Integrated PBL ovarian cancer – Flashcards
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Most prevalent cancer in women
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Breast
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3 types of ovarian cancer
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1 epithelium 2 germ cell 3 stroma
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3 types of epithelium cancer
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1 serous - columnar ep filled with serous fluid. Usually bilateral. P53 2 mucinous - large cystic masses, cervical, 3 endometrioid - glands, that resemble endometrium. 15-20% co exists with endometriosis
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Likely diagnosis=
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Endometrioid - Not linked to endometriosis as too old - low grade - frequent mutations in PTEN, KRAS, Beta- catenin
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Endometriosis info
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Presents of uterine glands outside of the uterus. 25/30 years Painful sex, periods, chronic pelvic pain Often goes to ovaries and uterine ligaments -> subfertility from ectopic estrogen release
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Endometriosis management (+ surgical)
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- COC - GnHR agonist - mirena - bilateral oopherectomy - Ovarian cystectomy - excise endometriosis
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Risk factors for ovarian cancer
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Age Smoking Obesity Braca1/2 Family hx Endometriosis
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Ovarian cancer presentation (+DDx)
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Elderly Vague symptoms 3-4 months Undiagnosed untill wide spread Pressure symptoms: (similar to IBS in younger pt). Dyspepsia e.g bloating, early satiety, urinary frequency, pelvic pain. DDx: peptic ulcer, reflux, gastric cancer. Try antacids e.g. Alkaline bile salts and alginates
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Ovarian cancer presentation
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Cachexia Abdo acites - fluid full of tumor cells Abdo/pelvic mass Metastatic lesions
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What test would you do to find out if it's ovarian cancer?
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Abdo/ trans vag ultrasound CA125 (>35Ul/ml) Menopausal status
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CA125 AKA mucin 16
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Cancer antigen / carbohydrate antigen Circulates in blood = blood test Used to diagnose (not alone) and monitor 85% accurate; 50% in early stage Can also be raised I'm PID, fibroids, endometriosis, cirrhosis and pregnancy
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Braca1
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Human protein that helps maintain DNA integrity by repairing damaged DNA
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Omentectomy, what is it and why is it done?
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Removes the fatty lay of tissue in the upper abdomen - the omentum. Small clusters of ovaian cancer are shed and implant onto the peritoneal surface, forming number out nodules. No barriers into abdo.
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Risk of malignancy index (RMI). Calculated in this case from?
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Used to see the likelihood a mass/cyst is malignant Calculated from 1) transvag/abdo US 2) menopausal status 3) CA125 >35Ul/ml Score exceeding 200 is significant to malignancy
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Management of ovarian cancer
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Staging at surgery Exploratory laparoscopy Total abdominal hysterectomy - bilateral salpingo- oopherectomy Explore for mets
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FIGO (federation of gynaecology and obstetrics) staging of ovarian cancer
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1 one or both ovaries 2 one or both ovaries + pelvis extension 3 one or both ovaries + abdo extension 4 one or both ovaries + distal mets
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Non surgical treatment of ovarian cancer at different stages
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Stage 1 low risk - no chem Stage 1 high risk - cisplatin Stage 2-4 cisplatin + paclitaxcel (chemo- alkylating agents. Platinum bases, covalent,y binds to DNA, cross linking strands) Recurrence - sign of doubling CA125 conc Cause of death - malignancies in bowel at lots of diff points
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Paclitaxel
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Natural taxane. Prevents depolymerisation of cellular microtubules which result in DNA, RNA and protein synthesis inhibition
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CANCER: what is it?
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Uncontrollable growth/division of cells; normally controlled by check points internally and growth factors externally Genetic and environmental hits Affecting tissue/organ locally then proceed to spread around body
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CANCER: environmental causes
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Radiation Infection Carcinogenic chemicals
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CANCER: molecular causes
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Activated oncogene or mutated tumor suppressor gene (x2) Types of mutation: insertion, deletion, missense (diff a'a'), nonsense (premature stop), chromosomal translocation
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Neoplasia/naoplasm:
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New growth
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Most commonly diagnoses cancers:
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Breast Lung Prostate Bowel
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Highest rates of cancer death:
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Lung prostate/breast Bowel
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How does cancer kill?
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Compress local structures Block vital structures Rupture & bleed Cachexia (greedy for nutrients)
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Cancer screening:
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Done on general population to find people at high risk and catch early/asymptomatic = save lives
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Screening sensitivity is
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The possibility than individual with the disease is screened positive
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Screening specificity:
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The probability that an individual without the disease is screened negative
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How are grade and stage assessed?
