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year 1 > CARDIO DRUGS > Flashcards

CARDIO DRUGS Flashcards

1
Q

what effect do nitrates have

A

venorelaxation - reduced preload
arteriolar relaxation - reduced afterload
increased coronary blood flow - dilates collateral vessels redirecting blood towards ischaemic areas

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2
Q

what is the pharmacology of nitrates

A

interact with SH groups in smooth muscle cells to liberate NO
NO activated guanylate cyclase causing increased cAMP which activates protein kinase G —> relaxation

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3
Q

what are 3 side effects of nitrates

A

postural hypotension/collapse
headaches
tolerance - 8hr free day

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4
Q

what is GTN used for

A

angina ST

+ aspirin in ACS prophylactically

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5
Q

how is GTN administered

A

sublingual spray or tablet

transdermal patch

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6
Q

what is isosorbide mononitrate used for

A

angina for sustained effect

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7
Q

how is isosorbide mononitrate administered

A

oral

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8
Q

what is the pharmacology of CCBs

A

prevent opening of L-type Ca2+ channels in heart and smooth muscle to cause decreased Ca2+ entry
this slows conduction through AV node (upstroke in SA node AP) and causes negative inotropic effect (less Ca2+ in plateau phase of ventricular AP - phase 2)

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9
Q

what effect do CCBs have

A

vasodilation

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10
Q

amlodipine
nifedipine
felodipine
are examples of what

A

dihydropyridines - CCBs

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11
Q

what are some side effects of dihydropyridines

A 
ankle oedema
dizziness
flushing
headaches
tachycardia and palpitation
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12
Q

what are dihydropyridines used for

A

hypertension

angina

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13
Q

name 2 rate limiting CCBs

A

verapamil

diltiazem

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14
Q

what are rate limiting CCBs used for

A

hypertension
post MI
Angina (diltiazem)
Verapamil (SVT arrhythmias e.g. AF)

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15
Q

what are some side effects of rate limiting CCBs

A

head ache
constipation (verapamil)
risk of heart block

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16
Q

why is amlodipine preferred for hypertension, especially in heart failure/heart block

A

smooth muscle selective - minimised unwanted cardiac effects

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17
Q

why should verapamil be avoided in HF

A

cardiac selective

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18
Q

what is the pharmacology of beta blockers

A 
block b1 +/- b2 adrenoreceptors
prevents coupling of NA through Gs proteins
decreases cAMP
decreases PKA
decreases CICR via RyR2 proteins
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19
Q

what is the effect of beta blockers

A

negative chronotropic effect
negative inotropic effect
decreased O2 demand/workload

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20
Q

why are B1 selective preferred

A

B2 adrenoreceptors cause vasodilation of coronary arteries so if blocked opposite will occur

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21
Q

atenolol
bisoprolol
metoprolol
are examples of what

A

b1 selective

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22
Q

when are b1 selectives used

A

Chronic HF
MI treatment LT and ST (metoprolol for immediate)
angina (unstable)
hypertension (no longer 1st line - reduces MAP and renin release from kidneys)

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23
Q

what are some side effects of beta blockers

A

tiredness
cold peripheries
bradycardia/heart block

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24
Q

why can BBs worsen HF in short term

A

person may rely on sympathetic stimulation to maintain adequate perfusion of body tissues

