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Patho I > Chapter1 > Flashcards

Chapter1 Flashcards

1
Q

What are the 4 aspects of diesease

A

etiology
pathogenesis
molecular/morphologic changes
clinical manifestations

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2
Q

increased demand or stimulation can lead to what cell adaptation

A

hyperplasia and hypertrophy

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3
Q

decreased nutrients and decreased stimulation can lead to what cell adaptations

A

atrophy

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4
Q

chronic irritation can lead to what cell adaptations

A

metaplasia

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5
Q

what type of stimuli can lead to cellular swelling and fatty changes classified as acute reversible injuries

A

acute and transient reduced O2, chemical injury, microbial infection

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6
Q

progressive and severe reduced O2, chemical injury, microbial infection can cause what

A

cell death

necrosis or apoptosis

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7
Q

what can lead to intracellular accumulations; calcifications

A

metabolic alterations, genetic or acquired; chronic injury

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8
Q

what stimulates hypertrophy

A

hormones and growth factors increase the demand

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9
Q

how come heart and skel m hypertophy more

A

striated mm have a limited capacity for division

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10
Q

what is the the cause of increased size in cells

A

increased production of cellular proteins

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11
Q

what are factors that have been proven to trigger hypertrophy

A

increased work load

TGFbeta, insulin-like GF(IGF-1), fibroblast growth factor, alpha adrenergic agonists, endothelia-1 and Ang II

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12
Q

What are the 2 main biochem pathways invovled with muscle hypertrophy

A

phosphoinositide-3kinase AKt pathway

signaling downstream of GPCRs

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13
Q

Why do drug abusers constantly have to increase the amount of intake for the same response

A

hypertrophy in sER in hepatocytes because increasing number of enzymes which detoxify drugs
cytochrom p-450

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14
Q

what are the types of physiologic hyperplasias

A

hormonal hyperplasia and compensatory

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15
Q

most forms of pathologic hyperplasia are caused by what

A

excesses of hormones or GF on target cells

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16
Q

what are common causes of patholigc atrophy

A 
decreased workload
loss of innervation
diminished blood supply
inadequate nutrition
loss of endocrine stimulation
pressure
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17
Q

severe decreased workload induced atrophy can lead to what other disease

A

osteoporosis from increased bone resorption

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18
Q

What is senile atrophy

A

reduced blood supply caused nu atherosclerosis in brain and heart

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19
Q

what is marasmus

A

profound protein-calorie malnutrition

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20
Q

what is cachexia

A

marked muscle wasting

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21
Q

what causes cachexia in chronic inflammatory disease patients

A

chronic overproduction of inflammatory cytokine tmor necrosis factor TNF
responsible for appetite suppression and lipid depletion, culminating in muscle atrophy

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22
Q

describe atrophy secondary to pressure

A

tumors compressing surrounding tissues, compromise of blood because of the pressure on the blood vessel

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23
Q

In atrophic muslces describe cellular components

A

decrease in cell size and organelles, like fewer mitochondria and myofilaments. reduced amounts of rER

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24
Q

what cellular mechanism causes atrophy

A

decreased protein synthesis and increased protein degradation

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25
Q

what pathway leads to degradation of cell proteins

A

ubiquitin-proteasome pathway

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26
Q

what activates ubiquitin ligases

A

nutrient deficiency and disuse

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27
Q

what is the mechanism behind cachexia due to cancer

A

the ubiquitin proteasome pathway

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28
Q

what is autophagy

A

when the starved cell eats its own components in an attempt to find nutrients and survive

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29
Q

what is the most common form of epithelial metaplasia

A

columnar to swuamous, like respiratory tract

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30
Q

What induces squamous metaplasia in respiratory epithelium

A

retinoic acid , Vit A

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31
Q

What is the metaplasia involved in Barrets Esophagus

A

squamous to columnar because of refluxed gastric acid

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32
Q

what type of cancers commonly arise when there are metaplastic changes from squamous to columnar

A

glandular, (adeno)carcinomas

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33
Q

What is CT metaplasia

A

formation of cartilage, cone or adipose in tissues that normally do not have these elements

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34
Q

what is myositis ossificans

A

bone formation in muscle

after intramuscular hemorrhage

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35
Q

what are causes of hypoxia

A

ischemia, CV failure, decrease O2 capacity in blood (anemia or CO)

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36
Q

what are physical agents that can cause cell injury

A

mechanical trauma, extreme temperatures, sudden changes atmospheric P, radiation, electrical shock

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37
Q

general groups of causes of cell injury

A

O2 deprivation, physical agents, chemical agnets, infectious agents, immunologic reactions, genetic derrangements
nutritional imbalances

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38
Q

What are the cellular morphalogic changes seen with decreased amounts of ATP

A

swelling of cell

blebbing of plasma membrane, detachment of ribosomes from ER and clumping of nuclear chromatin

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39
Q

what cellular changes are associated with necrosis

A

depletion ATP

rupture of lysosomal and plasma membranes

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40
Q

necrosis is the principial outcome of what

A

ischemia, exposure to toxins, various infections, trauma

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41
Q

describe changes in cell size that lead to necrosis? apoptosis?

