Angina & athlerosclerosis Flashcards Preview

Yr 2 - Pharmacology > Angina & athlerosclerosis > Flashcards

Flashcards in Angina & athlerosclerosis Deck (109):
1

What is angina?

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

2

What is abdominal angina?

Post prandial (after eating) abdominal pain

3

What is ludwig's angina?

A serious infection of the floor of the mouth

4

What is vincent's angina?

trench mouth and necrotic gum tissue

5

What is angina tonsillaris?

An inflammation of the tonsils

6

What is herpangina?

Pharyngeal blisters caused by Coxsackie A virus or echovirus

7

What is angina pectoris?

Pain localised to the chest 

Acute or chronic (on tablets)

8

What causes angina?

  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)

 

9

What are the 3 types of angina pectoris?

  • 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

10

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

10 years old

11

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

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

12

What is coronary heart disease?

Athlerosclerosis in the coronary arteries 

(most common cause of death in UK)

13

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

Having the right balance

14

What happens to the HDL:LDL ratio with age?

Decreases = increased MI risk

15

What happens to HDL:LDL ratio with statins?

Increases = less MI risk 

(although other drugs that increase the ratio )

16

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

Decrease because less obese!

17

What are the 3 stages of developing atheroma?

  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

18

What causes activation of platelets?

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

19

What is a coronary artery bypass graft?

takes a blood vessel from another part of the body

20

List 3 alternative treatments for surgical treatment of atheroma:

  • Rotational bur
  • Balloon
  • Stent (wire coil)

21

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

>95mmHg

22

What are the potential complications of hypertension (6)?

  • 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

23

What is primary hypertension:

what % of cases does it make up?

What are its two main causes?

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

24

What is secondary hypertension:

what % of cases does it make up?

What are the 4 main causes?

  • 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)

25

What are the consequences of hypertension?

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

26

What does ALLHAT trial stand for?

The antihypertensive and lipid lowering to prevent heart attack trial

27

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

There was an excess no. of deaths

28

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

Thaizide diuretic (chlorthalidone)

ACE inhibitor (lisinopril)

Ca channel blocker (amlodipine)

All of equal efficacy

29

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

Type II

30

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

70%

31

Which % of type II diabetes patients are obese?

55%

32

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

60%

33

What is polypharmacy?

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)

34

What are arrhythmias?

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

35

What depolarises in the PQ wave?

the atria & AV node

36

What depolarises in the QRS complex?

the heart

37

what repolarises in the T wave?

the wall

38

What happes in phase 4? (DIASTOLIC)

NaK pump = inward flow of K+ 

Na channel closed

= gradual depolarisation of cells

39

What happens in Phase 0?

Na channels open = inward influx of Na = rapid depolarisation

40

What happens in phase 1?

Rapid repolarisation

= transient outward current 

Cl current = SNS regulated

 

41

What happens in phase 2?

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

42

What happens in phase 3?

Repolarisation

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

43

What is a 'normal'/sinus arrhythmia?

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

What is atrial flutter?

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

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45

What is atrial fibrilation?

irregular but on finer physical state than flutter

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46

What is paroxymal supraventricular tachycardia?

Episodic ventricular tachycardia from nodal re-entry

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47

What is ventricular tachycardia?

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

48

What is polymorphic ventricular tachycardia?

Ventricular tachycardia with unstable (changes with time) ECG 

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49

What is ventricular fibrillation?

- frequently follows polymorphic ventricular tachycardia

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

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50

What are the main 3 causes of arrythmias?

  • 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

What does EAD stand for?

Early after depolarisation

52

What is an EAD?

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

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53

What does DAD stand for?

Delay after depolarisation

54

What is a DAD?

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

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55

How can purkinje fibres cause a ectopic focus?

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

56

What is a unidirectional block?

A cell can only depolarise other cells it is touching

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57

What is re-entry?

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

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58

What is a circus rhythm?

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

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59

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

Defibrillation 

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

60

Which 4 things determine the refractory period (4)?

