METABOLIC DISORDERS (manla) Part 1 Flashcards
The sum of tissue activity in terms of physical and chemical changes that happens inside your body associated with the use of protein, fat, carbohydrate, vitamins, minerals, water, and hormones in whatever is taken by the body.
METABOLISM
T/F
Everything is metabolized before it exits in your bowel or excretion (saliva, sweat, anything that comes out of the body is a product of metabolism).
T
Metabolic disorders may be caused by abnormal functions of glands:
• Pituitary
• Thyroid
• Parathyroid
• Adrenal
• Pancreas
Cretinism
A. Hypothyroidism
B. Hyperthyroidism
A
o Juvenile myxedema
A. Hypothyroidism
B. Hyperthyroidism
A
Myxedema
A. Hypothyroidism
B. Hyperthyroidism
A
Exophthalmic goiter - One where in the eyes are bulging
A. Hypothyroidism
B. Hyperthyroidism
B
Toxic adenoma
Tumor
Grows inside
Impinging your esophagus and having
a difficulty in speaking, breathing, and swallowing
A. Hypothyroidism
B. Hyperthyroidism
B
Primary hyperparathyroidism
Secondary hyperparathyroidism
What abnormal functions of glands?
PARATHYROID GLANd
“There is really something wrong with the gland
itself”
A. Primary hyperparathyroidism
B. Secondary hyperparathyroidism
A
It’s only a secondary to or a result of another
condition”
A. Primary hyperparathyroidism
B. Secondary hyperparathyroidism
B
Hypofunction of the gland, Hyperfunction of the gland
What abnormality?
ADRENAL GLAND
Diabetes Mellitus
What organ?
PANCREAS
Addison’s disease (chronic) - Take 6 years to develops
A. Hypofunction of the gland
B. Hyperfunction of the gland
A
Waterhouse-Friderichsen syndrome (acute)
*Symptoms suddenly appear
A. Hypofunction of the gland
B. Hyperfunction of the gland
A
Cushing’s syndrome
A. Hypofunction of the gland
B. Hyperfunction of the gland
B
Adrenogenital syndrome
A. Hypofunction of the gland
B. Hyperfunction of the gland
B
Adaptation syndrome
A. Hypofunction of the gland
B. Hyperfunction of the gland
B
Secretes insulin
Diabetes Mellitus
Disturbance in protein metabolism (2)
o Marasmus
o Kwashiorkor
Disturbance in carbohydrate metabolism (2)
o Hurler’s syndrome
o HEREDITARY FRUCTOSE INTOLERANCE
Disturbance in non-lipid metabolism (3)
o Letterer-Siwe disease
o Hand-Schuller-Christian Disease
o Eosinophilic granuloma
Master gland of the body
PITUITARY GLAND
Decreased secretion of pituitary hormone
HYPOPITUITARISM
Clinical Features of Hypopituitarism:
o Dwarfism
o Sparse hair
o Wrinkled skin
o Delayed tooth eruption
o Microdontia
o Malocclusion
o Short roots
o Retarded growth of jaws
o Thin eyebrows
o Thin lips
o Immobile expression
o Loss of eyelashes
True or false
One of clinical features of HYPOPITUITARISM are:
o Malocclusion
o Short roots
o Retarded growth of jaws
o Immobile expression
T
T/F
ACROMEGALY is a Rare
T
Due to oversecretion of growth hormone AFTER closure of epiphyseal plates.
ACROMEGALY
Due to oversecretion of growth hormone BEFORE closure of epiphyseal plates.
GIGANTISM
• Hyperhidrosis
• Muscle weakness
• Paresthesia
• Carpal tunnel syndrome
• Dysmenorrhea
• Decreased libido
• Sleep apnea
• Hypertension
• Heart disease
• Skin tag formation
CLINICAL FEATURES of HYPERPITUITARISM
ORAL MANIFESTATIONS
• Enlarged mandible and maxilla
• Diastemas
• Condylar hyperplasia
• Dental malocclusion
• Complete posterior crossbite
• Thick oral mucosa
• Increased salivary gland tissue
• Macroglossia
• Prominent lips
• Speech abnormalities
HYPERPITUITARISM
TREATMENT of HYPERPITUITARISM
• Normalize the level of growth hormones
• Preserve the pituitary gland function
HYPERTHYROIDISM Two kinds
- Exophthalmic
- Toxic Adenoma
Diffused hyperplasia of thyroid gland
A. Exophthalmic
B. Toxic Adenoma
A
Tumor of thyroid gland
A. Exophthalmic
B. Toxic Adenoma
B
Secretes growth hormones
THYROID GLAND
Hyperfunction of thyroid gland
HYPERTHYROIDISM
HYPERTHYROIDISM CHARACTERISTICS (3)
T3
T4
TSH
triiodothyronine
A. T3
B. T4
C. TSH
A
thyroxine
A. T3
B. T4
C. TSH
B
thyroid-stimulating hormones
A. T3
B. T4
C. TSH
C
Results when there is excessive stimulation of thyroid gland by excessive secretion of thyroid hormone.
