pharm comprehensive final

Parasympathetic nervous system affect on pupils, salivary glands, HR, bronchioles, stomach, BV, liver, intestines and bladder

-Pupils constrict - don’t need to see well when relaxing

-Increased salivation - to digest food

-Decreased HR -

-Bronchioles constrict - don’t need to breathe better when relaxing

-Stomach stimulates digestion

-Blood vessels dilate = decreased BP - bc muscles dont need more O2

-Liver released bile & increases glucose storage - digest

-Increased peristalsis - digest

-Bladder contracts - promotes urination - bc relaxed

what is the primary neurotransmitter for the PNS

Ach, Acetylcholine

what is the primary receptor on target tissues for the PNS

muscarin receptors on target tissues for Ach

what is bethanechol used for

treatment of urinary retention, to make pt pee -> ONLY IF NO BLOCKAGE

how does bethanechol work

acts on musc receptors in bladder to initiate contraction to initiate peeing

what are common side effects of bethanechol

since it is an cholinergic drug = increased secretion

• increased salivation, sweating, abd cramping, HYPOtension

what is the pharmacological class of bethancehol

parasympathomimetic, muscarinic agonist

what are symptoms of a cholinergic crisis

Excess salivation, lacrimation, urination, defection, gastric upset, emesis & muscle weakness

what is the pharmacological class for atropine

parasympatholytic, an anti-cholinergic (muscarinic antagonist)

what is the MOA for atropine

inhibits effects of Ach in body, inducing FIGHT OR FLIGHT

uses for atropine

to INCREASE HR, to BRONCHODILATE, to decrease secretions (anti-chol) and to dilate pupils

SE of atropine

bc its an anti-cholinergic: can cause urinary retention, constipation, dry mouth, TACHY, palpations

SNS effect on pupils, bronchioles, heart, blood vessels, glucose, GI, bladder

Pupils dilate (to see better in times of emergency)

-Bronchioles dilate to (to breathe better)

-Tachycardia

-Blood vessels dilate (INCREASED BP)

-Increased glucose production (for energy)

-GI system relaxes (decreased peristalsis)

-Bladder and uterus relax

primary neurotransmitter for SNS

EPI/NE

primary receptor for SNS

adrenergic receptors on target cells

where are alpha 1 receptors

on blood vessels and smooth muscle

what does Epi/NE binding to A1 cells cause

causes VASOCONSTRICTION = INCREASED BP

where are beta 1 cells located

on heart (bc 1 heart)

what does epi/NE binding to b1 cells cause

INCREASED HR

what drug is a beta 1 receptor blocker

metoprolol (decreases HR)

where are beta 2 receptors located

on the lungs and airways

what does epi/NE binding to B2 receptors cause

bronchodilation

what prototype is a beta2 agonist

albuterol

what are the 3 main uses for phenylephrine

• nasal decongestant

• pupil dilation

• to increase BP (anti-hypotensive)

what is the pharmacological class of phenylephrine

sympathoMIMETIC

AE of phenylephrine

burning of mucosa, rebound congestion, reflex bradycardia

BBW for phenyleperhine

death can occur with IV infusion → use other routes

what is prazosin used for (the TC)

anti-HTN, to decrease BP

what is the pharmacological class of PRAZOSIN

A1 receptor ANTAGONIST, sympatholytic

what is the MOA for prazosin

causes a RAPID decrease in perioheral resistance, vasodilating BVs = reduction of BP

what is the major AE for prazosin, and what intervention is done to decrease its effects

It causes orthostatic hypotension, so the first dose should be given at bedtime to avoid syncope/unconsciousness = FIRST DOSE EFFECT

what are two types of nociceptive pain

somatic - surface pain, including burns, cuts, scrapes

visceral - deep pain, including appendicitis and abdominal pains

what does neuropathic pain feel like

pins and needles, bruning, tingling, painful cold, electric shock like.

what does substance P do in the body

it enhances the transmission of a pain signal in the spinal cord and promotes inflammatory responses

what are the two opioid receptors

Mu and Kappa

what does activation of the Mu receptor cause

pain relief, EUPHORIA, RESPIRATORY DEPRESSION

what does activation of the Kappa receptor cause

pain relief, sedation, dysphoria

what is the class and action of morphine

opioid, binds to Mu and Kappa receptors to produce profound analgesia

SE of morphine

RESPIRATORY DEPRESSION, sedation, urinary retention, N/V, CONSTIPATION (admin stool softener), hallucinatinos

what do you need to monitor before and after giving morphine

BP, HR, RR

how fast does naloxone work

immediately

what is the class/MOA of naloxone

opioid receptor antagonist, blocks and replaces opoids at Mu and Kappa receptor sites

when do you administer naloxone in regards to a pt’s RR

if their RR < 10

Cox 1 pathway

protective functions

cox 2 pathway

inflammation and pain

class and MOA for aspirin

salicylate (5-ASA), NSAID → inhibits synthesis of inflammatory and pain prostaglandins

uses for aspirin

anticoag properties to prevent stroke/MI, pain, fever, inflammation

AE of aspirin

bleeding, GI discomfort, Stevens Johnson syndrome (NSAID)

CI/Interaction for Aspririn

CI in children bc it can cause REYES syndrome

uses for acetaminophen

anti-pyretic and analgesic (NOT ANTI-INFLAMM)

MOA for acetaminophen

inhibits synthesis of pain prostaglandins in the BRAIN

AE of acetaminophen

Stevens johnson syndrome (rash/blisters on face), severe liver injury, anaphylaxis

• DRUG IS HEPATOTOXIC!!!

antidote for acetaminophen

acetadote

classes and MOA for sumatriptan

5-HT (serotonin) receptor drug - vasoconstrictor of intracranial arteries = anti-migraine

SE of sumatriptan

tingling, tightness, pressure in chest, warm flushing sensation = “TRIPTAN RUSH”

nursing considerations for sumatriptan

NOT PREGNANCY SAFE

• not preventative, can only take after symptoms start

uses for ibuprofen

analgesic, anti-inflamm and anti-pyretic

MOA of ibuprofen

inhibits conversion of arachidonic acid to COX - inhibiting production of inflammation and pain prostaglandins

SE of ibuprofen

GI issues, can worsen all bleeding (inc. peptic ulcers)

CI/Caution for ibuprofen

has allergy cross sensitivity with aspirin (NSAIDS)

what organ is acetaminophen hard on

liver → HEPATOTOXIC

what organ is ibuprofen hard on

KIDNEYS

stevens johnson syndrome

blisters and rash along face, neck, trunk

• an allergic rxn to NSAIDS, acetaminophen and sulfa drugs

what is important pt education for all corticosteriods

MUST TAPER OFF of them.

• stop abruptly could cause addisons disease

• long term use causes cushings disease

S+S of cushing’s

moon face, buffalo hump, abdominal obesity, muscle wasting and thin extremities, stretch marks, hirsutism

class and action of prednisone

corticosteroid, decreases inflammation and suppresses the immune system

CI for prednisone (and all corticosteriods)

active infection!!!!

7 S’s of corticosteriods

• SWOLLEN

• SEPSIS (beware if infxn)

• SUGAR (HYPERgly)

• SKINNY (extremities)

• SIGHT (monitor vision changes)

• SLOWLY (taper)

• STRESS (need to adjust dose)

what does activation of SNS cause in the nose

constriction of arterioles = open airways

• SYMPATHOMIMETIC DRUGS = open airways

what does activation of the PNS do in the nose

dilates arterioles, increasing mucous production = stuffy nose

what cells drive the allergic response

mast cells, which release histamine which cause symptoms

• IgB antibody binds to mast cell. Then the allergen binds to the antibody on the mast cell = triggering mast cell to release histamine = causes symptoms

what is the medical term for hay fever

allergic rhinitis

PC of diphenhydramine (and what that means)

1st generation H1 antagonist, antihistamine

• CAUSES DROWSINESS

uses for diphenhydramine

for minor allergies and pre-medication for certain meds, chemo and blood transfusions

SE of diphenhydramine

drowsiness (diminishes with long term use), paradoxical excitation in kids and anticholinergic effects

CI for diphenhydramine

bc of anticholinergic effects, it tries everything out so dont use in obstructions

• BPH, GI obstructions, asthma

class of loratadine (and what that means)

2nd generation H1 antagonist

• IS NON-DROWSY

MOA/USES for loratadine

long acting, treats minor symptoms of allergy when taken 1x/day

CI for loratadine

for kids under 2

can you overdose on loratadine

yes, can cause problems to many organ systems

fluticasone PC and MOA

corticosteroid, so decreases inflammation in nasal passages = reduces congestion

CI for fluticosone (and other corticosteriods)

pts with active infections

pt. education for fluticasone

not for immediate relief

• spray in nose 1-2/day

• bc nasal route = can cause epistaxis and nasal irritation

class/MOA for dextromethorphan

cough suppressant, acting in the medulla WITHOUT euphoric effects (15-30 min onset)

CI for dextromethorphan

• kids under 6

• pts with chronic cough (from COPD or asthma) → bc they need to clear these secretions from their throats

• NO GRAPEFRUIT!

classes for oxymetazoline

nasal decongestant, SYMPATHOMIMETIC

MOA for oxymetazoline

via A1 receptor stimulation, causes constriction of nasal mucosa arterioles = drying out mucous membranes within minutes

SE/AE of oxymetazoline

rebound congestion, dryness or stinging of nasal mucosa

SNS effect on bronchioles

BRONCHODILATE.= breathe better

PNS effect on bronchioles

BRONCHOCONSTRICT = dont need to breathe hard when resting

common S+S of pulmonary distress

dyspnea, increased WOB (nasal flaring, accessory muscle use, retractions, orthopnea, paroxysmal nocturnal dyspnea)

what does asthma entail

inflammation and muscle tightening (bronchoconstriction) of airway, with excess mucous production

status asthmaticus

exercise induced asthma

what is bronchospasm

muscle around airways constrict, narrowing airways

inflammation/mucous r/t asthma

the lining of airways is swollen with THICK, STICKY mucous clogging airways making it harder to breathe

S+S of asthma attack

cough, WHEEZE, chest tightness, intense breathlessness

what is COPD, and what are the two subcategories

the chronic, irreversible airflow obstruction leading to hypoxia from decreased gas exchange

• two forms = chronic bronchitis and emphysema

Chronic bronchitis

BLUE BLOATER (overweight and cyanotic)

• mucous in airways and inflammation = daily productive cough

EMPHYSEMA

PINK PUFFER (older and thin, quiet chest)

• PERMANENT ENLARGEMENT AND DESTRUCTION OF ALVEOLI

• bronchioles lose elasticity, so alveioli dilate to allow air flow

  • ultimately overdilate, causing breakdown of alv.

most common cause of COPD (emphysema and chronic bronchitis)

chronic smoked tobacco use