ISCHEMIC HEART DISEASE

Presenter: Dr. Mounika

Moderator: Dr. Jayapal Rao
MD,HOD,Dept of Pathology
 ISCHEMIC
HEART DISEASE
 PLAN OF STUDY
1. Need for study 8.Investigations
2. Definition 9. Complications
3. Risk factors 10.DD
4. Pathogenesis 11.Management
5. Effects of Ischemia 12. Conclusion
6. Angina 13. Homoeopathic
7. MI approach
14. Bibliography
 Need for study
• EPIDEMOLOGY:
• IHD causes more deaths and disability
and incurs greater economic costs than
any other illness in the developed world.
IHD is the single most important cause of
premature death in developed world. It is
serious, chronic, life-threatening illness.
• With urbanization in the developing world,
the prevalence of risk factors for IHD is
increasing rapidly in these regions such
that a majority of the global burden of IHD
is now occurring in low-income and
middle-income countries. Population
subgroups that appear to be particularly
affected are men in South Asian countries,
especially India.
 Speciality of cardiac muscle?
• No fatigue?
• No tetanus?
 Blood supply
The two coronary arteries, left and right,
arise from the left and right sinus of
Valsalva, respectively. In 10% of
individuals the circulation is considered as
"left dominant" as the circumflex artery
gives off the posterior descending artery.
In 90%, the circulation is right dominant as
the posterior interventricular artery is given
off from the right coronary artery
Supply to heart occurs during
Systole or Diastole?
Factors that maintain circulation
• Pumping action of heart
• Elastic recoil of the arteries\
• Pressure gradient
• Respiration
• Muscular exercise
• Effect of gravity
 Factors regulating nutrition &
action of heart

• O2 supply
• Blood pressure
• Temperature
• Inorganic ions
• Neuroharmones
 Factors influencing coronary
circulation

• Mean aortic pressure

• Cardiac output
• Metabolic factors
• O2 supply
 Conduction & nerve supply

• Autorhythmic
• Sympathetic & parasympathetic
 DEFINITION OF IHD
• The World Health Organisation has
defined ischaemic heart disease (IHD) as
myocardial impairment due to imbalance
between coronary blood flow and
myocardial requirements.
• The most common cause of IHD is
atherosclerotic coronary artery
disease[CAD]
 Aetiology
MAJOR RISK FACTORS
• CONSTITUTIONAL • Acquired
• Age • Hyperlipidaemia
• Sex • Hypertension
• Genetic • DM
• Familial • Smoking
 Minor risk factors
• Environmental influences
• Obesity
• Infections
• Harmones
• Physical inactivity
• Stressful life
• Role of alcohol
• Homocystinuria
 PATHOPHYSIOLOGY OF
MYOCARDIAL ISCHAEMIA

Myocardial ischaemia occurs as a result of

imbalance between O2 supply and
demand.
Etiopathogenesis

1.Coronary atherosclerosis:
• Distribution:[ SVD, TVD]
• Location.
• 2. Superadded changes in coronary
atherosclerosis:
• Acute changes
• coronary artery thrombosis
• platelet aggregation
3.Non atherosclerotic causes:
• Vasospasm,
• Arteritis
• Embolism
• Trauma
• Aneurysm
• Compression.
 Effects of Myocardial Ischemia: Depending
on suddenness of onset , Duration,
Degree, Location, Extent of area affected
by ischemia.

• Asymptomatic state
• Angina pectoris
• Acute myocardial infarction
• Chronic ischemic heart disease
• Sudden cardiac death
 ANGINA
• It is derived from the greek word
STRANGULATION.
• It is a syndrome “SENSE OF BAND
AROUND CHEST”. Patient presses his
sternum with clenched fist to locate the
pain.
• Progressive constriction of coronary
arteries cardiac pain called angina.
 The types of angina include
• 1. Stable angina,
• 2. Unstable angina,
• 3. Prinzmetal’s angina
• 4. Post infarction angina
 Stable angina or effort angina

• Also called Heberdeen’s angina, it occurs

on known physical effort, and is relieved
with rest, standing or sublingual
nitroglycerine.

Modalities
• Temperature,
• Emotions,
• Diurnal
• Even sometimes smoking, sexual act,
shaving, straining at stool
Some cases pain is absent , Angina-
equivalent symptoms breathlessness,
fatigue, symptoms of decreased cardiac
output.
 Variants:
• Start-up or Walk- through angina,
• Nocturnal angina,
• Decubitius angina,
• Post Prandal angina,
• Ammunition factories.
Class
New York Heart Association Functional Classification Canadian Cardiovascular Society
Functional Classification
I 
Patients have cardiac disease but without Ordinary physical activity, such
the resulting limitations of physical activity. as walking and climbing stairs,
Ordinary physical activity does not cause does not cause angina. Angina
undue fatigue, palpitation, dyspnea, or present with strenuous or rapid
anginal pain.  or prolonged exertion at work or
recreation. 
II 
Patients have cardiac disease resulting in Slight limitation of ordinary
slight limitation of physical activity. They are activity. Walking or climbing
comfortable at rest. Ordinary physical stairs rapidly, walking uphill,
activity results in fatigue, palpitation, walking or stair climbing after
dyspnea, or anginal pain.  meals, in cold, or when under
emotional stress or only during
the few hours after awakening.
III 
Patients have cardiac disease resulting Marked limitation of
in marked limitation of physical activity. ordinary physical activity.
They are comfortable at rest. Less than Walking one to two blocks
ordinary physical activity causes on the level and climbing
fatigue, palpitation, dyspnea, or anginal more than one flight of
pain.  stairs in normal
conditions. 

IV 
Patients have cardiac disease resulting Inability to carry on any
in inability to carry on any physical physical activity without
activity without discomfort. Symptoms discomfort—anginal
of cardiac insufficiency or of the anginal syndrome may be present
syndrome may be present even at rest. at rest. 
If any physical activity is undertaken,
discomfort is increased. 
• Physical examination in patients with
angina pectoris is often normal. However,
there may be indication of coronary risk
factors like xanthelasma or xanthomas.
Palpation may reveal thickened arteries
and reduced or absent pulses as signs of
generalised atherosclerosis. LV
enlargement, S3 or S4 gallop.
 INVESTIGATIONS
• 1. X-ray chest for cardiomegaly or
pulmonary congestion. 2. Lipid profile 3.
Blood sugar, serum uric acid and urine
examination
• Electrocardiogram : In 50% of patients
with angina, the resting ECG is normal
between anginal episodes. During an
anginal episode transient ST-T depression
may be noted which disappears with rest
or with sublingual nitroglycerine
 Prinzmetal angina
• Also called variant angina, it was
described by Prinzmetal in 1959. The pain
usually occurs at rest at night or in the
early morning hours. It is associated with
ST elevation on the ECG, responds to
sublingual nitroglycerine, and is caused by
spasm of the coronary artery.
• Exercise stress testing may fail to induce
ischaemic changes. The spasm can be
induced by smoking, hyperventilation . The
cause of spasm may be increased alpha-
adrenergic activity during the early
morning hours or platelet aggregation.
Coronary angiography may reveal normal
coronary arteries.
 Unstable angina
• Also called intermediate coronary
syndrome and Preinfarction angina, it is a
serious form of angina and needs special
attention since 20% of these patients are
likely to develop fatal or nonfatal
myocardial infarction within 4 months.
There is a higher incidence of left main
coronary artery disease in these patients.
• Unstable angina includes (i) angina of
recent onset (less than 60 days); (ii) stable
angina with symptoms more severe in
intensity, frequency or duration and more
easily provoked; (iii) angina at rest; (iv)
angina following myocardial infarction
(within days or weeks).
• ST-T depression in the ECG is common...
About 25% of these patients have
coronary artery thrombosis. In the others,
spasm plays an important role. Patients
have associated severe coronary artery
obstructive disease.
 Management
• Thrombolytic agents
• PTCA
• CABG
 Post infarction angina
• Some patients with myocardial infarction
develop angina 2 days to 8 weeks
following the acute infarction. Most
patients have multivessel disease or
partially recanalised coronary arteries with
residual myocardial ischaemia.
MYOCARDIAL INFARCTION

The area of muscle that has either zero

flow or so little flow that it cannot sustain
cardiac muscle function process called
Infacrtion.
• Myocardial infarction is a serious
complication of atherosclerotic coronary
heart disease. In most patients (80-95%) it
results from thrombotic occlusion of the
infarct-related vessel. Myocardial
ischaemia and necrosis set in within about
20-40 minutes
• This occurs as a wave-front starting from
the subendocardial region and progressing
to the subepicardial region. The entire
process usually takes 6 hours to complete.
Therefore any intervention for limiting
infarct size should be initiated in this "time
window" of 6 hours.
Etiopathogenesis:

Mechanism of Myocardial ischemia:

Diminished coronary blood flow, Increased
myocardial demand, Hypertrophy of heart
without increase in coronary blood flow.
• Infarcts may be transmural versus
subendocardial infarcts: Transmural
most common type 95%. Subendocardial
infarct genesis is due to reduced coronary
perfusion without critical stenosis
 Transmural Sub-endocardial
• Full thickness • Inner 1/3 to half of ventricular
wall
• Superimposed thrombus in • Decreased circulating blood
atherosclerosis volume( shock, Hypotension,
Lysed thrombus)
• Focal damage • Circumferential
 Types of infarcts:

• 1. Acc to anatomical region of left

ventricle: Anterior, lateral, septal,
circumferential or combinations.

• 2. Acc to degree of thickness : Transmural,

Subendocardial.

• 3. Acc to age old, new [ healed & fresh].

Location of infarcts:

Infarcts are most frequently located in left

ventricle . Right ventricle is less
susceptible to infarction due to its thin wall
less metabolic requirement.
 3 common regions of MI:

• 1. Stenosis of left anterior descending coronary

artery is most common[40% to 50%]

• 2. Stenosis of right coronary artery[30% to 40%]

• 3. Stenosis of left circumflex coronary

artery[ 15% to 20%]
Morphology[ Pathological changes]
light microscopy
• First 0-6hrs- Streching of fibres.
• 6-12hrs after MI – Coagulative
necrosis & neutrophils begins
• Up to 3 days = Coagulative necrosis,
neutrophils
• 1-2 weeks = Granulation tissue
• ≥ 3 weeks = fine scar
• ≥ 2 months = dense scar
 CLINICAL FEATURES
• The presenting symptoms vary from
severe pain in the chest to minimal
symptoms with the disease being
unrecognised. In most patients, there is
substernal pain of varying intensity,
radiating to the arms, jaws or back or the
epigastric region, with sweating. The pain
lasts for 20 minutes or more and is
unrelieved or partially relieved by
sublingual nitroglycerine
• The discomfort may be felt as
compression of chest or a burning
sensation, associated with anxiety and
feeling of impending death. Continuing
discomfort is a symptom of ongoing
ischaemia and evolving infarction. As the
infarction is completed, the pain may
subside completely..
• In 15-30% of patients the infarction may go un
recognised because of absence of typical
symptoms. About 5% of such patients have
silent infarction. This is common in diabetics
and elderly patients. In others, breathlessness
as in acute left ventricular failure, syncope,
giddiness, fatigue, abdominal pain, nausea
and vomiting and unexplained hypotension
may be the presenting manifestation
 C/F
• Pain
• Indigestion
• Apprehension
• Shock
• Oliguria
• Low grade fever
• Acute pulmonary oedema
• Physical examination reveals a pale
patient who is sweating, restless, in agony
due to pain, and tossing in the bed in an
attempt to get relief. The pulse may be
rapid or slow, and regular or irregular.
Bradycardia may be a prominent feature in
the early hours especially in those with
inferior wall infarction
Blood pressure may be normal, low or high.
Auscultation may reveal S3 or S4 gallop.
Paradoxical splitting of the second heart sound
may be made out. Right ventricular infarction
may result in increased jugular venous
pressure and signs of right heart failure.
 Cardiac reserve

• Maximum amount of cardiac output that

can increase above normal. It is 400%
blood per min more than body requires.
 Coronary steal syndrome
• The degree of cellular death = degree of
ischemia x degree of metabolism of heart .
[ Increase exertion –
Increase metabolism- decrease blood
supply to ischemic areas leaving the blood
through coronary vessels.]
 INVESTIGATIONS

• Leucocytosis with polymorphonuclear

reaction and high ESR due to tissue
necrosis are present during the first week.
• Electrocardiographic changes : The earliest
changes are ST elevation occurring with the
onset of chest pain. Q waves appear when
transmural infarction occurs. ST segment
changes start reversing early (within 24
hours or so) and T waves begin to get
inverted.).
• Anterior wall infarction is diagnosed by
changes in leads V1 to V4,
• Lateral by changes in L1, aVL, V5 and V6,
and
• Inferior wall infarction by changes in L2, L3
and aVF
• Posterior wall LV infarction is diagnosed by
ST depression, upright T wave and tall R
wave in V1 and V2.
• The initial ECG changes may be present
in only about 50-75% of patients. In
others, a typical history and serial serum
enzyme changes provide diagnostic help.
Serial ECGs improve the diagnostic yield
to 85%.
• Serum enzymes: Necrosis of myocardial
cells releases enzymes in the blood.
• SGOT (AST) starts to rise within a few
hours, reaching a peak at 24 hours and
declining over the next 48-72 hours; it is
not specific for cardiac muscle injury since
it is present in red blood cells, liver and
skeletal muscle.
• Serum creatinine phosphokinase (CPK) rises
immediately 4 to 6hrs ; it falls to normal values
within 48 hours. This enzyme is also not
specific for cardiac cells and is present in
skeletal muscle and brain tissue. The CPK
isoenzyme, CPK-MB, is more specific for
cardiac tissue; its levels have been related to
the extent of myocardial infarction.
• Serum LDH levels increase late after
myocardial infarction. The increase starts
during the first day, peak levels are
achieved during the 3rd or 4th day, and
they may remain high for 14-15 days. LDH
cardiac isoenzyme (LDH1) is more
specific.
• Troponin level is increased in AMI 4 to
6hrs and is a more sensitive indicator of
myocardial neurosis high for 7 to 10 days.
MANAGEMENT

Almost 30-35% of patients with AMI die

due to arrhythmias, LV failure and
cardiogenic shock. Half of these deaths
occur in the first 1-2 hours after onset of
symptoms and 70-80% in the first 24
hours. Further, the Time window for
salvaging the ischaemic myocardium at
risk of necrosis is about 6 hours
 Reperfusion

• An occluding thrombus is responsible for

myocardial infarction in almost 85% of
patients. It is known that the infarction is
completed after several hours. An attempt
should therefore be made to remove the
obstruction and achieve reperfusion to re-
establish blood flow to the jeopardised
myocardium and so limit the size of the
infarct.
Cell injury induced by free radicals, particularly
reactive oxygen species, is an important
mechanism of cell damage in many pathologic
condition ischemia-reperfusion injury (induced
by restoration of blood flow in ischemic tissue) .
On perfusion excess of sodium and calcium
ions due to cell membrane damage.
• For approximately 30 minutes after the
onset of even the most severe ischemia,
myocardial injury is potentially reversible.
Thereafter, progressive loss of viability
occurs that is complete by 6 to 12 hours.
The benefits of reperfusion are greatest
when it is achieved early, and are
progressively lost when reperfusion is
delayed
Ischemic Heart Disease
• Thrombolytic agents, viz. streptokinase,
urokinase, acetylated streptokinase, and
tPA. It achieves recanalisation in about
50% of patients, recanalisation rates are
reportedly higher (75%). A major factor is
the high cost of the drug.
• All thrombolytic agents should be given within
4-6 hours after the onset of chest pain. Some
of the complications that can occur include
reperfusion arrhythmias and bleeding.
Thrombolysis is generally avoided in patients
following recent operations, those with recent
cerebrovascular accidents, those who have
bleeding diathesis or following
cardiopulmonary resuscitation.
• Thrombolytic agents help in reducing
short-term mortality and improving LV
function. Following thrombolytic therapy,
intravenous Herapin is given for the next
24-48 hours to prevent reocclusion..
• PTCA has been used as a method of
reperfusion with a success rate of 90-
95%.. It is a procedure of immense value
in patients with cardiogenic shock, severe
LV failure and large anterior myocardial
infarction.
• INDICATIONS OF PTCA:
• Coronary arteriography is indicated in (1)
patients with chronic stable angina
pectoris who are severely symptomatic
despite medical therapy and who are
being considered for revascularization,
i.e., a percutaneous coronary intervention
(PCI) or coronary artery bypass grafting
(CABG)
• patients with troublesome symptoms that
present diagnostic difficulties in whom
there is a need to confirm or rule out the
diagnosis of IHD.
• Coronary bypass surgery as a method of
reperfusion is limited to patients who do
not respond to thrombolytic therapy and
continue to get angina and are not suitable
candidates for PTCA. Complications and
mortality are higher.
• Anastomosis of one or both of the internal
mammary arteries or a radial artery to the
coronary artery distal to the obstructive
lesion is carried out. For additional
obstructions that cannot be bypassed by
an artery, a section of a vein (usually the
saphenous) is used to form a connection
between the aorta and the coronary artery
distal to the obstructive lesion.
• Occlusion of venous grafts is observed in
10–20% of patients during the first
postoperative year, in approximately 2%
per year during 5- to 7-year . Long-term
patency rates are considerably higher for
internal mammary and radial artery
implantations than saphenous vein grafts
• The survival benefit is greater in patients
with abnormal LV function (ejection
fraction <50%) the fraction of end diastolic
volume.
 Complications of Acute Myocardial
Infarction
• Arrhythmias
•  Heart failure
• Cardiogenic shock
• Sudden death. Rupture of interventricular
septum
• Thrombosis in LV causing cerebral
embolism
• Rupture of ventricle into pericardial sac causing
cardiac tamponade
• Deep vein thrombosis in legs causing
pulmonary embolism
• Pericarditis during massive infarction
• Aneurysm of ventricle with thrombosis and
thrombo-embolic phenomenon
• Dressler’s syndrome (post myocardial infarction
syndrome)
Dressler’s syndrome occurs a few days to
6 weeks following myocardial infarction
and is characterised by fever,
Pleuropericarditis, joint pains and raised
ESR. It results from an autoimmune
reaction to the necrosed myocardial tissue
 ASYMPTOMATIC [SILENT] CORONARY
ARTERY DISEASE

• Several autopsy studies in accident victims

or in military personnel dying in the
battlefield, stress testing in asymptomatic
individuals subjected to executive health
check-ups, and coronary angiographic
studies in individuals may have coronary
artery disease without any symptoms. In
many of them the first event may be sudden
cardiac death or myocardial infarction.
• Some of these patients exhibit higher
thresholds to electrically induced pain,
others show higher endorphin levels, and
still others may be diabetics with
autonomic dysfunction.[ Endorphins are
derived from a substance found in Pitutary
gland , naturally and have pain relieving
properties.]
• In addition, patients with asymptomatic
ischemia after suffering a myocardial
infarction are at greater risk for a second
coronary event. The widespread use of
exercise ECG during routine examinations
has also identified some of these
heretofore unrecognized patients with
asymptomatic CAD
 CHRONIC IHD

• Ischemic Cardiomyopathy or Diffuse

fibrosis in the myocardium
characterstically found in elderly age
group.CHF is gradually developed
decompensation over a period of years
• [Chronic anaemia]
 
SUDDEN CARDIAC DEATH AND
CARDIAC ARREST
• It is estimated that in 20% or more of
patients with coronary artery disease, the
first presenting feature may be sudden
cardiac death, defined as death within few
minutes to 2 hours after onset of
symptoms. The usual cause is ventricular
fibrillation or cardiac asystole and
occasionally electromechanical
dissociation.
 Differential Diagnosis
• 1. Pericarditis Hours to days; may be
episodic Sharp Retrosternal or toward
cardiac apex; may radiate to left shoulder
May be relieved by sitting up and leaning
forward <cough, swallowing, lying in
leftsided supine.
• Pericardial friction rub
• Aortic dissection : Abrupt onset of
unrelenting pain Tearing or ripping
sensation; knifelike Anterior chest, often
radiating to back, between shoulder
blades.
• Pulmonary embolism: Abrupt onset;
several minutes to a few hours Pleuritic
Often lateral, on the side of the embolism
Dyspnea, tachypnea, tachycardia, and
hypotension, haemoptysis.
• Esophageal reflux -10–60 min, Burning
Substernal, epigastric, Worsened by
postprandial recumbency.
• Relieved by antacids.
• Esophageal spasm- 2–30 min ,Pressure,
tightness, burning retrosternal, Can closely
mimic angina,
• Peptic ulcer- Prolonged Burning
Epigastric, substernal relieved with food or
antacids.
• Acid peptic disease: < Early mrng
[ acid secretions are not neutralised by
food.]
• Musculoskeletal disease- Variable, Aching
< movement
• May be reproduced by localized pressure
on examination[ chondrosternal,
costochondral .]
• Emotional and psychiatric conditions –
tightness & aching; may be fleeting
Variable; may be retrosternal, Situational
factors may precipitate symptoms
• Anxiety or depression often detectable
with careful history
 Prognosis
Depends on:

• 1.Number of diseased vessels

• 2. Degree of LV dysfunction
 MANAGEMENT [ADAPTATION]

• Myocardial ischemia is caused by a

discrepancy between the demand of the
heart muscle for oxygen and the ability of
the coronary circulation to meet this
demand. Most patients can be helped to
understand this concept and utilize it in the
rational programming of activity.
• Many tasks that ordinarily evoke angina
may be accomplished without symptoms
simply by reducing the speed at which
they are performed. Patients must
appreciate the diurnal variation in their
tolerance of certain activities and should
reduce their energy requirements in the
morning, immediately after meals, and in
cold or inclement weather.
On occasion, it may be necessary to
recommend a change in employment or
residence to avoid physical stress.
However, with the exception of manual
laborers, most patients with IHD can
continue to function merely by allowing
more time to complete each task. In some
patients, anger and frustration may be the
most important factors precipitating
myocardial ischemia. If these cannot be
avoided, training in stress management
may be useful.
• A treadmill exercise test to determine the
approximate heart rate at which ischemic
ECG changes or symptoms develop may
be helpful in the development of a specific
exercise program.
 EXERCISES
A regular program of isotonic exercise
[muscles contract & there is movement]
that is within the limits of each patient's
threshold for the development of angina
pectoris and does not exceed 80% of the
heart rate associated with ischemia on
exercise testing should be strongly
encouraged.
• Avoid Isometric exercises[muscle
contract increase in tension but does not
move]
 CONCLUSION

• Chest discomfort is one of the most

common challenges for clinicians in the
office or emergency department. The
differential diagnosis includes conditions
affecting organs throughout the thorax and
abdomen, with prognostic implications that
vary from benign to life-threatening.
• Failure to recognize potentially serious
conditions such as acute ischemic heart
disease, aortic dissection, tension
pneumothorax, or pulmonary embolism
can lead to serious complications,
including death. Conversely, overly
conservative management of low-risk
patients leads to unnecessary hospital
admissions, tests, procedures, and
anxiety.
•
 Homoeopathic approach
• Physiological action basis said by
Dr.Richard Hughes:
Aconite: “In all diseases of heart
characterised by increased action when
leftside is chiefly involved.”[ Physiologically
cardiac depressent][ Fear, anxiety, mental
restlessness]
Dr. Clark: Rapidity of action relieved
sometimes so painful & distressing spasm
of heart.
Arsenic: For incidence of cardiac cachexy.
Nights are troubled by oppression and
anguish.
Dr. Clark: Ars.Iod: Act on heart muscle
arresting degeneration & restoring vitality.
 Dr. Boerick- “Same character of
pain as in Angina”
• Cactus: “Pain as if constricted by Iron
band”[ It is a stimulant on ganglionic
centres in the cardiac walls.]
• Haemotoxylon: Sense of constriction is
characteristic. “ Sensation as if bar lay
across chest”
• Lactrodectus. Mactans: Picture of Angina,
constriction of chest muscles.
 Hydrocyanic acid: Spasmodic
constriction& tightness in chest, torturing
pain in chest.
• Anacardium: Also has band like
sensation.
• Glonine : Nitroglycerine[ palliative non
homoeopathic]
• Amy.Nitrosum:For palliation in Coronary
spasm.
• Tabacum: Prove the most homoeopathic
drug for Angina pectoris, Constriction of
heart.[ Nausea, vomiting ,death like pallor]
• Camphor: As a heart stimulant for
emergency use is most satisfactory
remedy.[ collapse]
• Veratrum: Best heart stimulant.
• Iberis:Posess efficacy in cardiac
diseases.Wakes at 2 am with palpitation.
• Ophidia [Naja, Bothrops][ Symptoms of
thrombotic phenomena]
• Craetagus: Solvent power upon
crustaceous and calcareous deposits in
arteries.
• Type A Personality: Aggressiveness,
Competitive drive, Ambitiousness, Sense
of urgency [ risk factors & modalities].
Environmental influences. Helpful in
selection of remedy.
 BIBLIOGRAPHY

• Textbook of pathology by Dr. Harshmohan

• API textbook of medicine
• Harrisons Internal medicine.
• Textbook of medical physiology by Guyton
 THANKYU
• THANKYU