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Disease Processes
| Question | Answer |
|---|---|
| What is hypoxia? | Lack of oxygen |
| What is hypoxaemia? | Lack of oxygen in blood |
| What is ischemia? | Lack of blood supply |
| What is re-perfusion? | Restoration of blood flowing lack of blood supply |
| What are the 3 types of cells (well-differentiated)? | 1. Labile (constantly dividing) 2. Stable (divide when stimulus) 3. Permanent (never divide) but can adapt to get bigger or can make new connections |
| Examples of labile cells | Epithelial in skin, GIT, repro, urinary and exocrine ducts. haeomopoietic stem cells |
| Examples of stable cells | Epithelial in liver, kidney, lung + pancreas. smooth muscle cells, fibroblasts, endothelial cells |
| Examples of permanent cells | cardiac and skeletal myocytes, CNS neurons |
| Connective cell types | Mycocytes, endothelium, cartilage (chondrocytes), bone, fibroblasts, fat |
| Epithelial cells | Glandular epithelium, simple sq (alveoli), strat sq (skin), simple col (secretion/absorption), pseudostratified (upper resp), transitional (urinary), strat cub/col (mammary glands, germ clls etc) |
| 'Other' tissues | Mesothelium, melanocytes, germ cells, lymphoid tissue, bone marrow, glial cells & neurons. RBCs, neutrophils, lymphocytes and macrophages |
| What is autophagy? | cell breaks down/destroys old, damaged, abnormal substances in its cytoplas, good for withstanding stress. Reduces metabolic requirements by getting rid of damaged mitochondria and producing autophagic vacuoles to break down content LOSE ABILITY AS AGE |
| What is apoptosis? | Programmed cell death - Active dismantling - Condensation of cytoplasm & nucleus - Break up within apoptotic bodies - Phagocytosis - No inflammation or scarring - Happens every day - vital in embryogenesis |
| What is necrosis? | All organelles and cell itself starts to swell due to cellular disruption and ionic dysfunction -> suddenly explodes toxic contents Kills neighbouring cell |
| What is an infarct and how does it occur? | An area of necrosis |
| Differences between necrosis and apoptosis? | Apoptosis = pathology and physiology Necrosis = only pathology Apoptosis = active Necrosis = passive Apoptosis = does not cause inflammation or disturb surrounding cells Necrosis = infarct |
| Tissue patterns of necrosis | 1. coagulative: hypoxic death 2. liquefactive: localised bacterial infections 3. caseous: TB lesions 4. fat; adipose tissue |
| What is atrophy? | decrease in tissue size |
| What determines whether a stimulus causes atrophy or infarction? | Depends on cell health (age) and severity, rapidity, duration of stressor Ie. Even in a young person, severe sudden stress can cause immediate necrosis For older cells, lower threshold for necrosis |
| What effect does aging have on cells and organs? | - Less able to undergo autophagy -> less able to withstand stress -Less ability to divide -> shrinkage -More occurrence of necrosis and apoptosis -> loss of functional tissue RISK FACTOR FOR ORGAN FAILURE |
| Define types of cellular adaptation and understand when these processes are not possible/reversible | Metaplasia = one normal cell to another Hyperplasia = excessive cell division Autophagy = cell breaks down/destroys old, damaged substances in cytoplasm Hypertrophy = increase in cell size TYPICALLY, ALL REVERSIBLE! PATHOLOGICAL OR PHYSIOLOGICAL |
| Benign vs malignant tumours | Metastatic ability vs not Encapsulated vs infiltrative Homogenous vs heterogenous Well-differentiated vs. varying differentiation |
| Describe the pathogenesis of the 2 most common primary lung cancers | 1. original ->metaplasia->dysplasia->CIS->inasive cnoma 2. original -> hyperplasia->dysplasia->CIS->invasive carcinoma |
| What are the 3 features of acute inflammation? | Hyperaemia (vasodilation inc permeability) Oedema (exudate) Neutrophils |
| What are the 3 possible outcomes of acute inflammation? | Resolution Organisation Chronic inf |
