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Renal First Aid USMLE Step 1 > Renal Path > Flashcards

Renal Path Flashcards

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USMLE® Step 1 flashcards
1
Q
  • Symptoms: Disorientation, stupor, coma. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hyponatremia

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2
Q
  • Symptoms: Irritability, delirium, coma (neurological). Lab Values: ** Pathophysiology: ** Treatment: *
A

Hypernatremia

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3
Q
  • Symptoms: Secondary to metabolic alkalosis. Hypokalemia, hypovolemia, increased aldosterone in compensation. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hypochloremia

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4
Q
  • Symptoms: Secondary to non-anion gap acidosis. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hyperchloremia

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5
Q
  • Symptoms: Peaked T waves, wide QRS, arrhythmias. Lab Values: ** Pathophysiology: Potassium-sparing diuretics, ARBs/ACE inhibitors, beta-antagonists. Treatment: *
A

Hyperkalemia

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6
Q
  • Symptoms: U waves on ECG, flattend T waves, arrhythmias, paralysis. Lab Values: ** Pathophysiology: Thiazides, loop diuretics. Treatment: *
A

Hypokalemia

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7
Q
  • Symptoms: Delirium, renal stones, abdominal pain, not necessarily calciuria. Lab Values: ** Pathophysiology: Caused by sarcoidosis, thiazides, metatstatic cancer, squamous cell carcinoma. Treatment: *
A

Hypercalcemia

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8
Q
  • Symptoms: Tetany, neuromuscular irritability. Lab Values: ** Pathophysiology: Caused by loop diuretics (ethacrynic, furosemide). Treatment: *
A

Hypocalcemia

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9
Q
  • Symptoms: Delirium, decreased deep tendon reflexes, cardiopulmonary arrest. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hypermagnesemia

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10
Q
  • Symptoms: *Neuromuscular irritability, arrhythmias. * Lab Values: ** Pathophysiology: ** Treatment: *
A

Hypomagnesemia

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11
Q
  • Symptoms: High-mineral ion product causes renal stones, metatstic calcifications. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hyperphosphatemia

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12
Q
  • Symptoms: Low-mineral ion product causes bone loss, osteomalacia. Lab Values: ** Pathophysiology: ** Treatment: *
A

Hypophosphatemia

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13
Q
  • Symptoms: ** Lab Values: Low pH, low HCO3 (primary), immediate compensatory decrease in PCO2 (hyperventillation). Pathophysiology: MUDPILES (Methanol, Uremia, Diabetic ketoacidosis, Propylene glycol, Iron tablets and INH, Lactic acidosis, Ethylene glycol, Salicylates. Anion gap = Na - (Cl + HCO3). Treatment: *
A

Anion gap metabolic acidosis

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14
Q
  • Symptoms: ** Lab Values: Low pH, low HCO3 (primary), immediate compensatory decrease in PCO2 (hyperventillation). Pathophysiology: HARD-ASS (Hyperalimentation, Addison’s disease, Renal tubular acidosis, Diarrhea, Acetazolamide, Spirnolactone, Saline infusion) Treatment: *
A

Non-anion gap metabolic acidosis

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15
Q
  • Symptoms: ** Lab Values: High pH, high HCO3 (primary), immediate compensatory increase in PCO2 (hypoventillation). Pathophysiology: Loop diuretics, thiazides, vomiting, antacid use, hyperaldosteronism. Treatment: *
A

Metabolic alkalosis

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16
Q
  • Symptoms: ** Lab Values: Low pH, high PCO2 (primary), gradual compensatory increase in HCO3 reabsorption. Pathophysiology: Airway obstruction, acute lung disease, chronic lung disease, opioids/narcotics/sedatives, weakning of respiratory muscles. Treatment: *
A

Respiratory acidosis

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17
Q
  • Symptoms: ** Lab Values: High pH, low PCO3 (primary), gradual compensatory decrease in HCO3 reabsorption. Pathophysiology: Hyperventilation (high altitude exposure), aspirin ingestion, pneumonia, pulmonary embolism. Treatment: *
A

Respiratory alkalosis

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18
Q
  • Symptoms: ** Lab Values: Plasma glucose above 160-200 mg/dL. Pathophysiology: All transporters saturated at 350mg/dL (Tm). Treatment: *
A

Glucosuria

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19
Q
  • Symptoms: Pellagra (dermatitis, diarrhea, dementia). Lab Values: Increase trytophan in urine and decrease absorption from gut. Pathophysiology: Autosomal recessive. Defective neutral amino acid transporter in instetinal and renal epithelial cells. Unable to synthesize niacin without its tryptophan precursor. Treatment: *
A

Hartnup disease

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20
Q
  • Symptoms: Associated with hypokalemia and risk for calcium-containing kidney stones. Lab Values: ** Pathophysiology: *Defect in collecting tubule’s ability to excrete H+. * Treatment: *
A

Renal tubular acidosis type 1

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21
Q
  • Symptoms: Associated with hypokalemia and hypophosphatemic rickets Lab Values: ** Pathophysiology: Defect in proximal tubule HCO3 reabsorption. Treatment: *
A

Renal tubular acidosis type 2

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22
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: ** Treatment: *
A

Renal tubular acidosis type 3

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23
Q
  • Symptoms: Associated with hyperkalemia and inhibition of ammonium excretion in the proxmial tubule. Leads to decrease urine pH to due to decrease buffering capacity. Lab Values: ** Pathophysiology: Hypoaldosteronism or lack of collecting tubule response to aldosterone. Treatment: *
A

Renal tubular acidosis type 4

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24
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Caused by glomerulonephritis, ischemia, or maglinant hypertension. Presence of casts indicates the hematuria is of renal origin. Treatment: *
A

RBC casts in urine

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25
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Bladder cancer, kidney stones. Treatment: *
A

Hematuria without casts

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26
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Caused by tubulointerstital inflammation, acute pyelonephritis, or transplant rejection. Presents of casts indicates pyuria is of renal orign. Treatment: *
A

WBC casts in urine

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27
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Acute cystitis Treatment: *
A

Pyuria without casts

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28
Q
  • Symptoms: ** Lab Values: Muddy brown. Pathophysiology: Caused by acute tubular necrosis. Treatment: *
A

Granular casts in urine

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29
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Caused by advaned renal diseaase or chronic renal failure. Treatment: *
A

Waxy casts in urine

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30
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Nonspecific. Treatment: *
A

Hyaline casts in urine

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31
Q
  • Symptoms: *{{Hematuria with RBC casts},} azotemia, oliguria, {{hypertension and edema}} (due to salt retention), and proteinuria (
A

Nephritic syndrome

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32
Q
  • Symptoms: *Peripheral and {{periorbital edema}}, hypertension, and {{dark urine (hematuria with RBC casts)}} that occurs 2-4 weeks after streptococcal pharyngitis. * Lab Values: LM: glomeruli enlarged and hypercellular, PMNs, {{“lumpy-bumpy”}} appearance. EM: {{subepithelial immune complex (IC) humps}}. IF: granular appearance due to IgG, IgM, and C3 deposition along GBM and mesangium. Elevated ASO titers. Pathophysiology: Nephritic syndrome (proliferation). Type III hypersensitivity. Treatment: * Usually resolves on its own…subendothelial hump moves to subepithelial
A

Acute poststreptococcal glomerulonephritis

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33
Q
  • Symptoms: {{Rapidly deteriorating renal function (days to weeks)}}. Lab Values: LM and IF: {{cresent-moon shaped due to parietal cell proliferation}}. Pathophysiology: Nephritic syndrome. {{Cresents consists of fibrin and plasma proteins}} with glomerular parietla cells, monocytes and macrophages. {{Due to Goodpasture syndrome, Wegener’s granulomatosis, and microscopic polyangiitis.}} Treatment: *
A

Rapidly progressive glomerulonephritis

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34
Q
  • Symptoms: Nephritic syndrome. Lab Values: LM: {{“wire looping” of capillaries.}} EM: {{subendothelial}} and intramembranous IgG based ICs often with C3 deposition.}} IF - granular. {{PAS staining. Full house deposition (all Ig’s!)}} Pathophysiology: Nephritic syndrome. {{Due to SLE or membranoproliferative glomerulonephritis}}.{{ Most common cause of death in SLE. Can concurrently present as nephrotic and nephritic syndrome}}. Treatment: *
A

