Endocrine Flashcards

1
Q

What is an adipokine? Name some examples?

A

Protein or hormone secreted from adipose cells

Ex: TNF alpha, leptin, adiponectin

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2
Q

How does leptin work?

A

Inhibits neurotransmitters that increase appetite and slow metabolism and stimulates neurons that decrease appetite and increase energy expenditure

Promotes weight loss

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3
Q

How does adiponectin work?

A

Most abundantly secreted adipokine in circulation
Lower levels w increased fat mass
Closely associated w insulin sensitivity
Low levels of adiponectin associated with chronic inflammatory states like obesity, insulin resistance, type 2 DM, cardiovascular disease

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4
Q

What is role of TNF-alpha in obesity?

A

This is a cytokines secreted by lots of cells including adipocytes

Obesity increases macrophage migration into adipose tissue, causing increased TNF alpha expression in overweight individuals

This causes local insulin resistance. It also decreases uptake of FFA into adipocytes and promoted lipolysis and release of FFA into circulation. FFA levels increase in circulation and negatively impact insulin sensitivity

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5
Q

MOA of slentrol (dirlotapide) and mitratapide (Yarvitan)?

A

Microsomal transport protein inhibition at intestines. Means that lipids don’t get assembled into apoprotein B, which means they don’t get absorbed
More importantly, the increased lipid causes secretion of satiety signals from gut (like pancreatic peptide Y, PYY) and inhibition of voluntary food intake

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6
Q

Examples of human weight loss drugs?

A

Sibutramine (Meridia)- inhibit serotonin and NE reuptake

Oralistat (Xenical)- increases fecal fat excretion

Phenteramine (Adipex-P)- increases metabolism similar to speed

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7
Q

What breeds are predisposed to hyperlipidemia?

A

HTG- schnauzer, beagle

HCH- Shelties, Dobies, Rotties, Briards, rough-coated collie, Pyrenees

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8
Q

What are some uncommon causes of hyperlipidemia?

A

Phenobarbital therapy, parvo, hypernatremia (maybe), Leishmania, lymphoma, hepatic insufficiency

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9
Q

How do omega 3 FA work to treat hyperlipidemia

A

Increased beta oxidation, reduced lipogenesis, and activation of LPL

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10
Q

MOA of niacin?

A

Not super known but inhibits hormone sensitive lipase and inhibits diacylglycerol acetyltransferase= reduced triglyceride synthesis

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11
Q

What side effects known for niacin in dogs? W

A

Myotoxicity maybe hepatotoxicty. Also erythema and pruritus

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12
Q

How does gemfibrozil work?

A

This is a fibric acid derivative. It inhibits peroxisome proliferator activated receptor alpha. This is a transcription factor that regulates lipid and lipoprotein synthesis and catabolism

Essentially it does a bunch of things that result in decreased triglyceride levels

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13
Q

Why no use statins in dogs?

A

Bc they’ll work on cholesterol not triglyceride

Also when used with fibrates there is an increased risk of hepatotoxicty

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14
Q

Which breed predisposed to primary hyperparathyroidism?

A

keeshonds

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15
Q

Do dogs with primary hyperthyroidism develop CKD bc of hypercalcemia?

A

NO! For some reason these dogs seem protected from renal failure

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16
Q

What are common co-morbidities of primary hyperparathyroidism?

A

UTI-30%

Cystic calculi- 30%

17
Q

You have a patient w normal PTH and high calcium. What’s the diagnosis?

A

Primary hyperparathyroidism

As calcium levels rise PTH should become undetectable

18
Q

When do you do pretreatment w calcitriol for PHP?

A

When total calcium greater than 15 or more than one parathyroid mass. They have a higher risk of post procedure hypocalcemia

19
Q

What sort of tumor causes primary hyperparathyroidism?

A

Histologically classified as adenoma, hyperplasia, or carcinoma. Doesn’t matter bc they don’t met or invade and recurrence is 10% regardless of tumor type

20
Q

What is desmopressin?

A

Synthetic analog of natural anti-diuretic hormone. Has increased ADH activity and prolonged duration of action, decreased pressor actions, fewer side effects than natural hormone.

21
Q

What route of admin is best for desmopressin?

A

Maybe SC bc can give smaller amts more efficaciously and it lasts longer but you can do oral and conjunctival as well.

22
Q

When do you consider doing a desmopressin response test?

A

When you’ve limited Ddx to central DI, nephrogenic DI or primary polydipsia

23
Q

What results on desmopressin response test tell you it’s central DI?

A

> 50% reduction of water intake and polyuria strongly suggest diagnosis of central DI. But lack of any reduction in PU/PD is probably due to nephrogenic DI.

24
Q

What are adverse effects of desmopressin?

A

Fluid retention, hyponatremia, decreased plasma osmolality. Water intoxication rarely can cause CNS disturbances. Give furosemide if it happens

25
Q

Who gets diabetic nephropathy?

A

Cats more commonly than dogs. Usually proteinuria and hypertension are the manifestations and azotemia is a late consequence

Don’t see it that much in dogs bc they don’t live long enough

26
Q

What is the mechanism of diabetic neuropathy?

A

Polyol pathway via aldose reductase promotes formation of sorbitol from glucose and then to fructose via sorbate dehydrogenase. Fructose accumulates in the nerves of cats and results in accumulation of glycation end products

Demyelination and splitting and ballooning of myelin are common in these cats

27
Q

Why don’t cats get diabetic cataracts?

A

Less aldose reductase activity in the lens. Maybe that’s the cause

28
Q

Which is the primary ketone in dogs and cats?

A

Beta hydroxybutryrate. Also, it’s not measured on urine dipstick!

29
Q

Definition of obesity

A

Exceeding ideal body weight by 15-20%

30
Q

What’s the pathogenesis of megaesophagus and decreased thyroid?

A

Unknown! May or may not recover fxn too

31
Q

What’s mechanism of peripheral neuropathy w hypoT4?

A

Usually metabolic. Maybe consequence of impaired axial transport

If they have vestibular dz, it could be due to compression of facial and vestibular n as they cross internal acoustic meatus (unknown why)