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Clin Path > Endocrine Ch 11 D&P > Flashcards

Endocrine Ch 11 D&P Flashcards

1
Q

What is the main sensor or regulator of parathyroid cheif cells, C-cells and renal epithelial cells in regards to Calcium balance and where is it located?

A

Its the ionized calcium sensing receptor (CaSR) and its present along the nephron on renal epithelial cells.

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2
Q

When the CaSR senses Calcium what happens?

A

There is a decrease in NaCl, Ca and Mg reabsorption in the proxinal convuluted tubule and a decrease in water reabsorption in the collecting duct.

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3
Q

What is the relationship between Mg and Ca balance?

A

Mg is an agonist of the CaSR and severe Mg depletion decreases PTH secretion and increases resistance to PTH, and it impairs Calcitriol synthesis (form of vitamin D).
- So BLUF, to Get Ca you need Mg.

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4
Q

*What are the functions of PTH and what does it respond to?

A

Responds to hypocalcemia (note also high Phos as in renal dz may cause a decrease in Ca and this indirectly high Phos can stim increased PTH release):

  • Net effect of PTH is increased serum Ca, decreased Phos, and increased renal excretion of Phos via the following mechs, MUST KNOW THESE 5 THINGS:
    1. Ca release from bone
    2. Phos excretion by kidney
    3. Accelerate formation of active Vit D (1, 25 dihydroxycholecalciferol by stim of 1-alpha-hydroxylase enzyme activity in the kidney)
    4. Ca reabsorption from the gut
    5. Ca reabsorption by renal tubules
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5
Q

What happens with Ca balance in primary hyperparathyroidism? What are the effects on the different organs?

A

This is like a parathyroid tumor > increased PTH > increase Ca and Phos from intestine and bone; increased renal reabsorption of Ca but increased renal loss of Phos; increased renal activation of vitamin D. > end result in increased Ca:Phos ratio in the blood.

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6
Q

What happens in primary hypoparathyroidism?

A

This may be d/t agenesis, surgical removal, atrophy.
You have decreased Ca and Phos from the intestine and bone, increased renal excretion of Ca and decreased renal excretion of Phos and reduced renal activation of Vitamin D.

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7
Q

What happens in renal secondary hyperparathyroidism (ie renal failure)?

A

You get metabolic acidosis due to decreased functional nephrons, which increases the iCa fraction , and this is mitigated by the reduced activation of Vit D to 1, 25 DHC by the kidney so over all there is decreased serum Ca and increased retention of Phos by the kidney.

  • The decreased serum Ca leads to secondary increase in PTH resulting in increased Ca and Phos resorbed from the bone.
  • THE BLUF: Renal failure causes dec serum Ca++ and that drives renal secondary hyperparathyroidism.
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8
Q

How does nutritional secondary hyperparathyroidism occur?

A

Increased PTH d/t decreased dietary intake of Ca and/or Vit D malabsorption or a diet high in Phos (ie dietary Ca-Phos-Vit D imbalance > renal retention of Ca, renal excretion of Phos and bone resorption (rubber jaw, FOD) > low normal serum Ca and Phos.
- This condition may also be caused by Vit D dependent / Type II rickets.

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9
Q

What does calcitonin do and where does it come from?

A

Thyroid parafollicular C cells.
Produced in response to hypercalcemia.
It tries to decrease serum Ca and Phos via:
-Inhibition of PTH bone resorption
-Increased Phos excretion by kidney
BLUF: It works with but oppostite of PTH to maintain serum Ca++ within precise limits and tempers the PTH action on bone.

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10
Q

What are the steps in Vitamin D metabolism?

A

Its made in the skin or ingested in food > enters serum and goes to the liver > Its called Vitamin D3 or just Vitamin D at this point > Hydroxylation in the liver to 25-Hydroxycholecalciferol > To kidney and its hydroxylated a second time by 1 alpha hydroxylase to 1-2-5 DI-hydroxycholecalciferol under regulation by PTH > This is the METABOLICALLY ACTIVE form > promotes Ca and Phos absorption in the INTESTINE and resorption of BONE,
BUT works against / antagonizes PTH’s action on the kidney.

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11
Q

What are the three forms of serum Ca++?

