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Renal/Resp Pathology > Renal > Flashcards

Renal Flashcards

1
Q

what nephron structures does the cortex contain?

A

glomeruli, proximal and distal tubules

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2
Q

what nephron structures does the medulla contain?

A

loops of Henle and collecting ducts

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3
Q

follow the course of renal blood supply from renal artery to afferent arteriole

A

renal artery –> segmental artery –> lobar artery –> interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole

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4
Q

capillary loops supplying tubules of juxtamedullary nephrons

A

vasa recta

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5
Q

capillary loops supplying tubules of cortical nephrons

A

tubular plexus

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6
Q

which layer of the glomerular filtration barrier is the size barrier?

A

capillary endothelium

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7
Q

which layer of the glomerular filtration barrier is the negative charge barrier?

A

basement membrane

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8
Q

which layer of the glomerular filtration barrier contains heparin sulfate?

A

basement membrane (negative charge barrier)

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9
Q

which portion of the nephron has brush borders?

A

proximal tubule

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10
Q

difference between cortical and juxtamedullary nephrons?

A

cortical nephrons have short loops of Henle that only have a descending thin limb; juxtamedullary nephrons have long loops with both ascending and descending thin limbs

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11
Q

thin segments of loop of Henle are lined with what type of cells?

A

simple squamous epithelium

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12
Q

which portion of nephrons passively reabsorbs water?

A

thin descending loop of Henle

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13
Q

concentrating segments of the nephron

A

thin descending loop of Henle and collecting duct

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14
Q

segments of the nephron that are water impermeable

A

thin ascending loop of Henle, thick ascending loop of Henle, early distal convoluted tubule

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15
Q

what segment of the nephron do loop diuretics (furosemide) work on, and what transporter do they target?

A

thick ascending loop of Henle, Na+/K+/2Cl- cotransoprter

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16
Q

what segment of the nephron do thiazides work on, and what transporter do they target?

A

early distal convoluted tubule, Na+/Cl- cotransporter

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17
Q

what segment of the nephron does aldosterone work on, and what is its mechanism of action?

A

late distal tubule, aldosterone causes insertion of sodium channels in lumen

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18
Q

what segment of the nephron does ADH work on, and what is its mechanism of action?

A

collecting ducts, ADH inserts aquaporin water channels in lumen

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19
Q

mechanism of diabetes insipidus

A

absence of ADH leads to excretion of water, leading to polyuria and hypotonic urine

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20
Q

what are JG cells?

A

specialized smooth muscle cells in the afferent arteriole, produce renin

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21
Q

what part of the JG apparatus senses Na and Cl concentrations?

A

macula densa

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22
Q

role of macula densa

A

part of JG apparatus, detects Na and Cl concentration for JG cells

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23
Q

when do JG cells secrete renin?

A

when renal blood pressure decreases, when NaCl delivery to distal tubule decreases, and when sympathetic tone increases

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24
Q

what kind of cells in kidney release erythropoietin?

A

interstitial cells

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25
Q

does renal tubular disease lead to acidosis or alkalosis and why?

A

acidosis because of failure of H+ ion excretion

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26
Q

explain the 60-40-20 rule of fluid distribution in body

A

60% of body weight is water
40% of body weight is intracellular fluid
20% of body weight is extracellular fluid

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27
Q

explain the mechanism of tuberoglomerular feedback

A

in response to an elevation of perfusion pressure, increased fluid is filtered, leading to increased delivery of NaCl to the macula densa –> increase in vascular resistance

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28
Q

what molecules increase GFR?

A

nitric oxide and prostaglandins

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29
Q

what molecules decrease GFR?

A

norepinephrine, epinephrine, endothelin, angiotensin II

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30
Q

what hormone increases Na+ reabsorption in the proximal tubule? what enzyme does it target?

A

angiotensin II, Na+/H+ countertransporter

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31
Q

what hormone increases Na+ reabsorption in the late distal tubule?

A

aldosterone

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32
Q

what hormone increases water reabsorption in the collecting duct?

A

ADH

33
Q

what are the effects of PTH?

A

decreased phosphorus reabsorption and increased calcium reabsorption

34
Q

clinical picture of Liddle syndrome (5)

A
  1. hypertension
  2. hypokalemia
  3. metabolic alkalosis
  4. low plasma renin
  5. low aldosterone
35
Q

pathogenesis of Liddle syndrome

A

mutation in renal ENaC leading to constitutive expression –> increased reabsorption of sodium –> hypertension

36
Q

agent used to treat Liddle syndrome

A

amiloride

37
Q

inheritance of Liddle syndrome

A

autosomal dominant

38
Q

Gitelman and Bartter syndromes: inheritance, common clinical presentation (2), presentation unique to Bartter syndrome

A

autosomal recessive; hypokalemia and metabolic alkalosis; hypercalciuria

39
Q

pathogenesis of Bartter syndrome

A

reabsorptive defect in thick ascending loop of Henle, affects Na+/K+/2Cl- cotransporters

40
Q

pathogenesis of Gitelman syndrome

A

reabsorptive defect of Na+/Cl- cotransporter in distal convoluted tubule

41
Q

which Mendelian hypertension disease causes hypokalemia, metabolic alkalosis, AND hypercalciuria?

A

Bartter syndrome

42
Q

define respiratory acidosis vs alkalosis

A

resp. acidosis: pCO2 > 40 mmHg

resp. alkalosis: pCO2 < 40 mmHg

43
Q

define metabolic acidosis vs alkalosis

A

metab. acidosis: HCO3- < 24 mmol/L

metab. alkalosis: HCO3- > 24 mmol/L

44
Q

compensation equation for metabolic acidosis

A 
pCO2 = 1.5[bicarbonate] + 8
pCO2 = last 2 digits of pH
45
Q

compensation equation for metabolic alkalosis

A

pCO2 = 0.9[bicarbonate] + 9

46
Q

compensation equation for respiratory acidosis

A

acute: bicarb increases 1 mmol/L per 10 mmHg increase in PaCO2
chronic: bicarb increases 4 mmol/L per 10 mmHg increase in PaCO2

47
Q

compensation equation for respiratory alkalosis

A

acute: bicarb decreases 2 mmol/L per 10 mmHg decrease in PaCO2
chronic: bicarb decreases 4 mmol/L per 10 mmHg decrease in PaCO2

48
Q

_________ in plasma osmolarity and _________ in blood volume trigger increased ADH release

A

increase, decrease

49
Q

which cancer can release ADH?

A

small cell lung

50
Q

equation for GFR using serum creatinine

A

GFR ~ 100/Cr

51
Q

_________ is the most important stimulus for aldosterone secretion relating to sodium balance, and it is dependent upon __________ secretion

A

angiotensin II, renin

52
Q

the systemic response to decreased ECF volume involves ________ and ________ activation, activation of ________, and increased ________

A

baroreceptor, sympthetic nerve, RAAS, ADH

53
Q

what is FENa?

A

how much filtered sodium is excreted

54
Q

in kidney disease, there is ____ serum calcium, ____ serum phosphorus, feedback to _____, leading to _____

A

low, retention of, parathyroid gland, high PTH release

55
Q

classic presentation of glomerular disease (3)

A

hematuria, loss of GFR, proteinuria

56
Q

classic presentation of nephrotic syndrome (4)

A

proteinuria, hypoalbuminemia, edema, hyperlipidemia

57
Q

classic presentation of nephritis (4)

A

mild proteinuria, hematuria (RBC casts), hypertension, edema

58
Q

hematuria accompanying a URI

A

IgA nephropathy

59
Q

kidney problem associated with Henoch-Schonlein purpura

A

IgA nephropathy

60
Q

cola-colored urine

A

post-streptococcal glomerulonephritis

61
Q

subepithelial “hump-like” immune complex deposits on EM

A

post-streptococcal glomerulonephritis

62
Q

crescentic glomerulonephritis

A

rapidly progressive glomerulonephritis

63
Q

pathogenesis of Goodpasture’s syndrome

A

rapidly progressive glomerulonephritis caused by antibodies against GBM and alveolar basement membrane (may present as pulmonary-renal syndrome)

64
Q

vasculitis that is C-ANCA positive and renal biopsy shows crescentic glomerulonephritis WITHOUT immune deposits, with sinusitis, nasal lesions, and hemoptysis

A

Wegener’s granulomatosis

65
Q

vasculitis that is P-ANCA positive and renal biopsy shows crescentic glomerulonephritis with necrotizing granulomatous inflammation, asthma, eosinophilia

A

Churg-Strauss syndrome

66
Q

vasculitis that is P-ANCA positive and renal biopsy shows crescentic glomerulonephritis without granulomatous inflammation and no asthma

A

microscopic polyangiitis

67
Q

3 primary nephrotic glomerular disease

A

membranous nephropathy, focal segmental glomerulosclerosis (FSGS), minimal change disease

68
Q

most common cause of nephrotic syndrome in children

A

minimal change disease

69
Q

nephrotic syndrome associated with Hodgkin’s lymphoma

A

minimal change disease

70
Q

what two nephrotic syndromes cause effacement of the podocyte foot processes?

A

minimal change disease and focal segmental glomerulosclerosis (FSGS)

71
Q

diagnose: child with proteinuria >3.5 g/day, effacement of the podocyte foot processes on EM

A

minimal change disease

72
Q

most common cause of nephrotic syndrome in Caucasian adults

A

membranous nephropathy

73
Q

secondary causes of membranous nephropathy

A

hepatitis B, SLE, solid tumors, drugs

74
Q

nephrotic syndrome that shows spike and dome appearance on EM, thickened GBM

A

membranous nephropathy

75
Q

most common cause of nephrotic syndrome in African Americans and Hispanics

A

focal segmental glomerulosclerosis (FSGS)

76
Q

nephrotic syndrome associated with HIV

A

focal segmental glomerulosclerosis (FSGS)

77
Q

glomerular disease that can present with nephrotic and nephritic features

A

membranoproliferative glomerulonephritis

78
Q

common cause of diffuse proliferative glomerulonephritis

A

SLE

Renal/Resp Pathology (4 decks)

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