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Pathophysiology > Endocrine: Module II > Flashcards

Endocrine: Module II Flashcards

1
Q

The pancreas has both ____ and ____ function

A

Endocrine

Exocrine

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2
Q

3 cell types of Islets of Langerhans

A

Alpha
Beta
Delta

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3
Q

Function of alpha cells

A

secrete glucagon

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4
Q

Function of beta cells

A

Secrete insulin

Co-secrete amylin

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5
Q

Function of delta cells

A

Secrete somatostatin and gastrin

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6
Q

What is the function of glucagon?

A

Prevents hypoglycemia by mobilizing “metabolic fuels”

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7
Q

Target tissue of glucagon: (3)

A

Liver –> stimulates glycogenolysis and glucogensis

Fat tissue –> stimulates lypolysis

Muscle –> proteolysis

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8
Q

The breakdown of glycogen is called…

A

Glycogenolysis

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9
Q

The formation of glucose is called….

A

Glucogenesis

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10
Q

The breakdown of amino acid is called….

A

Proteolysis

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11
Q

4 Factors that stimulate glucagon secretion from pancreas

A
  1. Hypoglycemia
  2. Exercise
  3. Stress
  4. Fasting
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12
Q

1 Factor that inhibits glucagon secretion from pancreas

A
  1. Hyperglycemia
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13
Q

Amylin: when is it secreted and what is its function?

A
  • Co-secreted with insulin during feeding

- Suppresses glucagon

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14
Q

Main function of insulin

A

Prevents hyperglycemia –> promotes “metabolic fuel” storage

  • Dec blood glucose levels
  • Dec blood levels of amino acids and FFA/ketones
  • Dec serum potassium levles
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15
Q

What is the target tissue of insulin?

A
  1. Liver
  2. Muscle
  3. Adipose tissue
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16
Q

What happens in the liver when insulin is increased and decreased?

A

Insulin increased: glucose uptake, formation of glycogen, lipid/protein synthesis

Insulin Decreased: ketogenesis, glycogenolysis

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17
Q

What happens in the muscles when insulin is increased and decreased?

A

Insulin increased: glucose uptake, formation of glycogen, amino acid uptake, protein synthesis

Insulin decreased: lypolysis

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18
Q

What happens in adipose tissue when insulin is increased and decreased?

A

Insulin increased: glucose uptake, glucose to form glycerol phosphate, fat storage

Insulin decreased: lypolysis

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19
Q

Factors that stimulate insulin secretion (4)

A
  1. Hyperglycemia
  2. Increased serum levels of FFA, amino acids
  3. GI/digestive hormones
  4. Parasympathetic stimulation of pancreatic beta cells
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20
Q

Factors that inhibit insulin secretion (4)

A
  1. Hypoglycemia
  2. Negative feedback loop: increased insulin levels
  3. Sympathetic stimulation of pancreatic beta cells
  4. Prostaglandins (PGE2)
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21
Q

Excessive insulin levels will _____ the number of insulin receptors.

A

Decrease

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22
Q

In obesity do we see up regulation or down regulation of insulin receptors?

A

Down regulation

Adipose tissue down regulate insulin receptors -> decreased insulin sensitivity

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23
Q

What is the response to decreased insulin sensitivity in response to feeding:

A
  1. Glucose levels remain elevated despite app. release of insulin
  2. Additional insulin is released in attempt to lower blood glucose
  3. Prolonged insulin exposure promotes additional “down-regulation” of receptors
  4. RESULT: insulin resistance progresses –> this is a cycle
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24
Q

What are the 3 “poly’s” of diabetes?

