Metabolism

Question 1

What percentage of horses can present anhidrosis and in what weather conditions?

Answer 1

25% in hot humid environment

Question 2

What are the clinical signs of anhidrosis?

Answer 2

Hyperthermia, poor performance, total or partial loss of ability to sweat, increased respiratory rates (3-5 times normal), and dry, thin hair coats with areas of alopecia

Question 3

What is the name of the catabolic process leading to break down of fatty acid to actyl-CoA, prior entering to the citric acid cycle?

a. Glycolysis
b. Ketosis
c. Pentose phosphate pathway
d. Beta-oxidation

Answer 3

d. Beta-oxidation

Fatty acid breakdown includes three major steps:

• Lipolysis of and release from adipose tissue
• Activation and transport into mitochondria
• β-oxidation

β-oxidation occurs mainly in the mitochondria.

Question 4

What is the effect of PTH in response to decreased extracellular fluid calcium ion concentration?

a. PTH stimulates bone resorption by the osteoblasts, causing release of calcium into the extracellular fluid
b. PTH increases reabsorption of calcium and phosphate by the renal tubules, leading to decreased excretion of calcium and phosphate in the urine
c. PTH is necessary for conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, which, in turn, increases calcium absorption by the intestines
d. PTH increases absorption of cholecalciferol (vitamin D3) by the skin, leading to increase calcium absorption by the intestines

Answer 4

c. PTH is necessary for conversion of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, which, in turn, increases calcium absorption by the intestines

Question 5

Where in the cell is Ach made?

What is the precursor and the enzyme use to produce it?

Answer 5

Ach is made from acetyl CoA and choline, they use the enzyme choline acetyltransferase and is made in the cytoplasm of axons, then transported in vesicles to be released in the synaptic cleft.

Question 6

What is secondary hyperparathyroidism? And what can it be caused by?

Answer 6

It is an increase in the parathyroid hormone related to vitamin D deficiency. Parathyroid hormone is stimulated by hypocalcemia (could be nutritional) .and chronic renal disease, which results in osteomalacia (trying to remove Ca from the bone).

Question 7

What is the most common cause of primary hyperparathyroidism?

Answer 7

Primary abnormalities in the parathyroid such as neoplasms. Clinical finding could include hypercalcemia (with possible metastatic calcification) and bone density loss.

Question 8

What can cause hypoparathyroidism?

Answer 8

Loss or destruction of the parathyroid gland. Clinical observations include hypocalcemia and hypophosphatemia.

Question 9

What is the treatment for hypoparathyroidism?

Answer 9

Vitamin D supplementation and Ca supplementation if needed.

Question 10

How does parathyroid (PTH) increases plasma Ca concentration?

Answer 10

Increases Ca intestinal absorption by increasing the amount of calbindin, which binds Ca and increases its absorption from the GI. It also stimulates osteoclasts to break down Ca from the bones and reabsorb it. The other way is by decreasing the amount of Ca excreted in urine and increases renal phosphate excretion (in loop of Henle and proximal part of the distal collecting tubules).

Question 11

Where does Vit D (Vit D3) come from and where is it processed?

Answer 11

Vitamin D comes from exposure to UV light in the skin, or by ingestion of cholecalciferol (less common). Once absorbed it goes to the liver and turns into 25-hydroxycholecalciferol, then it goes to the kidneys, where PTH turns it into 1-25-dihydroxycholecalciferol. Lastly it goes to the gut to stimulate Ca absorption (through calbindin).

Question 12

What is glucagon and what is its main purpose?

Answer 12

It is a hormone that comes from the alpha cells in the Langerhans islets from the Pancreas. It stimulates glycogenolysis and gluconeogenesis therefore increasing blood glucose concentration. It also stimulates Fat breakdown so that fatty acids are released for energy.

Question 13

What is somatostatin and what does it do to glucagon an insulin?

Answer 13

Somatostatin is the Growth Hormone Inhibitory Hormone (GHIH) that comes from the D cells from the Langerhans islets in the pancreas (it also comes from the hypothalamus). Somatostatin is a negative feedback by inhibiting glucagon and insulin secretion, it is released when there is food intake (suppresses hunger)..

Question 14

How does blood glucose affect carbohydrate and fat metabolism?

Answer 14

Increased blood glucose (BG) stimulates insulin release which stimulates carbohydrate metabolism and decreases fat metabolism. When BG is low the opposite happens.

Question 15

Where does insulin come from?

Answer 15

The beta cells in the Langerhans islets from the Pancreas.

Question 16

What is the receptor to which insulin binds to create its effect? What is the cascade effect that it has?

