Immunology (+hep)

Question 1

Diseases and viruses that cause hepatitis. Which is the most common viral cause

Answer 1

-Hep A, B, C
-epstein barr virus =most common
-Toxins from overdose of paracetamol
-autoimmune disease (less common)
-Wilson’s disease (rare)

Question 2

transmission of Hep A, B, C, D, E. which is the most common. which is emerging

Answer 2

most common = A
emerging = E
-Hep B, C & D: Parenteral (blood- transfusion, IV) sexually, perinatally
-Hep A and E -Enteral (faecal/oral)

Question 3

Difference between acute and chronic liver damage. (symptoms and causes)

Answer 3

-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

Question 4

which hep infection usually follows seafood poisoning

Answer 4

hep A

Question 5

what biomarkers and enzymes are elevated in hepatitis

Answer 5

-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

Question 6

which Hep viruses have vaccinations

Answer 6

hep A and B

Question 7

what is the maximum dose of paracetamol in a day. how much causes acute liver damage. how much is fatal

Answer 7

• 4g is the maximum / 24hrs
• 10-15g can cause acute liver damage
• 25g is fatal

Question 8

signs and symptoms of chronic liver disease (lots)

Answer 8

-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

Question 9

what enzyme is raised in chronic drinkers

Answer 9

gamma GT =gamma glutamyl transpeptidase (bone type and liver type)
AST > ALT

Question 10

serological markers for hep B. which is a sign of active viral replication

Answer 10

-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

Question 11

why clotting is affected in those with liver disease. which clotting factors are in the liver

Answer 11

-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

Question 12

why GA is not good for hepatitis patients -what syndrome may it cause

Answer 12

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

Question 13

which LA is to be avoided in hepatitis and which is fine. which should be limited

Answer 13

-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

Question 14

which antibiotics, antifungals and NSAIDs to avoid in liver disease.

Answer 14

-Miconazole =avoid
-Fluconazole = decreased dose (not metabolised properly)
-Avoid erythromycin, clindamycin and tetracycline
-reduce metronidazole
-NSAIDs fine but reduce paracetamol

Question 15

why portal hypertension in liver disease patients can affect dentistry

Answer 15

-risk of haematemesis (vomiting)
-Many of these patients take prophylactic B blockers (propranolol to reduce pressure) Propranolol reduces plasma clearance of epinephrine. Hypertensive crisis

Question 16

differences between innate and adaptive immunity

Answer 16

1. 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

Question 17

what are the 3 professional phagocytic immune cells

Answer 17

neutrophils, macrophages, natural killer cells

Question 18

what are the professional antigen presenting cells

Answer 18

dendritic, macrophages, B cells
(these are the only cells that express MHC class II)

Question 19

CD4 and CD8 T cells functions. what MHC molecules they express

Answer 19

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

Question 20

what are the functions of Th1, Th2, Th17, Tfh and T reg, Which cytokines mediate them

Answer 20

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

Question 21

Roles of interluikins 1,2,4,8,6,12,10. which is the growth stimulating factors

Answer 21

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

Question 22

examples of host physical barriers. what enzymes are found in saliva

Answer 22

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

Question 23

Difference between allergic and autoimmune response

Answer 23

-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)

Question 24

What types of hypersensitivity reactions does penicillin cause. How penicillin causes hypersensitivity

Answer 24

-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

Question 25

How is type 1 hypersensitivity caused. What cells are involved. Examples of this reactions (atopy and environmental agents). Signs and consequences of the reaction

Answer 25

-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

Question 26

How is type 2 hypersensitivity caused. Give examples.

Answer 26

* 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

Question 27

How does autoimmune haemolytic anaemia, blood group incompatibility and penicillin cause haemolytic anaemia.

Answer 27

1. Autoimmune haemolytic anemia: Autoantibodies bind to RBCs, activate complement and phagocytosis, causing RBC death. 2. Blood group incompatibility: Incompatible reaction during transfusions causes antibodies to attack antigens on RBCs. 3. Penicillin: ring can react with AA. Modify proteins on RBCs. Labelled for destruction -associated with thrombocytopenia

Question 28

What are type III hypersensitivity reaction mediated by. What is involved. Give examples of type III.

Answer 28

-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

Question 29

What are type IV hypersensitivity reactions mediated by. Examples of type IV

Answer 29

-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

Question 30

Coeliac disease has features of both an allergic and autoimmune disease. How is it caused. symptoms. The allele predisposition

Answer 30

-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)

Question 31

Which type of diabetes has a link to other inflammatory diseases, like periodontal disease and CVD. Why

Answer 31

-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.

