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PHAR 123 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What does the URT consist of?

A

Nose and Nasal cavities
paranasal sinuses
pharynx
larynx

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2
Q

What does the LRT consist of?

A

Trachea
bronchi and smaller bronchioles
lungs and alveoli

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3
Q

What is the role of the nose and nasal cavities?

A

Provide airway for respiration
Moistens and warms air
filters inhaled air
contains olfactory receptors
involved in speech

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4
Q

T or F. The nose is the most effcient way to get air?

A

False, the mouth is but, mouth gives much less moisture and less filtering.

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5
Q

Describe the Paranasal sinuses and its possible functions?

A

Air containing cavities in the skull, lined with mucous membrane
Decrease weigth of skull, increases resonance of voice, bufer agaisnt facial trauma, insulates sensitive structures from rapid temperature fluctuations, humidifies and heats air, imunological defense

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6
Q

What are the tonsils?

A

Immunocompetent organ first line of defence

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7
Q

What is pleurisy?

A

Inflammation of the pleura

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8
Q

What is the effect on the alveoli for COPD?

A

Nothing, alveoli themselves are not affected

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9
Q

What is the affect on the alveoli in emphysema?

A

Thinning of walls, less elastic, air traping leading to alveoli destruction

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10
Q

What is poor compliance?

A

Problem getting air in, restrictive disease

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11
Q

What is poor elasticity?

A

Air can get in but air trapping from poor gas exchange occurs

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12
Q

What is the effect of lower oxygen?

A

Higher BP, restriction

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13
Q

What is the conducting system?

A

All sites involved in conducting air into the lungs

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14
Q

What are the respiratory zones?

A

Where gas exchange occurs

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15
Q

What is plmonary ventilation?

A

Inspiration and expiration

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16
Q

WHat is external respiration?

A

lungs

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17
Q

What is internal respiration?

A

Tissues taking up oxygen

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18
Q

What does V/Q = 0 indicate?

A

blocking of airflow from lugns to alveoli, pressure not enough

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19
Q

what does V/Q = infinity indicate?

A

blocking blood flow, ventilation is good but perfusion not enough

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20
Q

WHat does any mismatch of V/Q cause?

A

hypoxemia

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21
Q

Normal breathing

A

eupnea

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22
Q

breathing that stops at night

A

apnea

23
Q

shortness of breath

A

dyspnea

24
Q

rapid breathing

A

tachypnea

25
Q

forced inhalation using external muscles

A

costal breathing

26
Q

deep breathing using abdominal muscles

A

Diaphragmatic breathing

27
Q

What is type 1 respiratory failure?

A

Inability of lungs to preform adequate gas exchange, oxygen saturation falls below 90%, CO2 levels remain normal or can be low

28
Q

Potential causes of type 1 respiratory failure?

A

lung disorder, pneumonia, pulmonary edema, fibrosis, embolism, hpyertension

29
Q

What is type 2 respiratory failure?

A

ventilatory failure; occurs when breathing is not suffeceint to rid the body of CO2. Leads to hypercapnia

30
Q

WHat is an obstructive disease FEV1/FVC look like

A

Low FEV1/FVC, normal FVC.
FEV1 lower b/c cannot breath out air quickly but with sustained effort will be able to breathe out all air to maintain a normal FVC

31
Q

What is a restrictive disease FEV1/FVC look like?

A

normal FEV1/FVC ratio but low FVC.

32
Q

WHat is FEV1?

A

forced expiratroy volme in 1 second

33
Q

What is FVC?

A

forced vital capacity

34
Q

WHat FEV1/FVC is diagnostic of asthma?

A

<0.7

35
Q

What are cardinal symptoms of COPD?

A

dyspnea, chronic cough, sputum production

36
Q

MOA of short-acting beta-adrenergic agonists? Drugs?

A

Bind to B2 receptors in lung causing hyperpolarixation f Ca activated K channels in airway, stimulation of ATP –> cAMP –> removal of calcium from muscle
Secondary MOA:
Reduces mediator release from mast cells
Reduces microvascular leakage after exposure to mediators
Enhances mucociliary clearance
Reduces neurotransmission of cholinergic nerves

Most used agent, rescue medication
Salbutamol and Terbutaline B2 selective, Epinepherine is non-selective

37
Q

Side effects of SABAA?

A

tachycardia
palpitations
dizziness
termor
–> tolerance typically develops these side effects

38
Q

MOA of short-acting muscarinic antagonists? drugs?

A

Ach in lungs causes bronchoconstriction and increased mucous secretiong; increases states of inflamation –> Ipratropium competitve antagonist of endogenous ach at muscarinic receptors
Inhbits M3-Gq-PLC-IP3-CA2+ pathway
not coomonly utilized in asthma
add-on during asthma attacks
rescue medication
Ipratropium

39
Q

Side effects of SAMA?

A

Cough
headache
dizziness
dry mouth
DI with anti-cholinergic load

40
Q

MOA of inhaled steroids? Drugs?

A

bind to glucocorticoid receptors, move into nucleus, inhibit histone acetyltransferase and increase histone deacetylase 2
HAT acetylates inflammatroy proteins, HDAC2 deacetylates inflammatory proteins
Beclomethasone, fluticasone, budesonide, mometasone, ciclesonide
First line controller medication

41
Q

Side Effects of steroid?

A

oral thrush
hoarseness of voice

longterm high dose:
adrenal supresson
increased glucsoe elvels
pneumonia
osteoporosis
DI with desmopressin can lead to hyponatremia risk

42
Q

Long-acting beta-adrenergic agonists details? Drugs?

A

Common controller medications
added after coticosteroid
less rapid acting than short-acting agents but last longer
same MOA, SE, and DI as SABA
Salmeterol, Formoterol

43
Q

What is unique about Formoterol?

A

Actually works veru quickly, can be used as both a reliever and controller

44
Q

MOA of Leukotriene receptor antagonist? Drug?

A

Cysteinyl-leukotriene receptors cause mucous secretion, bronchoconstrition and eosinophil recruitment when activated
ANtagonize the receptor and prevent these effects
Montelukast
Used in very mild asthma as an ORAL controller medication

45
Q

Side Effects of LRAs?

A

Minimal; no DIs

46
Q

Describe theophylline

A

Rarely used
Oral last-line controller medication
difficult dosing
Bronchodilation via:
- inhibiton of phosphodiesterase –> increase cAMP
- atangonizes adenosine receptors
- increases interleukin 10 levels
- preventin creation of pro-inflammatory mediators

47
Q

Side effects of Theophylline?

A

Tachycardia
Arrhythmias
Significant GI
DI with 3A4 substrate and 1A2 substrate

48
Q

Describe Biologics.

A

Injectable gents targeting alergic response or inflammatory mediators
last-line use
includes:
MAB’s
Omalizumab –> inhibits IgE
Mepolizumab, reslizumab, benralizumab  inhibits interleukin -5
Dupilumab –> inhibits interleukin 4 and 13

49
Q

Describe use of SABA’s and LABA’s in COPD

A

Same agents as asthma
slightly less effective than SAMA and LAMA in COPD
given scheduled rather than prn

50
Q

Describe SAMA and LAMA in COPD

A

used more than SABA and LABA
SAMA same drug (ipratropium)
LABA drugs include:
tiotropium
aclidinium
glycopyrronium
umeclidinium

51
Q

DEscribe inhaled steroid in COPD

A

Same agents as asthma
Main difference is they are utilized in end stage of COPD

52
Q

Main therapies of COPD? Severe? excerbations? rare?

A
  1. SABA and LABA
  2. SAMA and LAMA
    Severe:
  3. inhaled coticosteroids
    Exacerbations:
  4. oral steroids
  5. antibiotics
    Rarely used:
  6. Theophylline (methylxanthines)
53
Q

Categorize asthma treatments in Releiver, controller, exacerbations, and novel therapy.

A

Reliever: SABA and SAMA
Controller: ICS, LABA, LTRAs, theophylline
Exacerbations: orla steroids
Novel therapy: biologics

PHAR 123 (18 decks)

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