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Annika Muller Inglés 177 fichas

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  1. 1FREE RADICALSHighly reactive substances with an unpaired e- in their outer field.
    Want to pair that e- and react with normal intracellular components, e.g. DNA, stripping them of their electron.
    Made through generation of our energy when we use oxygen.
  2. 2MITOCHONDRIA- Induce cell death
    - Drive differentiation?
    - Surrounded by double membrane
    - Have cristae
    - Generate energy
  3. 3AUTOPHAGY"self eating"
    When a cell is shrinking bc slowly decreasing blood or nutrient supply
    If blood flow or nutrient levels restored = cell can be big again
    Only way to get rid of damaged mitochondria
    ability ↓ with age
  4. 4APOPTOSISProgrammed cell death (cell suicide)
    Gradual/slow gives cells time to adapt
    Physiological & pathological
    Active
    A single cell can die
    Does not stimulate inflammation
    No scarring
  5. 5NECROSISMore catastrophic form of cell death
    Sudden and complete
    Pathological
    Passive
    Kills neighbouring cells
    Stimulates inflammation
    Scarring
  6. 6-VEs OF NECROSIS- Neighbouring cells induced to undergo necrosis
    - Area of necrotic tissue = infarct
    - Stimulation of acute inflammation response to necrosis
    - Loss/reduced function of tissue
  7. 7MITOCHONDRIA AND AGINGaging = accumulate mitochondria that produce ↓ energy/ATP but ↑free radicals
    When FR react with lipids/proteins they can cause damage = dysfunction of the cell. Cell might choose to die by apoptosis.
    Free radicals can also react with our DNA causing (many)mutations- CARCINOMAS.
  8. 8INFARCTwhen neighboring cells die by necrosis
    Often bc of sudden disruption in blood
    • Ischaemic
    • Haemorrhagic
  9. 9NEOPLASIA"new abnormal growth"
    tumors
  10. 10CANCER INCIDENCE>90% cancers are Carcinomas
    Most cancers ↑ incidence as age ↑
    Cells that are dividing have ↑ chance of mutation
    Epithelial tissues are capable of dividing & some continuously divide
    Epithelial tissues are on the front line
    Cancer = many mutations = over time
  11. 11WHERE IS EPITHELIAL TISSUEskin
    Entire GI tract
    ducts
    breast tissue
    respiratory
    reproductive
    urinary systems
  12. 12LABILE CELLSconstantly dividing
    Epithelial e.g. Skin, GIT, reproductive, urinary bladder, lining of exocrine ducts
  13. 13STABILE CELLS(QUISCENT)
    - Epithelial e.g. Liver, kidney, lung, pancreas
    - Smooth muscle cells, fibroblasts, endothelial cells
    - Able to divide when stimulated
    - Ability to divide decreases with age
  14. 14PERMANENT CELLSNON DIVIDING
    - Cardiac & skeletal myocytes, neurons
    - If we lose these cells to apoptosis we’ve permanently lost some functional reserve
    - Not going to see primary cancers here unless super rare cancer in a child (blast)
    - site of metastases
  15. 15DYSPLASIAGenotype and phenotype are abnormal.
    mutation
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  16. 16LEIOMYOMACell of origin: Smooth muscle
    Malignant version: Leiomyosarcoma
  17. 17LipomaCell of origin: adipocyte or fat cell
    Malignant version: Adiposarcoma or liposarcoma
  18. 18HemangiomaCell of origin: endothelial cell
    Malignant version: hemangiosarcoma
  19. 19Neurofibroma (fibroma)Fibroblasts (in this case around a peripheral nerve)
    Fibrosarcoma
  20. 20ChondromaCartilage (chondrocyte)
    Chondrosarcoma
  21. 21OsteomaBone cell (osteoblast/osteocyte)
    Osteosarcoma
  22. 22AdenomaGlandular (secretory) epithelial cell
    Adenocarcinoma
  23. 23CystadenomaGlandular (secretory) epithelial cell growing in a cystic pattern
    Cystadenocarcinoma
  24. 24PapillomaEpithelial cell growing with finger-like projections
    Papillocarcinoma or papillary carcinoma
  25. 25TeratomaGerm cell
    Testicular teratoma is always malignant. Rarely a female teratoma will accumulate more mutations & develop into a teratocarcinoma
  26. 26Most benign tumours are not life threatening, can you think of an example of when a benign tumour may be deadlyIn brain can be lethal if they cannot be completely surgically removed.
    If deep within the brain or close to major blood vessels will not be easily cut out. Slow growing tumours = more resistant to current treatments that target rapidly dividing cells.
  27. 27*LeukaemiaHaematopoietic cells
  28. 28*LymphomaLymphocytes, lymphoid tissue
  29. 29*MelanomaMelanocytes
  30. 30*GliomaGlial cells e.g. astrocytes
  31. 31*MesotheliomaMesothelial cell
  32. 32*Testicular tumoursTypically, germ cell or an embryonic germ cell precursor that mutated during embryogenesis
  33. 33-blastomaNever a normal cell to begin with
    typically childhood cancers
  34. 34MALIGNANT TUMORSCan metastasize
    Infiltrative/invasive growth pattern
    Heterogeneous (differing degrees of differentiation, proliferation & aggression)
    Some cells grow quickly and can outstrip the growth of their blood supply and thus undergoing necrosis in areas.
  35. 35BENIGN TUMOURSDo not metastasize
    Encapsulated
    Homogenous
    Well differentiated
    GENERALLY, slower growing but many exceptions
  36. 36Why are osteosarcomas more common than other sarcomas especially in young people?The bones of young people are still growing & are therefore at greater risk. We stop growing taller soon after puberty at which point the risk of osteosarcomas diminishes.
  37. 37Hypertrophycells increase in size
  38. 38Hyperplasiacells increase in number, divide more
    Metaplasia and Hyperplasia increase the risk of dysplasia and tumour formation
  39. 39Metaplasiachange from one normal well-differentiated cell type into a different normal well-differentiated cell type
    Metaplasia and Hyperplasia increase the risk of dysplasia and tumour formation
  40. 40What is the immature scar tissue called and what is it composed of?Granulation tissue which includes macrophages removing/eating cellular debris; fibroblasts secreting collagen protein (the future scar) and angiogenesis (new capillaries to supply oxygen, glucose and growth factors.
  41. 41What type of epithelium lines the conductive regions of the airways and what function(s) does it have?Simple ciliated (initially pseudo-stratified columnar, then columnar then cuboidal) with goblet cells producing mucous interspersed.
  42. 42Why does chronic inflammation increase the risk of cancer formation when it occurs in sites where we have epithelial cells?The epithelial cells will also respond to growth factors and repeatedly divide in a futile attempt to repair. This increased proliferation (cell division) of epithelial cells puts them at risk of making mistakes when copying their DNA and passing on mutations. CARCINOMAS
  43. 43WHAT IS CHORNIC INFLAMMATION?Occurs when a stimulus causing cellular injury remains/repeatedly applied or when our immune system attacks something that it shouldn’t. We get ongoing cellular injury, either caused by the stimulus or our body’s immune cells (lymphocytes) and repeated attempts at repair.
  44. 44what are 3 ways cancers can spread?1. Via lymph (lymphatic spread)
    2. Via blood (haematogenous)
    3. Via direct seeding e.g. floating in pleural or peritoneal fluid
  45. 45Why are carcinomas the most common adult cancer?Epithelial cells are either labile or stable. They are also exposed to stress. Anything that enters our body has to cross an epithelial barrier unless it is directly injected.
  46. 46Most common site of metastatic cancersThe lungs are the most commonly affected organ as all venous blood returns to them & cancers usually spread first in the lymphatic & venous systems
  47. 47Why is the liver a common site of metastatic or 2ndary cancers?Largest visceral + major metabolic organ = large amount of arterial blood
    Rich venous supply
    Rich lymphatic supply
    Everything we ingest goes to liver via portal venous system. ? not as important idk
  48. 48Brain and bone for 2ndary and metastatic cancersnot as common as lungs or liver
    once more hematogenous mets (cancer embolus's) go to areas with a lot of arterial blood (brain and bone)
  49. 49What imaging modalities used for horseshoe kidney and adult polycystic kidney disease?Planar imaging – Seen due to fat surrounding kidney (observe kidney size, shape, position)
    US/CT - Good but not functional
    CT-IVP or NM renogram- functional
    US – non radiation
  50. 50SIGNS + SYMPTOMS OF CANCERS OF THE KIDNEY, URETER, + BLADDERPatients with urinary cancers often present with blood in the urine, mild flank pain, an abdominal mass or obstruction.