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Imaging (CT, MRI, XR). *TNM* T umor size N umber M ets histology
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Radio therapy
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Used if cancer is local and early stage Works by damaging DNA through ionising DNA atoms or inducing free radicle formation
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Chemotherapy
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If cancer has systemic spread Last chance cure or given as an adjunctive to kill and residual cancer cells Spreads around the body and acts on normal cells as well - given in cycles (nb also reduces the risk of resistance)
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Gestational diabetes mellitus
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Pregnancy is an anti-insulin state - require high levels of glucose for fetal growth and increased material metabolism 3% of pregnancies Increased insulin resistance -> high blood glucose
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What hormones in pregnancy affect insulin
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Human placental hormone Progesterone (Estrogen)
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Pathophysiology of GDM
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Increased cortisol/ HPL hormone interact with insulin receptors -> increased insulin resistance (+preg hormones) = ++ fat metabolism & ++++ maternal blood glucose = ++++ fetal blood glucose -> increased fetal insulin = anabolism, glycogen synthesis, lipogenesis = macrosoma
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NICE fasting glucose levels
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7mmol/L Or 7.8 2hrs after glucose load (glucose tolerance test)
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Maternal complications of GDM:
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Infections Worse cardiac function Worse renal function Retinopathy Misscarrage Still birth Future T2DM Caesarian delivery more likely
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Fetal complications of GDM:
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Neonatal hypoglycemia Neonatal respiratory distress syndrome Shoulder dystocia Fat baby Neural/cardiac tube defects
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Tx of GDM:
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Weightloss, exercise Metformin Insulin
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Types of fertility aids
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In vitro fertilisation +- Intra cytoplasmic sperm injection Intra uterine insemination
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IVF procedure
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1 ovarian stimulation with FSH and hCG 2 egg collection with US help 3 egg + sperm (can be injected ICSI) 4 grow for 2 days 5 transfer into uterine cavity + progesterone or hCG given 6 check for preg 2/52
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Who gets IVF ?
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Infertile woman under 40 - 3 cycle Infertile woman over 40 - 1 cycle
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Complications of IVF
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Multiple pregnancies Hyper stimulation Ectopic preg Complications of egg and sperm retrieval/implantation
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Heart failure epidemiology
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1-2% of the population Average age 75 Significant mortality
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Heart failure compensatory mechanisms
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Frank statins law - increased filling volume for re stretch Hypertrophy (ventricular remodelling Neurohormonal - RAAS, norad, ANP eventually fails and becomes pathological
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Forward heart failure
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Decreased cardiac output and tissue perfusion
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Backward heart failure
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Pooling in the venous system which can cause pulmonary/peripheral oedema
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Left sided heart failure (forwards/backwards)
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Forwards: Poor peripheral pulse Renal failure Confusion Backwards: -lungs Pulmonary oedema Frothy cough PND Orthopnea - Right heart failure
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Right heart failure
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Forward? Backwards: - systemic congestion Peripheral oedema Pleural effusion Kidney failure Confusion Paroxysmal nocturnal dyspnoea - Portal congestion Hepatosplenomegaly - cardiac crisis Ascites
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HF investigations
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Hx & Ex Previous MI -> echo No previous MI -> Brain natriuretic peptide -> if high, echo ECG CXR BNP released from stretched cardio myocytes
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CA125 & HF
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CA125 seen to be raised in HF (moderate - severe) Correlation with BNP levels High CA125 = predictive of mortality/prognostic
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Pre load:
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Tension in myocytes at the end of diastole
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Afterload:
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The stress of the myocytes during systole/ejection
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Hydrostatic pressure
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The intra vascular pressure forcing fluid out into interstitial space. Higher at arteriole end
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Oncotic pressure
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Pressure exerted by intra vascular proteins drawing solutes and fluid back into the blood
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Ejection fraction =
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Stroke volume x EDV Plot these against each other = frank stalins law that falls into la place's law
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Frank stalins law
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states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully
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La places law
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wall tension (T) is proportionate to the pressure (P) times radius (r) for thin-walled spheres or cylinders
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Left ventricular hypertrophy caused by...
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Because the ventricle is struggling to eject the blood contained within, the ventricle dilates, increasing its end-diastolic volume. As heart is weak struggles to keep up with la places law. increased wall tension in the dilated ventricle stimulates growth in the heart dilation of the chambers leads to collagen damage, including fibrosis and slipping of the muscle fibers Continual sympathetic activation leads to desensitization of adrenergic receptors. ++ angiotensin II = increase extra cellular fluid and peripheral resistance Thickness causes decreased EDV and back up to right = cor pulmonale
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What is a randomised control trial
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Interventional study (oppose to observational e.g. Cohort, case control) Identity efficacy of intervention by: - administering tx to one group non to a control group - has a measurable end point - does the intervention make a difference to the end point?
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What kind of bias can be seen in this kind of study
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Selection bias
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How can you reduce selection bias?
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Complete randomisation of groups
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Why do we have overseas trial committees
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To assess and monitor progression Access data Decide whether the trial should be stopped early -> strong efficacy, high mortality, unethical
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On treatment analysis
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Analysis includes only participants that took the treatment
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Intention to treat analysis
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Analysis of all patients who were intended to take the treatment, even if they have dropped out.
