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YEAR 2 CR > year 2 CR > Flashcards

year 2 CR Flashcards

1
Q

how to check if pt has antibodies against RBC cell membrane

A

direct coombes test

direct antiglobulin test

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2
Q

cause of autoimmune hemolytic anemia

A

idiopathy
drig (methylodpa, penicilin,
blood truasfusion
systemic lupus erythematosus

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3
Q

pr segment

A

0.04s

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4
Q

p wave

A

0.08

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5
Q

pr interval

A

0.12 to 0.22

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6
Q

qrs size

A

less 0.12

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7
Q

QT interval

A

male less than 0.45 females less than 0.47

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8
Q

isoelectric segment is

A

PR segment

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9
Q

1 large square is how many seconds

A

0.2

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10
Q

1 s,mall square is how many seconds

A

0.04

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11
Q

how to measure rate on ECG using squares

A

how many Rs in 30 squares and musltiply by 10 or number of Rs in 15 squares multiply by 5

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12
Q

characteristics of sinus rhytms

A

RR interval is regular

each P gives rise to a QRS

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13
Q

which lead is the stadnard lead

A

lead II

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14
Q

whta happens in the heart durin the PR interval

A

time from SA node to AV node (atrial depolarization)

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15
Q

diagnosis if RR interval irregular but normal P waves

A

heart block

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16
Q

Dx if QRS is enalrged

A

heart block because the signal travel theoght he myocytes and not the purkinjee fibres, so it takes longer to deporalise the ventricles.

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17
Q

shape of P wave in V1

A

biphasic

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18
Q

when is the QRS segment positive

A

in leads I and II

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19
Q

what are the two main layers of the VENTRICULES

A

endocardial muscle and epicardial muscle

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20
Q

which layer of hte ventricular muscle is innervated by pirkinjeefibres

A

the endocardial mucle. thats why it deporalises first and you see t wave so the delay and depolarization fo the epicardial muscle.

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21
Q

when woyld the ST segment change

A

if htere is a difference in contractility in the epicardail adn endocardial muscle

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22
Q

which ventricular layer is more susceptible to iscemia

A

the endocardial.

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23
Q

effetc of iscehmia on endocardial tisuse

A

slows AP. so if epicaridal muscle has a normal prfusion then you would get an inverted T wave on lead II

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24
Q

is inverted T wave a source for concern

A

not in kinds, its begning, but sign of PE or sichemia in adults.
normal if seen on lead I due to oreitnation of the heart.

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25
Q

hypersegmented nucleus seen in what condition

A

pernicious anemia

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26
Q

cause of large t wave

A

hyperkalemia, which prolongs the endocardial AP nore than epicardial

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27
Q

HR to classific as bradycardia

A

less than 60bpm

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28
Q

HR to classific as bradycardia

A

mroe than 100bpm

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29
Q

when is bradycardia not a source for concern

A

atheletes, pts on BB, vagal tone from drug abusers, hypoglycemia, brain injury

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30
Q

poem for heart conditions on ECG

A

if R is far from P then you have first degree, (HB)
long long long drpo then you have washenback (mobitz1) same as II degree HB
if some ps dont get through then you have mobits 2 same as 2nd degrese HB
if P and Q dont agree then you have mobitx 3

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31
Q

junctional rythm

A

when SA node is damaged and AV node takes over

no P wave, or inverted in lead II, bradycardia.

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32
Q

ventricular tachycardia

A

rapid irregular rythm
QRS regular
no p wave,
ST and long WRS.

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33
Q

vfib

A

nimporte quoi

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34
Q

atrial flutter

A

RR are regualrrly irregualr, pacemaker pulses form SA node byt nimpore qcomment
P wave becoms F (fñutter) wave.

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35
Q

atrial fib

A

RR irregularly irregulear. pacemaker oulses from around atrium

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36
Q

cause of ventrcular tachycardia

A

caridomyopathy, alcohol, caffeie, CAD,

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37
Q

risk of ventricualr tachycardia

A

cardia arrest

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38
Q

risk of v fib

A

EMERGNCY NEED A defibrillatory

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39
Q

bunble branch block pathophys

A

ischemia ot psoteiror and anterior interventricualr muscles. long QRS. you have a nothc on the r wave

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40
Q

STEMI on ecg

A

new ST elevation in 2 or more adjacent ecg leads

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41
Q

cause of stemi

A

ischeia of coronary artery, failure of vernticular AP to propagate into some parts of ventriculr msucle.

