Endocrine system disease
DR: JAMA
Endocrine System
 The endocrine system is all the organs of the body that are
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endocrine glands.
An endocrine gland secretes hormones.
Hormones are molecules that are secreted into the blood.
Hormones are substances that are secreted by one group of
cells that affects the physiology of another group of cells
(organs).
The endocrine system is controlled by the pituitary gland
and the hypothalamus.
Compared to most other organs in the body, endocrine
organs are well vascularized.
Thyroid gland
 Anatomy of thyroid gland: The thyroid gland is
situated in the neck anterior to the thyroid
cartilage.
 It weighs around 15-20g in the adult. The thyroid
gland has two lobes, the right and the left, joined
by an isthmus.
 Physiology: It secretes mainly thyroxin (T4) and a
small amount of triiodothyronine (T3).
Hypothyroidism
 Hypothyroidism is more common in females.
 It can be due to either:
a. Primary disorders of the thyroid gland (primary
hypothyroidism) or
b. Decreased TSH secretion by the pituitary gland
(secondary hypothyroidism)
Cause of hypothyroidism
 Autoimmune disease
 Treatment for hyperthyroidism.
 Thyroid surgery.
 Radiation therapy.
 Medications.
Clinical feature
 Weakness.
 Constipation
 Cold intolerance
 Large tongue
 Dry coarse skin
 Poor memory
 Pallor
 Poor concentration
 Hair loss
 Carpal tunnel syndrome
 Puffy face, hand, and feet
 Delayed relaxation of deep
 Myxedema
 Weight gain, poor appetite
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 Hypothermia
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 Goiter
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 Hoarse voice
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reflexes
Bradycardia
Hypertension
Ischemic heart disease
Pericardial effusion
Oral manifestation
1. Delayed eruption
2. Enamel hypoplasia in both dentitions.
3. Anterior open bite
4. Macroglossia
5. Micrognathia
6. Thick lips
7. Dysgeusia
8. Mouth breathing
Management
 Hypothyroidism should be treated with oral
levothyroxine.
The treatment is generally started with low
dose (50-100μg daily) and gradually
increased.
 In elderly, a smaller starting dose (25 μg) is
preferred to 32`avoid cardiac side effect.
Complication of hypothyroidism
 Goiter.
 Heart problems.
 Mental health .
 Peripheral neuropathy
 Myxedema.
 Infertility.
Hyperthyroidism
 Hyperthyroidism means the thyroid makes too
much thyroid hormone.
 thyroid is a gland in the front of the neck . It
controls the metabolism, which is how body
turns food into energy. It also affects heart,
muscles, bones, and cholesterol.
Cause
 Graves' Disease
 Functioning adenoma ("hot nodule") and toxic
multinodular goiter (TMNG)
 Excessive intake of thyroid hormones.
 Abnormal secretion of TSH.
 Thyroiditis (inflammation of the thyroid gland)
 Excessive iodine intake.
Clinical features
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Sudden weight loss.
Rapid heartbeat (tachycardia)
Increased appetite
Nervousness, anxiety and irritability
Tremor
Sweating
Changes in menstrual patterns
Increased sensitivity to heat
Goiter
Fatigue, muscle weakness
Difficulty sleeping
Skin thinning
Oral manifestation of hyperthyroidism
1. Accelerated dental eruption in children
2. Maxillary or mandibular osteoporosis
3. Enlargement of extra glandular thyroid tissue(mainly
in the lateral posterior tongue)
4. Increased susceptibility to caries
5. Periodontal disease
6. Burning mouth syndrome
7. Development of connective-tissue diseases like
Sjögren’s syndrom or systemic lupus erythematosus
Investigation of hyperthyroidism
 Serum total and unbound (free) T3 and T4 are
increased and TSH level is suppressed.
 TSH stimulation test
 ESR may be increased in sub acute thyroiditis.
 Ultrasonography .
 radioisotope iodine scanning
 serology
Management
Treatment of hyperthyroidism depends on the
cause and severity of the disease
 Beta blockers
 Iodides
 Antithyroid drugs (methimazole)
 Radioactive iodine
 Surgery (subtotal thyroidectomy)
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Complication
Hyperthyroidism can lead to a number of
complications:
 Heart problems.
 Brittle bones.
 Eye problems.
 Red, swollen skin.
 Thyrotoxic crisis.
Calcium metabolism
 The total amount of calcium is about 2 % of the body weight.
 Most of it (99%) is in the bones.
