Endocrine Generalities

1)First statement: JA
Second statement: Kylee
When GH-producing tumors occur in childhood, the disease that results is called
gigantism rather than acromegaly. A child's height is determined by the length of the so-
called long bones in the legs. In response to GH, these bones grow in length at the growth
plates—areas near either end of the bone. Growth plates fuse after puberty, so the
excessive GH production in adults does not result in increased height. Since our patient is
a 25 year old male and has passed through the stage of puberty, therefore, growth plates
have already fused causing no change in his height.

2)First statement: Karen

The following blood tests were requested prior to surgery to differentiate the endocrine system
disorder
○ Primary endocrine disorders: defects at the level of the target endocrine organ
○ Secondary endocrine disorders: defects at the level of the pituitary gland
○ Tertiary endocrine disorders: defects at the level of the hypothalamus

● 5 TYPES OF CELLS IN THE ANTERIOR PITUITARY GLAND BY IMMUNOCHEMICAL

TESTS:
○ Somatotrophs: secrete GH
○ Lactotrophs or mammotrophs: secrete PRL
○ Thyrotrophs: secrete TSH
○ Gonadotrophs: secrete FSH, LH
○ Corticotrophs: secrete ACTH

● FBS: 127 mg/dL (N.V.: 80-100 mg/dL)

○ GH is a hyperglycemic hormone
● 2-hr post glucose load: 201 mg/dL (N.V.: <140 mg/dL)
○ GH is a hyperglycemic hormone
● Plasma growth hormone 2 hrs after 75g glucose ingestion: 35 ng/mL (N.V.: <1
ng/mL)
○ Confirmatory test for acromegaly
○ Glucose Suppression Test - OGTT (75g glucose)
○ Blood is collected every after 30 minutes for 2 hrs, fasting sample is required
○ A normal response for this test is a suppression of GH less than 1 ng/mL
○ If GH fails to decline less than 1 ng/mL, it is acromegaly
○ Failure of GH to be suppressed below 0.3 ug/L accompanied by an elevated IGF-1
is diagnostic of acromegaly
○ Principle: GH is decreased in hyperglycemia
● Serum IGF-1: 945 ng/mL (N.V.: 117-329 ng/mL)
○ Insulin-like Growth Factor-1 or Somatomedin C
○ Screening test for acromegaly
○ Produced in the liver
○ Relatively long circulating half-life
○ Increased in patients with acromegaly; low in GH deficiency
● TSH: 0.80 u IU/mL (N.V.: 0.25-4.0 u IU/mL); FT4: 22 pmol/L (N.V.: 11.5-23.0 pmol/L);
FT3: 3.30 pmol/L (N.V.: 2.5-5.8 pmol/L)
○ It is essential to obtain TSH, FT3 and FT4 to eliminate primary hypothyroidism as a
cause for the elevated prolactin
● LH: 2.0 u IU/mL (N.V.: 1.9-9.4 u IU/mL); FSH: 6.0 m IU/mL (N.V.: 1-10.5 m IU/mL);
Testosterone: 7.5 nmol/mL (N.V.: 6.5-8.4 nmol/mL)
 ○ LH and FSH: g
○ Gonadotropins
○ FSH aids in spermatogenesis
○ LH stimulates Leydig cells to produce testosterone
● 8 AM Cortisol: 500 nmol/L (N.V.: 166-620 nmol/mL)
○ Principal glucocorticoid
○ Synthesis regulated by ACTH
○ Secretion is diurnal and is associated with a person’s sleep-wake cycle
○ High levels in the morning (8-10 am) and lowest at night (10 pm-12 am)
● Prolactin: 30 ng/mL (N.V.: 1-15 ng/mL)
○ Pituitary lactogenic hormone; a stress hormone (possible reasons for elevation in
question number 3)

Second statement: Noeri

3) First question: Chesca
Most postoperative complications involved after transphenoidal surgery include the occurence
of increased urine output and electrolyte imbalances due to a syndrome of inappropriate anti
diuretic hormone secretion (SIADH). Secretion of anti diuretic hormone is affected in this case
due to the manipulation of the pituitary gland which function also for the secretion of hormones
directly related to water and osmole balance.

