CVS medication Flashcards
reversible risk factors of cv
- Smoking
- Obesity
- Diet
- Alcohol
- Exercise
- Hypertension
- Hyperlipidaemia
- Diabetes
Irreversible risk factors of cv diseases
- Age
- Sex
- Family history
If high risk of CVS diseases, what tests or
medical treatment to reduce risk
- Family history
- Test cholesterol
- Test blood pressure
- Test for diabetes 2 (atherosclerosis)
- Control and reduce total cholesterol
- Control hypertension
- Anti platelet drugs like aspirin
Primary vs secondary prevention
Primary = before CV disease
Secondary = after presenting with CV disease like angina, MI, stroke
what is the worst risk factor for CV diseases?
SMOKING
what type of drug is aspirin
antiplatelet drug
how long do you need to stop aspirin before a procedure
7 days
how does aspirin inhibit platelet aggregation?
altering balance between thromboxane A2 and prostacyclin
is thromboxane or prostacyclin a platelet aggregator
thromboxane
- platelet aggregation
- blood clots
- vasoconstriction
what do statins do?
statins inhibit cholesterol synthesis in the liver by targeting an enyme
what can statins not be used with
Cannot use with antifungals Fluconazole
what happens when there is too much statin in the body
myositis muscle inflammation
what class of drugs are beta blockers
Anti-arrhythmic
Beta-blockers 2 examples
Atenolol
Propranolol
function of B blockers
mainfunction as an anti arrhythmic drug
treat High BP
Angina
Heart attack
Irregular heart rhythm
Reduces cardiac muscle excitability, lowers risk of heart attack
what to watch out for when someone is using b blockers
- cannot use b blockers with asthma
- must raise pt slowly cause postural hypotension
- makes heart failure worse , negative ionotropy
atenolol targets which adrenergic receptor
beta 1
propranolol targets which adrenergic receptor
beta 1 and beta 2
beta 1 vs beta 2
beta 1 - increase HR
beta 2 - vasodilation+ bronchodilation
Beta 1 receptors refer to the receptors located in the heart and kidney, where they are involved in the regulation of heart rate, cardiac contractility, and plasma renin release,
while beta 2 receptors refer to receptors that mediate relaxation of smooth muscle,
why can you not use beta blockers on asthma patients?
blocking airway β2-receptors can cause severe and sometimes fatal bronchoconstriction in people with asthma
example of an anticoagulant
warfarin
heparin
DOAC
Rivaroxaban
Apixaban
Dabigatran
Edoxaban
anticoagulant vs antiplatelet
antiplatelet
- longer bleeding time, not enough platelets to clot
anti coagulant
- normal bleeding time ,but higher risk of post treatment bleeding
- not enough fibrin to form stable clot
Antiplatelets prevent blood cells called platelets from clumping together to form a clot. Anticoagulants inhibitis coagulation cascade by interfering with proteins in your blood called factors
NOAC vs trad anticoagulants
NOAC
- Shorter half life
- No test required
- Short course
- No significant drug interactions
what r the two types of diuretics
Thiazide diuretics
Loop diuretics - furosemide
when are diuretics used
High BP
Heart failure
Oedema
Renal failure
to lower BP and cardiac workload
mechanism of diuretics
Remove salt and water
Reduces plasma volume, reducing cardiac workload
how do ACE inhibitors lower BP
Inhibits conversion of angiotensin I to II
Prevents aldosterone dependent reabsorption of salt and water
Decrease vol of blood = BP falls
side effects of ACE inhibitors
- cough
- hypotension
- swelling of tongue lips
- angioedema
- lichenoid rxn
what drug type has the suffix -pril
ace inhibitors
how do angiotensin II blockers work
angiotensin II is a vasoconstrictor
without that, cannot constrict so lowers bp
what is losartan
angiotensin II blocker
what does aldosterone do?
