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exam 2 Flashcards

1
Q

heart failure

A

complex clinical syndrome that results in insufficient blood volume/oxygen supply to the tissues and organs

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2
Q

HF occurs with

A

reduced EF of the LV or defect in filling

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3
Q

decreased CO leads to

A

decreased tissue perfusion

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4
Q

ejection fraction

A

the amount of blood pumped out of LV

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5
Q

heart failure etiology

A
  • associated with CV disease
  • some cases are reversible
  • most HF is chronic, progressive
  • management includes lifetsyle changes and medication
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6
Q

echocardiogram diagnosis…

A

HF

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7
Q

causes of HF

A
  • long standing hypertension
  • overuse of heart muscle
  • coronary artery disease
  • MI
  • valve disorders
  • fluid volume overload like kidney failure
  • dysrhythmias
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8
Q

risk factors of HF

A
  • hypertension (modifiable, if treated and managed incidence can be reduced by 50%)
  • CAD
  • comorbidities
  • genetics (50% of cardiomyopathy genetically linked)
  • septal defects
  • infection
  • toxins
  • dysrythmias
  • alcohol
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9
Q

cardiomyopathy

A

weakening of heart muscles
30% linked to HF

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10
Q

Stage A HF

A

risk factors but no symptoms

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11
Q

stage B HF

A

structural heart disease with no symptoms
tx: ACE inhibitors or ARBs in all patients; beta blockers in selected patients

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12
Q

stage C HF

A

structural disease w/ previous or current symptoms
tx: ACE inhibtiors and beta blockers, sodium restriction, diuretics, and digoxin

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13
Q

stage D HF

A

refractory symptoms requiring special interventions
tx: cardiac resynchronization if bundle-branch block present, revascularization, aldosterone antagonist, nesiritide, inotropes, VAD, transplant, hospice

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14
Q

class I HF

A

no limit on physical activity

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15
Q

class II HF

A

slight limitation of physical activity
comfortable at rest
ordinary activity results in fatigue, palpitations, and SOB/dyspnea

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16
Q

class III HF

A

marked limitation of physical activity
comfortable at rest
less than ordinary activity causes fatigue, palpitations, and SOB/dyspnea

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17
Q

class IV HF

A

unable to perform activity w/o discomfort

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18
Q

types of HF

A
  • left sided systolic
  • left sided diastolic
  • right sided
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19
Q

left sided systolic HF is

A

heart failure w/ reduced ejection fraction

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20
Q

left sided diastolic is

A

heart failure w/ preserved ejection fraction

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21
Q

problems with right ventricle will cause

A

backflow of blood into the rest of the body causing s/s systemically

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22
Q

problem in left ventricle will cause

A

backflow into the lungs leading to dyspnea and chest pain

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23
Q

left sided HF

A
  • most common form of HF
  • results from inability of LV to empty during systole and fill during diastole
  • blood backs into LA causing increased pulmonary hydrostatic pressure leading to fluid leakage in pulmonary capillary bed causing pulmonary edema and fluid
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24
Q

s/s of left sided HF

A
  • difficulty breathing at night (paroxysmal nocturnal dyspnea
  • elevated pulmonary capillary wedge pressure
  • cough
  • crackles
  • wheezing
  • tachypnea
  • elevated pulmonary capillary wedge pressure
  • restlessness
  • confusion
  • bloody sputum
  • exertional dyspnea
  • fatigue
  • cyanosis
  • S3 ventricular gallop
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25
Q

pathophys of HF w/ reduced EF

A
  • HF w/ reduced EF = systolic failure
  • inability to pump blood effectively
  • caused by impaired contractile function, increased afterload, or mechanical abnormalities
  • decreased LV ejection fraction (LVEF)
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26
Q

normal EF in LV is

A

55-75%

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27
Q

EF in LV w/ HF

A

<50%

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28
Q

pathophys of HF with preserved EF

A
  • diastolic HF
  • inability of the ventricles to relax and fill during diastole resulting in decreased stroke volume and CO
  • primary cause if HTN
  • same end result as systolic failure
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29
Q

pathophys of right sided HF

A
  • RV does not pump effectively
  • fluid back up in venous system
  • fluid moves into tissues and organs
  • left sided HF is most common cause
  • other causes: RV infarction, stenosis or regurgitation, valve disease, cor pulmonale (RV dilation and hypertrophy)
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30
Q

s/s of right sided HF

A
  • hepatomegaly
  • JVD
  • enlarged spleen
  • ascites
  • increased peripheral venous pressure
  • fatigue
  • anorexia and complaints of GI distress
  • weight gain
  • dependent edema
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31
Q

pathophys of biventricular failure

A
  • both right and left ventricular dysfunction
  • inability of both ventrciles to pump effectively
  • fluid build up and venous engorgement
  • decreased perfusion to vital organs
  • compensatory mechanisms
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32
Q

beneficial counterregulatory mechanisms

A
  • ANP and BNP
  • released in response to increased blood volume and ventricular wall stretching
  • causes diuresis, vasodilation, and lowered BP
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33
Q

elevated BNP =

A

mortality in HF, ineffective at moving excess fluid out

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34
Q

mild HF BNP =

A

300+

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35
Q

moderate HF BNP =

A

600+

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36
Q

severe HF BNP =

A

900+

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37
Q

ANP and BNP levels correlate w/

A

progression of HF

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38
Q

HF complications

A
  • pleural effusion
  • dysrhythmias and dyssynchronous contraction (atrial and ventricular, left ventricular thrombus)
  • hepatomegaly
  • cardiorenal syndrome
  • anemia
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39
Q

cardiorenal syndrome

A

decreased GFR and serum creatinine causing kidney dysfunction as a result of impaired BF to kidneys

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40
Q

anemia and HF

A

low BF to kidneys causing decrease in erythropoietin causing decreased ability to secrete blood

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41
Q

pulmonary edema

A
  • acute event reflecting a breakdown of physiologic compensatory mechanisms
  • as LV beings to fail, blood backflows into pulmonary circulation causing pulmonary interstitial edema resulting in hypoexmia
  • this leads to s/s like hypoexmia, SOB, low o2 sat, restlessness, anxiousness, cool skin, cyanosis, lung congestion, sputum production, tachypnea, etc.
  • limit exertion
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42
Q

management of pulmonary edema

A
  • easier to prevent than treat
  • early recognition: monitor lung sounds for s/s of decreased activity tolerance and increased fluid retention
  • minimize exertion and stress
  • oxygen; nonrebreatther
  • meds: diuretics (furosemide), vasodilators (nitroglycerin)
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43
Q

medical mangement of HF

A
  • vary according to severity of condition, comorbidities, and cause
  • treatment includes: oral and IV meds, lifestyle modifications, supplemental o2, and surgical interventions like ICD, LVAD, and transplants
  • education and counseling needed
  • advance directives
  • exercise
  • cardiac rehab
  • diet
  • fluid restriction diet
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44
Q

education and interventions for HF

A
  • nutrition (low sodium) = <2g/day
  • fluid restriction
  • daily weight
  • weight gain of 3+ pounds over 2 days or 3-5 pounds over a week should be reported
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45
Q

angiotensin II converting enzyme inhibitor

A

enalapril

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46
Q

angiotensin II receptor blockers (ARBs)

