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Pathology I MT I Chamberlin Spring 2014 > Week 2: Concepts in Pathology > Flashcards

Week 2: Concepts in Pathology Flashcards

1
Q

What is the difference between morphological pathology and theoretical pathology?

A 
Morphological = Macro or microscopic change (ie cancer)
Theoretical = Pre-cellular disease, a classification rather than specific diagnosis (ie multiple chemical sensitivity)
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2
Q

T or F?
A. Morbidity is death
B. Comorbidity is the co-occurrence of two or more related diseases
C. Idiopathic is a disease of unknown cause.
D. Iatrogenic is disease of natural causes

A

A. False. Morbidity = effects of disease. Mortality = death
B. True
C. True
D. False. Dr.-caused disease. 60% of diseases.

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3
Q

Clinical definition of death.

A

1) No spontaneous breath
2) No palpable pulse
3) No heart sounds on auscultation

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4
Q

T or F?
A. Signs are subjective, reported by patient
B. Symptoms are objective measurements
C. A self-limited disease goes away on its own.
D. Subclinical refers to a disease without expression

A

A. False. Signs are gathered through clinical exams or lab tests.
B. False. Symptoms are subjective, patient reported info.
C. True
D. True

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5
Q

Are these paired correctly?
A. Underlying cause = Pathogenesis
B. Course of disease = Etiology
C. Macro/micro damage = Morphology

A

A. =Etiology
B. =Pathogenesis
C. (Correct)

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6
Q

What is a functional disease?

A

Disease without gross or micro morphological changes (ie fibromyalgia)

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7
Q

What is a syndrome?

A

Group of signs and symptoms that occur together and characterize a particular abnormality or condition. Disease process with poorly understood pathogenesis.

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8
Q 
Eosin or Hematoxylin?
A. stains cytoplasm/RBC/collagen
B. stains structures blue/purple
C. stains nuclei/bacteria
D. stains structures pink/red
A

A. Eosin
B. Hematoxylin
C. Hematoxylin
D. Eosin

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9
Q

T or F?
A. Prussian blue reacts with cells and CT
B. Congo red reacts with amyloid and turns it pink/red
C. Gram stain reacts with bacteria
D. Trichrome reacts with iron

A

A. False. Prussian blue reacts with iron
B. True
C. True
D. False Trichrome reacts with cells and CT

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10
Q

Most common cause of cellular injury?

A

Hypoxia = lack of O2, commonly from ischemia (anemia, cardiac fail.) –> inability to produce ATP in ETC

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11
Q

Causes of cellular injury that are nutritional in nature?

A

1) Inadequate intake (Marasmus, Kwashiorkor)
2) Excessive caloric intake = obesity, atherosclerosis
3) Vitamin deficiency

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12
Q

Causes of cellular injury that are environmental in nature (the result of exposures)?

A

1) Chemical injury = drugs, poisons, pollution, occupational exposure
2) Infections = direct infection, toxins, host inflammatory response
3) Physical = trauma, burns, frostbite, radiation, pressure changes

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13
Q

Causes of cellular injury that are internally caused?

A

1) Immunological rxns = hypersensitivity rxn, autoimmune

2) Congenital = inborn metab. errors and genetic disorder

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14
Q

When does cloudy swelling occur? What happens?

A

Occurs when cells are incapable of maintaining ionic and fluid homeostasis.

  1. Decreased [ATP] and Na+ pump activity
  2. Causes Na and H2O to accumulate intracellularly. Ca also rises.
  3. Result is net isosmostic gain of water.
  4. Cellular degeneration no longer irreversible –> necrosis or apoptosis
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15
Q

Four critical intracellular systems that are susceptible to injury are?

A

DNA
Production of ATP via aerobic respiration
Cell membranes
Protein synthesis

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16
Q

Sources of Free Radicals

A

Metabolism, Redox reactions, Xanthene Oxidase, Free Iron, Neutrophils, Oxygen Therapy, UV light and irradiation, Drugs/toxins, Cigarette smoke and air pollution

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17
Q

Why is mitochondrial dysfunction is an important mechanism of cellular injury? What are the changes that occur in the cell?

