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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
liquefactive necrosis
enzymatic destruction of cells LYSOSOMAL enzymes tissue digestion Brain abcess pancreatitis
26
what type presents as cavitary lesions in brain
liquefactive
27
caseous
coag + liquefactive | TB/ histoplasmosis / nocardia
28
recap sizes of pulmonary mycosis
``` HBCP H small B medium C large P large ```
29
fat necrosis
necrosis of adipose tisse | chalky white app --- calcium depostiion
30
where can we see fat necrosis
breast (trauma) | peripancreatic fat
31
when TG break down what happens to the glycerol
used for energy | changes to DHAP----- glyc 3p------ glycolysis
32
what happens in hypercalcemia
hypercalcemia is activator of enzyme fat necrosis
33
how does saponifaction present on stain
DARK BLUE
34
what happens in alkaline ph to calcium
free calcium is DECREASED as it binds to COO-
35
fibrinoid necrosis
TYPE 3 ag ab complex deposit within vessel wall ----- leakage of fibrinogen BRIGHT PINK
36
examples of typ3 HSN
``` SHARP SLE HSP/ HSPN Arthus RPGN PAN/ PSGN ```
37
malignant htn assc with whch necrosis
fibrinoid | onion skin hyperplastic arteriosclerosis
38
DOC for HTN emergency
hydralazine / labetolol nifedipine
39
pre eclampsia
proteinuria + HTN >20 weeks gestation
40
pre eclampisa findings in <20 week gestation means
MOLAR preg
41
what is PANTT
``` PGI2 Ach Nitric oxide TpA Thrombomodulin ```
42
complication of pre eclampsia
coagulopathy due to spiral vessels abruptio placenta renal perf is dec----- r/o renal failure
43
abruptio placenta
``` premature seperation of placenta charc by PAINFUL bleeding R/f cocaine eclampsia pre e trauma smoking ``` 3rd trimestrer
44
DIC
delivery (abruptio placenta/ amniotic fluid embolism) Infection (ecoli/nisseria) Cancer (adeno/ aml m3 auer rods)
45
what activates coag cascade in adeno
mucin
46
placenta previa
attachment of placenta at lower segment of uterus (<2cm) to internal os painless bleeding in 3rd trimester treatmnt= C section
47
vasa previa
fetal vessels close tocervical os (umbilical cord)
48
triad of placenta previa
rupture of mebrane painless bleeding bradycardia***8
49
causes of schistocytes
``` sheared RBCs DIC TTP HUS HELLP MAHA (micro or macro) --- macro is with prosthetic valves ```
50
HELLP
hemolysis elevated liver enzyme low platelets ---- subcapsular hematoma rupture of this hematoma ---- hypotension
51
gangrenous necrosis
DRY ---- mimics coagulative ---- Gi tract / diabetic | WET ---- mimics liquefactive ---- superinfectino
52
Neural crest origin
``` MOTELPASS Melanocytes Odontoblast Tracheal cartilage Enterochromaffin cells / endocardial cushion Laryngeal cartilage Pia matter All ganglia/ adrenal medulla Schwann cells Spiral membrane ```
53
why is MCA is most commonly involved in embolism
its a direct continuation of ICA face motor/ sensory / broca/ werneckie
54
cytotoxic cd8 cells
cell mediated intracellular virally infected cells | cancer cells
55
intrisic vs extrinsic apoptosis
intrinsic --- mitochondria receptor mediated pathway damage via uv light heat ( thrombospondin / phosphatidylserine)
56
BCL2
inhibits release of cytochrome c antiapototic
57
bax bak
create pores --- increase cytochrome c release pro apoptotic
58
mutations with BCL2
over activation folliculr lymphoma t 14 18 DLBL CLL
59
CLL mannifestation
``` HATS Hypogamaglobulinemia AIHA Tx of DLBL ---- richters transformation SLL ```
60
extrinsic pathway
``` FAS FASL (CD95) death receptor ```
61
why is extrinsic pathway important
negative selection in T CELLS
62
BCL2 inhibitor
venetoclax
63
PD receptor
nevalumab | pembrolizumab
64
CTLA 4
ipilimumab
65
PD ligand
azetolezumab durvalumab avelumab
66
caspases
cysteine aspartic acid proteases

dr taher classes HK (24 decks)

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