Endocrine - Lecture v2 Lec 6

Hormones;
Endocrine & Metabolic

Disorders
nadia_hamdy@pharma.asu.edu.eg
3/20/2023 Clinical Bio, Prof. Nadia Hamdy, 2023 1

List of Endocrine Glands
• Hypothalamus & Pituitary gland in
the brain
• Thyroid gland (neck)
• Parathyroid glands (thyroid)
• Adrenal glands (top of kidney) Hormone functions
• Ovaries and testes (reproductive 1. Fetal differentiation of
glands) reproductive and CNS
• Islets of Langerhans (pancreas) 2. Growth and
development including
puberty
3. Maintaining
homeostasis
4. Maintaining optimal
levels of hormones
5. Metabolic function
Pituitary
• Master Gland
• Hypothalamus-pituitary
Axis (HPA)
• Makes stimulating
hormones (?SH)for other glands
• Anterior or posterior lope hormones

• Regulates
• Growth & Reproduction

Hypopituitarism
Growth Hormone (GH) deficiency; dwarfism
• Decreased activity of pituitary gland

• S/Sx
• Hypoglycemic seizures, neonatal jaundice, micro-penis,
undescended testicles
• Older-overweight, youthful facial features, high pitched
voices, skeletal & sexual maturation, hypoglycemia

Diagnosis and Treatment
• Radiographic view of pituitary gland

• Lab test
• IGF; Insulin-like Growth Factor
• Medications given to stimulate GH release and test GH
levels
• Treatment
• GH replacement therapy
• Follow-up and monitoring growth rate
• Educate society to treat child by age, not by size and
accept difference

Hyperpituitarism
• From pituitary adenoma or Hypothalamus tumor
• Excessive GH secretion, very rare in children;
gigantism, occurs before growth plates fuse (long
bones closure) so s/he is 7-8 feet tall
Or after growth plates fuse; acromegaly, then
overgrowth of facial structure occurs; fore head,
shoe size and ring size increase
• Treatment-surgery or radiation

Diabetes Insipidus (DI)
• Deficiency in ADH (Vasopressin; VP) released from
the posterior pituitary gland
• Inability to concentrate urine from decreased or
no antidiuretic hormone (ADH)
• Neurogenic (pituitary gland disruption)
• Nephrogenic (insensitive renal tubules to ADH)
• Associated with: head injuries, infections,
hypopituitarism, familial, tumors, surgery
• S/S: (abrupt onset) Polyuria, polydipsia, nocturia,
enuresis, dehydration, constipation, fever

Diabetes Insipidus
May be from
• Rx’s medication as side effects
• Head Trauma
• Pituitary Disorders
S/S:
• Excessive Urination; 5-15 L/day, thirst, dehydration
• Serum sodium concentration increases (hypernatremia)
• Plasma AVP (arginine vasopressin) level is decreased
• Urine specific gravity <1.010
• Blood fluid volume deficit; Monitor for Dehydration
• Daily Weights
Treatment – correct the cause

• IV hypertonic solution, increase Plasma Osmotic (PO) fluids like salts, ..,
Desmopressin acetate IM injections
Negative Feedback – Thyroid
• Thyroid gland regulates Metabolism

• Parathyroid gland regulates Ca
• Hypothyroidism
• Not enough hormone T4, T3
• Hyperthyroidism
• Too much hormone

Congenital Hypothyroidism (CH)
• Present @ birth (1:4000), Autosomal recessive
• From Absent or non-functioning thyroid (primary
hypothyroidism)
• S/Sx
Hypothermia, umbilical hernia, hypotonia, hoarse
cry, respiratory distress, prolonged jaundice,
lethargy, constipation, feeding difficulties