A

losartan

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47
Q

angiotensin receptor-neprilysin inhbitiors (ARNi)

A

sacubitril/valsartan

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48
Q

beta-adrenergic blocking agents (BB)

A

metoproplol

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49
Q

diuretics

A

furosemide

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50
Q

phosphodiesterase inhibitors (cardiotonic-inotropic agents)

A

milrinone

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51
Q

sinoatrial node modulators

A

ivabradine

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52
Q

cardiac glycosides

A

digoxin

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53
Q

sacubitril/valsartan (entresto)

A
  • angiotensin receptor- neprilysin inhibitors
  • significantly improves HF-associated morbidity and mortality
  • preferred over ACE and ARBs
  • inhbits enzyme neprilysin (degrades natriuretic peptides that help facilitate cardiac homeostasis) and blocks harmful effects of RAAS while keeping beneficial effects of NPs
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54
Q

ARNi contraindications

A
  • decrease dose w/ kidney/hepatic impairment
  • dont use with ACE inhbitiors
  • harmful if pregnant ! (contains ARB)
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55
Q

adverse effects of ARNis

A
  • hypotension
  • hyperkalemia
  • cough
  • dizziness
  • impaired kidney function
  • angioedema (higher risk in african americans)
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56
Q

monitoring/evalutation of ARNis

A
  • check BP
  • BUN, creatinine, and K+ monitoring
  • activity tolerance
  • symptoms mangement
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57
Q

interactions w/ ARNis

A

CYP inhibitors because it causes more breakdown of drug

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58
Q

milrinone

A
  • phosphodiesterase inhibitors (cardiotonic-inotropic agents)
  • IV med for short term use until device implantation or cardiac transplant
  • increases force of contraction (potent inotropic) of ventricles to improve EF
  • systemic and pulmonary vasodilator
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59
Q

contraindications of milrinone/phosphodiesterase inhibitors

A
  • allergy to milrinone or bisulfates
  • caution in pregnant women
  • severe aortic or pulmonic valve disease
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60
Q

adverse effects of milrinone/phosphodiesterase inhibitors

A
  • potentially fatal ventricular dysrythmias
  • hypotension (if BP or HR goes down, titrate down)
  • chest pain/angina
  • thrombocytopenia (low platelets)
  • hypokalemia
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61
Q

milrinone has a

A

long half life so be mindful of how drug is leaving the system

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62
Q

monitoring/evaluation for milrinone

A
  • accurate weight
  • creatinine clearance before dosing
  • continuous BP/HR monitoring
  • electrolytes
  • platelet count
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63
Q

interactions w/ milrinone

A

do not mix with over IV drugs

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64
Q

sinoatrial node modulators/ivabradine (corlanor)

A
  • adjunctive medication usually combined with max dose beta blockers
  • reduces hospitalizations in severe HF and reduced EF
  • inhibitors select channels of pacemaker of SA node, slowing firing and decreasing HR leading to reduced myocardial demand
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65
Q

ivabradine/SA node modulators adverse effects

A
  • bradycardia
  • hypotension
  • atrial fibrilation
  • phosphenes (halos/changes in vision)
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66
Q

ivabradine/SA node modulator contraindications

A
  • acute decomensated HF
  • hypotension
  • low HR
  • heartblock/ sick sinus syndrome/ pacemaker
  • severe hepatic disease
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67
Q

monitoring/evaluation of ivabradine/SA node modulator

A
  • check HR before admin
  • monitor HR and BP
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68
Q

interactions w/ ivabradine

A

cyp3a4 inducers/inhibitors

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69
Q

ACE inhibitors reminder

A
  • given for HF pts for drugs to be more effective
  • enalapril shows decreased mortality by blocking RAS production of angiotensin II to decreased vasconstriction and decreasing afterload of left ventrcile, decreases aldosterone secretion to excrete more water and lower volume
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70
Q

ARBs reminders

A
  • losartan
  • antagonist
  • improves afterload and decreases workload
  • check BP prior and 6 hrs after
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71
Q

beta-adrenergic blockers reminder

A
  • metoprolol succinate
  • suppresses the CNS, decreases catecholamines that damage myocardial cells
  • stops or slows ventricular remodeling
  • prevents ventricular fibrilation
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72
Q

digoxin (lanoxin)/cardiac glycosiddes

A
  • no longer first line of tx due to adverse effects
  • inotrope
  • moves Ca+ into cell and Na+/K+/ATPase out
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73
Q

contraindications for digoxin(lanozin)/cardiac glycosides

A
  • careful in older adults due to increased risk of toxicity
  • careful with impaired kidney function
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74
Q

adverse effects of digoxin (lanoxin)/cardiac glycosides

A
  • dig toxicity: PVCs, heart rythym disturbances (bradycardia, heart block, headache, confusion)
  • nausea/vomiting
  • vision changes
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75
Q

monitoring/evaluation of digoxin (lonaxin)/cardac glycosides

A
  • give w/ meals
  • check HR before admin
  • apical HR when giving for full minute (if <60 DO NOT GIVE!)
  • narrow therapuetic index so narrow range before toxicity
  • check serum levels (.5-2ng/mL)
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76
Q

digoxin interactions

A
  • herbs
  • st johns wort
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77
Q

diuretics

A

used in combo w/ other medications for the tx of HF
also used in management of conditions w/ fluid volume excess like edema (KD, HD, ascites), pulmonary edema, prevention of KF, and HTN

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78
Q

kidney pathohpys

A

kidney is composed of over 1million nephrons which are responsible for producing urine.
blood is filtered through glomerulus where it works through tubules where reabsorption of fluid and electrolytes occur and excretion of waste occurs.
some meds work on different areas of nephron to decrease reabsorption of Na+ and water increase urine output

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79
Q

loop diuretics/ furosemide (lasix)

A
  • rapid acting
  • CAN be given if kidney function is impaired (low GFR)
  • inhibits Na+ and Cl- reabsorption in loop of Henle
  • indicated in HF, pulmonary edema, hepatic (ascites), and kidney disease
  • works in 5 minutes, peaks in 30, and lasts for 2 hrs
  • provide patient a bed pan
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80
Q

contraindications of furosemide (lasix)/ loop diuretics

A
  • anuric patients
  • sulfonamide allergy
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81
Q

adverse effects of furosemide (lasix)/loop diuretics

A
  • electrolyte imablances
  • dehydration
  • ototoxicity if med pushed too quickly
  • hyperglycemia in diabetics
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82
Q

monitoring/evaluation of furosemide (lasix)/ loop diuretics

A
  • I&Os to assess efficacy
  • restrict Na+ in diet because lasix increases Na+ reabsorbtion
  • monitor K+ level (3.5 - 5.0 mEq/L) due to decreased K+ leading to hypokalemia
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83
Q

patient teaching for furosemide (lasix)

A
  • when to take the medication
  • potassium rich foods
  • check blood sugar
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84
Q

high K+ foods

A
  • prunes
  • apple sauce
  • spinach
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85
Q

hydrochlorothiazdie (HCTZ)/thiazide diuretics

A
  • slower onset than loop diuretics
  • long term management of HF and HTN
  • ceiling threshold (certain dosage yields max effect so increasing the dose may not do anything)
  • decreases reabsorption of Na+, Cl-, and H2O in distal convuluted tubule
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86
Q

contraindications for hydrochlorothiazide

A
  • less effective low GFR and ineffective if GFR <30mL/min
  • sulfonamide cross allergy
  • caution w/ hepatic imapirment
  • caution w/ pregnant patients
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87
Q

adverse effects of hydrochlorothiazide

A
  • electrolyte imbalances
  • hypotension
  • weakness/dizziness
  • diarrhea/constipation
  • erectile dysfunction
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88
Q

monitoring/evaluation for hydrochlorothiazide

A
  • check BP
  • check edema (listen to breath sounds if PE is present)
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89
Q

interactions w/ hydrochlorothiazide

A

may interactions w/ drugs and diet

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90
Q

spironolactone (aldactone)/potassium sparing diuretics

A
  • slow onset (several days)
  • works at distal tubule to decrease aldosterone-induced Na+ and H2O reasborption and K+ secretion
  • usually combined w/ other drugs to increase efficacy
  • DO NOT CRUSH, give slowly
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91
Q

contraindications for spirinolactone (aldactone)/ potassium sparing diuretics

A
  • caution if impaired kidney function (high K+)
  • severe hepatic impairment
  • avoid during 1st trimester of pregnancy
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92
Q

adverse effects of spirinolactone (aldactone)/ potassium sparing diuretics

A
  • HA, dizziness
  • abdominal cramping
  • diarrhea
  • gynecomastia
  • deepening voice
  • testicular atrophy
  • menstrual irregularities
  • risk GI bleed
  • BLACK BOX WARNING: tumorigenic
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93
Q

monitoring/evaluation for spironolactone (aldactone)/ potassium sparing diuretics

A
  • monitor K+ levels
  • risk digoxin or lithium toxicity
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94
Q

s/s of hypyerkalemia

A
  • heartblock
  • chest pain
  • dizziness
  • tall T waves (if hypokalemia check low T waves)
  • MONITOR
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95
Q

mannitol (osmitrol)/osmotic diuretics

A
  • IV infusion for rapid diuresis
  • increase osmotic pressure, pulling fluid from extravascular sites into blood stream therefore, increasing blood volume and decreasing reabsorption of water and electrolytes in tubules
  • used for acute kidney injury, increased intracranial pressure, and increase intraocular pressure
  • can give with decreased GFR or kidney function
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96
Q

what causes blood clots

A
  • hemostasis (blood stasis)
  • platelet aggregation
  • blood coagulation
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97
Q

thrombus formation

A

platelets and fibrin attach to plaque which initiates clot formation causing partial occlusion where if left untreated, leads to total occlusion

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98
Q

arterial thrombus

A
  • platelets initiate process followed by fibrin formulation and trapping the RBCs in the fibrin
  • usually associated with atherosclerotic plaque, hypertension, and turbulent BF
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99
Q

venous thrombosis

A
  • from platelet aggregation with fibrin attached to RBCs
  • usually associated with venous stasis
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100
Q

clinical manifestations of arterial thrombosis

A

arterial blood clots in the central, pulmonary, or cardiac system can produce cerebrovascular accident pulmonary embolism, or myocardial infarction, respectively

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101
Q

clinical manifestations of venous thrombosis

A
  • lead to DVT
  • include leg swelling, pain, palpitation, redness
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102
Q

major groups of drugs for thrombosis

A
  1. anticoagulants: prevent formation of new clots and prevent further growth of current clot
  2. antiplatelet: prevents platelet aggregation
  3. thrombolytic: attack and dissolve blood clots that have already formed
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103
Q

anticoagulants

A
  • inhibit clot formation
  • do not dissolve clot
  • used for both venous and arterial risks
  • venous risks: dvt, pulmonary embolism
  • arterial risks: coronary thrombosis, myocardial infarction (MI), cerebral vascular accident (CVA), stroke, artificial heart valve
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104
Q

4 types of anticoagulants

A
  1. heparin
  2. vitamin K antagonists
  3. direct thrombin inhibitors
  4. direct factor Xa inhibitors
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105
Q

heparin

A
  • pharmaceutical preparation
  • natural anticoagulant primarily in the mast cells in the peripheral CT
  • prototype anticoagulant
  • internal heparin resides within lungs and liver mainly
  • exogenous heparin resides within intestines or bovine lung or it is biologically made
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106
Q

regular heparin is given via

A

IV

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107
Q

low molecular weight is given via

A

subq

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108
Q

heparin action before thrombus formation

A
  • combines with antithrombin III (natural anticoagulant in the blood) to inactivate clotting factors (IX, X, XI) and XII
  • inhibits the conversion of prothrombin to thrombin
  • prevents the formation of a thrombus
  • prolongs clotting time
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109
Q

heparin action after thrombus formation

A
  • inhibits additional coagulation by inactivating thrombin which prevents the conversion of fibrinogen to fibrin
  • inhibits factor Xa
  • inhibits factors V and VIII and platelet aggregation
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110
Q

contraindications for heparin

A
  • major bleeding
  • trauma
  • hx of heparin induced thrombocytopenia (life threatening)
  • hypertension
  • renal or hepatic disease
  • alcoholism
  • GI ulcers
  • tubes
  • endocarditis
  • threatened abortion
  • dietary and medication interactions
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111
Q

adverse effects of heparin

A
  • dizziness
  • headache
  • bleeding
  • alopecia
  • ecchymosis
  • decreased platelets/thrombocytopenia
  • bleeding
  • drug interactions
  • bruning
  • itching
  • chills
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112
Q

administration of heparin

A
  • dose depends on route (either IV or SQ)
  • give SC and/or IV (NEVER PO as it is poorly absorbed in GI tract)
  • half life: usually 1-2 hrs
  • rapid onset reached in minutes
  • clotting returns to normal in 2-6hrs
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113
Q

heparin antidote

A

protamine sulfate

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114
Q

meds taht decrease effects of heparin

A
  • antihistamines
  • digoxin
  • nicotine
  • ntiroglycerin (IV)
  • tetracycline
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115
Q

herbs and foots taht increase effects of heparin

A
  • chamomile
  • garlic
  • ginger
  • ginko
  • ginseng
  • high-dose vitamin E
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116
Q

aPTT and heparin

A
  • prescribers use activated partial thromboplastin time that is sensitive to changes in blood clotting factors, except factor VII, to regulate heparin dosage
  • normal or control values indicate normal blood coagulation
  • therapuetic values indicate adequate coagulation indicate low levels of clotting factors and delayed blood coagulation
  • aPTT should be maintained between 1.5-2.5x the control or baseline value
  • normal control value is 25-35 seconds
  • therapeutic values of adequate anticoagulation are 45-70 seconds, approximately
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117
Q

low molecular weight heparin

A
  • combines with antithrombin III and inactivates factor XA but less able to inhibit thrombin
  • synthetic
  • smaller molecular structure
  • ex. ENOXAPRIN (LOVENOX) or DALTEPARIN SODIUM (FRAGMIN)
  • given subQ
  • monitor platelet count
  • half life is 2-4x longer than heparin
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118
Q

