Transcript Cardiomyopathy

ENDOCRINE DISEASE
Prof. M.K.Hamam
Oral Medicine
Diagnosis & Treatment
Burket’s
Tenth Edition
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1-
Endocrine Disorders
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Importance of hormones
Endocrine system
Hormonal disorders
Adrenal gland disorders
Addison’s disease
Dental evaluation, management
Thyroid disorders
anatomy
Location
Hormone
Hypothyroidism
Hyperthyroidism
Dental evaluation and management
Diabetes mellitus
2- liver diseases
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 .
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 .
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 ).
Pituitary gland
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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
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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 )
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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 .
B- Hyperpituitarism
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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 )
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
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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 .
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 .
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Disorders of adrenal gland
1- Adrenal cortex insufficiency
Etiology
1- Congenital
2- Acquired
A- Primary : Addison’s disease
B- Secondary :- ● to exogenous steroid therapy .
● to pituitary insufficiency .
( ACTH deficiency )
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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 .
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Clinical Features of Cushing’s
Syndrome
Round (“moon”) face.
A hump on upper back Buffalo hump
stretch marks on their abdomen (“striae”)
Hypertension
Prolonged wound repair
Obesity
Mental depression
Abdominal weight gain
Red, round ‘moon’ face
Thinning extremities
‘Buffalo hump’
High blood pressure
High blood sugar
Muscle weakness
Osteoporosis/Fractures
Infections
Blood clots
Visual field defects
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
Confusion
Concentration loss
Memory loss
Depression
Suicidal thoughts
Panic attacks
A – Primary Adrenal cortex insufficiency
Addison’s disease
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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
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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 .
Peutz–Jeghers syndrome: multiple
pigmented spots on :-
Addison disease: pigmentation of
the :-.
the skin.
the lower lip.
buccal mucosa
gingiva
the buccal mucosa.
lower lip
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2- Hypoglycemia
3- Weight loss , weakness
4- Addisonian’s 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 .
B- Secondary adrenal cortex insufficiency
( patient on glucocorticoid therapy )
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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
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Complications of glucocorticoid therapy
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A- Adreanal cortex atrophy :-
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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 .
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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
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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.
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Management of patient on steroid therapy .
Under local anaesthesia
1- patient on total replacement therapy : ‘’ Addison’s 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 : ( < 1hr. )
Emergency → 200 mg hydrocortisone I.V . → immediately before
appointment
No emergency → double the steroid dose the night and the whole day of
app.
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B- long appointment : ( > 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
11- Under General Anaesthesia
1- patient on total replacement therapy : ‘’ Addison’s disease ‘’
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2- patient received steroid during the previous 12 months .
100 - 200 mg I.V. hydrocortisone sodium succinate with premedication 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
Thyroid gland
●Thyroid glands secrete thyroxin ( T4 )and Tri- iodothyronine ( T3 ).
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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 .
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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.
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Hypothamus →→ secretes TRF → → Stimulates pituitary →→ secrete →→ stimulates TSH
→ Thyroid
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Inhibit ( -ve feed back )
secretes
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T3
& T4
stimulate
Thyroid
The precise role of thyroid hormones is not known . However , excessive secretion
increases the basal metabolic rate ( BMR )
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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 .
Hyperthyroidism:
Grave’s Disease
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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 .
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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 .
3- Thyroid crisis
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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.
2- Hypothyroidism
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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 )
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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
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Myxedema
Myxedema is defined as hypothyroidism acquired (not
inherited) in the adult.
Decreased metabolism “hypothyroid state”.
 Facial edema(myxedema).
 Coarse skin.
 Decreased mental acuity.
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Physical activity, and tolerance to cold, as well
Very uncommon  coma & die.
loss of hair
Weight gain
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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.
Diabetes Mellitus
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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 )
Comparison of Insulin-Dependent and
Non-Insulin Dependent Diabetes Mellitus
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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- < 7% it is normal , patient is not diabetic
B- 7-9 % patient is controlled .
C- > 13 % patient is not controlled .
3- Ketoacidosis
4- Glucosuria
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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.
Mangement of diabetic patients
A- Patient controlled by diet or diet & ant diabetic drugs .
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The dentist should reassure the patient to take his meal & ant diabetic
drugs
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B - Patient controlled by diet & insulin .
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These measurements are undertaken for the controlled patient only .but the
uncontrolled patient should be to the physician before any dental
procedure .
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1- Dental appointment should be in the morning about 1-2 hours after
breakfast
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And after the usual insulin dose .
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2- Premedication :- sedative or tranqllizer ( to decrease endogenous
adrenaline )
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3- Antibiotic cover when surgery is indicated .
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4- Avoid long appointments .
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5- Avoid excessive trauma during surgical procedure .
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6- Remove all septic foci and maintain good oral hygiene .
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7- Local anesthesia :- the lowest concentration of adrenaline
( vasoconstrictor is essential to decrease pain ) or use
prilocaine plus octapressin .
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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 .
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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 .
6- Diseases of the Liver
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.
Morbilliform
Symptoms
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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.
Symptoms
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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.
Hepatitis
It may be induced by : Chemical agents : phosphorus
 Drugs : isoniazed hyrochloride
 Collagen disease : lupus erythematous
 Viral infection :Infection mononucleosis
Cytomegalovirus
Coxsackie virus
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Hepatitis A,B,C,D,E Viruses .
What Is Hepatitis?
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Hepatitis means inflammation of the liver
– Hepat (liver) + itis (inflammation)= Hepatitis
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Viral hepatitis means there is a specific virus that
is causing liver to inflame (swell or become
larger than normal)
Inflammation
Walls ofscar
tissue begin
to form.
Healthy liver cells
become trapped
by a wall of scar
tissue
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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 .
Type
HBV
HCV
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
Target cell
Liver cells
Liver cell & lymphocyte
Vaccination
Available
Not available
Oncogenicity
can cause hepatocellular
Can cause hepatocellular
carcinoma
under study )
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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 .
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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 .
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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
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 • Highly infective
long time
individuals
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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 )
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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
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Dental implications
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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 .