  51. 51BEST IMAGING FOR CANCERS OF THE KIDNEY, URETERS, AND BLADDERUS best imaging as non-rad (paediatric pop)
    CT used for staging
  52. 52what is the difference between haematogenous/descending and urinary (ascending) infections of the kidneysDescending infections are likely to affect both kidneys diffusely and so lead to renal failure.
    Ascending infections are more likely to affect 1 kidney and usually only a segment of that kidney.
  53. 53Why are women more likely to get pyelonephritis (UTI)- shorter urethra
    - Absence of antibacterial properties found in prostatic fluid
    - hormonal changes affecting the adherence of bacteria to the mucosa, allowing it to spread along urinary tract
  54. 54why does glomerulonephritis affect both kidneys?These conditions are usually caused by blood-born stimuli and therefore affect all the glomeruli in both kidneys.
    Can affect entire kidney = reduction in function. As the function of both kidneys reduces, the clinical state of renal failure follows.
  55. 55What imaging is used for acute and chronic glomerulonephritis?Retrograde studies (unless infection present)
    Cystgram, urethrogram, urogram
    MCU – looking at reflux
    US used
  56. 56WHAT R SOME COMMON MANIFESTATIONS OF RENAL FAILURE?increased wastes
    increased RAAS
    Decreased activation of vitamin D
    Decreased response to PTH
    Acidosis
  57. 57what is RAASAngiotensin --> Angiotensin II is a potent vasoconstrictor leading to increased vascular tone/resistance.
    Aldosterone --> Aldosterone leads to the retention of salt and water thus increasing blood volume
  58. 58What may be the consequences of urinary stone formation?Pain (colic pain with peristaltic waves)
    Bleeding
    Obstruction of urine flow
    Predispose to infection
    Predispose to more stones
    dehydration
    staghorn stones ≈ metaplasia ≈ cancer
  59. 59Imaging: where are urinary stones most likely to form?PUJ
    VUJ
    Bony Pelvis
  60. 60What imaging is done for urinary stones?CT – dual energy, non-con to give composition of stone to aid urologist in treatment pathway.
    Plain Abdo- depending on stone make-up
    ESWL/ESRF - abbreviations to know
  61. 61How does atherosclerosis cause systemic hypertension?By reducing vessel contractility and increasing resistance to blood flow. Atherosclerosis can directly injure the kidney and increase RAAS activity which = greater hypertension from ↑ in blood volume + ↑vascular resistance
  62. 62How does systemic hypertension lead to atherosclerosis?Systemic Hypertension can lead to endothelial injury & the encouragement of turbulent blood flow
  63. 63What is the difference between angina and a heart attack?Both are caused by ischaemia but in angina blood is restored to the tissue before necrosis occurs.
  64. 64Explain the adaptations that smoking evokes (causes) in the conductive region of the airwaysCiliated epithelium of the conductive airways irritated = increased secretion of mucous and metaplasia to stratified squamous epithelium. = loss of the mucociliary escalator thus predisposing individuals towards obstruction from mucous, respiratory infections + injury from inhaled particulate.
  65. 65What is the most common malignancy diagnosed/found in the lungs?The most common malignancy found in the lungs is a secondary or metastatic cancer.
  66. 66RADIOGRAPHIC APPEARANCE OF PRIMARY LUNG CANCER VS SECONDARY LUNG CANCERPrimary: Solitary. Typically pulls hilar region (left normally higher than right)
    Secondary: Multiple nodules
  67. 67BronchopneumoniaOpportunistic infection of compromised individuals
    Common
  68. 68Lobar pneumoniabacteria of high virulence
    breathed in or travel to lungs via septicaemia
    Rare
  69. 69What are the possible outcomes of acute inflammation?Resolution, healing without scarring.
    Organisation, healing with scarring
    Chronic inflammation
  70. 70Radiographical appearance of broncho pneumoniaOriginates in upper airway and spreads to alveoli; appears as patchy appearance throughout lungs.
