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Pharmacology > Asthma/COPD/Colds/Allergies/GI > Flashcards

Asthma/COPD/Colds/Allergies/GI Flashcards

1
Q

destruction of walls in acinus diminishing SA for gas exchange and loss of elastic recoil

A

emphysema

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2
Q

asthma is ___ inflammatory response that results in ___ bronchial hyperreactivity to various stimuli

A

chronic

reversible

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3
Q 
W/ Asthma, inflammatory mediators act either directly on \_\_  or through \_\_  to produce an exaggerated bronchoconstrictive response with: 
1.
2. 
3.
4.
A

smooth muscle
neural pathways

  •   Edema
  •   Cellular infiltration
  •   Mucus plugs
  •   Epithelial denudation (late response)
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4
Q

describe the pathophysiology of exercise induced bronchoconstriction

A

-Inhalation of large volume of relatively cool, dry air alters
airway surface osmolality –> primary stimulus  

-Attenuated when the inspired air is humidified and brought closer to body temperature

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5
Q

describe the early asthmatic response

A
  • Immediate bronchoconstriction (↓ FEV) and vascular leakage caused by mediators from mast cells (histamine and cysteinyl leukotrienes (C4, D4).
  • LTB4 and other cytokines (IL-4, IL-5, TNF [tumor necrosis factor]) are responsible for recruitment of inflammatory cells involved in the late reaction (infiltration and activation).
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6
Q

describe the late asthmatic response

A

Delayed (4-6 hrs) bronchoconstriction and bronchial hyperreactivity following epithelial damage; mediated by ECP (eosinophil cationic protein), MBP (major basic protein), and cytokines from eosinophils and neutrophils

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7
Q

COPD inflammation is largely mediated by

A

macrophages-neutrophils-CD8 T lymphocytes

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8
Q

what mediators result in acute bronchospasm (bronchoconstriction, microvascular leakage, mucus secretion)

A

acetylcholine

leukotrienes**

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9
Q

what mediators result in chronic inflammation hyper-reactivity (inflammatory cell infiltration and activation and epithelial damage)

A

leukotrienes
LTB4
eosinophils
neutrophils

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10
Q

5 Asthma Treatment Goals

A
  1. Control chronic symptoms (including overnight) 
  2. Maintain normal activity (including exercise)
  3.   Maintain normal pulmonary function
  4.   Prevent acute episodes
  5.   Avoid adverse medication effect
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11
Q

describe the mechanism of bronchodilation w/ B-adrenergic receptors for asthma and COPD tx

A

B2: Gs= + AC= increase cAMP= bronchial muscle relaxation

*inhale is best route due to fast onset

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12
Q

Side Effects of B2 adrenergic or sympathomimietic drugs

A
  1. Skeletal muscle tremor (β2 receptors)
  2. Tachycardia, palpitations, anxiety, insomnia (β1 receptors)
  3. Dry mouth (anticholinergic- M)
  • Black Box Warning for salmeterol (LABA)
  • Increased risk of asthma related deaths
  • Should not be used without an inhaled corticosteroid
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13
Q

side effects of antimuscarinic agents used w/ asthma and COPD

A
  1. drying of upper mouth and airways

2. caution if comorbid glaucoma, symptomatic BPH, or bladder neck obstruction

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14
Q

How to glucocorticoids work

A
  1. inhibit T cell activation
  2. inhibit cytokine production
  3. inhibit eosinophil recrutiment
  4. inhibit mast cell migration
  5. inhibit mediators from eosinophils and mast cells
  6. vasoconstrict= reduce airway edema

*go to med bc they work everywhere

**anti-inflammatory

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15
Q

how to cromyolns work

A
  1. inhibit mediators from eosinophils and mast cells
  2. inhibit eosinophil chemotaxis

**anti-inflammatory

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16
Q

how to leukotriene inhibitors work

A
  1. inhibit leukotriene synthesis
  2. block leukotriene receptor

**anti-inflammatory

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17
Q

side effects of oral, parenteral corticosteriods w/ short course, high dose use?

