Endocrine: Module II Flashcards
The pancreas has both ____ and ____ function
Endocrine
Exocrine
3 cell types of Islets of Langerhans
Alpha
Beta
Delta
Function of alpha cells
secrete glucagon
Function of beta cells
Secrete insulin
Co-secrete amylin
Function of delta cells
Secrete somatostatin and gastrin
What is the function of glucagon?
Prevents hypoglycemia by mobilizing “metabolic fuels”
Target tissue of glucagon: (3)
Liver –> stimulates glycogenolysis and glucogensis
Fat tissue –> stimulates lypolysis
Muscle –> proteolysis
The breakdown of glycogen is called…
Glycogenolysis
The formation of glucose is called….
Glucogenesis
The breakdown of amino acid is called….
Proteolysis
4 Factors that stimulate glucagon secretion from pancreas
- Hypoglycemia
- Exercise
- Stress
- Fasting
1 Factor that inhibits glucagon secretion from pancreas
- Hyperglycemia
Amylin: when is it secreted and what is its function?
- Co-secreted with insulin during feeding
- Suppresses glucagon
Main function of insulin
Prevents hyperglycemia –> promotes “metabolic fuel” storage
- Dec blood glucose levels
- Dec blood levels of amino acids and FFA/ketones
- Dec serum potassium levles
What is the target tissue of insulin?
- Liver
- Muscle
- Adipose tissue
What happens in the liver when insulin is increased and decreased?
Insulin increased: glucose uptake, formation of glycogen, lipid/protein synthesis
Insulin Decreased: ketogenesis, glycogenolysis
What happens in the muscles when insulin is increased and decreased?
Insulin increased: glucose uptake, formation of glycogen, amino acid uptake, protein synthesis
Insulin decreased: lypolysis
What happens in adipose tissue when insulin is increased and decreased?
Insulin increased: glucose uptake, glucose to form glycerol phosphate, fat storage
Insulin decreased: lypolysis
Factors that stimulate insulin secretion (4)
- Hyperglycemia
- Increased serum levels of FFA, amino acids
- GI/digestive hormones
- Parasympathetic stimulation of pancreatic beta cells
Factors that inhibit insulin secretion (4)
- Hypoglycemia
- Negative feedback loop: increased insulin levels
- Sympathetic stimulation of pancreatic beta cells
- Prostaglandins (PGE2)
Excessive insulin levels will _____ the number of insulin receptors.
Decrease
In obesity do we see up regulation or down regulation of insulin receptors?
Down regulation
Adipose tissue down regulate insulin receptors -> decreased insulin sensitivity
What is the response to decreased insulin sensitivity in response to feeding:
- Glucose levels remain elevated despite app. release of insulin
- Additional insulin is released in attempt to lower blood glucose
- Prolonged insulin exposure promotes additional “down-regulation” of receptors
- RESULT: insulin resistance progresses –> this is a cycle
What are the 3 “poly’s” of diabetes?
- Polyuria –> excessive urine production
- Polydipsia –> excessive thirst
- Polyphagia –> increased appetite
Diabetes Mellitus Type I (insulin dependent)
Insulin insufficiency d/t result of pancreatic destruction of beta cells
Antibodies attach beta cells
Not associated w/ obesity
What happens in DM 1? (4 things)
- Hyperglycemia
(b/c cells unable to take up glucose) - Hyperlipidemia
- Increased ketone bodies/ketoacidosis
- Catabolic affect on muscle mass
Hyperlipidemia
–> in DM1
Increased lipoproteins in blood
- Lack of insulin is inhibitory to fat storage
- Promotes atherosclerotic changes in blood vessels
Describe the catabolic affects on muscle mass seen in DM 1
Body attempts to mobilie amino acids for “fuel” when insulin is low which results in muscle wasting, weight loss, and weakness/fatigue
What are 3 causes of insulin shock?
- Excessive insulin administration
- Increased physical activity
- Poor glucose monitoring/missed meals
Hypoglycemia produces ____, ______, and _____. (physical symptoms)
Hunger
Sweating
Irritability
Prolonged hypoglycemia =
diabetic coma/decrease CNS metabolism
Can lead to death
Treatment for insulin shock
Administer glucose to restore blood glucose levels
What is the major cause of DM Type 2?
Obesity
DM Type 2 is associated with _____ insulin ____.
