C 1.11 MANAGEMENT OF ADULTS AND CHILDREN AS IN-PATIENTS, INCLUDING THE MEDICALLY AT-RISK PATIENT Flashcards
Cardinal features of inflammation
Redness (rubor) Swelling (tumour) Pain (dolor) Heat (calor) Altered function (functiolaesa)
Immune system made up of:
x3
cells - immunocytes, various different types
Proteins
Soluble substances
All designed to identify and destroy pathogens
Organs of the immune system
Primary organs :lymphoid: - Thymus - Bone marrow Secondary tissues: - spleen - tonsils - lymph vessels - lymph nodes - adenoids - skin - liver
Apoptosis
Programmed cell death
Immunocytes
Bone marrow-derived white blood cells
- Myeloid leukocytes
- Lymphoid leukocytes
Macrophages and polymorphonuclear leukocytes -
Phagocytic - non-specifically ingest and destroy microbes
B-lymphocytes
recognise foreign proteins (antigens)
Differentiated B-lymphocytes (plasma cells) secrete antibodies (immunoglobulins) that specifically bind to and eliminated pathogens
T-Lymphocytes
Bind to antigens presented on the surface of antigen presenting cells (langerhans, macrophages, dendritic cells) and eliminated intracellular pathogens (eg viruses) out of reach of antibiodies.
T-cytotoxic lymphocytes (that express CD8 surface receptor) destroy damaged cells including virally infected and cancer cells.
T-helper cells express the CD4 cell surface receptor, producing a wide range of cytokines that enhance other immune cells function
Natural Killer Cells
NK lymphocytes produce cytokines and cause direct lysis of infected or damaged cells
Polymorphonuclear leukocytes/Granulocytes
Neutrophils Eosinophils Basophils Mast cells Characterised by variable shapes of their nuclei and presence of granules in their cytoplasm. Granules contain immune mediators.
Immune proteins - Cytokines
heterogenous group of small proteins, signalling molecules used in lots of biological functions including inflammation, differentiation, activation, proliferation, apoptosis. Include interleukins (ILs), interferons (IFNs), Tumour necrosis factor (TNF), Cehmokines, and colony stimulating factors (CSFs)
Immune proteins - Complement proteins
Plasma proteins
Activated as a proteolytic cascade - coat surface of pathogens, stimulating their lysis or phagocytosis by immune cells.
Complement activation precepitates inflammation: recruiting blood and immune cells to the area
Sickle cell anaemia
- trait
- disease
Normal Hb is HbA, Defective sickle haemaglobin - HbS
Sickle cell disease - Autosomal recessive inheritance 2 HbS genes (HbSS)
Sickle cell Trait - HbSA - innocuous - usually asymptomatic and rarely anaemia or other complications, unless exposed to extreme hypoxia (e.g. v poor anaesthesia)
Trait confers relative immunity against the malaria parasite during childhood in the critical period between the decline of the passively acquired maternal immunity and the development of the actively acquired immunity.
25% of African population carry HbS gene, also affects people of Middle East and Mediterranean origin.
Hb in RBCs - 4 components 2 beta chains and 2 alpha chains. In fetal Hb 2 alpha chains and 2 others
HbS molecules form due to substitution of valine for glutamic acid in the beta chain of Hb leading to increased rigidity of red cells and classic sickle appearance. This results in haemolysis and vaso-occlusion, leading to tissue infarction. Precipitated by deoxygenation (i.e. when in low flow vessels) or acidosis…
Haemolysis causes: (severity varies)
- anaemia (generally 6-8g/dL) although tends to be asymtomatic due to hyperdynamic circulation (increased circulatory volume) and lower oxygen affinity of HbS, so oxygen released to the tissues more readily then HbA
- high reticulocyte count (precursor to RBCs)
- gallstones
Fall in Hb can be due to
- Aplastic crisis - viral infection destroying erythrocyte precursors
- Acute sequestration crisis - liver and spleen engorged
- haemolysis due to drugs or infection
Vaso-occlusion
- causes avascular necrosis of bone marrow - bone pain crises, precipitated by hyposia, dehydration or infection
- splenic atrophy (increased susceptibility to infection - pneumococcus, salmonella and haemophilus)
- cerebral infarction (fits and hemiplegia
- retinal ischaemia - proliferative sickle retinopathy and visual loss
Acute chest syndrome most common cause of death - medical emergency - fever, cough, dyspnoea, pulmonary infiltrates on CXR. Caused by infection, fat embolism (from necrotic bone marrow),
Prognosis - median survival 40-50 years
Mainstays of treatment - oxygen, fluids, antibiotics, opioid analgesics, transfusions
Emotional stress can also play a part in precipitation of crises.
Dental management of Sickle Cell Disease
Routine treatment in non-crisis period only.
During crisis period - only treatment to manage pain and infection.
Preventative regime important - appropriate use of fluoride tooth pastes and fissure sealants.
Treatment should be planned for early in the morning, and kept as breif and stress free as possible.
Prophylactic antibiotics - pre-op co-amoxiclav or doxycycline and metronidazole deemed appropriate in patients undergoing oral surgery procedures, although little evidence to support this. Patients likely to be on low dose prophylaxis of antibiotics already.
Analgesia - paracetamol and codine recommended as NSAIDs and aspirin may contribute to acidosis which can precipitate crises, and patients may have altered renal function due to vascular damage to the kidneys.
LA with vasoconstrictor not contraindicated (although theoretically contribute to hypoxia and vascular stasis)
GA - hazardous - avoid wherever possible - change in oxygen PP, blood flow, pH and lowered temperature which accompany the anaesthetic may promote intravascular sickling and hence a painful, vaso-occlusive crisis. This needs to be considered and 5 mins of pre-op oxygen is advocated prior to anaesthesia.
IHS good for anxious patients as O2 delivered throughout, so no hypoxia risk
If very anxious then the risk of crisis precipitation due to stress may outweigh the risks of IVS - mainly risk of respiratory depression. ASA III - not in primary care, but by experienced sedationist. Give pre-IVS oxygenation 2-4L/min by nasal cannula for 5 mins, throughout procedure and recovery.for IHS pre-oxygenate, and post-operative oxygen should be given for 5mins after Nitrous oxide administration ceases.
Overdose drugs
Paracetamol: N-acetylcysteine Warfarin: Vit K Organophosphate weedkiller: Atropine Copper: Penicillamine Heparin: Protamine Salicylates: Activated Charcoal, Urine Alkalinisation Beta-blockers: Glucagone Theophylline: Activated charcoal Opioids: Naloxone Midazolam: Flumazenil
