Flashcards
Week 4
Flashcards do conjunto (67)
- 1What is are the physical/active barriers?Physical: skin, lungs, gut mucosa
Active barrier: cilia, secretions, anti-bacterial peptides - 2Describe the barriers of the gut-Layer of mucous that traps bacteria
-Paneth cells that secrete anti-microbial peptides
-Commensals which are non-invasive and compete with invading bacteria - 3Describe the features of the innate immune defence-Ready to rapidly activate at any time
-No memory
-Low specificity
-Generic response (reacts in the same way with each bacteria) - 4Describe the acute phase response-Vasodilation -> erythema
-Increased vascular permeability -> oedema
-Cytokines -> heat
-Nerve stimulation -> pain - 5What recognises threat in the innate system?Professional Antigen Presenting Cells:
-dendritic cells
-macrophages/monocytes
-mast cells - 6What recognises threat in the innate system?Phagocytes:
-macrophages
-neutrophils
Granulocytes:
-neutrophils
-eosinophils
-mast cells
-basophils - 7Describe macrophages-Detection, phagocytosis and destruction of pathogens
-Originate from blood monocytes
-Examples include: alveolar, kupffer cells, microglial and splenic macrophages - 8Describe dendritic cells-Captures and processes antigens
-Convert captured proteins into peptides
-Transports peptides to the CSM and presents them on major histocompatibility complex (MHC) molecules to T cells - 9What do granulocytes do?-All contain inflammatory proteins, toxic enzymes, oxygen radicals that kill pathogens
- 10How are pathogens recognised?-Recognised by Pattern Recognition Receptors (PPRRs)
-PRRs are on every innate cell
-PRRs recognise Pattern-Associated Molecular Patterns (PAMPs) that occur on pathogens - 11What are the different PRR?TLR: Toll-like receptors
NLR: Nucleotide oligomerisation receptors
CLR: C-type lectin receptors
RLR: RIG-1 like receptors - 12Describe the PRR signalling pathway-Different PRRs recognise different motifs on pathogen
-Intracellular signalling cascade
-Stimulates nucleus to produce cytokines and secrete them - 13What are cytokines?Chemical signals which modulate cell activity or attract cells (chemokines). They bind to cytokine receptors and activate them.
They can be pro/anti-inflammatory, influence cellular differentiation, direct cellular migration. - 14What are acute phase proteins?Opsonise and present pathogens to the immune system
- 15What are complements?-Cascade of proteins
-Opsonisation, killing, activation, chemoattraction - 16What are the key cytokine families?Inteferon
Chemokine
Tumour necrosis factor
Interleukin
Haematopoietins
Transforming growth factor beta - 17Describe the action of: -interferon family -chemokine family -tumour necrosis factor (TNF) familyInterferon: antiviral proteins
Chemokine: direct cell migration, adhesion and activated
TNF: regulate inflammatory and immune responses - 18Describe the action of: -interleukin family -haematopoietins -transforming growth factor beta familyInterleukin: variety of actions
Haematopoietins: promote cell proliferation and differentiation
Transforming growth factor beta family: regulation of immune cells - 19What is opsonisation?-Coating a pathogen to make it more visible to the immune system
-Opsonised by: complement, CRP and immunoglobulin
-Speeds up the rate of phagocytosis - 20Describe the ... pathway of complement activation? Classical Lectin AlternativeClassical: Initiated by antibody/antigen binding
Lectin: initiated by carbohydrate sugars
Alternative: activated when it makes direct contact with microbial polysaccharides
*All cleave a complement protein: C3 - 21Describe inflammation Describe cytolysisC3a triggers release of histamine
Formation of membrane attack complex (MAC) which creates holes in microbes - 22Describe opsonisation Describe chemotaxisC3b binds to microbial surface and promotes phagocytosis
C5a is a neutropil chemoattractant - 23What does inactivation of complement mean?Regulatory proteins which limit damage to host cells that can be caused by complement
- 24Describe the features of complement-Circulate inactive in the serum
-Sequentially cleave and activate next stage in complement cascade
-Allows amplification of immune response - 25From where is the thymus gland derived from in an embryo?Third pharyngeal pouch
