Final corrected Endocrine system pathology last new (2) (2).pdf

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2. Consists of
Endocrine Glands
Specialized cell clusters
Hormones
Target tissues

3. Are abiologically active chemicals
Transmitter substances, produced mainly
By the Endocrine glands of the body
Transported by the bloodstream
To the cells and organs on
Which it has a specific regulatory effects
Hormones act as chemical messengers
Stimulating certain life processes and
Retarding others

4. Increased activity of the target tissue
Often down regulates the activity of
The gland that secretes the
Stimulating hormone a process known as
Feedback inhibition
Hormones can be classified, based on
The nature of their receptors:
Hormones that trigger biochemical signals
Upon interacting with cell surface receptors:
This class is composed of two groups
1) Peptide hormones, such as growth hormone and
insulin
2) Small molecules, such as epinephrine.

5. Binding of these hormones to cell surface receptors
Leads to an increase in intracellular molecules,
Termed second messengers
Elevated levels of these compounds can change
Proliferation
Differentiation
Survival
Functional activity of cells

6. Hormones that diffuse across the plasma membrane and
Interact with intracellular receptors:
Many lipid-soluble hormones pass
Through the plasma membrane by diffusion
To interact with receptors in the cytosolor
The nucleus
The resulting hormone-receptor complexes bind
Specifically to promoter and
Enhancer elements in DNA affecting
The expression of specific target genes
Ex-.steroids -estrogen,progesterone,
Glucocorticoids
The retinoids-vitamin A
Thyroxine

7. The processes that may disturb
The normal activity of the endocrine system are:
Impaired synthesis of hormones
Release of hormones
Abnormal interactions between
Hormones and their target tissues
Abnormal responses of target organs
To their hormones

8. Can be classified as:
1) Diseases of
Underproduction
Overproduction of hormones
2) Diseases associated with the development of
Mass lesions which may be
Nonfunctional or
Associated with
Overproduction or
Underproduction of hormones

9. The Mechanisms of hormone release are:
Humoraldevelops in response to
Changing levels of ions or
Nutrients in the blood
Neural: isstimulated by nerves
Hormonal is stimulation received from other
hormones

10. A feedback system regulates the
Dysfunctions of the endocrine system that are
Hypofunction
Hyperfunction
Inflammation
Tumor
The feedback mechanism may be
Simple
Complex

11. Simple feedback occurs when
The level of one substance
Regulates secretion of a hormone
Ex. a lowserum calcium level stimulates
The parathyroid glands to secrete PTH
High serum calcium level inhibitsPTH secretion

12. Complex feedback occurs through the
Hypothalamic-pituitary adrenal target organ axis
Secretion of the hypothalamic
Corticotropin-releasing hormone
Releases pituitary ACTHwhich in turn
Stimulates adrenal cortisolsecretion
Subsequently, an
Increase in serum Cortisollevels
Inhibits ACTH by
Decreasing Corticotropin–releasing Hormone secretion or
ACTH directly

13. Feedback systems may
Fail to function properly
May respond to the wrong signals
Dysfunction of an endocrine gland
May manifest as:
Failure to produce adequate amounts of hormone
Excessive synthesis
Release

15. Released hormones may be:
Degraded at an altered rate
Inactivated by antibodies
Before reaching the target cell
Abnormal target cell responses include
Receptor-associated alterations
Intracellular alterations
Receptor-associated alterations are associated
With water-soluble hormones peptides and
Involve:

16. Decreased number of receptors, resulting in
Diminished or
Defective hormone-receptor binding
Impaired receptor function, resulting in
The presenceof antibodies against Specific
receptors,
Reducing Available Binding sites
Suppressingor
Exaggerating target cell response
Unusual expression of receptor function
Mimicking –imitate hormone action

17. Involve the
Inadequate synthesis of the hormones
Second messenger needed to convert the
Hormonal signal into intracellular events
Two different mechanisms may be involved:
Faulty response of target cells for
Water-soluble hormones to
Hormone -receptor binding
Failure to generate the required second messenger
Abnormal response of the target cell to the second
messenger
Failure to express the usual hormonal effect

18. Is the main integrative center
For the endocrine and nervous systems
It consolidates signals derived from
Upper cortical inputs
Autonomic function
Environmental signals such as
Light and temperature
Peripheral endocrine feedback
Releasing hormones:
Maintaining daily physiological cycles
Controlling appetite
Managing of sexual behavior
Regulating emotional responses