CH – Signs and Symptoms
• Anemia is due to decreased oxygen carrying requirement
• Retardation of mental development and growth manifest in later
infancy and largely irreversible
• Feeding problems, failure to thrive, constipation, a hoarse cry
• Protuberance of abdomen, dry skin, poor growth of hair and nails,
delayed eruption of deciduous teeth, umbilical hernia
• Delay in holding up the head, sitting, walking and talking
• Limb disproportionately short in relation to the trunk
• Severe mental deficiency, and low IQ
Endocrine disorders 11
Congenital Hypothyroidism
• Test- ideally 3-6 days old.
Test routinely after 24 hours of age (mandatory in every
state)
• Test blood T4 (thyroxine) & TSH
• High TSH + low T4 & T3 = Origin from the thyroid, not
from the pituitary
• Thyroxin-binding globulin (TBG) levels can be
measured in infants with suspected TBG deficiency.

• Management:
• Early diagnosis and treatment or mental retardation is
severe and permanent without treatment
• Levo-thyroxine
By (Pediatric) Endocrine specialist

• Life long treatment
• Monitor growth and development (mental and
physical)

Hypothyroidism
• Not enough hormone
• Lack of Iodine
• Pituitary disease
• Advancing age
Observation & Reporting
• Facial Myxoedema
• Weak/Fatigue
• Depression
• Wt. Gain
• Cold Intolerances
• Constipation
• Dry, Thick Skin

• Monitor:
• Weight
• Activity
• Limit Fatigue
• Cluster activities
• Plan rest periods
• Report Abnormal
• Medical Id bracelet
• Refer questions/concerns to nurse

Acquired Hypothyroidism Etiology
• Acquired
• 1:1000 school age children
• > 2 y.o.
• F>M
• Autoimmune thyroiditis (Hashimoto’s thyroiditis)
• Elevated TSH & decreased T4
• Iodine deficiency
• Iodine necessary for thyroid hormone synthesis
• Radiation/surgery to thyroid causes hypo function
• Drug/substance exposure as lithium for treatment
cause hypothyroidism
Acquired Hypothyroidism
• Increased risk with family history
• Goiter usually present
• Adverse effects after age 2-3 are reversible with
treatment
• Almost 30% Hashimoto’s spontaneously recover
(remission)

Acquired Hypothyroidism
• S/Sx-
• Everything slows down
• Cold intolerance, slow GI peristalsis, decreased
appetite, dry skin, coarse hair, hair loss, bradycardia,
fatigue, obesity, goiter, lethargy, delayed puberty,
abnormal menses, peripheral edema, decreased school
performance, enlarged tongue

Management
• Treatment: Levothyroxine
• Treat the disease not the symptoms
• TSH check at least yearly, better twice yearly.
• Drug therapy is lifelong
• Re-assure and educate parents

Hyperthyroidism
• Overactive Thyroid
• Causes:
• Graves’ Disease
• Excessive Intake of Thyroid Hormones
• Thyroiditis
• Excessive Iodine Intake
• Significantly Accelerated
Metabolism; increases BMR

Hyperthyroidism
• Thyroid hormone level increased (thyrotoxicosis – inc
BMR) high T4 & T3, low TSH
• Graves’ disease most common
• Preschool to teen-highly familial, F>M
• Autoimmune-immunoglobulins stimulate thyroid
• Thyroid hormone-producing tumors (thyroid or pituitary)
• Congenital-prenatally, mother has Graves’

