USMLE Step 1 Random Facts > Renal > Flashcards

Renal Flashcards

(90 cards)

Study These Flashcards
1
Q

nephrotic synd

A 
massive proteinuria (>3.5g/day, frothy urine), hyperlipidemia, fatty casts, edema; ass. w/ thromboembolism (bc of ATIII loss in urine; present w/ flank pain + hematuria), increase risk of infection
NO RBC OR RBC CASETS IN URINE

FSGS
membranous nephropathy
minimal change dz (lipoid nephrosis)
amyloidosis - ass w/ chronic conditions
MPGN
diabetic glomerulonephropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

nephritic synd

A

inflammatory!! (hypercellular, inflamed glomeruli from immune-complex dep)
hematuria, RBC casts in urine, azotemia, oliguria, HTN, mild proteinuria

PSGN
RPGN
DPGN
Berger's dz (IgA nephropathy)
Alport synd
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

FSGS

A
  • segmental sclerosis + hyalinosis (LM)
  • effacement of foot processes (EM)
  • adults (Hisp, Af Am)
  • NO response to steroids
  • ass w/ HIV, heroin abuse, obesity, sickle cell dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

membranous nephropathy

A
  • diffuse capillary + GBM thickening (bc immune-complex dep) (LM)
  • “spike-and-dome” appearance w/ SUBEPITHELIAL deposits [b/w epith cells + BM, under podocytes] (EM)
  • granular IF (w/ IgG + C3 dep)
  • SLE’s nephrotic presentation
  • idiopathic (85%)!!
  • also by use of NSAIDs/penicillamine, Hep C or B, DM
  • Caucasian adults
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

minimal change dz

A
  • NORMAL glomeruli (LM)
  • foot process effacement - bc of cytokine damage (EM)
  • selective loss of albumin, not Ig
  • may be triggered by recent infection/immune stim
  • children (usually idiopathic)
  • responds to steroids (ONLY ONE)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MPGN

A

type I:

  • granular IF (SUBENDOTHELIAL DEP)
  • tram-track appearance bc GBM splitting (from mesangial ingrowth)
  • thick capillary membranes
  • ass w/ HBV, HCV + subacute bacterial endocarditis

type II:

  • INTRAMEMBRANOUS DEP
  • ass w/ C3 nephritic factor (auto-Ab stabilizes C3 convertase)

**both have granular IF and LARGE HYPERCELLULAR GLOMERULI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

diabetic glomerulonephropathy

A

-hyaline arteriosclerosis
-NEG of GBM –> increased permeability, thickening
NEG of efferent arterioles –> increases GFR
GBM thickening, Kimmelsteil-Wilson nodules (ovoid hyaline mass; eosinophilic nodular glomerulosclerosis)
ACE inhibitors slow injury process!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

acute post-strep GN

A
  • type III HST
  • “lumpy-bumpy” appearance (glomeruli enlarged and hypercellular, neutrophils) (LM)
  • SUBEPITHELIAL immune complex humps (EM)
  • granular IF (IgG, IgM, C3 deposition) - decreased C3, normal C4
  • children
  • periph + periorbital edema
  • dark urine
  • after group A-beta strep infection of SKIN (impetigo) or PHARYNX - WEEKS after! + resolves spontaneously
  • elevated ASO titers, or anti-DNase B!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

RPGN

A
  • crescent-moon shape (consist of fibrin, plasma proteins like C3b, macrophages, glomerular parietal cells, monocytes) w/in BOWMAN’S SPACE (LM and IF)
  • poor prognosis

can result from:

  • Goodpasture’s synd (type II HST) - linear IF
  • Wegener’s granulomatosis (c-ANCA) - neg IF
  • microscopic polyangiitis, Churg Strauss (p-ANCA) - neg IF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Goodpasture’s synd

A

type II HST
Ab to GBM and alveolar BM
linear IF (C3 and IgG deposited along GBM)
hematuria/hemoptysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DPGN

A
  • due to SLE (most common cause of death in SLE) or MPGN
  • “wire looping” of capillaries (LM)
  • SUBENDOTHELIAL OR INTRAMEMBRANOUS IgG based immune complexes often w/ C3 dep
  • granular IF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Berger’s dz (IgA nephropathy)

A
  • related to Henoch-Schonlein purpura
  • mesangial prolif (LM); mesangial IC dep (EM)
  • IgA-based immune complex dep in mesangium (IF)
  • NORMAL complement levels
  • presents/flares w/ URI or acute gastroenteritis
  • follows mucosal infection (bc excess prod of IgA)
  • most common nephropathy worldwide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Alport synd

A
  • mut in type IV collagen –> split BM
  • X-linked
  • GN, deafness, eye problems (cataracts, etc.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

early prox tubule reabsorb/secrete?

A

all of glucose and AA
most of bicarb, Na, Cl, phosphate, water (ISOTONIC absorption)
65-80% Na reabsorbed
secretes ammonia (to buffer H)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PTH function in prox tubule

A

inhib Na/phosphate cotransport –> phosphate excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

thin descending LOH function?

