Plateau effect

Takes 4-5 half lifes for a medication to reach plateau effect.

Cryoprecipitate

• A frozen blood product prepared from plasma
• Each 15 mL unit typically contains 100 IU of factor VIII, 250 mg of fibrinogen, as well as von Willebrand factor (vWF) and factor XIII.
• Used commonly for DIC to keep fibrinogen levels > 1.0.
• 1 unit of cryo per 5kg patient weight will increase fibrinogen by about 100 mg/dL. Therefore number of bags = 0.2 x weight (kg) to provide about 100mg/dL fibrinogen.
• Many institutions use a standard dose of 10 units and then repeat if needed.

References

• http://en.wikipedia.org/wiki/Cryoprecipitate
• http://reference.medscape.com/drug/cryo-cryoprecipitate-999498
• http://www.transfusion.com.au/sites/default/files/iTRANSFUSE%202.2%20CRYO.pdf
• http://www.perthhaematology.com.au/cryo.ht

Sedation tips

• Don't use midazolam and olanzapine together as it can cause rapid onset respiratory depression. Clonazepam and olanzipine is a better combination.
• Chlorpromazine is also good. Non-addictive, and comes as a liquid.
  

HRT & progesterone

If you're prescribing HRT to someone, you should also be prescribing progesterone at the same time in the same way that you give laxatives to people on morphine.

(I don't know why - work this out at some stage)

SAAB drugs for use in acute coronary syndrome

• Statin
• Ace inhibitor
• Aspirin
• Beta blocker

Calcium channel blockers

Mechanism of action

Calcium channel blockers have a negative inotropic effect - they decrease the force of contraction of the myocardium.

They block L-type voltage gated calcium channels in the heart and blood vessels. This prevents calcium levels from increasing as much in the cells when stimulated, leading to less contraction.

They also decrease total peripheral resistance by dilating the blood vessels, and decreasing cardiac output by lowering the force of contraction. Because resistance and output drop, so does blood pressure. With low blood pressure, the heart does not have to work as hard; this can ease problems with cardiomyopathy and coronary disease.

Unlike with beta-blockers, the heart is still responsive to sympathetic nervous system stimulation, so blood pressure can be maintained more effectively.

Many calcium channel blockers also slow down the conduction of electrical activity within the heart by blocking the calcium channel during the plateau phase of the action potential of the heart. This causes a lowering of the heart rate and may cause heart blocks (negative chronotropic effect) of calcium channel blockers.

Classes

There are 2 classes of CCBs:

1. Dihydropyridines
   
   
   • Used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina because the vasodilation and hypotension can lead to reflex tachycardia.
     
   • This CCB class is easily identified by the suffix "-pine" e.g. Amlodepine, Felodipine.


2. Non-dihydropyridines
   
   
   
   • Relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina.
     
   • They have minimal vasodilatory effects compared with dihydropyridines.
     
   • Action is intracellular.
   • E.g. verapamil.
     

Indications

• Atrial fibrillation or flutter - to control heart rate via negative chronotropic effect.

Contraindications

• Avoided (or used with caution) in individuals with cardiomyopathy due to negative inotropic effect.
• Non-dihydropyridine CCBs should not be combined with beta-blockers because they are both negative inotropes and affect the AV node.
  

References:

• Wikpedia, http://en.wikipedia.org/wiki/Calcium_channel_blocker
  

Nilstat

Actions

Anti-fungal.

Indications

Treatment of candida.

References:

• AMH
  

Geris tutorial with the Prof

The acute geriatric admission

Principle 1 - Atypical presentation

Geriatric giants:

• Confusion
• Falls
• Incontinence
• Failure to cope

The reasons that the geriatric syndrome exists and that older people don't present with simple complaints the way younger people would is due to a combination of their underlying medical conditions as well as decreased reserve from multi-system failure and inability to compensate.

Principle 2 - Comorbidity

• Multiple Dxes and complex issues in Dx and management plan.
• Drugs and bugs - common precipitants of acute hospitalisation.

Principle 3 - Complications of immobility

Seven sins of immobilisation:

1. pressure sores
2. constipation and urosepsis
3. deconditioning
4. depression
5. malnutrition
6. venous thrombosis
7. bronchopneumonia
   

Prinicple 4 - Function

• Level of function and independence.
• Discharge planning on admission.

Rules of prescribing

• Rule of halves (impaired drug clearance, increased adverse effects)
• Rule of fives (polypharmacy)
• Medication untrial (adverse drug reactions)
• Medication trial (careful medical management)

Falls

• Syncope (Stokes Adams, postural hypotension, aortic stenosis, cerebrovascular disease, epilepsy, diabetic hypoglycaemia SPACED)
• Acute - drugs and bugs etc
• Chronic - 4 causes: drugs and disorders of eyes, cognition and gait

Incontinence

• Post void residual for retention (obstruction or neurological disorder)
• 5 causes: drugs, UTI, atrophic vaginitis, faecal impaction, prostate

Delirium

• Acute and fluctuating, inattention, altered LOC
• Reversible causes (drugs and bugs etc)

Marcain

Composition

Bupivacaine hydrochloride +/- Adrenaline

Actions

Bupivacaine is classed as a membrane stabilising agent and is a local anaesthetic of the amide type. Like all amines it causes a reversible blockade of impulse propagation along nerve fibres by preventing the inward movement of sodium ions through the nerve membrane.

Pharmacokinetics

Bupivacaine is a long acting, amide type local anaesthetic chemically related to lignocaine and mepivacaine. It is approximately four times as potent as lignocaine.

References:

• MIMS
  

Indomethacin

Drug class

NSAID

Action

Potent inhibitor of prostaglandin synthesis. Affords relief of symptoms but does not alter the progressive course of the underlying disease.

Uses

Arthritis and related inflammatory disorders; low back pain; postop bone pain; primary dysmenorrhoea, IBD.

Contraindications

NSAID sensitive asthma; active peptic ulcer, recurrent GI ulceration; pregnancy, lactation

Sold as

Athrexin

Arterial vs venous clots

Arterial clots

Arteries are thick blood vessels with fast flowing blood. Blood clots in arteries are typically triggered by underlying arteriosclerosis (roughening of the artery wall). Blood platelets get stuck to the roughened blood vessel wall and form a clot. Thus, the medication of choice in trying to prevent thrombosis in arteries are medications that act against platelets. The following medications are anti-platelet drugs:

• Aspirin (= ASA)
• Plavix (= Clopidogrel)
• Ticlid (= Ticlopidine)
• Aggrenox (= aspirin plus dipyridamole)

By interfering with platelet function, these drugs increase the patient's risk of bleeding, even though to a lesser degree than coumadin. The INR is not influenced by these drugs and vitamin K intake does not influence their effect.

Venous clots

Veins are thin blood vessels with slow flowing blood. Blood clots that form in veins (DVT, pulmonary embolism) are mainly made up of clotting proteins; platelets do not play a big role in venous clots. Warfarin is an effective anticoagulant by preventing the production of clotting factors in the liver, increasing the INR. It is therefore the drug of choice in venous thrombosis. Anti-platelet drugs do not play much of a role in preventing venous clots.

Occasionally, clots in arteries originate from one of the two left heart chambers and travel from there with the blood stream to the brain, the retina, or the extremities. This typically happens in atrial fibrillation. Such a clot is an arterial embolism that resembles the type of clots seen in veins i.e. they have little platelet participation. They are therefore best treated with warfarin, not with anti-platelet drugs, even though they are clots in arteries.

References:

• Thrombophilia Support page
  

INR & warfarin

If a patient's INR is > 3 (normal 0.8-1.2) then stop warfarin for a few days rather than reversing it with Vit K/FFPs.

Neostigmine methylsulfate

Actions

• An anticholinesterase agent which reversibly inhibits the hydrolysis of acetylcholine by competing with acetylcholine for attachment to acetylcholinesterase. As a result, acetylcholine accumulates at cholinergic synapses and its effects are prolonged and exaggerated.
  
• Produces a generalised cholinergic response, including miosis, increased tonus of intestinal and skeletal musculature, constriction of bronchi and ureters, bradycardia and stimulation of salivary and sweat glands.
  
• Used mainly for its direct cholinomimetic effect on skeletal muscle and to a lesser extent to increase the activity of smooth muscle.
• Because of its quaternary ammonium structure, neostigmine in moderate doses, does not cross the BBB to produce CNS effects. Extremely high doses, however, produce CNS stimulation followed by CNS depression.

Indications

• Reversal of the effects of neuromuscular blocking agents (e.g. tubocurarine, pancuronium).
  
• Prophylaxis and treatment of postoperative intestinal atony and urinary retention.
  
• Treatment of myasthenia gravis during acute exacerbations, when the condition is severe, or in neonates.

Pharmacokinetics

• For IV administration the elimination half-life is 47-60 minutes.
• For IM administration the elimination half-life is 50-91 minutes.
  
• Approximately 80% of a single IM dose of neostigmine is excreted in the urine in 24 hours, about 50% as unchanged drug and the remainder as metabolites.
  
• The major site of uptake is in the liver. It is metabolised partly by the hydrolysis of the ester linkage and partly by microsomal enzymes in the liver.