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Flashcards by laura.marsland, updated more than 1 year ago
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Created by laura.marsland
over 11 years ago
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| Question | Answer |
| List 3 oncogenes & associated malignancy | RAS (usually deactivated by GTP hydrolysis) - 90% of pancreatic adenocarcinomas & 50% of colon adenocarcinomas C-MYC - Translocation (8 - 14) - Burkitt's Lymphoma, breast & colon & lung Her2 - (cell membrane receptor) amplified in breast cancer |
| List 3 mechanisms for tumour cell spread | 1. Reduced interaction with other cells 2. Reduced interaction with stroma 3. Increased motility |
| What are CADHERINS & what is their association with invasion & metastasis | Calcium dependent glycoproteins present on the cell membrane - allow cells to interact with one another. Reduced/altered expression in some cancers allowing cells to move away from each other |
| What are INTEGRINS and what is their association with invasion & metastasis? | Cell surface glycoproteins. Reduced/altered expression in some cancers lead to reduced interaction between cell & stroma so cells able to move more freely |
| Describe the normal molecular events associated with Rb (a tumour suppressor gene) | When active (unphosphorylated) it is bound to and therefore sequesters E2F, which is usually involved in triggering cell division. If phosphorylated, it is inactive, detaches from E2F - which can then go on & initiate cell division & growth |
| List 3 functions of p53 (tumour suppressor gene) when NOT mutated | 1. Induces apoptosis in cells whose DNA defects are irreparable 2. Induces transcription of genes involved in DNA repair 3. Delays/stops progression through the cell cycle of cells with defective DNA/damaged cells |
| Define carcinogenesis | The process that results in the transformation of a normal cell into a neoplastic cell ~ by causing permanent non-lethal genetic alterations |
| List 3 differences in behaviour between benign & malignant cells | Retain function versus lost function No invasion versus ability to invade No metastasis versus metastasis |
| List 3 differentiating features of benign versus malignant cells, in terms of macroscopic appearance | No necrosis versus necrosis Well defined versus ill defined edge No haemorrhage versus haemorrhage |
| Differentiate between the microscopic features of benign versus malignant cells | Malignant - variation in nuclear size, shape & chromasia Loss of differentiation High mitotic count/activity |
| Differentiate between the microscopic features of benign versus malignant cells | Malignant - variation in nuclear size, shape & chromasia Loss of differentiation High mitotic count/activity |
| List the 3 requirements for tumour development | 1. There must be a change to DNA or gene expression 2. This change must lead to changes in cell growth & behaviour 3. This change must be non-lethal and passed on to daughter cells |
| What gene is implicated in Ataxia Telangiectasia and what does it normally do? | ATM (serine threonine kinase) - normally prevents progress through cell cycle if defects in DNA have not been repaired i.e. DNA repair checkpoints. It responds to defects in DNA (especially double strand breaks) by activating various proteins involved in apoptosis, cell cycle arrest & DNA repair |
| Define atherosclerosis | Intimal lesions of the arteries, caused by atheroma, that leads to hardening of the vessel wall |
| Define arteriolosclerosis | Small artery disease, hardening of arterioles, seen in DM & hypertension |
| Define atheroma | A chronic, intimal lesion of arteries that causes narrowing of the vessel lumen & weakening of the vessel wall |
| List the 4 constituents of an atherosclerotic plaque | Smooth muscle cells Inflammatory cells Extracellular matrix Lipids |
| BRIEFLY describe cellular events associated with atheromatous plaque development | 1. Endothelial injury 2. Lipid permeates & is oxidised 3. M.phages take up oxidised lipids (foam cells) 4. SMC migration & proliferation 5. Lipid accumulation 6. SMC calcification |
| List 4 complications of cerebral artery atheroma | TIA RIND CVA Vascular dementia |
| List 4 laboratory abnormalities that might be present in the setting of DIC | 1. Low platelets 2. Raised PT & APPT 3. Low fibrinogen 4. Raised FDPs |
| Define cellular INVOLUTION | Reduction in cell number (c.f. hyperplasia) |
| Give two examples of physiological hyperplasia | 1. Hormonal, e.g. endometrial 2. Compensatory, e.g. after partial hepatectomy |
| What type of inheritance does haemophilia A show? | X-linked recessive |
| List 2 types of physiological hypertrophy | 1. Hormonal, e.g. uterus (in combinations with hyperplasia) during pregnancy 2. Functional demand increased, e.g. mechanical or skeletal muscle |
| List 6 causes of cell atrophy | 1. Lack of nutrition 2. Denervation 3. Lack of blood flow 4. Reduced workload 5. Lack of endocrine stimulation 6. Ageing |
| Define metaplasia | Reversible change from one cell type to another. Can be pathological or physiological. |
| Define neoplasia | Abnormal growth of cells that continues even when the initiating stimulus is taken away |
| What is the definition of a 'thrombus' | A solid mass of blood constituents that forms in the vascular system within life. Composed of platelets, fibrin & blood cells |
| List the 3 components of Virchow's Triad | 1. Abnormal endothelial wall 2. Abnormal blood flow 3. Abnormal blood constituents |
| List the 5 potential fates of a thrombus | 1. Propagation 2. Fibrinolysis 3. Organisation 4. Recanalisation 5. Embolism |
| What is the definition of an embolism? | A mass which travels through the vascular tree & becomes lodged so as to obstruct blood flow |
| List 3 potential types/outcomes of pulmonary embolism | 1. Obstruction of medium or small PA with/without lung infarction 2. Massive/saddle embolism - obstruction of main PA - sudden death 3. Multiple small emboli - pulmonary hypertension |
| List 5 symptoms of PE | Breathlessness Collapse Chest pain Cough Haemoptysis |
| List 4 signs of PE | Tachycardia Tachypneoa Hypotension Raised JVP |
| List 7 types of embolism, other than thrombus | 1. Fat 2. Atheroma 3. Nitrogen 4. Tumour 5. Air 6. Amniotic fluid 7. Foreign material |
| Briefly describe DIC | Disseminated Intravascular Coagulation - complication of critical illness - multiple small emboli throughout vasculature, leads to exhaustion of clotting factors & resultant bleeding from e.g. skin, GIT, respiratory tract. Clots can also block organs - organ failure |
| What is the definition of haemostasis? | The maintenance of the blood in a fluid, clot-free state. Induction of rapid & localised haemostatic plug at the site of injury |
| What mechanisms keep blood from clotting normally? | 1. Intact endothelial wall 2. Dilution of clotting factors 3. Removal of active clotting factors by the liver 4. Anticoagulant mechanisms |
| Describe the role of the platelet in clotting (4 stages) | 1. Activation (on contact with subendothelial material 2. Adherence to subendothelial tissue via interaction with vWF 3. Aggregation (platelets clump together via interactions between GP2a-3b platelet receptor in combination with fibrinogen ) 4. Release of factors that stimulate continued further aggregation |
| What two roles does the endothelial wall play in preventing clotting? | 1. Physical barrier 2. Secretion of: a. Thrombomodulin b. Heparan c. Enzymes d. Prostacyclin |
| Differentiate between the actions of Tc & Th cells | Th (CD4) cells respond to MHC 2 proteins & secrete cytokines which initiate events that result in destruction of antigen (EXOGENOUS) Tc (CD8) cells respond to MHC 1 proteins & become activated and able to destroy antigen (ENDOGENOUS) |
| Differentiate between the actions of Th1 & Th2 lymphocytes | Th1 lymphocytes can activate macrophages but not help B cells Th2 lymphocytes can help B cells but not activate macrophages |
| List 2 functions of B cells in chronic inflammation | 1. Production of antibodies, which then mark antigens for opsonisation, interact with killer cells & trigger the classical complement pathway 2. Presenting of antigen to CD4 (Th) lymphocytes |
| List the 3 types of healing & repair | 1. Fibrous repair 2. Regeneration 3. Resolution |
| Define 'labile' cells | Continuously dividing throughout life E.g. skin, gut epithelium, cervix, endometrium, urinary tract |
| Define 'quiescent' cells | Generally not dividing (in Go) but can undergo rapid division if stimulated to do so E.g. osteocytes, chondrocytes, kidney cells, liver cells, fibroblasts, endothelial cells, smooth muscle cells |
| Define 'permanent' cells | Cannot divide in adult life. Have left the cell cycle E.g. cardiac muscle, neuronal, skeletal muscle |
| List the 5 stages of healing & repair | Angiogenesis Mitogenesis Chemotaxis & motility Fibrogenesis Remodelling |
| Describe the process of angiogenesis in healing & repair | Pre-existing capillaries bud into area OR develop from endothelial precursors VEG-F |
| What is granulation tissue? | The specialised tissue of healing & repair. Contains: 1. Fluid-rich 2. Antibodies & growth factors 3. Macrophages & myofibroblasts 4. Proliferating capillaries 5. Other inflammatory cells |
| Describe the processes of chemotaxis & mitogenesis in healing & repair | Fibroblasts migrate & proliferate Collagen laid down TGF-beta FIBROVASCULAR GRANULATION TISSUE |
| Describe the process of fibrogenesis in healing & repair | Fibroblasts continue to produce collagen. Fibroblasts align so that collagen is uniform, increasing tensile strength. FIBROUS GRANULATION TISSUE |
| Describe the remodelling process in healing & repair | MMPs cleave collagen PDG-F |
| List 2 factors that can stimulate apoptosis | 1. Extrinsic - e.g. TNF 2. Intrinsic - e.g. hormone withdrawal/growth stimulatory signal withdrawal |
| What factors comprise the anti-oxidant defence system? | Vit A, Vit E, Vit C, Glutathione |
| List the 3 features of acute inflammation | 1. Haemodynamic changes (RUBOR, CALOR) 2. Permeability changes in endothelium (TUMOR) 3. Recruitment & migration of neutrophils |
