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30 Cards in this Set
- Front
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•Definethe terms pathogen, virulence, infection and describe the types of infection. •Describehow microbes gain access to the body and how they do damage •Describehow microbes fool the bodies defence mechanisms and how they are transmitted•Describethe basic histology of the respiratory tract •Describethe defence mechanisms employed by the lung •Usingnamed examples describe some of the common or clinically important infectiveorganisms of the respiratory tract •Reviewantibiotic prescribing guidelines for respiratory tract infections (selfdirected). |
Pathogen: a disease causing microbe Virulence: Howinfectious something is (the ability to cause disease) Infection: the ability of a pathogen to get inside the body past the first line of defence |
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Types of Infection |
•Bacteria+ chlamidiae, Rickettsias andmycoplasmas •Fungi•Viruses•Prions (neurodegenerative) •Protozoa•Helminths(roundworms (nematodes), flatworms (tapeworms/cestodes) ,flukes (trematodes))Ectoparasites(insects and arachnids i.e. ticks, lice, fleas, spiders) |
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•Describe how microbes gain access to the body and how they do damage Routes of infection (basic) |
Inhalation Ingestion Sexualtransmission Bites Injections |
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Routes of infection (by system) •Describe how microbes gain access to the body and how they do damage |
Skin:Penetration(cuts, burns, insect bites) Respiratory system: Lungdefence mechanisms can be overcome (name some common problems) GI Tract: Ingestionof contaminated food/water: fecal oral route (dysentery, traveller's diarrhoea, typhoid, cholera) Urogenital tract: sexual transmission. STI colonise in UG tract. Women more prone than men |
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Transmission of disease (3 main types) |
Source Vertical - mother to fetus Horizontal - person to person Fomites (iPhones, toys) Zoomoses (animals) Community acquired Transmission within the body Gaining access to blood and lymph Locally proliferating Breaching epithelial barrier Person to person Skin shedding Coughing and sneezing Urination and defection |
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•Describe how microbes gain access to the body and how they do damage |
Entering or binding to cells –Releasing endotoxins/exotoxins –Release enzymes to break downtissue components or damage blood vessels (colagenases, haemolases) –Inducing host immune response –Inducing inflammation (which leadsto tissue damage) |
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•Describe the basic histology of the respiratory tract (Upper and Lower) |
Upper: Middle ear, larynx, pharynx, nasal cavity, sinuses. Lots of exposure to pathogens Lower: starts at bronchi and continues into the lungs. Essentially sterile. |
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Airway system (anatomy details) |
Trachea Left & right principal bronchus Lobar/secondary bronchus Segmentary/tertiary bronchus Intersegmental Terminal bronchioles Respiratory bronchioles Alveolar ducts Alveolar sacs |
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Airway layers (4) |
•Respiratory epithelium: pseudostratified columnar ciliated + basement membrane •Lamina propria:containing connective tissue, blood and lymph •Band of fibroelastic tissue at the base of the LP. This becomes more prominent and more muscular(smooth muscle) as the tubes get smaller to replace cartilage •Submucosa: seromucus glands, smooth muscle/elastinfibres •Cartilage: hyaline cartilage - c-shaped in trachea and less prominent as the tubes get smaller |
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General guide of airways: trachea to alveoli |
General guide: less cartilage and moresmooth muscle, fewer glands, flatter cells |
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Alveoli and alveolar epithelium (2 types) |
Alveoli - blind ended sacs with thin walls for gaseous exchange Type 1 pneumocytes: flattened squamous epithelial cells with thin cytoplasm to allow gaseous diffusion. Basement membrane fused with capillary basement membrane Type 2 pneumocytes: rounded cells with prominent secretory granules for production and secretion of surfactant |
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Host Defence mechanisms Nasopharynx |
Nasal hair Turbinates (concha) Mucocilliary apparatus Immunoglobulin A (IgA) secretion |
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Host Defence mechanisms Oropharynx |
Saliva Sloughing of epithelial cells (shedding dead cells) Local complement production |
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Host Defence mechanisms Trachea, bronchi |
Cough, epiglottic reflexes Sharp angled branching of airways Immunoglobulin production (IgG, IgM, IgA) |
