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HDT 2.2 > management of CVD > Flashcards

management of CVD Flashcards

1
Q

what is the symptoms of acute coronary syndrome?

A
  • unstable angina
  • non ST elevated myocardial infarction
  • ST elevated myocardial infarction
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2
Q

what is acute coronary syndrome?

A

when you have a group of symptoms related to the obstruction of the coronary arteries

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3
Q

what is a myocardial infarction?

A

it is a heart attack
formed usually by a blood clot in one of the coronary arteries or its branches
blood clot usually forms if there is plaque in the lining of the arteries

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4
Q

what increases with an MI

A

a cardiac enzyme called troponin

  • seen in serum levels 3-6 hours after MI and can stay for up to 14 days
  • cell damage causes this increase
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5
Q

what types of MI can you have?

A
  1. ST elevated
    there is a elevation of ST interval on 12 lead ECG
  2. Non ST elevated
    no change on 12 lead ECG
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6
Q

what are the causes of an MI?

A

a plaque will form
can have a stable plaque; leads to obstruction of blood flow and symptoms of angina
can have an unstable plaque; can rupture and form a thrombus

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7
Q

what are the modifiable and non-modifiable risks for an MI?

A

modifiable; diet, alcohol, exercise, BP, diabetes

non modifiable; agem gender, history, race

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8
Q

what are the symptoms of an MI?

A
  • have shortness of breath
  • wetting
  • crushing chest pain
  • pain starts at centre of chest and then moves to the arms neck and jaw
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9
Q

how can you treat ST elevation MI?

A
  • aspirin 300mg
  • coronary perfusion therapy ; angiography, drug therapy, fibrinolysis
  • pain relief and medical management; giving ticagrelor with aspirin or clopidogrel with aspirin
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10
Q

what kind of medication is prasugrel?

A

it is anti platelet medication

  • inhibits platelet activation
  • irreversibly binds of its active metabolite to ADP receptors on platelets

should use in combination with aspirin

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11
Q

what is ticagrelor?

A
  • ADP receptor antagonist

can cause dyspnoea and haemorrhage

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12
Q

what can cangrelor be used in combination with and what for?

A
  • used in combination with aspirin
  • used for reduction of thrombotic cardiovascular events in patients with CAD and having percutaneous coronary intervention
    haven’t had clopidogrel or ticagrelor treatment
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13
Q

what is the secondary prevention for an ST elevated MI?

A
  • aspirin at a low dose; ticagrelor may be used alongside this but only for up to 12 months
  • PPI to help reduce GI effects
  • beta blockers
  • ACE inhibitors
  • aldosterone antagonists
  • can use low dose of rivaroxaban
  • might need anti platelet therapy if they have a stent
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14
Q

what does it mean by unstable angina?

A

when they have the MI symptoms

but no rised levels of enzyme troponin and no ECG changes

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15
Q

what’s is NICE management of unstable angina?

A

can give 300mg aspirin loading dose and then continue it indefinitely
antithrombin therapy; can use unfractioned heparin
establish their risk score
1. if low ; conservative management and maybe an angiography
2. high risk; immediate angiography
for both offer aspirin with ticagrelor

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16
Q

what does non- ST elevated MI do?

A

it is the prevention of cross-linking and platelet binding

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17
Q

what is the secondary prevention of Non ST elevated MI and unstable angina?

A
  • dual anti platelet therapy
  • ACE inhibitors
  • beta blockers

can have cardiac rehabilitation

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18
Q

what is meant by stable angina?

A
  • chest pain or discomfort
  • when myocardium demands aren’t met by the blood supply

coronary arteries have narrowed and heart has to do more work

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19
Q

difference between stable and unstable angina?

A

stable angina; the pain can be precipitated by factors

unstable; can occur at any time and be seen as acute coronary syndrome

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20
Q

what is the aim of management of angina?

A
  • stop or minimise symptoms

- to improve quality of life

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21
Q

how long does anginal pain take to be relieved?

A
  • relieved by rest or GTN in about five minutes
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22
Q

what is the management for stable angina?

A
  • CCB or beta blocker
  • GTN for rapid symptom relief
    can use both CCB and BB together if one isn’t tolerated

can use ranolazine or ivabradine

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23
Q

what should be used when a CCB is being used with a BB or ivabradine?

A

make sure you use a slow release nifedipine, amlodipine or felodipine
you should only add a third anti-angina drug if the persons symptoms aren’t controlled with two drugs
only when other medicines are seen to be unsuitable use nicorandil; allows more blood flow and more oxygen to cells

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24
Q

what are the advantages of using nitrates?

A
  • tolerance
  • adjunctive therapy
  • you have short acting and long acting
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25
Q

what do nitrates do and when should they be used?

A

only be used if previous treatment is inadequate

- it mimics NO causing vasodilation improving blood flow and relaxing smooth muscle for release of NO

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26
Q

how are stents placed?

A

find the coronary arteries in the heart
using a catheter place the stent inside the artery with a balloon
the balloon will inflate opening up the arteries and widening the stent
the balloon is then removed allowing blood flow

27
Q

what problems should be discussed with patients after they have an MI?

A
  • using NSAIDs and ACE inhibitors
  • using nitrates
  • beta blocker side effects
  • should take aspirin with food
28
Q

what is patient care needed after an MI?

A
  • change diet, exercise and smoking cessation
  • cardiac rehabilitation
  • improving patient adherence is important
  • face any concerns or anxiety
29
Q

what side effects can nitrates have?

A

headache and continuous flushing

- postural hypotension

30
Q

what are some side effects of beta blockers?

A

headache, confusion, dizziness, constipation, bradycardia, nausea, fatigue

31
Q

what are some side effects of calcium channel blockers?

A

abdominal pain, drowsiness, flushing, nausea, vomiting, depression, angioedema

32
Q

what is anti-coagulant and anti-thrombotic drug? what is a thrombolytic agent?

A

anti-coagulant; drug to prevent blood clotting; targets coagulation cascade
anti-thrombotic - prevents thrombus formation
thrombolytic- agent that dissolves a blood clot

33
Q

what is good and bad about thrombosis?

A

good it it stops bleeding and is non-occlusive

bad is it can block blood supply causing embolism or chronic thrombosis

34
Q

what factors contribute to thrombosis?

A
  1. blood flow
  2. endothelial injury
  3. hyper coagulation
35
Q

what kind of drugs are most beneficial for preventing a clot

A

anti-fibrin drugs as some clots may have more fibrin present

36
Q

what kinds of thrombosis can you have?

A

you can have venous or arterial thrombosis
arterial; high shear and critical platelet number so use anti-platelet drugs
venous; low shear system so use anti-coagulants

37
Q

how does arterial thrombosis occur?

A

platelets interact with exposed endothelial cell s
they can roll and activate ADP
this causes thrombin to be produced and so a thrombus to form from collagen, fibrin and platelets

38
Q

what is the extrinsic pathway of coagulation?

A

when tissue damage causes TF:VIIa to occur and this will cause X to become factor Xa which is used to form thrombin

39
Q

what is the positive feedback cycle?

A

thrombin is used to make VIIa from VII

thrombin is used also to allow XI -> XIa and VIII -> VIIIa

40
Q

what are some anti-coagulant drugs?

A

heparin
warfarin
factor Xa inhibitor - rivaroxaban
thrombin inhibitor - dabigatran

41
Q

what is antithrombin III and what does it do?

A
  • it is physiological suicide inhibitor
    it binds with thrombin to induce thrombin inactivation
    produces a thrombin: AT complex which is inactive
    heparin is a cofactor that allows AT to bind better to thrombin
42
Q

what is warfarins MoA?

A

warfarin inhibits Vitamin K reductase and vitamin K epoxin reductase
this means factors are kept in their inactive form so cant be involved in coagulation cascade so cant form a fibrin clot

43
Q

what do interns do?

A

they mediate platelet adhesion to the injured cell wall and mediate platelet aggregation
important to maintain homeostasis and stop excess bleeding

44
Q

how does aspirin work?

A

it inhibits COX which produced TxA2
this means platelets cannot be activated and so function is disturbed
alongside clopidogrel they inhibit second mediators like ADP

45
Q

what does clopidogrel do?

A

it irreversibly blocks P2Y12 receptor

46
Q

what is tPA and uPA?

A

tPA is from endothelial cells and uPA from kidneys and they allow plasmin to be formed and increase its function for fibrin degradation

47
Q

how do transexamic acid and aminocaproic acid work?

A

they inhibit plasmin formation so inhibit fibrin degradation of the thrombus

48
Q

what are some common clot busters?

A
  • recombinant tPA
  • urokinase
  • streptokinase

they activate plasminogen

49
Q

what are the indication of thrombolytics?

A
  • acute MI
  • acute ischameic stroke
  • peripheral artery occlusion
  • DVT
50
Q

what are the different classes of anti-platelet drugs and what do they do?

