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141 Cards in this Set
- Front
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- 3rd side (hint)
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list the 3 ways chronic inflammation can be initiated
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1) de novo (primary)
2) repeated acute 3) following single acute |
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How does acute inflammation lead to chronic inflammation
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1) inability to completely eradicate antigen eg foreign body, incomplete drainage of abcess
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List the hallmarks of chronic inflammation
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1) recurring injury & repair
2) fibrosis & angiogenesis 3) mononuclear cells: lymphocytes, monocytes, macrophages |
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repeated cholelitiasis leading to repeated cholecystitis can lead to?
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chronic inflammation due to repeated acute inflammation resulting in obstruction, wall thickening, perforation
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list the 3 ways chronic inflammation can be initiated
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1) de novo (primary)
2) repeated acute 3) following single acute |
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List the 4 features of antigens leading to chronic inflammation
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1) low antigenicity
2) prolonged exposure to antigen (eg autoimmune endogenous antigens) 3) antigen that cannot be broken down (endogenous - uric acid crystals, exogenoug - silica, asbestos) 4) virulance factors preventing complete phagocytosis |
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How does acute inflammation lead to chronic inflammation
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1) inability to completely eradicate antigen eg foreign body, incomplete drainage of abcess
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How are giant cells formed
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multiple macrophages attempting to phagocise a large antigen eg silica
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List 3 types of giant cells, describe their nuclei
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1) Langhans (horseshoe)
2) Foreign body (diffuse) 3) Touton (xanthomas, form ring with surrounding lipid) |
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How does complement enhance phagocytosis
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Opsonisation: coating of agent by complement 3b or immunoglobulin
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What is the result of increased circulating proteins during acute inflammation
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1) Increased CRP is measurable and indicates inflammation
2) Increased fibrinogen causes erythrocyte clumping & rouleaux formation -> increased ESR |
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What are the 4 outcomes of acute inflammation
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1) resolution
2) repair 3) supurration (abcess formation) 4) chronic infection |
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What is mechanism LPS causes fever
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endotoxin (LPS) -> direct reset up of hypothalamus temp control OR leukocyte pyrogens (THF-a, IL1) -> production of PGs -> hypo reset up -> mechanisms for heat conservation (muscle work, adrenergic vasocontraction, piloerection)
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A burn patient's wounds develop a foul small and green discharge. Treatment with a quinolone is ineffective. What is it.
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Pseudomonas aeruginosa (nosocomial)
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A slimy infection forms around a pacemaker. What test can be performed to support your conclusions
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Probably Staphylococcus epidermidis. If coagulase, catalase -ve, gram +ve then confirmed.
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How is primary TB controlled
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Formation of granulomas by type IV hypersensitivity reaction to tuberculin in the lower lung fields:
1) Caseating necrosis (cheese like) and organism surrounded by epithelioid (activated) macrophages and lymphocytes. The mycobacteria remain dormant until calcification (Ghon focus including progression to hilar lymph nodes causing bronchial compression and calcified Ghon complex) or secondary infection of the upper lobes. Extrapulmonary spread is by haematogenous dissemination (meningitis, liver, GI, kidney) 2) Formation of Langhans giant cells with horseshoe multi-nuclei on granuloma surface |
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List the immunological steps of chronic inflammation
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1) Adhesion & extravasation of monocytes at inflammation site in response to cytokines (TNFa, IL1)
2) Activation of macrophages by IFa 3) Harbour large matter by giant cells (Langhans horseshoe nuclei, foreign body, touton) 4) Recurring injury (proteases, oxygen metabolites, coagulation factors, NO) 4) Repair: angiogenesis factors-> angioblasts, growth factors (PSGF, FGF), granulation (fibroblasts)-> maturation & contraction -> fibrosis (dense collegen & elastin) |
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Describe a granuloma
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Aggregate of epithelioid macrophages, giant cells with necrotic tissue surrounded by T cells and plasma cells
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Describe granulatomous inflammation
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1) type of focal chronic inflammation where foreign matter cannot be destroyed
2) Accumulations of macrophages transformed to epitheloid macrophages, lymphocytes fibrososis with or without central necrosis (caseation) |
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Describe the 2 types of mucosal repair processes
How is the process stimulated |
1) Regeneration: intact matric framework allowing restoration
2) Organisation: replacement of inflammatory cells by granulation tissue leading to fibrosis (scar tissue) 3) angiogenic & fibrogenic cytokines |
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What's happening in this lung
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1) neutrophils
2) fine fibrin meshwork Typical lobar pneumonia (acute infection) with S.pneumonae |