Question 32

What are primary and secondary immune tissues and give examples

Answer 32

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

Question 33

what is complement and the 3 functions

Answer 33

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

Question 34

why B cells are so diverse

Answer 34

1. antigen somatic recombination: gene rearrangement to get unique proteins to recognise specific antigens 2. class switching: (due to constant region of Ig changing) Same specificity to antigen but different functional characteristics. 3. somatic hypermutation: point mutations to improve affinity to antigen 4. switching between membrane bound and secreted antibodies (Ig M etc.): switching from B cell receptor, to acting as an antibody.

Question 35

difference between MHC class I and II. (where they are expressed, what they do)

Answer 35

1. 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. 2. 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

Question 36

how vaccines work

Answer 36

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

Question 37

explain primary and secondary immunodeficiency. and examples of diseases

Answer 37

1. 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 2. Secondary= acquired due to environmental factors. More common - immunosuppressive meds, malnutrition, chemotherapy, asplenia, major surgery, HIV infection, severe burns, radiotherapy, SLE, leukaemia

Question 38

what are monoclonal antibodies. how are they reduced and give example of biologic drugs

Answer 38

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

Question 39

symptoms and signs of immunodeficiency

Answer 39

-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

Question 40

what immunodeficiency is likely to cause bacterial infections of the tonsils, skin, chest

Answer 40

B cell defect

Question 41

what immunodeficiency is a common cause of fungal and viral infections

Answer 41

T cell defect

Question 42

which immunodeficiencies is a likely cause of abscesses

Answer 42

phagocytic cell defects and B cell defects

Question 43

What is SCID. which immune cells are impaired. what is there a mutation in

Answer 43

severe and combined immunodeficiency absent T cells, B cells may also be absent -viral, fungal and bacterial infections -mutation in adenosine deaminase gene

Question 44

What is Bruton's x-linked agammaglobulinemia. which immune cells are impaired.

Answer 44

low or absent B cells and reduced immunoglobulins absent tonsils recurrent bacterial infections (pyogenic bacteria)

Question 45

what is common variable immunodeficiency. which immune cells are impaired. what symptoms it can cause

Answer 45

low immunoglobulins (impaired IgA and IgG) recurrent infections (sinus, lungs, ears, eyes) can cause thyroid issues, alopecia, vitiligo high risk of malignancy (lymphoma)

Question 46

what is chronic granulomatous disease. symptoms

Answer 46

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.

Question 47

what may cause chronic mucocutaneous candidiases

Answer 47

-Failure to clear candida – nail, oral, vaginal Genetic defects [AIRE gene] Cytokine abnormalities Endocrine abnormalities [thyroid, parathyroid, adrenal] -Risk of oesophageal malignancy

Question 48

what is DiGeorge syndrome

Answer 48

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

Question 49

what drugs can lead to secondary immunodeficiency

Answer 49

-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

Question 50

what cells rituximab reduces

Answer 50

anti-CD20 & anti-TNFs - antibody reduction

Question 51

what diseases can lead to oral candida

Answer 51

-secondary immunodeficiency (HIV, drugs) -connective tissue disease -sjogren's disease -primary immunodeficiency -xerostomia -chronic hep C

Question 52

diseases that cause mouth ulcers

Answer 52

* 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

Question 53

diseases and drugs that can lead to gingivitis

Answer 53

-Cyclosporin -nifedipine, amlodipine -Scurvy -Anticonvulsants -Chronic granulomatous disease (primary immunodeficiency)

Question 54

what does C1 esterase deficiency cause. treatment

Answer 54

-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

Question 55

3 ways to test for allergies (type 1 hypersensitivity)

Answer 55

1. skin prick test - use agent, histamine and salty water. wheel at site shows they are allergic 2. Blood tests - IgE - (less sensitive) 3. Challenge tests: given allergen and observed closely (difficult to standardise)

Question 56

which are ester and amide LA. which is more common for allergy (although both rare)

Answer 56

-Allergy to esters (procaine & benzocaine) more common than amides (lidocaine, prilocaine, articaine, bupivicaine)

Question 57

symptoms of anaphylaxis and how to treat. what to do if no response

Answer 57

-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

Question 58

name antihistamine drugs.

Answer 58

cetrizine, loratidine, acravastine, chlorphenamine

Question 59

what are brown and blue inhalers uses

Answer 59

-Blue = for immediate relief. Relievers. Salbutamol. Beta adrenergic agonist -Brown = corticosteroid preventer inhalers. Beclomethasone

Question 60

oral presentation of allergies

Answer 60

Stomatits, Chelitis and lip swelling, Facial swelling, Oral lichenoid reactions - soreness in mouth / oral ulceration. facial dermatitis around mouth, red mouth

Question 61

what immune cells are affected by glucocorticoids / corticosteroids. name examples of drug names. Name side effects

Answer 61

-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

Question 62

What is adrenal suppression. which long-term drugs cause it. how much of the drug causes this

Answer 62

-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

Question 63

how glucocorticoids can cause osteoporosis. what is it. what drug treats it. and its side effect relevant to dentistry

Answer 63

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

Question 64

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

Answer 64

1. Inhibit IL2, disrupting T cells. Cyclosporin, tacrolimus 2. Interfere with DNA synthesis. Azathioprine (inhibit purine synthesis), methotrexate (inhibit dihydrofolate reductase) 3. Inhibits TNF-a and IL2. Inflixamab, adalimumab

Question 65

Action of azathioprine and methotrexate. side effects

Answer 65

-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.

Question 66

dental problems with immunosuppressants

Answer 66

1. Increased risk of infection, opportunistic and latent (eg. candida) 2. Increased risk of poor wound healing and wound infection 3. Increased malignancy - skin and lip cancer 4. Increased hepatic failure 5. may need pre-operative antibiotic cover (only if neutropenic, < 3 x 10^9 ) 6. adrenal atrophy due to prolonged corticosteroid therapy, must monitor blood pressure throughout treatment

Question 67

Name monoclonal antibody drugs for the treatment of osteoporosis

Answer 67

denosumab and romozosumab

Question 68

what is autoimmunity and self-tolerance

Answer 68

-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

Question 69

What is Addison's disease. causes and symptoms. what is addisonian crisis

Answer 69

-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

Question 70

cause of type 1 diabetes and oral signs

Answer 70

-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

Question 71

symptoms of hyperthyroidism and hypothyroidism.

Answer 71

-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

Question 72

what does carbimazole treat and its oral side effect

Answer 72

treats hyperthyroidism Carbimazole can cause agraulocytosis which can cause oral or oropharyngeal ulceration

Question 73

what is precipitate myxoedema coma. how it can be precipitated

Answer 73

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

Question 74

what is autoimmune neutropenia and symptoms

Answer 74

-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

Question 75

What is immune thrombocytopenia purpura. symptoms. treatment

Answer 75

-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)

Question 76

What is bullous pemphigoid

Answer 76

-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

Question 77

what is pemphigus vulgaris. what type of autoimmunity is it. symptoms

Answer 77

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

Question 78

what is goodpasture's syndrome. type of autoimmunity. complications

Answer 78

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

Question 79

list autoimmune diseases that affect the kidneys.

Answer 79

Wegeners granulomatosis, microscopic polyarteritis, SLE and Goodpastures

Question 80

list autoimmune disease that affect the liver

Answer 80

- Autoimmune hepatitis - Primary biliary cirrhosis

Question 81

List autoimmune diseases that affect the nervous system

Answer 81

-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

Question 82

what type of hypersensitivity is rheumatoid arthritis. extra-articular symptoms. what other autoimmune disease can manifest.

Answer 82

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

Question 83

List autoimmune connective tissue diseases

Answer 83

* Systemic lupus erythematosus * Scleroderma * Sjogren’s syndrome * Mixed connective tissue disease * Polymyositis and dermatomyositis

Question 84

Clinical features and dental aspects of systemic lupus erythematous. type of hypersensitivity. cutaneous features

Answer 84

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,

Question 85

what is scleroderma. skin Changes that occur and oral problems. issues using GA

Answer 85

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

Question 86

what is Sjögren's syndrome. What autoimmune disease is it associated with. Issues with GA

Answer 86

-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

Question 87

What is Behcet's syndrome. symptoms and oral considerations

Answer 87

-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

Question 88

what is multiple sclerosis, psoriases, vitiligo, acute rheumatic fever (all autoimmune diseases)

Answer 88

-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

Question 89

what is grave's disease

Answer 89

autoantibodies attack thyroid-stimulating-hormone receptor causing hyperthyroidism -bulging eyes

Question 90

What type of sensitivity is lichenoid reactions and causes

Answer 90

type IV medications - NSAIDs, oral hypoglycaemics, beta blockers, diuretics, anti-malarial metals (amalgam fillings), nickel, resins, acrylates