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Pharmacotherapy 1 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Why do we treat cholesterol?

A 
Cholesterol = precursor to hormones 
LDL = leads to atherosclerosis; low density 
VLDL = very low density 
Apo B = linked to HDL 
Apo A = linked to LDL 
Non-HDL = inc number → inc risk of ASCVD
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2
Q

Describe the CTT landmark lipid trial (purpose, result of cycle 1, and result of cycle 2)

A

-CTT = Cholesterol Tx Trialist
-Purpose = address uncertainties by developing meta-analyses to inc power of lipid trials
-Result of Cycle 1 = statins safe and improved CV outcomes; linear relationship b/w LDL lowering and CV outcome reduction
-Result of Cycle 2 = more intensive LDL lowering → better CV outcomes
-Each 39mg/dL dec ASCVD risk by 21%
-Each 1% dec in LDL results in about 1% dec in risk of ASCVD
—Moderate intensity = 30% dec ASCVD risk
—High intensity = 50% dec ASCVD risk

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3
Q

SAMS abbreviation and assess symptoms (timeline, nature)

A

Statin associated muscle symptoms

Usually bilateral, proximal muscles
Onset weeks to months after starting therapy
Resolves with discontinuation

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4
Q

Possible non-statin etiologies for muscle pain (5)

A
  • Hypothyroidism
  • Dec renal/hepatic fx
  • Rheumatologic disorders
  • Vitamin D deficiency (some studies show adding vitamin D makes pt more able to tolerate statin)
  • Primary muscle disease
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5
Q

If suspect myopathy/rhabdomyolysis

A

-Stop statin
-Check CK if severe SAMS and muscle weakness
-Assess for rhabdomyolysis
—CK >/= 10x ULN (men: 900; women: 700)
-Renal: inc SCr and/or inc UACR
-Can restart statin if rhabdomyolysis is reversible cause (drug interaction)
-Stop statin immediately if rhabdomyolysis is not reversible or can’t ID cause

If no reversible or identifiable cause, may need to stop statin indefinitely

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6
Q

What to do if pt has pain with a statin?

A

If pain with one statin, try lower dose with same statin. If still in pain, try a different statin. If still in pain, switch off statin therapy

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7
Q

SAMS management (what to do if you DON’T suspect myopathy or rhabdomyolysis)

A

-Stop statin
-Wait for SAMS to resolve
-Re-challenge with (select all that apply Q)
—Reduced dose of same statin
—Different statin
—Alternate dosing (intermittent)
-Monitor for re-emergence of SAMS
-Use max statin dose indicated and/or tolerated
-Moderate intensity statin + zetia may be alternative if high intensity statin isn’t tolerated
—And PCSK9 inh benefits those with familial Hyperlipidemia and ASCVD

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8
Q

Statins hepatotoxicity measurements/symptoms

A

LFTs at baseline

Measure again if hepatotoxicity symptoms arise with statin use

  • Unusual fatigue/weakness
  • Loss of appetite
  • Abdominal pain
  • Dark colored urine
  • Yellowing of skin/sclera
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9
Q

Statin blood glucose effects

A
  • Potent statins sometimes elevate BG
  • Possible to get diabetes with statin use
  • Several studies showed association —> led to FDA warning on statin label and generated discussion of risk vs benefit of statins in primary prevention
  • JUPITER study (elaborate on different card)
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10
Q

Elaborate on JUPITER study for statins/BG

A

-JUPITER study re-evaluated to say pts with at least 1 DM risk factor have a 28% inc risk of developing DM
—But benefit 39% dec in composite of MI, stroke, and hospital admin for unstable angina; and 17% dec in total mortality
—Equates to 134 vascular deaths avoided for 54 new cases of DM

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11
Q

Diabetes risk factors

A
  • African Americans, Hispanic, native Americans, Asian, Pacific Islander
  • Family history
  • Gestational DM
  • Baby > 9 lbs
  • PCOS
  • HDL < 35 and/or TG > 250
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12
Q

Statins/blood glucose: pts with no risk factors

A
  • No inc risk of developing DM
  • Statins produced 52% dec in MI, stroke, hospital admin for unstable angina; 22% dec in total mortality
  • Equates to 86 vascular deaths avoided with no new DM cases
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13
Q

What is considered ASCVD (select all that apply q)

A

Acute coronary syndrome (ACS) [recent = < 1 yr ago]
History of Myocardial infarction (MI, STEMI, NSTEMI)
Stable or unstable angina (SA or UA)
Stroke (CVA)
Peripheral Artery Disease (PAD)
Coronary/Arterial revascularization (stents)
Percutaneous transluminal coronary angioplasty (PTCA)
Coronary artery bypass graft (CABG)
Stroke or transient ischemia attack (TIA)
Peripheral arterial disease (PAD)

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14
Q

ASCVD = leading cause of

A

morbidity and mortality globally

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15
Q

Heart Dz in US

A

Leading cause of death in men and women
1 in every 4 deaths
Leading cause of death for most ethnicities (including AA, Hispanics, and whites)
Second to cancer in American Indians or Alaska Natives and Asians or Pacific Islanders

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16
Q

Stroke in US

A

1 out of 20 deaths
Happens every 40 seconds, & someone dies from it every 4 mins
87% are ischemic
Leading cause of long-term disabilities

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17
Q

ASCVD risk score calculator

A

Risk calculator developed by the NHLBI work group
Est the 10 year hard ASCVD risk of 1st event
Non-fatal MI, coronary heart disease death, fatal or non-fatal stroke

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18
Q

who to use risk calculator in

A

Developed using data from large, racially and geographically diverse, NHLBI-sponsored studies
Best used in
Non-Hispanic caucasians and African Americans
Aged 40-79
Pts with LDL 70-189mg/dL

Overestimates risk in Hispanics and Asians
Underestimates risk in American Indians (puerto ricans and south Asians)

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19
Q

what info is required to use ASCVD risk calc?

A 
Age
Sex
Race
Blood pressure
Cholesterol panel
DM: yes/no
Smoker: yes/no
On BP meds: y/n
On statin: y/n
On aspirin: y/n
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20
Q

screening pts

A

Adults 20+ years old, measure either fasting or non-fasting
If non-fasting results show TG >/=400, repeat with fasting panel
If LDL <70, measure direct rather than using Friedewald equation

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21
Q

Lifestyle management in hyperlipidemia

A 
Try first and then with cholesterol-lowering drugs
Adhere to a heart healthy diet
Regular exercise (2.5 hours/week)
Avoid ALL tobacco products
Maintain healthy weight
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22
Q

Heart healthy diet in hyperlipidemia

A

Emphasize fruits, veggies, and whole grains
Include low-fat dairy products, poultry, fish, legumes, non-tropical oils, and nuts
Limit intake of sweets, sugar-sweetened beverages, and red meats
Reduce % of calories from saturated (keep at 5-6%) and trans fat
Lower sodium intake (1500-2400 mg/day)
Follow DASH, USDA, or AHA dietary patterns & Mediterranean diet

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23
Q

DASH

A

dietary approaches to stop HTN

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24
Q

Exercise for dyslipidemia

A

2.5 hours/week or aerobic activity with moderate to vigorous intensity
Pt can build up this regimen if needed and exercise can be in 10 min increments
Examples
Brisk walking, swimming laps, raking leaves, dancing, heavy home cleaning

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25
Q

Approach to treatment

A

Guidelines say “if on max statin and LDL still > 100, adding Zetia may be reasonable”

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26
Q

Primary prevention

A

haven’t had an ASCVD event yet and trying to prevent it

LDL >/= 190
Diabetes
ASCVD risk elevation

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27
Q

secondary prevention

A

already had a heart attack/stroke and trying to prevent a second one

Clinical ASCVD

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28
Q

what are the 4 statin benefit groups?

A

Clinical ASCVD
LDL >/= 190mg/dL (Age >/= 20)
Diabetes (Age 40-75, LDL b/w 70-189 mg/dL)
ASCVD Risk Score elevation (age 40-75, LDL b/w 70-189 mg/dL)

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29
Q

Secondary ASCVD Prevention (for pts who already had ASCVD event) (3 broad groups w/n)

A

ASCVD + Not high risk Age = 75

ASCVD + Not high risk Age > 75

ASCVD + Very High Risk

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30
Q

ASCVD + Not high risk Age = 75

A

High-intensity statin
Goal: dec LDL by at least 50%
Threshold: LDL >/= 70; non-HDL >/= 100

If on max statin and not reaching threshold → initiate Zetia
If on statin + zetia and not reaching threshold → PCSK9-I

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31
Q

ASCVD + Not high risk Age > 75

A

Moderate-intensity statin or high-intensity statin
Goal: dec LDL by at least 30% (or 50%)
Threshold: LDL >/= 70; non-HDL >/= 100

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32
Q

ASCVD + Very High Risk

A

History of multiple (>/= 2) ASCVD events OR 1 major ASCVD + at least 2 high-risk conditions
High-intensity statin
Goal: dec LDL by at least 50%
Threshold: LDL >/= 70; non-HDL >/= 100

If on max statin and not reaching threshold → initiate Zetia
If on statin + zetia and not reaching threshold → PCSK9-I

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33
Q

Primary Severe Hypercholesterolemia (group)

A

LDL >/= 190

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34
Q

Risk Enhancing Factors

REF

A

Premature family history of ASCVD
—= 55 male relative; = 65 female relative

Primary hypercholesterolemia
—LDL 160-189; Non HDL 190-219

Race/Ethnicity (ex: south asian)

Persistently High LDL (>/= 160)

Chronic Inflammatory conditions
—Lupus, HIV, RA, Psoriasis

Premature menopause and preg-associated condn that inc ASCVD risk

CKD
—eGFR < 60 ml/min, not on dialysis or kidney transplant

Metabolic syndrome (must have at least 3)

Persistent TG > 175 mg/dL

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35
Q

DM In adults (w/ LDL 70-189)

2 broad groups

A

DM 20-39yo

DM 40-75yo

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36
Q

DM 40-75yo w/ low ASCVD risk, and only 2 REF

A

Minimum of moderate intensity statin

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37
Q

DM 40-75yo

ASCVD risk >/= 20% OR >/= 2 DM specific risk enhancing factors

A

high intensity statin (goal of 50% dec in LDL and Non-HDL >/=130)
If goal not met → Zetia if ASCVD risk at least 20%
Multi risk factors alone is not enough to initiate high-intensity statin in DM pts; must meet threshold of LDL at least 70.

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38
Q

DM 20-39yo

A

> /= 2 DM specific risk enhancing factors & LDL >/=70

Moderate intensity statin

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39
Q 
Primary Prevention (40-75yo w/o DM and with LDL >/= 70) 
(4 broad groups)
A

ASCVD Risk <5% “low risk”

ASCVD Risk >/=5% but < 7.5% “borderline risk”

ASCVD Risk >/= 7.5% but < 20% “intermediate risk”

ASCVD Risk >/= 20% “high-risk”

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40
Q

ASCVD Risk <5% “low risk”

A

Lifestyle modifications

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41
Q

ASCVD Risk >/=5% but < 7.5% “borderline risk”

A

> /= 2 ASCVD risk enhancing factors
Consider moderate intensity statin
Borderline pts with <2 REF or pts opposed to statin tx → use CAC to guide decision and convince the pt

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42
Q

ASCVD Risk >/= 7.5% but < 20% “intermediate risk”

A

> /= 2 ASCVD risk enhancing factors

Moderate-intensity statin

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43
Q

ASCVD Risk >/= 20% “high-risk”

A

High-intensity statin

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44
Q

Risk Factors for ASCVD

A 
Age 
>/= 45 men; >/= 55 women
Current Smoking 
HTN 
BP > 130/80 or use of antihypertensives 
Diabetes 
Sex (male > female)
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45
Q

Risk Enhancing Factors

REF

A

Premature family history of ASCVD
= 55 male relative; = 65 female relative
Primary hypercholesterolemia
LDL 160-189
Non HDL 190-219
Race/Ethnicity (ex: south asian)
Persistently High LDL (>/= 160)
Chronic Inflammatory conditions
Lupus, HIV, RA, Psoriasis
Premature menopause and preg-associated condn that inc ASCVD risk
CKD
eGFR < 60 ml/min, not on dialysis or kidney transplant
Metabolic syndrome (must have at least 3)

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46
Q

Metabolic syndrome (must have at least 3 of the following)

A

Inc waist (men >/= 40inches; women >/= 35 inches)
TG >/= 150 mg/dL
Elevated BP >/= 130/85 or antiHTN therapy
Elevated blood glucose >/= 100mg/dL fasting or on tax
Low HDL = 40 mg/dL in men; = 50 mg/dL in women
—Can inc HDL with exercise

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47
Q

Lipid/biomarkers

REF

A 
Persistent TG > 175 mg/dL
hsCRP >/= 2mg/dL 
Highly sensitive C reactive protein
Inflammatory marker
Lp(a) >/= 50mg/dL
ApoB >/=130mg/dL
Ankle brachial index (ABI) < 0.9
Compares BP between upper and lower limbs
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48
Q

Diabetes-Specific Risk Enhancing Factors

A 
Long duration (>/= 10 yr for T2DM or >/= 20 yr for T1DM 
eGFR < 60 ml/min
Albuminuria (>/= 30 mcg/mg) 
ABI < 0.9 
Retinopathy 
Neuropathy
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49
Q

High-Risk Conditions

A 
Age >/= 65
Heterozygous familial hypercholesterolemia 
Hx of CABG or PCI 
DM 
HTN 
CKD
Current smoking 
Hx of HF 
Persistently elevated LDL >/= 100mg/dL even with max statin &amp; Zetia
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50
Q

Low-Intensity Statins

A 
Simvastatin 10mg
Pravastatin 10-20mg
Lovastatin 20mg 
Fluvastatin 20-40mg 
Pitavastatin 1mg
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51
Q

Moderate-Intensity Statins

A 
Atorva 10-20mg
Rosuva 5-10mg
Simva 20-40mg 
Prava 40-80mg
Lova 40mg 
Fluva XL 80mg 
Pitava 2-4mg
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52
Q

High-Intensity Statins

A

Atorva 40-80mg

Rosuva 20-40mg

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53
Q

Atorva

A

Lipitor; 10,20,40,80mg

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54
Q

Rosuva

A

Crestor; 5, 10, 20, 40mg

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55
Q

Simva

A

Zocor; 5,10,20,40,80mg

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56
Q

Prava

A

Pravachol; 10,20,40,80mg

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57
Q

Fluva

A

Leschol/Leschol XL; 20,40mg (80mg XL)

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58
Q

Pitava

A

Livalo; 1,2,4mg

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59
Q

Lova

A

Mevacor; 10,20,40mg

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60
Q

CAC

A

(Coronary Artery Calcium)

Useful with pts reluctant to start tx and want more information to make informed choice
Concerned abt reinitiation of tx after dc due to ADE
Who are older with little risk burden (M 55-80; F 60-80)
With borderline risk and RF and REF to better inform tx decisions

