Canine Hyperadrenocorticism + Canine Hypoadrenocorticism, Pheochromocytoma Flashcards

1
Q

What layers of the adrenal gland does ACTH work on?

A
  • Zona Fasciculata (glucocorticoids)
  • Zona Reticularis (androgens)
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2
Q

Majority (80-85%) of dogs with Hyperadrenocorticism have a _________ tumor secreting excess ______

A

Pituitary, ACTH

(Pituitary tumor > adrenal tumor)

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3
Q

True or False: Most Pituitary dependent HAC are microadenomas

A

TRUE

(10-20% are macroadenomas which can cause compression and neuro signs)

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4
Q

What is an important consideration when taking a single ACTH and cortisol sample on a dog with PDH?

A

ACTH is secreted in bursts, if taking 1 sample ACTH and Cortisol can appear normal… look at AUC over time

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5
Q

What can be visualized on ultrasound of the adrenal glands in patients with PDH?

A

Bilateral hyperplasia due to excessive secretion of ACTH from the pituitary gland

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6
Q

What can be visualized on ultrasound of the adrenal glands in patients with ADH?

A

Unilateral hyperplasia or normal size of 1 gland, the other is atrophied and small

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7
Q

Do dogs with ADH have a benign or neoplastic tumor of the adrenal gland?

A

50:50 adenoma or carcinoma

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8
Q

What would you expect the CRH, ACTH, and cortisol levels to be in a patient with ADH?

A

↓ CRH
↓ ACTH
↑ Cortisol

(Adrenal gland secreting too much cortisol independent of feedback loop)

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9
Q

What can be visualized on ultrasound of the adrenal glands in patients with iatrogenic HAC?

A

Bilateral adrenal gland atrophy from exogenous steroids suppressing ACTH

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10
Q

At what age in dogs is HAC typically seen?

A

Middle to older age dogs

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11
Q

Is there a sex predilection for dogs with HAC/Cushings?

A

Yes, female > male

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12
Q

What breed of dogs are predisposed to developing HAC/Cushings?

A

PDH/ADH : poodles, dachshunds, terriers, GSD

+ labradoodles

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13
Q

What clinical signs can be seen in dogs with HAC?

A

(Cushings - 5 P’s!!)

  1. PU/PD/PP
  2. Pot belly
  3. Panting
  4. Muscle weakness
  5. Obesity
  6. Bilateral alopecia
  7. Calcinosis cutis
  8. Thin skin
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14
Q

True or False: Both hypothyroid and Hyperadrenocorticism patients tend to have thick skin

A

FALSE

HypoT = thick skin
HAC = thin skin

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15
Q

What are the associated complications in HAC/Cushings patients? (8)

A
  1. Hypertension
  2. Proteinuria
  3. Hypercoagulable state (PTE/ATE)
  4. UTI
  5. Calcium oxalate uroliths
  6. Pancreatitis
  7. Diabetes mellitus
  8. Poor wound healing
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16
Q

List the findings on CBC, Chem, and UA from a dog with HAC

A

CBC:
- Stress leukogram
- Thrombocytosis

Chem:
- ↑ ALKP, ↑ ALT, ↑ BA, ↑ Cholesterol, ↑ triglycerides
- mild ↑ BG
- ↑ Na, ↓ K

UA:
- USG: < 1.015, often < 1.008
- UTI (clinically silent, must do C&S)

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17
Q

HAC in dogs can cause hepatomegaly. How does this appear on ultrasound?

A

Hyperechoic liver

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18
Q

How is Urine Cortisol: Creatine ratio implemented in the diagnosis of HAC?

A
  • Screening test
  • High sensitivity, low specificity
  • If ↓ UCCR = unlikely HAC
  • If ↑ UCCR = not specific for HAC, can be a hint
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19
Q

What is the GOLD standard test for assessment of Iatrogenic HAC?

A

Iatrogenic HAC = Iatrogenic addisons

  • ACTH stim test
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20
Q

What results would you expect from an ACTH stim test performed on a PD-HAC patient?

A
  • Hypersecretion of cortisol levels in response to ACTH injection
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21
Q

What results would you expect from an ACTH stim test performed on a AD-HAC patient?

A
  • Hypersecretion of cortisol levels in response to ACTH injection
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22
Q

What is the GOLD standard test for diagnosing HAC?

