Lecture 6 Flashcards

1
Q

Dx Hypertension

A

TWO readings of at least 140/90 at TWO appointments

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2
Q

Primary Hypertension

A

Most Common
Unknown Etiology
Older People

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3
Q

Secondary Hypertension

A

Less Common
Has some cause
Younger People

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4
Q

Hypertension Results in

A

End organ damage- heart, kidneys, brain, eyes

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5
Q

Stage 1 Hypertension Numbers

A

140-159/90-99

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6
Q

Normal Tension Numbers

A
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7
Q

Stage 2 Hypertension Numbers

A

160-179/100-109

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8
Q

Pre-Hypertension

A

120-139/80-89

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9
Q

Hypertensive Emergency

A
>180/>110 AND have symptoms: 
Confusion
Chest Pain
Renal Failure
Visual Changes
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10
Q

Five Types of hypertension drugs

A
Diuretics (Thiazides, Loop)
Adrenergic Agents
CCB
ARB
ACEI
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11
Q

Thiazides: Mechanism

A

Act on distal Convuluted Tubule

Inhibit Na reabsorption

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12
Q

SE of Thiazides

A

Hypokalemia
Hyperuricemia
Xerostomia
Anorexia

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13
Q

Loop Diuretics: Mechanism

A

Act on Ascending Loop of Henle

Inhibit Na reabsorption

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14
Q

SE of Loop Diuretics

A

Hypokalemia

Hyperuricemia

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15
Q

What type of pts use Loop Diuretics

A

Hypertensive pts with CHF

Can cause rapid diuresis

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16
Q

Potassium Sparing Diuretics: Mech

A

Spirinolactone and Eplereone - Block Aldosterone Receptor

Amiloride and Triamterene - Block Na channels

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17
Q

Potassium Sparing D’s

A

Not as strong as other D’s- used as adjunct

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18
Q

SE of K Sparing D’s

A

Hyperkalemia

Arrythmia

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19
Q

Adrenergic Meds for Hypertensions: Types

A

A2 agonist
A1 antagonist
B blocker
B1 selective blocker

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20
Q

Adrenergic System Responses

A

A1 - Inc BP
A2 - Inhibits NE
B1 - Inc HR and Contraction
B2 - Inc vasoDILATION

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21
Q

A2 Agonist: Action

A

Inhibit Epi and NE –>

Vessel Dilation

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22
Q

SE of A2 Agonist

A

Drowsiness

Sedation

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23
Q

A1 Antagonist: Action

A

Block receptors in arteries and veins–> relax smooth muscle–> Reduce HTN

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24
Q

SE of A1 Antagonist

A

Postural Hypotension

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25
Q

Disadvantages of Non-selective B blockers and of Selective B1 Blockers

A

Non selective - reactive airway disease

Selective - hypotension and bradycardia

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26
Q

CCB’s: action

A

Inhibit movement of Ca into cardiac cells –> vasodilation and reduces afterload

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27
Q

Uses for CCB’s

A

Hypertension
Arryhthmias
Angina

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28
Q

SE’s of CCBs

A

Gingival growth
Excessive hypotension
Nausea/vomiting
Bradycardia

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29
Q

ACEI’s: Mech

A

Blocks ACE and thus blocks conversion of Angiotensin I to II
Angiotensin II produces vasoconstriction and stimulates aldosterone release and water retention

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30
Q

ACEI’s SE’s

A
Hypotension
URI
Nausea and vomiting
LICHENOID ORAL LESIONS
Drug interaction w/ NSAID's
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31
Q

ARB’s: Mech

A

Bind to Angiotensin II receptor and block action

–> blocks release of aldosterone

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32
Q

When is BP an EMERGENCY

A

> 180/110

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33
Q

ARB’s SE’s

A
Fewer than w/ ACEI's
Dizziness, fatigue, insomnia
URI's
Diarrhea 
muscle cramping
angioedema
34
Q

Meds to take after MI and Stent Placement

A

Clopidogrel - anti platelet
Felodipine - CCB
Nitroglycerine - vasodilator

35
Q

Stents, when need SBE Prophylaxis?

A

Only immediately after: 4-12 weeks post placement

36
Q

Types of PCI

A

Bare Metal Stent

Drug Eluting Stent

37
Q

Drugs to take with PCI’s

A

Aspirin and Clopidogrel (Plavix)

38
Q

Duration of Platelet Therapy drugs with each stent type

A

Bare Metal - 1 month, ideally a year

Drug-Eluting - 6 months, ideally a year

39
Q

With Bare Metal, at 6 weeks, what should you do

A

Bleeding risk low- continue dual-platelet therapy
High-risk surgery - just continue ASA
If Drug-eluting, defer all high risk procedures for 12 mo.

40
Q

LA recommendation for pts with MI/stent hx

A

Restrict Epi to 0.04 mg - 2.2 carps

41
Q

Angina

A

Mismatch of O2 needs of heart and delivery of it to heart

42
Q

Angina: Tx

A

100% O2
Sublingual Nitroglycerin 0.4mg
Should relieve in 3-5 min - if doesn’t, suspect MI!