Increased insulin resistance
Inefficient clearance of glucose from blood results in _____ insulin being secreted
MORE
How can one improve their diabetes type 2?
Diet changes and exercise
GTT stands for:
Glucose Tolerance Test
How do you perform a GTT? (steps)
- Baseline glucose level is established
- Administer glucose preparation
- Blood drawn in intervals (30 minutes) making sure to draw blood for at least 120 minutes
- Read values
Normal GTT values
fasting and 2 hours
Fasting: < 110 mg/dl
2 hours: < 140 mg/dl
DM GTT values
fasting and 2 hours
Fasting: > 126 mg/dl
2 hours: > 200 mg/dl
3 Hormones of the thyroid gland
- T4 (thyroxine)
- T3 (tri-iodothyronine)
- Calcitonin
3 Hormones of the thyroid gland
- T4 (thyroxine)
- T3 (tri-iodothyronine)
- Calcitonin
Where are thyroid hormones produced? What is this molecule that they produce?
thyroglobulin
produced in follicle cell
Where are thyroid hormones produced? What is this molecule that they produce?
thyroglobulin
produced in follicle cell
Describe how T3/T4 is released from the thyroid?
- TRH hormone released from hypothalamus
- Ant. pituitary releases TSH
- TSH stimulates endocytosis
- Enzymes separate T3/T4 and TGB
- T3/T4 diffuse into bloodstream
Stimuli for thyroid hormone release
- Metabolic demand determines rate
- TSH directly controls amt of T3/T4 released
- Pregnancy (growth)
- Gonadal and adrenocortical steroids (growth)
- Extreme cold temp (stress/energy production)
- Catecholamines (epi/NE) *stress
Thyroid hormone effects in the heart
Increased HR and CO (inotrophic and chronotropic)
Do this by increasing sensitivity to sympathetic system/epi
2 main forms of hyperthyroidism
- Primary hyperthyroidism
2. Secondary hyperthyroidism
Causes of a thyroid storm (7 causes)
- Infections, especially lung
- Thyroid surgery
- Stopping medications for hyperthyroidism
- Too high of thyroid dose (hypothyroidism)
- Tx w/ radioactive iodine
- Pregnancy
- Heart attack or other heart emergencies
What is the distinguishing symptom of “thyroid storm”
Temperature of 105-106
Iatrogenic hyperthyroidism (cause)
Excessive use of synthetic thyroxine
Lab results of Grave's Dz TSI TSH T3/T4 TRH
TSI: elevated TSH: decreased (inc. T3/T4 inhibit ant. pituitary from releasing TSH) T3/T4: elevated --> T3: 3-4x more --> T4: 2x more TRH: decreased
3 Types of primary hyperthyroidism
- Endogenous (Grave’s Dz)
- Iatrogenic
- Thyroid Storm
Thyroid hormone effects in the pituitary gland
- Inhibits TSH
- Stimulate release of GH
- Stimulate synthesis of pituitary hormones
Thyroid hormone effects in the GI
Maintain secretions of GI tract
Thyroid hormone effects in the liver
Promote TG and cholesterol metabolism
Regulate LDL homeostasis
Thyroid hormone effects in bone cells
Promote bone growth/devleopment synergistically with IGF-1/growth hormones
–> stimulate osteoblast/osteoclast activity
Thyroid hormone effects in muscle cells
- Promote muscle protein growth/development synergistically w/ other growth hormones
- Excess levels will promote catabolic metabolism of muscle to provide fuel for inc. BMR
Thyroid hormone effects in the CNS
- Stimulate myelin/axonal growth and development
- Stimulate sympathetic activity
* Overall systemic “overdrive”
Thyroid hormone effects in pulmonary system
Stimulates respiration centers in brain to increase ventilation
Thyroid hormone effects in vascular system
Decrease peripheral resistance of vascular system
Thyroid hormone effects overall
- Glycogenolysis
- Gluconeogenesis
- -> amino acids from muscle break down
- -> lipolyosis
What happens when one is deficient in thyroid function during the perinatal period?
Cognitive impairments (CNS doesn’t mature properly)
Describe how thyroid hormones effect growth/development
Stimulate GH release, necessary for IGF-1 function
CNS maturation is dependent on thyroid function ….
