MOD Flashcards
What gives rise to a diseased state in the most general form?
Failure of homeostasis on a cellular level due to the distrubance to the cells environment that translates into the observed morphological and physiological changes.
What are the two types of infact? and what gives rise to each type?
Red: Occurs when these is occlusion but there is a collateral blood supply/anastomoses which leads to extensive haemorage into the tissue. Loose tissue (like lungs) are prone to this and also when these is a high venous pressure/congestion.
White: Occurs only at end arteries (like in the conronary renal or retinal arteries)
What is ischaemic necrosis?
Cell death caused by a lack of blood supply
What are the types of hypoxia and their respective causes?
Hypoxemic- state of oxygen deficiency by there being a low oxygen content in the blood. (pulmonary effusion, low atmospheric oxygen content, reduced lung volume(congenitial, environmental) lung cancer)
Anemic hypoxia- Descreased ability to carry blood in the oxygen due to haemoglobin deficiency/impairment. (CO poisoning, iron deficiency)
-Ischemic hypoxia: occurs due to occlusion of blood flow to a particular tissue (can occur due to the vessell being blocked or damaged so thrombus, embolism, trauma, infection, low blood pressure).
-histiocytic: inability of cells to use the oxygen supplied to them (like cynanide poisoning)
What are some common causes of cell injury?
radiation, trauma, extremes of heat, lack of metabolites, current, pressure, toxins, microorganisms, autoimmune activity,hypoxia.
What is the result of cell injury?
it depends on the severity of the injury. slight injury will result in cell adaptation and severe injury will result in cell death.
Define necrosis
all the cell changes that occur after localised cell death due to irreversible damage to the cell and its components.
Define apoptosis
Apoptosis is individual controlled/programmed cell death that is induced.
What are the features of apoptosis and sequalae?
single cells become intensiely eosinophillic and visible are nucelar fragments, cell shrinkage and then blebbing. This keeps the entire contents of the cell in vesicles that prevents leakage. These vesicles are then phagocytosed by macrophages or neighbouring cells. The lack of leakage.
What are the features of necrosis and sequalae?
Cell damage: in the nucleus (pyknosis, karyolysis, karyorrhexis), swelling and lysis of cell components, myellin figures.
cell lysis: results in the cell contents passing into the surrounding tissue causing inflammation.
What are the types of necrosis? giving examples of when these would occur
Liquifying- more proteases released then protein resulting in surrounding tissue being dissolved. Occurs in tissue that lacks substantial supporting networks like the brain.
coagulative-More protein denaturation
caseous-
Fat-
What is the mechanism for apoptosis?
Apoptosis can be induced via either the intrinsic or extrinsic pathway. The intrinsic pathway.
intrinsic: DNA damage causes increase in mitochondrial permeability and the release of cytochrome c. This interacts with APAF1 and caspase 9 forming an apoptosome. This then activates a caspases.
Extrinsic: Binding of death ligands (trail) activates caspase activation.
How are free redicals formed?
free radicals are formed by a number of mechanisms. NADPH oxidase on leukocytes create them as part of the bodies immune response, Ischaimia and reperfusion injury, radiation can ionise water forming the hydroxyl free radicals, Electrons can leak across in the inner mitochondrial membrane and result in the creation of.
What are free redicals?
Free radicals are oxygen species with an unpaired electron making them hightly reactive.
What is the action of free radicals on cells?
Free radicals tend to target proteins and the cell membranes. Hydroxyl free radicals are most damaging to cell lipids and there is no mechansim for terminating these.
How do cells terminate free radicals?
Free radicals are terminated through a number of mechanisms. Firstly there are species within the body that can bind to free radicals like vitamins C, E and A.
There is a process of natural self termination through decay
There is also an enzyme system using SODs and Catalase to breakdown existing free radicals.
There are also storage proteins which bind transition metal elements preventing (in the case of iron) the heiber weiss and fenton reaction which create the hydroxyl radical).
What are heat shock proteins and what is their role?
Heat shock proteins are a group of chaperone proteins that are expressed by cells in response to high temperature; they assist in the refolding of denatured proteins, not only as a result of heat but also in response to physical and chemical stresses. The consequences of protein misfolding can be severe and there are a number of diseases that can result from faulty folding. In many cases, including some forms of cystic fibrosis.
What is ventilation/perfusion ratio and how can it effect blood oxygen saturation?
the ratio of oxygen in the lungs and blood supplied to the lungs. Optimally all blood should just be saturated with oxygen so if the blood flow through the pulmonary circulation increases or there is a decrease in oxygen uptake then it leads to a decrease in this value. The lower the value the lower the blood oxygen saturation.
What is myxedema? how does it arise?
Deposition of mucopolysaccharides. In hypothyroidism it arises systemically but in hyperthyroidism (graves) it occurs specifically in the pretibial region.
what are the inhibitors and inducers of apoptosis?
inhibitors: sex steroids, growth factors and cell matrix, Bcl-2
Inducers: Trail ligands, DNA damage, loss of growth factors, p53,
What are the features of reversible cell injury in hypoxia?
low oxygen, decrease in oxidative phosporylation, decrease in ATP, increase in glycolysis so decrease in glycogen and increase in pH. Leads to chromatin clumping. Low ATP causes a detachment of ribosomes, decrease in protein synthesis and an increase in lipid deposition. There is a decrease in Na/K atpase and so there in an influx of water and this leads to cellular swelling, ER swelling, Mitochondrial swelling, and blebs.
What are the features of irreversible cell damage in hypoxia.
There is a large influx of calcium ions (due to loss of NCX and no calcium atpase function). also there will be a release from the ER and mitochondrion. This leads to key cellular changes. damage to the chromatin and disruption to many cell processes.
What are the biochemical consequences of excessive alcohol intake?
Damage to GI tract and so poor absorption of nutrients (folate, and vitamins resulting in folate deficiency beri beri and pelagra), The Liver gets damaged and so becomes leaky so liver enzymes (ALTs and ASL and Gamma-GT) can be tested for in the blood, there can also be deposition of collagen in the liver and fat (mallory’s hyline). This will eventually lead to cirrhosis
What is the effect of paracetamol overdose and what is the protocol for dealing with an OD patient?
Saturates normal pathway so forms NAPQI which is toxic that damages hepatocytes, this is then conjugated with glutathione so the liver’s defences to damage are removed. Leads to death in 36-96 hours. if after 4 hours the blood paracetamol is high then N-acetyl-cysteine and after 2 hours charcoal can be given to absorb any in stomach.
What are the types of hypoxia and their respective causes?
Hypoxemic- state of oxygen deficiency by there being a low oxygen content in the blood. (pulmonary effusion, low atmospheric oxygen content, reduced lung volume(congenitial, environmental) lung cancer)
Anemic hypoxia- Descreased ability to carry blood in the oxygen due to haemoglobin deficiency/impairment. (CO poisoning, iron deficiency)
-Ischemic hypoxia: occurs due to occlusion of blood flow to a particular tissue (can occur due to the vessell being blocked or damaged so thrombus, embolism, trauma, infection, low blood pressure).
-histiocytic: inability of cells to use the oxygen supplied to them (like cynanide poisoning)
What are some common causes of cell injury?
radiation, trauma, extremes of heat, lack of metabolites, current, pressure, toxins, microorganisms, autoimmune activity,hypoxia.
What is the result of cell injury?
it depends on the severity of the injury. slight injury will result in cell adaptation and severe injury will result in cell death.
Define necrosis
all the cell changes that occur after localised cell death due to irreversible damage to the cell and its components.
Define apoptosis
Apoptosis is individual controlled/programmed cell death that is induced and energy dependent.
What are the features of apoptosis and sequalae?
single cells become intensiely eosinophillic and visible are nucelar fragments, cell shrinkage and then blebbing. This keeps the entire contents of the cell in vesicles that prevents leakage. These vesicles are then phagocytosed by macrophages or neighbouring cells. The lack of leakage.
What are the features of necrosis and sequalae?
Cell damage: in the nucleus (pyknosis, karyolysis, karyorrhexis), swelling and lysis of cell components, myellin figures.
cell lysis: results in the cell contents passing into the surrounding tissue causing inflammation.
What are the types of necrosis? giving examples of when these would occur
Liquifying- more proteases released then protein resulting in surrounding tissue being dissolved. Occurs in tissue that lacks substantial supporting networks like the brain.
coagulative-More protein denaturation
caseous-
Fat-
What is the mechanism for apoptosis?
Apoptosis can be induced via either the intrinsic or extrinsic pathway. The intrinsic pathway.
intrinsic: DNA damage causes increase in mitochondrial permeability and the release of cytochrome c. This interacts with APAF1 and caspase 9 forming an apoptosome. This then activates a caspases.
Extrinsic: Binding of death ligands (trail) activates caspase activation.
