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Chem and physics > Pharm Exam 1: Section 2 > Flashcards

Pharm Exam 1: Section 2 Flashcards

1
Q

Renin Angiotensin System
Maintains homeostasis in euvolemic state
Stimulated in low volume or low O2 state –> Sympathetic NS

A

Kidneys hold onto sodium and create thirst which increases volume and smooth muscle contraction
Increases BP and increases tissue perfusion in arterioles
If local tissue injury, A2 arrives and promotes vascular inflammation
Remodeling of cardiac and vascular tissues in myocardium occurs
Increased fibrous products in tissues –> hypertrophy
Hypertrophy –> CHF

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2
Q 
ACEI
Benzapril 
Captopril 
Enalapril 
Lisinopril

ARBS
Losartan
Valsartan

A

ACEI block Ace enzyme to prevent conversion of A1 to A2

ARBS don’t work on A2, work to block receptors for A2 at tissue level

Bradykinin: at high levels in lung –> cough
Prostaglandins: ACEI -> angioedema

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3
Q

ACEI and black people

A

Black people make less renin than other groups

ACEI less effective

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4
Q

ACEI & ARBS

How they work

A

Decrease production of A2 and aldosterone
Prevent vascular smooth muscle contraction -> decrease afterload (arteries)
Decrease Na and H2O retention in kidney -> decrease preload (veins) - less volume in system
Reduce vascular inflammation & remodeling bc A2 and its mechanisms are blocked
Aldosterone tells kidney to hold onto Na and K -> H2O follows salt - > increased volume. ACEI and ARBS block this mechanism

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5
Q

ACEI & ARBS

Pharmacokinetics

A

Well absorbed PO; better on empty stomach. Ok with food
Most are prodrugs (not active in own form but when they get to liver, they break down into metabolites that are active form)
* Must be used in people with intact hepatic system
* lisinopril & captopril not prodrugs

Used alone and in combo with diuretics -> tends to improve efficacy

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6
Q

ACEI & ARBS

Pharmacokinetics

A

Renal protection: decrease arterial resistance in glomeruli; when blood comes through kidney

Mild Insulin sensitization: ACEI & ARBS help cells recognize and use insulin- good for DM

Most excreted renal: used in pts w/ early renal failure and microalbuminuria in DM. If pt has more advanced renal failure, start at low dose, check electrolytes in 1 week to ensure no high K

Distributed to all tissues except CNS
Cross placenta, are in breast milk.

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7
Q

ACEI & ARBS

Adverse reactions

A

No reflex tachycardia bc no impact on CO

Hypotension

High K if dose too high

Cough: dry; don’t give another ACEI, can try ARB
-Cross -sensitivity so can happen with ARBS

Angioedema: typically when combined with other drugs like macrolides (zpack)

  • Occurs in face, mainly lips and mouth, sometimes forehead
  • If occurs, stop macrolide, stop ACEI for a couple of days
  • If just on ACEI, stop and start a different BP med; give antihistamine bc its a localized reaction
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8
Q

ACE & ARBS

Contraindication

A

ARBS excreted fecally more than renal
Cause with other BP meds
C/I in pregnancy; Category C

  • avoid K+ sparing diuretics bc ACEI causes changes with Na and K
  • If K is high in ACEI, double check, if still high -> reduce dose a little bit
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9
Q

ACE & ARBS

indications

A

HTN (esp w/ DM): 1st line agent
1st line for DM bc of renal protection

CHF: A2 and inflammation, remodeling -> cardiac changes; preload reducer, afterload reducer

Microalbuminuria: >19 is pathological; reason pts with DM but not HTN might be put on low dose ACEI or ARBS –> decrease arterial deconstruction in kidneys; helps improve perfusion bc less pressure in kidneys

Post MI, ACS, LVEF <40%

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10
Q

ACEI & ARBS

Monitoring

A

Potassium: make sure not elevated in first week and check again in 1 month

Angioedema esp w. macrolides
Don’t prescribe macrolide w/ ACEI if pt has infections

Check liver function

Check renal function

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11
Q

CCB

A

Most potent class of BP reduction

Nondihydropyridines: Type 1 receptors
- verapamil and diltiazem

Dihydropyridines: Type 2 receptors
- pines

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12
Q

CCB

Mechanism of action

A

Inhibit Ca+ movement at smooth muscle cell membrane

  • Arterial vasodilation
  • Decreased contractility
  • Decreased afterload
  • No impact on preload (no venous impact)

