Serotonin Syndrome

Serotonin syndrome is a serious and life-threatening reaction caused by excess serotonin in the CNS.

The classic triad

  1. Mental status changes (anxiety, restlessness, delirium, easy to startle)
  2. Autonomic hyperactivity (hyperthermia, hypertension, tachycardia, diaphoresis, vomiting, diarrhea)
  3. Neuromuscular abnormalities (hyperreflexia, myoclonus, tremor, muscle rigidity, and bilateral Babinski sign) – more pronounced in lower extremities
Serotonin Syndrome Neuroleptic Malignant Syndrome
Onset <24 H Days to weeks (not
Neuromuscular Hyperreactivity (tremor, clonus) Severe muscle rigidity, hyporeactivity (bradyreflexia)
Cause SSRIs, TCAs, MAOIs, other serotonergic drugs Dopamine antagonists (antipsychotics)
Lab findings None Elevated CK
Treatment STOP AGENT! Benzodiazepines +/- Propranolol STOP AGENT! + Bromocriptine +/- Dantrolene
Resolution Within 24h Days to week



Anticholinergic Mnemonic

The way to remember the effects of anticholinergic medications is using the mnemonic Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter.

  • Hot as a hare: increased body temperature
  • Blind as a bat: mydriasis (dilated pupils)
  • Dry as a bone: dry mouth, dry eyes, decreased sweat
  • Red as a beet: flushed face
  • Mad as a hatter: delirium

Common anticholinergic medications are dimenhydrinate (Gravol) and low-potency antipsychotics, benztropine, atropine and antihistamines.

Don’t forget about the other toxidromes!





A toxidrome is a syndrome (set of symptoms) caused by specific medications or toxins.

There are 5 big ones to know:

  1. Anticholinergic: low potency antipsychotics, oxybutynin, ACh receptor antagonists (ipratropium, atropine, scopolamine)
  2. Cholinergic: ACh recptor agonists (pilocarpine), AChEIs (organophosphates, phyostigmine)
  3. Opioid: Morphine, heroin, hydromorphone, etc
  4. Sympathomimetic: epinephrine, cocaine, amphetamine (Aderol), methylphenidate (Ritalin)
  5. Sedative-Hypnotic: Benzodiazepines, barbituates, “Z-drugs” (zopiclone, zolpidem), antihistamines

Alcohol and Benzodiazepine Withdrawal

The thing to remember with both alcohol and benzodiazepine withdrawal is that THEY CAN KILL YOU!

What to watch out for

Withdrawal seizures and alcoholic hallucinosis (hallucinations that develop within 12 – 24 h and resolve within 24 – 48 h)

Delirium Tremens (DTs): hallucinations, disorientation, tachycardia, hypertension, fever, agitation, and diaphoresis. Symptoms can persist for up to 7d

Wernicke’s Encephalopathy: Happens in hours to days, it has a classic triad

  1. Encephalopathy: profound disorientation, indifference and inattentiveness
  2. Oculomotor dysfunction: nystagmus, lateral rectus palsy, conjugate gaze palsies (affecting the CN III, VI and VIII nuclei)
  3. Gait ataxia: affecting the vermis of the cerebellum

How it works

Since alcohol and benzodiazepines both work on the GABA receptor (potentiating the effect of GABA by increasing the frequency of channel opening) they are cross-reactive. This means that you can treat alcohol withdrawal with a tapering dose of benzos (and you can treat benzo withdrawal also with a tapering dose of more benzos).

The thing to watch out for with someone who has chronically used benzodiazepines and has suddenly stopped is that the onset of symptoms will depend on the half-life of that particular drug.

  • Alprazolam (Xanax): 10 – 20 h
  • Lorazepam (Ativan): 10 – 25 h
  • Clonazepam (Rivotril): 20 – 50 h
  • Diazepam (Valium): 30 – 200 h

To minimize benzodiazepine withdrawal symptoms if someone has extended use (>3 months): taper by 1-20% over 6 or more weeks and/or switch to longer-acting agents.


Dopamine Pathways in the Brain (and schizophrenia)

There are 4 main dopamine pathways in the brain:

  1. Nigro-Striatal: substantial nigra to basal ganglia, involved in movement (what gets affected to cause EPS: tardive dyskinesia, akatisia)
  2. Meso-Limbic: VTA to nucleus accumbens, “reward” pathway (causes the positive symptoms of schizophrenia)
  3. Meso-Cortical: VTA to cortex, motivation and emotional response (thought to cause the negative symptoms of schizophrenia)
  4. Tubulo-Infundibular: hypothalamus to posterior pituitary (hypoprolactinemia in untreated individuals, but D2 blockade with antipsychotics can cause a hyperprolactenemia)


Antipsychotic medication can be divided into 2 classes

  1. Typical/First Generation
  2. Atypical/Second Generation

Typicals are characterized by strong D2 antagonism in the mess-limbic and meso-cortical pathways. This can also lead to significant extrapyramidal symptoms (EPS). They also have strong CYP-450 metabolism (which means lots of interactions with other drugs and grapefruits).

