Pharmacology Midterm

Question 1

What are the different routes of drug administration?

Answer 1

Enteral:
Oral - Most common; undergoes first pass
Sublingual - diffuses into the capillary network
Rectal - 50% first pass metabolism

Parenteral:
Intravenous - 100% absorption; No first pass
reactions: infection at site or too rapid delivery of high concentrated drug.

Intramuscular - aqueous solution or specialized depot formulation. Precipitates at site, dissolves slowly; provides sustained dose over extended period of time. (ie: depo provera; PCN)

Subcutaneous/Intradermal – vaccines; insulin shots

Others: Inhalation, Intranasal,
Intrathecal/Intraventricular, Topical & Transdermal*

*goes to blood

Question 2

What is the first pass effect?

Answer 2

The effect of Liver metabolism prior to reaching the systemic circulation.

Question 3

What are the effects of PH of a medium on drug absorption?

Answer 3

A drug passes through membranes more readily if uncharged.
Weak acids are better absorbed in the stomach, because of acid environment. (ph2)
Alkaline drugs are best absorbed in the small intestine which has higher ph. (ph8)

Question 4

What are the physical and patient associated factors influencing absorption of drugs?

Answer 4

Physical:
-blood flow to the absorption site
(more blood flow– more absorption)
-Surface area
(more sure area– more efficient absorption)
-Contact time at absorption site
(quick mov’t of drug through GI tract– less absorp.)

Patient:

• food in GI tract
• stomach acidity
• blood flow to GI tract

Question 5

What are two phases of drug metabolism? What are the chemical reactions involved in each phase?

Answer 5

Phase 1 Reaction:
Drugs are oxidized or reduced or hydrolyzed to a more polar form. *Most of phase 1 reactions utilize the Cytochrome P420 system of enzymes.

Phase 2 Reaction:
A polar group such as: ‘glutathione’ is conjugated to the drug; substantially increasing the polarity of the drug; making it excretable by the kidneys.
*Drugs undergoing Phase 2 reaction may have already undergone Phase 1 transformation.

Question 6

Define:

Agonist, Competitive Antagonist, Noncompetitive Antagonist & Physiologic Antagonist.

Answer 6

Agonist:
Drugs which alter the physiology of a cell by binding to plasma membrane or intracellular receptors.

Competitive Antagonist:
Competes with agonist for same receptors; during that time, agonists can not bind to the receptor.

Noncompetitive Antagonist:
Binds to a site other than the agonist binding domain; induces conformational shape changes in the receptor such that the agonist no longer recognizes the agonist binding domain.

Physiologic Antagonist:
Two agonists, in unrelated reactions, cause opposite effects. The effects CANCEL one another.

Question 7

Define:
Efficacy
Potency

Answer 7

Efficacy:
Degree to which a drug is able to induce MAXIMAL effects.
Potency:
The amount of drug required to produce 50% of the maximal response that the drug is capable of inducing.

Question 8

What are types of drug interactions? Define each.

Answer 8

Addition:
The response elicited by combined drugs is EQUAL TO the combined responses of the individual drugs.

Synergism:
The response elicited by combined drugs is GREATER THAN the combined responses of the individual drugs.

Potentiation:
A drug which has no effect, enhances the effect of a second drug. (ie: Augmentum)

Antagonism:
A drug inhibits the effect of another drug.
(ie: B-stimulant + B blocker = neutralization)

Question 9

Define: Tolerance, Dependence & Withdrawal

Answer 9

Tolerance:
Decreased response to a drug=> dose must be increased.

Dependence:
A patient NEEDS a drug to “function normally”.

Withdrawal:
Occurs when drug no longer administered. Sx’s are often the opposite of the effects of the drug.

Question 10

What are the effects of muscarinic receptors on different organs?

Answer 10

Eye: Pupil constriction
Cardio: Decreased heart rate
Respiratory: Bronchial constriction/Increased secretions
Genitourinary: Relax sphincters AND bl. wall contraction
Glands: Increased secretions - Sweat

Question 11

What are the uses of Pilocarpine & Donezepil?