Describe how thyroid hormones effect basal metabolic rate
Increase basal metabolic rate and O2 consumption
Also temp regulation (heat is produced d/t inc. BMR)
Inhibition of thyroid hormone release
- Negative feedback (serum levels of T3/T4)
- GHIH (somatostatin)
- Dopamine
What is the eventual fate of rT3 and T3 when they are no longer utilized?
Converted to T2, a completely inactive form of thyroid hormone
Where is the primary site of T4 –> T3 conversion?
The liver
If T4 is able to enter cell then it follows which 2 pathways?
- Binds to T4 receptor within cell nucleus
2. Undergo conversion to T3 or rT3 in cell cytoplasm/membrane
__% of thyroid hormone released is in form of T4. Only 0.03% is “bioavailable” and free and remainder is protein bound and has “____ ____” which allows for more difficult disassociation from carrier and thus ____ active than T3
80-90%
“Strong bind”
less
____% of thyroid hormone is released in the form of T3. Only 0.03% is “bioavailable” and free to enter cells while the remainder is _____ _____ and unable to enter cell until it disassociates. (acts as a circulating storage pool)
10-20%
protein bound
“Biological activity” on target cell of ___ is much greater than ___.
T3
T4
Free T3 and T4 are easily excreted by the _____.
Kidneys
Does T3/T4 usually circulate freely or bound to a carrier protein? Include percentages
- 9% bind to carrier protein (TGB, albumin, transthyretin)
0. 03% T4/T3 circulate freely and considered “active”
When iodine binds to the tyrosine/TGB molecule what is this process called?
Organification
How much of dietary iodine is “trapped” by the thyroid gland?
25%
Which tyrosine hormone is the active form and which is the inactive form?
T3 is active
T4 is inactive
Proper doses of calcium:
500 mg BID (so 1,000) total
What are the differences between calcium carbonate and calcium citrate?
Carbonate: cheaper, absorption best w/ food
Citrate: more expensive, slight advantage in absorption (w/ or w/o food) - especially in pts w/ reduced stomach acid
What are the two functions of the kidneys in calcium homeostasis/balance?
- Most calcium in glomerular filtrate is reabsorbed
2. Site of “conversion” of inactive vitamin D to active vitamin D (calcitriol)
Medications that impair absorption will ____ calcium secretion.
Increase
What are the two functions of bones in relation to calcium?
- Store calcium
2. Stimuli to increase calcium resorption (for osteoclast activity)
What are the 3 primary regulatory hormones that regulate ECF calcium?
- Parathyroid hormone (PTH)
- Calcitonin
- Calcitriol (active form of Vitamin D)
Where are parathyroid hormones synthesized and secreted from?
Parathyroid glands
What is the function of PTH?
Increase plasma (ECF) calcium levels
What are PTH’s two target tissues?
Bone and Kidney
What does an inc in PTH stimulate in the bone?
- Calcium resorption (stimulates osteocalstic activity)
What does an inc. in PTH stimulate in the kidneys?
- Stimulates conversion of inactive vitamin D to active (calcitriol)
- Converts 1,25 dihydroxyvitamin D
- Stimulates calcium resorption in tubules of kidneys
- Stimulates phosphate excretion
Stimulus for PTH release
Small decreases in plasma calcium
Inhibition of PTH release
Elevated plasma calcium and elevated calcitriol
negative feedback
Scientific (chemical) name for calcitrol
1,25-dihydroxyvitamin
What environmental exposure is necessary for vitamin D formation? What is another place you can get vitamin D from (not as necessary)
SUNLIGHT EXPOSURE!
Vitamin D2 is in eggs, dairy, fish oil, plants
Vitamin ___ or ___ are biologically inactive
D2 or D3
How are D2 and D3 converted to their active form, calcitriol?
Many steps in liver and kidney
Final step in kidney by PTH
Function of calcitriol?
Increase plasma calcium levels
–> also elevates phosphate levels in blood
What are the 3 target tissues of calcitriol?
- Intestine
- Bone
- Kidney
Calcitriol release is stimulated by:
Elevated PTH levels
Calcitriol is inhibited by?
Decreased PTH levels
Where is Calcitonin produced/secreted?
Parafollicular cells of thyroid gland
What is the function of calcitonin?
