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Pharmacology II > Pharm test 2 > Flashcards

Pharm test 2 Flashcards

1
Q

Sulfonylureas end in….

A

-ide; GlipizIDE, GlyburIDE, GlimepirIDE

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2
Q

What class of hypoglycemics are sulfonylureas?

A

Insulin secretagogues

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3
Q

What is the MOA of sulfonylureas

A

promote insulin release from beta cells of pancreas; also reduce hepatic glucose clearance and increase peripheral insulin sensitivity by prolonging half-life

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4
Q

What do sulfonylureas do in B cells?

A

close potassium channels leading to depolarization of cell, opening of Ca2+ ion channels and release of insulin

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5
Q

Where are sulfonylureas metabolized?

A

liver

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6
Q

What are the adverse effects of sulfonylureas?

A

HYPOglycemia, hyperinsulinemia, weight gain

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7
Q

Which sulfonylurea options are safer for patients with renal dysfunction and the elderly?

A

Glipizide and glimepiride

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8
Q

WHich medications interact with sulfonylureas and can lead to hyperglycemia?

A

glucocorticoids, diuretics, antipsychotics

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9
Q

Which medications interact with sulfonylureas and can lead to hypoglycemia?

A

B-blockers, sulfonamides, antifungals

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10
Q

Glipizide duration of action and dosing per day

A

14-16 hours and either once or twice a day

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11
Q

Glipizide XL duration of action and dosing per day

A

24 hours; once daily

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12
Q

Glimepiride duration of action and dosing per day

A

24+ hours; once daily or 4mg BID instead of 8mg once a day

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13
Q

MOA of meglitinides

A

prevent ATP-sensitive potassium channels from opening; controls postprandial glucose levels

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14
Q

Examples of meglitinides

A

prandin (repaglinide)
starlix (nateglinide)

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15
Q

Dosing of meglitinides

A

TID before meals

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16
Q

AEs of meglitinides

A

hypoglycemia, weight gain

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17
Q

Should meglitinides be taken if a meal is skipped?

A

NO! controls postprandial glucose levels; could lead to hypoglycemia

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18
Q

MOA of biguanides

A

decreased hepatic gluconeogenesis (decreased glucose production in the liver); increased glucose uptake by muscles; decreased glucose absorption via GI tract

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19
Q

A1C reduction by biguanides

A

approx. 1.5

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20
Q

AEs of biguanides

A

N/V, diarrhea, loss of appetite, weight loss, lactic acidosis

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21
Q

How do we avoid AEs of biguanides?

A

slow-titration and take with meals

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22
Q

Which patients should avoid taking biguanides?

A

Those at risk for lactic acidosis:
impaired renal function
topiramate use
>65 years old
future radiology studies with contrast
excessive alcohol intake

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23
Q

How long does a patient need to be off biguanides prior to an imaging test with contrast dye?

A

one week!

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24
Q

Which labs need to be checked with biguanide use?

A

eGFR and SCr

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25
Q

Renal-dependent dosing for biguanides

A

eGFR <30mL/min- advanced CKD; contraindicated
eGFR 30-45mL/min- generally not recommended, 500mg QD to BID at most
eGFR 45-60mL/min- max 1.5g/day in BID dosing; renal monitoring every 6 months
eGFR >60mL/min- normal dose up to 2g/day in BID dosing

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26
Q

MOA of thiazolidinediones (TZD)

A

activates PPAR-gamma leading to increased insulin sensitivity in the adipose tissue, muscle, and liver; also decreases hepatic glucose production

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27
Q

Examples of thiazolidinediones (TZD)

A

pioglitazone (Actos)
rosiglitazone (Avandia)

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28
Q

What patients should not the use TZDs?

A

those with symptomatic CHF, NYHA class III or IV heart failure
those with osteoporosis (decreased bone density with use)

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29
Q

AEs of thiazolidinediones

A

fluid retention/CHF
weight gain-edema
increased risk of bladder cancer (pioglitazone)
macular edema
decreased bone density and increased risk of fractures

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30
Q

Renal dosing for thiazolidinediones

A

No renal dosing! ok for use in patient with renal problems

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31
Q

MOA of SGLT-2 inhibitors

A

inhibit the reabsorption of glucose in tubular lumen of kidney

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32
Q

A1C reduction with SGLT2 inhibitors

A

0.4-1.1

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33
Q

Contraindications in using SGLT-2 inhibitors

A

DMI, DMII with low GFR (no use in renal failure!), bladder cancer

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34
Q

Avoid SGLT-2 inhibitor use if possible in patients with….

A

frequent UTIs or yeast infections, low bone density, foot ulcers, factors predisposing them to DKA (alcohol use)

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35
Q

When to consider the use of SGLT-2 inhibitors…

A

patients with inadequate glycemic control on two oral agents OR if metformin and insulin are not a therapeutic option

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36
Q

AEs of SGLT-2 inhibitors

A

volvovaginal candidias, UTIs, urinary frequency, hypotension (particularly in elderly or patients on diuretics), ketacidosis

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37
Q

Steglatro (Ertugliflozin) dosing/ renal dosing

A

once daily in the morning, contraindicated in GFR < 60

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38
Q

Canagliflozin (Invokana) dosing/renal dosing

A

Daily before first meal, contraindicated in GFR <45; no more than 100mg with GFR 45-59

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39
Q

Empagliflozin (Jardiance) dosing/renal dosing

A

Once daily in the morning, contraindicated in GFR <45

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40
Q

Which SGLT-2 inhibitor reduces the risk of cardiovascular death in patients with T2DM and CVD?

A

Empagliflozin (Jardiance)

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41
Q

Dapagliflozin (Farxiga) dosing/renal dosing

A

Daily AT ANY TIME, contraindicated in GFR <30 and active bladder cancer

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42
Q

Incretin

A

gut-driven peptide that are secreted after nutrient intake

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43
Q

GLP-1

A

glucagon-like peptide-1; responsible for 60-70% of postprandial insulin secretion

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44
Q

What degrades GLP-1?

A

DPP-4

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45
Q

MOA of GLP-1 agonists

A

incretin mimetics; enhances postprandial insulin secretion, reduces food intake by enhancing satiety, decreases postprandial glucagon secretion, promotes B-cell proliferation (stimulating more insulin production)

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46
Q

A1C reduction on GLP-1 agonists

A

0.55-1.38

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47
Q

Examples of GLP-1 agonists

A

Long acting: albiglutide (tanzeum), dulaglutide (trulicity), semaglutide (ozempic) liraglutide (victoza),
Short acting: lixisenatide (Adlyxin), exenatide (byetta, bydureon)

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48
Q

Which GLP-1 agonist has an oral form?

A

semaglutide (rybelsus)

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49
Q

AEs of GLP-1 agonists

A

N/V/D/C, weight loss, pancreatitis, increased satiety, possible thyroid tumors so contraindicated in pts with hx of thyroid or other endocrine cancers, hypoglycemia

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50
Q

Which GLP-1 agonist should be not be used in renal impairment?

A

Exenatide (Byetta, Bydureon)

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51
Q

Which GLP-1 agonist is approved to reduce the risk of cardiovascular events and cardiovascular mortality?

A

Liraglutide (Victoza)

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52
Q

Instructions for a missed dose of dulaglutide

A

If at least 72 hours before next scheduled dose- administer ASAP
If less than 72 hours before the next scheduled dose- missed dose is skipped and next dose is administered on regularly scheduled day
Then resume regular once a week dosing schedule

The day of weekly administration can be changed as long as the last dose was 3 days before.

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53
Q

MOA of DPP-4 inhibitors

A

inhibits DPP-4 from breaking down GLP-1 allowing for GLP-1 to exert its effects longer leading to decreased glucose levels; increases release of insulin postprandial and decreases secretion of postprandial glucagon

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54
Q

Which medications can be used in combination with DPP-4 inhibitors?

