Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharma > EXAM 2 Drugs > Flashcards

EXAM 2 Drugs Flashcards

1
Q

Metformin (Glucophage) Biguanides MOA

A

Decreases glucose production in the liver (gluconeogenesis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Metformin (Glucophage) Biguanides

TU:

A

Type 2 diabetes(considered drug of choice for initial therapy); prevention of Type 2 diabetes
in high risk patients; gestational diabetes; polycystic ovary syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Metformin (Glucophage) Biguanides

AD:

A

Decreased appetite, nausea, diarrhea, weight loss (average 7 to 8 lbs – may
be an added benefit of this drug), decreased absorption of vitamin B12 & folic
acid. Rarely lactic acidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Glipizide (Glipizide) Sulonylurea MOA

A
  • Primary: Stimulate the pancreatic β-cells to release insulin.
  • Secondary: Enhances the cellular sensitivity to the insulin (makes the insulin work better)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glipizide (Glipizide) Sulonylurea TU

A

• Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Glipizide (Glipizide) Sulonylurea AD

A

Can cause hypoglycemia; weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Repaglinide (Prandin) Meglitinides MOA

A

Primary: Stimulate the pancreatic β-cells to release insulin.
• Similar chemical structure and mechanism of action to sulfonylureas. Considered
alternatives to sulfonylureas. Do not give WITH sulfonylureas – they are too similar.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Repaglinide (Prandin) Meglitinides TU

A

Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Repaglinide (Prandin) Meglitinides AD

A

Can cause hypoglycemia; weight gain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pioglitazone (Actos) TZD MOA

A

Primary: Decreases insulin resistance. Increases the sensitivity to insulin in muscle, liver,
and fat cells. “Insulin sensitizers”
• Activates the peroxisome proliferators-activated receptor gamma (PPAR-gamma) receptors.
Basically it turns on insulin-responsive genes that help regulate carbohydrate and lipid
metabolism; increasing insulin sensitivity. This takes several weeks for benefits to be seen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pioglitazone (Actos) TZD TU

A

Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pioglitazone (Actos) TZD AD

A

• Can cause fluid retention, edema (precaution against use in mild HF & contraindicated in
severe HF). May cause resumption of ovulation in pts taking oral contraceptives. Raises HDL
and lowers triglycerides, which are good, but may also raise LDL. Probably NOT hepatotoxic
but liver function tests may still be monitored.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Canagliflozin (Invokana) SGLT-2 inhibitor MOA

A

Inhibit the enzyme α-glucosidase in the small intestine. This enzyme normally turns dietary
starch & sucrose into an absorbable form. Cause delayed glucose absorption. Decreased
post-prandial blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Canagliflozin (Invokana) SGLT-2 inhibitor TU

A

Type 2 diabetes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Canagliflozin (Invokana) SGLT-2 inhibitor AE

A

Oral absorption is minimal, so adverse effects are mostly GI related; fermentation (50%)
leads to flatulence, cramps, abdominal distention, borborygmus (rumbling bowel sounds), &
diarrhea. Liver dysfunction may be a concern with long-term, high dose therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sitagliptin (Januvia) DPP-4 inhibitors MOA

A

Glucose is filtered in the kidneys and then reabsorbed back into the
blood. Sodium-glucose transporter 2 (SGLT-2) is primarily the transporter (or pump) that is
responsible for reabsorbing the glucose back in to the blood. By blocking SGLT-2 less glucose
is reabsorbed and is excreted in the urine thereby reducing blood glucose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sitagliptin (Januvia) DPP-4 inhibitors TU

A

Type 2 Diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Sitagliptin (Januvia) DPP-4 inhibitors AE

A

genital yeast infections, urinary tract infections, increased urination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Exenatide (Byetta) Incretin mimetic MOA

A

Synthetic version of glucagon-like peptide-1 (GLP-1); normally, GLP-1 is released from cells
in the GI tract after a meal. GLP-1 increases insulin release and reduces production of
glucose by the liver as well as slows gastric emptying and suppresses appetite.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Exenatide (Byetta) Incretin mimetic TU

A

Type 2 diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Exenatide (Byetta) Incretin mimetic AE

