Random Flashcards
Nicardipine vs nifedipine?
They both have marked coronary and peripheral dilatation without AV or SA conduction depression
But nicardipine has minimal effect on cardiac muscle where nifedipine causes moderate depression of the cardiac muscles
esmolol
A. metabolism/half life/pharm
B. dosing
C. indications
A. blood borne esterases/9-10 minutes/cardioselective
B. 0.5mg/kg or infusion for HTN
SVT - 500ug/kg -> 50ug/kg/min x4 mins
if not controlled repeat loading dose then 100ug/kg/min for 4 minutes
repeat up to 200-300ug/kg/min
~if longer acting agent needed, use metoprolol
RF for steroids induced perianal itching
Female and young age, and with bouls dose.
The mechanism is unknown though it may be related to phosphate ester in chemical structure.
Fentanyl been used to decrease the incidence.
Max dose of vancomycin to prevent red man syndrome is
10 mg/min
The reaction (hypotension, Tachy, generalized pruritus, and red rash) related to non-immune mediated histamine release and related to the fast administration of a large molecular drug.
Other common anesthetic drug then steroids that causes genital burning and itching?
Fospropofol
It’s a prodrug of propfol in phosphate ester form (which though the cause of itchiness)
How histamine H2 receptors antagonists reduces the severity and risk or perioperative aspiration pneumonia?
They block histamine from inducing acidic gastric fluid secretion by partial cells which effectively raises gastric pH and therefore decrease risk of aspiration pnumonitis.
Onset of action and duration for H2 blockers
Onset. Duration
Cimetidine. 1-1.5 3-4
Ranitidine. 1 9-10
Famotidine. 1 10-12
In hours. So Ranitidine has longer elimination half life then cimetidine, faster onset, and it is more potent with fewer CV and CNS side effects.
Famotidine has longer half life then both.
The triad of cyanide toxicity are …
- Elevated PVO2
- Tachyphylaxis to sodium nitroprusside
- metabolic acidosis
Antidote for cyanide poison
Amyl nitrate
Converts Hb to MetHb which binds to cyanide and converting it to nontoxic cyanomethemoglobin
Anti thrombotic 2 classes are
Anti platelets (prevent platelet activation/aggregation)
Anticoagulants (reduce fibrin formation)
Anti platelets (which they prevent platelet activation/aggregation) are …
Anti platelets (prevent platelet activation/aggregation)
- ASA (irreversibly inhibit cyclooxygenase)
- ADP receptor inhibitors (clopidogrel, prasugrel, ticlopidine, ticagrelor)
- phosphodiestrase inhibitors (cilostazol)
- G2b-3a inhibitors (abciximab, eptifibatide, tirofiban)
Anticoagulants (which they reduce fibrin formation) are …
Anticoagulants (reduce fibrin formation)
- AT3 inhibitors (heparin, LMWH)
- heparin-like factor 10 inhibitors (fondaprinux)
- direct factor 10 inhibitors (rivaroxaban,apixaban)
- direct thrombin inhibitors (bivalirudin, hirudin, argatroban, dabigatran)
- Vit K antagonist (warfarin)
Diuretics that causes hyperchloremic metabolic acidosis?
Acetazolamide and K-sparing
There is no Diuretics that causes hypo-chloremic
Diuretics that causes hypochloremic metabolic acidosis ?
Loop + Thiazides
Contraction alkalosis occur due to a decrease in the extracellular volume around a constant extracellular HCO3. This combined with increased urinary H+ loss result into alkalosis
In Rx acute hyperkalemia, what are the driving K intercellular choices?
B-agonists
Insulin+D50
Bicarbonate
Hyperventilation (decreasing plasma CO2 leads to left shift of bicarb buffer system which lowers extracellular H+ and therefore shifts K into cell to maintain electrical neutrality).
Enzyme polymorphism and its associated anesthetic medication effect
CYP(2D6)
CYP(3A4)
MC1R
CYP(C19)
CYP(2C9)
(2D6) -> codeine, BB, anti arrhythmic, diltiqzem, tramadol
(3A4) -> most anesthetics, lidocaine, precedex
MC1R -> associated with red hair, leads to increase analgesia
(C19) -> PPI, antidepressants
(2C9) -> phenytoin, warfarin, ibuprofen
At what plasma levels of Mg causes ECG changes? What they are?
6-12 mgdL
Par prolongation + wide QRS (these changes occur before loss of deep tendon reflexes)
Associated with pain on injection?
Diazepam (not versed) Etomidate Methohexital Propfol Rocuronium
The mechanism is not entirely clear but studies point towards increase pain scale with; rapid injection, increase similar concentration of agent, or agents with either very high or low pH (propofol is thought due to release of bradykinin and not due to pH)
Chemistry derangements with thiazides
Hypo K, Mg, Na
Hyper Ca, urecemia, glycemia,
Increased TG, cholesterol, LDL production
MoA of
Thiazides
Furosemide
Spironolactone
Blocks Na/Cl at DCT
Blocks Na/K/Cl in loop of henle
Blocks aldo receptors in DCT
Large amount of licorice (عرق السوس) induces hyper aldosterone like effect through…
Inhibiting 11-beta-hydroxysteroid dehydrogenase which an enzyme converts cortisol to cortisone. Therefore large amount of cortisone act like aldosterone causing all symptoms of Conn syndrome.
Mydriatic drug that can cause anticholinergic toxicity?
Cyclopentolate
It’s used for ocular procedures and systemic absorption can cause (dysarthria, Tachy, disorientation, psychotic rxn, and convulsion)
It’s more common with use of 2% solution then 1% mixture
Drug used in treatment of glaucoma that can cause sever bronchospasm and bradycardia if systemic absorption occurs?
And other glaucoma treatment drug that can prolong Succinylcholine activity?
Timolol (nonselective BB)
Echothiophate (inhibits plasma butyrylcholinesterase which is called paudocholinesterase, the enzyme responsible for succinylcholine metabolism)
When to consider metoclopramide to prevent PONV or aspiration risk? And what’s its contraindication to use?
Diabetic patients undergoing outpatient procedures
First trimester in urgent situations (it counteract the effect of pregnancy progesterone mediated relaxation of LES)
Trauma patients
CI in bowel obstruction
Metoclopramide is a
Dopamine….
Seretonin …. at higher doses
Cholinergic … which enhances response of … in GI tissue
Dopamine antagonist
Seretonin antagonist
Cholenergic Agonist, enhances response to ACho (results in accelerated gastric emptying, decrease gastric fluid volume, increases LES tone, increase gastric contraction, and enhances peristalsis in duodenum and jejunum)
It has no effect on gastric pH
Glucagon MoA
Increases intracellular cAMP which results in increased intropy and chronotropy
Useful in treatment of BB toxicity because it dose not utilize alpha or beta adrenergic receptors
Medications/drug class causes hyperkalemia
Digitalis Heparin Mannitol Nonselective β-antagonists Pentamidine NSAIDs Succinylcholine Potassium-sparing diuretics Triamterene Trimethoprim
LMWH exerts its anticoagulation effect by inactivation of …
The …. is the best test to document the adequacy of anticoagulation with LMWH.
inactivation of factor Xa.
anti-Xa assay
St. John’s wort is an herbal medication that is taken by patients to treat depression. St. John’s wort induces P540 …
P450 3A4. This induction causes many anesthetic-related drugs to be metabolized including alfentanil and midazolam.
Name the four potassium sparing diuretics? their MoA?
Amiloride, triamterene, spironolactone, and eplerenone.
They work by blocking sodium reabsorption in the cortical collecting tubule and simultaneously increasing potassium reabsorption.
How mannitol can exert a renal protective effect?
Mannitol draws fluid into the renal tubule, which allows for continued patency and flushing of debris from the tubule. Accordingly, mannitol can exert a renal protective effect. In addition, mannitol transiently creates an osmotic gradient within the vasculature and can maintain circulating plasma volume and renal perfusion via this effect, further eliciting protective properties.
What is the contraindication for mannitol? whats alternative?
Mannitol is relatively contraindicated in patients with congestive heart failure (CHF) due to an initial increase in intravascular volume. Furosemide is the drug of choice when diuresis is recommended in this class of patients.
Difference mechanism of diuresis between Mannitol and ANP?
(ANP) induces diuresis via natriuresis,
Mannitol induces diuresis; not via an osmotic effect.
Medications that use cGMP as a second messenger
nitroglycerin, sodium nitroprusside, nitric oxide, and sildenafil.
Insulin and glucagon receptors use … as a second messenger
cAMP
NMDA receptor antagonists include, but are not limited to,
dextromethorphan, ketamine, memantine, methadone, nitrous oxide, and tramadol.
The NMDA receptor is an inotropic glutamate receptor that functions as a nonspecific ion channel when activated. Activation only occurs when … is bound to the receptor AND the cell is depolarized. The receptor’s effects are primarily mediated via increased intracellular …
glutamate and glycine
calcium
Antihistamine vs Antiacids vs PPI in their onset when given to decrease aspiration risk?
Cimetidine, ranitidine, and famotidine are common H2 blockers that are used to increase gastric pH. Additionally, they can reduce gastric volumes (except for ranitidine). When given orally these medications have an onset of action of approximately 1 hour. The pH raising effects of ranitidine are longer than those of cimetidine. Ranitidine lasts for 9 hours following administration. Intravenous cimetidine and famotidine typically work in under 30 minutes, but are not faster than oral antacid medications. Ranitidine in particular has an approximately 1 hour onset time for both IV and PO administration.
Antacids have a near immediate onset taking effect within 15-30 minutes of oral administration. Antacids work by neutralizing acid in the stomach. However, antacids may increase gastric volume and slow gastric emptying.
Proton pump inhibitors take 2-4 hours to initial effect when administered orally. Peak response may take up to 5 days. Proton pump inhibitors (PPI) act by binding to hydrogen potassium pumps. PPIs cause a permanent inhibition of proton pumps. Synthesis of new pumps takes about 24 hours, which explains the duration of action of PPI medications.
Amiodarone’s primary effect is … and itd clinical use for …
blockade of potassium channels. It also blocks calcium and sodium channels to a lesser effect as well as α- and β-adrenergic receptors.
refractory ventricular arrhythmias, sustained SVT with accessory pathway conduction, and atrial fibrillation/flutter/tachycardia with congestive heart failure (CHF). Recall that amiodarone is still the antiarrhythmic agent of choice in the setting of CHF or low ejection fraction.
The most common SE of Amiodarone?
bradycardia and hypotension, which occur in approximately 5 to 10% of the population. Risk factors include age >60 and higher dose therapy.
Others; hypothyroidism (20% of patients), life-threatening hyperthyroid storm, pulmonary toxicity (with a pulmonary fibrosis appearance), prolonged QT, and elevated liver function tests (LFTs). Pulmonary toxicity is one of the most lethal side effects of amiodarone therapy. It is dependent on cumulative dosage and may appear up to 45 days following discontinuation of the drug.
