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BDS 2 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

How does aspirin inhibit platelet aggregation?

A

Alter the balance between Throboxane A2 and Prostacyclin.

This is irreversible for the life of the platelet.

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2
Q

How does clopidogrel inhibit platelet aggregation?

A

Inhibits ADP induced platelet aggregation.

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3
Q

How does dipyridamole work on inhibiting platelet adhesion?

A

It inhibits phosphodiesterase (enzyme found in platelets).

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4
Q

Do antiplatelet drugs slow down or speed up the bleeding time during tooth extractions?

A

They prolong the bleeding time due to these drugs inhibiting platelet adhesion- a blood clot therefore cannot be formed.

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5
Q

What new antiplatelet drugs are used in conjunction with aspirin?

A

Prasugrel and Ticagrelor. These are only prescribed for acute coronary syndromes.

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6
Q

What three anticoagulant drugs are prescribed depending on the patient’s weight?

A

Rivaroxiban (1 daily), Apixaban (2 daily) and Dabigatran (2 daily).

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7
Q

How does warfarin work?

A

It is a coumadin based anticoagulant. Warfarin inhibits the synthesis of vitamin K dependent clotting factors. 2 7 9 and 10 (slow) and Protein C and Protein S fast).

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8
Q

What test is used to monitor warfarin and how does this test work?

A

INR test. ‘Prothrombin time’- measures the time it takes for your blood to clot. If your INR score is too high you are at an increased risk of bleeding.

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9
Q

What test is used to monitor warfarin and how does this test work?

A

INR test. ‘Prothrombin time’- measures the time it takes for your blood to clot. If your INR score is too high you are at an increased risk of bleeding. The therapeutic range is between 2 & 4.

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10
Q

What is haemophillia?

A

An inherited genetic disorder that impairs the bodies ability to create blood clots- this results in prolonged bleeding.

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11
Q

Give examples of drugs that you cannot take with warfarin?

A

Amoxicillin, metronidazole, erythromycin and NSAIDS.

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12
Q

What is a prodrug?

A

A biologically inactive compound which can be metabolised by the body to produce a drug.

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13
Q

Extrinsic activation - Vessel injury occurs then Factor 7 is released. This releases factor 10a which converts prothrombin into thrombin. This converts fibrinogen to fibrin.

A

.

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14
Q

Why should be avoid taking NSAIDS when taking warfarin?

A

NSAID will prolong action and inhibit platelets – avoid

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15
Q

What type of drugs are statins?

A

HMG coA reductase inhibitors.

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16
Q

What is an example of a prodrug?

A

Simvistatin.

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17
Q

What do statins do and what are the side effects of this medication? Name another medication that interacts with statins.

A

Inhibit cholesterol synthesis in the liver
 Reduce total cholesterol and LDL- cholesterol
 Side effects – possible myositis with some drug interactions – includes antifungals (fluconazole). cause plasma levels to go up drmatically and cuse myostitis.

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18
Q

Beta-adrenergic blockers (β-blockers)
 Atenolol – selective - β1 only
 Propranolol – non-selective – β1 and β2
 Many others (-olol)

Stop arrhythmias leading to cardiac arrest (Ventricular fibrillation – VF)
* Reduces heart muscle excitability

A

b2 receptor in lungs- also present in brain for anxiety, increases risk of getting asthma etc.

B1blocks adrenaline to heart- slows hert down and to make it function less well (heart attack patients dnt want their heart to be over stretched, they want electrical exitability of heart being less0.

beta blocker for heart attack patients. Cardiac arrthymias.

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19
Q

What are diuretics used for and name examples of them.

A

Antihypertensive and heart failure.

  • Loop diuretics (furosemide)
  • Thiazide diuretico (bendroflumethazide).
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20
Q

How do diuretics work and what are the side effects of them?

A 
Increase salt and water LOSS 
 Reduce plasma volume 
 Reduce cardiac workload
*Side effects – can lead to Na+/K+ imbalance if not monitored carefully
 Can lead to dry mouth in the elderly.
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21
Q

How does spironolactone work?

A

Spironolactone is an aldosterone receptor antagonist that acts in the renal distal tubule and collecting ducts, decreasing the reabsorption of sodium and water and decreasing the excretion of potassium.

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22
Q

What do nitrates do?

A

Nitrates dilate the veins and reduce preload to the heart. They dilate resistance arteries which reduces cardiac workload and reduces cardiac oxygen. They also dilate collateral coronary artery supply to reduce anginal pain.

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23
Q

How do calcium channel blockers work?

A

They act by reducing hypertension due to blocking calcium channels in smooth muscle.

2 drugs work on peripheral blood vessels (relaxation and vasodilation):
nifedipine and amlodipine.

Some more actively work on the heart muscle itself (slow conduction of pacing impulses):
verapamil.

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24
Q

What is the side effect most commonly associated with nifedipine, cyclosporin and phenytoin?

A

Overgrowth of gingival.

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25
Q

What do ACE inhibitors do and name some examples of them.

A

Ramapril, lisinopril and enalapril.
They inhibit the conversion of angiotensin 1 to angiotensin 2.
Prevents aldosterone dependent absorption of water and salt.

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26
Q

What are the side effects of ACE inhibitors?

A

Cough and hypotension.

Ora symptoms- angio-oedema and lochenoid reaction.

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27
Q

Name an example of angiotensin 2 blockers.

A

Losartan. They act in the same way as ACE inhibitors but by a different mechanism.

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28
Q

5 main groups of CVS medications?

A

ACE inhibitors, calcium channel blockers, diuretics, anticoagulants, beta blockers and nitrates.

29
Q

What are the two pathology processes dealing with acute coronary syndromes?

A
  • blood vessel narrowing (cramp) and blood vessel occlusion (severe pain). No or less blood is delivered to the body tissue which results in either cramping of the muscle or tissue death.
30
Q

Remember: a small change in vessel diameter has a large change in blood flow.

A

.

31
Q

What is ischamia?

A

An inadequate blood supply to tissues.

32
Q

What is infarction?

A

Tissue death as a response to artery blockage.

33
Q

Remember: boundaries and diagnosis of acute coronary syndromes are often difficult and if treated early there is more chance of survival.

A

.

34
Q

How to ACS diagnose?

A

History.
ECG findings - STEMI AND NSTEMI.
Biomarkers- troponin- troponin is released during MI from the cytosolic pool of the myocytes. This test measures the amount of the protein troponin in your blood. Troponin is found in cells in your heart muscle. When these cells are injured—most often because the heart isn’t getting enough oxygen and nutrients—they can release troponin and other substances into the blood.

35
Q

What is the difference between an nstemi and a stemi?

A

f there is a pattern known as ST-elevation on the EKG, this is called a STEMI, short for ST elevation myocardial infarction. If there is elevation of the blood markers suggesting heart damage, but no ST elevation seen on the EKG tracing, this is known as a NSTEMI.

36
Q

What is atherosclerosis?

A

A build up of plaque in the blood vessel wall. Plaque fissure erosion results in thrombosis. Genetics plays a big factor**

37
Q

Where are the coronary arteries situated?

A

The coronary arteries come off the aorta where the aortic valves open. The aortic valves cover the opening of the cornory arteries. The faster your heart rate gets, short diastolic time, less blood flow time to cornory arteries.

38
Q

What is angina and is there any relieving factors from the symptoms?

A

Angina is reversible ischamia of the heart muscle (narrowing of one or more of the coronary arteries resulting in a lack of blood supply to the heart tissue). “Classical” angina gets worse with exercise and “unstable” angina patients have symptoms even at rest with no biomarkers.

39
Q

What is the clinical presentation of angina?

A

“central crushing chest pain” with radiation to the arm, back or jaw.
incraese oxygen demand- cannot deliver efficient blood flow due to narrowing of blood vessles. Stops when you syop exercising.

ANGINA- DO NOT HAVE PERMANENT MUSCLE DAMAGE BUT HAVE SYMPTOMS OF MI, DIFFICULT TO DIAGNOSE THE TWO.

40
Q

What is the clinical presentation of “classical angina” and “unstable angina”.

A

“classical’- Gets worse during exercise so patients tend to work only within

41
Q

What is the clinical presentation of “classical angina” and “unstable angina”.

A

“Classical’- Gets worse during exercise so patients tend to work only within their limits. They usually have no pain at rest and there usually is gradual deterioration.

“Unstable”- Patients experience symptoms at rest with no biomarkers present.

42
Q

What is hyperdynamic circulation?

A

Hyperdynamic circulation is abnormally increased circulatory volume.

43
Q

How can you investigate angina?

A
  1. ECG
  2. Eliminate other diseases
  3. Angiography (die injected into artery to see blockage)
  4. Echocardiography
  5. Isotope studies
44
Q

How can you investigate angina?

A
  1. ECG (dne at exercise and rest).
  2. Eliminate other diseases: thyroid, anaemia and valve disease.
  3. Angiography (die injected into artery to see blockage).
  4. Echocardiography
  5. Isotope studies.
45
Q

What is present on an ECG when a person has angina?

A

ST segment depression.

46
Q

How do doctors use surgical therapy to treat angina?

A
  • Coronary artery bypass grafting. This is a major surgery and there is limited benefit (less in smokers who continue to smoke).
  • Angioplasty and Stenting- Lower risk but lower benefit and there is a risk of rupturing a blood vessel during the procedure.
47
Q

How do doctors use drug therapy to treat angina?

A
  • Hypertension (diuretics, calcium channel antagonists, ace inhibitors, beta blockers).
  • Reduce preload/ dilate coronary vessels (nitrates- short and long acting).
  • Emergency treatment- GTN spray.
48
Q

How do doctors use non-drug therapy to treat angina?

A
  • Live within limitations.

- Modify risk factors; stop smoking, exercise programme and improve diet to lower cholesterol.

49
Q

SMOKING CAUSES VASOCONSTRICTION.

A

.

50
Q

What is stenosis?

A

Stenosis is the term for a valve that doesn’t open properly. The flaps of a valve thicken, stiffen, or fuse together. As a result, the valve cannot fully open. Thus, the heart has to work harder to pump blood through the valve, and the body may suffer from a reduced supply of oxygen.

51
Q

What veins can be used for a coronary heart by pass?

A

Internal mammary artery and saphenous vein and radial artery.

52
Q

What is angioplasty and stenting? What is this risks associated with this procedure and what medication do you need to take after it.

A

Blow a ballon in aretery to squash plaques flat and put a stent in.
Risk of vessel rupture during this therapy and the patients will need dual anti platelet therapy but it depends with what stent type is used.
*Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup, a condition known as atherosclerosis.

53
Q

What is peripheral vascular disease?

A

PVD is “angina of the tissues”- usually the lower limb. Usually an atheroma in femoral/popliteal vessels. It is an MI risk so is treated in the same way as angina as it indicates arteriopath.

54
Q

What are the symptoms of peripheral vascular disease in patients?

A

“Claudication” pain in limb during exercise. Pain is relieved when rested. Feels like a burning, tired feeling/. Patients have limited function of this limb and poor wound healing. This can lead to necrosis and gangrene )chronic slow process).

55
Q

What is claudication distance?

A

The distance that a patient can walk on the flat before experiencing the pain of claudication is called the “claudication distance”.

56
Q

What does “arteriopath” mean?

A

Disease of the arteries.

57
Q

How can ischaemia lead to infarction?

A

Atheroma in blood vessels that have formed can cause a thrombosis to enlarge to rapidly block the vessel. This causes the plaque surface and platelets to detach to travel downstream and block vessels- results in infarction.

58
Q

Infarction:

  • Heart (coronary artery atheroma.
  • Limb- femoral and popliteal arteries.
  • Brain- carotid arteries.
A

.

59
Q

What are the five types of myocardial infarction?

A
  1. Spontaneous- plaque fissure/rupture (primary coronary event).
  2. MI secondary to ischaemia- balance of supply and demand.
  3. Sudden death with symptoms of ishamia and evidence of a ST elevation or thrombus.
  4. MI from PCI (angioplasty).
  5. MI from CABG.
60
Q

How to treat a MI?

A
  • reduce tissue loss from necrosis (angioplasty and thrombolysis).
  • bypass obstruction (CABG and fem/pop bypass).
  • aspirin and risk factor management.
61
Q

What does acute limb necrosis result in?

A
  • AMPUTATION.
62
Q

What is a brain infarction most commonly known as?

A

Stroke- usually an embolism from an atheroma. Occasionally a cerebral bleed. Rich in collateral blood supply (left/right, vertebral).

63
Q

What is a transient ischaemic attack?

A

A neurological dysfunction caused by an interruption in blood supply to the brain or the eye. This can happen for a short period of time and usually loss of function of the part of the brain involved occurs.

64
Q

What are the symptoms of a MI?

A
  • death, pain, nausea, sweaty, pale, “going to die feeling”.
65
Q

What on an ECG indicated an old MI?

A

-Q waves only indicate an old MI.

66
Q

What cardiac enzymes indicate that an MI has occurred?

A

Cardiac Enzymes
 Troponin
 Creatinine Kinase (CKmb)
 LDH & AST increase - not specific

67
Q

what is the primary and hospital care of a patient experiencing an MI?

A

Primary care
 aim to get patient to hospital!
 Analgesia, Aspirin & reassurance
 Basic life support if required  Cardiac arrest situation

Hospital
 Primary PCI
 acute angioplasty & stenting (if available)
 thrombolysis if indicated
 drug treatment to reduce tissue damage
 prevent recurrence/complications  Secondary prevention

68
Q

What are the complications of an MI?

A 
 Death
 Arrhythmias
 Heart Failure
 Ventricular hypofunction & thrombosis  papillary muscle rupture - valve disease!
 DVT & pulmonary embolism
 Complications of thrombolysis
69
Q

What medications can be given after an MI?

A 
Prevent next MI
 risk modification & aspirin   blocker
 ACE inhibitor
treat complications
 heart failure
 arrhythmias
 psychological distress

BDS 2 (19 decks)

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