Pharmacology/Toxicology Flashcards
(13 cards)
Niacin - mechanism for flushing and pruritus
Prostaglandin-mediated peripheral vasodilation –> can be reduced by ASA (take 30 min before niacin), which reduces PG production by inhibiting COX-1/2.
Methanol vs. Ethylene glycol poisoning
1) Methanol - side effects similar to ETOH
- HA, N/V, epigastric pain within 24 hours ingestion
- Vision loss, coma are severe consequences
- Optic disc hyperemia common finding
- AGMA
2) Ethylene glycol - similar to methanol but instead of damaging eyes it damages kidneys
Chronic alcoholism - most common electrolyte abnormality?
Hypomagnesemia, likely due to poor PO intake, ETOH induced renal losses, and diarrhea
Hypomagnesemia commonly occurs with hypokalemia –> well known cause of refractory hypokalemia
Hydroxychloroquine - use and side effects
DMARD, esp for SLE
Can cause retinal toxicity –> should have baseline ophthalmologic evaluation before starting and have annual reassessment after 5 years (toxicity arises ~ 5-7 years later)
Cyanide toxicity
Binds cytochrome oxidase and disrupts oxidative phosphorylation.
Commonly due to:
1) carbon and nitrogen containing compounds (eg wool and silk)
2) Industrial exposure (eg metal extraction in mining)
3) Medications (eg sodium nitroprusside)
4) House fires - smoke contains multiple toxins, HCN and CO being two major products of combustion in closed spaces.
Manifestations include:
Skin - flushing (cherry red), cyanosis (later)
CNS - AMS, seizures, coma
CV - arrhythmias
Respiratory - tachypnea followed by respiratory depression, PE
GI - Abd pain, N/V
Renal: metabolic acidosis (from lactic acidosis), renal failure
Treatment: hydroxocobalamin or sodium thiosulfate, which directly binds cyanide molecules. Alternate is induction of methemoglobinemia with nitrites to increase Fe3+ in circulating hemoglobin –> CN binds avidly so would provide alternate binding site.
Chemo-induced cardiotoxicity
Type 1 - a/w anthracyclines
Myocyte necrosis and destruction –> fibrosis, with progression to overt clinical HF, less likely to be reversible
Typie 2 - a/w trastuzumab
Myocardial stunning/hibernation w/o myocyte destruction, asymptomatic LV systolic dysfunction
MORE LIKELY to be reversible –> need baseline assessment w/ echo
Lead toxicity
Peripheral neuropathy –> primarily motor neurons with wrist/ankle drops
INH-associated anemia?
Pyridoxine (B6) deficiency –> sideroblastic anemia
Signs that distinguish benzo vs. opioid overdose
Both can present with slurred speech, unsteady gait, and drowsiness. Benzos however, lack respiratory depression and lack pupillary constriction.
Ethylene glycol presentation and treatment
Flank pain, hematuria, oliguria, AKI, and AGMA
Hypocalcemia and calcium oxalate deposition in kidneys
Treatment:
Fomepizole or ETOH to inhibit alcohol DH
Sodium bicarb to alleviate acidosis
HD in cases of of severe acidosis and/or end organ damage
Treatment of drug reaction (drug induced type 1 hypersensitivity)
Mild manifestations (eg only urticaria and pruritus without systemic symptoms) usually treated with antihistamines.
Those with more systemic symptoms (dyspnea, wheezes, stridor, diarrhea, cramps, anaphylaxis)–consider epinephrine and IV corticosteroids.
Medications that precipitate myasthenic crisis?
Abx: aminoglycosides, fluoroquinolones
BB, CCB, Mg
To bridge to slow acting steroid sparing meds (eg AZT) in myasthenic crisis should receive rapid acting plasma exchange or IVIG and high dose corticosteroids.
Nitrofurantoin side effects
Acute lung injury -> hypersensitivity pneumonitis with eos.
Long term –> interstitial lung disease
