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MOD 1 > chapter 2: cell response > Flashcards

chapter 2: cell response Flashcards

1
Q

4 aspects of disease process

A

etiology: cause
pathogenesis:biochem process
morphologic changes: struct alterations in cells/organs
clinical manifestations: conseq of changes

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2
Q

etiology

A

genetic: multifact

acquired

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3
Q

all forms of disease start with what

A

molecular or structural alterations in cells

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4
Q

reversible functional and structural responses to changes in physiologic states, some pathologic that allows cell to survive and continue to function

A

adaption

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5
Q

examples of adaptions

A 
hypertrophy
hyperplasia
metaplasia
pregnancy
atrophy
pathologic stimuli
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6
Q

cell death happens when and from what

A

adaption is not achieved
ischemia
ifection
toxins

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7
Q

nutrient deprivation triggers what

A

autophagy

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8
Q

calcium deposited at sites of cell death is called

A

pathologic calcification

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9
Q

what is the most common stimulus for hypertrophy

A

increased workload

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10
Q

uterine hypertrophy process

A

estrogenic hormones act on SM on estrogen receptors

-increased synthesis of SM cells

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11
Q

3 basic steps in molecular pathogenesis of cardiac hypertrophy

A

integrated actions of mechanical sensors
-GFs, IGF1, FGF, a adrenergic agonists

signal transduction

  • pi3 kinase/AKT pathway (exercised induced hypertrophy)
  • GPCR: pathologic hypertrophy

Activation of txn factors
-mef2, nfat, gata4

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12
Q

when does physiologic hyperplasia occur

A

when need to increase fnct capacity of hormone sensitive organs

need compensatory increase after damage or resection

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13
Q

examples of physiologic hyperplasia

A

erythropoietin in blood cells
liver regen
glandular epithelium prolif of female breast at puberty

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14
Q

pathologic hyperplasia from

A

excessive or inappropriate actions of hormones or GF acting on target cells

separate from cancer but can increase chance of cancer

can be from viral infections

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15
Q

pathologic hyperplasia example

A

endometrial hyperplasia
-abnormal menstrual bleeding

BPH

papillomaviruses

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16
Q

2 mechanisms of hyperplasia

A

GF driven proliferation of mature cells

increased output of new cells from tissue stem cells

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17
Q

atrpohy: physiologic

A

embryonic structures going away

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18
Q

atrophy: pathological causes

A

WINE Blood Pressure

decreased workload
loss innervation
inadequate nutrition
loss endocrine stim

decreased blood
increased pressure

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19
Q

atrophy of the brain

A

narrows gyri

widens sulci

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20
Q

cellular changes in atrophy

A

less mitochondria
reduced RER
decreased metabolic demand

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21
Q

mechanisms of atrophy

A

decreased protein syn

increased protein degradation

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22
Q

some cell debris within autophagic vacuoles resist digestion and persist in cytoplasm called

A

residual bodies
lipofuscin granules
-brown discoloration of tissue

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23
Q

types of caner in barrett esophagus

A

adenocarcinomas: glandular

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24
Q

myositis ossificans

A

bone formation in muscle

after intramuscular hemorrhage

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25
Q

reversible cell injury: 4 categories

A

reduced oxidative phos
cell swelling from change in ion concent and water influx
alterations in organelles
blebbing of PM

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26
Q

alterations in organelles during reversible cell injury

A

detachment of ribosomes from ER = decre prot syn

clumping of nuclear chromatin = dna damage

cytoskeletal damage

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27
Q

causes of cell injury

A

PICO NIG

physical agents
immunologic reactions: autoimmune (end) virus (exog)
chemical agents and drugs
oxygen deprivation

nutritional imbalance
infectious agents
genetic derangements: def of proteins

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28
Q

2 things recognized under light microscope in reversible injury

A

cellular swelling

fatty change

  • hypoxic injury
  • cells dep on fat metab
  • Lipid vacuoles in cytoplasm
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29
Q

first manifestation of almost all forms of cell injury

A

cell swelling

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30
Q

cell swelling if see small clear vacuoles in cytoplasm what is it and called

A

pinched off ER

hydropic change or vacuolar degeneration

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31
Q

morphology of necrosis

A

NIG DM

nuclear changes
increased eosinophilia in H&E stains
glass appearance

discontinuities in PM and organele membranes
myelin figures

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32
Q

caseous necrosis

A

tuberculosis infection
cheese like white appearacne
granuloma

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33
Q

fat necrosis

A

areas of fat destructrion from release of activated pancreatic lipases
chalky-white areas
FAs comine with calcium

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34
Q

immune reactions involving BVs
complex antigens and antibodies in wall of arterires
bright pink amorphous appearance H and E stains

A

fibrinoid necrosis

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35
Q

necrotic cells and cell debris left over provide site for deposition of calcium salts

A

dystrophic calcification

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36
Q

depletion of ATP to ______ of mormal levels has widespread effects on critical cellular systems

A

5-10%

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37
Q

mitochondrial damage from

A

increased Ca2+
ROS
oxygen deprivation
hypoxia and toxins

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38
Q

cyclophilin D

A

structural component of MPTP

-cyclosporine targets this to reduce injury to cell

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39
Q

3 major consequences of mitochondrial damage

A

formation of mitochondrial permeability transition pore
abnormal oxidative phos and ROS
mitochondrial leakage of apoptotic proteins

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40
Q

increased Ca2+ intracellular affect on mitochondria

A

1) opens MPTP and no ATP
2) activates enzymes: phospholipases,endonucleases, ATPases etc
3) apoptosis: direct activation caspases and increase mitochond perm

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41
Q

generation of free radicals

A

redox rxns in normal metabolic processes
absorption of radiant energy
rapid bursts of ROS from activated leukocytes
enzymatic metab of exogenous chemicals or drugs
transition metals
NO

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42
Q

redox rxns free radicals

A

O2*, H202, *OH

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43
Q

uv light and xrays can hydrolyze

A

water into *OH and H free radical

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44
Q

rapid bursts of ROS from activated leukocyte enzymes

A

NAPDH oxidase in PM

xanthine oxidase intracellular enzyeme

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45
Q

metab of drugs and chemicals can create

A

free radicals similar to ROS

CCL4–>CCL3

46
Q

transition metals and free radicals

A

iron and copper donate or accept free electorns during intracellular rxns and catalyze free radical fomration

47
Q

nitric oxide free radicals

A

can act as free radical and be converted to ONOO- (peroxynitrate anion) and NO2 and NO3-

48
Q

catalase function

A

decomposes H202

49
Q

what enzyme breaksdown O2*

A

superoxide dismutase

50
Q

glutathione peroxidase

A

breaks down H202

-can tell oxidized state of cell

51
Q

2 phenomena consistently characterized in irreversibility

A

inability to reverse mitochondrial dysfunction

profound disturbances in membrane function

52
Q

transaminases in blood is damage to

A

hepatocytes

53
Q

alkaline phosphatase in blood is damage to

A

bile duct epithelium

54
Q

protective response with cell injury and not enough oxygen getting to tissue

A

HIF-1

  • promotes new blood vessel formation and stimulates cell survival pathways
  • enhance anerobic glycolysis
55
Q

ischemia-reperfusion injury (4)

A

oxidative stress (ros)
intracellular calcium overload
inflammation (danger signals from dead cells)
activation of complement system (IgM in ischemic tissue gets bound by complement)

56
Q

chemical toxic inury (2)

A

direct toxicity
-mercury binding membrane proteins and cyanide posions cytochrome oxidase

conversion to toxic metabolites
-liver cytochrome P450 conversion to free radicals

57
Q

morphology of apoptosis

A

cell shrinkage: tightly packed organelles
chromatin condensation: most charact feature
formation of cytoplasmic blebs and apoptotic bodies

58
Q

sensors of apoptosis

A

BAD
BIM
PUMA
NOXA

59
Q

smac/Diablo

A

mitochondrial protein that can leak out and neutralize inhibitors of apoptosis
-IAPs normally block caspase 3 so smac/diablo allow apoptosis

60
Q

CD95

A

FAS

61
Q

what does FLIP do

A

inhibits extrinsic apoptosis by binding procaspase 8 and preventing cleavage
viruses use this

62
Q

apoptotic bodies are coated wtih ___ which are recognized by phagocytes

A

thrombospondin

63
Q

receptor and ligand for necroptosis

A

TNFL and TNFR

64
Q

process of necroptosis

A

ligand binds
RIP 1 and 3 and procaspase 8 recruited
downstream effects = ROS
-damge to mitochondria and reduced ATP

65
Q

necroptosis morphologically

A

resembles necrosis

loss atp, swellling of cell, lysosomal enzymes, rupture of PM

66
Q

physiologic necroptosis

A

bone growth plate

67
Q

pathologic necroptosis

A

parkinsons
acute pancreatisis
reperfusion injury

PAR

68
Q

pyroptosis

A

cell death with IL-1 release

-inflammasome

69
Q

autophagy vs microautophagy vs macroautophagy

A

auto: chaperone mediated, direct translocation across lysoomal membrane
micro: inward invag of lysosomal membrane
macro: sequestration and transporetation of portions of cytoslol in double membrane bound autophagic vacuole

70
Q

steps of autophagy

A

Formation of isolated membrane (phagophorre) and its nucleation from the ER

elongation of vesicle: LC3

maturation of autophagosome and fusion with lysosomes

71
Q

what are Atgsd

A

genes that code for products required for creation of autophagosome in autophagy

72
Q

autophagy in alzheimers

A

formation of autophagosome accelerated

defects in autophagy accelerate neurodegeneration

73
Q

huntingtons and autophagy

A

mutant huntintin impairs autophagy

74
Q

role of autophagy in infectious diseases and example

A

pathogens degraded by autophagy like shigella

75
Q

macrophage spefific dletion of Atg5 increases suscepti to what

A

tuberculosis

76
Q

abnormal intracellular accumulations

A

defect of packaging and transport–>inadeq removal–>fatty change in liver

defect in protein folding–>a1-antitrypsin

lack of enzyme leading to failure to degrade metab–>storage disease

ingestion of indigestible materials–>carbon and silica

77
Q

steatosis and casue

A

abnormal accum of TGs within parenchymal cells

  • alcohol abuse
  • nonalcoholic fatty liver disease: diabetes and obesity
78
Q

xanthomas

A

intracellular accum of cholesterol w/in macrophage (goes with hered hyperlipidemic states)

