everything you need to know cardiovascular system

7/31/2019 Everything You Need to Know Cardiovascular System

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ONN0809

Everything You Need to Know (at least) for

EDITORIAL

Apabila Ia mengkehendaki sesuatu urusan Ia katakan kepadanya: Jadilah, maka jadilah ia

(Al-Baqarah:117)

Dengan nama ALLAH yang MAHA PEMURAH lagi MAHA PENYAYANG

NAME

YEAR

MATRIC NO

ACADEMIC SESSION


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I know what I should love to do--to build a study; to write, and to think of nothing else. I want

to bury myself in a den of books. I want to saturate myself with the elements of which they are

made, and breathe their atmosphere until I am of it. Not a bookworm, being which is to give off

no utterances; but a man in the world of writing--one with a pen that shall stop men to listen to

it, whether they wish to or not. Dont give up, there is still time to study for the exam, GOODLUCK!

Onn Azli Puade

Medic 4

20011/2012

I studied the lives of great men and famous women; and I found that the men and women

who got to the top were those who did the jobs they had in hand, with everything they had of

energy and enthusiasm and hard work.

(Harry S Truman quotes-1884-1972)
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SYMPTOMS

CHEST PAIN

Definition

Is a feeling of uncomfortable or pain at the chest areaCauses

Cardiovascular

Myocardial infarction

Acute aortic dissection

Pericarditis

Gastrointestinal

Gastro-esophageal reflux

Peptic ulcer disease

Gastritis

Oesophageal spasm

Musculoskeletal

Persistent cough

Chest wall injuries

Costochondritis

Rib tumour, fracture

Herpes Zoster

Pulmonary

Pneumonia

Pulmonary embolisme

Pneumothorax

Central bronchial carcinoma

Inhaled foreign body

Further history regarding Chest Pain

1. Location of the painRetrosternally and radiates to jaw and left arm cardiac chest pain and oesophageal

refluxCentrally located and radiates to shoulder pericarditis

Radiates to back aortic dissection

2. Precipitating factorEffort, cold, food and emotion cardiac chest pain

Inspiration (due to movement of thorax) pleuritic chest pain

Posture gastro-oesophageal reflux

3. Relieving factorGTN oesophageal spasm and acute coronary syndrome

Antacid gastro-esophageal refluxAspirin pleuritic chest pain

4. Family and social historyAny history of diabetes, hypercholesterolemia, smoking and dietary intake that mght

become a risk factor for the cardiovascular disease

5. Associated symptomDyspnoea, orthopnoea and easy fatigue all points towards cardiovascular disease


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Pathogenesis and pathophysiology

Atherosclerotic plaque obstructing coronary artery

Reduce or diminished blood supply to region supply by the arteries

distal to the obstruction

Ischaemia of the myocardial cell

Release substance to elicit vasodilation as a compensatory mechanism

Still cannot receive adequate blood supply

Production of more chemical mediator by ischaemic myocardial cell

Histamine, serotonin and bradykinin released and entering vein of the hearts

The mediators accepted by chemoreceptor located at the pericardial layer

Sending Action Potential towards the lateral spinothalamic tract

The signal is either converged or facilitated at the spinal cord (referred pain1 theory)

RADIATING CHEST PAIN

Investigation

1. ECGTo view the electrical profile of this patient heart. Elevated ST segment elevation seen in

myocardial ischaemic, symmetrical T wave inversion in myocardial injury and abnormal

Q wave in myocardial infarction. It can also detect Pulmonary embolisme

2. Cardiac EnzymesLook out for Troponin T presence, creatinine kinase and CK-MB enzyme elevation

3. Chest X-rayObserve heart as well as lung field to exclude any heart enlargement and disease that

can cause pleuritic chest pain. Also to rule out the pain due to fracture or osteosarcoma

4. Blood cholesterolThe number one factor contributes to ACS which is hyperlipidaemia. Poor diet habit also

can cause elevation of total lipid in the blood

1Referred pain also known as synalgia is pain felt in a part of the body other than where it might be

expected due to sensory nerves from different parts of the body share common pathways when they

reach spinal cord. For diagram, see Guyton pg 605


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DYSPNOEA, ORTHOPNOEA2, PAROXYSMAL NOCTURNAL DYSPNOEA

3

Definition

Dyspnoea - Is an uncomfortable awareness of breathing or can be described as breathlessness

Causes

Cardiac failure left heart failure or congestive cardiac failure

Arrhythmia

Valvular Heart Disease

Pulmonary Hypertension

Further history regarding these symptoms

1. History or family history of hypertension?Systemic hypertension can leads to congestive cardiac failure but it occurs more likely to

the left heart before affecting right heart

2. Surgical historyHistory of chest surgery as well as tooth debridement and any invasive procedure will

increase tendency of getting systemic infection which likely to be affecting heart valve

3. Associated signs and symptomsCyanosis indicating heart failure

Cough with pink frothy sputum indicating pulmonary oedema, secondary to

pulmonary hypertension

Fever indicating infective endocardiis

4. Drug usedCertain drugs can cause arrhythmia such as beta blockers

5. Medical historyAny pulmonary disease such as obstructive, fibrosis and vascular disease can cause

pulmonary hypertension and in long standing case, it can leads to congestive cardiac

failure

2 Orthopnoea is breathlessness the prevents the patient from lying down so that the patient has to sleep

propped up in bed (by pillows) or sitting on the chair

3Paroxysmal Nocturnal Dyspnoea is severe dyspnoea that wakes the patient from sleep that the patient

is to forced to get up gasping for breath


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Further investigation regarding dyspnoea

1. Arterial Blood GasTo recognize the respiratory failure and the metabolic profile of the patient

2. Peak expiratory flow rateReduce in peak flow may indicates asthma or chronic airflow limitation

3. ECGEliminates probability of cardiac disease related to the symptoms. Look out for axis deviation to

rule out left or right ventricular enlargement

4. FBCTo rule out any pulmonary infection as well as anemia

Exudation of fluid to the alveolar space

(pulmonary oedema)

Lung is ventilated but not perfuse

V/Q mismatch

Respiratory acidosis

Increase carbon dioxide (indirectly) and

reduce oxygen (directly) level below 30

mmHg

Stimulate the chemoreceptor mainly the

aortic and carotid body

Ascend via vagus and glossopharyngeal

nerve

Terminates at the nucleus of the tractus

sollitarius

Stimulate the medullary respiratory area

Increase the respiratory effort as a

compensatory mechanism of respiratory

acidosis

DYSPNOEA

Recumbent position

Increase venous return to

the right heart

Increase afterload of the

right heart

Pulmonary congestion

Pulmonary hypertension

In recumbent position

ORTHOPNOEA

When sleeping

Woke up and gasping for

air

PAROXYSMAL NOCTURNAL

DYSPNOEA


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ANKLE SWELLING

Definition

Swelling of the lower limb may be unilateral or bilateral.

Causes

Local Swelling General Swelling

Acute swelling Chronic swelling

Trauma

DVT4

Cellulitis

Allergy Rheumatoid arthritis

Varicose vein

Obstruction to venous return

Lymphoedema

Caongenital malformations

Paralysis

Dependency

Congestive cardiac failure

Hypoproteinaemia

Renal failure

Fluid overload

Myxoedema

Further history regarding ankle swelling

1. Swelling locationBilateral swelling cardiac, renal and hepatic failure

Unilateral swelling trauma, venous disease, lymphatic disease

2. Associated and signs symptomsPain trauma, DVT, infection or complication of varicose veins

Red, swollen, hot and tender cellulitis

Wasting neurological damage

Frozen pelvis varicose vein, pelvic tumour

Dyspnoea, orthopnoea, PND, ankle oedema cardiac failure

Weight loss, diarrhea, steatorrhoea malabsorption

3. Past medical historyTrauma to the limb, recent pregnancy (DVT), abdominal or pelvic malignancy

4DVT or deep vein thrombosis is an obstruction of a vein by a clot within the deep veins of the calf of

the leg. May be caused by prolonged immobility, heart failure, pregnancy, injury and surgery predispose

to thrombosis by encouraging sluggish blood flow


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Further investigation regarding ankle sweling

