pharmacology

Question 1

phase 4

Answer 1

resting potential outward flux of K is dominant

Question 2

phase 0

Answer 2

upstroke, inward flux of Na is dominant

Question 3

phase 1

Answer 3

early repolarisation, outward flux of K is dominant

Question 4

phase 2

Answer 4

plateau, inward flux of Ca2+ is roughly balanced by outward flux of K

Question 5

phase 3

Answer 5

final repolarisation, outward flux of K is dominant

Question 6

sympathetic regulation of cardiac rate and force

Answer 6

noradrenaline and adrenaline activate beta 1 adrenoceptors in nodal and myocardial cells
coupling through G protein alpha subunit stimulates adenylyl cyclase to increase the intracellular concentration of cyclic AMP

Question 7

parasympathetic regulation of cardiac rate and force

Answer 7

acetylcholine activates M2 muscarinic cholinoreceptors largely in nodal cells
coupling through G protein via alpha subunits inhibits cyclase and reduces cAMP, via beta/gamma subunit dimer opens specific potassium channels in the SA node
decreased SA node action potential frequency and heart rate

Question 8

funny current

Answer 8

depolarising current, blocked HCN channels in SA ode slows heart rate

Question 9

excitation contraction coupling in cardiac muscle - contraction

Answer 9

ventricular action potential
opening of voltage actived Ca2+ channels during phase 2
Ca2+ influx into cytoplasm
Ca2+ release from the sacroplasmic reticulum
Ca2+ binds to troponin C and shifts tropomyosin out of the actin cleft
cross bridge formation between actin and myosin resulting in contraction via the sliding filament mechanism

Question 10

excitation contraction coupling in cardiac muscle - relaxation

Answer 10

repolarisation in phase 3 and 4
voltage activated Ca2+ channels close
Ca2+ efflux occurs by the Na/Ca exchanger
Ca2+ release from the sarcoplasmic reticulum stops, active sequestration of Ca2+ from the cytoplasm now dominates
Ca2+ dissociates from troponin C
cross bridges between actin and myosin break resulting in relaxation

Question 11

nitrates

Answer 11

organic nitrates relax all smooth muscle via their metabolism to nitric oxide

Question 12

calcium channel blockers

Answer 12

block or prevent opening of channels in excitable tissues in response to depolarisation and limit increase of Ca, causes vasodilation

Question 13

haemostasis

Answer 13

arrest of blood loss form a damaged vessel at the site of injury involves a sequence

Question 14

primary haemostasis

Answer 14

local vasoconstriction, platelet adhesion, activation and aggregation

Question 15

inactive factors

Answer 15

X

II - prothrombin

Question 16

active factor

Answer 16

IXa
Xa
IIa - thrombin

Question 17

active cofactor

Answer 17

VIIIa

Va

Question 18

arterial thrombus

Answer 18

white thrombus - mainly platelets in a fibrin mesh
forms an embolus if it detaches often causes a stroke
primary treatment is antiplatelet drugs

Question 19

venous thrombus

Answer 19

red thrombus - white head, jelly like red tail fibrin rich
embolus usually in the lung
primary treatment is anticoagulant

Question 20

rivaroxiban

Answer 20

directly inhibits factor Xa

Question 21

LMWH and fondaparinux

Answer 21

inactivate foactor Xa via antithrombin III

Question 22

Dabigatran

Answer 22

directly inhibits factor IIa

Question 23

heparin

Answer 23

inactivates factor IIa via antithrombin III

Question 24

warfarin

Answer 24

structurally related to vitamin K with which it competes for binding to hepatic vitamin K reductase preventing production of the active hydroquinone
renders factors II, VII, IX and X inactive
slow onset
low therapeutic index
long half life 40 hours