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Flashcards in Endocrine Deck (61):
1

What is the endocrine system?

collection of glands that produce hormones that regulate metabolism, growth and development, tissue function, sexual function, reproduction, sleep, and mood, among other things.

2

What is a hormone

A hormone is any member of a class of signaling molecules produced by glands that are transported by the circulatory system to target distant organs to regulate physiology and behaviour.

Could also act more locally as paracrine or Autocrine messengers to incite local effects

3

Are hormones always present?

Most are present in body fluids at all times, but in greater or lesser amounts depending on needs of the body

4

Paracrine vs Autocrine action

Autocrine- When hormones act locally on the same cells from which they were produced (ex- insulin inhibits further release from beta cells)

Paracrine- Acts locally on cells other then those that produced the hormone (sex steroids acting on ovary)

5

What are the Major organs of the Endocrine system?

Hypothalamus, pineal, pituitary, thyroid, thymus, adrenal, kidney, pancreas, ovaries, testes

6

Key Hormones of Hypothalamus

• Cortic0tropin releasing hormone (CRH)
-> Stimulate adrenocorticotropic hormone (ACTH) release from anterior pituitary

• Thyrotropin releasing hormone (TRH)
-> Stimulates TSH release from anterior pituitary (primarily)

• Growth Hormone Releasing hormone (GHRH)
-> Stimulates GH release from ANt. Pituitary

• Gonadotropin releasing hormone (GnRH)
-> Stim Ant. pituitary to release (LH) and FSH)

• Somatostatin
-> inhibits TSH and GH from Ant. Pituitary

• Vasopression (AKA ADH)
-> Acts on Kidney to Inc water reabsorption

Dopamine
-> Inhibit prolactin released from anterior pituitary

7

Key Hormones of Anterior Pituitary

• Growth Hormone (GH)
-> cell reproduction

• Adenocorticotropic (ACTH)
-> Stimulates corticosteroid (glucocorticoid and mineralcorticoid) and androgen synthesis and release from adrenocortical cells.

• Thyroid stimulating hormone
-> stimulate thyroid to release T3 and T4

• Follicle stimulating hormone
-> Stim ovaries and testes

• Lutemizing hormone- menstrual cycle, or sperm production
• Prolactin

8

Posterior Pituitary

• Oxitocin- stimulates contraction of uterus, milk ejection (breasts)
• Antidiuretic Hormone (AKA Vasopressin)- Inc water reabsorption by kidney

9

Thyroid

• Thyroid Hormone
o T3- increases metabolic rate, inc protein/bone turnover
o T4- increases responsivenbess to catecholamines necessary for fetal infant growth

10

Adrenal Cortex

• Glucocorticoids (cortisones) -> Is a Corticosteroids

• Mineral Corticoids (aldosterone- Increases Na absorption and K loss and H+ excretion by kidneys) ->Is a Corticosteroids

• Androgens (testosterone)

11

Adrenal Medulla

Adrenaline (epinephrine)
Noradrenaline (norepinephrine)

12

2 Basic Problems of Endocrine Pathology

• Hypersecretion- increase hormones production
• Hyposecretion decreased or no hormone production
o Inappropriate target cell response

13

Possible Etiology for Hypersecretion

1) Excessive trophic stimulation → inc hormones
2) Defect in the negative feedback loop∴no longer
stops/shuts off, so continuous production of hormones
3) Secretory cell tumor (tumor in gland, more cells/larger
organ) → release excess secretion of hormones

14

Possible Etiology from Hyposecretion

1) metb defect Es missing, inhibited
2) immune disorder Ab targeting glands and/or receptors
3) Sx/Tx for hypersectretion remove part of the organ∴ less
hormone secretion
4) Receptor defects (not enough binding)
5) No trophic stimulation → atrophy
6) Dietary deficiency eg/ iodine deficiency→ non-functional T3 and T4

15

Thyroid hormones

triiodothyroine T3 and thyroxine T4

NOTE The normal thyroid gland produces about 80% T4 and about 20% T3, however, T3 possesses about four times the hormone "strength" as T4.

16

Location and shape of the Thyroid

L: below the larynx in the anterior middle portion of the neck

S: shield-shape structure, left and right lobes composed of a large number of tiny, saclike structures called follicles

17

What is the function of the Thyroid

the sole fx of the thyroid is to make thyroid hormone. This hormone has an effect on nearly all tissues of the body where it inc cellular activity. The primary fx of the thyroid is to regulate the body’s metb

18

What stimulates the Thyroid?

What is the key element required by T

The secretion of the thyroid hormone is regulated by the hypothalamic-pituitary thyroid feedback system: Hypothalamus produces TRH→stimulates the anterior pituitary to release TSH→TSH acts on thyroid gland to produce T3 and T4

19

What is the key element required by Thyroid?

the process of thyroid synthesis, iodine is needed.

