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Cardiorespiratory 2 PBL > PBL 3 > Flashcards

PBL 3 Flashcards

1
Q

define C reactive proteins

A
  • this is an annular pentameric protein which is found in the blood plasma, it rises in response to inflammation.
  • The protein is made in the liver, it can cause pain redness, and swelling of the injured and affected area
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2
Q

define tacypnoea

A

this is abnormally fast rapid breathing, greater than 20 breaths per minute

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3
Q

define BMI

A

– weight/height squared, uses your height and weight to work out if you are healthy

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4
Q

Define myocardial infraction

A

– this is when a portion of the heart is deprived of oxygen due to a blockage of a coronary artery, thus the myocytes that are supplied with oxygen begin to die

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5
Q

define atheroscerolsos

A

this is a disease in which the plaque builds up inside the arteries, it is the process by which the atheroma undergoes changes and the plaque builds up

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6
Q

describe the process of atherosclerosis

A
  • initiated by endothelial damage which is induced by factors such as hypertension, hyperlipidaemia or smoking
  • the endothelial permeability alters and macromolecules such as low density lipoprotein and cell adhesion factors which result in monocytes and T lymphocyte migration
  • the endothelial dysfunction results in the intimal accumulation of lipid laden macrophages and T lymphocytes
  • growth factors stimulate the migration of smooth muscle cells from tunica media and these proliferate becoming foam cells that engulf the lipid this results in a raised pale cellular lesion that is called a fatty streak
  • this turns into an atheromatous plaque, this results in a development of a fibre cap between the endothelium and accumulating constituents of a lipid rich core
  • fibrous cap is made up of the smooth muscle cells and extracellular matrix synsthesed by these cells comprised of dense collagen, elastic fibres and proteoglycans
  • beneath and to the side of the fibrous cap and surrounding a lipid rich necrotic core of foam cells extracellular lipid and otters debris are inflammatory cells, more smooth muscle and peripheral neovascularisation
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7
Q

what is angina caused by

A
  • caused by myocardial ischaemia which results in a mismatch between myocardial blood flow and oxygen demand
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8
Q

What are the risk factors for angina

A
  • Tobacco use – can allow deposits of cholesterol to collect and block blood flow
  • Diabetes – not enough insulin is produced therefore glucose builds up and thus diabetes increases the risk of coronary artery disease which leads to angina and heart attacks
  • High blood pressure – high blood pressure damages arteries by accelerating hardening of the arteries
  • High blood cholesterol or triglyceride levels – cholesterol can narrow arteries throughout the body including those that supply the heart, LDL can increase the risk of angina and heart attacks
  • Family history
  • Older age
  • Lack of exercise – inactive lifestyle contributes to high cholesterol, high blood pressure, type 2 diabetes and obesity
  • Obesity – obesity raises the risk of angina and heart disease and its associated with high blood cholesterol levels
  • Stress – stress can increase your risk of angina and heart attacks
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9
Q

what are the surgical treatment options for angina

A

Percutaneous Coronary Intervention (PCI)

  • A stent is put into a narrowed coronary artery
  • Increases O2 delivery to myocardium
  • Used when angina no longer responds to medication

Coronary Artery Bypass Graft

  • Graft is taken from elsewhere (great saphenous vein)
  • Used to route around the blocked coronary artery
  • Used when angiography revealed PCI can’t help
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10
Q

what lifestyle advice should be given

A
  • Have a balanced diet
  • Cut down on alcohol
  • Lose weight
  • Exercise regularly
  • Stop smoking
  • Reduce stress level
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11
Q

what will the changes be in the ECG exercise

A
  • ST depression – shows that there is myocardial ischemia,
  • T wave inversion or tall pointed upright T wave which is indication of the beginning of a MI
  • Normal without exercise
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12
Q

why does the patient feel chest pain during exercise

A
  • Has stable angina
  • When exercising the heart increases in pumping thus it needs an increase in oxygenation but cannot get that as the coronary arteries are narrowed due to the narrowing of the arteries such as in atherosclerosis which can prevent the heart from receiving more oxygen
  • This can cause myocardial ischemia which can cause the chest pain
  • When he isn’t exercising the oxygen demand isn’t as high therefore the myocytes get enough oxygen and thus he does not experience the pain
  • May also go to the neck jaw, shoulder or back of the arm
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13
Q

what drugs is he currently taking and what drugs could be given to him

A
  • Aspirin
  • calcium channel blocker
  • statin

others

  • ACE
  • Beta Blockers
  • long acting nitrate
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14
Q

what is the mechanism of action of aspirin

A

– this is used to reduce the chance of heart attacks and a stroke, it is an NSAID,

  • it causes a decreased production of prostaglandins and TXA2,
  • it does this by inactivation of the COX enzyme
  • reduces the chance of clot formation as TXA2 is responsible for the aggregation of platelets that form blood clots
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15
Q

what is the mechanism of action of statins

A
  • stains competitively inhibit HMG-CoA reductase therefore they decrease, therefore this decreases the production of cholesterol, reduces the build up of fatty plaques in the arteries,
  • they also increase LDL uptake this is because there is a reduced level of cholesterol so cells seek to compensate this and draw the LDL out of circulation
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16
Q

what is the mechanism of action of ACE

A
  • given to those below the age of 55,
  • inhibit angiotensin II leads to vasodilation of small resistance arteries reduces the SVR and reduces the blood pressure
  • (ARBs could be given instead these have less side effects than ACEs, including less cough angioedema and potassium rentention)
  • Examples include benzepril, captopril, enalapril
17
Q