Answer 11

Pilocarpine –Treatment of Glaucoma

Donezepil – Alzheimer’s disease

Question 12

What is the MOA of indirect-acting cholinergic agonists? what are the disease in which these are used?

Answer 12

• They inhibit the enzyme (AChE) anticholinesterases; thereby prolonging the lifetime of Acetylcholine.
• Used in Tx. of Myasthenia Gravis (Edrophonium)
• Used in Tx. of Alzheimer’s (Donezepil)

Question 13

What are the two drugs that treat organophosphate poisoning? What are their actions?

Answer 13

Pralidoxime – hydrolyzes the phosphate bond & reactivates the enzyme.
Atrophine – Blocks the effects of excess acetylcholine.

Question 14

What are the effects & common side effects of cholinergic antagonists?

Answer 14

Effects:
-Blurred vision
-Reduced sweating / Flushing
-Reduced motility & secretions
-Cardio -- Increased heart rate
-Respiratory -- Bronchial dilation & decreased scrtns.
G/U -- Urinary retention

Side Effects: Blurred vision, Dry eyes, Dry eyes, Constipation & Urinary retention.

Question 15

Uses of: Atropine, Scopolamine, Ipratropium, & Succinylcholine?

Answer 15

Atropine- preanesthetic/prevents resp. secrestions
Scopolamine - prevents motion sickness (before sx’s)
Ipratropium - treats COPD/induces bronchodilation
Succinylcholine - For intubation/rapid onset/short duration. *Only depolarizing agent.

Question 16

What are the effects of stimulation of A1, B1 & B2 adrenoceptors? What are the effects of blocking them?

Answer 16

Stimulating:
A1 - Vasocontriction, increased peripheral resistance, increased BP, Mydriasis (dilated pupils), increased closure of the internal sphincter of UB.

A2 - Inhibition of Norepinephrine release, inhibition of acetylcholine release, inhibition of insulin release.

B1 - Tachycardia, increased lipolysis, increased myocardial contractility, increased release of renin.

B2 - Vasodilation, slightly decreased peripheral resistance, Bronchodilation, increased muscle & liver glycogenolysis, increased release of glucagon & relaxed uterine smooth muscle.

Question 17

What are the uses of Epinephrine, Dobutamine, Albuterol & Methylphenidate?

Answer 17

Epinephrine (Adrenaline) - A1, A2, B1, B2/ used in anaphylactic shock, or intense asthma.

Dobutamine (Debutrex) - B1/ stimulates heart congestive failure.

Albuterol (Ventolin) -B2/ Bronchodilator

Methylphenidate (Ritalin) - ADHD, appetite control

Question 18

What are the drugs to treat pheochromocytoma and benign prostatic hyperplasia? Which receptor do they act on?

Answer 18

Phenoxybenazmine (Dibenzyline)
TREATS: PHEOCHROMOCYTOMA
(A catecholamine-secreting tumor of adrenal medulla, to treat hypertensive episodes.)
-blocks both a1 & a2 andrenergic receptors causing vasodilation & lowering of blood pressure.

Doxazosin (Cardura)
TREATS: HYPERTENSION & BENIGN PROSTATE HYPERPLASIA Can cause orthostatic hypotension
-a1 blocker

Tomsulosin (Flomax)

• a1A blocker
• Relaxes smooth muscle in the urinary bladder neck & prostate; thus improving urine flow in BENIGN PROSTATE HYPERPLASIA

Question 19

What are uses & contraindications of Non-Selective B-blocker?

Answer 19

All are used in Hypertension
-Angina; Cardiac Arrythmias; M.I.; CHF; Hyperthyroidism; Glaucoma.
*Also serves as prophylaxis of migraines
(Propanolol & Sotalol)
Contraindicated in: ASTHMA

Question 20

Give examples and uses of Selective B-blockers.

Answer 20

Metoprolol – Hypertension; M.I.; Angina Pectoris

Atenolol – Same

Question 21

Give example and advantage of using Mixed a & b - blockers in the tx. of HTN.

Answer 21

Labetalol – a1, b1, and b2 blocker

• For HTN EMERGENCIES
• Preeclampsia

Carvedalol – a1, b1, and b2 blocker
- For HTN & CHF

Question 22

Why the use of B-blocker in diabetic patients should be with caution?

Answer 22

Because B-blockade leads to decreased glycogenolysis & decreased glucagon secretion. *Monitoring of glucose is essential; pronounced hypoglycemia may occur after insulin injection.

Question 23

What are the effects botulinum toxin & spider venom on acetylcholine release?

Answer 23

Inhibits acetylcholine release, nerve impulses are blocked, causing the flaccid (sagging)

Question 24

What are the effects of cocaine & Imipramine on norepinephrine reuptake?

Answer 24

They both BLOCK reuptake of norepinephrine, serotonin.

Question 25

Central Nervous System (Drugs) What are the MOA of Carbidopa, Bromocriptine, & Amantidine in Parkinson's disease?

Answer 25

Carbidopa ( MOA ): Diminishes decarboxylation of L-dopa in peripheral tissues thereby prevents its peripheral biotransformation. Decreasing required dose of L-dopa by about 75%. Amantidine ( MOA ): Enhances the synthesis, release or reuptake of dopamine from the surviving neurons. ** Also an antiviral drug effective in tx. of Influenza. Bromocriptine ( MOA ): Powerful dopamine receptor agonist that can stimulate postsynaptic dopamine receptors that are still present & functional.

Question 26

What are the MOA of Benzodiazepines & Barbiturates? | What are the withdrawal sx's of Benzos?

Answer 26

Benzodiazepines (MOA): Bind to a specific site on Neuronal GABA receptors. *This binding enhances the affinity of GABA receptors for GABA, resulting in more frequent openings of the chloride channels. *The increased influx of chloride causes increased inhibition. Withdrawal: confusion, anxiety, agitation & restlessness Barbiturates (MOA): Enhance the function of y-aminobutyric acid (GABA) in the CNS by enhancing the duration of chloride channel openings. *Hyperpolarizes the cell and causes an increase in inhibition of CNS

Question 27

What are the uses of diazepam? What is the drug which competitively antagonizes benzodiazepines; thereby reverses their sedative effects?

Answer 27

Used for: Anxiety disorders Skeletal musc. spasms/ or spasticity from digenerative disorder, such as MS and CP. Antagonist: Flumazenil: to reverse the sedative effects of benzos after aneasthesia or overdose of benzos.

Question 28

What is the MOA of local anesthetics? What are effects of epinephrine when used with local anesthetics?

Answer 28

MOA -- Local anesthetics block the sodium channels in the nerve membrane Epinephrine slows their systemic absorption.

Question 29

What are the therapeutic uses of lidocaine?

Answer 29

Lidocaine can be used in IV to treat cardiac arrythmias (ventricular tachycardia)

Question 30

Classification of antidepressant drugs. Which group is most widely used?

Answer 30

Selective Serotonin re-uptake inhibitors (SSRIs) | IE: Fluoxetine/Prozac

Question 31

What is the MOA of SSRI's? Give examples.

Answer 31

MOA: Selectively inhibit reuptake of serotonin. - Increase the concentration of norepinephrine or serotonin the synaptic cleft; by inhibiting the reuptake of neurotransmitters. - Others -- block their metabolic degradation OR incrase their release.

Question 32

What is the MOA of Tricyclic antidepresseants (first group of antidepressants discovered; but not used so much presently) & side effects?

Answer 32

MOA: Block the reuptake of biogenic amines, including norepinephrine & serotonin. Side effects: - (Anticholinergic effects) Dry mouth, constipation, urinary retention, blurred vision. -- Most common. - Weak a1 antagonist -- orthostatic hypotension/ decreased constriction. - Weak H1 antagonist -- histamine reaction/causing sedation

Question 33

What is the danger of eating tyramine-rich foods while taking MAO-inhibitors? What is the side effect of Trazodone?

Answer 33

Normally tyramine is rapidly inactivated by MAO in the gut. Those taking MAO inhibitors are unable to inactivate the tyramine; this can lead to a fatal hypertensive crisis. The tyramine causes release of norepinephrine, which can lead to an increase of BP & cardiac arrhythmias. Effects of Trazodone: Can cause priaprism in males-- penis tissue may die.

Question 34

What are the use, precautions & adverse effects of Lithium?

Answer 34

Uses: bipolar d/o - Low therapeutic index/ must have blood monitored if with chronic use. - Associated with contraction of hypothyroidism & nephrogenic diabetes insipidus ( ADH is not functioning resulting in less retention of water in the kidneys causing increased frequency/copious urine output.

Question 35

What are the two classes of neuroleptics? Which class does reduce both negative & positive sx's of schizophrenia?

Answer 35

Typical: Block dopamine, muscarinic cholinergic, a-adrenergic, & H1 histaminergic receptors. *Dopamine antagonism produces antipsychotic effect*. Note: -A decrease in Dopamine cause an increase in Prolactin. -With prolonged use can cause EXTRAPYRAMIDAL effects

Question 36

What are EXTRAPYRAMIDAL effects of typical neuroleptics/what are presentations of each?

Answer 36

Dystonia: spasms of the muscles of the face, tongue, neck & back Akathisia: motor restlessness Tardive dyskenasia: Stereotyped voluntary mov'ts. such as lip smacking, jaw mov'ts., darting of the tongue. Parkinsonism; tremor, rigidity & shuffling gait Neuroleptic Malignant Syndrome: Catatonia, rigidity, stupor, fluctuating BP, fever & dysarthria

Question 37

Uses of Chlorpromazine & Haloperidol?

Answer 37

Chlorpromazine: *Schizophrenia Also used for: Nausea, vomiting & Hiccoughs Haloperidol: Schizophrenia Also used for: Tourette's syndrome, & Huntington's disease

Question 38

What are the advantages of using atypical antiphycotics/What are the adverse effects & precautions while Clozapine?

Answer 38

Atypical use: Reduce both the negative & positive symptoms of schizophrenia, while causing a minimum pyramidal side effects. Clozapine: Can cause severe agranulocytosis (increase of infection). Should have WBC count checked on a weekly basis.

Question 39

Neuroleptic Malignant Syndrome--Symptoms & Treatments

Answer 39

A rare potentially fatal neurologic side effect of antipsychotic medication. Causing catatonia, rigidity, stupor, fluctuating BP, fever, dysarthria.

Question 40

Define narcotics. Classify them. What is the danger of using mixed group while withdrawn from a strong agonist?`

Answer 40

- Opiate drugs that act on specific receptors in the CNS to reduce perception of pain. * Act upon 3 receptors: * *Mu (mostly), Kappa, & Delta - Strong Agonists: All work on the Mu receptor Common ==> (Morphine - MI or Renal Pain) - Weak Agonists: Codeine ==> used for suppressing cough & pain. *Less potent than morphine -Mixed Agonists/Antagonists: They are agonist at the *Kappa receptor (giving them analgesic activity) And are antagonist at the *Mu receptor ** Using mixed group in patients that were on strong agonists or morphine can cause acute withdrawal!!

Question 41

Drug for Narcotic Overdose?

Answer 41

Naloxone (Narcan)

Question 42

What are the actions of Morphine on CNS, Eye, Respiration, Cardiovas. GI & GU systems? What are the withdrawal symptoms of narcotics?

Answer 42

CNS: Drowsiness & Sedation Eyes: Pupillary constriction by direct action on the brain nucleus of the oculomotor nerve (Pinpoint Pupil) Resp.: Resp. depression by direct action on the CNS *Can cause death in high doses. CV: No Effect GI: Increased resting tone of the smooth musc.; resulting in decrease mov't. of stomach & intestinal contents leading to spasm & constipation. GU: Increases the tone & produces spasm of the smooth musc. in GU tract; leading to urinary retension. **Withdrawal ==> (Autonomic hyperactivity) Diarrhea, vomiting, chills, fever, tearing, runny nose, tremor, abd. cramps -pain can be severe.

Question 43

MOA & adverse effects of Phenytoin?

Answer 43

MOA: Blocks voltage gated sodium channels by selectively binding to the channel. Adverse Effects: Gingival Hypertrophy & megaloblastic anemia (low Vit B12 or Folic Acid)

Question 44

Drugs For: Tonic-Clonic, Absence, Myoclonic, Febrile Seizures, & Status Epilepticus?

Answer 44

``` T/CL : Phenytoin; Carbamazepine Abs: Ethsuximide Myo: Valproic Acid Feb. Seiz: Diazepam Status Epilep: Phenytoin; Diazepam ```

Question 45

What is the MOA of H2-receptor antagonist on GI Tract? Give examples.

Answer 45

Prevents histamine-induced acid release by blocking H2 receptors: Cimetidine(Tagamet): inhibits cytochrome P-450 thereby causing an increased conc. of Warfarin, Theophline, Phenytoin, Diazepam, Propranolol etc. Ranitidine(Zantac): Less inhibition of P-450 Famotidine(Pepcid): No inhibition of P-450

Question 46

What is the MOA of Proton Pump Inhibitor on GI tract? Give Examples.

Answer 46

Inhibit H+ -K+ ATPase enzyme (Proton Pump) of the parietal cell thereby suppressing secretion of hydrogen ions into the gastric lumen. *Reduces acid production TREATS: GERD, Duodenal ulcer, & hypersecretory states. *Omeprazole (Prilosec) *Lansoprazole (Prevacid)

Question 47

Use of Misoprostol? Adverse Effect?

Answer 47

Increases HCO3- & mucin release. Reduces acid secretion used for prevention of ulcers caused by aspirin & other NSAIDs. Adverse Effect: Abortion(uterine contraction); diarrehea

Question 48

``` What are mechanism of antidiarrheal actions of Diphenoxylate with Atropine & of Bismuth Subsalicylate? Bismuth Subsalicylate (Pepto) ? ```

Answer 48

Diphenoxylate w/Atropine: - Diphenoxylate is an agonist at opiate receptors in GI tract & Atropine blocks muscarinic receptors. Both actions inhibit peristalsis. INDICATION: Diarrhea Bismuth Subsalicylate: -Decreases flow of fluids & electrolytes into the bowel, reduces inflammation within the intestine, may kill the organisms that can cause diarrhea.

Question 49

List important drugs used in the tx. of Ulcerative Colitis & Crohn's disease.

Answer 49

_Steroids & Anti-inflammatory Drugs_ Mesalamine (5- aminosalicylic Acid) Sulfasalazine *Infliximab -- A monoclonal antibody that binds to & inhibits TNF-a, a proinflammatory protein produced by immune cells. Used to treat moderate to severe Crohn's Disease that is refractory to other medical tx.' also used to treat rheumatoid arthritis.

Question 50

MOA of Infliximab?

Answer 50

*Infliximab -- A monoclonal antibody that binds to & inhibits TNF-a, a proinflammatory protein produced by immune cells. Used to treat moderate to severe Crohn's Disease that is refractory to other medical tx.' also used to treat rheumatoid arthritis.

Question 51

Important laxatives & cathartics? MOA of Lactulose?

Answer 51

Bulk forming agents: Psyllium- nondigested plant cellwall absorbs water into feces. Stimulant laxative & cathartics: Bisacodyl (Dulcolax) Increases water & electrolytes in feces & increases intestinal motility. Sorbitol -- Same MOA Lactulose: Hyperosmolarity draws water into colon *Good for Pt. w/severe Lv disease

Question 52

List Antiemetic drugs. What are the MOA & examples of serotonin antagonist?

Answer 52

Meclizine (Antivert) Chlorpromazine (Thorazine) Methylprednisolone (Medrol) ** Dolasetron (Anzemet): Serotonin antagonist inhibiting the action of serotonin at the 5-HT3 receptor in the small bowel, vagus nerve, & chemoreceptor trigger zone.