  71. 71Radiographical appearance of lobar pneumoniaNormal and infected alveolar in lobe; shows airbronchogram in lung (normal air-filled alveolar surrounded by infected)
  72. 72Radiographical appearance of viral pneumoniaInflammation of alveolar interstitium, appears as reticular pattern radiographically
  73. 73What aetiological agent is common to all COPD's Chronic Obstructive Airway DiseasesSmoking
  74. 74COPD's x4Chronic Obstructive Airways Diseases
    Asthma
    Chronic Bronchitis
    Bronchiectasis
    Emphysema
  75. 75What is emphysema?Irreversible and progressive destruction of alveolar walls
  76. 76Define bronchiectasis and explain how it developsirreversible, progressive dilatation of the bronchi and bronchioles caused by chronic necrotizing infections.
    The infections destroy the elastic tissue and lead to obstruction and scarring.
  77. 77What is the definition of chronic bronchitisChronic productive cough persisting for at least 3mnths and in 2 consecutive yrs
    Airway changes are similar to chronic asthma but the cause is more likely to be smoking and there is usually increased history of pulmonary infections
  78. 78What radiographic changes may occur as a result of COPDs; what adjustments in technique may be requiredIn emphysema: Barrel shaped chest in very thin patient. Overinflated lungs with flattened diaphragm. Bullae.
    Radiographically: Reduce exposure, usually 110-120 kVp/AEC (2 outer chambers) and use +/- buttons (not fat/skinny) to reduce mAs by 2 (50%).
  79. 79What are the 2 major risk factors for the development of venous thrombiStasis & Hypercoagulability
  80. 80Superficial vein thrombiSuperficial venous thrombi do not usually embolise.
    Superficial thrombi frequently give symptoms including pain and swelling.
  81. 81Deep vein thrombi (DVT)frequently embolize.
    may be asymptomatic or give mild symptoms like swelling distal to the clot.
    often very large and not strongly attached to the wall of the vein and so they can embolise as a very large mass causing catastrophic outcomes.
  82. 82A DVT that forms an embolus is likely to to travel to where?Femoral or Iliac vein > Inferior vena cava > Right atria -> right ventricle >Pulmonary arteries >LUNGS
  83. 83What is the possible radiographic appearance of a PE? (pulmonary embolism?)Westermark sign: Increased blood flow to unaffected side & reduced blood flow to affected side so affected side looks more prominent, it has reduced blood flow due to the clot
  84. 84causes of left ventricular heart failureValve disease
    IHD
    Systemic hypertension
  85. 85causes of right ventricular heart failureLeft-sided heart failure
    Pulmonary hypertension caused by pulmonary disorders like emboli and COPDs like emphysema
  86. 86Forward effects of heart failurefall in blood pressure = RAAS = sodium and water reabsorption (aldo) + increasing blood volume = (angio) vasoconstriction = increased vascular resistance
  87. 87RAAS acronymrenin-angiotensin-aldosterone system
  88. 88Backward effects of left ventricular heart failure- Pulmonary congestion = ↑hydrostatic pressure = oedema = dyspnoea (difficulty breathing) wen laying down for example.
    - Pulmonary gongestion = ↑resistance to blood flow entering lungs = greater workload on R Ventricle = hypertrophy and failure of R ventricle
  89. 89Backward effects of right ventricular heart failurecongestion + peripheral oedema with cyanosis.
    Distended jugular veins, oedema of the legs + ascites.
    Organs that contribute alot of venous blood to the vena cava will experience congestion and injury inc. necrosis
  90. 90Radiographic appearance of Left-Sided Heart FailureLeft ventricle enlarged (boot-shaped)
    Interstitial oedema (bat’s wing)
    Pleural effusions – blunt costophrenic angles
  91. 91Radiographic appearance of Right-Sided Heart FailureRight ventricle & atria enlarged (round ball shaped)
    Enlarged vena cava & right mediastinum
  92. 92Explain the bimodal age distribution of osteosarcoma. 75% happen in young ppl. WHy?Bone is actively growing in young people and most osteosarcomas occur in the actively growing epiphyseal plates. Increased proliferation= cancer risk factor.
    elderly people = frequently suffer from Paget’s disease + bone infarcts.
