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Flashcards in HISTOPATH Deck (232):
1

softer and paler due to DYSTROPHIC CALCIFICATION

Calcium Phosphate Stones

2

Gross:

Pus and little microabscesses in the kidney; hyperemia and yellowish discoloration

Acute pyelonephritis

3

Thin-walled cystic structure; 15-20 cm diameter. Loss of pyramids. Thin cortex.

Far-advanced cases of obstruction; irreversible

4

VHL is a 1) and encodes protein for 2) complex which normally degrades and controls growth factors such as Hypoxia Inducing Factors (HIF-1)

1) tumor suppressor gene

2) ubiquitin ligase

5

Macrophage accumulation in cortex

Xanthogranulomatous Pyelonephritis:

6

Histology:

placenta-like; 

malignant 1) (well-demarcated cell borders,are not multinucleated and have smaller nuclei) and malignant 2) (mutlinucleated large cells)

1) cytotrophoblasts; 

2) synctiotrophoblasts;

Choriocarcinoma

7

1)  and 2) can NOT cause obstruction;

3) can as they are sloughed off and this obstruction would NOT be seen on X-ray

All three are complication of pyelonephritis 

1) Perinephric abscess

2) pyonephrosis

3) papillary necrosis

8

Risk of SPONTANEOUS HEMORRHAGE

Angiomyolipoma

9

Grossly: yellow tumor w/ gelatinous center.

Renal Cell Carcinoma (RCC)

10

Outlines of tubules WITHOUT nuclei

Necrosis

11

Histology: clear cytoplasm in cells, arranged in nests.

Clear Cell Carcinoma:

12


Histology:

Atypical pleomorphic cells that surround a fibrovascular core

Papillary Carcinomas In-Situ:

13

A Cauliflower-like lesion on a freely movable stalk

Papillar transitional carcinoma; not invasive

14

Renal Oncoytoma--> Large eosinophilic cells;
Abundant 1) w/o 2)

(compare to Chromophobe RCC)

1) mitochondria

2) perinuclear clearing

Chromophobe has halo around nuclei;

15

Polysaccharide capsule => 70 serotypes

Interferes with COMPLEMENT ACTIVATION

Klebsiella

16

Sclerosis in FSGS: EC collagen deposition in the 1) and 2) 

mesangium and capillary loops

17

Mutation in 1) -->↑HIF-1 (transcription factor) which promotes cell growth (↑PDGF) and angiogenesis (↑VEGF).

VHL

18

Cystinuria decreased reabsorption of cystine and other dibasic amino acids (?)

lysine, ornithine, and arginine

19

Glomeruloid-like structures with BV in the center and epithelial cells around it.
 

Schiller Duval Bodies; seen in yolk sac tumor
 

20

Dominant-negative inactivating mutation of WT1 gene

Denys-Drash Syndrome:

21

Wilms tumor Histology:

Triphasic combination of 1)  + 2)  + 3).

1) dense blue cells (blastema);

2) stroma 3)  epithelial cell types (abortive tubules or glomeruli)

22

Papillary necrosis seen in 1) is which type of necrosis:

diabetics; coagulative; 

23

Polyomavirus

H&E-->1) 
EM-->2) .

nuclear enlargement and intranuclear inclusions;

2) cystalline-like lattices on EM

24

Milk-alkali syndrome-->those who take lots of antacids and drink milk

Hypercalcemia (and thus METASTATIC) leading to nephrocalcinosis

25

Macrophage accumulation surrounding struvite stones

Xanthogranulomatous Pyelonephritis

26

Easily palpable abdominal mass (visible), can cause intestinal obstruction

Wilms Tumor

27

Pyonephrosis vs. Perinephric abscess

Both are complications of acute pyelonephritis;

Pyonephrosis has acute inflammation but NOT encapsulated and confined to kidney

Perinephric abscess extends through the renal capsule into perinephric fat and encapsulated

28

TUBULAR effects first in hydronephrosis--> result 1)

1) impaired concentrating ability; dilute urine; no effect on GFR

29

ANP 1) sodium reabsorption so the kidney can eliminate sodium and decrease body volume

decreases

30

Post-obstructive diuresis--> sodium content?