 The normal total serum calcium level is 9-10.5 mg/dL (2.2-
2.6 mmol/L). Half of this is present in free form (ionized
calcium) and the remainder is bound with proteins mainly
albumin.
 The total serum calcium level is low in conditions in which
hypoalbuminemia exists, however, free calcium level is
normal.
 The ionized calcium is responsible for the physiological
functions of the calcium such as nerve function and muscle
contraction.
hypocalcaemia
 A low calcium level may result from a problem with the
parathyroid glands, as well as from diet, kidney
disorders, or certain drugs.
 As hypocalcemia progresses, muscle cramps are
common, and people may become confused, depressed,
and forgetful and have tingling in their lips, fingers, and
feet as well as stiff, achy muscles.
 Usually, the disorder is detected by routine blood tests.
Causes of hypocalcaemia
 Vitamin D deficiency.
 Chronic renal failure.
 Magnesium deficiency.
 Alcoholism.
 Biphosphonate therapy - drugs used to treat high
blood calcium levels or pills used to treat
osteoporosis.
 Certain types of leukemia or blood disorders.
Sign and symptoms
 memory loss
 muscle spasms
 numbness and tingling in the hands, feet, and face
 depression
 Hallucinations
 Seizures .
 Anxiety .
 Papilledema.
 psychosis
Investigation
 Serum calcium is low.
 Serum phosphorus is elevated
 Serum parathyroid hormone level is elevated
 ECG .
Treatment of hypocalcemia
Calcium and vitamin D supplements may be used
Hypercalcaemia
 Hypercalcemia is a condition in which the
calcium level in blood is above normal. Too much
calcium in blood can weaken bones, create
kidney stones, and interfere with the way heart
and brain works.
 Hypercalcaemia most commonly results from
overactive parathyroid glands.
Cause
 Adenoma
 Hyperplasia
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 Carcinoma
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 Tumors producing PTH
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related proteins
(malignancy of lung,
ovary, kidney)
 Hematological
malignancies (Myeloma,
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lymphoma, leukemia)
Sarcoidosis
Vitamin D excess
Hyperthyroidism
Milk alkali syndrome
Immobilization
Clinical features
 Constipation
 Nausea
 Decrease appetite
 Abdominal pain
 Peptic ulcer disease
 Kidney stones
 Bone aches and pains
 Fractures
 polyuria, polydipsia, renal colic and nephrolithiasis.
Oral manifestation of hypercalcimae
 Jaw bone dimeniralilztion
 Loss of lamina dura
 Osteitis fibrous cystica
Investigation
 Serum calcium and serum PTH levels are measured.
 High PTH level is present in primary
hyperparathyroidism while it is low in malignancies
where parathyroid related protein (PTHrP) is raised.
 Other tests are done to detect the presence of
malignancies if suspected.
 Measurement of thyroid hormones and vitamin D levels
may be required.
 ECG
Management
 Calcimimetics.
 Bisphosphonates.
 Prednisone.
 IV fluids and diuretics.
Complication of hypercalcemia
Hypercalcemia complications may include:
 Osteoporosis.
 Kidney stones.
 Kidney failure.
 Nervous system problems.
 Abnormal heart rhythm (arrhythmia).
PARATHYROID DISORDERS
 There are four parathyroid glands situated posterior to
the thyroid gland. These produce parathyroid hormone
(PTH) which is a peptide comprising of 84 amino acids.
 The secretion of PTH is regulated by the ionized
calcium levels in serum. The important physiological
roles of PTH are:
a. It promotes resorption of calcium from bones
b. It promotes resorption of calcium from renal tubules
c. It inhibits the absorption of phosphate by the renal
Hypoparathyroidism
 Hypoparathyroidism is an uncommon condition in
which body secretes abnormally low levels of
parathyroid hormone (PTH).
 PTH plays a key role in regulating and maintaining
a balance of body's levels of two minerals —
calcium
phosphorus.
Cause
 Acquired hypoparathyroidism.
 Autoimmune disease.
 Hereditary hypoparathyroidism.
 Extensive cancer radiation treatment of face or
neck.
 Low levels of magnesium in blood,.
Clinical feature
 Burning (paresthesias) in fingertips, toes and lips
 Muscle aches affecting legs, feet, abdomen or face
 spasms of muscles, particularly around the mouth, also in
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the hands, arms and throat
Fatigue or weakness
Patchy hair loss, such as thinning of the eyebrows
Dry, coarse skin
Brittle nails
Headaches
Depression.