A
  1. Ionized (biologically active form (50%) - almost always increased in hypercalcemic conditions and decreased only if hypocalcemia is severe)
  2. Protein bound Ca++ (40%; mostly albumin and it buffers changes in Ca++)
  3. Chelated or complexed Ca (ie with Mg, phosphate, citrate, bicarb, sulfate, lactate, anions; 10%)
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12
Q

What are the effects of acid base status on iCa++ ?

A
  • Alkalosis > decreases in serum iCa++ (metabolic alkalosis&raquo_space; subclinical hypocalcemia; Milk fever in cows is d/t alkalizing diet providing more cations like Na, K, Ca and Mg than anions).
  • Acidosis > Increases serum iCa++
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13
Q

Relationship between hypoalbuminemia and hypocalcemia?

A

Hypocalcemia is found in hypoalbuminemic conditions but clinical signs don’t occur cause iCa++ is normal.

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14
Q

How does dietary intake of Ca++ affect serum Ca concentration?

A

It doesn’t really directly affect the serum levels.

But it may affect PTH and bone, renal and GI absorption.

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15
Q

What is unique about Ca in horses?

A

They have a higher serum total Ca and iCa and poorly regulated intestinal absorption of Ca, high urinary fractional clearance of Ca, low serum Conc. of Vitamin D metabolites and increased Ca setpoint. THink of calcium carbonate in horse urine.
- You may also get hypercalcemia with renal dz in horses, in contrast to other species.

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16
Q

Where is phosphorus primarily regulated?

A

Kidney. Phosphaturia may occur when tubular resorption maximum is exceeded.

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17
Q

What is the influence of PTH on phosphorus?

A

Decreases it by decreasing tubular resorption, thus increasing phospaturia.

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18
Q

Does diet influence serum phosphate?

A

Yes, Dietary intake may directly influence serum phosphorus.

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19
Q

What are the three things that result in abnormal serum phosphorus?

A

Altered dietary concentrations.
Decreased renal excretion.
Hormonal imbalances.
Basically the stuff that affects serum Calcium.
Note hemolyzed serum can affect serum Phos and its also higher in young animals.

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20
Q

Whats the active form if magnesium and what does it do? How is it regulated?

A

iMg is the biologically active fraction. Its important in support of enzyme activity. Its a cofactor for many enzymes.
- Depends on dietary intake, regulated by mineralicorticoids and PTH.

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21
Q

In what situations are Mg abnormalities most common?

A

Primarily in ruminants.

Also in Insulin treated dogs with DKA

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22
Q

What are the causes of primary hyperparathyroidism?

A

Fxnl parathyroid neoplasms.

Idiopathic hyperplasia of parathyroid

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23
Q

What are serum PTH concentrations in primary hyperparathyroidism? What about Ca and Phos?

A

PTH is high, may be WNL but would still suggest hyperparathyroidism of dog is hypercalcemic and hypophosphatemic and NOT azotemic.
Ca is high and Phos is low usually, but phos may increase as renal mineralization takes place and renal failure develops.

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24
Q

What lesions are seen with hypoparathyroidism?

A

Bony lytic lesions,
soft tissue mineralization and
increased serum ALK Phos and
usually isosthenuric.

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25
Q

What is pseudohyperparathyroidism associated with? What is Ca and PHos in this conditoin?

A

Neoplasia.
Tumors may produce PTHrp, a vitamin D like steroid, a prostaglandin or osteoclast activating factor.
Ca is high and Phos may be very low, but Phos may increase after nephrocalcinosis and renal failure set in. Serum PTH would be low in this condition.
NOTE: High Phos is a big clue you have some sort of increase in PTH or PTHrp somewhere.

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26
Q

Name some tumors that commonly result in hypercalcemia?

A

Lymphoma
Apocrine gland adenocarcinoma (PTHrp)
Multiple myeloma (osteoclast activating factor)
Occasionally other neoplasms like carcinomas, SCC, nasal etc.

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27
Q

What are 8 common causes of hypercalcemia BESIDES primary and pseudohyperparathyroidism?

