Pgo - 20: Disorders Of The Endocrine System - Growth, Puberty

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hormones - secretes in high or low cons?

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low

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autocrine

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influence on secreted cell itself

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paracrine

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influence on adjacent cells

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Classic hormones (produced by specialised glands) are divided into three groups

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1) low molecular (amine) hormones (catecholamines, thyroid hormones, prostaglandins, leucotrienes, dopamine, serotonine, GABA, melatonin ...)
2) steroid hormones (e.g. gluco- and mineralcorticoids)
3) polypeptidic and protein hormones (e.g. insulin, leptin)

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another groups of hormones

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A) hypothalamic hormones
B) gastrointestinal hormones
C) opioid peptides
D) tissue growth factors (EGF, NGF, PDGF, ILGF)
E) atrial natriuretic hormone (ANF)
F) transforming growth factors and hematopoetic and other growth factors
G) endothelial factors (endothelins, EDRF)
H) cytokines (interleukins, interferon, TNF)

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Hormonal patterns of secretion

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they have specific rates and patterns of secretion (diurnal, pulsatile, cyclic patterns, pattern that depends on the level of circulating substrates)

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general characteristics of hromones

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1) spesific rates & patterns of secretion
2) feedback systems
3) affect only cells with appropriate receptors
4) excreted by kidney, deactivated by liver or by other mechanisms

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elevated or depressed hormone levels may be caused by

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1) failure of feedback systems
2) dysfunction of endocrine gland or endocrine function of cells
3) degradation of hormones at an altered rate or they may be inactivated by antibodies before reaching the target cell
4) ectopic sorces of hormones

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examples of dysfunction of endocrine gland or endocrine function of cells

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a) secretory cells are unable to produce or do not obtain an adequate quantity of required hormone precursors
b) secretory cells are unable to convert the precursors to the appropriate active form of hormon
c) secretory cells may synthetize and release excessive amounts of hormone

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failure of the target cells to respond to hormone may be caused by:

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1) receptor-associated disorders
2) intracellular disorders

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Receptor-associated disorders causing failure of the target cells to respond to hormone

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1) decrease in the number of receptors
2) impaired receptor function (decreased sensitivity to hormone)
3) Ab against spesific receptor function
4) unusual expression of receptor function

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intracellular disorders causing failure of the target cells to respond to hormone

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1) inadequate synthesis of the second messengers
2) number of intracellular receptors may be decreased or they may have altered affinity for hormones
3) alterations in generation of new mesenger RNA or absence of substrates for new protein synthesis

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manifestation of deficiency of hypothalamic hormones
1) adult women
2) adult men

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1) In adult women: menses cease- absence of GnRH
2) In adult men: spermatogenesis is impaired-absence of GnRH

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SIADH

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Syndrome of inappropriate ADH secretion
It is characterised by high levels of ADH in the absence of normal physiologic stimuli for its release

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causes of elevated ADH

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ectopically produced ADH (cancer of the lung, leukemia, response to surgery, inflammation of lung tissue, psychiatric disease, drugs-barbiturates, general anaesthesia, diuretics...)

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clinical presentation of rapid decrease of serum Na+ from 140 to 130 mmol/l

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thirst, anorexia, dyspnea on exertion, fatigue occur

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serum sodium levels below 110 to 115 mmol/l are likely to cause

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severe and sometimes irreversible neurologic damage

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diabetes insipidus

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an insufficiency of ADH leading to polyuria and polydipsia

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3 forms of diabetes insipid us

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1) neurogenic or central form - amount of ADH production
2) nephrogenic form - inadequate response to ADH
3) psychogenic form - extremely large volumes of fluid intake >> inhibition of ADH production

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pathophysiology of diabetes insipid us

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partial to total inability to concentrate urine due to chronic polyuria >> washout of renal medullary concentration gradient

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Hypopituitarism - cause

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idiopathic, organic damage of adenohypophysis or hypothalamus, e.g. pituitary infarction= Sheehan syndrome, pituitary apoplexy, shock, DM, head trauma, infections, vascular malformations, tumors

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Hyperpituitarism - cause

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adenoma of adenohypophysis
hypothalamic form of hyperpituitarism

