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VET377 > Endocrine 2 and 3 > Flashcards

Endocrine 2 and 3 Flashcards

1
Q

For the diagram below:

i) Name structures 1, 3, 5, 13
ii) 7 is systemic effects
iii) 10,11,12 name the triggers
iiii) The other numbers are the hormones
iv) Name the two ions excreted and 2 ions retained

A
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2
Q

For the image below:

i) For 1-6 state zones
ii) For 6, 7 and 8 state what is produced in these zones

A
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3
Q

What are the three main actions of gluco-corticoids?

A
  1. Hyperglycaemia with secondary hyperinsulinaemia
  2. Muscle atrophy
  3. Anti-inflammatory action
  4. Increased lipolysis (combined with hyperinsulinaemia) meaning increased intra-abdominal deposition (pot bellied appearance) and decreased subcutaneous fat deposition (leads to thin and inelastic skin)
  5. Effects on electrolytes + kidney: Increased GFR and inhibition of ADH release = polyuria, Na retention and increased K excretion = uncommon
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4
Q
A
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5
Q

Describe the pathophysiology of pituaritary dependant hypercortisolism (PDH):

A

Occurs in 80-85% of cases. Microadenoma or adenocarcinoma. Get bilateral adrenal hyperplasia + exaggerated responses to ACTH stimuli.

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6
Q

Breifly explain why hypercortisolism due to adrenalcortical tumour results in atrophy of the contralateral gland:

A

Adenoma or adenocarcinoma occurs in one of the adrenal glands. This leads to excessive release of cortisol that then results in atrophy of the contralateral gland

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7
Q

Breifly explain what causes iatrogenic hypercortisolism and why it is important not to stop the administration of these drugs suddenly:

A

Corticosteroid administration results in hypothalamus and pituaritary gland negative feedback. This results in bilateral adrenal gland atrophy due to absence of ACTH.

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8
Q

Provide an example of something that will predispose an animal to PDH (pituaritary-dependant hypercortisolism) or AT (adrenocortical tumour):

A

PDH: poodles, Dachs, terriers

AT: any dog above 20kg

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9
Q

What are the clinicopathologic changes suspected with hyperadrenocorticism? (THIS WILL BE IN EXAM)

A
  1. Stress leukogram -lymphopenia, neutrophilia, monocytosis, eosinopenia
  2. Policythemia - hypoxia secondary to chronic respiraotry insufficency
  3. ALP - due to isoenzyme C-ALP induction seen in 90% of cases
  4. Increased ALT and GGT - 50 to 80% of cases - secondary to vacuolar hepatopathy due to incrased glycogen storage + hepatocyte hypoxia
  5. Increased bile acids - about 30% of cases - mild hepatic insufficiency
  6. Increased glucose - increased in baout 30% of cases - mild hepatic insufficiency glucocorticoid induced hepatopathy
  7. Hyperlipaemia
  8. Decreased urea - seocndary to PU
  9. Decreased creatinine - reduced muscle catabolism
  10. Iso and hyposthenuria - gluco-cortiocid hormones inhibited by ADH secretion + cortisol may inhibit responsiveness of renal tubules to ADH
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10
Q

Is a stress leukogram sufficient enough to justify a test for hyperadrenocortism?

A

No as it has very low specificity

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11
Q

What is a test with high sensitivity good for?

A

Good test for screening

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12
Q

What is a test with high specificity good for?

A

A good test for confirming that an animal does not have the disease of interest

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13
Q

What is a test with high specificity good for?

A

Good test for confirming that an animal has a disease

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14
Q
  1. When is a dose dexamethosone supression test useful?
  2. Fill in the blanks on the test below
A

i) The test is usefull as a screening test if iatrogenic hyper-adrenocorticism is not expected

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15
Q

Comment on the specificity and the sensitivity of the low-dose dexamethasone supression test:

A

Sensitivity is high

Specificity is medium-low

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16
Q
  1. When is the ACTH stimulation test used?
  2. Fill in the blanks below
A
  1. Gold standard test for diagnosis of iatrogenic HAC
17
Q

Describe the specificity and the sensitivity of the ACTH stimulation test:

A

Moderate to low sensitivity

Moderate specificity = false positive results with stress

18
Q
  1. When should the urinary cortisol to creatine ratio test be used?
  2. Can it be used as the only test in the diagnosis of HAC?
A
  1. High sensitivity = if negative HAC ruled out. The low specificity = frequent false positives. This makes it a good initial screening test for HAC
  2. However this test should not be used as only test to diangose HAC
19
Q

When should a high dose dexamethasone supression test be used?

A

A HDDS is a test used to distinguish between PDH and AT in dogs with confirmed spontanous hyperadrenocorticism.

20
Q

When useful is a basal cortisol concentration test?

A

It has limited diangostic value - pulsatile ACTH secretion results in variable cortisol concentrations

21
Q

How useful is the measurement of endogenous ACTH concentration?

A

ACTH can be helpful in differentiating PDH from AT

22
Q

What are the four lobes in the equine pituitary gland?

A

Adenohypophysis = pars distalis (PD), pars intermedia (PI), pars tuberalis (PT)

Neurohypophysis = pars nervosa (PN)

23
Q

What type of cell type is present in the pars intermedia?

A

The PI receives innervation from dopaminergic neurons (it is poorly vascularised) - dopamine interacts to cause a decrease in hormone synthesis.

24
Q

Where is PC1 and PC2 produced?

A

Prohormone convertase 1 - PC1 cleaves POMC to yield ACTH + other products (in PD and PI)

Prohormone convertase 2 - PC2 acts on the products of PC1 to yield smaller peptides

25
Q

Where does the majority of plasma ACTH in healthy horses originate from?

A

Originates from the pars distalis

26
Q

What is pars pituaritary intermedia sysfuncton? Briefly explain how it arises:

A

PPID - enlarged pituitary gland due to hyperplasia and hypertrophy of the PI - neurodegenerative disease w/loss of inhibitory dopaminergic disease

27
Q

What are the clinical signs that are seen with PPID?

A

Hypertrichosis (excessive hair growth)

Lightening of coat colour

Late or incomplete shed

Retention of guard hairs

28
Q

What is an important consideration in using basal plasma ACTH concentraion fro diagnosis of PPID?

A

Most practical diagnostic test for PPID - collection of a single sample - however significant variation between laboratories

29
Q

Briefly explain what is involved in an overnight dexamethaosne supression test (ODST) and how it cam be interpeted?

A

Involves giving a low dose of dexamethosone, wating 24 hours and then later measuring cortisol levels. Expect high cortisol levels in a dog with PPID. Quite high sensitivity and specificity.

30
Q

Briefly explain what the results of a TRH stimulation test would look like in a dog with PPID:

A

TRH recepotrs are expressed on both Pi melanotropes and PD corticotropes - TRH leads to increased in [ACTH] in both normal and PPID animals. Response is significantly greater in PPID horses.

31
Q

What is the main target of aldosterone?

A

Kidneys

32
Q

What are the main renal effects of aldosterone?

A
  • Increased renal excretion of K+ (indirectly H+)
  • Increased renal retention of Na+ (indrectyl H2O and Cl-)
33
Q

What activates and what inhibits aldosterone?

A

Activated by: decreased extracellular fluid volume, decreased systemic blood presure, decreased Na, increased K+

Inhbitied by: Increased ANP

34
Q

Briefly describle the pathogenesis of secondary hypoadrenocorticism:

A
  1. Carcinoma, trauma, severe inflammations = decreased ACTH production
  2. Decreased glucocorticoids - with normal mineralocorticoids
35
Q

Describe the pathogenesis of primary hypoadrenocorticism:

A
  • In early onset hypocorticism crises only occurs with increased stimuli (stress, trauma)
  • Clinical syndrome occurs when 85-90% of adrenocrotical tissue is destroyed –> deficiencies of mineralcortcoids + glucocorticoids
36
Q

What are the two main triggers of primary hypoadrenocorticism?

A
  1. Immune mediated destruction of adrenal cortex
  2. Lymphomatous infiltration (++ in cats)
37
Q

What are the ten main abnormalities that are seen in cases of hypoadrenocortism?

A
  1. Electrolytes: Increased K+, decreased Na+ = Na+/K+ < 27, decreased Cl-
  2. Anemia: Mild, non-regenerative, due to gastro-intestinal hemorrhages
  3. Hypoalbuminaemia: due to gastro-intestinal bleeding (nobody knows why)
  4. Leukogram: opposite of stress leukogram due to cortisol insufficiency - lymphocytosis and eosinophilia
  5. Increase urea: pre-renal azotemia, secondary to GI haemorrhages
  6. Increased phosphorus: decreased GFR
  7. Decreased USG: not present in dehydrated patients - USG < 1.03 - chronic urinary sodium loss can cause renal medullary washout
  8. Metabolic acidosis: Due to decreased H+ excretion, reduced tissue perfusion secondary to hypovolaemia
  9. Increased calcium - unkown pathogenesis
  10. Decreased glucose - due to hypocortisolism - reduced liver gluconeogenesis + increased tissue uptake
38
Q

What test is considered gold standard in diagnosis of hypoadrenocorticism?

A

ACTH stimulation test: Sensitivity: 60-85%, specificity: 85-90%

VET377 (60 decks)

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