water reabsorption
nitrates function
vasodiltors
-Dilate veins reduce preload
-Dilate arteries reduce cardiac workload
-Dilate coronary artery reduce angina heart pain
what is commonly used for heart pain/ angina
nitrates
what is glyceryl trinitrate used for
Short acting for emergency of angina
angina pectoris vs ischemia
Angina pectoris = chest pain or discomfort that keeps returning, caused by myocardium not receiving enough blood and oxygen
Ischemia = restricted blood flow AND OXYGEN to cardiac muscle
Nifedipine vs Verapamil
Nifedipine – peripheral blood vessels (adrenoreceptors)
Verapamil – heart muscle
both are calcium channel blockers
what are Nifedipine and Verapamil
calcium channel blockers
what do calcium channel blockers do?
Blocks calcium channels in smooth muscle
Relaxation and vasodilation
Slow conduction in heart
side effects of calcium channel blockers
Can lead to gingival hyperplasia must monitor OH
what does warfarin inhibit
Warfarin inhibits synthesis of vitamin K dependent clotting factors
factor 2 7 9 10
protein c and s
what is the difeerence between factors 2 7 9 10 and protein c/s
2 7 9 10 (slow)
Protein C and protein S (fast)
why is heparin used together during the initial 1-2 days of warfarin use
- Anticoagulant medication is introduced.
- The medication’s primary effect is to reduce the synthesis of vitamin K-dependent clotting factors, including Protein C and Protein S.
- This reduction in Protein C and Protein S levels means there are fewer anticoagulant factors to counteract the procoagulant factors, leading to a temporary imbalance.
- As a result, the blood becomes “hypercoagulable,” meaning it has an increased tendency to form clots.
what is INR
INR is the ratio of (healthy prothrombin to thrombin time) : (patient prothrombin to thrombin time)
what is the ideal INR
Warfarin patient ideal INR 2-4
what can you not take with warfarin?
- ASSUME ALL drugs interact with warfarin
- Avoid NSAIDs
- Avoid analgesics
- Test INR AFTER antibiotics
- Local anaesthesia okay tho
can you use LA on warfarin patients?
yes
Coronary arteries
- Right
- Left anterior descending
- Circumflex
Perfusion of heart during diastole or systole
diastole
what happens to perfusion of cardiac muscles when HR increases
Importance is that as heart rate increases, the time period for diastole decreases, compromising perfusion of cardiac muscles
what is the difference betwee gradual and rapid occlusion of the BVs
If narrowing of blood vessels is gradual, higher chance of developing alternative blood supply.
If blockage is rapid and sudden, the blood supply immediately cut off catastrophic results
where does Atherosclerosis tend to occur
- Areas of stress
- Turbulent blood flow
- Change in blood flow
- Damages the lining of inner walls of BV, causing build up of fat and plaque
3 types of atherosclerosis
- Atherosclerosis with blood clot (most commonly seen in MI)
- Atherosclerosis (gradual narrowing)
- Spasm (vasospastic angina)
how to classify if its a reversible or irreversible damage to cardiac muscle
Reversible if <20min total occlusion
Permanent cardiac muscle damage if >20min
4 types of acute coronary syndromes
Stable angina
Unstable angina
NSTEMI
STEMI
what does STEMI stand fir
ST elevation MI
How to diagnose acute coronary syndromes
- look at history, see if ST elevated or normal, look at troponin levels
what does Troponin tell us
- tells us if its MI if elevated
- does not rise quickly
- takes about 24-48h after MI to peak
- cannot get clear diagnosis immediately
- if patient has a raised troponin level upon admission, possible that they had a MI in the last 24h
diff between stable and unstable angina
Stable angina
Atherosclerotic plaque
Unstable angina
Atherosclerotic plaque with clot Partial occlusion
which angina tends to occur during execrise
stable angina
is angina reversible
yes
which type of ACS id there Subendocardial infarct ie inner wall of cardiac muscle
NSTEMI
where does STEMI occur
