Pathology Flashcards

Question

Wound healing

Answer 1

INFLAMMATORY - immediate until 2-3days - local vasoconstriction - thrombus formation and fibrin mesh - platelets line damaged endothelium, release ADP/platelet derived growth factor/cytokines/histamine/serotonin/prostaglandins - ADP causes thrombus aggregation - cytokines attract lymphocytes and macrophages - histamine causes increased capillary permeability PROLIFERATIVE - day 3-week 3 - fibroblast activity, producing collagen type 3 and ground substance using vitC - angiogenesis, re-epithelialisation of wound surface, formulation of granulation tissue REMODELLING - maturation of collagen from type 3 to type 1 - decrease wound vascularity and wound contraction

Answer 2

Primary intention - NOT acute inflammatory reaction - fibin-rich haematoma, then neutrophils at margin of wound within 24hrs and move towards clot - epithelial cells move from wound edge and deposite basement membrane in 24-48hr - macrophages replace neutrophils at day3 - granulation tissue invasion - neovascularisation maximal at day5 - fibroblast proliferation at week 2 - scar devoid of inflammatory cells by week4 Secondary intention - where wound edges not opposed, heals from bottom upwards - by granulation, contraction, epithelialisation - requires myofibroblasts

Answer 3

At week 1, skin is 10% strength vs un-wounded, at 3months is 80% Growth factors involved - EGF, TGF, VEGF, PDGF, FGF, IGF Promoted by good blood supply, vitamin C, zinc, protein, insulin, UV light Inhibited by glucocorticoids, infection, extreme temperatures

Answer 4

Matures over 2 years - immature is pink, hard, raised, itchy Mature - atrophic / hypertrophic (excess scar tissue not extending beyond boundaries of original wound, due to granulation tissue) / keloid (excess scar tissue beyond boundaries, due to persistant type 3 collagen) Treatment of keloid/hypertrophic: - excision of scar, laser, steroid injection, pressure, silicon gel sheeting, radiation, vitaminE Reduce surgical scarring: monofilament sutures, removal of sutures at day3-5, tensionless suturing, fine sutures and steri-strips, subcuticular technique

Answer 5

= abnormal, uncontrolled, uncoordinated growth, which persists after cessation of stimuli Malignant neoplasia = invasion, rapid growth, metastases, poor differentiation

Answer 6

Carcinoma - epithelial origin Sarcoma - mesenchymal origin Teratoma - neoplasm with multiple germ cell layers (ovarian is benign, testicular is malignant) Choristoma - non-malignant mass of normal tissue in ectopic location Hamartoma - non-malignant mass of disorganised but mature tissue indigenous to site

Answer 7

Gompertzian - in early stages exponential growth, but slows as grows Majority of growth occurs before clinically detectable Radiologically needs to have - 10mm size, 10^9 cells 2^n = number of cells produced after n generations of division 2^45 is usually fatal (after 45 generations), but there is also concurrent tumour loss

Answer 8

* Establishment of autonomous lineage - resisting signals that inhibit growth, acquisition of independence from signal-stimulating growth, using oncogenes * Obtaining immortality - normal cells have finite no of divisions (40-60) determined by progressive shortening of telomere, but ca cells do not undergo telomeric shortening * Evasion of apoptosis (p53) * Angiogenic competence * Ability to invade * Ability to disseminate and implant * Evading detection and elimination * Genomic instability

Answer 9

Extent to which neoplastic cells resemble normal cells Benign = well differentiated (morphologically and functionally similar to mature normal cells) Anaplasia = lack of differentiation High-grade tumour = poorly differentiaed

Answer 10

ONLY cancers that can't are BCCs and gliomas LYMPHATIC - most carcinomas, eg endometrial, cervical BLOOD - most sarcomas, renal cell ca, choriocarcinoma BODY CAVITY - ovarian ca, breast ca, pseudomyxoma peritonei

