Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physio Test 4 > Endocrine Day 5- Adrenal and Ca > Flashcards

Endocrine Day 5- Adrenal and Ca Flashcards

1
Q

What is the master stress hormone of the body?

Where is it released from?

What does it stimulate?

A
  • CRH= master sex hormone
  • Released from PARAventricular nucleus
  • Stimulates corticotrophs to release ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is effect of ACTH?

A
  • ACTH causes adrenal cortex to release hormones
    • cortisol (type of glucosteroid)
    • aldosterone (mineralocorticoid)
      • allows us to increase Na/h2o reabsorption from tubule
      • cortisol can also act like aldosterone at kidney, causing increase H2O/Na reabsorption
    • androgen precursor
    • angiotensin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is ACTH?

A
  • Adrenocorticotropic Hormone derived from precursor pro-opiomelanocortin (POMC) from pit corticotroph cells by enzymatic clevage of precursor products
  • POMC–> ACTH intermediate–> ACTH
    • ACTH can be further cleaved into MSH and CLIP (only mention MSH)
  • MSH can cause increase melanin release by bindign to melanin receptors
    • ACTH is very similar to MSH so it can also bind to receptors in very high concentrations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the cellular zones of the adrenal cortex?

A
  • C=connective tissue capsule
  • ZG=zona glomerulosa produces aldosterone (mineralocorticoids)
  • ZF=zona fasciculata produces cortisol (glucocorticoids)
  • ZR=zona reticularis produces adrenal androgens
  • M=adrenal medulla produces norepi and epi (most central area)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are 2 major enzymes involved in synthesis of cortisol, aldosterones, and androgens by the cortex? What can happen if you’re deficient in either enzyme?

A
  • Two major enzymes
    • 21 alpha hydroxylase
    • 11 beta hydroxylase
  • If deficient in either enzyme, won’t be able to make mineralocorticoids (aldosterone) or glucocorticoids (cortisol)
  • This will force the pathway into andonergic pathway, causing increase in systemic androgens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can stimulate ACTH secretion (also increase CRH)

A
  • Cortisol decrease
    • adrenalectomy
  • sleep-wake transition- need cortisol to get out of bed
  • stress
    • hypoglycemia
    • anesthesia
    • sx- contributing factor to puffiness post op is excess cortisol
    • trauma
    • infection
    • pyrogens
  • Psych disturbance- both anxiety/depression can increase cortisol and incrase cortisol can cause anxiety/depression
    • anxiety
    • depression
  • alpha agonists- NE/E incrase cortisol
  • beta adrenergic antagonist
  • serotnin
  • ADH- stress hormone
    • causes constriction of vessels, raising BP
    • corticotorphs also have ADH receptors
  • gaba
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What inhibits ACTH secretion?

A

Cortisol increase <– main one

enkphalins

opiates

acth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What time of day is largest release in ACTH/cortisol?

A

8 am

  • Helps when glycogen stores decreased after sleep
  • BP may be a bit lower, surge of cortisol helps compensate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Low cortisol level is ____

High cortisol level is____

A

anabolic; catabolic

  • Low levels cortisol are anabolic and promote gluconeogenesis and storage of glucose as glycogen
  • Higher livels of cortisol are catabolic and promote breakdown of muscle/fat (proteolysis and lipolysis)
    • glycogenolysis also occurs in liver in order to increase substrates glucose, aa, ffa, aa for use in stress response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is RAAS system role in aldosterone production?

A

RAAS system produces angiotensin II which increases aldosterone which increases Na/H2O reabsorbtion and K secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is cushing disease?

A
  • Cushing disease is due to pituitary tumor over-secreting ACTH and causing excess cortisol secreiton
  • Causes
    • swelling on face
    • body fat redistrubted to back of neck and trunk
    • proteolysis of connective tissue collagen elements, leading to appearance of purple striae
    • hyperglycemia
    • impaired immune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is cushing’s syndrome?

A
  • Another version cushing disorder but called cushing syndrome
  • due to adrenal cortical tumor over-producing cortisol
  • excess cortisol drives same s/s as seen in previous cuhsing’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is congenital adrenal hyperplasia?

A
  • Cuased by 21-alpha hydroxylase deficiency
  • blocks biosynthetic pathway to produce cortisola nd aldosterone
  • forced substrates into androgen pathway
  • lack of cortiosl negative feedback causes excess ACTH release that stimulates excess androgen production
    • has virilizing effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is treatment for congenital adrenal hyperplasia?

A
  • Give cortisol
  • Not having cortisol is life-threatening
  • by reinstating negative feedback, ACTH levels drop and reduce andronergic pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is addion’s disease?

A
  • Autoimmune attack on adrenal cortex destorys cells making cortisol
  • develops cortisol deficiency
    • increased output ACTH from pituitary from loss negative feedback
      • can’t survive without cortisol
  • Highly pigmented skin due to melatonin from stimulation of MSH/increased ACTH levels
    • not hazardous but diagnostic tool
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does calcium regulation look like in body?

A
  • 1000 mg calcium ingested daily
    • GI tract net uptake= 175 mg
    • Bone net even (500 mg in, 500 mg out)
    • Kidney excretes 175 mg from kidney
  • insures that amount Ca in blood remains constant around 900 mg in ECF
17
Q

What are the 3 main types of bone cells

A
  • Osteoblasts
  • Osteoclasts
  • Osteocytes (which are absorbed osteoblasts)
18
Q

What are osteoblasts?

A
  • osteoblasts are found on surface of bone
  • deposit Ca and phosphate into bone
  • involved in movment of Ca PO4 out of bone, into fluid and into circulation
19
Q

What are osteoclasts?

A
  • liberate ca/phosphate from bone aka breakdown bone
20
Q

What are osteocytes?

A
  • Absorbed osteoblasts
21
Q

What are the osteocystic/osteoblastic membranes role in Ca regulation?

A
  • membrane is target for PTH and calcitiol (active form of VIt D)
    • acts on membrane to cause rapid movmeent of Ca of PO4 into blood= rapid phase Ca/Po4 mobilization
  • To replace bone fluid Ca and PO4 later, PTH stimulates slow phase of Ca mobilization by activating osteoclasts that will digest (reabsorb) bone and liberate Ca PO4 into bone fluid
22
Q

What exists outside of calcified bone?

A
  • Bone fluid exists between blasts and bone
23
Q

What is parathyroid hormone?

A
  • peptide hormone synthesized by parathyroid glands
    • 4 parathyroid glands embedded posteirorly in 4 lobes thyroid gland
24
Q

What cell scretes PTH?

A

Chief cells in parathyroid gland

25
Q

What is the main target of PTH?

A
  • Osteoclasts of bone (although indirectly)
    • PTH actually binds to osteoblasts, in turn osteoblasts secrete cytokines and stimulate osteoclasts to digest bone, which moves Ca/PO4 out of bone and into blood stream
  • kidney tubules
  • gut (via D3)

INCREASES the availability of Ca in blood

26
Q

What happens with removal of parathyroid glands?

A
  • Loss of ability to regulate Ca which untreated, will result in rapid death
    • (just need to supplement with external Ca)
27
Q

What cells monitor Ca concentrations?

A

Chief cells

  • When Ca levels decline in blood, chief cells increase output of PTH to restore Ca concentration
  • Ca and PTH have inverse relationship
28
Q

What is the summary of sites of action of PTH?

A
  • Bone: promote Ca and phosphate resorption (into blood)
    • increases remodeling of bone
  • Kidney: calcium reabsorption, phosphate excretion (need to decrease phosphate levels so crystals dont’ form in blood)
    • involved in final hydroxylation of 25-hydroxy vit d3
  • Intestine: indirect effects via dihydroxy vit D3
29
Q

What is PTH’s effect on plasma calcium and phosphate?

A

Increase Ca, decrease phosphate

30
Q

What is pathway for formation of VIt D3?

A
  • 7-Dehydrocholesterol in skin changes sturcutre when exposed to UV light
  • Vit D3 is delivered to liver, acted on by 25-hydroxylase
  • then taken to kidney
    • PTH activates enzyme 1-hydroxylase
    • creates active form VIT D3 aka calcitriol
      • main target is GI tract to stimulate uptake of ca/po4 from gut, into circulation
31
Q

Summary of Vit D3?

Active form?

Principal sites of action?

Cellular mechanism of action?

A
  • Active form- 1,25 dihydroxy cholecalciferol
  • Princaripal site:
    • intestine: promote ca /po4 absorption
    • bone: calcium and phosphate resorption
      • shor tterm effect: synergism with PTH
      • promotes mineralization (indirectly)
  • Cellular mechanism of action
    • promotes nuclear transritpion
    • role of ca binding proteins
32
Q

What is calcitonin? Where is it produced?

A
  • Calcitonin is synthesized by parafollicular cells or C-cells that are dispersed throughout thyroid tissue and reside next to thyroid follicles
  • Calcitonin increases net disposition of Ca and phosphate into bone by inhibiting osteoclastic activity., leaving osteoblastic activity unopposed
  • Calcitonin not too important in adults, but very important in kids for growing
33
Q

SUmmary of calcitonin action?

A
  • Principle sites of action
    • bone
      • inhibtion of osteoclsts
      • net deposition of calcium and phosphtae
      • decreased remodeling
    • kidney
      • ca, phosphate excretion
    • intestine
      • decreased Ca absorption
  • Effect on plasma Ca, phosphate
    • decreased Ca decreased phosphtae
  • Control of calcitonin secretion
    • directly related to plasma Ca
    • role of age
34
Q

What is hypoparathyroidism

A
  • Decrease in plasma Ca and increase phosphate
  • Bone: decrease remodeling. density normal
  • Muscle: tetany
    • not sufficient Ca in blood stream, not available to interfere with movement of Na into muscle
    • Na freely flows into muscle cells, causing muscle cell contraction and causes tetany
35
Q

What is hyperparathyroidism?

A
  • Excessive PTH output d/t tumor
  • Plasma: Ca increase, phosphate decrease
  • Bone:
    • remodeling increase (excessive to where osteoporosis occurs)
  • Muscles
    • hypotonia: due to blocked Na channels in membrane, get flaccid muscle activity leading to hypotonia
  • Kidney:
    • nephrocalcinosis (kidney stones)
    • renal insufficiency
36
Q

What is rickets?

A
  • Vita D3 deficiency (not eating enough/making enough)
  • Decreased Ca, decreased Phosphate (can’t absorb)
  • Bone:
    • decrease mineralization
    • deformities: wide epiphyses
  • Muscle:
    • tetany

Physio Test 4 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions