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Therapeutics I > HTN > Flashcards

HTN Flashcards

1
Q

What is HTN?

A

Elevation in pressure from normal

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2
Q

What is systolic vs diastolic?

A

Cardiac contraction and after contraction when the cardiac chambers are filling

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3
Q

What is MAP? Who do you calculate it?

A

Average pressure throughout cardiac cycle of contraction

MAP=1/3 SBP + 2/3 DBP
MAP= CO x PVR
CO=HR x SV

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4
Q

How does increasing CO lead to high BP?

A
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5
Q

How does increasing PVR lead to high BP?

A
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6
Q

What are the infrarenals of the RAAS?

A
  1. Renal purfusion pressure
  2. Catecholamines
  3. Angiotensin II
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7
Q

What are the extrarenals of RAAS?

A

Na+, K+, Cl-

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8
Q

Describe the presynaptic regulations of HTN?

A
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9
Q

Describe the postsynaptic regulations of HTN?

A
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10
Q

Describe the endothelial mechanisms?

A

Vasodilating substances → prostacyclin, bradykinin, nitric oxide
Vasoconstricting substances → angiotensin IIand endothelin I

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11
Q

What are the consequences of HTN?

A
  1. Stroke
  2. MI
  3. HF
  4. Angina
  5. Vision loss
  6. Kidney failure
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12
Q

What are some modifiable risk factors?

A
  1. Smoking
  2. DM
  3. Obesity/Physical inactivity
  4. DIet
  5. High cholesterol
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13
Q

What is normotensive?

A
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14
Q

What is elevated BP?

A
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15
Q

What is Stage 1 BP?

A
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16
Q

What is Stage 2 BP?

A
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17
Q

What is HTN crisis number?

A
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18
Q

What is essentinal HTN?

A

No underlying cause

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19
Q

What is secondary HTN?

A

Identifiable cause

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20
Q

What is resistant HTN?

A

≥130/80 mm Hg with concurrent use of 3 antiHTN meds of different classes

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21
Q

What is masked HTN?

A

Elevated BP at home despite office BP lower than 140/90

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22
Q

What is white coat HTN?

A

Normal BP at home but elevated in office

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23
Q

What are the environmental causes of essential HTN?

A
  1. Obesity
  2. Sodium intake
  3. Potassium intake
  4. PE
  5. Alcohol intake
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24
Q

What are common causes of secondary HTN?

A
  1. Renal disease
  2. Renovascular disease
  3. Aldosteronism
  4. Obstructive sleep apnea
  5. Drugs or alcohol
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25
Q

What are some med that can cause elevated BP?

A
  1. Alcohol
  2. Amphetamines
  3. Antidepressants
  4. Caffeine
  5. Decongestants
  6. Oral contraceptives
  7. NSAIDs
  8. Recreational drugs
  9. Systemic corticosteroids
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26
Q

What are the clinical presentations of HTN?

A
  1. Asymptomatic
  2. Elevated BP
  3. Require 2 or more measurements taken during 2 or more clinical encounters is required for diagnose
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27
Q

What are the clinical evals of HTN?

A
  1. Comprehensive med hisotry
  2. Physical examination
  3. Laba and diagnostics
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28
Q

What are the goals of evaluation?

A
  1. Identify secondary causes
  2. Identify CV risks and cormorbidity
  3. Assess for the presence or absence of HTN associated complications
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29
Q

What are some historical features to be aware of in primary HTN? Secondary?

A

P: Lifestyle factors, family history
S: Obstructive sleep apnea, weight

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30
Q

What are goals for HTN according to ACC/AHA? Alone? DM? CKD? Elderly?

A
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31
Q

What are the ACC/AHA goals of HTN? Why is it not used as often?

A
  1. Each patient is unique
  2. Balance benefit and harm

Insurance don’t abide by it

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32
Q

What is the purpose of trials of HTN?

A

Reducing morbidity and mortality of disease states and medications

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33
Q

What is the algorithm for normal BP?

A
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34
Q

What is the algorithm for elevated BP?

A
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35
Q

What is the algorithm for stage 1 HTN?

A
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36
Q

What is the algorithm for stage 2 HTN?

A
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37
Q

What needs to be considered when someone reaches stage 2?

A

2 antiHTN of different classes

Those ≥160/100 should be treated promptly

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38
Q

What are some non-pharm strategies for HTN?

A
  1. Weightloss
  2. DASH
  3. Sodium reduction
  4. Potassium supplements
  5. Increased physical activity
  6. Reduction in alcohol consumption
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39
Q

What are the weight loss goals?

A

IBW, expect about 1 mmHg for every 1 kg reduction in body weight (max: 5)

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40
Q

What consists of the DASH diet?

A

fruits, veggies, whole grains, low-fat dairy

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41
Q

What is the goal for Na+ intake?

A

<1500 mg/d

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42
Q

What is the goal for potassium supplements?

A

3500-5000 mg/d

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43
Q

What is the alcohol intake rec?

A

Men: ≤2
Women: ≤1

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44
Q

Who would respond more to sodium reduction?

A
  1. Blacks
  2. Older people
    Most fast foods are processed and have high sodium
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45
Q

What are strategies for reducing sodium?

A
  1. Fresh foods
  2. Use food labels
  3. Sub
  4. Control
46
Q

How do you calculate heart rate reserve?

A

Max HR- resting HR
Usually 220-age

47
Q

What are the types of physical activity?

A

Aerobic
Dynamic resistance
Isometric resistance

48
Q

What is aerobic?

A

Brisk walking, swimming, rowing, jumping rope, cycling, running

49
Q

What is dynamic resistance?

A

Concentric and eccentric contractions (joint movement)

Bicep curls, tricep dip, squats

50
Q

What is isometric resistance?

A

Contracting a muscle for a prescribed amount of time

Planking, wall sit

51
Q

What is considered a standard drink?

A

12 fl oz (beer) = 1.5 fl ox (double shot) = 5 fl oz (wine)

52
Q

What are alternative strategies for HTN (limited evidence)?

A
  1. Probiotics
  2. Increased protein and fiber
  3. Ca2+ supplements
53
Q

What is 1st line diuretic for HTN?

54
Q

What are the adrenergic HTN drugs?

A
  1. Non selective a atangonist
  2. alpha 1 blocker
  3. beta blockers
  4. centrally acting
55
Q

What are the vasodilators for HTN?

A

CCB
Direct acting VD
K+ channel openers

56
Q

What is the initial med for non-black?

A
  1. TZD
  2. CCB (DHP)
  3. ACEI
  4. ARB
57
Q

What is the initial med for blacks?

A

TZD or CCB

58
Q

How do we decide med for basic HTN patients?

59
Q

What is the MOA of thiazides?

A
  1. Inhibit reabsorption of Na+ in the DCT
  2. Increases the excretion of sodium and water and potassium
60
Q

What are the thiazides used for HTN?

A
  1. Chlorthalidone (stronger and higher efficacy)
  2. HCTZ
  3. Indapamide
  4. Metolazone (not really used)
61
Q

What are some pearls to know about TZD?

A
  1. first line of HTN
  2. PO QAM to avoid nocturnal diuresis
  3. May worsen gout
  4. Decreased efficacy withCrCl <30mL/min
  5. Sulfonamide allergy
62
Q

What is the MOA of CCB? what the difference between the two classes?

A

Blocks inward flow of Ca2+ through L channels of arterial smooth muscle

DHP: dilate arteries not veins
Non-DHP: reduce HR and contractility, not used for HTN

63
Q

What are some pearls for DHP?

A
  1. Peripheral edema on arterial and increased venous pressure → edema
  2. Nifedipine may cause yo-yoing
  3. Avoid use in patients with patients with HFrEF (amlodipine or felodipine)
  4. Potent peripheral VD
64
Q

What are some Non-DHP pearls?

A
  1. ER products for HTN (not commonly used)
  2. Avoid use in HFrEF
  3. Avoid with beta blockers
  4. For arterial tachyarrhythmia
  5. CYP3A4 substrates and moderate inhibitors DDI
65
Q

What are the DHP drugs?

66
Q

What are the nonDHP?

67
Q

What is the MOA of ACEI?

A
  1. Block the conversion of angiotensin II
  2. Increase bradykinin blocking breakdown

Coughing, angioedema

68
Q

ACEI drugs?

69
Q

ACEi Pearls?

A
  1. Strong rec for: stroke, CAD, HF, CKD, DM, albuminuria
  2. Reduce proteinuria
  3. DDI with ARB or renin inhibitor
  4. Hyperkalemia
  5. Angioedema
  6. Fetal toxicity
  7. Reduce dose 50% who are on diuretic or elderly
  8. Reno-protective
70
Q

What is the MOA of ARBS?

A

Blocks angiotensin II receptor (AT1) → vasodilation

71
Q

Types of ARBs?

72
Q

ARB pearls?

A
  1. No increased production of BK
  2. DDI with renin inhibitors and ACEis?
  3. hyperkalemia
  4. Risk for AKI
  5. Angioedema
  6. Fetal toxicity
  7. Reduce dose 50% who are on diuretic or elderly
73
Q

What need to be considered in black patients with HTN?

A
  1. Most require ≥2 AHTN med to achieve BP control
  2. TZD and CCBs are more effective
  3. ACEi are less effective and higher risk of angioedema
74
Q

What are some thing to be aware of for HTN geriatrics?

A

Less intensive BP control
High burden of comorbidity and limited life expectancy

75
Q

TZD and geriatrics?

A

Increased SIADH (electrolyte abnormalities)

76
Q

CCB and geriatrics?

A

Greater hypotensive response

Constipation

No CNS effect

77
Q

ACEis and getriatrics?

