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Pharmacology > Pharmacology Final > Flashcards

Pharmacology Final Flashcards

1
Q

What are dietary supplements?

A

Products intended to enhance a or supplement the diet such as botanicals, vitamins, or minerals

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2
Q

Explain the Dietary supplement Health and Education Act of 1994 and 2000 update (DSHEA)

A
  • Regulatory act for dietary supplements
  • Requires all products to be clearly labeled as “dietary supplements”
  • Product must state “not intended to diagnose, treat, cure, or prevent any disease.”
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3
Q

Explain the Dietary Supplement and Nonprescription Drug Consumer Protection Act of 2007

A

Must now include contact info so consumers can report AE

Manufacturers must evaluate identity, purity, potency, and consumption of products with labels that reflect accurately

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4
Q

What are the 4 phases of pharmacokinetics?

A

Absorption

Distribution

Metabolism (biotransformation)

Excretion

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5
Q

Explain absorption.

A
  • moving a drug from the site of admin to the bloodstream.
  • The primary factor to determine the onset of the drug action and the intensity of the drug action
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6
Q

Explain distribution.

A
  • Movement of medication to the body’s tissues
  • Key factors that influence circulation, permeability of cell membrane, plasma binding protein, Blood brain barrier
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7
Q

Explain metabolism.

A

Drugs are changed into new, less active chemicals

Aka biotransformation

Primary site is the liver

P450 system: determine the speed at which a drug is metabolized. Contributes to drug-drug interactions

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8
Q

Explain excretion.

A

Removing the drug from the body

Primary site is the kidney

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9
Q

Nursing Process: What should you obtain during assessment?

A

Obtain a thorough medication hx, allergies, and past medical conditions

Physical exam: weight, age, anything r/t the disease state or known drug effects

Level of education

Social supports

Financial support

Pattern of health care

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10
Q

Nursing Process: What is done during planning?

A

Set goals and desired patient outcomes

Minimize factors that contribute to medication errors

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11
Q

Nursing Process: Implementation

A

Focus entirely on the task of med admin

Rights of med admin

Provide comfort measures/coping with effects of drug therapy

Patient education

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12
Q

Nursing Process: Evaluation

A

Assess the patient for expected therapeutic outcomes and determine if any AE occurred

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13
Q

What is a half-life?

A

The length of time required for the plasma concentration to decrease by one half after administration

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14
Q

Why is a narrow therapeutic index important to be aware of?

A

Therapeutic drug monitoring used when drugs have a low safety margin (aka narrow therapeutic index/window)

Plasma concentration levels need to be monitored (via labs)

Peak, trough, random drug level

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15
Q

List anticholinergic effects.

A

s/s: dry mouth, constipation, urinary retention, blurred vision, palpitations, tachycardia

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16
Q

What is the MOA and routes for Aspirin (Salicylates)?

A

irreversible inhibition of COX-1 and COX-2, PO and rectal

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17
Q

What are salicylates used for?

A

Reduce mild to moderate pain and inflammation

Fever

Prevention of thromboembolic events

Off label: colorectal cancer prevention

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18
Q

What are the AE of salicylates/ASA?

A

GI: n/v, dyspepsia, heartburn, epigastric discomfort

Clotting: bleeding (increases w/ dose)

Renal impairment

Salicylism

Reye’s syndrome

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19
Q

List salicylate/ASA interactions.

A

Other salicylates

Other drugs that’s cause bleeding

Alcohol

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20
Q

List nursing considerations for salicylates/ASA.

A

Monitor s/s bleeding

Take with food/milk and 8oz water

Recommend PPI w/ long term therapy

Monitor: I&Os, BUN, and creatinine

Monitor for salicylism

Discontinue 1 week before surgery

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21
Q

What is the MOA and route for NSAIDs (ibuprofen)?

A

reversible inhibition of COX 1&2, PO

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22
Q

What are the uses for ibuprofen?

A

Reduce mild-moderate pain and inflammation

Fever

Dysmenorrhea

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23
Q

What are the AE of ibuprofen/NSAIDs?

A

GI (common)

Renal impairment w/ chronic use

BBW

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24
Q

List contraindications of ibuprofen/NSAIDs.

A

Allergy

Bleeding

Corticosteroids

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25
Q

List interactions for ibuprofen/NSAIDs.

A

Anticoagulants (bleeding)

NSAIDS

Alcohol

Corticosteroids

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26
Q

Drug Schedule Law: Explain the Controlled Substance Act of 1970.

A

Ranks drugs for abuse potential in categories 1-5.

Drugs w/ abuse potential

Hospitals, pharmacies, and prescribers have to register with the DEA and use registration numbers to purchase prescribed drugs

They must maintain records of all quantities purchases and sold

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27
Q

What is the MOA and route for morphine (opioid agonist)?

A

reacts with MU and Kappa receptors, po, iv, im, sc, sl, rectal, epidural, intrathecal

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28
Q

What are the uses for opioid agonists like morphine?

A

Relief of acute or chronic severe pain

Suppress cough

Slow GI motility with severe diarrhea

Sedation

Part of general anesthesia

Euphoria and intense relaxation (reason for abuse)

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29
Q

What are the AE of opioid agonists (morphine)?

A

Respiratory depression w/ apnea

(Monitor RR before admin and hold if less than 12. Admin antagonist if RR falls below 10 (naloxone)

CNS depression

GI: constipation and n/v

Urinary retention

Hypotension

Cough suppression

Pruritus

BBW: abuse

Tolerance

Pupil constriction

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30
Q

List contraindications for morphine (opioid agonist).

A

allergy and premature infants

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31
Q

For morphine/opioid agonists use caution in those with?

A

Respiratory dysfunction

GI/GU surgery

GI issue that slow motility

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32
Q

List interactions of opioid agonists.

A

other CNS depressants

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33
Q

What is the OD treatment?

A

Naloxone

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34
Q

What are nursing considerations when administering opioid agonists like morphine?

A

Monitor full set of v/s

Assist w/ ambulation to prevent falls and injury

Encourage fluid and fiber. Patient may need laxative

Monitor for urinary retention

Admin IV push slowly

Give on a fixed schedule not PRN

Administer before pain become severe

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35
Q

What is the MOA and route for opioid antagonist naloxone?

A

binds to MU and KAPPA but does NOT activate them, IV, IM, SC, nasal.

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36
Q

What are the uses for naloxone?

A

OD

Reversal of post op effects

Opioid addiction

Reversing neonatal depression

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37
Q

Opioid antagonists like Naloxone reverse these 4 things.

A

Analgesia

Sedation

Euphoria

Respiratory depression

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38
Q

Corticosteroids (prednisone) uses.

