M5 RESPIRATORY Flashcards
(90 cards)
1
Q
RISK FACTORS
allergens, genetics (atopy)
A
ASTHMA
2
Q
RISK FACTORS
alpha-1 antitrypsin deficiency (anti protease)
A
COPD
3
Q
KEY INFLAMMATORY CELLS
Eosinophils
mast cells
Th2 lymphocytes
A
ASTHMA
4
Q
KEY INFLAMMATORY CELLS
Neutrophils
macrophages
CD8+ T-cells
A
COPD
5
Q
AIRWAY OBSTRUCTION
Reversible (spontaneously or with treatment)
A
ASTHMA
6
Q
AIRWAY OBSTRUCTION
Irreversible (progressive, fixed obstruction; partial reversibility possible)
A
COPD
7
Q
SYMPTOMS
- Episodic wheezing
- dyspnea
- cough (often nocturnal/early morning)
A
ASTHMA
8
Q
SYMPTOMS
- chronic cough
- sputum
- progressive dyspnea (worsens with exertion)
A
COPD
9
Q
STRUCTURAL CHANGES
- Airway remodeling (subepithelial fibrosis, smooth muscle hypertrophy)
- Goblet cell hyperplasia
Goblet cell - produces mucus
A
ASTHMA
10
Q
STRUCTURAL CHANGES
- Alveolar destruction (emphysema caused by a-1 antitrypsin)
- Mucus gland hyperplasia (too much mucus production)
- Airway fibrosis
A
COPD
11
Q
CLASSIFICATION
- Primarily given to treat the bronchospasm RIGHT AWAY
- induce relief of acute bronchospasm
- SHORT-ACTING
A
RELIEVERS
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
13
Q
BRONCHODILATORS | B2 AGONISTS | SHORT-ACTING
RELIEVERS:
only SUBCUTANEOUS
A
TERBUTALINE
14
Q
BRONCHODILATORS | B2 AGONISTS
CONTROLLERS:
only ORAL
A
BAMBUTEROL
15
Q
BRONCHODILATORS | B2 AGONISTS
- 1st line relievers in BA
- ALTERNATIVE relievers in COPD
A
RELIEVERS
16
Q
BRONCHODILATORS | B2 AGONISTS
- ALTERNATIVE/ADJUNCTIVE controllers in BA
- 1st line controllers with inhaled glucocorticosteroids for COPD
A
CONTROLLERS
17
Q
BRONCHODILATORS | B2 AGONISTS | TOXICITY
easily overcome by the routine administration of supplemental oxygen
A
WORSENED HYPOXEMIA
18
Q
BRONCHODILATORS | B2 AGONISTS | TOXICITY
precipitation of ____
A
cardiac arrythmia
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
20
Q
BRONCHODILATORS | METHYLXANTHINES
MOA
A
Adenosine antagonism, PE ihibition
21
Q
BRONCHODILATORS | METHYLXANTHINES
MOA:
Inhibition of ____ appears to be the most involved in relaxing airway smooth muscle
A
PDE3
22
Q
BRONCHODILATORS | METHYLXANTHINES
MOA:
inhibition of ____ in inhibiting release of cytokines and chemokines, thus decreasing immune cell migration and activation
A
PDE4
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
24
Q
BRONCHODILATORS | METHYLXANTHINES
MOA:
inhibition of cell surface receptors for ____
A
ADENOSINE
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
