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RENAL Pathology > HISTOPATH > Flashcards

HISTOPATH Flashcards

1
Q

softer and paler due to DYSTROPHIC CALCIFICATION

A

Calcium Phosphate Stones

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2
Q

Gross:

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

A

Acute pyelonephritis

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3
Q

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

A

Far-advanced cases of obstruction; irreversible

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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

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5
Q

Macrophage accumulation in cortex

A

Xanthogranulomatous Pyelonephritis:

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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

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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

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8
Q

Risk of SPONTANEOUS HEMORRHAGE

A

Angiomyolipoma

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9
Q

Grossly: yellow tumor w/ gelatinous center.

A

Renal Cell Carcinoma (RCC)

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10
Q

Outlines of tubules WITHOUT nuclei

A

Necrosis

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11
Q

Histology: clear cytoplasm in cells, arranged in nests.

A

Clear Cell Carcinoma:

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12
Q

Histology:

Atypical pleomorphic cells that surround a fibrovascular core

A

Papillary Carcinomas In-Situ:

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13
Q

A Cauliflower-like lesion on a freely movable stalk

A

Papillar transitional carcinoma; not invasive

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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;

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15
Q

Polysaccharide capsule => 70 serotypes
•
Interferes with COMPLEMENT ACTIVATION

A

Klebsiella

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16
Q

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

A

mesangium and capillary loops

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17
Q

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

A

VHL

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18
Q

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

A

lysine, ornithine, and arginine

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19
Q

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

A

Schiller Duval Bodies; seen in yolk sac tumor

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20
Q

Dominant-negative inactivating mutation of WT1 gene

A

Denys-Drash Syndrome:

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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)

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22
Q

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

A

diabetics; coagulative;

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23
Q

Polyomavirus

H&E–>1)
EM–>2) .

A

nuclear enlargement and intranuclear inclusions;

2) cystalline-like lattices on EM

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24
Q

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

A

Hypercalcemia (and thus METASTATIC) leading to nephrocalcinosis

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25
Q

Macrophage accumulation surrounding struvite stones

A

Xanthogranulomatous Pyelonephritis

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26
Q

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

A

Wilms Tumor

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27
Q

Pyonephrosis vs. Perinephric abscess

A

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

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28
Q

TUBULAR effects first in hydronephrosis–> result 1)

A

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

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29
Q

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

A

decreases

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30
Q

Post-obstructive diuresis–> sodium content?

A

Unilateral Obstruction–>HIGH NaCl in urine;

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31
Q

Histology: papillae lined by epithelial cells.

A

Papillary Renal Cell Carcinoma

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32
Q

“nodular accumulation of eosinophilic material within glomeruli

A

KW bodies seen in Diabetic nephropathy

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33
Q

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

A

Prostate Adenocarinoma

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34
Q

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

A

Uric acid stone; uric acid increased in URINE;

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35
Q

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

A

Wilms Tumor

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36
Q

Neutrophilic microabcesses in renal interstitium

A

acute pyelonephritis

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37
Q

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

A

N-terminal amino acid

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38
Q

Beckwith-Wiedmann Syndrome:

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

A

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

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39
Q

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

A

1) acute pyelonephritis
2) encapsulated
3) perinephric fat

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40
Q

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;

A

Hyalinosis seen in FSGS

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41
Q

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

Widespread in moist environments

A

Pseudomonas Aeruginosa

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42
Q

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

(b) Familial form: Trisomy 7.
•
Both forms associated w/ activating mutations in MET.

A

Papillary Renal Cell Carcinoma (15% of RCC)

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43
Q

Gynecomastia and hyperthyroidism.
•
Hemoptysis

A

Choriocarcinoma

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44
Q

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

A

Granuloma

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45
Q

Bladder cancer:

  • Chromosome 9 deletions –> lose p16 (INK4a) or p15.
  • P53 mutations;

what is p16? p15?

A

p16–>encodes inhibitor of a cyclin-dependent kinase

they are both tumor suppressor genes

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46
Q

Chonic pyelo histopath:

1) infiltration of interstitium;

Thyroidization which are 2) within 3);

4)

A

Lymphocyte;

2) eosinophilic hyaline casts
3) tubules
4) Fibrosis

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47
Q

Gleason Grading system used for 1_

A

Prostate cancer

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48
Q

Fibrosis surrounding dilated tubules with hyaline casts

A

Chronic pyelonephritis

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49
Q

Hylaine arteriolosclerosis seen in: 1)

KW bodies seen in:2)

A

1) afferent and efferent arterioles
2) glomeruli causing glomerusclerosis

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50
Q

Precursor lesion–>PIN

A

Prostatic Intraepithelial Neoplasia for prostate cancer

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51
Q

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

A

GI diseases or in vegan diets.

