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Fichas

Histopathology

Rory Purves 3rd year Inglés 123 fichas

Fichas del conjunto (123)

  1. 1Define cirrhosisIrreversible destruction of the liver architecture associated with fibrosis and nodule formation which may follow necrosis
  2. 22 RFs for liver cell adenoma1. Being female
    2. OCP use
  3. 3Often misinterpreted as metastasesbile duct malformations
  4. 4focal nodularhyperplasiatumour like malformation
    central scar
    more common in women
  5. 5Causes of HCCcirrhosis
    Hep b/c
    ash/nash
    autoimmune hepatitis
    chronic biliary disease
  6. 6Fibrolamellar HCC - differencesyounger patients
    no background cirrhosis
    better prognosis
  7. 7angiosarcomamost common sarcoma of the liver
    mostly in older men
  8. 8Hepatoblastomachildren under 5
    AFP often raised
    lobulated appearance
  9. 9Hep Ano carrier state
  10. 10Hep Btransmission via bodily fluids
    Can lead to cirrhosis and HCC
  11. 11Hep Cusually forms a chronic disease
    often causes cirrhosis and can lead to HCC
  12. 12Hep Efood/waterborne
    severe in pregnant women
  13. 13Autoimmune Hephigh ALT, IgG
    ANA positive
  14. 14Primary Sclerosing cholangitispresents in young/middle age males
    common in patients with UC
    inflammation of the large bile ducts
    AMA neg, well recognised in children
    Can be p-ANCA positive
  15. 15Primary biliary cholangitispresents in middle aged females
    AMA pos, IgM pos, Alk Phos raised
    inflammation of the small bile ducts
  16. 16Wilson's diseaseAutosomal recessive mutation on Chr 13
    aberrant storage of copper in the liver
    presents in childhood
  17. 17HaemochromatosisAutosomal recessive mutation of HFE gene on Chr 6
    increased iron absorption and storage in the liver
    leads to cirrhosis and risk of HCC
  18. 18A1AT deficiencymutation in A1AT gene on chr14
    leads to accumulation in the liver
  19. 19Secretory portion of the mammary glandsTDLU - terminal duct lobular units
  20. 20Markers used to identify myoepithelial cellsSMM
    p63
    CK5/6
  21. 21Fibrocystic changecommon in women 25-45
    caused by hormonal changes
    benign, not clinically significant
  22. 22Fibroadenomamost common benign tumour between 25-30
    increases in size during pregnancy
    decreases in size with age
  23. 23Breast carcinoma classification criteria2 criteria
    invasion of basement membrane? yes - invasive, no - in situ
    Morphology - Ductal or lobar
  24. 24Breast carcinoma genetic factorsBRCA1 - chr17, also causes ovarian cancer
    BRCA2 - chr13
  25. 25Phylloides tumourcomposed of mesenchymal and epithelial elements
    mesenchymal component is malignant, metastasises through haematogenous route
    recurrence is common
  26. 26Breast lump Red flag symtomsTethered - carcinoma
    bloody discharge - ductal papilloma/carcinoma
    peau d'orange - carcinoma
    microcalcification - DCIS
  27. 27Coronary artery occlusionone or more lesions causing 75% reduction in CSA of at least one major epicardial artery
    90% of patients with IHD
  28. 28MITransmural - at least nearly full thickness of ventricular wall in distribution of one CA
    Subendocardial - inner 1/3 or 1/2 at most of ventricular wall, can be beyond perfusion territiry of one CA
    irreversible injury in 20-40mins
  29. 29Detection of MICKMB test
    Lactate
    Troponin 1 and T
    ECG, echo
  30. 30Mitral annular calcificationcan lead to mitral regurg
    source of throbi/emboli
    prone to IE
    women over 60
  31. 31Rheumatic heart diseaseoften occurs after Group A (beta haemolytic) streptococcal pharyngitis
    chronic rheumatic valvular disease - most important consequence of RF, always involves mitral, often aortic
  32. 32Bacterial Endocarditisforms friable vegetation in left heart valves, tricuspid in IVDUs
    preventable using prophylactic antibiotics
