M5 RESPIRATORY Flashcards

(90 cards)

1
Q

RISK FACTORS

allergens, genetics (atopy)

A

ASTHMA

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2
Q

RISK FACTORS

alpha-1 antitrypsin deficiency (anti protease)

A

COPD

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3
Q

KEY INFLAMMATORY CELLS

Eosinophils
mast cells
Th2 lymphocytes

A

ASTHMA

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4
Q

KEY INFLAMMATORY CELLS

Neutrophils
macrophages
CD8+ T-cells

A

COPD

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5
Q

AIRWAY OBSTRUCTION

Reversible (spontaneously or with treatment)

A

ASTHMA

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6
Q

AIRWAY OBSTRUCTION

Irreversible (progressive, fixed obstruction; partial reversibility possible)

A

COPD

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7
Q

SYMPTOMS

  • Episodic wheezing
  • dyspnea
  • cough (often nocturnal/early morning)
A

ASTHMA

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8
Q

SYMPTOMS

  • chronic cough
  • sputum
  • progressive dyspnea (worsens with exertion)
A

COPD

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9
Q

STRUCTURAL CHANGES

  • Airway remodeling (subepithelial fibrosis, smooth muscle hypertrophy)
  • Goblet cell hyperplasia

Goblet cell - produces mucus

A

ASTHMA

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10
Q

STRUCTURAL CHANGES

  • Alveolar destruction (emphysema caused by a-1 antitrypsin)
  • Mucus gland hyperplasia (too much mucus production)
  • Airway fibrosis
A

COPD

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11
Q

CLASSIFICATION

  • Primarily given to treat the bronchospasm RIGHT AWAY
  • induce relief of acute bronchospasm
  • SHORT-ACTING
A

RELIEVERS

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12
Q

CLASSIFICATION

  • Primarily PROPHYLACTIC drugs (PREVENTION)
  • Given to decrease the severity, duration, frequency of subsequent attacks of BA or COPD
  • LONG-acting
A

CONTROLLERS

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13
Q

BRONCHODILATORS | B2 AGONISTS | SHORT-ACTING

RELIEVERS:
only SUBCUTANEOUS

A

TERBUTALINE

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14
Q

BRONCHODILATORS | B2 AGONISTS

CONTROLLERS:
only ORAL

A

BAMBUTEROL

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15
Q

BRONCHODILATORS | B2 AGONISTS

  • 1st line relievers in BA
  • ALTERNATIVE relievers in COPD
A

RELIEVERS

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16
Q

BRONCHODILATORS | B2 AGONISTS

  • ALTERNATIVE/ADJUNCTIVE controllers in BA
  • 1st line controllers with inhaled glucocorticosteroids for COPD
A

CONTROLLERS

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17
Q

BRONCHODILATORS | B2 AGONISTS | TOXICITY

easily overcome by the routine administration of supplemental oxygen

A

WORSENED HYPOXEMIA

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18
Q

BRONCHODILATORS | B2 AGONISTS | TOXICITY

precipitation of ____

A

cardiac arrythmia

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19
Q

BRONCHODILATORS | B2 AGONISTS | TOXICITY

induction of ____ reflected by loss of protection afforded by acute treatment with beta agonist
- resolved by LABA

A

tachyphylaxis

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20
Q

BRONCHODILATORS | METHYLXANTHINES

MOA

A

Adenosine antagonism, PE ihibition

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21
Q

BRONCHODILATORS | METHYLXANTHINES

MOA:
Inhibition of ____ appears to be the most involved in relaxing airway smooth muscle

A

PDE3

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22
Q

BRONCHODILATORS | METHYLXANTHINES

MOA:
inhibition of ____ in inhibiting release of cytokines and chemokines, thus decreasing immune cell migration and activation

A

PDE4

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23
Q

BRONCHODILATORS | METHYLXANTHINES

  • A SELECTIVE PDE4 inhibitor that has shown efficacy in reducing the frequency of exacerbations of COPD
  • APPROVED TREATMENT FOR COPD BUT NOT FOR ASTHMA
  • has better therapeutic index than Theophylline
A

ROFLUMILAST

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24
Q

BRONCHODILATORS | METHYLXANTHINES

MOA:
inhibition of cell surface receptors for ____

A

ADENOSINE

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25
# **BRONCHODILATORS | METHYLXANTHINES** has been shown to **PROVOKE CONTRACTION** of isolated airway smooth muscle and **release** of **histamine** from airway mast cells
ADENOSINE
26
# **BRONCHODILATORS | METHYLXANTHINES** **80%** Theophylline - an **amino** derivative
Aminophylline
27
* ALTERNATIVE bronchodilator in **severe BA attacks** (IV infusion) * CONTROLLER treatment in BA (alternative) * Respiratory **stimulant** in COPD
METHYLXANTHINES
28
# **BRONCHODILATORS | METHYLXANTHINES** **therapeutic serum levels** of THEOPHYLLINE
5-15 mg/L
29
# **BRONCHODILATORS | METHYLXANTHINES** **serum level** that will produce TOXIC effect (**seizures**)
> 40 mg/L
30
# **BRONCHODILATORS** * BLOCKS **M3** * ROUTE: **inhalation** * USES: * 1st line broncho**dilator** in COPD * ALTERNATIVE adjunctive bronchodilator in BA (as **reliever**)
ANTICHOLINERGICS
31
# **BRONCHODILATORS | ANTICHOLINERGICS** effective as ALBUTEROL in patients with COPD who have at least **partially reversible obstruction**
IPRATROPIUM
32
* induce OPENING of **INWARD Cl- channels** leading to **influx** of Cl- into mast cells ➡️ MORE DIFFICULT to **stimulate** to **release histamine** * stabilizing effect is seen AFTER at least **3-4 weeks** of treatment * inhibit both **antigen-** and **exercise-induced** bronchospasm in asthmatic patients
MAST CELL STABILIZERS
33
# **MAST CELL STABILIZERS** MOA: induce **opening** of ___
inward Cl- channels
34
# **MAST CELL STABILIZERS** MOA: inhibit both ____ and ____ bronchospasm in asthmatic patients
antigen- and exercise-induced
35
# **MAST CELL STABILIZERS** CROMONES
Nedocromil Cromolyn sodium / Na cromoglycate
36
* mgt of **allergic conditions** * allergic type BA * allergic rhinitis
MAST CELL STABILIZERS
37
# **MAST CELL STABILIZERS** SIDE EFFECTS
induce bronchospasm
38
# **MAST CELL STABILIZERS** REMEDY for side effect
pre treatment with SABA (1 puff) before taking a puff of cromone
39
* **Leukotriene** modifiers * **Glucocorticosteroids**
ANTI-INFLAMMATORY AGENTS
40
# **ANTI-INFLAMMATORY AGENTS** * ALTERNATIVE controllers in **persistent BA** * mgt of **NSAID-induced BA**
LEUKOTRIENE MODIFIERS
41
# **ANTI-INFLAMMATORY AGENTS | LEUKOTRIENE MODIFIERS** Lipooxygenase (LOX) inhibitor
Zileuton
42
# **ANTI-INFLAMMATORY AGENTS | LEUKOTRIENE MODIFIERS** LTD4 antagonist
lukast (Montelukast, Zafirlukast)
43
# **ANTI-INFLAMMATORY AGENTS | LEUKOTRIENE MODIFIERS** SIDE EFFECTS: **lukast** — shown to unmask the sx of ____ (form of **eosinophilic vasculitis)
CHURGG-STRAUSS SYNDROME
44
# **ANTI-INFLAMMATORY AGENTS | LEUKOTRIENE MODIFIERS** SIDE EFFECTS: **recent**
psychotic features, increase suicidality
45
# **ANTI-INFLAMMATORY AGENTS** MOA: * inhibits synthesis of **phospholipase A2** * inhibit **late phase allergic reaction** which occurs **2-8 hours** AFTER the **onset** of **allergic/asthmatic attack**
GLUCOCORTICOSTEROIDS
46
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** ____ converts **lipids** to **arachidonic acid**
PHOSPHOLIPASE A2
47
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** LOCALLY-acting inhaled
Budenoside, Beclomethasone Fluticasone Triamcinolide
48
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** * as **MDIs** and **nebules** * PRIMARY INDICATION: 1st line CONTROLLERS for BA (**persistent** type of BA) * ADJUNCTIVE controllers in COPD
Locally acting inhaled
49
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** PREVENTION: for **oropharyngeal candidiasis**
gargle after each use
50
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** SIDE EFFECTS
Oral thrush — Oropharyngeal. candidiasis Vocal cord nodule Hoarseness of voice
51
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** * **SHORT**-acting, **LOW** potency * as SHORT COURSE treatment for **acute attacks** (NMT 10days)
SYSTEMIC GCs — ORAL
52
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** SYSTEMIC GCs — **ORAL**
Prednisone Prednisolone
53
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** * 1st line in mgt of **status asthmaticus** * indicated for **severe asthma exacerbation**
SYSTEMIC GCs — PARENTERAL
54
# **ANTI-INFLAMMATORY AGENTS | GLUCOCORTICOSTEROIDS** SYSTEMIC GCs — **PARENTERAL**
Hydrocortisone IV (Solu-Cortef) Methylprednisolone IV (Solu-Medrol)
55
# **TARGETED MONOCLONAL ANTIBODY** TARGET: **Omalizumab**
IgE
56
# **TARGETED MONOCLONAL ANTIBODY** TARGET: **Reslizumab**
IL-5
57
# **TARGETED MONOCLONAL ANTIBODY** TARGET: **Tezepelumab-ekko**
thymic stromal lymphopoietin (TSLP)
58
# **TARGETED MONOCLONAL ANTIBODY** * SQ * can **reduce frequency** of acute exacerbation * can reduce **corticosteroid requirement**
OMALIZUMAB
59
# **TARGETED MONOCLONAL ANTIBODY** * IV
Reslizumab
60
# **TARGETED MONOCLONAL ANTIBODY** * SQ * MOST RECENT antibody for **severe asthma**
Tezepelumab-ekko
61
a **protective reflex** that **clears** the **airways** of irritants, mucus, or foreign particles
COUGH
62
Cough **starts** when ____ (mainly in the throat, larynx, trachea, and bronchi) are **triggered** by **irritants** like dust, mucus, or infection
sensory receptors
63
# **COUGH** AFFERENT PATHWAY: **signals** are sent VIA the ___ to the **cough center** in the **brainstem (medulla)**
vagus nerve
64
# **COUGH** EFFERENT PATHWAY: the brain sends signals to ____ — diaphragm, intercostal muscles, and abdominal muscles
RESPIRATORY MUSCLES
65
a **VIRAL INFECTION** of the upper respiratory tract, primarily caused by **virus**
COMMON COLD
66
# **COMMON COLD** IMMUNE RESPONSE: **infected cells** RELEASE ____, triggering an immune response. This causes inflammation, mucus production, and swelling of the nasal tissues
CYTOKINES & CHEMOKINES
67
# **COUGH** they are **self-limiting** and usually resolve within ____
7 - 10 days
68
an **allergic reaction** in the **nasal passages** triggered by allergens such as pollen, dust mites, or pet dander
ALLERGIC RHINITIS
69
# **ALLERGIC RHINITIS | PHYSIOLOGY** upon **initial exposure**, the immune system **identifies** the allergen as **harmful** and produces **IgE antibodies** that bind to mast cells in the nasal mucosa
SENSITIZATION phase
70
71
# **ALLERGIC RHINITIS | PHYSIOLOGY** on **re-exposure**, allergens BIND to these IgE antibodies, causing mast cells to **release histamine** and other mediators. this leads to sneezing, nasal itching, rhinorrhea (runny nose), and nasal congestion
EARLY PHASE REACTION
72
73
# **ALLERGIC RHINITIS | PHYSIOLOGY** **several hours later**, inflammatory cells like **eosinophils** and **T cells** infiltrate the area, causing **prolonged inflammation** and **congestion**
LATE PHASE REACTION
74
# **ALLERGIC RHINITIS | PHYSIOLOGY** the process is driven by ____-dominant immune response and involves cytokines like IL-4, IL-5, and IL-13
Th2
75
# **DRUGS | COMMON COLDS** PROBLEM **A1 agonist**
rhinitis medicamucosa
76
# **DRUGS | COMMON COLDS** A1 agonist — NASAL DECONGESTANT
Pseudoephedrine Phenylephrine Peopylhexedrine Oxymetazoline
77
# **DRUGS | COMMON COLDS | NASAL DECONGESTANTS** A2 agonis — LOCAL VASOCONSTRICTORS
Clonidine Apraclonidine Brimonidine
78
# **DRUGS | COMMON COLDS | NASAL DECONGESTANTS** RULE for **nasal decongestants; local vasoconstrictors**
avoid some antihistamines ➡️ prolong SE of colds
79
# **DRUGS | ALLERGIC COLDS** ____ + ____
nasal decongestant + H1 antihistamines
80
# **DRUGS | COUGH AND MUCUS PRODUCTION** MOA: increase **water portion** of the mucus ➡️ **decreased viscosity** of mucus
MUCOREGULATORS — Bromhexine, Carbocisteine, Ambroxol
81
# **DRUGS | COUGH AND MUCUS PRODUCTION** MOA: BREAK **disulfide linkages** between mucus molecules ➡️ **less viscous** mucus (easy to expectorate)
MUCOLYTICS — N-acetylcysteine (NAC)
82
# **DRUGS | COUGH AND MUCUS PRODUCTION** MUCOLYTICS: also used for the mgt of **paracetamol toxicity**
N-acetylcysteine (NAC)
83
# **DRUGS | COUGH AND MUCUS PRODUCTION** MOA: **stimulate bronchial glands** to **secrete more** of the **water portion** of the mucus
EXPECTORANTS — Guaifenesin
84
# **DRUGS | COUGH AND MUCUS PRODUCTION** EXPECTORANT: * mgt of **chronic bronchitis** * given in **high doses** to **induce vomiting**
Guaifenesin (Glyceryl guaiacolate)
85
# **DRUGS | COUGH AND MUCUS PRODUCTION** * cough **suppressants** * for **NON-productive** * **excessive** cough * harmful (dangerous cough — with **blood**, TB)
ANTITUSSIVES
86
# **DRUGS | COUGH AND MUCUS PRODUCTION** ANTITUSSIVE: MOA — decrease the **sensitivity** of **peripheral cough receptors**
PERIPHERAL ACTING — Butamirate citrate
87
# **DRUGS | COUGH AND MUCUS PRODUCTION** ANTITUSSIVE: MOA — **suppress** the **cough center** (hyperpolarize the cough center)
CENTRALLY acting
88
# **DRUGS | COUGH AND MUCUS PRODUCTION** ANTITUSSIVE | CENTRALLY ACTING: **NARCOTIC**
Codeine Noscapine
89
# **DRUGS | COUGH AND MUCUS PRODUCTION** ANTITUSSIVE | CENTRALLY ACTING: **NON-NARCOTIC**
Dextromethorphan
90
# **DRUGS | COUGH AND MUCUS PRODUCTION** ANTITUSSIVE | CENTRALLY ACTING: **ANTIHISTAMINE**
Diphenhydramine