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Modules > Renal > Flashcards

Renal Flashcards

1
Q

Renal Clearance (Cx)

A 
= Ux*V/ Px
Volume of plasma cleared per unit time (ml/min)
Px, Ux= mg/ml 
V= urine flow rate 
Cx reabsorption , etc
Cl inulin = GFR
Cl pah = RPF
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2
Q

GFR

A

clearance of inulin
about 100 ml/min
= Kf (Pgc - Pbs)- (oncgc- oncbs) but oncbs = 0 mostly
Ccr = GFR but overestimates by about 10-15% bc of secretion in the PCT

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3
Q

Osmolality

A

285-295 mOsm/kg water

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4
Q

Water division between body and compartments

A

60-40-20
60% of body
40% ICF
20% ECF (75% interstitial, 25% plasma)

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5
Q

eRPF (effective renal plasma flow)

A

Clearance of PAH (para-aminohippuric acid)
100% cleared (secreted by carrier and saturable transport in the PCT)
underestimates RPF by about 10%

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6
Q

RBF

A

= RPF /(1-Hct)

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7
Q

FF

A

GFR/RPF

20%

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8
Q

Filtered load

A

GFR * Plasma concentration

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9
Q

What is the effect of prostaglandins on afferent arteriole?

A

dilate (increase GFR, increase RPF, FF constant)

NSAIDS block this path

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10
Q

At what plasma glucose does glucosuria begin?

A

200 mg/dL

Can be decreased in normal pregnancy (decrease ability of PCT to reabsorb glucose)

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11
Q

At what plasma glucose are transporters saturated ?

A

375 mg/dL

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12
Q

Henderson Hasselbach

A

pH = 6.1 + log (HCO3-)/ 0.03 PCO2

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13
Q

Winter’s formula

A

compensation metabolic acidosis

Pco2= 1.5 (HCO3) + 8 +- 2

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14
Q

Anion gap formula

A

8-12
(Na)- (HCO3- + Cl-)
Correct for albumin

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15
Q

Excreted load

A

= Px * GFR - [] reabsorbed

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16
Q

Most common site of ureter obstruction in fetus?

A

Uteropelvic junction (last to canalize)

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17
Q

What is horseshoe kidney associated with?

A
  • uteropelvic junction obstruction, hydronephrosis, renal stones, chromosomal aneuploidy syndromes (turner, wiliams, patau, etc); infection, and rarely renal cancer
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18
Q

Excretion Rate

A

Ux*V

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19
Q

Reabsorption

A

Filtered - excreted

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20
Q

Secretion

A

excreted - filtered

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21
Q

RBC casts

A

Glomerulonephritis, malignant hypertension

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22
Q

WBC casts

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection

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23
Q

Fatty casts/oval fat bodies

A

nephrotic syndrome

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24
Q

Granular casts (muddy brown)

A

acute tubular necrosis

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25
Q

Waxy casts

A

ESRD/chronic renal failure

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26
Q

Hyaline casts

A

nonspecific, can be normal esp in concentrated urine samples

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27
Q

Mechanism of action mannitol?

A

osmotic diuretic
Increases tubular fluid osmolaltiy –> increases fluid flow
Also decreases intracranial pressure

28
Q

Clinical use of mannitol?

A

Increased ICP, drug overdose (increases renal flow)

29
Q

Toxicity of mannitol?

A

Pulmonary edema

Dehydration

30
Q

When is mannitol contraindicated?

A

HF (pulmonary edema)

Anuria

31
Q

What is the mechanism of acetazolamide?

A

Carbonic anhydrase inhibitor
Acts in PCT
Decreases HCO3/Na reabsorption
Decreases total body HCO3 stores

32
Q

What are the clinical uses of acetazolamide?

A

Glaucoma (CA in cilliary body in eye)
Urinary alkalinzation (excrete weak acids; cystein and uric acid stones)
Pseudotumor cerebri (CA in choroid plexus)
Altitude sickness

33
Q

What is the toxicity of acetazolamide?

A 
Hyperchloremic metabolic acidosis
Parathesias
NH3 toxcity (encephalopathy with hepatic impairment)
Sulfa allergy 
CaPh stones
34
Q

What is the mechanism of furosemide action?

