Pharmcology 3 exam

• 3 NSAIDS?

  Ibuprofen, diclofenac, acetyl salicylic acid
• CA NSAIDS?

  Inflammation, fever and antiplatelet activity
• MOA NSAIDS?

  Inhibition of COX 1 and 2.

  Arachidonic acid is released directly from the cell membrane phospholipids by the enzyme phospholipase A2.

  Arachidonic acid is metabolised by COX 1 or 2 into unstable intermediates PGG2 and PGH2 which are the enzymatically transformed to different prostaniod species in different tissues.

  Includes prostaglandins linked to fever, pain and pyretic effects.

  Thromboxane which stimulates vasoconstriction and platelet adhestion
• COX 1?

  Is expressed in most tissues including blood platelets and primarily involved in tissue homeostasis including platelet aggregation. Inhibition will disrupt homeostasis of numerous physiological systems
• COX 2?

  mainly found in inflammatory cells upon activation they are responsible for the production of prostaglanoid mediators of inflammation, fever, gastric mucosa secretion and inhibition of gastric acid secretion.

  Inhibition will mostly have anti-inflammatory, antipyretic and analgesic effects
• Adverse effects NSAIDS?

  Gi disturbances, skin reactions, reversible renal insufficency, prolonged use can increase BP and risk of stroke
• 3 Opioids?

  Morphine, codeine, and oxycodone
• CA opioids?

  mod to severe pain, management of palliative care and active cancer treatment
• MOA opioids?


  4 main opioid receptors: MOP, KOP, NOP and DOP.

  MOP receptors are responsible for the most of the anaglestic effects of opioids but also for some of the major side effects:
• MOP receptors are responsible for most of the analgesic effects of opioids
• MOP receptors are also responsible for some major side effects
• The ligand binds to the Gi receptors, inhibiting adenylyl cyclase and decreasing cAMP
• This process produces 2 main effects:

  • Inhibit opening of calcium channels, reducing calcium entry into the presynaptic terminal and reducing transmitter release (glutamate and substance P which modulate pain perception in the spinal cord)
  • Promote opening of potassium channels, increasing potassium conductance out of the cell and hyperpolarizing the membrane, decreasing neuronal excitability (less likely to produce an action potential)
• Adverse effects Opioids?

  Nausea, vomiting, constipation, drowsiness, respiratory depression, tolerance and dependence can occur
• 3 Benzos?

  Diazepam, lorazepam, clonazepam
• CA Benzos?

  Anxiety, insomnia, alcohol withdrawal and epilepsy
• MOA Benzos?

  Act as a positive allosteric modulator on GABA a receptor

  bind to the BZD site on GABA-a receptor producing a confirmation change, allowing GABA to bind. when GABA binds it increases the frequency of the chloride channels opening allowing more chloride into the cell, hyperpolarizing it resulting in a decreased neuronal excitability.

  a1 is associated with the sedative effects of BZDS.

  a2-3 associated with the anxiolytic effects of BZDs
• Adverse effects of BZds?

  drowsiness, lethargy and fatigue. Tolerance and dependence can occur
• 3 TCAs?

  Amitriptyline, nortriptyline, imipramine
• CA TCAS?

  depression, anxiety, panic attacks, PTSD and migraine prophylaxis
• MOA TCAS?

  Block the reuptake of amines mostly 5HT and NE by the nerve terminals by competitive binding to the amine transporter (SERT and NET).
• TCA Adverse effects?

  Tachycardia, arrhythmias, anticholinergic effects, sexual dysfunction and sedation
• 3 SSRIs?

  Sertraline, fluoxteine, citalopram
• CA ssris?

  Depression, anxiety and OCD
• MOA ssris?

  Inhibit the reuptake of 5HT into serotonergic neurons therefore potentiating transmitter action.

  MOA of all antidepressant involve the immediate neurochemical effects followed by slow adaptive changes causing a downregulation in the monoamine receptors, producing the therapeutic effects
• Adverse effects Ssris?

  Due to non selective block

  insomnia, anxiety, nausea, vomiting and sexual dysfunction

  Serotonin syndrome can occur during antidepressant switching
• 3 SNRIs?

  Venlafaxine, desvenlafaxine, duloxetine
• SNRIs CA?

  depression, panic disordre, anxiety and social phobia
• MOA SNRIS?

  inhibit the reuptake of NE into noradrenergic neurons and 5HT into serotonergic neurons increasing availability of neurotransmitters in the synaptic cleft therefore potentiating neurotransmitter action.
• Adverse effects of SNRIs?

  due to non selective block

  headache, nausea, sleep problems, sexual dysfuntion

  Overdose can cause CNS depression, seizures and cardiac dysrhythmias
• MOA inhibitors 2?

  Phenelzine, tranylcypromine
• MAO inhibitor MOA?

  MAO is an enzyme that degrades excess 5HT and NE and dopamine within the nerve terminal. Inhibiting this enzyme causes a rapid and sustained increase in 5HT, NE and dopamine levels. Resulting in an increased rate in their spontaneous leakage from the nerve terminals into the synapse, potentiating neurotransmission
• 2 forms of MAO?

  MAO-A - has substrate preference of 5HT and NE

  MAO-B - Has substrate preference for dopamine
• Adverse effects MAO inhibitors?

  Postural hypotension, tremors, insomnia, increased appetite leading to extreme weight gain and antimuscarinic effects
• CA mirtazapine?

  Major depression and PTSD
• Mirtazapine MOA?

  primary action is block auto and hetero inhibitory receptors blocking the inhibition of serotonergic and noradrenergic neurons leading to increased release of neurotransmitters.
• MOA mirtazepine continued?

  The block of the presynaptic a2 autoreceptors on the noradrenergic nerve terminals will increase NE release. Which then act on post synaptic a1 receptors which will stimulate 5-HT release.

  The block of presynaptic a2 heteroreceptors on serotonergic nerve terminals will increase 5-HT release.

  Also simultaneously blocks 5HT2a and 5HT3 receptors will reduce the unwanted effects mediated through these receptors (sexual dysfunction and nausea) but remain the therapeutic benefit of 5HT1a receptors.
• adverse effects mirtazepine?

  Sedation, increased appetite and weight gain
• typical antipsychotics CA?

  Schizophrenia, positive symptoms, mania, aggressive behavior, persistent hiccups
• MOA typical antipsychotics?

  Antagonism of D2 receptors in the mesolimbic pathway which causes antipsychotic actions and reduced aggression, antiemetic effects and apathy.

  Relieve positive symptoms- hallucinations, delusions, thought disorders.

  Normally dopamine suppresses ACH release however when the D2 receptors are blocked, ach release is increased and it becomes overactive which is associated with extrapyramidal symptoms.

  As they are non selective they also bloc muscarinic, adrenergic and histamine receptors leading to side effects and often limit patient adherence.