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USMLE Step 1 Systems > Renal > Flashcards

Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

Cystinuria

A

AR - mutation of specific transmembrane channel - can’t absorb Lysine, Arg, Cystine, Ornithine

Sx: Recurrent Nephrolithiasis (2-3rd decade) - due to cystine unable to be reasorbed by kidneys and precipitating in urine as hexagonal cystine crystals

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2
Q

Histo: Hypercellular Glomerulus
U/A: 1+ protein, TR blood, RBC casts

Dx and Lab findings?

A

Poststreptococcal Glomerulonephritis
1. Anti streptococcal Ab: anti-streptolysin O, anti-DNAse B, anti-cationic proteinase

  1. Low C3, Low total, nl C4
    Presence of cryoglobulins.

Deposition of IC with leukocyte infiltration and mesangial proliferation

Histo: hypercellular glomerulus
Electron microscopy” “humps” of IC (IgG, IgM, C3)

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3
Q

What characterizes Goodpasture’s?

A

Renal + Pulm

anti-GBM Ab
Histo: crescent formation

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4
Q

What characterizes Wegener’s (GPA)

A

Renal (may progress to RPGN pauci immune) + Pulm + Upper resp (epistaxis, sinusitis)

anti-ANCA
Histo: crescents

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5
Q

What lab characterizes Drug induced interstitial nephritis

A

high serum eosinophil count

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6
Q

How is histology of Aspergillus different from Rhizopus?

A

Both fungi form V shaped branching hyphae:
Aspergillus: septated hyphae
Rhizopus: non-septated

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7
Q

What are the three presentations of Aspergillosis and how to treat?

A
  1. Invasive - in immunocomp’ed (HIV, leukemia)
    - pulm infection.
    - spreads hematogenously to skin, paranasal sinuses, kidney, endocardium, brain
    Tx: Amphotericin B
  2. Aspergillomas (fungal balls) - grow in pre-existing cavities in lungs (tb, bronchiectasis)
    Tx: surgerical removal
  3. Allergic bronchopulm aspergillosis - in asthma pts
    - wheezing, migratory pulm infiltrate
    Tx: corticosteroids
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8
Q

What is presentation of Rhizopus?

A

Mucormycosis - in Diabetes pts or immunocomp’ed

= paranasal infection/rhinosinusitis

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9
Q

Structures derived from metanephric diverticulum vs. metanephric mesoderm?

A

Metanephric

Diverticulum = collecting system -> collecting duct, calyces, renal pelvis, ureters

Mesoderm = glomeruli, PCT, loop of Henle, DCT

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10
Q

Recurrent stone formation from a young age suggests what disease? What diagnostic test?

A

Cystinuria.

(+) NItroprusside test.

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11
Q

What happens to GFR and FF with efferent arteriolar constriction?

A

GFR: increases, but will eventually decrease

  • increase in GFR due to increased hydrostatic pressure
  • as it goes on longer, RPF decreases and increase in oncotic pressure, eventually overwhelming the increase in hydrostatic pressure and GFR decreases

FF: GFR/RPF
- increases.

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12
Q

Concentration of substances as filtrate runs along proximal tubule (which increase, decrease, stay the same?)

A

Increase (Secreted, Not Resorbed): PAH, Creat, Inulin, Urea

No Change (reabsorbed in concentrations equal with water): Na, K

Decrease (reabsorbed): bicarb, glucose, amino acids

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13
Q

Cresentic Glomerulonephritis with no Ig or complement deposits on immunofluoro.

A

Type III RPGN - ANCA associated antibodies in serum; ‘pauci-immune”a

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14
Q

How does SIADH present?

A

Euvolemic Hyponatremia.

SIADH -> more water in, hypoNa -> transient hypervolemia -> suppress RAA and stimulates naturesis -> euvolemic state, worsen hypoNa

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15
Q

Ca, Phos, PTH changes in ESRD?

A 
High Phos (can't excrete) 
Low Ca (can't make 1,25OH vit D bc 1 alpha hydroxylase in kidneys messed up) 
High PTH
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16
Q

How to calculate Renal Blood Flow?

A

RBF = (PAH clearance which is RPF) / (1-hemocrit)

PAH clearance = urine PAH * urine flow rate / plasma PAH

Q1556

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17
Q

Vasopressin would decrease renal clearance of what?

A

Urea.

Vasopressin (ADH) increases permeability to water and urea. Urea gets reabsorbed more.

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18
Q

Renal cell carcinoma both sporadic and hereditary cases are associated with what?

A

VHL deletions/mutation on chr 3p.

Hereditary - associated with VHL.; AD. 1. cerebellar hemangioma 2. clear cell renal carcinoma 3. pheochromocytoma

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19
Q

Poststreptococcal Glomerulonephritis - immunofluorescence shows?

A

Deposits of IgG, IgM, C3 - starry sky appearance

Electron Microscopy - subepithelial humps of antigen-antibody complexes

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20
Q

Abnormal Bleeding in ESRD caused by what? How are the PT, PTT, Platelet, and bleeding time?

A

Uremic toxins - cause qualitative plt disorder - impair plt aggregation.

PT, PTT, Platelet counts are normal!
Bleeding time increased.

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21
Q

What renal disease associated with painless hematuria after a URI/acute gastroenteritis?

A

IgA Nephropathy

Sx: episodic hematuria, Rbc casts
Dx: IgA deposits in mesangium
Associated with: HSP (palpable purpura, abd pain, arthralgias, igA nephropathy)

22
Q

What renal disease characterizes Goodpasture’s?

A

Rapidly Progressive Glomerulonephritis (RPGN)
Light Microscope: crescent
IF: linear

Antibodies to glomerular basement membrane and alveolar basement membrane.

23
Q

What is pathognomonic for Diabetic Nephropathy?

A

Kimmelstiel-Wilson nodule. - nodular glomerulosclerosis, most commonly in periphery of glomerulus.

Progression: Glomerular Hyperfiltration -> Increase mesangial matrix and thickening of GBM.

24
Q

How are the following substances handled in the kidney: PAH, inulin, glucose, sodium, urea?

A

PAH: RBF - filtered and secreted
Inulin: GFR - freely filtered; not reabsorbed or secreted
Na: 300), transporters are maxed out and it shows up in urine.

25
Q

What condition associated with IgG4 antibodies to phospholipase A2?

A

Membranous Nephropathy - Nephrotic Syndrome

LM - diffuse capillary and GBM thickening
IF - granular - Immune complex deposition
EM - spike and dome - subepithelial deposits

26
Q

Crohn’s predisposes to what type of kidney stones?

A

Oxalate stones, due to reduced Ca-oxalate binding in the intestine.

Crohn’s -> terminal ileum, loss of bile acids -> fat malabsorption -> excess lipids in bowel lumen, which bind Ca -> less Ca in lumen able to bind oxalate and allow for Ca oxalate excretion in bowel -> more oxalate is absorbed -> kidney stones.

27
Q

Clearance =

A

(Urine Conc x Urine Flow Rate)/ Plasma Conc.

28
Q

RCC - what cell type and histo?

A

Proximal Tubule cells*

Cuboidal or Polygonal cells with clear abundant cytoplasm (due to lipid and carbs) and eccentric nuclei.

29
Q

What in the tonicity of urine in different parts of the nephron?

A

PCT: isotonic
Desc. limb (impermeable to solute): becomes hypertonic
Asc. limb (impermeable to water): becomes hypotonic
DCT (impermeable to water, reabsorb solute): still hypotonic

Q1607

30
Q

GFR post nephrectomy - 1 kidney left?

A

Compensatory Hyperfiltration and Hypertrophy of Nephrons.

Total GFR increases from 50% to 80% within several weeks.

31
Q

What changes to the afferent and/or efferent arterioles will increases GFR and decrease RBF?

A

Constriction of efferent arteriole.

32
Q

Cause, signs, histo of Acute Tubular Necrosis

A

ATN =

  1. ischemia (prolonged Hypotension, Shock, Postsurgical patients)
  2. nephrotoxic 2/2 toxic substances

Histo: Focal necrosis of Tubular epithelium in renal medulla

Muddy Brown Casts, High Cr, etc

(vs. acute interstitial nephritis 2/2 drug: interstitial renal inflammation - fever, rash, eosinophilia, azotemia, CVA)

33
Q

Left sided variocele + membranous glomerulopathy = why?

A

L sided variocele often indicates malignant tumor or thrombus in the L renal vein.

Membranous Glomerulopathy or any nephrotic syndrome predisposes to hypercoagulable state and thrombus formation due to LOSS OF ANTICOAGULANTS, such as Antithrombin III.

34
Q

What is necessary for acute pyelonephritis to develop?

A

Vesicourethral reflux.
Ex: recurrent episodes of cystitis can weaken vesicourethral junction leading to reflux and ascending infection

Note: suppression of endogenous flora, colonization of urethra, and attachment to bladder mucosa are factors for development of cystitis.

35
Q

Membranous Nephropathy

A

Most common cause of Nephrotic Syndrome

  1. Systemic disease - SLE, tumors, DM
  2. Drugs - gold, penicillamine, NSAIDS
  3. Infection - HBV, HCV, etc.
  4. Idiopathic
LM = GBM thickening (no increased cellularity) 
EM = "spike and dome" appearance with subepithelial deposits - silver stain
IF = granular as result of IC deposition- IgG and C3
36
Q

How does GFR and FF change in acute ureteral diameter constriction/obstruction?

A

GFR: decreases bc hydrostatic pressure in bowman’s space is increased

FF: decreases bc GFR decreases (RBF does not change)

37
Q

Marked, one-sided kidney atrophy is suggestive of?

A

Renal Artery Stenosis!
- HTN, CAD/Atherosclerotic co-morbidities

Could also be fibromuscular dysplasia if women 20-30 years old. Would show “string of beads” narrowing of renal artery.

38
Q

What is seen with the recovery phase of ATN?

A

Hypokalemia.

Initiation Stage: Ischemic injury precipitated by other cause

Maintenance Stage: Oliguria, HyperK, Fluid overload, Inc BUN/Cr

Recovery: Increase in urine output leading to high volume diuresis - hypoK, hypoMg, hypoPO4, hypoCa due to slowly recovering function.

39
Q

Isoniazid - mechanism and resistance?

A

Mech: Dec. synthesis mycolic acid. Bacterial catalase-peroxidase needed to convert INH to active metabolite

Resistance: Decreased activity of bacterial catalase-peroxidase.

40
Q

Equation for FF? RPF?

A 
FF = GFR/RPF 
RPF = (1-hemocrit)(RBF)
41
Q

Acute vs. Chronic renal compensation for resp acidosis?

A

Acute - HCO3 < 30

Chronic - HCO3 > 30.

42
Q

MCD is _____ type of proteinuria.

A

Selective - LMW secreted - albumin and transferrin (vs. higher weight ones like Igs and macroglobulin)

Normal barrier:
Size - fenestrated endothelium, GBM
Charge - podocytes repel (-) charge.

43
Q

Thiazide Adverse Effects

A

HYPER:

  • hyperglycemia
  • hyperuricemia: precipitate gout
  • hyperlipidemia
  • hypercalcemia

HYPO

  • hypoK
  • hypotension
44
Q

How does ADH help generate medullary concentration gradient?

A

In medullary segment of collecting duct, ADH increases urea transporters. Urea gets reabsorbed from collecting duct -> med interstitium -> thin loop of Henle (recycled).

Helps increase conc gradient for more water absorption.

45
Q

Name two causes of aminoaciduria and how to differentiate

A
  1. Hartnup disease
    - aminoaciduria of neutral amino acids only.
    - tryptophan def -> niacin def -> pellagra.
  2. Fanconi syndrome: PCT
    - general aminoaciduria.
    - glycosuria
    - hypophosphatemia
    - hypouricemia
46
Q

NSAIDS associated with what?

A

Chronic Renal Injury
1. Papillary Necrosis (flank pain, gross hematuria, passage of tissue fragments in urine)

  1. Interstitial Nephritis (inc. creat, tubular dysfxn, fanconi syndrome)

Glomerular and vascular abnl, if any, are mild.

Key Words: chronic pain.

47
Q

How to treat Nephrogenic DI?

A
  1. HCTZ - more PCT reabsorption of H20
  2. Indomethacin - inhibit prostaglandin - decrease RBF
  3. Amiloride - if Li induced DI
  4. Hydration
48
Q

In the case of severe hypovolemia, what happens to RPF, GFR, FF?

A

RPF: severely decreased

GFR: decreased (not as big a decrease as RPF because ATII system activated which constricts efferent arteriole)

FF: GFR/RPF: increased

Normal FF ~ 1/5 RPF.

49
Q

When you have blockage of RPF in the renal artery - what increases?

A

RPF dec
GFR dec, but to a less extent (RAAS activated which constricts efferent arteriole)

Increased FF.

50
Q

Membranous Nephropathy

A

Most common nephrotic syndrome in adults. Most commonly idiopathic, can be associated with antibody to phospholipase A2, or solid tumors.

LM: thickened GBM -> thickened capillary loops
EM: “spike and dome” due to subEPIthelial deposits.

51
Q

What other condition may lead to a similar picture as nephrogenic diabetes insipidous?

A

Hypercalcemia of malignancy.

HyperCa adversely affects renal concentrating ability.

USMLE Step 1 Systems (11 decks)

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