- 26What is DiGeorge syndrome?-Genetic syndrome caused by deletion of part of chromosome 22
Common features:
-Cardiac abnormality
-Abnormal facies
-Thymic aplasia
-Cleft palate
-Hypoparathyroidism
*Susceptible to reccurent infections due to an underdeveloped immune system - 27Describe the histological features of the cortex of the thymus-Located peripherally within each follicle
-Stains more darkly (more basophilic)
-More lymphocytes
-Epithelial reticular network
-Epithelial cells are connected by desmosomes (keratin is present in the cytoplasm) - 28Describe the histological features of the medulla-Located centrally within each follicle
-Fewer lymphocytes
-More epithelial cells
-Includes Hassal's corpuscles (flat non-secreting epithelial cells in concentric layers which are keratinised) - 29What are the anatomical relations of the thymus?-Located in thoracic superior mediastinum
-Posterior to manubrium of sternum
-Can extend superiorly into the neck and inferiorly into the anterior mediastinum (in front of fibrous pericardium) - 30Describe the vasculature of the thymusArterial: anterior intercostal and internal thoracic
Venous: left brachiocephalic, internal thoracic, inferior thyroid veins - 31What is the function of the thymus throughout life?-Active in children
-From puberty onwards, it begins to atrophy and is replaced by adipose. Produces fewer T cells - 32What is the blood-thymus barrier?-Epithelial cells+ basement membrane+ perocytes which form a sheath around capillaries forming a barrier
-Prevents entry of antigenic material
-Thymus only has efferent lymphatics, not afferent - 33What is MALT? What type of tissue is located here?Musoca Associated Lymphoid Tissue
Small aggregations of lymphocytes which form lymphoid follicles. These produce IgA and secrete plasma - 34Where is MALT found?-Tonsils, Peyers patches, appendix
- 35How do MALT areas differ histologically from surrounding cells?-Aggregations are large and confluent
-Found underneath villi and epithelia
-Populated by T/B cells, plasma cells and macrophages
-M cells are present in intestinal MALT - samples antigens in the lumen and delivers to lymphoid tissue - 36What is tonsillitis?-Inflammation of the palatine tonsils due to infection which is accompanied by enlarged jugulodigastric lymph nodes.
-Severe forms can lead to deviation of the uvula (quinsy) which can obstruct the pharynx
-Severe forms are treated with a tonsilectomy - 37Describe the spleen-Only lymphoid organ that filters the blood
-Filters dead erythrocytes + platelets, reacts to blood-borne pathogens by producing ab's
-Friable structure
-Easily damaged by blunt trauma
-Produces RBCs in children - 38Describe the white pulp-20% of the spleen
-Lymphoid aggregates (T/helper cells, B cells) and macrophages around the arteries - 39Describe the red pulp-80% of the spleen
-Vascular with parenchyma, vascular sinuses and sinusoids - 40Describe the location of the spleen-Upper L quadrant of the abdomen
-Covered by diaphragm and ribs 9-11 (cannot be palpated unless enlarged)
-Mid-axillary line
-Intraperitoneal - 41What are the anatomical relations of the spleen?Anterior: stomach
Posterior: diaphragm, left lung, ribs 9-11
Inferior: left colic (splenic) flexure
Medial: L kidney, tail of pancreas - 42Describe the vasculature of the spleenArterial: splenic artery (from coeliac trunk). Branches into 5 vessels which do not anastomose forming vascular segments
Venous: splenic vein with superior mesenteric vein to form hepatic portal vein - 43Why might the spleen be enlarged?-Hypersplenism
-Haemolytic anaemia
-Portal hypertension
-Malignancy
-Bacterial infections - 44Explain why a person who has had a splenectomy can survive if the spleen is important immunologically-Liver and bone marrow can take over some functions
-Person is more susceptible to some bacterial infections
-Requires life-long antibiotics - 45What sides of the body drain into which 2 lymph vessels?Right lymphatic duct: drain the R upper quadrant of the body (RHS of head, neck, R upper limb)
Thoracic duct: drains lymph from the rest of the body
Both enter at the internal jugular junction (where internal jugular and subclavian veins meet) - 46What is the difference upon palpation of lymph nodes that are infected, or malignant?Infected: painful, tender
