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Yr 2 - Pharmacology > Angina & athlerosclerosis > Flashcards

Angina & athlerosclerosis Flashcards

1
Q

What is angina?

A

A restriction in blood supply (most often talked about in heart but can even occur in the mouth!)

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2
Q

What is abdominal angina?

A

Post prandial (after eating) abdominal pain

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3
Q

What is ludwig’s angina?

A

A serious infection of the floor of the mouth

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4
Q

What is vincent’s angina?

A

trench mouth and necrotic gum tissue

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5
Q

What is angina tonsillaris?

A

An inflammation of the tonsils

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6
Q

What is herpangina?

A

Pharyngeal blisters caused by Coxsackie A virus or echovirus

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7
Q

What is angina pectoris?

A

Pain localised to the chest

Acute or chronic (on tablets)

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8
Q

What causes angina?

A
  1. Restricted blood supply = increased metabolite build up = decreased oxygen supply and increased cardiac work
  2. narrowing of the coronary artery (atheroma, thrombus etc.)
  3. **vasospasm of the coronary artery **(overly reactive vessels and drugs - e.g. cocaine & smoking)
  4. **severe anaemia **(cannot carry enough oxygen to the heart)
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9
Q

What are the 3 types of angina pectoris?

A
  • Chronic stable = exercise induced -> normally take medication
  • Unstable = sudden rupture of athleroscelrotic plaque -> blocks down stream arteries
  • Prinzmetal’s (angina inversa) = vasospasm = oversensitivity to vasoconstrictors
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10
Q

From which age do athlerosclerotic plaques start to build up from?

A

10 years old

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11
Q

What are the risk factors for coronary heart disease (8)?

A
  • Diabetes
  • Family history
  • high blood pressure
  • High LDL cholestrol & low HDL cholestrol
  • male
  • Lack of regular exercise
  • Obesity
  • Smoking
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12
Q

What is coronary heart disease?

A

Athlerosclerosis in the coronary arteries

(most common cause of death in UK)

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13
Q

Which is more important… having good (LDL) or bad (HDL) lipoproteins or having the right balance of LDL and HDL?

A

Having the right balance

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14
Q

What happens to the HDL:LDL ratio with age?

A

Decreases = increased MI risk

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15
Q

What happens to HDL:LDL ratio with statins?

A

Increases = less MI risk

(although other drugs that increase the ratio )

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16
Q

Does eating fewer saturated fats in your diet increase or decrease your risk for CHD?

A

Decrease because less obese!

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17
Q

What are the 3 stages of developing atheroma?

A
  1. Damage to epithelia
  2. Cholesterol accumulation = inflammatory response -> produces foam cells
  3. Foam cell degeneration = increased stiffness of artery wall = shear stress = continued worsening damage
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18
Q

What causes activation of platelets?

A
  • contact with intima matrix (sheds microparticles = attracts monocytes = proliferate & differentiate = phagocytes)
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19
Q

What is a coronary artery bypass graft?

A

takes a blood vessel from another part of the body

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20
Q

List 3 alternative treatments for surgical treatment of atheroma:

A
  • Rotational bur
  • Balloon
  • Stent (wire coil)
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21
Q

What diastolic blood pressure is required for someone to be hypertensive?

A

>95mmHg

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22
Q

What are the potential complications of hypertension (6)?

A
  • Stroke (athlerosclerosis)
  • kidney disease
  • eye disease
  • diabetes
  • pre-eclampsia (hypertension & protein in urea, swelling of feet, ankles, face & hands, severe headache, vision problems & pain just below ribs -> occurs if problem with placenta)
  • erectile dysfunction
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23
Q

What is primary hypertension:

what % of cases does it make up?

What are its two main causes?

A
  • 90-95% cases (essential/idiopathic)
  • obesity (BMI>25)
  • genetic
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24
Q

What is secondary hypertension:

what % of cases does it make up?

What are the 4 main causes?

