Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Systemic Veterinary Pathology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

In the endocrine pancreas, what do the Alpha and Beta cells secrete?

A

A: Glucagon in response to hypoglycemia
B: Insulin in response to hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does insulin affect glucose, lipids, protein, and ketone levels in the body?

A

Insulin will decrease glucose, decrease lipolysis, decreased proteolysis, decreased ketogenesis, and decreased gluconeogenesis. Iti will increase glucose oxidation, increase glycogenesis, and increased lipogenesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does glucagon affect glucose, lipids, protein and ketone levels in the body?

A

Glucagon will increase lipolysis, proteolysis, ketogenesis. It will decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type I Diabetes Mellitus

A

No insulin is produced by beta cells due to degeneration of islet cell and hypoplasia usually because of an autoimmune condition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type II Diabetes Mellitus

A

Insulin is still produced, but the receptors are desensitized. These are on cells that allow glucose to be brought into cells to be used as energy . Insulin antagonism and anti-insulin antibodies can also play role.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hyperglucagonemia in diabetes mellitus

A

This is characterized by excess glucagon production/secretion by the alpha cells of the pancreas. It can increae the oxidation of fatty acid in hepatocytes leading to ketoacidosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How could deficiencies in islet cells be created?

A
  1. Immune mediated disease
  2. Neoplasia
  3. Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which hormones can act as insulin antagonizer in type II diabetes mellitus?

A
  1. Growth hormone
  2. Glucagon
  3. Glucocorticoids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In diabetic cats, what is a common accumulation in the pancreatic islets of their pancreas?

A

Amyloid derived from islet amyloid polypeptide (IAPP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In diabetic dogs, what clinical sign occurs with the eyes and why?

A

Cataracts due to glucose being converted to sorbitol and fructose in the lens leading to swelling and degeneration of the lens fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Emphysematous cystitis in diabetic dogs, what is it and what is happening?

A

It is an infection of the bladder wall caused by gas-forming bacteria or fungi. Diabetes dogs are suffering from hyperglycemia which causes the body to want to excrete as much glucose as possible in the urine leading to glucosuria. Glucose fermenting bacteria appear in the bladder and form gas which damages the wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is insulinoma and what clinicopathologic finding is usually seen in a patient with this?

A

An insulinoma is a functional tumor ( if benign= adenoma, if malignant= adenocarcinoma) in the pancreas that affects the beta cells and causes an excess of insulin to be produced/secreted. This can lead to hypoglycemia which can manifest into collapse and/or seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

If a ferret has an insulinoma, what would the gross appearance of the pancreas be? Why?

A

Nodular hyperplasia. The current theory is that when they are fed diets high in carbohydrates, the blood sugar continually spikes causing overstimulation of the beta cells=hyperplasia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the best way to diagnose an insulinoma?

A

There will be hypoglycemia even with normal to increased blood levels of insulin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a gastrinoma and what lesion commonly accompanies it?

A

A gastrinoma is a rare invasive tumor in the pancreatic islets that affects the gastrin secreting G cells. This causes hypersecretion of gastric acid in the stomach leading to the development of peptic/gastric ulcers. Also called ““Zollinger-Ellison syndrome”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are chemoreceptors and where are they?

A

These detect fluctuations in oxygen, carbon dioxide, and pH levels in the blood. They are located in the aortic arch (aortic body) and near the bifurcation of the carotid arteries (carotid body).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a chemodectoma and what gross appearance will it have?

A

It is a tumor of either the aortic or carotid body. In animals, it is most commonly of the aortic variety in dogs, especially brachycephalic breeds. It presents as a solid white mass surrounding the aorta in the pericardial sac and it indistinguishable from a thyroid carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the major differences between aortic body and carotid body chemodectomas?

A

Aortic chemodectomas are non-functional and usually adenomas, but take up space and can cause pressure on the atria/vena cava.
Carotid chemodectomas are also non-functional, slow growing, unilateral, adenocarcinomas or adenomas. They can invade certain cranial nerves and the external jugular vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the etiology of chemodectomas?

A

The current theory is that brachycephalic dog breeds are in a constant state of hypoxia leading to hyperplasia of the aortic/carotid bodies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two functional cell types in the thyroid gland and what do they secrete?

A
  1. Thyroid follicular cells: Thyroxine ( T4) and Triiodothyronine(T3)
  2. Thyroid C cells (parafollicular): calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are the thyroid hormones regulated by the adenohypophysis?

A

The thyrotroph basophil cells of the adenohypophysis (pars distalis) release thyroid stimulating hormone (TSH) after the hypothalamus releases thyrotropin releasing hormone (TRH). The TSH from the adenohypophysis stimulates thyroid follicular cells to release T3 and T4 which usually raise increases the body’s metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain the main functions of T3, T4, and reverse T3.

A

T3 is responsible for most of the biologic effects in the body and has a longer half-life than T4.
T4 is the primary hormone secreted by the thyroid.
Reverse T3 is biologically inactive or protein bound hormone and represents the majority of hormone in the body, The free hormone levels in the blood represent the true thyroid status of the patient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What happens to T4 when a patient is suffering from renal disease or has protein restriction in a neonate?

A

It will be preferentially mono deiodinated to reverse T3.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In early hypothyroidism, why would serum T3 levels sometimes be within normal limits?

A

There is a possibility that the disease has not progressed enough to lower the serum levels, however, the T3 levels in the tissues may be lower than normal therefore not providing those tissue with enough hormone to function properly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

If there is chronic TSH stimulation, what gross and histologic appearance will the thyroid gland have?

A

TSH is released from the adenohypophysis and will stimulate the thyroid to secrete T3 and T4. In excess, this would overstimulate the thyroid causing hyperplasia and reduced luminal colloid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

If there is reduced TSH stimulation, what gross/histologic appearance will the thyroid gland have?

A

The thyroid gland will not be secreting as much T3 and T4 and will result in atrophy of the gland with increased luminal colloid as more T3/T4 is stored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

If there is chronic thyroxine (T4) administration, what will the thyroid gland look like grossly/histologically?

A

This will cause there to be a decrease in T4 secretion which will cause atrophy of the thyroid gland and an increase in appearance of colloid due to more storage of T4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

If there is an iodine deficiency, what will the thyroid gland look like grossly/histologically?

A

Iodine is required for the synthesis of T3 and T4. There will be a decrease in T3 and T4 which will cause the pituitary gland to ramp up (negative feedback lost) and release more TSH to stimulate the thyroid to produce more T3 and T4. Chronic stimulation of TSH will cause follicular hyperplasia of the thyroid gland and there would be decreased colloid because the cells are not making any T3/T4 to be stored.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

If there is an excess in iodine, what will the thyroid gland look like grossly and histologically?

A

Too much iodine means that there will be a reduction of T3/T4 synthesis in the thyroid gland. Because there is less T3/T4 in the blood, the adenohypophysis will start to release more TSH and stimulate the thyroid gland in excess leading the follicular hyperplasia and reduced luminal colloid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why would decreased total serum T4 levels not confirm a diagnosis of hypothyroidism?

A

There is a disease called euthyroid sick syndrome which can decrease the T3/T4 levels without there being hypothyroidism. You would want to test FREE T4 levels as it is more sensitive and specific. Testing for high TSH concentration along with low to borderline serum T4 levels is diagnostic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

In a dog with clinical hypothyroidism, what could the gross appearance of the thryoid gland be?

A
  1. Idiopathic follicular collapse and luymphocytic thyroiditis= thyroid atrophy
  2. Thryoid ademona/carcinoma with iodine defeciency/excess= Thryoid hyperplasia
  3. Secondary hypothryoisim due to a pituiary proglme = thryoid gland atorphy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the common cutaneous changes in a dog with hypothyroidism?

A
  1. Bilateral alopecia
  2. Hyperkeratosis
  3. Hyperpigmentation
  4. Myxedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What vascular disease may accompany hypothyroidism in dogs?

A

Atherosclerosis: Thyroid hormones are important for maintaining cholesterol levels, blood pressure, c reactive protein levels, and the renin-angiotensinogen system. Less of these hormones tend to increase cholestrol levels, blood pressure, and crp levels while decreasing vasodilatory substeances and inhibition of angiotensinogen Ii receptors. This can all lead to increase risk of atherosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In cats with clinical hyperthyroidism what will the gross appearance of the thyroid glands be?

A

Bilateral (usually) nodular, multifocal, hyperplasia with a possible adenoma or carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

In feline hyperthyroidism, what cardiac lesion is usually present? Why?

A

Hypertrophic cardiomyopathy due to the elevated thyroid hormones that stimulate the heart to pump faster and more forcefully in order to keep up with the increased metabolic needs, requiring more blood to be pumped to maintain the same HR and blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are four differential diagnoses for goiter ( or enlarged, hyperplastic thyroid gland that is non neoplastic and non inflammatory) in neonatal sheep?

A
  1. Iodine dificient diet
  2. Excess dietar iodine
  3. INgetion of goitrogenic compounds
  4. Congenital dyshormonogenic goiter ( a defect in thyroglobulin synthesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the difference between hyperplastic and colloid goiter?

A

Hyperplastic goiter: There is excessive TSH stimulation

Colloid goiter There is diminished TSH stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are two differential diagnosis for a mass surrounding the aorta in a dog?

A
  1. Chemodectoma

2. Ectopic thyroid carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Is a dog or a cat more likely to have a follicular cell carcinoma?

A

A dog, cats are more likely to have an adenoma.

40
Q

In aged bulls that are chronically fed a dairy ration, what will the histological/gross appearance of the thyroid gland be?

A

A dairy ration diet contains excess calcium. Excess serum calcium increases the production of calcitonin in the C cells of the thyroid gland. Overstimulation of the c-cells leads to hyperplasia of the cells=enlarged thyroid gland

41
Q

What are the hormone responsible for Ca+ homeostasis? Where are they produced and what is their action of the kidney, bone, and intestine?

A
  1. Parathryoid hormone: Produced by the chief cells in the parathyroid gland. Decreases renal reabsorption of phosphate, increases absorption of Ca+ in the intestine and mobilizes bone Ca+ into the blood.
  2. Calcitonin: Produced by the C-cells in the thyroid gland. Decreases absorption of Ca+ in intestines, decreases resorption of phosphate, and increased Ca+ deposited in bone.
  3. Vitamin D3: Comes from the diet. It increase Ca+ retention in the bone ( mineralization) and increases Ca+ absorption of Ca+ and phosphorus in the intestine.
42
Q

What are some examples of primary hyperfunction of the parathyroid gland?

A

A functional chief cell adenoma which would cause fibrous osteodystrophy due to unregulated increase in PTH secretion that would cause increased calcium mobilization from the bone with decreased phosphorus resorption.

43
Q

What are some examples of primary hypofunction of the parathyroid gland?

A
  1. Invasive/destructive neoplasm
  2. Iatrogenic via surgical removal of the parathyroid glands
  3. Lymphocytic parathyroiditis
44
Q

How does primary hypoparathyroidism result in tetany, seizures, and neuromuscular excitability?

A

There is reduced action of PTH which would cause decreased Ca+ mobilzation from bone causing there to be less of Ca+ in the blood.

45
Q

Whare are some causes of secondary hyperparathyroidism, how would the parathyroid gland appear grossly?

A
  1. Nutritional: a Ca+ or Vitamin D deficiency or excess of phosphorus in the diet woul cause an increase in PTH secretion in order to increase the Ca+ in the blood and cause bilateral symmetric hyperplasia of the parathyroid glands.
  2. Renal: If the glomerular filtration decreases for whatever reason, phosphorus is retained which causes the ionized blood Ca+ to decrease. In order to bring the Ca+ level backup, PTH is secreted in excess which could cause bilateral symmetric hyperplasia of the parathyroid glands.
46
Q

What would a persistent elevation of PTH do to the body?

A

It would cause a increase activity in osteoclasts which basically break down bone to release Ca+ into the bloodstream.

47
Q

Explain how vitamin D/calcitriol is related to the kidney and parathryoid gland.

A

D3 stimulates calcium uptake at the distal tubule luminal membrane in the kidney in response to high PTH levels. A cytosolic vitamin D-dependent calcium-binding protein (calbindin-D) sequesters calcium, which allows more calcium to enter the cell and more efficient diffusion of calcium across the cell. The ATP-dependent plasma membrane Ca2+ pump in the basolateral membrane pumps calcium out of the distal tubule cells into plasma. Therefore; vitamin D increases a number of blood Ca+ in response to increased PTH telling the kidney to activate vitamin D>

48
Q

What is humoral hypercalcemia of malignancy and what neoplasms are associated with this condition?

