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Pharm Flashcards

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1
Q

Bioavailability (f)?

A

proportion of administered drug which reaches the systemic circulation.
Determined by extent of absorption and amount of drug that is subject to pre-systemic metabolism.
f = AUC oral/AUC IV

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2
Q

Dose rate = ?

A

Elimination (Clearance) rate

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3
Q

Plasma concentration of a drug at steady state = ?

A

Clearance (CL)

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4
Q

What is first pass metabolism?

A

The extent of metabolism occurring after the drug is absorbed but before it reaches the systemic circulation.
Many drugs undergo 1st pass met in liver/gut wall.

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5
Q

When does steady state occur?

What is the time to reach steady state dependent on?

A

When amount of drug administered is equal to the amount of drug eliminated in the same period = 4.5. half lives
Time to reach steady state is dependent on the half life of the drug.

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6
Q

Time to reach steady state is dependent on the dose. T/F

A

False.

Dependent on half life.

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7
Q

Formula for half life?

A

t1/2 = Vdx07/Cl

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8
Q

What is first order kinetics?

A

The same time is taken to remove half the drug independent of the dose e.g. 10 mg vs. 10 g

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9
Q

Formula for desired concentration (Css)

A

Css = maintenance dose rate/ CL

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10
Q

Why do we give a loading dose? Formula for loading dose?

A

Dose given with the aim of immediately achieving steady state concentrations (quicker therapeutic range).
Loading dose = [target concentration) x VD (L)

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11
Q

Formula for clearance

A

CL = Vd x 0.7 / t1/2

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12
Q

What is zero order elimination?

A

a constant amount of drug is eliminated per unit of time (linear line in opposite direction, [drug]/time) e.g. EtOH

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13
Q

What is saturable metabolism? Examples of drugs.

A 
Drug concentrations rise disproportionately (non linear) compared with dose. 
EtOH
Aspirin
Clonidine
Fluoxetine
Methotrexate
Paroxetine
Phenytoin
Verapamil
Propafenone
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14
Q

Clockwise hysteresis loop curve. What explains the concentration effect/response loop?

A

Rapid tolerance to a drug develops. Response for a given plasma concentration is initially high but decreases as the tolerance develops. E.g. cocaine, pseudoephedrine

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15
Q

Anti-clockwise hysteresis loop curve. What explains the concentration effect/response loop?

A

There is a delay in the distribution of the drug from plasma to its site of action

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16
Q

What is the extraction ratio (ER)? Examples of high extraction drugs vs. low?

A

The fraction of drug removed in a single pass the organ (liver/renal) of elimination.

ER = 1 - [concentration out/concentration in]

CL = ER x blood flow

Bioavailability = fraction absorbed x (1- ER)

Low extraction drugs:
Diazepam
Warfarin

High extraction:
morphine
bb
ccb
ergot alkaloids
nitrates
perhexiline
prazsin
tcas
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17
Q

In patients with liver disease, what is the higher concentrations and greater effects of drugs due to?

A

Increased bioavailability.

Bioavailability = fraction absorbed x (1-ER)

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18
Q

What physiological changes occur in the elderly causing impacts of hepatic drug metabolism?

A

Decrease in blood flow 20-50%
Marked fall in cyp P450 activities and drugs
Vd - decreased lean mass and increased body mass

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19
Q

What is potency?

A

Measure of drug activity expressed in terms of the amount required to produce an effect of given intensity.
Highly potent drug e.g. fentanyl, alprazolam evokes a larger response at low concentration.

It is the first curve on the graph to have an effect

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20
Q

The clearance of drugs that are weak acids or bases are affected by changes in urine pH. What happens to the clearance of the basic/acid drug if:
Urine made more acidic
Urine made more alkaline

A

Urine made more acidic:
Basic drug CL increased
Acidic drug CL decreased

Urine made more alkaline:
Basic drug CL decreased
Acidic drug CL increased

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21
Q

TCA toxicity:
Clinical
ECG
Tx

A 
Clinical:
Coma
Sedation
Hypotension - as alpha 1 receptors blocked
Seizures 
Dilated pupils
Tachycardia

ECG:
Monomorphic VT as Na channels in phase 0 of action potential is blocked
Prolonged QRS > 120 ms
RAD

Tx:
NAHCO3 1 mmol/kg
Aim is serum alkalinisation as it binds TCA and excretes

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22
Q

Anticholinergic (anti-muscarinic)toxicity: Drugs, Clinical, Ix, Tx?

A 
Pure Anticholinergics:
Atropine
Benztropine
Benzhexol
Anticholinergic plants e.g. Brugmansia sp
Angel's Trumpet

Drugs with anticholinergic effects:
TCA
Antihistamines
Anti-psychotics

Clinical:
Peripheral:
Dry mouth
Dry skin
Mydriasis
Tachycardia
Urinary retention
GI ileus (decreased bowel sounds)
Hyperthermia

Central: 
Hallucinations
Delirium
agitation
aggression
Sedation
Seizures

Tx:
Physostigmine 2 mg IV
Repeat if partial response
DO not use in drugs with partial anticholinergic effects 
AE: Seizures and arrhythmias
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23
Q

Cholinergic toxicity: Drugs, Clinical, Ix, Tx?

A

Acetylcholine esterase inhibitors e.g. donepezil, rivastigmine, neostigmine (MG), organophosphorous pesticides, chemical warfare nerve agents
Acetylcholine receptor agonists e.g. nicotine, mushrooms

Clinical:
CNS excitation - delirium, coma, seizures
Neuromuscular excitation - fasiculations, weakness and paralysis
Autonomic - salivation, lacrimation, diaphoresis, flushing, miosis
Resp - bronchorrhea, broncoconstriction
CVS- bradycardia, HT, arrhythmias
Metabolic - hypokalaemia, hyperglucaemia, metabolic acidosis
GI - abdo pain, vomiting and diarrhea

Tx:
Atropine 1.2-3mg (used in bradycardia, anticholinergic). Continue until target end point achieved. May require up to 100 mg.

Targets:
Chest clear, no wheeze
HR > 80 bpm
SBP > 80 mmHg
Pupils no longer constricted
dry axillae
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24
Q

Methaemoglobinaemia. Causes, Clinical, Ix, Tx?

A

Occurs when ferrous iron in blood is oxidized to ferric form.

Causes:
Local anaes e.g. articaine, benzocaine, lignocaine, prilocaine, procaine
Abx- sulfamethoxazole, clofazimine, dapsone
Anti-malarials - chloroquine, primaquine
Prodrugs or sources of nitric oxide - Na nitrite (laxatives), Na nitrate, Na nitroprusside, GTN and amyl nitrite

Clinical:
Relate to concentration
20%

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25
NMS: Causes, Clinical, Ix, Diagnostic criteria, Tx?
Due to dopamine receptor blocking drug or withdrawn from doapine therapy e.g. levodopa and bromocriptine in PD. Almost all antipsychotics have been associated with NMS. Presentation: Tetrad - hyperthermia - EPS, lead pipe rigidity, bradykinesia or akinesia, dystonias, abnormal movements and posture, dysphagia, tremor - Autonomic effects - tachy, HT, labilae BP, diaphoresis, tachpneoa - CNS: drowsiness, confusion, coma, muism, incontinence ``` Ix: CK ++ Leucocytosis Low Fe Metabolic acidosis EEG: diffuse slowing consistent with metabolic encephalopathy ``` Diagnostic criteria: DSM IV consist of i) severe muscle rigidity, ii) elevated temperature, iii) diaphoresis, incontinence, dec GCS etc ``` Tx: bromocriptine 2.5 mg PO. Increase up to 5 mg as needed. Resp support IVF Cooling ```
26
Serotonin toxicity: Causes, Clinical, Diagnostic criteria, Tx?
Causes: Serotonin re-uptake inhibitors e.g. escitalopram, fluoxetine, sertraline, paroxetine, fluvoxamine, opoioids, herbal (st John's wart) MAOI e.g. phenelzine, moclebemide, linezolid, methylene blue Serotonin releasing drugs e.g. amphetamines Others: Lithium, tryptophan Clinical: Triad - neuromuscular excitation e.g. hyperreflexia, clonus, ocular clonus, myoclonus, shivering, tremor, hypertonia or rigidity - Autonominc - hypethermia, diaphoresis, flushing, mydriasis, tachycardia - CNS - agitation, anxiety, confusion Tx: Cyproheptadine 12 mg Sedation with bezos
27
Sympathomimetic syndrome. Drugs, Presentation, Tx?
Catecholamines e.g. adrenaline, dopamine Indirect sympathomimetics e.g. pseudoephedrine Amphetmines, cocaine Xanthines e.g. theophylline, caggeine MAOIs e.g. moclobemide NA reuptake inhibitors e.g. duloxetine, venlafaxine, reboxetine Presentation: CVS e.g tachy etc CNS e.g. excitation, seizures, euphoria NM- hyperreflexia, tremor, rhabdo Autonomic - hyperthermia, diaphoerisis, flushing, pallor metabolic effects- hypoK, hyperGly, acidosis GI e.g, N/V Tx: GTN infusion or Phentolamine or Sodium nitroprusside
28
Drugs implicated in DRESS
``` Aromatase anti-epileptics o Carbamazepine o Phenytoin o Lamotrigine o Phenobarbital Minocycline allopurinol Dapsone Abacavir Nevirapine ```
29
Carbamazepine and oxcarbezine. Which HLA testing recommended prior to commencing?
HLA-B*1502
30
Allopurinol. Which HLA test is recommended?
HLA-B*5801
31
Abacavir. Which HLA test is mandatory?
HLA-B*5701
32
What is Pharmacokinetics? ADME
``` What the body does to the drugs. Absorption Distribution Metabolism Elimination ```
33
What is pharmacodynamics?
What the drug does to the body
34
A drug is highly protein bound to albumin. Pt develops nephrotic syndrome. What is the pharmacokinetic effect of hypoalbuminaemia?
Increased free drug level
35
Most common adverse effect of interferon?
Neuropsychiatric disturbance followed by flu like symptoms
36
which drug used in combination with an SSRI may result in more severe adverse outcomes of serotonin syndrome?
MAOI e.g. moclobemide, phenelzine | - carries the greatest risk
37
Bevacizumab. Target site? Indication?
VEGF monoclonal Ab | Metastatic colorectal Ca
38
MOA of Levodopa with carbidopa or benserazide?
Levodopa is converted to dopamine in the brain and peripheral tissues, and replenishes depleted striatal dopamine. It is given with a peripheral dopa decarboxylase inhibitor (benserazide or carbidopa) to reduce peripheral dopamine production and also reduce adverse effects (eg nausea, vomiting, hypotension).
39
Ropinirole MOA. AE?
Doapmine agonist | Impulse control disorders
40
MOA of Nimodipine?
Dihydro CCB. | Crosses BBB to prevent cerebral vasospasm i.e. aneurysms
41
Non selective BB?
Carvidilol Propanolol Sotalol Timolol (glaucoma) - reduce intra-occular pressure
42
The concentration of Drug A is reduced when drug B is added and increased when Drug B is removed. What is the mechanism for this interaction?
Protein binding displacement The main drugs involved in drug binding are albumin and alpha-acid glycoprotein. Only free drug is active, metabolized and renally excreted. Plasma protein levels correlate with the degree of protein binding and levels of bound drug only. Measured drug levels include protein bound and free. Protein binding is only significant if drug is highly protein bound and there is a large change in plasma protein levels
43
In methyl Alcohol poisoning, what are the effects due to?
Systemic effects of formaldehyde are due to its metabolic conversion to formate -> metabolic acidosis, circ shock, resp insuff, acute renal failure. Formaldehyde - skin, eye and resp irritant - inhaled vapours cause narrowing of the bronchi and accumulation of fluids in the lungs - erosive injury to GIT, esp pharynx, epiglottis, oesophagus and stomach
44
What is the difference between efficacy and potency?
Efficacy = max response achieved by a drug Potency = measure of drug activity expressed in terms of the amount required to produce an effect of given intensity
45
Which analgesics are renally excreted?
Oxycodone and active metabolite oxymorphone Tramadol Gabapentin Pregabalin Morphine - renally excreted glucuronide metabolites Codeine
46
Which analgesics are hepatic cleared?
Buprenorphine | Fentanyl
47
What electrolyte disturbance does Lithium induce?
HyperNa | Litium induces nephrogenic DI
48
Which drugs cause hyponatraemia and SIADH?
Carbemazepine Valproate Sertraline Quetiapine
49
Salicylate poisoning: Presentation Ix
``` Vomiting Air hunger Tininitus Confusion Palpitations ``` ``` Ix: HyperNa HAGMA Mild hypoglycaemia Ketones in UA ```
50
MOA Cinecalcet?
Reduces PTH levels by increasing sensitivity of ca receptors on PTH glands
51
Protein binding. | Do changes in protein binding affect drug effect?
In most cases, protein binding displacement due to another highly protein bound drug, does not result in an increased drug effect.
52
The fraction of an unbound drug in plasma is..
usually not affected by drug concentration | dependent on the affinity of the drug for the binding protein
53
What are the 3 binding proteins and their respective actions?
Albumin - binds acidic drugs e.g. warfarin. Has 6 binding sites, 2 for drugs. Alpha acid glycoprotein - binds basic drugs e.g. disopyramide, lignocaine. Has one binding site. Lipoprotein - bind lipid drugs e.g. amphotericin B, cyclosporin.
54
What happens if the unbound fraction in plasma of warfarin is increased?
the unbound fraction at steady state would increase. clotting synthesis rates would not be altered. Total warfarin clearance would double. Unbound warfarin clearance would not change.
55
What happens is the unbound fraction of phenytoin in renal failure patients is increased from 0.1 to 0.2?
The therapeutic range in terms of unbound drug should double. The therapeutic range in terms of total drug should be reduced from 10-20mg/L to 5-10 mg/L.
56
Linear pharmokinetics means?
steady state drug concentration is proportional to the dose
57
Which process are saturable and can result in non-linear pharmcokinetics?
drug metabolism protein binding renal tubular secretion
58
Saturation of a drug metabolising enzyme occurs when?
the drug concentration is above the Km. | Km is the measure of the affinity of the substrate for the enzyme.
59
Saturation of protein binding occurs when?
The drug concentration approaches the concentration of the protein binding sites.
60
Alcohol pharmacokinetics.
A blood EtoH concentration of 0.05% about one standard drink will maintain steady state. Blood concentrations causing impaired driving performance means alcohol metabolism is saturated.
61
Common electrolyte abnormality associated with bactrim?
Hyperkalaemia | Hyponatraemia
62
How is Dabigatran excreted?
Renal excretion. | CI if egfr
63
Zero order kinetics First order Saturable
Zero order kinetics - elimination is constant e.g. EtOh First order - amount cleared dependent on amount in body - each t1/2, 50% cleared Saturable - change in dosing regime = large change in drug level - use small dose changes and monitoring e.g. phenytoin, aspirin, theophylline, clonidine
64
Dosing in elderly. Pharmacokinetic change?
Decreased Vd - due to decreased lean body mass, decrease H2O and increased fat Decreased clearance - due to decreased renal and heaptic function decreased PB due to decreased albumin Polypharmacy = drug interactions
65
Dosing in elderly. Pharmacodynamic changes?
Impaired homeostatic response - senistivity to effect e.g. orthostatic hyoptension Alterations in receptor function -> less rpedicatable effect Idiosyncratic reactions more common Co-morbidities -> more CI Polypharmacy - pharmacodynamics drug interactions e.g. aspirin and warfarin
66
Pharmacokinetic changes in pregnancy
Clearance increased - increased CO and haptic and renal blood flow. Hormones -> enyme induction Increased Vd by 20% Decreased protein binding therfore lower measured drg levels but free levels are unchanged
67
Pharmocodynamic issues in pregnancy?
All drugs cross placenta to some extent | All drugs diffuse into breast milk
68
Agonist. | Full vs. partial
Enhances target receptors usual actions e.g. slabutamol Full agonsit = elicits max response with suff high dose Partial agonist = unbale to elicit max response despite max dose
69
Antagonsit. | Competitive vs. non-competitive
Inhibits target receptor's usual action Competitve antagonsit binds reversibly to receptor. Max effect still achievable with higher doses of agonist Non-competitive antagonist (selfish) - binds irreversibly to receptor - max effect not achievable with agonsit
70
Why does hydralazine, procainamide, isoniazid cause drug induced lupus?
slow acetylation

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