Pharmacology Flashcards

1
Q

define volume of distribution

A

D (total drug in body (mg)) divided by c (plasma concentration (mg/L)) unit would be litres.

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2
Q

Pharmacodynamics

A

What the drug does to the body. relates to the study of a drugs effect and mechanism within the body

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3
Q

what is a “therapeutic dose”

A

the amount/dose of drug required to produce desired change in their disease or condition.

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4
Q

describe the mode of action “absorption/administration”

A

absorption= the movement of the drug from the site of administration to the blood stream. (Passive absorption, facilitated absorption, active transport, pinocytosis)

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5
Q

define tachyphylaxis

A

an acute, rapid, sudden, decrease in response to a drug after its administration, rendering it less effective.

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6
Q

define “half life”

A

is the time it takes the body to reduce the amount of drug in the plasma by half.

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7
Q

intropes

A

Inotropes increase the contractility of the heart.

Inotropes increase CO, thereby increasing MAP and maintaining perfusion to vital organs and tissues. Inotropes increase CO by increasing both SV and HR.

noradrenaline
adrenaline
ephedrine

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8
Q

describe the mode of action “metabolism”

A

metabolism= the process of transformation of the drug within the body to take it from being lipophilic to more hydrophilic so that it can be excreted from the body by the kidneys.

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9
Q

spinals related to cardiac effects

A

blocks the nerves in the thoraco-lumbar region (sympathetic) resulting in blocking sympathetic reflexes and parasympathetic takes over decreasing the blood pressure.

(total spinal= respiratory muscle paralysis, respiratory depression, apneic, cardiac arrest).

management of total spinal= intubation/establish patent airway, why? Because of total spinal affecting respiratory muscle function and subsequent loss of spontaneous breathing

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10
Q

propofol

A

Painful on injection, decreases cardiovascular system, respiratory depressant, alters EEG monitoring (epileptic movement), short acting, induction and sedation agent. • CNS
o Excitatory movement upon induction
o Euphoria at low doses -> abuse potential
CVS
o Decreases BP
o Blunts baroreceptor reflexes
Resp
o Resp depression
o Blunted response to hypercarbia & hypoxia
o Hiccups
Anaphylaxis
Pain on injection- pH difference with blood
Propofol infusion syndrome- form of metabolic acidosis
Bacterial contamination

doses= 1.5-2.5mg/kg for induction. 20ml/200mg ampules.
1-1.5 mg/kg/min

pharmacokinetics = (ADME) IV adminitration. Works on GABA receptors. metabolised in the liver. excreted by kidneys in urine.

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11
Q

intralipid

A

bolus of 1.5mls/kg over 1 minute
Infusion of 15ml/kg/hr
IF CVS IS STILL UNSTABLE= repeat boluses unto 3 in total and 5 mins between and double infusion rate.
Do not exceed 12ml/kg
The theory states that highly lipid-soluble drugs, including local anaesthetics and non-local anaesthetic drugs, are absorbed into the lipid emulsion of the plasma and removed from tissues affected by toxicity. reversing cardiotoxic effects of local anaesthetics.

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12
Q

describe the parasympathetic nervous system

A

the parasympathetic nervous system refers to our “rest and digest” involuntary reflexes such as vasodilation, devrease in heart rate and contractility, constriction of bronchioles and constriction of pupils. the nerve fibers come from the cranial-sacral region and have longer per-ganglionic fibres and shorter post-ganglionic fibres. acetylcholine is the neurotransmitter released at both junctions. the pre-ganglionic junction is a nicotinic receptor and the post-ganglionic fibre is a muscarinic receptor (cholinergic).

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13
Q

adrenaline

A

a potent alpha and beta agonist. comes in amplues of either 1:1000 (1ml) or 1:10000 (10ml) and both contain 1 mg.
bolus dose for anaphylaxis in 100mcg (1 ml of 1:10,000).
bolus dose for cardiac arrest is 1mg.

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14
Q

atropine

A

increases heart rate.
Anti muscurinic, anti cholinergic antagonist that blocks the receptors of the parasympathetic fibres allowing the sympathetic system to take over and increase heart rate. Drys secretions (mouth) and blurred vision. Dose = 20mcg/kg bolus. 600mcg or 0.6mg in an ampule of 1ml

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15
Q

olol’s

A
labetalol = alpha and beta blocker
metopralol = beta blocker
esmalol = beta blocker
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16
Q

ketamine

A

induction agent. non-respiratory depressant and hardly any effect on the cardiovascular system. Increases intra cranial and ocular pressure. Analgesic agent. Hallucinations. Induction agent shocked patients (very low BP, hypovalemic). PCAs. Doses = 1mg/kg. IV (induction dose) 10-20mg/kg.

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17
Q

define “bio availability”

A

is the percentage of drug that is a absorbed

18
Q

describe the sympathetic nervous system

A

the sympathetic nervous system refers to our “fight or flight” involuntary reflexes such as vasoconstriction (alpha 1), increased heart rate and contractility (beta 1), dilatation on bronchioles (beta 2) and dilation of pupils. the nerve fibres come from the thoraco-lumbar region and have shorter pre-ganglionic fibres and longer post-ganglionic fibres. noradrenaline is the neurotransmitter released at the post ganglionic junction to stimulate the alpha and beta receptors (adrenergic). acetylcholine is released and the pre-ganglionic junction and is considered nicotinic.

19
Q

describe the mode of action “distribution”

A

distribution= the movement of drugs within the body

20
Q

Paracetamol

A

Paracetamol= analgesic and Anti pyretic. Weak anti inflammatory effect. inhibitor of the synthesis of prostaglandins. Side effects= paracetamol-induced liver intoxication from large doses. 15mg/kg 4-6 times a day

21
Q

volitile

A

Volatile anaesthetics exert their effects at multiple sites throughout the central nervous system.

It appears that volatile agents preferentially increase power of GABAA receptors and two-pore domain K+ channels

22
Q

midazolam

A

(benzodiazapam works at the gaba receptor). Comes in 5 mg/5 ml ampule. 1-2 mg IV bolus for sedation and amnesia. Oral = 0.5mg/kg. CNS depression and addiction from long term use.
reversed by flumazenal

23
Q

side effects vs adverse effects

A

Side effects= drug effect other than the therapeutic effect that is usually undesirable but not harmful.

Adverse effects – including allergic reactions= undesirable and potentially harmful drug effect other than the therapeutic effect.

24
Q

amiodarone

A

anti-arrhythmic. acts on the nodal cells in the myocardium to regulate fast rhythms and has little effect on the BP.

25
Q

suxamethonium

A

is a depolarising neuromuscular blockade and aggressive nicotinic agonist that works by attaching to the nicotinic receptor at the neuromuscular junction to create the depolarisation of the nerve (sodium channels open) causing the “twitching” of muscles, and then remains on the receptor and blocking it rendering it unable to receive acetylcholine for depolarisation and therefore causing neuromuscular blockade (muscle relaxation).
dose= 100mg/2ml ampules. 1-1.5 mg/kg intubation dose for adults. 1ml from the ampule (50mg) dilutes into 5ml makes 10mg/ml.

side effects = bradycardia, increased intracranial pressure, increased intraoccular pressure, rise in potassium esp. in patients with burns, crush injury, trauma, renal failure, MH trigger, high reaction rate, sux apneoa, muscle aches and pains

26
Q

Dantrolene

A

acts within skeletal muscle by acting as a receptor antagonist to the ryanodine receptor, to depress calcium ion release which reduces excitation-contraction coupling in skeletal muscle.

27
Q

non-depolarising Muscle relaxants

A

Rocuronium = .5 - 1 mg per kg for intubating dose. 50mg or above for RSI dose competitive non depolarising. At neuromuscular site, ACh normally produces electrical depolarization of the postjunctional membrane of motor end-plate, which leads to conduction of muscle action potential and subsequently induces skeletal muscle contraction. Rocuronium acts by competing for cholinergic receptors at the motor end-plate. Rocuronium acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur.

28
Q

meteraminol

A

potent alpha agonist

29
Q

salbutamol

A

selective beta 2 agonist. You still get tachycardia because its not pure (stimulates both beta 1 and 2). beta 2 dilates the brocheoles and beta 1 increased heart rate and contractility.

30
Q

neostigmine

A

anticholinesterase (prevents break down of acetylcholine (neuro transmitter). used to reverse muscle paralysis from non-depolarising muscle relaxant. inhibits the break down of acetylcholine at both the neuromuscular junction and the parasympathetic pathway resulting in bradycardia. often given with atropine, a anticholinergic and antimuscarinic antagonist which blocks the cholinergic receptors and allows the sympathetic pathway to increase the heart rate.

31
Q

define “first pass metabolism”

A

it is drug metabolism that occurs in the intestines and liver during oral absorption of drugs into the systemic circulation.

32
Q

antibiotics

A

Antibiotics fight bacterial infections either by killing bacteria or slowing and suspending its growth. They do this by: attacking the wall or coating surrounding bacteria. high anaphylaxis rate.

33
Q

ephidrine

A

alpha and beta agonist. comes in 30mg/1ml. diliuted into 10mls saline and bolus of 1mL increments= 3mg/1mL bolus

34
Q

define toxicity

A

refers to how harmful or poisonous a drug can be to a person. Drug toxicity occurs when the drug dose is too high or if the liver and/or kidneys fail to excrete the drug.

35
Q

phenylephrine

A

alpha agonist

36
Q

Opioids

A

pin point pupils, constipation, resp depression, disorientation, itching (intrathecal morphine), tolerance, urinary retention, risk of addiction, sedation, hallucinations, neausea and vomiting. works on the mew receptors.

Tramadol= acts on mu opioid receptor, blocking the neuron from communicating pain to the brain. Side effects= constipation, nausea and vomiting, respectively depression. You may have increased levels of serotonin (a hormone in your body). This can cause a condition called serotonin syndrome

37
Q

Pharmacokinetics

A

relates to the study of how a drug moves within the body commonly relating to the terms absorption/administration, distribution, metabolism and elimination (ADME)

38
Q

define multimodal

A

decrease the narcotic side effects by using multiple different pain relief to lessen the dose or narcotics.

39
Q

Local anaesthetics

A

Local anaesthetics = Local anaesthetics act by preventing the generation and transmission of impulses along nerve fibres and at nerve endings; depolarisation and ion exchange are inhibited. This is achieved by anesthetics reversibly binding to and inactivating sodium channels. Sodium influx through these channels is necessary for the depolarization of nerve cell membranes. When a nerve loses depolarization and capacity to propagate an impulse, the individual loses sensation in the area supplied by the nerve. Testing indicates that ropivacaine is comparable to (or slightly more potent than) bupivacaine in blocking sensory fibres and less active in blocking motor fibres (less on heart).

Lignocaine is short acting. With adrenaline 5-7mg/kg. Without = 3mg/kg
Ropivocaine is longer acting. 2.5 mg/kg
Bupivicaine longer acting

40
Q

define tolerance

A

the ability of the body to alter its response to drug affects so that the effects are minimised over time.

41
Q

describe the mode of action “elimination”

A

elimination= the removal of drugs from the body

42
Q

describe the central nervous system and peripheral nervous system

A

CNS contains the brain and the spinal cord and the PNS contains the cranial and spinal nerves and is the communication lines from the CNS to the body. the PNS is broken down into sensory (afferent) and motor (efferent) systems. The motor (efferent) pathway then gets broken down into autonomic (involuntary) and somatic (voluntary). the autonomic system then gets further divided into the sympathetic nervous system and the parasympathetic nervous system.