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Clinical > The cardiac system > Flashcards

The cardiac system Flashcards

1
Q

What are the 6 main differences between cardiac and skeletal muscle?

A
  1. Cardiac has a long action potential whereas skeletal has a short one
  2. Skeletal muscle can have tetanus but cardiac cannot due to the long A.P. the heart must relax before it contracts again
  3. Some cardiac cells have an unstable AP
  4. The intercalated disks of cardiac muscles have alternating gap junctions and desmosomes
  5. Where skeletal muscle have multiple nuclei per cell cardiac has only one but acts as a syncytium
  6. Calcium from outside of the cell can regulate contraction strength as it does not saturate troponin
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2
Q

describe the process of non-pacemaker action potential

A
  • Resting membrane potential: high resting PK+
  • Initial depolarisation: Increase in PNa+
  • Plateau: increase in PCa2+ (l-type), decrease in PK+
  • Repolarisation: Decrease in PCa2+ (l-type), increase in PK+
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3
Q

Describe the process of a pacemaker action potential

A
  • Action potential: Increase in PCa2+ (L-type)
  • Pacemaker potential (pre-potential): Gradual decrease of PK+, early increase in PNa+ and a late increase in PCa2+ (t-type)
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4
Q

What type of drugs modulate electrical activity?

A
  • Ca2+ channel blockers: decrease the force of contraction

- Cardiac glycosides: Increase the force of contraction

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5
Q

What (other than drugs) modulate electrical activity?

A
  • Temperature (increases about 10 beats/min/*C)
  • Hyperkalaemia: fibrillation + heart block
  • Hypokalaemia: Fibrillation + heart block
  • Hypercalcaemia: Increases force of contraction + HR
  • Hypocalcaemia: Decreases force of contraction + HR
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6
Q

name the different parts of the heart that are for conducting

A
  • sinoatrial node: pacemaker (fastest)
  • atrioventricular node: delay box
  • Bundle of His
  • Purkinje fibres: rapid conducting system
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7
Q

What does the P wave correspond to?

A

atrial depolarisation

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8
Q

What does the QRS complex correspond to?

A

Ventricle depolarisation

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9
Q

What does the T wave correspond to?

A

Ventricle repolarisation

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10
Q

What is an atheroma?

A

The formation of large focal elevated lesions (plaques) in the intima of large and medium sized arteries

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11
Q

What is the earliest significant lesion and when does it form?

A

The earliest significant lesion is a fatty streak which forms in young children. It is a yellow linear elevation of the intimal lining and comprises of masses of lipid-laden macrophages. It has no clinical significance and may go away, however, patients are at risk of going on to form atheromatous plaques.

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12
Q

What are the early atheromatous plaques and when are they formed?

A

Formed in young adults, early atheromatous plaques are smooth yellow patches in the intima made of lipid-laden macrophages and can progress to form established plaques

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13
Q

What are fully developed atheromatous plaques?

A

They have a central lipid core with a fibrous tissue cap and is covered by the arterial endothelium. They are soft, highly thrombotic and often have a rim of foamy macrophages.

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14
Q

Why are the macrophages in atheromatous plaques described as foamy?

A

Due to the uptake of oxidised lipoproteins via specialised membrane bound scavenger receptors

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15
Q

Where do the atheromatous plaques tend to form

A

Bifurcations or at branching points (turbulent flow)

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16
Q

What is the fibrous tissue cap composed of?

A

There is collagen (produced by smooth muscle cells) in the cap to provide structural strength along with inflammatory cells recruited from the endothelium.

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17
Q

What happens in late development of the atheromatous plaques?

A

There is extensive dystrophic calcification and the plaques are confluent and cover large areas.

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18
Q

What are the risk factors of atheroma?

A
  • Hypercholesterolaemia
  • Smoking
  • Hypertension
  • Diabetes mellitus
  • Male
  • Elderly
  • Obesity
  • sedentary lifestyle
  • Low socioeconomic status
  • Low birthweight
  • Role of microorganisms
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19
Q

How is an atheromatous plaque formed?

A
  1. A microscopic injury to the endothelial lining of the artery
  2. Chronic inflammation and healing response of the vascular wall to the agent causing injury
    - Accumulation of lipoproteins (LDL) in the vessel wall
    - Monocyte adhesion to the endothelium results in migration to the intima and transformation into foamy macrophages
    - Platelet adhesion
    - Factor release from activated platelets
    - Smooth muscle cell proliferation, extracellular matrix production and T cell recruitment
  3. Chronic/ episodic exposure of the arterial wall to these processes cause the formation of atheromatous plaque
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20
Q

What are the causes of endothelial injury?

A
  • Haemodynamic disturbances (turbulent flow)

- Hypercholesterolaemia

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21
Q

How are the injured endothelial cells functionally altered?

A
  • Enhanced expression of cell adhesion molecules (ICAM-1, E-selection)
  • High permeability for LDL
  • Increased thrombogenicity
  • Inflammatory cells in the intima causes plaques
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22
Q

What is plaque growth initiated by?

A

small areas of endothelial loss

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23
Q

What are the clinical manifestations of progressive lumen narrowing due to high grade plaque stenosis?

A
  • Stenosis of 50-75% of the vessel lumen causes a critical reduction in blood flow in a distal arterial bed which, in turn, causes reversible ischaemia
  • e.g. stenosis of the atheromatous coronary artery can cause stable angina
  • Very severe stenosis causes ischaemic pain at rest (unstable angina)
  • e.g. ileal, femoral, popliteal artery stenosis results in intermittent claudication (peripheral arterial disease)
  • Longstanding tissue ischaemia results in atrophy of affected organ
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24
Q

What are the clinical manifestations of an acute atherothrombotic occlusion?

A
  • Major complications: rupture of plaque results in an acute event
  • Rapture exposes highly thrombotic plaque contents (collagen, lipid, debris) to the bloodstream which results in the activation of a coagulation cascade and thrombotic occlusion in a very short time
  • Total occlusion causes ischemia which leads to necrosis of tissue
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25
Q

What are the clinical manifestations of embolisation of the arterial bed?

A
  • Detachment of thrombus fragments from thrombosed atheromatous arteries which embolise distally to ruptured plaque
  • Embolic occlusion of small vessels cause small infarcts in organs
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26
Q

What are the clinical manifestations of ruptured atheromatous abdominal aortic aneurism?

A
  • Media beneath atheromatous plaques generally weakened
  • This results in gradual dilation of the vessel
  • Slow but progressive, seen in elderly, often asymptomatic
  • Sudden rupture results in a massive retroperitoneal haemorrhage
  • Mural thrombosis results in an embolism to the legs
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27
Q

What are the clinical manifestations of a vulnerable atheromatous plaque?

A
  • Typically have a thin fibrous cap, a large lipid core and prominent inflammation
  • Pronounced inflammatory activity results in degradation and weakening of the plaque which results in an increased risk of plaque rupture
  • Secretions of proteolytic enzymes, cytokines and reactive oxygen species by plaque inflammatory cells
  • Highly stenotic plaques often have a large fibrocalcific component with little inflammation
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28
Q

What is the preventative therapy of atheroma?

A
  • Stop smoking
  • Control blood pressure
  • Weight loss
  • Regular exercise
  • Dietary modifications
  • Cholesterol lowering drugs
  • Surgical options
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29
Q

What are the complications of Hypertension?

A
  • Brain: stroke, haemorrhage, cognitive decline
  • Heart: LV hypertrophy, coronary heart disease, congestive heart failure and MI
  • Kidneys: Renal failure, dialysis, transplantation and proteinurea
  • Peripheral vascular disease
  • Retinopathy (eyes)
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30
Q

What is the definition of hypertension?

A

-Blood pressure above which the benefits of treatment outweigh the risks

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31
Q

What is the definition of stage 1 hypertension?

A
  • Clinical blood pressure: 140/90 or higher

- ABPM: 135/85 or higher

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32
Q

What is the definition of stage 2 hypertension?

A
  • Clinical blood pressure: 160/100 or higher

- ABPM: 150/95 or higher

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33
Q

What is sever hypertension?

A

Clinical BP: 180/110 or higher

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34
Q

What are the underlying causes of secondary hypertension?

A
  • Chronic renal disease
  • Renal artery stenosis
  • Endocrine disease, cushings, Conn’s syndrome, phaeochromocytoma, GRA
  • Pregnancy (pre-eclampsia)
  • Coarctation of the aorta
  • Sleep apnoea
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35
Q

What are the drugs that ca cause hypertension?

A
  • NSAIDs
  • Oral contraceptives
  • Corticosteroids
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36
Q

What are the risk factors of hypertension?

A
  • Smoking
  • Diabetes myelitis
  • Renal disease
  • Male
  • Hyperlipidaemia
  • Previous MI or stroke
  • LV hypertrophy
  • Age
  • genetics
  • Environment
  • Weight
  • Alcohol intake
  • Race
  • Diet
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37
Q

What is the aetiology of Hypertension?

A
  • Polygenic: Major genes, Poly genes

- Polyfactorial: environmental, individual and shared

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38
Q

What do you have to think about if you’re thinking of treating hypertension?

A
  • Identifying true hypertension
  • Assess risk (look at risk factors)
  • Assess end organ damage
  • screen for treatable causes
  • treatment should be started at an overall CVD risk of 20%/10 years
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39
Q

When should the young (under 80) with stage 1 hypertension be given treatment?

A

If they have one of the following

  • established cardiovascular disease
  • target organ damage
  • renal disease
  • diabetes
  • CV risk > 20%/10 years
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40
Q

When should the young be given treatment with stage 2 hypertension?

A

whenever they have it

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41
Q

What is the step 1 treatment for over 55 year olds or Afro-Caribbeans?

A
  • Calcium channel blocker (CCB)

- if CCB not suitable or if there is evidence or a high risk of HF: Thiazide-like diuretic

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42
Q

What is step 1 treatment for under 55’s

A

ACEI/ARB

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43
Q

What is step 2 treatment?

A

Add thiazide-like diuretics to CCB or ACEI/ARB

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44
Q

What is step 3 treatment?

A

-Add all three classes (CCB, ACEI, Diuretic) together

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45
Q

What is step 4 treatment?

A
  • Blood K+ < 4.5mmol/l: low dose spirnolactone

- Blood K+ > 4.5mmol/l: higher dose thiazide-like diuretic

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46
Q

Give an example of an ACEI

A

Rampril

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47
Q

What does ACEI do?

A

competitively inhibit the actions of ACE

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48
Q

What are the contraindications of ACEI?

A
  • Renal artery stenosis
  • Renal failure
  • Hyperkalaemia
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49
Q

What are the adverse drug reactions of ACEI

A
  • Cough
  • First dose hypo-tension
  • taste disturbance
  • Renal impairment
  • angioneurotic oedema
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50
Q

What are the drug-drug interactions of ACEI?

A
  • NSAIDs (precipitate acute renal failure)
  • Potassium supplements (Hyperkalaemia)
  • Potassium sparing diuretics (Hyperkalaemia)
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51
Q

give 4 examples of ARB (angiotensin II agonists)

A

Losartan, Valsartan, Candesartan, Irbesartan

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52
Q

What does ARB do?

A

competitively block the actions of angiotensin II at the angiotensin ATI receptor

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53
Q

What advantage does ARB have over ACEI?

A

No cough

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54
Q

Give two examples of vasodilator calcium channel blockers

A

Amlodipine and Felodipine

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55
Q

Give two examples of rate limiting calcium channel blockers

A

Verapamil and Diltiazem

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56
Q

What are the contraindications of CCBs?

A
  • Acute MI

- HF, bradycardia

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57
Q

What are the adverse drug reactions of CCBs?

A
  • Flushing
  • Headache
  • Ankle oedema
  • Indigestion and re-flux esophagus
  • Rate limiting: Bradycardia and/or constipation
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58
Q

Name two Thiazide type diuretics

A

Indamide and clortidone

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59
Q

Where has Thiazide type diuretics proven beneficial?

A

MI an stroke reduction

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60
Q

What does thiazide type diuretics do?

A

Urinary excretion of sodium but it may take weeks to be fully effective

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61
Q

What are the adverse drug reactions of thiazide type diuretics?

A
  • Gout

- Impotence

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62
Q

Give two examples of vasodilators

A

Minoxidil and Hydralazide

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63
Q

Give an example of an alpha-adrenoreceptor antagonist

A

Doxazosin

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64
Q

What does alpha-adrenoreceptors do?

A

selectively blocks post-synaptic alpha 1-adrenoreceptors

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65
Q

What are the adverse reactions of alpha-adrenoreceptors?

A
  • First dose hypertension
  • Dizziness
  • dry mouth
  • headache
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66
Q

Give two examples of centrally acting agents

A

Methyldopa and Moxonidine

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67
Q

What are the adverse reactions of Methyldopa?