AP duration

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

Recovery time of Na channel

Sympathetic drive

61

What are the 6 mechanisms of anti-arrhytmic drugs?

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

What is the mneumonic for Antiarrhythmic drugs?

Quick Lids Flecking At Amiable Dilatants

Quinone Lidocaine Flecainide Atenolol Amidorone Diltiazem

63

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

Na channel blockers

64

What type of drugs is II?

Beta blocker

65

What type of drug is III?

K channel blocker

66

Which type of block is IV?

Ca channel blocker

67

How does magnesium effect electrical activity?

Decreases Ca reentry through sarcolemma

= ATP binding agent 

 

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

68

How does Adenosine effect electrical activity?

Increases K in atrial tissues

 

69

What is adenosine used for?

Used for supraventricular tachycardia

 

70

What are the side effects of adenosine?

transient flushing & breathlessness

71

What is the sicilian gambit?

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

72

What is a syndrome?

a number of associated symptoms

73

What are the 6 main characteristics for heart failure?

  • 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

What % of the population odes heart failure effect?

2-5%

75

Why does the risk of heart failure increase with age?

Loss of ability to repair itsnelf

76

What are the causes of heart failure (4)?

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

What is the 5 year mortality rate for heart failure?

50%

78

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

Distended jugulars in neck

Peripheral odema (pulmonary)

79

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

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

What are the two main treatment aims?

Improve symptoms

Improve survival

81

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

Diuretics (decrease blood volume)

Digoxin

Angiotensin Converting Enzyme (ACE) inhibitors

82

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

ACE inhibitors

Spirondactone

Beta blockers

 

83

List 3 classes of inotropic drugs:

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

Sympathomimetics e.g. dobutamine

Phosphodiesterase inhibitors

84

List 5 adrenoreceptor sympathomimetics:

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

85

What is the effect of adrenaline at low dose?

Vasodilation

86

What is the effect of adrenaline at high dose?

Vasoconstriction

87

What are 3 clinical uses of adrenaline?

Anaphylactic shock

Cardiogenic shock

Cardiac arrest

88

What are 2 clinical uses of noradrenaline?

Severe hypotension

Septic shock

89

What can reflex bradycardia mask?

direct stimulation on SAN

90

What are 3 clinical uses of dopamine?

Acute heart failure

Cardiogenic shock

Acute renal failure

91

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

Stimulates heart

Decreased vascular resistance

92

what does a high dose of dobutamine cause?

vasoconstriction 

n.b. = vasodilation in kidneys via D1 receptors

93

What are 3 clinical uses of dobutamine?

Acute heart failure

Cardiogenic shock

Refractory heart failure

94

What does dobutamine do?

Cardiac stimulation with modest vasodilation

95

What are 2 clinical uses of isoproterenol?

Bradycardia

Atrioventricular block

96

What are the effects of isoproterenol?

Cardiac stimulation

Vasodilation with little change in pressure

97

When are sympathomimetics used to treat heart failure?

Last ditch treatment for those in hospital awaiting a transplant

98

When are transduction sympathomimetics useful?

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

99

When are loop diuretics useful in treating heart failure?

Pulmonary and refractive odema

Kidney failure

100

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

Ototoxicity

Hypovolemia

Hypokalemia

Hypomagnesia

101

What is the action of thiazide diuretics?

Distal tubule = direct vasodilator

102

What are the 2 side effects of thiazide diuretics?

K loss

Hypotension

103

When are K sparing diuretics useful in heart failure?

control K loss (aldosterone antagonist)

104

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

Hyperkalaemia

Oestrogen like effects (with spirolactone)

105

What do ACE inhibitors control?

K loss 

Hypertension

106

What are the side effects of ACE inhibitors?

Cough

hypotension

Hyperkalemia

107

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

Better tolerated

No cough (no effect on bradykining)

Decreased BP

108

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

tetragenic (birth defects)

 

n.b. it also has less vasodilation than ACE

109