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Principles of Disease > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

Etiology

A

Underlying causes and modifying factors responsible for the initiation and progression of disease

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2
Q

Pathogenesis

A

mechanisms of development and progression of disease, account for the cellular and molecular changes that give rise to the specific functional and structural abnormalities that characterize any disease

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3
Q

What are 8 causes of Cell injury?

A
  1. hypoxia and ischemia
  2. toxins
  3. infectious agents
  4. immunologic reactions
  5. Genetic abnormalities
  6. Nutrient imbalances
  7. Physical agents
  8. Aging
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4
Q

What is hypoxia and what is ischemia?

A

hypoxia refferes to oxyegen deficiency and ischemia is a reduced blood supply. The most common cause of hypoxia is ischemia from an arterial obstruction. Both deprive tissues of oxygen but ischemia also results in nutrient deficiencies

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5
Q

Describe reversible injury

A

the stage of cell injury at which deranged function and morphology of the injured cells can return to normal if the damaging stimulus is removed

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6
Q

why do cells in reversible cell injury usually become swollen?

A

they intake water as a result of the failure of energy dependent ion pumps in the plasma membrane, leading to inability to maintain ionic and fluid homeostasis

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7
Q

Cellular swelling is due to increased _________ of the ________ _________

A

permeability of the plasma membrane

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8
Q

what are the two main morphological changes that occur with reversible cell injury?

A
  1. cellular swelling

2. fatty change

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9
Q

what is fatty change?

A

especially in organs that are involved in lipid metabolism such as the liver, triglyceride containing lipid vacuoles in the cytoplasm

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10
Q

The cytoplasm of injured cells may also become more _________ (redder) with progression towards necrosis

A

eosinophilic

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11
Q

what are 4 other morphological changes during cellular injury?

A
  1. plasma membrane alterations (blebbing, blunting etc)
  2. mitochondrial changes such as swelling and phospholipid rich densities
  3. dilation of the ER
  4. nuclear alterations such as clumping of chromatin
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12
Q

normal cell function depends on what ?

A

nutrients, oxygen glucose, amino acids, and removal of wastes

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13
Q

when the adaptive ability of the cell is exceeded cell ______ develops

A

injury

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14
Q

mild cell injury leads to _____ changes but if more injury occurs then _______ follows

A

functional changes then degeneration

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15
Q

what is a static state with cell injury?

A

they function at a sub optimal level

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16
Q

compensated state

A

insufficient function is sufficient to maintain life of the body

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17
Q

irreversible cell injury is characterized by changes at the __________ level

A

microscopic

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18
Q

do necrotic cells function?

A

no

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19
Q

necrosis in living organims

A

local cell death

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20
Q

somatic death

A

death of whole body

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21
Q

what ate the most important targets of injurious stimuli are ?

A

the mitochondria sites of ATP generation, cell membranes, protein synthesis, cytoskeleton, cell genetic apparatus

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22
Q

what are the overall 4 mechanisms of cell degeneration?

A
  1. Depletion of ATP
  2. impaired cell membrane function
  3. intracellular accumulations
  4. genetic abnormalities
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23
Q

what are some ways impaired cell energy production can occur?

A

hypoxia, hypoglycemia, enzyme inhibition, uncoupling of oxidation phosphorylation

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24
Q

hypoxemia

A

decrease ability of blood to carry oxyegn or insuficient hemoglobin to bind oxygen

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25
Q

hypoglycemia

A

low glucose levels in the blood

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26
Q

enzyme inhibition

A

anything which interfers with vital enzymes in the repiratory chain will lead to insuficient ATP

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27
Q

uncoupling oxidative phosphorylation

A

anything that alters how enzymes and chemical reactions are organized on the mitochondrial membrane will lead to decreased ATP production

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28
Q

cells have a _________ concentration of some solutes than surrounding environment

A

higher

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29
Q

with impaired energy production cells _____ water

A

gain

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30
Q

why does intracellular accumulation of water occur?

A

because lack of ATP leads to dysfunction of cell membrane and sodium pump, sodium and water moves in the cell

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31
Q

swelling of mitochondria causes what?

A

uncoupling of oxidative phosphorylation, alters arrangement of respiratory enzymes of mitochondria

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32
Q

why would cells switch to anaerobic glycolysis?

A

if a lack of oxygen has led to impaired energy, production of lactic acid occurs

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33
Q

defective energy production affects which cells first?