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Hypopituitarism - def

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insufficient secretion of one (selective form), more than one or all (panhypopituitarism) hormones of adenohypophysis

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Sheehan syndrome

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pituitary infarction

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if all hormones are deficient = panhypopituitarism: the patients suffer from:

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1) corticol deficiency (lack of ACTH)
2) thyroid hormone deficiency (lack of TSH)
3) ADH deficiency (diabetes insipidus)
4) deficiency of FSH & LH (gonadal failure and loss of secondary sex characteristics)
5) decrease in GH (decrease in somatomedin - affect children growth)
6) absence of prolactin (postpartum women unable to lactate)

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ACTH deficiency >> within ....... symptoms of cortisol insufficiency are developed

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2 weeks

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hypoglycemia in ACTH deficiency

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it is caused by increased sensitivity of tissues to insulin, decreased glycogene reserves, decreased gluconeogenesis

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clinical signs of ACTH deficiency

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1) nausea, vomiting, anorexia, fatigue, weakness
2) hypoglycemia (it is caused by increased sensitivity of tissues to insulin, decreased glycogene reserves, decreased gluconeogenesis)
3) in women, loss of body hair and decreased libido due to decreased adrenal androgen production
4) limited maximum aldosteron secretion

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within ..........symptoms of TSH deficiency are developed

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4-8 weeks

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symptoms of TSH deficiency

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- cold intolerance
- dryness of skin
- decreased metabolic rate
- mild myxedema
- lethargy

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symptoms of FSH and LH deficiences in female of reproductive age

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- amenorrhea
- atrophic changes of vagina, uterus and breasts

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symptoms of FSH and LH deficiences in postpubertal men

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- atrophy of the testicles
- decreased beard growth

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consequence of excessive secretion of prolactin in
1) men
2) women

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1) In men: impotency, decreased libido
2) In women: amenorrhea, galactorrhea

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manifestation of excessive secretion of somatotrophine (growth hormone) in
1) adults
2) adolescents

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1) adults: acromegaly
2) adolescents: gigantism (in adolescents whose epiphyseal plates have not yet closed)

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pathomechanism of excessive secretion of somatotrophine (growth hormone) in adults

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- c.tissue proliferation
- bony proliferation
- increased phosphate reabsorption in tubules
- impairment of carbohydrate tolerance
- increased metabolic rate
- hyperglycemia

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hyperglycemia in excessive secretion of somatotrophine (growth hormone) in adults is due to

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- it is a result of GH inhibition of peripheral glucose uptake and increase hepatic glucose production >> compensatory hyperinsulinism >> insulin resistance >> diabetes mellitus

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central form of Cushing

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Cushings disease: excessive secretion of ACTH

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symptoms and signs of Cushing's disease

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1) weight gain
2) glucose intolerance (DM2)
3) polyuria (osmotic polyuria)
4) protein wasting
5) hyperpigmentation
6) hypertension
7) suppression of the immune system
8) alteration of mental status (irritability, depression, schizophrenia)
9) symptoms/signs of increased adrenal androgens in women
10) hyperglycemia, glycosuria, hypokalemia, metabolic alkalosis
11) excessive secretion of thyreotrophin & gonadotrophin is rare

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why is there weight gain in Cushing's

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- accumulation of adipose tissue in the trunk, facial, and
cervical areas (truncal obesity, moon face, buffalo hump)
- weight gain from Na and water retention

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manifestation of Cushing's disease protein wasting in
1) bone
2) skin

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1) bone:
- loss of protein matrix >> osteoporosis
- increased blood calcium consentration >> renal stones
2) skin
- loss of collagen >> thin, weakened integumentary tissues >> purple striae, rupture of small vessels
- thin, atrophic skin is easily damaged, leading to skin breaks and ulceration

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cause and manifestation if hyperpigmentation in Cushing's

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due to very high levels of ACTH - manifestation in mucous membranes, hair and skin

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cause of hypertension in Cushing's disease

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results from permissive effect of cortisol on the actions of the catecholamines (KA) >> vascular sensitivity to KA >> vasoconstriction >> hypertension

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Cushing's disease: symptoms/signs of increased adrenal androgens in women

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- increased hair growth (facial hair)
- acne
- oligoamenorrhea
- changes of the voice