Nondihydropines: slow AV node conduction; verapamil can be given sublingual; monitor BP closely; slow HR

Dihydropines: vasodilator; little/no effect on HR; may cause reflex tachycardia if BP drops too low

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13
Q

CCB

Pharmacokinetics

A

All absorb well PO, OK with food

Nondihydropines
- rapid metabolism and bioavailability quickly (verapamil)

Dihydropines: varying ,metabolism and absorption
- Amlodipine 65-90%: well absorbed; high metabolism (works quickly), long half-life
Isradipine 15%: poor absorption and bioavailability

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14
Q

CCB

Pharmacokinetics

A

Rarely cross blood brain barrier; don’t have sedative properties
All cross placenta
Excreted in breast milk, except Nifedipine
Hepatic metabolism: broken down in liver
Fecal and renal excretion
Short 1/2 life if not sustained release formulation; need to be taken multiple times daily
Norvasc (amlodipine): long half life; good agent to use for daily dosing

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15
Q

CCB

Adverse reactions

A

Nondihydropine: chronotropic effect - low HR and arrhythmia related to low HR or alteration in conduction or velocity

Peripheral edema: vasodilation lets blood pool -> vascular permeability; elderly more prone

Constipation: gut is primarily smooth muscle; effects musculature and contraction of gut; peristalsis slows; elderly more prone

Worsen GERD - interferes with muscle contraction of lower esophageal sphincter -> increased reflux

Flushing, HA, low BP, edema, reflex tachycardia

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16
Q

CCB

A

Sustained release formulas are most effective; most predictive metabolism and lowest rate of side effects; most predictive bioavailability; long acting prevents BP fluctuations

Amlodipine: not sustained release; long acting and stable when crushed (good for pt w/ dysphasia); not excreted quickly; can be given once daily

C/I in pt w/ HF!!! Not used immediately post ACS. Can worsen wolf Parkinson white syndrome (conduction disturbance)

Category C
Amlodipine Category D

Check hepatic function before therapy: metabolized almost entirely in liver

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17
Q

CCB

Indications

A

Tachycardia dysrhythmias
-rate control for SVT, afib, (verapamil & diltiazem)

HTN

migraine prophylaxis (30% improvement)

Vasospastic angina (stable) bc of vasodilation effects

Raynauds: peripheral arterial spasms in cold weather; vasodilation

Esophageal spasm: lower esophageal sphincter relaxes w/ vasodilation of smooth muscle

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18
Q

Diuretics
Thiazides
Loop diuretics
K+ sparing

A

Decrease volume
decreased preload
decreased pressure arterial bed

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19
Q

Diuretics

Thiazides

A

Inhibit Na, K, Cl, and bicarb reabsorption in distal tubule of nephron. H2O follows electrolytes out of body.

Effect is increased Ca and uric acid

Electrolyte imbalance: low K
Increased glucose bc of dehydration

Muscle cramps: due to increased Ca, paresthesias, impotence.

Avoid in gout to prevent uric acid buildup

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20
Q

Diuretics

Thiazides

A

Chlorthalidone (Hygroton): very long 1/2 life (~50 hrs), very effective

Hydrochlorothiazide (Microzide, Hyrodiuril)

Indapaminde (Lozol)

Metolazone (Zaroxolyn): not as effective in pt with renal impairment; with gfr < 25 or low creatinine clearance NOT effective

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21
Q

Diuretics

Loop

A

Work in loop of Henle in kidney; action happens sooner in kidneys than later in tubules where thiazides work. Have more substantial diuretic effect; helpful for pt with kidney function impairment and low gfr

Furosemide (lasix)
Bumetanide (Bumex)

More substantial diuresis
0.5 - 1 hr 1/2 life

More K loss; will need to replace K more often than with thiazide

Indicated for edema with CHF

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22
Q

Diuretics

K sparing

A

Alter Na reabsorption in distal tubules in nephron further than where K is reabsorbed; reason K sparing diuretics let go of Na and not K

Triamterene
Spironolactone

Improve edema in CHF
Na depletion: watch for low Na
Avoid in ACE or ARB bc they hold onto K –> hyperkalemia

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23
Q

Diuretics

A

Preload reducers

Long term: reduce volume -> decreased SVR and afterload

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24
Q

Diuretics

Pharmacokinetics

A

Triamterene not absorbed as well as others. All effect electrolytes

Enter blood AND extracellular spaces

Liver metabolizes diuretics; Furosemide is both hepatic and non hepatic

All excreted in urine, some feces

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25
Q

Diuretics

Adverse reactions

A

Electrolyte imbalances

Glucose intolerance

Hyperuricemia: concern for gout pt

Dehydration and hypotension -> falls

Drug interactions

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26
Q

Diuretics

C/i

A

No K sparing diuretics in pt with renal impairment -> high K; Creatinine clearance < 25 - 30 avoid

Patients w/ gout: high uric acid -> flairup

High risk for falls: urge to go to bathroom is high

Dehydration

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27
Q

Diuretics

Indications

A

HTN: 1st line

Prevent CV complications: decrease volume and likelihood of developing CHF

Selection based EGFR
> mid 40s ml/min: Thiazides (good egfr)
< mid 40s ml/min: Loops (moderately low egfr)
If profoundly low send to nephrology

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28
Q

Diuretics

Indications

A

Edematous conditions
CHF: in addition to ACE (except K sparing)

Hepatic cirrhosis: abd ascites and lower extremity edema due to hepatic congestion

Renal impairment: Loop are most effective

Premenstrual edema: Gyn prescribes
Take 3-5 days before menses; stop once menses begins

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29
Q

Beta adrenergic blocker

“olol”

A

Beta 1: CV; SA node, atria, ventricles - increase HR or increase rate of contraction

Beta 2: Pulmonary; mediate smooth muscle contraction and constriction

Nonselective beta blockers: influence cells in lungs and in heart -> bronchiole smooth muscle contraction will exacerbate asthma symptoms

Nebivolol: most selective can affect poor metabolizers and not affect BP –> build up in system (not used often)

Atenolol: second most selective

Metoprolol: third most selective

All 3 have long half lives

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30
Q

Beta blockers

Mechanism of action

A

Prevent catecholamines (epi, norepinephrine) and beta agonists (albuterol) from binding to sites of activity

Receptor site located on CV, renal, opthalmologic, and respiratory systems

Some effect in pancreas and metabolism of fat -> elevated triglycerides and cholesterol and lower HDL
DM pts might have elevated hA1C bc of effect on pancreas

SA node to reduce HR to slow automaticity of heart

AV junction to reduce conduction velocity so impulse is not conducted quickly through junction

Atria and ventricles to reduce contractile force (negative isotropism) to decrease workload and O2 demand of heart

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31
Q

Beta blockers

Pharmacokinetics

A

Well absorbed PO, first pass metabolism

Widely distributed into tissues, placenta, and breast milk

CNS penetration with Timolol, Metoprolol, and Propranolol -> sedation

Nebivolol is very lipophilic, some CNS penetration -> some sedation

Hepatic metabolism

Excreted in bile, feces, urine

Nadolol, atenolol, and nebivolol require dose adjustments in diminished renal function; excreted in urine

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32
Q

Beta blockers

Adverse reactions

A

Bronchospasm: shouldn’t prescribe in pulmonary diseases

Most are pregnancy category C or D

Sotalol, Acebutolol, Pindolol are Category B

Metoprolol has very low excretion in breast milk; safer for breastfeeding mom

Rebound symptoms with discontinuation; taper slowly

Impotence: no erection, inability to maintain erection; beta blocker not first choice in men unless not sexually active (CHF)

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33
Q

Beta Blockers

Indications

A

Long term angina management

Rate control in dysrhythmias

Heart failure & HTN: reduce workload of heart and decrease O2 demand

Post ACS: reduce workload of heart and decrease O2 demand

Migraine prophylaxis, hyperthyroidism: tx of racing heart while leveling out thyroid levels

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34
Q

Beta Blockers

C/i

A

Pulmonary disease

AV block or sick sinus syndrome: slowed condition and prolonged PR intervals

Avoid in pt w/ DM or pre DM: will negatively impact glucose control

Children: atenolol and propranolol have approved dosing schedules

Induce cytochrome P2D6 which is used to metabolize Prozac and Paxil; pick a different SSRI if pt needs to be on beta blocker

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35
Q

Alpha Receptors
Sympathetic NS: fight or flight
Parasympathetic: Rest and relax

A

Alpha Receptors stimulated by norepinephrine (SNS) from brain

Alpha 1 receptors:

  • vascular walls, heart, eye, salivary glands, sphincters, Kidney, ureter, bladder, male sex organs
  • increased HR, increased urgency to void

Alpha 2 receptors:

  • arterioles of the skin and mucosa (dry mouth), pancreas
  • fat cells (inhibit lypolysis)
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36
Q

Alpha Agonists
Mechanism of action
Alpha 1

A

Alpha 1 agonists: epi and norepi signal heart, smooth muscle and CNS

Primary receptor on vascular smooth muscle: potent vasoconstrictor, increase HR

Naturally occurring catecholamines: epi, norepi, and dopamine

Nasal spray: oxymetazalone: typical decongestant -> spray in nare; phenylephrine

PO ephedrine: decreases nasal decongestion and treats bronchospasm in asthma; banned in 2003 due to risk of insomnia, stroke, HTN, urine retention

Pseudoephedrine: vasoconstriction in nasal passages and elsewhere in body; decreases nasal congestion but not used with HTN or arrhythmias
* must present ID to pharmacist to purchase due to use in making meth

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37
Q

Alpha Agonists
Mechanism of action
Alpha 2

A

Stimulate alpha 2 receptors in brain that activate inhibitory neurons to prevent release of norepi
Prevent/reduce central sympathetic tone

Inhibit cardiac acceleration and vasoconstriction centers in brain

Decrease peripheral outflow of norepi -> vasodilation
Decreased PVR, RVR, HR, BP

Compensatory effects: Na and H2O retention to increase volume -> edema in brain

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38
Q

Alpha 2 agonists

A

Clonidine (Catapres): PO or weekly patch; SL in hypertensive crisis; epidural by anesthesia

Guanabenz (Wytensin): not typically used

Methyldopa (Aldomet): can change central concentration in brain; affect tissue concentration in serotonin, dopamine, epi, norepi

  • prescribed for mood changes
  • preferred BP med for pregnant women; Category B
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39
Q

Alpha 2 Agonists

Pharmacokinetics

A

Methyldopa is most poorly absorbed

Methyldopa and clonidine enter brain

All are renally excreted

Methyldopa: Category B for pregnancy

Methyldopa and metabolites accumulate in renal failure and prolonged hypotension

40
Q

Alpha 1 Agonist

Adverse reactions

A 
Tachycardia
Increased cardiac workload
Increased O2 demand
Dysrhythmias
Headache
Sedation
41
Q

Alpha 2 Agonist

Adverse reactions

A

Xerostomia (dry mouth)
Hypotension
Sedation

42
Q

Alpha 1 agonist

Indications

A 
Sepsis
Anaphylaxis
Post CABG hypotension
Anesthesia induced hypotension
Nasal decongestion
43
Q

Alpha 2 agonist

Indications

A

Moderate of resistance HTN
Clonidine:
ETOH, opioid, heroine, tobacco withdrawal
Epidural
Hot flashes, decreases norepi rush to periphery causing vasodilation and decreasing increased HR with hot flashes

44
Q

Alpha Agonists

C/i

A 
Dry eye syndrome
Antipsych meds
TCAs, MAOIs, interact bc central acting
Beta blockers can cause malignant HTN
ETOH, benzos, antihistamines: poor choice bc central acting; Ok for withdrawal but NOT ok for people actively drinking alcohol
Caution:
Renal impairment
Recent MI
Severe CAD
Bc HTN and vasoconstriction can be life threatening if given
45
Q

Alpha Agonist

indications

A 
Low dose: renal low flow states (dopamine)
High dose dopamine: sepsis
Nasal decongestion
Hypotension
ETOH and drug withdrawal
Menopause
46
Q

Alpha blockers

Mechanism of Action

A

Indirect action: centrally acting in brain
* reduce sympathetic secretion of norepi

Direct action: peripheral action

  • block Alpha 1 receptors in blood vessels and relaxing them to decrease SVR
  • prostate and neck of bladder
47
Q

Alpha blockers

Non selective

A

Regitine (Phentolomine)
Dibenzyline (Phenoxybenzamine)

Reflex cardiac stimulation: cause reflex tachycardia

Rarely used except for Pheochromocytoma: tumor in adrenal gland -> dump huge amounts of epi

48
Q

Alpha blockers
Selective
“osin”

Doxazosin (cardura)*
Prazosin (minipress)*
Terazosin (Hytrin)*
Tamulosin (flomax)
Alfuzosin (urizatral)
Silodosin (rapaflo)*
A

Block effects of catecholamines in smooth muscle receptors: cause vasodilation

  • treat HTN and BPH

Tamulosin and Alfuzosin: very selective for subtypes in neck of bladder and prostate; increase outflow without increasing contraction. Cause smooth muscle at neck of bladder and around prostate area to relax so men with BPH can pee easier

