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MD1 Revision > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the normal value for end systolic volume?

A

75 mL

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2
Q

What is the normal value for stroke volume?

A

100 mL or less

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3
Q

What is the normal value for end diastolic pressure?

A

15 mmHg

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4
Q

What is the normal value for early diastolic pressure?

A

5 mmHg

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5
Q

Why does the gradient of the diastolic left ventricular pressure-volume curve increase more steeply with increase left ventricular volume?

A

Ventricle gets filled to its physical capacity > exponentially greater increase in pressure

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6
Q

What is the Frank-Starling relationship?

A

Greater pre-load on cardiac muscle fibres prior to contraction > increase in force of contraction
Within limits, more the heart fills with blood during diastole, the greater the force of contraction during systole
Pre-load is proportional to end diastolic volume
Therefore, the greater the end diastolic volume, the more forceful the contraction

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7
Q

What determines end diastolic volume?

A

Duration of ventricular diastole

Venous return

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8
Q

Why can the duration of ventricular diastole be short?

A

Heart rate increase > less filling time

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9
Q

What will happen to contractility if there is acidosis?

A

Decreases

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10
Q

What will happen to contractility if there is parasympathetic nerve deactivation?

A

Increases to small extent, as parasympathetic nervous system more important in heart rate and atrioventricular node firing

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11
Q

What will happen to contractility if there is caffeine intake?

A

Increases to small extent

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12
Q

What will happen to contractility if there is hypercapnia?

A

Decreases

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13
Q

Why does left ventricular pressure never reach maximal capacity during systole?

A

Aortic valve releases pressure when left ventricular pressure is greater than in aorta
In effect, aorta acts as release valve

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14
Q

Describe the blood distribution in the circulation

A 
Veins = 65%
Arteries = 13%
Capillaries = 5%
Lungs = 10%
Heart = 7%
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15
Q

Why is atrial pressure more sensitive to changes in volume than venous pressure?

A

Veins more compliant > taking blood out of veins will have less effect on pressure change

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16
Q

What is mean circulatory filling pressure?

A

Eventual average systemic pressure if heart stopped and blood settled in vessels

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17
Q

What is mean circulatory filling pressure determined by?

A

Volume of blood

Compliance of vessels

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18
Q

What effect would an increase in cardiac output have on venous pressure?

A

Decrease venous pressure

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19
Q

What effect would an increase in total peripheral resistance have on the volume of blood in the arterial and venous systems?

A

No effect

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20
Q

What effect would decreasing venous pressure have on cardiac output?

A

Decrease cardiac output due to reduced filling pressure

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21
Q

What is central venous pressure?

A

Pressure in great veins just outside heart

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22
Q

Why might central venous pressure rise?

A

Systemic venous congestion during right heart failure

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23
Q

Why might central venous pressure fall?

A 
Shock = systemic vasodilation
Venous return poor
- Blood loss
- Upright posture
- Inadequate muscle and respiratory pumps
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24
Q

What effect would an increase in contractility have on cardiac output and venous pressure?

A

Increase cardiac output

Decrease venous pressure

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25
Q

What substances produced by the endothelium alter muscle contraction?

A

Nitric oxide = vasodilator
Endothelin = vasoconstrictor
Prostacyclin = vasodilator

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26
Q

What is antagonist potency mostly determined by?

A

Potency

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27
Q

Which antagonists stop binding?

A

Competitive antagonists

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28
Q

Which antagonists stop activation?

A

Non-competitive antagonists

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29
Q

What does propranolol do?

A

Competitive antagonist of beta-adrenoceptors = beta-blocker

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30
Q

What are the factors affecting drug distribution?

A

Molecular size
Ability to bind plasma proteins
Lipid solubility

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31
Q

What is volume of distribution?

A

Volume of fluid in which amount of drug in body would need to be uniformly distributed to produced observed concentration in blood

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32
Q

How do you work out the volume of distribution?

A

Total amount of drug in body/drug blood plasma concentration

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33
Q

What does a small volume of distribution indicate?

A

Drug binds strongly to plasma proteins

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34
Q

What does a large volume of distribution indicate?

A

Drug take up by cells and binds to tissues > greater distribution

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35
Q

How does pH affect lipid solubility and thus the passage of drugs?

A

Drugs more lipid-soluble if uncharged

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36
Q

At which pH are acidic drugs more lipid soluble?

A

Low pH

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37
Q

At which pH are basic drugs more lipid soluble?

A

High pH

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38
Q

How is acetylcholine synthesised?

A
  1. Choline transported into cell by choline carrier
  2. Choline + acetyl-CoA > acetylchole
  3. Acetylcholine loaded into synaptic vessel
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39
Q

How is noradrenaline synthesised?

A
  1. Tyrosine transported into cell
  2. Converted to L-DOPA
  3. Converted to dopamine
  4. Transported into synpatic vesicle
  5. Converted to noradrenaline
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40
Q

How is adrenaline synthesised?

A

Noradrenaline converted to adrenaline in synpatic vesicle

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41
Q

What is co-transmission?

A

Autonomic nerves often release more than one neurotransmitter

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42
Q

How is acetylcholine inactivated?

A

Inactivated and degraded by acetylocholinesterase on effector tissue surface

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43
Q

How is noradrenaline inactivated?

A

Uptake 1 = reuptake via high affinity receptor

Uptake 2 = taken up via low affinity receptor by post-synaptic tissue > degraded

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44
Q

What is phenylephrine?

A

Alpha-adrenergic receptor agonist

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45
Q

How does adrenaline increase blood pressure?

A

Alpha and beta-adrenergic receptor agonist > vasoconstriction and tachycardia

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46
Q

How do anitcholinesterases work?

A

Decreased breakdown of acetylcholine > increased levels of acetylcholine in synaptic cleft > increased acetylcholine action

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47
Q

What is myasthenia gravis?

A

Autoimmune condition where Abs produced against nicotinic acetylcholine receptors (on neuromuscular junctions)
Abs bind to receptors
- Receptor internalisation and degradation
- Activation of complement > destruction of neuromuscular junction synapse architecture

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48
Q

How can myasthenia gravis be treated?

A

Use anticholinesterases
Effective in early stages
Decreased breakdown of acetylcholine > more in synpase > more chance of binding to remaining receptors

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49
Q

What are the effects of muscarinic receptor agonism?

A 
Salivation
Lacrimation
Urination
Defecation
Sweating
Bradycardia
Vasodilation
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50
Q

What are indirectly acting sympathomimetics?

A

Taken up by neuron > displace noradrenaline from synaptic vesicles > more noradrenaline displaced into synapse

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51
Q

What are some stimuli that induce histamine release?

A 
Ag via IgE
Complement fragments C3a and C5a
Neuropeptides
Cytokines and chemokines
Bacterial components
Physical trauma
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52
Q

What is the triple response to histamine?

A

Reddening
Wheal
Flare

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53
Q

What causes reddening in response to histamine?

A

Vasodilation

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54
Q

What causes a wheal in response to histamine?

A

Increased vessel permeability > local oedema

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55
Q

What causes a flare in response to histamine?

A

Spreading response through sensory fibres

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56
Q

What type of histamine receptors do classic antihistamines act on?

A

H1 receptors

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57
Q

Why do H1 receptor antagonists cause sleepiness?

A

Antagonise H1 receptors in cerebral cortex > reduce neuronal excitation
Bloch acetylcholine receptors > excess acetylcholine > drowsiness

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58
Q

What was the problem with using terfenadine as a non-sedative H1 receptor antagonist?

A

Cause rare, sudden ventricular arrhythmia

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59
Q

From which cells in the gastrointestinal tract is histamine released?

A

Enterochromaffin-like (ECL) cells

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60
Q

What two things does bradykinin mediate?

A

Pain

Inflammation

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61
Q

What triggers release of bradykining?

A

Pre-kallikrein cleaved to kallikrein by activated factor XII
Kallikrein becomes kininogen
Kininogen activated to bradykinin

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62
Q

What are the actions of bradykinin?

A 
Potent endothelium-dependent vasodilator
Contraction of non-vascular smooth muscle in bronchus and gut
Increase of vascular permeability
Sensitises pain nerve endings
Natriuresis
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63
Q

What are the effects of bradykinin on blood pressure and how?

A

Decreases blood pressure through

  • Vasodilation
  • Natriuresis
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64
Q

How do ACE inhibitors cause cough?

A

ACE normally breaks down bradykinin

ACE blocked > build up of bradykinin > bronchoconstriction > dry cough

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65
Q

What are the physiological roles of nitric oxide?

A

Flow-dependent vasodilation
Inhibits platelet adhesion and aggregation
Neurotransmitter

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66
Q

How is arachidonic acid stored?

A

Esterified and stored in membrane phospholipids

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67
Q

How is arachidonic acid liberated from membranes?

A

Increase in intracellular Ca > hospholipase A2 activated > breaks bond between arachidonic acid and phospholipid

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68
Q

What is the difference in expression between COX1 and COX2?

A

COX1 expression constitutive
COX2 expression inducible
- Expressed in response to inflammation

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69
Q

Which cells express high levels of lipoxygenase?

A

Inflammatory cells

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70
Q

What are the stable prostaglandins?

A

PGE2
PGD2
PGF2

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71
Q

What are the functions of PGE2?

A

Vasodilation
Pyrogenesis
- In hypothalamus, increases temperature set-point
Angiogenesis

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72
Q

What are the indications for non-steroidal anti-inflammatory drugs (NSAIDs)?

A

Anti-inflammatory
Analgesia
Antipyretic

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73
Q

Why is paracetamol often preferred over aspirin as an anti-pyretic?

A

Highly selective for COX2

Won’t cause gastric irritation/ulceration

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74
Q

Describe how bradykinin and PGE2 work in synergy to intensify pain

A

PGE2 > vasodilation > increased blood flow
Bradykinin > vascular leakiness
PGE2 increases sensitivity to pain caused by bradykinin

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75
Q

How is the set point raised during fever originating from inflammation?

A

Inflammation > macrophage activation > cytokines > PGE2 synthesis in hypothalamus > increase temperature set point

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76
Q

What are the gastro-protective roles of PGE2?

A

Promote blood flow
Increase mucus secretion
Reduce gastric acid secretion

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77
Q

How do NSAIDs cause gastric irritation?

A

Inhibit PGE2

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78
Q

Where is prostacyclin (PGI2) produced?

A

Endothelial cells

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79
Q

What is the function of PGI2?

A

Reduce platelet activation

Vasodilation

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80
Q

Where is TXA2 produced?

A

Platelets

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81
Q

What is the function of TXA2?

A

Increase platelet activation

Vasoconstriction

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82
Q

How do PGI2 and TXA2 differ in function?

A

Oppose actions of each other

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83
Q

How does aspirin differ to other NSAIDs?

A

Irreversibly inactivates COX

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84
Q

What effect can aspirin have on COX in platelets?

A

Irreversibly inactivate COX in platelets

Since platelets have no nucleus, won’t resynthesise COX for entire lifespan of 8 days

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85
Q

What effect does inactivation of COX in platelets by aspirin have?

A

TXA2 levels reduced more than PGI2 levels > endothelium-mediated vasodilation and decreased platelet activation

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86
Q

What are aspirin-triggered lipoxins?

A

Acetylation of COX2 alters its activity > produces aspirin-triggered lipoxins
Active

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87
Q

What is the suggested mechanism for cardio-protection from intake of fish oil?

A

Fish oil increases synthesis of PGI3

PGI3 has prostacyclin-like activity > suggested that it decreases incidence of coronary artery disease

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88
Q

What types of cells is 5-lipoxygenase activity only seen in?

A

Inflammatory cells

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89
Q

What is the link between leukotriene activity and asthma?

A

Leukotrienes potent bronchoconstrictors, also causing bronchospasm

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90
Q

What is the link between leukotriene and hayfever?

A

Allergic response > leukotriene release > nasal tissue oedema > nasal congestion

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91
Q

How can leukotriene action be blocked?

A

Leukotriene receptor antagonists

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92
Q

Why do coaguation factors normally not cause thrombosis in vessels?

A

Circulate as pro-enzymes

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93
Q

What are the three phases of haemostasis?

A

Primary haemostasis
Secondary hamostasis
Fibrinolysis

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94
Q

What happens in primary haemostasis?

A

Vasoconstriction
Platelet adhesion
Platelet aggregation

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95
Q

What happens in secondary haemostasis?

A

Activation of coagulation factors

Formation of fibrin

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96
Q

What happens in fibrinolysis?

A

Activation of fibrinolysis

Lysis of clot

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97
Q

What makes up Virchow’s triad?

A

Endothelial injury
Abnormal blood flow
Hypercoagulability

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98
Q

What is required to trigger the coagulation system?

A

Tissue factor

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99
Q

What molecules can inactivate thrombin?

A

Protein C

Anti-thrombin

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100
Q

What is the pharmacological mechanism of warfarin?

A

Inhibits reduction of vitamin K > no activation of vitamin K-dependent factors

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101
Q

What is the pharmacological mechanism of heparin?

A

Binds antithrombin > doesn’t cleave thrombin

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102
Q

What is the difference between risk and rate?

A 
Risk = probability of disease occurring in a disease-free population during a specified time period
Rate = probability of disease occurring in disease-free population during sum of individual follow-up periods
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103
Q

What is risk a measure of?

A

Incidence

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104
Q

What is person-time?

A

Makes explicit time population at risk actually spent being at risk

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105
Q

What are the benefits of using person-time?

A

Adjusts for loss of participants to follow

Risk can potentially underestimate true incidence

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106
Q

What is hazard, in relation to rate?

A

Type of rate that’s continuously updated as longitudinal study progresses
Rate that applies to an exact point in time = instantaneous rate

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107
Q

If absolute risk is isolated, how is it possible to provide an indication of association between a risk and an outcome?

A

Generate relative risk = risk ratio

Relative risk = risk among exposed/risk among unexposed

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108
Q

What is attributable risk?

A

Indicates absolute magnitude of change in risk/rate of outcome

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109
Q

How is attributable risk calculated?

A

Risk among exposed - risk among unexposed

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110
Q

What does attributable risk percentage represent?

A

Percentage of incident disease among exposed people that was due to exposure

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111
Q

What is population attributable risk?

A

Additional/excess risk of outcome in population, due to exposure

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112
Q

How do you calculate population attributable risk?

A

Risk in whole population - risk among unexposed

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113
Q

What does the population attributable risk percentage represent?

A

Proportion of incident disease among the whole population due to exposure

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114
Q

What is the population attributable risk percentage also known as?

A

Preventable fraction

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115
Q

When do chemoreceptors start to act in the context of blood pressure control?

A

When blood pressure falls below 60 mmHg

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116
Q

Where are baroreceptors located?

A

Carotid sinus
Aortic arch
Pre-glomerular arterioles

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117
Q

What is the carotid sinus?

A

Thin spot of wall in internal carotid artery
More compliant
More sensitive to changes in stretch due to change in pressure

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118
Q

Where are chemoreceptors located?

A

Carotid and aortic bodies outside arteries

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119
Q

What do chemoreceptors respond to?

A

Low flow
Low O2
High CO2
Low pH

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120
Q

What components of the cardiovascular system are responsive to parasympathetic signals?

A

Heart rate

Conduction speed at the sinoatrial node

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121
Q

How can a stroke occur from an atrial thrombus?

A

Atria starts beating at sinus rhythm, may have to pump against higher pressure due to decreased ventricular compliance
Thrombus may dislodge and travel up to brain
Cerebral embolism > stroke

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122
Q

How do systolic and diastolic blood pressures vary with age?

A

Systolic pressure increases

Diastolic pressure increases until 60, then decreases

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123
Q

Why does pulse pressure increase with age?

A

Decreasing compliance > increased systolic and decreased diastolic

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124
Q

Why does compliance decrease with age?

A

In arteries

  • More collagen
  • Less elastin
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125
Q

How does blood pressure vary with sex?

A

Males > females

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126
Q

How does blood pressure vary with body size?

A

Larger body size > higher blood pressure

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127
Q

What is the diurnal variation in blood pressure?

A

Lower at night

Less variability at night

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128
Q

What is the population paradox?

A

More deaths occur in people at moderate risk (large group) than in people at high risk (small group)

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129
Q

What are social permissions?

A

What doctors are allowed to do, that others can’t

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130
Q

Why are explicit ethical principles needed?

A

To address vulnerability inherent in patient’s position, by affirming particular ethical obligations of doctors to protect and respect patients
Provide counter to negative culture of medicine

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131
Q

What are the basic ethical principles?

A 
Beneficence
Non-maleficence
Respect for autonomy
Respect for privacy
Justice
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132
Q

What is the difference between moral confusion and moral distress?

A

Moral confusion = feeling unsure what’s right thing to do, and not knowing how to resolve it
Moral distress = feeling unable to do what you think is right and feeling compelled to do what you think is wrong

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133
Q

What are the targets for parasymathetic control of heart rate?

A

Sinoatrial and atrioventricular nodes via acetylcholine action on muscarinic cholinergic receptors

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134
Q

What is the effect of muscarinic receptor blockade on heart rate in healthy young individuals?

A

Increases it

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135
Q

What are the targets for sympathetic control of heart rate?

A

Sinoatrial node
Conducting pacemaker tissue
Myocardial cells

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136
Q

What is the effect of sympathetic release of noradrenaline and adrenaline on the heart?

A

Bind to beta-adrenoceptors > directly increase heart rate and contractility

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137
Q

What are the phases of the sinoatrial node pacemaker action potential?

A 
Phase 0
- Depolarisation
- Ca in
Phase 3
- Repolarisation
- K out
Phase 4
- Spontaneous depolarisation
- Na and Ca in
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138
Q

Why don’t the pacemaker cells have a stable resting membrane potential?

A

Leaky funny current Na channel

Uses Ca for depolarisation

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139
Q

Describe the mechanism for parasymathetic slowing of the sinoatrial node

A

Acetylcholine acts on muscarinic receptors on sinoatrial node > decrease in cAMP > K channels open > K efflux > slows Na and Ca fluxes > slower phase 4 > takes longer to reach threshold potential > slows rate of conduction of atrioventricular node

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140
Q

Describe the mechanism of sympathetic acceleration of the sinoatrial node

A

Noradrenaline and adrenaline act on beta1-adrenoceptors on sinoatrial node > increase in cAMP > opening of Ca channels > increased slope of phase 4 at sinoatrial and atrioventricular nodes > increased rate of firing from sinoatrial node and more rapid conduction to atrioventricular node

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141
Q

What are the phases of the ventricular pacemaker action potential?

A 
Phase 0
- Depolarisation
- Na in
Phase 1
- Rapid repolarisation
- K out
Phase 2
- Plateau
- Ca in
- K out
Phase 3
- Repolarisation
- K out
Phase 4
- Stable membrane potential
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142
Q

What are the mechanisms underlying dysrhythmias?

A

Altered impulse formation
Altered impulse conduction
Triggered activity

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143
Q

What is altered impulse formation?

A

Abnormal generation of action potentials at sites other than sinoatrial node

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144
Q

What is altered impulse conduction?

A

Conduction block

Re-entry > extra beats

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145
Q

What triggers activity in dysrhythmias?

A

Early/late after-depolarisations due to excess sympathetic activation

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146
Q

What is the molecular mechanism of class 1 anti-dysrhythmics?

A

Na channel block > reduces phase 0 slope and peak of ventricular action potential

  • 1a = moderate block
  • 1b = weak block
  • 1c = strong block
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147
Q

What is the molecular mechanism of class 2 anti-dysrhythmics?

A

Beta-adrenoceptor antagonism > decrease rate and conduction

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148
Q

What is the molecular mechanism of class 3 anti-dysrhythmics?

A

K channel blockade > delay phase 3 of ventricular action potential

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149
Q

What is the molecular mechanism of class 4 anti-dysrhythmics?

A

Ca channel blockade > reduces rate and conduction

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150
Q

What effects do beta-adrenoceptor antagonists have on Purkinje fibres?

A

Membrane stabilising effects - local anaesthetic-type action

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151
Q

What are patients on K channel inhibitors at an increased risk of experiencing and why?

A

K channel inhibition > K takes longer to leave cells > prolonged repolarisation time > prolonged action potential > more chance of triggered events

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152
Q

What is the drug class of lignocaine?

A

Class 1b

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153
Q

What do the side effects of lignocaine depend on?

A

Concentration of drug

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154
Q

What are the side effects of lignocaine, with increasing concentrations?

A 
Lip and tongue numbness
Light headedness
Visual disturbance
Muscular twitching
Convulsions
Coma
Respiratory arrest
Cardiovascular depression
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155
Q

Other than as an anti-dysrhythmic, what else is lignocaine used as?

A

Anti-dysrhthmic

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156
Q

What are the adverse effects of beta-adrenoceptor antagonists?

A 
Bradycardia
Reduced exercise capacity
Hypotension
Atrioventricular conduction block
Bronchoconstriction
Hypoglycaemia
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157
Q

Other than as an anti-dysrhythmic, what else are beta-adrenoceptor antagonists used in?

A

Hypertension
Heart failure
Angina
Anxiety

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158
Q

What is the drug class of amiodarone?

A

K channel inhibitor

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159
Q

What are the side effects of amiodarone?

A

Reversible photosensitisation
Skin discolouration
Hypothyroidism
Pulmonary fibrosis with long term use

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160
Q

What is the dug class of verapamil?

A

Ca channel blocker

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161
Q

What are the side effects of calcium channel blockers?

A 
Facial flushing
Peripheral oedema
Dizziness
Bradycardia
Headache
Nausea
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162
Q

Other than as an anti-dysrhythmic, where else are calcium channel blockers used?

A

Hypertension

Angina

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163
Q

What are the goals for the treatment of hypertension?

A

Reduce blood pressure to <140/85 mmHg

If diabetes/renal disease present, reduce blood pressure to <130/80 mmHg

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164
Q

What are the controlled variables contributing to blood pressure?

A

Heart rate
Stroke volume
Total peripheral resistance

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165
Q

What are the effects of angiotensin II?

A

Vasoconstriction
Aldosterone > salt and water retention
Cell growth
Increased sympathetic activity

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166
Q

What is the mechanism of action of ACE inhibitors?

A 
Block angiotensin I and angiotensin II conversion
- Reduce vascular tone > vasodilation
- Reduce aldosterone productionn
- Reduce cardiac hypertrophy
Prevent breakdown of bradykinin
- Increase action of bradykinin
   - Vasodilation
   - Cardioprotection
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167
Q

What are the adverse effects associated with ACE inhibitors?

A 
1st dose hypotension
Dry cough
Loss of taste
Hyperkalaemia
Acute renal failure
Pruritis
Foetal malformations
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168
Q

What are the types of angiotensin receptor antagonists?

A

AT1 antagonists - clinically useful

AT2 antagonists - not clinically useful

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169
Q

What do AT1 antagonists do?

A

Reduce vasoconstriction
Reduce aldosterone release
Reduce cardiac hypertrophy
Reduce sympathetic activity

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170
Q

What are the adverse effects of angiotensin receptor antagonists?

A

Hyperkalaemia
Headache
Dizziness

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171
Q

How do beta-adrenoceptor antagonists decrease blood pressure?

A

Reduce cardiac output
- Reduce heart rate
- Reduce contractility
Reduce renin release

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172
Q

How do different beta-adrenoceptor antagonists vary?

A

Selectivity
Intrinsic sympathomimetic activity
Lipid solubility

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173
Q

What are the adverse effects of using beta-adrenoceptor antagonists?

A

Cold extremities
Fatigue
Dreams, insomnia
Bronchoconstriction

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174
Q

When is the use of beta-adrenoceptor antagonists contraindicated?

A 
Diabetes
Asthma
Take care with
- Heart failure
- Metabolic syndrome
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175
Q

What type of calcium channels to calcium channel blockers block?

A

Voltage-gated L-type Ca channels in

  • Vasculature
  • Myocardium
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176
Q

What are the adverse effects of calcium channel blockers?

A

Oedema
Flushing
Headache
Bradycardia

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177
Q

How do thiuzide diuretics act to lower blood pressure?

A

Inhibit Na/Cl co-transporter in distal tubule > decrease Na and Cl reabsorption > increases Na and water excretion from kidney and K from collecting ducts > lower blood volume and reduced blood pressure

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178
Q

What are the adverse effects of thiuzide diuretics?

A

Hypokalaemia
Gout
Hyperglycaemia
Allergic reaction

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179
Q

What is the suffix of ACE inhibitors?

A

-pril

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180
Q

What is the suffix of angiotensin receptor antagonists?

A

-sartan

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181
Q

What is the suffix for beta-adrenoceptor antagonists?

A

-olol

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182
Q

What is the disadvantage of tetracycline use?

A

Short-half life

Must administer 4 times/day

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183
Q

How is the disadvantage of tetracycline overcome?

A

Semi-synthetics; eg: doxycycline

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184
Q

Why was penicillin-G replaced by penicillin-V?

A

Penicillin-G acid labile
- Must be given IV
Penicillin-V acid stable
- Available orally

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185
Q

What are the advantages of dicloxacillin and flucloxacillin over methicillin?

A

Less toxic

Capable of oral administration

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186
Q

What are the principles of selective toxicity?

A

Antibiotics should target organism but not damage host

187
Q

What antibiotic class targets the bacterial cell wall?

A

Beta-lactams

Glycopeptides

188
Q

What antibiotic class targets bacterial ribosomes?

A

Aminoglycosides

Chloramphenicol

189
Q

What antibiotic class targets bacterial nucleic acids?

A

Rifamycins

Quinolones

190
Q

What antibiotic class targets bacterial cell membranes?

A

Polymyxins

Polyenes - for fungi

191
Q

What antibiotic class targets bacterial folic acid synthesis?

A

Sulphonamides

Trimethoprims

192
Q

What is a cross-sectional study?

