year 2 CR Flashcards
how to check if pt has antibodies against RBC cell membrane
direct coombes test
direct antiglobulin test
cause of autoimmune hemolytic anemia
idiopathy
drig (methylodpa, penicilin,
blood truasfusion
systemic lupus erythematosus
pr segment
0.04s
p wave
0.08
pr interval
0.12 to 0.22
qrs size
less 0.12
QT interval
male less than 0.45 females less than 0.47
isoelectric segment is
PR segment
1 large square is how many seconds
0.2
1 s,mall square is how many seconds
0.04
how to measure rate on ECG using squares
how many Rs in 30 squares and musltiply by 10 or number of Rs in 15 squares multiply by 5
characteristics of sinus rhytms
RR interval is regular
each P gives rise to a QRS
which lead is the stadnard lead
lead II
whta happens in the heart durin the PR interval
time from SA node to AV node (atrial depolarization)
diagnosis if RR interval irregular but normal P waves
heart block
Dx if QRS is enalrged
heart block because the signal travel theoght he myocytes and not the purkinjee fibres, so it takes longer to deporalise the ventricles.
shape of P wave in V1
biphasic
when is the QRS segment positive
in leads I and II
what are the two main layers of the VENTRICULES
endocardial muscle and epicardial muscle
which layer of hte ventricular muscle is innervated by pirkinjeefibres
the endocardial mucle. thats why it deporalises first and you see t wave so the delay and depolarization fo the epicardial muscle.
when woyld the ST segment change
if htere is a difference in contractility in the epicardail adn endocardial muscle
which ventricular layer is more susceptible to iscemia
the endocardial.
effetc of iscehmia on endocardial tisuse
slows AP. so if epicaridal muscle has a normal prfusion then you would get an inverted T wave on lead II
is inverted T wave a source for concern
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.
hypersegmented nucleus seen in what condition
pernicious anemia
cause of large t wave
hyperkalemia, which prolongs the endocardial AP nore than epicardial
HR to classific as bradycardia
less than 60bpm
HR to classific as bradycardia
mroe than 100bpm
when is bradycardia not a source for concern
atheletes, pts on BB, vagal tone from drug abusers, hypoglycemia, brain injury
poem for heart conditions on ECG
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
junctional rythm
when SA node is damaged and AV node takes over
no P wave, or inverted in lead II, bradycardia.
ventricular tachycardia
rapid irregular rythm
QRS regular
no p wave,
ST and long WRS.
vfib
nimporte quoi
atrial flutter
RR are regualrrly irregualr, pacemaker pulses form SA node byt nimpore qcomment
P wave becoms F (fñutter) wave.
atrial fib
RR irregularly irregulear. pacemaker oulses from around atrium
cause of ventrcular tachycardia
caridomyopathy, alcohol, caffeie, CAD,
risk of ventricualr tachycardia
cardia arrest
risk of v fib
EMERGNCY NEED A defibrillatory
bunble branch block pathophys
ischemia ot psoteiror and anterior interventricualr muscles. long QRS. you have a nothc on the r wave
STEMI on ecg
new ST elevation in 2 or more adjacent ecg leads
cause of stemi
ischeia of coronary artery, failure of vernticular AP to propagate into some parts of ventriculr msucle.
which is worse stemi or nstemi
nstemi
when you have ST elevation in some leads, what happens to ST in other leads
ST recipriolca depression
causes of st depression
coronary iscehmia, hypokalemia, loss of strnght in endocardial muscele.
