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  2. 2. Anaemias and leukaemias
  3. 3. Anaemia <ul><li>types (etiology): </li></ul><ul><li>1) iron deficiency </li></ul><ul><ul><li>most common type </li></ul></ul><ul><ul><li>chronic menstrual blood loss, peptic ulcer, haemorrhoids </li></ul></ul><ul><li>2) pernicious anaemia </li></ul><ul><ul><li>macrocytic anaemia </li></ul></ul><ul><ul><li>+/- neurological disease </li></ul></ul><ul><ul><li>folate insufficiency </li></ul></ul>
  4. 4. Anaemia <ul><li>3) leukaemia </li></ul><ul><ul><li>cause of normocytic anaemia </li></ul></ul><ul><ul><li>childhood! </li></ul></ul><ul><li>4) sickle cell trait </li></ul><ul><li>5) thalasaemia </li></ul>
  5. 5. Anaemia <ul><li>clinical features </li></ul><ul><li>tab 22.2, 3, 4 </li></ul><ul><li>mucosal disease </li></ul><ul><li>glossitis </li></ul><ul><li>recurrent aphthae </li></ul><ul><li>candidiosis and angular stomatitis </li></ul>
  6. 6. Anaemia <ul><li>dangers of general anesthesia </li></ul><ul><ul><li>any reduction of oxygenation -> irreparable brain damage, myocardial infarction -> gen. anesthesia should be provided in hospital </li></ul></ul><ul><li>lowered resistence to infection </li></ul><ul><ul><li>oral candidiosis </li></ul></ul><ul><ul><li>osteomyelitis </li></ul></ul>
  7. 7. Sickle cell disease and sickle cell trait <ul><li>people of African, Afro-Caribbean and Mediterranean or Middle Eastern origin </li></ul><ul><li>sickle cell diease = homozygotes </li></ul><ul><li>sickle cell trait = heterozygotes </li></ul><ul><li>abnormal Hb (HbS) with the risk of haemolysis, anaemia and other effects </li></ul><ul><li>in heterozygotes sufficient normal Hb (HbA) is formed to allow normal life </li></ul>
  8. 8. Sickle cell disease and sickle cell trait <ul><li>Sickle cell disease: </li></ul><ul><li>complications from polymerisation of deoxygenated HbS (less soluable than HbA) </li></ul><ul><li>-> chronic haemolysis -> chronic anaemia </li></ul><ul><li>exacerbation of sickling raises blood viscosity -> blocking of capillaries and sickling crisis </li></ul><ul><li>tab 22.5 </li></ul><ul><li>+ abnormal susceptibility to infections (Pneumococcal, Meningococcal) and osteomyelitis </li></ul>
  9. 9. Sickle cell disease and sickle cell trait <ul><li>dental aspects of sickle cell disease and s.c.trait: </li></ul><ul><li>Hb ≤ 10g/dl -> v. s. homozygote </li></ul><ul><li>s.c. trait: gn anaesthesia with full oxygenation </li></ul><ul><li>s.c. disease: </li></ul><ul><li>+/- oral mucosa pale or yellowish due to jaundice </li></ul><ul><li>+/- radiographics changes in skull and jaws </li></ul><ul><li>prompt atb treatment </li></ul>
  10. 10. Sickle cell disease and sickle cell trait <ul><li>painfull crisis with analgesics </li></ul><ul><li>rigorous dental care necessary due to ↑ susceptibility to infection </li></ul>
  11. 11. The thalassaemias <ul><li>α -thalassaemias Asians, Africans and Afro-Caribbean </li></ul><ul><li>ß-thalassaemias Mediterranean (Greeks) </li></ul><ul><li>diminished synthesis of globin chains -> resulting relative excess of other chains -> precipitation in ery -> +/- haemolysis </li></ul><ul><li>severity of disease depends on the numbers of affected genes </li></ul><ul><li>minor = heterozygotes </li></ul><ul><li>major = heterozygotes </li></ul>
  12. 12. The thalassaemias <ul><li>thalassaemia minor: </li></ul><ul><li>mild, but persistent microcytic anaemia, otherwise asymptomatic </li></ul><ul><li>+/- splenomegaly </li></ul>
  13. 13. The thalassaemias <ul><li>thalassaemia major: </li></ul><ul><li>severe hypochromic, microcytic anaemia </li></ul><ul><li>great enlargement of liver and spleen </li></ul><ul><li>skeletal abnormalities (marrow expansion) </li></ul><ul><li>life saving transfusions, but iron depositions in tissues -> haemosiderosis -> dysfunction of glands and other organs -> xerostomia </li></ul>
  14. 14. Leukaemia <ul><li>leukaemic white blood cells production -> supress of other cell lines of the marrow </li></ul>
  15. 15. Leukaemia <ul><li>acute leukaemia </li></ul><ul><li>ALL most common leukaemia of children </li></ul><ul><li>AML in adults </li></ul><ul><li>tab 22.7 </li></ul><ul><li>splenomegaly, hepatomegaly, +/- lymphadenopathy </li></ul><ul><li>mucosal pallor, abnormal gingival bleeding </li></ul><ul><li>tab 22.8 </li></ul>
  16. 16. Leukaemia <ul><li>management: </li></ul><ul><ul><li>biopsy of gingival swelling </li></ul></ul><ul><ul><li>vigorous oral hygiene to controll the bacterial population before complications develop </li></ul></ul><ul><ul><li>extractions avoided, if necessary – blood transfusion, generous atb cover </li></ul></ul>
  17. 17. Leukaemia <ul><li>chronic leukaemia </li></ul>
  18. 18. Leukopenia and agranulocytosis <ul><li>leukopenia </li></ul><ul><li>WBC ≤ 5000³/l </li></ul><ul><li>different causes tab 22.10 </li></ul><ul><li>chance haematological finding x severe - immunodeficiency </li></ul>
  19. 19. Leukopenia and agranulocytosis <ul><li>agranulocytosis </li></ul><ul><li>clinical effects of severe neutropenia: fever prostration, mucosal ulceration </li></ul><ul><li>drug induced leukopenias </li></ul><ul><li>tab 22.12 </li></ul>
  20. 20. Leukopenia and agranulocytosis <ul><li>aplastic anaemia </li></ul><ul><li>failure of production of all bone marrow cells (pancytopenia) </li></ul><ul><li>systemic and oral effects: purpura, anaemia, susceptibility of infection </li></ul><ul><li>cause: unknown, ai, drug induced </li></ul><ul><li>management: stop drugs, give atb and transfusions </li></ul>
  21. 21. Haemorrhagic diseases
  22. 22. Haemorrhagic diseases <ul><li>haemorrhagic diseases = purpura (platelet deffects) and clotting deffects </li></ul>
  23. 23. Haemorrhagic diseases <ul><li>Investigation of a history of excessive bleeding: </li></ul><ul><ul><li>careful history essential tab. 23.1 </li></ul></ul><ul><ul><li>most of the haemorrhagical diseases are hereditary! </li></ul></ul><ul><ul><li>bleeding for up to 24hrs after an extraction usually due to local causes or a minor defect of haemostasis -> more prolonged bleeding is significant </li></ul></ul>
  24. 24. Haemorrhagic diseases <ul><li>Clinical examination: </li></ul><ul><ul><li>signs of anaemia and purpura </li></ul></ul><ul><ul><li>examination of the mouth -> planning of the operation </li></ul></ul><ul><ul><li>haemophilia – all essential extractions carried out at a single operation with fVIII cover </li></ul></ul><ul><ul><li>radiographs (to prevent complications) </li></ul></ul>
  25. 25. Haemorrhagic diseases <ul><li>Laboratory investigations: </li></ul><ul><ul><li>tab 23.2 </li></ul></ul><ul><ul><li>essential is look for anaemia </li></ul></ul><ul><ul><li>blood grouping </li></ul></ul>
  26. 26. Haemorrhagic diseases <ul><li>A) Purpura </li></ul><ul><li>typical result of platelet disorders </li></ul><ul><li>bleeding time prolonged but clotting function normal (with exception of of vW disease) </li></ul>
  27. 27. Haemorrhagic diseases <ul><li>general features of purpura: </li></ul><ul><ul><li>purpura = bleeding into the skin or mucous membranes causing petechiae or ecchymoses or „spontaneous bruising“ </li></ul></ul><ul><ul><li>haemorrhage immediately follows the trauma and ultimately stops spontaneously as a result of normal coagulation </li></ul></ul><ul><ul><li>thrombocytopenia = platelets ≤ 100 000 mm³ </li></ul></ul><ul><ul><li>spontaneous bleeding uncommon until platelets ≤ 50 000 mm³ </li></ul></ul>
  28. 28. Haemorrhagic diseases <ul><ul><li>typical site palate </li></ul></ul><ul><ul><li>+/- excessive gingival bleeding or blood blister </li></ul></ul><ul><ul><li>tab 23.3 </li></ul></ul>
  29. 29. Haemorrhagic diseases <ul><li>ITP </li></ul><ul><li>IgG auto Ab </li></ul><ul><li>↓ number of platelets </li></ul><ul><li>children or young adult women </li></ul><ul><li>first sign could be profuse gingival bleeding or postextraction haemorrhage </li></ul><ul><li>+/- spontaneous bleeding into the skin </li></ul>
  30. 30. Haemorrhagic diseases <ul><li>management: </li></ul><ul><ul><li>corticosteroids </li></ul></ul><ul><ul><li>transfusions of platelets </li></ul></ul><ul><ul><li>anti…??? </li></ul></ul>
  31. 31. Haemorrhagic diseases <ul><li>AIDS </li></ul><ul><li>ai thrombocytopenia can be early sign </li></ul><ul><li>drug associated purpura </li></ul><ul><li>aspirin + others interfere with platelet function </li></ul><ul><li>others act as haptens -> immune destruction of platelets or suppress marrow function </li></ul><ul><li>tab 23.4 </li></ul>
  32. 32. Haemorrhagic diseases <ul><li>localised oral purpura </li></ul><ul><li>sometimes blood blister without haemostatic defect </li></ul><ul><li>choking sensation („angina bullosa haemorrhagica“) </li></ul><ul><li>rupture -> ulcer </li></ul><ul><li>systemic purpura should be excluded </li></ul>
  33. 33. Haemorrhagic diseases <ul><li>von Willebrand´s disease </li></ul><ul><li>both by prolonged bleeding time and deficiency of fVIII </li></ul><ul><li>usually inherited, AD </li></ul><ul><li>deficiency of fVIII mild -> purpura more common manifestation </li></ul>
  34. 34. Haemorrhagic diseases <ul><li>B) Clotting disorders </li></ul><ul><li>tab 23.5 </li></ul>
  35. 35. Haemorrhagic diseases <ul><li>Haemophilia A </li></ul><ul><li>most common, severe </li></ul><ul><li>fVIII deficiency </li></ul><ul><li>6/100 000 </li></ul><ul><li>severe haemophilia typically effects in childhood – bleeding into muscles or joints after minor injuries </li></ul><ul><li>mild haemophilia (fVIII ≥ 25%) – no symptoms until an injury, surgery or dental extraction </li></ul>
  36. 36. Haemorrhagic diseases <ul><li>severe and prolonged bleeding can also follow local anaesthetic injections! (inferior dental blocks!) </li></ul>
  37. 37. Haemorrhagic diseases <ul><li>clinical features: </li></ul><ul><ul><li>positive family history </li></ul></ul><ul><ul><li>30% patients negative history! </li></ul></ul><ul><ul><li>bleeding starts after a short delay (normal platelet and vascular responses) -> persistent bleeding, can continue for weeks </li></ul></ul><ul><ul><li>haemarthroses </li></ul></ul><ul><ul><li>intracranial haemorrhage! </li></ul></ul><ul><ul><li>deep tissue bleeding -> obstruction of airways! </li></ul></ul><ul><ul><li>HBV, HCV+! </li></ul></ul><ul><ul><li>+/- formation of anti fVIII Ab </li></ul></ul>
  38. 38. Haemorrhagic diseases <ul><li>principles of management: </li></ul><ul><ul><li>radiographs (local status, prevention of complications) </li></ul></ul><ul><ul><li>admission to hospital </li></ul></ul><ul><ul><li>replacement therapy </li></ul></ul><ul><ul><li>as much surgical work as possible in one session 23.6 </li></ul></ul><ul><ul><li>for dental extraction fVIII level 50-75% </li></ul></ul><ul><ul><li>postoperatively: atb, risk of bleeding greatest 4-10 days postoperatively </li></ul></ul>
  39. 39. Haemorrhagic diseases <ul><ul><li>aspirin and related analgesics avoided! </li></ul></ul><ul><ul><li>extractions in mild haemophilia with antifibrinolytic drugs </li></ul></ul>
  40. 40. Haemorrhagic diseases <ul><li>Christmas disease (haemophilia B) </li></ul><ul><li>fIX </li></ul><ul><li>inherited </li></ul><ul><li>more stable -> replacement therapy in longer intervals </li></ul><ul><li>other the same as in haemophilia A </li></ul>
  41. 41. Haemorrhagic diseases <ul><li>Acquired clotting defects </li></ul><ul><li>a) vitamin K deficiency </li></ul><ul><li>causes: obstructive jaundice, malabsorption </li></ul><ul><li>surgary delayed to haemostasis recover </li></ul><ul><li>+/- vitamin K </li></ul>
  42. 42. Haemorrhagic diseases <ul><li>b) anticoagulant treatment </li></ul><ul><li>coumarin (warfarin) </li></ul><ul><li>dental extraction save with INR 2-3 </li></ul><ul><li>few teeth extracted in one session, trauma should be minimal, sockets can be sutured </li></ul><ul><li>anticoagulation should not be stopped </li></ul><ul><li>for large surgery -> stopped with agreement of physician </li></ul><ul><li>short term: heparin (acts only about 6hrs) -> surgery delayed for 12-24hrs </li></ul>
  43. 43. Haemorrhagic diseases <ul><li>c) liver disease </li></ul><ul><li>obstructive jaundice </li></ul><ul><li>extensive liver damage (viral hepatitis, alcoholism) </li></ul><ul><li>haemorrhage can be severe and difficult to control </li></ul><ul><li>-> vitamin K </li></ul><ul><li>antifibrinolytic agents </li></ul><ul><li>fresh plasma infusion </li></ul>
  44. 44. Lymphomas
  45. 45. Lymphomas <ul><li>any type of lymphocytes, most frequently B cells </li></ul><ul><li>all malignant </li></ul><ul><li>Hodgkin + non Hodgkin lymphomas (NHL) </li></ul><ul><li>relatively frequently involve cervical lymph nodes x rare in the mouth </li></ul>
  46. 46. Lymphomas <ul><li>A) NHL </li></ul><ul><li>adults predominantly affected </li></ul><ul><li>nondescript, soft, painless swelling +/- ulcerated </li></ul><ul><li>histologically: </li></ul><ul><li>+ invasion of adjacent tissues </li></ul><ul><li>+ if traumatised – inflammatory cells can obscure the lymphomatous nature of the tu </li></ul>
  47. 47. Lymphomas <ul><li>management: </li></ul><ul><ul><li>biopsy! </li></ul></ul><ul><ul><li>staging! </li></ul></ul>
  48. 48. Lymphomas <ul><li>Burkitt´s lymphoma </li></ul><ul><li>nasopharyngeal (T cell) lymphoma – mlg midline granuloma </li></ul><ul><li>MALT! </li></ul><ul><li>+ local manifestation of gn disease </li></ul>
  49. 49. Cervical lymphadenopathy
  50. 50. Cervical lymphadenopathy <ul><li>dental and periodontal infections most common cause </li></ul><ul><li>lymphomas </li></ul><ul><li>HIV infection </li></ul><ul><li>tab 26.1 </li></ul><ul><li>investigation: recent viral illness – lymphadenopathy resolves after some months </li></ul>
  51. 51. Cervical lymphadenopathy <ul><li>TBC </li></ul><ul><li>Mcb tuberculosis + atypical Mcb </li></ul><ul><li>clinical features: </li></ul><ul><li>pathology: granulomas, Mcb -> Mcb culture or DNA tests </li></ul><ul><li>management: suspicion of TBC – affected nodes should be excised intact </li></ul>
  52. 52. Cervical lymphadenopathy <ul><li>Syphilis </li></ul><ul><li>lymph nodes enlarged, soft and rubbery </li></ul><ul><li>primary or secondary stage </li></ul><ul><li>Treponema pallidum in a direct smear or by serological finding </li></ul><ul><li>management: atb </li></ul>
  53. 53. Cervical lymphadenopathy <ul><li>Cat scratch disease </li></ul><ul><li>tab 26.4 </li></ul><ul><li>pathology: destruction of lymph node architecture, necrosis and lymphocytic infiltration, formation of histiocytic granulomas and central suppuration </li></ul><ul><li>WS staining </li></ul><ul><li>x deep mycoses </li></ul>
  54. 54. Cervical lymphadenopathy <ul><li>management: history, clinical features, exclusion of other causes, disease is mild and self limiting, +/- suppuration and sinus formation </li></ul>
  55. 55. Cervical lymphadenopathy <ul><li>Lyme disease </li></ul><ul><li>transmitted by insects, deer ticks </li></ul><ul><li>tab 26.5 </li></ul><ul><li>management: history + clinical picture </li></ul><ul><li>confirmed serologically </li></ul><ul><li>atb! </li></ul>
  56. 56. Cervical lymphadenopathy <ul><li>Infectious mononucleosis </li></ul><ul><li>self-limiting lymphoproliferative disease </li></ul><ul><li>tab 26.6 </li></ul><ul><li>+/- more persistent lymphadenopathy which may mimic a lymphoma </li></ul><ul><li>management: peripheral blood picture (atypical lymphocytes), Paul-Bunnell test, anti EBV Ab, ampicillin or amoxicilin should be avoided! </li></ul>
  57. 57. Cervical lymphadenopathy <ul><li>AIDS </li></ul><ul><li>soon after infection transient glandular fever like-illness </li></ul><ul><li>later +/- wide spread lymphadenopathy (GLS) </li></ul><ul><li>-> AIDS </li></ul>
  58. 58. Cervical lymphadenopathy <ul><li>Toxoplasmosis </li></ul><ul><li>intestinal parasite of many domestic animals (cats) </li></ul><ul><li>management: serologically, antimicrobial treatment </li></ul>
  59. 59. Cervical lymphadenopathy <ul><li>Mucocutaneous lymph node syndrome (Kawasaki´s disease) </li></ul><ul><li>tab 26.8 </li></ul><ul><li>management: clinical and ECG finding </li></ul><ul><li>aspirin, γ -globulin </li></ul>
  60. 60. Cervical lymphadenopathy <ul><li>Drug-associated lymphadenopathies </li></ul><ul><li>occasional toxic effect of long term treatment with the antiepileptic drug, phenytoin can mimic lymphoma </li></ul><ul><li>management: </li></ul>