THYROTOXICOSIS
Other Characteristics:
o Heat intolerance
o Hyperhidrosis
o Nervousness
o Palpitations, highly emotional o Diarrhea
o Anxiety
o Weight loss
o Menstrual dysfunction
o Thin and brittle hair
HYPERTHYROIDISM
EYE CHANGES
• Exophthalmos
• Bright eyed stare or wide-eyed stare
• Facial expression of surprise
• Upper lid retraction
• Lid lag on normal blinking
HYPERTHYROIDISM
CARDIAC MANIFESTATIONS
• One of the earliest and most consistent feature
• Hyperthyroidism is an increased metabolic activity which
puts great demand on the heart: o Increase stroke volume
o Pulse rate
o Cardiac output
HYPERTHYROIDISM
ORAL MANIFESTATIONS
• Premature eruption of deciduous teeth
• Premature exfoliation
• Premature eruption of permanent teeth
• Osteoporosis of jaws
• Burning tongue
• Erosion of teeth
HYPERTHYROIDISM
HYPERTHYROIDISM TREATMENT
*Drug therapy
o E.g., thiocarbamades
*Radioactive iodine administration
*Reduce stress to minimize the occurrence of THYROID
CRISIS
T/F
Use of Epinephrine and Atropine is contraindicated in patients with hyperthyroidism due to patient’s increased sensitivity to epinephrine
T
T/F
Use of Epinephrine and Atropine may precipitate THYROID STORM which is a thyroid hormone induced hypermetabolism that is life threatening
T
Thyroid can’t produce amount of
hormones pituitary calls for
Primary Hypothyroidism
Thyroid isn’t being
stimulated by pituitary to produce hormones
Secondary Hypothyroidism
occurs in infancy
A. Cretinism
B. Juvenile Myxedema
C. Myxedema
A
occurs in childhood
A. Cretinism
B. Juvenile Myxedema
C. Myxedema
B
in adults
A. Cretinism
B. Juvenile Myxedema
C. Myxedema
C
• Mental defects
• Generalized edema
• Face is wide
• Underdeveloped mandible and maxilla is overdeveloped
• Brittle hair and fingernails
• Atrophic sweat glands
CLINICAL FEATURES OF CRETINISM:
• Delayed eruption
• Retained deciduous teeth
CLINICAL FEATURES OF JUVENILE MYXEDEMA:
• Is the atrophy of thyroid gland
• Unknown cause
• Edematous lips, nose
eyelids
• Large tongue
• Interfered speech
CLINICAL FEATURES OF MYXEDEMA IN ADULTS:
Increased secretion of parathyroid hormone
HYPERPARATHYROIDISM
Hyperplastic parathyroid gland causes ____
hyperparathyroidism
Characterized by:
• Increased in number of cells
• Increase in size of cells
HYPERPARATHYROIDISM
Consistent abnormal findings:
• Hypercalcemia
• Increased parathormone level
These 2 are needed for the confirmation of the diagnosis of _______.
HYPERPARATHYROIDISM
ETIOLOGY •
Unknown
Other beliefs:
o Irradiation
o Decreased estrogen o Hereditary
HYPERPARATHYROIDISM
CLINICAL FEATURES
• Fatigue
• Weakness
• Nausea (GROANS)
• Anorexia (GROANS)
• Polyuria (STONES)
o Urinal stones
• Thirst (GROANS)
• Depression (MOANS)
• Constipation (GROANS)
• Bone pain (BONES)
• Headaches (MOANS)
HYPERPARATHYROIDISM
Lesions are found in the:
• Kidney (stones)
• Skeletal System (bones)
• Gastrointestinal System (groans) • Nervous System (moans
HYPERPARATHYROIDISM
ORAL RADIOGRAPHIC FEATURES
• Bone demineralization of mandible and maxilla
HYPERPARATHYROIDISM
GI MANIFESTATIONS
• Peptic ulcer
HYPERPARATHYROIDISM
NEUROLOGIC MANIFESTATIONS
• Coma
• Parathyroid crisis
• Loss of memory
• Depression
HYPERPARATHYROIDISM
ORAL MANIFESTATIONS
• Chief oral finding: well
defined cystic radiolucency of the jaw, monocular (1 big circle) or multilocular (many small circles)
• Loosening of teeth
• Cortical plate of bones:
thinning
• Partial loss of lamina
dura
HYPERPARATHYROIDISM
HISTOPATHOLOGY
• Extravasation of red blood cells, thus the tumor appears reddish brown
• Thus, it is termed “BROWN TUMOR”
HYPERPARATHYROIDISM
SHAFER:
• Radiographic features of primary hyperparathyroidism:
o Ground glass appearance
o Loss of lamina dura
o Abnormal alveolar bone
An inherited disorder of connective tissue, characterized by joints which are hypermobile and skin that is hyperflexible
EHLERS-DANLOS SYNDROME
• Due to defects in collagen metabolism
• This condition has been classified to 8 forms:
o The EDS type VIII is the periodontal form where:
o There is fast progress of periodontal disease resulting to complete tooth loss by the 2nd or 3rd
decade of life
EHLERS-DANLOS SYNDROME
ETIOLOGY AND PATHOGENESIS
• Hereditary
• Defect in formation and structure of type III collagen
• Decrease in collagen hydroxylase
• Defect in collagen metabolism
• Disorder in copper metabolism
EHLERS-DANLOS SYNDROME
CLINICAL FEATURES
• Classical: (Skin)
o Hyperplastic skin
o Skin is velvet in
appearance.
o Skin is easily bruised,
very fragile.
o Minor trauma will
cause ecchymoses, bleeding, CIGARETTE
PAPER scar formation.
EHLERS-DANLOS SYNDROME
CLINICAL FEATURES
On joints:
o Hypermobility
o Dislocation of joints
o Back knee
o Flat feet
o Kyphoscoliosis
o Skeletal deformities
EHLERS-DANLOS SYNDROME
OROFACIAL FEATURES:
• Narrow maxilla
• Flattened midface
• Wide nasal bridge
• Hypertelorism
• Epicanthal folds
• Hollowed appearance of eyes
• Scarring of the forehand and
chin
• Fragile gingiva
• Problematic mucosal tissues
• TMJ dysfunction
• Tongue can extend too much
(tip to nose)
EHLERS-DANLOS SYNDROME
DENTAL FINDINGS:
• Deep anatomic grooves
• Very high cusps height of
molars and premolars
• Stunted or dilacerated roots
EHLERS-DANLOS SYNDROME
EHLERS-DANLOS SYNDROME TREATMENT
• Monitor the heart because usually patients die due to aneurysms
• Sudden bursting of arteries which is aneurysms
PROGNOSIS
• Wound healing is usually delayed
• Prolonged bleeding
• Osteoarthritis develops in repeated TMJ luxations
EHLERS-DANLOS SYNDROME
Also called Chronic Cortical Insufficiency
ADDISON’S DISEASE (CHRONIC)
• Low level of adrenal cortex hormones
• Primary symptom: BRONZE SKIN
o Bronzing of the Skin
ADDISON’S DISEASE (CHRONIC)
• Clinical manifestations of
o Bronze skin
o Pigmented mucous membranes
o Deep chocolate pigmentation of oral mucosa
from buccal area to angles of mouth spreading to gingiva tongue and lips
ADDISON’S DISEASE (CHRONIC)
When there is bilateral hyperplasia of adrenal glands it is called?
CUSHING’S SYNDROME
CLINICAL MANIFESTATIONS:
• Mooning of the face
• Round shoulders thus a “Buffalo hump” at the base of the
neck
• Altered hair distribution
• Muscular weakness
• Hypertension
• Glycosuria
• Albuminuria
CUSHING’S SYNDROME
Dexamethasone Test:
• Low dose at 12 PM fails to suppress 8 AM cortisol production
• High dose at 12 PM suppresses ACTH - producing pituitary adenoma only
CUSHING’S SYNDROME
ORAL MANIFESTATIONS
• Osteoporosis
• Premature cessation of epiphyseal growth
CUSHING’S SYNDROME
Hormone involved:
o Insulin
o Other endocrine glands also play a role in its
production
DIABETES MELITUS
• A disorder of carbohydrate metabolism
• Characterized by hyperglycemia and glycosuria
DIABETES
There is a disturbance in:
o Use of glucose by tissues
o Release of glucose by liver
o Production and release of pancreatic, pituitary
and adrenocortical hormones
o This disturbance lowers the resistance of tissue
to infection
DIABETES
EFFECTS ON THE ORAL CAVITY
• Periodontitis
• If untreated, periodontal abscess, inflamed, painful,
hemorrhagic gingival papillae
DIABETES MELITUS
CLINICAL MANIFESTATIONS
• 3P’s: Polyuria, Polydypsia, Polyphagia
• Due to excessive fluid loss: dry mouth
DIABETES MELITUS
T/ F
• There are no oral manifestations for patients with controlled diabetes
• But controlled diabetic patients should only undergo dental operations only after consultations with the physician who is treating the patient
T
diffuse hyperplasia of thyroid gland
Exophthalmic Goiter
tumor of thyroid gland
Toxic Adenoma
Lipid Reticuloendotheliosis (2)
→ Gaucher’s Disease
→ Niemman-Pick Disease
• Coronal pulp stones that are
floating
• Irregular composition of
dentinal tubules
• Denticles
• Enamel hypoplasia
EHLERS-DANLOS SYNDROME
