Hypothalamic, Adrenal, Pituitary, Thyroid, Adrenal, Hypothalamus, Pituitary Flashcards
What is the overall function of the endocrine system? How would you define the endocrine system?
Function: processes involved in maintaining physiological equilibrium (homeostasis)
-tissues or glands that secrete hormones into blood –> bind to specific receptors that allows the hormone to exert effect
–> only affect tissues with appropriate receptor
-negative feedback system regulates most hormone secretion
How is the endocrine system diff than the NS?
–> NS: neurotransmitters, neurohormone
–> endocrine: hormones
- What is meant by the lock & key relationship? How does that “relationship” influence hormone delivery and action throughout the body?
-tissues or glands that secrete hormones into blood –> bind to specific receptors that allows the hormone to exert effect
–> only affect tissues with appropriate receptor
What is set point?
In endocrinology, a set point is the physiological value around which a normal range fluctuates. For example, body weight and body temperature are set points that the endocrine system contributes to regulating. A set point is also the level at which a physiological state tends to stabilize, such as body temperature or weight.
What is a negative feedback loop?
-way the system maintains homeostasis
-secretion of specific hormones are turned on or off by specific physiological changes
EX: plasma glucose levels and insulin/glucagon response
Difference between steroid and non-steroid hormones and delivery to target tissues/organs/mech of action
A steroid hormone will actually enter the target cell and act directly on the DNA of the cell. A non-steroid hormone will land on a receptor on the cell surface, but not enter the cell. In this case a second messenger will carry out the work, but the hormone stays outside the cell.
How does the hypothalamus influence the Ant Pituitary?
Hypothalamus: major link between nervous and endocrine systems
-pituitary gland attached to hypothalamus by infundibulum
FUNCTIONS OF HYPOTHALAMUS:
-synthesizes and secretes regulatory hormones: releasing hormones (stimulate anterior pituitary hormone release) and release inhibitory hormones (inhibit release of anterior pit. hormones)
-directs pituitary gland (hypophysis)
-regulatory hormones need to travel through hypophyseal portal system to reach ant. pit.
GnRH–> FSH, And, LH
GHRH–> growth hormone
Somatostatin (GHIH)–> inhibits GH release
TRH–> TSH and prolactin
Dopamine–> inhibits prolactin release
CRH–> ACTH
PRH–> prolactin
Hypothalamus and posterior pituitary:
-synthesizes two hormones stored in post. pit.
–> oxytocin and vasopressin (ADH)
VASOPRESSION;
-regulates blood volume and salt concentration (plasma osmolality)
-the cells of the supraoptic and paraventricular nuclei are osmoreceptors
-released by post pit in response to low blood volume (baroreceptors sense low BP)
-increased plasma osmotic pressure (osmoreceptors in hypothalamus sense increased solute in blood)
-alcohol is a diuretic–> less ADH is produced–> less water retention
Pituitary disorders:
IN GENERAL:
-too much or too little hormone release
-hyperpituitarism
–>acromegaly/gigantism (inc. GH)
–> Cushing’s disease (inc. cortisol)
-hypopituitarism
–> Diabetes insipidus (decreased ADH)
COMMON SYMPTOMS:
-headache
-visual changes
-lethargy/fatigue
-nausea and vomiting
-nasal drainage
-behavior changes
-changes in sense of smell
TUMORS:
-pituitary tumors account for 10-15% of intra-cranial tumors
-majority are adenomas: benign
Gigantism vs Acromegaly
From anterior pituitary
GIGANTISM
- excessive
secretion of GH in
children
-epiphyseal plate not yet closed
ACROMEGALY
-GH secretion excessive in adults
-most often in 4th decade
-slow but continuous progression
Cortisol release and functions
-normally controlled by hypothalamus
–> CRH
-CRH triggers ant pit ot secrete ACTH into vascular system–> ACTH is carried in the blood to the adrenal cortex, stimulating the synthesis of cortisol
FUNCTIONS:
-counter regulatory to insulin: promotes hyperglycemia
-decreases bone formation (decrease osteoblast function) and decreases intestinal Ca++ absorption
-acts as a diuretic
-influences immune function (inhibits production/release of inflammatory mediators)
Cushing’s disease etiology
-associated with the adrenal and pituitary glands
-hypersecretion of cortisol
CAUSES:
(Pituitary cushing’s)
-pituitary adenoma- secretees ACTH
-ACTH dependent = disease
(Adrenal cushing’s)
-adrenal adenoma- secretes cortisol
–> exogenous corticosteroids (iatrogenic cushing’s syndrome)
-ACTH-indepedent- Syndrome
Cushing’s disease S/S
INCREASED CORTISOL
-central obesity
–> rapid weight gain with sparing of limbs
–> moon face and buffalo hump fat distribution
-skin
–> thinning and capillary fragility
–> bruising
–> striae
–> poor wound healing
-muscle wasting and weakness
-tachycardia; hypertension
-osteoporosis
–> impaired GI ca++ absorption (antagonizes vit D)
-hyperglycemia/DM (stress response)
-immunosuppression–> increased infection risk
Cushing’s disease similarities with DM
-hyperglycemia
-immunosuppression
-poor wound healing
-hypertension
Cushing’s disease medical treatment (steroids)
–>DISEASE: pituitary tumor excision via trans-sphenoidal surgery
–> SYNDROME: adrenal tumor excision- adrenalectomy
-Iatrogenic: decrease corticosteroids dosing
What is the primary function of the thyroid gland?
Thyroid follicles produces T3 and T4
-T4 to T3 ratio is 15 to 1
-T4 is a pro-hormone that is converted to the active T3
PRIMARY FUNCTIONS:
-growth and development
-increased catecholamine effect
-increased BMR
-important for brain and muscular development
-CV: increased HR/contractility and cardiac output
-CNS: increased arousal rates
Hyperthyroidism S/S
EXCESSIVE SECRETION OF:
-thyroxine (T4) and/or triiodithyronine (T3)
S/S:
-unintended weight loss and diarrhea
-anxiety and nervousness and tremors
-heat intolerance
-fatigue/muscle weakness
-palpitations/tachycardia/afib /hypertension
-hyperglycemia
-osteopenia (long term)
Hypothyroidism S/S
-lethargy
-fatigue
-bradycardia
-edema
-weight gain
-cold intolerance
-dry skin/brittle hair and fingernails
-goiter
Differences between T3 and T4
T3
-active form of T4
-iodine is necessary for formation of T4 and T3
-T4 converted to T3 which is active
T4
-much more abundant than T3
-considered a pro-hormone
-not active
Hyperthyroidism medical treatment:
-radioiodine therapy- often leads to hypothyroidism
MEDS:
-thyrostatics:
–> inhibit iodination of thyroglobulin (inhibit T3 and T4 production)
–> inhibit conversion of T4 to T3
-beta blockers
-thyroid surgery: thyroidectomy- not very common because medical therapy is effective
Steps of thyroid hormone release-HPA axis:
TRH from hypothalamus to pituitary
TSH from pituitary to thyroid gland
Thyroid gland releases T3 and T4 –> target tissues: heart, liver, bone, CNS
Function of iodine for thyroid
required for production of thyroid hormones
Graves Disease S/S; which gland/hormones are involved?
(type of hyperthyroidism- excessive T3 or T4)
-autoimmune disease: thyroid autoantibodies activate the TSH-receptor (pituitary) –> increase in thyroid hormone
-can also be caused by a pituitary tumor
SYMPTOM:
-Graves’ opthalmopathy (exopthalmos/proptosis)
—>bulging of eye anteriorly
—>Thyroid Eye Disease (due to inflammation)
Relationship between parathyroid hormone and OP
PTH FUNCTION:
-regulates serum calcium
-increases blood calcium concentration when it is too low (hypocalcemia) by stimulating osteoclasts to release more ca from bone
-decreases secretion of Ca by kidney
-activates vitamin D, which stimulates uptake of Ca from the intestine (diet)
-** opposite effect as calcitonin which is produced by thyroid gland (lowers blood Ca levels)
PTH and Calcitonin relationship and connection to serum calcium
Thyroid gland produces calcitonin:
-calcitonin produced in response to hypercalcemia–> helps to decrease serum Ca++ (deposition of calcium salt in bone)
-opposes the action of PTH –> PTH increases serum calcium (osteoclasts degrade bone matrix and release calcium into blood)
Risks and Causes of OP
- “…a systemic skeletal disease characterized by
low bone mass and micro-architectural deterioration of bone tissue leading to enhanced bone fragility and a consequent increase in fracture risk”
RISKS
-inadequate nutritional absorption:
–> Vitamin D deficiency
-lack of physical activity or fall risk
-weight loss
-cigarette smoking
-alcohol consumption (>2 drinks/day)
-stress
-history of falls
-older age
-gender
-white and asian ethnicity
-prior fracture
-family history of OP
SECONDARY CAUSES:
-prolonged corticosteroid use
-hypogonadism: body’s sex glands produce little or no sex hormones
-hyperparathyroidism (increased production of PTH–> increased serum calcium)
-chronic liver and renal disease
-inflammatory diseases (IBS, MS, COPD)
-diabetes mellitus
-dementia
-all fractures are associated with morbidity
What condition is associated with hypofunction of the adrenal glands?
