Cardiovascular Disease Flashcards
Cardiovascular conditions; CVD risk factors; ACS diagnosis; MI; Antiplatelets; Beta blockers; Statins; Renin angiotensin system; ACE inhibitors; ARBs; Angina; Nitrates; CCBs; Anticoagulants; Parental anticoagulants; Oral anticoagulants; Direct oral anticoagulants.
9 CVD conditions
Angina MI Heart valve disease Vascular disease Arrythmias Cardiomyopathy Congenital heart failure Heart failure Pericardial disease
10 risk factors for CVD
Smoking Obesity Family history Diabetes Hypertension Inactive lifestyle Drugs Electrolyte imbalance Hyperlipidaemia Increased age
Process of ACS diagnosis
onset of what symptom, type of MI or painful condition called…based on what feature of ECG + test result
Pt admitted with chest pain
Diagnosed with ACS
Continuing ST elevation = STEMI
Abnormal ST/T wave with increased/decreased troponin levels = NSTEMI or Unstable angina
Normal ECG with increased/decreased troponin = Stable angina
What occurs in myocardial infarction?
what tissue, lack of what leading to what
Myocardial/cardiac muscle ischaemia leading to necrosis of myocardium
What leads to MI?
pathophysiology of clot formation
Rupture or erosion of artherosclerotic plaque within tunica intima layer of artery.
Dislodged plaque results in thrombus formation.
Thrombus partially or fully occludes artery decreasing or cutting off blood supply to myocardium.
What 3 generic tests are carried out to diagnose MI?
3 blood tests for diagnosis
ECG
Blood chemistry: U&Es, FBC, Troponin
Chest X-ray
What 4 groups of drugs should patients following MI be prescribed?
BARS: Beta blocker Anti-platelet Renin angiotensin system blocker Statin
What are the 2 types of MI and describe their cause, what they occlude?
(thrombus)
NSTEMI - Atheromatous plaque with partially occluding thrombus, may cause occlusion of small coronary arteries due to platelet aggregation.
STEMI - artheromatous plaque that completely occludes coronary artery.
Which 2 hormones are involved in the mechanism of platelets and do they stimulate/inhibit aggregation?
Thromboxane - activates platelet aggregation
Prostacyclins - inhibits platelet aggregation
Name 4 mechanisms of platelets in clotting
Adhesion
Shape change
Secretion
Aggregation
What is a drug interaction and ADR of all anti-platelets?
Interaction - SSRIs as seritonin is involved in platelet formation
ADR - GIT bleeds
What is the function/mechanism of asprin?
enzyme, hormone, inhibits ? in regards to platelets
Non-selective COX1 inhibitor
Inhibits production of thromboxane thus preventing platelet aggregation
What is an ADR of asprin and how is it caused?
GIT irritation
Caused by inhibition of cytoprotective prostaglandins resulting in decreased stomach acid secretion and unregulated blood flow. Increasing risk of GIT ulcer formation.
5 contraindications of asprin use
Dyspepsia Active GIT ulcer Under 16 yrs Hypersensitivity Severe hepatic impairment
2 drug interactions of asprin
Anticoagulants
NSAIDs
Name 3 anti platelet drugs
Asprin
Clopidogrel
Ticagrelor
What is the function/mechanism of clopidogrel?
binds to what preventing what
Inhibits platelet aggregation
Acts as a ADP receptor antagonist preventing the binding of fibrin with platelets = no aggregation.
What organ is clopidogrel metabolised by?
Liver
5 ADRs of clopidogrel
Nausea/vomiting GIT discomfort Rash Thrombocytopenia (low thrombocyte count <150000 mc/L) GIT bleeds
3 drug interactions of clopidogrel
NSAIDs
Anticoagulants
PPIs
3 contraindications for the use of clopidogrel
Hypersensitivity
Active bleed
Severe hepatic impairment
How does ticagrelor work?
Inhibits platelet aggregation
What does ticagrelor do to liver enzymes?
Reversibly inhibits liver enzymes
Which one of the 3 antiplatelet medications requires a loading dose of 180mg before BD doses?