Signs and Symptoms
• Goiter
• Exophthalmos (bulging eyes)
• Tachycardia, sweating, tremors, warm skin
• Nervousness, irritability, mood swings
• Decreasing school performance-decreased
concentration
• Increased appetite with weight loss
• Heat intolerance, muscle weakness
• Fine hair, hyper-reflexia
• Easily fatigued, unable to sleep
Treatment
• Lab-
• TSH, T3, T4
• Thyroid scan
• Drug therapy (side-effects problems)
• Methimazole (MTZ) . Thioamides
• Propylthiouracil (PTU)
• Radiation
• Thyroidectomy
• Often not a lifelong disease – treatment continued
for 6-months to 2-years then individualized to
patient
• Patients who have been treated for hyperthyroidism
need to be followed closely because they may
develop Hypothyroidism, signs of seizures, or tetany.
• Follow up care includes:
• Check thyroid function test every 4-6 weeks
• Follow up on medications and dose adjustment
Iodine Deficiency Disorders (IDD)
• Endemic goiter
• Endemic cretinism
• Intellectual disability
• Growth retardation
• Neonatal hypothyroidism
• Increased early and late pregnancy loss
• Increased perinatal and infant mortality
Iodine Deficiency Disorders (IDD)
• Most common preventable cause of mental deficits in the world
• The WHO estimated that 20 million people in the world had
varying degrees of preventable brain damage due to effects of
iodine deficiency on fetal brain development
• Population at risk for IDD caused by low levels of iodine in the
soil was estimated to be 1 billion, approximately 20% of whom
have goiter
• Estimates of prevalence of neonatal hypothyroidism in various
regions where goiter is endemic range from 1 to 10%, as
compared with only 0.025% in iodine-sufficient regions
• Correction of iodine deficiency before pregnancy
• Severe hypothyroidism in infancy termed cretinism
• Maternal hypothyroidism is a factor contributing to cretinism
IDD – Signs and Symptoms
• Delayed closure of fontanelles, head to be large in relation to the body
• Naso-orbital configuration remains infantile
• Maldevelopment of femoral epiphyses  waddling gait
• The teeth are malformed and susceptible to caries
• A broad, flat nose, wide set eyes, periorbital puffiness, large protruding
tongue, sparse hair, rough skin, short neck, and protuberant abdomen
with umbilical hernia
• A small but significant number (3-7%) of infants with congenital
hypothyroidism have other birth defects, mainly atrial and ventricular
septal defects in their heart
Treatment of CH from IDD
• The rule in the treatment of congenital hypothyroidism is early diagnosis
and thyroid hormone replacement.
• Most important treatment variables are the dose and timing of thyroxine
therapy (Levothyroxine).
• Initial thyroxine dose 10-15 ug/kg/day, Can be given as a single weekly
dose
• Endemic cretinism can be prevented by appropriate iodine
supplementation. Iodization of salt is the usual method.
• Calcium supplements may be useful, Vitamin D therapy is necessary, and
IV calcium gluconate is recommended.
Diseases of the Thyroid
1. hypothyroid diseases;
Cretinism: hypothyroidism in infancy and childhood
leads to stunted growth and in-intelligence.
Can be corrected by giving thyroxine if started early
enough.
Myxedema: hypothyroidism in adults leads to
lowered metabolic rate and vigor (fatigue,
mental impaitment, depression, cold intolerance, dry
skin, wt gain).
Corrected by giving thyroxine.
Goiter: enlargement of the thyroid gland
(cough, hoasrdeness, trouble swallowing).
Can be caused by:
1. inadequate iodine in the diet with
resulting low levels of T4 and T3;
2. an autoimmune attack against components of the 3/20/2023
thyroid gland (called Hashimoto's thyroiditis). 29
2. hyperthyroid diseases;
(George W. Bush; bulging eyes,
high BP, hand tremors, increased
sweating, nervousness, insomnia,….)
A- Graves´ disease. An immune
disease in which autoantibodies
bind to and activate the
thyroid-stimulating hormone
receptor, leading to continual
stimulation of thyroid hormone
synthesis. Result in excessive
production of thyroid
hormones. Graves´ disease is
an example of an autoimmune
disease.
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3/20/2023
•PTH reduces the reabsorption of phosphate from the
proximal tubule of the kidney, which means more
phosphate is excreted through the urine.
•A high level of PTH in the blood is known as

