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EXAM 1 PATH (cell injury and cell death) Flashcards

1
Q

What are the cells four adaptations to stress?

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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2
Q
  • Increase in cell size
  • Usually enlarges entire organ
  • Caused by increased workload or hormonal stimulation
A

Hypertrophy

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3
Q
  • Increase in numbers of cells
  • usually increase size of organ
  • EX: breast enlargement during puberty; enlargement of endocrine organs; prostatic and endometrial hyper_____
A

Hyperplasia

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4
Q
  • Changes in cell/tissue (usually epithelial), from one type to anther
  • Usually in response to mechanical or chemical stress; may be physiologic
A

Metaplasia

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5
Q

-Decrease in cell size
-May cause shrinkage of organ
Causes:
-decreased workload (immobilization)
-denervation
-decreased blood supply
-loss of nutrition
-decreased endocrine stimulation
-aging

A

Atrophy

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6
Q

A type of cell death that is:
-always pathologic
-usually affects larger groups of cells; may be visible grossly
-often accompanied by inflammation
-causes enzymatic destruction of cell contents with disruption of cell membrane
-leakage of cell enzymes may be detectable by lab tests
-cell just falls apart
Ex: cardiac infarction

A

Necrosis

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7
Q

A type of cell death that is:

  • individual or programmed
  • nuclear dissolution with formation of apoptotic bodies
  • these bodies are rapidly cleared by macrophages
  • no trace of destroyed cell because membrane stays in tact
  • may be pathologic or physiologic
A

Apoptosis

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8
Q

What are causes of cell injury?

A
  • Hypoxia
  • Chemical injury
  • Physical injury
  • Infectious agents
  • Immunologic reactions (inflammation, autoimmune/allergic reactions)
  • Genetic/congenital defects
  • nutritional disorders
  • aging
  • idiopathic (we have no fucking clue)
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9
Q

A 62 year old man complains of increased frequency and difficulty of urinary voiding. Physical examination and imaging studies show a moderately enlarged prostate gland, and needle biopsy shows increased numbers of glands without evidence of cancer. The process is most accurately characterized as:

A

Hyperplasia

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10
Q

What are the four main mechanisms of cell injury?

A
  • Free radical damage (chemical injury)
  • Depletion of ATP
  • Damage to DNA and proteins (may cause apoptosis)
  • Alteration in calcium balance
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11
Q

What are the major cell structures that are the targets of cell injury?

A
  • Membranes (altered permeability)
  • mitochondria (ability to produce energy)
  • nucleus (chromatin) (ability to replicate)
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12
Q

What is a free radical?

A
  • any molecule with an unpaired electron

- unstable and reactive

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13
Q

What are free radicals created by?

A
  • Normal cell processes
  • radiation
  • chemicals and drugs
  • inflammation
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14
Q

What is a reactive oxygen species?

A

A type of free radical derived from oxygen, normal respiration

  • catalyzed by iron and copper
  • Exacerbated by some drugs: antimalarials, sulfonamides, nitrofurantoin
  • Causes: oxidative stress
  • EX: H202, Superoxide (O2-0, hyrdoxyl radica (OH-)
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15
Q

What are the effects of free radicals?

A
  • Peroxidation of membrane lipids (defects in membrane permeability)
  • Cross-linking/fragmentation of proteins (structural damage, loss of enzyme activity)
  • DNA damage (neoplastic transformation, when damage is irreversible: apoptosis)
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16
Q

What are the major causes of ATP depletion?

A
  • Hypoxia
  • Malnutrition
  • Mitochondrial damage
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17
Q

What are the major effects of ATP depletion?

A 
Increased membrane permeability:
-failure of ion pumps
-decreased phospholipid synthesis 
Accumulation of lactic acid 
-due to increase in glycolysis 
-decrease in cell pH
Decrease in protein synthesis
-due to structural alteration in rough ER
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18
Q

What are the causes of defective membrane permeability?

A
  • Ischemia (low blood supply
  • Chemical and microbial toxins
  • ROS
  • Complement
  • Increased intracellular calcium
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19
Q

What happens after defective membrane permeability?

