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Exams > Pharmacology finals COPIED > Flashcards

Pharmacology finals COPIED Flashcards

1
Q

What is dipyridamole?

A

a coronary vasodilator and a relatively weak antiplatelet drug.

inhibits platelet adhesion to the vessel wall.

Used combined with aspirin.

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2
Q

what’s the Mx of an acute migraine?

A

oral triptan and an NSAID/ paracetamol

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3
Q

What is the prophylaxis mx of migraines?

(2 attacks or more per month)

A

either

Topiramate

or

Propranolol (not for asthamatics)

(pizotifen is NOT recommended)

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4
Q
A
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5
Q

mech of action,

clinical indications,

potential adverse effects
of cimetidine, famotidine, ranitidine

(histamine H2-receptor antagonists)

A

drugs compete with histamine for binding to H2 receptors on gastric parietal cells.

Reduce volume and conc of gastric acid. This also proportionally decreases pepsin. (Gastric acid is the pepsinogen-pepsin catalyst)

cimetidine - weak antiandrogenic activity; can cause gynecomastia in elderly men.

cimetidine - WELL-KNOWN - inhibits P450 enzymes, therefore care with polypharmacy.

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6
Q

mech of action,

clinical indications,

potential adverse effects
of omeprazole

(proton pump inhibitor)

A

inhibitors of proton-pump, Strong inhibitors of gastric acid

Choice drug for peptic ulcers

Choice drug for GERD

Choice drug for Zollinger-Ellison syndrome

Choice drug for long-term NSAID therapy

hypomagnesemia can occur with long-term PPI therapy.

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7
Q

mech of action,

clinical indications,

potential adverse effects
of calcium carbonate

(gastric antiacid)

A

chemically neutralize stomach acid.

Commonly used for acid indigestion and dyspepsia.

Can cause some constipation, can cause rebound acid secretion.

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8
Q

mech of action,

clinical indications,

potential adverse effects
of sucralfate,

(cytoprotective drug)

A

this polysaccharide adhers to ulcer craters , inhibits pepsin-catalyzed hydrolysis of mucosal proteins. Helps form a protective barrier.

Used to treat peptic ulcers, but not so effective as H2blockers or PPIs, so only indicated with patients who can’t tolerate the others.

Take 2 hours between other drugs.

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9
Q

mech of action,

clinical indications,

potential adverse effects
of metoclopramide

others; prochlorperazine, domperidone

(acts peripherially - prokinetic drug

and acts centrally - antiemetic)

A

Blocks dopamine D2 receptors; this prevents the relaxation of GI smooth muscle produced by dopamine. Also increases acetylcholine from cholinergic motor neurons in the enteric nervous system.

>> tone and motility in the oesophagus and stomach. (therefore opioid induced sickness)

Also >> gastric emptying.

NB> also increases resting pressure of lower oesophageal sphincter, therefore << acid reflux.

Indications: GERD, diabetic gastroparesis, intractable hiccup, also antiemetic.

Adverse effects: CNS reactions. CONTRAINDICATED with px with seizures.

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10
Q

mech of action,

clinical indications,

potential adverse effects
of psyllium

(bulk forming laxative)

A

Indigestible hydrophilic drug

absorbs water and increases mass of stool. This stimulates mech peristalsis.

Also used to treat diarrhoea

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11
Q

mech of action,

clinical indications,

potential adverse effects
of docusate sodium

(stool softener)

A

facilitate movement of water into fatty intestinal material, thus softening stool.

Indicated for hard, dry stool, prevent aggravation of haemorrhoids, helping px avoid straining.

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12
Q

mech of action,

clinical indications,

potential adverse effects
of milk of magnesia

(osmotic laxative)

A

poorly absorbed salt that osmotically attracts water.

Administer to px to evacuate the bowel in prep for surgery.

Danger> loss of fluids and electrolytes

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13
Q

mech of action,

clinical indications,

potential adverse effects
of senna, bisacodyl

(stimulant - secretory laxatives )

A

Alter fluid secretion and stimulates peristalsis

Bisacodyl; used to evacuate the bowel. Can cause cramping and electrolyte/ fluid depletion. SHORT term use only.

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14
Q

mech of action,

clinical indications,

potential adverse effects
of ondansetron

(phenothiazines)

A

Selective 5-HT3 receptor antagonist; competitively block 5-HT3 receptors. I.e. blocks stimuli from the chemoreceptor trigger zone.

