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Pathophysiology Endocrine > Module #2: Endocrine Pancreas and Thyroid/Parathyroid Physiology > Flashcards

Module #2: Endocrine Pancreas and Thyroid/Parathyroid Physiology Flashcards

1
Q

What type of functions does the pancreas have?

A

endocrine

exocrine

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2
Q

Which pancreatic cells are responsible for its endocrine functions?

A

Islets of Langerhans

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3
Q

Name the types of Islets of Langerhans cells and their function

A

alpha = secrete glucagon

beta = secret insulin (co-secretion of amylin)

delta = secrete somatostatin (different from hypothalamus) and gastrin

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4
Q

What does glucagon do?

A

prevents hypoglycemia

mobilizes “metabolic fuels”

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5
Q

How does glucagon prevent hypoglycemia/mobilize metabolic fuels?

A

increase blood glucose levels

“catabolic” hormone that mobilizes fuel (glucose and FFA)

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6
Q

What are the target tissues of glucagon?

A

Liver

Fat Tissues

Muscle

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7
Q

What does glucagon do to the liver?

A

stimulate glycogenolysis (breakdown glycogen) and glycogenesis (glucose formation)

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8
Q

What does glucagon do to fat tissue?

A

stimulate lypolysis

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9
Q

What does glucagon do to muscle tissue?

A

stimulate proteolysis (breakdown for amino acid release)

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10
Q

What does glucagon do in response to hypoglycemia?

A

glucagon tries to make fuel so it increases:

glucose

free fatty acids and associated ketones

amno acids

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11
Q

What are the factors that stimulate glucagon secretion from the pancreas?

A

Hypoglycemia

Exercise

Stress

Fasting

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12
Q

What is a factor that inhibits glucagon secretion from the pancreas?

A

Hyperglycemia

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13
Q

What does Amylin do and when is it secreted?

A

supresses glucagon

co-secreted w/ insulin during feeding

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14
Q

What is the function of insulin?

A

prevent hyperglycemia

promote “metabolic fuel” storage

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15
Q

How does insulin function to prevent hyperglycemia and promote metabolic fuel storage?

A

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

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16
Q

What are the target tissues of insulin?

A

Liver

Muscle

Adipose Tissue

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17
Q

What response does insulin elicit in the liver?

A

increase: glucose uptake, formation of glycogen, lipid/protein synthesis
decrease: ketogenesis, glycogenolysis

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18
Q

What response does insulin elicit in muscles?

A

increase: glucose uptake, formation of glycogen, amino acid uptake, protein synthesis
decrease: glycogenolysis

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19
Q

What response does insulin elicit in adipose tissue?

A

increase: glucose uptake, glucose to form glycerol phoshate (part of TG formation), fat storage (formation)
decrease: lypolysis

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20
Q

What are the factors that stimulate insulin secretion from the pancreas?

A

Hyperglycemia

Increased serum levels of FFA, amin acids

GI/digestive hormones

Parasympathetic stimulation of pancreatic beta cells

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21
Q

What are the factors that inhibit insulin secretion from the pancreas?

A

Hypoglycemia

Negative feedback loop –> increased insulin levels

Sympathetic stimulation of pancreatic beta cells

Prostaglandins (PGE2)

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22
Q

How does the body regulate insulin receptors?

A

down regulate

up regulate

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23
Q

What will be the physiologic response to excessive insulin levels?

A

decrease the number of insulin receptors

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24
Q

What happens in obese people that leads to type 2 (non-insulin dependent) diabetes?

A

Adipose tissue down regulates insulin receptors –> decreased insulin sensitivity

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25
Q

What is the decreased insulin sensitivity response to feeding that leads to the vicious cycle of obesity/Type 2 diabetes?

A

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

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26
Q

What is the very basic definition of diabetes mellitus?

A

disruption of regulation of blood glucose levels

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27
Q

What are the different types of diabetes mellitus?

A

DM Type 1 aka juvenile-onset or insulin dependent

DM Type 2 aka adult onset or non-insulin dependent

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28
Q

What are the 3 poly’s of diabetes?

A

polyuria = excessive urine production

polydipsia = excessive thirst

polyphagia = increased appetite

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29
Q

What is DM Type 1?

A

insulin insufficiency due to result of pancreatic destruction of beta cell Islets of Langerhans

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30
Q

What is a suggested cause of DM Type 1?

