ENDOCRINE DISEASEENDOCRINE DISEASE

Prof. M.K.HamamProf. M.K.HamamOral MedicineOral MedicineDiagnosis & TreatmentDiagnosis & TreatmentBurket’sBurket’sTenth EditionTenth Edition

1- 1- Endocrine Disorders Endocrine Disorders    Importance of hormonesImportance of hormones Endocrine systemEndocrine system Hormonal disordersHormonal disorders Adrenal gland disordersAdrenal gland disorders Addison’s diseaseAddison’s disease Dental evaluation, managementDental evaluation, management Thyroid disordersThyroid disorders anatomy - Locationanatomy - Location HormoneHormone HypothyroidismHypothyroidism HyperthyroidismHyperthyroidism Dental evaluation and management Dental evaluation and management Diabetes mellitus Diabetes mellitus 2- liver diseases 2- liver diseases

Introduction Introduction

Endocrine system are inherently hierarchically organized .Endocrine system are inherently hierarchically organized .

The hypothalamus controls the pituitary gland activities which in The hypothalamus controls the pituitary gland activities which in turn regulate other endocrine gland secretions . turn regulate other endocrine gland secretions .

Hypothalamus secretes releasing and inhibiting factors .Hypothalamus secretes releasing and inhibiting factors .

Among the releasing hormone is Among the releasing hormone is corticotrophin releasing corticotrophin releasing factor factor

( CRF ) ( CRF ) , which stimulates the release of , which stimulates the release of adreno corticotrophic adreno corticotrophic hormone ( ACTH ) hormone ( ACTH ) from the pituitary gland . from the pituitary gland .

Hierarchical arrangement Hierarchical arrangement

ACTH acts on adrenal ACTH acts on adrenal cortex to cause the cortex to cause the release of cortisolrelease of cortisol

( hydrocortisone )( hydrocortisone )

Hypothalamus secretes Hypothalamus secretes → CRF stimulates → → CRF stimulates → pituitary gland pituitary gland secretes→ ACTHsecretes→ ACTH

stimulates → stimulates → Adrenalcortex → Adrenalcortex → Secretes → Cortisol .Secretes → Cortisol .

Negative feed back Negative feed back regulatoryregulatory

All endocrine system All endocrine system functions as a closed functions as a closed loop . In most endocrine loop . In most endocrine system ,negative feed system ,negative feed back regulatory their back regulatory their function . function .

For example , For example , hypothalamushypothalamus and and pituitary glandpituitary gland stimulate stimulate the secretion of cortisol the secretion of cortisol from adrenal cortex . from adrenal cortex . While cortisone inhibits While cortisone inhibits hypothalamus and hypothalamus and pituitary gland secretionpituitary gland secretion

( negative feed back ). ( negative feed back ).

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

A- Disorders of pituitary gland A- Disorders of pituitary gland ( Dwarfism ) ( Dwarfism )

General manifestation General manifestation 1- Impaired growth of child ( GH ) 1- Impaired growth of child ( GH ) 2- Hypoadrenocorticism ( ACTH )2- Hypoadrenocorticism ( ACTH ) 3- Hypothyroidism ( TSH ) 3- Hypothyroidism ( TSH ) 4- Failure of ovulation , amenorrhea . ( FSH )4- Failure of ovulation , amenorrhea . ( FSH ) 5- Impotence , defective spermatogenesis .5- Impotence , defective spermatogenesis .

( LH ) ( LH ) 6- Failure of lactation 6- Failure of lactation

( - prolactin ) ( - prolactin )

Oral manifestation :- Oral manifestation :- 1- Delayed shedding & eruption of teeth .1- Delayed shedding & eruption of teeth . 2- Microdontia : if occurs2- Microdontia : if occurs before before odontogensis .odontogensis . 3- Crowding and malocclusion with normal size of teeth. If 3- Crowding and malocclusion with normal size of teeth. If

occurs occurs afterafter odontogenesis. odontogenesis. Dental implication :- Dental implication :- Stress, surgery , GA,infection ,sedative ,hypnotic , and Stress, surgery , GA,infection ,sedative ,hypnotic , and

trauma trauma May precipitate hypo pituitary coma . May precipitate hypo pituitary coma . Hypo pituitary is related to decrease TSH & ACTH , so Hypo pituitary is related to decrease TSH & ACTH , so

the patient cannot the patient cannot tolerate stresstolerate stress. . Hypo pituitary coma is manged by :- Hypo pituitary coma is manged by :- 1- 200 mg hydrocortisone sodium succinate I.V. 1- 200 mg hydrocortisone sodium succinate I.V. 2- 25-50 mg dextrose ( if there is hypoglycemia ) 2- 25-50 mg dextrose ( if there is hypoglycemia ) 3- Oxygen 3- Oxygen 4- Call ambulance for hospital admission .4- Call ambulance for hospital admission .

B- HypB- Hypererpituitarism pituitarism

Children Children ( before epiphysis closure ) → ( before epiphysis closure ) → GigantismGigantism 1- well proportional individual but huge . 1- well proportional individual but huge . 2- teeth spacing ( if occur after odontogensis ) 2- teeth spacing ( if occur after odontogensis ) Adult :- ( after epiphyseal closure ) Adult :- ( after epiphyseal closure ) → → Acromegaly Acromegaly 1- large hand , feet , malar bone , supraorbital ridges , tongue , lip, 1- large hand , feet , malar bone , supraorbital ridges , tongue , lip,

mandible prognathism ) mandible prognathism ) 2- Teeth : spacing ( food impaction ) 2- Teeth : spacing ( food impaction ) hyper cementosis ( teeth fracture , or difficulty in extraction hyper cementosis ( teeth fracture , or difficulty in extraction

))

A 12 year old boy, 6’5”, with his mother, and his hand (left) in comparison with that of a grown man, 6’1”

All long bones in the body effected before closure of epiphyseal growth plates

Dental implication Dental implication 1- systemic problem associated with 1- systemic problem associated with

hyperpituitrism may complicate the dental hyperpituitrism may complicate the dental treatment as :- treatment as :-

Hypertension Hypertension Diabetes mellitus Diabetes mellitus Hypercalcemia Hypercalcemia Cardiomyopathy . Cardiomyopathy . 2- Hazards of GA related to breathing problem 2- Hazards of GA related to breathing problem

where :- where :- Tongue is large Tongue is large Epiglottic opening is narrow . Epiglottic opening is narrow . Kyphosis . Kyphosis . Thymus gland is enlarged Thymus gland is enlarged So it is better to avoid supine position .So it is better to avoid supine position .

Adrenal gland Adrenal gland

Adrenal gland secrete :-Adrenal gland secrete :-

A - From medulla A - From medulla

1- Epinephrine ( adrenaline ) 1- Epinephrine ( adrenaline )

2- nor epinephrine ( noradrenalin ) 2- nor epinephrine ( noradrenalin )

B- From Cortex B- From Cortex

1-1- Glucocorticoids ( cortisol ) Glucocorticoids ( cortisol )

2- Mineralocorticoids ( aldosterone ) 2- Mineralocorticoids ( aldosterone )

3- Sex hormones .3- Sex hormones .

Disorders of adrenal gland Disorders of adrenal gland 1- Adrenal cortex insufficiency 1- Adrenal cortex insufficiency Etiology Etiology 1- Congenital 1- Congenital 2- Acquired 2- Acquired A- Primary : A- Primary : Addison’s disease Addison’s disease B- Secondary :- ● to exogenous steroid B- Secondary :- ● to exogenous steroid

therapy . therapy . ● ● to pituitary insufficiency .to pituitary insufficiency .

( ACTH deficiency )( ACTH deficiency )

11-Adrenal cortex hyperfunction :11-Adrenal cortex hyperfunction : Etiology Etiology A- Cushing disease A- Cushing disease It is due to pituitary gland adenoma resulting It is due to pituitary gland adenoma resulting

in increase ACTH in increase ACTH That stimulate adrenal cortex . That stimulate adrenal cortex . B- Cushing syndrome : B- Cushing syndrome : It is due primary adrenal adenoma .It is due primary adrenal adenoma . C- Iatrogenic Cushing syndrome C- Iatrogenic Cushing syndrome It is due to exogenous corticosteroid therapy .It is due to exogenous corticosteroid therapy .

Clinical Features of Cushing’s Clinical Features of Cushing’s SyndromeSyndrome

Round (“moon”) face.Round (“moon”) face. A hump on upper back Buffalo humpA hump on upper back Buffalo hump stretch marks on their abdomen (“striae”)stretch marks on their abdomen (“striae”) HypertensionHypertension Prolonged wound repairProlonged wound repair ObesityObesity Mental depressionMental depression

Abdominal weight gainRed, round ‘moon’ faceThinning extremities‘Buffalo hump’

High blood pressure

High blood sugar

Muscle weakness

Osteoporosis/Fractures

Infections

Blood clots

Visual field defects

Easy bruisingThinning skinPoor wound healingAcnePurple striaeHirsutismFemale baldingMenstrual irregularity

Sleep disordersExcessive hungerExcessive thirstFrequent urinationSweating

AnxietyConfusionConcentration lossMemory lossDepressionSuicidal thoughtsPanic attacks

A – A – Primary Adrenal cortex insufficiencyPrimary Adrenal cortex insufficiency

Addison’s disease Addison’s disease

DefinitionDefinition It is adrenal cortex insufficiency ( atrophy ) leading to It is adrenal cortex insufficiency ( atrophy ) leading to

failure of cortisol and aldosterone secretion . failure of cortisol and aldosterone secretion . Auto immune disease : due to circulating antibodies Auto immune disease : due to circulating antibodies

directed against adrenal cortex . directed against adrenal cortex . Tuberculosis Tuberculosis Sarcoidosis Sarcoidosis Hemorrhage Hemorrhage Histoplasmosis Histoplasmosis Malignancy . Amyloidosis Malignancy . Amyloidosis

Clinical Features Clinical Features Manifestations related to Manifestations related to low level low level of of

aldosterone aldosterone 1-1- S Sodium & water depletionodium & water depletion 2- Reduced extracellular volume & hypotension .2- Reduced extracellular volume & hypotension . 3- Retained potassium & hydrogen ions 3- Retained potassium & hydrogen ions 4- Hyperkalemia & acidosis .4- Hyperkalemia & acidosis . Manifestaion related to low level of cortisol Manifestaion related to low level of cortisol 1- Stimulation pituitary gland to 1- Stimulation pituitary gland to secrete pro-opio secrete pro-opio

melanocortinmelanocortin . So there is . So there is increased level increased level of :- of :- Melanocyte stimulation activity which lead Melanocyte stimulation activity which lead to increase to increase

skin & oral melanin pigmentation .skin & oral melanin pigmentation . ACTH . ACTH .

Peutz–Jeghers syndrome: Peutz–Jeghers syndrome: multiple pigmented spots on :-multiple pigmented spots on :-

Addison disease: Addison disease: pigmentation of the :-.pigmentation of the :-.

the buccal mucosa.

the lower lip.

the skin.

buccal mucosa

lower lip

gingiva

2- Hypoglycemia 2- Hypoglycemia 3- Weight loss , weakness 3- Weight loss , weakness 4- 4- Addisonian’s Crisis ( Addisonian’s Crisis ( adrenal crisis adrenal crisis )) It is manifestationIt is manifestation by sever exacerbation of symptoms as by sever exacerbation of symptoms as

hypotension , headache , dehydration , weakness , nausea , hypotension , headache , dehydration , weakness , nausea , vomiting . vomiting .

It is precipitated It is precipitated by factors that increase the body demand for by factors that increase the body demand for cortisol such :- cortisol such :-

as surgery , stress , infection , trauma , G.A . as surgery , stress , infection , trauma , G.A . The patient may die if not treated immediately . The patient may die if not treated immediately . Laboratory finding Laboratory finding Cortisol , Sodium Cortisol , Sodium

ACTH , Potassium . ACTH , Potassium .

B- B- Secondary adrenal cortex insufficiency Secondary adrenal cortex insufficiency ( patient on ( patient on glucocorticoid therapy glucocorticoid therapy ))

Pharmacological action of glucocorticoids Pharmacological action of glucocorticoids 1-Owing to their anti- inflammatory and immune- 1-Owing to their anti- inflammatory and immune-

suppressive action , suppressive action , There are prescribed for management of :- There are prescribed for management of :- Allergic diseases . Allergic diseases . Autoimmune diseases : ( Lupus erythematosus , Autoimmune diseases : ( Lupus erythematosus ,

pemphigus vulgaris ,…..)pemphigus vulgaris ,…..) 2- they are prescribed as replacement therapy in patients 2- they are prescribed as replacement therapy in patients

with with Addison ‘s disease Addison ‘s disease

Complications of glucocorticoid therapy Complications of glucocorticoid therapy A- Adreanal cortex atrophy :- A- Adreanal cortex atrophy :- The long term low dose steroid ( 10 mg prednisone for one The long term low dose steroid ( 10 mg prednisone for one

month ) or short term high dose steroid results in adrenal month ) or short term high dose steroid results in adrenal cortex suppression ( atrophy ).cortex suppression ( atrophy ).

Adrenal cortex secretion is under the Adrenal cortex secretion is under the control of ACTH control of ACTH secreted by pituitary gland .secreted by pituitary gland .

Exogenous steroid Exogenous steroid received by the patient for received by the patient for management of certain allergic or skin disease results in management of certain allergic or skin disease results in suppression of ACTH release suppression of ACTH release . In turn , endogenous . In turn , endogenous adrenal cortex secretion is suppressed and the adrenal adrenal cortex secretion is suppressed and the adrenal glands under atrophy .glands under atrophy .

..

Patients with adrenal cortex Patients with adrenal cortex atrophy cannot atrophy cannot tolerate stress , tolerate stress , surgery , G.A , infection , and trauma . There is increase in the surgery , G.A , infection , and trauma . There is increase in the body with such high levels of endogenous corticosteroids body with such high levels of endogenous corticosteroids ( 300 mg ) , so the patient suffers ( 300 mg ) , so the patient suffers adrenal crisis adrenal crisis ..

Causes of adrenal crisis Causes of adrenal crisis :- :- 1-Adrenal insufficiency (A- cong. Adrenal ins .B- Primary : 1-Adrenal insufficiency (A- cong. Adrenal ins .B- Primary :

Addison's disease .& C-Secondary: ,exogenous steroid , Addison's disease .& C-Secondary: ,exogenous steroid , surgical excision of gland , pituitary insufficiency ) + certain surgical excision of gland , pituitary insufficiency ) + certain condition ( stress, G.A ., infection , surgery , trauma ) → condition ( stress, G.A ., infection , surgery , trauma ) → adrenal crisis .adrenal crisis .

2- Sudden withdrawal of exogenous steroid2- Sudden withdrawal of exogenous steroid

How to avoid adrenal atrophy ? How to avoid adrenal atrophy ? 1- alternate day : 1- alternate day : on the day off therapy on the day off therapy , the adrenal , the adrenal

pituitary axis is allowed to function and produce endogenous pituitary axis is allowed to function and produce endogenous cortisol .cortisol .