A

Blocks the NKCC pump in the TAL
Sulfonamide diuretic
Stimulates PGE release to vasodilate afferent arteriole

35
Q

What is furosemide used for?

A

Edematous states
HT
Hypercalcemia

36
Q

What is the toxicity of furosemide?

A

OH DANG!
Ototoxicity
Hypokalemia

Dehydration
Allergy to sulfa
Nephritis (interstitial)
Gout

37
Q

When would you use ethacrynic acid?

A

Diuresis in sulfa allergic patients
Same action as furosemide
Phenoxyacetic acid derivative

38
Q

What is the mechanism of HCTZ?

A

Blocks the NCC pump in the early DCT

39
Q

Clinical use of HCTZ

A

HT, HF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis

40
Q

Toxicity of HCTZ

A 
Hypokalemic metabolic alkalosis
Hyponatremia
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalemia
(hyperGLUC)
sulfa allergy
41
Q

Mechanisms of action of Spirnolactone?

A

competitive MR inhibitors

42
Q

Mechanism of action of triamterene/amiloride?

A

Block the ENaC channel

43
Q

Clinical use of K sparring diuretics

A

Hyperaldosteronism
K depletion
HF (even without frank edema can be useful to decrease aldosterone and its fibrotic action on the heart)
Ca based nephrolithiasis

44
Q

Toxicity of K sparring diuretics?

A

Hyperkalemia (arrythmia)
Hyperchloremia acidosis
Spirnolactone can have actions on other endocrine receptors causing gynocomastia (testosterone) and other anti-androgenic effects

45
Q

What are the mechanisms of action of ACE inhibitors?

A

Block ACE which converts ANGI to ANGII and metabolizes bradykinin into inactive metabolites

46
Q

Clinical uses of Ace inhibitors?

A 
HT
HF
Proteinuria 
Diabetic nephropathy (decreases constriction of efferent arteriole caused by NEG, decreased intraglomerular pressure slowing GBM thickening and mesangial expansion)
Prevent unfavorable heart remodeling
47
Q

What are the toxicities of ACE inhibitors?

A 
CATCHH
Cough (bradykinin)
Angioedema 
Teratogen (renal malformations)
Increase Creatinine (decrease in GFR)
Hyperkalemia 
Hypotension
48
Q

When are ACE inhibitor counterindicated?

A

Cl esterase deficiency

Bilateral renal artery stenosis (decrease GFR)

49
Q

What is the mechanism for ARBs?

A

Block the binding of ang II to ATI Rs (Gq)

50
Q

Clinical use of ARBs?

A

HT
HF
Proteinuria
Diabetic nephropathy with intolerance to ACE inhibitors (angioedema, cough)

51
Q

Toxicities of ARBs?

A 
Teratogen
Increase CK
Hypotension
Hyperkalemia
Decrease renal function
52
Q

Mechanism of action of aliskiren?

A

binds and inhibits the action of renin

53
Q

What is the clinical use of aliskiren?

A

HT

54
Q

What is the toxicity of aliskiren?

A

Hyperkalemia
Decreased renal function
Hypotention

55
Q

When is aliskiren counterindicated?

A

Diabetics taking ACEs or ARBs

56
Q

What are weak acid drugs that are excreted by alkalinization of the urine?

A

aspirin, phenobarbitol, methotrexate, and TCAs

57
Q

What are weak bases that are improved by acidification of the urine?

A

amphetamines

58
Q

What drugs cause DI?

A

lithium, demecocycline

59
Q

What drugs cause Fanconi syndrome?

A

Expired tetracycline

60
Q

Hemorrhagic cystitis is caused by which drugs?

A

cyclophosphamide, ifosfamide

61
Q

Interstitial nephritis is caused by which drugs?

A

Methicillin, furosemide, and NSAIDs

62
Q

What can you administer with cyclophosphomide to prevent hemorrhagic cystitis?

A

mesna

63
Q

What drugs cause SIADH?

A

carbamazipine
Cyclophosphomide
SSRIs
Can’t concentrate Serum sodium

64
Q

Pentad for TTP?

A 
FAT RN
Fever
Anemia
Thrombocytopenia
Renal failure
Neurological issues
65
Q

What is the test for citrate stones?

A

sodium cyanide nitroprusside +

break disulfide bonds to release cysteine

Modules (19 decks)

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