Cardiology 5

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  1. Giant Cell Arteritis AKA:
    temporal arteritis (if extracranial branches of carotid involved)
  2. Giant Cell Arteritis: clinical findings:
    Systemic panarteritis affecting med- lg vessels in pts >50
  3. Giant Cell Arteritis: 50% of pts have:
    polymyalgia rheumatica
  4. HA, scalp tenderness, visual sx, jaw claudication/ throat pain =
    Giant Cell Arteritis
  5. Sequela of Giant Cell Arteritis:
    Blindness due to opthalmic artery occlusion
  6. Giant Cell Arteritis labs
    High ESR, CRP & Interleukin-6 ; mild norm/norm anemia w/ thrombocytosis; temporal art bx is diagnostic
  7. Giant Cell Arteritis Tx
    prevention of blindness, Prednisone 60 mg ASAP & cont for 1-2 mos before taper dosage
  8. Giant Cell Arteritis pts: higher risk of:
    Thoracic aortic aneurysms are 17X more frequent
  9. Paroxysmal digital ischemia from exagd response of digital arterioles to cold or emotional stress (fingers, toes, ears & nose) =
    Raynaud Phenomenon
  10. Raynaud prevalence
    Primarily affects young women
  11. Raynaud: Excessive vasoconstriction =
  12. Raynaud: Subsequent vasodilation =
    cyanosis then rubor (white to blue to red)
  13. Raynaud Tx
    Lifestyle changes (gloves), CCB/ nitrates for chronic vasodilation; tx underlying condition
  14. Raynaud can be:
    primary or secondary to other disease states (scleroderma/SLE)
  15. Single largest killer of US men & women
  16. CHD causes what % of US deaths?
    1 in 5
  17. Pts with CHF: prognosis
    70% women & 80% of men under 65 will die within 8 years
  18. CHF effect on risk of sudden heart failure death:
    increases risk x8
  19. lifetime risk devt of A-fib
    1 in 4
  20. Inferior MI: EKG correlation
    (II, III, aVF); RCA; left circumflex if left dominant
  21. Anterior MI: EKG correlation
    (V2-V5); LAD
  22. Lateral MI: EKG correlation
    (I, aVL, V5-V6); Left circumflex
  23. Inferolateral MI: EKG correlation
    (II, III, aVF, I, aVL); Large RCA, or Left dominant Left circumflex
  24. Anterolateral MI: EKG correlation
    (V4-V6, I, aVL); Left circumflex
  25. Most common causes of heart failure:
    Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy (diastolic non-compliant CHF more common in hypertension than Systolic (end stage hypertensive dz))
  26. Structural causes of heart dz
    myocardial dz; pericardial dz
  27. Types of myocardial dz
    Cardiomyopathy; myocarditis
  28. 3 functional categories of cardiomyopathy
    dilated; hypertrophic; restrictive
  29. 3 types of myocarditis
    infectious; toxic; idiopathic
  30. 3 types of pericardial dz
    Pericarditis; Pericardial effusion / tamponade; Pericardial constriction
  31. ACC/AHA CHF Guidelines: Stage A
    At risk without known disease
  32. ACC/AHA CHF Guidelines: Stage B
    Heart disease-asymptomatic
  33. ACC/AHA CHF Guidelines: Stage C
    Prior or current symptoms
  34. ACC/AHA CHF Guidelines: Stage D
    Advanced or refractory
  35. CHF risk factors
    Age; Hypertension; Tobacco abuse; Diabetes mellitus; Obesity; ETOH/Substance abuse
  36. CHF precipitators
    Coronary artery dz/MI; Valvular or congenital heart dz; Hypertension….diastolic dysfn; ETOH/substance abuse; Viral Infxns; PG; Idiopathic
  37. MI pathophysiology (4 steps)
    1 plaque rupture; 2 plt activation aggregation; 3 fibrin generation; 4 thrombus formation
  38. 2 pathways for ischemic heart dz progression
    Progressive intraluminal narrowing; Sudden disruption/fissuring of plaques
  39. Progressive intraluminal narrowing tend to:
    to produce collateral blood supply & more likely to cause worsening stable/unstable angina (>75%)
  40. Sudden disruption/fissuring of plaques likely to:
    to rupture, causing ACS (Acute Coronary Syndrome) or Acute MI (25-75%)
  41. Tobacco: CAD risks
    2x risk for 1/2 to 1 pack/day; 3x risk for > 1 pack/day; risk declines 50% after one year of tobacco cessation
