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Auburn ECC > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What enzyme converts pyruvate to lactate?

A

Lactate Dehydrogenase

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2
Q

List the 7 stimuli for PTH secretion

A

Hypocalcemia, epinephrine, isoproterenol, dopamine, secretin, prostaglandin E2, and stimulation of nerve endings in the parathyroid gland

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3
Q

What inhibits PTH secretion?

A

High serum and intercellular iCa via increased arachidonic acid and possibly subsequent eicosanoid production. Calcitriol also inhibits PTH mRNA synthesis

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4
Q

What is the principal stimulus for PTH secretion?

A

Hypocalcemia

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5
Q

What are the clinical hallmarks of myxedema coma in human beings?

A

Altered mental status, inadequate thermoregulation, decreased respiratory and cardiac function, concurrent disease

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6
Q

T/F- Coma is commonly seen with myxedema coma?

A

False- it is rarely seen; more commonly disorientation, confusion, lethargy

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7
Q

What are the proposed mechanisms of altered mental status in myxedema coma?

A

Decreased blood flow and O2 delivery to the brain, hyponatremia, lack of direct effect of thyroid hormone on the brain, disruption of integrity of the BBB

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8
Q

What are the proposed mechanisms of altered thermoregulation in myxedema coma?

A

inadequate thyroid hormone function in the hypothalamus, decrease in calorigenic effect of thyroid hormones, hypoperfusion and hypotension

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9
Q

List things that contribute to hypoventilation in myxedema coma?

A

Decreased respiratory system responsiveness to hypoxia and hypercapnia, obesity, muscle weakness, pneumonia, pericardial or pleural effusion, ascites

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10
Q

Why does systolic hypotension occur commonly in people with myxedema coma?

A

secondary to bradycardia, decreased cardiac output, hypovolemia

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11
Q

Why might diastolic hypertension occur with myxedema coma?

A

peripheral vasoconstriction and central shunting of blood secondary to hypothermia and low O2 consumption

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12
Q

List mechanisms of edema formation with myxedema coma

A

accumulation of the glycosaminoglycan hyaluronic acid in the dermis, impaired renal perfusion due to decreased cardiac output, excessive secretion of ADH causing hyponatremia/fluid retention/edema

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13
Q

Proposed risk factors in dogs for development of myxedema coma?

A
  • Rottweiler dogs, middle age, untreated hypothyroidism, concurrent disorder (most commonly infection)
  • POSSIBLY steroid or NSAID administration
  • Risk factors in people- recent surgery, burns, CO2 retention, hypothermia, infection, hypoglycemia, GI hemorrhage, stroke, trauma, medications
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14
Q

T/F- female dogs are at an increased risk for developing myxedema coma?

A

False, although in people females are at an increased risk

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15
Q

Name some clinical signs associated with chronic untreated hypothyroidism

A

weight gain, obesity, lethargy, mental dullness, weakness, hyperkeratosis, alopecia, thin hair coat

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16
Q

What are the most common clinicopathologic abnormalities in hypothyroid dogs? What additional abnormalities are found in people but not necessarily dogs?

A
  • mild nonregenerative anemia, hypercholesterolemia, lipemia, increased ALP
  • people: hyponatremia, hypoglycemia
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17
Q

What is a pheochromocytoma?

A

Tumor of the chromaffin cells of the adrenal medulla

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18
Q

What do the chromaffin cells of the adrenal medulla do?

A

They synthesize, store, and secrete catecholamines in response to sympathetic stimulation.

They are also termed APUD cells as they are responsible for amine precursor uptake and decarboxylation

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19
Q

In humans, most pheochromocytomas secrete what catecholamine?

A

Norepinephrine

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20
Q

What percentage of dogs with a pheochromocytoma are symptomatic?

A

30-50% have clinical signs attributable to the tumor

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21
Q

What are common clinical signs seen with a pheochromocytoma?

A 
Hypertension
Weakness
Collapse
Lethargy
Vomiting
Diarrhea
PU/PD
Tachypnea
Abdominal distension
Syncope
Tachyarrhythmias
Bradyarrhthymias
Abdominal pain
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22
Q

What percentage of dogs with a pheochromocytoma have invasion into the caudal vena cava?

A

15-38%

23
Q

What arrhythmias can be seen with a pheochromocytoma?

A 
Third degree AV block
Second degree AV block secondary to hypertension
SVT
Paroxysmal tachycardia
Ventricular ectopy
24
Q

True or False:

Most pheochromocytomas are incidental findings

A

TRUE

The same is true in humans

25
Q

What laboratory findings can be seen in dogs with a pheochromocytoma?

A

Lab findings are generally unremarkable but may see mild, nonregenerative anemia, increased PCV due to catecholamine stimulation of the bone marrow, stress leukogram secondary to catecholamine release.

Dogs may also be hyperglycemic and hypercholesterolemia from catecholamine stimulation

26
Q

What percentage of dogs with a pheochromocytoma will have proteinuria?

A

50%, likely from hypertensive glomerulopathy

27
Q

What are the 3 basic categories of treatment for myxedema coma?

A

supportive care, thyroid supplementation, and treatment of concurrent diseases

28
Q

Which form of levothyroxine has a higher bioavailability and and results in a more rapid response to tx for myxedema coma?

A

IV at a dose of 5 mcg/kg q 12 hrs

Adverse effects include arrhythmias, angina pectoris, pneumonia

29
Q

Endogenous TSH concentrations are normal in approximately how many hypothyroid dogs?

A

63%

30
Q

What are the 3 basic categories of treatment for myxedema coma?

