All Flashcards

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
Ondansetron mechanism of action?
- blocks serotonin receptors in chemoreceptor trigger zone
26
What does Saline Cathartic do? ## Footnote Pharmacotherapy w/ Laxatives
pulls water into stool (sennosides) - implies accelerated, stronger, and more complete bowel empyting through osmosis
27
What do laxatives do (bulk forming)? ## Footnote Pharmacotherapy w/ Laxatives
- promotes defecation - prevents and treats constipation - Metamucil + surfactnat type (docusate sodium)
28
What to monitor with laxatives?
monitor for retrosternal pain (bulking from behind) + possible bowel perforation
29
Treatment with laxatives? ## Footnote Pharmacotherapy w/ Laxatives
- simple, chroni constipation - accelerate removal of ingested toxic substances - accelerate removal of dead parasites - cleanse bowel prior to diagnostic or surgical procedures
30
Metamucil considerations ## Footnote Pharmacotherapy w/ Laxatives
- 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
31
Most common opioids for diarrhea + why? ## Footnote Pharmacotherapy of Diarrhea
- opioids = most effective for controlling severe diarrhea - common opioids: codeine + diphenoxylate with atropine (Lomotil)
32
Diphenoxylate w/ Atropine (Lomotil): therapeutic + pharmacologic classification ## Footnote Pharmacotherapy of Diarrhea
- antidiarrheal - P = opioid
33
diphenoxylate with atropine (Lomotil): therapeutic effects + uses
- moderate to severe diarrhea - not recommended for infants - low-maintenance dose can by continued for up to 10 days - approved for children 2yr+
34
diphenoxylate with atropine (Lomotil): mechanism of action
acts on smooth muscle cells of intestine to slow peristalsis
35
diphenoxylate with atropine (Lomotil): Adverse effects
- dizziness - lethargy, drowsiness, - anticholinergic effects of atropine
36
diphenoxylate with atropine (Lomotil): Considerations
- 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**
37
what is used to treat IBD? ## Footnote Pharmacotherapy of IBD
- 5-ASA agents - immunosuppressants - biologic therapies - anti-inflammatory drugs
38
Goals of IBD pharmacotherapy?
- reduce symptoms - keep in remission (immunosuppressive agents) - alter progression of disease
39
What is used for induction therapy with Crohn's Disease?
**- 5-aminosalicylic acid (5-ASA) agents** - sulfasalazine, olsalazine, balsalazide, mesalamine severe: corticosteroids maintenance: immunosuppresive agents
40
# Sulfasalazine + Sulfonamides Sulfonamide is basis of what groups of drugs? ## Footnote IBD Pharmacotherapy
- sulfonylureas - sulfonamide antibiotics - loop + thiazide diuretics
41
Contraindications / Precautions with Suflasalazine
**- sulfonamide / salicylate** hypersensitivity - urinary obstruction - can worsen blood dyscrasias - hepatic impairment - dehydration - diabetes/ hypoglycemia
42
Actions of Antibiotic (Abx) Drugs
- 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
43
Abx: bactericidal vs bacteriostatic?
Bactericidal = kill bacteria bacteriostatic = slow growth of bacteria
44
Abx: Nursing Considerations
- 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
45
how long to observe pt for possible allergic reactions after parenteral admin?
observe for 30 mins, esp after first dose - monitor for hypersensitivity - make sure pt knows s/s of allergic rxn
46
Abx nursing considerations: food
- 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
47
What SEs of Abx to look for?
- skin, teeth, tendons, ears, kidneys - assess renal + hepatic function (esp in elderly) = 2.2lb or 1kg/day
48
How to choose abx + how long?
look @ location + shape - bony locations = harder for abx to get to, e.g., sinus infection = 10-14 days; ear infections ~5 days
49
Role of Penicilins - Nurse's job
- 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
50
Cephalosporin Therapy: Role of Nurse
- assess presence/hx of bleeding disorders - assess renal + hepatic function (esp in elderly) - assess for persistent diarrhea in children - avoid alcohol
51
Why assess for presence/hx of bleeding disorders when taking cephalosporin abx?
- can reduce prothrombin levels through interference w/ vitamin K metabolism
52
why avoid alcohol when taking cephalosporins?
some cephalosporins cause disulfiram (Antabuse)-like reaction with alcohol -- will start to severely vomit
53
Tetracyline Therapy: Nursing Considerations
- **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)
54
Macrolide Therapy: Nurse's Role
- 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
55
# toxicity? SEs? last name? Aminoglycosides
- more toxic than most abxs - have potential for serious AEs - last names don't work with this family and macrolides
56
Adverse effects of aminoglycosides
- ototoxicity, worse if given with lasix - nephrotoxicity, worse if given with Zovirax (acyclovir) - neuromuscular blockage, including resp paralysis
57
# what are they for? how do they work? Fluoroquinolines
- 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"
58
Fluoroquinolines - route, food + others
- 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
59
Who can't you give fluoroquinolones?
- Cipro, teenagers or atheletes, will cause tendon rupture - children + lactacting or pregnant women - crosses into breast milk
60
Which fluoroquinolone can cause photophobia?
norfloxacin -- sensitivity to lights
61
Sulfonamides - what are they + why are they used?
- 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
62
Sulfonamides - Abx allergy?
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
63
Sulfonamides: Prototype drug
trimethoprim-sulfamethoxazole = tmp/smz - bactrim, septra, cotrimoxazole - potential for allergic rxn
64
Trimethoprim-sulfamethoxazole: mechanism of action ## Footnote Sulfonamides
to kill bacteria by inhibiting metabolism of folic acid
65
Trimethoprim-sulfamethoxazole: Adverse Effects
- skin rashes - N/V - agranulocytosis or thrombocytopenia (caution w/ pernicious anemia) - photosensitivity
66
Trimethoprim-sulfamethoxazole: primary uses ## Footnote Sulfonamides
- broad spectrum (TMP/SMX) for UTIs - pneumocystis carinii pneumonia - shigella of small bowel - acute episodes of chronic bronchitis
67
Sulfonamide Therapy: Role of Nurse
- 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
68
# mech of action, primary use, AEs vancomycin (Vancocin)
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**
69
Superinfections - Acquired Resistance, how does it happen?
- 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**
70
Superbugs: Antibiotic Resistant Organisms (ABO)s
- **methicillin-resistant staphylococcus-aureus (MRSA) --> won't respond to fluoroquinolones, macrolides, aminoglycosdies, tetrocyclines** - VRE - CBO/CBE - ESBL - PCNs & Cephalosporins rendered useless - VRSA or VISA
71
What is multidrug-resistance?
when organism is resistant to more than 1 drug
72
Nursing Considerations for Acquired Resistance
- 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
73
What does using a single, specific abx do?
reduces antagonism +** reduces resistance **
74
Superinfection: S/S
- 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)
75
what are super infections?
- 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
76
Characteristics of Fungal Infections
- 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
77
what environments do fungal bac love?
dark, moist environments with lots of sugar
78
Fungal infections & immunocompromised
- DM, HIV, Cancer - systemic fungal infection may be rapidly fatal - may experience freq fungal infections and require aggressive pharmacotherapy
79
nystatin (Mycostain, Nystop): interactions ## Footnote Superficial Fungal Infections
unknown drug interactions + symptomatic overdose treatment
80
nystatin (Mycostain, Nystop): considerations
- 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)
81
drugs similar to nystatin: Griseofulvin (Gris-PEG)
- 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
82
Griseofulvin (Gris-PEG): SEs ## Footnote drug similar to nystatin
- phototoxicity - SJS - urticaria - dizziness - really decr effectiveness of OCP - alcohol = disulfiram-like reaction
83
If in doubt, what do you do?
**Check blood glucose** - if pt isn't feeling well - went for exam, didn't get breakfast - sweating, confused
84
Why should you watch for hypoglycemia with beta blockers?
it masks s/s of hypoglycemia
85
Short-acting insulin - types, onset, peak, duration
regular insulin: Humulin R or Novolin R onset: 0.5-1h (30 min before meal) peak: 2-3 h duration: 8h
86
Rapid Acting insulin - onset, peak, duration
Lispro (Humalog), Aspart (Novorapid), Glulisine (Apidra) onset: 0-15 min before meal peak: 0.5-1hr (**best to be eating)** duration: 3-4h
87
which insulin is given in pregnancy & in IV form?
regular insulin - for gestation diabetes
88
human regular insulin - Humulin R, Novolin R: AEs + SAEs
AEs: - irritation at injection site - lipodystrophy - weight gain SAEs: - hypoglycemia - rebound hyperglycemia - hypokalemia - always watch K+ levels, goes up in DKA
89
Insulin Therapy: Considerations
- 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
90
Insulin Therapy - Injections, what to know
- 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
91
# R Role of Nurse in Insulin Therapy?
- be familiar w/ **onset, peak, duration of action** of prescribed insulin - be aware of i**mportant aspects** of each specific insulin - not all insulin types compatible - know s**/s hypoglycemia + hyperglycemia**
92
Compatibility of Insulins?
- some may not be mixed tgt in single syringe, e.g., Lantus - **clear insulin always drawn into syringe first**
93
Considerations for all oral antidiabetic agents (T2D)
- 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
94
Sulfonylureas - what do they do?
