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BDS2 BAMS > CVS medication > Flashcards

CVS medication Flashcards

1
Q

reversible risk factors of cv

A
  • Smoking
  • Obesity
  • Diet
  • Alcohol
  • Exercise
  • Hypertension
  • Hyperlipidaemia
  • Diabetes
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2
Q

Irreversible risk factors of cv diseases

A
  • Age
  • Sex
  • Family history
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3
Q

If high risk of CVS diseases, what tests or

medical treatment to reduce risk

A
  • Family history
  • Test cholesterol
  • Test blood pressure
  • Test for diabetes 2 (atherosclerosis)
  • Control and reduce total cholesterol
  • Control hypertension
  • Anti platelet drugs like aspirin
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4
Q

Primary vs secondary prevention

A

Primary = before CV disease

Secondary = after presenting with CV disease like angina, MI, stroke

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5
Q

what is the worst risk factor for CV diseases?

A

SMOKING

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6
Q

what type of drug is aspirin

A

antiplatelet drug

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7
Q

how long do you need to stop aspirin before a procedure

A

7 days

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8
Q

how does aspirin inhibit platelet aggregation?

A

altering balance between thromboxane A2 and prostacyclin

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9
Q

is thromboxane or prostacyclin a platelet aggregator

A

thromboxane
- platelet aggregation
- blood clots
- vasoconstriction

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10
Q

what do statins do?

A

statins inhibit cholesterol synthesis in the liver by targeting an enyme

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11
Q

what can statins not be used with

A

Cannot use with antifungals Fluconazole

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12
Q

what happens when there is too much statin in the body

A

myositis muscle inflammation

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13
Q

what class of drugs are beta blockers

A

Anti-arrhythmic

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14
Q

Beta-blockers 2 examples

A

 Atenolol
 Propranolol

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15
Q

function of B blockers

A

mainfunction as an anti arrhythmic drug

treat High BP

Angina

Heart attack

Irregular heart rhythm

Reduces cardiac muscle excitability, lowers risk of heart attack

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16
Q

what to watch out for when someone is using b blockers

A
  1. cannot use b blockers with asthma
  2. must raise pt slowly cause postural hypotension
  3. makes heart failure worse , negative ionotropy
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17
Q

atenolol targets which adrenergic receptor

A

beta 1

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18
Q

propranolol targets which adrenergic receptor

A

beta 1 and beta 2

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19
Q

beta 1 vs beta 2

A

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,

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20
Q

why can you not use beta blockers on asthma patients?

A

blocking airway β2-receptors can cause severe and sometimes fatal bronchoconstriction in people with asthma

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21
Q

example of an anticoagulant

A

warfarin
heparin

DOAC
 Rivaroxaban
 Apixaban
 Dabigatran
 Edoxaban

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22
Q

anticoagulant vs antiplatelet

A

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

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23
Q

NOAC vs trad anticoagulants

A

NOAC
- Shorter half life
- No test required
- Short course
- No significant drug interactions

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24
Q

what r the two types of diuretics

A

 Thiazide diuretics
 Loop diuretics - furosemide

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25
Q

when are diuretics used

A

High BP

Heart failure

Oedema

Renal failure

to lower BP and cardiac workload

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26
Q

mechanism of diuretics

A

Remove salt and water
Reduces plasma volume, reducing cardiac workload

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27
Q

how do ACE inhibitors lower BP

A

Inhibits conversion of angiotensin I to II

Prevents aldosterone dependent reabsorption of salt and water

Decrease vol of blood = BP falls

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28
Q

side effects of ACE inhibitors

A
  • cough
  • hypotension
  • swelling of tongue lips
  • angioedema
  • lichenoid rxn
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29
Q

what drug type has the suffix -pril

A

ace inhibitors

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30
Q

how do angiotensin II blockers work

A

angiotensin II is a vasoconstrictor

without that, cannot constrict so lowers bp

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31
Q

what is losartan

A

angiotensin II blocker

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32
Q

what does aldosterone do?

A

water reabsorption

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33
Q

nitrates function

A

vasodiltors

-Dilate veins reduce preload

-Dilate arteries reduce cardiac workload

-Dilate coronary artery reduce angina heart pain

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34
Q

what is commonly used for heart pain/ angina

A

nitrates

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35
Q

what is glyceryl trinitrate used for

A

Short acting for emergency of angina

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36
Q

angina pectoris vs ischemia

A

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

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37
Q

Nifedipine vs Verapamil

A

Nifedipine – peripheral blood vessels (adrenoreceptors)

Verapamil – heart muscle

both are calcium channel blockers

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38
Q

what are Nifedipine and Verapamil

A

calcium channel blockers

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39
Q

what do calcium channel blockers do?

A

Blocks calcium channels in smooth muscle

Relaxation and vasodilation

Slow conduction in heart

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40
Q

side effects of calcium channel blockers

A

Can lead to gingival hyperplasia must monitor OH

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41
Q

what does warfarin inhibit

A

Warfarin inhibits synthesis of vitamin K dependent clotting factors
factor 2 7 9 10
protein c and s

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42
Q

what is the difeerence between factors 2 7 9 10 and protein c/s

A

 2 7 9 10 (slow)
 Protein C and protein S (fast)

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43
Q

why is heparin used together during the initial 1-2 days of warfarin use

A
  1. Anticoagulant medication is introduced.
  2. The medication’s primary effect is to reduce the synthesis of vitamin K-dependent clotting factors, including Protein C and Protein S.
  3. 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.
  4. As a result, the blood becomes “hypercoagulable,” meaning it has an increased tendency to form clots.
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44
Q

what is INR

A

INR is the ratio of (healthy prothrombin to thrombin time) : (patient prothrombin to thrombin time)

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45
Q

what is the ideal INR

A

Warfarin patient ideal INR 2-4

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46
Q

what can you not take with warfarin?

A
  • ASSUME ALL drugs interact with warfarin
  • Avoid NSAIDs
  • Avoid analgesics
  • Test INR AFTER antibiotics
  • Local anaesthesia okay tho
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47
Q

can you use LA on warfarin patients?

A

yes

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48
Q

Coronary arteries

A
  1. Right
  2. Left anterior descending
  3. Circumflex
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49
Q

Perfusion of heart during diastole or systole

A

diastole

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50
Q

what happens to perfusion of cardiac muscles when HR increases

A

Importance is that as heart rate increases, the time period for diastole decreases, compromising perfusion of cardiac muscles

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51
Q

what is the difference betwee gradual and rapid occlusion of the BVs

A

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

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52
Q

where does Atherosclerosis tend to occur

A
  • 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
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53
Q

3 types of atherosclerosis

A
  1. Atherosclerosis with blood clot (most commonly seen in MI)
  2. Atherosclerosis (gradual narrowing)
  3. Spasm (vasospastic angina)
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54
Q

how to classify if its a reversible or irreversible damage to cardiac muscle

A

Reversible if <20min total occlusion
Permanent cardiac muscle damage if >20min

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55
Q

4 types of acute coronary syndromes

A

Stable angina

Unstable angina

NSTEMI

STEMI

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56
Q

what does STEMI stand fir

A

ST elevation MI

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57
Q

How to diagnose acute coronary syndromes

A
  • look at history, see if ST elevated or normal, look at troponin levels
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58
Q

what does Troponin tell us

A
  • 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
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59
Q

diff between stable and unstable angina

A

Stable angina
Atherosclerotic plaque

Unstable angina
Atherosclerotic plaque with clot Partial occlusion

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60
Q

which angina tends to occur during execrise

A

stable angina

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61
Q

is angina reversible

A

yes

62
Q

which type of ACS id there Subendocardial infarct ie inner wall of cardiac muscle

A

NSTEMI

63
Q

where does STEMI occur

A

Transmural infarct ie full thickness of wall

64
Q

which ACS has elevated troponins

A

NSTEMI AND STEMI

65
Q

How to relieve symptoms of STABLE angina

A

Can relieve by decreasing oxygen requirements. Can do so by stopping exercise or increasing blood flow

66
Q

for angina pectoris, does the ecg have st rise or fall

A

usually depression but can have rise that correlates with periods of exercise

67
Q

test foe ischaemia of the heart in real time

A

an exercise ECG

68
Q

signs and symptoms of angina

A
  • central crushing pain
  • radiation of pain to arm neck back, jaw sometimes
  • referred pain
  • pain during exercise
  • pain relieved by rest
69
Q

what causes a mismatch in oxygen delivery and oxygen requirement

A
  • anaemia – reduced oxygen carrying capacity
  • hyperthyroidism – increased oxygen requirement by tissues high metabolism
70
Q

people who have angina pectoris are likely to have what other medical complications

A

anaemia, hyperthyroidism, hypovolaemia

71
Q

how to solve angina

A
  1. decreasing oxygen requirements
  2. Increase oxygen delivery
  3. Explanation of illness
  4. Modify risk factors
  5. Drug therapy
72
Q

Investigations for angina

A

o ECG
o angiography
o echocardiography
o eliminate diseases that increase cardiac workload

