FNPII Adult Cardiac

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  1. How is HTN diagnosed?
    SBP > 140 and DBP >90 based on the average of two or more seated BP readings on two or more office visits.
  2. Describ:

    Stage 1 HTN

    Stage 2 HTN
    Pre-HTN = SBP 120-139 / DBP 80-89

    Stage 1 HTN = SBP 140-159 / DBP 90-99

    Stage 2 HTN = SBP >=160 / DBP >= 100
  3. When would a diagnosis of secondary HTN be considered?
    New onset of DBP after the age of 60.  Consider renovascular disease.  
  4. When is HTN diagnosed?
    When EITHER SBP >=140 or DBP >=90
  5. Each increment of 20 mm Hg sytolic or 10 mm Hg diastoloic...
    Doubles the risk of cardiovascular disease in 40-70 year olds.
  6. When is secondary HTN considered?
    Young onset of HTN <30 or older onset >50.
  7. What are causes of reversable HTN?
    • Obesity, obstructive sleep apnea, renovascular disease, chronic steroid therapy, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, coartation of the aorta, thyroid disease, parathyroid disease, and excess ETOH intake.
    • Drugs: NSAIDS, Cox-2 Inhibitors, Diet pills, oral contraceptives, erythropoietin, cocaine, amphetamines, steroids, tacrolimus, cyclosporine, ephedra, licorice, smoking, chewing tobacco.  
  8. When is malignant HTN diagnosed?
    SBP>=180 / DBP >= 110 and evidence of acut target organ damage. 
  9. What is considered evidence of target organ damage in HTN?
    • Papilledema, hemorrhages, or exudates on funduscopic exam.
    • Change in mental status or neurological deficts on exam.
    • EKG consistent with myocardial ischemia or infarction.
    • Chest xray showing heart failure or aortic disection.  
    • Renal dysfunction evidenced by hematuria, proteinuria, and elevated serum creatinin. 
  10. A displaced PMI and S4 heart sound may indicate?
    Left ventricular hypertrophy.
  11. Signs of heart failure include:
    An S3 gallop, pulmonary crackles, JVD, and periferal edema.
  12. What are risk factors of CVD?
    Age, gender, postmenopausal status, diet, activity level, ETOH, caffeine use, smoking, dyslipidemia, diabetes, family history and  current meds. 
  13. What is pseudo-HTN?
    When too much calcification in the vessel wall does not allow the cuff to proper compress the vessel wall. 
  14. What is one of the earliest EKG indications of HTN?
    Left atrial enlargement.  Echo is most usefull in detecting increasing Left ventricular thickness.
  15. What is Isolated Systolic Hypertension? (ISH)
    SBP >160 with normal DBP 86 or less as a consequence of atherosclerocitic thickening of the vessels.  Effects nearly half of all adults >65 y/o.
  16. Treatment for PRE-HTN?
    • Lifestyle modification.
    • No meds unless compelling reason. 
  17. For most patients with stage 1 HTN, what is the initial treatment?
    • Lifestyle modifications
    • Thiazide type diuretic
  18. What measures represent goal BP measures for a non-diabetic and diabetic or renal patient?
    Non-diabetic < 130/90

    Diabetic / renal < 120/80
  19. What type of agent is favorable when deciding to treat HTN?
    An agent with once daily dosing with atleast 50% of its action in the last 12 hours.
  20. What treatment should be considered if BP is >20/10 mm Hg above goal pressure?
    Initiating therapy with two agents one of which is thiazide diuretic. 
  21. When should aspirin therapy be initiated?
    After goal BP is achieved, otherwise patient risks hemoragic stroke. 
  22. When should re-checks be scheduled after initiating BP therapy?
    Schedule a repeat BP check and electrolyte check 2-3 weeks. Serum Potassium and creatinine levels should be checked several times per year. 
  23. To prevent CVD, what is the desirable level of trigycerides?
    150 mg / dL.
  24. What is the desirable level of TOTAL cholesterol in the blood?
    Less than 200 mg /dL
  25. What are Triglycerides?
    Trigylcerides are the large lipid molecules formed from dietary fats.
  26. What is the typical presentation of metabolic syndrome?
    Increased BMI, elevated systolic BP, Hyper triglycerdemia, hyerglycemia, and low levels of HDL-C.  Any three of the above qualifies the patient as metabolic syndrome. 
  27. What constitutes discontinuing a statin?
    Liver enzymes 3X normal.
  28. After prescribing a statin, when should liver enzyme monitoring begin?
    Initially at 6-12 weeks, then every 6 months.
  29. Why is the pressence of diaphoresis worrisome with chest pain?
    Because it may indicate a significant drop in cardiac output during the episode of pain causing decreased perfusion to the skin.
  30. What is orthopenia?
    SOB that begins when the patient is in a supine position.
  31. Paroxysmal nocturnal dyspnea relates to what condition?
    SOB that occurs 2 to 4 hours into sleep.  Concurrent with redistribution of body fluids and a subsequent rise in left atrial pressure.  