Diffuse proliferative glomerulonephritis

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35
Q
  • Symptoms: {{Child with skin rash on buttocks and legs (palpable purpura)}}, arthralgia, intestinal hemorrhage, abdominal pain, and melena. Follows URIs. {{Association with IgA nephropathy}}. Lab Values: LM: mesangial proliferation. EM: mesangial IC deposits. IF: {{IgA-based deposits in mesangium}}. Pathophysiology: Due to IgA immune complex formation. Most common form of childhood systemic vasculitis. Multiple lesions of the same age. Treatment: *
A

Henoch-Schonlein purpura

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36
Q
  • Symptoms: Recurrent hematuria with RBC casts following URIs or acute gastroenteritis. Lab Values: LM: {{mesangia}} proliferation. EM: {{mesangial}} IC deposits. IF: IgA-based deposits in mesangium. Pathophysiology: {{IgA nephropathy.}} {{Antibody deposition in mesangial cells}} lead proliferation and nephritic syndrome. {{Associated with celiac sprue and Henoch-Schonlein purpura.}} Treatment: *
A

Berger’s disease

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37
Q
  • Symptoms: Male child with deafness, nephritic syndrome (hematuria with RBC casts, hypertension), ocular disorders. Lab Values: EM: splitting of lamina densa. Pathophysiology: X-linked recessive. Nephritic syndrome. Mutation in type IV collagen leading to split basement membrane. Treatment: *
A

Alport’s syndrome

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38
Q
  • Symptoms: {{Typically seen in young males. Hematuria, hemoptysis - NO SINUSITIS}}. Lab Values: LM: hypercellularity, crescents, fibrin. IF: {{linear pattern}} of IgG and C3 deposition. EM: no deposits, but there is glomerular basement membrane disruption. Pathophysiology: Type II hypersenstivitiy. {{Autoantibodies to basement membrane (type IV collagen).}} May progress to rapidly progressive glomerulonephritis. Treatment: *
A

Goodpasture’s syndrome

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39
Q
  • Symptoms: {{Massive proteinuria}} (> 3.5g/day, frothy urine), {{hyperlipidemia,}} fatty casts, {{peripheral edema}}, anasarca (generalized edema). {{Hypercoag}} (due to antithrombin III loss in urine). Increased risk of infection (due to immunoglobin loss). Lab Values: ** Pathophysiology: Leaky basement membrane allowing protein (ex. Albumin) to leak out. Treatment: *
A

Nephrotic syndrome

40
Q
  • Symptoms: Occurs at all ages. Peripheral edema, proteinuria, lipiduria, but does {{NOT respond to steroids}}. Lab Values: LM: {{segmental sclerosis and hyalinosis}}. Pathophysiology: Most common glomerular disease in {{IV drug abusers (heroin) or HIV patients.}} Also secondary to pamidronate. Treatment: *Doesn’t respond to steroids.
A

Focal segmental glomeruloscerlosis

41
Q
  • Symptoms: Nephrotic syndrome; hyperlipidemia, edema, proteinuria > 3.5 g/day, hypoalbuminemia, hypercoagulability, increased infection. Lab Values: LM: diffuse capillary and GBM thickening. EM: spike and dome appearance with subepithelial deposits (IgG and C3). IF: granular. SLE’s nephrotic presentation. Pathophysiology: DISC! Caused by drugs (penicillamine), infections (HepB and C), systemic diseases (SLE, DM), solid cancers (lung, colon). Most common cause of adult nephrotic syndrome. Treatment: *
A

Membranous glomerulonephritis

42
Q
  • Symptoms: Triggered by a recent infection or immunization. Most common in children. Heavy proteinuria, lipiduria, peripheral edema. Lab Values: LM: normal glomeruli. EM: foot process effacement, no IC deposits. Selective loss of albumin, not globulins due to GBM polyanion loss. Pathophysiology: Liver compensates for protein loss by liberating lipids. Must do EM to make diagnosis. Treatment: *Steroids.
A

Minimal change disease (lipoid nephrosis)

43
Q
  • Symptoms: Nephrotic syndrome; hyperlipidemia, edema, proteinuria > 3.5 g/day, hypoalbuminemia, hypercoagulability, increased infection. Lab Values: LM: congo red stain, apple-green biriferingence. Pathophysiology: Associated with chronic inflammatory conditions (multiple myeloma, TB, RA). Treatment: *
A

Amyloidosis

44
Q
  • Symptoms: Nephrotic and nephritic syndrome. Lab Values: Subendothelial IC with granular IF. Type I LM: tram-track apperance due to GBM splitting caused by mesangial ingrowth. Type II EM: “ribbon like, dense deposits”. C3 will be low with type II. Pathophysiology: Nephritic and nephrotic. Type I due to HBV, HCV, and HIV (classic complement, Ig complexes). Type II due to C3 nephritic factor which stimulates C3 production (alternative complement pathway) and deposition in GBM (SLE, endocarditis, CLL). Treatment: *
A

Membranoproliferative glomerulonephritis

45
Q
  • Symptoms: Nephrotic syndrome. Kimmelstiel-Wilson syndrome. Lab Values: LM: mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis. Pathophysiology: Nonenzymatic glycosylation (NEG) of GBM leads to increased permeability and thickening. NEG of efferent arterioles leads to increased GFR and mesangial expansion. Treatment: *
A

Diabetic glomerulonephropathy

46
Q
  • Symptoms: May lead to postrenal failure, hydronephrosis and pyelonephritis. Most common stone. Lab Values: Radiopaque on X-ray. Pathophysiology: Precipitates at low or neural pH. Hypercalcemic conditions (cancer, sarcoid, increased PTH) increases stone formation. Calcium oxalate or calcium phosphate. Oxalate crystals result from ethylene glycol (antifreeze) oor vitamin C abuse. Treatment: *Encourage fluid intake. Lithotripsy (ultrasound).
A

Calcium stone

47
Q
  • Symptoms: May lead to postrenal failure, hydronephrosis and pyelonephritis. Lab Values: Radiopaque on X-ray. Magnesium ammonium phosphate. Pathophysiology: Precipiates at increased pH. Caused by inection with urease-positive magnesium or radiolucent bugs (Proteus, Staph, Klebsiella). Forms staghorn calculi that can be a nidus for UTIs. Worsened by alkaluria. Treatment: *Lithotripsy (ultrasound).
A

Struvite stone

48
Q
  • Symptoms: May lead to postrenal failure, hydronephrosis and pyelonephritis. Lab Values: Radiolucent on X-ray. Pathophysiology: Precipitates at low pH. Secondary to hyperuricemia Often seen in diseases with increased cell turnover, like leukemia. Treatment: *Lithotripsy (ultrasound).
A

Uric acid stone

49
Q
  • Symptoms: May lead to postrenal failure, hydronephrosis and pyelonephritis. Lab Values: Radiopaque on X-ray. Detect with nitroprusside. Pathophysiology: Precipiates at low pH. Secondary to cystinuria (inability to reabsorb dibasic amino acids). Treatment: *Alkalinization of the urine.
A

Cystine stone

50
Q
  • Symptoms: Leads to acute postrenal failure and pyelonephritis. Lab Values: ** Pathophysiology: Results from complete or partial urinary tract obstruction. Causes dilation up to the obstruction and in chronic cases parenchymal thinning. Caused by stone formation, endometriosis, metastatic squamous cell carcinoma of cervix, BPH (bilateral hydronephrosis in elderly male). Treatment: *
A

Hydronephrosis

51
Q
  • Symptoms: ** Lab Values: Less than 3 cm in size, common finding at autopsy. Pathophysiology: ** Treatment: *
A

Cortical adenoma

52
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: *Assocaited with tuberous sclerosis. Hamartomas composed of fat, smooth muscle, and blood vessels. * Treatment: *
A

Renal angiomyolipoma

53
Q
  • Symptoms: *Most common in men 50-70 years of age. Increase incidence with smoking and obesity. Manifests with hematuria with casts, palpalble mass, secondary polycythemia, flank pain, fever, and weight loss. Hypertension due to renin. * Lab Values: Polygonal clear cells filled with lipids and carbohydrates. Gross yellow appearance; upper pole of kidney. Pathophysiology: Most common renal malingancy; associated with von Hippel-Lindau with a 3p deletion. Asosciated with paraneoplastic syndromes (ectopic EPO, renin (HTN), ACTH (cushing), PTHrP, and prolactin). Can invade renal vein/IVC and spread hematogenously (pulmonary embolization). Metastasizes to lung and bone. Treatment: *
A