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Waterhouse-Friderichsen syndrome - causes

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acute adrenal insufficiency
- infection
- trauma
- hemorrhage
- thrombosis

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prostation =

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very strong fatigue
(see in acute adrena insufficiency)

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causes of hyperthyroidism

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- Graves disease
- exogenous hyperthyroidism (iatrogenic, iodine induced)
- thyroiditis
- toxic nodular goiter
- thyroid cancer

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common characteristics of all forms of hyperthyroidism

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metabolic effect of increased circulating levels of thyroid hormones >> increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by sympathetic division of the autonomic nervous system;
1) endocrine
2) reproductive
3) gastrointestinal
4) integumentary

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The major manifestations of hyperthyroidism and mechanisms of their onset - endocrine

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- enlarged thyroid gland (TG) with systolic or continous bruit over thyroid due to increased blood flow
- cortisol degradation – due to increased metabolic rate
- hypercalcemia and decreased PTH secretion - due to excess bone resorption
- diminished sensitivity to exogenous insulin- due to increased hyperglycemia (glycogenolysis and gluco-neogenesis)

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The major manifestations of hyperthyroidism and mechanisms of their onset - reproductive

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- oligomenorrhea or amenorrhe due to hypothalamic or pituitary disturbances
- impotence and decreased libido in men

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The major manifestations of hyperthyroidism and mechanisms of their onset

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- weight loss and associated increase in appetite due to increased catabolism
- increased peristalsis  less formed and more frequent stools - due to malabsorption of fat
- nausea, vomiting, anorexia, abdominal pain
- increased use of hepatic glycogen stores and adipose and protein stores
- decrease of tissue stores of vitamins
- hyperlipid – acidemia (due to lipolysis)

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The major manifestations of hyperthyroidism and mechanisms of their onset

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- excessive sweating, flushing, and warm skin
- heat loss
- hair faint, soft, and straight, temporary hair loss
- nails that grow away nail beds

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hypothyroidism - definition

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deficient production of TH by the thyroid gland and/or  their action to the tissue

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primary hypothyroidism is caused by

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1. congenital defects or loss of thyroid tissue
2. defective hormone synthesis - due to: autoimmune thyroiditis, endemic iodine deficiency, antithyroid drugs

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secondary hypothyroidism is caused by

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1. insufficient stimulation of the normal gland
2. peripheral resistance to TH

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myxedema

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increased amount of protein and mucopolysaccharides in dermis >> increased water binding >> nonpitting edema, thickening of the tongue, and the laryngeal and pharyngeal mucous membranes >> thick slurred speech and hoarseness

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cause of goiter

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decrease in TH, causing increased production of TSH

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general manifestations of hypothyroidism

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low basal metabolic rate, cold intolerance, slightly lowered basal body temperature

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neurologic manifestation of hypothyroidism + mechanism

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- confusion, syncope, slowed thinking, memory loss, lethargy, hearing loss, slow movements
- cerebellar ataxia

Mechanism involved
- decreased cerebral blood flow  cerebral hypoxia
- decreased number of beta-adrenergic receptors

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endocrine manifestation of hypothyroidism + mechanism

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- increased TSH production (in primary hypothyroidism)
- increased serum prolactin levels with galactorrhea
- decreased rate of cortisol turnover, but normal cortisol levels

Mechanism involved
- decreased TH >> increased TSH
- stimulation of lactotropes by TRH >> increased prolactin
- decreased deactivation of cortisol

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reproductive manifestation of hypothyroidism

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- decreased androgen secretion in men
- increased estriol formation in women due to altered
metabolism of estrogens and androgens
- anovulation, decreased libido
- spontaneous abortion

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hematologic manifestation of hypothyroidism + mechanism

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- decreased RBC mass >> normocytic, normochromic anemia
- macrocytic anemia due to vitamin B12 deficiency and inadequate folate absorption

Mechanism involved
- decreased metabolic rate >> decreased oxygen requirement >> decreased erythropoietin production

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pulmonary manifestation of hypothyroidism + mechanism

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- dyspnoea - due to pleural effusions
- myxedematous changes of respiratory muscles >> hypoventilation

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renal manifestation of hypothyroidism + mechanism

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- decreased renal blood flow >> decreased GFR >> decreased renal excretion of water >> increased total body fluid >> dilutional hyponatremia
- decreased production of EPO

mechanisms involved
- hemodynamic alteration
- mucinous deposits in tissue

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gastrointestinal manifestation of hypothyroidism + mechanism

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- decreased appetite, constipation, weight gain
- decreased absorption of most nutrients
- decreased protein metabolism, glucose uptake
- increased sensitivity to exogenous insulin
- increased concentration of serum lipids

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musculoskeletal manifestation of hypothyroidism + mechanism

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- muscle aching and stiffness
- slow movement and slow tendon jerk reflexes
- decreased bone formation and resorption bone density
- aching and stiffness in joints

mechanisms involved
- decreased rate of muscle contraction and relaxation

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integumentary manifestation of hypothyroidism + mechanism

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- dry flaky skin
- dry, brittle head and body hair
- reduced growth of nails and hair

mechanisms involved
- reduced sweat and sebaceous gland secretion

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3 types of hyperparathyroidism

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1) primary - PTH secretion is autonomous and not under the usual feedback control mechanism
2) secondary - compensatory response of parathyroid glands to chronic hypocalcemia
3) tertiary - loss of sensitivity of hyperplastic parathyroid gland level of autonomous secretion of PTH

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The main manifestations of hyperparathyroidism
and mechanisms of their onset

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a) renal colic, nephrolithiasis, recurrent urinary tract infections, renal failure:
b) abdominal pain, peptic ulcer disease
c) pancreatitis
d) bone disease
e) muscle weakness, myalgia
f) neurologic and psychiatric alterations
g) polyuria, polydipsia
h) constipation
i) anorexia, nausea, vomiting
j) hypertension

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (j) hypertension

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due to secondary renal disease

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (g) polyuria

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they result from direct effect of hypercalcemia on renal tubule >> increased responsiveness to ADH

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - h) constipation

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is due to decreased peristalsis induced by hypercalcemia (smooth muscle weakness)

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (i) anorexia, nausea, vomiting

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due to stimulation of vomiting center by hypercalcemia

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (c) pancreatitis

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due to hypercalcemia

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (d) bone disease

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osteitis fibrosa and cystica; osteoporosis results from PTH hypersecretion stimulated bone resorption and metabolic acidosis

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (e) muscle weakness, myalgia

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probably due to PTH excess and its direct effect on striated muscle and on nerves  myopathic changes, suppressed nerve conduction

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (f) neurologic and psychiatric alterations

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result from hypercalcemia >> neuropathy develops

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (a) renal colic, nephrolithiasis, recurrent urinary tract infections,
renal failure

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they result from hypercalcemia, calciuria, hyperphosphaturia, proximal tubular bicarbonate leak, urine pH > 6

Mechanism: calcium phosphate salts precipitate in alkaline urine in renal pelvis, and in collecting ducts

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The main manifestations of hyperparathyroidism
and mechanisms of their onset - (b) abdominal pain, peptic ulcer disease

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result from hypercalcemia >> stimulated hypergastrinemia >> elevated HCl secretion

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causes of hypoparathyroidism

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damage to the parathyroid gland due to thyroid surgery

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consequences of hypoparathyroidism

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a) depressed serum calcium level and increased serum phosphate level
b) lowering of the threshold for nerve and muscle excitation
c) dry skin, loss of body and scalp hair, hypoplasia of developing teeth, horizontal ridges on the nails, cataracts, basal ganglia calcifications (Parkinsonian sy.)
d) hyperphosphatemia

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hypoparathyroidism - a) depressed serum calcium level and increased serum phosphate level >> mechanisms involved

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- decreased resorption of Ca from GIT, from bone and from renal tubules
- increased reabsorption of phosphates by the renal tubules

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hypoparathyroidism - b) lowering of the threshold for nerve and muscle excitation - manifestation

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muscle spasms, hyperreflexia, clonic - tonic convulsions, laryngeal spasms - tetany

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hypoparathyroidism - d) hyperphosphatemia - manifestation

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inhibition of renal enzyme necessary for the conversion of vitamin D to its most active form >> further depression of serum calcium level by reducing GIT absorption of calcium.