Acts both peripherally and centrally (vomiting centre)

Indicated for : cancer chemotherapy-induced emesis.

Adverse effects: headache, constipation, and diarrhoa.

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15
Q

mech of action,

clinical indications,

potential adverse effects
of dronabinol

(marijuana derivatives)

A

used for cancer chemotherapy induced emesis when other drugs have failed.

Used as an appetite stimulant for anorexic HIV patients

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16
Q

mech of action,

clinical indications,

potential adverse effects
of promethazine

(antihistamine)

A

H1 Antihistamine

treats nausea and vomiting induced by medications, anesthetics, and a wide range of other stimuli.

Rectal suppository or injection.

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17
Q

Which cells secrete gastrin?

A

G cells in the stomach’s antrum

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18
Q

What hormone stimulates the parietal cells?

A

Gastrin

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19
Q

Gastrin and acetylcholine also stimulates the release of ……. from paracrine cells

A

Histamine

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20
Q

What is the relationship between histamine and gastric acid production?

A

histamine stimulates H2 receptors located on parietal cells and provokes acid secretion.

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21
Q

What is used primarily for the treatment of motion sickness?

A

Scopalamine - muscarinic receptor antagonist similar to atropine.

Been used by astronauts.

Skin patch slow 72 hr release.

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22
Q

mech of action,

clinical indications,

potential adverse effects
of misoprostol,

(cytoprotective drug)

A

Prostaglandin E1 analogue

expensive. Inhibits gastric acid secretion, promotes mucus and bicarbonate.

Primary indication: prevention of gastric and duodenal ulcers with px who take NSAIDs long term.

contraindicated in PREGNANCY (stimulates uterine contractions)

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23
Q

H. Pylori tx

A

Triple therapy

PPI + two or more antimicrobial agents

eg. amoxicillin + clarithromycin

or metronidazole + clarithromycin

5 days + 5 days treatment programme

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24
Q

What’s the treatment for GERD?

(causing oesophagitis)

A

<< gastric acidity (two main groups previously mentioned)

increase the compromised oesophageal sphincter pressure (metoclopramide)

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25
Q

Summary

peptic ulcer meds

A

Histamine H2 receptor antagonists, or a proton pump inhibitor, or a cytoprotective agent

+

antibiotics for H.pylori

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26
Q

Diagram of vomiting pathways

A
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28
Q

Treatment of Crohn’s

A

Control flare-ups

steroids, immunosuppresants (eg. azathioprine)

otherwise biological agents; infliximab (targets TNF)

Surgery

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29
Q

ranitidine

A

H2 histamine receptor antagonist

blocks histamine and thus decreasing the amount of acid released by cells of the stomach.

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30
Q

What is mesalazine used for?

(5-aminosalicyclic acid) 5-ASA

A

treatment of choice for maintenance of mild-to-moderate ulcerative colitis.

(also reduces risk of colorectal cancer)

Also used inconjunction with antibiotics for the treatment of diverticulitis.

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31
Q

What is Hyosine used for?

(and MOA)

A

Motion sickness and vesibulocochlear dysfunction.

Targets the vomiting centre and vestibulocochlear nuclei.

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32
Q

How does cyclizine work and indications?

A

Histamine (H1) receptor antagonist

Targets the vestibulocochlear nuclei

Labyinthine disorder, vertigo, migraine

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33
Q

Key mechanism of Warfarin (coumarin compounds)

A

Vitamin K antagonist

Vitamin K is used to synthesis coagulation factors II (prothrombin), VII, IX, and X

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34
Q

Can Warfarin be used in pregnancy?

A

No because it crosses the placenta

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35
Q

Does Warfarin act immediately?

A

No because pool of circulating clotting factors needs to be depleted first.

Synthesis of new factors is then inhibited.

(takes 3-5 days to reach maximal effect)

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36
Q

What’s the management of acute thromboembolic disorders?

A

LMWH (Low molecular weight heparin) plus warfarin, and then withdraw LMWH when warfarin is effective.

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37
Q

Patient advise for Warfarin

A
  • Any signs of bleeding, including ecchymoses.
  • Contraindicated in pregnancy (fetal warfarin syndrome)
  • Avoid physical activities such as kick boxing
  • Don’t >>> green vegetables (vit K)
  • Avoid grapefruit juice, cranberry juice
  • Avoid major weight changes
  • Avoid aspirin, NSAIDs
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38
Q

Some common uses of Warfarin

A

Long-term treatment of DVT

Patients with AF

Patients with artificial heart valves.