A
  • 10% of cases
  • renal/renovascular disease
  • endocrine disease (e.g. phaeochomocytoma- tumour of adrenal medulla, cushings syndrome - excess cortisol, acromegaly - excess aldosterone, hypo/hyperthyroidism, pregnancy)
  • coarcation of aorta (malformation of aorta)
  • iatrogenic (hormonal/oral contraceptive & NSAIDs)
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25
Q

What are the consequences of hypertension?

A

Hypertrophy of ventricular (esp. left) wall -> muscle has to work harder for long time = increased risk of sudden cardiac death

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26
Q

What does ALLHAT trial stand for?

A

The antihypertensive and lipid lowering to prevent heart attack trial

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27
Q

why in the ALLHAT trial was the alpha blocker doxazosin discontinued?

A

There was an excess no. of deaths

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28
Q

In the ALLHAT trial what was discovered about the efficacy of the following drugs:

Thaizide diuretic (chlorthalidone)

ACE inhibitor (lisinopril)

Ca channel blocker (amlodipine)

A

All of equal efficacy

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29
Q

Which type of diabetes is hypertension often found in conjunction with?

A

Type II

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30
Q

Which % of type II diabetic patients die from cardiovascular disease?

A

70%

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31
Q

Which % of type II diabetes patients are obese?

A

55%

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32
Q

Which % of type II diabetic patients need polypharmacy to achieve tight control of their hypertension?

A

60%

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33
Q

What is polypharmacy?

A

using low doses of different drugs to produce a synergistic effect on blood pressure and have few side effects (each drug has its own unique side effects)

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34
Q

What are arrhythmias?

A

Regional differences in action potentials between nodal tissue, atria and ventricles

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35
Q

What depolarises in the PQ wave?

A

the atria & AV node

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36
Q

What depolarises in the QRS complex?

A

the heart

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37
Q

what repolarises in the T wave?

A

the wall

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38
Q

What happes in phase 4? (DIASTOLIC)

A

NaK pump = inward flow of K+

Na channel closed

= gradual depolarisation of cells

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39
Q

What happens in Phase 0?

A

Na channels open = inward influx of Na = rapid depolarisation

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40
Q

What happens in phase 1?

A

Rapid repolarisation

= transient outward current

Cl current = SNS regulated

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41
Q

What happens in phase 2?

A

Plateu = balance of electrical charges (outward K current = inward Na & Ca current -> NaCa exchanger)

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42
Q

What happens in phase 3?

A

Repolarisation

= increased K currents & inactivation of inward Na & Ca currents

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43
Q

What is a ‘normal’/sinus arrhythmia?

A

Variations in heart rate with breathing (originate from SAN = normal conduction)

No cause for concern unless rate changes are extreme! Treatment not needed!

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44
Q

What is atrial flutter?

A

Atrial rentry without conduction block (not every p = qrs) -> cannot repolarise until after a contraction has occured

45
Q

What is atrial fibrilation?

A

irregular but on finer physical state than flutter

46
Q

What is paroxymal supraventricular tachycardia?

A

Episodic ventricular tachycardia from nodal re-entry

47
Q

What is ventricular tachycardia?

A

High ventricular rate (atrial driven or re-entry) e.g. after ischaemic heart disease -> heart failure

48
Q

What is polymorphic ventricular tachycardia?

A

Ventricular tachycardia with unstable (changes with time) ECG

49
Q

What is ventricular fibrillation?

A
  • frequently follows polymorphic ventricular tachycardia

= fine re-entry = fatal! Completely unco-ordinated pumping of the heart = no blood pumped (CPR helps in this case)

50
Q

What are the main 3 causes of arrythmias?

A
  • Abnormality in action potential

(genetic, drugs, ischaemia, electrolyte disturbances)

  • Abnormality in conduction

(anatomy, ischaemia, electrolyte disturbances, secondary to AP and electrial activity)

  • Abnormality in excitability

(increased sympathetic drive & surgery)

51
Q

What does EAD stand for?

A

Early after depolarisation

52
Q

What is an EAD?

