5. bleeding disorder


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5. bleeding disorder

  1. 1. HEMOSTASIS, BLEEDING AND CLOTTING DISORDER Presented by : Nik Khairiyah Bt Raja Mohammed Mohamad Nizar B. Muhamad Yatim Nuradibah Bt Shahrul Nuramalina Bt Ahmad Ehsan
  2. 2. In the absence of blood vessel damage : platelets are repelled from each other and from endothelium of blood vessel. endothelial cell secretes prostacyclin and nitric oxide (NO) -act as vasodilator & inhibit platelet aggregation. plasma membrane of endothelial cell contain enzyme (CD39) - breakdown ADP to AMP + Pi.
  3. 3. Normal Hemostasis Def : consequence of tightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while introducing the rapid formation of a localized hemostatic plug at the site of vascular injury. - from Robbins Basic Pathology 8th edition Mechanism vasocontriction formation of platelet plug coagulation cascade fibrinolysis
  4. 4. Normal hemostasis
  5. 5. Coagulation cascade
  6. 6. Normal hemostasis
  7. 7. Bleeding Disorder Def : Bleeding disorders is a general term for a wide range of medical problems that lead to poor blood clotting and continuous bleeding. characterized clinically by abnormal bleeding, which can either be spontaneous or become evident after some inciting event. can result from : defects in the blood vessel abnormalities in the blood itself blood clotting factor platelet Source from : National Haemophilia Association
  8. 8. Source from : Nelson Essential of Pediatrics 5th edition
  9. 9. Diagnostic approach 1) Identify clinical features a) age of onset - neonate - toddler - adolescent b) family history - family tree - gender c) bleeding history - previous surgical / dental procedure - presence of systemic disorder - drug history - unusual pattern or inconsistent history d) pattern of bleeding - mucous membrane bleeding & skin haemorrhage - bleeding into muscles or into joints - scarring and delayed haemorrhage Source from : Tom Lissauer, Graham Clayden Illustrated Textbook of Paediatric 3rd edition
  10. 10. 2) Screening test Test Mechanism Tested Normal Value Disorder Bleeding time (BT) Hemostasis, capillary & platelet function 3-7 min beyond neonate Thrombocytopenia, von Willebrand disease Platelet count Platelet number 150 000 – 450 000 / mm^3 Thrombocytopenia Prothrombin time (PT) Extrinsic & common pathway < 12 sec beyond neonate; 12-18 sec in term neonate Defect in Vit K-dependent factor, liver disease, DIC Activated partial thromboplastin time (APTT) Intrinsic & common pathway 25-40 sec beyond neonate; 70 sec in term neonate Hemophilia, von Willebrand disease, DIC Source from : Nelson Essential of Pediatrics 5th edition
  11. 11. in neonate (term infant), the level of all clotting factors except factor VIII & fibrinogen are LOWER, much lower in preterm infants. therefore, the results have to be compared with normal values in infants of a SIMILAR GESTATIONAL & POSTNATAL AGE. sometimes necessary to exclude an Inherited Coagulation Factor Deficiency by testing the coagulation of both parents.
  12. 12. Thank you….
  14. 14. WHAT IS PLATELET ? Oblong disk shape Size- 2-4 µm on the long axis Volume- 5-12 fL Produced in bone marrow by megakaryocte cell Platelet count in blood- 150,000-350,000 µL Life span- ???? Function- ??