Memory problems
Oral manifestation of Hypoparathyroidism
1. Dental abnormalities:
- Enamel hypoplasia in horizontal lines
- Poorly calcified dentin
-Widened pulp chambers
- Dental pulp calcifications
- Shortened roots
- Hypodontia
- Delay dental development
2. Mandibular tori
3. Chronic candidiasis
4. Paresthesia of the tongue or lips
5. Alteration in facial muscles.
Investigation
 The serum calcium is low, serum phosphate is
high, and serum alkaline phosphatase is normal.
 The PTH levels are low. It is normal or high in
pseudohypoparathyroidism.
 The magnesium level is measured to rule out
hypomagnesemia.
Treatment
 Oral calcium carbonate tablet.
 Vitamin D.
 Dietary steps
 Rich in calcium.
 Low in phosphorus-rich items.
 Intravenous infusion.
Risk factor
Factors that may increase risk of developing
hypoparathyroidism include:
 Recent neck surgery, particularly if the thyroid was
involved.
 A family history of hypoparathyroidism.
 Having certain autoimmune or endocrine conditions,
such as Addison's disease — a condition characterized by
a deficit in hormone production by the adrenal glands
Hyperparathyroidism
 Hyperparathyroidism is an excess of parathyroid
hormone in the bloodstream due to over activity of one
or more of the body's four parathyroid glands.
 These glands are about the size of a grain of rice and are
located in neck
Cont...
 Primary hyperparathyroidism is caused by
hypersecretion of PTH. In majority of cases, this is due to
autonomous hypersecretion of PTH. Primary
hyperparathyroidism (adenoma or hyperplasia) may be familial
and part of multiple endocrine neoplasia
 Secondary hyperparathyroidism is characterized
by the hypersecretion of PTH due to stimulation
byhypocalcemia .There is hyperplasia of all parathyroid glands.
 Tertiary hyperparathyroidism hyperplastic
parathyroid glands (as in case of secondary hyperparathyroidism)
may result in adenoma formation and autonomous PTH
Clinical feature
 Fragile bones that easily fracture (osteoporosis)
 Kidney stones
 Excessive urination
 Abdominal pain
 Tiring easily or weakness
 Depression.
 Bone and joint pain
 Frequent complaints of illness with no apparent cause
 Nausea, vomiting or loss of appetite
Oral manifestation
1. Dental abnormalities:
-Widened pulp chambers
- Development defects
- Alterations in dental eruption
-Weak teeth
- Malocclusions
2. Brown tumor
3. Loss of bone density
4. Soft tissue calcifications
Investigation
 In primary hyperparathyroidism serum PTH level is
elevated, serum calcium is high and phosphate is low.
Serum alkaline phosphatase is raised if bone disease is
present.
 In secondary hyperparathyroidism, PTH level is elevated.
 Serum calcium is low and phosphate is high.
 Bone X-ray may show demineralization.
 Skull X-ray .
 Radioimaging and ultrasound neck are needed to localize
and diagnose parathyroid tumors.
Management
 Surgery.
 Calcimimetics.
 Hormone replacement therapy.
 Bisphosphonates.
Pituitary gland
 Anatomy: The pituitary gland is situated in the sella
turcica.
 The gland is connected to the hypothalamus with
pituitary stalk .
 The pituitary gland has two lobes anterior and posterior.
Portal vessels carry blood from the hypothalamus to the
anterior lobe while the posterior lobe receives nerve
fibers from the hypothalamus.
 Physiology: The anterior lobe of pituitary gland secretes
growth hormone (GH), prolactin (PRL),
adrenocorticotropic hormone (ACTH), thyroid stimulating
hormone (TSH),follicle stimulating hormone (FSH) and
luteinizing hormone (LH).
 The secretion of these hormones is controlled by the
hypothalamus.
 The hypothalamus stimulates or inhibits the secretion of
anterior pituitary hormones through the release of substances
in the portal vessels.
 Anti-diuretic hormone (ADH) and oxytocin are synthesized
in the hypothalamus and transported through the nerve axons
to the posterior pituitary.
Hypopituitarism
 Hypopituitarism may be caused by hypothalamic
dysfunction or pituitary disease.
 There may be single or multiple hormonal deficiencies.
 Hypopituitarism is a rare disorder in which the pituitary
gland either fails to produce one or more of its
hormones or doesn't produce enough of them.
Cause
 adenoma, granulomas, metastatic carcinoma and brain
tumors such as craniopharyngioma and meningioma.
 Pituitary tumor.
Other causes are
 Trauma .
