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Medicine Phase 2A (OWN) > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

At what percentage stenosis would you typically get symptoms of angina?

A

> 70%

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2
Q

Give a genetic cause of stable angina

A

Hypertrophic cardiomyopathy

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3
Q

If blood flow is reduced/ there is myocardial thickening, which part of layer of the heart is most affected?

A

Subendocardium

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4
Q

Why is chest pain felt with stable angina?

A

Subendocardial ischaemia leads to the release of adenosine and bradykinin which stimulate myocardial nerve fibres and alter pain sensation

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5
Q

Describe the symptoms of stable angina

A

Pressure/ squeezing pain that radiates to the left arm, jaw and shoulders
SOB
Diaphoresis

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6
Q

Describe vasospastic angina

A

Ischaemia from coronary artery vasospasms as smooth muscle around the arteries constrict
There is no correlation with exertion and all layers are affected

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7
Q

What ECG changes would you expect to see in stable and unstable angina?

A

ST segment depression from subendocardial ischaemia

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8
Q

What ECG changes would you expect to see in vasospastic angina?

A

ST segment elevation

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9
Q

How would you treat angina and in which case would you give calcium channel blockers?

A

Nitroglycerin spray, give CCB in vasospastic angina

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10
Q

How does the formation of an atherosclerotic plaque lead to a myocardial infarction?

A

Damage to the tunica intima of the endothelium- fat, cholesterol, proteins, calcium, WBCs accumulate and a hard fibrous cap forms
The cap breaks and exposes soft interior which platelets can adhere to and completely block the artery

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11
Q

Which area of the heart is supplied by the right coronary artery?

A

Posterior wall, septum and papillary muscles of the L ventricle

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12
Q

Which area of the heart is supplied by the L circumflex artery?

A

Lateral wall of the L ventricle

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13
Q

Which area of the heart is supplied by the L anterior descending artery?

A

Anterior wall and septum of L ventricle

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14
Q

Where is the first area affected in an MI and what ECG changes would you expect to see at this stage?

A

Inner 1/3 of myocardium- subendocardial infarct
ST segment depression
NSTEMI

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15
Q

What typically happens 3-6 hours after an MI?

A

Effects become transmural and ECG shows ST elevation: STEMI

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16
Q

Give 5 symptoms of a myocardial infarction

A 
Crushing chest pain- referred to L arm and jaw
Diaphoresis
Nausea
Fatigue
Dyspnoea
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17
Q

How would you diagnose a myocardial infarction?

A

Myocardial cells in the blood stream:
Troponin I and T - elevated 2-4 hours, peak at 48 hours, stay elevated for 7-10 days
CK-MB- elevated for 2-4 hours, peak at 24 hours, normal at 48 hours

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18
Q

Give 5 possible complications of myocardial infarction

A

Arrhythmias- damage to cells disrupts signals
Cariogenic shock- can’t pump enough blood
Pericarditis-1-3 days
Myocardial rupture- macrophages invade, granulation tissue, 3-14 days
Scarring- after 2 weeks

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19
Q

Give 3 types of therapy used to treat MI

A

Fibrinolytic therapy- medications
Angioplasty- surgical removal
Percutaneous coronary intervention- stent

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20
Q

Describe the risk of reperfusion injury after an MI

A

Influx of calcium- damaged cells contract but become stuck

Formation of reactive oxygen species which can damage cells

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21
Q

Give examples of medications that may be given after or in order to prevent an MI

A 
Antiplatelets- aspirin
Anticoagulants- heparin
Nitrates- relax coronary arteries and lower preload
Beta blockers- slow HR
Pain medication
Statins- improve lipid profile
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22
Q

Give the ejection fraction with the percentages for normal and HF

A

Stroke volume/ total volume
Normal= 50-70%
Systolic HF= < 40%

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23
Q

Why is the ejection fraction normal in diastolic HF?

A

Stroke volume and total volume are both low so fraction is not affected

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24
Q

Give 5 causes of L sided heart failure

A 
Long standing HTN
Ischaemic HD
Dilated cardiomyopathy
Concentric hypertrophy - diastolic HF 
Restrictive cardiomyopathy- diastolic HF
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25
Q

How does L sided heart failure lead to a build up of fluid?

A

Less blood to the kidneys activates the Renin-angiotensin aldosterone system and causes fluid retention
This is in order to increase BP, increase filling and therefore contraction strength
Fluid leaks from blood vessels causing oedema

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26
Q

How does pulmonary oedema occur as a result of L sided heart failure and what symptoms does this cause?

