Endocrine Flashcards
What is hypersomatotropism better known as? What is the difference between the two?
Acromegaly, growth hormone excess. Acromegaly is the clinical syndrome characterised by exposure to GH production over a long period of time. Hypersomatotropism is a more accurate description for all, where clinical signs may vary depending on length of exposure.
Which species and signalment is over represented in cases of acromegaly / hypersomatotropism ?
Feline, male, senior cats (8-14yrs)
What do somatotrophic cells secrete? Where are they found in the body?
Growth hormone, pituitary
Why do cats with acromegaly often present with diabetes mellitus?
Growth hormone is secreted by the tumour. This hormone is a diabetogenic hormone as it antagonises the effects of insulin. Leading to insulin resistance and diabetes.
What is a proxy for growth hormone measurement in the investigation of hypersomatotropism?
IGF-1 (insulin like growth factor)
Production of growth hormone from the pituitary is stimulated and inhibited by different peptides. Which peptides are they? Where are they produced from?
Growth hormone releasing protein GHRP (hypothalamus) increases production. Somatostatin inhibits production (hypothalamus).
In dogs, growth hormone can be produced from two glands. Name both.
Pituitary and mammary
In central versus nephrogenic diabetes insipidus, how does ADH differ?
Central is the reduced production of viable adh, nephrogenic is reduced activity of adh
What is the most common cause of canine primary hypothyroidism ? What are other differentials for primary hypothyroidism ?
Lymphocytic thyroiditis (thyroid tissue is destroyed in an immune mediated process, and tissue replaced by fibrous connective tissue). Other causes include idiopathic atrophy (atrophy of the gland and adipose tissue replaces viable tissue), follicular cell hyperplasia and infiltrative neoplasia
Describe the phenomenon known as euthyroid sick syndrome?
Concurrent illness in the body causes a fall in thyroid hormone levels.
Which tests would be helpful to diagnose hypothyroidism. Alongside total t4?
free T4 and TSH
Describe the three ways in which parathyroid hormone increases serum calcium
Conversion of vitamin D to its active form, vitamin D3 which increases absorption of calcium from GI tract, renal conservation of calcium and calcium release from boney stores
How can an ultrasound examination of the adrenal glands (bilaterally) help to differentiate between pituitary and adrenal dependent hyperadrenocorticism?
Bilateral enlargement of adrenals hint at pituitary, as negative feedback cancelled out by the pituitary adenoma. Unilateral enlargement and opposing atrophy indicate adrenal dependent, with the tumour on the larger gland. Negative feedback suppresses ACTH production, but this does not affect circulating cortisol
Describe the pathophysiology of Glucagonoma.
Rare tumour of the alpha cells within the islets of langerhans in the pancreas. They cause an erosive crusting skin rash called superficial necrolytic dermatitis (SND). The rash occurs most often on footpads causing pain, pruritis, interdigital erythema, crusting and fissuring of footpads.
Describe how bioactive vitamin D is produced. What else is it known by? What action does it illicit?
- Vitamin D3 obtained from diet
- Liver hydroxylates vitamin D3 to become vitamin D2
- Vitamin D2 travels to the kidneys via the blood stream
- Inside the proximal renal tubules, vitamin D2 is hydroxylated by 1-alpha-hydroxylase
- Known as calcitriol
- Will stimulate serum calcium levels
Which three mechanisms contribute to the regulation of active vitamin D (calcitriol) production?
- Negative feedback mechanism of circulating products. High PTH, low calcium, low phosphorus, low calcitriol will upregulate 1-alpha-hydroxylase activity (producing more calcitriol). The reverse is seen with low PTH and high calcium, phosphorus and calcitriol.
- Intracellular mechanism within all target cells. Production of 24-hydroxylase which catalyses the inactivation of calcitriol. High levels will reduce calcium and phosphorus by reducing calcitriol. Low levels will allow for more active calcitriol.
- Biding of calcitriol to carrier proteins.
Where in the stomach is gastrin produced.
