Endocrine

Question 1

What is a secondary endocrine disease/disorder?

Answer 1

when there is damage/ infection to the pituitary glands or thalamus.

Question 2

What is a primary endocrine disease/disorder?

Answer 2

when damage/infection occurs to the endocrine gland itself

Question 3

what are the 3 main pancreatic cells and the things they secrete?

Answer 3

Alpha cells: secrete glucagon
Beta cells: secrete insulin
delta cells: Secrete stomatotatin ( from the islets of langerhans)

Question 4

adrenal: where is the Zona fasiculata and what does it secrete

Answer 4

middle layer of the adrenal cortex that secretes glucocorticoids such as cortisol a stress hormone.

Question 5

where is the zona glomerulosa and what does it secrete?

Answer 5

zona glomerulosa is the outermost layer of the adrenal cortex that secretes mineralocorticoids like aldosterone a hormone that influences Na retention.

Question 6

Where is the zona reticularis and what does it secrete?

Answer 6

The zona fasiculata is the inner most layer of the adrenal cortex which secretes androgens the precursors for the sex hormones.

Question 7

what hormones does the adrenal medulla secretes?

Answer 7

the adrenal medulla secretes catecholamines such as epinephrine and Norepinephrine.

Question 8

name the thyroid gland hormones and some of their effects….

Answer 8

T3 & T4 are thyroid hormones htat increase BMR, +protein synthesis and degradation, +glycogenolysis and lipolysis, and + HR foc and CO

Question 9

what is Hypothyroidism?

Answer 9

Primary cause: congenital dysgensis of the precursors for noni-onated salts and cell receptor insensitivity to TSH
secondary: Adenohypophysis produces less TSH.
clinical manifestations:
- Cold intolerance, weight gain, low BP, low BMR, hyperlipidemia, bad memory, high TSH and TRH and decreased T3 T4,
Tx: hormone replacement of T3 T4

Question 10

what is cretinism?

Answer 10

• hypothyroidism in babies
• w/o adequate t3 and T4 at age >1month causes lasting neurological deficits
  clinical manifestaiton: irreversible cognative delays if not treated, neonatal jaundice, thickening tongue and lips, bradycardia/hypotension, poor muscle tone

Question 11

myxedma

Answer 11

hypothyroidism in adults do that a lack of t3 t4 w/o Tx
clinical manifestations:
- non pitting edema, alt mental status, cold intolerance
tx:
- T3 T4 supplements

Question 12

Goiter

Answer 12

Caused by a lack of iodine, TSH is still present and stims the thyroid to make T3 and T4 but no iodine present to actually make T3 T4.
Tx; iodine supplements

Question 13

Hyperthyroidism:
primary and secondary causes

Answer 13

primary: graves disease, causes an increased antibody expression that stimulates the TSH receptors on follicular cells to make MORE T3 and T4
Secondary: tumour in the adenohypophysis gland that increases TSH/TRH secretion.

Question 14

Hyperthyroidism manifestations and treatments

Answer 14

• increase BMR, heat intolerance, restlessness/insomnia, Amenorrhea ( women), thyroidmegaly, expothalamus ( blugging eyes)
  tx:
  primary: Beta blockers ( manages increases SNS ), drugs to inhibit T3 T4 production, removal of the gland,, T3/T4 replacement therapy
  secondary: remove tumour

Question 15

what are some regulatory mechanisms for cortisol release?

Answer 15

• circadian rhythm: more cortisol released in early mornings and decreases during the day, negative feedback loop of the relases of ACTH and CRH ( circadian cycle),

Question 16

Hypocortisolemia

Answer 16

• decreased amount of cortisol in circulation affecting the zona fasiculata and zona glomerulosa

Question 17

primary hypocortisolemia?

Answer 17

Addison’s disease: decreased production of cortisol and aldosterone
manifestations: hypovolemia, hyperkalemia, hyponatremia, hypoglycaemia, N/V/D/C, hyper-pigmentation of skin due to increased ACTH/POMC, vitiligo*

Question 18

Secondary hypocortisolemia?

Answer 18

Due to the reduced output from the adenohypophysis, reduced release of ACTH due to a tumour or Iatrogenic cause from prolonged exogenous cortical/related steroid will inhibit the hypothalamus from making CRH & the adenohypohysis from making ACTH.

Question 19

Congenital adrenal hyperplasia
(adenogenital syndrome)

Answer 19

-autosomal recessive body can not produce 21-hydroxylase to make cortisol and aldosterone
- instead precursors are converted into androgens
manifestation: virlization of women, enhanced manliness.

Question 20

Hypercortisolemia disorders….

Answer 20

Cushings disease/syndrome: onset age 40
- iatorgenic or caused by the over use of cotisol slows or completely stops the relase of CRH or ACTH resulting in excessive cortisol production
manifestations:
- buffalo humps, moon face, muscle weakness, + production of androgens, poor concentration, hyperglycemia

Question 21

What hormone reduces the secretion of growth hormone and where is it released from?

Answer 21

Somatostatin secreted by the delta cells in the pancreas

Question 22

what does hyper secretion of growth hormone cause?

Answer 22

Giantism: occurs when there is a benign tumour on the anterior pituitary prior to the fusion of the epiphyseal plate.
manifestations:
- increased bone growth, increased cartilage growth, delayed puberty, really tall, excessive bone deposition in the hands and face, cardiomegaly, and CV disorders

Question 23

what does the hypo secretion of GH cause?

Answer 23

Dwarfism: can be congenital or acquired. there is a lack of GH secreted and receptors do not respond and a lack of IGF produced.
- normal birthweught, reduced long bone growth, shorter axial skeleton, poor joint mobility, fat/muscle mass decreased, hypoglycemia
Tx: hormone replacement

Question 24

What is acromegaly?

Answer 24

Benign pituitary gland tumour after the epiphyseal plate. Onset is ages 20-40,
- increased bone/cartilage growth, arthritis, peripheral neuropathies, cardiomegaly, CV disorders.
Tx: tumour removal