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61
Q

CAC interpretation

A

0: withhold statin and reassess in 5-10yr
1-99: initiate statin in pts >/= 55yo
>/= 100 or 75th percentile: start statin

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62
Q

Pt with CI to high intensity statin or do not tolerate ADE

A

Go to moderate intensity statin or to whatever intensity is tolerated
If no statin is tolerated → add non-statin tx

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63
Q

Triglycerides classification

A

Normal <150
Moderate 150-499
Severe >/= 500

Don’t solely tx TG unless “severe”

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64
Q

Moderately elevated TG treatment (20+ years old)

A

Lifestyle (obesity; metabolic syndrome)
—Waist circumference: men > 40, women > 35
TG > 150; high BP, high BG, low HDL: men < 40, women < 50

Rule out secondary factors

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65
Q

secondary factors to rule out for elevated TG tx

A

DM
Chronic liver disease or CKD (ckd is GFR <60)
Hypothyroidism
Meds that inc TG

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66
Q

Moderately elevated TG treatment (40-75 yo)

A

All steps for >20 yo
If persistently elevated TG level and ASCVD risk >/= 7.5% when tested on 2 separate occasions (different appointments)
Then consider statin therapy
May intensify if TG stays elevated

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67
Q

Severely elevated TG treatment (40-75 yo)

A

All steps for moderate

TG >/= 500 mg/dL, consider statin therapy (moderate) and can add fibrate but NOT bile acid sequestrant (bc they inc TG levels)

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68
Q

TG >/=1000

A

really need to change diet (do all of the following)

Moderate statin 
Very low fat diet
Avoid refined carbs and alcohol 
Inc omega 3 FAs
*can initiate fenofibrate if needed to prevent pancreatitis (a risk when TG >/= 500)
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69
Q

Meds that can inc TG (13)

A 
Oral estrogen
Tamoxifen
Raloxifene
Retinoids
Immunosuppressives
***Beta blockers (at high doses)***
Atypical antipsychotics 
Protease inhibitors 
***Glucocorticoids***
***BAS***
Cyclophosphamide
Interferons
***High dose thiazides***
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70
Q

Hyperlipidemia TX (list the 4 main points)

A

Monitor response
Safety
Monitoring for adverse
Patient education

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71
Q

Monitoring response of hyperlipidemia tx

A

Recheck lipid panel in 4-12 weeks after initiation or dose adjustments

How is adherence? Are they meeting goal? Are they achieving thresholds?

Then recheck lipid panel every 3-12 months if at/reaching goal

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72
Q

Statins Pt and provider discussion points (4)

A

Indications
Benefits
Risk of SAMS
Pt concerns and preferences

  • *check CK at baseline in case of muscle complaints
  • future appts: discuss adherence, statin response, reaffirm benefit, address any SAMS
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73
Q

SAMS (statin associated muscle symptoms?)

4

A

Myalgia (most common; subjective)
Myopathy
Myositis (rare)
Rhabdomyolysis (rare)

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74
Q

Rhabdomyolysis

A

Suspect if CK > 10 x ULN + signs of renal injury (inc SCr and inc UACR)
UACR: urine albumin to creatinine ratio
Pt complaints of severe muscle pain; usually in large muscle groups like thighs

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75
Q

other reasons CK gets elevated

A

Muscle cramps, injury, exercise
Baseline levels can be as high as 10x the ULN

NORMAL RANGE
Men: 25-90 IU/L
Women: 10-70 IU/L

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76
Q

Safety: statins and diabetes

A

-Evaluate for new-onset diabetes
-Risk of diabetes not a contraindication to statin therapy; benefit outweighs the risk
-For people at risk for diabetes, recommend lifestyle modifications to prevent DM
Exercise
Healthy diet
Moderate weight loss

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77
Q

Statins drug interactions

A
  • Multiple CYP P450 interactions
  • Most can be managed with mitigation strategy
  • Be aware of what statin uses what P450 pathway
  • DO NOT USE GEMFIBROZIL
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78
Q

Atorvastatin. List brand name, CYP and pt education

A

Lipitor; 3A4 (not as much as lova and simva); can take any time of day, avoid grapefruit juice; high intensity statin

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79
Q

Rosuvastatin. List brand name, CYP, and pt edu

A

Crestor; high intensity statin; 2C9; can take any time of day

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80
Q

Pitavastatin. List brand name, CYP, and pt edu

A

Livalo; 2C9 (minor 2C8); can take any time of day

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81
Q

Simvastatin. List brand name, CYP, and pt edu

A
  • Zocor; 3A4; take at bedtime, avoid grapefruit juice
  • Don’t use 80mg dose unless pt is already stable on it and not having ADEs (no new rxs for it bc so many ADEs)
  • Max dose if giving with amiodarone or amlodipine or ranolazine is 20mg

No more than 10mg simva daily with verapamil and diltiazem

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82
Q

Lovastatin. List brand name, CYP, and pt edu

A
  • Mevacor; 3A4; take at bedtime, avoid grapefruit juice
  • Max dose with diltiazem, verapamil, Danazol, or amlodipine is 20mg lova
  • max dose with amiodarone is 40mg lova
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83
Q

Pravastatin. List brand name, CYP, and pt edu

A

Pravachol; no CYP; take at bedtime

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84
Q

Fluvastatin. List brand name, CYP, and pt edu

A

Lescol; 2C9 (minor 2C8 & 3A4); take with evening meal

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85
Q

Niacin. What ya know about it?

A

-Nicotinic acid inc HDL and dec TG
-Flushing from highest to lowest chance
IR > SR > ER
-Titrate niacin doses slowly
-Take 325mg enteric coated aspirin 30 min before taking niacin to minimize flushing
-Tolerance to flushing will inc over time
-Take with food
-If miss a dose, just skip it

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86
Q

Niacin safety and monitoring

A

-Associated with hepatotoxicity (usually w/SR)
-Inc BG (watch in DM pts)
-Gout (esp big toe; too much uric acid)
-Monitor at baseline, up-titration, q6months
—LFTs
—Fasting BG or A1c
—Uric acid
-Don’t use if LFTs > 2-3x ULN (she will provide this info) or if persistent severe cutaneous symptoms, hyperglycemia, acute gout, unexplained ab pain/GI symptoms or if new onset of A-fib or weight loss

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87
Q

BAS basic info and dosing

A

-Can inc TGs
-Bind in GIT, trap cholesterol, and excrete it
-Colestipol (Colestid)
—5-20g (max 30g) [powder and tab]
-cholestyramine (Questran, Prevalite)
—4-16g (max 24g) [powder]
-colesevelam (Welchol)
—2.6-3.8g (max 4.4g) [powder and tab]

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88
Q

BAS pt edu

A

-Mix with non-carbonated beverages (juice, milk, water)
-Add drink to powder and drink immediately
-Drink before meals BID
-Drink a large glass of water with tablets
-Titrate dose to minimize side effects (should lessen over time)
-Dose must be separated from other meds
—Take other meds 1 hr before or 4 hrs after (select all that apply Q)

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89
Q

BAS ADEs and associated conditions

A

Associated with

  • Pancreatitis
  • GI upset
  • Multiple drug interactions (absorption)

ADEs
-Constipation, abdominal pain, bloating, fullness, nausea, gas (less so with colesevelam)

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90
Q

BAS monitoring

A

-before starting, 4-6 weeks after starting, at 3 months, then every 6-12 months
—Fasting lipid panel
—Don’t use if baseline TG >/= 300 mg/dL
—Use with caution if TG 250-299
—Discontinue if TG > 400