Unilateral Obstruction-->HIGH NaCl in urine;

31

Histology: papillae lined by epithelial cells.

Papillary Renal Cell Carcinoma

32

“nodular accumulation of eosinophilic material within glomeruli

KW bodies seen in Diabetic nephropathy

33

Susceptible locus: chromosomes 1 and 10 (tumor suppressor gene) 
Sporadic-->Hypermethylation of Glutathione S-transferase p1 (GSPT1), which is a known GENOME CARETAKER GENE

Men with BRCA2 gene mutation--> higher risk

Prostate Adenocarinoma

34

Tumor lysis syndrome-> causes what type of stone? is it increased in urine or serum?

Uric acid stone; uric acid increased in URINE;

35

Grossly:

Large, tan and fleshy appearance w/ lots of cystic areas and areas of hemorrhage

Wilms Tumor

36

Neutrophilic microabcesses in renal interstitium

acute pyelonephritis

37

Hb A1c-->Glucose attached non-enzymatically to 1) 

N-terminal amino acid

38

Beckwith-Wiedmann Syndrome:

Mutation in 1) --> loss 2) in maternal gene leading to 3) of IGF-2.

1) WT2 gene cluster 2) genomic imprinting 3) overexpression

39

 

Both are complications of 1);

Pyonephrosis has acute inflammation but NOT 2) and confined to kidney

Perinephric abscess extends through the renal capsule into 3) and encapsulated

1) acute pyelonephritis

2) encapsulated

3) perinephric fat

40

1) : homogenous and eosinophilic;

EM shows hyaline is EXTRACELLULAR and amorphous; due to plasma proteins insudated from the circulation into glomerular structures, usually a consequence of endothelial or capillary wall injury;

Hyalinosis seen in FSGS

41

Gram (-) bacillus.
True aerobe; polar flagella for motility;

Widespread in moist environments

Pseudomonas Aeruginosa

42

a) Sporadic form: Trisomy 7&17; loss of Y in males;

(b) Familial form: Trisomy 7.

Both forms associated w/ activating mutations in MET.

Papillary Renal Cell Carcinoma (15% of RCC)

43

Gynecomastia and hyperthyroidism.

Hemoptysis

Choriocarcinoma

44

macrophages with abundant pink cytoplasm, usually surrounded by giant cells and a rim of lymphocytes

Granuloma

45

Bladder cancer:

•Chromosome 9 deletions --> lose p16 (INK4a) or p15.

•P53 mutations;

what is p16? p15?

p16-->encodes inhibitor of a cyclin-dependent kinase

they are both tumor suppressor genes

46

Chonic pyelo histopath:

1) infiltration of interstitium; 

Thyroidization which are 2) within 3); 

4)

Lymphocyte;

2) eosinophilic hyaline casts

3) tubules

4) Fibrosis 

47

Gleason Grading system used for 1_

Prostate cancer

48

Fibrosis surrounding dilated tubules with hyaline casts

Chronic pyelonephritis

49

Hylaine arteriolosclerosis seen in: 1)

KW bodies seen in:2)

1) afferent and efferent arterioles

2) glomeruli causing glomerusclerosis

50

Precursor lesion-->PIN

Prostatic Intraepithelial Neoplasia for prostate cancer

51

Hyperoxaluria—either hereditary (primary oxaluria) or acquired by intestinal overabsorption in pts w/ ___

GI diseases or in vegan diets.

52

hallmark of prostate CANCER histo

Prominent nucleoli; 

53

Urate Nephropathy: 1) and 2) deposition of crystalline monosodium urate; seen grossly as 3) streaks in the 4)

Tubular and interstitial 3) YELLOW 4) PAPILLAE

54

Gross: Stones are smooth, hard, yellow and

Uric acid stone

55

Prostate adenocarcinoma

Susceptible locus: 1) 

Sporadic-->2), which is a known GENOME CARETAKER GENE

Men with BRCA2 gene mutation--> higher risk

1) chromosomes 1 and 10 (tumor suppressor gene) 

2) Hypermethylation of Glutathione S-transferase p1 (GSPT1)

56

Sheets/nests of separated by fibrous bands infiltrated by lymphocytes


Clear cytoplasm that contains glycogen.