A

passive reabsorp of water (via medullary hypertonicity)

concentrating segment –> makes urine HYPERTONIC!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

thin desc LOH impermeable/permeable to?

A

imperm to Na

perm to urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

thick ascending LOH reabsorb?

A

active reabsorption of Na, K, Cl
indirectly reabsorb Mg, Ca (by + lumen potential from K backleak) - paracellular
10-20% Na reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

thick ascending LOH impermeable to?

A

WATER

makes urine LESS concentrated as it ascends

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

early distal convoluted tubule (DCT) reabsorb?

A

ACTIVE reabsorb of Na, Cl (urine hypotonic)
5-10% Na reabsorbed
MOST DILUTE SEGMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PTH effect on DCT?

A

increase Ca/Na exchange –> Ca reabsorb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

DCT impermeable to?

A

water (unless vasopressin levels adeq to promote reabsorp) and urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

collecting ducts reabsorb?

A

Na in exchange for K, H secretion (reg by aldosterone)
3-5% Na reabsorbed
HYPERTONIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Potter synd?

A 
clubfeet
flat face w/ low-set ears, other facial deformities
pulmonary hypoplasia (most common cause of death)

caused by bilat renal agenesis*** (mostly), ARPKD, posterior urethral valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
most bladder cancers are?
transitional cell carcinoma aka UROTHELIAL carcinoma
26
GFR calc measured by?
inulin | creatinine can estimate
27
PAH best measure of?
RPF; underestimated by ~10%
28
horseshoe kidney trapped under what artery?
IMA
29
RBF =
RPF/(1-hematocrit) = (PAH clearance)/(1-hematocrit) or (renal artery pressure - renal vein pressure)/renal vascular resistance
30
no ureteric bud =
bilat kidney agenesis
31
horseshoe kidney ass w/ what?
Turner's synd
32
what property of glomerular filtration barrier lost in nephrotic synd?
charge barrier
33
what keeps negative charge barrier?
BM + heparan sulfate
34
renal clearance =
(U x V)/P
35
FF =
GFR/RPF normally 20%
36
filtered load =
GFR x plasma concentration
37
glucose reabsorpt?
prox tubule via Na/glucose co-transport @160 mg/dL --> glucosuria (threshold) @350 mg/dL --> all transporters fully saturated
38
Hartnup disease is?
deficiency of tryptophan --> decreased vit B3 --> pellagra
39
in PCT, ATII action is?
stim Na/H exchange --> increased Na, H2O, HCO3 reabsorption; secrete H causes contraction alkalosis!
40
TF/P > 1 when
solute absorbed less quickly than water | ex. PAH, Creatinine, inulin, urea, Cl
41
TF/P = 1 when
solute + water reabsorbed @ same rate | ex. K, Na
42
TF/P < 1 when
solute reabsorbed faster than water | ex. HCO3, AA, glucose
43
functions of ATII
potent vasoconstrictor constricts efferent arterioles --> maintains GFR by increasing FF stim aldosterone prod, ADH release increases PCT Na/H activity --> contraction alkalosis stim hypothal --> thirst
44
ANP effect in kidney
increase GFR | decrease renin
45
JG cells are modified what?
modified SM of afferent arteriole
46
in renal artery stenosis what happens to JG cells
JG cells of affected kidney(s) --> hypertrophy + hyperplasia bc increased release of renin
47
what part of kidney converts to active vit D
PCT
48
afferent arteriole mediators
prostaglandins - vasodil | NSAIDS - oppose prostaglandins
49
efferent arteriole mediators
AT II - vasoconstriction | ACE inhib - oppose AT II
50
protein effects in glomerulus
if increased - increases glomerular capillary oncotic pressure --> decreased GFR, FF; no change RPF if decreased - decreases glomerular capillary oncotic pressure --> increased GFR, FF; no change RPF
51
impt function of ATII to prevent further decrease in vol loss
compensatory Na reabsorp. @ PCT and DCT!!!
52
increased serum Mg levels -->
decreased DTRs, bradycardia, lethargy, etc.
53
winter's formula
PCO2 = 1.5(HCO3) + 8 +/- 2
54
anion gap =
Na - (Cl + HCO3) normal = 8-12 mEq/L
55
increased anion gap metab acidosis
``` MUDPILES! Methanol (formic acid) Uremia DKA Propylene glycol INH or Iron tablets Lactic acidosis (ex. in shock) Ethylene glycol (oxalic acid) Salicylates (LATE) ```
56
normal anion gap metab acidosis
``` HARDASS! Hyperalimentation (ex.overeating, parenteral nutrition) Addison's dz Renal tubular acidosis Diarrhea Acetazolamide Spironolactone Saline infusion ```
57
RTA type 1
