Module #2: Endocrine Pancreas and Thyroid/Parathyroid Physiology Flashcards
What type of functions does the pancreas have?
endocrine
exocrine
Which pancreatic cells are responsible for its endocrine functions?
Islets of Langerhans
Name the types of Islets of Langerhans cells and their function
alpha = secrete glucagon
beta = secret insulin (co-secretion of amylin)
delta = secrete somatostatin (different from hypothalamus) and gastrin
What does glucagon do?
prevents hypoglycemia
mobilizes “metabolic fuels”
How does glucagon prevent hypoglycemia/mobilize metabolic fuels?
increase blood glucose levels
“catabolic” hormone that mobilizes fuel (glucose and FFA)
What are the target tissues of glucagon?
Liver
Fat Tissues
Muscle
What does glucagon do to the liver?
stimulate glycogenolysis (breakdown glycogen) and glycogenesis (glucose formation)
What does glucagon do to fat tissue?
stimulate lypolysis
What does glucagon do to muscle tissue?
stimulate proteolysis (breakdown for amino acid release)
What does glucagon do in response to hypoglycemia?
glucagon tries to make fuel so it increases:
glucose
free fatty acids and associated ketones
amno acids
What are the factors that stimulate glucagon secretion from the pancreas?
Hypoglycemia
Exercise
Stress
Fasting
What is a factor that inhibits glucagon secretion from the pancreas?
Hyperglycemia
What does Amylin do and when is it secreted?
supresses glucagon
co-secreted w/ insulin during feeding
What is the function of insulin?
prevent hyperglycemia
promote “metabolic fuel” storage
How does insulin function to prevent hyperglycemia and promote metabolic fuel storage?
decrease blood glucose levels –> increase glucose uptake into cells throughout body
decrease blood levels of amino acids, FFA, ketones
decrease serum potassium levels –> promote potassium uptake into cells
What are the target tissues of insulin?
Liver
Muscle
Adipose Tissue
What response does insulin elicit in the liver?
increase: glucose uptake, formation of glycogen, lipid/protein synthesis
decrease: ketogenesis, glycogenolysis
What response does insulin elicit in muscles?
increase: glucose uptake, formation of glycogen, amino acid uptake, protein synthesis
decrease: glycogenolysis
What response does insulin elicit in adipose tissue?
increase: glucose uptake, glucose to form glycerol phoshate (part of TG formation), fat storage (formation)
decrease: lypolysis
What are the factors that stimulate insulin secretion from the pancreas?
Hyperglycemia
Increased serum levels of FFA, amin acids
GI/digestive hormones
Parasympathetic stimulation of pancreatic beta cells
What are the factors that inhibit insulin secretion from the pancreas?
Hypoglycemia
Negative feedback loop –> increased insulin levels
Sympathetic stimulation of pancreatic beta cells
Prostaglandins (PGE2)
How does the body regulate insulin receptors?
down regulate
up regulate
What will be the physiologic response to excessive insulin levels?
decrease the number of insulin receptors
What happens in obese people that leads to type 2 (non-insulin dependent) diabetes?
Adipose tissue down regulates insulin receptors –> decreased insulin sensitivity
What is the decreased insulin sensitivity response to feeding that leads to the vicious cycle of obesity/Type 2 diabetes?
Glucose levels remain elevated despite “appropriate” release of insulin
additional insulin is released in attempt to lower blood glucose levels
prolonged insulin exposure promotes additional “down-regulation” of receptors
Result = insulin resistance (decreased sensitivity) progresses
What is the very basic definition of diabetes mellitus?
disruption of regulation of blood glucose levels
What are the different types of diabetes mellitus?
DM Type 1 aka juvenile-onset or insulin dependent
DM Type 2 aka adult onset or non-insulin dependent
What are the 3 poly’s of diabetes?
polyuria = excessive urine production
polydipsia = excessive thirst
polyphagia = increased appetite
What is DM Type 1?
insulin insufficiency due to result of pancreatic destruction of beta cell Islets of Langerhans
What is a suggested cause of DM Type 1?
suggested to be autoimmune disorder –> antibodies attack beta cell islets of Langerhans
** early treatment of immunosuppresive drugs may show significant improvement
Is DM Type 1 associated w/ obesity?
No
What are the consequences of decreased insulin?
Hyperglycemia
Hyperlipidemia
Increased ketone bodies/ketoacidosis
Catabolic affect on muscle mass
Why does decreased insulin lead to hyperglycemia?
cells are unable to take up glucose from blood
What are the signs and symptoms of hyperglycemia?
polyuria
polydipsia
What are the renal thresholds of hyperglycemia?
plasma glucose > 180-200 mg/dL = glucose dumping in urine
plasma glucose > 350 mg/Dl = transport max for glucose in PCT
Why does decreased insulin lead to hyperlipidemia?
inhibitory to fat storage
What is a consequence of hyperlipidemia?
promotes atherosclerotic changes in blood vessels
Why does decreased insulin lead to an increase of ketone bodies/ketoacidosis?
formed from increased FFA metabolism in the liver –> metabolic acidosis
Why does decreased insulin have a catabolic affect on muscle mass?
the body attempts to mobilize amino acids for “fuel” formation
What are the signs and symptoms of catabolism of muscles when there is a decrease in insulin?
muscle wasting
weight loss
weakness
fatigue
What is insulin shock?
Hypoglycemic reaction
What causes hypoglycemia of insulin shock?
excessive insulin administration
increased physical activity
poor glucose monitoring/missed meals, etc.
What are some signs/symptoms of hypoglycemia/insulin shock?
hunger
sweating
irritability
What are some consequences of prolonged hypoglycemia?
diabetic coma/decreased CNS metabolism –> giddiness, coma, death
When is hypoglycemia/insulin shock considered a medical emergency?
symptoms are severe
seizures
convulsions
loss of consciousness
repeated episodes
What is the treatment for hypoglycemia/insulin shock?
administer glucose to restore blood glucose levels
What is DM Type 2 associated with?
increased insulin resistance
obesity
usually adult onset
What does increased insulin resistance do?
obesity/inactivity creates viscous cycle of inefficient blood glucose clearance –> more insulin secretion
–> cycle –> increased insulin resistance
What is increased insulin resistance caused by?
decreased insulin receptor function
decreased insulin receptor number
What are 2 important ways to improve insulin sensitivity?
Diet changes
Exercise
Describe Glucose Tolerance Test (GTT)?
Establish baseline glucose level
Administer glucose prep
Blood draw in intervals (0 and 120 = minimum; usually draw every 30 minutes)
According to the WHO in 1999 what are considered normal values of GTT?
fasting = < 100 mg/dL
2 hrs = < 140 mg/dL
According to the WHO in 1999 what are considered DM values of GTT?
fasting = > 126 mg/dL
2 hrs = > 200 mg/dL
What hormones are produced in the thyroid gland?
T4 - thyroxine
T3 - tri-iodothyronine
Calcitonin
Where is un-iodinated TGB (thyroglobulin) produced?
follicle cells
What happens to TGB molecule, how is it modified?
Tyrosine is synthesized into it
Describe “Iodide trapping”
TSH sensitive iodide pump transports iodide into follicular cells
How much dietary iodine is trapped by the thyroid gland?
25%
What happens to the iodide once it is in the thyroid?
Binds to tyrosine/TGB molecule = organification
How are the thyroid molecules formed?
Once iodide binds to tyrosine/TGB molecules they then bind aka couple together to form T3 and T4
Where are T3 and T4 stored?
Colloid
Which thyroid hormone is the active form and which thyroid hormone is the inactive form?
T3 = active form
T4 = inactive form
How much T3/T4 is circulated bound to a carrier protein?
99.9%
What are the carrier proteins that bind to T3/T4 in the blood stream?
TGB
albumin
Transthyretin
Approximately how much of T4 and T3 circulate “freely”?
.03% each
What is “free” T3 or T4 considered?
active
Besides being active and doing its thing, what else can happen to free T3/T4?
Easily excreted by the kidneys
Approximately how much thyroid hormone is released as T3?
