Cellular Pathology Flashcards

1
Q

Robbins List Causes of Cell Injury

A

Oxygen Deprevation (Vascular)

Chemical Agents (Intoxication)

Infectious Agents (Infectious)

Immunologic Reactions (Inflammatory)

Genetic Factors (Congenital)

Nutritional Imbalances (Environmental, Metabolic)

Physical Agents (Trauma)

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2
Q

4 types of adaptions

A

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

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3
Q

Hypertrophy

A

Increase in cell size

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4
Q

Hyperplasia

A

Proliferation

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5
Q

Atrophy

A

Decrease in cell size

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6
Q

Metaplasia

A

change of one type of differentiated cell into another type of differentiated cell

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7
Q

Hx GERD. What cellular change might you see at the gastroesophageal junction

A

Protective metaplasic changes result in intestinal epithelium at lowe GE junction

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8
Q

45 year old M with barretts esophagus. What might you see?

A

A small region of red, velvet-like mucosa in the lower esophagus

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9
Q

27 year old M with N x 1 week, scleral icterus, and elevated AST and ALT

A

Defect in cell membrane

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10
Q

19 year old previously healthy collapeses playing bball. Died.

Age related atheromatous plaque buildup

MI due to CAD

Septal hypertrophy (congenital)

Congenital narrowing of the aorta with poor blood flow to the legs

Cardiac myxoma (pedunculated tumor within the L atrium)

A

Septal Hypertrophy

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11
Q

6 types of necrosis

A

Coagulative

Liquefactive

Gangrenous

Caseous

Fat necrosis: Saponification

Fibroid necrosis

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12
Q

Coagulative Necrosis

A

Seen in ischemia/ infarcts in most tissues (except brain)

Due to ischemia or infarction: proteins denature, then enzyme degredation

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13
Q

Liquefactive necrosis

A

Seen in bacterial abcesses, brain infarcts (due to increased fat content)

Due to neutrophil release lysosomal enzynes that digest tissue. Enzymatic degredation first, then proteins denature

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14
Q

Gengrenous Necrosis

A

Seen in distal extremity after chronic ischemia

Due to:

Dry: ischemia

Wet: superinfection

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15
Q

Caseous Necrosis

A

Seen in TB, systematic fungi

Due to macrophages wall off the infecting microorganisms lead to granular debris

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16
Q

Fat necrosis

A

Seen in enzymatic acute pancreatitis (saponification of pancreatic fat) and nonenzymatic traumatic (eg breaest injury)

Damaged cells release lipase which breaks down triglycerides in fat cells

Chalkiness

17
Q

Fibrinoid necrosis

A

Immune reaction in vessels

Immune complexes combine with fibrin leading to vessel wall damage

18
Q

Diseases due to misfolded proteins (think neurodegenerative)

A

Huntingtons

Parkinsons

Alzheimers

19
Q

Failure to degrade a metabolite due to inherited enzyme deficiencies

A

storage diease

20
Q

Cellular accumulation of normal substance

A

most neurodegenerative dz, fatty liver: acquired by inadequate removal of a normal substance

21
Q

Cellular accumulation of abnormal endogenous substance

A

cystic fibrosis, alpha1antitrypsin, other. Accumulation of an abnormal endogenous substance as a result of genetic or acquired defect

22
Q

Failure to degrade a metabolite

A

inborn errors of metabolism/ storage dz. Failure to degrade a metabolite due to inherited enzyme deficiencies

23
Q

accumulation of abnormal exogenous substance

A

pneumoconioses, scoliosis, asbestosis, berylliosis. deposition and accumulation of an abnormal exogenous substance

24
Q

Dystrophic calcification

A

dystrophic calcification is encountered in areas of necrosis of any type. It is virtually inevitable in the atheromas of advanced atherosclerosis, associated with intimal injury in the aorta and large arteried and is characterized by the accumulation of lipids

25
Q

Metastatic calcification

A

deposition of calcium salts in normal tissues is known as metastatic calcification and is almost always secondary to some derangement in calcium metabolism (hypercalcemia)

26
Q

54 year old F. Fatigue, C, HTN, kidney stones, PE/nl, PTH, Ca/PO4 elevated

widespead calcifation of the interstitial tissue in her kidneys, lungs, and GI tract. What type of calcification

A

metastatic calcification

27
Q

SLE

A

Positive anti-ds-DNA antibodies

28
Q

68 year old M smoker dies of chron bronchitis. No other medical problems. What is least likely to be observed in the lungs?

Patchy squamous metaplasia

Thickened bronchial walls

Granulomatous inflammation

neutrophil infiltration

mucoid gland enlargement

A

granulomatous inflammation

29
Q
A