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Renal Path MC > Renal 1 > Flashcards

Renal 1 Flashcards

1
Q

% of CO that goes to kidneys

A

25%

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2
Q

signifies end stage renal disease

A

GFR

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3
Q

size of particles normally filtered by kidneys

A
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4
Q

5 functional units of kidney

A

vascular supply, glomerulus, tubules, interstitium, collecting system

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5
Q

most of vasculature located within this area of kidney

A

cortex/glomeruli

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6
Q

sole blood supply of tubules

A

efferent arterioles (glomerular damage causes major problems downstream)

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7
Q

this portion of kidney is at greatest risk for ischemic and ischemic infarction

A

tubules

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8
Q

this portion of kidney is relatively avascular and has lower hematocrit

A

medulla

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9
Q

treatment for HTN caused by kidney problem

A

ACE inhibitor

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10
Q

this causes pre-renal vascular disease

A

decreased blood flow to glomeruli

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11
Q

this is result of pre-renal vascular disease

A

decreased GFR, loss ability excrete nitrogen waste, increase BUN and Cr, conservation water and Na (expanded intravascular volume and HTN)

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12
Q

this causes glomerular kidney disease

A

damage glomerular architecture (commonly immune related), vascular disease glomerular capillaries

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13
Q

result of glomerular disease (due to damage to architecture)

A

loss GFR and selective permeability (will see protein and RBC)

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14
Q

characteristic features of renal disease due to decrease in GFR

A

increase BUN and Cr, oliguria, dilution hyponatremia, increased K and phosphate, hypocalcemia, AG metabolic acidosis

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15
Q

additional problems in glomerular disease due to alteration in membrane filtration

A

proteinuria, hematuria, GN

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16
Q

this is characterized by HTN, Na conservation, azotemia W/O proteinuria or hematuria

A

pre-renal disease

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17
Q

these cells in kidney can regenerate

A

tubular epithelium

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18
Q

these are responsible for concentrating abnormal constituents of the glomerular filtrate, like toxins, lipids, proteins

A

tubular cells (epithelium sheds and tubular casts form)

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19
Q

major goal/function of tubules

A

urine concentration

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20
Q

hallmarks of tubular disease

A

loss of urine concentrating ability (end-stage), metabolic acidosis, formation tubular casts

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21
Q

this causes metabolic acidosis in tubular disease

A

loss of bicarb

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22
Q

interstitial disease is associated with this

A

loss EPO and anemia

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23
Q

interference with blood flow of this area of kidney causes production of renin and angiotensin II -> leading to HTN

A

interstitium

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24
Q

this is result of loss of prostaglandin production in interstitial disease

A

renal vasoconstriction, vascular insufficiency, HTN

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25
Q

loss of this % of GFR signifies renal insufficiency -> azotemia, anemia, HTN

A

50-80%

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26
Q

this signifies renal failure

A

GFR

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27
Q

decrease in GFR with resulting increase in BUN and Cr

A

azotemia

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28
Q

this condition, with early treatment, can have reversible glomerular damage

A

acute post-streptococcal GN

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29
Q

loss of protein (>3.5 g/day) w/o other evidence of filtration or vascular abnormality

A

nephrotic syndrome

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30
Q

loss of tubular function in isolated tubular syndrome causes this to occur

A

increased intraglomerular pressure (secondary to tubular collapse/damage), decrease GFR

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31
Q

Henderson-Hasselbalch equation

A

6.1 + log (HCO3/ .03*PCO2)

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32
Q

normal pH value

A

7.4

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33
Q

increase in PCO2 (hypoventilation) causes this

A

respiratory acidosis

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34
Q

decrease in PCO2 (hyperventilation) causes this

A

respiratory alkalosis

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35
Q

two conditions that will lead to metabolic acidosis

A

retention acids renal failure, loss bicarb tubular disease

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36
Q

increase in total acids leads to this

A

metabolic acidosis

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37
Q

vomiting leads to this

A

metabolic alkalosis (lose acids)

38
Q

diarrhea leads to this

A

metabolic acidosis (loss of bicarb)

39
Q

normal value for HCO3

A

25 mmol

40
Q

normal value for CO2

A

40 mmHg

41
Q

metabolic or respiratory problem will cause CO2 and bicarb (very slightly) to change in same direction?

A

respiratory

42
Q

condition with increased CO2, slightly increased HCO3

A

respiratory acidosis

43
Q

condition with decreased CO2, slightly decreased HCO3

A

respiratory alkalosis

44
Q

metabolic or respiratory problem has change in HCO3 but CO2 remains normal?

A

metabolic

45
Q

condition with decreased HCO3 and normal CO2

A

metabolic acidosis

46
Q

condition with increased HCO3 and normal CO2

A

metabolic alkalosis

47
Q

to normalize ratio in compensation for A/B problem…will HCO3 and PCO2 change in same or opposite direction?

A

SAME

48
Q

when anion gap is present, this must occur to keep anions equal to cations

A

Cl decreases

49
Q

this occurs to account for decreased bicarb if no anion gap is present

A

Cl increases (hyperchloremic metabolic acidosis)

50
Q

is metabolic acidosis with or without anion gap considered normochloremic?

A

with AG

51
Q

does tubular or glomerular acidosis cause increase in Cl?