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When is empirical antibiotic therapy commonly given
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1) community acquired pneumonia
2) ventilator associated pneumonia 3) fever with neutropenia 4) meningitis 5) pyelonephritis or UTI |
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What is the difference between pathogen directed therapy and susceptibility directed therapy
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1) PDT: pathogen known, susceptibility unknown. Need recent antibiotic history, history of infection by resistance organisms, local geographic susceptibility/resistance knowledge
2) SDT: use narrowest spectum drug organism is susceptible to 3) Do not use concentrations close to the break point |
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How are the parameters of the concentration v time curve important for aminoglycosides/quinolones v beta-lactams
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1) for aminoglycoside/quinolone ratio of Cmax : MIC matters because they are concentration dependent killers (ie infusion is best, followed by frequent doses)
2) For beta lactams time above MIC is important, NOT concentration |
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What are the pros and cons of using multiple antibiotics
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pros - synergy, prevent resistance, decreased risk of ineffective treatment
cons: increased risk of ARs and allergy |
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What is syncope and list the major causes
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Sudden transient loss of consciousness
Cardiogenic: arrhythmia, MI Peripheral vascular: vasovagal, situational Cerebrovascular: subarrachnoid haemorrage, subclavian steal |
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What is atopic march and what serum levels are affected
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Allergies: food -> dermatitis -> asthma -> seasonal rhinitis
Raised IgE |
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What are the 4 forms of antibiotic therapy
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empirical
prophylaxis directed susceptibility |
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When are prophylatic perioperative ab's most effective
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5x if clean wound (no inflammation, GI contents, urine, puss, trauma)
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What class is commonly used for prophylactic ab therapy and why
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1st gen cephalosporins because
1) less chance of penicillin resistance 2) covers staph & strep |
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What is a time dependent killer and what dosing is needed
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Killing maximised the longer time spent above MIC
Frequent or infusion or long acting (ceftriaxone) |
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M cells ?
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Microfold cells have the unique ability to take up antigen from the lumen of the small intestine via endocytosis or phagocytosis, and deliver it via transcytosis to dendritic cells (an antigen presenting cell) and T lymphocytes located in a unique pocket-like structure on their basolateral side.
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Define bacteraemia
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Presence of bacteria in the blood
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How is SIRS diagnosed
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fever >38 (or < 36)tachycardia
tachypnoea > 20 tachycardia >90 WCC > 12,000 or < 4,000 |
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What is sepsis
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A systemic response to infection
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What are the signs of severe sepsis
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Beginnings of shock: hypoperfusion manifested by oligourea, altered consciousness or delerium, lactic acidosis, coagulopathy (DIC due to endothelial injury caused by inflammation)
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What is septic shock
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Severe sepsis combined with refractory hypoperfusion (unresponsive to fluid resuscitation)
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What is the cause of purpurea in meningitis
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Infection -> endothelial damage -> DIC -> haemorrage
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How is serum bacteriacidal
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Activation of complement by classical (antibody mediated) alternative (direct) or mannin pathways -> lysis (MAC), opsonisation (c3b coat), inflammation
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Describe how HepB replicates
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1) DNA virus enters by phagocytosis
2) Host chaperones take DNA to nucleus 3) mRNA forms 4) longest mRNA replicated to DNA by reverse transcriptase |
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What arre the components of LPS and how is it a virulence factor
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O-antigen, protein A and core: directs phagocyte attack away and masks underlying bacterial wall antigens.
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Which hepatitis is most prevalent & which causes most chronic & acute deaths
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Hep B most prevalent and greatest incidence of acute disease deaths. Hep C least likely to cause fulmanent deaths but from chronic liver disease.
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What is activated whenLPS is released
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1) macrophages -> complement (MAC and opsonisation and cytokines and leucocytes (neutrophils, kupfer cells)-> more LPS release), inflammation, endothelial damage
2) coagulation and DIC |
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What is HepaDNA virus
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Hep B - a DNA virus
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What are the 3 zones of a full thickness burn
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hyperaemia (increased blood flow)
stasis (decreased blood flow but salvagable) coagulation (necrosis) |
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Compare the prognosis of chronic v non-chronic infected people with Hep B. Note incidence percentages of outcomes.