A

suggested to be autoimmune disorder –> antibodies attack beta cell islets of Langerhans

** early treatment of immunosuppresive drugs may show significant improvement

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31
Q

Is DM Type 1 associated w/ obesity?

A

No

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32
Q

What are the consequences of decreased insulin?

A

Hyperglycemia

Hyperlipidemia

Increased ketone bodies/ketoacidosis

Catabolic affect on muscle mass

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33
Q

Why does decreased insulin lead to hyperglycemia?

A

cells are unable to take up glucose from blood

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34
Q

What are the signs and symptoms of hyperglycemia?

A

polyuria

polydipsia

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35
Q

What are the renal thresholds of hyperglycemia?

A

plasma glucose > 180-200 mg/dL = glucose dumping in urine

plasma glucose > 350 mg/Dl = transport max for glucose in PCT

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36
Q

Why does decreased insulin lead to hyperlipidemia?

A

inhibitory to fat storage

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37
Q

What is a consequence of hyperlipidemia?

A

promotes atherosclerotic changes in blood vessels

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38
Q

Why does decreased insulin lead to an increase of ketone bodies/ketoacidosis?

A

formed from increased FFA metabolism in the liver –> metabolic acidosis

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39
Q

Why does decreased insulin have a catabolic affect on muscle mass?

A

the body attempts to mobilize amino acids for “fuel” formation

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40
Q

What are the signs and symptoms of catabolism of muscles when there is a decrease in insulin?

A

muscle wasting

weight loss

weakness

fatigue

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41
Q

What is insulin shock?

A

Hypoglycemic reaction

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42
Q

What causes hypoglycemia of insulin shock?

A

excessive insulin administration

increased physical activity

poor glucose monitoring/missed meals, etc.

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43
Q

What are some signs/symptoms of hypoglycemia/insulin shock?

A

hunger

sweating

irritability

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44
Q

What are some consequences of prolonged hypoglycemia?

A

diabetic coma/decreased CNS metabolism –> giddiness, coma, death

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45
Q

When is hypoglycemia/insulin shock considered a medical emergency?

A

symptoms are severe

seizures

convulsions

loss of consciousness

repeated episodes

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46
Q

What is the treatment for hypoglycemia/insulin shock?

A

administer glucose to restore blood glucose levels

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47
Q

What is DM Type 2 associated with?

A

increased insulin resistance

obesity

usually adult onset

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48
Q

What does increased insulin resistance do?

A

obesity/inactivity creates viscous cycle of inefficient blood glucose clearance –> more insulin secretion
–> cycle –> increased insulin resistance

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49
Q

What is increased insulin resistance caused by?

A

decreased insulin receptor function

decreased insulin receptor number

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50
Q

What are 2 important ways to improve insulin sensitivity?

A

Diet changes

Exercise

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51
Q

Describe Glucose Tolerance Test (GTT)?

A

Establish baseline glucose level

Administer glucose prep

Blood draw in intervals (0 and 120 = minimum; usually draw every 30 minutes)

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52
Q

According to the WHO in 1999 what are considered normal values of GTT?

A

fasting = < 100 mg/dL

2 hrs = < 140 mg/dL

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53
Q

According to the WHO in 1999 what are considered DM values of GTT?

A

fasting = > 126 mg/dL

2 hrs = > 200 mg/dL

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54
Q

What hormones are produced in the thyroid gland?

A

T4 - thyroxine

T3 - tri-iodothyronine

Calcitonin

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55
Q

Where is un-iodinated TGB (thyroglobulin) produced?

A

follicle cells

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56
Q

What happens to TGB molecule, how is it modified?

A

Tyrosine is synthesized into it

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57
Q

Describe “Iodide trapping”

A

TSH sensitive iodide pump transports iodide into follicular cells

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58
Q

How much dietary iodine is trapped by the thyroid gland?

A

25%

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59
Q

What happens to the iodide once it is in the thyroid?

A

Binds to tyrosine/TGB molecule = organification

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60
Q

How are the thyroid molecules formed?

A

Once iodide binds to tyrosine/TGB molecules they then bind aka couple together to form T3 and T4

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61
Q

Where are T3 and T4 stored?

A

Colloid

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62
Q

Which thyroid hormone is the active form and which thyroid hormone is the inactive form?

A

T3 = active form

T4 = inactive form

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63
Q

How much T3/T4 is circulated bound to a carrier protein?

A

99.9%

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64
Q

What are the carrier proteins that bind to T3/T4 in the blood stream?