A

Back up of blood increases pressure in the pulmonary artery leading to oedema, this causes:
Dyspnoea
Rales
Blood can leak into the alveoli

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27
Q

How can R sided heart failure occur as a result of an atrial or ventricular septal defect?

A

Blood is shunted L to R
Increase fluid volume in R atrium/ ventricle leads to concentric hypertrophy
Ischaemia- systolic dysfunction
Small volume- diastolic dysfunction

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28
Q

How can chronic lung disease lead to R sided heart failure?

A

Pulmonary HTN makes it harder for R side to pump against pressure, this causes Cor Pulmonalae
As a result there is systemic vein congestion:
Jugular venous distention
Hepatosplenomegaly- cirrhosis/ liver failure
Ascites
Pitting oedema

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29
Q

How would you treat heart failure?

A

ACE inhibitors

Diuretics

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30
Q

Give 4 risk factors for hypertension

A

Old age
Obesity
Salt-heavy diet
Sedentary lifestyle

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31
Q

Give 4 causes of secondary HTN

A 
Low renal blood flow:
Atherosclerosis
Vasculitis
Aortic dissection
Fibromuscular dysplasia (non-inflammatory, non-atherosclerotic growth of the artery)
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32
Q

Give the BP values for a hypertensive crisis

A

Systolic >180mmHg

Diastolic >120mmHg

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33
Q

Describe atrial flutter

A

Atria contract at high rates of around 300bpm

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34
Q

Give the difference between type I and type II atrial flutter

A

I- moves around tricuspid valve counterclockwise

II- exact location less defined

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35
Q

How might ischaemia lead to atrial flutter?

A

Heart cells are more irritable and this changes their properties to reentrant circuit is more likely to develop

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36
Q

Why is ventricular bpm usually <180 bpm and what implication does this have in atrial flutter?

A

AV node has a relatively long refractory period, so there is an atrial:ventricular ratio where QRS complex will only appear once every 2/3 atrial contractions

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37
Q

Give 4 symptoms of atrial flutter

A

SOB
Chest pain
Dizziness
Nausea

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38
Q

What is the risk in atrial flutter as there is ineffective contraction?

A

Blood stagnates and forms clots which can go to the brain and cause a stroke

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39
Q

How can atrial flutter lead to heart failure?

A

Prolonged tachycardia causes ventricles to decompensate

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40
Q

How would you treat atrial flutter?

A

Anticoagulants
Beta blockers
Calcium channel blockers

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41
Q

Describe bundle branch block

A

Electrical signal blocked along the bundle branches due to fibrosis:
Ischaemia, MI, myocarditis
HTN, coronary artery disease, cardiomyopathies

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42
Q

What happens if there is a R bundle branch block? What ECG changes would be seen?

A

Electrical impulse travels down L bundle branch and L ventricle contracts, the R ventricle then contracts late
There is therefore a wide QRS complex
V1- M shape
V6- W shape (MARROW)

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43
Q

What ECG changes would you expect to see in L bundle branch block?

A

V1- W shape

V6- M shape (WILLIAM)

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44
Q

Describe long QT syndrome

A

Abnormally long depolarisation in some heart cells

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45
Q

What causes long QT syndrome?

A

Dysfunctional L-type calcium channels which let in more calcium ions and causes early after-depolarisation so ventricles depolarise and contract prematurely which causes reentrant tachycardia (150-250bpm)

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46
Q

Give 3 symptoms of long QT syndrome

A

Palpitations
Dizziness
Syncope

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47
Q

Give 2 causes of long QT syndrome

A 
Congenital
Medication- class IA and III anti-arrthymics
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48
Q

Describe Wolf-Parkinson-White syndrome

A

An accessory pathway is present connecting the atria and ventricles, this is called the bundle of Kent and leads to the pre-excitation of ventricles

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49
Q

What ECG changes would you expect to see with Wolf-Parkinson-White syndrome?

A

Short PR interval

Long QRS complex

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50
Q

How can Wolf-Parkinson-White syndrome facilitate arrhythmias?

A

Atrial arrhythmia + bundle of Kent means that ventricular rate is equal to the atrial rate and therefore cariogenic shock occurs as there is no time for the heart to refill

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51
Q

Describe the causes of aortic dissection

A

Chronic HTN- stress, increase in blood volume

Weakened aortic wall

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52
Q

With aortic dissection, where may blood back up into and what effects could this have?