A
  • Cell membrane: Cell swelling/lysis
  • Mitochondrial membrane: depletion of ATP, release of apoptotic proteins
  • Lysosomal membrane: release of proteolytic enzymes/nucleases (CAUSES A SHIT TON OF FUCKING PROBLEMS)
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20
Q

What are the mechanisms for an increase in intracellular calcium?

A
  • release of organelle calcium stores

- influx across cell membrane

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21
Q

What are the effects of an increase in intracellular calcium?

A
  • Damage of mitochondria
  • Activation of enzymes: proteases, phospolipases, nucleases, ATPase (all of these get activated because of influx, most of these will end up breaking things down in the cell)
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22
Q

What are the sub cellular response mechanisms to stress?

A
  • autogaphy (eats bad parts of cells)
  • induction of smooth endoplasmic reticulum
  • increase in mitochondria
  • remodeling of cytoskeleton
  • neutralization of free radicals
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23
Q

What is autophagy?

A
  • The cell eats itself
  • Lysosomal digestion of a portion of cytoplasm and organelles
  • Usually in response to chronic nutrient deprivation
  • May progress to apoptosis if injury is severe enough
24
Q

What is does the Smooth ER do in response to stress?

A

-Metabolizes drugs and chemicals
-Increases metabolic capacity
EX: development of tolerance to effects of certain drugs due to induction of hepatic SER