A

supportive care, thyroid supplementation, and treatment of concurrent diseases

31
Q

What complications may be seen intraoperatively during adrenalectomy for removal of a pheochromocytoma?

A 
Hypotension
Hypertension
Tachycardia
Ventricular arrhythmias
Hemorrhage
32
Q

What is the reported perioperative mortality rate for dogs undergoing elective adrenalectomy vs emergency adrenalectomy due to acute adrenal hemorrhage?

A

Elective: 6%
Emergency: 50%

33
Q

In a study by Barthez in JVIM from 1997 what percentage of dogs with pheochromocytoma had each of the following:
Metastasis
Local invasion
Concurrent neoplasia

A

Metastasis: 15%
Local invasion: 39%
Concurrent neoplasia: 54%

34
Q

What postoperative complications can be seen in dogs with pheochromocytomas and how common are postoperative complications?

A

Vary from 30-51% depending on the study

Hypotension
Bradycardia
Ventricular arrhythmias
Tachypnea
Vomiting
Cardiopulmonary arrest
DIC
Incisional dehiscence
Hemorrhage
35
Q

What is the prognosis for a dog with a pheochromocytoma?

A

Guarded

Patients that survive the postoperative period and have complete resection of the tumor may have 18 months to 4 years

36
Q

Which form of levothyroxine has a higher bioavailability and and results in a more rapid response to tx for myxedema coma?

A

IV at a dose of 5 mcg/kg q 12 hrs

Adverse effects include arrhythmias, angina pectoris, pneumonia

37
Q

What is the reported survival rate for dogs with myxedema coma?

A

87% (in a case series of 8 dogs)

38
Q

List things that are associated with a poor prognosis in humans with myxedema coma

A

persistent hypothermia, advanced age, severity of concurrent disease, degree of mental alteration

39
Q

what is the general rule for Na decrease in response to hyperglycemia (pseudohyponatremia)

A

1 meq/L decrease in Na for every 62 mg/dl increase in glucose OR
1.6 meq/L decrease in Na for every 100 mg/dl increase in glucose
(both in Hopper)

40
Q

What is Hyperglycemic Hyperosmolar syndrome or HHS?

A

Its a complication of DM characterized for severe hyperglycemia (>600mg/dl), minimal or absent urine ketones and serum osmolality of >350mOsm/kg.

41
Q

Pathogenesis of HHS

A
  1. Hormonal alterations
  2. Reduction in the GFR
  3. Influence of concurrent diseases
42
Q

what hormones are involved in the Pathogenesis of HHS

A

Epinephrine, glucagon, cortisol and growth hormone

43
Q

Why can hyperglycemia be only present if there is a reduction of GFR?

A

Severe hyperglycemia can occur only in the presence ofreduced GFR, because there is no maximum rate of glucose loss via the kidney. That is, all glucose that enters the kidney in excess of the renal threshold will be excreted in the urine

44
Q

Name concurrent disesases that commonly predispose to HHS

A

CHF, CKD

neoplasia, infection, endocrinopathies, pancreatitis and liver disease.

45
Q

Indicate the formulas to calculate: Osmolality, effective Osmolality and corrected sodium

A 
Serum osm(calc) = 2(Na+ )+(BUN÷ 2.8)+(glucose ÷18)
Effective osm = 2(Na+ )+(glucose ÷18)
Na+(corr) = Na+(meas) + 1.6([measured glucose – normal glucose] ÷ 100)
46
Q

What is the initial ideall choice of fluid therapy for HHS?

A

Isotonic saline (0.9% saline) is typically the initial fluid of choice because it both addresses the fluid deficits and replaces glucose with sodium in the extracellular space, thus preventing a rapid shift in osmolality

47
Q

At what rate should we correct hypernatremia?

A

no more than 1 mEq/L/hr

48
Q

True or False

We can use the same protocol of regular insuline than in DKA

A

FALSE Ideally we should reduce the hyperglycemia slower, so we can use half the doses we use for DKA.

49
Q

How often is it recommended to monitor Potassium, phosphorus and Magnesium in HHS

A

4 to 6 times a day

50
Q

What is the most common clinical signs of hypophosphatemia in cats and dogs respectively?

A

cat (hemolysis), dog (seizure)

51
Q

What are common clinicopathologic findings related to DKA in dogs and cats? 1. CBC, 2. Chem, 3. Electrolyte

A

CBC

  1. dog: non-regenerative anemia, neutrophilia with left shift, thrombocytosis
  2. cat: anemia, neutrophilia with left shift

Chem

  1. dog & cat: persistent hyperglycemia
  2. dog: increased ALP, ALT, AST, Chol, azotemia
  3. cat: increased ALT, Chol, azotemia

Electrolyte

  1. K: initially extraceullar hyperkalemia, followed by hypokalemia on treatment
  2. P: initially hyperphosphatemia, followed by hypophosphatemia on treatment
  3. Magnesium: usually decreased in cat, dog usually do not have decreased iMg on initial examination
  4. hyponatremia
52
Q

What’s the indication of bicarbonate therapy in DKA patient?

A

only arterial pH remains less than 7.0 after 1 hours of fluid therapy

53
Q

True or false: ketonuria may not be detected because of nitroprusside reagent in the urine dipstick reacts with acetoacetate and not with beta-hydroxybutyrate (this is dominant ketone body in DKA)

A

True

54
Q

20% dogs with DKA have aerobic bacterial growth on culture of urine obtained by cystocentesis. What are 2 reasons explained in Silverstein?

A
  1. likely a result of diabetic immunosuppression

2. decreased ability to mobilize white blood cells to the site of infection

Auburn ECC (26 decks)

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