A
  1. hyperglycemia
  2. sodium retention
  3. hypertension
  4. hypokalemia
  5. GI bleeding
  6. CNS distrubance
  7. insomnia
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18
Q

side effects of oral, parenteral corticosteriods w/ chronic use

A
  1. immunosuppression
  2. growth suppression
  3. thinning of skin
  4. osteoporosis
  5. cataract formation
  6. adrenal gland suppression
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19
Q

side effects of inhaled steroids

A

*less systemic effects but still local effects possible

  1. thrush
  2. dysphonia/hoarseness– vocal cord weakness
    * 1 and 2 due to improper administration technique

HD:

  1. monitor for HPA axis (for adrenal gland suppression)
  2. bone density (osteoporosis)
  3. eyes (cataracts, glaucoma)
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20
Q

Advantages: Oral (vs inhalational administration of corticosteroids) administration increases compliance (esp. in children). Few adverse effects since __ are produced only at sites of inflammation. Relative to corticosteroids, less effect on airway symptoms / reactivity / inflammation, but equal in reducing frequency of exacerbations.

A

leukotriene inhibitors

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21
Q

Side effects of leukotriene inhibitors

A
  1. some are non-responders
  2. Zileuton may cause problems with liver dysfunction, so must perform regular liver function tests; must be given four times daily.
  3. Zafirlukast can interfere with warfarin metabolism.
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22
Q

• Mechanism: Anti-inflammatory action via prevention of antigen-induced release of inflammatory mediators from sensitized mast cells. Also inhibit pulmonary afferent nerve fiber receptors that contribute to cough and reflex bronchoconstriction and can suppress the activating effects of chemotactic peptides (cytokines) on neutrophils, eosinophils, and monocytes

A

cromolyn sodium

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23
Q

• Advantage: Has action to reduce both early and late phase bronchospastic response, useful in exercise-induced and antigen-induced asthma, as well as nonspecific airways reactivity. Minimal risk of systemic adverse effects

A

cromolyn sodium

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24
Q

Side effects of cromolyn sodium

A
  1. Limited to use as prophylactic agent, must be given prior to expected exposure to precipitant of asthma attack as it will NOT abort an attack once initiated;
  2. less effective in severe asthma.
  3. bronchospasm,
  4. wheezing,
  5. cough [these effects can be minimized by drinking water and/or by using of β2 agonist prior to treatment
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25
Q
  • Mechanisms of action: Bronchodilator and anti-inflammatory via various mechanisms including:
  • Inhibition of phosphodiesterase-nonselective (high concentrations)
  • Effect on calcium transport
  • Adenosine antagonist
  • Effect on prostaglandin synthesis
A

Theophylline

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26
Q

• Advantage: Prolonged duration of action (oral) - administration at dinner can target nocturnal asthma. Rapid onset of action if given intravenously (but rarely used today).

A

Theophylline

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27
Q

Side effects of theophylline

A
  1. Low margin of safety (generally avoid switching brands),
  2. risk of adverse effects related to blood level:
  3. insomnia,
  4. GI disturbances (nausea, vomiting),
  5. headache,
  6. anxiety;
  7. seizures and
  8. arrhythmias (at higher levels).
  9. NOT available via inhalational route. Requires monitoring of serum concentration levels.
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28
Q

• Mechanism: Inhibition leads to increases in cAMP levels in pulmonary inflammatory cells (neutrophils, T-lymphocytes, macrophages) resulting in suppression of a myriad of inflammatory responses underlying COPD (chemotaxis, phagocytosis, and release of proinflammatory mediators [lipid mediators, cytokines, chemokines, reactive oxygen species, and hydrolytic enzymes]).

A

PDE-4 inhibitor
(rolumilast)

NOTE: not also a bronchodilator like theophylline (a nonselective PDE inhibitor).