  33. 33Vascular supply of myocardiumLeft trunk: LAD - apex, ant wall of LV, ant 2/3 of VS
    LCX - lateral wall of LV
    RCA: RV, posterior1/3 of ventricular septum, post-basal wall of LV
  34. 34Nephrotic syndromeAcute: haematuria, oliguria, azotemia, hypertension
  35. 35Minimal change glomerulopathymost common cause of NS in children
  36. 36membranous glomerulonephritismost common cause of nephrotic syndrome in adults
    85% idiopathic
  37. 37Glomerular nephritislarge deposition of immune complexes in glomerular wall
  38. 38Main cause of acute nephritis in children?acute proliferative glomerulonephritis
    arises following group A beta-haemolytic streptococcal infection
  39. 39presentation of combined nephritic-nephrotic picturemembranoproliferative glomerulonephritis
  40. 40Acute tubular necrosisfocal necrosis and desquamation of the cells into the tubular lumen
    can lead to acute renal failure
  41. 41UTI - patient RFs, symptoms and organismselderly, female, catheters, malformations
    dysuria, frequency
    e. coli and proteus
  42. 42Acute Pyelonephritis - presentation, pathogenesisfever and raised creatinine (due to reduced eGFR)
    inflammatory infiltrate into the interstitium and tubular lamina
  43. 43Chronic pyelonephritis - appearance of the kidneysdepressed in scarred areas, pseudo-bulging in the intact parenchyma
    symptoms present bilaterally but scarring is asymmetrical
    a cut would show dilated, blunted or deformed calyces
    dilated 'colloid' filled tubules are present - thyroidisation of the kidneys
  44. 44Most common cause of abnormal mass in newbornmulticystic renal dysplasia
  45. 45ADPKDautosomal dominant
    presents bilaterally in middle age - haematuria, UTI, abdo mass, HTN
    can cause chronic renal failure
    management - supportive, treat HTN, dialysis transplant when required
  46. 46ARPKD (infantile)Large abdo masses at birth
    associated with liver abnormalities
    causes - CRF, HTN, PHTN, death shortly after birth if severe
  47. 47CRF/CKDoften unrecognised or coexists with other conditions
    Can be asymptomatic until end stage renal disease
    Caused by: Diabetes and hypertension
  48. 485 stages of CRF1 - GFR >90 with other evidence of damage
    2 - GFR 60-89 with other evidence of damage
    3 - A; GFR 45-59 with or without evidence of kidney damage, B; GFR 30-44 polyuria, anaemia, hypertension
    4 - GFR 15-29 with or without other evidence of kidney damage
    5- GFR <15 established renal failure
  49. 49Acute renal failurerapid reduction in renal excretory function (within 48)
    less than 0.5ml/kg urine output for >6hrs
    presentation - metabolic acidosis, increased urea
  50. 50Nephrolithiasisstone formation in the kidney or renal tract
    recurrance 40-70%
    75% calcium oxalate, hypercalcaemia, idiopathic calcuria
  51. 51Renal cell carcinomaRFs: regular + heavy metals, von hippel lindau syndrome
    presentation: paraneoplastic syndrome, referred back pain, haematuria, palpable masses
  52. 52Urinary bladder tumours90% in urothelium
    differential RF - industrial exposure to arylamines (dyes, aluminium)
  53. 53Epithelial tumours of the bladder - red flag symptompainless haematuria
  54. 54Bronchopneumonia - patient, symptoms and organismsextremes of age
    presents with flu like symptoms
    Staph, haemophilus I, klebsiella
  55. 55Lobar pneumonia - patients, symptoms and organismsyoung adults
    high grade fever
    Strep
  56. 56TB - distinguishing featuresZN stain
  57. 57Oncogenes in bronchocarcinomaC-myc in small cell carcinoma
    K-ras in adenocarcinoma
  58. 58Clinical features for Bronchocarcinomasweight loss, non-productive cough
    HAEMOPTYSIS, paraneoplastic syndrome from ectopic tumours:
    ACTH & ADH - SmCC
    PTH - SqCC
  59. 59Causes of perinatal deathsSpontaneous pre-term delivery and hypertensive disorders (pre-eclampsia) 29%
    prematurity - 62%
    foetal abnormalities - 12%
