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Pharmacology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Common abbreviations

A

By mouth - PO
Three times a day - tid
Every 6 hours - Q6h
Drop - gtt
After meals/after eating - pc
Before meals - ac
Give immediately (within 5 min) - STAT
Should be available within 30 min - ASAP
As needed - PRN

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2
Q

Metric table

A

1 tsp = 5mL
1 Quart = about 1 L
2.2 Lbs = 1 kg
1 fluid ounce = 30 mL
1 TBS = 15 mL
1 Gram = 1000 mg
1 mg= 1000 mcg
o 1,000 mcg= 1 mg
o 1,000 mg= 1G
o 1,000 G= 1kg
o 1oz= 30 mL= 2 tbsp
o 5mL= 1 tsp
o 1 mL= 1 cc

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3
Q

Pharmacological and therapeutic classifications

A

Pharmacologic
More specific description of how a drug produces its effect in the body (MOA)
Therapeutic
What a particular drug does clinically in treating a disease. Pathology they are intended to treat (Indication)

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4
Q

Scheduled drugs rationale

A

Schedule I - most potential for risk of abuse and dependence
Heroin, LSD, peyote
Only for research purposes
Schedule II
Morphine, Dilauded, Methadone, Oxycodone, Fentanyl
Requires prescription - must be written in ink or typed, requires office visit for refill, requires signature not a stamp
Schedule III
Anabolic steroids, codeine, Ketamine
Schedule IV
Xanax, valium, versed, Ativan
Schedule V
Antidiarrheal, antitussive, analgesic
OTC cough medications with limited narcotics

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5
Q

Narrow therapeutic index

A

Requires frequent assessment to prevent adverse effects and toxicity
Includes blood draws-peak and trough
Example drugs: lithium, vancomycin, theophylline

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6
Q

Drug half-life

A

Time it takes for 50% of the drug to be eliminated in your body
Short half life
Quickly reduced by half, decreasing the risk for toxicity
Quick acting
Ideal for fast relief
Higher risk for dependency
Lower risk for toxicity
Long half life
Takes longer to be reduced by half
May take longer to “kick in”
Ideal for long term relief
Lower risk for dependency
Higher risk for toxicity

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7
Q

Median effective dose

A

The effective dose for 50% of patients

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8
Q

Factors that affect absorption of drugs

A

Drug formulation and dose
Site of administration (enteral/parenteral)
Lipid solubility and pH
First pass effect
Food and drug interactions
Blood flow
pain/stress, etc

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9
Q

Agonist/antagonist defined

A

Agonist drugs
Binds to the receptor and produces the same response as an endogenous chemical (opioid). Helps work WITH the effect of another drug or body system.
Partial agonist or agonist-antagonist drugs
Produce a weaker response than an agonist
Antagonist drugs
Has an affinity for a receptor but displays little or no response. Prevents a response from occurring; works AGAINST the effect of another drug or body system. May be used to prevent effects eliciting from a previously administered medication (Naloxone)

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10
Q

Medication reconciliation

A

Keeping track of polypharmacia
Track interactions

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11
Q

Nurses’ responsibilities during medication errors

A

Report it
Assess pt

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12
Q

Pregnancy categories

A

o A- aokay (no fetal risk in controlled studies)
o B- better ask (no rist to fetus despite possible animal risk)
o C- caution (adverse effects in animals, but no human studies
o D- danger (studies show risks to mother and fetus)
o X- never (fetal abnormalities)

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13
Q

CAM therapies that increase the risk of bleeding

A

o ginger, garlic, St Johns Wort

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14
Q

How do drugs effect neurotransmitters

A

o They increase or decrease the action of NTs, they don’t add more NTs.
o Drugs affect the ANS in: synthesis, storage, influence the release, bind to receptors, prevent
destruction

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15
Q

Antidotes for acetaminophen, insulin, opioids, warfarin, heparin, enoxaparin, digoxin

A

Acetaminophen - acetylcysteine
Insulin - dextrose, glucagon
Opioids - Naloxone (Narcan)
Warfarin - Vitamin K
Heparin - Protamine
Enoxaparin - Protamine sulfate
Digoxin - Digoxin-specific antibody antigen-binding fragments (DSFab), digiband/digifab