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29
Q

• Advantage: Administered once daily via oral route. Reduces numbers of exacerbations in patients with severe COPD along with modest improvement in lung function. Reserve for refractory disease.

A

PDE-4 inhibitor

rolumilast

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30
Q

side effects of PDE-4 inhibitor

rolumilast

A
  1. Nausea and
  2. diarrhea most common side effects leading to discontinuation;
  3. weight loss in 8%.
  4. Psychiatric effects also observed (6% → insomnia, depression, anxiety
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31
Q

• Mechanism: A recombinant humanized monoclonal antibody that will bind free IgE in the circulation, preventing IgE attachment to mast cells and basophils and blocking the cellular response to allergens.

A

Omalizumab

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32
Q

• Advantages: An option for patients with moderate to severe persistent asthma, with high levels of antigen-specific IgE (i.e., a strong allergic component), who have been inadequately controlled despite maximal therapy with other asthma medications. Some studies have shown omalizumab treatment led to reduced inhaled corticosteroid use and decreased asthma exacerbations.

A

Omalizumab

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33
Q

• Mechanism: Splits disulfide linkages between mucoproteins resulting in decreased viscosity of pulmonary mucus secretions - BUT no evidence that thinning secretions induces clinical improvement. Also possesses antioxidant properties.

A

mucolytics

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34
Q

side effects of mucolytics

A
  1. trigger bronchospasm (always give w/ bronchodilator)
  2. N/V
  3. stomatitis
  4. rhinorrhea
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35
Q

black-box warning due to risk of anaphylaxis

A

Omalizumab

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36
Q

• Mechanism: Bronchodilation via action blocks vagal nerve component (parasympathetic) to oppose bronchospastic response and increased mucus secretion.

A

antimuscarinic agent (ipratroprium)

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37
Q

• Advantage: Relatively rapid onset of action. May be more effective than β-adrenergic agonists in COPD (bronchitis or emphysema)

A

antimuscarinic agent (ipratroprium)

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38
Q

in viral cold symptoms] [primary use in allergic rhinitis, minor role

A

antihistamines

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39
Q

(vasoconstrictors) [primary use in allergic

rhinitis and viral cold infections]

A

decongestants

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40
Q

[some use in coughs associated with viral

cold symptoms, allergic rhinitis, asthma, COPD]

A

antitussives

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41
Q

[some utility in viral cold infections-COPD]

A

expectorants

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42
Q

[some utility in viral cold infections-COPD]

A

mucolytics

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43
Q

describe the CV effects from histamine

A

H1 (increase IP3/DAG)

  • vasodilation via increased No synthesis= hypotension, nasal congestion, reflex tachycardia
  • increased cap. permeability (edema, hives, shock, rhinorrhea)

H2 (increased cAMP)
-cardiac stimulation and vasodilation

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44
Q

describe the GI effects from histamine

A

H1:
-SmM contraction= cramps

H2:
-increase gastric acid secretion

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45
Q

describe the bronchiolar SmM effects from histamine

A

H1:

-Bronchoconstriction— hyperactive responds in asthma

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46
Q

describe the neuron effects from histamine

A

H1

stimulate nerve endings- pain, itching

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47
Q

Describe the anaphylactic reaction effects from histamine

A

H1:

-Urticaria, abdominal cramps, laryngospasm, bronchospasm, decreased BP, shock

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48
Q

tx of anaphylatic rxn from histamine

A

Histamine plus other mediators are released from mast cells necessitating treatment with epinephrine

  • Antihistamines, while effects are additive with epinephrine,
    are not sufficient alone
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49
Q

how does cromolyn sodium affect histamine

A

prevents histamine release from mast cells

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50
Q

describe H1 receptor blocking agents for an antihistamine agent

A

-Reversible and competitive block with neglible H
blocking effects

1st generation agents: have additional blocking actions
at non H

2nd generation agents relatively selective for H1
receptors

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51
Q

uses/effects of antimuscarinic receptor blocking agents for an antihistamine agent

A
  1. Sedation (more in 1st generation bc less CNS penetration in 2nd generation)
  2. Prevent N/V and motion sickness: block M and H1 (1st gen. only)
  3. block of secretions: may be beneficial or SE: dry mouth, UR, blurred vision, constipation (1st gen only)
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52
Q

use of sodium channel block for antihistamine

A

local anesthetic action

-most often used topically first

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53
Q

α1-adrenergic receptor block (esp. promethazine) can cause what when used for an antihistamine

A

orthostatic hypotension in suspected individuals

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54
Q

compare 1st and 2nd generation antihistamines

A

1st:

  • more sedation*
  • more CNS penetration*
  • more antimuscarinic actions*
  • prevent N/V/motion sickness*
  • Metabolized by liver
  • short duration of action (4-8hrs)*

2nd:

  • highly H1 selective
  • less sedation
  • no block of secretions
  • no prevention of N/V/motion sickness
  • less antimuscarinic actions
  • longer actions (12-24 hrs)
  • metabolic and/or renal elimination
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55
Q

2nd generation antihistamines

A
  • fexofenadine/ Allergra
  • cetirizine/ Zrytec
  • loratadine/ Claritin
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56
Q

use of antihistamines

A
  1. allergic reactions (rhinitis and urticaria) – H1 receptor block
    * 1st and 2nd generation OTC

Chronic use may diminish clinical effectiveness - can try
switch to different class)

*1st generations have additional uses

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57
Q

what is the best drug class to help w/ allergic disordres

A

antihistamines

*helps w/ sneezing, pruritus, rhinorrhea, congestion (a little)

NOT w/ inflammation

Rapid onset!

(2nd best= corticosteroids but slower onset ie.nasal steroids)

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58
Q

additional uses of 1st generation antihistamines

A
  1. Cough suppression (Na channel blocker)??
  2. Motion sickness (H1 and M block)
  3. N/V (H1 and M block)–Meclizine-dimenhydrinate
  4. Sleep aid for insomnia (H1 and M block)– diphenhydramine- doxylamine
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59
Q

Side effects of antihistamines

A
  1. Sedation (mostly 1st gen.)
  2. Additive CNS depression w/ alcohol and other CNS depressants (more with 1)
  3. Antimuscarinic actions: dry mouth
  4. paradoxical excitation
  5. postural hypotension
  6. GI: Decreased appetite, N/V, constipation
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60
Q

what are 1st generation antihistamines

A

Dimenhydrinate
Diphenhydramine/Benadryl
Meclizine

61
Q

what is the main inflammatory mediatory in RSV colds that leads to symptoms

A

bradykinins

*Mast cell mediators (histamine) have MINOR role in the viral inflammatory response so antihistamines have minimal efficacy for treating cold sx

62
Q

Most common cold symptoms appear 1-3 days after infection and can be explained by the actions of BK including:

A
  1. Pain via activation of nociceptors
  2. Nasal stuffiness via dilation of blood vessels
  3. Nasal fluid hypersecretion via increased capillary
    permeability plus parasympathetic reflex mechanisms
  4. Cough via activation of irritant sensory receptors
63
Q

main inflammatory mediators of allergies vs viral colds

A

Allergies: LTs, Histamine

Viral Colds: BK

64
Q

what is the MOA for topical decongestants

A

stimulate alpha1- receptors of nasal BV dilated by histamine or BK–> vasoconstriction

  • promotes drainage, improves breathing
  • *PROMT effect relative to oral decongestants
65
Q

SE of topical decongestants

A
  1. Rebound congestions (rhinitis medicamentosa) due to ischemia-local irritation (restrict to 2x/day for 3-4 days)
66
Q

ex of topical decongestants

A
  1. Phenylephrine (Neosynephrine)– most effective, shorter duration
  2. Oxymetazoline (Afrin)– longer acting, use 2x day
67
Q

describe the MOA of oral decongestants

A

Stimulate α1 receptors of nasal BV dilated by histamine or bradykinin –> vasoconstriction
-increases neuronal release of NE