hyperparathyroidism; cancer.
•A low level of PTH in the blood is known as

hypoparathyroidism.
-Causes include surgical misadventure (during routine
thyroid surgery), autoimmune disorder, and inborn errors
of metabolism.
-Treatment with Ca or calcitriol (vit D).
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Adrenal Gland & its disorders
• Adrenal cortex • Adrenal medulla
– Catecholamines
Cushing's Syndrome • epinephrine
• Glucocorticoid (cortisol) hormone excess • Norepinephrine
Congenital Adrenal Hyperplasia (CAH)
Increased adr. =
• Deficiency of cortisol Phaeochromocytom
Adrenal Insufficiency a
• Acute Adrenocortical Insufficiency
• Chronic Adrenocortical Insufficiency (Addison’s
disease)
• Adrenal gland destruction
• Mineralocorticoids
• aldosterone
• Sex steroids: Androgens, estrogens & progestins
Clinical Bio, Prof. Nadia Hamdy, 2023 32
Anterior
Adrenal Pathway
pituitary
ACTH:
ACTH
Inhibition
Adrenocorticotropic hormone
Adrenal cortex
*Negative feedback loop
Cortisol

Cushing’s Syndrome
• Adrenocortical hyperfunction
• Excess glucocorticoids (especially cortisol) or ACTH
• Rare in children (mostly F 30-50 years old)
• Etiology
• Primary – Malignant adrenal tumor
• Secondary – Pituitary adenoma (>8-yo)
• adrenocorticotropic hormone (ACTH)
• Ectopic (nonpituitary) ACTH-secreting tumor
• Iatrogenic – excessive/prolonged steroid therapy
(most common cause)

S/Sx Cushing’s
• Alters metabolism: Catabolism of protein, dec.
absorption of Ca, inc. appetite, salt-retaining
• Poor wound healing, easily bruised, muscle wasting,
demineralization of bone, osteoporosis, fat accumulation
(protruding abdomen, “buffalo hump”, “moon face”), edema,
HTN, fatigue, hirsutism, acne, impaired glucose tolerance,
mood swings, oligomenorrhea/amenorrhea
• Cushingoid appearance reversible with treatment =
a moon face, buffalo hump, acne, obese torso, and thin, easily
bruised skin, all representing the cumulative effect of high-
dose steroids.

Cushing’s treatment
• Surgical removal of tumor
• cortisol replacement is then required
• malignant adrenal tumor prognosis is poor
• pituitary tumor cure rate ~25%
• Irradiation
• Pharmacologic
• block steroid synthesis, mainly used with ectopic
tumors that can not be resected
• Tapered withdraw of pharmacologically prescribed
glucocorticoids

Congenital Adrenal Hyperplasia (CAH)
1:5000-15000 live births - Autosomal recessive

(chromosome 6)
Adrenals enlarged – still cannot produce cortisol
(insufficiency) & overproduce androgen
• Form 1: salt-losing
• Form 2: non-salt-losing (simple virilization)

CAH
• Form 1: salt-losing
• Blockage of cortisol & aldosterone production-excessive salt
& fluid excretion
• Adrenal crisis (may be life threatening) recurrent emesis,
dehydration, metabolic acidosis, hypotension,
hypoglycemia, circulatory collapse
• Form 2: non-salt-losing (simple virilization)
• Overproduce androgen
• Females: Ambiguous genitalia-enlarged clitoris, fused labia,
urogenital sinus
• Males: Precocious genital development
• Precocious puberty, tall stature early then short d/t
premature epiphyseal closure

CAH Treatment
• hydrocotisone (corticosteroid) to suppress ACTH
• given early enough will reverse physical symptoms
• inc. dose required with acute illness, injury, surgery
• Salt-losing:
• aldosterone
• supplementary dietary salt

Acute Adrenal Insufficiency
• Adrenocortical insufficiency (Acute)
• Etiology
• Primary
Addison’s disease (chronic)
Infection/trauma to adrenal gland: TB, AIDS, fulminating
infections (meningococcemia, fungal)
• Secondary
Pituitary tumors, surgery, radiation
Exogenous steroids stopped abruptly
Diagnosis
• Based on clinical symptoms
• Confirm: improvement with cortisol therapy

Acute Adrenocortical Insufficiency
Clinical Manifestations & Treatment
• Symptoms acute and sudden
• BP drops, minimal pulse, elev temp, severe
dehydration & hypoglycemia, seizures, death
• Cortisol replacement
• IV fluids and glucose
• Antibiotic tx for specific infection
• Blood transfusion (hemorrhagic)

• D.M Three Types
• Type 1
• Onset early in life
• Pancreas not producing enough insulin
• Insulin injections
• Type 2
• Adults
• Body doesn’t use insulin well
• Diet/exercise/PO meds
• Gestational (GDM)
• During pregnancy
• Generally goes away after birth

DMI-Etiology
• Autoimmune disease in which islet cell
antibodies lead to the destruction of the
pancreatic beta cells (in islets of Langerhans)
and eventually to a relative lack of insulin
(>90% beta cells are destroyed)
• Disorder of carbohydrate metabolism resulting
from the decrease in insulin production

DM type 1-Etiology
• Influenced by 3 major factors
• Genetic susceptibility to develop - chromosome 6
• Environment - viruses or chemicals in diet may
damage beta cells
• Immunologic processes - Increase of circulating
antibodies in pancreatic islet cells (inflammatory
process) As the beta cells are destroyed, antibodies
will decrease

Hypoglycemia
Observations & Reporting
• Blood Sugar < 60
• Cold, clammy skin
• Irritability
• Rapid, shallow breathing
• Rapid pulse
• Vision Changes
• Convulsions
• Faintness
DM-I Onset
• Relatively acute with rapid progression and
deterioration of the child
• Hyperglycemia
• “Poly-triad”
• Polyuria
• Polydipsia
• Polyphagia
• Weakness
• Low BP
• Kussmaul Breathing
•3/20/2023
BG>125 Clinical Bio, Prof. Nadia Hamdy, 2023 46
Hyperglycemia
• Poor control/unknown disease
• Symptoms:
• lethargic, sleepy, slowed responses, confusion
• tachypnea, hungry, dehydrated
• weak pulse, flushed, dry skin, thirsty, HA
• abdominal pain, N/V, blurred vision, shock
Management:
• Good insulin control
• Frequent monitoring
• Correct dosing
• Refrigerated, non-expired insulin
• Appropriate diet
• Regular exercise Clinical Bio, Prof. Nadia Hamdy, 2023
3/20/2023 47
Diabetic Ketoacidosis: DKA
• Dangerous Complication
• Too Many Ketones; Serum ketones present
• Body Acidic, wt loss, nausea, vomiting
• Up to 1000
• Serum glucose – >300 mg/dL, BG > 400
• Acidosis (pH</=7.30 + bicarb < 15mEq/L)
• Glycosuria, ketonuria; Sweet “fruity-like” (acetone) breath & urine
• Electrolyte disorder; Tachypnea/Kussmaul (deep & rapid)
respirations (d/t inc. CO2)
• Dehydration, flushed ears and cheeks
• Coma: serum osmolality > 350mOsm/kg
• potential for cerebral edema-life threatening
Hypoglycemia
• Causes
• Insulin excess
• Decrease in food intake
• Increased activity
• Alcohol consumption
• Rapid onset of symptoms

• Hyperglycemia-chronic complications
• Hypertension
• Deceleration in linear growth and maturation
• Dry, rough skin with poor turgor
• Poor wound healing-impaired immune function
• Decreased acuity and blurred vision Retinal vascular
changes (diabetic retinopathy)
• Heart disease, renal failure, peripheral vascular disease,
neuropathy
• Accelerated atherosclerosis, hepatomegaly
• 30% will develop hypothyroidism

Exercise • Benefits
• Improved cardiovascular health
• Improved glucose tolerance
• Increased insulin sensitivity
• Reduced hyperinsulinemia
• Reduces overall blood sugar
• Reduced body fat and weight
• Exercise precautions
• Plan, ideally 60-90 minutes after a meal
• Consume additional snacks
• Consume snacks before and during strenuous exercise/sports
• Monitor glucose levels closely
• Avoid strenuous exercise in evening or just before going to bed
• Avoid
3/20/2023 with glucose levels
Clinical>Bio,
240 mg/dl
Prof. Nadia Hamdy, or
2023 ketouria present 51
Sick day rules for DM
• Q 4-6 hour glucose monitoring and urine ketone
checks around the clock
• Insulin must be taken even if anorexia, N/V
• Regular insulin supplemented if hyperglycemia and
ketonuria are present
• Increased fluids, especially if ketosis,
hyperglycemia, or fever present

