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RUSVM SAM 1 > Hyper/Hypo Adrenocortistism > Flashcards

Hyper/Hypo Adrenocortistism Flashcards

1
Q

Excessive production of glucocorticoids by the adrenal glands

A

Hyperadrenocortisim

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2
Q

What are the three forms of HAC

A 
Pituitary dependent (PDH) 
Adrenocortical neoplasia (AT) 
Iatrogenic
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3
Q

What is the most common type of HAC?

A

Pituitary dependent

Accounts for 80-85% of cases

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4
Q

What type of HAC causes bilateral adrenocortical hyperplasia?

A

Pituitary dependent

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5
Q

What type of HAC causes bilateral adrenal atrophy?

A

Iatrogenic

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6
Q

What type of HAC has and enlarged adrenal gland with atrophy of the contralateral gland

A

Adrenocortical tumors (AT)

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7
Q

Species predisposed to HAC?

A 
Poodles
Boxer 
Dashunds 
Schnauzers 
Boston terriers 
German shepherds
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8
Q

At what age do you usually see HAC?

A

Middle aged to old dog, ave 12yrs

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9
Q

What is not a clinical finding associated with HAC?

PU/PD 
Bilaterally symmetrical alopecia 
Pendulous abdomen 
Seborrhea 
Calcinosis cutis
A

Seborrhea - associated with hypothyroidism

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10
Q

What would you expect to find on a CBC, chem panel and UA of a cushings patient

A

CBC- polycythemia, stress leukogram

Chem- increased ALP, hypercholesterolemia, mildly increase ALT and glucose

UA- decreased specific gravity, proteinuria
USG <1.025

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11
Q

What may you see on a radiograph of a HAC patient?

A

Hepatomegaly –corstiol makes the liver larger

Distended bladder- PU/PD

Mineralization
Osteopenia

Metastasis of adrenal tumors

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12
Q

Would you expect to see an increased BP in cushings patient?

A

50-80% of patients are hypertensive

Maybe du to PLN

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13
Q

T/F: baseline cortisol can be normal in cushings dogs

A

True

Secretion in episodic

Mean daily cortisol is increased but individual measurement can be normal

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14
Q

What would the urine cortisol: creatinine ratio be in a cushings patient?

A

Would be increased

Urine cortisol excretion increases with adrenal secretion of cortisol

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15
Q

T/F: a high urine cortisol: creatinine ratio can be diagnostic for cushings

A

False

Positive test makes cushings a possibility, but is not diagnostic

However, a negative test makes cushings unlikely

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16
Q

What is the low dose dexamethasone suppression test?

A

Dexamethasone inhibits release of ACTH from pituitary

Normal - cortisol suppressed

Cushings- no suppression

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17
Q

Low Dose Dex suppression test

50% suppression at 4 hrs with lack of suppression at 8hrs.
What is your interpretation?

A

Pituitary dependent hyperadrenocortisim

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18
Q

Low Dose Dex suppression test

No suppression at 8hrs or 4hrs.
What is your interpretation?

A

Cushings

Could be either AT or PDH

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19
Q

What is the test of choice for iatrogenic cushings?

A

ACTH stimulation test

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20
Q

What are the cons of the ACTH stimulation test?

A

Expensive

Compounded gels are not recommended.

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21
Q

What is the high dose Dex suppression text?

A

About 10x dose of LDDST
Cannot be used to diagnose cushings, test to differentiate between PDH and AT

Suppression =PDH
No suppression= inconclusive

Cannot definitely diagnose AT

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22
Q

What would you use an Endogenous corticotrophin to diagnose?

A

To differentate between PDH and AT

Cannot be used to diagnose cushings b/c of overlap in ACTH in normal animals and PDH animals

Normal 20-100pg/mL
PDH 40-500pg/mL
AT <20pg/mL

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23
Q

T/F: ultrasound can be used to differentiate malignant from benign adrenal tumors

A

False

Can usually only determine malignancy this way if there is invasion of the vena cava or liver metastases

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24
Q

What test would be the BEST to diagnose cushings in a case with only mild clinical signs or lab abnormalities only

A

ACTH stim

Also good for

  • patients with concurrent nonadrenal illness
  • patients with suspected iatrogenic cushings
  • patients on phenobarbital
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25
Q

What test would be BEST to diagnose a cushings case in a patient with severe clinical signs and no evidence of non adrenal illness?

A

LDDS

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26
Q

What would be the BEST test to diagnose a suspected adrenal tumor?

A

LDDS

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27
Q

Which test is the BEST at differentiating PDH vs AT HAC, is this the most practical clinically?

A

Endogenous ACTH.

Not most clinically practical because test is expensive and sample required very careful handling. See more often in University setting.

Clinically, abdominal radiographs are used to visualize AT

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28
Q

You run LDDS, ACTH stim, Endogenous ACTH and they all come back negative, but the dog has classical cushingoid appearance.

What could be the problem with this dog?

A

Noncortisol hormones and cushings

-> derangement of steroid pathway and overproduction of precursors

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29
Q

If you think a dog has noncortisol cushings, how would you confirm your diagnosis?

A

Perform ACTH stimulation and assay noncortisol hormones (Eg progestin)

30
Q

What are the medical therapy treatments for cushings?

A 
Mitotane 
Selegiline 
Ketoconazole 
Trilostane 
Cyprohetadine 
Bromocriptine
31
Q

What is the MOA of mitotane ?

A

Destroy zona fasciculata and reticularis of adrenal gland -> permanent atrophy

Inhibits cholesterol side chain cleavage.

32
Q

What is the dosage of mitotane and how would you monitor this therapy?

A

Starting dose - 50mg/kg/day, divided BID with meals

Maintenance - 50mg/kg/week

Monitor - ACTH stim within 5-10days then 1 and 3 months after diagnosis

33
Q

What is the MOA of selegiline

A

Irreversible inhibitor of monoamine oxidase type B -> restore central dopamine concentration

-> decrease the clinical signs of cushings, but does not have any effect on the tumor

34
Q

Which therapy may be a good option for patients whose owners do not want to used Lysodren due to side effects or the high cost of Trilostane

A

Selegiline (Anipryl)

35
Q

When is Anipryl use appropriate?

A

Patients with mild cushings signs but are negative on lab tests

May have a role in patients that test positive for cushings but have no clinical signs

Cognitive dysfunction

Behavior - pee in the right places

36
Q

What is the MOA of trilostane?

A

Competitive inhibitor of 3B-hydroxysteroid dehydrogenase —> inhibit synthesis of steroids (cortisol and aldosterone)

37
Q

T/F: Mitotane and Trilostane are reversible drug therapies

A

False

Only trilostane is reversible

38
Q

What drug should you do periodic monitoring of electrolytes because it can cause a hyperkalemia ?

A

Trilostane

39
Q

How does ketoconazole treat cushings?

A

Inhibit steroid biosynthesis
-> imidazole antifungal drug

EXPENSIVE

40
Q

What are adverse effects of ketoconazole ?

A

Excessive glucocorticoids deficiency -> cessation of therapy

Vomiting, diarrhea, anorexia, and elevated liver enzymes

41
Q

What is the MOA of cyprohetadine? How does this treat cushings?

A

Antiserotonin, anticholinergic, and antihistamine effects

Increased serotonin theroeticallly associated with excess pituitary ACTH

42
Q

What are the non-drug therapies for cushings?

A

Surgical

  • transsphenoidal hypophysectomy - very difficult and requried lifelong thyroid pred replacement
  • bilateral adrenalectomy

Radiation therapy

43
Q

What is the treatment of pituitary macroadenomas ?

A

Radiation therapy
-reduce tumor size and clinical signs.

Often still require medical therapy to control cushings disease

44
Q

What is the treatment f choice for adrenal tumors?

A

Adrenalectomy
- are often vascular and invasive even if benign

50% malignant -> very poor prognosis

45
Q

How can you reduce risk of thromboembolism post-adrenalectomy

A

Treatment with dexamethasone, heparin, plasma, and Hetastarch- over first 5 days

46
Q

What are some complications associated with PDH?

A

Hypertension, PTE, CNS signs, infections, recurrence of disease, CHF

47
Q

What are the 5P’s of HAC?

A 
Panting 
PU
PD
PP 
Potbelly
48
Q

What is the signalment of hypoadrenocorticism ?

A

Med to lg breed dogs

Younger

49
Q

Release of aldosterone from the adrenal gland has what effect?

A

Increased Na and water reabsorption
Increased K secretion into urine

Increase blood volume

50
Q

Aldosterone release from the adrenal gland is stimulated by?

A

Angiotensin II

51
Q

Deficiency in aldosterone results in…?

A

HYPO natermia and chloremia

HYPER kalemia

52
Q

What are the major regulators of aldosterone secretion?

A

Plasma K levels and RAAS

53
Q

Where does aldosterone exert its effect?

A

DCT and collecting duct

-> increase Na reabsorption

54
Q

What is the signalment of Addison’s disease?

A

Dog, young to middle aged

F>M

55
Q

Clinical signs of Addisons?

A 
“Ain’t doing right” 
Waxing and waning 
Anorexia 
Lethargy 
Dehydration 
Weakness
Polyuria
56
Q

What does an addisons crisis appear like?

A

Collapse, bradycardia, melena

57
Q

What is “typical” hypoadrenocorticism ?

A

Deficient in both mineralalocortocoids and glucocorticoids

Due to primary lesions - usually immune mediated adrenal gland destruction

58
Q

What is the normal function of glucocorticoids? What will you see in a deficiency?

A

Normal fx: increase blood glucose, gluconeogensis, glycogenolysis, muscle/fat catabolism

Deficiency: anorexia, lethargy, fasting hypoglycemia

59
Q

What is atypical hypoadrenocorticism? What are the two causes?

A

Low glucocorticoids

  • pituitary lesion so there is not enough ACTH
  • early in a typical addisons, before it progresses to include mineralocorticoids
60
Q

What is iatrogenic hypoadrenocorticism ?

A

Abrupt discontinuation of glucocorticoids without time for the atrophied adrenals to respond

61
Q

Poodle 1.5yrs, history of lethargy and poor appetite

PE: recumbency and minimally responsive, positive skin tent, sunken eyes, tacky mm.

TPR: hypothermic and bradycardia

What’s you DDx, and what diagnostics would you run to confirm?

A

Hypoadrenocorticism

QATS - mild hypoglycemia, azotemia, USG 1.018

CBC, chem, UA
ECG

62
Q

Poodle 1.5yrs, history of lethargy and poor appetite

PE: recumbency and minimally responsive, positive skin tent, sunken eyes, tacky mm.

TPR: hypothermic and bradycardia

What type of supportive care would you give this patient?

A

Heat
IV catch with fluids
Emerg hyperkalemia treatment

63
Q

What type of fluids should be given to addisons patient?

A

Saline

Can have hyperkalemia, do NOT give fluids with K

64
Q

What could you do to treat a hyperkalemia in an addisons patient?

A

Saline
Calcium gluconate: cardioprotective
Regular insulin with concurrent dextrose (draws potassium into cells and some diuretic effect)
Bicarb - patient are acidotic

65
Q

What CBC, Chem and UA results would you expect in an Addisons patient?

A

CBC - NO stress leukogram

Chem- azotemia, hyponatremia, hyperkalemia

UA- isosthenuric

66
Q

What test is diagnostic or hypoadrenocorticism

A

ACTH stimulation test

Endogenous ACTH levels
-can be used to differentiate type

67
Q

Endogenous ACTH is high in ________________ hypoadrenocorticism and low in _________forms

A

Primary; secondary and tertiary

68
Q

What is the treatment for an acute Addisonian crisis ??

A

Restore blood volume rapidly: 0.9% NaCl

Address life-threatening hyperkalemia: shock dose fluids then insulin/glucose, Ca gluconte, or Bicarb if nessessary

GIVE GLUCOCORTICOIDS ** dexamethasone **

Give mineralocorticoids - DOCP/Fludricortisone

69
Q

Which therapy for mineralocorticoids, also has some glucocorticoid effect?

A

Fludrocortisone

70
Q

T/F: glucocorticoids maintence therapy is needed by all addisons patients

A

False

More likely needed with DOCP

71
Q

For maintenance therapy fo glucocorticoids, addisons patients should receive what type of dose?

A

Physiologic dose (0.25/kg/day)

All owners should have some to give under conditions of stress (0.5-1.5 mg/kg/day)

72
Q

How do you treat atypical hypoadrenocorticism ?

A

Glucocorticoids supplementation

RUSVM SAM 1 (26 decks)

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