Ticagrelor
4 ADRs of ticagrelor
Dysponea
Nausea/vomiting
Rash
Bruising
4 drug interactions of ticagrelor and the reason for them
Clarythromycin Simvastatin Digoxin Rifampicin Caused by drug being metabolised/inhibiting liver enzymes
3 contraindications for ticagrelors use
Active bleed
Pregnancy
Moderate-severe hepatic impairment
How do beta blockers work?
Reduce oxygen requirement of cardiac muscle cells
True or false, beta blockers require titrating to a max tolerated dose?
True
4 mechanisms of how beta blockers work
Slow heart rate
Decrease heart contractility
Decrease blood pressure
Improve coronary oxygenation
4 ADRs of beta blockers
Fatigue
Bradycardia
Hypotension
Bronchospasm
4 contraindications for beta blockers use
Acute heart failure
Symptomatic bradycardia/ hypotension
Severe asthma/ COPD
Hypersensitivity
4 drug interactions with beta blockers
Veranapril
NSAIDs
Topical beta blockers
Anti-hypertensives
What is the function of statins?
Lower concentration of lipids in circulation
5 mechanisms of statins
Inhibit HMG-CoA enzyme Stabilise plaque Decrease cholesterol by improving clearance of LDL Improve endothelial function Prevent thrombus formation
2 ADRs of statins
Myopathy (muscle disease)
Hepatoxicity
What 3 interactions occur with statins?
eat, enzyme
Grapefruit
Metabolised by CYP enzymes check BNF
Amylodapine
4 management interventions for NSTEMI
Angiogram
Angioplasty
Coronary artery bypass grafting (CABG)
Percutaneous coronary intervention (PCI)
2 types of stent
Metal stent
Drug emitting
4 functions of renin angiotensin system
Regulation of BP and volume, blood sodium and water concentration
Where is renin produced and what does it stimulate where?
Kidneys
Stimulates angiotensin production in liver
Where is angiotensin produced and what does it stimulate where?
Liver
Stimulates the release of aldosterone from the adrenal cortex
Where is aldoserone produced and what does it stimulate where?
Adrenal cortex
Stimulates the uptake of sodium and water in the kidneys
What stimulates the release of atrial natriuretic hormone and what is it’s function?
Release stimulated by increased blood volume
Negatively feeds back into RAAS to inhibit aldosterone production causing maintenance of blood water and sodium concentration
2 classes of drugs involved in the renin angiotensin aldosterone system
Angiotensin converting enzyme (ACE) inhibitors
Angiotensin receptor blockers (ARBs)
Explain mechanism of ACE inhibitors
system involved in, what stage, which hormone
Renin angiotensin aldosterone system
Intercepts at lungs preventing conversion of angiotensin I to angiotensin II
What two things should be monitored when taking ACE inhibitors?
Kidney function and BP
Explain the mechanism of ARBs
which system, where by doing what
Renin angiotensin system
Acting as competative angiotensin II receptor antagonists
4 ADRS of ACEIs and ARBs
Dry cough
Dizziness
Hyperkalaemia
Angiodema
3 drug interactions with ARBs and ACEI
NSAIDs
K sparing diuretics
K supplements
4 contraindications for ACEI and ARBs use
Pregnancy
Renal stenosis
Hereditary angiodemia
Hypersensitivity
What 5 drugs may be given to someone with angina?
Asprin Angiotensin converting enzyme inhibitors Calcium channel blockers Statins Nitrates
What is angina and what is it caused by?
Chest pain felt due to ischaemia of coronary arteries reducing oxygen supply to cardiac muscle cells, caused by coronary artery disease
What are 2 events that may bring on symptoms of angina?
Physical activity
Obstruction of blood flow
What do drugs for angina aim to stimulate?
Smooth muscle relaxation
4 types of angina
Stable
Unstable
Variant
Microvascular
3 features of stable angina
?expected, trigger, duration, relief with?