A

Pericardial space- pericardial tamponade
Mediastinum- if tunica media tears
Back into the true lumen and renal/ subclavian arteries may be compressed by false lumen causing a low blood flow to the kidneys and arms

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53
Q

Give 5 symptoms of aortic dissection

A 
Sharp chest pain which radiates to the back
Weak pulse in downstream artery 
Difference in BP between L and R arms 
Hypotension
Shock
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54
Q

How would you treat aortic dissection?

A 
Surgically:
Removal of dissected aorta
Wall constructed with synthetic graft
Sometimes propped open with stent
BP medications: beta blockers
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55
Q

Give 5 causes of pericarditis

A 
Idiopathic 
Viral
Dressler syndrome- after MI
Ureic pericarditis- high blood urea
Autoimmune- immune system attacks pericardium
Cancer/ radiation
Medications- penicillin/ anticonvulsants
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56
Q

Describe the process of chronic pericarditis

A

Immune cells cause fibrosis of the pericardium making it stiff and restrictive so the heart struggles to relax/ expand
This leads to a decrease in stroke volume and an increase in heart rate

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57
Q

Give 2 symptoms of pericarditis and 2 symptoms of a large pericardial effusion

A

Fever
Chest pain: worse on heavy breathing and better leaning forward

Decreased heart sounds
Decreased cardiac output
SOB, low BP, dizziness

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58
Q

What would you hear through a stethoscope with pericarditis?

A

Thickened layers rub against each other, this is called a friction rub

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59
Q

What ECG changes would you expect to see with pericarditis?

A

Acute: ST elevation, PR depression, T wave starts to flatten, eventually returns to normal
Pericardial effusions: low QRS complex voltage
Alterans- QRS complexes have different heights as a result of the heart swinging back and forth in fluid

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60
Q

How would you treat pericarditis?

A

Relieve pain
Treat cause
Pericardial effusion- pericardiocentesis

61
Q

Describe the difference between organic PVD and functional PVD

A

Organic- obstruction/ blockage of peripheral vessels

Functional- constriction of peripheral vessels

62
Q

How ischaemia due to PVD lead to claudication?

A

Ischaemic cells release adenosine which is a signalling molecule that affects nerves in this area and this is felt as pain

63
Q 
Which artery would you suspect in PVD with pain in:
Hip/ buttocks
Thigh
Upper 2/3 of calf
Lower 1/3 of calf
Foot
A 
Aorta/ iliac 
Iliac/ common femoral
Superficial femoral
Popliteal
Tibial
64
Q

Give 2 symptoms of peripheral vascular disease other than pain

A

Ulcers on the feet that do not heal normally

Colour changes- elevation pallor and dependent rubor

65
Q

Give 4 risk factors for peripheral vascular disease

A

Smoking
Diabetes
Dyslipidemia
HTN

66
Q

How would you diagnose PVD?

A

Listening to iliac arteries with a stethoscope for “whoosh” or bruit, due to narrowing
Doppler ultra sound to look at blood flow
Ankle-brachial index (ABI) - comparison of two BPs

67
Q

Give the equation for the ABI and the value used to diagnose PVD

A

Systolic BP in ankle/ systolic BP in arm <0.9

68
Q

Give 3 causes of aortic valve stenosis

A

Stress over time- damages endothelial cells around the valves which leads to fibrosis and calcification
Bicuspid aortic valve- more stress per leaflet
Chronic rheumatic fever- repeated damage and repair causes commissural fusion

69
Q

Explain why you hear an “ejection click” and murmur with aortic stenosis

A

Ventricle contracts and pressure increases until valve eventually opens- ejection click
Blood is moving through a narrow opening causing a murmur

70
Q

What type of murmur do you hear with aortic stenosis?

A

Crescendo-Decrescendo murmur as it gets louder and then quieter as blood flow subsides

71
Q

What is the result of increased ventricular pressure in aortic stenosis?

A

Concentric left ventricular hypertrophy- new sarcomeres are added in parallel to existing ones

72
Q

What is microangiopathic haemolytic anaemia and why does it occur in aortic stenosis?

A

Damage to WBCs as they are forced through the smaller valve and split into schistocytes leading to haemoglobinuria

73
Q

What is the treatment for aortic stenosis or regurgitation?

A

Valve replacement

74
Q

Describe the causes of aortic regurgitation

A

Aortic root dilation- leaflets are pulled apart
Causes: idiopathic, aortic dissection, aneurysms, syphilis
Valvular damage- infective endocarditis, chronic rheumatic fever
Fibrosis- cannot form a seal and blood leaks through

75
Q

What type of murmur would you hear with aortic regurgitation?

A

Early decrescendo diastolic murmur due to blood flowing back through the valve

76
Q

Why do you get an increase in pulse pressure with aortic regurgitation?

A

Increase in L ventricular blood volume due to back flow, therefore increase in stroke volume and systolic BP
Less blood in aorta during diastole therefore a drop in diastolic BP

77
Q

Give the symptoms of a hyperdynamic circulation as found in aortic regurgitation

A

Bounding pulse, head bobbing, capillary beds of fingernails pulsate (Quincke’s sign)

78
Q

What is myxomatous degeneration and how can it cause mitral valve prolapse?

A

Weakened connective tissue which increases the leaflet area and increases the chordae tendineae length which can then rupture- this can cause the posterior leaflet to fold into the atrium

79
Q

Give the signs and symptoms of mitral valve regurgitation

A

Usually asymptomatic

Heart murmur- mid-systolic click and systolic murmur

80
Q

Give 3 causes of mitral valve regurgitation

A

Damaged papillary muscles as a result of an MI
L sided HF leading to left ventricular dilation
Rheumatic fever-chronic rheumatic HD- leaflet fibrosis

81
Q

How can mitral valve regurgitation cause L sided heart failure?

A

With every contraction some blood goes back to the L atrium, this then drains back into the ventricle which increases preload causing eccentric hypertrophy

82
Q

Give the main cause of mitral valve stenosis

A

Rheumatic fever- commissural fusion

83
Q

What are the consequences of mitral valve stenosis?

A

Increased volume in atrium therefore increased pressure
Dilation due to increased pressure, leading to pulmonary congestion and oedema- Dyspnoea
Pacemaker cells stretch due to dilation and become more irritable and prone to atrial fibrillation- stagnant blood- thrombosis
There is also extra blood in the pulmonary system causing HTN

84
Q

How can mitral valve stenosis lead to dysphagia?

A

If atria dilates enough due to increased load, it can compress the oesophagus

85
Q

How would you treat mitral valve disease?

A

Valve repair

Surgical replacement of the valve

86
Q

What are the two factors that ultimately determine blood pressure?

A

Resistance to flow and cardiac output

87
Q

What are the two sub-types of hypovolemic shock?

A

Hemorrhagic and non-hemorrhagic

88
Q

Give an example of non-hemorrhagic shock

A

Severe dehydration

89
Q

Approximately how much blood can be lost before there is a likely risk of shock

A

20% loss (around 1L)

90
Q

What chemicals are released as a result of decreased cardiac output?

A

Catecholamines
-adrenaline and noradrenaline
ADH
Angiotensin II

91
Q

What is mixed venous oxygen saturation and how is it affected in hypovolemic and cariogenic shock?

A

Amount of oxygen bound to haemoglobin returning to the R side of the heart from the tissues
Decreased MVO2

92
Q

What is the most common cause of cardiogenic shock?

A

Acute myocardial infarction- muscle cells die leading to weaker contractions and therefore decreased stroke volume

93
Q

Describe distributive shock

A

Damaged endothelial cells leading to excessive dilation of blood vessels and leaky blood vessels

94
Q

How does increased dilation of blood vessels cause distributive shock?

A

Increased dilation of blood vessels decreases resistance to flow causing a drop in BP

95
Q

How does septic shock occur?

A

Endotoxins (lipopolysaccharides) found in the outset membrane of gram negative bacteria lead to lower perfusion

96
Q

How does the damage of endothelial cells by bacterial endotoxins lead to vasodilation?

A

Endothelial cells release vasodilators such as nitric oxide

They activate the complement pathway causing mast cells to release histamine

97
Q

What is the procoagulant produced by endothelial cells?

A

Tissue factor

98
Q

Why does low vascular resistance lead to reduced oxygen perfusion to the tissues?

A

Blood is moving too fast to unload the oxygen, there is a drop in oxygen despite increased blood flow

99
Q

Give the three sub-types of distributive shock

A

Septic
Anaphylactic
Neurogenic shock

100
Q

Describe the formation of the atrial septum in a foetus

A

Septum primum grows, osmium primum is present
Septum primum fuses with the endocardial cushion and closes the gap completely, ostium secundum appears
Septum secundum forms with foramen ovale present

101
Q

What is the most common cause of an atrial septal defect?

A

Septum secundum doesn’t grow enough during development

102
Q

Which conditions are atrial septal defects strongly associated with?

A

Foetal alcohol syndrome

Down’s syndrome

103
Q

Describe the movement of blood with an atrial septal defect and how this affects oxygen saturation

A

Higher pressure in left side of the heart means blood is shunted from L to R
Increased oxygen saturation in R atrium, R ventricle, pulmonary artery

104
Q

How does the extra blood in the R side of the heart affect the pulmonary valve with atrial septal defect?

A

Delayed pulmonic valve closure

105
Q

What causes a ventricular septal defect?

A

If upward growing muscular ridge and downward growing membranous region don’t fuse- commonly defect in membranous region

106
Q

Describe blood flow with a ventricular septal defect and how this affects oxygen saturation

A

Blood flows from R ventricle to lungs since pressure is higher in L ventricle than R
Blood is shunted from L ventricle to right since pressure is higher in L
Increased oxygen saturation in R ventricle and pulmonary artery

107
Q

How might pulmonary HTN occur with a ventricular septal defect and what are the implications of this?

A

Increased blood shunted to R side of the heart can cause pulmonary HTN, if pressure on R side then exceeds the left, blood is shunted from R to L, this is called Eisenmenger’s syndrome
Non-oxygenated blood is pumped into the systemic system- cyanosis

108
Q

Describe dilated cardiomyopathy

A

Dilation of the heart chambers means contractions are weaker, decreasing stroke volume and causing biventricular congestive heart failure

109
Q

How does dilated cardiomyopathy affect the heart valves

A

Stretches out the valves that separate the ventricles causing mitral or tricuspid valve regurgitation

110
Q

Give 2 conditions caused by dilated cardiomyopathy

A

Valve regurgitation

Arrhythmias- stretching cells causes irritation

111
Q

Give 5 causes of dilated cardiomyopathy

A 
Idiopathic
Genetic mutation
Infection
Alcohol abuse
Drugs
Peripartum cardiomyopathy- pregnancy
112
Q

How would you treat dilated cardiomyopathy?

A

L ventricular assist device

Heart transplant

113
Q

Give 5 causes of secondary HTN (other than kidney or endocrine disorders)

A 
Anaemia
Drugs
Cancers
Pregnancy
Neurological disorders
Hormonal contraceptives
114
Q

Give 4 causes of kidney related secondary HTN

A

PKD
Chronic glomerulonephritis
Renovascular HTN
Renal tumours

115
Q

Give 5 endocrine disorders which cause HTN

A 
Neurogenic HTN
Hyper/hypothyroidism
Acromegaly
Hyperparathyroidism
Hyperaldosteronism (Conn's syndrome)
116
Q

What ECG changes would you expect to see with atrial fibrillation?

A

“Scribble” instead of P wave
Irregular QRS complex intervals
100-175bpm

117
Q

Give 4 risk factors for atrial fibrillation

A

CVD
Diabetes
Obesity
Genetics

118
Q

What is tissue heterogeneity?

A

Cells develop different properties

119
Q

Describe the difference between the multiple wavelet theory and the automatic focus theory to explain atrial fibrillation

A

Multiple wavelet theory suggests multiple cells responsible firing off ‘wavelets’ which may trigger other ‘wavelets’
Automatic focus theory suggests one specific area initiates AF located in the cardiac muscle around the pulmonary veins

120
Q

Describe the difference between paroxysmal, persistent and longstanding persistent AF

A

Paroxysmal comes and goes
Persistent > 7 days
Longstanding persistent >12 months

121
Q

Why do repeated episodes of paroxysmal AF lead to persistent AF?

A

Stress
Calcium overload
Progressive fibrosis

122
Q

Give 5 symptoms of AF

A 
Fatigue
Dizziness
SOB
Weakness
Palpitations
123
Q

Give a common complication of AF and explain why this is a risk

A

Stroke, as blood stagnates making it more likely to clot

124
Q

How would you diagnose AF?

A

Persistent AF: ECG

Paroxysmal AF: Holter monitor which is a portable device monitoring heart activity for an extended period of time

125
Q

How would you treat AF?

