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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

once adrenaline activates B1 ADRs, what happens?

A

stimulates adenylyl cyclase which inc conc. of cAMP which inc SAN AP frequency (due to inc in CA++)

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2
Q

what happens once Ach binds to M2 muscarinic receptors?

A

inhibits adenylyl cyclase so dec conc of cAMP which dec SAN AP frequency

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3
Q

what determines the pacemaker potential

A

depolarisation

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4
Q

give 2 examples of B-ADR agonists & antagonists

A

. adrenaline & dobutamine

. all beta blockers

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5
Q

what is an example of a partial antagonist

A

propranolol

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6
Q

what conditions do B-ADR agonists treat

A

stimulate sympathetic activity so cardiac arrest or heart failure

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7
Q

what conditions do beta-blockers treat

A

slow down HR etc so arrhythmias-A.fib, tachy etc, heart failure, angina, HT

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8
Q

give 3 common side effects of beta blockers

A

cold extremities, bronchospasm, hypoglycaemia

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9
Q

what is digoxin used for

A

heart failure, A.fib

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10
Q

how do calcium sensitisers work

A

open K+ channels causing vasodilation so red. after load

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11
Q

what are lipids transported by

A

lipoproteins

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12
Q

describe a lipoprotein

A

spherical- hydrophobic core with cholesterol & triglycerides and hydrophilic coat with apoproteins

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13
Q

what are the 4 types of lipoprotein

A

HDL, LDL, very LDL, chylomicrons

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14
Q

why is LDL bad?

A

LDL become oxidised to OXLDL which is taken up by macrophages creating a fatty streak- inflammatory response deposits collagen=atheromatous plaque formed

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15
Q

why is HDL good?

A

HDL accepts excess LDL and brings to liver to be converted to hepatocytes

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16
Q

how does haemostasis occur

A

vascular wall damage exposes collagen & tissue factor > 1y haemostasis (vasoconstriction, platelet adhesion, activation/aggregation of fibrinogen) > activation of blood clotting factors and formation of stable clot

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17
Q

describe 1y homeostasis

A

activated platelets synthesises and release thromboxane A2

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18
Q

what does thromboxane A2 do?

A

causes the release of serotonin binds to vessels= vasconstriciton
causes release of ADP= activating platelets and prompting coagulation of blood

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19
Q

fill in the blanks for the Amplifying Cascade;

fibrinogen > _____ > fibrin >

A

thrombin

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20
Q

what is the aggregative & adhesive factor

A

collagen

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21
Q

give the 4 clotting factors

A

2,7,9,10

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22
Q

how are clotting factors converted to their activated form (2a,7a,9a,10a)?

A

an enzyme with VitK Reductase cofactor

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23
Q

what do ECGs show

A

cardiac rate, rhythm, chamber size, electrical axis of heart

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24
Q

when does an electrode generate an upward deflection on ECG

A

when depolarisation moves toward +ve electrode

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25
Q

what is isopotential

A

flat line- no electrical activity

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26
Q

what are the 3 limb leads

A

right arm-left arm
right arm- left leg
left arm-left leg

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27
Q

what are the 3 augmented leads

A

aVR, aVF, aVL

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28
Q

what is unique about the aVR ECG recording

A

it is upside down

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29
Q

True/False…

Limb leads & augmented leads are horizontal

A

false…
they are VERTICAL
chest leads are HORIZONTAL

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30
Q

what do each of the 6 chest leads represent

A

V1 &V2: septal
V3& V4: anterior heart
V5 &V6: lateral aspect of heart (e.g. LV)

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31
Q

P wave…

A

atrial depolarisation- <0.12s

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32
Q

QRS complex…

A

ventricular depolarisation- <0.1sec

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33
Q

T wave…

A

ventricular repolarisation

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34
Q

QT interval…

A

depolarisation & repol of Vs

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35
Q

ST segment…

A

systole

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36
Q

TP segment…

A

diastole

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37
Q

PR interval…

A

AV node delay- (-0.12-0.2sec)

38
Q

what does ST depression show

A

ischaemia

39
Q

what does ST elevation show

A

infarction

40
Q

how to place chest leads

A

V1 next to sternal angle on right

41
Q

What are signs of a normal axis of heart

A

lead 1: +ve deflection

aVF: +ve deflection

42
Q

signs of left axis deviation

A

lead 1: +ve deflection

aVF: -ve deflection

43
Q

signs of right axis deviation

A

lead 1: -ve deflection

aVF: +ve deflection

44
Q

extreme right axis deviation

A

lead 1: -ve deflection

aVF: -ve deflection

45
Q

how do you analyse a rhythm strip

A
  1. Patient details
  2. Check date & time of ECG
  3. Check calibration of ECG paper
  4. Determine axis
  5. Workout rate and rhythm
    a. Is electrical activity present?
    b. Is rhythm regular?
    c. HR? (300 divided by no of big boxes between 1 QRS and next)
    d. Is P-wave present?
    e. What is PR interval like
    f. Is there a QRS after p-wave
    g. QRS duration normal (< 3 small squares)
  6. Look at individual leads for ST or T wave changes
46
Q

what are the 4 anti-cholesterol drugs

A

statins, fibrates, PCSK 9 inhibitors, ezetimibe

47
Q

give examples, used for what, 2 side effects and action of statins

A
  • simvastatin, atorvastatin
  • hyperlipidaemia, angina, CVA
  • risk of MI, renal failure
  • HMG co-enzyme A reductase inhibitors (rate limiting step of cholesterol synthesis= inc in LDL receptors)
48
Q

give an example of a fibrate?

A

bexafibrate

49
Q

what is the suffix of PCSK 9 inhibitors & an example

A

occumab

- evolocumab

50
Q

how do PCSK 9 Inhibitors work

A

inc no of LDL receptors

51
Q

how does ezetimibe work

A

inhibits cholesterol absorption by converting it to bile salts

52
Q

which anti-cholesterol drug is best to treat familial hypercholesterolaemia

A

PCSK 9 inhibitors

53
Q

what are the 4 drug sub-groups to treat hypertension

A

diuretics
beta-blockers
vasodilators
mineralocorticoid antagonists

54
Q

what are the 2 types of diuretics

A

thiazide and loop

55
Q

how do diuretics work

A

block Na re-absorption so inc urine output

56
Q

give an example of a loop diuretic and a thiazide diuretic

A

loop=furosemide

thiazide= bendroflumethiazide

57
Q

beta blockers can be non-selective and…

A

cardioselective

58
Q

how do beta blockers work

A

selective: block binding of adrenaline to either B1 OR B2 ADRs= lower HR, contractility etc so low BP
non-selective: same but block B1 & B2

59
Q

what is the main side effect of b-blockers

A

cold extremities

60
Q

what are 4 vasodilation drugs to reduce BP

A

ca-channel inhibitors
ACEI
alpha blockers
ARBs (angiotensin receptor blockers)

61
Q

give 2 examples of Ca-channel blockers

A

Diltiazem, verapamil

62
Q

how do Ca-channel blockers work

A

block Ca channels reducing AP and electrical conduction to heart (slower HR), also cause vasodilation

63
Q

what is a common side effect of Ca-channel blockers

A

ankle oedema

64
Q

what is an example of an alpha blocker and how does it work

A

Doxazosin

blocka a-ADRs= vasodilation

65
Q

give an example of an ACEI & ARB and how they work

A

Lisinopril (suffix=pril), Losartan
blocks conversion of angiotensin 1 > angiotensin 2 so no aldosterone= more Na+ leaving system so less water retention which means less volume in system= lower BP

66
Q

True/False..

You can give pregnant women ARBs/ACEI

A

False..

do not give these to pregnant women/ renal dysfunction pts

67
Q

Spironolactone is an example of what drug group

A

Mineralocorticoid Antagonists

68
Q

how do mineralocorticoid antagonists act

A

block aldosterone receptor

69
Q

what type of drugs are given for anti-anginas treatment

A

vasodilators, slow HR medicine, metabolic modulators

70
Q

what are 2 types of vasodilators for anti-anginas tx

A

nitrates, nicorandil

71
Q

give 3 examples of nitrates

A

GTN, isosorbide, mononitrate

72
Q

what types of drug slow HR

A

b-clockers, Ca channel blockers, ivabridine

73
Q

True/False…

Ivabradine acts on AVN

A

False..

acts on SAN

74
Q

how does renolazine (metabolic modulator) act

A

dec Ca load on heart

75
Q

what type of drugs are given in MI

A

anti-thrombotic drugs; anti platelet drugs, anticoagulants, fibrinolytic

76
Q

what is a side effect of ivabradine

A

altered vision

77
Q

name 3 anti-platelets

A

aspirin, clopidogrel, ticagrelor

78
Q

name 3 anticoagulants

A

warfarin, heparin, DOACs

79
Q

what is the difference between anti platelets, anti coagulants & fibrinolytics

A

in their action;
anti-platelets: inhibit platelet agglutination and hence thrombus formation- effective in arterial circulation
anti-coagulants: suppress synthesis of clotting factors by binding to antithrombin-3/ inhibiting vitK reductase
fibrinolytic: dissolve formed clot

80
Q

give an example of a fibrinolytic

A

streptokinase

81
Q

what is the biggest risk for anti-thrombotic drug

A

haemorrhage

82
Q

what are the 4 classes of anti-arrhythmic drugs

A 
class 1: Lignocaine, Quinidine, flecainide 
class 2: non-selective b-blocker
class 3: amiodarone, sotalol
class 4: verapamil (Ca-channel blocker)
83
Q

what is the no1 non-selective beta blocker

A

propanolol

84
Q

how do class 1 anti-arrhythmic drugs work

A

block Na+ channels reducing the current

85
Q

how do class 3 anti-arrhythmic drugs work

A

AP prolongation

86
Q

what 2 drugs are given for anti-fibrillation

A

b-blocker, digoxin

87
Q

how does digoxin work

A

delays conduction between atria and ventricles

88
Q

vomiting, yellow vision, bradycardia, arrhythmias are all part of which drug toxicity

A

digoxin

89
Q

what 7 drugs are given in heart failure?

A 
ACEI, ARBs
BBs
mineralocorticoid antagonists 
diuretics
digoxin
Neprilysin Inhibitors (Nis)
90
Q

how does Nis act

A

blocks angiotensin 2 binding to its receptor

91
Q

what is the first line tx for inc TGAs

A

fibrates- agonist of receptor which inc lipase which hydrolyses TAGs

92
Q

what are fibrinolytic used for

A

open occluded arteries- opposes coagulation cascade

Cardiovascular (12 decks)

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