**NO REBOUND congestiong bc drugs are delivered systemically

68
Q

side effects of oral decongestants

A

Systemic actions can cause:

  1. headaches,
  2. nausea,
  3. dizziness,
  4. increased BP
  5. palpitations

*at chronic or high doses

(use w/ caution if hx of HTN or arrhythmia)

69
Q

examples of oral decongestants

A
  1. Pseudoephedrine (Sudafed)- safest/effective vasoconstrictor oral agent
  2. Phenylephrine (Sudafed PE) - substrate for hepatic MAO so variable interpatient blood levels
70
Q

Why is sudafed such a hassel to get from the pharmacy?

A

similar compound to methamphetamine (just remove a hydroxyl group and you have meth)

71
Q

antitussives target what?

A

cough center mu (u) receptors in CNS

72
Q

Antitussives are best used when?

A
  1. Reduce frequency of cough, esp. dry, non-productive cough
  2. Excessive coughing can be discomforting, self-perpetuating
73
Q

MOA for antitussives and examples

A

*both central and peripheral actions
1. Most effective agents are agonists at endogenous µ-
opioid receptors to depress the cough center in brain stem (ex. codeine, dextromethorphan, hydrocodone)

  1. Diphenhydramine (Benylin, OTC) is generally less effective, working
    through antihistaminic and/or local anesthetic actions
74
Q

Effective antitussives at lower doses - less physiological /

psychological dependence

A

opioid drugs (controlled substances)

ie. codeine, hydrocodone (in Tussionex)

75
Q

Side effects of Codeine, hydrocodone when used as an antitussive

A
  1. nausea
  2. drowsiness
  3. constipation
  4. allergic rxns (pruritus less common)
76
Q

Most commonly used OTC cough suppressant.

Variable effectiveness

A

Dextromethorphan (in Robitussin DM)

77
Q

Antitussive agent that is an opioid agonist, but does not depress respiration or
predispose to addiction (only l-isomers do this)

A

Dextromethorphan (in Robitussin DM)

78
Q

Side effects of Dextromethorphan (in Robitussin DM)

A

Mild

  1. drowsiness
  2. GI upset
  3. can produce PCP-like effects and coma at doses 50-100x therapeutic value (Robo-tripping)
79
Q

Dextromethorphan (in Robitussin DM) has what effects at a low/therapeutic dose (15-30 mg) vs drug abuse dose (500-1500mg)

A

15-30mg: antitussive: block mu receptors

500-1500mg- blcok of NMDA glutamate receptors

80
Q

Safe and somewhat effective antitussive

A

Diphenhydramine (Benylin, OTC)

81
Q

Side effects of Diphenhydramine (Benylin, OTC)

A
  1. Sedation
  2. antimuscarinic effects

*gerater propensity for SE than dextromethorphan

82
Q

Tetracaine (local anesthetic) congener antitussive

A

Benzonatate (Tessalon Perles)

83
Q

Guidelines for tx of cough in adult due to common cold

A
  1. 1st generation antihistamine/decongestant (e.g.,
    brompheniramine / pseudoephedrine)
  2. Naproxen (tid x 5 days): blocks inflammation that
    stimulates cough afferents

**2nd generation antihistamines ineffective

84
Q

Guidelines for tx of cough in adult due to upper airway cough syndrome (postnasal drip)

A

1st generation antihistamine/decongestant (e.g.,

brompheniramine / pseudoephedrine)

85
Q

“-prazole”= blocks ___

“-itidine”= blocks ___

A

-prazole blocks ATPase –> PPI
(in parietal cell)

-itidine blocks H2 receptor–> H2 antagonist

86
Q

___ is the tx of choice for ACUTE ulcers and given along these agents will lead to ulcer healing
___ is necessary to reduce rates of recurrence though

