Cell Injury & Adaptation Flashcards

(49 cards)

1
Q

What is the difference between reversible and irreversible cell injury?

A

Reversible: Cell can recover if stress is removed
Irreversible: Leads to cell death

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2
Q

What causes hydropic swelling?

A

Increased water inside the cell due to failure of the Na⁺/K⁺ ATPase pump → Na⁺ builds up → water follows.

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3
Q

What are the cellular effects of hydropic swelling on organelles?

A

ER: Swelling, ribosomes detach → ↓ protein synthesis
Mitochondria: Swelling → ↓ ATP production
Plasma membrane: Blebbing (still reversible)
Nucleus: Nucleolar segregation → disrupted rRNA processing

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4
Q

What is ischemia?

A

A condition where blood flow (and thus oxygen) is restricted or reduced, causing hypoxia and ATP depletion.

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5
Q

What is oxidative stress?

A

Imbalance between reactive oxygen species (ROS) production and antioxidant defenses.

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6
Q

What are 3 major ROS molecules?

A

Superoxide (O₂⁻)
Hydrogen peroxide (H₂O₂)
Hydroxyl radical (OH∙)

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7
Q

Which ROS is most reactive and damaging?

A

Hydroxyl radical (OH∙)

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8
Q

What does lipid peroxidation result in?

A

Membrane damage due to ROS attacking unsaturated fatty acids.

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9
Q

How do ROS damage proteins?

A

By oxidizing sulfur and nitrogen-containing amino acids → fragmentation, cross-linking, and degradation.

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10
Q

How do ROS affect DNA?

A

They cause strand breaks, base modifications, and cross-links → mutations and cell death.

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11
Q

What enzymes protect against ROS damage?

A

SOD (Superoxide dismutase) – converts O₂⁻ → H₂O₂
Catalase – converts H₂O₂ → H₂O + O₂
Glutathione peroxidase (GPX) – detoxifies H₂O₂ and lipid peroxides

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12
Q

What vitamins act as ROS scavengers?

A

Vitamin C, Vitamin E, Retinoids (Vitamin A derivatives)

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13
Q

What role does nitric oxide (NO) play in oxidative stress?

A

Can be protective or damaging; reacts with O₂⁻ to form peroxynitrite (ONOO⁻), a harmful compound.

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14
Q

What is the role of p53 in oxidative stress?

A

Repairs DNA or promotes cell survival
If stress is severe, promotes cell death by impairing oxidant defenses

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15
Q

What are the main cellular adaptations to stress?

A

Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia

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16
Q

What is atrophy and what causes it?

A

A decrease in cell size or function caused by:
Disuse
Ischemia
Nutrient deficiency
Hormone loss
Aging
Chronic inflammation
Pressure (e.g., bed sores)

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17
Q

What is the cellular mechanism behind atrophy?

A

↓ Protein synthesis
↑ Protein degradation (via ubiquitin-proteasome pathway)

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18
Q

Differentiate between reversible cell shrinkage and irreversible cell loss in atrophy.

A

Reversible: cells reduce in size but can recover
Irreversible: excessive cell death (e.g., Alzheimer’s) leads to permanent tissue atrophy

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19
Q

What is hypertrophy?

A

An increase in cell size (and organ size) in response to increased demand or trophic signals.

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20
Q

Give examples of physiological vs pathological hypertrophy.

A

Physiological: Exercise, pregnancy
Pathological: Hypertension, valve disease → cardiac hypertrophy

21
Q

What signaling pathway promotes muscle hypertrophy?

A

The Akt pathway, which promotes protein synthesis and inhibits apoptosis.

22
Q

What is hyperplasia and when does it occur?

A

Increase in cell number due to:
Hormonal stimulation (e.g., endometrium)
Increased demand (e.g., bone marrow at high altitude)
Chronic injury/inflammation
Immune response (e.g., lymphoid hyperplasia)

23
Q

What is metaplasia?

