Pharm Flashcards

1
Q

SSRI
AE (early and late)

A

Ex: Fluoxetine, paroxetine, sertraline, escitalopram, citalopram, fluvoxamine

Early AE: Nausea, anxiety, insomnia - will go away
Late AE: decreased all 3 sexual responses (libido, sexual arousal, and orgasm) - wont go away
Use with alcohol can cause depression

Safe for breastfeeding moms
1st line in children and adolescents however there is a “black box warning” for increased risk of suicidal thinking and behavior, so started on low dose.
Continue to 6 months after remission of depressive symptoms

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2
Q

SNRI
AE

A

Ex: Venlafaxine, Duloxetine, Desvenlafaxine

AE:
- Itching or rash
- Increased BP or HR

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3
Q

Bupropion
MOA, Use, AE

A

MOA: Norepinephrine & dopamine reuptake inhibitor

Use: Used for depression, smoking cessation.
AE: increase sz threshold for anorexic/bulimic patients. Favorable sexual side effect

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4
Q

Indomethacin
MAO, Use, AE

A

NSAID

Use:
1. Tocolytic used at <32 weeks, poses greater risk of used >32 weeks
2. 1st line for gout

AE: Chronic renal disease, GI bleed

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5
Q

Alternative medicine

A

Saw Palmetto: Benign prostatic hyperplasia
Garlic: Hypercholesterolemia
St. John’s wort: Depression
Glucosamine & Chondroitin: Osteoarthritis

Ginkgo biloba: used as a memory booster. AE: increased risk of bleeding and plt dysfunction (#1), seizures, HA, irritability, restlessness, D/N/V

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6
Q

ADAPT
what is is, tx

A

Cause: most commonly 1st gen antipsychotic

Acute dystonia: sustained muscular contraction –> Benztropine, Diphenhydramine

Akathesia: restlessness, pacing, tapping –> Benztropine, Benzo, Beta blocker

Parkinsonism: rigidity, mask facies, shuffling gait, tremor –> Benzotropine, Amantadine

Tardive dyskinesia: lip-tongue smacking, repetitive/uncontrolled –> stop med, switch to 2nd gen antipsychotic (Clozapine), Valbenazine

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7
Q

Steroids
AE for skin, Endocrine, Eyes, Neuro, Immune, GI, Cardio

A
  • Skin: Atrophy, easy bruising
  • Endocrine: adrenal insufficiency, hyperglycemia, linear growth impairment, osteoporosis
  • Eyes: cataracts
  • Neuro: behavior and sleep disturbances
  • Immune: Neutrophilia, immuosuppresssion
  • GI: Gastrisitis, ulcers, GI bleed
  • Cardio:HTN
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8
Q

Inhaled steroids
AE and its Tx

A

AE: oral candidiasis (thrush) which can be removed, showing areas of inflammation.
Comp: esophagitis
Tx: Topical antifungal (nystatin suspension or clotrimazole). Resistant form can be treated with oral fluconazole.

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9
Q

HTN Meds
AE of Loops, Thiazide, ACE, ARB
How to stop if possible

A

Loops
AE: OHHH DANG - Ototoxicity, HypoK, HypoH+ HypoMg, Dehydration, Sulfa allergies, Nephritis, Gout

Thiazides
AE: HyperGLUC (glucose, lipids, uric acid, calcium) and Hypo Na, K, H+, Pancreatitis, Sulfa allergies
Although it causes hypercalcemia, doesn’t cause constipation

ACEs:
AE: CATCHH - cough, angioedema, teratogen, high creatinine (decrease GFR), HyperK, Hypotension, and Pancreatitis

ARB’s:
AE: caTCHH: teratogen, high creatinine (decrease GRF), hyperK and hypotension and Pancreatitis

Can stop if stable BP below target BP for at least a year with good adherence to nonpharmacologic measures. Discontinue 1 medication at a time. Can decrease dose daily or take every other day over 1-2 months. Abrupt discontinuation of a short-acting drug can cause rebound hypertension.

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10
Q

Doxycycline
Use, AE

A

Lymes, Rocky Mountain, acne vulgaris

AE: photosensitivity, Effect bone and teeth in kids

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11
Q

Isotretinoin
4 AE

A

Nodulocystic acne may initially flare up and subsequently improve within the first few weeks of isotretinoin therapy.

