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Pharmacology > Respiratory, GI, and Infectious Diseases > Flashcards

Respiratory, GI, and Infectious Diseases Flashcards

1
Q

In what ways can drug therapy help respiratory conditions in relation to PT

A
  • Breath more easily
  • Become more engaged in respiratory muscle training & various exercises
  • Reduce anxiety
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2
Q

What is the goal of respiratory drugs

A
  • Maintain airflow
  • Control secretions & irritation
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3
Q

Acute problems associated with respiratory drugs

A
  • Nasal congestion
  • Coughing
  • Seasonal allergies
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4
Q

Chronic problems associated with respiratory drugs

A
  • Asthma
  • Chronic bronchitis
  • Emphysema
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5
Q

List drugs used for respiratory irritation & secretion control

A
  • Anti-tussives
  • Decongestants
  • Mucolytics/Expectorants
  • Anti-histamines
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6
Q

Describe anti-tussives

A
  • Help to suppress cough associated with a cold or other throat irritations
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7
Q

Side effects of anti-tussives

A
  • Sedation
  • Dizziness
  • GI upset
  • Dependence on opioids
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8
Q

List some anti-tussives

A
  • Benzonatate: local anesthetic
  • Codeine, Hydrocodone, & Hydromorphone: suppression of cough reflex
  • Dextromethorphan: inhibition of cough reflex
  • Diphenhydramine: anti-histamine
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9
Q

Describe decongestants

A
  • Help to relieve runny nose & stuffy head feeling
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10
Q

Side effects of decongestants

A
  • More apparent at high doses or during prolonged use
  • Headaches
  • Dizziness
  • Nausea
  • Insomnia
  • Increased BP
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11
Q

Lists the nasal sprays and oral dosages of decongestants

A
  • Nasal sprays: Oxymetazoline & Phenylephrine
  • Oral: Ephedrine, Pseudoephedrine, & Phenylephrine
  • They bind alpha receptors in blood vessels of nasal mucosa = vasoconstriction
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12
Q

Lists 1st and 2nd generation anti-histamines

A
  • 1st gen: Diphenhydramine, Doxylamine, & Hydroxyzine
  • 2nd gen: Cetirizine, Loratadine, & Fexofenadine
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13
Q

Side effects of 1st generation anti-histamines

A
  • Sedation
  • Fatigue
  • Dizziness
  • GI distress
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14
Q

Describe mucolytics and expectorants

A
  • Mucolytics: decrease viscosity of secretions
  • Expectorants: Help to eject mucus
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15
Q

Side effects of mucolytics and expectorants

A
  • Mucolytics: Nausea, vomiting, oral mucosa inflammation
  • Expectorants: GI upset
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16
Q

List chronic respiratory problems and the goal

A
  • COPD
  • Asthma
  • Cystic fibrosis
  • Goal is to maintain airway patency
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17
Q

Describe beta adrenergic drugs

A
  • Beta agonists that stimulate beta 2 receptors
  • Cause relaxation of bronchiole smooth muscle
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18
Q

List short and long acting beta adrenergic drugs

A
  • Short: Albuterol & Levalbuterol
  • Long: Salmeterol, Formoterol, & Vilanterol
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19
Q

Side effects of beta adrenergic drugs

A
  • Excessive use = airway irritation
  • Tolerance
  • Cardiac irregularities
  • Nervousness, tremor
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20
Q

Ways to administer beta adrenergic drugs

A
  • MDI (metered dose inhalers): inhalation technique is critical
  • Nebulizers: may be beneficial for patients who cannot master the technique needed for MDI delivery
  • DPI (dry powder inhalers)
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21
Q

Describe xanthine derivative

A
  • No longer recommend due to weak efficacy & side effects
  • Produce bronchoodilation by inhibiting PDE in bronchial smooth muscle
  • PDE inhibition = decreased function of inflammatory cells & mediators
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22
Q

List xanthine derivatives and their side effects

A
  • Theophylline & Aminophylline
  • Side effect: toxicity
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23
Q

Describe anti-cholinergic drugs

A
  • Have large role in COPD
  • Drugs: Ipratropium & Tiotropium
  • Vagus nerve releases Ash into respiratory smooth muscle and blocks stimulus which prevents bronchoconstriction
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24
Q

Side effects of anti-cholinergic drugs

A
  • Dry mouth
  • Constipation
  • Tachycardia
  • Confusion
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25
Q

Describe glucocorticoids

A
  • Stop inflammation
  • IV: for severe acute episodes of bronchoconstriction
  • Oral: for more prolonged use
  • Inhaled: prolonged use, less systemic exposure
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26
Q

Side effects of glucocorticoids

A
  • Psychiatric disturbances
  • HTN
  • Hyperglycemia
  • Long term: muscle wasting, osteoporosis, loss of adrenal function, skin breakdown
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27
Q

Describe Cromones

A
  • Help prevent bronchospasm
  • Taken prophylactically
  • Prevent release of histamine
  • Cromolyn (Nasalcrom)
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28
Q

Describe leukotriene inhibitors

A
  • Leukotrienes are inflammatory mediators
  • Zileuton (Zyflo): inhibits production of leukotrienes
  • Montleukast (Singular): blocks receptor for leukotrienes
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29
Q

Describe management for asthma

A
  • Bronchial smooth muscle spasm, airway inflammation, & mucous plugging of airways
  • Traditional Tx: bronchodilators, Xanthine derivatives, & steroids only in severe cases
  • Current Tx: 1st line is inhaled glucocorticoids (fluticasone, budesonide, beclomethasone), can be combined with bronchodilators
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30
Q

Describe management of COPD

A
  • Chronic respiratory symptoms (cough, SOB, sputum production), persistent airflow obstruction
  • Long acting anti-cholinergics
  • Long acting beta agonists
  • Short acting rescue inhalers
  • Inhaled glucocorticoids in severe disease
  • Bronchodilators are the primary treatment
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31
Q

Slide 21

A
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32
Q

Describe the uses and the harms of gastric acidity & secretion

A
  • Acidity helps to activate protease & controls growth of bacteria in the intestine
  • Harmful: if produced in excessive amounts can cause ulcers & hemorrhage of the stomach lining; peptic ulcers can occur
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33
Q

Describe antacids

A
  • Help control acidity & secretion
  • Contain a base which helps to neutralize acid by binding H+ in the stomach
  • Aluminum containing, magnesium containing, calcium carbonate containing, sodium bicarbonate containing
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34
Q

Side effects of antacids

A
  • Constipation
  • Electrolyte imbalances
  • Altered PH in body fluids
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35
Q

Describe H2 receptor blockers

A
  • Help control acidity & secretion
  • Histamine stimulates stomach cells to increase gastric acid secretion
  • H2 blockers bind receptor & prevent histamine from stimulating stomach cells
  • Famotidine, Mizatidine, Cimetidine
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36
Q

Side effects of H2 receptor blockers

A
  • Headache
  • Dizziness
  • Discontinuation can cause acid rebound
  • Electrolyte imbalances
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37
Q

Absorption of some antibiotics is decreased by _______-_______ in the presence of aluminum or magnesium antacids

A
  • 50-90%
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38
Q

Describe proton pump inhibitors

A
  • Help control acidity & secretion
  • Drugs: Omeprazole, Lansoprazole, Pantoprazole, & Esomeprazole
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39
Q

Side effects of proton pump inhibitors

A
  • Acid rebound if discontinued
  • Decreased bone mineralization
  • Increased risk of C. diff
  • Decrease absorption
  • Pneumonia risk
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40
Q

Describe helicobacter pylori

A
  • Gram negative bacteria
  • Research suggests it can cause gastroduodenal ulcers
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41
Q

Lists drugs that help control acidity & secretion

A
  • Anticholinergics: decrease the release of gastric acid & no longer used due to side effects; SE = dry mouth, constipation, urinary retention
  • Metoclopramide: stimulates motility in upper GI tract; SE = restlessness, drowsiness, fatigue
  • Prostaglandins: stimulates gastric mucus secretion & inhibits gastric secretion, not often used; SE = diarrhea
  • Sucralfate: forms protective gel in stomach & sticks to ulcers & shields them from stomach acid; SE = constipation
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42
Q

What causes diarrhea

A
  • Fast movement of food through GI tract which can lead to dehydration
  • Normal movement of food through GI tract = absorption of nutrients & water
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43
Q

