Patho Exam 2 drug

Upper Respiratory Tract Disorder

Anti- histamines

• MOA: block histamine release from receptors

• Indications: allergies, cold and flu symptoms, and others

• Treat: edema, inflammation, itch, rash, red/watery eyers, runny nose, sneezing

  • First generation

    • indications: induce sleep, prevent motion sickness, reduce anxiety

    • SE: sedation, dry mouth, dizziness, low BP

    • diphenhydramine (Benadryl)

    • Route: IM, IV, Po

    • nursing considerations: caution while driving, avoid alcohol

  • Second generation

    • much less sedating (doesn’t affect receptors in CNS)

    • cetirizine (Zyrtec0; loratadine (Claritin), fexofenadine (Allegra)

    • Route: PO

Asthma Meds

agonist

• chemical that binds to a receptor to produce a biological response

• produces an effect

antagonist

• chemical that may bind to a receptor, that blocks a receptor to a natural agonist

• does not produce a response

adrenergic amines

• drugs that stimulate the sympathetic nervous system (adrenergic nervous system)

• sympathomimetic drugs (sympathetic nervous system activation- epinephrine, norepinephrine)

  • alpha receptors

  • beta receptors

Muscarinic

• think parasympathetic nervous system and acetylcholine receptor

Cholinergic

• mimic the action of the neurotransmitter acetylcholine the primary transmitter of nerve impulses within the parasympathetic nervous system

Bronchodilators: short acting and long term inhaled beta 2- adrenergic agonists

• MOA: stimulates the beta 2 adrenergic receptors in the smooth muscle of the bronchi and bronchioles

  • enzyme adenyl cyclase causes increased production of cyclic AMP, resulting in bronchodilation

  • albuterol ( Proventil, Ventolin)

• Muscle tremor is the most frequent adverse effect

• Major adverse effects: excessive cardiac and CNA stimulation

  • symptoms of cardiac stimulation include angina, tachycardia, and palpitations

  • symptoms of CNS stumulation consist of agitation, anxiety, insomnia, seizures and tremors

Bronchodilators: Anticholinergics- muscarinic receptor antagonists

• muscarinic receptors antagonists bind to muscarinic receptors and inhibit acetylcholine mediated bronchospasms

• anticholinergics are most useful in long term management

  • ipratropium (Atrovent) is chemically related to atropine and blocks the muscarinic acetylcholine receptors in the smooth muscles of the bronchi in the lungs, inhibiting bronchoconstriction and mucus secretion

  • tiotropium (Spiriva): blocks action of acetylcholine in the bronchial smooth muscle

    • reduces bronchoconstrictive substance release

    • does not relieve acute bronchospasm

  • AE:

    • cough, nervousness, nausea, GI upset, headache, dizziness

    • vary depending on medication used

Xanthines

• MOA: relaxes bronchial smooth muscle, promoting bronchodilation and suppresses air-way responsiveness to stimuli that trigger bronchospasm-

• theophylline (Elixophyllin, Theo-24, Theochron)

• 2nd line of IV drug therapy

• not recommended for acute exacerbation of disease

• narrow therapeutic range→ review serum theophylline to determine theophylline dosages

• AE: cardiac and CNS simulation, toxic levels → convulsions (give diazepam (Valium) to control seizures

• Theophylline stimulates the chemoreceptor trigger in the medulla oblongata → N+V

Anti-inflammatory agents: corticosteroids

• not a rescue med

• MOA: suppresses the release of inflammatory mediators, block the generation of cytokines and the recruitment of eosinophils

  • increase the number and sensitivity of beta 2 adrenergic receptors, which restores the effectiveness of beta 2 bronchodilators

• suppresses airway inflammation, decrease mucous secretion, decrease edema of airway mucosa, promotes repair of damged epithelium, decrease airway reactivity

Anti-inflammatory Agents: Leukotriene modifiers

• montelukast (Singulair) is leukotriene modifier or leukotrine receptor antagonist; black box warning- cause cause neuropsychiatric events

• leukotrienes are proinflammatory mediators produced by the immune system during trauma, infection and inflammation, cysteinyl leukotrienes are a family of inflammatory lipid mediators

