Quiz 2- Glucocorticoid and Etc! Flashcards
(189 cards)
1
Q
A
2
Q
Hydrocortisone
A
Glucocorticoid
3
Q
Glucocorticoid Drugs:
A
*Hydrocortisone, Cortisone
*Prednisone, Prednisolone
*Methylprednisolone
*Dexamethasone
4
Q
Cortisone
A
Glucocorticoid
5
Q
Hypothalamus (detects stress) and releases:
A
Corticotropin releasing hormone (CRH)
- CRH then travels to Anterior Pituitary
6
Q
Anterior Pituitary (below the brain)
A
- Once CRH gets to Anterior Pituitary
- It releases Adrenocorticotropic Hormone (ACTH)
7
Q
Adrenal Cortex (top of the kidneys)
A
- ACTH is released into the adrenal cortex.
- It then releases cortisol (stress hormone)
8
Q
Where is cortisol released?
A
Adrenal Cortex
9
Q
HPA Axis hormones released:
A
Corticotropin Releasing Hormone (CRH)–> Adrenocorticotropin hormone (ACTH)–> Cortisol
- Hypothalamus–> Anterior Pituitary-> Adrenal Cortex
10
Q
Glucocorticoid
A
steroidal (synthetic) drugs (mimic or modify natural hormones)
11
Q
Which part of the HPA Axis produces glucocorticoid?
A
Adrenal cortex
12
Q
Glucocorticoid molecular characteritsics, enzymes, metabolism
A
- Glucocorticoid are:
- lipophilic
- nuclear receptor binding
- some are prodrugs
13
Q
Glucocorticoid as an Endogenous substance (not synthetic)
A
- stimulates gluconeogenesis: making glucose from proteins and fats to raise blood glucose
- stimulates protein
degradation: break down of proteins for energy - facilitates lipolysis :breakdown of fat stores for energy
14
Q
How is Glucocorticoid related to inflammation?
A
- Inhibits prostaglandin synthesis (COX-2): reduce swelling and pain
- Suppress Histamine release: reduce allergic reaction
- Suppression of Phagocytes/ Lymphocytes: lowers immune activity
15
Q
Glucocorticoid as a drug
A
- HIGH EFFICACY FOR TISSUE INFLAMMATION.
- think how it inhibits COX2
- suppress Histamine
- lowers immune system (suppression of phagocytes/ lymphocytes)
16
Q
Glucocorticoid Drugs:
A
*Hydrocortisone, Cortisone
*Prednisone, Prednisolone
*Methylprednisolone
*Dexamethasone
17
Q
Hydrocortisone
A
Glucocorticoid
18
Q
Cortisone
A
Glucocorticoid
19
Q
Prednisone
A
Glucocorticoid
20
Q
Prednisolone
A
Glucocorticoid
21
Q
Methylprednisolone
A
Glucocorticoid
22
Q
Dexamethasone
A
Glucocorticoid
23
Q
What are DMARD?
A
disease-modifying anti-rheumatic drugs
24
Q
Where is DMARD the main primary tx?
A
- used in Rheumatoid Arthritis to reduce joint damage
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Is glucocorticoid a DMARD?
