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
-Hep B, C & D: Parenteral (blood- transfusion, IV) sexually, perinatally
-Hep A and E -Enteral (faecal/oral)
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 max
-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
explain primary and secondary immunodeficiency. and examples of diseases
- Primary= inherited mutations in genes that control immune responses (defects in TLR signalling, T/B cell development etc.) Rare.
eg. SCID, Bruton’s X linked agammaglobulinemia, combined variable, hyper IgE syndrome, Papillon lefevre syndrome - Secondary= acquired due to environmental factors. More common - immunosuppressive meds, malnutrition, chemotherapy, asplenia, major surgery, HIV infection, severe burns, radiotherapy, SLE, leukaemia
what are monoclonal antibodies. how are they reduced and give example of biologic drugs
Monoclonal = a specific antibody made by cloning a unique white blood cell.
-used for diagnosis and therapies (biologics for autoimmune diseases)
~10x the size of normal proteins – expensive/ difficult to maintain however target specific molecules
-Immunise a mouse with an antigen you are interested in. Take B cells and fuse them with cancer/ myeloma cells to make a hybridoma so that they are immortal so they can be cultured. Select for antigen-specific hybridoma and genetically modify them so that humans don’t recognise them as foreign.And clone these cells
E.g. Rituximab (anti CD20) kills tumour cells in lymphoma
Infliximab (anti-TNF) blocks inflammation in rheumatoid arthritis
Impilimumab (anti-CTLA-4) blocks immunosuppression in melanoma
symptoms and signs of immunodeficiency
-Increased infection - Serious, Persistant (chronic candida), Unusual sites, Recurrent (pneumonia, sinus infections, ear infections, liver abscesses, osteomyelitis, cellulitis, sepsis)
-increased autoimmune disease - endocrine disease, skin problem (vitiligo, alopecia, telangiectasia)
-malignnacy
-damage from infection (bronchiectasis)
-liver abscess, pneumocystis, aspergillus
-eczema, thrombocytopenia, congenital heart disease
-antibiotics have little effect
-oral hairy leukoplakia, severe gingivitis, tooth loss, mouth ulcers, dry mouth, tonsillitis
what immunodeficiency is likely to cause bacterial infections of the tonsils, skin, chest
B cell defect
what immunodeficiency is a common cause of fungal and viral infections
T cell defect
which immunodeficiencies is a likely cause of abscesses
phagocytic cell defects and B cell defects
What is SCID. which immune cells are impaired. what is there a mutation in
severe and combined immunodeficiency
absent T cells, B cells may also be absent
-viral, fungal and bacterial infections
-mutation in adenosine deaminase gene
What is Bruton’s x-linked agammaglobulinemia. which immune cells are impaired.
low or absent B cells and reduced immunoglobulins
absent tonsils
recurrent bacterial infections (pyogenic bacteria)
what is common variable immunodeficiency. which immune cells are impaired. what symptoms it can cause
low immunoglobulins (impaired IgA and IgG)
recurrent infections (sinus, lungs, ears, eyes)
can cause thyroid issues, alopecia, vitiligo
high risk of malignancy (lymphoma)
what is chronic granulomatous disease. symptoms
a genetic disorder where phagocytes are unable to kill bacteria and fungi so highly susceptible to frequent and sometimes life-threatening infections.
-can cause gingivitis and tooth loss, recurrent abscesses, bowel inflammation
-Fever, Chest pain when breathing, Swollen lymph nodes, ongoing runny nose.
-Skin rash, swelling or redness.
-Swelling and redness in the mouth.
-Vomiting. Diarrhea. Stomach pain. Bloody stool.
