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Cell Metabolism > Pathology > Flashcards

Pathology Flashcards

1
Q

Atrophy

A

Shrinkage of cell by loss of substance

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2
Q

Reasons for atrophy

A

Disuse, inadequate nutrients, lack of endocrine stimulus, poor blood supply, denervation, aging

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3
Q

Hypertrophy

A

Increase in SIZE of cell –> increasing organ size

Grows by creating more stuff (lipids, proteins glycogen, anabolic reactions)

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4
Q

Hyperplasia

A

Increase in NUMBER of cells

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5
Q

Reasons for hypertrophy and hyperplasia

A

Increased functional demand

Increase, work demand, metabolic demand, excess endocrine stimulus

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6
Q

Metaplasia

A

Replacement of one cell type with another cell type, usually less differentiated

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7
Q

Reasons for metaplasia

A

Increased capacity for tissue survival, persisting injury
Loss of normal cell function
Maintained if compromised–> Dysplasia

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8
Q

Causes of Cell Injury

A 
Oxygen deprivation
Chemical agents
Infectious agents
Immunologic reactions
Genetic factors
Nutritional imbalances
Physical agents
Radiation
Calcium
Aging
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9
Q

Oxygen Deprivation Categories

A

Ischemia- Tissue isnt receiving enough oxygen
Hypoxia- Cells are deprived
Anoxia- Complete loss of oxygen/blood

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10
Q

What negative outcomes occur due to hypoxia?

A

Decreases ATP
Failure of sodium-potassium pump, calcium pump
Hydropic degeneration –> Cellular swelling, membrane loses ability to regulate ion permeability
Reduced pH
Mitochondrial swelling
If not corrected cell will lyse

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11
Q

Reperfusion Injury

A

Rapid restoration of blood flow to ischemic tissue
Most damage occurs from mitochondrial dysfunction and subsequent free radical production
-Lipid peroxidation
-Alteration of DNA and proteins

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12
Q

Creation of Reactive Oxygen Species

A

Reduction of molecular oxygen creates superoxide O2-
Superoxide Dismutase creates H2O2
Hydrogen peroxide can then be converted to water by Catalase or Glutathione (Antioxidant enzyme)
If hydrogen peroxide is not converted it will form a hydroxyl radical

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13
Q

Asphyxial Injuries

A

Failure to receive or use oxygen

Suffocation, strangulation, chemical (CO and propane), drowning

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14
Q

What causes negative affects due to Calcium? And how is this propagated in the cell?

A

Ischemia and toxins increase intracellular Calcium in the Mitochondria, and smooth ER
Results in activation of cellular enzymes
Phospholipase & protease –> Membrane damage
Endonuclease –> Nuclear damage
ATPase–> reduced ATP

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15
Q

How can aging injure the cell

A

Environmental and metabolic insults –> DNA damage –> Mutations
Telomere shortening –> Decreased cell replication –> cell loss
Abnormal protein homeostasis –> Decrease functional proteins –> Decrease cell functions

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16
Q

What can accumulate in a cell due to injury?

A 
Lipid (triglycerides, cholesterol)
Protein
Glycogen
Water Pigments (melanin bilirubin)
Calcium (calcified heart valves)
Urate (deposits in joints)
17
Q

What are features of reversible cell injury?

A 
Cellular swelling
Fatty change (TG accumulate due to excessive intake, defective transport)
Altered ion flux
Mitochondrial swelling
Pynknosis
Membrane alterations (blebbing)
18
Q

Features of Irreversible Cell Injury

A

Same as reversible plus…
Increased eosinophilia
Greater nuclear changes

19
Q

Necrosis

A

Cell death associated with loss of cell integrity and leakage of cell contents eliciting local damage (inflammation)

20
Q

Apoptosis

A

Cell activates enzymes that degrade clls DNA, nuclear and cytoplasmic proteins.
Membrane remains intact and is phagocytosed, no inflammation

21
Q

Necrosis Nuclear changes

A

Pyknosis - Clumping of chromatin in the nucleus
Karyorrhexis- Fragmentation of nucleus
Karyolysis- Nuclear dissolution and chromatin lysis

22
Q

Necrosis Calcification occurs because

A

Dead cells can be degraded into fatty acids which bind calcium, resulting in calcification

23
Q

Dystrophic Calcification

A

Can happen in any necrosis

Likely to occur with atheroma with atherosclerosis (atrioventricular valves)

24
Q

Metabolic Calcification

A

Consequence of hypercalcemia
Can occur in any tissue
Bone destruction, Vit D disorders, renal failure

25
Q

Patterns of Tissue Necrosis (6)

A 
Coagulative Necrosis
Liquefactive Necrosis
Caseous Necrosis
Fat Necrosis
Fibrinoid Necrosis
Gangrenous Necrosis
26
Q

Coagulative Necrosis occurs in? Result from?

A

Kidneys, heart, spleen, and adrenal gland
Protein denaturation
-Albumin changes into an opaque state

27
Q

Liquefactive Necrosis

A

Neurons and glial cells

Hydrolytic enzymes

28
Q

Caseous Necrosis

A

Combination of coagulative and liquefactive

Often enclosed in granuloma

29
Q

Fat necrosis

A

Pancreas, breast, abdominal organs
Action of lipases (saponification)
FFA + Calcium

30
Q

Fibrinoid Necrosis

A

Arteries

Complexes of antigens and antibodies are deposited on the walls of arteries

31
Q

Gangrenous Necrosis, 2 types

A

Result of hypoxia, limbs not organs
Dry
-Insufficient blood, coagulative, dry, crusty, black
Wet
-Infection, liquefactive, cold, swollen, black, foul odor, pus

32
Q

Apoptosis Cell Morphology

A

Cell shrinkage, pyknosis, apoptotic bodies

33
Q

Causes of Apoptosis, Physiologic

A 
During embryogenesis
Hormone deprivation
Proliferating populations
End of usefulness
Elimination of WBC
34
Q

Causes of Apoptosis, Pathologic

A

DNA damage
Accrual of misfolded proteins
Injury from infection

35
Q

Apoptosis, Intrinsic path

A

Mitochondrial, depends on mito membrane permeability
Injurious stimuli (loss of growth factor, DNA damage, protein misfolding)
BCL-2 inhibition –> BAX/BAK activation–> Cytochrome C leaves mito–>Caspases activated

36
Q

Apoptosis, Extrinsic

A

Death receptor activated by TNF–> caspases

37
Q

What do caspases cause?

A

Nuclear fragmentation
Cytoplasmic blebbing
Formation of apoptotic bodies
Phagocytosis of bodies

38
Q

Autophagy

A

Lysosomal digestion of cells components
Survival in times of starvation
Excessive autophagy will activate apoptosis

Cell Metabolism (16 decks)

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