Table of Contents

1. ID
2. GI
3. Pulmonology

ID
Treatment Regimens
SSTI
- Purulent
- Abscess, etc.
- Mainly caused by S. aureus
- Drain abscess + culture abscess
- Non-purulent
- Cellulitis, etc.
- Mainly caused by Streptococcus species
- No cultures needed
- Duration of therapy
- 5-10 days (shorter is better)

Drug Coverage Dose Notes

Cephalexin Streptococcus + 500-1000 mg PO q6 Minimal ADRs, no

MSSA safety concerns

NO MRSA Frequent dosing

required

Clindamycin Streptococcus + 300 mg PO TID C. difficile concern

MSSA + MRSA
Minimal ADRs, no
safety concerns

Doxycycline Streptococcus + 100 mg PO BID ADRs: Teeth staining,

MSSA + MRSA photosensitivity,
esophageal irritation,
potential DDI with
divalent cations

Avoid in
children/pregnancy

Sulfamethoxazole- Streptococcus + 1 DS tablet PO BID ADR: Renal

trimethoprim MSSA + MRSA dysfunction,
(Bactrim) hyperkalemia, rash,
SJS/TEN (often
associated with high
doses or IV dosing)

DDI: Warfarin
amoxicillin Streptococcus Often added to
Bactrim to improve
NO staphylococcus streptococcus
coverage

Augmentin Streptococcus + ADRs: Diarrhea

MSSA

NO MRSA

linezolid Streptococcus + Very broad antibiotic

MSSA + MRSA
ADRs:
thrombocytopenia,
serotonin syndrome

Oral vancomycin No systemic

bioavailability (mainly
for C. difficile
infections)

Necrotizing Fasciitis
● Type 1: polymicrobial
● Type 2: Monomicrobial (GAS > MRSA)
● Surgical intervention needed ASAP

Type I polymicrobial and Type II monomicrobial empiric therapy:

Drug Coverage Dose Notes

Vancomycin or Broad gram + Standard doses for

Linezolid coverage all drugs except
clindamycin (900 mg
+ Broad gram - and IV q8 = high dose)
anaerobic coverage
Zosyn or carbapenem
or [ceftriaxone + NOT for spectrum of
metronidazole] activity = toxin
inhibition
+

clindamycin

Type II definitive therapy:

Group A Streptococcus (S. pyogenes)

Drug Dose Notes

Penicillin G 4 million units IV q 4

hours for 10-14 days
+
900 mg IV/PO q8 for
Clindamycin 10-14 days

MRSA

Drug Dose Notes

Vancomycin Trough goal of 15

mg/L

Linezolid 600 mg IV/PO q12

Daptomycin 6-8mg/kg IV q24

Ceftaroline 600 IV q12

Vibrio vulnificus (saltwater)

Drug

Doxycycline + ceftriaxone

Aeromonas (Freshwater)

Drug

Doxycycline + ciprofloxacin

Pyomyositis
● Usually S. aureus
● MRI most effective in confirming diagnosis

Empiric Coverage

Drug

Vancomycin

Empiric Coverage (immunocompromised)

Drug

Vancomycin

Zosyn or Unasyn or carbapenem

Bite wounds

Pre-emptive antibiotic (animal or human bites)

● Duration = 3-5 days

Drug

Amoxicillin + clavulanate

OR

Ampicillin-sulbactam

Osteomyelitis
● Acute = days-2 weeks - Treat for 4-6 weeks
● Chronic = > 4 weeks - Treat for > 6 weeks
○ Treatment duration begins when removal of necrotic bone/tissue is complete
● MRI is most sensitive and specific
● WBC, CRP, and ESR can be used to help monitor improvement but not diagnostic
alone.
● Recommend withholding antibiotics until cultures are obtained
● OVIVA = IV and oral antibiotics similar results when adequate source control is
achieved
● Monitoring
○ Vancomycin - levels and AKI
○ nafcillin/oxacillin - AKI (AIN), hepatotoxicity, blood dyscrasias
○ Daptomycin - rhabdomyolysis (CK levels)
○ Fluoroquinolones - separate from divalent cations, QT prolongation
○ All antibiotics - C. difficile infections

Definitive treatment regimens

Organism Drug Dose Notes

Streptococcus Penicillin ceftriaxone 2g IV q24

species OR
ceftriaxone

MSSA or CoNS nafcillin/oxacillin nafcillin/oxacillin

OR 2g IV q4
cefazolin
Cefazolin 2g IV q8

MRSA or CoNS Vancomycin Target AUC 400-600

OR
daptomycin 8-10mg/kg IV q24

GNR (not ceftriaxone Ceftriaxone 2g IV q24

pseudomonas)
Osteomyelitis with hardware
● Add on rifampin 450mg IV/PO BID - to help penetrate biofilm on prosthetic
● Remove hardware whenever possible

Septic Arthritis
● Risk factors
○ Rheumatoid or osteoarthritis
○ Joint prosthesis
○ Intra-articular corticosteroid use
● Microbiology
○ S. aureus (MSSA or MRSA)
■ Trauma
■ Surgery
■ Prosthesis
■ SSTI
■ Arthritis
■ IVDU
○ Streptococci
■ Cellulitis
■ Asplenia
○ Neisseria gonorrhea
■ Sexually active
■ Younger
■ Complement deficiency
○ GNRs
■ Elderly
■ Immunocompromised
■ Gastrointestinal disorder
■ Recurrent UTIs

Empiric Treatment

Risk Factors Antimicrobial regimen

None Nafcillin/oxacillin 2g IV q4

MRSA risk factors, Vancomycin (target trough of 15)

trauma, surgery OR
prosthesis Linezolid 600 mg IV/PO q12
OR
Daptomycin 6-8mg/kg IV q24

Young, sexually Ceftriaxone 2g IV q24

active

IVDU Cefepime 2g IV q8
OR
Ceftazidime 2g IV q8
Diabetic Foot infection or DFI
● Inpatient treatment
○ Empiric coverage (MSSA/MRSA + GNR (+/- pseudomonas) + anaerobes
■ Vancomycin+ceftriaxone+metronidazole
■ Vancomycin+cefepime+metronidazole
■ Vancomycin+ciprofloxacin+metronidazole
■ vancomycin+zosyn/meropenem
● Duration
○ With source control = 0-5 days
○ Mild = 1-2 weeks
○ moderate/severe = 2-3 weeks
○ Osteomyelitis = >6 weeks
7
Meningitis
● Signs and Symptoms
○ Classic Triad = fever, altered mental status, nuchal rigidity
● Pathogens of meningitis
○ < 1 month old = L. monocytogenes
○ 1 month - 23 months = S. pneumonia, N. meningitidis
○ 2-50 years = S. pneumonia, N. meningitidis
○ > 50 years = S. pneumonia, N. meningitidis, L. monocytogenes

Antibiotic Treatment

Suspected Organism Drug Dose Notes

Streptococcus Ceftriaxone Ceftriaxone 2 g q12

Pneumoniae OR
Vancomycin (if Vancomycin trough
ceftriaxone resistance goal of 15 mg/L
> 10%)

N. meningitis ceftriaxone Ceftriaxone 2 g q12

H. influenzae ceftriaxone Ceftriaxone 2 g q12

Listeria Ampicillin Ampicillin 2g IV q4

Monocytogenes

Corticosteroid treatment
● Given before or with first dose of antibiotics (diminished effects if given later)
● Usually given for patients with S. pneumoniae meningitis (usually always)
● Decreases mortality and hearing loss
● Treatment
○ Dexamethasone 0.15mg/kg q6 for 2-3 days

Antibiotic prophylaxis
 ● For household contacts/very close contact
● Recommended agents
○ Rifampin
○ Ciprofloxacin
○ Ceftriaxone

Sepsis
● Identification
○ qSOFA
■ HAT
● Hypotension (SBP < 100)
● Altered mental status
● Tachypnea (RR > 22/min)
● Rivers Trial
○ Found lower mortality rate in EGTD group but results have not been
reproduced in other studies.
● Treatment
○ Fluids
■ Administer 30 mL/kg of crystalloids within 3 hours
■ crystalloids>colloids
● Dextrose 5%, 10%
● NaCl 0.9%, 0.45%
○ Avoid when Na and Cl levels are high
○ Avoid in AKI and nephrotoxicity (use plasmalyte or
lactated ringers instead)
● Lactated Ringers
● Plasmalyte
○ Antibiotics
■ Get cultures before starting antibiotics
■ Administer antibiotics within 1 hour
■ Start broad then de-escalate → Anti-MRSA
○ MAP
■ MAP goal > 65 mmHg
● (SBP + 2DBP) / 3 = MAP
■ Vasopressors
● Norepinephrine (1st line)
● Vasopressin (2nd line)
● Epinephrine (2nd line)
● Dopamine
● Phenylephrine
■ Inotropes have no place in sepsis (only used in HF)
○ Corticosteroid
■ No need for corticosteroids if fluids + vasopressors restore
hemodynamic stability.
■ If needed: hydrocortisone 200mg/day

MDRO
● Acquisition of DNA is the major method of acquiring resistance:
 ○ Conjugation (pili mating)
○ Transduction (bacterial viruses spreading DNA from bacteria to bacteria)
○ Transformation (bacteria pickup DNA from environment)
● Types of resistance
○ Enzymatic inactivation
■ Beta-lactamases
● Gram (+) secrete large quantities in the environment
● Gram (-) small amounts inside cell at high concentration
■ Aminoglycoside modifying enzymes
○ Non-enzymatic mechanisms
■ Decreased permeability
● Gram (+) = thicker cell wall = less permeability
● Gram (-) = reduced number of porin channels
■ Efflux pumps
● Mutations can increase # of efflux pumps to pump drug outside
of cell
■ Alteration of target site
● Decreases binding affinity of antibiotic to its target
● Definition
○ Resistant to at least one antibiotic from three or more classes
● Enterobacterales
○ Resistance is common
■ ESBL
● E. coli most common ESBL
● Treatment of ESBL is use of carbapenems
■ Carbapenem resistance
● Carbapenemases or porin mutation + high level AmpC
production
● Most common mechanism for carbapenem resistance is
KPC (klebsiella pneumoniae carbapenemase)
● Use of polymyxin
○ Generally not preferred due to nephrotoxicity and neurotoxicity
○ No gram + activity

Organism Drug Notes

MRSA Older Treatments: Both newer treatment are one time dose
Vancomycin
Linezolid
Daptomycin
Ceftaroline
Tetracycline
Bactrim

Newer Treatments:
Oritavancin
dalbavancin

Carbapenem Avycaz (ceftazidime Vabomere

Resistance + avibactam) - No pseudomonas
 Vabomere
(meropenem +
vaborbactam)

Recarbio
(imipenem/cilastatin
- relebactam)

Fetroja (cefiderocol)

Pseudomonas MDRO Avycaz (ceftazidime Zerbaxa

+ avibactam) - has no activity vs. CRE or ESBL
- 1000x higher affinity towards PBP in
Recarbio pseudomonas
(imipenem/cilastatin - DOC for pseudomonas
- relebactam)

Fetroja (cefiderocol)

Zerbaxa
(Ceftolozane -
tazobactam)