20

Two types of Goiter

Endemic and Toxic

21

Describe pathology of an Endemic Goiter

need iodine to form hormone... iodine deficiency d/t lack of iodine in diet→dec production of T3 and T4 → compensatory inc in TSH to create more T3 and T4 →hyperplasia in the thyroid inc in size and number d/t inc of TSH, making lots of un functional T3 and T4.
-> Too much TSH causing too much load on the cells
-> cells spread/grow and divide→goiter

22

What causes a toxic Goiter?

there is excess production of thyroid hormones from functionally autonomous thyroid nodules, which do not require stimulation from thyroid stimulating hormone (TSH)

toxicity from inc levels of hormone d/t hyperactivity. End result is a large nodular gland

23

Describe Hyperthyroidism and the clinical presentation

AKA Grave's Disease

mostly auto immune
is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone.
- most common Hyperthyroidism 80-90%,
- most often seen in young women
- If you see the following 3 things, they indicate
Graves disease:
1) hyperthyoidism
2) goiter
3) exopthalmus protruding eyeballs, fluid deposits in fat pads and protruding eyeballs

24

Pathology of Graves Disease

AKA hyperthyroidism

TSAb Thyroid Stimulating Ab mimics TSH and binds to Thyroid receptors → stimulates T3 and T4, but stays there and doesn't disassociate normally d/t inability of Es to breakdown the structure of the TSAb. RESULT= lots of T3 and T4

- Body compensates negative feedback by dec TSH → test shows elevated T3 and T4 and low TSH

25

Describe Thyrotoxicosis

- If you don’t treat hyperthyroidsm/grave’s disease, it results in inc T3 and T4 → general inc in metb→ excessive metabolic heat→ compensitory heat loss mechanisms causing →flushed skin + perspiration
- intolerance to any inc in body temp
- excitable, irritable, insomnia, anxiety
- inc demand for energy (inc metb requires inc
glucose), O2, →inc Heart Rate and Cardio Output
- and waste removal, hyperventilation to expel CO2
- altered metb pathways fat and protein used causing weight loss

26

Tx options Hyperthyroidism

o 1 of 3 options
• antithyroid drugs (e.g. TAPAZOLE to suppress hormone synthesis
• radioiodine therapy
• Sx for large goiters
(not first line, only when other tx doesn't
work)

27

Etiology of Hypothyroidism

1. primary thyroid hyposecretion
2. secondary pituitary or
3. tertiary hypothalamus
- 95% is primary
- mainly d/t radiation and Sx for hyperactivity
- dec in metabolic rate

28

Problems associated with Hypothyroidism

• Dec body temp
• Dec in CO
• Dec in CNS Fx
• Weak muscle action (d/t Dec ATP)
• Inc Weight (less metabolization equals more storage glucose/lipids)

29

What is Hashimoto’s thyroiditis

(most common hypothyroid state ~95%)
• ~90% in middle aged women
• autoimmune destruction of gland
• Antithyroid Abs block TSH binding
• Lymphocyte infiltrates
• No stimulation of Thyroid leads to atrophy and size reduction

30

Tx of Hypothyroidism?

Tx
• If endemic goiter -> dietary I
• P.O T4 Thyroxine (why not T3?)

31

The adrenal Cortex: outer layer - stimulated by pituitary ACTH
→ secretes?

1) mineral corticoids → aldosterone
2) glucocorticosteroids → cortisol
3) androgens→Testosterone, DHT stimulates testosterone

Main

32

The adrenal Medulla: middle layer – stimulated by Sympathetic Nervous System → secrets?

1) epinephrine
2) non- epinephrine

33

Etiology of Hyperfunction of Adrenal Gland

o Cortical tumor or hyperplasia -> inc cortisol, Dec ACTH
o Anterior pituitary tumor or hyperplasia of AP -> Inc ACTH
o Ectopic tumor (secretory) ACTH tumor (eg in lung)

34

What is Cushing Syndrome?

(Table 41-4)

- glucocorticoid hypersecretion→excessive hormone mainly cortisol:
1) excessive fat and protein catabolism (break down
2) gluconeogenesis, production of glucose from non-carbohydrates
3) anti-inflm effects because it’s a steroid

35

Characteristic features of Cushing Syndrome?

->facial, neck and abdm fat deposits
rounded moon face
weak muscles (d/t protein catabolism)

Na and water retention →HTN and hypokalemia low K d/t excretion of K, in normal concentrations cortisol doesn’t effect electrolytes, but if high concentration of cortisol, it acts like aldosterone (mineral fx)
- Overall, prolonged hyperglucemia d/t gluconeogenesis glucose in excess →causing insulin resistance ; IGT (Impaired Glucose Tolerance)
- Other mnfts: androgen hyper secretion sometimes: females develop male sex characteristics
both males and female are susceptible to infections because one fx of the hormone is to suppress inflm response→excessive hormone
- rounded moon face, and buffalo hump (on the traps)
- female: secondary male sex characteristics, balding, facial hair etc d/t hypersecretions of androgens
- mineral cortisoids→aldosterone hypersecretion
- 30-50 years
- x2 likehood in women

36

Tx of Cushing disease

• Excise Tumor
• Irradiate pituitary
• Drugs for ectopic tumors
• Adrenalectomy?

37

What is Conn syndrome

• Aldosterone Hypersec (mineral corticoids)
• Uncommon

38

Etiology of conns syndrome

• Usually cortical adenoma
• Idiopathic cortical hyperplasia
• Renin secreting renal tumor (Not ectopic)

- problem with mineral cortisoids→ excessive aldosterone secretion

39

MNFTS of Conns

• HTN (major problem) D/T Na and water retention→inc blood vol→inc BP→HTN

- Hypokalemia and alkalosis d/t excretion of H ions minor fx of aldosterone is excrete H ions → excess aldosterone = excess excretion H ions, both K and H ions are positive, causing a higher pH∴alkalosis

40

TX of Conns

• Adrenalectomy for adenoma (unilateral)
• Drugs for hyperplasia
o Aldosterone receptor antagonist
• NA diet restriction

41

What is Addison's Disease?

- chronic primary adrenocortical deficiency
- relatively rare
- hyposecretion
- ↓dec in all 3 groups of Hormones

42

Etiology of Addison's

1) auto immune
2) infection
3) tumor (not of the cells that secrete hormones, but of the cells that are non-secretary, need space so damage normal surrounding tissue → dec hormone

• High dose glucocorticoid Tx -> dec ACTH
• Cortex must sustained substantial damage
???

43

MNFTS of Addisons

• Fluid loss (Na, CL) -> hypovolemia -> Dec CO -> hypotension-> weakness/chronic fatigue
Lack of cortisol • low stress tolerance, hypoglycemia
• Decreased General adaptive syndrome AS
• Addisonian crisis: acute insuff of hormones d/t stress (can be fatal)

44

Tx of Addisons

• Acute
o IV fluids
o IV glucocorticoids
• Chronic
o Glucocorticoids
o Mineral corticoids

45

What are tropic hormones and where are the majority produced?

Tropic hormones are hormones that have other endocrine glands as their target. Most tropic hormones are produced and secreted by the anterior pituitary.

46

What are the two non trophic hormones from the pituitary

Growth Hormone (effects bones and muscles) and Prolactin (affects mammary glands)

47

What is the control system for all tropic hormones?

The model of ALL tropic hormones is a NEGATIVE FEEDBACK LOOP

48

What is the most common location and cause of pituitary disorders?

Anterior pituitary and adenomas

49

Describe hyperactivity of the anterior pituitary

- adenomas (tumor) of secretitory cells trophic will cause other glands to secrete and non-trophic hormones directly cause eg/ prolactinin and growth hormone
- hyperactivity of all “target gland” eg/ TSH and ACTH

50

Describe hyperactivity of the posterior pituitary?

Syndrome of inappropriate ADH (SIADH)
- Excessive ADH or
- ADH like substances coming from ectopic tumors
(eg/ tumors in the lungs, thymus, lymph nodes)
- Too much ADH = excessive water retention→inc
BP STOPS RENIN-ANGIOTENSION LOOP also dilute components in the blood→dilute Na called dilutional hyponatremia

51

What might come from removing the adrenal gland?

Hyposecretiion of associated hormones

52

Does the pituitary directly control the pancreas?

No,

Adrenal and Thyroid yes

53

What are the two non trophic hormones from the pituitary

Growth hormone and Prolactin

54

Where are the common disorders of pituitary?

D/t what?

• Mostly Anterior Pituitary
• Posterior pituitary less common
• Most d/t adenomas

55

How will a tumor effect the Anterior pituitary?

• Adenomas (tropic hormones & non tropic hormones)
o Tumor could be functional (secretory) or non – secretory tomur
• Hyperactivity of target gland?

56

How will hyperactivity of the posterior pituitary MNFTS?

Syndrome of inappropriate ADH (SIADH, pg 743)
• Hypersecretion of ADH
• Ectopic tumors (eg in lungs)
o ADH-like substances
• Increase water retention
o Dilutional hyponatremia
• Renin and aldosterone secretion decreased
o Impaired Na reabsorption

57

Tx for hyperactivity of the pituitary?

• Mild: restrict fluids
• Diuretics
• ADH antagonists

58

What does ACTH stimulate?

Mainly cortisol

(but apparently also some androgens?)

59

What does Cortisol do?

Increase BG by stimulation Gluconeogenesis

Suppress immune and inflm

Aids in metabolism of carbs, fat and proteins

Minor effect- high levels of cortisol may act like aldosterone (inc in Na and water retention)

60

What does Aldosterone do

Minor effect- Inc H ion excretion

Inc in Na causes dec in potassi

61

Why does addison cause weight loss

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