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91
Q

CAI general comments, usual dose, and available preparations

A
  • Zetia (add on therapy. Not first line)
  • Generally well tolerated
  • Usual daily dose: 10mg
  • Available preparations: Zetia or Vytorin (combo with simva)
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92
Q

CAI monitoring, drug interactions, and ADEs

A

Monitor before starting and when clinically needed

  • LFTs
  • Discontinue if persistent ALT elevations >3x ULN

Drug interactions
-Gemfibrozil, cyclosporine, cholestyramine

Safety/ADEs
-No serious ADEs; arthralgia, diarrhea, possible gallstones (cholelithiasis)

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93
Q

Fibrates (meds, pt edu)

A
  • Gemfibrozil (Lopid)
  • Fenofibrate (Tricor)
  • Generally well tolerated

-Pt education
-Not all fenofibrate formulations are bioequivalent
-LoFibra, original Tricor (54 or 160mg) and Lipofen
—Take with food
-New tricor (48 or 145mg), Antara, or gemfibrozil
—Without regard to food
-Triglide
—Without regard to food; no chipped/broken tabs
-Trilipix
—Without regard to food; indicated with statins

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94
Q

Fibrates monitoring

A

-Before starting, within 3 months, then q6months
-MUST MAKE RENAL ADJUSTMENTS
SCr and eGFR
—Don’t use if eGFR < 30 mL/min
—Discontinue if eGFR dec persistently to = 30 mL/min
—If eGFR 30-59 mL/min, dose of fenofibrate shouldn’t exceed 54 mg/day

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95
Q

Omega 3 FAs

A

-Lovaza (rx)
-Fish oil supplements
—Dose: 2-4g EPA + DHA daily can dec TG by 35%
—Make sure dose is reached if taking OTC

Associated with

  • Fishy taste (refrigerate to minimize taste)
  • GI disturbances
  • Inc bleeding risk (minor)

Monitoring
-No labs required, confer with pts on side effects

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96
Q

Utilizing the Friedewald equation, calculate a patient’s LDL

A

Most cases, LDL is calculated not directly measured

  • LDL = TC - [HDL + (TG/5)]*
  • Equation is invalidated if TG >/= 400

Non HDL = TC - HDL

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97
Q

BP

A

amt of tension exerted by blood against the arterial walls measured in mmHg
Amt of force req for the heart to circulate the blood through the body

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98
Q

SBP

A

systolic; max blood pressure during ventricular systole (cardiac contraction)

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99
Q

DBP

A

minimal blood pressure in the vasculature at the end of diastole (cardiac relaxation)

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100
Q

Primary/Essential HTN

A 
Unknown cause 
No secondary cause IDed 
Abt 90% of htn pts 
Multifactorial 
Genetics may play a role
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101
Q

Secondary HTN

A 
Consequence of another disorder 
Could be result of… 
CKD**
Primary aldosteronism** 
Obstructive sleep apnea**
Cushing’s syndrome 
Aortic dissection 
Pheochromocytoma 
Pregnancy 
Thyroid disease 
drugs/substances 
Sudafed, amphetamines, BC bills, NSAID, Sodium, alcohol, cyclosporine
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102
Q

White coat HTN

A

Ambulatory blood pressure monitoring (ABPM)
Records bp at preset intervals over 24-48 hr
Used to confirm/exclude white coat htn

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103
Q

types of HTN

A 
Isolated systolic HTN (ISH) 
Isolated diastolic HTN 
Pulmonary htn 
Pseudohypertension 
Masked htn 
white coat HTN 
primary/secondary HTN
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104
Q

HTN Prevalence & Epidemiology

A

~33% of americans dx
Only about 54.4% of HTN pts at goal
Most common among AA, elderly, low socioeconomic classes
Normotensive adults >55 have 90% chance of developing htn in their lifetime

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105
Q

Normal BP & Tx options

A

<120 & <80

Lifestyle modifications for prevention

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106
Q

Elevated BP & Tx options

A

120-129 & <80

Lifestyle modifications

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107
Q

Stage 1 HTN & Tx options

A

130-139 or 80-89

Antihypertensive + lifestyle if ASCVD risk >/= 10%

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108
Q

Stage 2 HTN & Tx options

A

> /= 140 or >/= 90

Antihypertensives + lifestyle regardless of ASCVD risk

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109
Q

urgency/emergency BP

A

> /= 180 or >/= 120

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110
Q

Risk Factors for HTN

A 
Race
Family history 
Increased sodium or alcohol intake 
Obesity &amp; wt gain 
Sedentary lifestyle 
Diabetes 
Dyslipidemia 
Personality traits 
Vit D deficiency 
Smoking 
Secondary factors: drugs
111
Q

Complications of HTN

A

Major modifiable risk factor for premature CVD
Starting at 115/75 mmHg, CVD risk doubles with every 20 mmHg inc of SBP or every 10 mmHg inc in DBP

Strokes, headache, convulsion, elevated sugar lvl, hpertensive retinopathy, MI, HF, chronic renal failure

112
Q

Dx of HTN

A

Not based on single elevated measurement; Avg of two or more properly measured readings taken at two or more visits used

113
Q

Evaluation of HTN

A 
Physical exam 
Lab testing (Urinalysis, Lipid panel, TSH, EKG)
114
Q

Goals of Tx for HTN

A

Reduce HTN associated morbidity & mortality
Dec: CVD, renal dz, MI/Stroke, HF

BP goal
<130/80

115
Q

Lifestyle modifications HTN

A

Lower BP in ALL HTN/elevated BP pts
w/ normal bp: encourage following lifestyle modifications for prevention
Wt reduction, DASH, dec sodium intake, inc potassium, physical activity, moderation of alcohol consumption (1.5 oz liquor, 5 oz wine, 12 oz beer)
DASH: dietary approaches to stop HTN diet
= 2300 mg sodium to lower; = 1500 mg lowers further
=1500 mg sodium recommended for…
Pt with HTN, DM, CKD, AA, age 51+

116
Q

Volume depleters (Diuretics) HTN

A

Thiazide & Thiazide-like
Loops
K+ sparing
Ald Antag

117
Q

Thiazide & Thiazide-like HTN ADE

A

HCTZ, Chlorthalidone

Doses > 50 don’t show much more dec in BP but inc ADE

Electrolyte disturbances 
Hyperuricemia (may precipitate gout) 
Hyperglycemia, glucose intolerance 
Sexual dysfx 
Rare cross-reactivity with sulfa allergies 
May inc lipids at higher doses
118
Q

HTN: Thiazide and Thiazide-Like Monitoring & Pt Edu

A 
Uric acid level (usually <6) 
BG
Electrolytes
Lipids
GFR

EDU: Take in morning; Watch for cramps/muscle weakness

119
Q

HCTZ (HTN)

A

(Microzide, Hydrodiuril) – 12.5-25 mg / day

Does not work as well at eGFR < 30

120
Q

Chlorthalidone

A

(Thalitone) – 12.5-25 mg / day

Preferred over HCTZ
Works okay for eGFR > 10 (no adj req)
Longer t1/2
Proven dec in CVD risk

121
Q

HTN: Thiazide and Thiazide-Like MOA

A

Inhib Na reabs in DCT → inc excretion of Na, H2O, and K
Dec SBP by 15-20 mmhg
Dec DBP by 5-10 mmhg