73
Q

ECG vs echocardiography

A

ECG = electrical system of heart, produces wave like diagram

Echocardiography = mechanical system of heart, check heart valves or ventricles, ultrasound picture of heart

74
Q

CABG procedure

A
  • 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
75
Q

which BVs taken for cabg

A

usually take the saphenous vein in leg, or mammary artery in chest, or radial artery in arm

76
Q

Angioplasty + stenting procedure

A
  • 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
77
Q

diff between cabg and angioplasty

A

angio - lower risk
- but lower benefits

78
Q

danger of cabg

A

stop heart

79
Q

danger of angioplasty

A
  • danger of vessel rupture
80
Q

PCI

A

percutaneous intervention

81
Q

why need antiplatetlet therapy for angioplasty + stenting

A
  • platelets tend to stick to stent
  • coat stent with chemicals that inhibit platelet adhesion
82
Q

when can cabg not be done

A
  • can only be done if the site of blockage is close to the artery origin
83
Q

what is Peripheral vascular disease

A
  • same as angina but instead of heart, affects the tissues in the body
84
Q

where does Peripheral vascular disease usually occur

A
  • lower limbs
  • arms
85
Q

atheroma vs atherosclerosis

A

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.

86
Q

claudication pain

A
  • claudication pain/ cramps in limbs on exercise
  • claudication pain equivalent to angina pain in heart
87
Q

arteriopath

A
  • someone who has atherosclerosis in their legs has high risk of atherosclerosis in their heart to due to “arteriopath”
88
Q

what happens in px with Peripheral vascular disease

A
  • poor wound healing
  • tissues necrosis
  • amputation
  • aggravated by high bp and smoking
  • chronic lack of oxygen -> necrosis
89
Q

how to Reduce oxygen requirement in Treatment of angina

A

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)

90
Q

how to surgically
Increase oxygen delivery in Treatment of angina

A

a. angioplasty + stent
b. CABG = coronary artery bypass graft

91
Q

4 drugs frequently used in treatment of angina

A

Aspirin
Hypertension drugs
nitrates
GTN emergency nitrate

*refer to summary notes section drug therapy

92
Q

what type of drug is aspirin

A

antiplatelet drug to reduce MI risk

93
Q

How does ischaemia turn into infarction?

A
  • atheroma becomes full clot
  • embolization
94
Q
  • embolization
A

o plaque detaches and travels to distal site, blocking vessels fully

95
Q

Infarction occurs in which organs

A

heart limbs brain

96
Q

what do you call infarction in the brain

A

embolic stroke

97
Q

which arteries are blocked in limb infarction

A

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

98
Q

how does embolic stroke occur

A

platelet detaches from atherosclerosis in carotid arteries

embolising upwards into the cerebral circulation

99
Q

what is transient ischaemic attacks

A

less than 24h mini/mild stroke

100
Q

in stroke is there always permanent damage?

A

no. damage is variable. sometimes reversible if its a mild stroke and depends on the region of the brain too

101
Q

how does a mini stroke (TIA) occur?

A

solely platelet embolisation
platelets usually removed quickly from circulation (24h) and vessels will open again

*embolizationcan be plaque or platelets

102
Q

how to reduce tissue loss from necrosis

A

open blood flow asap

thrombolysis or PCI

103
Q

what drugs often used in thrombolysis

A

streptokinase or tissue plasminogen activator

104
Q

timeframe for thrombolysis

A

delayed admission (up to 6h after symptoms)

105
Q

why is further risk management for MI patients so important

A

because patient who is presenting with MI will likely have widespread atherosclerotic disease and is at risk of further MI

106
Q

when Can you not thrombolysis

A
  • recently had an open wound or surgery because clots dissolve
  • severe hypertension, as thrombolysis will exacerbate active bleeding
107
Q

why is cardiac pain more distressing than somatic tissue pain?

A

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

108
Q

ecg in normal vs MI

A

st elevation sometimes (stemi)

Q wave much larger

109
Q

12 lead ECG helps you diagnose what?

A

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

110
Q

how does MI differ from cardiac arrest?

A

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.

111
Q

will MI lead to cardiac arrest?