| What are the 3 main components of granulation tissue & their role/purpose in repair? | Fibroblasts (secrete collagen) Macrophages (clean up dead cells) Angiogenesis (new blood vessels) |
| What are the consequences of healing through organisation? | Function lost, possible distortion of surrounding tissue due to contraction |
| What are the 3 main causes of chronic inflammation? | 1. Unresolved acute (stimulus still there) 2. Repeated acute 3. Special cases * |
| Define the 3 general features of chronic inflammation | 1. Persistent injury 2. Ongoing attempts at repair 3. Lymphocytes |
| Describe the possible negative consequences of chronic inflammation. | 1. Risk of hyperplasia if epithelial cells present 2. Loss of function 3. Eventually healing by organisation |
| Sterile vs non sterile sites | Sterile = no microbes/microorganisms; blood, brain & CSF, bone/marrow, lower resp, upper urogenital Non = skin, GIT, upper resp, lower urogenital |
| Innate vs adaptive | Innate = fast response, not specific Acquired = slow, memory |
| Cancer superpowers | |
| What is metaplasia | change from one normal cell to another normal cell |
| Hyperplasia | Excessive cell division |
| Neoplasia | Prescence/formation of new, abnormal growth of tissue (irreversible) |
| Tumour | A swelling of a part of the body caused by an abnormal growth of tissue (benign or malignant) |
| When does necrosis occur? | as a result of ischaemic events or haemorrhagic events |
| Metaplasia in epithelial cells of lower oesophagus | stratified sq to simple glandular columnar cells after being exposed to stomach acid reflux |
| Metaplasia in epithelial cells of ectocervix | simple columnar glandular to stratified sq after being exposed to the ectocervix |
| 3 routes of metastasis | 1. Blood 2. Lymph vessels 3. Direct seeding |
| Common sites of metastasis | 1. Lung (closest to heart) 2. Liver (venous and arterial blood supply) 3. Blood / brain |
| What is the response to necrosis? | Acute inflammation and healing by organisation |
| Innate vs acquired defence | Innate; first line, prevent opportunistic infection, fast response, non specific, neutrophils + macrophages Acquired; slow response, memory, T and B lymphocytes and antibodies |
| Sterile vs non sterile sites | Sterile: no microbes/microorganisms, blood, brain and CSF, lower resp, upper urogenital Non: skin, GIT, upper resp, lower urogenetial |
| What is an oedema? | Increased fluid in interstitial tissue |
| What is an effusion? | increased fluid in body cavities |
| What is hyperaemia? | Active increase in blood flow to an area |
| What is congestion? | Passive build up of blood in low pressure circuits |
| What is an exudate? | active, inflammatory extravascular fluid with high protein conc (inflammatory response) |
| What is a transudate? | passive, extravascular fluid with low protein conc |
| Acute vs chronic inf | |
| Colloidal pressure stuff | |
| Describe the pathogenesis of the 2 most common primary lung cancers | Original + smoking -> metaplasia -> mutations -> CIS -> Invasive carcinoma Original + smoking -> hyperplasia -> dysplasia etc |
| Dysplasia def | Prescence of abnormal cells within a tissue/organ (pre-cancerous) |
| Ulcer def | A lesion or sore (area of necrosis) on a body surface |
| Abscess def | Area of necrosis in an organ |
| Resolution def | Healing without scarring, involving restoration of structure and function |
| Organisation def | Healing by scarring/fibrosis, functional tissue lost and replaced with scar tissue |
| What are the 3 features of acute inflammation? | 1.Hyperaemia – after acute inf & chem mediators are released, vasodilation occurs & blood vessel wall permeability increases 2.Oedema – exudate begins repair 3.Neutrophils – leukocytes activated (polymorphonuclear cells e.g. monocytes & macrophages) |
| What are the 3 possible outcomes of acute inflammation? | 1. Organisation 2. Resolution 3. Chronic inflammation |