19. Controls
Body temperature
Hunger
Thirst
Fatigue
Sleep
Circadian Rythmes

20. In turn-the hypothalamus delivers signals to
The pituitary gland which
Releases hormones that directly affects
The functions of
The thyroid gland
The adrenal gland
The gonads
Influencing growth
Milk production
Water balance

24. Controls theendocrinesystem in three ways-
1) Neurons in the paraventricular and supraopticnuclei
Send their axons to form the posterior pituitary gland
Where they secrete oxytocin and vasopressin
2)Neurons in the periventricular, paraventricular, and
Arcuate nuclei send axons to the median eminence,
To secrete pituitary hormone releasing hormones,
Which regulate the anterior pituitary gland.
3)The hypothalamus controls autonomic outputs to
Many peripheral endocrine tissues,
Which further regulate their secretion

26. Releasing and Inhibiting hormones are:
Thyrotropin-releasing
Gonadotropin-releasing
Growth hormone-releasing
Corticotrophin -releasing
Somatostatinand
Dopamine hormones
These hormones release into the blood via
The capillaries travel to the pituitary gland
Oxytocinand vasopressinare also hypothalamic
hormones

27. Magnocellular neurons are
Neuroendocrine cells among the largest cells
In the hypothalamus
They synthesize the hormones
Arginine vasopressin
Oxytocin
Send axons into the neurohypophysis
The pathway from the hypothalamus to
The posterior pituitary is called
The hypothalamo-neurohypophysealtract

28. Is a system of blood vessels
The bridge of capillaries
At the base of the brain, connecting
The hypothalamus with the anterior pituitary.
Its main function is to quickly transport and
Exchange hormones between
Arcuate nucleus of the hypothalamus and
Anterior pituitary gland.
This network, allows hypothalamic hormones
To be transported to the anterior pituitary
Without entering the systemic circulation.

32. Secreted hormone Produced by Effect
Thyrotropin-releasing
hormone(TRH)
Prolactin-releasing
hormone TRH, or PRH
Parvocellular
neurosecretorycells
paraventricularnucleus
StimulatesThyroid
Stimulating Hormone
TSHandProlactin
Releasefromanterior
pituitary
Corticotropin-releasing
hormone(CRH)
Parvocellular
neurosecretorycells of the
paraventricularnucleus
StimulateAdrenocorticot
ropic
hormone(ACTH)release
fromanterior pituitary
Dopamine(DA)
(Prolactin-inhibiting
hormone) PIH
Dopaminneurons of the
arcuatenucleus
Inhibitprolactinrelease
fromanteriorpituitary

33. Secreted hormone Produced by Effect
Growth hormone–
releasing
hormone(GHRH)
somatocrinin
Neuroendocrinecells of
the arcuatenucleus
Stimulategrowth
hormone GH release
fromanterior pituitary
GonadotropinReleasing
Hormone
GnRH
Somatostatin
(growth-hormone-
inhibiting hormone)SS,
GHIH
Neuroendocrinecells of
thePreopticArea
Neuroendocrinecells
Of the Periventricular
nucleus
StimulateFolicle
Stimulating Hormone
FSH release from
anterior pituitary
StimulateLuteinizing
stimulating Hormone LH
release from anterior
pituitary
InhibitGHrelease
fromanteriorpituitary
Inhibit moderately
TSHrelease
fromanterior pituitary

34. Oxytocin(OXY or
OXT)
Magnocellular
neurosecretorycellsof
the paraventricular
nucleus and Supra
optic nucleus
Uterine Contraction
Lactation
Letdown effect
Vasopressin
AntidiureticHormone
ADH
Magnocellular
neurosecretorycellsof
the paraventricular
nucleus and Supra
optic nucleus
Increase in the
permeability to water
of the cells ofdistal
tubule andcollecting
duct in the kidney and
thus -allows water
reabsorptionand
excretion of
concentrated urine

37. Often referred to as
„master gland ”
Together with the hypothalamus, it
Orchestrates the complex regulatory
Functions of multiple endocrine glands

38. Has Two divisions:
Anterior pituitary-adenohypophysis
Secretes 7 hormones
1. TSH Thyroid-stimulating hormone
2. ACTHAdrenocorticotropichormone
3. FSHFollicle-stimulating hormone
4. LHLuteinizing hormone
5. GHGrowth hormone
6. PRLProlactin
7. MSHMelanocyte-stimulating hormone

39. TSH -stimulates the thyroid to produce
Thyroid hormone
ACTH -stimulates the adrenal cortex to produce
Corticosteroids: aldosteroneand cortisol
FSHFollicle-Stimulating Hormone stimulates
Follicle growth
Ovarian estrogen production
Sperm production
Androgen-binding protein

40. LHLuteinizing Hormone has a role in
Ovulation and the growth of the Corpus luteum
Stimulatesandrogen secretion by interstitial cells in testes
GHpromotes body growth by:
Binding to receptors on the surface of liver cells
This stimulates them to release
Insulin -like growth factor-1IGF-1-somatomedin
IGF-1 acts directly on the ends of the
Long bones promoting their growth

41. PRL ProlaktinDuring pregnancy helps in
The preparation of the breasts for
Future milk production.
After birth, promotes the synthesis of milk.
MSH Alpha Melanocyte-Stimulating Hormone
Stimulates melanin secretion -
Melanineis the pigment that gives human
Skin, Hair, eyes their color.
Melanin is produced by cells called melanocytes
Freckles are small, concentrated areas of
Increased melanin production

42. Posterior pituitary-Neurohypophysisproduces
8.ADH antidiuretichormone, or Vasopressin
9. Oxytocin
ADH acts on the collecting ducts of
The kidney to facilitate the reabsorption
Of water into the blood.
Thus it acts to reduce the volume of urine
Oxitocineacts on certain smooth muscles:
Stimulating contractions of the uterus at the time of birth.
Stimulating release of milk when the baby begins to
suckle

45. The adrenal cortex secretes
Mineralocorticoids
Glucocorticoids
Sex steroid hormones –androgens
Progestins
Estrogens
Androgens and estrogens produced by the
Adrenal is a minor fraction of the total amount
Of these steroids produced in the body
Glucocorticoidsand mineralocorticoidsare
Produced almost exclusively in the adrenal cortex

46. Aldosterone,a mineralocorticoid
Regulates the reabsorptionof sodium and
The excretion of potassium by the kidneys
Affected by ACTH, aldosteroneis mainly
Regulated by RAAS
Cortisol, a glucocorticoid, stimulates
Gluconeogenesis
Increases protein breakdown
Free fatty acid mobilization,
Suppresses the immune response,
Facilitates an appropriate response to stress

47. The adrenal medulla produces
The catecholamines-Epinephrine
Norepinephrine, which cause
Vasoconstriction
Stimulates fight-or-flight response
Dilation of bronchioles
Increased BP
Blood glucose level
HR

48. Abnormalities of the pituitary gland result from
Oversecretion
Under secretion
Abnormalities of posterior and anterior lobes
Can occur independently
Oversecretionmost commonly involves
ACTH leading to Cushing’s syndrome or
GH leading to acromegaly.

49. Under secretion
Involves the anterior pituitary hormones
Deficient production of the ADH-
Diabetes insipidus-the most common
Disorder of the posterior lobe in which
Abnormally large volumes of
Dilute urine are excreted

50. GH hypersecretion
Usually is the result of
Benign pituitary adenoma
More often in Males
Mean age: 40-50 years
Macroadenoma~ 70-75%
Micoadenomas~ 25-30%
1st symptom onset, -dg. ~ 7-12 years
Progressive form –more common among youngs

51. Acralbony overgrowth
Increased foot and hand size –
Increased shoe/glove size
Ring tightening
Proximal muscle weakness

52. Carpal tunnel syndrome CTS-tingling sensation
Pins and needles
Numbness
Pain in the hand and fingersdu to the
Compression of the median nerve
That controls sensation and movement in the
hands

53. Face Frontal bossing
Large fleshy nose
Thicker mouth
Macroglossia
Widened space between the
Lower incisor teeth
Mandibularenlargement –prognathism
Oily skin -Hyperhydrosis
Deep sounding voice
Generalizatedorganomegaly-
Cardiomegaly
Liver and spleen enlargement

56. Cardiovascular system:
Left ventricular hypertrophy
Coronary heart disease
Cardiomyopathywith arrhythmias
Diastolic dysfunction
Hypertension

57. Splanchnomegaly
Glucose-intolerance –
Diabetes mellitus
Increased risk for colon polyps-
Colon tumors
Upper airway obstruction–du to
Increased Thyroid gland,
Tongue