A

TGB

albumin

Transthyretin

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65
Q

Approximately how much of T4 and T3 circulate “freely”?

A

.03% each

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66
Q

What is “free” T3 or T4 considered?

A

active

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67
Q

Besides being active and doing its thing, what else can happen to free T3/T4?

A

Easily excreted by the kidneys

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68
Q

Approximately how much thyroid hormone is released as T3?

A

10 - 20%

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69
Q

Which form of T3 is considered bioavailable?

A

active free form (.03%)

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70
Q

How does active T3 elicit its physiologic response?

A

enters cell, binds to receptor w/in the nucleus

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71
Q

When can carrier bound T3 enter a cell to elicit its response?

A

it must disassociate from the carrier protein

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72
Q

What allows easier disassociation of T3 from the carrier protein?

A

Loose bind; T3 = more active than T4

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73
Q

Approximately how much thyroid hormone is released as T4?

A

80 - 90%

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74
Q

Which form of T4 is considered bioavailable?

A

active free form (.03%)

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75
Q

How does T4 ellicite its response the cell?

A

Bind to T4 receptors w/in the cell nucleus

undergo conversion to T3 or rT3 in cell cytoplasm/membrane

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76
Q

How does the activity of T4 compare to T3?

A

T4 activity is much less than T3

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77
Q

Where is T4 converted to T3?

A

Primary site of T4 –> T3 = Liver

generally in target tissues (muscles, liver, kidney, etc.)

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78
Q

What happens after T4 is converted to T3?

A

can be utilized in the cell

can exit and bind in another cell

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79
Q

What is rT3?

A

reverse T3, the inactive form of T3

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80
Q

What happens after T4 is converted to rT3?

A

exits the cell

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81
Q

When is “bound” T4 able to enter a cell?

A

must dissociate from the carrier protein

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82
Q

Why does T4 have a more difficult disassociation from carrier?

A

strong binding –> T4 = less active compared to T3

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83
Q

What happens to rT3 and T3 that aren’t utilized?

A

converted to T2 (completely inactive thyroid hormone)

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84
Q

Describe the signaling pathway of thyroid hormone release from thyroid gland

A

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)

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85
Q

What are the stimuli for thyroid hormone release?

A

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)

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86
Q

What are the inhibitors of thyroid hormone release?

A

Serum levels of T3/T4 inhibit TSH release from anterior pituitary

GHIH (somatostatin)

Dopamine (prolactin inhibiting hormone)

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87
Q

Generally, what are the functions of thyroid hormones T3/T4?

A

Growth/Development

Control rate of metabolism

Regulate/influence every organ of the body

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88
Q

What is T3/T4 required for during growth and development?

A

normal skeletal growth

maturation of all cells

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89
Q

What other hormones does T3/T4 stimulate that are required for growth/development?

A

Stimulates GH release, which is necessary for IGF-1 function

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90
Q

What is CNS maturation dependent on?

A

thyroid function during prenatal period

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91
Q

What happens if there is a deficiency of T3/T4 during the peri-natal period?

A

CNS impairment (cognitive impairment)

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92
Q

How does T3/T4 control metabolism?

A

increases BMR (basal metabolic rate)

increases O2 consumption of the body

temperature regulation

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93
Q

The BMR of which tissues is NOT increased by T3/T4?

A

Brain

Spleen

Testes

94
Q

What does thyroid hormone do in all cells except the brain, gonads, spleen?

A

increase cellular respiration = increase BMR (basal metabolic rate)

95
Q

What does elevated BMR do?

A

increases O2 consumption

increases heat production

increases demand for fuel

96
Q

What does elevated BMR do to the liver?

A

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)

97
Q

What is thyroid hormone action on the heart?

A

increase HR and Cardiac Output by increasing sensitivity to sympathetic system/epinephrine (ionotropic and chronotropic)

98
Q

What is the thyroid hormone action on the vascular system?

A

decrease total peripheral resistance of the vascular system

99
Q

What is the thyroid hormone action on pulmonary organs?

A

stimulate respiration centers in brainstem –> increase ventilation

100
Q

What is the thyroid hormone action in the CNS?

A

stimulate myelin/axonal growth and development

stimulate sympathetic activity

101
Q

What is the thyroid hormone action on adipose tissue (fat cells)?

A

increase lipolysis –> mobilize FFA for metabolic fuel

102
Q

What is the thyroid hormone action in muslce?