Can often be stained immunologically by c-kit

Seminoma

57

Reinke crystals--. rod like cytoplasmic inclusions

Leydig Cell Tumor

58

Granulomatous Prostatitis--> Rxn following 1)

Transurethral resection (TUR) of prostate for nodular hyperplasia

59

H&E-->nuclear enlargement and intranuclear inclusions;
EM-->cystalline-like lattices on EM.

Polyoma virus; seen in Immunocompromised such as renal transplants; causes acute pyelonephritis, UTI

60

Germline deletion of WT1 (tumor suppressor gene) of 11p13—two-hit hypothesis

Wager Syndrome:

61

Mutation in ____; causes kidney stones due to hypercalciuria, aminoaciduria, and phosphaturia;

Dent’s Syndrome; chloride channels

62

Grossly

Abnormal bumpy kidney shape; Scarring at upper and lower poles

Fibrosis and loss of cortex

Chronic Pyelonephritis:

63

BPH vs. Prostate cancer histo

BPH has nodules; prostate cancer NO nodules;

64

Gouty tophus-->a focal accumulation of 1)  surrounded by 2)

Urate crystals in the adrenal medulla w/ 3) around them.

4)  around the crystals (host response).

urate crystals;

2) inflammatory cells (macrophages) 

3) giant cells

4) fibrosis

65

A 17-year-old woman has a right flank mass which is draining thick yellow fluid.
You examine the fluid microscopically and see white pyramidal crystals

Xanthogranulomatous pyelonephritis; notice fistula; also struvite crystal (white pyramidal crystal)

66

A 55-year-old man with a long history of diabetes has proteinuria and decreased GFR. A renal biopsy shows pink nodules in his glomerui composed of:

Glycated proteins

67

Renal pelvis absesses and papillary necrosis caused by hyaline deposition in tubules;

Both complication of ?;

diabetic nephropthy

68

Angiomyolipoma

Due to loss of: 

suppressor function of TSC1 or TSC2 genes

69

Histology: papillary fronds (can be low or high grade).

Urothelial Carcinoma: Renal Pelvis

70

EM of ____-->_____ of renal tubular epithelial cells contain abundant calcium deposits.

Nephrocalcinosis; MITOCHONDRIA

71

Cystoscope: cauliflower-like lesions.

Develops as low grade papillary tumor

Papillary Carcinomas In-Situ:

72

Hallmark: halos around the nuclei

Chromophobe RCC; remember it is malignant as oppsed to oncocytoma

73

Hydronephrosis Pathophysiology

the BACK PRESSURE leads to: Renal atrophy (more tubular) Decreased inner medullary blood flow.

74

Bladder cancer gross:

Gross:
Large fungating mass invading the muscle,
YELLOW amorphous necrosis

75

Renal atrophy (more tubular) Decreased inner medullary blood flow.

Hydronephrosis Pathophysiology

76

Calcification of the interstitium

metastatic nephrocalcinosis

77


Clinical Sign of Invasive Bladder Cancer

1)

Frequency, urgency, and dysuria

PAINLESS hematuria—unless there is obstruction

78

Wedge-shaped scars mixed w/ relatively normal renal tissue

Nephrocalcinosis

79

Papillary Renal Cell Carcinoma

a) Sporadic form: 1) 

(b) Familial form: 2)

Both forms associated w/ 3) in MET.

