HISTOPATH Flashcards
1
Q
softer and paler due to DYSTROPHIC CALCIFICATION
A
Calcium Phosphate Stones
2
Q
Gross:
Pus and little microabscesses in the kidney; hyperemia and yellowish discoloration
A
Acute pyelonephritis
3
Q
Thin-walled cystic structure; 15-20 cm diameter. Loss of pyramids. Thin cortex.
A
Far-advanced cases of obstruction; irreversible
4
Q
VHL is a 1) and encodes protein for 2) complex which normally degrades and controls growth factors such as Hypoxia Inducing Factors (HIF-1)
A
1) tumor suppressor gene
2) ubiquitin ligase
5
Q
Macrophage accumulation in cortex
A
Xanthogranulomatous Pyelonephritis:
6
Q
Histology:
•
placenta-like;
malignant 1) (well-demarcated cell borders,are not multinucleated and have smaller nuclei) and malignant 2) (mutlinucleated large cells)
A
1) cytotrophoblasts;
2) synctiotrophoblasts;
Choriocarcinoma
7
Q
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
A
1) Perinephric abscess
2) pyonephrosis
3) papillary necrosis
8
Q
Risk of SPONTANEOUS HEMORRHAGE
A
Angiomyolipoma
9
Q
Grossly: yellow tumor w/ gelatinous center.
A
Renal Cell Carcinoma (RCC)
10
Q
Outlines of tubules WITHOUT nuclei
A
Necrosis
11
Q
Histology: clear cytoplasm in cells, arranged in nests.
A
Clear Cell Carcinoma:
12
Q
Histology:
Atypical pleomorphic cells that surround a fibrovascular core
A
Papillary Carcinomas In-Situ:
13
Q
A Cauliflower-like lesion on a freely movable stalk
A
Papillar transitional carcinoma; not invasive
14
Q
Renal Oncoytoma–> Large eosinophilic cells;
Abundant 1) w/o 2)
(compare to Chromophobe RCC)
A
1) mitochondria
2) perinuclear clearing
Chromophobe has halo around nuclei;
15
Q
Polysaccharide capsule => 70 serotypes
•
Interferes with COMPLEMENT ACTIVATION
A
Klebsiella
16
Q
Sclerosis in FSGS: EC collagen deposition in the 1) and 2)
A
mesangium and capillary loops
17
Q
Mutation in 1) –>↑HIF-1 (transcription factor) which promotes cell growth (↑PDGF) and angiogenesis (↑VEGF).
A
VHL
18
Q
Cystinuria decreased reabsorption of cystine and other dibasic amino acids (?)
A
lysine, ornithine, and arginine
19
Q
Glomeruloid-like structures with BV in the center and epithelial cells around it.
A
Schiller Duval Bodies; seen in yolk sac tumor
20
Q
Dominant-negative inactivating mutation of WT1 gene
A
Denys-Drash Syndrome:
21
Q
Wilms tumor Histology:
•
Triphasic combination of 1) + 2) + 3).
A
1) dense blue cells (blastema);
2) stroma 3) epithelial cell types (abortive tubules or glomeruli)
22
Q
Papillary necrosis seen in 1) is which type of necrosis:
A
diabetics; coagulative;
23
Q
Polyomavirus
H&E–>1)
EM–>2) .
A
nuclear enlargement and intranuclear inclusions;
2) cystalline-like lattices on EM
24
Q
Milk-alkali syndrome–>those who take lots of antacids and drink milk
A
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
