Skip to content
  • Categories
  • Recent
  • Popular
  • World
Skins
  • Light
  • Brite
  • Cerulean
  • Cosmo
  • Flatly
  • Journal
  • Litera
  • Lumen
  • Lux
  • Materia
  • Minty
  • Morph
  • Pulse
  • Sandstone
  • Simplex
  • Sketchy
  • Spacelab
  • United
  • Yeti
  • Zephyr
  • Dark
  • Cyborg
  • Darkly
  • Quartz
  • Slate
  • Solar
  • Superhero
  • Vapor

  • Default (No Skin)
  • No Skin
Collapse

isurg

  1. Home
  2. Pathology Mocks
  3. Mock16 Colon Cancer

Mock16 Colon Cancer

Scheduled Pinned Locked Moved Pathology Mocks
1 Posts 1 Posters 5 Views
  • Oldest to Newest
  • Newest to Oldest
  • Most Votes
Reply
  • Reply as topic
Log in to reply
This topic has been deleted. Only users with topic management privileges can see it.
  • A Offline
    A Offline
    admin
    wrote last edited by admin
    #1

    Stem
    60-year-old male with rectal bleeding. Rectal examination revealed external haemorrhoids. FIT (faecal immunochemical test) is 100 (positive). Colonoscopy + biopsy revealed adenocarcinoma with melanosis coli. Histological examination of the specimen revealed a lesion invading up to muscularis propria. Patient has a history of CHD.

    How can you stage colorectal cancer?

    By using Dukes' staging
    TNM

    What's the stage of this?

    According to the case the tumour invade up to muscularis propria but so it will be B1
    No lymph node or distant metastasis.

    Which is more important in clinical use?

    TNM.
    Modified Duke Staging System
    A: Tumour penetrates into the mucosa of the bowel wall, but no further.
    B1: Tumour penetrates into, but not through the muscularis propria, (the muscular layer) of the bowel wall.
    B2: Tumour penetrates into and through the muscularis propria of the bowel wall.
    C1: Tumour penetrates into, but not through the muscularis propria of the bowel wall; there is pathologic evidence of colon cancer in the lymph nodes.
    C2: Tumour penetrates into and through the muscularis propria of the bowel wall; there is pathologic evidence of colon cancer in the lymph nodes.
    D: The tumour, which has spread beyond the continues of the lymph nodes (to organs such as the liver, lung or bone).

    What is the age for screening for colorectal carcinoma?

    Between 50 to 59 years.

    What is the faecal immunochemical test (FIT)?

    FIT detects small amounts of blood in stool samples using antibodies specific to human haemoglobin. It is less likely to detect globin from upper gastrointestinal bleeding than guaiac-based tests as it targets the globin component of haemoglobin, which degrades as it passes through the gut.
    FIT for screening is quantitative and the threshold for an abnormal result is set locally.

    What are haemorrhoids?

    Swollen and bulging veins in the lower rectum and anus.

    How do they occur?

    The anal cushions function normally when they are fixed to their proper sites within the anal canal by fibromuscular ligaments, which are the anal remnants of the longitudinal layer of the muscularis propria from the rectum (Treitz's ligaments).
    When these submucosal fibres fragment (as by prolonged and repeated downward stress related to straining during defecation), the anal cushions are no longer restrained from engorging excessively with blood and may result in bleeding and prolapse.

    What's the pathogenesis of thrombosed piles?

    Acute thrombosis results from sudden raised pressure causing rupture of the vascular plexus leading to a blood clot at the anal verge.
    Any activity requiring excessive abdominal straining such as over-exercising can cause this

    Define melanosis coli? What's its significance?

    It is a disorder of pigmentation of the wall of the colon
    Often identified at the time of colonoscopy.
    It is benign
    May have no significant correlation with disease.
    Associated with chronic laxative use

    Why does coronary artery get thrombosed?

    Due to coronary artery atherosclerosis

    How does atherosclerosis occur?

    Endothelial injury, and resultant endothelial dysfunction, leading to increased permeability, leukocyte adhesion, and thrombosis
    Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall
    Platelet adhesion
    Monocyte adhesion to the endothelium, migration into the intima, and differentiation into macrophages and foam cells
    Lipid accumulation within macrophages, which release inflammatory cytokines
    Smooth muscle cell recruitment due to factors released from activated platelets, macrophages, and vascular wall cells
    Smooth muscle cell proliferation and ECM production

    What are its risk factors?
    Non-modifiable (constitutional)

    Genetic abnormalities
    Family history
    Increasing age
    Male gender

    Modifiable

    Hyperlipidaemia
    Hypertension
    Cigarette smoking
    Diabetes
    Inflammation

    What are the common sites of atherosclerosis and their effects?

    Large and medium vessels

    Effects?

    Coronary arteritis (cause decrease blood supply, MI)
    Cerebral arteries (cause CVA)
    In Renal (renal failure)
    In lower limb (can cause ischemic limb)
    In blood supply of small intestine (can cause ischemic colitis)

    Can you define a thrombus? What's its function?

    A thrombus is solid constituent of blood and its healthy response to injury intended to prevent bleeding

    What's the mechanism of thrombus formation?

    An atheromatous plaque is suddenly disrupted by intra-plaque haemorrhage or mechanical forces
    This will expose sub-endothelial collagen and necrotic plaque contents to the blood.
    Then Platelets adhere, aggregate. and are activated, releasing thromboxane A2, adenosine diphosphate (ADP), and serotonin-causing further platelet aggregation and vasospasm.
    Activation of coagulation by exposure of tissue factor and other mechanisms adds to the growing thrombus.
    Finally, within minutes, the thrombus can evolve to completely occlude the coronary artery lumen

    Mention 4 differences between a thrombus and a clot?
    Thrombus

    Occurs in flowing/circulating blood
    Firmly attached to vessel wall
    Friable and dry
    Pale, red or mixed
    May show lines of Zahn

    Clot

    Occurs in stagnant blood
    Loosely attached
    Soft and moist
    Red or yellow appearance
    No lines of Zahn

    How does myocardial infarction occur?

    Within seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in adenosine triphosphate (ATP) and accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes
    The functional consequence is a rapid loss of contractility, which occurs within a minute or so of the onset of ischemia. Ultrastructural changes (including myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling) also become rapidly apparent.
    These early changes are potentially reversible. Only severe ischemia lasting at least 20 to 40 minutes causes irreversible damage and myocyte death leading to coagulation necrosis

    1 Reply Last reply
    0
    • A admin moved this topic from Pathology

    Hello! It looks like you're interested in this conversation, but you don't have an account yet.

    Getting fed up of having to scroll through the same posts each visit? When you register for an account, you'll always come back to exactly where you were before, and choose to be notified of new replies (either via email, or push notification). You'll also be able to save bookmarks and upvote posts to show your appreciation to other community members.

    With your input, this post could be even better 💗

    Register Login
    Reply
    • Reply as topic
    Log in to reply
    • Oldest to Newest
    • Newest to Oldest
    • Most Votes


    • Login

    • Don't have an account? Register

    • Login or register to search.
    • First post
      Last post
    0
    • Categories
    • Recent
    • Popular
    • World