| What are the 3 main components of granulation tissue & their role/purpose in repair? | 1. Fibroblasts – secrete collagen 2. Macrophages – remove debris 3. Angiogenesis – making new blood vessels |
| What are the consequences of healing through organisation? | Function lost, possible distortion of surrounding tissue due to contraction |
| What are the 3 main causes of chronic inflammation? | 1. Unresolved acute (stimulus still there) 2. Repeated acute 3. Special cases * |
| Define the 3 general features of chronic inflammation? | 1. Persistent injury 2. Ongoing attempts at repair 3. Lymphocytes |
| Describe the possible negative consequences of chronic inflammation. | 1. Risk of hyperplasia if epithelial cells present 2. Loss of function 3. Eventually healing by organisation |
| What is ischaemia | Lack of blood supply to a part of the body |
| What is a haemorrhage | rupture of blood |
| what is thrombus | a blood clot that forms on the wall of a blood vessel or in the heart when blood platelets, proteins, and cells stick together. |
| what is embolua | undissolved mass travelling in the blood. (e.g. blood clot that has broken off - thromboembolism, clumps of cancer cells, clumps of microbes - septic, gas bubbles, fat droplets, amniotic fluid, foreign material) |
| aneurysm def | An abnormal, localised dilatation of an artery or ventricle |
| atheroma def | An abnormal, localised dilatation of an artery or ventricle |
| Atherosclerosis | The chronic inf. Process within the wall of an artery (ongoing injury, attempts at repair, inflammatory cells plus oxidised lipis etc) |
| stasis | Stasis: A stoppage or slowdown in the flow of blood or other body fluid, such as lymph. |
| Superficial vs deep vein thrombi | Superficial: pain due to nerve endings, ulceration of ovrrlying skin, oedema downstream, not fatal, rarely embolise Deep: asymptomatic, embolise, can kill instantly, can occur quickly |
| Risk factors for DVT | Stasis and hypercoagulation |
| Main risk factor for athersclerosis | Systemic hypertension, age, male gender, genetics, smoking, diabetes etc |
| How do the kidneys contribute to systemic hypertension? | |
| What vascular pathologies does atherosclerosis predispose towards? | thrombus, emboli, aneurysm |
| Renal physiology | |
| Explain RAAS | |
| What is anemia? | Excessive loss of RBCs |
| Origin of leukemia? | Haemopoietic stem cells |
| Venous vs arterial thrombi | Venous = excessive stasis or increased coagulation Arteries = turbulent blood flow (systemic hypertension) triggering atherosclerosis |
| What are the vascular consequences of atherosclerosis? | Reduced vascular elasticity, increased vascular resistance, swellin/bleeding in plaque |
| What is systemic hypertension a risk factor of? | Atherosclerosis and left ventricular heart failure? |
| What is pulmonary hypertension a risk factor for? | Right sided heart failure |
| Why do we receive a transudate in chronic inf? | Only increase in hydrostatic pressure due to hyperaemia but no increased vascular permeability OR decrease in colloidal pressure (lack of plasma proteins) |
| Where do thrombi end up if they embolise? | For veins - lungs Arteries not sure |
| How do the kidneys contribute to systemic hypertension? | Overactivation of RAAS |
| What vascular pathologies does atherosclerosis predispose towards? | Thrombus, embolus, aneurysm |
| What are the possible consequences of having atherosclerosis in the abdominal aorta, coronary arteries, carotid & cerebral arteries? | 1. Abdominal aorta atherosclerosis -> aneurysm -> rupture -> hypovolemic shock 2. Carotid and cerebral arteries; ischaemic stroke 3. Coronary arteries -> ischaemic heart disease -> angina, MI etc. |
| Describe the inflammation & repair that occurs following an MI. | Acute inflammation and healing through organisation, due to the nature of the tissue (permanent). |
| Briefly describe what complications can occur following an MI. | Predisposes to thrombus (procoagulant), arrhythmia (scar does not conduct electrical impulses), aneurysm (weakened tissue), increased risk of heart failure (decreased functional reserve) |
| List the causes of left- versus right-sided heart failure (HF). | left: IHD, systemic hypertension, aortic/mitral valve disease, pericarditis right: LSHF, pulmonary hypertension |
| Forward effects of HF | Renal response to reduced CO - Reduced renal perfusion - Angiotensin II - increased vascular resistance and induces the - Aldosterone causes kidneys to retain salt (Na+) and water (H2O) leading to inc blood volume |
| Backward effects of LSHF + symptoms | Pulmonary Congestion Increased hydrostatic pressure (leading to transudates) Pulmonary oedema Dyspnoea, cough with blood tinged phlegm |
| Backward effects of RSHF+ symptoms | Systemic venous congestion Increased hydrostatic pressure Peripheral oedema Liver/spleen/kidney disease (pressure necrosis from congestion) Oedema in lower limbs and ascites/abdominal effusion Jugular distention |
| List some of the common causes & possible consequences of endocarditis. | Valve disease – bacterial or autoimmune (rhemuatic heart disease) Results in valve stenosis and incompetemce |
| List some of the common causes & possible consequences of pericarditis. | Extension of acute inf, foreign (cancer), autoimmune disease Impaired diastole and systole -> heart failure |
| List the main impacts of ageing on the cardiovascular system? | Increased risk of atherosclerosis (-> ischaemic heart diseases, systemic hypertension) Lose functional reserve -> hypertrophy, stress and increased risk of failure -> ischaemic events Heart valves prone to calcification with age |
| What 2 things are typically present within an atheroma? | Fat deposit + calcium |
| Why do thrombi form on atherosclerotic lesions and within anyeurysms? | Less anticoagulants and turbulent blood flow |
| Difference between MI and BI? | MI=coagulative necrosis BI=liquefactive necrosis |
| What are the scars in the brain made of? | Glial cells |
| What factors influence prognosis for cancer patients? | Rate of growth, removability, rate of division |
| What cellular adaptations are caused by smoking? | Hyperplasia of GOBLET CELLS Metaplasia of CILLIATED EPITHELIUM |
| Does metaplasia always precede dysplasia? | No |
| Smooth muscle benign tumour | Leiomyoma |
| Benign tumour in endothelium | Haemangioma |
| Benign tumour in secretory epithelium | Adenoma |
| Benign tumour in cystic / secretory epithelium | Cystadenoma |
| Finger like benign tumour | Papilloma |
| Brnign tumour of germ cells | Teratoma |
| Malignant tumour of haemopoietic stem cells | Leukaemia |
| where might the acute inflammatory process be life threatening? | |
| where might the acute inflammatory process be life threatening? | |
| Describe the innate defences in the conductive & respiratory portions of the lungs. | ANYTHING NOT A LYMPHOCYTE (EPITHELIAL BARRIERS, CILIA, MUCOUS, COUGHING/SNEEZING) |
| How are the lungs affected by left ventricular failure? | BACKWARD EFFECTS - PULMONARY CONGESTION (INC IN HYDROSTATIC PRESSURE -> PULMONARY OEDEMA) |
| How do lung diseases contribute to right ventricular failure? | REDUCING VENTILATION . INCREASIN RESISTANCE. PULMONARY CIRCUIT. IN COPDS AND PNEUMOCOMINOSIS AND PULMONARY EMBOLI |
| Where do most pulmonary emboli (PE) travel from? | Deep vein thrombi |
| List definitions of the 4 main COPDs | 1. Bronchiestasis 2. C |
| What type of reaction occurs in atopic asthma, what occurs acutely in the airways and chronically if asthma is not well-controlled? | |
| What is pneumoconiosis, which particles are commonly implicated in Australia & what can they cause. | |
| What is pneumonia & what are the major differences between lobar & bronchopneumonia | |
| What is compliance | expandibility of lungs |
| What is atelactasis? | the collapse of a lung or part of a lung, also known as a lobe |
| main causes & possible consequences). of COPDS | |
| What is a COPD? | Impaired airflow due to complete or partial obstruction at any level of the bronchial tree |
Created by:
jrichardss