Predictable, able to be reproduced
Triggered by emotional/physical stress
Short in duration
Relief with rest
3 features of unstable angina
?expected, trigger, duration
Unexpected, change in stable angina
Spontaneous, can occur at rest
Duration >30mins
4 features of variant angina
?expected, trigger, duration, causes what
Sudden onset, no warning
No identified trigger, can occur at rest
Duration >15mins
Causes lasting heart damage
3 features of microvascular angina
?expected, trigger, duration
Unpredictable
No identified trigger
>10-30 mins
Explain the mechanism of nitrates for angina
chemical, conversion to which substrate, for which enzyme, to convert to which substance, which stimulates what
Convert nitrate ions into nitric oxide
Nitric oxide is the substrate for guanylate cyclase enzyme
Guanylate cyclase converts nitric oxide into guanosine monophosphate cGMP
cGMP stimulates smooth muscle relaxation
What is GTN spray used for?
Relief of angina chest pain
Secondary prevention for angina related to exercise
What does GTN stand for?
Glyceryl trinitrate
6 ADRs of nitrates
Postural hypotension Flushing Reflex tachycardia Tolerance Headache Nausea
2 drug interactions with nitrates
Phosphodiesterase type 5 inhibitors (pulmonary hypotension)
Anti-hypertensives
How does GTN work?
Stimulates vasodilation, widening lumen of coronary arteries improving blood supply to coronary arteries
5 steps f GTN spray use
Chest pain occurs Stop, sit, rest Spray GTN sublingually - wait 5 mins Chest pain persists = spray GTN sublingually again - wait 5 minutes Pain persists = call 999
4 ADRs of GTN
Headache
Dizziness
Nausea/vomiting
Low BP
What is the action of nicorandil?
Dual action as a nitrate and potassium channel agonist
Explain the mechanism of nicorandil
binds to what, stimulates what having what overall effect
Binds to potassium channels - indirectly blocking calcium channels + directly stimulating increase in coronary perfusion and vasodilation
Nitrate aspect binds to calcium channels on smooth muscle - lowing ventricular filling pressure and SVR
Both increase blood supply and oxygen to cardiac muscle
4 ADRs of nicorandil
Headache
Nausea
Diziness
Fatigue
2 drug interactions with nicorandil
Antihypertensives
Phophodiesterase type 5 inhibitors
2 contraindications of nicorandil’s use
Low BP/pulmonary oedema
How do calcium channel blockers work?
Relax smooth muscle and decrease HR
What are calcium channel blockers and alternative medication to?
Beta blockers
Explain mechanism of calcium channel blockers
where is the receptor located, what do they stop, what effect do they have
Bind to calcium channels on smooth muscles
Block influx of calcium ions
Results in smooth muscles remaining relaxed
Name 3 classes of calcium channel blockers
Benzothiazepines
Dihydropyridines
Phenyalkylamines
Action of dihydropyridines
selective to what, used for treatment in what, cause what
Selective to smooth muscles
Used to treat hypertension
Cause reduction in stroke volume
Action of phenylalkylamine
selective to what, cause what
Selective to myocardium
Cause vasodilation
Action of benziorhiazepines
selective to what, cause what
Selective to cardiac muscle
Cause vasodilation
5 ADRs of calcium channel blockers
Oedema Hypotension Bradycardia Headache Constipation
3 drug interactions with calcium channel blockers
Amlodipine enzyme inducers/inhibitors
Anti-hypertensives
Verapamil
What 2 parts of the clotting cascade to be aware of?
Factor Xa
Thrombin
What 2 parts of the clotting cascade is factor Xa involved in?
Intrinsic and extrinsic pathway
What is thrombin what does it produce and what is that required for?
(clotting cascade)
Enzyme that produces the protein fibrin required for binding to platelets allowing their aggregation
9 ideal features of anticoagulants
Wide therapeutic range No food or drug ADRs Oral administration Rapid onset/offset of action Predictable effect with weight determined dosing No routine monitoring Reversible Cost effective Suitable for pts with renal/hepatic impairment
Name two parenteral anticoagulants
Heparin
Low molecular weight heparin
What is protamine used for?
Reversal agent for heparin
Explain heparin’s mechanism of action in preventing clotting
(binds to what, inactivates what, preventing what 2 conversions)
Binds to antithrombin
Inactivates factor Xa
Prevents conversion of prothrombin to thrombin, fibrogen to fibrin preventing clotting
Via what route and method is heparin administered?
