Immunology (+hep) Flashcards
Diseases and viruses that cause hepatitis. Which is the most common viral cause
-Hep A, B, C
-epstein barr virus =most common
-Toxins from overdose of paracetamol
-autoimmune disease (less common)
-Wilson’s disease (rare)
transmission of Hep A, B, C, D, E. which is the most common. which is emerging
most common = A
emerging = E
-Parenteral (via blood- transfusion, IV sexual) transmission - Hep B, C & D
-Enteral (faecal/oral) transmission – Hep A and E
Difference between acute and chronic liver damage. (symptoms and causes)
-acute: immune response to virus. Also due to alcohol
-Causes jaundice, feel ill, dark urine, rarely fatal
-chronic: Due to chronic Hep C and alcohol abuse. virus difficult to clear by immune system, where neither wins. cirrhosis due to chronic damage to the liver with fibrosis and scarring in an attempt to regenerate. Many symptoms affecting whole body
which hep infection usually follows seafood poisoning
hep A
what biomarkers and enzymes are elevated in hepatitis
-ALT - alanine transaminase (enzymes released by damaged liver cells)
-AST - aspartate transaminase
-alkaline phosphatase (made in bile duct),
-bilirubin (liver unable to clear it, causes jaundice),
[but do not predict severity of disease]
-albumin is reduced
which Hep viruses have vaccinations
hep A and B
what is the maximum dose of paracetamol in a day. how much causes acute liver damage. how much is fatal
- 4g is the maximum / 24hrs
- 10-15g can cause acute liver damage
- 25g is fatal
signs and symptoms of chronic liver disease (lots)
-encephalopathy (brain not working properly), reduced attention span, reverse sleeping pattern
-Ascites - abdominal swelling -bloating
-Portal hypertension – Veins expand at bottom of oesophagus causing hypertension, If these burst it can cause vomiting of blood.
-Loss of lean body mass – shoulders
-impaired clotting. increased bruising, stretch marks, thin skin
-jaundice- yellow skin and sclera, dark urine, greasy stools
-Spider Naevi – central arteriole radiating from spider. Disappears temporarily if press it as blood empties. Only appears above SVC in upper thorax
-Liver hand flap = tremor when hand is extended
-enlarged salivary glands
Palmar erythema – red palms [also in arthritis]
-Gynaecomastia – developing breast tissue in males, as osetrogen not metabolised
-Dupuytren’s contracture – wing finger/ middle finger always flexed [also due to anti-epyletic drugs]
-finger clubbing
what enzyme is raised in chronic drinkers
gamma GT =gamma glutamyl transpeptidase (bone type and liver type)
AST > ALT
serological markers for hep B. which is a sign of active viral replication
-heb B surface antigen - marker of ongoing infectivity
-anti heb B surface antigen = confers protection from infection
-heb B core antigen - detected when there are antibodies to it
-hep B e antigen = sign of active viral replication
why clotting is affected in those with liver disease. which clotting factors are in the liver
-impaired clotting due to changes in clotting factors and platelets (low platelets)
-clotting affected as factors 2,7,9, 10, 11, 12 and vitamin K are in liver
why GA is not good for hepatitis patients -what syndrome may it cause
Severe jaundice undergoing GA may lead to hepato-renal syndrome - renal failure secondary to liver failure
-those with cirrhosis can’t be treated in GDP, should be sedated in specialised units as small doses may lead to coma as not metabolised well
which LA is to be avoided in hepatitis and which is fine. which should be limited
-avoid amides as metabolised in liver. Avoid lidocaine. But if ester allergy then:
-Articaine = better option, as metabolised in plasma. 2 cartridges
-Prilocaine better option as metabolised in lungs and kidneys. Limit 2 cartridges
which antibiotics, antifungals and NSAIDs to avoid in liver disease.
-Miconazole =avoid
-Fluconazole = decreased dose (not metabolised properly)
-Avoid erythromycin, clindamycin and tetracycline
-reduce metronidazole
-NSAIDs fine but reduce paracetamol
why portal hypertension in liver disease patients can affect dentistry
-risk of haematemesis (vomiting)
-Many of these patients take prophylactic B blockers (propranolol to reduce pressure) Propranolol reduces plasma clearance of epinephrine. Hypertensive crisis
differences between innate and adaptive immunity
- Innate: first line of defence. Rapid, Basic level of protection, Fixed, constant during exposure Limited specificity (reaction to all bacteria of a species), No memory. Neutrophils, macrophages, dendritic cells, mast cells, NK
2.Adaptive: Slow to develop, Highly specific and respond to wider range of pathogens, Variable, Improves upon exposure, Has memory. Long-lasting protection against infection. T cells, B cells, antibodies
what are the 3 professional phagocytic immune cells
neutrophils, macrophages, natural killer cells
what are the professional antigen presenting cells
dendritic, macrophages, B cells
(these are the only cells that express MHC class II)
CD4 and CD8 T cells functions. what MHC molecules they express
CD4 = provide help by recruiting more immune ells. (Th1, Tfh etc.) express MHC class II
CD8 = express MHC class I. cytotoxic. kill infected cells. cannot work without 4
what are the functions of Th1, Th2, Th17, Tfh and T reg, Which cytokines mediate them
Naïve T cells = have not encountered an antigen before so have not been activated. They can only go to secondary lymphoid tissues if activated
Th 1= macrophage recruitment
-IL12, IFN Y
Th2 = mast cells for allergies
-IL4
Th 17 = innate reinforcement (AMP, neutrophils)
-IL1B
Tfh = B cells
-IL6
T reg = supresses T cells
-IL10
Roles of interluikins 1,2,4,8,6,12,10. which is the growth stimulating factors
IL-1 = inflammatory response
IL-2= T cell division and proliferation (growth stimulating factor)
IL 4= allergy cells and enhance barrier function at mucosal surfaces
IL8 = Neutrophil chemotaxis
IL6= B cell activation, by T helper cells
IL12= T cell activation
IL10- suppress T cell activity, prevent autoimmunity
examples of host physical barriers. what enzymes are found in saliva
1-Skin: keratin, high cell turn over, cell-cell junctions with small gaps and little intercellular material, low pH so inhibits growth of pathogens and favours immune cells.
2-Mucosal tissues: secrete mucous to coat bacteria and prevent attachment, ciliated epithelium so cilia eject bacteria, large surface area.
3-Saliva: lysozyme digest cell walls. Lactoferrin removes iron required by bacteria. Phospholipase digests cell membranes. Fluid flushes out infection.
4-Urine - flush out pathogens
5-Acidic GI tract with digestive enzymes to inhibit cell growth
Difference between allergic and autoimmune response
-A state of altered reactivity in which the body reacts with an exaggerated immune response to a foreign agent
1-Allergy: reaction to an otherwise harmless extrinsic antigen. (Type 1 hypersensitivity)
2-Autoimmune: reaction to an otherwise tolerated intrinsic antigen (type 2,3,4 hypersensitivity)
What types of hypersensitivity reactions does penicillin cause. How penicillin causes hypersensitivity
-Type 1,2 and 3
-Type 1: Beta lactam ring can react with amino groups on proteins. Penicillin-protein complex can initiate IgE response in some people.
-Type 2: ring can react with AA. Modify proteins on RBCs. Labelled for destruction so causes haemolytic anaemia
How is type 1 hypersensitivity caused. What cells are involved. Examples of this reactions (atopy and environmental agents). Signs and consequences of the reaction
-Rapid response to an allergen (pollen, food, penicillin etc.)
-Mediated by IgE
-Allergens can reach the bloodstream and activate mast cells throughout the body.
Atopy trait = genetic tendency to develop allergy. -Eg. asthma, eczema, hives
Environmental = dust, pollen, food, wasp stings
Consequences:
1. Increased capillary permeability: itching, rash, rhitinis, laryngeal oedema and bronchiole constriction causing suffocation, peripheral oedema causing hypotension and heart attack
2. smooth muscle contraction -coughing, urinary urgency, vommitting, cramps, anaphylaxis, wheezing
How is type 2 hypersensitivity caused. Give examples.
- IgG (mainly) or IgM binding to an antigen
-causing activation of complement, resulting in cytotoxicity of host cells.
-pre-existing antibodies bind to graft
eg-autoimmune haemolytic anaemia, thrombocytopenia purpura, pemphigus vulgaris, acute rheumatic fever
How does autoimmune haemolytic anaemia, blood group incompatibility and penicillin cause haemolytic anaemia.
- Autoimmune haemolytic anemia: Autoantibodies bind to RBCs, activate complement and phagocytosis, causing RBC death.
- Blood group incompatibility: Incompatible reaction during transfusions causes antibodies to attack antigens on RBCs.
- Penicillin: ring can react with AA. Modify proteins on RBCs. Labelled for destruction
-associated with thrombocytopenia
What are type III hypersensitivity reaction mediated by. What is involved. Give examples of type III.
-IgG mediated
-reactions against soluble antigens in the circulation
-Activates complement and macrophages. Sensitises mast cells. Causing inflammation and tissue injury.
Eg. Serum sickness, Arthur reaction and oral erythema multiforme (crusty blistering of oral mucosa), systemic lupus erythematous, rheumatoid arthritis
What are type IV hypersensitivity reactions mediated by. Examples of type IV
-Host T cells attack foreign antigen. Pro-inflammatory mediators released by T cells. IFNY.
-Delayed reaction as takes a while for T cells to be recruited
eg. TB, Crohn’s, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, metal ion sensitivity, contact dermatitis, lichenoid reactions
Coeliac disease has features of both an allergic and autoimmune disease. How is it caused. symptoms. The allele predisposition
-Inflammation of upper small intestine, in response to gluten. Loss of vili, increase in renewing epithelial cells, severe inflammation, tissue damage.
-HLA-DQ2
-a-gliadin in gluten isn’t usually recognised, but its modification in the disease causes an inflammatory reaction to it causing gut damage
-low energy, oedema, anaemia, diarrhoea/ constipation, aphthous ulcers. dermatitis herpetiformis (particularly the elbows)
Which type of diabetes has a link to other inflammatory diseases, like periodontal disease and CVD. Why
-Type 2
-Increased blood glucose leads to reduced sensitivity to insulin, so production is impaired. Local release of cytokine causes localised and systemic inflammation.
-Heightened systemic inflammation in type 2 as cytokine and chemokines can enter the circulation. And excess glucose in circulation can act on receptors that lead to proinflammtory mediator expression
-so may also be associated with periodontitis or CVD for example.
What are primary and secondary immune tissues and give examples
1-Primary immune tissues: produce immune cells in haematopoiesis.
-Bone marrow and thymus
2-Secondary immune tissues: sites where immune responses are initiated. Antigens are presented here.
-Tonsils, spleen, lymph nodes, Peyer’s patch, MALT
what is complement and the 3 functions
a cascade that enhances antibodies and phagocytic cells to clear infection. Activated C3 convertase.
-Complement components are proteins in the blood and tissue fluid that cause:
1. Chemotaxis: recruitment of neutrophils to site of infection, causing inflammation
2. Opsonisation: coating bacteria to promote antigen uptake by phagocytes.
3. Membrane attack complex: AMPs disrupt the cell membrane and destroy the pathogen
why B cells are so diverse
- antigen somatic recombination: gene rearrangement to get unique proteins to recognise specific antigens
- class switching: (due to constant region of Ig changing) Same specificity to antigen but different functional characteristics.
- somatic hypermutation: point mutations to improve affinity to antigen
- switching between membrane bound and secreted antibodies (Ig M etc.): switching from B cell receptor, to acting as an antibody.
difference between MHC class I and II. (where they are expressed, what they do)
- MHC class I = expressed by most nucleated cells (so not RBCs)
-intracellular antigens are presented by this route
-present the antigen to cytotoxic CD8 T cells. - MHC class II = only expressed by professional antigen presenting cells. (dendritic, macrophage B cells)
-extracellular antigens presented by this route
-presented to CD4 helper T cells
how vaccines work
It teaches your body to make antibodies that protect you against the pathogen if you were to become exposed to it
- It contains a weakened or inactivated microbe, or an agent that resembles its toxins or surface proteins. It elicits an immune response, so that our body has memory and is immune to secondary exposure
Memory B and T cells= -memorize the characteristics of the antigen during initial infection so in secondary infections, it triggers an accelerated and stronger immune response, where IgG predominates
-protects the individual getting disease, prevents you spreading it to other people, protects communities