Answer 11

Inherited syndromes (all autosomal dominant) - retinoblastoma, MEN, neurofibromatosis 1+2, von Hippel-Lau syndrome Inherited autosomal recessive syndromes of defective DNA repair - xeroderma pigmentosum, Fanconi's anaemia Familial cancers - breast, ovarian, HNPCC

Answer 12

BRCA-1 - on long arm of chrom 17 - 80% lifetime risk breast ca, 50% ovarian ca BRCA-2 - on long arm of chrom 13 - 45% breast ca, 25% ovarian ca - also predisposes to prostate and pancreatic ca Other cancer genes - HNPCC, RB (retinoblastoma), p16 (melanoma)

Answer 13

Hereditary non-polyposis colonic cancer, aka Lynch syndrome Autosomal dominant inheritance 5 genes 80% lifetime risk colonic ca, 30-50% endometrial ca, 10% ovarian ca

Answer 14

Chronic inflammation - crohn's, UC Pre-cancerous conditions - leukoplakia, cervical dysplasia, pernicious anaemia Carcinogenic agents - asbestos - mesothelioma, GI tract ca - diethylstilbestrol (synthetic oestrogen) - vaginal clear cell ca - high fat/low fibre - colonic ca - aniline dye - bladder ca - HPV 16/18 - cervical ca - anabolic steroids or HepB - hepatocellular ca

Answer 15

hCG - trophoblastic (choriocarcinoma), non-seminomatous germ cell tumour Calcitonin - medullary ca of thyroid Catecholamines - phaeochromocytoma AFP - hepatocellular ca, non-seminomatous germ cell tumour CEA (carcinoembryonic antigen) - colonic, pancreatic, gastric, lung PSA - prostate Immunoglobulins - multiple myeloma Ca125 - ovarian ca, primary peritoneal ca Ca19-9 - colonic, pancreatic Ca15-3 - breast

Answer 16

Symptom complexes in ca patients - not due to spread of ca but due to endocrine function or immunological response Cushing's - small cell lung, pancreatic SIADH - small cell lung, intracranial Carcinoid syndrome - bronchial adenoma, pancreatic, gastric Polycythaemia - renal cell, cerebellar haemangioma, hepatocellular ca, fibroid Myasthenia - bronchogenic ca Acanthosis nigrans - lung, uterine ca Dermatomyositis - bronchogenic, breast Trousseau's - pancreatic

Answer 17

Transcription factor that regulates cell cycle - activates DNA repair, initiates apoptosis Tumour suppressor On chrom17 Li-Fraumeni syndrome - AD disorder linked to p53 mutation, 25x greater chance of malignancy by age 50

Answer 18

Anti-platelet - prostacyclin - NO - ADPase Anti-coagulant - thrombomodulin - anti-thrombin III - tissue factor pathway inhibitor Fibrinolytic - tissue-type plasminogen activator (t-PA)

Answer 19

Pro-platelet - von Willebrand factor Pro-coagulant - thromboplastin Anti-fibrinolytic - plasminogen activator inhibitor

Answer 20

Platelets contain fibrinogen, fibronectin, PDGF, histamine, serotonin, factor V and VIII Platelet aggregation induced by vWF, ADP, thromboxane A2 PRIMARY HAEMOSTATIC PLUG - platelet aggregation, reversible SECONDARY HAEMOSTATIC PLUG - thrombin binds to platelets, irreversible FIBRIN BINDS TO PLUG - ADP mediated activation of platelets, causes changes to their surface receptor for fibrinogen, so fibrin can form and bind to the plug

Answer 21

INTRINSIC: - from contact activation (surface damage) - using factors XII XI IX VIII (12, 11, 9, 8) - both activate factor X (test using PTT - play table tennis inside, 25-29s) EXTRINSIC: - from tissue factor (III) released in trauma and inflammation - using factors III (TF), VII (3 +7 = 10) - both activate factor X (test using PT - play tennis outside, 12s) COMMON: - activated factor X, causes prothrombin -> thrombin (II) (Ca and factor V (co-factor) are needed here) - which then cleaves fibrinogen -> fibrin (I) (factors 2, 7, 9, 10 are vitamin K dependent)