    The person awakens suddenly with SOB, stands or sits up for 10 to 30 minutes to reset.
  32. Significantly elevated BP with no evidence of TOD...
    NOT an emergency.
  33. What does a displaced PMI and an S4 heart sound indicate?
  34. When is HTN diagnosed?
    When a the average of at least two seated BP measurements on at least two or more vistits exceeds 90 DBP or 140 SBP.
  35. What is isolated systolic HTN?
    SBP > 160 with a normal DBP.  Occurs in 1/2 of adults over 65 y/o.  Due to atherosclerotic thickening of the vessels. 
  36. When should you consider using an ACEI?
    • ACEI in the presence of:
    • Heart failure
    • MI Limits cardiac remodeling!
    • Diabetes
    • Renal insufficiency
    • NOT in Pregnancy!
  37. Describe s/s of PE?
    • Location:
    • Over Lung area

    • Charactaristics:
    • Stabbing; may be cyanotic, dsypnea, or cough with hemoptysis; sudden onset

    • Worse with inspiration
    • Better with analgesics
  38. Describe dissecting aoritc aneurysm?
    • Location: 
    • Retrosternal, upper abdom, or epigastric.  May radiate to back neck and shoulders.

    • Charactaristics:
    • Excruciating, tearing, may be accompanied by BP diffences betweeen L arm and right arm.

    • Nothing makes it worse
    • Relieved by analgesics.
  39. Describe MI?
    • Location:
    • Across chest; may radiate to jaw, neck, arms and back.

    • Charactaristics:
    • Pressure, burning, aching, tightness; may be accompanied by SOB, diaphoriesis, weakness, anxiety; nausea; sudden onset; last 1 to 2 hours.

    • Aggravated by exertion and anxiety
    • Relieved by NARCOTIC analgesics - Morphine
  40. Describe acute anxiety/
    • Location:
    • Anywhere in the chest.

    • Charactaristics:
    • Dull or stabbing pain, usually accompanyied by hyperventilation or breathlessness, sudden onset, may last less than a minute or for several days.

    • Aggravated by increased resp. rate, stress and anxiety.
    • Relieved by slowing of resp rate, stress relief. 
  41. Describe Costocondritis...
    • Location:
    • Anywhere in the chest.
    • Charactaristics:
    • Sharp, continuous or gradual; chest may be tender to the touch;  gradual or sudden onset.

    • Aggravated by: Movement, palpation
    • Relieved by: Time; analgesics or heat application
  42. Which chamber of the heart poses a risk of emolization?
    L atrium
  43. What is the primary reason to prescribe coumadin for a-fib?
    Prevent stroke
  44. What is a contraindication for Beta Blockers? 
    Asthma or COPD
  45. Calcium channel blockers....
    The largest CCB family is the dihydropyrines. Act primarilily on the arterioles.

    • Verapamil and dilitiazem are CCBs but from different families. 
    • Act on arterioles AND the heart.  Verapamil increases digoxin levels by 60%.

    Useful in treating Raynauds.
  46. When should diruetics NOT be used?
    Gout and DM
  47. Name identifiyable causes of HTN?
    • Sleep apnea
    • Drug-induced or related causes
    • Chronic kidney disease
    • Primary aldosteronism 
    • Renovascular disease
    • Chronic steroid therapy and Cushing’s syndrome
    • Pheochromocytoma - tumor of adrenal gland - results in too much epi and nor-epi
    • Coarctation of the aorta
    • Thyroid or parathyroid disease 
    •      Hyperthyroid - heart beats faster - incr BP
    •      Hypothyroid - incre stiffness vasculatur Diastolic HTN.
  48. What tests would you order for Pt with HTN?
    • Routine Tests
    • • Electrocardiogram 
    • • Urinalysis 
    • • Blood glucose, and hematocrit 
    • • Serum potassium, creatinine, or the
    • corresponding estimated GFR,     and
    • calcium Lipid profile, after
    • 9- to 12-hour fast, that includes high-density and  low-density lipoprotein cholesterol, and triglycerides 

    • Optional tests
    • • Measurement of
    • urinary albumin excretion or albumin/creatinine ratio 
    • More extensive testing for identifiable causes is not generally indicated unless BP control is not achieved
  49. Do not want to give what drug post MI?
  50. Do contraceptives raise BP?

    Does HRT Raise BP?
    Contraceptives - yes

    HRT - No
  51. Potential unfavorable effects of 
    Thiazide Diuretics
    Beta Blockers
    ACEI and ARBs
    Aldosterone and K sparing diruetics
    • Thiazide diuretics should be used cautiously in gout or a
    • history of significant hyponatremia.

    • BBs should be generally avoided in patients with asthma,
    • reactive airways disease, or second- or third-degree heart block.

    ACEIs and ARBs are contraindicated in pregnant women or those likely to become pregnant.

    • ACEIs should not be used in individuals with a history
    • of angioedema.

    Aldosterone antagonists and potassium-sparing diuretics can cause hyperkalemia.
  52. What are some rare family history related clotting disorders that  can influence PVD and ultimately create a DVT?
    • •Factor V Leiden mutation
    • •Protein C deficiency
    • •Protein S deficiency
    • •Anti thrombin III deficiency
    • •Homocycteinemia
    • •Prothrombin gene mutation
  53. PE mostly come from?
    90% PE come from DVT.
  54. What is the treatment for DVT?
    • •Referral to hospital or vascular surgeon
    • •LMWH-Dalteparin/Fragmin or enoxaparin BID
    • •Warfarin overlapped
    • •Continue warfarin 6 months to lifetime
  55. Where Superficial Throbophlebitis  aka Superficial vein thrombosis (SVT) typically found?

    What are there charactaristics?
    • •Thrombus and inflammation of the superficial veins.
    • •Greater or lesser saphenous veins

    • •Hardening of vein
    • •Redness, warmth and tenderness over vein
    • •No significant edema of extremity
    • •SVT is a clinical diagnosis
  56. What is the technical name for statins?
    HMG CoA Reductase Inhibitors (Statins)
  57. What do bile acid sequesterants do?
    Primarily decrease LDL by binding to bile acids in the intestinal tract.

    GI upset is common
  58. Examples of Fibric Acids...
    • •Gemfibrozil  600 mg BID
    • •Fenofibrate  200 mg QD
    • •Clofibrate  1000 mg BID
    • •Fenofibric  45-135 mg
  59. Cholesterol absorbtion inhibitor
    •Ezetimibe  10 mg  daily
  60. Differentiate stable Angina vs Unstable
    • Angina syptoms are worse with:
    • Patient activity, heavy meals, cold weather, and resolve with rest and nitro.

    • Unstable Angina 
    • •Inc. in frequency of CP
    • •Inc. in severity of CP
    • •Inc in duration of CP
    • •Chest Pain at rest > 20 min < 30 min
    • Not relieved by rest and nitro
    • •CP is provoked by a lower level of Pt activity

    • •CP awakens the
    • patient at night
  61. What does Levines sign look like?
    Image Upload77% having MI
  62. How long can troponin levels stay elevated after an MI?

    How do you diagnose an MI in a patient with known unstable angina?
    Post MI troponin levels maybe elevated for 2 weeks.

    33% of patients with unstable angina have elevated troponins but NORMAL CKMB.
  63. Describe the following labs in MI?
    •CBC w/diff
    •Liver/lipid panel
    •TSH/ glucose 
    • LDH ( lactase dhydrogenase)
    • •Found in heart muscle, RBC and kidney
    • •With acute MI, LDH becomes detectable by 12 hours post
    • CP, peaks 24-48 hours and remains 10-14 dys following MI
    • •Can be used to help R/O MI when symptoms present > 24 hrs (along with Troponin).

    • • Other labs to consider
    • •CRP (C Reactive Protein)- acute inflammation
    • •BNP- substance which is secreted from the ventricles in
    • response to pressure d/t CHG
    • •Homocysteine- inflammation
    • •CBC with diff (in anemia)- lack hemoglobin to transport O2
    • •BMP
    • •Liver panel/ lipid panel/ TSH (hyper)/Glucose
  64. What is Bilirubin?
    • Waste producte of RBC breakdown.
    • Unconjugated, AKA Free, AKA indirect must go to liver to be broken down into direct or watersoluable Bili to be excreated. 
  65. Explain the difference between prehepatic jaundice and hepatic jaundice. 
    Elevated indirect bilirubin levels indicate prehepatic jaundice, such as hemolytic jaundice, or certain types of hepatic jaundice involving inability to conjugate bilirubin.

    Elevated direct bilirubin levels indicate other types of hepatic jaundice, such as in viral or alcoholic hepatitis, or posthepatic jaundice, as in biliary obstruction.
  66. What is kernicterus?
    •Elevated uncojugated bili due to neonate’s inability to clear bili

    •Elevated dependant on age and rise of bili

    •>30 = brain damage
  67. Describe ALP?
    • •Found in the kidneys, biliary
    • tract, epithelium, intestinal mucosa and the placenta

    •Determines liver and bone disorders

    • •Significantly elevated in bile duct
    • obstruction/ bile duct disease
  68. What is GGT?
    • •Enzyme produced in bile ducts
    • •Alcohol causes elevation
    • –Inc. heavy drinkers absence liver disease
    • –Detects presence alcohol even with small amt. ingested
    • –Important evaluation and management of alcoholism
    • * GGT also used to differentiate
    • liver from skeletal disease when the ALP is elevated
  69. In what diseases will there be an increase in basophil production?
    •Increases seen with leukemia or Hodgkin’s
  70. Describe monocytes?
    2-6% of leukocyte count

    Phagocytic cells that remove debris from body

    • Increase tests for:
    • TB, leprosy, lipid storage dz, ubacute bacterial endocarditis, monocytic leukemia, malaria, RMSF

    Decreased in RA, HIV
  71. What are signs and symptoms of hypokalemia?
    • •Depressed T’s
    • •Elevated P’s
    • •Cardiac irritability
    • •Neuromuscular changes (tetany, coma)
  72. S/S of HYPERkalemia
    • •Peaked T’s
    • •Flattened P’s
    • •Cardiac arrest
    • •Bradycardia
    • •Nueromuscular weakness, tremors, flaccid paralysis
  73. S/S of hyponatremia?
    • •Anorexia
    • •N & V
    • •Muscle cramps
    • •Seizures
    • •Lethargy
    • •Apathy, confusion, decreased sensation
  74. Hypernatremia
    • •Diabetes insipidus
    • •Tracheobronchitis
    • •Primary aldosteronism
    • •Coma
    • •Cushings
  75. Hypercalcemia
    • •Hyperparathyroidism and cancer most common
    • reason.
    • •Prolonged immobilization
    • •Excessive Vit. D intake
    • •Paget’s dz
    • •8.6-10mg/dl (nl CA); 4.65-5.28
    • (ionized)
    • •>13 cardiotoxicity, arrythmias and coma
  76. Hypocalcemia
    • •Pseudo (reflection of low albumin)
    • •Hypoparathyroidism (usually due to accidental surgical removal of the glands, irradiation,GI disorders
    • •Hyperphosphatemia (laxitives, renal failure)
    • •Renal failure
    • •Vit D deficiency
    • •< 6 may produce tetany and convulsions
  77. Increased Ionized Cal:
    • •Hyperparathyroidism
    • •PTH producing tumors
    • •Increased Vit D intake
  78. Decreased Ical
    • •Hyperventilation (with Tx
    • of ICP)
    • •HCO3 admin in metabolic acidosis
    • •Acute pancreatitis
    • •Hypoparathyroidism 
    • •Vit D deficiency
    • •TSS
    • •Fat embolism
    • •>7 coma
  79. What is Prinzmetal's angina?
    Episodes unrelated to activities that increase oxygen demand. Cyclic often occurs during sleep, intensifies quickly and lasts longer than stable angina. S/S palpitations, syncope, bradycardia. Relief: Exercise
  80. Who may experiance a "silent MI"?
  81. What is the most important precaution in patients taking Digoxin?

    What are the symptoms of digoxin toxicity?
    Dysrhythmias secondary to hypokalemia due to diuretic use.

    Anorexia, nausea, vomitting, visual disturbances, blurred vision, yellow tinge to vision, appearance of halos around dark objects.
  82. How long do you have to administer thrombolytics for MI?
    Within 3 hours; 30 minutes best.
  83. What is the treatment for heart failure?
    • •If severe send to ED/ cardiologist
    • •Start diuretic therapy: mild (HCTZ); severe (loop diuretics with K replacement)
    • •Ace inhibitors for all LV systolic dysfunction
    • •Beta Blockers (decrease cardiac work load & reduce sympathetic stim, decrease afterload)
    • •Weigh q day
    • •Na restricted diet
    • •Consider inotropic agents: digoxin, IV Tx: Dobutamine, Amrinone, Nesiritide
  84. Where does an ischemic strok from emboli originating in the L atria in A-fib usually occurr?
    In a branch of the middle cerebral artery.
  85. Describe the stages of HTN retinopathy?
    Grade 1Generalised arteriolar constriction - seen as `silver wiring` and vascular tortuosities.

    Grade 2As grade 1 + irregularly located, tight constrictions - Known as `(AV) nicking` or `AV nipping`

    Grade 3As grade 2 + with cotton wool spots and flame-hemorrhages

    Grade 4As above but with swelling of the optic disk (papilledema)
Card Set:
FNPII Adult Cardiac
2012-10-11 18:16:35
FNP Upstate

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