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Basics of Path > Cell Adaptation, Injury, and Death > Flashcards

Cell Adaptation, Injury, and Death Flashcards

1
Q

What are 3 cellular mechanisms of hypertrophy?

A
  1. Gene activation
  2. Protein synthesis
  3. Production of organelles
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2
Q

What is the mechanism for hyperplasia?

A

Production of new cells from stem cells

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3
Q

When do hyperplasia and hypertrophy occur together?

A

Uterus - pregnancy

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4
Q

Permanent tissue can only undergo _________.

A

Hypertrophy

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5
Q

What are 3 main permanent tissue?

A
  1. Cardiac myocytes
  2. Skeletal muscle
  3. Nerves
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6
Q

Pathologic hyperplasia can lead to cancer. What is the exception?

A

BPH

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7
Q

Atrophy

A

A decrease in size and number of cells

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8
Q

By what mechanisms does atrophy occur?

A
  1. Ubiquitin-proteosome degradation of cytoskeleton
  2. Autophagy of cellular components -vacuoles/ lysosomes
  3. Apoptosis
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9
Q

Metaplasia

A

Change in cell type to handle stress

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10
Q

Barrett Esophagus

A

Change of esophageal squamous epithelium to columnar (non-ciliated, mucinous) epithelium of stomach - acid reflux

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11
Q

How does metaplasia occur?

A

Reprogramming stem cells, reversible with removable of driving stressor

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12
Q

Metaplasia can progress to dysplasia and cancer except for ____________.

A

Apocrine metaplasia - seen w/ fibrocystic change of breast

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13
Q

_________ deficiency can result in metaplasia.

A

Vitamin A - necessary for maintenance of specialized epithelium i.e. conjunctiva (squamous thickening keratomalacia)
Night blindness, immune deficient (maturation), metaplasia

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14
Q

Myositis ossificans

A

Mesenchymal tissue metaplasia
Inflammation (trauma) of sk muscle –> Bone
**doesn’t grow off bone

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15
Q

Dysplasia

A

Disordered cellular growth - proliferation of precancerous cells (CIN) - from longstanding pathologic hyperplasia or metaplasia

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16
Q

Is dysplasia reversible?

A

Yes

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17
Q

If stress persists, what does dysplasia proceed to?

A

Carcinoma (irreversible)

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18
Q

Aplasia

A

Failure of cell production during embryogenesis - unilateral renal agenesis

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19
Q

Hypoplasia

A

Dec. in cell production during embryogenesis - small organ - streak ovary in Turner syndrome

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20
Q

Likelihood of injury depends on what 3 things?

A

Stress, severity, and type of cell affected

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21
Q

What type of cell is most affected by hypoxia?

A

Nerve cells

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22
Q

Hypoxia

A

Low oxygen delivery to tissue - Low ATP - cellular injury

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23
Q

What are the 3 major causes of hypoxia?

A

Ischemia, hypoxemia, dec. carrying ability of blood (anemia, CO)

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24
Q

What are 3 mechanisms of ischemia?

A
  1. Block artery
  2. Block hepatic vein - Budd-Chiari Syndrome
  3. Shock
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25
Q

Hypoxemia

A

Low partial pressure of oxygen in the blood (PaO2 < 60 mmHg or SaO2 <90%)

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26
Q

What are common causes of hypoxemia?

A
  1. High altitude,
  2. Inc PACO2 (hypovent, COPD)
  3. Interstitial fibrosis
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27
Q

Anemia

A

Dec in RBC mass

PaO2 normal and SaO2 normal (%)

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28
Q

CO poisoning

A

CO binds Hb more avidly than O2

PaO2 normal, SaO2 decreased - cherry red skin

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29
Q

Methemoglobinemia

A

Iron in heme is oxidized to Fe3+ - can’t bind O2
PaO2 is normal, SaO2 decreased - oxidant stress (sulfa and nitrate drugs) or newborns
Cyanosis w/ chocolate-colored blood - IV methylene blue

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30
Q

Hypoxia impairs ___________. which results in decreased ATP.

A

Oxidative phosphorylation

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31
Q

What 3 key things does low ATP disrupt.

A
  1. Na-K pump (Na/H2O builds up)
  2. Ca pump (Ca builds up in cytosol)
  3. Aerobic glycolysis (lactic acid)
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32
Q

What are the findings of reversible injury?

A
  1. Cellular swelling

2. Loss of microvilli, membrane blebbing and swelling of RER (dec protein synthesis)

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33
Q

What are the findings of irreversible damage?

A
  1. Plasma membrane damage
    ~Ruptured cell, leaking enzymes, and Inc Ca
  2. Mitochondrial membrane damage (Inner membrane) e transport - cytochrome c
  3. Lysosome membrane damage - autophagy
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34
Q

Morphologic hallmark of cell death is loss of _________.

A

Nucleus

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35
Q

Loss of nucleus can occur via which 3 mechanisms?

A

Pyknosis, karyorrhexis, and karyolysis

36
Q

Pyknosis

A

Nucleus shrinks down

37
Q

Karyorrhexis

A

Nucleus breaks down into pieces

38
Q

Karyolysis

A

Nucleus breaks down farther into building blocks

39
Q

Necrosis

A

Death of a large group of cells, followed by acute inflammation

40
Q

Necrosis is always due to underlying _________ process.

A

Pathologic

41
Q

Coagulative necrosis

A

Necrotic tissue that remains firm - cell shape/organ structure are preserved, nucleus disappears

42
Q

Ischemic infarction of any solid organ leads to _____________.

A

Coagulative necrosis - not brain

43
Q

Area of infarcted tissue is often ______-shaped and _____.

A

Wedge

Pale

44
Q

Red infarction

A

Blood re-enters a loosely organized tissue

45
Q

Liquefactive necrosis

A

Necrotic tissue becomes liquefied - enzymatic lysis of cells and proteins

46
Q

What are the characteristic instances of liquefactive necrosis?

A
  1. Brain infarction (microglial)
  2. Abscess (neutrophils)
  3. Pancreatitis (pancreatic enzymes)
47
Q

Why does a brain infarction result in liquefactive necrosis?

A

The microglial cells contain hydrolytic enzymes

48
Q

Gangrenous necrosis - dry

A

Coagulative necrosis that resembles mummified tissue - Ischemia of lower limb and GI

49
Q

Gangrenous necrosis - wet

A

Coagulative necrosis w/ superimposed infection - liquefactive

50
Q

Caseous necrosis

A

Soft, friable necrotic tissue “cottage cheese like” appearance - TB infection or fungal
Characteristic granulomatous inflammation - combo

51
Q

Fat necrosis

A

Necrotic adipose tissue w/ chalky-white appearance - deposition of calcium – saponification (FA + Ca)

52
Q

What two types of necrosis are seen with pancreatitis

A

Fat (peripancreatic fat) and Liquefactive (pancreas)

53
Q

Where is fat necrosis seen?

A
  1. Trauma to fat e.g. breast

2. Pancreatitis-mediated damage of peripancreatic fat

54
Q

Saponification

A

FA released by trauma or lipase join w/ Ca (dystrophic calcification)

55
Q

Dystrophic Calcification

A

Dead/dying tissue is a deposit site for Ca - serum Ca and PO4 is normal

56
Q

Metastatic Calcification

A

Serum Ca or serum PO4 is elevated and forces Ca into tissues which then precipitates out

57
Q

Fibrinoid necrosis

A

Necrotic damage to blood vessel wall - leaking of protein into vessel wall – bright pink staining

58
Q

What is fibrinoid necrosis characteristic of?

A
  1. Malignant HTN
  2. Vasculitis
  3. Preeclampsia (30 yo woman)
59
Q

Apoptosis

A

Energy-dependent, genetically programmed cell death - single cell or small groups of cells

60
Q

What are 3 morphological characteristics of apoptosis?

A
  1. Dying cell shrinks (eosinophilic)
  2. Nucleus condenses and fragments
  3. Apoptotic bodies fall from cell and are removed by macrophages (no inflammation)
61
Q

Apoptosis is mediated by __________ which activate ___________ and ______________.