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39
Q

Name three LMWHs

A

enoxaparin

dalteparin

tinzaparin

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40
Q

Key mechanism of heparin

A

inactivates clotting factors by potentiating the activity of an endogenous anticoagulant (antithrombin III)

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41
Q

Can Heparin be given orally?

A

No because heparin and related anticoagulants are not absorbed from the gut (large molecules) and so much be administered by IV.

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42
Q

What is antithrombin?

A

an endogenous anticoagulant (potent inhibitor of coagulation)

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43
Q

What is the principal component of fibrinolysis?

A

Enzyme plasmin

(generated from inactive precursor plasminogen)2

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44
Q

What are the key adverse effects of Heparin?

A

Bleeding

thrombocytopenia

(hyperkalemia)

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45
Q

What’s the antidote for warfarin-induced bleeding

A

Phytonadione (vitamin K1)

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46
Q

Clinicial uses for Warfarin

A

Long term management of DVT, AF, and artificial heart values.

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47
Q

What is the INR for recurrent embolization or artificial heart valves?

What is the INR for warfarin (generally)

A

3 - 4.5

2-3

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48
Q

Name three LMWH

A

enoxaparin

dalteparin

tinzaparin

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49
Q

How does Dabigatran work?

A

Direct thrombin inhibitor

(thrombin is used in the pathway of transforming fibrinogen to fibrin)

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50
Q

How does LMWH compare to unfractionated heparin in it’s modus operandi?

A

Primarily deactive factor X

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51
Q

What’s the advantages of LMWH compared to standard heparin?

A

can be administered subcutaneously.

more predictable anticoagulation activity (aPTT monitoring not required)

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52
Q

What is HIT?

A

Heparin-induced-thrombocytopenia

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53
Q

Tell me about HIT 1

A

occurs in 25% of patients. Direct interaction between heparin and platelets, leading to platelet aggregation. Mild and reversible.

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54
Q

Tell me about HIT 2

A

less common, more serious.

Immunoglobulin mediated platelet inactivation.

High risk of thrombotic complications and mortality.

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55
Q

How does Fondaparinux work?

A

Indirect Factor Xa inhibitor

It selectively binds to antithrombin (an endogenous anticoagulant)

which

inactivates Xa resulting in a strong inhibition of thrombin generation and clot formation.

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56
Q

How Warfarin monitored?

A

Prothrombin Time (PT)

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57
Q

What does INR stand for?

A

International normalized ratio

INR = (PT observed / PT control)

PT = prothrombin time

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58
Q

What is the antidote to unfractionated heparin and LMWH?

A

Protamine sulfate

(+ve charged protein than combines with -ve charged heparin)

** measure aPTT to monitor **

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59
Q

How do you monitor

(a) Heparin
(b) Warfarin
(c) Dabigatran

A

(a) Heparin - aPTT

(b) Warfarin - PT - Prothrombin Time (remember the INR equation for warfarin)

(c) Dabigatran - TT (thrombin clotting time)

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60
Q

What initiates the formation of platelets along the vascular wall?

A

injury and the expose of the blood to extravascular collagen.

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61
Q

What activates the intrinsic pathway?

A

surface contact with a foreign body or extravascular tissue (i.e. collagen)

62
Q

What activates the extrinsic pathway in the coagulation cascade?

A

a complex tissue factor called thromboplastin.

63
Q

Where does the intrinsic and extrinsic pathways converge?

A

Factor X - major rate-limiting step

64
Q

What does the activation of factor X lead to?

A

the formation of Thrombin

65
Q

What three factors combined often lead to thrombic changes?

A
  • sluggish blood flow
  • inflammation
  • abnormalities in vascular endothelium
66
Q

What’s the difference between arterial thrombi and venous thrombi?

A

arterial thrombi (white); more platelet aggrevation driven

venous thrombi (red); more coagulation driven

67
Q

Aspirin; clinical usages and action as an antiplatelet drug

A

Acute coronary syndrome

Thrombic strokes; acute and prophylaxis

shown to prevent MI with angina.

Artificial heart valves, percutaneous coronary angioplasty.

ACTION: inhibits the synthesis of prostaglandins from arachidonic acid.