shape of QRS in leads I and II
upriht
whats special about AVR wave shapes
all are negatve
where might ST be normally elevated
in v1 v2
what happens to r wave as you move from v1 to v6
it keeps increasing
s wave in chest leads disapears where
v6
causes of macrocytic anemia
penicious anemia (intrisnce factor def due to autoimmune) folate def b12 def hemolytic disease (herediatry speherocytosis, G6PD, automiimune)
what does primary hemostasis resut in the formation of
platelet plug
what does secondary hemostasis result in the formation of
fibrin clot
tell me about how platelets are derived from HSC
HSC
myeloid progenotir
megakrocytes
platelets
diameter of paltelets
1-4 um
do platelets have a a nucleus
no
normal values of platlets
150-400x10^9
lifespan of platelets
8 to 10 days
dx of thrombocytopeniea
less than 150 x 10^9 plateelets
where are platelets made
bone. marrow
what are the two steps of primary hemostasis
lcoal vasoconstriction
formation of the paltelet plug
how does primary hemostasis local vasconstriciton work
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
in what conditiondo you get high endothelin release
hypertension
exaplin formation of platelet plug
- CT is under endothelium
- is endothelium is damaged then CT is exposied..
- VWF from plasma binds the colalgen
- 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)
when are platelets activated
when they bind firbinogen
whahts the platelet release reactin
platelets are activated when they bind firbonegn.
platelets become spiky and entangled.
platelets release ADP, TXA2, serotonin from granules (platelet release reaction)
goal of the platelet releae reaction
to attract more platelets to the site.
to induce unbound platelets to express g2b/g3a
whats a platelet plug made of
fibirnogen and ertyhrocyte.
defin bleeding time
time to form an effective platelet plug and stop bleeding
normal bleeding time
1-9 mims
when is bleedig time longer
female
kids
why is aspirin anticoagulatnt
cyclogenase makes prostaglandin makes tormboxane (procoagulatnt.
aspirin is cuclogenase inhibitor. so no procoagulatn
goal of secondary homnetstatis
formation of fibrin clot throuhg the coagulation cascade
components of the coagulation cascade
3 steps.
- extrisic coagultion pathways
- intrinsic coagulation pathway
- common pathway
whats the initiation phase a part of
extrinsic pathway
expalin initiation phase
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
common coagulation pathway
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
does thrombin polymerises all fibrinogen
nah only the bound ones.
otherwise, DIC (due to sepsis)
whats hagemans facotr
factor 12
whast teh intrinsic coagulation pathway
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)
goal of bradykinin
extrvarsion of water into tissue
so swlling
leukocyte leade blood, enter tissue to fight pathogen
veins consrict.
what pathywas are measured by prothombin time
extrinsic and common
Prothormbin time?
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.
actiuvated partial thromboplastin time measures what pathways
instrinsic and common paheay
APPT how does it work
blood drain. add calcium and kyaline which triggers factor 12a.
what does bleeding time assess
platelet plug formation.
INR measures adm nromal values
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.
hemophilia A is dercreased inw aht factor
8
hemophilia B is dercreased inw aht factor
9
inheritence of hemophila A
x linked so mostly in males
what happens in hemophilia 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.
what happens in hemophilia B
less levels of factor 9 so less htombin amplification
how to remove clots
plasmin: breaks down fibrin and lyses clot.
plasminogen: inactivates plasmin
plasminogen is part of the platelet plug
palsminogen is kept inactive by
alpha 2 antipalsmimn so when tissue is helaed, you get inhibition of alpha 2 antiplasmin.
TPA is relased by
endothelial cells. converts palsminogen to palsmin.
what are ddimers
fibrin fragmentws. high in DVT
vitamin K required for
factors 7 9 10 bc modifies protein to allow binding of ca2plus
when is vitamin k deficient
liver disease, pooe deit, high INR
classic anticoagulanta
heparin
warfarin
antithrombin
DOACs direct antithrombin inhibitor
heparin
binds anad activates antithrombin which inhibits thombin and factor 10a
given in IV becasue absorbed poorly.
short half life
give conitnously
warfarin
competes with site that bind vitmain k so reduces effecicay of clotting factors 7, 9 10
and inrease PT
warfarin effect on PT
increases
antithrombin
plasma protein binds and inactivates enzymof coagulation adn prevents spontaneous clotting
DOACs direct antithrombin inhibitor
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