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16
Q

Anticholinergic side effects

A

S/E: dry mouth, blurry vision, constipation, urinary retention, photophobia, ortho hypotension

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17
Q

Adrenergic agonist and sympathomimetic drugs defined

A

o indications: shock, hypotension, hypo-shock, allergic rhinitis (hayfever), pre-labor (relaxes sm)
o aka agonists/ sympathomimetic
o catecholamines- share same chemical structure as NE.
o noncatecholamines- dextroamphetamine (Adderall)
o nursing care: watching pt very closely, take before 4 pm so no insomnia

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18
Q

Medication therapeutic goal for treating Parkinson’s disease

A

Overall purpose: treat symptoms, delay progression, no cure for disease
Patho: loss of dopaminergic neurons in the SNpc
dopamine replacement sinimet (levodopa/carbidopa)

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19
Q

SSRI patient teaching (Zoloft/sertraline?)

A

o generally first line of treatment, major differences in tolerability
o watch for signs of Serotonin syndrome:
▪ caused by multiple medications that affect the metabolism, synthesis, or reuptake of
serotonin
▪ buildup of serotonin in neurons
▪ SE: agitation/confusion/restlessness, flushing or diaphoresis, lethargy, nausea, vomiting,
diarrhea, muscle twitching/tremors, hyperthermia, tachycardia
-takes weeks to works
-suicide risk
- no sudden stop

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20
Q

EPS causes and types

A

Causes: antipsychotic medications (phenothiazines, nonphenothiazines, dopamine system stabilizers)
- Acute dystonia
muscle spasms (back, neck, tongue, and face), dislocate joints, impair respirations due to laryngospasm
- Akathisia (inability to rest or relax)
Paces, trouble sitting still, or difficulty sleeping, Repetitive movements: rocking or crossing/uncrossing arms and legs. May be mistaken for anxiety and agitation. *Symptom management with beta-adrenergic blockers, anticholinergics, or benzodiazepines
- Parkinsonism
Tremor, loss of fine motor skills, muscle rigidity, stooped posture, shuffling gait
- Tardive dyskinesia (TD) - face and tongue

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21
Q

Antiseizure drugs general patient teaching-Epilepsy specifically

A

Avoid alcohol, OTC drugs, other CNS depressants and herbal medications
Avoid nicotine
If diabetic, monitor blood glucose

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22
Q

Opioid side/adverse effects

A

Sedation, euphoria, intense relaxation, nausea, vomiting, constipation, urinary retention, pruritus (itching), respiratory depression, orthostatic hypotension, increased intracranial pressure, risk of physical and psychological dependence, dizziness, hallucinations, anxiety, tolerance

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23
Q

Important nursing assessments for opioid administration

A

Pain
Vitals
Monitor for respiratory depression
watch for addiction, assess pain before and after administration

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24
Q

Statin (atorvastatin-Lipitor) side effects and patient teaching

A

o helps with dyslipidemia, CAD
o SE: Muscle weakness/pain, headaches, GI upset, Rhabdomyolysis (dangerous levels of muscle
breakdown, can clog kidneys), Myopathy (muscle weakness)
o Also can be hard on liver (might need liver function tests)
o avoid grapefruit juice
o take at night (cholesterol synthesis)
- cola pee

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25
Q

Loop diuretic (furosemide-Lasix) side effects, patient teaching

A

furosemide (Lasix)
Block reabsorption of Na, K and Cl in loop of Henle.
SE: Hypokalemia, Orthostatic hypotension, ototoxicity.
Teach: Take K supplements
Give slow 10mg/min to avoid ototoxicity.
weigh daily, measure i/os, safety c orthostasis, take in AM

26
Q

Thiazide diuretic patient teaching

A

Thiazide
-thiazide (Microzide)
- Block reabsorption of Na, Cl, in distal tubules.
Less K loss
Orthostatic hypotension, hypokalemia
weigh daily, measure i/os, safety c orthostasis, take in AM
no ototoxicity

27
Q

Signs and symptoms, nursing assessment of fluid overload

A

o Colloids- (proteins pull water into blood vessels and expands plasma volume). Given primarily
for hypovolemic shock, hemorrhage and burns. Be mindful of fluid overload.- auscultate lung
sounds for crackles.
o water intake must equal output
- swelling/edema
- distended jugs
- cold/clammy skin
- confusion

28
Q

ARB mechanism of action

A

o Treat HTN and heart failure (effect RAAS)
o End in -sartan
o Prevent angiotensin II from binding to receptor=vasodilator and piss out electrolytes
o NO COUGH
o orthostatic hypotension, dizziness, N/V/D.

29
Q

Calcium Channel Blocker mechanism of action

A

o Antagonizes calcium channels
o Ends in -pine,amil. verapamil (Calan)
o Effects:
▪ Vascular smooth muscle: dilates peripheral arterioles
▪ Myocardium: reduces force of myocardial contraction that (can lower BP)
▪ Cardiac conduction: slows speed of electrical conduction

30
Q

Beta-blocker mechanism of action, side effects-metoprolol (Lopressor)

A

Lopressor MOA: Inhibits beta1 receptors, slowing heart rate and reducing blood pressure
S/E: bradycardia (hold for HR<60) and heart block, N/V, dizziness, fatigue, insomnia, orthostatic hypotension
o MOA: decrease heart rate and myocardial contractility; reducing cardiac output and workload
o SE: hypotension, bradycardia, exercise intolerance, fatigue
o Contraindications: pt with asthma
o Pt teaching: check pulse for one minute

31
Q

ACE inhibitor mechanism of action and side effects

A

-pril
MOA: block angio 1->2=Reduce afterload on the heart and lower blood pressure by decreasing
aldosterone therefore enhancing excretion of sodium and water
hypotension, cough, hyperkalemia and renal failure

32
Q

warfarin (Coumadin)patient teaching

A

Take at the same time every day, either morning or evening
Avoid vitamin K
PT or INR frequently drawn, ideally 2-3
Common serious side effects - bleeding

33
Q

Nitroglycerin administration and patient teaching

A

o Relax arterial (dilation) and venous smooth muscle (help reduce heart workload, reduce O2
demand)
o used for angina, MI, CAD
o SE: headache, hypotension
o 1 tab sublingual Q5min x3 (if pain not decreased, believed to be MI)

34
Q

enoxaparin (Lovenox) administration

A

Only administer in the abdomen, 2 inches (5cm) from the umbilicus
o Low molecular weight heparins
o More stable
o It can be given SubQ twice a day. Pt can inject themselves and go home.
o Treatment for DVT and PE.
o It has more predictable dosing and monitor parameters, more prefered for home use.
o Heparin works faster than warfarin

35
Q

NSAID, aspirin (Acetylsalicylic Acid [ASA]) side effects

A

o aspirin (Acetylsalicylic Acid) ASA
▪ blocks COX 1 and 2
▪ SE: N/V/D, bruising, bleeding
Salicylism: vomiting, tinnitus, confusion, hyperthermia, respiratory alkalosis, metabolic acidosis, and multiple organ failure.
▪ It can treat pain, fever, headache, and inflammation. It can also reduce the risk of heart
attack.
o NSAID
▪ blocks COX 1
▪ ibuprofen (Advil, Motrin) max dose is 3200 mg/day
▪ SE: N/V/D,

36
Q

acetaminophen (Tylenol) side effects, patient teaching

A

o inhibits COX
o antipyretic (#1)
o direct access to heat monitoring center in brain
o max dose 3 grams/day
o teach to read labels!
o interferes c metabolism of warfarin
S/E: sweating, stomach pain, diarrhea, constipation, nausea, headache, can cause Steven Johnson Syndrome, hepatotoxic

37
Q

Corticosteroid (glucocorticoids) side effects (prednisone)

A

o used to treat severe inflammation and other conditions
o dampens immune response (immunosuppressant)
o must taper dose to avoid adrenal insufficiency (adrenal gland atrophys following
corticosteroid therapy)
o have several serious SE with long-term use: renal insufficiency, hyperglycemia, mood
changes, cataracts, PUD (peptic ulcer disease), electrolyte imbalances, osteoporosis, impaired
wound healing, bruising, weight gain, Cushings disease (buff hump, moon face, crouching eagle mountain tiger)

38
Q

How are anti-infectives classified

A

o anti-infective drugs classified by their susceptible organisms, chemical structure and
mechanism of action. (anti- bacterials, virals, protozoans, etc)

39
Q

Antibiotic patient teaching

A

o teach pts to don’t stop until finished and space out doses and avoid alcohol
o may influence effectiveness of birthcontrol
o probiotics to prevent diarrhea
o report fever that doesn’t diminish within 3 days, SOB, dizzy, drowsy, skin/sclera yellowing
(liver toxicity)
o allergic reactions: itching, rashes, swelling
o may develop drug resistance by selection- the hardier microbes see what the drug looks like
and will make little “pacmen” to eat up the abx.
o acquired resistance; ability of organism to become unresponsive over time to abx

40
Q

Who is at risk for fungal infections

A

o immunosuppressed (cancer, HIV, autoimmune disorders, etc)

41
Q

Antineoplastic therapy patient teaching

A

o may be used for curing, palliative, or prophylaxis
o total cure means every malignant cell must be removed or killed through surgery, radiation or
drugs or by pts immune system
o chemo tx uses multiple drugs in order to allow for lower doses, fewer SE and greater success
▪ hit different processes in the cell cycle (kills more of the cancer cells)
o problems with chemo may limit therapy c most antineoplastic drugs
o avoid extreme temps of food and liquids bc they may cause trauma, avoid mouth washes bc
of alcohol content- stomatitis
o discuss and explore the meaning of hair loss before pt can deal c their feelings- alopecia
o use tylenol bc it doesn’t cause bleeding when immunosuppressed (No NSAIDs (can affect
clotting))- HA
o soft toothbrush, use electric razor, emery board for nail care, avoid foods that are difficult to
chew or have extreme temps- prevent bleeding
o teach handwashing, no visitors (usually), no fresh fruit or flowers

42
Q

Glucocorticoid inhalation side effects

A

o Inhaled for long term prophylaxis of asthma
o Reduce inflammation (histamine, leukotrienes)
o SE: dry mouth, thrush, gross taste, cataracts (if taken long term), hoarseness
o May take a few weeks to work
o Rinse mouth to avoid thrush

43
Q

Inhalation/intranasal route rationale

A

o Faster onset of action, can’t become addicted or have toxic levels
o Larger surface area
o Local, less systemic effects
o more blood flow

44
Q

Decongestant usage-different types/routes

A

o Most oral decongestants are sympathomimetics (adrenergic drugs)
o Oral have a longer onset of action
o Intranasal drugs are deliverd via sprays directly to their site of action which offers rapid and
efficient relief.
o Oral more likely for systemic effects

45
Q

SABA side effects (albuterol)

A

o Beta-2 adrenergic agonists (short-acting Beta Agonist (SABA))
o SABAx 2: SNS, activate B2 receptors, bronchodilation, airways widen
o Acute bronchospasm- most effective drug
o MOA: activate B2 receptors- bronchodilation, stimulates SNS, widens airways
o SE: increased HR, dysrhythmias, tremor, anxiety, h/a, throat irritation, bitter taste in mouth, can
cause hyperglycemia
o Use at first sign/symptom of asthma attack, only for accute attacks (rescue inhaler)

46
Q

PPI administration, patient teaching

A

o omeprazole (Prilosec) classification
▪ PPI (acid reducer)
▪ Binds to the enzyme that is responsible for secreting hydrochloric acid
▪ Several drug/drug interactions: coumadin (Warfarin), antivirals, antidepressants
▪ Administration: 20-30 min before meal on empty stomach (1-2 times a day)
▪ Most PPIs end in “prazole”

47
Q

H2-receptor antagonist mechanism of action

A

o Decreases acid secretion from parietal cells
o Most end in “tidine”
o Take c meal or at bedtime, best c food
o Don’t take at same time as PPIs or antacids

