Session 9 Flashcards
(31 cards)
What causes cystic fibrosis?
An autosomal recessive defect in the CFTR gene affecting exocrine glands.
What are the clinical consequences of cystic fibrosis?
Defects in chloride ion transport causing mucus to become thick and dehydrated; lungs are predisposed to colonisation and infection by several different organisms.
What organisms typically cause infection in cystic fibrosis?
Haemophilus influenzae, Staphylococcus aureus, Pseudomonas aeruginosa, Candida albicans, Aspergillus fumigatus, Mycobacteria.
What type of Pseudomonas is often the causative organism in infections in cystic fibrosis patients?
Mucoid Pseudomonas aeruginosa.
What infections often cause acute exacerbation of COPD?
Infections of the lungs due to S. pneumonia, H. influenzae, Moraxella catarrhalis, Ps. aeruginosa or E. coli.
How can viral lung infections predispose COPD patients to acute exacerbation?
Viral infection causes inflammation which makes it easier for bacteria to colonise, bacterial infection may set in and trigger an acute exacerbation.
How may diabetes dispose patients to infection?
Hyperglycaemia and acidaemia impair the humoral immunity and polymorphonuclear leukocyte and lymphocyte functions; micro- and macro-vascular disease reduces tissue perfusion so neutrophil response is lowered; neuropathy reduces sensation so areas of skin may go unnoticed.
What ENT infections are often found in diabetic patients?
Malignant or necrotising otitis externa, rhinocerebral mucormyosis.
What is the causative organism in necrotising or malignant otitis externa?
Pseudomonas aeruginosa
What are usually the causative organisms in UTIs found in diabetic patients?
Enterobacteriaceae (e.g. E. coli) or Pseudomonas aeruginosa.
What skin and soft tissue infections are often found in diabetics?
Cellulitis, folliculitis, foot ulcers and necrotising fasciitis.
What is the typical causative organism in cellulitis?
Staphylococcus aureus or group A beta-haemolytic Strep. species.
What is the typical causative organism in folliculitis?
Staphylococcus aureus.
What is the typical causative organism in diabetic foot ulcers and necrotising fasciitis?
Usually polymicrobial due to: Staphylococcus aureus, beta-haemolytic streptococcus sp, enterobacteriaceae and several anaerobes.
What is the sensitisation phase in a hypersensitivity reaction?
The first encounter with the antigen which is clinically silent.
What is the effector phase of a hypersensitivity reaction?
An encounter with an antigen after the first where clinical pathology occurs on re-exposure.
What are the features of type I hypersensitivity reactions?
- Allergic reactions
- Occur within 30 mins and are usually harmless
- IgE or IgM mediated
What are the features of type II hypersensitivity reactions?
- Antibody mediated
- Occur in 5-12 hours
- IgG and IgM mediated
- Tissue antigens
What are the features of type III hypersensitivity reactions?
- Immune complex mediated
- Occur within 3-8 hours
- IgG and IgM mediated
- Soluble antigens
What are the features of type IV hypersensitivity reactions?q
- Non-antibody mediated
- Caused by environmental infectious agents and self antigens
- Occur within 24-48 hours
Describe the hygiene hypothesis.
Children with an urban upbringing are more likely to develop allergies than children with a rural upbringing due to factors such as lower exposure to allergens, better sanitation, etc.
What is clinical cross-reactivity with respect to allergies?
People with one allergy are more likely to be allergic to certain other allergens due to the similarity of the allergens. E.g. people with cows milk allergies are very likely to also be allergic to goats milk.
Describe the key features of mast cells.
Large nucleus, little cytoplasm, many granules, found near vessels and in mucosal membranes of vessels, activated by an IgE-dependent mechanism, activation causes release of contents.
What occurs at the first exposure of an allergen in an allergic reaction?
Mast cells are armed with antigens ready for a second exposure: antigen-specific IgE binds to mast cells and sensitises them to the antigen; no mast cells are activated so it is clinically silent.