How are free redicals formed?
free radicals are formed by a number of mechanisms. NADPH oxidase on leukocytes create them as part of the bodies immune response, Ischaimia and reperfusion injury, radiation can ionise water forming the hydroxyl free radicals, Electrons can leak across in the inner mitochondrial membrane and result in the creation of.
What are free redicals?
Free radicals are oxygen species with an unpaired electron making them hightly reactive.
What is the action of free radicals on cells?
Free radicals tend to target proteins and the cell membranes. Hydroxyl free radicals are most damaging to cell lipids and there is no mechansim for terminating these.
How do cells terminate free radicals?
Free radicals are terminated through a number of mechanisms. Firstly there are species within the body that can bind to free radicals like vitamins C, E and A.
There is a process of natural self termination through decay
There is also an enzyme system using SODs and Catalase to breakdown existing free radicals.
There are also storage proteins which bind transition metal elements preventing (in the case of iron) the heiber weiss and fenton reaction which create the hydroxyl radical).
What are heat shock proteins and what is their role?
Heat shock proteins are a group of chaperone proteins that are expressed by cells in response to high temperature; they assist in the refolding of denatured proteins, not only as a result of heat but also in response to physical and chemical stresses. The consequences of protein misfolding can be severe and there are a number of diseases that can result from faulty folding. In many cases, including some forms of cystic fibrosis.
What is ventilation/perfusion ratio and how can it effect blood oxygen saturation?
the ratio of oxygen in the lungs and blood supplied to the lungs. Optimally all blood should just be saturated with oxygen so if the blood flow through the pulmonary circulation increases or there is a decrease in oxygen uptake then it leads to a decrease in this value. The lower the value the lower the blood oxygen saturation.
What is myxedema? how does it arise?
Deposition of mucopolysaccharides. In hypothyroidism it arises systemically but in hyperthyroidism (graves) it occurs specifically in the pretibial region.
what are the inhibitors and inducers of apoptosis?
inhibitors: sex steroids, growth factors and cell matrix, Bcl-2
Inducers: Trail ligands, DNA damage, loss of growth factors, p53,
What are the features of reversible cell injury in hypoxia?
low oxygen, decrease in oxidative phosporylation, decrease in ATP, increase in glycolysis so decrease in glycogen and increase in pH. Leads to chromatin clumping. Low ATP causes a detachment of ribosomes, decrease in protein synthesis and an increase in lipid deposition. There is a decrease in Na/K atpase and so there in an influx of water and this leads to cellular swelling, ER swelling, Mitochondrial swelling, and blebs.
What are the features of irreversible cell damage in hypoxia.
There is a large influx of calcium ions (due to loss of NCX and no calcium atpase function). also there will be a release from the ER and mitochondrion. This leads to key cellular changes. damage to the chromatin and disruption to many cell processes.
What are the biochemical consequences of excessive alcohol intake?
Damage to GI tract and so poor absorption of nutrients (folate, and vitamins resulting in folate deficiency beri beri and pelagra), The Liver gets damaged and so becomes leaky so liver enzymes (ALTs and ASL and Gamma-GT) can be tested for in the blood, there can also be deposition of collagen in the liver and fat (mallory’s hyline). This will eventually lead to cirrhosis
What is the effect of asprin overdose? what is the treatment?
Acetylesalicylic acid overdose stimulates resp centre in brian resulting in resp alkalosis. -ve feeback causes fall in pH. Interfers with normal metabolism which contributes to acidosis. inhibits COX1 and COX 2 causing GI bleeding due to lack of mucins and also descrease platelet aggregation.
activated charcoal, intravenous dextrose and normal saline, sodium bicarbonate, and dialysis
Describe the mechanism of action of heparin?
Binds to anti-thrombin and activates it resulting in a 1000 fold increase in rate of clearence of key components to the clotting cascade.
Describe the mechanism of action of asprin
Inhibits COX1 and 2. This results in the suppressed production of prostaglandins and thromboxane which stops platelate aggreagation and stop fever and pain.
Can also result in Upper GI bleeding.
Describe the mechanism of action of warfarin.
Takes the place of Vitamin K in the formation of gla-residues resulting in the absence of several key components of the clotting clascade i.e factor VII and X.
How do platelets adhere to each other and to the cell wall?
Endothelium normally produce NO which inhibits thrombus formation. Also they express various proteins inhibtting platelet aggregation.
Von willibrand factor anchors cells to collagen but isnt normally exposed to collagen when in the lumen.
