Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
WEEK 20:
Cardiovascular Therapeutics:
| Question | Answer |
|---|---|
| oxygenated blood is supplied to heart by | coronary arteries |
| ischaemic heart disease (IHD) | atherosclerotic plaque that develop within coronary vessels leading to reduction in blood supply to myocardium |
| symptoms severity of IHD depends on (3) | extent of reduced blood flow, rate at which blood flow is reduced, and duration of ischaemia - presenting as angina or acute MI |
| factors that increase formation of atherosclerotic plaques (BAD HEART) (8) | BMI >30, Age >65, Diabetes, Hypertension (most common), E (alcohol), An increase LDL+ and decrease HDL, Relatives, and Tobacco use |
| types of risk factors for IDH (2) | modifiable (eg diabetes) and non modifiable (eg age) |
| causes of IHD (2) | reduction on O2 supply (eg atherosclerosis) and increase in oxygen demand (eg tachycardia) |
| types of ischaemia | mild transient ischaemia and prolonged ischaemia |
| milk transient ischaemia | patient presents with pain (angina pectoris) and once imbalance resolved there is no permanent damage to myocardium |
| prolonged ischaemia | irreversible cell damage leading to necrosis of heart muscle - MI and scar formation leading to impaired function |
| types of IHD conditions (4- angina and infarction) | unstable and stable angina, subendocardial infarction (NSTEMI) and transmural infarction (STEMI) |
| stable angina | predictable attack (eg when walking up stairs) that is relieved by rest and is due to an atheroma which obstructs flow of blood, reducing maximal capacity of coronary artery. There is stable plaque with strong fibrous cap that prevents it from rupturing. |
| unstable angina | irregular acceleration of symptoms with rapid progression caused by a rupture of the surface of an atherosclerotic plaque with platelet drug formation/ thrombus which reduces blood flow. Urgent treatment needed due to discomfort and can lead to MI. |
| subendocardial infarction (NSTEMI) | caused by rupture of surface of atherosclerotic plaque with platelet formation/ thrombus which reduces blood flow leading to cell necrosis which is equal to/ more than 30 minutes of ischaemia. symptoms develop at rest. |
| Transmural infraction (STEMI) | caused by rupture of the surface of an unstable atherosclerotic plaque which occludes the entire lumen (total occlusion) with platelet formation/ thrombus which reduces blood flow. symptoms develop at rest and with exertion. |
| types of MI | transmural infarction and subendocardial infarction |
| difference between NSTEMI and STEMI (3 each) | STEMI has more affected myocardium, ST elevation, and total occlusion of coronary vessel BUT NSTEMI has less affected myocardium, non ST elevation, and partial occlusion in coronary vessel |
| pharmacological management of angina (2) | prevention (drugs to reduce risk of atherosclerosis) and pharmacological treatment (drugs to relieve pain of angina and avert onset of angina attack with history of condition) |
| treatment of angina aimed to do what | maintain oxygen balance by increasing oxygen supply to myocardium or decreasing oxygen demand to myocardium |
| describe B-adrenoceptor antagonist as a treatment for angina | block the effects of noradrenaline/ adrenaline released during stress/exercise leading to reduced demand/ cardiac work (decreased HR and stroke volume) |
| B-adrenoceptor antagonists are not suitable for | asthmatics (due to B2 activity leading to bronchoconstriction) |
| examples of B-adrenoceptor antagonists (3) (suffix) | propranolol, atenolol, metoprolol - olol |
| organic nitrates as a treatment for angina | vasodilators that act on peripheral circulation rather than coronary circulation with their main effect via general venous and arterial dilation in order to reduce oxygen demand and increase supply |
| nitrates mechanism of action | GTN enters vascular smooth muscle and is converted into NO (by mtALDH2) and NO then activates guanylyl cyclase which then converted GTP into cGMP which is used to convert myosin-LC-PO4 into myosin-LC leading to smooth muscle relaxation |
| common nitrates used in clinic (2) | glyceryl trinitrate (GTN)/ nitroglycerin and isosorbide dinitrate + isosorbide mononitrate |
| glyceryl trinitrate (GTN)/ nitroglycerin | given via sublingual or transdermal route with high first pass metabolism (broken down by liver before reaching blood = bad), rapid onset and short duration of action to treat acute attacks |
| isosorbide dinitrate + isosorbide mononitrate | given via oral administration with a greater resistance to first pass metabolism, slower onset of action used to treat angina attacks before they occur (prophylaxis) |
| issues with nitrate tolerance as a treatment for angina | anginal pain can become unresponsive to medication especially with prophylactic use but is reversible with drug free periods |
| how is unresponsiveness to nitrates overcome | drug free periods |
| calcium channel blockers mechanism of action | block L type voltage gated Ca2+ channels to cause negative inotropic and chronotropic effects on heart cells and relaxation of arterial smooth muscle |
| effect of calcium channel blockers on nodal cells | blocks Ca2+ channel leading to negative chronotropic effect and reduced after load so cardiac work reduces and myocardial oxygen demand decreases |
| examples of calcium channel blockers | non dihydropyridines and dihydropyridines |
| examples of non dihydropyridines (2) | verapamil (cardio-selective and an antiarrhythmic) and diltiazem (produces cardiac and vascular effects and is an antiarrhythmic) |
| examples of dihydropyridines (end in pine) (2) | nifedipine and amlodipine which are vascular selective |
| potassium channel opener | nicorandil opens KATP in vascular smooth muscle so K+ leaves causing hyperpolarisation of the plasma membrane which reduces calcium entry (electrical excitability) so smooth muscle relaxes (vasodilates) |
| examples of antiplatelet drugs | aspirin and clopidogrel |
| acute MI | sudden block of major coronary artery (usually left/ left circumflex) due to thrombosis (which is usually triggered by rupture of atherosclerotic plaque) resulting in ischaemia and tissue damage |
| MI pathophysiology | after 30 minutes of ischaemia (which decreases ATP, increases CA2+ leading to arrhythmias and decreased cardiac output so tissue dies) MI occurs |
| consequences of myocardial ischaemia | no O2 means anaerobic respiration in myocardial cells so lactic acid made leading to tissue necrosis |
| difference between MI and myocardial ischaemia | MI = prolonged reduction in O2 to heart but myocardial ischaemia is reduced blood flow leading to reduced O2 supply to heart (leads to MI) |
| symptoms of MI (6) | prolonged chest pain, profuse sweating, nausea, SOB, vomiting, or even asymptomatic |
| lab evaluation findings of MI | based on blood levels of proteins which leak out of irreversibly damaged myocytes |
| acute MI pharmacological treatment (3) | fibrinolytic drugs (eg alteplase/ streptokinase which converts plasminogen into plasmin which breaks down fibrin), antiplatelet drugs, and others eg statins/ beta blockers |
| age of peak incidence of symptomatic IHD in men | 50-60 |
| age of peak incidence of symptomatic IHD in women | 60-70 |
| types of angina | stable and unstable |
| effect of calcium channel blockers on cardiac myocytes (muscle cells) | block Ca2+ channels leading to negative ionotropic effect and reduced after load so cardiac work reduces and myocardial oxygen demand decreases |
| aspirin as secondary prevention of arterial thrombus formation | give low dose (75mg) daily |
| aspirin as management of unstable angina and MI | give 300mg |
| how to use clopidogrel | is a P2Y12 antagonist which stops platelets from sticking together, used alongside aspirin |
| troponin in the bloodstream indicates | MI |
| fibrinolytic drugs | eg streptokinase/ alteplase treat acute MI by converting plasminogen into plasmin which lyses fibrin |
Created by:
kablooey
Popular Medical sets