Answer 16

Insulin binds to the alpha-subunits of the insulin receptor on the outside of the cell.
The cascade effect starts by activating the beta subunits (in the cell membrane) which phosphorylate tyrosine kinase. Tyrosine kinase which phosphorylates other intracellular enzymes (insulin receptor substrates), which leads to a number of effects such a glucose transport, protein synthesis, fat synthesis, glycogen synthesis and growth and gene expression.

Question 17

How long does insulin lasts in plasma and who degrades it?

Answer 17

Half life of insulin is 10-15 min and is degraded by insulinase in kidney, liver and muscles.

Question 18

What are the different positive feedbacks for insulin secretion?

Answer 18

The following conditions will increase insulin secretion

• High blood glucose
• The aminoacids Arginine and Lysine
• GI hormones such as gastrin, secretin and cholecystokinin and GIP (gastric inhibitory peptide)
• Prolonged increases in glucagon, cortisol and growth hormone will cause increase in BG therefore, an increase in insulin.

Question 19

How does insulin affect protein metabolism?

Answer 19

It stimulates protein synthesis with the presence of amino-acids.

It draws the amino-acids into the cells and increases
translation of messenger RNA for protein synthesis. It decreases the rate of protein catabolism and depresses the rate of gluconeogenesis.

Question 20

How does insulin affect fat metabolism?

Answer 20

Low BG will increase fat breakdown for fatty acid release.
Fatty acids are converted into cholesterol and phospholipids by the liver which can eventually lead to ketosis and ketoacidosis in the absence of insulin.

Question 21

How does insulin affect carbohydrate metabolism?

Answer 21

Promotes muscle cell glucose uptake, liver uptake of glucose and eventual storage through increase of glycogen synthase. Gluconeogenesis is also inhibited by insuline.

Question 22

What is T3?

Answer 22

Triiodothyronine, is the active form of thyroid hormone, it gets converted from T4 in the tissues where it is needed.
It is responsible for transcription of genes.

Question 23

What is T4?

Answer 23

Thyroxine, is the most released form from the thyroid and gets converted to T3 in the tissues.

Question 24

What are the main functions of thyroid hormone?

Answer 24

• Activate nuclear transcription of large number of genes
• Increase cellular metabolic activity and basal metabolic rate by increasing activity in the mitochondria
• Increase active transport of ions through cell membrane
• Promote growth and development of brain,
• Stimulates carbohydrate and fat metabolism
• Increases protein synthesis and need for vitamins
• Increases respiration, blood flow, cardiac output and HR

Question 25

How do you measure thyroid function?

Answer 25

Measure TRH or TSH stimulation test. A baseline of T3 and T4 is obtained, then 1mg of TRH or 5 IU of TSH are administered, T3 should double at 2 hrs and T4 should double at 4 hrs.
Free T4 can also be used if only single point time collections are available.

Question 26

What are examples of glucocorticoids?

Answer 26

Cortisol (most potent, 95% of all glucocorticoide activity) and corticosterone.

Synthetic glucocorticoids:

• dexamethasone (30 times more potent than cortisol)
• methylprednisolone (5 times more potent than cortisol)
• prednisone (4 times more potent than cortisol)
• cortisone (same potency as cortisol)

Question 27

Which is the most important mineralocorticoid?

Answer 27

Aldosterone - does 90% of all mineralocorticoid activity

Desoxycorticosterone, corticosterone and cortisol also ave slight mineralocorticoid activity.
Synthetic - 9-alpha-fluorocortisol is slightly more potent than aldosterone.

Question 28

What other name does the posterior pituitary have?

What hormones are released from it?

Answer 28

Neurohypophysis.
Releases ADH (Anti Diuretic Hormone or Vasopressin), and Oxytocin

Question 29

What other name does the anterior pituitary have?

What hormones are released from it?

Answer 29

Adenohypophysis.

Releases TSH, GH, LH, FSH, ACTH (corticotropin), Prolactin.

Question 30

Why is Growth Hormone important?

Answer 30

It is important for growth and increased metabolic rate. It reduces fat storage by increasing fat metabolism and its usage for energy. It increases protein synthesis and decreases glucose utilization.

Question 31

How does GH work to stimulate growth?

Answer 31

It stimulates the liver to produce somatomedins (IGF - Insulin Growth Factor) which stimulate growth.

Question 32

What regulates GH secretion?

Answer 32

Factors that will increase GH release:

• Poor nutrition (starvation)
• High cortisol level (exercise, stress, excitement)
• Hypoglycemia or low concentrations of fatty acids
• Trauma
• Ghrelin