A
  1. PAR1 inhibitors; stop PAR1 which is a receptor for thrombin
  2. alphaIIbbeta3 inhibitors which stop platelet interaction with fibrinogen and induce bleeding
  3. cyclooxyrgenase inhibitors; no formation of TxA2
  4. phospodiesterase inhibitors; block platelet activation and stops aggregation
51
Q

how does atherosclerosis occur?

A

LDLs travel through endothelial barrier into the artery and it is oxidised
the macrophages are attracted to oxidised LDL so enter the artery space and phagocytes these oxidised LDLs
you get a foam cell full of lipids and these build up in the artery wall
theyll expand but if not enough HDL to remove the LDL they’ll keep growing
foam cells release lipid content when they die attracting cytokines and release growth factors which increases collagen synthesis hardening the plaque
this causes narrowing and hardening of arteries

52
Q

what is the structure of lipoproteins?

A

transport lipids around body
has a coat containing apoproteins; mediate lipoproteins binding
transport pathways are endogenous or exogenous
and you can have VLDL, HDL, LDL lipoproteins

53
Q

what is the exogenous lipid pathway?

A

lipid enters from the diet
it is then emulsified by the bile acids in the GIT
the lipids (cholesterol esters, TG) are absorbed into chylomicons
the TaGs are hydrolysed by lipoprotein lipase and then become free fatty acids then are absorbed/stored in fat and muscle tissue

54
Q

what is the endogenous lipid pathway?

A
  1. the liver will make C and TG from exogenous pathway
  2. they are secreted into VLDLs; VLDL bind to blood vessel wall receptors to break down TG
  3. TG hydrolysed by lipoprotein lipase and free fatty acids produced to be absorbed/stored in fat and muscle tissue
  4. LDLs contain mainly CE due to TG breakdown
  • cholesterol from cell turnover absorbed into HDL
  • cholesterol esters transferred to LDL and VLDL
  • increased HDL promotes LDL removal
55
Q

what are normal lipid levels?

A 
cholesterol, should be <5 mmol/l-1
LDL-chol <3; HDL >1.2 
if you have abnormal levels of lipid then its dyslipidaemia 
-> more LDL 
-> less HDL
56
Q

what types of hyperlipidaemia can you have?

A

its when you have high amount of lipoproteins

  1. primary; genetic
    - six phenotypes
    - for HL IIa ; more LDL and for HL IIb; more VLDL and LDL
  2. secondary; metabolic disorders
    - > diabetes, renal disease, alcoholism
57
Q

what are some HMG CoA reductase inhibitors?

A

statins ; atorvastatin is high intensity and pravastatin is low intensity
prevent cholesterol synthesis by inhibiting HMG CoA reductase
too much decreased cholesterol can mean what increased HMG CoA enzyme and LDL receptors so more cholesterol and LDL receptors expressed on hepatocytes

58
Q

what are PCSK9 inhibits?

A

PCSK9s they break down LDL receptors on the hepatocytes so LDL isn’t taken up to be broken down
an inhibitor inhibits this and so there’s more LDL uptake into hepatocytes and decreased plasma LDL so less blood cholesterol
- used with statin has an increased beneficial risk

59
Q

what are fibrates?

A

they enter cells and activate nucleus to activate transcription
activate receptors
more lipoprotein lipase more less VLDL production and so less TGs
so more HDL and more uptake of LDL
this benefits decreasing risk of heart disease

60
Q

what are bile acid-binding resins and what do they do?

A

it binds to bile acid so bile acids cannot emulsify lipids
- resins aren’t absorbed so lose cholesterol and bile acids and lipids
so more LDL receptors and less LDL in plasma so more TG

61
Q

what is the action of ezetimibe?

A

inhibits intestinal absorption of cholesterol
no receptor uptake
can use with statin
has a higher potency than resins dose
need 10mg
no effect on fat soluble vitamin asborption

62
Q

what is the prescribing guidelines for hyperlipidaemia?

A

first line is statins and can use PCSK9 inhibitors or ezetimibe
can use vibrate of bile acid resin as second line or nicotinic acid

watch for fibrates + statin

63
Q

what is nicotinic acid?

A

it decreases synthesis of TG and so less VLDL and less LDL
so more HDL
use with statins and resins to decrease mortality

can cause upset GI or flush

64
Q

how does fish oil help hyperlipidaemia?

A

it prevents TG increase but allows cholesterol increase
decreases clotting

made up of omega 3 TGs

HDT 2.2 (10 decks)

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