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DT III > renal mak > Flashcards

renal mak Flashcards

1
Q

nephrotic syndrome characteristics

A

edema, intial normal GFR, >3.5g/d proteinuria, lipiduria

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2
Q

if these foot processes which were there are now effaced, why then do we get so much leakage of protein

A

effacement changes the BM, making it more permeable to allow proteins to leak across

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3
Q

the major EM finding on a renal biopsy of a 5y/o w/ nephrotic syndrome who responded to corticotherapy is

A

fusion of foot processes (minimal change glomerulopathy)

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4
Q
  1. 10yo Girl was brough by her parents to their family physician. History revealed that the child had a sore throat for about 10d prior to the office visit. Initial laboratory tests ordered by the family physician revealed an elevated BUN and creatinine. A microscopic urinalysis showed hematuria w/ dysmorphic RBC’s. The light microscopic appearance of the renal biopsy showed hypercellularity, w/ PMN’s present, and there were subepithelial electron dense “humps” seen by electron microscopy. What additional laboratory finding is most likely to be present in this setting:
A

c. Elevated anti-streptolysin O titer

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5
Q

focal seqmental glomerulosclerosis of the kidney characteristics

A

b. It is not as common as minimal change disease in children
c. There is effacement of podocytes plus segmental scarring
d. It tends to recur after transplantation
e. Less than half of patients have some response to corticosteroids

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6
Q

light microscopic findings on renal biopsy suggests the worst immediate prognosis

A

d. Glomerular crescents (proliferation of parietal epithelium)

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7
Q

Major clinical feature associated w/ the renal biopsy finding on immunofluorescence microscopy of mesangial IgA deposistion in a 35yo man following a “flulike” illness is: (IgA nephropathy)

A

hematuria

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8
Q

Hyaline arteriolosclerosis of the kidney is most likely to be associated with which of the following conditions

A

Renal artery stenosis in the opposite kidney

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9
Q

The microscopic findings at autopsy of hyalinized glomeruli, interstitial fibrosis and focal tubular atrophy, and arteriolar thickening in a 75yo woman w/ normal renal function most strongly suggests:

A

d. Benign nephrosclerosis

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10
Q

Nephritic Sx Pathogenesis

A

inflammatory rupture of glomerular capillaries w/ bleeding into the urinary space

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11
Q

Nephritic Sx Clinical

A

mild to mod proteinuria and edema

  • *gross hematuria**
  • red cell casts*
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12
Q

Nephritic Sx Diseases

A
  1. Acute Proliferative
  2. Nonstrep Acute
  3. Rapidly Progressive (RPGN)

Glomerulonephritis

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13
Q

Acute Proliferative

A

1-4 weeks post GAS (kids)

immune complex mediated–> coarse IF

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14
Q

Acute Proliferative Morph

A

LM: proliferation w/ neutrophils and monocyte infiltration

IF: Granular deposits

EM: “humps” in epithelial side of BM

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15
Q

Acute Proliferative clinical

A

kids 6-10yo, 1-2 weeks post sore throat

hematuria, oliguria, periorbital edema, HTN, mild proteinuria and red cell casts

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16
Q

Nonstrep Acute

A

same as Acute, just after another disease

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17
Q

RPGN

A

severe, death w/in weeks if untreated

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18
Q

RPGN path

A

ruptures in GBM triggers Crescent formation

immunologically mediated

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19
Q

Crescent

A

proliferation of parietal epithelia cells lining Bowman’s capsule due to infiltration by monocytes and macrophages

contain fibrin

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20
Q

Type I RPGN

A

Anti-GBM antibody, linear IF

Goodpasture’s Sx

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21
Q

Goodpasture’s Syndrome

A

anti-GBM ab also xreact with pulmonary alveolar BM

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22
Q

Type II RPGN

A

immune complex deposition granular IF

lupus, post infections, Henroch Scheloin

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23
Q

Type III RPGN

A

NO anti-GBM or immune complexes

circulating ANCA

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24
Q

RPGN gross

A

large, pale kidneys with cortical petechial hemes

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25
Q

RPGN clinical

A

hematuria, RBC, proteinuria, htn , edema

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26
Q

Nephrotic Syndrome

A

increased BM permeability leading to loss of plasma protein

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27
Q

Nephrotic Syndrome clinical

A

severe proteinuria >3.5g/day, hyperlipidemia, edema

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28
Q

Nephrotic Syndrome diseases

A

Membranous nephropathy, minimal-change disease, Focal Segmental Glomerulosclerosis, Membranoproliferative Glomerulonephritis

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29
Q

Membranous Nephropathy

A

idiopathic, autoimmune

immune complex mediated with diffuse thickening of glomerular capillary wall

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30
Q

Membranous Nephropathy EM

A
  • deposits btwn GBM and epithelial cells
  • spikes protruding from GBM
  • spikes and domes
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31
Q

Membranous Nephropathy clinical

A

INITIAL mild proteinuria, hematuria, mild HTN –> severe goes to sclerosis, inc Creatinine, HTN worse

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32
Q

Minimal Change disease

A

kids in 2-6 following RI selective to albumin

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33
Q

Minimal change disease

A

no immune complexes seen, but responds to steroids

effacement of foot processes of visceral epithelial cells on EM

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34
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

idiopathic, adaptive response to loss of renal tissue

poor steroid response

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35
Q

FSGS path

A

visceral epithelial damage

w/ hyalinosis and sclerosis

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36
Q

FSGS light microscopy

A

focal sclerosing, segmental, affected capillary loops collapse

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37
Q

FSGS EM

A

effacement of foot processes, detachment of epithelial cells and denudation of GM

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38
Q

MPGN Type I

A

immune complexes in glomerulus w/ activation of both complement pathways

secondary is always Type I

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39
Q

MPGN Type II

A

dense deposit disease

alternative complement only (C3 only)

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40
Q

MPGN LM

A

proliferation of mesangial cells and capillary endothelium

**tramtrack splitting*

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41
Q

MPGN Type I EM

A

subdendothelial deposits

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42
Q

MPGN Type II EM

A

ribbonlike dense material in GM

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43
Q

MPGN clinical

A

nephrotic syndrome + hematuria

bad reoccurrence

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44
Q

Berger’s Disease

IgA nephropathy

A

hematuria in young adult, following UTI, lasts several days, slow progression to CRF

45
Q

Alport Syndrome

A

X-linked recessive abnormal a5 collagen IV mutation

Hematuria and Red casts with Nerve Deafness and Eye Disorders

46
Q

Alport syndrome morph

A

GMB thinning initially

late: GBM alternating thick and thin, splitting and layering of lamina densa

47
Q

Thin BM Lesion

Benign Familial Hematuria

A

thinning of GMB, asymptomatic, no big deal

48
Q

Chronic Glomerulonephritis

A

contracted kidneys with granular, thinned cortex leading to atrophy of the tubules

49
Q

End Stage Renal disease

A

sclerosis, fibrosis, inflammation, hylanized sclerotic vessels, atrophy of tubules

50
Q

Henoch Schonlein Purpura

A

3-8yo following URI w/ IgA deposited in the glomerular mesangium

51
Q

DM nephropathy clinical

A

nonnephrotic proteinuria, nephrotic syndrome, CRF

52
Q

AMyloidosis

A

deposits in mesangium and capillary walls

presents with nephrotic syndrome

53
Q

Nephrosclerosis pathogenesis

A

medial and intimal thickening due to hemodynamic changes, aging, and genetics

hyaline deposition in arterioles

54
Q

when does Nephrosclerosis cause renal insufficiency

A

AA, severe HTN, underlying disease (DM)

55
Q

Malignant HTN gross morph

A

“flea bitten” appearance of kidney from petechial hemes on cortical surface w/ associated edema

56
Q

Malignant HTN histo morph

A

fibronoid necrosis of arterioles with eosinophilic granules

57
Q

Malignant HTN hyperplastic arteriolitis

A

onion-skinning appearance due to proliferation of concentrically arranged SM cells and collagen

58
Q

Renal artery stenosis

A

UNILATERAL constriction decreases intrarenal circulation/blood pressure

59
Q

Renal artery stenosis pathway

A

JGA cells rls renin–> angiotensin II (htn) –> aldosterone (hypernatremia and hyperH2O)

60
Q

Kidney embryo germ layer

A

intermediate mesoderm at Day 22

61
Q

Kidney embryo derivation

A

mesoderm–>intermediate mesoderm-> lateral urogenital ridge–> nephrogenic cords–>

meso: mesonephric duct (Wolffian)
meta: kidney/uretric bud

62
Q

Ureteric bud

A

Day 32

forms 1-3m collectuing tubules and ducts, major and minor calyces, renal pelvis, ureters

63
Q

metanephric blastema

A

glomeruli, tubules, bowman’s space

64
Q

Final kidney

A

T12-L3 rt lower than lt

week 12 but placenta still does waste

65
Q

hydronephrosis

A

dilation of the calyces and and pelvis due to obstruction of urine flow by aberrant/accessory renal arteries

66
Q

horseshoe kidney

A

inferior mesenteric artery disrupts kidney ascent leading to fused lower poles

67
Q

Wilms tumor

A

nephroblastoma 11p13,

more likely in horseshoe kidney

68
Q

multicystic dysplastic kidney

A

Nephrons fail to develop and ureteric bud
fails to branch so collecting ducts never
form

69
Q

Autosomal Recessive Polycystic Kidney Disease

A

Cysts form from collecting ducts

70
Q

Autosomal DominantPolycystic Kidney Disease

A

Cysts form from all segments of the nephron

71
Q

Renal agenesis

A

Failure of kidney development (bilateral renal
agenesis) due to the failure of formation of the
ureteric bud

Potter Syndrome

72
Q

Potter Syndrome

A

anuria, oligohydroamnios, pulm hypoplasia

craniofacial abnormalities, noncompatible with life

73
Q

WAGR syndrome

A

aniridia, hemihypertrophy, wilms tumor

74
Q

Ureteropelvic junction obstruction

A

Most common site of obstruction
Presents prenatally as hydronephrosis; may present as a palpable
abdominal mass. Evaluate with US, VCUG

75
Q

HUS

A

Endothelial injury (Shiga like toxin)→ platelet activation and thrombosis

76
Q

TTP

A

Platelet aggregation from very large multimers of vWF due to deficiency of ADAMST13

77
Q

HUS sx

A

kids

Severe oliguria, and hematuria, Microangiopathichemolytic anemia, Thrombocytopenia

78
Q

TTP sx

A

adults

Pentad of fever, neurologic symptoms, microangiopathichemolytic anemia, thrombocytopenia, renal failure

79
Q

TTP/HUS acute kidney effects

A

Cortical necrosis, subcapsular petechiae, thickened walls

80
Q

TTP/HUS chronic kidney effects

A

scarring of cortex, tramtracking, thickening of everything

81
Q

cholesterol emboli

A

Arterial seeding of fragmented atherosclerotic plaque to small arterioles
•Clear clefts of cholesterol seen embolizedto small vessels

82
Q

Sickle-cell Disease Nephropathy

A

Hematuria, Proteinuria, Diminished concentrating ability

83
Q

Diffuse Cortical Necrosis

A

Follows catastrophic conditions such as abruptioplacentae, septic shock

Massive ischemic (coagulative) necrosis

84
Q

HH EQUATION

A

pH=pKa + log (A-)/(HA)

85
Q

respiratory acidosis cause

A

respiratory distress, no breathing

86
Q

respiratory alkalosis cause

A

hyperventilating

87
Q

how to look at ABG

A
  1. Look at pH.
  2. Look at PCO2
  3. What is the primary disorder (respiratory or metabolic)
  4. Calculate anion gap
  5. Look for compensation
  6. Look for clues to mixed disorders – multiple problems can coexist.
88
Q

Anion Gap

A

4-12 normal

high: ketone, lactic acid, ethylene glycol poisoning

89
Q

Anion Gap equation

A

Na - (Cl + HCO3)

90
Q

Metabolic Acidosis

A

pH less than 7.4 HCO3 less than 24

91
Q

Metabolic Acidosis Respiratory Compensation

A

PCO2 less than 40

92
Q

Respiratory Acidosis

A

pCO2 greater than 40

93
Q

Respiratory Acidosis Metabolic Compensation

A

HCO3 greater than 24

94
Q

Metabolic Alkalosis

A

pH >7.40, HCo3 greater than 24

95
Q

Metabolic Alkalosis Respiratory Compensation

A

PCO2 greater than 40

96
Q

Respiratory Alkalosis

A

pH >7.40, PCO2 less than 40

97
Q

Respiratory Alkalosis Metabolic Compensation

A

HCO3 less than 24

98
Q

Mixed Disorder Clues

A
  1. pH is normal but PCO2 or HCO3- is abnormal
  2. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap.
  3. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder
99
Q

Mixed Disorders rule of thumb

A
  • When the PCO2 is elevated and the [HCO3-] reduced, respiratory acidosis and metabolic acidosis coexist.
  • When the PCO2 is reduced and the [HCO3-] elevated, respiratory alkalosis and metabolic alkalosis coexist
100
Q

diarrhea/renal failure acid base disorder

A

non anion gap metabolic acidosis

101
Q

Metabolic Acidosis diseases

A

Lactic acidosis, ketoacidosis, loss of bicarb, ingested toxins

anion gap

102
Q

Metabolic Alkalosis

A

vomiting, diuretic, increased mineralcorticoid effect, increased intake of alkali

103
Q

Respiratory Acidosis

A

CNS depressant, neuromuscular disorders, obstructive lung disease

104
Q

Respiratory Alkalosis

A

Hyperventilation (anxiety, CNS infection)
Salicylates!!
SIRS
Pulmonary disease (acute PE and acute flair of asthma).
Hypoxia

105
Q

Chronic Kidney disease definition

A

GFR 3 months.

106
Q

CKD sx

A

Usually none. Fatigue. Nocturia. Swelling. Confusion.

107
Q

drug to preven protein excretion

A

ACEI

108
Q

metabolic acidosis tx

A

sodium bicarb

109
Q

calcium acetate MOA

A

binds phosphate to keep it under

DT III (2 decks)

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