49
Q

Alpha blockers

Pharmacokinetics

A

Impact both venous and arterial receptors: impact both preload and afterload

Reflex tachycardia with some pts

Improved lipid profiles and insulin sensitivity

Diastolic BP most profoundly effected: orthostatic hypotension common (1st dose): educated to take right before going to bed

Well absorbed PO
Metabolized in liver
Whole drug is inactive and when broken down, metabolites are active. Long lasting effects bc heavily bound to protein

Doxazosin has first pass metabolism in liver

Prazosin and terazosin have 3-4 active metabolites

Heavily protein bound, liver metabolism

50
Q

Alpha blockers

Adverse reactions

A

All accentuated with ETOH, nitrates or antihypertensive meds

Hypotension

Syncope

Reflex tachycardia

Fluid retention in periphery: effect on arterial and venous beds

Nasal congestion and dry mouth

51
Q

Alpha blockers

C/i

A

CHF: venous dilation, decreased preload, not as much volume back to heart

Peripheral edema: venous dilation

Pregnant or lactating

Impaired renal function: doses accumulate -> persistent hypotension over long period of time

52
Q

Alpha blockers

Indications

A

HTN (not first line drug)

BPH

Ureteral stones in ureter (off label use)
Doxazosin, terazosin, tamrulosin

53
Q

Alpha blockers

Monitoring

A

Weight: first indication of fluid status change -> weight gain

WBC and LFTs at initiation: liver metabolism

If BPH: PSA and digital rectal exam (DRE): evaluate size of prostate with DRE to determine effectiveness of alpha blocker on prostate
May take weeks for full effect (6-8 weeks)

54
Q

Heart failure

A

ACE or ARB: reduce afterload, prevent remodeling of cardiac musculature

Beta blocker: reduce mortality in pt with CHF bc decrease O2 demand and workload of heart

Diuretic: reduce preload to decrease workload of heart; don’t want to decrease too low bc don’t have venous return

Nitrates: for more advanced heart failure; relax cardiac blood vessels, impact O2 supply and demand

55
Q

HTN
Treatment goals
> 60: < 150/90
< 60: < 140/90

A

1: >60 yo 150/90 - no need to adjust meds if no s/s
2: <60 yo DBP > 90 - initiate treatment
3: <60 yo SBP > 140 - initiate treatment
4: > 18 yo w/ CKD BP >140/90 - initiate treatment
5: > 18 yo w/ DM BP >140/90 - initiate tx
6: nonblack w/ and w/out DM: tx includes thiazide, CCB, ACEI, or ARB
7: black w/ and w/out DM: tx includes thiazide or CCB
8: > 18 yo w/ CKD: tx includes ACEI or ARB to improve kidney outcomes (regardless of race)
9: If goal BP not met in 1 month, increase dose or add 2nd drug from recommended class. Add up to 3 drugs. Refer to specialist if still not controlled after 3.

First is ALWAYS lifestyle choices

56
Q

HTN

A

First line therapy
Black: thiazide and/or CCB
Nonblack: thiazide, ACE or ARB, CCB (alone or in combo)

57
Q

ACC & AHA

A

Recommend BP <130/90

58
Q

HTN

Selecting tx plan

A

Maximize first drug: start low hydrochlorothiazide, increase from 12.5mg to 25mg until effects work

Add 2nd drug before maximizing 1st drug: start lisinopril
If not controlled, add diuretic

Start 2 drugs in different classes - usually if very uncontrolled

If still not controlled with diuretic, ACEI, ARB, CCB add
Beta blocker or
Aldosterone antagonist or
Alpha blocker if also have BPH or
Refer to HTN specialist

Pt w/ DM should receive ACE or ARB
Pt w/ renal failure should receive ACE or ARB

59
Q

Cardiac Glycosides

Bufalin, Oufalin
Digoxin (derived from fox glove plant)

A

Increase contractile force of heart

Inhibit Na pump of heart via ATPase

  • permit buildup of Na and Ca intracellulary
  • cardiac muscle shortens
  • increased force -> better CO
60
Q

Na - K pump

A

ATP is broken down to ADP –> energy released causing Na-K pump to push Na out of cell and K into cell
Digoxin binds to ATPase (enzyme breaks ATP-ADP) -> Na builds up in cell.
Na leaks out of Ca channel pump -> buildup of K due to buildup of Na.
Buildup of Ca and K -> intracellularly -> increased contractile force -> better CO