A

Another name for this is pseudohypoparathyroidism where a tumor released a PTH-related peptide that can cause the blood Ca+ levels to increase too much ( Hypercalcemia) leading to soft tissue mineralization in the kidneys, lungs, stomach, and heart. T cell lymphomas and apocrine gland of anal sac adenocarcinoma will do this. The parathyroid gland will respong to the increased PTH-rp but not secretiing PTH leading to atrophy of the C cells and the parathyroid gland as a whole.

49
Q

What is milk fever and how does it relate to dairy cow diet?

A

Milk fever is parturient hypocalcemia that occurs when there is excessive calcium in the diet. The increased calcium in the blood causes more calcitonin to be released from the C-cells in the parathyroid gland. Calcitonin helps bone absorb Ca+ and makes it more difficult for calcium stores to be mobilized for milk production. The pool of osteoclasts for PTH to stimulate is not big enough. The small osteoclast pool results from feeding a high level of dietary calcium during the nonlactating period, which suppresses parathyroid gland secretion of PTH and stimulates parafollicular C-cell secretion of calcitonin.

50
Q

Zona glomerulosa

A

Mineralocorticoids like aldosterone

51
Q

Zona fasciculata

A

Glucocorticoids like cortisol and corticosterone

52
Q

Zona reticularis

A

Sex steroid hormones like progesterone, estrogen, and androgen

53
Q

How is aldosterone secreted?

A

Decrease in blood volume increases renin secretion from the kidney which catalyzes the conversion of angiotensin 1 to angiotensin 2- angiotensin 2 acts on the zona glomerulosa to secrete aldosterone.

54
Q

How does aldosterone effect the distal convoluted tubule of the kidney?

A

Increases sodium absorption from the glomerular filtrate and increases potassium secretion.

55
Q

How is glucocorticoid secreted?

A

When an animal is stressed, ACTH is released from the adenohypophysis of the pituitary gland. The ACTH stimulates the zona fasciculata ( and the whole ardrenal cortex) of the adrenal cortex to produce and secrete cortisol.

56
Q

What effect do glucocorticoids have on the liver?

A

Increase protein catabolism which provides amino acids for the liver to use in gluconeogenesis. It will also increase the glycogen storage.

57
Q

What effect do glucocorticoids have on muscle?

A

Increase protein degradation (catabolism) and decreases protein synthesis

58
Q

What effect do glucocorticoids have on fat stores?

A

They increase lypolysis to provide more glycerol for the liver to create more glucagon and decrease the glucose utilization of the lipids.

59
Q

When a patient as hyperadrenocorticism and they just were out of surgery, what do we need to be aware of?

A

That the animal is stressed and secreting glucocorticoids. Glucocorticoids suppress inflammation and immunological responses which can increase the risk of infection. In addition, they inhibit fibroblast proliferation and collagen synthesis which can make it difficult for a wound to heal.

60
Q

What hormones are secreted by the adrenal medulla?

A

Norepinephrine and epinephrine which are both catecholamines

61
Q

When a dog is suffering from hypoadrenocorticism, what will be happening with it’s electrolytes?

A

Hypoadrenocorticism is characterized by a decreased secretion of mineralocorticoids form the zona glomerulosa. Mineralocorticoids like aldosterone excrete Ka+ out of body and absorb Na+ and water, so the patient will be hyperkalemia=bradycardic, and hypoatremic and hypochloremic, probably dehydrated as well.

62
Q

What would the gross/microscopic appearance of the adrenal glands be in a dog with hypoadrenocorticism?

A

Bilateral atrophy of all three zones of the adrenal cortex. Most likely from immune mediated destruction or lack of stimulation. Microscopically, we will see lymphocytic and plasmacytic inflammation with thin cortices.

63
Q

How would a horse acquire bilateral adrenocortical hemorrhage?

A

Severe adrenocortical hemorrhage and necrosis resulting in adrenal insufficiency is caused by vascular derangements and ischemia associated with the primary disease in patients with septicemia or endotoxic shock.