Antrum of the stomach by G-cells
Which cells in the stomach are responsible for gastric acid secretion?
Parietal cells.
What is diaphoresis?
Excessive sweating, can occur in people as a result of hypoglycaemia
What is the Somogyi phenomenon?
Proposed in 1930s, hypoglycaemia in the evening followed by hyperglycaemia in the morning. Postulated to be due to counter regulatory hormones secreted overnight. Disputed after continuous blood glucose monitoring technology available. Other theories include dawn phenomenon where insulin secretion reduces overnight.
Describe the length of activity of neutral protamine hagedorn insulin, and porcine lente insulin
Are rapidly absorbed and considered intermediate acting, can be considerably less than 12hrs. Individual activity varies.
Describe the activity of protamine zinc insulin and glargine insulin
Slow onset and prolonged activity. Nadir can be up to 22hrs post administration
How and why do ketone bodies form, in the pathophysiology of diabetic ketoacidosis?
1) Ketone bodies are the by-products of fat metabolism. Fatty acids and glycerol are released into the blood from fat cells. The liver breaks down the fatty acids to form 3 by products (acetone, acetoacetic acid and beta hydroxybuteric acid) which can be used by cells to respire.
2) in DM, these are formed due to low insulin and hyperglycaemia. Glucose is not taken up into cells. The liver upregulates the catabolism of fatty acids as a source of energy. This leads to a build up of ketone bodies, as synthesis outweighs excretion
What is meant by the term “osmotic diuresis” in relation to the pathophysiology of diabetic ketoacidosis ?
ketone body production increases in a state of dka. Synthesis outweighs excretion and ketone bodies build up. This leads to ketonuria and an osmotic diuresis. Acidaemia also increases renal excretion. This can lead to clinical dehydration.
What does the pineal gland produce? Where is it located?
Produces melatonin which is essential for circadian rhythms and the sleep-wake cycle. It is in the central brain between the two hemispheres and near the thalamus.
Which test is non-invasive, can be competed at home and is highly sensitive for HAC?
Urine sample collection, Urine cortisol:urine creatinine ratio
Which diagnostic test is completed in the clinic and is highly sensitive for HAC?
LDDST
A patient is having an ACTH stimulation test. The response is exaggerated. What diagnostic information does this yield?
Not Addisons. Could be HAC however not very sensitive as responses vary. Could be HAC, in conjunction with consistent clinical signs, LDDST and UCCR.
Anatomically, which layer of the adrenal gland produces mineralocorticoids?
Zona glomerulus
Anatomically, which layer of the adrenal gland produces glucocorticoids?
Zona fasciculata
Anatomically, which layer of the adrenal gland produces androgens?
Zona reticularis
Anatomically, which layer of the adrenal gland produces adrenaline/noradrenaline?
Medulla
What action does gastrin have on parietal cells?
Gastric acid secretion and mucosal growth
Other than gastrin, which two other ligands can stimulate gastric acid secretion?
Acetylcholine and histamine
An excess of which hormone causes Zollinger-Ellison syndrome?
Gastrin
Define what is meant by a paracrine gland
A gland that produces a hormone that acts locally, in close vicinity to the gland
Which type of tumour represents the most common cause of canine hyperadrenocorticism ?
Pituitary adenoma (rarely carcinoma)
What makes atypical hyperadrenocorticism different from typical HAC?
Atypical is due to increase in cortisol precursor molecules. Means most tests will be normal despite classic clinical signs and exam. Typical HAC is excessive cortisol.
How does renal secondary hyperparathyroidism manifest?
In early dz, lower GFR. This leads to phosphorus retention as excretion reduces. An increase in the phosphaturic hormone, FGF-23, tries to increase excretion of phosphorus. It will also reduce calcitriol production. A fall in calcitriol leads to reduced calcium levels, which stimulates PTH production. As CKD progresses, the patient can develop hyperparathyroidism due to excess PTH secretion in response to phosphorus imbalance.