-clusters of foamy cells in subepithelial of CT of skin and tendons

79
Q

cholesterolosis

A

focal accum of cholesterol-laden macrophages in lamina propria of gallbladder

80
Q

niemann pick disease

A

lysosomal storage disease

  • defect in enzyme directing cholest trafficking
    • results cholest in multiple organs
81
Q

protein accumulation in cell morphology

A

eosinophilic, rounded droplets, vacoules or aggregates in cytoplasm

82
Q

causes of excess intracell protien (5)

A

reabsorption of droplets in prox renal tubules
-renal disease with lost protein through glomerulus

plasma cells secrete too much normal proteins like Igs
-large eosinophilic inclusion called russel bodies

defective intracell transport and secretion critical proteins
-a1 antitrypsin deficiency

accumulation of cytoskeletal proteins

  • keratin filaments and neurofilaments
  • alcoholic hyaline
  • neurofibrillary tangle

aggregation of abnormal proteins

83
Q

hyaline change intracell

A

-glassy pink appearance in H&E stain

84
Q

hyaline change extracellular

A

long-standing hypertension and diabetes

-wall of arterioles become hylinized

85
Q

glycogen intracell morph

A

clear vacuoles within cytoplasm
stain best with carmine or PAS
-rose to violet color

86
Q

in diabetes glycogen accumulates in

A

kidney, liver, b cells islets of langerhans, heart muscle cells

katie Lynn breaks hearts

87
Q 
lipofuscin
-makeup
-derived from 
sign of 
color
what pts
A

lipids and phospholipids in complex with proetins
-derived through lipid peroxidation
sign of free radical injury and lipid perox
yellow-brown pigment
-in liver and heart of aging patiens
-patients with severe malnutirtion and cancer cachexia

88
Q

when black pigment inserted into tissue in pts with alkaptonuria it is called

A

ochronosis

89
Q

too much iron caues ___ to accumulate wihtin cells

-local

A

hemosiderin

-local excess in bruise

90
Q

systemic overload of iron hemosiderin called

A

deposited in many organs and tissues

hemosiderosis

91
Q

causes of hemosiderosis

A

increased absorption dietary iron due to error of metab

hemolytic anemias
repeated blood transufusions

92
Q

dystrophic calcification

A

deposition occuring locally in dying tissues

93
Q

dystrophic calcification occur in what tissue and what diseases

A

commonly in aging or damaged heart valves

almost always present in atheromas of atherosclerosis

94
Q

dystophic calcification morphology

A

fine white granules or clumps

95
Q

metastatic calcification

A

deposition of calcium salts in normal tissue because of hypercalcemia

96
Q

causes of hypercalcemia

A

increased PTH: PT tumor or exog PTH related protein from malignant tumor

increased resoption of bone tissue

renal failure
-retention phosphate and 2ndasry hyperPTism

vitamin D related disorders

97
Q

resorption of bone tissue due to tumor of bone marrow disease

A

myeloma and leukemia

98
Q

resoption of bone tissue or accelerated bone turnover

A

pagets disease

99
Q

resoprtion of bone diffuse skeletal metastasis

A

breast cancer

100
Q

vitamin D disorder sarcoidosis

A

macrophages activate vit D precursor

101
Q

Vit D idiopathic hypercalcemia of infacny

A

williams syndrome

102
Q

Werner syndrome

A

premature aging

defective gene product is DNA helicase

103
Q

genetic instability in somatic cells causes aging what disease

A

bloom syndrome and ataxia telengiectasia

104
Q

tumor suppressor genes INK4 and P16 coded by what gene locus

A

CDKN2a

105
Q

deficit of protein for folding increases aging rapidly

A

heat shock protein

106
Q

rapamycin

A

inhibits mTOR

increases lifespan in rats

107
Q

insulin and IGF produced in response to what and does what

A

GH
-promotes anabolic state
downstream signaling of kinases
-AKT and mTOR

108
Q

sirtuins

A

deacetylases, increase longevity, inhibit metabolic activity, reduce apoptosis, increase insulin sensitivtity and glucose metab.

109
Q

sirtuin ___ contrbutes to metabolic adaption of caloric resrtiction
-promotes genomic integrity by activating DNA repair enzymes through deacylation

A

6

110
Q

caloric constriction effect

A

reduce signal intensity of IGF-1
-reduced cell damage
lower rate of cell growth and metab

MOD 1 (6 decks)

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