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Physiology Exam III > Endocrine + Bone > Flashcards

Endocrine + Bone Flashcards

1
Q

What are the functions of the thyroid gland?

A
  • secrete thyroid hormone from follicle cells (metabolism)

- secrete calcitonin from parafollicular cells (regulate circulating Ca2+)

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2
Q

Is the thyroid gland highly vascularized or barely vascularized?

A

highly!

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3
Q

How are thyroid hormones produced?

A
  • iodine from diet attaches to tyrosine to form MIT or DIT
  • T3 = MIT + DIT
  • T4 = DIT + DIT
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4
Q

Is more T3 or T4 produced in the thyroid gland? Why?

A
  • more T4 is made

- only small amount of free hormone –> pituitary respond to and regulates free hormone

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5
Q

What form is of thyroid hormone is T3? T4?

A

T3 = active form

T4 = storage form (can be converted to T3)

both are mainly bound to plasma proteins (TBG - thyroxin binding globulin)

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6
Q

What is TRH (thyrotropin releasing hormone)?

A
  • regulates thyroid via endocrine feedback loop
  • released from hypothalamus –> blood –> pituitary
  • increased activity of transporters –> increases iodine –> increased production of T3/T4 (determined by TSH release)
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7
Q

What is hyperthyroidism?

A
  • body wasting, nervousness, tachy, tremor, ++ heat production, high BMR, affects reflexes and brain development
  • TSH is low
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8
Q

What is hypothyroidism?

A
  • fetal/neonatal: mental retardation, dwarfism, short limbs (tx at birth has good prognosis)
  • adult: mental + physical slowing, poor resistance to cold myxedema, low BMR
  • TSH is high
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9
Q

What is the relationship between TSH and thyroid hormone?

A
  • decreased free TH (increased binding hormones) –> increases production of TSH –> increases TH production until levels return to normal
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10
Q

What are deiodinase isozymes?

A
  • cause deiodination (require selenium)
  • D1 converts T4 to T3 in the liver, kidney, and thyroid (most important)
  • D2 converts T4 to T3 in the brain, pituitary, brown fat, heart, skeletal muscle
  • D3 converts T4 to rT3 in the placenta, skin, brain
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11
Q

What cellular affect does thyroid hormone have?

A
  1. T3/T4 enters nucleus
  2. Binds to TH-receptor
  3. CoActivators are recruited to T3-bound TH-R
  4. Gene expression is altered (silenced)
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12
Q

Why is T3 the favorite child?

A
  • 4x more biologically potent than that weakling T4

- 10x greater affinity for receptors than T4

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13
Q

What causes hypothyroidism?

A
  • primary (problem w/thyroid): thyroid ds, lack of thyroid, Hasimotos (autoimmune destruction)
  • secondary (problem w/TSH): anterior pituitary d/o, hypothalamus d/o
  • iodine deficiency (decreases TH, increases TSH –> gland hypertrophies –> goiter)
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14
Q

What causes hyperthyroidism?

A
  • Graves’ (most common): antibodies stimulate TSH receptor –> excess T3/T4 –> goiter
  • Solitary adenoma (lg amts of TH)
  • Hashimotos in early stages (increased TH secretion)
  • TSH-secreting pituitary tumor
  • mutations causing activation of TSH receptor
  • administration of T3/T4
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15
Q

What other parts of the body does thyroid hormone affect?

A
  • adipose tissue (stims lipolysis)
  • heart (chrono/inotropic)
  • muscle (inc protein breakdown)
  • bone (+ growth + skel dvlpt)
  • NS (+ brain dvlpt)
  • gut (inc carb absoprtion)
  • metabolic (inc met rate, stim O2 consumption by metabolically active tissues)
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16
Q

How does bone growth occur?

A
  • new bone forms at end of shaft to increase length
  • exceptions: mesenchymal cells form bone directly in clavicles, mandibles, certain skull bones
  • growth stops when epiphyses unit w/shaft + form epiphysial closure (cartilage cells stop proliferating)
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17
Q

How is bone balanced?

A
  • bone growth ends at puberty but bone is still dynamic (10y turnover)
  • in a healthy person, resorption = formation
  • -> PTH inc remodeling, estrogen dec resoption
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18
Q

What is PTH?