IV via continuous infusion
What is the half life of heparin?
1-2 hours
Via what organ is heparin cleared from the body?
Liver
What is the name of the monitoring that is required when pt is on heparin?
(aPPT)
Activation partial thromboplastin time (aPPT)
What is activation partial thromboplastin time a measure of?
Time it takes the blood to clot
What is a normal activation thromboplastin time?
in secs
60-70secs
Why is a aPPT activator added to heparin?
To narrow the reference range
Define ‘the reference range’
heparin
Time taken for a pt on heparins blood to clot
What is an ideal reference range for someone on heparin?
in secs
30-40secs
Above how many seconds for aPPT and PPT does spontaneous bleeding occur?
aPPT= >70seconds PPT= >100 seconds
Explain the mechanism of action of low molecular weight heparin as an anticoagulant
(binds to what, effecting what in the clotting cascade)
Binds to antithrombin
Effecting factor Xa
Give 7 reasons why low molecular weight heparin is preferred to heparin
(dosing, half life, monitoring- in which pts, clearance, effect on platelets, reduces risk of what)
Given OD/ BD
Half life: 5-7 hours
Monitoring: only in certain pts - children with poor renal function/low weight; pts with creatinine clearance <30ml/min
Less inhibition of platelets
Lower risk of heparin induced thrombocytopenia (HIT)
What is vitamin K and what is it needed for?
solubility, clotting cascade
Fat soluble vitamin
Needed for the production of clotting factors in the clotting cascade
What is the mechanism of action of direct oral anticoagulants?
(act on what in clotting cascade)
Direct effect on thrombin and factor Xa in clotting cascade
Name 4 main direct oral anticoagulants
Apixaban
Dabigatran
Endoxaban
Rivaroxaban
Which 1 of the 4 direct oral anticoagulants effects thrombin?
Dabigatran
Which 3 of the 4 oral anticoagulants effect factor Xa?
Apixaban
Endoxaban
Rivaroxaban
How does dabigatran interfere with the clotting cascade? What type of drug is it?
(clue: what does it require to become active)
Interferes with thrombin
It is a prodrug needing first pass metabolism to be activated.
What is praxbind the reversal drug for?
Dabigatran
What is an ADR of dabigatran?
Dyspepsia
2 interactions of dabigatran
ATP inhibitor/inducer
Anti-platelets
7 contraindications for dabigatran’s use
Hypersensitivity Possit box Creatinine clearance <30ml/min Active bleed Surgery Hepatic impairment Prosthetic heart valve
What is the mechanism of rivaroxaban, apixaban, endoxaban in the clotting cascade?
(inhibits what, interupting what, stopping what)
Inhibit factor Xa
Interrupt intrinsic and extrinsic pathway of clotting cascade
Stop formation of thrombin preventing the development of thrombi.
What is andexXa a reversal drug for?
Factor Xa inhibiting drugs
9 ADRs of rivaroxaban, apixaban, endoxaban
Nausea/vomiting Diarrhoea Jaundice Alopecia Rash Hepatic impairment Pyrexia Headache Haemorrhage
5 contraindications for rivaroxaban, apixaban, endoxaban’s use
Hypersensitivity Pts with poor adherence Bleeding complications Creatinine clearance of <15ml/min Active bleed
What type of anticoagulant is warfarin?
Oral anticoagulant
What is warfarin’s mechanism of action?
enzyme it effects, vit …
Inhibits vitamin K reductase that activates vitamin K
Where does warfarin metabolism occur?
Liver CYP enzymes
True or false the effects of warfarin can last after the end of dose?
True
What monitoring test is required when a patient is on warfarin?
International normalised ratio
4 ADRs of warfarin
Bleeding
Nausea/vomiting
Liver dysfunction
Jaundice
5 contraindications of warfarin
Pregnancy Haemorrhagic stroke Hypersensitivity Active bleed Surgery <72 hrs
What 2 groups of drugs interact with warfarin?
Anti-coagulants
Non-prescription drugs - herbal remedies, vitamins, alternative medicines, OTCs