LMWH indicated for

A
  • DVT
  • PE
  • prevention of complications of MI
  • prevention of thrombosis secondary to surgery, ischemic complications of unstable angina, and MI
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119
Q

contraindications of LMWH

A
  • stroke
  • peptic ulcer
  • blood anomilies
  • low platelet count
  • do not give if having eye surgery, brain, or spinal surgery
  • caution with: hemophilia, dissecting, aneurysm, peptic ulcer disease
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120
Q

enoxaprin (lovenox)/ LMWH

A
  • prevention of DVT, PE, complications of MI
  • subq injection or IV (rare)
  • adverse reaction: bleeding, thrombocytopenia
  • antagonist: protamine sulfate
  • avoid aspirin!!!!!
  • monitor platelet count
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121
Q

interventions and teachings for heparin

A
  • monitor for bleeding (bruised gums, abdominal pain, coffee-ground emesis, tarry stools
  • avoid use of NSAIDs, aspirin, or med with salicylates
  • use electric razor
  • brush with soft toothbrush
122
Q

teaching/monitoring for enoxaparin(lovenox)

A
  • provide instruction for self-admin
  • DO NOT expel air bubble - purpose to make sure full dose is delivered to patient
  • avoid use of NSAIDs, aspirin, or med w/ salicylates
  • monitor for signs of bleeding
  • brush with soft toothbrush
  • use electric razor
123
Q

direct thrombin inhibitors

A
  • inhibit thrombin from converting fibrinogen to fibrin
  • ex. Dabigatran (Pradaxa), argatroband (Acova), bivalirudin (angiomax), desirudin (iprivask)
124
Q

dabigatran (pradaxa)/ direct thrombin inhibitors action

A
  • inhibits thrombin, preventing thrombus formation, preventing strokes, embolism in patients w/ A-fib
  • given in conjunction with ASA for pt w/ coronary angioplasty
125
Q

dabigatran (pradaxa) / direct thrombin inhibitors use

A

for patients who cannot take heparin or are pregnancy risk C (black box?)

126
Q

dabigatran (pradaxa) / direct thrombin inhibitors contraindications

A
  • pts with bleeding
  • caution with renal failure
  • oral capsule use within 30 days of opening
  • not to be used with other anticoagulants
127
Q

adverse side effects of dabigatran (pradaxa) / direct thrombin inhibitors

A
  • bleeding
  • abdominal pain
  • gastritis
  • anemia
128
Q

warfarin (coumadin)/ vitamin K antagonist

A
  • inhibits hepatic synthesis of vitamin K, affects clotting factors II, VII, IX, and X
  • well absorbed in GI tract
  • half life 42hrs and lasts around 1-7 days
  • uses to prevent thrombolytic conditions such as thrombophlebitis, pulmonary embolism, embolism formation caused by atrial fib, long term therapy
  • may be used after heart attack, stroke, or VTE
  • given orally about 2-5mg for 2-3 days until drug levels are in blood and then it is adjusted via INR labs
129
Q

side effects/adverse effects of warfarin (coumadin)/vitamin K antagonist

A
  • bleeding
  • anorexia
  • abdominal cramps
  • nausea/vomiting
130
Q

lab testing for warfarin

A
  • international normalized ratio reports PT results
  • normal INR = 1.3-2
  • patients on warfarin need to maintain INR 2-3
  • monitor at regular intervals
131
Q

warfarin antidote

A
  • vitamin K
  • 24-48 hrs for efect
  • for acute bleeding, fresh frozen plasma is indicated
132
Q

drugs that decrease the effects of warfarin

A
  • chlordiazepoxide
  • haloperidol
  • IV lipid emulsions
  • isotretinoin
  • meprobamate
  • spironolactone
133
Q

drugs that increase effects of warfarin

A
  • acetaminophen
  • allopurinol
  • amiodarone
  • alteplase
  • androgens
  • aspirin
  • NSAIDs
  • antithrombin
  • cephalosporins!
134
Q

herbs and foods that increase warfarin (coumadin)

A
  • angelica
  • cat’s claw
  • chamomile
  • cranberry juice
  • garlic
  • ginko
  • green tea
  • tumeric
135
Q

herbs that decrease warfarin (coumadin)

A
  • ginseng
  • st. john’s wort
  • vitamin K (broccoli, brussel sprouts, cabbage, cauliflower, chives, tomatoes, turnips, green peppers)
136
Q

nursing implications for warfarin (coumadin) / vitamin K antagonist

A
  • monitor INR!
  • assess for bleeding (urine, emesis, stool, cuts)
137
Q

education for warfarin

A
  • take med as directed at the same time
  • lab work for INR
  • limit food high in vitamin K
  • caution activity that can cause bleeding
  • advise pt to report s/s of bleeding
  • no alcohol or OTC. meds, or herbal products
  • no aspirin or NSAIDs
  • carry ID describing med regimen
138
Q

direct factor Xa inhibitors

A
  • binds directly to inhibit production of thrombin which inactivate clotting factosr (Xa) and inhibits production of THROMBIN
  • ex. Rvaroxaban (Xarelto) prototype, apixaban (eliquis), edoxaban (savaysa)
  • rapidly absorbed and highly bound to protein
  • inhibit platelet activation and formation of fibrin clotting by inhibition of factor Xa
  • used for secondary prevention of venous thrmoboemolism and stroke prevention in pts with nonvalvular afib
139
Q

adverse effects of direct factor Xa inhibitors

A

bleeding is most common

140
Q

contraindications of direct factor Xa inhibitors

A

those with a known hypersensitivity to the drug

141
Q

nursing implications for direct factor Xa inhibitors

A
  • monitor albumin and platelets
  • assess bleeding
  • numerous drugs and herbs that either increase or decrease effects so monitor!
142
Q

drugs that increase effects of rivaroxaban (xarelto) / direct factor Xa inhibitors

A
  • anticoags
  • apixaban
  • asa
  • antiplatelet agents
  • anti-inflammatory agents
  • thrombolytics
  • vtiamin E
142
Q

drugs that decrease effects of rivaroxaban (xarelto) / direct factor Xa inhibitors