A

Hypoglycemia (14 – 35%), nausea (45%), diarrhea (13%), feeling jittery (9%). Reduce dose of
oral medications when starting to avoid hypoglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the Duration and Onset of: Lispro Insulin (Humalog)

A

Duration: 2-4 hrs
Onset: 10-30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the Duration and Onset of: Aspart Insulin (Novolog)

A

Duration: 2-4 hrs
Onset: 10-30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the Duration and Onset of: Glulisine Insulin (Apidra)

A

Duration: 2-4 hrs
Onset: 10-30 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the Duration and Onset of: Regular Insulin (HumulinR, Novolin R)

A

Duration: 6-10 hrs
Onset: 30-60 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the Duration and Onset of: NPH (Humulin N, Novolin N)

A

Duration: 12-18 hrs
Onset: 60-120 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the Duration and Onset of: Detemir Insulin (Levemir)

A

Duration: up to 24 hours
Onset: 60-120 mins

28
Q

What is the Duration and Onset of: Glargine Insulin (Lantus)

A

Duration: longer than 24 hours
Onset: 70 mins

29
Q

What are the SSRI drugs

A 
Escitalopram (Lexapro) SSRI
Fluoxetine (Prozac) SSRI
Sertraline (Zoloft) SSRI\
Paroxetine (Paxil) SSRI
Citalopram (Celexa) SSRI

Effective For Sadness Panic Compulsion

30
Q

What are the MOA and AE of SSRI

A

MOA: inhibits reuptake of serotonin in the CNS nerve terminals

AE: Stomach upset, sexual dysfunction, serotonin syndrome, suicidal thoughts

31
Q

What are the SNRI Drugs

A

Duloxetine (Cymbalta) SNRI
Venlafaxine (Effexor) SNR

Vexed and Depressed

32
Q

What are the MOA and AE of SNRI

A

MOA: • SNRI’s inhibit the reuptake of serotonin and norepinephrine into CNS nerve terminals causing
an increase in serotonin and norepinephrine concentrations in the CNS

AE: insomnia, nervousness, dry mouth, anorexia, mild CV effects, sexual dysfunction,
sweating, HTN

BAD SNRI
Body weight, Anorexia, Decrease blood pressure, Suicidal thoughts, Nausea, Reproductive, Insomnia

33
Q

What are the TCA drugs

A

Amitriptyline (Elavil) TCA

Nortriptyline (Pamelor) TCA

34
Q

What are the TCA drugs MOA and AE

A

MOA: TCAs inhibit reuptake of norepinephrine and serotonin into CNS nerve terminals.
• Thus, TCAs initially increase concentrations of these neurotransmitters in the CNS
TCAs: Tachycardia, Cardiac effects, Anticholinergic effects, sexual dysfunction
AE:
• Weight gain, sexual dysfunction
• Anticholinergic side effects: Blockade of acetylcholine at the muscarinic receptors can cause
dry mouth, blurred vision, urinary retention, constipation, tachycardia, and confusion.
• Cardiovascular: increased adrenergic activity (they increase norepinephrine levels) can result in cardiac overstimulation, which can be life threatening in an overdose situation.
• Antihistamine side effects: Blockade of histamine at the H1-receptors in the CNS can cause sedation & drowsiness (Some tolerance may develop to this side effect.)
• α1-blockade: orthostatic hypotension ⇒ increased risk of falls in the elderly.
• Seizures: Lowers seizure threshold.

35
Q

What are the MOA-inhibitors MOA and AE

A

MOA: Inhibit both of the enzymes, monoamine-oxidase-A (MAO-A) & monoamine-oxidase-B (MAO-B).
• The monoamine-oxidase enzymes are present in the liver, intestines, and in some nerve terminals.

AE: Orthostatic hypotension, dizziness, sexual dysfunction, sleep disturbance

36
Q

What are the benzodiazepines drugs?