43
Q

Anti-Angina Drugs

A

Nitroglycerin
CCB’s
B-Blockers

44
Q

NTG Mech

A

Activate guanylyl cyclase and increase cGMP to cause Vasodilation!

45
Q

NTG SE’s

A

Severe headaches
Flushing, hypotension, light-headedness
Syncope
Localized burning or tingling where places sublingually

46
Q

MI

A

ischemia leading to myocardial muscle tissue death

47
Q

Disrhythmias associated with MI

A

Premature ventricular contractions
Ventricular tachycardia
Ventricular fibrillation
Asystole

48
Q

CHF: Mech

A

Heart is unable to fill/eject blood to meet bodily demands

49
Q

Right Side CHF vs Left Side CHF

A

Right Side - Systemic Edema

Left Side- Pulmonary Congestion

50
Q

CHF Classes

A

1 - symptomatic w/ greater thn normal activity
2 - symptomatic w/ normal activty
3 - symptomatic w/ minimal activity
4 - symptomatic w/out any activity

51
Q

CHF Tx

A

Digoxin
Diuretics
ACEI’s

52
Q

Digoxin

A

Most common CHF drug

53
Q

Digoxin: Mech

A

Inc force and strength of contraction of myocardium- allows heart to do more work w/out inc use of O2–> more efficient

54
Q

Digoxin SE’s

A

Narrow therapeutic index
Arryhthmias
Visual changes
Nausea vomiting

55
Q

Digoxin Pts

A

Check for SE’s, minimize Epi, monitor for bradycardia

Tetracycline and Erythromycin can Inc digoxin levels!!!

56
Q

First line against CHF

A

ACEI’s and ARB’s

57
Q

Signs of poor control of CHF

A

Shortness of breath
Peripheral Edema
Fluctuations in body weight

58
Q

CHF pts

A

Continue all meds on day of procedure
Obtain cardiology clearance
Minimize BP and HR fluctuation

59
Q

Atrial Fibrillation

A

Multiple areas in atria depolarize - can lead to rate in the 180s
7x increase risk of CVA
Higher possibility of thrombus formation

60
Q

Acute A Fib Tx

A

48 hrs- Anticoagulant for 3 weeks, then Cardiovert

61
Q

Stable/Chronic A Fib Tx

A

CCB and B-Blockers to control rate

Anticoagulant

62
Q

AntiArrhythmic Agents

A

Work by depressing parts of the heart that are causing abnormal beating
Dec depolarization velocity, propogation

63
Q

Classes of AntiArrhythmic Agents

A

I - Na blockers
II - B Blockers
III - K Blockers
IV - Ca Blockers

64
Q

Antiarrythmic agents Caution

A

Have narrow TI - so only use if arrhythmi is preventing proper heart function

65
Q

Hyperlipidemia

A

Can cause inc in Chylomicrons
VLDL’s
LDL’s

66
Q

Hyperlipidemia: Tx

A

Lifestyle changes
HMG CoA Reductase Inhibitors (statins)
Intestinal absorption inhibitors
Gemfibrozil

67
Q

Statins: Mech and SE’s

A
Inhibit HMG CoA Reductase, the rate limiting enzyme in cholesterol synthesis
SE's: GI issues
Muscle pain
Skin rash
Can inc effect of warfarin
68
Q

Ezetimibe

A

Inhibits intestinal absorption of Cholesterol

69
Q

Gemfibrozil

A

Increases lipolysis of triglycerides and inhibits secretion of VLDL’s from liver

70
Q

SE’s of Gemfibrozil

A
Gall stones (cholelithiasis)
Taste perversion, hyperglycemia
71
Q

Valve disease: Pressure overload problem

A

Mitral or Aortic Stenosis

72
Q

Valve disease: Volume Overload problem

A

Mitral or Aortic Regurgitation

73
Q

Heart Murmur: Systole

A

Aortic and pulmonary stenosis or

Mitral or tricuspid regurgitatoin

74
Q

Heart Murmur: Diastole

A

Aortic or pulmonary regurgitation or

Mitral or tricuspid stenosis

75
Q

Aortic Stenosis

A
Leads to ventricular hypertrophy
Increased risk for MI
Symptoms: Angina
Syncope
Dyspnea
76
Q

Aortic Stenosis Prognosis

A

75% die in 3 years if don’t replace valve

77
Q

Aortic Stenosis Mgmt

A

Heart rate control w/ B Blockers, CCB, Digoxin

BP Control w/ ACEI and ARB

78
Q

Surgical Tx of Aortic Stenosis

A

Mechanical valve - last 20-30 years, long-term anticoagulant

Biologic Valve - last 10-15 years, long-term anticoagulation NOT needed

79
Q

Pacemakers

A

Used for Sick Sinus Syndrome
Tx for Long-term bradycardia
Can pace atria, ventricles, or both

80
Q

ICD

A

Provide shocks w/in 15 seconds if sense disrhythmia

For patients with V fib, increase risk of cardiac death, or advanced CHF

81
Q

Dental treatment for people with Aortic Stenosis

A

DON’T TREAT - refer to OMS, continue all meds

82
Q

Monopolar Cautery

A

DON’T EVER USE- can reset ICD