A

RA, SLE, IBD< inflammatory disorders, allergic conditions, asthma, derm disorders, suppression of allograft rejection

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39
Q

What are the AE of corticosteroids/prednisone?

A

Adrenal insufficiency

Infection

Peptic ulcers

Osteoporosis

Behavioral changes

Hyperglycemia

Cushing syndrome

Sodium/water retention

diminished growth in children

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40
Q

List interactions for corticosteroids/prednisone.

A

Hypoglycemic

Nsaids

Alcohol

Diuretics

Vaccines

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41
Q

List contraindications for corticosteroids/prednisone.

A

Allergy

Systemic fungal infections and infections not controlled by meds

Diabetes

Peptic ulcers

Children, pregnancy, lactation

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42
Q

Explain the nurse’s role in anesthesia (what to monitor, assessment preop).

A

Preop assessment :

Contraindications and cautions

Known allergies

Family hx or personal hx of malignant hyperthermia

Weight

Vitals

ECG

Skin assessment

Bowel sounds

Have emergency equipment available

Monitor temperature

Monitor: HR, RR, BP, ECG, cardiac output and AE

Institute safety precautions

Provide comfort measures

Provide pain relief

Skin care and turning

Offer support and encouragement

Provide education

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43
Q

What is the therapeutic use for the prostaglandin inhibitor misoprostol?

A

GI indication is prevention of gastric ulcers caused by long term NSAID therapy.

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44
Q

What is the MOA and route for misoprostol? Keep in mind when to give this medication.

A

inhibits gastric acid secretion and increases bicarb and mucus production in the stomach (protects the stomach lining), PO x4/day w/ meals and at bedtime while on NSAIDS

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45
Q

What are the AE of misoprostol?

A

GI: most common id diarrhea. And abd pain, n/, dyspepsia

GU: miscarriages, excessive bleeding, spotting, cramping

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46
Q

List contraindications for misoprostol. (only 1).

A

pregnancy category x

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47
Q

What is the MOA of antacids (sodium bicarb)?

A

Inorganic chemicals that neutralize stomach acid

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48
Q

Why are antacids not recommended as a primary drug?

A

Not recommended as primary drug class because they do not promote ulcer healing

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49
Q

What are AE of antacids?

A

Acid rebound

Constipation

Diarrhea

Fluid retention and heart failure

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50
Q

List contraindications for antacids.

A

Allergy

Renal impairment

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51
Q

List interactions/instructions specific to antacids.

A

Need to separate antacids from other drugs by two hours

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52
Q

Explain H. Pylori treatment (how is it treated, barriers to compliance).

A

Antibiotics should be given. Usually, a combination of antibiotics is used concurrently to eradicate and decrease resistance.

Use a minimum of two antibiotics perferably 3 and an antisecretory agent (PPI, H2 antag)

Barriers to compliance :

  • Can require up to 12 pill/day for 14 days
  • GI AE
  • Expensive
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53
Q

Explain issues with laxative use. (why does misuse occur, causes, consequences).

A

Misuse occurs from misconceptions of what constitutes normal bowel function

Causes:
-Misconception that bowel movements must occur daily

-Can perpetuate their own use

-Bowel replenishment after evacuation can be 2-5 days; often mistakes for constipation

Consequences: cathartic dependence

-Diminished defecatory reflexes leading to further reliance on laxatives

-Electrolyte imbalance, dehydration, and impaction

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54
Q

What is the MOA for lubricant laxatives (docusate)?

A

used to make defecation easier without stimulating the GI tract.

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55
Q

Lubricant laxatives like docusate are expected to produce a soft stool in _____ to _____ hours after onset of treatment.

A

Produces a soft stool 24-48 hours after onset of treatment

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56
Q

What is the treatment for IBS-C? (constipation predominant IBS)

A

lubiprostone

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57
Q

What is the treatment for IBS-D? (diarrhea predominant IBS)

A

aloesetron

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58
Q

What is the MOA for lubiprostone (IBS-C treatment).

A

activates chloride channels in the intestinal luminal cells (this increases fluid and motility)

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59
Q

What is the MOA for aloestron (IBS-D treatment).

A

inhibits serotonin receptors in the GI tract leading to decreased perception of abdominal pain and discomfort and decreased motility, BBW.

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60
Q

What is the MOA and routes for Hydantoins (phenytoin)?

A

stabilize nerve membranes by influencing ionic channels in the cell membrane (decrease excitability and hyperexcitability). Reduce the tonic-colonic muscular and emotional response to stimulation , PO/IV

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61
Q

What are the AE of Hydantoins (phenytoin)?

A

CNS depression: drowsiness, confusion, fatigue

Increased r/f suicide ideation

GI: gingival hyperplasia, constipation, dry mouth

Bone marrow suppression

Skin reactions (could be serious)

Sever liver toxicity

BBW

Toxicity: nystagmus, ataxia, sedation, blurred/double vision

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62
Q

What is the therapeutic serum level for hydantoins (phenytoin)?

A

10-20

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63
Q

List contraindications of hydantoins (phenytoin).

A

Allery

Pregnancy/lactation

Coma, depression, psychosis

Older adults

Impaired liver or renal function

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64
Q

List interactions for hydantoins (phenytoin).

A

Alcohol or other CNS depressants

Oral contraceptives

Primrose and gingko

IV phenytoin is incompatible with dextrose solutions

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65
Q

What are some nursing considerations when administering hydantoins?

A

Educate not to drive or preform hazardous activity if experiencing CNS effects

Obtain regular dental check ups

Brush teeth with soft bristles

Do not stop taking abruptly

Monitor: CNS and rash

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66
Q

What are 4 treatment goals for status epilepticus?

A
  • maintain ventilation
  • correct hypoglycemia
  • terminate seizures: IV benzos
  • initiate or continue long term suppression drugs
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67
Q

What are the uses for carabmazepine?

A
  • management of generalized and focal seizures
  • monotherapy or in combination with another AED
  • off label: neuropathic pain
  • take several weeks to achieve optimal effects
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68
Q

What is the MOA for carabmazepine?

A

inhibits polysynaptic responses and blocks sodium channels to prevent the formation of repetitive action potential in the abnormal focus

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69
Q

What are the AE of carbamazepine?

A

CNS: double vision, vertigo, HA< ataxia, drowsiness, dizziness

GI: n/v

Elevated liver enzymes

Dermatologic: rash, photosensitivity, alopecia

BBW: dermatologic reactions.

Association of congenital abnormalities

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70
Q

List contraindications for carbamazepine.

A

Allergy to drug or tricyclic antidepressants

Liver disease

HLA-B*1502 gene

Pregnancy and lactation

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71
Q

List interactions for carbamazepine.

A

CNS depressants and alcohol

Grapefruit juice

St john’s wort

Decrease effectiveness of contraceptives and gives false negatives on pregnancy tests

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72
Q

What are nursing considerations for carbamazepine?

A

Begin with low dose and gradually increase

Give at bedtime if possible

Give with meals for GI s/s

Educate about not doing hazardous activity

Use sunscreen

Fall precautions

Monitor: WBC, CBC, skin, edema

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73
Q

Neurotransmitters affected with Alzheimer’s Disease (Hallmark of AD).

A

Beta-amyloid and neuritic plaques

Neurofibrillary tangles

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74
Q

Pharmacotherapy of Alzheimer’s. (what is the main goal of pharmacotherapy for AD, which 2 drug classes are used, name prototypes).

A

Drugs are used to slow memory loss

2 drug classes used:

  1. Reversable indirect acting cholinesterase inhibitors
    (donepezil, galantamine, rivastigmine)
  2. Neuronal receptor blocker (NMDA receptor antagonist)
    (memantine)
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75
Q

Indirect acting cholinesterase inhibitors: donepezil, what is the goal of this medication, MOA, and route.

A

Goal: improve ADLS and improve behaviors and cognition

May delay or slow progression… not treat!

MOA: blocks acetylcholinesterase

Route: PO

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76
Q

What are AE for donepezil?

A

cholinergic side effects, CNS effects, CV (bradycardia, hypotension, heart block)

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77
Q

List the only contraindication for donepezil.

A

allergy

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78
Q

Use caution for donepezil in cases of:

A

pregnancy/lactation/renal and hepatic dysfunction

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79
Q

List interactions for donepezil.

A

anticholinergic drugs, drugs that can reduce response to cholinesterase inhibitors

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80
Q

Centrally acting muscle relaxants: baclofen. What is the MOA/routes?

A

works in the CNS to interfere with the reflexes that are causing the muscle spasms. Possibly by increasing gamma aminobutyric

take PO dose with food/milk, available PO or intrathecal pump

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81
Q

List contraindications of baclofen.

A

allergy, caution in patients older than 65

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82
Q

What are the AE of baclofen (centrally acting muscle relaxants)?

A

CNS depression

GI/GU: nausea, dry mouth, constipation, urinary retention

CV: hypotension and arrhythmias

Tapered slowly

Physical dependence

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83
Q

Regular Insulin is also recognized as short-acting. What is the MOA? What are appropriate routes?

A

identical to insulin produced by the beta cells of the pancreas. Promotes cellular utake and use of glucose. Promotes glucose storage. Promotes uptake of potassium into cells.

SQ injection, regular can be given IV

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84
Q

What are AE of regular insulin?

A

Hypoglycemia

Injection reactions

lipodystrophy

Hypokalemia

Cough and throat pain (inhaled route only)

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85
Q

When mixing insulin, explain how it should be mixed.

A

short before intermediate (clear before cloudy)

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86
Q

Biguanides: metformin. What is the MOA and routes? Why is this the preferred drug for Type II DM?

A

Preferred drug for type II DM because safety and effectiveness

decreases hepatic glucose production. Increases uptake of glucose. Improves insulin sensitivity of peripheral cells.

PO (regular or sustained release), solution.

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87
Q

What are biguanides like metformin used for?

A

Maintain blood sugar levels WNL in patients with type II dm where diet and exercise are ineffective.

Off label: PCOS

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88
Q

What are AE of metformin?

A

GI

Allergic skin reactions

BBW: lactic acidosis

Lactic acidosis s/s: malaise, myalgia, hyperventilation, severe abd pain.

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89
Q

List contraindications for metformin.

A

Allergy

Impaired renal function

Metabolic acidosis

2 days prior and 2 days after IV contrast

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90
Q

List interactions for metformin. (only 2).

A

Alcohol

Iv contrast

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91
Q

Explain treatment of hypoglycemia. (prototype, what it is used for, moa, AE, contraindications, interactions).

A

Glucagon

Uses:

Emergency treatment of severe hypoglycemia in patients who are unable to swallow or are unconscious

MOA: increases blood glucose levels. Decreases insulin releases. Accelerates breakdown of glycogen in the liver.

AE:

GI upset and n/v

Hyperglycemia

Contraindications:

Depleted glycogen stores

Interactions

Antagonizes effects of antidiabetic drugs

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92
Q

What is the MOA and routes for Levothyroxine?

A

synthetic form of T4, increases metabolic rate. PO/IV

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93
Q

What is levothyroxine used for?

A

hyperthyroidism, goiters, thyroid cancer, myxedema coma

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94
Q

What are the AE of levothyroxine?

A

Rare at therapeutic doses

Hyperthyroidism

BBW: not for weight loss use

Esophageal atresia

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95
Q

List contraindications of levothyroxine.

A

Allergy

Thyrotoxicosis

Acute MI

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96
Q

Antithyroid agent: Thioamides. What are the 2 prototypes and MOA?

A

MOA: lowers thyroid hormone by preventing formation of thyroid hormone, inhibit conversion of t3 to t4.

Prototypes: propylthiouracil (PTU) and methimazole.

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96
Q

List interactions of levothyroxine.

A

Take in the am on an empty stomach

Many drugs decrease absorption and serum levels of levothyroxine

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97
Q

What are the AE of thioamides like PTU and methimazole?

A

n/v, liver toxicity. Arthralgia. Hypothyroidism. Bone marrow suppression.

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98
Q

List contraindications for PTU/methimazole.

A

allergy, pregnancy, lactation

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99
Q

List interactions for PTU/methimazole.

A

increases actions of anticoagulants

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100
Q

What do iodine solutions do to thyroid cells? List route and 2 main AE.

A
  • cause thyroid cells to become oversaturated with iodine and stop producing thyroid hormone.
  • route: po
  • ae: iodism, stained teeth
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101
Q

What is the MOA and route for radioactive iodine? State the main AE overall.

A

MOA: taken up by thyroid cells which are then destroyed by the beta radiation

Route: PO

AE: hypothyroidism

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102
Q

When is radioactive iodine contraindicated?

A

hypersensitivity, pregnancy (cat. x), lactation

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103
Q

The patient asks the nurse, “when will I see the full effects of radioactive iodine?” the nurse knows that effects will take __-___ months and the patient should take radiation precautions.

A

2-3 months.

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104
Q

List 5 drug classes used for dyslipidemia. Including other lipid lowering agents (there are 3 others).

A

HMG-CoA reductase inhibitors (statins)

Bile acid sequestrants

Cholesterol absorption inhibitors

PCSK9 inhibitors

Other lipid lowering agents: Niacin, omega 3, fibrates

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105
Q

HMG-CoA reductase inhibitors (statins): atorvastatin. What are the uses, MOA, and PO (any special instructions?)

