Lecture 1 Cell Reaction To Injury Flashcards

1
Q

study of suffering

A

pathology

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2
Q

old fashioned term that use to include sins, evil spirits and gods along with other causative agents

A

cause

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3
Q

a summary of ALL factors leading to a diseased state, including predispositions and environmental influence

A

etiology

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4
Q

the mechanism of development of disease state

A

pathogenesis

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5
Q

structural alterations on cellular, tissue, and organ level

A

morphologic changes

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6
Q

symptoms and signs directly associated with a diseased state

A

clinical significance

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7
Q

homeostatic processes include adaptation to significant changes in what 3 phenomenons

A
  1. availability of the substrate
  2. physical condition
  3. accumulation of the waste
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8
Q

when cells manage to stay grossly functional we call that

A

adaptation

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9
Q

when the cells i dysfunctional but capable of getting back to the functional state this is called

A

reversible injury

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10
Q

when the cell cannot return to functional state

A

irreversible injury (cell death is imminent)

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11
Q

what 2 main stimuli lead to cell adaptation or injury

A
  1. change in demand

2. hypoxia

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12
Q

what are the three elements of “change in demand”

A
  1. workload
  2. hormonal stimulation
  3. nervous stimulation
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13
Q

what are the two types of hypoxia

A
  1. inadequate tissue oxygenation

2. inadequate blood oxygenation

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14
Q

what are the 3 causes of inadequate tissue oxygenation?

A
  1. ischemia
  2. hypovolemia
  3. heart failure
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15
Q

what are the 4 causes of inadequate blood oxygenation?

A
  1. Respiratory Injury
  2. Anemia
  3. CO Poisoning
  4. High Altitude
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16
Q

What is the main organelle hit in the cell during hypoxia

A

Mitochondria (and subsequently ATP production)

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17
Q

What metabolic pathway is still alive in cell hypoxia?

A

Anaerobic glycolysis, but it forms lactic acid, increasing anion gap, and dropping pH

18
Q

As a result of cellular hypoxia, the Na/K pump also dies allowing for what ions to move in what direction?

A

K leaves & Na/Calcium/H20 get in
(cell swells)
(protein synthesis also stops)

19
Q

chemical injury can alter what two cellular functions

A
  1. membrane permeability

2. co-factor/enzyme function

20
Q

besides mechanical injury, high body temperature does what inside the cell

A

denatures proteins

21
Q

low cell temperature does what inside the cell?

A

inactivates proteins

22
Q

ionizing UV radiation does what

A
  1. produces free radicals

2. damages DNA

23
Q

Give some sources of free radicals

A
  1. normal metabolic process
  2. from ionizing radiation
  3. enzyme degradation from pharm drugs
  4. Transitional metals (Iron, copper)
  5. Nitric Oxide (NO)
24
Q

Free radical presence can cause

A
  1. lipid peroxidation
  2. protein damage
  3. DNA damage
25
Free radicals can be eliminated by....
1. Antioxidants (vitamins, etc.) 2. Natural decay 3. Enzymes (that themselves become disabled) 4. Special enzyme (Super Oxide Dismutase)
26
what type of virus leads to cell death
Cytolytic (Adeno, HSV)
27
what type of virus leads to proliferation of cells
Oncogenic (HPV, EBV)
28
what are the 4 nutrients that if imbalanced, can lead to cell injury or adaptation
1. calories 2. proteins 3. vitamins 4. minerals
29
what are the 2 immunological reactions to cell injury/adaptation
inflammation and autoimmune disease
30
as we age, what occurs with cells
inability to repair, and effectively replicate
31
failure of cell production
aplasia
32
absence of organ or limb in fetal develope as a result of asplasia is called...?
agenesis
33
later in life, absence of tissue is result of loss of what type of cell?
progenitor cells (bone marrow)
34
what is the term for the less extreme aplasia, where there is a decrease in cell production
hypoplasia (usually due to lack of hormones, i.e. turners/kleinfelters)
35
decrease in the size of the organ or tissue due to shrinking cell size
atrophy
36
atrophy is an active and specific response, not just passive cell loss....true or false
true
37
what does each cell undergo first in atrophy
decreased protein synthesis (some however are upregulated)
38
which protein synthesis is upregulated in atrophy?
contractile proteins like ubiuitin and cortisol and thyroxine (insulin opposes these two)
39
is gene expression altered in cell atrophy?
yes
40
the cell decreases in its utilization of what food?
fats (hence lipid deposits in infarcted cardiomyosites)
41
what new granule is present that now contains degraded organelles in atrophy?
autophagic granules