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1) Chronic, carier state, 5-15% of infected cases, 200x likely to develop hepatocellular carcenoma, infective
2) Non-chronic: 85-95% resolved in a few weeks or 1% fulminant. |
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What skin appendages are lost in a deep partial thickness and full thickness burn
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1) deep partial: full depth of dermis destroys pilosebaceous units but spares sweat glands
2) full thickness destroys hypodermis destroys sweat glands |
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Explain how HepB carriers are diagnosed
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Persistent HepBs positive. If seroconversion to HepBe -ve then little viral replication, few symptoms (polyarteritis nodosum, glomerulonephritis) but if not, chronic active disease -> elevated transaminases, cirrhosis, carcinoma.
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What are 3 signs of an inhalation burn injury
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1) hoarseness
2) carbonaceous sputum 3) facial and mucous membrane burns |
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What does the presence of anti HBe antibody indicate
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No chronic infection. IgMs for HBs present around 8-12 weeks, HBc present around 14 weeks. HBs should drop dramatically by 20 weeks.
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What are the 3 types of wound healing
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primary intention: minimal tissue loss, margins are close with minimal contraction
secondary intention: large degree of tissue loss and separation of margins resulting in granulation tissue containing smooth muscle, contraction and epithelisaton. tertiary: autograft, allograft |
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What does the presence of elevated HBs-antigen in the absence of anti-HBs after 24 weeks indicate, What other marker indicates active disease?
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Elevated HBs-pantigen means chronic disease. Elevated HBe antigen indicates active chronic disease.
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What are the 4 stages of wound healing
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1) coagulation (platelets, fibrin)
2) inflammation 3) granulation (epithelisation, vascularisation, fibrogenesis) 4) contraction (vascular regression, remodelling, collagen and ECM deposition) |
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S.pneumoniae commonly causes respiratory infection yet S.aureus rarely does. why
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Mode of transmission: Strep.p is airborne, Staph.a is by contact. Also, Strep.p has polysacharride capsule evading macrophage endocytosis
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What is an immediate complication of a burn
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barrier loss
infection |
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What is an intermediate complication of a burn
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fluid loss
shock |
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What is a delayed complication of a burn
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Poor perfusion -> infection
Scar contractures -> loss of flexibility |
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List 3 protazoa that cause diarrhoea
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Giardia intestinalis
Cryptosporidium parvum Entamoeba histolytica |
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Which cell type is responsible for the production of the mediators stimulating bronchoconstriction in allergic asthma?
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mast
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List 3 helminths that cause diarrhoea
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Trichuris trichiura, Strongyloides stercoralis, hookworms
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Which immunoglobulin isotype activates the cell type that secretes bronchoconstrictors in allergic asthma?
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IgE
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Describe the pathogenesis diarrhoea and malabsorption caused by Giardia
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1) blanketing (T-cell & macrophage (IL1, IL6, TNF alpha) activation, villous atrophy, crypt deepening -> increased secretion & decreased reabsorption)
2) chemical (deconjugation of bile salts, inhibition of pancreatic enzymes (lipase, proteases, disaccharidases-> hyperosmolarity, bacterial overgrowth, steatorrhoea) -> pale diarrhoea with flatus 3) |
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B cells undergo isotype switching in an allergic asthmatic response due to the cytokines IL-4 and IL-13. Which cell type is responsible for the production of these cytokines?
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Th2
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Why is diarrhoea due to chronic Ghiardia even after eradication difficult to resolve
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1) Atrophied villi take time to regrow
2) depleted folate levels inhibit regrowth of villi (need folate supplementation) |
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Chemokines, low molecular weight proteins which are secreted by a variety of cell types (e.g., fibroblasts, macrophages, dendritic cells) during inflammatory responses, are primarily known for their ability to:
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Attract cells of the immune system into areas of inflammation
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give one diarrhoea producing example of:
a) amoeba b) flagellate c) cilliate d) sporozite |
a) entamoeba hystolytica
b) ghiardia c) balantidium d) cryptosporidium |
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How is the atopic status of a patient best determined?
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Measuring the size of the response to an allergen in a skin prick test
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Hayfever and Farmer's lung are both inflammatory conditions of the respiratory tract caused by hypersensitivity responses to inhaled allergens. Compare and contrast the immunological mechanisms by which each condition arises.
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Hayfever is a type I hypersensitivity reaction, in which initial exposure to the allergen induced an IgE antibody response (mediated by activation of TH2 cells). This allergen specific IgE binds to Fc recpetors on the surface of mast cells (especially in the respiratory sub-mucosa). Subsequent exposure to the allergen results in allergen cross-liinking the IgE bound to the mast cells which causes the mast cells to degranulate. Inside these granules are inflammatory mediators; the most impostant of which in hayfever is histamine. Histamine causes vasodilation and increased vascular permeability causing the characteristic redness, runny nose and itchy eyes associated with hayfever.
Farmer’s Lung is a type III hypersensitivity reaction cause by the deposition in the lungs of immune complexes produced in response to an inhaled allergen (often Actinomycetes species). Unlike hayfever where IgE is the main antibody, IgG is the major antibody in Farmer’s lung. These IgG molecules combine with allergen in the lungs and initiate an inflammatory response with complement activation and recruitment of neutrophils to the area along with vasodilation and increased vascular permeability. |
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How are entamoeba hystolytica cysts released in the gut. Where do they end up.
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1) low pH, proteases release trophozites into SI
2) colon is colonized -> dysentry (blood) or ulceration (hystolysis) -> bowel perforation & death if untreated or asymptomatic 3) migration to liver or brain causing abcesses |
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Joseph Lee, presents to A&E with severe shortness of breath and a bilateral expiratory wheeze. Pulmonary function tests reveal a forced expiratory flow rate of 25% of predicted and a forced expiratory volume in one second (FEV1) of 30% of predicted. His condition improves dramatically with the administration of nebulised salbutamol and ipratropium. However 4 hours later (while still in hospital), his condition worsens again. What is the most likely explanation for this deterioration?
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Type I hypersensitivity reactions (such as asthma) can demonstrate a late phase response some hours after the initial response. While the initial response is largely due to pre-formed mediators such as histamine; the late phase response is due to newly synthesised mediators; as well as cells such as eosinophils recruited to the site of inflammation in response to those mediators released initially
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A woman with blood group O+ develops dyspnea, fevers and lumbar pain shortly after receiving a blood transfusion. It is determined that she was accidentally given A+ donor blood. This acute reaction is an example of which type of hypersensitivity reaction?
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Type II (antibody mediated). Preformed host antibodies react against antigen on donor red blood cells, resulting in an acute haemolytic transfusion reaction.
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Give 3 examples of type IV delayed hypersensitivity reactions
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1) contact dermatitis
2) tuberculin hypersensitivity (Mantoux test) 3) granulomatous hypersensitivity |
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A patient shows an afferent pupillary defect. What are the likely ddx
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Compression of the optic nerve by tumour
Glaucoma |
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If a child presents underweight and his mother says it's worms, is it more likely to be Enterobius or Trichuris.
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Trichuris: whipworms
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What changes in visual fields are associated with
1) a pituitary tumour 2) a retro-chiasmal lesion |
1) pituitary tumour affects the optic chiasm, affecting the medial retina hence bitemporal hemianopia
2) retrochiasmal will affect the ipsilateral temporal retina (hence the nasal field) and the contralateral nasal retina (hence the contralateral temporal field) |
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A bowel infection producing gas following bowel perforation is most likely? describe features
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B.fragilis, G- bacilis anaerobe, commensal with virulence factors (capsule, adhesion, superoxidase dismutase),
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List 5 ocular changes caused by UVL
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Cataracts
Pterygium BCC, SCC (eyelid, conjunctiva) melanoma (retine) photokeratitis (acute) |
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Describe Campylobacter jejuni
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G- bacillis, strict microaerobe, needs CO2, flagellated, endo & exo toxins, uncooked chicken & unpasturised milk
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What type of lesion is this and name some others of this class
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Solar lentigo: basal melanocyte proliferation
also melanocyte hyperpigmentation (freckle) and benign naevus (can be junctional nests along the epidermal junction or compound with nests within the dermis and the junction) |
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List the important Chlostridium species
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difficile (spores, enterotoxin), botulinium, perfingens, tetani
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What are the 2 classes of melanoma
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1) Superficial spreading in 70% of white pop cases (can progress to nodular)
2) Acral lentigenous in Asians |
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What are toxins A & B and what produces them
