1: Cell Response And Adaptations Flashcards

1
Q

Etiology

A

Initiating cause of a disease

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2
Q

Pathogenesis

A

Sequence of molecular, biochemical, and cellular events that lead to disease development

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3
Q

Four steps of disease leading to S/S

A
  1. Etiology
  2. Pathogenesis
  3. Morphological changes
  4. Clinical manifestation (S/S)
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4
Q

Disease

A

Any deviation from normal structure/function of a part/organ/system as manifested by characteristic symptoms and signs

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5
Q

Disorder

A

A derangement or abnormality of function; a morbid physical or mental state

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6
Q

Neoplasm

A

A new + abnormal growth, specifically when uncontrolled and progressive

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7
Q

Syndrome

A

A set of sx that occur together - the sum of signs of any morbid state

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8
Q

When can cardiac-specific enzymes be detected in the blood after MI?

A

As early as two hours, but sometimes not until 4-12 hours later

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9
Q

Myelin figures

A

Phospholipids derived from damaged cell membranes that appear in reversible cell injury

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10
Q

Major mechanism of apoptosis

A

Mitochondrial pathway

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11
Q

Three anti-apoptotic and three pro-apoptotic proteins

A

Anti: BCL2, BCL-XL, MCL1
Pro: cytochrome C, BAX, BAK

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12
Q

Function of anti-apoptotic proteins

A

Keep mito outer membrane impermeable to prevent leakage of cytochrome C into cytosol

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13
Q

How does BAX-BAK complex function?

A

Oligomerize within outer mito membrane and promote mito permeability

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14
Q

Regulated apoptosis initiators: two other names

A

Sensors, BH3-only proteins

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15
Q

BH3 only protein functions

A

Sensors of cell stress and damage to regulate balance between pro- and anti-apoptotic proteins

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16
Q

Examples of regulated apoptosis initiators/BH3-only proteins

A

BAD, BIM, BID, Puma, Noxa

17
Q

How is extrinsic pathway of apoptosis initiated?

A

FasL binds Fas receptor (a TNFR)

18
Q

What cell types express FasL?

A

CD4 T cells and some CD8 T cells

19
Q

What protein can inhibit extrinsic mechanism of apoptosis? How?

A

FLIP: binds pro-caspase-8 but cannot cleave and activate it

20
Q

Pyroptosis

A

Programmed cell death + IL-1 and fever

21
Q

Necroptosis

A

Necrosis through a controlled molecular pathway

22
Q

Characteristics of necroptosis

A

Loss of ATP, swelling of cell, ROS generation, lysosomal enzyme release, rupture of plasma membrane

23
Q

Does necroptosis utilize caspases?

24
Q

Some clinical settings where necroptosis occurs

A

Steatohepatitis, acute pancreatitis, ischemia-reperfusion injury, neurodegenerative diseases

25
Mechanism of pyroptosis
Microbe enters cell -> activate inflammasome -> activates caspase 1 -> forms IL-1
26
Ferroptosis
Cell death triggered by excess intracellular Fe or ROS that overwhelms the antioxidant defenses -> lipid peroxidation -> cell death resembling necrosis
27
Autophagy
Survival mechanism to maintain the integrity of cells by recycling essential metabolites and clearing debris
28
What condition is autophagy usually associated with?
Atrophy
29
Disease states where dysregulation of autophagy occurs
CA, IBD, neurodegenerative disorders
30
Principle cell targets of injury
Mito, cell membrane, machinery for protein synthesis, DNA
31
Where is most intracellular Ca sequestered?
Mito and ER
32
Some initiators of cell adaptations
Physiologic changes (H’s, GFs), metabolic alterations, physical injury, infection, chronic irritation
33
Two checkpoints in mitosis and what they do
G2-M: check for damaged or Unduplicated DNA | G1-S: check for damaged DNA
34
When things accumulate in a cell, where can they accumulate?
Cytoplasm, in organelles, in nucleus
35
How does caloric restriction increase longevity (two ways)
1. Reduces signal intensity of IGF-1 pathway 2. Increases sirtuins-> contributes to metabolic adaption of caloric restriction + promote genomic integrity by activating DNA repair enzymes