Second question: Carissa

Desmopressin- analogue of vasopressin
Upon binding of desmopressin to V2 receptors in the basolateral membrane of the cells of the
distal tubule and collecting ducts of the nephron, adenylyl cyclase is stimulated. The resulting
intracellular cascades in the collecting duct lead to increased rate of insertion of water channels,
called aquaporins, into the lumenal membrane and enhanced the permeability of the membrane
to water.
Pancreas
1)Isa
Normally, the carbohydrates in the food we eat - or the glycogen stores of the body - are
converted into glucose and used by the body as its primary source of energy. Drastically
decreasing one’s carbohydrate intake forces the body to use other substances as a source of
energy. A small amount of carbohydrate is still needed because glucose is the preferred energy
source of the brain. The high amount of fat intake causes a switch of energy source. The liver
converts fat into fatty acids and ketone bodies, which now serves as the main energy source of
the body. Increased ketone bodies in the blood is called ketosis; thus, this type of diet is called
ketogenic diet. Ketosis is different from ketoacidosis, which is a complication of type 1 diabetes
mellitus. Research is still being done regarding whether or not a long-term ketogenic diet is
harmful to the body.

2)Lara & Kate

Normal Values:
BP: 120/80 mmHg
CR: 60-100/min
RR: 12-20/min
Blood Glucose: 100mg/dL
Serum Potassium: 3.5-5.0 mEq/L
Serum Sodium: 135-145 mEq/L
Serum Chloride: 96-106 mEq/L
Arterial Blood gas: pH 7.38-7.42
pCO2: 38-42 mmHg
HCO3: 22-28 mmol/L or mEq/L

Type 1 Diabetes is a catabolic disorder wherein circulating insulin is very low or absent, plasma
glucagon is elevated, and the pancreatic beta cells fail to respond to all insulin-secretory stimuli.
The pancreas shows lymphocytic infiltration and destruction of insulin-secreting cells of the
islets of Langerhans, causing insulin deficiency. Extreme insulin deficiency leads to osmotic
diuresis and dehydration as well as elevated free fatty acid levels and diabetic ketoacidosis
(DKA), which may be life-threatening.
Symptoms continue to progress to dehydration, resulting in low blood volume, increased pulse
rate, and dry flushed skin. The plasma pH begins to drop as acetone and ketones breakdown.
When the plasma level reaches 7.2, the respiratory center is stimulated, and the patient's
breathing becomes shallow and rapid (Kussmaul respiration) with a fruity odor. This is the
body's way of trying to prevent a further decline in pH. The increased loss of CO2 from the lungs
reduces plasma carbonic acid to acceptable levels. Metabolic acidosis occurs when the body's
buffer system is unable to maintain normal pH with the assistance of the respiratory
compensatory mechanisms.

Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and
develops when insulin levels are insufficient to meet the body’s basic metabolic requirements.
Insidious increased thirst (ie, polydipsia) and urination (ie, polyuria) are the most common early
symptoms of diabetic ketoacidosis (DKA). Fruity or acetone breath, nausea/vomiting,
dehydration, deep, rapid breathing (Kussmaul), lethargy, weakness, headache also can present
as symptoms of DKA.
- ketogenesis due to insulin deficiency leads to increased serum levels of ketones and
ketonuria
 - acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids
that cause metabolic acidosis
- respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid
respirations (Kussmaul breathing)
- acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis
patients

Thyroid
1)Sha & Leandro

The T4 test and the TSH test are the two most common thyroid function tests. They’re usually
ordered together. The T4 test is known as the thyroxine test. A high level of T4 indicates an
overactive thyroid (hyperthyroidism). Symptoms include anxiety, unplanned weight loss,
tremors, and diarrhea. Most of the T4 in your body is bound to protein. A small portion of T4 is
not and this is called free T4. Free T4 is the form that is readily available for your body to use.
Sometimes a free T4 level is also checked along with the T4 test.

The TSH test measures the level of thyroid-stimulating hormone in your blood. The TSH has a
normal test range between 0.4 and 4.0 milli-international units of hormone per liter of blood
(mIU/L).

The Hypothalamic-pituitary-thyroid Axis

Levels of thyroid hormones in serum are tightly regulated by the hypothalamic-pituitary-thyroid

axis. Hypothalamic TSH-releasing hormone (TRH) is secreted mainly from the
paraventricular nucleus in the hypothalamus and reaches the median eminence through axonal
transport. TRH is then carried via the hypothalamic portal vein to thyrotrophs, which
produce TSH, where it binds to TRH receptors and stimulates the genes that express the TSH
β subunits. Apart from these thyrotropic effects, TRH also regulates the conjugation of the TSH
α and β chains and glycosylation of the TSH molecule to control its biological activity. Mature
TSH is secreted from the pituitary gland and reaches the thyroid gland, where it
stimulates thyroid hormone production and release.

Since there is an increased amount of TSH (10 mIU/L) based on the laboratory result, this will
stimulate the thyroid gland to also produce an increased amount of thyroid hormone.

2)in hypothyroidism: Becca

In hyperthyroidism: Ayra
3)A.Floen
Graves disease is an autoimmune disease characterized by hyperthyroidism. Activates thyroid
gland TSH receptor and stimulates hormone synthesis and release.
DRUGS
NaI - inhibits the iodination of tyrosine and release of thyroid hormone.; decreases the size and
as well as the vascularity of the gland. Also used in the management of thyroid storm as well as
the preparation of patients that will undergo surgical resection of a hyperactive thyroid.
*radioactive iodine - large doses are enough to damage hyperactive thyroid without harming
other tissues. Permanently curing thyrotoxicosis without surgery. pak
Propranolol - aside from controlling tachycardia and other cardiac abnormalities from severe
thyrotoxicosis, it also inhibits the peripheral converstion of T4 to T3.
PTU - (thioamides) - sulfur containing thioamides that inhibits thyroid synthesis by blocking
peroxidase ractions, iodination of tyrosine residues, and coupling of DIT diiodotyrosine and MIT
monoiodotyrosine, and peripheral conversion of T4 to T3. but doesnt inhibit release of hormone.
Methylprednisone - since Graves is an autoimmune disease, steroid’s immunosuppresive
effects may help calm the tits of the antibodies that stimulate TSH receptors. Also by inhibitng
the peripheral conversion of T4 to T3.
B. Jarah

Figure 41-5
1. Iodide is actively transported into the gland against chemical and electrical gradients by
a sodium-iodide symporter (NIS) located in the basolateral membrane of thyroid
epithelial cells.
 2. One iodide ion is transported uphill against an iodide gradient while two sodium ions
move down their electrochemical gradient. The driving force for this secondary active
transporter is Na+ / K+ ATPase
3. After entering the gland, iodide rapidly moves to the apical plasma membrane and is
transported into the lumen of the follicles by sodium-independent iodide/chloride
transporter called Pendrin
4. Iodide is oxidized and incorporated into tyrosine residues within thyroglobulin. A single
iodination forms MIT and a second iodination of the same residue produces DIT. [Two
DIT molecules = T4; One MIT and one DIT = T3] Coupling occurs between iodinated
tyrosines that remain part of the primary structure of thyroglobulin catalyzed by the
enzyme Thyroid Peroxidase
5. Once thyroglobulin has been iodinated, it is stored in the lumen of the follicle as colloid
6. Release of T4 and T3 into the bloodstream is initiated by endocytosis of colloid from the
follicular lumen by the processes of macro- and pinocytosis. Endocytotic vesicles fuse
with lysosomes and thyroglobulin is degraded
7. MIT and DIT molecules are rapidly deiodinated within the follicular cell by the enzyme
Iodotyrosine deiodinase -> specific for MIT and DIT and cannot use T4 and T3 as
substrates
8. T4 and T3 are transported across the basal side of the cell and enter the blood

Drugs:
1. Sodium Iodide
- Expression of NIS gene is inhibited by Iodide and stimulated by TSH
2. Propanolol
- Inhibits peripheral conversion of T4 to T3 (T4 is the primary product but T3 is the active
form)
- Peripheral conversion relies through the action of Thyronine-specific deiodinases
particularly Type 1 Deiodinase (D1), which occurs in tissues with high blood flow and
rapid exchange with plasma, such as the liver, kidneys, and thyroid gland.
3. Propylthiouracil
- Blocks peroxidase reactions therefore inhibiting iodination of tyrosine residues (Thyroid
peroxidase involved in iodine-tyrosine coupling - Step 4)
4. Methylprednisolone
- Also inhibits peripheral conversion (same with Propanolol)