Transmural infarct ie full thickness of wall
which ACS has elevated troponins
NSTEMI AND STEMI
How to relieve symptoms of STABLE angina
Can relieve by decreasing oxygen requirements. Can do so by stopping exercise or increasing blood flow
for angina pectoris, does the ecg have st rise or fall
usually depression but can have rise that correlates with periods of exercise
test foe ischaemia of the heart in real time
an exercise ECG
signs and symptoms of angina
- central crushing pain
- radiation of pain to arm neck back, jaw sometimes
- referred pain
- pain during exercise
- pain relieved by rest
what causes a mismatch in oxygen delivery and oxygen requirement
- anaemia – reduced oxygen carrying capacity
- hyperthyroidism – increased oxygen requirement by tissues high metabolism
people who have angina pectoris are likely to have what other medical complications
anaemia, hyperthyroidism, hypovolaemia
how to solve angina
- decreasing oxygen requirements
- Increase oxygen delivery
- Explanation of illness
- Modify risk factors
- Drug therapy
Investigations for angina
o ECG
o angiography
o echocardiography
o eliminate diseases that increase cardiac workload
ECG vs echocardiography
ECG = electrical system of heart, produces wave like diagram
Echocardiography = mechanical system of heart, check heart valves or ventricles, ultrasound picture of heart
CABG procedure
- new blood vessels usually taken from the leg are grafted into aorta to carry blood past the obstruction
- major surgery
- limited benefits esp in smokers
- includes stopping of the heart temporarily
- ## mortality risk
which BVs taken for cabg
usually take the saphenous vein in leg, or mammary artery in chest, or radial artery in arm
Angioplasty + stenting procedure
- cannula placed in femoral artery in leg or the radial/brachial artery in arm, cannula passed through the vascular system to the site of narrowing
- cannula blows up balloon which stretches a stent in place to keep the blood vessels open
diff between cabg and angioplasty
angio - lower risk
- but lower benefits
danger of cabg
stop heart
danger of angioplasty
- danger of vessel rupture
PCI
percutaneous intervention
why need antiplatetlet therapy for angioplasty + stenting
- platelets tend to stick to stent
- coat stent with chemicals that inhibit platelet adhesion
when can cabg not be done
- can only be done if the site of blockage is close to the artery origin
what is Peripheral vascular disease
- same as angina but instead of heart, affects the tissues in the body
where does Peripheral vascular disease usually occur
- lower limbs
- arms
atheroma vs atherosclerosis
Atheroma refers to the fatty deposits or plaques that develop within the inner lining of arteries Atheroma is an early stage in the development of atherosclerosis.
Atherosclerosis is a more advanced and complex disease involving the buildup of atheromas and other elements.
claudication pain
- claudication pain/ cramps in limbs on exercise
- claudication pain equivalent to angina pain in heart
arteriopath
- someone who has atherosclerosis in their legs has high risk of atherosclerosis in their heart to due to “arteriopath”
what happens in px with Peripheral vascular disease
- poor wound healing
- tissues necrosis
- amputation
- aggravated by high bp and smoking
- chronic lack of oxygen -> necrosis
how to Reduce oxygen requirement in Treatment of angina
a. reduce afterload
b. reduce preload
c. correct mechanical issues (heart valve failure or septal defects, they cause less blood to be pumped into circulation, heart has to pump harder to maintain cardiac output)
how to surgically
Increase oxygen delivery in Treatment of angina
a. angioplasty + stent
b. CABG = coronary artery bypass graft
4 drugs frequently used in treatment of angina
Aspirin
Hypertension drugs
nitrates
GTN emergency nitrate
*refer to summary notes section drug therapy
what type of drug is aspirin
antiplatelet drug to reduce MI risk
How does ischaemia turn into infarction?
