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Chapter 1 Flashcards

1
Q

what are the four aspects of disease

A

cause/etiology
pathogenesis
molecular and morphologic changes
functional derangements and clinical manifestations

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2
Q

hypertrophy

A

increase in size of cells

cardiac and skeletal mm (these cannot undergo hyperplasia)

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3
Q

hypertrophy triggered by

A

GFs: TGFbeta, IGF1, FGF
vasoactive agents: alpha adrenergic agonists
endothelin 1, angiotensin II

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4
Q

hypertrophy is signaled by

A

P3K/AKT- physiologic

GPCRs- pathologic

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5
Q

hyperplasia

A

increased cell #

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6
Q

physiologic hyperplasia

A

hormonal (proliferation of breast tissue in puberty and pregnancy)
compensatory (liver regeneration)

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7
Q

pathologic hyperplasia

A

endometrial hyperplasia
benign prostatic hyperplasia
viral infections

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8
Q

autophagy

A

residual bodies called lipofuscin granules

brown atrophy

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9
Q

myositosis ossificans

A

bone in mm

usually after intramuscular hemmorage

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10
Q

periductal mastits

A

type of metaplasia in smokers
effects breast tissue and lactiferous ducts
can get pockets which form abcesses

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11
Q

metaplasia mechanism

A

signals generated by GFs, ECM, retinoic acid
base cells responsible for regeneration if apical cells die
base cells regenerate to produce a different type of epithelium

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12
Q

reversible cell injury signs

A 
decreased ATP
cell swelling
mitochondria and cytoskeleton abnormalities
blebbing of plasma membrane
detachment of ribosomes from ER
clumping of chromatin
loss of membrane integrity
fatty change (in hypoxic and toxic injuries)
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13
Q

nucleus in necrosis

A

pyknosis -> karyorrhexis -> karyohysis

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14
Q

ischemic tissue

A

increased esonophilia staining sue to low cytoplasmic RNA and denatured proteins

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15
Q

myelin figures

A

replace dead ischemic cells
large whorled phospholipid masses
phagocytosed
can calcify to form Ca soaps

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16
Q

karyolysis

A

faded/abscent nuclei

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17
Q

pyknosis

A

nuclear shrinkage and increased basophilia

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18
Q

karyorrhexis

A

fragmented nuclei

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19
Q

coagulative necrosis

A

architecture of dead tissue persists for days-weeks
firm texture
injury denatures enzymes as well so proteolysis cannot occur
eosinophilic, anucleated cells persist
infart

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20
Q

liquefactive necrosis

A

digestion of dead cells -> liquid viscous mass
focal bacterial or fungal infections
creamy yellow/green pus (color due to dead leukocytes)
brain due to ischemia

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21
Q

caseous necrosis

A

foci of TB
cheese like appearance
ganulomas

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22
Q

fat necrosis

A

clinical term
focal areas of fat destruction
usually due to release of activated pancreatic lipases in pancreatitis
can get fat saponification

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23
Q

fibrinoid necrosis

A

immune rxns involving blood vessels
complexes of Ags and Abs deposit on wall of aa -> immune complex
immune complex and fibrin(leaked from vessels) -> bright pink and amorphous appearance

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24
Q

decreased ATP

A

plasma membrane energy dependent Na pump cannot fnx
cellular energy dependent metabolism altered
failure of Ca pump (increased intracellular Ca)
decreased protein synthesis
proteins unfold

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25
plasma membrane energy dependent Na pump failure
Na enters and accumulates K diffuses out cell swelling and dilation of ER
26
cellular energy dependent metabolism altered
decreased ox phos -> decreased ATP/increased AMP -> PFK & phosphorylases -> increased anerobic glycolyssi -> deplete glycogen stores & build up of lactic acid -> low pH -> activate lytic enzymes
27
increased intracellular Ca
MPTP activates phospholipases, proteases, endonucleases, ATPases apoptosis via caspases and MPTP
28
Fenton rxn
Fe2 + H202 -> Fe3 +OH- +OHradical | OH radicals most damaging
29
CCL4
created into radical by sET inhibits protein synthesis steatosis of liver
30
antioxidants
vit A,E,C and glutathione
31
catalase
2H202 -> O2 + H20
32
SODs
O2 radicals -> H202
33
lipid peroxidation
occurs in membranes double bonds attacked by ROS produces peroxides -> more peroxidation
34
oxidative modification of proteins
FR promote oxidation of AA side chains | can damage active site of enzymes disrupt structure or enhance degradation
35
lesions in DNA
single and double stranded breaks x-linking formation of adducts cell aging
36
O2 radical mechanism of production
incomplete reduction of O2 during OxPhos | phagocyte oxidase in leukocytes
37
O2 radical mechanism of inactivation
conversion of H202 and O2 by SOD
38
O2 radical pathologic effects
stimulated production of degradative enzymes in leukocytes & other cells may directly damage lipids, proteins, and DNA acts close to site of production
39
H202 mechanism of production
by SOD from oxygen | by peroxidases in peroxisomes
40
H202 mechanisms of inactivation
conversion to water and O2 by catalase
41
H202 pathologic effects
can be converted to OH radical and OCL - which destroy microbes and cells can act distant from production
42
OH radical mechanism of production
generated from water by hydrolysis radiation fenton rxn from 02
43
OH radical mechanism of inactivation
conversion of water by glutathione peroxidase
44
OH radical pathology
most reactive oxygen derived FR | principal ROS responsible for damaging lipids, proteins, and DNA
45
ONOO radical mechanism of production
production by interaction of O2 radical and NO | generated by NO synthase
46
ONOO- mechanism of inactivation
conversion of HNO2 by peroxisomes
47
ONOO- pathology
damages lipids, proteins, and DNA
48
anti-apoptotics
Bcl-2, Bcl-x, Mcl-1 control mitochondrial permeability part of Bcl Family
49
BH3-only proteins
stress/damage sensors part of Bcl family Bim, Bid, Bad activate Bax and Bak
50
Bax and Bak
form oligomers and insert into mitochondrial membrane making it leaky so cytochrome C can escape to cytoplasm
51
cytochrome C
binds Apaf1 to from apoptosome whihc activates caspase 9 which will activate executioner caspases (6&3)
52
extrinsic/death receptor mediated
death receptors part of TNF receptor family FasL will bind 3 Fad receptors activates caspase 8/10 which will activate exucutioner caspases (6&3)
53
changes to promote phagocytosis
phosphotidylserine thrombospondin Abs chemotaxis
54
lipid accumulation
steatosis liver, heart, mm, kidney caused by toxins, malnutrition, DM, obesity, anorexia, alcoholism clear vacuoles, stain w/ sudan IV or oil red-o
55
cholesterolosis
focal accumulations of cholesterol laden macrophages in lamina propria of gall bladder
56
nieman-pick disease
lysosomal storage disease | mutation in cholesterol trafficking
57
protein accumulation
rounded, eosinophilic droplets, vacuoles, or aggregates in cytoplasm alpha-antitrypsin deficences
58
accumulation of thin filiments
rigor mortis
59
karatin
found in epithelial cells | accumulates in alcoholic hyaline in liver
60
neurofiliaments
accumulate in neurofibrillary tangles like in alzheimers
61
desmin filiments
mm
62
vimentin filiments
CT
63
glial filiments
astrocytes
64
hyaline changes
homogenous glossy pink appearance when stained w/hematoxylin and eosin histo term, not specific to cause
65
glycogen accumulation
appears as clear vacuoles in cytoplasm dissolves in aqueous fisative DM, glycogen storage diseases
66
hemosiderin granules
excess Fe binds ferratin locally -> bruise systemic -> hemosiderosis extreme -> hemochromatosis
67
dystrophic calcification
occurs despite normal serum Ca levels and in absence of defective Ca metabolism areas of necrosis
68
examples of dystrophic calcification
atherosclerosis aging/damages heart valves heterotopic bone lamellated configurations called psammoma bodies
69
metastatic calcification
normal tissues due to hypercalcemia accentuates dystrophic calcification causes high PTH from PT or from tumor destruction of bone tissue (cancer, pagets) Vit D disorders, sarcoidosis, idiopathic hypercalcemia of infancy renal failure (retention of phosphate) aluminum intoxication

PBD1 (6 decks)

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