-Microscope : Perfect differentiation cytologically & histologically(smilar to origin). -No spread or recurrence if well excised. -Suspect malignancy if : sudden enlargement, invasion of capsule, loss of intercellular cement substance, or pleomorphism & anaplasia started to appear. 11- GENERAL CHARACTERS OF MALIGNANCY ? - Rapid rate than benign & invasive (infiltrative) mode. - Grossly in solid organ : large, irregular, non-capsulated, firm, fleshy with hemorrhage & necrosis. - Grossly on a surface either fungating with broad base, infiltrative forming a stricture ring in a tube or ulcerative ( large, irregular, necrotic floor, indurated base, with raised everted edges). - Microscope : invading malignant cells with features of anaplasia (Changes in morphology & pattern (arrangement) in malignant tumours as pleomorphism,Hyperchromasia, increase N/C ratio, mitosis & giant cells and loss of polarity.) forming sheets or masses of variable grades of differentiation (ACCORDING TO CELLULAR ARRANGEMENT)into grade 1, 2, 3, 4.numerous thin vessels in fibrous stroma. - Recurrence after excision, lethal (fatal) course,ended by cachexia. Spread : direct, lymphatic , blood or transcoelomic. 12- Mechanism of spread of malignant tumours? -Mechanism of invasion (direct or distant) : attachment to BM, degradation using collagenases & cathepsin B released from either tumour cells or activated fibroblasts followed by motility through pseudopodia. -Vascular dissimination & homing : survived tumour cells move in blood singly or as emboli covered by blood cells till reach the target organ, then invade vessel wall by similar mechanism as above. 13- LYMPHATIC SPREAD ? - Mechanism of spread & vascular dissimination ( as above). -Commoner in carcinoma & 2 types : (a) EMBOLISM: tumour emboli pass in lymph reaching subcapsular sinus of lymph node, forming mass destroy LN, causing LN enlargement , firmness & fixation. (b)PERMEATION: tumour invade lymph as solid columns causing lymphatic obstruction & edema, occur in breast, bronchi & prostate (non-pitting). 14- ORGAN METASTASIS (haematogenous spread) ? -Mechanism of vascular invasion : attachment to vascular BM, degradation using collagenases & cathepsin B released from either tumour cells or activated fibroblasts followed by motility through pseudopodia. -Vascular dissimination & homing : survived tumour cells move in blood singly or as emboli covered by blood cells till reach the target organ, then invade vessel wall by similar mechanism as above. -Tumour cells reach blood either directly through invasion of thin vessels commoner in sarcoma, or indirectly through lymphatics as in carcinoma. -Routes: 1- Tumour emboli reach systemic venous blood implanted into lungs. 2- Tumour emboli reach portal vein implanted into liver. 3- Tumour emboli reach aorta from lung or Lt heart implanted into brain, bone, liver….. 4- Through vertebral plexus of veins, emboli reach CNS & vertebrae directly. -Commonest organs are liver,lungs,brain & bone, rare in heart,intestine & pancreas. -Metastasis appear as well defined , multiple nodules. In bone osteolytic lesion causing bone fracture & pancytopenia except in metastasis of to prostatic cancer where it is osteosclerotic (dense Ca due to alkaline phosphatase) .
Posted on: Sat, 29 Nov 2014 12:34:12 +0000
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