61
Q

Digoxin and K

A

ATPase has higher affinity to K than digoxin -> ATPase will bind to K more readily than digoxin
If pt has change that might be related to digoxin, ALWAYS check digoxin levels
High K -> ATPase binds to K -> digoxin less effective
Low K -> digoxin binds to ATPase bc not enough K -> digoxin toxicity

Always check K before giving digoxin dose or if pt has change that could be related to digoxin

62
Q

Cardiac glycosides

Mechanism of action

A

Impact electrical forces of cardiac tissue

Decreased automaticity (enhanced vagus nerve stimulation -> decreased automaticity in SA node)

Decrease conduction velocity

  • AV node conduction slows
  • cardiac muscle cells: decrease ectopic foci in heart that require decreased automaticity
  • more effective in atrial muscle cells, SA node, and AV node. less effective in ventricular cells perkinje fibers
63
Q

Cardiac glycosides

A

Decreased renin activity (vasodilation)

Effect all smooth excitable muscle and tissue and CNS

Chemoreceptor trigger zone (center of brain that cause vestibular disturbances) -> n/v, diarrhea, visual disturbances

64
Q

Cardiac glycosides

Pharmacokinetics

A

Slower absorption with food/meals

Bioavailability varies with brand; can cause therapeutic changes. Ask pt if going to a different pharmacy or if pill looks different

Absorbed into all tissues, but highest in heart, kidney and liver

Excreted unchanged in urine

36 - 48 hr half life (long half life - toxicity can last for 5-10 days)

Steady state after 4-7 days of dosing

65
Q

Cardiac glycosides

Interactions

A

Nondihydropines: interact bc they adjust HR and effect conduction system of heart. Add onto effects of Digoxin
verapamil and diltiazem

Antiarrhythmics: work on conduction of heart, potentiate digoxin s/s
Quinidine and amiodarone

66
Q

Cardiac glycosides
Adverse reactions

Therapeutic level: 0.9-1.2ng/ml

A

Noncardiac s/s occur first bc of penetration into CNS in chemo receptor trigger zone

Anorexia, n/v/d

Fatigue, malaise, HA, visual changes (yellow tint, green halos)

Bradycardia, AV block (assess pt, listen to heart, know rate, rhythm, periodically check EKG to ensure not creating heart block) with medication

Toxic level (>2): with diuretics, hypokalemia,

67
Q

Cardiac glycosides

C/i

A

AV block bc atrial conduction isn’t getting through to ventricles

Bradycardia

Hypertrophic sub aortic stenosis: digoxin increases force of contraction -> worsened hypertrophy

Renal failure (low dose ok for impairment)

Electrolyte imbalance: high K reduces effect; low K causes toxicity

WPW syndrome: increases afib likelihood bc digoxin blocks normal pathway of atria

68
Q

Cardiac glycosides

Indications

A

Rapid afib

SVT

HF w/ severe dysfunction (EF <40); not 1st line HF med

69
Q

Nitrates

IV 
sublingual
inhaled
Transdermal: paste; patch
ER tabs
A

Nitric oxide relaxes all blood vessels

  • arterial and venous
  • afterload and preload reducers
  • venous and arterial pooling

Decrease myocardial O2 demand

Decrease myocardial O2 supply

Less impact on atherosclerotic vessels (need higher doses)

PO formulation: less potent vasodilation; sustained longer action bc metabolized in liver; metabolites break down and active

70
Q

Nitrates

PO

A

Pt who require higher or consistent dosing
Ex: pt using sublingual nitroglycerin in outpt setting frequently or pt needs lots of refills)

Hepatic metabolism: decreases vasodilation potency

Iserbidedinitrate and iserbidemonitrate

71
Q

Nitrates

C/i

A

Increased ICP: Vasodilation of blood vessels in brain; worsens increased ICP

Dehydration/volume depletion: preload already low, nitroglycerin worsens preload; if pt has CHF -> worsened

Anemia

Use of drugs for erectile dysfunction: potentiate vasodilation -> hypotension

72
Q

Nitrates

Adverse drug reactions

A

HA

Hypotension: arterial vasodilation

Reflex tachycardia: don’t treat tachycardia until BP is taken care of)

Skin irritation: patches and creams
Educate to rotate site; don’t put it on arms and legs bc as you move, blood flow is increased to extremities and drug gets absorbed more

73
Q

Nitrates

indications

A

Angina

Post MI

HF: not 1st line

74
Q

Antiarrhythmics

A

Goal: eliminate or decrease ectopic foci or conduction of ectopic impulses
-based on action potential and ion exchange (Na, Ca, K)

Depressed or accelerated conduction

Alternate pathways

Re-entry phenomena: Wolf Parkinson White

Uni or bidirectional

75
Q

Antiarrhythmic Drug Classes

Amiodarone: fibrosis

multiple drug interactions: look up if unsure

Work in tandem with cardiologist

Monitor EKG, ADR, labs

Wean; don’t stop abruptly

A

Class 1: Na channel blockers: reduce influx of Na into cells

Class 1a: Work in atrial tissue, SA node, AV nodes to reduce rapid firing of ectopic foci; lengthen action potential
Norpace, procainamide, quinidine

Class1b: work in ventricular tissue; last result for severe refractory ventricular tachycardia; shorten action potential
Lidocaine, phenytoin

Class 1C: little/no action potential increase
Flecainide, propafenone

Class 2: prolong refractory period; slightly negative inotropic effect (decreased contraction)
Esmolol, metoprolol, atenolol

Class 3: block K channels (decreased automaticity of ventricles)
Amiodarone, sotalol, dofetilide

Class 4: CCB
verapamil, diltiazem

76
Q

Serum lipids

Influenced by:

A

Genes

Diet

Activity

Smoking

Medication

Comorbidities: DM, HTN, arthritis, lupus

77
Q

Triglycerides

A

like carbs that have not been metabolized
> 300-400 considered pre DM

genetic

ETOH abuse

menopause bc of decreased estrogen

Educate to decrease carb intake

Beta blockers slow carb metabolism -> high triglycerides

78
Q

Hepatic LDL

A

made in liver -> arteries and arterioles create plaque

HMG-CoA/mevalonate: substance reduced by lipoprotein lipase and converts to mevalonate. Statins block conversion to HMG-CoA to reduce LDL production

Liver has receptors for LDL bc receptors pull LDL from blood to make more LDL to be sent out to periphery. Lower LDL level -> liver makes more LDL receptors -> absorb more LDL into liver -> less LDL in circulation

LDL receptors take up triglycerides some cholesterol meds will lower LDL and triglycerides too

HDL clearance: good cholesterol, removes. some LDL from circulation and back to liver so it can be metabolized or broken down

79
Q

Antilipidemics

Statins

A

Inhibit HMG CoA reductase -> prevent conversion mevalonate

Most effective lipid lowering agent

Lowers LDL

Raises HDL

Lowes triglycerides

Pregnancy category X

Very strong CYP450 inducers: many interactions

80
Q

Statins

CYP3A

A

CYP3A metabolism

Statin levels increased w/ meds that inhibit CYP3A
Nondihydropines (verapamil and diltiazem)
Erythromycin
Azoles (antifungals, diflucan)
Prozac
Protease inhibitors (hiv meds)

CYP3A inducers: lower statin levels
Rifampin (tb and resp infections)
Dilantin and phenobarbital

81
Q

Statins

Adverse drug reactions

A

HA, fatigue, GI distress, myalgia (order creatinine kinase (CK))

Myopathy
D/c med or reduce dose
Rhabdomyolysis
renal failure

Increased LFTs

82
Q

Antilipidemics

Indications

A

1: Pt w/ ASCVD
2: Pt w/ LDL > 190mg/dl (regardless if no other comorbidities)

3: DM
40-75 yo
no ASCVD
LDL 70-189

4: no ASCVD; no DM
LDL 70-189
> 7.5% 10 year ASCVD

5: measure lipids, return LDL to target

83
Q

Statin Treatment

Group 1

A

ASCVD (includes ACS, MI, angina, CAD, revascularization, TIA, stroke)

Age: < 75: high intensity statin therapy

  • atorvastatin 40-80
  • rosuvastatin 20-40mg

Age > 75: moderate intensity if not a high intensity candidate bc of hepatic disease, can elevate liver enzymes

84
Q

Statin treatment

Group 2

A

Pt w/ LDL > 190mg/dl

high intensity statin

moderate intensity if not a good candidate for high intensity; intended to lower cholesterol by 30-49%-atorvastatin 10-20mg
-rosuvastatin 5-10mg