  42. Most common causes of heart failure:
    Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy
  43. Which type of non-compliant CHF is more common in HTN?
    Diastolic more than Systolic (end stage hypertensive dz)
  44. What precipitates conduction system problems?
    Coronary artery dz/MI (ischemia induced); congenital; anything that causes CHF
  45. CAD signs/symptoms
    Chest pain/pressure/tightness; Jaw/ neck/ throat/scapular/ arm pain; SOB/ Dyspnea on exertion; N&V; Diaphoresis; Fatigue
  46. Deoxygenated blood draining from the heart itself enters the right atrium via:
    the coronary sinus & thebesian veins
  47. Second most common cause of sudden death in young adults
    Anomalous coronary arteries (4-15% of young people with sudden cardiac death); 1-2% of population
  48. Which valves do/do not have chordae/papillary mx?
    AV valves do; semilunar valves do not
  49. period of ventricular contraction
  50. period of ventricular relaxation
  51. the load that stretches the cardiac muscle prior to contraction
  52. the resistance against which the left ventricle must contract
  53. ability of cardiac muscle to shorten, when given a load
    myocardial contractility
  54. myocardial contractility is increased by:
    sympathetic stimulation/action
  55. myocardial contractility is decreased by:
    myocardial injury
  56. afterload comprises:
    blood volume/viscosity; resistance in aorta & other peripheral vessels
  57. Preload is increased by:
    inspiration or increasing venous return to right heart)
  58. Amount of blood remaining after ejection:
    end systolic volume
  59. In diastole, _____% of ventricular filling occurs before atrial contraction
  60. SV=
    EDV (end diastolic volume) – ESV (end systolic volume)
  61. CO =
    HR x SV (normal about 5 L/min)
  62. Adult normal cardiac blood volumes:
    SV=70ml, EDV=135ml, ESV=65ml, CO=5L total blood
  63. volume of blood ejected from each ventricle during one minute
    Cardiac output
  64. volume of blood ejected with each heartbeat
    Stroke volume
  65. Starling’s Law:
    SV increases as the EDV increases
  66. Ejection Fraction formula:
    EF% = SV/EDV
  67. A quantitative measure of contractility
    Ejection Fraction
  68. Normal EF
    67% (at DUMC: >55%)
  69. Annulus:
    fibrous ring surrounding each of the 4 cardiac valves; fn: to provide structural support to the heart
  70. narrowing or obstruction to forward flow while valve is open
  71. backward leakage during time when valve is closed
    Regurgitation / Insufficiency
  72. S1 = _____ valve closing
    Mitral (Systole)
  73. S2 = _____ valve closing
    Aortic valve closing (diastole)
  74. S3 may indicate:
    CHF (sounds like: Ken-Tuc-Key)
  75. S4 may indicate:
    HTN or CAD (sounds like: Tenn-es-see)
  76. Which heart sound is always pathological?
  77. Left & right coronary arteries arise from what part of the aortic root?
    Sinuses of Valsalva
  78. Branches off the left main coronary artery
    LAD; Left circumflex
  79. Right Dominant: Septum supplied by:
    Distal branches from RCA (supply the septum 70%)
  80. Left Dominant: Septum supplied by:
    Distal branches from LCx (supply the septum 20%)
  81. SA Node is supplied by:
    RCA 60% of the time & by LCX 40% of the time
  82. AV node supplied by:
    dominant artery (RCA or LCx)
  83. small vascular channels that interconnect the normal coronary arteries
    Collateral Vessels
  84. Function of collateral vessels in normal myocardium