Answer 22

Protein C - physiological anticoagulant - degrades factor Va and VIIIa - activated by thrombin Protein S - anticoagulant - cofactor with activated protein C for the degradation of factor Va and VIIIa - binds to complement factors

Answer 23

Variant of factor V that cannot be inactivated by protein C -> hypercoagulant state Autosomal dominant 5% prevalence in caucasians 30% of patients with DVT or PE have

Answer 24

By generation of plasmin Plasminogen -> plasmin via Hageman dependent pathway, plasminogen activators (tissue-type PA and urokinase-like PA)

Answer 25

Physiological ↓ in platelet levels - due to haemodilution Hypercoagulant - ↑levels of coagulant factors ↑ fibrinogen ↑ ESR Fibrinolytic system - placenta secretes PAI-2 which inhibits fibrinolytic system, ↑ anti-thrombin III, ↑ FDPs - activity remains low in labour but returns to normal 1hr after delivery of placenta

Answer 26

Endothelial injury Stasis Hypercoagulability

Answer 27

PRIMARY (genetic) disorders - protein C or S deficiency - anti-thrombin III deficiency - factor V Leiden SECONDARY (acquired) - pregnancy - COCP - antiphospholipid antibodies - nephrotic syndrome - Trousseau's syndrome - heparin induced thrombocytopenia syndrome

Answer 28

Venous, arterial or cardiac Based on Virchow's triad - endothelial injury, stasis, hypercoagulability Fate - propagation / embolisation / dissolution / organisation and recanalization

Answer 29

= Hughes' syndrome Triad for definition - thrombosis (arterial or venous), recurrent miscarriage (>3 consecutive at <10 weeks), antiphospholipid antibodies Autoimmune Also see PET, preterm deliveries, thrombocytopenia, livedo reticularis Primary if no other autoimmune conditions, secondary if also eg SLE Fetal loss due to pro-coagulant state, and decreased level of annexin-V (anticoagulant on normal placental villi) Treat - aspirin, and anticoagulants LMWH

Answer 30

Heterogenous antibodies directed against anionic phospholipids or their binding proteins (prothrombin, factor V, protein C and S, annexin V) Lupus anticoagulant and anticardiolipin antibodies 2-5% of normal obstetric population, 15% of those with recurrent miscarriage, 30% if SLE

Answer 31

Formation of antibodies that bind to heparin-platelet complex So activates platelets -> low platelet count, thrombosis Treat with lepirudin (thrombin inhibitor)

Answer 32

= consumptive coagulopathy Causes - cancer, massive tissue injury, massive haemorrhage, infection, liver disease, placental abruption, pre-eclampsia, amniotic fluid embolism Features - ↑PT, ↑APTT, high levels FDPs, ↑ soluble fibrin complex, ↓ fibrinogen, high D-dimer, thrombocytopenia, fragmented RBCs (schistocytes) on blood film

Answer 33

eg pulmonary thromboembolism - 60% silent, -> cor pulmonale (RV failure) Fat embolism - neurological symptoms, pulmonary insufficiency, anaemia, thrombocytopenia Air embolism - eg decompression sickness Amniotic fluid embolism - 1 in 8000 - 80,000 deliveries - 60% mortality rate

Answer 34

5-10% term pregnancies Gestational TP - benign, no treatment, will return to normal post delivery TTP = thrombotic thrombocytopenic purpura - thrombocytopenia with microangiopathic haemolytic anaemia and renal impairment - platelet consumption disorder - treatment is plasma exchange (NOT platelet transfusion) If PLT >80 - regional anaesthesia safe if >50 - LMWH is safe

Answer 35

Immune thrombocytopenic purpura Haemolytic uraemic syndrome Thrombotic thrombocytopenic purpura Bone marrow suppression Gestational thrombocytopenia HELLP syndrome SLE and antiphospholipid syndrome DIC HIV