A

Uses:

Adjuncts with diet and exercise for the treatment of increased cholesterol and LDL levels that are unresponsive to diet alone

MOA:

Liver responds to the loss of LDL by making more receptors wihc removes the LDL from the blood

Route: PO. Should be given at night because cholesterol biosynthesis is higher.

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106
Q

What are the AE of atorvastatin?

A

Generally, well tolerated

GI most common

Increased liver enzymes and liver failure

Myopathy

Rhabdomyolysis

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107
Q

List contraindications of atorvastatin.

A

pregnancy (cat. x), allergy, liver disease, breastfeeding

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108
Q

Antihistamines. Name the prototype for 1st gen and 2nd gen.

A

1st: diphenhydramine
2nd: cetirizine

109
Q

What is the MOA of anthistamines?

A

h1 receptor antagonists. They block histamine from reaching its receptor, thus relieving allergy s/s.

110
Q

List contraindications of antihistamines.

A

allergy, pregnancy/lactation

111
Q

What are AE of antihistamines?

A

CNS: drowsiness (more common w/ gen 1), dizziness. Young children may experience CNS stimulation instead of depression.

GI: n/v

Anticholinergic effects (more common w/ gen 1)

112
Q

List interactions for antihistamines. (only 2)

A

CNs depressants, alcohol

113
Q

Beta2 adrenergic agonists: albuterol (SABA). They are most effective and preferred for relieving acute bronchospasms. What is their MOA/routes?

A

activate the sympathetic nervous system which relaxes the smooth muscle, resulting in bronchodilation

po, inhaled, parenteral

114
Q

What are the AE of albuterol?

A

CV: tachycardia, palpitations, tremors

CNS stimulations, nervousness, sweating, flushing

Paradoxical bronchospasm

LABA BBW

115
Q

List contraindications for albuterol (beta 2 agonist only has 2)

A

Allergy

Tachydysrhythmias

116
Q

List interactions for albuterol. (only 2).

A

beta blockers, caffeine

117
Q

2 key education points for albuterol are?

A
  • LABA not for relief of an acute attack
  • if taking a glucocorticoid use this beta first
118
Q

Inhaled corticosteroids: budesonide. Why are they used? What is the MOA?

A

Use:

Preferred drug for long term management of asthma in children and adults

Not for acute attack use! need to be used on a daily schedule.

MOA: decreases inflammation in the airways

119
Q

List contraindications of budesonide. (2 only)

A

allergy, emergency use (not for emergencies)

120
Q

What are AE of budesonide?

A

Hoarseness, sore throat, coughing, dry mouth, oral fungal infection

Long term has potential to affect bone physiology. Decreased growth in children and osteoporosis in adults.

121
Q

What are the interactions for budesonide? (trick question)

A

no known

122
Q

Smoking cessation: varenicline. How long is this medication given. What is the MOA and route.

A
  • given for 12-24 weeks
  • MOA: activates nicotinic acetylcholine receptors in the brain and blocks nicotine from reaching the brain
  • route: PO
123
Q

What are AE of varenicline?

A

n/v, dry mouth, strange dreams, HTN

Seizures and neuropsychiatric events

124
Q

List contraindications and interactions of varenicline.

A
  • contraindicated in allergies
  • interactions: increased effects of alcohol
125
Q

Define withdrawal, tolerance, addiction, and physical dependence.

A

Withdrawal: s/s that occur in physically dependent individuals when they discontinue drug use

Tolerance: a state in which a dose of a drug elicits a smaller response than it did initially

Addiction: a chronic, relapsing brain disease

Physical dependence: a state in which abstinence syndrome will occur if drug use is discontinued

126
Q

Alcohol deterrent: disulfiram. List uses. (3).

A

Taking disulfiram with alcohol results in a syndrome named disulfiram-alcohol reaction

Can only be given to patients who fully understand and are motivated to maintain sobriety

Prevents impulse drinking does not cure alcohol abuse

127
Q

MOA and route for disulfiram.

A

MOA: irreversibly inhibits the enzyme acetaldehyde dehydrogenase causing toxic acetaldehyde to build up in the blood

Route: PO

128
Q

AE of disulfiram.

A

Extreme doses can cause neurological toxicity, psychosis, and hepatotoxicity

129
Q

Interactions for disulfiram.

A

Interactions: alcohol. s/s begin 5-10 min after alcohol ingestion. All alcohol products must be strictly avoided (cough syrups, mouthwash, vitamins, etc…)

130
Q

Uses of potassium sparing diuretics like spironolactone.

A

Mild diuretics

Useful in patients who are high risk for hypokalemia

Used as adjuvants for the management of edema and sodium retention associated with HF, nephrotic syndrome, and liver disease

131
Q

MOA of spironolactone and route.

A

MOA:

Inhibit the actions of aldosterone in the distal tubule and collecting ducts

Route: PO

132
Q

AE of spironolactone.

A

Hyperkalemia

Gynecomastia, impotence, diminished libido- males

Menstrual irregularities, hirsutism, breast tenderness- females

Decreased fertility

BBW

133
Q

Contraindications of sprironolactone.

A

Allergy

Anuria, severe renal impairment, pregnancy, and hyperkalemia

134
Q

Interactions for spironolactone.

A

Potassium supplements, ACE inhibitors, ARBs

Avoid foods high in potassium

135
Q

Thiazide diuretics: hydrochlorothiazide (HCTZ). Why are they used? 3 listed.

A

Mild diuretics

1st line treatment of mild to moderate HTN

Edema r/t heart, liver, and renal failure

136
Q

MOA of HCTZ (thiazide diuretics) and the routes.

A

MOA: block the chloride pump which keeps chloride and sodium in the distal tubule to be excreted in the urine

Route: PO and one is available IV

137
Q

AE of HCTZ.

A

GI upset

Hypotension

Fluid and electrolyte imbalances: hypokalemia, hypercalcemia

Uremia: possible gout attack

Hyperglycemia w/ long term use

138
Q

Contraindications for HCTZ.

A

Allergy to thiazides and sulfonamides

Fluid and electrolyte imbalance and severe renal disease

139
Q

Interactions for HCTZ.

A

Other antihypertensive drugs

Digoxin

140
Q

ACE inhibitors are first line treatment for HTN. What is their MOA and routes? What 3 things are they used for?

A

MOA: works in the lungs to block conversion of angiotensin 1 to angiotensin 2

Routes: PO (enapril also IV)

Uses:
HTN

HF

Acute MI

141
Q

AE of ACE Inhibitors.

A

CV: hypotension, reflex tachycardia, angina

GI: irritation

Hyperkalemia

Persistent dry cough

Angioedema

BBW: r/f congenital effects if taken during pregnancy

142
Q

Interactions for ACE inhibitors.