A

those with the highest metabolic rate, highest oxygen demand
ex. brain cells

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34
Q

cell membrane damage is caused by _____ ________

A

free radicals

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35
Q

free radicals

A

highly reactive particles haveing an unpaired electron in their outer shell, also known as oxidative stress, by product of metabolism

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36
Q

final compounds of the activated complement pathway can lead to _____ ________ _______

A

damaged cell membranes

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37
Q

what causes direct lysis of the cell membrane?

A

enzymes with lipase acitivity, certain viruses, physical and chemical agents

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38
Q

cell shape changes from bioconcave to _________ with impaired membrane function

A

spherocytes (spheroidal)

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39
Q

how does deposition of lipofuscin occur?

A

resulted from free radical peroxidation of lipids in subcellular membranes

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40
Q

deleterious effects can be ________ or ________

A

exogenous (outisde) or endogenous (inside)

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41
Q

what are exogenous injurious agents usually from?

A

drugs toxic chemicals, heavy metals, infectious agents etc

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42
Q

triglyceride accumate in the cytoplasm of parenchymal cells in organs such as the liver this is called what?

A

fatty degradation, fatty change or steatosis

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43
Q

when does fatty liver disease occur?

A

when free fatty acids are carried in the portal blood from the intestine to the liver where they are processed to form triglycerides, phospholipids and cholesterol esters

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44
Q

normal liver cells contain _______ triglycerides

A

little

45
Q

when would the balance be upset be favouring triglyceride accumulation in the liver?

A
  • Increased mobilization of adipose tissue, increased amounts of fatty acids reach the liver (as in starvation or diabetes mellitus)
  • Overactivity of certain enzymes so increase in conversion of fatty acids into tryglycerides (induced by alcohol consumption)
  • The oxidation of triglycerides to other forms is decreased (occurs in anemia and hypoxia)
  • Apoprotein synthesis is decreased (as in protein malnutrition or with specific hepatotoxins
46
Q

whats the bodys mechanism for ridding excess iron?

A

no mechanism

47
Q

iron occasionally accumulates in tissues as ___________

A

hemosiderin

48
Q

how does local accumulation of iron occur?

A

when hemoglobin is broken down at sites of hemorrhage, bruises undergoe as they resolve

49
Q

how do bruises happen?

A

area of hemorrhage within the tissue, caused by blunt trauma, blood escapes the vessels and moves into tissue space

50
Q

contusion

A

bruise

51
Q

hemochromatosis

A

rare inherited defect in iron metabolism, free ferric accumulates and is reduced to produce toxic free radicals

52
Q

jaundice is a sign of what?

A

increased bilirubin, yellow pigmented skin

53
Q

is jaundice a disease?

A

not itself but a sign of disease

54
Q

hemolysis

A

desruction of RBCs

55
Q

Jaundice can result from 3 mechanisms

A
  1. hemolysis
  2. hepaocellular dysfunction
  3. obstruction to bile flow
56
Q

is bilirubin secreted in the urine?

A

no because its lipid soluble

57
Q

obstruction to bile flow is called

A

cholestasis

58
Q

cholestasis within the liver is called ______ or outside the liver _________

A

intrahepatic, extrahepatic

59
Q

what happens when bilirubin is depleted in parenchymal cells ?

A

causes cellular injury

60
Q

what are other substances which can accumulate within cells as a result of metabolic derangements

A

proteins, glycogen, cholesterol, carbon, melanin

61
Q

DNA abnormalities can either be ________ or __________

A

inherited or aquired

62
Q

inherited

A

having a genetic basis

63
Q

acquired

A

somatic

64
Q

somatic refers to ______

A

body, cells of tissue as apposed to germ line

65
Q

failure of synthesis of structural proteins can cause?

A

necrosis

66
Q

failure of growth of regulating proteins can cause ?

A

cancer

67
Q

failure of enzyme synthesis can cause ?

A

congenital disease

68
Q

microscopic morphological changes which indicate reversible injury are?

A

cellular swelling and fatty change

69
Q

_______ hours need to pass before necrosis is visible by light microscopy

A

6-8

70
Q

what is the appearance of necrosis a result of?

A

concurrent enzymatic digestion of the cell and denaturation proteins

71
Q

what are the 3 morphological evidence types of necrosis?

A
  1. gross evidence
  2. cytoplasmic
  3. nuclear
72
Q

gross evidence of necrosis includes ?

