Renal Pathology Flashcards

1
Q

Infectious aetiology of nephritic types of glomerular disease?

A

Post streptococcal GN-MC

IgA nephropathy

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2
Q

Autoimmune aetiology of nephritic type of glomerular disease?

A

Good pastures syndrome, wegeners granulomatosis, microscopic polyarteritis-rapidly progressive crescentic GN

SLE- diffuse proliferative GN

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3
Q

Circulating immunocomplex deposition mechanism producing nephritic glomerular disease?

A

IgA nephropathy-mesangium
Post strep GN-sub epithelial
Diffuse proliferative-sub endothelial

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4
Q

Antibodies directed against GBM antigens mechanism in nephritic type of glomerular diseases?

A

Good pastures-rapidly progressive GN

Anti-BM ab against collagen in lungs and kidneys

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5
Q

Granular IF finding seen in which nephritic type of glomerular diseases?

A

IgA glomerulopathy-mesangium
Post strep-sub epithelial
Diffuse proliferative-sub endothelial
[wire looping of capillaries]

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6
Q

Specific test to confirm post streptococcal GN?

A

Anti-DNAse B titres -+ streptozyme test

ASO - degraded by oil in skin

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7
Q

Specific test to confirm diffuse proliferative GN?

A

Serum ANA test-rim pattern-confirms anti-dsDNA antibodies

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8
Q

Specific test to confirm good pastures-rapidly progressive GN?

A

HLA-DR2 +

Hemoptysis–>CRF

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9
Q

Nephritic type of glomerular diseases that progress to CRF?

A

All but post streptococcal GN which usually resolves in children

Highest incidence in rapidly progressive glomerulonephritis

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10
Q

Infectious aetiology of nephrotic syndrome type glomerular diseases?

A

Focal segmental glomerulosclerosis
Diffuse membranous glomerulopathy-HBV/syphilis/plasmodium malariae
Type 1MPGN- HCV/HBV

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11
Q

Malignancy aetiology of nephrotic type of glomerular diseases?

A

Focal segmental glomerulosclerosis- Hodgkin’s lymphoma

Diffuse membranous glomerulopathy-HL, carcinoma

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12
Q

T cell production of cytokines mechanism in nephrotic types of glomerular diseases?

A

Minimal change disease

Cytokines-loss of negative charge on GBM

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13
Q

Immune complex deposition mechanism in nephrotic type of glomerular diseases?

A

Diffuse membranous glomerulopathy-sub epithelial
Type 1 MPGN-sub endothelial
Type 2 MPGN-intra membranous

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14
Q

Autoimmune aetiology of nephrotic type of glomerular diseases?

A

Diffuse membranous glomerulopathy

Type 2 MPGN- C3 nephritic factor autoantibodies bind to C3 convertase-constant stimulation-deplete levels

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15
Q

Tram tracks on EM in nephrotic type of glomerular diseases?

A

Type 1 MPGN and type 2 MPGN caused by splitting of GBM by in growth of mesangium

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16
Q

Specific test for minimal change disease?

A

Positive fat stains in glomerulus and tubules

Fusion of podocytes in EM

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17
Q

Specific clinical features seen in minimal change disease but not other types of nephrotic type of glomerular disease?

A
Selective proteinuria (only albumin not globulin) 
Normotensive
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18
Q

Drugs that cause diffuse membranous glomerulopathy?

A

Captopril, gold therapy

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19
Q

Specific test for diffuse membranous glomerulopathy?

A

Silver stain-spike and some pattern

Diffuse thickening of membranes

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20
Q

Which is the only type of nephrotic type of glomerular disease that does not progress to CRF?

A

Minimal change disease

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21
Q

Nephritic type of glomerular diseases?

A

Based on site of IC deposition:

  1. Sub endothelial- diffuse proliferative GN
  2. Basement membrane- rapidly progressive cresentric GN
  3. Sub epithelial- Post strep GN
  4. Mesangium- IgA glomerulopathy
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22
Q

Hereditary glomerular diseases?

A

Alport syndrome and thin basement membrane disease

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23
Q

Type of inheritance in hereditary glomerular diseases?

A

Alport syndrome- X linked recessive and autosomal dominant/recessive
Thin basement membrane disease-AD

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24
Q

Clinical features in alport syndrome vs. thin basement membrane disease?

A

Sensorineural hearing loss and ocular findings in alport syndrome; hematuria and mild proteinuria in both

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25
Q

Diagnosis of alport syndrome vs. thin basement membrane disease?

A

Alport syndrome-EM/monoclonal ab to detect GBM defects

Thin basement membrane disease-extremely thin BM

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26
Q

Gross and microscopic findings in chronic glomerulonephritis?

A

Shrunken kidneys

Glomerular sclerosis and tubular atrophy

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27
Q

Most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis followed by diffuse membranous glomerulopathy

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28
Q

Cause of acute renal failure following haemorrhage?

A

Hypovolemia-> pre renal azotemia-> most common cause of acute tubular necrosis

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29
Q

Drug most commonly responsible for acute tubular necrosis?

A

Gentamicin; amino glycosides

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30
Q

In which subtype of acute tubular necrosis can acute renal failure be reversed?

A

Nephrotoxic- tubular basement membrane not disrupted- tubular cell regeneration possible

Ischemic-bm disrupted

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31
Q

Lab findings in acute tubular necrosis?

A

Oliguria (~400ml/day)
Pigmented renal tubular casts
Hyperkalemia, increased anion gap metabolic acidosis
Hypokalemia (diuresis phase) and infection

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32
Q

Reason for administration of dopamine low dose in ATN?

A

Increases renal blood flow

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33
Q

Distinguishing conditions of oliguria with good tubular function?

A

Pre renal azotemia and acute glomerulonephritis

Urine sedimentation- RBC casts and hematuria in acute glomerulonephritis

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34
Q

Distinguish between conditions producing oliguria with bad tubular function?

A

Post renal azotemia and acute tubular necrosis

Urine sedimentation:
Acute tubular necrosis-pigmented tubular casts

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35
Q

Conditions with good tubular function and oliguria?

A

Prerenal azotemia

Acute glomerulonephritis

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36
Q

Conditions with bad tubular function and oliguria?

A

Post renal azotemia and acute tubular necrosis

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37
Q

Common causes of tubulointerstial nephritis?

A

Acute pyelonephritis
Lead poisoning
Urate nephropathy
Multiple myeloma

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38
Q

Aetiology of acute pyelonephritis?

A

E.coli most common cause

Enterococcus 2ndMC

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39
Q

Mechanism of TIN in cancer patients receiving aggressive therapy?

A

Urate nephropathy with deposition of urate crystals in tubules and interstitium

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40
Q

Mechanism of TIN in persons with chronic pain?

A

Aspirin- decreases renal blood flow by blocking prostaglandin release

Acetaminophen-free radical damage

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41
Q

Mechanism of TIN with patients on rifampin/penicillin?

A

Drug induced nephropathy-type 1 and 4 hypersensitivity reaction

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42
Q

Mechanism of TIN in young girls?

A

Acute/chronic pyelonephritis-short urethra

Vesicoureteral reflux with ascending infection

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43
Q

Mechanism of TIN in elderly

Male?

A

BPH- lower urinary tract obstruction-chronic pyelonephritis

44
Q

Mechanism of TIN in chronic lead poisoning?

A

Decreases renal excretion of uric acid-urate nephropathy

Direct toxicity

45
Q

Mechanism of TIN in multiple myeloma patients?

A

Bence Jones proteinuria-foreign body giant cell reaction in tubular lumen in PT

Nephrocalcinosis- calcification of collecting duct 2 to hypercalcemia due to lytic lesions

Primary amyloidosis-light chains to amyloid

46
Q

Clinical findings in acute pyelonephritis vs. chronic pyelonephritis?

A

Acute: Spiking fever, flank pain
Increased frequency of urination
Painful urination

Chronic: history
Reflux nephropathy->HTN in children
CRF

47
Q

Gross and microscopy findings in acute pyelonephritis vs. chronic?

A

Acute- abscess in cortex and medulla; micro abscess in tubules

Chronic-reflux: U shaped scars overlying blunt calyx
Obstructive: dilation of calyx with diffuse thinning of cortical tissue
Thyroidisation (eosinophilic material) of tubules with atrophy

48
Q

Specific diagnosis of acute vs chronic pyelonephritis?

A

Acute- WBC casts, pyuria/bacteruria and hematuria

Chronic-IV pyelogram-U shaped scars overlying blunt calyx

49
Q

Causes of renal papillary necrosis?

A

APN, analgesic nephropathy, DM and sickle cell disease/trait

50
Q

Lab diagnosis of renal papillary necrosis?

A

Sloughing of renal papillae- hematuria, proteinuria, flank pain

IVP- ring defect

51
Q

Most common cause of chronic renal failure?

A

DM

51
Q

Mechanism for normocytic anaemia in chronic renal failure?

A

Decreased erythropoietin

51
Q

Mechanism of osteomalacia vs. osteoporosis in chronic renal failure?

A

Osteomalacia- loss of mineralised bone due to hypovitaminosis D-hypocalcemia

Osteoporosis-metabolic acidosis-excess H+ buffered by bone

52
Q

Mechanism of cystic lesions in jaw/ osteitis fibrosa cystica in chronic renal failure?

A

Hypovitaminosis D->hypocalcemia->+ PTH-> secondary hyperparathyroidism->increases bone resorption

53
Q

Mechanism of HTN and CCF in chronic renal failure?

A

Salt retention and volume overload

54
Q

Mechanism of hyperkalemia and hyponatremia in chronic renal failure?

A

Volume overload- dilution hyponatremia/Na loss

Hyperkalemia- very low GFR and metabolic acidosis shifts K+ from ICF to ECF

55
Q

Mechanism of hypocalcemia in chronic renal failure?

A

Hypovitaminosis D-decreased synthesis of 1-alpha hydroxylase in PT

Hyperphosphatemia- drives Ca into bones and soft tissues [metastatic calcification]

56
Q

Mechanism of free water clearance =0 in chronic renal failure?

A

Tubular dysfunction- loss of concentration and dilution

57
Q

Specific test to diagnose chronic renal failure?

A

Increased serum cystatin C(>1.3mg/flow)

Only filtered not secreted; cysteine protease inhibitor produced by all nucleated cells

58
Q

Mechanism of prolonged bleeding time in chronic renal failure?

A

Platelet aggregation defect [qualitative]

59
Q

Pathogenesis of benign nephrosclerosis vs. malignant HTN?

A

Benign nephrosclerosis-hyaline arteriolosclerosis in arterioles of renal cortex

Malignant HTN-vascular damage to arterioles and small arteries->hyperplastic arteriolosclerosis and fibrinoid necrosis

60
Q

Risk factors for malignant HTN?

A

BNS
Haemolytic uremic syndrome
Thrombotic thrombocytopenic purpura
Systemic sclerosis

61
Q

Features of hypertensive encephalopathy in malignant HTN?

A

Cerebral edema
Papilledema
Retinopathy-exudates, flame hemorrhages
Potential for intracerebral bleed

62
Q

Morphology of kidney in benign nephrosclerosis?

A

Small kidney; granular cortical surface

63
Q

Aetiology of renal infarction?

A

Embolisation from L. Heart
Atheroembolic disease
Vasculitis; polyarteritis nodosa

64
Q

Diagnosis of anuria in a pregnant woman followed by ARF?

A

DIC limited to renal cortex 2 to abruptio placentae, preeclampsia–> bilateral pale renal infarcts

65
Q

Aetiology of hydronephrosis in children vs. adults?

A

Children-congenital bladder neck obstruction/urethral valve defect

Adult-renal stones, BPH

66
Q

Dilated ureter and renal pelvis; compression atrophy of renal medulla and cortex with post renal azotemia. Diagnosis?

A

Hydronephrosis

67
Q

Most common metabolic abnormality producing stones?

A

Hypercalciuria w/o hypercalcemia- increased GI absorption of Ca

68
Q

Factors that promote formation of calcium renal stones?

A

Hypercalciuria; decreased urine volume
Reduced urine citrate-citrate chelates ca; Urinary pH alteration-alkaline pH favours ca and Po4 stones;

Dairy products-rich in oxalate/phosphate; primary HPTH

69
Q

Most common type of stone in adults and its aetiology?

A

Calcium oxalate stone–>pure vegan diet, vitamin C deficiency and Crohn’s disease

70
Q

Most common type of renal stones in children?

A

Calcium phosphate stones–> dairy products and distal renal tubular acidosis

71
Q

Uncommon types of renal stones?

A

Uric acid and cystine

72
Q

Stones associated with proteus infection? [urine is alkaline and smells of ammonium]

A

Magnesium ammonium phosphate stone

73
Q

Rationale behind treatment of calcium stones with hydrocholothiazide and cellulose phosphate?

A

Hydrochlorothiazide- causes hypercalcemia; decreases urine ca

Cellulose phosphate binds to ca in intestine

74
Q

Rationale behind treatment of Uric acid stones with alkaline pH and allopurinol?

A

Allopurinol-decreases synthesis of Uric acid

Alkaline pH-makes Uric acid soluble in urine

75
Q

Rationale behind using antibiotic and surgical removal in struvite stones?

A

Antibiotic-eliminates urease producer

Surgical removal-size of struvite stone

76
Q

Colicky pain radiating to ipsilateral groin and gross hematuria. Diagnosis?

A

Renal stones

77
Q

Best test to diagnose renal stones?

A

SpiralCT scan (unenhanced)

78
Q

Bilateral renal cell carcinoma, hemangioblastoma of cerebellum and retina. Diagnosis with inheritance pattern?

A

Von hippel-Lindau disease. Autosomal dominant associated with chromosome 3

79
Q

Gross and microscopy of most common type of renal cell carcinoma?

A

Gross: yellow tumour on upper pole >3cm
Microscopy: clear cells with lipid and glycogen

80
Q

Triad of renal cell carcinoma?

A

Hematuria-abdominal mass-flank pain

81
Q

Mechanism of left sided and variocele and extension to heart in renal cell carcinoma?

A

Predisposition to invasion of renal vein; renal vein-IVC-heart

Renal vein blocked-drainage of spermatic vein blocked-variocele

82
Q

Mechanism of secondary polycythemia and hypercalcemia in RCC?

A

Ectopic production of hormones:
EPO- 2 polycythemia Vera
PTH related protein-hypercalcemia

83
Q

Most common site of metastasis of RCC?

A

Lung- cannon ball appearance on radiograph

84
Q

Most common cause of renal pelvis cancer and RCC?

A

Smoking

85
Q

Renal stones and chronic infection predispose to what type of cancer?

A

SCC of renal pelvis

86
Q

Most common primary renal tumour in children? [2-5 years]

A

Wilms tumour

87
Q

Syndromes associated with Wilms tumour?

A

WAGR

Beckwith-wiesemann syndrome

88
Q

Clinical features of WAGR syndrome?

A

Wilms tumour-aniridia-genitourinary-retardation (mental)

89
Q

Clinical features of beckwith-wiedemann syndrome?

A

Wilms tumour, macroglossia, enlarged body organs (liver adrenal pancreas) and hemihypertrophy of extremities

90
Q

Child with unilateral flank mass and HTN. Diagnosis?

A

Wilms tumour; HTN due to renin secretion

91
Q

Bilateral renal cell carcinoma, hemangioblastoma of cerebellum and retina. Diagnosis with inheritance pattern?

A

Von hippel-Lindau disease. Autosomal dominant associated with chromosome 3

92
Q

Gross and microscopy of most common type of renal cell carcinoma?

A

Gross: yellow tumour on upper pole >3cm
Microscopy: clear cells with lipid and glycogen

93
Q

Triad of renal cell carcinoma?

A

Hematuria-abdominal mass-flank pain

94
Q

Mechanism of left sided and variocele and extension to heart in renal cell carcinoma?

A

Predisposition to invasion of renal vein; renal vein-IVC-heart

Renal vein blocked-drainage of spermatic vein blocked-variocele

95
Q

Mechanism of secondary polycythemia and hypercalcemia in RCC?

A

Ectopic production of hormones:
EPO- 2 polycythemia Vera
PTH related protein-hypercalcemia

96
Q

Most common site of metastasis of RCC?

A

Lung- cannon ball appearance on radiograph

97
Q

Most common cause of renal pelvis cancer and RCC?

A

Smoking

98
Q

Renal stones and chronic infection predispose to what type of cancer?

A

SCC of renal pelvis

99
Q

Most common primary renal tumour in children? [2-5 years]

A

Wilms tumour

100
Q

Syndromes associated with Wilms tumour?

A

WAGR

Beckwith-wiesemann syndrome

101
Q

Clinical features of WAGR syndrome?

A

Wilms tumour-aniridia-genitourinary-retardation (mental)

102
Q

Clinical features of beckwith-wiedemann syndrome?

A

Wilms tumour, macroglossia, enlarged body organs (liver adrenal pancreas) and hemihypertrophy of extremities

103
Q

Child with unilateral flank mass and HTN. Diagnosis?

A

Wilms tumour; HTN due to renin secretion