A
  • Sedation
  • drowsiness
  • Dry mouth
  • Nasal congestion
  • Oethostatic hypotension
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68
Q

What is the definition of stable angina?

A

A discomfort in the chest and/or adjacent areas with myocardial ischaemia but without myocardial necrosis.

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69
Q

What is the overall pathophysiology of angina?

A

A mismatched supply of O2 and metabolites to the myocardium and the myocardial demand for them.

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70
Q

What are the 4 causes of angina?

A
  • A reduction in blood flow
  • Reduced O2 transport: anaemia
  • Pathological increased demand for O2
  • Thyrotoxicosis
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71
Q

What is the reduction in blood flow to the myocardium caused by?

A
  • Obstructive coronary atheroma
  • Coronary artery spasm
  • coronary inflammation/ arteritis
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72
Q

What might increase the myocardial demand for O2?

A

LV hypertrophy: as seen in persistent hypertension, significant aortic stenosis and hypertrophic cardiomyopathy.

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73
Q

What is the characteristics of the pain of angina?

A
  • Site: retrosternal
  • character: tight band/ pressure/ heaviness
  • Radiation: neck and/or jaw, down arms
  • Aggregation: exercise, emotional stress
  • relieving factors: rapid improvement with GTN (1-3mins) or physical rest
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74
Q

What other symptoms will there be if there is no pain?

A
  • Breathlessness on exertion
  • Excessive fatigue for activity undertaken
  • Near syncope on exertion
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75
Q

What 6 features make angina less Likely?

A
  • Sharp/ stabbing pain: pleuritic or pericardial (worse in different positions)
  • Associations with body movements or respiration
  • very localised site
  • No pattern to pain, particularly if occurring at rest
  • Begins sometime after rest
  • Lasting for hours
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76
Q

What are the risk factors of angina?

A
  • age
  • gender
  • creed
  • family history
  • Genetic factors
  • smoking
  • Life style: diet and exercise
  • Diabetes myelitis
  • Hypertension
  • Hyperlipidaemia
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77
Q

What bloods would you have done to diagnose angina?

A
  • full blood count
  • lipid profile
  • fasting glucose
  • electrolytes
  • liver and thyroid tests
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78
Q

What is the reason for taking a CXR in angina?

A

It shows pulmonary oedema

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79
Q

What will an electrocardiagram show in angina?

A
  • Evidence of an MI: pathological Q waves

- LV hypertrophy: high voltages, lateral ST-segment or “strain pattern”

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80
Q

What are the advantages of a myocardial perfusion test?

A

Superior to ETT in detection of CAD, localisation of ischaemia and assessing size of affected area

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81
Q

What are the disadvantages of the myocardial perfusion test?

A
  • Expensive

- Involves radioactivity

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82
Q

What are the drugs that are used for pharmacological induced stress?

A
  • adenosine
  • dipyramidamole
  • dubutamine
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83
Q

What happens in a myocardial perfusion test if the heart is normal?

A

It takes up the tracer both before and after stress

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84
Q

What happens in a myocardial perfusion test if the heart is ischaemic?

A

tracer seen at rest but not after stress

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85
Q

What happens in a myocardial perfusion test if there was an infarction?

A

Tracer would not be seen at rest or stress

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86
Q

What happens in a myocardial perfusion test if there is angina?

A

Tracer would not be seen at rest but would be seen in stress

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87
Q

What are the general measures of treatment of stable angina?

A

address risk factors: BP, cholesterol, lifestyle

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88
Q

What drugs are used to treat angina?

A
  • statins
  • ACEI
  • Aspirin
  • beta blockers
  • calcium channel blockers
  • IK channel blockers
  • Nitrates
  • Potassium channels blockers
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89
Q

When do you consider the use of statins in the treatment of angina?

A

If the total cholesterol is > 3.5 mmol/l

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90
Q

What do statins do?

A

They reduce the deposition of LDL-cholesterol in atheroma reducing plaque ruptures and ACS

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91
Q

When are ACE inhibitors used in the treatment of angina?

A

If there is an increased cardiovascular risk and atheroma

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92
Q

What do ACE inhibitors do in the treatment of angina?

A

They stabilise the endothelium and also reduce plaque ruptures

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93
Q

What is the alternative drug for aspirin in the treatment of angina?

A

Clopidogrel

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94
Q

What does aspirin do in the treatment of angina?

A

It protects the endothelium and reduces platelet activation/ aggregation

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95
Q

What are the beta blockers for?

A

to achieve resting HR, reducing myocardial work and has anti-arrhythmic effects

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96
Q

What do the CCBs do?

A

achieve resting heart rate and it is central acting

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97
Q

What does IK channel blockers do?

A

achieve resting heart rate. Ivabradine reduces sinus rhythm

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98
Q

What do nitrates do?

A

produces vasodilation

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99
Q

Name a potassium channel blocker

A

nicorandil

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100
Q

What is a percutaneous coronary investigation (PCI)

A

A surgeon crosses a stenotic lesion with a guide wire and squashes the atheromatous plaque into the walls with a balloon and stent

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101
Q

what medication is needed if this coarse of action is taken?

A

-take aspirin and clopidigrel together whilst the endothelium covers the stent. Disease modifying drugs are still needed though.

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102
Q

Does this work?

A

There is no evidence of an improved prognosis in angina

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103
Q

When is coronary artery bypass grafting (CABG) the best option?

A

In diffuse multivessel

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104
Q

What is the advantages of CABG?

A

Good lasting benifit

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105
Q

What is the disadvantages of CABG?

A

you must continue the disease modification medications and the graft deteriorates after 10 years.

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106
Q

name 7 problems that can cause defects in blood flow

A
  • Thromboembolism
  • Atheroma
  • Hyperviscosity
  • Spasm
  • External compression (tumour)
  • Vasculitis
  • Vascular steel (vessel steels blood from another)
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107
Q

What are the three factors that cause thrombosis?

A
  • Changes in the blood vessel wall
  • Changes in the blood constitutes
  • Changes in the pattern of blood flow
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108
Q

What are the outcomes of thrombosis?

A
  • resolution
  • Organisation/ recanalisation
  • Death
  • Propagation which leads to an embolism
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109
Q

What is an embolism?

A

Movement of abnormal material in the blood stream and its implantation in the vessel, blocking the way

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110
Q

What are the different types of embolism?

A
  • Thrombosis
  • Systemic thrombosis
  • Paradoxical embolism
  • Fat embolism
  • Gas embolism
  • tumour
  • trophoblast
  • septic material
  • Amniotic fluid
  • Foreign bodies
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111
Q

what are the sources of a thrombosis?

A
  • Mural thrombosis
  • aortic aneurysm
  • atheromatous plaques
  • valvular vagitation
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112
Q

What is a paradoxical embolism?

A

In the venous circulation and causes what is effectively known as a stroke

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113
Q

What is a systemic thrombosis?

A

It travels to a wide verity of sites: lower limbs (most common), brain, other organs

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114
Q

What are the consequences of a systemic thrombosis?

A

depends on vulnerability of effected tissue to ischaemia, calibre of occluded vesicle, collateral circulation but usually infarction occurs

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115
Q

What are the most common signs of a fat embolism?

A
  • confusion
  • renal disease
  • rash
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116
Q

From where to where does standard limb lead 1 go (negative to positive)?

A

Right arm to left arm

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117
Q

From where to where does standard limb lead 2 go (negative to positive)?

A

From the right arm to the left leg

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118
Q

From where to where does standard limb lead 3 go (negative to positive)?

A

Left arm to left leg

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119
Q

What type of events are transmitted better on an ECG? fast or slow events?

A

Fast

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120
Q

What is the heart doing at each point in the ECG?

A

-P wave: SA node depolarises
-Q wave: the AV node depolarises and the interventricular septum depolarises from left to right
-R wave: Atrial relaxation and the bulk of the ventical depolarises from the endocardial to the epicardial surface
-S wave: The upper part of the interventricular septum depolarises
T wave: ventricle repolarisation

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121
Q

What does each wave of the ECG signify?

A

P wave: atrial depolarisation
QRS complex: Ventricle depolarisation
T wave: ventricle repolarisation

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122
Q

Why is the T wave positive?

A

The action potential is longer in the endocardial cells than the epicardial cells and the wave for repolarisation runs in the opposite direction to the wave of depolarisation

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123
Q

What does STEMI mean?

A

ST elevated myocardial infarction

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124
Q

What does NSTEMI mean?

A

Non ST elevated myocardial infarction

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125
Q

What is worse a STEMI or a NSTEMI and why?

A

A STEMI as an elevated ST segment seems to indicate something has gone seriously wrong

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126
Q

What are the 5 major stages of heart development?

A
  1. Bilateral Heart primordia
  2. Primitive heart tube
  3. Heart looping
  4. Arterial and ventricular septation
  5. Outflow tract septation
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127
Q

When does the primordial heart start to develop?

A

at the beginning of week 4 as the embryo is rapidly growing and so diffusion is not fast enough

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128
Q

What is the real name foe paired endothelial strands and when and where do they appear?

A

angioblastic cords appear in the carcinogenic medoderm in the third week

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129
Q

What is the pericardium derived from?

A

intra-embryonic coelom

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130
Q

What is each layer of the pericardium developed from?

A
  • parietal (fibrous + serous): somatic mesoderm

- Visceral (Serous): Splanchnic mesoderm

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131
Q

Where does each horn of the sinus venosus get blood from?

A
  • The yolk sac (viteline v.)
  • The placenta (Umbilical v.)
  • Body of the embryo (common cardinal v.)
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132
Q

Where do the aortic arches arise from?

A

The aortic sac

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133
Q

Where do the aortic arches terminate?

A

dorsal aorta

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134
Q

Why does the heart loop?

A

The bulbous cordis and the ventricle grows faster than the other regions forming a U-shaped bulboventricular loop

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135
Q

What is dextrocardia?

A

Heart tube loops to the left side instead of the right

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136
Q

When is atrial and ventricular septation seen?

A

around the 27-30th day of embryonic development

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137
Q

When does the partitioning of the primordial atrium into left and right start?

A

At the end of week 4

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138
Q

What is the opening between the septum primum and the endocardial cushion

A

Ostium primum

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139
Q

What is the role of the oval foreman before birth?

A
  • Allows most of the blood o pass through the right atrium to the left atrium (non-functioning lung)
  • Prevents passage of blood in the opposite direction
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140
Q

What are the roles of the oval foremen after birth?

A
  • normally closes (increased pulmonary blood flow and shift of pressure to the left atrium)
  • Septum primum fuses with septum secundum
  • Oval fossa of an adult heart is a ruminant of the oval foremen
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141
Q

Name the four clinically significant types of atrial septum defects

A
  1. Foremen secundum defect
  2. Endocardial cushion defect
  3. Sinus venosus defect
  4. common atrium
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142
Q

What is the opening in the muscular ventricular septum called?

A

Interventricular foremen

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143
Q

How does the interventricular foremen close?

A

Aorticopulmonary septum rotates and fuses with the muscular ventricular septum

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144
Q

When does the partitioning of the bulbous cordis and truncus arteriosus happen?

A

During the 5th week of development

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145
Q

What are the early pacemakers?

A

Primordial atrium and then sinus venosus

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146
Q

When does the SA node develop?

A

During the 5th week

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147
Q

What is the aetiology of CHD?

A
  • Rubella infection in pregnancy
  • Maternal alcohol abuse
  • Maternal drug treatment and radiation
  • genetics
  • Chromosomal: down’s syndrome and turner’s syndrome
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148
Q

What are the causes if transposition of great vessels?

A
  • Failure of aorticopulmonary septum to take a spiral coarse

- Defect migration of neural crest cells

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149
Q

What is the first stage of the cardiac cycle?

A

Late diastole: both sets of chambers are relaxed and the verticals fill passivly

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150
Q

What is the second stage of the cardiac cycle?

A

Atrial systole: Atrial contraction forces a small amount of additional blood into the ventricals

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151
Q

What is the third stage of the cardiac cycle?

A

isovolumic ventricular contraction: first phase of ventricular contraction pushes AV valves closed bat does not create enough pressure to open the semilunar valves

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152
Q

What is the fourth stage of the cardiac cycle?

A

ventricular ejection: as ventricular pressure rises and exceeds the pressure in the arteries, the semilunar valve opens and blood is ejected

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153
Q

What is the fifth stage of the cardiac cycle?

A

isovolumic ventricular relaxation: as the ventricles relax, pressure in the ventricles falls, blood flows back into cusps of the semilunar valves and snaps them closed

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154
Q

What is the first heart beat noise?

A

The mitral and the tricusped valves closing

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155
Q

What is the second heart beat noise?

A

The aortic and the pulmonary valves closing

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156
Q

What is it that the sympathetic nervous system releases?

A

Noradrenaline plus circulating adrenaline from adrenal medulla

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157
Q

What receptors do adrenaline and Noradrenaline act on in the heart?