Injury to endothelium exposes the VMF to the collagen in the basement membrane. This leads to aggragation of platelets. Also change in blood flow can lead to clots as can thrombin, ADP and thromboxane.
Why must the clotting system be finely tuned?
Due to the consequence being bleeding out or the blood setting solid. This process needs tight regulation at several points.
Describe the clotting cascade.
Extrinsic: tissue factor 3–>7–>10
Intrinsic: 12–> 11–> 9–>10–>thrombin–> fribrinogen to fibrin and XIII.
9–>10 is upregulated my VIII.
XIII forms cross links in the fibrin.
Define heamostasis.
The process of stopping bleeding through various mechanisms (fibrinolytic, platelets, vasclular auto-occulsion in severance)
Define thrombosis
Formation of a solid mass of blood in the circulatory system in a living person.
What is the effect of thrombus in the venous system?
Initially congestion and swelling. The temperature of the tissue will increase due to more blood being present. Eventually the pressure in the tissue will match that of the arterial supply leading to no blood entering and therefore ischimia and necrosis.
What is the effect of thrombus in the systemic circulation?
Leads to ischimic necrosis due to the tissue being deprived of oxygen straight away.
What is Virchow’s triad?
3 factors that lead to thrombus formation.
Blood flow- stagnation/turbulence like in AF or an aneurysm.
Blood components- disruption of clotting factors that can arise from pregnancy, post-op smokers and drinkers.
Vessel wall intergrity- injury, inflammation, compression, atheroma, spasm.
What are the outcomes of a thrombus?
Lysis: complete restoration of blood flow to the affected region, no permanent damage to tissue, only happens for small clots.
Recanalisation: partial re-establishment of blood flow through developement of new lumens through the thrombus.
Organisation: lumen remains blocked and there is in-growth of capillaries and fibroblasts.
Propagation: Thrmbus in vessel disrupts blood flow further down system leading to another thrombus forming.
Thromboemboli: The thrombus breaks off and travels in the blood stream to a site distal to its point of origin.
What is an embolism?
Blockage of blood vessel by a solid liquid or gas at a site distant to its point of origin.
What can cause an embolism?
iaterogenic (medical equipment air from injection, medical equipment and drugs causing) , tumour cells, nitrogen from decompression, throat getting cut, amniotic fluid, thromboembolism
What is a DVT? how is it managed? prevented? pathophysiology? risk factors?
deep vein thrombosis, arises in the deep veins of the legs typically.
managed through the use of oral warfarin and IV heparin.
prevented through TED stockings,early mobilisation post surgery and sub cut heparin.
Pathophysiology: Formed by abnormal blood flow in the legs, results in clotting formation and then this can progress through propagation and grow in size. If a bit breaks off can lead to pulmonary embolism.
Describe pulmonary emboli.
originate from thromboemboli in the venous network that travel into the RA–>RV–> pulmonary circulation.
Cannot reach systemic circulation due to being to large to pass through the cappilaries.
If small will have a very small effect only causing SOB.
Medium=coughing up blood/pulmonary odema
Massive=fatal
recurrent= pulmonary hypertension and RV hypertrophy.
Treated by filter in atria and by prophylactic anticoagulants.
Describe common congenital disorders of blood coagulation.
VIII deficiency (Haemophillia A) IX deficiency (Haemophilia B) Both are x linked and interupt the intrinsic clotting pathway. Common in populations where a high frequency of consanguineous marriage is present. VWD- VWF is absent and this is essential for platelet adhesion. Has a site for factor 8 and collagen. All can present with spontaneous haemorrage into joints and soft tissue, early onset OA. Most common cause of death is HIV and Hep C contracted from blood products pre-screening. 12% of patients can develop an immune response to the treatment of factor replacement. Non congenital auto immune response can develop in individuals.
Describe DIC, its treatment, causes and presentation
Common state of in which hemorrhage and thrombosis occur simultaneously as a result of another pathology. The clotting leads to depletion of factors leading to hemorrhage.
Causes include infection, neoplasm, trauma, liver disease.
Pathogenesis: endothelial damage and tissue trauma lead to the initial clotting.
Death occurs in 40% of cases. systemic disruption of normal activity in all organs.
Describe common causes of thrombocytopaenia.
Reduction of platelet number in the blood.
Drop in platelet production: megaloblastic anemia, infections, chemotherapy, alcohol, liver cirrosis.
Increased in platelet destruction: AI thrombocytopenic purpura, DIC,
Platelet sequestration: hypersplenism
Describe common causes of thrombophillia
Congenital deficiency in antithrombin, protein c and s deficiency.
Describe common acquired disorders of coagulation
Liver disease: Leads to failure of factor synthesis.
Vitamin K deficiency: lack of green vegetables in diet, its fat soluble so requires bile for absorption. Needed to make gamma carboxyglutamate residues of 2, 7, 9, and 10 also protein c and s.
Describe causes of acute inflammation and the purpose of
Causes: infection, toxins, hypersensitivity, physical/chemical agents, necrosis.
Purpose: decrease the total damage to the body, deal with the initial cause as quickly as possible, innate stereotyped response to tissue injury.
What are the macroscopic features of acute inflammation?
Rubor, calor, dolar, tumor, and loss of function
Describe the vascular phase of acute inflammation and the factors that can cause this.
Initially a transient vasoconstruction:
Then a vasodilation: histamine for first half hour then bradykinin and leukotriene.
Increase in endothelium permeability: histamines and leukotrienes cause endothelial contraction, vegf causes an increase in transcytosis.
Drop in blood velocity: This is due to the increase in endothelium permeability so less blood can flow through.
Describe where histamine is produced and the effects of
Produced: in mast cells, platelats, and basophils in response to trauma, C3A and IL1.
Effects: Vasodilation, increase in endothelial contraction, pain,
Describe the exudation formation in acute inflammation
Formed due to increased endothelium permeability. This allows proteins to pass into the fluid. Due to colloid osmotic effect the proteins take water into the extracellular space with them. This leads to oedema. This is due to starlings law of the cappilaires.
What is the benefit and disadvantages of forming of exudate?
Removal of toxins by dilution, increasing the supply of nutrients to the site of injury, increases the flow of neutrophils and antibodies to the site of injury. Increases lymph drainage increasing the immune response to any pathogens.
Disadvantages: result in compression of surrounding tissue, can be more harmful by decreasing blood volume if systemic reaction like in anaphylaxis.
How are neutrophils brought into the site of injury?
Neutrophils enter the site of inflammation through 4 steps.
margination: occurs due to blood stasis and involves the neutrophils moving from the circulation to the vessel wall.
Rolling: binding via selectins moves the neutrophils by allowing intermittant binding to the endothelium.
Adhesion: binding to the endothelium via intergrins.
Emigration: firstly diapedesis occurs where the neutrophil passes through the vessel wall. This requires moving of the endothelial cells by relaxing junctions and dissolving of the basement membrane using mmps. Chemotaxis then occurs allowing the neutrophil to move up the gradient of various chemicals (C5A, LTB4 and bacterial peptides).
what is the neutrophil mechanism of action?
phagocytosis of pathogens
Killing of pathogen: O2 dependant (using myeloperioxidase halide system). and O2 independant (using proteases and lysozymes).
What are the systemic markers and consequences of acute inflammation?
Fever (due to released endogenous pyrogens like IL1, TNF alpha and prostoglandin) Raised WBCC (in response to the tissue trauma and the type of WBC can indicate the cause of tissue injury) shock (due to too much exudate being formed dropping blood pressure). Markers of acute inflammation will be CRP alpha 1 antitrypsin, and serum amyloid A protein.
Describe resolution of acute inflammation
The initial causes of tissue damage must be removed. This leads to a decrease in exudate formed. The exuadate formed in tissue space is drained via the lymph or reabsorbed by the blood. Decrease in exudate formation and chemicals released results in less margination and chemotaxis of WBC. Tissue damage must be repaired for full resolution. If there is architercural damage then there will be scar tissue produced as the body attempts to regenerate.
How can drugs modifiy acute inflmammation?
Asprin inhibits the production of various arachnidonic acid derivatives and so acts to reduce the pain and inflammation.
Adrenaline acts to vasoconstrict at high concentrations by activating alpha 1 receptors and this results in the increases in BP during shock.
Describe Lobar pneumonia
Most usually caused by streptococcus pneumonia.
progression is congestion that includes vascualr engorgement hyperemic few WBC and many bacteria (first 24hours), then Red hepatizisation where RBCs are extravasated into tissue then grey which the RBC disintergrate followed by resolution.
Usually acute
Treatment is antibiotics
Describe acute appendicitis
Symptoms: pain, vomiting, fever and if abdomen has general pain suspected peritonitis.
Cause: primary obstruction of the appendix lumen resulting in swelling of the tissue. Ichimia and necrosis follow due to the swelling and perforation results in bacteria entering the peritonium and can lead to sepsis. Most common causes of blockage are trauma, fecal matter.
