Usmle Step 1 Fa Renal Pathology

Front 1

Type I RTA
(a) defect
(b) effect
(c) causes
(d) treatment

Back 1

(a) Various defects leading to inability to secrete H+ (basol HCO3/CL exchanger, cytoplasmic CA< apical H+ATPase or H+/K+ATPase, basolat K/Cl transp, reduced titratable buffers)
(b) urine pH >5.5; hypokalemia
(c) amphoterecin, light chains in multiple myeloma
(d) oral admin of HCO3

Front 2

Type II RTA
(a) defect
(b) effect
(c) causes
(d) treatment

Back 2

(a) Defect in proximal tubule reabsorption of HCO3 (Na/HCO3 transporter or BB CA or generalized defect in PT -Fanconi's or protein overload toxicity))
(b) Urine pH initially >5.5 due to loss of filtered HCO3; when serum HCO3 equal to threshold, the PT tubules reclaim HCO3 causing urine pH to drop; hypokalemia may occur (incr Na+ presentation at DT)
(c) carbonic anhydrase inhibitors, primary hyperparathyroidism, proximal tubule nephrotoxic drugs/chemicals (aminoglycosides, heavy metals)
(d) thiazides to produce volume depletion which incr renal threshold for HCO3 reclamation

Front 3

Type IV RTA
(a) defect
(b) effect
(c) causes

Back 3

(a) hypoaldosteronism
(b) causes hyperkalemia, inhibition of ammonia (high K+ leads to decr ammoniagenesis) excretion in proximal tubule leading to urine pH decr and decr buffering capacity
(d) destruction of HGA (hyaline arteriosclerosis of afferent arterioles in DM, acute or chronic tubulointerstial inflam)

Front 4

Possible causes of RBC casts in urine

Back 4

Glomerular inflammation (nephritic syndromes)
Ischemia
Malignant HTN
Presence of casts indicates renal origin

Front 5

Possible causes of WBC casts in urine

Back 5

Tubulointerstitial diseases
Acute pyelonephritis
Glomerular disorders

Front 6

Possible causes of granular (muddle brown) casts in urine

Back 6

Acute tubular necrosis

Front 7

Possible causes of waxy casts in urine

Back 7

Advanced renal disease/CRF

Front 8

Possible causes of hyaline casts in urine

Back 8

Nonspecific

Front 9

Acute cytitis: results from macroscopic urinalysis?

Back 9

WBC's no casts

Front 10

Bladder cancer: results from macroscopic urinalysis?

Back 10

RBC's no casts

Front 11

Define nephritic syndrome

Back 11

Inflammatory process involving glomeruli, leading to hematuria, azotemia, RBC casts in urine, oliguria, hypertension, and proteinuria (3.5g/day)

Front 12

Name major nephritic syndromes

Back 12

Acute poststreptococcal glomerulonephritis
Rapidly progressive (crescentic) glomerulonephritis
Diffuse proliferative glomerulonephritis (SLE)
Berger's disease (IgA glomerular nephropathy)
Alport's Syndrome

Front 13

Define nephrotic syndrome

Back 13

Presents w/massive proteinuria (>3.5d, frothy urine), hyperlipidemia, edema

Front 14

Name the major nephrotic syndromes

Back 14

Membranous glomerulonephritis (diffuse membranous GN)
Minimal change disease
Amyloidosis
Diabetic glomerulonephropathy
Focal Segmental glomerulosclerosis
Membranoproliferative glomerulonephritis

Front 15

Alport's Syndrome
(a) etiology
(b) clinical presentation
(c) EM
(d) Treatment

Back 15

(a) XLD absence of type IV collagen
(b) nephritis (hematuria; may have RBC casts); hearing loss; eye problems (cataracts, etc)
(c) Thickening or attenuation of GBM w/longitudinal splitting
(d) ACEI's, renal transplant

Front 16

Fabry's disease
(a) etiology
(b) clinical presentation
(c) diagnosis
(d) treatment

Back 16

(a) XL lysosomal storage dz; deficiency of alpha galactosidase. Accumulates in tissues.
(b) Proteinuria/hematuria
purples papules (trunk, lower genitalia)
heart problems (LVH, arrythmias, premature CAD)
Corneal opacities
(c) incr levels of ceramide and digalactosidase in urine
(d) recomb alpha galactosidase

Front 17

Minimal change disease
(a) Etiology/epidemiology
(b) secondary diseases
(c) clinical presentation
(d) LM
(e) EM
(f) treatment

Back 17

(a) unknown; usually following an upper resp tract infx
Mainly in young children
(b) Hodgkin's; hypersensitivity
(c) Nephrotic presentatoin (edema, wt gain, selective proteinuria, hyperlipidemia)
(d) normal glomeruli
(e) fusion of podocyte foot processes
(f) predinisone
Cyclophosph or chlorambucil if resistant to steroids

Front 18

Focal Segmental Glomerulosclerosis
(a) associations
(b) clinical presentation
(c) LM
(d) IF
(e) EM
(f) treatment/outcome

Back 18

(a) heroine use, morbid obesity, HIV, HTN, mainly adults
(b) Nephrotic syndrome w/microscopic hematuria
(c) sclerosis w/in capillary tufts (focal, segmental) w/hyalniosis
(d) IgM and C3 in sclerotic regions
(e) Fusion of epithelial foot processes
(f) prednisone; most progress to ESRD in 5-10yr

Front 19

Membranous glomerulonephritis
(a) epidemiology
(b) secondary diseases
(c) clinical presentation
(d) LM
(e) EM
(F) complications
(g) treatment

Back 19

(a) adults; immune complex dz of unknown etioloty
(b) SLE, malignancy, infection (Hep B, syphilis, drugs
(c) nephrotic syndrome w/azotemia
(d) LM: diffuse capillary wall and BM thickening
(e) subepithelial deposits (spike and dome w/methenamine stain)
(f) renal vein thrombosis
(g) cyclophos, ACEI, transplant (little response to steroids)

Front 20

Acute Poststreptococcal Glomerulonephritis
(a) epidemiology/etiology
(b) clinical presenation
(c) gross
(d) LM
(e) EM
(f) outcomes

Back 20

(a) children due to GAS infx
(b) nephritis syndrome 1-2 wks post infx; periorbital edema
(c) inflammation of all glom and both kidneys; punctate surface hemorrhages
(d) LM shows hypercellulra glom w/prol of mes/epi (normal BM)
(e) subepithelial humps ("lumpy bumpy")
(f) resolves spontaneously

Front 21

Rapidly Progressive Glomerulonephritis
(a) epidemiology
(b) etiology
(c) clinical presentation
(d) LM
(e) outcomes

Back 21

(a) adolescents and young adults (type II); >40 usually type III
(b) Type I: antiGBM ab (goodpasture's)
Type II: Immune c omplex (SLE, IgA, HSP, Wegener's)
(c) rapidly progressive nephritic syndrome
(d) crescents b/w Bowman's space and glomerulus (fibrin and prolif of parietal cells in bowman's space)
(e) dialysis and/or transplant; rapid course to renal failure

Front 22

Membranoproliferative glomerulonephritis Type I
(a) epidemiology
(b) secondary diseases
(c) clinical presentation
(d) LM
(e) EM
(f) course and therapy

Back 22

(a) adults (involves both classic and alternative pathway)
(b) hep C, hepB, lupus
(c) more often presents w/nephrotic pattern
(d) splitting of BM, expansion of mesangial matrix "tram track"
(e) subendothelial electron dense depositis
(f) corticosteroids and antiplatelet drugs, usually progresses slowly to CRF

Front 23

Membranoproliferative glomerulonephritis Type II
(a) epidemiology
(b) secondary diseases
(c) clinical presentation
(d) LM
(e) EM
(f) course and therapy

Back 23

(a) younger adults (only involves alternative complement pathway)
(b) HepC,B, HIV, SLE
(c) nephritic or macroscopic hematuria or chronic renal failure
(d) "tram track" appearance due to splitting of BM and expansion of mesangial matrix
(e) dense deposits within BM
(f) corticosteroids/antiplatelet drugs; usually slowly progress to CRF

Front 24

IgA nephropathy aka Buerger's
(a) epidemiology
(b) secondary diseases
(c) clinical presentation
(d) LM
(e) EM
(f) labs
(g) course and therapy

Back 24

(a) most common primary GN in world; in adults and young adults; M>F
(b) May be a part of henoch schloenlein purpura or manifest after infx
(c) hematuria w/in 1-2 days of URI
(d) Focal proliferative w/mesangial expansion
(e) mesangial IgA deposits
(f) incr IgA and normal complement

Front 25

5 types of SLE involving kidneys (general presentations)

Back 25

Type I: mild mesangial proliferation (asymptomatic or low grade proteinuria)
Type II: Mesangial nephritis (low grade hematuria and/or proteinuria)
Type III: focal proliferative nephritis (nephritic urinary sediment, proteinuria)
Type IV: Diffuse proliferative : Mot severe. Nephritic and nephritic
Type V: membranous nephropathy (nephrotic syndrome)

Front 26

Histology of the 5 types of SLE nephropathies

Back 26

Type I: normal
Type II: mesangiall FS glom involv; incr mesangial matrix
Type III: Less than half glomeruli involved
Type IV: All glom involv; mesangial prolif
-LM: wire loop abnormality (omm complex thicken BM)
-EM/IF: subendothelial imm complex deposition
Type V: similar to membranous glomerulonephritis (Subepithelial)

Front 27

Treatment of SLE nephropathies

Back 27

Type I to II: no treatment
Type III to V: aggressive immunosuppression w/corticosteroids, cyclophos, azathioprine, chlorambucil

Front 28

Diabetic nephropathy
(a) epidemiology
(b) clinical presentation
(c) LM
(d) labs
(e) treatment

Back 28

(a) ESRD more prevalent in TIIDM but more change of getting in TIDM
~20yrs after onset of DM; M>F, AA, NA>whites
(b) nephrotic syndrome and retinopathy invariably present
(c) microalbuminemia (early) and proteinuria (late)
(d) Thick GBM (NE glycosylation); mesangial damage; Kimmelstiel Wilson "wire loop" nodules
(e) strict control of DM and HTN; no effective treatment once proteinuria; progress to ESRD

Front 29

Goodpasture's
(a) etiology
(b) presentation
(c) histology
(d) treatment

Back 29

(a) anti GBM antibodies
(b) pulmonary hemorrhage; nephritic presentation and rapidly progressive GN
(c) antiGBM Abs (linear Ig staining of BM)
(d) plasma exchange and coeticosteroids

Front 30

4 major types of kidney stones

Back 30

Calcium (oxalate, phosphate or both)
Ammonium magnesium phosphate (struvite)
Uric acid
Cystine

Front 31

Calcium based kidney stones
(a) cause
(b) appearance
(c) notes

Back 31

75% of all renal stones; calcium oxalate, phosphate, or both
(a) conditions that cause hypercalcemia (cancer, incr pTH, incr vitD, milk alkali syndrome) can lead to hypercalcuria and stones
(b) radiopaque
(c) oxalate crystals can result from ethylene glycol (antifreeze) or vitC abuse

Front 32

Struvite stones
(a) composition
(b) cause
(c) appearance

Back 32

(a) ammonium magnesium phosphate
(b) infection w/ urease positive bugs (Proteus, staph, klebs) which make urine more alkaline causing precipitation of magnesium ammonium phosphate salts
(c) can form staghorn calculi; radiopaque or radiolucent

Front 33

Uric acid stones
(a) associations
(b) appearance

Back 33

(a) strong association w/gout and often seen as a result of diseases with increases cell turnover (leukemia and myeloproliferative disorders)
(b) radiolucent

Front 34

Cystine stones
(a) causes
(b) appearance

Back 34

(a) most often due to secondary cysteinuria
(b) hexagonal shaped stones; rarely form staghorn calculi; faintly radioopaque; treat w/alkalinization of urine

Front 35

Cortical adenoma
(a) description
(b) gross
(c) micro

Back 35

(a) benign tumor of the kidney; common finding at biopsy
(b) yellow, encapsulated cortical nodules
(c) may be identical to renal cell carcinoma, distinguished by size

Front 36

Angiomyolipomas
(a) composition
(b) disease association

Back 36

(a) hamartomas; composed of fat, smooth muscle, and blood vessels
(b) particularly common in patients with tuberous sclerosis

Front 37

Renal cell carcinoma
(a) epidemiology
(b) risk factors/associations
(c) symptoms
(d) gross
(e) micro
(f) prognosis

Back 37

(a) 90% of all renal cancers; 50-70YO no sex prediliction
(b) incr incidence with smoking and obesity
Associated w/paraneoplastic syndromes(ectopic EPO, ACTH, PTHrP, prolactin)
Von Hippel Lindau and gene deletion on Ch3
(c) "classic" triad: hematuria, palpable mass, costovertebral pain; also secondary polycythemia, flank pain, fever, wt loss
(d) usually upper pole; solitary w/necrosis and hemorrhage; often invades renal vein and extends into vena cava and heart
(e) high incidence of mets on presentation

Front 38

Wilm's tumor
(a) epidemiology
(b) cause
(c) symptoms
(d) gross
(e) micro
(f) prognosis

Back 38

(a) most common renal malignancy of early childhood
(b) deletion of tmor suppressor gene WT1 on C11
(c) huge, palpable flank mass, hemihypertrophy; nausea, hematuria, intestinal obstruction
(d) Large, demarcated mass; usually unilateral but may be bilateral if familial
(e) embryonic glomerular and tubular structures surrounded by spindle cells
(f) 90% survival when treated with Sx/Rx/Cx

Front 39

WAGR complex

Back 39

Wilm's tumor
Aniridia
Genitourinary malformation
Mental motor retardation

Front 40

Transitional cell carcinoma
(a) epidemiology
(b) symptoms
(c) associations

Back 40

(a) MCC tumor of urinary tract system
(b) painless hematuria
(c) phenacetin, smoking, aniline dyes, and cyclophosphamide

Front 41

Pyelonephritis (acute)
(a) risk factors
(b) epidemiology
(c) symptoms
(d) urine
(e) gross
(f) micro

Back 41

(a) urinary obstruction, vesicoureteral reflux, pregnancy, intrumentation, diabetes mellitus
(b) F<40 most common; over 40, men due to BPH
(c) fever, CVA tenderness, WBC casts (dysuria, frequency, urgency_
(d) WBCs and WBC casts (casts are pathognomonic)
(e) yellow microabscesses in cortex w/relative sparing of glomeruli
(f) suppurative and tubular necrosis

Front 42

Chronic pyelonephritis
(a) cause
(b) symptoms
(c) gross
(d) microscopic

Back 42

(a) reflux nephropathy most common
(b) present with renal failure or HTN
(c) irregular scarring , coarse, asymmetric at corticomedullary jct and blunted calyx
(d) chronic inflammation w/eosinophilic casts (thyroidization)

Front 43

Diffuse cortical necrosis
(a) describe
(b) cause
(c) associations

Back 43

(a) acute generalized infarction of cortices of both kidneys
(b) likely due to combo of vasospasm and DIC
(c) associated w/obstetric catastrophes and septic shock

Front 44

Drug induced interstitial nephritis
(a) describe
(b) symptoms
(c) cause

Back 44

(a) acute interstitial renal inflammation
(b) fever, rash, eosinophilia, hematuria 2 wks after drug admin
(c) penicillins derivatives, NSAIDs, diuretics act as haptens

Front 45

Acute Tubular Necrosis
(a) 3 stages
(b) associations
(c) outcomes

Back 45

(a) inciting event, maintenance (low urine), recovery
(b) renal ischemia (shock, sepsis), crush injury, toxins
(c) 2-3 wk recovery, death most often occurring in renal phase; treat w/dialysis; MCC of ARF

Front 46

Renal papillary necrosis
(a) define
(b) major associations

Back 46

(a) sloughing of renal papillae leading to gross hematuria and proteinuria
(b) DM, acute pyelonephritis, chronic phenacetin use, sickle cell anemia

Front 47

Gouty nephropathy
(a) describe
(b) diagnosis

Back 47

(a) urate crystals in tubules inducing tophus formation and chronic inflammatory rxn
(b) birefringent needle shaped crystals

Front 48

Acute urate nephropathy
(a) describe
(b) cause

Back 48

(a) precipitation of crystals in collecting ducts causing obstruction
(b) lymphoma and leukemia, esp after chemo

Front 49

Exstrophy of bladder
(a) describe
(b) associations

Back 49

(a) absence of anterior musculature of bladder and abdominal wall; failure of mesoderm to grow over anterior bladder
(b) incr incidence of adenocarcinoma; site of severe chronic infx

