PHRM 1203 END OF SEM EXAM LATEST UPDATE
Pharmacodynamics - ANSWER what the drug does to the body, describes site of action
of drug and MOA and side effects
Pharmacokinetics - ANSWER what the body does to the drug, describes relationship
between the drug dose and the concentration in the body
ADME - ANSWER absorption, distribution, metabolism, excretion
factors influencing absorption - ANSWER food, some medications, acidity of stomach,
nausea and vomiting, route
factors that influence distribution - ANSWER hydrophilic or lipophilic, (hydro philiic
doesn't distribute everywhere whereas lipophilic does and bbb), perfusion of body
tissues
Metabolism - ANSWER protective mechanism to eliminate toxins from body, liver is
major organ, involves converting fat-soluble medications to water-soluble medications
first pass metabolism - ANSWER generally occurs with oral administration, drug enters
the portal circulation to liver before systemic circulation, undergoes metabolism before
going back to system circulation, results in reduced bioavailability (higher
concentration given) examples include morphine, labetalol, propranolol and salbutamol
Excretion - ANSWER liver and kidneys are main organs for drug elimination, takes 4-5
half lives for a drug to be eliminated from body, poor kidney function can cause water
soluble medications to accumulate (smaller doses given)
TDM - ANSWER conducted for medications that can cause toxicity, takes 4-5 half lives
for a drug to reach a steady state of concentration, TDM can be conducted for drugs
with a narrow therapeutic range (small window where drugs are effective for patient)
reasons for TDM - ANSWER to optimise drug therapy and reduce potential for toxicity,
some are taken at trough level (before next dose, drug at lowest level), others are taken
every few hours, TDM must be taken once the drug reaches steady state concentration
types of drugs for TDM - ANSWER high risk of toxicity, narrow therapeutic range,
unpredictable response, correlation between drug concentration or plasma, those able
to be measured in blood or plasma
examples of TDM drugs - ANSWER antimicrobials (gentamicin, vancomycin)
anti-epileptic agents (carbamazepine, phenobarbitone), cardiovascular agents
(digoxin), anticoagulants (wafarin, heparin), psychotropic agents (lithium), respiratory
agents (caffeine)
suitable first line agents in uncomplicated elevated blood pressure in non-pregnant
,adults - ANSWER low-dose thiazide, angiotensin converting enzyme (ACE) inhibitors
(end in -pril), angiotensin II receptor blockers (ARBs also known as sartans, generic
names end in -sartan)
What are ACE inhibitors? - ANSWER one of the main medications used in the
management of hypertension and their site of action is the angiotensin I and angiotensin
II receptor, can be used to manage Chronic heart failure and for heart attacks
How does angiotensin II increase BP? - ANSWER Renin is released when there is a
decrease in sodium concentration in the body or in response to hypotension, when the
enzyme renin is released into circulation-angiotensin II is produced, angiotensin I is
converted to angiotensin II via the angiotensin converting enzyme, angiotensin II is a
vasoconstrictor hormone and via its action on the cortex of the adrenal glands,
stimulates the secretion of aldosterone, a mineral corticoid, aldosterone increases
sodium re-absorption, this resuts in increased blood pressure, blood volume and a
decrease in urine output
MOA for ACEI - ANSWER they block the conversion of angiotensin I to angiotensin II
(causes vasodilation), they enhance the excretion of sodium and chloride ions in the
urine due to reduced aldosterone secretion, they prevent the breakdown of bradykinin
which is a vasodilating agent that reduces peripheral resistance, this reduces the
vasoconstrictor effect resulting in lower blood pressure
common side effects of ACEi - ANSWER hypotension, hyperkalaemia, cough, dizziness,
headache, tiredness, nausea, renal impairment, andioedema
contraindication of ACEi - ANSWER patients with history of hypersensitivity to ACEi,
patients with angioedema, patients with bilateral or unilateral renal artery stenosis,
pregnancy
pregnancy and ACEi - ANSWER use in second and third trimester can cause fetal renal
dysfunction oligohydramnios and possible fetal death, captopril and enalapril appear
safe to use
examples of ACEi - ANSWER common ACEi in Australia include perindopril, ramipril,
trandolapril, lisinopril
what are ARA - ANSWER angiotensin receptor antagonsits, closely related to ACEi
MOA of ARA - ANSWER selectively bind to angiotensin II receptor which prevents
angiotensin II from binding to receptor, this blocks the action of Angiotensin II
side effects and contraindication of ARA - ANSWER similar to ACEi, hypotension,
hyperkalaemia, NO COUGH, dizziness, headache, tiredness, nausea, renal impairment,
avoid in pregnancy and breastfeeding
two classifications of calcium channel blockers - ANSWER 1. dihydropyridines which
cause vasodilation in the peripheral blood vessels which helps to lower blood pressure
(these are preferred treatment of hypertension)
, 2. non-dihydropyridines which reduce the heart rate and contractility while having a
lower peripheral vasodilation effect
two classifcations of non-dihydropyridine calcium channel blockers - ANSWER 1.
benzothiazipines (dilitiazem) causes both peripheral vasodilation, albeit to a lesser
extent, reduces heart rate and cardiac contractility
2. phenylalkylamines (verapamil) has its greatest effects on reducing heart rate and
contractility with the lesser effects on peripheral vasodilation compared to the other
classes
Examples of dihydropyridines - ANSWER six in Australia however clevidipine and
nimodipine are not used, nifedipine is relatively short acting so has a controlled release
can CCB be used during pregnancy - ANSWER probs not, requires specialist advice
where are the beta receptors located - ANSWER 1. B1 receptors are predominantly
located in the heart, kidneys and smooth muscle in the gastrointestinal tract
2. B2 receptors are predominantly located in the lungs
b-blockers in pregnancy - ANSWER b-blockers can cause bradycardia in fetus and
neonate, however, labetalol is fine and is main choice when treating hypertension in
pregnancy, atenolol should be avoided in early stages of pregnancy
Cardio selective beta blockers - ANSWER atenolol, bisoprolol, metoprolol and nebivolol,
they have a greater affinity for b1 receptors, used with caution in patients who have well
controlled asthma or COPD
non selective b blockers - ANSWER block b1 and b2 receptors, include propranolol, can
cause bronchospasm and should not be used in patients with asthma or chronic
obstructive airway disease (causes bronchospasm)
nonselective b-blockers that block b1, b2 and a1 - ANSWER carvedilol and labetalol
two types of b blockers - ANSWER lipid soluble and water soluble, lipid soluble can
cause sleep disturbances, nightmares and hallucinations as they cross the bbb
side effects and contraindications of b blockers - ANSWER bradycardia (not used in
patients with bradycardia or a slow heart rate), they can worsen peripheral arterial
disease, need to be used in caution with diabetic patients as they mask the signs of
diabetic hypoglycemia, poorly controlled asthma as they cause bronchospasm
cause of asthma - ANSWER asthma is a chronic lung disease caused by inflammation or
swelling in the airways, this then causes muscles in the surrounding airways to tighten,
which leads to wheezing, shortness of breath, chest tightness and coughing
goals of asthma treatment - ANSWER symptom control and relief, prevention of
exacerbation and acute asthma, improve and maintain lung function and quality of life
Pharmacodynamics - ANSWER what the drug does to the body, describes site of action
of drug and MOA and side effects
Pharmacokinetics - ANSWER what the body does to the drug, describes relationship
between the drug dose and the concentration in the body
ADME - ANSWER absorption, distribution, metabolism, excretion
factors influencing absorption - ANSWER food, some medications, acidity of stomach,
nausea and vomiting, route
factors that influence distribution - ANSWER hydrophilic or lipophilic, (hydro philiic
doesn't distribute everywhere whereas lipophilic does and bbb), perfusion of body
tissues
Metabolism - ANSWER protective mechanism to eliminate toxins from body, liver is
major organ, involves converting fat-soluble medications to water-soluble medications
first pass metabolism - ANSWER generally occurs with oral administration, drug enters
the portal circulation to liver before systemic circulation, undergoes metabolism before
going back to system circulation, results in reduced bioavailability (higher
concentration given) examples include morphine, labetalol, propranolol and salbutamol
Excretion - ANSWER liver and kidneys are main organs for drug elimination, takes 4-5
half lives for a drug to be eliminated from body, poor kidney function can cause water
soluble medications to accumulate (smaller doses given)
TDM - ANSWER conducted for medications that can cause toxicity, takes 4-5 half lives
for a drug to reach a steady state of concentration, TDM can be conducted for drugs
with a narrow therapeutic range (small window where drugs are effective for patient)
reasons for TDM - ANSWER to optimise drug therapy and reduce potential for toxicity,
some are taken at trough level (before next dose, drug at lowest level), others are taken
every few hours, TDM must be taken once the drug reaches steady state concentration
types of drugs for TDM - ANSWER high risk of toxicity, narrow therapeutic range,
unpredictable response, correlation between drug concentration or plasma, those able
to be measured in blood or plasma
examples of TDM drugs - ANSWER antimicrobials (gentamicin, vancomycin)
anti-epileptic agents (carbamazepine, phenobarbitone), cardiovascular agents
(digoxin), anticoagulants (wafarin, heparin), psychotropic agents (lithium), respiratory
agents (caffeine)
suitable first line agents in uncomplicated elevated blood pressure in non-pregnant
,adults - ANSWER low-dose thiazide, angiotensin converting enzyme (ACE) inhibitors
(end in -pril), angiotensin II receptor blockers (ARBs also known as sartans, generic
names end in -sartan)
What are ACE inhibitors? - ANSWER one of the main medications used in the