  • High-potency typicals: only slightly anticholinergic & minimally sedating but have more weight gain and a higher risk of EPS
  • Low-potency typicals: more quite sedating and more anticholinergic (bradycardia, GI upset) but have a lower risk of EPS

Atypicals have less risk for EPS, but carry a higher risk for metabolic side-effects and weight gain. While they bind to D2 receptors (like typicals), atypicals have higher affinity for serotonin (5HT) receptors.

Clozapine is a little different from the other atypicals in that is has been shown to have a shorter half-life, which is thought to be why it doesn’t produce as many EPS. However it has the very specific (and serious) risk of agranulocytosis.

Bacteria involved in bite wounds

With bites you need to consider not only the ton of different bacteria inhabiting the mouth of whatever/whoever was the biter, but also the flora of whatever part of the body was bitten. Mouths tend to be a schmogourbord of Gram positives and negative, aerobes and anaerobes. The two bugs to specifically keep in mind when thinking about bites are Eikenella in human bites and Pasturella in animal bites (especially cat bites).

Amox-clav is a fairly good choice for bites (of both the human and animal variety) but you need to remember that if the bite if say, on the ear, you’ll also need coverage for pseudomonas. To make matters a little more confusing Eikenella is resistant to clindamycin, macrolides, metronidazole, and fluoroquinolones. So if the bitten person is allergic to penicillins, clindamycin just won’t do.

Where diuretics work in the nephron

The nephron is composed of distinct areas that are specific to regulating different electrolytes.

An overview of nephron anatomy

Loop diuretics: blocks the sodium/potassium/chloride transporter in the ascending loop of Henle, potassium-wasting
Thiazide diuretics: blocks the sodium/chloride transporter in the distal tubule, potassium-wasting
Amiloride: directly blocks sodium channels in the collecting duct, potassium-sparing
Spironolactone: blocks the aldosterone receptors in the cortical collecting duct. This causes a decrease in sodium and water reabsorption and decreases potassium secreting (therefore is potassium-sparing)

Determinants of Glomerular Filtration Rate (GFR)

GFR should be ~100 mL/min

Calculating GFR
(140 – age) x lean body weight (kg) / sCr (umol/L)

What determines GFR

  1. Renal blood flow: effective circulating volume, cardiac output
  2. Resistance to flow: vascular tone of afferent and efferent arterioles
  3. Permeability of glomerular basement membrane

Drugs that increase GFR

  • Prostaglandin: vasodilator (afferent > efferent)
  • Angiotensin II: vasoconstrictor (efferent > afferent)
  • Norepinephrine: vasoconstrictor, increases blood pressure
  • ANP: afferent vasodilator, efferent vasoconstrictor

Drugs that decrease GFR

  • NSAIDs: afferent vasoconstriction
  • ACE Inhibitors: decrease efferent vasoconstriction
  • Angiotensin Receptor Blockers (ARBs): decrease efferent vasoconstriction

Insulin Regimens and Dosing

Insulin dosing has to be one of the most (seemingly) unnecessarily complicated dosings in medicine. Not only are there 4 ways to dose it (BID, QID with rapid, QID with fast, QID with extended-release) there are three different companies, all naming their insulins slightly differently. But how can you remember whether to give Humalog, Humulin N, Humulin R, NovoRapid, Novolin Toronto, NPH, Lantus, or some combination of the above?

This is a master illustration to help organize insulin dosing and amounts.

Total Daily Dose

0.3 – 0.6 units/kg
Start low, titrate up

BID (conventional therapy)

2/3 : 1/3 rule
2/3 breakfast : 1/3 supper
2/3 long : 1/3 fast

QID (with either Rapid or Fast-acting and either long or extended)

Breakfast: 20-25% long, 15-20% rapid
Lunch: 15-20% rapid
Supper: 15-20% rapid
Bedtime: 25-30% long

Antibiotic classes and mechanism

These are the different classes of medications and their mechanism of action. I’ve sorted them by which ones are exclusively Gram + or Gram – and which ones do both.

Here’s a handy mnemonic for remembering the antibiotics that act on the ribosomes (I find they’re the most confusing to remember):

Buy AT 30

CELL for 50