Cumulative ID
Treatments
AOM
● Risk factors
○ Age (pediatric)
○ daycare/siblings
○ No breastfeeding
○ Lower socioeconomic status
○ Exposure to cigarette
○ Winter
○ Anatomic abnormality
○ 1st episode < 6 months
● Treatment consideration
○ Severe AOM:
■ moderate to severe ear pain (otalgia) > 48 hours OR fever > 39 C
■ Initiate antibiotic treatment
○ Mild to moderate AOM
■ Mild otalgia AND temperature < 39 C
■ Age < 2 = initiate treatment
■ Age > 2 = observe for 48 hours UNLESS bilateral AOM
● Treatment duration
○ Age < 2 = 10 days
○ Age > 2 = 5-7 days
Antibiotic Treatment for no prior risk (No antibiotics in prior month, no conjunctivitis, no history
of recurrent AOM, no risk factors of antibiotic resistance)

Drug Dose Notes

Amoxicillin (Amoxil) High 90 mg/kg/day divided in BID First-line

dose or TID

Amoxicillin/clavulanate 90/6.4mg/kg/day divided BID First-line

(Augmentin) high dose

Antibiotic treatment for prior risk (antibiotics taken in past 30 days, failed response to
amoxicillin, concurrent conjunctivitis, history of recurrent AOM, increased risk of antibiotic
resistance (daycare, not vaccinated, living in area with high prevalence of resistance

Drug Dose Notes

Amoxicillin/clavulanate 90/6.4mg/kg/day divided BID First-line

(Augmentin) high dose

Cefdinir, cefpodoxime, Alternative therapy

cefuroxime, ceftriaxone

Pain Treatment
● Should normally always be given to relieve pain

Drug Dose Notes

acetaminophen 15 mg/kg/dose up to QID NTE 4000 mg/day

ibuprofen 10 mg/kg/dose up to QID NTE 2400 mg/day

UTI
- Cystitis
- Dysuria
- Urinary frequency
- Suprapubic pain
- Pyelonephritis
- All symptoms of cystitis
- Fever
- Flank pain
- Costovertebral angle (CVA) tenderness
- N/V

Cystitis - first line

Drug Dose Duration Notes

Nitrofurantoin 100mg PO BID 5 days

(Macrobid)
Bactrim 1 tab PO BID 3 days

Fosfomycin (Monurol) 3 gm PO for 1 dose 1 day

Cystitis - second line

Drug Dose Duration Notes

Amoxicillin, 3-7 days

cephalexin, cefdinir,
cefaclor,
cefpodoxime-proxetil

Ciprofloxacin, 3 days
levofloxacin

Cystitis - pregnancy

Drug Dose Duration Notes

amoxicillin

Amoxicillin -
clavulanate

cephalexin

Pyelonephritis - outpatient

Drug Dose Duration Notes

ciprofloxacin 7 days

levofloxacin 5 days

Bactrim 14 days

Pyelonephritis - inpatient

Drug Dose Duration Notes

ceftriaxone 7-14 days

Ciprofloxacin, 7-14 days

levofloxacin

Gentamicin, 7-14 days

tobramycin

Pyelonephritis - inpatient (risk for drug resistance)

Drug Dose Duration Notes

cefepime 7-14 days No enterococcus
activity

ertapenem 7-14 days ESBL

No enterococcus or
P. aeruginosa

meropenem 7-14 days ESBL, enterococcus,

and P. aeruginosa

Bacteriuria without symptoms

● Do not treat/screen unless:
○ Pregnant
○ Undergoing urological surgical procedure

GI
Portal Hypertension and Complications of Liver
● Portal hypertension
○ Results in development of varices
○ Most common cause is liver cirrhosis which is mostly caused by alcohol

Drug Notes

Propranolol

Nadolol

Carvedilol

Ascites
● Results from hypoalbuminemia due to lower protein synthesis from liver damage which
results in fluid escape to vascular space
● Non-pharmacologic
○ Low sodium diet ( < 2 g daily )
○ Fluid restriction ( < 1000 mL intake a day )
○ Paracentesis (draw out fluid from body)
○ TIPS

