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Basic Pathology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

common causes of cell injury

A
  • hypoxia and anoxia (primary cause)
  • free radicals
  • toxins
  • infection
  • immunologic or inflammatory responses
  • genetic and metabolic disturbances
  • traumatic injury
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2
Q

time course of cell injury:

1) homeostasis
2) cell injury
3) reversible changes:
- _____
- _____
- _____
4) cell death
5) irreversible changes:
- _____
- _____
- _____

A

ATP depletion;
biochemical dysfunction;
early ultrastructural changes: cytoplasmic swelling, vacuolation;

late ultrastructural changes;
early light microscopic changes: pyknosis;
late light microscopic changes: karyorrhexis, karyolysis

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3
Q

hypoxic injury and cellular swelling

A

reduces oxygen delivery to the cell –> inhibits cell’s ability to create adequate ATP –> water moves into cell (bc pumps aren’t working w/o ATP) –> swelling and vacuolation; can be reversible if oxygen delivery is restored

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4
Q

ischemic hypoxia

A

decreased blood flow therefore decreased oxygen (ex: pinched blood vessel); most common

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5
Q

ischemic anoxia

A

no blood flow (ex: blocked blood vessel)

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6
Q

anemic hypoxia

A

red blood cells can’t deliver sufficient oxygen to cells (ex: sickle cell anemia, carbon monoxide poisoning)

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7
Q

reactive oxygen species:

____ and _____ generated

A

internally; externally

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8
Q

normal metabolic processes (e.g., mitochondrial electron transport chain) and immune responses generate ___

A

free radicals

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9
Q

free radicals can cause damage to molecules by ____ through oxidation (called oxidative damage)

A

stealing their electrons

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10
Q

a free radical is an atom or group of atoms that have ____, making them extremely ___

A

1 or more unpaired electrons; reactive

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11
Q

___ and ___ forms of reactive oxygen species

A

radical; non-radical

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12
Q

ROS’s are typically neutralized by ____

A

internally produced anti-oxidants

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13
Q

ROS’s are produced in larger amounts with ____

A

injury and aging (oxidative stress)

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14
Q

ROS’s can break ____

A

covalent bonds in molecules

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15
Q

radical forms have an ____

A

unpaired electron- donates to or acquires electron from cellular molecules

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16
Q

ROS associated injury

A
  • lipid peroxidation
  • protein degradation
  • DNA damage
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17
Q

ROS sources

A
  • mitochondria
  • inflammation
  • exercise
  • cigarette smoke
  • pollution
  • certain drugs, pesticides
  • solvents
  • reperfusion
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18
Q

direct toxic injury and examples

A

disrupt cellular function;
lead: CNS toxicity;
mercury: CNS toxicity;
carbon monoxide: anemic hypoxia

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19
Q

indirect toxic injury and examples

A

toxic after metabolism;
ethanol: CNS and liver toxicity (can also have direct toxicity);
ethambutol (TB drug): toxic optic neuropathy;
cyclosporine: renal toxicity

20
Q

infectious injury direct cellular damage

A

ex: virus targets cell and causes cell to rupture; bacteria releases toxin that damages the cell

21
Q

infectious injury indirect cellular damage via immune response

A

collateral damage that comes along with the immune response to an infection; typically normal

22
Q

genetic and metabolic injury can be ___ or ____; they disrupt normal cell function; examples?

A

acquired; congenital;

sickle cell anemia, fatty liver disease, hepatolenticular degeneration, type 2 diabetes mellitus

23
Q

traumatic injury examples in the eye

A
  • blunt force trauma
  • sharp force trauma
  • penetrating trauma
  • ionizing radiation
24
Q

____ is a response to stress

A

adaptation

25
Q

adaptation attempts to restore ____; result of altered ____; type depends on cell and stressor

A

homeostasis; gene expression

26
Q

atrophy

A

decreased cell size; can be result of injury/decreased use

27
Q

hypertrophy

A

increased cell size; can be result of exercise, pregnancy; left ventricular hypertrophy caused by obesity/hypertension

28
Q

hyperplasia

A

increased cell number; ex: calluses form due to mechanical irritation, pregnancy

29
Q

metaplasia

A

conversion of one cell type to another; in ectropion the exposed conj. may begin to keratinize due to exposure to external environment

30
Q

dysplasia

A

disorderly growth; not an adaptation but rather damage; a precursor to cancer

31
Q

intracellular and extracellular accumulations as adaptation

A
  • water
  • lipids
  • cholesterol
  • calcium
  • pigments
  • ex: bilirubin, lipofuscin
32
Q

primary theories of aging

A
  • accumulation of injurious events
  • genetically controlled program
  • likely a combination of both
33
Q

as we age, our cells produce less ____ and more ____, which further reduces the ability to produce ____

A

ATP; free radicals; ATP

34
Q

necrosis

A

initiated by (external) cell injury, leads to inflammation; group of cells; type of necrosis that occurs depends on the type of tissue in which it occurs

35
Q

apoptosis

A

programmed cell death; initiated by suicide gene activation; single cell; orderly and non-inflammatory; body can recycle materials; developmentally necessary; ordered cell turnover; can also result from injury

36
Q

coagulative necrosis

A
  • kidneys, heart, adrenal glands

- begins with ischemia, leads to protein denaturation, cellular lysis, and clotting

37
Q

liquefactive necrosis

A
  • neurons and glial cells of the brain
  • cells release hydrolytic enzymes which digest tissues into a wet/runny wound
  • may form abscess or cysts
38
Q

caseous necrosis

A
  • cheese-like
  • tuberculosis pulmonary infection
  • combination of coagulative and liquefactive necrosis
39
Q

gangrenous necrosis

A

clinical term; large area of affected tissue

40
Q

dry gangrene

A

large area with coagulative necrosis

41
Q

wet gangrene

A

large area with liquefactive necrosis

42
Q

gas gangrene

A

associated with anaerobic bacteria that produce gas

43
Q

fat necrosis

A
  • breast, pancreas, and other abdominal organs

- action of lipases may cause saponification (changing of tissue into soapy texture)

44
Q

somatic death

A

sufficient death of cells/tissues of vital organs: heart, brain, kidneys;
occurs when the death of the tissue exceeds the body’s ability for normal life processes

45
Q

postmortem changes; useful for investigating unobserved deaths

A
  • algor mortis: cooling of the body
  • livor mortis: pooling of the blood
  • rigor mortis: muscle contraction
  • postmortem autolysis (endogenous) and putrefaction (exogenous)

Basic Pathology (21 decks)

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