122
Q

(HTN) Loops MOA

A

Block Na/K/Cl cotransport in thick ascending limb of loop of henle
Reserved for pts with co-existing renal insufficiency or HF (fluid overload)
Can push a loop until you get the diuresis you need BUT unlike thiazides, people don’t get used to loop diuresis

123
Q

(HTN) loops ADE

A

Electrolyte disturbances (hypokalemia most often)
Watch for cramps/muscle weakness as sign
Only need to supplement K if pt is actually low
Hyperuricemia: may precipitate gout

124
Q

Furosemide (loop, HTN)

A

(Lasix) 20-80 mg/day (divided doses)

125
Q

Bumetanide (loop, HTN)

A

(Bumex) 0.5-4mg/day (divided doses) 40x more potent than furosemide

126
Q

Torsemide (loop, HTN)

A

(Demadex) 5-10mg/day

127
Q

Loop (HTN) monitoring

A

Sulfa allergy
Electrolytes, esp K
Dehydration

128
Q

Loop pt edu (HTN)

A

Take qam and early afternoon to avoid nocturnal diuresis (don’t recommend taking after 6pm)
Watch for cramps/muscle weakness

129
Q

Potassium sparing diuretics (HTN) MOA

A

Block Na channels from late distal convoluted tubule to collecting duct
Dec intracellular Na —> K retention and dec Ca, Mg, and H excretion
Directly inh K secretion

130
Q

When to use K sparing in HTN

A

If previous diuretic tx caused hypokalemia (counteracts K wasting with thiazides)
Triamterene/HCTZ (Maxzide/Dyazide) 37.5/25mg (both)
Maxzide 75/50mg
Dyazide 50/25mg
AVOID in pts with eGFR <45

131
Q

Triamterene (k sparing, HTN)

A

(Dyrenium) 50-100mg/day

132
Q

Amiloride (k sparing, HTN)

A

(Midamor) 5-10 mg/day

133
Q

(HTN) K sparing ADEs

A

Electrolyte disturbances
Gynecomastia
Come back within 1 month to see if working/ADEs

134
Q

K sparing monitoring parameters & pt edu (HTN)

A 
Electrolytes
Renal function (eGFR <45)

edu:
Take in morning; avoid excessive K intake

135
Q

Aldosterone antagonists MOA & ADE (HTN)

A

In distal renal tubules; inc NaCl and water excretion while conserving K and H ions

ADE: Electrolyte disturbances (hyperkalemia)
Gynecomastia (spironolactone)

136
Q

Ald antag monitoring (HTN)

A

K, Na, renal fx
K should be <5 when starting therapy**
Bc K levels will inc so don’t want too high even before therapy starts

Not recommended with CrCL <30 mL/min in general population. Why?
Not going to work as well. If not clearing quicker, hold onto drug, inc risk of arrhythmias (get baseline K)

137
Q

Ald antag pt edu (HTN)

A

Take qam; watch for cramps/muscle weakness

138
Q

Spironolactone (ald antag, HTN)

A

(Aldactone) 50-200mg/day

139
Q

Eplerenone (ald antag, HTN)

A

(Inspra) 25-100mg/day

140
Q

Adrenergic inhibitors (HTN)

A

(Peripheral, central, alpha/beta receptors)

141
Q

Betaxolol (HTN)

A

(Kerlone)

cardioselective b-blocker

142
Q

Bisoprolol(HTN)

A

(Zebeta) 2.5-10mg/day

cardioselective b-blocker

143
Q

Esmolol(HTN)

A

iv only

cardioselective b-blocker

144
Q

Acebutolol(HTN)

A

Sectral

cardioselective b-blocker

145
Q

Metoprolol(HTN)

A

(Lopressor, Toprol XL) 50-400mg/day

cardioselective b-blocker

146
Q

Atenolol(HTN)

A

(Tenormin) 25-100 mg/day

cardioselective b-blocker

147
Q

Nebivolol(HTN)

A

(Bystolic) 5-40 mg/day

cardioselective b-blocker

148
Q

B-blockers

149
Q

Cardioselective B-blockers

A

MANBABE or BBEAMAN

betaxolol, bisoprolol, esmolol, acebutolol, metoprolol, atenolol, nebivolol

150
Q

non-selective b blockers

A

nadolol, propranolol, timolol

151
Q

Nadolol (HTN)

152
Q

Propranolol (HTN)

A

Inderal) 40-480 mg/day

153
Q

Timolol (HTN)

A

(Blocadren)

154
Q

beta & alpha 1 blockers

A

carvedilol & labetolol

155
Q

Carvedilol (HTN)

A

(Coreg) 12.5-50mg/day

156
Q

Labetalol (HTN)

A

(Trandate) 200-2400 mg/day

157
Q

Beta blocker MOA HTN

A

Inh beta-adrenergic receptors —> dec CO and dec renin release —> dec peripheral vascular resistance
Dec HR/FOC/AV conduction rate
Not usually first line unless co-morbid conditions
Taper to discontinue
Bc up regulation —> reflex tachycardia
May mask signs of hypoglycemia (EXCEPT sweaty palms)

158
Q

Beta blocker ADEs

HTN

A

Bradycardia
Bronchial constriction (at high dose, even cardio selective do this bc lose selectivity)
Discontinuation syndromes (rebound tachycardia)
CNS fatigue/insomnia/depression/bizarre dreams
Sexual dysfunction (Not in Bystolic bc inc NO production)
Worsening depression
Weight gain
Exercise intolerance

159
Q

Beta blocker cautions (HTN)

A

Bradycardia
Diabetics (tight glycemic control)
Asthma/COPD
Noncompliance

160
Q

Beta blocker contraindications

HTN

A 
HR < 60bpm
SBP <90 mmHg
Severe asthma
Heart block
Acute decompensated HF
161
Q

Beta blocker monitoring

HTN

A

HR (want slower but not too much slower to where clots form and then it gets pumped somewhere and causes heart attack or stroke)

162
Q

Beta blocker counseling points

HTN

A

Pts with diabetes- monitor BG

Compliance to avoid rebound HTN

163
Q

Antihypertensive agents are almost equally _______, producing good antihypertensive response in ___ to ___ % of pts

A

Efficacious; 30-50%

164
Q

Selection criteria for Tx for HTN

A
  • Indication & Contraindications

- Allergies, past medical history, comorbidities, pt preference, etc

165
Q

If monotherapy is warranted in HTN in the absence of comorbidities, what are the preferred drugs to start with due to improved CV endpts?

A
  • Thiazide-like diuretics, or DHP CCB (FIRST LINE)

- ACEI/ARB are also acceptable for monotherapy

166
Q

When is combo tx initially preferred? HTN

A

Stage 2 HTN

ASCVD risk >/= 10%

167
Q

What do you typically start with to treat HTN?

A

Thiazide or ACEI/ARB or DHP CCB (or a combo of these)

168
Q

What do you typically start with to treat HTN in AAs?