- atheroma becomes full clot
- embolization
- embolization
o plaque detaches and travels to distal site, blocking vessels fully
Infarction occurs in which organs
heart limbs brain
what do you call infarction in the brain
embolic stroke
which arteries are blocked in limb infarction
femoral and popliteal arteries in leg/knee
b. atheroma, claudication pain
c. leading to complete obstruction or embolization
d. lastly necrosis or ischemic tissue loss
how does embolic stroke occur
platelet detaches from atherosclerosis in carotid arteries
embolising upwards into the cerebral circulation
what is transient ischaemic attacks
less than 24h mini/mild stroke
in stroke is there always permanent damage?
no. damage is variable. sometimes reversible if its a mild stroke and depends on the region of the brain too
how does a mini stroke (TIA) occur?
solely platelet embolisation
platelets usually removed quickly from circulation (24h) and vessels will open again
*embolizationcan be plaque or platelets
how to reduce tissue loss from necrosis
open blood flow asap
thrombolysis or PCI
what drugs often used in thrombolysis
streptokinase or tissue plasminogen activator
timeframe for thrombolysis
delayed admission (up to 6h after symptoms)
why is further risk management for MI patients so important
because patient who is presenting with MI will likely have widespread atherosclerotic disease and is at risk of further MI
when Can you not thrombolysis
- recently had an open wound or surgery because clots dissolve
- severe hypertension, as thrombolysis will exacerbate active bleeding
why is cardiac pain more distressing than somatic tissue pain?
it is much more distressing because of the different pain signalling path. cardiac pain from thalamus and ancient basal brain to the cortex, brain cannot ignore these signals
ecg in normal vs MI
st elevation sometimes (stemi)
Q wave much larger
12 lead ECG helps you diagnose what?
a 12 lead ECG is that it tells you whereabout in the heart the MI is taking place, so you can diagnose electrical issues with the heart
how does MI differ from cardiac arrest?
MI, or myocardial infarction, is when the blood supply to part of the heart is blocked, causing damage to the heart muscle. (heart attack)
Cardiac arrest is when the heart stops functioning due to an electrical issue, and it can be fatal if not immediately reversed.
will MI lead to cardiac arrest?
not always only sometimes if there’s like post MI arrythmias
- Cardiac arrest can be recognised in a patient having MI by a sudden loss of consciousness -> CPR immediately
Complications of MI
- death
- post MI arrhythmias that can lead to VF
- heart failure
- ventricular hypofunction and mural thrombosis
- deep vein thrombosis and pulmonary embolism
- refer to notes for more info
how to reduce penumbra tissue damage in infarction
o inflammation medication can reduce swelling and increase blood flow to surrounding normal tissues, making the final area of cardiac damage smaller
what 4 types of vascular pathology are there
Atherosclerosis
Atheroma
Peripheral vascular disease
Aneurysms
risk factors for vascular pathology rmb at least 3
hyperlipademia
chronic periodntitis
age
males /gender
genetics
hemodynamics
hypertension
how does chronic periodontitis link to vascular pathology
– C reactive protein produced due to chronic inflammation, risk for atherosclerosis
what gene is mutated that might cause vasuclar pathology
mutation of LDL receptor gene, causes hypercholesterolaemia
what happens when endothelial cells of BV are activated
- increased cell surface receptors for increased permeability
- increased cell adhesion molecules
- increased procoagulants
- turbulent flow
- cytokines
- complement
- lipid products
2 stages of atheroma
chronic inflammatory
healing
describe the chronic inflammatory stage 4 marks
1.increased cell surface receptors for lipids to permeate
- lipids move out of the blood and settle in the tunica media of BV walls
- increased cell adhesion molecules for macrophages and t cells to attach to BV walls, causing inflammation
- macrophages engulf lipids, producing foam cells
describe the healing phase
Proliferation of smooth muscle cells
Growth factors
Atheroma has
Fibrous cap
Fatty fibrous plaque
Dystrophic Calcification
If the atheroma ruptures, may release the substances into bloodstream causing thrombosis
thrombosis vs embolism
thrombosis is a blood vlot that causes blockage
embolism caused when a thrombus or a piece of thrombus breaks off from where it formed and travels to another area of your body
4 effects of atherosclerosis
angina
MI
thrombosis
embolism
AAA
abdominal aortic aneurysms
Results from atherosclerosis
Commonest
Plays a role in peripheral vascular disease
Huge vessel aneurysm, causes pressure on surrounding organs and can produce more problems when it ruptures
where do aneurysms commonly occur
Brain mostly
Blood vessel
Cardiac wall
what causes aneurysms
Developmental
Degenerative
Traumatic
Accident
Infections
Aging
what is the appearance of cardiac muscle cells in coagulation necrosis?
