Bryan - Sa Med - Adrenal Disease - Fall 3Rd Year

Front 1

What is the distribution between pituitary-dependent and adrenal-dependent hyperadrenocorticism in dogs?

Back 1

80-85% pituitary
15-20% adrenal

Front 2

Predict the following in pituitary-dependent hyperadrenocorticism:
Adrenal size
Circulating ACTH
Circulating cortisol

Back 2

Adrenal size (normal to bilaterally enlarged)
Circulating ACTH (HIGH)
Circulating cortisol (HIGH)

Front 3

Predict the following in adrenal-dependent hyperadrenocorticism:
Adrenal size
Circulating ACTH
Circulating cortisol
ADH

Back 3

Adrenal size (unilaterally enlarged w/contralateral hypoplasia)
Circulating ACTH (LOW)
Circulating cortisol (HIGH)
ADH (LOW)

Front 4

What are the most common clinical signs associated with hyperadrenocorticism in dogs?

Back 4

PU/PD/PP
Pendulous abdomen
Alopecia (& other cutaneous signs)
(also lameness, weakness, panting, UTI signs)

Front 5

What are some common clinpath signs associated with hyperadrenocorticism in dogs?

Back 5

Hypercholesteremia
Diabetes mellitus
Increased ALP (ALT also may increase but not as markedly as ALP)
Hypertension

Front 6

Which of the following is NOT associated with hyperadrenocorticism in dogs?
a) Pyoderma
b) Hypotension
c) Congestive heart failure
d) SARDS
e) Diabetes insipidus

Back 6

b) Hypotension
c) Congestive heart failure (usually a CONCURRENT disease)
e) Diabetes insipidus

Front 7

Which of the following ARE associated with hyperadrenocorticism in dogs?
a) hypothyroidism
b) proteinuria
c) hypovolemia
d) anterior uveitis
e) thrombocytosis

Back 7

a) hypothyroidism
b) proteinuria
e) thrombocytosis

(note - should be HYPERvolemia and Sudden Acute Retinal Degeneration)

Front 8

Cushing's disease is a ____________ disease.

Back 8

clinical

Front 9

T or F:
An ACTH stim test with a low post stimulation result is highly indicative of adrenal disease absence.

Back 9

False!
Due to its low sensitivity, ACTH stim test is really a screening test only (miss 40% of positives).

Front 10

T or F:
A LDDS test that successfully suppresses is highly indicative of adrenal disease absence.

Back 10

True!
LDDS has good sensitivity!

Front 11

Which of the following is the most likely result of a LDDS test in a patient with pituitary dependent HAC?
a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value
c) drops under 50% at 4h but increases afterwards
d) drops under 50% at 4 and 8 h.

Back 11

c) drops under 50% at 4h but increases afterwards

Front 12

Which of the following is the most likely result of a LDDS test in a normal patient?
a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value
c) drops under 50% at 4h but increases afterwards
d) drops under 50% at 4 and 8 h.

Back 12

d) drops under 50% at 4 and 8 h.

Front 13

Which of the following is/are the most likely results of a LDDS test in adrenal dependent HAC?
a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value
c) drops under 50% at 4h but increases afterwards
d) drops under 50% at 4 and 8 h.

Back 13

a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value

Front 14

T or F:
An animal testing negative on the urine cortisol:creatinine test has a high chance of NOT having adrenal disease.

Back 14

True!
Urine cortisol:creatinine has a great negative predictive value

Front 15

Which of the following is/are the most likely results of a HDDS test in adrenal dependent HAC?
a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value
c) drops under 50% at 4h but increases afterwards
d) drops under 50% at 4 and 8 h.

Back 15

a) no suppression whatsoever

Front 16

Which of the following is/are the most likely results of a HDDS test in pituitary-dependent HAC?
a) no suppression whatsoever
b) does not suppress under 50% of initial cortisol value
c) drops under 50% at 4h but increases afterwards
d) drops under 50% at 4 and 8 h.

Back 16

d) drops under 50% at 4 and 8 h (in 75%; 25% will still not suppress)

Front 17

T or F:
If a dog has signs of Cushing's but ACTH stim, LDDS, and HDDS are all negative, the dog likely does not have Cushing's.

Back 17

False!
Gotta rule-out Atypical HAC - do ACTH stim and measure OTHER steroid hormones!

Front 18

Which of the following are NOT common treatments for a dog with Cushing's?
a) Transphenoidal hypophysectomy
b) Bilateral adrenalectomy
c) Adrenolytic mitotane protocol
d) Melatonin protocol
e) Ketoconazole protocol

Back 18

a) Transphenoidal hypophysectomy (unless you're Dutch...)
b) Bilateral adrenalectomy
c) Adrenolytic mitotane protocol
e) Ketoconazole protocol

Front 19

As measured by serum cortisol, what is the goal of mitotane therapy?

Back 19

Want cortisol BELOW REFERENCE RANGE after ACTH stimulation

Front 20

Which cells does mitotaine effect?
a) zona glomerulosa
b) zona fasiculata
c) zona reticularis
d) medullary parenchyma

Back 20

b) zona fasiculata
c) zona reticularis

Front 21

Central Diabetes Insipidus, Keratoconjunctivitis Sicca, and Hypothyroid are side-effects to which Cushing's treatment? Which of the conditions is irreversible?

Back 21

Transphenoidal hypophysectomy (hypothyroid is irreversible)

Front 22

Your dog is on mitotaine therapy and stops eating and begins vomiting. What is your next step?
a) continue therapy
b) increase dose 25%
c) discontinue mitotaine
d) reduce dose 25%

Back 22

c) discontinue mitotaine (YOU'RE GIVING THE DOG ADDISON'S; administer glucocorticoids)

Front 23

What is the mechanism of action for trilostane? How is its efficacy monitored?

Back 23

Trilostane inhibits steroid production (monitor via ACTH stim 2-6 hrs post pill)

Front 24

T or F:
Radiotherapeutic ablation of microadenomas greatly lessens the clinical signs of pituitary-dependent Cushing's.

Back 24

False!
May improve neuro signs but doesn't help the Cushing's.

Front 25

T or F:
Mitotane and trilostane are of little use to adrenal-dependent Cushing's.

Back 25

True! They usually don't work well and are $$$$$$$$$$$$$$$$$.

Front 26

Removal of which adrenal is the most difficult?

Back 26

Right side!

Front 27

T or F:
During a unilateral adrenalectomy, pre, peri, and post-op glucocorticoids should be administered.

Back 27

True!
Give dex or hydrocortisone to not interfere with ACTH stim tests!

Front 28

What are options for inoperable adrenal tumors? What is the mechanism of action for each?

Back 28

Melatonin
Lignins
(both are steroid enzyme inhibitors)

Front 29

If a cat has Cushing's, which form is the most likely?

Back 29

Pituitary

Front 30

T or F:
In terms of signalment in dogs, small breeds get pituitary-dependent HAC while large breed get adrenal.

Back 30

True (kinda)
Boxers get pituitary dependent

Front 31

Which of the following tests work with feline Cushing's?
a) ACTH stim
b) LDDS test
c) HDDS test
d) endogenous ACTH

Back 31

c) LDDS test (at levels like a HDDS in dogs)
c) HDDS test (higher dex levels than in dogs)
d) endogenous ACTH

Front 32

Which forms of treatments have success in treating feline Cushing's?
a) Mitotane
b) Ketoconazole
c) Trilostane
d) bilateral adrenalectomy
e) unilateral adrenalectomy
f) Hypophysectomy

Back 32

c) Trilostane
d) bilateral adrenalectomy
f) Hypophysectomy

Front 33

What are the mineralocorticoids? Which is the most potent?

Back 33

Cortisol
11-deoxycorticosterone
Aldosterone (most potent)

Front 34

Which of the following can lead to increased aldosterone secretion?
a) high renal blood pressure
b) low renal blood pressure
c) increased NaCl
d) decreased NaCl
e) high plasma K

Back 34

b) low renal blood pressure
d) decreased NaCl
e) high plasma K

Front 35

What effect does aldosterone have on the kidney?

Back 35

Causes Na retention as well as release of K and H+.

Front 36

T or F:
Hyperaldosteronism typically affects both dogs and cats.

Back 36

False! pretty rare disease but affects cats more than dogs

Front 37

Choose primary or secondary hyperaldosteronism...
...renin-dependent.

Back 37

Secondary

Front 38

Choose primary or secondary hyperaldosteronism...
...associated with heart failure.

Back 38

secondary

Front 39

Choose primary or secondary hyperaldosteronism...
...associated with neoplasia.

Back 39

primary

Front 40

What is the common signalment for hyperaldosteronism?

Back 40

older female cat with low K and high BP

Front 41

What are major clinical signs of hyperaldosteronism?

Back 41

Weakness
PU/PD
Cardiac arrthymias
Hypertension
Retinopathy

Front 42

Which are common tests for hyperaldosteronism?
a) serum K
b) Serum aldosterone
c) aldosterone:renin ratios
d) serum renin

Back 42

b) Serum aldosterone

Front 43

What are acceptable treatments for hyperaldosteronism?

Back 43

Adrenalectomy
Medical management (ACE inhibitors, spironolactone, Ca channel blockers)

Front 44

Which drug is an aldosterone antagonist?

Back 44

Spirinolactone

Front 45

What is the prognosis for hyperaldosteronism treatment?

Back 45

If kidneys are OK, GOOD PROGNOSIS!

Front 46

What is the precursor to all catecholamines? How is catecholamine production regulated?

Back 46

Tyrosine (converted into L-dopa by tyrosine kinase); norepinephrine inhibits this by negative feedback

Front 47

Which of the following are NOT effects of catecholamines?
a) increased gluconeogenesis
b) vasodilation
c) bronchodilation
d) increase heart rate
e) increased renin release

Back 47

a) increased gluconeogenesis (should be glycogenolysis)
b) vasodilation (should be vasoconstriction)

Front 48

Pheochromocytomas are tumors of ____________ cells.

Back 48

CHROMAFFIN

Front 49

Why is catecholamine release from pheochromocytomas variable?

Back 49

no innervation to the tumor

Front 50

T or F:
Pheochromocytomas cause clinical signs mostly due to their mass effects and not catecholamine release.

Back 50

False!
Mass effects, hemorrhage, and catecholamine release all cause clinical signs.

Front 51

What proportion of pheochromocytomas are malignant? What proportion are incidental findings?

Back 51

50% malignancy; up to 60% incidental findings though!

Front 52

What are common signs associated with pheochromocytoma?
a) palpable abdominal mass
b) tachycardia
c) pain
d) abdominal distention
e) hypertension

Back 52

b) tachycardia
e) hypertension

Front 53

T or F:
Stress or fear can exacerbate signs of pheochromocytoma.

Back 53

False!

Front 54

How is pheochromocytoma diagnosed?

Back 54

Clinical signs then essentially ruling-out Cushing's once an adrenal mass is found.

Front 55

What pre-op stabilization should be considered before excision of a pheochromocytoma?

Back 55

Phenoxybenzamine (anti-hypertensive)
Beta blockers (if tachyarrthymias)

Front 56

T or F:
Hypoadrenocorticism usually manifests as a deficiency in mineralocorticoids and glucocorticoids.

Back 56

True! (although one part in the notes says that it is primarily glucocorticoids)

Front 57

T or F:
Primary hypoadrenocorticism is the most common form in small animals and involves atrophy of certain zones of the pituitary gland.

Back 57

False!
It is the most common form but it involves ADRENAL ATROPHY

Front 58

What is the most common cause of hypoadrenocorticism in small animals?
a) iatrogenic
b) idiopathic
c) immune-mediated
d) infarct to adrenals
e) idiocracy

Back 58

b) idiopathic (but immune-mediated is the leading theory right now; also iatrogenic is a main issue with SECONDARY hypo-AC)

Front 59

What is the common signalment for a small animal with hypoadrenocorticism?

Back 59

YOUNG ADULT *******

Front 60

What are common presenting or clinical signs for a dog with hypoadrenocorticism?

Back 60

Lethargy
GI signs (anorexia, vomiting, diarrhea, melena, wt loss)
Weakness/trembling
PU/PD
muscle wasting
bradycardia
hypothermia

Front 61

What are some significant laboratory findings for a dog with hypoadrenocorticism?

Back 61

Absence of stress leukogram
Increased K, decreased NaCl
Mild non-regenerative anemia

Front 62

Which lab abnormalities in hypoadrenocorticism are due to decreased corrtisol?
a) hyperkalemia
b) hypoglycemia
c) anemia
d) hypocholesteremia
e) metabolic acidosis

Back 62

b) hypoglycemia
c) anemia
d) hypocholesteremia

Front 63

Which lab abnormalities in hypoadrenocorticism are due to decreased mineralocorticoids?
a) hyperkalemia
b) hypoglycemia
c) anemia
d) hypocholesteremia
e) metabolic acidosis

Back 63

a) hyperkalemia
e) metabolic acidosis

Front 64

What radiographic finding should likely be noted on a dog with hypoadrenocorticism?

Back 64

Microcardia (due to hypovolemia)

Front 65

Predict the ACTH stim test results of a dog with primary hypoadrenocorticism and of a dog with secondary hypoadrenocortism.

Back 65

Both should have baseline cortisol VERY low and NO STIMULATION WHATSOEVER

Front 66

How can primary hypoadrenocorticism be differentiated from secondary?

Back 66

Use endogenous ACTH test; primary should have high ACTH, secondary should have low ACTH

Front 67

What medical response should be given in a patient in an Addisonian crisis?

Back 67

Shock dose of crystalloid (maybe w/Ca);
IV dexmeth or hydrocortisone;
Insulin + glucose (if hyper K);
Address any acidosis
Give gastric protectants

Front 68

T or F:
Mineralocorticoids should always be included when treating acute hypoadrenocorticism.

Back 68

False! Only give them if there are electrolyte abnormalities, once the patient is stabilized.

Front 69

What drug can be given to address electrolyte abnormalities when managing chronic hypoadrenocorticism?

Back 69

DOCP (desoxycorticosterone pivalate)

Front 70

A patient with well-managed Addison's suddenly has a crisis around July 4th. What gives?

Back 70

Inability of body to respond to stress - need to up the pred dose in times of stress!

Front 71

How does hypoadrenocorticism present differently in cats than in dogs?

Back 71

No vomiting or PU/PD in cats!

Front 72

How is testing for hypoadrenocorticism different between dogs and cats?

Back 72

Cats - lower dose given and test at 0, 30, 60 min.
Dogs - higher dose given and test at 0, 2, and 3 hrs.