Teratogenicity: 2 negative pregnancy test beforehand, 2 concurrent methods of contraception (1 month before, during and month after)
Other AE: dry skin & mucous membranes, myalgias, pseudotumor cerebri (with other tetracycline used)

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12
Q

OCP
MOA

A

Combined hormone contraception –> constant elevated systemic levels of estrogen and progesterone –> negative feedback of hypothalamus (decrease pulsatile release) and anterior pituitary (decrease LH, FSH)

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13
Q

Doxorubicin (AE)
Trastuzumab (AE)

A

AE: Cardiotoxicity (strongly related to cumulative doses and is irreversible)
Monitor with Radionuclide ventriculography: quantitating LVEF.
Performed at baseline before chemotherapy and before each subsequent dose of chemotherapy.
Regimen is dependent on baseline cardiac function…CI if EF <30%.
Decrease in EF by >10% warrants discontinuation of therapy.
________________________________________________
Trastuzumab
Monoclonal antibody against HER-2
AE:
- Decline in LVEF –> HF. This cardiotoxicity is reversible and there is complete recovery after treatment discontinuation.

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14
Q

Methotrexate
AE

A

AE: inhibits DHFR which is needed to convert folic acid into folinic acid –> folate deficiency –> macrocytic anemia
Tx: Folinic acid (Leucovorin)

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15
Q

TCA
Toxicity Sx , Tx

A

Ex: Amitriptyline, Nortriptyline

CNS: AMS, Seizures, Respiratory depression

Cardio: Sinus Tachy, hypotension, Prolonged PR/QRS/QT interval, Arrhythmia

Anti-cholinergic: Dry mouth, dry skin (inhibits diaphoresis) blurry vision, dilated pupils, urinary retention, flushing, hyperthermia, constipation

Tx: Oxygen, Intubation, IVF, Activated charcoal (if within 2 hrs), IVF sodium bicarbonate for QRS interval widening or ventricular arrhythmia (blocks fast Na channels and neutralized TCA

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16
Q

Fentanyl
MOA, AE

A

MOA: Short-acting opioid analgesic
AE: Respiratory depression, Exacerbated hypotension

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17
Q

Ketamine
MOA, AE

A

MOA: NMDA receptor antagonist/phencyclidine derivative
Preferred med for awake intubation of difficult airways. Provided dissociation, amnesia, and analgesia
AE: hypertension

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18
Q

Propofol

A

MOA: GABA receptor agonist
Rapid onset sedation and amnesia
AE: Respiratory depression, hypotension, loss of airway reflex

19
Q

Rocuronium
Succinylcholine
MOA, AE

A

Neuromuscular blocking agents used for sedation.
Both cause paralysis, loss of upper airway tone, cessation of all respiratory efforts

20
Q

Parkinsonism drugs
Levodopa (MOA)
Amantadine (MOA, Toxicity)
Pramipexol (MOA, toxicity)

A

Levodopa
MOA:
- dopamine immediate precursor
- Can cross BBB and be converted to dopamine.
- Rapidly metabolizes peripherally to dopamine and 3-O-metyldopa.
- Excess peripheral dopamine –> N/V, tachyarrhythmia, postural hypotension

  • Carbidopa blocks peripheral conversion and increases amount of dopamine going to the brain. This decreases peripheral AE but not central AE.
    _______________________________________________AAmantadine:
  • Increases dopamine release and decreases dopamine reuptake
    Toxicity = Psychosis, ataxia, livedo reticularis.
    _______________________________________________
    Pramipexole
  • Dopamine agonist
    Toxicity: impulse control disorder (eg,
    gambling), postural hypotension, hallucinations/confusion.
21
Q

Metformin

A
  • Decrease hepatic glucose production
  • Decrease intestinal glucose absorption
  • Increase peripheral glucose uptake/utilization
  • Decrease Lipogenesis

AE: Diarrhea, lactic acidosis, Vit B12 deficiency

22
Q

Amiodarone
AE

A

MOA: K channel blocker
- Pulmonary toxicity (responsible for most deaths). Tx - discontinuation
- Photosensitivity
- Blue-grey skin discoloration
- Bone marrow suppression
- Abnormal liver function test

  • Thyroid dysfunction:
    —Hypo: inhibits conversation of T4 to T3
    —Hyper: increase thyroid hormone synthesis or release of preformed thyroid hormones.
23
Q

SERM
Names, MOA, AE

A

Tamoxifen and Raloxifene

MOA: competitive inhibitor of estrogen binding
Mixed agonist/antagonist action

Tamoxifen: adjuvant tx for breast cancer
Raloxifene: postmenopausal osteoporosis

AE:
Both: Hot flashes, Venous thromboembolism, Tamoxifen: Endometrial hyperplasia & carcinoma and uterine sarcoma
— Regular screening is not proven beneficial, so only evaluate if sx develop.

24
Q

Rituximab
MOA

A

IgG monoclonal antibody against CD20 (a surface molecule presenting on developing and mature B-cells).
This binding on CD20 –> Fc receptor – mediated B-cell cytotoxicity & antibody-dependent B-cell phagocytosis, which significantly reduces B cell population.
Reduced B cells –> reduced inflammation

25
Q

Lithium
AE causing poluria
other AE

A

Polyuria (causes nephrogenic diabetes insipidus): Inability to concentrate the urine d/t inadequate arginine vasopressin (AVP) aka ADH.
AVP is released in response to rising plasma osmolality. This facilitates renal water reabsorption by increasing expression of the aquaporin 2 water channels. Lithium inhibits function of these channels –> less water reabsorption.

Lithium induced hypothyroidism.
- Interferes with the synthesis and release of thyroid hormone, causing a range of thyroid moralities that typically occur in the first two years of treatment.
- Tx: Levothyroxine.

26
Q

Clozapine
Use, AE

A
  • Treatment resistant schizophrenia/schizoaffective disorder
  • Schizophrenia with persistent suicidality

AE:
- Heme: agranulocytosis/neutropenia (ANC monitoring required)
- Cardiac: myocarditis, QTC prolongation
- Metabolic: insulin resistance/DM
- GI: constipation/adynamic ileus

27
Q

Valproic acid
AE

A

1st line for Juvenile myoclonic epilepsy
AE:
- Dose-related thrombocytopenia
- Hepatotoxicity
- Pancreatitis
- Teratogen

28
Q

Carbamazepine
AE

A
  • Diplopia
  • Ataxia
  • Blood dyscrasias (agranulocytosis, aplastic anemia)
  • Liver toxicity
  • Teratogenesis (cleft lip/palate, spina bifida), - induction of cytochrome P-450
  • SIADH –> hyponatremia
  • Stevens- Johnson syndrome
29
Q

Cholinergic Toxicity (Parasympathetic) vs anticholinergic
Sx

A

Cholinergic: Organophosphates
D - diarrhea vs Constipation
U - urination vs urinary retention
M - Constricted pupils vs Dilated pupils
B - bradycardia vs tachycardia, prolonged QRS, arrhythmia
E - emesis
L - lacrimation, sweating vs anhidrosis, flushed
L - Lethargy
S - Saliva vs dry mouth

30
Q

Stimulant intoxication
sx

A

CNS: Agitation, psychosis, insomnia, dilated pupils

Cardio: tachycardia, HTN

GI: dry mouth, bruxiam, anorexia

Derm: diaphoresis

Tx: Benzo for agitation. Antipsychotics for psychosis

31
Q

Salicylate poisoning (Sx, Tx)
Acetaminophen poisoning (Sx, Tx)

A

Salicylate
Sx:
Tachypnea –> respiratory alkalosis
N/V
Cochlear toxicity –> Tinnitus
Cerebral tissue injury and neuroglycopenia –> cerebral edema and AMS
Inhibition of cellular metabolism –> hyperthermia and lactic acidosis

Tx:
Acidosis facilitates proton uptake by salicylate anion making it uncharged and free to pass through electrically neutral cell walls.
- Bicarbonate acts as a base to bind free hydrogen ions in the blood –> trapping it within the bloodstream –> decrease tissue absorption
- Bicarbonate also alkalinizes the urine, to reduce renal tubular absorption and increase urinary excretion.
- Can also give glucose and activated charcoal (if within 2-4hrs of ingestion)
________________________________________________
Acetaminophen
Path: depletion of intrahepatic glutathione –> accumulation of NAPQI
Sx: Asx –> N/V/Fatigue –> elevated liver enzymes –> change in coagulation, AKI

Tx:
- Activated charcoal (if within 2-4hrs of ingestion)
- N- acetylcysteine (most effective when given within 8 hrs)

32
Q

Alcohol
Ethylene Glycol
Sx, Tx,
Methanol Tx

A

Alcohol
Preferred screening question:
The single-item screening question “How many times in the past year have you had 5 (4 for women) or more drinks in a day?

Ethylene Glycol
Antifreeze, engine coolant, bake fluids
Sweet tasting alcohol
Sx:
- AMS
- Intoxication effects and GI irritation
- Ethylene is metabolized into oxalic and glycolic acid –> metabolic acidosis
- Oxalic acid metabolites bind to serum calcium and form calcium oxalate –> hypocalcemia –> seizures
- Calcium oxylate crystals precipitate –> tubular obstruction–> AKI
Tx:
- Fomepizole (best) or ethanol to prevent conversion into acid.
- Na Bicarb
- Hemodialysis

Methanol toxicity is also treated with fomepizole

33
Q

Opioid (overdose tx)
Benzo (overdose tx)