A

acid suppression

Abx

87
Q

what type of organism is H. pylori

A

Gram Neg bacilli

facultative anaerobe

88
Q

what is 1st line tx for H. pylori

A 
Triple therapy (10-14 days)
-PPI BID + Clarithromycin + Amoxicillin ( or Metronidazole if PCN allergy)
89
Q

what is 1st Line alternative OR salvage therapy for H. pylori

A 
Quadruple therapy (0-14 days)
PPI + Bismuth + Tetracycline + Metronidazole
90
Q

Anti-secretory drug categories for PUD

A

PPIs
H2 antagonist

*all antisecretory agents cause an increase in gastric pH

91
Q

Cyctoprotective drugs for PUD

A

Sucralfate (Carafate®) Misoprostol (Cytotec®)–> “-prostol”= prostaglandin inhibitor

92
Q

describe the MOA for PPIs

A

Prodrug–> enters systemic circulation–> diffuse into parietal cells–> activated in canaliculi to sulfenamide–> then trapped

  • Irreversible inactivates H+K+ATPase
  • Only inactivates active pumps –> 2-5 days for steady state effect
93
Q

when should you take a PPI

A

Best BEFORE a meal–> Cp max then coincides w/ max pump secretion

94
Q

how are PPIs metabolized?

A

CYP450 enzyme in rapid first pass metabolism –> consider lower dose in pts w/ severe hepatic disease

95
Q

uses of PPIs

A
  1. GERD (most effective agent)
  2. PUD (faster sx relief than healing H2 antagonists)
  3. NSAID induced ulcers (prevention and tx)– often used in critcically ill
  4. Prevention of stress gastritis
  5. Zollinger-Ellison syndrome
96
Q

Side effects from PPIs

A
  • remarkably safe
  • Mild
    1. HA
    2. abdominal pain
    3. Constipation
    4. diarrhea
97
Q

side effects from chronic use of PPIs (over 1 yr, erosive esophagitis)

A
  1. Hypergastrinemia – no tolerance but may contribute to rebound increases in gastric acidity upon stopping– tapper
  2. increase fx risk? decreased Ca2+ absorption
  3. decreased Mg2+ absorption
98
Q

Drug-drug interactions w/ PPIs

A
  • due to actions on CYP450

- Omeprazole may inhibit conversion of antiplatelet agent clopidogrel to active form

99
Q

MOA of H2 receptor antagonists

A

Competitive reversible block of H2 receptors – basolateral

membrane

100
Q

compare the actions of H2 receptor antagonists and PPIs

A
  1. H2 antagonists less efficacious than PPIs – generally requires bid dosing
  2. More rapid onset of action than PPIs in acute gastritis

3.  Better at block of nocturnal (H2) than meal-stimulated
(ACh-gastrin) acid secretion

101
Q

describe the PK of H2 receptor antagonists

A
  1. Rapidly absorbed (advantage in acute gastritis)
  2.   Major route of elimination is renal excretion
  3.   Dosage reduction in renal dysfunction (esp. in elderly)
102
Q

uses of H2 receptor antagonists

A
  1. GERD if infrequent (if frequent requires BID)
  2. PUD– largely replaced by PPIs
  3. Stress-related gastritis- reduce bleeding when given IV
103
Q

Side effects of H2 receptor antagonists

A

Generally well tolerated

  1. CNS dysfunciton- AMS (more common w/ cimetidine w/ renal dysfxn)
  2. Endocrine effects w/ Cimetidine - gynecomastia
104
Q

drug drug interactions w/ H2 receptor antagonists

A

Cimetidine inhibition of CYP450 metabolism, which increase the effects or toxicity of many drugs

105
Q

MOA of Sucralfate (Carafate)

A

Sulfated disaccharide Aluminum salt selectively binds to necrotic ulcer tissue to form a protective barrier

  • Activated by acidic pH – give on empty stomach – 2-4 / day
  •   Not absorbed
106
Q