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toxin A & B by C.difficile: enterotoxins, cytokine release, secretory diarrhoea, necrosis
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What is this skin condition and explain
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1) predominance of single melanocytes in the epidermal layer
2) abnormally large nuclei, hyperchromic with eosinic nucleoli 3) lymphocytic infiltrate 4) mitoses 3) |
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What is the typical morphology of SCC's
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Scaly ulcerated keratinous lesions
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Describe the properties and the symptoms of E.coli
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G- bacillis has O-antigen due to lipopolysacharride, H-antigen due to flagella, exotoxins producing diarrhoea and/or haemolysis, adhesins
1) EPEC (enteropathogenic E. coli) •ETEC (enterotoxigenic E. coli) GI - diarrhoea without blood 2) EHEC (enterohemorrhagic E. coli) 3) EAEC (enteroadherent E. coli) UTI, pyelonephritis haemolytic uremic syndrome |
•EHEC (enterohemorrhagic E. coli)
•ETEC (enterotoxigenic E. coli) •EPEC (enteropathogenic E. coli) •EIEC (enteroinvasive E. coli •EAEC (enteroadherent E. coli |
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What is this lesion and what is the most common risk factor
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SCC :
1) dysplastic squamous epithelial cells penetrating the dermis 2) keratinisation 3) keratin horn pearl |
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List the virulence factors of H.pylori
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CUFMAV
CagA, urease, flagella, mucinase, adhesins, VacA |
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Describethe morphology of BCC
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1) Pearly papule with central ulcer not healing
2) telangiectasia 3) Hx of bleeding |
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What is this skin cancer and why
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BCC because
1) Islands of peripheral palisading cells with haphazard central cells |
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Describe the ABC approach to diagnosing melanoma
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A = asymmetry
B = border (irregular) C = colour (varies) D = diameter (>6mm or changing ie radial growth phase) E = elevation -> evolution to vertical growth phase and invasion |
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What is the typical progression of melanoma from a benign lesion
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1) junctional nevus
2) compound nevus 3) SSM 4) Nodular melanoma |
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Describe the Clark system of melanoma grading
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1) Epidermis
2) Papillary dermal impingement - radial phase 3) Penetration of papillary dermis and impingement on reticular dermis - start of vertical growth phase (80% 5Y survival) 4) Reticular dermis invaded 5) Subdermal fat invaded (<50% 5Y survival) |
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What types of biopsies are done on melanomas and which is preferred
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1) shave
2) punch 3) excisional with 1cm margin if 1cm depth to fascia or 2 cm margin if 2-3 cm depth to fascia |
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List 2 primary and secondary public health skin cancer strategies
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1) primary: sunsmart (mass education), sunalert (UV index forecasts, national skin cancer week
2) secondary: regular GP screening of high risk groups, teaching regular self examination |
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How can Campylobacter be identified within a group of gut flora
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Antibiotic resistance (Skirrow's test). Other commensals die.
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What loss of function occurs with full thickness burns
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Thermoregulation (loss of sweat glands)
Sensation Vitamin D production Excretion Barrier |
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Two types of haemolysis are possible for Strep. Describe
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Beta, strong haemolysis (S.pyrogenes)
Alpha, weak haemolysis (S.pneumoniae) |
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What are the mechanisms of burn injuries
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Thermal
Chemical Inhalation of hot gasses Cold Electrical Radiation |
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What are the phases of wound healing following a partial thickness burn
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Vascular constriction
Coagulation Inflammation (neutrophils 24h followed by macrophages for 2-3 days) Granulation Angiogenesis Epithelisation Contraction and remodelling (centripetal contraction occurs after 5 days for 2 weeks, type I collagen deposition 2-4 weeks) Remodelling continues up to 12 months |
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List 3 types of exotoxins
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1) cytotoxins (kill host cells to release contents: iron, nutrients)
2) enterotoxins 3) neurotoxins |
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Describe type I immune response sensitisation phase
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1) Dendritic cell presents antigen to Th
2) IL's released (3, 4,5) producing IgE B cells and activated eosinophils 3) IgE binds to mast cells - primed |
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Describe endotoxin and how this is a virulence factor
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Desctruction of Gram- cell releases endotoxin:
1) lipid A in lipopolysacharride component of cell wall causes inflammation (activates macrophages) 2) toxin causes cell lysis, releases iron & nutrients |