A
  1. Hypervitaminosis D
  2. Ingestion of Cholecalciferol containing rodenticides (the drug version of this is calcitriol - active vitamin D3).
  3. Ingestion of Vitamin D containing plants (sestrum, solanum, tricetum)
  4. Renal dz in horses (in health the horse kidney secretes lots of Ca which decreases in dz resulting in retention and mineralization
  5. Renal failure in dogs is infrequent cause of hypercalcemia (ie young dogs w/ familial renal dz not old dogs with chronic renal dz).
  6. Canine adrenal insufficiency (Low Na, High K+, High Phos, Azotemia, High Ca associated with glucocorticoid deficiency).
  7. Bone dz accompanied by osteolysis
  8. Granulomatous dz (like Blasto; d/t excess production of active vitamin D by macrophages)
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28
Q

What value may mask hypercalcemia?

A

Hypalbuminemia, if total calcium is being measured.

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29
Q

What are 5 common causes of hypocalcemia associated with sickness?

A

Sickness in general, sepsis in foals, enterocolitis in adult horses, acute pancreatitis, may cause it.
Hypoalbuminemia.
Alkalosis.

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30
Q

What are some other causes of hypcalcemia (9) (aside from the sickness ones mentioned above)?

A 
C cell thyroid neoplasm (calcitonin producing).
Eclamsia / milk fever
EDTA
Hypomagnesemia (grass tetany)
Hypoparathyroidism
Malabsorption
Phosphate enema
Renal failure
Toxicosis (blister beetle or Ethylene glycol)
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31
Q

What are the mechs by which renal dz results in hypocalcemia?

A
  • Decreaesd 1 alpha hydroxylase and decreased 1, 25 dihydroxycholecalciferol formation; soft tissue mineralization due to hyperphosphatemia
  • Ethylene glycol d/t chelation of Ca by oxxalate
  • Post renal urinary obstruction in cats (hypoCa, hyperPhos)
  • Uremic acidosis may temper the hypocalcemia causes acidosis results in hypercalcemia usually (iCa++ is increased).
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32
Q

How does hypoparathyroidism occur and what does it result in terms of Ca and Phos?

A

Spontaneously or following surgical removal of thyroid and parathyroid glands (ie surgically tx’d hyperthyroid cats). PTH is decreased (or may be WRI)

  • Phos is WRI or a little high
  • Serum iCa++ low;
  • if serum iCa++ is low but PTH is high they have parathyroid independent
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33
Q

What is the mechanism of hypocalcemia in pancreatitis?

A

unknown but could be related to formation of calcium soaps or increased calcitonin or calcitonin like activity, decreased PTH etc..
Usually there is a concurrent acidosis which keeps the iCa++ normal or low normal.

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34
Q

What is milk fever?

A

Parturient paresis in cattle, or peurpural tetany in bitch, mare or ewe. Related to demand for Ca in lactation. Usually also hypophosphatemic.

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35
Q

What is grass tetany and what is seen with it?

A

Hypomagnesemia, and it usually is accompanied by hypomagnesemia.

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36
Q

What is 1 common cause each of hypocalcemia in cat, horse and bull?

A

Cat > phosphate enema
Horse > Blister Beetle/Canthardin toxicosis
Bull > Thyroid C cell / calcitonin secreting neoplasm

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37
Q

What is the most common cause of hyperphosphatemia (8)?

A 
Decreased GFR (prerenal, renal or post renal azotemia)
Hypervitaminosis D
Nutritional secondary hyperparathyroidism (excess phosphorus in diet).
Hypoparathyroidism (high Phos, Low Ca).
PHosphate enemas
Osteolytic bone dz
Young animals
Hemolysis
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38
Q

*What are the two forms of Nutritional secondary hyperparathyroidism and associated abnormalities in Ca and Phos?

A
  • High Phosphorus diet (resulting in Low Ca and HIGH Phos).

- Low Ca or low vitamin D diet (which would result in LOW Ca AND LOW Phos).

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39
Q

How common is Hypophosphatemia and what are some common causes (5)?

A

Its uncommon.

  • Primary and pseudo hyperparathyroidism may cause it.
  • Nutritional secondary hyperparathyroidism (low Ca++ or Vitamin D in diet).
  • Inadequate dietary Phos intake
  • Milk fever / eclampsia
  • Hyperinsulinemia / Insulin admin
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40
Q

How common is hypermagnesemia and what are some common causes?