A

necrosis- swelling

apoptosis- reduced/shrinking

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42
Q

describe changes in PM in necrosis and apoptosis

A

necrosis- disrupted

apoptosis- intact, altered structure

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43
Q

describe changes in cellular elements in necrosis and apoptosis

A

necrosis- enzymatic digestion, may leak out of cell

apoptosis- intact, may be release in apoptotic bodies

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44
Q

is necrosis physiologic or pathologic

A

invariable pathologic

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45
Q

what is cellular swelling the result of

A

failure of energy dependent ion pumps in the PM

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46
Q

what type of cells undergoe fatty changes as a type of reversible injury

A

cells involved in dependent on fat metabolism

haptocytes and myocardial cells

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47
Q

small clear vacuoles seen on microscopic evaluation are respresentations fo what

A

distended pinched off segments of the ER

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48
Q

What are the ultrastructural changes of reversible cell injury

A

plasma membrane alterations
mitochondrial changes
dilation of ER
nuclear alterations

49
Q

what are the plasma membrane alterations in reversible cell injury

A

blebbin, blunting and loss of microvilli

50
Q

what are the mitochondrial changes in reversible cell injury

A

swelling and appearance of small amorphous densities

51
Q

what does dilation of the ER mean

A

detachment of polysomes, intracytoplasmic myelin figures

52
Q

what are the nuclear alterations seen in reversible cell injury

A

disaggregation of granular and fibrillar elements

53
Q

why is necrosis associated with inflammation

A

when the contents leak out, inflammation occurs in surrounding tissue

54
Q

how early can we detect necrosis of muscles

A

2 hours after because release the MD BB MM enzymes

55
Q

how do necrotic cells stain in H&E stains

A

increased eosinophilia
loss of cytoplasmic RNA (binds to hematoxylin)
denatrured cytoplasmic proteins (bind eosin)

56
Q

why do necrotic cells have a more glassy homogenous appearance

A

loss of glycogen particles

57
Q

What are myelin figures

A

whorled phospholipid masses- from damaged cell membranes

58
Q

what causes calcium soaps

A

calcification of fatty acid residues like the myelin figures

59
Q

loss of DNA because of enzymatic degradation by endonucleases is called what and looks how microscopically

A

karyolysis

basophilia of chromatin may fade

60
Q

what is pyknosis

A

apoptotic cell death- nuclear shrinkage and increased basophilia
chromatin condenses into soli dhrunken basophilic mass

61
Q

what is karyorrhexis

A

pyknotic nucleus undergoes fragmentation- day or two the nucleus in necrotic cell totally disappears

62
Q

what is coagulative necrosis

A

architecture of dead tissue is preserved for some days. firm texture
injury denatures structural proteins AND enzymes so blocks proteolysis

63
Q

a localized area of coagulative necrosis is called what

A

infarct

64
Q

What is liquefactive necrosis

A

digestion of dead cells resulting into liquid viscous mass

65
Q

what causes liquefactive necrosis

A

focal bacterial, fungal infections because the microbes stimulate accumulation WBCs and liveration of enzymes from these cells

66
Q

what is pus

A

the dead leukocytes

67
Q

what type of cell death results in liquefactive necrosis

A

hypoxic cell death in the CNS

68
Q

What is gangrenous necrosis

A

lost blood supply and necrosed. involves multiple tissue planes

69
Q

what is wet gangrene

A

when there is more liquefactive necrosis because of the degradative ensymes of bacteria and attracted leukocytes

70
Q

what is caseous necrosis

A

necrotic area appears collection of fragmented/lysed cells and amorphous granular debris enclosed within distinctive border.
“granuloma”

71
Q

what is fat necrosis

A

focal areas of fat destruction

from release of activated pancreatic lipases into the substance of the pancreas and peritoneal cavity

72
Q

what disease process commonly involves fat necrosis

A

acture pancreatitis

73
Q

Describe changes seen in acute pancreatitis

A

pancreatic enzymes leak out of acinar cells and liquefy membranes of fat cells. released lipases split TG esters in the fat cells. FA combine with Ca to produce chalky white areas

74
Q

what is saponification

A

the chalky white areas in caseous necrosis

75
Q

what is fibrinoid necrosis

A

immune rxns of blood vessels

immune complex deposits link with fibrin resulting in a bright pink and amorphous appearance in H&E stains “fibrinoid”

76
Q

what type of syndromes commonly include fibrinoid necrotic changes

A

immunologically mediated vasculitis syndromes

77
Q

what does the cellular response to injurious stimuli depend on

A

nature of injury, duration, severity

78
Q

the consequences of cell injury depend on

A

type, state and adaptability of injured cell

79
Q

what cellular components are most frequently damaged by injurious stimuli

A

mitochondria, cell membranes, machinery of protein synthesis and packaging and the DNA in nuclei