A

tubular (lose bicarb, no anion gap)

52
Q

anion gap greater than this value signifies there is an unknown acid or acid is increased

A

> 27 mmol

53
Q

this condition increases K levels

A

acidosis (H+ exchanged for K)

54
Q

condition with bilateral renal a genesis -> incompatible with life, many stillborn infants (head and extremity malformations)

A

Potter’s syndrome/oligohydramnios

55
Q

true hypoplasia is rare, but most small kidneys are due to this

A

scarring

56
Q

what part of kidney is most commonly fused in horseshoe kidney?

A

lower poles

57
Q

does horseshoe kidney lie anterior or posterior to great vessels?

A

anterior

58
Q

this form of polycystic kidney disease is most commonly in children

A

autosomal recessive

59
Q

this cystic renal disease is associated with renal cell carcinoma

A

acquired cysts

60
Q

this is abnormal in multi cystic renal dysplasia (dysplasia of renal components)

A

metanephric differentiation

61
Q

abnormal structures in kidney including islands of cartilage, undifferentiated mesenchyme, immature collecting ducts

A

multicystic renal dysplasia

62
Q

associated conditions with multi cystic renal dysplasia

A

ureteropelvic obstruction, ureteral agenesis

63
Q

hereditary disorder with multiple expanding cysts in both kidneys (ENLARGED kidneys, filled with serous/hemorrhagic fluid) -> presents in 4-5 decade

A

ADPKD

64
Q

what causes renal failure in ADPKD?

A

expanding cysts destroy parenchyma

65
Q

mutations associated with ADPKD

A

PKD1 (chromosome 16), PKD2 (chromo 4)-> polycystin (in cilia of tubular epithelial cells…secrete fluid)

66
Q

where do cysts in ADPKD arise from?

A

tubular epithelium

67
Q

morphology of ARPKD

A

small cysts cut surface, dilated elongated channels replacing medulla/cortex, dilation collecting tubules

68
Q

secondary complications of medullary sponge kidney

A

calcification, hematuria, infection and renal calculi

69
Q

cause of acquired cystic disease

A

dialysis

70
Q

cause of renal artery stenosis (uncommon cause of HTN)

A

atheromatous plaque at origin of renal artery

71
Q

stenosis of renal arteries NOT associated with atherosclerosis -> more common in women, 3rd-4th decade

A

fibromuscular dysplasia

72
Q

pathology of fibromuscular dysplasia

A

fibrous/fibromuscular thickening intima, media, adventitia

73
Q

hallmark of renal disease

A

dilutional hyponatremia with inappropriate Na loss

74
Q

tubular disease leads to this A/B condition

A

non-AG metabolic acidosis

75
Q

causes of interstitial disease

A

infection, drug toxicity, HS reaction, accompanying tubular or glomerular disease

76
Q

characteristic of collection system obstruction

A

oliguria/anuria w/o glomerular or tubular dysfunction

77
Q

result of longstanding obstruction of collecting system

A

ascending destruction tubular/interstitial, loss GFR

78
Q

mechanism of most glomerular diseases

A

immunologic mechanism/deposition of substances (alters BM)

79
Q

mechanism of most tubular or interstitial diseases

A

toxic mechanism, infection, or obstruction

80
Q

signs of renal insufficiency

A

azotemia, anemia, HTN

81
Q

causes of acute renal insufficiency/acute renal failure

A

pre-renal vascular insufficiency, ATN, acute GN

82
Q

possible courses of slowly progressive GN

A

asymptomatic proteinuria/hematuria, nephrotic syndrome, GN (nephritic), crescentic GN (rapidly progressive)

83
Q

global symptoms/indicators of renal failure

A

oliguria, HTN, electrolyte imbalance, metabolic acidosis

84
Q

possible causes of pre-renal problem leading to renal insufficiency

A

hypotension, CHF, renal artery stenosis, arteriolosclerosis, PAN, scleroderma

85
Q

electrolyte disturbances in acute renal syndrome

A

hyponatremia/calcemia, hyperkalemia/phosphatemia

86
Q

changes in urine due to acute renal syndrome

A

decreased production, increased osmolality

87
Q

non-renal systemic complication associated with renal failure and azotemia -> due to loss of normal renal function or build up of waste metabolites

A

uremia

88
Q

mechanism of how nephrotic syndrome leads to HTN

A

hypoalbuminemia -> anasarca -> decreased intravascular volume -> RAS activation -> Na and water retention (DIURETICS to treat edema can be FATAL b/c IVV already low)

89
Q

these are direct results of protein loss in nephrotic syndrome

A

reversal albumin:globulin ratio, increased infection (loss of complement/low weight globulin), hyper coagulable state, hyperlipidemia/lipiduria (loss lipoproteins)

90
Q

lipid appears as these in urine due to loss of lipoproteins -> tubular cells that have reabsorbed the lipid and are shed (lipid casts)

A

oval fat bodies

91
Q

hallmarks of chronic renal failure/uremia

A

interstitial fibrosis, vascular insufficiency, loss GFR, tubular dysfunction

92
Q

systemic symptoms of chronic renal failure/uremia

A

anemia, bleeding diatheses, renal osteodystrophy, neurological symptoms

Renal Path MC (5 decks)

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