A

Leads to severe membrane damage and irreversible cell injury

1) Decrease in oxid. phosphorylation causes decreased ATP and increases permeability of mitochondria
2) Release of cytochrome c is a trigger for apoptosis
3) The Na/K/ATPase pumps start to fail
4) Influx of Na and H2O and efflux of K
5) Cellular swelling, swelling of the ER

18
Q

T or F: ATP depletion results in
A. Increased cell membrane permeability
B. Efflux of Ca
C. Ca triggers 2nd messenger to activate a wide spectrum of enzymes
D. Proteases breakdown protein, ATPase depletes ATP, phospholipases cause cell injury, and endonucleases cause DNA damage

A

A. True
B. False. Influx of Ca
C. True
D. True

19
Q

What are the nuclear changes associated with irreversible cell injury/death?

A 
Pyknosis = degeneration and condensation of nuclear chromatin (Greek pyknono = to thicken up, to become dense)
Karyorrhexis = nuclear fragmentation (Greek rhexis = bursting)
Karyolysis = dissolution of the nucleus
20
Q

What Type of Necrosis: Appearance
A. Soft, friable “cottage cheese” appearance
B. Chalky white appearance
C. Dry (no tissue fluid) gangrene looks like ____
D. Wet (tissue fluid) gangrene looks like ____
E. Necrotic CT that resembles fibrin

A 
A. Caseous
B. Fat
C. Coagulative
D. Liquifactive
E. Fibrinoid
21
Q

What Type of Necrosis: Where It Is Found
A. Most common in kidney, liver, heart
B. In abscesses, brain infarcts, & pancreatic necrosis
C. Caused by lipases acting on adipocytes
D. Common in lower extremities, g.b., GI tract

A

A. Coagulative
B. Liquifaction
C. Fat
D. Gangrenous

22
Q

What Type of Necrosis: Mechanism
A. From acute immunologic injury (hypersensitivity rxn)
B. Hydrolytic/proteolytic enzymes, zymogens –> autolysis
C. Combination of liquefaction and coagulation
D. Seen w/ granulomatous diseases like TB

A

A. Fibrinoid
B. Liquifaction
C. Caseous
D. Caseous

23
Q 
What Type of Necrosis: Random
A. Most common form of necrosis
B. Responsible for mosquito reminder (cyst from denaturing and coagulation of proteins in cytoplasm)
C. Eosinophilic (pink) pattern
D. General term for dead tissue
A

A. Coagulative
B. Coagulative
C. Fibrinoid
D. Gangreous

24
Q

T or F? Apoptosis
A. Specialized form of cell death with inflamm. response
B. Triggered by lack of growth factors/hormones (mitochondrial pathway)
C. Usually affects large numbers of cells
D. Triggered by receptor-ligand signals (Fas, TNF) (Extrinstic pathway)

A

A. False. NO INFLAMMATORY RESPONSE!
B. True
C. False. Usually affects single cells / small groups of cells
D. True

25
Q

Sequence of Apoptosis: Put in Order and Fix Errors

  1. Membrane breakdown (Peroxidation of lipids)
  2. Chromatin condensation and fragmentation
  3. Cell swells & has dense eosinophilic cytoplasm
  4. Cell bursts
  5. Phagocytosis by macrophages
A
  1. Cell SHRINKS (and has dense eosinophilic cytoplasm)
  2. Chromatin condensation and fragmentation
  3. FORMATION OF MEMBRANE BLEBS
  4. BREAKDOWN OF CELL INTO APOPTOTIC BODIES
  5. Phagocytosis of apoptotic bodies by macrophages
26
Q

T or F: Gene regulation of Apoptosis
A. p53 arrests cell cycle and weighs DNA damage
B. Bcl-2 stimulates apoptosis in response to DNA injury
C. p53 prevents release of cytochrome c from mito.
D. cyt c binds to pro-apoptotic protease activating factor (Apaf-1) to trigger apoptosis

A

A. True
B. False. p53 does this (if DNA repair is not possible)
C. False. bcl-2 does this
D. True

27
Q

What are the stages of dysplasia in order of morbidity? Is all dysplasia pathological?

