Monoamine Oxidase Inhibitor Side Effects
Monoamine Oxidase Inhibitors (MOA) are a class of antidepressants that includes Isocarboxazide (Marplan), Phenelzine (Nardil), Tranylcypromine (Parnate), and Selegiline (Emsam).
MAO inhibitors are prone to drug interactions that inhibit its breakdown and could lead to hypertensive crisis, serotonin syndrome, or increased psychosis.
⭐ Patients taking MAO inhibitors must avoid tyramine-rich foods, including aged cheese, pickled herring, yeast extract, air-dried meats, sauerkraut, soy sauce, fava beans, and some red wines and beers as it can precipitate hypertensive crisis. Foods can become high in tyramine when they have been aged, fermented, pickled, or smoked.
Morphine Side Effects
💊 Morphine is considered the classic opioid analgesic with which other painkillers are compared. Like other medications in this class, morphine has an affinity for delta, kappa, and mu-opioid receptors.
💊 This drug produces the majority of its analgesic effects by binding to the mu-opioid receptor within the central nervous system (CNS) and the peripheral nervous system (PNS).
💊 Morphine can potentially be a lethal medication when not used properly. It causes a host of symptoms related to depression of the CNS. Severe respiratory depression is the most feared complication of morphine in cases of overdose. Immediate injection of naloxone is required to reverse the effects of morphine.
Phenytoin Side Effects
Phenytoin has a narrow therapeutic window (10-20 mg/L) and requires serum drug monitoring to prevent toxicities. Check out this awesome mnemonic on how to remember its side effects!
SNRI Side Effects
Serotonin and norepinephrine reuptake inhibitors (SNRIs) are a class of antidepressants that work by blocking serotonin and norepinephrine reuptake in the synapse (as the name suggests).
🗒️ It is important to educate patients that there is an increased risk of suicidal thinking and behavior in children, adolescents, and young adults during the first few months of therapy and it may take up to 8 weeks before therapeutic effects are recognized.
SSRIs Side Effects
💊 Selective serotonin reuptake inhibitors (SSRIs) work by inhibiting 5-HT reuptake by the presynaptic cleft, thus increasing serotonin levels in the synapse. It is commonly used to treat depression, a condition thought to be linked to low levels of serotonin, dopamine, and norepinephrine.
⭐ As you can see, this mnemonic is similar to the mnemonic on the side effects of SNRIs. Since they both block serotonin reuptake, they exhibit very similar side effect profiles except SNRIs can also impact blood pressure (increase or decrease) due to the norepinephrine reuptake inhibition. SSRIs do not affect blood pressure.
In addition, SSRIs can cause weight gain in adults on long-term therapy, while SNRIs cause less of this long-term weight gain and are more associated with weight loss.
Statin Side Effects
Statins are the drugs of choice in treating increases in non-HDL and LDL cholesterol, as they have shown a reduction in cardiovascular disease and mortality.
Statins inhibit the enzyme HMG-CoA reductase, which prevents the conversion of HMG-CoA to mevalonate. This is the rate-limiting step in cholesterol synthesis.
Tricyclic Antidepressant (TCAs) Side Effects
Tricyclic antidepressants (TCAs) are drugs used to treat depression, bipolar disorder, and other conditions such as chronic pain and insomnia. They primarily work by blocking norepinephrine and serotonin (5HT2) reuptake. They also block acetylcholine and histamine receptors which contribute to their side effect profile.
👉🏻 Muscarinic M1 block: anticholinergic side effects including dry mouth, blurry vision, constipation, and urinary retention
👉🏻 Histamine 1 receptor block: sedation and weight gain
👉🏻 Adrenergic alpha block: postural hypotension, tachycardia, and erectile disfunction
👉🏻 Sodium channel block: QTc prolongation, arrhythmias
👉🏻 Serotonin uptake block: weight gain
Valproate Side Effects
💊 Valproic acid is used in seizures, bipolar disorder, and migraine prophylaxis. It works by increasing the availability of gamma (y)-aminobutyric acid (GABA), an inhibitory neurotransmitter.
🖇️ Divalproex sodium is a compound of sodium valproate and valproic acid. Divalproex dissociates to valproate in the GI tract.
🖇️ Use special caution with the combination of valproic acid and lamotrigine due to the risk of serious rash called Stevens-Johnson Syndrome.
Warfarin Factor Half-Lives
Warfarin is an oral anticoagulant most frequently used to control and prevent thromboembolic events. ACCP recommends that patients newly started on warfarin be bridged with LMWH or unfractionated heparin for 5 days AND until therapeutic INR is achieved.
🌟High-yield fact🌟 The presence of a therapeutic INR does not confer protection from clot formation and expansion during the first few days of warfarin therapy, so if your patient’s INR is 2.0 on day 3, it is recommended to continue bridging until day 5.
This recommendation is based on the fact that the anticoagulant activity of warfarin depends on the clearance of functional clotting factors already present in the body.
Warfarin works by inhibiting new clotting factors from forming but requires that the old factors be cleared from the body. The clearance of these clotting factors is determined by their half-lives. The earliest changes in the International Normalized Ratio (INR) are typically noted 24 to 36 hours after a dose of warfarin is administered. These changes are due to the clearance of functional factor VII, which is the vitamin K–dependent clotting factor with the shortest half-life (6 hours: after 3-5 half-lives or 24-36 hours it will be eliminated from the body). The factor with the longest half-life, prothrombin or factor II, will take 5 days to clear from the body, hence why we need to bridge for at least 5 days AND until therapeutic INR is achieved.
This is a high-yield question that is often asked on exams and clinical rotations. This mnemonic helps you remember which vitamin K-dependent factors warfarin affects.
Warfarin, brand name Coumadin, is an anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent clotting factors, which include Factors II, VII, IX, and X, and the anticoagulant proteins C and S.