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1
Q

Physiology of Upper Gastrointestinal Tract

A
  • stomach secretes acid, enzymes, and hormones that are essential to digestive physiology
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2
Q

What are the natural defenses of the stomach?

A
  • somatostatin
  • bicarbonate ion
  • mucus
  • prostaglandin E2
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3
Q

What do prostaglandin antagonists include?

A
  • NSAIDs/ASA (damages GI mucosa directly)
  • corticosteroids
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4
Q

Peptic ulcer risk factors

A
  • infection w/ H. pylori
  • close family hx of PUD
  • drugs
  • blood group O
  • smoking tobacco
  • excessive caffeine
  • psychological stress (thought to be primary cause of PUD)
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5
Q

what drugs increase risk of peptic ulcer disease (PUD?)

A
  • glucorticoids
  • NSAIDs
  • platelet inhibitors
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6
Q

PUD: NSAID-induced risk factors

A
  • long-term use
  • advanced age
  • hx of ulcers
  • corticosteroids
  • anticoagulants
  • alcohol + smoking
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7
Q

Goals of PUD pharmacotherapy

A
  • relieve symptoms
  • promote healing
  • prevent complications
  • prevent future recurrence
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8
Q

what do PPIs end in? and what do they do?

A

“-prazole”
- PPIs block gastric acid secretion
- choice of drug therapy in PUD + gastroesophageal reflex disease

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9
Q

H2 -receptor antagonists - what do they do?

A

suppress gastric acid secretion & are widely prescribed for treating PUD + gastroesophageal disease

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10
Q

what are the H2-receptor antagonists?

A
  1. ranitidine (Zantac)
  2. cimetidine (Tagamet)
  3. famotidine (pepcid)
  4. nizatidine (axid)
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11
Q

H2 receptor antagonists - Pharmacokinetic properties

A
  • rapid absorption from SI
  • 30 minute onset of action
  • half-life from 1-4h
  • no known effects on fetus
  • excreted primarily from kidneys
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12
Q

what are antacids?

A

= alkaline substancse that neutralize stomach acid to treat symptoms of heartburn

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13
Q

Antacids Pharmacotherapy: AEs

A
  • constipation
  • @ high doses, aluminum products bind w/ phosphate in GI tract = LT use can result in phosphate depletion
  • high risk in: malnourished, alcoholics, renal disease
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14
Q

Symptoms of bowel obstruction

A

abdominal distension, n/v, bloating, tender
SNT - soft, non-tender, no distention?

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15
Q

Antacids: Contraindications / precautions

A
  • prolonged use with low serum phosphate
  • avoid w/ suspected bowel obstruction
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16
Q

Antacids: Drug Interactions

A
  • don’t take with other meds – will interfere w/ absorption
  • anticholinergic drugs incr effects of antacids
  • aluminum + calcium antacids may inhbit absorption of dietary iron
  • decr absorption of some drugs
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17
Q

Antacids decrease the absorption of which drugs?

A
  • cimetidine
  • fluoroquinolones
  • digoxin
  • isoniazid
  • chloroquine
  • NSAIDs
  • iron salts
  • phenytoin
  • tetracycline
  • thyroxine
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18
Q

Considerations w/ Antacids

A
  • PMH
  • watch kidney labratory values
  • monitor for bowel changes & worsening symptoms
  • **hold drug + notify prescriber **if pt has symptoms of appendicitis, undiagnosed GI bleeding, or suspected obstruction
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19
Q

What helps with simple nausea, such as motion sickness?

Pharmacotherapy of N/V

A
  • anticholinergic agents (scopolamine)
  • antihistamines (dimenhydrinate/diphenhydramine)
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20
Q

What helps with chemotherapy-induced N/V?

Pharmacotherapy of N/V

A
  • serotonin (5-HT3) receptor antagonists (Zofran)
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21
Q

what is the primary indication for the use of antiemetic medication?

A

chemotherapy-induced nausea and vomiting

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22
Q

what is used for antineoplastic therapy?

Pharmacotherapy of N/V

A
  • phenothiazine (methotrimeprazine / Nozinan)
  • hydroxyzine (Atarax)
  • dopamine antagonists –> Metoclopramide (Reglan)
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23
Q

Ondansetron - Therapeutic + Pharmacological classification?

A

therapeutic: antiemetic
pharmacologic: serotonin (5-HT3) receptor antagonist

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24
Q

Therapeutic use of ondansetron/ Zofran?

A
  • treatment of serious N/V
  • used at least 30 min prior to chemotherapy + continued for several days after
  • off-label use for cholestatic or opioid-induced pruritus
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25
Q

Ondansetron mechanism of action?

A
  • blocks serotonin receptors in chemoreceptor trigger zone
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26
Q

What does Saline Cathartic do?

Pharmacotherapy w/ Laxatives

A

pulls water into stool (sennosides)
- implies accelerated, stronger, and more complete bowel empyting through osmosis

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27
Q

What do laxatives do (bulk forming)?

Pharmacotherapy w/ Laxatives

A
  • promotes defecation
  • prevents and treats constipation
  • Metamucil + surfactnat type (docusate sodium)
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28
Q

What to monitor with laxatives?

A

monitor for retrosternal pain (bulking from behind) + possible bowel perforation

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29
Q

Treatment with laxatives?

Pharmacotherapy w/ Laxatives

A
  • simple, chroni constipation
  • accelerate removal of ingested toxic substances
  • accelerate removal of dead parasites
  • cleanse bowel prior to diagnostic or surgical procedures
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30
Q

Metamucil considerations

Pharmacotherapy w/ Laxatives

A
  • know PMHx
  • assess BMs + GI functioning
  • mix power + granules w/ at least 8 ounces of pleasant-tasting liquid immediately before use, drinks lots of h2o
  • immediately report complaints of retrosternal pain after taking drug to prescriber
  • smaller, more frequent doses spaced throughout day to relieve discomfort
  • monitor warfarin + digoxin levels closely
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31
Q

Most common opioids for diarrhea + why?

Pharmacotherapy of Diarrhea

A
  • opioids = most effective for controlling severe diarrhea
  • common opioids: codeine + diphenoxylate with atropine (Lomotil)
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32
Q

Diphenoxylate w/ Atropine (Lomotil): therapeutic + pharmacologic classification

Pharmacotherapy of Diarrhea

A
  • antidiarrheal
  • P = opioid
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33
Q

diphenoxylate with atropine (Lomotil): therapeutic effects + uses

A
  • moderate to severe diarrhea
  • not recommended for infants
  • low-maintenance dose can by continued for up to 10 days
  • approved for children 2yr+
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34
Q

diphenoxylate with atropine (Lomotil): mechanism of action

A

acts on smooth muscle cells of intestine to slow peristalsis

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35
Q

diphenoxylate with atropine (Lomotil): Adverse effects

A
  • dizziness
  • lethargy, drowsiness,
  • anticholinergic effects of atropine
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36
Q

diphenoxylate with atropine (Lomotil): Considerations

A
  • know PMHx + Sx
  • complete assessment of BM + GI function (freq + consistency of stools)
  • report abdo distension + s/s decr peristalsis
  • want to find SNTnoD –> softness, non-tender, no distension
  • monitor s/s dehyration, esp young children
  • maintain safe env’t bc can cause drowsiness/dizziness
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37
Q

what is used to treat IBD?

Pharmacotherapy of IBD

A
  • 5-ASA agents
  • immunosuppressants
  • biologic therapies
  • anti-inflammatory drugs
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38
Q

Goals of IBD pharmacotherapy?

A
  • reduce symptoms
  • keep in remission (immunosuppressive agents)
  • alter progression of disease
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39
Q

What is used for induction therapy with Crohn’s Disease?

A

- 5-aminosalicylic acid (5-ASA) agents
- sulfasalazine, olsalazine, balsalazide, mesalamine

severe: corticosteroids
maintenance: immunosuppresive agents

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40
Q

Sulfasalazine + Sulfonamides

Sulfonamide is basis of what groups of drugs?

IBD Pharmacotherapy

A
  • sulfonylureas
  • sulfonamide antibiotics
  • loop + thiazide diuretics
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41
Q

Contraindications / Precautions with Suflasalazine

A

- sulfonamide / salicylate hypersensitivity
- urinary obstruction
- can worsen blood dyscrasias
- hepatic impairment
- dehydration
- diabetes/ hypoglycemia

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42
Q

Actions of Antibiotic (Abx) Drugs

A
  • affect target organism’s structure, metabolism, or life cycle
  • goal = eliminate pathogen
  • may be used for prophylactic treatment of people with suppressed or compromised immune systems
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43
Q

Abx: bactericidal vs bacteriostatic?

A

Bactericidal = kill bacteria
bacteriostatic = slow growth of bacteria

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44
Q

Abx: Nursing Considerations

A
  • make sure pt finishes all abx
  • don’t share
  • keep away from children (safety lid + lock)
  • educate about abx decreasing effects of oral contraceptives and use back up BC – will decr efficacy of hormone-based BC
  • teach pts to wear medic-alert bracelets if allergic
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45
Q

how long to observe pt for possible allergic reactions after parenteral admin?

A

observe for 30 mins, esp after first dose
- monitor for hypersensitivity
- make sure pt knows s/s of allergic rxn

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46
Q

Abx nursing considerations: food

A
  • teach when to take w/ food & when to avoid certain foods (i.e., Ca/iron - tetras)
  • take probiotics (1-2x/day) to counter antibiotic
  • replacement of normal colon flora w/ probiotic supplements or cultured dairy products
  • most best taken on empty stomach
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47
Q

What SEs of Abx to look for?

A
  • skin, teeth, tendons, ears, kidneys
  • assess renal + hepatic function (esp in elderly) = 2.2lb or 1kg/day
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48
Q

How to choose abx + how long?

A

look @ location + shape
- bony locations = harder for abx to get to, e.g., sinus infection = 10-14 days; ear infections ~5 days

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49
Q

Role of Penicilins - Nurse’s job

A
  • assess previous drug rxn to penicilin (animal products exposed to abx)
  • avoid cephalosporins if pt has severe penicilin allergy
  • monitor for hyperkalemia + hypernatremia (incr risk in pt w/ DM/ on dialysis)
  • monitor cardiac status, including ECG changes
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50
Q

Cephalosporin Therapy: Role of Nurse

A
  • assess presence/hx of bleeding disorders
  • assess renal + hepatic function (esp in elderly)
  • assess for persistent diarrhea in children
  • avoid alcohol
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51
Q

Why assess for presence/hx of bleeding disorders when taking cephalosporin abx?

A
  • can reduce prothrombin levels through interference w/ vitamin K metabolism
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52
Q

why avoid alcohol when taking cephalosporins?