A
  • estrogens
  • progestins
143
Q

herbs that increase rivaroxaban (xarelto) / direct factor Xa inhibitors

A
  • aflalfa
  • anise
  • grapefruit juice
144
Q

st johns wort and rivaroxaban

A

decreases effects

145
Q

antiplatelet drugs

A
  • prevent thrombosis in arteries by suppressing platelet aggregation
  • mainly for prophylactic use for MI, stroke prevention, or repeated MI prevention of stroke
  • long term, low dose aspirin
146
Q

aspirin and surgery

A

stop 7 days before surgery due to prolonged antiplatelet activity

147
Q

antiplatelet drugs examples

A
  • clopidogrel (plavix) - frequently used after Mi w/ aspiring (PROTOTYPE)
  • aspirin (ecotrin)
  • abciximab (reopro)
  • dipyridamole (persantine) or w/ ASA (aggrenox)
  • prasugrel (effient)
  • ticagrelor (brillinta)
148
Q

clopidogrel (plavix) / antiplatelet drug

A
  • prevents platelet aggregation blocks ADP to the receptor
  • excreted in urine and feces
  • discontinue 7 days b4 surgery
  • onset 1-2hrs
  • peak time 2-3 hrs
  • used for MI, stroke, and PAD, or after placement of stent
149
Q

contraindications of clopidogrel (plavix) / antiplatelet drugs

A
  • bleeding
  • intracranial hemorrhage
  • liver disease (check LFTs)
  • peptic ulcers
150
Q

side effects of clopidogrel (plavix)

A
  • abdominal pain
  • flulike symptoms
  • dizziness
  • headaches
  • fatigue
151
Q

adverse effects of clopidogrel (plavix)

A
  • pruritus
  • rash
  • purpura
  • diarrhea
  • severe neutropenia
152
Q

nursing implications for clopidogrel (plavix)

A
  • assess for s/s of stroke, peripheral vascular disease or MI
  • assess thrombotic issues
  • monitor bleeding times
  • monitor H/H and neutrophils
153
Q

patient education for clopidorgrel (plavix)

A
  • take medication as direct
  • call provider for fever, weakness, chills, or unusual bleeding
154
Q

drugs that increase clopidogrel effects

A
  • ASA
  • NSAID
  • platelet inhibitors
  • thrombolytics
  • atoravastatin
  • bariutates
  • rifampin
155
Q

drugs that decrease effects of clopidorgrel (plavix)

A
  • amiodarone
  • diliazem ABX
  • omeprazole
  • SSRIs
156
Q

herbs that increase effects of Clopidogrel (plavix)

A
  • garlic
  • ginko
  • ginger
  • green tea
  • horse chestnut
  • st jogns wort
157
Q

aspirin (ecotrin)

A
  • antiplatelet
  • oral, often used as adjunctive med
158
Q

adverse effects of aspirin (ecotrin)/ antiplatelet

A
  • bleeding
  • GI upset
  • tinnitus
  • hearing loss
159
Q

contraindications for aspirin (ecotrin)

A
  • third trimester prgenancy (category D risk)
  • bleeding disorders
  • thrombocytopenia
160
Q

meds that effect aspirin

A
  • caffeine may increase aspirin absorption
  • coticosteroids may increase ASA excretion and decrease effects of ASA
  • can reduce hypertensive action of beta blockers
161
Q

abciximab (reo pro)

A
  • antiplatelet
  • prevents binding of fibrinogen to active platelets
  • monitor: HR, BP, bleeding, stool monitor, gastric bleeding, monitor puncture sites
  • pregnancy risk
  • contraindicating in patients with active bleeding
  • use caution w/ renal or hepatic problems, thrombocytopenia, hx of stroke, uncontrolled HTN
  • advise patient to no use with other anticoags
  • if using other meds, assess bleeding
162
Q

prasugrel (effient)

A

demonstrated improved cardiac outcome for acute coronary syndromes

163
Q

ticagrelor (brillinta)

A

latest ADP receptor antagonist

164
Q

prasugrel (effient) and ticagrelor (brillinta) use

A
  • reduce rate of CV death, MI, and stroke in patient w/ previous hx
  • BLACK BOX WARNING: significant fatal hemorrhage
  • more potent than clopidogrel
165
Q

dipyridamole (presantine)

A
  • antiplatelet
  • inhibits platelet adhesion
  • oral route
  • pregnancy risk
  • use: prevention of thromboemoblism after cardiac valve replacement, given w/ warfarin
  • combination of drug with ASA prevents strokes in people with previous TIAs
  • combination of dipyridamole and aspirin indicated for prevention of stroke
166
Q

thrombolytics

A

purpose is to dissolve thrombi so these drugs stimulate conversion of plasminogen to plasmin, a proteolytic enzyme that breakds down fibrin, the framework of a thromus, main use of thrombolytic agents is for management of acute, severe, thromboembolic disease, such as MI, PE, and iliofemoral thrombosis

167
Q

use of thrombolytics

A
  • acute severe thromboemolic disease
  • after acute MI
  • stroke
  • pulmonary embolus
  • DVT
  • non coronary artery occlusion
168
Q

thrombolytic admin

A

within 3-4 1/2 hours of thromboti stroke symptoms (AHA)

169
Q

risk of thrombolytics

A

brain hemorrhage

170
Q

contraindications for thrombolytics

A
  • severe uncontrolled HTN
  • aneurysm
  • internal bleeding
  • intracranial or intraspinal surgery or trauma in past 3 months
  • recent surgery
  • use of oral anticoags
  • can increase risk of cerebral embolism in people with afib and aflutter
171
Q

nursing implications for thrombolytis

A
  • assess for cardiac dysrythmias
  • bradycardia
  • PVCs
  • Vtach
  • check for bleeding
172
Q

common thrombolytics

A
  • alteplase (tPA) or Activase (give with ischemic stroke)
  • tenecteplase (TNK-tPA) or TNKase
173
Q

aminocaproic acid (amicar)

A

controls bleeding from overfose of tPA
antidote for tPA

174
Q

idarucizumab (praxbind)

A

antidote for dabigatran

175
Q

protamine sulfate

A

antidote for heparin

176
Q

vitamin K

A

antidote for warfarin

177
Q

what is hypertension

A

chronic disorder causing increased pressure on arteries

178
Q

signs and symptoms of HTN

A
  • chest discomfort
  • sweating
179
Q

risk factors for HTN

A
  • age
  • family hx
  • diabetes
  • kidney disease
180
Q

consequences of high BP

A
  • stroke (can cause blood vessels to burst or clog easily)
  • HF (heart can enlarge and fail to supply blood)
  • sexual dysfunction (ED in men or lower libido in women)
  • vision loss (damage of vessels in eye)
  • heart attack (can cause vessels to narrow and stiffen)
  • kidney disease/failure (can damage arteries and impair ability to filter blood)
181
Q

HTN crisis

A

> 180 SBP and/or >120 DBP

182
Q

elevated BP

A

120-129/<80

183
Q

stage 1 HTN

A

130-139/80-89

184
Q

stage 2 HTN

A

> 140/>90

185
Q

how is HTN diagnosed

A

3 elevated readings over time

186
Q

determinants of BP

A
  • CO
  • preload
  • afterload
  • contractility
187
Q

cardiac output

A
  • HR x SV
  • refers to total amount of blood ejected by one of the ventricles in L/min
  • SV = 60-90 mL/beat
  • 4-8L/min = normal CO
188
Q

stroke volume

A

impacted by preload, afterload, and contracility
amount of blood ejected from one of the ventrciles per heartbeat
average resting SV = 60-130mL

189
Q

preload

A

amount of blood in heart right before contraction

190
Q

afterload

A

resistance to ejection of blood from ventricle

191
Q

contractility

A
  • how well the heart pumps as a muscle
  • increase in contractility = higher stroke volume
  • enahnced by catecholamins, sympathetic neuronal activity, and meds like digoxin, dopamin, etc.
  • depressed by hypoexmia, acidosis, and beta adrenergic blocking agents like metoprolol
192
Q

diastolic

A

refers to resistance

193
Q

beta 1 receptors

A

in cardiac tissue that can stimulate increased cardiac activity and HR

194
Q

beta 2 receptors

A

in smooth vessels in muscle in blood vessels in bronchi, periphery, and uterine muscles

195
Q

beta 3 receptors

A

in kidneys to help stimulate renin-angiotensin-aldosterone system

196
Q

beta 2Gs

A

Gs coupled receptors increse cAMP and cause smooth muscle relaxation

197
Q

kidney BP regulation

A
  • control fluid volume
  • RAAS
  • control Na+ and H2O elimination/retention effecting CO and systemic BP
198
Q

blood vessel regulation of BP

A
  • baroreceptors in aorta and carotid sinus
  • vasomotor center in medulla
  • catecholamines (norephinephrine, released for sympathetic nerve terminals)
  • epinephrine released from adrenal medulla (increases BP via vasoconstriction)
199
Q

renin-angiotensin-aldosterone system

A
  • in reponse to low BP or low Na+ (indicating low fluid volume) the RAAS can kick in to compensate
  • liver releases angiotensinogen into the blood and in response the kidney secretes an enzyme renin
  • angiotensinogen and renin combine creating angiotensin I
  • when angiotensin I gets to our lungs, ACE (angiotensin coverting enzyme) gets released
  • ACE and angiotensin I combine to form angiotensin II which works on adrenal glands and kidneys
  • when angiotensin II gets to adrenal gland it creates aldosterone which allows BP regulation to occur and reabsorption of Na+ and in turn increase amount of fluid on board
  • kidneys will cause vasoconstriction in arterioles of kidney causing an increase in BP as the arteries narrow the BP increases
200
Q

response to hypotension

A
  • SNS is stimulated
  • adrenal medulla secretes epinephrine and norepinephrine
  • angiotensin II and aldosterone are fored
  • kidneys retain fluid
  • BP is increased
201
Q

response to hypertension

A
  • increased renal secretion
  • fluid loss decreases circulating volume causing lower CO and lower arterial pressure, causing decreased BP
202
Q

first line treatment for HTN

A
  • diet
  • stress reduction
  • exercise
  • decrease salt
  • decreased alcohol
  • smoking cessation
203
Q

captipril is a

A

angiotensin converting enzyme (ACE) inhibitor

204
Q

losartan is a

A

angiotensin II receptor blocker

205
Q

amlodipine is a

A

calcium channel blocker

206
Q

propranolol is a

A

beta blocker antiadrenergic (BB)

207
Q

nitroprusside (IV) is a

A

vasopressor

208
Q

hydralazine is a

A

direct vasodilator

209
Q

examples of ACE inhibitors

A
  • THINK PRIL
  • captorpil (capoten), enalapril maleate (vasotec)
  • lisinopril (prinivil, zestril)
  • benazepril hydrochloride (lotensin)
  • fosinopril (monorpil)
210
Q

uses of ACE inhibitors

A
  • HTN
  • HF
  • MI
211
Q

ACE inhibitors increases risk of

A

cough
hyperkalemia
angioedema
neutropenia

212
Q

fetus and ACE inhibitors

A

significant risk to fetus if taken during pregnancy

213
Q

ACE overview

A
  • prevents ACE from converting angiotensin I to II causing vasoconstriction
  • decreases BP
  • increase K+ and causes loss of Na+ and fluid
  • causes little change in CO or rate and decreases peripheral resistance
214
Q

ACE BLACK BOX

A

fetus developmental harm

215
Q

contraindications of ACE inhibitors

A
  • BLACK BOX: pregnancy (death to fetus), prevention of pregnancy if on medication
  • K+ sparnig diuretics such as spirinolactone (aldactone)
  • salt substitutes that contain K+ risk of hyperkalemia
216
Q

administration of ACE inhbiitors

A
  • take captopril 1hr before meal
  • other ACEs can be taken with or without meals
  • increases concentration of digoxin and lithium
217
Q

african american adults one ACE inhibitors

A
  • does not respond when taken alone
  • responds well when taken with a diuretic
218
Q

Angiotensin II receptor blockers (ARBs)

A
  • one of the recommended classes as first line agents for HTN
  • blocks vasoconstriction that raises BP and BLOCKS angiotensin II
  • selectively binds with angiotensin II receptors in vascular smooth muscle and adrenal cortex to block vasoconstriction and release of aldosterone
  • increases renal flow
  • action blocks BP from raising in response to renin angiotensin system
  • overall decreases BP
219
Q

ARB examples

A
  • ALL END IN SARTAN
  • losratan (cozaar)
  • valsartan (diovan)
  • irbesartan (avapro)
  • candesartan (atacand)
220
Q

uses of ARBs

A
  • HTN
  • HF
  • stroke prevention
  • pt’s who cannot take ACE inhibitors
221
Q

adverse effects of ARBs

A
  • dizziness
  • muscle cramps
  • heart burn
  • diarrhea
  • angioedema
  • less likely to produce dry cough and angioedema but can happen
  • do not need to lower dose in older adults
  • NOT for children
222
Q

ARBS are NOT used for

A

monotherapy in african americans

223
Q

black box warning of ARBs

A

can cause death to fetus

224
Q

nursing considerations for ARBs

A
  • assess efficacy by checking BP
  • assess kidney and hepatic labs
  • high first pass effect
  • avoid herbs and supplements
  • monitor K+
225
Q

calcium channel blockers

A
  • block calcium vessels
  • lead to vasodilator of vascular smooth muscle
  • decrease force of contraction
  • decrease myocardial oxygen consumption
  • decrease HR
  • slow conduction through AV node
  • can be used for monotherapy in african americans
  • safe in pregnancy
226
Q

examples of CCBs

A
  • amlodipine (norvasc) (DO NOT TAKE W/ ST JOHNS WORT it is an inducer of CYP450
  • nifedipine (procardia) (DO NOT TAKE W GRAPEFRUIT JUICE)
  • diltizem (cardizem)
  • verapamil (calan sr)
227
Q

uses of CCBs

A
  • HTN
  • coronary artery disease (CAD)
  • angina
228
Q

side effects of CCBs

A
  • flush
  • fatigue
  • headache
  • edema of feet and hands
  • dizziness
  • ankle edema
  • bradycardia, AV block
  • nausea
  • abdominal pain
229
Q

contraindications for CCBs

A
  • sick sinus syndrome (SSS)
  • heart block
  • hypersensitivity
  • grapefruit juice (w/ nifedipine and verapamil)
  • hepatic impairment
  • stopping med abruptly (don’t stop taking nifedipine abruptly)
230
Q

beta-adrenergic blockers

A
  • inhibit activities of sympathetic nervous system
  • block beta I receptors in heart
  • decrease HR (negative chronotropic)
  • decrease myocardial contractility (negative inotropic)
  • decrease rate of conduction in AV (neg dromotropic)
  • alpha block adds vasodilation in meds like labetalol (reduces renin release which decreases angiotensin II causing vasodilation and promotes excretion of NA and water)
  • dilates blood vessel and decreases vascular resistance
231
Q

beta blocker examples

A
  • ALL END IN -OLOL
  • propanolol (inderal)
  • metoprolol (lopressor)
  • atenolol (tenormin)
  • esmolol (brevibloc)
  • acebutolol (sectral)
  • betaxolol (kerlone)
  • metoprolol succinate (toprol-xl)
  • penbutolol sulfate (levatol)
232
Q

cardio selective beta blockers (beta 1)

