nurs 116 - lec 5

glucocorticoid side effects

none or minimal

• acute tx only (high dose, IV/IM, short term)

• local route (ex injection into joint)

risk of systemic effects

• long term tx

• systemic route (PO, IV, IM)

• cushing syndrome

how to stop glucocorticoid tx?

negative feedback - NO ABRUPT STOPPAGE

• wean until 0 bc if it suddenly stops, the body will think it had enough and will stop producing it

cushing syndrome ss

red cheeks

fat pads

abd stretch marks

bruise easy (lose platelets, WBC)

muscle wasting

why is cushing syndrome so dangerous?

by the time you realize it, it’s already too late

what is liver steatosis

fat build up in liver

acute inflammation time frame

-occurs within 15 min (allergy)

-leaves in less than 10 days

chronic inflammation time frame

acute inflammation (15 min) → more than 10 days

chronic inflammation steps

1) clotting occurs with cells (WBC, collagen, fibroblasts)

2) granulation restores vascular supply → epithelial cells fill in granulation tissue

3) restored epithelium thickens and forms scar tissue

why is chronic inflammation bad?

-tissue destruction bc of repetitive inflammatory cascade → effects fx

-secretion of regenerative mediators (ex. tissue growth factors) leads to neoplasms (cancer)

-scar tissue formation

• less vascular (less perfusion)

• less flexible (tears easier)

• less strong (80% of former strength)

what is the most common allergy in yeg?

allergic rhinitis, 40% of pop

allergic rhinitis ss, bw and tx

ss: rhinitis (nasal discharge and swelling), conjunctivitis (eyes), sneezing, snoring, itching, headache from nasal-sinus infection

bw: high eosinophils

tx: 1) antihistamines pre/during exposer; 2) intranasal corticosteroids (insufflation) for nasal mucosa inflammation

allergic rhinitis drugs “flat mom butt”

fluticasone

mometasone

budenoside

atopic dermatitis characteristics (3)

allergic disease, autoimmune profile

• high IgE in plasma

lichenification: scar formation

risk of super infection: bacterial + viral

what is the cause of eczema (skin mutation)?

filaggrin gene mutation in skin → more water escapes → allergens get in easier

can you grow out of atopic dermatitis?

yes

do you use soap when treating dermatitis?

no, will dry out skin

atopic dermatitis tx

topical glucocorticoids

antihistamines

antibiotics/virals for infections

risk factors of psariosis

family hx + triggers

psoriasis skin changes

hyperkeratosis (thickening of skin)

thinned stratum granulosum

vasodilation

dilated dermal papillae

psoriasis ss and tx

ss: dry scaly skin patches, non pruritic (itchy = no histamine)

tx: glucocorticoids (local→ systemic as needed), moisturizing cream

eczema vs psoriasis

eczema: intense itching, oozing & crusting, appears on flexural skin surfaces

psoriasis: itching less severe, scaling, appears on extensor skin surfaces

what is arthritis

joint inflammation

what is rheumatoid arthritis (RA)

chronic systemic rheumatic (inflammatory) disease

autoimmune

risk factors of RA

family hx, gender

steps for RA

1) WBC and pro-inflammatory mediators

2) dysfunction of synovial cavity (pannus)

3) destruction of surrounding tissue (bone, cartilage)

4) thickening and deformity of affected tissue → autoimmune

pannus joint

-no cartilage

-bone erosion

-swollen synovial membrane

RA ss, bw and tx

ss: synovial join inflammation, anorexia

bw: high c-reactive protein

tx: NSAIDs, glucocorticoids (PO)

RA biologic drugs: response modifying agent

stops cytokines

end in “mab”

parenteral

RA biologic drugs: DMARDS (disease modifying anti-rheumatic drugs)

enhance anti-inflammatory mediators (ex. adenosine)

methotrexate

parenteral

what is osteoarthritis (OA)

degenerative disorder of articular cartilage

wear and tear arthritis (fewer joints affected)

OA risk factors

mechanical stress, obesity, age, gender

how does estrogen effect bones to prevent OA?

it protect bones so menopause increases risk

OA steps

cartilage changes

1. less proteoglycans

2. less collagen

3. inflammatory mediator release (cytokines, prostaglandins) → more inflammation

4. cartilage tissue destruction → bone-bone articulating surface

bone spurs

bone overgrowth caused by bone-bone contact which stim more growth (+ feedback)

OA tx drug classes

NSAIDS, glucocorticoids (local)

OA local glucocorticoid treatment

cortisone joint injection using ultrasound

inflammatory bowel disease (IBD)

group of chronic inflammatory conditions in GI tract

canada has the highest incidence in the world

crohn’s vs. ulcerative IBD

crohn’s: gums → bums, patchy inflammation

ulcerative colitis: inner lining of bowel/lg int, continuous

IBD ss, dx

ss: tummy pain, weight loss, fever, tiredness

dx: flare-ups affect skin, eyes, liver, joint/use x-rays and stool samples

T or F: there is a cure for IBD

F

what is a fistula

abnormal connection b/w 2 organs which makes the area less flexible → pain

IBD trigger

endogenous GI host flora (antigen) → inflammation

IBD tx drug classes

-DMARDS → biologics

-glucocorticoids

sulfasalazine tx, drug class, drugs, admin + subjugates

IBD

DMARD: biologic

azulfidine, salazopyrun

PO: activate metabolites → 5-ASA, sulfapyridine

5-ASA drugs (“mat”) + fx

mesalamine, asacol, teva

treat IBD, esp ulcerative colitis

local NSAID effect

PO, rectal (long-sustaining tablet)

sulfapyridine tx, s/e?

treat IBD

systemic ADME + anti-inflammatory = side effects

what is asthma

chronic inflammatory airway disorder (not autoimmune)

how many canadians have asthma

10%

risk fx for asthma

family hx, triggers

asthma inflammation pathway

1. inflammation, degranulation

2. WBC signaling, esp T + interleukins

   • th2 helper cells→ signal B to make IgE→ cross link→ degranulation

3. bronchial inflammation, bronchoc, mucous prod (makes it hard for inhaled med to reach target)

what does an epithelial injury in the bronchi cause?

chronic hypersensitivity of bronchial airways

asthma attack ss

hard to breathe

tachycardia

anxiety, panic

fatigue

systemic effects of asthma

fast inhale, slow exhale → traps air in alveoli

• hyperinflated lungs with minimal gas exchange

• ventilation-perfusion mismatch (lots of blood, little O2)

• low O2, high CO2

• hypoxemia, hypercarbia, high pulmonary pressure → increased RVEDP → low CO

asthma management tx

-stabilize inflammation, reduce # of attacks

-maintenance drugs (controllers)

-meds should be as local as possible

-daily

what type of drugs do you need for asthma attack tx

rescue drugs (relievers)

asthma tx MUST HAVES

rx for maintenance and rescue drugs

know when to call 911

asthma inhaled anti-inflammatory drug classes

glucocorticoids, mast cell stabilizers, leukotrine modifiers (PO)

using glucocorticoids for asthma

1st line maintenance tx

• prophylaxis against attacks

inhaled every day (nebulizers in clinical settings)

prophylaxis

preventative tx

asthma: glucocorticoid drug names (bad bitch flute)

budenoside

beclomethasone

fluticasone

asthma tx: mast cell stabilizers fx

inhibits histamine

asthma: mast cell stabilizer drug + characteristics

cromolyn

• inhaler

• slow onset

• dose 3-4/day

• not common

• synergy with glucocorticoids

what do leukotriene mods do?

block leuko receptors

modify inflammatory response pre-exposure

asthma tx: leuko mod drug + characteristics

montelukast (singulair)

PO

systemic effect

slow onset

prophylaxis

synergy tx

short exposure to decrease side effects for long term use

asthma tx: biologics-monoclonal antibodies drug + characteristics

xolair (omalizumab)

SC

longterm tx plan

high affinity for IgE

• binds free IgE/decreases mast-cell bound IgE (no degranulation)

rescue asthma tx drug classes

beta 2 adrenergic agonists, anticholinergics

beta 2 adrenergic agonist properties

rescue asthma tx

potent

stimulate SNS B2 receptors

fast

beta 2 adrenergic agonist drug names '“betas are for sale”

formoterol (oxeze)

salbutamol (ventolin)

anticholinergic drug class properties

less potent

antagonist PNS (bronchod) to allow SNS to take effect

slow onset

synergy w beta 2 adrenergic agonist

anticholinergics drug name

atrovent (iptraprotrium)

asthma attack ER admin tx

oscar’s banana split makes a great apple

O2

beta 2 adrenergy agonists/nebulizer is best

• ventolin

sympathomimetics, IV

• epinephrine → vasoc for perfusion

magnesium sulfate, IV

• vaso/bronchod

anticholinergic, nebulizer

• synergy

• atrovent

glucocorticoid, IV

• dexamethasone

antihistamine, IV

• benadryl

asthma tx: magnesium sulfate (MgSO4) - class, admin

drug class: electrolyte, enzymatic activator, calcium channel blocker

IV

titrate to effect for severe bronchoc

rescue med

what does inhibition of ca channel do? (asthma)

inhibit in smooth musc → no depol → bronchod → stabilize mast & t-cells → decreased pro/inflammatory mediators

side effect of mgso4 asthma tx

hypotension

what does mgso4 cause to be released?

enhanced release of NO → vasod, pulm vasod → improved gas exchange

how do you treat a local allergy like contact dermatitis?

antihistamine, topical (ex. benadryl cream)

how to treat known allergen with systemic exposure present?

antihistamine, non-drowsy (ex reactin - 1tb)

how to treat eye symptom exposure

antihistamine, topical to eye (ex. patanol, eye drops)

what do you do if allergen exposure anticipated in high doses?

prophylaxis w leuko mods → singulair, 1tb x 2 days pre-exposure

what is anaphylaxis

systemic inflammation & severe vasod

anaphyalxis ss

airway: SOB

skin: hives

brain: anxiety

heart: hypotension

stomach: nausea

asthma attack vs. anaphylaxis

asthma: airway/breathing; no hives, swelling, vomiting or diarrhea

• tx focused on airway/breathing

ana: systemic vasod & bronchoc; breathing issues most prominent

• tx focused on perfusion, airway/breathing

what do you do when you are unsure if a person is having an asthma attack or is in anaphylaxis?

administer epinephrine then albuterol

air trapping

bc of bronchoc + edema mucous, gas exchange can’t be completed

dx?

OA/wear and tear

dx?

RA → MUST HAVE SWOLLEN SYNOVIAL MEMB