- 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
95
examples of sulfonylureas
- glipizide (Glucotrol) - glyburide (Diabeta, Micronase) - glimepiride (Amaryl)
96
Sulfonylureas: Contraindications/Precautions
- sensitivity to sulfa drugs or thiazide diuretics - renal or hepatic disease - if used during pregnancy, discontinue at least 1 month b4 delivery
97
Sulfonylureas: Drug Interactions
- alcohol - oral anticoagulants, MAOIs, probenecid, sulfonamides - chloramphenicol, salicylates, clofibrate - rifampin - thiazides / sulfonamide-based drugs - ginseng, garlic, black cohosh, juniper berries, fenugreek, coriander, dandelion root
98
How long do biguanades need to be taken to reach therapeutic effect? ## Footnote T2D
6-12 weeks
99
What does Biguanades (metformin) do?
- 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 ## Footnote T2D
100
how long do biguanades (metformin) need to be held when contrast dye is needed? ## Footnote T2D
48h before and 48h after to prevent lactic acid buildup
101
Biguanades/metformin: Contraindications / precautions
- 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
102
Adrenergic Agonists: Catecholamines
- 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
103
why can't catecholamines be taken PO?
"eats" cates b4 enter bldstream & to target tissue - broken down before it is absorbed
104
Adrenergic agonists: noncatecholamines
- may be taken PO - not destroyed as rapidly - better able to enter brain + affect CNS
105
Epinephrine: Considerations ## Footnote Nonselective adrenergic agonists - activate alpha, beta receptors, for bronchospasm, cardiac arrest + hypotension
- 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)
106
Alpha 1 Agonists - Phenylephrine: Contraindications / precautions ## Footnote to relieve nasal decongestion + elevate BP
- severe HTN - pre-existing bradycardia - advanced CAD - nitroglycerin - narrow-angle glaucoma - hyperthyroidism - diabetes
107
Alpha 1 Agonists - Phenylephrine: treatment of overdose
- phentolamine - anti-dysrhythmic drugs
108
Alpha 1 Agonists - Phenylephrine: Considerations
- 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
109
Muscarinic Antagonists - what is used?
belladonna - natural source of alkaloids w/ anticholinergic activity
110
Muscarinic Antagonists - Uses
- 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
111
Muscarinic Antagonists - AEs
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
112
Anticholinergic syndrome: what is it & what's the antidote?
= 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
113
Nicotinic antagonists: Neuromuscular blockers - what do they work on?
work on muscle, NOT CNS or motor/sensory perceptions
114
Nicotinic antagonists: Neuromuscular blockers - how do they work?
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
115
Nicotinic antagonists: Neuromuscular blockers - Depolarizing ## Footnote Succinylcholine
- 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
116
Nicotinic antagonists: Neuromuscular blockers - Nondepolarizing ## Footnote Tubocararine
- given to produce muscle paralysis during longer surgical procedures - occupies Ach receptors and causes muscle paralysis w/o depolarization (no contraction - = flaccid paralysis
117
Succinylcholine: AEs
- complete paralysis of diaphragm/intercostal muscles - watch for resp paralysis - tachycardia - hypotension - urinary retention
118
Succinylcholine: Serious AEs
- malignant hyperthemia - muscles rigid, skin hot - resp depression - apnea - dysrhythmias
119
Succinylcholine: Black Box Warning
- children w/ congenital musculoskeletal diseases at greater risk for cardiac arrest - no way to predict which pts at risk
120
Succinylcholine: therapeutic effects + uses
- 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)
121
Tubocurarine - what is it for?
- 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**
122
what is first-dose phenomenon?
- when the SNS is blocked, PNS dominates - hypotension / orthohypotension d/t decr blood flow to brain; syncope - reflex tachycardia and nasal congestion also occur
123
How to prevent first-dose phenomenon?
prevention by initial therapy begun with low doses and usually given at bedtime
124
# what do they do? Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers
- block peripheral catecholamines - used concurrently w/ drugs like diuretics - relax smooth muscle bladder (detrusor) and prostate - incr urine flow
125
Alpha-Adrenergic Antagonists: Selective Alpha1 Blocker - what do they do to** arterioles**?
Block vasoconstriction on vascular smooth muscle (afterload) which decr BP directly
126
Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - what do they do to **veins**?
Block vasoconstriction which decr venous return (preload) to heart and lowers BP indirectly
127
Alpha-Adrenergic Antagonists: Selective Alpha1 Blockers - **Therapeutic uses**
1. Benign prostatic hyperplasia 2. Pheochromocytoma 3. HTN
128
# What selective agents are used? Selective Alpha1 Blockers: BPH therapeutic use | Alpha-Adrenergic Antagonists
2 selective agents used in BPH 1. Alfuzosin (uroxatral) 2. tamsulosin (Flomax) don't cure condition, need surgery
129
# what is it? Selective Alpha1 Blockers: Pheochromocytoma | Alpha-Adrenergic Antagonists
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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Selective Alpha1 Blockers: HTN | Alpha-Adrenergic Antagonists
used to treat severe HTN
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Beta-Adrenergic Antagonists: Selective
- block only beta1 receptors - cardioselective - fewer noncardiac SEs - little effect on bronchial smooth muscle - can be safely given to pts w/ asthma and COPD
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Beta-Adrenergic Antagonists: Nonselective
- block beta1 and beta2 receptors - produce more SEs than selective beta1 antagonists - serious SE = bronchoconstriction (caution in pts w/ COPD + asthma)
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what to not do with beta-adrenergic antagonists?
- don't stop suddenly, will go into rebound tachycardia / rebound HTN --> can lead to stroke - stay away from grapefruit juice + statins (ARBs)
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When should you not give beta-adrenergic antagonists?
- hypotension - bradycardia - in 2nd-3rd degree heart block
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Beta-Adrenergic Antagonists: Therapeutic Uses
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
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How does it take for body to adapt to Beta-Adrenergic Antagonists?
in about 6 weeks, pts will feel like shit
137
Beta-Adrenergic Antagonists: AEs
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
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Propranolol: Considerations ## Footnote Non-selective Beta1 Blockers
- 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
Propranolol: names of nonselective beta blockers
"-olol" - carvedilol (Coreg) - labetalol (Normodyne, Trandate) - sotalol (Betapace, Sorine): watch for widening QRS complex
140
Calcium Channel Blockers: Vascular smooth muscle effects
- 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
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What do CCBs do?
stop the influx of Ca into vascular smooth muscle
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CCBs: Myocardium effects
reduces force of myocardial contraction (negative inotropic effect) - reduces inward movement of calcium during plateau phase of action potential
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CCBs: Cardiac conduction effects
negative chronotropic effect - SA node generates fewer action potentials - slows automaticity - decr hR
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Nifedipine: Drug Interactions ## Footnote Dihydropyridine CCBs: selective for vascular smooth muscle & used to treat HTN + angina pectoris
- 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
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# ``` Nifedipine: Treatment of Overdose ## Footnote Dihydropyridine CCBs
- rapid-acting vasopressors such as dopamine, dobutamine - calcium infusions
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Verapamil: Drug Interactions ## Footnote nondihydropyridines: act on both vascular smooth muscle + myocardia
- 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
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Drugs similar to verapamil (Calan, Isoptin, Verelan)
Diltiazem (Cardizem, Dilacor, Taztia XR, Tiazac) - treatment of atrial dysrhythmias + HTN, stable, and vasospastic angina - same profile as verapamil - migraine prophylaxis off-label
148
What are ACE inhibitors? | what are they used for? what do they do?
- = 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) ## Footnote Drugs affecting renin-angiotensin-aldosterone system
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How to decide which drug to use for HTN? | primary vs secondary htn treatment
primary: due to genetics, treatment = hydrochlorothiazide secondary - drug of choice = ACE for kidney protection / heart if CVS problems
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Indications for ACE inhbitoris? ## Footnote Drugs affecting renin-angiotensin-aldosterone system
- 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
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ACE inhibitors - serious AEs & contraindications? ## Footnote Drugs affecting renin-angiotensin-aldosterone system
- 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
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Lisinopril: therapeutic effects + uses ## Footnote ACE inhibitor/ antiHTN
- HF - HTN - acute MI
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What is the prototype drug for ACEI? | therapeutic classification & pharmacological classification?
lisinopril (Prinivil, Zestril) therapeutic classification: antihypertensive pharmacologic classification: ACEI
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Lisinopril: mechanism of action? ## Footnote ACEI/ antiHTN
- binds to and inhibits action of ACE - decr in serum angiotensin II reduces aldosterone, which results in less sodium and water retetion
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Lisinopril - what are the AEs? ## Footnote ACEI/ antiHTN
- cough - headache - dizziness - orthostatic hypotension
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Lisinopril: what are the serious AEs? ## Footnote ACEI/antiHTN
- angioedema - agranulocytosis (abnormal bld levels) - hepatotoxicity
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Lisinopril - contraindications? ## Footnote ACEI/antiHTN
- pregnancy - category D - angioedema - hyperkalemia - serious renal impairment
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lisinopril - any nursing considerations? | KNOW THIS!!! ## Footnote ACEI/anti-HTN
- check renal labs and K+ levels for hyperkalemia - monitor BP before administration and 30min to 1 hour after
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lisinopril - drug interactions?
- 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)
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lisinopril - treatment of overdose?
- normal saline or vasopressor - hemodialysis
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Angiotensin II receptor blockers (ARBs) - what are they used for? how do they work?
- 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
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what are the indications for ARBs? contraindications?
- 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
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What is the prototype drug for ARBs? | therapeutic & pharmacologic classification?
prototype = losartan (Cozaar) therapeutic classification: antiHTN pharmacologic: angiotensin II receptor blocker
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losartan - what are the therapeutic effects/uses? ## Footnote ARBs
- HTN - CVA prophylaxis - prevention of diabetic neuropathy - off-label use for HF
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losartan - what is the mechanism of action?
- 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)
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losartan - any drug interactions?
- decr antiHTN activity w/ NSAIDs - additive hypotensive action w/ diuretics & other hypotensives - hyperkalemia --> K+ supplements, potassium-sparing diuretics - additive hypotensive effect (alcohol)
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# [](http://)[](http://) Etiology & Pathogenesis of HTN - what does HTN damage?
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)
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What is the first line treatment option for HTN? and which drug is 1st choice?
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
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What do diuretics do? are there any AEs?
decr blood volume and decr BP AEs: - dehydration - hyponatremia - hypokalemia (less w/ K+ sparing diuretics) - nocturia (if taken too late in day) - orthostatic hypotension
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What diuretics are used for HTN?
- 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
ACEI - what are the adverse effects? ## Footnote blocking renin-angiotensin-aldosterone system leads to decr in BP
- persistent cough - postural hypotension - hyperkalemia - angioedema
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Adrenergic antagonists - beta blockers AEs?
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
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ARBS - what does it do and AEs?
- inhibits effects of angiotensin II - similar effects to ACEI - drug = losartan fewer AEs than ACEI - hypotension - angioedema (more rare) - more expensive - no cough
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Vasodilators - how do they lower BP?
- 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 ## Footnote relax arteriolar smooth muscle --> decr resistance, and therefore decr afterload
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Vasodilators - AEs?
- reflex tachycardia and hypotension - compensatory incr in HR due to suden drop in BP - fluid retention - can be minimized with beta blockers and diuretics
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Vasodilators - what agents are used?
- hydralazine - diazoxide - nitroprusside
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Prototype drug for direct-acting vasodilators? | Therapeutic + pharmacologic classification
therapeutic: antiHTN pharmacologic: direct vasodilator prototype drug = hydralazine (Apresoline)
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hydralazine (Apresoline) - what is the therapeutic effects and uses? ## Footnote vasodilator
- moderate to severe HTN - hypertensive emergencies - acute HF
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hydralazine (Apresoline) - what is the mechanism of action?
- causes peripheral vasodilation - decr peripheral vascular resistance, HR & CO - decr afterload - selective for arterioles (selective for afterload)
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hydralazine (Apresoline) - what are the nursing considerations?
- 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)
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Statins - what are they used for?
- 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
Prototype drug for statins?
atorvastatin (Lipitor) therapeutic: antihyperlipidemic pharmacologic: HMG-CoA reductase inhibitor
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atorvastatin - what are the uses and what is the mechanism of action?
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
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atorvastatin - what are the s/s of hepatotoxicity?
- RUQ tenderness - changes in stool - jaundice - bleeding/ bruising - abdominal distention
185
Bile acid sequestrants - what are they used for?
- 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
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atorvastatin (Lipitor) - what are the nursing considerations?
- 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
What is the prototype drug for bile acid sequestrants?
cholestyramine (Questran) therapeutic: antihyperlipidemic pharmacologic: bile acid sequestrant
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cholestyramine (Questran): what are the therapeutic uses & what's the mechanism of action?
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
cholestyramine - what are some nursing considerations?
- 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
What is fibric acid used for?
- 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
what is the prototype drug for fibric acid?
gemfibrozil (Lopid) therapeutic: antihyperlipidemic pharmacologic: fibric acid agent (fibrate)
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gemfibrozil: what is the therapeutic use & mechanism of action?
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
gemfibrozil (Lopid) - what are the adverse effects?
- GI: abdominal cramping, diarrhea, nausea, dyspepsia (indigestion) - headache - dizziness - peripheral neuropathy - diminished libido ## Footnote fibric acid
194
gemfibrozil (Lopid) - what are the serious adverse effects?
- cholelithiasis (gallstones) - anemia - eosinophilia (high #) - bleeding
195
gemfibrozil (Lopid) - what are the contraindications/ precautions with this medication?
- gallbladder disease - serious liver impairment - renal impairment
196
gemfibrozil (Lopid) - any drug interactions?
- 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
gemfibrozil - What are some considerations?
- monitor lab tests - consult prescriber if inadequate response after 3 months - educate pt that drug will cause bloating and gas - watch for bleeding
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Pathophysiology of HF: what are the locations and types of HF?
location: - left-sided: pulmonary edema - right-sided: peripheral edema types of failure: - systolic failure: decr contractility, decr EF - diastolic: decr ventricular filling, normal EF
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What are cardiac glycosides used for?
- 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
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what are the considerations with HF?
- 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
what are ARNIs?
**= ARB + neprolysing agents ** - decrease mortality by 40% --> will see massive improvement
202
what is the prototype drug for cardiac glycosides?
digoxin (Lanoxin, Lanoxicaps) therapeutic: drug for HF pharmacologic: cardiac glycoside, inotropic agent
203
digoxin - indications and mechanism of action?
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
what are the adverse effects of digoxin?
- general malaise - dizziness, headaches - N/V, anorexia **- visual disturbances (blurred or yellow vision)**
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what are the serious adverse effects of digoxin?