Answer 36

Due to antibodies against platelet surface glycoproteins 1-2:10,000 pregnancies Antiplatelet IgG - can cross placenta and cause fetal thrombocytopenia Treatment - corticosteroids, immunoglobulins, splenectomy, azathioprine, platelet transfusion

Answer 37

Area of ischaemic necrosis caused by occlusion of either arterial supply or venous drainage to tissue Causes - thrombosis, embolism, vasospasm, expansion of atheroma, extrinsic compression of vessel Red (haemorrhagic) - due to venous obstruction White (anaemic) - due to arterial obstruction

Answer 38

SIRS = 2 of: - temp <36 or >38 - tachycardia >90 - tachypnoea >20 - WBC <4 or >12 Sepsis is SIRS if result of infection Severe sepsis is if also evidence of failure of >1 organ system MODS = 2 or more failed organ systems, 60% mortality

Answer 39

= collection of pus (dead and dying WBCs) surrounded by acute inflammatory response and pyogenic membrane Contains hyperosmolar material that draws fluid in and increases pressure, causing pain If related to surgical wound, usually takes 7-10 days to form Outcome - resolution by I+D, antibiotics, chronic abscess (with plasma cells and lymphocytes), fistula, sinus

Answer 40

Host response Virulence and inoculums of infective agent Vascularity and tissue health Presence of foreign body Presence of antibiotics during decisive period

Answer 41

Clean (if +abx prophylaxis infection rate is 2%) Clean-contaminated (" 10%) Contaminated (" 20%) Dirty (" 40%)

Answer 42

Systemic state of low tissue perfusion, inadequate for normal cellular respiration Pathogenesis: - lack of O2 -> anaerobic respiration -> lactic acid -> metabolic acidosis - consumption of cellular glucose stores -> cessation of anaerobic respiration -> cell lysis -> hyperkalaemia - hypoxia and acidosis activate immune and coagulation systems -> increased capillary permeability Cardio - decreased preload and afterload cause reflex tachycardia and vasoconstriction, reduced perfusion -> hypothermia Resp - metabolic acidosis so increased RR and minute ventilation (to excrete CO2), -> compensatory respiratory alkalosis Renal - reduced glomerular filtration, oliguria, activation of renin-angiotensin system, vasoconstriction Hormonal - ADH and cortisol release

Answer 43

Metabolites (H and K) that build up during tissue hypoperfusion are flushed back into systemic circulation -> acute lung injury -> acute renal injury -> MODS

Answer 44

HYPOVOLAEMIC - haemorrhoagic, non-haemorrhagic, 3rd spacing CARDIOGENIC - MI, arrhythmia without output OBSTRUCTIVE - tamponade, PE, pneumothorax DISTRIBUTIVE - septic, anaphylactic, neurogenic ENDOCRINE - adrenal insufficicency, hypo/hyperthyroidism

Answer 45

When normal vital signs but continued tissue hypoperfusion Due to low mixed venous oxygen saturation, persistent lactic acidosis Or global hypoperfusion - see base deficit, lactate

Answer 46

Based on response to 250-500ml IV fluid challenge: RESPONDER - sustained improvement, no active bleeding or fluid loss TRANSIENT RESPONDER - improve but then revert back to previous state over 20 mins (have ongoing fluid loss) NON-RESPONDER - show no improvement

Answer 47

Normal CVP = 5-15cm H2O After IV fluid challenge - should get CVP rise of 2-5, then drifting back over 20 mins - if no response then underfilled - large sustained response then overfilled

Answer 48

From RA Measure of O2 delivery and extraction by tissues Normal value 50-70% If <50% - inadequate oxygen delivery, or increased oxygen extraction If >70% - in sepsis due to decreased utilisation of O2 at cellular level

Answer 49

Leads to acidosis, hypothermia, coagulopathy Degree of haemorrhage - <15% is within limits of compensatory mechanism (at expense of GI tract, muscle, skin) 15-30% decompensation starts 30-40% BP falls >40% severe

Answer 50

Primary - immediate Reactionary - delayed but within 24hr of event, can be due to dislodgement of clot/vasodilation/normalisation of BP Secondary - within 7-14 days of primary event, caused by sloughing of vessel wall