A

Examines sample of population selected and information obtained at 1 point/period in time
No follow up of subjects
Each subject contributes data only once

193
Q

How is data collected in cross-sectional studies?

A

Questionnaires
Examinations
Investigations
Prevalence is especially looked at

194
Q

What are the advantages of cross-sectional studies?

A

Relatively cheap

Easy

195
Q

What are the disadvantages of cross-sectional studies?

A

Often need for representative sample, as study mainly descriptive
Weak evidence of causality because no explicit data on temporal relationships

196
Q

What is a case-control study?

A

Comparison of previous exposure status between cases and controls
Looks at effect of exposure on outcome of interest

197
Q

What is the purpose of matching during a case-control study?

A

Matched on bases of confounders to reduce potential for bias

198
Q

What are the advantages of case-control studies?

A

Gives explicit knowledge about temporal relationship between exposure and outcome
Useful for studying rare outcomes

199
Q

Why is relative risk unmeasurable in case-control studies?

A

Relative risk = measure of incidence

Case-control studies retrospective > no data on incidence

200
Q

What is used as an approximation of relative risk in case-control studies?

A

Odds ratio

201
Q

What are cohort studies?

A

Longitudinal studies done with follow-up of subjects to collect incidence data
Compares outcomes between exposed and not exposed to risk factor > relative risks derived

202
Q

What are the advantages of cohort studies?

A

Explicit and detailed knowledge about temporal relationship between exposure and outcome
Can include multiple exposures and outcomes
Cohorts can be established as part of routine clinical care

203
Q

What are the disadvantages of cohort studies?

A

Difficult to study rare outcomes

Not cheap nor easy

204
Q

Why is a retrospective cohort study still considered a longitudinal study?

A

Researchers begin study at time where cohort has already been established and data available bout exposure in past

205
Q

What is bias?

A

Unintentional error, due to systematic difference between/among groups > under-/overestimation of true results

206
Q

What are the two main types of bias?

A

Selection

Information (measurement)

207
Q

What is selection bias?

A

Systematic difference in characteristics of people selected for study and those not selected

208
Q

How is selection bias minimised?

A

Representative sample
Cases and controls from same source
Maximise response
Minimise subjects lost to follow-up

209
Q

What is information bias?

A

Systematic differences in way information collected between/among groups being compared

210
Q

What is recall bias?

A

Information bias where cases more likely to recall presence of exposure due to already established prejudice about association between risk factor and outcome

211
Q

How is information bias minimised?

A

Ensuring methods for collecting information uniform between/among groups being compared

212
Q

What is confounding?

A

Influences relationship between exposure and outcome
3rd variable that
- Independently affects outcome
- Related to exposure

213
Q

What are the two universal confounders?

A

Age

Sex

214
Q

How is confounding minimised?

A 
In design and execution of stages of study
- Matching by confounder
- Restriction
In analysis
- Stratification
- Multivariate analyses
215
Q

What are the three layers of the heart?

A

Epicardium
Myocardium
Endocardium

216
Q

What are the sub-layers of the epicardium?

A 
Squamous epithelium
Sub-epicardial connective tissue
- Blood vessels
- Fat
- Nervous tissue
217
Q

What makes up the myocardium?

A

Muscle cells

Capillaries

218
Q

What are the sub-layers of the endocardium?

A

Endothelial layer
Subendocardial connective tisse
Conducting tissue

219
Q

Describe the cell size, location of nucleus, and fibre structure of cardiac muscle cells

A

Small cells
Central nucleus
Branching fibres
- Joined to each other by intercalated discs
Richly vascularised
WBCs between myocardial cells and capillaries

220
Q

What is the role of intercalated discs?

A

Anchors actin filaments in 1 cell’s sarcomere to sarcomere in another cells via fascia adherens

221
Q

How can intercalated discs come apart?

A

Removing Ca supply

222
Q

What are Purkinje fibres?

A

Larger, modified cardiac muscle cells with limited contractile machinery

223
Q

Where are Purkinje fibres found?

A

Bundles in subendocardium

224
Q

What is the role of the endothelium?

A

Inhibits clotting by secreting inhibitors
Secretes clotting factor into subendothelial tissue
Releases vasoactive substances

225
Q

Apart from constriction and relaxation, what is the role of smooth muscle in the tunica media of vessels?

A

Secretes connective tissue

  • Extracellular matrix
  • Collagen
  • Elastin
  • Ground substance
226
Q

Which layer is the vasa vasorum located in?

A

Adventitia

227
Q

Where are the elastic arteries generally found?

A

Closest to heat, where there’s highest blood pressure fluctations

  • Aorta
  • Carotid arteries
228
Q

What is the purpose of the many layers of elastin in elastic arteries?

A

Can stretch due to higher blood pressure
When heart relaxes, layers of elastin in media store energy > compress blood > restores energy to blood during diastole > blood pressure never drops to 0
Allows blood flow to be continuous

229
Q

What is the diastolic blood pressure due to?

A

Elastic energy applied to blood

230
Q

What is the primary role of muscular arteries?

A

Distribute blood to tissue

Regulate blood pressure through contractions of media

231
Q

How is capillary flow regulated?

A

Single smooth muscle cell sphincters

232
Q

What is the structure of capillaries?

A 
Single endothelial cells rolled into tubed
Sealed to each other by tight junctions
Basal lamina = thick connective tissue
Sometimes media = pericyte
Adventitia = few collagen fibres
233
Q

How do the layers of veins differ from those of arteries?

A

Same layers
Media thinner
Adventitia thicker
have 1-way valves

234
Q

What type of vessel is the preferred site of diapedesis of leukocytes?

A

Venules

- Affected by histamines and other cytokines

235
Q

Where are the lymphatic vessels located in relation to the blood vessels?

A

On venous side

236
Q

How are lymphatics distinguished from veins?

A

Absence of RBCs

Presence of WBCs

237
Q

What are the risk factors for developing atherosclerosis?

A 
Hyperlipidaemia
Hypertension
Smoking
Toxins
Haemodynamic factors
Immune reactions
Viruses
238
Q

What is the pathophysiology of atherosclerosis?

A

Endothelial injury/dysfunction > LDL entry and oxidation via ROS > cytokine production > recruitment of monocytes > phagocytosis of lipics and formation of foam cells > recruitment of lymphocytes > recruitment of smooth muscle cells from tunica media and formation of ECM > degeneration of components of plaque > lipid-rich necrotic core > initial remodelling of vessel wall preserves lumen diameter > continued endothelial dysfunction > vessel stenosis, impaired vasodilation, plaques vulnerable to rupture, local pro-thrombotic environment

239
Q

What is the definition of the metabolic syndrome?

A

Central obesity + any 2 of following

  • Raised triglycerides
  • Reduced HDL
  • Raised blood pressure
  • Raised fasting plasma glucose
240
Q

What are the complications of atherosclerosis?

A

Ischaemia
Infarction
Aneurysm

241
Q

Why can ischaemia follow atherosclerosis?

A

Fixed vessel narrowing

Acute plaque event

242
Q

Why can infarction follow atherosclerosis?

A

Occlusion by plaque/thrombus

243
Q

What are the types of aneurysms?

A

True
- Saccular
- Fusiform
False = extravasation into extravascular connective tissue

244
Q

What causes aneurysms?

A

Atherosclerosis
Congenital weakness in wall
Systemic hypertension
Infection in artery wall

245
Q

Describe the mechanism of hyaline arteriolosclerosis?

A

Age-related change caused by endothelial stress > deposition of plasma proteins and increased collage in vessel wall > arteriole wall thickens with homogenous eosinophilic hyaline > lumen narrows

246
Q

What can cause cardiac remodelling and hypertrophy?

A

Myocardial infarction
Cardiac damage
Volume overload
Pressure overload

247
Q

What effect on left ventricular mass and left ventricular wall thickness does concentric hypertrophy have?

A

Increased left ventricular mass

Increased left ventricular wall thickness

248
Q

What effect on left ventricular mass and left ventricular wall thickness does remodelling have?

A

Normal left ventricular mass

Increased left ventricular wall thickness

249
Q

What effect on left ventricular mass and left ventricular wall thickness does eccentric hypertrophy have?

A

Increased left ventricular mass

Normal relative wall thickness

250
Q

What is concentric hypertrophy?

A

Increased wall thickness without left ventricular enlargement
Often due to pressure overload
More sarcomeres in parallel

251
Q

What is eccentric hypertrophy?

A

Increased chamber size and normal relative wall thickness
Often due to volume overload
Myocyte stretching - more sarcomeres in series

252
Q

Describe LaPlace’s law

A

Wall stress = pressure pulling heart apart
- Stress counteracted by desmosomes joining myocytes
- Increasing wall thickness reduces wall stress because it increases number of desmosomes
Pressure greater determinant of wall stress than volume

253
Q

What is decompensation

A

Occurs in long-term following hypertrophy
Characterised by
- Reduced systolic function and cardiac output
- Increased left ventricular end diastolic pressure
- Eventual cardiac failure

254
Q

What are some environmental causes of concentric and eccentric hypertrophy?

A

Concentric: pressure overload due to high afterload
- Hypertension
- Aortic stenosis
Eccentric: volume overload due to high preload
- Mitral and aortic regurgitation
- Ventricular septal defect

255
Q

What are two genetic causes of ventricular hypertrophy?

A

Hypertrophic cardiomyopathy > thickened septum

Fabry’s disease

256
Q

How is left ventricular hypertrophy clinically identified?

A 
Forceful apex beat
S3 and S4 heart sounds
ECG
Chest x-ray
Echocardiogram
MRI
257
Q

What are the causes of left ventricular remodelling?

A 
Renin-angiotensin-aldosterone
Adrenergic nervous system
Endothelin
Cytokines
Local factors
258
Q

What are the causes of right ventricular hypertrophy?

A

Congenital
Pulmonary hypertension
Right heart valves

259
Q

Describe the pathology of hypertrophic cardiomyopathy?

A

Increased left ventricular wall thickness, especially of septum > left ventricle outflow tract obstruction > cellular hypertrophy > myocyte disarray

260
Q

What is athlete’s heart?

A

Eccentric hypertrophy with normal cardiac function

Usually regresses with deconditioning but may not regress > ventricular arrhythmia and sudden cardiac death

261
Q

What are the four determinants of cardiac output?

A

Contractility
Preload
Afterload
Heart rate

262
Q

Describe the length-tension relationship in muscle fibres

A

Increased sarcomere length > increased force of contraction

263
Q

How is left ventricular end diastolic pressure measured?

A

Measure pulmonary wedge pressure = ventricular pressure = atrial pressure

264
Q

How is right ventricular end diastolic pressure measured?

A 
Non-invasive = JVP
Invasive = across tricuspid valve
265
Q

How do pulmonary artery wedge pressure and JVP reflect preload?

A

Pulmonary artery wedge pressure = left ventricular end diastolic pressure
JVP = right ventricular end diastolic pressure

266
Q

Why does cardiac failure happen?

A

Usually due to decreased cardiac output arising from systolic failure = loss of contractility

267
Q

How does cardiac failure happen?

A 
Loss of myocardial muscle
- Ischaemic heart disease
- Cardiomyopathy
Pressure overload
- Aortic stenosis
- Hypertension
Volume overload
- Valve regurgitation
- Shunts
268
Q

How may cardiac failure worse by inappropriate homeostatic adaptations?

A

Increased end diastolic pressure and thus end diastolic volume to maintain same cardiac output
However, increased end diastolic volume > more fluid in left ventricle > more fluid in left atrium > more pressure in left atrium > pulmonary hypertension > pulmonary oedema

269
Q

What are the homeostatic mechanisms to combat cardiac failure?

A

RAAS stimulation > Na and water retention > peripheral/pulmonary oedema
Corresponding K loss and vasoconstriction

270
Q

Why is long term sympathetic stimulation of the heart unfavourable?

A

Vasoconstriction
Ventricular arrhythmias
Direct toxic effect

271
Q

What is the pathophysiology of diastolic heart failure?

A

Normal systolic function
Reduced left ventricular compliance due to
- Infarct
- Chronic hypertension
- Hypertrophy
Increased left ventricular end diastolic pressure required to fill left ventricle > increase in pulmonary venous pressure > pulmonary congestion/oedema

272
Q

Why is overdosing of diuretics unfavourable for cardiac function in patients with heart failure?

A

Drop in blood pressure to do compromised systolic function > cardiogenic shock

273
Q

How is peptidoglycan synthesised?

A

Synthesised from intermediates in cytoplasm on inner aspect of plasma membrane
Building block transported to exterior membrane and linked to growing peptidoglycan chain

274
Q

How does vancomycin work?

A

Binds to terminal D-Ala-D-Ala in peptidoglycan building block
Prevents cell wall synthesis

275
Q

What types of bacteria is vancomycin effective against?

A

Gram positive bacteria only, because can’t cross Gram negative outer membrane

276
Q

What is the basis of vancomycin resistance in enterococci?

A

Enterococci change terminal D-Ala to D-Lac > vancomycin can’t bind

277
Q

What is the mechanism of action of penicillin?

A

Has similar structure to D-Ala-D-Ala
Binds to and deactivates penicillin-binding proteins > no cross-linking
Defective synthesis of cell wall
Bacteria starts to break down its own cell wall

278
Q

What do beta-lactamases do?

A

Have similar structures to penicillin binding proteins
Beta-lactam antibiotic binds to beta-lactamase > hydrolysed
Unstable antibiotic > can’t fulfill role in disrupting cell wall synthesis

279
Q

What are the two mechanisms of resistance to beta-lactams?

A

Beta-lactamases

Altered penicillin-binding proteins

280
Q

What are the two types of beta-lactamase expression?

A

Expressed on plasmids
- Susceptible to clavulanic acid
Chromosomal expression
- Susceptible to ticarcillin

281
Q

Which beta-lactam is Pseudomonas aeruginosa susceptible to?

A

Ticarcillin

282
Q

What is the mechanism of beta-lactam resistance in methicillin-resistant Staphylococcus aureus (MRSA)?

A

Altered penicillin binding proteins

283
Q

Why is the combination of clavulanic acid and amoxycillin effective?

A

Clavulanic acid binds to beta-lactamase > inhibits it

Amoxycillin can now act

284
Q

How do aminoglycosides work?

A

Bind to 30S ribosomal subunit

Distort reading frame > altered proteins > early termination

285
Q

How does chloramphenicol work?

A

Binds to 50S ribosomal subunit

Interferes with peptidyl transfer

286
Q

How do macrolides work?

A

Bind to 50S ribosomal subunit

Interfere with translocation

287
Q

What are the mechanisms of resistance to aminoglycosides?

A

Efflux = drug pumped out of cell
Gram negative bacteria may modify outer membrane to reduce drug entry
Enzymatic modification > reduced entry
Ribosomal mutation > reduced drug binding

288
Q

Why is metronidazole only effective against strict anaerobes?

A

Strict anaerobes produce nitro-reductase > needed for activation of metronidazole into active form

289
Q

What is intrinsic resistance?

A

Resistant to antibiotic naturally

290
Q

What is acquired resistance?

A

Mutation

Horizontal gene transfer

291
Q

How does transfer of genes between bacteria occur?

A

Transformation
Phage-mediated transduction
Plasmid- mediated conjugation

292
Q

Why are multiresistance plasmids a major problem?

A

Potential for transfer between completely unrelated bacteria

Can lead to simultaneous acquisition of resistance to multiple antibiotics in 1 genetic event

293
Q

What is a benefit and risk of using digoxin?

A

Increases contractility but increases risk of dysrhythmias

294
Q

How does digoxin work?

A

Inhibits Na/K ATPase
Increased intracellular Na > decreased Ca exit
Increase Ca in sarcoplasmic reticulum
Increase Ca release with each action potential

295
Q

What is the drug class of digoxin?

A

Glycosides

296
Q

What are the adverse effects of using glycosides in heart failure?

A 
Low therapeutic index
Affect all excitable tissues
- Gut: anorexia, nausea, diarrhoea
- CNS: drowsiness, confusin, psychosis
- Cardiac: ventricular dysrhythmias
Increased toxicity
- Hypokalaemia
- Hypercalcaemia
- Renal impairment
297
Q

How do beta1 agonists increase contractility?

A

Agonist binds beta1-adrenoceptor > in creased cAMP > phosphorylation of Ca channel > increased Ca entry

298
Q

What is dobutamine?

A

Selective beta1-adrenoceptor agonist

299
Q

What are the adverse effects associated with beta-adrenoceptor agonists?

A

Increased cardiac work

Risk of arrhythmias

300
Q

How do phosphodiesterase inhibitors work?

A

Block action of phosphodiesterase > increased cAMP > increased protein kinase activity > more open Ca channels > increased intracellular Ca > increased contractility

301
Q

What is the effect on adrenoceptors during chronic heart failure?

A

Chronic overactivation of beta1-adrenoceptors with sympathetic compensation for reduced cardiac output > reduced beta1-adrenoceptor expression and impaired beta1-adrenoceptor coupling > reduced sensitivity to beta1- adrenoceptor agonists/sympathetic drive

302
Q

What are the three main mechanisms leading to heart failure?

A

Decreased contractility due to loss of functional myocardial muscle
Pressure overload (afterload too high) due to
- Aortic stenosis
- Hypertension
Volume overload (preload too high) due to
- Valve regurgitation
- Shunts

303
Q

What are the compensatory responses to a fall in cardiac output?

