Pituitary Gland Disorders

Question 1

Pituitary gland: anatomy and hormones they produce.

Answer 1

It is a gland located in the bony structure, sella turnica located at the base of the skull.
It has 2 parts
Anterior part originates from the Rathke’s pouch
Posterior part originates from the floor of the 3rd ventricle.
Blood supply- superior hypophyseal artery.
Anterior pituitary produces; prolactin, ACTH, LH, FSH, TSH, GH, melanocyte-stimulation hormone.
Posterior pituitary produces; oxytocin and ADH

Question 2

Functions of all the pituitary hormones.

Answer 2

Prolactin- promotes milk production from mammary glands
ACTH- Stimulates the production of adrenal gland hormones
GH- promotes growth of body tissues
TSH- stimulates the thyroid hormones to release its hormones
FSH- stimulates the production of ovarian follicles
LH- stimulates androgens and progesterone production in the gonads
MSH- stimulates the production of melanin by melanocytes
Oxytocin- contraction of uterine muscles during birth
ADH-stimulates reabsorption of water in the kidneys

Question 3

Neurohypophysis disorders- Diabetes insipidus; definition, etiology and classification

Answer 3

Diabetes insipidus is the disorder of the posterior lobe of the pituitary gland characterized by a deficiency of anti diuretic hormone or vasopressin. Great thirst (polydipsia) and large volume of dilute urine characterize the disorder.

Etiology/Causes- It is caused by problems with a chemical called vasopressin (AVP), which is also known as an anti diuretic hormone.

Central diabetes insipidus-> Head trauma or surgery, pituitary or hypothalamic tumor, intracerebral occlusion or infection.

b) Nephrogenic diabetes insipidus-> Systemic diseases involving the kidney, multiple myeloma, sickle cell anemia, pyelonephritis, poly cystic kidney disease
Dipsogenic diabetes insipidus-> due to malfunction of the thirst mechanism. Damage to the hypothalamus or pituitary may lead to this condition.

Gestational diabetes insipidus-> which occurs during pregnancy as a result of the placenta producing vasopressinase: an enzyme that breaks down vasopressin, it leads to ADH deficiency.

Question 4

Symptoms, diagnostic criteria

Answer 4

Symptoms
Polyuria with urine output of 5 to 15 L daily, polydipsia,especially desire for cold fluids, anorexia and epigastric fullness, nocturia and related fatigue from interrupted sleep, decrease of appetite, dryness of skin and mucous membranes, pharyngitis,gastritis and constipation.

.Diagnostic criteria
Insufficient ADH release despite serum osmolarity
Increase osmolarity in response to ADH
- Specific gravity of urine is less than 1005.
- Osmolarity of urine is less than 100mOsmol/kg
5 to 10 liters of urine per day (polyuria)
a)vasopressin response test
Plasma osmolality rises above normal > 300 mosm/kg with urine osmality < 300 Mos/kg
b)nephrogenic diagnostic criteria
plasma osmolality >300mosm/kg with urine osmolality between 300 -700 mosm/kg
- Polydypsia
- Dehydration

Question 5

Treatment

Answer 5

• Fluid replacement
  • When oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patient’s serum.
  
  • Desmopressin is the drug of choice. A synthetic analogue of antidiuretic hormone (ADH),available in subcutaneous, IV, intranasal, and oral preparations. Administered 2-3 times per day. Frequent electrolyte monitoring is recommended during the initial phase of treatment.
    • synthetic vasopressin and the nonhormonal agents chlorpropamide, carbamazepine, thiazides, and nonsteroidal anti-inflammatory drugs (NSAIDs).
    Monitoring
    • Monitor for fluid retention and hyponatremia during initial therapy. Follow the volume of water intake and the frequency and volume of urination, and inquire about thirst. Monitor serum sodium, 24-hour urinary volumes, and specific gravity. Request posthospitalization follow-up visits with the patient every 6-12 months.
    Dietary measures
    • Adequate and balanced intake of salt and water. A low-protein, low-sodium diet can help to decrease urine output.
    Postoperative setting
    • After pituitary surgery, patients should undergo continuous monitoring of fluid intake, urinary output, and specific gravities, along with daily measurements of serum electrolytes.
    • Administer the usual dose of desmopressin and give (hypotonic) IV fluids to match urinary output and fall of specific gravity of urine.

Question 6

Prolactin disorders, clinics and treatment

Answer 6

Hyperprolactinemia is the increased production of prolactin >250ml
Etiology: drugs, adenoma of the pituitary gland, severe primary hypothyroidism
Clinics: galactorrhea, menstrual irregularities, infertility, weakness, impotence, visual field abnormalities
Treatment: Dopamine agonist- bromocriptin which stimulates D2 receptors or lactotroph inhibiting prolactin synthesis and release.
Pergolide or Carbegoline twice a week low dose in 4 parts.

