Infarction: Definition, Causes, Types, Pathogenesis,Treatment and MCQs for NEET, GPAT, CSIR NET JRF

INTRODUCTION :-

1. Infarction is the process of tissue necrosis, usually of coagulative type, resulting from ischemia; the localized area of necrosis so developed is called an infarct.
2. It occurs because of the occlusion (blockage or closing of blood vessels) of either of its arterial supply or its venous drainage.

CAUSES OF INFARCTION :-

1. Most commonly, infarcts are caused by interruption in arterial blood supply called ischemic necrosis.
2. Nearly, all infarcts are caused by thrombotic or embolic occlusion.
3. Stagnant hypoxia infarcts are less commonly produced by venous obstruction.
4. Nearly 99% of infarcts are caused by thrombolic events, and almost all are the result of arterial blockage.

TYPES OF INFARCTS :-

A.] According to their color :

• Pale or anemic due to arterial occlusion and are seen in compact organs such as heart, kidney, spleen.
• Red or hemorrhagic, seen in soft tissues and are caused either by pulmonary arterial obstruction (eg. in the lungs) or by arterial or venous occlusion (eg. in the intestine).

B.] According to their age :

• Recent or fresh.
• Old or healed.

C.] According to the absence or presence of infection :

• Bland, when free of bacterial contamination.
• Septic, when infected.

PATHOGENESIS :-

The process of infraction takes place as follows :-

1. Localized hyperanemia caused because of the obstruction of blood supply.
2. Within few hours, the affected part become swollen due to oedma and haemorrage. More extensive in lungs and spleen and less in kidney and heart.
3. Cellular changes such as cloudy swelling and degradation appears early.
4. Their is a progressive proteolysis of necrosis tissue and their is lysis of RBC.
5. An acute inflammatory reaction and hyperaemia appears.
6. Blood pigments, haemotidin and haemosiderin , liberated by the lysis of RBC are deposited in the infarct.
7. Following this, their is a progressive in growth of granular tissue from the margin of infarct so that eventually the infarct is replaced by the fibrous scar.

TREATMENT :-

Aspirin
All patients with a suspected myocardial infarction should be given aspirin. It is a powerful antiplatelet drug, with a rapid effect, which reduces mortality by 20%. Aspirin, 150-300 mg, should be swallowed as early as possible. General practitioners should give aspirin or advise the patient to take an aspirin when they are called by a patient who may be suffering a myocardial infarction. There is no need to wait for an electrocardiograph (ECG). If the patient has not already taken aspirin, it should be given in the ambulance or emergency room.

Streptokinase
Streptokinase produces generalized systemic fibrinolysis and is the drug most commonly used in Australia. Despite reducing mortality by 25%, only about 30% of patients have their coronary flow restored to normal within 90 minutes of treatment. This increases to over 50% by 3 hours and up to 80% by 5-7 days.

An intravenous infusion of 1.5 million units is given over 30-60 minutes. Most patients will develop hypotension if streptokinase is given quickly, but this is usually easily overcome by slowing the infusion and giving fluid.

Streptokinase is derived from Streptococci and will produce an antibody reaction. These antibodies appear after 2-3 days and persist for some years. The presence of antibodies reduces the efficacy of subsequent doses of streptokinase and increases the potential for anaphylaxis. The present consensus is that streptokinase should be used only once per patient. All patients should be informed about being treated with streptokinase and ideally given a card or other form of record so that this information is available should they have another infarction.

Fibrinolytic therapy
The mainstay of treatment is fibrinolytic therapy. This is given to dissolve the thrombus in the artery and restore flow. There are two fibrinolytic drugs commonly used in Australia – streptokinase and tissue plasminogen activator (tPA).

Fibrinolytic therapy should be given to all patients with appropriate indications and no contraindications .

The indications for fibrinolytic therapy are symptoms of myocardial ischaemia, of less than 12 hours’ duration, with ECG changes of ST elevation or left bundle branch block. Patients without these ECG changes should not be given fibrinolytic therapy.

MULTIPLE CHOICE QUESTIONS [MCQs] :-

1.] White infarct is seen in ?

a. Lung

b. Intestine

c. Heart

d. Ovary

2.] White infarcts are seen in the following except ?

a. Liver

b. Kidney

c. Spleen

d. Heart

3.] Pale infarct is seen in all except ?

a. Lungs

b. Spleen

c. Kidney

d. Heart

4.] Hemorrhagic infarction is seen in ?

a. Venous thrombosis

b. Thrombosis

c. Embolism

d. All of the above

5.] Heart failure cells are seen in ?

a. Chronic venous congestion of liver

b. Chronic venous congestion of lung

c. Acute venous congestion of lungs

d. Acute venous congestion of liver

6.] Necrosis with putrefaction is called as ?

a. Desiccation

b. Gangrene

c. Liquefaction

d. Coagulative necrosis

7.] What is the another name for a stroke ?

a. Heart attack

b. Brain attack

c. Myocardial infarction

d. None of the above

8.] An ischemic  stroke occurs when a blood clots blocks a blood vessel to the brain ?

a. True

b. False

9.] Chicken fat clot is ?

a. Postmortem clot

b. Thrombus

c. Infarct

d. All of the above

10.] What is the most commonly involved coronary artery in myocardial infarction (MI) ?

a. Right coronary artery (RCA)

b. Left anterior descending artery (LAD)

c. Left circumflex artery (LCA)

d. Posterior descending artery (PDA)

SOLUTIONS :-

1.] (c) Heart

2.] (a) Liver

3.] (a) Lungs

4.] (d)

5.] (b) Chronic venous congestion of lung

6.] (b) Gangrene

7.] (b) Brain attack

8.] (a)

9.] (a) Postmortem clot

10.] (b) Left anterior descending artery (LAD)

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REFERENCES :-

1.] Textbook Of Pathology By Harsh Mohan; 7th edition; Page no. 111 – 114.

2.] Robbin’s Basic Pathology; 5th edition; Page no. 114 – 116.