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  1. hyperpigmentation of LEs
    chronic venous insufficiency
  2. cell death and necrosis occur in
    venous stasis ulcers
  3. Risk factors for DVT
    • immobility
    • age
    • L heart failure
    • venous stasis
    • trauma
    • IV meds
    • Vein wall damage
    • Pregnancy 
    • Oral contraceptives
    • Malignancy 
    • Genetic coagulopathies
    • Hypercoagulation
  4. Superior Vena Cava Syndrome (SVCS)
    progressive occlusion of SVC leads to venous distention in UEs and head
  5. localized dilation or outpouching of vessel wall or cardiac chamer
  6. True aneurysms
    involve all 3 layers of arterial wall; weakening of vessel wall
  7. embolism
    Obstruction of vessel by an embolus or a bolus of matter that is circulation in bloodstream
  8. Thrombus
    blood clot that remains attached to vessel wall
  9. PAD
    atherosclerotic disease that decreases perfusion to the limbs, especial LEs
  10. Thromboangiitis obliterans is a type of PAD that is also known as
    Buerger disease

    young men who are heavy cigarette smokers
  11. Paynaud phenomenon and disease
    characterized by attacks of vasospasm in small arteries and arteriols of fingers and (less commonly) the toes
  12. hypertension
    • 2 or more diastolic BPs on 2 or more consecutive visits of 90 or more
    • average of 2 or more visits is >140 systolic
  13. Primary HTN is also known as
    idiopathic HTN
  14. Primary HTN cause
    none specific
  15. HTN results from
    combination of genetic and environmental factors mediated by host of neurohumoral effects likely responsible for development

    affects 90-95% of HTN cases
  16. Secondary HTN
    caused by any system disease that increases peripheral resistance in BV or cardiac output
  17. Secondary HTN renal disorders
    • renovascular disease
    • renin producing tumors
    • renal failure
  18. Endocrine disorders secondary HTN
    • acromegaly
    • thyroid disturbances
    • adrenal disorders
  19. Vascular disease secondary HTN
  20. Neurologic disorders secondary HTN
    leasions requiring higher systolic BP to maintain perfusion
  21. Complicated HTN
    damages walls of BV
  22. possible renal complications of complicated HTN
    • parenchymal damage
    • renal arteriosclerosis
    • renal insufficiency and failure
  23. CV complications of complicated HTN
    • LV hypertrophy
    • angina
    • CHR
    • CAD
    • MI
    • sudden death
  24. cerobravasuclar complications in complicated HTN
    • TIA
    • CVA
    • Cerebral thrombosis
    • Aneurysm
    • Hemorrhage
  25. malignant HTN
    rapid progression in which diastolic is >140
  26. orthostatic or postural hypotension
    decrease in both systolic and diastolic arterial BP on standing from a reclining position

    may be r/t anatomic variation with aging, antihypertensive and antidepressent therapy, fluid volume depletion, venous pooling
  27. abnormal thickening or hardening of vessel walls
  28. form of arteriosclerosis. thickening caused by hardening of soft deposits of intraarterial fat and fibrin that reduce lumen size. inflammatory disease
  29. begins with injury to endothelial cells of arteries
  30. Atherosclerosis development
    • Endotheial cell injury:
    • decreased antithrombolytics and vasodilators
    • growth factors stimulate smooth muscle proliferation
    • macrophages recruited to site and oxidize LDL with enzymes to produce foam cells
    •             foam cells form fatty streak continued               inflammation
    •                    Fibrous plaque overlays foam cells

    HTN develops if systemic vascular resistance elevates
  31. CAD
    diminishes bloodflow to myocardium

    persistent ischemia or complete occlusion= infarction or death of deprived mycardial cells/tissue


    Adipokines: hormones released from adipose cells

    Adiponectin: antiatherogenic hormone

    Decreased in obesity

    Anti-inflammatory effect, protects vascular endothelium

    Decrease of hormone increases CV risk
  32. Myocardial ischemia
    • atherosclerois is most common cause
    • Angina
    • Stable
    • Temporary ishcemia
    • exertion, vessels cant dilate in response to dmand
    • NTG and rest effective
    • Normal EKG, negative enzyme levels
  33. MI
    • unstable
    • advanced, reversible occurs at rest, NTG inffective

    normal transient, ST depression and T wave inversion, negative enzymes
  34. what happens in mi
    coronayr arteries cannot compensate for lack of o2: pronounced Q waves, ST elevation later, CPK-MB, LDH, SGOT, Troponins i and T indicate severity
  35. Subendocardial mi
    usually non-ST segment elevation (non-STEMI)

    ST depression, T wave inversion w/o Q waves
  36. Transmural MI
    marked elevation in ST segments on EKG (STEMI)
  37. __________ most common complication of 90% of MIs
  38. Pericarditis
    idiopathic, common with infections, connective tissue diesases or radiation therapy
  39. pericardial effusion
    • accumulation of fluid in pericardial cavity 
    • possible w/ all forms of pericarditis
  40. Cardiac tamponade
    pressure from fluid causes cardiac compression 

    first structures to be affected are RA and RV where diastolic pressures are normally lowest
  41. cardiomyopathies
    diverse group of diseases that affect myocardium, result of ischemic disorders, HTN, valvular dysfunction
  42. Dilated cardiomyopathy
    • assocated with alcoholism, pregnancy, infection 
    • LV chamber volume and size increases
    • mitral valve incompetence
  43. hypertrophic cardiomyopathy
    • hypertrophy of LV and IV septum
    • chamber volume normal or decreased
    • mitral valve incompetent
  44. REstrictive cardiomyopathy
    myocardium inflitrated with amyloid, hemosiderin or glycogen deposits

    AV valve incompetence
  45. valvular orifice constricted or narrowed
    valvular stenosis
  46. valve leavelets or cuspid fail to close completely; blood flow continues when valve should be closed
    valvular regurgitation/insufficiency/incompetence
  47. aortic stenosis
    • rheumatic heart disease
    • congenital malformation
    • calcification causes LV failure
    • dyspnea
    • angina
  48. Mitral stenosis
    • acute rehumatic fever
    • bacterial endocarditis causes LA and RV hypertrophy
    • RV failure
    • CP
    • Orthopnea
    • Pulmonary HTN
  49. MItral regurgitation
    • rhumatic heart disease
    • mitral valvue prolapse
    • CAD causes LHF
    • pulmonary HTN 
    • dyspnea
    • RV, LV and LA hypertrophy
  50. Tricuspid regurgitaion
    pulmonary HTN causes RHF, peripheral edema, ascitis
  51. Rheumatic heart disease
    Sequel to pharyngeal infection with group A betahemolytic streptococci

    causes carditis of all 3 layers of heart wall, endocardial inflammation, vegitative growth

    Fever, lymphadenopathy, anti-streptolysi o titer (ASO)
  52. Inefective Endocarditis
    caused by staph aureus, viruses, fungi

    prior damage to valves leads to thromotic endocarditis, blood-brone microbes colonize damage valve and vegetate

    Fever, murmur, petechial lesions of skin and mucosa, bacteremia, osler's nodes
  53. Left side heart failure
    LV fails, increased pressure and volume in LA, fluid transferred from capillaries to alveoli causing pulmonary edema

    orthopnea, decreaed UO, s3 gallop, blood-tinged sputum
  54. r sided failure ( cor pulmonale)
    L failure, decreaed RV emptying, increaesd vol and prssure in RA, increased volume in distensible organs, peripheral edema and serous effusion

    GI disorders, JVD, dependent edema ascitis
  55. High-Output failure
    inability of the heart to adequately supply blood with nutrients, despite adequate blood and normal myocardial activity 


    Septicemia causes systemic vasodilation and fever

Card Set:
2014-11-17 15:40:25
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