48
Q

psyllium husk (Metamucil) administration, general laxative patient teaching

A

o Drink lots of water and increase fiber intake
o Move more
o Moves water into the colon, and blocks water absorption back into the body in the colon
o Bulk forming (Metamucil)
▪ May take 1-3 days to work
▪ Eat things like prunes (natural laxative)
▪ May help decrease cholesterol (LDL)- binds to bile acids, binds to cholesterol

49
Q

Vitamin indications

A

o B12- vegetarians, pernicious anemia
o B1 thiamine- beriberi (paresthesia, neuralgia (nerve pain), loss of reflexes/sensation)
o B3 niacin- pellagra (fatigue, dry skin, anorexia)
o B9 folic acid- pregnancy
o C- scurvy
o D- osteoporosis
o K- clotting disorders
o calcium- elderly
o iron- vegetarian
o K+- pts on diuretics

50
Q

metformin (Glucophage) mechanism of action, side effects

A

o management of type 2 diabetes
o type of biguanides (most common): decreases hepatic production of glucose (gluconeogenesis)
and reduces insulin resistance. protects pt against cardiac disease
o doesn’t promote insulin release from pancreas
o GI related SE, avoid alcohol, low risk for hypoglycemia

51
Q

NPO guidelines for diabetics

A

o no DM meds if NPO (check c dr)

52
Q

Insulin (rapid, short, intermediate, long) administration guidelines

A

o lispro (Humalog): rapid- 5-15min, 15min, 1-3 hrs, 3 hrs
o regular insulin (Novolin R): short- 30min-60, 30min, 2-4 hrs, 5-7 hrs
o isophane insulin suspension (NPH): intermediate twice a day, 1-2 hr, 4-12 hrs, 18 hrs
o insulin glargine (Lantus): long acting-, once a day-evening, 2 hr, no peak, 24 hrs

53
Q

What type of insulins are Lispro (Humalog), aspart (Novolog), regular (R), NPH, glargine (Lantus),

A

o lispro (Humalog): rapid
o aspart (Novolog): rapid-acting
o regular (R): only type that can be given IV
o NPH: intermediate
o glargine (Lantus): long (never mix c other insulins)

54
Q

New diabetic patient education

A

o check BG daily, and keep within normal range
o know signs of hypo and hyper glycemia
o take meds as directed
o self foot checks
o cannot cure it, only treat it
o get good exercise, lifestyle changes

55
Q

Drugs that cause male sexual dysfunction

A

o SSRIs, TCA, ACE inhibitors, beta blockers, alpha blockers, thiazide diuretics cause erectile
dysfunction

56
Q

tadalafil (Cialis) patient teaching

A

o Treatment for erectile dysfunction
o phosphodiesterase-5 inhibitors (PDE5)- relaxation of sm, arterial dilation in corpus cavernosum
o SE: hypotension, priapism (erictile for more than 4 hrs.)- dangerous blood flow. Contact dr!
o contraindications; if taking nitrates, (dangerous hypotension-death),

57
Q

finasteride (Proscar) mechanism of action

A

o Tx for benign prostatic hyperplasia
o 5-alpha reductase inhibitor: blocks conversion of testosterone to the more potent hormone (DHT)
which prostate gland enlargement is dependent on.

58
Q

isotretinoin (Accutane) patient teaching

A

o must sign a pledge, can cause serious birth defects
o inhibits sebacious glands
o 2 forms of birth control- unknown MOA, must take for at least 8-12 weeks.
o SE: suicidal thoughts, depression- alert dr!

59
Q

Eye gtt administration

A

2 gtts at most (can’t absorb more)
don’t mix 2 drugs, wait 5 minutes between
place in conjunctiva
don’t contaminate tip of the dropped
wait to put in contacts for at least 15 min
little pressure on tear duct decreases systemic effects
inner to outer corner

60
Q

Ear gtt administration

A

Ear drops
cleanse ear
remove visible cerumen
make sure gtts are warm (room temp)
lie c infected side up
lie still for 10-15 minutes afterward

Pharmacology (9 decks)

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