A

the heart is reactivated (it fails to depolarise fully = longer action potential = increased following refractory period following contraction)

53
Q

What does DAD stand for?

A

Delay after depolarisation

54
Q

What is a DAD?

A

spontaneous Ca release inside cell = too much Ca = activates Ca/Na exchanger = another depolarisation

55
Q

How can purkinje fibres cause a ectopic focus?

A

Anterograde movement of abnomal electrical activity = interferes with normal conduction & heart contraction

56
Q

What is a unidirectional block?

A

A cell can only depolarise other cells it is touching

57
Q

What is re-entry?

A

Re-entered beat passes the conduction defect before the next normal beat = cycles & changes rhythm of heart

58
Q

What is a circus rhythm?

A

A region of slow conduction = part of AP reaches tissue after its conducted (after the refractory period) = second small AP

59
Q

How can we correct unidirectional blocks, re-entry and circus rhythm?

A

Defibrillation

= forces depolarisation of tissue = total resynchronisation (if timing is wrong must reapply!)

60
Q

Which 4 things determine the refractory period (4)?

A

AP duration

Average membrane potential (recruitment of ion channels -> must return to resting)

Recovery time of Na channel

Sympathetic drive

61
Q

What are the 6 mechanisms of anti-arrhytmic drugs?

A

Stop automaticity (the tissue becoming a pacemaker):

  • Increase membrane threshold
  • Hyperpolarise membrane
  • Block sympathetic activity
  • Inhibit Na & Ca entry

Stop re-entry:

  • Convert unidirectional block to bidirectional block
  • Abolish unidirectional block
62
Q

What is the mneumonic for Antiarrhythmic drugs?

A

Quick Lids Flecking At Amiable Dilatants

Quinone Lidocaine Flecainide Atenolol Amidorone Diltiazem

63
Q

What type of drugs are 1a, 1b & 1c?

A

Na channel blockers

64
Q

What type of drugs is II?

A

Beta blocker

65
Q

What type of drug is III?

A

K channel blocker

66
Q

Which type of block is IV?

A

Ca channel blocker

67
Q

How does magnesium effect electrical activity?

A

Decreases Ca reentry through sarcolemma

= ATP binding agent

n.b. magnesium levels are decreased in ischemic cells = ventricular arrhythmias

68
Q

How does Adenosine effect electrical activity?

A

Increases K in atrial tissues

69
Q

What is adenosine used for?

A

Used for supraventricular tachycardia

70
Q

What are the side effects of adenosine?

A

transient flushing & breathlessness

71
Q

What is the sicilian gambit?

A

Anti-arrythmic therapy logically based on know sites of action of a drug and arrhythmias mechanism (pattern recognition)

72
Q

What is a syndrome?

A

a number of associated symptoms

73
Q

What are the 6 main characteristics for heart failure?

A
  • Progressive cardiac dysfuntion
  • Breathlessness
  • Tiredness
  • Neurohormonal disturbances (e.g. corticotropin releasing hormone, vasopresssin, growth hormone releasing hormone)
  • Odema (pitting odema = press thumb firmly & doesnt bounce back)
  • sudden death
74
Q

What % of the population odes heart failure effect?

A

2-5%

75
Q

Why does the risk of heart failure increase with age?

A

Loss of ability to repair itsnelf

76
Q

What are the causes of heart failure (4)?

A

Volume overload (valve regurgitation)

Pressure overload (systemic hypertension/outflow obstruction)

Loss of muscle (post MI, chronic ischaemia, connective tissue diseases, infection & poisons)

Restricted filling (pericardial disease = stiff heart, restrictive cardiomyopathy & tachyarrhythmia)

77
Q

What is the 5 year mortality rate for heart failure?

A

50%

78
Q

In which two ways can you determine increased right atrial pressure?

A

Distended jugulars in neck

Peripheral odema (pulmonary)

79
Q

What is the outcome of increased right atrial pressure (3)?

