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PBD1 > Chapter 1 > Flashcards

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
Q

plasma membrane energy dependent Na pump failure

A

Na enters and accumulates
K diffuses out
cell swelling and dilation of ER

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26
Q

cellular energy dependent metabolism altered

A

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

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27
Q

increased intracellular Ca

A

MPTP
activates phospholipases, proteases, endonucleases, ATPases
apoptosis via caspases and MPTP

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28
Q

Fenton rxn

A

Fe2 + H202 -> Fe3 +OH- +OHradical

OH radicals most damaging

29
Q

CCL4

A

created into radical by sET
inhibits protein synthesis
steatosis of liver

30
Q

antioxidants

A

vit A,E,C and glutathione

31
Q

catalase

A

2H202 -> O2 + H20

32
Q

SODs

A

O2 radicals -> H202

33
Q

lipid peroxidation

A

occurs in membranes
double bonds attacked by ROS
produces peroxides -> more peroxidation

34
Q

oxidative modification of proteins

A

FR promote oxidation of AA side chains

can damage active site of enzymes disrupt structure or enhance degradation

35
Q

lesions in DNA

A

single and double stranded breaks
x-linking
formation of adducts
cell aging

36
Q

O2 radical mechanism of production

A

incomplete reduction of O2 during OxPhos

phagocyte oxidase in leukocytes

37
Q

O2 radical mechanism of inactivation

A

conversion of H202 and O2 by SOD

38
Q

O2 radical pathologic effects

A

stimulated production of degradative enzymes in leukocytes & other cells
may directly damage lipids, proteins, and DNA
acts close to site of production

39
Q

H202 mechanism of production

A

by SOD from oxygen

by peroxidases in peroxisomes

40
Q

H202 mechanisms of inactivation

A

conversion to water and O2 by catalase

41
Q

H202 pathologic effects

A

can be converted to OH radical and OCL - which destroy microbes and cells
can act distant from production

42
Q

OH radical mechanism of production

A

generated from water by hydrolysis
radiation
fenton rxn
from 02

43
Q

OH radical mechanism of inactivation

A

conversion of water by glutathione peroxidase

44
Q

OH radical pathology

A

most reactive oxygen derived FR

principal ROS responsible for damaging lipids, proteins, and DNA

45
Q

ONOO radical mechanism of production

A

production by interaction of O2 radical and NO

generated by NO synthase

46
Q

ONOO- mechanism of inactivation

A

conversion of HNO2 by peroxisomes

47
Q

ONOO- pathology

A

damages lipids, proteins, and DNA

48
Q

anti-apoptotics

A

Bcl-2, Bcl-x, Mcl-1
control mitochondrial permeability
part of Bcl Family

49
Q

BH3-only proteins

A

stress/damage sensors
part of Bcl family
Bim, Bid, Bad
activate Bax and Bak

50
Q

Bax and Bak

A

form oligomers and insert into mitochondrial membrane making it leaky so cytochrome C can escape to cytoplasm

51
Q

cytochrome C

A

binds Apaf1 to from apoptosome whihc activates caspase 9 which will activate executioner caspases (6&3)

52
Q

extrinsic/death receptor mediated

A

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
Q

changes to promote phagocytosis

A

phosphotidylserine
thrombospondin
Abs
chemotaxis

54
Q

lipid accumulation

A

steatosis
liver, heart, mm, kidney
caused by toxins, malnutrition, DM, obesity, anorexia, alcoholism
clear vacuoles, stain w/ sudan IV or oil red-o

55
Q

cholesterolosis

A

focal accumulations of cholesterol laden macrophages in lamina propria of gall bladder

56
Q

nieman-pick disease

A

lysosomal storage disease

mutation in cholesterol trafficking

57
Q

protein accumulation

A

rounded, eosinophilic droplets, vacuoles, or aggregates in cytoplasm
alpha-antitrypsin deficences

58
Q

accumulation of thin filiments

A

rigor mortis

59
Q

karatin

A

found in epithelial cells

accumulates in alcoholic hyaline in liver

60
Q

neurofiliaments

A

accumulate in neurofibrillary tangles like in alzheimers

61
Q

desmin filiments

A

mm

62
Q

vimentin filiments

A

CT

63
Q

glial filiments

A

astrocytes

64
Q

hyaline changes

A

homogenous glossy pink appearance when stained w/hematoxylin and eosin
histo term, not specific to cause

65
Q

glycogen accumulation

A

appears as clear vacuoles in cytoplasm
dissolves in aqueous fisative
DM, glycogen storage diseases

66
Q

hemosiderin granules

A

excess Fe binds ferratin
locally -> bruise
systemic -> hemosiderosis
extreme -> hemochromatosis

67
Q

dystrophic calcification

A

occurs despite normal serum Ca levels and in absence of defective Ca metabolism
areas of necrosis

68
Q

examples of dystrophic calcification

A

atherosclerosis
aging/damages heart valves
heterotopic bone
lamellated configurations called psammoma bodies

69
Q

metastatic calcification

A

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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