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dr taher classes HK > cvs 21 > Flashcards

cvs 21 Flashcards

1
Q

most susceptible to cell injury

A

neurons (inc O2 demand)

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2
Q

least susceptible to cell injury

A

skeletal muscle

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3
Q

most common cause of hypoxia is

A

ischemia

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4
Q

swelling of the cell is caused by

A

decrease in Na/K atpase pump function

also swelling of ER — blebformation

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5
Q

when o2 supply is decreased ATP decreases and what happens to pH

A

low pH

clumping of nuclear chromatin

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6
Q

other complications of low atp in cell

A

dettachment of ribosomes — dec protein synthesis

lipid deposition

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7
Q

myelin figures

A

made up of phospholipids whch make up cell membrane

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8
Q

hibernating myocardium

A

chronic myocardial ischemia —dec myocardial metabolism and function —- tries to match with the coronary blood flow — can lead to systolic dysf

once revascularized it may improve too

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9
Q

irreversible cell injury

A

damage to cell membrane due to constatnt influx of water
loss of membrane phospholipids
protective amino acids like glycine lost

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10
Q

influx of calcium leads to

A

dense mitochondria - reduce mitochondrial functioning

mitochondrial vacuolization

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11
Q

what activate enzymes and what enzymes are these

A

calcium

endonucleases protease

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12
Q

what is the significant change in irreversble cell injury

A

pyknosis ( condensation of nuclear chromatin)
karyorhexis (fragmentation by endonucleas)
karyolysis (nucleus break down)

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13
Q

what can cause hypoventilation

A 
opiods
barbiturates
CNS injury
C3 C4 C5 keeps diaphragm alive
Nm disease
obesity hypoventilation synd
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14
Q

A-a gradient in hypoventilatino

A

normal

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15
Q

when can diffusion of O2 get affected

A

fibrosis — restrictive lung disease

barrier is thick

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16
Q

always pathological

A

necrosis

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17
Q

necessary for homeostasis

A

apoptosis

removal of cancer cells for ex by CD8 and NK cells

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18
Q

swelling of cell

A

necrosis

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19
Q

cellular shrinkge a

A

apoptosis

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20
Q

inflammation

A

necrosis

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21
Q

step ladder pattern on gel electrophoresis

DNA LADDERING

A

apoptosis

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22
Q

coagulative necrosis

A

most common type (necrosis)
LOSS of nucleus but cellular outline is preserved

all tissue except brain

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23
Q

what does eosin staining show in coag necrosis

A

PINK RED discolouration

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24
Q

sheehan syndrome is an example of

A

coag necrosis

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25
Q

liquefactive necrosis

A

enzymatic destruction of cells
LYSOSOMAL enzymes tissue digestion

Brain abcess pancreatitis

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26
Q

what type presents as cavitary lesions in brain

A

liquefactive

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27
Q

caseous

A

coag + liquefactive

TB/ histoplasmosis / nocardia

28
Q

recap sizes of pulmonary mycosis

A 
HBCP 
H small 
B medium 
C large
P large
29
Q

fat necrosis

A

necrosis of adipose tisse

chalky white app — calcium depostiion

30
Q

where can we see fat necrosis

A

breast (trauma)

peripancreatic fat

31
Q

when TG break down what happens to the glycerol

A

used for energy

changes to DHAP—– glyc 3p—— glycolysis

32
Q

what happens in hypercalcemia

A

hypercalcemia is activator of enzyme fat necrosis

33
Q

how does saponifaction present on stain

A

DARK BLUE

34
Q

what happens in alkaline ph to calcium

A

free calcium is DECREASED as it binds to COO-

35
Q

fibrinoid necrosis

A

TYPE 3 ag ab complex
deposit within vessel wall —– leakage of fibrinogen

BRIGHT PINK

36
Q

examples of typ3 HSN

A 
SHARP 
SLE
HSP/ HSPN
Arthus
RPGN
PAN/ PSGN
37
Q

malignant htn assc with whch necrosis

A

fibrinoid

onion skin hyperplastic arteriosclerosis

38
Q

DOC for HTN emergency

A

hydralazine / labetolol nifedipine

39
Q

pre eclampsia

A

proteinuria + HTN >20 weeks gestation

40
Q

pre eclampisa findings in <20 week gestation means

A

MOLAR preg

41
Q

what is PANTT

A 
PGI2
Ach
Nitric oxide
TpA
Thrombomodulin
42
Q

complication of pre eclampsia

A

coagulopathy due to spiral vessels
abruptio placenta
renal perf is dec—– r/o renal failure

43
Q

abruptio placenta

A 
premature seperation of placenta 
charc by PAINFUL bleeding 
R/f 
cocaine
eclampsia
pre e
trauma 
smoking

3rd trimestrer

44
Q

DIC

A

delivery (abruptio placenta/ amniotic fluid embolism)
Infection (ecoli/nisseria)
Cancer (adeno/ aml m3 auer rods)

45
Q

what activates coag cascade in adeno

A

mucin

46
Q

placenta previa

A

attachment of placenta at lower segment of uterus (<2cm) to internal os
painless bleeding in 3rd trimester

treatmnt= C section

47
Q

vasa previa

A

fetal vessels close tocervical os (umbilical cord)

48
Q

triad of placenta previa

A

rupture of mebrane
painless bleeding
bradycardia***8

49
Q

causes of schistocytes

A 
sheared RBCs 
DIC
TTP
HUS
HELLP
MAHA (micro or macro) --- macro is with prosthetic valves
50
Q

HELLP

A

hemolysis elevated liver enzyme low platelets —- subcapsular hematoma

rupture of this hematoma —- hypotension

51
Q

gangrenous necrosis

A

DRY —- mimics coagulative —- Gi tract / diabetic

WET —- mimics liquefactive —- superinfectino

52
Q

Neural crest origin

A 
MOTELPASS
Melanocytes
Odontoblast
Tracheal cartilage
Enterochromaffin cells / endocardial cushion
Laryngeal cartilage 
Pia matter
All ganglia/ adrenal medulla
Schwann cells 
Spiral membrane
53
Q

why is MCA is most commonly involved in embolism

A

its a direct continuation of ICA

face motor/ sensory / broca/ werneckie

54
Q

cytotoxic cd8 cells

A

cell mediated intracellular virally infected cells

cancer cells

55
Q

intrisic vs extrinsic apoptosis

A

intrinsic — mitochondria

receptor mediated pathway
damage via uv light
heat ( thrombospondin / phosphatidylserine)

56
Q

BCL2

A

inhibits release of cytochrome c

antiapototic

57
Q

bax bak

A

create pores — increase cytochrome c release

pro apoptotic

58
Q

mutations with BCL2

A

over activation
folliculr lymphoma t 14 18
DLBL
CLL

59
Q

CLL mannifestation

A 
HATS
Hypogamaglobulinemia
AIHA
Tx of DLBL ---- richters transformation
SLL
60
Q

extrinsic pathway

A 
FAS FASL (CD95)
death receptor
61
Q

why is extrinsic pathway important

A

negative selection in T CELLS

62
Q

BCL2 inhibitor

A

venetoclax

63
Q

PD receptor

A

nevalumab

pembrolizumab

64
Q

CTLA 4

A

ipilimumab

65
Q

PD ligand

A

azetolezumab
durvalumab
avelumab

66
Q

caspases

A

cysteine
aspartic acid
proteases

dr taher classes HK (24 decks)

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