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Year 1 Medicine Newcastle > Case 2 > Flashcards

Case 2 Flashcards

1
Q

Pathogenesis

A

The way a disease develops

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2
Q

Syncope

A

Fainting or passing out caused by the temporary drop in the amount of blood that flows to the brain

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3
Q

Epidermis

A

The outermost layer of skin tat acts as a barrier to the outside world

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4
Q

parasympathetic innervation

A

Slowing of the heart rate by the vagus nerve

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5
Q

Atrophy

A

Decrease in size and number of cells within a tissue or organ

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6
Q

Ischaemia

A

Reduction in blood flow to a specific organ or tissue

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7
Q

Hypertrophy

A

A large increase in cell size to increase tissue or organ size

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8
Q

Hyperplasia

A

A large increase in cell number to increase the tissue or organ size

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9
Q

Metaplasia

A

a reversible change in which a differentiated cell type is exchanged for another

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10
Q

Mesenchymal Stem cells

A

stem cells found in the connective tissue

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11
Q

Hypoxia

A

Reduced oxygen delivery to the tissues

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12
Q

Hypoxaemia

A

reduced p.p of oxygen in the blood

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13
Q

What are the requirements of a cell to function properly

A 
Internal Homeostasis
Constant Energy Supply
Controlled cell division
Intact Plasma membrane
Safe and effective function of cellular activities 
Genomic integrity
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14
Q

What restricts a cell from functioning properly

A 
Failure of membrane functional integrity (Damage to ion pumps, bacterial toxins)
Membrane damage (free radicals)
Blockage of metabolic pathways (interruption of proteins synthesis, respiratory poisons, hormone factor lack)
DNA damage or loss (Ionising radiation, chemo, free radicals)
Mechanical disruption (Trauma, Osmotic pressure)
Energy failure (Oxygen or glucose lack, mitochondrial failure)
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15
Q

What are the consequences of anaerobic respiration in a cell

A

This results in a build up of acid through metabolic acidosis that denatures proteins

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16
Q

Free Radicals

A

Chemical radicals characterised by a single unpaired electron in the outer shell and are highly reactive

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17
Q

hat happens in a paracetamol overdose

A

Paracetamol contains free radicals that are usually removed but in this case damage hepatocytes (cells in the liver) and can cause chemical hepatitis

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18
Q

Necrosis

A

the pathological cell or tissue death in a living organism resulting in an inflammatory response

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19
Q

Coagulative necrosis

A

Cell death caused by ischaemia in any organ except the brain

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20
Q

infarction

A

Obstruction of the blood to an organ or tissue and resulting in localised cell death of that tissue

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21
Q

Liquefactive necrosis

A

Where necrotic tissue liquefies and hydrolytic enzymes leak from the dead cells

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22
Q

Gangrene

A

Necrosis when there is visible decay of tissue

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23
Q

Fibrinoid necrosis

A

When small blood vessels are under extreme pressure that results in necrosis of the muscle wall and seepage of plasma into these wall deposits

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24
Q

Fat necrosis

A

occurs in the pancreatitis release of lipases or in the breast due to direct trauma to adipose tissues

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25
Q

Apoptosis

A

The falling off of cells- doesn’t produce an inflammatory response

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26
Q

pyknosis

A

The shrinkage of the nucleus in a necrotic cell

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27
Q

Karyorrhexis

A

The fragmentation of nuclear material

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28
Q

Dysplasia

A

Increased cell proliferation, abnormal morphology and decreased differentiation

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29
Q

Dystrophic calcification

A

The calcification of necrotic or degenerative cells anywhere in the body

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30
Q

Metastatic calcification

A

The deposition of calcium in otherwise healthy tissues due to elevated levels of calcium

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31
Q

isovolumetric contraction

A

An increase in pressure with no change of volume

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32
Q

What ion initiates an impact in cardiac myocytes?

A

An influx of Ca2+

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33
Q

What ion movement occurs on the downward slope of an action potential in a myocardial cell

A

The closure of Ca 2+ alongside a delayed release of K+ ions

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34
Q

What happens between action potentials in myocardial cells

A

There is an influx of Na+ to pacemaker cells

The Ca2+ channels recover from activation

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35
Q

What is different in the shape of an action potential in a ventricular myocyte

A

the downwards slope has a bump in it where there are Ca2+ channels opening to maintain the action potential despite an efflux of K+ and Na+ from the myocytes

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36
Q

What effect does the sympathetic nervous system have on heart rate

A

Increases heart rate by releasing noradrenaline

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37
Q

What effect does the parasympathetic nervous system have and why?

A

It releases Ach which decreases the opening of Na+ channels and increases K+ channels so more K+ leaves the cell whilst less Na+ enters
This hyperpolarises the membrane and results in longer refractory periods

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38
Q

What is the parasympathetic nerve of the heart and how does it affect heart rate?

A

Vagus nerve- slows it down

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39
Q

Venous return

A

The volume of blood returning to the heart

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40
Q

Cardiac Output

A

The volume of blood pumped per minute- average around 5L

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41
Q

Preload

A

The degree of stretch as a result of the ventricles filling up with blood

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42
Q

Ejection fraction

A

The percentage of blood that is pumped in comparison to the initial preload

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43
Q

What changes occur in the heart in a response to heavy exercise

A

Increased cardiac output
Increased atrial booster pump action to increase venous return by more forceful atria contraction and a shorter diastole period
Increased ventricular suction
increased myocardial contractility and sympathetic response to increase HR

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44
Q

What are the good lipids- HDL or LDL

A

HDL

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45
Q

What is Starling’s law of the heart

A

The initial fibre length in diastole is proportional to the force of contraction
More venous return means higher end diastolic volume
So the muscle must stretch and increase contractility in order to counter this

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46
Q

What controls homeometric (extrinsic) factors of the heart and how

A

The sympathetic nervous system- by increasing the contractility of the heart without increasing fibre length through increasing Ca2+ conc.

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47
Q

Infarction

A

An insufficient blood supply carrying oxygen and metabolic needs leading to cell of tissue necrosis

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48
Q

Atheroma

A

A fatty deposit of the inner lining of the blood vessel wall and can cause an ischaemia

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49
Q

thrombosis

A

a local clot formation as a result of a thrombus

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50
Q

embolus

A

A local clot being carried elsewhere in the body

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51
Q

Spasms

A

Contractions of the muscle within blood vessels

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52
Q

What makes tissues more susceptible to ischaemias?

A

Previous damage
a single blood supply source
Brain and heart tissues more susceptible

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53
Q

How can non-vascular ischaemias occur

A

a decrease in deoxygenated blood flow from hypotension, carbaminohaemoglobin or anaemia
Or increased tissue demand

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54
Q

What are myocardial infarctions

A

A sudden rupture of fatty deposits within the coronary arteries

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55
Q

How can an blocking of the coronary arteries result in myocardial problems

A

Usually through an atheroma
Less blood therefore less ATP and acidic build up
Fewer Na+ and Ca2+ move out so less water moves out with them and cell oedema can occur
necrosis begins to occur and rapid action needs to be taken to reverse this process
If not reversed the cells are replaced with scar tissue which is much less adapted to it’s function and structually weaker
Build up of lactate and serotonin activates pain receptors in the chest
After an episode can create stunned myocardium that doesn’t contract as well but will recover if a small enough area

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56
Q

Modifiable risk factors of ischaemic heart disease

A 
Smoking
Diet
Reduced physical activity 
Overweight/obesity 
High blood pressure 
High cholesterol levels 
Excessive alcohol consumption 
Excessive stree
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57
Q

Non-modifiable risk factors of ischaemic heart disease

A 
Increasing age
Gender- male (prior to age 60)
Ethnicity (South Asians)
Family history 
Social deprivation
Type 2 diabetes
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58
Q

chronic ischaemic heart disease

A

slow progressing heart disease due to the atherosclerosis of arteries over time
Angina is a symptom

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59
Q

Acute coronary syndrome

A

Rapid plaque distribution that leads to occlusion of the coronary arteries

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60
Q

Stable angina

A

The most common presentation of angina
narrowed coronary arteries due to atherosclerotic plaques
the heart doesn’t receive enough oxygen during exercise to match the workload
there is then a build up of metabolites that leads to chest pain that is gripping in nature and may radiate to the arms or jaw
breathlessness alongside palpitations may occur
normally relieved by rest or nitroglycerides

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61
Q

Variant angina

A

More often in females than males
Spasm of the coronary arteries
can occur without provocation and results in the heart not getting enough blood, even at rest
there is then a build up of metabolites that leads to chest pain that is gripping in nature and may radiate to the arms or jaw
breathlessness alongside palpitations may occur

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62
Q

silent angina

A

same pathophysiology as other forms of angina except there is no chest pain or symptoms
possibly as a result of low pain levels or damaged nerves

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63
Q

How is angina managed and treated?

A

Lifestyle modifications such as stopping smoking, exercising and eating healthy
taking medications that dilate vessels, slow heart rate or reduce heart contractility
A stent or bypass graft can surgically deal with it

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64
Q

Acute coronary syndrome

A

An umbrella term for unstable angina, Non-ST elevation myocardial infarctions and ST elevation myocardial infarctions
they are all caused by acute disruption of coronary plaque that leads to sudden artery occlusion via platelet aggression

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65
Q

Which acute coronary artery syndrome has complete occlusion?

A

STEMIs

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66
Q

what are the symptoms of acute coronary syndrome

A

Central chest pain, dyspnoea and nausea although not all have chest pain and silent MIs may occur
they may also present with pre-snycope and may look pale and clammy

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67
Q

What would the blood marker of troponin T show in the coronary arteries during acute coronary syndrome?

A

there would be a significant rise for STEMIs and NSTEMIs but not unstable angina as there is no myocardial necrosis

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68
Q

What would an ECG show for a STEMI?

A

an ST elevation

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69
Q

What is immediate management for acute coronary syndrome?

A

Oxygen, a vasodilator and analgesia

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70
Q

How can you manage acute coronary syndrome in the long term?

A

Lifestyle changes and medications in a similar way to angina

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71
Q

What is the acronym for the complications that need to be addressed following an MI?

A 
D eath
A rrhythmias 
R upture of ventricular septum 
T amponade-fluid accumulation
H eart failure- damage or necrosis of muscle 
V alve disease- mitral regurgitation 
A neurysm of the ventricle 
D Dressler's syndrome (percarditis)
Thrombo E mbolism- mural thrombus 
R eccurence
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72
Q

How long is each large square on an ECG?

A

200ms

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73
Q

How long is each tiny square on an ECG?

A

40ms

74
Q

How many large squares constitute a second on an ECG?

A

5

75
Q

What are the first two things you should be looking at on an ECG?

A

Rate and rhythm

76
Q

What should the heart rate be and ho do you classify it if not?

A

Should be between 60-100

<60 is bradycardia and 100< is tachycardia

77
Q

How do you work out the rate?

A

300 divided by the number of large boxes between R waves

78
Q

What is sinus arrhythmia

A

This is an irregularity in heart rate due to the fact that, when you breathe in, the heart rate increases

79
Q

What is an ectopic beat?

A

The sensation of skipping a heart beat due to a premature beat

80
Q

What occurs in the heart to produce a P wave?

A

Atrial depolarisation

81
Q

What occurs in the heart during the QRS complex?

A

Ventricular depolarisation

82
Q

What occurs in the heart during T waves?

A

Ventricular repolarisation

83
Q

Where is the PR interval and what does it show if it is longer?

A

Beginning of the P wave to the beginning of the QRS complex

If it is longer than 200ms then it could suggest AV nodal damage

84
Q

How wide is a normal QRS interval?

A

70-100ms

85
Q

What does a narrow QRS interval suggest and how does the P wave help is in determining which one?

A 
A supraventricular problem-
SAN problem (normal P wave)
Atrial problem (abnormal fluttery P wave)
AV node/ junction problem (No P wave or abnormal short PR interval)
86
Q

What does a wide QRS complex suggest the problem is?

A

A problem of ventricular origin

87
Q

What does the ST segment suggest?

A

An abnormal ST segment can be an indicator of MI

88
Q

Where is the ST segment?

A

From the end of the QRS complex to the beginning of the T wave

89
Q

How is the QT interval measured?

A

The time between the beginning of the QRS complex and the end of the T wave

90
Q

What does an abnormal QT interval suggest?

A

Electrical instability

91
Q

How can you classify each level of heart block on an ECG?

A

First- slight AV nodal damage and lengthened PR interval
Second- Occasionally missing QRS complexes
Third- No correlation between P wave and QRS complex as AV node is dead

92
Q

How does AF show on an ECG?

A

No P waves and irregular rhythm

93
Q

Hypovolaemic shock

A

When an individual loses more than a fifth of their blood

94
Q

Cardiogenic shock

A

Mechanical or electrical failures of the ventricles that physically compresses the heart to reduce cardiac function

95
Q

Septic shock

A

Blood pressure drops as bacterial toxins increase vasodilation

96
Q

Anaphylactic shock

A

Exaggerated immune response

97
Q

What are symptoms of shock?

A 
Anxious, tired, apathy or exhaustion
Intense thirst 
Decreased arterial systolic, diastolic and pulse pressures with a rapid and weak pulse 
Physically collapsed veins 
Pale or cold with moist skin
98
Q

What can occur if the compensatory mechanisms against shock don’t work effectively?

A

Refractory shock- irreversible shock that ensues death

99
Q

How can hypovolaemic shock occur?

A

It may be caused by a haemorrhage, blood plasma loss due to burns or severe fluid loss through things such as vomiting or diarrhoea

100
Q

What occurs in the body in severe cases of shock?

A 
Brain- confused/anxious
Heart rate- >140bpm
respiration rate- >35/min
Negligible urine production
Major decrease in BP and pulse pressure
101
Q

How are compensatory mechanisms initiated in a response to haemorrage?

A

There is a decreased venous return and cardiac output
the arterial BP also falls
This is sensed by venous and atrial receptors that decrease baroreceptor firing rates alongside chemoreceptors
This increases sympathetic activity

102
Q

What does increased sympathetic activity result in in a response to shock?

A

Increased vasoconstriction of arteries and veins
Increased HR
Increased cardiac contractility
Increased stimulation of the renin-angiotensin system in the kidney to decrease urine formation and maintain arterial pressure

103
Q

Autotransfusion

A

A compensatory mechanism for shock where up to 500ml of fluid may move from the interstitium into the circulation following a severe haemorrhage

104
Q

How does autotransfusion occur?

A

The drop in capillary presure causes the movement of fluid
The increase in sympathetic activity brought on by the baro and chemo receptors in response to shock results in the liver undergoing glyconeogenesis to increase the plasma and interstitial osmolarity in order to move water from the interstitial space into the main plasma

105
Q

What results in irreversible shock due to a dramatic decrease in BP?

A

Vascular failure-adrenergic receptors become desensitised, neurotransmitters depleted
Heart failure- acidosis goes negative,Ca2+ channels decrease and so does contractility
CNS activity decreases- prolonged ischaemia leads to decreased neuronal activity and decreased sympathetic output

106
Q

What is the medical model of health

A

Health is the absence of disease, illness or injury

107
Q

What is the functional model of health?

A

Health is the ability to function a normal social role

108
Q

What is the idealist model of health?

A

Health is the complete state of physical, mental and social wellbeing

109
Q

What is sickness?

A

The social experience of ill health, how a specific health problem impacts upon society such as missing work

110
Q

What is illness?

A

The subjective experience, can be psychological and may not have biological basis or signs

111
Q

End diastolic volume

A

The amount of blood in a ventricle at the end of diastole

112
Q

End diastolic pressure

A

The pressure the fluid left in the ventricle after diastole exerts on the ventricular chambers

113
Q

Preload

A

The degree of stretch in the ventricles at the end of diastole

114
Q

What does the Frank-Starling curve show

A

How the preload affects the stroke volume, increased preload means increased SV however a convex curve relationship

115
Q

Afterload

A

The stress on the ventricle all when contracting to eject blood out of the ventricle

116
Q

What increases afterload

A

High BP or aortic stenosis

117
Q

What causes systolic heart failure?

A

When the left ventricle is unable to eject blood effectively during systole

118
Q

What can increase the likelihood of systolic heart failure?

A

Increased afterload as it can result in hypertrophy of the heart muscle
Damaged muscle as a result of an MI or cardiomyopathy

119
Q

What is a symptom of systolic heart failure and how?

A

As a result of a decreased stroke volume in systolic heart failure there is an increase in fluid left behind in the ventricles and thus preload
this excess pressure cant be cleared as the heart is failing and as a result there is a backing up in the venous system and a pulmonary oedema may form, causing breathlessness

120
Q

What is diastolic heart failure?

A

This is when the chambers are unable to fill with blood during diastole

121
Q

Compliance

A

How easy it is for a chamber to expand when it is filled with a volume of blood

122
Q

What causes a reduction in compliance

A

Impaired ventricular relaxation- old age and increased collagen fibres
Hypertrophy- high afterload

123
Q

What symptoms are shown in diastolic heart failure

A

There is backing up into the venous system which results in a build of tissue fluid and oedemas here and can result in breathlessness
This can increase at night or when lying down

124
Q

What is a symptom of right ventricular failure

A

An increased JVC, pitting peripheral oedema and kidney congestion

125
Q

hat is the most common cause of right ventricular failure?

A

Left ventricular heart failure as high pulmonary pressure causes excessive afterload, causing it to work harder and eventually fail

126
Q

What increases your risk of heart failure?

A 
History of ischaemic heart disease, MI or valvular disease 
Hypertension
Diabetes
Alcohol excess
Smoking
127
Q

What investigations can you do for heart failure?

A

An electrocardiogram, echocardiogram or chest X-ray

128
Q

What could a chest X-ray show for left sided heart failure?

A

A pulmonary oedema so a build up of fluid in the lungs which looks fuzzy on the X-ray

129
Q

Ho can you treat heart failure?

A

Lifestyle changes such as reducing smoking, increasing exercise and healthy diet
Most drug treatments reduce the compensatory effects that occur such as the RAA system
You may also fit them with a pacemaker or implantable defibrillator as severe heart failure can disrupt heart rhythms

130
Q

What are the advantages and disadvantages of x-rays and plain radiography

A

Advantages- simple, cheap and quick
Disadvantages- very small amount of harm through exposure to ionising radiation, you can’t use it on reproductive organs, the thyroid or pregnant women due to their being high cell turnover, it’s only a 2D photo

131
Q

What are the advantages and disadvantages of a CT scan

A

Adv.- generates a 3D image of multiple x-rays, very quick and not resource heavy
Disadv.- they struggle to sho accurate images of soft tissues such as muscles, ligaments and tendons, a lot of ionising radiation is produced

132
Q

What are the advantages of MRI

A

No ionising radiation- can be used on high cell turnover areas
Offers extreme, in depth detail, especially of soft tissue and nervous system injuries

133
Q

What are the disadvantages of MRI

A

Aren’t useful for parts of the body where there is no water such as bones
metallic objects can result in catastrophic accidents so patients who have pacemakers, metal clips, implants are limited
The scanners are extremely expensive
Take a lot longer to image and are very resource heavy
Certain patients find the machines very difficult as they are claustrophobic and loud

134
Q

What are the advantages and disadvantages of ultrasound

A

Adv- Cheap and portable machines and can be used in many different clinical scenarios, no risk of ionising radiation
Dis- Scans vary greatly in quality and depend on many things such as the patients BMI, if the surrounding tissues are covered by things such as bone then the structure cannot be seen

135
Q

How does echocardiography work?

A

An ultrasound probe is placed between patients ribs and the functioning of valves can be viewed in real time in order to quantify contractility of the walls
Backflow can be assessed using the doppler effect

136
Q

How does a coronary angiography work?

A

A peripheral artery is punctured with a hollow needle and a coronary catheter ire is passed through
this is then threaded through the artery and into the aortic root
A dye is then injected into each of the coronary roots and radiography is used to image any blockages as the dye and flow of it will show up on the scan

137
Q

Infective endocarditis

A

An infection of the endocardial surface of the heart (the inner lining including the valves)

138
Q

What can cause endocardial damage?

A 
Turbulent blood flow from valve problems
Congenital heart disease
Cardiomyopathy
Cardiothoracic surgery
Implanted foreign material (prosthetic heart valves, pacemaker leads)
139
Q

How can bacteria enter the heart and potentially fester within an endocardial thrombus?

A

Through poor dental hygiene, sepsis, intravenous drugs or recent surgery

140
Q

What is the most common bacteria to cause endocarditis?

A

staphylococcus aureus- very common in intravenous drug users

141
Q

What bacteria is very common in causing endocarditis after valvular surgery?

A

staphylococcus epidermis

142
Q

What are the symptoms of subacute endocarditis?

A

an onset fever, tiredness, night sweats and weight loss- can often lead to acute endocarditis

143
Q

What are the symptoms of acute endocarditis

A

severe febrile illness (fever), heart murmurs, embolic events, cardiac and renal failure

144
Q

What vascular problems can endocarditis lead to?

A

The bacteria from the endocarditis can break off and travel through the circulation as a septic embolus
They can deposit and cause micro-abscesses known as Janeway lesions
Haemmorhages may be seen in the mucous membranes, subconjunctiva and splinter haemorrhages in the nails
large emboli can block blood vessels and potentially cause severe complications

145
Q

hat immunological problems can arise from endocarditis

A

Immunoglobins made by the immune system bind to bacteria in order to remove them
they may clump together to form an immune complex multiple may deposit in tissues around the body and cause inflammation
this can deposit in the hands to form Osler’s nodes that are similar to Janeway’s lesions but tender
They may also cause kidney damage
They can be seen in roth spots in retinal fundoscopy

146
Q

How can you diagnose endocarditis?

A

The Duke criteria is a tool that examines blood cultures, echocardiograms and clinical presentation
Echocardiograms can be used to detect vegetations and assess valve damage

147
Q

How can you treat endocarditis?

A

Antibiotic treatment depends on whether the patient has their own valves and the causative bacterium
people at risk of it receive antibiotic prophylaxis hen undergoing surgery to prevent it

148
Q

What is the first treatment for chronic heart disease?

A

An ACE inhibitor and a beta blocker

149
Q

What does digoxin do as a ‘positive inotrope’

A

It’s an antiarrhythmic drug that increases vagal tone to the heart
as a positive inotrope it increases intracellular Ca2+

150
Q

When should digoxin be used

A

Supraventricular arrhythmias- chronic AF and chronic heart failure (improves symptoms but not mortality)

151
Q

What are the pharmacokinetics of digoxin?

A 
Clinical onset of around 30min
Bioavailability of 75%
Peak effect 1-5h
Half life- 36h
elimination- 70% renal
152
Q

What are the side effects of digoxin?

A 
Ectopic beats
Arrhythmias
Cardiac conduction problems
Cerebral impairment
Other problems such as vomiting and diarrhoea
153
Q

What does an ST depression suggest?

A

ischaemia (may be unstable angina or NSTEMI)

154
Q

What does an ST elevation suggest?

A

STEMI

155
Q

What produces the first heart sound S1?

A

The closure of the mitral and tricuspid valves

156
Q

What produces the second heart sound S2?

A

The closure of the aortic and pulmonary valves

157
Q

What is stenosis of a heart valve?

A

The narrowing of a heart valve

158
Q

What is regurgitation?

A

The unnatural backwards flow of blood through a valve

159
Q

What are the symptoms of mitral regurgitation?

A

Shortness of breath, fatigue and palpitations with an increased risk of AF and heart failure

160
Q

What can cause mitral regurgitation?

A

Left ventricular dilation which can dilate the valve
Annular calcification: the calcification of the mitral valve generally due to age
Infective endocarditis
Prolapse of the valve
MI can rupture the chordae tendinae or papillary muscles
Rheumatic heart disease

161
Q

What are the symptoms of aortic stenosis

A

Chest pain, breathlessness, syncope and fatigue

162
Q

What is the most common cause of aortic stenosis

A

Age related calcification

163
Q

What are the symptoms of aortic regurgitation

A

Shortness of breath, palpitations and anginal chest pain

164
Q

What causes a collapsing pulse

A

Aortic regurgitation

165
Q

What conformational changes in the heart can result from mitral stenosis

A

Enlarged left atrium

166
Q

What can aortic regurgitation cause

A 
Increases the risk of AF
High pressure in pulmonary system 
Shortness of breath 
Haemoptysis 
Right heart failure
167
Q

What is malar flush

A

A red flush in the face due to a build up of CO2 as a result of a back pressure of blood

168
Q

Where are the positive and negative electrode respectively on lead 2 of an ECG

A

negative on the right hand and positive on the left ankle

169
Q

What occurs in the heart due to dilated cardiomyopathy

A

Ventricular enlargement and loss of contractility in the heart muscle without any thickening

170
Q

What are the symptoms of dilated cardiomyopathy

A

Arrhythmias
Sudden cardiac death
Blood clots develop as blood flows slower than before

171
Q

How can you investigate dilated cardiomyopathy

A

Chest X-rays, ECGs, Echocardiograms, MRIs, angiographies or cardiac biopsies

172
Q

What is the difference between sporadic dilated cardiomyopathy and familial

A

Sporadic is caused by an insult such as myocarditis, toxins or an autoimmune response whereas familial has gene origin

173
Q

How do you treat dilated cardiomyopathy

A 
Diuretics 
ACE inhibitors 
Beta blockers 
Anticoagulation 
Pacemakers or implantable defibrillators
174
Q

What is hypertrophic obstructive cardiomyopathy

A

This is when the septum becomes large and bulky and prevents things from flowing out of the left ventricular outflow tract

175
Q

What are most cases of hypertrophic cardiomyopathy attributed to

A

Genetic

176
Q

What are the symptoms of hypertrophic cardiomyopathy

A

Most patients are asymptomatic but some may present with
Chest pain
Dyspnoea
Syncope

177
Q

What investigations can be done to examine hypertrophic cardiomyopathy

A

An ECG with ST and T wave changes
Echocardiography
Cardiac MRI
Genetic analysis

178
Q

What is restrictive cardiomyopathy

A

This is when the ventricle is not thicker, just stiffer

179
Q

What is the most at risk group of restrictive cardiomyopathies

A

The elderly

180
Q

What is Kussmaul’s sign and what does it indicate

A

This is a rise in JVP with inspiraton and is a sign of restrictive cardiomyopathy

Year 1 Medicine Newcastle (8 decks)

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