A
  • parathyroid hormone

- increases Ca2+ resorption, decreases phosphate reabsorption

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19
Q

What is PTHrP?

A
  • parathyroid related protein
  • binds to same receptor as PTH - acts as a paracrine factor
  • proper eruption of teeth
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20
Q

What is the role of Vitamin D on Ca2+?

A
  • inc retention in kidney
  • inc uptake in gut
  • stims osteoblast production in bone –> stims osteoclasts –> Ca2+ resorption
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21
Q

What is calcitonin?

A

decreases Ca2+ retention (opposes osteoclasts –> dec plasma Ca2+) by inhibiting absorption in gut, inhib osteoclasts + stimulating osteoblasts, + inhibiting renal tubule reabsorption (excrete Ca2+)

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22
Q

How does estrogen affect bones?

A
  • normally inhibits osteoclast development indirectly (inhibs IL-1, IL-6, TNFa)
  • after menopause –> deficiency causes bone loss
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23
Q

Where is calcium found?

A
  • mainly in bone (stable)
  • small amount exchangeable
  • binding is proportional to plasma level
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24
Q

What causes hypercalcemia?

A
  • hyperparathyroidism, cancer

- leads to anorexia, NV, depression, coma, constipation

25
Q

What causes hypocalcemia?

A
  • hypoparathyroidism, VitD deficiency, kidney ds, malabsorption
26
Q

What happens when plasma Ca2+ is low?

A
  1. Inc PTH secretion –> inc plasma PTH
    2a. Kidneys increases Ca2+ reabsorption (decrease urinary excretion) + increase vitD (–> intestines increase Ca2+ absorption)
    2b. Bone increases resorption (–> increased Ca2+ release into plasma)
  2. Restoration of plasma Ca2+ to normal
27
Q

What is osteoporosis?

A
  • abnormal loss of bone (remaining bone is intact)
  • excess osteoclast activity
  • -> fractures, widow’s hump
28
Q

What is osteopetrosis?

A
  • abnormal hardening of bone
  • d/t defective osteoclasts (unopposed actions of osteoblasts)
  • hematologic abnormalities
  • -> dense, thick bones
29
Q

What is osteomalacia?

A
  • abn bone frmn d/t inadequate mineralization in adults + growth plates closed (Rickets) in kids > vit D deficiency
  • -> weakness of wt-brg bones, dental defects, hypoclacelmia, bow-legged
30
Q

What is Paget’s Disease?

A
  • abn bone remodeling d/t uncontrolled/abn osteoclast

- -> deformity, fractures

31
Q

What are the functions of the endocrine system?

A
  • energy balance
  • metabolic rate (storage + brkdn of metabolites)
  • homeostasis (blood vol, osmolarity, glc, electrolytes)
  • reproduction
  • G&D
  • environmental adaptation (temp, stress)
32
Q

What are the two types of hormones in the endocrine system?

A
  • proteins (AA derivatives): ACTH, insulin, GH, glucagon, LH, FSH, TSH, HCG, T3, T4, epi
  • steroids (cholesterol derivatives): glucocorticoids, androgens, estrogens
33
Q

What does the anterior pituitary do?

A

Secretes:

  • ACTH
  • LH
  • FSH
  • estrogen + progesterone
  • testosterone
  • tSH
  • prolactin
  • GH
34
Q

What is panhyperpituitarism?

A

excess of all anterior pituitary hormones:

  • amenorrhea (prolactin)
  • hyperthyroidism (TSH)
  • gigantism (GH)
  • infertility (LH + FSH)
35
Q

What is panhypopituitarism?

A

deficiency of all anterior pituitary hormones:

  • no lactation (prolactin)
  • dwarfism (GH)
  • hypothyroidism (TSH)
36
Q

What does the Posterior Pituitary do?

A
  • paraventricular + supraoptic nuclei: vasopressin/ADH, oxytocin (pregnancy, lactation)
37
Q

What’s the deal with growth hormone (GH)?

A
  • produced in anterior pituitary
  • trophic hormone (stimulates liver to release IGF-1)
  • highest lvls during sleep
  • release is pulsatile
  • stimulated by low blood glc, arginine, catecholamines, CHRH
  • Inhibited by glc, IGF-1
38
Q

What are some causes of dwarfism?

