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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
Minimal change disease: o Path-
normal appearing glomeruli by light microscopy, no immune complexes; USE EM to see epithelial foot processes
26
Minimal change disease: o Therapy-
good response to corticosteroid therapy
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• Focal and segmental glomerulosclerosis-
fibrotic change going on; common cause of nephrotic syndrome in adults; may be idiopathic or secondary to other glomerular diseases, scarring
28
• Focal and segmental glomerulosclerosis- | o Path-
segmental sclerosis of some glomeruli characterized by increased mesangial matrix collagen with obliteration of capillary loops
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• Focal and segmental glomerulosclerosis- | o Therapy-
poor response to corticosteroid treatment- renal failure in 50% after 10 yrs
30
• Membranous nephropathy (glomerulonephritis)- most common in adults age -----------; may be
30-50yrs primary and limited to kidney or secondary to infection malignancy, SLE (systemic lupus erethemat) or drugs
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Membranous nephropathy: o Path-
immune complexes in the epithelial side of GBM demonstrable by immunofluorescence and EM
32
Membranous nephropathy: o Therapy-
poor roseponse to corticosteroid treatment with 40% developing renal failure in 2-20 yrs
33
• Glomerular disease in diabetes mellitus-
minimal proteinuria progresses over 10-15 yrs to severe proteinuria
34
Glomerular Disease in diabetes mellitus: o Path-
thick glomerular basement membranes, diffuse increase in mesangial matrix and formation of mesangial nodules (the latter is nodular glomerulosclerosis or Kimmelstiel-Wilson lesion).
35
Nephritic Syndrome: • Characterized by
acute onset of hematuria, oliguria/azotemia, and hypertension
36
Nephritic Syndrome: • Proliferation of cells within --------- accompanied by ------------→severe capillary wall injury, results --------------
glomeruli inflammatory cells in blood passing into urine as well as GFR
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Acute postinfectious (poststrep.) glomerulonephritis- common to occur soon after
S. pharyngitis infection
38
``` Acute postinfectious (poststrep.) glomerulonephritis o Path- ```
proliferation of endothelial and mesangial cells with neutrophil infiltrate; immune complexes in GBM and mesangium
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``` Acute postinfectious (poststrep.) glomerulonephritis • Progression to chronic renal disease in more likely in ```
adults
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• IgA Nephropathy-
usually in children and young adults; hematuria 1-2 days after non-specific upper respiratory tract viral infection
41
IgA Nephropathy: o Path- increased
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
• Crescentic/Rapidly Progressive Glomerulonephritis-
acute clinical syndrome, progressive loss of renal function, severe oliguria; death from renal failure in weeks to months if untreated
43
Crescentic/Rapidly Progressive Glomerulonephritis: o Path-
crescentic glomerulonephritis due to proliferation of epithelium with histiocyte infiltration
44
Crescentic/Rapidly Progressive Glomerulonephritis: • Several different disorders-
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
Crescentic/Rapidly Progressive Glomerulonephritis: o May be associated with
antibodies directed against a glomerular basement antigen
46
Chronic (End-Stage) Renal Disease- | • Loss of ----------- leading to ------------,
glomeruli and tubules fibrosis
47
Chronic renal disease:
damaged glomeruli become completely sclerotic (global sclerosis)→ adaptive changes→injury and progressive renal failure
48
Chronic renal disease: o Routine exam-
proteinuria, hypertension or azotemia
49
chronic renal disease: o Therapy-
without treatment→ poor prognosis, renal dialysis and kidney transplant necessary for patient survival
50
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • -------------------- of kidney and renal pelvis caused by ---------------------------
Suppurative inflammation bacterial infection, affects tubules, interstitium and pelvis→typically secondary to bacterial infection
51
Acute Pyelonephritis- aka Tubulointerstitial nephritis o Infection from urinary bladder→
renal pelvis and kidney
52
Acute Pyelonephritis- aka Tubulointerstitial nephritis: o Less common route in infection→
hematogenous spread of bacteria
53
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Predisposing conditions-
female, pregnant, immunosuppressed, diabetes mellitus
54
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Clinically-
sudden onset of pain at costovertebral angle and systemic infection, dysuria, frequency and urgency
55
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Path-
patchy insterstitial tubular neutrophilic inflammation
56
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Etiology-
predisposing conditions
57
Acute Pyelonephritis- aka Tubulointerstitial nephritis: • Prognosis-
repeated bouts of acute inflammation of continuous inflammation may lead to chronic pyelonephritis
58
chronic pyelonephritis: o Characterized by
mononuclear inflammatory infiltration and irregular scarring
59
Drug- Induced Interstitial Nephritis- | • Path-
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
Acute Tubular Necrosis- | • Clinical-
rapid onset of renal failure, reduced urine output, electrolyte imbalances, reversible over a period of wks as damaged tubular epithelium regenerates
61
Acute Tubular Necrosis- • Etiology-
injury to tubular epithelial cells from ischemia or a toxin
62
Acute Tubular Necrosis- • Pathology-
dilation of tubules, interstitial edema, necrosis of epithelium
63
Acute Tubular Necrosis- • Treatment-
dialysis, supportive care
64
Acute Tubular Necrosis- • Prognosis-
full recovery unless preexisting kidney disease
65
• Arterionephrosclerosis- contributing factors are ---------------, may lead to ----------------
hypertension and diabetes gradual onset of chronic renal failure
66
Arterionephrosclerosis: o Path-
kidneys are symmetrically atrophic with moderate reduction in size, kidney surface has an even fine granularity and cortex is thin
67
Arterionephrosclerosis: o Histopathology-
narrowing of lumen of arterioles and arteries caused by hyaline type of arteriolosclerosis
68
Arterionephrosclerosis: • Clinic:
* Tubular atrophy and interstitial fibrosis | * Global sclerosis of glomeruli
69
• Arterionephrosclerosis associated with
malignant hypertension
70
Arterionephrosclerosis | o Clinical-
relatively rapid onset of renal failure with increased intracranial pressure leading to headache, nausea, vomiting and visual impairment o
71
Arterionephrosclerosis Path-
arterioles show hyperplastic arteriolosclerosis, reducing blood flow and causing necrosis of glomeruli
72
• Thrombotic Microangiopathies- Defect:
o TTP- acquired defect in ADAMTS13
73
• Widespread involvement of other organs in
TTP
74
Thrombotic microangiopathies: o HUS-
endothelial cell injury due to Shiga-toxin from E. coli or Shigella→ platelet activation • Renal involvement predominates; occurs most often in children
75
Thrombotic microangiopathies o Path-
similar in both disorders with microthrombus formation in capillaries
76
-------------; may form ---------- of pelvis and calyceal system
staghorn calculi” cast
77
Types of stones- | • Magnesium ammonium phosphate-
pts have persistently alkaline urine; infection proteus predisposes to these stones
78
Types of stones- | • Uric acid- occur in
pts with gout, leukemia (high cell turnover) or persistently acid urine

Gen Path Exam 2 (12 decks)

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