CPPS 304 UPDATED FINAL EXAM 2026 QUESTIONS AND
SOLUTIONS RATED A+
✔✔How can H1 receptor antagonists (antihistamines) be used most effectively? -
✔✔most effective when used on a regular basis for managing seasonal allergies
✔✔Should H1 receptor antagonists be used to treat acute anaphylactic attacks? -
✔✔no
need larger intervention(ex. epinephrine)
✔✔Why can HI receptor antagonists not be used to treat anaphylaxis - ✔✔when
anaphylactic response is detected histamine has already been released and bound to
receptors (no point in antihistamines)
downstream effects of histamine need to be addressed
✔✔Routes of administration of antihistamines (2) - ✔✔oral
topical (dermal, ophthalmic)
✔✔Types of oral antihistamines - ✔✔1 gen (sedating):
diphenhydramine (Benadryl)
2 gen (non-sedating):
loratadine (Claritin) - do not cross BBB
✔✔Side effects of antihistamines (2) - ✔✔- sedation (common with 1 gen)
- anticholinergic effects (common with 1 gen)
ex. dry mouth
✔✔COX pathway - ✔✔arachidonic acid converted to PGH2 via COX
PGH2 converted to:
PGE2
TxA2 (via thromboxane synthase)
PGI2 (via prostacyclin synthase)
✔✔What does TxA2 (thromboxane A2) mediate - ✔✔platelet aggregation
vasoconstriction
✔✔What does PGI2 (prostacyclin) mediate - ✔✔platelet inhibition
vasodilation
✔✔What does PGE2 mediate - ✔✔fever
vasodilation
pain
inflammation
mucous production
,✔✔What does blocking the formation of PGE2 cause - ✔✔analgesia (pain-relief)
anti-inflammatory
antipyretic (fever-relief)
decreased mucous release - GI ulceration
✔✔What type of drug inhibits PGE2 formation - ✔✔NSAIDs
✔✔Consequence of NSAIDs - ✔✔GI ulcers
✔✔COX1 vs COX2: expression - ✔✔COX1 - constitutive
COX2 - inducible
✔✔COX1 vs COX2: location - ✔✔COX1: everywhere
COX2: predominantly in inflamed tissue
✔✔COX1 vs COX2: role - ✔✔COX1: protection, maintenance
COX2: proinflammatory, mitogenic
✔✔COX1 vs COX2: specific functions - ✔✔COX1: GI cytoprotection (mucous
production), platelet aggragation
COX2: inflammation, carcinogenesis
✔✔What was the goal of selective COX2 inhibitors? (2) - ✔✔designed to maximize anti-
inflammatory activity and minimize GI problems
✔✔Problem with selective COX2 inhibitors? - ✔✔unexpected cardiovascular
complications
- increased platelet aggregation = blood clots
✔✔Examples of NSAIDs (2) - ✔✔ibeprofin
acetylsalicylic acid (ASA - aspirin)
✔✔Effects of prostacyclin agonists and example - ✔✔- anti platelet effects
- vasodilation
- may cause bleeding
example: Epoprostenol
✔✔What can prostacyclin agonists be used to treat - ✔✔pulmonary hypertension -
constricted vessels put strain on heart and can result in right heart failure
✔✔Difficulty with epoprostenol - ✔✔difficult to administer - must be done through
catheter/infusion pump
,✔✔TRASI - ✔✔thromboxane receptor antagonist and synthase inhibitor (double
whammy)
✔✔Example of a TRASI - ✔✔picotamide - used in Europe for patients with peripheral
artery disease
✔✔What does PGF2a (prostaglandin) mediate - ✔✔promotes uterine contraction
promotes outflow of aqueous humour from the eye
✔✔What can PGF2a analogues be used to treat (3) - ✔✔promotes abortion -
misoprostol
promotes secretion of GI mucous
management of glaucoma - aqueous humour secretion (latanoprost)
✔✔How are leukotrienes produced - ✔✔produced from arachidonic acid via
lipoxygenase pathway
✔✔Examples of leukotrienes - ✔✔LTC4, LTD4, LTE4
✔✔What do leukotrienes promote? - ✔✔inflammation
allergy
bronchoconstriction
✔✔What do leukotriene receptor antagonists do and example - ✔✔decrease
bronchconstriction and inflammation
ex. montelukast - treats asthma
✔✔5-lipoxgenase inhibitor - ✔✔zileuton - treats astma
not in canada
✔✔Other name for seretonin - ✔✔5-hydroxytryptamine (5HT)
