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PathoPharm > Module 7 - Respiratory > Flashcards

Module 7 - Respiratory Flashcards

1
Q

What are the structures of the upper respiratory system?

A

Nose
Mouth
Sinuses
Pharynx
Larynx

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2
Q

What are the structures of the lower respiratory system?

A

Trachea
Bronchi
Bronchioles
Alveoli

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3
Q

What is the primary drive of breathing?

A

Elevated CO2 levels in blood make it more acidic –> medulla oblongata respiratory sensors feel this and control rate and depth of breathing to remove CO2 from blood

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4
Q

What is the secondary drive for breathing?

A

When O2 is low in blood, chemoreceptors in the carotid sinuses and aortic arch sense hypoxic conditions and send signals to medulla oblongata that more O2 is needed

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5
Q

Define ventilation

A

The amount of air in the alveoli - NOT the amount in the lungs!

Aka - the air that is available to perform gas exchange

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6
Q

Define perfusion

A

The amount of blood in the pulmonary capillaries of the lungs

Aka - how much blood is available to perform gas exchange

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7
Q

What are some factors that affect ventilation?

A
  • Resistance to airflow
  • Lung compliance (elasticity)
  • Lung volume and capacity (atelectasis)
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8
Q

TLC

A

Total Lung Capacity

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9
Q

FEV1

A

Forced Expiratory Volume (in 1 second)
(The total amount of air that can be expelled in 1 second)

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10
Q

FVC

A

Forced Vital Capacity (the total amount of air that can be exhaled by a person)

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11
Q

PEF

A

Peak Expiratory Flow

Maximum speed of exhalation

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12
Q

Define hypoxemia

A

reduction in the partial pressure of O2 in the blood to below 60mmHg - causes cyanosis

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13
Q

What are signs/symptoms of hypoxia?

A

Agitation, confusion, euphoria, impaired judgement, convulsions, delirium, stupor, coma, combative behavior

Hypotension and bradycardia

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14
Q

What are compensatory mechanisms when a person becomes hypoxemic?

A

Increase in vasoconstriction and BP in an effort to conserve O2 while still perfusing tissues

^Sympathetic NS is activated by low PO2 and causes that vasoconstriction

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15
Q

Define hypercapnia

A

Increase in arterial PCO2 to above 50mmHg

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16
Q

Compensations for hypercapnia

A
  • Increased rate/depth of breathing to expel CO2
  • Vasodilation to increase perfusion of alveoli
  • HA, warm and flushed skin
  • Disorientation, somnolence, coma
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17
Q

What are antitussives?

A

Drugs that decrease the sensitivity of cough receptors by acting on the medullary cough center of brain

CNS depressants so CI w/ head injury or when a productive cough is desired

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18
Q

What are expectorants?

A

Decreases mucous viscosity and allows for more productive cough - allows us to cough out the stuff that’s stuck in the cough

19
Q

What are mucolytics?

A

Breaks disulfide bonds in mucus to make it less sticky –> liquifies mucus

Dont give to pts at risk of bronchospasm (ie asthma or peptic ulcer patients)

20
Q

What are decongestants?

A

Increases vasoconstriction –> less leaky/swollen/edematous nasal passageways

21
Q

What are three varieties of decongestants?

A
  • Oral (systemic)
  • Topical nasal sprays*
  • Topical steroid sprays*

*Can cause increased HR and BP, insomnia, and nervousness especially in people who already struggle with these

Can take days to weeks to fully kick in, and beware rebound nasal congestion

22
Q

Pseudoephedrine (Sudafed)

A

“fed up” with congestion

Why: Decrease nasal congestion and rhinitis

Patho: Alpha-1 agonist, vasoconstriction of respiratory tract mucosa

SE: Insomnia, palpitations, nervousness

Caution: Cardiac pts, HTN, hyperthyroid, monitor for rebound congestion, only use for 3-5 days

23
Q

Phenylephrine (Coricidin)

A

Topical nasal spray - immediate onset of action + local effect (not systemic)

Increases vasoconstriction so:

Caution: cardiac pts, HTN, hyperthyroid, monitor for rebound, and limit use to 3-5 days

If pt has any nose booboos beware vasoconstriction

24
Q

Fluticasone (Flonase)

A

Topical nasal Steroid - anti-inflammatory effect to upper airways but takes time for full effect (over weeks)

SE: Burning, itching

Cautions: Immunocompromised ptst, asthma (can exacerbate bronchospams), stop smoking

25
Q

Antihistamines

A

Claritin and benedryl

SE: sedation, confusion, cant see poop spit pee

Cautions: respiratory disease due to thickened mucus secretions

26
Q

What is the difference b/w asthma and COPD?

A

Asthma: REVERSIBLE airway obstruction
COPD: CHRONIC obstruction of airways (two types - emphysema vs chronic bronchitis)

27
Q

What are some similarities? b/w asthma and COPD?

A

Similarities:
- Bronchoconstriction
- Inflammation, mucosal edema
- Excessive mucus production

28
Q

Extrinsic Asthma

A
  • Only triggered by external allergens
  • Type I hypersensitivity response
  • IgE binds to allergens and basophils + mast cells –> degranulation
29
Q

Triggers of intrinsic asthma

A
  • Cold air
  • Exercise
  • Viral upper respiratory infx
  • mediated by /local/ IgE production
  • Typically appears later in life
  • Some correlation w/ obesity, hx of smoking, family hx
  • Attacks typically happen at night or early morning when waking up
30
Q

Peak flow meter usage

A

Peak Flow Meters measure PEF - if pt blows in green zone, their asthma is well controlled. If in yellow, they should implement management strategies (use your meds, avoid exposure to triggers, if meds don’t work call doc). If red, go to ER

31
Q

Beta-2 Agonists

A

Dilates bronchi and increase rate/depth of respirations. SABAs and LABAs.

  • SABA, quick relief (albuterol) (good for asthma bc acute relief for acute symptoms)
    -LABA, prophylactic (salmeterol) (good for COPD bc chronic problem)

SE: Tachycardia, palpitations, tremors, HA, cardiac arrhythmias, chest pain, nervousness + anxiety, insomnia, N/V, hypokalemia, dizziness, hypersensitivity rxns

*common with SABAs

32
Q

SABA meaning

A

Short Acting Beta Agonist

33
Q

LABA

A

Long Acting Beta Agonist

34
Q

Antcholinergics for asthma and COPD

A

1) Acetylcholine causes bronchoconstriction
2) Anticholinergics block Ach and parasympathetic NS
3) Smooth muscle relaxation
4) Airways dilate

Useful for patients who can’t tolerate Beta-2 agonists, but not as effective

35
Q

Xanthines (Theophylline)

A

Anticholinergic (cant see spit poop pee) (inhibit parasympathetic NS –> SE = nervousness, F or F, tachycardia)

Good for both asthma and COPD

Narrow therapeutic index - monitor drug levels! Avoid caffeine as it can increase risk of toxicity

36
Q

Why are corticosteroids used for asthma and COPD?

A

Gradually reduces inflammation over time by decreasing the # of mast cells in airways.

Often combined with bronchodilators for combined use as maintenance therapy

37
Q

Antileukotriene - Montelukast

A
  • Blocks leukotrienes from signaling lung cells
  • ppx and chronic asthma tx
  • Not for acute tx
  • Monitor HA, NVD, elevated LFTs, myalgias
38
Q

COPD Points

A

Causes alveoli to lose their elasticity –> cant expel air all the way –> air trapping
Inflammation and fibrosis of bronchial walls

  • Asthma is reversible but COPD is not
  • Leads to pulmonary insufficiency, pulmonary HTN, cor pulmonale
39
Q

Cor Pulmonale

A

Right sided heart failure due to lung disease and increased pulm. resistance

40
Q

Emphysema

A

Pink Puffers (barrel chest)
- Abnormal distension of air spaces
- Alveoli are destroyed (apoptosis, oxidative stress)
- Hyperventilation
- Trying to blow off CO2

41
Q

Chronic Bronchitis

A

Blue Bloaters (chronic cough and cyanosis)
- Increased mucus secretion causes airway obstruction and inflammation of bronchioles
- Chronic productive cough

42
Q

Symptoms of pneumonia

A
  • cough
  • fever
  • chills
  • SOB
  • chest pain
  • increased sputum
43
Q
A

PathoPharm (1 decks)

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