2- single morning dose of exogenous steroid 1.5 hrs. after 2- single morning dose of exogenous steroid 1.5 hrs. after arising . Cortisol level is normally high in the morning . Thus if arising . Cortisol level is normally high in the morning . Thus if steroid is given at this time it steroid is given at this time it does not to does not to tend to suppress tend to suppress ACTHACTH and and adrenal gland adrenal gland secretion . secretion .

How to avoid adrenal crisis ? How to avoid adrenal crisis ? 1-1- Careful case history :- Careful case history :- It should be remember that It should be remember that not only not only patient under patient under current current

treatment treatment are not at risk of adrenal crisisare not at risk of adrenal crisis but but also patient who also patient who had steroid therapy during had steroid therapy during the last year the last year ( normal function of ( normal function of adrenal gland is restored within adrenal gland is restored within 9-12 month9-12 month. ). )

2- Supplementary corticosteroid should be given2- Supplementary corticosteroid should be given before before and and during during period of stress ( G.A. Trauma ,…… ) period of stress ( G.A. Trauma ,…… )

3- Gradual withdrawal of steroid therapy to allow for the 3- Gradual withdrawal of steroid therapy to allow for the restoration of adrenal function.restoration of adrenal function.

Management of patient on steroid therapy Management of patient on steroid therapy . . Under local anaesthesia Under local anaesthesia 1-1- patient on total replacement therapy : ‘’ Addison’s patient on total replacement therapy : ‘’ Addison’s

disease ‘’disease ‘’ Hospitalization Hospitalization It is better to over treat ( i.e. high dose of steroid ) during surgery It is better to over treat ( i.e. high dose of steroid ) during surgery

rather that to have Adrenal crisis . rather that to have Adrenal crisis . 2- patient received steroid during the previous 12 months . 2- patient received steroid during the previous 12 months . 200 mg hydrocortisone orally 2 hours pre-operative 200 mg hydrocortisone orally 2 hours pre-operative or or 200 mg hydrocortisone I.V . Immediately pre operative . 200 mg hydrocortisone I.V . Immediately pre operative . 3- patient currently on steroid therapy :- 3- patient currently on steroid therapy :- A- Short appointment : ( < 1hr. ) A- Short appointment : ( < 1hr. ) Emergency → 200 mg hydrocortisone I.V . → immediately before Emergency → 200 mg hydrocortisone I.V . → immediately before

appointment appointment No emergency → double the steroid dose the night and the whole No emergency → double the steroid dose the night and the whole

day of app.day of app.

B- long appointment : ( > 1 hr. ) B- long appointment : ( > 1 hr. ) Emergency → 200 mg hydrocortisone I.V. immediately Emergency → 200 mg hydrocortisone I.V. immediately

before app. before app. 200 mg hydrocortisone I.M. 6 hrs . For 24 200 mg hydrocortisone I.M. 6 hrs . For 24

hrs . hrs . No emergency →No emergency → Triple Triple the dose the night before and the the dose the night before and the

whole day of app. whole day of app. then gradual tapping to regular dose then gradual tapping to regular dose

over the 2th of 3over the 2th of 3rd rd postoperative days postoperative days

11- Under General Anaesthesia 11- Under General Anaesthesia 1- patient on total replacement therapy : ‘’ Addison’s 1- patient on total replacement therapy : ‘’ Addison’s

disease ‘’disease ‘’ 2- patient received steroid during the previous 12 2- patient received steroid during the previous 12

months . months . 100 - 200 mg I.V. hydrocortisone sodium succinate with 100 - 200 mg I.V. hydrocortisone sodium succinate with

pre-medication and then every 6 hrs . For 24-72 hrs . Then pre-medication and then every 6 hrs . For 24-72 hrs . Then continue normal medication . continue normal medication .

3- patient currently on steroid therapy :- 3- patient currently on steroid therapy :- Monitor blood pressure during surgery & recovery .Monitor blood pressure during surgery & recovery . I.V. steroid should be given if there isI.V. steroid should be given if there is fall fall in blood pressure in blood pressure

Thyroid gland Thyroid gland

●●Thyroid glands secrete Thyroid glands secrete thyroxin thyroxin ( ( T4 T4 )and )and Tri- iodothyronine Tri- iodothyronine ( ( T3T3 ). ). Thyroid gland Thyroid gland secretion is under the control of secretion is under the control of pituitary glandpituitary gland

which secretewhich secrete ( TSH ) ( TSH ) . The release of . The release of TSHTSH from pituitary gland is from pituitary gland is regulated by thyrotrophine releasing factor (regulated by thyrotrophine releasing factor ( TRF TRF ) from ) from hypothalamus . hypothalamus .

Negative feed back mechanism Negative feed back mechanism similar to the pituitary adrenal similar to the pituitary adrenal axis is also regulating the thyroid gland secretion and the axis is axis is also regulating the thyroid gland secretion and the axis is called called pituitary thyroid axis.pituitary thyroid axis.