Trisomy 7&17; loss of Y in males;

2) Trisomy 7

3) activating mutations

80

HALLMARK: CENTRAL SCAR; Tan/orange well-circumscribed tumor

Renal Oncoytoma

81

 

  1. Hereditary forms (mutations in podocyte genes) --> podocin, alpha-actinin-4, TRPC6
  2. Overwork/Stress: *mostly perihalar variant*
  3. Congenital: unilateral agenesis;
  4. Acquired: reflux nephropathy
  5. Obesity (not enough kidney to support the body weight).
  6. Reduced O2 in blood from Sickle Cell Disease, cyanotic congenital heart disease

 

FSGS

82

Hereditary forms (mutations in podocyte genes)  podocin, alpha-actinin-4, TRPC6

Sporadic: Overwork/Stress such as obesity or sickle cell

Focal Segmental Glomerulosclerosis 

83

Tubules have eosinophilic hyaline casts called thyroidization.

Chronic Pyelonephritis:

84

Lesions (hemartomas) composed of fat, smooth muscle and blood vessels.

Angiomyolipoma

85

unilateral agenesis of kidney can lead to 

FSGS

86

 

•Chromosome 9 deletions --> lose tumor suppressor gene p16 (INK4a) or tumor suppressor gene p15.
•P53 mutations; normal function is to prevent apoptosis

•Genetic changes (mutations) in bladder cancer:

87

loss of sequence on short arm of chromosome 3 (where VHL is) and then second allele undergoes 1)

somatic mutation or hypermethylation;

regarding Renal Cell carcinoma

88

Large gram (-) bacilli

Produce BRICK RED COLONIES

Serratia

89

Seminoma

Sheets/nests of separated by fibrous bands infiltrated by 1)

2) cytoplasm that contains glycogen.
Can often be stained immunologically by 3)

1) lymphocytes; 2) Clear;

3) c-kit

90

Lancefield Group D strep, but more ovate than other streptococci

Enterococcus

91

changes in visceral epithelial cells: effacement of foot processes, vacuolization, retraction, and cell detachment from GBM

Focal Segmental Glomerulosclerosis

92

Both sporadic and familial RCC associated w/ LOSS of 1) on 2)

1) VHL gene

2) chromosome 3

93

Histology:

Sheets of undifferentiated cells; necrosis and hemorrhage

Embryonal Carcinoma

94

Hemorrhagic mass w/ necrosis (testicular tumors)

Choriocarcinoma; Embryonal Carcinoma

95

Immunoglobulin A deposition in mesangial cells

IgA nephropathy

96

GFR is 50% ↓; normal BUN and creatinine; generally asymptomatic

Stage 1: Diminished Renal Reserve

97

GFR is 50-80% ↓;

Azotemia, anemia (↓EPO), and HTN.

Present initially w/ polyuria and nocturia

Stage 2: Renal Insufficiency

98

Stage 3: Chronic Renal Failure

GFR 1) of normal.

Edema, 2), and 3)

1) <20% 2)metabolic acidosis

3) hyperkalemia.

99

GFR <5% of normal;

Uremia:

↑BUN (↑nitrogenous waste); Nausea, anorexia, pericarditis, encephalopathy, asterixis, and platelet dysfunction

Stage 4: End Stage Renal Disease

100

low EPO production by renal peritubular interstitial cells cuases 1; seen in 2)

anemia; Chronic Renal Disease

101

Associated w/ berry aneurysms

Autosomal DominantPKD

102

Mutations: (two loci; loss of function)

PC1 (membrane receptor)

 PC2 (Ca2+ channel activity

ADPKD1 and 2 gene

103

present in infants as worsening renal failure and HTN

Autosomal Recessive PKD

104

Mutation in PKHD1 gene --> fibrocystin (membrane receptor

AR PKD

105

Associated/ congenital hepatic fibrosis and hepatic cysts

AR PKD

106

renal stone formation (nephrolithiasis

Medullary Sponge Kidney

107

Fetal appearance --> immature glomeruli and tubules

Multicystic Renal Dysplasia

108

Lung hypoplasia

Flat face w/ low set ears

defects in the extremities

Potter Sequence

Bilateral Renal Agenesis

109

compensatory hypertrophy of the existing kidney.

Unilateral Agenesis

110

aspirin and phenacetin causes:

Papillary Necrosis

111

↑risk of transitional papillary carcinoma of the renal pelvis

Analgesic nephropathy

112

Inherited Renal Cyst diseases that lead to chronic renal failure

Medullary Cystic Disease

Polycystic Kidney Disease (PKD)

113

NON-inherited Cystic Disease

Multicystic Renal Dysplasia

Medullary Sponge Kidney

114

NORMAL anion gap (i.e. hyperchloremic—since Cl- compensating) metabolic acidosis.

Renal Tubular Acidosis

115

Pts have HIGH urine pH;

HYPOkalemia and ↑risk of calcium phosphate stones (recall: alkaline stones).

Type 1: Distal Tubule

116

amphotericin B toxicity.

Type 1: Distal Tubule

117

Sjogren’s,

analgesic nephropathy

Type 1: Distal Tubule

118

↑risk of calcium phosphate stones (

Type 1: Distal Tubule

119

Defects in PCT --> ↓HCO3- reabsorption -> ↑excretion of HCO3- in urine --> metabolic acidosis

Type 2: Proximal Tubule

120

Causes:

Fanconi’s Syndrome and CA inhibitors

Type 2: Proximal Tubule

121

LOW urine pH;

HYPOkalemia;

Type 2: Proximal Tubule

122

EM--> FIBRILLAR deposits; light chain form in NON-FIBRILLAR

Amyloid Nephropathy

123

LM Stain w/ congo red

Amyloid Nephropathy

124

Amyloid Nephropathy

amorphous, a-cellular, and undigestable material in the 1) and 2)

1) mesangium

2) renal tubules

125

Angulated and tubular casts surrounded by macrophages, including multinucleate cells

light chain cast nephropathy

126

Rheumatoid arthritis

Chronic TB

serum Amyloid A protein; inflammatory

127

Clear cytoplasm that contains glycogen.

Seminoma

128

Germ Cell Tumors Seen in older men
 

Spermacytic Seminomas:

129

precocious puberty

Leydig Cell Tumor

130

sex cord-stromal tissues of the testicle

Leydig Cell Tumor

Sertoli Cell Tumors

131

Choriocarcinoma vs. Leydig cell tumor s/s

Choriocarcinoma--> gynecomastia and hemoptysis

Leydig cell--> Gynecomastia and precocious puberty

132

capillary surrounded by an epithelial layer

Schiller duval bodies; yolk sac tumor

133

elevated AFP

Yolk sac tumor

134

Elevated bHCG

Choriocarcinoma

135

stained immunologically by c-kit

Seminoma

136

Drug Hypersensitivity (type I HYPERSENSITIVTY

Acute Tubulointerstitial Nephritis

137

EOSINOPHILS IN URINE!!

Acute Tubulointerstitial Nephritis

138

↑IgE levels and basophils; 

EOSINOPHILS IN URINE!!

Acute Tubulointerstitial Nephritis

139

Fatty change initially, followed by necrosis

Carbon Tetrachloride Poisoning

140

Ballooning and hydropic or vacuolar degeneration of PCT

Ethylene glycol:

141

↑urine volumes but ↓GFR; usually benign

Nonoligouric AKI: 50% of AKI pts

142

SLIGHT OLIGURIA w/ a ↑in BUN

Initiation PhaseAKI (FIRST 36 HRS)

143

OLIGURIA;

HYPERkalemia;

Metabolic acidosis (inability to excrete urea, K+ and H+)

Maintenance Phase AKI

144

Hyaline and pigmented (brown) granular casts in the distal tubules and collecting ducts

Tamm-Horsfall protein; SEEN IN AKI

145

Interstitial edema, leukocytes within dilated vasa recta, epithelial regeneration

AKI

146

granular casts in the distal tubules and collecting ducts

AKI

147

acute pancreatitis, septic shock

Ischemia Acute Tubular Necrosis

148

Aminoglycosides, radioCONTRAST dyes

NEPHROTOXIC Renal tubular acidosis

149

Urate (tumor lysis syndrome),

Acute Tubular Necrosis;

Uric acid stones

150

Ethylene glycol

 nephrotoxic acute tubular necrosis

151

Grossly:

Pale cortex and hyperemic medullary regions

Acute Tubular Necrosis

152

Large proteinaceous casts (can be either light chain deposition disease or Bence Jones).

Light-Chain amyloid Deposition Disease

153

damages cell cytoskeleton

Proteases such as calpain

154

damges cell membrane

phospholipase c

155

cysts in the medullary collecting ducts; affects tubules

Medullary Cystic Disease

156

Parenchymal fibrosis --> leads to SHRUNKEN kidneys and worsening renal failure.

Medullary Cystic Disease

157

POLYURIA

HYPOkalemia

 

Recovery Phase AKI

158

Acute Tubulointerstitial Nephritis types of Hypersensitivity

TYPE I

159

Unilateral defect in children;

Generally have

Renal Hypoplasia

160

Myoglobinuria from crush injury to muscle

Direct toxic tubular injury; AKI

161

Hb or Myoglobin casts in TUBULES

crush injury causing AKI

162

Defect in metanephric differentiation;

persistence of cartilage, undifferentiated mesenchyme, and immature ductules

 

Multicystic Renal Dysplasia

163

obstruction etiology such as ureteropelvic or ureteral atresia

Multicystic renal dysplasia

164

gentamicin

nephrotoxic aki

165

aki findings:

1) ___ casts in distal tubules and coll. ducts

2) ___ protein;

3) Interstitial edema

___ within dilated vasa recta

Hyaline pigmented GRANULAR;

tamm horsfall protein;

Leukocytes

166

leukocytes within dilated vasa recta

AKI

167

Hypotension and shock

Pre-renal azotemia

168

nuclear shrinkage (EM changes in necrosis)

pyknosis

169

karyolysis

nuclear degradation (EM changes in necrosis

170

DNA ladder

Apoptotis

171

caspase-3 and caspase-6

executioner proteases

172

necrotic cell death usually forms a (1) 

SMEAR

173

 karyolysis: nuclear degradation

necrosis; NOT apoptosis

174

 FLIP 2

bind to caspace 8 and block its cleavage; anti-APOPTOTIC

175

caspace 8

Extrinsic pathway--> initiator

176

caspace 9

Intrinsic pathway--> initiator

177

BAX and BAK activated by BID and BAD

Pro-apoptotic

178

BCL-2

ANTI-apoptotic

179

INC. cyt C release

INC BAX and BAK (pro-apop)

DEC. BCL-2 (anti-apop)

180

Bcl-2 binds to and inhibits ___ preventing Cytochrome C release thus inhibiting the ___ pathway

Bcl-2 binds to it and inhibits APAF-1 preventing Cytochrome C release thus inhibiting the INTRINSIC pathway

181

APAF-1

normally activates caspace 9; inhibited by Bcl-2 which is anti-apoptotic

182

FAS-L binds to 

CD95 (fas-R); extrinsic pathway

183

FAS binds to FasL and interacts with FADD which activates caspace 8

184

BP systolic >220 or diastolic >120 w/ NO evidence of end organ damage

Hypertensive Urgency

185

BP systolic >220 or diastolic >120 + end organ damage

Hypertensive Emergency

186

hyaline arteriolosclerosis of afferent and efferent in 1)

only AFFERENT 2)

1) diabetic nephropahty

2) essential HTN

187

individual cells apoptose

Intrinsic Pathway

188

groups apoptose

Extrinsic Pathway

189

very high BP causes hemolysis of RBCs seen on slides:

schistocytes

190

chromatin condensation; nuclear shrinkage (pyknosis)

apoptosis

191

caspace 3 activity or endonuclease 

detect apoptosis

192

release of PDGF (malignant hypertension)

myointimal proliferation--> ↑ hypertension--> Fibrinoid necrosis

193

structure maintained but NO nuclei

coagulative necrosis

194

Macula densa release 1) which tells JGA cells to INC. renin release

1)prostaglandins

195

annexin V binds to phosphatidylserine once it moves to the outer membrane; stain to detect ?