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25
give an example of a non-selective BB
propranolol
26
what are non-selective BBs used for
anti-arrhythmic | thyrotoxicosis
27
what are side effects of non-selective BBs
``` worsening of claudication - stops vasodilation in skeletal muscle vessels bronchospasm in asthmatics tiredness cold peripheries bradycardia/heart block ```
28
why should you be cautious with BB and insulin dependent diabetics
BBs may mask hypoglycaemia as sympathetic nervous system suppressed
29
why can BB cause tiredness
cardiac output (B1) and skeletal muscle perfusion (B2) in exercise are regulated by B adrenoreceptors
30
Give an example of a drug that selectively blocks HCN channels to slow down funny current and therefore reduce heart rate and oxygen demand
ivabradine
31
when are HCN channel blockers used
angina as an alternative to BBs
32
what are some side effects of ivabradine
``` head aches blurred vision dizziness tiredness weakness hypotension ```
33
give 2 examples of a K channel agonist
nicorandil | minoxidil
34
how do K channel agonists work
open Katp channels in vascular smooth muscle and antagonise ATP causing hyper polarisation this switches off L-type Ca2+ channels resulting in relaxation
35
what type of vessels do K channel agonists primarily vasodilate
arteries
36
what are some side effects of K channel agonists
``` headache flushing dizziness reflex tachycardia (give alongside BB) salt and water retention (give alongside loop diuretic) ```
37
true/false | Minoxidil also has NO donor activity to bring about venorelaxation
false | Nicorandil does
38
what is nicorandil used for
Angina - if still symptomatic despite optimal treatment with other drugs
39
what is used if HR still fast after a BB
+ ivabradine
40
why do BBs have little effect at rest
sympathetic stimulation not very active during rest
41
give an example of a selective B1 agonist
dobutamine
42
give an example of an alpha and beta agonist
Adrenaline
43
what is the pharmacology of B-adrenoreceptor agonists
activate b-adrenoreceptors to enhance coupling of NA through Gs proteins increases [cAMP] positive chronotropic and positive inotropic effect increased CO and increased O2 demand of heart
44
what are some side effects of BBs
hypertension tachycardia arrhythmia
45
when are B agonists used
cardiac arrest (adrenaline IV) emergency asthma/anaphylactic shock (adrenaline IM) acute HF/cardiogenic shock (Dobutamine, IV) post cardiac surgery
46
how does adrenaline redirect blood flow to heart
constricts BVs in skin, mucosa and abdomen
47
why are B agonists considered toxic
LT stimulation of sympathetic system causes HF
48
what kind of drugs are Prazosin and Doxazosin
alpha-1 adrenoreceptor antagonists
49
what is the pharmacology of a-1 adrenoreceptor antagonists
block sympathetic/hormonal effect on alpha receptors causing reduced sympathetic drive vasodilation, reduced MAP and TPR
50
what are some side effects of alpha-1 antagonists
``` postural hypotension flushing tachycardia nasal congestion impotence ```
51
when are alpha adrenoreceptor antagonists used
hypertension with prostatic hypertrophy
52
what kind of drugs are atropine and hyoscine
Muscarinic receptor antagonists
53
how do muscarinic receptor antagonists work
reduction of vagal tone by competing with ACh - reduces parasympathetic drive to the heart --> increased HR
54
what are some side effects of atropine
dry mouth urinary retention blurred vision
55
when are muscarinic receptors used
bradycardia (e.g. following MI where vagal tone raised) anaesthesia adjunct antispasmodic anti cholinesterase poisoning
56
when is isoprenaline used
heart block
57
when are calcium/magnesium chlorides used
VT due to hyperkalaemia VF digoxin toxicity
58
name a drug that inhibits PDE in cardiac and smooth muscle causing increased cAMP and therefore increased contractility
amrinone
59
how do ACEIs work
inhibit conversion of AT I to AT II by inhibiting ACE reduces BP secondary to vasodilation prevents degradation of bradykinin - potent vasodilator increased fluid excretion due to decreased aldosterone
60
where is the greatest vasodilation effect of ACEIs and therefore improved perfusion
kidney heart brain
61
what do all ACEIs end in
-pril
62