A

NSAIDS, other antihypertensives.

143
Q

ARBS: losartan (-sartan). What is the MOA, route, and what are they used for?

A

MOA: binds w/ angiotensin II receptors in vascular smooth muscle and the adrenal gland results in vasodilation and prevents secretion of aldosterone

Uses:

HTN, stroke prophylaxis, prevention of type II diabetic neuropathy

Off label: HF

Route: PO

144
Q

AE of losartan.

A

HA, dizzy, syncope

Gi irritation

Nasal congestion and s/s of respiratory tract infection

Angioedema and acute renal failure

145
Q

Contraindications for losartan.

A

allergy, pregnancy

146
Q

Interactions for losartan.

A

NSAIDs, other antihypertensives.

147
Q

Calcium Channel Blockers: amlodipine. What is the MOA and routes.

A

Moa: selectively blocks calcium channels in vascular smooth muscle

Route: PO and IV

148
Q

Contraindications for amlodipine (CCB).

A

Allergy

Heart block, HF, brady dysrhythmias

Renal or hepatic dysfunction

Pregnancy and lactation

149
Q

AE of amlodipine (CCBs).

A

CNS: dizzy, lightheaded, HA

GI: nausea, constipation, hepatotoxicity

CV: hypotension, bradycardia, edema, heart block

Skin flushing

150
Q

Interactions for amlodipine.

A

Other antihypertensives

Alcohol

Grapefruit juice

151
Q

Beta blockers: (-lol). What is the MOA. Why is it used. What are the routes.

A

Moa: diminished myocardial contractility (decreases cardiac output). Prevents release of renin by the kidneys

Uses: HTN, angina, dysrhythmias, glaucoma, HF, MI, migraine prophylaxis

Off label: stage fright and PTSD

Routes: PO and IV

152
Q

AE of beta blockers.

A

n/v, diarrhea

Fatigue and insomnia, confusion

bronchospasm, stevens Johnson syndrome, anaphylaxis

Hypotension and bradycardia

Hypoglycemia

BBW: withdrawal treatment gradually over several weeks

Loss of libido and erectile dysfunction

153
Q

Contraindications for beta blockers.

A

COPD and asthma, bradycardia, severe HF

154
Q

What are the treatment goals for Parkinson’s Disease?

A

To increase the ability of the patient to perform normal ADL and decrease the chance of falls that could cause injury.

Therapy is aimed at management of s/s to provide optimal functioning for as long as possible.

Drugs do not offer a cure but significantly reduce s/s for a time in many patients

155
Q

Dopaminergic agents: levodopa and carbidopa. Why is it used? What is the MOA? What is the only contraindication?

A

Uses:

Relieve s/s of idiopathic and secondary Parkinson’s disease

MOA: taken up by dopaminergic nerves to be converted to dopamine

Contraindications: allergy

156
Q

Interactions of levodopa and carbidopa.

A

Interactions:

Dopamine antagonists, iron salts, high protein meals

MAOIs

157
Q

AE of levidopa/carbidopa.

A

GI: n/v, anorexia

CNS: muscle twitching, tremors, ataxia. Psychosis, hallucinations, paranoia

CV: orthostatic hypotension

Anticholinergic effects

BBW

158
Q

Other information r/t levolevoddopa/carbidopa. (3 key points).

A

2-3 weeks of therapy needed before improvement is observed

Beneficial effects tend to diminish

Amantadine can help with the involuntary movement, tremors, and twitching

159
Q

Immune modulators: interferon beta-1b. Why is it used? What is the MOA? What is the route (any special instructions?).

A

Uses:

Treatment of relapsing forms of MS

MOA: unknown. May inhibit the movement of leukocytes across the blood brain barrier

Route: Subq every other day

160
Q

Contraindications of interferon beta-1b?

A

allergy, pregnancy, caution in people with suicidal tendencies/other mental health disorders.

161
Q

AE of interferon beta- 1b.

A

Flu like s/s

Bone marrow suppression

Injection site reactions

Increased liver enzymes and toxicity

162
Q

Interactions of interferon beta 1b.

A

Do not administer with any other drugs that may suppress the immune system

163
Q

Other info for interferon beta 1b ( what do nurses monitor?)

A

Monitor for depression and suicidal ideations

Monitor CBS and LFTs before treatment and periodically

164
Q

Calcitriol. What are the uses. What is the MOA and routes?

A

Use:

Hypocalcemia, chronic kidney disease, hypoparathyroidism

MOA: elevates serum calcium levels, decreases elevated blood levels of phosphorus and decreases bone resorption

Route: po and IV

165
Q

Contraindications for calcitriol.

A

Hypercalcemia

Vit. D toxicity

166
Q

AE of calcitriol.

A

GI: n/v, dry mouth, constipations, metallic taste

Hypercalcemia

167
Q

Calcium supplements: Calcium carbonate. What are the uses? What is the MOA?

A

Uses:

Prevention and treatment of hypocalcemia

Osteoporosis

Pregnancy, lactation

Gastric hyperacidity

MOA: restore normal serum levels of calcium

168
Q

Contraindications for calcium carbonate.

A

Cardiac dysrhythmias, renal calculi, hypercalcemia, low phosphate levels

169
Q

AE of calcium bicabonate.

A

Hypercalcemia

Constipation

Kidney stones

IV: pain at site, hypotension, heat wave, fainting, dysrhythmias

170
Q

Interactions for calcium bicarbonate.

A

Calcium decreases absorption of thyroid hormones, and some antibiotics

Zinc rich foods decrease absorption

171
Q

Recommended dietary allowance for calcium supplements, what else is this supplement usually given with?

A

RDA: 1000-1200 mg/day

Often given w/ vit. D

172
Q

Calcitonin. What are the uses, what is the MOA, what are the 3 routes?

A

Uses:

Does NOT prevent osteoporosis

Postmenopausal osteoporosis

Paget’s disease and hypercalcemia secondary to hyperparathyroidism

Antihypercalcemic agent

MOA: acts similar to calcitonin produced by the thyroid glands. Inhibits bone resorption, decreases serum CA levels, increases excretion of phosphate, calcium, and sodium from the kidneys

Route: SC, IM, intranasal

173
Q

Contraindications of calcitonin.

A

lactation, allergy to med/fish

174
Q

AE of calcitonin.

A

Flushing of face and hands, n/v, rash

Hypocalcemia

Nasal dryness

Hypersensitivity

Decreased therapeutic effects over time

175
Q

Bisphosphonates: alendronate. What are the uses. What is the MOA.

A

Uses:

Osteoporosis prevention and treatment in post-menopausal people

Age related osteoporosis in males

Glucocorticoids related osteoporosis

MOA: decreases bone resorption

176
Q

What are the contraindications for alendronate.

A

Allergy

Hypocalcemia

177
Q

AE of alendronate.

A

Hypocalcemia

GI: n/v, pain, constipation, diarrhea, esophagitis, ulceration

Osteonecrosis of the jaw

178
Q

Interactions of alendronate.

A

Empty stomach

Take on full glass of water

Remain upright 30 min after taking

Diet needs adequate amount of vit d, calcium, and phosphates

179
Q

SERMS: raloxifene. What are the uses. What is the MOA. What are some contraindications.

A

Uses:

Prevention and treatment of osteoporosis in postmenopausal people

Breast cancer prophylaxis of estrogen dependent or receptor positive breast cancers

MOA: activates estrogen receptors in endometrial tissue and bones. Decreases bone resorption and bone loss. Blocks access to estrogen receptors in breast tissues.

Contraindications:

Pregnancy (cat. X)

Lactation

Hx of thromboembolism

Allergy

180
Q

What are AE of raloxifene (SERMS).

A

Increased risk of thromboembolic events

Hot flashes

Endometrial cancer

BBW: thromboembolism

181
Q

DMARDS I: methotrexate. They are antimetabolite drugs and work by interfering with a normal metabolic process. What is their MOA and uses.

A

Uses:

RA

SLE

Malaria

Cancer

MOA: immunosuppression

182
Q

Contraindications for methotrexate.

A

Allergy

Liver or renal insufficiency

Visual field damage

183
Q

AE of methotrexate.

A

Liver damage

Bone marrow suppression

GI ulcers

Pulmonary fibrosis

Eye damage

184
Q

Interactions for methotrexate.

A

Antacids

Hepatotoxic drugs

Alcohol

185
Q

Other information for someone taking methotrexate.

A

Need routine eye exams

Drink 8-12 8oz glasses of water per day

Cat. X drug

If on methotrexate they need a weekly folic acid supplement

186
Q

Heparin. What is the MOA, routes, and uses.

A

MOA: factor Xa thrombin inhibitor. Binds with antithrombin. Blocks the formation of prothrombin. Prevents formation of fibrin clots within minutes of IV admin.
Uses:

IV is 1st line for acute thromboembolic disorders

Also used to maintain line patency in heparin locks and arterial lines

Route: SQ and Iv

187
Q

Labs for heparin. (which labs, how often are they measured, what’s normal, what is the therapeutic range?)

A

Aptt or ptt is used to measure heparin

Meausred daily and 6-8 hours after dosage change

Normal: 25-40 seconds

Therapeutic: 1.5-2 x baseline (60-80 sec)

188
Q

AE of heparin.

A

Bleeding

BBW

Heparin induced thrombocytopenia (HIT)

Hypersensitivity reactions

189
Q

Antidote for heparin.

A

protamine sulfate.

190
Q

Contraindications for heparin.

A

Active bleeding

Severe HTN

Recent trauma

Intracranial hemorrhage

191
Q

Interactions of heparin.

A

Other anticoagulants and antiplatelet

Several herbs

192
Q

Warfarin. Why is it used? MOA, route, and main AE.

A

Uses:

Long term prophylaxis of arterial thromboembolism

MI

Stroke

A fib

Prosthetic valves

MOA: inhibits 2 enzymes involved in Vit. K formation

Route: PO

Pregnancy cat: X

AE:

Bleeding

BBW

Toxicity

193
Q

What is the antidote for warfarin?

A

Vit. K

194
Q

Contraindications for warfarin.

A

Recent trauma

Active internal bleeding

Bleeding disorders

Intracranial hemorrhage

Sever HTN

195
Q

Interactions for warfarin.

A

Numerous drugs, several herbs, foods high in vit. K

196
Q

Nitrates: isosorbide dinitrate and nitroglycerin. What is the MOA.

A

Moa: relaxes and dilates veins, arteries, and capillaries. Allows for increased blood flow. Lowers BP. Decreases vasospasms of the arteries.

197
Q

Nitrates: short-acting and long-acting. Name prototype for each.

A

Short acting: nitroglycerine

Long acting: isosorbide dinitrate

198
Q

AE of nitrates.

A

CNS: HA, dizzy, weakness

GI: n/v

Skin: flushing, contact dermatitis

CV: hypotension, orthostatic hypotension, syncope, reflex tachycardia

Tolerance with long actings

199
Q

Contraindications for nitrates.

A

Phosphodiesterase-5 inhibitors

Alcohol

200
Q

Beta blockers: propranolol. What is it used for. MOA/routes.

A

Used for angina prophylaxis

Moa: decreases cardiac workload by lowering BP, slowing HR, and reducing contractility

Not effective in vasospastic angina

Uses:

HTN, HF, stable angina, post-acute MMI

Off label: migraine prophylaxis and unstable angina

MOA: selectively blocks beta

Route: PO and IV

201
Q

AE of propranolol.

A

CV: bradycardia, hypotension

CNS: fatigue, dizziness

GI: n/v

Respiratory: bronchospasm

BBW

202
Q

Contraindications for propranolol.

A

Severe bradycardia, heart block, shock

203
Q

Interactions of propranolol.

A

other antihypertensives.

204
Q

Cardiac glycosides: digoxin. What are the uses. What is the MOA. What are the routes.

A

Uses:

Alleviates s/s

Increases exercise tolerance

MOA: inhibits enzyme responsible for sodium and potassium ion exchange. This increases intracellular calcium and allows more Ca to enter myocardial cells

Increased force of myocardial contraction

Increased CO and renal perfusion

Slowed HR decreased conduction velocity through the AV node

Route: PO and IC

205
Q

Digoxin has a narrow margin of safety. What is the therapeutic range, how often should digoxin levels be drawn after a dose?

A

range: 0.5-2
levels drawn 6-12 hours after a dose

206
Q

Antidote for digoxin toxicity.

A

digoxin immune fab

207
Q

AE of digoxin.

A

CV: arrhythmias, bradycardia

CNS: drowsiness, HA< weakness, vision changes

GI: n/v, anorexia

Digoxin toxicity: anorexia, n/v, malaise, depression, arrhythmias.

208
Q

Contraindications of digoxin.

A

Allergy

Heart block

Acute MI

Ventricular dysrhythmias

Renal insufficiency

Caution in pregnancy and lactation

209
Q

Interactions for digoxin.

A

St john’s wort and psyllium

Ginseng, hawthorn, black licorice

Potassium losing diuretics

Refer to pharmacist because many meds increase digoxin levels

210
Q

Other info. Hold digoxin if pulse is less than ___.

A

Hold if apical pulse less than 60

Bioavailability can differ

211
Q

Phosphodiesterase III inhibitors: milrinone. What are the uses? What is the MOA? What is the route?

A

Uses:

Short term treatment of acute decompensated HF

Therapy is limited to 2-3 days and requires continuous monitoring

MOA: inhibits phosphodiesterase II which increases Ca levels in the cell. Increases contractility and cardiac output

Route: IV.

212
Q

Contraindications for milrinone. Interactions as well.

A

Contraindications:

Allergy to milrinone or bisulfites

Interactions:

Can not combine milrinone with furosemide

213
Q

Class 1b antidysrhythmic: lidocaine. What are the uses? What is the MOA? What are the routes?

A

Uses:

Treatment of life-threatening ventricular arrhythmias during MI or cardiac surgery

Treatment of refractory ventricular arrhythmias

MOA: blocks sodium ion channels. Shortens the duration of the action potential.

Route: IM, IV

214
Q

What is the narrow therapeutic range for lidocaine?

A

1.5-5

215
Q

AE of lidocaine.

A

CNS: dizzy, drowsiness, fatigue, twitching, mouth numbness, slurred speech

GI: changes in taste, n/v

CV: proarrhythmic, hypotension, vasodilation, cardiac arrest

216
Q

Contraindications of lidocaine.

A

Allergy

Bradycardia

Heart block

HF

Hypotension

Shock

Electrolyte disturbances

217
Q

Interactions of lidocaine.

A

Other antiarrhythmics

Beta blockers

Phenytoin

218
Q

Class IV antidysrhythmic: CCB (verapamil). Uses. MOA. Routes.

A

Uses:

Only effective against atrial dysrhythmias

MOA: blocks movement of calcium ions in the cardiac and smooth muscle cells

Route: PO, IV

219
Q

AE of verapamil.

A

CNS: dizzy, fatigue, depression, HA

GI: constipations, n/v

CV: hypotension, HF, shock, arrhythmias, edema

220
Q

Contraindications of verapamil.

A

Allergy

Heart block

Severe HF

Hypotension

221
Q

Interactions for verapmail.

A

Alcohol

Grapefruit juice

Beta blockers

222
Q

Antimicrobials and cancer. Define difference between bactericidal and bacteriostatic.

A

Bactericidal: destroys bacteria

Bacteriostatic: prevents growth

223
Q

Cephalosporins: cefazolin. What are the routes, what is the MOA.

A

Route: PO, IM, IV

MOA: causes bacteria to build weak cell walls when dividing. Bacteriostatic or bactericidal depending on the dose

224
Q

Categories for cefazolin.

A

5 generations

Increasing activity against gram (-)

Increasing resistance to beta lactamases

Increasing ability to reach CSF

225
Q

AE of cefazolin.

A

GI s/s

Allergic reactions

Injection site reactions

CNS: HA, dizzy

Nephrotoxicity

Superinfections

226
Q

Contraindications of cefazolin.

A

Allergy to drug or PCN

227
Q

Interactions for cefazolin. Only 1.

A

alcohol

228
Q

Metronidazole. What are the routes. What is the MOA. What are the main AE.

A

Route: PO, IV

MOA: inhibits DNA and RNA synthesis. Bactericidal

AE:

Nausea, dry mouth, HA

Neurotoxicity

BBW: cancer in lab animals

229
Q

Contraindication and interaction for metronidazole.

A

Contraindications:

Allergy

Interactions:

Alcohol (disulfiram-like reaction)

230
Q

Other information for metronidazole. (what else is it used for, what happens to urine)

A

Used for protozoal infections, PUD, and infections caused by obligate anaerobic bacteria. Causes harmless darkening of urine

231
Q

Drugs used for tuberculosis. RIPES.

A

R- rifampin

I- isoniazid

P- pyrazinamide

E- ethambutol

S- streptomycin

232
Q

Alkylating agents: cisplatin and cyclophosphamide. What is the MOA. What are the routes.

A

MOA: non-cell cycle specific. Kills cancer cells by altering the shape of the DNA double helix and preventing the DNA from duplicating during cell division

They are broad spectrum and used against many types of malignancies

Route: po and IV

233
Q

AE of cisplatin/cyclophosphamides (alkylating agents).

A

GI

Skin

Hematologic

Secondary cancers, cardiotoxicity, hepatotoxicity, renal toxicity, pulmonary fibrosis

Infertility

Strong vesicants

Cancer cells can develop resistance w/ prolonged treatment

234
Q

Interactions of alkylating agents.

A

Anticoagulants

Agents that cause: Bone marrow suppression, cardiotoxicity, hepatotoxicity, renal toxicity

St john’s wort

235
Q

Nursing considerations for alkylating agents.

A

Pre medicate with an antiemetic

Monitor: I&Os, labs, s/s infection

Admin mesna (prevent hemorrhagic cystitis) cyclophosphamide

Admin amifostine (prevent renal toxicity) cisplatin

Educate on no live virus vaccines

236
Q

Targeted therapies: monoclonal antibodies. (What do antineoplastic drugs specifically do? what is the MOA of monoclonal antibodies)

A

Antineoplastic drugs that have been specifically engineered to attack cancer antigens of a specific cancer

Once a MAB binds to the cancer antigen it either directly kills the cancer cell or marks it for the destruction by other immune responses

Example: monoclonal antibodies that target breast cancer with HER2

237
Q

SSRI: fluoxetine. What are the uses. What is the MOA. What is the route.

A

First choice of drugs for depression

Use:

Depression and anxiety

OCD

Panic attacks

Bulimia

PMDD

PTSD

Social phobias and social anxiety disorder

MOA: blocks reuptake of serotonin

Route: PO

238
Q

Fluoxetine can take up to how many weeks to reach therapeutic effects?

A

4 weeks for peak effec

239
Q

AE of fluoxetine.

A

GI: n/v, diarrhea, dry mouth

CNS: HA, dizzy, insomnia, nervousness, anxiety, tremors, agitation, mania

GU: painful menstruation and sexual dysfunction

Weight gain

Bruxism

BBW: suicide

Serotonin syndrome

Withdrawal

240
Q

Contraindications for Fluoxetine.

A

Allergy

SNRIs, MAOIs, TCAs

241
Q

Interactions for Fluoxetine.

A

SNRIs, MAOIs, TCAs

St john’s wort

Primrose

Grapefruit juice

242
Q

Bupropion. What is the MOA. What are the uses.

A

Moa: weekly blocks reuptake of norepinephrine and dopamine
Use:

Depression

Prevention of seasonal affective disorder

Smoking cessation

Not used for anxiety

243
Q

What are the benefits of bupropion.