A

Thiazide or DHP CCB

169
Q

HTN Treatment initiation therapy dependent factors

A 
CVD risk
Safety
Efficacy
Tolerability 
Cost
Pt centered concerns
Degree of HTN lowering needed
170
Q

HTN Tx initiation: general non-black population

A

Thiazide or DHP CCB or ACEI/ARB

171
Q

HTN Tx initiation: general black population

A

Thiazide or DHP CCB

172
Q

HTN Tx initiation: if BP >20/10 above goal

A
  • Use combo therapy
  • ACEI/ARB + DHP CCB (ACCOMPLISH trial)
  • Thiazide + ACEI/ARB or DHP CCB
173
Q

HTN w/o Compelling indications

A

Tx based on the degree of elevated BP

174
Q

Stage 1 HTN (without compelling indications)

A

-Monotherapy
-Thiazide, ACEI/ARB, CCB (thiazide = most common)
—CCB and thiazide are equally best… use before ACEI/ARB
-IF AA → THIAZIDE OR CCB

175
Q

Stage 2 HTN (without compelling indications)

A

-2-drug combo including a thiazide (Thiazide + ACEI/ARB/CCB)
-Doses should be titrated & addn drugs added until goal BP achieved
-Combo pdts used to dec pill burden & improve compliance
Ex: lisinopril/HCTZ, losartan/hctz, olmesartan/amlodipine

176
Q

General HTN Tx Approach

A
  • Initiate tx if BP > goal
  • If monotherapy → thiazide or DHP CCB
  • If two drugs → Thiazide & ACEI/ARB or Thiazide & CCB or CCB & ACEI/ARB
  • If AA with combo tx → one needs to be DHP CCB or Thiazide → doesn’t have to be both though
177
Q

HTN w/ Compelling Indications

A

-Amend initial tx in presence of underlying condn requiring specific antihypertensive agents independent of BP control
-Require certain antiHTN drug classes for high risk cond
—Drug selection for compelling indications is based on favorable outcomes from clinical trials
—Combination of agents may be required

178
Q

HF (compelling indication w HTN ) (ACEI/ARB)

A

ACEI/ARB to inhibit cardiac remodeling → ACEI preferred over ARB
-If using ARB: valsartan, losartan, candesartan have best evidence for dec preload/afterload

179
Q

HF (compelling indication w HTN ) (BB)

A

B-Blocker: monitor HR (<60bpm = too low)

-Use CASH MONEY BILLIONAIRES only: metoprolol succinate (Toprol XL), Carvedilol, Bisprolol

180
Q

HF (compelling indication w HTN ) (Other drugs besides ACE/ARB/BB)

A

-ALD antagonist: eplerenone or spironolactone
-Loops: for fluid overload → good with dec GFR; keep inc dose until fluid overload is dec, then dec dose while still in hosp
—Improves symptoms & exercise tolerance
—DOES NOT IMPROVE MORBIDITY AND MORTALITY
-Thiazides: not useful for monotx, but useful add-on for diuretic resistance
—Metolazone (good w/ low GFR for combo tx)

181
Q

IN AA PT WITH HF (w HTN)

A

Bidil (isosorbide dinitrate/hydralazine) recommended

  • Added to standard tx with b-blocker and ACEI in AA pt that is persistently symptomatic
  • Also for pts who cannot tolerate ACEI/ARB
  • Reduces mortality but to a lesser extent than ACEI
182
Q

Stable Ischemic Heart Dz (compelling indications w HTN)

A
  • B-blocker, ACEI/ARB, and thiazide have evidence for prevention of CV complications of HTN
  • Choice of agent depends on… compelling indications, dz states, tolerability
  • Can substitute long-acting non-DHP CCB (verapamil XR/diltiazem XR) for B-blocker to dec contractility & HR
  • May add on DHP CCB in chronic stable angina → but not if on non-DHP already
183
Q

Post MI therapy (Stable Ischemic Heart Dz; compelling indication)

A

-B-blockers → reduce reinfarction & sudden death
—Dec recurrence of CV events, improve O2 supply/demand ratio, most beneficial in first 3 yr

-ACEI → reduce risk of death, hospitalization, recurrent MI, progression to HF, inhib cardiac remodeling

-Can add DHP-CCB or ald antag
—Eplerenone if MI + HF

-Most common tx: B-Blocker, ACEI, + Statin post-MI

184
Q

Diabetes (compelling indication w HTN) (what it causes)

A
  • Most common cause of ESRD
  • HTN is second most common cause of ESRD
  • Intensive BP control in DM pt significantly reduces complications
185
Q

TX of DM w/ HTN

A

-All first-line agents
-Usually start with ACEI/ARB → ACEI = some renal protection
—Decrease progression of diabetic nephropathy and reduce albuminuria
—MUST USE IF PT ALREADY HAS ALBUMINURIA
-RAAS Drugs & CCBS → improve and/or do not worsen insulin sensitivity
-B-Blocker → may worsen insulin sensitivity; can mask hypoglycemia symp
-Diuretics → hypokalemia & worsening glucose tolerance

186
Q

CKD (compelling indication w HTN)

A

-CKD → eGFR <60; presence of albuminuria
-ACEI/ARBs (CKD w HTN)
—Limited rise in SCr
—Used in CKD pt with stable renal Fx

187
Q

Secondary Stroke Prevention (compelling indication w HTN)

A

-Pt with stroke usually only med compliant for ~3mo
-AntiHTN tx reduce risk of stroke by 30-40%
-Ischemic stroke
—Considered form of HTN associated target-organ damage

188
Q

First line monotherapy for Secondary Stroke Prevention (compelling indication w HTN)

A

ACEI/ARB or Thiazide

189
Q

Combo tx for Secondary Stroke Prevention (compelling indication w HTN)

A

ACEI + thiazide preferred

Also okay → ACEI + CCB

190
Q

When to treat HTN in pts with prior stroke but previously untreated for HTN

A

Do not start tx unless BP > 140/90

191
Q

HF (compelling indication w HTN Tx summary)

A

ACEI/ARB + BBlocker

If fluid overload → Loop → thiazide for resistance

192
Q

Stable Ischemic Heart Dz (compelling indication w HTN Tx summary)

A

ACEI/ARB + BBlocker

193
Q

DM (compelling indication w HTN Tx summary)

A

ACEI/ARB if albuminuria

CCB, thiazide

194
Q

CKD (compelling indication w HTN Tx summary)

195
Q

Secondary Stroke Prevention (compelling indication w HTN Tx summary)

A

ACEI/ARB and/or Thiazide

Tx HTN if BP > 140/90

196
Q

Pregnancy (in HTN)

Define and list drugs

A

-Chronic HTN: high BP prior to pregnancy or diagnosed before 20th week gestation
-If antiHTN taken prior to pregnancy, transition to methyldopa (DAVD), long acting nifedipine, hydralazine (DAVD), and/or labetalol
—All shown safe in pregnancy
—Do NOT use ACEI/ARB or direct renin inh

197
Q

Pregnancy in HTN recommendations (not specific drugs)

A

-Recommend HTN tx if severe (SBP >/=160; diastolic >/= 110)
—Should dec risk of maternal stroke/pre-eclampsia
-Goal BP during pregnancy not clearly est
-Overall goal: minimize short term HTN risks to mother while avoiding potentially harmful therapy to fetus

198
Q

Older adults (in HTN) prevalence and drugs

A

-HTN prevalence inc with age
—65+ pt more likely to have CVD and renal insufficiency
—80+ significantly inc risk of isolated systolic hypertension

-ISH: thiazides or long acting DHP-CCB is first line
—Nifedipine preferred but most use amlodipine
—May also use ACEI/ARBs
—BB less efficacious as initial agents in elderly

199
Q

Older adults (in HTN) ADEs and dosing

A

-Predisposed to orthostatic hypotension from volume depletion and sympathetic inhibition
—Usually initiate with DHP-CCB, with addition of ACEI/ARB or diuretic if needed
-Lower starting doses and slower titrations to prevent ortho hypo

200
Q

Children and adolescents in HTN (facts)

A

-CANT USE INDAPAMIDE IN CHILDREN (18+ only)
-HTN defined as BP >95 percentile according to gender, age, and height on at least 3 occasions
—Secondary HTN (most commonly renal disease) is most common cause
—Essential HTN is second most common cause in children 11+ yo