when are ACEIs used
``` hypertension HF - reduced afterload LV dysfunction post MI stroke prevention diabetic nephropathy ```
63
what are some side effects of ACEIs
``` dry irritant cough taste disturbance angioneurotic oedema hyperkalaemia due to potassium retention - reduced aldosterone renal dysfunction hypotension ```
64
when are ACEIs/ARBs contraindicated
renal artery stenosis | pregnancy/child bearing potential
65
what should be used in pregnancy induced hypertension
BB or CCB
66
true / false | angioneurotic oedema is more common in black people
true
67
what do all ARBs end in
-sartan
68
how do ARBs work
competitively block agonist action of angiotensin II at AT1 receptors preventing vasoconstriction, aldosterone release and sympathetic activation reduced BP secondary to vasodilation
69
why is there no dry cough with ARBs
no effect on bradykinin metabolism
70
what are some side effects of ARBs
dizziness syncope hyperkalaemia renal dysfunction
71
where do thiazide diuretics inhibit reabsorption
distal tubule
72
where do loop diuretics inhibit reabsorption
ascending loop of henle
73
what are some side effects of diuretics
``` hypokalaemia hyponatraemia thirst headaches dizziness arrhythmia impotence ankle oedema ```
74
when are diuretics contraindicated
diabetics - hyperglycaemia | history of gout - increased uric acid
75
what kind of diuretic is bendroflumethiazide
thiazide-like
76
what kind of diuretic is furosemide
loop
77
when would a thiazide diuretic be used
hypertension (mild diuresis) HF (mild or congestive) severe resistant oedema (with a loop agent)
78
when would a loop diuretic be used
hypertension (strong diuresis) acute pulmonary oedema chronic HF or congestive
79
how can hypokalaemia be avoided
potassium sparing diuretic e.g. spironolactone | K+ supplements
80
when and how are statins given
oral at night
81
how do statins work
competitively inhibit HMG CoA reductase to decrease hepatic cholesterol synthesis decreased cholesterol conc in hepatocytes results in increase in LDL receptor expression enhanced LDL clearance
82
give 4 effects of statins
decrease inflammation decrease thrombosis reversal of endothelial dysfunction stabilisation of atherosclerotic plaque
83
what are some side effects of statins
myopathy Rhabdomyolysis renal failure GI disturbance Insomnia
84
when are statins used
``` hypercholesterolaemia MI long term primary and secondary prevention of CVD events Angina/TIA diabetes ```
85
when are statins contraindicated
pregnancy | homozygous familial hypercholesterolaemia - LDL receptors lacking - no effect
86
What kind of drugs are Bezafibrate Gemfibrozil
fibrates
87
when are fibrates used
1st line treatment in low HDL cholesterol - hypertriglyceridaemia
88
how do fibrates work
decrease triglyceride levels by increasing rate of removal slight decrease in LDL and HDL by decreasing liver production of particle that carried them in blood agonists of PPAR-alpha to enhance transcription of gene encoding LPL
89
what is a possible side effect of fibrates
hyositis - combine with statin
90
aspirin tirofiban and clopidogrel are examples of what
antiplatelets
91
do anti platelets break down clots that are already formed?
no
92
how does aspirin work
irreversibly blocks COX-1 enzyme in platelets to inhibit production of TXA2 - mediator for platelet aggregation and clot formation therefore prevents aggregation and cross linking (adhesion)
93
when is aspirin used
``` immediate MI treatment post PCI/post CABG stroke/TIA prevention of athero-thrombotic events MI longterm ```
94
what are some side effects of aspirin
bronchospasm (aspirin sensitivity) GI irritation Haemorrhage
95
when should you be cautious with aspirin
asthma | uncontrolled hypertension
96
how does clopidogrel work
blocks P2Y12 receptors on platelets to prevent ADP binding to receptor prevents platelet aggregation and cross linking
97
when is clopidogrel used
immediate MI | prevention of atherothrombotic events
98
how does tirofiban work
blocks GP IIA/IIB receptors on platelets to prevent fibrinogen binding inhibits conversion to fibrin
99
when is tirofiban used
preventative of MI in unstable angina patients - IV short term + aspirin + heparin
100
give an example of a fibrinolytic drug
streptokinase
101