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42
Q

which is worse stemi or nstemi

A

nstemi

43
Q

when you have ST elevation in some leads, what happens to ST in other leads

A

ST recipriolca depression

44
Q

causes of st depression

A

coronary iscehmia, hypokalemia, loss of strnght in endocardial muscele.

45
Q

shape of QRS in leads I and II

A

upriht

46
Q

whats special about AVR wave shapes

A

all are negatve

47
Q

where might ST be normally elevated

A

in v1 v2

48
Q

what happens to r wave as you move from v1 to v6

A

it keeps increasing

49
Q

s wave in chest leads disapears where

A

v6

50
Q

causes of macrocytic anemia

A 
penicious anemia (intrisnce factor def due to autoimmune)
folate def
b12 def
hemolytic disease (herediatry speherocytosis, G6PD, automiimune)
51
Q

what does primary hemostasis resut in the formation of

A

platelet plug

52
Q

what does secondary hemostasis result in the formation of

A

fibrin clot

53
Q

tell me about how platelets are derived from HSC

A

HSC
myeloid progenotir
megakrocytes
platelets

54
Q

diameter of paltelets

A

1-4 um

55
Q

do platelets have a a nucleus

A

no

56
Q

normal values of platlets

A

150-400x10^9

57
Q

lifespan of platelets

A

8 to 10 days

58
Q

dx of thrombocytopeniea

A

less than 150 x 10^9 plateelets

59
Q

where are platelets made

A

bone. marrow

60
Q

what are the two steps of primary hemostasis

A

lcoal vasoconstriction

formation of the paltelet plug

61
Q

how does primary hemostasis local vasconstriciton work

A

No and PG12 are normally released by healthy endothelial cells. to cause vasodilation.

if endothelium is damaged, no release. so vasconstriciton.
also, endothelin is released to cause vasocontrictin, smooth muscle cell proliferation and the release of noradrenaline.

so overlall, bleeds less

62
Q

in what conditiondo you get high endothelin release

A

hypertension

63
Q

exaplin formation of platelet plug

A
  1. CT is under endothelium
  2. is endothelium is damaged then CT is exposied..
  3. VWF from plasma binds the colalgen
  4. platelets bind VWF via GP1b
    platelets that bind VWF express G2b/G3a receptor.
    fibrinogen binds the g2b/g3a receptor so formatiom of paltelet. cluster.
    platelets are activated when they bind firbonegn.
    platelets become spiky and entangled.
    platelets release ADP, TXA2, serotonin from granules (platelet release reaction)
64
Q

when are platelets activated

A

when they bind firbinogen

65
Q

whahts the platelet release reactin

A

platelets are activated when they bind firbonegn.
platelets become spiky and entangled.
platelets release ADP, TXA2, serotonin from granules (platelet release reaction)

66
Q

goal of the platelet releae reaction

A

to attract more platelets to the site.

to induce unbound platelets to express g2b/g3a

67
Q

whats a platelet plug made of

A

fibirnogen and ertyhrocyte.

68
Q

defin bleeding time

A

time to form an effective platelet plug and stop bleeding

69
Q

normal bleeding time

A

1-9 mims

70
Q

when is bleedig time longer

A

female

kids

71
Q

why is aspirin anticoagulatnt

A

cyclogenase makes prostaglandin makes tormboxane (procoagulatnt.

aspirin is cuclogenase inhibitor. so no procoagulatn

72
Q

goal of secondary homnetstatis

A

formation of fibrin clot throuhg the coagulation cascade

73
Q

components of the coagulation cascade

A

3 steps.

  1. extrisic coagultion pathways
  2. intrinsic coagulation pathway
  3. common pathway
74
Q

whats the initiation phase a part of

A

extrinsic pathway

75
Q

expalin initiation phase

A

vessel damage causes release of Tissue factor3. on subendothelial tissue

TF3 changes F7 to F7a

F7a (and calcliun) chaneges facotr 10 to 10a

10a changes prothomon to throbim but at low levels so needs amplification

thrombin converts:
5 to 5a (imcreases P-T)
8 to 8a
11 to 11a

11a changes 9 to 9a

8a and 9a increase conversion 10 to 10a which changes more P to T

76
Q

common coagulation pathway

A

conversion from P to T is actually part of the comon pathways.

lead to sequece of rxns between prot to T crosslinking.

so P goes to T using 10a and CAlcium.

thombin changes fibrinogen to fibrin. also thormbin makes factor 13 whcih goes into 13a.

and 13agoes from fibrin to crosslinking fibrin

77
Q

does thrombin polymerises all fibrinogen

A

nah only the bound ones.

otherwise, DIC (due to sepsis)

78
Q

whats hagemans facotr

A

factor 12

79
Q

whast teh intrinsic coagulation pathway

A

12 to 12a which increases kallikerins (bradkykinene

12 a changes 11 to 11a

11a chanegs 9 to 9a

9a and calcium from x to xa

xa feeds into p to T (common pathway)

80
Q

goal of bradykinin

A

extrvarsion of water into tissue
so swlling
leukocyte leade blood, enter tissue to fight pathogen
veins consrict.

81
Q

what pathywas are measured by prothombin time

A

extrinsic and common

82
Q

Prothormbin time?

A

blood test in tube with citrate which chelates CA2plus and prevents clotting by blocking fctor 10a.

add excess calcium adn tisue factor

measures time taken for sample to clot measured using otpical instrument.

concerted to INR.

83
Q

actiuvated partial thromboplastin time measures what pathways

A

instrinsic and common paheay

84
Q

APPT how does it work

A

blood drain. add calcium and kyaline which triggers factor 12a.

85
Q

what does bleeding time assess

A

platelet plug formation.

86
Q

INR measures adm nromal values

A

0.8 to 1.2

derived from PT.
assess coagulability of blood. for at risk pts aim for 2 to 3 (if pts on warfarin/heparin)

high INR means slow clotting.

87
Q

hemophilia A is dercreased inw aht factor

A

8

88
Q

hemophilia B is dercreased inw aht factor

A

9

89
Q

inheritence of hemophila A

A

x linked so mostly in males

90
Q

what happens in hemophilia A

A

less fcto 8 which is not part of initiation phase, onlhy used for thombin amplification.
so less thormbin formation and clos are weak adn easily disloged.

91
Q

what happens in hemophilia B

A

less levels of factor 9 so less htombin amplification

92
Q

how to remove clots

A

plasmin: breaks down fibrin and lyses clot.
plasminogen: inactivates plasmin

plasminogen is part of the platelet plug

93
Q

palsminogen is kept inactive by

A

alpha 2 antipalsmimn so when tissue is helaed, you get inhibition of alpha 2 antiplasmin.

94
Q

TPA is relased by

A

endothelial cells. converts palsminogen to palsmin.

95
Q

what are ddimers

A

fibrin fragmentws. high in DVT

96
Q

vitamin K required for

A

factors 7 9 10 bc modifies protein to allow binding of ca2plus

97
Q

when is vitamin k deficient

A

liver disease, pooe deit, high INR

98
Q

classic anticoagulanta

A

heparin
warfarin
antithrombin
DOACs direct antithrombin inhibitor

99
Q

heparin

A

binds anad activates antithrombin which inhibits thombin and factor 10a

given in IV becasue absorbed poorly.

short half life

give conitnously

100
Q

warfarin

A

competes with site that bind vitmain k so reduces effecicay of clotting factors 7, 9 10
and inrease PT

101
Q

warfarin effect on PT

A

increases

102
Q

antithrombin

A

plasma protein binds and inactivates enzymof coagulation adn prevents spontaneous clotting

103
Q

DOACs direct antithrombin inhibitor

A

like dabagitran
factor 10a inhibitor
less s e but mroe expansive

hard to stop effect so porblmeatic in emergencyes. so hard predictor worse than warfarin

NOAC: better predicting than warfaring nut

YEAR 2 CR (3 decks)

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