Answer 51

Packed red cells - 330ml RBC, 250mg iron, stored at 2-6 degrees, 5 week shelf life Fresh frozen plasma - stored at -40degrees, shelf life 2 years Cryoprecipitate - rich in factor VIII and fibrinogen Platelets - stored at 20-24degrees, shelf like 5 days

Answer 52

Single transfusion - haemolytic (ABO incompatibility) - febrile (graft vs host response from residual leukocytes in blood) - allergic - infection - air embolism - thrombophlebitis - transfusion-related acute lung injury (from FFP) Massive transfusion - coagulopathy - hypocalcaemia, hyper/hypokalaemia, hypothermia, iron overload

Answer 53

FFP if PT>1.5x normal Cryoprecipitate if fibrinogen <0.8 Platelets if <50 TXA Aprotinin Recombinant factor VIIa

Answer 54

Every 3 years in 25-49yo Every 5 years in 50-65yo False negative 10% Borderline/mild dyskariosis 10% Moderate/severe dyskariosis 2% Inadequate 10%

Answer 55

Form of cervical dysplasia, premalignant Major aetiology HPV 16 and 18 Most spontaneously regress, or progression to cancer takes 15years Cytology - nuclear enlargement, increased nuclear:cytoplasmic ratio, nuclear pleomorphism, hypochromasia, increased mitotic activity

Answer 56

Usually coexists with squamous disease Multifocal in 15%

Answer 57

9:100,000, commonest gynae ca worldwide Mean age presentation is 52yo, but bimodal distribution with peaks in late 30s and early 60s 99.7% of cervical ca due to all types of HPV (70% due to 16 and 18) Squamous cell 80% Adenocarcinoma 15% <1% small cell ca (neuroendocrine, poor pronosis as early spread), clear cell ca, glassy cell ca

Answer 58

Stage 0 - ca in situ Stage 1 - 1A - limited to cervix, micro-invasive - treat with LLETZ/trachelectomy/hysterectomy - 1B - visible lesion - need radical hysterectomy and lymphadenectomy Stage 2 - invades beyond uterus but not to pelvic floor or lower 1/3 vagina - 2A without parametrial - 2B with parametrial - treat with radiation, cisplatin-based chemotherapy, and hysterectomy Stage 3 - extends to pelvic side wall or lower 1/3 vagina or hydronephrosis - 3A - no side wall - 3B - side wall or hydronephrosis - treat with radiation therapy and cisplatin-based chemo Stage 4 - extends beyond true pelvis - 4A - bladder and rectum - 4B - distant mets - radiation + chemo

Answer 59

= leiomyomas Oestrogen dependent benign tumours Arise from uterine smooth muscle No evidence that can become malignant, risk to leiomyosarcoma 0.25% Microscopically, tumor cells resemble normal cells (elongated, spindle-shaped, with a cigar-shaped nucleus) and form bundles with different directions (whorled). These cells are uniform in size and shape, with scarce mitoses. Degeneration due to outgrowing blood supply - hyaline most common, or red in pregnancy Intravenous leiomyomatosis is variant fibroid - can metastasize via haematological spread, in any organ

Answer 60

Ectopic endometrium (stroma + glands) Frequently in POD and ovaries In women of fertile age, 1-2% Unknown aetiology - theories oestrogen dependent, genetic, transplantation, retrograde implantation from menstruation Can be associated with cancers eg clear cell carcinoma Dysmenorrhoea, dyspareunia, dyschezia, dysuria, chronic pelvic pain, infertility in 40% Ca125 elevated Histologically see haemosiderin-laden macrophages

Answer 61

1 - superficial lesions and filmy adhesions 2 - deep lesions at cul-de-sac 3 - all above + endometriomas on ovaries 4 - all above + extensive adhesions