DDX: Based on examination and raised WBC count. also and US or Xray can be used.
Treatment: surgery to remove appendix
Describe alpha one anti-trypsin deficiency
Genetic mutation that results in the lack of a protease inhibitor that protects against inflammatory enzymes i.e neutrophil elastase. Sypmtoms would be SOB wheezing and emphysema.
Describe hereditary angio-oedema.
Genetic lack of C1 esterase which inhibits the actions of bradykinin. This lead to swelling of the GI tract genitals and face.
high mortality.
Define chronic inflammation
Chronic response to injury with associated fibrosis
Describe sarcoidosis
Granuloma formation and accumulation typically in lungs and lymph however it can occur in any tissue.
Symptoms: SOB, wheezing, fatigue, weight loss TATT, conduction abnormalities.
DDX:disease of exclusion
Causes: typically idiopathic but is associated with a number of other conditions
Describe TB
Caused by the mycobacterium TB and typically affects the lungs.
symptoms: cough, blood tinged sputum, fever, weightloss sypmtoms often much more severe in HIV. can erode into pulmonary artery resulting in massive bleeding and systemic spread resulting in millary tb.
DDX: chest xray and cultures. TB are acid fast and so stain accordingly however they have a slow rate of binary fission.
Treatment: antibiotics however there are many resistantant strains (MDR-TB)
Risk factors: poor ventilation, over crowding, poor immune response, poor diet, smokers, HIV
Immune response: macrophages, and lymphocytes and fibroblasts aggregate to form granulomas which are langerhan’s ginat cells.
leads to caseous necrosis.
Describe leprosy
Leprosy is caused by the mycobacterium leprae and is a granulomatous disease of peripheral nerves and URT.
DDX: skin lesions muscle weakness, loss of sensation, flat nose.
Describe syphillis
4 stage disease contracted via sexual activity.
Tertiary: occurs 3-15 years after initial disease contraction but only 1/3 of people develop. 50% of which develop gummatous which is charachterised by the formation of chronic gummas which are soft granulomas that can vary is size and occur in most tissue but is common in skin bone and liver. 33% go on to form neurosyphillis which can present with a mirad of symptoms depending on where in the brain the disease attackes. CV syphillis can lead to aortitis leading to aneurysym formation.
Describe foreign body reactions
granuloma classed as a foreign body granuloma.
Describe wegener’s granulomatosis
vasculitis of medium blood vessels that can occurs in any organ. Upon biopsy often granulomas are discovered in tissue.
pathophysiology: thought to involve cANCA
What is the action of helicobacter pylori?
Causes: stomach ulceration in 20% and stomach cancer in 2% of cases of infection.
Pathophysiology: tunnel into stomach mucus and produce urease which produces NH3 resulting in stomach acid neutralisation. This and other products damage the cells of the stomach mucosa.
Stomach ulcer treatment?
Removal of cause: antacids and H2 antagonists, antibiotics for H.pylori,
Compare and contrast crohns and U.C
stool has blood in UC and in C has fat
fever in c and only in severe UC
fistulas in C and weightloss in C
UC is usually continuous from rectum to colon.
Describe the consequences of chronic inflammation
can result in fibrosis, atrophy, loss of function, continued stimulation of immune response.
What causes chronic inflammation to arise?
chronic infection/irriations (de novo)
acute–>chronic transition
What is a macrophage and what is its typical function?
A macrophage is an immune cell of the body which appears in chronic inflammation as monocytes travel from blood into tissue becoming macrophages. They can create new granules and and involved in phagocytosis, APC and cytokine production
Describe granulomas and their composition
A granuloma is a special type of cell aggregation composed on epitheloid histiocytes sounded by lymphocytes. They often form in response to large objects that frustrate phagocytosis. Giant cells can form through merging of macrophages and they are different based on the causes of inflammation.
what cells are involved in chronic inflammation and their role?
Touton giant cells: due to fat necrosis.
Langerhans giant cell: Due to TB
Foreign body giant cell: friustrated phagocytosis of foreign body.
Macrophage: present in chronic inflammation, APC phagocytosis, and cytokine production.
B Lymphocyte: produce plasma cells which produce antibodies.
T lymphocyes: helper and cytotoxic
NK cells: Kill cells based on changes in MHC on cell surfaces/ due to cellular distress
Eosinophils: produce histamine and are a sign of allergic reactions and parasites/chronic inflammation.
Fibroblasts/myofibroblasts: produce collagen and so produce fibrosis and also cause tissue contraction.
