265 - respiratory disorders Flashcards
role of the lungs in regulating BP?
production of angiotensin converting enzyme (pulmonary epithelium)
what are the three types of cells found in the alveoli?
type I pneumocytes - simple squamous epithelial cells
type II pneumocytes - secrete surfactant
alveolar macrophages
what are the mechanisms of respiration in the body?
- neurological (nervous) regulation
- chemical regulation
- mechanical regulation
which part of the brain is responsible for voluntary control of respiration?
the cerebral cortex
which parts of the brain are responsible for involuntary control of respiration?
medulla and pons
what are the medullary centres that control respiration, what do they do?
dorsal respiratory group - controls inspiration/the diaphragm
ventral respiratory group - rhythmicity of breathing
what are the pontine respiratory centres and what do they do?
apneustic center
pneumotaxic centre
together they help to coordinate smooth respiratory rhythm (they send signals to the medulla to smooth it
what influences the respiratory centres in the medulla to increase or suppress breathing?
- higher centres of the brain (voluntary control, pain, emotion, temperature) these signals travel via the pontine centres to the medullary centres
- chemoreceptors - central and peripheral
- mechanoreceptors in lungs also nose etc - eg irritant receptors and stretch receptors in lungs, receptors in muscles trigger increased RR during exercise
where are the peripheral chemoreceptors located and what do they detect?
in the carotid and aortic bodies
detect arterial O2, CO2 and pH and increase/suppress breathing accordingly
where are the central chemoreceptors located and what do they detect and respond to?
located on the surface of the medulla
detect pCO2 in arterial blood and pH of CSF
primarily respond to changes in pH in CSF
what factors affect the mechanical regulation of respiration?
- alveolar surface tension (surfactant)
2, elasticity lungs/chest wall - compliance (ability to expand) and elastic recall (ability to relax back)
- airway resistance
- work of breathing
what is asthma?
a disease characterised by chronic airway obstruction
what is asthma characterised by?
bronchoconstriction
oedema of the airways
mucous hypersecretion
epidemiology of asthma?
Accounts for (approx.) 29% of the burden of disease due to respiratory conditions
some triggers for asthma?
colds and flu dust pollution cigarette smoke paint fumes foods moulds and funghi stress
pathophysiology of asthma, from initial exposure to an allergen to the rupture of mast cells
- initial exposure
- specific IgE produced
- minimal signs and symptoms
- IgE binds to mast cells, ready
- reexposure - antibodies bind to antigen
- IgE triggered, causes mast cell degranulation
- mast cells release chemical mediators of inflammation
what are the chemical mediators released by degranulating mast cells?
HPLP - the harry potter album! histamine prostaglandin luekotrienes platelet activating factor
how do the chemical mediators released by mast cells trigger the s+s of asthma?
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
clinical manifestations of asthma
chest tightness cough dyspnoea wheezing anxiety tachypnoea tachycardia
complications of asthma?
Status Asthmaticus (potential death) Cor pulmonale Atelectasis Respiratory infection Pneumothorax
what is cor pumonale?
abnormal enlargement of the right side of the heart because of lung disease/pulmonary HTN
what is atelectasis?
collapsed lung, often due to airway obstruction
what is status asthmaticus?
acute severe asthma attack, not responsive to bronchodilators
asthma meds: what sorts of relievers are there, what are their mechanisms of action?
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
four effects of asthma relievers?
increased airway diameter
decreased resistance
increased gas exchange
decreased work of breathing
what are the adverse effects of SABAs, and what are they due to?
tachycardia tremors palpitations flushing headaches HTN
due to the effect of stimulation of all B2 receptors as well as beta-1
what are the adverse effects of anti-cholinergics, and what are they due to?
urinary retention
dry mouth
constipation
tachycardia
due to antagonist action on all muscarinic receptors
main anticholinergic/antimuscarinic used in treatment of asthma?
ipratropium
when are anticholnergics generally used in treatment of asthma?
usually in conjunction with SABA in a severe acute episode - slower onset but longer lasting
classes of medications for asthma prevention?
corticosteroids
leukotriene receptor antagonists
mast cell stabilisers
LABAs
routes, MOA of corticosteroids in prevention of asthma?
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
examples of corticosteroids used to treat asthma?
prednisolone
fluticasone
budesonide (Pulmoncort)
adverse effects of inhaled corticosteroids?
thrush
hoarseness
URTI - upper respiratory tract infection
pharyngitis
rhinitis
adverse effects of oral corticosteroids?
Headaches Dyspepsia Nausea Dizziness Insomnia Liver Dysfunction
MOA of leukotriene receptor antagonists in prevention of asthma?
acts directly on the leukotriene receptors to cause bronchodilation through direct action on bronchial muscles
examples of leukotriene receptor antagonists used to treat asthma?
Montelukast
Zafirlukast
adverse effects of leukotriene receptor antagonists?
Headaches Nausea Dizziness Insomnia Gastric upset
MOA of mast cell stabilisers in prevention of asthma?
indirect acting antihistamines prevent the release of substances that cause the bronchospasm
examples of mast cell stabilisers used to treat asthma?
Nedocromil
Cromoglycate
adverse effects of mast cell stabilisers?
Headaches
Dry mucosa
Nausea
MOA of LABAs in prevention of asthma?
difference between LABAs and SABAs?
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
examples of LABAs used to treat asthma?
seretide
what are the discharge considerations for a patient who has experienced an acute exacerbation of asthma?
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
what is an asthma management plan?
how often do patients need to have this reviewed?
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.
what does an asthma management plan include?
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.
criteria for the prescription of corticosteroids or other preventer medications?
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.
what is COPD?
a disease characterised by persistent respiratory symptoms and airflow limitations, due to airway or alveolar abnormalities
what is COPD usually caused by?
significant exposure to noxious particles or gases
most commonly cigarette smoke, then pollutants
epidemiology of COPD?
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
risk factors for COPD
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
pathophysiology of COPD
- noxious stimuli
- abnormal and prolonged inflammatory response
- 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 - gas trapping→hyperinflation, gas exchange abnormalities, airflow limitation
- signs and symptoms (dyspnoea, cough, hypoxaemia, hypercapnia, cor pulmonale)
signs and symptoms of COPD?
dyspnoea
chronic cough
sputum production
hypoxaemia
hypercapnia
cor pulmonale
fatigue
weight loss
what is air trapping in COPD?
air gets trapped in the alveoli during expiration because of excess mucous and loss of elastic recoil in airways, so they collapse during expirtation
what are the major complications of COPD?
pulmonary hypertension and cor pulmonale
ischemic heart disease
heart failure
osteoporosis
explain the pathophysiology of pulmonary hypertension and cor pulmonale associated with COPD?
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)
management of COPD?
- smoking cessation/decreased pollutant exposure (remove respiratory irritant/trigger for inflammation)
- corticosteroids to manage inflammatory response, SABAs to manage airway constriction
- supplemental oxygen to treat dyspnoea in patients with severe resting chronic hypoxaemia
- non-invasive ventilation (CPAP, BIPAP) to treat tachnypnoea in patients with severe chronic hypercapnia
- pulmonary rehabilitation (exercise, self- management interventions)
- influenza and pneumococcal vaccination to reduce risk of exacerbations
what is pneumonia?
an inflammation of lung parenchyma which causes an alteration in gas exchange
causes of pneumonia?
aspiration of oropharyngeal secretions composed of bacterial flora or gastric content
inhalation of contaminants
contamination from systemic
circulation
classifications of pneumonia?
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.
difference between typical and atypical pneumonia?
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.
clinical manifestations of pneumonia?
Fever, Rigors, Sweats
Malaise
Anorexia
Fatigue
Cough
Purulent sputum
Pleuritic chest pain (Pleurisy)
Dyspnoea
Sometimes haemoptysis (Rusty sputum)
clinical diagnosis of pneumonia?
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
management of pneumonia?
improve oxygenation
IV Fluids for dehydration or low blood pressure
empirical antibiotics (eg. penicillin like Amoxicillin)
treatment of symptoms (analgesia/antipyretic/antiemetic)
potential complications of pneumonia?
hypoxia
pleural empyema
pneumonic shock
septic shock
pleural effusion
abscess
what is pleural empyema?
the collection of pus in the pleural cavity (it’s a form of pleural effusion)
pathophysiology of pneumonia?
- inflammation of the lung caused by trauma/infection/alveolar oedema/vascular congestion
- damage to epithelial cells (causes sputum changes)
- accumulation of cellular debris and exudate
- consolidation
- decreased lung compliance
- hypoxia
- respiratory acidosis
normal SaO2 for a pt with COPD?
88-92%