A

sulfonylureas, metformin, TZDs, insulin
NO COMBO use with GLP-1 agonists

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55
Q

All DPP-4 inhibitors require renal dosing EXCEPT…

A

linagliption

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56
Q

Changes in weight with DPP-4 inhibitors

A

none, they are weight neutral. Also do not cause satiety

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57
Q

Dosing of DPP-4 inhibitors

A

Taken once daily, well-absorbed with oral administration, ok to take with meals

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58
Q

AEs of DPP-4 inhibitors

A

usually well tolerated, nasopharyngitis, headache, pancreatitis, risk of severe joint pain, increased risk of heart failure with alogliptin and saxagliptin

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59
Q

Which DPP-4 inhibitors increase the risk of heart failure?

A

Alogliptin (Nesina) and saxagliptin (Onglyza)

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60
Q

Examples of DPP-4 inhibitors

A

Alogliptin (Nesina), Saxagliptin (Onglyza), Sitagliptin (Januvia), Linagliptin (Tradjenta)

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61
Q

DPP-4 inhibitors end in

A

-gliptin

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62
Q

Insulin analogues

A

made by recombinant DNA technology, administered SubQ, IV, or inhalation

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63
Q

Concentration of insulins

A

all have concentration of 100 units/mL except glargine (Toujeo) which is 300 units/mL

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64
Q

Regular insulin onset, peak, duration

A

Onset: 1/2-1 hour
Peak: 2-4 hours
Duration: 6-8 hours

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65
Q

Lyspro/Aspart/Glulisine onset, peak, duration

A

Onset: <15 minutes
Peak: 1-2 hours
Duration: 4-6 hours

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66
Q

NPH onset, peak, duration

A

Onset: 1-2 hours
Peak: 6-10 hours
Duration: 12+ hours

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67
Q

Detemir onset, peak, duration

A

Onset: 1 hour
Peak: around 12 hours
Duration 12-24 hours

68
Q

Glargine onset, peak, duration

A

Onset: 1.5 hours
Peak: flat, no peak
Duration: 24 hours

69
Q

AEs of insulin

A

lipodystrophy- may cause wide glycemic oscillations and hypoglycemia

70
Q

Lipoatrophy

A

large, often deep retracted scar on skin from serious damage to SubQ tissue

71
Q

Lipohypertrophy

A

thickened “rubbery” tissue swelling; mostly firm but occasionally presents as a soft lesion

72
Q

S/S of hypoglycemia

A

Headache, anxiety, tachycardia, confusion, vertigo, diaphoresis, shakiness, increased appetite, blurred vision, weakness/fatigue

73
Q

Hypothyroidism

A

permanent condition requiring lifelong treatment, commonly autoimmune (Hashimoto’s)

74
Q

Two conditions that may not require thyroid hormone replacement

A

Transient hypothyroidism (painless or subacute thyroiditis)
Reversible hypothyroidism (due to a drug that can be discontinued) ex: amiodarone

75
Q

Liothyronine

A

T3 analogue, takes effect rapidly, Cytomel: 25-75mcg PO QD

76
Q

How soon can a dose of liothyronine be increased?

A

1-2 weeks

77
Q

Levothyroxine

A

T4 analogue; standard choice of therapy

78
Q

MOA of levothyroxine

A

diffueses into cell nucleus and binds to thyroid receptor proteins attached to DNA on the effector organs; bound to thyroxine-binding globulin in the plasma, must dissociate prior to entry into cells, T4 then deiodinated into T3 in the cells

79
Q

When does levothyroxine reach it’s steady state?

A

6-8 weeks

80
Q

What labs do you check for hypothyroidism?

A

TSH and T4

81
Q

What can decrease the absorption of T4?

A

calcium, iron salts, aluminum-containing antacids, PPIs, sucralfate

82
Q

How is levothyroxine metabolized?

A

via conjugation with glucoronides and sulfates and excreted in bile

83
Q

Dose changes to levothyroxine in pregnancy

A

dose needs to be increased; free T4 is important for normal fetal development

84
Q

AEs of levothyroxine

A

cardiovascular side effects: palpitations, tachycardia; increased appetite, nervousness, tremor, weight loss, diarrhea, diaphoresis- think hyperthyroid sx’s

85
Q

Ways to avoid AEs of levothyroxine

A

start with low dose and increase gradually

86
Q

Dosing for levothyroxine

A

1.6mcg/kg/day OR
25-50mcg standard dosing

87
Q

When should T4 be taken

A

on an empty stomach, ideally 60 minutes before breakfast with water OR three hours after the evening meal

other meds are best 4 hours after dose.

88
Q

When should soft gels be used in treatment of hypothyroidism?

A

Patients with atrophic gastritis and after bariatric surgery; soft gels may be less dependent upon gastric pH

89
Q

combination T4/T3 therapy

A

DO NOT USE
physiological ratio of T4:T3 is 13:1-16:1
combo meds such as Liotrix and desiccated thyroid extract are supraphysiologic at 4:1 ratio

90
Q

How does furosemide interact with levothyroxine

A

Decreases T4 binding to TBG

91
Q

How does amiodarone interact with levothyroxine?

A

impaired conversion of T4 to T3

92
Q

Hyperthyroidsim

A

excessive production of thyroid hormones from the thyroid gland; many times autoimmune (Grave’s disease)

93
Q

Symptomatic treatment of hyperthyroidism

A

beta-blockers (atenolol); decrease symptoms from increased sympathetic tones

94
Q

Antithyroid medications

A

Thioamides

95
Q

Examples of Thioamides

A

Propylthiouracil (PTU) and methimazole (Tapazole)

96
Q

MOA of thioamides

A

inhibit thyroid peroxidase; do not inhibit thyroid hormones

97
Q

How long does it take thioamides to attain euthyroid state

A

3-8 weeks

98
Q

Methimazole (Tapazole)

A

exclusively used for longer duration of action and less side effects; used during 2nd and 3rd trimesters of pregnancy

99
Q

Prophylthiouracil (PTU)

A

used during 1st trimester of pregnancy- high binding leads to less crossing of the placenta; not recommended for pediatric patients due to hepatotoxicity; should be a short dose with close patient monitoring; only for those who cannot take methimazole or have surgery or radioactive iodine treatment

100
Q

AEs of Thioamides

A

skin rash, vasculitis, hypothyroidism, lupus-like syndrome, agranulocytosis (increased risk of infection), hypoprothrombinemia (Increased risk of bleeding), hepatotoxicity

reversible with discontinuation of meds

101
Q

Monitoring on thioamides

A

periodically assess free T4 and total T3 levels- first check not before 4 weeks then every 4-6 weeks until stabilized and then every 3-6 months

also monitor calcium levels

102
Q

Lugol’s solution

A

potassium iodine (10%) and iodine (5%); inhibits synthesis and release of T3 and T4; used to treat thyroid storms; not used in primary care

103
Q

Absorption changes in children

A

different water content and degree of vascularization on skin, muscle, and fat leads to erratic absorption via IM and rectal administration

also lower gastric acidity, gastric emptying time, GI motility, pancreatic enzyme activity, and increased GI surface area with younger age can lead to different bioavailability

104
Q

Distribution changes in children

A

changes in body composition (total body water and adipose tissue) and differing plasma protein binding, tissue binding, and blood flow to organs changes distribution

105
Q

Metabolism changes in children

A

limited data

106
Q

Elimination and Excretion changes in children

A

Immature enzyme development and liver/renal function- decreased renal blood flow, GFR, and tubular function

protein binding in neonates is low, the less bound a drug is the more efficient it can transverse cell membranes or diffuse
- affects drugs efficiency

107
Q

Specific changes in premature infants

A

Incomplete glial development enhances the permeability of the BBB and permits drugs and bilirubin to enter the CNS more readily

108
Q

Specific drug differences in children: valproic acid

A

higher incidence of valproic acid- associated hepatotoxicity in young infants

109
Q

Specific drug changes in children- valproic acid

A

higher incidence of valproic acid-associated hepatotoxicity in young infants

110
Q

Specific drug changes in children- diphenhydramine

A

greater frequency of paradoxical CNS reactions in infants

111
Q

Specific drug changes in children: atypical antipsychotics

A

higher incidence of weight gain in adolescence

112
Q

Specific drug changes in children: warfarin

A

altered concentration-versus-effect profiles for warfarin in children with congenital heart disease

113
Q

Important considerations for pharmacology in children

A

weigh risks vs. benefits
consider long term effects
consider dosage formulations

114
Q

Specific drug changes in children: fluoroqinolones (ciprofloxacin)

A

risk of severe degenerative arthropathy so contraindicated in children <18 years old
should not be used if alternate treatment exists

115
Q

Specific drugs changes in children: antidepressants

A

increased risk of suicidality in children however risk of suicide in patients with untreated depression is much higher

116
Q

Specific drug changes in children: controlled substances for ADHD

A

delayed onset of puberty (conflicting data)

117
Q

Specific drug changes in children: inhaled steroids

A

conflicting data about height reduction (1cm reduction)

118
Q

APAP gtts vs. APAP liquid

A

3x as concentrated

119
Q

What should you use for the best dosage recommendation?

A

manufacturers package insert
DONT use Young or Clark’s rules as they are not accurate
physiologically children are not small adults

120
Q

What is the most common form of dosing calculation for children?

A

body weight-based dosing
mg/kg/day or mg/kg/dose

121
Q

What is the most accurate method of dosing calculation for children?

A

Body surface area: use for narrow-therapeutic index drugs

122
Q

KIDs List

A

released in 2020; Key potentially Inappropriate Drugs in Pediatrics; weak and strong recommendations based on evidence
67 drugs and 10 excipients

123
Q

Specific drugs to avoid in children: Salicylates (ASA)

A

KIDs list shows weak recommendations but AAP recommends against it for <18 years old due to risk of Reye syndrome; however proven benefit for some pediatric populations

124
Q

Specific drugs to avoid in children: Tetracycline

A

tooth discoloration & enamel hypoplasia <8 years old; delayed skeletal development and bone growth in premature infants

125
Q

Drugs to avoid in children: codeine

A

respiratory depression; death

126
Q

Guidelines for use of cold and cough medications in children

A

AAP- no OTC cough or cold medicine should be given to < 6 years old
FDA- children under 2 should not be given medication containing decongestants or antihistamine
Manufactures- no cold products for children <4 years old

127
Q

Pharmacokinetic changes in obese children

A

changes in tissue compositon; increased blood volume/cardiac output, impaired liver and kidney functions all decrease the volume of distribution and clearance of many medications

physicochemical properties of a drug (lipid solubility and relative protein binding) leads to different effects on PK

128
Q

Other medications not to use in children

A

benzocaine, ceftriaxone, gentamycin ophthalmic ointment, lidocaine 2% viscous, macrolides, topical corticosteroids, tramadol

129
Q

Current recommendations for weight-based dosing in children

A

for children <18 who are <40kg (88lbs) use weight-based dosing

for children >40kg use weight-based design unless the dose exceeds recommended adult dose

130
Q

Common errors in prescribing medications

A

incorrect dosage
incorrect frequency
underdosing or overdosing
inappropriate medication selection for indication
incorrect route of administration
failure to screen drug interactions or monitor side effects

131
Q

Ways to minimize prescribing errors

A

Use EMR to send prescriptions
Put pts age and weight on prescription is dose is dependent on weight

132
Q

Placenta-and-fetal unit changes in PK

A

placenta affects the amount of drug that crosses the placental membrane, the amount of drug metabolized
Fetus: affects the distribution and elimination of drug

both are additional compartments for distribution

133
Q

GI absorption in pregnancy

A

-decreased gastric motility- delayed absorption of medications unless a drug is slow to dissolve
-decreased GI surface area
-reduction in gastric secretions and increase in gastric mucus secretion leads to increased gastric pH- decrease in absorption of medications that need acidic pH
- N/V in pregnancy from increased progesterone levels so meds should be taken when nausea is minimal

BUT OVERALL MINIMAL EFFECT ON BIOAVAILABILITY AND THERAPEUTIC EFFECT OF MOST ORAL DRUGS

134
Q

Lung absorption in pregnancy

A

Increased cardiac and tidal volume in pregnancy; but not studies have showed increased toxicity of inhaled medications

135
Q

Transdermal absorption in pregnancy

A

increased during pregnancy but deemed safer than oral or IV (limited data available)

136
Q

Changes in distribution in pregnancy

A

increase in total body water and body fat leads to increased volume of distribution of hydro and lipophilic drugs

decreased plasma albumin leads to decreased albumin binding which leads to increased free drug concentration leading to more distribution in tissues

Efficacy and toxicity are related to unbound drug concentration in plasma

137
Q

What drugs are significantly affected by changes in distribution in pregnancy?

A

Tacrolimus and phenytoin

138
Q

Changes in elimination in pregnancy

A

increased progesterone levels stimulate hepatic microsomal enzyme systems leading to increased elimination of some hepatically eliminated medications decreasing elimination of others

rate of renal blood flow increases by 50% and GFR increases which leads to drugs excreted by the kidney having an increase in elimination (ex: cefazolin and clindamycin)

139
Q

CYP450 changes in pregnancy

A

from increase in progesterone levels

140
Q

Four factors affecting the ability of a drug to cross the placenta

A

lipid-soluble drugs cross more freely than water-soluble
ionisation of the drug affects placental transfer
molecular weight of the drug- lighter weigh tor smaller drug molecules cross the placenta easier
protein binding status- unbound drugs cross placenta easier

141
Q

Teratogenicity

A

ability of a drug to cause defects in fetus

142
Q

Safe antibiotics in pregnancy

A

penicillin, cephalosporins, erythromycin- considered safe
higher-dose regimens may be needed since they are cleared quicker due to increased GFR

143
Q

Antibiotics to avoid in pregnancy

A

aminoglycosides and tetracyclines
avoid nitrofuratoin in near term preganancies
chloramphenicol is safe only topically

144
Q

Metronidazole in lactation

A

may give breast milk an unpleasant taste

145
Q

Pregnancy and lactation labeling rules

A

Must give information on pregnancy, lactation, and female and male reproductive potential

146
Q

Lactation labeling

A

If not systemically absorbed- must state that fact
If systemically absorbed, label must include:
relevant information on presence of drug in human milk
effects of drug on breast-fed child
effect of drug on milk production
risk and benefit statement

147
Q

Absorption changes in geriatrics

A

least affected
possibly slower but still complete
the more drugs a patient takes the higher risk for drug-drug interactions that interfere with absorption

148
Q

Distribution changes in geriatrics

A

Bady fat increases with age- drugs that are lipid soluble may stay in blood longer since there are more fat stores where it can be distributed
decrease in muscle mass leads to less total body water- blood levels of a drug that this water-soluble may be higher than expected
decrease in albumin- causes lower amount of protein binding and leads to more active drug circulating in the blood

149
Q

Clearance changes in geriatrics

A

liver and kidneys are affected by age
blood flow to the liver decreases which can reduce the clearance of some drugs by 30-40%
GFR decline is extremely variable
SCr is not reliable but still important to assess (older adults have decreased muscle mass and muscle metabolism so less creatinine production)

