exam 1 Flashcards Preview

Renal > exam 1 > Flashcards

Flashcards in exam 1 Deck (114):
1

what do intercalated celled do?

reabsorb K and secrete H

2

what do principle cells do?

reabsorb Na and water and secrete K

3

which parts of the nephron are impermeable to water?

thin ascending loop, thick ascending loop & early distal tubule

4

where do loop diuretics act?

thick ascending loop

5

what controls the permeability in the late distal tubule and collecting duct?

ADH

6

More ADH->

more permeable to water

7

are the LDT, Corticol collecting duct, medullary collecting , proximal tubule duct permeable to urea?

LDT NO
CCD NO
MCD YES
PT YES

8

in the descending loop is fluid concentrated or dilute

concentrated due to water reabsorbed by osmosis

9

in the ascending loop if fluid concentrated or dilute

dilute due to Na, K & Cl being reabsorbed

10

glomerular filtration occurs through

passive diffusion of water & small molecules into bowman's capsule & proximal tubule

11

secretion occurs primarily through

proximal tubule via active transport

12

where does water & solute reabsorption occur?

throughout the nephron

13

where does drug reabsorption occur?

primarily in the distal tubule & collecting ducts

14

normal BUN

5-20mg/dL

15

normal BUN:creatinine

10-15:1

16

urea crosses membrane by

passive diffusion

17

normal SCr

0.5-1.5mg/dL

18

as GFR declines, what happens to SCr?

SCr concentrations rise
- Cr is primarily eliminated through glomerular filtration

19

Jaffee reaction

- reacts with noncreatinine chromogens in the serum which may result in falsely elevated SCr
- NOT present in the urine

20

normal CrCl for men

90-139mL/min

21

normal CrCl

80-125mL/min

22

cystatin C is synthesized

by all nucleated cells in the body at a constant rate

23

why may cystatin C provide an ideal marker of GFR?

it is independent of age and gender

24

pts receiving corticosteriods for renal transplants may have

dose dependent increases in cystatin C

25

abnormal substances in the urine

blood, protein, glucose, ketones, urobilinogen, bilirubin, WBCs

26

what plays a main role in AKI in regards to ischemia?

vasoconstriction

27

urine pH

4.5-7.8

28

normal specific gravity of urine

1.003-1.03

29

suggestive of UTIs

nitrates & leukocyte esterase

30

excretion of protein in healthy adults

30-150mg/d

31

is albumin filtered?

no, it is too big and negatively charged

32

MDRD can be inaccurate-

underestimating GFR >60mL/min

33

relationship between GFR and Cr is ____ at lower levels

weaker

34

what is one of the most common causes of chronic kidney disease?

chronic glomerulonephritis (starts with the glomerulus)

35

most common cause of glomerulopathies

antibody mediated injury

36

causes of chronic glomerulonephritis (descending)

- crescentic GN
- focal segmental glomerulosclerosis
- membranoproliferative G
- IgAN
- membranous nephropathy
- post=streptococcal GN

37

focal segment glomerulosclerosis is often associated with what?

HTN & DM

38

nephritic main symptom

hematuria

39

nephrotic main symptom

proteinuria >3.5g/day

40

what are the 2 main causes of nephritic syndrome?

- post-strep & SLE

41

what are the most common kidney diseases?

urinary tract infections

42

calculi

kidney stones

43

kidney structures affected by pyelonephritis

tubules
interstitium
pelvis

44

acute pyelonephritis complications

papillary necrosis
pyonephrosis
perinephric abscess

45

what can cause papillary necosis?

DM or urinary tract obstruction

46

acute pyelonephritis can be caused by sepsis or it can

cause sepsis

47

pyuria

puss in the urine

48

polyomavirus nephropathy can lead to

renal transplant failure

49

chronic pyelonephritis is associated with

involvement of calyces & pelvis

50

first sign of inability to concentrate urine

polyuria & nocturia
(as in unilateral or partial hydroonephrosis)

51

permanent renal atrophy aka

hydronephrosis or obstructive uropathy

52

most common out pt drug leading to nephrotoxicity

NSAIDs

53

what kind of acute renal failure can be prevented?

hemodynamically mediated
(NSAIDs & ACEI)

54

out patient first signs of nephrotoxicity

symptoms of uremia(malaise, anorexia, vomiting or fluid overload (edema)

55

general indicators of proximal tubular injury

1. metabolic acidosis w/ bicarbonaturia
2. glycosuria w/out hyperglycemia
3. hypophosphatemia & hypouricemia due to incr urinary loss of phosphorus & uric acid

56

general indicators of distal tubular injury

1. polyuria from inability to concentrate urine
2. metabolic acidosis from impaired urine acidification
3. hyperkalemia from impaired k+ excretion

57

what is a organic anion transporter (OAT) inhibitor?

probenicid- can decrease ctytotoxicity of neucleotide antivirals & cephalosporins if administered together

58

where does drug metabolism mostly occur?

proximal tubule

59

methoxyfluorane is metabolized to

-fluoride and oxalate
- fluoride has been shown to act in ascending limb & collecting duct
- example of toxic drug metabolism

60

ampho B

- induces MEDULLARY tubular damage due to imbalance between increased cellular energy & inadequate oxygen delivery

61

aminoglycoside nephrotoxicity is due to

volume depletion (& concentrated accumulation)

62

methotrexate nephrotoxicity

acidic urine leads to precipitation of methotrexate

63

what can help with aminoglycoside accumulation

Ca supplements inhibit drug transport across lumen

64

what can help with ampho B toxicity

furosemide. decrease cell energy needs by reducing cell membrance transport activity

65

hemodynamically mediated renal faiure

results from a decr in blood flow-> insufficient perfusion presure

66

reduced glomerular capillary hydrostatic pressure

ACEI & ARBs

67

angII effects

constricts EFFERENT arteriole (inc. pressure & GFR)

68

inhibition of renal prostaglandin production

NSAIDs
- PGs cause vasodilation to compensate & protect from ischemia & hypoxia

69

calcineurin inhibitors (cyclosporine & tacrolimus) increase

potent vasoconstrictors & decrease vasodilators!

70

systemic polyarteritis nodosa

- renal vascular alteration
- a vasculitis with involvement of small & medium sized renal arteries following methamphetamine abuse

71

thrombus formation

- renal vascular alteration
- seen with oral contraceptives, cyclosporin, mitomycin C, cisplating & quinine

72

drug induced glomerular disease is

-uncommon
- defined as proteinuria >3.5g/d w/ or w/out renal insufficiency

73

drug induced kidney injury most commonly effects

the tubules
- acute tubular necrosis

74

minimal change glomerular disease

- NSAIDs associated w/ T-cell infiltrate & cell-mediated immunity
- increase glomerular capillary permeability to PROTEINS

75

focal segmental glomerulosclerosis (FSGS)

- patchy areas of glomerular sclerosis

76

most common drug cause of FSGS

heroin

- can also include bisphoshonates, zoledronat & AIDs

77

most common drug induced GLOMERULAR lesion

membranous nephropathy

78

membranous nephropathy

- immune complexes deposit
- parenterol gold - most common
- also penicillamine, captopril & NSAIDs

79

most common membranous nephropathy is caused by

parenterol gold

80

toxicity of AGs is directly proportional to

number of cationic charges

81

AGs cause accumulation of

phospholids

82

cisplatin nephrotoxicity

- minding of platium to proximal tubular cell-> disruption of cell enzyme activity & uncouples oxidative phosphorylation
- can cause hypoMGemia

83

radiocontrast media causes

oxidative stress
- N-acetylcysteine may help
- one of the most common causes of hospital acquired renal failure

84

acute allergic interstitial nephritus

- PCN-methicillin
-NSAID-fenoprofen

85

chronic interstitial nephritis

- lithium (inability to conc. urine)
- cyclosporin & tacrolimus (fibrosis)

86

nephrolithiasis aka

kidney stones
- triamterene HCTZ
-laxative abuse

87

acute kidney injury=

acute kidney failure
- sudden impairment of kidney function resulting in retention of N & other wastes

88

BUN comes from

liver protein metabolism

89

creatinine comes from

muscles

90

prerenal

block blood flow to kidneys

91

renal/intrinsic

in the kidneys

92

postrenal

blockage of urine outflow

93

GFR is often reduced in

prerenal & renal

94

if BUN:SCr ration is unchanged, problem is

renal!

95

if BUN:SCr ration is increased, problem is

prerenal!

96

most common form of AKI

prerenal

97

autoregulation is adversely effected by

-atherosclerosis
- HTN
- old age
-NSAIDs
-ACEI/ARBs

98

most common cause of heptorenal syndrome

liver cirrhosis

99

hepatic renal syndrome

blood is trapped in splanchnic ciculation, so kidneys are activated (vasoconstriction) due to hypovolemia-like conditions

100

endogenous nephrotoxins

myoglobin
hemoglobin
uric acid
myeloma light chains

101

diagnosis of AKI

SCr rise of at least 0.3mg/dL or 50% w/in 24-48 hours ore a reduction in urine output to 0.5ml/kg/hr >6hours

102

Na absorption

-prerenal- can still absorb Na
- renal- cannot absorb Na

103

hypervolemia

oligouria/anuria, Na & water retention, weight gain, dependent edema, incr jugular vein pressure, PULMONARY EDEMA, acute lung injury

104

hypovolemia

recovery phase & polyuria, osmotic diuersis

105

proximal tubules contain a large amount of

carbonic anhydrase

106

CA type 4

luminal & basolateral membranes
carbonic acid-> water & CO2

107

CA type 2

cytoplasm
- CO2+ water-> carbonic acid

108

CA inhibitors

-prevents reabsorption of bicarb
- makes blood more acidic

109

osmotic agents

mannitol & urea
- creates osmotic driving force & keeps water from leaving urine
- incr in excretion of nearly all electrolytes

110

what can be used for dialysisdisequilibrium syndrom

mannitol

111

thiazides work where?

distal tubule; inhibit Na-Cl cotransporter

112

some thiazides are also

weak CA inhibitors & can also increase bicarb excretion

113

traimterene & amiloride moa

block Na transport chains in the late tuble & collecting duct

114

what are the most effective drugs to produce diuresis in AKI?

mannitol & loop diuretics