- cell outline remains
- nuclei removed
- darker staining
- lost of striation
- macrophages that removes necrotic tissue
- lymphocytes
what happens after coagulation necrosis
Granulation tissue formation after the necrotic tissue has been removed,
the granulation tissue is not able to function the same as normal cardiac muscle
first step in healing process
what occurs during granulation tissue formation
fibroblasts produce collagen
angiogenesis
growth factors VEGF cytokines hormones
what happens after granulation tissue is removed
fibrous scar tissue replaces, tissue remodeeling
example of a Chronic coronary disease
Congestive heart failure
what is Congestive heart failure caused by
IHD – ischaemic heart disease
Hypertension
Valvular disease
how does chronic heart diseases occur (2 types)
1 Hypertension or atherosclerosis
Increased resistance in BVs
Heart needs to pump stronger to overcome resistance
Cardiac muscle hypertrophy ie becomes much larger
There is an increase in demand for oxygen and nutrients for cardiac muscle but not enough blood flow
So ischaemia and injury to myocytes
- cell injury -> necrosis
is - Haemangioma benign or malignant
neither
3 types of tumour vascular malformation
- Capillary
- Cavernous
- Sturge Weber syndrome
causes of Vascular malformations
developmental
what are vascular malformations
blood filled spaces
If there is intraosseous malformation, may be increased bleeding during tooth extractions
For Sturge weber in oral cavity, need specialised oral settings otherwise if poke any of these blood filled spaces, can cause extensive bleeding
where and who is kaposi sarcome usually found in?
oral cavity of HIV, herpes virus 8 patients
what is kaposi sarcome
Low grade sarcoma of lymphatics and blood vessels
diseases of the valves 3 examples
calcific aortic stenosis
rhematic valvulitis
infective endocarditis
rhematic heart disease
when the valves are diseased , how does it affect the opening and closing of the valves?
Stenosis failure to open
Insufficiency failure to close
Vegetations lumps on valve cusps
insufficiency
failure to close tight, can cause oxy and deoxy blood to mix
what is rhematic heart disease caused by
- Cross rxn btwn host proteins and Streptococcus A antigens
- Hypersensitivity type 2 and 4 rxn
Aschoff bodies
present in rheumatic fever
- inflammation in all 3 layers of the heart
- pancarditis
- lesions in heart
- area of fibrinoid necrosis
- T cells
- modified macrophages with caterpillar looking nucleus (Anitschkow cells)
what is rheumatic valvultis
inflammation of the valves, occurs in the endocardium
vegetations along the lines of closure
thickening and fusion causing valves to not be able to open fully
what is the result of rheumatic valvulitis
Results in aortic dilation
Atrial fibrillation -> blood flows in all diff directions and speeds -> RBCs hit against the walls of the atrium -> set up thrombi on walls of atrium
may result in infective endocarditis
When do you need to prescribe antibiotic prophylaxis for infective endocarditis?
causes of Infective endocarditis in oral setting
Oral pathogens
Streptococcus
staphylococcus
non dental are
Microbial infection of heart valves
Damaged valves
Prosthetic heart valves
congenital heart disease
what is infective endocarditis
Inflammation of the endocardium and valves. Usually caused by bacterial infection.
what type of necrosis in rheumatic valvulitis
fibrinoid valvulitis
What comprises of the vegetations on the cusps in IE?
Vegetations contain fibrin inflammatory cells and pathogens that can eventually cause infective emboli