85
Q

Statin treatment

Group 3

A

Pt w/ DM; 40-75yo; no ACVSD; LDL 70-189
Tx bc usually have metabolic syndrome (HTN, DM, HLD)
DM pt: increased risk for stroke and MI
Higher incidence of first fatal MI

Age 40-75: moderate intensity statin

  • atorvastatin 10-20mg
  • rosuvastatin 5-10mg

If DM and hypercholesterolemia- perform risk assessment
If risk >7.5% -> high risk statin

86
Q

Statin treatment

Group 4

A

Pt w/ no ASCVD or DM; LDL 70-189; >7.5% 10yr ASCVD risk; 40-75 yo

Moderate to high intensity
primary care emphasis

87
Q

Bile Acid Resin

A

Not absorbed in GI tract

Bind with bile acids and cholesterol in intestine -> form insoluble product that is excreted w/ cholesterol. Stops bile acid from returning to liver to make more cholesterol

Liver makes bile acids from cholesterol; bile is stored in gall bladder

Eat fatty meal, gall bladder releases bile acids to break down fats -> fats go to liver -> synthesized into cholesterol

When LDL goes down, liver increases LDL receptor sites -> more LDL is taken out of blood and into liver to be broken down

Decrease LDL

Increase HDL

Can increase triglycerides

Used for people with liver disease who can’t take statins

88
Q

Bile acid resins

Wlchol (colesevelam)
Questran (cholestyramine)

A

Powders that are mixed and taken with meal

Safest agent for pt w/ hepatic disease

Oatmeal and shredded wheat (soluble fibers) decrease bile acids bc soluble fiber travel slowly through intestine and absorb H2O, bile acids, and cholesterol -> reduced cholesterol absorbed for cholesterol synthesis

Don’t take w/ other meds for 2 hrs before or after bc will get excreted with insoluble waste

89
Q

Bile acid resin

Adverse reaction

A

No LFT monitoring required

GI complaints; take stool softener or Metamucil @ different time of day; prune juice

  • constipation
  • diarrhea
  • bloating
  • flatulence: simethicone, gas x
90
Q

Fibric acid derivatives

Mechanism of action

A

Used to reduce triglycerides by enzymatic destruction of lipoproteins that transport triglycerides

  • lower triglycerides
  • increase hdl
  • little impact on LDL
91
Q

Fibric acid derivatives
Gemfibrizol (Lopid)
Fenofibrate (tricor)

A

GI adverse reactions:

myopathies when take w/ statin
hepatic toxicity esp w/ statins
gall stones bc so much cholesterol coming back to liver

Interactions: anticoagulants

92
Q

Cholesterol absorption inhibitors

Ezetimibe (Zetia)

A

Decrease absorption of cholesterol in the small intestine

Decreased storage of cholesterol in liver
-decreased LDL

Very effective in combo w/ statins

No impact on CV events; unclear if helpful

Adverse reactions mostly in combo w/ statins

93
Q

Niacin

A

B vitamin

100-300x recommended daily dose improved cholesterol; never use it to lower LDL

Increases HDL
lowers LDL slightly
Lowers triglycerides

Start at low dose: 50-100mg did
Titrate slowly up to 1.5g.day

94
Q

Niacin

Adverse reactions

A

Flushing of face and neck; similar to hot flashes
Can take ASA to reduce prostaglandins -> reduced flushing

Acanthosis Nigricans: hyperpigmentation of neck, groin, axilla.
Indicates pre-DM -> niacin altering metabolism profoundly
Can’t give to people who already have disorder

Check uric acid, glucose, LFTs
check before beginning therapy and check 6-12 weeks after completing titration

95
Q

Niacin

C/i

A

Peptic ulcer disease

Gout: bc of uric acid

DM: bc worsens glycemic control

96
Q

Omega 3 fatty acids

A

Lowers triglycerides
Increases HDL slightly

Lovazza: concentrated fish oil; less GI s/s, less fish breath
FDA approved (insurance might cover)

OTC flaxseed/fish oil

  • antiplatelet effects
  • fish breath

Need to be taken at high doses to be effective; minimum of 3g/day

97
Q

Cholesterol Drugs

A 
First: lifestyle changes
Almost all: metabolized by liver
Many interactions: grapefruit juice
Most are c/I in pregnancy
Monitor LFTs and lipids before q 4-6 weeks for several months
Not for use during pregnancy and breastfeeding
Diet and exercise before medicating
Less fatty food
Exercise 30min/day 5x/week

Chem and physics (8 decks)

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