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Block 9 Week 5 > Fung > renal path > Flashcards

Fung > renal path Flashcards

1
Q

what are the 3 metabolic fxns of the kidney?

A
  1. excrete ions (water, Na, Ca, P)
  2. maintain acid-base balance
  3. excrete toxic metabolic waste pdts
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2
Q

what are the 2 endocrine fxns of the kidney?

A
  1. secrete EPO & PGs

2. regulate vitamin D metabolism

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3
Q

how does the kidney regulate BP?

A

secretes renin

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4
Q

what are the 3 main renal fxns?

A
  1. metabolism
  2. endocrine
  3. regulate BP
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5
Q

if you have a histo slide w/ glomeruli, what part of the kidney are you in?

A

cortex

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6
Q

what is the endothelium of the renal cortex?

A

fenestrated endothelial cells

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7
Q

where is the endothelium of the renal cortex located?

A

adjacent to the lamina rara interna of the GBM

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8
Q

what is another name for visceral epithelium?

A

podocytes

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9
Q

where are the podocytes?

A

adjacent to the lamina rara externa of the GBM (externa > epi)

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10
Q

what is unique about podocytes?

A

foot processes separated by filtration slits

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11
Q

how many layers does the GBM have?

A

3

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12
Q

what are the layers of the GBM?

A

lamina rara interna
lamina densa
lamina rara externa

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13
Q

the GBM is composed of what 6 things?

A
  1. type IV collagen
  2. laminin
  3. heparan sulfate
  4. fibronectin
  5. entactin
  6. glycoproteins
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14
Q

what does the mesangium do?

A

supports the glomerular tuft

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15
Q

where is the mesangium?

A

btwn capillaries in the cortex

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16
Q

what does the mesangium contain?

A

matrix similar to the basement membrane

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17
Q

what 4 things are special about mesangial cells?

A
  1. contractile
  2. phagocytic
  3. secrete mediators
  4. lay down matrix
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18
Q

what are mesangial cells similar to?

A

vascular smooth muscle cells & pericytes

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19
Q

how can you tell the DCT apart from the PCT?

A

the DCT has a wider lumen

the PCT has fatter cells and is cloudier in the lumen

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20
Q

what structures are in the renal medulla (think histo)?

A

collecting ducts & tubules

NO GLOMERULI

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21
Q

T/F: renal disease is always caused by primary reasons

A

FALSE

tons of diverse causes

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22
Q

what are the 4 basic patterns of rxns in response to glomerular injury?

A
  1. hypercellularity
  2. BM thickening
  3. hyalinosis
  4. sclerosis
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23
Q

define diffuse

A

involving ALL glomeruli

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24
Q

define focal

A

involving SOME glomeruli

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25
Q

define global

A

involving a WHOLE glomerulus

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26
Q

define segmental

A

involving PART of a glomerulus

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27
Q

what is most glomerular injury d/t (generally)?

A

immunologic causes

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28
Q

what are the 3 ways immunologic causes can injury a glomerulus?

A
  1. ab rxn in situ w/i glomerulus
  2. circulating ab deposits w/i glomerulus
  3. cytotoxic ab directed against the glomerulus
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29
Q

when cytotoxic ab are directed against the glomerulus, what pathway is activated?

A

complement

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30
Q

when circulating ab gets deposited in the glomerulus, what types of ag are involved (generally)?

A

endogenous
AND
exogenous

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31
Q

when ab reacts in situ w/i the glomerulus, what types of ag are involved?

A

intrinsic glomerular ag
AND
ag planted w/i the glomerulus

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32
Q

what is the biggest difference btwn CIRCULATING ab & IN SITU ab deposits?

A

the circulating deposits are actually immune COMPLEXES w/ ab & ag
(in situ means that the ag is already IN the glomerulus, so the ab just comes in and reacts w/ that)

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33
Q

what clinical presentations can glomerular injury lead to?

A 
nephrotic syndrome
nephritic syndrome
rapidly progressive glomerulonephritis
chronic renal failure
asymptomatic hematuria
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34
Q

define azotemia

A

BUN or Cr elevation, either prerenal, intrinsic, or postrenal

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35
Q

what is acute renal failure?

A

rapid decline in GFR

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36
Q

how long is “rapid” in acute renal failure?

A

hours to days

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37
Q

what are the 3 characteristics of acute renal failure?

A
  1. azotemia
  2. fluid & electrolyte imbalance
  3. oliguria or anuria
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38
Q

what types of fluid & electrolyte imbalances can be found w/ acute renal failure?

A 
hyponatremia
hyperkalemia
hyperphosphatemia
hypocalcemia
metabolic acidosis
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39
Q

what are the 4 causes of acute renal failure?

