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semester 2 2019 > 265 - respiratory disorders > Flashcards

265 - respiratory disorders Flashcards

1
Q

role of the lungs in regulating BP?

A

production of angiotensin converting enzyme (pulmonary epithelium)

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2
Q

what are the three types of cells found in the alveoli?

A

type I pneumocytes - simple squamous epithelial cells

type II pneumocytes - secrete surfactant

alveolar macrophages

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3
Q

what are the mechanisms of respiration in the body?

A
  1. neurological (nervous) regulation
  2. chemical regulation
  3. mechanical regulation
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4
Q

which part of the brain is responsible for voluntary control of respiration?

A

the cerebral cortex

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5
Q

which parts of the brain are responsible for involuntary control of respiration?

A

medulla and pons

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6
Q

what are the medullary centres that control respiration, what do they do?

A

dorsal respiratory group - controls inspiration/the diaphragm

ventral respiratory group - rhythmicity of breathing

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7
Q

what are the pontine respiratory centres and what do they do?

A

apneustic center

pneumotaxic centre

together they help to coordinate smooth respiratory rhythm (they send signals to the medulla to smooth it

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8
Q

what influences the respiratory centres in the medulla to increase or suppress breathing?

A
  1. higher centres of the brain (voluntary control, pain, emotion, temperature) these signals travel via the pontine centres to the medullary centres
  2. chemoreceptors - central and peripheral
  3. mechanoreceptors in lungs also nose etc - eg irritant receptors and stretch receptors in lungs, receptors in muscles trigger increased RR during exercise
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9
Q

where are the peripheral chemoreceptors located and what do they detect?

A

in the carotid and aortic bodies

detect arterial O2, CO2 and pH and increase/suppress breathing accordingly

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10
Q

where are the central chemoreceptors located and what do they detect and respond to?

A

located on the surface of the medulla

detect pCO2 in arterial blood and pH of CSF

primarily respond to changes in pH in CSF

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11
Q

what factors affect the mechanical regulation of respiration?

A
  1. alveolar surface tension (surfactant)

2, elasticity lungs/chest wall - compliance (ability to expand) and elastic recall (ability to relax back)

  1. airway resistance
  2. work of breathing
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12
Q

what is asthma?

A

a disease characterised by chronic airway obstruction

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13
Q

what is asthma characterised by?

A

bronchoconstriction
oedema of the airways
mucous hypersecretion

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14
Q

epidemiology of asthma?

A

Accounts for (approx.) 29% of the burden of disease due to respiratory conditions

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15
Q

some triggers for asthma?

A 
colds and flu
dust
pollution
cigarette smoke
paint fumes
foods
moulds and funghi
stress
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16
Q

pathophysiology of asthma, from initial exposure to an allergen to the rupture of mast cells

A
  1. initial exposure
  2. specific IgE produced
  3. minimal signs and symptoms
  4. IgE binds to mast cells, ready
  5. reexposure - antibodies bind to antigen
  6. IgE triggered, causes mast cell degranulation
  7. mast cells release chemical mediators of inflammation
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17
Q

what are the chemical mediators released by degranulating mast cells?

A 
HPLP - the harry potter album!
histamine
prostaglandin
luekotrienes
platelet activating factor
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18
Q

how do the chemical mediators released by mast cells trigger the s+s of asthma?

A

histamine and prostaglandin cause vasodilation and increased vascular permeability leading to airway oedema

leukotrienes cause bronchoconstriction

platelet activating factor causes increased mucous production

together this all leads to bronchospasms and airway obstruction

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19
Q

clinical manifestations of asthma

A 
chest tightness 
cough 
dyspnoea
wheezing
anxiety
tachypnoea
tachycardia
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20
Q

complications of asthma?

A 
Status Asthmaticus (potential death)
Cor pulmonale
Atelectasis
Respiratory infection
Pneumothorax
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21
Q

what is cor pumonale?

A

abnormal enlargement of the right side of the heart because of lung disease/pulmonary HTN

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22
Q

what is atelectasis?

A

collapsed lung, often due to airway obstruction

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23
Q

what is status asthmaticus?

A

acute severe asthma attack, not responsive to bronchodilators

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24
Q

asthma meds: what sorts of relievers are there, what are their mechanisms of action?

A

short-acting beta-2 agonists - stimulate B2 receptors found in smooth muscles of airways, inhibits smooth muscle and causes bronchodilation

anticholinergics (anti-muscarinic) - blocks ACh from binding to muscarinic receptors in airways, inhibiting smooth muscle contraction

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25
Q

four effects of asthma relievers?

A

increased airway diameter

decreased resistance

increased gas exchange

decreased work of breathing

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26
Q

what are the adverse effects of SABAs, and what are they due to?

A 
tachycardia
tremors
palpitations
flushing
headaches
HTN

due to the effect of stimulation of all B2 receptors as well as beta-1

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27
Q

what are the adverse effects of anti-cholinergics, and what are they due to?

A

urinary retention
dry mouth
constipation
tachycardia

due to antagonist action on all muscarinic receptors

28
Q

main anticholinergic/antimuscarinic used in treatment of asthma?

A

ipratropium

29
Q

when are anticholnergics generally used in treatment of asthma?

A

usually in conjunction with SABA in a severe acute episode - slower onset but longer lasting

30
Q

classes of medications for asthma prevention?

A

corticosteroids

leukotriene receptor antagonists

mast cell stabilisers

LABAs

31
Q

routes, MOA of corticosteroids in prevention of asthma?

A

oral or inhaled (less systemics SEs when inhaled)

inhibit synthesis of inflammatory mediators by inhibiting PLA2 enzyme → no PGs, leukotrienes, histamine → reduced/ no asthma signs and symptoms

32
Q

examples of corticosteroids used to treat asthma?

A

prednisolone
fluticasone
budesonide (Pulmoncort)

33
Q

adverse effects of inhaled corticosteroids?

A

thrush

hoarseness

URTI - upper respiratory tract infection

pharyngitis

rhinitis

34
Q

adverse effects of oral corticosteroids?

A 
Headaches
Dyspepsia
Nausea
Dizziness
Insomnia
Liver Dysfunction
35
Q

MOA of leukotriene receptor antagonists in prevention of asthma?

A

acts directly on the leukotriene receptors to cause bronchodilation through direct action on bronchial muscles

36
Q

examples of leukotriene receptor antagonists used to treat asthma?

A

Montelukast

Zafirlukast

37
Q

adverse effects of leukotriene receptor antagonists?

A 
Headaches
Nausea
Dizziness
Insomnia
Gastric upset
38
Q

MOA of mast cell stabilisers in prevention of asthma?

A

indirect acting antihistamines prevent the release of substances that cause the bronchospasm

39
Q

examples of mast cell stabilisers used to treat asthma?

A

Nedocromil

Cromoglycate

40
Q

adverse effects of mast cell stabilisers?

A

Headaches
Dry mucosa
Nausea

41
Q

MOA of LABAs in prevention of asthma?

difference between LABAs and SABAs?

A

stimulate B2 receptors found in smooth muscles of airways, inhibits smooth muscle and causes bronchodilation

not used for acute attacks, they’re long acting (up to 12 hrs)

often used in conjunction with corticosteroids for asthma management

42
Q

examples of LABAs used to treat asthma?

A

seretide

43
Q

what are the discharge considerations for a patient who has experienced an acute exacerbation of asthma?

A

patients cannot be dc until they demonstrate 4 hours of being symptom free

determine the effectiveness of his inhaler technique

eduation including need for asthma plan

arrange follow-up: recheck within 3 days by usual GP
plus comprehensive assessment in 2–4 weeks to review the treatment regimen

44
Q

what is an asthma management plan?

how often do patients need to have this reviewed?

A

an individualised plan which helps to the person with asthma deal and manage asthma episodes

review the written asthma action plan every year, and whenever there is a significant change in treatment or asthma status.

45
Q

what does an asthma management plan include?

A

includes usual asthma and allergy meds

clear instructions on how to change medication (including when and how to start a course of oral corticosteroids)

when and how to get medical care, including during an emergency

name of the person preparing the plan

the date.

46
Q

criteria for the prescription of corticosteroids or other preventer medications?

A

asthma symptoms twice or more during the past month

waking due to asthma symptoms once or more during the past month

an asthma flare up in the previous 12 months.

47
Q

what is COPD?

A

a disease characterised by persistent respiratory symptoms and airflow limitations, due to airway or alveolar abnormalities

48
Q

what is COPD usually caused by?

A

significant exposure to noxious particles or gases

most commonly cigarette smoke, then pollutants

49
Q

epidemiology of COPD?

A

fourth main contributor for disability in Australia

fourth major cause of death in the world

7.5% of australians over 40, increases with age to about 25% of those over 75

50
Q

risk factors for COPD

A

smoking

genetic factors - alpha 1- antitrypsin deficiency

age

female gender

occupational exposure/exposure to particles

pollution

lower socioeconomic status

history of respiratory disease: asthma and chronic bronchitis

51
Q

pathophysiology of COPD

A
  1. noxious stimuli
  2. abnormal and prolonged inflammatory response
  3. increase in cytokines, WBC activity
    4a. persistent bronchial inflammation, excess goblet cells, leading to bronchial oedema, mucous hypersecretion, airway scarring/remodelling, increased infection risk
    4b. breakdown in lung parenchyma leading to destruction of alveolar wall, loss of elastic recoil, and enlargement of air spaces
  4. gas trapping→hyperinflation, gas exchange abnormalities, airflow limitation
  5. signs and symptoms (dyspnoea, cough, hypoxaemia, hypercapnia, cor pulmonale)
52
Q

signs and symptoms of COPD?

A

dyspnoea

chronic cough

sputum production

hypoxaemia

hypercapnia

cor pulmonale

fatigue

weight loss

53
Q

what is air trapping in COPD?

A

air gets trapped in the alveoli during expiration because of excess mucous and loss of elastic recoil in airways, so they collapse during expirtation

54
Q

what are the major complications of COPD?

A

pulmonary hypertension and cor pulmonale

ischemic heart disease

heart failure

osteoporosis

55
Q

explain the pathophysiology of pulmonary hypertension and cor pulmonale associated with COPD?

A

airway remodeling and air trapping → reduced gas exchange capacity → increase in PaCO2 → hyperventilation

compensatory hyperventilation will eventually fail → hypoxaemia → pulmonary vasoconstriction occurs to overcome this reduced perfusion → pulmonary hypertension occurs→the right ventricle and subsequently right atrium are overworked and become
enlarged over time (cor pulmonare)

56
Q

management of COPD?

A
  1. smoking cessation/decreased pollutant exposure (remove respiratory irritant/trigger for inflammation)
  2. corticosteroids to manage inflammatory response, SABAs to manage airway constriction
  3. supplemental oxygen to treat dyspnoea in patients with severe resting chronic hypoxaemia
  4. non-invasive ventilation (CPAP, BIPAP) to treat tachnypnoea in patients with severe chronic hypercapnia
  5. pulmonary rehabilitation (exercise, self- management interventions)
  6. influenza and pneumococcal vaccination to reduce risk of exacerbations
57
Q

what is pneumonia?

A

an inflammation of lung parenchyma which causes an alteration in gas exchange

58
Q

causes of pneumonia?

A

aspiration of oropharyngeal secretions composed of bacterial flora or gastric content

inhalation of contaminants

contamination from systemic
circulation

59
Q

classifications of pneumonia?

A

1) CAP - Acquired out of hospital
2) HAP – Pneumonia > 48 hours after admission or within 7-10 days after discharge
3) VAP – Patients in ICU ventilated
4) Pneumonia in the immunocompromised, chemotherapy, HIV infection and transplantation.

60
Q

difference between typical and atypical pneumonia?

A

typical caused by organisms such as Streptococcus pneumoniae which accounts for 60 to 70% of all bacterial CAP cases.

atypical caused by Mycoplasma pneumoniae, Chlamyodophila pneumoniae and respiratory viruses.

61
Q

clinical manifestations of pneumonia?

A

Fever, Rigors, Sweats

Malaise

Anorexia

Fatigue

Cough

Purulent sputum

Pleuritic chest pain (Pleurisy)

Dyspnoea

Sometimes haemoptysis (Rusty sputum)

62
Q

clinical diagnosis of pneumonia?

A

Full history and physical examination

Oxygen Saturations

Sputum culture

Chest x-ray to confirm diagnosis

Blood tests –FBC (High or low white cell count),

U+Es (Glucose: Low Na, high urea/creatinine)

LFT’s: Often abnormal (High ALT and ALP), low albumin

C-reactive protein

Microscopic culture and sensitivity

63
Q

management of pneumonia?

A

improve oxygenation

IV Fluids for dehydration or low blood pressure

empirical antibiotics (eg. penicillin like Amoxicillin)

treatment of symptoms (analgesia/antipyretic/antiemetic)

64
Q

potential complications of pneumonia?

A

hypoxia

pleural empyema

pneumonic shock

septic shock

pleural effusion

abscess

65
Q

what is pleural empyema?

A

the collection of pus in the pleural cavity (it’s a form of pleural effusion)

66
Q

pathophysiology of pneumonia?

A
  1. inflammation of the lung caused by trauma/infection/alveolar oedema/vascular congestion
  2. damage to epithelial cells (causes sputum changes)
  3. accumulation of cellular debris and exudate
  4. consolidation
  5. decreased lung compliance
  6. hypoxia
  7. respiratory acidosis
67
Q

normal SaO2 for a pt with COPD?

A

88-92%

semester 2 2019 (16 decks)

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