A

Beta 1 receptors on the sinoatrial node

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158
Q

What does the binding of adrenaline and Noradrenaline to beta 1 receptors do to the heart?

A

Increases the slope of action potential increasing the heart rate (tachycardia)

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159
Q

What does the parasympathetic system release and from where?

A

acetylcholine from the Vegas nerve

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160
Q

What receptors does acetylcholine work on in the heart?

A

Muscurinic receptors on the sinoatrial node

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161
Q

What does the binding of acetylcholine to muscurinic receptors do to the heart?

A

It hyperpolarises cells and decreases and decreases the slope of the pacemaker potential decreasing the heart rate (bradycardia)

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162
Q

What is preload?

A

The energy of contraction is proportional to the initial length of cardiac muscle

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163
Q

What is preload effected by in vivo?

A

It is effected by the end diastolic volume

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164
Q

What happens to stroke volume if there is a decreased venous return

A

decreased EDV and therefore decreased stroke volume

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165
Q

What is afterload?

A

The load against which the muscle tries to contract

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166
Q

What happen to stroke volume if the total peripheral resistance increases?

A

Aortic pressure will increase and so the ventricles will have to work harder to push open the aortic valve and it will have less energy to do the useful bit of contraction i.e. stroke volume will decrease

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167
Q

How does the sympathetic nervous system effect stroke volume?

A

It increases contractility: gives stronger, shorter contractions

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168
Q

How does the parasympathetic system effect stroke volume?

A

It has little effect, probably because the vagus nerve doesn’t innervate the ventricular muscles

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169
Q

How does hypercalcemia effect stroke volume?

A

it increases stroke volume

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170
Q

How does hypocalcaemia effect stroke volume?

A

it decreases stroke volume

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171
Q

How does ischaemia effect stroke volume

A

it decreases stroke volume

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172
Q

How do barbiturates effect stroke volume?

A

it decreases stroke volume

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173
Q

What structures are anterior to the heart?

A
  • Sternum
  • Left costal cartilages 4-7
  • Anterior edges of lungs and pleura
  • Thymic ruminants
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174
Q

What structures are posterior to the heart

A
  • Esophagus
  • Descending aortic arch
  • Thorasic vertebrae 5-8
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175
Q

What structures are lateral to the heart?

A
  • Lungs

- Phrenic nerve

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176
Q

What structures are inferior to the heart?

A

Central tendon of the diaphragm

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177
Q

What are the layers of the heart wall (in order of inside to outside)?

A
  • Endocardium
  • Myocardium
  • Intercalated disks
  • Epicardium
  • Epithelium
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178
Q

What tissues make up the Endocardium?

A
  • Simple squamous epithelium
  • Basement membrane
  • Connective tissue
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179
Q

What is the role of the Endocardium?

A
  • Lines the heart chambers

- Forms valves

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180
Q

Describe the myocardium

A
  • Cardiac muscles (myocytes)
  • Striated muscles, lots of mitochondria
  • Rich capillary bed
  • myocytes connected by intercalated disks
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181
Q

Describe intercalated disks

A
  • Complex junctions that connect myocytes
  • Desmosomes: connects at horizontal interface to bind myocytes together
  • Gap junctions: connects at vertical interface for electrical communication, this is essential to the cardiac cycle
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182
Q

Describe the Epicardium

A
  • connective tissue, basement membrane and simple squamous epithelium
  • The epicardium contains the main branches of the coronary arteries
  • -may be fatty
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183
Q

What is the endothelium?

A

The same layer as the visceral pericardium

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184
Q

What holds the heart in place?

A
  • Hangs by great vessels within the fibrous pericarium
  • Dense connective tissue bag
  • Attachments: Central tendon of diaphragm, sternum, roots of great vessels
  • Lined by serous pericardium
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185
Q

What is the serous pericardium made from?

A

Epithelium

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186
Q

What does the serous pericardium do?

A

It secretes pericardial fluid (lubricant) that allows freedom of movement during the cardiac cycle

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187
Q

What are the three layers of a basic blood vessel?

A
  1. Tunica intima
  2. Tunica media
  3. Tunica adventisia
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188
Q

What type of cells does the tunica intima have?

A
  • Simple squamous epithelium
  • Basement membrane
  • connective tissue
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189
Q

What is the tunica media made up of?

A
  • Smooth muscle

- Elastic tissue

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190
Q

What is the tunica adventitia made up of?

A

Fibrous connective tissue

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191
Q

What are the differences between arteries and veins?

A
  • Arteries have a smaller diameter than accompanying veins
  • Arteries have thicker walls
  • Arteries have a thick tunica media and a thin tunica adventitia
  • Veins have a thin tunica media and a thick tunica adventitia
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192
Q

What are the three types of arteries?

A
  • Elastic
  • Muscular
  • Arterioles
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193
Q

What type of vessel is elastic arteries

A

Large conducting

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194
Q

Give some examples of elastic arteries

A
  • The aorta
  • The common carotid
  • Pulmonary
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195
Q

What do elastic arteries do?

A
  • Pressure reservoir
  • Stretched during systole
  • During diastole the heart relaxes, the pressure falls and the artery recoils maintaining pressure on the blood
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196
Q

Why are elastic arteries so stretchable and able to recoil?

A

There is an excessive amount of elastic fibres in the tunica media in the form of layers (laminae). These layers are stretched by smooth muscles

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197
Q

What type of vessel are muscular arteries?

A

distrabuting

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198
Q

Give some examples of muscular arteries

A
  • Coronary arteries
  • Radial
  • Femoral
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199
Q

What do muscular arteries do?

A

Control the distribution of blood to regions

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200
Q

What are muscular arteries composed of?

A
  • T. intima: endothelial cells, BM
  • Thick T. media has smooth muscle cells
  • No elastic lamina between the muscle cells in the T. media
  • Elastic fibres are concentrated in two defined sheets called the internal elastic lamina (IEL) just under the spithelium and the extenal/outer elastic lamina (OEL) between the T. media and the T. adventitia
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201
Q

What do arterioles do?

A
  • they are terminal branches which supply blood to the capillary bed
  • Controls blood flow to the capillary beds (local)
  • Controls blood pressure (systemic)
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202
Q

What are arterioles made of?

A
  • T. intima: endothelium, BM, no IEL
  • 1-2 layers of smooth muscle in the t. media
  • no t. adventitia
  • Rich sympathetic nerve innervation
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203
Q

What do capillaries do?

A

main exchange site for nutrients and gasses

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204
Q

What are capillaries made up of?

A
  • Very thin walled
  • T. intima only: endothelium on BM
  • no T. media
  • no T. adventitia
  • Pericytes: incomplete layers of cells surrounding the BM, they have contractile properties which help control the flow of blood in the capillaries
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205
Q

Is the BP in capillaries low or high?

A

Low

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206
Q

What are the three types of capillaries?

A
  • Continuous
  • Fenestrated
  • Discontinuous
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207
Q

What is the role of continuous capillaries?

A
  • Control of what is exchanged
  • Material must pass through the cell or between the cell (junctions can control)
  • Selective transport mechanisms
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208
Q

How do the protein diaphragms in some of the fenestrations filter molecules?

A

-MW and/ or charge

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209
Q

How is there free passage of fluid and cells in discontinuous capillaries?

A

There are gaps between the endothelial cells (and BM)

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210
Q

Where would you find continuous capillaries?

A

Muscles

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211
Q

Where would you find fenestrated capillaries

A

endocrine glands, kidney, renal capuscle

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212
Q

Where would you find discontinuous capillaries?

A

Liver, spleen and bone marrow

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213
Q

What are sinusoids?

A
  • Large diameter discontinuous capillaries
  • Found where a large amount of exchange is taking place (liver, some endocrine glands)
  • T. intima contains a large amount of phagocytic cells
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214
Q

What is the structure of veins?

A
  • Thin T. intima
  • IEL or OEL is thin ir absent
  • T. media is very thin or absent
  • T. adventitia: collagenous tissue valves (to prevent backflow) endothelial projections into the lumen
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215
Q

Describe superficial veins

A
  • Thick walled

- No surrounding support

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216
Q

Describe Deep veins

A
  • Thin walled

- Surrounding support from the deep fascia and muscles

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217
Q

What does the lymphatic system do?

A
  • Drains tissue fluid from lost blood capillaries
  • Drains into the venous system
  • Nodes found alongside major veins and around the origin of major arteries
  • Valves direct flow
  • Clinically important in tumour cell metastasis
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218
Q

Describe lymph capillaries

A
  • Blind ended capillaries
  • Lines by very thin endothelium
  • No fenestrations
  • Absent/ rudimentary basal lamina
  • Lumen maintained at negative hydrostatic pressure
  • Anchoring filaments: fine collegenous filaments link endothelial cells to surrounding tissue keeping lumen open
  • No red blood cells in lumen
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219
Q

What does ischaemia mean?

A

relative lack of blood supply to a tissue/organ leading to inadequate O2 supply to meet the needs of the tissue or argan

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220
Q

What is hypoxic hypoxia?

A
  • Low inspired O2 level

- Normal inspired O2 but low PaO2

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221
Q

What is anaemic hypoxia?

A

normal inspired O2 but blood abnormal

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222
Q

What is stagnant hypoxia?

A

Normal inspired O2 but abnormal delivery

  • Local e.g. occlusion of vessel
  • systemic e.g. shock
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223
Q

What is cytoxic hypoxia

A

Normal inspired O2 but abnormal at tissue level

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224
Q

What factors effect Oxygen supply?

A
  • Inspired O2
  • Pulmonary function
  • Blood constitutes
  • Blood flow
  • Integrity of vasculature
  • Tissue mechanisms
  • Supply issues
  • Demand issues
  • Localised accumulation of lipid and fibrous tissue in the intima of arteries
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225
Q

What sort of supply issues affect oxygen delivery?

A
  • coronary artery atheroma
  • Cardiac failure (flow)
  • Pulmonary function- other disease or pulmonary oedema
  • Anaemia
  • Previous MI
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226
Q

What sore of demand issues affect oxygen delivery?

A
  • Heart as high as intrinsic demand

- Exertion/ stress increases the demand

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227
Q

What are the clinical consequences of ischaemia?

A
  • MI
  • TIA
  • Cerebral infarction
  • Abnormal aortic aneurysm
  • Peripheral vascular disease
  • Cardiac failure
  • coronary disease
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228
Q

What are the different effects ischaemia has?

A
  • Functional
  • Acute (you will see the changes)
  • Chronic (may go unnoticed for a while)
  • Acute on chronic (sudden worsening of a chronic event)
  • Biochemical
  • Cellular
  • Clinical
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229
Q

What are the functional effects Ischaemia has?

A
  • Blood/ O2 supply fails to meet the demand due to decreased supply, increased demand or bith
  • Related to rate of onset
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230
Q

What are the biochemical effects ischaemia has?

A

-Decreased O2 leads to anaerobic respiration which can causes cell death (the change in biochemistry leads to cell death)

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231
Q

What are the cellular effects ischaemia has?

A

-Different tissue have variable O2 requirements and are variably susceptible to ischaemia

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232
Q

What are the clinical effects of ischaemia?

A
  • Dysfunction
  • Pain
  • Physical damage (specialised cells are effected the most)
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233
Q

What is the outcome of ischaemia?

A
  • No clincal effect
  • Resolution verses therapeutic intervention
  • May lead to infarction
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234
Q

What is infarction?

A

Ischaemic necrosis within a tissue/organ in a living body produced by occlusion of either the arterial supply or venous damage

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235
Q

What is the aetiology of infarction?

A
  • Thrombosis
  • Embolism
  • Trauma
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236
Q

What are the four thing the scale of damage depends on?

A
  1. time period
  2. Tissue/ organ
  3. Pattern of blood supply
  4. Previous disease
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237
Q

What happens if a myocardial infarction happens for seconds?

A

Anaerobic metabolism, onset of ATP depletion

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238
Q

What happens if a myocardial infarction happens for less than 2 minutes?

A

Loss of myocardial contractility (heart failure)

239
Q

What happens if a myocardial infarction happens for a few minutes?

A
  • Ultrastuctural changes (myofibulator relaxation, glycogen depletion, cell and mitochondrial swelling)
  • Changes are reversable
240
Q

What happens if a myocardial infarction happens for 20-40 minutes?

A

Myocyte necrosis (irreversible)

241
Q

What happens if a myocardial infarction happens for more than 1 hour?

A

Injury to the micovasculature

242
Q

What is the appearance of infarcts at less than 24 hours?

A
  • No change on visual inspection

- A few hours to 12 hours post insult, see swollen mitochondria on electron microscopy

243
Q

What is the appearance of infarcts at 24-48 hours?

A
  • Pale infarct: myocardium, spleen, kidney, solid tissue
  • Red infarct: Lung, liver or loose tissues
  • Microscopically: acute inflammation initially at the edge of the infarct, loss of specialised features
244
Q

What is the appearance of infarcts at about 72 hours?