80
Q

ATP depletion is associated with what types of injuries

A

hypoxic and chemical

81
Q

what is the main way that ATP is made in mammalian cells

A

oxidative phosphorylation of ATP from ETC in mitochondria

82
Q

what is the second way that ATP is made

A

glycolytic pathway from using glycogen

83
Q

What tissues can survive longer in oxygen deprivation

A

liver (greater glycolytic capacity)

84
Q

how does depleted ATP lead to cell swelling

A

ATP dependent Na K pump stops functioning and Na accumulates in cell so water flows in

85
Q

anaerobic glycolysis leads to what

A

accumulation of lactic acid and inorganic phosphates which reduces intracell pH–> decreased activity of cellular enzymes

86
Q

what are the 2 major consequences of mitochondrial damage

A

formation of high conductance channel in mitochondrial membrane- loss of membrane ptential
proteins that are sequestered between inner and outer membranes could leak out and cause apoptosis

87
Q

when the mitochondria loses its membrane potential what happens

A

failure of oxidative phosphorylation and progressive depletion ATP

88
Q

how does cyclosprine affect mitochondrial pore

A

targets component cyclophilin D

89
Q

what are the proteins that the mitochondria sequesters between membranes

A

cytochrome C and proteins that indirectly activate apoptosis inducing enzymes called caspases

90
Q

Ishcemia and certain toxins change Ca how

A

increase in cytosolic Ca [ ] because release of Ca from intracell stores and later influx

91
Q

Increased intracell Ca causes what

A

opening of mitochondrial permeability transition pore
activates enzymes which have deleterious effects (protesases, endonucleases and ATPases)
induction apoptosis by activation of caspases

92
Q

Chemical and radiation injury and ischemia-reperfusion use what mechanism for cell injury

A

free radicals

93
Q

what is so bad about free radicals

A

have ractions with proteins, lipids carbs. initiate autoctalytic reactions

94
Q

What are ROS

A

reactive oxygen specias, oxygen derived free radicals

95
Q

excess ROS lead to what

A

oxidative stress

96
Q

where are ROS produced physiologically

A

leukocytes, neutrophils, macrophages and during mitochondrial respiration

97
Q

What are the intermediates produced during reduction-oxidation for normal respiration

A

O2,one electron
H2O2, two electrons
OH, three electrons

98
Q

ultraviolet and X-rays hydrolyze what

A

water into OH and H

99
Q

what is a common enzyme that produces O2-

A

xanthine oxidase

100
Q

enzymatic metabolis of exogenous chemicals or drugs create what

A

free radicals that have similar effects to ROS

101
Q

how do transition metals contribute to free radicals

A

iron and copper donate of accept free electrons during the reactions and catalyze free radical formation

102
Q

What is the doubled edge sword of NO

A

produced by endothelial cells for dilation

can act as free radical and can be convereted to highly reactive peroxynitrite anion ONOO- as well as NO2- and NO3-

103
Q

how do antioxidants attack free radicals

A

block initiation of free radical formation or inactivate free radicals

104
Q

what are our antioxidants in our body

A

Vit E Vit A and ascorbic acid and glutathione

105
Q

what transport proteins can bind to the metal ions

A

transferrin, ferritin, lactoferrin and ceruloplasmin

106
Q

what does catalase degrade

A

H2O2, found in peroxisomes

107
Q

whatdoes superoxide dismutase degrade

A

O2 to H2O2

108
Q

what are the types of SOD

A

manganese SOD in mitochondria

copper-zinc SOD in cytosol

109
Q

what does glutathione peroxidase break down

A

H2O2+ 2GSH to GSSG

110
Q

how do we detect cells ability to detoxify ROS

A

the ratio of oxidized glutathione GSSG to the reduced from GSH

111
Q

what are the 3 main effects of ROS

A

lipid peroxidation in membranes
oxidative modification of proteins
lesions in DNA

112
Q

what do free radicals do to amino acid side chains

A

incude disulfide bonds and oxidation of the protein backbone

disrupt conformation and enhance proteasomal degradation of unfolded or misfolded proteins

113
Q

what type of lesions do free radicals do to the DNA

A

single and double strand breaks in DNA, cross linking and formation of adducts

114
Q

when is oxidative DNA damage seen alot

A

cellular aging

115
Q

what type of products have a detergent effect on PM

A

the lipid breakdown products like FFA, acyl carnitine and lysophospholipids

116
Q

what are the causes of membrane breakdown

A

ROS
decreased phospholipid syntehsis
increased phospholipid breadown
cytoskeletal deformities

117
Q

loss of mitochondrial membrane ultimately leads to what

A

apoptosis

118
Q

loss of PM ultimately leads to what

A

depletion energy and loss of cellular contents from cell rupture
necrosis

119
Q

injury to lysosomal membranes leads to what

A

leakage of enzymes
RNases DNases proteases, phosphotases, glucosidases and cathepsins
leading to enzymatic degradation of proteins, DNA, RNA glycogen and thus necrosis

Patho I (6 decks)

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