- ventricular dysrhythmias - AV block (chambers stop talking to other chambers --> heart block) - atrial dysrhythmias - sinus bradycardia
206
What are organic nitrates used for? | short-acting, long-acting?
- to termine or prevent angina episodes - short-acting: to stop angina attacks - long-acting: to prevent angina attacks
207
organic nitrates: what is the mechanism of action?
- 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
organic nitrates: adverse effects?
- hypotension - headache - tolerance
209
prototype drug for organic nitrates? | indications too
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
nitroglycerin - what is the mechanism of action?
- 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
# MI pharmacologic management Beta-Adrenergic Blockers - what does it do?
- 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
# MI pharmacologic management Angiotensin-converting enzyme (ACE) inhibitors - what does it do? | when to use, what to watch for
- 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
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# MI pharmacologic management Aspirin - what is for? | dosage?
- 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
# MI pharmacologic management Thrombolitics: what are they used for? | timing? risks?
- 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
# MI pharmacologic management what is used to preevnt and treat MI + thrombotic stroke? any others?
- 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
Coagulation Modifiers: Thrombolytics - what do they do?
aka fibrinolytics - alteplase (tPa), tenecteplase (TNK-tPa) - dissolves bonds that hold existing thrombi together
217
Coagulation modifiers: Antifibrinolytics - what do they do?
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
Anticoagulants - what are the parental and oral drugs?
parental: - heparin - low-molecular-weight heparins (only subcu) - fondaprinuxn (chemically r/t LMWH) - direct thrombin inhibitors oral (preferred route): - warfarin - dabigatran
219
What are some considerations for anticoagulants?
- 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
What are the 5 contraindications for all blood thinners?
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
What are the INR levels for warfarin?
- below 1 if not going for surgery/is normal - between 2-3 if at risk for clotting
222
Anticoagulants - patient education?
- 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
oral anticoagulants- what is the prototype drug?
warfarin (Coumadin) therapeutic: anticoagulant pharmacologic: vitamin K antagonist
224
warfarin - therapeutic effects/uses & mechanism of action
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
What are some considerations for warfarin?
- 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
Warfarin - pt education?
- monitor for signs of bleeding - apply firm pressure x 5 min venous & x10 mins for arterial needle sticks - reduce risk of trauma
227
Heparin - classifications, therapeutic uses/effects & mechanism of action?
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
Heparin - any considerations?
- 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
What are ADP receptor blockers? | what do they do?
- 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
ADP Receptor Blockers/P2Y12 Inhibitors - what are the agents?
reversible: - Ticlopidine (Ticlid) BID - stroke prophylaxis - cangrelor irreversible - MI & stroke - clopidogrel (Plavix) - prasugrel
231
Adverse effects of ADP receptor blockers?
- bleeding - neutropenia/agranulocytosis - thrombotic thrombocytopenic purpura
232
ADP receptor blockers: prototype drug?
clopidogrel (Plavix) therapeutic: antiplatelet agent pharmacologic: ADP receptor blocker 3 new P2Y12 receptor inhibitors: prasugrel, cangrelor, ticagrelor
233
clopidogrel: therapeutic uses/effects?
- **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
clopidogrel - mechanism of action?
- inhibits ADP receptors on platelets and prolongs bleeding time by irreversibly inhibiting platelet aggregation - CYP450 interaction
235
What are the drawbacks of clopidogrel?
- 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
Thrombolytics - what are they called?
"-plase" or "-nase"
237
What are some thrombolytics?
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
What risks do thrombolytics have?
risk of bleeding may outweight benefits - watch for s/s hemorrhagic stroke (LOC)
239
Antifibrinolytics: therapeutic uses / effects?
- aplastic anemia - hepatic cirrhosis - postop cardiac surgery (@ risk for excessive bleeding - certain carcinomas - hemophilia A - excessive post surgical bleeds
240
Antifibrinolytics - what are they for?
- 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
Ferrous Sulfate - Adverse effects?
- N/V - **brown stains on teeth from liquid** - darkened stools - constipation
242
Ferrous sulfate - contraindications/precautions?
- hemochromatosis - PUD - regional enteritis - ulcerative colitis
243
Considerations for Ferrous Sulfate?
- 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
Ferrous sulfate - patient and family education
- 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
what foods to not take with ferrous sulfate?
avoid taking with: - milk - eggs - antacids - caffeine beverages
246
cyanocobalamin - what is it for?
T: agent for anemia P: vitamin supplement - for vit b12 deficiency anemia
247
cyanocobalamin - adverse effects?
- rashes - itching - other signs of allergy
248
cyanocobalamin - serious adverse effects?
- sodium retention with possible worsening HF - anaphylaxis - hypokalemia & potential dysrhythmias
249
Cyanocobalamin - contraindications / precautions?
- suspected sensitivity to cobalt - severe pulmonary disease - heart disease pregnancy category A, category C when used parenterally
250
cyanocobalamin - any drug interactions?
can decrease absorption - ethanol/ alcohol - aminosalicylic acid - omeprazole - neomycin - chloramphenicol
251
cyanocobalamin - any considerations?
- 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
What are the symptoms of anxiety disorders? ## Footnote NEED TO KNOW!!!
- apprehension - worry, fear - palpitations - SOB - heartburn - dry mouth - excess sweating
253
What can high levels of anxiety/ "panic attack" can be misconstrued as? ## Footnote NEED TO KNOW!!!
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
Anxiety disorders - how do you ensure an accurate diagnosis? ## Footnote NEED TO KNOW!!!
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
Benzodiazepines - what are they ?
- 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
Benzodiazepines - what are the cautions with them? ## Footnote NEED TO KNOW!!!
- 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
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what are the 5 "Bs" to be aware of with benzodiazepines? ## Footnote NEED TO KNOW!!!
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)
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benzodiazepines - prototype drug?
lorazepam (Ativan) therapeutic: antianxiety agent, sedative - hypnotic, antiseizure agent pharmacologic: benzodiazepine, GABA receptor agonist
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lorazepam - uses & mechanism of action?
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)
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What are some nursing considerations for lorazepam? ## Footnote NEED TO KNOW!!!
- 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
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What are the adverse effects of phenobarbital?
- oversedation - "hangover" effect, lethary - hallucinations - blood dyscrasias - hypocalcemia - hepatic disease - N/V/D/C - paradoxical excitation in children or older adults
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Barbituates - what are they and what are they for?
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
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what are the serious AEs of phenobarbital? | KNOW THIS!!!!
- **coma** - **SJS** - **angioedema** - **periorbital edema** - ** thrombophlebitis**
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Phenobarbital - any nursing considerations? ## Footnote NEED TO KNOW!!!
- 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
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What are the causes of depression? does it coexist with other conditions? ## Footnote NEED TO KNOW!!!
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
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Depression - what is it? ## Footnote NEED TO KNOW!!!
a mood disorder - persistant disturbance in emotion that impairs ability to effectively deal with ADLs - 2 primary types of mood disorders = depression & bipolar disorder
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Assessment of Depression - how long does it take for mood to improve? ## Footnote NEED TO KNOW!!!
- 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
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Assessment of Depression - what is the nurse's role? ## Footnote NEED TO KNOW!!!
- careful monitoring of talk of suicide - weekly or daily patient contact - careful monitoring of medications
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tricyclic antidepressants - what are they used for? and how?
- once mainstay treatment of depression, but have many AEs - block reuptake transport of norepinephrine and serotonin @ synapses
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Tricyclic antidepressants - what are the disadvantages? ## Footnote NEED TO KNOW!!!
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
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tricyclic antidepressants - prototype drug?
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
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imipramine - any contraindications? ## Footnote NEED TO KNOW!!!
- MI, heart block, dysrhythmias - asthma, GI disorders, alcoholism, schizophrenia, bipolar disorder - avoid use w/ alcohol - seizure disorders
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imipramine - any precautions? ## Footnote NEED TO KNOW!!!
d/t sympathomimetic effect - suicidal tendencies - urinary retention - prostatic hyperplasia - cardiac/hepatic disease - increased intraocular pressure - hyperthyroidism - parkinson disease
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what are selective serontin reuptake inhibitors?
- 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
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imipramine - any considerations? ## Footnote NEED TO KNOW!!!
- monitor for suicidal ideation - be sure pt swallows each dose - encourage compliance - monitor for urinary retention / constipation - treat for dry mouth
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SSRIs - prototype drug? what is it used for?
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
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what is serotonin syndrome? | SSRIs ## Footnote NEED TO KNOW!!!
- 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
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Fluoxetine - AEs?
- **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
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fluoxetine - contraindications / precautions
- bipolar disorder - cardiac dysfunction - diabetes - seizure disorders - carefully observe peds pts for hyperkinesia and personality changes/disorders - late pregnancy
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Monoaime Oxidase Inhibitors - what are they for?
- 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 ## Footnote NEED TO KNOW!!!
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MAOIs - what to avoid? | to avoid incidence of AEs
- 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**
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Fluoxetine - drug interactions
- **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
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what are the AEs of MAOIs?
- dizziness/orthostatic hypotension - drowsiness/headache - sexual dysfunction - anorexia/ diarrhea
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what are the serious AEs of MAOIs?
- **hypertensive crisis (foods with tyramine)** - dysrhythmias - SIADH- like symptoms (h2o retention) ## Footnote NEED TO KNOW!!!
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what is the difficulty with MAOIs?
high incidence of AEs & high level of NON-compliance
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What considerations are there for MAOIs?
- 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 ## Footnote NEED TO KNOW!!!
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what precautions are there for MAOIs?
- epilepsy - severe, frequent headaches - HTN - dysrhythmias - suicidal tendencies
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What is the choice of antiepileptic drug therapy (AED) dependent on?
- 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 ## Footnote NEED TO KNOW!!!
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Benzodiazepines - how & what are they used for? | how do they work for seizures?
- 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 ## Footnote NEED TO KNOW!!!
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What are some considerations for benzodiazepines?
- 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 ## Footnote NEED TO KNOW!!!
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Hydantoins - what are they used for?
- most effective in management of most types of seizures, including general seizure, but have many AEs - desensitize sodium channels
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hydantoin - prototype drug?
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
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dibenzazepines - what are they for?
- drug of choice for many tonic-clonic and partial seizures - acute mania - off-label: symptomatic treatment of neuropathic pain, hiccups, severe symptoms of dementia
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Phenytoin - any considerations? ## Footnote NEED TO KNOW!!!
- 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
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dibenzazepines - prototype drug?
carbamazepine (carbatrol, tegretol, others) - t = antiepiletic drug - p = iminostilbene, neuronal sodium channel modulator - inhibits sodium channels, blocks repetitive, sustained firing of neurons
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carbamazepine - any contraindications/precautions? | dibenzazepines ## Footnote NEED TO KNOW!!!
- hypersensitivity - increased ocular pressure - lupus - cardiac/hepatic disease - HTN - older adults (watch narrow safety margin) - pregnancy - category D
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Valproic acid - what is it?
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
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valproic acid - what are the drug interactions?
- 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
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what are some considerations w/ valproic acid? ## Footnote NEED TO KNOW!!!
- 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
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What is bipolar disorder?
- 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 ## Footnote need to know!
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what are some nonpharmacological interventions for bipolar disorder? ## Footnote need to know!
- identifying triggers: lack of sleep, excessive stress, poor nutrition - support groups - ECT
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What are some pharmacological interventions for bipolar disorder? ## Footnote need to know!
- medications - highly individualized based on severity and predominant symptoms
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Lithium - how are they used in BD?
- conventional therapy for tx of BD - mood stablizers - traditional treatment = lithium carbonate
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lithium - any drug interactions?
- **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
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Lithium - any considerations? ## Footnote need to know!
- 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**
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what are s/s lithium toxicity? ## Footnote need to know!
- 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
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what is the etiology of schizophrenia?
- 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) ## Footnote need to know!
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what has become the drugs of choice for schizophrenia treatment? ## Footnote need to know!
2nd generation (atypical) antipsychotics
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How to manage pyschoses with medications? | initial treatment
- 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
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# what is it? Antipsychotic drugs AEs - Extrapyramidal SEs (EPS)
- refers to locations in CNS associated with postural and automatic movements includes: - acute dystonia - akathisia - parkinsonism - tardive dyskinesia (TD) common with typical anti-psychotics
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What is tardive dyskinesia?
- 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
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Extrapyramidal SEs (EPS) - what is it? cause?
- 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)
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# what is it? s/s? treatment? Antispychotics AEs: Neuroleptic malignant syndrome (NMS)
- 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
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Antipsychotics AEs: adverse effects on reproductive system
- major cause of nonadherence - sexual, menstrual, breast dysfunction
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Nonphenothiazines - what are they? use?
- 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
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nonphenothiazines - prototype drug
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
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haloperidol - adverse effects ## Footnote need to know!
- anticholinergic symptoms (blurred vision, dry eyes, glaucoma) - weight gain - headache - anemia - phototoxicity * *** most likely to produce EPS (> than phenothiazines)**
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haloperidol - serious adverse effects?
- tachycardia - cardiac arrest - laryngospasm - respiratory depression - seizures - agranulocytosis / leukopenia/ leukocytosis - neuroleptic malignant syndrome (NMS)
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what is neuroleptic malignant syndrome (NMS)?
- = 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
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2nd-gen (atypical) antipsychotics - prototype drug?
- 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
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Risperidone: considerations?
- 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
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which drugs are similar to risperidone (Risperdal)? | 2nd-gen (atypical) antipsychotics
1. quetiapine (Seroquel) 2. olanzapine (Zyprexa) 3. clozapine (Clozari, FazaClo) ## Footnote need to know!
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dopamine system stabilizers (DSS) - what are they?
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
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aripiprazole (Abilify) - any considerations?
- monitor for EPS symptoms/ anticholinergic effects - ensure adequate nutrition, fluid - monitor for s/s NMS - watch labs (liver - hepatic pathway, CYP)
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aripiprazole (Abilify) - what does patient include? ## Footnote need to know!
- 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
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What to consider for all pysch meds? ## Footnote need to know!
know s/s of and which drugs cause: - TD (Tardive dyskinesia) - EPS - NMS - SES/SS (Serotonin syndrome)
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Signs & Symptoms of Serotonin Syndrome?
- 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