A

Opioid overdose Tx: Naloxone

Benzo overdose Tx: Flumazenil but can precipitate seizures

34
Q

Drainage cleaner
Sx

A

Alkaline solution –> injure upper GI tract and airway
Emesis, dysphasia (drooling from avoiding swallowing) , stridor

35
Q

Benefits of smoking cessation
Methods, MOA , and AE

A

Smoking cessation can lower risk of all-cause mortality and cardiovascular events within 5yrs
- Smoking cessation can reverse or reduce loss of bone density and decrease the risk of fractures within 10yrs
- Weight changes are not significant

Varenicline
- MOA: partial nicotine receptor agonist
- Most effective than either bupropion or combined nicotine replacement therapy
- AE: disordered sleep, abnormal dreams, nausea

Bupropion
- Decrease postcessation weight gain
- Good choice of patients with unipolar depression
- AE: can worsen HTN
- CI in patients with seizure or eating disorder

Nicotine patches and nasal spray:
- decrese craving and daytime withdrawal sx
- No real AE

36
Q

Phencyclidine Toxicity
Sx, Tx

A

NMDA receptor agonist
Sx
- Agitation, hallucinations
- Combative
- Bizarre behavior lasting 8 hrs
- Traumatic injuries
- HTN, Tachycardia, Ataxia, Prominent Nystagmus

Tx: 1st line Benzo , Adjunctive Haloperidol

37
Q

Macrolide

A

Inhibit protein synthesis by bind to the 23S rRNA of the 50S ribosomal subunit Bacteriostatic.

38
Q

Phenytoin
MOA, AE

A

MOA: Blocks Na+ channels

AE:
PHENYTOIN:
P450 induction
Hirsutism
Enlarged
gums
Nystagmus - Tx: reduce dosage
Yellow-brown skin
Teratogenicity (fetal hydantoin syndrome)
Osteopenia
Inhibited folate absorption
Neuropathy
Rare adverse reactions including Stevens-Johnson syndrome, DRESS syndrome, SLE-like syndrome. Toxicity leads to diplopia, ataxia, sedation.

39
Q

Dobutamine
MOA

A

MOA: beta 1 receptor agonist –> increased production of cAMP –> positive inotropic effect (increase contractibility) and positive chronotropic effects (increased HR)
Decrease SVR

40
Q

DM meds

A

Basil insulin is typically added first to control nocturnal and fasting hyperglycemia through its continuous suppression of baseline hepatic gluconeogenesis.
Options include intermediate-acting NPH (neutral protamine hagedorn) which is given twice a day, or long-acting insulin given once a day.
Although both are equally effective in controlling fasting hyperglycemia, NPH carries a higher risk of hypoglycemia. In contrast, insulin glargine has no significant effect making the risk of hypoglycemia lower.

SLT-2: decreases reabsorption of Na + glucose –> more Na in the renal tubules –> decrease RAAS –> reduced constriction of efferent arterioles –> decrease GFR

41
Q

Vancomycin
MAO, AE MOA

A

MOA: Inhibits transpeptidase from cross linking a growth peptidoglycan chain by binding to the D-ala-D-ala terminus.
Resistance occurs when D-ala-D-ala terminus is replaced with D-ala-D-lactase –> decrease vancomycin binding

Drug-induced direct mast cell activation through a non-IgE mediated pathway. Vancomycin binds to Mas-related G protein receptor X2 found on mast cells, triggering the release of preformed vasoactive mediators (histamine).

42
Q

Beta-blockers (propranolol)
Uses
Toxicity (Pathophys, Sx,Dx, Tx)

A

Can be used for tremors (essential tremor, tremors secondary to hyperthyroidism)

Toxicity
Excessive blockage –> decrease intracellular cAMP

Sx of Beta 1blockade:
- Cardiac suppression with bradycardia & hypotension
- Confusion due to cerebral hypoperfusion

Sx of Beta 2 blockade:
- Broncospam
- Hypoglycemia (impaired gluconeogenesis/glycogenolysis)
- Confusion & seizures due to hypoglycemia

DX:
- ECG: sinus node dysfunction and AV block
- Clinical presentation

TX:
- IV fluids for hypotension
- Atropine for bradycardia
- Glucagon to direct counteract toxicity (increasing cAMP)
- Calcium gluconate sometimes given to increase blood pressure

43
Q

Bisphosphonates
MOA, AE, preliminary testing

A

Alendronate, ibandronate, risedronate, zoledronate

MOA: Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity.

AE:
- Esophagitis (if taken orally, patients are advised to take with water and remain upright for 30 minutes)
- Osteonecrosis of jaw
- Atypical femoral stress fractures
- Hypocalcemia (decrease bone resorption) so must confirm Ca and Vit D levels before starting