List and describe antidiarrheal agents

A
  • Opioid Derivatives: Decrease GI motility, Reduce fluid loss through absorption of salt and water, Drugs = Diphenoxylate, Loperamide; SE = nausea & constipation
  • Bismuth salicylate: Stimulates water and electrolyte reabsorption, Also decreases gastric acid secretion; SE = no serious SE
  • Bile acid Sequestrants: Useful for diarrhea caused by excessive bile acid secretion
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44
Q

Describe laxatives & the different forms

A
  • Promote evacuation of bowel when no obstruction exists in GI system
  • Bulk forming: absorb water & swell in GI tract, stretches GI tract & stimulates peristalsis
  • Stimulants: irritate gastric mucosa
  • Hyperosmotic laxatives: draws mater into bowel & small intestine, stimulating peristalsis
  • Lubricants & softeners: helps water enter still which softens stool & allows for easier defecation
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45
Q

Describe Emetics

A
  • Induce vomiting
  • Given for poisonings or toxic ingestions
  • Stimulate emetic center in the brain
  • Ipecac, apomorphine
46
Q

Describe Antiemetics

A
  • Antihistamines (meclizine)
  • Anticholinergics (scopolamine)
  • Dopamine blockers
  • Serotonin receptor blockers
47
Q

Describe digestants

A
  • Help to digest food
  • Pancreatic enzymes (amylase, lipase)
  • Bile salts: help with lipid digestion & absorption
48
Q

Describe Cholelitholytics

A
  • Ursodiol- helps to decrease cholesterol content of bile, can aid in dissolution of gallstones
49
Q

Slide 33

A
50
Q

Describe bacteria

A
  • Unicellular organisms
  • Depend on nourishing medium to survive
  • Gram positive: Staph, Strep, & Enterococcus
  • Gram negative: E. coli, Pseudomonas, & Klebsiella
51
Q

Describe antibiotics

A
  • Used to treat many different bacteria
  • Many different classes of antibiotics, each with their own spectrum of activity
  • Choose based on: Comorbidities/Allergies, Bacterial strain, Physician/patient preference, Cost, Inpatient vs outpatient
  • Usually start broad & narrow based on culture
52
Q

Define selective toxicity, bactericidal, & bacteriastatic

A
  • Selective toxicity: drug kills the bacteria but not the hosts own cells
  • Bactericidal: ability to kill or destroy bacteria
  • Bacteriostatic: ability to limit growth & proliferation of bacteria but does not kill
53
Q

How do antibiotics work

A
  • Inhibition of cell wall formation & function: Penicillins, cephalosporins, carbapenems, vancomycin
  • Inhibition of bacterial protein synthesis: Tetracyclines, aminoglycosides, clindamycin, linezolid
  • Inhibition of bacterial DNA/RNA synthesis & function: Sulfonamides, fluoroquinolones
54
Q

Describe Penicillins

A
  • 1st antibiotic invented
  • Many forms of natural & semisynthetic penicillin: all share common structure called beta lactate ring
  • MOA: impairs construction of bacterial cell wall
  • 1st line for ear infections & strep
  • SE: rash, GI distress, & allergic reactions
55
Q

Describe Cephalosporins

A
  • MOA: Similar to penicillins in that they impair cell wall formation
  • Divided into 1st, 2nd, 3rd and 4th generation depending on spectrum of activity
  • Useful for UTIs, intra-abdominal infections, skin infections (earlier generations)
  • SE: allergic reactions with small chance of cross reactivity with penicillins, GI distress
56
Q

Other agents that inhibit cell wall synthesis

A
  • Carbapenems: Slightly broader spectrum of activity than penicillins or cephalosporins
  • Vancomycin: Good gram positive coverage, Can be nephrotoxic
  • Colisitin, Cycloserine, Ethambutol: Not commonly used due to serious side effects
57
Q

Describe Aminoglycosides

A
  • Bactericidal
  • Effective against gram negatives
  • Tobramycin, gentamicin
  • SE: oototxicity & nephrotoxicity
58
Q

Describe Macrolides

A
  • Bacteriostatic
  • Covers both gram + and gram -
  • Azithromycin= used for pneumonia and COPD
  • SE: GI distress
59
Q