Side effects of Sucralfate (Carafate)

A

few side effects

  1. constipation
107
Q

MOA of Misoprostol (cytotec)

A

Prostaglandin analog - acts on epithelial cell to ↓ H+

secretion - ↑ mucus-bicarbonate

108
Q

what is Misoprostol (Cytotec) used

A

NSAID induced ulceres

109
Q

Side effects of Misoprostol (Cytotec)

A
  1. diarrhea
  2. uterine stimulation/cramping
  3. CONTRAINDICATED in pregnancy bc of increase uterine motility
110
Q

Most effective agent for preventing NSAID-induced ulcers:

A

PPIs

Omeprazole (prilosec) or Esomeprazole (nexium)

111
Q

Antacids raise pH of stomach contents to ___

112
Q

PK of antacids

A
  1. should be nonabsorbable– wil raise urinary pH about 1 when used in ulcer tx
  2. should be long-acting but must be given every 2 hrs
113
Q

side effects of antacids

A

no adverse effects

but diarrhea- constipation is common

114
Q

drug-drug interactions of antacids

A

None generally avoid by spacing dose around other drugs

115
Q

examples of gastric antacids

A
  1. Calcium (as carbonate- Tums)
  2. Aluminum
  3. Magnesium (Milk of Magnesium)
116
Q

adverse reactions of calcium antacids

A
  1. rebound secretion
  2. safe but not for chronic use
  3. CONSTIPATION
  4. hypercalcemia
117
Q

adverse reactions of aluminum antacids

A
  1. CONSTIPATION

2. chronic intake may lead to CNS toxicity

118
Q

adverse reactions of magnesium antacids

A
  1. osmotic DIARRHEA

2. retention of Mg if renal disease

119
Q

avoid sodium bicarbonate antacid/neutralizing agent if:

A
  • pregnant
  • CHF
  • HTN
  • edema
  • renal failure

*conditions exacerbated by fluid retention

120
Q

drugs associated w/ inducing constipation

A
  1. Antimuscarinic agents
  2. drugs w/ antimuscarinic SE (1st generation antihistamines, tricyclic antidepressants, typical antipsychotic agents)
  3. Antacids (calcium and aluminum)
  4. Ca2+ channel blockers (esp. verapamil)
  5. opioid analgesics
  6. 5HT3 antagonists
121
Q

Laxative classification by mechanism of action

A

1st- bulk forming
2nd- Saline (osmotic): increases fluid volume
3rd- stimulant (irritant): stimulates enteric nerves

Prevent: Wetting agents: moistens to ease passage

122
Q

management of simple constipation

A
  1. proper diet (20-30g daily)
  2. exercise (esp. abdominal muscles)
  3. adequate fluid intake (6-8 8oz/day)
123
Q

what laxative is usually recommended first

A

Psyllium

fiber/bulk forming

124
Q

Psyllium MOA

A

physiologic mechanism: facilitates passage and stimulate peristalsis via absorption of water –> bulk expansion

125
Q

adverse reactions w/ psyllium

A

may combine and interact w/ other drugs (ie. digoxin/salicylates) so space dosing

126
Q

MOA of saline (osmotic) cathartics

A

Non-absorbable ions –> osmotic retention of intestinal

water –> increased peristalsis

127
Q

examples of saline (osmotic) cathartics

A
  1. milk of magnesia, magnesium citrate
  2. polyethylene Glycol- electrolyte solutions (PEGs)- Miralax
  3. Lactulose
  4. Phosphage enema–> reserved for fecal impaction
128
Q

when is milk of magnesia most commonly used

A
  1. Most used for mild to moderate constipation

2 Avoid in renal dysfunction as long term use can lead to electrolyte imbalances

129
Q

•  Bowel cleansing prior medical procedures
•  Contain Na+-K+ salts to prevent net transfer of
electrolytes

A

High volume solutions of polyethylene glycol (saline osmotic cathartics)

130
Q

-For difficult to treat constipation
•  Daily dose for treatments less than 2 weeks duration
•  Excessive use may lead to electrolyte depletion

A

smaller volume solutions of polyethylene glycol (saline osmotic cathartics)

131
Q

MOA of lactulose

A

Dissacharide metabolized by colonic bacteria to low

MW acids –> osmotic diarrhea –> increased peristalsis

132
Q

examples of stimulant laxatives

A
  1. Bisacodyl
  2. Senna
  3. Castor Oil
133
Q

MOA of Bisacodyl (stimulant laxative)

A

↑ peristaltic activity via local irritation (PG-NO) –> accumulation of water and electrolytes –> ↑ motility

134
Q

adverse reactions of Bisacodyl (stimulant laxative)

A

potentially dangerous side effects

  1. electrolyte/fluid deficiencies
  2. severe cramps

*most widely abused class- but safe for chronic use
in recommended doses

135
Q

MOA of castor oil

A
  1. Contains a triglyceride that is hydrolyzed in the gut to
    ricinoleic acid

-  Acts primarily in the small intestine –> stimulate fluid/
electrolyte secretion and speed intestinal transit

136
Q

Castor bean also contains __, an extremely toxic glycoprotein

137
Q

examples of Stool-wetting agents and Emollients

A
  1. Docusate (colace)
  2. Lubricant (mineral oil)

*used for prevention

138
Q

A surfactant that acts as stool-softener (facilitates

admixture of aqueous and fatty substances)

A

Docusate (colace)

*Often used in combination with stimulant laxative
when initiating opioid analgesic therapy

ROLE IS PRIMARY PREVENTION

139
Q

Coats fecal contents preventing colonic absorption of fecal water

A

Lubricant (mineral oil)

140
Q

Peripherally acting opioid antagonists for patients taking opioids for non- cancer pain that have failed laxative therapy

A
  1. Methylnatrexone (Relistor)- expensive but doesn’t cross BBB
  2. Naloxegol (Movantik)- binds primarily to opioid receptors in GI tract only
141
Q

drugs that induce diarrhea

A
  1. Abx (esp. broad spectrum)
  2. Colchicine
  3. Digoxin
  4. Magnesium antacids
  5. Misoprostol
  6. Muscarinic agonists
  7. Resperine
  8. SSRIs
142
Q

Classes of drugs that tx diarrhea

A
  1. Opioids
  2. Polycarbophil
  3. Adsorbents
  4. Probiotics
143
Q

MOA of Loperamide (Imodium)

A 
Opioid receptor agonist affecting intestinal motility (µ),
intestinal secretion (δ), and absorption (µ and δ) 
-anti-secretory activity against cholera toxin (good for travelers diarrhea)
144
Q

side effects of Loperamide (Imodium)

A
  1. can cross BBB and cause:
    - CNS (euphoria and decreased RR)
    - Cardiac toxicity (prolonged QT)
  2. CNS depression (esp. in children)
  3. paralytic ileus
  4. may worsen Shigella infections

*low addition liability for acute use due to water solubility (difficult to dissolve and then inject)

145
Q

what drug is approved by the FDA to use for diarrhea AND constipation

A

Polycarbophil (Mitrolan)

146
Q

examples of Adsorbents

A 
Charcoal
Bismuth subsalicylate (pepto Bismol), Kaolin, pectin
147
Q

what drug has an association w/ Reye’s Syndrome in children under 12y/o

A

bismuth subsalicylate

*AVOID USE

148
Q

Taken after each loose bowel movement until controlled

  • Manages mild to moderate diarrhea
  • “Formed stools” and perception of decreased fluidity, but small effect on fluid volume excreted
A

adsorbents

149
Q

MOA of probiotics

A

Suppress growth of pathogenic organisms –> restore

normal flora –> possible role in antibiotic-associated, viral, or Traveler’s diarrhea

Pharmacology (31 decks)

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