  60. 60Pre-eclampsia - clinical pres, autopsy findingsunexplained high maternal BP and proteinuria
    IUGR and assymetrical growth
    infarct on placenta
  61. 61Acute choriomanionitisacute inflammation of foetal membranes
    common after PROM
    risk of ascending infection to mother
  62. 623 layers of testistunica vaginalis/outer serosa
    tunica albuginea
    tunica vasculosa
  63. 63Leydig cells - distribution and functionadjacent to SNTs
    produce testosterone in presence of LH
  64. 64Stages of development in germ cells1. spermatogonium
    2. primary spermatocyte
    3. secondary spermatocyte
    4. spermatid
    5. spermatozoon
  65. 65germ cell tumour - presentation, RFsPainless unilateral testis enlargement, secondary hydrocele, symptoms from metastases - retroperitoneal mass, gynaecomastia
    Cryptorchidism, genetic predisposition, testicular dysgenesis
  66. 66Classification of GCTsIn situ - intratubular germ cell neoplasia
    invasive - Seminoma, NSGCT, mixed
  67. 67Subtypes of seminomaclassical - most common in 40s, mos
    Spermatocytic - older age group, prognosis is better than classical
  68. 68NSGCTs -4 subtypesembryonal carcinoma
    Yolk sac tumour
    Choriocarcinoma
    Teratoma
  69. 69Embryonal carcinoma20-30
    usually associated with other GCT
  70. 70Yolk sac tumourMost common GCT in <3yrs
    in adults, associates with embryonal carcinoma
    serum AFP is raised
  71. 71Choriocarcinomahighly malignant
    raised serum HCG levels
  72. 72Teratomacan differentiate into any of the 3 germ layers
    2nd most common in children
    good prognosis
    adult pure form is rare, treated as malignant as they have a high metastatic potential
  73. 73Mixed GCT14% of all GCTs
    treated as a NSGCT
  74. 74Prognosis for testicular cancerType dependant - seminoma worse than NSGCT
    staging:
    1. contained within testicle, no spread. 1s means raised markers post surgery
    2. nearby lymph nodes in abdo/pelvis. S1 raised markers
    A- lymph nodes <2cm
    B- 2-5
    C- >5
    3. A- distant lymph spread (collarbone, lumgs)
    B- nearby/distant nodes with high markers S2
    C- same as B but higher markers S3, OR spread to another organ
    Size in seminoma - <40mm good, <40 bad
    Invasion of the reti-testis
    Vascular invasion
  75. 75BPH - patient, symptoms, causesv common in men over 50
    urinary retention
    caused by androgens (DHT)
  76. 76Prostate carcinoma - patient, etiologymen over 50
    hormone androgen receptor
    genes 1q24-25 and 1st degree relatives
  77. 77Staging of prostate carcinomaA- non palpable
    B- palpable
    C- Extracapsular extension
    D- metastatic
  78. 78Diagnosis of prostate carcinomaRaised PSA level according to age:
    50-59; >3
    60-69; >4
    70+; >5
    digital PR exam
    Imaging
    Biopsy
  79. 79Complications of reflux oesophagitisstricture - fibrosis of smooth muscle reduces compliance of oesophagus. can be caused by achalasia
    Barretts - replaced lining with glandular mucosa due to reflux of stomach acid. Raises SCJ above GOJ - barretts distance
    Neoplasia: SCC - 20% 3:1 m:f, poor prognosis
    Adenocarcinoma - 80% good prognosis if early stage staged using TNM
  80. 80TNM stagingT - tumour; depth of invasion
    N - nodes; involvement of lymph nodes
    M - metastases
  81. 81Achalasiadestruction of myenteric ganglion cells
    complication: SCC, stricture
    immobilisation due to lack of peristalsis
  82. 82Common UGI infectionsCandida - old age, immunosuppressed; cottage cheese in oesophagus
    HSV - immunosuppressed, old age not enough
    Chagas disease - reduviid bug from central/south america; causes pseudo-achalasia, cardiomyopathy
  83. 83ABC classification for gastritisA- autoimmune
    B- bacterial
    C- chemical
  84. 84Reactive gastritisChemical most common;
    often caused by nsaids and alcohol;
    look for vessel dilation in foveolar epithelium
  85. 85HP gastritiscomplications: ulcer, MALT lymphoma and carcinoma
    often present in antrum, moves in caudal direction as epithelium is destroyed
  86. 86MALT lymphomaresult of chronic HP, treat by eradicating HP with PPI, Abx +/- bismuth
  87. 87Gastric carcinomamost common in antrum, with higher HP levels
    HP is class 1 carcinogen
  88. 88Adenocarcinoma of the stomachM:F - 3:1
    RFs: poor diet, HP
    if advanced - <20% 5yr survival
    early - 90%
    Intestinal or diffuse type
    Diffuse can be treated with Her2 therapy
    TNM staging
  89. 89GISTcaused by mutations in tyrosine kinase genes (KIT)
    treat with surgery and TKIs (imatinib)
    Most common in stomach
  90. 90Coeliac diseasecomplications: malabsorption - anaemia low albumin; ulcerative jejunitis; neoplasm - EATL, SIadenoC
    pathology: flat micosa, reduction in vilous height to crypt depth ratio from 5:1 to 3:1
  91. 91GiardiasisMost common SI protozoal infection
    Contaminated waterspread
    immunocompromised patients
    mucosa can be normal and inflamed
  92. 92SI neoplasiaDuodenal in FAP
    adenocarcinoma - rare; autoimmune conditions
    Lymphomas - B&T cell, Burkitts (ilieum), EATL
    Neuroendocrine tumours - SI has 5% 5 yr survival
  93. 93HPV16&18 - malignancy
    6&11 - genital warts
    spontaneously clears unless immunosuppression - leads to chronic infection and progression to malignancy
    brush smear to check for HPV
  94. 94Cervical squamous cell carcinoma - causes, pathophysiologyoften begins with persistent HPV infection
    high risk types integrate proteins e6&7 - inhibiting p53 and retinoblastoma, leading to dysplasia of squamous epithelium
  95. 95Grading of CSCCCIN 1,2&3-
    1. Mild, lower 1/3
    2. moderate 2/3
    3. severe whole thickness (Carcinoma in situ)
    after CIN3 = invasive SCC
  96. 96Treatment of CSCCif CIN1/2 then LLTx of transition zone (retain fertility)
    if CIN3 or invasive, hysterectomy and pelvic lymph node resection (infertile)
    if possible keep ovaries to prevent early menopause
  97. 97Adenomyosis - pathogenesisendometrial tissue located within the myometrium - 'islands' of endometrium
    causes smooth muscle inflammation and menorrhagia
  98. 98Endometriosisendo tissue on serosa outside of the uterus
    causes metaplasia of serosal cells to endometrial cells
    causes 'chocolate cysts' due to no drainage for bleeding
  99. 99Endometrial carcinoma - red flag and RFsPostmenopausal bleeding
    normal + nulliparous, infertility
  100. 1002 types of EC1. more common, endometrioid carcinoma
    oestrogen excess; often obese without children
    2. serous cell carcinomas
    elderly with atrophic endometrium, tend to be higher grade, not related to oestrogen excess
  101. 101Grading of endometrioid carcinomasSimple hyperplasia
    complex hyperplasia - complex architecture
    Atypical complex hyperplasia - glands increase in size and abnormal nuclear activity lining the glands
    Carcinoma - cells lining glands show invasion
  102. 102Grading of ECFIGO staging
    1 confined to uterine body
    2 invading cervix
    3 not beyond true pelvis
    beyond true pelvis +/- bladder/rectum
  103. 103Fibroid leiomyomabenign SM tumour - subserosal, intramural, submucosal
    often multiple
    can produce abnormal bleeding, discomfort
    growth stimulated by oestrogen exposure
  104. 104Leiomyosarcomausually single
    haemorrhage, frequent mitoses
  105. 105Ectopic pregnancy - signs, treatment and RFpositive urine test but negative US;
    salpingectomy;
    Scarring or structural abnormality can predispose (chlamydia, gonorrhoea, PIV) although often no history
  106. 106metastatic ovarian tumours - pathogenesisDirect spread from gastric carcinoma, haematogenous from breast
  107. 107types of ovarian tumourSurface epithelium - most common, can form different endothelial phenotypes, usually cystic, can be benign, malignant or borderline
    germ cell - benign mostly, can form teratoma: totipotent, solid with cysts, often single component e.g. dermoid
    Sex-cord stromal tumours - can be granulomas or fibromas
  108. 108Crohns disease - epidemiology, pathologycommon in north america/europe
    RR for siblings is 13-36x, most common 15-30yrs
    both ileum and caecum in 40-50%
    Skip lesions, cobblestone and crypt abscesses all characteristic
  109. 109Crohns - complications and treatmentadhesions, perforation, perirectal disease, malabsorption, small bowel adenocarcinoma
    5-asa, steroids, immunosuppression, monoclonal antibodies against tnf (infliximab), surgical resection
  110. 110UCRR for siblings is 7-17x
    max incidence 20-50, another peak at 60-70
    histology is crypt abscesses with neutrophils in the crypt and gland branching
  111. 111Toxic megacolon - presentation, cause, complications and treatmenthigh fever, tachycardic, diarrhoea;
    paralysis of the motor function of the transverse colon
    perforation, massive haemorrhage, colon cancer
    5-asa, steroids, immunosuppression, surgery
  112. 112inflammatory polypsseen in UC and CD
    look like adenomas, microscopically inflammatory, hyperplastic mucosa
  113. 113hamartomatous polypsbenign tumour like lesions
    juvenile polyps - cystic glands with normal or inflamed epithelium, germ line SMAD4 mutation (18q21-22 in 25-30%), usually child less than 8; 80% in rectum, usually presents with bleeding or rarely prolapse
    Peutz-Jegher - polyps and pigmentation of the oral mucosa, lips, palm, genitalia; autodom, can lead to intussusception and partial/complete obstruction. Can lead to adenoma/carcinoma
  114. 114Neoplastic polypsAdenoma
    premalignant- classification: tubular
    tubulovillous - villi-elongated crypts
    villous - more than 75% villous
    Flat/depressed adenoma - high malignant potential, associated with a familial colon cancer (HNPCC) or FAP
    malignant potential is proportional to villosity, size, degree of dysplasia
  115. 115hyperplastic polypsmost common polyp in adults
    asymptomatic, no mlaignant potential unless mixed types
  116. 116Leimyomatous polypon muscularis mucosae
    symptoms: anaemia, bleeding due to ulceration, epigastric pain
  117. 117Colorectal cancer - site characteristicsright colon - polypoid, discomfort/anaemia
    left colon - anular and obstructing, bleeding/mucus, colicky pain, change in bowel habit
  118. 118Classification of CR cancersDukes:
    A - into wall tissue, but not through
    B - through muscularis propria into fat
    C - 1 prsence in lymph nodes
    2 involves apical node
    D - metastases
    TNM
  119. 119TNM classificationT
    1- invades submucosa
    2- invades muscularis propria
    3 - into subserosa/pericolic/perirectal tissues
    4- invades other organs/structures and /or perforates visceral peritoneum
    N
    0 - no lymph node spread
    1 - 1-3 regional lymph nodes
    2 - 4+ regional lymph nodes
    M
    0 - no mets
    1 - mets
  120. 120Stage groupings1 - T1 or 2, N0, M0: begun to spread but within inner lining
    2 - T3 or 4, N0, M0: spread to tissues near the colon/rectum, no lymph nodes
    3 - any T, N1/2, M0: spread to lymoh nodes but not distant parts of the body
    4 - M1: metastasised, mostly lung and liver
  121. 121HNPCCautodom
    carcinoma develops a lot younger
    right sided, abnormalities in 4 repair genes
  122. 122Amsterdam criteria for HNPCC3+ family members with cr cancer, at least 2 1st degree relatives
    2 successive generations
    1 must have occured before 50
    FAP has been excluded
  123. 123FAPwithout intervention all will develop colon cancer
    multiple polyps throughout colon
    none at birth, develop over time

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3rd year Fichas sobre Histopathology, creado por Rory Purves el 24/04/2017.
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