  15. 15. Classification of platelet disorders Quantitative disorder Abnormal distribution Dilution effect Decreased production (leukemia and some anemia) Increased destruction Qualitative disorders Inherited disorders (rare) Acquired disorders (medication, chronic renal failure, cardiopulmonary bypass)
  16. 16. Glanzmann’sthrombasthenia Bernard-Soulier syndrome PRIMARY ITP TTP TAR syndrome Wiskott-Aldrich syndrome Neonatal isoimmune SECONDARY Malignancy Aplastic anemia DIVC Sepsis Drug-induced Hemolytic-uremic syndrome Hypersplenism Autoimmune(SLE) HIV
  17. 17. THROMBOCYTOPENIA Defined as reduced in the platelet count< 150, 000µL that characterized by spontaneous bleeding, a prolonged bleeding time, and a normal PT and PTT. The risk of bleeding depends on the level of the platelet count: Mild thrombocytopenia (platelet <150 000 cells/µL) Moderate thrombocytopenia (platelet 20 000 - 50 000 cells/µL) Severe thrombocytopenia (platelet <20 000 cells/µL)
  18. 18. Sign and symptom bruising, petechiae, purpura and mucosal bleeding (epistaxis @ gum bleeding) major haemorrhage like severe GI bleeding, intracranial bleeding or haematuria is less common normal platelet count may present in platelet dysfunction
  19. 19. Congenital (Fanconianaemia, Wiskot-Aldrich Syndrome Decreased production of platelets Acquired (aplastic anaemia, marrow infiltration, drug induced ) Increased platelets destruction Immunologic destruction (ITP, SLE , Alloimmune neonatal thrombocytopenia) Aetiology Nonimmunologicdestruction (HUS, TTP,DIC, CHD) Sequestration Hypersplenism Dilutional Massive blood transfusion
  20. 20. 1.IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP) DEFINITION Isolated thrombocytopenia with otherwise normal blood count in a patient with no clinically apparent associated conditions that can cause thrombocytopenia (such as HIV infection, SLE, lymphoproliferative disorders, alloimmune thrombocytopenia, and congenital or hereditary thrombocytopenia). Caused by immune- mediated destrcuction of circulating platelet d/t anti-platelet autiantibodies There are two clinical subtypes of ITP: Acute ITP. Chronic ITP (starts after the disease has been present for > 6 months).
  21. 21. Feature of Acute and Chronic ITP
  22. 22. PATHOGENESIS Inappropriate immune recovery follows an acute viral infection in children. Autoantibodies (IgG or IgM) directed against platelet membrane antigens (especially glycoprotein complex IIb/IIIa). Phagocytosis of antibody-coated platelets by the reticuloendothelial system. Increased destruction of platelets – Thrombocytopenia.
  23. 23. CLINICAL MANIFESTATIONS Onset is usually sudden for acute ITP and in chronic ITP, it is insidious onset. Petechiae or purpura Feet, legs, arms, and buttocks. Mucosal bleeding. Palatal petechiae, epistaxis, hematuria, menorrhagia, GI bleeding. Rarely, intracranial hemorrhage may occur in long standing severe thrombocytopenia.
  24. 24. DIAGNOSIS History taking. Physical examination. Signs of bleeding (petechiae and purpura). Mucosal bleeding. Investigations. Full blood count. Low platelet count. Histological findings. Platelets are normal in size or may appear larger than normal. Normal red blood cells morphology. Normal white blood cells morphology. Coagulation tests. Prolong bleeding time, normal PT and PTT.
  25. 25. Not all children with acute ITP need hospitalization. Treatment is indicated if there is: Life threatening bleeding episode (e.g. ICH) regardless of platelet count. Platelet count < 20,000/mm³ with mucosal bleeding. Platelet count < 10,000/mm³with any bleeding. Choice of treatment: Oral prednisolone - 4 mg/kg/day for 7 days, taper and discontinue at 21 days. IV Methylprednisolone - 30 mg/kg/day for 3 days. IV Immunoglobulin - 0.8 g/kg/dose for 1 day OR 250 mg/kg for 2 days. IV Anti-Rh(D) immunoglobulin - (50 – 75 µ/kg) in Rhesus positive patients – may cause haemolytic anaemia. TREATMENT & MANAGEMENT
  26. 26. Splenectomy is only for life threatening in acute ITP For chronic ITP: Repeated treatment with IV immunoglobulin or IV anti-D or high dose pulse steroids are effective in delaying the need for splenectomy Splenectomy is effective in inducing remission in 70-80% of childhood chronic ITP
  27. 27. COMPLICATION Intracranial hemorrhage - 50% mortality rate. Risk of ICH highest in: Platelet count < 20 000/mm³. History of head trauma. Uses of aspirin (inhibitor of platelet aggregation). Presence of cerebral arteriovenous malformation. 50% of all ICH occurs after 1 month of presentation, 30% after 6 months.
  28. 28. 2. Hemolytic Uremic Syndrome (HUS) Related to TTP in which the number of platelets suddenly decreases, RBC are destroyed and the kidney stop functioning HUS is rare, but can occur with certain bacterial infection (E.coli or shigelladysenteriae) and with the use some drugs (quinine, cyclosporine, mitomycin C) Toxin producing organism such as E.coli cause endothelial damage that activates localized clotting, leading to platelet aggregation and consumption Common in infants, young children and pregnant women
  29. 29. 3.Thrombotic Thrombocytopenic Purpura (TTP) Resembles hemolytic uremic syndrome but occur more commonly in adults than in children Spontaneous aggregation of platelets and activation of coagulation in small blood vessels In TTP, platelet consumption, precipitated by a congenital or acquired deficiency of metalloproteinase that cleaves vWF
  30. 30. THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP) HEMOLYTIC – UREMIC SYNDROME (HUS) Severe deficiency of the vWF – cleavage protease Platelet activation Platelet thrombi formation.
  31. 31. 4.Marrow infiltration eg: leukemia A progressive, malignant disease of the blood forming organs, marked by distorted proliferation and development of leukocytes and their precursors in the blood and the bone marrow Overproduction of these white cells, which are immature or abnormal forms, suppresses the production of normal WBC, RBC and platelets Lead to increase susceptibility to infection,anemia and bleeding
  32. 32. Clinical presentation Result from infiltration of bone marrow or other organs with leukemic blast cells Mostly presents insidiously over several weeks with some or all of following signs and symptoms: Malaise Infections Pallor Abnormal bruising Hepatosplenomegaly Lymphadenopathy Bone pain
  33. 33. Progress rapidly in some children Blood count is abnormal, low hemoglobin,thrombocytopenia and evidence of circulating blast cells in most children Bone marrow examination to confirm the diagnosis
  34. 34. 5.Disseminated Intravascular Coagulation (DIC) Disorder characterized by coagulation pathway activation leading to diffuse fibrin deposition in the microvasculature and consumption of coagulation factors and platelets. Occurs as secondary complication of variety diseases. Caused by the systemic activation of coagulation pathways, leading to formation of thrombi throughout the microcirculation and widespread thromboses. There is consumption of platelets and coagulation factors and secondarily activation of fibrinolysis. As consequence, there is depletion of the elements required for hemostasis ( consumptive coagulopathy) May be acute or chronic. Initiated through the tissue factor pathway.
  35. 35. The commonest causes of activation of coagulation are severe sepsis or shock due to circulatory collapse, e.g in meningococcal septicemia or extensive tissue damage from trauma or burn. Infectious Meningococcemia Other gram –vebact (Salmonella, E.coli, Haemophilus) Virus (CMV, herpes, hemorrhagic fevers) Rickettsia, Malaria and fungus Tissue injury CNS trauma, crush injury Multiple fracture with fat emboli Profound shock of asphyxia Hypothermia/hyperthermia Massive burns Malignancy Acute promyelocytic leukemia Acute monoblastic or myelocytic leukemia widespread malignancies (neuroblastoma) Causes of DIC Venom/ toxin Snake bites Insect bites Microangiopathic disorder Severe TTP/ hemolytic uremic syndrome Giant hemangioma Hereditary thrombotic disorders Antithrombin iii def. Homozygous protein C def. GIT disorder Fulminant hepatitis severe IBD Reye syndrome Newborn Maternal toxemia G. B strep. Infection Abruptioplacentae Congenital viral disease (CMV, herpes) Miscellaneous Severe acute graft rejection Acute hemolytic transfusion reaction Heparin induced thrombosis
  36. 36. Pathophysiology of DIC Endothelial injury Massive tissue destruction sepsis Release of tissue factor Platelet aggregation Activation of plasmin Widespread microvascular thrombosis Proteolysis of clotting factor Consumption of clotting factors and platelets fibrinolysis Vascular occlusion Fibrin split products Microangiopathic hemolytic anemia Ischemic tissue damage Inhibition of thrombin, platelet aggregation and fibrin polymerization bleeding
  37. 37. Clinical Course The diagnosis of DIC usually suspected clinically and confirmed by a laboratory finding of a decline in platelets and fibrinogen associated with elevated PT time, PTT time, levels of fibrin(ogen) degradation products and D-dimers. There is also marked reduction of naturally occuring anticoagulants, protein C, S and antithrombin. In severely ill patient, there will be sudden occurrence of bleeding from venepuncture or incision site, gastrointestinal or pulmonary hemorrhage, petechiae or ecchymosis or evidence of peripheral gangrene or thrombosis.
  38. 38. Clinical course Depending on the balance between clotting and bleeding tendencies. In acute DIC (e.g., associated with obstetric complication) is dominated by a bleeding diathesis. In chronic DIC (e.g., as occur in an individual with cancer) tends to present with symptom related to thrombosis. Typically, the abnormal clotting occurs only in the microcirculation, although large vessels are involved occasionally.
  39. 39. Treatment Treat the disorder inducing the DIC first such as sepsis. Support the patient by correcting hypoxia, acidosis and poor perfusion. Replace depleted blood clotting factors, platelets and anticoagulant proteins by transfusion. Heparin may be used to treat significant arterial or venous thrombotic disease unless sites of life-threatening bleeding coexist. Thus, the use of heparin remains controversial. Treatment with anticoagulants or coagulants contained in fresh-frozen plasma usually needed in acute case. Drotregocinalfa (recombinant activated protein C) reduces mortality in adults with DIC and sepsis.
  40. 40. Disorder Of Platelet Function Bernard-Soulier syndrome Deficiency of glycoprotein Ib complex (vWF receptor) Autosomal recessive coagulapathy Abnormally large platelets Glanzmannthrombasthenia Deficiency of glycoprotein IIb-IIIa (fibrinogen receptor) Bleeding time is prolonged
  42. 42. Topic classification
  43. 43. Case study A 15 years old girl comes to your clinic with complain of heavy menses (menorrhagia). She also complain sometimes she had mild nose bleed (epistaxis) and easy bruising. She had previous surgical history of tonsillectomy at 6 years of age, which required blood transfusion for excessive bleeding. Her mother required a hysterectomy after giving birth to her younger brother because of excessive hemorrhage. Her mother is planning for her brother to join for circumcision in this school holiday.
  44. 44. Haemophilia – overview A group of blood disorders in which there is defect in clotting factors 70% are X-linked recessive disorder. 30% spontaneous mutation. The bleeding patterns of haemophilia are similar. Types : A:Deficiency in factor VIII (classic haemophilia) B: Deficiency in factor IX (Christmas disease) C: Deficiency in factor XI
  45. 45. Haemophilia - classification
  46. 46. Haemophilia – clinical manifestation Haemarthrosis(spontaneous bleeding in muscle or joints - painful) Illiapsoas bleeding Joint Swelling Easy bruising Epistaxis Haematuria Intracranial hemorrhage
  47. 47. Haemophilia - investigation Full blood count Activated partial thromboplastin time (aPTT) – PROLONGE Normal Prothrombin Time, Platelet Count, Bleeding Time. Specific factor assay : VIII or IX - LOW Joint x-ray Further Investigation Hepatitis B, Hepatitis C, HIV serology Diagnosis for carrier status for genetic counseling
  48. 48. Haemophilia - treatment First aid: Pressure, Rest, Ice, Elevation (PRICE) Blood transfusion – severe blood lost Factor concentrates; continuous infusion (severe) or intermittent bolus (prophalaxis). Factor VII given every 8-12 hours Factor IX given every 12-24 hours Desmorpressin acetate (DDAVP); mild & moderate, not for severe. Antifibrinolytics: Aminocaproic acid (Amicar) Fresh Frozen plasma (high risk for virus)
  49. 49. Haemophilia - complication Factor concentrate infusion at home as prophylaxis; Repeated venopuctures Need for venous access Availability Cost Developed Inhibitors ?????? Joint destruction; inflammation, swelling, fibrosis. Acquisition of virus (Hep B, Hep C, Hep D & HIV)
  50. 50. Haemophilia - inhibitors It’s a IgG antibodies directed against transfused factor VIII (30%), rarely happens with factor IX (2%) Making treatment for haemophilia difficult. Can be low titer Porcine factor VIII or continue infusion of factor VIII. Can be high titer  recombinant factor VIIa as bypassing agent.
  51. 51. Von willerbrand disorder - overview Most common hereditary deficiency caused abnormality in von Willerbrand protein. Functions on both primary & secondary homestasis. 1. To act as bridge between subendothelial collagen and platelets 2. Bind and protect factor VIII from rapid clearance then delivers it to site of injury.
  52. 52. Von willerbrand disorder - types Type I (70%-80%) – Quantitative, Partial decrease in quantity vWF Mild clinical symptoms Type 2 (15%-20%)– Qualitative, Decrease affinity toward Factor VIII and platelet Type 3 – Quantitative, Absence of von Willerbrand factor Severe clinical symptoms Lack of response to Desmorphine (DDAVP)
  53. 53. Clinical menifestation Asymptomatic Mucous membrane bleeding Epistaxis Cutaneus bleeding Gingival bleeding Menorrhagia
  54. 54. investigation Full Blood Count – platelet normal aPTTPROLONGE or normal Factor VIII LOW or normal. von Willerbrand Factor activity (ristocetin cofactor) Ristocetin, an antibiotic that causes vWF to bind to platelet taken from plasma. In healthy people, platelet rapidly agglutinate. von Willerbrand Factor antigen Measure vWF protein and binding sites. Not accurate.
  55. 55. treatment Desmopressin (DDAVP) – Treatment of choice for patients with vWD types 1 and 2 . Concentrate of von Willerbrand Factor (Humarate P) when high levels of vWF are needed but cannot achieved with DDAVP (type 3) Contraceptive for menorrhagia Clot-stabilizing medications  (antifibrinolytic medications) -
  56. 56. Prognosis & complications Lifelong tendency toward easy bruising, frequent epistaxis, and menorrhagia. Register with Malaysia Hemophilia Society. Carry medic-alert bracelet or chain & carry books diagnosis, types etc.
  57. 57. Vitamin k deficiency 3 main types of VK are K-1, phylloquinone, derived from plants; K-2, menaquinone, produced by the intestinal flora K-3, menadione which is a synthetic, water-soluble form used for treatment. Required for synthesis of Plasma factor II, VII, IX, and X Hemorrhagic disease in infant that breastfeed exclusively. Give parenteral vitamin K (0.5 to 1 mg) to all newborns shortly after birth.
  58. 58. Hepatic failure Severe impairment of hepatic functions or severe necrosis of hepatocytes in the absence of pre-existing liver disease Fatal for most affected children. The mortality rate may reach 80-90% in the absence of liver transplantation.
  59. 59. Sources: Nelson, Essential of Peadiatrics Tom, Illustrated Textbook Paediatric Paediatric Protocol for Malaysians Hospitals http://www.emedicne.com/ Thank you for your attention.. Questions?
  60. 60. Fiqh medic Should children with severe clotting disorder undergo circumcisions? Can we infuse bovine or porcine products in medical treatment? ?
  61. 61. answers von Willerbrand Disorder Circumcision is not compulsory, can if only procedure is monitored by specialist & prohylaxis is available. Can use porcine or bovine products as it has already undergone multiple process. Proceed with halal product if available.
  64. 64. A vessel defect either congenital or acquired resulting in abnormal bleeding despite an otherwise normal coagulation factor and platelet.
  66. 66. VASCULAR- NON HEAMATOLOGIC Child abuse Other trauma Vasculitis Ulcer Varices Ehler- Danlos syndrome Telangiectasia Angiodysplasia
  67. 67. 1. Child abuse Trauma to blood vessels Physically Cutaneous purpuraand petechiae
  68. 68. 2. OTHER TRAUMA ULTRAVIOLET RADIATION-severe sunburn INFECTIOUS-bacterial, rickettsial, viral, protozoa,parasitic infections EMBOLIC NEOPLASTIC- Langerhans cell histiocytosis DRUG RELATED- penicillin, phenytoin ALLERGIC- allergic/ contact dermatitis Hematology Basic principle and practice, 4th edition.
  69. 69. Langerhans cell histiocytosis Rocky mountain spotted fever Contact dermatitis Penicillin allergy
  70. 70. 3. VASCULITIS Henoch-Schonlein purpura DEFINITION Vasculitis of unknown etiology characterized by inflammation of small blood vessel associated with leukocytic infiltration of tissue, hemorrhage, and ischemia. EPIDEMIOLOGY Incidence 13/100 000 children occur in children age 3-15 years. boys>girls ETIOLOGY Unknown. Likely mechanism thought to be an immune-complex mediated disease with deposits of IgA in the glomerular capillaries, dermal capillaries and GI tract. Mesangial deposition of IgA and C3 in the kidney.
  71. 71. CLINICAL MANIFESTATION Rash of palpable purpura: below the waist on the butocks and lower extremeties. Can be accompanied by edema of the calves,dorsum of the feet, scalp, and scrotum or labia. 2. Athritis: acute, tend to affect the lower extremeties; ankle and knees. joint swelling.
  72. 72. 3. Gastrointestinal : mild to moderate crampy abdominal pain, abdominal distension, bloody diarrhea, intussusception or abdominal perforation. 4. Renal: heamaturia, hypertension LABORATORY AND IMAGING STUDIES Elevated ESR, CRP and WBC count. Normal platelet count Urinalysis ( Hematuria) Serum BUN and Creatinine Stool sample. CT scans show multifocal areas of bowel-wall thickening, mesenteric edema, vascular engorgement, and nonspecific lymphadenopathy. Renal biopsy may show IgAmesangial deposition and occasionally IgM, C3, and fibrin. Patients with IgA nephropathy may have elevated plasma antibody titers against H. parainfluenzae.
  73. 73. Diagnosis Presence of 2 of 4 criteria: Palpable purpura- raises, palpable hemorrhagic skin lesions in the absence of thrombocytopenia. Bowel angina - diffuse abdominal pain or the diagnosis of bowel ischemia Diagnostic biopsy- histologic changes showing granulocytes in the walls of arterioles or venules Pediatric age group- age < 15 years at onset of symptoms Treatment: Corticosteroid NSAID
  74. 74. 5. VARICES Varices?-Varices are dilated blood vessels ( veins) usually in the esophagus or stomach.- eg due to Portal hypertension. The varices are fragile and can rupture easily, resulting in a large amount of blood loss. Symptoms of bleeding varices include: Vomitting of blood Black, tarry, or bloody stool Low blood pressure Rapid heart rate Shock (in severe cases)
  75. 75. 6. ULCER Clinical manifestation: Burning epigastric several hour after meal & night. GI bleed (hematemesis,melena) Risk facor: H. Pylori infection Drugs Family history Head trauma Burn injury Investigation: Endoscopy-mandatory with alarm symptoms Test for H.Pylori FBC ESR Amylase and lipase Treatment: Omeprazole-clarithromycin-metronidazole (associate with H.pylori) Antacids Proton pump inhibitor
  76. 76. 7. EHLER- DANLOS SYNDROME Congenital disorder of defect in collagen synthesis. Patient’s skin lacks its normal resistance to traction and can be easily pulled away from underlying structures. This condition places blood vessels at great risk for disruption even with minor trauma
  77. 77. Cutaneous findings – hyperextensible and fragile skin, poor wound healing, easy bruising,molluscoidpseudotumors. Systemic features – joint hypermobility, scoliosis, significant risk of spontaneous arterial, intestinal or uterine rupture
  78. 78. Diagnosis clinical observation. Both DNA and biochemical studies skin biopsy Management There is no known cure for Ehlers Danlos Syndrome. The treatment is supportive. Close monitoring of the cardiovascular system.
  79. 79. MARFAN SYNDROME An autosomal dominant disorder of the connective tissue. Clinically symptoms mostly involve three systems: Cardiac ( dissecting aorta, aortic valve regurgitation, mitral valve prolapse) MSK ( dolichostenomalia, arachnodactyly, abnormalities of the sternum, kyphoscoliosis) Ophtalmology (dislocated lens, cataracts) Diagnosed by : [ Diagnostic criteria for Marfan syndrome ]- **presence of 2 major criteria(organ systems) and 1minor criteria ( third organ system). [ NELSON ESSENTIALS of PEDIATRICS, 5th EDITION; page223 ]
  80. 80. Pectuscarinatum Thin and tall body habitus arachnodactyly Pectusexcavatum
  81. 81. 8. TELANGIECTASIA Congenital defects of the vessel wall that can result to abnormal bleeding tendency. Eg: Hereditary hemorrhaghictelangiectasia Progressive degenaration of the vessel wall leading to development of widespread angiomatous lesion. On PE, small violaceous non pulsatiletelangiectasias can be found over lips and mucous membrane.( They blanch with pressure). This disease not limited to the skin– Telangiectasias in lung, liver.
  82. 82. 9. ANGIODYSPLASIA angiodysplasia is a small vascular malformation of the gut. it resembles telangiectasia. common cause of unexplained GI bleeding (recurrent bleeding per rectum) and anemia. cecum or ascending colon Diagnosis of angiodysplasia is often accomplished with endoscopy, either colonoscopy or EGD.
  83. 83. Colonoscopy of angioydsplasia in the Sigmoid colon
  84. 84. THANK YOU !