we started the second week of endocrine with a look at parathryoid and calcium issues. calcium levels are regulated hormonally by 3 main agents: PTH from the parathyroid, activated vitamin D from the kidneys, and calcitonin from the thyroid. PTH has four main actions: increases osteoclastic activity, increases reabsorption of calcium in the kidneys, decreases reabsorption of phosphate in the kidneys, and stimulates activation of vitamin D in the kidneys. whereas PTH has the effect of raising serum calcium levels, calcitonin (secreted from the C cells of the thyroid) lowers them by inhibiting osteoclastic bone resorption.
parathyroid hormone can be secreted in excess in many conditions, categorized by 1º, 2º, 3º. 1º is usually due to a parathyroid adenoma and results in osteoporosis, kidney stones, abdominal symptoms, and fatigue (bones, stones, groans, moans). it may also be asymptomatic and found by elevated serum calcium levels. hypercalcemia can also be caused by other conditions such as multiple sclerosis and sarcoidosis, in which case PTH levels would be low due to negative feedback to the parathyroid. 2º hyperparathyroid is often due to renal failure, which causes chronically low levels of calcium, resulting in compensatory PTH secretion. 3º refers to hypercalcemia from autonomous PTH secretion.
on the other end, hypoparathyroidism is mainly caused by surgical procedures-- such as removing part of the thyroid in grave's disease. signs and symptoms might include neuromuscular instability, parkinsons-like movements, and muscle tetany. the characteristic signs on a PE are chvosek (tapping on the TMJ causes contraction of the periorbital or perioral muscles) or trousseau's sign (carpal pedal spasm from occluding forearm blood supply).
the thyroid gland produces thyroid hormone mostly in the form of T4, most of which is bound to TBG in the blood. hypothyroidism can be due to primary causes (autoimmune dysfunction of the thyroid itself), secondary (dysfunction of anterior pituitary secretion of TSH), or tertiary (dysfunction of hypothalamic secretion of TRH), though the latter two are relatively rare. primary hypothyroidism can affect newborns, and cretinism can develop if thyroid hormones are low during the first few weeks of life, resulting in mental retardation, short stature, puffy facial features, among other symptoms.
for adults, hypothyroidism occurs more frequently in females, and is most commonly due to autoimmune disease, although outside the US can also be attributed to iodine deficiency. besides the signs and symptoms related to slowed metabolism (decreased circulation, energy, hair loss, etc), one might also notice follicular hyperkeratosis-- red bumps over the hair follicles on the outer arms, which is related to a defect in vitamin A synthesis, as well as diminished DTR's. lab values would show decreased levels of T4 but increased levels of TSH. secondary hypothyroidism results from pituitary dysfunction, causing low TSH and T4/T3 levels but high TRH levels. patients might present with signs of general pituitary dysfunction, or an intracranial mass (such as pituitary adenoma symptoms).
hyperthyroidism manifests with signs of metabolic excess such as heat intolerance, weight loss, irritability, warm/moist skin, muscle tremors, high cardiac output, etc. the most common cause is autoimmune via antibodies to the thyroid's TSH receptors as in grave's disease. grave's patients might also present with pretibial myxedema, a skin thickening specific to the legs. hyperthyroid states are diagnosed by testing for antibodies against the thyroid as well as checking radioactive iodine uptake. high uptake plus positive antibodies means primary / autoimmune hyperthyroid. high uptake plus negative antibodies can mean plummer's syndrome, toxic thyroid nodules that can stimulate thyroid hormone production. low uptake plus negative antibodies can indicate thyroiditis.
four types of thyroid cancer have been identified: papillary is the most common and has a relatively good prognosis. follicular is more malignant and makes up 15% of thyroid cancers. medullary involves proliferation of c-cells and subsequent elevation of calcitonin levels. anaplastic / undifferentiated type is the most rare and has the worst prognosis.
questions
physiology...
1. what are the three hormones that are in charge of calcium regulation and where are they secreted from?
2. what steps would be taken in order to make a diagnosis of hyperparathyroid from a patient with high calcium levels?
3. what are the four main actions of PTH?
4. what are the actions of calcitonin and where is it secreted from?
hyperparathyroid states...
5. what is 1º hyperparathyroidism usually due to?
6. what are the signs and symptoms of 1º hyperparathyroidism?
7. besides hyperparathyroidism, what are some other causes of hypercalcemia?
8. in general, how high or low are PTH levels in hypercalcemia that is not of parathyroid origin?
9. what is the most common cause of 2º hyperparathyroidism?
10. what is the mechanism of pathogenesis for 2º hyperparathyroidism?
11. what is the hallmark of 3º hyperparathyroidism?
hypoparathyroid...
12. what is the most common cause of hypoparathyroidism?
13. what are the signs / symptoms of hypoparathyroidism?
14. what are the classic PE findings for hypoparathyroidism?
15. describe the first sign from question 14.
16. describe the second sign from question 14.
thyroid physiology review...
17. which cells in which gland is TSH made in?
18. TSH levels are mainly regulated by...
19. what are the three proteins that carry thyroid hormones in the blood?
hypothyroidism intro...
20. what is the difference between primary, secondary, and tertiary hypothyroidism?
21. what is peripheral hypothyroidism?
22. what are some etiologies for primary hypothyroidism?
23. hypothyroid is the number one reversible cause of...
24. what is cretinism and what are its manifestations?
primary hypothyroidism...
25. which gender is hypothyroidism more common in?
26. what are the most common causes of adult hypothyroidism in the US and the world?
27. what is follicular hyperkeratosis and what is it due to?
28. what is a common PE finding for hypothyroidism?
29. what are the lab values for the thyroid hormones in hypothyroidism?
secondary hypothyroidism...
30. what is a condition associated with secondary hypothyroidism?
31. what are the signs / symptoms of a patient with secondary hypothyroidism?
32. what åre the typical lab values for a patient with secondary hypothyroidism?
33. what is a contraindication for thyroid hormone replacement therapy?
hyperthyroidism...
34. what are some of the symptoms of hyperthyroidism?
35. what are some PE findings for hyperthyroidism?
36. what is the most common cause of hyperthyroidism?
37. what is the mechanism for the condition in question 36?
38. what is a symptom associated with the condition in question 36 that manifests on the extremities?
39. how is the cause of hyperthyroidism determined diagnostically?
40. according to the method in question 39, primary hyperthyroid would be characterized by...
41. according to the method in question 39, plummer's syndrome would be characterized by...
42. according to the method in question 39, thyroiditis would be characterized by...
other thyroid pathologies...
43. what are the 4 types of thyroid cancer?
44. which thyroid cancer is the most common?
45. which is more malignant, follicular or papillary?
46. the medullary type is characterized by proliferation of which cell?
47. how does anaplastic thyroid cancer present?
answers
1. PTH from parathyroid, calcitonin from thyroid, and activated vitamin D from the kidneys.
2. recheck. check for high ionized calcium levels. check for high PTH levels.
3. stimulates osteoblastic activity
inhibits reabsorption of phosphate in the kidneys
stimulates reabsorption of calcium in the kidneys
stimulates activation of vitamin D in the kidneys
4. secreted from C cells of the thyroid, decreases serum calcium by decreasing bone resorption via osteoclasts.
5. parathyroid adenoma.
6. bones, stones, abdominal moans, groans.
7. multiple sclerosis, paget's disease, vitamin D intoxication, sarcoidosis.
8. low because of negative feedback to the parathyroid.
9. renal disease.
10. depressed serum calcium leads to overcompensation via PTH secretion.
11. development of autonomous hypersecretion of PTH, causing hypercalcemia.
12. surgically induced.
13. neuromuscular instability, parkinsons-like movements, tetany.
14. chvosek and trousseau's sign.
15. tapping around the TMJ causes contraction of muscles around the mouth or eyes.
16. "carpal pedal spasm" resulting from occluding blood supply to forearm for several minutes.
17. thyrotroph cells of the anterior pituitary.
18. T3 levels.
19. TBG, transthyretin, albumin.
20. primary is a dysfunction in secretion of the thyroid gland itself, secondary is dysfunction in secretion of TSH from AP, tertiary is dysfunction in secretion of TRH from hypothalamus.
21. peripheral resistance to thyroid hormones, or reduced T4 to T3 conversion, or excess rT3.
22. congenital
iodine deficiency related (goitrogens)
thyroid ablation
23. depression.
24. primary hypothyroid during the first few weeks of life, resulting in mental retardation, short stature, puffy facial features, dry skin, myxedema.
25. females.
26. autoimmune, and iodine deficiency.
27. red bumps over the hair follicles on the outer arm, due to vitamin A synthesis defect.
28. diminished DTR's
29. high TSH, low T4.
30. sheehan's.
31. symptoms of deficiency of other pituitary hormones, or intracranial mass.
32. high TRH, low TSH, low T4 and T3.
33. adrenal cortisal insufficiency / addison's, MI, thyrotoxicosis
34. heat intolerance
irritability
weight loss
exophthalmos
35. may have goiter
warm, moist skin
conjunctival injection
high cardiac output
tremor
fast DTR's
36. grave's disease.
37. antibody against TSH receptor causes constant stimulation of thyroid gland.
38. skin thickening on the legs: pretibial myxedema.
39. testing for antibodies to thyroid plus radioactive iodine uptake.
40. high uptake and positive antibodies.
41. high uptake and negative antibodies.
42. low uptake and negative antibodies.
43. papillary, follicular, medullary, anaplastic.
44. papillary.
45. follicular.
46. c cells that produce calcitonin.
47. rapid and painful enlargement of the thyroid, poor prognosis.
Showing posts with label CPD III. Show all posts
Showing posts with label CPD III. Show all posts
Monday, May 10, 2010
Monday, May 3, 2010
CPD III- endocrine II: adrenals
some review of kidney / adrenal physiology. the adrenals are endocrine organs that lie on top of the kidneys and are divided into the adrenal cortex and medulla. the adrenal medulla can be described as "a gland within a gland" and mostly secretes epinephrine, although nor-epinephrine and small amounts of dopamine are also secreted. the adrenal cortex is subdivided into three "zones", each secreting a different hormone- the zona glomerulosa secretes minerocorticoids such as aldosterone, zona fasiculata secretes glucocorticoids such as cortisol, and the zona reticularis secretes sex steroids such as DHEA, androgens, and small amounts of estrogen / cortisol.
addison's disease refers to adrenal hypofunction and can be primary or secondary. primary is due to damage to the adrenal cortex itself, usually due to autoimmune causes. this can result in decreased cortisol as well as aldosterone production, leading to hypoglycemia, hyponatremia, and hyperkalemia. the serum levels of ACTH will be extremely high but levels of cortisol will be extremely low in these patients. signs and symptoms might include weakness, dehydration, anorexia, hypotension, hyperpigmentation due to stimulation of melanocytes by ACTH. primary addison's can be confirmed with the ACTH stimulation test- patients with a damaged adrenal cortex will not respond to exogenous ACTH administration. secondary addison's is a shortage of ACTH, usually from damage to the pituitary from trauma, surgery, radiation, or tumors. this patient would have low levels of cortisol as well, but also low levels of ACTH and normal aldosterone secretion. also, because ACTH levels are low, melanocytes would not be stimulated and this results in hypopigmentation, contrasting with the hyperpigmentation seen in primary addison's.
an addisonian crisis results when a patient who has been taking exogenous glucocorticosteroids is unable to produce cortisol intrinsically due to lower ACTH levels when the glucocorticosteroids have been stopped. this patient may take weeks to months to acclimate, during which severe symptoms of weakness, nausea/vomiting, dehydration, hypoglycemia may occur.
cushing's syndrome is on the opposite side from addison's, representing adrenal hyperfunction. most cases are iatrogenic, from long term exogenous use of glucocorticosteroids. cushing's disease is a specific type which involves a pituitary adenoma that produces ACTH. ACTH may also be produced in ectopic cancer sites- lung cancer cells in particular. patients with cushing's will present with weight gain, especially around the abdomen, as well as moon facies, buffalo hump, and hypertension. aldosterone production may also be affected, leading to hypokalemia and hypertension as well. diagnosis can be confirmed by the dexamethasone test, in which the cortisol production in response to dexamethasone is measured-- normally it is suppressed, but in cushing's patients, it is unaffected.
conn's syndrome is hyperfunction of the adrenals specific to the zona glomerulosa- resulting in aldosterone hyperproduction. this generally results in hypertension and hypokalemia and is due to a adrenal adenoma. lab results might include high serum aldosterone, low potassium, and low renin (suppressed in response to high blood volume). a patient suspected of conn's might go through the aldosterone suppression test, in which IV fluid is introduced into the body and aldosterone levels are monitored-- if they are not inhibited as they should be in response to the extra fluid volume, they probably have conn's syndrome.
congenital adrenal hyperplasia is an underproduction of cortisol due to a deficiency of enzymes that regulate cortisol production. due to the shunting of cortisol precursor to androgen precursors such as 17-hydroxyprogesterone, these patients will have signs and symptoms of androgenism: hirsuitism, abnormal menses and infertility in females and precocious sexual development in males. they might also have short stature due to the premature closure of the epiphyseal growth plates. lab tests would look for increased levels of 17-ketosteroids and treatment involves exogenous administration of cortisol.
a pheochromocytoma is an catecholamine producing adenoma of the adrenal medulla which results in increased renin secretion, leading to severe hypertension which is resistant to blood pressure lowering regimens. the classic presentation is a patient with episodes of hypertension with intermittent episodes of hypotension, with headache, sweating, mental status changes, and hypermetabolism. a pheochromocytoma is generally diagnosed by the 24 hour urinary catecholamine test, meta-nephrine levels, and the clonidine suppression test.
questions
physiology...
1. what are the three zones of the adrenal cortex?
2. what do the cells of the adrenal medulla secrete?
3. what do the three zones of the adrenal cortex secrete?
4. describe the chain of production of ACTH.
addison's disease...
5. what is primary addison's disease?
6. what is the most common cause of primary addison's disease?
7. why might primary addison's lead to hypotension?
8. what are the signs and symptoms of primary addison's disease?
9. which areas of the body are more prone to developing hyperpigmentation in primary addison's?
10. what is the characteristic lab picture of a patient with primary addison's?
11. what are some other lab markers that might be abnormal in a patient with primary addison's?
12. what is the test that can be performed that will confirm the diagnosis of primary addison's?
13. what is the etiology of secondary addison's?
14. what is the sign that can differentiate secondary and primary addison's?
addisonian crisis...
15. what is an addisonian crisis?
16. what are the symptoms of an acute addisonian crisis?
cushing's syndrome...
17. what is the difference between cushing's syndrome and cushing's disease?
18. what are the causes of cushing's disease?
19. what is a potential cause for cushing's disease not related to the pituitary or adrenals?
20. what are the signs and symptoms for cushing's syndrome?
21. what are the lab findings for a patient with cushing's?
22. what is a test that can confirm the diagnosis of cushing's syndrome? how does it work?
conn's syndrome...
23. what is conn's syndrome?
24. what is the typical presentation of a patient with conn's syndrome?
25. what are the abnormal lab results of a patient with conn's syndrome?
26. what is a test that confirms the diagnosis of conn's syndrome?
congenital adrenal hyperplasia...
27. what is CAH?
28. what is the most common enzyme involved in CAH?
29. why might CAH lead to virilization?
30. how might CAH affect females?
31. how might CAH affect males?
32. why might CAH lead to short stature?
33. what is the lab test that can help diagnose CAH?
pheochromocytoma...
34. what is a pheochromocytoma?
35. what is the classic presentation of a patient with a pheochromocytoma?
36. what are the signs and symptoms of a patient with a pheohromocytoma?
37. what are the lab tests useful in diagnosing a pheochromocytoma?
38. what is a test that can be used to confirm the diagnosis of a pheochromocytoma?
answers
1. zona glomerulosa, fasiculata, reticularis.
2. mostly epinephrine, some nor-epinephrine, a little dopamine.
3. glomerulosa: minerocorticoids such as aldoesterone
fasiculata: glucocorticoids such as cortisol
reticularis: androgens such as DHEA
4. hypothalamus secretes CRH in response to stress, triggering pituitary to release ACTH, which acts on the adrenal glands.
5. adrenal insufficiency due to a damaged adrenal gland.
6. autoimmune destruction of the adrenal cortex.
7. because damage might include the zona glomerulosa, which would result in an underproduction of aldosterone, a hormone that facilitates water reabsorption in the kidneys.
8. WOAHH:
weakness
often dehydrated
anorexia
hypotension
hyperpigmentation / bronze skin
9. palmar creases, buccal mucosa, elbows and knees.
10. extremely low cortisol levels and high ACTH levels.
11. hypoglycemia, hyponatremia, hyperkalemia.
12. ACTH stimulation test: patients with primary addison's should not respond to administration of ACTH exogenously.
13. insufficient ACTH production by the anterior pituitary due to trauma, surgery, radiation, tumors.
14. secondary patients have pallor instead of hyperpigmentation because of low ACTH levels.
15. removal of long term exogenous administration of glucocorticoids leading to inability to produce cortisol due to low ACTH levels.
16. weakness
nausea/vomiting
dehydration
hypoglycemia
17. cushing's syndrome refers to adrenal hyperfunction generally whereas cushing's disease is a type of cushing's syndrome that refers to a pituitary adenoma.
18. generally from longterm exogenous administration of glucocorticoids.
19. ectopic sites that produce ACTH, such as lung cancer cells.
20. weight gain, especially mid abdominal
moon facies / buffalo hump
hypertension
21. hyperglycemia
secondary diabetes
hypertension / hypokalemia
22. 6 hour or overnight dexamethasone suppression test. normally cortisol production should be inhibited by administration of dexamethasone.
23. an increase in aldosterone production from an adrenal adenoma without cortisol increases.
24. hypertension.
25. high serum aldosterone
hypokalemia
low serum renin
26. aldosterone suppression test: administer extra IV fluid and watch for the lack of aldosterone suppression.
27. underproduction of cortisol due to deficiency of enzymes related to cortisol synthesis.
28. 21-hydroxylase.
29. because the decreased cortisol precursor production will lead to increased synthesis of other precursors, one of which is an androgen precursor, 17-hydroxyprogesterone.
30. symptoms of androgenism: hirsuitism, abnormal menses, infertility.
31. precocious development.
32. because high androgen levels also lead to premature closure of the epiphyseal growth plates.
33. serum levels of 17-ketosteroids such as 17-hydroxyprogesterone.
34. catecholamine producing tumor.
35. episodes of severe hypertension followed by hypotension.
36. headache
diaphoresis
mental status changes
hypermetabolism
postural hypotension
37. 24 hour urinary catecholamines and meta-nephrines
38. clonidine suppression test.
addison's disease refers to adrenal hypofunction and can be primary or secondary. primary is due to damage to the adrenal cortex itself, usually due to autoimmune causes. this can result in decreased cortisol as well as aldosterone production, leading to hypoglycemia, hyponatremia, and hyperkalemia. the serum levels of ACTH will be extremely high but levels of cortisol will be extremely low in these patients. signs and symptoms might include weakness, dehydration, anorexia, hypotension, hyperpigmentation due to stimulation of melanocytes by ACTH. primary addison's can be confirmed with the ACTH stimulation test- patients with a damaged adrenal cortex will not respond to exogenous ACTH administration. secondary addison's is a shortage of ACTH, usually from damage to the pituitary from trauma, surgery, radiation, or tumors. this patient would have low levels of cortisol as well, but also low levels of ACTH and normal aldosterone secretion. also, because ACTH levels are low, melanocytes would not be stimulated and this results in hypopigmentation, contrasting with the hyperpigmentation seen in primary addison's.
an addisonian crisis results when a patient who has been taking exogenous glucocorticosteroids is unable to produce cortisol intrinsically due to lower ACTH levels when the glucocorticosteroids have been stopped. this patient may take weeks to months to acclimate, during which severe symptoms of weakness, nausea/vomiting, dehydration, hypoglycemia may occur.
cushing's syndrome is on the opposite side from addison's, representing adrenal hyperfunction. most cases are iatrogenic, from long term exogenous use of glucocorticosteroids. cushing's disease is a specific type which involves a pituitary adenoma that produces ACTH. ACTH may also be produced in ectopic cancer sites- lung cancer cells in particular. patients with cushing's will present with weight gain, especially around the abdomen, as well as moon facies, buffalo hump, and hypertension. aldosterone production may also be affected, leading to hypokalemia and hypertension as well. diagnosis can be confirmed by the dexamethasone test, in which the cortisol production in response to dexamethasone is measured-- normally it is suppressed, but in cushing's patients, it is unaffected.
conn's syndrome is hyperfunction of the adrenals specific to the zona glomerulosa- resulting in aldosterone hyperproduction. this generally results in hypertension and hypokalemia and is due to a adrenal adenoma. lab results might include high serum aldosterone, low potassium, and low renin (suppressed in response to high blood volume). a patient suspected of conn's might go through the aldosterone suppression test, in which IV fluid is introduced into the body and aldosterone levels are monitored-- if they are not inhibited as they should be in response to the extra fluid volume, they probably have conn's syndrome.
congenital adrenal hyperplasia is an underproduction of cortisol due to a deficiency of enzymes that regulate cortisol production. due to the shunting of cortisol precursor to androgen precursors such as 17-hydroxyprogesterone, these patients will have signs and symptoms of androgenism: hirsuitism, abnormal menses and infertility in females and precocious sexual development in males. they might also have short stature due to the premature closure of the epiphyseal growth plates. lab tests would look for increased levels of 17-ketosteroids and treatment involves exogenous administration of cortisol.
a pheochromocytoma is an catecholamine producing adenoma of the adrenal medulla which results in increased renin secretion, leading to severe hypertension which is resistant to blood pressure lowering regimens. the classic presentation is a patient with episodes of hypertension with intermittent episodes of hypotension, with headache, sweating, mental status changes, and hypermetabolism. a pheochromocytoma is generally diagnosed by the 24 hour urinary catecholamine test, meta-nephrine levels, and the clonidine suppression test.
questions
physiology...
1. what are the three zones of the adrenal cortex?
2. what do the cells of the adrenal medulla secrete?
3. what do the three zones of the adrenal cortex secrete?
4. describe the chain of production of ACTH.
addison's disease...
5. what is primary addison's disease?
6. what is the most common cause of primary addison's disease?
7. why might primary addison's lead to hypotension?
8. what are the signs and symptoms of primary addison's disease?
9. which areas of the body are more prone to developing hyperpigmentation in primary addison's?
10. what is the characteristic lab picture of a patient with primary addison's?
11. what are some other lab markers that might be abnormal in a patient with primary addison's?
12. what is the test that can be performed that will confirm the diagnosis of primary addison's?
13. what is the etiology of secondary addison's?
14. what is the sign that can differentiate secondary and primary addison's?
addisonian crisis...
15. what is an addisonian crisis?
16. what are the symptoms of an acute addisonian crisis?
cushing's syndrome...
17. what is the difference between cushing's syndrome and cushing's disease?
18. what are the causes of cushing's disease?
19. what is a potential cause for cushing's disease not related to the pituitary or adrenals?
20. what are the signs and symptoms for cushing's syndrome?
21. what are the lab findings for a patient with cushing's?
22. what is a test that can confirm the diagnosis of cushing's syndrome? how does it work?
conn's syndrome...
23. what is conn's syndrome?
24. what is the typical presentation of a patient with conn's syndrome?
25. what are the abnormal lab results of a patient with conn's syndrome?
26. what is a test that confirms the diagnosis of conn's syndrome?
congenital adrenal hyperplasia...
27. what is CAH?
28. what is the most common enzyme involved in CAH?
29. why might CAH lead to virilization?
30. how might CAH affect females?
31. how might CAH affect males?
32. why might CAH lead to short stature?
33. what is the lab test that can help diagnose CAH?
pheochromocytoma...
34. what is a pheochromocytoma?
35. what is the classic presentation of a patient with a pheochromocytoma?
36. what are the signs and symptoms of a patient with a pheohromocytoma?
37. what are the lab tests useful in diagnosing a pheochromocytoma?
38. what is a test that can be used to confirm the diagnosis of a pheochromocytoma?
answers
1. zona glomerulosa, fasiculata, reticularis.
2. mostly epinephrine, some nor-epinephrine, a little dopamine.
3. glomerulosa: minerocorticoids such as aldoesterone
fasiculata: glucocorticoids such as cortisol
reticularis: androgens such as DHEA
4. hypothalamus secretes CRH in response to stress, triggering pituitary to release ACTH, which acts on the adrenal glands.
5. adrenal insufficiency due to a damaged adrenal gland.
6. autoimmune destruction of the adrenal cortex.
7. because damage might include the zona glomerulosa, which would result in an underproduction of aldosterone, a hormone that facilitates water reabsorption in the kidneys.
8. WOAHH:
weakness
often dehydrated
anorexia
hypotension
hyperpigmentation / bronze skin
9. palmar creases, buccal mucosa, elbows and knees.
10. extremely low cortisol levels and high ACTH levels.
11. hypoglycemia, hyponatremia, hyperkalemia.
12. ACTH stimulation test: patients with primary addison's should not respond to administration of ACTH exogenously.
13. insufficient ACTH production by the anterior pituitary due to trauma, surgery, radiation, tumors.
14. secondary patients have pallor instead of hyperpigmentation because of low ACTH levels.
15. removal of long term exogenous administration of glucocorticoids leading to inability to produce cortisol due to low ACTH levels.
16. weakness
nausea/vomiting
dehydration
hypoglycemia
17. cushing's syndrome refers to adrenal hyperfunction generally whereas cushing's disease is a type of cushing's syndrome that refers to a pituitary adenoma.
18. generally from longterm exogenous administration of glucocorticoids.
19. ectopic sites that produce ACTH, such as lung cancer cells.
20. weight gain, especially mid abdominal
moon facies / buffalo hump
hypertension
21. hyperglycemia
secondary diabetes
hypertension / hypokalemia
22. 6 hour or overnight dexamethasone suppression test. normally cortisol production should be inhibited by administration of dexamethasone.
23. an increase in aldosterone production from an adrenal adenoma without cortisol increases.
24. hypertension.
25. high serum aldosterone
hypokalemia
low serum renin
26. aldosterone suppression test: administer extra IV fluid and watch for the lack of aldosterone suppression.
27. underproduction of cortisol due to deficiency of enzymes related to cortisol synthesis.
28. 21-hydroxylase.
29. because the decreased cortisol precursor production will lead to increased synthesis of other precursors, one of which is an androgen precursor, 17-hydroxyprogesterone.
30. symptoms of androgenism: hirsuitism, abnormal menses, infertility.
31. precocious development.
32. because high androgen levels also lead to premature closure of the epiphyseal growth plates.
33. serum levels of 17-ketosteroids such as 17-hydroxyprogesterone.
34. catecholamine producing tumor.
35. episodes of severe hypertension followed by hypotension.
36. headache
diaphoresis
mental status changes
hypermetabolism
postural hypotension
37. 24 hour urinary catecholamines and meta-nephrines
38. clonidine suppression test.
CPD III- endocrine I: hypothalamus, pituitary
this lecture began our introduction to diagnosis of endocrine disorders, courtesy of dr. marcus miller.
the hypothalamus is the endocrine organ that receives information from the CNS and in turn stimulates the pituitary to release hormones. it carries a set of hormones as well, including TRH, CRH, GnRH, GHRH, somatostatin, ADH, oxytocin, and dopamine. [quick note: somatostatin acts as a GHRH antagonist, and dopamine acts as a prolactin antagonist] the hypothalamus is connected via nerves as well as blood to the pituitary, which is divided into 3 lobes, anterior (makes up 80%), intermediate, and posterior. the posterior pituitary acts as a storage for ADH and oxytocin, and the intermediate lobe also contains hormones such as the melanocyte stimulating hormone. because of the pituitary's location in the sella turcica, pituitary adenomas might lead to bitemporal hemianopsia due to the upward growth and subsequent impingement on the optic chiasm.
the anterior pituitary's general function is to stimulate peripheral endocrine organs such as the thyroid and regulate growth and lactation. it does this by release of a variety of hormones, including growth hormone, LH / FSH, TSH, prolactin, and ACTH. ACTH is responsible for stimulating cortisol production from the adrenals. LH stimulates ovulation and progesterone production in females and prolactin has the opposite effect, while also stimulating lactation.
the posterior pituitary is made up of modified nerve fibers, axons, and glial cells extending from the supraoptic and paraventricular nuclei from the hypothalamus. as mentioned before, the axons of the posterior pituitary store two hormones made in the hypothalamus, ADH and oxytocin. ADH's main action is in the kidney, stimulating water reabsorption in the distal tubules, while oxytocin stimulates lactation and uterine contraction, among other things.
hypopituitarism means decreased output of pituitary hormones and can be due to a variety of causes-- oftentimes the cause for panhypopituitarism (equal reduction in all AP hormones) is iatrogenic-- either through radiation to the head or surgery that reduces blood flow. other causes might include destructive processes such as inflammation or infection, hemochromatosis, malignancy. hypopituitarism can also result in dwarfism, which comes in several varieties as well- if resulting from panhypopituitarism, body proportions will be normal, while a selective GH deficiency might result in abnormal proportions. achondroplastic dwarfism is a third type that is not related to hypopituitarism (and therefore is unresponsive to GH supplication).
some pituitary pathologies: pituitary apoplexy is a hemorrhage into a pre-existing adenoma, resulting in a sudden onset headache and diplopia. severe cases might also lead to ischemic necrosis and may even result in death. the most common cause of ischemic necrosis is sheehan's syndrome, although patients with this syndrome may have a range of outcomes, ranging from asymptomatic to death. sheehan's syndrome is a situation where the already hypoxic pituitary in pregnant women (due to an increase in pituitary size without increased vasculature) is further compromised by obstetric hemorrhage, leading to vasospasm and ischemic necrosis.
pituitary adenomas are the most common cause of hyperpituitarism, although a good portion of pituitary adenomas are non functional and can remain undetected. they can be macro (greater than 1cm) or micro (less than 1cm) and comprise 10% of all intracranial neoplasms. functional adenomas are generally composed of one cell type and secrete a single hormone. the most common functional adenomas are: prolactinoma, ACTH producing, gonadotropin producing, and growth hormone producing.
the most common type of adenoma produces prolactin and is composed of weakly staining acidophilic cells-- within which prolactin can be detected in the secretory granules. in females, the effects of a prolactinoma are what one would expect from increased prolactin levels: amenorrhea, diminished libido, ovarian cysts (due to inhibition of ovulation), galactorrhea. in males, prolactinomas might manifest asymptomatically, or decreased libido. prolactinomas might be diagnosed by high serum prolactin levels, and an MRI will confirm the presence of one as small as 2mm.
growth hormone producing adenomas are the second most common type. they are measured / diagnosed primarily by increased IGF-1 levels, from increased hepatic production due to GH stimulation. GH excess can lead to a variety of signs/symptoms, including diabetes, HTN, hyperglycemia, CHF, gonadal dysfunction, and muscle weakness. if the adenoma is functional before growth plate closure, the result is pituitary giantism, in which body size is increased and arms / legs are disproportionately long. if the adenoma is function after growth plate closure, the result is acromegaly, which has its own characteristics: enlarged hands, feet, face (nose broadens, teeth get further apart, jaw protrudes), and organomegaly. GH producing adenomas are diagnosed via IGF-1 levels as well as the GH suppression test, in which GH levels do not drop as they should in response to glucose administration.
empty sella syndrome describes any condition in which the sella turcica is enlarged but not filled with pituitary tissue. risk factors include pregnancy, obesity, and hypertension. ESS is caused by increased intracranial pressure which leads to CSF entering the sella turcica, compressing the pituitary against its walls. presentation might be asymptomatic, or may have papilledema. ESS might also be due to a surgical procedure or radiation which has enlarged the sella turcica.
excess ADH production may be related to posterior pituitary dysfunction and can result in dysfunction in the water balance in the body. syndrome of inappropriate ADH describes such a condition, which can also be caused by ectopic sites, generally from cancer cells. the signs and symptoms might be limited to reduced urine, and the diagnosis might be made by highly concentrated urine, decreased plasma osmolality, and hyponatremia.
diabetes insipidus is a condition which results from ADH deficiency; either from an underproduction from the hypothalamus (central) or dysfunctional ADH receptors in the kidney (nephrogenic). DI results in polyuria and polydipsia, with the polyuria generally exceeding the polydipsia. central might be caused by surgery/trauma, tumors, infection, sheehan's syndrome, while nephrogenic might be caused by chronic renal disease, lithium, among other things. a useful test for distinguishing central, nephrogenic DI, and psychogenic polydipsia is the water deprivation test. after depriving water, patients with psychogenic polydipsia will have increased osmolality while the other two conditions will not. after administration of ADH, psychogenic polydipsia and central DI will increase urine osmolality (increased reabsorption produces more concentrated urine), whereas nephrogenic will remain the same.
questions
hypothalamus and pituitary...
1. what is the relative prevalence of endocrine issues related to the hypothalamus, pituitary, and thyroid?
2. what are the hormones released by the hypothalamus?
3. what is the effect of these hormones on the pituitary?
4. where is the pituitary gland located?
5. what is the pituitary gland covered by?
6. how might a pituitary adenoma lead to loss of peripheral vision?
7. what are the divisions of the pituitary? which division predominates?
8. describe the general function of the posterior pituitary.
9. describe the function of the intermediate pituitary.
10. dopamine exerts inhibitory control over which other hormone?
anterior pituitary...
11. what are the hormones released by the anterior pituitary?
12. what is a better marker for checking growth hormone activity than a simple serum growth hormone level test?
13. describe the general function of the hormones released by the anterior pituitary.
14. what does ACTH do?
15. what does LH do in males and females?
16. what does prolactin do?
posterior pituitary...
17. describe the structure / content of the posterior pituitary.
18. what are the two hormones that are stored in the axons of the posterior pituitary?
19. what does ADH do?
20. what does oxytocin do?
hypopituitarism and dwarfism...
21. most cases of hypopituitarism are the result of...
22. what are some other potential causes of hypopituitarism?
23. what are the two types of pituitary dwarfism?
24. what is achondoplastic dwarfism?
acute pituitary pathologies...
25. what is pituitary apoplexy?
26. what are the symptoms of a pituitary apoplexy?
27. what are the complications of a severe case of pituitary apoplexy?
28. sheehan's syndrome is the most common cause of...
29. describe the pathophysiology of sheehan's syndrome.
pituitary adenoma...
30. pituitary adenomas are the most common cause of...
31. pituitary adenomas are usually...
32. what percentage of intracranial neoplasms are pituitary adenomas?
33. what age range is most common for pituitary adenomas?
34. functional adenomas are usually...
35. what is the difference between a macro and microadenoma?
36. are males more likely to present with a macro or microadenoma?
37. what are the most common types of functional adenomas?
prolactinoma...
38. most prolactinomas are composed of...
39. prolactin can be detected within...
40. what are the signs and symptoms of a prolactinoma in females?
41. what percentage of secondary amenorrhea cases are due to prolactinomas?
42. what are the signs / symptoms of a prolactinoma in males?
43. what are some labs and imaging techniques useful in diagnosing prolactinomas?
44. what is a naturopathic treatment option for prolactinoma?
growth hormone producing adenoma...
45. persistent oversecretion of GH stimulates...
46. what are the signs and symptoms of a GH producing adenoma?
47. how is a GH producing adenoma classified if it is functional before vs. after growth plate closure?
48. describe the body proportions of a patient with pituitary gigantism.
49. what are the signs and symptoms of a patient with acromegaly?
50. what are the lab tests used to diagnose GH producing adenomas?
51. how can a GH producing adenoma be differentiated from hyperglycemia?
corticotroph adenoma...
52. what is a corticotroph adenoma?
53. what is the difference between cushing's syndrome and cushing's disease?
empty sella syndrome...
54. what is the empty sella syndrome?
55. what are the risk factors for ESS?
56. what is the etiology of ESS?
57. what are the signs/symptoms of ESS?
58. what is secondary ESS?
syndrome of inappropriate ADH...
59. what is SIADH?
60. what are some etiological factors that might lead to SIADH?
61. what are the signs / symptoms of SIADH?
62. what are the lab results for SIADH?
diabetes insipidus...
63. what are the two causes of diabetes insipidus?
64. what are the signs and symptoms of DI?
65. what are some etiologies of central DI?
66. what is a drug that might cause nephrogenic DI?
67. what is a test that can distinguish between central DI, nephrogenic DI, and psychogenic polydipsia?
68. what is one possible treatment for DI?
answers
1. hypothalamus problems are much rarer than pituitary and thyroid.
2. TRH
CRH
GnRH
GHRH
somatostatin
dopamine
ADH
oxytocin
3. stimulates pituitary, except for somatostatin and dopamine.
4. the sella turcica.
5. dura mater, except for the a thin opening which conveys a stalk from the hypothalamus.
6. the upward growth of a pituitary tumor will impinge on the optic chiasm, which will block the optic pathways responsible for peripheral vision bilaterally.
7. anterior, intermediate, posterior lobes. anterior is 80%.
8. storage unit for oxytocin and ADH.
9. also contains hormones or precursor to hormones such as melanocyte stimulating hormone and a hormone that increases aldosterone production.
10. prolactin.
11. growth hormone
LH and FSH
TSH
prolactin
ACTH.
[G L/F T P A] [go left, pa]
12. IGF-1 levels.
13. stimulates peripheral endocrine organs and regulates growth and lactation.
14. stimulates cortisol production in the adrenals.
15. stimulates ovulation and progesterone production in females, stimulates testosterone production in males.
16. promotes lactation and suppresses ovulation and fertility.
17. a modified neural network consisting of modified glial cells, nerve fibers, and axonal processes extending from the supraoptic and paraventricular nuclei of the hypothalamus.
18. ADH and oxytocin.
19. stimulates water reabsorption in distal tubules of nephron.
20. regulates lactation and uterine contraction.
21. radiation or surgery which reduce blood flow to the brain.
22. destructive lesions
destructive processes
impingement from malignancy
infection
hemochromatosis
sarcoidosis
23. resulting either from deficiency of all AP hormones or just GH, in which body proportions remain normal and abnormal, respectively.
24. genetic dysfunction of fibroblasts that results in abnormal cartilaginous development.
25. sudden hemorrhage into an existing pituitary adenoma.
26. sudden onset headache and diplopia.
27. ischemic necrosis, death.
28. ischemic necrosis of the pituitary.
29. in pregnant women, the anterior pituitary enlarges without corresponding vasculature increase. this hypoxic state combined with an obstetric hemorrhage can cause vasospasm of the blood supply and ultimately ischemia and necrosis.
30. hyperpituitarism.
31. non functional, isolated lesions with no associated neoplasms.
32. 10%.
33. 30-60.
34. made of one cell type that produces one hormone.
35. greater than or less than 1 cm.
36. macro because of the greater chance of adenoma remaining undetected due to the lack of hormonal feedback as compared to women.
37. prolactinoma, ACTH cell adenoma, gonadotropin adenoma, growth hormone adenoma
[pro act gon grow] [functionally proactive: go and grow!]
38. weakly staining acidophilic cells.
39. secretory granules within cytoplasm of cells.
40. diminished menses or amenorrhea
diminished libido
infertility
ovarian cysts
galactorrhea
[prolact amen libido infertility cysts galact] [amen; all infertile cysts in the galaxy now have libidos]
41. roughly 25%.
42. asymptomatic, or decreased libido / sperm count.
43. serum prolactin and MRI.
44. botanicals that have phytoestrogenic or progesterone agonist effects.
45. hepatic secretion of IGF-1
46. hyperglycemia, DM, HTN, CHF, gonadal dysfunction, muscle weakness/arthritis. [sugar sugar blood blood nads muscles]
47. before: pituitary giant
after: acromegaly
48. bigger body size with disproportionately long arms and legs.
49. disproportionately large hands, feet, face
enlargement of heart, thyroid, liver, adrenals
jaw protrusion
spreading of teeth
broadening of nose
"spade like" hands
50. IGF-1 levels and the GH suppression test.
51. in the GH suppression test of a hyperglycemic patient, GH will be suppressed, but won't be in a patient with a GH producing adenoma.
52. an adenoma that produces ACTH, leading to adrenal hypersecretion of cortisol.
53. cushing's syndrome describes a state of hypercortisolism, of which cushing's disease is a specific type related to a corticotroph adenoma.
54. any condition that leads to an enlarged sella turcica not filled with pituitary tissue.
55. obese females
multiple pregnancies
hypertension
[fat fetus food]
56. increased intracranial pressure leads to CSF entering the sella turcica and compressing pituitary against wall.
57. asymptomatic, may see papilledema.
58. ESS due to surgical procedure or radiation that has enlarged the sella turcica.
59. excess secretion of ADH by ectopic sites.
60. cancer (lung, breast, prostate), head trauma, narcotics.
61. oliguria with no other signs.
62. highly concentrated urine, low plasma osmolality, hyponatremia.
63. deficiency of ADH either by hypothalamus underproduction or kidney unresponsiveness.
64. polyuria, polydipsia.
65. trauma
surgery
tumor
infection
sheehan's
66. lithium.
67. the water deprivation test.
68. oxytocin.
the hypothalamus is the endocrine organ that receives information from the CNS and in turn stimulates the pituitary to release hormones. it carries a set of hormones as well, including TRH, CRH, GnRH, GHRH, somatostatin, ADH, oxytocin, and dopamine. [quick note: somatostatin acts as a GHRH antagonist, and dopamine acts as a prolactin antagonist] the hypothalamus is connected via nerves as well as blood to the pituitary, which is divided into 3 lobes, anterior (makes up 80%), intermediate, and posterior. the posterior pituitary acts as a storage for ADH and oxytocin, and the intermediate lobe also contains hormones such as the melanocyte stimulating hormone. because of the pituitary's location in the sella turcica, pituitary adenomas might lead to bitemporal hemianopsia due to the upward growth and subsequent impingement on the optic chiasm.
the anterior pituitary's general function is to stimulate peripheral endocrine organs such as the thyroid and regulate growth and lactation. it does this by release of a variety of hormones, including growth hormone, LH / FSH, TSH, prolactin, and ACTH. ACTH is responsible for stimulating cortisol production from the adrenals. LH stimulates ovulation and progesterone production in females and prolactin has the opposite effect, while also stimulating lactation.
the posterior pituitary is made up of modified nerve fibers, axons, and glial cells extending from the supraoptic and paraventricular nuclei from the hypothalamus. as mentioned before, the axons of the posterior pituitary store two hormones made in the hypothalamus, ADH and oxytocin. ADH's main action is in the kidney, stimulating water reabsorption in the distal tubules, while oxytocin stimulates lactation and uterine contraction, among other things.
hypopituitarism means decreased output of pituitary hormones and can be due to a variety of causes-- oftentimes the cause for panhypopituitarism (equal reduction in all AP hormones) is iatrogenic-- either through radiation to the head or surgery that reduces blood flow. other causes might include destructive processes such as inflammation or infection, hemochromatosis, malignancy. hypopituitarism can also result in dwarfism, which comes in several varieties as well- if resulting from panhypopituitarism, body proportions will be normal, while a selective GH deficiency might result in abnormal proportions. achondroplastic dwarfism is a third type that is not related to hypopituitarism (and therefore is unresponsive to GH supplication).
some pituitary pathologies: pituitary apoplexy is a hemorrhage into a pre-existing adenoma, resulting in a sudden onset headache and diplopia. severe cases might also lead to ischemic necrosis and may even result in death. the most common cause of ischemic necrosis is sheehan's syndrome, although patients with this syndrome may have a range of outcomes, ranging from asymptomatic to death. sheehan's syndrome is a situation where the already hypoxic pituitary in pregnant women (due to an increase in pituitary size without increased vasculature) is further compromised by obstetric hemorrhage, leading to vasospasm and ischemic necrosis.
pituitary adenomas are the most common cause of hyperpituitarism, although a good portion of pituitary adenomas are non functional and can remain undetected. they can be macro (greater than 1cm) or micro (less than 1cm) and comprise 10% of all intracranial neoplasms. functional adenomas are generally composed of one cell type and secrete a single hormone. the most common functional adenomas are: prolactinoma, ACTH producing, gonadotropin producing, and growth hormone producing.
the most common type of adenoma produces prolactin and is composed of weakly staining acidophilic cells-- within which prolactin can be detected in the secretory granules. in females, the effects of a prolactinoma are what one would expect from increased prolactin levels: amenorrhea, diminished libido, ovarian cysts (due to inhibition of ovulation), galactorrhea. in males, prolactinomas might manifest asymptomatically, or decreased libido. prolactinomas might be diagnosed by high serum prolactin levels, and an MRI will confirm the presence of one as small as 2mm.
growth hormone producing adenomas are the second most common type. they are measured / diagnosed primarily by increased IGF-1 levels, from increased hepatic production due to GH stimulation. GH excess can lead to a variety of signs/symptoms, including diabetes, HTN, hyperglycemia, CHF, gonadal dysfunction, and muscle weakness. if the adenoma is functional before growth plate closure, the result is pituitary giantism, in which body size is increased and arms / legs are disproportionately long. if the adenoma is function after growth plate closure, the result is acromegaly, which has its own characteristics: enlarged hands, feet, face (nose broadens, teeth get further apart, jaw protrudes), and organomegaly. GH producing adenomas are diagnosed via IGF-1 levels as well as the GH suppression test, in which GH levels do not drop as they should in response to glucose administration.
empty sella syndrome describes any condition in which the sella turcica is enlarged but not filled with pituitary tissue. risk factors include pregnancy, obesity, and hypertension. ESS is caused by increased intracranial pressure which leads to CSF entering the sella turcica, compressing the pituitary against its walls. presentation might be asymptomatic, or may have papilledema. ESS might also be due to a surgical procedure or radiation which has enlarged the sella turcica.
excess ADH production may be related to posterior pituitary dysfunction and can result in dysfunction in the water balance in the body. syndrome of inappropriate ADH describes such a condition, which can also be caused by ectopic sites, generally from cancer cells. the signs and symptoms might be limited to reduced urine, and the diagnosis might be made by highly concentrated urine, decreased plasma osmolality, and hyponatremia.
diabetes insipidus is a condition which results from ADH deficiency; either from an underproduction from the hypothalamus (central) or dysfunctional ADH receptors in the kidney (nephrogenic). DI results in polyuria and polydipsia, with the polyuria generally exceeding the polydipsia. central might be caused by surgery/trauma, tumors, infection, sheehan's syndrome, while nephrogenic might be caused by chronic renal disease, lithium, among other things. a useful test for distinguishing central, nephrogenic DI, and psychogenic polydipsia is the water deprivation test. after depriving water, patients with psychogenic polydipsia will have increased osmolality while the other two conditions will not. after administration of ADH, psychogenic polydipsia and central DI will increase urine osmolality (increased reabsorption produces more concentrated urine), whereas nephrogenic will remain the same.
questions
hypothalamus and pituitary...
1. what is the relative prevalence of endocrine issues related to the hypothalamus, pituitary, and thyroid?
2. what are the hormones released by the hypothalamus?
3. what is the effect of these hormones on the pituitary?
4. where is the pituitary gland located?
5. what is the pituitary gland covered by?
6. how might a pituitary adenoma lead to loss of peripheral vision?
7. what are the divisions of the pituitary? which division predominates?
8. describe the general function of the posterior pituitary.
9. describe the function of the intermediate pituitary.
10. dopamine exerts inhibitory control over which other hormone?
anterior pituitary...
11. what are the hormones released by the anterior pituitary?
12. what is a better marker for checking growth hormone activity than a simple serum growth hormone level test?
13. describe the general function of the hormones released by the anterior pituitary.
14. what does ACTH do?
15. what does LH do in males and females?
16. what does prolactin do?
posterior pituitary...
17. describe the structure / content of the posterior pituitary.
18. what are the two hormones that are stored in the axons of the posterior pituitary?
19. what does ADH do?
20. what does oxytocin do?
hypopituitarism and dwarfism...
21. most cases of hypopituitarism are the result of...
22. what are some other potential causes of hypopituitarism?
23. what are the two types of pituitary dwarfism?
24. what is achondoplastic dwarfism?
acute pituitary pathologies...
25. what is pituitary apoplexy?
26. what are the symptoms of a pituitary apoplexy?
27. what are the complications of a severe case of pituitary apoplexy?
28. sheehan's syndrome is the most common cause of...
29. describe the pathophysiology of sheehan's syndrome.
pituitary adenoma...
30. pituitary adenomas are the most common cause of...
31. pituitary adenomas are usually...
32. what percentage of intracranial neoplasms are pituitary adenomas?
33. what age range is most common for pituitary adenomas?
34. functional adenomas are usually...
35. what is the difference between a macro and microadenoma?
36. are males more likely to present with a macro or microadenoma?
37. what are the most common types of functional adenomas?
prolactinoma...
38. most prolactinomas are composed of...
39. prolactin can be detected within...
40. what are the signs and symptoms of a prolactinoma in females?
41. what percentage of secondary amenorrhea cases are due to prolactinomas?
42. what are the signs / symptoms of a prolactinoma in males?
43. what are some labs and imaging techniques useful in diagnosing prolactinomas?
44. what is a naturopathic treatment option for prolactinoma?
growth hormone producing adenoma...
45. persistent oversecretion of GH stimulates...
46. what are the signs and symptoms of a GH producing adenoma?
47. how is a GH producing adenoma classified if it is functional before vs. after growth plate closure?
48. describe the body proportions of a patient with pituitary gigantism.
49. what are the signs and symptoms of a patient with acromegaly?
50. what are the lab tests used to diagnose GH producing adenomas?
51. how can a GH producing adenoma be differentiated from hyperglycemia?
corticotroph adenoma...
52. what is a corticotroph adenoma?
53. what is the difference between cushing's syndrome and cushing's disease?
empty sella syndrome...
54. what is the empty sella syndrome?
55. what are the risk factors for ESS?
56. what is the etiology of ESS?
57. what are the signs/symptoms of ESS?
58. what is secondary ESS?
syndrome of inappropriate ADH...
59. what is SIADH?
60. what are some etiological factors that might lead to SIADH?
61. what are the signs / symptoms of SIADH?
62. what are the lab results for SIADH?
diabetes insipidus...
63. what are the two causes of diabetes insipidus?
64. what are the signs and symptoms of DI?
65. what are some etiologies of central DI?
66. what is a drug that might cause nephrogenic DI?
67. what is a test that can distinguish between central DI, nephrogenic DI, and psychogenic polydipsia?
68. what is one possible treatment for DI?
answers
1. hypothalamus problems are much rarer than pituitary and thyroid.
2. TRH
CRH
GnRH
GHRH
somatostatin
dopamine
ADH
oxytocin
3. stimulates pituitary, except for somatostatin and dopamine.
4. the sella turcica.
5. dura mater, except for the a thin opening which conveys a stalk from the hypothalamus.
6. the upward growth of a pituitary tumor will impinge on the optic chiasm, which will block the optic pathways responsible for peripheral vision bilaterally.
7. anterior, intermediate, posterior lobes. anterior is 80%.
8. storage unit for oxytocin and ADH.
9. also contains hormones or precursor to hormones such as melanocyte stimulating hormone and a hormone that increases aldosterone production.
10. prolactin.
11. growth hormone
LH and FSH
TSH
prolactin
ACTH.
[G L/F T P A] [go left, pa]
12. IGF-1 levels.
13. stimulates peripheral endocrine organs and regulates growth and lactation.
14. stimulates cortisol production in the adrenals.
15. stimulates ovulation and progesterone production in females, stimulates testosterone production in males.
16. promotes lactation and suppresses ovulation and fertility.
17. a modified neural network consisting of modified glial cells, nerve fibers, and axonal processes extending from the supraoptic and paraventricular nuclei of the hypothalamus.
18. ADH and oxytocin.
19. stimulates water reabsorption in distal tubules of nephron.
20. regulates lactation and uterine contraction.
21. radiation or surgery which reduce blood flow to the brain.
22. destructive lesions
destructive processes
impingement from malignancy
infection
hemochromatosis
sarcoidosis
23. resulting either from deficiency of all AP hormones or just GH, in which body proportions remain normal and abnormal, respectively.
24. genetic dysfunction of fibroblasts that results in abnormal cartilaginous development.
25. sudden hemorrhage into an existing pituitary adenoma.
26. sudden onset headache and diplopia.
27. ischemic necrosis, death.
28. ischemic necrosis of the pituitary.
29. in pregnant women, the anterior pituitary enlarges without corresponding vasculature increase. this hypoxic state combined with an obstetric hemorrhage can cause vasospasm of the blood supply and ultimately ischemia and necrosis.
30. hyperpituitarism.
31. non functional, isolated lesions with no associated neoplasms.
32. 10%.
33. 30-60.
34. made of one cell type that produces one hormone.
35. greater than or less than 1 cm.
36. macro because of the greater chance of adenoma remaining undetected due to the lack of hormonal feedback as compared to women.
37. prolactinoma, ACTH cell adenoma, gonadotropin adenoma, growth hormone adenoma
[pro act gon grow] [functionally proactive: go and grow!]
38. weakly staining acidophilic cells.
39. secretory granules within cytoplasm of cells.
40. diminished menses or amenorrhea
diminished libido
infertility
ovarian cysts
galactorrhea
[prolact amen libido infertility cysts galact] [amen; all infertile cysts in the galaxy now have libidos]
41. roughly 25%.
42. asymptomatic, or decreased libido / sperm count.
43. serum prolactin and MRI.
44. botanicals that have phytoestrogenic or progesterone agonist effects.
45. hepatic secretion of IGF-1
46. hyperglycemia, DM, HTN, CHF, gonadal dysfunction, muscle weakness/arthritis. [sugar sugar blood blood nads muscles]
47. before: pituitary giant
after: acromegaly
48. bigger body size with disproportionately long arms and legs.
49. disproportionately large hands, feet, face
enlargement of heart, thyroid, liver, adrenals
jaw protrusion
spreading of teeth
broadening of nose
"spade like" hands
50. IGF-1 levels and the GH suppression test.
51. in the GH suppression test of a hyperglycemic patient, GH will be suppressed, but won't be in a patient with a GH producing adenoma.
52. an adenoma that produces ACTH, leading to adrenal hypersecretion of cortisol.
53. cushing's syndrome describes a state of hypercortisolism, of which cushing's disease is a specific type related to a corticotroph adenoma.
54. any condition that leads to an enlarged sella turcica not filled with pituitary tissue.
55. obese females
multiple pregnancies
hypertension
[fat fetus food]
56. increased intracranial pressure leads to CSF entering the sella turcica and compressing pituitary against wall.
57. asymptomatic, may see papilledema.
58. ESS due to surgical procedure or radiation that has enlarged the sella turcica.
59. excess secretion of ADH by ectopic sites.
60. cancer (lung, breast, prostate), head trauma, narcotics.
61. oliguria with no other signs.
62. highly concentrated urine, low plasma osmolality, hyponatremia.
63. deficiency of ADH either by hypothalamus underproduction or kidney unresponsiveness.
64. polyuria, polydipsia.
65. trauma
surgery
tumor
infection
sheehan's
66. lithium.
67. the water deprivation test.
68. oxytocin.
Sunday, April 25, 2010
CPD III: kidneys, part II
the second week on the kidney: beginning with tubular disorders. the normal function of the renal tubules is reabsorption of various electrolytes, thus many tubular disorders result in excess amounts of these materials in the urine. fanconi's syndrome is a congenital or acquired syndrome that is often fatal by the 20's that leads to dysfunction of the proximal tubule, resulting in cystinosis, glucosuria, phosphaturia, aminoaciduria, bicarbonate wasting. cystinuria and aminoaciduria are failed reabsorption of cysteine or amino acids in general, leading to excess excretion in the urine. in both, cystine crystals might form and create symptoms similar to that of a patient with renal colic. wilson's disease is a rare congenital disease that involves copper deposition in the tubules, along with the liver, brain, and RBC's. the pathognomonic sign for wilson's disease is the "kayser fleischer" rings seen in the eye.
renal glucosuria is a tubular dysfunction that results in spilling of glucose into the urine despite normal or low blood glucose levels. it is often asymptomatic and might be found by glucose in the urine after a 24 hour fast. renal acidosis is another condition that involves acidosis which might be due to impaired secretion of H+ in the distal tubule or impaired reabsorption of bicarbonate in the proximal tubule. the latter might be associated with potassium wasting and muscle dysfunction as well. potassium absorption can also be affected by tubular dysfunction, as seen in bartter's and liddle's syndrome. nephrogenic diabetes insipidus is a congenital and generally fatal disease that might show up in infants in which the kidney's ADH receptors are dysfunctional, resulting in polydipsia, polyuria and hypotonic urine.
diabetic nephropathy is a complication that occurs in about 1/3 of cases of diabetes mellitus which involves glycosylation of the nephron and the dysfunction that results. it might occur 15-20 years after a diagnosis of DM and might be heavily influenced (or prevented) by diet and lifestyle factors early on. the first signs are not overt and may include increased GFR and mild proteinuria. patients with stage II DN will see a drop in GFR, more noticeable proteinuria (resulting in edema symptoms as well), and increasing hypertension. stage III is the last stage, the last few years of a ~20 year process which involves greatly reduced GFR, massive proteinuria, hypertension, and retinopathy. patients with severe DN are at increased risk for infections as well due to the higher glucose levels in the urine.
polycystic kidney disease is a hereditary disorder that results in multiple bilateral cysts that increase size and decrease function of the kidneys. it can manifest as proteinuria, mild hematuria, low back pain, infection, and colic due to formation of stones. late stage, it might also be accompanied by hepatic involvement such as portal HTN and esophageal varices. it will show proteinuria and hematuria on lab diagnosis, as well as pyuria which might appear even without infection. 50% of patients with PKD will end up with renal failure in 10 years.
interstitial tubular disorder is another possible tubular dysfunction that occurs due to drug toxicity or hypersensitivity- most commonly from seizure medication. these drugs can affect both the tubules and the interstitial space, causing a variety of symptoms including that of tubular dysfunction, renal failure, UTI, as well as a host of dermatological manifestations depending on the causative agent. labs might resemble an infection without the presence of bacteria: eosinophilia, proteinuria, hematuria. a patient with ITD would present clinically with enlarged kidneys.
cystitis is a UTI of the bladder, commonly due to vaginal uptake in women and chronic bacterial prostatitis in men. it manifests mostly through urinary symptoms: frequency, urgency, dysuria, occasional hematuria, and possibly suprapubic or lower back pain. there are generally no remarkable PE findings other than general achiness. a UA might show turbid urine and possibly hematuria.
if acute infection reaches the kidneys, acute pyelonephritis results. this condition is more common in girls / pregnant women or patients who have urethral instrumentation. it is most commonly due to e.coli, klebsiella, enterobacter and proteus, which may be present in a urine culture in excess of 100,000 / ml. symptoms include fever/chills/nausea/vomiting, as well as kidney tenderness and enlargement, and possible urinary symptoms as well. lab tests might show neutrophilia, bacteruria, and presence of WBC casts is a pathognomonic sign.
untreated or poorly managed acute pyelonephritis might lead to chronic pyelonephritis, which in turn may lead to chronic renal failure if fibrosis is widespread enough. these patients have a vague and inconsistent clinical presentation, sometimes having fever, abdominal/flank pain, and obstructive symptoms. a PE for a patient with CP should include checking for HTN and anemia symptoms, as well as edema, CVA tenderness, and palpation of the kidney and bladder. definitive diagnosis is made by IVU.
interstitial cystitis is a disorder of the bladder lining, related to dysfunction of the GAG layer. rather than an infectious origin, IC is commonly triggered by such foods as cranberry juice, potassium rich foods, coffee, alcohol, tomatoes, etc. it presents as a more severe cystitis, with urgency, frequency, and severe abdominal pain which can be severe enough to limit sexual activity. diagnosis is made by excluding other bladder conditions and can be made definitively by bladder wall biopsy, which would show hunnel's patches: tiny ulcerations.
a urinary calculi is a stone in the ureter, commonly made of calcium oxalate, struvite, uric acid, or cystine. they appear more frequently in men and are often idiopathic, although several risk factors have been identified- such as low water intake, excess vitamin C intake, and a sedentary lifestyle. people with UC will present with episodes of severe, colicky flank pain that may radiate down to the thigh, as well as hematuria and urinary symptoms. a UA might show hematuria, pyuria, and crystals-- a 6 sided crystal points to a stone made of cystine.
some notes on cancers of the kidney and bladder: most kidney tumors are adenocarcinomas, which are commonly caused by drugs and environmental toxins and might present asymptomatically due to the high functional reserve of the kidneys. wilm's tumor mostly affects children and may present as an asymptomatic mass. neuroblastoma is a systemic, often fatal condition which affects the kidney as well and can be identified by blackness around the eyes. bladder tumors are most often caused by cigarette smoking, and can cause hematuria, secondary infection, flank pain with obstructive symptoms. the conventional treatment strategy is sloughing off of cancer cells via instillation of BCG within the bladder.
questions
various tubular disorders...
1. what is fanconi's syndrome?
2. what is the prognosis for patients with fanconi's syndrome?
3. what is cystinuria?
4. patients with cystinuria can present similarly to which condition?
5. what is aminoaciduria?
6. cystine renal stones in a patient with aminoaciduria might indicate...
7. how is aminoaciduria diagnosed?
8. what is wilson's disease?
9. wilson's disease might present similarly to...
10. what is the pathognomonic sign for wilson's disease?
11. what is the prognosis for patients with wilson's disease?
12. if diagnosed early, what might be of benefit to patients with wilson's disease?
more tubular disorders...
13. what is renal glucosuria?
14. how is renal glucosuria diagnosed?
15. what is renal acidosis?
16. renal acidosis from proximal tubule dysfunction often accompanies which disease?
17. distal tubule dysfunction is often accompanied by...
18. what is bartter's syndrome?
19. what is liddle's syndrome?
20. what is nephrogenic diabetes insipidus?
21. what are the signs and symptoms of nephrogenic diabetes insipidus?
diabetic nephropathy...
22. what is diabetic nephropathy?
23. describe the hallmarks of the first stage of diabetic nephropathy. how long after DM diagnosis is the onset?
24. what are the hallmarks of the second stage of diabetic nephropathy?
25. what are the hallmarks of the third stage of diabetic nephropathy?
26. patients with diabetic nephropathy are more prone to...
27. what is the treatment strategy for patients in stage I DN?
28. what is the survival rate for stage II or III DN patients who need dialysis?
polycystic kidney disease...
29. what is polycystic kidney disease?
30. what are the signs and symptoms of PKD?
31. what are some symptoms that might appear late in the course of PKD?
32. what are the lab results for PKD?
33. what is the prognosis for PKD?
interstitial tubular disease...
34. what is ITD?
35. what are medications that commonly trigger ITD?
36. what are the signs and symptoms of ITD?
37. what are some typical lab results for a patient with ITD?
38. what is a PE finding one might find on a patient with ITD?
renal / urinary tract infections...
39. what are some general symptoms of a lower UTI?
40. what are some general symptoms of an upper UTI?
41. blood borne infections are more likely seen in which demographic?
42. what are some physiological mechanisms that fight against infections in the urinary tract?
43. what are some factors that predispose an individual to getting a UTI?
cystitis...
44. what is a common etiology of cystitis for females?
45. what is the most common etiology of cystitis for males?
46. what are the typical cystitis PE findings?
47. what are the signs and symptoms of cystitis?
48. what are some lab findings for cystitis?
acute pyelonephritis...
49. which demographic is AP most common in?
50. which microorganisms are most commonly implicated in AP?
51. what are the signs and symptoms of AP?
52. what are the lab markers one might see with an AP patient?
53. a urine culture might show...
chronic pyelonephritis...
54. CP accounts for what percentage of renal failure cases?
55. what is CP caused by?
56. how does CP lead to renal failure?
57. what is the symptom picture for CP?
58. CP symptoms might appear similarly to what other condition?
59. what should be checked for on a PE of a patient with CP?
60. definititve diagnosis of CP is made by...
61. what are some strategies for improving kidney health?
interstitial cystitis...
62. what gender is more affected by IC?
63. what is the pathophysiology of IC?
64. what are some common foods that irritate IC?
65. how does IC present clinically?
66. 60% of patients with IC experience...
67. how long does IC generally take to diagnose?
68. what are the diagnostic criteria for IC?
69. what is the pathognomonic sign for IC?
70. what is unique about the UA for patients with IC?
urinary calculi...
71. which gender is more prone to UC?
72. 75% of urinary calculi are due to what etiology?
73. 20% of urinary calculi are due to...
74. what are the most common types of stones found in UC?
75. what are the signs and symptoms of UC?
76. what might be found on a urinalysis of UC?
77. 6 sided crystals in a UA of UC is indicative of...
78. what are some risk factors for UC?
cancer...
79. what percentage of kidney tumors is represented by adenocarcinomas?
80. what are some etiological agents in adenocarcinoma of the kidneys?
81. what are the signs / symptoms of adenocarcinoma?
82. wilm's tumor is most common in which demographic?
83. wilm's tumor most commonly presents as...
84. what is a characteristic sign for neuroblastoma?
85. what is a common etiology for bladder cancer?
86. what are the signs and symptoms of bladder cancer?
answers
1. congenital or acquired dysfunction of proximal tubule that results in cystinosis, glucosuria, phosphaturia, aminoaciduria, and bicarbonate wasting.
2. most die in 20's.
3. impaired reabsorption of cysteine in the tubules which causes increased urinary excretion and formation of cystine calculi.
4. renal colic.
5. impaired absorption of all amino acids.
6. chronic renal failure.
7. excess amino acids and cystine crystals on UA.
8. a rare congenital disorder which involves copper deposition in various places in the body such as the renal tubules, liver, brain, RBC's.
9. hepatitis.
10. kayser fleischer rings.
11. generally poor due to late diagnosis.
12. treatment with zinc.
13. inherited condition that involves low blood glucose combined with excess excretion of glucose.
14. normal or low serum glucose but glucose in urine after overnight fast.
15. chronic acidosis which results either from impaired resorption of bicarbonate in proximal tubule or impaired secretion of H+ in distal tubule.
16. fanconi's syndrome, wilson's disease, multiple myeloma, vitamin D deficiency, heavy metal toxicity.
17. potassium wasting and the resulting muscle dysfunction.
18. hypokalemia due to dysfunction in thick ascending loop of henle.
19. rare disorder that resembles primary aldosteronism with hypertension and hyperkalemic alkalosis.
20. dysfunction of ADH receptors on the kidney.
21. polydipsia, polyuria, hypotonic urine.
22. a complication that occurs in about a third of cases of diabetes mellitus resulting from glycosylation of the nephron.
23. may appear 15-20 years after DM diagnosis; undetectable increase in GFR, mild proteinuria.
24. decreased GFR
proteinuria
edema due to low protein
hypertension.
25. azotemia (increases seen in BUN and creatinine)
GFR less than 1/3
massive proteinuria
hypertension
retinopathy
26. infections due to higher glucose levels in urine, neurogenic bladder, hypertension.
27. watch diet: low sugars, high vegetables
monitor blood pressure
watch for retinal fundus changes
28. 2-3 years.
29. an autosomal dominant or recessive disease that results in multiple bilateral cysts that increase the size and reduce the function of the kidneys.
30. asymptomatic, or
lumbar pain
hematuria
infection
colic due to stones [back blood bugs stones] [bloody stones on the back of bugs]
31. hepatic symptoms: portal HTN, esophageal varices.
32. proteinuria, occasional hematuria, pyruria (even without infection)
33. 50% chance for kidney failure in 10 years.
34. acute renal failure due to drug reaction / hypersensitivity that affects tubules and interstitial tissue.
35. seizure medications.
36. variable:
UTI sxs
tubular dysfunction sxs
oliguria
urticaria, photosensitivity, erythema nodosum, epidermal necrolysis
37. eosinophilia, proteinuria, hematuria, but no bacteria.
38. enlarged kidneys.
39. more urinary symptoms: dysuria, frequency, urgency, hematuria, etc. suprapubic pain.
40. kidney tenderness, fever/chills, N/V, sometimes diarrhea.
41. IV drug users.
42. immune response via WBC's and antibodies, urine acidity, and voiding.
43. congenital malformations (hypospadias)
poor or ineffective hygiene
frequent intercourse, anal sex
high urine pH
catheterization
low water intake
high carb diet / diabetes
44. uptake of bacteria from vagina.
45. chronic bacterial prostatitis.
46. patient in general distress and malaise, but not as severe as pyelonephritis.
47. dysuria, urgency, frequency, nocturia
suprapubic and lower back pain
48. turbid urine and occasional hematuria.
49. girls / pregnant women, or patients with catheterization.
50. e.coli, klebsiella, proteus, enterobacter.
51. fever/chills, N/V
flank pain, kidney tenderness and enlargement
urinary frequency / urgency in 1/3.
52. elevated neutrophils, bacteria, WBC casts in the urine.
53. more than 100,000 organisms / ml.
54. 2-3%.
55. recurrent acute pyelonephritis.
56. CP leads to fibrosis which decreases renal function, ultimately leading to chronic renal failure.
57. vague, inconsistent. may have
fever
flank / abdominal pain
obstructive symptoms
58. chronic interstitial nephritis.
59. signs of HTN, anemia, edema, CVA tenderness, palpation of kidneys and bladder.
60. IVU.
61. drink more water (up to half your weight??)
regulate protein intake
reduce unnecessary medications
62. females 10:1.
63. disruption of interior lining of the bladder, related to dysregulation of GAG layer. may also be abnormal accumulation of mast cells.
64. cranberry
coffee / tea
alcohol / tobacco
tomatoes
potassium
65. as a more severe cystitis:
frequency, urgency (enough to keep housebound) and severe abdominal pain
66. pain with intercourse.
67. 4.5 years on avg.
68. exclusion of other bladder conditions
irritative voiding
specific cystography changes or
aggravation from potassium
69. hunner's patches: tiny ulcerations seen in bladder wall biopsy.
70. consistently free of bacteria, unlike many other bladder conditions; not infective.
71. 3-4 times more common in males.
72. idiopathic.
73. uric acid abnormalities.
74. calcium oxalate, struvite, uric acid, cystine.
75. hematuria
episodes of severe, spastic, colicky pain that may radiate from flank to thigh
urinary symptoms: urgency, frequency, dysuria.
76. may have hematuria, pyuria, crystals.
77. cystine crystals.
78. low fluid intake
sedentary lifestyle
excess vitamin C
low vitamin B6, mg
79. 86%.
80. drugs
heavy metals
radiation
viruses
lifestyle factors: smoking, coffee, etc.
81. often asx because of high functional reserve of kidneys, but may present with colic, hematuria.
82. children.
83. asymptomatic mass.
84. black under the eyes.
85. smoking.
86. hematuria
infection
obstructive symptoms, flank pain
renal glucosuria is a tubular dysfunction that results in spilling of glucose into the urine despite normal or low blood glucose levels. it is often asymptomatic and might be found by glucose in the urine after a 24 hour fast. renal acidosis is another condition that involves acidosis which might be due to impaired secretion of H+ in the distal tubule or impaired reabsorption of bicarbonate in the proximal tubule. the latter might be associated with potassium wasting and muscle dysfunction as well. potassium absorption can also be affected by tubular dysfunction, as seen in bartter's and liddle's syndrome. nephrogenic diabetes insipidus is a congenital and generally fatal disease that might show up in infants in which the kidney's ADH receptors are dysfunctional, resulting in polydipsia, polyuria and hypotonic urine.
diabetic nephropathy is a complication that occurs in about 1/3 of cases of diabetes mellitus which involves glycosylation of the nephron and the dysfunction that results. it might occur 15-20 years after a diagnosis of DM and might be heavily influenced (or prevented) by diet and lifestyle factors early on. the first signs are not overt and may include increased GFR and mild proteinuria. patients with stage II DN will see a drop in GFR, more noticeable proteinuria (resulting in edema symptoms as well), and increasing hypertension. stage III is the last stage, the last few years of a ~20 year process which involves greatly reduced GFR, massive proteinuria, hypertension, and retinopathy. patients with severe DN are at increased risk for infections as well due to the higher glucose levels in the urine.
polycystic kidney disease is a hereditary disorder that results in multiple bilateral cysts that increase size and decrease function of the kidneys. it can manifest as proteinuria, mild hematuria, low back pain, infection, and colic due to formation of stones. late stage, it might also be accompanied by hepatic involvement such as portal HTN and esophageal varices. it will show proteinuria and hematuria on lab diagnosis, as well as pyuria which might appear even without infection. 50% of patients with PKD will end up with renal failure in 10 years.
interstitial tubular disorder is another possible tubular dysfunction that occurs due to drug toxicity or hypersensitivity- most commonly from seizure medication. these drugs can affect both the tubules and the interstitial space, causing a variety of symptoms including that of tubular dysfunction, renal failure, UTI, as well as a host of dermatological manifestations depending on the causative agent. labs might resemble an infection without the presence of bacteria: eosinophilia, proteinuria, hematuria. a patient with ITD would present clinically with enlarged kidneys.
cystitis is a UTI of the bladder, commonly due to vaginal uptake in women and chronic bacterial prostatitis in men. it manifests mostly through urinary symptoms: frequency, urgency, dysuria, occasional hematuria, and possibly suprapubic or lower back pain. there are generally no remarkable PE findings other than general achiness. a UA might show turbid urine and possibly hematuria.
if acute infection reaches the kidneys, acute pyelonephritis results. this condition is more common in girls / pregnant women or patients who have urethral instrumentation. it is most commonly due to e.coli, klebsiella, enterobacter and proteus, which may be present in a urine culture in excess of 100,000 / ml. symptoms include fever/chills/nausea/vomiting, as well as kidney tenderness and enlargement, and possible urinary symptoms as well. lab tests might show neutrophilia, bacteruria, and presence of WBC casts is a pathognomonic sign.
untreated or poorly managed acute pyelonephritis might lead to chronic pyelonephritis, which in turn may lead to chronic renal failure if fibrosis is widespread enough. these patients have a vague and inconsistent clinical presentation, sometimes having fever, abdominal/flank pain, and obstructive symptoms. a PE for a patient with CP should include checking for HTN and anemia symptoms, as well as edema, CVA tenderness, and palpation of the kidney and bladder. definitive diagnosis is made by IVU.
interstitial cystitis is a disorder of the bladder lining, related to dysfunction of the GAG layer. rather than an infectious origin, IC is commonly triggered by such foods as cranberry juice, potassium rich foods, coffee, alcohol, tomatoes, etc. it presents as a more severe cystitis, with urgency, frequency, and severe abdominal pain which can be severe enough to limit sexual activity. diagnosis is made by excluding other bladder conditions and can be made definitively by bladder wall biopsy, which would show hunnel's patches: tiny ulcerations.
a urinary calculi is a stone in the ureter, commonly made of calcium oxalate, struvite, uric acid, or cystine. they appear more frequently in men and are often idiopathic, although several risk factors have been identified- such as low water intake, excess vitamin C intake, and a sedentary lifestyle. people with UC will present with episodes of severe, colicky flank pain that may radiate down to the thigh, as well as hematuria and urinary symptoms. a UA might show hematuria, pyuria, and crystals-- a 6 sided crystal points to a stone made of cystine.
some notes on cancers of the kidney and bladder: most kidney tumors are adenocarcinomas, which are commonly caused by drugs and environmental toxins and might present asymptomatically due to the high functional reserve of the kidneys. wilm's tumor mostly affects children and may present as an asymptomatic mass. neuroblastoma is a systemic, often fatal condition which affects the kidney as well and can be identified by blackness around the eyes. bladder tumors are most often caused by cigarette smoking, and can cause hematuria, secondary infection, flank pain with obstructive symptoms. the conventional treatment strategy is sloughing off of cancer cells via instillation of BCG within the bladder.
questions
various tubular disorders...
1. what is fanconi's syndrome?
2. what is the prognosis for patients with fanconi's syndrome?
3. what is cystinuria?
4. patients with cystinuria can present similarly to which condition?
5. what is aminoaciduria?
6. cystine renal stones in a patient with aminoaciduria might indicate...
7. how is aminoaciduria diagnosed?
8. what is wilson's disease?
9. wilson's disease might present similarly to...
10. what is the pathognomonic sign for wilson's disease?
11. what is the prognosis for patients with wilson's disease?
12. if diagnosed early, what might be of benefit to patients with wilson's disease?
more tubular disorders...
13. what is renal glucosuria?
14. how is renal glucosuria diagnosed?
15. what is renal acidosis?
16. renal acidosis from proximal tubule dysfunction often accompanies which disease?
17. distal tubule dysfunction is often accompanied by...
18. what is bartter's syndrome?
19. what is liddle's syndrome?
20. what is nephrogenic diabetes insipidus?
21. what are the signs and symptoms of nephrogenic diabetes insipidus?
diabetic nephropathy...
22. what is diabetic nephropathy?
23. describe the hallmarks of the first stage of diabetic nephropathy. how long after DM diagnosis is the onset?
24. what are the hallmarks of the second stage of diabetic nephropathy?
25. what are the hallmarks of the third stage of diabetic nephropathy?
26. patients with diabetic nephropathy are more prone to...
27. what is the treatment strategy for patients in stage I DN?
28. what is the survival rate for stage II or III DN patients who need dialysis?
polycystic kidney disease...
29. what is polycystic kidney disease?
30. what are the signs and symptoms of PKD?
31. what are some symptoms that might appear late in the course of PKD?
32. what are the lab results for PKD?
33. what is the prognosis for PKD?
interstitial tubular disease...
34. what is ITD?
35. what are medications that commonly trigger ITD?
36. what are the signs and symptoms of ITD?
37. what are some typical lab results for a patient with ITD?
38. what is a PE finding one might find on a patient with ITD?
renal / urinary tract infections...
39. what are some general symptoms of a lower UTI?
40. what are some general symptoms of an upper UTI?
41. blood borne infections are more likely seen in which demographic?
42. what are some physiological mechanisms that fight against infections in the urinary tract?
43. what are some factors that predispose an individual to getting a UTI?
cystitis...
44. what is a common etiology of cystitis for females?
45. what is the most common etiology of cystitis for males?
46. what are the typical cystitis PE findings?
47. what are the signs and symptoms of cystitis?
48. what are some lab findings for cystitis?
acute pyelonephritis...
49. which demographic is AP most common in?
50. which microorganisms are most commonly implicated in AP?
51. what are the signs and symptoms of AP?
52. what are the lab markers one might see with an AP patient?
53. a urine culture might show...
chronic pyelonephritis...
54. CP accounts for what percentage of renal failure cases?
55. what is CP caused by?
56. how does CP lead to renal failure?
57. what is the symptom picture for CP?
58. CP symptoms might appear similarly to what other condition?
59. what should be checked for on a PE of a patient with CP?
60. definititve diagnosis of CP is made by...
61. what are some strategies for improving kidney health?
interstitial cystitis...
62. what gender is more affected by IC?
63. what is the pathophysiology of IC?
64. what are some common foods that irritate IC?
65. how does IC present clinically?
66. 60% of patients with IC experience...
67. how long does IC generally take to diagnose?
68. what are the diagnostic criteria for IC?
69. what is the pathognomonic sign for IC?
70. what is unique about the UA for patients with IC?
urinary calculi...
71. which gender is more prone to UC?
72. 75% of urinary calculi are due to what etiology?
73. 20% of urinary calculi are due to...
74. what are the most common types of stones found in UC?
75. what are the signs and symptoms of UC?
76. what might be found on a urinalysis of UC?
77. 6 sided crystals in a UA of UC is indicative of...
78. what are some risk factors for UC?
cancer...
79. what percentage of kidney tumors is represented by adenocarcinomas?
80. what are some etiological agents in adenocarcinoma of the kidneys?
81. what are the signs / symptoms of adenocarcinoma?
82. wilm's tumor is most common in which demographic?
83. wilm's tumor most commonly presents as...
84. what is a characteristic sign for neuroblastoma?
85. what is a common etiology for bladder cancer?
86. what are the signs and symptoms of bladder cancer?
answers
1. congenital or acquired dysfunction of proximal tubule that results in cystinosis, glucosuria, phosphaturia, aminoaciduria, and bicarbonate wasting.
2. most die in 20's.
3. impaired reabsorption of cysteine in the tubules which causes increased urinary excretion and formation of cystine calculi.
4. renal colic.
5. impaired absorption of all amino acids.
6. chronic renal failure.
7. excess amino acids and cystine crystals on UA.
8. a rare congenital disorder which involves copper deposition in various places in the body such as the renal tubules, liver, brain, RBC's.
9. hepatitis.
10. kayser fleischer rings.
11. generally poor due to late diagnosis.
12. treatment with zinc.
13. inherited condition that involves low blood glucose combined with excess excretion of glucose.
14. normal or low serum glucose but glucose in urine after overnight fast.
15. chronic acidosis which results either from impaired resorption of bicarbonate in proximal tubule or impaired secretion of H+ in distal tubule.
16. fanconi's syndrome, wilson's disease, multiple myeloma, vitamin D deficiency, heavy metal toxicity.
17. potassium wasting and the resulting muscle dysfunction.
18. hypokalemia due to dysfunction in thick ascending loop of henle.
19. rare disorder that resembles primary aldosteronism with hypertension and hyperkalemic alkalosis.
20. dysfunction of ADH receptors on the kidney.
21. polydipsia, polyuria, hypotonic urine.
22. a complication that occurs in about a third of cases of diabetes mellitus resulting from glycosylation of the nephron.
23. may appear 15-20 years after DM diagnosis; undetectable increase in GFR, mild proteinuria.
24. decreased GFR
proteinuria
edema due to low protein
hypertension.
25. azotemia (increases seen in BUN and creatinine)
GFR less than 1/3
massive proteinuria
hypertension
retinopathy
26. infections due to higher glucose levels in urine, neurogenic bladder, hypertension.
27. watch diet: low sugars, high vegetables
monitor blood pressure
watch for retinal fundus changes
28. 2-3 years.
29. an autosomal dominant or recessive disease that results in multiple bilateral cysts that increase the size and reduce the function of the kidneys.
30. asymptomatic, or
lumbar pain
hematuria
infection
colic due to stones [back blood bugs stones] [bloody stones on the back of bugs]
31. hepatic symptoms: portal HTN, esophageal varices.
32. proteinuria, occasional hematuria, pyruria (even without infection)
33. 50% chance for kidney failure in 10 years.
34. acute renal failure due to drug reaction / hypersensitivity that affects tubules and interstitial tissue.
35. seizure medications.
36. variable:
UTI sxs
tubular dysfunction sxs
oliguria
urticaria, photosensitivity, erythema nodosum, epidermal necrolysis
37. eosinophilia, proteinuria, hematuria, but no bacteria.
38. enlarged kidneys.
39. more urinary symptoms: dysuria, frequency, urgency, hematuria, etc. suprapubic pain.
40. kidney tenderness, fever/chills, N/V, sometimes diarrhea.
41. IV drug users.
42. immune response via WBC's and antibodies, urine acidity, and voiding.
43. congenital malformations (hypospadias)
poor or ineffective hygiene
frequent intercourse, anal sex
high urine pH
catheterization
low water intake
high carb diet / diabetes
44. uptake of bacteria from vagina.
45. chronic bacterial prostatitis.
46. patient in general distress and malaise, but not as severe as pyelonephritis.
47. dysuria, urgency, frequency, nocturia
suprapubic and lower back pain
48. turbid urine and occasional hematuria.
49. girls / pregnant women, or patients with catheterization.
50. e.coli, klebsiella, proteus, enterobacter.
51. fever/chills, N/V
flank pain, kidney tenderness and enlargement
urinary frequency / urgency in 1/3.
52. elevated neutrophils, bacteria, WBC casts in the urine.
53. more than 100,000 organisms / ml.
54. 2-3%.
55. recurrent acute pyelonephritis.
56. CP leads to fibrosis which decreases renal function, ultimately leading to chronic renal failure.
57. vague, inconsistent. may have
fever
flank / abdominal pain
obstructive symptoms
58. chronic interstitial nephritis.
59. signs of HTN, anemia, edema, CVA tenderness, palpation of kidneys and bladder.
60. IVU.
61. drink more water (up to half your weight??)
regulate protein intake
reduce unnecessary medications
62. females 10:1.
63. disruption of interior lining of the bladder, related to dysregulation of GAG layer. may also be abnormal accumulation of mast cells.
64. cranberry
coffee / tea
alcohol / tobacco
tomatoes
potassium
65. as a more severe cystitis:
frequency, urgency (enough to keep housebound) and severe abdominal pain
66. pain with intercourse.
67. 4.5 years on avg.
68. exclusion of other bladder conditions
irritative voiding
specific cystography changes or
aggravation from potassium
69. hunner's patches: tiny ulcerations seen in bladder wall biopsy.
70. consistently free of bacteria, unlike many other bladder conditions; not infective.
71. 3-4 times more common in males.
72. idiopathic.
73. uric acid abnormalities.
74. calcium oxalate, struvite, uric acid, cystine.
75. hematuria
episodes of severe, spastic, colicky pain that may radiate from flank to thigh
urinary symptoms: urgency, frequency, dysuria.
76. may have hematuria, pyuria, crystals.
77. cystine crystals.
78. low fluid intake
sedentary lifestyle
excess vitamin C
low vitamin B6, mg
79. 86%.
80. drugs
heavy metals
radiation
viruses
lifestyle factors: smoking, coffee, etc.
81. often asx because of high functional reserve of kidneys, but may present with colic, hematuria.
82. children.
83. asymptomatic mass.
84. black under the eyes.
85. smoking.
86. hematuria
infection
obstructive symptoms, flank pain
Monday, April 19, 2010
CPD III: kidneys part I
the kidney unit in CPD III. we started with some introductory notes about diagnosis and the general symptom picture. labs that are helpful in the diagnosis of kidney conditions include urinalysis (can detect infection, RBC's, casts, etc), CBC, and chem screen (BUN and creatinine are useful measures of glomerular function). imaging studies might include xray, US, IVU, depending on the condition suspected. some typical symptoms associated with kidney conditions: UTI's commonly present with a triad of symptoms, urinary frequency, urgency, dysuria. chills/fever in association with these symptoms might indicate involvement of the upper urinary tract. urethral discharge in males is most likely due to GC/chlamydia infection. nocturia might be indicative of BPH, or simply reflect excess nighttime fluid consumption- consider nocturia seriously if it is a sudden change for the patient. enuresis, bedwetting, can be primary or secondary- patients with secondary enuresis might only have episodes followed by breaks of 6 months or more and are more likely due to psychological as opposed to physiological factors. incontinence comes in three flavors- overflow from incomplete emptying due to obstruction, stress from increased pressure, and urge from decreased CNS inhibition.
renal colic, or kidney stones, often cause severe unilateral pain in a crescendo-decrescendo pattern that radiates from the kidney / flank area to the lower abdomen and bladder, and sometimes as far down as the knee. patients might also present with nausea/vomiting, hematuria, and urinary frequency, as well as chills/fever if an infection is involved. diagnosis is made by UA and imaging, in particular US and IVU.
polyuria can be a physiologic response to an increased osmolar load, in which case the major concern is loss of electrolytes. it can also point to certain underlying pathologies such as diabetes insipidus, which leads to an underproduction of ADH by the pituitary. nephrogenic diabetes insipidus can also result in polyuria- in this condition, the kidney's ADH receptors are non functioning.
oligouria and anuria are conditions of decreased urine and can be from pre-renal, renal, or post renal causes. pre-renal causes can include dehydration, as well as any condition that decreases blood flow to the kidney such as CHF or hemorrhage. renal causes are grouped under the acronym VINDICATE: vascular lesions, inflammatory lesions, neoplasm, degenerative conditions, intoxication, congenital disorders, autoimmune, trauma, endocrine causes. post renal: MINNT-- malformations, inflammatory, neoplasm, neurological, trauma.
some notes about the various colors of urine and what they might indicate: normal color is yellow, although bright / concentrated yellow might indicate dehydration or B vitamins. overly clear might indicate glomerular dysfunction as in chronic glomerulonephritis, or simply polydipsia. cloudy white might be indicative of infection as the cloudiness might be bacteria or pus. red might be RBC's but can also be from certain foods such as beets.
as the kidneys are primarily responsible for maintaining fluid volume in the body, systemic edema symptoms often point to kidney filtration issues. pitting edema refers to a type in which fluid can be displaced, forming transient "pits", whereas in non-pitting, fluid can not be displaced- this is often due to local trauma such as a bee sting. in general edema formation can occur via four mechanisms- increased capillary pressure, increased capillary permeability, decreased plasma proteins, and lymph obstruction. edema symptoms may also point to other organ systems, in particular heart dysfunction (recall that RCHF leads to systemic edema), thyroid (hypothyroid myxedema), hepatic (look for jaundice, ascites, palmar erythema), and might even be due to a worm found in pork, trichinosis if seen periorbitally.
acute renal failure describes a situation marked by rapidly increasing azotemia plus oliguria / anuria. as with azotemia, the cause may be pre-renal (CHF), renal (glomerulonephritis), or post renal (bladder outlet obstruction, BPH). clinically, it manifests as lethargy, pulmonary edema, CHF, hypertension, and oliguria. diagnosis is made via chem screen, CBC, and UA-- most helpful is the rapid and steady increase of creatinine (as well as BUN). if oliguria / anuria persists for more than 3 days, this is an indicator of poor prognosis; conventional emergency treatment might require dialysis and complete kidney rest.
whereas acute renal failure might produce sudden increases in BUN / creatinine, chronic renal failure might show mild elevations for month long periods. there are many risk factors that contribute to CRF, such as glomerulonephritis, cardiovascular disease, SLE, pyelonephritis, etc. clinical presentation can be divided by the stage of disease: CRF initially presents with nonspecific / vague symptoms, or fatigue / mental haze. the intermediate stage presents with bad taste in mouth, muscle spasm/convusion/neuropathy, pruritis, nausea / vomiting. the late stage presents with cardiovascular issues such as hypertension, CHF, pericarditis, as well as skin issues such as uremic frost and yellow/brown complexion. in addition to the BUN / creatinine levels, one might expect to see normochromic / normocytic anemia (deficient erythropoetin production), waxy casts on a UA, and imbalanced electrolytes. these patients are generally put on dialysis long term (200,000 in the US) with dietary / fluid intake monitoring- in particular, avoiding high protein intake.
nephrotic syndrome results from a dysfunctional or damaged glomerular basement membrane, leading to loss of proteins and hyperlipidemia. it can be primary from diseases such as immune complex nephritides, or secondary to systemic illness such as diabetes mellitus. patients might present with frothy urine, marked edema periorbitally and peripherally, muscle wasting due to lack of protein, and respiratory symptoms. diagnosis is made by UA, chem screen, CBC- UA might show proteins, cellular elements, casts. chem screen might show hyperlipidemia, hyperalbuminemia, and CBC might show microcytic anemia.
acute glomerulonephritis is another form of glomerular dysfunction, this time from immune complex deposition from previous infection, such as an untreated strep throat infection. it commonly affects children and young adults and is relatively rare in adults over 50. although it has mild proteinuria as nephrotic syndrome does, the hallmark of AG is hematuria and presence of RBC casts in the UA. the decreased glomerular function also leads to increased sodium retention, which ultimately increases blood volume and may lead to hypertension or CHF. children have a good chance of recovery from AG but will always have an increased risk for HTN-- thus an adult who has unexplained HTN might have had acute glomerulonephritis earlier in life. chronic glomerulonephritis might result from longstanding acute glomerulonephritis and might develop insidiously- patients might asx, but with occasional proteinuria and hematuria, with RBC casts on a UA. steadily increasing BUN might also be observed over months or years.
goodpasture's is a near fatal glomerular disease that has a predilection for young males. the hallmark signs are lung and renal hemorrhage that results in hemoptysis and hematuria. labs have the combined characteristics of nephrotic syndrome and glomerulonephritis: hematuria / RBC's, but also with protein / casts in UA, along with increased BUN / creatinine. patients might also present with headache, malaise, and anorexia. the prognosis for goodpasture's is poor, and patients with this condition rarely live past their 20's.
idiopathic primary renal hematuric/proteinuric syndrome is diagnosed when there is mild gross or microscopic hematuria and proteinuria without any clear explanation. the etiology may be related to IgA towards the glomeruli, as well as buerger's disease and febrile URI's. this condition has a preference for males and children-- most recover but like acute glomerulonephritis have an increased lifetime risk for hypertension and renal insufficiency.
henoch-schoenlein purpura is similar to IPRHPS but with marked skin, GI, and joint involvement- the characteristic purpura lesions are symmetrically distributed on the extensor surfaces. GI symptoms might include abdominal pain, vomiting, and joint pain may occur at the ankles, hands, feet. HSP generally follows a viral infection, such as an acute viral URI. lab findings might show hematuria / proteinuria, occult blood, and increased ESR. HSP is self limiting, generally within 6 weeks, although 10-20% of patients might develop chronic renal failure.
questions
diagnosis...
1. what are some helpful lab tests to consider when ruling in or out kidney related pathologies?
2. what are two components of a chem screen that can give an indication of kidney function?
3. what are the imaging techniques used to diagnose kidney conditions?
4. what is the "triad of symptoms" seen in UTI's?
5. what might chills/fever indicate in a patient with the triad of symptoms for a UTI?
6. leukocyte casts in a UA might indicate...
7. what is the most common cause of urethral discharge in males?
8. what might nocturia be indicative of?
9. what is the difference between primary and secondary enuresis?
10. what are the different types of incontinence?
renal colic...
11. describe the pain sensation in renal colic.
12. describe the typical radiation patterns seen in renal colic pain.
13. what are some concomitant symptoms seen in renal colic?
14. what is a typical PE of a patient with RC?
15. what would labs show for RC?
16. what are the imaging studies used to diagnose RC?
polyuria...
17. what are some pathological conditions associated with polyuria?
18. why does diabetes insipidus cause polyuria?
19. what is nephrogenic diabetes insipidus?
oligo / anuria...
20. what are some prerenal causes of oligouria or anuria?
21. what are some renal causes of oligouria / anuria?
22. what are some post renal causes of oligouria / anuria?
what might be indicated by urine that is...
23. colorless.
24. cloudy white.
25. yellow.
26. orange.
27. red.
28. blue/green.
29. brown/black.
edema...
30. what is the difference between pitting and non-pitting edema?
31. what is a common cause of non-pitting edema?
32. what are four pathophysiological mechanisms for edema formation?
33. what are some hepatic symptoms or conditions that might be associated with edema?
34. what is a thyroid related etiology for edema?
35. what is the relationship between edema and pork?
acute renal failure...
36. what is acute renal failure?
37. what are the major etiologies of acute renal failure?
38. what are some "pre-renal" causes of acute renal failure?
39. what are some "renal" causes of acute renal failure?
40. what are some "post-renal" causes of acute renal failure?
41. what are some of the signs and symptoms of acute renal failure?
42. what are some labs that aid in the diagnosis of acute renal failure?
43. if anemia is present in acute renal failure, what type of anemia would it be?
44. what is a marker for prognosis of acute renal failure?
45. what is the conventional treatment strategy for acute renal failure?
chronic renal failure...
46. what are some risk factors for CRF?
47. how many patients in the US are currently on dialysis long term?
48. what are the early signs / symptoms for CRF?
49. what are the intermediate stage signs/symptoms for CRF?
50. what are the late stage signs/symptoms for CRF?
51. what are the lab tests used to diagnose CRF?
52. what are some electrolyte imbalances one might expect to see in CRF?
53. what is the connection between CRF and chronic anemia?
54. what are some treatment strategies for CRF?
nephrotic syndrome...
55. what is nephrotic syndrome?
56. which gender is more affected by nephrotic syndrome?
57. what are the etiologies of nephrotic syndrome?
58. what are the signs and symptoms of nephrotic syndrome?
59. what might one expect to find on a UA of a pt with NS?
60. what might one expect to find on a chem screen of a pt with NS?
61. what is the connection between nephrotic syndrome and hyperlipidemia?
62. what might be a finding on a CBC of a pt with NS?
63. what are some PE findings for NS?
acute glomerulonephritis...
64. what is AG? what are the hallmarks of AG?
65. what age group is most commonly affected by AG?
66. what is the etiology of AG?
67. how long after an episode of untreated strep throat might AG appear?
68. what are the signs/symptoms of AG?
69. what is the lab finding that is diagnostic for AG?
70. what might be seen in fundoscopy of a pt with AG?
71. what is the prognosis for children with AG?
chronic glomerulonephritis...
72. what is chronic glomerulonephritis?
73. what is a typical presentation for chronic glomerulonephritis?
goodpasture's syndrome...
74. which demographic is most commonly affected by goodpasture's syndrome?
75. what are the hallmark signs and symptoms of GS?
76. what are the concomitant symptoms of GS?
77. what are common lab findings for GS?
78. what is the prognosis of goodpasture's syndrome?
idiopathic primary renal hematuric/proteinuric syndrome...
79. what is IPRHPS?
80. what are some possible etiologies of IPRHPS?
81. what demographic is most closely associated with IPRHPS?
82. what might be a predisposing factor for IPRHPS?
83. what might lab findings show for IPRHPS?
84. what is the prognosis for IPRHPS?
henoch-schoenlein purpura...
85. what is HSP?
86. what is the etiology of HSP?
87. what are the signs and symptoms of HSP?
88. what are some lab findings one might expect to find with HSP?
89. what is the prognosis of HSP?
answers
1. UA, culture, CBC, chem screen.
2. BUN and creatinine: both excreted by the kidneys and therefore can be a rough indicator for glomerular function.
3. Xray, US, IVU.
4. urinary frequency, urgency, pain.
5. upper UTI.
6. renal parenchyma infection.
7. GC chlamydia.
8. early disease, excess fluid consumption in evening, BPH, interstitial cystitis.
9. in secondary, there might be a period of dryness (over 6 months)-- more likely due to psychological factors.
10. overflow (obstruction of urinary tract leads to incomplete emptying), stress (increased intraabdominal pressure), urge (decreased CNS inhibition).
11. severe, unilateral, crescendo-decrescendo pain.
12. from flank/kidney around to lower abdomen, follows course of urinary tract and sometimes radiates down further, as far as knee.
13. chills/fever
N/V
hematuria
frequency
14. unremarkable or flank tenderness.
15. hematuria with or without pyuria / bacteruria.
16. xray, US, IVU (for kidney and ureter).
17. diabetes insipidus, nephrogenic diabetes insipidus, psychogenic polydipsia.
18. in DI, the pituitary underproduces ADH, a hormone that allows for water reabsorption in the kidney- thereby leading to greater urine output.
19. a condition where the kidney's receptors for ADH are not functioning.
20. dehydration, hemorrhage, CHF.
21. VINDICATE:
vascular lesions
inflammatory lesions
neoplasm
degenerative
intoxication
congenital disorders
autoimmune (most common)
trauma
endocrine
22. MINNT:
malformations
inflammation
neoplasms
neurological disorders
trauma
23. polydipsia, chronic glomerulonephritis, diabetes inspidis/mellitus.
24. phosphates, epithelial cells, bacteria/pus.
25. B vitamins.
26. urobilinogen, bile, pyridium, carrots.
27. beets, or RBC's.
28. certain drugs (thymol, phenol, indigo blue), pseudomonas.
29. bilirubin, hemoglobin.
30. in pitting, fluid can be displaced and transient "pits" are formed. in non-pitting, edema is so severe that fluid can not be displaced.
31. trauma causes coagulation of proteins such as fibrinogen.
32. increased capillary pressure (blood clots, CHF)
increased capillary permeability (CHF)
decreased plasma proteins (burns, nephrosis, low protein intake)
lymph obstruction (lymph node removal, parasites)
33. jaundice
ascites
spider nevi
red nose
palmar erythema
34. there is a marked increase in water retention in hypothyroid myxedema.
35. trichinosis is a worm found in pork that is associated with periorbital edema.
36. rapidly increasing azotemia plus oliguria.
37. 60-70% extrinsic factors: trauma, drugs, surgery, obstruction, etc.
20-30% due to intrinsic factors: acute glomerulonephritis, SLE, goodpasture's, etc.
38. renal failure that results from inadequate renal perfusion due to factors upstream from the kidney: CHF, hemorrhage, etc.
39. decreased renal blood flow, reduced glomerular filtration, or renal obstruction.
40. bladder outlet obstruction, BPH, tumors.
41. lethargy
pulmonary edema
CHF
hypertension
oliguria
42. chem screen: steadily increasing creatinine is diagnostic. also see BUN increase.
CBC to check for anemia and infection
UA to check for RBC's, WBC's, casts.
43. normocytic normochromic.
44. oliguria / anuria for more than 3 days indicates very poor prognosis; may be fatal.
45. dialysis to allow kidney to recover, or severe limitation of fluid and electrolyte intake.
46. glomerulonephritis
cardiovascular diseases such as arteriosclerosis, HTN
SLE, diabetes
congenital abnormalities (polycystic kidney)
pyelonephritis
47. about 200,000.
48. non-specific
fatigue
nocturia
mental haze
49. muscle twitching, aches, convulsions
neuropathy
bad taste in mouth
N/V
pruritis
50. uremic frost
GI ulcers / bleeding
tissue wasting
yellow / brown skin
hypertension / CHF / pericarditis
51. chem screen would show mild / moderate elevations of BUN/creatinine over months
CBC would show normocytic / normochromic anemia,
UA might show waxy casts
52. decreased calcium, increased phosphorous, potassium, CO2.
53. kidney failure leads to improper erythropoetin production.
54. dietary and fluid intake monitoring - decrease protein and increase carb intake.
55. damage to the glomerular basement membrane that causes hyponaturia, proteinuria, hypoalbuminemia, lipiduria, hyperlipidemia.
56. males.
57. primary nephrotic disease such as immune complex nephritides or underyling systemic disease such as diabetes mellitus.
58. frothy urine
edema
muscle wasting
abdominal pain
SOB/DOE
[basement pee edema muscle stomach breath] [basement flooded with pee- use your stomach muscles and blow it out]
59. cellular elements, protein, casts.
60. hyperalbuminemia and hyperlipidemia.
61. the liver increases lipid production (cholesterol) concurrently with protein production in an attempt to normalize protein levels from the protein loss incurred in nephrotic syndrome.
62. microcytic anemia.
63. periorbital and peripheral edema
muscle wasting
parallel white lines on nails
orthostatic hypotension
64. glomerular dysfunction which causes decreased GFR and increased Na retention, leading to hematuria and hypertension.
65. young children older than 3 or young adults. rare in >50yos.
66. previous infection which causes immune complex deposition in glomeruli.
67. 1-6 weeks.
68. hematuria / oliguria
flank pain
mild edema
hypertension
69. RBC casts on a UA.
70. retinal hemorrhages.
71. 90% chance of recovery but increased risk for HTN remains throughout lifetime.
72. diffuse sclerosis of glomeruli and insidious loss of kidney function.
73. asx, with no abnormal lab results except for occasional proteinuria and hematuria. steadily increasing BUN over years.
74. young males 9:1.
75. renal and lung hemorrhage-- hemoptysis and hematuria.
76. headache, malaise, anorexia.
77. increased BUN/creatinine, RBC, protein on UA, microcytic anemia on CBC.
78. poor, patients rarely live past 20's.
79. presence of protein and RBC's in urine with no explanation.
80. glomerular IgA deposition, buerger's disease.
81. 6:1 males, children/young adult most common.
82. febrile URI.
83. hematuria, proteinuria, increased IgA.
84. many children recover but have an increased lifetime risk for hypertension and renal insufficiency.
85. similar to IPRHPS but with skin, joint, and GI involvement.
86. often follows a viral infection, acute URI.
87. symmetrically distributed purpura on extensor surfaces
arthritis
GI distress- vomiting, pain, occult blood
hematuria, proteinuria
88. increased ESR
hematuria / proteinuria
occult blood
89. self limiting in 1-6 weeks. 10-20% have chronic renal failure.
renal colic, or kidney stones, often cause severe unilateral pain in a crescendo-decrescendo pattern that radiates from the kidney / flank area to the lower abdomen and bladder, and sometimes as far down as the knee. patients might also present with nausea/vomiting, hematuria, and urinary frequency, as well as chills/fever if an infection is involved. diagnosis is made by UA and imaging, in particular US and IVU.
polyuria can be a physiologic response to an increased osmolar load, in which case the major concern is loss of electrolytes. it can also point to certain underlying pathologies such as diabetes insipidus, which leads to an underproduction of ADH by the pituitary. nephrogenic diabetes insipidus can also result in polyuria- in this condition, the kidney's ADH receptors are non functioning.
oligouria and anuria are conditions of decreased urine and can be from pre-renal, renal, or post renal causes. pre-renal causes can include dehydration, as well as any condition that decreases blood flow to the kidney such as CHF or hemorrhage. renal causes are grouped under the acronym VINDICATE: vascular lesions, inflammatory lesions, neoplasm, degenerative conditions, intoxication, congenital disorders, autoimmune, trauma, endocrine causes. post renal: MINNT-- malformations, inflammatory, neoplasm, neurological, trauma.
some notes about the various colors of urine and what they might indicate: normal color is yellow, although bright / concentrated yellow might indicate dehydration or B vitamins. overly clear might indicate glomerular dysfunction as in chronic glomerulonephritis, or simply polydipsia. cloudy white might be indicative of infection as the cloudiness might be bacteria or pus. red might be RBC's but can also be from certain foods such as beets.
as the kidneys are primarily responsible for maintaining fluid volume in the body, systemic edema symptoms often point to kidney filtration issues. pitting edema refers to a type in which fluid can be displaced, forming transient "pits", whereas in non-pitting, fluid can not be displaced- this is often due to local trauma such as a bee sting. in general edema formation can occur via four mechanisms- increased capillary pressure, increased capillary permeability, decreased plasma proteins, and lymph obstruction. edema symptoms may also point to other organ systems, in particular heart dysfunction (recall that RCHF leads to systemic edema), thyroid (hypothyroid myxedema), hepatic (look for jaundice, ascites, palmar erythema), and might even be due to a worm found in pork, trichinosis if seen periorbitally.
acute renal failure describes a situation marked by rapidly increasing azotemia plus oliguria / anuria. as with azotemia, the cause may be pre-renal (CHF), renal (glomerulonephritis), or post renal (bladder outlet obstruction, BPH). clinically, it manifests as lethargy, pulmonary edema, CHF, hypertension, and oliguria. diagnosis is made via chem screen, CBC, and UA-- most helpful is the rapid and steady increase of creatinine (as well as BUN). if oliguria / anuria persists for more than 3 days, this is an indicator of poor prognosis; conventional emergency treatment might require dialysis and complete kidney rest.
whereas acute renal failure might produce sudden increases in BUN / creatinine, chronic renal failure might show mild elevations for month long periods. there are many risk factors that contribute to CRF, such as glomerulonephritis, cardiovascular disease, SLE, pyelonephritis, etc. clinical presentation can be divided by the stage of disease: CRF initially presents with nonspecific / vague symptoms, or fatigue / mental haze. the intermediate stage presents with bad taste in mouth, muscle spasm/convusion/neuropathy, pruritis, nausea / vomiting. the late stage presents with cardiovascular issues such as hypertension, CHF, pericarditis, as well as skin issues such as uremic frost and yellow/brown complexion. in addition to the BUN / creatinine levels, one might expect to see normochromic / normocytic anemia (deficient erythropoetin production), waxy casts on a UA, and imbalanced electrolytes. these patients are generally put on dialysis long term (200,000 in the US) with dietary / fluid intake monitoring- in particular, avoiding high protein intake.
nephrotic syndrome results from a dysfunctional or damaged glomerular basement membrane, leading to loss of proteins and hyperlipidemia. it can be primary from diseases such as immune complex nephritides, or secondary to systemic illness such as diabetes mellitus. patients might present with frothy urine, marked edema periorbitally and peripherally, muscle wasting due to lack of protein, and respiratory symptoms. diagnosis is made by UA, chem screen, CBC- UA might show proteins, cellular elements, casts. chem screen might show hyperlipidemia, hyperalbuminemia, and CBC might show microcytic anemia.
acute glomerulonephritis is another form of glomerular dysfunction, this time from immune complex deposition from previous infection, such as an untreated strep throat infection. it commonly affects children and young adults and is relatively rare in adults over 50. although it has mild proteinuria as nephrotic syndrome does, the hallmark of AG is hematuria and presence of RBC casts in the UA. the decreased glomerular function also leads to increased sodium retention, which ultimately increases blood volume and may lead to hypertension or CHF. children have a good chance of recovery from AG but will always have an increased risk for HTN-- thus an adult who has unexplained HTN might have had acute glomerulonephritis earlier in life. chronic glomerulonephritis might result from longstanding acute glomerulonephritis and might develop insidiously- patients might asx, but with occasional proteinuria and hematuria, with RBC casts on a UA. steadily increasing BUN might also be observed over months or years.
goodpasture's is a near fatal glomerular disease that has a predilection for young males. the hallmark signs are lung and renal hemorrhage that results in hemoptysis and hematuria. labs have the combined characteristics of nephrotic syndrome and glomerulonephritis: hematuria / RBC's, but also with protein / casts in UA, along with increased BUN / creatinine. patients might also present with headache, malaise, and anorexia. the prognosis for goodpasture's is poor, and patients with this condition rarely live past their 20's.
idiopathic primary renal hematuric/proteinuric syndrome is diagnosed when there is mild gross or microscopic hematuria and proteinuria without any clear explanation. the etiology may be related to IgA towards the glomeruli, as well as buerger's disease and febrile URI's. this condition has a preference for males and children-- most recover but like acute glomerulonephritis have an increased lifetime risk for hypertension and renal insufficiency.
henoch-schoenlein purpura is similar to IPRHPS but with marked skin, GI, and joint involvement- the characteristic purpura lesions are symmetrically distributed on the extensor surfaces. GI symptoms might include abdominal pain, vomiting, and joint pain may occur at the ankles, hands, feet. HSP generally follows a viral infection, such as an acute viral URI. lab findings might show hematuria / proteinuria, occult blood, and increased ESR. HSP is self limiting, generally within 6 weeks, although 10-20% of patients might develop chronic renal failure.
questions
diagnosis...
1. what are some helpful lab tests to consider when ruling in or out kidney related pathologies?
2. what are two components of a chem screen that can give an indication of kidney function?
3. what are the imaging techniques used to diagnose kidney conditions?
4. what is the "triad of symptoms" seen in UTI's?
5. what might chills/fever indicate in a patient with the triad of symptoms for a UTI?
6. leukocyte casts in a UA might indicate...
7. what is the most common cause of urethral discharge in males?
8. what might nocturia be indicative of?
9. what is the difference between primary and secondary enuresis?
10. what are the different types of incontinence?
renal colic...
11. describe the pain sensation in renal colic.
12. describe the typical radiation patterns seen in renal colic pain.
13. what are some concomitant symptoms seen in renal colic?
14. what is a typical PE of a patient with RC?
15. what would labs show for RC?
16. what are the imaging studies used to diagnose RC?
polyuria...
17. what are some pathological conditions associated with polyuria?
18. why does diabetes insipidus cause polyuria?
19. what is nephrogenic diabetes insipidus?
oligo / anuria...
20. what are some prerenal causes of oligouria or anuria?
21. what are some renal causes of oligouria / anuria?
22. what are some post renal causes of oligouria / anuria?
what might be indicated by urine that is...
23. colorless.
24. cloudy white.
25. yellow.
26. orange.
27. red.
28. blue/green.
29. brown/black.
edema...
30. what is the difference between pitting and non-pitting edema?
31. what is a common cause of non-pitting edema?
32. what are four pathophysiological mechanisms for edema formation?
33. what are some hepatic symptoms or conditions that might be associated with edema?
34. what is a thyroid related etiology for edema?
35. what is the relationship between edema and pork?
acute renal failure...
36. what is acute renal failure?
37. what are the major etiologies of acute renal failure?
38. what are some "pre-renal" causes of acute renal failure?
39. what are some "renal" causes of acute renal failure?
40. what are some "post-renal" causes of acute renal failure?
41. what are some of the signs and symptoms of acute renal failure?
42. what are some labs that aid in the diagnosis of acute renal failure?
43. if anemia is present in acute renal failure, what type of anemia would it be?
44. what is a marker for prognosis of acute renal failure?
45. what is the conventional treatment strategy for acute renal failure?
chronic renal failure...
46. what are some risk factors for CRF?
47. how many patients in the US are currently on dialysis long term?
48. what are the early signs / symptoms for CRF?
49. what are the intermediate stage signs/symptoms for CRF?
50. what are the late stage signs/symptoms for CRF?
51. what are the lab tests used to diagnose CRF?
52. what are some electrolyte imbalances one might expect to see in CRF?
53. what is the connection between CRF and chronic anemia?
54. what are some treatment strategies for CRF?
nephrotic syndrome...
55. what is nephrotic syndrome?
56. which gender is more affected by nephrotic syndrome?
57. what are the etiologies of nephrotic syndrome?
58. what are the signs and symptoms of nephrotic syndrome?
59. what might one expect to find on a UA of a pt with NS?
60. what might one expect to find on a chem screen of a pt with NS?
61. what is the connection between nephrotic syndrome and hyperlipidemia?
62. what might be a finding on a CBC of a pt with NS?
63. what are some PE findings for NS?
acute glomerulonephritis...
64. what is AG? what are the hallmarks of AG?
65. what age group is most commonly affected by AG?
66. what is the etiology of AG?
67. how long after an episode of untreated strep throat might AG appear?
68. what are the signs/symptoms of AG?
69. what is the lab finding that is diagnostic for AG?
70. what might be seen in fundoscopy of a pt with AG?
71. what is the prognosis for children with AG?
chronic glomerulonephritis...
72. what is chronic glomerulonephritis?
73. what is a typical presentation for chronic glomerulonephritis?
goodpasture's syndrome...
74. which demographic is most commonly affected by goodpasture's syndrome?
75. what are the hallmark signs and symptoms of GS?
76. what are the concomitant symptoms of GS?
77. what are common lab findings for GS?
78. what is the prognosis of goodpasture's syndrome?
idiopathic primary renal hematuric/proteinuric syndrome...
79. what is IPRHPS?
80. what are some possible etiologies of IPRHPS?
81. what demographic is most closely associated with IPRHPS?
82. what might be a predisposing factor for IPRHPS?
83. what might lab findings show for IPRHPS?
84. what is the prognosis for IPRHPS?
henoch-schoenlein purpura...
85. what is HSP?
86. what is the etiology of HSP?
87. what are the signs and symptoms of HSP?
88. what are some lab findings one might expect to find with HSP?
89. what is the prognosis of HSP?
answers
1. UA, culture, CBC, chem screen.
2. BUN and creatinine: both excreted by the kidneys and therefore can be a rough indicator for glomerular function.
3. Xray, US, IVU.
4. urinary frequency, urgency, pain.
5. upper UTI.
6. renal parenchyma infection.
7. GC chlamydia.
8. early disease, excess fluid consumption in evening, BPH, interstitial cystitis.
9. in secondary, there might be a period of dryness (over 6 months)-- more likely due to psychological factors.
10. overflow (obstruction of urinary tract leads to incomplete emptying), stress (increased intraabdominal pressure), urge (decreased CNS inhibition).
11. severe, unilateral, crescendo-decrescendo pain.
12. from flank/kidney around to lower abdomen, follows course of urinary tract and sometimes radiates down further, as far as knee.
13. chills/fever
N/V
hematuria
frequency
14. unremarkable or flank tenderness.
15. hematuria with or without pyuria / bacteruria.
16. xray, US, IVU (for kidney and ureter).
17. diabetes insipidus, nephrogenic diabetes insipidus, psychogenic polydipsia.
18. in DI, the pituitary underproduces ADH, a hormone that allows for water reabsorption in the kidney- thereby leading to greater urine output.
19. a condition where the kidney's receptors for ADH are not functioning.
20. dehydration, hemorrhage, CHF.
21. VINDICATE:
vascular lesions
inflammatory lesions
neoplasm
degenerative
intoxication
congenital disorders
autoimmune (most common)
trauma
endocrine
22. MINNT:
malformations
inflammation
neoplasms
neurological disorders
trauma
23. polydipsia, chronic glomerulonephritis, diabetes inspidis/mellitus.
24. phosphates, epithelial cells, bacteria/pus.
25. B vitamins.
26. urobilinogen, bile, pyridium, carrots.
27. beets, or RBC's.
28. certain drugs (thymol, phenol, indigo blue), pseudomonas.
29. bilirubin, hemoglobin.
30. in pitting, fluid can be displaced and transient "pits" are formed. in non-pitting, edema is so severe that fluid can not be displaced.
31. trauma causes coagulation of proteins such as fibrinogen.
32. increased capillary pressure (blood clots, CHF)
increased capillary permeability (CHF)
decreased plasma proteins (burns, nephrosis, low protein intake)
lymph obstruction (lymph node removal, parasites)
33. jaundice
ascites
spider nevi
red nose
palmar erythema
34. there is a marked increase in water retention in hypothyroid myxedema.
35. trichinosis is a worm found in pork that is associated with periorbital edema.
36. rapidly increasing azotemia plus oliguria.
37. 60-70% extrinsic factors: trauma, drugs, surgery, obstruction, etc.
20-30% due to intrinsic factors: acute glomerulonephritis, SLE, goodpasture's, etc.
38. renal failure that results from inadequate renal perfusion due to factors upstream from the kidney: CHF, hemorrhage, etc.
39. decreased renal blood flow, reduced glomerular filtration, or renal obstruction.
40. bladder outlet obstruction, BPH, tumors.
41. lethargy
pulmonary edema
CHF
hypertension
oliguria
42. chem screen: steadily increasing creatinine is diagnostic. also see BUN increase.
CBC to check for anemia and infection
UA to check for RBC's, WBC's, casts.
43. normocytic normochromic.
44. oliguria / anuria for more than 3 days indicates very poor prognosis; may be fatal.
45. dialysis to allow kidney to recover, or severe limitation of fluid and electrolyte intake.
46. glomerulonephritis
cardiovascular diseases such as arteriosclerosis, HTN
SLE, diabetes
congenital abnormalities (polycystic kidney)
pyelonephritis
47. about 200,000.
48. non-specific
fatigue
nocturia
mental haze
49. muscle twitching, aches, convulsions
neuropathy
bad taste in mouth
N/V
pruritis
50. uremic frost
GI ulcers / bleeding
tissue wasting
yellow / brown skin
hypertension / CHF / pericarditis
51. chem screen would show mild / moderate elevations of BUN/creatinine over months
CBC would show normocytic / normochromic anemia,
UA might show waxy casts
52. decreased calcium, increased phosphorous, potassium, CO2.
53. kidney failure leads to improper erythropoetin production.
54. dietary and fluid intake monitoring - decrease protein and increase carb intake.
55. damage to the glomerular basement membrane that causes hyponaturia, proteinuria, hypoalbuminemia, lipiduria, hyperlipidemia.
56. males.
57. primary nephrotic disease such as immune complex nephritides or underyling systemic disease such as diabetes mellitus.
58. frothy urine
edema
muscle wasting
abdominal pain
SOB/DOE
[basement pee edema muscle stomach breath] [basement flooded with pee- use your stomach muscles and blow it out]
59. cellular elements, protein, casts.
60. hyperalbuminemia and hyperlipidemia.
61. the liver increases lipid production (cholesterol) concurrently with protein production in an attempt to normalize protein levels from the protein loss incurred in nephrotic syndrome.
62. microcytic anemia.
63. periorbital and peripheral edema
muscle wasting
parallel white lines on nails
orthostatic hypotension
64. glomerular dysfunction which causes decreased GFR and increased Na retention, leading to hematuria and hypertension.
65. young children older than 3 or young adults. rare in >50yos.
66. previous infection which causes immune complex deposition in glomeruli.
67. 1-6 weeks.
68. hematuria / oliguria
flank pain
mild edema
hypertension
69. RBC casts on a UA.
70. retinal hemorrhages.
71. 90% chance of recovery but increased risk for HTN remains throughout lifetime.
72. diffuse sclerosis of glomeruli and insidious loss of kidney function.
73. asx, with no abnormal lab results except for occasional proteinuria and hematuria. steadily increasing BUN over years.
74. young males 9:1.
75. renal and lung hemorrhage-- hemoptysis and hematuria.
76. headache, malaise, anorexia.
77. increased BUN/creatinine, RBC, protein on UA, microcytic anemia on CBC.
78. poor, patients rarely live past 20's.
79. presence of protein and RBC's in urine with no explanation.
80. glomerular IgA deposition, buerger's disease.
81. 6:1 males, children/young adult most common.
82. febrile URI.
83. hematuria, proteinuria, increased IgA.
84. many children recover but have an increased lifetime risk for hypertension and renal insufficiency.
85. similar to IPRHPS but with skin, joint, and GI involvement.
86. often follows a viral infection, acute URI.
87. symmetrically distributed purpura on extensor surfaces
arthritis
GI distress- vomiting, pain, occult blood
hematuria, proteinuria
88. increased ESR
hematuria / proteinuria
occult blood
89. self limiting in 1-6 weeks. 10-20% have chronic renal failure.
Sunday, April 11, 2010
CPD III: male genitalia
the first lecture of this semester-- male genitalia. some diagnostic notes: besides palpating all the obvious structures of the male genitalia for structural abnormalities, discharge, masses, it is also useful to palpate the lower abdominal area for hernias. if there is a mass, transillumination is useful to determine whether the mass is solid or liquid. a prostate exam is indicated if benign prostatic hypertrophy or cancer is suspected, and will elicit the sensation of needing to pee if performed correctly.
urethritis is inflammation of the urethra generally caused by infection: potentially from the bladder, kidneys, or prostate. in young patients it is more likely to be STI derived and the microorganisms most commonly implicated are GC, trich, ecoli, and ureaplasma. GC causes a thick yellow/green discharge while other types can cause a whitish mucoid discharge. a positive diagnosis for urethritis due to GC necessitates treatment via antibiotics and reporting to public health agencies due to the risk of infecting others. cystitis can present similarly to urethritis in that both have urinary frequency, urgency, and pain. it is most commonly caused by recurring chronic bacterial prostatitis and is diagnosed via dipstick and a 3 part urinalysis (3 parts to roughly determine whether the source of infection is the bladder, kidney, prostate).
lower urinary tract infections are often related to congenital structural anomalies of the genitalia that might predispose to infection via urinary stasis or aiding in incubation of bacteria. hypospadias and epispadias are abnormal openings of the urethral meatus on the underside and topside of the penis, respectively, and can both lead to greater chance of lower urinary tract infection. balanopasthitis is inflammation of the glans penis and foreskin and occurs more frequently in uncircumscribed men. phimosis is an inability to retract the foreskin of the penis.
infection from herpes simplex is a relatively common problem and is a societal challenge in that it often presents asymptomatically but is communicable via skin contact. if symptoms do appear, they can appear 3-14 days after the initial exposure to the virus and generally manifest as painful, itchy vesicles on the head or shaft of the penis, which then disappear in 3-5 days. recurrences can occur, on average 4 times a year and are much milder than the initial onset of symptoms. HSV infections are diagnosed via the TZANK smear and treated with valtrex/lysine in the allopathic world and lauric acid in the naturopathic world.
infection from HPV, in particular strains 6 and 11, can cause genital warts after a latent period of months to years. they are highly communicable via sexual contact (60% likelihood of transmission per sexual encounter) and manifest as multiple soft, raised, painless, pruritic masses in various areas.
erythroplasia of queyrat is a premalignant lesion on the glans or the corona of the penis and appears as a well circumscribed red/velvety area. the treatment is generally surgical removal. priapism is prolonged, often painful erection in the absence of sexual stimulation that may occur from certain systemic conditions such as sickle cell anemia, pelvic tumors or infections, recreational drug use. it is treated by cold compresses to reduce blood flow to the area. peyronie's disease is a distortion or deviation of the penis caused by hardening of the corpus cavernosa. the biggest concern with this disease is that it makes intercourse virtually impossible. it is treated as a connective tissue disorder.
there are a number of conditions that might produce painless scrotal masses. transillumination is a useful technique to determine whether the mass is filled with serous fluid, blood, or other substances-- a hematocele is a mass filled with blood secondary to trauma that will not transilluminate, while a hydrocele is a mass filled with serous fluid that will transilluminate. scrotal edema might occur in patients who have systemic edema as in RCHF. varicoceles of the panpiniform plexus might occur, causing a dragging sensation in the patient and feeling like a "bag of worms" upon PE.
testicular torsion is a twisting of the testes within the scrotal sac that leads to a torsion of the epididymis, leading to severe unilateral pain. it can affect young boys (10-16) as well as adults, and can be due to congenital defects, undescended testicles, sexual arousal / activity, trauma, among other factors. patients who present with this might have experienced similar pain in the past that represents torsion and detorsion of the testicle. it is diagnosed by doppler and PE, which might show a negative prehn's sign- lifting the testicle provides no relief of pain.
a positive prehn's sign would indicate epididymitis, inflammation of the epididymis due to reflux of urine or infection via lymphatics (again, source of infection is from kidneys, prostate, bladders). patients with acute epididymitis present with severe scrotal pain and tenderness that can radiate along the spermatic cord and to the flank. the likely infectious agent for patients under 35 is GC / chlamydia and for over 35, e. coli. a CBC might show leukocytosis and a dipstick might show bacteruria and pyuria. chronic epididymitis might result after repeated episodes of acute epididymitis, and differs in presentation from AE in that there is swelling and thickening of the scrotum but not pain.
cryptorchidism is a condition that involves undescended testicles, which can be in a variety of locations. the "true" variant is in the abdomen, "incomplete" in the inguinal canal, "ectopic" is outside of the normal course of descent", and "hypermobile" is the most common, where the testicle descends and retracts from the scrotum to the inguinal canal. if untreated, it may lead to failure of spermatogenesis from improper temperature regulation and an increased cancer risk as well. it is diagnosed by PE, with some help from valsalva to determine whether the testicle can retract or not. a common treatment given to aid in the normal descent of the testes is HCG.
tumors can also develop in the scrotum, generally of the types seminoma, mixed cell, teratoma, and embryonal carcinoma. they will present as a firm, smooth, non tender mass that does not transilluminate. labs might show increased AFP, HCG, LDH. those with cryptorchidism have a much greater chance to develop scrotal tumors, and blacks/asians have a lower chance.
some notes on diagnosis of prostate conditions: normal size is 4cm by 4cm and normal consistency is rubbery. palpation is done by a digital rectal exam, which is contraindicated in acute prostatitis due to risk of spreading infection. if the medial sulcus is absent upon palpation, this indicates prostatic hypertrophy. prostatic symptoms can be grouped into two categories: obstructive result from swelling of the prostate and result in difficulty urinating, and irritative result from infection or inflammation and result in urgency, dysuria, discomfort. elevated PSA levels are used to indicate damage to the prostate, although this test has a high possibility for false negatives.
acute bacterial prostatitis is an obstruction of the urethra distal to the prostate and is generally due to ecoli, klebsiella, enterococcus, or pseudomonas. it manifests with symptoms of an infection (fever, etc.) plus a host of urinary symptoms including dysuria, frequency, urgency, possibly nocturia and hematuria. it might also present with low back and perianal pain. PE would reveal a swollen, warm, firm prostate, and copious discharge would follow exam. CBC would show leukocytosis / left shift, dipstick would show leukocytes and bacteria, and culture of prostatic secretions would reveal presence of bacteria. chronic bacterial prostatitis presents similarly, but slightly more "toned down"-- but more urgent that urethritis, according to dr. thom. it is diagnosed by prostatic secretion (presence of WBC, bacterial culture), and the three glass method.
benign prostatic hypertrophy is an enlargement of the periurethral glands and stroma that results in obstructive symptoms such as frequency, urgency, nocturia. if obstruction is severe enough, it can eventually lead to renal failure. PE might result in an enlarged, boggy prostate with an absence of a median furrow. labs might show increased BUN/creatinine levels, leukocytosis, and increased PSA, although these might be elevated falsely due to the manual exam itself. conventionally, hypertrophied prostate may be alleviated by surgical removal of hypertrophied parts, although this is generally only a short term solution. dr. thom advocates the use of hot/cold hydrotherapy as an effective treatment for most prostate conditions.
finally, adenocarcinoma is cancer of the prostate which is more likely to occur with old age, african american race, obesity, increased testosterone levels. it can be asymptomatic, or have gradually developing obstructive symptoms- as well as bone pain from metastasis, commonly to the hip. diagnosis is by palpation of a stony, hard mass with irregular nodules, and can be confirmed with biopsy. elevated total PSA levels can aid in diagnosis and higher proportion of free PSA level is an indicator of better prognosis. alk phos and acid phosphatase levels may also be elevated.
questions
physical exam...
1. what are the structures that require palpation in a male genitalia exam?
2. what is a useful diagnostic technique for determining the structure of abnormal masses in the male genital region?
3. what are the two most common prostate problems requiring a prostate exam?
4. what sensation will the patient feel if the prostate is properly palpated?
urethritis...
5. what are 3 potential sources of infection that may cause urethritis?
6. describe the typical presentation of a patient with urethritis.
7. what is the most likely etiology of urethritis for a young and old patient?
8. if the etiology is infection, what are the most likely microorganisms for urethritis?
9. what is the quality of the discharge in urethritis?
10. what are some ddx's for urethritis?
11. what is the treatment for infectious urethritis?
cystitis...
12. what is the most common cause of cystitis?
13. what are the symptoms of cystitis?
14. how is cystitis diagnosed?
lower urinary infections and congenital anomalies...
15. what is epispadias?
16. what is a common complication of epispadias and why?
17. what is hypospadias?
18. what is balanopasthitis?
19. what is a predisposing factor for balanopasthitis?
20. what is phimosis?
herpes simplex infections...
21. when do symptoms of HSV infections appear?
22. what is the typical presentation for symptomatic HSV infections?
23. compare the severity of recurrence of HSV infections vs. the original infection.
24. on average, how many recurrences a year do patients with HSV infection have?
25. how are HSV infections diagnosed?
26. what are the allopathic and naturopathic treatments for HSV?
genital warts...
27. what is the most common cause of genital warts?
28. what is the variant of [question 27] that causes most cases of genital warts?
29. describe the pathogenesis of genital warts.
30. describe the symptom picture of a patient with genital warts.
31. how long after exposure to [question 27] does it take for symptoms to appear?
erythroplasia of queyrat...
32. what is erythroplasia of queyrat?
33. what is the appearance of erythroplasia of queyrat?
34. what is the treatment for erythroplasia of queyrat?
priapism...
35. what is priapism?
36. what is the etiology of priapism?
37. what is the treatment goal for priapism?
peyronie's disease...
38. what is peyronie's disease?
39. what is the biggest concern with peyronie's disease?
40. what is the treatment strategy for peyronie's disease?
painless scrotal masses...
41. what is a hematocele? how is it diagnosed?
42. what is a hydrocele and how is it diagnosed?
43. what are acute hydroceles from and when do they usually occur?
44. when do chronic hydroceles usually occur?
45. when might one see scrotal edema?
46. what is the diagnostic sign for varicoceles?
47. what is the sensation for a patient with varicoceles?
48. what is a spermatocele?
testicular torsion...
49. what is the typical age for testicular torsion?
50. what are some etiologies for testicular torsion?
51. describe the typical symptom picture for testicular torsion.
52. what is a common finding for the history of a patient with testicular torsion?
53. what are some concomitant symptoms in testicular torsion?
54. what is a PE test useful to diagnose testicular torsion?
55. diagnosis of testicular torsion...
epididymitis...
56. what is the mechanism for pathogenesis of acute epididymitis?
57. what is the most likely etiology of acute epididymitis for patients under and over 35?
58. what are some factors that can trigger the onset of symptoms for AE?
59. what are the signs and symptoms of AE?
60. what are the labs used to diagnose AE and what are their findings?
cryptorchidism...
61. what are the different variants of cryptorchidism? which is the most common?
62. if untreated, cryptorchidism may lead to...
63. what is a PE test that can differentiate between types of cryptorchidism?
64. what is one hormonal treatment for cryptorchidism?
65. what is the treatment for retractile cryptorchidism for pre-pubescent boys?
scrotal tumors...
66. what are the most common types of scrotal tumors?
67. which demographic groups have a lower incidence of scrotal tumors?
68. what is a factor that increases the risk for scrotal tumors?
69. what are the signs and symptoms for scrotal tumors?
70. labs for ST's might show...
71. what is the prognosis for a seminoma?
prostate conditions diagnosis...
72. describe "obstructive symptoms" related to prostate.
73. how might obstructive symptoms be related to low energy?
74. what are "irritative symptoms" and what are they caused by?
75. which conditions can result in both irritative and obstructive symptoms?
76. what is the average size of the prostate?
77. what might one notice upon palpation of a hypertrophied prostate?
78. what might a "mushy" consistency indicate?
79. what might an "indurated" consistency indicate?
80. what might a "stony hard" consistency indicate?
81. when might a digital rectal exam be contraindicated and why?
82. what do elevated PSA levels indicate?
prostatitis...
83. what is ABP and what is it generally due to?
84. what are the signs and symptoms of ABP?
85. what are the PE findings for ABP?
86. what are some labs that might aid in the diagnosis of ABP?
87. compare the presentation of chronic bacterial prostatitis with ABP and urethritis.
88. describe the symptom picture of a patient with chronic bacterial prostatitis.
89. how is CBP diagnosed?
90. what is chronic non bacterial prostatitis?
91. what is the characteristic symptom for chronic non-bacterial prostatitis?
benign prostatic hypertrophy...
92. when is BPH likely to occur?
93. what are the structures affected in BPH?
94. describe the symptom picture of a patient with BPH.
95. what is a complication of BPH?
96. what are the PE findings for BPH?
97. what are the lab findings for BPH?
98. what is an important factor to consider regarding the PSA test?
99. what is a naturopathic treatment for BPH?
adenocarcinoma of the prostate...
100. what is the prognosis for adenocarcinoma of the prostate?
101. what are some risk factors for adenocarcinoma of the prostate?
102. what are the signs / symptoms for A of P?
103. what are the PE findings for A of P?
104. how is a definitive diagnosis for A of P made?
105. what is the relationship between age of diagnosis and prognosis?
106. what is the relationship between PSA levels and prognosis?
107. what are the labs used to diagnose adenocarcinoma of the prostate?
answers
1. penis, glans, testes, lower abdominal wall, epididymis.
2. transillumination.
3. BPH and cancer.
4. the urge to pee.
5. kidneys, bladders, prostate.
6. urinary urgency, frequency, pain, discharge.
7. young: STD. old: BPH or prostate issue.
8. GC, e.coli, trich, ureaplasma.
9. yellow/green, purulent in GC. whitish mucoid in non-specific.
10. congenital anomalies or urinary tract obstruction that cause urinary stasis, or bladder cancer.
11. antibiotics because of the risk of spreading.
12. chronic bacterial prostatitis.
13. frequency, urgency, dysuria, low back pain, hematuria.
14. midstream urinalysis, dipstick, urine culture.
15. congenitally displaced urethral meatus on dorsal side of the penis.
16. infection due to urinary stasis.
17. same as urethral meatus on the ventral side of the penis.
18. inflammation of the glans penis and foreskin.
19. uncircumcision.
20. inability retract foreskin of penis.
21. 3-14 days after infection.
22. itchy and painful vesicles on the head or shaft of penis that heal in 3-5 days.
23. recurrence is generally milder and shorter.
24. four a year.
25. TZANK smear.
26. allopathic: valtrex, lysine. naturopathic: lauric acid.
27. HPV.
28. strains 6 and 11, low risk for developing cancer.
29. viral particles penetrate the skin and mucosal surfaces of the genital area via micro-abrasions acquired through sexual contact.
30. soft, raised masses that are generally painless and pruritic.
31. months to years.
32. a premalignant lesion on the glans or the corona.
33. well circumscribed red/velvet area.
34. surgical removal.
35. prolonged erection not related to sexual stimulation.
36. idiopathic in 1/3, 2/3 related to other systemic conditions (sickle cell, pelvic tumors, infections, drugs)
37. reduce blood flow to the area via cold compresses.
38. hardening of the corpus cavernosa which results in distortion or deflection of the penis.
39. inability for intercourse.
40. treat as any other connective tissue disorder.
41. blood filled mass in the scrotum from trauma that does not transilluminate.
42. serous fluid filled mass in the scrotum that transilluminates.
43. inflammation of epididymis or testes, between 2-5 years old.
44. middle aged men.
45. in patients with systemic edema: congestive heart failure, nephrotic syndrome, ascites, etc.
46. feels like a "bag of worms". does not transilluminate.
47. none or a heavy, dragging sensation.
48. cystic tumor of the epididymis containing sperm.
49. 10-16.
50. congenital anomaly, undescended testicle, sexual arousal/activity, trauma.
51. spontaneous, severe, scrotal pain.
52. similar episodes in the past that resolved spontaneously.
53. N/V
abdominal pain
fever
urinary frequency
[stomach stomach hot pee]
54. the prehn sign- if lifting the testicle does not relieve the pain, it is likely testicular torsion. if it does, it is likely epididymitis.
55. doppler to assess blood flow.
56. reflux of urine into the epididymis, or infection via lymphatics.
57. under 35: GC, chlamydia. over 35: e.coli.
58. strenuous activity, sexual activity, urethral instrumentation.
59. severe scrotal pain that can radiate up spermatic cord to flank
swelling and extreme tenderness
erythematous scrotal skin that is freely movable
fever
60. CBC might show leukocytosis, UA might show bacteruria, pyuria.
61. true, incomplete, ectopic, hypermobile- most common.
62. failure of spermatogenesis and increased cancer risk.
63. asking the patient to valsalva and feel for retraction-- indicates hypermobile type.
64. HCG.
65. wait for puberty for testicle to descend fully.
66. seminomas, mixed cell types, embryonal carcinoma, teratoma.
67. blacks and asians.
68. cryptorchidism.
69. a smooth, firm, painless enlargement that does not transilluminate.
70. increased AFP, HCG, LDH.
71. 80% 5 year survival.
72. swelling of prostate leads to obstruction of urethra leads to difficulty urinating.
73. the nocturia that might result can lead to a decreased quality of sleep.
74. irritation of the prostate rather than swelling, leads to urgency, dysuria, perineal discomfort.
75. BPH, chronic prostatitis.
76. 4cm by 4cm.
77. absence of the medial sulcus palpating east-west, larger size palpating north-south.
78. congestion from lack of intercourse or infection.
79. nodules from infection.
80. tumor.
81. acute prostatitis, because it might spread the infection.
82. damage to the epithelium of the vasculature of the prostate, from cancer, infection, infarction, or trauma.
83. obstruction of the urethra distal to the prostate, generally from infection by e.coli, klebsiella, enterococcus, pseudomonas.
84. that of any infection (fever etc) plus
frequency, urgency, dysuria, nocturia
lower back and perianal pain
arthralgia / myalgia
85. warm, tender, firm, swollen prostate. copious discharge after exam.
86. CBC might show leukocytosis with left shift. dipstick might show leukocytes and bacteria. culture of prostatic secretions might show increased bacteria.
87. more urgent than urethrtitis, more toned down than ABP.
88. many of the same symptoms as ABP. may also include intense local discomfort in the scrotum, severe tenderness to palpation.
89. WBC's in prostatic secretions, "three glass method", bacterial culture.
90. inflammation of the prostate not overtly related to bacterial infection, although some connection to chlamydia might exist. more common than chronic bacterial.
91. milky white discharge.
92. over 70yo.
93. peri-urethral glands and stroma.
94. obstructive symptoms. frequency, urgency, nocturia.
95. renal failure if obstruction is severe enough.
96. enlarged, boggy, spongy, maybe lumpy. loss of median furrow.
97. increased BUN/creatinine, leukocytosis, elevation of PSA.
98. the marked increased after a manual exam.
99. hydrotherapy.
100. 97% 5 year survival.
101. old age
african american
positive family history
increased testosterone levels
high fat/low fiber diet
obesity
102. asymptomatic, or gradually developing obstructive symptoms
bone pain from metastasis
103. stony hard mass with irregular nodules.
104. biopsy.
105. the older age the diagnosis is made, the less likely it is that the patient will die from it.
106. higher free PSA levels correlate with lower chance for cancer.
107. elevated total PSA, alk phos (if spread to bone), acid phosphatase.
urethritis is inflammation of the urethra generally caused by infection: potentially from the bladder, kidneys, or prostate. in young patients it is more likely to be STI derived and the microorganisms most commonly implicated are GC, trich, ecoli, and ureaplasma. GC causes a thick yellow/green discharge while other types can cause a whitish mucoid discharge. a positive diagnosis for urethritis due to GC necessitates treatment via antibiotics and reporting to public health agencies due to the risk of infecting others. cystitis can present similarly to urethritis in that both have urinary frequency, urgency, and pain. it is most commonly caused by recurring chronic bacterial prostatitis and is diagnosed via dipstick and a 3 part urinalysis (3 parts to roughly determine whether the source of infection is the bladder, kidney, prostate).
lower urinary tract infections are often related to congenital structural anomalies of the genitalia that might predispose to infection via urinary stasis or aiding in incubation of bacteria. hypospadias and epispadias are abnormal openings of the urethral meatus on the underside and topside of the penis, respectively, and can both lead to greater chance of lower urinary tract infection. balanopasthitis is inflammation of the glans penis and foreskin and occurs more frequently in uncircumscribed men. phimosis is an inability to retract the foreskin of the penis.
infection from herpes simplex is a relatively common problem and is a societal challenge in that it often presents asymptomatically but is communicable via skin contact. if symptoms do appear, they can appear 3-14 days after the initial exposure to the virus and generally manifest as painful, itchy vesicles on the head or shaft of the penis, which then disappear in 3-5 days. recurrences can occur, on average 4 times a year and are much milder than the initial onset of symptoms. HSV infections are diagnosed via the TZANK smear and treated with valtrex/lysine in the allopathic world and lauric acid in the naturopathic world.
infection from HPV, in particular strains 6 and 11, can cause genital warts after a latent period of months to years. they are highly communicable via sexual contact (60% likelihood of transmission per sexual encounter) and manifest as multiple soft, raised, painless, pruritic masses in various areas.
erythroplasia of queyrat is a premalignant lesion on the glans or the corona of the penis and appears as a well circumscribed red/velvety area. the treatment is generally surgical removal. priapism is prolonged, often painful erection in the absence of sexual stimulation that may occur from certain systemic conditions such as sickle cell anemia, pelvic tumors or infections, recreational drug use. it is treated by cold compresses to reduce blood flow to the area. peyronie's disease is a distortion or deviation of the penis caused by hardening of the corpus cavernosa. the biggest concern with this disease is that it makes intercourse virtually impossible. it is treated as a connective tissue disorder.
there are a number of conditions that might produce painless scrotal masses. transillumination is a useful technique to determine whether the mass is filled with serous fluid, blood, or other substances-- a hematocele is a mass filled with blood secondary to trauma that will not transilluminate, while a hydrocele is a mass filled with serous fluid that will transilluminate. scrotal edema might occur in patients who have systemic edema as in RCHF. varicoceles of the panpiniform plexus might occur, causing a dragging sensation in the patient and feeling like a "bag of worms" upon PE.
testicular torsion is a twisting of the testes within the scrotal sac that leads to a torsion of the epididymis, leading to severe unilateral pain. it can affect young boys (10-16) as well as adults, and can be due to congenital defects, undescended testicles, sexual arousal / activity, trauma, among other factors. patients who present with this might have experienced similar pain in the past that represents torsion and detorsion of the testicle. it is diagnosed by doppler and PE, which might show a negative prehn's sign- lifting the testicle provides no relief of pain.
a positive prehn's sign would indicate epididymitis, inflammation of the epididymis due to reflux of urine or infection via lymphatics (again, source of infection is from kidneys, prostate, bladders). patients with acute epididymitis present with severe scrotal pain and tenderness that can radiate along the spermatic cord and to the flank. the likely infectious agent for patients under 35 is GC / chlamydia and for over 35, e. coli. a CBC might show leukocytosis and a dipstick might show bacteruria and pyuria. chronic epididymitis might result after repeated episodes of acute epididymitis, and differs in presentation from AE in that there is swelling and thickening of the scrotum but not pain.
cryptorchidism is a condition that involves undescended testicles, which can be in a variety of locations. the "true" variant is in the abdomen, "incomplete" in the inguinal canal, "ectopic" is outside of the normal course of descent", and "hypermobile" is the most common, where the testicle descends and retracts from the scrotum to the inguinal canal. if untreated, it may lead to failure of spermatogenesis from improper temperature regulation and an increased cancer risk as well. it is diagnosed by PE, with some help from valsalva to determine whether the testicle can retract or not. a common treatment given to aid in the normal descent of the testes is HCG.
tumors can also develop in the scrotum, generally of the types seminoma, mixed cell, teratoma, and embryonal carcinoma. they will present as a firm, smooth, non tender mass that does not transilluminate. labs might show increased AFP, HCG, LDH. those with cryptorchidism have a much greater chance to develop scrotal tumors, and blacks/asians have a lower chance.
some notes on diagnosis of prostate conditions: normal size is 4cm by 4cm and normal consistency is rubbery. palpation is done by a digital rectal exam, which is contraindicated in acute prostatitis due to risk of spreading infection. if the medial sulcus is absent upon palpation, this indicates prostatic hypertrophy. prostatic symptoms can be grouped into two categories: obstructive result from swelling of the prostate and result in difficulty urinating, and irritative result from infection or inflammation and result in urgency, dysuria, discomfort. elevated PSA levels are used to indicate damage to the prostate, although this test has a high possibility for false negatives.
acute bacterial prostatitis is an obstruction of the urethra distal to the prostate and is generally due to ecoli, klebsiella, enterococcus, or pseudomonas. it manifests with symptoms of an infection (fever, etc.) plus a host of urinary symptoms including dysuria, frequency, urgency, possibly nocturia and hematuria. it might also present with low back and perianal pain. PE would reveal a swollen, warm, firm prostate, and copious discharge would follow exam. CBC would show leukocytosis / left shift, dipstick would show leukocytes and bacteria, and culture of prostatic secretions would reveal presence of bacteria. chronic bacterial prostatitis presents similarly, but slightly more "toned down"-- but more urgent that urethritis, according to dr. thom. it is diagnosed by prostatic secretion (presence of WBC, bacterial culture), and the three glass method.
benign prostatic hypertrophy is an enlargement of the periurethral glands and stroma that results in obstructive symptoms such as frequency, urgency, nocturia. if obstruction is severe enough, it can eventually lead to renal failure. PE might result in an enlarged, boggy prostate with an absence of a median furrow. labs might show increased BUN/creatinine levels, leukocytosis, and increased PSA, although these might be elevated falsely due to the manual exam itself. conventionally, hypertrophied prostate may be alleviated by surgical removal of hypertrophied parts, although this is generally only a short term solution. dr. thom advocates the use of hot/cold hydrotherapy as an effective treatment for most prostate conditions.
finally, adenocarcinoma is cancer of the prostate which is more likely to occur with old age, african american race, obesity, increased testosterone levels. it can be asymptomatic, or have gradually developing obstructive symptoms- as well as bone pain from metastasis, commonly to the hip. diagnosis is by palpation of a stony, hard mass with irregular nodules, and can be confirmed with biopsy. elevated total PSA levels can aid in diagnosis and higher proportion of free PSA level is an indicator of better prognosis. alk phos and acid phosphatase levels may also be elevated.
questions
physical exam...
1. what are the structures that require palpation in a male genitalia exam?
2. what is a useful diagnostic technique for determining the structure of abnormal masses in the male genital region?
3. what are the two most common prostate problems requiring a prostate exam?
4. what sensation will the patient feel if the prostate is properly palpated?
urethritis...
5. what are 3 potential sources of infection that may cause urethritis?
6. describe the typical presentation of a patient with urethritis.
7. what is the most likely etiology of urethritis for a young and old patient?
8. if the etiology is infection, what are the most likely microorganisms for urethritis?
9. what is the quality of the discharge in urethritis?
10. what are some ddx's for urethritis?
11. what is the treatment for infectious urethritis?
cystitis...
12. what is the most common cause of cystitis?
13. what are the symptoms of cystitis?
14. how is cystitis diagnosed?
lower urinary infections and congenital anomalies...
15. what is epispadias?
16. what is a common complication of epispadias and why?
17. what is hypospadias?
18. what is balanopasthitis?
19. what is a predisposing factor for balanopasthitis?
20. what is phimosis?
herpes simplex infections...
21. when do symptoms of HSV infections appear?
22. what is the typical presentation for symptomatic HSV infections?
23. compare the severity of recurrence of HSV infections vs. the original infection.
24. on average, how many recurrences a year do patients with HSV infection have?
25. how are HSV infections diagnosed?
26. what are the allopathic and naturopathic treatments for HSV?
genital warts...
27. what is the most common cause of genital warts?
28. what is the variant of [question 27] that causes most cases of genital warts?
29. describe the pathogenesis of genital warts.
30. describe the symptom picture of a patient with genital warts.
31. how long after exposure to [question 27] does it take for symptoms to appear?
erythroplasia of queyrat...
32. what is erythroplasia of queyrat?
33. what is the appearance of erythroplasia of queyrat?
34. what is the treatment for erythroplasia of queyrat?
priapism...
35. what is priapism?
36. what is the etiology of priapism?
37. what is the treatment goal for priapism?
peyronie's disease...
38. what is peyronie's disease?
39. what is the biggest concern with peyronie's disease?
40. what is the treatment strategy for peyronie's disease?
painless scrotal masses...
41. what is a hematocele? how is it diagnosed?
42. what is a hydrocele and how is it diagnosed?
43. what are acute hydroceles from and when do they usually occur?
44. when do chronic hydroceles usually occur?
45. when might one see scrotal edema?
46. what is the diagnostic sign for varicoceles?
47. what is the sensation for a patient with varicoceles?
48. what is a spermatocele?
testicular torsion...
49. what is the typical age for testicular torsion?
50. what are some etiologies for testicular torsion?
51. describe the typical symptom picture for testicular torsion.
52. what is a common finding for the history of a patient with testicular torsion?
53. what are some concomitant symptoms in testicular torsion?
54. what is a PE test useful to diagnose testicular torsion?
55. diagnosis of testicular torsion...
epididymitis...
56. what is the mechanism for pathogenesis of acute epididymitis?
57. what is the most likely etiology of acute epididymitis for patients under and over 35?
58. what are some factors that can trigger the onset of symptoms for AE?
59. what are the signs and symptoms of AE?
60. what are the labs used to diagnose AE and what are their findings?
cryptorchidism...
61. what are the different variants of cryptorchidism? which is the most common?
62. if untreated, cryptorchidism may lead to...
63. what is a PE test that can differentiate between types of cryptorchidism?
64. what is one hormonal treatment for cryptorchidism?
65. what is the treatment for retractile cryptorchidism for pre-pubescent boys?
scrotal tumors...
66. what are the most common types of scrotal tumors?
67. which demographic groups have a lower incidence of scrotal tumors?
68. what is a factor that increases the risk for scrotal tumors?
69. what are the signs and symptoms for scrotal tumors?
70. labs for ST's might show...
71. what is the prognosis for a seminoma?
prostate conditions diagnosis...
72. describe "obstructive symptoms" related to prostate.
73. how might obstructive symptoms be related to low energy?
74. what are "irritative symptoms" and what are they caused by?
75. which conditions can result in both irritative and obstructive symptoms?
76. what is the average size of the prostate?
77. what might one notice upon palpation of a hypertrophied prostate?
78. what might a "mushy" consistency indicate?
79. what might an "indurated" consistency indicate?
80. what might a "stony hard" consistency indicate?
81. when might a digital rectal exam be contraindicated and why?
82. what do elevated PSA levels indicate?
prostatitis...
83. what is ABP and what is it generally due to?
84. what are the signs and symptoms of ABP?
85. what are the PE findings for ABP?
86. what are some labs that might aid in the diagnosis of ABP?
87. compare the presentation of chronic bacterial prostatitis with ABP and urethritis.
88. describe the symptom picture of a patient with chronic bacterial prostatitis.
89. how is CBP diagnosed?
90. what is chronic non bacterial prostatitis?
91. what is the characteristic symptom for chronic non-bacterial prostatitis?
benign prostatic hypertrophy...
92. when is BPH likely to occur?
93. what are the structures affected in BPH?
94. describe the symptom picture of a patient with BPH.
95. what is a complication of BPH?
96. what are the PE findings for BPH?
97. what are the lab findings for BPH?
98. what is an important factor to consider regarding the PSA test?
99. what is a naturopathic treatment for BPH?
adenocarcinoma of the prostate...
100. what is the prognosis for adenocarcinoma of the prostate?
101. what are some risk factors for adenocarcinoma of the prostate?
102. what are the signs / symptoms for A of P?
103. what are the PE findings for A of P?
104. how is a definitive diagnosis for A of P made?
105. what is the relationship between age of diagnosis and prognosis?
106. what is the relationship between PSA levels and prognosis?
107. what are the labs used to diagnose adenocarcinoma of the prostate?
answers
1. penis, glans, testes, lower abdominal wall, epididymis.
2. transillumination.
3. BPH and cancer.
4. the urge to pee.
5. kidneys, bladders, prostate.
6. urinary urgency, frequency, pain, discharge.
7. young: STD. old: BPH or prostate issue.
8. GC, e.coli, trich, ureaplasma.
9. yellow/green, purulent in GC. whitish mucoid in non-specific.
10. congenital anomalies or urinary tract obstruction that cause urinary stasis, or bladder cancer.
11. antibiotics because of the risk of spreading.
12. chronic bacterial prostatitis.
13. frequency, urgency, dysuria, low back pain, hematuria.
14. midstream urinalysis, dipstick, urine culture.
15. congenitally displaced urethral meatus on dorsal side of the penis.
16. infection due to urinary stasis.
17. same as urethral meatus on the ventral side of the penis.
18. inflammation of the glans penis and foreskin.
19. uncircumcision.
20. inability retract foreskin of penis.
21. 3-14 days after infection.
22. itchy and painful vesicles on the head or shaft of penis that heal in 3-5 days.
23. recurrence is generally milder and shorter.
24. four a year.
25. TZANK smear.
26. allopathic: valtrex, lysine. naturopathic: lauric acid.
27. HPV.
28. strains 6 and 11, low risk for developing cancer.
29. viral particles penetrate the skin and mucosal surfaces of the genital area via micro-abrasions acquired through sexual contact.
30. soft, raised masses that are generally painless and pruritic.
31. months to years.
32. a premalignant lesion on the glans or the corona.
33. well circumscribed red/velvet area.
34. surgical removal.
35. prolonged erection not related to sexual stimulation.
36. idiopathic in 1/3, 2/3 related to other systemic conditions (sickle cell, pelvic tumors, infections, drugs)
37. reduce blood flow to the area via cold compresses.
38. hardening of the corpus cavernosa which results in distortion or deflection of the penis.
39. inability for intercourse.
40. treat as any other connective tissue disorder.
41. blood filled mass in the scrotum from trauma that does not transilluminate.
42. serous fluid filled mass in the scrotum that transilluminates.
43. inflammation of epididymis or testes, between 2-5 years old.
44. middle aged men.
45. in patients with systemic edema: congestive heart failure, nephrotic syndrome, ascites, etc.
46. feels like a "bag of worms". does not transilluminate.
47. none or a heavy, dragging sensation.
48. cystic tumor of the epididymis containing sperm.
49. 10-16.
50. congenital anomaly, undescended testicle, sexual arousal/activity, trauma.
51. spontaneous, severe, scrotal pain.
52. similar episodes in the past that resolved spontaneously.
53. N/V
abdominal pain
fever
urinary frequency
[stomach stomach hot pee]
54. the prehn sign- if lifting the testicle does not relieve the pain, it is likely testicular torsion. if it does, it is likely epididymitis.
55. doppler to assess blood flow.
56. reflux of urine into the epididymis, or infection via lymphatics.
57. under 35: GC, chlamydia. over 35: e.coli.
58. strenuous activity, sexual activity, urethral instrumentation.
59. severe scrotal pain that can radiate up spermatic cord to flank
swelling and extreme tenderness
erythematous scrotal skin that is freely movable
fever
60. CBC might show leukocytosis, UA might show bacteruria, pyuria.
61. true, incomplete, ectopic, hypermobile- most common.
62. failure of spermatogenesis and increased cancer risk.
63. asking the patient to valsalva and feel for retraction-- indicates hypermobile type.
64. HCG.
65. wait for puberty for testicle to descend fully.
66. seminomas, mixed cell types, embryonal carcinoma, teratoma.
67. blacks and asians.
68. cryptorchidism.
69. a smooth, firm, painless enlargement that does not transilluminate.
70. increased AFP, HCG, LDH.
71. 80% 5 year survival.
72. swelling of prostate leads to obstruction of urethra leads to difficulty urinating.
73. the nocturia that might result can lead to a decreased quality of sleep.
74. irritation of the prostate rather than swelling, leads to urgency, dysuria, perineal discomfort.
75. BPH, chronic prostatitis.
76. 4cm by 4cm.
77. absence of the medial sulcus palpating east-west, larger size palpating north-south.
78. congestion from lack of intercourse or infection.
79. nodules from infection.
80. tumor.
81. acute prostatitis, because it might spread the infection.
82. damage to the epithelium of the vasculature of the prostate, from cancer, infection, infarction, or trauma.
83. obstruction of the urethra distal to the prostate, generally from infection by e.coli, klebsiella, enterococcus, pseudomonas.
84. that of any infection (fever etc) plus
frequency, urgency, dysuria, nocturia
lower back and perianal pain
arthralgia / myalgia
85. warm, tender, firm, swollen prostate. copious discharge after exam.
86. CBC might show leukocytosis with left shift. dipstick might show leukocytes and bacteria. culture of prostatic secretions might show increased bacteria.
87. more urgent than urethrtitis, more toned down than ABP.
88. many of the same symptoms as ABP. may also include intense local discomfort in the scrotum, severe tenderness to palpation.
89. WBC's in prostatic secretions, "three glass method", bacterial culture.
90. inflammation of the prostate not overtly related to bacterial infection, although some connection to chlamydia might exist. more common than chronic bacterial.
91. milky white discharge.
92. over 70yo.
93. peri-urethral glands and stroma.
94. obstructive symptoms. frequency, urgency, nocturia.
95. renal failure if obstruction is severe enough.
96. enlarged, boggy, spongy, maybe lumpy. loss of median furrow.
97. increased BUN/creatinine, leukocytosis, elevation of PSA.
98. the marked increased after a manual exam.
99. hydrotherapy.
100. 97% 5 year survival.
101. old age
african american
positive family history
increased testosterone levels
high fat/low fiber diet
obesity
102. asymptomatic, or gradually developing obstructive symptoms
bone pain from metastasis
103. stony hard mass with irregular nodules.
104. biopsy.
105. the older age the diagnosis is made, the less likely it is that the patient will die from it.
106. higher free PSA levels correlate with lower chance for cancer.
107. elevated total PSA, alk phos (if spread to bone), acid phosphatase.
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