150
Q

CYP450 changes in geriatrics

A

system becomes easily overwhelmed in older patients leading to slower drug metabolism

151
Q

Cockcroft-Gault Equation

A

calculates creatinine clearance
CrCl (mL/min) = (140-age) x lean body weight (kg)/serum creatinine (mg/dL) x 72 (x0.85 if female)

152
Q

Drugs with decreased hepatic clearance in geriatrics

A

acetaminophen, codeine, warfarin

153
Q

Drugs with decreased renal clearance in geriatrics

A

amoxicillin, atenolol, furosemide, hydrochlorothiazide, metformin

154
Q

Drugs associated with falls in geriatrics

A

antihistamines, antihypertensives

155
Q

Drugs associated with confusion in geriatrics

A

corticosteroids

156
Q

Drugs with significant anticholinergic effects in geriatrics

A

antidepressants (tricyclics) and antihistamines

157
Q

Factors leading to polypharmacy

A

clinical practice guidelines
chronic disease managment
multiple prescribers or pharmacies
direct to consumer marketing
treating surrogate markers
uncertain treatment goals
clinical uncertainty
lack of communication
adverse drug event or new symptom?
treating side effects of another Rx
increased use of OTC, herbal supplements, complementary or alternative medications

158
Q

Consequences of polypharmacy

A

increased risk of adverse drug reactions
reduced medication adherence
increase risk of serious drug-drug interactions
increased health care costs
reduced functional ability and ability to perform independent ADLs
increased risk of cognitive impairment, falls, malnutrition, urinary incontinence

159
Q

How to streamline the medication review process

A

define or confirm clinical indications for all meds taken
adjust dosage for renal function
assess relative risks and benefits for each med
identify adverse drug events
evaluate drug-drug and drug-disease interactions

160
Q

9 questions to address pharmacology in the elderly

A

Is each medication necessary?
Is the drug contraindicated in the elderly?
Are there duplicate medications?
Is the patient taking the lowest effective dose?
Is the medication intended to treat the side effect of another medication?
Can the drug regimen be simplified?
Are there potential drug interactions?
Is the patient adherent?
Is the paitent taking OTC medications, herbal products, or another person’s medications?

161
Q

Safe prescibing tips

A

review medicaiton list at every visit
evaluate patient adherence
consider new symptoms or complaints as possible drug-related problem and investigate
use Beers criteria when considering new presciptions
ensure each medication has a clear indication
ask about use of OTCs
start low and go slow when prescribing
consult other health care professionals

162
Q

Mnemonic to remember polypharmacy principles

A

TIDE
T: Time
I: individualize
D: drug interactions
E: educate

T; allow sufficient time to addres and discuss medication issues each visit
I: apply PK and PD principles to regimens by adjusting doses for renal and heplatic imparment and starting medications at lowest possible dose
D: consider potential drug-drug and drug-disease interactions
E: educate the patient and caregiver about side effects and monitoring parameters

163
Q

Role of nursing in polypharmacy

A

Obtain a thorough drug history
teach patietn when to contact prescriber
use one pharmacy
identify risks and develop individualized interventions
teach patient to dispose of old medications
collaborate with patient, family, and prescriber on treatment goals
provide effective teaching on role of drug thearpy in reaching goals
take steps to promote adherance
avoid drugs on Beers list
monitor for desired levels and labs when appropriate
monitor for drug-drug and drug-disease interactions
reduce symptoms and improve QOL
communicate with patient’s other providers

164
Q

Ways to promote adherence in geriatrics

A

simplify drug regimen
provider clear and concise verbal and written instructions
use approprate dosage forms
containers clearly labeled and easy to open
daily reminders, timers, pill dispensers
support systems
frequent monitoring

165
Q

DPP4 inhibitors end in

A

-gliptin

166
Q

SGLT-2 inhibitors end in…

A

-flozin

Pharmacology II (3 decks)

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