A
  • metoprolol (lopressor)
  • atenolol (tenormin)
  • esmolol (brevibloc)
233
Q

nonselective beta blockers (beta 1 and 2)

A

propranolol

234
Q

alpha and beta blockers

A
  • carvedilol (coreg)
  • labetalol (trandate)
235
Q

side effects of beta blockers

A
  • marked decrease in BP
  • insomnia
  • depression
  • nightmares
  • sexual dysfunction
236
Q

BLACK BOX FOR BETA ADRENERGICS

A

abrupt withdrawal for those with CAD can cause angina, ventricular arrythmias, and MI

237
Q

nursing considerations for beta blockers

A
  • assessment of BP
  • assess first dose phenomenon
  • asses for fluid retention if not used in conjunction w/ diuretic
  • patient education
  • never stop taking beta blockers (can cause rebound effect)
  • report dizziness or feeling faint
238
Q

vasodilators

A
  • used in severe HTN not responsive to other meds
  • maintains control of BP
  • acts directly on smooth muscle to cause vasodilation decreasing BP
  • doesn’t inhibit CV reflexes and tachycardia
  • renin release will occur
  • nitroprusside is most potent arterial and venous vasodilator
  • DO NOT TAKE W/ VIAGRA
  • rapid onset and short acting
239
Q

ICU settings and nitroglycerine (IV)

A

reduces afterload
VS q5-15min
hemodynamic monitoring

240
Q

nitroprusside metabolizes

A

thiocyanate
measure levels if use >72hrs
toxicity: n/v, muscle spasms and seizures w/ poisoning or toxicity

241
Q

BLACK BOX warning for vasodilators

A

can cause angina or precipitate pericardial effusion causing cardiac tamponade

242
Q

hydralazine and minoxidil acts

A

mainly on arterioles

243
Q

hydralazine and minoxidil both have a

A

limited effect on HTN when used alone

244
Q

vasodilators have potential to

A

stimulate the SNS and trigger relflexive compensatory mecnaisms (vasoconstriction, tachycardia, and increase CO) raising BP

245
Q

you can give vasodilators with drugs taht

A

inhibit excessive sympathetic stimulation (e.g., propanolol, and adrenergic blocker)

246
Q

diuretics

A
  • first line for mild HTN
  • help kidneys get rid of excess water and salt
  • reduces the volume of blood that needs to pass through the blood vessels - results decrease BP
  • category of diuretics depends on where kidney functions
  • combination diuretics which include more than one variety used together
  • used in conjunction with antihypertensive medication due to the fluid retention
247
Q

diuretic examples

A
  • hydrochlorothizaide (microzide) is most common
  • furosemide (lasix) - loop diuretic used for renal insufficiency
  • spironolactone (aldactone) used for pts with renal insufficiency, K+ sparring-
248
Q

which diuretics are first line treatment

A

thiazide diuretics used with ACE, ARBs, or CCB

249
Q

direct renin inhibitors

A
  • aliskiren
  • directly inhibits renin - decreases conversion of angiotensin to angiotensin I, stops RAS leading to decrease B/P
  • aldosterone is not stimulated to release causing increased risk of hyperkalemia
  • do not use with ACE or ARBs, can lead to severe renal impairment
250
Q

contraindications for direct renin inhibitors

A

chronic kidney disease
use of ACE or ARBs

251
Q

nursing considerations for direct renin inhibitors

A
  • assess BP
  • monitor K+
  • check for difficulty swallowing, breathing
  • assess for angioedema
  • assess renal function (output and serum levels)

patient teaching:
- If taken with high fat meals, effect of medication will decrease
- Report any sign of difficulty breathing, dizziness, swelling in tissue around eyes or mouth to health care provider

252
Q

normal GI function

A
  • gastric mucosa is equipped with cell destructive and cell protective measures
  • dysfunction from an imbalance between destructive and protective measures
253
Q

destructive measures of GI tract

A
  • gastric acid
  • pepsin can cause damage to lining of stomach
  • H. pylori and NSAIDs
254
Q

protective measures of GI tract

A
  • mucous
  • dilution of gastric caid
  • prostaglandin E
  • mechanisms to prevent diffusion of HCl from stomach back into mucousal lining
255
Q

cellular functions of GI tract

A
  • parietal cells line membrane of stomach
  • made of acetylcholine, gastrin, and histmaine activating cell receptors of pariteal cells
  • enzyme moves gastric acid production into the cells into the stomach
  • histamine 2 receptor antagonists will block histamine binding receptors
  • proton pump inhibitors will prevent effectivenss
  • pepsin is the conversion of pesinogen to pepsin to digest proteins (prevention of conversion will decrease pepsin which can be damaging to stomach lining)
256
Q

GERD

A
  • stomach acid or bile backs up into the esophagus irritating the lining
  • usually from incompetent lower esophageal sphincter
  • contributing factors: coffee, acidic foods, greasy foods, chocolate, alcohol
257
Q

s/s of GERD

A
  • pyrosis/heartburn (worsening when bending over)
  • regurgitation
  • hoarseness
  • dry cough
  • globus sensation
  • dyspepsia
  • dysphagia
  • epigastric pain
258
Q

gastric ulcer

A
  • common in older adult
  • chronic condition
  • pain WORSE when EATING
  • heartburn, bloating, indigestion, nausea
  • dull, achy, abdominal pain
  • painless bleeding (emesis), longer to heal
  • pain could mimic heart attack
  • assess for perforation
259
Q

duodenal ulcer

A
  • can occur at any age
  • chronic
  • pain relieved by eating
  • heartburn, bloating, burning sensation in throat
  • severe abdominal pain
  • pain worse at night because they are not eating
  • assess for perforation
260
Q

peptic ulcer disease

A
  • esophagous, stomach, or duodenum
  • most cases from H. pylori or NSAIDs
  • s/s: nausea, heartburn, epigastric pain
261
Q

h. pylori is from

A

fecal oral route

262
Q

peptic ulcer disease/lab tests

A
  • endoscopy
  • h. pylori breath, blood, or stool test
  • check for blood
  • endoscopy with biopsy
  • can rule out cancer
  • rapid urease testing w/ hx
  • barium contrast if endoscopy can’t be done due to obstruction
  • CBC
263
Q

meds for PUD may

A

increase or decrease destructive factors

264
Q

antacid example

A

mylanta

265
Q

histmaine 2 receptor antagonists example

A

cimetidine (tagamet)

266
Q

proton pump inhibitors example

A

omeprazole (prilosec)

267
Q

mylanta (aluminum hydroxide/magnesium hydroxide/ simethicom) / antacids

A
  • alkaline that neutralizes stomach acids by raising pH
  • prevents conversion of pepsinogen to pepsin
  • simethicone antiflatulent
  • indcations: used to prevent or treat PUD, GERD, esophagitis, heartburn, gastritis, GI bleed, stress ulcers, pain relief prn
268
Q

contraindications of mylanta

A
  • renal failure or creatinine clearance <30
  • appendicitis
  • inflamed bowel
269
Q

adverse effects of mylanta

A
  • aluminium based so may cause constipation, hypophosphatemia, and osteomalacia
  • magnesium based so may cause hypermagnesemia and diarrhea
270
Q

monitoring for mylanta

A
  • labs for Mg+ and PO34-
  • bone scans to monitor for osteomalacia
  • monitor for symptom relief
271
Q

patient teaching for mylanta

A
  • timing: DO NOT TAKE W/ OTHER DRUGS, will prevent or decrease absorption of other drug
  • take 1-3hrs after meals or at bed time, not for long term use
  • interactions w/ anticholinergics
272
Q

tums are

A

calcium based which can cause hypercalcemia

273
Q

histamine 2 receptor antagonists/cimetidine (tagamet)

A
  • inhbits actions of histmaine at H2 receptors on parietal cells of stomach
  • indicated for PUD, GERD, GI bleed from stress ulcers, esophagitis, zollinger-ellison disease
274
Q

adverse effects of histamine 2 receptor antagonists (cimetidine/tagamet)

A
  • diarrhea
  • drowsiness
  • headache
  • confusion
  • gynecomastia
275
Q

contraindications for cimetdidine (tagamet)

A
  • renal impairment
  • hepatic impairment
  • preganant/lactating
276
Q

monitoring for cimetidine (tagamet)

A
  • creatinine clearance
  • LFTs
  • symptom relief
277
Q

patient teaching for cimetidine

A
  • take med at bed time or w/ dinner
  • CYP inhibitors so use with famotidine and rantidine is a problem
  • no use w/ antacids (NOTHING AT SAME TIME AS ANTACIDS)
  • some drugs need acidic environment like tetracycline
278
Q

proton pump inhibitors (PPIs)/omeprazole (prilosec)

A
  • all end in -azole
  • BEST DRUG
  • stronger, faster, and longer relief than H2RAs
  • most potent inhibitors of gastric acid secretion
  • prevents the H+K+ATPase enzyme from pumping or release of gastric acid from parietal cells into stomach
279
Q

indications for PPIs or omeprazole (prilosec)

A
  • PUD
  • GERD
  • Zollinger-ellison syndrome
280
Q

adverse effects of omeprazole (prilosec)

A
  • nausea
  • diarrhea
  • headache
  • bone fractures (in high dose or long term use)
281
Q

contraindications/cautions w omeprazole (prilosec)

A
  • hypersensitivity
  • plavix usage
  • benzos
  • warfarin
  • phenoytoin
  • do not crush or chew med
282
Q

monitoring for omeprazole

A

symptom relief

283
Q

patient teaching for omeprazole

A
  • take 30 minutes before meals
  • do not crush or chew, can give med in NG or PEG tube if placed
284
Q

misoprostol (cytotec)

A
  • synthetic prostaglandin E
  • often given w/ NSAIDs
  • RA, osteoarthritis can be on long term NSAIDs so they will take this with NSAIDs to decrease GI bleed/ulcer risk
285
Q

adverse effects of misoprostol

A
  • BLACK BOX WARNING FOR FETUS
  • diarrhea
  • abdominal cramping
  • nausea/vomiting
  • headache
  • uterine cramping
  • vaginal bleeding
286
Q

sucralfate

A
  • prevent (lower dose) and treat PUD
  • binds to ulcer making barrier
  • adverse effects: dry mouth, constipation
287
Q

antibiotics

A

combo drug therapy to tx H. pylori
2 abx and acid reducer

288
Q

dismuth subsalicylate

A
  • pink bismuth
  • adverse effects include: dark stools and ringing in ear
289
Q

contraindicatiosn for bismuth salicylate

A
  • someone allergic to salicylate
  • no children (risk of reye’s)
290
Q

older adults age 65+

A
  • largest consumers of healthcare
  • more prone to abx resistant infections
  • limited testing on older adults in drug trials
  • common health problems: arthritis, heart disease, decreased sensory perception, bone disorders, DM
291
Q

polypharmacy

A
  • use of multiple medications due to multiple conditions
  • can cause multiple interactions due to many different forms of medication
  • prevention: use 1 pharmacy, have docor look over meds, reconciliation on every visit
292
Q

risk to benefit ratio

A

does the risk of taking the drug equate to benefit

293
Q

age related changes to pharmacodynamics

A
  • what drug does to body
  • lifestyle changes
  • receptor sites (less receptor sites on cells or reduced affinity, receptor sites are where drug binds and exerts action
  • longer drug action
  • beta blockers have decreased function of beta receptors so not as effective on older adults
  • digoxin toxicity more common due to prolonged time the drug is in the body
294
Q

absorption in older adults

A
  • less gastric acidity
  • decreased blood and surface area for absorption to occur
  • delayed gastric processes
  • decreased circulation and muscle mass for IM injections
295
Q

distribution in older adults

A

getting drug to where it is going to act
- decreased CO, decreased BF, and body mass and fluids
- lower albumin leading to decreased ability for drug to get to where it needs to

296
Q

metabolism in older adults

A
  • liver gets smaller
  • causes longer half life
297
Q

excretion in older adults

A
  • decreased kidney BF, functioning nephrons, and GFR
  • higher risk of adverse reactions
  • check creatinine clearance and GFR
298
Q

other changes with agining

A
  • anticholinergic and sedative drugs (increase risk of functional decline and falls, assess risk to benefit ratio, confusion, impaired memory, etc. ex. ipratropium, benadryl)
  • more susceptible to infecitons secondary to decline in ROS
  • decreased cytokines
  • s/s of infection change from low temp, confusion, etc.
299
Q

medication adherance

A
  • increased reminders
  • diminished vision
  • economic factors, getting drugs, cost
  • start slow and low to diminish adverse reactions
300
Q

beers criteria

A
  • based on 5 categories of potentially inappropriate meds used in adults
  • potentially inappropriate meds
  • inappropriate for certain disease or syndromes
  • meds that need caution
  • potentially inappropriate drug-drug interactions
  • meds who dosages should be adjusted based on renal function
301
Q

long covid

A
  • continuing covid s/s 16%
  • 65 million people worldwide have long covid
  • SOB
  • dyspnea
  • xray and other tests and nothing is there
  • long covid can resolve in 1 year
  • usually from prolonged inflammatory resopnse
  • pre-existing conditions make you more at risk

path/pharm (4 decks)

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