APOPTOSIS

196

pinkish fibrin like material in BV wall;

fibrinoid necrosis

197

myelin figure are phospholipid masses

necrosis!

198

caspaces cleave after ? 

aspartic acid in aa chain

199

detect necrosis by?

cell proteins and membranes that leak into tissues

200

endothelial cell damage from HIGH BP releases 1) which then causes release of 2); result--> Fibrinoid necrosi

1) vWF

2) PDGF

201

“string of beads” pattern

Fibromuscular dysplasia:

202

Fibromuscular dysplasia

Renal Vascular HTN

203

Renal artery vasculitis such as 1)  are causes of Fibromuscular dysplasia; 

1) Takayasus and Giant cell

204

Thickening of MEDIAL arterial smooth muscle, which alternates w/ atrophy

Fibromuscular dysplasia

205

STAGE 2 Renovascular HTN

Stenotic kidney--> dec renin;

Normal--> dec renin; 

 

206

abdominal aortic aneurysms

Renal Vascular HTN

207

cholesterol clefts

embolus e.g. abdominal aortic aneurysm

208

Tubules show marked ischemic atrophy w/o extensive interstitial fibrosis


Fibromuscular dysplasia

209

95% from atherosclerosis

renovascular stenosis

210

renal VEIN renin is INC. in ischemic vs. normal kidney

Stage 1 renovascular HTN

211

C/I for Renovascular stenosis

ACE inhibitors; captopril, etc

212

ACE made in

pulmonary and renal ENDOTHELIAL CELLs

213

HTN leads to renal hypoperfusion of BOTH KIDNEYS

STAGE 3 Renovascular HTN

214

AREAS of clear space where lipid is washed out; 

cholesterol clefts--> embolus in renovascular HTN

215

Affects arterioles and arteries

Diabetic Macroangiopathy

216

Diabetic Mircoangiopathy

LESION AT LEVEL OF CAPILLARY and consist of increased accumulation of capillary basement membrane material

217

NONENZYMATIC glycosylation of proteins of the vascular BM

hyaline arteriololosclerosis

218

Glucose reacts with proteins form 1) which activate 2) which activate immune system

1) AGE 2) RAGE

219

increases RAGE thus INC. immune response to hyperglycemia;

oxygen free radicals

220

 NOT measured by urine dipstick

microalbuminuria

221

HYALINE change and EPITHELIAL CELL LOSS; leads to ___ necrosis

Tubular lesion in diabetic microangiopathy; PAPILLARY NECROSIS 

222

glomerulosclerosis and increased mesangial matrix from hyperglycemia causes:

DECRESED GFR

223

Glomerular changes in microangiopathy diabetes:

Hyperglycemia 1) in the glomeruli and activates2) 

 

 

↑TGF-beta;

2)  protein kinase C

 

224

 

Microangiopathic Diabetes vs. Macro

Capillaries, tubules, and glomeruli are micro;

renal arteries and arterioles are MACRO

225

Metabolizes glucose into sorbitol via aldose reductase and then to fructose via Sorbitol Dehydrogenase

Polyol pathway

226

↓myoinositol and ↓ Na/K ATPase leads to IMPAIRED axonal transport.

Polyol pathway

227

Extracellular matrix proteins in the GBM and mesangium causes 

MICROANGIOPATHY diabetes

228

Glycation of proteins OR polyol pathway prodcuts such as Sorbitol leads to;

 

HYALINIZATION of tubules

229

Degree of protein glycation measured by:

HbA1c

230

Hyaline changes are (macro/microangiopathic)

Atherosclerosis is (macro/micro)

Hyaline--> MICRO

Ather--> MACRO

231

Diabetic nephropathy:

Tubular lesion hallmark

Hyaline change

Epithelial cell loss (necrosis)

232

Develop nephrotic syndrome due to Diabetic nephropathy: what stage?

Stage 4: MACROalbuminuria