1. FBCLow Hb indicating trauma or fracture secondary to large haematoma. Large haematoma also

associated with reduced platelet count

2. Chest X-rayFinding suggestive cardiomegaly, pulmonary oedema and pleural effusions

3. Limb X-rayMay show fracture, tumour or gas in the tissues associated with gas gangrene

4. VenographyWill confirm Deep Vein Thrombosis

5. LymphangiographyMay demonstrate the cause lymphoedema, e.g hypoplasia or obstruction

Right heart failure

Reduce afterload of the right heart

Blood congested in the right heart

Backflow of the blood in the Inferior Vena Cava, precipated by

gravity

Blood become congested in the lower limb, precipated by left

heart pumping

Increase hydrostatic pressure

Exudation of interstitial fluid to extravascular space

ANKLE SWELLING


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EASY FATIGUE, INTERMITTENT CLAUDICATION5, SYNCOPE

6

Definition

Is a state of increased discomfort and decreased efficiency due to prolonged or excessive

exertion

Causes

Cardiac Failure Lack of Sleep Anemia Depression Hypoglycemia Peripheral vascular disease


Cardiac failure

Low cardiac output

Poor blood supply (oxygen) to the skeletal muscle

Exercise/strenuous work

Anaerobic respiration produces energy and lactic acid

Increase level of lactic acid

Lactic acidosis

Discomfort and hurt at the skeletal muscle

FATIGUE

5Intermittent claudication is related to the claudication distance which is the distance the patient walk

until the pain in one or both calves, thighs and buttocks can be felt6

Syncope is a transient loss of consciousness due to the reduce blood supply to the cerebral artery

Walking

Pain in the thigh and

calves

INTERMITTENT

CLAUDICATION

Poor blood supply to the

carotid artery

Poor blood supply to the

cerebral artery

Transient loss ofconsciousness

SYNCOPE


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PALPITATION

Definition

Awareness of the heartbeat

Causes

Cardiac arrhythmia

Premature ventricular contraction

Premature atrial contraction

Atrial fibrillation

Sinus tachycardia

Anxiety/emotional stress

Caffeine

Nicotine

Alcohol

Supraventricular tachycardia Ventricular tachycardia


Cardiac failure

Inadequate cardiac output

Reduced blood supply (Oxygen) to the body tissue

Ischaemic tissue release substance

Stimulate the sympathetic activity as a

compensatory mechanism

Increase heart rate to increase cardiac output

Hyperdynamic circulation

Ventricular tachycardia

Awareness of the heart beat due to the

hyperdynamic circulation

PALPITATION


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SIGNS

CACHEXIA, POOR WEIGHT GAINED

Definition

Is a condition of abnormally low weight, weakness and general bodily decline associated withchronic disease

Causes

Systemic disease

Malignancy

Cardiac failure

Chronic respiratory disease

Malabsorption

Renal failure

Liver failure

Endocrine

Hyperthyroidism

Diabetes mellitus

Addisons Disease

Infective

Infective endocarditis

Tuberculosis

HIV

Helminth infection

Psychiatric

Anorexia Nervosa

Depression

Systemic Infection

Inflammatory reaction

Release of TNF-

Stimulate the release of the

cachectin factor

Cachectin factor enters blood

circulation

Suppress appetite center of the

hypothalamus

Lost of appetite

CACHEXIA

Cardiac failure

Reduced blood supply to the

body

Compensatory mechanism

Stimulate the sympathetic

nervous system

Long standing sympathetic

stimulation

Growth retardation

POOR WEIGHT GAINED/CARDIAC

CACHEXIA


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ANAEMIA AND PALLOR7

Definition

Is defined as a haemoglobin concentration of less than 13.5 g/dl in adult males and 11.5 g/dl in

adult females

Causes

Microcytic (MCV 95 fl)

Iron deficiency

Anaemia of chronic disease

Thalassaemia

Acute blood loss

Haemolytic Anaemia

Mixed deficiencies

Secondary anaemia*

Bone marrow failure

Pregnancy

Megaloblastic anaemia

Alcoholism

Liver disease

Hypothyroidism

Addisons disease

Hyperthyroidism

Marrow infiltration


7 Pallor is an abnormal paleness of the skin due to the deficiency of haemoglobin especially in the

mucous membrane of the sclerae

Systemic Infection (infective

endocarditis)

Inflammatory reaction

Release of TNF-

Suppress the bone marrow

Reduce production of red

blood cell

Reduce total haemoglobin in

the blood

Normocytic nomochromic

anaemia

PALLOR


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ARTERIAL PULSE NORMAL AND ABNORMAL PULSE

