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Phase 1 - S2 Cardiovasular System > Clinical Conditions > Flashcards

Clinical Conditions Flashcards

1
Q

What heart murmur is heard in aortic stenosis

A

Systolic

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2
Q

What heart murmur is heard in aortic Regurgitation

A

Diastolic

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3
Q

What heart murmur is heard in mitral stenosis

A

Diastolic

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4
Q

What heart murmur is heard in mitral Regurgitation

A

Systolic

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5
Q

What causes aortic stenosis

A

Fibrosis, calcification, congenital (bicuspid), rheumatic fever

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6
Q

What causes mitral stenosis

A

Rheumatic fever or valve fusion

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7
Q

What causes aortic Regurgitation

A

Aortic root dilation, rheumatic fever

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8
Q

What causes mitral valve be Regurgitation

A

Weakening of the tissue, MI damaging papillary muscles, rheumatic fever, fibrosis, LV dilation

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9
Q

What can be seen due to a bounding pulse

A

Quinke’s sign and head bobbing

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10
Q

What happens to the blood viscosity in multiple myeloma and what does this result in

A

It increases giving slugging in the peripheries as its harder for the heart to pump the blood

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11
Q

Give some examples of acute phase proteins

A

CRP, complement factors, fibrinogen, ferritin

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12
Q

What are the acyanotic heart defects

A

PDA, atrial septum defect, ventricular septum defect, coarctation of the aorta

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13
Q

What is coarctation of the aorta

A

Narrowing of the aorta

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14
Q

What is PDA

A

Patent ductus arteriosus - hen the ductus arteriosus doesn’t close so blood flows from the aorta to the pulmonary artery

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15
Q

What does atrial septum defect result in

A

An increase in blood flow to the RA giving right heart failure due to pulmonary hypertension

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16
Q

What is the most common heart defect

A

Ventricular septum defect

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17
Q

What are the cyanotic heart defects

A

Hypoplastic left heart syndrome, transposition of the great arteries, tetralogy of fallot, tricuspid atresia and pulmonary atresia

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18
Q

What is hypoplastic left heart syndrome

A

Underdevelopment of the left side of the heart

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19
Q

Why is transposition of the great arteries not fatal during pregnancy

A

As the shunts mean that oxygenated blood is still circulated around the body

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20
Q

What are the 4 features of tetralogy of fallot

A

Overriding aorta, pulmonary artery stenosis, ventricular septum defect and RV hypertrophy

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21
Q

What is tricuspid atresia

A

When there no passage between RA and RV so the RV is underdeveloped

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22
Q

What is pulmonary atresia

A

No RV outlet so blood flow back through the RA to LA

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23
Q

How does the electrical activity of ventricular myocytes change in hyperkalaemia

A

The membrane potential is more positive, this inactivates more sodium Channels so there is also a slower upstroke

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24
Q

What is used to treat hyperkalaemia

A

Calcium gluconate with glucose

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25
Q

How does the electrical activity of ventricular myocytes change with hypokalaemia

A

The action potential lengthens giving delayed depolarisations

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26
Q

What type of drug is propranolol

A

Beta blocker

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27
Q

What drugs are used in hypertension

A

ACE inhibitors, calcium blockers, beta blockers, alpha blockers, diuretics

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28
Q

What blood pressure is classed as hypertension

A

140/90

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29
Q

What is essential hypertension

A

An unknown causes for the rise in bp

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30
Q

What is secondary hypertension

A

When there is a known cause for hypertension e.g. Renovascular disease, conn’s syndrome, Cushing’s syndrome, phaechromocytoma

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31
Q

What causes cardiogenic shock

A

MI, arrthymias, heart failure

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32
Q

What is cardiogenic shock

A

When the ventricles cant empty properly

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33
Q

What is mechanical shock

A

Where the ventricles cant fill properly

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34
Q

What causes mechanical shock

A

PE, cardiac tamponande

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35
Q

What is distributive shock

A

Excessive vasodilation causing a fall in TPR

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36
Q

What causes distributive shock

A

Anaphylactic shock or septic shock

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37
Q

What is hypovoleamic shock

A

Where there is reduced blood volume so a lower CO

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38
Q

What causes hypovoleamic shoc k

A

Haemorrhage, burns, vomiting, diarrhoea

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39
Q

How long should the PR interval be

A

0.12 - 0.2 seconds

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40
Q

How long should the QRS complex be

A

0.12 seconds

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41
Q

What does a long QT interval mean

A

The ventricles are taking longer to repolarise

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42
Q

What does a longer QRS complex mean

A

The ventricles are taking longer to depolarise - so the normal depolarisation route (His - Purkinjie system) may not being used

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43
Q

What is sinus rhythm

A

Where every p wave is followed by a QRS complex, with a normal heart rate

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44
Q

How is first degree heart block seen

A

Prolonged PR interval

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45
Q

How is second degree heart block (Mobitz type 1) seen

A

Increasing prolonged PR interval until a QRS complex is suddenly dropped

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46
Q

How does second degree heart block (Mobitz type 2) present on an ECG

A

Normal PR interval with a QRS complex suddenly dropped

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47
Q

How is third degree heart block seen on an ECG

A

No coordinated contractions of the atria and ventricles. Usually shows a wider QRS complex as the ventricular escape rhythm takes

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48
Q

What is heart block

A

Slower/failure of conduction between the atria and ventricles via the AVN

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49
Q

What is a superventricular rhythm

A

Where the heart rhythm results from the SAN, AVN or ectopic atrial sites

50
Q

What is a STEMI

A

Where there is complete occlusion of a coronary artery resulting in an MI giving ST elevation on an ECG

51
Q

What is an NSTEMI

A

Where there is a large occlusion of a coronary artery resulting in ST depression on an ECG

52
Q

How does angina show on an ECG

A

ST depression

53
Q

How can you tell the difference between an NSTEMI and angina

A

An NSTEMI with show troponin on a blood test but angina wont as there’s no cell death

54
Q

How does high potassium affect an ECG trace

A

Gives a high T wave which leads to ventricular fibrillation

55
Q

What doe slow potassium look like on an ECG

A

Low T wave

56
Q

Weeks after an MI what is seen on an ECG

A

Pathological Q wave

57
Q

Describe the appearance of a pathological Q wave

A

1/4 the height of the R wave and 2 small squares tall

58
Q

What are the cardiac causes of chest pain

A

Ischaemia, pericarditis

59
Q

describe ischaemic chest pain

A

dull, retrosternal which may radiate to the neck, jaw and shoulders

60
Q

is ischaemic pain visceral or somatic pain

A

visceral

61
Q

describe chest pain caused by pericarditis

A

sharp, retrosternal which is worse coughing/inhaling but better sitting up

62
Q

what is heard on auscultation in pericarditis

A

coarse noise called the pericardial rub

63
Q

what is seen on an ECG in pericarditis

A

elevated, saddle shaped ST

64
Q

what are the respiratory causes of chest pain

A

pneumonia and PE

65
Q

describe chest pain caused by pneumonia

A

pain is to the sides of the chest

66
Q

is chest pain caused by pneumonia somatic or visceral pain

A

somatic as the irregular surfaces of the infection rub on the pleural sacs

67
Q

describe chest pain caused by PE

A

sharp, well localised pain

worse on inspiration

68
Q

describe chest pain caused by acid reflux

A

the acid from the stomach running up the oesophagus gives a centralised burning pain which is made worse lying down or eating certain foods

69
Q

what are musculoskeletal causes of chest pain

A

rib fracture or costochondritis

70
Q

what is costochondritis

A

inflammation of the costal cartilages giving a sharp, localised pain which hurts on palpating and breathing in

71
Q

what is radiating pain

A

pain that starts in one place and moves around

72
Q

what is referred pain

A

when pain is experienced somewhere away from the site of origin. the afferent pain signals are sent to the brain but these get mixed with the signals from the dermatomes T1-4 and so the efferent signals are sent down these pathways

73
Q

what is percutaneous coronary intervention

A

when a balloon is inserted into the coronary artery via the femoral or radial artery. the balloon is then inflated and this crushes the plaque into the artery walls. a metal stent then keeps the artery dilated

74
Q

what is acute coronary syndrome

A

when there is a sudden reduction of blood flow to the heart

75
Q

why cant stable angina be a cause of acute coronary syndrome

A

as stable angina occurs over time and cant suddenly cut off the blood supply

76
Q

what is the difference between a STEMI and NSTEMI

A

STEMI is when the artery is fully occluded causing infarction whereas an NSTEMI is where the plaque occludes most of the artery

77
Q

how can you tell the difference between an NSTEMI and unstable angina

A

troponin is released during an NSTEMI as there is infarction

78
Q

what is stable angina

A

ischaemia occurring during exercise as the blood demand of the heart increases however the occlusion of the artery doesn’t allow enough blood to reach the heart

79
Q

what will help relieve symptoms of stable angina

A

GTN spray

80
Q

what is used to treat stable angina

A

aspirin, beta blockers, statins, ACE inhibitors, CABG

81
Q

what is heart failure

A

a state in which the heart fails to maintain an adequate circulation for the needs of the body

82
Q

give some causes of heart failure

A

ischaemic heart disease, hypertension, valve disease, alcohol, amyloidosis

83
Q

what are the clinical features of left heart failure

A

dyspnoea, orthopnoea, pulmonary oedema, tachycardia

84
Q

why do you get pulmonary oedema in left heart failure

A

the left side of the heart cant pump blood out so it bacs up into the lungs increasing the pressure in the vessels in the lungs so more fluid passes out

85
Q

why can you cough up blood in left heart failure

A

the increase pressure in the lungs damages the capillaries

86
Q

what are the systolic causes of left heart failure

A

ischaemia, hypertension (hypertrophy results in ischaemia due to lack of blood supply), dilated cardiomyopathy (dilation of the muscle as it was hypertrophic but this couldn’t be sustained)

87
Q

what are the diastolic causes of left heart failure

A

hypertrophy leads to a smaller volume in the ventricles, or the walls are less compliant

88
Q

what are the features of right heart failure

A

jugular venous distension, systemic oedema, fatigue, dyspnoea, ascites and hepatosplenomegaly

89
Q

why is ascites and hepatosplenomegaly seen in right heart failure

A

the oedema surrounds the organs and enlarges them as well as fluid entering the peritoneal cavity

90
Q

what causes right heart failure

A

secondary to left heart failure

chronic lung disease

91
Q

what is cor pulmonale

A

chronic lung disease causing right heart failure due to an increased vascular resistance due to vasoconstriction to prevent perfusion of the alveoli which are no longer ventilated

92
Q

what is left ventricular systolic dysfunction

A

this is systolic left heart failure where there is reduced LV output despite less LV capacity

93
Q

what is heart failure with preserved ejection fraction

A

left sided diastolic heart failure

this is where there is reduced cardiac output but normal ejection fraction

94
Q

what is a palpitation

A

noticeably rapid, strong or irregular heartbeat

95
Q

what neuro-humoral activation is activated by heart failure

A
  • sympathetic nervous system
  • RAAS
  • natriuretic hormones
  • ADH
  • bradykinin
96
Q

what is given to patients with angina

A
  • beta blockers
  • calcium blockers
  • organic nitrates (GTN spray)
97
Q

how do organic nitrates work?

A

they produce organic nitrates which are venodilators lowering the preload as the heart fills less reducing the force of contraction needed

98
Q

name 3 anti-thrombic drugs

A

heparin, warfarin, aspirin

99
Q

what conditions increase the risk of thrombus formation

A

atrial fibrillation, MI, prosthetic heart valves

100
Q

what is adenosine used to treat

A

supraventricular tachycardias

101
Q

how does adenosine work

A

acts on alpha 1 to enhance potassium conductance

102
Q

what is used to treat heart failure

A

cardiac glycosides, beta agonists, ACE inhibitors

103
Q

how do cardiac glycosides work and name one

A

digoxin. they block Na/K/ATPases causing an increase in intracellular sodium causing the NCX to slow down. this means less calcium is pumped out of the cell so more is stored in the SER increasing the force of contraction.

104
Q

what drug is used in heart failure with AF

A

cardiac glycosides

105
Q

what are the 4 classes of anti-arrhythmic drugs

A
  • sodium channel blockers
  • beta blockers
  • potassium channel blockers
  • calcium channel blockers
106
Q

give an example of a beta agonist

A

dobutamine

107
Q

give an example of a potassium channel blocker

A

amiodrane

108
Q

give an example of a beta blocker

A

propranolol

109
Q

give an example of a sodium channel blocker nd describe how it works

A

lidocaine. they blocker sodium channels during depolarisation to prevent the channels being activated again too soon and then dissociate in time for repolarisation

110
Q

what types of arrhythmias are there

A

bradycardia, tachycardia, atrial flutter, atrial fibrillation, ventricular fibrillation

111
Q

what are the causes of tachycardia

A

ectopic pacemaker activity, after depolarisations, re-enter loops

112
Q

what are the causes of bradycardia

A

sinus bradycardia and conduction block

113
Q

what is acute peripheral atrial disease

A

sudden blockage of an artery causing ischaemia

114
Q

amputation will need to occur how long after acute peripheral arterial disease if the ischemia is not reversed

A

6 hours

115
Q

what are the symptoms of acute peripheral arterial disease

A

6 P’s (pain, paralysis, perishing cold, paraesthesia, pulseless, pallor)

116
Q

what is chronic peripheral arterial disease

A

slow narrowing of an artery giving rise to collateral circulation over time

117
Q

what are the symptoms of chronic peripheral arterial disease

A
  • possibly non if the collateral circulation Is sufficient
  • intermittent claudication
  • rest pain
  • ulceration
118
Q

when is rest pain worsened and how is this relieved

A

lying in bed its worsened as gravity can no longer help bring blood to the foot and heat increases the metabolic rate so hanging the foot out of bed helps

119
Q

true or false: ischemia can result from thyrotoxicosis

A

true - there is an increased metabolic rate so the person become tachycardic but as the coronary arteries fill in diastole it means the heart receives less oxygen

120
Q

what are the pulses you can feel in the leg

A
  • dorsalis pedis
  • femoral
  • popliteal
  • posterior tibial artery
121
Q

what are varicose veins

A

veins with incompentant valves as the walls of the veins are weak and become dilated separating the valves

122
Q

what are the complications of varicose veins

A

haemorrhage, thrombophlebitis (inflammatory response), oedema, skin pigmentation, lipodermatosclerosis, ulceration

Phase 1 - S2 Cardiovasular System (16 decks)

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