A

promote muscle protein growth/development (works synergistically w/ other GH)

excess levels –> catabolic metabolism of muscles to provide fuel for increased BMR

103
Q

What is the thyroid hormone action on bones?

A

promote bone growth/development (synergistically w/ other GH)

stimulate osteoblast/obsteroclast activity

104
Q

What is the thyroid hormone action in the liver?

A

promote TG (triglyceride) and cholesterol metabolism

regulate LDL homeostasis

105
Q

What is the thyroid hormone action in the GI system?

A

Maintain secretions of GI tract

106
Q

What is the thyroid hormone action on the pituitary gland?

A

Inhibit TSH

Stimulate the release of GH

Stimulate synthesis of pituitary hormones

107
Q

What are the sings and symptoms of hyperthyroidism in the thyroid?

A

enlargement of the thyroid gland (goiter)

108
Q

What are the sings and symptoms of hyperthyroidism in the cardiovascular system?

A

Palpitations

Hypertension

Increased pulse pressure

Tachycardia

Increased Cardiac Output

109
Q

What are the sings and symptoms of hyperthyroidism in the pulmonary system?

A

Elevated respiration rate

110
Q

What are the sings and symptoms of hyperthyroidism in the CNS?

A

Hyperactivity

Fine tremor

Increased nervousness (excitable, irritable, apprehensive)

Increased sympathetic activity

111
Q

What are the sings and symptoms of hyperthyroidism in the integumentary system?

A

Warm moist skin

Excessive sweating

Thin/fine hair

112
Q

What are the general sings and symptoms of hyperthyroidism?

A

Weight loss despite food intake

Loss of muscle mass

Fat loss

113
Q

What are the sings and symptoms of hyperthyroidism in muscles?

A

Proximal Weakness

114
Q

What are the sings and symptoms of hyperthyroidism in the eyes?

A

Exophthalmos aka proprtosis

can be caused by: sympathetic hyperactivity, infiltrative changes

115
Q

What are the sings and symptoms of hyperthyroidism in the GI tract?

A

Increased motilities

increased bowel movements

116
Q

What is another name for primary hyperthyroidism?

A

Thyrotoxicosis

117
Q

What are the forms of primary hyperthyroidism?

A

Endogenous (Grave’s Disease)

Iatrogenic hyperthyroidism

Thyroid Storm

118
Q

What happens in Grave’s Disease?

A

excessive TSI (thyroid-stimulating immunoglobulins) bind to TSH receptors and stimulate the release of T3/T4

119
Q

What will you see in labs of pts w/ Grave’s disease?

A

TSI = elevated

TSH = decreased (increased T3/T4 inhibit release of TSH)

T3/T4 = elevated (T3 = 3-4x; T4 = 2x)

TRH = decreased

120
Q

What causes Iatrogenic hyperthyroidism?

A

Excessive use of synthetic thyroxine

121
Q

What is thyroid storm?

A

rare but life threatening form of hyperthyroidism

122
Q

What are the sings/symptoms of thyroid storm

A

Hallmark hyperthyroidism signs/symptoms

distinguishing sign = 105-106 degree fever

123
Q

What are some causes of Thyroid Storm (7)?

A

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

124
Q

What is a rare secondary hyperthyroidism disease?

A

TSH secreting adenomas

125
Q

What will secondary hyperthyroidism labs look like?

A

TSI = normal

TSH = elevated (tumor)

T3/T4 = elevated (T3 = 3-4x; T4 = 2x)

TRH = decreased

126
Q

When/How do you get Hypothyroidism?

A

Adult-onset

Congenital

127
Q

What are the cardiac symptoms of adult onset hypothyroidism?

A

Bradycardia –> decrease cardiac output

Hypotension

Elevated peripheral resistance to maintain blood pressure

128
Q

What are the pulmonary symptoms of adult onset hypothyroidism?

A

Decreased respiration rate

129
Q

What are the CNS symptoms of adult onset hypothyroidism?

A

Hypoactive –> lethargic, confusion, slow speech hoarse voice, diminished memory function

Decreased DTR’s (deep tendon reflex)

130
Q

What are the integumentary symptoms of adult onset hypothyroidism?

A

Cool dry skin –> reduced heat production associated w/ decreased BMR

slow wound healing

dry brittle hair

Myxedema

131
Q

What is Myxedema?

A

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)

132
Q

What happens to your weight when you have adult onset hypothyroidism?

A

Gain weight despite reduced appetite/food intake

133
Q

What are the GI symptoms of adult onset hypothyroidism?

A

Decreased Motility

Constipation (decreased BMs)

Protruding abdomen

134
Q

What are the muscle symptoms of adult onset hypothyroidism?

A

Stiffness/achiness of muscles/joints –> muscle cramps

Drooping eyelids

135
Q

What are the bone symptoms of adult onset hypothyroidism?

A

Potential for anemia due to suppression of bone marrow function

136
Q

Is there thyroid enlargement associated with adult onset hypothyroidism?

A

Sometimes

137
Q

What is another name for congenital onset hypothyroidism?

A

Cretinism

138
Q

What are the symptoms that are specifically associated with congenital onset hypothyroidism?

A

Cognitive impairment

Gross Dwarfism

139
Q

Why will you have cognitive impairment with congenital onset hypothyroidism?

A

T3/T4 are necessary for CNS development

140
Q

What are the signs/symptoms of gross dwarfism?

A

impaired skeletal growth

short limbs

141
Q

What are some signs @ birth that are suggestive to screen for congenital onset hypothyroidism?

A

High birth weight

Hypothermia

Jaundice

142
Q

What is considered the critical window of intervention for treatment of congenital onset hypothyroidism?

A

4 months

143
Q

What is the most common form of primary adult onset hypothyroidism?

A

Hashimoto’s thyroiditis

144
Q

What are the other less common forms of primary adult onset hypothyroidism?

A

Iodine deficiency

Thyroidectomy

Radiation damage in treatment of hyperthyroidism

145
Q

What is Hashimoto’s thyroiditis and why does it cause hypothyroidism?

A

Autoimmune disorder

Gradual destruction of functional thyroid tissue

146
Q

What will you see in the labs of a pt with primary adult onset hypothyroidism?

A

TSH = elevated (low circulation of T4/T3)

T3/T4 = low –> T4 is converted to T3 as body demands

147
Q

What will you see in the labs of a pt with secondary hypothyroidism?

A

All are low

TSH = low –> anterior pituitary/hypothalamus damage

T3/T4 = low

148
Q

What is goiter?

A

An enlargement of the thyroid gland

149
Q

Why is the thyroid enlarged in goiter?

A

Elevated TSH levels trying to stimulate the thyroid gland

150
Q

Can you predict thyroid function based on goiter alone?

A

NO

Can be normal, elevated, or diminished

151
Q

What is goiter caused by in Grave’s disease (hyperthyroidism)?

A

immuoglobulin (TSI) stimulating thyroid gland to produce T3/T4

152
Q

What is goiter caused by in Hashimoto’s (hypothyroidism)?

A

elevated TSH trying to stimulate thyroid gland to produce T3/T4

153
Q

What is goiter caused by in Iodine deficiency?

A

elevated TSH trying to stimulate thyroid to produce T3/T4 –> dietary iodine is lacking

154
Q

What are the 3 hormones that control calcium homeostasis/balance?

A

PTH

Calcitriol

Calcitonin

155
Q

What is the function of calcium?

A

Mineralization of bone matrix

Formation of bone and teeth

Normal physiological functions

Milke production (lactogenesis)

156
Q

What are the normal physiological functions that are dependent on stable levels of calcium in the blood?

A

Maintain membrane permeability

Maintain excitability of nerve and muscle

Release of neurotransmitters

Muscle contractions

Coagulation of blood

157
Q

Where is most calcium stored?

A

98-99% in bone

**phosphate also stored in bone

158
Q

Where is calcium found when its not stored in bone?

A

Circulating in the ECF (extracellular fluid)

159
Q

What are the forms of calcium circulating in the ECF, and how much of each do you have?

A

50% = free form of ionized calcium Ca2+

45% = bound to albumin (protein)

5% = bound to phosphate/citrate

160
Q

Is there any intracellular calcium?

A

Yes, but thousand’s of times less than extracellular fluid

161
Q

What is the function of intracellular fluid calcium?

A

Intracellular signaling = action potentials, secondary messenger systems, etc

Enzyme secretion

Muscle contraction

162
Q

Where in the body is there a constant large exchange of calcium?

A

GI tract

Bone

Kidney

163
Q

How tightly are extracellular fluid calcium levels maintained?

A

w/ in a narrow window

164
Q

What are the normal values of calcium in the extracellular fluid?

A

8 - 10 mg/dL

165
Q

What levels of calcium are considered hypercalcemia?

A

> 10.5 mg/Dl

166
Q

What are the 3 levels of hypercalcemia and what are their values?

A

Mild = 10.5 - 11.9 mg/dL

Moderate = 12 - 13.9 mg/dL

Severe (crisis) = 14 - 16 mg/dL

167
Q

What is the differences between calcium homeostasis and balance?

A

homeostasis = short term equilibrium

balance = long term maintenance of bone density

168
Q

What is the goal of calcium balance in the body?

A

intake/intestinal absorption = excretion

169
Q

What is the goal of calcium homeostasis?

A

maintenance of extracellular fluid (ECF) calcium levels

170
Q

How fast can PTH exert its influence on plasma calcium levels?

A

w/ in 1 - 2 hours

But not the only physiological influence of calcium levels in the blood

171
Q

Which organs maintain ECF calcium levels?

A

GI tract

Kidney

Bone

172
Q

What is important about the GI tract in terms of calcium homeostasis?

A

site of absorption of dietary/supplementary calcium

173
Q

What are the 2 forms of supplemental calcium?

A

Calcium carbonate

Calcium citrate

174
Q

Which form of supplemental calcium has a better rate of absorption?

A

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

175
Q

What are the characteristics of calcium carbonate?

A

Cheaper

Absorbs best w/ food

176
Q

What are the characteristics of calcium citrate?

A

More expensive

May have slightly better absorption w/ or w/o food

Good for pts w/ reduced stomach acid

177
Q

What are the 2 functions of the kidneys in calcium homeostasis/balance?

A

Reabsorption of calcium in glomerular filtrate

Site of conversion of inactive vitamin D to active vitamin D (calcitriol)

178
Q

Where in the kidney is calcium reabsorbed?

A

90% in PCT

8 - 9% in DCT/collecting ducts

179
Q

What will impair calcium absorption, and what do they do?

A

Pathology and Meds

Increase calcium excretion

180
Q

What are the 2 functions of the bones in calcium homeostasis/balance?

A

Calcium Storage

Stimuli to increase calcium reabsorption (osteoclastic activity) –> increase ECF calcium

181
Q

What are the primary regulatory hormones of ECF calcium and phosphate?

A

PTH = parathyroid hormone

Calcitonin

Calcitriol = active form of vitamin D

182
Q

What are the secondary influencing hormones that regulate ECF calcium?

A

GH

Thyroid hormones

Adrenal/Gonadal steroid hormones

183
Q

Where is Parathyroid Hormone (PTH) made/released?

A

synthesized and released from parathyroid glands

184
Q

What is the function of PTH?

A

increase plasma (ECF) calcium levels

185
Q

What are the target tissues of PTH?

A

Bone

Kidney

186
Q

What does PTH stimulate in the bone?

A

osteoclastic activity –> promotes calcium resorption from bone

promotes phosphate release from bone

187
Q

How quickly does PTH work?

A

Immediately stimulate osteoclastic activity (minutes)

Increase plasma (ECF) calcium w/ in 1 - 2 hours

188
Q

What does PTH stimulate in the kidneys?

A

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

189
Q

What is the physiologic purpose of excreting phosphate and bicarbonate when stimulated by PTH in the kidneys?

A

prevents hyperphosphatemia as body is trying to restore calcium levels

190
Q

What is PTH release stimulated by?

A

small decreases of plasma (ECF) calcium

191
Q

What is PTH release inhibited by?

A

Elevated plasma (ECF) calcium

Elevated “activated” vitamin D (calcitriol) –> negative feedback

192
Q

What is calcitriol?

A

active form of vitamin D3

193
Q

Where is vitamin D2 formed?

A

absorbed from foods –> eggs, dairy, fish oil, plants

194
Q

Where is vitamin D3 formed?

A

Skin w/ exposure to UV (sun) light

195
Q

Is D2 and D3 biologically active?

A

No

Needs to be activated in liver/kidney (final step in kidney via PTH)

196
Q

What is the function of calcitriol?

A

Increase plasma (ECF) calcium levels

Other roles in immunity and reproductive functions

197
Q

What are the target tissues of calcitriol?

A

Intestine

Bone

Kidney

198
Q

What does calcitriol stimulate in the intestine?

A

Calcium absorption in the small intestine

Phosphate absorption in the small intestine

199
Q

What does calcitriol stimulate in bone?

A

osteoclastic activity –> promotes calcium resorption from bone

phosphate release from bone

200
Q

What does calcitriol stimulate in the kidney?

A

Calcium resorption in tubules of kidneys

Phosphate resorption in kidneys

201
Q

What is calcitriol release stimulated by?

A

Elevated PTH levels

202
Q

What is calcitriol release inhibited by?

A

Decreased PTH levels

203
Q

Where is calcitonin produced/secreted?

A

Parafollicular cells of the thyroid gland

204
Q

What is the function of calcitonin?

A

Decrease plasma (ECF) calcium levels –> “tones down” plasma levels of calcium

minor role compared to PTH/calcitriol

205
Q

What are the target tissues of calcitonin?

A

Bone

Kidney

206
Q

What does calcitonin do in bone?

A

inhibits osteoclasts –> inhibits calcium resorption

207
Q

What does calcitonin do in the kidneys?

A

stimulates calcium/phosphate excretion in the renal tubules

208
Q

What is calcitonin release stimulated by?

A

Large increases of plasma (ECF) calcium

209
Q

What is calcitonin release inhibited by?

A

Decreased levels of plasma (ECF) calcium

210
Q

What are the common causes of hyperparathyroidism?

A

neoplasms that secrete PTH

211
Q

What are the symptoms of hyperparathyroidism?

A

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

212
Q

What would you see in the labs of a pt with Hyperparathyroidism?

A

Hypercalcemia

Hypercalciuria

Hypophosphatemia

Potential to develop into metabolic acidosis

213
Q

What is hypercalcemia due to in hyperparathyroidism?

A

Increased resorption of calcium from bone

decreased renal excretion of calcium

increased intestinal absorption of calcium

214
Q

What is hypercalciuria due to in hyperparathyroidism?

A

excessive hypercalcemia –> kidney filtration is “overloaded”, the excess calcium excreted into urine

215
Q

What is hypophosphatemia due to in hyperparathyroidism?

A

Increased phosphate excretion in kidneys

216
Q

Why would hyperparathyroidism potentially cause metabolic acidosis?

A

PTH increases excretion of bicarbonate in the kidneys

217
Q

What causes kidney stones to form in hyperparathyroidism?

A

hypercalciuria and alkaline urine are ideal for kidney stone formation

218
Q

What causes muscle weakness, fatigue, lethargy in hyperparathyroidism?

A

hypercalcemia –> decreased Na+ permeability –> decreased tissue excitability

219
Q

What causes polyuria, nocturia and polydipsia (increased thirst) in hyperparathyroidism?

A

hypercalcemia inhibits action of ADH in kidney –> increased urinary excretion

220
Q

What causes confusion, drowsiness and coma in hyperparathyroidism?

A

hypercalcemia alters conductivity/function of CNS tissue –> death

221
Q

What causes the nausea, vomitting, and constipation in hyperparathyroidism?

A

hypercalcemia decreases GI peristalsis and stimulates vomit centers in brainstem

222
Q

What could happen due to the decreased bone density?

A

Fractures due to increased bone reabsorption

**would take a long time

223
Q

What is hypoparathyroidism caused by?

A

Surgical removal

Damage

Not as common

224
Q

What does hypoparathyroidism cause?

A

Low levels of calcium = hypocalcemia

No significant effect on bone

225
Q

What are the symptoms of hypoparathyroidism?

A

Neuromuscular excitability

Muscle Spasms

Tetany = severe, intermittent tonic contractions and muscular pain

Cardiac Dysfunction

226
Q

What will hypocalcemia do to tissues throughout the body?

A

increase excitability of tissue

227
Q

What are the motor signs of nerve irritability?

A

Tetany

Seizures

228
Q

How do you assess for motor nerve irritability?

A

Chyostek’s sign = tap anterior to external acoustic meatus –> hyper excitability of facial muscles (eye + mouth)

229
Q

What are other signs of motor nerve irritability?

A

Hyper-reflexia

Muscle Spasms

Laryngeal Spasms

230
Q

What are the sensory signs of nerve irritability?

A

Paraesthesis = tingling, tickling, prickling, pricking, or burning of a person’s skin with no apparent long-term physical effect

231
Q

What are the signs of hyperphosphatemia?

A

Soft tissue deposits

Itchiness (pruritis)

Joint Pain

Pathophysiology Endocrine (3 decks)

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