A
  • Macroscopically: a pale infarct will be yellow/ white and red peripherally and a red infarct will have little change
  • Microcopically: chronic inflammation; macrophages remove debris, granulation tissue, fibrosis
245
Q

What is the end result o the appearance of an infarction?

A
  • Scar replaces area of tissue damage
  • Shape depaends of territory of occluded vessel
  • reperfusion injury
246
Q

What is the reparation process?

A
  • Cell death
  • Acute inflammation
  • Macrophage phagocytosis of dead cells
  • Granulation tissue
  • Collagen deposition
  • Scar formation
247
Q

What are transmural infarcts?

A

ischaemic necrosis affects full thickness of the myocardium

248
Q

What is subendocardial infarction?

A

Ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

249
Q

What are acute infarcts?

A

Classified according to whether there is elevation but a significantly elevated troponin level (STEMI and Non-STEMI)

250
Q

What are the complications of myocardial infarctions?

A
  • Sudden death
  • Arrhythmias
  • Angina
  • Cardiac failure
  • Cardiac rupture
  • Re-infarction
  • pericarditis
  • Pulmonary embolism secondary to DVT
  • papillary muscle dysfunction
  • Mural thrombosis
  • Ventricular aneurysm
  • Dressler’s syndrome
251
Q

What is aneurysm disease?

A
  • Dilation of all layers of the aorta
  • Increasing diameter> 50% (abdominal aorta 3 cm)
  • Most (95%) are infarenal (below the level of the two renal arteries)
  • You also get aneurisms caused by trauma (false aneurism) which tends to be be radial and femoral arteries
252
Q

What are the causes of aneurysm disease?

A
  • Degenerative disease
  • Connective tissue disease
  • Infection
253
Q

What are the risk factors?

A
  • Male sex
  • Age
  • Smoking
  • Hypertension
  • Family history
254
Q

What is the normal presentation of an aneurysm?

A
  • Asymptomatic
  • Feel mass on examination
  • Family history
  • Incidentally found on scan
255
Q

Who is screening offered to?

A

65+ men

256
Q

What is the outcome of screening?

A
  • Normal aorta: discharged
  • Small AAA (3.0-4.4 cm): will be invided to annual USS scans
  • Medium AAA (4.4-5.5cm): will be invited to monthly USS scans
  • Large AAA (>5.5): sent to nearest vascular surgery unit
257
Q

What are the symptoms of an impending rupture of an aortic aneurysm?

A
  • Increasing back pain

- Tender AAA

258
Q

What are the symptoms of a rupture of an aortic aneurysm?

A
  • Abdo/back/flank pain
  • Painful pulsetile mass
  • Haemidynamic instability (single episodes or progressive)
  • Hypoperfusion (peripherally shut off, cold, confused)
259
Q

What are the unusual presentations of an AAA?

A
  • Distal embolism
  • Aortocaval fistula (erodes into the vena cava)
  • Aortoentric fistula (erodes into bowel)
  • Urteric occlusion
  • Duodenal obstruction
260
Q

At what size of AAA is treatment offered?

A

5.5 cm (3-15% chance of rupture)

261
Q

What investigations are done for AAA to tell if they are a candidate for repair?

A
  • Full history and examination
  • Bloods
  • ECG
  • SCHO
  • PFTs
  • MPS
  • CPEX
  • End of bed test
  • patient prefereance
262
Q

What are the advantages of USS?

A
  • Cheap
  • no radiation
  • no contrast
263
Q

What are the disadvantages of USS?

A
  • Operator dependent

- Inadequate for surgical planning

264
Q

What are the advantages of CT/MRI?

A
  • quick
  • not operator dependent
  • gives a detailed anatomy and so necessary for surgical planning
265
Q

What are the disadvantages of CT/MRI?

A
  • Contrast

- Radiation

266
Q

What are the requirements of a stroke?

A

-A neurological loss of deficit (function)
-Of sudden onset
Lasts more than 24 hours
-Of vascular origen

267
Q

What is a transient ischaemia attack?

A

A neurological loss of deficit that lasts less than 24 hours

268
Q

What are the causes of a stroke?

A
  • Blockage of a vessel with thrombus or clot
  • Disease of the vessel wall
  • Disturbance of the normal properties of the blood
  • Rupture if the vessel wall
  • Carotid stenosis
  • Carotid disease
  • Cardioemolic stroke
  • Small vessel stroke
  • Carotid dissection
269
Q

What are the symptoms of a stroke?

A
  • Loss of power
  • Loss of sensation
  • Loss of speech
  • Loss of vision
  • Loss of coordination
270
Q

What are the four different stroke sub-types?

A
  • TACS (total anterior circulation stroke)
  • PACS (Partial anterior circulation stroke_
  • LACS (Lacunar stroke)
  • POCS (Posterior circulation stroke)
271
Q

What are the signs of a TACS?

A
  • weakness
  • sensory deficits
  • Homonymous hemianopia (loss of vision)
  • Higher cerebral dysfunction
272
Q

What are TACS usually due to?

A

The occlusion of proximal MCA or ICA

273
Q

What is the criteria for PACS:

A 
2 of:
-Weakness
-Sensory deficit 
-Higher cerebral dysfunction
or
-Restricted motor/ sensory deficit
274
Q

Where are most PACS occlusions located?

A

In the branches of MCA

275
Q

Where is the occlusion of LACS?

A

In the white matter

276
Q

Where does POCS affect?

A
  • Brainstem
  • Cerebellar lobe
  • Occupital lobe
277
Q

What are the criteria for POCS?

A
  • Bilateral motor/ sensory deficit
  • Disordered conjugate eye movement
  • Isolated homonyous hemianopia
  • Isolated cranial nerve palsy with contralateral motor/sensory deficit
  • Coma
  • Disordered breathing
  • Tinnitus
  • Vertigo
  • Horner’s
278
Q

What are the risk factors of stroke?

A
  • High blood pressure
  • Arterial fibrillation
  • Age
  • Race
  • Family history
279
Q

What investigations are done for stoke?

A
  • Blood tests (full blood count, Lipids)
  • ECG
  • CT
  • MRI (shows ischaemic stoke better than CT does)
  • Cardiac doppler
280
Q

Describe normal blood flow

A
  • Cells are held in the centre of the flowing blood surrounded by plasma
  • There is a pressure gradient resistant to the blood flow due to the decreasing diameter
  • Muscular arteries are less complaint than elastic arteries and are more compliant than veins
281
Q

name the defects in blood flow

A
  • Thromboembolism
  • Atheroma
  • Hyperviscosity
  • Spasm
  • External compression
  • Vasculitis
  • Vascular steel
282
Q

What is virchow’s triad?

A
  • Changes in the blood vessel wall
  • Changes in blood constitutes
  • Changes in the pattern of blood flow
283
Q

What is thrombosis?

A

Formation of a solid mass from the constitutes of blood within the vascular system during life

284
Q

What are the risk factors for a thromboembolism?

A
  • Cardiac failure
  • Severer trauma/ burns
  • Post-op
  • Naphrotic syndrome
  • Disseminated malignancy
  • Oral contraceptive
  • Increasing age
  • Bed rest/ immobilisation
  • Obesity
  • PMH
  • DVT
  • Propholaxis for surgical paients at risk
285
Q

What is critical limb ischaemia?

A
  • Atherosclerotic disease of the arteries supplyong the lower limbs
  • Less commonly vasculitis, buerger’s disease
  • Same disease process as coronary and carotid atherosclerotic disease (systemic disease)
286
Q

What are the risk factors of critical limb disease?

A
  • Male
  • Age
  • Smoking
  • Hypercholesterolaemia
  • Hypertension
  • Diabetes
287
Q

What are the symptoms of stage I critical limb ischaemia?

A
  • Asymptomatic

- Incomplete blood vessel obstruction

288
Q

What are the symptoms of stage II CLI?

A
  • Mild limb claudication
  • Stage IIA: claudication when walking distances more than 200 meters
  • Stage IIB: claudication when walking leass than 200 meters
289
Q

What are the symptoms of stage III CLI?

A
  • Rest pain

- Mostly in the feet

290
Q

What are the symptoms of stage IV CLI?

A

Necrosis and/or gangrene of the limb

291
Q

What are the signs of chronic ischaemia?

A
  • Ulceration
  • Pallor
  • Hair loss
292
Q

What is the Buerger’s test?

A
  • Elevate legs: pallor, get sever ischaemia if more than 20 degrees
  • Hang feet over the edge of the bed: slowly regain colour, dark red colour (hyperanaemic sunset foot)
293
Q

What is the management of peripheral arteries disease?

A
  • Antiplatlet
  • Statin
  • BP control (target 140/85)
  • Smoking cessation
  • Exercise
  • Diabetes control
294
Q

What imaging investigations are doen to look at peripheral arterial disease?

A
  • Duplex
  • CTA/MRA
  • Digital subtraction angiogram
295
Q

What does a surgical bypass for peripheral limb disease require?

A
  • Inflow
  • A conduit: vein from leg or arms (autologous), synthetic (PTFE/Dacron)
  • Outflow
296
Q

What are the risks of complications in a surgical bypass?

A
  • Bleeding
  • Wound infection
  • Pain
  • Scarring
  • DVT
  • PE
  • MI
  • CVA
  • LRTI
  • Death
  • Damage to nearby vein, artery, nerve
  • Distal emboli
  • Graft failure (stenosis, occlusion)
297
Q

What is the pathopysiology of acute limb ischaemia?

A
  • Arterial ambolis: MI, AF, proximal atherosclerosis (not DVT/PE)
  • Thrombosis: usually thrombosis of previously diseased artery
  • Trauma
  • Dissection
  • Acute anaurism thrombosis i.e. popliteal
298
Q

What is the history of acute limb ischaemia?

A
  • History of chronic limb ischaemia
  • Risk factors for CLI
  • Cardiac history
  • Onset/duration of symptoms
  • Functional status/ SH
299
Q

What si the presentation of acute limb ischaemia?

A
  • Pain
  • Pallor
  • Perishingly cold
  • Paraesthesia
  • Paralysis
  • Pulses
300
Q

What is the management of ALI?

A
  • ECG
  • Bloods
  • Nil by mouthe
  • Analgesia
  • Anticoagulate
301
Q

What is the pathophysiology of diabetic foot disease?

A
  • Miscrovascular peripheral artery disease
  • Peripheral neuropathy
  • Mechanical imbalance
  • Susceptibility to infection
302
Q

How must diabetics with diabetic foot disease take care of their feet?

A
  • Always wear shoes
  • Check fir of footwear
  • Cheack pressure points/plantar surface of foot regularly
  • Prompt and regulate woundcare of skin breaches
303
Q

What si the management of diabetic foot disease?

A
  • Prevention
  • Good wound care
  • Tracking infection- consider systemic antibiotics
  • Investigate for osteomylitis, gas gangrene, necrotising fascitis
  • Revascularisation
  • Amputation
304
Q

How is the aortic sac formed?

A
  • Extension of the truncus arteriosus of the primordial heart tube
  • First arteries to appear in the left and right primitive aorta
  • Each primitive aorta has a ventrical part and a dorsal part
  • After the fusion of the two endocardial tubes the two ventrical aortae partly fuse to form the aortic sac
  • Aortic branches arise from the aortic sac
305
Q

When do the pharyngeal arteries develop?

A

The 4th and 5th week

306
Q

How many aortic arches are there?

A

6

307
Q

What happens to aortic arch 1 and 2

A

the 1st and 2nd arch disappear early, remnant of the first arch forms part of the maxillary artery

308
Q

What happens to the aortic arch 3?

A

Constitutes the commencement of the internal carotid artery and is therefore named the carotid arch

309
Q

What happen to the 4th aortic arch?

A

The 4th right arch forms the right subclavian artey and the 4th left arch constitutes the distal part of the aortic arch

310
Q

What happen to the 5th aortic arch?

A

The 5th aortic arch either never forms or forms incompletely and then regresses

311
Q

What happen to the 6th aortic arch?

A
  • Left side: Left pulmonary artery and ductus areriosus

- Right side: right pulmonary artery

312
Q

What are most great artery anomalies normally the result of?

A

persistence of aortic arches that should normally regress

313
Q

What is varicose veins?

A
  • Torturous dilated superficial veins
  • Primary VVs: valvular dysfunction
  • Sights: Long saphenous, short saphenous
314
Q

What gender is varicose veins more common in?

A

females

315
Q

What are the signs and symptoms of Varicose veins?

A
  • Cosmesis
  • Localised or generalised discomfort in the leg
  • Nocturnal crams
  • Swelling
  • Acute haemorrhage
  • Superficial thrombophlebitis
  • Pruritus (itching)
  • Skin changes
316
Q

What is the treatment of varicose veins?

A
  • Surgery: high tie, stripping, multiple stab avulsions
  • Injection (sclerotherapy)
  • Minimally invasive procedures
  • Compression
  • Conservative (may include compression)
317
Q

What are the relative contraindications of superficial venous surgery?

A
  • Previous DVT (collaterals)
  • Arterial insufficiency
  • Patient co morbidity
  • Morbid obesity
318
Q

What are the complications in surgery for varicose veins?

A
  • Minor haemorrhage
  • Thrombophlebitis, haematoma
  • Wound problems, sever pain
  • Sural/saphenous nerves
  • damage to deep veins, arteries, nerves, DVT
319
Q

What are the minimally invasive treatments for varicose veins?

A
  • Foam sclerotherapy: chemical reaction with endothelium
  • Endovenous laser ablation: thermal ablation
  • Radiofrequency ablation: thermal ablation
320
Q

What are the results of the minimally invasive treatment options for varicose veins?

A
  • Short to medium term just as effective clinically as surgery
  • Long term results awaited
  • Cost-effectiveness: not known
321
Q

What are the signs and symptoms of chronic venous insufficiency?

A
  • Ankle oedema
  • Telangectasia
  • Venous eczema
  • Haemosiderin pigmentation
  • Hypopigmentation “atrophie blache”
  • Lipodermatosclerosis
  • Venous ulceration
322
Q

What is the pathophysiology of chronic vascular disease?

A
  • Venous hypertension
  • Venous engorgmnt and stasis
  • Imbalance of starling forces and fluid exudate
323
Q

What is the aetiology of chronic vascular disease?

A

Failure of calf muscle to pump:

  • Superficial venous reflux
  • Deep venous reflux
  • Venus obstruction
  • Neuromuscular
  • Obesity
  • Inactivity
324
Q

What is a leg ulcer?

A

Breach in the skin between the knee and the ankle joint, present for over 4 weeks

325
Q

What investigations do you do for a leg ulcer?

A
  • ABPI

- Dluplex

326
Q

What is the treatment of chronic venous Insufficiency?

A
  • Multi-layered granulated, elastic, high grade, comression therapy
  • Non-adherent dressings
  • Systemic and tropical therapy
  • Exercise (calf muscle pump)
327
Q

What is primary lymphoedema?

A
  • Congenital
  • Praecox
  • Tarda
328
Q

What is secondary lymphoedama?

A
  • Malignancy
  • Surgery
  • Radiotherapy
  • Infection
329
Q

How do you get MAP (main arterial pressure)?

A

CO (cardiac output)+ TPR (total peripheral resistance)

330
Q

What happens if MAP (main arterial pressure) is too low or high?

A
  • Too low: Syncope (feinting)

- Too high: Hypertension

331
Q

What are barroreceptors?

A

Stretch receptors (in the walls of the blood pressure- the aortic arch and the carotid sinus) detect blood pressure

332
Q

Where is the integrating centre for the arterial baroreflex?

A

The medula

333
Q

What is the Glossopharyngeal nerve?

A

The nerve that supplies the carotid sinus

334
Q

What does the Vegas nerve do?

A

Control the pacemaker which decreases heart rate

335
Q

What are central chemoreceptors?

A

respond to CO2 and O2 conc. in the blood

336
Q

What do chemoreceptors in muscles respond to?

A

metabolites in the local blood flow

337
Q

When are joint receptors activated?

A

when you move joints more frequently which is taken as physical activity

338
Q

What do high centres do?

A

tells the medullary cardiovascular centres that you are about to do some work and to get ready

339
Q

What is the reason you don’t fall down all the time?

A

arterial barorreflex

340
Q

What are the effects of standing on blood pressure?

A
  • Increased hydrostatic pressure causes pooling of blood in veins/venules of feet/ legs
  • Decreased VR, decreased preload, decreased SV, decreased CO, decreased MAP
  • Decreased baroreceptor firing
341
Q

What is the valsava manouver?

A

Forced expiration against a closed glottis

342
Q

Talk through the valsava manouver

A
  • Increased thoracic pressure is transmitted through the aorta
  • Increased thoracic pressure, decreased VR, decreased SDV, decreased SV, decreased CO, decreased MAP
  • Decreased MAP is transmitted by baroreceptors which initiate reflex increased CO and increased TPR
  • Decrease in thoracic pressure is transmitted through the aorta
  • VR restored so SV increased (massivly), so increased effects not worn off (BP is higher here than before)
  • Back to normal
343
Q

What do elastic arteries do?

A

act as a pressure reservoir: they damp down pressure variations

344
Q

What is the pressure wave effected by?

A
  • Stroke volume
  • Velocity of ejaculation
  • Elasticity of arteries
  • TPR
345
Q

Does the pressure rise or fall as it goes down the vascular tree?

A

fall

346
Q

What is the pressure at the start of the arteries

A

~95mmHg

347
Q

What is the pressure at the end of the arteries?

A

~90mmHg

348
Q

What is the pressure in the arterioles?

A

~40mmHg

349
Q

What fraction of the systemic BP is the pulmonary BP?

A

~1/5

350
Q

What are the fastest vessels

A

The bigger ones

351
Q

How does gravity affect the driving pressure from the arteries to the veins?

A

It doesn’t

352
Q

What does gravity do to blood flow?

A
  • Causes venous distention in the legs
  • Decreases EDV, preload, SV, CO and MAP
  • Can cause orthostatic (postural) hypotension
  • Causes venous collapse in the neck (because the pressure is lower) and can be used to estimate central venous pressure
353
Q

What does the skeletal muscle pump do?

A
  • Sustained muscle contraction (weight lifting): stops blood getting back to heart
  • Rhythmic muscle contraction (running): Helps get the blood get back to the heart
354
Q

What is the respiratory pump?

A

The harder and the deeper you breath the more blood that is sucked back into the heart

355
Q

What is venomotor tone?

A
  • The state of contraction of smooth muscle surrounding the venules and veins
  • Mobilises captaincy
356
Q

What is the systemic filling pressure created by?

A

Ventricles and transmitted through the vascular tree to the veins

357
Q

What happen to the systemic filling pressure during exercise?

A

It increases

358
Q

Describe the gross structure of the capillary system

A
  • Specialised for exchange
  • Lots of them
  • Thin walled (presents a smaller diffusion barrier)
  • Small diameter (bigger surface area:volume ratio)
359
Q

Describe the ultrastructure of the capillary system

A
  • Continuous: No clefts or channels e.g. the brain or clefts only e.g. muscle
  • Fenestrated: clefts and channels e.g. intestine (specialised for fluid exchange)
  • Discontinuous: clefts and massive channels e.g. liver (due to proteins being produced
360
Q

Describe the anti-clotting mechanisms of the endothelium

A
  • Formation of a platelet plug (send out signals to fibrinogen)
  • Formation of Fibrin from fibrinogen by the enzyme thrombin
  • Fibrin clot forms
  • Produces tissue factor pathway inhibitor (TFPI): stops thrombin production
  • Expresses thrombomodulin: binds excessive thrombin
  • Secretes tissue plasminogen activator (t-PA): digests vlots
361
Q

What is the purpose of the anticlotting mechanisms of the endothelium?

A
  • Stops blood contacting collagen (by forming a physical barrier): no platlete aggregation
  • Produces prostacyclin and NO: both inhibit platelete aggregation
362
Q

How does exchange take place?

A
  • Diffusion: self-regulating, Non-saturable, Non-polar substances across membranes, polar substances across clefts/channels
  • Carrier mediated transport e.g. glucose transporter (GLUT 3 etc.)
  • Bulk flow
  • Starling forces: capillary hydrostatitc pressure vs ISF hydrostatic pressure, it varries between capillary beds but overall it’s ~20l is lost and ~17l is regained
363
Q

What does the lymph system do?

A
  • Lymph drains into the low pressure part of the systemic circulation
  • If starling’s forces are not working then you can get an oedema
364
Q

How can you get an oedema?

A
  • Lymphatic obstruction e.g. due to filariasm surgery
  • Raised CVP e.g. due to ventricular failure
  • Hypoproteinaemia e.g. due to nephrosis, liver failure, nutrition
  • Increased capillary permeability (inflammation) e.g. rheumatism
365
Q

What is the function of the kidney?

A
  • Excretion of waste product
  • Maintenance of ion balance
  • Regulation of pH
  • Regulation of osmolarity
  • Regulation of plasma volume
366
Q

How is it that the kidneys are one of the main factors which effect the long term control of blood pressure?

A

-Controlling plasma volume is used to regulate MAP

367
Q

How is it that the kidneys control how much water is lost and how much is retained

A
  • The fluid that has been filtered out has either been filtered or modified: either reabsorbed into the blood or secreted out
  • The clever renal counter-current system creates a very high osmollarity outside the collecting duct
  • Control over sodium transport determines how big that osmolarity gradient is
  • control over the permeability of the water determines if water follows that osmotic gradient or not
368
Q

What does it mean when sodium is pumped out of the filtrate of the kidney?

A
  • The conc. of the filtrate decreases as you go on

- This results in a larger conc. gradient

369
Q

What does making the collecting duct very permeable or impermeable to water do

A
  • Permeable: lots of water re-absorption, little urine and it conserves plasma volume
  • Impermeable: little re-absorption, lots of urine (diuresis) and a reduction in plasma volume
370
Q

Where is the renin-angiotensin-aldosterone system produced?

A

The juxtaglomerular (granule cells) of the kidney

371
Q

What are the triggers of the renin-angiotensin-aldosterone system?

A
  • Activation of the sympathetic nerves to the juxtaglomerular apparatus
  • Decreased distension of afferent arterioles (the renal baroreflex)
  • Decreased delivery of Na+/Cl- through the tubule
372
Q

What happens if the renin-angiotensin-aldosterone system is triggered?

A

Rennin is produced

373
Q

What does renin do?

A
  • Converts inactive angiotensin to angiotensin I

- Which in turn is converted b y angiotensin converting enzymes to angiotensin II

374
Q

What does angiotensin do?

A
  • Stimulates the release of aldosterone from the adrenal cortex: increases Na+ re-absorption in the loop of henle and therefore reduces diuresis and increases plasma volume
  • Increases the release of ADH
  • Is a vasoconstrictor
375
Q

Why is the renin-angiotensin-aldosterone system a negative feedback system?

A
  • Multiple mechanisms detect any decrease in MAP
  • Stimulates release of renin
  • This evokes multiple mechanisms which increase MAP
376
Q

Where is the Anti-diuretic hormone produced and released?

A
  • Produced: The hypothalamus

- Released: The posterior pituitary

377
Q

What are the triggers of ADH?

A
  • A decrease in blood volume (as sensed by cardiopulmonary baroreceptors and relayed via medullary cardiovascular centres)
  • An increase in osmolarity of interstitial fluid (sensed by the osmoreceptors in the hypothalamus)
  • Circulating angiotensin II
378
Q

What is the function of ADH?

A
  • Increases the permeability of the collecting duct to water, therefore decreases diuresis and increases plasma volume
  • Causes vasoconstriction (hence its alternative name vasopressin), therefore increases MAP
379
Q

How is ADH a negative feedback system?

A
  • Multiple mechanisms to decrease any decrease in MAP
  • Stimulates the release of ADH
  • This evokes multiple mechanisms which increase MAP
380
Q

Where is the Atrial natriuretic and the brain netriuretic peptide produced and released?

A

produced in and released from the myocardial cells in the atria and (despite its name) the ventricles respectivly

381
Q

What are the triggers for Atrial natriuretic and the brain netriuretic peptide?

A

Increased distension of the atrium and the ventricals

382
Q

What are the functions of the Atrial natriuretic and the brain netriuretic peptide?

A
  • Increases exertion of Na+ (natriuretic), therefore water as well
  • Inhibits the release of renin
  • Acts on the medullary CV centres to reduce MAP
383
Q

What does varying the radius of resistance vessels do?

A

Control the TPR an therefore regulate MAP

384
Q

How does the sympathetic nerves regulate arterial resistance?

A
  • Releases nor-epinephrine
  • Binds to alpha 1 receptors
  • Causes arteriolar constriction
  • Therefore decreases flow through that tissue and tends to increase TPR
385
Q

How does the parasympathetic nerves regulate arterial resistance?

A

Usually no effect (with the exception of genitalia and salivary glands_

386
Q

Give an example of and state the effect of epinephrine binding to beta 2 receptors

A
  • e.g. skeletal and cardiac muscle
  • Causes arteriolar dilation
  • Increases flow through that tissue and tends to decrease TPR
387
Q

What does angiotensin II do for regulation of arterial resistance?

A
  • Produced in response to low blood volumes
  • Causes arteriolar constriction
  • Therefore increases TPR
388
Q

What does Atrial natriuretic peptide and brain natriuretic peptide (pro-diuretic hormone) do for regulation of arterial resistance?

A
  • Released in response to high blood volume
  • Causes arteriolar dilation
  • Therefore decreases TPR
389
Q

What does active (metabolic) hyperaemia do for intrinsic control of arterial resistance?

A
  • Increase metabolic activity and causes increased concentration of metabolites
  • Sensed by the endothelium which triggers the release of the EDRF (endothelium derived relaxing factor- Nitric oxide)
  • Causes arteriolar dilation
  • Increases flow to wash out metabolites
  • An adaption to match blood supply to the metabolic needes of the tisuue
390
Q

What is pressure flow autoregulation?

A
  • Decreased MAP causes a decreased flow
  • Metabolites accumulate
  • Triggers release of EDRF
  • Arterioles dilate and flow is restored to normal
391
Q

What is reactive hyperaemia?

A
  • Occlusion of blood supply causes a subsequent increase in blood flow
  • An extreme version of autoregulation
392
Q

Explain the coronary circulation regulation of peripheral resistance

A
  • Each time the heart contracts it cuts off its own blood supply
  • But it still has to cope with increased demand during exercise
  • Shows excellent active hyperaemia
  • Expresses many beta 2 receptors
  • These swamp any sympathetic arteriolar constriction
393
Q

How does the cerebral circulation regulate arterial resistance?

A
  • Needs to be kept stable, whatever

- Shows excellent autoregulation

394
Q

How does the Pulmonary circulation regulate arterial resistance?

A
  • Decreased O2 causes arteriolar constriction
  • i.e. the opposite response to most tissue
  • Ensures that blood is directed to the best ventilated parts
395
Q

How does the renal circulation regulate arterial resistance?

A
  • The main function id filtration which depends on pressure
  • Change in MAP would have a big effect on blood volume
  • Shows excellent pressure autoregulation
396
Q

What is the aetiology of mitral stenosis?

A
  • Rheumatic heart disease
  • Congenital mitral stenosis
  • systemic conditions: systemic lupus erythematous or rheumatoid arthritis
397
Q

What should be the size of the mitral valve normally?

A

4-6cm2

398
Q

What is the size of a stenosed mitral valve?

A

<2cm2

399
Q

What are the consequences of a stenosed mitral valve?

A

A-V pressure gradient increases

  • LA pressure increases
  • Pulmonary venous and capillary pressure increases
  • Pulmonary vascular resistance increases
  • Pulmonary aortic pressure increases and pulmonary hypertension develops
  • RH dilation with tricusped regurgitation and pulmonary regurgitation (this is when people start to suffer)
400
Q

What does the severity of mitral stenosis increase with?

A
  • Trans-valvular pressure gradient
  • Trans-valvular flow rate (affected by cardiac output and heart rate)
  • Trachycardia (exercise, acute illness, pregnancy, atrial fibrillation etc.)
401
Q

What are the clinical manifestations of mitral stenosis?

A
  • Dyspnoea: mild exertional pulmonary oedema (cardinal symptom)
  • Haemoptysis: rupture of thin walls
  • Systemic embolisation: LA and LA appendage enlargement
  • Infection endocarditis
  • Chest pain
  • Hoarseness (compression of the left recurrent laryngeal nerve)
402
Q

What should you find in the clinical examination if there is mitral stenosis?

A
  • Mitral facies (red cheeks and nose)
  • Pulse is normal
  • JVP- prominent wave
  • Trapping apex beat and diastolic thrill
  • Right ventricular heave
403
Q

What investigations should be done for mitral stenosis?

A
  • ECG: thickness and scarring of the leaflets, fusion of the commissures
  • Cardiac catheterisation
  • CXR
404
Q

What is the treatment of mitral stenosis?

A
  • Diuretics and restriction of sodium intake
  • Atrial fibrillation: sinus rhythm restoration or ventricular rate control
  • Anticoagulation: all those with atrial fibrillation and debatable in sinus rhythm
  • Valvotomy (balloon vs surgical)
  • MVR
405
Q

What is the aetiology of mitral regurgitation?

A
  • Rheumatic heart disease
  • Mitral valve prolapse
  • Ineffective endocarditis
  • Degenerative
  • Functional MR due to left ventricular and annular dilation
406
Q

What does mitral regurgitation effect?

A
  • preload
  • Afterload
  • LV contractility
  • Results in annular enlargement which increases regurgitation volume
407
Q

How does the left ventricle compassionate for the increased regurgitation volume?

A
  • Acute: end systolic pressure and end systolic volume decreases and wall tension also decreases
  • Chronic: end diastolic volume increases, end systolic volume returns to normal and an eccentric LV hypertrophy developes
408
Q

What does left atrium compliance do?

A
  • Reduced: marked rise in pressure, thickening of the atrium and myocardium, increases in pulmonary vascular resistance and remodelling of the vasculature with pulmonary hypertension
  • Increased: marked volume enlargement, lesser changes in pulmonary vasculature, develops atrial fibrillation
  • A combination of the two
409
Q

What is the clinical manifestations of mitral regurgitation?

A
  • Acute (valve perforation, chordal/ pap muscle): breathlessness, pulmonary oedema, cardiac shock
  • Chronic: fatigue, exhaustion (low CO), right heart failure, dyspnoea or palpitations due to atrial finrillation
410
Q

What clinical examinations does one do for mitral regurgitation?

A
  • Pulse: normal or reduces in heart failure
  • JVP: prominent if right heart failure is present
  • Brisk and hyperdynamic apex beat
  • Right ventricular heave
411
Q

What investigations are done for mitral regurgitation?

A
  • ECG
  • CXR
  • Cardiac catheterisation
412
Q

What is the symptoms of mitral regurgitation?

A
  • Acute MR: preload and afterload reduction may be lifesaving (sodium nitrprusside, dobutamine, IABP)
  • Chronic MR: lack of evidence that any therapy is beneficial for haemodynamic improvement, LV function improvement preservation
  • Mitral valve apparatus repair or replace
413
Q

What is the aetiology of aortic stenosis?

A
  • Degenerative (common): linked to atherosclerosis
  • Rheumatic (less common)
  • Bicuspid (commonest congenital heart condition)
414
Q

What is the pathophysiology of aortic stenosis?

A
  • Increased LV systolic pressure
  • severe concentric hypertrophy and left ventricular hypertrophy
  • Increased LV end-diastolic pressure (LA pressure rises, pulmonary hypertension)
  • Increased myocardial O2 consumption
  • Myocardial ischaemia
  • LV failure
415
Q

What are the symptoms of Aortic stenosis?

A
  • Long asymptomatic phase
  • Chest pain
  • Syncope/ dizziness
  • Breathlessness on exertion
  • Heart failure
416
Q

What would be found in a clinical examination of aortic stenosis?

A
  • Pulse: small volume and slowly rising
  • JVP: prominent if RH failure is present, low BP
  • Vigorous and sustained apex beat
  • RV heave
  • Normal S1 with a less audible S2
417
Q

What investigations are done for aortic stenosis?

A
  • ECG
  • CXR
  • Cardiac catheterisation
418
Q

What is the aetiology of aortic regurgitation?

A
  • Aorta: dilated aorta (marfans, hypertension), connective tissue disorder
  • Leaflets: bicuspid aortic valve, rheumatic heart disease, endocarditis, myomatous degeneration
419
Q

What is the pathophysiology of aortic regurgitation?

A
  • LV accommodates both stroke volume and regurgitatant volume
  • Increased LV end-diastolic volume and LV systolic pressure
  • LV hypertrophy and LV dilation
  • Myocardial ischaemia
  • LV failure
420
Q

What is the treatment for aortic stenosis?

A
  • Limited for those who develop heart failure

- Aortic valve replacement

421
Q

What are the symptoms for aortic regurgitation?

A
  • Chronic: long asymptomatic phase, exertional breathlessness
  • Acute AR: poorly tolerated as well as tension cannot adapt
422
Q

What treatments are done for aortic regurgitation?

A
  • Vasodilator therapy shown to display the timing for surgical intervention
  • Aortic valve replacement or repair
423
Q

What are the things that go under acute coronary syndromes?

A
  • Unstable angina
  • NSTEMI
  • STEMI
  • Sudden cardiac death
424
Q

What causes acute coronary syndromes?

A

Plaque rupture and thrombosis

425
Q

What is the main difference between acute coronary syndromes symptoms and angina symptoms?

A

Angina only happens on exertion where as ACS will almost always give symptoms at rest

426
Q

What are the risk factors for coronary artery disease?

A
  • Age
  • Gender
  • creed
  • Family history
  • Genetic factors
  • Previous angina
  • Cardiac events or intervention
  • Smoking
  • Diabetes mellitus
  • Hyperlipidaemia
  • Hypertension
  • Lifestyly: diet and exercise
427
Q

What will unstable angina start off as?

A

angina on effort, but progressive increasing frequency and severity, often provoked by less exertion and/or then at rest

428
Q

What will NSTEMI start off as?

A

myocardial ischaemia symptoms occurring at rest

429
Q

What is the immediate treatment of unstable angina and non-ST elevation MI

A
  • Morphine (or dimorphine)
  • Oxygen
  • Nitroglycerine (GTN spray or tablet)
  • Aspirin 300mg orally (crush/chew)
430
Q

What are the causes of cardiac ischaemia?

A
  • Atherosclerosis
  • Embolism
  • Coronary thrombosis
  • Aortic dissection
  • Arteritides
  • Congenital
431
Q

What are the manifestations of ischaemic heart disease?

A
  • Angina
  • MI
  • Arrhythmias
  • Chronic heart failure
  • Sudden death
432
Q

What are the dangerous patterns of coronary heart disease?

A
  • Left main stem stenosis

- 3 vessel coronary artery disease

433
Q

What are the indications for coronary artery bypass grafting?

A
  • Symptomatic (any CAD pattern)

- Prognostic (LMSS, 3VDx)

434
Q

How are patients selected for CABG?

A
  • Adequate lung function
  • Adequate mental function
  • Adequate hepatic function
  • Ascending aorta OK
  • Distal coronary targets OK
  • LV EF>20%
435
Q

What are the conduits for CABG?

A
  • Reversed saphenous vein
  • Internal mammary arterties
  • Radial arteries
436
Q

What are the problems related to a sternotomy?

A
  • Wire infection
  • Painful wires
  • Sternal dehiscence
  • Sternal malunion
437
Q

What are the post-op problems in cardiac surgery?

A
  • Cardiac tamponade
  • Death
  • Stroke
438
Q

What are the primary and secondary features of cardiac tamponade following cardiac surgery?

A
  • Primary: Raised CVP, raised heart rate, low BP

- Secondary features: Oliguria, increased oxygen requirements, metabolic acidosis

439
Q

What is the treatment of tamponade following surgery?

A

chest re-opening

440
Q

What are the causes of valvular heart disease in an adult?

A
  • Degenerative
  • Congenital
  • Infective
  • Inflammatory
  • LV or RV dilation
  • Trauma
  • Neoplastic
  • Paraneoplastic
441
Q

What is rheumatic fever?

A
  • A relapsing illness
  • Related to streptococcal infections
  • The hallmark pathology is pancarditis
  • Skin and joint malfunctions
442
Q

How is rheumatic fever treated?

A

Asprin and bed rest

443
Q

What are the indications for surgery in endocarditis?

A
  • Sever valvular regurgitation
  • Large vegetation
  • Persistent pyrexia
  • Progressive renal failure
444
Q

What is the cardiopulmonary bypass?

A
  • Blood drained from the RA and returned to the ascending aorta
  • Heart and lung function taken over by CPB mchine
  • Systemic anti-coagulation needed
  • Induced hypothermia
445
Q

What are the options of heart valves prothesis?

A
  • Biological valve
  • Mechanical valve
  • Mitral valve repair
446
Q

What are the advantages and disadvantages of a biological valve?

A
  • No warfarin required

- Wears out after 15 years

447
Q

What are the advantages and disadvantages of a mechanical valve?

A
  • Warfarin required

- Valve lasts >40 years

448
Q

What is dilated cardiomyopathy?

A
  • A structural and functional description, the ventricular function is impaired
  • Can be a primary problem or the end result of ant pathological insult to the myocardium
449
Q

Excluding ischaemia and valvular causes, what is the aetiological backround of dilated cardiomyopathy?

A
  • Genetic and familial DMC: SCN5A gene, muscular dystrophy
  • Inflammatory, infectious, autoimmune, postpartum
  • Toxic: drugs, exogenous chemicals, endocrine
  • Injury, cell loss, scar replacement
450
Q

What are the symptoms of dilated cardiomyopathy?

A
  • progressive, slow onset
  • Dyspnoea
  • Fatigue
  • Orthopnoea
  • PND
  • Ankle swelling
  • Weight gain of fluid overload
  • Cough
451
Q

What will you find when examining someone with dilated cardiomyopathy?

A
  • Poor superficial perfusion
  • Thready pulse
  • Irregular if in AF
  • SOB at rest
  • Narrow pulse pressure
  • JVP elevated +/- TR waves
  • Displaced apex
  • S3 and S4
  • MR murmur often
  • Pulmonary oedema
  • Pleural effusions
  • Ankle oedema
  • Acites
  • Hepatomegally
452
Q

What are the investigations someone does for a dilated cardiomyopathy?

A
  • Repeated ECG noting LBBB if present
  • CXR
  • N terminal pro brain natriuetic peptide
  • Basic bloods: FBC, U and E
  • Echo
  • CMRI
  • Coronary angiogram
  • Sometimes biopsy depending on the time coarse of cardiomyopathy
453
Q

What are the general measures of treatment for dilated cardiomyopathy?

A
  • Correct anaemia
  • Remove exacerbating drugs e.g. NSAIDS
  • Correct an endocrine disturbance
  • Advise on fluid and salt intake, reduce it
  • Advise on managing weight to identify fluid overload
  • AF nurse referral
454
Q

What are the more specific measures for the management of Dilated cardiomyopathy?

A
  • ACEI, ATII blockers, diuretics
  • Beta blockers
  • Spironolactone
  • Anticoagulants as required
  • SCD risk assessment with ICD or CRT-D/P implant
  • Cardiac transplant
455
Q

What is restrictive and infiltrative cardiomyopathy?

A
  • Describes the physiology of filling and myocyte relaxation capacity
  • The systolic function may or may not be impaired
456
Q

What is the aetiology of restrictive and infiltrative cardiomyopathy?

A
  • Non infiltrative: familial, forms of HCM, scleroderma, diabetic, pseudoxanthoma, elasticum
  • infiltrative: amyloid, sarcoid
  • Storage diseases: haemachromatosis, Fabry disease
  • Endomyocardial: fibrosis, carcinoid, radiation, drug effects
457
Q

What is the pathology of restrictive and infiltrative cardiomyopathy?

A
  • The inability to fill well a ventricle whose wall has reduced compliance
  • Relaxation of the ventricular wall is an active process that needs functioning intact myocytes, it is not passive
458
Q

What are the specific measures of management for restrictive and infiltrative cardiomyopathy?

A
  • Limited diuretic use as low filling pressures will cause problems
  • Beta blockers limited ACEI use
  • Anticoagulants required
  • SCD risk assessment with ICD or CRT-D/P implant
  • Cardiac transplant
459
Q

What is hypertrophic cardiomyopathy?

A
  • Morphological decription
  • Impaired relaxation is a common feature
  • Systolic function is usually adequate albeit with some functional abnormality
460
Q

What are the symptoms of hypertrophic cardiomyopathy?

A
  • Asymptomatic for many
  • Fatigue
  • Dyspnoea
  • Anginal like chsst pain
  • Exertional pre syncope
  • Syncope related to arrhythmias or LVOT obstruction
461
Q

What are the examination findings for hypertrophic cardiomyopathy?

A
  • Can be none
  • Notched pulse pattern
  • Irregular pulse if in AF or ectopy
  • Double impulse over apex, thrills and murmurs, often dynamic, LVOT murmur will increase with valsalve and decrease with sqautting
  • JVP can be very raised in very restrictive filling
462
Q

What are the general measures of management of hypertrophic cardiomyopathy?

A
  • Avoid heavy exercise
  • Avoid dehydration
  • Explore FH and first degree relatives, ECGs and Echos may be required
  • Consider genetic testing
  • Regular FU to re appraise the risk and progress
463
Q

What are the more specific measures of management of hypertrophic cardiomyopathy?

A
  • Drugs to try and enhance relaxation, variable results but often if symptomatic, beta blockers, verapamil, disopyramide
  • If in AF anticoagulise
  • Obstructed form: surgical or alcohol septal ablation
  • ICD if required based on risk stratification
464
Q

What is myocarditis?

A
  • Acute or chronic inflammation of the myocardium
  • Can be associated with pericarditis
  • Can impair myocardial dunction, conduction and generate arrhythmia
465
Q

What are the causes of myocarditis?

A
  • Viral
  • Bacterial
  • Fungal
  • Protozoal
  • Parasitic
  • Toxins
  • Hypersensitivity
  • Autoimmune activation
466
Q

What are the specific viruses that can cause myocarditis?

A
  • Adenovirus
  • Coxsackeivirus, enterovirus
  • Cytomegalovirus
  • Parvovirus B19
  • Hepatitis C virus
  • HIV
  • Herpesvirus
  • EBV
  • Mixed infections
467
Q

What are the specific bacterial causes of myocarditis?

A
  • Mycobacterial species
  • Chlamydia pneumoniae
  • Streptococcal species
  • Mycoplasma pneumoniae
  • Treponema pallidum
468
Q

What are the symptoms of myocarditis?

A
  • Heart failure, SOB, CP in only 26%
  • Shorter coarse of a few weeks
  • May not have fever
  • Signs of HF
469
Q

What are the general measures of myocarditis management?

A
  • Supportive treatment of HF and support for brady and tachy arrhythmias
  • Immunotherapy if biopsy or other Ix point to a specific diagnosis
  • Stop possible drugs or toxic agent exposure
470
Q

What are the key causes of pericarditis?

A
  • Viral
  • Bacterial
  • Post MI
  • Perforation
  • Dissection of proximal aorta
  • Neoplasia
471
Q

What are the symptoms of pericarditis?

A
  • chest pain with pleuritic features and postual features, sitting forward usually improves it lying back makes it worse
  • Fever
472
Q

What are the signs of pericarditis?

A
  • Temp up
  • Pericardial rub LSE
  • Look for JVP as if effusion is pressent
  • Low BP
  • Muffled HS and raised JVP should make you think not just pericarditis but effusion
  • High fever and very unwell despite no effusion may suggest bacterial
473
Q

What are the general measures of treatment of pericarditis?

A
  • Viral is concervative
  • Idiopathic gets clochicine and limited use of NSAIDs
  • Bacterial must be drained even if small effusion and antimicrobials, high death rate
  • If large effusion present and some haemodynamic effects then drain
474
Q

What are the symptoms of a pericardial effusion?

A
  • Overt
  • Fatigue
  • SOB
  • Dizzy with low BP
  • Occasionally chest pai
475
Q

What are the signs of pericardial disease?

A
  • Overt
  • Pulsus paradoxus
  • JVP raised
  • Low BP
  • +/- rub
  • +/- muffled HS
  • Pulmonary oedema is ver rare in pericardial effusions/ tampaonade
476
Q

What is the key test for pericardial effusions?

A

urgent echo

477
Q

What is the treatment for pericardial effusions?

A

drainage

478
Q

What are the causes of restrictive pericarditis?

A
  • Idiopathic
  • Radiation
  • Post surgery
  • Autoimmune
  • Renal failure
  • Sarcoid
479
Q

What is the pathology of restrictive endocarditis?

A

Impairment of filling although myocardium is normal most of the time

480
Q

What are the symptoms of constrictive pericarditis?

A
  • Fatigue
  • SOB
  • Cough
481
Q

What are the sings of constrictive pericarditis?

A
  • More of right HF with oedema
  • Ascitis
  • High JVP
  • Jaundice
  • Hepatomegallly
  • AF
  • TR
  • Plural effusion
  • Pericardial knock
482
Q

What is the treatment of constrictive pericarditis?

A

careful and limited diuretics and pericardectomy

483
Q

What is the clinical presentation of heart failure?

A

A clinical syndrome comprising of dyspnoea, fatigue or fluid retention due to cardiac dysfunction, either at rest or on exertion, with accompanying neurohormanal activation

484
Q

What factors increase the risk of chronic heart failure?

A
  • Treatment of acute MI
  • Ageing population
  • Incidence of: Hypertension, CHD, Obesity, diabetes, HLP
485
Q

What decreases the risk of chronic heart failure?

A

Treatment of:

  • HLP
  • Hypertension
  • CHD
  • Diabetes
  • Obesity
  • CHF
486
Q

What are the symptoms of heart failure?

A
  • Breathlessness
  • Fatigue
  • Oedema
  • Reduced exercise capacity
487
Q

What are the signs of heart failure?

A
  • Oedema
  • Tachycardia
  • Raised JVP
  • Chest crepitations or effusion
  • 3rd heart sound
  • Displaced or abnormal apex beat
488
Q

What can cause heart failure?

A
  • If sufficiently severe almost any structural cardiac abnormality will cause heart failure
  • LV systolic dysfunction- many causes
  • Valvular heart disease
  • LV diastolic dysfunction/ HF with preserved systolic function/ HF with normal ejection fraction
  • Cardiac arrhythmias
  • Pericardial constriction or effusion
  • Myocardial ischaemia/ infarction (usually via LVSD)
  • Restrictive cardiomyopathy eg amyloid, HMC
  • Right ventricular failure: primary or secondary to pul. hypertension
489
Q

What are the causes of LV systolic dysfunction?

A
  • Ischaemic heart disease (usually MI)
  • Dilated cardiomyopathy (DCM): means LVSD not due to IHD or secondary to other lesions ie valves/ VSD
  • Severe aortic valve disease or mitral regurgitation
490
Q

What are the causes of Dilated cardiomyopathy?

A
  • Inherited
  • Toxins: e.g. alcohol, catecholamines
  • Viral: acute myocarditis or chronic DCM
  • Other infections: HIV, chaga’s disease, Lyme’s disease
  • Systemic disease: sarcoidosis, haemachromatosis, SLE, mitochondrial dis.
  • Muscular dytrophies
  • Peri-partum cardiomyopathy
  • Hypertension
  • Isolated non compaction
  • Tachycardia related cardiomyopathy
  • RV pacing induced cardiomyopathy
  • End-stage hypertrophic cardiomyopathy
  • End stage arrythmogenic RV cardiomyopathy
491
Q

What is class 1 HF?

A
  • No limitations for exercise

- Symptoms usually during activity

492
Q

What is class 2 HF?

A
  • Mild limitation for exercise

- Comfortable with rest or mild with exertion

493
Q

What is class 3 HF?

A
  • Moderate limitation for exercise

- Comfortable only at rest

494
Q

What is class 4 HF?

A
  • Severe limitation of exercise

- Any physical activity brings only discomfort and symptoms occur at rest

495
Q

What are the types of heart failure?

A
  • Systolic heart failure (HFrEF): decreased pumping action of the heart, which results in fluid back up in the lungs and heart failure
  • Diastolic heart failure (HFpEF): Involves a thickened and stiff heart muscle. As a result, the heart does not fill with blood properly. This results in fluid backup in the lungs and heart failure
496
Q

What drugs are used to improve the symptoms of HF?

A
  • Loop diuretics

- Digotoxin

497
Q

What drugs are used to improve symptoms and survival of HF?

A
  • ACE inhibitors/ ARBs
  • Spirnolactone
  • Valsartan-sacubitrasl
498
Q

What drugs are used to improve survival of HF?

A
  • Beta-blockers

- Ivabridine

499
Q

What drugs are used for blocking detrimental hormone changes (beta blockers)?

A
  • Carvedilol
  • Bisoprolol
  • Metoprolol
500
Q

Give examples of an ACE inhibitor

A

Ramipril, Enalapril, Lisinopril

501
Q

Give examples of angiotensin antagonists

A
  • Valsartan
  • Losartan
  • Elite II
502
Q

What blocks Aldesterone?

A

Sprinolactone

503
Q

What does Neprolysin do?

A

prevents the metabolism and enhances ANP/BNP actions (which are potent naturitic agents and vasodilators)

504
Q

What type of drug is digoxin and what does it do?

A

Positive inotrope: improves the ablility of the heart to pump and so improves cardiac status

505
Q

What does Hydralazide do?

A

It is an arterial dilator that has been shown to improve cardiac function

506
Q

What are the names of some nitrovasodilators?

A
  • Isobride Mono

- Dinitrate

507
Q

Give an example of a Loop diuretic

A

Furosemide

508
Q

What are the drug reactions of Loop diuretics?

A
  • Dehydration
  • Hypotension
  • Hypokalaemia, hyponatraemia
  • Gout
  • Impaired glucose tolerance, diabetes
509
Q

What drugs does Frusemide interact with?

A
  • NSAIDs (renal toxicity)
  • Aminoglycosides (Aural and renal toxicity)
  • Lithium (renal toxicity)
  • antihypertensives (profound hypotension)
  • Vancomycin (renal toxicity)
510
Q

What drugs reduce mortality in HF?

A
  • Angiotensin Blockade
  • Beta receptor blockade
  • Aldosterone blockade
  • ANP/BNP enhancement
511
Q

What are the adverse drug reactions of ACE inhibitors?

A
  • First dose hypotension
  • Cough
  • Angioedema
  • Renal impairment
  • Renal failure
  • Hyperkalaemia
512
Q

What are the drug- drug interactions of ACEI?

A
  • NSAIDs (acute renal failure)
  • Potassium supplements (hyperkalaemia)
  • Potassium sparring diuretics (hyperkalaemia)
513
Q

What are the side effects of Digoxin?

A
  • Arrhythmia
  • Nausea
  • Confusion
514
Q

Describe the tunica intima

A
  • Layer of endothelial cells
  • Subendothelial layer: collagen and elastic fibres
  • Separated from tunica media internal elastic membrane
515
Q

Describe the tunica media

A
  • Smooth muscle cells

- Secrete elastin in the form of sheets, or lamellae

516
Q

Describe the tunica adventitia

A

-Thin connective tissue layer
-Collagen fibres and elastic fibres (not lamellae)
The collagen in the adventitia prevents elastic arteries from stretching beyond their physiological limits during systole

517
Q

What is the definition of an aneurysm?

A

A localised enlargement of an artery caused by a weakening of the vessel wall

518
Q

What are the different types of aneurysm?

A
  • True aneurysms: Saccular and fusiform
  • False aneurysm
  • Dissecting aneurysm
519
Q

What is a true aneurysm?

A

Weakness and dilation of the wall, it involves all three layers

520
Q

What is a true aneurysm associated with?

A
  • Hypertension
  • Atherosclerosis
  • Smoking
  • Collagen abnormalities (Marfan’s cystic medial necrosis)
  • Trauma
  • Infection (mycotic/ syphillis)
521
Q

What is a false aneurysm?

A

Rupture of the wall of the aorta with the haematoma either contained by the thin adventitial layer or by the surrounding soft tissue

522
Q

What are the signs and symptoms of an aortic aneurysm?

A
  • Asymptomatic
  • Shortness of breath or even heart failure (AR)
  • dysphagia and hoarseness (ascending aorta, chronic)
  • Sharp chest pain radiating to back- between shoulder blades- possible dissection
  • Pulsatile mass
  • Hypotension
523
Q

what causes an aortic dissection?

A
  • Hypertension
  • Atherosclerosis
  • Trauma
  • Marfan’s syndrome
524
Q

What are the symptoms of an aortic dissection?

A
  • Tearing, sever chest pain (radiating to back)
  • Collapse (tamponade, acute AR, external rupture)
  • Bewasre inferior ST elevation
525
Q

What are the signs of an aortic dissection?

A
  • Reduced or absent peripheral pulses (BP mismatch between sides)
  • Hypo/hypertension
  • Soft early diastolic murmur (AR)
  • Pulmonary oedema
  • CXR usually shows a widening mediastinum
  • Diagnostics can be confirmed by echo-cardiogram or CT scanning
526
Q

What are the treatment options for aortic dissection?

A
  • type A: sugery

- Type B: Meticulous blood pressure control, sodium nitroprusside plus beta blocker

527
Q

What is the presentation of aortic fibrillation?

A
  • Asymptomatic
  • Palpitations, dyspneoa, chest pain
  • Embolism
528
Q

What are the investigations done for aortic fibrillation?

A
  • Documenting arrhythmia on ECG: 12 leads for 24 hour recording event recorder
  • Blood test especially thyroid
  • Echo cardiogram
529
Q

What are the rate control drugs used for aortic fibrillation?

A
  • Digoxin
  • Beta blocker
  • Ca-antagonists + warfarin (or aspirin if low risk)
530
Q

What are the rhythm control drugs used for aortic fibrillation?

A

Class IC/ III drugs +/- DC cardioversion

531
Q

What are the electrical approaches for the treatment of aortic fibrillation?

A
  • Pace and ablation of AV node

- Substrate modification e.g. pulmonary ostial ablation, maze procedures

532
Q

What is the treatment of atrial flutter?

A
  • Control ventricular rate and thromboembolic risk
  • Usually crdiovert
  • Prevent with AA drugs or RFA of cavotricusped isthmus
533
Q

What are the symptoms of ventricular tachycardia?

A
  • Palpitations
  • Chest pain
  • Dyspnoea
  • Dizziness
  • Syncope
534
Q

How does one stop ventricular tachycardia?

A
  • Cardiac arrest protocol
  • DC cardio-aversion
  • Drugs
535
Q

How does one prevent ventricular tachycardia

A
  • Treat underlying cause
  • AA drugs
  • ICD
536
Q

What is the most usual underlying cause of ventricular tachycardia?

A

structural heart disease

537
Q

What are the different types of arrhythmia?

A
  • Sinus arrhythmia
  • Supraventricular arrhythmia: atrial fibrillation, SVT (junctional)
  • Ventricular arrhythmia: ventricular tachycardia, ventricular fibrillation
  • Heart block
538
Q

What are the electrophysiological properties of class IA drugs?

A

Fast sodium-channel blockade

539
Q

Give some examples of class IA drugs

A
  • Quinidine
  • Procainamide
  • Dispyramide
540
Q

What are the electrophysiological properties of class IB drugs?

A

Intermediate sodium-channel blockade

541
Q

Give some examples of class IB drugs

A
  • Lidocain
  • Mexoletine
  • tocainide
542
Q

What are the electrophysiological properties of class IC drugs?

A

Slow sodium-channel blockade

543
Q

Give some examples of class IC drugs

A
  • Flecainide

- Propafenone

544
Q

What are the electrophysiological properties of class II drugs?

A

B-Adrenergic receptor antagonism

545
Q

Give some examples of class II drugs

A
  • Atenolol

- Bisoprolol

546
Q

What are the electrophysiological properties of class III drugs?

A

Prolong refractoriness

547
Q

Give some examples of class III drugs

A
  • Amiodarone
  • Bretylium
  • Sotalol
548
Q

Give some examples of class IV drugs

A
  • Diltiazem

- Verapamil

549
Q

What is class IA drugs used for?

A
  • atrial fibrillation
  • Premature atrial contractions
  • Premature ventricular contractions
  • Ventricular tachycardia
  • Wolff-Parkinson-white syndrome
550
Q

What are the side effects of class IA drugs (quinidine)?

A
  • Cinchonism (blurred vision, tinnitus, headache, psychosis)
  • Cramping
  • Nausea
  • enhances digitalis toxicity
551
Q

What is class IB drugs used for?

A

-Ventricular arr

552
Q

What is class IB drugs used for?

A

-Ventricular disrythmias only (premature ventricular contractions, ventricular tachycardia, ventricular fibrillation)

553
Q

What are the side effects of class IB drugs?

A

Tocainide can cause pulmonary fibrosis

554
Q

What is class Ic drugs used for?

A
  • Severe ventricular disrhythmias

- atrial fibrillation/ flutter

555
Q

What are the side effects of class Ic drugs?

A
  • Can induce life threatening VT

- beta blocking and calcium channel blocking activity can worsen heart failure

556
Q

What are class II drugs used for?

A
  • General myocardial depressant for both supraventricular and ventricular disrhythmias
  • Now first line for atrial fibrillation
557
Q

What are class III drugs used to treat?

A

arrythmias that are tricky to treat

558
Q

What are class IV drugs used to treat?

A

Paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

559
Q

What does digoxin do?

A
  • Inhibits the sodium-potassium ATPase pump
  • Positive inotrope- improves strength of cardiac contraction
  • Allows more calcium to be available for contraction
  • Used for heart failure and atrial fibrillation
560
Q

What are the signs of digoxin toxicity?

A
  • Nausea and vomiting
  • Xanthopsia (see an orange glow)
  • Bradycardia
  • Tachycardia
  • Arrhythmias: VT and VF
561
Q

What do you do to treat digoxin toxicity?

A

Digibind

  • Digoxin immune antibody
  • Binds with digoxin, forming complex molecules
  • Excreted in urine
562
Q

What does adenosine do?

A

Slows conducting through the AV node

-Used to convert paroxysmal supraventricular tachycardia to sinus rhythm

563
Q

What are the indications for anticoagulation?

A

-Atrial fibrillation: risk of stroke, peripheral emboli

564
Q

What drugs are used for anticoagulation?

A
  • Warfarin
  • Dabigatran
  • Rivaroxaban
  • Apixaban
565
Q

What does Warfarin do?

A

Inhibits the production of clotting factors II, VII, IX and X

566
Q

What are the drugs that interact with Warfarin?

A
  • Aspirin (inhibition of platelets)
  • Heparin antimetabolics (inhibition of clotting factors)
  • Barbiturates and phenytoin (induction of metabolising enzymes (cytochrome P450))
  • Vitamin K (promotes clotting factors)
  • Cholestyramine (reduced absorption)
567
Q

What are the adverse effects of warfarin?

A
  • Bleeding
  • Tetratogenic
  • Avoid in first and third trimesters
  • Retroplacental bleeding and fetal intracerebral bleeding
568
Q

What is the mutation for down’s syndrome?

A

Trisomy 21

569
Q

What are the heart problems that can happen due to down’s syndrome?

A
  • Atrio-ventricular septal defects

- Duodenal atresia

570
Q

What is the mutation for turner’s syndrome?

A

45X

571
Q

What are the results of turner’s syndrome?

A
  • coartication of the aorta
  • Shortened stature
  • gonadal dysgenesis
  • Puffy hands
572
Q

What can neck webbing indicate?

A
  • Turner’s syndrome
  • Noonan syndrome
  • CFC syndrome
  • Leopard syndrome
  • Costello syndrome
573
Q

What is the mutation for Noonan syndrome?

A

(chromosome 12)

  • PTPN11 gene
  • SOS1
  • KRAS
  • BRAF
  • RAF1
  • MEK1
574
Q

What are the features of Noonan syndrome?

A
  • Pulmonary stenosis
  • Shoert stature
  • Neck webbing
  • Cryptorchidism
  • Characteristic face
575
Q

What is cardio-facio-cutaneous (CFC)?

A
  • Noonan-like
  • Ectodermal problems
  • Developmental delay
576
Q

What is leopard syndrome?

A
  • Noonan like
  • Multiple lentigenes
  • Deafness
577
Q

What is Costello syndrome?

A
  • Noonan like
  • Thickened skin fold
  • Susceptible to warts
  • Cardiomyopathy
  • Later cancer risk
578
Q

What are the mutations that cause Leopard syndrome?

A
  • PTPN11

- RAF1

579
Q

What are the mutations that cause CFC?

A
  • SOS1
  • KRAS
  • BRAS
  • MEK1
  • MEK2
580
Q

What are the mutations that cause Costello syndrome?

A
  • HRAS
  • KRAS
  • BRAF
  • MEK1
581
Q

What are the mutations that cause NFNS?

A

Neurofibromin

582
Q

What are the mutations that cause NF1?

A

Neurofibromin

583
Q

What is the criteria for 22q11 deletion syndrome?

A
  • C: Cardiac malformation
  • A: Abnormal facies
  • T: Thymic hypoplasia
  • C: Cleft palate
  • H: Hypoparathyroidism
  • 22: 22q11 deletion
584
Q

What is 22q11 deletion syndrome?

A

It encompasses both DiGoeorge syndrome and schprintzen syndrome

585
Q

What is DiGeorge syndrome?

A
  • Thymic hypoplasia
  • Hypoparathyroidism
  • Outflow tract cardiac malformation
  • Usually sparodic
586
Q

What is schprintzen syndrome?

A
  • Cleft palate/ palatal insufficiency
  • Outflow tract cardiac malformation
  • Characteristic face
587
Q

What is Williams syndrome?

A
  • Aortic stenosis (supravalvular)
  • Hypercalcemia
  • 5th finger clinodactyly
  • cocktail party manner
  • Deletion of elastin in chromosome 7
  • Deletion of contiguous genes
  • LIM kinase
588
Q

What is cardiovascular connective tissue disease?

A
  • Marfan
  • Loeys-dietz
  • Ehlers danlos
  • FTAA
589
Q

What is familiar arrhythmias?

A
  • Long QT
  • Brugada
  • CPVT
  • ARVC
590
Q

What is familial cardiomyopathy?

A
  • HCM

- DCM

591
Q

What is Marfan syndrome?

A

-Autosomal dominant
-Multisystem
-Connective tissue
-Fibrillin 1 gene
-Chromosome 15q21
Chromosome 3p22

592
Q

What does Marfan’s effect?

A
  • Cardiovascular system: aortic dilatation/ dissection
  • Eyes: ectopia lentis
  • Skeletal: ULSR and SHR, scoliosis/ kyphosis, pectus deformity, thumb and wrist, foot and ankle, reduced elbow extension
  • Skin: striae
  • Repiratory: pneumothorax
  • Dural ectasia
  • Mitral valve prolapse
  • Myopia (near sighted)
  • Face
  • Protusio acetabuli
593
Q

What other thing have Marfan’s like symptoms?

A
  • Loeys-Dietz syndrome
  • Marfan’s syndrome 2
  • Familiar thoracic aortic aneurism
  • MASS phenotype

Clinical (5 decks)

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