68
Q

What’s the most important prostaglandin affecting platelet aggregation?

A

prostacyclin and TXA2

(prostaglandin I2 (PGI2)

Aspirin irreversibly inhibits cyclooxygenase; enzyme that catalyzes TXA2 synthesis.

69
Q

Adverse effects of aspirin

A

GI bleeding

hypoprothrombinaemia; therefore increased bleeding risks

70
Q

When is clopidogrel indicated?

A
  • px who can’t tolerate aspirin
  • used in COMBINATION with aspirin for ACS
71
Q

When are the representative drugs steptokinase, alteplase indicated?

A

intravenously to degrade thrombi in px with

MI, thromvotic stroke, PE

Primary means of restoring coronary blood flow if angioplasty facilities not available.

72
Q

Adverse reactions with aspirin?

A

GI irritation, bleeding,

hypersensitivity reactions,

tinnitus

73
Q

Adverse reactions to streptokinase

A

bleeding, hypersensitivity reactions,

and reperfusion arrhymias (of interest)

anaphylactic shock can occur with streptokinase, therefore cannot be used repeatedly on same patient.

74
Q

what is t-PA and give an example drug

A

Alteplase

drugs that are ‘recombinant forms of human tissue plasminogen activator’

tissue-Plasminogen Activator

75
Q

How do Rivaroxaban, Apixaban, Edoxaban work?

A

Direct Factor Xa inhibitor

76
Q

How does Dagibatran work?

A

Direct thrombin inhibitor.

77
Q

What’s best for arterial thrombosis? Anticoagulants or antiplatelets?

A

Antiplatelets

78
Q

Some advantages of NOACs/ DOACs

A
  • few interactions with food/ drugs
  • predictable anticoagulant effect
  • no need for routine monitoring
79
Q

Which pathway does Warfarin affect?

A

Both intrinsic and extrinsic

80
Q

MOA of Heparin

A

binds to body’s own anticoagulant (antithrombin III)

This complex inhibits factor Xa (and other factors)

81
Q

What is Dipyridamole?

What is it indicated for?

A

Dipyridamole a coronary vasodilator and a relatively weak antiplatelet drug.

Dipyridamole is used in COMBO with aspirin to prevent ischaemic stroke in px with history of thrombotic stroke, and persons experiencing TIAs.

82
Q

What is Dipyridamole?

A

Dipyridamole is an antiplatelet medication that also has vasodilating properties that can make it unsuitable for use in those with severe coronary artery disease, unstable angina, recent myocardial infarction.

Can be combined with aspirin as an option to prevent occlusive vascular events in patients who have had a TIA, or ischaemic stroke.

83
Q
A
84
Q

What kind of drug is Salbutamol?

A

Acts on the Beta 2 adrenergic receptors in the smooth muscle. It is a Beta 2 agonist drug.

85
Q

What other drug (not salbutamol) is commonly used to treat asthma?

A

Ipratropium Bromide

86
Q

What kind of drug is Ipratropium Bromide?

A

anti cholinergic bronchodilator

87
Q

What group of drugs do respiratory consultants use for the management of asthma (2)?

Name two.

A

Xanthines

  • aminophylline
  • theophyline

Corticosteroids

88
Q

How quickly does Salbutamol act, and how long does it last for?

A

2-5 mins

about two hours

89
Q

What’s the typical dose of prednisolone for an acute asthma attack?

A

40-60mg orally

or

IV hydrocortisone 100mg if oral tablets not tolerated.

90
Q

A common side effect from Salbutamol

A

tachycardia

91
Q

What kind of neb would you use for an acute asthma attack (and dose)

A

5mg Salbutamol via O2 driven Nebuliser

92
Q

What could you mix with Salbutamol for an acute asthma attack (and dose)?

A

ipratropium bromide 500ug (micrograms)

93
Q

If usual meds are ineffective for acute asthma attack, what is worth trying?

A

magnesium sulphate

2g over 20 minutes via 200ml saline (mark saline bag with time)

94
Q

What drugs can trigger an asthma attack?

A

B-Blockers

NSAIDS

95
Q

What is Cromolyn sodium and how does it work?

A

Mast cell stabilizer

Stabilizes the plasma membrane of mast cells and eosinophils to prevent the release of histamine, leukotrienes, and other inflammatory mediators.

(works by blocking flux of Calcium into the cells).

96
Q

How are corticosteroids used to manage asthma?

