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CPR 2 Exam 3 > Renal Pathology - Dr. Dobson Part 1 > Flashcards

Renal Pathology - Dr. Dobson Part 1 Flashcards

1
Q

most sensitive time in utero

A

week 3-9 peaking 4th and 5th

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2
Q

cause most commonly for glomerular and tubular and interstitial renal disorders

A

Glomerular = immunological

Tubular + interstitial = toxic or infectious

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3
Q

glomerular capillary filtration barrier 3 layers

A
  1. endothelium :
  2. BM :
  3. foot processes Podocytes:
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4
Q

glomerular endothelium is made up of what

A

fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin

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4
Q

glomerular endothelium is made up of what

A

fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin

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5
Q

glomerular endothelium is made up of what

A

fenestrated and permeable to water, small solutes, small proteins (not cells, large proteins, plts)
= - charges (repel albumin

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6
Q

the endothelial cells of Bowmans capsule release what chemical substances

A
  1. NO = vasodilator
  2. Endothelin-1 = vasoconstrictor
    (control Renal plasma flow RPF)
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7
Q

the basement membrane is composed of what

A
  • charge matrix
    = charge selective barrier
    = also size barrier
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8
Q

kidney role in endocrine ways

A

erythropoietin, renin, PGE, regulates Vit D metabolism

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9
Q

6 warning signs of kidney disease

A
  1. Cr and BUN high
  2. GFR < 60
  3. blood, protein in urine
  4. high BP
  5. high urination, painful urination
  6. puffy eyes or hands or feet
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10
Q

distal tubule role

A

secretes H+ and reabsorbs the HCO-3

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11
Q

buffers for H+

A

HPO4 and NH3 = H2PO3 + NH4+

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12
Q

Azotemia

A

elevated BUN and Cr

from decreased GFR

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13
Q

Uremia

A

Azotemia that has sx

uremic frosting can be seen

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14
Q

BUN is made how

A

Urea N broken down in liver from protein making BUN

it then goes to the kidneys

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15
Q

ideal BUN : Cr ratio

A

10:1 - 20:1

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16
Q

prerenal azotemia

A 
CHF
burns
GI hemorrage
Shock, stress
dehydration
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17
Q

renal level azotemia

A 
GN
Pylo
DM
Nephrotoxic drugs 
renal failure 
anabolic steroids
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18
Q

Post renal azotemia

A

stones , neoplasm
bladder urethral abnormality
bladder outlet obstruction (BPH)

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19
Q

GFR is what and normal

A

how much blood passes glomeruli each minute
- estimated from serum cr
= 90mL/min/1.73m2 or higher

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20
Q

proteinuria Nephritic syndrome SX

A
  1. hematuria + RBC casts
  2. HTN
  3. low GFR
  4. mild proteinuria
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21
Q

Proteinuria Nephrotic Syndrome

A
  1. heavy proteinuria
  2. hypoalbuminuria = edema
  3. hyperlipidemia, lipiduria
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22
Q

dip stick use

A

usually only in EM

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23
Q

AKI

A

rapid decline in GFR (hours to days)
= fluid electrolyte dysregulation
= high CR and BUN
= low or no urine can happen (ATI)

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24
Q

CKD

A

low GFR under 60 for at least 3mos,

= also albuminuria can happen

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25
Q

CKD is end stage of what

A

chronic renal parenchymal disease

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26
Q

CKD usually effects what pts

A

DM and HTN

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27
Q

Wilms tumor effects

A

developmental abnormalities in kidney and urinary tract

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28
Q

most common cause of chronic kidney disease in children

A

renal dysplasias and hypoplasias

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29
Q

Prune Belly Syndrome prevalence and 5 common SX

A

male

  1. Hydroureteronephrosis
  2. Vesicourereral reflux (VUR) bilateral
  3. renal dysplasia
  4. cryptochidism bilateral
  5. UTIs common
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30
Q

Bilateral agenesis

A

usually un stillborn infants

only compatible with life if unilateral

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31
Q

unilateral agenesis of kidney can progress to what

A

glomerular sclerosis or hypertrophy nephrons

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32
Q

renal hypoplasia is common when

A

in low birth weight infants

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33
Q

ectopic kidney can be found where

A

pelvis, iliac fossa, abd or thoracic cavities, contralateral positions

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34
Q

Vesicoureteral reflux (VUR)

A

most common and serious anomaly
= high chance of pylo + loss of renal function
= can cause congenital vesicouterine fistulae (dilation of ureter)

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35
Q

Ureteropelvic Junction Obstruction (UPJ) SX children

A

most common cause of hydronephrosis in infants

  1. UTI
  2. Hematuria
  3. FTT
  4. Sepsis
  5. azotemia
  6. Hydronephrosis
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36
Q

Ureteropelvic Junction Obstruction (UPJ) what happens

A

ureter gets obstructed and compressed by a renal artery like the inferior segmental artery

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37
Q

Ureteropelvic Junction Obstruction (UPJ) SX adults

A

women

  1. UTI
  2. hematuria
  3. ABD pain or V from intermittent obstruction
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38
Q

3 sites that have high risk of constriction of the ureter

A

Ureteropelvic junction (as it exits kidney)
Crossing the iliac artery and pelvic brim
When entering bladder

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39
Q

renal diverticuli

A

pouches forming in bladder or ureter
= 1cm-10cm
= can cause infection and rare carcinoma

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40
Q

Extrophy of bladder

A

NO anterior wall development for abd and bladder

= exposed bladder mucosa

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41
Q

Extrophy of bladder can cause what

A

the exposed mucosa can go through colonic glandular metaplasia (adenocarcinoma) + infections to upper GU

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42
Q

urachal cyst

A

the urachal canal and bladder is connected by allantois that is obliterated however if not it makes the urachus cyst (metaplastic glandular epithelium cyst on umbilicus)

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43
Q

urachal cyst can become

A

adenocarcinoma

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44
Q

Malformation of urethral groove

A

ventral (Hypospadias) or dorsal (epispadias) opening of penis

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45
Q

Hypospadias and epispadias can cause what

A

ascending infection of urinary tracts

or if as base of penis can cause X ejactulation

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46
Q

Cryptorchidism

A

partial or complete failure of testes to descend into scrotal sac
= usually unilateral

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47
Q

Cryptorchidism can cause what

A

testicular cancer

= also can at times present in hypospadias

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48
Q

4 diseases that usually effect the glomerulous

A
  1. DM
  2. HTN
  3. SLE
  4. Fabry disease
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49
Q

Basement membrane layers

A
  1. Lamina rara interna (loose)
  2. Central Lamina densa
  3. Lamina rara externa (loose)
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50
Q

layers from capillary to urine lumen (tubule)

A
  1. capillary fenestrated endothelium
  2. BM (3 layers)
  3. Podocytes and foot processes (visceral epithelial cells)
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51
Q

Acute response to glomerular injury is what

A
  1. mesangial and endothelial cells swell and proliferate + WBCs come proliferate = Endocapillary proliferation
  2. glomerular epithelial cells proliferation from injury that causes plasma proteins leakage into urine —-> activate coagulation = CRESCENTS formation + WBCs go into these
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52
Q

Chronic Response to glomerular injury

A

THICKENING OF BM or CAPILLARY WALLS :

  1. immune complexes deposition, fibrin, amyloid, cryoglobulins deposition in GBM
  2. Protein synthesis in GBM= Diabetic Glomerulosclerosis
  3. More layers (matrixes) form in BM = Membranoproliferative Glomerulonephritis (MPGN)
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53
Q

Hyalinosis

A

ECM amorphous material leak into glomerulous
= can obliterate capillary lumens if glomerular tuft
= usually from endothelial or epithelial injury + end stage

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54
Q

Sclerosis

A

EXM collagenous matrix leak deposition in mesangial cells or capillary loops
= in Diabetic Glomerulosclerosis
= can obliterate capillaries

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54
Q

Sclerosis

A

EXM collagenous matrix leak deposition in mesangial cells or capillary loops
= in Diabetic Glomerulosclerosis
= can obliterate capillaries

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55
Q

Podocytopathy

A

loss of podocytes which have limited replication capability
= seen in FSGF and diabetic neuropathy
= causes proteinuria

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56
Q

Podocytopathy can happen from what things happening

A

immune complex deposition

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57
Q

when does progressive renal disease happen

A

once nephrons are destroyed so GFR is 30%-50% normal = progression starts independent or original disease

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58
Q

progressive renal disease causes what 2 things to happen

A
  1. Sclerosis : secondary FSGS, after many renal injuries (proteinuria + loss of renal function)
  2. Tubulointerstitial Injury : interstitial inflammation (in GN) + Tubulointerstitial fibrosis (Diabetic nephropathy)
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59
Q

decline in renal function is more correlated to what

A

extent of tubulointerstitial damage then glomerular damage

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60
Q

Acute Proliferative (Post-infectious and Infection-Associated) GN is what and caused by

A

immune complexes + glomerular cell proliferation

= most common for strep (Group A B-hemolytic Strep (GABH)

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61
Q

Acute Proliferative (Post-infectious and Infection-Associated) GN immunoflorescent staining

A

speckles from granular deposits of C3 (N that cause “humps”)

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62
Q

Rapidly Progressive GN (Crescentic) is what

A

fast loss of renal function (NEPHRITIC) + oliguria

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63
Q

Rapidly Progressive GN (Crescentic) Immunoflorescent stain

A

crescents glomeruli seen (know what this looks like) from PAS
= proliferating epithelial cells and WBS in BC

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64
Q

Type 1 Anti-GMB Abs is what

A

GOODPASTURE SYNDROME
= AB against a3 of collagen4
= can effect lungs (pulmonary hemorrhage)

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65
Q

Type 1 Anti-GMB Abs prevalence

A

male 20yo, often smokers

= autoimmune

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66
Q

glomerular lesions are formed from what 3 autoimmune diseases and what is seen in this

A
  1. Goodpasture
  2. Microscopic polyangiitis
  3. Granulomatosis with polyangiitis (Wegner’s)
    = glomerular necrosis + crescent formation** + scarring sclerosis
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67
Q

Rapid Progressing GN (RPGN) types

A
  1. Type 1 Anti-GMB Abs = (GP syndrome)
  2. Type 2 Immune complex = (SLE, Henoch - Schönlein Purpura, IgA nephropathy BERGER, post-infectious GN)
  3. Type 3 Pauci- Immune = (Wegner GPA + Microscopic PA, Membranous nephropathy, Minimal change disease, FSGS, MPGN)
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68
Q

Type 2 Immune complex RPGN is what and SX

A

SLE

  • fever
  • skin, jonts, kidney , serous membranes
  • hematuria, RBC casts, htn (NEPHRITIC)
69
Q

DX SLE

A

AB to dsDNA (Smith Ag = Sm Ag)

70
Q

SLE and kidney

A

50% pts
GN and Tubulointerstitial nephritis
= immune complex deposit on BM —-> WIRE LOOP when cap wall thickens
= crescents in BC

71
Q

Henoch - Schönlein Purpura SX

A
  1. ABD pain + GI bleeding, V
  2. blood + protein urine
  3. RASH : pupuric rash (Vesicles) on legs, butt, arms
  4. joint pain
72
Q

Henoch - Schönlein Purpura and kidney

A

nephritic or nephrotic, RPGN + many crescents
= IGA deposited mesagial cells (like in IgA nephropathy)
= usually follows URI
= atrophy

73
Q

Henoch - Schönlein Purpura prevalence

A

3yo -9yo children syndrome

can happen in adults = more severe

74
Q

fibrillary GN SX

A
  1. blood + protein in urine
  2. BUN and Cr high
  3. edema
  4. granular IgG, C3, kappa + lambda light chains SEEN **
    • DNAJB9**
75
Q

IgA nephropathy is also called

A

Bergers disease

76
Q

IgA Nephropahty (Bergers)

A

IgA deposits in the mesangial regions

- hematuria

77
Q

IgA Nephropahty (Bergers) is very similar to what disease

A

Henoch-Schönlein purpura

78
Q

IgA Nephropahty (Bergers) is associated to what diseases

A

Celiacs

Hepatobiliary clearance of IGA problems (Liver disease)

79
Q

IgA Nephropahty (Bergers) immunoflorescents stain

A

grandular IgA deposition on mesangial cells

80
Q

RPGN Type 3 Pauci- Immune SX

A

WEGNER (GPA)

  1. necrotizing granuloma of URT
  2. necrotizing grnulomatous vasculitis (lungs, airways)
81
Q

RPGN Type 3 Pauci- Immune happens from

A

T-cells responding to inhaled or other envir thing

= PR3- ANCA

82
Q

RPGN Type 3 Pauci- Immune TX

A

immunosuppression

83
Q

post strep GN deposition location

A

immune complexes deposition on subepithelial spaces + many N and glomerular cells proliferate

84
Q

RPGN nephritic or nephrotic

A

nephritic

85
Q

highest molecular weight protein

A

immunoglobulins only in non-selective proteinuria

86
Q

most common causes of secondary nephrotic syndrome

A

DM
SLE
Amyloidosis

87
Q

most common primary nephrotic syndrome causes

A
  1. FSGS (all ages)
  2. Minimal change disease (children)
  3. membranous nephropathy (adults)
88
Q

Membranous nephropathy happens how

A

75% primary = autoimmune

(other causes)

  • drugs like gold, NSAIDS, Penicillin
  • tumors
  • SLE
  • HEP B, HEPC, schistosomiasis
89
Q

Primary Membranous nephropathy causes

A

anutoABs to M-type Phospholipase A 2 Receptor (PLA2R)

90
Q

Membranous nephropathy immunoflorescents staining and deposition location

A

thickening of capillary wall**

Ig deposits on subepithelial side of BM (IgG)

91
Q

Minimal change disease what happens

A

diffuse effacement of foot processes (flattening)

= minimal changes to glomerulus

92
Q

Membranous nephropathy associated with what 5 diseases

A
  1. respiratory infections
  2. corticosteroids
  3. eczema, rhinitis
  4. HLA haplotypes for atrophy
  5. Hogdkin lymphoma
93
Q

Focal Segmental Glomerulosclerosis prevalence

A

most common nephrotic syndrome

esp in AA and hispanic

94
Q

Focal Segmental Glomerulosclerosis secondary causes for this

A
  1. HIV , heroin, Sickle cell, morbid obese
  2. other necrotizing lesions like IgA nephropathy, focal GN
  3. slit diaphragm protein mutation
95
Q

Focal Segmental Glomerulosclerosis what happens

A
  1. effacement of foot processes
  2. proteins accumulate in mesangial matrix
  3. focal + segmental sclerosis (TGF-B fibrosis)
96
Q

Focal Segmental Glomerulosclerosis immunoflorescence stain and location

A
  1. collapse of cap loops, increase matrix, plasma protein on cap walls —-> hyalinosis
  2. foam cells + lipids
  3. IgM + C3 can be deposited in mesangium
97
Q

Focal Segmental Glomerulosclerosis can lead to

A

tubular atrophy and interstitial fibrosis

98
Q

2 diseases that can lead to FSGS and difference

A
  1. DM = global mesangial sclerosis

2. HIV = focal segmental GN

99
Q

Membranoproliferative GN type 1 and type 2

A

TYPE 1 : deposition of IgG** + Complement

TYPE 2 : dense deposite disease**, C3 GLOMERULOPATHY (complement activation and excretion)

100
Q

Membranoproliferative GN type 1 and type 2 is associated with

A
  1. SLE, HEP B, HEP C, schistosomiasis, HIV
  2. a-1 antitrypsin def
  3. hodgkins
101
Q

Membranoproliferative GN type 1 and type 2 immunoflorescence

A

WBC to mesangium
= double-contour, tram track appearance (split membrane appearance)
=lobular look glomeruli
=

102
Q

Membranoproliferative GN type 2 WHAT is seen

A

LOW C3 , only normal C1 and C4
LOW Factor B, Properdin
(C3 nephritic factor in circulation C3NeF)**

103
Q

Alport Syndrome SX

A

hematuria —-> Chronic RF
nerve deafness
eye disorders

104
Q

Alport Syndrome what causes this

A

mutation in collagen 4 subunits (in GBM, lens, cochlea)

esp subunits a3, a4, a5

105
Q

Alport Syndrome inheritance

A

X linked most common

can be AD or AR

106
Q

Alport Syndrome staining look

A

thickening and thinning spots on the BM of glomeruli + lamina densa splitting
= basket-weave apperance

107
Q

Alport Syndrome can progress to what

A

global or focal segmental Glomerulosclerosis , vascular sclerosis, tubular atrophy, interstitial fibrosis

108
Q

Thin Basement Membrane Nephropathy (Benign Familial Hematuria)

A

asymptomatic hematuria

diffuse thinning of GBMm however normal renal function

109
Q

Diabetic Nephropathy first sign

A

low amounts of albumin in urine (30mg-300mg/day) (which will show - dip stick, you need urine microscopy)

110
Q

Diabetic nephropathy prevalence

A

more in T1D, however still in T2D AA, native americans, hispanic

= can progress to ESRD

111
Q

glomerulus in Diabetes

A

most in T1D

Glomerular capillary BM (GBM) thickening) + mesangial widening + tubular BM thickening

112
Q

Diabetic Nephropathy is also called what

A

intercapillary glomerulosclerosis OR Kimmelstiel- Wilson disease

113
Q

Diabetic Nephropathy what is seen in the arteries and tubules

A

hyalinosis in capillaries

tubular atrophy + interstitial fibrosis (glomerulosclerosis)

114
Q

acute kidney injury (AKI) Ischemic vs nephrotoxic

A

Ischemic : from low BF

Nephrotoxic : from endogenous agents

115
Q

muddy brown granular casts are seen when

A

AKI on microscopes

116
Q

Initiation Phase of AKI

A

decrease of Urine output and increase BUN (oliguria can happen, from low BF + low GFR)

117
Q

Maintenance Phase AKI

A

decrease urine (40-400ml/day = oliguria), NA and Water overload, rising BUN, hyperkalemia, metabolic acidosis,

118
Q

Recovery Phase AKI

A

increase in urine V up to 3L/day (from still damaged tubules), HYPOkalemia, tubules recover over time, BUN and Cr decrease

119
Q

HALLMARKS of tubulointerstitial disorders

A
  1. X nephritic X nephrotic syndrome
  2. X concentration in urine (polyuria or nocturia), salt wasting,
  3. metabolic acidosis = cant excrete acids
120
Q

acute pyelonephritis

A

bacterial infection
usually from UTI
= suppurative inflammation

121
Q

Chronic pyelonephritis

A

usually also bacterial infection + vesicoureteral reflux, obstruction

122
Q

acute pyelonephritis SX

A

CVA tenderness
fever, high WBCs
Dysuria, polyuria

123
Q

pyelonephritis is usually from what

A

E. Coli

124
Q

TX pyelonephritis

A

E. Coli Cystitis :
= 1 dose AB FOSFOMYCIN
= 3day TMP/SMZ
= nitrofurantoin

125
Q

kidney viral infection happens from what usually

A

Polyomavirus usually from allograft kidney from immunosuppression = Polyomavirus-associated-nephropathy(PVAN)

126
Q

other viral infections of kidneys primary

A

BK virus

JC virus

127
Q

complications of pyelonephritis

A
  1. Papillary necrosis : coagulative necrosis of pyramids (yellow grey-white)
  2. Pyonephrosis: almost or complete obstruction usually high in GU tract
  3. Perinephric abscess : suppurative inflammation through renal capsule to perinephric tissue
128
Q

Papillary necrosis is seen in what patients with pyelonephritis

A
  1. DM
  2. Sickle cell
  3. Obstruction
129
Q

Pyonephrosis is what

A

almost or complete obstruction of GU tract esp high up

= suppurative exudate cant drain and fills pelvis, calyces, ureter + pus

130
Q

what diseases effect chronic tubulointersititial inflammation and scarring of CALYCES + pelvis

A

Chronic pyelonephritis + Analgesic nephropathy

131
Q

dilation of calyces Vesicoureteral reflux vs obstruction

A

obstruction dilates more and basically all calyces from the high P backflow

132
Q

blood agar and MacConkey agar is used when

A

for pus or urine samples

133
Q

Proteus Mirabilis on blood agar

A

thin waves of concentric circles form

134
Q

Proteus Mirabilis UTI TX

A

UTI : 3day trimethoprim/sulfamethoxazole (TMP/SMZ)

or 3day fluroquinolone (ciprofloxacin)

135
Q

complicated UTI TX

A

ABs for 10-21 days

136
Q

TX acute Pyelonephritis uncomplicated

A 
(Gentamycin or ceftriaxone can be given 1 time before starting)
1. Fluoroquinolone**
OR
2. TMP/SMZ
OR 
3. cephalosporin
(7-14days)
137
Q

acute kidney injury top causes

A
  1. Pyelonephritis

2. toxin or drug induced tubulointerstitial nephritis

138
Q

Drug or Toxin induced Tubulointerstitial nephritis happens from what

A

Sulfonamides, synthetic penicillin (methicillin, ampicillin), synthetic AB (Rifampin), diuretics, NSAIDS, allopurinol, cimetidine

139
Q

Drug or Toxin induced Tubulointerstitial nephritis injury happens how

A
  1. cause interstitial inflammation (acute hypersensitive nephritis)
  2. cause ATI
  3. injuries cumulate take years to become CKD (goes unrecognized)
140
Q

Drug induced ACUTE Tubulointerstitial nephritis SX

A

2-40days after

  1. fever
  2. high E
  3. rash 25%
  4. renal problems (blood, protein, WBCs esp E)
  5. high Cr or AKI (50%)
141
Q

NSAIDS and kidney

A

inhibits COX2 including in the kidney

= can cause several renal injuries

142
Q

nephropathy with hyperuricemia happens in which 3 diseases

A
  1. Acute uric acid nephropathy
  2. Chronic urate nephropathy
  3. Nepholithiasis (stones)
  4. Tumor Lysis Syndrome (effecting tubules and high uric acid, usually from tumor cells undergoing chemo)
143
Q

hypercalcemia and kidney

A

diseases like hyperPTH

can lead to stones and chronic tubulointerstitial disease

144
Q

ADTKD (AD Tubulointerstitial Kidney Disease)
also called
causes

A

(medullary cystic kidney disease)

= progressive renal failure in adults inherited as AD

145
Q

ADTKD (AD Tubulointerstitial Kidney Disease) MUTATIONS 4

A
  1. MUC1 (distal nephrons)
  2. UMOD (thick ascending LOH)
  3. REN (Juxtaglomerular apparatus)
  4. HNF1B (hepatocyte TF regulating other genes)
146
Q

multiple myeloma and kidney + 4 reasons effects happen

A

renal insufficiency due to

  1. Bence- Jones proteinuria + nephropathy
  2. Amyloidosis
  3. Light Chain deposition disease
  4. Hypercalcemia + Hyperuricemia
147
Q

cancer that can cause membranoproliferative GN

A

leukemia and lymphoma

148
Q

cancer that can cause minimal change disease

A

Hodgkins

149
Q

cancer that can cause membranous nephropathy

A

carcinomas

150
Q

cancer that can cause monoclonal immunoglobin / light chain deposition disease

A

Multiple Myeloma

151
Q

Uromodulin (Tamm-Horsfall protein) function

A

protein in kidney (guardian)

  1. modulate ion channel activity + balance
  2. systemic inflammatory responce
  3. tubular communication
  4. bacterial adhesion protection
  5. mineral crystallization
152
Q

Uromodulin (Tamm-Horsfall protein) THP mutation can cause

A
  1. UTI recurrent
  2. kidney stones
  3. htn
  4. hyperuricemia
  5. AKI / CKD
153
Q

organ that can impair renal function

A

LIVER DISEASE **

also Heart Disease

154
Q

Hepatorenal syndrome steps

A
  1. PORTAL HTN (from liver disease)
  2. vasodilators made
  3. lower renal BF
  4. renin/angiotensin activation
  5. lower renal BF more = renal failure
155
Q

Hepatorenal syndrome is usually from what

A

Portal HTN from cirrhosis, severe alcoholic hep, or tumor at times, fulminant hepatic failure

156
Q

most common disease or system in body that effects

A

vascular disease (HTN, vasculitis)

157
Q

Nephrosclerosis strong association

A

HTN (DM makes it worse)

158
Q

Nephrosclerosis kidney looks like

A 
grain leather (sugar coating) look on surface
\+ reduced size from cortical scarring
159
Q

renal artery stenosis causes what

A

HTN from the renin production activated (when ischemia in kidney)

160
Q

Fibromuscular Dysplasia (FMD)

A

thickening in medium and large As (renal, carotid, splanchnic, vertebral) = hyperplasia + fibrosis —-> luminal stenosis

161
Q

Fibromuscular Dysplasia (FMD) in renal artery can be caused by + angiography look

A

renovascular htn

= beads on string on adjacent vessels —-> vascular outpouching (aneurysms) that can rupture

162
Q

Focal FMD vs Multifocal FMD

A

Focal FMD : tubular narrowing (stenosis), focal lesions
= intimal fibroplasia

Multifocal FMD : 90%, many lesions + STRING ON BEADS

163
Q

thrombotic microangiopathy is what

A

syndrome that includes TTP/HUS and thrombi on caps and arterioles (including in kidney) = MICROANGIOPATHIC HEMOLYTIC ANEMIA

164
Q

thrombotic microangiopathy is what

is caused by what

A
  1. Shiga toxin- mediated HUS (E. coli H0517)
  2. Atypical HUS
  3. TTP (ADAMTS13)
165
Q

Typical Hemolytic Uremic Syndrome is what and from what

A

Epidemic, Classic, +Diarrhea

1. GI E. Coli O157:H7 infection

166
Q

Typical HUS SX

A

hematemesis, melena, oliguria, hematuria, thrombocytopenis, hemolytic anemia, HTN, neurologic changes

167
Q

Atyical Hemolytic Uremic Syndrome is what and caused by 4

A

Non-Epidemic, -Diarrhea

  1. Factor H def. Factor I def, def CD46 (prevent complement)
  2. Anti-phospholipid syndrome (can be from SLE)
  3. post-pregnancy complications
  4. systemic sclerosis, malignant htn
168
Q

TTP PENTAT

A
  1. fever
  2. neurologic changes, headache
  3. thrombocytopenia
  4. microangiopathic hemolytic anemia
  5. renal problems (renal failure)
169
Q

TTP happens because of

A

ADAMT13 mutation of ABs against it** (cleaves vWF for proper plt aggregation)

170
Q

TTP looks like what in kidney

A

massive ischemic necrosis in CORTEX

171
Q

Bilateral renal artery disease can cause what and important to recognize for

A

see in angiography
can cause chronic ischemia + renal insufficiency (even with no htn)

= surgery to revascularize to prevent more renal decline

172
Q

3 renal problems that can occur in sickle cell pts

A
  1. hematuria
  2. poor concentrated urine = hyposthenuria
  3. Patchy papillary necrosis

CPR 2 Exam 3 (5 decks)

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