Anat Pathology

• Rheumatic fever


  Caused by an immunological reaction to group A beta-hemolytic streptococcus (streptococcus pyogenes) infection in the throat
• Rheumatic fever development


  1. Child develops sore throat/pharyngitis

  2. Wait 2-4 weeks without antibiotics

  3. Immune system attacks heart, neurons, joints, skin due to molecular mimicry
• Jones criteria for rheumatic fever

  • Joint disease (migratory polyarthritis)
  • Carditis (endocarditis, myocarditis, pericarditis)
  • Subcutaneous nodules
  • Erythema marginatum
  • Sydenham's chorea
• Diagnosis of rheumatic fever

  Clinically - 1 major + 2 minor criteria OR 2 major criteria
• Rheumatic fever


  • Acute condition affecting young people 5-15 years old, especially in crowded/poor areas
  • Causes regurgitation murmurs acutely, stenotic murmurs chronically
• Prevention of rheumatic fever

  Treat pharyngitis early with penicillin to prevent immune reaction
• Infective endocarditis


  Inflammation of the endocardium and heart valves, caused by bacteria, fungi, viruses, or parasites
• Acute vs subacute infective endocarditis

  • Acute - highly virulent bacteria (e.g. Staphylococcus, Streptococcus) rapidly destroy healthy valve
  • Subacute - less virulent bacteria (e.g. viridans streptococci, Enterococcus) attack damaged valve
• Infective endocarditis development


  1. Vegetations form on valves, containing pathogens, platelets, and fibrin

  2. Vegetations damage valve leaflets and chordae tendineae

  3. Can lead to regurgitation murmurs, bacteremia, septic emboli, and organ abscesses
• Infective endocarditis can occur in patients with prosthetic valves, indwelling catheters, or poor dental hygiene
• Infective endocarditis


  Infection of the endocardium, which has the heart valves
• Infective endocarditis


  • Can occur if I have a damaged valve from a previous disease, if I'm immunocompromised, had a dental procedure with poor oral hygiene, have a prosthetic valve, or have an indwelling catheter - all of these are sources of bacterial invasion of the blood
• Infective endocarditis progression


  1. Bacteria/fungi invade the blood and settle on the heart valves, forming vegetations containing pathogens, platelets and fibrin

  2. Vegetations damage the valve leaflets and chordae tendineae

  3. This leads to regurgitation murmurs like mitral, tricuspid or aortic regurgitation
• Symptoms of infective endocarditis


  Fever, new regurgitation murmur, fatigue, joint pain, Roth spots, glomerulonephritis, petechiae, Splinter hemorrhages, Janeway lesions, Osler nodes, septic embolization, splenomegaly, neurological symptoms
• Diagnosis of infective endocarditis

  Clinically by modified Duke's criteria - need 2 major or 1 major + 3 minor criteria. Includes positive blood cultures, positive echocardiogram findings, predisposing conditions, embolic/immunological phenomena
• Empiric treatment of infective endocarditis

  Start with Vancomycin, penicillin, or ampicillin + gentamicin, then adjust based on culture results
• Gentamicin is nephrotoxic and ototoxic
• Fever and new murmur

  Equals infective endocarditis until proven otherwise
• Rheumatic fever occurs in younger patients (5-15 years old), while infective endocarditis is more common in older patients (40-65 years old)
• Rheumatic fever is diagnosed by Jones criteria, while infective endocarditis is diagnosed by modified Duke's criteria
• Rheumatic fever is treated with penicillin, while infective endocarditis requires empiric antibiotics followed by targeted treatment based on culture results
• Lipoprotein metabolism


  1. Exogenous pathway

  2. Endogenous pathway
• Exogenous pathway


  Path by which cholesterol, triglycerides and other lipids are transported to different tissues from the diet
• Endogenous pathway


  Path by which cholesterol and lipids synthesized in the body are transported to different tissues
• Exogenous pathway


  1. Digestion in small intestine

  2. Chemo receptors detect fats

  3. Cholecystokinin released

  4. Gallbladder contracts to release bile

  5. Bile emulsifies fats

  6. Pancreatic lipase breaks down triglycerides

  7. Monoglycerides and fatty acids absorbed

  8. Resynthesized into triglycerides

  9. Packaged into chylomicrons
• Bile


  • Contains cholesterol, phospholipids, water, bilirubin, bile salts/acids
  • Bile salts emulsify fats
• Chylomicrons


  Lipoproteins that transport dietary lipids from intestine to tissues
• Chylomicrons are about 500 times smaller than the initial fat globules in the intestine
• Monoglycerides and fatty acids are absorbed into intestinal cells and resynthesized into triglycerides
• Triglycerides are packaged with cholesterol, cholesterol esters, phospholipids and apoprotein B-48 into chylomicrons
• Chylomicrons are released into circulation
• Cholesterol esters


  Molecules containing cholesterol and phospholipids
• Packaging of molecules


  1. Cholesterol

  2. Phospholipids

  3. Triglycerides

  4. Cholesterol esters

  5. Packaging into a structure
• Triglycerides


  Prominent component of the packaged molecule
• Apo B48


  Protein associated with the packaged molecule
• Chylomicron


  The packaged molecule that is pushed into circulation
• Absorption of chylomicron


  1. Absorbed into lacteals

  2. Transported through lymphatic system

  3. Emptied into blood via thoracic duct
• HDL (High Density Lipoprotein)


  Donates proteins (Apo E, Apo C2) to the chylomicron
• Apo E


  Binds to LDL receptors
• Apo C2


  Activates lipoprotein lipase