    Nonfunctional because no pressure gradient is present
  85. S/S of conduction problems
    palpitations; dizziness; presyncope/ syncope
  86. Myocardial dz categories
    Cardiomyopathy; Myocarditis
  87. MI Pathophysiology steps
    1. Plaque rupture; 2. Plt activation/aggregation; 3. Fibrin generation; 4. Thrombus formation
  88. Cardiac ischemia risk factors
    Age; Gender ? FH; Sedentary Lifestyle; Tobacco; HTN; DM/insulin resistance; Hyperlipidemia
  89. DM increases risk/incidence of:
    Diffuse dz; small vessel dz; CHF & death rates post MI; death or MI post CABG & PCI
  90. Recommended for sedentary lifestyle
    Devoted exercise 30 min/day, 5 d/wk; initially under med supervision
  91. Causes of coronary ischemia leading to chest pain
    Atherosclerosis; Vasospastic disorders; stenosis or HCM; Coronary thrombosis/ embolization; Acute aortic dissection
  92. Causes of noncardiac CP
    Pericarditis; myocarditis; MVP; chostocondritis; C- or T-spine dz/thoracic outlet; GI/gall bladder; PE; pneumonia; pneumothorax
  93. Before a dx of CAD, diabetics risk of MI =
    risk of non-diabetic with prior MI
  94. Almost all MI’s result from:
    coronary atherosclerosis & superimposed coronary thrombosis
  95. Antithrombotics include:
    Fibrinolytics, anticoagulants, antiplatelet drugs
  96. Use of fibrinolytics
    STEMI only
  97. Anticoagulants: acute & chronic
    Acute: UFH, LMWH, DTIs; chronic: warfarin
  98. UFH vs LMWH re: inactivating thrombin
    UFH > LMWH
  99. Beta blockers AEs
    Hypotension; Decrease HR, heart block; May worsen HF symptoms; CNS (fatigue, malaise, depression); Bronchospasm (use ß1 selective agents)
  100. Irreversibly binds to ADP receptor on platelets; Full reversal requires removal of plts
  101. Fibrinolytics: absolute CI
    Prior hemorrhagic CVA; any cerebrovascular events < 1 year; active internal bleeding; Known intracranial neoplasm; suspected aortic dissection
  102. Fibrinolytics: relative CI
    BP > 180/110; Use of anticoags w/ INR > 2; Noncompressible vascular punctures; Prolonged CPR (> 10 minutes); PG or Menstruation; Trauma < 2-4 weeks prior; Major surgery < 3 weeks prior
  103. UFH: main risk =
  104. UFH: used for:
    Both STEMI and NSTEMI
  105. ATPIII/heparin has greatest effect on:
    Factor II (thrombin)
  106. Can use to monitor LMWH
    Factor Xa
  107. UFH/LMWH AEs
    Bleeding, HIT, osteoporosis
  108. UFH vs LMWH: which inhibited by PF4 (thus limited effect vs ACS)?
  109. UFH vs LMWH: req dose adjustment for renal:
  110. Catheter thrombosis during PCI
  111. Bivalirudin used in STEMI in place of:
    UFH / LMWH
  112. Add warfarin for:
    pts w/ USA or NSTEMI w/anticoag indication (to maintain INR 2.0-3.0)
  113. Clopidogrel dosing
    usu loading & maint doses
  114. Clopidogrel AEs
    Bleeding; Thrombocytopenia; Leukopenia; TTP
  115. Clopidogrel: who gets:
    All STEMI/NSTEMI (2-4 wks to 1 yr)
  116. GP IIb/IIIa inhibs: who gets:
    STEMI pts going for PCI
  117. GP IIb/IIIa inhibs: not recommended if:
    PCI is not planned
  118. Fredrickson phenotype I
    Serum conc of chylomicrons elevated; trigs are elevated to >99th percentile
  119. Fredrickson phenotype IIa
    Serum LDL chol elevated; the total chol is >90th percentile. Triglyceride and/or apolipoprotein B may also be ≥ 90th percentile
  120. Fredrickson phenotype IIb
    Serum LDL & VLDL elevated; TC and/or trigs may be ≥ 90th percentile and apolipoprotein B ≥ 90th percentile