A

A reversible change from one differentiated cell type to another better suited to stress (e.g., bronchial columnar → squamous in smokers)

24
Q

What is the clinical concern with metaplasia?

A

It’s protective but functionally inferior and can become preneoplastic if the stress persists.

25
What is dysplasia?
Disorganized cell growth and abnormal differentiation — often seen as precancerous.
26
Name three features of dysplastic tissue.
Loss of uniform architecture Nuclear atypia Loss of normal maturation
27
What is intracellular storage and when is it harmful?
Retention of materials in cells (normal or abnormal). Harmful when: Enzymes are missing (e.g., lysosomal diseases) Overload of normal substances (e.g., iron, fat, glycogen)
28
Name two harmful examples of intracellular lipid accumulation.
Fatty liver in alcoholism or diabetes Atherosclerosis from cholesterol buildup
29
What is lipofuscin and what does it indicate?
“Wear-and-tear” pigment from oxidative stress. Accumulates with age in neurons, heart, and liver.
30
What is anthracosis?
Inhaled carbon pigment stored in lungs (benign but visible in smokers/urban dwellers).
31
What is hemochromatosis?
A genetic disorder causing excessive iron absorption and storage → organ damage and ↑ cancer risk.
32
What is dystrophic calcification?
Calcium deposition in damaged tissues (e.g., atherosclerotic plaques) without hypercalcemia.
33
What is metastatic calcification and its causes?
Widespread calcium deposits in normal tissues due to hypercalcemia (e.g., chronic kidney disease, vitamin D toxicity).
34
What is muscle atrophy?
A reduction in muscle mass, strength, and function due to decreased protein synthesis and/or increased protein degradation.
35
What level of muscle mass loss is fatal?
Loss of ~40% of lean body mass is fatal; even 5% can impair function.
36
What are common causes of muscle atrophy?
Disuse (immobilization) Chronic diseases (e.g., cancer, CHF, COPD) Aging (sarcopenia) Malnutrition Inflammation (e.g., RA, AIDS)
37
What types of muscle fibers are most affected in aging-related atrophy (sarcopenia)?
Type II (fast-twitch) fibers.
38
What cellular changes occur in sarcopenia?
Reduced protein synthesis Loss of spinal motor neurons Hormonal decline (↓ IGF-1, testosterone, GH)
39
What system is the primary driver of protein degradation in muscle atrophy?
The ubiquitin–proteasome system (UPS).
40
Which transcription factor activates atrophy-related genes?
FOXO (forkhead box O) transcription factors.
41
What is the role of myostatin in muscle atrophy?
Myostatin inhibits muscle growth; ↑ myostatin = ↑ FOXO → ↑ protein breakdown.
42
Name key proteolytic systems involved in muscle protein degradation.
Ubiquitin–Proteasome System Caspase-3 Calpain (cleaves actomyosin) Autophagy-lysosome pathway
43
How does cancer cause muscle wasting (cachexia)?
Tumors release cytokines (e.g., TNF-α, IL-6), promoting lipolysis and proteolysis → muscle atrophy.
44
How does cardiac cachexia affect muscle?
Preferential loss of Type I (slow-twitch) fibers due to hypoxia and poor perfusion.
45
What role does inflammation play in disease-related muscle loss?
Chronic inflammation increases cytokines (TNF-α, IL-1β, IL-6), which activate protein degradation pathways.
46
What is the role of the Akt pathway in muscle?
Promotes hypertrophy by stimulating protein synthesis and inhibiting FOXO. Inhibition of Akt → muscle atrophy
47
Can muscle atrophy be reversed?
Yes, if the underlying cause is treated and muscle use is restored (due to satellite cell involvement in regeneration).
48
How do ACE inhibitors help with sarcopenia?
By preserving muscle strength, possibly through reducing angiotensin II–related catabolic signaling.
49
What is reperfusion injury?
Tissue damage that occurs when blood supply returns to tissue after ischemia, due to ROS burst, inflammation, and calcium overload.