A
  1. Hyperplasia - regrowth of liver, skin (can be healthy)
  2. Metaplasia
  3. Dysplasia - not all pathological but can become so
  4. Neoplasia (cancer)
28
Q

Diseases associated with amyloidosis?

A 
B cell proliferations
Chronic inflammation
Chronic renal failure
Alzheimer's disease
Type II diabetes
Prion diease
29
Q 
Name the blot test used to test for:
A. Protein 
B. RNA mutation
C. DNA mutation
D. Test multiple mutations, multiple diseases with combination of above
A

A. Western blot
B. Northern blot
C. Southern blot
D. Dot blot

30
Q

Marasmus or Kwashiorkor?
A. Decrease in total protein intake
B. Prominent bones, loose skin, decrease in subQ fat
C. Bloated belly, poor wound healing, xerosis, itchy rash
D. Decrease in total caloric intake

A

A. Kwashiorkor
B. Marasmus
C. Kwashiorkor
D. Marasmus

31
Q

What type of vitamin deficiency is responsible for:
A. Scurvy
B. Megaloblastic anemia, neuropathy, spinal cord degeneration
C. Pellagra
D. Bleeding diathesis

A

A. C
B. B-12
C. Niacin B3
D. K

32
Q

How do the treatments of wet and dry gangrene differ?

A

Dry gangrene = no tissue fluid = leave it alone it will autoamputate
Wet gangrene = tissue fluid = hospitable to pathogens = must amputate

33
Q

What do caspases do, and why are they important?

A

Apoptosis is mediated by a cascade of caspases. Caspases digest nuclear and cytoskeletal proteins. They also activate endonucleases

34
Q

What is steatosis, and what are its two main causes in the western world?

A

Abnormal accumulation of TAG in liver, heart, muscle, kidneys, macrophages of arteries.
Usually due to cellular metabolic damage and increased lipids.
Caused by alcoholism or hyperlipidemia

35
Q

What is the pathological significance and appearance of Lipofuscin?

A

Endogenous pigment - wear and tear pigment, generated by free radicals from redox rxns as we age. Not pathological.

36
Q

What is hemosiderosis, and why is it seen in venous stasis ulcers of the lower extremity?

A

Accumulation of hemosiderin in bodily tissues as a result of the breakdown of red blood cells. Dead red blood cells release iron that is stored as hemosiderin. Hemosiderin collects in the skin (pigmentation = bruising) and is slowly removed. Seen in any wound where blood cells are being destroyed.

37
Q

Calcification: Dystrophic or Metastatic?
A. Occurs when there is elevated serum calcium or phosphate
B. Can be caused by atheroma, TB, damaged heart valves, psammoma bodies
C. Local calcification of non-viable tissues
D. Can be caused by bone cancer, milk abuse, antacid abuse

A

A. Metastatic
B. Dystropic
C. Dystropic
D. Metastatic

38
Q

What type of vitamin deficiency is responsible for:
A. Rickets and osteomalacia
B. Megaloblastic anemia and Neural Tube Defects (NTD)
C. Squamous metaplasia, immune deficiency, night blindness

A

A. Vit D
B. Folate
C. Vit A

39
Q

What is the mechanism of Steatosis?

A

Too much free fat coming into the liver. Too much FA synth. and impaired FA oxid.
Excess esterification of FA –> TAG
Too little apoprotein synth, failure of lipoprotein secretion
Liver hypoxia.

40
Q

What happens to amyloids after staining with Congo red? How are they distinguished from other tissues?

A

Congo red turns amyloid red/pink but under polarized light it appears green. This differentiates the amyloid from other proteins found in cytoplasm.

Pathology I MT I Chamberlin Spring 2014 (3 decks)

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