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Pathology > 1.2 types of injury > Flashcards

1.2 types of injury Flashcards

1
Q

Types of injury (8)

A 
hypoxia
microbial
physical
chemical
oxygen/free readicals
genetic
immune
nutritional
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2
Q

hypoxia

A

not enough oxygen

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3
Q

anoxia

A

no oxygen

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4
Q

number one killer

A

hypoxia_..storkes, infarctions

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5
Q

decrease input_..global hypoxia (as opposed to foca/local hypoxia)

A

restriction of all oxygen-whole body deprevation

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6
Q

examples of global hypoxia (9)

A 
lack of air,        
inability to take in air,            
inability to transport O2 from the lungs to the blood, 
anemia, 
CO, 
cyanide, 
pump failure, 
dec blood volume, 
inc vascular space
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7
Q

lack of air

A

drowning,

gasses that displace o2 (like evaporating liquid nitrogen)

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8
Q

inability to take in air

A 
external suffocation (cut of O2 only_takes longer), 
strangulation (cuts off O2 and carotids), 
plugged pipes (blocked trachea)
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9
Q

anemia

A

low hemoglobin/rbc

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10
Q

CO

A

irreversibly binds heme and shifts o2 binding curve_.person will be cherry red, the venous blood will be red like arterial blood

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11
Q

cyanide

A

uncouples oxidative phosphorylation - blocks cytochrome c oxidase

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12
Q

pump failure

A

can’t move blood around - heart is not pumping enough blood - cardiogenic shock

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13
Q

increased vascular space

A

but the same volume remains so this results in spetic shock - decrease pressure

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14
Q

decreased blood volume

A

bleeding out

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15
Q

most common cause of local hypoxia

A

ischemia (dec blood flow) ex. Coronary artery gets ischemic causing heart not to get enough blood

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16
Q

ischemia is worse than hypoxia bc

A

not only less o2 delivery but also don’t get metabolites needed for glycolysis and waste is not carried away like lactic acid

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17
Q

hypoxia is low o2 so there is a switch to_.

A

glycolysis

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18
Q

lactate pH and ATP, ADP in ischemia

A

lactate inc,
pH dc,
ATP dec,
ADP inc

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19
Q

Causes of ischemia

A

arterial occlusion, venous occlusion,

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20
Q

arterial occlusion (4)

A

artherosclerosis,
thrombosis,
embolization,
external pressure

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21
Q

venous occlusion

A

thrombosis–usually anastomotic channels are able to overcom this but in the kidney there is only one renal vein so thrombosis can cause blood to stop coming out, flow goes to zero, infac

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22
Q

how do you tell if venous or arterial occlusion

A

arterial - pale when it dies,

venous - engorged with blood and hemorrhaged

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23
Q

Effects of hypoxia

A

dec mitocondrial oxidated phosphorylation, dec ATP, dec activity of ATP dependent fn, in clycolysis dec pH and dec glycogen, ribosome detachment so dec protein synthesis

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24
Q

Anaerobic glycolysis

A

glucose + 2 adp –> 2 lactate + 2 atp (only 2 atp)

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25
Q

Aerobic glycolysis

A

glucos + 6O2 (this is not used in glycolysis) + 36 adp —> 6 CO2 + 6 H2O + 36 ATP (glycolysis + oxidative phosphorylation)

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26
Q

aerobic organs

A

brain and heart

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27
Q

problem with aerobic atp production

A

free radicals due to the use of O2, but normally we have defenses for it

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28
Q

reperfusion injury

A

an area the is occluded has blood with O2 returned to it, but that O2 forms free radicals by endothelial cells and leukocytes from inflammation causing more damage

29
Q

What is a free radical

A

an atom/molecule with an unpaired electron that makes it extremely reactive and reactions lead to creation of more free radicals (chain reaction)

30
Q

importance of free radicals

A

react with and modify cellular constituents, initiate chain reactions when they react with adjacent atoms and molecules amplifying their effect

31
Q

how are free radicals made

A

additions of electors to molecular oxygen (reduction in ETC), cytochrom p450 metabolism

32
Q

important oxygen radicals

A

superoxide aniion, hydrogen peroxide, hydroxyl radical (o2-, h2o2, oh’)

33
Q

which ROI reacts w/ pretty much anything

A

Oh’

34
Q

what is bad about superoxide

A

its ability to dismutate and frorm hydrogen peroxided that can then, with iron, from the hydrocxyl radical; it also reduces iron to the ferrous state