| List 4 roles of the macrophage in chronic inflammation | 1. Secrete factors involved in tissue destruction (e.g. proteases) & repair (e.g. VEG-F) 2. Secrete cytokines to recruit inflammatory mediators (e.g. PAF) 3. Phagocytosis 4. Antigen presenting (MHC 1 & 2) |
| List 6 non-immunological defences | 1. Skin sebum 2. Low pH of stomach & vagina 3. Mucociliary clearance system 4. Complete emptying of the bladder & inhibition of urine flow up the ureters 5. Commensal flora, e.g in vagina & bowel & skin 6. Skin |
| Describe what are meant by 'haemodynamic changes' in acute inflammation | Vasodilation due to vasodilatory mediators, e.g.NO, leads to hyperaemia - RUBOR & CALOR |
| Describe what is meant by 'changes in endothelial permeability' in acute inflammation | In response to histamine & PAF, endothelial cells swell & partially retract, allowing fluid, salt & protein (e.g. albumin, immunoglobulins) to enter damaged area (TUMOR). Inflammatory fluid is known as exudate |
| List and describe 3 types of exudate | 1. Purulent (pus containing) 2. Fibrinous (fibrinogen containing) 3. Transudate (low protein content) |
| Describe the process of 'neutrophil migration & recruitment' in acute inflammation | 1. Margination 2. Adhesion 3. Emigration 4. Chemotaxis |
| Describe the process of phagocytosis by neutrophils in acute inflammation | 1. Neutrophils recognise dead/foreign material via mannose receptors or opsonins & Fc/C3b & bind to it - engulf it into phagosome 2. Fuse with lysosome - phagolysosome - series of reactions (O2 dependent & non O2 dependent) - lysis |
| List 7 outcomes of acute inflammation | 1. Resolution 2. Suppuration 3. Organisation & repair 4. Chronic inflammation 5. Death 6. Septicaemia 7. Calcification |
| Describe the process of resolution of acute inflammation | 1. Exudate drains to lymphatics 2. Plasmin degrades fibrin 3. Neutrophil apoptosis 4. Regeneration |
| What is caseous necrosis? | An accumulation of an amorphous structure within an area of debris |
| Describe the pathophysiology of fat necrosis | Results from the action of lipases into adipose tissue. Free fatty acids accumulate & precipitate as calcium salts (saponification). E.g. pancreatitis/trauma |
| Define gangrene & list two types | A type of necrosis that is visible grossly. Mostly coagulative? Dry gangrene Mostly liquefactive or in a wet body cavity? Wet gangrene |
| Describe coagulative necrosis | 1. Cell death but basic shape & architecture remains 2. Solid consistency maintained 3. Necrotic cells removed by inflammatory cells 4. Tissue regeneration from neighbouring cells or scar tissue |
| Describe liquefactive necrosis | 1. Complete dissolution of necrotic tissue 2. Massive infiltration of neutrophils & abscess formation 3. Release of reactive oxygen species & proteases (ISCHAEMIC NECROSIS IN BRAIN) |
| What are heat shock proteins? | A class of functionally related proteins which are upregulated when cells are exposed to elevated temperatures or other stressors. Protect proteins from stress-related damage and remove damaged proteins. |
| List 3 reversible mechanisms of cell damage | Reversible: 1. Reduced protein synthesis 2. Loss of ATP - e.g. inhibition of Na/K pump 3. Anaerobic metabolism - lactic acid build up |
| List 2 irreversible mechanisms of cell injury | 1. Massive intracytoplasmic calcium influx 2. Activation of enzymes, e.g. ATPase |
| List 5 factors that lead to generation of free radicals | 1. Normal cellular metabolism 2. Nitric Oxide 3. Transition metal, e.g. Fe+++ 4. Toxins - e.g. carbon tetrachloride 5. Irradiation |
| List 4 mechanisms of removal of free radicals | 1. Spontaneous decay 2. Anti-oxidants, e.g. vitamin A/E/glutathione 3. Transport proteins, e.g. ferritin 4. Enzymes, e.g. catalase |
| List 3 mechanisms of free radical-induced damage | 1. Membrane lipid peroxidation 2. Interaction with proteins 3. DNA damage |
| Define 'free radical' | Any species capable of independent existence that contains one or more unpaired electrons |
| Describe the role of the complement system | Part of the innate immune system A triggered enzyme cascade, ultimately resulting in the activation of a MEMBRANE ATTACK COMPLEX, which lyses invaders. Functions: opsonization, chemotaxis, cell lysis & clumping of antigen-bearing agents |
| List 3 complement proteins and state their role | 1. C3b - binds to the surface of pathogens targets them for opsonisation by phagocytes 2. C5a - chemotactic - recruits inflammatory cells 3. C5b - initiates membrane attack complex (C5b, C6, C7, C8 & C9) |
| List the 6 causes of cellular injury & give an example of each | Immune - e.g. cytokines Physical - e.g. direct trauma/heat Infectious - e.g. prions Nutritional - e.g. malnutrition Chemical - e.g. arsenic & reduced ATP Hypoxic - e.g. ischaemic (MI) |
| List 3 differences between necrotic & apoptotic cell death? | 1. Pathological versus Physiological/pathological 2. Enzymatic destruction versus internally controlled 3. Cell contents leak out versus nuclear dissolution 4. Death of contiguous groups of cells versus death of single cells |
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