1. Gather all the pertinent information in order to understand a patient’s condition
2. Understand why certain diagnostic tests were performed and what were the results
3. Develop a relationship with other health professionals. We all work as a team in order to make the patient feel better.
4. Comprehensive Clinical Pharmacy Notes: Make them less wordy, create tables in order to show objective lab values and the trend associated with them
5. Digoxin dosing: Be cautious in elderly patients, better to go low and slow. Use IBW and not total body weight!
6. Keep your work-ups organized. It would be easier for another pharmacist covering for you or in case the patient gets transferred.
Attended a presentation on Delirium.
Delirium is not dementia. It is sudden change in usual behavior with:
Fluctuation: comes and goes in the course of a day
Inattention: easily distracted, difficulty focusing
Almost any medication or medical illness or change in environment can lead to delirium
Some causes: metabolic (hyponatremia, hypoglycemia, hypoxaemia)
Drugs: digoxin, lithium
CNS:opioids, benzodiazepines, anticholinergics, antihistamines, corticosteroids, anticonvulsants, alcohol, antidepressants, caffeine
CVS: clonidine, nifedipine, nitroprusside, beta-blockers, digoxin, antiarrhythmics, nicotine
GI: H2 blockers, metoclopramide
Antimicrobials: acyclovir, amphotericin B, cephalosporins, ciprofloxacin, septra
Antipsychotics: agent of choice. Literature supporting efficacy is limited. No benefit when used for prophylaxis.
Benzodiazepines: masks symptoms of delirium through sedation, does not treat delirium, increases its risk. Benefit is seen with acute agitation.
Haloperidol agent of choice, IV causes less EPS than oral form (pyridium metabolite)
Chlorpromazine: not recommended due to high anticholinergic activity, CSF conc. is 5X more than plasma, main role to control intractable hiccoughs
Methotrimeprazine: potential analgesic effect, causes sedation and lowers BP
Atypicals (olanzapine, risperidone, quetiapine equally effective to haloperidol)
Role of atypicals: used with underlying parkinsons disease, prolonged QT interval, when experiencing EPS
Calculating maintenance dose:
Add up first 24 hour dose requirement
Give 50% of this dose over the next 24 hrs in 4 divided doses e.g. Q6H
Reduce maintenance dose by 25% each day if symptoms remain controlled
Continue prn regimen as needed for breakthrough doses
Causes: Infection: UTI, pneumonia
Structural: Subarachnoid haemorrhage, urinary retention
Environmental: being in hospital or the ED
As health care professionals we can help by treating the cause of delirium: e.g. manage pain, fluids for hydration or review medications,
signs/symptoms: cough with yellow or green mucus, which may have traces of blood
sharp or stabbing chest pain made worse by deep breathing or coughing
fever with chills
rapid, shallow breathing
SOB. Other symptoms may include: headache, sweating, clammy skin, loss of appetite, feeling of weakness or fatigue, confusion
Hypophosphatemia causes: alcoholism, diarrhea, starvation, Vit D deficiency
Symptoms: bone pain, confusion, muscle weakness
Secondary prevention of stroke:
The GOLD Standard: ASA (ATTC 2009) NNT=125
ASA+ Dipyridamole SR (ESPS-2, ESPRIT) better than ASA, Ticlopidine (TASS)
Similar to ASA = Clopidogrel (CAPRIE), Warfarin (WARSS), Clopidogrel + ASA (MATCH, CHARISMA)
(Source: Loewen P Undergrad Lecture 3rd year Therapeutics)
The serum anion gap = Sum of serum chloride and bicarbonate concentrations subtracted from the serum sodium concentration.
Used in the detection and analysis of acid-base disorders, assessment of quality control in the chemical laboratory, and detection of such disorders as multiple myeloma, bromide intoxication, and lithium intoxication.
The normal value can vary widely, reflecting both differences in the methods that are used to measure its constituents and substantial interindividual variability.
Low values most commonly indicate laboratory error or hypoalbuminemia but can denote the presence of a paraproteinemia or intoxication with lithium, bromide, or iodide.
Elevated values most commonly indicate metabolic acidosis but can reflect laboratory error, metabolic alkalosis, hyperphosphatemia, or paraproteinemia. Metabolic acidosis can be divided into high anion and normal anion gap varieties, which can be present alone or concurrently.
Why is ACEI beneficial in heart failure, left ventricular dysfunction, acute MI, chronic kidney disease?
reduces aldosterone (which also facilitates collagen deposition and fibrosis)
Angiotensin II promotes VSMC (Vascular smooth muscle cell) growth and migration and glomerular hyperfiltration leading to microalbumin angioedema (nose, throat, larynx – airway obstruction may be fatal)
Renin release is increased by decrease in renal arterial pressure, decrease in sodium in the distal tubule.
alpha-1 blocker: vasoconstriction and increase in contractility
Verapamil and diltiazem: have a more cardiac depressant effect (cardiac arrhthmias and bradycardia)
Venous thromboses are mainly composed of RBC
Arterial ones are mainly composed of platelets
Virchow’s triad: Causes — Stasis, vascular injury, hypercoagulopathy
Drug related causes of VTE: Estrogens/progestins: Hormone replacement therapy, oral contraceptive therapy, SERMs (tamoxifen, raloxifen)
Initial treatment of DVT/PE:
IV UH or SC LMWH or SC fondaparinux or SC UH immediately
Give first dose of warfarin on same day
UH/LMWH: minimum 5 days
Continue until INR > or = 2 for at least 48 hours
Baseline INR, then daily or every 2 days until stabilized in therapeutic range
Baseline CBC, then daily or every 2-3 days while on UH/LMWH (bleeding, HIT)
LMWH associated with less HIT and osteoporosis
poor renal function: UH preferred
Fatal PE is the # 1 cause of maternal mortality worldwide in pregnancy. Risk 5X greater during postpartum period than during pregnancy.
UH, LMWH and warfarin are safe choice in a nursing mother
Approaches to angina drug therapy
antianginal: nitrates, b-blockers and CCBs
vascular protection: antiplatelet agents (ASA), ACEI, lipid lowering therapy
Statins: increased clearing of LDL, not much effect on HDL. promotes plaque stability, reduction in inflammation at site
Activity of key enzymes involved in cholesterol synthesis peaks between midnight and 2 am.
Statins decrease risk of major coronary events by 30%
Stroke by 20%
All cause mortality 12-15%
ACS management: Clopidogrel in addition to ASA for 1-12 months post ACS (duration of dual ASA and clopidogrel based on if coronary stents inserted and type of stent).
B-blocker use post-MI decrease morbidity and mortality