Renal cell carcinoma

54
Q
  • Symptoms: Presents with huge, palpable flank (renal) mass and/or hematuria. Associated with hemihypertrophy syndromes. WAGR complex: Wilms’ tumor, aniridia (no iris), genitourinary malformation, and mental-motor retardation. Lab Values: 11p WT1 tumor supressor gene deletion. Tubule formation means better prognosis (less anaplasia). Pathophysiology: *Autosomal dominant. Most common renal malignancy of early childhood (ages 2-4). * Treatment: *Dactinomycin
A

Wilms’ tumor

55
Q
  • Symptoms: Elderly patient with painless hematuria without casts (major buzz word for bladder cancer). Lab Values: Papillary growth lined by transitional epithelium with mild nuclear atypia and pleopmorphism. Pathophysiology: Most common tumor of urinary trat system (can occur in renal calyces, renal pelvis, ureters, and bladder). Associated with Phenacetin, Smoking, Analine dyes, and Cyclophosphamide (problems with your Pee SAC). Treatment: *
A

Transitional cell carcinoma

56
Q
  • Symptoms: Presents with pyuria with WBC casts, fever, CVA tenderness, nausea, and vomiting. Lab Values: PMN infilitration into renal interstitium. Pathophysiology: Affects cortex with relative sparing of glomeruli/vessels. Most common cause is E. coli. Treatment: *
A

Acute pyelonephritis

57
Q
  • Symptoms: Presents with pyuria with WBC casts, fever, CVA tenderness, nausea, and vomiting. Lab Values: Lymphocytic invasion with fibrosis. Pathophysiology: Coarse, asymmetric corticomedullary scarring (U shaped, different sized kidneys), blunted calyx. Tubules contain eosinophilic casts (thyroidization of kidney). Vesicoureteral reflux required for development. Treatment: *
A

Chronic pyelonephritis

58
Q
  • Symptoms: Acute interstitial renal inflammation. Associated with feer, rash, hematuria, CVA tenderness, pyuria (typically eosinophils) and azotemia occuring 1-2 weeks after drug administration. Lab Values: Eosinophilia, granulomas. Pathophysiology: Diuretics, NSAIDS, penicillins, sulfonamides, rifampin act as haptens inducing hyperensitivity. Usually methacillin. Treatment: *
A

Drug-induced intersitital nephritis

59
Q
  • Symptoms: Acute generalized cortical infarction of both kidneys. Likely due to a combination of vasospasm and DIC. Lab Values: ** Pathophysiology: Associated with obstetric catastrophes (e.g. abruptio placentae) and septic shock. Treatment: *
A

Diffuse cortical necrosis

60
Q
  • Symptoms: 3 stages: inciting event, maintenance phase (oliguric, lasts 1-3 weeks with risk of hyperkalemia), recovery phase (polyuric; BUN and serum creatinine fall; risk of hypokalemia). Lab Values: *Granular (“muddy brown” casts. Coagulative necrosis. Intrinsic renal failure (
A

Acute tubular necrosis

61
Q
  • Symptoms: *Acute onset of gross hematuria, proteinuria. * Lab Values: ** Pathophysiology: May be triggered by a recent infection or immune stimulus. Associated with diabetes mellitus, acute pyelonephritis, chronic phenacetin use (acetaminophen), sickle cell anemia, and chronic obstruction. Treatment: *
A

Renal papillary necrosis

62
Q
  • Symptoms: Abrupt decline in renal function with an increase in creatinine and BUN over a period of several days. Lab Values: ** Pathophysiology: ** Treatment: *
A

Acute renal failure

63
Q
  • Symptoms: ** Lab Values: Urine osm >500, urine Na 20. Pathophysiology: Due to a decrease in RBF (hypotension) leading to decreased GFR. Sodium, water, and urea retained in kidney in an attempt to conserve volume so BUN/creatinine ratio rises. Treatment: *
A

Prerenal azotemia

64
Q
  • Symptoms: ** Lab Values: *Epithelial/granular casts. Urine osm 20, Fe(Na) >2%, serum BUN/Cr
A

Instrinsic renal failure

65
Q
  • Symptoms: ** Lab Values: Urine osm 40, Fe(Na) >4%, serum BUN/Cr >15. Pathophysiology: Due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies). Develops only with bilateral obstruction. Treatment: *
A