  121. Increased Apo A-I prodn has what effect in animals?
    Anti-atherogenic (reduced atherosclerosis progression; regression of existing dz)
  122. Rationales for screening:
    High chol & CHD are common; rel btw TC & LDL & risk of CHD & coronary mortality; lowering LDL in mod/hi risk pt => few CV events; dyslipidemia (not LDL) common in early onset CHD; screen tests commonly avail
  123. Mechanisms by which oxidized LDL causes atherogenesis
    Endothelial damage; changes in vasc tone; Monocyte/ macrophage recruitment; increased LDL uptake by macrophages (foam cell formation); Induction of GF; Increased plt aggregation; Formation of auto-Abs to oxidized LDL
  124. HDL antiatherogenic properties include:
    Reverse chol transport; antioxidation; protection vs thrombosis; maintenance of endothelial fn; maintenance of low blood viscosity thru permissive action on red cell deformability
  125. Process whereby excess cholesterol in cells and in atherosclerotic plaques is removed
    Reverse cholesterol transport
  126. Mgmt of Low HDL-C
    Wt reduction & inc physical activity; LDL-C is primary target of tx; Non-HDL-C is secondary target of tx (if trigs ³200 mg/dL); consider nicotinic acid or fibrates
  127. Fredrickson phenotype III
    Serum VLDL remnants & chylomicrons elevated; TC & trigs >90th percentile
  128. Fredrickson phenotype IV
    Serum VLDL elevated; TC may be >90th percentile & may also see trigs >90th percentile or low HDL
  129. Fredrickson phenotype V
    Elevated serum chylomicrons & VLDL; triglycerides >99th percentile
  130. Hypertriglyceridemia & CHD: Assoc disorders
    Accumul of chylomicron remnants & VLDL remnants; generation of small, dense LDL-C; assoc w/ low HDL-C; increased coagulability (inc plasminogen activator inhibitor (PAI-1); inc factor VIIc; activation of prothrombin to thrombin
  131. ATPIII chol screening for pt w/o CHD:
    LDL < 160 & 0-01 risk factor; or LDL <130 & >1 risk factor: rescreen in 5 yrs
  132. ATPIII risk determination Step 1
    1. Fasting lipid level
  133. ATPIII risk determination Step 2
    2. determine CHD equivalents
  134. ATPIII risk determination Step 3
    3. Major CHD factors other than LDL
  135. ATPIII risk determination Step 4
    4. If >1 non-LDL CHD factor (in pt w/o CHD or equivalent): use modified Framingham criteria
  136. ATPIII risk determination Step 5
    5. Detn risk category to establish LDL goal, when to initiate tx lifestyle changes, & when to consider drug tx
  137. ATP III criteria: Metabolic syndrome
    3 of 5: abd obesity (waist men >40 in & women >35 in; trigs ≥150 or tx for hi trigs; HDL <40 (M) & <50 (F) or tx for low HDL; BP ≥130/85 or tx for hi BP; FPG ≥100 or tx
  138. IDF metab syndrome defn
    Inc waist girth plus any 2: 1. Trigs >150 or tx; HDL <40 (M) & <50 (F) or tx; SBP >130, DBP >85, or HTN tx; FPG >100 or prior dx type 2 DM
  139. Summary: CV risk factors in DM pts
    Type I: hi trigs & HTN; Type 2: dyslipid, HTN, ins resistance, obesity, FH atherosclerosis; SMK NOT risk factor for I or 2
  140. 3 levels of prevention
    Primary: remove risk factors; secondary: early detection & tx; tertiary: reduce complications
  141. (A) fat contribute to CV dz; (B) fat may be cardioprotective
    A. Saturated & trans fat; B. monounsaturated & polyunsaturated fat
  142. Lipids carried by LPs for:
    energy utilization; lipid deposition; steroid hormone prodn; bile acid formation
  143. Lipoprotein consists of:
    esterified & unesterified chol, trigs, phospholipids, & protein
  144. Protein components of the lipoprotein =
    apolipoproteins or apoproteins.
  145. Apolipoproteins =
    cofactors for enzymes and ligands for receptors
  146. Defects in apolipoprotein metabolism lead to:
    abnormalities in lipid handling
  147. Very large particles that carry dietary lipid =
  148. Chylomicrons are assoc with:
    Apolipoproteins (including A-I, A-II, A-IV, B-48, C-I, C-II, C-III, and E)
  149. LDL carries:
    cholesterol esters
  150. LDL assoc with:
    apolipoprotein B-100.