Malignant: painless, hard, fixed - 47Which lymph nodes are routinely examined?Neck, axillary, inguinal
- 48What is a sentinel node?-First few lymph nodes which a tumour drains into
-Determines stage of cancer, prognosis, guides treatment - 49What are the anatomical relations of the thoracic duct? What happens if it is damaged?-Starts from T12
-At T5 it crosses over to LHS
-Drains into systemic circulation at the angle of the left subclavian and internal jugular vein (left venous angle)
-If damaged, lymph can accumulate in the pleural cavity (chylothorax) - 50How are neutrophils activated?-Inflammed or infected tissues release inflammatory cytokines
-Released systemically forming a gradient which leads back to the site of injury
-PAMP and DAMP is released - 51How do neutrophils migrate from the circulation to the tissues?1) Rolling/tethering- selectins loosely bind to neutrophils. Gives time for firm adhesion molecules to attach
2) Triggering
3) Firm adhesion
4) Extravasation- neutrophil enters the ECM between 2 epithelial cells - 52How do neutrophils recognise pathogens?1) Neutrophil receptors bind to PAMPs or DAMPs
2) The signal is transduced via second messengers
3) Cellular response: increased cytokine production and phagocytosis
4) Change in gene expression - 53What is a phagolysosome?When a phagosome (pathogen in vacuole) fuses with a lysosome (vacuole with low pH, toxic granules and free radicals)
NOTE: some bacteria are able to grow inside macrophages such as salmonella - 54What do granules contain?-Proteases/proteinases
-Bacteriocidal proteins
-Superoxides (free radicals) - 55What happens if the granules get out of the cell? (ie. the neutrophil undergoes necrosis)-Digests all components of the ECM
-Activates and recruits other immune cells
-Damages other local cells eg. epithelium - 56What is the role of reactive oxygen species? (in relation to bacteria)-Damage bacteria
-Need proteinases to kill the bacteria
-Lower the pH of the phagolysosome, optimising conditions for the proteinases - 57What is a NET (neutrophil extracellular trap)?-Occurs when cell has reached phagocytic capacity but infection/inflammation is still present
-Cell extrudes unravelled DNA coated in bactericidal proteins
-Traps and kills bacteria - 58What happens during the inflammation resolution?-Anti-inflammatory signals are released such as IL-10 (produced by macrophages)
-Attracts some neutrophils away from inflammation (retrograde chemotaxis)
-Some neutrophils are phagocytosed by macrophages (efferocytosis)
-When retrograde chemotaxis or efferocytosis fails, cells undergo necrosis - 59What is pus?When there are too many neutrophils for macrophages to clear
- 60What is leukocyte adhesion deficiency?Defect in the integrins which allow binding and entry of neutrophils into tissues
- 61How long is the time-frame for risk of neutropenia after chemotherapy?10-14 days
- 62Neutropenia can be caused by decreased production in the bone marrow. What are some causes?-Aplastic anaemia
-Cancer
-Hereditary disorders eg. congenital neutropenia
-Radiation (chemo) - 63Neutropenia can be caused by increased destruction. What are some causes?AI neutropenia (rare)
Chemotherapy - 64Neutropenia can be caused by marginalisaiton and sequestration. What are some causes?-Haemodialysis (AKA dialysis)
-Hypersplenism (associated with RI) - 65Describe benign ethnic neutropenia-Present in people of African descent and some ethnic groups in the Middle East
-No infections despite what would be considered mild neutropenic levels
-Bone marrow can produce sufficient cells during challenge
-No treatment is needed - 66Describe Alpha 1 Anti-trypsin Deficiency-Results in unopposed neutrophil action
-Abnormal structure of alpha 1 anti-trypsin which is an inhibitory protein that controls neutrophil elastase
-Neutrophil elastase destroys bacteria/host tissue and localises to NETs
-Results in emphysema in the lungs - 67Describe chronic granulomatous disease-Failure to produce reactive oxygen species
-Results in recurrent and severe infections
-Granulomas form in tissues
-Presents from 1-2 yrs old
-Diagnosed via a blood test
Informações
- Descrição
- Barrier immunity & innate recognition Anatomy of the lymphatic system The neutrophil in infection and inflammatory disease
- Criado por
- Dolu Falowo
- Visualizações
- 5
- Avaliação