A
  1. Polyuria –> excessive urine production
  2. Polydipsia –> excessive thirst
  3. Polyphagia –> increased appetite
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25
Q

Diabetes Mellitus Type I (insulin dependent)

A

Insulin insufficiency d/t result of pancreatic destruction of beta cells

Antibodies attach beta cells

Not associated w/ obesity

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26
Q

What happens in DM 1? (4 things)

A
  1. Hyperglycemia
    (b/c cells unable to take up glucose)
  2. Hyperlipidemia
  3. Increased ketone bodies/ketoacidosis
  4. Catabolic affect on muscle mass
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27
Q

Hyperlipidemia

–> in DM1

A

Increased lipoproteins in blood

  • Lack of insulin is inhibitory to fat storage
  • Promotes atherosclerotic changes in blood vessels
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28
Q

Describe the catabolic affects on muscle mass seen in DM 1

A

Body attempts to mobilie amino acids for “fuel” when insulin is low which results in muscle wasting, weight loss, and weakness/fatigue

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29
Q

What are 3 causes of insulin shock?

A
  1. Excessive insulin administration
  2. Increased physical activity
  3. Poor glucose monitoring/missed meals
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30
Q

Hypoglycemia produces ____, ______, and _____. (physical symptoms)

A

Hunger
Sweating
Irritability

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31
Q

Prolonged hypoglycemia =

A

diabetic coma/decrease CNS metabolism

Can lead to death

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32
Q

Treatment for insulin shock

A

Administer glucose to restore blood glucose levels

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33
Q

What is the major cause of DM Type 2?

A

Obesity

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34
Q

DM Type 2 is associated with _____ insulin ____.

A

Increased insulin resistance

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35
Q

Inefficient clearance of glucose from blood results in _____ insulin being secreted

A

MORE

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36
Q

How can one improve their diabetes type 2?

A

Diet changes and exercise

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37
Q

GTT stands for:

A

Glucose Tolerance Test

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38
Q

How do you perform a GTT? (steps)

A
  1. Baseline glucose level is established
  2. Administer glucose preparation
  3. Blood drawn in intervals (30 minutes) making sure to draw blood for at least 120 minutes
  4. Read values
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39
Q

Normal GTT values

fasting and 2 hours

A

Fasting: < 110 mg/dl

2 hours: < 140 mg/dl

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40
Q

DM GTT values

fasting and 2 hours

A

Fasting: > 126 mg/dl

2 hours: > 200 mg/dl

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41
Q

3 Hormones of the thyroid gland

A
  1. T4 (thyroxine)
  2. T3 (tri-iodothyronine)
  3. Calcitonin
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41
Q

3 Hormones of the thyroid gland

A
  1. T4 (thyroxine)
  2. T3 (tri-iodothyronine)
  3. Calcitonin
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42
Q

Where are thyroid hormones produced? What is this molecule that they produce?

A

thyroglobulin

produced in follicle cell

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42
Q

Where are thyroid hormones produced? What is this molecule that they produce?

A

thyroglobulin

produced in follicle cell

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43
Q

Describe how T3/T4 is released from the thyroid?

A
  1. TRH hormone released from hypothalamus
  2. Ant. pituitary releases TSH
  3. TSH stimulates endocytosis
  4. Enzymes separate T3/T4 and TGB
  5. T3/T4 diffuse into bloodstream
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44
Q

Stimuli for thyroid hormone release

A
  1. Metabolic demand determines rate
  2. TSH directly controls amt of T3/T4 released
  3. Pregnancy (growth)
  4. Gonadal and adrenocortical steroids (growth)
  5. Extreme cold temp (stress/energy production)
  6. Catecholamines (epi/NE) *stress
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45
Q

Thyroid hormone effects in the heart

A

Increased HR and CO (inotrophic and chronotropic)

Do this by increasing sensitivity to sympathetic system/epi

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46
Q

2 main forms of hyperthyroidism

A
  1. Primary hyperthyroidism

2. Secondary hyperthyroidism

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47
Q

Causes of a thyroid storm (7 causes)

A
  1. Infections, especially lung
  2. Thyroid surgery
  3. Stopping medications for hyperthyroidism
  4. Too high of thyroid dose (hypothyroidism)
  5. Tx w/ radioactive iodine
  6. Pregnancy
  7. Heart attack or other heart emergencies
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48
Q

What is the distinguishing symptom of “thyroid storm”

A

Temperature of 105-106

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49
Q

Iatrogenic hyperthyroidism (cause)

A

Excessive use of synthetic thyroxine

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50
Q 
Lab results of Grave's Dz
TSI
TSH
T3/T4
TRH
A 
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
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51
Q

3 Types of primary hyperthyroidism

A
  1. Endogenous (Grave’s Dz)
  2. Iatrogenic
  3. Thyroid Storm
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52
Q

Thyroid hormone effects in the pituitary gland

A
  1. Inhibits TSH
  2. Stimulate release of GH
  3. Stimulate synthesis of pituitary hormones
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53
Q

Thyroid hormone effects in the GI

A

Maintain secretions of GI tract

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54
Q

Thyroid hormone effects in the liver

A

Promote TG and cholesterol metabolism

Regulate LDL homeostasis

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55
Q

Thyroid hormone effects in bone cells

A

Promote bone growth/devleopment synergistically with IGF-1/growth hormones
–> stimulate osteoblast/osteoclast activity

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56
Q

Thyroid hormone effects in muscle cells

A
  1. Promote muscle protein growth/development synergistically w/ other growth hormones
  2. Excess levels will promote catabolic metabolism of muscle to provide fuel for inc. BMR
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57
Q

Thyroid hormone effects in the CNS

A
  1. Stimulate myelin/axonal growth and development
  2. Stimulate sympathetic activity
    * Overall systemic “overdrive”
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58
Q

Thyroid hormone effects in pulmonary system

A

Stimulates respiration centers in brain to increase ventilation

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59
Q

Thyroid hormone effects in vascular system

A

Decrease peripheral resistance of vascular system

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60
Q

Thyroid hormone effects overall

A
  1. Glycogenolysis
  2. Gluconeogenesis
    - -> amino acids from muscle break down
    - -> lipolyosis
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61
Q

What happens when one is deficient in thyroid function during the perinatal period?

A

Cognitive impairments (CNS doesn’t mature properly)

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62
Q

Describe how thyroid hormones effect growth/development

A

Stimulate GH release, necessary for IGF-1 function

CNS maturation is dependent on thyroid function ….

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63
Q

Describe how thyroid hormones effect basal metabolic rate

A

Increase basal metabolic rate and O2 consumption

Also temp regulation (heat is produced d/t inc. BMR)

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64
Q

Inhibition of thyroid hormone release

A
  1. Negative feedback (serum levels of T3/T4)
  2. GHIH (somatostatin)
  3. Dopamine
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65
Q

What is the eventual fate of rT3 and T3 when they are no longer utilized?

A

Converted to T2, a completely inactive form of thyroid hormone

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66
Q

Where is the primary site of T4 –> T3 conversion?

A

The liver

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67
Q

If T4 is able to enter cell then it follows which 2 pathways?

A
  1. Binds to T4 receptor within cell nucleus

2. Undergo conversion to T3 or rT3 in cell cytoplasm/membrane

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68
Q

__% 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

A

80-90%
“Strong bind”
less

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69
Q

____% 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)

A

10-20%

protein bound

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70
Q

“Biological activity” on target cell of ___ is much greater than ___.

A

T3

T4

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71
Q

Free T3 and T4 are easily excreted by the _____.

A

Kidneys

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72
Q

Does T3/T4 usually circulate freely or bound to a carrier protein? Include percentages

A
  1. 9% bind to carrier protein (TGB, albumin, transthyretin)

0. 03% T4/T3 circulate freely and considered “active”

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73
Q

When iodine binds to the tyrosine/TGB molecule what is this process called?

A

Organification

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74
Q

How much of dietary iodine is “trapped” by the thyroid gland?

A

25%

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75
Q

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

A

T3 is active

T4 is inactive

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75
Q

Proper doses of calcium:

A

500 mg BID (so 1,000) total

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75
Q

What are the differences between calcium carbonate and calcium citrate?

A

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

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75
Q

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

A
  1. Most calcium in glomerular filtrate is reabsorbed

2. Site of “conversion” of inactive vitamin D to active vitamin D (calcitriol)

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75
Q

Medications that impair absorption will ____ calcium secretion.

A

Increase

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75
Q

What are the two functions of bones in relation to calcium?

A
  1. Store calcium

2. Stimuli to increase calcium resorption (for osteoclast activity)

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75
Q

What are the 3 primary regulatory hormones that regulate ECF calcium?

A
  1. Parathyroid hormone (PTH)
  2. Calcitonin
  3. Calcitriol (active form of Vitamin D)
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75
Q

Where are parathyroid hormones synthesized and secreted from?

A

Parathyroid glands

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75
Q

What is the function of PTH?

A

Increase plasma (ECF) calcium levels

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75
Q

What are PTH’s two target tissues?

A

Bone and Kidney

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75
Q

What does an inc in PTH stimulate in the bone?

A
  1. Calcium resorption (stimulates osteocalstic activity)
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75
Q

What does an inc. in PTH stimulate in the kidneys?

A
  1. Stimulates conversion of inactive vitamin D to active (calcitriol)
  2. Converts 1,25 dihydroxyvitamin D
  3. Stimulates calcium resorption in tubules of kidneys
  4. Stimulates phosphate excretion
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75
Q

Stimulus for PTH release

A

Small decreases in plasma calcium

75
Q

Inhibition of PTH release

A

Elevated plasma calcium and elevated calcitriol

negative feedback

75
Q

Scientific (chemical) name for calcitrol

A

1,25-dihydroxyvitamin

75
Q

What environmental exposure is necessary for vitamin D formation? What is another place you can get vitamin D from (not as necessary)

A

SUNLIGHT EXPOSURE!

Vitamin D2 is in eggs, dairy, fish oil, plants

75
Q

Vitamin ___ or ___ are biologically inactive

A

D2 or D3

75
Q

How are D2 and D3 converted to their active form, calcitriol?

A

Many steps in liver and kidney

Final step in kidney by PTH

75
Q

Function of calcitriol?

A

Increase plasma calcium levels

–> also elevates phosphate levels in blood

75
Q

What are the 3 target tissues of calcitriol?

A
  1. Intestine
  2. Bone
  3. Kidney
75
Q

Calcitriol release is stimulated by:

A

Elevated PTH levels

75
Q

Calcitriol is inhibited by?

A

Decreased PTH levels

75
Q

Where is Calcitonin produced/secreted?

A

Parafollicular cells of thyroid gland

75
Q

What is the function of calcitonin?

A 
Decrease plasma (ECF) calcium levels
**Minor role...if not working properly, it doesn't reflect a large change in plasma calcium levels
75
Q

Target tissue of calcitonin and what it does at those tissues

A

Kidney - inhibits calcium resorption by inhibiting osteoclasts
Bone - stimulates calcium and phosphate excretion

75
Q

Calcitonin release stimulated by:

A

Large increases of plasma calcium

75
Q

Calcitonin is inhibited by:

A

Decreased levels of plasma calcium

75
Q

What is a common cause of hyperparathyroidism?

A

Neoplasms secreting PTH

75
Q

What would you see on labs in a pt w/ hyperparathyroidism?

A
  1. Hypercalcemia
  2. Hypercalciuria (calcium in urine)
  3. Hypophosphatemia (low levels of phosphate in blood)
  4. Potentially metabolic acidosis
75
Q

What is the common cause of hypoparathyroidism?

A

Surgical removal or damage

75
Q

Where are T3 and T4 stored?

A

Stored in the colloid

75
Q

Describe how T3/T4 is released from the thyroid?