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Describe the type I immediate immune response
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1) IgE on mast cells binds to antigen
2) primary mediators: histamine, NCF (neutrophil chemotactic factor), ECF (eosinophil chemotactic factor) 3) secondary mediators: arachadonic acid derivatives causing vasodilation and inflammation 4) cytokines released stimulate late phase response |
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Describe Giardia lamblia
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1) cyst and flagellated trophozoite forms
2) faecal oral route 3) colonisation, mechanical irritation (deepening pits, shrinking villi), possible toxins -> inflammation |
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What are the mechanisms of type II hypersensitivity
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Typically antibody attack of cell surface antigens (RBC's, thyroid) causing
cytotoxicity by 1) tagging, complement activation and opsonisation 2) IgG binds to cell surface antigen and neutrophil causing cell death 3) IgG binds to cellular receptor altering its function |
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What are the distinguishing features of acute inflammation (ie regarding duration, lymphocytes recruited etc)
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1) time: short, limited
2) exudation of fluid, plasma proteins 3) neutrophils 4) resolves when offending agent eliminated |
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What is type III hypersensitivity
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IgG immune complexes (lupus, glomerulonephritis)
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What are the distinguishing features of chronic inflammation
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1) time: long, continuing
2) blood vessel proliferation, fibrosis, necrosis 3) macrophages & lymphocytes |
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What type of hypersensitivity is the tuberculin reaction
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Type IV where
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What is the difference between exuadate & oedema
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Exudate: increased vascular permeability to neutrophils (prurulent), fibrin (fibrinous)
Oedema: interstitial fluid |
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What are the 3 stages of acute inflammation
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1) vasodilation: increased vascular calibre (IL1, TNFa)
2) permeability of exudate: oedema, proteins (complement) and passage of neutrophils 3) infiltration of leukocytes (initially neutrophils, later monocytes and other lymphocytes) |
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The5 cardinal signs of inflammation
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1) rubor
2) dolor (pain) 3) calor 4) tumor (oedema) 5) loss of function |
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What is the mechanism causing the cardinal signs of inflammation
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1) endothelial cells release NO if injured or mast cells release histamine
2) arteriolar smooth muscle relaxes 3) increased calibre, blood flow, permeability 4) red, hot, swollen |
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What are the 3 main differences between G+ and G-
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1) thick peptidoglycan layer G+
2) LPS G- 3) teichoic acid (G+ |
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List the common features of Hep B & C. How are they different
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1) Transmission by direct contact
2) Icsohedral capsid with lipid envelope Difference: Hep C is a single strand RNA virus, Hep B is DNA virus |
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What is a serotype
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The specific antigenicity of a viral surface protein (capsid or envelope)
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compare Hep A & Hep B viruses
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1) nucleic acid: Hep A (RNA), Hep B (DNA
2) both icsohedral capsids: Hep A (naked), Hep B (enveloped) 3) Hep A: picnorvirus, Hep B: HEPADNA virus |
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compare Hep A, Hep B, Hep C with regards to incidence of acute infections, chronic infections, fulminant disease deaths
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1) acute: Hep A & Hep B
2) chronic Hep B & Hep C 3) fulminant disease deaths: mostly Hep B, some Hep A |
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What are the 3 antigens tested for with Hep B
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1) HBsAg
2) HBcAg (core) 3) HBeAg (core) |
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How is HepB similar to retroviruses
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Both use reverse transcriptase to produce DNA from RNA. (first step for retros, last step for HepB)
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A pregnant woman has Hep B. what is the likely course of the disease in her child
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1) Perinatal transmission resulting in infection without immune response calledthe immune tolerant phase with rising HBsAg, HBeAg during the immunotolerant phase. anti-HBe appears during the clearance phase with increasing aninotransferase levels. This can progress to hepatocarcinoma
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In testing for Hep A, what is the time sequence of events
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1) IgM but no IgG - acute infection (3-6 weeks), faeces still infective
2) IgM and IgG present - recovery phase > 6 weeks, non-infective 3) IgG only: past infection, immunne |
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If HBsAg+ > 6 months, what are the 3 possible outcomes and which is most likely