Definition

Is a series of pressure waves within an artery caused by contractions of the left ventricle

corresponding with the heart rate which is usually palpated at the radial arteryNormal heart rate

60 100 bit/minute

Abnormal pulse

1. Rate and rhythmRhythm\Rate Tachycardia Bradycardia

Regular Congestive cardiac failure

Constrictive pericarditis

Hypovolaemic shock

Myocardial ischaemia

Sick sinus syndrome

3rd

degree AV block

2nd

degree AV block

Myocardial infarction

Hypothyroidism

Drugs (-blockers, digoxin)

Irregular Atrial fibrillation

Pulmonary embolisme

Myocardial ischaemia

Left atrial enlargement

Mitral valve disease

Atrial fibrillation

2nd

degree AV block type I

2. VolumeType Description

Thready pulse Difficult to be felt and are not palpable

e.g. hypovolaemic shock

Weak pulse Is not palpable when slight pressure

applied

e.g. hypovolemc shock, atherosclerotic

plaque, congestive cardiac failure

Bounding pulse Feels full and spring like even under

moderate pressure

e.g. aortic regurgitation

3. Charactera) Pulsus alternans alternating weak and strong pulse due to left ventricular failureb) Pulsus parvus et tardus slow uprising of the carotid upstroke in Aortic stenosisc) Pulsus bisferiens a double waveform due to aortic stenosis/regurgitationd) Spike and dome pulse double carotid impulse due to hypertrophic obstructive

cardiomyopathy


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HYPERTENSION

Definition

Hypertension is elevation of blood pressure8

above the normal range expected in a particular

age group

Classification

*Primary hypertension/essential hypertension is due to unknown causes

*Secondary hypertension is due to certain disease that leads to rise in blood pressure

Complication of hypertension

1. Congestive cardiac failure/left ventricular failure2. Hypertensive retinopathy3. Atherosclerosis4. Hypertensive nephropathy5. Cerebral haemorrhage6. Artery berry aneurysm7. Abdominar aorta aneurysm8. Aortic aneurysm9. Ischaemic heart disease

Regulation of Blood Pressure

8Blood pressure can be define as the pressure of the blood against the arterial wall or total peripheral

resistance times cardiac output

characteristic Benign Malignant

aetiology usually primary* primary or secondary*

blood pressure diastolic 90-120, very slow rise diastolic >120, very rapid rise

age middle age, elderly young, middle age

course very slow (years) rapid (months)

incidence common uncommon

Total Peripheral

Resistance

Cardiac

OutputX

Cardiac Factor

Heart rate

Contractility

Blood volume

Mineralocorticoids

Sodium

Humoral Factor

Vasoconstrictor

Vasodilator

Neural Factor

Vasoconstrictor

Vasodilator

The goal of antihypertensive drugs is to reduce or

inhibit both factors that are increasing TPR as well

as CO

The goal of antifailure drugs is to reduce the TPR as

well as increasin cardiac out ut.


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HEART FAILURE9

LEFT HEART FAILURE

Failure of the left heart to pump oxygenated blood to meet up body blood requirement

Causes1. Ischaemic heart disease2. Systemic hypertension3. Aortic or mitral valve disease4. Non ischaemic myocardial disease

Pathogenesis

9 Can be define as failure of the heart pumping out the blood to all over the body to meet adequate

tissue perfusion

Symptoms Signs

- Exertional dyspnoea- Orthopnoea- Paroxysmal nocturnal dyspnoea- Syncope- Intermittent claudication- Easy fatigue

- Tachypnoea- Central cyanosis- Hypotension- Cardiac cachexia- Sinus tachycardia- Displaced apex beat- Left ventricular S3 sound- Sign of pulmonary oedema

Increase cardiac workload

Increase wall stress

Cell stretch (Frank Starling

mechanism)

Hypertrophy/dilation

Contraction of the heart become less

efficient due to thicken wall

LEFT HEART FAILURE

Systemic hypertension

(pressure overload)

Valvular heart disease

(pressure or volume overload)

Ischaemic heart disease

(volume overload)


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RIGHT HEART FAILURE

Failure of the right heart to drain deoxygenated blood and to pump the blood to the pulmonary

circulation

Causes- Severe pulmonary hypertension- Atrial Septal Defect- Tricuspid regurgitation- Pulmonary stenosis- Pulmonary regurgitation- Myocardial disease of the right heart- Causes of left heart failure