A

Acts as a stimulant and suppresses appetite

Does not cause weight gain

Increases sex desire and pleasure

Available in ER

244
Q

What are the AE of bupropion?

A

CNS: HA< insomnia, agitation, tremor, seizures, psychosis

CV: tachycardia

GI: N/V, weight loss

BBW: suicide

245
Q

Contraindications for buproprion.

A

Allergy

Seizure disorders or hx of anorexia nervosa

246
Q

Interactions for bupropion.

A

SSRIs, SNRIs, MAOIs, TCAs

St john’s wort

Other herbal therapies

247
Q

MAOIs: phenelzine. How long might it take to see therapeutic effects? What is the route?

A

May take 12 weeks for therapeutic effects

Route: PO

248
Q

AE of MAOIs.

A

CNS: dizzy, nervousness, insomnia, blurred vision, mania

GI: n/v, diarrhea, constipation, weight gain, dry mouth, liver toxicity

GU: sex dysfunction, incontinence, urinary retention

CV: hypotension, palpitations, dysrhythmias, angina, HTN crisis

BBW: suicide

Withdrawal

249
Q

Interactions for MAOIs.

A

Tyramine

St. John’s wort

Other herbs

Check w/ prescriber before taking any other meds

250
Q

Atypical antipsychotics: risperidone. What is the MOA. What are the AE.

A

Moa: moderate blockade of dopamine receptors. Strong blockade for serotonin

AE:

metabolic effects (weight gain diabetes, dyslipidemia)

GI: n/v, constipation, increased salivation

251
Q

Movement disorders. Acute dystonia. (Manifestations, timeframe, treatment.)

A

Manifestations: severe painful spasms of muscles in neck and body

Timeframe: early in the course of treatment

Treatment: anticholinergic drugs (diphenhydramine and benztropine)

252
Q

Movement disorders. Parkinsonism. (Manifestations, timeframe, treatment).

A

Manifestations: bradykinesia, mask like face, drooling, tremor, rigidity, shuffling gait, stooped posture

Timeframe: first month of therapy

Treatments: anticholinergic drugs and amantadine

253
Q

Movement disorders. Akathasia. (Manifestations, timeframe, treatments).

A

Manifestations: inability to rest and relax. Pacing. Trouble sleeping. Trouble remaining still. Repetitive movements.

Timeframe: first 2 months of therapy

Treatments: benzos and betablockers

254
Q

Movement disorders. Tardive dyskinesia. (Manifestations, timeframe, treatment).

A

Manifestations: twisting, writing, worm-like movements of the tongue, face, and neck. Lip smacking. Tongue darting

Timeframe: during long term treatment and may persist for years after the drug is discontinued.

Treatment: deutetrabenazine and valbenazine

255
Q

Estrogen. What are the uses.

A

Hormone replacement therapy

Palliation for menopause discomfort

Hypogonadism and ovarian failure therapy

Contraception

Osteoporosis

Estrogen sensitive cancers

Acne

256
Q

AE of estrogen.

A

GU: breakthrough bleeding, menstrual irregularities, dysmenorrhea, changes in libido

GI: n/v, abd cramps, bloating, acute pancreatitis, gallbladder disease, jaundice, hepatic adenomas

CNS: HA

Genral: fluid retention, chloasma

257
Q

Contraindications for estrogen.

A

Estrogen dependent cancers

Hx or thromboembolic disorders

Heavy smokers

Hepatic dysfunction

Pregnancy and lactation

258
Q

BBW for estrogen.

A

Breast cancer

r/f endometrial cancer

Not used for dementia of CVD treatment

Increase r/f stork and thromboembolic disorders and dementia in those 65+

259
Q

Progestins. What are the uses, what are the AE.

A

Uses:

Postmenopausal hormone therapy

Contraception

Functional uterine bleeding

Amenorrhea

Infertility

AE:

Similar to estrogens

Teratogenic effects

Vaginal bleeding

Depression/mood swings

Breast tenderness

Bloating

260
Q

Contraindications for progestins.

A

endometriosis, same as estrogens.

261
Q

BBW for progestins.

A

Increased r/f stroke, DVT, PE, and MI

Breast cancer

Increase r/f dementia

Not approved for treatment of CVD or dementia

262
Q

IUDs. Hormonal (how long is it good for, when is it placed)

A

Among the most effective contraceptive available

Placed within 7 days of onset of menses

Good for 3-6 years

263
Q

Nonhormonal IUDs. When is it placed, good for how long? what are AE?

A

Among most effective contraceptives

Places within 7 days onset of menses

Good for 10 years

Heavy periods and cramping

264
Q

Tocolytics: magnesium sulfate. What are they used for? If combined with glucocorticoids they can accelerate _____?

A

Uterine relaxants

Suppression of preterm labor

If used in combo with glucocorticoids can accelerate lung development

Also used to buy time to treat infection

265
Q

Testosterone. What are contraindications? Warning r/t drug.

A

Class III controlled substance

Contraindications

Allergy

Pregnancy and lactation

Breast cancer

Warning

Risk of CV events and need to evaluate the patient carefully for appropriate use of the drug

266
Q

AE of testosterone.

A

Androgenic effects: acne, edema, hirsutism, deep voice, oily skin and hair, weight gain, penile enlargement, testicular atrophy

Prepubescants: virilization and reduced height

Postpubescents: inhibition of testicular function, gynecomastia, priapism, baldness, prostate issues, changes in libido

Antiestrogen effects: flushing, sweating, menstrual irregularities, no menses, hirsutism, clitoris growth, emotional liability

Other: HA, dizzy, sleep disorders, fatigue, rash

GI: hepatocellular cancer or hepatitis

BBW: topical forms for virilizations in children wo come in contact

Inappropriate use: CV events and prostate issues

267
Q

PDE5 Inhibitors: sildenafil. What is the MOA.

A

increases nitrous oxide levels in the corpus cavernosum

268
Q

Contraindications and interactions for sildenafil.

A

Contraindications:

Pregnancy and lactation

Penile implants

Not to be used to increase sexual performance in people with vaginas

Interactions

Nitrates

Alpha blockers

Grapefruit juice

269
Q

AE of sildenafil.

A

Hypotension

Priapism

Headache, flushing, dyspepsia, UTI, diarrhea, dizzy, rash

Rare: opic neuropathy, sudden hearing loss, risk for melanoma

270
Q

Onset of sildenafil.

A

Sildenafil: 27 minutes… take one-hour before anticipated sexual stimulation

271
Q

Alpha blockers. What are they used for? what is the MOA.

A

Use: benign prostatic hyperplasia

Moa: blockade of alpha receptors relaxes smooth muscle in the bladder neck, prostate capsule, and prostatic urethra

all end in -sin.

Pharmacology (16 decks)

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