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Y1 Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Muscle contraction mechanism

A
  1. L type Ca2+ channels open (due to depolarisation), allowing Ca2+ influx
  2. Ca2+ binds to troponin C and cause troponin-tropomyosin complex to move away from myosin binding site on actin
  3. allows troponin-tropomyosin complex to bind to actin and cause muscle contraction
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2
Q

Muscle relaxation mechanism

A
  1. L type Ca2+ channels close
  2. Ca2+ actively transported out of the cell via NCXR
  3. Ca2+ actively transported back into SR via SERCA
  4. reduction in Ca2+ causes troponin-tropomyosin to block myosin binding site, preventing myosin from binding -> muscle relaxation
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3
Q

Examples of beta adrenoceptor agonists

A

Adrenaline
Noradrenaline
Dobutamine

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4
Q

What type of adrenoceptor are adrenaline and noradrenaline

A

Mixed adrenoceptor - acts on beta and alpha adrenergic receptors

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5
Q

Which adrenergic receptor is adrenaline more effective

A

beta adrenergic

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6
Q

Which adrenergic receptor is noradrenaline more effective in

A

alpha adrenergic

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7
Q

What type of adrenergic receptor is dobutamine selective for

A

beta 1

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8
Q

Effects of beta adrenergic agonists

A
  1. positive chronotropic
  2. positive inotropic
  3. positive dromotropic
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9
Q

What is the overall effect of beta adrenergic receptor agonists

A

Increases HR and force of contraction (contractility) hence increases cardiac output
Increases O2 consumption of the heart muscle

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10
Q

Use of adrenaline

A

cardiac arrest

anaphylactic shock

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11
Q

What are the additional effects of adrenaline except from positive chronotropic and inotropic effects

A

Acts on alpha 1 adrenergic receptors - Constriction of arterioles in skin / gut / mucosa to redirect more blood to the heart

Acts on beta 2 adrenergic receptors - Dilatation of coronary arteries to increase blood flow

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12
Q

What is cardiac arrest

A

When the heart suddenly stops pumping, can be due to coronary artery disease blocking the coronary arteries

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13
Q

Side effects of adrenaline

A

tremor
arrhythmias
headache

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14
Q

Why does adrenaline have additional effects

A

because it is a non-selective beta agonists and it can also bind to alpha adrenergic receptorss

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15
Q

Uses of dobutamine

A

Acute heart failure

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16
Q

What is acute heart failure

A

Weakening of heart’s ability to contract

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17
Q

Side effects of dobutamine

A

Tachycardia
headache
palpitations

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18
Q

Examples of non-selective beta blockers

A

propanalol
nadalol
pindolol

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19
Q

Examples of selective beta blockers

A

atenolol
bisoprolol
metoprolol

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20
Q

What does the effect of beta blockers depend on

A

the degree of sympathetic stimulation because beta adrenergic receptors are used only during sympathetic stimulation (when not used, blocking it has no effect bc it is not producing an effect anyways)

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21
Q

Effect of beta blockers

A

Decreases HR and force of contraction hence cardiac output

Decreases O2 consumption

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22
Q

Uses of beta blockers

A

Angina - first line treatment apart from CCB
Arrhythmias - supraventricular tachycardia and AF - first line treatment
Compensated heart failure
Post MI management

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23
Q

How does beta blockers help with arrhythmias

A

Decreases excessive sympathetic activity and conduction velocity through AV node

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24
Q

What should you be aware of in using beta blockers for compensated heart failure

A

Use low doses only

Because some patients may have compensated heart failure by using sympathetic drive

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25
Which beta blocker is used in heart failure
carvedilol
26
Side effects of beta blockers
``` bronchospasm aggravation of heart failure bradycardia hypoglycaemia fatigue ```
27
Why may beta blockers cause hypoglycaemia
Because B2 recepors in liver controls the release of glucose
28
Effects of muscarinic antagonists
No effect on force of contraction | Increases HR
29
What type of drug is atropine
muscarinic antagonist
30
Use of muscarinic antagonist
First line treatment for bradycardia
31
Contraindications for beta blockers
Asthma | Use of verapamil
32
Side effect of ACE inhibitors
hyperkalaemia cough angio-oedema first dose hypotension
33
Example of thiazide diuretic
hydrochlorothiazide indapamide Bendrofluazide
34
Which conditions contraindicate the use of thiazide diuretics
Hypokalaemia Hypercalcaemia Hyponatraemia Addison's disease
35
Mechanism of action of diuretics
Increases urination hence loss of fluid, including Na+ -> loss of plasma volume -> lower blood pressure Decreases excretion of Ca2+
36
What conditions do thiazide diuretics treat
heart failure - to relief resistant oedema | resistant hypertension - last line of treatment for hypertension
37
Side effects of diuretics
dehydration postural hypotension gout (painful form of arthritis) impotence
38
Which medication is used to treat digoxin toxicity
Digibind
39
Example of angiotensin receptor blocker
candesartan | Losartan
40
Mechanism of action of cardiac glycoside
Blocks Na+/K+ channel so there is no Na+ gradient for NCXR hence Ca2+ cannot be moved out of cell
41
Inotropic drugs
Cardiac glycoside PDE inhbitors Levosimendan
42
Mechanism of PDE inhibitors
PDE deactivates adenylyl cyclase which lowers cAMP | Inhibit PDE -> more cAMP -> more Ca2+
43
Effect of PDE inhibitors
Positive inotropic | Vasodilation
44
Use of digoxin
Last line of treatment for Acute and chronic heart failure
45
Side effects of digoxin
``` Heart block Arrhythmia disturbs colour vision diarrhea nausea ```
46
Anti hypertensive drugs
ACE inhibitors Calcium Channel Blockers Diuretics beta blockers (not used anymore unless present with other comorbidities)
47
Effect of ACE inhibitors
Venous dilatation -> decrease in preload Vasodilation -> decrease in SVR -> decrease in BP Decrease in release of aldosterone -> less Na+ and water reabsorption -> lower BP
48
Examples of ACE inhibitors
Ramipril Lisinopril enalapril
49
Uses of ACE inhibitors
``` Hypertension - first line treatment for those with type 2 diabetes Heart failure (left ventrircular systole dysfunction) - first line treatment Post MI managemnet ```
50
Side effects of ACE inhibitors
``` Dry cough (most common) Hyperkalaemia hyponatraemia Initial dosage hypotension Angio-oedema (life threatening) ```
51
What drug can be used if ACE inhibitors are not well tolerated
Angiotensin Receptor blocker
52
What conditions contraindicates the use of ACE inhibitors
Chronic kidney disease Severe valve disease Pregnancy
53
What type of drug is Losartan and Candesartan
Angiotensin receptor inhibitor
54
What causes dry cough when using ACE inhibitors
bradykinin
55
Effect of Calcium channel blockers
Negative inotropic Negative chronotropic (bc phase 0 of nodal action potential depends on L type Ca2+ channels) Vasodilation
56
Why is calcium channel blockers used against hypertension
Blocks L type Ca2+ channels on vascular smooth muscle less Ca2+ influx -> less CICR -> less Ca2+ binds with CaM -> less activation of myosin LCK -> less phosphorylation of myosin LC -> less muscle contraction
57
Examples of CCB
Verapamil - selective for cardiac L type Ca2+ channels Amlodipine - selective for smooth muscle L type Ca2+ channels Dilitiazem - intermediate selectivit.y
58
Use of CCB
Hypertension (amlodipine) - first line treatment Angina (verapamil) - used with GTN when beta blockers are contraindicated Arrhythmia (verapamil / dilitiazem)
59
Drugs for angina
Beta blockers - first line CCB - if beta blocker not tolerated Nitrates - if beta blocker not tolerated ACE inhibitors - for patients with diabetes
60
Side effects of amlodipine
hypotension dizziness swollen ankles
61
How does Nitric Oxide affect the vasculature
It diffuses into smooth muscle from endothelium, activating cGMP to inhibit myosin LCK and stimulate myosin phosphatase
62
Mechanism of organic nitrates
at low dose - venodilation | at high dose - vasodilation
63
Effect of organic nitrates
1) decreased preload 2) decreased afterload 3) vasodilation of collateral arteries in patients with angina
64
Why are organic nitrates used in angina
In angina patients, collateral vessels develop between healthy and diseased vessels. Nitrates cause vasodilation of those collateral vessels so redirect blood flow to ischaemic area
65
Uses of organic nitrate
Angina - if beta blockers not tolerated | Acute MI
66
How do patients with angina benefit from using nitrates
1) increased blood flow to ischaemic area | 2) decrease preload and afterload so lower O2 requirement
67
Side effects of Nitrates
Headaches Hypotension Fainting
68
Examples of nitrates
GTN | Isosorbide mononitrate - prophylaxis for angina
69
Drugs for heart failure (first line)
Diuretics Beta blockers ACE inhibitors AT inhibitors if ACE inhibitors not tolerated
70
What is haemastasis
Arrest of blood loss from injury
71
List the 3 main steps of blood clot
1) injury / damage to the vessel 2) Primary haemastasis - local vasoconstriction and formation of soft plug 3) Activation of coagulation cascade and formation of solid clot
72
Describe primary haemastasis
1) damage to the blood vessel exposes collagen (at connective tissue layer) and thromboplastin 2) Platelets bind to collagen and becomes activated 3) Activated platelets release TXA2 4) TXA2 causes local vasoconstriction 4) TXA2 binds to TXA2 receptors (TP receptors) on platelets, causing platelets to release 5-HT and ADP 5) ADP binds to P2Y12 receptors to cause - attract more platelets - increased expression of GP receptors so binds more fibrinogen between platelets -> forms soft plug - exposes acidic phospholipids that stimulate coagulation cascade 5) 5-HT binds to HT receptors to cause local vasoconstriction
73
Describe coagulation cascade
Inactive factor X -> Active Xa by tenase Active Xa and Va is part of prothrombin Inactive factor II -> Active IIa by prothrombin = thrombin Thrombin converts fibrinogen to fibrin = solid blood clot
74
Where are P2Y12 receptors found
On platelets
75
What is thrombosis
Pathological haemastasis
76
Pathology of thrombosis
Virchow's trial - abnormal blood flow - increased coagulability of blood - injury to vessel
77
What conditions can cause abnormal blood flow
Atrial fibrillation / HF -> slow blood flow | Slow blood flow more likely to clot
78
What conditions causes increased coagulability of blood
``` Pregnancy Physical inactivity dehydration prolonged bed rest / long flight smoking alcohol obesity ```
79
What is thrombophilia
Inherited or acquired condition that makes the blood more likely to clot
80
Difference between arterial and venous thrombus
Arterial - platelets enriched ; white | Venous - red ; fibrin and erythrocytes enriched
81
In which type of thrombus is anticoagulants normally used in?
Venous thrombus
82
What type of drug is used for arterial thrombus
Antiplatelets because it is enriched with platelets
83
Types of anticoagulants
Warfarin Heparin LMWH DOAC
84
Mechanism of action of warfarin
Blocks Vitamin K+ reductase (competes with vitamin K).
85
Why is vitamin reductase needed in clotting
Vitamin reductase converts oxidised form of vitK into reduced form Reduced form of vitK is needed in gamma carboxylation which converts inactive factors X, II, IV, VII to active form
86
Uses of anticoagulants
prevention of venous thrombosis and embolism
87
Features of warfarin
Slow onset of action (2-3 days) | Long half life
88
Risk of using warfarin
Haemorrhage low therapeutic ratio conditions that increases risk of haemorrhage
89
What does low therapeutic ratio mean
The therapeutic window is small; dose that gives therapeutic effects is close to dose that cause toxicity
90
What factors potentiate effects of warfarin (increase risk of haemorrhage)
``` liver disease increased metabolism of clotting factors Drugs - aspirin - NSAID - drugs that reduce vitamin K ```
91
Why shouldn't aspirin be used with warfarin
It inhibits platelet functions which potentiates the effect of warfarin and increases risk of haemorrhage
92
What measures the time it takes for blood to clot
INR
93
How should the use of warfarin be monitored
By monitoring INR
94
Contraindications for warfarin
third / late trimesters of pregnancy | patients that are due to have surgery
95
How to manage overdose of warfarin
Give vitamin K (as phytomenadione) | Give plasma clotting factors
96
Mechanism of action of heparin
binds to antithrombin IIIa and increases its affinity for active factors Xa and IIa Antithrombin IIIa inactivates those factors
97
Administration of warfarin
Orally
98
Use of warfarin (except for prevention of venous thrombosis and embolism)
arterial thrombosis in patients with synthetic valves / atrial fibrillation
99
Use of LMWH (except for prevention of venous thrombosis and embolism)
ACS; patients with NSTEMI that need immediate angiography
100
Administration of heparin
IV - for immediate effect | SC - delayed an hour
101
Side effects of heparin and LMWH
Haemorrhage Osteoporosis Hypoaldosteronism - hyperkalaemia Hypersensitivity reactions
102
Difference between heparin and LMWH
LMWH does not inactivate factor IIa | Lower risk of haemorrhage, osteoporosis, HIT
103
What is HIT