hypoaldosteronism/
hypocortisolism (ADDISON’S DISEASE)
Hypercalcemia symptoms:
-too much calcium in the blood
GROANS: GI symptoms like pain, nausea, and vomiting. Hypercalcemia can lead to peptic ulcer disease and pancreatitis.
BONES: Bone related complications like bone pain, increases the risk of developing osteoporosis, arthritis and pathological fractures.
STONES: Renal stones causing pain
MOANS: refers to fatigue and malaise
THRONES: polyuria, polydipsia, constipation
PSYCHIC OVERTONES: lethargy, confusion, depression, and memory loss
Diagnosis of OP:
DEXA SCAN:
-A DEXA (dual-energy X-ray absorptiometry) scan is a bone density test that uses high and low energy X-rays to measure bone strength and thickness.
NORMAL BMD/ABNORMAL (T-SCORE RATING SYSTEM)
-healthy: 1.0 g/cm^2
-low: -1.0 to -2.5 SD below that of young, normal adult
-OP: < -2.5 to -3.0 SD below young normal adult
-severe OP: </= to 3.0
What drugs are prescribed for OP?
Bisphosphonates
-prevent action of osteoclasts
-attaches to bony surfaces undergoing active resorption and inhibits the action of osteoclasts
Selective Estrogen Receptor Modulators (SERMs)
Calcitonin
-deposition of calcium salt in the bone
-inhibits bone resorption
PTH
-stimulates bone formation more than bone resorption
Physical therapist role in the management of OP/prevention of osteoporosis:
EDUCATION:
-stop smoking
-calcium
-vitamin D
-medication
-weight-bearing exercise
-check your risk factors
-reduce alcohol
EXERCISE:
-resistance training: 2-3 days/week
-60-80% 1rm (8-12 REPS) for major muscle groups
-aerobic: moderate 40-60% HRR to vigorous (60-85% of HRR)
TIME: 30-60 minutes (> 150 min/week is the goal)
-emphasize extension based exercise and avoid flex/rotation (scapular squeezes, prone hip extension)
-don’t forget balance, posture, and flexibility
What is the FRAX?
Fracture Risk Assessment Tool
The Fracture Risk Assessment Tool (FRAX) is a free online tool that estimates a patient’s 10-year probability of major bone fractures, especially if they have osteoporosis. FRAX uses bone mineral density (BMD) and other risk factors to calculate the likelihood of hip, forearm, vertebral, or humerus fractures, as well as other major fractures.
Diabetes insipidus:
Excretion of large volume of urine (polyuria) & excessive thirst (polydipsia) & increased appetite (polyphagia)
CAUSES:
1) posterior pit doesn’t secrete ADH (central/neurogenic DI)
2) Insensitivity of kidney to ADH (nephrogenic DI)
DIAGNOSIS:
-no hyperglycemia
-dilute urine
-hypernatremia and increased plasma osmolality (lots of solute, not a lot of water)
-S/S: Polydipsia, polyuria, polyphagia
-hypovolemia; dehydration
–> dizziness, hypotension
–>seizures
-muscle weakness
Addison’s disease: reduced cortisol (pituitary gland)
-autoimmune disorder
-weight loss
-low blood pressure
-patches of darker skin
-weakness
-extreme fatigue
-N/V
-craving for salt
-dizziness upon standing