Describe Tetracyclines

A
  • Bacteriostatic
  • Gram + and gram - coverage
  • Doxycycline: useful in tick borne disease, skin infections
  • SE: Gi distress, Calcium binding in teeth, sensitivity to UV rays
60
Q

Describe Linezolid

A
  • Effective against gram positives including MRSA
  • Can cause serotonin syndrome when used with other agents
  • SE: Thrombocytopenia
61
Q

Describe Clindamycin

A
  • Covers both gram + and some gram -
  • Good for penetrating wounds, infection in the female genitourinary tract
  • SE: GI distress & C. diff infection
62
Q

Describe Fluoroquinolones

A
  • Coverage of both gram + and gram -
  • Good for respiratory tract, UTIs, bone infections
  • SE: GI distress, insomnia, tendonitis
63
Q

Describe Sulfamethoxazole-trimethoprim

A
  • Covers both gram + and gram - bacteria
  • SE: hepatotoxicity & nephrotoxicity
64
Q

Describe Metronidazole

A
  • Coverage of anaerobic bacteria
  • SE: GI distress & confusion
65
Q

Side effects of Rifampin, Dapsone, & Clofazimine

A
  • Change in urine color
  • Liver dysfunction
  • Blood dyscrasias
66
Q

Describe Daptomycin

A
  • Binds to cell membrane and depolarizes cell
  • Used for skin and other infections
  • Activity against MRSA
  • SE: GI distress & myopathy
67
Q

Describe Nitrofurantoin

A
  • Reduced to toxic metabolite that inhibits bacterial function
  • Both gram + and gram - coverage
  • Used for UTIs
  • SE: GI distress & neurotoxicity
68
Q

Describe the types of skin & soft tissue infections

A
  • Impetigo: red sores on the face, normally caused by staph, treated with topical mupirocin
  • Cellulitis: most common bacteria (staph & strep), Cephalexin, amoxicillin for treatment
  • Abscess: coverage for staph & strep with addition of MRSA, Tx drugs = Doxycycline, Bactrim, Vancomycin
69
Q

Describe the types of pneumonia

A
  • Bacteria in the lungs, causes inflammation of lung parenchyma
  • Aspiration: coverage for strep & anaerobic, Tx drugs = Augmentin, Zosyn
  • Community acquired: coverage for strep & some gram -, Levofloxacin, Cefdinir + azithromycin
  • Hospital acquired: coverage for gram + and gram -, concerns for MRSA & pseudomonas, Vancomycin, Cefepime
70
Q

Describe the types of urinary tract infection

A
  • Cystitis: Lower urinary tract infection, Most common bacteria: E. coli, Fluoroquinolone, cephalosporins, bactrim, nitrofurantoin
  • Pyelonephritis: Infection of kidney, Can lead to long term damage if not treated,
    Fluoroquinolone, cephalosporins, bactrim
71
Q

Guidance of antibiotics

A
  • Try to pick an antibiotic that covers normal causative bacteria: Need to consider patient allergies and co-morbidities
  • If inpatient, will typically obtain a culture: This helps you to narrow antibiotics
  • Try to narrow antibiotics as soon as possible
72
Q

Describe antibiotic resistance

A
  • Bacteria can have natural or acquired defense mechanisms that make them resistant to some antibiotics
  • Beta Lactamase enzyme: found in some bacteria and helps the bacteria destroy penicillins and cephalosporins
  • Bacteria can also modify the drug binding site, prevent drug absorption, or develop pumps that expel the drug
73
Q

Examples of resistance

A
  • MRSA: methicillin resistant staph aureus
  • VRE: vancomycin resistant enterococcus
  • MDRO: multiple drug resistant organism
74
Q

How do we treat resistant bacteria

A
  • Switch to an antibiotic the bacteria is susceptible to
  • For some resistance, we have developed drugs to overcome the resistance
  • Beta-lactamase inhibitors- prevent bacterial enzyme from breaking down the drug: Augmentin- amoxicillin + clavulanic acid
75
Q

Slide 55

A
76
Q

List in order the contact precautions

A
  • Perform hand hygiene
  • Wear gloves
  • Wear gown
  • Used for MRSA, VRE, & scabies
77
Q

List in order the contact special enteric precautions

A
  • Used for C. diff infections
  • Hand hygiene must be with soap & water
  • Wera gloves
  • Wear gown
78
Q