Postrenal failure

66
Q
  • Symptoms: Renal proximal tubular necrosis. Lab Values: ** Pathophysiology: Usage of expired tetracyclines. Treatment: *
A

Fanconi’s syndrome

67
Q
  • Symptoms: Nausea, anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction associated with renal failure. Lab Values: Increased BUN and creatinine in serum. Increased bleeding time and normal PC/PT/PTT/TT. Pathophysiology: ** Treatment: *
A

Uremia

68
Q
  • Symptoms: Fluid rtention (CHF, pulmonary edema, HTN), hyperkalemia, metabolic acidosis, uremia, aneima (failure of EPO), renal osteodystrophy (failure of Vit D), dyslipidemia (increase TGs), growth retardation and developmental delay. Lab Values: ** Pathophysiology: Acute form (acute tubular necrosis) or chronic form (HTN and diabetes). Treatment: *
A

Consequences of renal failure

69
Q
  • Symptoms: Subperiosteal thining of bones caused by chronic renal failure. Secondary hyperparathyroidism. Lab Values: ** Pathophysiology: *Failure of vitamin D hydroxylation leading to calcium wasting and phosphate retention. Hyperphosphatemia also independently decreases serum calcium, whereas decreased 1,25 vitamin D decreases intestinal calcium absroption. * Treatment: *
A

Renal osteodystrophy

70
Q
  • Symptoms: ADULT. Multiple, large, bilateral cysts that ultimately destroy the kidney parenchyma. Flank pain, hematuria, malignant hypertension, urinary infection, and progressive renal failure. Lab Values: Surface of kidneys is irregular because the cysts are in the proximal convoluted tubules. Pathophysiology: Chromosome 16. PKD1 or PKD2 mutation. Death from complications of chronic kidney disease or HTN (due to increased renin production). Associated with polycystic liver disease, berry aneurysms, and mitral valve prolapse. Treatment: *
A

Autosomal dominant polycystic kidney disease

71
Q
  • Symptoms: INFANTILE presentation in parenchyma. Associated with congenital hepatic fibrosis. Significant renal failur ein utero can lead to Potter’s syndrome. Concerns beyond neonatal peroid include HTN, portal H TN, and progressive renal insufficiency. Lab Values: Surface of kidneys are smooth because the cysts are in the collecting ducts in the medulla. Pathophysiology: ** Treatment: *
A

Autosomal recessive polycystic kidney disease

72
Q
  • Symptoms: Most common renal cystic disease in children; unilateral. Enlarged renal mass with cartilage and immature colecting ducts. May progress to renal failure. Lab Values: ** Pathophysiology: ** Treatment: *
A

Renal dysplasia

73
Q
  • Symptoms: Cortical and medullary cysts from long-standing dialysis. Lab Values: ** Pathophysiology: ** Treatment: *
A

Acquired polycystic kidney disease

74
Q
  • Symptoms: Benign, common (40% of eldery), incidental finding. Lab Values: Thin, nonehancing, cortical, fluid filled. Pathophysiology: ** Treatment: *
A

Simple cysts

75
Q
  • Symptoms: Sometimes lead to fibrosis and progressive renal insufficiency with inability to concentrate urine. 70% develop kidney stones, poor prognosis. Lab Values: Ultrasound shows small kidney. Pathophysiology: ** Treatment: *
A

Medullary cystic disease

76
Q
  • Symptoms: Oligohydroaminos leading to limb deformities, facial deformities, and pulmonary hypoplasia. Lab Values: ** Pathophysiology: Bilateral renal agnesis caused by malformation of ureteric bud. Treatment: *
A

Potter’s syndrome

77
Q
  • Symptoms: Progressive glomerular sclerosis. Often patients have adequate renal function. Remaining kidney undergoes compensatory hypertrophy. Lab Values: ** Pathophysiology: ** Treatment: *
A

Unilateral renal agensis

78
Q
  • Symptoms: Fusion of the kidneys at the lower pole; can’t ascend past the IMA. Normal renal function but may be predisposed to renal calculi. Lab Values: ** Pathophysiology: Common congenital anomaly (1 in 750). Treatment: *
A

Horseshoe kidney

79
Q
  • Symptoms: Aneima, anorexia, malaise, uremia, proteinuria, HTN, azotemia. Secondary hyperparathyroidism. Lab Values: Bilateral shrunken kidneys. Hyalinization of glomeruli, interstitial fibrosis, atrophy of tubules, and lymphocytic infilitrate. Broad waxy casts. Pathophysiology: End stage renal disease of multiple causes (SLE, DM). Treatment: *Dialysis and transplantation.
A

Chronic glomerulonephritis

80
Q
  • Symptoms: Pyuria with no WBC casts. Typically a young female with dysuria. Lab Values: ** Pathophysiology: Caused by E. coli, S. saphrophyticus, cyclophosphamide. Treatment: *
A

Acute cystitis

81
Q
  • Symptoms: Renal failure. Lab Values: ** Pathophysiology: Chronic-drug-induced tuberointerstitial nephritis. Most commonly from acetominophen or other analgesics. Treatment: *
A

Chronic tuberointerstitial nephritis

82
Q
  • Symptoms: Renal papillary necrosis, HTN, renail failure, and transitional cellc arcinoma of pelvis and bladder. Lab Values: ** Pathophysiology: Due to aluminium in the dialysate. Treatment: *
A

Chronic dialysis toxicity

83
Q
  • Symptoms: Hypertension due to elevated renin. Secondary hyperaldosteronism. Lab Values: ** Pathophysiology: Caused by atherosclerosis (elderly male). Treatment: *
A

Renal artery stenosis

84
Q
  • Symptoms: Hypertension due to elevated renin in a YOUNG FEMALE. Secondary hyperaldosteronism. Lab Values: ** Pathophysiology: Leads to renal artery stenosis. Treatment: *
A

Fibromuscular dysplasia

85
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Hyalinzation of arterioles leading to ischemia and shrunken kidney. Treatment: *
A

Effect of essential hypertension on kidney

86
Q
  • Symptoms: ** Lab Values: Flea-bitten kidney. Pathophysiology: Hyperplasia of the vessel media; “onion skinning”. Treatment: *
A

Effect of malignant hypertension on kidney

87
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Caused by methysergide (ergot alkaloid for migraine headaches). Fiborsis leads to entrapment of the ureters. Treatment: *
A

Retroperitoneal fibrosis

88
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Due to schistosomiasis (history of snails). Metaplasia of transitional epithelium to squamous. Treatment: *
A

Squamous cell carcinoma of the bladder

89
Q
  • Symptoms: Arises from urachal remininant. Lab Values: Present at the DOME of the bladder. Pathophysiology: Associated with extrophy of the bladder (mucosal surface exposed to environment; glandular metaplasia of epithelial). Treatment: *
A

Adenocarcinoma of the bladder

90
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Seen in young females in bladder. Treatment: *
A

Embryonal rhabdomyosarcoma

91
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Prolapse of bladder into vagina. Common in middle-aged to elderly women. Treatment: *
A

Cystocele

92
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Can complicate urinary tract outlet obstruction due to BPH. Treatment: *
A

Acquired diverticuli of the bladder

93
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Due to 12th rib. Treatment: *
A

Left kidney laceration

94
Q
  • Symptoms: ** Lab Values: ** Pathophysiology: Due to the failure of recanalization at the uteropelvic junction. Treatment: *
A

Fetal unilateral hydronephrosis

95
Q
  • Symptoms: Cystic dilation of medullary collecting ducts; at inreased risk of kidney stones and UTIs. Limited to the medulla; no other significant symptoms or consequences. Relatively common and benign. Lab Values: ** Pathophysiology: Congenital. Treatment: *
A

Medullary sponge kidney

96
Q
  • Symptoms: Signs of renal failure, peripheral gangrene, or livedo reticularis following an invasive vascular procedure (angioplastic, aortic surgery). Lab Values: ** Pathophysiology: Due to embolization of cholesterol crystals. Treatment: *
A

Atheroembolic renal disease

97
Q
  • Symptoms: Oligohydroaminos leading to limb deformities, facial deformities, and pulmonary hypoplasia. Lab Values: ** Pathophysiology: Due to defect in urogenital sinus. Treatment: *
A

Posterior urethral valves

Renal First Aid USMLE Step 1 (5 decks)

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