A

Favorable side effect profiles, hyperkalemia

78
Q

Beta blockers and geriatrics?

A

Less hemodynamic response and more bradycardia

79
Q

What are some thing to be aware of for HTN pregnancies?

A
  1. BP decline 1st trimester than slowly rises
  2. ARB and ACEi are fetotoxic
  3. Nifedipine, labetalol, methyldopa, hydralazine
  4. Preeclampsia are risk facotrs
80
Q

What are comorbidities of HTN?

A
  1. Stable ischemic heart disease
  2. A fib
  3. HF
  4. PAD
  5. CKD
  6. DM
  7. CVD
  8. Metabolic syndrome
81
Q

HTN treatment for stable ischemic heart disease?

A

GDMT w/ beta blocker (not for HTN but for disease state)

82
Q

What is the guideline for HFrEF?

A

Find optimal regimen for HF not HTN

ACEi or ARB, ARNI, MCR antagonists, diuretics, GDMT beta blockers

Don’t use Non-DHP

Goal: <130/80

83
Q

What is the guideline for HfpEF?

A

Goal: <130/80
ACEi or ARB, beta blocker, MRA

Volume overload treatment with diuretics

84
Q

How does HTN effect CKD?

A

Major contributor to decline in GFR

30% of patients have masked HTN

85
Q

Guidelines for CKD?

86
Q

What is the difference between acute intracerbral hemorrhage and ischemic stroke? Secondary stroke prevention?

A

Hem: Increased BP → pressure in vessels → leakage in brain
Stroke: Lack of O2 → damage → treatment is permissive HTN
Secondary: management of stroke

87
Q

How do you treat PAD with HTN?

A

Normal patient

88
Q

How do you treat DM with HTN?

A
  1. First line
  2. With albuminuria: ACEi/ARB
89
Q

What is metabolic syndrome? What is the treatment?

A

Metabolic dysregulation by visceral fat accumulation, insulin resistance, hyperinsulinemia, hyperlipidemia

Thiazides due to increased insulin resistance

Don’t use beta blockers → deterioration of glucose tolerance and dyslipidemia

90
Q

What is the most common cormorbidie associated with HTN?

91
Q

What is the goal for Afib HTN?

A

Control HTN to aid a fib prevention

ARB

92
Q

What is the standard for clinical monitoring of HTN?

A
  1. Reevaluation 2-4 weeks after initiating or changing therapy
  2. Once at goal → monitor every 3-6 months

Self monitoring and ABP can be used in combo

93
Q

How do we monitor ADRs?

A

Pharmacist must know common side effects and lab parameters

94
Q

How do you lab monitoring for HTN?

A
  1. 2-4 weeks after agent initiation or dose increase
  2. Every 6-12 months for stable patients
  3. More intensive follow up for aldosterone antagonists → K+ and renal function evaluation within 3 days then again for 1 week
95
Q

What are the signs and symptoms of HTN to look out for?

A
  1. Ischemic chest pain
  2. Vision
  3. One side weakness
  4. Slurred speech
  5. Loss of balance

Ey exam
Proteinurina

96
Q

Recommendations for non adherence?

A
  1. Focus on clinical outcomes
  2. Empowerment
  3. Implement a team
  4. Advocate for health policy reform
97
Q

Preferred HTN combos?

A
  1. ACEI/CCB
  2. ARB/CCB
  3. ACEi/thiazide
  4. ARB/thiazide
98
Q

How do you diagnose resistant HTN?

A
  1. Failure to achieve BP control with 3 meds
  2. BP control but requires ≥4 meds
99
Q

Risk factors of resistant HTN?

A
  1. Older
  2. Obesity
  3. CKD
  4. Black
  5. DM
100
Q

Common 3 drug regimen?

A

CCB, RAAS inhibitors, Chlorthalidone

101
Q

What are recommended combo with spironolactone?

A

Hydralazine or minoxidil

102
Q

What is the treatment algorithm for resistant HTN?

A

Confirm resistance → Exclude pseudo resistance → Identify and reverse lifestyle factors → discontinue substances → screen for secondary causes → pharm treatment → refer to specialist

103
Q

What diuretics are more potent than HCTZ?

A

Chlorthalidone and indapimide

104
Q

What can be used in place of thiazides if patient has decreased renal function?

105
Q

What are guidelines for alpha-1 blockers?

A

Sodium and H2O retention
First dose phenomenon

106
Q

What are guidelines for central a2 blockers?

A

Significant CNS activity
Induce HTN crisis

107
Q

What are guidelines for renin inhibitors?

A

DDI with RAAS inhibitors
Long acting

108
Q

What are guidelines for loop?

109
Q

What are guidelines for K+ sparing?

A

Avoid CKD
For thiazide induced hypokalemia

110
Q

Overall algorithm for HTN?

111
Q

Overall algorithm for HTN with cormorbidieis?

Therapeutics I (32 decks)

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