Hypothamus →Hypothamus →→→ secretes TRF → secretes TRF → →→ Stimulates pituitary → Stimulates pituitary →→→ secrete → secrete →→→ stimulates TSH stimulates TSH → Thyroid → Thyroid

Inhibit ( -ve feed back ) T3 & T4 Inhibit ( -ve feed back ) T3 & T4 secretes secretes stimulate stimulate

ThyroidThyroid

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

Disorders of thyroid gland :-Disorders of thyroid gland :- HyperthyroidismHyperthyroidism ( thyrotoxicosis ) ( thyrotoxicosis ) Types :- Types :- Grave ‘s disease Grave ‘s disease : characterized by : diffused enlargement of : characterized by : diffused enlargement of

thyroidthyroid gland . gland . : exophthalmos . : exophthalmos . Nodular Goiter Nodular Goiter : characterized by : less sever nodular enlargement : characterized by : less sever nodular enlargement

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

Hyperthyroidism: Hyperthyroidism: Grave’s DiseaseGrave’s Disease

Oral manifestation Oral manifestation Normal growth of jaws Normal growth of jaws Early shedding of deciduous teeth Early shedding of deciduous teeth Early eruption of permanent teeth . Early eruption of permanent teeth . Osteoporosis . Osteoporosis . Dental implication Dental implication 1-Treated1-Treated thyrotoxic patient present no problem in dental thyrotoxic patient present no problem in dental

treatment . treatment . Untreated patient may have tachycardia and arrhythmia that Untreated patient may have tachycardia and arrhythmia that

can lead to heart failure .can lead to heart failure .Adrenergic receptors are very sensitive to adrenaline , so Adrenergic receptors are very sensitive to adrenaline , so local local

anesthesia anesthesia should beshould be free free from adrenaline . Prilocaine from adrenaline . Prilocaine containing octapressin is an alternative .containing octapressin is an alternative .

2- G.A ( risk of arrhythmia )2- G.A ( risk of arrhythmia )3- anti- thyroid drugs ( thiocarbamides ) induces 3- anti- thyroid drugs ( thiocarbamides ) induces agranulocytosisagranulocytosis

→oral & oropharyngeal →oral & oropharyngeal ulcerationulceration . .

3- Thyroid crisis 3- Thyroid crisis

It is an exaggerated manifestation of hyperthyroidism . It is an exaggerated manifestation of hyperthyroidism . Precipitation factors .Precipitation factors . Stress Stress , , infection infection , , surgery surgery . . Clinical manifestation :-Clinical manifestation :- nausea , vomiting , profuse sweating ,Tremor ,Tachycardia ,Fever , nausea , vomiting , profuse sweating ,Tremor ,Tachycardia ,Fever ,

hypotension ,Finally heart failure and death. hypotension ,Finally heart failure and death. How to avoid thyroid crisis . How to avoid thyroid crisis . Stress , ( Tranquilizers :benzodiazepine potentiate the antithyroid Stress , ( Tranquilizers :benzodiazepine potentiate the antithyroid

drugs )drugs ) Acute infection should be managed immediately . Acute infection should be managed immediately . How to manage thyroid crisis ?How to manage thyroid crisis ? call ambulance call ambulance for hospitalization since medical treatment will for hospitalization since medical treatment will

include :-include :- Hydrocortisone 200 mg i.vHydrocortisone 200 mg i.v Glucose i.vGlucose i.v Ice pack , wet pack , fans Ice pack , wet pack , fans Antithyroid Antithyroid drugs and adrenergic antagonizer ( propanolol )drugs and adrenergic antagonizer ( propanolol ) N.B :-N.B :- The dentist should cool the patient with cold towels and give 100-300 mg .i.v . 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. Hydrocortizone and will be ready to initate cardiopulmonary resuscitation if indicated.

2- Hypothyroidism2- Hypothyroidism

Less common than hyperthyroidismLess common than hyperthyroidism Females.Females. Children Children CretinismCretinism (inherited or acquired)(inherited or acquired) Adult Adult MyxedemaMyxedema (acquired). (acquired). Causes :Causes : Thyroid ,Congenital absence or defect Thyroid ,Congenital absence or defect Iatrogenic Iatrogenic Iodine deficiency Iodine deficiency Chronic thyroditisChronic thyroditis Pituitary ( secondary)Pituitary ( secondary) Hypothalamic (tertiaryHypothalamic (tertiary ) )

Cretinism Cretinism In childhoodIn childhood severe developmental defects (unless recognized and severe developmental defects (unless recognized and

treated early). treated early). Clinical manifestations Clinical manifestations

– Growth retardation Growth retardation – Mental retardation Mental retardation – Mongoloid faces.Mongoloid faces.– Protuberant abdomenProtuberant abdomen– Delayed bony and dental development.Delayed bony and dental development.– Defective development and maturation of the CNSDefective development and maturation of the CNS– Delayed eruption of teeth. Delayed eruption of teeth. – MicrognathiaMicrognathia– Macroglossia Macroglossia – Malocclusion , anterior open bite Malocclusion , anterior open bite – Puffy , enlarged , protruded lip.Puffy , enlarged , protruded lip.– Short & flat nose Short & flat nose

MyxedemaMyxedema Myxedema is defined as hypothyroidism acquired (not Myxedema is defined as hypothyroidism acquired (not

inherited) in the adult. inherited) in the adult. Decreased metabolism “hypothyroid state”.Decreased metabolism “hypothyroid state”.

Facial edemaFacial edema(myxedema)(myxedema).. Coarse skin.Coarse skin. Decreased mental acuity.Decreased mental acuity. Physical activity, and tolerance to cold, as wellPhysical activity, and tolerance to cold, as well Very uncommon Very uncommon coma & die coma & die.. loss of hair loss of hair Weight gain Weight gain

Dental implication Dental implication Myxedema coma Myxedema coma Precipitating factor Precipitating factor Trauma , surgery , infection , G.A Trauma , surgery , infection , G.A Sedative ( diazepam ) analgesic ( codeine ) . The Sedative ( diazepam ) analgesic ( codeine ) . The

respiratory center is hypersensitive to these drugs , they respiratory center is hypersensitive to these drugs , they should be avoided or the dose must be reduced . should be avoided or the dose must be reduced .

Manifestation Manifestation Hypothermia , Hypofuntion , Bradycardia , Epileptic Hypothermia , Hypofuntion , Bradycardia , Epileptic

seizures seizures Management Management Call ambulance for hospitalization Call ambulance for hospitalization Artificial respiration Artificial respiration 200 mg hydrocortisone i.v.200 mg hydrocortisone i.v.

Diabetes Mellitus Diabetes Mellitus

DefinitionDefinition It is an endocrine disorder , characterized by persist rise in It is an endocrine disorder , characterized by persist rise in blood glucose blood glucose

level level , , Resulting from absolute or relative deficiency of insulin . Insulin reduces Resulting from absolute or relative deficiency of insulin . Insulin reduces

blood sugar level by : - blood sugar level by : - Glucose oxidation Glucose oxidation Glycogensis .Glycogensis . Increase uptake of glucose by cells Increase uptake of glucose by cells Etiology :- Etiology :- 1- Primary ( idiopathic ) 1- Primary ( idiopathic ) A- insulin dependent ( juvenile onset ) A- insulin dependent ( juvenile onset ) B- Non – insulin dependent ( maturity onset ) B- Non – insulin dependent ( maturity onset ) 2- Secondary 2- Secondary A- Pancreatic damage ( Chronic pancreatitis , Hemochromatosis . )A- Pancreatic damage ( Chronic pancreatitis , Hemochromatosis . ) B- Genetic syndrome ( insulin resistance ) B- Genetic syndrome ( insulin resistance ) C- Endocrinal ( Acromegaly , Cushing , pheochromocytoma , Steroid C- Endocrinal ( Acromegaly , Cushing , pheochromocytoma , Steroid

therapy ) therapy )

Comparison of Insulin-Dependent and Comparison of Insulin-Dependent and Non-Insulin Dependent Diabetes Non-Insulin Dependent Diabetes MellitusMellitus

Manifestations of diabetes are due to :- Manifestations of diabetes are due to :- 1- hyperglycemia 1- hyperglycemia 2- Ketoacidosis 2- Ketoacidosis 3- vascular wall disease 3- vascular wall disease 4- Advanced glycosylated end products ( AGEs ) 4- Advanced glycosylated end products ( AGEs ) 5- hyperlipidemea 5- hyperlipidemea DiagnosisDiagnosis 1- Glucose tolerance test . 1- Glucose tolerance test . 2- High glycsylated hemoglobin ( reflects blood sugar level in 2- High glycsylated hemoglobin ( reflects blood sugar level in

the last 3 months ). If :- the last 3 months ). If :- A- < 7% it is normal , patient is not diabetic A- < 7% it is normal , patient is not diabetic B- 7-9 % patient is controlled . B- 7-9 % patient is controlled . C- > 13 % patient is not controlled . C- > 13 % patient is not controlled . 3- Ketoacidosis 3- Ketoacidosis 4- Glucosuria 4- Glucosuria

Oral manifestations .Oral manifestations . No specific pathogonomic features . No specific pathogonomic features . More obvious in uncontrolled diabetics . More obvious in uncontrolled diabetics . 1- Dry mouth 1- Dry mouth 2- 2- Atrophy of Atrophy of filiform papilla filiform papilla & enlarged & enlarged hyperemic fungiform hyperemic fungiform

papillae papillae .. 3-3- Burning Burning sensation of the tongue . sensation of the tongue . 4- Periodontal disease ( 4- Periodontal disease ( periodontal abscess periodontal abscess in uncontrolled ) in uncontrolled ) 5- Occasionally 5- Occasionally enlargedenlarged salivary glands . salivary glands . 6- Increased rate of 6- Increased rate of dental caries dental caries . . 7- odontalgia ( due to 7- odontalgia ( due to pulp necrosis pulp necrosis ) ) 8-8- Grinspan syndrome Grinspan syndrome : ( it consists of ) : ( it consists of ) Diabetes Diabetes Hypertension Hypertension Lichenoid reaction.Lichenoid reaction.

Mangement of diabetic patients Mangement of diabetic patients A- Patient controlled by diet or diet & ant diabetic drugs . A- Patient controlled by diet or diet & ant diabetic drugs . The dentist shouldThe dentist should reassure reassure the patient to take the patient to take his meal his meal & ant & ant

diabetic drugs diabetic drugs B - Patient controlled by B - Patient controlled by diet & insulin diet & insulin . . These measurements are undertaken for the These measurements are undertaken for the controlledcontrolled patient patient

only .but the only .but the uncontrolled patient uncontrolled patient should be to the physician should be to the physician beforebefore any dental procedure . any dental procedure .

1- Dental appointment should be in the morning about 1-2 hours 1- Dental appointment should be in the morning about 1-2 hours after breakfast after breakfast

And after the usual insulin dose . And after the usual insulin dose . 2- Premedication :- sedative or tranqllizer ( to decrease endogenous 2- Premedication :- sedative or tranqllizer ( to decrease endogenous

adrenaline ) adrenaline ) 3- Antibiotic cover when surgery is indicated . 3- Antibiotic cover when surgery is indicated . 4- Avoid long appointments .4- Avoid long appointments . 5- Avoid excessive trauma during surgical procedure .5- Avoid excessive trauma during surgical procedure . 6- Remove all septic foci and maintain good oral hygiene .6- Remove all septic foci and maintain good oral hygiene .

7- Local anesthesia :- the lowest concentration of 7- Local anesthesia :- the lowest concentration of adrenaline ( vasoconstrictor is essential to decrease adrenaline ( vasoconstrictor is essential to decrease pain ) or use prilocaine plus octapressin .pain ) or use prilocaine plus octapressin .

8- G.A ( by anaesthetist ) 8- G.A ( by anaesthetist ) 9- Hospitalization ( multiple extraction, massive 9- Hospitalization ( multiple extraction, massive

infection , patient is receiving more than 60 units insulin infection , patient is receiving more than 60 units insulin / day . / day .

10 – Unconsciousness in dental surgery is frequently due 10 – Unconsciousness in dental surgery is frequently due to hypoglycemia . 25 gm glucose orally or 20 ml of 20% to hypoglycemia . 25 gm glucose orally or 20 ml of 20% dextrose i.v. will relieve hypoglycemia rapidly . dextrose i.v. will relieve hypoglycemia rapidly .

If this is ineffective , call the ambulance .If this is ineffective , call the ambulance .

Effect of low glucose level Effect of low glucose level Brain use only glucose , if its level falls Brain use only glucose , if its level falls 1- neuroglycopenia → irritability , tremor , confusion & 1- neuroglycopenia → irritability , tremor , confusion &

loss of concentration . loss of concentration . 2- Adrenaline release → tachycardia , palpation & 2- Adrenaline release → tachycardia , palpation &

sweating . sweating . HypoglycemicHypoglycemic shock is more dangerous than shock is more dangerous than

hyperglycemic hyperglycemic shock because of neuroglycopenia .shock because of neuroglycopenia .

6- Diseases of the Liver6- Diseases of the Liver

A- Jaundice (icterus):A- Jaundice (icterus):

Jaundice : excessive bilirubin in the Jaundice : excessive bilirubin in the circulation. circulation. – HemolyticHemolytic jaundicejaundice: hemolysis of red : hemolysis of red

blood cells.blood cells.– ObstructiveObstructive jaundicejaundice: obstruction in the : obstruction in the

biliary tree: stones, infectious or biliary tree: stones, infectious or neoplastic lesions.neoplastic lesions.

– HepatocellularHepatocellular jaundicejaundice: liver disease.: liver disease.

Morbilliform

SymptomsSymptoms

Excess of bilirubin.Excess of bilirubin. Color of the skin, oral mucous membrane, and Color of the skin, oral mucous membrane, and

sclera.sclera. Hepatocellular disease: a deficiency of Hepatocellular disease: a deficiency of prothrombinprothrombin

and and clotting factorsclotting factors.. Decreased tolerance to anesthetics and medications.Decreased tolerance to anesthetics and medications. History of contact with hepatitis pt. History of contact with hepatitis pt. Refer to Refer to

physician.physician.

Symptoms Symptoms

Symptoms of all hepatitis A, B, C, D, and Non- B Symptoms of all hepatitis A, B, C, D, and Non- B are same (hepatitis A). are same (hepatitis A).

More than half of all the types of hepatitis are More than half of all the types of hepatitis are either either subclinicalsubclinical or or mildmild enough to escape enough to escape diagnosis. diagnosis.

Malaise, arthralgia, myalgia, anorexia, nausea and Malaise, arthralgia, myalgia, anorexia, nausea and fever. fever.

Morbilliform skin rash.Morbilliform skin rash.

HepatitisHepatitis

It may be induced by :- It may be induced by :- Chemical agents : phosphorus Chemical agents : phosphorus Drugs : isoniazed hyrochloride Drugs : isoniazed hyrochloride Collagen disease : lupus erythematous Collagen disease : lupus erythematous Viral infection :- Viral infection :-

Infection mononucleosis Infection mononucleosis

Cytomegalovirus Cytomegalovirus

Coxsackie virus Coxsackie virus

Hepatitis A,B,C,D,E Viruses .Hepatitis A,B,C,D,E Viruses .

What Is Hepatitis?What Is Hepatitis? Hepatitis means inflammation of the liverHepatitis means inflammation of the liver

– Hepat (liver) + itis (inflammation)= HepatitisHepat (liver) + itis (inflammation)= Hepatitis Viral hepatitis means there is a specific Viral hepatitis means there is a specific

virus that is causing liver to inflame (swell virus that is causing liver to inflame (swell or become larger than normal)or become larger than normal)

InflammationInflammation

Walls ofscar tissue begin to form.

Healthy liver cells become trapped by a wall of scar tissue

Definition :- Definition :- Inflammation in the liver induced by viral infection Inflammation in the liver induced by viral infection Types :- Types :- Hepatitis A transmitted by food , not serious .Hepatitis A transmitted by food , not serious . Hepatitis B Hepatitis B Hepatitis CHepatitis C Hepatitis D ( delta ) Hepatitis D ( delta ) Hepatitis E : water borne spread .Hepatitis E : water borne spread .

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

Clinical manifestations Clinical manifestations Prodromal phase :- high fever , malaise , anorexia , nausea Prodromal phase :- high fever , malaise , anorexia , nausea Icteric phase :- Icteric phase :- 1- 1- Jaundice develops within 5 days then fever gradually subsides .Jaundice develops within 5 days then fever gradually subsides . 2- cteric colour of sclera , nail bed , oral mucous membrane 2- cteric colour of sclera , nail bed , oral mucous membrane

specially floor of mouth and palate . specially floor of mouth and palate . 3- Hepatomegaly & tenderness of liver .3- Hepatomegaly & tenderness of liver . 4- Spleenomegaly & lymphadenopathy . 4- Spleenomegaly & lymphadenopathy . 5- Spider angioma 5- Spider angioma 6- Cholesterol deposition along lower eye lid . 6- Cholesterol deposition along lower eye lid . 7- Bleeding tendency 7- Bleeding tendency 8- Dark urine and light colored stools . 8- Dark urine and light colored stools .

Recovery phase :- Recovery phase :- It is very long with HBV , HCV and the disease may be complicated It is very long with HBV , HCV and the disease may be complicated

by :-by :- 1- Acute fulminate infection .1- Acute fulminate infection . 2- Chronic infection .2- Chronic infection . 3- Liver cirrhosis .3- Liver cirrhosis . 4- Hepatocellular carcinoma . 4- Hepatocellular carcinoma . Diagnosis :- Diagnosis :- Case history ( blood trasfusion , contact with infected individual )Case history ( blood trasfusion , contact with infected individual ) Clinical examination : icteric colour Clinical examination : icteric colour Laboratory investigation . Laboratory investigation .

1- Serological tests 1- Serological tests There are 3 antigens characteristic for HBV . There are 3 antigens characteristic for HBV . HBsAgHBsAg : Surface antigen . : Surface antigen . HBcAgHBcAg : Cora antigen . : Cora antigen . HBeAg HBeAg : Envelope antigen . : Envelope antigen . There are There are 3 antibodies 3 antibodies produced in response to the produced in response to the

previously mentioned previously mentioned antigensantigens : : Anti-HBsAnti-HBs : antibody : antibody Anti- HBc Anti- HBc : antibody : antibody Anti- HBe Anti- HBe : antibody : antibody

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

Generally , the Generally , the antibodiesantibodies riserise after disappearance of after disappearance of their their antigensantigens

N.B . The presence of :- N.B . The presence of :- Anti – HBs antibodies means :-Anti – HBs antibodies means :-

1- past infection with HBV 1- past infection with HBV

2- Vaccination of HB . 2- Vaccination of HB . Anti – HBe and HBs Ag means :- Anti – HBe and HBs Ag means :-

Healthy carrier ( will not manifest the disease ) Healthy carrier ( will not manifest the disease ) HBsAg then later Anti – HBc level rise means HBsAg then later Anti – HBc level rise means . .

Active hepatitis .Active hepatitis . Anti – HBc , HBsAg and absence of anti- HBs means : Anti – HBc , HBsAg and absence of anti- HBs means :

Chronic carrier ( may manifest the disease ) Chronic carrier ( may manifest the disease )

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

Indicated mainly for diagnosis of HCV Indicated mainly for diagnosis of HCV

Dental implicationsDental implications

There are There are 3 major problems 3 major problems facing the dentists , facing the dentists , when dealing with hepatitis patients . when dealing with hepatitis patients .

1- Bleeding and clotting disorders due to liver disease. 1- Bleeding and clotting disorders due to liver disease. 2- Cross infection 2- Cross infection .( infection control ,vaccination , accidental needle .( infection control ,vaccination , accidental needle

prick ) prick )

3- Defective detoxification of drugs . 3- Defective detoxification of drugs .