Week 6 Tissue Injury- Nelson Flashcards

1
Q

Hypertrophy

A

increased SIZE of cell leads to increase in size of organ or tissue

Results from increased production of cellular proteins

increased demand or stimulation

Ex: Thickness of left ventricle, uterus after pregnancy

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2
Q

Hyperplasia

A

increased NUMBER of cells leads to increase in organ or tissue

occurs if the cells of the organ can divide

increased demand or stimulation

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3
Q

Atrophy

A

decreased nutrients and decreased stimulation

Decrease in cell SIZE and NUMBER resulting in reduced size of tissue or organ

Common causes:
Decreased workload
loss of innervation
diminished blood supply
inadequate nutrition
loss of endocrine stimulation
pressure
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4
Q

Metaplasia

A

chronic irritation
adaptive response in which one differentiated type of cell is replaced by another cell type

Reprogramming of stem cells in normal tissue OR reprogramming of undifferentiated mesechymal cells

External stimuli

Ex: normal columnar epithelium changed to squamous metaplasia in lungs (loosing cilia) in smokers

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5
Q

Necrosis

A

loss of membrane integrity
Microscopic changes:
nucleus fades away, shrinks, cell content leaked out

specific proteins and enzymes can be detected in blood as diagnostic test

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6
Q

Apoptosis

A

Characterized by induction of REGULATED enzymatic suicide program that active intrinsic enzyme to degrade cells own DNA and nuclear/ cytoplasmic proteins

Causes:
DNA damage
accumulation of misfolded proteins
viral infection

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7
Q

Coagulative necrosis

A

architecture of dead tissue is preserved (infarct)

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8
Q

Liquefactive necrosis

A

digestion of the dead tissue results in liquid viscous mass, typically seen in focal bacteria or fungal infections. Lots of pus filled with neutrophils

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9
Q

Gangenous necrosis

A

clinical term, not specific. usually applied to necrosis of a limb undergoing coagulative ischemic necrosis

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10
Q

caseous necrosis

A

cheese-like necrosis associated with necrotizing granulomas

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11
Q

fat necrosis

A

focal areas of fat destruction

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12
Q

Fibrinoid necrosis

A

necrosis seen in immune reactions involving vessels

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13
Q

Describe mechanism of cell injury due to depletion of ATP

A

ATP is required for all synthetic degradative processes in the cell

caused by reduced blood supply of oxygen and nutrients, mito changes or exposure to certain toxins

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14
Q

Describe mechanism of cell injury due to mitochondrial damage

A

mito supply ATP to the cell through oxidative phosphorylation

damage caused by oxygen deprivation, oxygen free radials, increased cytosolic Ca+

results in defect in mito membrane, failure of ETC, depletion of ATP, formation of reactive oxygen species
escape of mitochondrial membrane proteins (cytochrome C)

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15
Q

Describe mechanism of cell injury due to influx of calcium and loss of calcium homeostasis

A

this may cause

mito membrane defect, no ATP generation, activation of lytic enzymes, induce apoptosis

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16
Q

Describe mechanism of cell injury due to oxygen derived free radials

A

Caused when production of ROS increases, scavenging systems are ineffective, or oxidative stress

may cause wide variety of conditions and diseases (chemical and radiation injury, ischemia reperfusion, cancer, aging, degenerative diseases

17
Q

Mechanism of cell injury due to defects of membrane permeability

A

can occur due to ROS, decreased phospholipid synthesis (or increased breakdown), cytoskeleton abnormalities

Results in
mito membrane damage (decreased ATP)
Plasma membrane damage loss of osmotic balance, and cellular components,
release of lytic enzymes if lysosomal membranes compromised

18
Q

When does injury become irreversible?

A

mitochondrial dysfunciton (depletion of ATP) and profound distrubance in membrane function (rupture of lysosomal and plasma membranes)

19
Q

Define autophagy

A

a survival mechanism during nutrient deprivation can cannibalize itself and recycle the digested contents

20
Q

What are the four main pathways of abnormal intracellular accumulations?

A
-abnormal metabolism
(fatty change in liver associated with alcohol abuse)
defect in protein folding/transport
(excess cholesteral causing atherosclerotic vascular disease)
lack of enzyme
(glycogen storage diseases)
ingestion of indigestible materials
(Exogenous pigments like a tatoo)
21
Q

Dystrophic calcifications

A

occurs in areas of necrosis

NORMAL serum calcium levels

22
Q

Metastatic calcification

A

due to herpcalcemia secondary to disordered calcium metabolism
ELEVATED serum calcium levels
found in normal tissues

23
Q

Cellular aging

A

result of progressive decline in cellular function and viability casued by genetic abnormalities and the accumulation of cellular and molecular damage due to effects of exposure to exogenous influences

24
Q

Biochemical markers:

AST

A

found in liver, heart, skeletal muscle, brain and kidneys

25
Q

Biochemical markers

ALT

A

liver

26
Q

Biochemical markers

ALP

A

bile duct damage

27
Q

Biochemical markers

Troponin 1

A

cardiac muscle