A

Decreased CO > decreased BP > baroreflex > increased sympathetic outflow
- Beta-adrenoceptor activation > increased renin > increased angiotensin II > increased aldosterone > Na retention > volume expansion > increased preload
- Alpha-adrenoceptor activation + angiotensin II > vasoconstriction > increased afterload
Increased preload + afterload > increased oxygen demand > worsening function > myocardial remodelling

304
Q

Which drugs can reduce preload during congestion?

A

Venodilators
Diuretics
Aldosterone receptor antagonists
ADH receptor antagonists

305
Q

What is the drug class of nitrates?

A

Venodilators

306
Q

What is the drug class of frusemide?

A

Loop diuretics

307
Q

What is the drug class of spironolactone?

A

Aldosterone receptor antagonists

308
Q

What does spironolactone do?

A

Inhibit aldosterone action on cortical and distal tubules
Spares K
Shows increase in long term survival

309
Q

Which drugs can reduce afterload?

A 
Arterial vasodilators
- Prone to reflex tachycardia
ACE inhibitors and ARBs
AT1 antagonists
Beta-adrenoceptor antagonists
310
Q

Which drugs are first line therapy for heart failure?

A

ACE inhibitors and ARBs

311
Q

In which grades of heart failure are ACE inhibitors and ARBs effective?

A

All

312
Q

What effect do ACE inhibitors and ARBs have on heart failure?

A

Improve symptoms
Delay progression of remodelling
Decrease constriction and fluid retention
Slows progression of hypertrophy

313
Q

What are the side effects of using beta-adrenoceptor antagonists for heart failure?

A 
Hypotension
Fatigue
Bronchoconstriction
- Contraindication for asthma
Cold extremities
- Contraindicated in peripheral vascular disease
May cause/mask signs of hypoglycaemia
- Contraindicated for diabetes
314
Q

What is the difference between a clot and a thrombus?

A

Clot forms in static blood in vitro

Thrombus forms in vivo

315
Q

What is thrombosis?

A

Pathological formation of haemostatic plug in blood vessel in absence of blood loss

316
Q

What are the three main stages of physiological haemostasis?

A
  1. Vasoconstriction: exposed collagen on damaged vessel wall > platelets stick to collagen > become activated > release ADP and serotonin > serotonin powerful vasoconstrictor
  2. Platelet adhesion and activation: granule contents secreted > mediators synthesised > platelets aggregate and adhere
  3. Fibrin formation: thrombin cleaves fibrinogen
317
Q

What are some stimuli for platelet activation?

A

Collagen
Thrombin
Thromboxane
ADP

318
Q

How is blood coagulation controlled?

A

Enzyme inhibitors > cascade inhibition

Fibrinolysis by plasmin

319
Q

Which drugs can affect fibrin formation?

A

Procoagulant drugs
Injectable anticoagulants
Oral anticoagulants

320
Q

How does heparin work?

A

Injected

Enhances activity of antithrombin > inhibits and inactivated factor Xa and thrombin

321
Q

What version of heparin has a longer half life?

A

Low molecular weight heparin

322
Q

How does warfarin work?

A 
Oral administration
Inhibits reduction of vitamin K > prevents activation of clotting factors
- II
- VII
- IX
- X
Delayed onset of action
323
Q

How is the anti-coagulant effect of heparin monitored?

A

APTT = activated partial thromboplastin time

Measure of intrinsic pathway

324
Q

Which drugs may lead to increased warfarin activity?

A 
Aspirin
- Impaired platelet aggregation
NSAIDs
- Competition for plasma protein binding
Alcohol
- Competition for cytochrome p450 pathway
325
Q

How is the anti-coagulant effect of warfarin monitored?

A

PT = prothrombin time
Time for clot formation after addition of Ca and tissue factor
Measure of extrinsic pathway

326
Q

What is the INR?

A

Ratio of patient PT to normal PT

327
Q

Which drugs can affect platelet activation and adhesion?

A

ADP receptor antagonists
Thromboxane synthesis inhibitors
Glycoprotein IIb/IIIa receptor antagonists

328
Q

What is the drug class of clopidogrel?

A

ADP receptor antagonists

329
Q

How is streptokinase used?

A

Activates plasminogen
Used IV
Single use - antigenic and can activate immune system upon re-exposure because derived from bacteria

330
Q

How is alteplase used?

A

Human recombinant tPA
Not antigenic
IV infusion because has short half life

331
Q

How does aortic stenosis arise?

A

Progressive narrowing of aortic valve due to fibrosis and calcification

332
Q

How does the left ventricle respond to aortic stenosis?

A

Pressure overload of left ventricle > concentric hypetrophy > walls thicken > less compliance > diastolic dysfunction > increased left ventricular end diastolic pressure required to fill left ventricle > cardiac failure

333
Q

What are the two main types of causes of aortic regurgitation?

A 
Damage of aortic leaflets
- Endocarditis
- Rheumatic fever
Dilatation of aortic root
- Marfan's syndrome
- Aortic dissection
- Collagen vascular disorders
- Syphilis
334
Q

Describe the progression of acute severe aortic regurgitation>

A

Sudden increase in left ventricular end diastolic pressure and left atrial pressure > acute pulmonary oedema > cardiogenic shock > early surgery needed to prevent death

335
Q

What are the causes of mitral regurgitation?

A

Myxomatous degeneration > mitral valve prolapse
Ruptured chordae tendineae > flail leaflet
Infective endocarditis
Myocardial infarct > ruptured papillary muscle
Rheumatic fever
Collagen vascular disease
Cardiomyopathy

336
Q

What is usually the cause of acute ischaemia?

A

Increased demand for oxygen that isn’t met

337
Q

What are the causes of infarction?

A 
Arterial occlusion
- Thrombotic
- External compression in dissection
Venous occlusion
Systemic reduction in tissue perfusion
338
Q

What does the size of an infarction depend on?

A 
Size of artery occluded
Duration of occlusion
Vulnerability of cells to ischaemia
Whether artery carrying oxygenated/deoxygenated blood
Nature of arterial supply
Oxygen content of blood
State of systemic circulation
339
Q

What are usually the causes of haemorrhagic infarcts?

A

Dual circulation/natural collateral circulation
Reperfusion
Venous occlusion

340
Q

What can cause endothelial dysfunction/injury?

A

Direct trauma
Atherosclerosis
Immunological/infective inflammation of endothelium/endocardim
Endocardium after MI

341
Q

What can cause hypercoagulability?

A 
Post operative and post traumatic states
Genetic
Certain malignancies; eg: adenocarcinoma of pancreas
High oestrogen levels
- Peri-partum
- Oral contraceptives
Post myocardial infarction
Antiphospholipid Ab syndrome
Obesity
342
Q

What can cause changes in blood flow?

A

Turbulence; eg: aneurysm

Slowing

343
Q

What is gangrene?

A

Necrosis complicated by bacterial infection that eats dead organic matter = saprophytic

344
Q

What is primary gangrene?

A

Gas gangrene

345
Q

What is secondary gangrene?

A

Wet gangrene > complicating acute appendicitis/cholecystitis/infarction of small bowel
Dry gangrene > infarction of toes/foot/leg

346
Q

How does randomisation help to deal with confounding?

A

Aims to make treatment groups identical in all aspects other than intervention

347
Q

How is information bias dealt with?

A

Blinding - reduces preconceived ideas relating to intervention being undertaken

  • Single blind
  • Double blind
348
Q

What is intention to treat analysis?

A

Deals with selection bias
Assumes subjects remained in their randomised group, regardless of what they did in real life
Always underestimates any treatment effect

349
Q

What is survival analysis?

A

During follow up
Explicit capture of outcomes and their time of occurrence
Measures time to event
Usually plotted on the Kaplan-Meier curve

350
Q

What is the number needed to treat?

A

Number of people needed to undergo intervention in order to prevent outcome in one
Marker of efficiency of intervention

351
Q

How is the number needed to treat calculated?

A

1/absolute risk or rate reduction

352
Q

What is the number needed to treat affected by?

A

Relative effect

Underlying likelihood of outcome

353
Q

How does social gradient affect health?

A

Life expectancy shorter and disease more common down social ladder

354
Q

How does stress affect health?

A

Stressful circumstances and inability to cope damaging to health > can lead to premature death

355
Q

How does work affect health?

A

More control over work > better health

356
Q

How does unemployment affect health?

A

Job security increases health

357
Q

How does social support affect health?

A

Social support improves health

358
Q

How does food affect health?

A

Good diet and adequate food supply improve health

359
Q

What are the four stages of health transition?