  151. HDL carries:
    cholesterol esters
  152. HDL is associated with:
    apolipoproteins A-I, A-II, C-I, C-II, C-III, D, and E
  153. One mechm by which LDL promotes atherosclerosis
    oxidative modification
  154. VLDL carries:
    endogenous trigs (& to a lesser degree chol)
  155. Major apolipoproteins assoc with VLDL:
    B-100, C-I, C-II, C-III, and E
  156. Intermediate density lipoprotein (IDL) carries:
    chol esters & triglycerides
  157. IDLs are assoc with:
    apolipoproteins B-100, C-III, and E
  158. Fn of CETP
    transfers oxidized lipids from LDL to HDL
  159. The oxidized lipids in HDL are reduced by:
    HDL apolipoproteins
  160. The liver wrt reduced lipids
    Liver takes up reduced lipids from HDL more rapidly than from LDL
  161. Hypoalphalipoproteinemia =
    Low serum HDL; assoc w/ increased risk of overt CHD
  162. Framingham: MI risk
    MI risk increases by 25 percent for every 5 mg/dL decrement in HDL below median values
  163. Low HDL: risk factors
    SMK; sedentary;obese; insulin resistant/ DM; hypertriglyceridemia; chronic inflammatory dz
  164. Cardioprotective HDL =
    >60 mg/dL (>75 assoc w/ longevity syndrome)
  165. Strategies for HDL metab as tx target
    Increase apo A-I prodn; promote reverse chol transport; delay HDL catabolism
  166. Effect of ETOH (wine, beer) on HDL-C
  167. Theoretical effect of CTEP inhibitors
    Lower LDL; increase HDL
  168. Familial Dyslipidemias
    Fredrickson phenotypes III, IV, & V
  169. high levels of trigs may directly promote:
  170. high levels of trigs assoc w/ increases in:
    fibrinogen, clotting factors VII & X, & blood viscosity
  171. ATP III: normal trigs
  172. ATP III: borderline high trigs
  173. ATP III: high (trigs)
  174. ATP III: very high (trigs)
    =/> 500
  175. Primary concern w/ ATPIII borderline high:
    Metabolic syndrome
  176. Primary concern w/ ATPIII High category
  177. Primary concern w/ ATPIII Very High category
  178. ATP III recommends Chol screening how often?
    at least every 5 yrs for pts 20 or older
  179. Pts w/ borderline-high chol & <2 risk factors should be rescreened:
    within 1-2 yrs
  180. Framingham risk factors
    Age, TC, HDL, BP, & SMK
  181. Framingham focuses on which lipid:
    TC (but LDL is primary tx target)
  182. Framingham 10-yr CHD risk categories
    r >20%, 10-20%, and <10%
  183. Low HDL-C is an Independent Predictor of CHD Risk even when:
    LDL-C is Low
  184. Metab syndrome/girth increases genetic susceptibility to:
    dyslipidemia, hypertension, type 2 DM
  185. Goals of Diagnosing HTN
    Detect & stage HTN severity; detect TOD; assessing overall CV risk; detect secondary causes of HTN
  186. HTN stats
    1 in 3 in US = HTN; 66 mil in US 20 yo & older; 95% are essential HTN; 2005 in US, direct & indirect cost of HTN = $59.7 Billion
  187. HTN pt awareness stats
    63% aware of the dx; only 45% receiving tx; 34% under ctrl using a threshold criterion of 140/90
  188. Factors of essential HTN:
    Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse
  189. Primary HTN: other factors:
    Variable plasma renin activity; variable symp n.s. response & catecholamines; insulin resistance & DM; inadequate dietary K+ & Ca+ ; resistant vessels
  190. Renal artery stenosis in HTN: MOA
    Excessive renin release in response to decrease in renal blood flow & perfusion pressure
  191. Renal vascular HTN: 2 pathologic processes (resulting in stenosis)
    85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition)
  192. Fibromuscular dysplasia (FMD) is characterized by:
    fibrous thickening of the intima, media, or adventitia of the renal artery
  193. Congenital abnormality which results in narrowing of the aorta, usually in the ascending region, which increase PVR due to the stenosis
    Coarctation of the Aorta
  194. Coarctation of the Aorta: incidence
    Rare (1:10,000) & usually accompanies other abnormalities such as bicuspid aortic valve or Turner Syndrome
  195. Hyperaldosteronism: most common etiologies:
    unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia
  196. If Pheochromocytoma undiagnosed:
    Outpouring of catecholamines during unrelated surgical/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80%
  197. Obstructive sleep apnea & HTN
    HTN = response to chronic, intermittent hypoxia during nocturnal apneic episodes
  198. Cushing Syndrome: tx for HTN
    HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
  199. HTN & chronic kidney dz: epidemiology
    HTN is second most common cause of chronic kidney disease (> 25% of cases)
  200. Most easily recognized treatable risk factor for stroke, MI, CHF, peripheral vascular dz, aortic dissection, atrial fibrillation & end-stage kidney disease