A

Inadequate tissue perfusion (stress causes heart dilation = decreased coronary output)

Volume overload

Cardiac remodelling (enlarged ventricles, spherical shape & decreased efficiency of contraction = easier to distend further)

80
Q

What are the two main treatment aims?

A

Improve symptoms

Improve survival

81
Q

Which drugs do we use to improve the symptoms of heartfailure (3)?

A

Diuretics (decrease blood volume)

Digoxin

Angiotensin Converting Enzyme (ACE) inhibitors

82
Q

Which 3 drugs do we use to improve survival for heart failure patients?

A

ACE inhibitors

Spirondactone

Beta blockers

83
Q

List 3 classes of inotropic drugs:

A

Cardiac glycosides (e.g. digoxin) = cardiotonic steroids

Sympathomimetics e.g. dobutamine

Phosphodiesterase inhibitors

84
Q

List 5 adrenoreceptor sympathomimetics:

A
  • Adrenaline (β > α)
  • Noradrenaline (β1=α1 > β2=α2)
  • Dopamine (β1=β2 > α1)
  • Dobutamine (β1 > β2 > α1)
  • Isoproterenol (β1=β2)
85
Q

What is the effect of adrenaline at low dose?

A

Vasodilation

86
Q

What is the effect of adrenaline at high dose?

A

Vasoconstriction

87
Q

What are 3 clinical uses of adrenaline?

A

Anaphylactic shock

Cardiogenic shock

Cardiac arrest

88
Q

What are 2 clinical uses of noradrenaline?

A

Severe hypotension

Septic shock

89
Q

What can reflex bradycardia mask?

A

direct stimulation on SAN

90
Q

What are 3 clinical uses of dopamine?

A

Acute heart failure

Cardiogenic shock

Acute renal failure

91
Q

what does a low dose of dopamine cause (2)?

A

Stimulates heart

Decreased vascular resistance

92
Q

what does a high dose of dobutamine cause?

A

vasoconstriction

n.b. = vasodilation in kidneys via D1 receptors

93
Q

What are 3 clinical uses of dobutamine?

A

Acute heart failure

Cardiogenic shock

Refractory heart failure

94
Q

What does dobutamine do?

A

Cardiac stimulation with modest vasodilation

95
Q

What are 2 clinical uses of isoproterenol?

A

Bradycardia

Atrioventricular block

96
Q

What are the effects of isoproterenol?

A

Cardiac stimulation

Vasodilation with little change in pressure

97
Q

When are sympathomimetics used to treat heart failure?

A

Last ditch treatment for those in hospital awaiting a transplant

98
Q

When are transduction sympathomimetics useful?

A

When other therapies fail (no real benefit over other treatment and 27% increase in morbidity)

99
Q

When are loop diuretics useful in treating heart failure?

A

Pulmonary and refractive odema

Kidney failure

100
Q

What are the side effects of loop diuretics (4)?

A

Ototoxicity

Hypovolemia

Hypokalemia

Hypomagnesia

101
Q

What is the action of thiazide diuretics?

A

Distal tubule = direct vasodilator

102
Q

What are the 2 side effects of thiazide diuretics?

A

K loss

Hypotension

103
Q

When are K sparing diuretics useful in heart failure?

A

control K loss (aldosterone antagonist)

104
Q

What are the side effects of K sparing diuretics (2)?

A

Hyperkalaemia

Oestrogen like effects (with spirolactone)

105
Q

What do ACE inhibitors control?

A

K loss

Hypertension

106
Q

What are the side effects of ACE inhibitors?

A

Cough

hypotension

Hyperkalemia

107
Q

Why are angiotensin II receptor blockers preferable to ACE inhibitors (3)?

A

Better tolerated

No cough (no effect on bradykining)

Decreased BP

108
Q

What is the key side effect of angiotensin II receptor blockers?

A

tetragenic (birth defects)

n.b. it also has less vasodilation than ACE

109
Q
A

Yr 2 - Pharmacology (18 decks)

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