Flashcards in Post storyline quiz answers Deck (17):
Why can the effects of epinephrine be seen a few seconds after injection, whilst the effects of thyroid hormone requires a few hours?
Epinephrine - membrane bound G protein coupled receptor. Fast and dynamic. Upon activation they quickly involve G-proteins to generate second messengers. Procress from hormone-receptor binding to physiological function takes a few seconds.
Thyroid hormone - nuclear receptor. Enters the cell and activates transcription factor. This leads to mRNA formation which is then translated into protein to exert function. Process of making a new protein takes at least 30 minutes and effect may appear hours later.
Why is it difficult to make insulin tablets that can be taken orally in contrast to steroid hormones?
Insulin = protein. Many proteolytic enzymes are present in stomach that can digest (pepsin).
Steroid hormones are cholesterol derivatives. The GI tract facilitates steroid hormone absorption by secretion of bile salts.
How do tyrosine kinases work?
Catalyzes transfer of phosphate-donating molecule to a tyrosine residue of a protein.
Which endocrine processes influence the response of the liver and muscle to fasting?
Fasting - imbalance between consumption and uptake of energy
In order to keep the blood glucose level stable, the endocine and ANS elicit an integrated response that leads to the release of glucagon and adrenaline from the pancreas and adrenal medulla
Glucose is stored in the liver and muscle in the form of glycogen. Liver cells have glucagon and adrenaline receptors. The liver cells convert glycogen into glucose molecules in glycogenolysis.
When these stores become depleted, glucagnon encourage liver and muscle cells to produce more glucose via gluconeogenesis.
Adrenaline and glucagon regulate the metabolism through lipolysis (beta oxidation of fatty acids). Beta oxidation does not increase blood glucose but can make ketone bodies through formation of Acetyl-CoA. Circulating ketone bodies can be used as a source of energy.
Mechanism of foot ulceration
There are two main reasons for development of foot ulcers in diabetes.
A. Peripheral neuropathy: This complications leads to impaired sensation in patients with diabetes. So the patients don't feel pain after minor foot injury. This leads to continues tissue damage in their feet.
B. Vasuclar abnormality and endothelial dysfunction. These leads to poor perfusion of injured fingers and feet. Poor perfusion means slow repair of damaged tissues.
Prevention of foot ulceration is crucial in management of diabetes.
PTH is released in response to a [---] in plasma calcium
What roles do T3 and T4 play
Control metabolic rate
Development of CNS
Cellular and biochemical pathways for TH synthesis
The thyroid is composed of thyroidal cells that are lined up around a liquid called colloid. Synthesis of thyroid hormone requires several steps.
1. Iodide should be trapped in the thyroid gland. This is done by the aid of a sodium-iodide exchanger (symporter) in thyroidal cells.
2. Iodide will be then transported into the colloid in the outer side of the thyroidal follicular cells.
3. Thyroidal cells also synthetize a protein rich in tyrosine which is called thyroglobulin and secret it into the colloid.
4. At this location an enzyme called thyroperoxidase (TPO) takes iodide and converts in into iodine free radical.
5. This free radical is reactive and interacts with the tyrosine residues of the thyroglobulin (remember that thyroglobulin is rich in tyrosine amino acids).
6. This iodination of thyroglobulin makes iodinated tyrosine derivatives such as thyroxine (T4) and 3-iodothyronine (T4).
7. These iodinated compounds are attached to the thyroglobulin and are not free.
8. However, iodinated thyroglobulin can undergo endocytosis and enters the cell. Inside the cells proteolytic enzymes break down iodinated thyroglobulin and release free T4 and T3
What would happen to TSH levels if exogenous thyroxine was administered?
Suppresses TSH secretion by the pituitary through negative feedback loop
What would happen to TSH levels if exogenous TSH was administered?
TSH stimulates the thyroid gland to secrete thyroxine - leading to decreased TSH production by the pituitary due to negative feedback loop. q
What would happen to TSH levels if there was surgical removal of the thyroid gland?
Surgical removal decreases T3 and T4. There would be no negative feedback loop to suppress TSH release - TSH levels should go up.
How does the body regulate plasma calcium levels?
This requires good interaction between several organs.
Bones - reservoir of calcium
Gut - absorption of calcium from dietary sources
Also activation of vitamin D (formation of 1,25(OH)2 from the kidney). Gut has a receptor for the active form of vit D to increase calcium absorption.
Kidneys - change in rate of tubular calcium reabsorption
The endocrine and parathroid glands connect the activity of these organs.
How does atomic explosions increase rate of thyroid cancer?
Radioactive iodine is a major urianium, plutonium fission product.
Iodide is actively trapped by thyroid cells. This can emit ionizing radiation and induce DNA mutation in thyroid cells.
If one of these mutations affects an oncogene, it can lead to uncotrolled proliferation of thyroidal cells and cancer.
Consequences of iodine deficiency
Potential side effects from injecting cortisol analogues
Although glucocorticoids are very good anti-inflammatory drugs, they can cause harm to the body as well. The following are the main side-effects of prolonged glucocorticoid therapy:
1. Immunosuppression - more prone to serious infection (e.g. pneumonia).
2. Metabolic effects: Glucocotricoids can trigger temporary and possibly long term increase in blood glucose (diabetes mellitus). Calcium absorption may be suppressed and osteoporosis may result.
3. Wound healing requires a certain amount of cytokine production to recruit fibroblasts. Wound healing can be delayed during glucocorticoid therapy.
4. Psychological effects of glucocotricoids can be striking and may prevent some people from using them as therapy. They can cause mood changes and in some rare cases even psychosis.
What are the clinical presentations of 21-hydroxylase deficiency?
With low 21-hydroxylase activity, our body cannot make enough glucocorticoids and mineralocorticoids.
This stimulates the pituitary gland to release more ACTH.
High ACTH then leads to hypertrophy of the adrenal cortex.
A large adrenal cortex means that more sex hormones (e.g. androgens) are synthetized as shown in below figure.
The clinical phenotype of congenital adrenal hypertrophy is related to either:
a. Low glucocorticoid and aldosterone level,
b. high sex hormone synthesis (mainly androgens).
Clinical presentation depends on severity of the enzyme deficiency and the gender:
If the defect is severe it may result in water and salt wasting (aldosterone deficiency) and stress intolerance (cortisol deficiency).
Females with severe 21-hydroxylase deficiency have ambiguous genitalia at birth due to high level of androgens in their fetal stage.
Females with mild 21-hydroxylase deficiency are identified later in childhood because of precocious pubic hair and infertility.
Males with mild deficiencies of 21-hydroxylase also present with early development of pubic hair and precocious puberty.