A
  1. Age of pestilence and famine
  2. Age of receding pandemics
  3. Age of degenerative and man-made diseases
  4. Age of delayed degenerative diseases
360
Q

What are the most powerful class of diuretics?

A

Loop diuretics

361
Q

What is the mechanism of action of loop diuretics?

A

Acts on thick ascending limb of loop of Henle
Inhibits Na/K/2Cl carrier
Reduction in hypertonicity of blood > reduced water absorption into blood
Increased Na in distal tubule > increase osmotic pressure in tubule > reduced water reabsorption from tubule > torrential urine flow

362
Q

What are the pharmacokinetics of loop diuretics?

A

Well absorbed from gut
Plasma protein bound
Reaches site of action via secretion from blood into nephron
Duration = 3-6 hrs

363
Q

What are the adverse effects of loop diuretics?

A

K loss from distal tubule

H excretion > metabolic alkalosis

364
Q

What are the clinical uses of loop diuretics?

A 
Ion/water overload in
- Acute pulmonary oedema
- Chronic heart failure
- Ascites
- Renal failure
Hypertension
365
Q

What is the mechanism of action of thiazide diuretics?

A

Acts on distal tubules to inhibit Na/Cl co-transporter

366
Q

What are the adverse effects of thiazide diuretics?

A

K loss from collecting ducts

Increased plasma uric acid > gout

367
Q

What are the clinical uses of thiazide diuretics?

A

Hypertension

Severe resistant oedema - in combination with loop diuretic

368
Q

When are potassium sparing diuretics used?

A

In combination with K losing diuretics to prevent K loss in patients with heart failure

369
Q

How does spironolactone work?

A

K sparing diuretic
Competitive antagonist of aldosterone receptor > reduced activation of Na channels and reduced stimulation of Na pump synthesis

370
Q

How do amiloride and triamterene work?

A

K sparing diuretics

Block luminal Na channels in collecting tubules and ducts > inhibition of Na reabsorption and inhibition of K secretion

371
Q

What are osmotic diuretics?

A

Pharmacologically inert
Filtered but not reabsorbed
Exert osmotic pressure

372
Q

Where do osmotic diuretics work?

A

Water permeable part of nephron

  • Proximal tubules
  • Descending loop of Henle
  • Collecting tubules
373
Q

When are osmotic diuretics used?

A

Raised intracranial pressure
Raised intraocular pressure
Prevention of acute renal failure

374
Q

How does gentamicin cause renal toxicity?

A

In apical membrane of proximal tubule
Alters generation of 2nd messengers > altered intracellular Ca > impaired mitochondrial respiration > cell injury
Nephrotoxicity can impair excretion > further renal damage

375
Q

What are the three fates of cholesterol made in the liver?

A

Ester formation and storage in liver for export in VLDL
Bile acid formation
Incorporation into membranes

376
Q

Which lipoproteins contain the most cholesterol?

A

LDL then VLDL

377
Q

What is familial hypercholesterolaemia?

A

Inherited dominant disorder
Mutation in LDL receptor gene
Failure of LDL receptors to take LDL from circulation
Elevated circulatory LDL

378
Q

Describe the different areas supplied by the coronary arteries

A

Anterior and anterior 2/3 septum = left anterior descending territory
Lateral = lateral circumflex territory
Posterior/inferior and 1/3 septum = posterior descending artery/right coronary artery territory

379
Q

What does oxygen supply to the myocardium depend on?

A

Oxygen content of blood

Myocardial blood flow

380
Q

Which section of muscle is most susceptible to ischaemia, and why?

A

Subendocardial muscle because subjected to greatest pressure, potentiallly impairing blood flow

381
Q

How is oxygen supply increased during periods of exertion?

A

In normal state, myocardium removes almost as much oxygen from blood as possible
So vasodilation to increase blood flow to meet increased oxygen demand

382
Q

Define ischaemic heart disease

A

Group of conditions in which there’s an imbalance between myocardial oxygen supply and demand > myocardial hypoxia and accumulation of waste products

383
Q

Which conditions are included under the umbrella of ischaemic heart disease?

A 
Chronic coronary syndromes
- Stable angina
- Chronic cardiac failure
- Some arrhythmias
Acute coronary syndromes
- Unstable angina
- Sudden cardiac death
- Myocardial infarction
384
Q

Which part of coronary arteries does atherosclerosis primarily affect?

A

Epicardial parts

385
Q

How does atherosclerosis with stable plaque cause stable angina?

A

Chronic remodelling of vessel wall > fixed vessel stenosis and endothelial dysfunction > impaired release of vasodilators > inadequate vasodilation of smaller vessels > inability to increase flow during times of increased demand > stable angina

386
Q

What is an acute plaque event?

A

Ruptured plaque > blood exposed to subendothelial tissues > platelets activated by exposed collagen > vasoconstriction, primary haemostasis, secondary haemostasis > thrombus formation > acute narrowing of vessel lumen > acute ischaemia > acute coronary syndromes

387
Q

What is sudden cardiac death?

A

Unexpected fatal even occurring within 1 hour of beginning of symptoms/without symptoms in apparently healthy subjects/whose disease was not so severe as to predict such an outcome

388
Q

Desribe the progression of a myocardial infarction

A

ATP depletion > generation of ROS > altered Ca homeostasis > irreversible cell injury if continuing ischaemia

389
Q

What are the potential complications of a myocardial infarct after minutes to hours?

A

Damaged myocytes unstable > arrhythmia

Damaged myocytes can’t contract properly > cardiac failure

390
Q

What are the potential complications of a myocardial infarct after days?

A

Damaged myocytes unstable > arrhythmias
Damaged myocytes being destroyed > cardiac failure
Damaged wall isn’t moving normally > mural thrombus
Wall necrotic and weakened > rupture
Inflammatory mediators abound > fibrinous pericarditis

391
Q

How can the myocardial wall rupture?

A

Rupture of free ventricular wall > blood into pericardium = haemopericardium > compresses heart until it stops = cardiac tamponade
Rupture of papillary muscle > new onset murmur > mitral regurgitation > cardiac failure > acute severe cardiac failure = cardiogenic shock
Rupture of interventricular septum > new onset murmur > ventricular septal defect > cardiac failure > cardiogenic shock

392
Q

What are the potential complications of a myocardial infarct after weeks?

A

Damaged myocytes cleared, leaving islands of viable myocytes in healing tissue > arrhythmia
Damaged myocytes won’t be replaced > cardiac failure
Damged wall not moving normally > mural thrombus
Collagen deposition > wall strong again > flexible to wall stress > stretch > thin > bulge out > aneurysm > mural thrombus

393
Q

What are the potential complications of a myocardial infarct after months?

A

Arrhythmia
Cardiac failure
Aneurysm formed won’t regress - unlikely to rupture > mural thrombus

394
Q

What cellular changes occur in a myocardial infarct within 30 minutes?

A

Reversible ischaemia

395
Q

What cellular changes occur in a myocardial infarct within 12 hours?

A

Cell death and release of troponin

396
Q

What cellular changes occur in a myocardial infarct within 12-24 hours?

A

Necrosis

Start of acute inflammation

397
Q

What cellular changes occur in a myocardial infarct within 1-3 days?

A

Peak of acute inflammation

398
Q

What cellular changes occur in a myocardial infarct within 3-7 days?

A

End of acute inflammation
Start of repair by granulation tissue
Collage at 7 days

399
Q

What cellular changes occur in a myocardial infarct within 1-8 weeks?

A

Vascular granulation tissue > fibrous granulation tissue

400
Q

What cellular changes occur in a myocardial infarct after eight weeks?

A

Established fibrosis

401
Q

Outline the general treatment regime for dyslipidaemia

A

Establish fasting plasma lipid profile for diagnosis
Consider cardiovascular disease status and risk factors
Treat secondary causes
Manage modifiable risk factors

402
Q

What is the rate limiting step in cholesterol synthesis?

A

HMG-CoA > mevalonic acid by HMG-CoA reductase

403
Q

How does high cholesterol in the body lead to decreased endogenous cholesterol synthesis?

A

Negative feedback inhibits action of HMG-CoA reductase

404
Q

How does the body compensate in response to a decrease in endogenous cholesterol synthesis due to statin use?

A

Compensatory increase in hepatic LDL receptors > increased clearance of LDL from blood > decreased plasma total cholesterol and LDL > increased plasma HDL

405
Q

What is poor compliance to statins attributed to?

A

Perceived lack of efficacy due to no short term feeling of efficacy

406
Q

Why do serumu aminotransferases need to be measured every two to four months whillst on statins?

A

In case toxicity cause by drug-drug interactions

407
Q

Why might a patient on statins experience muscle pain?

A

Statin use can lead to minor increases in creatine kinase > breaks down muscle

408
Q

What are the adverse effects of statin use?

