Renal Patho and Diuretics Flashcards

1
Q

the average kidney has how many nephrons?

A

1 million

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2
Q

4 measures of kidney function or damage

A

-serum creatinine
-blood urea nitrogen (BUN)
-creatinine clearance
-GFR

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3
Q

true or false: we lose nephrons as we age

A

true

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4
Q

compensatory response to renal injury (9 steps)

A

renal injury -> decrease # of nephrons -> compensatory inc in size and function of remaining nephrons -> glomerular and tubular lesions -> loss of nephrons > compensatory capacity -> progressive dec in GFR -> azotemia -> uremic syndrome

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5
Q

what two disease states account for > 60% of renal failure cases in US?

A

HTN and diabetes

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6
Q

3 primary causes of intrinsic acute kidney injury

A

sepsis
ischemia
nephrotoxins

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7
Q

common key elements of progressive nephropathies (slide 24 of 45; 3 red arrows)

A

-increased glomerular capillary pressure
-proteinuria
-glomerulosclerosis

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8
Q

2 key abnormalities that give rise of CKD-MBD

A

-impaired phosphate excretion
-decreased production of vitamin D3

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9
Q

hematuria is seen in

a. nephritic syndrome
b. nephrotic syndrome

A

a. nephritic syndrome

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10
Q

proteinuria is seen in

a. nephritic syndrome
b. nephrotic syndrome

A

b. nephrotic syndrome

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11
Q

nephrotic syndrome (3 things to know from table; slide 31)

A

-edema
-proteinuria
-low serum albumin

(usually see proteinuria and edema)

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12
Q

nephritic syndrome (2 things to know from table; slide 31)

A

-hematuria
-red blood cell casts are present

(usually see blood, inflammation (blood urea))

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13
Q

what is glomerulonephritis?

A

inflammation of glomeruli

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14
Q

true or false: glomerulonephritis is only acute

A

false (has both acute and chronic forms)

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15
Q

primary cause of glomerulonephritis

A

Alport syndrome

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16
Q

“presents flank pain with painful urination” refers to which condition?

A

pyelonephritis

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16
Q

what is pyelonephritis?

A

inflammation of kidney tissue

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16
Q

secondary causes of glomerulonephritis

A

infections, drugs, autoimmune disorders (vasculitis, Lupus)

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17
Q

pyelonephritis may lead to _____

A

sepsis

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17
Q

cause of pyelonephritis

A

bacteria from blood or urinary tract (i.e. bacterial infection)

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18
Q

70-75% of acute intersistial nephritis is caused by _____, 4-10% is caused by _____

A

drugs; infection

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19
Q

main drug class associated with interstitial nephritis

A

penicillins

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20
Q

autosomal dominant (adult) polycystic kidney disease is caused by inherited mutation of which two genes?

A

PKD1 (polycystic kidney disease 1) or PKD2 gene in renal tubular cells

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21
Q

autosomal recessive (childhood) polycystic kidney disease is caused by a mutation in what gene?

A

PKHD1 - fibrocystin (polyductin)

22
Q

nephrolithiasis is also known as _____ _____

A

kidney stones (renal calculi)

23
Q

are kidney stones more prevalent in men or women?

A

men

(lifetime prevalence 10% men, 5% women)

24
Q

nephrolithiasis arises from a supersaturation of solutes, mainly which one?

A

calcium

25
Q

70-80% of nephrolithiasis is what composition?

A

calcium oxalate or calcium phosphate

26
Q

uric acid is ___-___% of the composition of kidney stones

A

10-15%

27
Q

primary treatment for kidney stones (4 of them)

A

-analgesics
-hydration
-lithotripsy (shock waves)
-surgical removal

28
Q

prevention of kidney stones (2 methods)

A

-diet (hydration; elim Ca supplements)
-diuretics

29
Q

carbonic anhydrase inhibitors act on what part of the nephron?

A

PCT

30
Q

acetazolamide 3 structural things to know

A

-sulfamoyl group essential for diuresis
-sulfamoyl N unsubstituted to retain activity
-derivatives with high partition coeff and lowest pKa have > potency

31
Q

true or false: CA inhibitors have high efficacy as diuretics

A

false (low efficacy)

32
Q

drug that treats acute mountain sickness

A

acetazolamide

33
Q

how does acetazolamide treat acute mountain sickness?

A

the metabolic acidosis produced by the drug counteracts the respiratory alkalosis than can result from hyperventilation in this condition. (drug is taken prophylactically for several days before)

34
Q

osmotic diuretics site of action (2 of them)

A

PCT and descending loop of Henle

35
Q

true or false: mannitol has a risk of hyponatremia

A

false (hypernatremia)

36
Q

3 orally active osmotic diuretics

A

-isosorbide
-glucose
-glycerine

37
Q

loop diuretics main site of action

A

thick ascending limb of Loop of Henle

38
Q

which transporter do loop diuretics inhibit?

A

Na+-K+-2Cl- symporter

39
Q

SAR for loop diuretics (inhib NaK2Cl symporter) (3 things to know; slide 25 of 49)

A

-substituent at 1 position must be acidic
-sulfamoyl group in the 5 position is essential for optimal diuretic activity
-activating group in the 4 position

40
Q

5 toxicities of loop diuretics

A

-dehydration
-hypokalemic metabolic acidosis
-ototoxicity
-hyperuricemia
-hypomagnesemia

(2 and 3 were highlighted on slides)

41
Q

thiazides act primarily on ___, and the ___ secondary

A

DCT; PCT

42
Q

thiazides inhibit which transporter?

A

Na+-Cl- symporter

43
Q

thiazides reduce _____ reuptake

A

potassium

44
Q

Inhibitors of renal epithelial Na+ channels (ENaC inhibitors) act at what location? (2 of them)

A

-late DCT
-collecting duct

45
Q

clinical use of ENaC inhibitors

A

-adjunct treatment w thiazide or loop diuretic in heart failure or hypertension

46
Q

toxicities of ENaC inhibitors (2 of them)

A

hyperkalemia (most important bc potassium sparing)
hyperchloremic metabolic acidosis

47
Q

loop diuretics have weak _____ _____ activity

A

CA inhibitory

48
Q

MRA location of action (2 of them)

A

-late DCT
-collecting duct

49
Q

two subclasses of Na+-Cl- symport inhibitors

A

-thiazides
-hydrothiazides

50
Q

what is the difference in structure between thiazides and hydrothiazides?

A

thiazides have a double bond at C3-C4, hydrothiazides have no double bond

51
Q

renal epithelial Na+ channel inhibitors (2 drugs)

A

-amiloride
-triamterene

52
Q

which drug is available IV?

a. conivaptan
b. tolvaptan

A

a. conivaptan

(tolvaptan is oral)

53
Q

which is more selective for V2 receptors?

a. conivaptan
b. tolvaptan

A

b. tolvaptan

54
Q

only diuretics that do no act within the tubular lumen

A

mineralocorticoid receptor antagonists (MRA)

55
Q

two main vasopressin antagonists drugs

A

conivaptan
tolvaptan