Answer 62

Presence of endometrial glands in myometrium 20%

Answer 63

Related to prolonged oestrogen stimulation of endometrium Simple, complex or atypical (atypical highest rate of progression to malignancy endometrial adenocarcinoma, 25-50%) Treatment - progestogens for simple/complex - TAH + BSO for atypical

Answer 64

Endometrial hyperplasia Hypertension Ovarian ca, breast ca Diabetes Tamoxifen, oestrogen Late menopause Early menarche Obesity Nulliparity

Answer 65

Carcinoma - non-endometroid (papillary serous or clear cell, both poorly differentiated with poorer prognosis) - or endometroid Sarcoma From pluripotent stem cells in endometrium HOMOLOGOUS if contain endometrial tissue only - stromal or glandular, HETEROLOGOUS if they contain extra-uterine tissue such as skeletal muscle or cartilage, PURE if differentiation occurs along one cellular pathway only - for instance, an endometrial stromal sarcoma, MIXED if differentiation occurs along more than one cellular pathway - for instance containing both endometrial stromal sarcoma and endometrial adenocarcinoma Poor prognosis

Answer 66

1 - limited to uterus, 85-90% 5 year survival 1A - invasion <1/2 myometrium 1B - invasion >1/2 myometrium 2 - cervical stromal invasion, 65% 5yr survival 3 - extension beyond uterus but confined to pelvis, 45-60% 5yr survival 3A - invasion of serosa, adnexa, peritoneal fluid 3B - vaginal invasion 3C - nodal involvement 4 - distant mets, 15% 5yr survival 4A - mucosa of rectum and bladder 4B - distant mets including abdominal and/or inguinal lymph

Answer 67

5% prevalence Based on Rotterdam criteria, need 2/3 of: - oligo-ovulation - excess androgen activity - polycystic ovaries on imaging (>12 follicles in each ovary measuring 2-9mm in diameter, or ovarian volume >10ml) High androgen activity due to - high LH, decreased SHBG, increased insulin, extra-ovarian production of androgens (eg Cushing's, CAH) High LH:FSH ratio 2:1 or more Higher risk of endometrial hyperplasia/neoplasia, insulin, resistance, dyslipidaemia

Answer 68

EPITHELIAL 85% - serous (75%), mucinous, Brenner's (transitional cells, secrete oestrogen, mostly benign, can be bilateral), clear cell, differentiated, endometroid (assoc with endometriosis), fibroma STROMAL 5% - sertoli-leydig (testosterone secreting, usually benign), thecofibroma, granulosa (oestrogen secreting, see Kall-Exner bodies) GERM CELL 5% (or 70% in under 20s) - germinoma, endodermal sinus tumour (secretes AFP and a-antitrypsin), choriocarcinoma (secretes hCG), teratoma, embryonal (secretes LDH)

Answer 69

From peritoneal, endometrium, breast, and GI tract cancers Krukenberg cancer = secondary ovarian from GI primary, characterised by mucin-secreting signet-ring cells, usually affects both ovaries

Answer 70

Includes dermoid cysts (from all 3 germ cell layers), mature teratomas, struma ovarii (mostly thyroid tissue, can cause hyperthyroidism), carcinoid component Benign teratoma is the commonest ovarian tumour (40%) - bilateral in 10-15% - 1% undergo malignant transformation

Answer 71

Biochemical: - ca125 (elevated in 50% with early disease, 80% with late) - ca119 or CEA in mucinous - AFP in germ cell - B-HCG in choriocarcinoma - LDH in dysgerminoma Cytokeratins - CK 7 positive - CK 20 negative Risk of malignancy index (RMI) = CA125 x menopausal status x ultrasound features - premenopausal = 1, post = 3 - >1 USS feature seen = 3 - RMI>200 highly indicative of malignancy

Answer 72

aka chronic atrophic vulvitis Autoimmune All ages but common after menopause See - narrowed introitus, labial atrophy, epidermal atrophy, hydropic degeneration of basal layer, dermal inflammation, sclerotic stroma 5% have association with squamous vulval carcinoma

Answer 73

1 - limited to 1 or both ovaries 1A - 1 ovary, peritoneal washings -ve 1B - both ovaries, peritoneal washings -ve 1C - capsule ruptures, peritoneal washings +ve 2 - pelvic extensions 2A - implants on uterus 2B - implants on pelvic structure 2C - peritoneal washings +ve 3 - peritoneal implants beyond pelvis or with extension to small bowel/omentum 3A - microscopic implants 3B - macroscopic <2cm 3C - macroscopic >2cm 4 - distant metastasis

Answer 74

aka hyperdysplastic dystrophy Secondary to pruritus See - acanthosis of vulval squamous epithelium, hyperkeratosis, thickened epithelium, increased mitotic activity in basal and prickle cell layer

Answer 75

See - epithelial nuclear atypia, increased mitosis, lack of surface differentiation 90% associated with HPV 10-30% assoc with another primary squamous neoplasm in vagina or cervix

Answer 76

Non-invasive intraepithelial adenocarcinoma Not usually associated with underlying invasive malignancy Can be assoc with adenocarcinoma arising from urethra, rectum or Bartholin's gland Lesion - sharp demarcation, erythematous, pruritic

Answer 77

4% of gynae cancers, 3/100,000 women, median age 74yo Usually presents with itching Types - SCC 85%, melanoma 5%, BCC, adenocarcinoma, sarcoma

Answer 78

1 - confined to vulva 1A - lesions <2cm with stromal invasion <1mm 1B - lesions >2cm, stromal invasion >1mm 2 - extension to adjacent perineal structures, eg 1/3 lower vagina, 1/3 lower urethra, anus 3 - positive inguino-femoral nodes 3A - <2 lymph node mets 3B - >2 lymph node mets 3C - with extracapsular spread 4 - extension to upper urethra and vagina 4A - upper vagina, upper urethra, bladder, rectum 4B - distant mets including pelvic lymph nodes

Answer 79

1% of gynae cancer Primary carcinoma uncommon Associated with HPV Types - 90% SCC, adenocarcinoma, germ cell, sarcoma Botryoides

Answer 80

BP >140/90 with proteinuria, after 20w gestation 2-3% of pregnancies (HTN in 10-15%) 2% of those with PET -> eclampsia Unknown aetiology Pathophysiology ?due to poor placentation -> utero-placental resistance and abnormal placental function - vasoconstricted - plasma contracted - intravascular coagulation - endothelial dysfunction (↑ capillary permeability, ↑ vascular tone, ↑ fibronectin, platelet thrombosis) - biochemical - ↓NO, ↓ thromboxane A2, angiotensin and endothelin, ↓prostacyclin

Answer 81

Mild - BP >140/90 - proteinuria 300mg/24hr Severe - BP >160/110 - proteinuria >5g/24hr Features - headache, visual disturbance, epigastric/RUQ pain, vomiting, ankle swelling, seizures - hyper-reflexia, clonus, oliguria - deranged LFTs, low platelets, abnormal renal function, deranged clotting, elevated urinary protein

Answer 82

Age >40 BMI >30 Family hx Primip Multiple pregnancy Previous hx Hydatidiform mole Pre-existing HTN Renal disease Diabetes Antiphospholipid syndrome

Answer 83

Haemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome Placental abruption FGR Eclampsia Pulmonary oedema DIC Commonest causes of death in PET - cerebral haemorrhage, ARDS

Answer 84

Features - pruritus of limbs and trunk (palms and soles especially), no rash, abnormal LFTs, rare to have jaundice Multifactorial poorly understood pathogenesis Complications - vitK deficiency, PPH, pre-term delivery, intrapartum fetal distress, intrauterine fetal death 1-4%, fetal intracranial haemorrhage Risk of recurrence 90% in future pregnancies

Answer 85

Usually after 30w gestation RFs - primigravida, obesity, male fetus, multiple pregnancy 10-20% maternal mortality, 20-30% fetal mortality Features - vomiting, abdo pain, jaundice, abnormal LFTs, profound hypoglycaemia, hyperuricaemia, coagulopathy Complications - fulminant hepatic failure, encephalopathy

Answer 86

Haemolysis, elevated liver enzymes, low platelets 20% of those with severe PET Pathogenesis - endothelial cell injury, microanngiopathic platelet activation and consumption Effects on pregnancy - abruption, acute renal failure, hepatic necrosis, liver rupture, subcapsular liver haematoma Perinatal mortality 10-60%, maternal 1% Risk of recurrence in future pregnancies low, but risk of PET high (75%)

Answer 87

Dilated cardiomyopathy From 8mo gestation to 5mo postpartum Assoc with congestive HF, ↓LVEF, cardiac arrhythmias, thromboembolism Cause unknown, diagnosis of exclusion Maternal mortality 25-50% Management - diuretics, B-blockers, ACEi, anticoagulation, or if refractory then LV assist device or heart transplant

Answer 88

Positive if agglutination occurs Indirect - detects antibodies against RBCs present in patient's serum, used for antibody screening (cross-matching and antenatal screening) Direct - detects antibodies bound to RBC surface antigens, indicates immune-mediated attack o RBCs - alloimmune haemolysis (haem disease of newborn) - autoimmune haemolysis (SLE, idiopathic, secondary to lymphoproliferative disease or infection) - drug-induced immune-mediated haemolysis (methyldopa, penicillin, quinidine)

Answer 89

To measure fetal RBCs in maternal circulation Normally fetal maternal haemorrhage is <4ml at delivery Anti-D immunoglobulin - 500IU neutralizes 4ml of RH+ve RBC - should be given within 72hr of sensitisation in non-sensitised Rh-ve women - provides protection for 6 weeks

Answer 90

Hypopituitarism - caused by ischaemic necrosis due to blood loss and hypovolemic shock during and after childbirth Signs - absence or difficulty with lactation, amenorrhea / oligomenorrhea and features of hypothyroidism (tiredness, weight gain etc) due to reduced TSH.

Answer 91

Due to direct effect of progesterone on the endometrium - endometrial epithelial cells become increasingly vacuolated and thrown into pseudo-papillary folds giving a hyper-secretory impression, evidence of decidualisation around spiral arteries and under the surface of the epithelium - glandular hyperplasia, intra-nuclear cytoplasmic invaginations which may resemble viral inclusions - in normal intra-uterine pregnancy, ectopic pregnancy, progestogen therapy and can also occur in the endocervix

Answer 92

COCP - glandular atrophy Copper IUD - mononuclear cell infiltration, irregular polymorphs near the surface, foci of haemorrhage and squamous metaplasia may be present, cyclical changes persist Progesterone IUS - progestogenic effects including decidual change and inactive or weakly secretory glands with thinning of the endometrial lining

Answer 93

= yolk sac Rapidly growing Intraperitoneal spread Germ cell tumours Typically produce AFP Occur in young women See Schiller-duval bodies

Answer 94

= the seminoma in males - commonest malignant germ cell tumour; occur in young women between the ages of 13 - 30 years - 10-15% are bilateral; solid tumours which typically present with abdominal mass or pressure symptoms - lymphatic spread to the para-aortic nodes - very radio-sensitive - no reliable serum marker but commonly see elevated LDH, occasionally hCG - karyotyping recommended

Answer 95

- usually a secondary from a uterine tumour - primary ovarian choriocarcinoma is rare and develops from germ cells - solid tumours, typically unilateral with cytotrophoblasts and syncytiotrophoblasts on histological examination - produce HCG

Answer 96

Triad of benign ovarian tumour (typically thecoma/fibroma), ascites and pleural effusion Thecomas may produce oestrogen with a presentation similar to that described for granulosa tumours. Less likely to rupture Fibromas with > 3 mitoses per 10 high power fields are considered fibrosarcomas

Answer 97

Concentric lamellated calcified structures, most commonly in papillary thyroid carcinoma (PTC), meningioma, and papillary serous cystadenocarcinoma of ovary Contain calcium

Pathology Flashcards

(122 cards)