List in order the airborne isolation precautions

A
  • Used for tuberculosis & chicken pox
  • Perform hand hygiene
  • Wear N95 respirator
  • Keep door closed at all times
79
Q

List in order the droplet isolation precautions

A
  • Used for influenza, mumps, & pertussis
  • Perform hand hygiene
  • Wear gloves
  • Wear surgical mask
  • Wear face shield or goggles
80
Q

List in order the enhanced precautions

A
  • Used for COVID-19
  • Perform hand hygiene
  • Wear gown
  • Wear respirator (N95, PAPR, P100)
  • Wear face shield or goggles
  • Wear gloves
  • Keep door closed
  • Visitation should be limited
81
Q

Describe the structure and function of viruses

A
  • Unicellular micro-organisms
  • Nucleic acid core + protein shell
  • Can’t replicate or synthesize proteins
  • Relies on host metabolic process to function
82
Q

Describe ways viruses transmit

A
  • Inhaled droplets
  • Contaminated food & water
  • Direct contact from infected people
  • Direct inoculation by bites
83
Q

Describe antiviral drugs

A
  • Target specific steps in the viral replication process
  • Limited number of approved drugs
  • Hard to design because you need to kill the virus without killing the human cells
84
Q

Describe the process of viral replication

A
  • Adsorption: virus attaches to host cell surface
  • Penetration/Uncoating: enters host cells & coating on virus is removed
  • Biosynthesis: virus takes control of cells machinery to initiate synthesis for new viral enzymes & proteins
  • Maturation & release: parts of virus are assembled into mature virus & released from host cell
85
Q

Describe herpes

A
  • Creeping or spreading skin lesions caused by virus
  • 8 types but most common include: HSV type 1, HSV type 2, Varicella-Zoster, Epstein-Barr, & Cytomegalovirus
  • Once infected the virus stays for life
86
Q

Describe Acyclovir and Valacyclovir

A
  • Used to treat herpes & varicella-zoster
  • SE: GI upset, Headaches, Dizziness, Kidney crystallization if given IV
87
Q

List anti-herpes drugs

A
  • Acyclovir
  • Valacyclovir
  • Cidofovir
  • Docosanol
  • Foscarnet
  • Ganciclovir
  • Valganciclovir
  • Imiquimod
  • Trifluridine
88
Q

Describe Cidofovir

A
  • Used to treat cytomegalovirus retinitis in people with AIDS, severe adenovirus, acyclovir resistant HSV
  • SE: Nephrotoxicity, neutropenia, GI upset, headache
89
Q

MOA of Cidofovir, Acyclovir, and Valacyclovir

A
  • Taken into virus infected cells & converted in acyclovir triphosphate: this inhibits DNA polymerase enzyme & impairs replication
  • Virus also incorporates drug into DNA strands which stops further DNA production
90
Q

Describe Docosanol

A
  • Topical drug used to treat herpes lesions around the mouth
  • MOA: Acts on host cells to prevent virus from absorbing; needs to be applied early in course
  • SE: local skin irritation & headache
91
Q

Describe Foscarnet, Ganciclovir and Valganciclovir, Imiquimod, and Trifluridine

A
  • Foscarnet: For CMV retinitis, Work similar to acyclovir
  • Ganciclovir and Valganciclovir: Treats CMV and other problems in AIDs patients
    Imiquimod: Topical agent, Enhances production of interferons
  • Trifluridine: Eye drops for herpes keratitis
92
Q

Describe the 3 strands of influenza

A
  • A: fevers, chills, malaise, headache, & sore throat
  • B: fevers, chills, malaise, headache, & sore throat
  • C: minor illness
93
Q

List anti-influenza drugs

A
  • Oseltamivir
  • Baloxavir
94
Q

Describe Oseltamivir

A
  • Effective against influenza A & B
  • Best if given within 48hrs of symptom onset
  • MOA: inhibits neuraminidase, interferes with biosynthesis
  • SE: CNS effects (hallucinations) & GI problems
95
Q

Describe Baloxavir

A
  • Used to prevent & treat influenza A & B
  • MOA: Inhibits endonuclease activity of selective polymerase acid protein, inhibits viral gene transcription, results in inhibition of virus replication
  • SE: diarrhea & vomiting
96
Q