Front 50

MCC of bladder obstruction in men

Back 50

BPH or carcinoma

Front 51

MCC of bladder obstruction in women

Back 51

Cystocele of bladder

Front 52

Acute renal failure (3 types)

Back 52

Abrupt decline in renal fct w/increased Cr and BUN over a period of several days

Front 53

Prerenal ARF
(a) cause
(b) expected urine osm
(c) expected urine Na
(d) expected FeNa
(e) expected BUN/Cr ratio

Back 53

(a) decreased RBF (like hypotension) causes decr GFR, incr sodium and water retention of kidney; BUN/Cr increase in the attempt to conserve volume
(b) >500
(c) <10
(d) <1%
(e) >20

Front 54

Renal ARF
(a) cause
(b) expected urine osm
(c) expected urine Na
(d) expected FeNa
(e) expected BUN/Cr ratio

Back 54

(a) usually due to tubular necrosis/ischemia/toxins; debris is obstructing tubule causing backflow and decr GFR; urine has epithelial/granular casts; BUN absorption impaired
(b) <500
(c) >20%
(d) >2%
(e) <15

Front 55

Postrenal ARF
(a) cause
(b) expected urine osm
(c) expected urine Na
(d) expected FeNa
(e) expected BUN/Cr ratio

Back 55

(a) outflow obstruction (stones, BPH, neoplasia) but only if bilateral
(b) <350
(c) >40
(d) >4%
(e) >15%

Front 56

Fanconi's syndrome
(a) describe
(b) cause
(c) complications (cause)

Back 56

(a) decr proximal tubule transport of AA, glucose, phosphate, uric acid, protein, and electrolytes
(b) congenital or acquired (Wilson's disease, glycogen storage disease, drugs like cisplatin, expired tetracycline)
(c) Rickets (decr phosphate reabsorption)
Metabolic acidosis (decr bicarb reabsorption)
Increased distal Na reabsorption leading to hypokalemia (decr early Na reabsorption)

Front 57

ADPKD
(a) description
(b) cause
(c) presentation
(d) outcomes
(e) associations

Back 57

(a) multiple, large, bilateral cysts; enlarged kidneys
(b) flank pain, hematuria, HTN, urinary infx, progressive renal failure
(c) flank pain, hematuria, hypertension, urinary infx, progressive renal failure
(d) AD mutation in APKD2
(e) death from uremia or HTN due to incr renin
(f) polycystic liver disease, berry aneurysm (HTN), mitral valve prolapse

Front 58

ARPKD
(a) clinical presentation
(b) associations

Back 58

(a) infantile presentation in parenchyma
(b) hepatic cysts and fibrosis

Front 59

Dialysis cysts description

Back 59

Cortical and medullary cysts resulting from long standing dialysis

Front 60

Simple cysts description

Back 60

Benign incidental finding; cortex only

Front 61

Medullary cystic disease description

Back 61

Medullary cysts; US shows small kidney; poor prognosis

Front 62

Medullary sponge disease

Back 62

collecting duct cysts; good prognosis

Front 63

Low Na+ symptoms

Back 63

Disorientation, stupor, coma

Front 64

High Na+ symptoms

Back 64

Neurologic; irritablity, delirium, coma

Front 65

Low Cl- symptoms

Back 65

Secondary to metabolic alkalosis, hypokalemia, hypovolemia, incr aldoesterone

Front 66

High Cl- symptoms

Back 66

Secondary to non anion gap acidosis

Front 67

Low K+ symptoms

Back 67

U waves on ECG, flattened T waves, arrhythmias, paralysis

Front 68

High K+ symptoms

Back 68

Peaked T waves, wide QRS, arrythmias

Front 69

Low Ca2+ symptoms

Back 69

Tetany, neuromuscular irritability

Front 70

High Ca2+ symptoms

Back 70

Delirium, renal stones, abdominal pain, not necessarily calciuria

Front 71

Low Mg2+ symptoms

Back 71

Neuromuscular irritability, arrythmias

Front 72

High Mg2+ symptoms

Back 72

Delirium, decreased DTR's, cardiopulmonary arrest

Front 73

Low phosphate symptoms

Back 73

Low mineral ion product causes bone loss and osteomalacia

Front 74

High phosphate symptoms

Back 74

High mineral ion product causes renal stones and metastatic calcifications