Ha Em a Tho Pathology

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HAEMATOPATHOLOGY



Anaemias and leukaemias



Anaemia

types (etiology):

1) iron deficiency

±

most common type ± chronic menstrual blood loss, peptic ulcer,

haemorrhoids

2) pernicious anaemia

± macrocytic anaemia

± +/- neurological disease

± folate insufficiency



Anaemia

3) leukaemia

± cause of normocytic anaemia

±

childhood! 4) sickle cell trait

5) thalasaemia



Anaemia

clinical features

tab 22.2, 3, 4

mucosal disease

glossitis

recurrent aphthae candidiosis and angular stomatitis



Anaemia

dangers of general anesthesia

± any reduction of oxygenation irreparable brain

damage, myocardial infarction gen. anesthesia

should be provided in hospital

lowered resistence to infection

± oral candidiosis

± osteomyelitis



Sickle cell disease and sickle cell trait

people of African, Afro-Caribbean and

Mediterranean or Middle Eastern origin

sickle cell diease = homozygotes sickle cell trait = heterozygotes

abnormal Hb (HbS) with the risk of

haemolysis, anaemia and other effects in heterozygotes sufficient normal Hb (HbA) is

formed to allow normal life




Sickle cell disease:

complications from polymerisation of

deoxygenated HbS (less soluable than HbA)

chronic haemolysis chronic anaemia

exacerbation of sickling raises blood viscosity

blocking of capillaries and sickling crisis

tab 22.5 + abnormal susceptibility to infections

(Pneumococcal, Meningococcal) and

osteomyelitis




dental aspects of sickle cell disease and s.c.trait:

Hb 10g/dl v. s. homozygote

s.c. trait: gn anaesthesia with full oxygenation

s.c. disease:

+/- oral mucosa pale or yellowish due to

jaundice +/- radiographics changes in skull and jaws

prompt atb treatment




painfull crisis with analgesics

rigorous dental care necessary due to

susceptibility to infection



The thalassaemias

-thalassaemias Asians, Africans and Afro-

Caribbean

ß-thalassaemias Mediterranean (Greeks)

diminished synthesis of globin chains resulting relative excess of other chains

precipitation in ery +/- haemolysis

severity of disease depends on the numbersof affected genes

minor = heterozygotes

major = heterozygotes



The thalassaemias

thalassaemia minor:

mild, but persistent microcytic anaemia,

otherwise asymptomatic +/- splenomegaly



The thalassaemias

thalassaemia major:

severe hypochromic, microcytic anaemia

great enlargement of liver and spleen

skeletal abnormalities (marrow expansion)

life saving transfusions, but iron depositions in

tissues haemosiderosis dysfunction of glands and other organs xerostomia



Leukaemia

leukaemic white blood cells production

supress of other cell lines of the marrow



Leukaemia

acute leukaemia

ALL most common leukaemia of children

AML in adults

tab 22.7

splenomegaly, hepatomegaly, +/-

lymphadenopathy mucosal pallor, abnormal gingival bleeding

tab 22.8



Leukaemia

management:

± biopsy of gingival swelling

±

vigorous oral hygiene to controll the bacterialpopulation before complications develop

± extractions avoided, if necessary blood

transfusion, generous atb cover



Leukaemia

chronic leukaemia



Leukopenia and agranulocytosis

leukopenia

WBC 5000³/l

different causes tab 22.10

chance haematological finding x severe -

immunodeficiency




agranulocytosis

clinical effects of severe neutropenia: fever

prostration, mucosal ulceration

drug induced leukopenias

tab 22.12




aplastic anaemia

failure of production of all bone marrow cells

(pancytopenia) systemic and oral effects: purpura, anaemia,

susceptibility of infection

cause: unknown, ai, drug induced management: stop drugs, give atb and

transfusions



Haemorrhagic diseases




haemorrhagic diseases = purpura (platelet

deffects) and clotting deffects




Investigation of a history of excessive bleeding:

± careful history essential tab. 23.1

± most of the haemorrhagical diseases are hereditary!

± bleeding for up to 24hrs after an extraction usually

due to local causes or a minor defect of haemostasis

more prolonged bleeding is significant




Clinical examination:

± signs of anaemia and purpura

± examination of the mouth planning of the

operation

± haemophilia all essential extractions carried out

at a single operation with fVIII cover

± radiographs (to prevent complications)




Laboratory investigations:

± tab 23.2

± essential is look for anaemia

± blood grouping




A) Purpura

typical result of platelet disorders

bleeding time prolonged but clotting functionnormal (with exception of of vW disease)




general features of purpura:

± purpura = bleeding into the skin or mucous

membranes causing petechiae or ecchymoses or

spontaneous bruising ± haemorrhage immediately follows the trauma and

ultimately stops spontaneously as a result of

normal coagulation

± thrombocytopenia = platelets 100 000 mm³ ± spontaneous bleeding uncommon until platelets

50 000 mm³




± typical site palate

± +/- excessive gingival bleeding or blood blister

± tab 23.3




ITP

IgG auto Ab

number of platelets children or young adult women

first sign could be profuse gingival bleeding or

postextraction haemorrhage +/- spontaneous bleeding into the skin




management:

± corticosteroids

± transfusions of platelets

± anti???




AIDS

ai thrombocytopenia can be early sign

drug associated purpura aspirin + others interfere with platelet

function

others act as haptens immune destructionof platelets or suppress marrow function

tab 23.4




localised oral purpura

sometimes blood blister without haemostatic

defect choking sensation (angina bullosa

haemorrhagica)

rupture ulcer

systemic purpura should be excluded




vonWillebrand´s disease

both by prolonged bleeding time and

deficiency of fVIII

usually inherited, AD

deficiency of fVIII mild purpura more

common manifestation




B) Clotting disorders

tab 23.5




Haemophilia A

most common, severe

fVIII deficiency 6/100 000

severe haemophilia typically effects in

childhood bleeding into muscles or jointsafter minor injuries

mild haemophilia (fVIII 25%) no symptoms

until an injury, surgery or dental extraction




severe and prolonged bleeding can also follow

local anaesthetic injections! (inferior dental

blocks!)




clinical features: ± positive family history

± 30% patients negative history!

± bleeding starts after a short delay (normal platelet and vascular

responses) persistent bleeding, can continue for weeks ± haemarthroses

± intracranial haemorrhage!

± deep tissue bleeding obstruction of airways!

± HBV, HCV+!

± +/- formation of anti fVIII Ab




principles of management: ± radiographs (local status, prevention of

complications)

± admission to hospital

± replacement therapy

± as much surgical work as possible in one session

23.6

± for dental extraction fVIII level 50-75% ± postoperatively: atb, risk of bleeding greatest 4-10

days postoperatively




± aspirin and related analgesics avoided!

± extractions in mild haemophilia with

antifibrinolytic drugs




Christmas disease (haemophilia B)

f IX

inherited more stable replacement therapy in longer

intervals

other the same as in haemophilia A




Acquired clotting defects

a) vitamin K deficiency

causes: obstructive jaundice, malabsorption surgary delayed to haemostasis recover

+/- vitamin K




b) anticoagulant treatment coumarin (warfarin)

dental extraction save with INR 2-3

few teeth extracted in one session, traumashould be minimal, sockets can be sutured

anticoagulation should not be stopped

for large surgery stopped with agreementof physician

short term: heparin (acts only about 6hrs)

surgery delayed for 12-24hrs




c) liver disease

obstructive jaundice

extensive liver damage (viral hepatitis,alcoholism)

haemorrhage can be severe and difficult to

control

vitamin K

antifibrinolytic agents

fresh plasma infusion



Lymphomas



Lymphomas

any type of lymphocytes, most frequently B

cells

all malignant

Hodgkin + non Hodgkin lymphomas (NHL)

relatively frequently involve cervical lymph

nodes x rare in the mouth



Lymphomas

A) NHL

adults predominantly affected

nondescript, soft, painless swelling +/-ulcerated

histologically:

+ invasion of adjacent tissues + if traumatised inflammatory cells can

obscure the lymphomatous nature of the tu



Lymphomas

management:

± biopsy!

± staging!



Lymphomas

Burkitt´s lymphoma

nasopharyngeal (T cell) lymphoma mlg

midline granuloma

MALT!

+ local manifestation of gn disease



Cervical lymphadenopathy




dental and periodontal infections most

common cause

lymphomas

HIV infection

tab 26.1

investigation: recent viral illness lymphadenopathy resolves after some months




TBC

Mcb tuberculosis + atypical Mcb

clinical features: pathology: granulomas, Mcb Mcb culture

or DNA tests

management: suspicion of TB

C affectednodes should be excised intact




Syphilis

lymph nodes enlarged, soft and rubbery

primary or secondary stage Treponema pallidum in a direct smear or by

serological finding

management: atb




Cat scratch disease

tab 26.4

pathology: destruction of lymph nodearchitecture, necrosis and lymphocytic

infiltration, formation of histiocytic

granulomas and central suppuration

WS staining

x deep mycoses




management: history, clinical features,

exclusion of other causes, disease is mild and

self limiting, +/- suppuration and sinus

formation




Lyme disease

transmitted by insects, deer ticks

tab 26.5 management: history + clinical picture

confirmed serologically

atb!




Infectious mononucleosis

self-limiting lymphoproliferative disease

tab 26.6 +/- more persistent lymphadenopathy which

may mimic a lymphoma

management: peripheral blood picture(atypical lymphocytes), Paul-Bunnell test, anti

EBV Ab, ampicillin or amoxicilin should be

avoided!




AIDS

soon after infection transient glandular fever

like-illness

later +/- wide spread lymphadenopathy (GLS)

AIDS




Toxoplasmosis

intestinal parasite of many domestic animals

(cats)

management: serologically, antimicrobial

treatment




Mucocutaneous lymph node syndrome

(Kawasaki´s disease)

tab 26.8

management: clinical and ECG finding

aspirin, -globulin




Drug-associated lymphadenopathies

occasional toxic effect of long term treatment

with the antiepileptic drug, phenytoin can

mimic lymphoma

management:

Ha Em a Tho Pathology

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