  93. 93Why is the bone so commonly affected by metastases?Bone very vascular = arterial metastases easily distributed to bone + it is a good site for tumor cells to become trapped. Bone metastases found in 25%+ of ppl who die from cancer and 75% of ppl who die from breast cancer.
    there r other factors that attract certain cancers to the bones.
  94. 94Radiographic signs and modalities for osteosarcomaSunburst sign (Codmans Triangle) from periosteal lifting
    Plain radiography for diagnosis, MR for initial staging (assessing interosseous tumor size) then CT for further staging and during treatment.
  95. 95What are the radiographic signs for multiple myeloma Radiographic modalitiesMultiple, small, punched-out, round lesions within the skull, spine, and pelvis.
    Diagnosis is via blood (pathology) however imaging is undertaken with MRI (gold-standard) for detection of bone marrow involvement.
    Planar imaging – A typical skeletal survey
  96. 96What are 2 complications of Paget's disease of bone and why might they occurpathologic fractures (weak bone less resistant to external forces)
    narrowing of foramina = obstructs CSF flow -> hydrocephalus OR = compression of cranial nerves ->deafness or visual disturbances
  97. 97How does Paget's Disease change radiographically?The early phase features osteolytic (lucent) regions which are later followed by coarsened trabeculae and bony enlargement. Sclerotic changes occur much later in the disease process.
  98. 98osteoporosis risk factorsA low starting peak bone mass which is determined by genes, nutrition + physical activity during development. Once peak bone mass is reached bone is lost through ageing, reduced physical activity, sarcopenia, amenorrhea and loss of oestrogenic activity after the menopause
  99. 99what are the consequences of renal failure on the skeletal system?In failure, the kidney may not be able to synthesize the active metabolite of vitamin D = the gut cannot absorb calcium from food, which results in low levels of serum/blood calcium. (under mineralization of bone & soft tissue calcification)
  100. 100Under what circumstances would acute osteomyelitis become chronic?chronic inflamm = stimulus remains
    bone fragments may become necrotic as their blood supply is compromised by the infection. These dead pieces of bone act like foreign bodies (like a splinter) and keep the inflammation going.
  101. 101What is the radiographic appearance of osteomyelitisThe earliest changes are seen in adjacent soft tissues +/- muscle outlines with swelling and loss or blurring of normal fat planes. An effusion may be seen in an adjacent joint.
    Regional osteopenia, periosteal reactions, loss of trabecular bone
  102. 102What is a pathologic fracture & what are some common causesA # that occurs in a bone already affected by disease + requires less force to break.
    osteoporosis, osteomalacia, Paget’s, chronic renal failure, primary & secondary tumours, osteomyelitis and joint diseases.
  103. 103the radiographic healing timeline for fractures1. The inflammatory phase
    (hematoma, immediately after injury)
    2. The repairing phase
    (cartilage + tissue develops over 2/3wks)
    3. Bone remodeling
    (final phase)
  104. 104Why is scaphoid imaging undertaken 10-14 days post injuryRepairing phase – looking for callus formation
  105. 105Goutcommon systemic metabolic disorder
    pain and inflammation
    ↑ incidence with age
    big toe in men
    rare in wmn b4 menopause then in hands
  106. 106Osteoarthritis (OA)Wear & tear resulting in loss of cartilage.
    little inflammation but swelling = pain
    tends to affect weight bearing joints
    most likely to occur in elderly, overweight or netballers, AFL + runners
  107. 107Rheumatoid arthritis (RA)Autoimmune destruction of joints that may affect any synovial joint in the body
    irreversible joint deformation
    chronic + systemic inflammation
    Affects women more than men
    typically 1st diagnosed middle age
  108. 108radiographic signs of osteoarthritisSoft tissue swelling
    Loss of joint space (weight-bearing joints)
    Osteophytic lipping
    Sclerotic changes
  109. 109radiographic signs of rheumatoid arthritisSoft tissue swelling
    Calcifications at joint
    Changes in joint alignment
    Bone erosions
  110. 110Why only some of the secondary deposits in the liver are pigmented?The pigment is melanin, the well-differentiated secondaries still produce melanin while the poorly differentiated ones do not so appear pale. Cancers show heterogeneity
  111. 111Is the gastrointestinal site considered to be a sterile site?No, from mouth to anus it is populated with a variety of organisms that are essential for the maintenance of health.