Pathogenesis

Symptoms Signs

- Peripheral swelling- Abdominal distension- Anorexia- Nausea

- Raised Jugular Venous Pressure- Right ventricular heave- Right ventricular S3- Pansystolic murmur- Hepatomegaly- Pulsatile liver- Oedema

Pulmonary hypertension,

pulmonary stenosis

(pressure overload)

Stronger contraction of the right heart to

overcome the pressure/volume

Increase cardiac workload

Increase wall stress

Cell stretch (Frank Starling mechanism)

Hypertrophy

Contraction of the heart become less efficient

due to thicken wall

RIGHT HEART FAILURE

Atrial Septal Defect,

tricuspid regurgitation

(volume overload)


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ONN0809

CONGENITAL HEART DISEASE

Definition

Is an abnormality of the heart or great vessel that is present from birth

Causes

Can be divided to 3 different causes

1. Genetic factorI. Chromosomal aberrations Down Syndrome or Robersonian translocationII. Mendelian inheritance single gene mutation that is passes generation to

generation

2. Maternal factori. Maternal or placental infectionToxoplasma gondii, rubella virus or

cytomegalovirus are the most common

ii. Insulin dependant diabetes exposed the fetus to the high level of glucose andinduced fetal hyperinsulinaemia which can leads to cardiac defect or neural tube

defect (diabetic embyopathy)

iii. Hypertension hypertensive embryopathyiv. Lifestyle intake of alcohol, drugs and smoking

3. Environmental factori. Chemical exposure inhalation of corrosive chemical substanceii. Radiation hazardous and non-hazardous radiation such as X ray, uvray etc

prove to cause anomalies such as microcephaly, blindness

4. Multifactorial any collection of above symptomsClassification

Congenital Heart Disease

Acyanotic Cyanotic

Without shunt With shunt

- Coarctation of aorta (5%)

- Congenital aortic stenosis (4%)

- Pulmonary stenosis (8%)

- Bicuspid aortic valve

- Dextocardia

- Atrial Septal defect (10%)

- Ventricular Septal Defect (42%)

- Patent Ductus Arteriosus (7%)

- Tetralogy of Fallot (5%)

- Eisenmenger Syndrome

- Pulmonary Atresia

- Transposition of Great Arteries (4%)


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Normal fetal circulation

due to the rudimentary structure of the lung and liver, blood has to bypass both of thisorgans receives blood supply mainly from umbilical vein from maternal blood via placenta

blood will go directly to the IVC via ductus venosus and 50% more will enters the liversinusoids blood will enters the heart through IVC directly to the right atrium and then some to theleft atrium via foramen ovale which opens the structure interatrial septum, some to the

right ventricle, left ventricle and some to the lung (approx. 10%) from the left ventricle, blood is pumped to the aorta from the right ventricle, blood will be pumped to the pulmonary trunk and straight tothe aorta via ductus arteriosus From aorta, blood will drains to the umbilical artery and lastly back to placenta intomaternal circulation.

* For pathological point of view of Congenital Heart Disease, simply imagine the circulation inadult is same as above

Atrial septal defect

a congenital defect of the heart in which there is a hole in the partition separating the two atria

Ventricular septal defect

a congenital defect of the heart which there is a hole between the 2 ventricles

Patent Ductus Arteriosus

a condition in which the ductus arteriosus is failed to close

Coarctation of aorta10

a congenital narrowing of the short segment of the aorta which commonly occurs just beyond

the origin of the subclavian artery from the aorta

Tetralogy of Fallot

Characterized by

1. Pulmonary stenosis2. VSD3. Overriding of Aorta4. Right Ventricular Hypertrophy

10Sorry for unable to list all the signs, symptoms, pathogenesis and investigation for congenital heart

disease details. Kindly refer to the pathology book


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ONN0809

ISCHAEMIC HEART DISEASE

Definition

Defined clinically as Acute Coronary Syndrome (ACS) is a collections of syndromes due to

imbalance of Oxygen supply and Oxygen requirement

Syndromes

1. Angina pectoris refer to the chest pain in which are divided to 3 different types asstated below;

i. Typical or Stable Anginaii. Prinzmetal or Variant Anginaiii. Cresendo or Unstable Angina