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52
Q

hallmark of prostate CANCER histo

A

Prominent nucleoli;

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53
Q

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

A

Tubular and interstitial 3) YELLOW 4) PAPILLAE

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54
Q

Gross: Stones are smooth, hard, yellow and

A

Uric acid stone

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55
Q

Prostate adenocarcinoma

Susceptible locus: 1)

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

Men with BRCA2 gene mutation–> higher risk

A

1) chromosomes 1 and 10 (tumor suppressor gene)
2) Hypermethylation of Glutathione S-transferase p1 (GSPT1)

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56
Q

Sheets/nests of separated by fibrous bands infiltrated by lymphocytes

Clear cytoplasm that contains glycogen.

Can often be stained immunologically by c-kit

A

Seminoma

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57
Q

Reinke crystals–. rod like cytoplasmic inclusions

A

Leydig Cell Tumor

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58
Q

Granulomatous Prostatitis–> Rxn following 1)

A

Transurethral resection (TUR) of prostate for nodular hyperplasia

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59
Q

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

A

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

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60
Q

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

A

Wager Syndrome:

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61
Q

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

A

Dent’s Syndrome; chloride channels

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62
Q

Grossly
•
Abnormal bumpy kidney shape; Scarring at upper and lower poles
•
Fibrosis and loss of cortex

A

Chronic Pyelonephritis:

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63
Q

BPH vs. Prostate cancer histo

A

BPH has nodules; prostate cancer NO nodules;

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64
Q

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).

A

urate crystals;

2) inflammatory cells (macrophages)
3) giant cells
4) fibrosis

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65
Q

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

A

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

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66
Q

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:

A

Glycated proteins

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67
Q

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

Both complication of ?;

A

diabetic nephropthy

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68
Q

Angiomyolipoma

Due to loss of:

A

suppressor function of TSC1 or TSC2 genes

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69
Q

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

A

Urothelial Carcinoma: Renal Pelvis

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70
Q

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

A

Nephrocalcinosis; MITOCHONDRIA

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71
Q

Cystoscope: cauliflower-like lesions.

Develops as low grade papillary tumor

A

Papillary Carcinomas In-Situ:

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72
Q

Hallmark: halos around the nuclei

A

Chromophobe RCC; remember it is malignant as oppsed to oncocytoma

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73
Q

Hydronephrosis Pathophysiology

A

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

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74
Q

Bladder cancer gross:

A

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

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75
Q

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

A

Hydronephrosis Pathophysiology

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76
Q

Calcification of the interstitium

A

metastatic nephrocalcinosis

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77
Q

Clinical Sign of Invasive Bladder Cancer

1)

Frequency, urgency, and dysuria

A

PAINLESS hematuria—unless there is obstruction

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78
Q

Wedge-shaped scars mixed w/ relatively normal renal tissue

A

Nephrocalcinosis

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79
Q

Papillary Renal Cell Carcinoma

a) Sporadic form: 1)
(b) Familial form: 2)

Both forms associated w/ 3) in MET.

A

Trisomy 7&17; loss of Y in males;

2) Trisomy 7
3) activating mutations

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80
Q

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

A

Renal Oncoytoma

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81
Q
  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
A

FSGS

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82
Q

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

Sporadic: Overwork/Stress such as obesity or sickle cell

A

Focal Segmental Glomerulosclerosis

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83
Q

Tubules have eosinophilic hyaline casts called thyroidization.

A

Chronic Pyelonephritis:

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84
Q

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

A

Angiomyolipoma

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85
Q

unilateral agenesis of kidney can lead to

A

FSGS

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86
Q
  • Chromosome 9 deletions –> lose tumor suppressor gene p16 (INK4a) or tumor suppressor gene p15.
  • P53 mutations; normal function is to prevent apoptosis
A

•Genetic changes (mutations) in bladder cancer:

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87
Q

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

A

somatic mutation or hypermethylation;

regarding Renal Cell carcinoma

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88
Q

Large gram (-) bacilli

Produce BRICK RED COLONIES

A

Serratia

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89
Q

Seminoma

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

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

A

1) lymphocytes; 2) Clear;
3) c-kit

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90
Q

Lancefield Group D strep, but more ovate than other streptococci

A

Enterococcus

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91
Q

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

A

Focal Segmental Glomerulosclerosis

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92
Q

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

A

1) VHL gene
2) chromosome 3

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93
Q

Histology:
•
Sheets of undifferentiated cells; necrosis and hemorrhage

A

Embryonal Carcinoma

94
Q

Hemorrhagic mass w/ necrosis (testicular tumors)

