the kidney unit in CPD III. we started with some introductory notes about diagnosis and the general symptom picture. labs that are helpful in the diagnosis of kidney conditions include urinalysis (can detect infection, RBC's, casts, etc), CBC, and chem screen (BUN and creatinine are useful measures of glomerular function). imaging studies might include xray, US, IVU, depending on the condition suspected. some typical symptoms associated with kidney conditions: UTI's commonly present with a triad of symptoms, urinary frequency, urgency, dysuria. chills/fever in association with these symptoms might indicate involvement of the upper urinary tract. urethral discharge in males is most likely due to GC/chlamydia infection. nocturia might be indicative of BPH, or simply reflect excess nighttime fluid consumption- consider nocturia seriously if it is a sudden change for the patient. enuresis, bedwetting, can be primary or secondary- patients with secondary enuresis might only have episodes followed by breaks of 6 months or more and are more likely due to psychological as opposed to physiological factors. incontinence comes in three flavors- overflow from incomplete emptying due to obstruction, stress from increased pressure, and urge from decreased CNS inhibition.
renal colic, or kidney stones, often cause severe unilateral pain in a crescendo-decrescendo pattern that radiates from the kidney / flank area to the lower abdomen and bladder, and sometimes as far down as the knee. patients might also present with nausea/vomiting, hematuria, and urinary frequency, as well as chills/fever if an infection is involved. diagnosis is made by UA and imaging, in particular US and IVU.
polyuria can be a physiologic response to an increased osmolar load, in which case the major concern is loss of electrolytes. it can also point to certain underlying pathologies such as diabetes insipidus, which leads to an underproduction of ADH by the pituitary. nephrogenic diabetes insipidus can also result in polyuria- in this condition, the kidney's ADH receptors are non functioning.
oligouria and anuria are conditions of decreased urine and can be from pre-renal, renal, or post renal causes. pre-renal causes can include dehydration, as well as any condition that decreases blood flow to the kidney such as CHF or hemorrhage. renal causes are grouped under the acronym VINDICATE: vascular lesions, inflammatory lesions, neoplasm, degenerative conditions, intoxication, congenital disorders, autoimmune, trauma, endocrine causes. post renal: MINNT-- malformations, inflammatory, neoplasm, neurological, trauma.
some notes about the various colors of urine and what they might indicate: normal color is yellow, although bright / concentrated yellow might indicate dehydration or B vitamins. overly clear might indicate glomerular dysfunction as in chronic glomerulonephritis, or simply polydipsia. cloudy white might be indicative of infection as the cloudiness might be bacteria or pus. red might be RBC's but can also be from certain foods such as beets.
as the kidneys are primarily responsible for maintaining fluid volume in the body, systemic edema symptoms often point to kidney filtration issues. pitting edema refers to a type in which fluid can be displaced, forming transient "pits", whereas in non-pitting, fluid can not be displaced- this is often due to local trauma such as a bee sting. in general edema formation can occur via four mechanisms- increased capillary pressure, increased capillary permeability, decreased plasma proteins, and lymph obstruction. edema symptoms may also point to other organ systems, in particular heart dysfunction (recall that RCHF leads to systemic edema), thyroid (hypothyroid myxedema), hepatic (look for jaundice, ascites, palmar erythema), and might even be due to a worm found in pork, trichinosis if seen periorbitally.
acute renal failure describes a situation marked by rapidly increasing azotemia plus oliguria / anuria. as with azotemia, the cause may be pre-renal (CHF), renal (glomerulonephritis), or post renal (bladder outlet obstruction, BPH). clinically, it manifests as lethargy, pulmonary edema, CHF, hypertension, and oliguria. diagnosis is made via chem screen, CBC, and UA-- most helpful is the rapid and steady increase of creatinine (as well as BUN). if oliguria / anuria persists for more than 3 days, this is an indicator of poor prognosis; conventional emergency treatment might require dialysis and complete kidney rest.
whereas acute renal failure might produce sudden increases in BUN / creatinine, chronic renal failure might show mild elevations for month long periods. there are many risk factors that contribute to CRF, such as glomerulonephritis, cardiovascular disease, SLE, pyelonephritis, etc. clinical presentation can be divided by the stage of disease: CRF initially presents with nonspecific / vague symptoms, or fatigue / mental haze. the intermediate stage presents with bad taste in mouth, muscle spasm/convusion/neuropathy, pruritis, nausea / vomiting. the late stage presents with cardiovascular issues such as hypertension, CHF, pericarditis, as well as skin issues such as uremic frost and yellow/brown complexion. in addition to the BUN / creatinine levels, one might expect to see normochromic / normocytic anemia (deficient erythropoetin production), waxy casts on a UA, and imbalanced electrolytes. these patients are generally put on dialysis long term (200,000 in the US) with dietary / fluid intake monitoring- in particular, avoiding high protein intake.
nephrotic syndrome results from a dysfunctional or damaged glomerular basement membrane, leading to loss of proteins and hyperlipidemia. it can be primary from diseases such as immune complex nephritides, or secondary to systemic illness such as diabetes mellitus. patients might present with frothy urine, marked edema periorbitally and peripherally, muscle wasting due to lack of protein, and respiratory symptoms. diagnosis is made by UA, chem screen, CBC- UA might show proteins, cellular elements, casts. chem screen might show hyperlipidemia, hyperalbuminemia, and CBC might show microcytic anemia.
acute glomerulonephritis is another form of glomerular dysfunction, this time from immune complex deposition from previous infection, such as an untreated strep throat infection. it commonly affects children and young adults and is relatively rare in adults over 50. although it has mild proteinuria as nephrotic syndrome does, the hallmark of AG is hematuria and presence of RBC casts in the UA. the decreased glomerular function also leads to increased sodium retention, which ultimately increases blood volume and may lead to hypertension or CHF. children have a good chance of recovery from AG but will always have an increased risk for HTN-- thus an adult who has unexplained HTN might have had acute glomerulonephritis earlier in life. chronic glomerulonephritis might result from longstanding acute glomerulonephritis and might develop insidiously- patients might asx, but with occasional proteinuria and hematuria, with RBC casts on a UA. steadily increasing BUN might also be observed over months or years.
goodpasture's is a near fatal glomerular disease that has a predilection for young males. the hallmark signs are lung and renal hemorrhage that results in hemoptysis and hematuria. labs have the combined characteristics of nephrotic syndrome and glomerulonephritis: hematuria / RBC's, but also with protein / casts in UA, along with increased BUN / creatinine. patients might also present with headache, malaise, and anorexia. the prognosis for goodpasture's is poor, and patients with this condition rarely live past their 20's.
idiopathic primary renal hematuric/proteinuric syndrome is diagnosed when there is mild gross or microscopic hematuria and proteinuria without any clear explanation. the etiology may be related to IgA towards the glomeruli, as well as buerger's disease and febrile URI's. this condition has a preference for males and children-- most recover but like acute glomerulonephritis have an increased lifetime risk for hypertension and renal insufficiency.
henoch-schoenlein purpura is similar to IPRHPS but with marked skin, GI, and joint involvement- the characteristic purpura lesions are symmetrically distributed on the extensor surfaces. GI symptoms might include abdominal pain, vomiting, and joint pain may occur at the ankles, hands, feet. HSP generally follows a viral infection, such as an acute viral URI. lab findings might show hematuria / proteinuria, occult blood, and increased ESR. HSP is self limiting, generally within 6 weeks, although 10-20% of patients might develop chronic renal failure.
questions
diagnosis...
1. what are some helpful lab tests to consider when ruling in or out kidney related pathologies?
2. what are two components of a chem screen that can give an indication of kidney function?
3. what are the imaging techniques used to diagnose kidney conditions?
4. what is the "triad of symptoms" seen in UTI's?
5. what might chills/fever indicate in a patient with the triad of symptoms for a UTI?
6. leukocyte casts in a UA might indicate...
7. what is the most common cause of urethral discharge in males?
8. what might nocturia be indicative of?
9. what is the difference between primary and secondary enuresis?
10. what are the different types of incontinence?
renal colic...
11. describe the pain sensation in renal colic.
12. describe the typical radiation patterns seen in renal colic pain.
13. what are some concomitant symptoms seen in renal colic?
14. what is a typical PE of a patient with RC?
15. what would labs show for RC?
16. what are the imaging studies used to diagnose RC?
polyuria...
17. what are some pathological conditions associated with polyuria?
18. why does diabetes insipidus cause polyuria?
19. what is nephrogenic diabetes insipidus?
oligo / anuria...
20. what are some prerenal causes of oligouria or anuria?
21. what are some renal causes of oligouria / anuria?
22. what are some post renal causes of oligouria / anuria?
what might be indicated by urine that is...
23. colorless.
24. cloudy white.
25. yellow.
26. orange.
27. red.
28. blue/green.
29. brown/black.
edema...
30. what is the difference between pitting and non-pitting edema?
31. what is a common cause of non-pitting edema?
32. what are four pathophysiological mechanisms for edema formation?
33. what are some hepatic symptoms or conditions that might be associated with edema?
34. what is a thyroid related etiology for edema?
35. what is the relationship between edema and pork?
acute renal failure...
36. what is acute renal failure?
37. what are the major etiologies of acute renal failure?
38. what are some "pre-renal" causes of acute renal failure?
39. what are some "renal" causes of acute renal failure?
40. what are some "post-renal" causes of acute renal failure?
41. what are some of the signs and symptoms of acute renal failure?
42. what are some labs that aid in the diagnosis of acute renal failure?
43. if anemia is present in acute renal failure, what type of anemia would it be?
44. what is a marker for prognosis of acute renal failure?
45. what is the conventional treatment strategy for acute renal failure?
chronic renal failure...
46. what are some risk factors for CRF?
47. how many patients in the US are currently on dialysis long term?
48. what are the early signs / symptoms for CRF?
49. what are the intermediate stage signs/symptoms for CRF?
50. what are the late stage signs/symptoms for CRF?
51. what are the lab tests used to diagnose CRF?
52. what are some electrolyte imbalances one might expect to see in CRF?
53. what is the connection between CRF and chronic anemia?
54. what are some treatment strategies for CRF?
nephrotic syndrome...
55. what is nephrotic syndrome?
56. which gender is more affected by nephrotic syndrome?
57. what are the etiologies of nephrotic syndrome?
58. what are the signs and symptoms of nephrotic syndrome?
59. what might one expect to find on a UA of a pt with NS?
60. what might one expect to find on a chem screen of a pt with NS?
61. what is the connection between nephrotic syndrome and hyperlipidemia?
62. what might be a finding on a CBC of a pt with NS?
63. what are some PE findings for NS?
acute glomerulonephritis...
64. what is AG? what are the hallmarks of AG?
65. what age group is most commonly affected by AG?
66. what is the etiology of AG?
67. how long after an episode of untreated strep throat might AG appear?
68. what are the signs/symptoms of AG?
69. what is the lab finding that is diagnostic for AG?
70. what might be seen in fundoscopy of a pt with AG?
71. what is the prognosis for children with AG?
chronic glomerulonephritis...
72. what is chronic glomerulonephritis?
73. what is a typical presentation for chronic glomerulonephritis?
goodpasture's syndrome...
74. which demographic is most commonly affected by goodpasture's syndrome?
75. what are the hallmark signs and symptoms of GS?
76. what are the concomitant symptoms of GS?
77. what are common lab findings for GS?
78. what is the prognosis of goodpasture's syndrome?
idiopathic primary renal hematuric/proteinuric syndrome...
79. what is IPRHPS?
80. what are some possible etiologies of IPRHPS?
81. what demographic is most closely associated with IPRHPS?
82. what might be a predisposing factor for IPRHPS?
83. what might lab findings show for IPRHPS?
84. what is the prognosis for IPRHPS?
henoch-schoenlein purpura...
85. what is HSP?
86. what is the etiology of HSP?
87. what are the signs and symptoms of HSP?
88. what are some lab findings one might expect to find with HSP?
89. what is the prognosis of HSP?
answers
1. UA, culture, CBC, chem screen.
2. BUN and creatinine: both excreted by the kidneys and therefore can be a rough indicator for glomerular function.
3. Xray, US, IVU.
4. urinary frequency, urgency, pain.
5. upper UTI.
6. renal parenchyma infection.
7. GC chlamydia.
8. early disease, excess fluid consumption in evening, BPH, interstitial cystitis.
9. in secondary, there might be a period of dryness (over 6 months)-- more likely due to psychological factors.
10. overflow (obstruction of urinary tract leads to incomplete emptying), stress (increased intraabdominal pressure), urge (decreased CNS inhibition).
11. severe, unilateral, crescendo-decrescendo pain.
12. from flank/kidney around to lower abdomen, follows course of urinary tract and sometimes radiates down further, as far as knee.
13. chills/fever
N/V
hematuria
frequency
14. unremarkable or flank tenderness.
15. hematuria with or without pyuria / bacteruria.
16. xray, US, IVU (for kidney and ureter).
17. diabetes insipidus, nephrogenic diabetes insipidus, psychogenic polydipsia.
18. in DI, the pituitary underproduces ADH, a hormone that allows for water reabsorption in the kidney- thereby leading to greater urine output.
19. a condition where the kidney's receptors for ADH are not functioning.
20. dehydration, hemorrhage, CHF.
21. VINDICATE:
vascular lesions
inflammatory lesions
neoplasm
degenerative
intoxication
congenital disorders
autoimmune (most common)
trauma
endocrine
22. MINNT:
malformations
inflammation
neoplasms
neurological disorders
trauma
23. polydipsia, chronic glomerulonephritis, diabetes inspidis/mellitus.
24. phosphates, epithelial cells, bacteria/pus.
25. B vitamins.
26. urobilinogen, bile, pyridium, carrots.
27. beets, or RBC's.
28. certain drugs (thymol, phenol, indigo blue), pseudomonas.
29. bilirubin, hemoglobin.
30. in pitting, fluid can be displaced and transient "pits" are formed. in non-pitting, edema is so severe that fluid can not be displaced.
31. trauma causes coagulation of proteins such as fibrinogen.
32. increased capillary pressure (blood clots, CHF)
increased capillary permeability (CHF)
decreased plasma proteins (burns, nephrosis, low protein intake)
lymph obstruction (lymph node removal, parasites)
33. jaundice
ascites
spider nevi
red nose
palmar erythema
34. there is a marked increase in water retention in hypothyroid myxedema.
35. trichinosis is a worm found in pork that is associated with periorbital edema.
36. rapidly increasing azotemia plus oliguria.
37. 60-70% extrinsic factors: trauma, drugs, surgery, obstruction, etc.
20-30% due to intrinsic factors: acute glomerulonephritis, SLE, goodpasture's, etc.
38. renal failure that results from inadequate renal perfusion due to factors upstream from the kidney: CHF, hemorrhage, etc.
39. decreased renal blood flow, reduced glomerular filtration, or renal obstruction.
40. bladder outlet obstruction, BPH, tumors.
41. lethargy
pulmonary edema
CHF
hypertension
oliguria
42. chem screen: steadily increasing creatinine is diagnostic. also see BUN increase.
CBC to check for anemia and infection
UA to check for RBC's, WBC's, casts.
43. normocytic normochromic.
44. oliguria / anuria for more than 3 days indicates very poor prognosis; may be fatal.
45. dialysis to allow kidney to recover, or severe limitation of fluid and electrolyte intake.
46. glomerulonephritis
cardiovascular diseases such as arteriosclerosis, HTN
SLE, diabetes
congenital abnormalities (polycystic kidney)
pyelonephritis
47. about 200,000.
48. non-specific
fatigue
nocturia
mental haze
49. muscle twitching, aches, convulsions
neuropathy
bad taste in mouth
N/V
pruritis
50. uremic frost
GI ulcers / bleeding
tissue wasting
yellow / brown skin
hypertension / CHF / pericarditis
51. chem screen would show mild / moderate elevations of BUN/creatinine over months
CBC would show normocytic / normochromic anemia,
UA might show waxy casts
52. decreased calcium, increased phosphorous, potassium, CO2.
53. kidney failure leads to improper erythropoetin production.
54. dietary and fluid intake monitoring - decrease protein and increase carb intake.
55. damage to the glomerular basement membrane that causes hyponaturia, proteinuria, hypoalbuminemia, lipiduria, hyperlipidemia.
56. males.
57. primary nephrotic disease such as immune complex nephritides or underyling systemic disease such as diabetes mellitus.
58. frothy urine
edema
muscle wasting
abdominal pain
SOB/DOE
[basement pee edema muscle stomach breath] [basement flooded with pee- use your stomach muscles and blow it out]
59. cellular elements, protein, casts.
60. hyperalbuminemia and hyperlipidemia.
61. the liver increases lipid production (cholesterol) concurrently with protein production in an attempt to normalize protein levels from the protein loss incurred in nephrotic syndrome.
62. microcytic anemia.
63. periorbital and peripheral edema
muscle wasting
parallel white lines on nails
orthostatic hypotension
64. glomerular dysfunction which causes decreased GFR and increased Na retention, leading to hematuria and hypertension.
65. young children older than 3 or young adults. rare in >50yos.
66. previous infection which causes immune complex deposition in glomeruli.
67. 1-6 weeks.
68. hematuria / oliguria
flank pain
mild edema
hypertension
69. RBC casts on a UA.
70. retinal hemorrhages.
71. 90% chance of recovery but increased risk for HTN remains throughout lifetime.
72. diffuse sclerosis of glomeruli and insidious loss of kidney function.
73. asx, with no abnormal lab results except for occasional proteinuria and hematuria. steadily increasing BUN over years.
74. young males 9:1.
75. renal and lung hemorrhage-- hemoptysis and hematuria.
76. headache, malaise, anorexia.
77. increased BUN/creatinine, RBC, protein on UA, microcytic anemia on CBC.
78. poor, patients rarely live past 20's.
79. presence of protein and RBC's in urine with no explanation.
80. glomerular IgA deposition, buerger's disease.
81. 6:1 males, children/young adult most common.
82. febrile URI.
83. hematuria, proteinuria, increased IgA.
84. many children recover but have an increased lifetime risk for hypertension and renal insufficiency.
85. similar to IPRHPS but with skin, joint, and GI involvement.
86. often follows a viral infection, acute URI.
87. symmetrically distributed purpura on extensor surfaces
arthritis
GI distress- vomiting, pain, occult blood
hematuria, proteinuria
88. increased ESR
hematuria / proteinuria
occult blood
89. self limiting in 1-6 weeks. 10-20% have chronic renal failure.
No comments:
Post a Comment