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PA > Unit 1 Pharm Final > Flashcards

Unit 1 Pharm Final Flashcards

1
Q

Name the two types of primary ligands.

A

Agonists and antagonists.

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2
Q

A ligand that binds a receptor and activates it.

A

Agonist

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3
Q

A ligand that binds a receptor and produces no response.

A

Antagonists

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4
Q

Name the three types of agonists ligands.

A

Full Agonist
Partial Agonist
Inverse Agonist

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5
Q

Name the two types of antagonist ligands.

A

Competitive

non-competitive

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6
Q

This ligand binds to a receptor and produces a response opposite of the agonist.

A

Inverse agonist

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7
Q

Which antagonist is non-reversible, competitive or non-competitive? Why?

A

Non-competitive is non-reversible due to covalent bonds.

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8
Q

What are the three ways receptors are classified? Which one is the most common?

A
  • according to the ligand with which they interact (most common)
  • Signal Transduction mechanism
  • Cellular Location
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9
Q

Which receptor acts the fastest?

a) ligand gated channels-ionotropic
b) G-protein coupled receptors
c) Nuclear Receptors

A

Ligand gated channels - ionotropic

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10
Q

Name at least two receptor binding forces.

A
  • Ionic
  • Hydrogen
  • Hydrophobic
  • Van der Waals Forces
  • Covalent
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11
Q

Define Efficacy.

A

The ability of a drug to produce a cellular effect.

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12
Q

The amount of drug required to produce an effect is referred to as what?

A

Potency

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13
Q

The region between median lethal dose (LD50) and median effective dose (ED50) is called the?

A

Therapeutic Index

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14
Q

A patient takes an oral medication, the medication goes to the gut, into the hepatic portal vein, and then metabolized by the liver before entering systemic circulation.

This process reduces the effectiveness of the medication and is called what?

A

The First Pass Effect

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15
Q

Name at least two routes of drug administration that bypass the first pass effect.

A
  • Sublingual
  • IV
  • SQ
  • IM
  • Intrathecal
  • Intraperitoneal
  • IO
  • Inhalation
  • Topical
  • Transdermal
  • Transmucosal
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16
Q

Drugs administered rectally roughly bypass the first pass effect by how much?

A

About 50%

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17
Q

Define Bioavailability.

A

Fraction of the administered drug dose that reaches systemic circulation in active form.

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18
Q

What is the equation for bioavailability?

A

BA = AUC oral / AUC iv X 100

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19
Q

Cytochrome P450 3A4 or CYP 3A4 is inhibited by what acidic fruit / juice?

A

Grapefruit Juice

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20
Q

The majority of metabolism from CYP P450 occurs with which sub-enzyme?

A

CYP 3A4 (~50%)

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21
Q

Phenobarbital, rifampin, phenytoin, carbamazepine, and St. John’s Wart are all inducers of what?

A

CYP P450

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22
Q

Name at least one CYP P450 inhibitor.

A
  • Cimetidine
  • Ketoconazole
  • Ritonavir
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23
Q

Volume of fluid in which drug dose dissolved to have the same concentration as it does in the plasma is called what?

A

Volume of Distribution

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24
Q

What is the formula for Volume of Distribution?

A

Vd = Q(amount of drug in the body) / Cp (pasma concentration

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25
Q

Volume of distribution X Plasma Concentration = ?

This is the formula for what?

A

Dose

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26
Q

What types of comounds affect volume of distribution?

A

Weak bases

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27
Q

Volume of distribution is affected by Ion trapping, this leads to a drug being highly concentrated within the cell and less concentrated in the plasma.

Define Ion Trapping.

A

Ion Trapping: weak bases are less ionized in the plasma but become ionized inside the cells which leads to them being trapped.

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28
Q

When distribution is limited to a specific compartment, you would expect the volume of distribution to increase or decrease?

A

Decrease

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29
Q

Volume of distribution X Plasma Concentration (desired) = ?

This is the formula for?

A

Loading Dose

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30
Q

How many half-lifes does it take to reach steady state?

A

5 Half-lifes

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31
Q

Define steady state.

A

Steady state is when the rate of elimination = the rate of administration.

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32
Q

Plasma protein binding affects the distribution of a drug.

Acidic drugs interact with?
Basic drugs interact with?

A

Acidic drugs interact with Albumin

Basic drugs interact with glycoproteins and B-globulins

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33
Q

How do you change / affect plasma protein binding?

A

Add another drug, add competition for binding.

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34
Q

A drug with a low pKa will absorb in what kind of solution?

A drug with a high pKa?

A

Low pKa = low pH = absorption in acidic solution

High pKa = high pH = absorption in alkaline solution

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35
Q

What is the importance of knowing the half-life?

A

Important for achieving steady state. Which is 5x the half-life

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36
Q

T1/2 = 0.693/ke is the equation for?

A

Half-life

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37
Q

Explain the process of NSAID related to systemic PUD.

A

NSAIDs inhibit COX, this decreases prostaglandins, which causes an increase in gastric acid and a decrease in bicarbonate, mucous, and blood flow.

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38
Q

When NSAIDs are trapped in gastric epithelial cells this is referred to as what kind of PUD?

A

Topical related PUD

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39
Q

What do G cells secrete?

A

Gastrin

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40
Q

Somatosatin is released from what kind of cell?

A

D cells (usually from the GI mucosa)

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41
Q

How do you diagnose an H. pylori infection?

A

Urea Breath Test

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42
Q

Describe the two treatment options for an H. pylori infection.

A
  1. Bismuth-based Quadruple Therapy
    - Bismuth Subsalicylate
    - Metronidazole
    - Tetracycline
    - PPI
  2. Clarithromyacin-base Quadruple Therapy
    - Amoxicillan
    - Clarithromycin
    - Metronidzaole
    - PPI
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43
Q

What are the protective properties of somatostatin?

A
  • stimulates mucus secretion
  • stimulates bicarbonate release
  • decreases acid secretion (gastric acid / HCl)
  • Increases mucosal blood flow
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44
Q
  • Continued chest pain
  • dysphagia
  • odynophagia
  • unexplained weight loss
  • choking

These would be alarming symptoms for what common GI disorder?

A

Gastroesophageal Relux Disease (GERD)

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45
Q

What is the common suffix seen to help identify a medication as a proton pump inhibitor?

A

“PRAZOLE” or “RAZOLE”

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46
Q

What is the mechanism of action (MOA) for a PPI?

A

Binds to and irreversibly inactivates the H+/K+ ATPase channel in gastric parietal cells to inhibit gastric acid secretion.

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47
Q

What must be active in order for a PPI medication to function properly?

A

The H+/K+ ATPase pumps must be active for a PPI to bind to and inactivate.

48
Q

Why should you not take omeprazole with clopidogrel (plavix)?

A

Omeprazole inhibits the CYP enzyme that allows Plavix to be active.

49
Q

List the short term adverse effects of a PPI medication.

A
  • Nausea
  • Vomiting
  • Abdominal Pain
  • Constipation
  • Diarrhea
  • Flatulence
50
Q

What are the more serious, long term adverse effects of a PPI medication?

A
  • Block B12 absorption
  • Osteoporosis (interferes with Ca2+ absorption)
  • Infection (C. Diff = most common)
  • Carcinoid Tumor (ECL Hyperplasia)
  • Possible malabsorption of magnesium
51
Q

PPI’s are considered pregnancy category B, except for one. What is that medication and what is the category?

A

Omeprazole - Category C

52
Q

What is the identifying suffix for Histamine Receptor Antagonists (H2RAs)

A

“TIDINES”

53
Q

What is the MOA of a H2RA medication?

A

Block the histamine receptors on the parietal cells leading to decreased acid secretion.

54
Q

Which H2RA medication is know for having an interaction with other medications which increases the pH level and alters the absorption of other medications?

A

Cimetidine

55
Q

What is the H2RA medication Rob has referred to as being the “shitty one”? Why is that?

A

Cimetidine - causes gynecomastia and CYP inhibition

56
Q

What are some side effects of H2RA medications?

A
  • mental status change (elderly), hallucinations, and confusion
  • Decreased effectiveness over time
  • rebound acid secretion with discontinuation
57
Q

H2RA medications belong to what pregnancy category?

A

B

58
Q

Which antacid should not be used in pregnancy?

A

Sodium Bicarbonate (alka seltzer, baking soda) - causes metabolic alkalosis

59
Q

Mylanta and Maalox (Aluminum and Magnesium hydroxides), What are some adverse side effects with these medications?

A

Magnesium - causes diarrhea sx
Aluminum - causes constipation sx

These medications can cause hypermagnesemia and hypophosphatemia

60
Q

What are some side effects of Calcium Carbonate?

A
  • Constipation

- Metabolic Alkalosis

61
Q

What is the MOA of Antacids?

A

Medications are inorganic bases that chemically neutralize the acid in the stomach leading to an overall increased pH.

62
Q

List three different cytoprotective medications.

A
  • Sucralfate (carafate)
  • Misoprostol (cytotec)
  • Bismuth Subslicylate (Pepto Bismol)
63
Q

What is the MOA of sucralfate?

A

Adheres to the ulcer craters.

64
Q

When should Sucralfate be taken?

A

2 hours before a meal

65
Q

What are some adverse side effects of Sucralfate?

A
  • Renal insufficiency
  • constipation
  • laryngospasms
66
Q

What is the MOA of misoprostol?

A

Prostaglandin E1 analog, used for NSAID PUD.

67
Q

What is the black box warning for misoprostol?

A

Pregnancy warning, can cause premature uterine contractions.

68
Q

What is the MOA and unique adverse effect of Bismuth Subsalicylate?

A

MOA - coats and protects ulcer craters

Adverse Effect - causes black colored stools

69
Q

What is the MOA of Muscarinic Antagonist drugs?

A

Anti-spasmodic medications

70
Q

What is the MOA of metoclopramide?

A

Blocks dopamine (D2) receptors to prevent relaxation of GI smooth muscle, this increases propulsive activity, tone, and motility. This also accelerates gastric emptying.

71
Q

What are three adverse effects of metoclopramide?

A
  • Gynecomastia
  • Restlessness
  • Parkinsonism
72
Q

What are the contraindications for metoclopramide?

A
  • Seizure disorders
  • Pheochromocytoma
  • GI Hemorrhage
73
Q

What is the black box warning for metoclopramide?

A

Tardive Dyskinesia (risk increases with treatment duration)

74
Q

Name the different types of laxatives.

A
  • Bulk forming
  • Surfactants
  • Osmotic Laxatives
  • Stimulant Laxatives
  • Lubiprostone
75
Q

What is the MOA for bulk forming laxatives?

A

Indigestible hydrophilic material that absorbs H2O in the lumen.

76
Q

Surfactants are more commonly referred to as what?

A

Stool Softeners

77
Q

MOA of action for surfactants?

A

Incorporate H2O into fatty intestinal material

78
Q

MOA of osmoitc laxatives?

A

Retain water in lumen, which leads to increased lumen pressure, and peristalsis.

79
Q

MOA of stimulant laxatives?

A

Act directly on the intestinal mucosa, leading to altered fluid secretion and stimulated peristalsis.

80
Q

Lubiprostone MOA is what?

A

Secretes Cl- into the lumen to increase motility.

81
Q

What are the antidiarrheal agents?

A
  • opioids
  • locally acting
  • alosetron
82
Q

What is the MOA for opioid antidiarrheal?

A

Opioid receptors leading to sustained segmental contraction of smooth muscle.

83
Q

What is the MOA of 5HT3 Serotonin Receptor Blockers?

A

Block 5HT3 receptors which prevents peripheral and central stimulation of the vomiting pathway.

84
Q

Name the different types of hypertension medications.

A
  • Thiazide Type Diuretics
  • Loop Diuretics
  • Potassium Sparring Diuretics
  • ACE-I
  • Angiotensin Receptor Blockers
  • Aliskiren
  • Calcium Channel Blockers
  • Reserpine
  • Guanethidine
  • Alpha 1 Selective Blockers
  • Beta Adrenergic Blockers
  • Centrally Acting Antihypertensives
  • Direct Acting Vasodilators
85
Q

Which HTN medications are contraindicated in pregnancy?

A
  • ACE-I
  • ARBS
  • Aliskiren
86
Q

What are the electrolyte effects with Thiazide Type Diuretics?

A
  • Hypokalemia
  • Hypomagnesemia
  • Hypercalcemia
  • Hyperuricemia
  • Hyperglycemia
87
Q

What are the electrolyte effects with Loop Diuretics?

A
  • Hypokalemia
  • Hyponatremia
  • Hypomagnesemia
  • Hypocalcemia
  • Hyperuricemia
  • Hyperglycemia
88
Q

What are the electrolyte effects with Potassium Sparring Diuretics?

A
  • Hyperkalemia

- Hyponatremia

89
Q

What are the electrolyte effects with ACE-I?

A
  • Hyperkalemia
90
Q

What are the electrolyte effects with ARBs?

A
  • Hyperkalemia
91
Q

What is the MOA of an ACE-I?

A

Stop angiotensin I from converting into angiotensin II and therefore prevent downstream effects of vasodilation from aldosterone.

Also blocks bradykinin, which leads to a dry cough and angioedema.

92
Q

What are the adverse effects of ACE-I?

A
  • Hyperkalemia
  • Dry Cough
  • Angioedema
  • Acute Kidney Failure
  • Serum Lithium
93
Q

Contraindications of ACE-I?

A

Bilateral renal stenosis and pregnancy.

94
Q

What is the MOA of B-Blockers?

A

Decreases CO, renin release, and systemic vascular resistance by decreasing sympathetic discharge.

95
Q

What is the identifying suffix for B-blockers?

A

“OLOL”

96
Q

What are the contraindications of B-Blockers?

A
  • Heart block
  • Bradycardia
  • COPD
  • Asthma
97
Q

What HTN medications do not work as well in black patients?

A
  • B-blockers
98
Q

What HTN medication works better in black patients?

A
  • Hydralazine
99
Q

What is a side effect of alpha-1-selective blockers?

A

Orthostatic hypotension

100
Q

Compare ACEI and ARBs

A
  • Equal efficacy, cardio and renoprotectivity
  • 1st HTN drugs
  • Lower cough and angioedema with ARBs (better tolerated)
  • Contraindications are the same, no pregnancy and no bilateral renal stenosis
  • Both have short and long half-life options
  • ARB are more expensive.
101
Q

First line HTN treatment for non-black patients

A
  • Thiazide-type diuretic
  • Calcium Channel Blocker
  • Angiotensin-Converting Enzyme Inhibitor (ACEI)
  • Angiotensin Receptor Blocker (ARB)
102
Q

First Line HTN treatment for general black population

A

Thiazide-type or CCB

103
Q

First line HTN treatment for black patient with diabetes.

A

Thiazide-type or CCB

104
Q

First line HTN treatment for chronic kidney disease population

A
  • ACE-I

- ARB

105
Q

Vasodilator causes tachycardia, what drug can counter this effect?

A

B-blocker

106
Q

Why is HDL good?

A

Reverse cholesterol transport and vaso-protective

107
Q

What is LDL bad?

A

Increases risk of atherosclerosis and oxidizes to make foam cells.

108
Q

What is the MOA of STATINs?

A

Inhibits HMG-CoA Reductase competitively and decreases cholesterol pool. The liver will make more LDL receptors to compensate, and will increase LDL removal.

109
Q

What are some side-effects of HMG-CoA inhibitors?

A
  • increases LFTs
  • Increases Creatine Kinase
  • Muscle pain (rhabdo)
  • Cognitive impairment
  • Increases blood glucoseST
110
Q

Statin monitoring?

A

Liver enzymes and creatine kinase

111
Q

When should a statin be taken?

A

Taken at night except those with long half-lives (atorvastatin, pitavastatin, rosuvastatin)

112
Q

What is the CYP metabolism for different statin drugs?

A

CYP 3A4 = lovastatin, simvastatin, atorvastatin

CYP 2C9 = Fluvostatin and Rosuvastatin

113
Q

Niacin causes facial flusiing what should be given to reverse this effect?

A

Aspirin 30 minutes before taking niacin.

114
Q

What are the 5 rights?

A
  • Right Drug
  • Right Dose
  • Right Route
  • Right Patient
  • Right TIme
115
Q

What does Rx mean?

A

Rx = Latin for recipe - proceeds physician recipe for prescribing medication

116
Q

What does Sig mean?

A

Sig = used on Rx blanks to mark directions

117
Q

What makes up the different parts of a prescription?

A
  • Superscripts: date, name, address, weight, age, and RX
  • Inscription: drug anem, strength/conc., or the name and amount of each ingredient to be compounded
  • Subscription: pharmacists instructions
  • Signatura: instructions to the patient
  • Name and signature of the prescriber

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