A

Choriocarcinoma; Embryonal Carcinoma

95
Q

Immunoglobulin A deposition in mesangial cells

A

IgA nephropathy

96
Q

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

A

Stage 1: Diminished Renal Reserve

97
Q

GFR is 50-80% ↓;

Azotemia, anemia (↓EPO), and HTN.

Present initially w/ polyuria and nocturia

A

Stage 2: Renal Insufficiency

98
Q

Stage 3: Chronic Renal Failure
•
GFR 1) of normal.
•
Edema, 2), and 3)

A

1) <20% 2)metabolic acidosis
3) hyperkalemia.

99
Q

GFR <5% of normal;

Uremia:

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

A

Stage 4: End Stage Renal Disease

100
Q

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

A

anemia; Chronic Renal Disease

101
Q

Associated w/ berry aneurysms

A

Autosomal DominantPKD

102
Q

Mutations: (two loci; loss of function)

PC1 (membrane receptor)

PC2 (Ca2+ channel activity

A

ADPKD1 and 2 gene

103
Q

present in infants as worsening renal failure and HTN

A

Autosomal Recessive PKD

104
Q

Mutation in PKHD1 gene –> fibrocystin (membrane receptor

A

AR PKD

105
Q

Associated/ congenital hepatic fibrosis and hepatic cysts

A

AR PKD

106
Q

renal stone formation (nephrolithiasis

A

Medullary Sponge Kidney

107
Q

Fetal appearance –> immature glomeruli and tubules

A

Multicystic Renal Dysplasia

108
Q

Lung hypoplasia

Flat face w/ low set ears

defects in the extremities

A

Potter Sequence

Bilateral Renal Agenesis

109
Q

compensatory hypertrophy of the existing kidney.

A

Unilateral Agenesis

110
Q

aspirin and phenacetin causes:

A

Papillary Necrosis

111
Q

↑risk of transitional papillary carcinoma of the renal pelvis

A

Analgesic nephropathy

112
Q

Inherited Renal Cyst diseases that lead to chronic renal failure

A

Medullary Cystic Disease

Polycystic Kidney Disease (PKD)

113
Q

NON-inherited Cystic Disease

A

Multicystic Renal Dysplasia

Medullary Sponge Kidney

114
Q

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

A

Renal Tubular Acidosis

115
Q

Pts have HIGH urine pH;

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

A

Type 1: Distal Tubule

116
Q

amphotericin B toxicity.

A

Type 1: Distal Tubule

117
Q

Sjogren’s,
•
analgesic nephropathy

A

Type 1: Distal Tubule

118
Q

↑risk of calcium phosphate stones (

A

Type 1: Distal Tubule

119
Q

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

A

Type 2: Proximal Tubule

120
Q

Causes:

Fanconi’s Syndrome and CA inhibitors

A

Type 2: Proximal Tubule

121
Q

LOW urine pH;

HYPOkalemia;

A

Type 2: Proximal Tubule

122
Q

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

A

Amyloid Nephropathy

123
Q

LM Stain w/ congo red

A

Amyloid Nephropathy

124
Q

Amyloid Nephropathy

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

A

1) mesangium
2) renal tubules

125
Q

Angulated and tubular casts surrounded by macrophages, including multinucleate cells

A

light chain cast nephropathy

126
Q

Rheumatoid arthritis
•
Chronic TB

A

serum Amyloid A protein; inflammatory

127
Q

Clear cytoplasm that contains glycogen.

A

Seminoma

128
Q

Germ Cell Tumors Seen in older men

A

Spermacytic Seminomas:

129
Q

precocious puberty

A

Leydig Cell Tumor

130
Q

sex cord-stromal tissues of the testicle

A

Leydig Cell Tumor

Sertoli Cell Tumors

131
Q

Choriocarcinoma vs. Leydig cell tumor s/s

A

Choriocarcinoma–> gynecomastia and hemoptysis

Leydig cell–> Gynecomastia and precocious puberty

132
Q

capillary surrounded by an epithelial layer

A

Schiller duval bodies; yolk sac tumor

133
Q

elevated AFP

A

Yolk sac tumor

134
Q

Elevated bHCG

A

Choriocarcinoma

135
Q

stained immunologically by c-kit

A

Seminoma

136
Q

Drug Hypersensitivity (type I HYPERSENSITIVTY

A

Acute Tubulointerstitial Nephritis

137
Q

EOSINOPHILS IN URINE!!

A

Acute Tubulointerstitial Nephritis

138
Q

↑IgE levels and basophils;

EOSINOPHILS IN URINE!!

A

Acute Tubulointerstitial Nephritis

139
Q

Fatty change initially, followed by necrosis

A

Carbon Tetrachloride Poisoning

140
Q

Ballooning and hydropic or vacuolar degeneration of PCT

A

Ethylene glycol:

141
Q

↑urine volumes but ↓GFR; usually benign

A

Nonoligouric AKI: 50% of AKI pts

142
Q

SLIGHT OLIGURIA w/ a ↑in BUN

A

Initiation PhaseAKI (FIRST 36 HRS)

143
Q

OLIGURIA;

HYPERkalemia;

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

A

Maintenance Phase AKI

144
Q

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

A

Tamm-Horsfall protein; SEEN IN AKI

145
Q

Interstitial edema, leukocytes within dilated vasa recta, epithelial regeneration

A

AKI

146
Q

granular casts in the distal tubules and collecting ducts

A

AKI

147
Q

acute pancreatitis, septic shock

A

Ischemia Acute Tubular Necrosis

148
Q

Aminoglycosides, radioCONTRAST dyes

A

NEPHROTOXIC Renal tubular acidosis

149
Q

Urate (tumor lysis syndrome),

A

Acute Tubular Necrosis;

Uric acid stones

150
Q

Ethylene glycol

A

nephrotoxic acute tubular necrosis

151
Q

Grossly:
•
Pale cortex and hyperemic medullary regions

A

Acute Tubular Necrosis

152
Q

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

A

Light-Chain amyloid Deposition Disease

153
Q

damages cell cytoskeleton

A

Proteases such as calpain

154
Q

damges cell membrane

A

phospholipase c

155
Q

cysts in the medullary collecting ducts; affects tubules

A

Medullary Cystic Disease

156
Q

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

A

Medullary Cystic Disease

157
Q

POLYURIA

HYPOkalemia

A

Recovery Phase AKI

158
Q

Acute Tubulointerstitial Nephritis types of Hypersensitivity

A

TYPE I

159
Q

Unilateral defect in children;

Generally have

A

Renal Hypoplasia

160
Q

Myoglobinuria from crush injury to muscle

A

Direct toxic tubular injury; AKI

161
Q

Hb or Myoglobin casts in TUBULES

A

crush injury causing AKI

162
Q

Defect in metanephric differentiation;

persistence of cartilage, undifferentiated mesenchyme, and immature ductules

A

Multicystic Renal Dysplasia

163
Q

obstruction etiology such as ureteropelvic or ureteral atresia

A

Multicystic renal dysplasia

164
Q

gentamicin

A

nephrotoxic aki

165
Q

aki findings:

1) ___ casts in distal tubules and coll. ducts
2) ___ protein;
3) Interstitial edema

___ within dilated vasa recta

A

Hyaline pigmented GRANULAR;

tamm horsfall protein;

Leukocytes

166
Q

leukocytes within dilated vasa recta

A

AKI

167
Q

Hypotension and shock

A

Pre-renal azotemia

168
Q

nuclear shrinkage (EM changes in necrosis)

A

pyknosis

169
Q

karyolysis

A

nuclear degradation (EM changes in necrosis

170
Q

DNA ladder

A

Apoptotis

171
Q

caspase-3 and caspase-6

A

executioner proteases

172
Q

necrotic cell death usually forms a (1)

A

SMEAR

173
Q

karyolysis: nuclear degradation

A

necrosis; NOT apoptosis

174
Q

FLIP 2

A

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

175
Q

caspace 8

A

Extrinsic pathway–> initiator

176
Q

caspace 9

A

Intrinsic pathway–> initiator

177
Q

BAX and BAK activated by BID and BAD

A

Pro-apoptotic

178
Q

BCL-2

A

ANTI-apoptotic

179
Q

INC. cyt C release

A

INC BAX and BAK (pro-apop)

DEC. BCL-2 (anti-apop)

180
Q

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

A

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

181
Q

APAF-1

A

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

182
Q

FAS-L binds to

A

CD95 (fas-R); extrinsic pathway

183
Q

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

A
184
Q

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

A

Hypertensive Urgency

185
Q

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

A

Hypertensive Emergency

186
Q

hyaline arteriolosclerosis of afferent and efferent in 1)

only AFFERENT 2)

A

1) diabetic nephropahty
2) essential HTN

187
Q

individual cells apoptose

A

Intrinsic Pathway

188
Q

groups apoptose

A

Extrinsic Pathway

189
Q

very high BP causes hemolysis of RBCs seen on slides:

A

schistocytes

190
Q

chromatin condensation; nuclear shrinkage (pyknosis)

A

apoptosis

191
Q

caspace 3 activity or endonuclease

A

detect apoptosis

192
Q

release of PDGF (malignant hypertension)

A

myointimal proliferation–> ↑ hypertension–> Fibrinoid necrosis

193
Q

structure maintained but NO nuclei

A

coagulative necrosis

194
Q

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

A

1)prostaglandins

195
Q

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

A

APOPTOSIS

196
Q

pinkish fibrin like material in BV wall;

A

fibrinoid necrosis

197
Q

myelin figure are phospholipid masses

A

necrosis!

198
Q

caspaces cleave after ?

A

aspartic acid in aa chain

199
Q

detect necrosis by?

A

cell proteins and membranes that leak into tissues

200
Q

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

A

1) vWF
2) PDGF

201
Q

“string of beads” pattern

A

Fibromuscular dysplasia:

202
Q

Fibromuscular dysplasia

A

Renal Vascular HTN

203
Q

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

A

1) Takayasus and Giant cell

204
Q

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

A

Fibromuscular dysplasia

205
Q

STAGE 2 Renovascular HTN

A

Stenotic kidney–> dec renin;

Normal–> dec renin;

206
Q

abdominal aortic aneurysms

A

Renal Vascular HTN

207
Q

cholesterol clefts

A

embolus e.g. abdominal aortic aneurysm

208
Q

Tubules show marked ischemic atrophy w/o extensive interstitial fibrosis

A

•
Fibromuscular dysplasia

209
Q

95% from atherosclerosis

A

renovascular stenosis

210
Q

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

A

Stage 1 renovascular HTN

211
Q

C/I for Renovascular stenosis

A

ACE inhibitors; captopril, etc

212
Q

ACE made in

A

pulmonary and renal ENDOTHELIAL CELLs

213
Q

HTN leads to renal hypoperfusion of BOTH KIDNEYS

A

STAGE 3 Renovascular HTN

214
Q

AREAS of clear space where lipid is washed out;

A

cholesterol clefts–> embolus in renovascular HTN

215
Q

Affects arterioles and arteries

A

Diabetic Macroangiopathy

216
Q

Diabetic Mircoangiopathy

A

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

217
Q

NONENZYMATIC glycosylation of proteins of the vascular BM

A

hyaline arteriololosclerosis

218
Q

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

A

1) AGE 2) RAGE

219
Q

increases RAGE thus INC. immune response to hyperglycemia;

A

oxygen free radicals

220
Q

NOT measured by urine dipstick

A

microalbuminuria

221
Q

HYALINE change and EPITHELIAL CELL LOSS; leads to ___ necrosis

A

Tubular lesion in diabetic microangiopathy; PAPILLARY NECROSIS

222
Q

glomerulosclerosis and increased mesangial matrix from hyperglycemia causes:

A

DECRESED GFR

223
Q

Glomerular changes in microangiopathy diabetes:

Hyperglycemia 1) in the glomeruli and activates2)

A

↑TGF-beta;

2) protein kinase C

224
Q

Microangiopathic Diabetes vs. Macro

A

Capillaries, tubules, and glomeruli are micro;

renal arteries and arterioles are MACRO

225
Q

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

A

Polyol pathway

226
Q

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

A

Polyol pathway

227
Q

Extracellular matrix proteins in the GBM and mesangium causes

A

MICROANGIOPATHY diabetes

228
Q

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

A

HYALINIZATION of tubules

229
Q

Degree of protein glycation measured by:

A

HbA1c

230
Q

Hyaline changes are (macro/microangiopathic)

Atherosclerosis is (macro/micro)

A

Hyaline–> MICRO

Ather–> MACRO

231
Q

Diabetic nephropathy:

Tubular lesion hallmark

A

Hyaline change

Epithelial cell loss (necrosis)

232
Q

Develop nephrotic syndrome due to Diabetic nephropathy: what stage?

A

Stage 4: MACROalbuminuria

RENAL Pathology (21 decks)

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