BMJ best practice diseases Flashcards
Acute bronchitis- what is it?
Describe the symptoms, examination, diagnostic tests and treatment (acute and ongoing) relevant.
Productive cough for upwards of 30days.
Fever, wheezes, rhonchi.
No history of chronic resp issues
Tests: Peak flow and chest x-ray
Treatment: acute: short acting beta-2- agonist as a bronchodilator.
Ongoing: short acting beta-2- agonist, if symptoms persist (and patient produces purulent sputum) add antibiotics.
Describe acute bronchitis and how it is caused. Also describe the pathophysiology of acute bronchitis.
Acute bronchitis is a lower respiratory tract infection. It is characterised by inflammation of the bronchioles. It is caused by a viral infection such as the ones that cause URTI (e.g. rhinovirus).
The pathophysiology of acute bronchitis is the inflammation of the bronchioles increasing mucus secretion (productive cough) and may cause oedema.
The infection will clear within a few days however the bronchioles will not be repaired for several weeks meaning the cough will continue.
Describe acute respiratory distress syndrome and the pathophysiology of ARDS.
ARDS is a non-cardiogenic pulmonary oedema. It often complicates critical illness.
ARDS causes diffuse alveolar damage. Alveolar spaces are flooded with proteinaceous fluid, inflammatory cells and inflammatory mediators.
The alveoli become flooded due to alveolar-capillary membrane injury. Hyaline membranes are formed and surfactant function decreases.
Describe the symptoms of ARDS.
What tests would you perform to diagnose ARDS and what are they likely to show?
Acute onset. Low oxygen saturation. Respiratory failure.
Critically ill patient, dyspnoea, frothy sputum, increased resp rate, low lung compliance.
On examination- may present as basilar or diffuse rales (crackles that do not clear after cough).
Tests performed-CXR, ABG, sputum, urine and blood cultures and lipase
On a chest X-ray, bilateral opacities would be seen.
Patients PaO2 (inspired oxygen) would be less than 300.
ABG would show low O2 sats.
Sputum, blood and urine culture would be positive if there is an underlying infection.
Lipase would be elevated in cases of acute pancreatitis.
Describe the treatment of ARDS.
Keep tidal volume high. This would involve use of oxygen masks. (6cc per kg).
Keep fluid balance neutral to slightly negative. Some patients may require a bicarbonate infusion if there pH is low.
Optimise ventilation.
Describe acute respiratory failure. Mention the two types.
Inability of the lungs to perform gas exchange causing hypoxia with or without hypercapnia (CO2 retention).
There are two types of resp failure, type 1 or type 2.
Type 1 is hypoxia without hypercapnia with an arterial pressure of less than 60mmHg.
Type 2 resp failure is hypoxia with hypercapnia. This is with an arterial partial pressure of greater than 50mmHg of carbon dioxide.
Describe the pathophysiology of acute respiratory failure.
Metabolic demands aren’t met because of the inability for gas exchange to occur at the lungs.
Caused by an underlying condition which can be any form of lung disease e.g. oedema, COPD, embolism, shunt etc.
Type 2- hypercapnic. Failure of Co2 exchange, causing increased Co2 in the arteries and respiratory acidosis. To compensate for this, renal bicarbonate retention occurs. Type 2 resp failures occurs with lung problems that limit exchange of Co2 from blood to atmosphere. This can occur in the obstruction of airways, secretions in the small airways and alveoli and chest wall abnormalities.
Describe the symptoms, examination and test and treatment of acute respiratory failure.
Direct trauma to the thorax or neck. dyspnoea Confusion Tachypnoea Accessory breathing muscle use Stridor Inability to speak Retraction of intercostal muscles Loss of airway/gag reflex. Cyanosis
Examination and tests:
Pulse oximetry- SpO2 less than 80%
ABG- pH
Describe allergic bronchopulmonary aspergillosis. Why does this reaction occur. Which people are generally more susceptible to it.
Hypersensitivity reaction that occurs when the bronchi become colonised by Aspegillus Fumigatus in an otherwise immunocompetent person. Patient usually have previous diagnosis of asthma, cystic fibrosis or atopy.
Exposure of an atopic person to it will cause the release of IgE and IgG antibodies.
Describe the symptoms, people who are most susceptible too, tests and treatment of allergic bronchopulmonary aspergillosis.
Symptoms include wheeze, cough, mucus plugs, fever, pleuritic pain, finger clubbing, cyanosis, weight loss. Causes of these include bronchial obstruction, airway inflammation and mucoid impaction that can lead to bronchiectasis, fibrosis and respiratory comproimise.
Groups that are most at risk are young adults/teenages, people with a history of atopy, asthma or CF.
Tests performed are:
skin tests for sensitivity to aspergillus. Shows positive wheal and flare reaction.
Serum total IgE- Elevated
Full blood count-Elevated
Chest X-ray- Upper/middle lobe infiltrates.
Treatment:
First of all give a corticosteroid. Manage the asthma and CF. In adjunction to this you could prescribe an azole antifungal.
Describe an alpha-1-antitrypsin deficiency.
Autosomal co-dominant genetic disorder. It results in AAT allele mutations at the protein inhibitor locus (PI).
It causes ineffective activity of the specific protease inhibitor alpha-1-antitrypsin. This is the enzyme responsible for neutralising neutrophil elastase and for preventing inflammatory tissue damage in the lungs.
Can result in hepatic failure.
Describe the symptoms, tests and treatment for alpha-1-antitrypsin deficiency.
Symptoms- productive cough. SOB on exertion. Chest hyperinflation. Wheeze. Jaundice. Current cigarette smoker. Exposure to gas/fumes or dust. Hepatomegaly (abnormal enlargement of the liver). Ascites (accumalation of fluid in the peritoneal cavity). Confusion. Generally affects males in the 32-41 age range.
Tests
Plasma AAT level- reduced plasma level
Describe anaphylaxis
Acute, severe, life threatening allergic reaction. Reaction is caused by release of immune and inflammatory mediators from basophils and mast cells.
Describe the pathophysiology of anaphylaxis.
The clinical symptoms derive from pro-inflammatory and vasoactive mediators and cytokines released by massive degranulation or release from basophils and mast cells. Classically, this cascade is initiated by an IgE-mediated hypersensitivity reaction.
Allergens are introduced into the body by various routes: ingestion, inhalation, parenteral, or skin contact. On first exposure, a susceptible person forms IgE antibodies specific to the antigen presented. IgE antibodies attach to high-affinity Fc receptors on basophils and mast cells.
On subsequent exposure, binding of antigen to the IgE antibodies leads to bridging and triggers the degranulation of mast cells. Histamine, prostaglandin D2, leukotrienes, platelet-activating factor, tryptase, nitric oxide, and eosinophil and neutrophil chemotactic factors have diverse effects on target organs and lead to the clinical manifestations of anaphylaxis. These manifestations include increased vascular permeability, vasodilation, and myocardial dysfunction, leading to hypotension and cardiovascular collapse, as up to 50% of intravascular volume can shift to the extravascular compartment in minutes. Altered smooth muscle tone results in bronchospasm and asthma in the respiratory tract, and may also lead to uterine cramps. Activation of the autonomic nervous system causes tachycardia, anxiety, and mucus hypersecretion. Increased platelet aggregation and subsequent recruitment of more immune cells complete the picture of the systemic inflammatory response.
NSAIDs may also trigger cell activation by altering arachidonic acid metabolism. Activation of complement, the complement peptides (anaphylatoxins) such as C3a and C5a, and their direct action on mast cells and basophils may lead to mediator release, producing symptoms indistinguishable from the classic IgE-mediated reaction
Describe the symptoms, tests and treatment of anaphylaxis.
Symptoms- wheezing, rhinitis (or coryza), flushing, dyspnoea, ACUTE IN ONSET, urticaria (hives/rash), stridor and hoarseness of voice, possible nausea and vomiting, abdominal cramping or pain, tachycardia, dizziness, sense of impending doom.
Tests- serum tryptase level
skin test
Treatment- acute in onset- INTRAMUSCULAR ADRENALINE