No, but they have "DMARD- like" effect because they protect joints by reducing inflammation and damage
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Glucocorticoid therapeutic effects
- Affects multiple systems in the body-> not just joints
- Important for growth (in utero for liver + gut maturation)
- Stops insulin from being used properly
-Anti allergic (suppresses Histamine)
-Anti inflammtory effect and immunosuppression (reduced pain, swelling, stiffness and physical disability)
- Helps blood vessel work properly and reduces permeability (histamine suppuression)
27
Glucocorticoids Adverse Effects: (Part 1)
- risk for infection (suppression of phagocytes/ lymphocytes)
- myopathy(muscle weakness)
- osteonecrosis/osteoporosis
- mood changes/ anxiety, depression, even psychosis
- long term use can suppress natural cortisol production
28
Glucocorticoids Adverse Effects: (Part 2)
- Metabolism:
- weight gain/ obesity
- fluid retention/edema
-cushing syndrome
- impaired glucose metabolism
- insulin resistance + beta cell dysfunction
- stomach; gastric ulcer if taken with NSAID
- Hirsutism (excess hair growth) and skin thinning
- eyes (cataract and glaucoma)
- increased CV risk
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Cushing syndrome
cause of chronic use of glucocorticoid
S &S:
- moon face, buffalo hump (fat on upper back), high blood sugar and skin thinning
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Allergy symptoms include:
Rash
Lacrimation
Runny nose
Sneezing
Red eyes
Itching
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Local allergy, contact dermatitis Tx:
Antihistamine- Topical
ie.) Benadryl (diphenhydramine) cream
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known allergen, systemic exposure Tx:
Antihistamine- non-drowsy preferred
ie.) Reactin (cetirizine
33
eye symptoms allergy:
Antihistamine- topical to eye
ie.) Patanol (olopatadine)
34
If allergen exposure is anticipated in high doses: (local/ systemic)
Leukotriene modifiers
ie.)Singulair (1 tab x 2 days pre-exposure)
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Anaphylaxis:
high histamine => systemic inflammatory response => severe inflammation & vasodilation
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Signs and Symptoms of Anaphylaxis"
- evidence of allergy
- bronchoconstriction (tight airways-> wheezing, difficulty breathing) &
-hypotension (low BP due to vasodilation-> dizziness, fainting)
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What are we most concerned of during Anaphylaxis:
- Bronchoconstriction and Hypotension (due to vasodilation)
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Tx of Anaphylaxis:
- focuses on ABC's
- Epinephrine, IM; IV (sympathomimetic effect)
-Dexamethasone, IV (glucocorticoid; suppresses histamine release)
-antihistamines, IV
- IV fluids (for Cardiac Output)
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Signs and Symptoms of Anaphylaxis (more info)
-Coughing
Shortness of breath
Wheezing
Chest pain/tightness
Tightening of throat
Difficulty swallowing
-Hives
Swelling
Itchiness
Widespread redness
Warmth
(skin may feel hot due to increased blood flow)
- Anxiety
Confusion
Headache
Feeling that something is about the happen
- Faint
Pale
Blue color : Lack of O2 in the bloodstream
Dizziness: sign of hypotension
Weak pulse
Shock
Loss of consciousness
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Epinephrine
non-selective adrenergic agonist (alpha, beta)
- cause vasoconstriction, bronchodilation and increase HR
-sympathomimetic
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Epinephrine as tx:
Onset: rapid
Timing: 15-20 mins (often we give repeated doses until pt is rescued)
- has an antihistamine effect in which (it constricts BV to reduce swelling and increase BP + relaxes muscle in the airways)
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Epinephrine Drug can come as:
Epipen, Adrenalin
ROA: IV or IM (EpiPen)
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Glucocorticoid Drugs that have no or minimal side effects:
- topical Voltaren PRN
- intranasal Avamys PRN (as needed)
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Glucocorticoid Use Risk of Systemic Effects if:
- long term treatment (chronic use)
- systemic route
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How does ROA affect glucocorticoid's side effects:
- PO Glucocorticoid: risk of systemic side effects
- Topical/ Intranasal Glucocorticoid: minimal/ no side effects
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Negative Feedback of HPA Axis:
- When someone is in Glucocorticoid therapy, hypothalamus + anterior pituitary gland recognizes that we have enough hence reduced secretion of CTH, ACTH and eventually cortisol (from adrenal cortex)
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What is crucial thing to do when someone is in Glucocorticoid and we want to stop tx?
- No abrupt stoppage; because body has relying on that therapy for so long that if you stop that completely--> can cause adrenal insufficiency (fatigue, low bp and shock)
- we must slowly titrate "weaning protocol" until 0mg and adrenal gland starts producing cortisol again
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When does Cushing Syndrome occur?