Decrease plasma (ECF) calcium levels **Minor role...if not working properly, it doesn't reflect a large change in plasma calcium levels
Target tissue of calcitonin and what it does at those tissues
Kidney - inhibits calcium resorption by inhibiting osteoclasts
Bone - stimulates calcium and phosphate excretion
Calcitonin release stimulated by:
Large increases of plasma calcium
Calcitonin is inhibited by:
Decreased levels of plasma calcium
What is a common cause of hyperparathyroidism?
Neoplasms secreting PTH
What would you see on labs in a pt w/ hyperparathyroidism?
- Hypercalcemia
- Hypercalciuria (calcium in urine)
- Hypophosphatemia (low levels of phosphate in blood)
- Potentially metabolic acidosis
What is the common cause of hypoparathyroidism?
Surgical removal or damage
Where are T3 and T4 stored?
Stored in the colloid
Describe how T3/T4 is released from the thyroid?
- TRH hormone released from hypothalamus
- Ant. pituitary releases TSH
- TSH stimulates endocytosis
- Enzymes separate T3/T4 and TGB
- T3/T4 diffuse into bloodstream
rT3
reverse T3
Inactive form of T3 and usually exits cell
Stimuli for thyroid hormone release
- Metabolic demand determines rate
- TSH directly controls amt of T3/T4 released
- Pregnancy (growth)
- Gonadal and adrenocortical steroids (growth)
- Extreme cold temp (stress/energy production)
- Catecholamines (epi/NE) *stress
2 Main functions/actions of thyroid hormones
- Necessary for growth/development
- Control rate of metabolism
- -> therefore regulate/influence EVERY ORGAN OF THE BODY
Thyroid hormones act on all target tissue except for:
- Brain
- Spleen
- Gonads
Thyroid hormone effects in the heart
Increased HR and CO (inotrophic and chronotropic)
Do this by increasing sensitivity to sympathetic system/epi
Thyroid hormone effects in fat cells
Increase lipolysis - mobilize FFA for metabolic fuel
Symptoms of hyperthyroidism
+/- goiter
Cardiac: palpations, tachycardia, inc. CO, inc. pulse pressure, HTN
Pulmonary: inc. RR
CNS: hyperactive, fine tremor, nervousness, inc. sympathetic activity
Integumentary: warm, moist skin, excessive sweating, thin/fine hair
Wt loss: loss of muscle mass, weakness, fat loss
Eyes: exophthalmos
GI: inc. motility (inc. BM)
2 main forms of hyperthyroidism
- Primary hyperthyroidism
2. Secondary hyperthyroidism
Cause of Grave’s Dz (primary endogenous hyperthyroidism)
Excessive TSI (thyroid-stimulating immunoglobulins) bind to TSH receptors and stimulate release of T3/T4
What is the significant effect of hypoparathyroidism?
Hypocalcemia
*and hyperphosphatemia
3 Hormones of the thyroid gland
- T4 (thyroxine)
- T3 (tri-iodothyronine)
- Calcitonin
Where are thyroid hormones produced? What is this molecule that they produce?
thyroglobulin
produced in follicle cell
Which tyrosine hormone is the active form and which is the inactive form?
T3 is active
T4 is inactive
How much of dietary iodine is “trapped” by the thyroid gland?
25%
When iodine binds to the tyrosine/TGB molecule what is this process called?
Organification
Where are T3 and T4 stored?
Stored in the colloid
Describe how T3/T4 is released from the thyroid?
- TRH hormone released from hypothalamus
- Ant. pituitary releases TSH
- TSH stimulates endocytosis
- Enzymes separate T3/T4 and TGB
- T3/T4 diffuse into bloodstream
Does T3/T4 usually circulate freely or bound to a carrier protein? Include percentages
- 9% bind to carrier protein (TGB, albumin, transthyretin)
0. 03% T4/T3 circulate freely and considered “active”
Free T3 and T4 are easily excreted by the _____.
Kidneys
“Biological activity” on target cell of ___ is much greater than ___.
T3
T4
____% of thyroid hormone is released in the form of T3. Only 0.03% is “bioavailable” and free to enter cells while the remainder is _____ _____ and unable to enter cell until it disassociates. (acts as a circulating storage pool)
10-20%
protein bound
__% of thyroid hormone released is in form of T4. Only 0.03% is “bioavailable” and free and remainder is protein bound and has “____ ____” which allows for more difficult disassociation from carrier and thus ____ active than T3
80-90%
“Strong bind”
less
If T4 is able to enter cell then it follows which 2 pathways?
- Binds to T4 receptor within cell nucleus
2. Undergo conversion to T3 or rT3 in cell cytoplasm/membrane
rT3
reverse T3
Inactive form of T3 and usually exits cell
Where is the primary site of T4 –> T3 conversion?
The liver
What is the eventual fate of rT3 and T3 when they are no longer utilized?
Converted to T2, a completely inactive form of thyroid hormone
Stimuli for thyroid hormone release
- Metabolic demand determines rate
- TSH directly controls amt of T3/T4 released
- Pregnancy (growth)
- Gonadal and adrenocortical steroids (growth)
- Extreme cold temp (stress/energy production)
- Catecholamines (epi/NE) *stress
Inhibition of thyroid hormone release
- Negative feedback (serum levels of T3/T4)
- GHIH (somatostatin)
- Dopamine
2 Main functions/actions of thyroid hormones
- Necessary for growth/development
- Control rate of metabolism
- -> therefore regulate/influence EVERY ORGAN OF THE BODY
Describe how thyroid hormones effect basal metabolic rate
Increase basal metabolic rate and O2 consumption
Also temp regulation (heat is produced d/t inc. BMR)
Describe how thyroid hormones effect growth/development
Stimulate GH release, necessary for IGF-1 function
CNS maturation is dependent on thyroid function ….
What happens when one is deficient in thyroid function during the perinatal period?
Cognitive impairments (CNS doesn’t mature properly)
Thyroid hormones act on all target tissue except for:
- Brain
- Spleen
- Gonads
Thyroid hormone effects overall
- Glycogenolysis
- Gluconeogenesis
- -> amino acids from muscle break down
- -> lipolyosis
Thyroid hormone effects in the heart
Increased HR and CO (inotrophic and chronotropic)
Do this by increasing sensitivity to sympathetic system/epi
Thyroid hormone effects in vascular system
Decrease peripheral resistance of vascular system
Thyroid hormone effects in pulmonary system
Stimulates respiration centers in brain to increase ventilation
Thyroid hormone effects in the CNS
- Stimulate myelin/axonal growth and development
- Stimulate sympathetic activity
* Overall systemic “overdrive”
Thyroid hormone effects in fat cells
Increase lipolysis - mobilize FFA for metabolic fuel
Thyroid hormone effects in muscle cells
- Promote muscle protein growth/development synergistically w/ other growth hormones
- Excess levels will promote catabolic metabolism of muscle to provide fuel for inc. BMR
Thyroid hormone effects in bone cells
Promote bone growth/devleopment synergistically with IGF-1/growth hormones
–> stimulate osteoblast/osteoclast activity
Thyroid hormone effects in the liver
Promote TG and cholesterol metabolism
Regulate LDL homeostasis
Thyroid hormone effects in the GI
Maintain secretions of GI tract
Thyroid hormone effects in the pituitary gland
- Inhibits TSH
- Stimulate release of GH
- Stimulate synthesis of pituitary hormones
Symptoms of hyperthyroidism
+/- goiter
Cardiac: palpations, tachycardia, inc. CO, inc. pulse pressure, HTN
Pulmonary: inc. RR
CNS: hyperactive, fine tremor, nervousness, inc. sympathetic activity
Integumentary: warm, moist skin, excessive sweating, thin/fine hair
Wt loss: loss of muscle mass, weakness, fat loss
Eyes: exophthalmos
GI: inc. motility (inc. BM)
2 main forms of hyperthyroidism
- Primary hyperthyroidism
2. Secondary hyperthyroidism
3 Types of primary hyperthyroidism
- Endogenous (Grave’s Dz)
- Iatrogenic
- Thyroid Storm
Cause of Grave’s Dz (primary endogenous hyperthyroidism)
Excessive TSI (thyroid-stimulating immunoglobulins) bind to TSH receptors and stimulate release of T3/T4
Lab results of Grave's Dz TSI TSH T3/T4 TRH
TSI: elevated TSH: decreased (inc. T3/T4 inhibit ant. pituitary from releasing TSH) T3/T4: elevated --> T3: 3-4x more --> T4: 2x more TRH: decreased
Iatrogenic hyperthyroidism (cause)
Excessive use of synthetic thyroxine
What is the distinguishing symptom of “thyroid storm”
Temperature of 105-106
Causes of a thyroid storm (7 causes)
- Infections, especially lung
- Thyroid surgery
- Stopping medications for hyperthyroidism
- Too high of thyroid dose (hypothyroidism)
- Tx w/ radioactive iodine
- Pregnancy
- Heart attack or other heart emergencies
What is a cause of secondary hyperthyroidism?
TSH secreting adenomas (rare)
What does lab work look like with secondary hyperthyroidism? TSI TSH T3/T4 TRH
TSI: normal
TSH: elevated
T3/T4: elevated
TRH: decreased
What are the differences between primary and secondary hyperthyroidism in terms of labs
In primary:
TSI is elevated
TSH is decreased
In secondary
TSI is normal
TSH is increased
*Differences seen because in secondary, the ant. pituitary is effected while in primary, the thyroid is effected
Hypothyroidism can be ____ ____ or ______.
Adult-onset
Congenital
Symptoms of adult onset hypothyroidism
Cardiac: bradycardia, dec. CO, hypotension, inc. peripheral resistance
Pulm: dec. RR
CNS: hypoactive (lethargic, confused, slow speech), decreased DTRs
Integumentary: cool dry skin, slow wound healing, dry brittle hair, myxedema
Wt. gain
GI: dec. motility –> protruding abdomen
Muscle: stiffness, cramps, drooping eyelids
Bone: anemia
+/- goiter
What is myxedema
Puffy appearance of face, hands, feet
Enlarged tongue d/t deposits in oral cavity
What causes puffy appearance in hypothyroidism?
Muccopolysaccharides attract water in skin/connective tissue
What are the different symptoms of congenital hypothyroidism?
Same as adult-onset but usually include in addition to those:
- Cognitive impairment
- Gross dwarfism
What is congenital hypothyroidism also called?
Cretinism
What are some early detection signs that would cause a provider to screen for hypothyroidism?
High birth weight
Hypothermia
Jaundice
Hashimoto’s Thyroiditis (autoimmune)
Primary adult onset
Gradual destruction of functional thyroid tissue
What do the labs look like in Hashimoto’s Thyroiditis
TSH: elevated (d/t low circulating T3/T4)
T3/T4: low
What do labs look like in secondary hypothyroidism?
ALL ARE LOW
TSH: low
(d/t ant. pituitary damage)
T3/T4: low
*Disfunctional feedback response
How do goiters usually come about?
D/t elevated TSH levels trying to stimulate the thyroid gland
In which instances is TSH elevated and you might see a goiter? (2)
- Puberty
2. Pregnancy
Do goiters predict whether thyroid function is normal, elevated, or diminished?
NO!!
What is the cause of a goiter in Grave’s Dz?
D/t TSI stimulating thyroid gland to produce T3/T4
What is the cause of a goiter in Hashimoto’s?
D/t elevated TSH trying to stimulate thyroid gland to produce T3/T4
What is the cause of a goiter in Iodine deficiency?
D/t elevated TSH trying to stimulate thyroid to produce T3/T4
Functions of calcium (HINT: 8)
- Mineralization of bone matrix
- Formation of bone and teeth
- Maintain membrane permeability
- Maintain excitability of nerve and muscle
- Release neurotransmitters
- Muscle contractions
- Coagulation of blood
- Milk production
Where is the majority of calcium stored?
98-99% in bone
- -> 99% of that is in mineralized form
- -> 1% in a pool ready to go into blood stream
Percentage of calcium in “free” form, bound to protein, and bound to phosphate in the extracellular fluid
50% in free form
45% bound to protein
5% bound to phosphate/citrate
The very small amount of intracellular calcium is responsible for: (3 things)
- Intracellular signaling
- Enzyme secretion
- Muscle contraction
What are normal serum calcium values?
8-10 mg/dl
What are hypercalcemia leves? (mild, mod, severe)
Hypercalcemia: >10.5 mg/dl
Mild: 10.5-11.9 mg/dl
Moderate: 12- 13.9 mg/dl
Severe “crisis”: 14-16 mg/dl
Contrast calcium homeostasis with calcium balance?
Calcium homeostasis is short-term equilibrium while calcium balance is a long term maintenance of bone density.
The ECF is maintained through calcium exchange between three organs:
GI tract
Kidneys
Bone
What are the 2 forms of calcium supplementation?
- Calcium carbonate
2. Calcium citrate
% of calcium absorption in ____ related to the amount of calcium injested at one time
Inversly
Proper doses of calcium:
500 mg BID (so 1,000) total
What are the differences between calcium carbonate and calcium citrate?
Carbonate: cheaper, absorption best w/ food
Citrate: more expensive, slight advantage in absorption (w/ or w/o food) - especially in pts w/ reduced stomach acid
What are the two functions of the kidneys in calcium homeostasis/balance?
- Most calcium in glomerular filtrate is reabsorbed
2. Site of “conversion” of inactive vitamin D to active vitamin D (calcitriol)
Medications that impair absorption will ____ calcium secretion.
Increase
What are the two functions of bones in relation to calcium?
- Store calcium
2. Stimuli to increase calcium resorption (for osteoclast activity)
What are the 3 primary regulatory hormones that regulate ECF calcium?
- Parathyroid hormone (PTH)
- Calcitonin
- Calcitriol (active form of Vitamin D)
What are the 3 secondary regulatory hormones that regulate ECF calcium?
- GH
- Thyroid hormones
- Adrenal/gonadal steroid hormones
Where are parathyroid hormones synthesized and secreted from?
Parathyroid glands
What is the function of PTH?
Increase plasma (ECF) calcium levels
What are PTH’s two target tissues?
Bone and Kidney
What does an inc in PTH stimulate in the bone?
- Calcium resorption (stimulates osteocalstic activity)
What does an inc. in PTH stimulate in the kidneys?
- Stimulates conversion of inactive vitamin D to active (calcitriol)
- Converts 1,25 dihydroxyvitamin D
- Stimulates calcium resorption in tubules of kidneys
- Stimulates phosphate excretion
Stimulus for PTH release
Small decreases in plasma calcium
Inhibition of PTH release
Elevated plasma calcium and elevated calcitriol
negative feedback
Scientific (chemical) name for calcitrol
1,25-dihydroxyvitamin
What environmental exposure is necessary for vitamin D formation? What is another place you can get vitamin D from (not as necessary)
SUNLIGHT EXPOSURE!
Vitamin D2 is in eggs, dairy, fish oil, plants
Vitamin ___ or ___ are biologically inactive
D2 or D3
How are D2 and D3 converted to their active form, calcitriol?
Many steps in liver and kidney
Final step in kidney by PTH
Function of calcitriol?
Increase plasma calcium levels
–> also elevates phosphate levels in blood
What are the 3 target tissues of calcitriol?
- Intestine
- Bone
- Kidney
Calcitriol release is stimulated by:
Elevated PTH levels
Calcitriol is inhibited by?
Decreased PTH levels
Where is Calcitonin produced/secreted?
Parafollicular cells of thyroid gland
What is the function of calcitonin?
Decrease plasma (ECF) calcium levels **Minor role...if not working properly, it doesn't reflect a large change in plasma calcium levels
Target tissue of calcitonin and what it does at those tissues
Kidney - inhibits calcium resorption by inhibiting osteoclasts
Bone - stimulates calcium and phosphate excretion
Calcitonin release stimulated by:
Large increases of plasma calcium
Calcitonin is inhibited by:
Decreased levels of plasma calcium
What is a common cause of hyperparathyroidism?
Neoplasms secreting PTH
What are some symptoms of hyperparathyroidism?
Precipitation/deposits of calcium/phosphate in tissues –> results in tissue dammage/organ dysfunction
- Kidney Stones
- Muscle weakness
- Polyuria, nocturia, polydispia
- Confusion, drowsy, coma
- Nausea, vomitting, constipation
- Potential dec. bone density
What would you see on labs in a pt w/ hyperparathyroidism?
- Hypercalcemia
- Hypercalciuria (calcium in urine)
- Hypophosphatemia (low levels of phosphate in blood)
- Potentially metabolic acidosis
What is the common cause of hypoparathyroidism?
Surgical removal or damage
What is the significant effect of hypoparathyroidism?
Hypocalcemia
*and hyperphosphatemia
Symptoms of hypoparathyroidism
- Neuromuscular excitability
- Muscle spasms, tetany
- Cardiac dysfunction
