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?

A

Nope

24
Q

Some clinical settings where necroptosis occurs

A

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

25
Q

Mechanism of pyroptosis

A

Microbe enters cell -> activate inflammasome -> activates caspase 1 -> forms IL-1

26
Q

Ferroptosis

A

Cell death triggered by excess intracellular Fe or ROS that overwhelms the antioxidant defenses -> lipid peroxidation -> cell death resembling necrosis

27
Q

Autophagy

A

Survival mechanism to maintain the integrity of cells by recycling essential metabolites and clearing debris

28
Q

What condition is autophagy usually associated with?

A

Atrophy

29
Q

Disease states where dysregulation of autophagy occurs

A

CA, IBD, neurodegenerative disorders

30
Q

Principle cell targets of injury

A

Mito, cell membrane, machinery for protein synthesis, DNA

31
Q

Where is most intracellular Ca sequestered?

A

Mito and ER

32
Q

Some initiators of cell adaptations

A

Physiologic changes (H’s, GFs), metabolic alterations, physical injury, infection, chronic irritation

33
Q

Two checkpoints in mitosis and what they do

A

G2-M: check for damaged or Unduplicated DNA

G1-S: check for damaged DNA

34
Q

When things accumulate in a cell, where can they accumulate?

A

Cytoplasm, in organelles, in nucleus

35
Q

How does caloric restriction increase longevity (two ways)

A
  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