heparin induced thrombocytopenia - increases risk of thrombosis; a side effect of heparin and less commonly LMWH
104
Administration of LMWH
IV
105
Example of LMWH
enoxaparin | dalteparin
106
Why is heparin more preferred in renal failure
Because LMWH requires renal excretion
107
Examples of DOAC - direct inhibition of thrombin
Dabigatran
108
Examples of DOAC - direct inhibition of Xa
Rivaroxiban Apixaban fondaparinux
109
Examples of antiplatelets
Aspirin Clopidogrel Prasugrel Ticagrelor
110
Mechanism of action of aspirin
Irreversibly blocks COX which synthesizes TXA2 | Only start producing TXA2 again when affected platelets are replaced
111
Use of aspirin
Prevention of arterial thrombosis and embolism Acute coronary syndrome Treatment for acute ischaemic attack
112
Administration of aspirin
Orally
113
Side effects of aspirin
GI bleeding and ulceration | Reye's syndrome - more common in children
114
Contraindications for aspirin
Children | Previous GI ulceration history
115
Mechanism of action of clopidogrel
Blocks P2Y12, prevents ADP from binding
116
Use of clopidogrel
Prevention of arterial thrombosis and embolism | Acute coronary syndrome
117
Mechanism of action of fibrinolytics
Activates plasminogen which converts into plasmin that breaks down fibrin hence lyses the blood clot
118
Use of fibrinolytics
Used when PCI is not available promptly | To reopen occluded arteries in MI / stroke
119
Examples of fibrinolytics
Streptokinase Duteplase Alteplase
120
What to do if haemorrhage occurs while using anticoagulants
Stop anticoagulant and reverse effect Heparin - protamine Warfarin - vitamin K (phynometadione) / plasma of clotting factors
121
What is atherosclerosis associated to
Increased LDL, decreased HDL
122
Why is LDL the bad cholesterol
Involved in formation of atherosclerotic plaque
123
Why is HDL the good cholesterol
HDL can accept excess cholesterol and transport it back to liver to use it in bile
124
Mechanism of action of statins
HMG CoA reductase inhibitors
125
Effects of statins
``` Decrease LDL Decrease TAG Increase HDL Decrease thrombosis, inflammation Reverse dysfunction of endothelium Stabilize atherosclerotic plaque ```
126
Examples of statins
Atorvastatin Simvastatin Prevastatin Fluvastatin
127
When should fluvastatin be used
When you don't know if the patient can tolerate statin or not
128
Why should fluvastatin be used in patients with unknown tolerance of statin
Because it has lowest efficacy
129
Uses of statin
First line prevention if the patient has high cholesterol
130
Why is statin prescribed at night
Because HMG CoA reductase has highest activity at night
131
Side effects of statin
``` Diarrhea Myopathy (rhabdomyolysis) Drug induced liver injury dizziness Headache ```
132
What life threatening myopathy can statin cause
rhabdomyolysis
133
What rare side effect may atorvastatin cause
angio-oedema
134
Mechanism of action of fibrates
Agonists of PPAR to induce transcription of genes that encode LPL
135
Examples of fibrates
Fenofibrate Bezafibrate Gemfibrozil
136
Why are fibrates worse than statin
Better than statin at increasing HDL and decreasing TAG but worse than statin at decreasing LDL
137
Side effects of fibrates
Diarrhea Nausea GI upset
138
When are fibrates used
when the patient has hypertriacylglyceridemia and low HDL
139
Mechanism of bile acid binding resin
Blocks reabsorption of bile acid so forces the body to use more cholesterol to produce bile Lower cholesterol -> more LDL receptors -> more LDL clearance
140
Is atropine a selective or non-selective muscarinic antagonist
Non-selective
141
Where are M2 receptors found and what does blocking them do
Heart; positive chronotropic effect
142
Where are M3 receptors found
Smooth muscles - vessels / bronchi Endocrine glands Exocrine glands
143
What decreases the effect of ACE inhibitors and what may occur
NSAIDs such as ibuprofen this causes blood pressures to still be high despite taking ACE inhibitors
144
Example of 5-HT antagonist to treat leg claudication
Naftidrofuryl
145
Mechanism of action of adenosine
Adenosine receptor agonist; binds to A1 receptor in AV node, inhibit adenylyl cyclase
146
Treatment for recurrent DVT or PE despite adequate anticoagulation
Insert inferior vena cava filter
147
What receptors do ACh released from preganglionic neurone act on
Nicotinic receptors | M1 receptors
148
Side effect of bile acid sequestrants
``` Vitamin deficiency Constipation Indigestion Abdominal cramps Bloating ```
149
What causes vitamin deficiency when using bile acid sequestrants
malabsorption of fat due to less micelles formed (caused by less bile acid) = malabsorption of fat soluble vitamins
150
What type of vitamin deficiency causes excessive bleeding
Vitamin K

Y1 Cardiovascular (6 decks)

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