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Pathology > EXAM 1 PATH (cell injury and cell death) > Flashcards

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
Q

How does increasing mitochondria assist cells in response to stress?

A
  • increases in number and sizes of mitochondria
  • often seen in hypertrophied cells
  • may affect mitochondrial function
  • more energy
26
Q

Explain the cell’s mechanism of remodeling the cytoskeleton in response to stress

A
  • changes in amount and configuration of filaments, microtubules, and contractile proteins
  • often in response to physical stress
  • may be affected by some drugs
27
Q

Explain the cell’s mechanism of neutralization of free radicals in response to stress

A 
Exogenous antioxidants (blueberries) 
Increased activity of antioxidant enzymes 
-superoxide dismutase 
-catalase 
-glutathione peroxidase
28
Q

What is ischemia/reperfusion injury?

A
  • 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
Q

What are the mechanisms of ischemia/reperfusion injury?

A

Increased activity of ROS:
-incomplete glucose metabolism of damaged mitochondria
-damage to cell antioxidants
Inflammation

30
Q

Where is ischemia/reperfusion injury seen clinically?

A

Heart attack and stroke

31
Q

What are reversible changes of cell injury and death morphology?

A
  • Cell swelling
  • fatty change (liver, heart)
  • mild/localized cytoplasmic eosinophilia
32
Q

What are irreversible changes of cell injury and death morphology?

A
  • Deep cytoplasmic eosinophilia

- Calcification

33
Q

What are nuclear changes of cell injury and death morphology

A
  • Dissolution (karyolysis)
  • Fragmentation (karyorrhexis)
  • Condensation and shrinkage (pyknosis)
34
Q

What are 6 types of tissue/organ necrosis?

A
  • Coagulative
  • Liquefactive
  • Gangrenous
  • Caseous
  • Fat
  • Fibrinoid
35
Q

What is coagulative necrosis?

A
  • 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
Q

What is liquefactive necrosis?

A

-complete digestion of necrotic cells, with liquefaction of tissue
Ex:
-some types of infectious disease (abscess)
-infarcts in CNS (stroke)

37
Q

What is Gangrenous necrosis?

A
  • 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
Q

What is Caseous necrosis?

A
  • 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
Q

What is fat necrosis?

A
  • enzymatic (lipase) destruction of adipose tissue and triglycerides
  • fatty acids combine with calcium to form chalky, soap-like deposits saponification
  • characteristic of pancreatitis
40
Q

What is fibrinoid necrosis?

A
  • 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
Q

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:

A

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
Q

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:

A

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
Q

What are physiologic causes and examples of apoptosis?

A

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
Q

What are pathologic causes and examples of apoptosis ?

A 
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
Q

What are the intrinsic mechanisms of apoptosis?

A

Injurious stimulus–>Activation of Bcl-2–>leakage of mitochondrial proteins–>
ACTIVATION OF CASPASES–>nucleases, proteases,–> apoptotic body–>clearance by macrophages

46
Q

What are the extrinsic mechanisms of apoptosis?

A

Binding of surface receptor and external (T-cell ligand)–> activation of adapter proteins–>
ACTIVATION OF CASPASES–>nucleases, proteases,–> apoptotic body–>clearance by macrophages

47
Q

What are common intracellular accumulations?

A
  • Fat
  • Cholesterol
  • Glycogen
  • Pigments (lipofuscin, carbon, melanin, iron)
  • Calcium
48
Q

Give examples of fat accumulations in cells

A
  • 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
Q

Give examples of cholesterol accumulations in cells

A
  • Macrophages (foam cells)
  • vascular smooth muscles (atherosclerosis)
  • subcutaneous tissue (xanthomas)
50
Q

Give examples of glycogen accumulation in cells

A
  • normal in hepatocytes (glycogen stores)
  • abnormal amounts and/or accumulation in other tissues in: Diabetes, glycogen storage diseases
  • can be physiologic
51
Q

Give examples of pigments (lipofuscin) accumulations in cells

A
  • 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
Q

Give examples of pigment (iron) accumulations in cells

A
  • 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
Q

Give examples of pigment (carbon) accumulations in cells

A 
Ubiquitous pigment 
-air pollutants
-tobacco smoke
Accumulates in: 
-lungs 
-medistinal lymph
Imparts black appearance in tissues
54
Q

What is dystrophic calcification?

A
  • 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
Q

What is metastatic calcification

A
  • 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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