when should streptokinase not be given
``` post streptococcal infection recent haemorrhage trauma severe diabetic retinopathy ulcers bleeding tendencies ```
102
how do fibrinolytics work
activate plasminogen to form plasmin - a protein which promotes fibrin degradation - opposes coagulation cascade
103
can streptokinase reopen occluded arteries/dissolve formed clots
yes
104
how does digoxin work
blocks sarcolemma Na/K ATPase by binding to alpha subunit so calcium unable to leave cell so more goes into SR - increased contractility
105
what is an indirect action of digoxin
stimulates vagal activity on the heart - slows conduction through AV node and prolongs AV node refractory period - decreased heart rate
106
when is digoxin used
isn't really used anymore AF Chronic HF (still symptomatic despite maximal treatment with other drugs)
107
what are the side effects of digoxin toxicity
``` nausea vomiting yellow vision bradycardia/heart block ventricular arrhythmias - increases ventricular irritability ```
108
why does hypokalaemia make digoxin toxicity worse
binds competitively with K
109
what is digoxin toxicity caused by
membrane depolarisation and oscillatory after potentials likely due to Ca2+ overload
110
what is spironolactone
potassium sparing diuretic
111
how does spironolactone work
aldosterone antagonist - blocks sodium and water reabsorption
112
when is spironolactone used
hypertension chronic HF oedema
113
what are side effects of spironolactone
nausea postural hypotension tiredness/fainting gynaecomastia
114
what is the name of the new drug which is a combination of ARB and Neprilysin
Sacubitril-Valsartan
115
what does Sacubitril-Valsartan do
blocks NP breakdown and so boosts NP levels (vasodilation)- will replace ACEIs - don't used in combination with ACEI
116
how does ezetimibe work
inhibits NPC1LA transport protein in enterocytes of duodenum reducing absorption of cholesterol decrease in LDL
117
how is ezetimibe administered
oral admin
118
when is ezetimibe used
+ statin when statin alone not achieving goal
119
what are some (rare) side effects of ezetimibe
diarrhoea abdominal pain headaches
120
when is ezetemibe contraindicated
breast feeders
121
colestyramine colestipol colsevelam are examples of what
bile acid binding resins
122
how do bile acid binding resins work
interrupt enterohepatic recycling of cholesterol non-absorbable so cause excretion of bile salts therefore resulting in more cholesterol being converted to bile salts - decreased absorption of bile salts and triglycerides - increased LDL receptor expression
123
what classes control rhythm and what classes control rate
1 and 3 - rhythm | 2 and 4 - rate
124
what phase do class 1 drugs act on
0
125
what phase do class 2 drugs act on
4
126
what phase do class 3 drugs act on
3
127
what phase do class 4 drugs act on
2
128
verapamil is what class of anti arrhythmic drug
4
129
atenolol and propranolol are what class of anti arrhythmic drug
2
130
lignocaine, flecainide, proprafenone, dysopyramide, hydroquinidine are what class of anti arrhythmic drug
1
131
amiodarone, sotalol, dronedarone and bretylium are what class of anti arrhythmic drugs
3
132
what do class I AADs do
Na channel blockers with preference to the most active (tachycardia areas) slow conduction, prolong depolarisation depress phase 0
133
what are class I AADs used for
``` paroxysmal AF (+ WPW) VT / VF ```
134
what do class II AADs do
BBs
135
what are class II AADs used for
paroxysmal AF | MI arrhythmias
136
what are class III AADs used for
WPW SVTs Paroxysmal SVT/VT
137
what do class III AADs do
K+ channel blockers | prolong repolarisation
138
what do class IV AADs do
CCBs
139
what are class IV AADs used for
SVT | AF without WPW
140
what kind of drug is levosimendan
calcium sensitiser
141
how does levosimendan work
binds to troponin C in cardiac muscle sensitising it to action of Ca2+ - inotropic also opens Katp channels in vascular smooth muscle causing vasodilation
142
what is levosimendan used for
acute decompensated HF
143
what are some side effects of amiodarone
phototoxicity pulmonary fibrosis thyroid abnormalities (hypo/hyper)
144
give the name of a drug that is a late sodium channel modulator
ranolazine
145
what are the effects of ranolazine
