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Nursing Year One > Phys II- Endocrine II > Flashcards

Phys II- Endocrine II Flashcards

1
Q

Follicular Cells

A
  • functional unit of thyroid

- lumen filled with colloid (stores TH)

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2
Q

Describe TH

A
  • T4 (thyroxine) or T3
  • made of tyrosine (made by body) and iodine (from diet), amine
  • lipophilic
  • tropic
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3
Q

C Cells

A
  • secrete calcitonin

- peptide hormone

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4
Q

TH Synthesis (4 steps)

A
  1. thyroglobulin uses exocytosis to move from follicular cells to colloid)
  2. Iodine to colloid from blood via pump
  3. Iodine attaches to tyrosine
  4. iodinated tyrosine molecules couple up to form TH
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5
Q

TH Storage

A
  • in colloid until secretion

- usually enough for several months

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6
Q

TH Secretion

A
  1. follicular cells phagocytize thyroglobulin colloid

2. T3 and T4 are now free to diffuse across plasma mem into blood using plasma protein (thyroxine-binding globulin)

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7
Q

Is T3 or T4 more potent? How much?

A

T3 (4x)

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8
Q

How is TH used?

A
  • target cells cleave iodine
  • liver/kidney
  • long term but slow acting
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9
Q

3 Effects of TH

A
  1. Metabolic
  2. Permissive
  3. Developmental
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10
Q

Metabolic Effects of TH

A
  • basal metabolic rate
  • stimulates Na/K+
  • heat generation
  • calorigenic
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11
Q

Permissive Effects of TH

A
  • works w SNS
  • increase target cells responsiveness toE and NE
  • increase HR and force by increasing beta-adrenoreceptors on heart
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12
Q

Developmental Effects of TH

A
  • normal NS development
  • essential for normal growth
  • stimulates release of GH
  • stimulates IGF-1 production
  • enhances effect of GH and IGF-1
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13
Q

Congenital Hypothyroidism

A
  • absence of TH in fetus

- poorly developed NS (compromised intellectual function)

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14
Q

What is the one condition resulting from hypothyroidism?

A

atrophy

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15
Q

What are the three conditions resulting from hyperthyroidism?

A
  1. Hypertrophy
  2. Hyperplasia
  3. Goiter
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16
Q

Hyperthyroidism

A
  • primary failure of thyroid
  • secondary to deficiency of TRH, TSH or both
  • too much iodine in diet
  • low TSH in blood
  • high T4/T3 in blood
  • often caused by Graves (autoimmune)
  • often goiter present
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17
Q

Cretinism

A

hyperthyroidism at birth causing CNS effects

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18
Q

How is Hyperthyroidism treated?

A
  • surgical removal
  • radioactive iodine
  • antithyroid
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19
Q

Symptoms of Hyperthyroidism

A
  • weight loss
  • heat intolerance
  • increased appetite
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20
Q

Hypothyroidism

A
  • high TSH

- low T4 and T3

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21
Q

Symptoms of Hypothyroidism

A
  • weight gain
  • cold sensitivity
  • fatigue
  • slow weak pulse
  • impaired mental function
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22
Q

Treatment of Hypothyroidism

A
  • replacement therapy

- dietary iodine

23
Q

Myxedema

A
  • hypothyroidism in adults
  • edema
  • sugar related
24
Q

Goiters

A
  • over stimulated thyroid
  • mostly hypo but can be hyper
  • treat with exogenous TH or dietary Iodine
25
Q

Grave’s Disease

A
  • improper TSI production
  • goiter
  • decreased TSH in blood
26
Q

Adrenal Medulla

A
  • inner

- E , NE

27
Q

Adrenal Cortex

A
  • outer

- steroid hormones (cholesterol)

28
Q

Three Divisions of the Adrenal Cortex

A
  1. Zona Glomerulosa
  2. Zona Fasciculata
  3. Zona Reticularis
29
Q

Zona Glomerulosa

A
  • outer

- aldosterone

30
Q

Zona Fasciculata

A
  • middle/largest
  • cortisol
  • DHEA
31
Q

Zona Reticularis

A
  • innermost
  • DHEA
  • cortisol
32
Q
  1. DHEA
  2. Cortisol
  3. Aldosterone
    Triggers…
A
  1. albumin
  2. corticosteroid-binding globulin
  3. albumin
33
Q

Three Adrenal Steroids

A
  1. Mineralcorticoids
  2. Gluticocorticoids
  3. Sex Hormones
34
Q
  1. What are Mineralcorticoids?
  2. What do they do?
  3. What happens when they are lacking?
  4. What stimulates their release?
A
    • aldosterone
    • influence NA+/K+ balance
    • action site on distal and collecting tubules of kidney
    • decreases Na+,
    • increases plasma K+
    • lowers BP
    • independent of ant pit 3.
    • w/o aldosterone you die within 2 days from shock
    • secretion increased by renin-angiotensin-aldosterone system
35
Q

Hypersecretion of Mineralcorticoids

A
  • adrenal tumor
  • chron’s
  • inipropriate increased activity of renin-angio… (secondary hypersecretion)
  • excessive Na+ retention or K+ depletion
  • high BP
36
Q
  1. What are Gluticocorticoids?
  2. What do they do?
  3. How are they regulated?
A
    • cortisol
    • glucose, lipid&protein metabolism
    • stimulates hepatic gluconeogenesis (glucose from non-carb)
    • inhibits glucose uptake
    • increase plasma glucose
    • stimulates protein degeneration (esp. in muscles)
    • lipolysis
    • adaptation to stress
    • anti-inflammatory
    • immunosupressive
    • diurnal rhythm (increased when awake)
    • negative feedback (CRH, ACTH)
37
Q

What organ does Gluticocorticoids not effec t?

A

brain

38
Q

What can supplementary gluticocorticoids be used to treat?

A
  1. inflammatory conditions

2. transplants

39
Q

Describe the Tropic Effects of Cortisol

A
  • permissive
  • permit (E) to induce vasoconstriction
  • prevents circulatory shock in stress
40
Q

Hyper-secretion of Cortisol

A
  • overstimulation of adrenal cortex by CRH, ACTH

- tumors

41
Q

Cushing’s

A
  • hyper-secretion of cortisol
  • buffalo hump
  • moon face
  • skinny arms and legs
  • thin/brittle skin
  • muscle weakness
  • immunosupressin
  • osteoperosis
  • striations
  • hyperglycemia
  • hypertension
  • adrenalectomy needed
42
Q

Sex Hormones

A
  • identical/similarf to gonad hormone s
  • DHEA
  • ACTH NOT FSH or LH
  • overpowered by testosterone
  • responsible for hair in women, growth spurt, and development/maintenance of sex drive
43
Q

DHEA Hyper-Secretion

A
  • Arenogenital Syndrome
  • male-like body hair
  • deepening of voice
  • muscular arms and legs
  • small breasts
  • no menstruation
  • cortisol insufficiency increases ACTH therefore DHEA
  • inhibits gonadotropins making women sterile
  • treated with glucorticoid therapy
44
Q

DHEA Hyper-secretion in newborn females

A
  • male external genetalia
45
Q

DHEA Hyper-Secretion in Pre-Pubertal Males

A
  • prepubertal males (pseudopuberty)
46
Q

The Adrenal Medulla can be described as…

A
  • modified SNS
47
Q

Epinephrine

A
  • fight or flight
  • helps SNS
  • maintenance of BP
  • increases blood glucose
  • increases blood fatty acids
  • gluconeogenesis (liver)
  • glycogenolysis (liver/ skeletal muscles)
  • inhibits insulin
  • increased glucagon secretion
48
Q

Stress and Hormones

A
  • coordinated by hypothalamus
  • activates SNS (and E)
  • activates CRH-ACTH-cortisol system
  • increase blood glucose and fatty acids
  • decreases insulin
  • increases glucagon
  • increases RAAS
  • increases vasopressin
  • no effect on BP or blood volume
  • ACTH helps with learning and behaviour
49
Q

Anabolism

A
  • build up/synthesis of larger macromolecules from smaller subunits
  • require ATP
  • excess stored for later
50
Q

Catabolism

A
  • breakdown of large energy rich molecules
    1. hydrolysis of larger into smaller
    2. oxidation of smaller to yield energy for ATP
51
Q

Pancreatic Hormones (from Islets of Langerhans)

A
  1. Beta- Cells
    • insulin
  2. Alpha-Cells
    • glucagon
  3. PP Cells
    • pancreatic polypeptide
52
Q

Insulin

A
  • anabolic
  • uptake of glucose (glycogen), fatty acids(triglycerides) , AA (proteins)
  • secretion increases in absorptive state
  • stimulated by blood glucose
53
Q

Diabetes Mellitus

A
  • increased blood glucose
  • glucose in urine
  • Type 1 (10%)- lack of secretion
  • Type 2 (90%)- reduced sensitivity in target cells, more insulin than normal
54
Q

Polyuria

A

extra glucose not reabsorbed by nephron is secreted and water is secreted as well (osmotic diuresis), sweet urine

Nursing Year One (31 decks)

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