A

Used on a long-term basis to prevent asthmatic attacks, rather than to treat acute bronchospasm.

97
Q

Some examples of steroid inhalers (4)

A

Beclomethasone

Budesonide

Fluticasone

Triamcinolone

98
Q

Why is it not advisable to give steroid inhalers to children?

A

Possibly suppress growth.

(another possible side effect; oral thrush from excessive steroid deposition in the mouth)

99
Q

What are the three groups of bronchodilators?

A

selective B2-adrenoceptor agonists

muscarinic receptor antagonists

theophylline

  • all relax bronchial smooth muscle, but only B2 agonists are used in acute asthmatic attacks.
100
Q

When are muscarinic antagonists indicated?

A

for COPD patients more than asthma patients.

101
Q

When are theophyllines used?

A

long-term basis to prevent bronchoconstriction (with asthma or emphysema)

102
Q

What are Salmeterol and Formoterol examples of, and when would they be prescribed?

A

Long-acting B2-receptor agonists (LABA), given twice daily by inhalation for the long-term treatment of asthma and emphysema.

Particularly useful in preventing nocturnal asthmatic attacks.

103
Q

How do Salmeterol and Formoterol work?

A

They inhibit the late phase of allergen-induced bronchoconstriction.

(occurs after the bronchodilating effects of shorter-acting drugs have dissipated).

104
Q

What type of drugs are Ipratropium and Tiotropium?

A

Muscarinic receptor antagonists

(NB. Ipratroprium is a derivative of atropine).

105
Q

Why would you use Ipratropium or Tiotropium in the management of COPD? (chronic bronchitis + emphysema)

A

Bronchodilating effect of ipratroprium is slower to develop than that of a B2-agonist, but it lasts longer.

106
Q

What is Advair (brand)?

A

Fluticasone (corticosteroid)

Salmeterol (long-acting B2-receptor agonist)

107
Q

What is Symbicort?

A

Budesonide (corticosteroid)

Formoterol ( long acting B2 receptor agonist)

108
Q

What is Montelukast an example of, and what is its mechanism?

A

Leukotriene receptor antagonist

They have a structure similar to cysteinyl leukotrienes, and they compete with these substances for the CysLT1 receptor.

109
Q

What is the clinical use of Montelukast and Zafirlukast?

A

Effective with patients with allergic asthma, including aspirin-sensitive asthma, and they maybe used to prevent exercised-induced asthma when taken at least two hours before the event.

Effects of this drug are accumulative.

Benefit children more than adults.

110
Q

Ipratropium is typically a less effective B2-agonist in asthmatic patients, so why is it used in moderate to severe asthma?

A

Because it has a greater bronchodilating effect when used synergically with another B2 agonist in moderate to severe asthmatics.

111
Q

How do the anticholinergic muscarinic receptor antagonists work?

(tiotropium and ipratropium)

A

They block the bronchoconstricting effect of the vagal nerve (parasympathetic)

112
Q

What are the adverse effects of

Leukotriene receptor antagonists

(eg. Montelukast)

A

Small number of patients can get hypersensitivity reactions.

Rare cases of liver injury.

NB> this group of drugs is highly bound to plasma proteins (>99%) and are extensively metabolized by hepatic cytochrome P450 enzymes.

113
Q

What is Salmeterol?

A

Long-acting B2-receptor agonist

114
Q

What is Formoterol?

A

Long-acting B2​-receptor agonist

115
Q

What is Advair?

A

Fluticasone and Salmeterol

116
Q

What is Symbicort?

A

Budesonide and Formoterol

117
Q

What the the LABAs Salmeterol and Formoterol good for treating?

A

Late phase of allergen-induced bronchoconstriction, therefore useful at preventing nocturnal asthmatic attacks.

118
Q

What is Combivent?

A

Albuterol and ipratropium

(used to treat COPD).

119
Q

Which drug lasts for 24 hours and is first -line treatment for COPD?

A

Tiotropium

120
Q

What is a side effect of tiotropium and ipratropium?

A

dry mouth

121
Q

Which drugs can inact with > therapeutic range of theophylline

A

Cimetidine

erthromycin

fluoroquinolone, isoniazid and verapamil.

122
Q

What is Omalizumab?

A

IgE antagonist given subcutaneously every 2-4 weeks in combination with inhaled corticosteroid therapy.

