Endocrine Flashcards

1
Q

Pathophysiology of canine diabetes mellitus

A

Pancreas does not make insulin (similar to type I in people). Usually immune-mediated or secondary to pancreatitis. Middle-aged dogs predisposed.

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2
Q

Canine diabetes mellitus treatment

A

Goal: control clinical signs and improve quality of life
No remission possible
Tx: Insulin (vetsulin) begin at 0.25-0.5 U/kg q12h, high fiber diet, glucose curves to guide treatment (helps void underdosage/overdosage)

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3
Q

How would glucose curves help identify the somogyi effect?

A

The somogyi effect is when the animal is on too much insulin. This leads to a drop in BG which the body responds by releasing glucagon to spike BG. On “spot checks” this may lead us to think the patient is being UNDERdosed.. but in reality the patient is being OVERdosed!

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4
Q

DKA pathophysiology

A

Mismanaged DM leading to a lack of insulin for glucose uptake. The cells are starved leading to fat breakdown and ketone build-up

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5
Q

DKA clinical pathology findings
Glucose ___
Potassium ___ or ___
Na ___
AG ___

A

Glucose HIGH
Potassium HIGH (no cellular uptake) or LOW (anorexia)
Sodium LOW (fluid shift into vasculature)
AG HIGH (KLUE)

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6
Q

DKA Treatment

A

IV fluids
Electrolyte correction
Fast acting insulin (CRI)
Dextrose (resolve the ketonemia)
Potassium ALWAYS given with insulin CRI

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7
Q

Hyperadrenocorticism (Cushings) etiology

A

Pituitary dependent tumor (85%) PDH
Adrenal dependent tumor (15%) ADH
Iatrogenic (excessive corticosteroids)

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8
Q

Cushing’s clinical signs

A

muscle weakness/atrophy, alopecia, comedones, abdominal distention, hepatomegaly, thin skin, calcinosis cutis

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9
Q

Cushing’s clinical pathology
_____ leukogram
_____ ALP, ALT, Triglycerides
_____ BUN
_____ Creatinine

A

stress leukogram (neutrophils and monocytes HIGH, lymphocytes and eosinophils LOW)
LOW BUN (cortisol inhibits ADH causing washout)
LOW Creatinine d/t muscle wasting

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10
Q

LDDST (how to perform, expected results for PDH vs ADH)

A

Baseline, 4 hr, 8 hr sample
PDH - will see suppression (drop in 4 hr) and then huge spike in 8 hr
ADH - will NOT see any suppression for any sample

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11
Q

ACTH stimulation test (expected results for cushings vs addisons)

A

Cushings - will see exaggerated response
Addisons- no response

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12
Q

Cushing’s Tx (two main drugs & their mechanism)

A

Mitotane - cytotoxic adrenocortical destruction
Trilostane - inhibit cortisol synthesis

can ultrasound abdomen to look for adrenal mass

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13
Q

Addison’s disease gender predelection

A

70% Female

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14
Q

Addison’s pathophysiology and clinical signs

A

Decreased production of cortisol and aldosterone

Anorexia, lethargy, thin condition, PU/PD, diarrhea, collapse, bradycardia (tall T waves), shaking, low SG

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15
Q

Addison’s clinical pathology
Anemia
Lack of ____ leukogram
K __
Na/Cl __
ALT/AST/ALP __
USG __

A

Lack of stress leukogram
High potassium
Low na/cl
High liver enzymes
USG < 1.030

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16
Q

Addison’s diagnosis (test and expected result)

A

ACTH Stim < 2 (baseline AND post-injection)

17
Q

Addison’s treatment

A

Fluids (normal saline best choice)
Hyperkalemia Tx (insulin + dextrose, calcium gluconate)

Prednisone (corticosteroid replacement)
Fludrocortisone (mineralocorticoid aka: aldoserone replacement)

18
Q

Canine hypothyroidism clinical signs

A

Weight gain, alopecia (trunk, tail, ventral thorax), pyoderma, hyperkeratosis, bradycardia, weak pulses, lethargy, obesity

19
Q

Hypothyroidism
TSH _
TT4_
FT4_

A

TSH high
TT4 low
FT4 low

Note: if TSH is in normal range and TT4/FT4 are both low, that is highly suspicious for hypothyroidism!

20
Q

Hypothyroidism Tx

A

Levothyroxine :)

21
Q

Low ___ and ___ leads to medullary washout and low USG.

A

BUN , Na

22
Q

Why do we see a low USG with addison’s disease?

A

low aldosterone - leading to low sodium - leading to medullary washout