A

Medication to control HR and reduce clotting
Pacemaker
Radio-frequency catheter oblation

126
Q

Define ventricular tachycardia

A

More than 3 consecutive PVCs

> 100 ppm but can experience up to 450bpm

127
Q

Give 5 symptoms of ventricular tachycardia and explain why these occur

A 
Less blood pumped out with each heartbeat as there is not enough time to refill, this causes:
Chest pain
Fainting
Dizziness
SOB
Sudden death
128
Q

Describe focal ventricular tachycardia

A

The cells have an abnormal automaticity, ventricular cells usually have an automaticity of 30bpm but these can become stressed/ irritated and the automaticity can increase past that of the SAN

129
Q

Give 4 examples of ways in which the ventricular cells can become irritated causing ventricular tachycardia

A

Medications
Illicit drugs
Electrolyte imbalances
Ischaemia

130
Q

Describe how reentrant ventricular tachycardia may occur

A

Heart cells are damaged/ dead and form scar tissue which is less conductive
Impulse travels around dead tissue in a loop, variability in conduction speed and refractory period can lead to reentrant loop occurring

131
Q

Describe the difference between monomorphic and polymorphic ventricular tachycardia

A

Monomorphic- reentrant and focal (one group responsible)

Polymorphic- multiple areas of ventricular cells are affected, signal is originating from different groups

132
Q

How would you treat ventricular tachycardia?

A

Cardioversion
Medication to lower HR to normal
Electrical pulse delivered to heart on R wave, avoid T wave as this is a vulnerable period
Radio-frequency catheter oblation
Device implantable cardioverter defibrilation

133
Q

What are the two types of true aneurysm?

A

Symmetrical- fusiform aneurysm

Asymmetrical- saccular/ berry aneurysm

134
Q

What is a pseudoaneurysm?

A

Gap in the artery wall and blood pools due to surrounding connective tissue

135
Q

What percentage of aneurysms are abdominal compared to thoracic?

A

60% abdominal

40% thoracic

136
Q

Where is the most common place to find an abdominal aneurysm?

A

Below renal arteries, above aortic bifurcation

There is less collagen and therefore the arteries are weaker

137
Q

Describe how obstruction of the vasa vasorum supplying the first section of the aorta can cause weakening of the aortic wall

A

Hyaline arteriosclerosis of the vasa vasorum
Narrowing of the lumen leads to ischaemia and smooth muscle atrophy
This weakens the aorta’s wall

138
Q

How can the formation of an atherosclerotic plaque cause weakening of an artery wall

A

Oxygen can’t penetrate the plaque and therefore cannot reach the wall

139
Q

Give 4 risk factors for aneurysms

A

Male
>60
HTN
Smoking

140
Q

How can syphilis cause an aneurysm?

A

Causes inflammation of the vasa vasorum (endarteritis obliterans), this causes narrowing of the vessels and so no blood flow

141
Q

How do mycotic aneurysms occur?

A

Caused by infection
Infection breaks off and travels to visceral, intercranial/ arteries feeding arms and legs
They weaken the vessel wall

142
Q

Give 3 bacteria and 2 fungi which can cause mycotic aneurysms

A

Bacteroides fragilis
Pseudomonas aeruginesa
Salmonella (any)

Aspergillus
Candida

143
Q

Which genetic disorders can lead to aneurysm formation?

A

Anything affecting the connective tissue
Marfan syndrome- elastic properties compromised
Ehlers Danlos syndrome- ability to form collage is impacted

144
Q

What effect can a thoracic aneurysm have on the aortic valve?

A

Pulls on the valve so it can’t close properly
Blood therefore flows back into the ventricle and there is aortic insufficiency
There may also be a cough if the L recurrent laryngeal nerve is stretched by the aneurysm

145
Q

Describe a brain aneurysm rupture

A

Blood pools into subarachnoid space, increases pressure which irritates the meninges
This causes a headache and inability to flex the neck forwards

146
Q

How can aneurysms cause blood clots?

A

Blood may be pulled into the extra lumen space

It is not moving as quickly as the rest of the blood- stagnates and is therefore likely to clot

147
Q

Give 3 signs/ symptoms of abdominal aortic aneurysms

A

Severe L flank pain
Pulsating mass with heartbeat
Hypotension

148
Q

How might a thoracic aneurysm present?

A

Usually asymptomatic

May be chest/ back pain

Medicine Phase 2A (OWN) (10 decks)

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