DM Diagnostic criteria
• Many go undiagnosed (~33%) for up to 6 years
• Classic symptoms + >200 mg/dL
• No classic symptoms
• 2 fasting plasma glucose levels of >125 mg/dL
• 2 oral glucose tolerance tests with 2-hour plasma
glucose levels plus one intervening value >200mg/dL

Laboratory tests
• Plasma glucose
• Normal adult – 80-120 mg/dL
• 1 week to 16 years: 60-105 mg/dl
• >16 years: 70-115 mg/dl
• Hemoglobin A1c (HbA1c)
• Should be performed every 3 months
• 3.9 - 7.7% is normal
• Significantly decrease/delay chronic, long-term
complications with tight control

Laboratory
• Fasting lipid profile
• > 2 years old after control of blood sugar obtained
• If values normal, should be assessed every 5 yr.
• Urinalysis
• Glucose (renal threshold for glucose 160 mg/dL),
ketones and protein negative
• Serum creatinine
• In children with proteinuria need 24 hr. urine collection
• Thyroid function tests

Diabetes Mellitus Type II
• Non-insulin dependent diabetes mellitus (NIDDM)
= insulin resistance + relative insulin deficiency + excess
glucose production by the liver
• “Adult onset diabetes” - >40 y.o. and over weight – now
known to affect record numbers of adolescents and
children – average age of onset in chn/adol is 13
• Risk factors – Obesity, genetic, African-Americans,
Hispanics, Native Americans, Japanese, puberty, polycystic
ovary syndrome, F>M
• Most diagnosed after puberty – common to be an
“accidental” diagnosis
• Common to have HTN, dyslipidemia, vaginal infection,
obesity, family history
??????
• DM type 2 & hyper lipoproteinemia type IV
• MODY
• LADA
• Metabolic syndrom
• DM Type 3 or 2.5

Hypocalcemia
• Parathyroid Hormone (PTH) vs Calcitonin
• S/Sx – dry, scaly skin, brittle hair, thin nails, tetany,
laryngeal stridor, muscle cramps, twitching, HA,
seizures, mood swings, confusion, diarrhea,
vomiting
• Treatment – maintaining normal serum calcium,
long-term Vit D (Cholecalciferol/Calcitriol) therapy,
calcium

Cases
Osteoporosis with age or thyroid disease
bones become fragile and fracture.
Bone loses density, should measure the amount of calcium and
minerals in the bone.
There are no symptoms in the early stages of osteoporosis.
Many times, people will have a fracture before learning that they
have the disease.
Pain almost anywhere in the spine can be caused by fractures of
the bones of the spine. These are called compression fractures.
They often occur without an injury. The pain occurs suddenly or
slowly over time.
There can be a loss of height (as much as 6 inches) over time. A

stooped posture or kyphosis (also called a dowager's hump)
develop.

Osteoporosis. High levels
of thyroid hormones
suppress the production
of TSH through
negative-feedback
mechanism.
The resulting low level of
TSH causes an increase
in the numbers of bone-
reabsorbing osteoclasts
resulting in osteoporosis.
60
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Precocious Puberty
• Early onset of Puberty (premature activation of
pituitary/hypothalamus)
• Ages for girls: 8-13
• Ages for boys: 9 1/2-14
• Development of secondary sex characteristics and
increased rate of growth and bone maturation
(initially tall for age, then short d/t early closure of
epiphysial plates)

