KINESIOL 1YY3 Chapter Notes - Chapter 1: Rheumatoid Arthritis, Airway Obstruction, Neuromuscular Disease

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Cardiovascular Disease

BP = CO x SVR

CO = HR x SV

Infarction

Necrosis due to ischaemia

Arterial

oMI

oStroke

oBowel infarction

oAcute limb ischaemia

Venous

oPE

oTorsion of vascular pedicle

oSigmoid volvulus

oTesticular torsion



Atherosclerosis

Arterial wall thickening and loss of elasticity



Stages

Endothelial cell injury

Inflammatory response in vessel wall

oOxidised LDL

Formation of stable atherosclerotic plaque

oVascular smooth muscle phenotype shift

Complication of stenosis or plaque rupture



Risk Factors

Non-Modifiable

oAge

oSex

oFamily history

oOthers - Type A personality,

oestrogen deficiency



Modifiable

oHypertension

oDiabetes Mellitus

oSmoking

oHypercholesterolaemia

oOthers - physical inactivity,

lipoprotein Lp(a)

Complications

Plaque-related Stenosis (angina, intermittent claudication)

Plaque rupture

oThrombosis (MI, stroke, acute limb ischaemia)

oEmbolism (MI, stroke, acute limb ichaemia)

Weakening of vessel wall (AAA)



Acute Coronary Syndrome

Unstable angina

oNo cardiac damage (normal

tropnin)

NSTEMI/STEMI

oCardiac damage (raised tropnin)



Acute Limb Ischaemia

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

Thrombosis (60%)

oHx of claudication/rest pain

oOnset over hours

oSigns of chronic

vascularinsufficiency

oHard arteries

oNo bruits



Embolism (30%)

oRecent MI, atrial fibrillation,

aneurysm

oOnset over seconds

oNo evidence of previous disease

oSoft artery

oBruits

Hypertension

140/90 (based upon additional risk factors)

160/100 (absolute)



Primary (essential) - 95%

oIdiopathic



Secondary

oRenal disease

oEndocrine disease

oPregnancy

oDrugs

Sequalae

HTN retinopathy

CVA

↑ Glucose levels

HTN encephalopathy

MI

HTN Cardiomyopathy

HTN Nephropathy



Cardiac Failure

A syndrome caused by any abnormality of the heart that may be characterised by a set of

haemodynamic,

neural, and endocrine abnormalities



LVF

Causes:

oIHD

oHypertension

oValve disease

oMyocardial disease

Consequences:

oImpaired pulmonary outflow

Congestion and oedema

oReduced renal perfusion

Salt and water retention +

ATN

oReduced CNS perfusion

(encephalopathy)



RVF

Causes:

oLeft-sided heart failure

(Congestive)

oChronic Lung Pathology - Cor

Pulmonale

Consequences:

oPortal, systemic and peripheral

congestion

oTricuspid regurgitation

oRenal congestion (R > L)



Cardiomyopathy

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Causes Features

Hypertr

ophic

Inherited (50% AD)

Sporadic cases

Pathology - heavy muscular hypertrophy with poor

compliance

Often asymmetrical septal hypertrophy

Sequelae:

- Arrhythmias - AF

- LV outflow obstruction

- CHF

- Sudden deathYoung man



Syncope, FH of sudden death, Jerky pulse and double

apical impulse, Ejection systolic murmur (+/- mild

mitral murmur)

Dilated Idiopathic

Genetic

Infections e.g. viral

myocarditis

Toxins - alcohol,

chemotherapy

Four-chambered hypertrophy and dilatation

Poor prognosis

Progressive CCF

Progressive loss of mycoytes causing dilation +

heart failure + arrhythmias

Restricti

  Pathology - restriction of ventricular filling with

myocardial fibrosis

ARVD Inflammation and

thinning of the right

ventricular wall

Usually due to

mutation in cell

adhesion genes

Key consequences:

- Arrhythmia

- CCF



Valve Disease

Congenital

Abnormalities e.g. Bicuspid valves



Acquired

Rheumatic fever/Endocarditis

Functional (e.g. Mitral/tricuspid valve

disease)

Degeneration (e.g calcific aortic stenosis)



Stenosis

Pressure overload + hypertrophy

Develops slowly



Regurgitation

Volume overload

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Document Summary

Arterial: mi, stroke, bowel infarction, acute limb ischaemia. Arterial wall thickening and loss of elasticity. Inflammatory response in vessel wall: oxidised ldl. Formation of stable atherosclerotic plaque: vascular smooth muscle phenotype shift. Non-modifiable: age, sex, family history, others - type a personality, oestrogen deficiency. Venous: pe, torsion of vascular pedicle, sigmoid volvulus, testicular torsion. Modifiable: hypertension, diabetes mellitus, smoking, hypercholesterolaemia, others - physical inactivity, lipoprotein lp(a) Plaque rupture: thrombosis (mi, stroke, acute limb ischaemia, embolism (mi, stroke, acute limb ichaemia) Nstemi/stemi: no cardiac damage (normal, cardiac damage (raised tropnin) tropnin) Embolism (30%: hx of claudication/rest pain, onset over hours, signs of chronic vascularinsufficiency, hard arteries, no bruits, recent mi, atrial fibrillation, aneurysm, onset over seconds, no evidence of previous disease, soft artery, bruits. Secondary: renal disease, endocrine disease, pregnancy, drugs. A syndrome caused by any abnormality of the heart that may be characterised by a set of haemodynamic, neural, and endocrine abnormalities. Causes: ihd, hypertension, valve disease, myocardial disease.

KINESIOL 1YY3 Chapter Notes - Chapter 1: Rheumatoid Arthritis, Airway Obstruction, Neuromuscular Disease

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