RESP Flashcards
Atopic Triad
Asthma
Hay fever
Eczema
Pathophysiology of asthma
Triggers:
Allergic: pollen, pets
Nonallergic: smoking, perfumes
Trigger taken by dendritic cell and presented to T-helper 2 cell. TH2 cells produce IL-4, IL-13 (cause plasma cells to release IgE. IgE activated mast cells to cause degranulation. Granules include histamine leukotriene, prostaglandin- type 1 hypersensitivty reaction -> bronchospasm, increased mucus production, oedema. This narrows airway and produces symptoms) and IL-5 (leads to activation of eosinophils which release more cytokines and leukotriene contibuting to symptoms as well.
Pathophysiology of Pulmonary embolism
Pulmonary embolism (PE) is a condition where a blood clot (thrombus) forms in the pulmonary arteries. This is usually the result of a deep vein thrombosis (DVT) that developed in the legs and travelled (embolised) through the venous system and the right side of the heart to the pulmonary arteries in the lungs. Once they are in the pulmonary arteries they block the blood flow to the lung tissue and create strain on the right side of the heart. DVTs and PEs are collectively known as venous thromboembolism (VTE).
RIPE
R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months
TOM TIP: Remember that isoniazid causes peripheral neuropathy and pyridoxine (vitamin B6) is usually co-prescribed prophylactically to help prevent this. An exam question might ask “they are started on R, I, P and E, what should also be prescribed?” The answer would be pyridoxine.
Chest X Ray TB
Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy
Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones
Disseminated Miliary TB give a picture of “millet seeds” uniformly distributed throughout the lung fields
Disease Course TB
The TB bacteria are very slow dividing with high oxygen demands and this makes them difficult to culture and treat. It is mostly spread by inhaling saliva droplets from infected people. It then spreads through the lymphatics and blood. Granulomas containing the bacteria form around the body.
Active TB is where there is active infection in various areas within the body. In the majority of cases the immune system is able to kill and clear the infection. The immune system may encapsulate sites of infection and stop the progression of the disease and this is referred to as latent TB. When latent TB reactivates this is known as secondary TB. When the immune system is unable to control the disease this causes a disseminated, severe disease and is referred to as miliary TB.
The most common site for TB infection is in the lungs where they get plenty of oxygen. Extrapulmonary TB is where it infects other areas:
Cystic fibrosis
Presentation of cystic fibrosis
Microbial colonises cystic fibrosis
Pseudomonas aeruginosa :
Prophylactic is flucloxacillin
Treatment is a nebulised antibiotic such as tobramycin
Oral ciprofloxacin is also used
Bronchiectasis Chest XRay
Signet ring sign
Criteria for pleural effusion
Lights Criteria
Criteria for pleural effusion
Lights Criteria
Someone with pharyngitis what do you need to rule out?
Rheumatic fever espically children
lifecycle/pathogenesis of malaria infection
Plasmodium protozoa injected by female Anopheles multiple in RBCs.
Haemolysis/RBC sequestration/Cytokine release
Liver stage – asexual reproduction of schizonts forming merozoites (this causes fever spikes)
Licensed nedication slow down proression of idiopathic pulmonary fibrosis
Pirfenidone
Nintedanib
Severity of asthma attacks