A
  • GH insensitivity
  • pygmies (normal GH but can’t produce IGF-1)
  • GH deficiency (hypopituitary dwarfism)
39
Q

What happens in GH excess?

A

(usually d/t GH-secreting adenoma)

  • gigantism (adenoma before puberty)
  • acromegaly (adenoma after puberty –> over stimulated bone of soft tissues)
40
Q

What type of cells are found in the endocrine pancreas?

A
  • alpha cella (secrete glucagon)
  • beta cells (secrete insulin, GABA, PTHrP)
  • delta cells (secrete somatostatin)
  • F type cells (secrete pancreatic polypeptide - PP)
41
Q

What is the purpose of insulin?

A
  • fuel storage

- decreases blood sugar

42
Q

How is insulin released?

A

pancreatic beta cell have glc sensors –> release insulin when glc is high:

  1. Glc is transported into cell via GLUT1 transporter
  2. Glc metabolized into brkdn products + ATP
  3. ATP causes closure of K channels –> cell deps
  4. Dep causes opening of Ca channels –> ca influx into cell
  5. Ca influx causes insulin vesicles to fuse to membrane + exocytose
  6. Insulin travels to liver, muscle/fat (via systemic circulation)
43
Q

What stimulates insulin release?

A
  • nutrients (oral glc)
  • hormones (incretins, glucagon, secretin)
  • parasym stimulation (Epi B2 receptors)
44
Q

What inhibits insulin?

A
  • insulin (negative feedback)

- sympathetic (NE, Epi a2 receptors)

45
Q

What effect does insulin have on receptors?

A

(autophosphorylation)

  • (acute) translocation of GLUT4 transporter to cm –> insulin enter cell –> glc moves into cell –> dec in plasma glc
  • (longer) enzyme phosphorylation cascades: activation/inhibition of metabolism, activation of lipid signaling, altered gene expression (gene transcriptase + prot synthesis)
46
Q

What does insulin inhibit in cellular glucose pathways?

A
  • glycogenolysis (breakdown of glycogen into glc)
  • gluconeogenesis (formation of new glc)
  • -> no more glc
47
Q

What does insulin stimulate in cellular glucose pathways?

A
  • glycogenesis (storage of glc as glycogen)
  • glycolysis (breakdown of glc)
  • glucose uptake
  • -> less glc, more glycogen
48
Q

What are normal fasting glc levels?

A

3.5-5.5 mM/L

70-99 mg/dL

49
Q

What are DM glc fasting levels?

A

> 7mM/L

>126mg/dL

50
Q

What’s bad about hypoglycemia?

A

pathological –> sympathetic CNS sx (confusion, HA, lethargy, seizures, coma)

51
Q

What’s bag about hyperglycemia?

A
  • pathological –> polydipsia, polyurea, dehydration, fatigue, blured vision, nausea, dKA, Kussmail hyperventilation, arrhythmia, stupor, coma
  • chronic: poor healing, atherosclerosis, blindness, kidney failure, amputations, heart disease
52
Q

What is Type I DM?

A
  • congenital: absent/impaired insulin secretion
  • onset <20yo
  • caused by beta cell antibodies
  • tx: intensive insulin tx
53
Q

What is Type II DM?

A
  • acquired (obesity): progressively impaired insulin secretion
  • onset usually >30yo
  • caused by insulin resistance that progresses to beta cell failure
  • tx w/diet/exercise, oral/injected agents, insulin
54
Q

What occurs in insulin resistance?

A

decreased insulin receptors

increased blood glc levels

55
Q

What occurs in a lack of insulin?

A

increased blood glc, fa (ketoacids), and aa levels

acid/base imbalance
HoTN

56
Q

What stimulates glucagon production?

A
  • hypoglycemia

glucagon fcns to increase blood glc

57
Q

What inhibits glucagon production?

A
  • increased glc

- insulin

58
Q

What does glucagon do?

A
  • increases glc, FA, ketoacids
  • increases glycogenolysis
  • increases gluconeogenesis
59
Q

What modulates appetite?

A
  • increases: ghrelin, opiods

- decreases: leptin, insulin, glucagon, histamine, serotonin

Physiology Exam III (3 decks)

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