what is the mechanism of action of beta blockers

A
  • first line treatment for stable angina, can have a combination of the two
  • B1 RECEPOT ANTAGONIST
  • Reduces heart rate and negative inotropic effect, this reduces blood pressure and myocardial oxygen demand
  • These drugs work on multiple different pharmalogical receptors
  • Ths increases end diastolic volume and increases ejection time
  • Examples include propranolol(nonselective), and atenolol(selective)
18
Q

what is the mechanism of action of long acting nitrates

A
  • NTG causes nitrates to be taken up
  • This causes increased production of nitric oxidise
  • Leads to produce of GTP which actives cyclic GMP
  • Leas to a lost of a phosphate from myosin
  • This leads to vasodilation
  • Examples include glyceryl trinitirate, isosorbide dinitrate
19
Q

describe what aspirin does

A

– this is used to reduce the chance of heart attacks and a stroke, it is an NSAID,

  • it causes a decreased production of prostaglandins and TXA2,
  • it does this by inactivation of the COX enzyme
  • reduces the chance of clot formation as TXA2 is responsible for the aggregation of platelets that form blood clots
20
Q

what is the difference between stable and unstable angina

A
  • Stable angina is the more common one this is when the attacks have triggers such as stress and exercise and stop within a few minutes of resting
  • Unstable angina is more serious and the attacks are more unpredictable, they don’t have a trigger and can continue despite resting
  • Unstable angina is a condition in which your heart does not get enough blood flow and oxygen and leads to a heart attack, this is because fatty deposits in the blood vessel rupture or a blood clot forms and this can quickly block or reduce flow through a narrowed artery and suddenly decrease blood flow to the heart muscle
21
Q

what are the two types of angina

A
  • There are two main types for angina, these are stable and unstable angina
22
Q

what is angia pectoris

A

Angina Pectoris is chest pain that is associated with

myocardial ischemia.

23
Q

what are the reversible and irreversible risk factors of CHD

A

Reversible

  • Smoking
  • Hypertension
  • Hyperlipidaemia
  • Obesity
  • Physical Inactivity
  • Poor Diet

irreversible

  • family history
  • older age
  • male
  • diabetes
24
Q

what are the causes of angina

A
  • imbalance of myocaridal oxygen and myocardial demand
25
Q

what causes an increase in myocardial oxygen supply

A

Coronary artery disease

  • Atherosclerosis
  • Vasospasm

Severe anaemia

26
Q

What causes an increase in myocardial oxygen demand

A

Left ventricular hypertrophy

  • Severe Hypertension
  • Aortic Stenosis
  • Aortic Regurgitation

Right ventricular hypertrophy

  • Pulmonary Hypertension
  • Pulmonary Stenosis

Rapid tachyarrhythmias

27
Q

why is there chest pain in angina

A

Atherosclerosis causes narrowing stenosis in the
coronary arteries.

Blood flow at rest is adequate for the myocardium
but in exercise, the blood flow is restricted by the
stenosis and ischaemia continues.

The pain is due to hypoxia in the myocardium
leading to formation of lactic acid & a lowering of
pH.

Pain endings in the myocardium are sensitive to a
low pH.

These pain fibres project to the spinal cord but as
we have no sensory awareness of our heart, the
pain is referred to the skin & muscle in the same
dermatomes as the afferents from the heart,
normally C3, 4 & 5.

Pain is thus referred most often to the left arm, but
may also radiate to the lower jaw, neck, right arm,
back & epigastrium.

28
Q

how do you diagnose angain

A 
HISTORY!!!
A thorough history is key to diagnosing angina
When asking about the chest pain:
- Site
- Character
- Radiation
- Duration
- Exacerbating factors

Features of classical stable angina from history:
1. Chest pain (Squeezing/Tightness) brought on by strenuous
activity, never at rest
2. Episodes last 2-5 minutes and is gradual in onset and
offset
3. Alleviated by rest or GTN

If a patient has all the classical signs of stable angina, a very likely
diagnosis can be made.

Further testing is only necessary in some cases where the history is not
consistent with angina or in high risk patients with atypical symptoms

29
Q

what are further tests that can be used for angina

A
  • ECG exercise - gold standard
30
Q

what would an ECG exercise test look like in angina

A

Planar or downward sloping ST Depression is diagnostic of angina

Other features of the ECG are used to judge severity and are prognostic
factors including tolerance of exercise, severity of ST depressions, exertional arrhythmias

31
Q

what are the features of unstable angina

A

Unstable angina is similar to stable angina, however it is a
medical emergency as it may indicate an impending MI. It
is defined as angina alongside one of these 3 features:

  1. It occurs at rest or with minimal exertion, usually lasting >10
    minutes.
  2. It is severe & of new onset, i.e. within the prior 4-6 weeks.
  3. It occurs with a crescendo pattern, i.e. distinctly more severe,
    prolonged or frequent than previously
32
Q

what is first line therpay for acute symptoms of angina

A

nitrates

33
Q

what are preventiative therpay given for angina

A

The optimal management of patients with stable angina
requires more than antianginal therapy. Therapies aimed at
preventing cardiovascular events are central to long-term
care.

Antiplatelet therapy – Aspirin is given as a protective
measure against clots that can lead to stroke and MI

Statins – These lower cholesterol levels which is a risk factor
for cardiovascular events

Lifestyle changes – smoking cessation, regular exercise and
loss of excess weight reduce risk of cardiovascular events

34
Q

What does ranoazine do

A

Ranolazine – Reduces left ventricular wall pressure

by blocking certain sodium channels in myocardium

Cardiorespiratory 2 PBL (10 decks)

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