A

some cephalosporins cause disulfiram (Antabuse)-like reaction with alcohol – will start to severely vomit

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53
Q

Tetracyline Therapy: Nursing Considerations

A
  • **decr **effectiveness of OCP - should use alt BC
  • incr potential for yeast infection while taking OCP + tetracyclines
  • caution w/ impaired liver/kidney function
  • take on empty stomach to incr absorption
  • may result in photosensitivity
  • watch for supra infection, e.g., pseudomembranous colitis
  • don’t take w/ milk products, iron supplements, magnesium-containing laxatives, or antacids (fluoros)
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54
Q

Macrolide Therapy: Nurse’s Role

A
  • watch liver (EES) erythromycin estolate
  • multiple drug-drug interactions w/ macrolides (CYP)
  • examine pt for hx of cardiac disorders - may exacerbate existing heart disease
  • cause metallic taste in mouth
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55
Q

toxicity? SEs? last name?

Aminoglycosides

A
  • more toxic than most abxs
  • have potential for serious AEs
  • last names don’t work with this family and macrolides
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56
Q

Adverse effects of aminoglycosides

A
  • ototoxicity, worse if given with lasix
  • nephrotoxicity, worse if given with Zovirax (acyclovir)
  • neuromuscular blockage, including resp paralysis
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57
Q

what are they for? how do they work?

Fluoroquinolines

A
  • initially for UTIs
  • bacteriocidal, affect DNA synthesis by inhibting 2 bacterial enzymes
  • activity against gram-neg pathogens, newer drugs have activity against gram-positive microbes
  • for infections of GI, GU, resp, skin + soft tissues
  • “-oxain’s”
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58
Q

Fluoroquinolines - route, food + others

A
  • decr 90% if taken with multivitamins or minerals such as Ca, Mag, Fe, Zinc ions (Tetras 50%)
  • IV = PO, easy transition to home
  • can cause C. Diff, dysrhythmias + liver failure (QT prolongation + arrythmias)
  • CNS disturbances affect 1-8% of pts
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59
Q

Who can’t you give fluoroquinolones?

A
  • Cipro, teenagers or atheletes, will cause tendon rupture
  • children + lactacting or pregnant women
  • crosses into breast milk
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60
Q

Which fluoroquinolone can cause photophobia?

A

norfloxacin – sensitivity to lights

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61
Q

Sulfonamides - what are they + why are they used?

A
  • bacteriostatic, inhibit folic acid
  • broad spectrum, but widespread use has led to incr resistance
  • used in combination to treat UTIs
  • anti-inflammatory properties can help w/ RA + UC
  • teratogenic - cause birth defects
  • don’t take when breastfeeding or pregnant
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62
Q

Sulfonamides - Abx allergy?

A

Rxn to sulfonamide abx could mean allergy to other sulfonamide meds
- DM sulfonylyreas (glyburide + glimepiride), NSAIDs (celecoxib), certain “h2o pills” (furosemide, chlorothiazide), IBD (sulfasalazine)
- allergy to those meds may cause sensitivity to abx, caution w/ 1st dose

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63
Q

Sulfonamides: Prototype drug

A

trimethoprim-sulfamethoxazole = tmp/smz
- bactrim, septra, cotrimoxazole
- potential for allergic rxn

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64
Q

Trimethoprim-sulfamethoxazole: mechanism of action

Sulfonamides

A

to kill bacteria by inhibiting metabolism of folic acid

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65
Q

Trimethoprim-sulfamethoxazole: Adverse Effects

A
  • skin rashes
  • N/V
  • agranulocytosis or thrombocytopenia (caution w/ pernicious anemia)
  • photosensitivity
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66
Q

Trimethoprim-sulfamethoxazole: primary uses

Sulfonamides

A
  • broad spectrum (TMP/SMX) for UTIs
  • pneumocystis carinii pneumonia
  • shigella of small bowel
  • acute episodes of chronic bronchitis
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67
Q

Sulfonamide Therapy: Role of Nurse

A
  • assess for anemia/ other hematological disorders (HgB & platelets) - can incr risk for hemolytic anemia + bld dyscrasias
  • assess renal function; sulfonamides may incr risk for crystalluria
  • use alt BC if on OCP
  • contraindicated w/ hx of hypersensitivity to sulfonamides (SJS)
  • teach how to decr effects of photosensitivity
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68
Q

mech of action, primary use, AEs

vancomycin (Vancocin)

A

mechanism of action: bactericidal, inhbits cell wall synthesis

primary use: reserved for severe/resistant gram-positive infection; effective for MRSA infections, used to treat for C. Diff

AES: ototoxicity (balance + dizziness), nephrotoxicity, red man syndrome, confusion/hallucinations, anaphylaxis

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69
Q

Superinfections - Acquired Resistance, how does it happen?

A
  • abx destroy sensitive bac, only insensitive (mutated) bac remain
  • free from competition from bac that were sensitive to drug, mutated bacteria thrives
  • client now develops infection that is resistant to conventional therapy
  • resistant bacteria can be transmitted to others
  • aka SUPERBUGS
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70
Q

Superbugs: Antibiotic Resistant Organisms (ABO)s

A
  • methicillin-resistant staphylococcus-aureus (MRSA) –> won’t respond to fluoroquinolones, macrolides, aminoglycosdies, tetrocyclines
  • VRE
  • CBO/CBE
  • ESBL - PCNs & Cephalosporins rendered useless
  • VRSA or VISA
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71
Q

What is multidrug-resistance?

A

when organism is resistant to more than 1 drug

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72
Q

Nursing Considerations for Acquired Resistance

A
  • pts take full course of abx
  • don’t save abx or share with others
  • abx don’t treat viral infections
  • overprescribing has led to ARO d/t loss of effectiveness
  • C&S prior to treatment preferable
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73
Q

What does using a single, specific abx do?

A

reduces antagonism +** reduces resistance **

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74
Q

Superinfection: S/S

A
  • diarrhea (c. diff or pseudomembranous colitis)
  • bladder pain + painful urination (e. coli / UTI)
  • abnormal vaginal discharge (yeast - candida)
  • red rash w/ satellite lesion (yeast - candida)
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75
Q

what are super infections?

A
  • secondary infections that occur when too many host flora are killed by abx
  • host flora stop pathogenic organisms
  • host flora killed by abx, microorganisms multiply
  • super opportunistic
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76
Q

Characteristics of Fungal Infections

A
  • not easily transmitted thru casual contact
  • serious fungal infections uncommon w/ healthy immune defense
  • more common in immunocompromised pts
  • treatment may req weeks to months of therapy due to resistance
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77
Q

what environments do fungal bac love?

A

dark, moist environments with lots of sugar

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78
Q

Fungal infections & immunocompromised

A
  • DM, HIV, Cancer
  • systemic fungal infection may be rapidly fatal
  • may experience freq fungal infections and require aggressive pharmacotherapy
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79
Q

nystatin (Mycostain, Nystop): interactions

Superficial Fungal Infections

A

unknown drug interactions + symptomatic overdose treatment

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80
Q

nystatin (Mycostain, Nystop): considerations

A
  • Hx + assessment
  • observe for improvement & report persistent infections
  • avoid occlusive dressings / ointment on moist, dark areas of body
  • teach pt to avoid sharing shoes, towels, or personal objects (esp w/ candida)
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81
Q

drugs similar to nystatin: Griseofulvin (Gris-PEG)

A
  • orally only (ineffective topically)
  • used to treat skin infections, e.g., jock itch, athlete’s foot, ringworm; fungal infections of scalp, fingernails, toenails
  • reserved for cases w/ nail, hair, or large body surface involvement
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82
Q

Griseofulvin (Gris-PEG): SEs

drug similar to nystatin

A
  • phototoxicity
  • SJS
  • urticaria
  • dizziness
  • really decr effectiveness of OCP
  • alcohol = disulfiram-like reaction
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83
Q

If in doubt, what do you do?

A

Check blood glucose
- if pt isn’t feeling well
- went for exam, didn’t get breakfast
- sweating, confused

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84
Q

Why should you watch for hypoglycemia with beta blockers?

A

it masks s/s of hypoglycemia

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85
Q

Short-acting insulin - types, onset, peak, duration

A

regular insulin: Humulin R or Novolin R

onset: 0.5-1h (30 min before meal)
peak: 2-3 h
duration: 8h

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86
Q

Rapid Acting insulin - onset, peak, duration

A

Lispro (Humalog), Aspart (Novorapid), Glulisine (Apidra)

onset: 0-15 min before meal
peak: 0.5-1hr (best to be eating)
duration: 3-4h

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87
Q

which insulin is given in pregnancy & in IV form?

A

regular insulin
- for gestation diabetes

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88
Q

human regular insulin - Humulin R, Novolin R: AEs + SAEs

A

AEs:
- irritation at injection site
- lipodystrophy
- weight gain

SAEs:
- hypoglycemia
- rebound hyperglycemia
- hypokalemia - always watch K+ levels, goes up in DKA

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89
Q

Insulin Therapy: Considerations

A
  • adminster only regular insulin via IV
  • assess alc intake & BG – will make them go up and down
  • medicine hx - herbs + dietary supplements, note meds that can alter effects of insulin
  • ensure pt has consumed or is capable of consuming adequate food to prevent hypoglycemmia rxn
  • assess K of insulin therapy, diet, and exercise, and how these affect serum glucose levels
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90
Q

Insulin Therapy - Injections, what to know

A
  • don’t admin if BG < 4 mmol, or if exhibting signs of hypoglycemia
  • rotate injection sites weekly to prevent lipodystrophy
  • check periodic hemoglobin A1C levels
  • assess s/s LT DM complications: eyes, heart, kidneys, feet
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91
Q

R

Role of Nurse in Insulin Therapy?

A
  • be familiar w/ onset, peak, duration of action of prescribed insulin
  • be aware of important aspects of each specific insulin
  • not all insulin types compatible
  • know s/s hypoglycemia + hyperglycemia
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92
Q

Compatibility of Insulins?

A
  • some may not be mixed tgt in single syringe, e.g., Lantus
  • clear insulin always drawn into syringe first
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93
Q

Considerations for all oral antidiabetic agents (T2D)

A
  • monitor BG (hypo- & hyperglycemia)
  • check s/s illness or infection
  • watch liver function
  • assess for adherence to therapy + ability for self-care
  • sulfonylureas contraindicated in women who are pregnant/breast-feeding, or persons w/ renal/liver disease
  • 2nd gen sulfonylureas have fewer drug-drug interactions
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94
Q

Sulfonylureas - what do they do?

A
  • stimulates insulin release from pancreas
  • incr sensitivity to insulin receptors
  • decr chance of prolonged hypoglycemia
  • 10% experience decr effectiveness after prolonged use
  • most SEs = minor + GI related
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95
Q

examples of sulfonylureas

A
  • glipizide (Glucotrol)
  • glyburide (Diabeta, Micronase)
  • glimepiride (Amaryl)
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96
Q

Sulfonylureas: Contraindications/Precautions

A
  • sensitivity to sulfa drugs or thiazide diuretics
  • renal or hepatic disease
  • if used during pregnancy, discontinue at least 1 month b4 delivery
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97
Q

Sulfonylureas: Drug Interactions

A
  • alcohol
  • oral anticoagulants, MAOIs, probenecid, sulfonamides
  • chloramphenicol, salicylates, clofibrate
  • rifampin
  • thiazides / sulfonamide-based drugs
  • ginseng, garlic, black cohosh, juniper berries, fenugreek, coriander, dandelion root
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98
Q

How long do biguanades need to be taken to reach therapeutic effect?

T2D

A

6-12 weeks

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99
Q

What does Biguanades (metformin) do?

A
  • decr glucose production by liver
  • incr insulin sensitivity at tissues
  • improve glucose transport into cells
  • don’t promote weight gain
  • usually first line of treatment

T2D

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100
Q

how long do biguanades (metformin) need to be held when contrast dye is needed?

T2D

A

48h before and 48h after to prevent lactic acid buildup

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101
Q

Biguanades/metformin: Contraindications / precautions

A
  • impaired renal function
  • HF, liver failure, hx of lactic acidosis
  • concurrent serious infection, e.g., septicemia
  • any condition that predisposes pt to hypoxemia
  • anemia, diarrhea, vomiting, fever, dehydration, gastroparesis, GI obstruction
  • hyperthyroidism, pituitary insufficiency, trauma
  • pregnancy + lactation
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102
Q

Adrenergic Agonists: Catecholamines

A
  • short duration of action
  • destroyed rapidly by monoamine oxidase (MAO)
  • COMT (catechol-O-methyltransferase) is one of several enzymes that degrade catecholamines, such as dopamine, epinephrine, norepinephrine
  • no PO - must be parenteral or inhalation d/t COMT in intestinal tract
  • doesn’t cross BBB
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103
Q

why can’t catecholamines be taken PO?

A

“eats” cates b4 enter bldstream & to target tissue
- broken down before it is absorbed

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104
Q

Adrenergic agonists: noncatecholamines

A
  • may be taken PO
  • not destroyed as rapidly
  • better able to enter brain + affect CNS
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105
Q

Epinephrine: Considerations

Nonselective adrenergic agonists - activate alpha, beta receptors, for bronchospasm, cardiac arrest + hypotension

A
  • assess underlying problem + preexisting conditions
  • hx / px (VS)
  • closely monitor resp status
  • use cardiac monitor/resuscitation equipment
  • monitor BP closely
  • inform prescriber of changes in I&O
  • monitor for hyperglycemia - insulin gtt
  • examine ocular + nasal mucosa
  • protect from light (brown bag/IV)
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106
Q

Alpha 1 Agonists - Phenylephrine: Contraindications / precautions

to relieve nasal decongestion + elevate BP

A
  • severe HTN
  • pre-existing bradycardia
  • advanced CAD
  • nitroglycerin
  • narrow-angle glaucoma
  • hyperthyroidism
  • diabetes
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107
Q

Alpha 1 Agonists - Phenylephrine: treatment of overdose

A
  • phentolamine
  • anti-dysrhythmic drugs
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108
Q

Alpha 1 Agonists - Phenylephrine: Considerations

A
  • examine IV site frequently
  • advise pt to remove contact lenses
  • dark eye protection after ophthalmic admin (dry out eyes + nasal airways)
  • avoid caffeine (w/ all adrenergic agonists)
  • contact HCP if palpitations or jittery/nervousness
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109
Q

Muscarinic Antagonists - what is used?

A

belladonna - natural source of alkaloids w/ anticholinergic activity

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110
Q

Muscarinic Antagonists - Uses

A
  • GI disorders such as IBS
  • opthalmic procedures
  • cardiac rhythm disorders
  • chemotherapy induced diarrhea
  • adjuncts to anesthesia (decr secretions)
  • asthma + COPD (bronchodilation effects)
  • antidotes for poisoning or overdose
  • urge incontinence (overactive bladder), helps w/ spasms - watch BPH
  • Parkinson disease
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111
Q

Muscarinic Antagonists - AEs

A

relatively high incidence of AEs - why it is rarely the drug of choice
- urinary retention
- xerostomia (dry mouth)
- tachycardia
- CNS stimulation
- dry eyes
- photophobia
- urinary retention in BPH

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112
Q

Anticholinergic syndrome: what is it & what’s the antidote?

A

= overdose of muscarinic antagonists
- dry mouth, difficulty swallowing
- visual changes, blurred vision, photophobia
- agitation + hallucinations

antidote = physostigmine
- generally only admin to pts showing severe symptoms

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113
Q

Nicotinic antagonists: Neuromuscular blockers - what do they work on?

A

work on muscle, NOT CNS or motor/sensory perceptions

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114
Q

Nicotinic antagonists: Neuromuscular blockers - how do they work?

A

motor end plate of muscle: causes relase of Ach to travel to receptors on skeletal muscle = muscle contraction

continuous depolarized state in which Ca doesn’t return to its storage depots =
- sustained muscle contraction + paralyzed condition necessary for certain surgical procedures

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115
Q

Nicotinic antagonists: Neuromuscular blockers - Depolarizing

Succinylcholine

A
  • given to produce muscle paralysis duringn short medical-surgical procedures
  • watch for contraction to signal access - preceded by contraction
  • initial contraction and then muscle is relaxed –> paralyzed
  • restlessness = no success
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116
Q

Nicotinic antagonists: Neuromuscular blockers - Nondepolarizing

Tubocararine

A
  • given to produce muscle paralysis during longer surgical procedures
  • occupies Ach receptors and causes muscle paralysis w/o depolarization (no contraction
  • = flaccid paralysis
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117
Q

Succinylcholine: AEs

A
  • complete paralysis of diaphragm/intercostal muscles - watch for resp paralysis
  • tachycardia
  • hypotension
  • urinary retention
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118
Q

Succinylcholine: Serious AEs

A
  • malignant hyperthemia - muscles rigid, skin hot
  • resp depression
  • apnea
  • dysrhythmias
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119
Q

Succinylcholine: Black Box Warning

A
  • children w/ congenital musculoskeletal diseases at greater risk for cardiac arrest
  • no way to predict which pts at risk
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120
Q

Succinylcholine: therapeutic effects + uses

A
  • surgical anesthesia
  • pseudochlinesterase
  • relaxes abdo muscles, or for relaxation prior to intubation
  • induces relaxation in less than 1 minute
  • muscle strength returns quickly after discontinuation of drug
  • pt can still feel pain, is aware of surroundings (use benzos + opioids)
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121
Q

Tubocurarine - what is it for?

A
  • nondepolarizing neuromuscular blockers (NDNBs)
  • tubocurarine = prototype, 9 others in class
  • used to relax skeletal muscles during surgical procedures
  • don’t cause sedation, analgesia, or loss of consciousness –> must use benzos, propofol & opioids in conjunction
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122
Q

what is first-dose phenomenon?

A
  • when the SNS is blocked, PNS dominates
  • hypotension / orthohypotension d/t decr blood flow to brain; syncope
  • reflex tachycardia and nasal congestion also occur
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123
Q

How to prevent first-dose phenomenon?

A

prevention by initial therapy begun with low doses and usually given at bedtime

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124
Q

what do they do?

Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers

A
  • block peripheral catecholamines
  • used concurrently w/ drugs like diuretics
  • relax smooth muscle bladder (detrusor) and prostate
  • incr urine flow
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125
Q

Alpha-Adrenergic Antagonists: Selective Alpha1 Blocker - what do they do to** arterioles**?

A

Block vasoconstriction on vascular smooth muscle (afterload) which decr BP directly

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126
Q

Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - what do they do to veins?

A

Block vasoconstriction which decr venous return (preload) to heart and lowers BP indirectly

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127
Q

Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - Therapeutic uses

A
  1. Benign prostatic hyperplasia
  2. Pheochromocytoma
  3. HTN
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128
Q

What selective agents are used?

Selective Alpha1 Blockers: BPH therapeutic use

Alpha-Adrenergic Antagonists

A

2 selective agents used in BPH
1. Alfuzosin (uroxatral)
2. tamsulosin (Flomax)

don’t cure condition, need surgery

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129
Q

what is it?

Selective Alpha1 Blockers: Pheochromocytoma

Alpha-Adrenergic Antagonists

A

small tumour of adrenal medulla, causes irregular secretion of Epi & NE
- excessive secretion of catecholamine in this condition causes severe HTN

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130
Q

Selective Alpha1 Blockers: HTN

Alpha-Adrenergic Antagonists

A

used to treat severe HTN

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131
Q

Beta-Adrenergic Antagonists: Selective

A
  • block only beta1 receptors
  • cardioselective
  • fewer noncardiac SEs
  • little effect on bronchial smooth muscle
  • can be safely given to pts w/ asthma and COPD
132
Q

Beta-Adrenergic Antagonists: Nonselective

A
  • block beta1 and beta2 receptors
  • produce more SEs than selective beta1 antagonists
  • serious SE = bronchoconstriction (caution in pts w/ COPD + asthma)
133
Q

what to not do with beta-adrenergic antagonists?

A
  • don’t stop suddenly, will go into rebound tachycardia / rebound HTN –> can lead to stroke
  • stay away from grapefruit juice + statins (ARBs)
134
Q

When should you not give beta-adrenergic antagonists?

A
  • hypotension
  • bradycardia
  • in 2nd-3rd degree heart block
135
Q

Beta-Adrenergic Antagonists: Therapeutic Uses

A

most therapeutic actions relate to CV system
- slow conduction velocity thru AV node
- decr HR (chronotropic)
- decr force of contractions (inotropic)
- during stress/exercise - prevents sympathetic stimulation to heart
- caution when admin CCBs concurrently bc may potentiate HF

136
Q

How does it take for body to adapt to Beta-Adrenergic Antagonists?