A 
Mild GI symptoms
Headache
Insomnia
Dizziness
Myopathy - rare
Hepatitis, liver failure - rare
Renal failure - rare
409
Q

What are the contraindications for statin use and why?

A

Pregnancy - impair foetal myelination

Infection, pre-surgery, post-trauma - drug-drug interactions

410
Q

What is the mechanism of action of bile acid sequestrants?

A

Bind bile acid > prevent gut reabsorption of cholesterol > increase in bile excretion > increased demand for cholesterol for bile acid synthesis > upregulation of hepatic LDL receptors > removal of LDL from plasma > more cholesterol metabolism

411
Q

What are the adverse effect of bile acid resins?

A 
Abdominal discomfort
Bloating
Constipation
Flatulence
Steatorrhoea
Decreases absorption of other drugs as not very specific
412
Q

What is the mechanism of action of ezetimibe?

A

Acts as sterol transporter to intestine > inhibit cholesterol absorption from intestine

413
Q

Why does ezetimibe not affect absorption of bile acids and fat soluble vitamins?

A

Extremely specific

414
Q

What is the mechanism of action of niacin?

A

Unclear

Normally used in combinations, usually after other combinations have been ineffective

415
Q

How does hiacin decrease the effects of atherosclerosis?

A

Decreases secretion of VLDL from liver
Reduces plasma LDL and triglycerides
Increases HDL
Lowers potentially atherogenic lipoprotein A

416
Q

What are the adverse effects of niacin use?

A 
Vasodilation
- Flushing
Hypotension
Nausea
Vomiting
417
Q

What is the mechanism of action of fibrates?

A

Agonist at nuclear receptors > regulates gene expression to increase synthesis of lipoprotein lipase > increased breakdwon of triglycerides

418
Q

What precautions must be taken when administering fibrates?

A

Mild elevation of serum aminotransferases

Monitor at 3 month intervals

419
Q

What are the common adverse effects of fibrate use?

A

Nausea
Dry mouth
Headache
Rash

420
Q

How does orlistat act to reduce blood triglyceride levels?

A

Lipase inhibitor > triglycerides excreted undigested

421
Q

Why does most of coronary perfusion occur in diastole?

A

During systole coronary arteries compressed

422
Q

What are the aims of stable angina treatment?

A

Prevent attacks
Relieve symptoms
Prevent progression to myocardial infarct

423
Q

What is the mechanism of action of nitrates?

A

Biotransformation > releases nitric oxide > vascular relaxation

424
Q

Where do nitrates act?

A

Mainly in veins to decrease preload

Also in large arteries to decrease afterload

425
Q

What is glyceryl trinitrate (GTN)?

A

Short acting nitrate
Given sublingually
- IV for emergency

426
Q

What is isosorbide dinitrate?

A 
Longer accting nitrate
Given orally 
For
- Anticipation of effort
- Prophylaxis
427
Q

What are the adverse effects of nitrate use?

A

Postural hypotension
Headache
Flushing
Reflex tachycardia

428
Q

What is the selectivity of verapamil?

A

1:1 vascular:cardiac selectivity
Can’t be used during heart failure
Can be used for angina and hypertension

429
Q

What is the selectivity of diltiazem and nifedipine?

A

Vascular selective
Used in angina and hypertension
Can also be used during heart failure

430
Q

What is the mechanism of action of calcium channel blockers in the use of ischaemic heart disease?

A

Blocks Ca entry into heart through L-type channels > decreased HR > increased filling time > increased preload > decreased contractility > decreased cardiac output > reduced oxygen demand
Vascular selective: blocks Ca entry into muscle cells of vessels > arterial dilation > reducd afterload

431
Q

What are the adverse effects of calcium channel blockers in angina?

A 
Flushing
Headache
Oedema
Nifedipine: hypotension
Verapimil: bradycardia, atrioventricular block
432
Q

How do atenolol and propanolol differ?

A

Atenolol cardio-selective beta1-adrenoceptor antagonist

Propanolol non-selective beta-blocker

433
Q

How does ivabradine work?

A

Blocks If > inhibits Na into cell > decreased velocity of diastolic depolarisation

434
Q

What are the indications for ivabradine use?

A

Patients with

  • Ischaemic heart disease
  • Left ventricular dysfunction, and
  • Heart rate of >70 bpm
435
Q

What are the adverse effects of ivabradine?

A

Brightness in visula field

Conduction abnormalities

436
Q

How is variant angina treated?

A

Relieve coronary spasm with short acting nitrate

Prophylaxis with vascular selective Ca channel blocker

437
Q

How is unstable angina treated?

A

Same as with stable angina

Aspiring to prevent thrombosis

438
Q

What are the methods of antimicrobial testing?

A 
Dilution methods
- Minimum inhibitory concentration
Diffusion methods
- Disc susceptibility test
E-test strips combine disc susceptibility test and minimum inhibitory concentration
439
Q

What is the rationale for using antibiotic combinations?

A

Temporary measure in ill patient
Delay emergence of resistance
Treat mixed infections
Achieve synergistic effect

440
Q

What are the mechanisms of synergy?

A

Block sequential steps of metabolic pathway
Inhibits enzymatic degradation
Enhance antimicrobial uptake by bacterial cell

441
Q

What are Jawetz’s laws of antibiotic synergy?

A

Bacteriostatic bacteriostatic = additive/indifferent
Bacteriostatic + bactericidal = antagonistic
Bactericidal + bactericidal = synergistic

442
Q

What did the Whitehall study show in relation to employment and increased risk of death from cardiovascular disease?

A

Lower employment grde associated with increased risk of death from cardiovascular disease

443
Q

What was attributed to the higher risk of mortality with a lower employment grade being because of?

A

60% - chronic stress related to lack of control within job
Lower income > decreased access to healthcare
Poorer diet
Less education
Smoking
Obesity
Less leisure time

444
Q

What are the two determinants of the psycho-biological stress response?

A

Stressors

Resistance/vulnerability factors

445
Q

Describe the formation of an X-ray image

A

Image = shadown on detector
X-ray hits detector > converts sliver-halide crystals to silver
More x-rays hit detector > blacker image

446
Q

Describe the concept of e-densities

A

How many x-rays get through an object dependent on electron density of object

447
Q

List the order of e-densities of different objects, from lowest (black) to highest (white)

A 
Air
Fat
Soft tissue
Bone
Contrast agents
Metal
448
Q

What is a silhouette sign?

A

Interface only seen if tissues of differing e-densities next to each other
Will produce silhouette sign

449
Q

Why is an erect P-A chest x-ray performed under full inspiration?

A

Lung fulll of air > good silhouette for other structures

450
Q

Why are chest x-rays usually perfromed in the P-A direction?

A

Heart closer to fil and less magnified - edges of heart less blurred
Patient instructed to hug x-ray cassette so scapulae moved away from chest wall

451
Q

Why are chest x-rays usually performed with the patient in the erect position?

A

Blood flow distribution in lungs can be assessed
Vessels nearer lung base larger than vessels more superior
Easier to see pleural effusions

452
Q

In left heart failure, how do the vessels in a chest x-ray look different than normal?

A

Pulmonary vascular redistribution

- Pulmonary vessels near hilum and apex become larger and more dilated due to congestion

453
Q

Why does hypertrophy occur?

A

Increased functional demand/stimulation by hormonal or growth factors

454
Q

What happens to cellular components during atrophy?

A

Cells decrease in size and activity
Removed by autophagy
Apoptosis

455
Q

When does atrophy become irreversible?

A

Cell loss and associated fibrosis

456
Q

What is involution?

A

Physiological atrophy involving apoptosis

457
Q

Define metaplasia

A

Change from one fully differentiated mature cell type to another - better able to withstand new environmental conditions

458
Q

What is the mechanism underlying cell metaplasia?

A

Cytokine/growth factor driven reprogramming of line of differentiation

459
Q

What are the causes of disturbed valve function?

A 
Congenital abnormalities
Myxomatous mitral valve
Degenerative changes due to calcifcation
Inflammatory
- Infection
- Immune mediated
460
Q

What are the possible complications of valve replacements?

A

Porcine valves susceptible to infective endocarditis
Prosthetic mechanical valves predispose to thrmobosis of valve
- Need to take anticoagulant drugs to prevent thrombosis

461
Q

Why does concentric hypertrophy develop?

A

Increased afterlad
Preserves systolic function temporarily
Ultimately thickened myocardium > impaired perfusion > ischaemia

462
Q

Why does eccentric hypertrophy develop?

A

Volume loads
Aids function up to a point
Predisposes myocardium to ischaemia

463
Q

What happens as myocardial hypertrophy worsens?

A 
Decompensation
Microscopically
- Fibrosis
- Apoptosis
Dilates > increased end diastolic volume

MD1 Revision (9 decks)

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