what may cause chronic mucocutaneous candidiases
-Failure to clear candida – nail, oral, vaginal
Genetic defects [AIRE gene]
Cytokine abnormalities
Endocrine abnormalities [thyroid, parathyroid, adrenal]
-Risk of oesophageal malignancy
what is DiGeorge syndrome
deletion on 22q11 gene
thymus doesn’t develop, so reduced or absent T cells
viral, fungal and bacterial infections
cardiac abnormalities
variable learning difficulties
speech difficulties
cleft palate
what drugs can lead to secondary immunodeficiency
-cytotoxic cancer drugs: kill all dividing cells, so will include bone marrow and lymphoid systems, depleting immune cells
-anti-convulsants - reduce B cells and neutrophils
-Carbimazole - can reduce neutrophils and cause mouth ulcers
-Immunosupressants:
o Cyclophosphamide
o Azathioprine
o Methotrexate
o Cyclosporin & Tacrolimus
o Prednisolone > 20 mg/day
o Biologics
what cells rituximab reduces
anti-CD20 & anti-TNFs - antibody reduction
what diseases can lead to oral candida
-secondary immunodeficiency (HIV, drugs)
-connective tissue disease
-sjogren’s disease
-primary immunodeficiency
-xerostomia
-chronic hep C
diseases that cause mouth ulcers
- Nutritional deficiencies
- Behcets syndrome
- SLE (systemic lupus erythematosis)
- Cancer
- Crohn’s disease
- Infection – viral (HSV), (bacterial)
- Trauma
- Haematological malignancy
- Medications e.g.methotrexate
- Oral dermatoses – lichen planus, pemphigoid, pemphigus
diseases and drugs that can lead to gingivitis
-Cyclosporin
-nifedipine, amlodipine
-Scurvy
-Anticonvulsants
-Chronic granulomatous disease (primary immunodeficiency)
what does C1 esterase deficiency cause. treatment
-Causes angiodema - Recurrent deep swelling with minor trauma
-Recurrent abdominal pain
vomitting
-Can have fatal laryngeal oedema
-No urticaria/ hives
-hoarse voice
-persistent cough
-dysphagia or tongue swelling.
-Long term treatment is with androgenic steroids and tranexamic acid. Treatment of acute attacks is replacement of the enzyme
Low C4
3 ways to test for allergies (type 1 hypersensitivity)
- skin prick test - use agent, histamine and salty water. wheel at site shows they are allergic
- Blood tests - IgE - (less sensitive)
- Challenge tests: given allergen and observed closely (difficult to standardise)
which are ester and amide LA. which is more common for allergy (although both rare)
-Allergy to esters (procaine & benzocaine) more common than amides (lidocaine, prilocaine, articaine, bupivicaine)
symptoms of anaphylaxis and how to treat. what to do if no response
-Severe allergic reaction. Sudden onset, rapid progression
-1 or both of Breathing difficulties or Hypotension. Skin changes often present (itchy or rash) Also dizziness, nausea, high HR
-remove trigger if possible, lay flat or slightly upright
-give IM 1:1000 adrenaline (0.5ml) in middle third of thigh.
-high flow oxygen, establish airway, apply monitoring.
-if no response, repeat IM adrenaline after 5 mins. IV fluid bolus
consider giving bronchodilator (salbutamol) after IM adrenaline
name antihistamine drugs.
cetrizine, loratidine, acravastine, chlorphenamine
what are brown and blue inhalers uses
-Blue = for immediate relief. Relievers. Salbutamol. Beta adrenergic agonist
-Brown = corticosteroid preventer inhalers. Beclomethasone
oral presentation of allergies
Stomatits, Chelitis and lip swelling, Facial swelling, Oral lichenoid reactions - soreness in mouth / oral ulceration. facial dermatitis around mouth, red mouth
what immune cells are affected by glucocorticoids / corticosteroids. name examples of drug names. Name side effects
-surpess T cells, inhibiting TNF-a and IL-1
-prednisolone, betamethasone, dexamethasone
-adrenal suppression, reflux, increased thirst and urination, hypertension, tachycardia, menstrual period changes, mood changes, weakness, osteoporosis, puffy face, seizures, increased risk of infection, delayed healing, ulcers, oedema of feet, skin atrophy
What is adrenal suppression. which long-term drugs cause it. how much of the drug causes this
-long-term use of glucocorticoids can supress the adrenal gland which can reduce ACTH so cortex not stimulated to make glucocortoids
-cannot produce sufficient corticosteroid in times of physiological stress (for example dental surgery)
-Patients potentially affected: Systemic steroids at or above 7.5 mg prednisolone
how glucocorticoids can cause osteoporosis. what is it. what drug treats it. and its side effect relevant to dentistry
Significant bone loss due to decreased function of osteoblasts, increasing fracture risk. Seen with daily prednisone doses > 5 mg.
-Patients take bisphosphonates to slow bone loss but have a risk of MRONJ (medication-related osteonecrosis of the jaw) which affects extractions and periodontal disease.
-Bisphosphonates remain in bone marrow for 10 years or more
There are 3 classes of non-glucocorticoids: 1) calcineurin inhibitors, 2) antimetabolites and 3) antibodies. name examples of drugs for each. what cells they interfere with
- Inhibit IL2, disrupting T cells. Cyclosporin, tacrolimus
- Interfere with DNA synthesis. Azathioprine (inhibit purine synthesis), methotrexate (inhibit dihydrofolate reductase)
- Inhibits TNF-a and IL2. Inflixamab, adalimumab
Action of azathioprine and methotrexate. side effects
-Non-glucocorticoid, anti-metabolites, interfere with DNA synthesis
1-Azathioprine = inhibits purine synthesis, essential for DNA. can cause liver toxicity.
-bone marrow suppression= Neutropenia, Thrombocytopenia, Agranulocytosis. Oral manifestations
2-Methotrexate = inhibits folic acid synthesis. binds dihydrofolate reductase and prevents synthesis of tetrahydrofolate.
dental problems with immunosuppressants
- Increased risk of infection, opportunistic and latent (eg. candida)
- Increased risk of poor wound healing and wound infection
- Increased malignancy - skin and lip cancer
- Increased hepatic failure
- may need pre-operative antibiotic cover (only if neutropenic, < 3 x 10^9 )
- adrenal atrophy due to prolonged corticosteroid therapy, must monitor blood pressure throughout treatment
Name monoclonal antibody drugs for the treatment of osteoporosis
denosumab and romozosumab
what is autoimmunity and self-tolerance
-self-tolerance: fighting foreign antigens but not own body’s antigens
-autoimmunity: failure of self-tolerance where body attacks self-antigens as has affinity to them/ breached checkpoints of T/B cell development/ has supressed Treg. Therefore causes tissue damage, altered physiological function
What is Addison’s disease. causes and symptoms. what is addisonian crisis
-autoimmune disease causing adrenal insufficiency causing lack of cortisol and aldosterone
-fatigue, depression, increased pigmentation of skin folds, buccal mucosa and scars
-crisis = collapse, abdominal pain, hypotension
cause of type 1 diabetes and oral signs
-destruction of beta pancreatic insulin producing cells - islets of langerhans
-less insulin produced, causing hyperglycaemia
-candia, dry mouth, sialosis, glossitis, periodontitis, increased risk of dry socket
symptoms of hyperthyroidism and hypothyroidism.
-hyper = weight loss despite increase appetite, diarrhoea, anxiety, tremor, sweating, eyes pushed forwards
-hypo = fatigue, weight gain despite decreased appetite, dry skin, hypothermia, cardiac failure, anaemia, constipation
what does carbimazole treat and its oral side effect
treats hyperthyroidism
Carbimazole can cause agraulocytosis which can cause oral or oropharyngeal ulceration
what is precipitate myxoedema coma. how it can be precipitated
a rare life-threatening clinical condition in patients with longstanding severe untreated hypothyroidism, demonstrate classic symptoms of hypothyroidism: fatigue; constipation; weight gain; cold intolerance; a deep voice; coarse hair; and dry, pale, cool skin.
-can be caused by analgesic and sedatives including GAs
what is autoimmune neutropenia and symptoms
-immune system attacks neutrophils so lack of them
-Oral ulceration, Increased risk of infection (pharyngitis, sinusitis), fevers, periodontitis
-Prophylaxis with anti-bacterials and anti-fungals
What is immune thrombocytopenia purpura. symptoms. treatment
-idiopathic (unknown cause) or due to virus
-abnormal decrease in platelets
-easy bruising and bleeding
* May need high dose steroids, splenectomy or rituximab (needs immune system to be switched off very quickly)
What is bullous pemphigoid
-common in elderly
-type II hypersensitivity, autoantibodies (IgG/ IgE) target basement membrane
-It usually starts with an itchy, raised rash. Progresses into large painful blisters on the skin and mouth.
-spreads to trunk, flexural structures
-treated with prednisolone and azathioprine
what is pemphigus vulgaris. what type of autoimmunity is it. symptoms
type II
blistering of skin and non-healing erosions of mucous membranes
Mouth blistering develops first. Then painful blistering of skin that is fragile and can burst so prone to infection
-impaired adhesion of keratinocytes
what is goodpasture’s syndrome. type of autoimmunity. complications
type II. antibodies targeted against basement membrane of lungs and kidney, causing glomerulonephritis and pulmonary haemorrhage
-can progress to chronic renal failure: bleeding tenancies, impaired drug excretion, hypertension, infections, anaemia, dysrhthmias due to electrolyte imbalance
list autoimmune diseases that affect the kidneys.
Wegeners granulomatosis, microscopic polyarteritis, SLE and Goodpastures
list autoimmune disease that affect the liver
- Autoimmune hepatitis
- Primary biliary cirrhosis
List autoimmune diseases that affect the nervous system
-Guillain-Barre – often post-infection involving progressive neuropathy. destruction of nerves
-CIDP
-Myasthenia gravis – inflammation around nerve junction so there is no signalling through them = impaired cell-cell interaction
-multiple sclerosis
what type of hypersensitivity is rheumatoid arthritis. extra-articular symptoms. what other autoimmune disease can manifest.
type 4 and 3
-T cells target synovial joint antigen causing joint inflammation, pain, destruction and loss of function
-extra-articular manifestations = muscle wasting, vasculitis, GI problems, Sjögren’s syndrome, scleritis, synovitis
List autoimmune connective tissue diseases
- Systemic lupus erythematosus
- Scleroderma
- Sjogren’s syndrome
- Mixed connective tissue disease
- Polymyositis and dermatomyositis
Clinical features and dental aspects of systemic lupus erythematous. type of hypersensitivity. cutaneous features
type III
Arthritis, Pleurisy, pericarditis, Glomerulonephritis, Anaemia, thrombocytopenia, Neurological disease, Cardiac disease, vasculitis
-Cutaneous features: Oral ulceration, Photosensitive rashes, Raynaud’s
Bleeding tendencies, renal disease affects drug metabolism, steroid use,
what is scleroderma. skin Changes that occur and oral problems. issues using GA
thickened areas of skin and sometimes problems with internal organs and blood vessels, caused by the immune system attacking the connective tissue under the skin and around internal organs and blood vessels
-oedema, fibrosis, atrophy, calcification on finger tips, raynauds, Oesophageal immotility (difficulty swallowing), TMJ problems, thickened stiffened tongue, constriction of oral orifice, widening of PDL without tooth mobility
-GA = dysphagia, pulmonary, cardiac and renal problems
what is Sjögren’s syndrome. What autoimmune disease is it associated with. Issues with GA
-dry eyes, dry mouth, gland enlargement (salivary, pancreatic, lung, vagina, lacrimal),
-fatigue, recurrent chest infection, impaired sense of taste, candida infection, angular stomatitis
-associated with rheumatoid arthritis
-GA = lung disease, anaemia
What is Behcet’s syndrome. symptoms and oral considerations
-blood vessel inflammation (vasculitis) throughout your body.
-mouth sores and ulcers, eye inflammation, skin rashes and lesions, genital sores, hypo function of salivary glands
-dry mouth: caries, gingivitis, fungal and viral infection. difficulty eating speaking and swallowing
what is multiple sclerosis, psoriases, vitiligo, acute rheumatic fever (all autoimmune diseases)
-multiple sclerosis= demyleination of brain and spinal cord nerves Common symptoms include tiredness, vision problems and problems with walking or balance.
-psoriases= flaky patches of skin which form scales
-vitiligo= lack of melanin, causing patches on skin
-acute rheumatic fever = affects the heart, joints, brain, and skin. Rheumatic fever can develop if strep throat, scarlet fever, and strep skin infections are not treated properly. can cause arthritis, myocarditis, scaring of heart valves
what is grave’s disease
autoantibodies attack thyroid-stimulating-hormone receptor causing hyperthyroidism -bulging eyes
What type of sensitivity is lichenoid reactions and causes
type IV
medications - NSAIDs, oral hypoglycaemics, beta blockers, diuretics, anti-malarial
metals (amalgam fillings), nickel, resins, acrylates