64
Q

What is the most common cause of hyperadrenocorticism in the dog?

A

A functional corticotroph pituitary adenoma that secretes ACTH, overstimulates the adrenal cortex ( mainly zona fasiculata) and causes bilateral adrenal cortical hypertrophy and hyperplasia ( cushing’s disease)

65
Q

What are two causes of hyperadrenocorticism in dogs that do not involve a pituitary adenoma?

A
  1. Iatrogenic administration of corticosteroids that causes bilateral adrenal cortical atrophy
  2. Functional adrenal gland adenoma that secretes glucocorticoids and causes unilateral adrenomegaly ( adrenal gland with the tumor) and contralateral cortical atrophy ( this gland stops producing glucocorticoids and atrophies) .
66
Q

What tests can you used to diagnose hyperadrenocorticism?

A
  1. ACTH stimulation test

2. Low dose dexamethasone suppression test

67
Q

How would a normal ACTH stimulation test took? What about a dexamethasone suppression test?

A

ACTH: You administer ACTH and the body’s cortisol level will rise.
DST: You administer the Dexamethasone and the cortisol level should decrease.

68
Q

How will an ACTH stimulation and DST look if the patient has a functional pituitary adenoma?

A

ACTH: Doesn’t really screen for this, but if the cortisol level increases, you know you have general cushing’s disease.
DST: The cortisol level will be suppressed

69
Q

How will an ACTH stimulation and DST look if the patient has a Iatrogenic hyperadrenocorticism condition?

A

ACTH: Cortisol level will stay the same
DST: Don’t’ use this test as the body already suppressed all the cortisol it could from the administration of the ACTH.

70
Q

How will an ACTH stimulation and DST look if the patient has a functional adrenal adenoma?

A

ACTH: If the cortisol level increases, you know that patient has cushing’s, but can’t tell why.
DST: Cortisol level will stay the same

71
Q

Which test should you use for iatrogenic hyperadrenocorticism?

A

ACTH stimulation Test

72
Q

How will a adrenocortical adenoma look different than adrenocortical carcinoma? Which is more common?

A

Adenoma (more common) will be well demarcated with unilateral nodule and partially completely encapsulated while the carcinoma will show vascular and capsular with metastasis.

73
Q

How would a functional versus non-functional adrenocortical compare morphologically?

A

It is not possible to distinguish non-functional versus functional grossly. However, a functional adrenocortical tumor would cause contralateral atrophy in the unaffected adrenal cortex.

74
Q

What cutaneous changes will you see in a dog with hyperadrenocorticism?

A
  1. Calcinosis cutis
  2. PIgmentation changes
  3. Bilaterally symmetric alopecia
  4. Thinning elasticity of skin
  5. Secondary infections like pyoderma and malassezia
75
Q

Microscopically, how would a canine liver look with hyperadrenocorticism?

A

There would be severe glycogen and lipid accumulation causing steroid hepatopathy. This would lead to severely high alkaline phosphatase levels. Vacuolization of hepatocytes would be seen.

76
Q

If a ferret had an adrenocortical neoplasm, how would it differ from that in a dog?

A

Since ferrets have an increased lyase activity with these types of neoplasm and dog do not, the tumor will secrete estradiol or androgenic steroid hormones. Lyases are needed in the synthesis of androgens and estradiols. The tumor would also cause unilateral adrenomegaly and not contralateral atrophy.

77
Q

In ferrets with adrenocortical neoplasms, what lesions will you see?

A
  1. Vulvar enlargement or prostatic gland squamous metaplasia
  2. Pyometra
  3. Endometrial hyperplasia
  4. Bilateral symmetric alopecia
  5. Anemia
  6. Thrombocytopenia
78
Q

What is the gross appearance of a pheochromocytoma?

A

It is located in the adrenal medulla and is surrounded by a thin, compressed, rim of the adrenal cortex. They are large, multilobular and can be encapsulated.

79
Q

What cardiac changes can you expect to see with a pheochromocytoma?
Why?

A
  1. Tachycardia
  2. Edema
  3. Cardiac Hypertrophy
  4. Hypertension

The tumor causes an excess of norepinephrine to be secreted from the adrenal medulla. This ramps up the sympathetic nervous system .

