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ENDOCRINE DISEASE

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Title: ENDOCRINE DISEASE


1
ENDOCRINE DISEASE
  • Prof. M.K.Hamam
  • Oral Medicine
  • Diagnosis Treatment
  • Burkets
  • Tenth Edition

2
  • 1- Endocrine Disorders
  •  
  • Importance of hormones
  • Endocrine system
  • Hormonal disorders
  • Adrenal gland disorders
  • Addisons disease
  • Dental evaluation, management
  • Thyroid disorders
  • anatomy -
    Location
  • Hormone
  • Hypothyroidism
  • Hyperthyroidism
  • Dental evaluation and management
  • Diabetes mellitus
  • 2- liver diseases

3
  • Introduction
  • Endocrine system are inherently hierarchically
    organized .
  • The hypothalamus controls the pituitary gland
    activities which in turn regulate other endocrine
    gland secretions .
  • Hypothalamus secretes releasing and inhibiting
    factors .
  • Among the releasing hormone is corticotrophin
    releasing factor
  • ( CRF ) , which stimulates the release of adreno
    corticotrophic hormone ( ACTH ) from the
    pituitary gland .

4
  • Hierarchical arrangement
  • ACTH acts on adrenal cortex to cause the release
    of cortisol
  • ( hydrocortisone )
  • Hypothalamus secretes ? CRF stimulates ?
    pituitary gland secretes? ACTH
  • stimulates ? Adrenalcortex ? Secretes ?
    Cortisol .

5
Negative feed back regulatory
  • All endocrine system functions as a closed loop
    . In most endocrine system ,negative feed back
    regulatory their function .
  • For example , hypothalamus and pituitary gland
    stimulate the secretion of cortisol from adrenal
    cortex . While cortisone inhibits hypothalamus
    and pituitary gland secretion
  • ( negative feed back ).

6
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7
Pituitary gland
  • The anterior lobe of pituitary gland produces .
  • 1- Adreno Corticotrophic Hormone ( ACTH )
  • 2- Melanocyte Stimulating Hormone ( MSH )
  • 3- Thyroid Stimulating hormone .( TSH )
  • 4- Growth Hormone ( GH )
  • 5- Follicle Stimulating Hormone ( FSH )
  • 6- Luteinizing Hormone ( LH )
  • 7- Prolactin

8
  • A- Disorders of pituitary gland ( Dwarfism )
  • General manifestation
  • 1- Impaired growth of child ( GH )
  • 2- Hypoadrenocorticism ( ACTH )
  • 3- Hypothyroidism ( TSH )
  • 4- Failure of ovulation , amenorrhea . ( FSH )
  • 5- Impotence , defective spermatogenesis .( LH
    )
  • 6- Failure of lactation
    ( - prolactin )

9
  • Oral manifestation -
  • 1- Delayed shedding eruption of teeth .
  • 2- Microdontia if occurs before odontogensis .
  • 3- Crowding and malocclusion with normal size of
    teeth. If occurs after odontogenesis.
  • Dental implication -
  • Stress, surgery , GA,infection ,sedative
    ,hypnotic , and trauma
  • May precipitate hypo pituitary coma .
  • Hypo pituitary is related to decrease TSH ACTH
    , so the patient cannot tolerate stress.
  • Hypo pituitary coma is manged by -
  • 1- 200 mg hydrocortisone sodium succinate I.V.
  • 2- 25-50 mg dextrose ( if there is hypoglycemia
    )
  • 3- Oxygen
  • 4- Call ambulance for hospital admission .

10
B- Hyperpituitarism
  • Children ( before epiphysis closure ) ? Gigantism
  • 1- well proportional individual but huge .
  • 2- teeth spacing ( if occur after odontogensis )
  • Adult - ( after epiphyseal closure ) ?
    Acromegaly
  • 1- large hand , feet , malar bone , supraorbital
    ridges , tongue , lip, mandible prognathism )
  • 2- Teeth spacing ( food impaction )
  • hyper cementosis ( teeth
    fracture , or difficulty in extraction )

11
A 12 year old boy, 65, with his mother, and his
hand (left) in comparison with that of a grown
man, 61 All long bones in the body effected
before closure of epiphyseal growth plates
12
  • Dental implication
  • 1- systemic problem associated with
    hyperpituitrism may complicate the dental
    treatment as -
  • Hypertension
  • Diabetes mellitus
  • Hypercalcemia
  • Cardiomyopathy .
  • 2- Hazards of GA related to breathing problem
    where -
  • Tongue is large
  • Epiglottic opening is narrow .
  • Kyphosis .
  • Thymus gland is enlarged
  • So it is better to avoid supine position .

13
Adrenal gland
  • Adrenal gland secrete -
  • A - From medulla
  • 1- Epinephrine ( adrenaline )
  • 2- nor epinephrine ( noradrenalin )
  • B- From Cortex
  • 1- Glucocorticoids ( cortisol )
  • 2- Mineralocorticoids ( aldosterone )
  • 3- Sex hormones .

14
  • Disorders of adrenal gland
  • 1- Adrenal cortex insufficiency
  • Etiology
  • 1- Congenital
  • 2- Acquired
  • A- Primary Addisons disease
  • B- Secondary - ? to exogenous steroid
    therapy .
  • ? to pituitary
    insufficiency .
  • ( ACTH
    deficiency )

15
  • 11-Adrenal cortex hyperfunction
  • Etiology
  • A- Cushing disease
  • It is due to pituitary gland adenoma resulting in
    increase ACTH
  • That stimulate adrenal cortex .
  • B- Cushing syndrome
  • It is due primary adrenal adenoma .
  • C- Iatrogenic Cushing syndrome
  • It is due to exogenous corticosteroid therapy .

16
  • Clinical Features of Cushings Syndrome
  • Round (moon) face.
  • A hump on upper back Buffalo hump
  • stretch marks on their abdomen (striae)
  • Hypertension
  • Prolonged wound repair
  • Obesity
  • Mental depression

17
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18
Easy bruising Thinning skin Poor wound
healing Acne Purple striae Hirsutism Female
balding Menstrual irregularity Sleep
disorders Excessive hunger Excessive
thirst Frequent urination Sweating Anxiety Confus
ion Concentration loss Memory loss Depression Suic
idal thoughts Panic attacks
Abdominal weight gain Red, round moon
face Thinning extremities Buffalo hump High
blood pressure High blood sugar Muscle
weakness Osteoporosis/Fractures Infections Bloo
d clots Visual field defects
19
A Primary Adrenal cortex insufficiency
Addisons disease
  • Definition
  • It is adrenal cortex insufficiency ( atrophy )
    leading to failure of cortisol and aldosterone
    secretion .
  • Auto immune disease due to circulating
    antibodies directed against adrenal cortex .
  • Tuberculosis
  • Sarcoidosis
  • Hemorrhage
  • Histoplasmosis
  • Malignancy . Amyloidosis

20
  • Clinical Features
  • Manifestations related to low level of
    aldosterone
  • 1- Sodium water depletion
  • 2- Reduced extracellular volume hypotension .
  • 3- Retained potassium hydrogen ions
  • 4- Hyperkalemia acidosis .
  • Manifestaion related to low level of cortisol
  • 1- Stimulation pituitary gland to secrete
    pro-opio melanocortin . So there is increased
    level of -
  • Melanocyte stimulation activity which lead to
    increase skin oral melanin pigmentation .
  • ACTH .

21
  • PeutzJeghers syndrome multiple pigmented spots
    on -
  • Addison disease pigmentation of the -.

the skin.
the lower lip.
buccal mucosa
gingiva
the buccal mucosa.
lower lip
22
  • 2- Hypoglycemia
  • 3- Weight loss , weakness
  • 4- Addisonians Crisis ( adrenal crisis )
  • It is manifestation by sever exacerbation of
    symptoms as hypotension , headache , dehydration
    , weakness , nausea , vomiting .
  • It is precipitated by factors that increase the
    body demand for cortisol such -
  • as surgery , stress , infection , trauma ,
    G.A .
  • The patient may die if not treated immediately .
  • Laboratory finding
  • Cortisol , Sodium

  • ACTH , Potassium .




23
B- Secondary adrenal cortex insufficiency
( patient on glucocorticoid therapy )
  • Pharmacological action of glucocorticoids
  • 1-Owing to their anti- inflammatory and immune-
    suppressive action ,
  • There are prescribed for management of -
  • Allergic diseases .
  • Autoimmune diseases ( Lupus erythematosus ,
    pemphigus vulgaris ,..)
  • 2- they are prescribed as replacement therapy in
    patients with Addison s disease

24
  • Complications of glucocorticoid therapy
  • A- Adreanal cortex atrophy -
  • The long term low dose steroid ( 10 mg prednisone
    for one month ) or short term high dose steroid
    results in adrenal cortex suppression ( atrophy
    ).
  • Adrenal cortex secretion is under the control of
    ACTH secreted by pituitary gland .
  • Exogenous steroid received by the patient for
    management of certain allergic or skin disease
    results in suppression of ACTH release . In turn
    , endogenous adrenal cortex secretion is
    suppressed and the adrenal glands under atrophy .
  • .

25
  • Patients with adrenal cortex atrophy cannot
    tolerate stress , surgery , G.A , infection , and
    trauma . There is increase in the body with
    such high levels of endogenous corticosteroids (
    300 mg ) , so the patient suffers adrenal crisis
    .
  • Causes of adrenal crisis -
  • 1-Adrenal insufficiency (A- cong. Adrenal ins .B-
    Primary Addison's disease . C-Secondary
    ,exogenous steroid , surgical excision of gland ,
    pituitary insufficiency ) certain condition (
    stress, G.A ., infection , surgery , trauma ) ?
    adrenal crisis .
  • 2- Sudden withdrawal of exogenous steroid

26
  • How to avoid adrenal atrophy ?
  • 1- alternate day on the day off therapy , the
    adrenal pituitary axis is allowed to function and
    produce endogenous cortisol .
  • 2- single morning dose of exogenous steroid 1.5
    hrs. after arising . Cortisol level is normally
    high in the morning . Thus if steroid is given at
    this time it does not to tend to suppress ACTH
    and adrenal gland secretion .
  • How to avoid adrenal crisis ?
  • 1- Careful case history -
  • It should be remember that not only patient under
    current treatment are not at risk of adrenal
    crisis but also patient who had steroid therapy
    during the last year ( normal function of
    adrenal gland is restored within 9-12 month. )
  • 2- Supplementary corticosteroid should be given
    before and during period of stress ( G.A. Trauma
    , )
  • 3- Gradual withdrawal of steroid therapy to allow
    for the restoration of adrenal function.

27
  • Management of patient on steroid therapy .
  • Under local anaesthesia
  • 1- patient on total replacement therapy
    Addisons disease
  • Hospitalization
  • It is better to over treat ( i.e. high dose of
    steroid ) during surgery rather that to have
    Adrenal crisis .
  • 2- patient received steroid during the previous
    12 months .
  • 200 mg hydrocortisone orally 2 hours
    pre-operative or
  • 200 mg hydrocortisone I.V . Immediately pre
    operative .
  • 3- patient currently on steroid therapy -
  • A- Short appointment ( lt 1hr. )
  • Emergency ? 200 mg hydrocortisone I.V . ?
    immediately before appointment
  • No emergency ? double the steroid dose the night
    and the whole day of app.

28
  • B- long appointment ( gt 1 hr. )
  • Emergency ? 200 mg hydrocortisone I.V.
    immediately before app.
  • 200 mg hydrocortisone
    I.M. 6 hrs . For 24 hrs .
  • No emergency ? Triple the dose the night before
    and the whole day of app.
  • then gradual
    tapping to regular dose over the 2th of
    3rd postoperative days

29
  • 11- Under General Anaesthesia
  • 1- patient on total replacement therapy
    Addisons disease
  • 2- patient received steroid during the previous
    12 months .
  • 100 - 200 mg I.V. hydrocortisone sodium
    succinate with pre-medication and then every 6
    hrs . For 24-72 hrs . Then continue normal
    medication .
  • 3- patient currently on steroid therapy -
  • Monitor blood pressure during surgery
    recovery .
  • I.V. steroid should be given if there is fall in
    blood pressure

30
Thyroid gland
  • ?Thyroid glands secrete thyroxin ( T4 )and Tri-
    iodothyronine ( T3 ).
  • Thyroid gland secretion is under the control of
    pituitary gland which secrete ( TSH ) . The
    release of TSH from pituitary gland is regulated
    by thyrotrophine releasing factor ( TRF ) from
    hypothalamus .
  • Negative feed back mechanism similar to the
    pituitary adrenal axis is also regulating the
    thyroid gland secretion and the axis is called
    pituitary thyroid axis.
  • Hypothamus ?? secretes TRF ? ? Stimulates
    pituitary ?? secrete ?? stimulates TSH ? Thyroid
  • Inhibit ( -ve feed back )
    T3
    T4 secretes


    stimulate


  • Thyroid
  • The precise role of thyroid hormones is not
    known . However , excessive secretion increases
    the basal metabolic rate ( BMR )



31
  • Disorders of thyroid gland -
  • Hyperthyroidism ( thyrotoxicosis )
  • Types -
  • Grave s disease characterized by diffused
    enlargement of thyroid

  • gland .

  • exophthalmos .
  • Nodular Goiter characterized by less sever
    nodular enlargement of

  • thyroid gland .

  • No exophthalmos
  • General manifestation
  • Warm moist skin
  • Tremors of hands and tongue
  • Exophthalmoses which may persist even after
    treatment .
  • Nervousness
  • Tachycardia . Due to increase BMR .

32
Hyperthyroidism Graves Disease
33
  • Oral manifestation
  • Normal growth of jaws
  • Early shedding of deciduous teeth
  • Early eruption of permanent teeth .
  • Osteoporosis .
  • Dental implication
  • 1-Treated thyrotoxic patient present no problem
    in dental treatment .
  • Untreated patient may have tachycardia and
    arrhythmia that can lead to heart failure .
  • Adrenergic receptors are very sensitive to
    adrenaline , so local anesthesia should be free
    from adrenaline . Prilocaine containing
    octapressin is an alternative .
  • 2- G.A ( risk of arrhythmia )
  • 3- anti- thyroid drugs ( thiocarbamides ) induces
    agranulocytosis ?oral oropharyngeal ulceration .

34
3- Thyroid crisis
  • It is an exaggerated manifestation of
    hyperthyroidism .
  • Precipitation factors . Stress , infection ,
    surgery .
  • Clinical manifestation -
  • nausea , vomiting , profuse sweating ,Tremor
    ,Tachycardia ,Fever , hypotension ,Finally heart
    failure and death.
  • How to avoid thyroid crisis .
  • Stress , ( Tranquilizers benzodiazepine
    potentiate the antithyroid drugs )
  • Acute infection should be managed immediately .
  • How to manage thyroid crisis ?
  • call ambulance for hospitalization since medical
    treatment will include -
  • Hydrocortisone 200 mg i.v
  • Glucose i.v
  • Ice pack , wet pack , fans
  • Antithyroid drugs and adrenergic antagonizer (
    propanolol )
  • N.B - The dentist should cool the patient with
    cold towels and give 100-300 mg .i.v .
    Hydrocortizone and will be ready to initate
    cardiopulmonary resuscitation if indicated.

35
2- Hypothyroidism
  • Less common than hyperthyroidism
  • Females.
  • Children ? Cretinism (inherited or acquired)
  • Adult ? Myxedema (acquired).
  • Causes
  • Thyroid ,Congenital absence or defect
  • Iatrogenic
  • Iodine deficiency
  • Chronic thyroditis
  • Pituitary ( secondary)
  • Hypothalamic (tertiary )

36
  • Cretinism
  • In childhood? severe developmental defects
    (unless recognized and treated early).
  • Clinical manifestations
  • Growth retardation
  • Mental retardation
  • Mongoloid faces.
  • Protuberant abdomen
  • Delayed bony and dental development.
  • Defective development and maturation of the CNS
  • Delayed eruption of teeth.
  • Micrognathia
  • Macroglossia
  • Malocclusion , anterior open bite
  • Puffy , enlarged , protruded lip.
  • Short flat nose

37
  • Myxedema
  • Myxedema is defined as hypothyroidism acquired
    (not inherited) in the adult.
  • Decreased metabolism hypothyroid state.
  • Facial edema(myxedema).
  • Coarse skin.
  • Decreased mental acuity.
  • Physical activity, and tolerance to cold, as well
  • Very uncommon ? coma die.
  • loss of hair
  • Weight gain

38
  • Dental implication
  • Myxedema coma
  • Precipitating factor
  • Trauma , surgery , infection , G.A
  • Sedative ( diazepam ) analgesic ( codeine ) . The
    respiratory center is hypersensitive to these
    drugs , they should be avoided or the dose must
    be reduced .
  • Manifestation
  • Hypothermia , Hypofuntion , Bradycardia ,
    Epileptic seizures
  • Management
  • Call ambulance for hospitalization
  • Artificial respiration
  • 200 mg hydrocortisone i.v.

39
Diabetes Mellitus
  • Definition
  • It is an endocrine disorder , characterized by
    persist rise in blood glucose level ,
  • Resulting from absolute or relative deficiency
    of insulin . Insulin reduces blood sugar level by
    -
  • Glucose oxidation
  • Glycogensis .
  • Increase uptake of glucose by cells
  • Etiology -
  • 1- Primary ( idiopathic )
  • A- insulin dependent ( juvenile onset )
  • B- Non insulin dependent ( maturity onset )
  • 2- Secondary
  • A- Pancreatic damage ( Chronic pancreatitis ,
    Hemochromatosis . )
  • B- Genetic syndrome ( insulin resistance )
  • C- Endocrinal ( Acromegaly , Cushing ,
    pheochromocytoma , Steroid therapy )

40
Comparison of Insulin-Dependent and Non-Insulin
Dependent Diabetes Mellitus
41
  • Manifestations of diabetes are due to -
  • 1- hyperglycemia
  • 2- Ketoacidosis
  • 3- vascular wall disease
  • 4- Advanced glycosylated end products ( AGEs )
  • 5- hyperlipidemea
  • Diagnosis
  • 1- Glucose tolerance test .
  • 2- High glycsylated hemoglobin ( reflects blood
    sugar level in the last 3 months ). If -
  • A- lt 7 it is normal , patient is not diabetic
  • B- 7-9 patient is controlled .
  • C- gt 13 patient is not controlled .
  • 3- Ketoacidosis
  • 4- Glucosuria

42
  • Oral manifestations .
  • No specific pathogonomic features .
  • More obvious in uncontrolled diabetics .
  • 1- Dry mouth
  • 2- Atrophy of filiform papilla enlarged
    hyperemic fungiform papillae .
  • 3- Burning sensation of the tongue .
  • 4- Periodontal disease ( periodontal abscess in
    uncontrolled )
  • 5- Occasionally enlarged salivary glands .
  • 6- Increased rate of dental caries .
  • 7- odontalgia ( due to pulp necrosis )
  • 8- Grinspan syndrome ( it consists of )
  • Diabetes
  • Hypertension
  • Lichenoid reaction.

43
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44
  • Mangement of diabetic patients
  • A- Patient controlled by diet or diet ant
    diabetic drugs .
  • The dentist should reassure the patient to take
    his meal ant diabetic drugs
  • B - Patient controlled by diet insulin .
  • These measurements are undertaken for the
    controlled patient only .but the uncontrolled
    patient should be to the physician before any
    dental procedure .
  • 1- Dental appointment should be in the morning
    about 1-2 hours after breakfast
  • And after the usual insulin dose .
  • 2- Premedication - sedative or tranqllizer ( to
    decrease endogenous adrenaline )
  • 3- Antibiotic cover when surgery is indicated .
  • 4- Avoid long appointments .
  • 5- Avoid excessive trauma during surgical
    procedure .
  • 6- Remove all septic foci and maintain good oral
    hygiene .

45
  • 7- Local anesthesia - the lowest concentration
    of adrenaline ( vasoconstrictor is essential to
    decrease pain ) or use prilocaine plus
    octapressin .
  • 8- G.A ( by anaesthetist )
  • 9- Hospitalization ( multiple extraction, massive
    infection , patient is receiving more than 60
    units insulin / day .
  • 10 Unconsciousness in dental surgery is
    frequently due to hypoglycemia . 25 gm glucose
    orally or 20 ml of 20 dextrose i.v. will relieve
    hypoglycemia rapidly .
  • If this is ineffective , call the ambulance .

46
  • Effect of low glucose level
  • Brain use only glucose , if its level falls
  • 1- neuroglycopenia ? irritability , tremor ,
    confusion loss of concentration .
  • 2- Adrenaline release ? tachycardia , palpation
    sweating .
  • Hypoglycemic shock is more dangerous than
    hyperglycemic shock because of neuroglycopenia .

47
6- Diseases of the Liver
48
A- Jaundice (icterus)
  • Jaundice excessive bilirubin in the
    circulation.
  • Hemolytic jaundice hemolysis of red blood cells.
  • Obstructive jaundice obstruction in the biliary
    tree stones, infectious or neoplastic lesions.
  • Hepatocellular jaundice liver disease.

49
Morbilliform
50
Symptoms
  • Excess of bilirubin.
  • Color of the skin, oral mucous membrane, and
    sclera.
  • Hepatocellular disease a deficiency of
    prothrombin and clotting factors.
  • Decreased tolerance to anesthetics and
    medications.
  • History of contact with hepatitis pt. ? Refer to
    physician.

51
Symptoms
  • Symptoms of all hepatitis A, B, C, D, and Non- B
    are same (hepatitis A).
  • More than half of all the types of hepatitis are
    either subclinical or mild enough to escape
    diagnosis.
  • Malaise, arthralgia, myalgia, anorexia, nausea
    and fever.
  • Morbilliform skin rash.

52
Hepatitis
  • It may be induced by -
  • Chemical agents phosphorus
  • Drugs isoniazed hyrochloride
  • Collagen disease lupus erythematous
  • Viral infection -
  • Infection mononucleosis
  • Cytomegalovirus
  • Coxsackie virus
  • Hepatitis A,B,C,D,E Viruses .

53
What Is Hepatitis?
  • Hepatitis means inflammation of the liver
  • Hepat (liver) itis (inflammation) Hepatitis
  • Viral hepatitis means there is a specific virus
    that is causing liver to inflame (swell or become
    larger than normal)

54
Inflammation
Walls ofscar tissue begin to form.
Healthy liver cells become trapped by a wall of
scar tissue
55
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56
  • Definition -
  • Inflammation in the liver induced by viral
    infection
  • Types -
  • Hepatitis A transmitted by food , not serious
    .
  • Hepatitis B
  • Hepatitis C
  • Hepatitis D ( delta )
  • Hepatitis E water borne spread .

57
HBV HCV
Type DNA virus RNA virus
Reverse transcriptase enzyme Present Absent
Present in All body fluids, saliva, CNS ,tears , semen , amniotic fluid All body fluids except semen ( still under study )
Mode of transmission Parental , sexual Parental. Sexual ( still under study )
Target cell Liver cells Liver cell lymphocyte
Vaccination Available Not available
Oncogenicity can cause hepatocellular Can cause hepatocellular carcinoma
58
  • Clinical manifestations
  • Prodromal phase - high fever , malaise ,
    anorexia , nausea
  • Icteric phase -
  • 1- Jaundice develops within 5 days then fever
    gradually subsides .
  • 2- cteric colour of sclera , nail bed , oral
    mucous membrane specially floor of mouth and
    palate .
  • 3- Hepatomegaly tenderness of liver .
  • 4- Spleenomegaly lymphadenopathy .
  • 5- Spider angioma
  • 6- Cholesterol deposition along lower eye lid .
  • 7- Bleeding tendency
  • 8- Dark urine and light colored stools .

59
  • Recovery phase -
  • It is very long with HBV , HCV and the disease
    may be complicated by -
  • 1- Acute fulminate infection .
  • 2- Chronic infection .
  • 3- Liver cirrhosis .
  • 4- Hepatocellular carcinoma .
  • Diagnosis -
  • Case history ( blood trasfusion , contact with
    infected individual )
  • Clinical examination icteric colour
  • Laboratory investigation .

60
  • 1- Serological tests
  • There are 3 antigens characteristic for HBV .
  • HBsAg Surface antigen .
  • HBcAg Cora antigen .
  • HBeAg Envelope antigen .
  • There are 3 antibodies produced in response to
    the previously mentioned antigens
  • Anti-HBs antibody
  • Anti- HBc antibody
  • Anti- HBe antibody

61
Antigen Appear Disappear Indicate
HBsAg Up to 6 weeks after exposure May disappear 1-6 w.after infection . Or lasts for 25 years in carriers Acute infection Chronic carriers
HBcAg Active stage of disease After resolution of disease .
HBeAg Active stage of disease After resolution of disease may persist for long time Highly infective individuals
62
  • Generally , the antibodies rise after
    disappearance of their antigens
  • N.B . The presence of -
  • Anti HBs antibodies means -
  • 1- past infection with HBV
  • 2- Vaccination of HB .
  • Anti HBe and HBs Ag means -
  • Healthy carrier ( will not manifest the
    disease )
  • HBsAg then later Anti HBc level rise means .
  • Active hepatitis .
  • Anti HBc , HBsAg and absence of anti- HBs means
  • Chronic carrier ( may manifest the disease
    )

63
  • 2- liver function test - elevation of -
  • A- serum glutamic pyruvic transaminase ( SGPT )
  • Alanine aminotransferase ( ALT )
  • B- Serum glutamic oxaloacetic transaminase ( SGOT
    )
  • Aspartic transferase ( AST )
  • C- Serum alkaline phosphatase .
  • D- Serum bilirubin .
  • 3- Polymerase Chain Reaction ( PCR )
  • Indicated mainly for diagnosis of HCV

64
Dental implications
  • There are 3 major problems facing the dentists ,
    when dealing with hepatitis patients .
  • 1- Bleeding and clotting disorders due to liver
    disease.
  • 2- Cross infection .( infection control
    ,vaccination , accidental needle prick )
  • 3- Defective detoxification of drugs .
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