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Flashcards

Histopathology

Kitty Wong Medicine English 190 cards

What are the malignant carcinomas of the thyroid? (PFAM)

Cards in this deck (190)

  1. 1How to differentiate between nephrotic vs nephritic syndrome?Nephrotic - Chronic effacement of BM / podocytes. Proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia. Damage not accompanied by inflammation or proliferation.
    Nephritic - Acute, non-selective proteinuria, haematuria, oliguria, HTN. Immuno-mediated inflammation, vascular, and epithelial damage +/- proliferation of glomerular cells.
  2. 2Minimal change disease is the most common childhood nephrotic syndrome What are the characteristic clinical / histo presentations?No detectable immune deposit under light microscopy. Asso. resp infx / immunization.
    CLIN: Periorbital oedema and pitting oedema.
    Rx: Steroids.
    (If resistant to rx --> Focal segmental)
  3. 3What histological change is seen in focal segmental glomerulosclerosis?Localised lesions in glomeruli showing partial hyalinization.
  4. 4Membranous glomerulonephritis is the most common nephrotic syndrome in adults. What is this due to?Immune-complex depositions in basement membrane.
    Thickened GBM and subepithelial deposits / spikes.
  5. 5What nephritic syndrome is associated with group A beta-haemolytic strep. infection?Acute proliferative glomerulonephritis.
    Common in childhood acute nephritis.
    Histo: endocapillary hypercellularity - glomeruli increased in size and number.
  6. 6What is the classic picture of membranoproliferative glomerulonephritis?Combined nephrotic - nephritic picture.
    Crescenteric depositions - rapidly progressing, renal failure.
  7. 7What is the histological picture in acute pyelonephritis?Infection backflow into tubules, glomeruli spared.
  8. 8What clinical picture is this: Complete anatomical distortion, scar tissue, thyroidisation of kidneys**.Chronic pyelonephritis & reflux /obstructive nephropathy.
  9. 9What histological changes are seen in hypertensive kidney disease? 1) Benign nephrosclerosis 2) Malignant HTN & accelerated nephrosclerosis1) Focal renal arteriole sclerosis, minimal scarring, granular surface***
    2) Malignant - Fibrous intimal thickening.
  10. 10What can cause cystic disease of the kidneys?1. Adult polycystic disease (AD)
    2. Infantile polycystic disease (AR)
    3. Simple renal cysts - asymptomatic
    4. Dialysis-associated cystic disease
  11. 11What is infantile polycystic disease associated with? What phenotype is especially worrying?Asso. Liver abnormalities.
    POTTER PHENOTYPE:
    Decreased urine in-utero, decreased lung development.
  12. 12Common causes of CKD / CRF?Renal: Glomerulonephritis, chronic pyelonephritis.
    Systemic: DM, HTN
  13. 13What are van mayer's complex and irregular ducts indicative of?Bile duct malformation (benign)
    White liver nodules often misinterpreted as mets.
  14. 14What benign liver neoplasm is associated with oral contraceptive use?Liver cell adenoma.
  15. 15What is this benign liver neoplasm? Tumour like malformation. Central scar with bland hepatocytes and malformed blood vessels.Focal nodular hyperplasia
  16. 16What malignant liver neoplasm produces bile?Hepatocellular carcinoma (HCC).
    ONLY CARCINOMA PRODUCING BILE.
  17. 17What is hepatocellular carcinoma (HCC) linked to? What is shown on LFTs and histology?Linked to hepatitis or any cause of liver cirrhosis.
    LFTs: Elevated AFP
    Histo: Thick liver plates and bile duct cells.
  18. 18In a young person with no background of cirrhosis, what is the likely malignant liver neoplasm?Fibrolamellar HCC
    Histology: Collagen with large HCC cells
    Rx: Surgical resection
  19. 19Hepatoblastoma is the most common childhood liver tumour in children <5y. What is seen on histology?Lobular appearance, different histological variation.
    Composed of tissue resembling fetal and mature liver cells or bile duct cells.
  20. 20Haemangioma is a benign vascular tumour of the liver; Angiosarcoma is a malignant vascular tumour. What are the main risks of developing this cancer?M > F
    Arsenic
    Anabolic steroids
    Others: thorotrast, vinyl chloride (plastic)
  21. 21What histological feature is seen in angiosarcoma of the liver?Chiamorphism (variation in cell size)
  22. 22Cholangiocarcinoma is malignancy of the biliary ducts. It is often progressive and associated with poor outcomes. What is it associated with?Chronic inflammation of bile ducts.
    Primary sclerosing cholangitis
    Parasites
    Pyogenic cholangitis
  23. 23What histological finding is seen on primary sclerosing cholangitis?Fibrosed bile ducts, deformed / strictures in biliary tree imaging.
    AMA -ve.
  24. 24Primary biliary cholangitis (PBC)Granulomas affecting small bile ducts causing cirrhosis.
    Common in middle-aged females.
    **AMA+ (PBC SPECIFIC)
    Raised IgM, raised Alk Phos
  25. 25What gene is mutated in alpha-1-antitrypsin deficiency? Aside from early onset emphysema, what liver problems can this cause?A1AT gene on chromosome 14.
    Leads to liver fibrosis / cirrhosis, increased HCC risk.
  26. 26What histological change is seen in reflux oesophagitis?Thickening of basal layer
    Increase in eosinophils / lymphocytes
    Vascular patille becomes flat
    Worse at bottom of oesophagus
  27. 27Achalasia is a stricture causing build-up of food and barium due to inflammatory destruction of myenteric ganglion cells. What histological feature is seen? What is the most important complication?Histo: Affects distal oesophagus - lymphocytes attracting ganglion cells.
    Complication: Squamous cell carcinoma due to prolonged epithelial chemical insult.
  28. 28What infection has: Macro - cheese like lesions Histo - spores-pseudohyphi (Esp. immunosuppressed patient)Candida
  29. 29What histological features would you see in an immunosuppressed patient with an upper GI infection by herpes simplex virus (HSV)?Viral nuclear inclusions and multi-nucleation
  30. 30How is Chagas disease transmitted? How does it affect the heart and the GIT?Transmitted in faeces of "blood sucking" reduviip bug via bite.
    Cardiac muscle inflammation - Cardiomyopathy
    Fibrotic strictures of GI smooth muscles - pseudo-achalasia
  31. 31What histological change is seen in Barrett's metaplasia? What correlates most with risk of malignancy?Metastatic replacement of oesophageal lining (squamous) by glandular mucosa.
    Length of lesion correlates with risk of malignancy (adenocarcinoma).
  32. 32What are the 3 types of Gastritis?A - Autoimmune
    Chronic Atrophic Gastritis
    (Neoplastic risk, F>M)
    B - Bacterial
    Chronic Superficial Gastritis
    (H.pylori, infx)
    C - Chemical, bile reflux, drugs (NSAIDs)
    Reflux / Reactive Gastritis
    (Foveolar hyperplasia, oedema, telangiectasia, lack of inflammatory cells)
  33. 33What are the 3 histological features of chemical / reactive gastritis?Mild - Foveolar Hyperplasia / BV Dilatation
    Moderate - SM spurring from muscularis mucosae
    Severe - Inflammation
  34. 34What does H.Pylori cause? (4)1. Chronic Active Gastritis
    2. Gastric ulcer
    3. MALT lymphoma
    (will regress if H.P eradicated)
    4. UGI Carcinoma (esp. Gastric Antrum)
  35. 35What are the 4 types of gastric neoplasia?1. Adenocarcinoma +++
    2. Lymphoma / MALT
    3. Neuro-endocrine tumour ('carcinoid')
    4. GI stromal tumour (GIST)
  36. 36What 2 types of adenocarcinomas are there for GI malignancy?1. Intestinal-Type Carcinoma
    Expresses HER2, responds well to rx.
    2. Diffuse-Type Carcinoma
    Does not express HER2, poor prognosis.
  37. 37What is GIST caused by? Where does it occur (most likely - least likely)?Tyrosine kinase gene (TKI / KIT) mutations.
    Stomach > Small intestine > Oesophagus / Large bowel
  38. 38What does GIST look like histologically? How is it treated?Histo: Spindly or round.
    Rx: Surgery +/- TKI inhibitors (e.g. Imatinib)
  39. 39Coeliac disease may present clinically with malabsorption (anaemia, low albumin) and failure to thrive which is improved by a gluten-free diet. What histological features can be seen?Flat mucosa, villous stunting (low height).
    Crypt hyperplasia.
    Increased intraepithelial lymphocytes (lymphocytosis).
    Infiltration of lamina propria by plasma cells and lymphocytes.
  40. 40What are some complications of coeliac disease?1. Refractory sprue - clonal lymphocytes predisposed to cancer.
    2. Ulcerative jejunitis.
    3. Neoplasia - EATL, small intestinal adenocarcinoma.
  41. 41What are 5 types of small intestinal neoplasias?1. Adenomas - FAP
    2. Adenocarcinoma - Coeliac, Crohn's, FAP
    3. Lymphoma - B (ileum Burkitt's); T (EATL)
    4. GIST
    5. Neuroendocrine - SI / appendix
  42. 42What are features of neuroendocrine small intestinal tumours?1. Small but can metastasise easily - carcinoids (nodule mets)
    2. Subtypes: Carcinoids, Small cell carcinoma (poor prog)
    3. Carcinoid Syndrome (Functional + liver mets)
  43. 43How is neuroendocrine tumours of the small intestine treated?No cure.
    Suppression with somatostatin analogues.
  44. 44What is the histopathological features seen in Crohn's Disease?Transmural inflammation (affecting all layers) with crypt abscesses and non-nerotising granulomas.
    Ulcers may penetrate into fissures in muscular propria.
    Healing causes fibrosis and stricture formation.
    Anywhere along GI tract - Cobblestone appearance / skip lesions.
  45. 45What histopathological features is seen in Ulcerative Colitis?Confined to large bowel.
    Crypt abscesses with neutrophils in crypt, crypt wall, lamina propria.
    Crypt architectural distortion with gland branching, shortening and loss of normal gland arrangement.
  46. 46What are the 4 types / classes of colorectal polyps?1. Inflammatory - pseudopolyps, benign lymphoid polyps.
    2. Hamartomatous - Juvenile polyp, Peutz-Jegher
    3. Neoplastic - Adenoma, adenocarcinoma.
    4. Others - Hyperplastic, lipoma. leiomyoma
  47. 47Histo: Inflammatory pseudopolypsInflammatory tissue, hyper plastic mucosa
    Seen in UC / Crohn's.
    Macroscopically like adenomas.
  48. 48Histo: HarmartomaBenign tumour like lesion with >2 cell types
  49. 49Histo: Juvenile Polyps Most common paediatric polyps. What is the gene mutation?Cystic glands with normal or inflamed epithelium. Often in rectum.
    Germ line SMAD4 mutation.
  50. 50Peutz-Jegher polyps defining features?GI polyps with pigmentations of oral mucosa, lips, palms, genitalia.
    May have dysplastic foci if developed into adenoma / carcinoma.
    May cause intussuception and partial / complete obstruction.
  51. 51Types of adenoma in order of increasing malignancy risk?(Order of increasing malig. risk)
    1. Tubular
    2. Villous
    3. Tubulovillous
    4. Flat / Depressed adenoma
    (asso. HNPCC, FAP)
  52. 52Histological features of hyperplastic polyp? Are these malignant?Rectosigmoid sessile nodule, mostly asymptomatic in 60s-70s.
    Benign - no malignant potential
    UNLESS mixed (hyperplastic adenomatous polyps, serrated adenomas)
  53. 53Histo: Leiomyomatous polypMuscularis mucosae affected.
    Rectum, jejunum, ileum.
  54. 54What is the genetic mutation causing familial adenomatous polyposis (FAP)?APC gene
    Characterised by multiple polyps throughout colon - absent at birth but develop over time.
    If not treated - will develop colon cancer.
  55. 55Hereditary non-polyposis colorectal cancer (HNPCC) is multiple right sided carcinoma that develops in the young. What is the genetic mutation in this condition? What is the diagnosis criteria used?Abnormalities in 4 mismatch repair genes (microsatellite instability)
    Dx: Amsterdam criteria
    1. >3 family members with colorectal ca.
    2. Affects family members from >2 successive generations.
    3. One of the colorectal ca. occurred prior to 50yo.
    4. FAP excluded.
  56. 56Where do breast pathologies universally arise from?The terminal duct lobular units (TDLU) / terminal ductule.
  57. 57How does the TDLU drain?TDLU --> Sub-segmental duct --> Segmental duct --> Collecting / Lactiferous duct --> Nipple
  58. 58What are the two layers of normal breast histology and their function?1. Inner epithelial cells - Milk production.
    Markers: cytokeratins, epithelial membrane antigens.
    2. Outer myoepithelial cells - Contracts and squeeze milk forwards.
    Markers: SMM, p63,m ck5/6.
  59. 59In what breast pathology do you get micro-calcifications?DCIS
    Fat necrosis (dystrophic calcification)
    Ischaemic or suppurative
  60. 60What sign is seen in benign fibrocystic change in breast pathology?T-Cup Sign
    Cyst with apocrine metaplasia.
  61. 61Histological features of fibroadenoma of breast?Proliferative ducts and connective tissue stoma with defined border between epithelial and mesenchymal cells.
  62. 62Histological features of Phylloides Tumour? Which part is malignant and what is the route of spread?Leaf-like, composed of epithelial and mesenchymal elements. (Basically if anything has both it's worse).
    Mesenchymal component is malignant and produce metastasis through haematogenous route.
  63. 63Histological features of DCIS and LCIS?DCIS - Large duct filled with neoplastic cells with central necrosis.
    LCIS - Lobules filled with neoplastic cells, confined to acinus.
    Both confined within basement membrane.
  64. 64Invasive breast carcinomas penetrates through the basement membrane. What are the histological features of: 1) Invasive ductal carcinoma NST 2) Invasive lobular carcinoma1) Invasive ductal - Neoplastic cells lined by single layer.
    2) Invasive lobular - Invaded BM into stroma.
  65. 65What causes aortic stenosis? (2) (Which one is more common?) What causes mitral stenosis?Aortic Stenosis:
    Bicuspid valve / Calcific aortic sclerosis ***
    Rheumatic Heart Disease
    Mitral Stenosis: Rheumatic Heart Disease
  66. 66What can cause aortic regurgitation? Which is the most common? (3)++ Aortic root dilatation (e.g. Aortitis, syphillis)
    Mucinous deterioration (Marfan's)
    Endocarditis
  67. 67What can cause mitral regurgitation? (4)1. Mitral dilatation
    2. Mucinous degeneration (Marfan's)
    3. Endocarditis
    4. Papillary cell rupture
    (Mitral annular calcification)
  68. 68What gross changes are seen in myocardial infarction?Occasional mottling --> Dark mottling --> Central yellow tan --> Gray white scar.
  69. 69Microscopic changes in myocardial infarction?1. Early coagulation necrosis / oedema / haemorrhage.
    2. Pyknosis of nucleic, hyper-eosinophilia, early necrophilic infiltrate.
    3. Coagulation necrosis, interstitial infiltrate of neutrophils.
    4. Dense collagenous scars.
  70. 70What is mitral annular calcification? What complications can it lead to?Degenerative calcific deposits in the ring of mitral valve.
    Complications:
    1. Source of thrombus / emboli.
    2. Prone to infective endocarditis.
  71. 71What histological characteristics can you see in mitral valve prolapse?Ballooning of valvular cusps with thickened and rubbery leaflets.
  72. 72What causes rheumatic fever? What histological deformity is seen?Group A Beta-haemolytic streptococcal pharyngitis.
    Inflammatory deformity of valves:
    Leaflet thickening, commissure fusion, shortening / thickening / fusion of chordae tendinae.
  73. 73Infective endocarditis - vegetations on valves disrupt function mechanically. Which heart valves are typically affected in bacterial endocarditis? What's a group that's particularly at risk?Most commonly left heart valves affected.
    Tricuspid valve is involved in IVDU.
  74. 74What epithelium lines the: 1) Nose to distal bronchi 2) Portion of larynx / nasal vestibules1) Pseudo-stratified ciliated columnar epithelium
    2) Stratified squamous epithelium
  75. 75What type of hypersensitivity is caused by mTB in pulmonary TB? What investigations to do?Type 4 hypersensitivity
    FbC lymphocytes, tuberculin, culture
  76. 76What risk factors predispose bronchogenic carcinomas?1. Cigarette smoking
    2. Asbestos - Mesothelioma
    3. Radiation - radon gas
    4. Oncogenes - C-myc in SCLC, K-ras in adenocarcinoma.
    5. Scarring?
  77. 77Classification of lung cancerSmall Cell Lung Cancer (20%)
    (Ectopic neuroendocrine)
    Non-small cell lung cancer (80%)
    Adenocarcinoma+++
    Squamous cell carcinoma++
    Large cell undifferentiated carcinoma
  78. 78Primary T immune system occurs in the bone marrow and thymus. What happens in this process? What do the T cells mature into? Antigen dependent or independent?T cell receptor (TCR) rearranged.
    Mature into:
    CD4+ = B cell activation
    CD+ = Cellular immunity, cytotoxic response
    Antigen independent
  79. 79Where does the secondary immune system occur? What is the aim of 2º immunity? Antigen dependent / independent?Lymphoid follicle, T zone in LN, spleen, GIT
    Adaptive immune response
    Antigen dependent process
  80. 80What is the tertiary immune system? Where does it occur?Immune competent mature lymphoid cells petrol body surfaces.
    Genital tract + Skin.
  81. 81B Lymphoid cell is naive in bone marrow to enter blood and secondary lymphoid follicles. How does it mature?Rearrangement of immunoglobulin gene - Polyclonal.
    (Clonal = Lymphoma)
    Expresses immunoglobulin on surface as part of B cell receptor.
  82. 82T cell activation is dependent on B cell proliferation in secondary-B lymphoid follicle. What 3 compartments are in the lymphoid follicle?1. Germinal Centre
    2. Mantle
    3. Marginal zone
  83. 83Where do B cells increase in size and number within the lymphoid follicle? Somatic hypermutation at the germinal centre creates what 2 zones?Germinal centre --> Centroblasts --> Centrocytes, plasma cells, marginal zone B cells.
    Dark - Apoptosis of non-advantageous mutations.
    Light - Expansion of advantageous mutations --> Ig / memory cells.
  84. 84Reactive lymph nodes are normal - what can be seen in them under histology?Capsule and subcapsule sinus with many germinal centres.
    T zone (paracortex) between germinal centres.
    Hilum-afferent blood vessels.
  85. 85Mucosa associated lymphoid tissue (MALT) contributes to local immunity. Where are these found? What is the process in reaction to antigens?Peyer's patches in ileum, GIT except stomach.
    B+T lymphocytes infiltrate surface epithelium --> Adapted M cells present antigens --> Formation of germinal centres --> IgA --> Strengthen immune response to neutralise bacteria.
  86. 86What viruses are associated with malignant lymphoma?1. EBV - Burkitt's, Hodgkin, Post-transplant / AIDS
    2. HTLV1 - T cell non-hodgkin's lymphoma
    3. Hep. C - Low grade B cell NHL
    4. HHV8, Kaposi Sarcoma Virus - Plasma cell malignancy
  87. 87B cell lymphomas: B cells can transform into a malignant cell and retain morphological and phenotypic similarities to parent cell. What staining is seen in Low vs High Grade B cell lymphomas?+ve CD20 antigen (B-cell lineage)
    Low Grade B cell lymphomas:
    Low Kai67 staining
    High Grade B cell:
    High Kai67 staining
  88. 88What is this pathology: Big neoplastic cells with round nuclei, eccentric, form sheets.Plasma cell neoplasms
  89. 89Single cell, TCR rearranged lymphoma?T-cell lymphoma.
  90. 90Reed sternberg cells are seen in Hodgkin's lymphoma. What specific immuno-phenotype is seen?PAX5, CD30.
  91. 91Diagnostic methods for lymphoma?Morphology
    H+E stain
    Immunohistochemistry (antibody)
    Flow cytometry
    Molecular techniques (PCR, FISH)
  92. 92What does FISH show in diagnosing lymphomas? What is an indicator of poor prognosis in Burkitt's lymphoma?Fluorescence indicates translocated genes, e.g. in Burkitt's lymphoma.
    C-MIC translocation --> Aggressive and poor prognosis.
  93. 93What is the gene abnormality in Osteogenesis Imperfecta? How does this present clinically?Point mutation --> defective T1 collagen synthesis.
    Early onset osteoporosis, brittle bones.
  94. 94What does a point mutation of fibroblast growth factor receptor (FGFR) cause? How does this present?Achondroplasia.
    Short limbs, trident hands, contracted base of skull.
    NORMAL PROPORTION: skull and thorax.
  95. 95What is osteopetrosis? What serious problem can this lead to? How does it present on bloods?Defect in osteoclastic unit --> Inability to resorb bone.
    Continual new bone formation leads to dense bones, compromising haematopoiesis as marrow disappears.
    --> Pancytopenia.
  96. 96In what age group does osteomyelitis occur? Why? What is the most common causative organism?18m - 18y due to vascular growth plates predisposing infection in metaphysis of bone.
    S. aureus+++
    Others: enterobacteria, E.faecalis, P.aeruginosa, strep, coag-ve staph, A.calcoaceticus.
  97. 97What is the most important cause of osteoporosis? Where are the classic fracture sites?Post-menopausal osteoporosis.
    Others: disuse, diet, drugs, endocrine.
    Compression vertebral #, #NOF, Colle's #
  98. 98What are the causes of rickets/osteomalacia? What's the difference?Causes: Intrinsic vit. D disturbance / deficiency***, CKD, Inborn errors of metabolism (hypophosphataemia)
    Childhood - Rickets - genu varum / valgum
    Adult - Osteomalacia
  99. 99What are "Looser's zones" and what do they indicate?Microfractures due to structural weakness.
    Osteomalacia* / Rickets
  100. 100What is Paget's Disease of the Bones? What cancer might it develop into?Excessive breakdown and formation of bone followed by disorganised bone remodelling --> Weak misshapen bones, pain, fractures, arthritis.
    Osteosarcoma
  101. 101What types of osteosarcomas (bone forming tumour) are there and what age do they present?1. High grade intramedullary tumours+++
    ~15y
    2. Periosteal tumours (2%) - 20s
    3. Parosteal tumours (5%) - broad age range
  102. 102What radiological features are seen in osteosarcoma? What sites does it affect or distinctly uncommon?Radiology: Tumour in medullary cavity towards metaphysis, lytic expansile lesions*
    V. Common: Around knee
    Distinctly uncommon: Rib, vertebral column, peripheral limbs.
  103. 103What histological features is seen in osteosarcoma?Disorganised sheets of malignant osteoblasts showing pleomorphism and nuclear hyperchromatism.
    **Tumour osteoid or bone**
    Interspersed with irregular islands of non-structural tumour bone.
  104. 104A patient has Ollier's disease. What multiple tumours does he have?Enchondroma.
  105. 105A patient has exostosis (outgrowth of cartilage on bone). What condition is this? How does it present?Osteochondroma.
    (Chondromyxoid fibroma, chondroblastoma).
    May be asymptomatic or can crush tendons / nerves, #.
  106. 106Chondrosarcoma is a malignant cartilage tumour. What maybe found concurrently?15% of chondrosarcomas arise from osteosarcomas.
  107. 107What is the cause of Hashimoto's thyroiditis?Autoimmune anti-thyroid antibodies causing lymphoctic destruction of thyroid.
  108. 108What is Graves' Disease?Autoimmune thyroid stimulating autoantibodies --> Hyper functional multi nodular goitre or adenoma, Hyperthyroidism.
  109. 109Benign tumours of the thyroid are usually euthyroid (e.g. Multi nodular goitre, follicular denoma). What complication can a large benign goitre cause? How to treat these tumours / nodules?Compression of trachea / oesophagus (dysphagia).
    Rx. Thyroid lobectomy.
  110. 110What are the malignant carcinomas of the thyroid? (PFAM)What are the malignant carcinomas of the thyroid? (PFAM)
  111. 111Which malignant thyroid carcinoma has this histological feature: Widely invasive thyroid and blood vessels.Follicular carcinoma
  112. 112Which malignant thyroid carcinoma has this histological feature: Papillae covered by epithelial cells with pale, empty nuclei.Papillary carcinoma.
  113. 113Which malignant thyroid carcinoma has this histological feature: Psammoma bodies and enlarged LNPapillary carcinoma
  114. 114Which malignant thyroid carcinoma has this histological feature: Calcitonin stainingMedullary carcinoma.
    Arises from C cells which secrete calcitonin.
    Neuroendocrine tumour.
  115. 115Which malignant thyroid carcinoma may show MEN II?Medullary Carcinoma
  116. 116Primary hyperparathyroidism may be caused by Adenoma***, Hyperplasia**, and Carcinomas. How can these be differentiated?Adenoma - 1 big, 3 small / normal.
    Hyperplasia - 4 big or variably sized.
    Carcinoma - Very high calcium, bone disease, renal stones, mets, adherent at surgery.
  117. 117What is the most common cause of 2º hyperparathyroidism?Chronic renal failure.
    Others: Vit D / calcium deficiency, malabsorption, low serum Mg, pseudohypoparathyroidism (genetic resistance to PTH).
    Hypocalcaemia --> Compensatory overactivity. Hyperplasia of all 4 glands.
  118. 118Aside from USS, what other scan can be used ix / dx 2º hyperparathyroidism?Sestamibi scan.
    Highlights hyperactive PT glands.
    Results variable in hyperplasia.
  119. 119What may acute adrenal crisis be precipitated by?Infection
    Trauma
    Surgery
  120. 120What investigation is used to check for pheochromocytoma?Urine catecholamines
    Serum catecholamines
  121. 121Multiple endocrine neoplasia (MEN) syndromes are genetically inherited (AD). What does the normal MEN1 gene do? Where does MEN1 affect?MEN 1 gene is tumour suppressor, so mutations --> endocrine hyperplasia / tumours.
    Pituitary adenoma, parathyroid hyperplasia, pancreatic tumours.
  122. 122Where does MEN 2A affect?Parathyroid hyperplasia***
    Medullary thyroid carcinoma
    Pheochromocytoma
  123. 123What does MEN 2B affect? What is the genetic mutation of MEN 2?Mucosal neuromas
    Marfanoid body habitus
    Medullary thyroid carcinoma
    Pheochromocytoma
    RET oncogene mutation on chromosome 10. Genetic testing + prophylactic surgery.
  124. 124Familial medullary thyroid carcinoma (FMTC) affects?Thyroid only.
  125. 125In perinatal autopsy, when is an XR mandatory?If suspected skeletal dysplasia and multiple malformations.
  126. 126What are the main causes of perinatal deaths?1. Prematurity (62%)
    2. Obstetric events (28%)
    3. Metal abnormalities (12%)
  127. 127What chromosomal disorders result from the following: 1) Trisomy 21 2) Trisomy 18 3) Trisomy 13 4) Triploidy 5) 45, X01) T21 - Downs
    2) T18 - Edward's
    3) T13 - Patau's
    4) Triploidy - mostly spontaneous miscarried / stillborn
    5) Turner's
  128. 128What maternal diseases can lead to perinatal birth?1) Diabetic mother
    2) Pre-eclampsia
    3) Others: maternal drug abuse, thrombophilia, autoimmune disorders, malformed uterus.
  129. 129What are the clinical signs of pre-eclampsia? On autopsy?Maternal high BP and proteinuria.
    Autopsy: IUGR, asymmetricla growth restriction, placenta pathology
  130. 130What does a single palmar crease indicate?Trisomy 21
  131. 131In what condition is this seen on perinatal pathology: Wrinkled glove like skin and potter faciesOligohydramnios (deficiency of amniotic fluids)
  132. 132What is Acute choriomanionitis?Acute inflammation of metal membranes.
    Common after premature rupture of membranes (PROM) and ascending infection.
  133. 133Paediatric pathology: A newborn has delayed meconium passage, abdominal distension and billows vomiting. Histology of his distal rectum revealed aganglionic nerve trunks. What is this condition?Hirschsprung's Disease
    Developmental failure of neural crest cells migration - absence of ganglion cells in distal rectum so stools can't pass properly.
  134. 134What is the gene mutation in cystic fibrosis and how is it inherited? How does it present clinically?Autosomal recessive CFTR gene mutation.
    Mucus plugging of lungs - Bronchiectasis
    Inspissated meconium (thick / congealed)
    Intestinal atresia
    Rectal prolapse
  135. 135What is the characteristic histological finding in cystic fibrosis?Mucus plugs extending deep into crypts.
  136. 136What is the autoimmune pathology behind Coeliac's disease? Who is it more common / frequent in? What are the longterm complications?Inflammatory T-cell response in small intestine to gliadine (gluten).
    Frequently in T1DM and trisomy 21.
    Osteoporosis, intestinal T-lymphoma.
  137. 137What is seen on histology for Coeliac's disease?Villous atrophy, increased intraepithelial lymphocytes, increased lamina propria inflammatory cells, crypt hyperplasia.
  138. 138Adult polycystic kidney disease is autosomal-dominant. What is the inheritance pattern in paediatric polycystic kidney disease and what is the gene mutation?Autosomal recessive PKHD1 gene mutation.
  139. 139What is the current practice for investigating paediatric malignancies?Request molecular investigations from cytogenetic laboratory as paediatric malignancies are often associated with underlying genetic changes.
    FISH, PCR, microarray, histological diagnosis // MDT.
  140. 140On histology and FISH, the lab found malignant small, round, blue tumours in the bones and soft tissues of the patient (paediatric). What is this condition?Ewing's sarcoma.
  141. 141In the testis: What does each section contain / function? 1. Parenchyma 2. Interstitium 3. Rete Testis1. Parenchyma - Containing 4 seminiferous tubules which have stromal cells and germ cells in various stages of development.
    2. Interstitium - Stromal elements + Leydig cells - Testosterone secretion.
    3. Rete Testis - Receives luminal contents of seminiferous tubules --> Ductile efferentis.
    --> Epididymis --> Vas deferens --> Prostatic urethra --> + seminal vesicle --> ejaculatory duct.
  142. 142What is the most common type of testicular cancer?Germ cell tumours (GCT)
  143. 143How may germ cell tumours present clinically?Painless unilateral enlargement of testis
    2º hydrocele
    Metastatic signs
    Retroperitoneal mass
    Gynaecomastia
  144. 144Which GCT has this histological feature: In-situ proliferation of neoplastic germ cells in seminiferous tubules.Intra tubular germ cell neoplasia
    (in situ GCT)
  145. 145Which GCT has this histological feature: Sheets of rounded cells with clear cytoplasm and variable lymphocytic infiltrate in stromaClassical seminoma
  146. 146Which GCT has this histological feature: Mixed population of small, intermediate, giant cells w/ increased mitotic rate.Spermatocytic seminoma.
    Only 3-5% of seminomas.
    Good prognosis. Usually older age.
  147. 147Which GCT has this histological feature: Aplastic cells arranged in glandular / alveolar / solid / papillary growth patterns.Embryonal carcinoma.
  148. 148Which GCT has this histological feature: Schiller-Duval bodies Raised AFP tumour markers include beta-SCG, LDSYolk sac tumour
  149. 149Which GCT has this histological feature: Cryototrophoblasts and syncitiotrophoblasts Raised HCGChoriocarcinoma (MTT)
  150. 150Which GCT has this histological feature: Tissues from any germ cell layers including mature (adult) and immature (foetal) tissue.Teratoma
  151. 151How might GCT spread?1. Direct - rete testis / epididymis
    2. Lymphatic - para-aortic & mediastinal LN
    3. Haematogenous - lung, liver, bone (teratoma)
  152. 152What are the tumours of the two zones of prostate? 1) Periurethral / inner zone 2) Outer zoneInner - Nodular hyperplasia
    (DHT - increased glandular + stromal component - urinary retention)
    Outer - Carcinoma
    Premalignant lesion (PIN) / Adenocarcinoma
  153. 153What histological features are seen in prostate adenocarcinoma? What's the aetiology?Glandular structures lined by single cell layer.
    Multifactorial aetiology:
    Androgen receptor
    1q24-25 genetic susceptibility
    Fat consumption
    Lycopene in tomatoes protective
  154. 154How is carcinoma of the prostate staged?A - Not palpable
    B - Palpable prostate only
    C - Extracapsular extension
    D - Metastatic
  155. 155What is the epithelial lining of the cervix 1) At birth 2) At puberty 3) In Adulthood1) At birth - Non-keratinising stratified squamous epithelium
    2) At puberty - Columnar glandular cells exposed to vagina
    3) Adult - Transformation zone of squamous metaplasia
  156. 156What is the strain of HPV that is: 1) High risk for cervical squamous carcinoma 2) Low risk for genital warts1) 16/18
    2) 6/11
  157. 157What is seen in histology on a cervical smear of a woman with HPV?Perinuclear halo - cervical smear exfoliated cells.
  158. 158How is cervical intraepithelial neoplasia (CIN) graded? (3)CIN-I : Disordered maturation in lower 1/3.
    CIN-II: 2/3 dysplastic.
    CN-III: Full thickness dysplastic changes.
    Carcinoma in-situ.
  159. 159What is adenomyosis? What would you see on histology?Endometrium grows / infiltrates myometrium; contractions + pain.
    Histo: Pockets of glandular tissue in myometrium.
  160. 160What is endometriosis? What does this increase the risk of?Endometrial tissue grows outside of uterus.
    Increased risk of ovarian cancer.
  161. 161How would endometrial carcinoma present clinically?Post-menopausal bleeding
    Obese / DM
    Nulliparous with non-ovulatory cycles
    HTN
    Infertility
  162. 162What are the types of endometrial carcinoma?Type 1 - Perimenopausal endometrial carcinoma - oestrogen excess
    In order of increasing risk: Simple < Complex < Atypical < Carcinoma
    Type 2 - Elderly - atrophic endometrium
  163. 163What types of fibroid / leiomyoma are there? (3)Subserosal
    Intramural
    Submucosal
  164. 164Histological features of Leiomyoma LeiomyosarcomaLeiomyoma: multiple, white-grey, whorled, uniform
    Leiomyosarcoma: single, necrosis, haemorrhage, frequent mitosis.
  165. 165What is the risk of ectopic pregnancy?Risk of rupture and fatal haemorrhage in oviduct implantation.
  166. 166What are the types of surface epithelial ovarian tumours?Cell type: Serous, mucinous, endometrioid
    Pattern of growth: cystic, solid, surface
    Amount of fibrous stroma
    Atypia / Invasiveness: benign, borderline, malignant
  167. 167Teratomas are totipotent germ cell ovarian tumours. What does it look like?Solid with minute cysts or predominantly cystic.
    Often a single component - e.g. dermoid cyst.
  168. 168What histological change is seen in infarcted myocardium?Necrotic muscle with loss of nuclei
    Oedema
    Fibre disarray - LINES OF ZAHN*
    (indicative of thrombus in heart / aorta)
    (Early - contraction then necrosis)
  169. 169What post-mortem changes are seen in the acute, subacute, and healed phase of MI?Acute - acute inflammatory cells.
    Subacute - necrotic tissue with inflammatory cells (macrophages)
    Healed - Fibrotic scar tissue, collagen bundles, fibroblasts.
  170. 170Antistreptolysin titre elevated is suggestive of...?Rheumatic heart failure (strep)
    Immune deposits --> Heart failure many years later as fibrotic damage lasts a long time.
  171. 171What does decreased pulmonary vascular markings suggest?Pulmonary atresia
  172. 172What is the Tetralogy of Fallot?Ventricular septal defect
    Pulmonary stenosis / atresia
    Right ventricular hypertrophy
    Overriding aorta
  173. 173How might a young person with DVT get a CVA?If they have ASD (e.g. septal defect).
    --> Paradoxical embolus: embolism that makes use of an abnormal communication in the vasculature.
  174. 174What are the causes of hypertension? (ERECT)E - Essential
    R - Renal
    E - Endocrine (Cushing's, Conn's, Pheochromocytoma)
    C - Coarctation of aorta
    T - Toxaemia of pregnancy.
  175. 175Histological features of atherosclerosis?Thickened intima
    Fragmented internal elastic lamina
    SM infiltration of intima
    Luminal narrowing
  176. 176What is Samter's Triad?Aspirin-exacerbated Respiratory Disease
    Triad:
    Nasal polyps + Asthma + Aspirin / NSAID sensitivity
  177. 177A bronchial washing of an SOB patient contains dumbbell-shaped structures which stained for iron stains. What are these?Asbestos bodies
  178. 178What markers are positive in intratubular neoplasia of testes?PLAP, C-Kit
  179. 179What markers are positive in embryonal carcinoma?Cytokeratin+
    CD 30+
  180. 180What biochemical markers are raised in prostate cancer?PSA, ALP.
  181. 181What may form renal stones?1. Calcium oxalate (smooth)
    2. Triple phosphate
    3. Urate (granular)
    4. Cysteine
  182. 182What histotypes are there of renal cell carcinoma?1. Clear cell***
    2. Papillary
    3. Chromophobe (atypical)
    Large epithelial cells of parenchyma.
  183. 183What is the histology show for transitional cell carcinoma (TCC) of renal pelvis?Low grade TCC growing in pushing fashion around medullary renal tubules.
  184. 184Fat accumulation in hepatocytes and pericellular spaces(Non-) Alcoholic fatty liver disease
  185. 185What markers separate autoimmune hepatitis apart from chronic hepatitis? HistoAutoimmune hepatitis = Chronic hepatitis + Raised ALT, raised IgG, Raised ANA+
    Histo: Main inflammation in portal tract with limiting plate.
    Destruction of limiting plate --> Interphase hepatitis.
  186. 186What is wilson's disease?AR inherited chromosome 13 mutation.
    Increased copper in liver / brain.
    Liver failure / neuro deficit. (CHILDHOOD)
  187. 187What does HFE gene mutation lead to? What is this condition?Haemachromatosis - HFE gene mutation on chromosome 6, AR inheritance.
    Iron overload and storage.
    Leads to cirrhosis, increase HCC risk.
  188. 188Radial scar in breast disease?Benign dense fibrous scar related to sclerosis adenosis.
    <1% breast cancer.
  189. 189What does bloody nipple discharge possibly indicate?Duct papilloma
    Carcinoma
  190. 190Failure to thrive with anti-gliadine and anti-tissue transglutaminase antibodies in bloodCoeliac's

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UoB 2018 Y3 pathology
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