80
Q

What are the major hormones produced by the pars distalis (adenohypophysis) and from where?

A
  1. ACTH
  2. Melanocyte-stimulating hormone
  3. Growth hormone
  4. Prolactin
  5. LH and FSH
  6. TSH
81
Q

What are the major hormones produced by the pars nervosa (neurohypophysis)?

A
  1. ADH (vasopressin)

2. Oxytocin

82
Q

What cell types are found in the adenohypophysis?

A
  1. Chromophobes
  2. Acidophils
  3. Basophils
83
Q

What is the mechanism of GH secretion from the pars distalis?

A

GHRH released from hypothalamus-adenohypophysis release GH from somatotrophs-GH acts on target tissues.

84
Q

What is the mechanism of ACTH secretion from the pars distalis?

A

CRH released from hypothalamus-adenohypophysis released ACTH from corticotrophs-ACTH acts on adrenal cortex to release cortisol from the zona fasciculata and sex steroids from the zona reticularis..

85
Q

What is the mechanism of TSH secretion from the adenohypophysis?

A

TRH released from hypothalamus-adenohypophysis secretes TSH from thyrotrophs-TSH acts on thyroid follicular cells.

86
Q

What is the mechanism by which hormones of the neurohypophysis are produced and excreted?

A

Hormones are synthesized in cell bodies in hypothalamus- they are transported by axonal processes of the hypothalamic-hypophyseal tract to axons in the neurophypohesis- released in the hypothalamophypohyseal protal system.

87
Q

If there is aplasia of the adenohypophysis what will the morphlogic appearance of target endocrine organs look like?

A

Adrenal cortex:Hypoplasia
Gonads: Hypoplasia
Thyroid follicular cells: Hypoplasia

88
Q

Why is there prolonged gestation in animals with panhypopituitarism?

A

Since there is a decreased amount of ACTH stimulating the adrenal cortex to secrete cortisol, 17alpha-hydroxylase in the placenta is not induced which leads to maintained progesterone levels as it is not converted to estrogen=maintained pregnancy.

89
Q

What does veratrum californicum do to sheep?

A

It can cause cyclopia in the lamb when the mother ingests it on day 12-14 of gestation. The toxins inhibit neural tube development which leads to craniofacial malformation , CNS and hypothalamic defect, and lack of thalamic control of the HPA axis.

90
Q

What is the clinical appearance of dogs with panhypopituitarism?

A

The dog will have a small skeleton with delayed growth plate closure. This is caused by a decrease amount of somatotropin secretion from the adenohypophysis and that is critical for interstitial cartilage growth.

91
Q

What is the clinical appearance of dogs with panhypopituitarism?

A

The dog will have a small skeleton with delayed growth plate closure. This is caused by a decrease amount of somatotropin (growth hormone) secretion from the adenohypophysis and that is critical for interstitial cartilage growth.

92
Q

Explain how pituitary dwarfism occurs in german shepherd dogs.

A

Autosomal recessive genes cause failure of the oropharyngeal ectoderm to differentiate.

93
Q

What is the most likely cause of panhypopituitarism in adult animals?

A

A neoplasm which reduces trophic stimulation of target organs and causes a mass effect that can lead to CNS problem and diabetes insipidus.

94
Q

If an animal has a functional adenoma of the pituitary gland, what will be the gross/microscopic appearance of the adrenal glands?

A

Bilateral adrenocortical hyperplasia, especially of the zona fasciculata and reticularis as the tumors tend to arise in corticotroph cells of the adenohypophysis. This will to lead to hyperadrenocorticism.

95
Q

If an animal has a non-functional adenoma of the pituitary gland, what will be the gross/microscopic appearc of the adrenal glands?

A

The tumor is compressive and reduces the secretion of pituitary hormones. There will be less TSH=decrease metabolic rate, loss of muscle and atrophy of skin due to a loss of anabolic effect of growth hormone, trophic atrophy of the adrenal cortex from loss of ACTH stimulation, and hypoglycemia.

96
Q

Where is the typical location of pituitary adenomas in the dog?

A

The pars distalis… adenohypophysis.

97
Q

Where is the typical location of a pituitary adenomas in horse?

A

The pars intermedia

Systemic Veterinary Pathology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions