discoid lupus is a chronic skin condition that manifests as erythematous, round, scaly lesions 5-10mm in diameter that are common on the cheeks, ears, scalp, and the bridge of the nose. the etiology is unclear, though sunlight seems to be a trigger. it is more common in females 3:1, and usually appears in the third decade. other symptoms may appear such as atrophy and telangiectasias, as well as mouth ulcers in some. ddx's might include SLE, seborrheic dermatitis, rosacea, lichen planus, most of which can be ruled in or out via atrophic features or distribution of lesions on the body.
systemic lupus erythematosus (SLE) is an autoimmune disease that affects many systems of the body that is thought to involve antinuclear antibodies and a type III hypersensitivity response. it has a predilection for females and african americans and affects 1 in 2000 people. etiology is unclear, although genetic factors are presumed, and some environmental triggers have been identified, such as certain medications (procainamide, hydralazine, quinidine), sunlight, infection, silicone implants.
the most characterizing symptom for SLE is the butterfly rash across the face, although this might be absent in some patients. because SLE is a systemic disease, it can manifest in many different ways- ulcerations in the mouth / nasal cavity, xerostomia, polyserositis (inflammation of the serous membranes, leading to pleuritis / peritonitis / etc), recurrent respiratory infections, kidney failure, and very commonly, polyarthralgia that are symmetric and non deforming. diagnosis is by presence of characterizing symptoms as well as ANA tests.
scleroderma is a condition that results from abnormal fibrosis and collagen deposition. it can come in different variants; the diffuse type is more severe, rapid onset, with more internal organ involvement and widespread skin thickening. on the other hand, the CREST variant is more common and less severe-- CREST stands for calcification, raynaud's, esophageal dysfunction, sclerodactyly, and telangiectasias. patients with scleroderma might have hard, taut, shiny skin and faces that resemble mask-like textures, as well as subcutaneous calcifications. joints might have a friction rub, especially the knees. esophageal issues resulting from LES dysfunction might result in dysphagia, acid reflux, and barrett's esophagus. cardiovascular changes might include arrhythmias and pericarditis, while respiratory changes might include pleurisy, pulmonary hypertension, and dyspnea. diagnosis is made by presence of characteristic major and minor symptoms: the one major symptom is sclerotamous skin changes proximal to the MCP joints, and the minor symptoms are sclerodactyly, pulmonary fibrosis, and digital pitting scars. lab tests commonly reveal positive antibodies- ANA and anti-centromere in most cases, and anti-Scl-70 might be present in 30%, indicating pulmonary fibrosis.
polymyalgia rheumatica is a seronegative musculoskeletal condition that mainly presents as muscle pain in the neck, shoulders, or pelvic girdle muscles (as opposed to the joints). it might also result in weight loss, profound morning stiffness, fever, malaise. lab findings would be seronegative, with an increased ESR, and possibly normochromic / normocytic anemia. it is often treated with a 5 day burst of steroids, which may alleviate symptoms greatly. a severe complication is temporal arteritis, which will cause a severe headache and could ultimately lead to blindness.
polyarteritis nodosa is a vasculitis of the small and medium sized artery, with secondary ischemia of the affected tissues. it is an autoimmune condition that affects middle aged males most commonly. this condition affects the whole body and therefore has a presentation that is difficult to diagnose because it mimics many other conditions. the most common symptoms are fever, headache, weight loss, asthma, chest / abdomen pain, renal issues (hypertension, edema, failure), peripheral neuropathy. labs would reveal high WBC count, proteinuria and hematuria.
mixed connective tissue disorder (MCTD) is a combination of scleroderma, lupus, and polymyositis that mostly affects females in the 4th decade of life. it can cause: sausage digits and lupus like rashes, non deforming arthritis, muscle weakness / pain, decreased peristalsis in the esophagus, dyspnea, pulmonary hypertension, pericarditis. diagnosis is by ANA and anti-U1RNP.
ankylosing spondylitis is an inflammatory arthritis that preferentially affects males 15-30 and is fairly well localized to the lower spine, SI joints, ribcage, and eyes. it is usually made worse by prolonged rest and better by motion-- thus morning activities are particularly difficult for AS patients, who present with severe heel pain. ribcage pain might prevent full respirations and cause asthma like symptoms. uveitis might occur as well, resulting in ciliary injection and photophobia. a patient with AS will have a loss of lumbar lordosis and compensatory thoracic accentuation, stooped posture, and abnormal gait. lab findings are seronegative, elevated ESR, and positive HLA-B27. diagnosis is made by xray of the SI joints. ddx's include herniated disc and DISH syndrome.
psoriatic arthritis is a type of arthritis that affects 20% of sufferers of psoriasis, resulting in inflammation of the DIP joints, sausage digits, and nail discoloration / pitting. there are different types that vary in distribution and severity; the most common (50% of cases) are symmetrical, presenting similarly to RA. next is asymmetrical, which is milder and affects less than 3 joints at a time. lab findings are seronegative, increased ESR / CRP, may have positive HLA B27.
reiter's syndrome, aka reactive arthritis, is an arthritis that is secondary to infection such as GU infection or gastroenteritis. it affects males preferentially and seems to have the HLA B27 connection as well. main symptoms are captured by the phrase "can't see, can't pee, can't dance with me"- uveitis, urethritis (milder than that of an STD), and arthritis which is generally an asymmetric polyarthralgia of the lower extremities. severe cases will also develop back pain. RS patients may also develop mucocutaneous, painless lesions in the mouth, tongue, glans penis, and bottom of the feet, as well as hyperkeratosis on the soles of the feet and palms.
osteoarthritis is the most common connective tissue disease that is degenerative in nature: meaning RF-seronegative, non-inflammatory. if under 45, OA is associated with males and if over 55 OA is associated with females. etiological factors are varied and can include microtrauma, infection, malabsorption, genetic factors, endocrine imbalances. the cartilage of an OA patient undergoes erosion via fissuring and pitting, causing osteophytes / bone spurs to form (as adaptive physiology to prevent movement of the affected joint). common locations are the knee, hip, fingers (PIP=bouchard's nodes, DIP=heberden's nodes), spine (C5-7 and L4-5 in particular). some features distinguish OA from RA: the morning stiffness is not as bad, and OA is more of a deep, poorly localized pain. PE findings might include joint swelling / effusion / crepitus, abnormal gait / ROM / deformation, and tenderness to palpation. OA diagnosis is made definitively by xray.
infectious arthritis is arthritis secondary to an infection: in young children this is commonly caused by staph, h. flu, and in adults it is commonly caused by staph, strep, pneumonia, or gonococci. the typical presentation is rapid onset of swelling / tenderness / decreased ROM / redness of a single joint with fever and leukocytosis. the most common location is the knee, but IA often affects the hip, shoulder, wrist, and phalanges. it is diagnosed by a CBC w/ differential and a synovial fluid biopsy.
lyme disease is an infectious condition caused by borelia burgdorferi carried by deer ticks, largely in the northeast. the characteristic symptom is the bullseye lesion: erythema chronicum migrans, which appears 3-30 days after exposure. lyme disease might also affect other systems, causing neurological symptoms (meningitis or encephalitis, chorea, ataxia, peripheral neuropathy), cardiovascular symptoms (AV blocks, pericarditis, cardiomegaly), and myalgias/arthalgias (sudden swelling of a single large joint). CDC recommends a two step diagnosis process: antibody titer test, then western blot.
the last condition of this week was osteomyelitis: infection of the bone via a longstanding condition such as prostatitis, UTI, or open wound. osteomyelitis develops slowly over the course of several months and presents as severe back pain and perivertebral spasm. it is not accompanied by fever or leukocytosis, and is diagnosed by elevated ESR and xray, which would show spotty demineralization of bone.
questions
discoid lupus...
1. what etiological factor commonly precedes the initial lesions of DL?
2. what is the most common age and gender that DL affects?
3. describe the skin lesions in DL.
4. where are the body areas commonly affected in DL?
5. what is a concomitant symptom in DL?
6. are anti-DNA antibodies present or absent?
7. what are some ddx's for DL?
8. how can most of the ddx's be ruled out?
SLE overview...
9. what is SLE?
10. what are the demographic / gender groups most likely to have SLE?
11. what are three etiological categories for SLE?
12. what are some environmental triggers for SLE?
13. what are the most common drugs that are associated with SLE?
14. what is the most characterizing symptom for SLE?
SLE symptom presentation and diagnosis...
15. 40% of SLE patients have...
16. SLE patients might have ulcerations in which locations?
17. what symptoms might cause a SLE patient to be confused with sjogren's?
18. what is the most common symptom of SLE? what condition presents in a similar way?
19. how might SLE manifest in the respiratory system?
20. what are common UA findings for SLE patients?
21. which serous membranes might be affected in SLE? what is this condition called?
22. how common is raynaud's in SLE patients?
23. what is the screening test for SLE?
scleroderma overview...
24. what is scleroderma?
25. how common is scleroderma in the US? which gender is more affected?
26. how does the age of onset for scleroderma compare to SLE?
27. what is the more severe variant of scleroderma? what is it characterized by?
28. what are the hallmarks of CREST syndrome?
scleroderma presentation...
29. describe the distribution of skin changes in scleroderma.
30. describe the morphology of skin changes in scleroderma.
31. what are some other skin changes that might accompany a scleroderma patient?
32. what is a PE sign that might be picked up in the joints of a scleroderma patient?
33. what are the typical GI manifestations of scleroderma?
34. what are the cardiovascular changes in scleroderma?
35. what are the respiratory manifestations of scleroderma?
scleroderma diagnosis...
36. which lab markers are present in over 90% of scleroderma patients?
37. how common is a positive anti Scl-70 antibody and what is it associated with?
38. what is the major diagnostic criteria for scleroderma?
39. what are the three minor diagnostic criteria for scleroderma?
polymyalgia rheumatica...
40. which gender and age is more prone to developing polymyalgia rheumatica?
41. describe the distribution of pain in PR.
42. what are some concomitant symptoms in PR?
43. in the shoulder girdle, are proximal or distal muscles more likely to be affected?
44. what are the lab findings associated with polymyalgia rheumatica?
45. what is a treatment that can serve as a diagnosis for PR?
46. what is an important, severe concomitant that might result from PR?
47. what are the diagnostic criteria for [46]?
48. [46] might lead to...
49. what is the prognosis for PR?
polyarteritis nodosa...
50. what is polyarteritis nodosa?
51. which gender and age is most commonly affected by PN?
52. what is the etiology of PN?
53. why is PN so difficult to diagnose?
54. what are the most common symptoms of PN?
55. what would labs for PN reveal?
mixed connective tissue disease...
56. MCTD is a combination of...
57. which age and gender is most commonly affected by MCTD?
58. what are the dermatological manifestations of MCTD?
59. how does MCTD manifest in the joints?
60. and the muscles?
61. and the esophagus?
62. pulmonary stuff?
63. heart?
64. what are the lab findings for MCTD?
ankylosing spondylitis...
65. what is AS?
66. which gender and age is most commonly affected by AS?
67. what is a genetic marker that is often positive in AS?
68. what are the body areas commonly affected by AS?
69. describe the severity of the morning symptoms of AS.
70. how does movement / rest affect AS patients?
71. why does AS present with asthma?
72. what are the eye symptoms that AS patients present with?
73. what are the PE findings for AS?
74. what are the lab findings for AS?
75. how is diagnosis of AS confirmed?
76. what are the ddx'es for AS?
77. what are the treatment goals for AS?
psoriatic arthritis...
78. what percentage of chronic psoriasis patients develop PA?
79. what percentage of PA patients develop ankylosing spondylitis?
80. describe the distribution and morphology of PA.
81. what are the different types of PA? which is most common?
82. what are the lab findings for PA?
reiter's syndrome...
83. what is reiter's syndrome? what is it also called?
84. what are the etiological agents identified for RS?
85. what is the difference between the people prone to developing sexually transmitted vs. dysenteric RS?
86. what are the signs / symptoms of RS?
87. how does the urethritis differ from that of an STD?
88. describe the arthritis in RS.
89. what are the dermatological manifestations of RS?
osteoarthritis...
90. how common is osteoarthritis?
91. what age and gender is most commonly affected by OA?
92. what are some etiological factors for OA?
93. describe what happens to the bones and joints in OA.
94. which vertebral junctions are particularly prone to developing [93]?
95. what are the most common locations for osteoarthritis?
96. what are Heberden's and Bouchard's nodes?
97. what are the symptoms/signs that differentiate OA from RA?
98. what are some PE findings for OA?
99. how is OA diagnosed?
100. what are the ddx's for OA?
101. what are the treatment strategies for OA?
infectious arthritis...
102. what are the most likely microorganisms responsible for IA in young children?
103. what are the most likely microorganisms responsible for IA in adults?
104. what is the typical presentation of IA?
105. what are the most common locations for IA?
106. how is IA diagnosed?
lyme disease...
107. what are the infectious agents in lyme disease?
108. what is the characteristic symptom of lyme disease? when does it appear?
109. what are the neurological signs of lyme disease?
110. what are the CV symptoms of lymedisease?
111. 50% of patients with lyme disease have...
112. what is the two step diagnostic method advocated for identification of lyme disease by the CDC?
113. what are some ddx's for lyme disease?
osteomyelitis...
114. what is the etiology of osteomyelitis?
115. describe the time course of osteomyelitis.
116. what are the signs and symptoms of osteomyelitis?
117. is osteomyelitis accompanied by fever? what about leukocytosis?
118. what labs are used to diagnose osteomyelitis?
answers
1. sunlight.
2. females in 30's.
3. erythematous, round, scaly papules with follicular plugging. 5-10mm.
4. cheeks, bridge of nose, scalp, ears.
5. many mouth ulcers.
6. absent.
7. SLE
rosacea
seborrheic dermatitis
photosensitivity
lichen planus
8. via lack of atrophic features or a different distribution pattern.
9. an type III hypersensitivity response which results in immune complex deposition and antinuclear antibody formation affecting many systems of the body.
10. young females, african americans.
11. genetic predisposition (not clarified), environmental triggers, drug reactions.
12. medications
stress
sunlight
infection
silicone implants
13. procainamide, hydralazine, quinidine.
14. butterfly rash.
15. photosensitive skin eruptions.
16. oral and nasal.
17. parotid enlargement and xerostomia.
18. polyarthralgia and arthritis, similar to rheumatoid arthritis presentation.
19. recurrent respiratory infections.
20. proteinuria, hematuria, cellular elements.
21. polyserositis: pleuritis, pericarditis (and myocarditis), peritonitis.
22. 1/3.
23. ANA test, UA.
24. rare chronic disease characterized by excess collagen deposition in various tissues.
25. 300,000 in US, 4 times more likely females.
26. slightly older; 30's to 40's.
27. diffuse scleroderma, a rare variant that develops rapidly and has widespread skin thickening and greater lung / GI damage.
28. calcinosis
raynaud's
esophageal dysfunction
sclerodactyly
telangiectasia
29. most commonly on the distal portions of upper extremities, but may be all over the body.
30. taut, shiny, hyperpigmented. face becomes mask like.
31. subcutaneous calcifications and telangiectasias.
32. friction rubs over joints, especially knees.
33. esophageal dysfunction which leads to dysphagia, acid reflux, and may progress to barrett's esophagus (1/3 of patients)
34. arrythmias, abnormal EKG, pericarditis.
35. fibrosis, pulmonary hypertension, pleurisy.
36. ANA, anti centromere antibodies,
37. 30%, pulmonary fibrosis.
38. scleromatous skin changes proximal to the MCP joint.
39. digital pitting scars, sclerodactyly, bibasilar pulmonary fibrosis.
40. females (2:1) over 50.
41. symmetric distribution in neck, shoulder, and pelvic girdle muscles.
42. morning stiffness
weight loss
fever, malaise
43. proximal.
44. seronegative, ESR over 40, may have normochromic/normocytic anemia.
45. if a 5 day burst of steroids helps, it is likely PR.
46. temporal arteritis.
47. age over 50, new onset, temporal artery abnormality (tenderness or diminished pulse), elevated ESR, biopsy.
48. blindness.
49. 90% recover within 2 years.
50. vasculitis of the small and medium arteries and secondary ischemia of the affected tissues.
51. middle aged males.
52. autoimmune/hyperimmune response.
53. because it mimics many other diseases and has a insidious onset.
54. fever
abdominal pain
peripheral neuropathy
renal hypertension / edema / failure
angina / MI / CV issues
weight loss
headache
asthma
55. high WBC's, proteinuria, hematuria.
56. scleroderma, lupus, polymyositis.
57. 80% females in 4th decade.
58. sausage fingers, lupus like rashes.
59. non deforming arthritis.
60. weakness, maybe tenderness.
61. decreased peristalsis.
62. dyspnea, hypertension.
63. pericarditis.
64. high ANA and high titers of anti-U1RNP.
65. an inflammatory arthritis primarily affecting spine and SI joints.
66. males 3:1, 15-30 years old.
67. HLA-B27.
68. heels, spine, rib cage, eyes.
69. prolonged morning stiffness, and heel pain that causes most AS patients to not want to walk.
70. prolonged rest makes worse, movement makes stiffness better.
71. because the rib pain makes breathing difficult.
72. uveitis: ciliary injection, photophobia.
73. reduced lumber range of motion, accentuated thoracic curve, loss of lumbar lordosis, stooped posture, abnormal gait, shallow breathing.
74. seronegative, increased ESR, positive HLA-B27.
75. xray of SI joints.
76. herniated disk, DISH syndrome.
77. prevent joint fusion via regular movement and stretching.
78. 20%.
79. 1/3.
80. DIP's, sausage digits, nail pitting and discoloration.
81. symmetric, asymmetric, arthritis mutilans, spondylitis, DIP predominant. symmetric accounts for 50%.
82. seronegative, increased ESR, CRP, may have positive HLA B-27.
83. reactive arthritis; arthritis that develops secondary to an infection elsewhere in the body such as a GU infection or gastroenteritis.
84. HLA-B27, male gender, white race (connected to HLA-B27)
85. sexually transmitted: young men, chlamydia trachomatis. dysenteric: women, children, elderly. shigella, salmonella, campylobacter, yersinia.
86. uveitis, urethritis, arthritis. [can't see, can't pee, can't dance with me]
87. less painful / more mild.
88. asymmetric polyarthritis that affects larger joints of lower extremities and toes.
89. mucocutaneous lesions- small, painless ulcers in the mouth, tongue, glans penis, bottom of feet. may also develop hyperkeratotic lesions on soles of feet and palms.
90. most common connective tissue disease.
91. under 45: males more affected. over 55: females more affected.
92. genetic, autointoxication, malabsorption, endocrine imbalance, microtrauma, surgery.
93. pitting/fissuring erosions of articular cartilage, formation of osteophytes / bone spurs.
94. C6-C7, L4-L5.
95. knee, hip, fingers.
96. H: DIP involvement. B: PIP involvement.
97. morning stiffness not as bad
deep, poorly localized pain
better with rest, worse with use
might have night time pain
98. tenderness to palpation
joint swelling / effusion / crepitus
ROM limitation / abnormal gait
valgus / varus deformities
99. lab tests are largely uninformative (may have increased ESR). diagnosis by xray.
100. psoriatic arthritis
ankylosing spondylitis
reiter's
RA
101. largely palliation of pain, although glucosamine sulfate can help if taken for a long time. exercise is the most helpful.
102. staph, h influenza, gram- bacilli. [staff, flu, negative]
103. staph, strep, pneumonia, gonococci. [staff, strip, new, gone]
104. rapid onset, unilateral, single hot / swollen / painful joint with fever and decreased ROM.
105. knee, shoulder, wrist, hip, phalanges.
106. CBC with diff: leukocytosis. biopsy of synovial fluid.
107. borelia burgdorferi carried through the deer tick.
108. erythema chronicum migricans, 3-32 days after tick bite.
109. lymphocytic meningitis, encephalitis, chorea, ataxia, cranial neuritis, peripheral neuropathy.
110. AV block, pericarditis, cardiomegaly
111. myalgias/arthralgias that present as sudden swelling of a single large joint.
112. test for antibody titers, then do western blot.
113. juvenile RA
hepatitis
herpes zoster
infectious arthritis
reiter's syndrome
114. an underlying condition that makes the patient more prone to chronic infection such as an open wound, chronic prostatitis or chronic UTI's.
115. slow onset over several months.
116. severe back pain and paravertebral spasm.
117. no.
118. increased ESR and xray would show cloudy/spotty demineralization of bone.
Monday, May 24, 2010
Monday, May 10, 2010
CPD III - thyroid and parathyroid conditions
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.
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.
Wednesday, May 5, 2010
GPA prep- respiratory and HEENT
URI: upper respiratory infection caused either by bacteria or a virus, leading to congestion, sneezing, rhinorrhea, discharge, malaise. if bacterial in origin, a URI might be more likely to present with fever / chills and yellow/green mucopurulent discharge. if viral in origin a URI might present with clear rhinorrhea. diagnosis is by the jones criteria, rapid strep test, and microscopic smear of exudates.
asthma: can be extrinsic (allergic, to molds, pollens, etc), or intrinsic (infectious, emotional, etc.). usually results in coughing (worse at night), wheezing, dyspnea, sputum production. PE findings might include tachypnea, tachycardia, accessory muscle use, and if severe, pulsus paradoxus and muscle wasting. lung auscultation will reveal prolonged expiratory phase with expiratory wheezing, diminished breath sounds. a skin exam might also be performed to confirm signs of atopy (eczema, dermatitis).
sinusitis is an inflammation of the sinuses due to infection or allergies. it can result in a painful pressure in the sinus area from the swelling of the mucous membranes if associated with a URI. typical signs and symptoms might include swelling / tenderness over the affected sinus, malaise, toothache, severe frontal headache, swollen eyelids. on PE, one might find erythematous nasal mucosa and sinuses that do not transilluminate. labs might be useful to rule out periapical abscess (using xray) or to confirm chronic sinusitis (using CT scan).
bronchitis is an inflammation of the bronchial tree, either secondary to an infection, asthma, irritant, or primary/chronic. if infectious in origin, bronchitis is likely due to a bacterial URI, while common irritants might be organic solvents, ammonia, dust, chlorine. symptoms are similar to an infectious URI: coryza, malaise, f/c, myalgia, etc. the cough often progresses from a dry, non-productive, to a sputum producing cough. on a respiratory exam, one might hear scattered rhonchi, crackling/wheezing, moist rales.
pneumonia is an acute infection of the lung, and can be from a variety of different sources- bacterial, viral, or mycoplasmal. adults are more likely to get bacterial pneumonia, while young adults and children are more likely to get mycoplasmal or viral. risk factors include cigarette smoke, young/old age, immunocompromised, recurrent URI's, physical debilitation. patients might present with fever / chills, nausea / vomiting, pleurisy / dyspnea, productive cough with rusty colored sputum and an increased pulse and respiratory rate. a lung exam might reveal signs of lung consolidation: dullness to percussion, increased tactile fremitus, whispered pectriloquy, and bronchial breath sounds / crackles. ddx's might include bronchitis, goodpasture's, asthma, cystic fibrosis.
some notes on the different types of headaches. doing a good history is vital to determining the cause of the headache, as well as determining the location and radiation patterns. tension headaches are more likely to be described as a band-like pain around the occiput, whereas migraines are more frontal. pain around or in the eyes might be due to a cluster headache, and pain in the face is likely from trigeminal neuralgia. unilateral head pain on the side of the head could be from temporal arteritis. papilledema or A/V nicking on a fundoscopic can indicate serious conditions such as intracranial hemorrhage or malignant hypertension, respectively.
hay fever aka allergic rhinitis is inflammation of the mucosa of the eyes and nasal passageways, leading to rhinorrhea, itchy / burning eyes and nasal congestion. it is often due to seasonal allergens such as pollen and will present bilaterally. a skin test might be useful to check for signs of atopy in the form of dermatitis, etc. differentials might include sinusitis, acute rhinitis, vasomotor rhinitis, and cocaine use.
conjunctivitis is an inflammation of the conjunctiva of the eyes and can be bacterial, viral (pink eye), or allergic / irritant in nature. signs include conjunctival injection (superficial dilated vessels away from the iris), pruritis, discharge, hyperemic and swollen lids. if symptoms are bilateral, the origin is more likely to be infectious or allergic while unilateral symptoms suggest toxic/chemical/mechanical causes. a culture of secretions can be useful in differentiating the cause of conjunctivitis: bacterial related secretions would contain PMN's, viral would contain leukocytes, and allergic would contain eosinophils.
strep throat is the result of infection via type A beta-hemolytic strep. it manifests as swollen, sore throat with fever and L/A. the jones criteria, used to diagnose strep, requires at least 2 of the following: fever above 100.4F po, no cough, pseudomembrane, tonsillar exudate. strep can also be diagnosed via a rapid strep test or throat culture. ddx's might include pharyngitis, mono, peritonsilar abscess, and diptheria.
vertigo is more of a symptom and can be due to several different causes, including benign paroxysmal positional vertigo, meniere's vestibular neuronitis, and other CNS disorders. episodic vertigo is more likely to be BPPV, while vertigo that lasts for hours / days is more likely to be meniere's or vestibular neuronitis. vertigo can also be associated with symptoms such as nausea / vomiting, tinnitus, and nystagmus-- which if unilateral and horizontal indicates benign causes and if variable indicates CNS disorders.
questions
URI...
1. what is the etiology of a URI?
2. what are some typical signs / symptoms of a URI?
3. what are some features that might distinguish a URI of bacterial vs. viral origin?
4. what labs should be performed for the diagnosis of a URI?
asthma...
5. what are three major features of asthma?
6. what is the difference between intrinsic and extrinsic asthma?
7. what are the major signs and symptoms of asthma?
8. what are some typical PE findings for asthma?
9. what signs might indicate a severe case of asthma?
10. what are the common findings for a lung exam on a patient with asthma?
11. why might a skin exam be performed on a patient suspected of having asthma?
sinusitis...
12. what is sinusitis?
13. what are the typical signs and symptoms of sinusitis?
14. what are some typical PE findings for sinusitis?
15. which labs might be performed to aid in a diagnosis of sinusitis?
bronchitis...
16. what is bronchitis?
17. what are the most common etiological agents for bronchitis?
18. the symptoms of infectious bronchitis are similar to...
19. describe the progression of the cough in infectious bronchitis.
20. severe cases of bronchitis might also present with...
21. what might be heard on a respiratory exam for bronchitis?
22. where in the lung might these sounds be heard?
pneumonia...
23. what is pneumonia?
24. what are three different types of pneumonia?
25. which type is most common in adults? young adults / children?
26. what are some risk factors for pneumonia?
27. what are the signs and symptoms for pneumonia?
28. what are the signs one would expect to find on a lung exam of a pneumonia patient?
29. what are some ddx's for pneumonia?
headaches...
30. what are some causes of head pain?
31. where do tension headaches usually present? how is the sensation described?
32. a frontal headache is more likely what type of headache?
33. a periorbital or deep orbital pain is most likely due to what type of headache?
34. pain in the face is likely due to...
35. unilateral head pain on the side of the head is likely due to...
36. patients with temporal arteritis might also present with what concomitant symptom?
37. what are some physical exams that one should perform on a patient that presents with head pain?
hay fever...
38. what is hay fever?
39. what are two useful questions to ask a patient suspected of hay fever?
40. what are the signs and symptoms of hay fever?
41. why might a skin test be performed in patients suspected of hay fever?
42. what are the differentials for hay fever?
conjunctivitis...
43. "pink eye" is...
44. what are the signs and symptoms of conjunctivitis?
45. what do bilateral vs. unilateral symptoms suggest about the origins of conjunctivitis?
46. what PE exams would be useful in diagnosing conjunctivitis?
47. what labs would you order with a patient suspected of conjunctivitis?
strep throat...
48. what is the etiology of strep throat?
49. what are the signs/symptoms of strep throat?
50. what are the jones criteria for diagnosing strep throat?
51. what are the lab tests used to diagnose strep throat?
52. what are the ddx's for strep throat?
vertigo...
53. episodic vertigo is more likely to be...
54. vertigo that lasts hours or days is more likely to be...
55. vertigo that is sudden onset and lasts for minutes is more likely to be...
56. what are the signs and symptoms associated with vertigo?
57. how can the type of nystagmus differentiate between potential causes of vertigo?
answers
1. viruses or bacteria invading upper respiratory tract, causing inflammation of the mucosa.
2. congestion, sneezing, rhinorrhea, post-nasal drainage, malaise.
3. bacterial more likely to have fever / chills and yellow green mucopurulent discharge. viral more likely to have clear rhinorrhea.
4. rapid strep test if jones criteria met, microscopic smear of exudates.
5. airway obstruction
inflammation
irritability / hypersensitivity
6. extrinsic is to allergy to external factors such as mold, pollen, etc. intrinsic is non allergic- from infections or emotional or other internal causes.
7. coughing, especially at night
wheezing, shortness of breath, DOE
sputum production
8. tachypnea, tachycardia, diaphoresis, wheezing, accessory muscle use.
9. weight loss, wasting, pulsus paradoxus.
10. prolonged expiratory phase, expiratory wheezing and diminished breath sounds.
11. to look for signs of atopy: dermatitis, eczema, other allergic skin conditions.
12. inflammation of the paranasal sinuses due to infection or allergy.
13. swelling / tenderness
malaise
toothache
frontal headache
swollen eyelids
14. erythematous nasal mucosa, sinuses do not transilluminate.
15. CT scan for chronic sinusitis
xray of teeth apices to rule out periapical abscess
CBC
16. an infection of the bronchial tree, either secondary to an infection, asthma, irritant, or primary / chronic.
17. infectious: bacterial URI
irritant: organic solvents, ammonia, dusts, chlorine
18. infectious URI symptoms: coryza, malaise, fever/chills, myalgia, etc
19. begins as dry and non productive, then develops into a productive cough.
20. 101-102 degree fevers.
21. scattered rhonchi, crackling/wheezing, moist rales.
22. at the base for crackling / rales.
23. infection of the lung.
24. bacterial, viral, mycoplasma.
25. bacterial most common in adults, mycoplasma in young adults and children.
26. immunocompromised
young or old age
recurrent URI's
cigarette smoke
physical debilitation
27. fever / chills
pleurisy / dyspnea
productive cough with rusty sputum
tachycardia, tachypnea
N/V
malaise / myalgia
28. increased tactile fremitus
dullness to percussion
bronchial breath sounds
whispered pectriloquy
crackles
[touch dull bronchial whisper crackle]
[fremitus dullness whisper bronchial crackles] [touch the dull whisker to hear the bronchial crackles]
29. bronchitis
asthma
cystic fibrosis
goodpasture's
30. vasomotor instability
muscle tension
hypoglycemia
infection
trauma
mass lesion
cerebral hemorrhage
31. occiput, band-like.
32. migraine
33. cluster
34. trigeminal neuralgia.
35. temporal arteritis.
36. polymyalgia rheumatica.
37. vitals, M/S, eye exam, sinsuses, neurological exam.
38. also known as allergic rhinitis; an inflammatory process involving the nasal and throat mucosa, as well as the conjunctiva in response to various allergens.
39. do your symptoms appear seasonally? are they bilateral?
40. rhinorrhea
burning, itchy, watery eyes
nasal / sinus congestion
41. to check for signs of atopy: dermatitis, eczema.
42. sinusitis, acute rhinitis, vasomotor rhinitis, cocaine use.
43. viral conjunctivitis.
44. superficial dilated vessels in conjunctiva
pruritis
discharge
hyperemia, swelling of lids
45. bilateral more likely allergic / infectious. unilateral more likely toxic/chemical/mechanical.
46. vitals, lymph nodes, EENT, (heart, lungs)
47. culture of secretion: bacterial would contain PMN's, viral would contain lymphocytes, allergic would contain eosinophils.
48. pharyngitis caused by group A beta-hemolytic streptococcus.
49. sore throat
fever
no cough
cervical L/A
injected / erythematous mucous membranes
exudate / pseudomembrane
50. fever over 100.4 po, no cough, tonsilar exudate, pseudomembrane.
51. rapid strep test and throat culture.
52. viral / bacterial pharyngitis
infectious mononucleosis
diptheria
peritonsilar abscess
53. BPPV
54. meniere's, vestibular neuronitis
55. brain or vascular disease.
56. spinning sensation/disequilibirum
nystagmus
N/V
tinnitus
57. unilateral horizontal nystagmus is more likely benign, variable nystagmus likely due to a CNS disorder.
asthma: can be extrinsic (allergic, to molds, pollens, etc), or intrinsic (infectious, emotional, etc.). usually results in coughing (worse at night), wheezing, dyspnea, sputum production. PE findings might include tachypnea, tachycardia, accessory muscle use, and if severe, pulsus paradoxus and muscle wasting. lung auscultation will reveal prolonged expiratory phase with expiratory wheezing, diminished breath sounds. a skin exam might also be performed to confirm signs of atopy (eczema, dermatitis).
sinusitis is an inflammation of the sinuses due to infection or allergies. it can result in a painful pressure in the sinus area from the swelling of the mucous membranes if associated with a URI. typical signs and symptoms might include swelling / tenderness over the affected sinus, malaise, toothache, severe frontal headache, swollen eyelids. on PE, one might find erythematous nasal mucosa and sinuses that do not transilluminate. labs might be useful to rule out periapical abscess (using xray) or to confirm chronic sinusitis (using CT scan).
bronchitis is an inflammation of the bronchial tree, either secondary to an infection, asthma, irritant, or primary/chronic. if infectious in origin, bronchitis is likely due to a bacterial URI, while common irritants might be organic solvents, ammonia, dust, chlorine. symptoms are similar to an infectious URI: coryza, malaise, f/c, myalgia, etc. the cough often progresses from a dry, non-productive, to a sputum producing cough. on a respiratory exam, one might hear scattered rhonchi, crackling/wheezing, moist rales.
pneumonia is an acute infection of the lung, and can be from a variety of different sources- bacterial, viral, or mycoplasmal. adults are more likely to get bacterial pneumonia, while young adults and children are more likely to get mycoplasmal or viral. risk factors include cigarette smoke, young/old age, immunocompromised, recurrent URI's, physical debilitation. patients might present with fever / chills, nausea / vomiting, pleurisy / dyspnea, productive cough with rusty colored sputum and an increased pulse and respiratory rate. a lung exam might reveal signs of lung consolidation: dullness to percussion, increased tactile fremitus, whispered pectriloquy, and bronchial breath sounds / crackles. ddx's might include bronchitis, goodpasture's, asthma, cystic fibrosis.
some notes on the different types of headaches. doing a good history is vital to determining the cause of the headache, as well as determining the location and radiation patterns. tension headaches are more likely to be described as a band-like pain around the occiput, whereas migraines are more frontal. pain around or in the eyes might be due to a cluster headache, and pain in the face is likely from trigeminal neuralgia. unilateral head pain on the side of the head could be from temporal arteritis. papilledema or A/V nicking on a fundoscopic can indicate serious conditions such as intracranial hemorrhage or malignant hypertension, respectively.
hay fever aka allergic rhinitis is inflammation of the mucosa of the eyes and nasal passageways, leading to rhinorrhea, itchy / burning eyes and nasal congestion. it is often due to seasonal allergens such as pollen and will present bilaterally. a skin test might be useful to check for signs of atopy in the form of dermatitis, etc. differentials might include sinusitis, acute rhinitis, vasomotor rhinitis, and cocaine use.
conjunctivitis is an inflammation of the conjunctiva of the eyes and can be bacterial, viral (pink eye), or allergic / irritant in nature. signs include conjunctival injection (superficial dilated vessels away from the iris), pruritis, discharge, hyperemic and swollen lids. if symptoms are bilateral, the origin is more likely to be infectious or allergic while unilateral symptoms suggest toxic/chemical/mechanical causes. a culture of secretions can be useful in differentiating the cause of conjunctivitis: bacterial related secretions would contain PMN's, viral would contain leukocytes, and allergic would contain eosinophils.
strep throat is the result of infection via type A beta-hemolytic strep. it manifests as swollen, sore throat with fever and L/A. the jones criteria, used to diagnose strep, requires at least 2 of the following: fever above 100.4F po, no cough, pseudomembrane, tonsillar exudate. strep can also be diagnosed via a rapid strep test or throat culture. ddx's might include pharyngitis, mono, peritonsilar abscess, and diptheria.
vertigo is more of a symptom and can be due to several different causes, including benign paroxysmal positional vertigo, meniere's vestibular neuronitis, and other CNS disorders. episodic vertigo is more likely to be BPPV, while vertigo that lasts for hours / days is more likely to be meniere's or vestibular neuronitis. vertigo can also be associated with symptoms such as nausea / vomiting, tinnitus, and nystagmus-- which if unilateral and horizontal indicates benign causes and if variable indicates CNS disorders.
questions
URI...
1. what is the etiology of a URI?
2. what are some typical signs / symptoms of a URI?
3. what are some features that might distinguish a URI of bacterial vs. viral origin?
4. what labs should be performed for the diagnosis of a URI?
asthma...
5. what are three major features of asthma?
6. what is the difference between intrinsic and extrinsic asthma?
7. what are the major signs and symptoms of asthma?
8. what are some typical PE findings for asthma?
9. what signs might indicate a severe case of asthma?
10. what are the common findings for a lung exam on a patient with asthma?
11. why might a skin exam be performed on a patient suspected of having asthma?
sinusitis...
12. what is sinusitis?
13. what are the typical signs and symptoms of sinusitis?
14. what are some typical PE findings for sinusitis?
15. which labs might be performed to aid in a diagnosis of sinusitis?
bronchitis...
16. what is bronchitis?
17. what are the most common etiological agents for bronchitis?
18. the symptoms of infectious bronchitis are similar to...
19. describe the progression of the cough in infectious bronchitis.
20. severe cases of bronchitis might also present with...
21. what might be heard on a respiratory exam for bronchitis?
22. where in the lung might these sounds be heard?
pneumonia...
23. what is pneumonia?
24. what are three different types of pneumonia?
25. which type is most common in adults? young adults / children?
26. what are some risk factors for pneumonia?
27. what are the signs and symptoms for pneumonia?
28. what are the signs one would expect to find on a lung exam of a pneumonia patient?
29. what are some ddx's for pneumonia?
headaches...
30. what are some causes of head pain?
31. where do tension headaches usually present? how is the sensation described?
32. a frontal headache is more likely what type of headache?
33. a periorbital or deep orbital pain is most likely due to what type of headache?
34. pain in the face is likely due to...
35. unilateral head pain on the side of the head is likely due to...
36. patients with temporal arteritis might also present with what concomitant symptom?
37. what are some physical exams that one should perform on a patient that presents with head pain?
hay fever...
38. what is hay fever?
39. what are two useful questions to ask a patient suspected of hay fever?
40. what are the signs and symptoms of hay fever?
41. why might a skin test be performed in patients suspected of hay fever?
42. what are the differentials for hay fever?
conjunctivitis...
43. "pink eye" is...
44. what are the signs and symptoms of conjunctivitis?
45. what do bilateral vs. unilateral symptoms suggest about the origins of conjunctivitis?
46. what PE exams would be useful in diagnosing conjunctivitis?
47. what labs would you order with a patient suspected of conjunctivitis?
strep throat...
48. what is the etiology of strep throat?
49. what are the signs/symptoms of strep throat?
50. what are the jones criteria for diagnosing strep throat?
51. what are the lab tests used to diagnose strep throat?
52. what are the ddx's for strep throat?
vertigo...
53. episodic vertigo is more likely to be...
54. vertigo that lasts hours or days is more likely to be...
55. vertigo that is sudden onset and lasts for minutes is more likely to be...
56. what are the signs and symptoms associated with vertigo?
57. how can the type of nystagmus differentiate between potential causes of vertigo?
answers
1. viruses or bacteria invading upper respiratory tract, causing inflammation of the mucosa.
2. congestion, sneezing, rhinorrhea, post-nasal drainage, malaise.
3. bacterial more likely to have fever / chills and yellow green mucopurulent discharge. viral more likely to have clear rhinorrhea.
4. rapid strep test if jones criteria met, microscopic smear of exudates.
5. airway obstruction
inflammation
irritability / hypersensitivity
6. extrinsic is to allergy to external factors such as mold, pollen, etc. intrinsic is non allergic- from infections or emotional or other internal causes.
7. coughing, especially at night
wheezing, shortness of breath, DOE
sputum production
8. tachypnea, tachycardia, diaphoresis, wheezing, accessory muscle use.
9. weight loss, wasting, pulsus paradoxus.
10. prolonged expiratory phase, expiratory wheezing and diminished breath sounds.
11. to look for signs of atopy: dermatitis, eczema, other allergic skin conditions.
12. inflammation of the paranasal sinuses due to infection or allergy.
13. swelling / tenderness
malaise
toothache
frontal headache
swollen eyelids
14. erythematous nasal mucosa, sinuses do not transilluminate.
15. CT scan for chronic sinusitis
xray of teeth apices to rule out periapical abscess
CBC
16. an infection of the bronchial tree, either secondary to an infection, asthma, irritant, or primary / chronic.
17. infectious: bacterial URI
irritant: organic solvents, ammonia, dusts, chlorine
18. infectious URI symptoms: coryza, malaise, fever/chills, myalgia, etc
19. begins as dry and non productive, then develops into a productive cough.
20. 101-102 degree fevers.
21. scattered rhonchi, crackling/wheezing, moist rales.
22. at the base for crackling / rales.
23. infection of the lung.
24. bacterial, viral, mycoplasma.
25. bacterial most common in adults, mycoplasma in young adults and children.
26. immunocompromised
young or old age
recurrent URI's
cigarette smoke
physical debilitation
27. fever / chills
pleurisy / dyspnea
productive cough with rusty sputum
tachycardia, tachypnea
N/V
malaise / myalgia
28. increased tactile fremitus
dullness to percussion
bronchial breath sounds
whispered pectriloquy
crackles
[touch dull bronchial whisper crackle]
[fremitus dullness whisper bronchial crackles] [touch the dull whisker to hear the bronchial crackles]
29. bronchitis
asthma
cystic fibrosis
goodpasture's
30. vasomotor instability
muscle tension
hypoglycemia
infection
trauma
mass lesion
cerebral hemorrhage
31. occiput, band-like.
32. migraine
33. cluster
34. trigeminal neuralgia.
35. temporal arteritis.
36. polymyalgia rheumatica.
37. vitals, M/S, eye exam, sinsuses, neurological exam.
38. also known as allergic rhinitis; an inflammatory process involving the nasal and throat mucosa, as well as the conjunctiva in response to various allergens.
39. do your symptoms appear seasonally? are they bilateral?
40. rhinorrhea
burning, itchy, watery eyes
nasal / sinus congestion
41. to check for signs of atopy: dermatitis, eczema.
42. sinusitis, acute rhinitis, vasomotor rhinitis, cocaine use.
43. viral conjunctivitis.
44. superficial dilated vessels in conjunctiva
pruritis
discharge
hyperemia, swelling of lids
45. bilateral more likely allergic / infectious. unilateral more likely toxic/chemical/mechanical.
46. vitals, lymph nodes, EENT, (heart, lungs)
47. culture of secretion: bacterial would contain PMN's, viral would contain lymphocytes, allergic would contain eosinophils.
48. pharyngitis caused by group A beta-hemolytic streptococcus.
49. sore throat
fever
no cough
cervical L/A
injected / erythematous mucous membranes
exudate / pseudomembrane
50. fever over 100.4 po, no cough, tonsilar exudate, pseudomembrane.
51. rapid strep test and throat culture.
52. viral / bacterial pharyngitis
infectious mononucleosis
diptheria
peritonsilar abscess
53. BPPV
54. meniere's, vestibular neuronitis
55. brain or vascular disease.
56. spinning sensation/disequilibirum
nystagmus
N/V
tinnitus
57. unilateral horizontal nystagmus is more likely benign, variable nystagmus likely due to a CNS disorder.
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.
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