35
Q

fenton rxn

A

O2 + e- –> O2- ,O2 - + Fe 3+ –> Fe 2+ + O2, 2 O2- –> H2O2, Fe 2+ + H2O2 –> Fe 3+ + OH ‘

36
Q

what does vit C do

A

makes situation worse turning Fe3+ to Fe2+. This ferrous iron lying around can react w/ h2o2 to from the deadly OH’ radical

37
Q

radical and cell death

A

when cells die these radicals leak out causing damage

38
Q

Lipid peroxidation happens with

A

free radicals and unsaturated fatty acids_.very bad bc of chain reactions eating up membranes

39
Q

4-hydroxylnanol (4- HNE)

A

highly toxic and damage cell resulting from chronic lipid oxidation

40
Q

AA with sulfur are

A

cysteine and methionine

41
Q

SH groups can be oxidized resultinging

A

S–S bond causing conformational changes, loss of enzyme activity, and protein crosslinking

42
Q

SH group modification changes enzyme activity by

A

inhibiting ca atpases in membrane, ER/SR causing cytosolic ca to rise leading to death, and also causes cytoskeletal crosslinking

43
Q

oxidant defenses

A

superoxide dismutase (cytoplasm, mitochondria, and plasma, catalase (peroxisomes), glutathione perosxidases (cytoplasm, plasma), glutathione reductase

44
Q

problem with catalase

A

in peroxisome for fatty acid oxidation so cant protect from cytosol free radicals

45
Q

glutathione peroxidase

A

2 red glut + h2o2 –> ox glut-glut + h2o req. selenium, lipid peroxides also substrate

46
Q

glutathione reductase

A

ox glut-glut + nadph –> 2 red glut + nadp

47
Q

reduced glutathione

A

directly scavenges radicals

48
Q

vit E (alpha tocopherol)

A

scavenges radicals in cell membranes

49
Q

ascorbic acid (vit C)

A

antioxidant in plasma (also reduced fe3+ to fe 2+)

50
Q

uric acid (purine metabolite)

A

antioxidant in plasma

51
Q

ferritin, transferrin, lactoferrin, and ceruloplasmin

A

bind fe 2 + and cu2+

52
Q

hemochromatosis

A

genetic condition with lots of free iron (should normally be bound)

53
Q

Physical injury (5)

A

electricity, radiation (free radicals), trauma, temperature, 357 magnum

54
Q

chemical injury

A

corrosives, toxins and poisons (free radicals), carcinogens, sensitizers

55
Q

direct cehmical injury

A

cyanide - direct inhibition of cyt C

56
Q

indirect cehmical injury

A

ccl4 (in p450 sys makes CCl3’ radical) acetaminophen( in p450 sys decreases GSH)

57
Q

Carbon tetrachloride

A

when reactive in liver forms lipid peroxidation

58
Q

slide 74

A

do you know it yet?????

59
Q

Microbial injury (6)

A

bacteria, viruses, fungi, parasites, richettsia, prions

60
Q

Genetic injury

A

chormosomal abnormalites, mutations deletions, interaction with environment

61
Q

Immune injury

A

allergy, anaphylaxis, autoimmune antiboides, antigen-antibody complexes, cell-mediated autoimmunity, transplant rejection

62
Q

morphology associated with reversible injury

A

cell swelling, mitochondrial swelling, small dense bodies in mitochondria, membrane blebbing and swelling, intracellular accumulations

63
Q

cell swelling

A

hydropic degeneration and cloudy swelling

64
Q

why do cells swell during ischemia

A

lack of blood supply–>dec oxygen –>na/k atp pumps cant work –> sodium keeps comingin and water follows sodium –>swelling

65
Q

tissue osmolality ___..due to catabolism within ischemic cells

A

increases

66
Q

Lipid accumulation in hepatocytes due to

A

impaired lipoprotein synthesis (ethanol protein malnutrition),
decreased fatty acid oxidation (hypoxia),
increased liberation of fat from peripheral stores (starvation)

67
Q

radiation can also cause

A

cataracts, esophageal stricture, pulomnary fibrosis, congenital malformations, sterility, nephritis, transversemyelitis, myocaridal fibrosis, constrictive pericarditis

68
Q

why is tylenol bad

A

acetaminophen–>benzoquinone–>depletes GSH–>protien thiol oxidation–>crosslinking membrane proteins–>cell death

Pathology (26 decks)

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