A

in about 6 weeks, pts will feel like shit

137
Q

Beta-Adrenergic Antagonists: AEs

A
  1. prevents hyperglycemia effect of catecholamines –> dangerous in pts w/ DM b/c can cause hypoglycemia + masks s/s hypoglycemia
    - decr amount of free fatty acids available during metabolic stress
  2. bronchoconstriction - cannot be used in pts w/ COPD, asthma
  3. rebound cardiac excitation may occur if beta blockers withdrawn abruptly - never stop w/o talking to HCP first
138
Q

Propranolol: Considerations

Non-selective Beta1 Blockers

A
  • monitor VS q15min to q1hr
  • Hx + Px - assess for asthma + COPD
  • review lab tests for kidney, liver, hematologic + cardiac functions
  • watch for ADRs in older adults + in pts w/ impaired renal function
  • monitor I/O & daily weights (esp in HF)
  • pt edu: decr salt intake, don’t stop drug suddenly
  • examine for impaired circulation: irregular rhythm, SOB, bilateral lower extremities edema
  • watch for widening QRS - immediate nursing attention
139
Q

Propranolol: names of nonselective beta blockers

A

“-olol”
- carvedilol (Coreg)
- labetalol (Normodyne, Trandate)
- sotalol (Betapace, Sorine): watch for widening QRS complex

140
Q

Calcium Channel Blockers: Vascular smooth muscle effects

A
  • prevents contraction of peripheral arterioles (vasodilation + decr BP)
  • afterload reduced - decr peripheral resistence + preload = lower myocardial oxygen demand + less workload for heart
  • dilation of coronary arteries = more bld flow to heart
141
Q

What do CCBs do?

A

stop the influx of Ca into vascular smooth muscle

142
Q

CCBs: Myocardium effects

A

reduces force of myocardial contraction (negative inotropic effect)
- reduces inward movement of calcium during plateau phase of action potential

143
Q

CCBs: Cardiac conduction effects

A

negative chronotropic effect
- SA node generates fewer action potentials
- slows automaticity
- decr hR

144
Q

Nifedipine: Drug Interactions

Dihydropyridine CCBs: selective for vascular smooth muscle & used to treat HTN + angina pectoris

A
  • may interact w/ drugs that induce or inhibit CYP 3A4
  • additive effect w/ other antiHTN drugs
  • incr risk of CHF w/ BB
  • incr serum levels of digoxin - bradycardia
  • syncope/drop in BP w/ alcohol
145
Q

```

Nifedipine: Treatment of Overdose

Dihydropyridine CCBs

A
  • rapid-acting vasopressors such as dopamine, dobutamine
  • calcium infusions
146
Q

Verapamil: Drug Interactions

nondihydropyridines: act on both vascular smooth muscle + myocardia

A
  • incr digoxin levels = incr risk bradycardia
  • additive hypotension / bradycardia with other antiHTN drugs
  • 3x plasma concentration of buspirone
  • risk of myopathy incr significantly w/ statins
  • verapamil incr carbamazepine (Tegretol) levels = neurotoxicity (ataxia/seizures)
  • grapefruit juice may incr levels
147
Q

Drugs similar to verapamil (Calan, Isoptin, Verelan)

A

Diltiazem (Cardizem, Dilacor, Taztia XR, Tiazac)
- treatment of atrial dysrhythmias + HTN, stable, and vasospastic angina
- same profile as verapamil
- migraine prophylaxis off-label

148
Q

What are ACE inhibitors?

what are they used for? what do they do?

A
  • = first-line agents in treatment of HTN and HF
  • block conversion of angiotenin I to angiotensin II (occurs in lungs)
  • results in decr in BP + HR
  • decrease in aldosterone secretion reduces blood volume
  • breaks down bradykinin (similar to histamine)

Drugs affecting renin-angiotensin-aldosterone system

149
Q

How to decide which drug to use for HTN?

primary vs secondary htn treatment

A

primary: due to genetics, treatment = hydrochlorothiazide
secondary - drug of choice = ACE for kidney protection / heart if CVS problems

150
Q

Indications for ACE inhbitoris?

Drugs affecting renin-angiotensin-aldosterone system

A
  • slows progression of HF
  • lower mortality of recent acute MI
  • prophylaxis for adverse cardiac events
  • prevent or delay progression of renal disease and retinopathy of diabetics
151
Q

ACE inhibitors - serious AEs & contraindications?

Drugs affecting renin-angiotensin-aldosterone system

A
  • contraindicated in hyperkalemia
  • caution when using ACEI with K+ sparing diuretics (don’t give with spironolactone)
  • watch K+ levels
  • angioedema most serious –> rapid swelling of throat, face, larynx, tongue that can lead to airway obstruction
  • all have black box warning regarding risk for major congenital defects, esp 2nd & 3rd trimester
152
Q

Lisinopril: therapeutic effects + uses

ACE inhibitor/ antiHTN

A
  • HF
  • HTN
  • acute MI
153
Q

What is the prototype drug for ACEI?

therapeutic classification & pharmacological classification?

A

lisinopril (Prinivil, Zestril)
therapeutic classification: antihypertensive
pharmacologic classification: ACEI

154
Q

Lisinopril: mechanism of action?

ACEI/ antiHTN

A
  • binds to and inhibits action of ACE
  • decr in serum angiotensin II reduces aldosterone, which results in less sodium and water retetion
155
Q

Lisinopril - what are the AEs?

ACEI/ antiHTN

A
  • cough
  • headache
  • dizziness
  • orthostatic hypotension
156
Q

Lisinopril: what are the serious AEs?

ACEI/antiHTN

A
  • angioedema
  • agranulocytosis (abnormal bld levels)
  • hepatotoxicity
157
Q

Lisinopril - contraindications?

ACEI/antiHTN

A
  • pregnancy - category D
  • angioedema
  • hyperkalemia
  • serious renal impairment
158
Q

lisinopril - any nursing considerations?

KNOW THIS!!!

ACEI/anti-HTN

A
  • check renal labs and K+ levels for hyperkalemia
  • monitor BP before administration and 30min to 1 hour after
159
Q

lisinopril - drug interactions?

A
  • decreased antiHTN activity and worsened renal disease (NSAIDs –> GI + GFR = kidneys)
  • synergistic hypotensive action (diuretics + other hypotensives)
  • hyperkalemia (K+ supplements, potassium-sparing diuretics)
  • pregnancy category C (1st trimester), category D (2nd & 3rd)
160
Q

lisinopril - treatment of overdose?

A
  • normal saline or vasopressor
  • hemodialysis
161
Q

Angiotensin II receptor blockers (ARBs) - what are they used for? how do they work?

A
  • act by inhibiting AT1 receptor and are used for HTN + HF
  • block angiotensin II form activating their target receptors in smooth muscle
  • cause vasodilation, reduce PR, decr BP
  • prevent aldosterone secretion
  • promote excretion of Na+ & h2o by kidneys
162
Q

what are the indications for ARBs? contraindications?

A
  • same as ACEI
  • HTN, HF
  • some approved to treat MI and prophylaxis of CVA
  • unlike ARBs, don’t cause cough
  • angioedema less common than ARBs
163
Q

What is the prototype drug for ARBs?

therapeutic & pharmacologic classification?

A

prototype = losartan (Cozaar)
therapeutic classification: antiHTN
pharmacologic: angiotensin II receptor blocker

164
Q

losartan - what are the therapeutic effects/uses?

ARBs

A
  • HTN
  • CVA prophylaxis
  • prevention of diabetic neuropathy
  • off-label use for HF
165
Q

losartan - what is the mechanism of action?

A
  • selectively blocks angiotensin AT1 receptors, resulting in decreased BP
  • blockade prevents cardiac remodelling and deterioration of renal function in pts with diabetes (protects heart & kidneys)
166
Q

losartan - any drug interactions?

A
  • decr antiHTN activity w/ NSAIDs
  • additive hypotensive action w/ diuretics & other hypotensives
  • hyperkalemia –> K+ supplements, potassium-sparing diuretics
  • additive hypotensive effect (alcohol)
167
Q

Etiology & Pathogenesis of HTN - what does HTN damage?

A

heart
- hypertrophy, MI, HF (watch for rapid weight gain, 5lbs/2-3 days), SOB, BLE edema

eyes:
- blindness –> have frequent eye checks

brain:
- stroke - assess for speech changes, drooping face, one-sided weakness

kidneys:
- kidney failure - watch for protein in urine (micro/macro-albuminuria)

168
Q

What is the first line treatment option for HTN? and which drug is 1st choice?

A

diurectics = often first choice of drug for treating mild to moderate HTN
- thiazide diuretic = first line treatment option for HTN
- multi-drug therapy often required

169
Q

What do diuretics do? are there any AEs?

A

decr blood volume and decr BP

AEs:
- dehydration
- hyponatremia
- hypokalemia (less w/ K+ sparing diuretics)
- nocturia (if taken too late in day)
- orthostatic hypotension

170
Q

What diuretics are used for HTN?

A
  • thiazide + thiazide-like diuretics (most common for HTN): hydrochlorothiazide
  • potassium-sparing diuretics: triamterene, spironolactone
  • loop (high-ceiling) diuretics: not usually used for HTN; furosemide, bumetanide (can cause K+ depletion)
171
Q

ACEI - what are the adverse effects?

blocking renin-angiotensin-aldosterone system leads to decr in BP

A
  • persistent cough
  • postural hypotension
  • hyperkalemia
  • angioedema
172
Q

Adrenergic antagonists - beta blockers AEs?

A

nonspecific causes bronchoconstriction - use w/ caution for pts w/ asthma / HF
- low doses: AEs uncommon

higher doses:
- fatigue, activity intolerance
- erectile dysfunction
- masks symptoms of hypoglycemia
- clinical depression

173
Q

ARBS - what does it do and AEs?

A
  • inhibits effects of angiotensin II
  • similar effects to ACEI
  • drug = losartan

fewer AEs than ACEI
- hypotension
- angioedema (more rare)
- more expensive
- no cough

174
Q

Vasodilators - how do they lower BP?

A
  • relax arterial smooth muscle directly = decr resistance (pressure coming back up) and decr afterload
  • affects veins and arteries
  • some drugs also affect veins, such as isosorbide dinitrate (long-acting nitrate) = decr preload

relax arteriolar smooth muscle –> decr resistance, and therefore decr afterload

175
Q

Vasodilators - AEs?

A
  • reflex tachycardia and hypotension
  • compensatory incr in HR due to suden drop in BP
  • fluid retention
  • can be minimized with beta blockers and diuretics
176
Q

Vasodilators - what agents are used?

A
  • hydralazine
  • diazoxide
  • nitroprusside
177
Q

Prototype drug for direct-acting vasodilators?

Therapeutic + pharmacologic classification

A

therapeutic: antiHTN
pharmacologic: direct vasodilator
prototype drug = hydralazine (Apresoline)

178
Q

hydralazine (Apresoline) - what is the therapeutic effects and uses?

vasodilator

A
  • moderate to severe HTN
  • hypertensive emergencies
  • acute HF
179
Q

hydralazine (Apresoline) - what is the mechanism of action?

A
  • causes peripheral vasodilation
  • decr peripheral vascular resistance, HR & CO
  • decr afterload
  • selective for arterioles (selective for afterload)
180
Q

hydralazine (Apresoline) - what are the nursing considerations?

A
  • Hx & Px (esp BP)
  • monitor lab tests for antinuclear antibody titer before and during therapy
  • monitor I&O - potential with fluid retention/edema
  • watch for adverse effects (i.e., palpitations/CP) - heart!!!
  • assess for rapid drop in BP and subsequent tachycardia (can put into shock)
181
Q

Statins - what are they used for?

A
  • for reducing blood lipid levels / for dyslipidemias
  • first-line therapy
  • can reduce LDL levels by 20-40%
  • raise HDL levels
  • primary prevention (no hx of cvs disease)
  • secondary prevention (slow progression and reduce mortality)
182
Q

Prototype drug for statins?

A

atorvastatin (Lipitor)
therapeutic: antihyperlipidemic
pharmacologic: HMG-CoA reductase inhibitor

183
Q

atorvastatin - what are the uses and what is the mechanism of action?

A

therapeutic uses:
- hypercholesterolemia
- family hypercholesterolemia

mechanism of action:
- inhibits HMG-CoA reductase (primary regulatory enzyme in cholesterol biosynthesis)
- liver makes less cholesterol and responds by making more LDL receptors to remove cholesterol from blood

184
Q

atorvastatin - what are the s/s of hepatotoxicity?

A
  • RUQ tenderness
  • changes in stool
  • jaundice
  • bleeding/ bruising
  • abdominal distention
185
Q

Bile acid sequestrants - what are they used for?

A
  • often combined w/ statins to reduce LDL cholesterol levels
  • GI SEs

bile breaks down fat –> bile acid sequestrants binds with bile acids so fat doesn’t get broken down/reabsorbed

186
Q

atorvastatin (Lipitor) - what are the nursing considerations?

A
  • obtain baseline lipid values
  • monitor LDL cholesterol values
  • assess lipid lab tests within 2-4 weeks of initiation of therapy/ change in dose
  • assess for signs of rhabdomyolysis or myopathies (generalized muscle pain/aches all over)
  • observe for digoxin toxicity
  • watch for hepatotoxicity
  • pregnancy - category X
    - no grapefruit juice
    - no alcohol (liver)
187
Q

What is the prototype drug for bile acid sequestrants?

A

cholestyramine (Questran)
therapeutic: antihyperlipidemic
pharmacologic: bile acid sequestrant

188
Q

cholestyramine (Questran): what are the therapeutic uses & what’s the mechanism of action?

A

therapeutic use:
- hypercholesterolemia (elevated LDL)

mechanism of action:
- binds to bile acids
- forms insoluble compounds containing cholesterol that is excreted in feces
- lowers LDL levels by increasing LDL receptors on hepatocytes

189
Q

cholestyramine - what are some nursing considerations?

A
  • completely dissolve powder before administration
  • increase fluid intake
  • assess for early signs of hypoprothrombinemia (watch bld)
  • monitor lab tests for therapeutic effectiveness
  • consult prescriber to see if supplemental vit A & D, and folic acid are required in LT care
  • A & D = fat-soluble vitamins, so can decr absorption, and cholestyramine binds to folic acid –> can lead to deficiencies
190
Q

What is fibric acid used for?

A
  • to lower triglyceride levels
  • have little effect on LDL cholesterol
  • most often used for elevated triglycerides and other “L”s are within good range
191
Q

what is the prototype drug for fibric acid?

A

gemfibrozil (Lopid)
therapeutic: antihyperlipidemic
pharmacologic: fibric acid agent (fibrate)

192
Q

gemfibrozil: what is the therapeutic use & mechanism of action?

A

therapeutic effect/use:
- hypertriglyceridemia and VLDL (very low-density lipoprotein)
- second-line therapy after statins

mechanism of action:
- exact mechanism unknown
- inhibits breakdown of stored fat

193
Q

gemfibrozil (Lopid) - what are the adverse effects?

A
  • GI: abdominal cramping, diarrhea, nausea, dyspepsia (indigestion)
  • headache
  • dizziness
  • peripheral neuropathy
  • diminished libido

fibric acid

194
Q

gemfibrozil (Lopid) - what are the serious adverse effects?

A
  • cholelithiasis (gallstones)
  • anemia
  • eosinophilia (high #)
  • bleeding
195
Q

gemfibrozil (Lopid) - what are the contraindications/ precautions with this medication?

A
  • gallbladder disease
  • serious liver impairment
  • renal impairment
196
Q

gemfibrozil (Lopid) - any drug interactions?

A
  • increased risk of myositis (inflammation) and rhabdomyolysis w/ some statins
  • incr risk of bleeding with anticoagulants: easily bruised, tarry/dark stool, vomit coffee grounds, check hematocrit/labs, hematuria, pain, stroke s/s
  • enhanced hypoglycemia effects w/ antidiabetic agents
197
Q

gemfibrozil - What are some considerations?

A
  • monitor lab tests
  • consult prescriber if inadequate response after 3 months
  • educate pt that drug will cause bloating and gas
  • watch for bleeding
198
Q

Pathophysiology of HF: what are the locations and types of HF?

A

location:
- left-sided: pulmonary edema
- right-sided: peripheral edema

types of failure:
- systolic failure: decr contractility, decr EF
- diastolic: decr ventricular filling, normal EF

199
Q

What are cardiac glycosides used for?

A
  • used in treating HF before ACEIs (ACEIs now first-line treatment)
  • incr force of myocardial contraction –> incr contractility
  • improves symptoms but doesn’t improve mortality
  • stabilizes cardiac conduction abnormalities (watch with other antiarrhythmics)
  • digitalization - incr dose gradually until tissues become saturated with medication and s/s of HF diminish
200
Q

what are the considerations with HF?

A
  • ensure pt monitors for dependent BLE edema
  • worsening SOB or new onset of SOB
  • evaluate # of pillows needed to sleep at night or if they are sleeping in recliner
  • weigh themselves everyday - same time, scale, clothes
    **- call HCP if 2lb weight gain in 1 day, or 5lbs in 2-3 days **
201
Q

what are ARNIs?

A

**= ARB + neprolysing agents **
- decrease mortality by 40% –> will see massive improvement

202
Q

what is the prototype drug for cardiac glycosides?

A

digoxin (Lanoxin, Lanoxicaps)
therapeutic: drug for HF
pharmacologic: cardiac glycoside, inotropic agent

203
Q

digoxin - indications and mechanism of action?

A

indications: HF
mechanism of action: inhibits sodium-potassium-ATPase
- as sodium accumulates in myocytes, calcium ions are released from storage areas to activate contractile elements

204
Q

what are the adverse effects of digoxin?

A
  • general malaise
  • dizziness, headaches
  • N/V, anorexia
    - visual disturbances (blurred or yellow vision)
205
Q

what are the serious adverse effects of digoxin?

A
  • ventricular dysrhythmias
  • AV block (chambers stop talking to other chambers –> heart block)
  • atrial dysrhythmias
  • sinus bradycardia
206
Q

What are organic nitrates used for?

short-acting, long-acting?

A
  • to termine or prevent angina episodes
  • short-acting: to stop angina attacks
  • long-acting: to prevent angina attacks
207
Q

organic nitrates: what is the mechanism of action?

A
  • nitric oxide = cell-signaling molecule and potent vasodilator
  • relaxes venous muscles –> redue preload = less work for heart
  • ## relaxes arterial muscle –> incr blood flow to myocardium, heart doesn’t have to blow so hard = afterload reduced
208
Q

organic nitrates: adverse effects?

A
  • hypotension
  • headache
  • tolerance
209
Q

prototype drug for organic nitrates?

indications too

A

nitroglycerin (Nitrstat, Nitro-Bid, Nitro-Dur, others)
therapeutic: antianginal
pharmacologic: organic nitrate, vasodilator

indications:
- acute angina/MI
- acute CHF/pulmonary edema
- severe HTN
- hypertensive emergency

210
Q

nitroglycerin - what is the mechanism of action?

A
  • forms nitric oxide @ vascular smooth muscle –> triggers cascade resulting in release of calcium ions
  • relaxes both arterial and venous smooth muscles = less cardiac return (less preload & afterload)
    -** dilates coronary arteries = incr O2 to myocardium (cardiac muscles)**
211
Q

MI pharmacologic management

Beta-Adrenergic Blockers - what does it do?

A
  • reduce myocardial demand
  • decr HR (- chronotropic), decr contractility (- inotropic), decr BP
  • counters effects of sympathetic stimulation
  • reduce contraction + strength of contractility (prevents dysrhythmias)
  • therapy usually continued for life
212
Q

MI pharmacologic management

Angiotensin-converting enzyme (ACE) inhibitors - what does it do?

when to use, what to watch for

A
  • given within 24h of onset of MI
  • prevents cardiac remodelling
  • suppress dysrhythmias
  • therapy usually continued for life
  • watch K+ levels and for angioedema
  • check labs for K+ & renal function
213
Q

MI pharmacologic management

Aspirin - what is for?

dosage?

A
  • 160-325 mg initially, and then 81mg daily
  • lower dose causes less GI bleeding
  • heparin and low-molecular-weight heparins (enoxaparin) used for acute treatment
214
Q

MI pharmacologic management

Thrombolitics: what are they used for?

timing? risks?

A
  • to dissolve active clots
  • only for use in early MI (best within 30 mins, no benefit after 24h)
  • severe risk of bleeding
  • alteplase (Activase)
215
Q

MI pharmacologic management

what is used to preevnt and treat MI + thrombotic stroke? any others?

A
  • clopidogrel (Plavix) and ticlopidine (Ticlid) used to prevent + treat MI & thrombotic stroke
  • GP IIb/IIa inhibitors used for MI + pts undergoing percutaneous coronary interventions (PCIs)
  • protease-activated receptor-I-antagonists, such as vorapaxar (Zontivity) = newly approved antiplatelet drugs used to reduce incidence of thrombotic events in pts with MI hx or clotting disorders
216
Q

Coagulation Modifiers: Thrombolytics - what do they do?

A

aka fibrinolytics - alteplase (tPa), tenecteplase (TNK-tPa)
- dissolves bonds that hold existing thrombi together

217
Q

Coagulation modifiers: Antifibrinolytics - what do they do?

A

aminocaproic acid & tranexamic acid
- inhibit activation of plasminogen to plasmin, prevent break-up of fibrin & maintain clot stability
- used to prevent excessive bleeding
- used to stabilize post surgical bleeds

218
Q

Anticoagulants - what are the parental and oral drugs?

A

parental:
- heparin
- low-molecular-weight heparins (only subcu)
- fondaprinuxn (chemically r/t LMWH)
- direct thrombin inhibitors

oral (preferred route):
- warfarin
- dabigatran

219
Q

What are some considerations for anticoagulants?

A
  • baseline blood tests
  • monitor aPTT every 6 hours when adjusting dose (follow PPOs in IHA)
  • monitor for signs of bleeding
  • apply firm pressure x5 min venous & x10 mins for arterial needle sticks
  • reduce risk of trauma
    -** keep heparin antidote readily available (protamine sulfate)**
220
Q

What are the 5 contraindications for all blood thinners?

A
  1. hemorrhagic stroke
  2. GI bleed
  3. trauma
  4. surgery - heparin stopped 24h before surgery, start again 24h after
  5. blood disorders, e.g., hemophilia
221
Q

What are the INR levels for warfarin?

A
  • below 1 if not going for surgery/is normal
  • between 2-3 if at risk for clotting
222
Q

Anticoagulants - patient education?

A
  • no razors, wax instead or use electric razor
  • soft bristled toothbrush
  • no high impact activities (will bruise more easily)
  • if bleeding, e.g., nosebleed or fingercut, > 30 min, go to hospital
  • if GI bleed (coffee ground emesis or melena), go to hospital
223
Q

oral anticoagulants- what is the prototype drug?

A

warfarin (Coumadin)
therapeutic: anticoagulant
pharmacologic: vitamin K antagonist

224
Q

warfarin - therapeutic effects/uses & mechanism of action

A

therapeutic effects/uses:
- prophylaxis arterial thromboembolism (prevention of CVA/MI)
- DVT/PE
- long-term indwelling catheters
- prevent thromboembolic events in high-risk patients

mechanism of action:
- inhibits 2 enzymes involved in formation of activated vit K
- inhibits synthesis of new clotting factors

225
Q

What are some considerations for warfarin?

A
  • assess for risk of thromboemboli
  • monitor PT/INR
  • monitor urine, stool, liver function, blood
  • monitor risk groups for nonadherence
  • teach pts to avoid, or eat sparingly, foods rich in vit K, such as broccoli, leafy greens, etc
226
Q

Warfarin - pt education?

A
  • monitor for signs of bleeding
  • apply firm pressure x 5 min venous & x10 mins for arterial needle sticks
  • reduce risk of trauma
227
Q

Heparin - classifications, therapeutic uses/effects & mechanism of action?

A

therapeutic class: anticoagulant
pharmacologic: indirect thrombin inhibitor

effects/uses:
- acute thromboembolic disorders
- DVT/PE
- unstable angina/evolving MI
- prophylaxis

mechanism of action:
- activates anti-thrombin III, which inhibits thrombin and to a lesser extent, factor Xa (prevents formation of clots)

228
Q

Heparin - any considerations?

A
  • baseline blood tests
  • monitor aPTT q6h when adjusting dose (follow PPOs in IHA)
  • monitor for signs of bleeding
  • apply firm pressure x 5min venous & x10 mins for arterial needle sticks
  • reduce risk of trauma
  • keep heparin antidote readily available (protamine sulfate)
229
Q

What are ADP receptor blockers?

what do they do?

A
  • aka P2Y12 inhibitors
  • antiplatelet agents prescribed for prevention & treatment of arterial thrombosis
  • inhibits aggregation (decr ability to clot, doesn’t come to spot of bleeding)
  • makes blood less “sticky”
230
Q

ADP Receptor Blockers/P2Y12 Inhibitors - what are the agents?

A

reversible:
- Ticlopidine (Ticlid) BID - stroke prophylaxis
- cangrelor

irreversible - MI & stroke
- clopidogrel (Plavix)
- prasugrel

231
Q

Adverse effects of ADP receptor blockers?

A
  • bleeding
  • neutropenia/agranulocytosis
  • thrombotic thrombocytopenic purpura
232
Q

ADP receptor blockers: prototype drug?

A

clopidogrel (Plavix)
therapeutic: antiplatelet agent
pharmacologic: ADP receptor blocker

3 new P2Y12 receptor inhibitors: prasugrel, cangrelor, ticagrelor

233
Q

clopidogrel: therapeutic uses/effects?

A
  • reduce risk of CVA/MI (doesn’t break down clot directly) - more preventative
  • reducing thrombolytic events post-CVA/MI
  • prevent DVT
  • prevent thrombi formation unstable angina / coronary stents
234
Q

clopidogrel - mechanism of action?

A
  • inhibits ADP receptors on platelets and prolongs bleeding time by irreversibly inhibiting platelet aggregation
  • CYP450 interaction
235
Q

What are the drawbacks of clopidogrel?

A
  • delayed onset of action
  • large inter-individual variability in platelet response
  • genetic polymorphism of metabolizing enzyme
  • drug-drug interactions (DDIs)
  • 2-step activation process catalyzed by series of ctyochrome P450 (CYP) isoenzymes
    –> prodrug, requires hepatic conversion to an active metabolite resulting in delayed onset of action and inter-individual variability
236
Q

Thrombolytics - what are they called?

A

“-plase” or “-nase”

237
Q

What are some thrombolytics?

A

streptokinase (SK)/ Urokinase (UK)
- older, slower, more side effects, cheap, allergenic
- for PE, MI, DVT

newer drugs have fewer side effects
- tenecteplase (TNK-tPA)
- alteplase (tPA)

238
Q

What risks do thrombolytics have?

A

risk of bleeding may outweight benefits - watch for s/s hemorrhagic stroke (LOC)

239
Q

Antifibrinolytics: therapeutic uses / effects?

A
  • aplastic anemia
  • hepatic cirrhosis
  • postop cardiac surgery (@ risk for excessive bleeding
  • certain carcinomas
  • hemophilia A
  • excessive post surgical bleeds
240
Q

Antifibrinolytics - what are they for?

A
  • aka hemostatics/tranexamic acid, to promote formation of clots
  • more commonly prescribed in surgical pts
  • occupies binding sites on plasminogen and plasmin
  • prevents digestion of fibrin clot by plasmin
  • stabilizes clot
241
Q

Ferrous Sulfate - Adverse effects?

A
  • N/V
  • brown stains on teeth from liquid
  • darkened stools
  • constipation
242
Q

Ferrous sulfate - contraindications/precautions?

A
  • hemochromatosis
  • PUD
  • regional enteritis
  • ulcerative colitis
243
Q

Considerations for Ferrous Sulfate?

A
  • assess VS for cellular hypoxia
  • give on empty stomach, if possible
  • if difficulty swallowing tablets or capsules, recommend a liquid formulation or less corrosive form, such as ferrous gluconate
  • prevent staining of teeth (rinse with h2o)
  • mix Feosol elixir w/ h2o
  • continue iron therapy for 2-3 months after normal Hgb
  • baseline levels for RBCs, hematocrit, hemoglobin, and serum ferritin
  • monitor BMs
244
Q

Ferrous sulfate - patient and family education

A
  • don’t take tablets or capsules within 1 hour of bedtime
  • don’t crush tablets or empty contents of capsule
  • take ferrous sulfate with full glass of water
  • rinse mouth with clear h2o immediately after ingestion
  • consume citrus fruit or tomato juice with iron preparations (except elixir form)
  • dark green or black stools = harmless SE
  • report constipation or diarrhea
245
Q

what foods to not take with ferrous sulfate?

A

avoid taking with:
- milk
- eggs
- antacids
- caffeine beverages

246
Q

cyanocobalamin - what is it for?

A

T: agent for anemia
P: vitamin supplement
- for vit b12 deficiency anemia

247
Q

cyanocobalamin - adverse effects?

A
  • rashes
  • itching
  • other signs of allergy
248
Q

cyanocobalamin - serious adverse effects?

A
  • sodium retention with possible worsening HF
  • anaphylaxis
  • hypokalemia & potential dysrhythmias
249
Q

Cyanocobalamin - contraindications / precautions?

A
  • suspected sensitivity to cobalt
  • severe pulmonary disease
  • heart disease

pregnancy category A, category C when used parenterally

250
Q

cyanocobalamin - any drug interactions?

A

can decrease absorption
- ethanol/ alcohol
- aminosalicylic acid
- omeprazole
- neomycin
- chloramphenicol

251
Q

cyanocobalamin - any considerations?

A
  • monitor lab tests; repeat test 5-7 days after start of therapy, and @ regular intervals during
  • monitor serum K+ levels during first 48h
  • pts w/ cardiac disease and those on parental cyanocobalamin @ risk for dysrhythmias, palpitations & CP - watch VS
  • be alert to s/s pulmonary edema
  • monitor effectiveness of pharmacotherapy
  • complete diet + drug hx
  • inquire into alcohol drinking patterns
252
Q

What are the symptoms of anxiety disorders?

NEED TO KNOW!!!

A
  • apprehension
  • worry, fear
  • palpitations
  • SOB
  • heartburn
  • dry mouth
  • excess sweating
253
Q

What can high levels of anxiety/ “panic attack” can be misconstrued as?

NEED TO KNOW!!!

A

often can be miscontrued as heart attack
- always rule out MI first (diagnostic tests & ECG)
- obtain hx of recent events that might trigger anxiety or that might indicate drug abuse

254
Q

Anxiety disorders - how do you ensure an accurate diagnosis?

NEED TO KNOW!!!

A

nurse needs to take complete hx:
- medications that may worsen/cause anxiety symptoms
- medical conditions that may be associated with anxiety
- consider nonpharmacological interventions that reduce environmental, physical, and emotional stressors prior to pharmacological intervention

255
Q

Benzodiazepines - what are they ?

A
  • drugs of choice for generalized anxiety disorder and short-term therapy of insomnia
  • off-label use: seizures, alcohol withdrawal, status epilepticus
  • metabolized in liver, excreted in kidneys
  • tolerance develops
  • potential for dependence
  • OD with alcohol may be fatal
  • “-azepam”
256
Q

Benzodiazepines - what are the cautions with them?

NEED TO KNOW!!!

A
  • change dose gradually - DONT stop abruptly
  • watch for suicidal ideation
  • may cause mania or psychosis
  • watch in use with dysfunctional kidneys, liver, CV, or pulmonary system
  • use cautiously with the elderly
257
Q

what are the 5 “Bs” to be aware of with benzodiazepines?

NEED TO KNOW!!!

A
  1. brain: sleepy, make person relaxed, put into dreamy state
  2. blood - cause blood dyscrasias
  3. drops BP
  4. bile (think liver)
  5. bonkers - more likely for elderly (e.g., gets agitated instead of relaxed)
258
Q

benzodiazepines - prototype drug?

A

lorazepam (Ativan)
therapeutic: antianxiety agent, sedative - hypnotic, antiseizure agent
pharmacologic: benzodiazepine, GABA receptor agonist

259
Q

lorazepam - uses & mechanism of action?

A

effects & uses:
- routine management of GAD
- reduce anxiety prior to surgery/medical procedure
- reduce anxiety in mechanically ventilataed patients
- off-label use for insomnia, seizures, ethanol withdrawal, status epilepticus

mechanism of action:
- potentiates GABA
- can cause diff levels of CNS depression: relaxation, sleep (higher doses), coma (higher doses)

260
Q

What are some nursing considerations for lorazepam?

NEED TO KNOW!!!

A
  • aspirate prior to injection (IM) & give slowly
  • assess for paradoxical CNS excitement
  • advise pt to stop smoking
  • watch CBC, liver function & renal function
  • teach nonpharmacological methods first, before anti-anxiety drugs
  • assess for S/S overdose or abuse
  • teach nonpharmacological methods of sleep & relaxation
  • assess for suicidal ideation
261
Q

What are the adverse effects of phenobarbital?

A
  • oversedation
  • “hangover” effect, lethary
  • hallucinations
  • blood dyscrasias
  • hypocalcemia
  • hepatic disease
  • N/V/D/C
  • paradoxical excitation in children or older adults
262
Q

Barbituates - what are they and what are they for?

A

therapeutic: sedative-hypnotics & anti-epileptic drug
pharmacologic: barbituate, GABA receptor agonist

prototype drug: phenobarbital (Luminal)

  • for status epilepticus (IV route) and ST management of insomnia
  • dependence high, overdose / withdrawal severe
263
Q

what are the serious AEs of phenobarbital?

KNOW THIS!!!!

A
  • coma
  • SJS
  • angioedema
  • periorbital edema
  • ** thrombophlebitis**
264
Q

Phenobarbital - any nursing considerations?

NEED TO KNOW!!!

A
  • monitor for resp depression
  • assess pt given IV barbituates q15 min
  • monitor for s/s blood dyscrasias
  • aspirate prior to injection
  • monitor therapeutic serum concentrations of drug (like dig, dilantin, lithium)
  • teach nonpharmacologic methods of relaxation/sleep
  • assess baseline hepatic + renal function and monitor during therapy
  • if pt develops fever, angioedema, and body rash - hold med & call MD
265
Q

What are the causes of depression? does it coexist with other conditions?

NEED TO KNOW!!!

A

causes:
- environmental
- situational
- hereditary
- no longer thought to be related to parenting or unresolved childhood

often does coexist with other conditoins
- anxiety disorders
- substance abuse
- HTN or arthritis

266
Q

Depression - what is it?

NEED TO KNOW!!!

A

a mood disorder
- persistant disturbance in emotion that impairs ability to effectively deal with ADLs
- 2 primary types of mood disorders = depression & bipolar disorder

267
Q

Assessment of Depression - how long does it take for mood to improve?

NEED TO KNOW!!!

A
  • 3 or more weeks of antidepressant therapy may be required before pt’s mood begins to improve
  • 6-8 weeks to reach maximal benefit
  • risk of attempted suicide highest in month before pharmacotherapy
  • majority of persons who commit suicide have been diagnosed with major depression
268
Q

Assessment of Depression - what is the nurse’s role?

NEED TO KNOW!!!

A
  • careful monitoring of talk of suicide
  • weekly or daily patient contact
  • careful monitoring of medications
269
Q

tricyclic antidepressants - what are they used for? and how?

A
  • once mainstay treatment of depression, but have many AEs
  • block reuptake transport of norepinephrine and serotonin @ synapses
270
Q

Tricyclic antidepressants - what are the disadvantages?

NEED TO KNOW!!!

A

many side effects
- anticholinergenic effects/ sympathomimetic effects
- orthostatic hypotension
- sedation (worsened w/ concurrent use of other CNS depressants)
- relatively high incidence of sexual dysfunction (often cause of cessation)

  • withdrawal symptoms if not tapered - don’t stop suddenly
  • may take 3 weeks to see effects & 6 weeks to see optimum benefits
271
Q

tricyclic antidepressants - prototype drug?

A

imipramine (Tofranil)
- therapeutic = tricyclic antidepressant
- pharmacologic = norepinephrine reuptake inhibitor
- for major depressive disorder

off-label uses:
- adjuvant tx of ca / neuropathic pain
- overactive bladder; ADHD; bulimia nervosa
- social anxiety disorder
- panic disorder

272
Q

imipramine - any contraindications?

NEED TO KNOW!!!

A
  • MI, heart block, dysrhythmias
  • asthma, GI disorders, alcoholism, schizophrenia, bipolar disorder
  • avoid use w/ alcohol
  • seizure disorders
273
Q

imipramine - any precautions?

NEED TO KNOW!!!

A

d/t sympathomimetic effect
- suicidal tendencies
- urinary retention
- prostatic hyperplasia
- cardiac/hepatic disease
- increased intraocular pressure
- hyperthyroidism
- parkinson disease

274
Q

what are selective serontin reuptake inhibitors?

A
  • drugs of choice for treating depression d/t low incidence of serious AEs
  • fewer sympathomimetic & anticholinergic effects
  • for variety of MH disorders: social anxiety, PTSD, GAD, panic disorder, OCD
275
Q

imipramine - any considerations?

NEED TO KNOW!!!

A
  • monitor for suicidal ideation
  • be sure pt swallows each dose
  • encourage compliance
  • monitor for urinary retention / constipation
  • treat for dry mouth
276
Q

SSRIs - prototype drug? what is it used for?

A

fluoxetine (Prozac, Sarafem)
therapeutic: anti-depressant, anti-anxiety
pharmacologic: SSRI

uses:
- depression
- bulimia
- pediatric depression
- panic attacks

mechanism of action:
- blocks uptake of serotonin @ neuronal presynaptic membrane
- enhances action of serotonin

277
Q

what is serotonin syndrome?

SSRIs

NEED TO KNOW!!!

A
  • when pt takes multiple medications (or overdose) that cause serotonin to accumulate in neurons in CNS
  • confusion, restlessness, tremors, lack of muscle control
  • conservative treatment to discontinue all serotonergic drugs
278
Q

Fluoxetine - AEs?

A
  • pediatric patients - personality disorder or hyperkinesia**
  • N/V/D/C
  • anorexia
  • cramping/flatulence
  • fluctuations in weight
  • sexual dysfunction
  • seizures
  • poor concentration
  • nightmares
  • hot flashes
  • palpitations
  • nervousness
  • serotonin syndrome
279
Q

fluoxetine - contraindications / precautions

A
  • bipolar disorder
  • cardiac dysfunction
  • diabetes
  • seizure disorders
  • carefully observe peds pts for hyperkinesia and personality changes/disorders
  • late pregnancy
280
Q

Monoaime Oxidase Inhibitors - what are they for?

A
  • effective antidepressants but rarely used d/t potentially serious AEs
  • off-label use for OCD, panic disorder, social anxiety disorder, migraine prophylaxis
  • potentiates effects of insulin, diabetic drugs

NEED TO KNOW!!!

281
Q

MAOIs - what to avoid?

to avoid incidence of AEs

A
  • avoid foods containing tyramine (MAO in food) - foods that have been aged or fermented
  • cheese, alcohol, condiments, certain aged meats, wine (think charcuterie board)
  • avoid L-tyrosine (a.a) - tyramine a component of tyrosine (found in some aged foods - fermented foods, e.g., sausages)
  • avoid caffeine
282
Q

Fluoxetine - drug interactions

A
  • increased extrapyramidal side effects (EPS) with certain antipsychotics
  • incr risk of toxicity with phenytoin, digoxin, carbamazepine
  • excessive sedation with other CNS depressants
  • incr risk of bleeding with warfarin, aspirin, NSAIDs
283
Q

what are the AEs of MAOIs?

A
  • dizziness/orthostatic hypotension
  • drowsiness/headache
  • sexual dysfunction
  • anorexia/ diarrhea
284
Q

what are the serious AEs of MAOIs?

A
  • hypertensive crisis (foods with tyramine)
  • dysrhythmias
  • SIADH- like symptoms (h2o retention)

NEED TO KNOW!!!

285
Q

what is the difficulty with MAOIs?

A

high incidence of AEs & high level of NON-compliance

286
Q

What considerations are there for MAOIs?

A
  • assess for suicidal ideation
  • encourage compliance
  • **avoid foods containing tyramine (MAO in food) - aged / fermented
  • avoid L-tyrosine (a.a.) - tyramine a component of tyrosine**
  • avoid caffeine

NEED TO KNOW!!!

287
Q

what precautions are there for MAOIs?

A
  • epilepsy
  • severe, frequent headaches
  • HTN
  • dysrhythmias
  • suicidal tendencies
288
Q

What is the choice of antiepileptic drug therapy (AED) dependent on?

A
  • dependent on seizure type and characteristics
  • medical hx
  • results of EEG & other diagnostic tests
  • cormorbid conditions
  • never stop taking without guidance of HCP - can cause withdrawal seizures

NEED TO KNOW!!!

289
Q

Benzodiazepines - how & what are they used for?

how do they work for seizures?

A
  • most important drugs in treatment of status epilepticus
  • control seizures by acting in limbic, thalamic, hypothalamic regions of CNS
  • limited applications (use for seizures when other drugs ineffective)
  • have resuscitation equipment available if administering by IV - monitor for CV collapse & resp depression

NEED TO KNOW!!!

290
Q

What are some considerations for benzodiazepines?

A
  • educate on s/s resp depression + cv collapse
  • assess for decr in seizure activity
  • maintain pt safety pre & post seizures (watch for triggers)
  • assess for hx of smoking (may req larger doses)
  • assess for urinary retention
  • don’t mix with other drugs parenterally

NEED TO KNOW!!!

291
Q

Hydantoins - what are they used for?

A
  • most effective in management of most types of seizures, including general seizure, but have many AEs
  • desensitize sodium channels
292
Q

hydantoin - prototype drug?

A

phenytoin (dilantin, phenytek)
- therapeutic: antiepileptic
- pharmacologic: hydantoin, neuronal sodium channel modulator

use = prophylactic therapy of all seizures except absence

mechanisms of action: delays influx of sodium ions in neurons, doesn’t elevate seizure threshold

293
Q

dibenzazepines - what are they for?

A
  • drug of choice for many tonic-clonic and partial seizures
  • acute mania
  • off-label: symptomatic treatment of neuropathic pain, hiccups, severe symptoms of dementia
294
Q

Phenytoin - any considerations?

NEED TO KNOW!!!

A
  • shake suspension well prior to administration
  • watch for extravasation with IV route
  • check bld levels regularly (like lithium, dig, tegretol)
  • monitor CBC (clotting)
  • watch for neurological changes & SE
  • monitor bld glucose in diabetics
  • assess folic acid deficiency
295
Q

dibenzazepines - prototype drug?

A

carbamazepine (carbatrol, tegretol, others)
- t = antiepiletic drug
- p = iminostilbene, neuronal sodium channel modulator

  • inhibits sodium channels, blocks repetitive, sustained firing of neurons
296
Q

carbamazepine - any contraindications/precautions?

dibenzazepines

NEED TO KNOW!!!

A
  • hypersensitivity
  • increased ocular pressure
  • lupus
  • cardiac/hepatic disease
  • HTN
  • older adults (watch narrow safety margin)
  • pregnancy - category D
297
Q

Valproic acid - what is it?

A

valproic acid (Depacon, Depakene, Depakote)
- anti-epileptic drug, anti-manic agent; GABA agonist
- for absence seizures/complex partial seizures; mania; migraine
- incr conc of GABA in brain

298
Q

valproic acid - what are the drug interactions?

A
  • additive sedation w/ CNS depressants & alcohol
  • more rapid metabolish w/ enzyme-indcuing AEDs
  • incr serum levels of TCAs
  • incr serum levels w/ aspirin, isoniazid, cimetidine (watch for bleeding)
  • decr absorption w/ cholestyramine
  • binds with some fat-soluble vitamins
299
Q

what are some considerations w/ valproic acid?

NEED TO KNOW!!!

A
  • monitor seizure activity & check serum levels
  • obtain baseline platelet counts & check PT/PTT/INR regularly during therapy
  • monitor for s/s hyperammonemia & bleeding
  • watch liver lab work
  • naloxone & hemodialysis for overdose treatment
300
Q

What is bipolar disorder?

A
  • alternates between extreme feelings of sadness and extreme mania
  • significantly impacts social and occupational functioning
  • nonadherence = serious problems (d/t highs –> believes they don’t need meds anymore

need to know!

301
Q

what are some nonpharmacological interventions for bipolar disorder?

need to know!

A
  • identifying triggers: lack of sleep, excessive stress, poor nutrition
  • support groups
  • ECT
302
Q

What are some pharmacological interventions for bipolar disorder?

need to know!

A
  • medications
  • highly individualized based on severity and predominant symptoms
303
Q

Lithium - how are they used in BD?

A
  • conventional therapy for tx of BD
  • mood stablizers
  • traditional treatment = lithium carbonate
304
Q

lithium - any drug interactions?

A
  • diuretics = incr risk of lithium toxicity (e.g., lasix)
  • NSAIDs, thiazide diuretics - can incr lithium levels
  • anti-thyroid drugs, drugs containing iodine can incr hypothyroid effect
  • halperidol causes incr neurotoxicity
  • SSRIs, MAOIs, dextromethorphan may result in SES
  • some herbal, food interactions
305
Q

Lithium - any considerations?

need to know!

A
  • monitor serum levels Q1-3 days initially & 2-3 months after
  • assess s/s bipolar disorder before and during treatment
    - obtain baseline thyroid, kidney, cardiac function, lyte levels
  • monitor for s/s lithium toxicity
  • assess daily weight changes, edema, changes in skin turgor
  • lithium = salt –> dehydration incr lithium & overhydration decr lithium levels (n/v/d, or exercising)
  • monitor sodium intake - take table salt to maintain osmotic hydration, but don’t overdo it
306
Q

what are s/s lithium toxicity?

need to know!

A
  • n/v
  • persistent diarrhea
  • coarse trembling of hands or legs
  • frequent muscle twitching, e.g., pronounced jerking of arms or legs
  • blurred vision
  • marked dizziness
  • difficulty walking
  • slurred speech
  • irregular heartbeat
  • swelling of feet or lower legs
307
Q

what is the etiology of schizophrenia?

A
  • precise etiology = unknown
  • genetic component: 5-10x greater risk if 1st-degree relative has disorder
  • neurotransmitter imbalance: overactive dopaminergic pathways in basal nuclei & association w/ dopamine type 2 (D2) receptors (antipsychotic drugs block receptors)

need to know!

308
Q

what has become the drugs of choice for schizophrenia treatment?

need to know!

A

2nd generation (atypical) antipsychotics

309
Q

How to manage pyschoses with medications?

initial treatment

A
  • first doses of antipyschotics may be higher than normal
    —> produces sedation if pti is agitated, aggressive, or posing dangers to others
  • most drugs provided orally
  • benzodiazepenes (lorazepam [Ativan]) –> provided IM to relax pt and may allow initial dose of antipsychotic to be reduced
  • benzos given oral after under control
  • acute symptoms usually resovle in 3-7 days
310
Q

what is it?

Antipsychotic drugs AEs - Extrapyramidal SEs (EPS)

A
  • refers to locations in CNS associated with postural and automatic movements
    includes:
  • acute dystonia
  • akathisia
  • parkinsonism
  • tardive dyskinesia (TD) common with typical anti-psychotics
311
Q

What is tardive dyskinesia?

A
  • syndrome of symptoms characterized by bizarre facial and tongue movements, stiff neck, and difficulty swallowing
  • result of dopamine blockage
  • common with typical antipsychotics
  • treatment = discontinue antipsychotics
  • include ambulatory tardive dyskinesias & oral tardive dyskinesias
312
Q

Extrapyramidal SEs (EPS) - what is it? cause?

A
  • variety of responses that originate outside the pyramidal tracts and in the basal ganglion of the brain
  • s/s: tremors, chorea, dystonia, akinesia, akasthisia
  • result of dopamine blockage
  • common w/ typical antipsychotics
  • treatment with anticholinergic drugs, e.g., benzotropine (Cogentin)
313
Q

what is it? s/s? treatment?

Antispychotics AEs: Neuroleptic malignant syndrome (NMS)

A
  • potentially fatal adverse reaction
  • symptoms: high fever, diaphoresis, muscle rigidity, tachycardia, BP fluctuations
  • condition can deteriorate to stupor or coma without quick, aggressive treatment
  • treatment: antipyretics, electrolytes, muscle relaxants
314
Q

Antipsychotics AEs: adverse effects on reproductive system

A
  • major cause of nonadherence
  • sexual, menstrual, breast dysfunction
315
Q

Nonphenothiazines - what are they? use?

A
  • 1st-gen antipsychotics, same therapeutic applications and similar SEs as phenothiazines
  • similar SEs to phenothiazines (less sedation, fewer anticholinergic SEs)
  • greater or equal incidence of EPS
316
Q

nonphenothiazines - prototype drug

A

haloperidol (Haldol)
- therapeutic: antipsychotic (1st-gen)
- pharmacologic: nonphenothiazine, dopamine antagonist

therapeutic use: high potency antipsychotic, treats acute + chronic psychotic disorders

mechanism of action: anticholinergic effects, alpha1-adrenergic blocking effects, blocks neurotransmission at dopamine D2 receptors

317
Q

haloperidol - adverse effects

need to know!

A
  • anticholinergic symptoms (blurred vision, dry eyes, glaucoma)
  • weight gain
  • headache
  • anemia
  • phototoxicity
  • * most likely to produce EPS (> than phenothiazines)
318
Q

haloperidol - serious adverse effects?

A
  • tachycardia
  • cardiac arrest
  • laryngospasm
  • respiratory depression
  • seizures
  • agranulocytosis / leukopenia/ leukocytosis
  • neuroleptic malignant syndrome (NMS)
319
Q

what is neuroleptic malignant syndrome (NMS)?

A
  • = life-threatening neurological disorder most often caused by adverse reaction to neuroleptic / antipsychotic drugs
  • typically consists of muscle rigidity, fever, sweating, autonomic instability, and cognitive changes
  • cognitive changes: delirium, associated with elevated plasma creatine phosphokinase
320
Q

2nd-gen (atypical) antipsychotics - prototype drug?

A
  • drugs of choice for schizophrenia

prototype drug = risperidone (Risperdal)
- pharmacologic: benzisoxazole & dopamine antagonist
therapeutic effects:
- 1993+: schizophrenia & related psychoses
- 2003: acute mania associated w/ bipolar disorder

mechanism: unknown; blocking binding of dopamine to its receptors? highest affinity for type D2, less on D1

321
Q

Risperidone: considerations?

A
  • if medications cause drowsiness - take @ bedtime
  • watch pt for orthostatic hypotension (rise slowly)
  • assess for EPS/ TD / akathesias/ NMS
  • educate pt for s/s of SEs + what to watch for, when to contact HCP
  • encourage sips of h2o / hard candies for dry mouth & anticholinergic-like symptoms
  • avoid alcohol & caffeine
  • incr fluids + fibre
  • watch liver lab results & educate pt on s/s liver involvement (jaundice/stool)
  • tell pt to report significant weight gain (5lb/week)
  • ensure pt knows that definite improvement may not be seen for 6-8 weeks
322
Q

which drugs are similar to risperidone (Risperdal)?

2nd-gen (atypical) antipsychotics

A
  1. quetiapine (Seroquel)
  2. olanzapine (Zyprexa)
  3. clozapine (Clozari, FazaClo)

need to know!

323
Q

dopamine system stabilizers (DSS) - what are they?

A

prototype drug: aripiprazole (Abilify)
- newer class of atypical antipsychotics
- exhibit both antagonist & partial agonist activity on dopamine receptors = decr ADEs
- minimal risk of EPS
- for schizophrenia control & decr s/s

324
Q

aripiprazole (Abilify) - any considerations?

A
  • monitor for EPS symptoms/ anticholinergic effects
  • ensure adequate nutrition, fluid
  • monitor for s/s NMS
  • watch labs (liver - hepatic pathway, CYP)
325
Q

aripiprazole (Abilify) - what does patient include?

need to know!

A
  • monitor for weight gain/ changes in sexual characteristics (lactation in men)
  • can result in non-compliance; tell pt not stop suddenly
  • teach + document what you shared with pt & what they need to protect their health
  • no alcohol use or illegal drug use
  • no caffeine use
  • no smoking
326
Q

What to consider for all pysch meds?

need to know!

A

know s/s of and which drugs cause:
- TD (Tardive dyskinesia)
- EPS
- NMS
- SES/SS (Serotonin syndrome)

327
Q

Signs & Symptoms of Serotonin Syndrome?

A
  • confusion
  • agitatoin or restlessness
  • dilated pupils (NMS)
  • headache
  • changes in BP and/or temp
  • N/V/D
  • rapid HR
  • tremor
  • loss of muscle coordination / twitching of muscles
  • shivering & goosebumps
  • heavy sweating

serious:
- high fever (super concerning)
- seizures
- irregular heartbeat
- unconsciousness

N220 (17 decks)

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