"distal" defect in collecting tubule ability to EXCRETE H+ [intercalated cells] urine pH > 5.5 hypokalemia increased risk for Ca phosphate kidney stones bc of increased urine pH + bone resorption
58
RTA type 2
``` "proximal" urine pH < 5.5 defect in PCT reabsorption of HCO3 hypokalemia increased risk of hypophosphatemic rickets may be ass w/ Fanconi synd ```
59
RTA type 4
"hyperkalemic" HYPOALDOSTERONISM or collecting tubule lack of response to aldost hyperkalemia --> impairs ammoniagenesis in PCT --> decreased buffering capacity + urine pH decreased
60
what 2 synd can present as both nephritic/nephrotic
DPGN MPGN SLE
61
diff b/w IgA neph + PSGN
IgA neph - few DAYS after URI infection | PSGN - few WEEKS after infection
62
complications of kidney stones
hydronephrosis (expansion of renal pelvis) | pyelonephritis
63
all kidney stones are radiopaque EXCEPT
Uric acid stones = radiolUcent (not seen on x-ray) | view on CT or US
64
lowest pH in nephrons is @
DCT | collecting tubules
65
2 factors that prevent crystallization of stones
- citrate (binds free Ca --> facilitates its excretion) | - fluids!
66
calcium phosphate stones
alkaline pH causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn's tx = citrate, thiazide diuretics
67
calcium oxalate stones
acidic pH **can result from ethylene glycol (antifreeze) or vit C abuse other causes: hypercalcemia (cancer, increased PTH, sarcoidosis), Crohn's tx = citrate, thiazide diuretics
68
common kidney stone presentation
calcium oxalate stones in pt w/ hypercalciuria + normal serum calcium (idiopathic hypercalciuria)
69
ammonium magesium phosphate stones (struvite)
alkaline pH infection w/ urease-positive bugs (Proteus, Staph, Klebsiella) staghorn calculi (nidus for UTIs)
70
uric acid stones
acidic pH radioLUCENT from hyperuricemia (gout); seen in dz w/ increased cell turnover like LEUKEMIA tx = alkalinization of urine
71
cystine stones
acidic pH HEXAGONAL crystals - of sulfur-containing compounds! 2ndary to cystinuria tx = alkalinization
72
RCC originates from what cells
PCT cells - clear cells! (filled w/ lipids + carbs)
73
RCC spread =
hematogenously by invading renal vein --> IVC
74
RCC ass w/ what paraneoplastic synd
ectopic EPO ACTH PTHrP prolactin
75
Wilm's tumor (nephroblastoma) contains what cells
embryonic glomerular structures (blastema)
76
acute pyelonephritis histo + casts
neutrophilic infiltrate | WBC casts
77
chronic pyelonephritis histo + casts
``` lymphocytic infiltration + corticomedullary fibrosis (scarring) eosinophilic casts (thyroidization of kidney) ```
78
drugs implicated in drug-induced interstital nephritis
1-2 wks after: penicillin derivatives, diuretics, sulfonamides, rifampin months after: NSAIDS chronic interstitial nephritis: lithium, cyclosporine
79
diffuse cortical necrosis ass w/?
obstetric complic (ex. placenta abruptio) septic shock ARDS
80
acute tubular necrosis features?
- 3 stages (inciting, maintenance, recovery) - inj + necrosis of tubular epith cells - ass w/ aminoglycosides, cisplatin, amphotericin B, foscarnet, heavy metals, ethylene glycol, crush injury (myoglobiuria), toxins, renal ischemia (shock, sepsis) - granular "muddy brown" casts seen**** - w/ drugs/toxins --> PCT suscept; w/ renal ischemia --> PCT + medullary segment of thick ascending limb suscept
81
in ATN, death occurs usually in what phase
inciting
82
maintenance phase of ATN =
oliguria risk of hyperkalemia 1-3 wks
83
recovery phase of ATN =
polyuria risk of hypokalemia (bc of high vol + hypotonic urine) BUN + serum creatinine fall
84
renal papillary necrosis ass w/
DM acute pyelonephritis + UT obstruction chronic phenacetin use (ex. acetominophen) sickle cell anemia/trait
85
prerenal azotemia =
- bc of decreased RBF (ex. hypotension, NSAIDs) - Na/H2O and urea retained to conserve vol - INCREASED BUN/creatinine ratio
86
intrinsic renal failure =
- cause = ATN or ischemia/toxins - patchy necrosis - epith/granular casts in urine - DECREASED BUN/creatine ratio
87
postrenal azotemia =
- due to outflow obstuction (stones, BPH, neoplasia, etc.) - forces BUN back into blood - ONLY w/ bilat obstruction - INCREASED BUN/creatinine ratio
88
features of uremia
``` pericarditis N/V asterixis encephalopathy platelet dysfunt (qualitative dysfunct; NORMAL platelet count) INCREASED BUN/creatinine ratio ```
89
histo in renal osteodystrophy
subperiosteal thinning of bones
90
medullary cystic disease
- AD - tubulointerstital fibrosis (cysts in medullary CD) - inability to conc urine - SHRUNKEN KIDNEYS on US
USMLE Step 1 Random Facts
flashcards
Decks in class (35)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions