Pathology

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jbaalmann
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55427
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Pathology
Updated:
2010-12-13 19:07:18
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Cardiology
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  1. Cardiac tamponade
    • compression of teh heart due to rapid accumulation fo fluid in ther pericardial sac
    • Prevents chamber from expanding fully; limits ability of heart to pump blood
  2. Pericarditis
    • inflammation of the pericardial sac lining due to viral (fibrinous), bactrial (purulent), or blood (hemorrhagic causes)
    • Pain tends to remain substernal with some referred; worsens upon laying down
  3. Hypovolemic hyponatremia
    • Not enough salt in the ECM
    • Hypotonic contraction: ECF volumer decreases, cell swells; decreased total Na in body
    • Happen when you lose Na in excess of water; decreased Na intake; inappropriate Na loss
    • Treat with IV saline
  4. Euvolemic Hyponatremia
    • Hypotonic expansion: slight increase in ECF, cell swells; normal total Na in body
    • Happens when you gain water in excess of salt; psychogenic polydipsia; SIADH; ecstasy
    • Treatment is to restrict water intake
  5. Hypervolemic hyponatremia
    • Hypotonic expansion: increase in ECF, cell swells; increased total Na in body
    • Happens when TBW increases disproportionately to total Na; renal and heart failure
    • Treatment is to restrict water and sodium intake
  6. Hypovolemic Hypernatremia
    • Too much salt in the ECM
    • Hypertonic contraction: ECF volume decreases and cell shrinks
    • Happens when you lose water in excess of sodium; diarrhea; vomiting; diuretics; decreased thirst
    • Treat by stabilizing hemodynamics, then replacing water deficit
  7. Euvolemic Hypernatremia
    • Too much salt in the ECM
    • Hypertonic contraction: ECF volume decreases and cell shrinks
    • Happens when water is lost from ICF and ISF but not vascular; diabetes insipidus
    • Treat with hypotonic fluids to replace water deficit
  8. Hypervolemic hypernatremia
    • Too much salt in the ECM
    • Hypertonic expansion: ECF volume increases, cell shrinks
    • Happens when you gain Na in excess of water; IV-hypertonic saline, excess aldoesterone
    • Treat with diuretics and IV-dextrose
  9. Patent Foramen Ovale
    • Not an ASD because no septal tissue is missing
    • Interatrial shunting cannot occur as long as LA pressure exceeds RA pressure
    • An elevation in RA pressure can cause R to L shunting
  10. VSD
    • Most common heart defect
    • Failure of ventricular septation (mostly in membranous portion of septum-most small defects in muscular portions spontaneously close); L to R shunting
    • Late cyanosis with shunt reversal
  11. ASD
    • Failure of atrial septation; most often of secundum type involving fossa ovalis
    • may be undetected until adulthood; usually unassociated with other anomalies (septum primum type may be associated with mitral and tricuspid valve anomalies)
    • Allows L to R shunting because pressure is higher in the left side; cyanosis results if it switches to R to L
    • SOB, easily fatigued, poor growth
  12. Patent Ductus Arteriosus
    • Failure to close after birth; normally closes 10-15 hours after birth and anatomically 2-3 days
    • Machine like murmur
    • Cyanosis in toes, but not fingers (L-R shunt because of pressure))
    • Indomethacin may induce closure
  13. Tetralogy of Fallot
    • Most common cyanotic CHD
    • VSD, pulm stenosis, overriding aorta (dextraposition of aorta), hypertrophy of RV
    • Cyanotic
    • Fail to thrive
  14. Pulmonary stenosis
    • Valves are abnormally small, ductus arteriosus remains open
    • Asymptomatic unless exertion
    • RV hypertrophy
  15. Coarctation of the aorta
    • Constriction of teh aorta, usually just above or below ductus arteriosus
    • Hypertension in upper extremities, hypotension in lower extremities; anastomoses develop between subclavian artery and aorta
    • Notching of ribs due to dilated intercostal arteries
  16. Aortic stenosis
    • Cusps of aortic valve fuse together
    • LV hypertrophy
  17. Transposition of the great arteries
    • failure of spiraling of conotruncal ridges (week 6)
    • RV pumps to aorta; LV pumps to pulm trunl; 2 systems working in parallel with no connections
    • To be compatible with life, must have persistent foramen ovale, VSD, or patent ductus arteriosus
    • Cyanosis
  18. Persistent truncus arteriosus
    • Failure of conotruncal ridges to fuse with one another
    • Outflow of entire heart through single vessel
    • Cyanosis
    • CHF
  19. What are 2 conditions that both reduce the excitability of a cell?
    • Hypercalcemia (shifts Na-activation curve to the right; increases threshold; requires larger depol)
    • Hyperkalemia (decreases availability of resting Na-channels)
  20. Catecholaminergic polymorphic ventricular tachycardia
    • Channelopathy
    • Decreased ability of SR to control Ca
  21. Brugada syndrome
    • Channelopathy
    • Reduced inward Na-current
  22. Short QT syndrome
    • Channelopathy
    • Increased IKR, IKS, and IK1
  23. Long QT syndrome
    • Channelopathy
    • Problems with Na-K channels
  24. Atrial Fibrillation
    • Channelopathy
    • Increased IKR, IKS, IK1
    • Impaired gap junctions
  25. Sinus Node Dysfunction
    • Channelopathy
    • Decreased If (Phase 4-time between APs)
  26. Causes of RV hypertrophy
    • Pulmonary hypertension
    • Pulmonary stenosis
  27. Causes of LV hypertrophy
    • Aortic stenosis
    • Chronic systemic hypertension
  28. Infective Endocarditis
    • Colonization or invasion of the heart valves or mural endocardium by a microbe
    • Strep viridians is most common in previously damaged or abnormal heart valves
    • S Aureus infects normal or abnormal valves (10-20%)
    • Enterococci and HACEK (Haemophilus, Actinobacillus, cardiobacterium, Eikenella, and Kingella) are all common causes
    • Prosthetic valve endocarditis is commonly caused by caogulase-negative staphylococci
  29. Complications of bacterial endocarditis
    • formation of vegetations composed to thrombotic debris and organisms
    • Acute is typically infection of previously normal heart valve by highly virulent, necrotizing, ulcerative, destructive legions causing organism
  30. Non-bacterial thrombotic endocarditis (NBTE)
    • Marantic endocarditis\
    • Precipitation of small amount of fibrin and other blood components on valve leafletss (small and sterile)
    • Majority of patients have other debilitating diseases
    • Vegetations can be colonized by microorganisms leading to IE
  31. Libman-Sacks endocarditis
    • Mitral and tricuspid valvulitis with small, sterile vegetations
    • Occasionally encountered with SLE
    • Lesions are small single or multiple, sterile, pink vegetations taht often have a warty appearance
    • Can be located on underside of AV valves, valvular endocardium, chords, ro mural endocardium of atria and ventricles
  32. Idiopathic vavlular diseases
    Aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency
    • Aortic stenosis: calcification of anatomically normal and congenitally bicuspid aortic valves
    • Aortic insufficiency: dilation of the ascending aorta, suually related to hypertension and aging
    • Mitral stenosis: rheumatic heart disease
    • Mitral insufficiency: myxomatous degeneration
  33. Rheumatic heart disease
    • Acute rheumatic fever is an inflamm disease that follows pharyngeal infection with group A strep (normall children); AI response to strep Ags (Strep0 and DNAase B) results in cross reaction to tissue Ags
    • Valve leaflets become deformed by chronic inflammation, fibrosis, and vascular proliferation
    • Particularly mitral stenosis; RHD is virtually the only cause of this
  34. Jones diagnostic criteris for RF
    • based upon preceding group A strep infection, plus 2 of the following:
    • Major (migratory polyarthritis, pancarditis, subcutaneous nodules, erythema marginatum, Sydenham's chorea)
    • Minor (fever, arthralgi, increase in acute phase reactants)
  35. Aortic Insufficiency
    • Decrescendo; louder on expiration
    • Murmur=diastolic
    • Increased aortic pulse pressure
    • LV hypertrophy, greater SV
  36. Aortic stenosis
    • crescendo-decrescendo; louder on expiration
    • murmur=systolic
    • decreased aortic pulse pressure; peak LV systolic pressure greater than aortic systolic pressure; paradoxial splitting of S2
    • LV hypertrophy
  37. Mitral insufficiency
    • holosytolic; louder on expiration
    • Murmur=systolic
    • LV hypertrophy
  38. Mitral stenosis
    • Decrescendo-crescendo; louder on expiration
    • Murmur=diastolic
    • increased LA presure; increased pulmonary venous pressure
    • Pulmonary edema; reduced O2 levels in lungs; pulmonary arteriolar constriction; RV hypertrophy
  39. Pulmonic insufficiency
    • Decrescendo; louder on inspiration
    • diastolic
    • increased pulse pressure in pulmonary artery
    • RV hypertrophy; greater SV
  40. Pulmonic stenosis
    • Crescendo-decrescendo; louder on inspiration
    • Systolic
    • decreased pulse pressure in pulmonary artery; peak RV systolic pressure is greater than systolic pressure in pulmonary artery; wide splitting of S2
    • RV hypertrophy
  41. Tricuspid insufficiency
    • Holosystolic; louder on inspiration
    • Systolic
    • RV hypertrophy
  42. Tricuspid stenosis
    • decrescendo-crescendo; louder on inspiration
    • diastolic
    • increased RA pressure; increased systemic vein pressure; increased cap pressure
    • Systemic organ edema; reduced O2 levels in systemic organs
  43. Renal parenchymal damage and hypertension
    Renal disease-->nephron damage-->impaired excretion of sodium and water-->increased blood volume-->increased venous pressure and return-->increased preload-->increased SV-->increased CO-->increased MAP
  44. Renovascular disease and hypertension
    Atherosclerotic plaques in renal arteries-->impaired renal blood flow-->increased renin secretion-->Ang II leads to vasoconstriction-->increased TPR-->increased MAP

    Also, Ang II-->aldosterone-->increased renal sodium reabsorption-->increased blood volume-->increased VR-->increased CO-->increased MAP
  45. Pheochromocytoma and hypertension
    • Catecholamine secreting tumor-->increased NE and epi-->arteriolar constriction-->increased TPR-->increased MAP
    • EPI and NE also-->venous constriction-->increased VR-->increased SV-->increased CO-->increased MAP
    • Epi and NE also-->increase HR-->increase CO-->increase MAP
  46. Endothelial cell dysfunction and hypertension
    endothelial cell damage-->decreased NO-->increased vasoconstriction-->increased MAP

    Also ET-1-->increased and sustained vasoconstriction-->increased MAP
  47. Polyarteritis nodosa
    • Vasculitis
    • Acute necrotizing vasculitis of medium-sized muscular arteries
    • Fibrinoid necrosis, mixed inflamm cells, thrombosis, infarction of organ
    • Presence of P-ANCA
    • RX: steroids, anti-inflamms, or immunosuppressives
  48. Hypersensitivity angiitis
    • Vasculitis
    • group of inflammatory lesions affecting small vessels that are thought to be in response to foreign substances
    • Localized (w/in skin--includes leukocytoclastic vasculitis, cutaneous vasculitis, and palpable purpura--fibrinoid necrosis, acute inflammation, and extravasation of RBCs) or generalized (systemic hypersensitivity polyarteritis--can be associated with SLE, RA, SS, HSP, malignancy, etc.; arterioles, small arteries; P and C-ANCA, RPGN, and renal failure)
  49. Churg-Strauss syndrome
    • systemic vasculitis with prominent eosinophilia
    • Young people with asthma or allergies
    • Necrotizing vasculitis of small and medium sized vessels--granulomas, eosinophilia, and fibrinoid necrosis
    • C-ANCA and P-ANCA
  50. Giant cell arteritis
    • Focal, chronic, granulomatous inflammation fo teh temporal artery
    • Most common form of vasculitis
    • Cordlike nodule vessels with narrow lumen, granulomatous inflammation with lymphs, plasma cells, macs, eosinophils, necrosis, fragmentation of elastic lamina, and fibrosis of the media and thick intima
    • Clinically, benign, self-limiting, muscle aches, rheumatica, visual symptoms, blindness
    • Treat with steroids
  51. Wegener granulomatosis
    • Vasculitis
    • Systemic necrotizing granulomatous vasculitis of unknown etiology
    • involes lungs, kindeys, and upper resp tract
    • Parenchymal necrosis, granulomatous inflammation, small arteries and capillaries
    • Clinically, hematuria, proteinuria, sinusitis, pneumonitis, pulmonary infiltrate, and C-ANCA
  52. Takayasu arteritis
    • Vasculitis
    • Inflammation of unknown etiology--affects large arteries (aorta and branches)
    • Pulseless disease
    • Constitutional symptoms, high asymmetrical BP, cardiac symptoms, CHF, syncope, dizziness
    • Treat with steroids or surgical reconstruction
  53. Kawasaki disease
    • Vasculitis
    • acute necrotizing vasculitis of infancy and early childhood
    • Fever, rash, conjunctival and oral lesions; lymphadenitis
    • Affects coronary arteries; can lead to aneurysms and death
    • May be associated with parvovirus B19
  54. Thromboangiitis obliterans/Beurger disease
    • Vasculitis
    • Occlusive inflamm disease of medium and small arteries in distal arms and legs
    • Cell-mediated immunity, collagen types II and III, acute inflammation, thrombosis, infarcts, gangrene, amputations
    • Intermittent caludication, painful ulcers, gangrene
  55. Atherosclerosis
    • Risk: age, gender, hyperlipidemia, hypertension, diabetes, CRP (same as for ischemic heart disease)
    • Endothelial injury-->adhesion of platelets-->release PDGF-->smooth muscle migrationa nd proliferation
    • Foam cells come from macs and smooth muscle cells-->HDL tries to help clear cholesterol from these accumulations
    • Smooth muscle cells migrate to intima, proliferate, produce ECM including collagen and proteoglycans
    • Atheroma formation leads to aneurysm and rupture, occlusion by thrombosis (dissolution, propagation, organization, canalization, or embolization), or critical stenosis
    • Treat with throbolytic drugs, angioplasty or stents, bypass grafts; timing of intervention is essential (<12 hours)

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