A
  1. Caspases
  2. Proteases (cytoskeleton)
  3. Endonucleases (DNA)
62
Q

What are the 3 pathways that can activate caspases?

A
  1. Intrinsic
  2. Extrinsic receptor-ligand
  3. CD8+ T cell via perforins and granzymes
63
Q

Intrinsic mitochondrial pathway

A

Cellular injury, DNA damage, or dec. hormal stim will inactivates Bcl2 -> Cytochrome c leaves from inner mitochondrial matrix into cytoplasm

64
Q

Extrinsic receptor-ligand pathway

A

FAS ligand binds FAS death receptor on target cell or

TNF binds TNF receptor

65
Q

How are free radicals generated pathologically?

A
  1. Ionizing radiation (OH*) hydroxyl
  2. Inflammation
  3. Metals (Cu and Fe)
  4. Drugs/chemicals
66
Q

What is the most damaging free radical?

A

The Hydroxyl radical OH*

67
Q

How does iron generate a free radical, and what is the most common?

A
  1. Fenton reaction

2. Hydroxyl

68
Q

How do free radicals cause damage?

A
  1. Peroxidation of lipids

2. Oxidation of DNA and proteins

69
Q

What are 3 ways the body can eliminate free radicals?

A
  1. Antioxidants (Vita A, C, E)
  2. Metal carrier proteins (transferrin)
  3. Enzymes
70
Q

What 3 enzymes are important for the elimination of free radicals?

A
  1. SOD (O2-)
  2. Glutathione peroxidase (OH*)
  3. Catalase (H2O2)
71
Q

Where is CCl4 commonly seen, and where is it converted to CCl3? What is the classic histologic finding?

A
  1. Dry Cleaning
  2. Liver
  3. Fatty Liver (RER swelling/no Apolipoprotein)
72
Q

What is the main way a reperfusion injury causes damage?

A

Return of oxygen and inflammatory cells to dead cells generates free radicals

73
Q

A patient undergoing a myocardial infarction is taken to the cath lab. After the artery is opened up, the cardiac enzymes continue to rise, why?

A

Reperfusion injury - damage to cardiac myocytes by free radicals

74
Q

Amyloid

A

Misfolded protein that deposits in extracellular space

75
Q

What are the common characteristics of amyloid

A
  1. Beta-pleated sheet config
  2. Congo red staining and apple-green birefringence under polarized light
  3. Tends to deposit around blood vessels
76
Q

Primary amyloidosis

A

Systemic deposition of AL amyloid - derived from Ig light chain

77
Q

What is primary amyloidosis associated with?

A

Plasma cell dyscrasias (more light than heavy chain)

78
Q

Secondary amyloidosis

A

Systemic deposition of AA amyloid derived from SAA

79
Q

SAA

A

Acute phase reactant that is increased in chronic inflammatory states, malignancy and familial mediterranean fever

80
Q

Familial Mediterranean fever

A

Dysfunction of neutrophils (AR) - fever and acute serosal inflammation –> High SAA during attacks deposits as AA amyloid

81
Q

Classic clinical findings of systemic amyloidosis (3)

A
  1. Nephrotic syndrome (most commonly involved)
  2. Restrictive cardiomyopathy or arrhythmia
  3. Tongue enlargement, malabsorption, and hepatosplenomegaly
82
Q

Senile cardiac amyloidosis

A

Non-mutated serum transthyretin deposits in heart - usually asymptomatic

83
Q

Familial amyloid cardiomyopathy

A

Mutated serum transthyretin deposits in heart - restrictive cardiomyopathy - 5% of AA

84
Q

Type II Diabetes

A

Amylin deposits in islets of pancreas - derived from insulin

85
Q

Alzheimer Disease

A

Abeta amyloid deposits in brain forming plaques - derived from beta-amyloid precursor protein (Chrom 21)

86
Q

Dialysis-associated amyloidosis

A

beta2-microglobulin deposits in joints - not filtered well

87
Q

Medullary carcinoma of thyroid

A

Calcitonin deposits within tumor - tumor cells w/ an amyloid background

Basics of Path (5 decks)

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