58. MorisTilletwas born in 1903 in Russia
In childhood he was nicknamed "The Angel"
Due to his angelic face
Was very clever, plaid chess
Knew 14 foreign languages
From 1917, the family lived in France
In age 20, Tilletnoticed swelling in his
Feet , hands, and head,
The acromegalywas diagnosed

59. Tillefled to the United States, where
He used his unusual appearance
Became a professional boxer in the ring
Acted as a giant,
Terrifying the opponents
He was twice recognized
World heavy weight champion in box
He turned his disadvantage
Into an advantage

64. პროგნატიზმი

67. Random GH level useless
Pulsate secretion
Age and gender-matched
IGF-Insulin like grows factor 1 levels increased
Failure of GH suppression
Age and gender-matched IGF-1 levels
Oral glucose tolerance test OGTT -
Failure of GH supression<1µg
Paradox GH rising after glucose or
TRH administration

68. Hypersecretionof IGF-I insulin like
Grows factor causes gigantism in children
When the epiphysealgrowth plates
Are open and acromegalyin adults
Acromegalyis the same disorder of
IGF-I excess, but occurs after
The growth plate cartilage fuses in adulthood
Gene on the X chromosome,GPR101
Was identified which was over expressed
1000-fold more than normal

69. Tall stature
Mild to moderate obesity (common)
Macrocephalymay precede linear growth
Headaches
Visual changes
Hypopituitarism
Soft tissue hypertrophy
Exaggerated growth of the hands and feet
Thick fingers and toes

70. Frontal bossing
Prognathism
Hyperhidrosis
Osteoarthritis -a late feature of IGF-I excess
Peripheral neuropathies -CTS
Cardiovascular disease
Benign tumors
Endocrinopathies

74. The higher and the smaller
men

78. It is hypofunctionof the pituitary gland.
It results from disease of the pituitary gland itself
Destruction of the anterior lobe of pituitary or
Of the hypothalamus
Panhypopituitarism
Total absence of all pituitary secretions -Is rare.
Postpartum pituitary necrosisis more likely to
Occur in women
With severe blood loss
Hypovolemia, and
Hypotension at the time of delivery

79. Hypopituitarismresults from
Impaired production of one or more
Anterior pituitary tropic hormone
Can be Inherited
Aquired
Pituitary Tumours are usually benign
Their location and effects on hormone production
Can be life threatening

80. A disease characterized
by panhypopituitarism
that causes progressive
exhaustion,, atrophy of
the gonads, thyroid, and
adrenal cortex,
Loss of body hair that
Results from
Atrophy or Destruction
of the anterior lobe of the
pituitary gland

81. Is characterized by growth and
Development disorders caused by
Insufficient secretion of
Growth hormone -GH
Growth is very slowed or delayed
Pituitary dwarfism is a consequence of
Decreased function of the pituitary gland
Occurred early in childhood before the
Ossification of bonecartilages

82. May be caused by:
Specific genetic mutations
Traumaincl. surgery ofthe pituitary gland
Tumors
Trauma or
Irradiationof theCNS
Leukemia
In most cases is idiopathic

85. Anabnormal slow growth rate
The body proportions are normal
Astature 20-25% lower than
The normalaverage age stature
The cranial perimeter is usually normal
Due to deficient degradation of fat,
Fat distribution in patientsis much higher
Especially around the waist
Rarely excess fat deposits in the thighs
Abdomen or in
The mammary glands can occur

86. Diminishedprotein synthesis
Themuscle mass -proportionallydecreased
Muscle strength isdecreased
Sexual organs
Are not sufficiently developed
Small in size
Themammaryglandsunderdeveloped
Amenorrhea is present
In males the testicles are not
Descended into the scrotum

87. Growth hormone deficiencyis present
Growth charts by age will help determine a
diagnosis.
X-ray of thehand fistis usedto determine
Bone age comparing it with
The child’s chronological age
Bone age in children with pituitary dwarfism
Is usually 2 or more yearsdelayedthan the
actualchronological age.

88. Located in the neck, anterior to the trachea
Weight range from 12 to 30g
Produces: FT4 ,FT3 active hormone
FT4 -Thyroxineis made
Exclusively in thyroid gland
T4 is the most important source of FT3
By peripheral tissue deiodination“ T4 to T3 “
More than 90% of the thyroid hormones
Physiological effects are due to
The binding of T3 to thyroid receptors
In peripheral tissues

90. Affects every single cell in the body
Modulates:
Oxygen consumption
Growth rate
Maturation and cell differentiation
Turnover of Vitamins
Hormones
Proteins
Fat
CHO -carbohydrates

91. Act by binding to Nuclear receptors, termed
Thyroid Hormone Receptors -TRs
Increasing synthesis of proteins
At mitochondrial level
Increases number and activity to increasing
Adenosine triphosphate-ATP production
At Cell membrane increases ions and
Substrates transmembraneflow

92. CALORIGENESIS
GROWTH, MATURATION RATE
C.N.S. DEVELOPMENT FUNCTION
CHO, FAT, PROTEIN METABOLISM
MUSCLE METABOLISM
ELECTROLYTE BALANCE
VITAMIN METABOLISM
CARDIOVASCULAR SYSTEM
HEMATOPOIETIC SYSTEM
GASTROINTESTINAL SYSTEM
ENDOCRINE SYSTEM
PREGNANCY



93. Hyper production of ThyreoidGlands hormones
State due to elevated circulating levels of free T3 and T4
Can be Primary
Secondary
Without Hyperthyroidism
Exogenous or factitious
Causes
Primary Hyperthyroidism
Grave´s disease
Toxic MultinodularGoiter
Toxic adenoma
Functioning thyroid carcinoma metastases
Activating mutation of TSH receptor
Struma ovary
Drugs: Iodine excess

94. Without hyperthyroidism:
Subacutethyroiditis
Silent thyroiditis
Other causes of thyroid destruction:
Amiodarone
Radiation
Infarction of an adenoma

95. Hyperactivity
Irritability
Tachycardia
Tremor
Dysphoria
Heat intolerance & sweating
Palpitations
Fatigue & weakness
Weight loss with increased appetite due the
hypermetabolism
Heat intolerance
Excessive sweating

96. Diarrhea
Polyuria
Sexual dysfunction
Atrialfibrillation
Goiter--struma
Warm and fleshed skin
Muscle weakness, myopathy
Lid retraction or lag
Gynecomastia
Exophtalmus
Pretibialmyxedema
Stimulation of the gut results in
Hypermotility
Malabsorption
Diarrhea

97. Underproduction of thyroid hormones-
Hypothyroidism
Primary
Secondary
Peripheral
Congenital

98. Causes:
Secondary
Pituitary gland destruction
Isolated TSH deficiency
Bexarotenetreatment
Hypothalamic disorders
Peripheral:
Rare, familial tendency

100. Tiredness
Weakness
Dry skin
Somnolence
Sexual dysfunction
Hair loss -alopecia
Difficulty concentrating
Bradycardia
Dyspnea
Puffy face
Hands
Feet
Peripheral edema
Serous cavity effusions

101. Clinical signs
Laboratory findings:
TSH plasma level -normal
Practically excludes abnormality
If TSH is abnormal, next step:
Total Free T4, T3
TSI Thyroid Stimulating Ig
TPO Thyroid PeroxidaseAb
AntimitochondrialAb
Plasma TgThyroglobulin
Radioiodine uptake
Thyroid scanning

102. Signs:
Bradycardia
Dry coarse skin
Diffuse alopecia
Peripheral edema
Delayed tendon reflex relaxation
Carpal tunelsyndrome
Serous cavity effusions.

104. FNA-Fine-needle aspiration
Thyroid ultrasound
TSH High usually means Hypothyroidism
Rare causes:
TSH-secreting pituitary tumor
Thyroid hormone resistance
Assay artifact
TSH low usually indicates Thyrotoxicosis

105. Is the most common cause of endogenous hyperthyroidism
Was described in 1835 by Robert Graves as the disease
characterized by
“Violent and long continued palpitations in females”
Enlargement of the thyroid gland
It is characterized by a triad of manifestations:
Thyrotoxicosis,caused by a diffusely enlarged
Hyper functional thyroid-in all cases.
An infiltrative ophthalmopathywith resultant
Exophthalmusin 40% of patients.
An infiltrative dermopathy-pretibialmyxedema-
Resulting from the deposition of hyaluronicacid-is rare.
Women are affected up to 7times more than men
A peak incidence is between 20 -40 ages

106. Ocular
manifestations: a
wide, staring
gaze and lid lag
are
present because
of Sympathetic
Overstimulation
of the levator
palpebrae
superioris
Truethyroid
ophthalmopathy
associated with
Proptosisis
seen only in
Graves disease

107. The volume of the retroorbitalconnective tissues and
Extraocularmuscles is increased as a result of:
1)Marked infiltration of the retro orbital space by
Mononuclear predominantly T cells
2) Inflammatory edema and
Swelling of extra ocular muscles
3) Accumulation of extracellular matrix components-
Spec. hyaluronicacid and chondroitinsulfate;
4) Increased numbers of adipocytes-
Fatty infiltration
The eyeball are displaced forward
Interfering with the function of
The extraocularmuscles.

108. Genetic factors are important
Rate in monozygotic twins is high as 60%
Is associated with the presence of
HLA haplotypes, specifiallyHLA-DR3 and
Polymorphisms in genes encoding the inhibitory
T cell receptor CTLA-4 and
The tyrosine phosphatasePTPN22
Is characterized by a breakdown in self-tolerance
To thyroid auto antigens of which the most
Important is the TSH receptor
The result is the production of multiple auto antibodies inc
Thyroid-stimulating immunoglobulin an IgGantibody
That binds to the TSH receptor and mimics the
Action of TSH stimulating adenylcyclase
With resultant increased release of thyroid hormones
This autoantibody, is relatively specific for GD

109. Thyroid growth-stimulating immunoglobulins:
These anti-TSH receptor antibodies prevent
TSH from binding to its receptor on thyroid
Epithelial cells and in so doing
May actually inhibit thyroid cell function
The coexistence of stimulating and inhibiting
Immunoglobulinsof the same patient is not unusual—
A finding that may explain why some patients with GD
Spontaneously develop episodes
Of hypothyroidism.

110. Four tiny glands, located in the neck,
Control the body's calcium levels.
Each gland is about the size of a grain of rice
Produce aparathyroid hormone-PTH.
PTH raises the blood calcium level by:
Breaking down the bone -where most of
The body's calcium is stored causing
Calcium release
Increasing the body's ability to absorb calcium
from food
Increasing the kidney's ability to hold on to
calcium that would otherwise be lost in the urine.

111. When the blood calcium level is too low,
PTH is released to bring the calcium level
Back up to normal
When the calcium level is normal or gets
A little too high, normal parathyroids
Will stop releasing PTH.
Proper calcium balance is crucial to the
Normal functioning of the heart,
Nervous system, kidneys, and bones.

114. -HPT is the most common type of PD
Leads to overproduction of parathyroid gland
Primary HPTis enlargement of one or
More of the parathyroid glands causes
Overproduction of the hormone.
This causes high calcium levels,
Can cause a variety of health problems
The most common treatment is -Surgery
Secondary hyperparathyroidism-
Another disease causes low calcium levels
Over time, increased parathyroid hormone levels
occur

115. Primary -a benign adenoma -the most common cause.
Hyperplasiaof two or more parathyroid glands
A cancerous tumor -a very rare
Secondary: Severe calcium deficiency.
Due the diet
Because the problems of calcium absorption by GIT
Severe vitamin D deficiency.
Vitamin D helps maintain appropriate calcium levels in
the blood.
Helps digestive system absorb calcium from the food.
The lack of vitamin D can cause drop of calcium levels
Chronic kidney failure.
The kidneys convert vitamin D into usable form.
Chronic kidney failure is the most common cause of
Secondary HPT

116. Most people with primary HPT have no symptoms
The mild symptoms are:
Muscle weakness
Fatigue
Increased need for sleep
Depression
Aches and pains in the joints and bones
More severe Symptoms are:
Loss of appetite
Nausea
Constipation
Confusion or impaired thinking and memory
Increased thirst and urination
Brittle bones
Easily bones fracture (osteoporosis)
Kidney stones

117. Laboratory
Testing the levels of calcium
PTH in blood
25-hydroxy-vitamin D blood test detects the
The lack vitamin D in the blood
Bone densitometry-DEXA to measure bone loss
Computed Tomography -CT scans
Magnetic Resonance Imaging –MRI
Surgery-removal of the heperactive
Parathyroid glands is highly effective
Medications -calcimimetics-Cinacalcet
Decrease the amount of PTH produced
By the parathyroid glands.
Dietary supplements calcium supplements
Vitamin D supplements