A

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
112
Q

Complications of MI

A
  • 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
113
Q

how to reduce penumbra tissue damage in infarction

A

o inflammation medication can reduce swelling and increase blood flow to surrounding normal tissues, making the final area of cardiac damage smaller

114
Q

what 4 types of vascular pathology are there

A

Atherosclerosis
Atheroma
Peripheral vascular disease
Aneurysms

115
Q

risk factors for vascular pathology rmb at least 3

A

hyperlipademia
chronic periodntitis
age
males /gender
genetics
hemodynamics
hypertension

116
Q

how does chronic periodontitis link to vascular pathology

A

– C reactive protein produced due to chronic inflammation, risk for atherosclerosis

117
Q

what gene is mutated that might cause vasuclar pathology

A

mutation of LDL receptor gene, causes hypercholesterolaemia

118
Q

what happens when endothelial cells of BV are activated

A
  • increased cell surface receptors for increased permeability
  • increased cell adhesion molecules
  • increased procoagulants
  • turbulent flow
  • cytokines
  • complement
  • lipid products
119
Q

2 stages of atheroma

A

chronic inflammatory
healing

120
Q

describe the chronic inflammatory stage 4 marks

A

1.increased cell surface receptors for lipids to permeate

  1. lipids move out of the blood and settle in the tunica media of BV walls
  2. increased cell adhesion molecules for macrophages and t cells to attach to BV walls, causing inflammation
  3. macrophages engulf lipids, producing foam cells
121
Q

describe the healing phase

A

 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

122
Q

thrombosis vs embolism

A

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

123
Q

4 effects of atherosclerosis

A

angina
MI
thrombosis
embolism

124
Q

AAA

A

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

125
Q

where do aneurysms commonly occur

A

Brain mostly
Blood vessel
Cardiac wall

126
Q

what causes aneurysms

A

Developmental
Degenerative
Traumatic
Accident
Infections
Aging

127
Q

what is the appearance of cardiac muscle cells in coagulation necrosis?

A
  • cell outline remains
  • nuclei removed
  • darker staining
  • lost of striation
  • macrophages that removes necrotic tissue
  • lymphocytes
128
Q

what happens after coagulation necrosis

A

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

129
Q

what occurs during granulation tissue formation

A

fibroblasts produce collagen
angiogenesis
growth factors VEGF cytokines hormones

130
Q

what happens after granulation tissue is removed

A

fibrous scar tissue replaces, tissue remodeeling

131
Q

example of a Chronic coronary disease

A

Congestive heart failure

132
Q

what is Congestive heart failure caused by

A

IHD – ischaemic heart disease
Hypertension
Valvular disease

133
Q

how does chronic heart diseases occur (2 types)

A

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

  1. cell injury -> necrosis
134
Q

is - Haemangioma benign or malignant

A

neither

135
Q

3 types of tumour vascular malformation

A
  • Capillary
  • Cavernous
  • Sturge Weber syndrome
136
Q

causes of Vascular malformations

A

developmental

137
Q

what are vascular malformations

A

blood filled spaces

If there is intraosseous malformation, may be increased bleeding during tooth extractions

138
Q

For Sturge weber in oral cavity, need specialised oral settings otherwise if poke any of these blood filled spaces, can cause extensive bleeding

A
139
Q

where and who is kaposi sarcome usually found in?

A

oral cavity of HIV, herpes virus 8 patients

140
Q

what is kaposi sarcome

A

Low grade sarcoma of lymphatics and blood vessels

141
Q

diseases of the valves 3 examples

A

calcific aortic stenosis
rhematic valvulitis
infective endocarditis
rhematic heart disease

142
Q

when the valves are diseased , how does it affect the opening and closing of the valves?

A

Stenosis failure to open

Insufficiency failure to close

Vegetations lumps on valve cusps

143
Q

insufficiency

A

failure to close tight, can cause oxy and deoxy blood to mix

144
Q

what is rhematic heart disease caused by

A
  • Cross rxn btwn host proteins and Streptococcus A antigens
  • Hypersensitivity type 2 and 4 rxn
145
Q

Aschoff bodies

A

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)

146
Q

what is rheumatic valvultis

A

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

147
Q

what is the result of rheumatic valvulitis

A

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

148
Q

When do you need to prescribe antibiotic prophylaxis for infective endocarditis?

A
149
Q

causes of Infective endocarditis in oral setting

A

Oral pathogens
Streptococcus
staphylococcus

non dental are
Microbial infection of heart valves
Damaged valves
Prosthetic heart valves
congenital heart disease

150
Q

what is infective endocarditis

A

Inflammation of the endocardium and valves. Usually caused by bacterial infection.

151
Q

what type of necrosis in rheumatic valvulitis

A

fibrinoid valvulitis

152
Q

What comprises of the vegetations on the cusps in IE?

A

Vegetations contain fibrin inflammatory cells and pathogens that can eventually cause infective emboli

BDS2 BAMS (27 decks)

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