Pathology
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Pathology - Details
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| 🇬🇧 | 🇬🇧 |
| What is stage iV? | Cancer has spread to other organs of the body, distant from the prmary tumour (including lymph nodes). De nova means new areas where roccuring breast cancer have reappeared in other areas of the body |
| What is stage iV? | Cancer has spread to other organs of the body, distant from the prmary tumour (including lymph nodes). De nova means new areas where roccuring breast cancer have reappeared in other areas of the body |
| What are the 3 areas that make up cellular pathology | Andrology, Ctyology and Histology |
| What is fixation? | Series of complex chemical reactions to preseve cells and thier components ina life - like state, allowing sample preperation and staining. |
| What are the aims of fixation? | To be able to see chemical and physical cellular characteristics, allowing for pattern observations and any morphological or chemical changes. Allow fixed in time for future analysis, comparison and observation. |
| What is putrification? | Decomposition of cell and compontents due to lysosomal activity as a result of micr - organism infection. |
| What is avoided by correct fixation? | Autolysis, putrification, loss of soluble substances, damage from fixing proceedure. Can still react with staining components. |
| What changes are visible in a fixed specimen? | Shrinking, Swelling and hardedning of cellular components |
| Why are chnages seen in fixation? | Dehydration of the sample after being cut from blood and nutrient supply, chemical reactions and cross link formations with the fixive used. |
| What is nuclear vacuolation? | Ghost nucleus appearance as swells and shrinks |
| What are the 3 types of fixation? | Physical, chemical and microwave. |
| How does 10% NBF work? | Forms side chain cross links with proteins on the methyl group and hydroxyl, fixing them in place Formeldahyde can form cross - links wirh purines and pyrimadines and some fats by bindign with hydrogen groups. |
| Why may we choose frozen fixation | Surgery diagnosis - benign or malignant? Identification of fats |
| What are the drawbacks of frozen fixation? | Not able to special stain Only benign or malignant cannot go into detail Not able to use IHC Delicate - manual staining |
| What factors affect fixation? | Time, temp, penetration rate, volue ratio, Specient sze, pH and buffers |
| What is the difference between somatic and germ line mutations? | Germ line in the gametes and somatic every other cell. Somatic is more common root cause of cancer |
| What are teh features of a benign tumour | Slow growing, non - life threatening, clear borders, may be encapsulated, does not metastasise, lower recurrance |
| What are the features of a malignat tumour? | Fast growing and life threatening, may metastasise to other areas, higher recurrance rate |
| What is a gain of function mutation? | When the genetic mutation of a gene leads to over- expression of a protien, causing it to be activated permenantly. |
| How are proto- oncogenes activated? | Deletion or point mutation, gene amplification and chromosonal translocation |
| What is gene amplification? | When multiple copies of genes are found on the chromosone leading to protein over - production. |
| How does chromosoal transloction contribute to cancer development? | Relocation next to promoter, causer over production. Fusion to actively transcribed gene mean that it is over transcription of protein. |
| How can nucleotide deletion or muttation affect cancer development? | It can lead to the production of a hyperactive protein. This sends false signals to the cell to proliferate |
| What are the 6 hallmarks of cancer? | Sustained proliferation signals, angiogenesis, Resisting cell death Evading growth supressors, invasion and metastasis, replication immortality. |
| What does the p53/MDM2/P14RAF pathway control? | Decreased cellular apoptosis and increased cellular proliferation. |
| Describe the p53/MDM2/P14RAF pathway in healthy cells | When no DNA damage is present p53 remains unphosphorylated, this allows it to bind to the MDM2 promoter reigon, stimulating the MDM2 expression. MDM2 regulates the levels of p53 in the cell, by binding with it to create an MDM2/p53 complex leading to p53 degredation. |
| Describe the p53/MDM2/p14ARF pathway in cells with DNA damage | If DNA is damged, P53 is phosphorylated, it cannot bind to MDM2 to form P53/MDM2 complex. This means that teh amount of P53 in the cell increases, and halts the G1-S transition, co stimulating other protein transcription, necessary for DNA repair. Once the DNA is repaired, P53 becomes unphosphorylated and can be degraded by the MDM2 protein. In the occurance of extensive DNA damage, P14RAF encoded by the CDK4N2a protein, inhibits the breakdown of p 53 and triggers the start of cellular apoptosis. |
| Describe the P16INK4a/CDK4/RB1 pathway in healthy cells. | Rb protein and E2F are bound in a complex. CDK4/6 and cyclin D when bound, partially phosphorylate the RB/E2F complex, causing the release of E2F, activating both the G1 - S phase transition in the cell cycle and P16INK4a tumor suppressor. P16INK4a causes the recombination of E2F and RB to limit further cell proliferation. |
| Describe the P14IN4a/CDK4/RB1 pathway in cancerous cells. | In the case of cancer, the incorrect or underexpression of People 16INk4a tumour supressor, means that there is no recombination of the RB and E2F proteins, meaning that proliferation is signalled to continue. CDK4/6 inhibitors are therefore, an area of cancer treataent being used in underexpression of p16INk4a. Overexpression of CDK4/6/Cyclin D can also lead to cancer development as overproliferation occurs. |
