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PATHOLOGY & PATHOPHYSIOLOGY DISORDERS OF THE HEART © DOUGANS INTERNATIONAL. All rights reserved.

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Page 1: PATHOLOGY & PATHOPHYSIOLOGY - Distanceforum.dougans-international.com/files/files/DISORDERS OF THE HEART.pdf · Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages

PATHOLOGY & PATHOPHYSIOLOGY

DISORDERS OF THE HEART

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DISORDERS OF THE HEART

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Disorders of the Heart

Ischaemia

Angina pectoris

Myocardial

infarction

Inflammation &

infection

Pericarditis

Endocarditis

Myocarditis

Degenerative

disorders

Heart failure

Heart valve

disorders

Congenital disorders

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DISORDERS OF THE HEART

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Incidence:

Heart disease is the most common cause of morbidity and

mortality today!

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RISK FACTORS FOR CARDIOVASCULAR DISEASES

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Controllable:

That which we have control over, e.g. lifestyle, stress and

smoking

Uncontrollable:

That which we have no

control over, e.g. age,

gender, family history and

race

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RISK FACTORS FOR CARDIOVASCULAR DISEASES

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Smoking:

A smoker’s risk of developing coronary artery disease is directly related to

the number of cigarettes smoked per day

Smoking decreases HDL levels and increase LDL levels

Smoking increases the levels of carbon monoxide in the blood which may

directly injure artery walls and lead to atherosclerosis

Smoking leads to constriction of arteries, aggravating the lack of blood flow

in areas where the arteries are already narrowed by atherosclerosis

Smoking increases the blood’s tendency to clot, thus increasing the risk for

stroke, heart attack and peripheral vascular disease

People who quit smoking have only half the risk of those who continue,

regardless of the number of years smoked before

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ISCHAEMIC HEART DISEASE (IHD)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

IHD = heart disease due to ischaemia (i.e. problems in the

coronary arteries)

Causes 20 to 30% of deaths in the western world

Usually due to atherosclerosis in the coronary arteries

Ischaemia = a deficiency in the blood supply to a part of the

body

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ISCHAEMIC HEART DISEASE (IHD)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Consequences of IHD:

Angina pectoris

Myocardial infarction

Sudden cardiac death due to

arrythmias (irregular heart

rhythm)

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ANGINA PECTORIS

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Definition:

Episodic chest pain caused by ischaemia of the myocardium

Pain goes away after a few minutes of rest

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ANGINA PECTORIS

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Management of angina pectoris:

Avoid risk factors for atherosclerosis

Medicines: nitrates (dilate the arteries)

Surgery if severe: coronary angioplasty, coronary artery bypass

(“bypass surgery”)

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MYOCARDIAL INFARCTION (MI)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Definition:

Necrosis of the myocardium as a result of severe ischaemia

Signs and symptoms:

Chest pain (same area as angina),

dyspnoea, nausea, vomiting,

syncope (fainting)

The pain is typically described as a

severe crushing or constricting

sensation in the chest

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MYOCARDIAL INFARCTION (MI)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Complications of MI:

Sudden death

Arrythmia (irregular heart rhythm)

Thrombosis inside the heart

Pericarditis

Chronic left heart failure

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MYOCARDIAL INFARCTION (MI)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Management of MI:

Oxygen

Analgesia (pain medication)

Nitrates (dilates arteries)

Fibrinolytic therapy (breaks down blood clots)

Anticoagulants (prevents blood clots)

B-antagonists (lowers the heart rate)

ACE inhibitors (lowers blood pressure)

Bed rest for 24 to 48 hours

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DISORDERS OF THE HEART

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Angina Pectoris Myocardial infarction

Pathogenesis:

Temporary blockage with

no tissue death,

especially after exercise

Complete blockage

resulting in tissue

necrosis

Signs & symptoms:

Symptoms last a few

minutes - pain, nausea,

sweating, dizziness and

shortness of breath

Symptoms last longer

than 30 minutes - severe

crushing pain

Alleviation of pain: Rest, nitro-glycerine Nothing

Treatment: Lifestyle changes Surgery plus lifestyle

changes

Complications: MI Death

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INFLAMMATION OF THE HEART

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Pericarditis Myocarditis Endocarditis

Aetiology: Viral, e.g. influenza,

HIV Viral Bacterial

Complications:

Scar tissue and

adhesions can form

that restrict the

heart movements

Heart failure and

sudden death

Heart failure,

damage to heart

valves, Rheumatic

fever

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INFECTIVE ENDOCARDITIS

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

The presence of valvular disease, prosthetic heart valves or

congenital heart defects provides an environment conducive to

bacterial growth on the endocardium

The bacteria form vegetations on damaged valves

Complications:

Damage to the valves, acute heart failure, emboli, infections in

other areas of the body

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RHEUMATIC FEVER

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Definition: An immune disorder that may occur 2 to 3 weeks after a

streptococcal throat infection

Aetiology: Autoimmune

Pathogenesis: Starts with a streptococcal throat infection (tonsillitis or

pharyngitis)

In some people the antibodies produced to fight the streptococcal

bacteria also attack body proteins (they cross-react). If this happens

you develop rheumatic fever. Your own antibodies then attack your

heart, joints, subcutaneous tissues and blood vessels.

Who is most at risk of getting rheumatic fever ?

School-aged children in developing countries

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STREPTOCOCCAL PHARYNGITIS (TONSILLITIS)

Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Signs and symptoms:

Sore throat, swollen tonsils

Throat is beefy red

Enlarged cervical lymph nodes

Fever

Headache

Nausea and vomiting

Rapid heartbeat

Malaise

In some children scarlet fever can develop: paleness around the mouth,

rest of face flushed. Red rash, redness in the skinfolds (rash is not itchy or

painful). Tongue white with red papillae (strawberry tongue).

Cough, laryngitis and a stuffy nose is not usually symptoms.

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Complications of rheumatic fever:

Heart valves can be damaged

Years after a bout of rheumatic fever, the patient can suffer from

heart disease due to the long-term effect of damaged valves on

the functioning of the heart

RHEUMATIC FEVER

Prevention of rheumatic fever:

When a child has tonsillitis or pharyngitis, the doctor should test

if it is a streptococcal infection. If it is, the child will require

antibiotics to prevent rheumatic fever

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Aetiology:

Congenital

Rheumatic fever

Endocarditis

Degeneration with ageing

HEART VALVE DISORDERS

Types of heart valve disorders:

Stenosis: This is abnormal rigidity of a valve

Regurgitation/incompetence: Failure of a valve to close fully

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Consequences of heart valve disorders:

HEART VALVE DISORDERS

If the valves are not working

properly, it means that the

heart has to work harder to

compensate

A serious valve disorder will

eventually lead to heart

failure

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

When the heart can not keep up with the demand of the body

Left sided heart failure or right sided heart failure or both

HEART/CARDIAC FAILURE

Aetiology:

Hypoxia, e.g. coronary artery disease, anaemia

Increased pressure: Left ventricle can fail if it has to pump against high

systemic blood pressure. Right ventricle can fail if it has to pump against

high pulmonary blood pressure.

Increased volume in the heart: aortic, tricuspid or mitral incompetence

Myocardial necrosis, e.g. MI

Deficient filling of the heart, e.g. mitral stenosis or pericarditis

Cardiomyopathy

Arrythmias

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Leads to increase pulmonary blood pressure and pulmonary

oedema

Signs and symptoms:

Dyspnoea on exertion

Orthopnoea

Paroxysmal nocturnal dyspnoea

Chronic cough

Tachycardia

Cyanosis

LEFT VENTRICULAR FAILURE

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Usually secondary to left cardiac failure

Signs and symptoms:

Ankle/sacral oedema

Increased JVP

Cyanosis

Enlarged and tender liver

Proteinuria

Nocturia

RIGHT CARDIAC FAILURE

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

Prevalence: Relatively common - 8 out of 1,000 live births

Aetiology:

Sporadic – no teratogenic factors can be identified

Maternal factors: Maternal rubella, maternal alcohol abuse,

intrauterine radiation, maternal use of certain medicines, e.g.

thalidomide

Genetic abnormalities ,e.g. Down’s syndrome

CONGENITAL HEART DISEASE

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

The most common congenital abnormality

Small or large defects

Management: Small defects often close spontaneously. Larger

defects will lead to cardiac failure, thus surgery is necessary.

VENTRICULAR SEPTAL DEFECTS

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Learner Study Guide – Pathology & Pathophysiology, Chapter 7, pages 55-62

VENTRICULAR SEPTAL DEFECTS

Source: www.dhg.org.uk,

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QUESTIONS