A
  1. glomerular injury
  2. interstitial injury
  3. vascular injury
  4. tubular injury
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40
Q

what are the 4 sx of acute renal failure?

A
  1. decreased/absent urine output
  2. lethargy
  3. fatigue
  4. nausea
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41
Q

what 5 categories can you use to distinguish btwn prerenal and renal acute renal failure?

A
  1. FENa+
  2. BUN/Cr
  3. Urine Na+
  4. Urine osmolality
  5. Specific gravity
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42
Q

how does FENa+ differ btwn prerenal and renal acute renal failure?

A

prerenal: 1%
renal: >1%

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43
Q

how does BUN/Cr differ btwn prerenal and renal acute renal failure?

A

prerenal: >20:1
renal: <20:1

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44
Q

how does Urine Na+ differ btwn prerenal and renal acute renal failure?

A

prerenal: 20mEq/L

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45
Q

how does urine osmolality differ btwn prerenal and renal acute renal failure?

A

prerenal: >500 mOsm/kg
renal: <400 mOsm/kg

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46
Q

how does specific gravity differ btwn prerenal and renal acute renal failure?

A

prerenal: >1.020
renal: <1.020

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47
Q

what is chronic renal failure?

A

diminished GFR for at least 3 months

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48
Q

what constitutes “diminshed” GFR in chronic renal failure?

A

<60 mL/minute/1.73m^2

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49
Q

what are the 3 characteristics of chronic renal failure?

A
  1. azotemia
  2. fluid & electrolyte imbalance
  3. uremia

(1 & 2 are the same as acute)

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50
Q

what is uremia?

A

a syndrome assoc w/ fluid, electrolyte, & hormonal imbalances + metabolic abnormalities

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51
Q

what are the sx of uremia?

A 
N/V 
fatigue
anorexia
weight loss
muscle cramps
pruritis
mental status change
visual disturbances
inc thirst
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52
Q

what are the 3 main causes of chronic renal failure?

A
  1. diabetes
  2. HTN
  3. renal parenchymal disease
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53
Q

how bad does GFR get w/ chronic renal failure?

A

<20-25% of normal

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54
Q

what is the difference btwn chronic renal failure & end stage renal disease in terms of GFR?

A

chronic renal failure is <5% of normal

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55
Q

what are the 4 sx of nephritic syndrome?

A
  1. hematuria (RBC casts)
  2. azotemia
  3. oliguria
  4. slight proteinuria
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56
Q

what characterizes nephritic syndrome?

A

INFLAMMATION of glomeruli

the i in nephritic means inflammation

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57
Q

what are the sx of acute proliferative glomerulonephritis?

A
  1. URI or skin infection 1-6 wks prior
  2. gross hematuria
  3. oliguria
  4. RBC casts
  5. peripheral edema
  6. HTN
  7. azotemia
  8. mild proteinuria
    (2, 3, 4, & 8 = nephritic syndrome)
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58
Q

what causes acute proliferative glomerulonephritis?

A

beta-hemolytic group A strep

Lancefield M types 1, 2, 4, 12, 47, 49, 57

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59
Q

what is another name for acute proliferative glomerulonephritis?

A

poststreptococcal glomerulonephritis (PSGN) (pathoma)

60
Q

what is the pathogenesis of acute proliferative glomerulonephritis?

A

circulating immune complexes are deposited in the glomerulus (subepithelial HUMPS)

61
Q

what findings will you see for acute proliferative glomerulonephritis on IF & EM?

A

IF: granular d/t immune complexes
EM: subepithelial humps d/t immune complexes

62
Q

what does acute proliferative glomerulonephritis look like on H&E?

A

hypercellular

inflamed glomeruli

63
Q

name the nephritides according to pathoma

A
  1. post-strep glomerulonephritis (acute proliferative)
  2. rapidly progressive glomerulonephritis
  3. IgA nephropathy (Berger)
  4. Alport syndrome
64
Q

what is the difference btwn the clinical course of acute proliferative glomerulonephritis in adults vs kids?

A

KIDS: 95% recover totally
ADULTS: only 60% recover

65
Q

what is the therapy for acute proliferative glomerulonephritis in kids?

A

maintain Na & water balance (i.e. supportive therapy bc most kids recover)

66
Q

what can acute proliferative glomerulonephritis progress to?

A

rapidly progressive glomerulonephritis

67
Q

what characterizes rapidly progressive glomerulonephritis?

A
  1. rapid & progressive loss of renal fxn
  2. oliguria
  3. nephritic sx
68
Q

what can you see on H&E & IF w/ rapidly progressive glomerulonephritis?

A

crescents in Bowman’s space made of FIBRIN & MACS

69
Q

what are the 3 types of rapidly progressive glomerulonephritis?

A
  1. Type I > anti-GBM ab
  2. Type II > immune complex
  3. Type III > pauci-immune
70
Q

what characterizes type I rapidly progressive glomerulonephritis?

A

LINEAR deposits of IgG/C3

71
Q

what is the treatment for type I rapidly progressive glomerulonephritis?

A

plasmapharesis

immunosuppression

72
Q

what are the causes of type II rapidly progressive glomerulonephritis?

A
  1. complication of post-infectious glomerulonephritis
  2. lupus nephritis complication
  3. IgA nephropathy
  4. idiopathic
73
Q

what is the treatment for type II rapidly progressive glomerulonephritis?

A

treat the UNDERLYING DISEASE!

DO NOT DO PLASMAPHARESIS

74
Q

what is the diff btwn type I & type II rapidly progressive glomerulonephritis on IF?

A

type I is LINEAR

type II is GRANULAR

75
Q

what kind of ab do you have in Type III rapidly progressive glomerulonephritis?

A

circulating
ANCA!
(pauci-ANCA = paul anka)

76
Q

what ANCA is assoc w/ Wegener?

A

PR3-ANCA

c-ANCA

77
Q

what ANCA is assoc w/ microscopic polyangiitis?

A

MPO-ANCA

p-ANCA

78
Q

what ANCA is assoc w/ Churg-Strauss?

79
Q

what causes most cases of type III rapidly progressive glomerulonephritis?

A

most cases are idiopathic

80
Q

what is the treatment for type III rapidly progressive glomerulonephritis?

A

steroids

cytotoxic agents

81
Q

what are the 4 things you need to remember about nephrOtic syndrome?

A
  1. massive proteinuria
  2. hypoalbuminemia (& hypogammaglobulinemia)
  3. edema
  4. hyperlipidemia / hypercholesterolemia
    (Pathoma says also loss of ATIII)
82
Q

T/F: proteinuria in nephrotic syndromes can be selective

83
Q

what are the 2 MAIN/broad causes of nephrotic syndromes?

A

primary glomerular disease
AND
systemic disease

84
Q

what are the 5 primary glomerular diseases that can be nephrotic?

A
  1. MCD
  2. FSGS
  3. MN
  4. MPGN
  5. DM
  6. SA
85
Q

what is the most frequent cause of nephrotic syndrome in kids?

86
Q

what does MCD look like on H&E?

A

normal glomeruli

87
Q

what does MCD look like on IF?

A

negative/normal (no immune complexes)

88
Q

what does MCD look like on EM?

A

effacement of foot processes of podocytes

89
Q

what do MCD & FSGS have in common?

A

no immune complex deposition so negative IF

effacement of foot processes on EM

90
Q

what is the biggest diff btwn MCD & FSGS?

A

FSGS has focal segmental glomerular sclerosis on H&E (hence the name)

91
Q

what is the pathophysiology of MCD?

A

immune dysfxn > cytokine > damage to visceral epithelial cells > proteinuria

92
Q

what is MCD assoc w/?

A

respiratory illness
post-immunization
atopic disorders

93
Q

what nephrotic syndrome can you give steroids to treat?

94
Q

what cancer is MCD assoc w/?

A

Hodgkin lymphoma

95
Q

T/F: MCD has highly selective proteinuria

A

TRUE

selective for albumin

96
Q

T/F: MCD is assoc w/ HTN & hematuria

A

FALSE
MCD is nephrOtic
HTN & hematuria are nephritic sx

97
Q

what age group is affected by membranous nephropathy?

98
Q

which 2 nephrotic syndromes are immune complex mediated?

A

membranous nephropathy
AND
membranoproliferative glomerulonephritis

99
Q

T/F: there is only primary membranous nephropathy

A

FALSE

primary & secondary

100
Q

what characterizes membranous nephropathy?

A

diffuse thickening of the glomerular capillary wall

thickened glomerular BM

101
Q

does membranous nephropathy have Ig deposits?

A

YES

subepithelial > spike & dome

102
Q

what does membranous nephropathy look like on H&E?

A

thickened glomerular BM

103
Q

what does membranous nephropathy look like on IF?

A

granular d/t immune complexes

104
Q

what does membranous nephropathy look like on EM?

A

spike & dome d/t subepithelial deposits

105
Q

what are the 3 clinical features of membranous nephropathy?

A
  1. insidious onset
  2. mild HTN & hematuria possible
  3. progression leads to glomerular sclerosis
106
Q

what is the treatment for membranous nephropathy?

A

treat underlying condition

does NOT respond to steroids

107
Q

what is FSGS characterized by?

A

focal & segmental sclerosis of the capillary tuft

108
Q

what are the 4 possible causes of FSGS?

A
  1. idiopathic
  2. secondary
  3. complication of focal glomerulonephritis
  4. adaptive response to loss of renal tissue
109
Q

what is FSGS thought to be a part of clinically & why?

A

thought to be a phase in MCD
accentuated diffuse epithelial cell change of MCD
cytokine-mediated or defects in slit diaphragm proteins

110
Q

T/F: you get hyalinosis & sclerosis w/ FSGS

A

TRUE

d/t entrapment of plasma proteins

111
Q

what does FSGS look like on H&E?

A

focal segmental sclerosis

112
Q

what does FSGS look like on EM?

A

effacement of foot processes

113
Q

what does FSGS look like on IF?

A

negative/normal (bc no immune complexes)

114
Q

T/F: idiopathic FSGS spontaneously remits

A

FALSE

“little tendency”

115
Q

does FSGS respond to steroids?

A

variable (poor)

116
Q

what are the sx of MPGN (generally)?

A
  1. nephrotic sx
  2. nephritic sx
  3. nephritic-nephrotic sx
  4. asymptomatic hematuria
117
Q

what characterizes MPGN?

A
  1. altered GBM
  2. proliferation of glomerular cells/mesangium
  3. leukocyte proliferation
118
Q

T/F: there is only one type of MPGN

A

FALSE

there are 2!

119
Q

what is type I MPGN?

A

immune complex deposition + activation of classical & alt complement pathways

120
Q

what can cause type I MPGN?

A

planted exogenous ag (HBV & HCV)

circulating immune complexes

121
Q

where are the deposits in type I MPGN?

A

subendothelial

122
Q

where are the deposits in type II MPGN?

A

intramembranous

123
Q

is type I or type II MPGN more common?

124
Q

what is type II MPGN?

A

dysregulation of alt complement pathway

125
Q

what is the pathophysiology of type II MPGN?

A

auto-ab (C3 nephritic factor) that stabilizes C3 convertase > overactivates complement > low circulating C3 + inflammation

126
Q

what does MPGN look like on H&E?

A

thickened glomerular BM w/ tram-track appearance

127
Q

T/F: most cases of MPGN spontaneously remit

A

FALSE

few spontaneous remissions w/ a slowly progressive & unremitting course

128
Q

T/F: steroids & immunosuppressives are the RX for MPGN

129
Q

what is the most common type of glomerulonephritis worldwide?

A

IgA nephropathy

130
Q

how do IgA nephropathy pts present?

A

w/ recurrent episodic gross or microscopic hematuria (episodes coincide w/ mucosal [resp or GI] infections)

131
Q

what is the systemic form of IgA nephropathy?

A

Henoch-Schonlein purpura

132
Q

where does the IgA immune complex deposit in IgA nephropathy?

133
Q

what form of IgA increases in IgA nephropathy?

A

polymeric forms of IgA1

134
Q

what causes IgA nephropathy?

A

genetic or acquired abnormality of immune regulation upon exposure to env agents in lungs & GI tract

135
Q

how does IgA nephropathy cause glomerular injury?

A

IgA & immune complexes get trapped in the mesangium > activate complement > injury

136
Q

what does IgA nephropathy look like on IF?

A

granular d/t IgA immune complex deposition

137
Q

T/F: IgA nephropathy pts may retain renal fxn for decades

138
Q

what can diabetic nephropathy cause?

A

kidney failure (one of the leading causes)

139
Q

what 3 glomerular syndromes is diabetic nephropathy assoc w/?

A
  1. non-nephrotic proteinuria
  2. nephrotic syndrome
  3. chronic renal failure
140
Q

what are the 3 manifestations of diabetic nephropathy?

A
  1. hyalinizing arteriolar sclerosis
  2. pyelonephritis
  3. tubular lesions
141
Q

what does diabetic nephropathy look like on H&E?

A

Kimmelstiel-Wilson nodules (sclerosis) = pathognomonic

142
Q

what is Alport syndrome?

A

X-linked inherited defect in type IV collagen

143
Q

what 3 things characterize Alport syndrome?

A
  1. hematuria progressing to renal failure
  2. sensory hearing loss
  3. ocular disorders
144
Q

what is familial renal disease (Alport) d/t?

A

defects in type IV collagen

145
Q

how does familial renal disease (Alport) clinically manifest?

A

familial asymptomatic hematuria

146
Q

what is the prognosis for familial renal disease (Alport)?

A

normal renal fxn

excellent prognosis

147
Q

what is the kidney lesion in familial renal disease (Alport)?

A

thinned & split glomerular BM

Block 9 Week 5 (3 decks)

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