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Aneuysms- Pathology

Definition: Congenital or acquired weakness of vessel wall media, resulting in a localized dilation or out pouching. The bulge in the aneurysm may burst and death may occur any time. 1. Atherosclerotic aneurysms: Weakening of media secondary to atheroma formation Occur in the abdominal aorta below the real arteries Associated with hypertension Half of aortic aneurysms > 6cm in diameter will rupture within 10 years 2.Aortic dissecting aneurysms Its due to cystic medial necrosis of tunica media. Blood from the vessel lumen enters the intimal tear and dissects through the layers of media. It presents with severe tearing pain. It may compress and obstruct the aortic the aortic branches (eg- renal or coronary arteries) HTN and Marfan syndrome are predisposing factors. 3. Syphilitic aneurysms: Involves ascending aorta Syphilitic (leutic) aortitis causes an obliterative endarteritis of the vasa vasoram. Leading to ischemia and smooth muscle atrophy of aortic media. May dilate the aortic ...

Temporal arteritis- Pathology

Most common form of vasculitis. Affects females more than males. Primarily affects the elderly population. Temporal arteritis is associated with HLA-DR4 Distribution of the disease: 1. Small and medium sized arteries 2. Cranial arteries (temporal, facial and ophthalmic arteries) 2. Aortic arch-giant cell aortitis (uncommon) Clinical features: 1. Throbbing headache- Mostly unilateral 2. Tender firm temporal arteries 3. Visual disturbances- Blurred vision, double vision, visual loss. 4. Facial pain 5. Fever, Malaise, Weight loss, muscle aches, anemia 6. Polymyalgia rheumatica: systemic flu like symptoms and joint involvement (pain, morning stiffness in neck, shoulders and hips). Laboratory findings- Elevated ESR Pathology- 1. Segmental granulomatous vaculitis 2. Fragmentation of internal elastic lamina 3. Intimal fibrosis with luminal narrowing. Diagnosis- Temporal arterial biopsy, classical presentation or rapid onset may be treated empirically Treatment - Corticosteroids

Wagers granulomatosis- Pathology, CVS

Wagner's granulomatosis is a kind of autoimmune disorder affecting the arteries. Medium sized and small arteries are involved. This is a kind of necrotizing vasculitis with granulomas. Its more common in males than in females. Mostly occurs at the age group of 40-60. Classically involves Nose, Sinuses, Lungs and kidneys. Clinical Features: Bilateral pneumonitis with nodular and cavity pulmonary infiltrates. Chronic sinusitis. Nasopharyngeal ulcerations. Focal necrotizing glomerulosclerosis and Crescentic glomerulosclerosis are the two important forms of Renal pathology observed. Microscopic picture: Fibrinoid necrosis, Neutrophils and granulomas. Lab findings: Cytoplasmic antineutrophil cytoplasmic auto antibodies(C-ANCA) Auto antibody against proteinase 3 Diagnosis is confirmed by biopsy Treatment is by giving immunosuppresive drugs like Cyclophosphamide.

Pathology- Cardiac Tumors

Cardiac Myxoma: It is derived from the Mesenchyme and usually arise within the left atrium near the fossa ovalis. It restrict the blood flow to left ventricle. Shows constitutional signs of fever, weight loss and anemia. Microscopic picture- Stellate shaped cells in the myxoid background. Complications- Embolism (mostly in the brain), Ball valve obstruction of valves. Cardiac Rhabdomyomas: Benign tumour arising from myocardium.. Associated with Tuberous sclerosis . Metastatic Disease: Most commonly from Lungs. This is more common than primary cardiac tumors.

Sequential changes in MI

Gross sequence of Changes in MI Time Predominant finding 0 to 18 hours No gross changes 18 to 24 hours Vague pallor and softening 1 to 7 days Yellow scar 7 to 28 days Central scar formation with red border Months Thick white Firm scar formation Microscopic changes in MI Survival Time Predominant Finding 1-4 hours Wavy myocyte fibers, contraction bands 4-24 hours Coagulative necrosis 1 to 3 days Neutrophil infiltration 3 to 7 days Macrophage infiltration 7 to 28 days Granulation tissue Months Fibrotic scar

Cell Injury

Reversible Injury: 1. Decreased synthesis of ATP by oxidative phosphorylation.   2. Decrease function of Na-K ATPase pump- Influx of sodium and efflux of potassium Swelling of cell and endoplasmic reticulum. 3. Glycolysis- Depletion of cytoplasmic glycogen, Increased lactic acid production Decreased PH of the cell 4. Decreased protein synthesis and detachment of ribosomes from rough endoplasmic reticulum. 5. Plasma membrane blebs and myelin figures Irreversible Injury: 1. Severe membrane damage- Massive influx of calcium into the cell- Large flocculant densities in the matrix. Efflux of intra cellular enzymes into circulation. 2. Mitochondrial dysfunction- Mitochondrial swelling Large densities in mitochondrial matrix Irreparable damage of oxidative phosphorylation Inability to produce ATP 3. Rupture of lysosomes- Release of lysosomal digestive enzymes into cytosol Activation of acid hydrolases followed by autolysis 4. Nuclear changes- Pyknosis- degeneration and condensation of n...

Important points about ANS phamacology

Atenolol is not lipid soluble therefore it has longer half life than Metaprolol which is lipid soluble. Carvedilol blocks both alpha and beta receptors and is the most common beta blocker used in chronic congestive heart failure because it has Antioxidant and Antimitogenic properties in addition. Esmolol has the shortest and Nadolol has the longest half life among all beta blockers. Beta Blockers must not be used in compensated (i.e) acute heart failure. Beta blockers that are excreted in kidneys (lipid insoluble): Nadalol, Satolol, Atenolol, Acebutalol, Bisprolol, Betaxolol, Celioprolol- Should be avoided in renal failure. Endogenous Norepinephrine is metabolized by COMT and MAO. Exogenous Norepinephrin is metabolized by reuptake. Hemicholimium- Blocks the reuptake of Choline Vesamicol- prevents entry of choline into storage vesicles. Glucagon is DOC in beta blockers overdose. Other drugs that are used- Norepinephrine and Calcium chloride. Cardioselective Beta Blocker used in Glaucom...

Alpha 1 Blockers

Alpha 1 receptors are located in- Eye radial (i.e dilator) muscle Arterioles and viens, Male sex oegans, Urinary bladder, Kidney and Liver. Alpha 1 receptors use G q Coupled secondary mediators and cause increase in phospholipase C, IP3, DAG and calcium levels in the cell. Alpha1 blockers: Selective Blockers- Prazosin, Doxazocin, Terazocin Non selective Alpha blockers (both alpha 1 and alpha 2 receptor blockers)- Phentolamine(competitive inhibitor), Phenoxybenzamine (non competitive inhibitor) Effects of Alpha1 receptor blockage: Eye- Miosis Arterioles and veins- Reduced sympathetic tone in blood vessels- This results in vasodilation, Decrease in preload and after load on heart, lowering of peripheral vascular resistance and thus a fall in blood pressure is noted. The drop in blood pressure causes a reflex tachycardia. Prazosin : Prazosin can lower BP rapidly so patients are recommended to relax for 1 hour after taking the first dose and...