A

LDDS test

(take blood sample, give Dexamethasone, then measure cortisol at 4 and 8 hrs)

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23
Q

What results would you expect from an LDDS test performed on a PD-HAC patient?

A
  • Dexamethasone will lower cortisol levels at 4 hrs (75% of cases), then elevates again by 8 hrs
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24
Q

What results would you expect from an LDDS test performed on a AD-HAC patient?

A

- Elevated cortisol @ 4 hrs and 8 hrs, no suppression
- Dexamethasone suppresses CRH and ACTH
- ADH is from adrenal mass secreting too much cortisol, so LDDS won’t be effective at suppressing cortisol

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25
Q

If measuring endogenous ACTH, what would you expect the levels to be in a dog with ADH vs PDH?

A

ADH: Low ACTH
PDH: High ACTH

26
Q

When would mitotane be used over trilostane in treatment of HAC?

A
  • Used for carcinogenic adrenal tumors to destroy mets
  • Destroys the adrenal cortex and can cause iatrogenic addisons
  • Addisons better than neoplasia i guess
27
Q

What hormone regulates glucocorticoid secretion?

A

ACTH

28
Q

What is the difference between typical vs atypical addisons?

A

Typical: deficiency in glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

Atypical: deficiency in glucocorticoids only

29
Q

How is the medical management different in typical vs atypical addisons?

A

Typical:
- Needs Dexamethasone/Prednisone + Fludrocortisone acetate or DOCP

Atypical:
- Only needs glucocorticoid replacement (Dexamethasone/Prednisone)

30
Q

Do typical or atypical Addisonians present with worse clinical signs?

A

Typical addisons (worse CS due to mineralocorticoid deficiency)

31
Q

What is the consequence of a mineralocorticoid deficiency?

A
  • Inability to conserve Na+ → hypovolemia and hypotension
  • Lack of aldosterone leads to K+ retention → myocardial excitability (cause of death)
32
Q

What is the main mineralocorticoid lacking in typical Hypoadrenocorticism patients?

A
  • Aldosterone
33
Q

What layers of the adrenal gland are affected in atypical hypoadrenocorticism patients?

A
  • only the zona fasciculata
  • Lack of glucocorticoids (cortisol)
34
Q

What layers of the adrenal gland are affected in typical hypoadrenocorticism patients?

A
  • Zona glomerulosa and Zona fasciculata
  • Lack of glucocorticoids (cortisol) + mineralocorticoids (aldosterone)
35
Q

What age of dogs present with hypoadrenocorticism?

A

Young to middle age

36
Q

Is there a sex predilection for dogs with hypoadrenocorticism?

A

Female > male

37
Q

What clinical signs can be seen in dogs with hypoadrenocorticism? (7)

A

Usually waxing/waning non specific CS
1. PU/PD
2. Poor appetite/anorexia
3. Vomiting/Regurg
4. Diarrhea
5. Shaking, shivering, tremors
6. Collapse
7. Hematemesis, hematochezia, melena

38
Q

What would you expect the following PE findings to be from a patient with hypoadrenocorticism?
HR:
Temp:
Femoral pulses:
CRT:
BP:

A

HR: ↓↓↓ Bradycardia
Temp: ↓↓↓ Hypothermia
Femoral pulses: ↓ weak
CRT: > 2, prolonged
BP: ↓↓↓ (from hypovolemia)

39
Q

What is the treatment protocol for fixing electrolyte imbalances associated with hypoadrenocorticism?

A

( ↓ Na, ↑ K ) Treating hyperkalemia

  • Calcium gluconate (heart protective)
  • Insulin (pushes K+ intracellularly to ↓ K+)
  • Dextrose IV (glucosuria will pull K+ into urine)
40
Q

What are the main electrolyte changes seen in patients with typical hypoadrenocorticism?

A

↑ K, ↓ Na, ↓ Cl

41
Q

What is the treatment plan for a patient with hypoadrenocorticism?

A
  1. IV fluids
  2. Address hyperkalemia (calcium gluconate, dextrose, insulin)
  3. Dexamethasone or Prednisone to replace glucocorticoids
  4. Fludrocortisone or DOCP to replace mineralocorticoids
42
Q

What clinical signs can patients with pheochromocytoma present with?