A
  1. TRH hormone released from hypothalamus
  2. Ant. pituitary releases TSH
  3. TSH stimulates endocytosis
  4. Enzymes separate T3/T4 and TGB
  5. T3/T4 diffuse into bloodstream
75
Q

rT3

A

reverse T3

Inactive form of T3 and usually exits cell

75
Q

Stimuli for thyroid hormone release

A
  1. Metabolic demand determines rate
  2. TSH directly controls amt of T3/T4 released
  3. Pregnancy (growth)
  4. Gonadal and adrenocortical steroids (growth)
  5. Extreme cold temp (stress/energy production)
  6. Catecholamines (epi/NE) *stress
75
Q

2 Main functions/actions of thyroid hormones

A
  1. Necessary for growth/development
  2. Control rate of metabolism
    - -> therefore regulate/influence EVERY ORGAN OF THE BODY
75
Q

Thyroid hormones act on all target tissue except for:

A
  1. Brain
  2. Spleen
  3. Gonads
75
Q

Thyroid hormone effects in the heart

A

Increased HR and CO (inotrophic and chronotropic)

Do this by increasing sensitivity to sympathetic system/epi

75
Q

Thyroid hormone effects in fat cells

A

Increase lipolysis - mobilize FFA for metabolic fuel

75
Q

Symptoms of hyperthyroidism

A

+/- 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)

75
Q

2 main forms of hyperthyroidism

A
  1. Primary hyperthyroidism

2. Secondary hyperthyroidism

75
Q

Cause of Grave’s Dz (primary endogenous hyperthyroidism)

A

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

76
Q

What is the significant effect of hypoparathyroidism?

A

Hypocalcemia

*and hyperphosphatemia

77
Q

3 Hormones of the thyroid gland

A
  1. T4 (thyroxine)
  2. T3 (tri-iodothyronine)
  3. Calcitonin
78
Q

Where are thyroid hormones produced? What is this molecule that they produce?

A

thyroglobulin

produced in follicle cell

79
Q

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

A

T3 is active

T4 is inactive

80
Q

How much of dietary iodine is “trapped” by the thyroid gland?

A

25%

81
Q

When iodine binds to the tyrosine/TGB molecule what is this process called?

A

Organification

82
Q

Where are T3 and T4 stored?

A

Stored in the colloid

83
Q

Describe how T3/T4 is released from the thyroid?

A
  1. TRH hormone released from hypothalamus
  2. Ant. pituitary releases TSH
  3. TSH stimulates endocytosis
  4. Enzymes separate T3/T4 and TGB
  5. T3/T4 diffuse into bloodstream
84
Q

Does T3/T4 usually circulate freely or bound to a carrier protein? Include percentages

A
  1. 9% bind to carrier protein (TGB, albumin, transthyretin)

0. 03% T4/T3 circulate freely and considered “active”

85
Q

Free T3 and T4 are easily excreted by the _____.

A

Kidneys

86
Q

“Biological activity” on target cell of ___ is much greater than ___.

A

T3

T4

87
Q

____% 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)

A

10-20%

protein bound

88
Q

__% 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

A

80-90%
“Strong bind”
less

89
Q

If T4 is able to enter cell then it follows which 2 pathways?

A
  1. Binds to T4 receptor within cell nucleus

2. Undergo conversion to T3 or rT3 in cell cytoplasm/membrane

90
Q

rT3

A

reverse T3

Inactive form of T3 and usually exits cell

91
Q

Where is the primary site of T4 –> T3 conversion?

A

The liver

92
Q

What is the eventual fate of rT3 and T3 when they are no longer utilized?

A

Converted to T2, a completely inactive form of thyroid hormone

93
Q

Stimuli for thyroid hormone release

A
  1. Metabolic demand determines rate
  2. TSH directly controls amt of T3/T4 released
  3. Pregnancy (growth)
  4. Gonadal and adrenocortical steroids (growth)
  5. Extreme cold temp (stress/energy production)
  6. Catecholamines (epi/NE) *stress
94
Q

Inhibition of thyroid hormone release

A
  1. Negative feedback (serum levels of T3/T4)
  2. GHIH (somatostatin)
  3. Dopamine
95
Q

2 Main functions/actions of thyroid hormones

A
  1. Necessary for growth/development
  2. Control rate of metabolism
    - -> therefore regulate/influence EVERY ORGAN OF THE BODY
96
Q

Describe how thyroid hormones effect basal metabolic rate

A

Increase basal metabolic rate and O2 consumption

Also temp regulation (heat is produced d/t inc. BMR)

97
Q

Describe how thyroid hormones effect growth/development

A

Stimulate GH release, necessary for IGF-1 function

CNS maturation is dependent on thyroid function ….

98
Q

What happens when one is deficient in thyroid function during the perinatal period?

A

Cognitive impairments (CNS doesn’t mature properly)

99
Q

Thyroid hormones act on all target tissue except for:

A
  1. Brain
  2. Spleen
  3. Gonads
100
Q

Thyroid hormone effects overall

A
  1. Glycogenolysis
  2. Gluconeogenesis
    - -> amino acids from muscle break down
    - -> lipolyosis
101
Q

Thyroid hormone effects in the heart

A

Increased HR and CO (inotrophic and chronotropic)

Do this by increasing sensitivity to sympathetic system/epi

102
Q

Thyroid hormone effects in vascular system

A

Decrease peripheral resistance of vascular system

103
Q

Thyroid hormone effects in pulmonary system

A

Stimulates respiration centers in brain to increase ventilation

104
Q

Thyroid hormone effects in the CNS

A
  1. Stimulate myelin/axonal growth and development
  2. Stimulate sympathetic activity
    * Overall systemic “overdrive”
105
Q

Thyroid hormone effects in fat cells

A

Increase lipolysis - mobilize FFA for metabolic fuel

106
Q

Thyroid hormone effects in muscle cells

A
  1. Promote muscle protein growth/development synergistically w/ other growth hormones
  2. Excess levels will promote catabolic metabolism of muscle to provide fuel for inc. BMR
107
Q

Thyroid hormone effects in bone cells

A

Promote bone growth/devleopment synergistically with IGF-1/growth hormones
–> stimulate osteoblast/osteoclast activity

108
Q

Thyroid hormone effects in the liver

A

Promote TG and cholesterol metabolism

Regulate LDL homeostasis

109
Q

Thyroid hormone effects in the GI

A

Maintain secretions of GI tract

110
Q

Thyroid hormone effects in the pituitary gland

A
  1. Inhibits TSH
  2. Stimulate release of GH
  3. Stimulate synthesis of pituitary hormones
111
Q

Symptoms of hyperthyroidism

A

+/- 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)

112
Q

2 main forms of hyperthyroidism

A
  1. Primary hyperthyroidism

2. Secondary hyperthyroidism

113
Q

3 Types of primary hyperthyroidism

A
  1. Endogenous (Grave’s Dz)
  2. Iatrogenic
  3. Thyroid Storm
114
Q

Cause of Grave’s Dz (primary endogenous hyperthyroidism)

A

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

115
Q 
Lab results of Grave's Dz
TSI
TSH
T3/T4
TRH
A 
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
116
Q

Iatrogenic hyperthyroidism (cause)

A

Excessive use of synthetic thyroxine

117
Q

What is the distinguishing symptom of “thyroid storm”

A

Temperature of 105-106

118
Q

Causes of a thyroid storm (7 causes)

A
  1. Infections, especially lung
  2. Thyroid surgery
  3. Stopping medications for hyperthyroidism
  4. Too high of thyroid dose (hypothyroidism)
  5. Tx w/ radioactive iodine
  6. Pregnancy
  7. Heart attack or other heart emergencies
119
Q

What is a cause of secondary hyperthyroidism?

A

TSH secreting adenomas (rare)

120
Q 
What does lab work look like with secondary hyperthyroidism?
TSI
TSH
T3/T4
TRH
A

TSI: normal
TSH: elevated
T3/T4: elevated
TRH: decreased

121
Q

What are the differences between primary and secondary hyperthyroidism in terms of labs

A

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

122
Q

Hypothyroidism can be ____ ____ or ______.

A

Adult-onset

Congenital

123
Q

Symptoms of adult onset hypothyroidism

A

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

124
Q

What is myxedema

A

Puffy appearance of face, hands, feet

Enlarged tongue d/t deposits in oral cavity

125
Q

What causes puffy appearance in hypothyroidism?

A

Muccopolysaccharides attract water in skin/connective tissue

126
Q

What are the different symptoms of congenital hypothyroidism?

A

Same as adult-onset but usually include in addition to those:

  1. Cognitive impairment
  2. Gross dwarfism
127
Q

What is congenital hypothyroidism also called?

A

Cretinism

128
Q

What are some early detection signs that would cause a provider to screen for hypothyroidism?

A

High birth weight
Hypothermia
Jaundice

129
Q

Hashimoto’s Thyroiditis (autoimmune)

A

Primary adult onset

Gradual destruction of functional thyroid tissue

130
Q

What do the labs look like in Hashimoto’s Thyroiditis

A

TSH: elevated (d/t low circulating T3/T4)

T3/T4: low

131
Q

What do labs look like in secondary hypothyroidism?

A

ALL ARE LOW
TSH: low
(d/t ant. pituitary damage)

T3/T4: low

*Disfunctional feedback response

132
Q

How do goiters usually come about?

A

D/t elevated TSH levels trying to stimulate the thyroid gland

133
Q

In which instances is TSH elevated and you might see a goiter? (2)

A
  1. Puberty

2. Pregnancy

134
Q

Do goiters predict whether thyroid function is normal, elevated, or diminished?

A

NO!!

135
Q

What is the cause of a goiter in Grave’s Dz?

A

D/t TSI stimulating thyroid gland to produce T3/T4

136
Q

What is the cause of a goiter in Hashimoto’s?

A

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

137
Q

What is the cause of a goiter in Iodine deficiency?

A

D/t elevated TSH trying to stimulate thyroid to produce T3/T4

138
Q

Functions of calcium (HINT: 8)

A
  1. Mineralization of bone matrix
  2. Formation of bone and teeth
  3. Maintain membrane permeability
  4. Maintain excitability of nerve and muscle
  5. Release neurotransmitters
  6. Muscle contractions
  7. Coagulation of blood
  8. Milk production
139
Q

Where is the majority of calcium stored?

A

98-99% in bone

  • -> 99% of that is in mineralized form
  • -> 1% in a pool ready to go into blood stream
140
Q

Percentage of calcium in “free” form, bound to protein, and bound to phosphate in the extracellular fluid

A

50% in free form
45% bound to protein
5% bound to phosphate/citrate

141
Q

The very small amount of intracellular calcium is responsible for: (3 things)

A
  1. Intracellular signaling
  2. Enzyme secretion
  3. Muscle contraction
142
Q

What are normal serum calcium values?

A

8-10 mg/dl

143
Q

What are hypercalcemia leves? (mild, mod, severe)

A

Hypercalcemia: >10.5 mg/dl

Mild: 10.5-11.9 mg/dl
Moderate: 12- 13.9 mg/dl
Severe “crisis”: 14-16 mg/dl

144
Q

Contrast calcium homeostasis with calcium balance?

A

Calcium homeostasis is short-term equilibrium while calcium balance is a long term maintenance of bone density.

145
Q

The ECF is maintained through calcium exchange between three organs:

A

GI tract
Kidneys
Bone

146
Q

What are the 2 forms of calcium supplementation?

A
  1. Calcium carbonate

2. Calcium citrate

147
Q

% of calcium absorption in ____ related to the amount of calcium injested at one time

A

Inversly

148
Q

Proper doses of calcium:

A

500 mg BID (so 1,000) total

149
Q

What are the differences between calcium carbonate and calcium citrate?

A

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

150
Q

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

A
  1. Most calcium in glomerular filtrate is reabsorbed

2. Site of “conversion” of inactive vitamin D to active vitamin D (calcitriol)

151
Q

Medications that impair absorption will ____ calcium secretion.

A

Increase

152
Q

What are the two functions of bones in relation to calcium?

A
  1. Store calcium

2. Stimuli to increase calcium resorption (for osteoclast activity)

153
Q

What are the 3 primary regulatory hormones that regulate ECF calcium?

A
  1. Parathyroid hormone (PTH)
  2. Calcitonin
  3. Calcitriol (active form of Vitamin D)
154
Q

What are the 3 secondary regulatory hormones that regulate ECF calcium?

A
  1. GH
  2. Thyroid hormones
  3. Adrenal/gonadal steroid hormones
155
Q

Where are parathyroid hormones synthesized and secreted from?

A

Parathyroid glands

156
Q

What is the function of PTH?

A

Increase plasma (ECF) calcium levels

157
Q

What are PTH’s two target tissues?

A

Bone and Kidney

158
Q

What does an inc in PTH stimulate in the bone?

A
  1. Calcium resorption (stimulates osteocalstic activity)
159
Q

What does an inc. in PTH stimulate in the kidneys?

A
  1. Stimulates conversion of inactive vitamin D to active (calcitriol)
  2. Converts 1,25 dihydroxyvitamin D
  3. Stimulates calcium resorption in tubules of kidneys
  4. Stimulates phosphate excretion
160
Q

Stimulus for PTH release

A

Small decreases in plasma calcium

161
Q

Inhibition of PTH release

A

Elevated plasma calcium and elevated calcitriol

negative feedback

162
Q

Scientific (chemical) name for calcitrol

A

1,25-dihydroxyvitamin

163
Q

What environmental exposure is necessary for vitamin D formation? What is another place you can get vitamin D from (not as necessary)

A

SUNLIGHT EXPOSURE!

Vitamin D2 is in eggs, dairy, fish oil, plants

164
Q

Vitamin ___ or ___ are biologically inactive

A

D2 or D3

165
Q

How are D2 and D3 converted to their active form, calcitriol?

A

Many steps in liver and kidney

Final step in kidney by PTH

166
Q

Function of calcitriol?

A

Increase plasma calcium levels

–> also elevates phosphate levels in blood

167
Q

What are the 3 target tissues of calcitriol?

A
  1. Intestine
  2. Bone
  3. Kidney
168
Q

Calcitriol release is stimulated by:

A

Elevated PTH levels

169
Q

Calcitriol is inhibited by?

A

Decreased PTH levels

170
Q

Where is Calcitonin produced/secreted?

A

Parafollicular cells of thyroid gland

171
Q

What is the function of calcitonin?

A 
Decrease plasma (ECF) calcium levels
**Minor role...if not working properly, it doesn't reflect a large change in plasma calcium levels
172
Q

Target tissue of calcitonin and what it does at those tissues

A

Kidney - inhibits calcium resorption by inhibiting osteoclasts
Bone - stimulates calcium and phosphate excretion

173
Q

Calcitonin release stimulated by:

A

Large increases of plasma calcium

174
Q

Calcitonin is inhibited by:

A

Decreased levels of plasma calcium

175
Q

What is a common cause of hyperparathyroidism?

A

Neoplasms secreting PTH

176
Q

What are some symptoms of hyperparathyroidism?

A

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
177
Q

What would you see on labs in a pt w/ hyperparathyroidism?

A
  1. Hypercalcemia
  2. Hypercalciuria (calcium in urine)
  3. Hypophosphatemia (low levels of phosphate in blood)
  4. Potentially metabolic acidosis
178
Q

What is the common cause of hypoparathyroidism?

A

Surgical removal or damage

179
Q

What is the significant effect of hypoparathyroidism?

A

Hypocalcemia

*and hyperphosphatemia

180
Q

Symptoms of hypoparathyroidism

A
  1. Neuromuscular excitability
  2. Muscle spasms, tetany
  3. Cardiac dysfunction

Pathophysiology (12 decks)

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