Pharm Flashcards
SSRI
AE (early and late)
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
SNRI
AE
Ex: Venlafaxine, Duloxetine, Desvenlafaxine
AE:
- Itching or rash
- Increased BP or HR
Bupropion
MOA, Use, AE
MOA: Norepinephrine & dopamine reuptake inhibitor
Use: Used for depression, smoking cessation.
AE: increase sz threshold for anorexic/bulimic patients. Favorable sexual side effect
Indomethacin
MAO, Use, AE
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
Alternative medicine
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
ADAPT
what is is, tx
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
Steroids
AE for skin, Endocrine, Eyes, Neuro, Immune, GI, Cardio
- 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
Inhaled steroids
AE and its Tx
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.
HTN Meds
AE of Loops, Thiazide, ACE, ARB
How to stop if possible
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.
Doxycycline
Use, AE
Lymes, Rocky Mountain, acne vulgaris
AE: photosensitivity, Effect bone and teeth in kids
Isotretinoin
4 AE
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)
OCP
MOA
Combined hormone contraception –> constant elevated systemic levels of estrogen and progesterone –> negative feedback of hypothalamus (decrease pulsatile release) and anterior pituitary (decrease LH, FSH)
Doxorubicin (AE)
Trastuzumab (AE)
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.
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Trastuzumab
Monoclonal antibody against HER-2
AE:
- Decline in LVEF –> HF. This cardiotoxicity is reversible and there is complete recovery after treatment discontinuation.
Methotrexate
AE
AE: inhibits DHFR which is needed to convert folic acid into folinic acid –> folate deficiency –> macrocytic anemia
Tx: Folinic acid (Leucovorin)
TCA
Toxicity Sx , Tx
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
Fentanyl
MOA, AE
MOA: Short-acting opioid analgesic
AE: Respiratory depression, Exacerbated hypotension
Ketamine
MOA, AE
MOA: NMDA receptor antagonist/phencyclidine derivative
Preferred med for awake intubation of difficult airways. Provided dissociation, amnesia, and analgesia
AE: hypertension
Propofol
MOA: GABA receptor agonist
Rapid onset sedation and amnesia
AE: Respiratory depression, hypotension, loss of airway reflex
Rocuronium
Succinylcholine
MOA, AE
Neuromuscular blocking agents used for sedation.
Both cause paralysis, loss of upper airway tone, cessation of all respiratory efforts
Parkinsonism drugs
Levodopa (MOA)
Amantadine (MOA, Toxicity)
Pramipexol (MOA, toxicity)
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.
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Pramipexole - Dopamine agonist
Toxicity: impulse control disorder (eg,
gambling), postural hypotension, hallucinations/confusion.
Metformin
- Decrease hepatic glucose production
- Decrease intestinal glucose absorption
- Increase peripheral glucose uptake/utilization
- Decrease Lipogenesis
AE: Diarrhea, lactic acidosis, Vit B12 deficiency
Amiodarone
AE
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.
SERM
Names, MOA, AE
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.
Rituximab
MOA
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
Lithium
AE causing poluria
other AE
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.
Clozapine
Use, AE
- 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
Valproic acid
AE
1st line for Juvenile myoclonic epilepsy
AE:
- Dose-related thrombocytopenia
- Hepatotoxicity
- Pancreatitis
- Teratogen
Carbamazepine
AE
- 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
Cholinergic Toxicity (Parasympathetic) vs anticholinergic
Sx
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
Stimulant intoxication
sx
CNS: Agitation, psychosis, insomnia, dilated pupils
Cardio: tachycardia, HTN
GI: dry mouth, bruxiam, anorexia
Derm: diaphoresis
Tx: Benzo for agitation. Antipsychotics for psychosis
Salicylate poisoning (Sx, Tx)
Acetaminophen poisoning (Sx, Tx)
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)
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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)
Alcohol
Ethylene Glycol
Sx, Tx,
Methanol Tx
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
Opioid (overdose tx)
Benzo (overdose tx)
Opioid overdose Tx: Naloxone
Benzo overdose Tx: Flumazenil but can precipitate seizures
Drainage cleaner
Sx
Alkaline solution –> injure upper GI tract and airway
Emesis, dysphasia (drooling from avoiding swallowing) , stridor
Benefits of smoking cessation
Methods, MOA , and AE
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
Phencyclidine Toxicity
Sx, Tx
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
Macrolide
Inhibit protein synthesis by bind to the 23S rRNA of the 50S ribosomal subunit Bacteriostatic.
Phenytoin
MOA, AE
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.
Dobutamine
MOA
MOA: beta 1 receptor agonist –> increased production of cAMP –> positive inotropic effect (increase contractibility) and positive chronotropic effects (increased HR)
Decrease SVR
DM meds
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
Vancomycin
MAO, AE MOA
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).
Beta-blockers (propranolol)
Uses
Toxicity (Pathophys, Sx,Dx, Tx)
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
Bisphosphonates
MOA, AE, preliminary testing
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