Question 7

Acromegaly and gigantism- definition, etiology

Answer 7

Acromegaly is caused by the pituitary gland overproducing growth hormone over time
NOTE:ACROMEGALY IS IN ADULTS (after puberty) AND GIGANTISM IS IN CHILD(before puberty and before the epiphyseal plates closes)
Etiology is normally due to pituitary and non-pituitary tumors

Question 8

Symptoms and diagnosis

Answer 8

Based on clinical signs and symptoms;
Enlargement of the hands and feet, coarsening of facial features, and thickened skin folds; increase in shoe, hat, glove, and ring size
Enlarged nose and mandible (prognathism and separation of teeth), sometimes causing underbite
Deeper voice
Hypertrophic tongue
Diasthema
Protracted jaw
Athropathy
Increased sweating
Obstructive sleep apnea
Enlarged internal organs, including heart, lung, spleen, liver, and kidneys
Menstrual problems (common) due to co-secretion of prolactin by GH producing tumor
Metabolic changes, i.e., impaired glucose tolerance (80%) and diabetes (13–20%)
NB; Patients with acromegaly have symptoms for ~9 years before the
diagnosis is made.
Labs
Initial test; Plasma insulin growth factor (IGF-1) level - elevated
Norms; Age 18 -374.1 ng/ml, Age 35-39 -180.1 ng/ml, After 70yrs; 92.7ng/ml

The confirmatory test is GH measurement after 100 g of glucose is given orally; if GH remains high (>5 ng/mL), it is positive and suggests acromegaly. Normally, glucose load should completely suppress levels of GH.
Elevated IGF levels

Instrumental
Pituitary MRI for location of tumor

Question 9

Treatment of GH disorders

Answer 9

1.A dopaminergic agonist- bromergocriptine (bromocriptine), causes a paradoxical inhibition of growth-hormone secretion in patients with acromegaly.
2. Somatostatin analogues: octreotide, sandostatin (clinical remissions in 90 % patients, normalization of GH level in 50 % of patients).
Side effects include nausea, diarrhea, gallstones, glucose intolorence.

3. SOMAVERT (pegvisomant for injection) is a prescription medicine for acromegaly. It is for patients whose disease has not been controlled by surgery, radiation, and/or other medical therapies, or patients for whom these options are not appropriate. The goal of treatment with SOMAVERT is to have a normal IGF-I level in the blood.

Question 10

Obesity: definition and classification.

Answer 10

Overweight and obesity are defined as abnormal or excessive fat accumulation in the body tissues. A body mass index (BMI) over 25 is considered overweight, and over 30 is obese.

Classification by egorov.

1. Alimentary
2. Endocrine
3. Cerebral

Classification according to stages of obesity.
According to brock’s index
1.weight excess<30%
2.weight excess 30-50%
3.weight excess 50-100%
4.weight excess>100%

Classification due to fat deposition.
Lower type
Upper type

Classification. According to body massBMI kg/m2.
Underweight-<18.5
Normal -18.5 – 24.9
Overweight (including obesity)-25.0 – 29.9
Obese I-30.0 – 34.9
Obesity II-35.0 – 39.9
Extreme Obesity-> 40 Obesity III

Question 11

Predisposing factors, clinics,regulation and treatment of obesity

Answer 11

Sex, social factors, diet, lifestyle, exercise patterns, endocrine disorders
Clinical signs.
1.Fast weight gain 20-30kg during 1-2 years
2.More frequent dysplastic localization of fat
3.presence of striae
4.signs of hypothalamic dysfunction (palpitations,hyperhydrosis ,hypertension).

TREATMENT.
Diet
The simplest way to reduce caloric intake is with a low-calorie diet.
1.1)eat 4 – 5 times a day, only in a direct time, not to eat between basic meal receptions;
2)eat only one portion;
3) limit a free liquid to 1,0 – 1,2 l/day;
4) not to eat with the aim of decreasing depression, not to eat ―for a company‖;
5)the total daily energy intake should be between 1600 – 800 Kcal.

Physical activity
most important for maintance of weight loss
Physical activity has to be:
1)Regular (30 – 45 – 60 min walking/day 7 days/week)
2)Bring only positive emotions
3)Group support
4)Any exercise is better than no exercise (bike, walk, dance)

Pharmacotherapy.
In patients with endocrine and cerebral pathology:
anti-inflammatory drugs (to treat encephalitis, arachnoiditis)
bromocreptin, peritol (to treat hypothalamic and pituitary disorders) and others.