A

Uncommon cause its readily excreted in kidney.

  • Herbivores with renal failure
  • Admin of Mg containing products to animals with renal failure
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41
Q

What are causes of Hypomagnesemia and who gets it?

A
  • Hypoparathyroidism, critical illness, diabetes mellitus, lactation tetany, PLE.
  • Think CALVES, adult cattle nad sheep.
  • Hypocalcemia may be refractory to txment until hypomagnesemia corrected.
  • Grass tetany related to decreased intake is classic presentation.
    (NOTE: Urine Mg may be useful dxic test)
42
Q

What is the balance of T3 and T4 in the normal thyroid gland and elsewhere; how is T3 derived and what affects it?

A

80% T4
20% T3 (this is more potent)
Most of the T3 in dogs and cats is derived from deiodination (via D1 enzyme - type I deiodinase) of T4 occuring OUTSIDE the thyroid gland. Like in Liver and Kidney, then its available to other tissues).
- D1 activity reduced in Hypothyroidism; increased in hyperthyroidism.
- D1 activity reduced in Illness and protein calorie malnutrition.
- There is also D2 enzyme in brain, pituitary and CNS in most species T3 produced via D2 is retained in the tissue
- D2 activity is increased in hypothyroidism and decreased in hyperthyroidism (opposite of D1)

43
Q

What is the relationship between TSH and free T4 - how is this maintained?

A
  • Serum TSH level is inversely proportional to circulating free T4.
    All T4 entering pituitary is converted to T3 (viaD2), and the generated T3 provides negative feedback on the cells that produce TSH in the pitutary.
44
Q

What are the basics of the hypothalamus - pituitary - thyroid axis?

A

Hypothalamus produces TRH > released into Pituitary portal system > Stims Anterior pituitary thyrotrope cells to produce TSH > Stimulates thyroid gland to produce T3 and T4 (mostly) into systemic circulation and mostly protein bound. free T4 provides negative feedback to the hypothlamus controlling TRH release. Extrathyroid tissue like the liver can also release T3 that has been converted from T4.

45
Q

With impending thyroid failure as in primary hypothyroidism or in iodine deficiency what is the status of T3 compared to T4?

A

T3 is maintained longer, it does not usually decline as fast as T4.

46
Q

Where does feedback work in the Hypothalamic - Pituitary - thyroid gland axis?

A

Negative feedback via T3 and T4 at the pituitary gland and hypothalamus.

47
Q

How does thyroid hormone circulate and how is it available?

A

Most (like 99%) circulates bound to plasma proteins like thyroid binding globulin (TBG), albumin etc. Free T3 and T4 are the non protein bound fractions that can enter tissues and have an action. They are a very small percentage in health. (0.1%) Measured as fT4 by equil dialysis.

48
Q

What are some examples of nonthyroidal illness that may cause decreased T4?

A
  • Hypoproteinemia (fT4 would be normal)
  • Age in dogs and horses
  • Severe illness
  • Admin of steroids and some other drugs
49
Q

What does total T4 measure?

A

Both bound and unbound T4. (f and TT4)

50
Q

What are the potential interpretations of a Total T4 WRI?

A
  • You can exclude hypothyroidism
  • In some cases if there are anti T4 autoantibodies present this may actually push the TT4 into or above the reference interval and hypothyroidism will not be detected (not sure how this occurs, maybe the Ab binds the T4 and makes it unavailable but its still detected in the test).
51
Q

What are the ways to interpret a decrease in TT4?

A
  • Hypothyroidism may or may not be present, this is not confirmatory
  • Nonthyroidal illness may be present (euthyroid sick)
  • Need to test for TSH and fT4 to determine if hypothyroid is present
  • (ie TT4 is a screening test, if its normal you are good, but if its low you need additional testing.)
52
Q

How do you interpret an increase in TT4?

A
  • Hyperthyroidism may be present
  • If you clinically suspect hypothyroid and they measure hyper on TT4, check for anti T4 antibodies, they are present in approximately 1% of hypothyroid individuals an may elevate the measured TT4.
53
Q

Should T3 be measured?

A
  • No value in this. Its the most hormonally active form of thyroid hormone and coorelate poorly with clincial dz cause it can be made or converted from T4 in thyroid as well as non thyroid tissue.
  • It may alos be antibody bound which increases serum levels but that ab bound portion thats measured can’t be used by the body, I think.
54
Q

How is free T4 measured?

A

Equilibrium dialysis.

55
Q

What are the potential artifacts of fT4?

A

It may underestimate fT4 in some cases.

  • Its usually increased in hyperthyroid cats (but can have a small percentage of false positives).
  • Interpret in conjunction with other thyroid tests
      • Despite limitations it has the highest single test diagnostic sensitivity, specificity and accuracy in detecting thyroid dz.
56
Q

Which breeds naturally have a lower basal serum T4 or fT4 concentrations?

A

Sighthounds like Greyhounds, Scottish deerhounds, Basenjis.

57
Q

Why test for TSH and how should it be done?

A

Its done in order to detect a lack of negative feedback on the pituitary gland or hypothalamus. (High in hypothyroid, low in hyperthyroid).

  • TSH is generally non detectable in hyperthyroid cats
  • SHould always be done with TT4 and FT4
  • *TSH has poor sensitivity as a screening test for hypothyroidism and the test is not that great
  • Elevated in dogs with primary hypothyroidism (75%) (chronically it may actually fall to normal).
58
Q

When do anti-thyroglobulin Ab’s occur and what is the signficance?

A
  • Remember thyroglobulin is made from tyrosine in the follicular cells to be secreted into the colloid and then made into thyroid hormone.
  • There is an ELISA to quantitate Abs to it.
  • If present it indicates thyroid autoimmunity and its HIGHLY SPECIFIC for the presence of thyroid dz.
  • Abs are present in half of dogs with hypothyroid and almost all dogs with thyroiditis. Antithyroglobulin ab’s may be present before onset of clinical dz.
  • Don’t confuse this with Anti T3 or T4 Ab’s discussed earlier.
59
Q

What is the significance of anti T3 and anti T4 antibodies?

A
  • Occur in low percentage of dogs with thyroiditis but also seen in normal animals.
  • The serum usually also Thyroglobulin positive but may be due to cross reactivity or the hapten affect (cause T3 and T4 contain thyroglobulin).
  • Main clinical signficance is that it may interfere with measure of T3 and T4 and so if detected YOU MUST MEASURE FREE T4 TO BE ACCURATE AND DETECT THYROID DZ.
60
Q

What is the purpose of measuring T4 response to TRH or TSH? (ie you administer it)

A

A test of thyroid reserve.

  • Mainly a research thing but considered gold standard to dx thyroid dz.
  • In a healthy animal when you admin TSH you get a two fold elevation in serum T4 in the second sample or exceed the upper limit of the normal reference interval for the euthyroid state.
61
Q

What is the best most accurate test for hypothyroidism?

A

Free T4. Very high sensitivity.
If you add TSH to fT4 you increase the specificity a little but you lose some sensitivity, so using both is a little less accurate.

62
Q

What does TRH stimulation test measure and how is it used?

A
  • May be used to test for pituitary and thyroid secretory reserve in dogs iwth hypothyroidism. (TRH stim only shows marginal elevations in T4 in euthroid dogs so no elevation would probably indicate hypothyroidism).
  • Most commonly used to dx hyperthyroid cats but not great even for this, poor discrim between hyperthyroidism and non thyroid illness.
    • Thyroid autonomy is considered to exist and hyperthyroidism, if the serum T4 fails to increase by 50% following administration of TRH (basically the thyroid gland is doing its own thing).
63
Q

What is the most common cause of hypothyroidism and how do you ideally test for it?

A

In dogs usually associated with thyroid atrophy or lymphocytic thyroiditis.

  • Total T4 often inadequate to dx it but if its WNL then you can exclude hypothyroidism (except in those few where T4 Abs falsely elevate the total T4 but dont reflect the usable T4).
  • if T4 is low, run a TSH and fT4. (TSH high)
  • low fT4 is highly specific for hypothyroidism.
64
Q

What is the cause of secondary hypothyroidism and how common is it?

A
  • Uncommon dz where TSH is inadequate usually d/t pituitary lesion
  • You would expect thyroid gland atrophy d/t inadequate stimulation
65
Q

What are some of the more common other lab abnormalities in hypothyroidism?

A

Normocytic, normochromic, non regenerative anemia.

Hypercholesterolemia

66
Q

What is the most common lesion in hyperthyroidism?

A

Nodular adenomatous thyroid hyperplasia or thyroid adenoma in older cats.

67
Q

What are the common lab abnormalities in hyperthyroidism (comment on renal function)?

A
  • Polycythemia
  • Increased Alk Phos, ALT
  • Hyperthyroidism causes an increase in cardiac output and GFR and so when you tx them they may decline and unmask renal dz. May be useful to measure UPC ratio, USG and TT4 prior to treatment to try and predict if renal dz is present.
68
Q

How does hyperthyroidism affect glucose in cats?

A

They may be glucose intolerant and have over diabetes mellitus but txment won’t fix it and may make it worse. May see fasting hyperglycemia and delayed response to glucose.

  • Fructosamine would be low d/t accelerated plasma protein / albumin turnover. (unless concurrent DM is present)
  • Fructosamine not really useful to measure in DM cats until hyperthyroid controlled.
69
Q

How is hyperthyroid generally dx’d in cats?

A
  • Use TT4 to screen - it will be elevated in most unless dz in mild.
  • Other tests: Free T4
  • T3 suppression test (serum T4 should decrease by at least 50%. but in hyperthyroid it doesn’t go down by much).
  • TRH stimulation test > If T4 fails to increase by at least 50% you can have thyroid autonomy/failure to respond to feedback, or hyperthyroidism.
    T3 suppresses TRH and TSH release from the hypothal and pit respectively. TRH stimulates the pit.
70
Q

Which pancreatic cells secrete insulin? What are the major target organs for insulin?

A

Beta cells of the islets of Langerhan.

Primarily liver, skeletal muscle and fat.

71
Q

Insulin promotes metabolism of which substrates, and how?

A

Anabolic metabolism of carbs, fats, proteins and nucleic acids by potentiating cellular uptake of Glucose, other monosaccharides, some AA, fatty acids, K+ and Mg.

72
Q

Insulin is NOT required for glucose uptake by which cells / tissues?

A

RBCs, neurons, enterocytes, pancreatic beta cells, renal tubular cells and the ocular lens.

73
Q

Where does glucagon come from and what are the effects of it?

A

Alpha cells of the islets in response to hypoglycemia.

  • Glucagon promotes gluconeogenesis and hepatic glycogenolysis to increase blood glucose
  • It also causes lipolysis and ketogenesis as ketones are used as fuel when glucose is low as in starvation or diabetes mellitus.
74
Q
  • What are the other hormones (4) that oppose the effects of insulin?
A

i. e. they try and keep the blood glucose high.
- Glucocorticoids antagonize insulin and promote gluconeogenesis, glycogenolysis and lipolysis and inhibit muscular protein synthesis.
- Catecholamines increase glycogenolysis, gluconeogenesis and lipolysis (essentially the same as steroids)
- Growth hormone inhibits glucose uptake by insulin responsive cells and promotes lipolysis
- Progesterone in high concentrations during later estrus and metestrus may cause excessive growth hormone release from hyperplastic ductular epi of the mammary gland and thus exert an anti insulin effect.

75
Q
  • What do the delta cells in the islets produce and what is the effect?
A

Delta cells of the islets produce Somatostatin, which inhibits glucagon and insulin secretion.

76
Q

Diabetes mellitus results when what happens?

A

Insulin secretion is inadequate or tissues fail to respond to insulin (ie resistance).
- Most DM dogs and cats have an absolute deficiency of insulin but some diabetic cats may have normal to increased serum insulin but have peripheral insulin resistance.

77
Q

How can you make the dx of DM with one blood or urine sample?

A

If both hyperglycemia and ketonemia, or glucosuria and ketonuria are present respectively.

78
Q

Other common lab abnormalities in DM other than glucose abnormalities?

A
  • Ketonemia, ketonuria and ketoacidosis
  • Lipemia
  • Osmotic diuresis with dehydration and electrolyte loss
  • Proteinuria (d/t lower UTI or glomerular dz)
  • Glycosylation of serum hemoglobin and serum protein (fructosamine)
79
Q

What are the time ranges of glycosylated Hgb and Fructosamine?

A

Hgb is two to three months

Fructosamine is two to three weeks

80
Q

What is the cause of hyperinsulinemia and what testing is done for this?

A

Fxnl Pancreatic beta cell tumor. (usually measure insulin to establish this)

  • Usually also measure glucose with this without fasting. (it should be below 60mg/dl before measuring insulin).
  • You can also do a insulin glucose ratio, subtract 30 and if its below 30 then that suggests hyperinsulin.
81
Q

What are the three types of hyperadrenocorticism?

A

Pituitary dependent
Adrenal dependent
Iatrogenic

82
Q

Which layers of the adrenal secrete which hormones?

A

Salt - Zona glomerulosa - Aldosterone
Sugar - Zona fasciculata - Cortisol (some reticularis too)
Sex - Zona reticularis - Androgens & estrogens

83
Q

How is glucocorticoid secretion stimulated from the start of the axis? Where is the feedback?

A

Corticotropin releasing hormone from the hypothalamus > ACTH from the anterior pituitary > Cortisol / Glucocorticoids from the adrenal gland.
Feedback: Cortisol inhibits release of CRH which in turn shuts down ACTH and it can inhibit ACTH release directly. (negative feedback.
- Exogenous steroids also suppress ACTH secretion.

84
Q

What are the other ancillary effects of steroids on metabolism?

A

They make more glucose and fat present in the blood (the opposite of insulin)

  • Antagonize insulin and promote gluconeogenesis and glycogenesis.
  • Decrease glucose uptake by tissues
  • INcrease lipolysis
  • Suppress wound healing, inflammation and immune fxn
85
Q

Where do mineralicorticoids come from and what is their function? How are they regulated?

A

Aldosterone - primary mineralicorticoid - secreted by zona glomerulosa of adrenal cortex.

  • Regualted by Renin - Angiotensin system (from kidney etc)
  • Stimulated by rising K+ levels (helps keep K+ in check)
86
Q

What is the primary target organ of Aldosterone?

A

The kidney where aldosterone promotes renal tubular absorption of Na+ and excretion of K+. (remember addisons animals are hyperkalemic).

87
Q

What is the most common form of hyperadrenocorticism?

A

Pituitary dependent Cushings from hyperplasia or neoplasia of the ACTH secreting corticotroph cells of the anterior pituitary. (it can occasionally come from the pars intermedia too.)

  • With this you would expect bilateral hyperplasia of the adrenal cortex.
  • Adrenal dependent cushings is less common and most often is d/t unilateral tumor.
88
Q

What is the most common cause of hypoadrenocorticism and what is typically deficient?

A

Adrenal gland failure. Rather than failure of ACTH secretion from the pituitary. But the cause isn’t always determined.
- Both mineralicorticoids and glucocorticoids are typically deficient.
(except in Atypical Addisons where only glucocorticoids are defecient - this condition is the “great pretender” cause it mimics other dz, GI dz etc. - this could be d/t a problem with ACTH secretion in pitutiary dz or a failure of specific zone of the adrenal; this may also occuring with acute withdrawal of steroids after chronic admin or overzealous txment of Cushings dz).

89
Q

Which exogenous steroid WILL NOT cross react with cortisol assays?

A

Dexamethasone - the others typically cross react.

90
Q

In assessing the adrenal glands regardless of what dz is suspect, what is usually always tested for?

A
  • Its always Cortisol that gets measured, whether its the ACTH stim test or Dex suppression test, or baseline cortisol or whatever, its Cortisol thats measured.
91
Q

What does the ACTH stim test measure, how is it performed and how is it interpreted?
*What is it used to diagnose (3)?

A
  • Its evaluating the ability of the adrenal gland to increase plasma cortisol in response to ACTH stim.
  • You check baseline cortisol, give ACTH, recheck cortisol and you should get a 2-3X increase in cortisol above baseline after admin.
  • With pit dependent cushings the response / cortisol level is higher than 2-3X, like above 20. You still need to do a Dex Suppression test to determine adrenal or pituitary dz.
  • With adrenal tumors the response is also abnormal - high but only in 50% of the cases.
  • With iatrogenic cushings dogs have no response and thus this is the test of choice for iatrogenic cushings.
  • It can be used to diagnose Addisons but doesn’t tell you if the problem is pitutary or adrenal (the animal would have little or no response to ACTH regardless).
92
Q

What is the low dose dexamethasone test used for?

A
  • Used to screen animals for pituitary dependent and adrenal dependent Cushings.
  • You suppress the adrenals with dex and see what response you get - cortisol should be very low normally after dex stim. (you have to wait like 8 hours after stim.)
  • With both pituitary and adrenal cushings the the cortisol is inadequately suppresssed, ie too high at 8 hours after admin. Its a very sensitive test.
93
Q

What is the High does dex suppression test?

A
  • Used to distinguish between pit and adrenal dependent Cushings.
  • Again measuring cortisol after a high does of Dex.
  • Normaly the cortisol is very low after suppression
  • In pituitary dz the Cortisol also suppresses very low (but not in about 25% of cases w/pituitary dz)
  • Most dogs with Adrenal tumors also fail to suppress
94
Q

What is the urine cortisol creatinine ratio used for?

A
  • Screening test for Cushings.
  • An increase is a sensitive indicator or naturally occuring Cushings but may also occur in dogs that are stressed.
  • You measure urine cortisol and creatnine in the same random sample.
95
Q

What is measuring endogenous ACTH useful for?

A

Distinguishing pituitary from adrenal dependent Cushings.
- In pituitary dz is WNL or high
- In adrenal dz ACTH is low
With Addisons dz that is pituitary dependent (Atypical Addisons) Plasma ACTH is decreased.
In regular adrenal dependent Addisons plasma ACTH would be increased.
Its hard to measure endogenous ACTH in practice.

96
Q

What are some of the other lab abnormalities in Cushings?

A

SMILED: Segs and Monos increased, Lymphocytes and Eosinophils decreased.

  • Elevated serum Alk Phos (both hepatic and steroid isoenzymes).
  • Hyperglycemia with glucosuria in horses but not in dogs.
  • Lipemia with increased serum Cholesterol
  • Dilute urine with USG indicating isosthenuria or hyposthenuria.
97
Q

What are the expected plasma cortisol concentration in pituitary dependent cushings with bilateral hypertrophied adrenals?

A
  • Baseline plasma cortisol may be WNL or elevated.
  • Most dogs will have exaggerated plasma cortisol response to ACTH stim.
  • Low dose dex will fail to suppress plasma cortisol in horses, dogs and cats with pituitary dependent cushings.
  • High dose dex test will suppress most dogs with pit dependent Cushings but it doesn’t suppress horses.
98
Q

What are the expected plasma cortisol concentrations / responses with Adrenal dependent cushings (ie tumor with the other side atrophied)?

A
  • Baseline cortisol WNL or increased
  • Response to ACTH stim is WNL or exaggerated
  • Cortisol DOES NOT suppress with either low or high dose dex suppression test
99
Q

What is baseline cortisol expected in iatrogenic Cushings with bilateral adrenal atrophy?

A
  • Baseline cortisol is WNL or decreased.

- There is no response to ACTH stim

100
Q

What are the expected lab findings with Addisons with cortical atrophy (or absence of lesions in the adrenal)?

A
  • Baseline cortisol is WNL or decreased

- There is NO response to ACTH stim

101
Q

What are the common lab abnormalities with Addison’s disease?

A
  • Hyponatremia and Hyperkalemia d/t Aldosterone deficiency.
  • Na+/K+ less than 23:1 highly suggestive of adrenal insufficiency
  • Na+/K+ less than 26:1 suggestive of adrenal insufficiency
  • NOTE even if Na and K are normal, that DOES NOT exclude adrenal insufficiency.
  • Hypercalcemia may be present
  • Lymphocytosis occasionally
  • Hypoglycemia (unless concurrent DM)
  • Adrenal glands may show cortical atrophy OR lesions may not be present in the adrenals.

Clin Path (14 decks)

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