 Surgery.
 Radiation .
 Encephalitis .
 stroke.
Clinical features
 Fatigue .
 Hot flashes, and inability
 Weight loss.
to produce milk for
breast-feeding in women
 Decreased facial or body
hair in men
 Short stature in children
 Decreased sex drive .
 Sensitivity to cold or
difficulty staying warm
 Decreased appetite.
 Facial puffiness
 Anemia
 Infertility
Oral manifestation Hypopituitarism
 Tooth eruption is delayed
 Root length is reduced
 Malocclusion
 Saliva gland are prone to hypo function
Investigation
 blood tests.
 Stimulation or dynamic testing.
 Brain imaging.
 Vision tests.
Management
 Remove underlying cause
Hormone replacement medications may include:
 Corticosteroids.
 Levothyroxine.
 Sex hormones.
 Growth hormone.
Hyperpituitarism
 Hyperpituitarism also called acromegaly and
gigantism. Hyper secretion of pituitary hormones
secondary to macro adenomas can interfere with
other pituitary hormone functions, resulting in
target organ hormone deficiencies.
Acromegaly
 Acromegaly is a hormonal disorder that develops when
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the pituitary gland produces too much growth hormone
during adulthood.
When this happens, the bones increase in size, including
those of hands, feet and face.
Acromegaly usually affects middle-aged adults.
Acromegaly is caused by an excess of the growth
hormone secreted by pituitary adenoma.
In most cases the adenoma is more than 1 cm in
diameter (macroadenoma).
Clinical features
 The most common symptoms are
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headache and sweating
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Enlarged hands and feet
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enlarged facial features
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Coarse, oily, thickened skin
Excessive sweating and body odor 
Small outgrowths of skin tissue 
Fatigue and muscle weakness
A deepened, husky voice due to 
enlarged vocal cords and sinuses
Severe snoring due to obstruction
of the upper airway
Impaired vision
Pain and limited joint mobility
Menstrual cycle irregularities in
women
Erectile dysfunction in men
Enlarged liver, heart, kidneys,
spleen and other organs
Increased chest size (barrel chest)
Oral manifestation
 Enlargement of tongue
 Spacing in the tooth
 Malocclusion
 Mandible increase in
thickness and length
 Chin is prominent
 Hypercementosis
 Enlarged jaw
Investigation
 The serum GH is measured during oral glucose
tolerance test. In normal subjects, plasma GH is
suppressed to below
2 mU/L.
 Failure of suppression of GH level or paradoxical rise
suggests acromegaly.
Management
Drugs used to lower the production or block the
action of GH include:
 Somatostatin analogues.
 Dopamine agonists.
 Growth hormone antagonist.
Complication
 High blood pressure (hypertension)
 Cardiovascular disease, particularly enlargement of the
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heart
Osteoarthritis
Diabetes mellitus
Precancerous growths (polyps) on the lining of colon
Sleep apnea.
Carpal tunnel syndrome.
Spinal cord compression
Vision loss
Gigantism
 Gigantism is abnormal growth due to an excess of growth
hormone during childhood.
causes
 The most common cause of too much growth hormone release is a
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noncancerous (benign) tumor of the pituitary gland. Other causes
include:
Carney complex
Multiple endocrine neoplasia type 1 (MEN-1)
Neurofibromatosis
If excess growth hormone occurs after normal bone growth has
stopped, the condition is known as acromegaly.
Gigantism is very rare.
Clinical features
 The child will grow in height, as well as in the muscles and
organs. This excessive growth makes the child extremely
large for his or her age.
Other symptoms include:
 Delayed puberty
 Double vision
 prominent jaw
 Gaps between the teeth
 Headache
 Increased sweating
 Large hands and feet with thick fingers and toes
 Weakness
Diagnosis
 Growth hormone test
 Thyroid hormone
 Prolactin hormone test
Treatment
SURGERY
Addison’s Disease
 Adrenal cortex secretes three major classes of steroids:
a. Glucocorticoids (cortisol)
b. Mineralocorticoids (aldosterone)
c. Adrenal androgens
Addison's disease
 Addison's disease is a disorder that occurs when body
produces insufficient amounts of certain hormones
produced by adrenal glands.
 In Addison's disease, the adrenal glands produce too little
cortisol and often insufficient levels of aldosterone as
well.
Cause Addison's disease
 Autoimmune
 Tuberculosis
 Histoplasmosis HIV/AIDS
 Bilateral adrenalectomy
 Intraadrenal hemorrhage
 Amyloidosis Hemochromatosis
 Metastatic carcinoma
Clinical feature
 Muscle weakness and
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fatigue
Weight loss and decreased
appetite
Darkening of skin
(hyperpigmentation)
Low blood pressure
fainting
Low blood sugar
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(hypoglycemia)
Nausea, diarrhea or
vomiting.
Muscle or joint pains
Irritability
Depression
Body hair loss or sexual
dysfunction in women.
Oral manifestation
 The oral mucosa can in turn develop black-bluish
plaques, mainly affecting buccal mucosa but it can also be
seen on the gums, palate, tongue and lips
Diagnosis
 ACTH stimulation test: Cortisol level fails to increase in
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response to exogenous ACTH.
ACTH level: This is high in Addison’s disease
Plasma rennin activity is high with low or low-normal
aldosterone level
Measurement of antibodies against steroid secreting cells
Tests for tuberculosis
CT/MRI to identify metastatic malignancy
Elisa for HIV
Management
 Oral corticosteroids.
 Corticosteroid injections.
 Androgen replacement therapy.
Cushing’s Disease
 Cushing’s disease is due to hypersecretion of ACTH by the
pituitary gland and it is the most common cause of Cushing’s
syndrome.
 Cushing’s syndrome is defined as a state of cortisol excess
due to any cause.
 ACTH causes increased production of corticosteroids by the
adrenal cortex.
 Cushing’s disease is usually benign small pituitary adenoma
(micro adenoma).
Clinical feature
 Moon face
 Buffalo hump
 hypertension.
 Osteoporosis.
 muscle wasting.
 Hyperglycemia.
 impaired wound healing and psychosis
 Weight gain .
Diagnoses for cushing’s syndrome
 Blood test to determine
 Blood glucose level
 White blood cell count and potassium level
 Abdominal CT
Treatment for cushing’s syndrome
 Laparoscopic adrenalectomy
Possible complication
 Diabetes
 High blood pressure
 Infections
 Kidney stones
 Mental illness
 Compression fractures.
Conn’s syndrome
conns syndrome Is a disease of the adrenal
glands involving excess production of a
hormone called aldosterone .
Cause for Conn’s syndrome
 Excess production of aldosterone by the tumor
leads to the development of Conn's syndrome
with high blood pressure and low potassium level.
Symptoms for Conn's syndrome
 Hypertension
 High aldesterone level in the blood act on the
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kidney to increase the loss of mineral potassium in
the urine.
Fall in blood potassium to lead
Tiredness
Muscle weakness
Passing of volume of urine (polyuria)
Diagnosis
 CT scan
 Radiologist inserts a small catheter into adrenal
vein.
Treatment
 Adrenalectomy
Diabetes mellitus
Diabetes is a metabolic disorder resulting in abnormally high
blood sugar levels (hyperglycemia)
 Blood sugar is normally
controlled by a hormone
called insulin that is
secreted by the pancreas.
Diabetes Mellitus
 Types Of Diabetes
 Type 1 Diabetes
 Type 2 Diabetes
Diabetes Mellitus
Type 1 Diabetes
 Once Known as insulin-dependent or juvenile
 Pancreas produces little or no insulin
 Accounts for 5-10% of diagnosed diabetes
 Need Insulin injections to survive
INSULIN DEPANDENT DIABETES
Diabetes Mellitus
It caused:
 Autoimmune.
 Genetic.
 Environmental factors.
Risk Factors:
Occurs equally among males and females
 Siblings of people with type 1 diabetes
 Children of parents with type 1 diabetes .
 Overweight
 Family History
Diabetes Mellitus
Type 1 Diabetes Symptoms
 Usually develop over short period
 Increased thirst, urination, constant hunger,
weight loss, blurred vision, and extreme
tiredness.
 If not diagnosed or treated with insulin, a
person can lapse into a life-threatening coma
Diabetes Mellitus
Treatment
 Daily injections of Insulin are basic therapy
 Injections must be balanced with meals and
daily activities
 Glucose levels must be closely monitored
through blood sugar testing
Diabetes Mellitus
Type 2 Diabetes
 Most common form
 About 90-95% of people have this type
 Usually develops in adults over 40 yrs old
 The pancreas produces insulin, but for some
reason , the body can’t use the insulin or are
insulin resistance.
•Diabetes Mellitus
Risk for Type 2 Diabetes
 over age 45
family history of diabetes
 overweight
 Lack of exercise regularly
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Metabolic syndrome (also called insulin
resistance syndrome).
 Hypertension.
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Abnormal lipid levels.
 History of gestational diabetes.
Type 2 Diabetes Symptoms
Develop gradually and are not as noticeable as type 1
Symptoms include
 feeling tired or ill.
 frequent urination (esp. at night).
 unusual thirst.
 weight loss.
 blurred vision.
 frequent infections.
 slow healing of sores.
Diabetes Mellitus
 Treatment of type 2:
 Diet
 Exercise
 Blood Testing
 Some take oral drugs or insulin to lower blood glucose
levels.
Diabetes Mellitus
 Medications
 Oral
 Tolbutamide
 Chloropropamide
 Tolazamide
 Acetohexamide
 Glyburide
 Glipizide
 Glucotrol
 GLUGOPHAGE
Oral manifestation of diabetes
 Gingivitis and periodontisis
 Periradicular osteolytic inflammatory lesion
 Loss of teeth
 Xerostomia (dry mouth )
 Lesions of oral mucosa and tongue .
Complication of diabetes
 Heart Disease is 2-4 times common in diabetics
 High Blood Pressure affects 60-65 percent of people with
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diabetes
blindness among adults 20-74 years .
At least 15% of all people with diabetes with eventually have
a foot ulcer/and or leg ulcer.
Gangrene is common in diabetes due to poor circulation of
lower extremities.
Periodontal disease 82%
Diabetes Complications
Foot/Leg/Heel Ulcers
Diabetic Emergencies in the Dental
Office
 The most common diabetic emergency
in the dental office is
Hypoglycemia.
Insulin Shock (Hypoglycemia)
 Occurs when insulin levels are too high
 Who have been prevented from eating at the expected
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time
Can occur if a pt accidentally or intentionally takes too
much insulin
Alcohol Intake
It is an Urgent medical emergency
Prolonged hypoglycemia can result in serious brain
damage
Insulin Shock (Hypoglycemia)
Signs and Symptoms
 Weak, Rapid Pulse
 Cold, clammy skin
 Weakness
 Headache
 Irritable, nervous behavior
 May appear intoxicated
 Coma (severe cases)
Management of hypoglycemia in dental
clinic
The patient is often aware of what happening and able to
warm the dentist. then give glucose tablets or powder or
sugar(at least four lamp) as sweetened drink, repeated if
symptoms are not relieved.
The dental practitioner should give the patient
approximately 15 g of oral carbohydrate in a form that
will be absorbed rapidly..
If consciousness has been lost and an intravenous line is
in place,25 to50ml of a 50% dextrose solution (D50) or
1 mg of glucagon. Can be given intravenously.
Management of hyporglacemia in
dental clinic
If an intravenous line is not in place,1 mg of glucagon
can be injected subcutaneously or intramuscularly at
almost any body site. Glucagon injection causes rapid
glycogenolysis the liver, releasing stored glycogen and
rapidly elevating blood glucose.
Following treatment, the signs and symptoms of
hypoglycemia should resolve in 10 to 15 minutes. The
patient should be observed for 30 to 60 minutes after
recovery.
Insulin Shock (Hypoglycemia)
in dental clinic
 Treatment
In the dental clinic, care is limited to activating the
emergency medical system.
 Airway
 Breathing
 Circulation
 Disability
 Asses Pt for trauma-protect C-spine if Ness.
 Administer O2 per assessment
 Monitor vital sing, Suction Airway if Necessary
 The patient should be transported to a hospital as soon as
Insulin Shock (Hypoglycemia)
Treatment BLS Cont.
 Obtain Medical HX
 Check Finger Glucose, if <60 and pt’s airway is
protected administer oral glucose
 Transport Pt in position of comfort
 Reassess vital signs as needed.
Comparison
 Hypoglycemia
 Hyperglycemia
 Onset Sudden
 Slower onset
 Skin cold, pale, moist
 Skin warm, red, dry
 Normal
 Weak, rapid pulse
 Acidic Breath
 Kussmaul Respiration's
 Weakness/
 Rapid Pulse
uncoordination
 Headache
 Irritable/Nervous
Behavior
 Polyuria, polydypsia,
polyphagia
 Nausea/Vomiting
 Falling Blood Pressure
TREAMENT AND MANAGEMENT OF
DIABETETTIC PATIENT IN DENTAL CLINIC
 Good history and examination
 Control of diabetic
 Other key dental treatment considerations(restoration,




extraction).
Antibiotic therapy specially tetracycline
Scalling technique
Root planing
Regular dental clinic visit