✔✔Types of serotonin receptors - ✔✔subtypes: 5HT-1 to 5HT-7
many sub-subtypes
mostly GPCRs
✔✔Main sites of action (3) - ✔✔GI tract (enterochromaffin cells) - major source of 5HT
platelets - results in platelet aggregation
Brain - key role in anxiety and depression
✔✔How do most antidepressants work? - ✔✔promote 5HT and other NT in the CNS
✔✔Mechanism of most antidepressants? - ✔✔inhibit reuptake pumps of serotonin,
noradrenaline, and sometimes dopamine (increases amount of NT in synapse)
, ✔✔example of SSRI - ✔✔fluoxetine
✔✔Look at 5HT receptor chart (last slide) - ✔✔
✔✔Chemotherapy - ✔✔treatment of disease by means of chemicals (drugs) that have a
specific toxic effect upon disease-producing microorganisms, or that selectively destroy
cancerous tissue
✔✔-static vs -cidal - ✔✔-static: stops bug from replicating (lets host immune system do
work of killing)
-cidal: kills bug directly
✔✔Most common targets by antibiotics (3) - ✔✔cell wall
DNA/RNA
ribosomes
✔✔How do antibiotics damage the cell wall/membrane - ✔✔cell wall synthesis inhibitors
drugs that damage cell membranes
✔✔How do antibiotics inhibit protein synthesis - ✔✔ribosomal inhibitors
✔✔How do antibiotics inhibit RNA - ✔✔RNA polymerase inhibitors
✔✔How do antibiotics inhibit DNA - ✔✔DNA gyrase inhibitors
purine synthesis inhibitors
inflict DNA damage
✔✔Cell wall synthesis inhibitors (3) - ✔✔B-lactams:
- penicillins (amoxicillin)
- cephalosporins
- carbapenems
✔✔What step of cell wall synthesis do B lactase target - ✔✔joining of peptidoglycan
rows to form a stable wall
causes leaks in cell
✔✔Most effective/most important class of antibiotics thus far - ✔✔cell wall inhibitors
since penicillin - 1928
✔✔general guidelines for choosing antibiotics (2) - ✔✔1. some drugs work better on
specific types of bacteria
ex. some penicillins work better on gram(+) bacteria over others
2. consider where the infection is located
SOLUTIONS RATED A+
✔✔How can H1 receptor antagonists (antihistamines) be used most effectively? -
✔✔most effective when used on a regular basis for managing seasonal allergies
✔✔Should H1 receptor antagonists be used to treat acute anaphylactic attacks? -
✔✔no
need larger intervention(ex. epinephrine)
✔✔Why can HI receptor antagonists not be used to treat anaphylaxis - ✔✔when
anaphylactic response is detected histamine has already been released and bound to
receptors (no point in antihistamines)
downstream effects of histamine need to be addressed
✔✔Routes of administration of antihistamines (2) - ✔✔oral
topical (dermal, ophthalmic)
✔✔Types of oral antihistamines - ✔✔1 gen (sedating):
diphenhydramine (Benadryl)
2 gen (non-sedating):
loratadine (Claritin) - do not cross BBB
✔✔Side effects of antihistamines (2) - ✔✔- sedation (common with 1 gen)
- anticholinergic effects (common with 1 gen)
ex. dry mouth
✔✔COX pathway - ✔✔arachidonic acid converted to PGH2 via COX
PGH2 converted to:
PGE2
TxA2 (via thromboxane synthase)
PGI2 (via prostacyclin synthase)
✔✔What does TxA2 (thromboxane A2) mediate - ✔✔platelet aggregation
vasoconstriction
✔✔What does PGI2 (prostacyclin) mediate - ✔✔platelet inhibition
vasodilation
✔✔What does PGE2 mediate - ✔✔fever
vasodilation
pain
inflammation
mucous production
,✔✔What does blocking the formation of PGE2 cause - ✔✔analgesia (pain-relief)
anti-inflammatory
antipyretic (fever-relief)
decreased mucous release - GI ulceration
✔✔What type of drug inhibits PGE2 formation - ✔✔NSAIDs
✔✔Consequence of NSAIDs - ✔✔GI ulcers
✔✔COX1 vs COX2: expression - ✔✔COX1 - constitutive
COX2 - inducible
✔✔COX1 vs COX2: location - ✔✔COX1: everywhere
COX2: predominantly in inflamed tissue
✔✔COX1 vs COX2: role - ✔✔COX1: protection, maintenance
COX2: proinflammatory, mitogenic
✔✔COX1 vs COX2: specific functions - ✔✔COX1: GI cytoprotection (mucous
production), platelet aggragation
COX2: inflammation, carcinogenesis
✔✔What was the goal of selective COX2 inhibitors? (2) - ✔✔designed to maximize anti-
inflammatory activity and minimize GI problems
✔✔Problem with selective COX2 inhibitors? - ✔✔unexpected cardiovascular
complications
- increased platelet aggregation = blood clots
✔✔Examples of NSAIDs (2) - ✔✔ibeprofin
acetylsalicylic acid (ASA - aspirin)
✔✔Effects of prostacyclin agonists and example - ✔✔- anti platelet effects
- vasodilation
- may cause bleeding
example: Epoprostenol
✔✔What can prostacyclin agonists be used to treat - ✔✔pulmonary hypertension -
constricted vessels put strain on heart and can result in right heart failure
✔✔Difficulty with epoprostenol - ✔✔difficult to administer - must be done through
catheter/infusion pump
,✔✔TRASI - ✔✔thromboxane receptor antagonist and synthase inhibitor (double
whammy)
✔✔Example of a TRASI - ✔✔picotamide - used in Europe for patients with peripheral
artery disease
✔✔What does PGF2a (prostaglandin) mediate - ✔✔promotes uterine contraction
promotes outflow of aqueous humour from the eye
✔✔What can PGF2a analogues be used to treat (3) - ✔✔promotes abortion -
misoprostol
promotes secretion of GI mucous
management of glaucoma - aqueous humour secretion (latanoprost)
✔✔How are leukotrienes produced - ✔✔produced from arachidonic acid via
lipoxygenase pathway
✔✔Examples of leukotrienes - ✔✔LTC4, LTD4, LTE4
✔✔What do leukotrienes promote? - ✔✔inflammation
allergy
bronchoconstriction
✔✔What do leukotriene receptor antagonists do and example - ✔✔decrease
bronchconstriction and inflammation
ex. montelukast - treats asthma
✔✔5-lipoxgenase inhibitor - ✔✔zileuton - treats astma
not in canada
✔✔Other name for seretonin - ✔✔5-hydroxytryptamine (5HT)
✔✔Types of serotonin receptors - ✔✔subtypes: 5HT-1 to 5HT-7
many sub-subtypes
mostly GPCRs
✔✔Main sites of action (3) - ✔✔GI tract (enterochromaffin cells) - major source of 5HT
platelets - results in platelet aggregation
Brain - key role in anxiety and depression
✔✔How do most antidepressants work? - ✔✔promote 5HT and other NT in the CNS
✔✔Mechanism of most antidepressants? - ✔✔inhibit reuptake pumps of serotonin,
noradrenaline, and sometimes dopamine (increases amount of NT in synapse)
, ✔✔example of SSRI - ✔✔fluoxetine
✔✔Look at 5HT receptor chart (last slide) - ✔✔
✔✔Chemotherapy - ✔✔treatment of disease by means of chemicals (drugs) that have a
specific toxic effect upon disease-producing microorganisms, or that selectively destroy
cancerous tissue
✔✔-static vs -cidal - ✔✔-static: stops bug from replicating (lets host immune system do
work of killing)
-cidal: kills bug directly
✔✔Most common targets by antibiotics (3) - ✔✔cell wall
DNA/RNA
ribosomes
✔✔How do antibiotics damage the cell wall/membrane - ✔✔cell wall synthesis inhibitors
drugs that damage cell membranes
✔✔How do antibiotics inhibit protein synthesis - ✔✔ribosomal inhibitors
✔✔How do antibiotics inhibit RNA - ✔✔RNA polymerase inhibitors
✔✔How do antibiotics inhibit DNA - ✔✔DNA gyrase inhibitors
purine synthesis inhibitors
inflict DNA damage
✔✔Cell wall synthesis inhibitors (3) - ✔✔B-lactams:
- penicillins (amoxicillin)
- cephalosporins
- carbapenems
✔✔What step of cell wall synthesis do B lactase target - ✔✔joining of peptidoglycan
rows to form a stable wall
causes leaks in cell
✔✔Most effective/most important class of antibiotics thus far - ✔✔cell wall inhibitors
since penicillin - 1928
✔✔general guidelines for choosing antibiotics (2) - ✔✔1. some drugs work better on
specific types of bacteria
ex. some penicillins work better on gram(+) bacteria over others
2. consider where the infection is located