2. Myocardial infarctionDue to the long standing myocardial tissue ischemic which leads to tissue injury before

infarction

3. Chronic ischaemic heart diseaseDevelops slowly as a progression of coronary artery narrowing but not completely

occluded

4. Sudden Cardiac deathDue to the tissue hypoxic and failure to remove the metabolites

Causes

1. Role of acute plaque change2. Role of inflammation3. Role of arterial thrombosis4. Role of vasoconstriction

Risk factors

1. Age (40-60 increase risk of getting IHD up to 5 folds)2. Sex (oestrogen proven to be protecting endothelial layer, female has lower risk)3. Genetic (hypertension and primary hyperlipidemia is the major cause)4. Secondary hyperlipidemia (increase circulating triglycerides contributes to the role of

thrombosis)

5. Smoking (contributes to the endothelial injury as well as role of inflammation)6. DM (decrease liver removal of LDL from circulation)7. Hypothyroidism (decrease the formation of LDL receptor in the liver)8. Nephrotic syndrome (increase hepatic production of lipids and lipoprotein)


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ONN0809


Hypertension

Increase afterload

Increase myocardial

demand

Oxygen supply/requirement

imbalance

Chronic ischaemia of

myocardial cell

Release pain producing

substance

Shear stress to the endothelial

Arterial damage

Accelerated atherosclerosis

Atheroma

Progressive gradual narrowing

of lumen

Angina Pectoris

Coronary spasm

Prinzmetal angina

Neuroendocrine imbalance

(catecholamines,

prostaglandin)

Coronary artery involves

Ischemia of the

myocardial cell

Injury of myocardial cell

Myocardial Infarction

Hyperlipidaemia

LDL deposits at the site

of injury

Exposure of the subendothelial

layer

Platelet aggregation

Fissuring or ulceration of the

platelet plaque

Platelet rupture

Embolisme

Sudden cardiac death

Chronic IHDIHD

Recovery with scarring

or fibrosis

Cardiac arrhythmiaChronic heart failure

Cardiac arrest

Acute heart failure

Cardiogenic shock

Cardiac rupture

Cardiac tamponade

DEATH


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ONN0809

RHEUMATIC HEART DISEASE

Definition

Is an acute, immunological mediated, multisystem inflammatory disease that occurs a few weeks after

an episode of Group A (-haemolytic) streptococcus pharyngitis that involves the heart

Causes

1. Chronic valvular disease mitral valve stenosis2. -haemolytic Group A streptococci3. Hypersensitivity reaction type II and III

Major and Minor Criteria for Diagnosing Rheumatic fever

Major Minor

Subcutaneous nodules

Polyathritis

Erythema Marginatum

Carditis

Sydenhams Chorea

Fever

Athralgia

Previous Rheumatic Fever

Raised ESR or C-reactive protein

Leukocytosis

Prolonged PR nterval

Pathogenesis (the exact pathogenesis is still unknown)

Streptococcus pyogenes

Infection of the throat (pharyngitis)

Immune response involving monocytes and

macrophage

M-proteins combine with HLA class II molecules

Presented to the CD4+ T cell

Travels in blood vessels and reaching heart tissue

Cross reaction occurs between M peptides,

myocardium and valvar tissue with the CD4+ T cell

Hypersensitivity reaction to the myocardium and

valvar tissue

Formation of Aschoff Body (characterized by

granular fibrinoid material, Aschoff giant cells,

lymphocytes, plasma cell, fibroblast and collagen)

Pancarditis/mitral valve stenosis

Chronic RHD


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ONN0809

Major Signs and their Pathophysiology

Cross reaction with host tissue

To cardiac tissue

Formation of Aschoff body

Pancarditis (pericardium,

myocardium or

endocardium)

Myocarditis

Tachycardia and

dilation

Cardiac failure

endocarditis

Slowly affecting

myocardium

Pericarditis

Inflammation of the

pericardial cavity

bread and butter

appearance

Chest pain and fever

To valvar tissue (mainly

mitral valve)

Formation of Aschoff

body

fish mouth appearance

Vegetation or fissuring

Mitral stenosis

To joint cartilage

Inflammation

Polyathritis

Maculopapular

rash

Erythema

Marginatum

Large Aschoff body

Subcutaneous

nodules

To skin

To subthalamic and caudate

nuclei

Sydenhams chorea

For better understanding

The streptococcus may share the same antigen

with human tissues, particularly cardiac cell

and valves.