- occurs when the body is exposed to excessive glucocorticoids for a long time whether endogenous overproduction or exogenous administration?
49
Cushing Syndrome S &S:
-Red cheeks,
- fat pads (buffalo hump), -abdominal stretch marks -bruise easily,
-pendulous abdomen
-thin arms and legs
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Health complications (due to excess cortisol):
- Neuropsychiatric disorders
- Arterial atherosclerosis and vascular disease
- Liver steatosis (fatty liver)
- Osteoporosis (femoral neck) - increased risk of hip fractures
- myopathy
- cardiac disease
- osteoporosis and vertebral fractures
- visceral obesity
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Long term/ Chronic inflammation
- more than 10 days and persistent**
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Chronic Inflammation Treatment:
=- often includes Glucocorticoids
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Chronic Inflammation Diseases:
- Allergic rhinitis
- Dermatitis
- Psoriasis
- Arthritis
- IBD (Inflammatory Bowel Disease)
- Asthma
- COPD
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Glucocorticoid Evaluation:
- clinical efficacy
- risk vs benefit
- local vs systemic use
- patient response
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Acute Inflammation
- less than 10 days and it gets better eventually ** unlike chronic where it is persistent
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Chronic Inflammation process
- 1.) Acute inflammation occurs
-2.) Followed by an innate response (called proliferation- rapid increase of: lymphocytes, macrophages, fibroblasts, endothelial cells, inflammatroy mediators and etc)
-3.) Tissue destruction by repetitive inflammation
-4.) Eventually- Scar tissue formation: where normal tissue is replaced by scar tissue (this tissue is less vascular, less flexible, less strong)
5.) this cycle (repeated many times) causes cellular tissue changes (leads to dysfunction of tissue, increase susceptibility to abnormal cell growth and cellular division (cancerous/ non-cancerous))
57
In chronic inflammation, where we see repeated cycles of tissue destruction and tissue formation; eventually this cycle will cause cellular tissue changes (3):
- dysfunction of the tissue:
loss of normal function
- susceptibility to unusual growth & altered: increased susceptibility to abnormal cell growth
- cellular division ie.)neoplasms: risk of tumor growth-> cancerous or non-cancerous
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Tissue Repair Process:
1.) Clotting occurs, caused by clotting proteins and plasma proteins, and a scab is formed
2.) Inflammatory chemicals are released from injury
3.) White blood cells seep into the injured area.
Epithelial cells (new skin cells) multiply and fill in over the granulation tissue . Granulation tissue restores the vascular supply
-->Restored epithelium thickens; the area matures and contracts (reducing the wound size)
Underlying area of scar tissue is less elastic and weaker than normal skin
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Allergic rhinitis
- common allergic condition caused by inhaled allergens
leading to nasal and sinus inflammation
- 40% population and often seasonal
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Allergic Rhinits triggers:
pollen, dust, dander (skin shed by dogs, cats/ animals)
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S&S of Allergic Rhinitis:
rhinitis, swelling, conjunctivitis, sneezing, snoring, itching, headache from nasal-sinus congestion
62
For Allergic Rhinits, when we do blood work- what will we see in high of?
- High eosinophils: indicate allergic reaction
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Allergic Rhinitis Tx:
Glucocorticoid- Intranasal
ie.) fluticasone (Flonase, Avamys)
ie.) mometasone (Nasonex)
ie.) budenoside (Rhinocort)
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Fluticasone (Flonase, Avamys)
Glucocorticoid- Intranasal
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Flonase
Glucocorticoid- Intranasal
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Avamys
Glucocorticoid- Intranasal
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mometasone (Nasonex)
Glucocorticoid- Intranasal
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Nasonex
Glucocorticoid- Intranasal
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budenoside (Rhinocort)
Glucocorticoid- Intranasal
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Rhinocort
Glucocorticoid- Intranasal
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Suffixes ending in - one, -ide
Glucocorticoids
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Suffixes ending in - dine, -mine
Antihistamines
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Seborrheic Dermatitis:
Inflammation of the epidermis
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Seborrheic Dermatitis Description:
- red, scaly patches, + not itchy
In Infants: called 'Cradle Cap'
In Adults: often returns as dandruff
75
Seborrheic Dermatitis Tx:
In infants: asymptomatic; usually parents are bothered
Tx of scalp: dandruff shampoo
Tx on body: a mild topical corticosteroid combined with an antifungal (ketoconazole)
76
Ketoconazole
- an antifungal
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Psoriasis
- chronic inflammatory dermatoses (in pattern/dermatoses)
- autoimmune basis
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Psoriasis Description:
- Red raised patches (papules + plaques) with a silvery scale
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Psoriasis is usually found in which areas?
(extensor surfaces)- like elbows and knees
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Seborrheic Dermatitis is usually found in which areas?
flexural areas (body folds→ wrists, back of the knees + inside elbows ), neck and groin
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Psoriasis S &S:
- itching, nail pitting, and symmetrical distribution on both sides of the body
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Clinical presentation of Psoriasis is enough to diagnose it- true or false?
true
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Psoriasis triggers:
-Upper respiratory infections
-Stress
-Cold
-Low sunlight
-Some drugs
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Psoriasis Pathology:
-Epidermal hyperplasia (thickening of the outer skin layer)
- Parakeratotic Scale (abnormal skin cells that have not fully matured)
-Accumulation of neutrophils within superficial epidermis (WBC build up in the upper skin)
85
Psoriasis Treatment
- Avoid rubbing/ scratching
- Emolients and moisturizers
- Sunlight exposure helps
- Topical steroids
- Vitamin D analogs (slow skin cell growth)
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Atopic dermatitis
- most common type of eczema
- allergy triggered (high plasma IgE)
- autoimmune tendency
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Atopic Dermatitis: Chronic inflammation of the skin
- pruritic (itchy)
- scar formation ‘lichenification’ thickened, roughened skin from repeated scratching
- deficient innate skin barrier
- risk of super-infection (bacterial/ viral)
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Atopic Dermatitis Tx:
moisturize +
- topical glucocorticoids
-Antihistamines
-antibiotics/antivirals if infection
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What is Atopic Triad?
- Atopic asthma
- Atopic dermatitis (eczema)
- Allergic rhinitis
; Each of these conditions can occur independently, but having one increases the likelihood of developing the others due to the shared genetic and environmental factors.
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Psoriasis- Chronic inflammation of the skin:
- Hyperkeratosis: excessive growth of the outer skin (forming scaly plaques)
- Thinned stratum granulosum: disrupted epidermal layer
- Dilated dermal papillae: increased blood flow to the skin
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Psoriasis Tx:
- Glucocorticoids
- DMARD's
- UV light
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Psoriasis can start locally (at site of skin) in "flare ups" and then become systemic (affecting the entire body)
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What is Photobiomodulation Therapy (PBMT) ?
- Regenerative potential in tissue engineering (used to stimulate tissue repair and regeneration)
- Stimulation of angiogenesis
- Increased collagen synthesis
- Mitochondrial ATP production
- Modulation of cytokines and growth factors (helps regulate cell growth, proliferation, differentiation, and healing)
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Eczema Vs Psoriasis:
Eczema: intense itching ,oozing and crusting , inflamed skin may leak flui, form crusts and scabs
- appear on flexural skin surface
Psoriasis: itching less severe, scaling (excessive skin build up), dry scaly patches
- appears on extensor skin surfaces
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Rheumatoid arthritis (RA
chronic, systemic autoimmune disease that causes inflammation of the joints and other organs
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RA risk factor:
Family hx, gender (more common in women bc decreased levels of estrogen), trigger
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Aside from joints, RA also affects:
Eye conditions
Dry mouth
Fatigue
Extreme tiredness
Lung scarring or nodules
Cause breathing problems
Heart disease
Digestive problems
Skin conditions
Inflammation
Cartilage damage
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Main issue of RA:
- dysfunction of the synovial cavity: "pannus"
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What is "pannus" formation'?
Thickened, inflamed tissue inside the joint cavity (cause pain, swelling and reduced joint function
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Effect of "pannus"?
- Pannus erodes bone, cartilage, and ligaments.
- Joints become swollen, painful, and deformed (abnormal change)
- loss of normal fx: As the joint structure is destroyed, movement becomes limited and painful
- making it PAINFUL*
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What does it mean when RA is considered as autoimmune disease?
- it means it is progressive and autoimmune destruction of healthy endogenous tissues
- The immune system continues attacking healthy tissues, worsening the damage over time.
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RA effects on the body: aside from pannus formation
Eye conditions
Dry mouth
Fatigue
Extreme tiredness
Lung scarring or nodules
Cause breathing problems
Heart disease
Digestive problems
Skin conditions
Inflammation
Cartilage damage
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S&S of Synovial Joint Inflammation:
- hands, knees, cervical spine (neck area)
- systemic symptoms (beyond just joints)
- generalized fatigue, anorexia (loss of appetite)
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When figuring out if inflammation is present. what will we check in BW?
C- reactive protein- a marker of inflammation in the blood
- a high CRP : active disease (maybe in terms of RA) and an ongoing systemic inflammation
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Tx of Rheumatoid Arthritis:
- NSAID's
- Glucocorticoids (PO route)
- DMARD's
- Biologic Response Modifiers (BRM's) --> IV, SC Route
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What are BRMs (biologic response modifiers)?
- decrease T & B cell response
- prevent autoimmune attack on joints
- ie.) Infliximab, Adalimumab, Ustekinumab
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Infliximab
BRMs - biologic response modifiers
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Adalimumab
BRMs - biologic response modifiers
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Ustekinumab
BRMs - biologic response modifiers
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What are DMARD's- disease-modifying anti-rheumatic drugs?
- inhibits nucleotide synthesis
-inhibits WBC synthesis & fx: reduce immune overactivity
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Methotrexate
DMARD
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What is Osteoarthritis (OA)?
- " wear & tear"
-degenerative disorder of articular cartilage.
- not autoimmune
-happens when the cartilage (the cushion between bones) wears down over time
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OA as a result of:
- "wear and tear": results from joint overuse and aging
- mechanical stress
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OA Risk factor:
- Mechanical stress (repeated joint use-> sports, labor, heavy lifting),
- obesity,
-age (more common in older adults)
gender (more common in women)
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Since OA is caused by a degenerative disorder of articular cartilage... how does cartilage changes occur?
- repetitive pro/inflammatory mediator release (cytokines, prostaglandins) => chronic inflammation
- => decreased proteoglycans (cartilage water binding protein)
Cartilage loses its ability to retain moisture
=> weakened collagen II network
Cartilage structure becomes fragile
=> cartilage tissue destruction (thins & breaks down) => bone-bone (joint surfaces rub together) in articulating surface!: Causes pain, stiffness, and reduced mobility
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Proteoglycan
Attracts H2O to keep cartilage hydrated & resilient
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Hyaluronic acid
Provides lubrication & shock absorption
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Type II collagen fibril
Maintain cartilage strength & structure
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Tx for OA:
- NSAIDs,
-Glucocorticoids (intra articular injection) ie.) Betamethasone (Celestone)
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Betamethasone (Celestone)
Glucocorticoid (IA)
- intrarticular because it contains large molecules that'll stay
- half life is 2-3 wks; then pt gets repeated doses
121
Articular carticular
-Normal function:
Covers the ends of bones, allowing smooth movement.
-OA effect:
Cartilage loss leads to friction between bones, causing pain.
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Meniscus
-Normal function:
Acts as a shock absorber in the knee joint.
-OA effect:
Can become damaged or thinned, leading to reduced cushioning.
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Normal Joint Space vs Joint Space Narrowing
-Bone spurs can occur and cause pain & limit movement
Joint space narrowing: as cartilage wears away, space between bones shrinks--> causing stiffness and pain
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Rheumatoid Arthritis vs Osteoarthritis:
Rheumatoid Arthritis:
- Bone erosion:the immune system attacks joint tissues, leading to bone damage (erosion)
- Swollen inflamed synovial membrane
- Osteoarthritis: bone ends rub together ,thinned cartilage
125
Inflammatory Bowel Disease (IBD)
a group of chronic inflammatory conditions that affect the digestive tract.
ie.) Crohn’s disease, Ulcerative Colitis
126
IBD Risk factors:
- family hx
triggers (environmental, bacterial)
127
IBD autoimmune?
YES!
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129
IBD systemic s&s:
fever, anemia, fatigue, weight loss, rash
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Crohn's disease:
can occur anywhere within the GI tract (mouth to anus)
131
Ulcerative Colitis (UC):
occurs in the large intestine
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IBD Tx:
- ●Glucocorticoids
- ●Aminosalicylate (help control inflammation in the intestines)
- ●DMARDs (Methotrexate)
- stem cell research (mesenchymal stem cells)
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Ulcerative colitis
- only affects the large intestine (specifically- the colon); starting from rectum and extending upward
134
UC description:
- ulcer (open sores)on the lining of the colon wall
- affects the innermost layer of the colon wall
- some areas of the intestinal lining survive between ulcerated regions
- loss of haustra
- crypt distortion: become irregularly shaped
135
Crohn's DIsease:
-anywhere in the GI tract; mostly the ileum (last part of the small intestine) that is mostly affected area
- thickening of colon wall
- cobblestone appearance of surface: bumpy and uneven
- fistula: abnormal tunnels can form
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Drug class: Aminosalicylates
anti- inflammatory drugs used to treat IBD
- they are PO administered
- prodrug (gets metabolized in the colon)
- 2 products: 5-ASA: salicylate (NSAID) + Sulfapyridine (DMARD)
ie.) Sulfasalazine (Azulfidine, Salazopyrin)
137
Aminosalicylate when metabolized in the colon produced 2 drugs; what are they?
salicylate (NSAID): reduce gut inflammation
AND
Sulfapyridine (DMARD): helps control immune system overactivity
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Asthma (aka bronchial asthma)
chronic inflammatory airway disorder (not autoimmune)
139
Asthma:risk factors
family hx, atopy (tendency for allergies, eczema, hay fever)
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Asthma Etiology:
1.) noxious stimuli trigger (allergens, particles, infection, stress, ….)
2.) ●reactivity of the airways to the stimuli => chronic hypersensitivity
3.) ●chronic inflammatory changes: epithelial injury (damages airway lining)
4.) ●high goblet cell activity (mucous)-->Globlet cells overproduce mucus-> worsening obstruction
141
Asthma Presentation:
- bronchial inflammation: swollen airways
- Bronchoconstriction: narrowed airways cause wheezing
-mucous production: blocks airflow
142
During Asthma: T- cell release?
Interleukin-4 (IL-4) and Interleukin 12 (IL- 3)--> that increase allergic responses
143
Bronchial Asthma (in a diagram)
T cell-> Release Interleukin-4 (IL-4) and Interleukin-13 (IL-13)-> increase allergic responses.
B cell-> activated B-cell-> produce IgE antibodies
FcERI: FcERI receptors in mast cells
Mast cell: IgE binds to FcERI receptors, making them react strongly to allergens
Allergen : Activation of mast cells (mediator release-> Histamine, leukotrienes, cytokines)-> cause inflammation
144
Early response (mins after exposure) of Asthma:
bronchospasm (airways tighten), edema (swelling), airflow obstruction (difficulty breathing)
145
Late response (hours later)
airway inflammation, airflow obstruction, airway hyperresponsiveness
146
Asthma Challenges:
1.) chronic bronchial inflammation: long-term swelling & mucus buildup
2. risk of acute attacks
(e.g. sudden extreme inflammatory response)
147
Asthma Tx Focus:
- stabilizing the bronchial inflammation & minimizing the number of attacks
●avoidance of triggers
●daily ‘maintenance’ drugs to decrease bronchial inflammation: ‘controllers’
●correct administration technique (inhalation equipment: inhalers)
●immunizations to decrease respiratory infection risk (e.g. Prevnar)
●recognizing the s&s of an attack
●asthma attack drugs: ‘rescue’ drugs (aka ‘relievers’)
●911 if attack persists
148
Prevnar
immunization to decrease respiratory infection risk
149
Asthma Line of Treatments: (3)
1.) ●Tx: ‘controllers’ -> long term Anti-inflammatory drugs
2.) Tx: rescue
3.) Severe attack "drugs"
150
Tx: ‘controllers’
- prevention against attacks
Drug class: Glucocorticoids
ie.) Pulmicort (Budenoside), Qvar (Beclomethasone), Flovent (Fluticasone)
151
Tx: "controllers" - Glucocorticoids, what are the adjunct tx?
- Mast cell stabilizers
ie.) Cromolyn (cromoglicic acid)
- Leukotriene modifiers: blocks leukotrienes, reducing infammation. ie.) Singulair (montelukast)
152
Pulmicort (Budenoside)
- Glucocorticoid, tx- asthma controller
153
Qvar (Beclomethasone)
Glucocorticoid, tx- asthma controller
154
Flovent (Fluticasone)
Glucocorticoid, tx- asthma controller
155
Cromolyn (cromoglicic acid)
- Mast cell stabilizers
- Adjunct tx for "asthma controller"
156
Singulair (montelukast)
- Leukotriene modifier
-Adjunct tx for "asthma controller"
157
Drug class for tx for asthma controller?
- Glucocorticoids
158
long term maintenance for severe asthma and allergic conditions?
Xolair (omalizumab)
- Xoliari has high affiinity for igE- thus preventing it from attaching to mast cells = reduction in mast cell response
159
Impaired gas exchange secondary to asthma
- As the inflammatory process continues, the bronchioles narrow due to cytokine release, and goblet cells increase mucus production-> trapping CO2 in the alveoli
160
What narrows during an asthma attack?
- Bronchioles
161
Gas exchange is inhibited as O2 can’t be inspired (enter properly) and CO2 can’t be expelled= air trapping
O2 can't enter
C02 can't get out
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Edema in Impaired Gas Exchange Secondary to Asthma:
The airway walls swell due to inflammation.
More swelling = Even less space for air to move
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Asthma Attack S &S:
○wheezing, shortness of breath, decreased/no air entry into lung lobes
○tachycardia
○anxiety, panic
○fatigue
164
Asthma Pathology (1):
limited inspiration (less air enters) + longer expiration phase (breathing out) => trapping of air in alveoli:
165
Asthma Pathology (2):
hyper-inflated lungs with low gas exchange
-Because trapped air can't escape, the lungs become overinflated (hyperinflation).
This reduces the ability of the alveoli to exchange oxygen (O₂) and carbon dioxide (CO₂)
The body gets less oxygen (hypoxia) and holds on to too much CO₂ (hypercarbia
166
Asthma Pathology (3):
ventilation-perfusion mismatch
- some alveoli are blocked by mucus and inflammation
-In asthma, some alveoli are blocked by mucus, inflammation, or swelling.
Air (oxygen) can’t reach those alveoli, so ventilation is reduced.
However, blood still flows to those areas, but it can’t pick up enough oxygen because the airways are blocked
167
Asthma Pathology (4):
causes hypoxemia & hypercarbia
- high pulmonary pressure will increased right ventricular end-diastolic pressure => low Cardiac Output
168
What are Tx: rescue drugs during Asthma:
- medications used during an asthma attack to quickly open the airways (bronchodilation) and improve breathing
169
Tx "rescue drugs" in Asthma
bronchodilator drugs, inhaled
-Drug Class: Beta 2- adrenergic agonists: very potent, stimulates SNS, fast-acting
- Drug Class: Anticholinergics: antagonize PNS--> allow more air flow; synergy with Beta-2 Adrenergic agonists
170
How does Beta -2 adrenergic agonists differ from Anticholinergics?
- Beta-2 agonists :open airways quickly
- Anticholinergics: provide longer-lasting bronchodilation
171
Beta -2 adrenergic Agonists
- potent, stimulate SNS, fast-acting.
ie.) Salbutamol (Ventolin)
○Albuterol (Ventolin)
○Formoterol (Oxeze, Turbohaler)
172
Salbutamol (Ventolin)
Beta-2 adrenergic Agonists
173
Albuterol (Ventolin)
Beta-2 adrenergic Agonists
174
Formoterol (Oxeze, Turbohaler)
Beta-2 adrenergic Agonists
175
Anticholinergics
-less potent, synergy with Beta 2- adrenergic agonist
ie.) Atrovent (Ipratropium)
176
Atrovent (Ipratropium)
Anticholinergics
177
Asthma Tx in severe attack:
- Oxygen (O₂) therapy is given immediately to correct low oxygen levels (hypoxemia)
- Beta2 adrenergic agonists, inhalation (nebulizer-> continuous mist inhalation. ie.) Ventolin
- Calcium channel blocker(smooth muscle)
- Anticholinergics, inhalation (nebulizer)
- Adrenergics/Sympathomimetics, IV ie.) Epinephrine (Adrenalin)
- Glucocorticoids, IV ie.) Dexamethasone
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Adjunct tx in Asthma severe attack:
Antihistamines, IV (e.g. Benadryl)
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Ventolin
- used in severe asthma attack
- Beta2 adrenergic agonists, inhalation (nebulizer-> continuous mist inhalation
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Magnesium sulfate (MgSO4), IV
- used in severe asthma attack
- calcium channel blocker (targets smooth muscle to relax--> stabilization of mast cells + t-cells)
Side effect: hypotension (although, we are concerned, it's okay because right now the problem is the airway)
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Anticholinergics, inhalation (nebulizer)
-used in severe asthma attack
- Synergy tx-> with Beta-2 agonists
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●Adrenergics/SympathomimeticsIV
-used in severe asthma attack
- ○Epinephrine (Adrenalin)
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Dexamethasone
- used in severe asthma attack
- a glucocorticoid
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Magnesium Sulfate (MgSO4)
- Drug classes: electrolyte; enzymatic activator; Calcium channel blocker
- ●inhibition of Ca channels in smooth muscle => reduced cellular excitability => bronchodilation
- ●stabilization of mast cells & T-cells => decreased pro/inflammatory mediators
- ●enhanced release of NO => vasodilation (relaxes blood vessels), pulmonary vasodilation = improved gas exchange
○side effects:
hypotension
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Do we titrate MgSO4 for severe bronchoconstriction?
Yes we do! Adjust the dose carefully base don how well the pt respomse
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Nitric Oxide
rescue drug to pt’s with angina to allow vasodilation (better O2 perfusion)
Side effect: hypotension
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How do we differentiate Asthma to Anaphylaxis?
- Asthma: focus is to bronchodilate (open up airway to make breathing easier)
- Anaphylaxis: focus is to vasoconstrict to maintain BP (maintain blood pressure and ensure adequate blood flow)
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Asthma vs Anaphylaxis Tx
ASTHMA:
- Bronchodilators
- Anti-inflammatory meds
- Long acting bronchodilators
- Leukotriene modifiers
- Allergen immunotherapy
Anaphylaxis:
- Epinephrine (Adrenaline)
- Antihistamines
- Corticosteroids
- Beta-agonists
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