201
Q

Children and adolescents in HTN (tx)

A

-Start with lifestyle changes then drug therapy in essential HTN
-drug therapy usually required for chronic secondary HTN
—Thiazide, ACEI/ARB, CCB are acceptable choices
—Avoid ACEI/ARBs in sexually active females
—Counsel on sexual side effects in younger male pts

202
Q

AA in HTN (basic facts and tx)

A
  • Affected at higher rate and target-organ damage is more prevalent
  • Inc need for combo therapy to reach BP goals
  • most effective: thiazides and DHP-CCBs as mono therapy (-ipines)
  • Combo of thiazide or CCB with ACEI/ARB/BB has significant inc antiHTN response
  • Inc risk of angioedema and cough from ACEI
203
Q

AntiHTN compliance

A 
HTN is chronic asymptomatic disease
Monitor BP response
Question pts about how they take meds
Pill counts
Monitor freq of refills
204
Q

How to improve HTN med compliance

A

Maintain pt contact
Keep med regimens simple and inexpensive
Dec BP slowly to dec adverse symptoms

205
Q

AntiHTN pt edu

A

-Benefits and ADEs
-Awareness of normal and abnormal BP
-Consequences of uncontrolled BP
-Need for chronic therapy
—Meds control BP without curing disease
-Benefits of lifestyle modifications and setting realistic goals

206
Q

PCP of HTN: collect

A
  • Pt characteristics (age, race, sex, pregnant)
  • Pt history (personal medical, family, social like eating habits/drinking/tobacco use)
  • Home BP readings
  • Current meds/any history of antiHTN use
  • BP, HR, height, weight, BMI
  • Electrolytes, SCr, BUN, lipid panel, glucose, ECG
207
Q

PCP of HTN: assess

A

Compelling indications
HTN related complications
10 yr ASCVD risk if indicated
Current meds that may cause/worsen HTN
BP goal and if it’s been achieved
Is current antiHTN regimen appropriate and effective
For resistant HTN if taking 3 or more antiHTN meds

208
Q

PCP of HTN: plan

A

-Tailored lifestyle modifications and weight mgmt
—Heart healthy diet; 150 min/wk of moderate to vigorous exercise
-Drug therapy regimen including specific antiHTN, dose, route, frequency, and duration; specify if need to continue/stop
-Monitor parameters including efficacy (BP, CV events, kidney health), safety (ADEs), timeframe
-Pt edu
-Self-monitoring BP, HR, weight- where and how to record
-Referrals to other providers if needed

209
Q

PCP of HTN: Implement

A
  • Provide pt edu regarding all elements of tx plan
  • Use motivational interviewing and coaching to inc adherence
  • Schedule follow up
210
Q

PCP of HTN: monitor and evaluate

A
  • Determine if reaching BP goal
  • Presence of ADEs
  • Occurrence of CV events and development/progression of kidney impairment
  • Pt adherence to tx plan using multiple sources of info
211
Q

Treatment of HTN crises (Define HTN crises)

A
  • HTN crises: clinical syndromes when severe HTN results in irreversible end-organ damage or death over a short period of time if untreated
  • Diagnosis of HTN crises: absolute BP measurement, rate of BP rise, and presence of coexisting complications
212
Q

HTN urgency and emergency characterized by…

A

Very elevated BP (usually >180-120) with or without end-organ damage

213
Q

HTN urgency

A

-Asymptomatic and no signs of target organ damage
-Give clonidine (or labetalol, captopril, furosemide) in office, then they can return to normal regimen; out-pt
—Adjust maintenance therapy or add therapy
-If BP >180/120 without evidence of progressive end-organ damage
-BP needs to be lowered in hours to days, but not immediately
—Initial goal: BP <160/100 over a few hours-days
—MAP shouldn’t be lowered by more than 25-30% over this time period
-Re-evaluate within 1-3 days; no longer than a week

214
Q

List HTN urgency drug tx and ADEs (4 drugs)

A

Clonidine (go-to choice)
ADE: hypotension, drowsiness, dry mouth

Labetalol
ADE: bronchoconstriction; heart block, orthostatic hypotension

Captopril
ADE: hypotension, bilateral renal artery stenosis

Furosemide
ADE: hypokalemia

215
Q

HTN emergency

A

-Has target organ damage; give IV drugs
-If BP >180/120 with end organ damage that’s either progressive or present at initial evaluation
—Requires immediate treatment in ICU
-Goal to dec and maintain diastolic BP 100-110 for 1-2 days
-Usually systolic BP should be dec gradually by no more than 25% within first hour
-If pt is stable, dec BP to <160/100 over 2-6 hours then gradually dec to goal over 24-48 hours
-Start oral therapy once goal is met

216
Q

List HTN emergency drug tx and comments

A

Nicardipine; contraindicated in advanced aortic stenosis; no dose adj needed for elderly

Clevidipine; contraindicated in pts with soybean, soy product, EGG/egg products allergies and in pts with defective lipid metabolism. Use low end dose range for elderly
-Defective lipid metabolism: pathological Hyperlipidemia, lipoid nephrosis or acute pancreatitis

Esmolol; contraindicated in pts on BBs, have bradycardia, and/or decompensated HF (monitor for bradycardia; may worsen HF); higher doses may block B2 receptors and impact lung function in reactive airway disease

Labetalol; contraindicated in reactive airway disease or COPD; especially useful in hyper-adrenergic syndromes; may worsen HF and shouldn’t be given in pts with 2nd or 3rd degree heart block or bradycardia

217
Q

Signs of end-organ damage

A

CV findings: left ventricular hypertrophy (LVH), possible acute HF, pulmonary edema
-Increased O2 consumption, detrimental to pts with coronary artery disease

GI findings: N/V

218
Q

HTN crises goals of therapy

A

Lower BP at a safe rate

219
Q

What are effects of overly aggressive dec in BP? (3)

A

Dec cerebral blood flow
-May lead to cerebral ischemia (leading to seizures, coma, stroke)

Dec in coronary perfusion
-Possibly leading to MIs or arrhythmias

Dec in renal blood flow
-May lead to renal impairment/failure

220
Q

ARBs “sartans” Drugs and dosing (4)

A

Candesartan (Atacand) – 8-32 mg/day – daily

Olmesartan (Benicar) – 20-40 mg/day – daily

Valsartan (Diovan) – 80-320 mg/day – daily

Losartan (Cozaar) – 50-100 mg/day – daily BID

221
Q

ARB MOA and ACEI indications for switching

A

-Inhib AT1R & venous dilation

  • Alt tx for pts with ACEI cough or if they are not tolerated
  • Cross-reactivity in ACEI angioedema is < 10% so still an option
  • Cut starting dose in half if given with diuretic
222
Q

ARB ADEs

A

Angioedema, hyperkalemia, <3% cough, renal dysfx

223
Q

ARB contraindications

A

-Same as ACEI
-Absolute CI
—Pregnancy (2nd & 3rd trimesters)
—Angioedema
—Bilateral renal artery stenosis
-Relative CI
—Cough, hyperkalemia, volume depletion, unstable renal fx

224
Q

ARB monitoring

A 
Same as ACEI 
BP
Electrolytes
SCr
HR
BUN
Baseline LFT
225
Q

Alpha-1 blockers (HTN)

226
Q

Doxazosin (HTN)

A

(Cardura) 1-16 mg/day

Alpha-1 blockers

227
Q

Prazosin (HTN)

A

(Minipress) 2-30 mg/day
Also used to treat PTSD nightmares
Can cause unwanted erections
Alpha-1 blockers

228
Q

Terazosin (HTN)

A

(Hytrin) 1-20 mg/day

Alpha-1 blockers

229
Q

Alpha1 blockers MOA

HTN

A

Block activation of postsynaptic a1 receptors by circulating catecholamines —> vasodilation
Usually for pts with HTN and BPH (benign prostatic hyperplasia)

230
Q

Alpha1 blockers ADEs

HTN

A

First dose syncope
Temporary loss of consciousness from fall in BP
Tell pt to stand slowly to dec risk of orthostatic hypotension
Caution: fall risk in elderly

Headache
Drowsiness
Fatigue
Weakness

231
Q

Alpha-2 agonists MOA

HTN

A

Stimulate a2 receptors in brain —> inh release of NE centrally —> dec sympathetic outflow and inc vagal tone —> vasodilation —> dec HR, CO, systemic vascular resistance, and plasma renin activity
Most effective w/diuretic to dec fluid retention
**use with caution in elderly

232
Q

Clonidine (Alpha-2 agonists HTN)

A

Catapres, 0.1-2.4 mg/day

233
Q

Methyldopa (Alpha-2 agonists HTN)

A

(Aldomet) 250-3000 mg/day

234
Q

Clonidine: DOA, uses

HTN

A 
DOA: 6-8 hrs (relatively short)
Dosed BID or TID
Should NOT be given once daily at night
Potentially would rebound HTN in the morning
Good at lowering BP and doing it quickly
Also given for ADHD
Good for refractory HTN
Not recommended in pregnancy
235
Q

Clonidine ADE HTN

A

Sedation
Dry mouth
Rebound HTN
Patch: skin irritation

236
Q

Methyldopa: ADEs

in HTN

A 
One of safest drugs in pregnancy
Side effects usually make clonidine better choice unless pregnant
Somnolence (drowsiness)
Postural hypotension
Hemolytic anemia
Positive antinuclear antibodies
Fever
Liver dysfunction
237
Q

Vasodilators in HTN

A

direct vasodilators, CCB, ACEI, ARBs, Direct Renin Inhibitors

238
Q

Direct vasodilators MOA HTN

A

Smooth muscle relaxation for vasodilation
Saved for special conditions
Particularly pts with CKD who need additional BP control

239
Q

DAVD ADEs HTN

A 
Headache
Tachycardia
Lupus-like syndrome (hydralazine)
Fluid retention (Minoxidil black box warning: max out a diuretic and 2 other antiHTN first)
Hirsutism (minoxidil)
240
Q

Hydralazine

A

(Apresoline) 10-300 mg/day

DAVD

241
Q

Minoxidil

A

(Loniten) 5-100 mg/day

DAVD

242
Q

CCB for HTN classes

A

DHPs (ipines) & Non-DHPs

243
Q

DHP CCB for HTN monitoring

A

Less effect on HR than non-DHPs

Monitoring
HR, Edema, LFTs (since hepatic elim)

244
Q

Amlodipine

A

(Norvasc) – 2.5-10 mg/day

DHP CCB

245
Q

Nifedipine LA

A

(Procardia XL, Adalat CC) – 60-120 mg/day

DHP CCB

246
Q

Clevidipine

A

IV only

DHP CCB

247
Q

Which DHPs are first gen, second gen, and third gen?

A

1st gen: nifedipine
2nd gen: isradipine, nicardipine, felodipine
3rd gen: amlodipine

248
Q

Non-DHPs MOA for HTN

A

Less peripheral and coronary arteriolar vasodilation, mostly neg inotropic and chronotropic effects (prefer XR in HTN tx)
Given more for arrhythmia and angina than in DHPs
Verapamil > diltiazem

Not first line therapy for HTN

May reduce proteinuria in pts with CKD

249
Q

Which non-DHP is a phenylalkylamine? A benzothiazepine?

A

Phenylalkylamine: verapamil
Benzothiazepine: diltiazem

250
Q

What are the cardiac and vascular effects of non-DHPs?

A

Cardiac: dec contractility, dec HR, dec conduction velocity
Vascular: relax smooth muscle

251
Q

Verapamil

A

nonDHP CCB

(Verelan, Calandras): 120-480 mg/day

252
Q

Diltiazem

A

(Cardizem, Cartia, Taztia): 180-360 mg/day

NonDHP CCB

253
Q

Non-DHP contraindications

A

2nd and 3rd degree heart block
Cardiogenic shock
Acute MI (diltiazem)
Systolic heart failure

254
Q

CCB ADEs htn

A 
Bradycardia
Tachycardia (nifedipine) 
Heart failure exacerbation
Constipation (mainly in verapamil)
Peripheral edema (esp Amlodipine 10)
Gingival hyperplasia (swollen gums)
AV node block
Hypotension (postural; get up slow) 
Reflex tachycardia (mostly nifedipine)
Headache &amp; Flushing (esp nifedipine from inc vasodilation) 
GERD
Fatigue
255
Q

CCB monitoring in HTN

A

HR
BP
EKG
LFTs

256
Q

What is not a counseling point for pt recently started on chlorthalidone?

A

May dec BG in diabetes (wrong bc CAN impact BG)

257
Q

Which condition is NOT a common side effect of nifedipine?

A

Constipation (more common in verapamil)

258
Q

ACEI useful in what comorbid conditions w HTN

A

HF
High CVD risk
Diabetic pts

259
Q

how to change start dose of ACEI in pt with HTN and taking diuretic

A

cut starting dose in ½

Start low and titrate up

260
Q

ACEI MOA (HTN)

A

Inhib ACE from converting ang I to ang II → vasodilation

261
Q

Benazepril

A

(Lotensin) – 10-40mg/day – daily BID

ACEI

262
Q

Captopril

A

(Capoten) – 12.5-150 mg/day – daily BID

ACEI

263
Q

Enalapril

A

(Vasotec) – 5-40mg/day – daily BID

ACEI

264
Q

Lisinopril

A

Prinivil, Zestril) – 10-40mg/day – daily

ACEI

265
Q

Contraindications for ACEI use in HTN

A

Absolute CI
Pregnancy (2nd & 3rd trimesters)
Angioedema
Bilateral renal artery stenosis

Relative CI
Cough, hyperkalemia, volume depletion, unstable renal fx

266
Q

ACEI monitoring in HTN

A 
BP
Electrolytes
SCr
HR
BUN
Baseline LFT
267
Q

Direct renin inh drug and MOA

A

Aliskiren (Tekturna) 150-300mg/day
Inh conversion of Ang I to Ang II by directly inh plasma renin activity
CYP3A4 substrate so watch for drug interactions

268
Q

Direct Renin inh ADEs

A 
Cough
Hyperkalemia
Elevated CK (muscle pain)
Dizziness
Diarrhea
Angioedema (switch pt off of all drugs that affect RAAS pathway)
269
Q

Direct Renin inh contraindications

A

Pregnancy

Taking other ACE-I or ARBs in diabetics

270
Q

Direct renin inh monitoring

A 
K
Renal function (BUN, SCr)
271
Q

Direct renin inh pt edu

A

Admin at same time every day consistent with regards to meals
High fat meal reduces abs
Renin inh have been reported to cause bradycardia but don’t know MOA

272
Q

What is a more common side effect of aliskiren?

273
Q

What are effects of blocking the response to beta-adrenergic stimulation?

A

Inc central sympathetic output

274
Q

Hypokalemia is NOT a possible ADE in which diuretic?

A

Eplerenone

Pharmacotherapy 1 (2 decks)

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