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1) Resolution (50% - most likely with Anti-HBs, Anti-HBc, Anti-HBe)
2) Chronic presistent (extrahepatic symptoms) with Anti-HBe, HBs, AntiHBc 4) chronic active (cirrhosis, carcinoma) with HBe, HBs and anti-HBc only |
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What are the likely serology results for an acute resolving Hep B infection
1) 6 weeks to 3 months 2) 3 - 6 months 3) > 6 months |
1) HBsAg+, HBeAg+, anti-HBc-, anti-HBs-
2) as above but IgM anti-HBc+, HBsAg+ reaches peak but HBeAg falling 3) IgM anti-HBc+, total anti-HBc+, anti-HBeAg present, no surface antigen or antibody but begins to rise after 8 months |
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What are the likely serology results for a chronic non-resolving resolving Hep B infection
1) 6 weeks to 3 months 2) 3 - 6 months 3) > 6 months |
1) HBsAg+
2) as above with IgM anti-HBc+ 3) HBsAg+ and anti-HBc+ |
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How is outcome of HepB infection related to age
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Chronic more likely
perinatal > children > adolescent > adult Acute is opposite |
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Describe symptoms of infection of the large intestine
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Large inflammatory bowel symptoms:
1) Diarrhoea: normal volume, + blood, + mucous, + leukocytes 2) Systemic: possible fever, severe LLQ pain |
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List 3 commin GI viruses
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1) rota
2) norwalk 3) adeno |
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List the types of virulance factors and their purpose as used by pathogenic GIT bacteria
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entry (flagella, spores)
establishment & adherence (fimbri, adhesins, flagella adhesion) invasion & colonization (secretion of anti-phagocytic proteins, o-antigen, capsule, biofilms) growth (siderophores) toxins (LPS (fever), enterotoxin (diarrhoea), cytotoxins (eg VacA of H.pylori) & haemolysin (allpha & beta) |
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How can non-pathogenic E.coli become pathogenic
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Phage transduction: Shigella genes transgerred to E.coli producing ECHC E.coli expressing: Shigella toxin, o-antigen & adhesion flagella -> bloody diarrhoea -> HUS (5%)
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How are the symptoms and responses of Giardia "typical" with respect to its site of infection
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Typical small intestine infection ie
diarrhoea: watery (osmotic), no dysentery systemic: no fever |
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Describe the immune response to Giardia and the consequences
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Overgrowth triggers macrophages -> IL1,6, TNF-a, IFN-Y -> inflammation, Tc, IgA -> villous atrophy, crypt deepening -> malabsorption, disacharridase inactivity (glucose malabsorption), pancreatic enzyme inhibition (fat, protein malabsorption), sodium & water malabsorption -> watery steatorrea, flatulance, dehydration, anaemia (macrocytic & microcytic), failure to thrive
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Stools are bulky, pasty, liquid, pale, smelly, hard to
flush - explain the mechanisms wrt a GI infection |
1) Bulky stools -> malabsorption due to inflammation of mucosa, destruction of villi, colonisation of gut wall, decreased mucosal disacharride production
2) fatty, smelly: pancreatic lipase inactivation due to uptake of bile salts 3) pale stools: giardia uptakes bile salts 4) liquid: osmotic & malabsorbtive diarrhoea, SI villous atrophy 5) smelly: bacterial fermentation of unabsorbed nutrient matter |
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How would serology indicate immunity to Hep B because of vaccination
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anti-HBsAg (+ve)
anti-HBcAg (-ve) HBsAg (-ve) HBcAg (-ve) |
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How would serology indicate immunity to Hep B because of past infection
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anti-HBsAg (+ve)
anti-HBcAg (+ve) antigens -ve |
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How would serology indicate chronic Hep B
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anti-HBsAg (-ve)
HBsAg (+ve) anti-HBcAg (+ve) |
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Why is Hep A vaccination effective after only a single course and Hep B requires 3
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Hep A - inactivated whole virus
Hep B - subunit |
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Describe the mechanisms of the symptoms of Giarditis
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diarrrhoea, flatulance, abdominal distension: colonisation of SI mucosa & microvillus atrophy (also exotoxins) prevents brush border enzymes breaking down disacharrides & peptides -> osmotic diarrhoea, bacterial metabolites (gas & distension)
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What test would a GP perform to test for H.pylori
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14C urea breath test
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Describe the rapid urease test for H. pylori
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Also known as CLO test
1) biopsy of stomach mucosa taken 2) placed in urea medium with indicator 3) pH rise indicates breakdown of urea to ammonia |
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Why does H.pylori only produce symptoms in certain individuals
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Depends on strain
Type II has flagella, mucins, urease, adhesins Type I also has VacA (cytotoxic exotoxin - mucosal necrosis and infiltration to lamina propria) and CagA exotoxin |
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