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Pathology > Injury & Necrosis > Flashcards

Injury & Necrosis Flashcards

1
Q

Reversible injury

A

ischemia

  • decreas ox phosphorylation
  • decrease ATP, increase glycolysis
  • decrease Na pump so ER swells, blebs, myelin figures, cell swelling
  • detach ribosome- decrease prot syn
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2
Q

Nutritional imbalance

A

protein calorie def

  • found in marasmus, kwashiorkor
  • anorexia nervosa

excess calorie intake

  • DMII
  • metabolic syndrome
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3
Q

Irreversible Injury

A

Cell death, mem injury

  • loss phospholipids
  • cytoskeletal alterations
  • free radicals
  • lipid breakdown
  • increase enz leakage
  • release lysosomes
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4
Q

Hypoxia

A
  • ischemia
  • atheroscelrosis most common cause
  • can also be due to resp failure, anemia, CO poisoning
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5
Q

Hypoxia Physical:

A

Phys:

trauma, temp changes, radiation, electric shock, P changes *Caisson’s disease

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6
Q

Chem agents & drugs

A

poisons- Arsenic, CN, Hg

alc, tobacco, IV

asbestos, CO, CCL4

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7
Q

infectious agents:

A
  • virus- influenza
  • bac- streptococci
  • plasmodia- malaria
  • rickettsia- Q fever
  • fungi- candida
  • worms- tape/hookworm
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8
Q

Immunological Rxn

A
  • autoimmune diseases
  • hypersensitivity rxn (butterfly rash in systemic lupus)
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9
Q

Genetic Defects

A
  • down syndrome
  • sickle cell anemia
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10
Q

Apoptosis

A

Regulation of cell numbers in development & systems

Also done to kill infectious agents

Cell mem is intact

No adjacent inflammation

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11
Q

Necrosis

A

Normal post mortem changes

Pathological

Cell mem is disrupted

Enzyme digestion

Frequently w/ adjacent inflammation

LIVING TISSUE

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12
Q

Hydropic Swelling Pathogenesis

A
  • Imparied cell vol reg
  • Injurious agents interfere w/ mem regulated process, increase Na+ perm
  • damage to pump directly
  • reversible

found in kidney= cell swelling

and liver= fatty changes (increase in fat)

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13
Q

EM features of subcellular level of reversible injury

A
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14
Q

Irreversible Cell Injury

A

Nucleaus= pyknosis

  • nuke shrinks & condenses chromatin
  • karyolysis, loss of basophilia
  • karyorrhexis, breakup of chromatin into small dense fragments w/ necrotic cell
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15
Q

Cytoplasm of necrotic cell

A

Hyper eosinophilia

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16
Q

EM features of irreversible injury

A

clumped nuke chromatin

mitochondrial swelling

Ca2+ deposition

myelin figures present

17
Q

Injury Review

A

Reversible

  • decrease pH
  • increase glycolysis
  • decrease prot syn
  • failulre of Na+/K+ pump
  • hydropic change

Irreversible

  • severe ATP depletion
  • nuke changes
  • mem changes
  • ROS
  • cytokskeleton abnormal
  • influx Ca2+
  • mitochondrial densities
18
Q

Coagulative necrosis

A
  • cell outlines are visible
  • no cell organelles
  • neutrophils remove these features after few days
  • due to ischemia/infarction
  • Seen everywhere except BRAIN
  • hypoxia blocks proteaolysis & lysosome digestion when it denatures structural prot!

Key: deep eosinophilia, no nuke

19
Q

Liquefactive Necrosis

A
  • tissue converted into liquied viscous mass
  • in brain due to hypoxia- loss CT support & lysosomes
  • Form abscess

KEY: look for empty space or inflammatory cells, no cell structure seen

20
Q

Gangrenous necrosis

A
  • limb or intestine loss of blood supply
  • loop of bowel twists,
  • dry gangrene
  • wet gangrene- w/ liquefactive
  • gas gangrene
21
Q

Gangrene Etiologies

A
  • a.. thromboembolism
  • DM vascular disease
  • atherosclerosis
  • indirect hyperthermic effect like frostbite
22
Q

Dry gangrene

A

Key: line of demarcation b/t necrotic tissue & healthy tissue

23
Q

Wet Gangrene

A

KEY: bac infectio in patient w/ diabetes

*antibiotics won’t work b/c poor transport in patient

24
Q

Gas gangrene

A

KEY: Clostridium perfringens

25
Q

Caseous Necrosis

A
  • TB but seen w/ fungi & Brucella bacteria
  • Associates w/ T lymphocytes & INF g
  • Do not show cell outlines but don’t liquefy
  • Dead cells- amorphous, granular & eosinophilic
  • Looks like clumpy cheese
  • Toxicity from mycobac cell wall
  • Also have dystrophic calcification

*dormant TB- caseation only in hilar LN

*active TB- all over lung

26
Q

Central Caseous necrosis

A
27
Q

Fat Necrosis

A

KEY= pancreatisis

  • digestive enz from pancrease released
  • phospholipases & proteases attack PM of adipocytes & trglycerides are released
  • pancreatic lipase hydrolyze triglycerides producing FA
  • FFA bind /w Ca2+ forming soaps which appear:
  • amorphous, basophilic deposits at edges
  • chalky & gloss appearance
28
Q

Fat Necrosis

A
29
Q

Fat Necrosis

A

Micro

30
Q

Fibrinoid Necrosis

A

KEY= BV!!!

  • Seen in immune rxns
  • When antigen-Ag complex deposit in vessel walls
  • Fibrin present as well
  • Malignant hyperT

Pathology (8 decks)

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