(however this drug can cause allergic reactions)

123
Q

Whats the MOA for theophylline?

A

acts at CNS and cellular level. Multiple actions on cell types and receptors.

124
Q

What is theophylline used for?

A

COPD (20%> in FEV1)

125
Q

theophylline helps with COPD; in which ways?

A

>20% FEV1

> diaphragmatic contactility

> central respiratory drive

> mucociliary clearance

< inflammation

(used when COPD not controlled)

126
Q

What is albuterol?

A

Short acting inhaled B2 -agonist

(also levalbuterol)

127
Q

What category are ipratropium and tiotropium and what are they primarily used for?

A

Muscarinic receptor antagonists

Primarily used to treat COPD

128
Q

What’s the management for mild, persistent asthma?

A

Corticosteroid inhaler

(may be fluticasone or budesonide)

129
Q

Why would you add a LABA?

A

If inhaled corticosteroid therapy is insufficient.

130
Q

What’s the advantage of B2 -agonists over nonselective B-receptor agonists?

A

They relax bronchial smooth muscle without producing so much tachycardia.

HOWEVER; higher doses can activate cardiac B1-receptors and cause tachycardia.

131
Q

What are the potential side effects of all B2-agonists?

A

tachycardia

tremor

nervousness

132
Q

What is an adrenergic agonist?

A

An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors.

133
Q

What is the problem with B-adrenoceptor agonists and diabetes?

A

They stimulate glycogenolysis and thus can cause hyperglycaemia.

134
Q

MOA of Cromolyn Sodium

A

Stabilize the plasma membrane of mast cells and eosinophils

  • mast cell stabilizer
135
Q

Indications of Cromolyn Sodium

A

Prophylactic use.

Indicated for exercise-induced asthma.

136
Q

What’s the use of LABAs?

A

Long-term treatment of asthma and emphysema. Particularly useful for preventing nocturnal asthmatic attacks.

Salmeterol and Formoterol inhibit the late phase of allergen-induced bronchoconstriction.

137
Q

Two examples of LABA

A

salmeterol

and

formoterol

138
Q

What is Advair?

A

Advair: Fluticasone and Salmeterol

139
Q

What is symbicort?

A

Symbicort: Budesonide and Formoterol

140
Q

MOA of theophylline

A

Acts at the CNS level

Also cellular level; blocks adenosine receptors, etc.

Drug is bronchodilating, anti-inflammatory, and immunosuppressant.

141
Q

Indications fo theophylline

A

Long term use is associated with 20% increase in FEV1.

Reduces dyspnea, increases diaphragmatic contractility.

Increases central respiratory drive.

Increases muociliary clearance, reduces inflammation.

Used to treat COPD that isn’t controlled by B2 agonist and tiotropium.

142
Q

Theophyline fo asthma?

A

Usage is declining. Use if other drugs not working.

143
Q

Drug interactions of theophylline

A

Cimetidine and erythromycin inhibit CYPP1A2 and increase theophylline plasma concentrations.

Significant when drug is high in therapeutic range.

Also fluoroquinolone, isoniazid and verapamil.

144
Q

If serum level of theophylline is too high, then….

A
  • 25mg/L ; seizures and serious arrhythmias.
145
Q

What is Montelukast?

A

Leukotriene receptor antagonist (they compete for the same leukotriene receptors)

146
Q

Indications of Montelukast?

A

Allergic asthma (including aspirin-sensitive asthma)

Prevention of exercise-induced asthma (take two hours before)

Accumulative effect. Benefits children more and adults.

Alternative for those not wishing to take steroids (although not so effective).

Not as effective as LABA as add-on to corticosteroids, but may be safer.

147
Q

Montelukast adverse effects?

A

use P450 pathway

Occasionally hypersensitivity reactions.

Rare – liver injury.

148
Q

Side effects of B2 agonists

A

Tachycardia, tremor, nervousness

149
Q

What do B1 agonists do?

A

stimulate cardiac muscle;

increasing rate (chronotropic)

and strength (inotropic),

and

conductivity (dromotropic)

150
Q

Why are the anticholinergics Ipratropium and tiotropium used in COPD?

A

the bronchodilating effects of ipratropium is slower to develop than that of a B2-agonist, but it lasts longer.

Improves quality of life in patients with moderate-severe COPD.

Tiotropium; first-line treatment for patients with mild to severe COPD.

Exams (3 decks)

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