Topic: Ischemia, Infarction, Aneurysm, Atherosclerosis, Infective Endocarditis Faculty: Medicine Course: BSc Nursing - 2nd year

1. ● Infective Endocarditis
● Ischemia, infarction and
aneurysm
● Atherosclerosis
Dr. Salman Ansari
Dept. of Pathology
Kanachur Institute of Medical Sciences

2. Contents
● Infective endocarditis
● Ischemia
● Infarction
● Aneurysm
● Atherosclerosis

3. INFECTIVE ENDOCARDITIS

4. Infective Endocarditis
- Infective endocarditis also called Bacterial Endocarditis
- Endo card itis
- Inside heart inflammation
- Definition: “Serious infection of the valves and mural
endocardium(internal wall of heart) by microorganisms”

5. Types
Depending on severity, there are 2 types
1. Acute Bacterial Endocarditis(ABE)
2. Subacute Bacterial Endocarditis(SABE)
- Acute BE: destruction of endocardium by highly virulent bacteria in
a previously normal heart, usually rapidly fatal in a period of 2-6
weeks
- Subacute BE: less virulent bacteria in a previously diseased
heart, gradual course over a period of 6 weeks to few months

6. Incidence
- Usually over 50 years of age
- Males affected more than females

7. Etiology
Causes: Infection with microorganisms
+
Predisposing factors

8. 1. Infective agents:
- 90% of cases by streptococci and staphylococci
- In ABE: most common is Staphylococcus Aureus
- In SABE: most common is Streptococcus viridans
1. Predisposing factors: 3 factors
- Conditions with bacteremia, septicemia, pyemia(any
infections)
- Underlying heart disease(ABE in normal heart, SABE in
previously diseased)
- Weak immunity

9. Pathogenesis
Damage to valves/endothelium
Bacteria stick to damaged valves/endocardium
Bacteria multiplies
Formation of “vegetation”

10. Morphology
Presence of vegetations on valves or endocardium
Gross:
- left heart usually, mitral valve most common
- Few mm to cm
- Grey-brown colour
- Single or multiple
- Breaks easily(friable)
- ABE in normal heart, SABE in diseased heart

12. Microscopy:
1. CAP
2. BACTERIA
3. WBCs

13. Clinical features
Fever, chills, weakness
Complications:
1. In heart(cardiac complications)
2. Can spread beyond heart to other organs(extracardiac
complications)

14. 1. Cardiac complications
- Valvular stenosis(thickening of valve)
- Perforation, rupture or aneurysm of
Valves
- Abscess
- Heart failure

15. 2. Extracardiac complications:
- Vegetations are friable and can break
- Emboli from left heart can go to other organs like
spleen, kidney and brain
- Emboli from right heart can go into lungs and cause an
abscess

17. Diagnosis:
● Modified Duke criteria
● Blood culture
● Echocardiography
Treatment:
i.v antibiotics for upto 6 weeks

19. ISCHEMIA

20. Ischemia
- Definition: lack of blood supply to tissues
- Ischemia leads to: -lack of oxygen(hypoxia)
-malnourishment of cells
-accumulation of waste products

21. Causes of ischemia
- Heart: Heart isn’t pumping properly(poor cardiac output)
- Arteries: block in arteries - atherosclerosis, embolism
- Veins: block in veins(thrombosis)

23. Clinical effects
● Acute limb ischemia
● Heart: angina pectoris, ischemic heart disease
● Bowel: mesenteric ischemia
● Acute or chronic brain ischemia

24. INFARCTION

25. Infarction
-Definition: Necrosis(death) of tissue, due to ischemia
- Area affected is called an infarct
- Causes of infarction: same as causes of ischemia

27. Red infarct

28. Pale infarct

29. Pathogenesis
- Increased blood flow initially
- affected part becomes swollen
- Cloudy swelling, cell degeneration, and cell death later
- Necrotic tissue breaks down
- WBCs come to site
- RBCs break down, so infarct becomes pale
- Granulation tissue grows, and infarct is replaced by scar

31. Morphology
Gross:
- Infarcts of solid organs are wedge-shaped
- Infarcts due to block in arteries are pale
- Infarcts due to block in veins are red
- Both become pale later on

35. Microscopic features:
- Ischemic necrosis
- Hemorrhage, neutrophils present
- Infarct replaced by scar later on

36. ANEURYSM

37. Aneurysms
- Definition: abnormal permanent dilation of blood
vessel due to weakening of wall
- Wall stretches like a balloon

38. Classification

42. C. Based on pathogenetic mechahisms:
- Atherosclerotic aneurysm
- Syphilitic aneurysm
- Dissecting aneurysm(dissecting hematoma)
- Mycotic aneurysm
- Berry aneurysm: affecting the circle of Willis in the brain

43. Effects of aneurysms
1. Rupture: can tear and bleed, which can lead to death
2. Compression: the enlarged artery can press on the
nearby structures
3. Arterial occlusion

45. ATHEROSCLEROSIS

46. Definition
- Athero sclerosis
Fatty paste hardening
- Definition: “thickening and hardening of large and
medium sized arteries due to fibrofatty plaques(called
atheromas)”
- Affects mainly the aorta, coronary arteries(heart) and cerebral
arteries(brain)

48. Etiology
Modifiable
Non-modifiable(constitutional)
Risk
factors
Additional risk factors

49. Modifiable risk factors
1. Hyperlipidemia: increase in serum cholesterol
➢ High levels of Low density lipoprotein(LDL) - “bad
cholesterol”
➢ Low levels of High-density lipoprotein(HDL) - “good
cholesterol”
1. Hypertension: increase in systolic and diastolic blood
pressure
2. Cigarette smoking: most important avoidable cause of
atherosclerosis

50. Non-modifiable/constitutional risk factors
● Age: risk increases with older age
● Sex: Males are more at risk
● Family history
● Race: blacks are at higher risk

51. Additional risk factors
- Stress
- Obesity
- Lack of exercise

53. Pathogenesis- “Response to Injury” hypothesis
Exposure to risk factors
-> Formation of fatty streaks
-> lipoprotein particles accumulate inside intima and macrophages
enter into the lesion
-> macrophages ingest the lipoprotein and transform into "foam
cells"
-> macrophages release cytokines and lead to smooth muscle
proliferation

54. -> some foam cells die - formation of lipid-rich core
-> fibrous tissue forms around lipid-laden macrophage - formation
of fibrous cap
-> this fully developed plaque/atheroma can undergo calcification
-> plaque can bulge into lumen of coronary artery and narrow it
-> thrombosis can occur, leading to complete block of blood vessel
and causing acute coronary syndrome

55. Pathogenesis(short version)
Exposure to risk factors formation of fatty streak
-> lipoproteins accumulate, macrophage migration
-> streak develops into a fully-developed atheroma
-> Atheroma can undergo calcification or
thrombosis(“complicated plaque”)
-> Leading to clinical events(acute coronary syndrome,
stroke, limb ischemia)

59. Morphological features
Gross:
- Site: lower abdominal aorta, coronary arteries, popliteal
arteries, internal carotid arteries and circle of Willis
- Appearance: yellow oval lesions

61. Microscopy:
Plaque is made up of:
- Superficial fibrous cap
- Necrotic core: cholesterol cleft, foam cells
- Shoulder: peripheral area below and on the sides of the
cap

63. Fibrous cap
Foam cell
Diagram of atheroma/plaque

64. Clinical effects
- Artery becomes narrow ischemia and atrophy
- Artery can get blocked suddenly infarction and necrosis
- Plaque can break thrombus and embolisation
- Artery wall can became weak and dilate aneurysm and
rupture

65. Clinical significance
Causes a number of diseases, such as:
- Heart -> ischemic heart disease, myocardial infarction
- Brain -> chronic ischemic brain damage, stroke
- Aorta -> aneurysm formation, thrombosis and
embolisation to other organs
- Small intestine -> ischemic bowel disease, infarction
- Lower extremities -> intermittent claudication, gangrene

68. Prevention
Primary prevention: Targeting modifiable risk factors to prevent occurrence
of disease
Secondary prevention: after the disease process has already started
- Stop smoking - most important avoidable cause
- Maintain serum cholesterol: reduce levels of LDL, increase levels of
HDL
- Can be done via diet and drugs
- Low cholesterol diet, cholesterol-lowering medications(statins)

69. - Control blood pressure - via lifestyle(diet and exercise)
and antihypertensive medications(ACE inhibitors, beta
blockers, calcium channel blockers)
- Diabetic control(through diet/exercise/medications)
- Regular exercise (brisk walking, cycling or swimming for
20 minutes two or three times a week) has a protective
effect.

70. References:
● Ramadas Nayak - Textbook of Pathology for Allied Health Sciences
● Harsh Mohan - Textbook of Pathology
Questions:
salman.s.ansari92@gmail.com