25
How does increasing mitochondria assist cells in response to stress?
- increases in number and sizes of mitochondria - often seen in hypertrophied cells - may affect mitochondrial function - more energy
26
Explain the cell's mechanism of remodeling the cytoskeleton in response to stress
- changes in amount and configuration of filaments, microtubules, and contractile proteins - often in response to physical stress - may be affected by some drugs
27
Explain the cell's mechanism of neutralization of free radicals in response to stress
``` Exogenous antioxidants (blueberries) Increased activity of antioxidant enzymes -superoxide dismutase -catalase -glutathione peroxidase ```
28
What is ischemia/reperfusion injury?
- Paradoxial exacerbation of injury to ischemic tissue following restoration of blood flow - even after the blood flow is fixed you still see problems - mostly because of free radical damage, they are still present even after returning blood flow
29
What are the mechanisms of ischemia/reperfusion injury?
Increased activity of ROS: -incomplete glucose metabolism of damaged mitochondria -damage to cell antioxidants Inflammation
30
Where is ischemia/reperfusion injury seen clinically?
Heart attack and stroke
31
What are reversible changes of cell injury and death morphology?
- Cell swelling - fatty change (liver, heart) - mild/localized cytoplasmic eosinophilia
32
What are irreversible changes of cell injury and death morphology?
- Deep cytoplasmic eosinophilia | - Calcification
33
What are nuclear changes of cell injury and death morphology
- Dissolution (karyolysis) - Fragmentation (karyorrhexis) - Condensation and shrinkage (pyknosis)
34
What are 6 types of tissue/organ necrosis?
- Coagulative - Liquefactive - Gangrenous - Caseous - Fat - Fibrinoid
35
What is coagulative necrosis?
- Main pattern in ischemic necrosis (infract) - Ghost outlines of cells without nuclear staining (the nuclei don't stain here, structure is there but not nuclei) - Tissue is grossly firm and/or discolored - Gradually replaced by macrophages and scar tissue
36
What is liquefactive necrosis?
-complete digestion of necrotic cells, with liquefaction of tissue Ex: -some types of infectious disease (abscess) -infarcts in CNS (stroke)
37
What is Gangrenous necrosis?
- Coagulative necrosis of an extremity due to prolonged ischemia - May be accompanied by liquefactive necrosis with secondary infection ("wet gangrene") - can be wet or dry
38
What is Caseous necrosis?
- From the german word of cheese - Tissue broken down to granular, cheese-like substance - Characteristic of tuberculosis and some fungus infections - occurs mostly in lungs - usually infectious agents (fungal, bacterial)
39
What is fat necrosis?
- enzymatic (lipase) destruction of adipose tissue and triglycerides - fatty acids combine with calcium to form chalky, soap-like deposits saponification - characteristic of pancreatitis
40
What is fibrinoid necrosis?
- Distinctive type of necrosis associated with immunologic disease - antigen-anitbody complexes combine with fibrin to form deeply eosinophilic "fibrinoid" - really hard to see grossly - associated with immune reactions
41
A 16 year old girl is diagnosed with epilepsy after suffering a grand mal seizure, and is started on phenobarbital. Serum drug level is in the therapeutic range two weeks after beginning the medication. At a checkup six months later, on the same dose, a repeat serum drug level is subtherapeutic. The decrease in serum drug level is most likely related to:
Increased drug metabolism due to hypertrophy of hepatic endoplasmic reticulum. - since the biopsy showed increased numbers of glands (and by extension gland cells). - Hypertrophy would show increase in size of individual gland cells - atrophy would show decrease in number of cells, and metaplasia would show a different type of tissue.
42
A 42 year old man complains of a cough. Chest x-ray shows a lung mass, which is surgically resected. Gross examination of the mass shows a yellow-white, granular cut surface. Culture of the mass is positive for the fungus Histoplasma. Microscopic examination of the mass will most likely show:
Caseous necrosis. - since the mass is composed of granular material and is associated with a fungal infection. - Gangrenous and coagulative necrosis would be associated with ischemia, and fibrinoid necrosis would be associated with an immune reaction. - Cancer would not normally coexist with a fungal infection.
43
What are physiologic causes and examples of apoptosis?
Withdrawal of growth factors: - breakdown of endometirume during menstruation - cell loss in proliferating populations (skin, intestinal mucosa) - elimination of inflammatory cells after inflammatory stimulus is eliminated - involution of cells/tissue during embryonic/fetal development
44
What are pathologic causes and examples of apoptosis ?
``` DNA damage: -radiation injury -chemotherapy -some viral infections Immune reactions: -graft-versus-host diseases (GVHD) -elimination of virus infected cells Accumulation of abnormal proteins -neurodegenerative dieseases ```
45
What are the intrinsic mechanisms of apoptosis?
Injurious stimulus-->Activation of Bcl-2-->leakage of mitochondrial proteins--> ACTIVATION OF CASPASES-->nucleases, proteases,--> apoptotic body-->clearance by macrophages
46
What are the extrinsic mechanisms of apoptosis?
Binding of surface receptor and external (T-cell ligand)--> activation of adapter proteins--> ACTIVATION OF CASPASES-->nucleases, proteases,--> apoptotic body-->clearance by macrophages
47
What are common intracellular accumulations?
- Fat - Cholesterol - Glycogen - Pigments (lipofuscin, carbon, melanin, iron) - Calcium
48
Give examples of fat accumulations in cells
- most common in liver - caused by anything that affects fat metabolism: chemicals (drugs, alcohol), diabetes, marked obesity, malnutrition - morphology-cells with fat vacuoles (clear on H&E stain)
49
Give examples of cholesterol accumulations in cells
- Macrophages (foam cells) - vascular smooth muscles (atherosclerosis) - subcutaneous tissue (xanthomas)
50
Give examples of glycogen accumulation in cells
- normal in hepatocytes (glycogen stores) - abnormal amounts and/or accumulation in other tissues in: Diabetes, glycogen storage diseases - can be physiologic
51
Give examples of pigments (lipofuscin) accumulations in cells
- yellow-brown protein-lipid complex "wear and tear pigment" - product of free-radical per oxidation of membrane lipids - increased with age and in atrophic tissues
52
Give examples of pigment (iron) accumulations in cells
- stored in tissues as iron-protein complexes (hemosiderin) - small amounts normal in liver and bone marrow - abnormal amounts (hemosiderosis) in: - -increased RBC breakdown (chronic hemorrhage, multiple blood diffusions, hemolytic anemia) - -Defects in iron metabolism (some types of anemia, hemochromatosis)
53
Give examples of pigment (carbon) accumulations in cells
``` Ubiquitous pigment -air pollutants -tobacco smoke Accumulates in: -lungs -medistinal lymph Imparts black appearance in tissues ```
54
What is dystrophic calcification?
- deposition of calcium in previously damaged or abnormal tissue (atherosclerosis, damaged cardiac valves, some tumors (psammonia bodies) - usually associated with normal systemic calcium metabolism
55
What is metastatic calcification
- deposition of calcium in normal tissue - always associated with defective calcium metabolism (parathyroid disease, bone disease, renal disease, vitamin D deficiency)

Pathology (4 decks)

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