A

unaided eye, coagulation necrosis, liquification, caseation and fat necrosis

73
Q

fat necrosis can be subdivided into ______ and ______

A

enzymatic and non enzymatic

74
Q

what is the main difference between enzymatic fat necrosis and non enzymatic fat necrosis?

A

enzymatic (particularly with pancreatic injuries , lipase into adjacent fat tissue in abdomen mesentery and omentum)

nonenzymatic (occurs in other fat deposits such as breast or subqutaneous tissue usually following trauma)

75
Q

cytoplasmic evience of necrosis requires what?

A

visualization with light or electron microscope

76
Q

what are the 3 signs of cytoplasmic evidence with necrosis?

A
  1. cytoplasm become homogenous and deeply staining, denaturation of cytoplasmic proteins, more pink (HE stain)
  2. may become vaculated and bubbly failure of sodium pump
  3. dystrophic cacification, abnormal deposits of calium slats in dead or dying tissues
77
Q

what is the most definitive indicator of necrosis?

A

nuclear evidence

78
Q

what is some nuclear evidence necrosis is occuring?

A

chromatin clumps, nucelus stains dark blue,pyknotic nuclei

79
Q

what is a pyknotic nucleus?

A

break up into fragments

80
Q

what does it mean when a tissue has a large functional reserve?

A

a large number of tissues need to be lost in order for organ function to be impaired

81
Q

loss in arterial blood supply can cause?

A

gangreen, frostbite, bacterial infections

82
Q

with a loss of tissue whats affected first (blood supply)?

A

furthest from circulatory system ex. toes, tials, ears, fingers

83
Q

if tissue is uninfected what does it look like?

A

dry, brittle, shriveled

84
Q

does necrotic tissue usually have inflamation?

A

little to none

85
Q

_____ _____ is necessary for inflamation

A

blood flow

86
Q

why is necrotic tissue an ideal growth medium for infection?

A

beyond reach of inflammatory cells and immune system

87
Q

can necrotic tissue become inflamed at all?

A

yes it can incite inflammation around edges of dead or dying cells where blood supply is still intact

88
Q

what is one of the major concerns for burn victims?

A

secondary bacterial infections

89
Q

what causes a fever?

A

realease of pyrogens (fever inducing agents

90
Q

what causes an increased white blood cell count?

A

inflammatory response accompanying necrosis

91
Q

there are currently ____ types of cell death

A

13

92
Q

apoptosis

A

cells can be programmed to die at certain times

93
Q

autophagy

A

cells can die because survival mechanisms have gone awry

94
Q

what are the 4 parts to physiological apoptosis?

A
  1. programmed cell death during embryogenesis
  2. hormaonally driven regression of tissues
  3. cell death in tissues with normal rapid turnover
  4. elimination of potentially harmful self reactive lymphocytes during maturation
95
Q

all cells have internal mechanisms for induing apoptosis, this is activated by what circumstances?

A
  • damage to DNA
  • accumulation of misfolded proteins
  • viral infections
  • pathologic atrophy of organs
96
Q

cells in the imune system are termed ________

A

cytotoxic (t cells)

97
Q

Tcells are capable of ?

A

inducing death through apoptosis in their neighbours if they detect abnormalities

98
Q

Necrosis is ______ while apoptosis is _______

A

passive and disorderly, active, organized and orderly

99
Q

apoptosis is largely mediated by ________

A

capsases

100
Q

executioner capsases

A

functional enzymes that degrade DNA and cell proteins

101
Q

what two things must occur in order for an abnormal cell to produce a tumour?

A

1) endogenous suicide signals as a result of DNA abnormalities
2) recognition and response from cytotoxic T-cells

102
Q

Necrosis is ____ cell death and can only occur within _____ beings

A

local, living

103
Q

rigor mortis

A

the stiffening of a dead body, occurs to reduction in ATP in the muscles

104
Q

post mortem livifity

A

gravitational settling of the blood in dependent lower parts, subsequent breakdown of hemoglobin produces the typical green discoloration of the skin

105
Q

post mortem livifity

A

gravitational settling of the blood in dependent lower parts, subsequent breakdown of hemoglobin produces the typical green discoloration of the skin

106
Q

post mortem blood clotting

A

result in formation of large clots in places such as the chambers of the heart

107
Q

putrefaction

A

results from the fermentation caused by saprophytic bacteria; gas accumulation may produce rupture of the stomach or a typical foamy liver which is full of gas bubbles

108
Q

autolysis

A

disintegration of tissues and organs as a whole which occurs after death due to action of enzymes.

Principles of Disease (8 decks)

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