  201. HTN in younger pts (< 50 yrs): Hemodynamic fault =
    vasoconstriction at the level of the resistance arterioles
  202. Isolated systolic HTN: associated risks
    BP of 160/60 (pulse pressure of 100 mmHg) carries 2x the risk of fatal coronary heart dz as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP)
  203. Diastolic BP age pattern
    Peaks in the early 50’s, then declines for men and women (Systolic BP continues to rise for both throughout life)
  204. Resistant Hypertension
    Defined as persistence of BP > 140/90 despite tx with full doses of 3 or more different classes of meds in rational combination (& including a diuretic); important to know pt is compliant
  205. 4 Categories of Resistant HTN
    Pseudoresistance; Inadequate medical regimen; Nonadherence or ingestion of pressor substances; secondary HTN
  206. Pseudoresistance:
    Usually caused by white coat effect superimposed on chronic HTN that is well controlled with meds outside the office
  207. Resistant HTN: Inadequate medical regimen
    Absence of appropriate diuretic; Renal fn impairment which affects drug clearance; monotherapy or inadequate dosing of meds
  208. Resistant HTN: Nonadherence or ingestion of pressor substances
    a. Medication nonadherence; b. Lifestyle modification noncompliance; obesity, high salt diet, excessive alcohol intake; c. Habitual use of tobacco, cocaine, meth, phenylephrine or NSAIDS (cause renal Na+ retention)
  209. Resistant HTN: Secondary HTN:
    If you’ve exhausted the first 3 categories, time to look for secondary cause of HTN
  210. Most commonly overlooked secondary causes of Resistant HTN:
    Chronic kidney dz & primary aldosteronism
  211. Hypertensive Urgency
    Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure
  212. Hypertensive Emergency
    Acute, severe elevation in BP; evidence of rapidly progressive TOD (eg, MI, pulmonary edema or renal failure); requires immediate, gradual reduction of BP (NOT to the normal range); always look for secondary causes
  213. Hypertensive Emergency: tx
    Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
  214. Malignant Hypertension:
    Type of Hypertensive Emergency; usually accompanied by other end organ damage
  215. Malignant Hypertension is most common in:
    Young adults, prior renal dz, AA males, PG, or collagen vascular dz
  216. Dz w/ Compelling Indications for tight HTN ctrl
    CHF; High Coronary Dz Risk; Chronic Kidney Dz; DM; Post-MI; Recurrent Stroke Prevention
  217. Beta blocker : MOA
    Blockade of parts of the symp NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
  218. Fn of Angiotensin II
    Normally stims release of Na+-retaining hormone aldosterone (adrenal corticol cells); normally amplifies vasoconstriction (systemic and renal)
  219. ACEI AEs
    Cough; Angioedema; Hyperkalemia; Rash; CI in PG; use cautiously in renal artery stenosis (RAS)
  220. ARBs: MOA
    Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
  221. ARBs AEs
    Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
  222. Diuretics: MOA
    Act to block Na+ (and K+) from being absorbed, thus increasing urine Na+. Water follows Na+ out of the body. Blood volume is less (lowering BP)
  223. Diuretics: AEs
    Hypokalemia; Volume depletion; Gout; increased insulin resistance; hyponatremia; increased chol levels
  224. CCBs: MOA
    Blocks vascular smooth mx contractility (resulting in vasodilatation & afterload reduction). Also result in coronary vasodilatation & are used in coronary artery spasm
  225. CCBs: Dihydropyridines (DHPs) vs nonDHPs
    DHPs more vascular selective; nonDHPs are more cardio-selective with more inhibitory effects on the SA/AV node
  226. BP =
    CO X PVR
  227. Essential HTN =
    established primary HTN
  228. Hallmark of essential HTN =
    elevated peripheral vascular resistance
  229. Variations in BP determined by:
    variations in ECF volume, heart contractility, & vascular tone
  230. Def of HTN = repeated readings of:
    SBP over 140 &/or DBP over 90
  231. Evidence supports tx of high risk pts at lower threshold of:
    of 130/80 mmHg.
  232. HTN: High risk groups include:
    DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG
  233. Factors of essential HTN affect:
    ECF volume, heart contractility, or vascular tone
  234. HTN contributes to what % of M/F AA deaths?
    30% M & 20% F
  235. Most common secondary cause of HTN
    Chronic renal dz (proteinuria, high creat)
  236. ?% of pts w/ chronic renal dz have HTN
Card Set:
Cardiology 5
2011-07-18 20:23:53
DPAP2012 Cardiology

Cardiology flashcards made by previous students
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