  • can cause sustained constriction of bronchioles and immediate hypersensitivity reactions

  • increases mucus secretion and mucosal edema

Anti-inflammatory agents: mast cell stabilizers

• MOA: prevent release of bronchoconstricitve and inflammatory substances, in response to allergens, other stimuli

• cromolyn (Nasal Crom, metered dose) stabilizes mast cells and prevents the release of bronchoconstrictive and inflammatory substances

• not effective in acute bronchospasm of status asthmaticus

Immunosuppressants: Monoclonal Antibodies

• omalizumab (Xolair)

• MOA: combines with free IgE blocking receptors on the surface of mast cells and basophils → less IgE available to combine with allergens

  • prevents IgE from attaching to the cells

  • Prevents development of inflammation

• Black box war: only administred only in health care settings under direct supervision of HCP who could initiate treatment for life-threatening anaphylaxis

Pain Meds

Non-opioids and adjuvants tramadol (Ultram), centrally acting analgesic

• MOA:

  • binds weakly to mu opioid receptors

  • inhibit reuptake of both norepi and serotonin

• Indication: treat moderate to severe pain, PO

• AE: usually none

  • drowsy, dizzy, headache, nausea, constipation, respiratory depression

  • rare: seizure when combine with other CNS depressants

Non-opioids and adjuvants gabapentin (Neurontin) and pregablin (Lyrica)

• anti- convulsants

• MOA: thought to spontaneously suppress neuronal firing

• Indications:

  • to complement effects of opioids

  • used specifically for neuropathic pain

• AE:

  • drowsy, dizzy, visual problems

  • can only be partially reversed with Naloxone

Non-opioids and adjuvants NSAIDS

• analgesic, anti-inflammatory, antipyetic

• non-steroidal anti-inflammatory drugs

  • nonselective COX inhibitors

  • Selective COX-2 inhibitors

• acetaminophen/Tylenol (APAP)

  • analgesic and antipyretic

  • Tylenol has NO anti-inflammatory properties

• used to treat mild-moderate pain

Types of NSAIDS

• aspirin (ASA): non selective COX inhibitor

• ibuprofen (Advil): non selective COX inhibitor

• napoxen (Aleve): non-selective COX inhibitor

• ketorolac (Toradol): non selective COX inhibitor

• celecoxib (Celebrex) : COX-2 selective NSAID

• Indications: used to treat mild-moderate pain; inflammation; fever; pain

NSAIDS: MOA

• anti-prostaglandins

• decreased prostaglandins

  • blocks a key enzyme: cyclooxygenase (COX)- an enzyme that is crucial to the production of prostaglandins

• 2 types of cyclooxygenase (COX)

  • COX-1: enzyme that protects the gastric mucosa and needed for thromboxane synthesis

    • ASA only Thromboxane activates platelets

    • COX- 2 enzyme responsible for inflammation and fever

Common SE of NSAIDS

• Non-selective COX inhibitor

  • ASA ibuprofen, naproxen

  • both COX-1 and COX-2 inhibited → prostaglandins AND thromboxane synthesis is blocked= analgesia, anti-pyretic, and anti-thrombotic

    • ASA is more anti-thrombotic than ibruprogen and naproxen

  • SE: GI upset, stomach ulcers, GI bleeding, rash, edema, kidney falure, increases in BP, inhibits platelet aggregation, SOA in asthma patients

• Selective COX-2 inhibitors

  • celecoxib (Celebrex)

  • only COX 2 blocked

  • COX-1 is not impacted as much (decrease risk of bleed)

  • Therefore: GI mucosa still protected and platelet function not impacted

  • no impact/ effect on platelets

  • However: serious cardiovascular thrombotic events

Black bow warnings with NSAIDS

• cardiovascular risk

  • NSAIDS may cause an increased risk of serious cardiovascular thrombotic events, MI, and stroke

  • risk may increase with duration of use

  • PTs with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk

• GI risk

  • increased risk of serious gastrointestinal AE including bleeding, ulceration, and perforation of the stomach or intestines which can be fatal

  • can occur at any time during use and without warning symptoms

  • elderly pt are at greater risk for serious GI events

Aspirin specific SE

• salicylate poisoning/toxicity

• ACUTE:

  • nausea/vomiting

  • seizures

  • cerebral edema

• Chronic

  • nausea/vomiting

  • tinnitus- ringing in the ears

  • hearing loss

Do not give to children less than 15 years of age. Risk of Reyes Syndrome

ketorolac (Toradol)

• Most potent NSAID

• Given IV or IM

• Indications: used to treat acute/ Short term moderate to severe pain

  • primarily used in the post-op setting

  • used for 5 days or less

  • reduces pain and inflammation

  • analgesic effect similar to morphine but without the respiratory depression

• SE consideration

  • similar risk of GI ulcers and higher risk of renal dysfunction (especially if patient has decreased renal function at baseline or are dehydrated)

acetaminophen (Tylenol)

• MOA: unknown

  • decreases prostaglandin synthesis in the CNS possibly

  • No anti-inflammatory properties

• Indications: mild to moderate pain and fever (anti-pyretic)

• Route: PO or IV (Ofirmev)

• Limitation

  • ceiling effect

  • No anti-inflammatory properties

AE: acetaminophen

• with normal doses: hardly any

• Large amounts: hepatic necrosis (acute), liver failure with chronic long term use and mild nephropathy

  • look for jaundice, elevated LFTs, and creatine levels

• adults dose restriction: 4g/24 hours

  • Hydrovodone with acetaminophen= Lortab/Norco

  • Oxycodone with acetaminophen= Percocet

morphine sulfate (opioid, Schedule 2) MS contin

• MOA: mu agonist: mimics the action of endogenous opioids at the mu receptors

  • morphine binds to the mu receptor and creates a response

• oral, liquid or pareneral

• Interations: alcohol and CNS depressants

• Indications: moderate to severe pain (5-8)

• AE: respiratory depression and CNS depression, constipation, drowsiness/fatigue, confusion, dry mouth, itching

• Nursing considerations: all opioids may impair the mental/ physical abilities, dont drive care

• Dosage percautions:

  • Normal PO starting dose: 30mg q3-4 hrs

  • Normal IV starting dose 1-4mg

hydromorphone (Dilaudid)

• Schedule 2

• Indications: Severe pain (8-10)

fentanyl (Duragesic)

• Indications: synthetic opioid for moderate-severe pain, surgical induction, and chronic pain

• PO, IV, IM, and transdermal

• extremely potent (0.1 mg IV fen= 10 mg IV morphine)

• Synthetic

codeine

• schedule 2

• Indications: mild to moderate pain, reduce coughing

• ONLY PO

• usualy combined with other analgesics (acetaminophen and aspirin)

• Precautions: not for children < 18 years old related to life threatening breathing problems

• AE: nausea

oxycodone

• Scheudle 2

• semi syntheitc derivative of codeine: PO ONLY

• Indications: moderate to severe pain, 10x more potent that codeine

hydrocodone

• Indications: moderate to severe pain and cough suppressant

  • teats round the clock chronic pain

  • analgesic effect similar to codein: 6x more potent than codeine

methadone

• full synthetic opioid analgesic

• Schedule 2

• longer half life than other opiods (higher risk for overdose)

• given PO

naloxone (Narcan) opioid antagonist

• MOA: binfs to opioid receptors but DOES NOT ACTIVATE (clogs them)

  • onset less than 2 min

  • Route: IV, IM, Intranasal

• Indications: antidote to reverse effects of morphine and morphine-like drugs

• AE:

  • abrupt reversal of opioid effects with recurrent pain

  • increased BP

Diabetes Drugs

Rapid acting- Insulin lispro

• starts working in 15 min onset

• peaks in 1 hour

• continues to work 2-4 hours

• Administered with meals to control postprandial meal glucose rises (give with food)

• must use with intermediate or long acting insulin

Short-acting insulin- insulin regular

• onset 30-60 mins

• peak 2-6 hours

• duration 3-8 hours

• given before meals to control postprandial hyperglycemia, but can also be given for longer acting glycemic control

  • tube feedings

  • insulin infusions

Intermediate acting insulin: NPH

• neutral protamine hagedron (NPH) insulin

  • protamine helps slow down absorption so that it last longer throughout the day

• onset 2-4 hours

• peak 4-10 hour

• duration 10-20 hours

• Cloudy insulin: lightly agitate before using (do not shake)- roll

• injected twice daily to help with glycemic control with meals and throughout the night

• can be given with short acting insulin

  • draw shorter acting first (clear), and then NPH (cloudy)

Long acting insulin: glargine

• Once a day dosing

• onset is about 70 mins and last all day

• controls blood sugar all day

• never mix with other insulins

• often given at night

Sulfonylureas

• glipizide, glyburide, glimepiride

• first category of oral drugs used to treat diabetes

• MOA: binding and closing the K-ATP channels in the pancreatic beta cells, stimulating secretion of insuling

  • increases bodys sensitivity or response to insulin

  • reduces the release of glucose from the liver

• SE: hypoglycemia

Biguanides (metformin)

• MOA: lowers blood glucose by decreasing production of glucose in liver

  • enhances glucose uptake and utilization by muscles

  • does not promote insulin release from pancreas

  • does not cause hypoglycemia

• Onset several days

• peak 2-4 weeks

• SE: abdominal bloating, N/V/D, risk for acidosis in patients with elevated creatine, do not use in patients with elevated ALT levels

• Nursing: monitor serum glucose levels, give 30 mins before meals

  • must be held for 48 hours post IV contrast usage

• Therapeutic use: glycemic control, prevent T2DM, polyscstic ovarina syndrome

• do not use with heart failure, kidney disease, liver disease, or excessive alcohol

GLP-1 agonist

• dulaglutide (Trulicity), liraglutide, exenatide (Victoza), semaglutide (Ozempic, Rybelsus)

• MOA: enhances glucose dependent insulin secretion

  • stimulate glucose-dependent release of insulin, inhibits prostpradnial reals eof glucagon, and suppresses appetite

  • slows gastric empyting

• use with metformin or other diabetic meds

• plasma level peaks in 2 hours, half life 2.5 hours

• SE: N/V/D, injection site reactions, headache, upper respiratory infections, weight loss

• Box warning: risk of thyroid c cell tumors

DPP4 inhibitors

• linagliptin, sazagliptin, sitagliptin

• MOA: inhibits dipeptidyl peptidase 4, an enzyme that inactives the incretin hormone

  • increases insulin release by enhacning the activity of incretins

  • reduce glucagon release

  • decreases hepatic glucose production

  • slow down digestion and decrease appetite

• SE: gastroinestinal problems (N/D, stomach pain), flu like symptoms, skine reaction, increased risk of pancreatitis

• indicated to use in combination with diet and lifestyle modifications

Sodium-glucose cotransporter 2 (SLGT2) inhibitors

• canagliflozin, empagliflozin (Jardiance), dapagliflozin (Farxiga)

MOA: prevents the kidneys from reabsorbing glucose back into the blood

• kidneys lower blood glucose levels and excess glu in the blood removed via urine

• kidney filter glu out of blood and then reabsorb glu back into blood → the protein that absorb glu are called sodium glucose transport proteins

• SLGT2 inhibitors block these proteins, less glu reabsorbed back into blood (decrease bld glu)

• SE: increased risk of UTI, genital mycotic infections, hypotension, fainting, dizzy, fatigue

• given PO, do not give to someone with ESRD or severe kidney disease

Glucagon

• hypoglycemia antidote

  • oral for awake patients that can swallow and talk

  • SC/IV/IM unconscious pts

• MOA: activates hepatic glucagon receptors, stimulates glycogenolysis, gluconeogenesis and release of glucose

• has short duration of action

  • half life 25-35 mins

• check finger stick after 15 min

alpha- glucosidase inhibitors

• acarbose

• MOA: blocks enzymes in small intestine that break down complex carbohydrates into monosaccharides

  • carbs must be in monosaccharide form to be absored

  • dely digestion and absorptionof glucos e

• if hypogylcemia occur treat with glucose NOT sucrose (table sugar) beacuse the drug will inhibit absorption of sucrose