10 - 20%
Which form of T3 is considered bioavailable?
active free form (.03%)
How does active T3 elicit its physiologic response?
enters cell, binds to receptor w/in the nucleus
When can carrier bound T3 enter a cell to elicit its response?
it must disassociate from the carrier protein
What allows easier disassociation of T3 from the carrier protein?
Loose bind; T3 = more active than T4
Approximately how much thyroid hormone is released as T4?
80 - 90%
Which form of T4 is considered bioavailable?
active free form (.03%)
How does T4 ellicite its response the cell?
Bind to T4 receptors w/in the cell nucleus
undergo conversion to T3 or rT3 in cell cytoplasm/membrane
How does the activity of T4 compare to T3?
T4 activity is much less than T3
Where is T4 converted to T3?
Primary site of T4 –> T3 = Liver
generally in target tissues (muscles, liver, kidney, etc.)
What happens after T4 is converted to T3?
can be utilized in the cell
can exit and bind in another cell
What is rT3?
reverse T3, the inactive form of T3
What happens after T4 is converted to rT3?
exits the cell
When is “bound” T4 able to enter a cell?
must dissociate from the carrier protein
Why does T4 have a more difficult disassociation from carrier?
strong binding –> T4 = less active compared to T3
What happens to rT3 and T3 that aren’t utilized?
converted to T2 (completely inactive thyroid hormone)
Describe the signaling pathway of thyroid hormone release from thyroid gland
TRH released from hypothalamus –> TSH release from anterior pituitary
TSH binds receptor on thyroid cell –> endocytosis of T3/T4 back into follicle cell
Enzymes separate T3/T4 from TGB
T3/T4 diffuse into bloodstream (90% T4, 10% T3)
What are the stimuli for thyroid hormone release?
Metabolic demand determines rate of release
TSH directly controls amount of T3/T4
Pregnancy
Gonadal and adrenocortical steroids
Extreme cold temperature environment
Catecholamines (epinephrine/norepinephrine)
What are the inhibitors of thyroid hormone release?
Serum levels of T3/T4 inhibit TSH release from anterior pituitary
GHIH (somatostatin)
Dopamine (prolactin inhibiting hormone)
Generally, what are the functions of thyroid hormones T3/T4?
Growth/Development
Control rate of metabolism
Regulate/influence every organ of the body
What is T3/T4 required for during growth and development?
normal skeletal growth
maturation of all cells
What other hormones does T3/T4 stimulate that are required for growth/development?
Stimulates GH release, which is necessary for IGF-1 function
What is CNS maturation dependent on?
thyroid function during prenatal period
What happens if there is a deficiency of T3/T4 during the peri-natal period?
CNS impairment (cognitive impairment)
How does T3/T4 control metabolism?
increases BMR (basal metabolic rate)
increases O2 consumption of the body
temperature regulation
The BMR of which tissues is NOT increased by T3/T4?
Brain
Spleen
Testes
What does thyroid hormone do in all cells except the brain, gonads, spleen?
increase cellular respiration = increase BMR (basal metabolic rate)
What does elevated BMR do?
increases O2 consumption
increases heat production
increases demand for fuel
What does elevated BMR do to the liver?
glycogenolysis = breakdown glycogen stores –> glucose
gluconeogensis = amino acids from muscle breakdown; lipolysis - glycerol from adipose tissue, FFA used as fuel (spare glucose for brain/CNS)
What is thyroid hormone action on the heart?
increase HR and Cardiac Output by increasing sensitivity to sympathetic system/epinephrine (ionotropic and chronotropic)
What is the thyroid hormone action on the vascular system?
decrease total peripheral resistance of the vascular system
What is the thyroid hormone action on pulmonary organs?
stimulate respiration centers in brainstem –> increase ventilation
What is the thyroid hormone action in the CNS?
stimulate myelin/axonal growth and development
stimulate sympathetic activity
What is the thyroid hormone action on adipose tissue (fat cells)?
increase lipolysis –> mobilize FFA for metabolic fuel
What is the thyroid hormone action in muslce?
promote muscle protein growth/development (works synergistically w/ other GH)
excess levels –> catabolic metabolism of muscles to provide fuel for increased BMR
What is the thyroid hormone action on bones?
promote bone growth/development (synergistically w/ other GH)
stimulate osteoblast/obsteroclast activity
What is the thyroid hormone action in the liver?
promote TG (triglyceride) and cholesterol metabolism
regulate LDL homeostasis
What is the thyroid hormone action in the GI system?
Maintain secretions of GI tract
What is the thyroid hormone action on the pituitary gland?
Inhibit TSH
Stimulate the release of GH
Stimulate synthesis of pituitary hormones
What are the sings and symptoms of hyperthyroidism in the thyroid?
enlargement of the thyroid gland (goiter)
What are the sings and symptoms of hyperthyroidism in the cardiovascular system?
Palpitations
Hypertension
Increased pulse pressure
Tachycardia
Increased Cardiac Output
What are the sings and symptoms of hyperthyroidism in the pulmonary system?
Elevated respiration rate
What are the sings and symptoms of hyperthyroidism in the CNS?
Hyperactivity
Fine tremor
Increased nervousness (excitable, irritable, apprehensive)
Increased sympathetic activity
What are the sings and symptoms of hyperthyroidism in the integumentary system?
Warm moist skin
Excessive sweating
Thin/fine hair
What are the general sings and symptoms of hyperthyroidism?
Weight loss despite food intake
Loss of muscle mass
Fat loss
What are the sings and symptoms of hyperthyroidism in muscles?
Proximal Weakness
What are the sings and symptoms of hyperthyroidism in the eyes?
Exophthalmos aka proprtosis
can be caused by: sympathetic hyperactivity, infiltrative changes
What are the sings and symptoms of hyperthyroidism in the GI tract?
Increased motilities
increased bowel movements
What is another name for primary hyperthyroidism?
Thyrotoxicosis
What are the forms of primary hyperthyroidism?
Endogenous (Grave’s Disease)
Iatrogenic hyperthyroidism
Thyroid Storm
What happens in Grave’s Disease?
excessive TSI (thyroid-stimulating immunoglobulins) bind to TSH receptors and stimulate the release of T3/T4
What will you see in labs of pts w/ Grave’s disease?
TSI = elevated
TSH = decreased (increased T3/T4 inhibit release of TSH)
T3/T4 = elevated (T3 = 3-4x; T4 = 2x)
TRH = decreased
What causes Iatrogenic hyperthyroidism?
Excessive use of synthetic thyroxine
What is thyroid storm?
rare but life threatening form of hyperthyroidism
What are the sings/symptoms of thyroid storm
Hallmark hyperthyroidism signs/symptoms
distinguishing sign = 105-106 degree fever
What are some causes of Thyroid Storm (7)?
Infections (esp. lungs)
Thyroid surgery in pts w/ overactive thyroid gland
Stopping meds given for hyperthyroidism
Too high of thyroid dose
Treatment w/ radioactive iodine
Pregnancy
Heart attack or heart emergencies
What is a rare secondary hyperthyroidism disease?
TSH secreting adenomas
What will secondary hyperthyroidism labs look like?
TSI = normal
TSH = elevated (tumor)
T3/T4 = elevated (T3 = 3-4x; T4 = 2x)
TRH = decreased
When/How do you get Hypothyroidism?
Adult-onset
Congenital
What are the cardiac symptoms of adult onset hypothyroidism?
Bradycardia –> decrease cardiac output
Hypotension
Elevated peripheral resistance to maintain blood pressure
What are the pulmonary symptoms of adult onset hypothyroidism?
Decreased respiration rate
What are the CNS symptoms of adult onset hypothyroidism?
Hypoactive –> lethargic, confusion, slow speech hoarse voice, diminished memory function
Decreased DTR’s (deep tendon reflex)
What are the integumentary symptoms of adult onset hypothyroidism?
Cool dry skin –> reduced heat production associated w/ decreased BMR
slow wound healing
dry brittle hair
Myxedema
What is Myxedema?
Puffy appearance of face, hands, feet –> infiltration of skin/connective tissue w/ muccopolysaccharides –> attacks H2O
Edema = non-pitting
Thickening/protrusion of the tongue (deposits in oral cavity)
What happens to your weight when you have adult onset hypothyroidism?
Gain weight despite reduced appetite/food intake
What are the GI symptoms of adult onset hypothyroidism?
Decreased Motility
Constipation (decreased BMs)
Protruding abdomen
What are the muscle symptoms of adult onset hypothyroidism?
Stiffness/achiness of muscles/joints –> muscle cramps
Drooping eyelids
What are the bone symptoms of adult onset hypothyroidism?
Potential for anemia due to suppression of bone marrow function
Is there thyroid enlargement associated with adult onset hypothyroidism?
Sometimes
What is another name for congenital onset hypothyroidism?
Cretinism
What are the symptoms that are specifically associated with congenital onset hypothyroidism?
Cognitive impairment
Gross Dwarfism
Why will you have cognitive impairment with congenital onset hypothyroidism?
T3/T4 are necessary for CNS development
What are the signs/symptoms of gross dwarfism?
impaired skeletal growth
short limbs
What are some signs @ birth that are suggestive to screen for congenital onset hypothyroidism?
High birth weight
Hypothermia
Jaundice
What is considered the critical window of intervention for treatment of congenital onset hypothyroidism?
4 months
What is the most common form of primary adult onset hypothyroidism?
Hashimoto’s thyroiditis
What are the other less common forms of primary adult onset hypothyroidism?
Iodine deficiency
Thyroidectomy
Radiation damage in treatment of hyperthyroidism
What is Hashimoto’s thyroiditis and why does it cause hypothyroidism?
Autoimmune disorder
Gradual destruction of functional thyroid tissue
What will you see in the labs of a pt with primary adult onset hypothyroidism?
TSH = elevated (low circulation of T4/T3)
T3/T4 = low –> T4 is converted to T3 as body demands
What will you see in the labs of a pt with secondary hypothyroidism?
All are low
TSH = low –> anterior pituitary/hypothalamus damage
T3/T4 = low
What is goiter?
An enlargement of the thyroid gland
Why is the thyroid enlarged in goiter?
Elevated TSH levels trying to stimulate the thyroid gland
Can you predict thyroid function based on goiter alone?
NO
Can be normal, elevated, or diminished
What is goiter caused by in Grave’s disease (hyperthyroidism)?
immuoglobulin (TSI) stimulating thyroid gland to produce T3/T4
What is goiter caused by in Hashimoto’s (hypothyroidism)?
elevated TSH trying to stimulate thyroid gland to produce T3/T4
What is goiter caused by in Iodine deficiency?
elevated TSH trying to stimulate thyroid to produce T3/T4 –> dietary iodine is lacking
What are the 3 hormones that control calcium homeostasis/balance?
PTH
Calcitriol
Calcitonin
What is the function of calcium?
Mineralization of bone matrix
Formation of bone and teeth
Normal physiological functions
Milke production (lactogenesis)
What are the normal physiological functions that are dependent on stable levels of calcium in the blood?
Maintain membrane permeability
Maintain excitability of nerve and muscle
Release of neurotransmitters
Muscle contractions
Coagulation of blood
Where is most calcium stored?
98-99% in bone
**phosphate also stored in bone
Where is calcium found when its not stored in bone?
Circulating in the ECF (extracellular fluid)
What are the forms of calcium circulating in the ECF, and how much of each do you have?
50% = free form of ionized calcium Ca2+
45% = bound to albumin (protein)
5% = bound to phosphate/citrate
Is there any intracellular calcium?
Yes, but thousand’s of times less than extracellular fluid
What is the function of intracellular fluid calcium?
Intracellular signaling = action potentials, secondary messenger systems, etc
Enzyme secretion
Muscle contraction
Where in the body is there a constant large exchange of calcium?
GI tract
Bone
Kidney
How tightly are extracellular fluid calcium levels maintained?
w/ in a narrow window
What are the normal values of calcium in the extracellular fluid?
8 - 10 mg/dL
What levels of calcium are considered hypercalcemia?
> 10.5 mg/Dl
What are the 3 levels of hypercalcemia and what are their values?
Mild = 10.5 - 11.9 mg/dL
Moderate = 12 - 13.9 mg/dL
Severe (crisis) = 14 - 16 mg/dL
What is the differences between calcium homeostasis and balance?
homeostasis = short term equilibrium
balance = long term maintenance of bone density
What is the goal of calcium balance in the body?
intake/intestinal absorption = excretion
What is the goal of calcium homeostasis?
maintenance of extracellular fluid (ECF) calcium levels
How fast can PTH exert its influence on plasma calcium levels?
w/ in 1 - 2 hours
But not the only physiological influence of calcium levels in the blood
Which organs maintain ECF calcium levels?
GI tract
Kidney
Bone
What is important about the GI tract in terms of calcium homeostasis?
site of absorption of dietary/supplementary calcium
What are the 2 forms of supplemental calcium?
Calcium carbonate
Calcium citrate
Which form of supplemental calcium has a better rate of absorption?
Both have about the same:
% of absorption = inverse to amount of calcium ingested at one time
ideally want to “spread out” supplement doses instead of single large dose
What are the characteristics of calcium carbonate?
Cheaper
Absorbs best w/ food
What are the characteristics of calcium citrate?
More expensive
May have slightly better absorption w/ or w/o food
Good for pts w/ reduced stomach acid
What are the 2 functions of the kidneys in calcium homeostasis/balance?
Reabsorption of calcium in glomerular filtrate
Site of conversion of inactive vitamin D to active vitamin D (calcitriol)
Where in the kidney is calcium reabsorbed?
90% in PCT
8 - 9% in DCT/collecting ducts
What will impair calcium absorption, and what do they do?
Pathology and Meds
Increase calcium excretion
What are the 2 functions of the bones in calcium homeostasis/balance?
Calcium Storage
Stimuli to increase calcium reabsorption (osteoclastic activity) –> increase ECF calcium
What are the primary regulatory hormones of ECF calcium and phosphate?
PTH = parathyroid hormone
Calcitonin
Calcitriol = active form of vitamin D
What are the secondary influencing hormones that regulate ECF calcium?
GH
Thyroid hormones
Adrenal/Gonadal steroid hormones
Where is Parathyroid Hormone (PTH) made/released?
synthesized and released from parathyroid glands
What is the function of PTH?
increase plasma (ECF) calcium levels
What are the target tissues of PTH?
Bone
Kidney
What does PTH stimulate in the bone?
osteoclastic activity –> promotes calcium resorption from bone
promotes phosphate release from bone
How quickly does PTH work?
Immediately stimulate osteoclastic activity (minutes)
Increase plasma (ECF) calcium w/ in 1 - 2 hours
What does PTH stimulate in the kidneys?
Conversion of inactive vitamin D –> active vitamin D (calcitriol)
Prolonged PTH release –> conversion of more 1,25 dihydroxyvitamin D (1,25 OH2D3) = calcitriol
Calcium resorption in tubules of kidneys
Stimulates phosphate (and bicarbonate) excretion in kidneys
What is the physiologic purpose of excreting phosphate and bicarbonate when stimulated by PTH in the kidneys?
prevents hyperphosphatemia as body is trying to restore calcium levels
What is PTH release stimulated by?
small decreases of plasma (ECF) calcium
What is PTH release inhibited by?
Elevated plasma (ECF) calcium
Elevated “activated” vitamin D (calcitriol) –> negative feedback
What is calcitriol?
active form of vitamin D3
Where is vitamin D2 formed?
absorbed from foods –> eggs, dairy, fish oil, plants
Where is vitamin D3 formed?
Skin w/ exposure to UV (sun) light
Is D2 and D3 biologically active?
No
Needs to be activated in liver/kidney (final step in kidney via PTH)
What is the function of calcitriol?
Increase plasma (ECF) calcium levels
Other roles in immunity and reproductive functions
What are the target tissues of calcitriol?
Intestine
Bone
Kidney
What does calcitriol stimulate in the intestine?
Calcium absorption in the small intestine
Phosphate absorption in the small intestine
What does calcitriol stimulate in bone?
osteoclastic activity –> promotes calcium resorption from bone
phosphate release from bone
What does calcitriol stimulate in the kidney?
Calcium resorption in tubules of kidneys
Phosphate resorption in kidneys
What is calcitriol release stimulated by?
Elevated PTH levels
What is calcitriol release inhibited by?
Decreased PTH levels
Where is calcitonin produced/secreted?
Parafollicular cells of the thyroid gland
What is the function of calcitonin?
Decrease plasma (ECF) calcium levels –> “tones down” plasma levels of calcium
minor role compared to PTH/calcitriol
What are the target tissues of calcitonin?
Bone
Kidney
What does calcitonin do in bone?
inhibits osteoclasts –> inhibits calcium resorption
What does calcitonin do in the kidneys?
stimulates calcium/phosphate excretion in the renal tubules
What is calcitonin release stimulated by?
Large increases of plasma (ECF) calcium
What is calcitonin release inhibited by?
Decreased levels of plasma (ECF) calcium
What are the common causes of hyperparathyroidism?
neoplasms that secrete PTH
What are the symptoms of hyperparathyroidism?
Precipitation/deposits of calcium phosphate –> tissue damage/organ dysfunction
Kidney Stones
Muscle weakness, fatigue, lethargy
Polyuria, nocturia, polydipsia (increased thirst)
Confusion, drowsy and coma
Nausea, vomitting, constipation
Potential decreased bone density
What would you see in the labs of a pt with Hyperparathyroidism?
Hypercalcemia
Hypercalciuria
Hypophosphatemia
Potential to develop into metabolic acidosis
What is hypercalcemia due to in hyperparathyroidism?
Increased resorption of calcium from bone
decreased renal excretion of calcium
increased intestinal absorption of calcium
What is hypercalciuria due to in hyperparathyroidism?
excessive hypercalcemia –> kidney filtration is “overloaded”, the excess calcium excreted into urine
What is hypophosphatemia due to in hyperparathyroidism?
Increased phosphate excretion in kidneys
Why would hyperparathyroidism potentially cause metabolic acidosis?
PTH increases excretion of bicarbonate in the kidneys
What causes kidney stones to form in hyperparathyroidism?
hypercalciuria and alkaline urine are ideal for kidney stone formation
What causes muscle weakness, fatigue, lethargy in hyperparathyroidism?
hypercalcemia –> decreased Na+ permeability –> decreased tissue excitability
What causes polyuria, nocturia and polydipsia (increased thirst) in hyperparathyroidism?
hypercalcemia inhibits action of ADH in kidney –> increased urinary excretion
What causes confusion, drowsiness and coma in hyperparathyroidism?
hypercalcemia alters conductivity/function of CNS tissue –> death
What causes the nausea, vomitting, and constipation in hyperparathyroidism?
hypercalcemia decreases GI peristalsis and stimulates vomit centers in brainstem
What could happen due to the decreased bone density?
Fractures due to increased bone reabsorption
**would take a long time
What is hypoparathyroidism caused by?
Surgical removal
Damage
Not as common
What does hypoparathyroidism cause?
Low levels of calcium = hypocalcemia
No significant effect on bone
What are the symptoms of hypoparathyroidism?
Neuromuscular excitability
Muscle Spasms
Tetany = severe, intermittent tonic contractions and muscular pain
Cardiac Dysfunction
What will hypocalcemia do to tissues throughout the body?
increase excitability of tissue
What are the motor signs of nerve irritability?
Tetany
Seizures
How do you assess for motor nerve irritability?
Chyostek’s sign = tap anterior to external acoustic meatus –> hyper excitability of facial muscles (eye + mouth)
What are other signs of motor nerve irritability?
Hyper-reflexia
Muscle Spasms
Laryngeal Spasms
What are the sensory signs of nerve irritability?
Paraesthesis = tingling, tickling, prickling, pricking, or burning of a person’s skin with no apparent long-term physical effect
What are the signs of hyperphosphatemia?
Soft tissue deposits
Itchiness (pruritis)
Joint Pain