Precocious Puberty
• Test: gonadotropin, LH, FSH, bone study, CT, MRI
(often no causative factor is found)
• Treatment:
• none-self resolving (monitor)
• Lupron Depot (synthetic luteinizing hormone releasing
factor)
• Education: parents and child, include discussions
about sexuality (child is fertile), same-age peers

??????
• Galactorrhea,
• Amenorrhea,
• alpha 21-hydroxylase defficiency

Prolactin (PRL)
• During pregnancy it helps in the preparation of the breasts for future milk
production. After birth, prolactin promotes the synthesis of milk.
• PRL secretion is stimulated by TRH, endogenous estrogen (increase

moderately physiologically in pregnancy) AND,
repressed by dopamine and exogenous estrogens.
• PRL levels are used, with other tests, to help determine:

1. the cause of galactorrhea (production of milk not in pregnancy).
2. Diagnose infertility and erectile dysfunction.
3/20/2023 64
• High levels are seen with:
1. Anorexia nervosa (Queen Victoria),
2. Drugs that block the effect of dopamine
through receptors (tranquilizers;
phenothiazines, butyrophenones,
metoclopramide, antihypertensive drugs;
depleting CNS catecholamine as reserpine),
tricyclic antidepressants, opiates, verapamil.
3. Hypothyroidism???? (normalized by T3),
4. Kidney disease and dialysis (from decreased
clearance, and disordered hypothalamic
regulation)
5. PCOS (polycystic ovary syndrome= obesity,
menstrual irregularities),
6. Prolactinomas.
7. Stress (hypoglycemia, MI, surgery, exercise,
sleep)
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• Low levels are seen with:
1. Hypopituitarism.
2. Dopamine treatment, L-dopa, and
ergot alkaloids derivatives.
66
3/20/2023
Cases
PCOS Symptom
 Oligomenorrhoea (defined as <9 periods per year)
 Infertility or subfertility
 Acne
 Hirsutism
 Alopecia
 Obesity or difficulty losing weight
 Psychological symptoms; mood swings, depression, anxiety, poor self-
esteem
 Sleep apnoea
 LH elevated, LH:FSH ratio increased (>2), with FSH normal;
 Free testosterone levels may be raised

Cases
Graves' disease have symptoms of an overactive thyroid, such as:
• Goiter (enlarged thyroid)
• Trouble sleeping
• Irritability or nervousness
• Heat sensitivity, increased sweating
• Hand tremors
• Rapid heartbeat
• Thinning of skin or fine, brittle hair
• Frequent bowel movements
• Weight loss without dieting
• Fatigue or muscle weakness
• Lighter menstrual flow and less frequent periods
• Problems getting pregnant

Cases
Hashimoto's thyroiditis
tends to occur in families.
It can be associated with other autoimmune conditions such as type 1
diabetes or celiac disease.
Hashimoto's thyroiditis is 5 to 10 times more common in women than in men
and most often starts in adulthood.
Blood drawn from people with Hashimoto's thyroiditis typically reveals an
increased number of antibodies against thyroid-specific proteins, including
thyroperoxidase and thyroglobulin.
T lymphocytes, a type of cell involved in the inflammation process, invade
the thyroid gland cause silent, painless inflammation that destroys it;
ultimately, the individual produces little or no thyroid hormone and becomes
hypothyroid.

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Hormones;

Endocrine & Metabolic

3/20/2023 Clinical Bio, Prof. Nadia Hamdy, 2023 1

• Anterior or posterior lope hormones

3/20/2023 Clinical Bio, Prof. Nadia Hamdy, 2023 3

• Decreased activity of pituitary gland

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• Radiographic view of pituitary gland

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Treatment – correct the cause

• Thyroid gland regulates Metabolism

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By (Pediatric) Endocrine specialist

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•A high level of PTH in the blood is known as

•A low level of PTH in the blood is known as

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1:5000-15000 live births - Autosomal recessive

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There can be a loss of height (as much as 6 inches) over time. A

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• PRL secretion is stimulated by TRH, endogenous estrogen (increase

• PRL levels are used, with other tests, to help determine:

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