A

Diazepam (Valium) Benzodiazepine
Lorazepam (Ativan) Benzodiazepine
Alprazolam (Xanax) Benzodiazepine
Temazepam (Restoril) Benzodiazepine

sleep drugs

37
Q

What are the MOA of Benzodiazepines drugs

A

Mechanism of Action
• Enhances the actions & binding of gamma-aminobutyric acid (GABA) to its CNS binding sites.
• GABA is an inhibitory CNS neurotransmitter that inhibits neuronal activity

38
Q

What are the TU of Benzodiazepines drugs

A
  • Anxiolytic – Reduces anxiety.
  • Insomnia, sedative/hypnotic (sleeping pill) – Do not use benzodiazepines with long half-lives, especially in the elderly. Use sleeping pills for short term treatment of insomnia only.
  • Seizure disorders – (diazepam, lorazepam) – Quick onset. Drugs of choice for status epilepticus.
  • Alcohol withdrawal – (lorazepam, chlordiazepoxide) – Lessen de-toxification symptoms.
  • Muscle spasm – (diazepam) – Relax the skeletal muscle spasticity by actions on the spinal cord.
39
Q

What are the AE of Benzodiazepines drugs

A
  • CNS depression: drowsiness, confusion, hangover feeling with agents with long half-lives.
  • Respiratory depression: especially if combined with other drugs that cause respiratory depression such as alcohol, opioids, and barbiturates.
  • Anterograde amnesia (forgetfulness): especially midazolam & triazolam.
  • Sleep-walking: Engaging in activities while not fully awake with no memory of the event (e.g. walking, eating, driving, etc.). This can obviously be very dangerous.
  • Abuse: Schedule IV controlled substance; some addiction potential exists.
  • Physical dependence / Withdrawal symptoms: Withdrawal symptoms include anxiety, insomnia, panic, sweating, tremors, agitation, HTN, muscle twitching, & fatal SEIZURES.
40
Q

What are the MOA of Benzodiazepines like drugs: Z Drug

A

*Zolpidem (Ambien®, Ambien Cr®)

Mechanism of Action
• Enhances the actions & binding of gamma-aminobutyric acid (GABA) to its CNS binding sites.
• GABA is an inhibitory CNS neurotransmitter that inhibits neuronal activity

41
Q

What are the TU of Benzodiazepines like drugs: Z Drug

A

*Zolpidem (Ambien®, Ambien Cr®)

  • Anxiolytic – Reduces anxiety.
  • Insomnia, sedative/hypnotic (sleeping pill) – Do not use benzodiazepines with long half-lives, especially in the elderly. Use sleeping pills for short term treatment of insomnia only.
  • Seizure disorders – (diazepam, lorazepam) – Quick onset. Drugs of choice for status epilepticus.
  • Alcohol withdrawal – (lorazepam, chlordiazepoxide) – Lessen de-toxification symptoms.
  • Muscle spasm – (diazepam) – Relax the skeletal muscle spasticity by actions on the spinal cord.
42
Q

What are the AE of Benzodiazepines like drugs: Z Drug

A

*Zolpidem (Ambien®, Ambien Cr®)

  • CNS depression: drowsiness, confusion, hangover feeling with agents with long half-lives.
  • Respiratory depression: especially if combined with other drugs that cause respiratory depression such as alcohol, opioids, and barbiturates.
  • Anterograde amnesia (forgetfulness): especially midazolam & triazolam.
  • Sleep-walking: Engaging in activities while not fully awake with no memory of the event (e.g. walking, eating, driving, etc.). This can obviously be very dangerous.
  • Abuse: Schedule IV controlled substance; some addiction potential exists.
  • Physical dependence / Withdrawal symptoms: Withdrawal symptoms include anxiety, insomnia, panic, sweating, tremors, agitation, HTN, muscle twitching, & fatal SEIZURES.
43
Q

What is the Benzodiazepine overdose antidote?

A

Flumazenil (Romazicon)

44
Q

What are the other sleep aids?

A

Diphenhydramine (Benadryl) Sleep aid
Sedating antihistamine; tolerance develops with routine use; strong anticholinergic side
effects

Buspirone (Buspar) Antianxiety
Mechanism of action is unclear but probably affects serotonin. Initial response in 1 – 3 weeks
• Advantages: no sedation, no abuse potential, no potentiation of other CNS agents
• Disadvantage: anxiolytic effects take many weeks to many months to develop fully

45
Q

What is the MOA of the 1st gen antipsychotics?

A

Haloperidol (Haldol) 1st gen

Block dopamine receptors (mainly D2) in certain areas of the brain.

46
Q

What is the MOA of the 2nd gen antipsychotics?

A

Risperidone (Risperidone) 2nd gen
Quetiapine (Seroquel) 2nd gen
Clozapine (Clozaril)

Block serotonin & dopamine receptors.
• The main differences between the 1st and 2nd generation antipsychotics are:
− 2nd generation agents generally block serotonin receptors and D1-receptors more than D2-receptors, thus they have a much lower risk of causing extrapyramidal side effects.
− Some 2nd generation agents may relieve negative symptoms of psychosis better than 1st
generation agents.

47
Q

Describe the mechanism of action of levodopa & carbidopa & why they are always used together.

A
  • Gold standard treatment
  • Levodopa is a metabolic precursor of dopamine.
  • Dopaminergic neurons convert levodopa to dopamine in the CNS. A certain level of active neurons must still be present to adequately convert the drug to active form

A large amount of levodopa is converted to dopamine before it is able to cross the blood brain barrier.

Carbidopa is a drug given with levodopa to prevent or block this conversion. It inhibits the enzyme, dopa decarboxylase. Carbidopa itself does not cross the blood brain barrier &
therefore does not inhibit the conversion of levodpa to dopamine in the CNS.

48
Q

What are the other parkinson’s disease meds?

A

Pramipexole (Mirapex) Dopamine Receptor Agonist
Entacapone (Comtan) COMT-inhibitor
Rasagiline (Azilect) Monoamine Oxidase-B inhibitor
Benztropine (Cogentin) Anticolinergic medication

49
Q

What are the anti-epilepsy drugs? (8)

A

a. Phenobarbital
b. Phenytoin
c. Carbamazepine
d. Valproic Acid
e. Fosphenytoin
f. Levetiracetam
g. Lamotrigine
h. Gabapentin

50
Q

What are MOA of the Mast cell stabilizer drug?

A

Cromolyn

Stabilized the mast cell membrane, thus preventing the release of inflammatory mediators stored in them

51
Q

What are TU of the Mast cell stabilizer drug?

A

Therapeutic Use
• Severe Acute Asthma: Not effective; once the mast cells release their contents, it is too late.
• Chronic Asthma: Considered alternatives or adjunct to inhaled corticosteroids; less effective than corticosteroids. May be used in Step 2 chronic asthma in fixed doses to reduce frequency and severity of attacks. May reduce inhaled corticosteroid requirements when used in combination.
• Exercise-Induced Bronchospasm: Considered an alternative treatment option; less effective than a β2-agonist.
• COPD: Currently, no role

52
Q

What are AE of the Mast cell stabilizer drug?

A

Excellent safety profiles: cough, bad taste, and headache.

53
Q

What are MOA of the Leukotriene Modifiers drug?

A

Montelukast

Leukotrienes worsening asthma symptoms. Leukotrienes cause edema in the airways, movement of immune cells to the airways, over-secretion of mucous, & bronchoconstriction. Leukotriene modifiers suppress leukotriene activity.

54
Q

What are TU of the Leukotriene Modifiers drug?

A

Therapeutic Use
• Severe Acute Asthma: Not effective
• Chronic Asthma: Considered an alternative to low dose inhaled corticosteroids; less
effective than corticosteroids. Also listed as an adjunctive option in Step 2.
• COPD: Currently, no role.
• Other: FDA approved for seasonal allergies

55
Q

What are AE of the Leukotriene Modifiers drug?

A

Side Effects / Drug Interactions
• Insomnia, agitation, anxiety, depression.
• Zileuton requires 4 times per day dosing and CYP3A4 drug interactions, therefore is used
less often than the others in this class

56
Q

What are MOA of the Cholinergic Antagonist drug?

A

Tiotropium (Spiriva)
Ipratropium (Atrovent)

Mechanism of Action
(MDI, nebulizer) (MDI)
(DPI)
• Block muscarinic receptors, reduce respiratory secretions & cause bronchodilation. Ipratropium is short-acting; tiotropium and aclidinium are long acting.

57
Q

What are TU of the Cholinergic Antagonist drug?

A

Tiotropium (Spiriva)
Ipratropium (Atrovent)

Therapeutic Use
• Acute Severe Asthma: Would not be used alone in acute severe asthma; slower onset of action than the β2-agonists. May be used in combination with a β2-agonist if patient dose not respond adequately to β2-agonist alone. Inhaled ipratropium generally produces a further improvement in lung function of 10% to 15% over inhaled β2-agonists alone.
• Chronic Asthma: Not shown to improve outcomes in chronic asthma therefore not used.
• COPD: Key bronchodilators in COPD, used inhaled at fixed doses to provide constant bronchodilation. Tiotropium bromide and aclidinium bromide are long-acting; it is more effective and more convenient than shorter-acting ipratropium. Anticholinergic bronchodilators may be better tolerated at the often very high dosages required in later stages of COPD. Synergy is achieved by combining cholinergic and β2-agonist bronchodilators.

58
Q

What are AE of the Cholinergic Antagonist drug?

A

Tiotropium (Spiriva)
Ipratropium (Atrovent)

Side Effects
• Dry mouth, metallic taste. Ipratropium bromide has very poor absorption via the lungs or GI tract so systemic side effects are minimal. Tiotropium and aclidinium have some anticholinergic side effects.

59
Q

What are MOA of the Inhaled Short Acting B2-Agonists (SABA) drug?

A

Albuterol (Proventil)

Most effective bronchodilators available
• Selectively activates β2 receptors causing smooth muscle relaxation (bronchodilation Side Effects

60
Q

What are TU of the Inhaled Short Acting B2-Agonists (SABA) drug?

A

Albuterol (Proventil)

Therapeutic Uses of inhaled, Short Acting β2-Agonists
• Acute Severe Asthma: Bronchodilator of choice for acute asthma symptoms. Usually dosed prn for quick relief of acute attacks. Often referred to as “rescue inhalers.” 66% of adults require only 3 doses of nebulizered albuterol (2.5 – 5mg q20 min per neb or 2 – 4 puffs q20min per MDI/DPI) to be discharged from hospital. If inadequate response to the first 3 doses, give 10 – 15 mg/h continuously. If using a rescue inhaler > 2 times a week should consider starting or intensifying anti-inflammatory
therapy.

  • Chronic Asthma: All asthmatics, regardless of severity, must be prescribed a fast-acting inhaled β2-agonist for quick-relief.
  • Acute COPD Exacerbations: Bronchodilator of choice for acute exacerbation of symptoms.

• COPD: Used inhaled at fixed doses to provide constant bronchodilation. Synergy is
achieved by combining anticholinergic and β2-agonist bronchodilators.

61
Q

What are AE of the Inhaled Short Acting B2-Agonists (SABA) drug?

A

Albuterol (Proventil)

Side effects are more common with systemic use and high inhaled doses: nervousness,
anxiety, tremor, tachycardia, and chest pain.
• Drugs selective for β2 receptors will be less likely to cause these cardiac side effects.
However, any drug can lose its selectivity with larger doses.

62
Q

What are MOA of the Inhaled Long Acting B2-Agonists (LABA) drug?

A
63
Q

What are TU of the Inhaled Long Acting B2-Agonists (LABA) drug?

A
64
Q

What are AE of the Inhaled Long Acting B2-Agonists (LABA) drug?

A
65
Q

What are MOA of the Oral bronchodilator drug?

A

Promotes bronchodilation by relaxing smooth muscle of the bronchi and strengthening diaphragm contractions. Exact mechanism unclear. May have very mild anti-inflammatory properties.

66
Q

What are TU of the Oral bronchodilator drug?

A

Severe Acute Asthma: The use of IV aminophylline in the management of acute respiratory distress has not been recommended for years. Benefits do not outweigh the risks.
• Chronic Asthma: May provide mild bronchodilation; much less effective than the β2 agonists. It is not the preferred treatment at any stage of asthma; currently listed as an alternative adjunctive drug only. Adding theophylline to inhaled corticosteroids is no more effective than doubling the dose of the inhaled corticosteroid.
• COPD: Considered an adjunct bronchodilator in patients not fully responding to the combination of inhaled anticholinergics + β2-agonists. Studies indicate, some synergistic bronchodilation may occur with this triple bronchodilator therapy.

67
Q

What are AE of the Oral bronchodilator drug?

A

….

Pharma (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions