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USMLE REVIEW > Renal > Flashcards

Renal Flashcards

1
Q

What fundamental problem creates Potter Sequence?

A

Oligohydromnios causes by bilateral renal agenesis (failure of ureteric buds to form)

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2
Q

What cells release renin?

A

Juxtaglomerular cells

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3
Q

3 stimuli to induce renin release

A

Decreased BP
Hypoosmolarity (low Na)
Catecholamines = B-adrenergic stimulation

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4
Q

Water distribution in water

A

60% body wt is water
2/3 of that is intracellular

1/3 is extracellular –1/4 of that is intravascular

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5
Q

At what blood glucose are all renal transporters saturated?

A

350 mg/dL

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6
Q

Vitamin deficiency resulting from Hartnup disease?

A

Hartnup = defective tryptophan transporter

Results in Niacin deficiency (B3) = pellegra

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7
Q

3 D’s of pellegra

A

Diarrhea
Dementia
Dermatitis

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8
Q

Which drugs inhibit the Na/Cl/K pump in thick ascending limb?

A

Loop Diuretics

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9
Q

Where are Ca and Mg reabsorbed in the kidney?

A

Thick ascending limb

More Ca+ absorbed in early distal tubule when PTH is present

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10
Q

Where does PTH act in the kidney?

A

Early distal convoluted tubule

Increases reabsorption of Ca+

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11
Q

What cells are located in the collect duct? what do they do?

A

Principle = reabsorb water and Na, secrete K

Alpha-intercalated = secrete H+

Beta-intercalated = secrete HCO3-

*Both intercalated reabsorb K+

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12
Q

What psych drug can block the function of aquaporins?

A

Lithium - can induce nephrogenic diabetes

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13
Q

What class of diuretic directly affects principle cells?

A

K+ sparing diuretics = spironolactone, eplerenone

*aldosterone antagonists

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14
Q

Treatment for acute altitude sickness?

A

Acetazolamide

Low partial pressure O2 at high altitude

So increase ventilation to oxygenate tissues

Blow off more CO2 causing Respiratory alkalosis

Compensate by getting rid of Bicarb… takes several days

Acetazolamide helps decrease bicarb and overcome alkalosis

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15
Q

Treatment for psueduotumor cerebri? (idiopathic intracranial HTN)

A

Acetazolamide

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16
Q

Which diuretics lose Ca+?

A

Loop Diuretics!

*Thiazides retain Ca+

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17
Q

Loop diuretic that is safe to give to a patient with a sulfa allergy?

A

Ethacrynic Acid

**Not a sulfonamide but has same action as furosemide

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18
Q

Common side effects of loop diuretics?

A 
Hypokalemia
Dehydration
Gout
Sulfa allergy
Ototoxicity
Nephrotoxicity
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19
Q

MOA of chlorthalidone

A

Thiazide diuretics

Inhibit NaCl reabsorption in early DCT

LOWERS Ca+ excretion!!

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20
Q

4 drugs used to treat HTN

A

Hydrochlorothiazide
ACE
ARB
Ca+ channel blocker

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21
Q

3 treatments to correct hyperkalemia

A

B-agonist (albuterol)
IV bicarbonate
IV insulin + dextrose

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22
Q

First treatment for severe hyperkalemia to prevent arrhythmias?

A

IV calcium

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23
Q

Correcting to rapidly may result in central pontine myelinolysis

A

Hyponatremia

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24
Q

Electrolyte imbalance causing peaked T waves

A

Hyperkalemia

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25
Electrolyte imbalance causing tetany
Hypocalcemia, hypomagnesemia
26
Electrolyte imbalances causing arrhythmias
Hyperkalemia Hypokalemia Hypomagnesemia
27
Electrolyte imbalance causing decreased deep tendon reflexes
Hypermagnesemia
28
Electrolyte imbalance causing flattened T waves, and U waves on ECG
Hypokalemia
29
Treatment for nephrogenic DI
Thiazides Indomethicin Amiloride
30
Treatment for Lithium-induced nephrogenic DI
Amiloride Li enters through ENA and blocks fusion of aquaporins with membrane Amiloride blocks ENA so Li can't even enter cell! Bang!
31
Differential for high anion gap acidosis
MUDPILES ``` Methanol Uremia DKA Propylene glycol Isoniazide/ Iron Lactic Acidosis Ethylene glycol Salycilates ``` **adding acids
32
How do you determine an anion gap?
[Na+] - [Cl-] - [HCO3-]
33
Differential for non-anion gap acidosis?
HARD ASS ``` Hyperalimentation Addison Disease Renal Tubular Necrosis Diarrhea Acetazolamide Spironolactone Saline infusion ```
34
``` EM = Subepithelial humps LM = Hypercellular glomeruli ```
Post strep glomerulonephritis
35
Decreased C3 High anti-streptolysin O High anti-DNase B
Recent strep infection
36
IgA based immune complex deposits in mesangium Mesangial proliferation
IgA nephropathy = Berger Disease
37
Thinning and splitting of basement membrane Mutation in type IV collagen
Alport Syndrome
38
Causes of rapidly progressive glomerulonephritis...
Goodpasture syndrome Wegeners (Granulomatosis with polyangiitis) Microscopic polyangiitis
39
Wire loop appearance on LM - pronounced basement membrane
Lupus nephritis = diffuse proliferative glomerulonephritis
40
Linear pattern of IgG deposition on IF
goodpasture
41
Lumpy-bumpy deposits of IgG, IgM, and C3 in the mesangium
Post strep glomerulonephritis | Nephritic
42
Deposits of IgA in the mesangium
Berger Disease = IgA nephropathy | Nephritic
43
Anti-GBM antibodies, hematuria, hemoptysis
Goodpasture
44
Crescent formation in the glomeruli
Rapidly Progressive Glomerulonephritis | Nephritic
45
Defining features of nephrotic syndrome
Proteinuria > 3.5 mg/day Hypoalbuminemia Peripheral Edema
46
Kimmelstiel-Wilson lesions
Diabetic glomerulonephropathy | Nephrotic
47
Most common nephrotic syndrome in children
Minimal Change (Nephrotic)
48
Most common nephrotic syndrome in adults?
Focal Segmental Glomerulosclerosis | Nephrotic
49
Effacement of epithelial foot processes
Minimal Change | Nephrotic
50
Nephrotic syndrome associated with Hep B
Membranoproliferative Glomerulonephritis | Both
51
Subendothelial hump and tram track appearance
Membranoproliferative Glomerulonephritis | Both
52
Segmental sclerosis and hyalinosis | Nephrotic
Focal segmental glomerulosclerosis | Nephrotic
53
Spiking of the GBM due to electron dense subepithelial deposits
Membranous Nephropathy
54
How can you distinguish prerenal azotemia from intrinsic renal failure?
Prerenal azotemia = increased Na+ retention and BUN reabsorption... thus decreased FeNa, and increased BUN/Creatinine ratio Intrinsic RF = can't reabsorb Na+ so FeNa is increased, can't reabsorb BUN so decreased BUN/Creatinine ratio
55
Muddy Brown/Granular Casts
Acute Tubular Necrosis
56
Fever Eosinophilis Azotemia Rash - diffuse maculopapular
Acute Interstitial Nephritis (aka Drug induced interstitial nephritis) *Most common cause is DRUGS
57
Hyaline cast
Concentrated urine | Not pathologic
58
Red cell cast
Glomerular bleeding (glomerulonephritis, vasculitis)
59
White cell casts
Acute pyelonephritis
60
Epithelial cell casts
Acute Interstial Nephritis
61
Fatty Cast
Nephrotic Syndrome
62
Waxy Cast
End stage renal stage = further degeneration of granular casts
63
HTN Hepatic cysts Intracranial aneurysms Mitral Valve Prolapse
ADPKD
64
urease-positive bacteria indicated in struvite stones? (Magnesium Phosphate stones)
Proteus Mirabils Klebsiella (S. sapro)
65
Radio opaque Enveloped shaped crystals Most common
Calcium oxalate stone *Tx = Thiazide diuretics (retain Ca+)
66
Coffin lid crystals in urine
Struvite Stone Radiopaque Staghorn calculi
67
Polycythemia Anemia Hypercalcemia
Renal Cell Carcinoma Von Hippo Lindau Chromosome 3
68
Most common renal malignancy of early childhood
Wilms Tumor (nephroblastoma)
69
Painless hematuria
Transitional cell carcinoma
70
Risk Factors for transitional cell carcinoma
Phenacetin Smoking Aniline Dyes Cyclophosphamide
71
Approximation for GFR
Inulin = freely filtered, and not secreted or absorbed
72
Approximation for RPF
PAH = is 100% excreted.... freely filtered and secreted
73
Preferentially dilate afferent arteriole
Prostaglandins Increased RPF Increased GFR FF is constant
74
Preferentially constrict efferent arteriole?
Angiotensin II Decreased RPF Increased GFR Therefore increased FF
75
EPO secretion by kidney
Released by interstitial cells in peritubular capillary bed in response to hypoxia
76
What cells hydroxylate vitamin D?
PCT
77
How do you determine predicted CO2?
PCO2 = 1.5[HCO3] + 8 +/- 2
78
Complication of hydronephrosis?
Possible atrophy of renal cortex and medulla
79
Pre-renal azotemia
Increased BUN/Creatinine ratio (>20) Decreased FENa BUN retained in kidney because trying to increase volume
80
Intrinsic Renal Failure
Decreased BUN/Creatinine ration because BUN reabsorption is impaired Increased FENa Generally due to acute tubular necrosis (muddy brown casts)
81
When would you see post-renal azotemia?
Due to outflow obstruction Develops only with bilateral obstruction Stone, BPH, neoplasia, congenital anomalies
82
Consequences of renal failure
MAD HUNGER ``` Metabolic Acidosis Dyslipidemia Hyperkalemia Uremia Na/H20 retention (HF, pulmonary edema, HTN) Growth retardation/ developmental Erythoropoietin failure (anemia) Renal osteodystrophy (damage to bone that occurs from renal failure) ```

USMLE REVIEW (25 decks)

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