| How does the EGF pathway work? | The EGF (epidermal growth factor) receptor is located on the lasma membrane of the cell. Once the EGF ligant is formed, it leads to the dimerisation (binding) of intracellular proteins, that become phosphorylated to trigger various proliferative pathways. |
| How can the EGF pathway be impacted in cancer cells? | Over expression of the EGF recptor can lead to accelerated dimerisation, leading to an increased proliferative signal within the cell. Autophosphorykation can occur intracellularly, so always switched on to trigger proliferation. Truncated forms of the EGF recpter, lacks the HER2 domain, which means a poorer prognosis for the patient and lower response to trastuzumab in treatment |
| What is the difference between a pathologic stage? | Pathologic staging is only detering following tissue / surgical ananlysis. Clinical staging is given based on signs and symptoms |
| What is the TNM system? What are the ranges for each component? | Stands for Tumour, Nodes and metastasis, It is used as a guideline for the staging of cancer. T= 0-4, N = 0-3 and M = 0-3 |
| What is stage 0 | Cancer is in situ, no evidence of cancerous cells, or atypical cells invading surrounding tissues |
| What is stage 1, including details on 1A and 1B | Evidence of spread to surrounding tissues. 1A= Tumour size up to 2cm and is contained within the breast. No Node involvement 1B = No tumour in the breast but cancerous cells between 0.2mm - 2cm are found in the lymph nodes |
| What is IIA staging? | When the cancer is invasive, but still within the breast tissue, but is also found in 1 -3 auxillary lymph nodes smaller that 0.2mm Tumour is between 2 - 5 cm and has not infiltrated the lymph nodes |
| What is IIB stage? | Tumour is between 2 - 5cm and small amounts of cells between 0.2mm and 2mm are found in the auxillary lymph nodes Tuour is 2-5cm and has spread to 1-3 or breast bone lymph nodes. |
| What is stage IIIA | Any size tumour / no tunour but caner found in 4-9 auxillary lymph nodes or if cancer is larger than 5cm and has spread to auxillary lymph nodes |
| What is stage IIIB | Cancer has spread to chest wall and or skin of breast and may have infiltrated up yo 9 auxillary lymph nodes. |
| What is stage IIIC? | May be no tumour but has spread to 10 or more lymph nodes within the chest area above or below the collar bone. |
| What is stage iV? | Cancer has spread to other organs of the body, distant from the prmary tumour (including lymph nodes). De nova means new areas where roccuring breast cancer have reappeared in other areas of the body |
| What is pleomorphism? | Variation in cell size and shape, including large or additional nuclei |
| What is atypical mitosis? | Abnormal seperation of chromatics that may produce tripolar or quadripolar in appearance. |
| What is loss of polarity? | Cellular disorganisation |
| What does dysplasia mean? | Abnormal growth of cells. Nornally charachaterised by when immature cells are near the surface. May revert if cellular stressor is removed. |
| What are the 4 causes of infalmmation | Infection, necrosis, immunological reaction, environmental/physical agents |
| What are the 2 types of inflammation | Acute and chronic |
| What is the purpose of inflammation | Localise and eliminate cause, limit tissue injury, restore tissue |
| What are the 5 main inflammation responses | Recognition, recruitment, removal, regulation and repair. |
| What are the 4 signs of acute inflammation? | Rubor (redness), calor (heat), tumour (swelling), dolor (pain) |
| What are the key differences between acute and chronic inflammation? | Hours vs weeks Neutophil vs leukocytes Vascular response vs none Innate vs cell mediated immunity Rapid vs prologned |
| What is serous exedate | Clear water like fluid, found in blisters |
| What is proteinaceous exedate? | Protein heavy such as anibodies |
| What is fibrinous exedate | Contains connective tissues such as fibrin that allows trapping of causing agent, activated by thromboplastins |
| What is purulent exedate | Whene exedate is infected. Pus |
| Why is serous exedate useful? | Dilutes toxins as is water based |
| What are the 3 leukocyte phases? | Adhession of leukocytes to endothelium at inflammatoion site Migration of leukocytes through vessel wall Movement of cells to the cause at the site |
| What does seorus inflammation look like? | Markd by blistering and outpouring of fluid into the skin, appears as gaps on stainig near the service epithelium. |
| What does fibrinous inflammation look like? | Occurs with more serious injury that leads to greater vasculat permiability, to allow for larger protein molecules to pass into the extracellular space |
| What is an abcess? | A collection of perulent tissue from an infection |
| What are ulcers? | Shedding of endothelium on tissues and organs following necrosis of tissue layers, often in GI tract and mouth |
| What will ulcers look like in staiing. | Crater appearajce, noting missing tissues. |
| What are the 3 main causes of chronic infammation? | Prolonged infection, autoimmunity, Non degeneratable materials. |
| What does chronic inflammation look like? | No cardinal signs of inflammation, Little vascular changes and higher amount of macrophages and lymphocytes rather than neutrophils. Will look more permenant damage on the slides, fusion if various strucrures over time/ |
| What is granulomatous inflammation> | Distinct pattern associated with chronic inflammation. ggragations of macrophages, thata hve transformed by monoclucleat leukocytes. Typically in lung tissues |
| What are th two types of granuloma? | Foreign body and Immune |