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Gen Path Exam 2 > Sweep 1.4 > Flashcards

Sweep 1.4 Flashcards

1
Q

some lung tumors can produce

A

ADH, ACTH, PTH (looks like parathyroid tumor)

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2
Q

• Pneumoconioses- a group of lung disorders caused by ———————–

A

inhalation of dusts; size, shape and conc. of particles are important factors and particles induce scarring

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3
Q

Pneumoconiosis: Coal workers-

A

nodular/diffuse fibrosis with coal macules; progressive massive fibrosis

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4
Q

Pneumoconiosis: o Silicosis-

A

most prevalent occupational disease in world – due to inhalation of silicone.

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5
Q

• Interstitium- formed by

A

collagen and blood vessels between tubules and glomeruli

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6
Q

Azotemia- elevation of ————– due to decreased —————-

A

blood urea nitrogen and creatinine levels

filtration of blood through the glomeruli (decreased glomerular filtration rate)

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7
Q

• Uremia- association of ———– with clinical signs and symptoms, including ——————–

A

azotemia

gastroenteritis, peripheral neuropathy, pericarditis, dermatitis, hyperkalemia and metabolic acidosis

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8
Q

o Acute nephritic syndrome: results from

A

glomerular injury and is characterized by acute onset of hematuria, mild to moderate proteinuria, azotemia and hypertension

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9
Q

o Nephrotic syndrome:

A

glomerular syndrome characterized by heavy proteinuria (>3.5g/day), hypoalbuminemia, severe edema, hyperlipidemia and lipiduria
o

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10
Q

Acute renal failure: sudden onset of

A

azotemia with oliguria/anuria

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11
Q

• Autosomal dominant (adult) polycystic kidney disease-

o Clinically-

A

1/500 people; characterized by multiple expanding cysts in both kidneys; gradual onset of renal failure in adult, hematuria, pain in flank around 4th decade, hypertension and UTIs; BIG KIDNEYS

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12
Q

• Autosomal dominant (adult) polycystic kidney disease- o Etiology-

A

defective gene is PKD1→ encodes polycystin-1

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13
Q

• Autosomal dominant (adult) polycystic kidney disease- o Extrarenal pathology-

A

1/3 of pts have cysts in liver, aneurysms may develop in circle of Willis

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14
Q

• Autosomal dominant (adult) polycystic kidney disease- o Histopathology-

A

cysts arise from all levels of nephron

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15
Q

• Autosomal recessive (childhood) polycystic kidney disease-

o Clinicaly-

A

rare; renal failure develops from infancy to several years of age; due to mutation in PKHD1 gene (defective protein)

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16
Q

• Autosomal recessive (childhood) polycystic kidney disease- o Extrarenal pathology-

A

liver cysts and progressive liver fibrosis

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17
Q

• Autosomal recessive (childhood) polycystic kidney disease- o Pathology-

A

numerous small uniform-size cysts from collecting tubules in cortex and medulla

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18
Q

o Mechanisms of glomerular injury-

A

immune complex deposits in glomerular basement membrane or mesangium, can be circulating immune complexes, or autoantibodies to glormerular components
o Path evaluation of kidney biopsies- PAS, trichrome and Jones stain
• Immunofluorescence- looking for immune deposits
• Electron microscopy- ID of immune complexes, cell and basement membrane morphological changes
o Nephrotic syndrome- heavy proteinuria, hypoalbuminemia, severe edema; caused by increase glomerular capillary permeability to plasma proteins

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19
Q

o Mechanisms of glomerular injury-

A

immune complex deposits in glomerular basement membrane or mesangium, can be circulating immune complexes, or autoantibodies to glormerular components

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20
Q

o Path evaluation of kidney biopsies-

A

PAS, trichrome and Jones stain

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21
Q

Path eval of kidney biopsies: • Immunofluorescence- looking for

A

immune deposits

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22
Q

Path eval of kidney biopsies• Electron microscopy-

A

ID of immune complexes, cell and basement membrane morphological changes

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23
Q

Path eval of kidney biopsies: o Nephrotic syndrome-

A

heavy proteinuria, hypoalbuminemia, severe edema; caused by increase glomerular capillary permeability to plasma proteins

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24
Q

• Minimal change disease- most common cause of

A

nephrotic syndrome in children

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25
Q

Minimal change disease: o Path-

A

normal appearing glomeruli by light microscopy, no immune complexes; USE EM to see epithelial foot processes

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26
Q

Minimal change disease: o Therapy-

A

good response to corticosteroid therapy

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27
Q

• Focal and segmental glomerulosclerosis-

A

fibrotic change going on; common cause of nephrotic syndrome in adults; may be idiopathic or secondary to other glomerular diseases, scarring

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28
Q

• Focal and segmental glomerulosclerosis-

o Path-

A

segmental sclerosis of some glomeruli characterized by increased mesangial matrix collagen with obliteration of capillary loops

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29
Q

• Focal and segmental glomerulosclerosis-

o Therapy-

A

poor response to corticosteroid treatment- renal failure in 50% after 10 yrs

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30
Q

• Membranous nephropathy (glomerulonephritis)- most common in adults age ———–; may be

A

30-50yrs

primary and limited to kidney or secondary to infection malignancy, SLE (systemic lupus erethemat) or drugs

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31
Q

Membranous nephropathy: o Path-

A

immune complexes in the epithelial side of GBM demonstrable by immunofluorescence and EM

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32
Q

Membranous nephropathy: o Therapy-

A

poor roseponse to corticosteroid treatment with 40% developing renal failure in 2-20 yrs

33
Q

• Glomerular disease in diabetes mellitus-

A

minimal proteinuria progresses over 10-15 yrs to severe proteinuria

34
Q

Glomerular Disease in diabetes mellitus: o Path-

A

thick glomerular basement membranes, diffuse increase in mesangial matrix and formation of mesangial nodules (the latter is nodular glomerulosclerosis or Kimmelstiel-Wilson lesion).

35
Q

Nephritic Syndrome: • Characterized by

A

acute onset of hematuria, oliguria/azotemia, and hypertension

36
Q

Nephritic Syndrome: • Proliferation of cells within ——— accompanied by ————→severe capillary wall injury, results ————–

A

glomeruli

inflammatory cells

in blood passing into urine as well as GFR

37
Q

Acute postinfectious (poststrep.) glomerulonephritis- common to occur soon after

A

S. pharyngitis infection

38
Q 
Acute postinfectious (poststrep.) glomerulonephritis
o	Path-
A

proliferation of endothelial and mesangial cells with neutrophil infiltrate; immune complexes in GBM and mesangium

39
Q 
Acute postinfectious (poststrep.) glomerulonephritis
•	Progression to chronic renal disease in more likely in
A

adults

40
Q

• IgA Nephropathy-

A

usually in children and young adults; hematuria 1-2 days after non-specific upper respiratory tract viral infection

41
Q

IgA Nephropathy: o Path- increased

A

IgA, can lead to Henoch-Schönlein purpura; mesangial deposition of immune complex with IgA, occasionally crescent epithelial cell proliferation (push glomerular tuft off to the side)

42
Q

• Crescentic/Rapidly Progressive Glomerulonephritis-

A

acute clinical syndrome, progressive loss of renal function, severe oliguria; death from renal failure in weeks to months if untreated

43
Q

Crescentic/Rapidly Progressive Glomerulonephritis: o Path-

A

crescentic glomerulonephritis due to proliferation of epithelium with histiocyte infiltration

44
Q

Crescentic/Rapidly Progressive Glomerulonephritis: • Several different disorders-

A

Anti-GBM antibody disease (12% of cases), Immune complex disease (44% of cases), Pauci-immune, lack of anti-GBM or immune complexes (44% of cases)

45
Q

Crescentic/Rapidly Progressive Glomerulonephritis: o May be associated with

A

antibodies directed against a glomerular basement antigen

46
Q

Chronic (End-Stage) Renal Disease-

• Loss of ———– leading to ————,

A

glomeruli and tubules

fibrosis

47
Q

Chronic renal disease:

A

damaged glomeruli become completely sclerotic (global sclerosis)→ adaptive changes→injury and progressive renal failure

48
Q

Chronic renal disease: o Routine exam-

A

proteinuria, hypertension or azotemia

49
Q

chronic renal disease: o Therapy-

A

without treatment→ poor prognosis, renal dialysis and kidney transplant necessary for patient survival

50
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • ——————– of kidney and renal pelvis caused by —————————

A

Suppurative inflammation

bacterial infection, affects tubules, interstitium and pelvis→typically secondary to bacterial infection

51
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis

o Infection from urinary bladder→

A

renal pelvis and kidney

52
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: o Less common route in infection→

A

hematogenous spread of bacteria

53
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Predisposing conditions-

A

female, pregnant, immunosuppressed, diabetes mellitus

54
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Clinically-

A

sudden onset of pain at costovertebral angle and systemic infection, dysuria, frequency and urgency

55
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Path-

A

patchy insterstitial tubular neutrophilic inflammation

56
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Etiology-

A

predisposing conditions

57
Q

Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Prognosis-

A

repeated bouts of acute inflammation of continuous inflammation may lead to chronic pyelonephritis

58
Q

chronic pyelonephritis: o Characterized by

A

mononuclear inflammatory infiltration and irregular scarring

59
Q

Drug- Induced Interstitial Nephritis-

• Path-

A

hypersensitivity to drugs; interstitial infiltration of mononuclear inflammatory cells; often with neutrophils and eosinophils; granulomas may be present NO GLOMERULI INVOLVEMENT; large doses of analgesics may lead to interstitial nephritis with papillary necrosis

60
Q

Acute Tubular Necrosis-

• Clinical-

A

rapid onset of renal failure, reduced urine output, electrolyte imbalances, reversible over a period of wks as damaged tubular epithelium regenerates

61
Q

Acute Tubular Necrosis- • Etiology-

A

injury to tubular epithelial cells from ischemia or a toxin

62
Q

Acute Tubular Necrosis- • Pathology-

A

dilation of tubules, interstitial edema, necrosis of epithelium

63
Q

Acute Tubular Necrosis- • Treatment-

A

dialysis, supportive care

64
Q

Acute Tubular Necrosis- • Prognosis-

A

full recovery unless preexisting kidney disease

65
Q

• Arterionephrosclerosis- contributing factors are —————, may lead to —————-

A

hypertension and diabetes

gradual onset of chronic renal failure

66
Q

Arterionephrosclerosis: o Path-

A

kidneys are symmetrically atrophic with moderate reduction in size, kidney surface has an even fine granularity and cortex is thin

67
Q

Arterionephrosclerosis: o Histopathology-

A

narrowing of lumen of arterioles and arteries caused by hyaline type of arteriolosclerosis

68
Q

Arterionephrosclerosis: • Clinic:

A
  • Tubular atrophy and interstitial fibrosis

* Global sclerosis of glomeruli

69
Q

• Arterionephrosclerosis associated with

A

malignant hypertension

70
Q

Arterionephrosclerosis

o Clinical-

A

relatively rapid onset of renal failure with increased intracranial pressure leading to headache, nausea, vomiting and visual impairment
o

71
Q

Arterionephrosclerosis

Path-

A

arterioles show hyperplastic arteriolosclerosis, reducing blood flow and causing necrosis of glomeruli

72
Q

• Thrombotic Microangiopathies-

Defect:

A

o TTP- acquired defect in ADAMTS13

73
Q

• Widespread involvement of other organs in

A

TTP

74
Q

Thrombotic microangiopathies: o HUS-

A

endothelial cell injury due to Shiga-toxin from E. coli or Shigella→ platelet activation

• Renal involvement predominates; occurs most often in children

75
Q

Thrombotic microangiopathies

o Path-

A

similar in both disorders with microthrombus formation in capillaries

76
Q

————-; may form ———- of pelvis and calyceal system

A

staghorn calculi”

cast

77
Q

Types of stones-

• Magnesium ammonium phosphate-

A

pts have persistently alkaline urine; infection proteus predisposes to these stones

78
Q

Types of stones-

• Uric acid- occur in

A

pts with gout, leukemia (high cell turnover) or persistently acid urine

Gen Path Exam 2 (12 decks)

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