improves blood flow so heart works more efficiently
146
what kind of drugs are Bosentan and ambrisentan
ETA receptor antagonists
147
what do ETA receptor antagonists do
antagonists of ETA receptor which endothelin acts on | vasodilators
148
what are ETARAs used for
pulmonary hypertension
149
what is ranolazine used for
angina
150
Digoxin Dobutamine Levosimendan have what effect on the force of contraction
increased force of contraction - inotropic drugs
151
antiplatelets anticoagulants fibrinolytic are all...
antithrombotics
152
give 4 types of anti-anginals
nitrates BBs CCBs K channel openers
153
give 4 types of antihypertensives
Diuretics (mainly thiazide) BBs CCBs vasodilators (alpha blockers, ACEIs, ARBs)
154
how are the doses of warfarin and heparin controlled
INR
155
how is warfarin reversed
vitamin K | dietary vitamin K can decrease action
156
how does warfarin work
blocks vitamin K reductase reduces hydroquinone form of Vit K (reduced form) reduced form is responsible for gamma-carboxylation of glutamate residues of clotting factor precursors II, VII, IX and X (2 7 9 10) this means the precursors remain inactive and the coagulation cascade is inhibited clot formation prevented
157
when is warfarin used | same as heparin and LMWH
``` DVT or PE NSTEMI AF TIA prophylaxis of embolism e.g. post op prosthetic valves ```
158
what are some side effects of warfarin
``` haemorrhage black/bloody stools dizziness weakness joint pain ```
159
what kind of drugs does warfarin interact with
hepatic metabolism of warfarin inhibitors platelet function inhibitors e.g. NSAIDs Vitamin K availability reducers/inhibitors
160
does warfarin have a high or low therapeutic index
low
161
when is warfarin contraindicated
liver disease - decreased clotting factors | first few months of pregnancy
162
can heparin be given orally
no - only IV
163
can warfarin be given orally
yes
164
what kinds of drugs are fondaparinux enoxaparin dalteparin
LMWH
165
how does heparin work
binds to antithrombin III increasing its affinity for clotting factors to increase rate of inactivation of clotting factors IIa and Xa inhibits coagulation cascade
166
how do LMWHs work
inhibit factor Xa by binding to antithrombin III factor Xa is upstream to IIa so should indirectly inhibit IIa (can't bind to ATIII and IIa at same time) inhibits coagulation cascade
167
why is heparin preferring to LMWH in renal failure
LMWH excreted via renal route
168
what are some side effects of heparin/LMWH
haemorrhage osteoporosis hypoaldosteronism hypersensitivity reactions
169
true / false | heparin only needs to bind to ATIII to inhibit Xa
true
170
true / false | LMLWH only needs to bind to ATIII to inhibit IIa
false | must bind to both ATIII and IIa to inhibit IIa
171
what should be done in the event of haemorrhage due to heparin/LMWH
discontinue drug | administer protamine sulfate - inactivated heparin
172
why are rivaroxaban and dabigatran preferred over heparin and LMWH
no need for IV and less haemorrhage risk
173
what are rivaroxaban and dabigatran
anticoagulants
174
when are rivaroxaban and dabigatran used
prophylaxis of venous thromboembolism PE or DVT post hip/knee replacement to prevent venous thrombosis
175
what are some side effects of rivaroxaban
haemorrhage | renal impairment
176
what are some side effects of dabigatran
haemorrhage | anaemia
177
when is rivaroxaban contraindicated
liver disease with coagulopathy
178
when is dabigatran contraindicated
patients under 50kg
179
how does rivaroxaban work
factor Xa inhibitor
180
what does factor Xa do
converts prothrombin (II) to thrombin (IIa)
181
how does dabigatran work
thrombin inhibitor (IIa inhibitor)
182
what is morphine
vasodilator
183
when is morphine used
relieve pain, anxiety and tachycardia caused by MI | acute MI treatment + anti-emetic
184
When is adenosine used
terminate paroxysmal SVT | SVT in acute phase
185
how does adenosine work
activates a1-adenosine receptors opens ACh-sensitive K+ channels (GIRK channels) causing hyper polarisation of the AV node suppressing impulse conduction - decreases HR
186
true/false | lidocaine can be used for SVT and VT management
false - used in VT but ineffective in SVT

year 1 (45 decks)

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