  112. 112Stratified squamous epithelium can be found in the... (x3)oral cavity, esophagus, + Anus
  113. 113Simple columnar epithelium is found in the... (x3)Stomach, small and large intestine
  114. 114Small Intestine epithelium:The surface of the small intestine has folds of mucosae composed of many villi each of which is lined by simple columnar epithelium with microvilli
  115. 115Oral-pharyngeal Cancer - Risk Factors - NomenclatureAlcohol, Smoking, HPV
    Usually starts with leukoplakia or adenoma & forms SCC or adenocarcinoma
  116. 116Upper oesophagus - Risk Factors - NomenclatureAlcohol, Smoking, HPV
    SCC
  117. 117Lower oesophagus - Risk Factors - NomenclatureChronic gastric reflux
    Adenocarcinoma
  118. 118Stomach - Risk Factors - NomenclatureChronic gastritis & ulcers usually caused by H. pylori infection, chronic use of NSAIDs, alcohol, smoking
    Adenoma, adenocarcinoma
  119. 119Colon - Risk Factors - NomenclatureGenetics, Smoking, Chronic inflammatory bowel diseases, diet low in fibre & high in fat
    Adenoma “polyp”
    adenocarcinoma
  120. 120Gall Bladder - Risk Factors - NomenclatureChronic inflammation usually from gall stones
    Adenocarcinoma
    SCC
  121. 121Pancreas - Risk Factors - NomenclatureChronic inflammation caused by stones, alcohol
    Adenocarcinoma usually from exocrine epithelial cell
  122. 122Liver - Risk Factors - NomenclatureCirrhosis caused by alcohol, iron-overload, infections, autoimmune disease, biliary disease
    Hepatocellular carcinoma
  123. 123What is the COMMON procedure for diagnosis of bowel cancerColonoscopy
  124. 124What are the main risk factors for the development of gastric ulcers and gastritis?Infection with H. pylori, alcohol, smoking, chronic use of NSAIDs
  125. 125What are the possible complications associated with gastric ulcers?Cancer, chronic blood loss leading to anaemia, acute massive blood loss, scarring/obstruction, perforation & pain
  126. 126What is a diverticulum?Blind-ended sack or out-pouch
  127. 127Congenital diverticulaAppendix
    Meckel’s diverticulum
  128. 128How can diverticulosis be caused by low fiber diets?When stools lack bulk, the muscle layers within the walls of the colon have to contract with more force to push the stool through. In response the muscle hypertrophies and the overlying tissues can be pushed between the muscle fibres forming pouches.
  129. 129Where is Zenker’s Diverticulum locatedOesphagus – A Zenker’s diverticulum is a pouch that forms in the throat at the very beginning of the digestive tract just above the upper esophageal sphincter (UES).
  130. 130Whether natural, congenital or acquired , diverticula are susceptible to:Material travelling along the tube can become trapped leading to stone formation, inflammation & pain. If the wall ruptures -> peritonitis and septicemia. If the inflammation becomes chronic, scar tissue can cause adhesions and fistulas to form between loops of bowel & other organs.
  131. 131What are the possible complications of chronic inflammatory bowel diseases?Cancer, blood loss, malabsorption, pain & bloating, scarring, adhesions & fistula formation
  132. 132What complications may occur from having gall stones?Pain; chronic inflammation increasing the risk or cancer; obstruction leading to malabsorption, jaundice, cirrhosis & pancreatitis.
  133. 133What is an ERCPEndoscopic retrograde cholangiopancreatography (ERCP) is a procedure that combines upper gastrointestinal (GI) endoscopy and x-rays to treat problems of the bile and pancreatic ducts.
  134. 134What is the difference between a cholecystectomy and a lap chole?A cholecystectomy is a surgical procedure to remove your gallbladder, whereas a lap chole is the same procedure however undertaken laparoscopically.
  135. 135What is cirrhosis and what are the common causes of cirrhosisChronic inflammation of the liver resulting in complete disruption of the The normal lobular structure = loss of function.
    Common causes = chronic alcohol intake, hepatitis, autoimmune disease, iron-overload (hemochromatosis), biliary disease, heart failure
  136. 136How do the effects of liver failure worsen the effects of cirrhosis?Cirrhosis > portal hypertension > congestion > increased hydrostatic pressure > oedema & ascites.
    Liver failure > decreased synthesis of plasma proteins > reduced colloidal osmotic pressure > oedema & ascites.
  137. 137What is the best imaging method for diagnosis of liver cancers?CT – with contrast.
  138. 138Most pancreatic cancers are derived from cells of the exocrine pancreas and 70% of these occur at the head of the pancreas where they cause what signs and symptoms?Pain, obstruction, malabsorption, autodigestion & enzymatic fat necrosis
  139. 139Type 1 diabetes diabetes mellitusautoimmune disease
    targets beta cells
    present in early childhood
    normal weight or underweight
    hyperglycemia = acute emergency
    insulin replacement therapy
  140. 140Type 2 Diabetesgenetic component can be overcome by environmental interventions
    overweight or inactive
    initially insulin insensitivity
    initially reversible with lifestyle changes
    vague symptoms- lethargy
    lose weight and exercise + {diet GI}
  141. 141What are some of the common consequences of chronic hyperglycaemia typically observed in diabetes mellitus?- Atherosclerosis + arteriosclerosis = thrombus, embolus + aneurysm
    peripheral vascular disease
    - ↓ blood supply or SOL (aneurysm) = atrophy of the brain
    - Ischaemic heart disease (angina, MI, heart failure)
  142. 142List some examples of SOLsTumours, haematomas, oedema/swelling (diffuse or localised), abscesses, hemorrhage, hydrocephalus, aneurysm, contrecoup injury etc.
  143. 143What is an SOL? (acronym)space-occupying lesions
  144. 144What determines whether atrophy or brain herniation occurs in response to a SOL?Generally the speed of the accumulation, if something accumulates gradually, the brain has time to adapt through atrophy whereas a fast accumulation will result in herniation.
  145. 145List some causes of brain atrophy.Senile (age)
    Alcohol/drug abuse
    Smoking
    Hypertension
    SOL's
    Diabetes
    Vascular Diseases
  146. 146What are burr holes?Burr holes are small holes that a Physician/Paramedic makes in the skull. Burr holes are used to help relieve pressure on the brain when fluid, such as blood, builds up and starts to compress brain tissue
  147. 147Why are space-occupying lesions (SOLs) so dangerous?If something is introduced slowly the brain compensates by reducing the amount of CSF, blood and by undergoing atrophy but these measures are limited. Once further adaptation is impossible, intracranial pressure will rise and the brain herniates.
  148. 148Epidural Haemorrhageoften result of rupture of dural arteries
    trauma to temporal bone = middle meningeal artery involved
    often high arterial pressure = rapid accumulation of blood/haematoma between the skull and dura
    ↑ICP = herniation + death
  149. 149Subdural Hematomasoften result of tearing of the bridging veins between dura mater + arachnoid layers
    displacement of the skull = tears
    elderly + those w/ brain atrophy @risk
    progress slowly = vague symptoms
    Large tears can = herniation + death
  150. 150What is the best imaging method for a SAHCT
  151. 1514 ways in which the brain and meninges may become infected1. Trauma/surgery including lumber puncture
    2. Through blood
    3. Extension from local sites (ears, eyes, sinuses etc.)
    4. Via the peripheral nervous system
  152. 152What is the anatomical difference between encephalitis and meningitis?Encephalitis = inflammation of the brain tissue itself
    Meningitis = inflammation of the meninges
    Leptomeningitis = Subarachnoid & pia
    Patchymeningitis = Dura mater
  153. 153Is meningioma an example of a benign or malignant tumour?Benign but being in the brain, they can still be lethal
  154. 154Which is the most common malignant tumour of the CNS in adults?In adults 50% metastatic carcinomas or melanomas & 50% are glioma/glioblastoma
    In children 1st = leukaemia 2nd =
    astrocytoma
  155. 155What is the best imaging method for diagnosis of brain cancers?MRI - may be of the brain, spinal cord, or both, depending on the type of tumour suspected. Better imaging delineation of tissues than CT
  156. 156Why is the brain often affected by metastatic cancer?The brain is very metabolically active and therefore receives a lot of arterial blood.
  157. 157What is a 'stroke'?Necrosis occurring in the brain from ischemia or hemorrhage
  158. 158What are the main fixed and modifiable risk factors predisposing towards atherosclerosis?↑ age + genetic predisposition
    male gender (menopause for females)
    some infections + uncontrolled diabetes
    smoking
    hypertension, reduced HDL but increased LDL, visceral adiposity
  159. 159How does imaging assist with determining how recent an intercranial bleed has occurred?initial evaluation of suspected stroke = noncon CT head. In the first 6 hours of a bleed, early ischemic changes appear as loss of gray–white differentiation, and on imaging acute blood is hyperdense (measured by Hounsfield units (HU)). The differentiation (HU) of blood changes over time
  160. 160What is cryptorchidism; what problems may arise from it?Undescended testes, which can be part of testicular dysgenesis syndrome. Undescended testes is more prone to trauma, cancer, infertility, and can cause psychological stress(prosthesis can overcome mass deficit from absence of testis).
  161. 161Penis Cancer - Nomenclature - Risk F- Papilloma (B) + SCC (M)
    - HPV + poor hygiene
  162. 162Prostate Cancer - Nomenclature - Risk F- Adenoma (B) + Adenocarcinoma (M)
    - genetics, ethnicity, environmental factors
    - most common cancer in males
  163. 163Transformation Zone (Cervix) Cancer - Nomenclature - Risk Factors- Papilloma, adenoma (B)
    SCC (M)
    - HPV, smoking, immune depletion
  164. 164Uterus (myometrium) Cancers - Nomenclature- Leiomyoma (B) Leiomyosarcoma (M)
    - sarcomas very rare and common benign version doesn't become malignant
  165. 165Uterus (endometrium) Cancers - Nomenclature - Risk Factors- Adenoma (B) Adenocarcinoma (M)
    - ↑ age, obesity, high estrogen, ethnicity, diabetes II
  166. 166Ovary (germ cell) Cancers - Nomenclature- Teratoma (B) Teratocarcinoma (M)
    - carcinoma can occur within the teratoma
  167. 167Ovary (surface epithelium) Cancers - Nomenclature - Risk Factors- Cystadenoma (B), Cystadenocarcinoma (M)
    - ovulation, obesity, genetics, HRT, fertility treatment, ↑age
  168. 168Breast Cancer - Nomenclature - Risk Factors- Fibroadenoma (B), Adenocarcinoma (M)
    - Female, ↑age, breast density, obesity, genetics, radiation, ↑alcohol consumption
  169. 169What are the preferred imaging method(s) for tumours of the reproductive system?US is imaging method of choice – either thru abdominal wall or transvaginally.
    CT used in Staging.
    MRI good for soft tissue
    PET/CT used to ascertain response to chemo following treatment
    Teratoma Testes – US is gold standard
  170. 170Which STI's often cause PID? (Pelvic Inflammatory Disease)Gonorrhoea & Chlamydia
  171. 171What conditions may result from PID? (Pelvic Inflammatory Disease)Ectopic pregnancy and infertility.
    Inflammation walls off the infected ovaries forming abscesses, these structures can rupture and cause peritonitis.
    The scarring can lead to adhesions and obstruction of other organs
  172. 172What imaging method is used in PID? (Pelvic Inflammatory Disease)US is best imaging method
    HSG used in both 1o and 2o infertility – 30% increase in pregnancy following HSG (and tube flush)
  173. 173How does PID predispose individuals to ectopic pregnancy?Infection = scarring of the fallopian tubes = inhibit/impair the transit of sperm/ova.
  174. 174What common conditions increase the likelihood of ectopic pregnancy?PID
    endometriosis
    leiomyoma.
    Inflammation in the GIT can also = adhesions and obstruction.
  175. 175What is Endometriosis?Endometrial glands present outside of the endometrium, they grow bc of ↑ oestrogen, differentiate in response to progesterone and bleed when ↓hormone levels. Bc of their location, the bloody material is trapped = pain and the body walls the area off in granulation tissue
  176. 176Would you expect the condition to get better or worse during pregnancy, why?Endometriosis often improve during pregnancy due to the loss of the menstrual cycle
  177. 177What are the preferred imaging method(s) for endo?laparoscopy = gold standard for diagnosis
    ↑ US + MRI to evaluate deep disease (90%+)

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Fichas sobre 020, creado por Annika Muller el 06/06/2023.
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Annika Muller
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