Drug Notes

spironolactone Drug of choice for ascites and more potent

than furosemide

ADRs: hyperkalemia, gynecomastia

furosemide Not effective for ascites as monotherapy

(often used with spironolactone)
Spironolactone:furosemide ratio = 100:40

ADRs: hypokalemia, lower BP, BUN/SCr

albumin Expands effective plasma volume to help
improve effect of vasopressors

Spontaneous bacterial peritonitis (SBP)

● Prevention
○ Norfloxacin, bactrim, or ciprofloxacin daily

drug notes

Cefotaxime (claforan) Drug of choice

ceftriaxone

ofloxacin

ciprofloxacin

Hepatorenal Syndrome or HRS

● Type 1 (aka HRS-AKI) more dangerous than Type 2 with a worse prognosis
● No cure for HRS, only palliative care

Drug Notes

Albumin IV

vasoconstrictors Non IV: enteral midodrine + SQ octreotide

IV: norepinephrine, vasopressin, terlipressin

Acute variceal bleeding

● Stabilize blood volume (hemodynamic stability)
● Airway management
● Fluid resuscitation with colloids (like albumin) → do not replace all lost volume with blood
● Bleeding control → octreotide (Sandostatin)
○ Do not use vasopressin or initiate beta blocker in acute setting

Prevention of Variceal Bleeding

● Non-selective beta blockers
○ Nadolol
○ Propranolol
○ Carvedilol
● Isosorbide mononitrate is NOT recommended
● If beta blocker intolerance: endoscopic variceal ligation (EVL) then add
pantoprazole

Hepatic encephalopathy
● Ammonia (NH3) is metabolized into urea by liver but in cirrhosis there is a buildup of
ammonia which leads to encephalopathy
● Not recommended:
○ Neomycin
○ Metronidazole
○ vancomycin
Drug Notes

Lactulose First line agent

Non-absorbable disaccharide that eventually
results in lactic acid which lowers GI pH, causing
NH3 → NH4+ preventing absorption of
ammonium.

ADRs: diarrhea

Rifaximin (Xifaxan) Lowers amount of urease-producing bacteria,

preventing ammonia production in gut

Drug induced Liver Injury or DILI

● Drug metabolism
○ Phase I: oxidation, reduction, hydrolysis
○ Phase II: glucuronidation, sulfation, glutathione
○ Phase III: transporters
● Mechanisms of injury
○ Intrinsic injury (direct injury to hepatocyte)
■ Dose-dependent injury
○ Idiosyncratic injury (modulation of immune reactions)
■ Allergic: hypersensitivity reaction
■ Metabolic: aberrant metabolism in susceptible patients
● Drugs associated with DILI
○ Antibiotics and antiepileptic drugs are the most common
● Histology
○ Hepatitis (hepatocellular) = ALT 3x > ULN
○ Cholestasis (bile ducts or canaliculi) = ALP 2x > ULN
○ Mixed = ALT 3x ULN AND ALP 2x ULN
● If DILI is suspected
○ Discontinue drug if:
■ ALT/AST > 3x ULN with symptoms
■ ALT/AST > 3x ULN AND (total bilirubin >2x ULN or INR > 1.5)
■ ALT/AST > 5x ULN for > 2 weeks
○ Automatically stopping drug when AST/ALT 3x > ULN without symptoms may
be unnecessary as liver can adapt and become tolerant
○ Do not rechallenge discontinued drug if
■ Enzymes increase 5x ULN
■ Immunologic reaction
● APAP
○ Metabolized into NAPQI by CYP2E1 which is normally scavenged by
glutathione
○ Ingestion of 7-10 grams of APAP can lead to lower glutathione levels → increased
NAPQI = hepatoxicity
○ Fasting
■ Can decrease glutathione sulfation and conjugation
○ Alcohol
■ Can decrease glutathione conjugation and induce 2E1
 ○ NAC is antidote for APAP toxicity
● Alcohol induced hepatitis
○ Best treatment: stop drinking → resolution occurs within weeks to months
● Herbal and dietary supplements or HDS
○ Body building and weight loss supplements are most commonly associated
with HDS

Toxicology
● Exposure history
○ Where patient was found
○ Where patient works
○ What is nature of exposure
○ Type of toxin
○ Amount of exposure
○ Onset of symptoms
● Toxidrome
○ Anticholinergic
■ Tachycardia
■ Fever
■ Dilated pupils
■ Constipation
■ Dry mucosal membranes
○ Cholinergic
■ Pinpoint pupils
■ Bowel sounds
■ Wet membranes
○ Opioid
■ Bradycardia
■ Bradypnea
■ Cold temperatures
■ Pinpoint pupils
■ Constipation
■ Dry mucosal membranes
○ Sympathomimetic
■ Tachycardia
■ fever
■ Tachypnea
■ Dilated pupils
■ Bowel sounds
■ Wet membranes
○ Sedative-hypnotic
■ Bradycardia
■ Bradypnea
■ Cold temperatures
■ Constipation
■ Dry membranes
● Type of antidotes
○ Chemical antagonist
■ Neutralizes toxicant
 ■ Example: protamine for heparin
○ Chelators
■ Used for heavy metals to prevent them from reacting with our body’s
cells
○ receptor/target antagonists
■ Antagonizes receptor and competes with substrate for receptor
■ Examples:
● Naloxone for opioids on mu receptors
● Flumazenil for benzodiazepines on GABA receptors
○ Binders
■ Andexanet alfa (Annexa) for eliquis and xarelto
■ Binds to and sequesters toxin to reduce their plasma concentration and
neutralize their effect
○ Dispositional antagonists
■ General strategies to alter PK
■ Examples:
● Whole bowel irrigation
● Gastric lavage
● Activated charcoal

toxicant antidote/treatment

acetaminophen NAC
● Sulfation, glutathione precursor,
glutathione substitute, improves multi-
organ failure
● Rumack-Matthew Nomogram
● IV and PO equivalent when
administered within 8-10 hours
○ IV preferred in:
■ Fulminant liver failure,
pregnancy, and
neonates
○ Oral not well tolerated (N/V)

Local anesthetics (bupivacaine, ropivacaine, Lipid emulsifier

-”caine”)

Heparin (UFH and LMWH) protamine

Factor Xa (Eliquis and Xarelto) Andexanet alfa (Annexa)

Theophylline, dapsone, carbamazepine, phenytoin, Activated charcoal

quinine → These People Drink Charcoal Quickly

ASA IV sodium bicarbonate

IV potassium
IV glucose
Activated charcoal
hemodialysis
Theophylline, urea, metformin/methanol, hemodialysis
barbiturates, lithium, ethylene glycol, valproic
acid, acetaminophen, carbamazepine, salicylic
acid → TUMBLE VACS

Anticholinergic toxicity (jimson weed, Physostigmine (acetylcholinesterase inhibitor

atropine, etc.) to increase acetylcholine levels)

Pulmonology Cumulative
Asthma
- Imbalance of cholinergic and adrenergic action
- Cholinergic = bronchoconstriction
- Adrenergic (Be) = bronchodilation

Drug Class Mechanism

Anticholinergics/LAMAs Anticholinergic → prevents bronchoconstriction

- Ipratropium (Atrovent) and are often long acting
- Tiotropium (Spiriva) Mainly targets M3 receptors
- Aclidinium
- Umeclidinium (incruse Ellipta)
- - “ium” drugs

SABAs Short acting beta 2 agonist → causes

- Terbutaline bronchodilation
- Albuterol
- Levalbuterol
- Pirbuterol
- Contains “but” in the name

LABAs Long acting beta 2 agonist → causes

- Salmeterol bronchodilation
- Formoterol
- Arformoterol
- Indacaterol
- Drugs that end in “terol”

Mast cell degranulation inhibitors Non-specific stabilizer of mast cells, inhibits

- Cromolyn sodium Cl- channel which prevents calcium influx and
stops mast cell degranulation

Glucocorticoids / ICS Anti-inflammatory effects in body and helps

- Beclomethasone increase beta 2 agonist effects by
- Budesonide upregulating B2 receptors and stimulate
- Fluticasone cAMP to augment bronchodilation
- Mometasone
- Ciclesonide
- Often ends in “sonide” or “sone”

Leukotrienes Blocks leukotriene receptor which is often

 - Montelukast associated with smooth muscle constriction in
- zafirlukast airways and immune system activation

Leukotriene synthesis blocker Inhibits 5-lipoxygenase which is needed for

- Zileuton/Zyflo leukotriene formation

omalizumab/Xolair Binds to IgE and prevents binding of IgE to

variety of cells to prevent immune activation

IL-5 monoclonal antibodies Neutralizes IL-5 cytokine which is involved in

- Mepolizumab, reslizumab eosinophil asthma

IL-4 antibody Blocks IL-4 receptor which blocks

- Dupilumab inflammation pathway

COPD
- Drugs to avoid with COPD
- Beta blockers
- Respiratory depressants
- Treatment guidelines
- Dyspnea pathway
- LABA or LAMA first → LAMA + LABA
- Exacerbation pathway
- LABA or LAMA first then:
- LABA + ICS (if eos > 300 or eos > 100 and > 2 moderate
exacerbations/1 hospitalization)
- LABA + LAMA
- If eos < 100 → add roflumilast or azithromycin
- If eos > 100 → add ICS
- If there is still no relief add roflumilast or
azithromycin
- Gold assessment tool
- A
- mMRC 0-1
- CAT < 10
- 0 or 1 exacerbation but no hospital admission
- Initiate bronchodilator
- B
- mMRC > 2
- CAT > 10
- 0 or 1 exacerbation but no hospital admission
- Initiate LABA or LAMA
- C
- mMRC 0-1
- CAT < 10
- 2 or more exacerbation or 1 exacerbation that leads to hospital
admission
- Initiate LAMA
- D
- mMRC > 2
 - CAT > 10
- 2 or more exacerbation or 1 exacerbation that leads to hospital
admission
- Initiate combinational therapy

Drug mechanism

Anticholinergics/LAMAs Anticholinergic → prevents bronchoconstriction

- Ipratropium (Atrovent) and are often long acting
- Tiotropium (Spiriva) Mainly targets M3 receptors
- Aclidinium
- Umeclidinium (incruse Ellipta)
- - “ium” drugs

SABAs Short acting beta 2 agonist → causes

- Terbutaline bronchodilation
- Albuterol
- Levalbuterol
- Pirbuterol
- Contains “but” in the name

LABAs Long acting beta 2 agonist → causes

- Salmeterol bronchodilation
- Formoterol
- Arformoterol
- Indacaterol
- Drugs that end in “terol”

Glucocorticoids / ICS Anti-inflammatory effects in body and helps

- Beclomethasone increase beta 2 agonist effects by
- Budesonide upregulating B2 receptors and stimulate
- Fluticasone cAMP to augment bronchodilation
- Mometasone
- Ciclesonide MONO-THERAPY ICS IS NOT
- Often ends in “sonide” or “sone” APPROPRIATE FOR COPD

Oral PDE4 inhibitor Prevents degradation of cAMP which helps

- Roflumilast (Daliresp) relax airways and decrease inflammatory
response

Cystic Fibrosis
- Respiratory management
- Bronchodilators
- Hypertonic saline
- Dornase alpha
- Chest percussion
- Inhaled antibiotics
- Nutrition support
- Enzyme supplement
- Fat soluble vitamins (ADEK)
- 110-200% caloric requirement
Drug mechanism

Ivacaftor (Kalydeco) Enhances Cl- channel conductance

Not for mono-therapy for patients with F508
deletions
Used in ages > 1

lumacaftor/ivacaftor (Orkambi) Chaperone + Cl- channel enhancement

Used for patients who are homozygous for
F508 deletions
For patients > 2 years old

tezacaftor/Ivacaftor (Symdeko) Chaperone + Cl- channel enhancement

Used for patients who are homozygous for
F508 deletions
For patients > 6 years old

Elexacaftor/tezacaftor/ivacaftor (Trikafta) Chaperone + Cl- channel enhancement

Used for patients who are homozygous or
heterozygous for F508 deletions
For patients > 12 years old

PAH
- 3 pathways
- NO
- raises cGMP levels inducing vasodilation
- IP
- activation of adenylyl cyclase which increases cAMP levels. Increased
cAMP activates PKA which inhibits myosin light chain kinase which
leads to smooth muscle relaxation and vasodilation
- Endothelin
- blocking receptors prevents vasoconstriction and endothelial cell
proliferation

Drug/Drug Class Mechanism

PDE5 inhibitors Prevents degradation of cGMP helping to

- Tadalafil (Adcirca) prolong the effects of the NO pathway
- Sildenafil (Revatio) (vasodilation)
Methylxanthine
- Theophylline
- Aminophylline
- Theophylline:aminophylline = 100:79

Endothelin receptor antagonist Prevents vasoconstriction in airway and

- Bosentan (Tracleer) - inhibits both prevents endothelial cell proliferation
ETa and ETb
- Ambrisentan (Letairis) - inhibits only
ETa
- Macitentan (Opsumit) - inhibits both
ETa and ETb
Prostanoids Induces IP pathway → vasodilation and anti-
- Epoprostenol proliferation
- Treprostinil
- Iloprost
Non-prostanoids
- selexipag

Soluble guanylate cyclase stimulators Sensitizes sGC to NO and directly stimulates

- Riociguat (Adempas) sGC via binding site different from NO
- Pyrrazopyridine moiety

Medicinal chemistry review

- Anticholinergic
- Essential features
- Quaternary nitrogen to interact with negative aspartate group
- Minimal of 2 methyl groups for hydrophobic pocket
- Ethylene bridge
- Ester to interact with tyrosine and threonine (hydrogen bond)
- Methyl of acetoxy group cannot be extended without blocking it
- Increase duration of action
- Bulky group attached to quaternary nitrogen
- Two aromatic groups attached to ester/reduced carbonyl
- Modify ring to make ester less susceptible to hydrolysis
- Replace ester with hydroxyl (reduced carbonyl)
- Adrenergic receptor agonist (SABA and LABA)
- Aromatic ring with polar groups
- Meta-phenol can be replaced with other hydrogen bonding groups
- Alcohol forms hydrogen bond to binding site
- Substituents at alpha carbon other than hydrogen will increase duration of
action due to MAO resistance
- Ammonium forms ionic bond to binding site
- N-alkyl groups affect target selectivity
- Larger N-alkyl groups leads to selectivity to receptor and slow MAO
metabolism
- Ring configuration
- Catechol
- Resorcinol
- Salicyl alcohol
- N-formamide
- Glucocorticoid
- Essential groups
- Pregnane skeleton
- Ring A-en-one system
- 17B-ketol side chain
- C-21 hydroxyl group
- Increase anti-inflammatory and mineralocorticoid activities
- 9a fluorine or 9a chlorine
- 21 OH
- Increase anti-inflammatory only
- 1-dehydro (flattens ring)
 - 6a methyl or 6a fluorine
- 11 beta hydroxyl
- Decreases mineralocorticoid
- 6alpha methyl
- 16a or 16b methyl
- 16a or 17a acetonide
- 16a OH
- Endothelin receptor antagonist
- Characterized by pyrimidine ring