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Host defence mech Terminal airways and alveoli |
Alveolar lining fluid made up of surfactant, Ig, complement Cytokines IL-1 and TNF Alveolar macrophages Neutrophils Cell mediated immunity |
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•Using named examples describe some of the common or clinically important infective organisms of the respiratory tract URTIs |
–Otitismedia, sinusitis, pharyngitis, tracheitis.–Very common; often viral inaetiology.Secondarybacterial (or fungal) infections are common |
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LRTIs |
–Bronchitis, bronchiolitis –Pneumonia (infection of lungparenchyma leading to inflammation & consolidation). –May be bacterial, viral or fungalin aetiology. –History isimportant to determine likely pathogens. |
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•Review antibiotic prescribing guidelines for respiratory tract infections When to give an appointment? |
Clinical assessment for: acute otitis media acute sort throat/acute pharyngitis/acute tonsillitis common cold acute rhinosinusitis (inflammation of the paranasal sinuses and the nasal cavity) acute cough/acute bronchitis |
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When to delay or not give antibiotics? |
acute otitis media acute sort throat/acute pharyngitis/acute tonsillitis common coldacute rhinosinusitis (inflammation of the paranasal sinuses and the nasal cavity) acute cough/acute bronchitis |
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When to do immediate prescribing strategy? |
–bilateralacute otitismedia in children younger than 2 years –acuteotitismedia in children with otorrhoea (AOM and OME) –acutesore throat/acute pharyngitis/acutetonsillitis when three or more Centor criteria are present. |
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Centor Criteria? |
–presence of tonsillarexudate –tender anterior cervicallymphadenopathy or lymphadenitis –history of fever (over 38◦C) –absence of cough |
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Streptococcal score card (Group A beta-haemolytic streptococci) |
–Age 5 to 15 years–Season (late autumn, winter, earlyspring)–Fever (≥38.3°C [≥101°F])–Cervical lymphadenopathy–Pharyngeal erythema, oedema, orexudateNosymptoms of a viral upper respiratory infection |
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Streptococcus pyogenes |
•(GroupA streptococcus) is a Gram-positive, non-motile, non-sporeforming coccusthat occurs in chains or in pairs of cells •It isestimated that between 5-15% of normal individuals harbour the bacterium, usually in therespiratory tract, without signs of disease. •Causespharyngitis |
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Scarletfever (mechanism) |
•Causedby group A streptococci –Havean M protein component used to inhibit phagocytosis –Havehaemolysins O and S as well as DNase, streptokinase and pyrogenictoxins–Cancause Toxic shock and tonsil abcesses |
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Scarlet fever (presentation and symptoms) |
•Scarlet fever presents with rash over trunk and abdomen then spreads to entire body •Pyrexia (raised T/fever) Lymphadenopathy (enlarged lymph nodes) Aches and nausea |
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Diptheria •Corynebacteriumdiphtheriae |
•Gram-positive,aerobic, nonmotile,rod-shaped bacteria •Irregular,club-shaped or V-shaped arrangements in normal growth •Theyundergo snapping movements just after cell division giving characteristic formsresembling Chinese letters or palisades. •Damageis caused by exotoxin A orB Produces B lactamase |
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Diptheria symptoms and prognosis |
•Severe pharyngitis and pseudomembrane that can cover the trachea •Symptoms–Myalgia–Fever–Pleuriticchest pain–Vomitting –Diarrohea•Mortality rate of 15% but up to 50%in hospital outbreaks |
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Pneumocystiscarinii |
•Generallylimited to immuno-compromised patients•FungusPneumocystis(carinii) jiroveci•Causeslethal pneumonia (Pneumocytis – PCP)•Neverbeen grown in culture – information comes from clinical cases/observations•Resemblesa protozoa in shape and contains cholesterol in cells walls rather than ergosterol•Antibodiesfound in most humans by age 4•Lowvirulence in healthy hosts |
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Pneumocystis carinii (Symptoms and prognosis) |
•Dyspnea•Cough•Alveolarinfiltrates•Causesloughing of cells and fluid build up•Deathis from progressive asphyxiation |
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Aspergillosis |
•Generallylimited to immuno-compromised patients•Fungus– Aspergillus•Conidiasmall enough to reach the alveoli •Afterattachment extracellular proteases and phospholipases produced•Colonisationleads to invasion of pulmonary tissues and penetration of blood vessels by septate hyphae•Mortalityfor invasive apsergillosis is 100% |