A
  1. Himb limb edema
  2. Collapse
  3. ABD distension
  4. Acute blindness
  5. Epistaxis
  6. Vomiting

(may be intermittent)

43
Q

What physical exam finding is not seen with pheochromocytoma?

A. Tachycardia
B. Retinal hemorrhage
C. Hypothermia
d. Hind limb edema

A

C. Hypothermia

(Pyrexia/Fever)

44
Q

List the physical exam findings that can be seen in patients with pheochromocytoma

A

- Normal PE is common
- Inc lung sounds due to pulmonary hypertension
- Tachycardia, arrhythmias, murmur
- High/normal BP
- ABD mass
- Pyrexia (fever)
- Signs of retinal hypertension
- Hind limb edema

45
Q

List the Ddx for systemic hypertension

A
  1. CKD
  2. HyperT
  3. Hyperadrenocorticism / Cushings
  4. Hyperaldosteronism / Conns
  5. Acromegaly
  6. Pheochromocytoma
46
Q

How can catecholamines be measured to diagnose pheochromocytoma?

A
  • Measure metabolites in urine/blood → Normetanephrine, Metanephrine, Vanillymandelic acid
47
Q

How is pheochromocytoma treated?

A
  1. Control hypertension (Phenoxybenzamine, Prazosin)
  2. Surgical removal (risky, massive arrhythmias) - treat with Esmolol
48
Q

What is the prognosis of pheochromocytoma?

A
  • 50% malignant in dogs, if benign and successful surgery can have normal life
  • Variable in cats
49
Q

Which of the following has a longer survival time: PDH or ADH?

A
  • PDH longer survival because it’s benign
  • ADH 50:50 adenoma or carcinoma with metastasis
50
Q

What diagnostics must be performed prior to surgery on a Cushings patient?

A

CT/MRI - assess for mets, invasion of CVC, angiography

51
Q

List the Ddx for a palpable adrenal mass

A
  1. Hyperadrenocorticism
  2. Hyperaldosteronism (Conns)
  3. Pheochromocytoma
  4. Non secretory adrenal tumors
52
Q

A patient is presenting with non specific, chronic, mild waxing and waning GI signs. Bloodwork shows hyperkalemia and hyponatremia. What is the 1st test you should run if suspect Addisons?

A
  • Start with basal cortisol
  • If ↑ cortisol, rules out Addisons = “pseudoAddisons”
  • If ↓ basal cortisol, confirm with ACTH stim test
53
Q

A patient presenting collapsed in an Addisonian crisis. What is the first test you should perform?

A

ACTH stim

54
Q

When should basal cortisol levels vs ACTH stim test be used in hypoadrenocorticism patients?

A
  • Basal cortisol if patient showing non specific CS of addisons
  • ACTH if in addisonian crisis, collapsed, or if basal cortisol comes back ↓
55
Q

A patient presenting collapsed in an Addisonian crisis is managed with fluids and started on Dexamethasone and DOCP. On 2 week recheck, the patient is hypokalemic and hypertensive. What could be the cause?

A

DOCP can cause hyperaldosteronism (too much aldosterone) resulting in ↓ K+ and ↑ BP

56
Q

What dog breed is susceptible to side effects from DOCP?

A

Labradoodles

57
Q

What is “pseudoAddisons”?

A

Patient presenting collapsed with CS of addisons, ↓ Na+, ↑ K+ but normal cortisol and aldosterone levels

58
Q

Bradycardia in a collapsed or shocky dog should raise suspicion of ____________

A

Hyperkalemia (Addisons)

59
Q

Is primary or secondary hypoadrenocorticism more common in dogs?

A

Primary - destruction of adrenal gland causing low cortisol

(Idiopathic, immune mediated, neoplasia, hemorrhagic infarction, iatrogenic)

60
Q

What is the cause of secondary hypoadrenocorticism in dogs?

A
  • Lack of ACTH secreted from pituitary (less common) results in atypical Addisons (loss of only glucocorticoids)
  • exogenous steroids
61
Q

What layers of the adrenal gland are affected by secondary hypoadrenocorticism?

A
  • Zona fasciculata only
  • Lack of glucocorticoids only (from lack of ACTH from pituitary)
62
Q

What is the most common cause of atypical Addisons?

A

(Secondary hypoadrenocorticism)

Addisons secondary to exogenous steroids (dec ACTH = atrophy of zona fasciculata, mineralocorticoids unaffected)