14. formation of glucose
from Non-
carbohydrate
substances
(this is imp in
young ppl, and
that's why elderly
will have low lean
body mass & more
adipose tissue)
Anti-
Insulin
effect
34. The most important mechanism
is through PTH .(How)? ●1.25-
Dihydroxycholecalciferol or
calcifrol takes a place through
PTH. ●Low calcium stimulates
PTH release and PTH is going to
mediate the process of calciferol
formation
35. • * PTH has a slower effect ,its effect peak in 3-4 hours and it is less
important in young individuals than calcitonin because their growth
turn over.
36.
37.
38.
39.
40.
41.
42.
43. • also act on the stomach to inhibit gastric emptying , and on
the brain's satiety center to induce loss of appetite.
48. • Glucocorticoids released by the adrenal cortex include:
1- Hydrocortisone: Commonly known as cortisol, it regulates how the
body converts fats, proteins, and carbohydrates to energy. It also helps
regulate blood pressure and cardiovascular function
2- Corticosterone: This hormone works with hydrocortisone to
regulate immune
49.
50. • in renal epithelial cells cortisol will be converted to cortisone by an
enzyme called 11β-hydroxysteroid dehydrogenase type 2 (
cortisone has minimal binding to that receptors )
51.
52.
53.
54. Features of Addison disease
• If the disease is secondary ( in hypothalamus or pituitary) ,
there will be no Excess secretion of ACTH , so there will not be
Hyperpigmentation feature.
70. • Sulfonylureas work on a receptor close to K+ channels on the
B-Cells of the pancreas, inhibiting these channels, causing
depolarization, allowing the entry of calcium to the cell, which
gets the granules to fuse to the cell membrane to secrete
insulin.
• *sulfonylureas are the 2nd line oral diabetic agents, given
when Metformin has failed to control the glucose levels, and
when the patient is underweight or at least not obese.
71.
72.
73. • What pharmacologists also did is develop DPP4 inhibitors, and
the advantage of these DPP4 inhibitors over Exanetide are
that DPP4 inhibitors are given orally and not in subcutaneous
injections.
78. Glucocorticoids receptors are widely distributed
through the body while mineralocorticoids receptors
are only limited to certain organs , particularly the
kidney and other excretory organs like the sweet
glands and the salivary ones, so mineralocorticoids
just regulate the processes of electrolytes and fluid
transport while Glucocorticoids have a much wider
role in the body.
79.
80. • Aldosterone is not the main regulator for sodium
reabsorption , the ACTH and rennin-angiotensin
II systems are the main regulator .
84. So in the replacement therapy, the basic concept
is to start with Hydrocortisone, if the patient is
having a sustained salt wasting, then you might
need to add the Fludrocortisone. (The mineralo-
mimetic drug is only added if Hydrocortisone is
not sufficient to stop the salt wasting).
92. Side effect of corticoids
• So imagine a pregnant woman who has asthma, it's almost
always these patients will develop gestational diabetes,
because you have to use corticosteroids in these patients if
they have sever flares of the disease.
102. Usually decreased TSH levels are associated with increased free T4
levels ,, however in some patients we might see ,increased T3 but
normal or decreased freeT4 ,,[T3 toxicosis]
110. # toxic multinodular
goiter: type of
multinodular goiter that
manifest with
thyrotoxicosis secondary
to the development of
autonomous nodules that
produce thyroid hormone
independent of TSH
stimulation
154. Actions of thyroid hormones
They stimulate the synthesis of a number of hormones
and enzymes. One such enzyme is cytochrome c
oxidase, a part of the electron transport chain. The ETC
is found in the inner mitochondrial membrane, and its
function is ATP synthesis. An increasein thyroid hormone
will lead to an increase in ATP production, and since ATP
production is associated with heat production patients
with hyperthyroidism will suffer from heat intolerance.
155.
156. 1) Iodide trapping: The first stage in the formation of
thyroid hormones is transport of iodides from the
blood into the thyroid gland. This is an active process
that requires energy. In the basal membrane there is
a sodium/potassium ATPase pump that creates a
sodium concentration outside the cell. A sodium
iodine symporter then carries the iodide (along with
sodium) into the follicular cell.
2) Oxidation of Iodide: This is conversion of the
iodide ions to an oxidized form of iodine. Iodide ion
is converted to I2 that is capable of combining
directly with tyrosine. Oxidation of iodide is
catalyzed by peroxidase/hydrogen peroxide system
Organification: The binding of iodine to the tyrosine
residues of the thyroglobulin molecule is called
organification of the thyroglobulin.This process is
catalyzed by the enzyme iodinase
Under normal
condition 70%
of tyrosine
residues of
thyroglobulin
are in the form
MIT and DIT
and 30% as
thyroxine (T4)
(only a minor
part is in the
form of T3)
157. *Propylthiouracil (PTU) inhibits peroxidase
enzyme as well as coupling of iodinated
tyrosine residues(Steps 2&4), that’s why it can
be used in the treatment of patients with
excessive thyroid function. In the figure PTU is
the thioamide.
158. 1) As a result of TSH stimulation,
follicular cells will extend pseudopods.
These pseudopods will entrap a part of
the colloid making an endosome
(pinocytic vesicles). The process by
which this happens is called pinocytosis.
The endosome contains thyroglobulin.
4) Most of the MIT and DIT are recycled
back into the colloid. Their iodine is
cleaved by deiodinase enzyme that makes
iodine available for making thyroid
hormones.