management of hypertension and their site of action is the angiotensin I and angiotensin
II receptor, can be used to manage Chronic heart failure and for heart attacks
How does angiotensin II increase BP? - ANSWER Renin is released when there is a
decrease in sodium concentration in the body or in response to hypotension, when the
enzyme renin is released into circulation-angiotensin II is produced, angiotensin I is
converted to angiotensin II via the angiotensin converting enzyme, angiotensin II is a
vasoconstrictor hormone and via its action on the cortex of the adrenal glands,
stimulates the secretion of aldosterone, a mineral corticoid, aldosterone increases
sodium re-absorption, this resuts in increased blood pressure, blood volume and a
decrease in urine output
MOA for ACEI - ANSWER they block the conversion of angiotensin I to angiotensin II
(causes vasodilation), they enhance the excretion of sodium and chloride ions in the
urine due to reduced aldosterone secretion, they prevent the breakdown of bradykinin
which is a vasodilating agent that reduces peripheral resistance, this reduces the
vasoconstrictor effect resulting in lower blood pressure
common side effects of ACEi - ANSWER hypotension, hyperkalaemia, cough, dizziness,
headache, tiredness, nausea, renal impairment, andioedema
contraindication of ACEi - ANSWER patients with history of hypersensitivity to ACEi,
patients with angioedema, patients with bilateral or unilateral renal artery stenosis,
pregnancy
pregnancy and ACEi - ANSWER use in second and third trimester can cause fetal renal
dysfunction oligohydramnios and possible fetal death, captopril and enalapril appear
safe to use
examples of ACEi - ANSWER common ACEi in Australia include perindopril, ramipril,
trandolapril, lisinopril
what are ARA - ANSWER angiotensin receptor antagonsits, closely related to ACEi
MOA of ARA - ANSWER selectively bind to angiotensin II receptor which prevents
angiotensin II from binding to receptor, this blocks the action of Angiotensin II
side effects and contraindication of ARA - ANSWER similar to ACEi, hypotension,
hyperkalaemia, NO COUGH, dizziness, headache, tiredness, nausea, renal impairment,
avoid in pregnancy and breastfeeding
two classifications of calcium channel blockers - ANSWER 1. dihydropyridines which
cause vasodilation in the peripheral blood vessels which helps to lower blood pressure
(these are preferred treatment of hypertension)
, 2. non-dihydropyridines which reduce the heart rate and contractility while having a
lower peripheral vasodilation effect
two classifcations of non-dihydropyridine calcium channel blockers - ANSWER 1.
benzothiazipines (dilitiazem) causes both peripheral vasodilation, albeit to a lesser
extent, reduces heart rate and cardiac contractility
2. phenylalkylamines (verapamil) has its greatest effects on reducing heart rate and
contractility with the lesser effects on peripheral vasodilation compared to the other
classes
Examples of dihydropyridines - ANSWER six in Australia however clevidipine and
nimodipine are not used, nifedipine is relatively short acting so has a controlled release
can CCB be used during pregnancy - ANSWER probs not, requires specialist advice
where are the beta receptors located - ANSWER 1. B1 receptors are predominantly
located in the heart, kidneys and smooth muscle in the gastrointestinal tract
2. B2 receptors are predominantly located in the lungs
b-blockers in pregnancy - ANSWER b-blockers can cause bradycardia in fetus and
neonate, however, labetalol is fine and is main choice when treating hypertension in
pregnancy, atenolol should be avoided in early stages of pregnancy
Cardio selective beta blockers - ANSWER atenolol, bisoprolol, metoprolol and nebivolol,
they have a greater affinity for b1 receptors, used with caution in patients who have well
controlled asthma or COPD
non selective b blockers - ANSWER block b1 and b2 receptors, include propranolol, can
cause bronchospasm and should not be used in patients with asthma or chronic
obstructive airway disease (causes bronchospasm)
nonselective b-blockers that block b1, b2 and a1 - ANSWER carvedilol and labetalol
two types of b blockers - ANSWER lipid soluble and water soluble, lipid soluble can
cause sleep disturbances, nightmares and hallucinations as they cross the bbb
side effects and contraindications of b blockers - ANSWER bradycardia (not used in
patients with bradycardia or a slow heart rate), they can worsen peripheral arterial
disease, need to be used in caution with diabetic patients as they mask the signs of
diabetic hypoglycemia, poorly controlled asthma as they cause bronchospasm
cause of asthma - ANSWER asthma is a chronic lung disease caused by inflammation or
swelling in the airways, this then causes muscles in the surrounding airways to tighten,
which leads to wheezing, shortness of breath, chest tightness and coughing
goals of asthma treatment - ANSWER symptom control and relief, prevention of
exacerbation and acute asthma, improve and maintain lung function and quality of life