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ONN0809

INFECTIVE ENDOCARDITIS

Definition

Is a disease of the heart valves particularly: the mural endocardium is only occasionally affected by late

spread from the valves

Causes

1. Gram positive bacteriaStreptococcus viridans

Streptococcus pyogenes

Streptococcus pneumonia

Staphylococcus aureus

Staphylococcus epidemidis

2. Gram negative bacteriaEischerichia coli

Pseudomonas sp.Klebsiella pneumonia

Haemophilus influenza

3. FungusCandida albicans

Aspergillus sp.

Signs and symptoms

Symptoms Signs

Fever

DyspnoeaEasy fatiguability

Splinter haemorrhage

Osler NodesJaneway lesion

Clubbing

Roths spots

Splenomegaly

Haematuria


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ONN0809


Endothelial damage

Exposure of subendothelial

collagen

Platelets deposition

Development of thrombi

Nonbacterial thrombotic

endocarditis

Clinical procedure

Provide bacterial entry to the

blood stream

Hypertension

Valvular dysfunctionDeposition of

immune complex

(SLE ad RHD)Cardiac

catheterization

High altitude Blood stasis

Tooth extraction

Endoscopy

Genitourinary

instrumentation

Cardiac surgery

I/V drug abuse

Virulent pyogenic bacteria

(staphylococcus aureus)

Acute Bacterial Endocarditis

Vegetation large and crumbling

Loose mixture of organisms and

fibrin mainly, with cellular debris

Rapid destruction of cusps and

chordae and spread of

suppuration to adjacent heart

muscle

Acute heart failure

Low grade bacteria (streptococcus

viridians)

Subacute bacterial endocarditis

Large firm vegetation, fairly dense

fibrin and platelet aggregation with

bacterial colonies, few leukocytes

Gradually increasing damage to

valve cusps

Minimal spread to adjacent

structures

Gradual heart failure


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ONN0809

NORMAL VALUES OF THE INVESTIGATION

Haematology

RBC Male (4.6 - 6.5 x 1012 /L)

Female (3.9 5.6 x 1012

/L)

White cell countAdult 4 11 x 109 /L

Infant (full term at birth) 10 25 x 109 /L

Infant (1 year) 4 18 x 109 / L

Basophil 0 0.1 x 109 /L (0 1%)

Eosinophil 0.01 0.44 x 109 /L (1 6%)

Neutrophil 2 7.5 x 109 /L (40 75%)

Monocyte 0.2 0.8 x 109 /L (2 10%)

Lymphocyte 1.3 3.5 x 109 /L (20 45%)

Fat

Cholesterol 3.6-6.3 mmol/L

HDL Male (0.78-1.81 mmol/L)

Female (0.78-2.2 mmol/L)

LDL Male (2.3-5.57 mmol/L)

Female (2.3-5.7 mmol/L)

Cardiac enzymes

Creatinine Kinase Male (


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THANK YOU FOR ALL THE LECTURES OF PPSP USMKK FOR ESPECIALLY AS STATED BELOW FOR CHECKING,

CORRECTING ALL THE FACTS WHICH WERE PUBLISHED AND FOR TEACHING MEDICAL STUDENT BATCH

2008/2009 2ND YEAR WITH HARDWORKING AND GREAT DEDICATION

1. ASSOCIATES PROF OTHMAN MANSOR2. DR THIN THIN WIN @ SAFIYA3. DR SAMARENDA S MUTUM4. DR ISKANDAR ZULKARNAIN ALIAS5. DR MOHD ASNIZAM ASARI

REFERENCE

1. PPSP lectures Lecture notes 2nd year 2008/20092. Oxford Concise Medical Dictionary, 6th edition definition3. Clinical Examination, 5thedition, Nicholas J Talley and Simmon OConnor clinical signs4. Differential diagnosis, 2nd edition, Andrew T Raftery and Eric Lim clinical signs and symptoms5. Pathology Basis f Disease, 7th Edition, Robbins and Cotran pathogenesis of diseases6. MIMS respiratory guide, Malaysia Edition 2004/2005

SPECIAL THANKS TO

KH CHEONG BASIC PRINCIPLE OF ECG

ROBIATUL AIDAWIYAH CARDIAC CYCLE

everything you need to know cardiovascular system

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