HIV and AIDS treatments

A
  • HIV is a retrovirus: impairs function of certain cells in the immune system, can lead to immune system compromise & increased risk of opportunistic infection
  • AIDS: life threatening as immune system can’t defend against invasive micro-organisms, can also have neuromuscular involvement
97
Q

Goals of treatment for HIV and AIDS

A
  • Control Proliferation: highly active antiretroviral therapy (HAART), aggressive drug regimens, very effective but does not cure HIV, adherence can be difficult as non-adherence = resistance
  • Treat/kill opportunistic infections
98
Q

Describe HIV-Integrase inhibitors

A
  • Drugs: Dolutegravir, Elvitegravir, Raltegravir
  • MOA: Inhibits enzyme required for HIV to splice viral DNA
  • SE: fever, headache, GI problems
99
Q

Describe HIV-Protease inhibitors

A
  • Drugs: Ataznavir, Ritonavir, Lopinavir
  • MOA: inhibits enzyme needed to manufacture specific HIV proteins, prevents HIV from maturing
  • SE: alterations in fat deposition, increases in cholesterol & triglycerides, diarrhea, headache, fatigue
100
Q

Describe HIV-Nucleoside reverse transcriptase inhibitors

A
  • Drugs: Zidovudine, Abacavir, Emtricitabine, Tenofivir
  • MOA: Inhibit replication and proliferation of HIV-type I, act on HIV reverse transcriptase and inhibit step in replication
101
Q

Side effects of HIV-Nucleoside reverse transcriptase inhibitors

A
  • Anemia, Granulocytopenia
  • Fevers/Chills
  • Nausea, dizziness
  • Headache, Fatigue
  • Peripheral neuropathies
  • Liver dysfunction
  • CNS toxicity
  • Allergies: Abacavir
102
Q

Describe HIV-Nonnucleoside reverse transcriptase inhibitors

A
  • Drugs: Nevirapine, efavirenz
  • MOA: inhibit transcription of RNA into DNA
  • SE: GI distress & skin rashes
103
Q

Describe treating of opportunistic infections

A
  • Maintaining good immune function is the best defense
  • Antimicrobial can be prescribed if immunocompromised progresses & infection develops
104
Q

Describe Hepatits

A
  • Long incubation period between infection & symptoms
  • 5 types: A-E with C the most common
105
Q

Describe interferons

A
  • Group of proteins that have several effects: demonstrate non-specific antiviral activity
  • Divided into 3 major classes: Type I = alpha & beta, used to treat chronic HBV & HCV, Type II = gamma, and Type III = lambda
  • SE: Flu like symptoms, mood disturbances, and autoimmune disorders
106
Q

Describe Ribavirin

A
  • Used against several viruses including RSV, secondary for influenza
  • Combined with interferons for treatment of chronic HCV
  • MOA: not fully understood, impairs viral messenger RNA synthesis
  • SE: anemia, alopecia, GI upset, mood disorders
107
Q

Describe direct acting anti-virals

A
  • Used to treat Hepatitis C
  • All are combination medications
  • Drugs: Harvoni, Zepatier, Epclusa, Mavyret, Vosevi
  • MOA: depending on the drug, target either polymerase or protease to inhibit viral replication
  • SE: flu like symptoms, arthritic pain, GI upset, anemia
108
Q

Describe Nirmatrelvir and ritonavir

A
  • Treatment for mild to moderate COVID-19
  • MOA: inhibits SARS-COV-2 main protease, resulting in inhibition of viral replication
  • SE: diarrhea & dyspepsia
109
Q

Describe Molnupiravir

A
  • Treatment of mil to moderate COVID-19
  • MOA: becomes incorporated into SARS-COV-2 RNA, resulting in errors in viral genome & inhibition of replication
  • SE: hypersensitivity reactions, diarrhea, & vomiting
110
Q

Describe viral resistance

A
  • Viruses can mutate and make pharmacologic agents ineffective
  • Antivirals should be used judiciously
  • Overcoming viral resistance continues to be a research focus
111
Q

Describe viral vaccines

A
  • Stimulate production of immune factors: Expose the body to a piece of the virus, but not the actual virus
  • Drawbacks: Can be only partially effective, May require boosters
112
Q

Slide 92

A

Pharmacology (12 decks)

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