Cushing's, Addison's and Pheochromocytoma Flashcards

1
Q

85-95% of endogenous cushing’s dogs and cats are due to ____.

A

Pituitary-induced micro or macroadenoma

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2
Q

Cushing’s pathogenesis

A

XS ACTH made in pituitary –> adrenals –> hypercortisolemia (pituitary escape from negative inhibition)

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3
Q

Adrenal steroidogenesis

A

ACTH –> adrenal cortex –> aldosterone, cortisol and sex steroids.

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4
Q

Atypical cushing’s

A

normal cortisol levels, cushings symptoms caused by xs intermediate metabolites from steroidogenesis

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5
Q

What are the three zones of the adrenal cortex?

A

Glomerulosa
Fasciculata
Reticularis

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6
Q

What hormone is made in the zona glomerulosa?

A

aldosterone

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7
Q

What hormone is made in the zona fasciculata?

A

cortisol

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8
Q

What hormone is made in the zona reticularis?

A

ketosteroids and cortisol

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9
Q

Aldosterone has an effect on _____.

A

Na and K production in the body

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10
Q

Pathophysiologic effects of xs cotisol?

A

Muscle/bone/tendon - weakness
liver - glycogen deposition; steroid hepatopathy
gut - hyperacid secretions
immune system - suppressed, prone to secondary infection (silent UTIs)
kidney - PU/PD because ^GFR and renal plasma flow
Brain - hyperirritable. Dog: panting!
Bloodstream - mature neutrophilia, lymphopenia, eosinopenia, monocytosis, thrombocytosis, and increased RBCs
Lipid metabolism - increased cholesterol

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11
Q

Breed and age incidence of Hyperadrenocorticism?

A

toy and miniature breeds (poodles and dachshunds)

age: 3-13 range, avg 8 years old

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12
Q

main endogenous causes of Hyperadrenocorticism?

A
pituitary dependent (high ACTH, high cortisol)
adrenal dependent (low ACTH, high cortisol)
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13
Q

exogenous cause of Hyperadrenocorticism?

A

iatrogenic - large doses of glucocorticoids (act like cortisol)

** must wean off these drugs because will have trouble making cortisol with removal of drug.

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14
Q

Physical features of Hyperadrenocorticism?

A

Panting (dogs)
PU/PD
pendulous abdomen (due to muscle weakness)
stria (stretch marks) from weakening/thinning of skin
truncal alopecia with hyperpigmentation
acne formation - keratin plugging of hair follicles
easily bruise
calcinosis cutis
cushings wrinkles
general muscle weakness- myotonia!
lethargy
polyphagia
testicular atrophy and hepatomegaly in the dog due to glycogen accumulation
hypercoagulable

Other: pulmonary calcification, prothrombotic tendency, hypertension, proteinuria, glomerulopathy (can be permanent)

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15
Q

Hyperadrenocorticism lab findings?

A

mature neutrophilia, eosinopenia, and lymphopenia
Polycythemia
high liver enzymes (hepatomegaly due to glycogen accumulation)
glucose (if also have DM)
+/- pyuria —> UTI
+/- hematuria
Proteinuric (glomerulopathy)
hypertension (glomerulopathy)
high cholesterol/TGs (lipemia)
high cortisol
adrenal/pulmonary calcification (gritty lungs on necropsy)

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16
Q

Cushing’s imaging

A
radiographs
early phase pyeologram 
arteriography
abdominal U/S
pituitary CT/MR
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17
Q

If unilateral adrenal tumor is resected, the ipsilateral adrenal will be atrophied so expect _____ post-op.

A

adrenocortical insufficiency - supplement glucocorticoids

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18
Q

pituitary macroadenomas are hard to resect; try to remove whole pituitary which means will have _____ post-op.

A

diabetes insipidus (no renal ADH) or another hypoendocrinopathy

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19
Q

Cushing’s diagnosis

A
Urine cortisol/Cr ratio (if negative, rules out cushing's, if positive, could be something other than cushing's) 
ACTH stim test***
LDDT - low dose dex suppression 
HDDT
Plasma ACTH - \$\$$ and time
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20
Q

Most common signs of cushing’s in a dog?

A

PU/PD, pendulous abdomen, and panting

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21
Q

ACTH stim test

A

hyperstimulation of ACTH (cortisol) is positive for cushings. (>20)
Doesn’t specify if pituitary or adrenal cushings, do LDDT/HDDT to determine which.

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22
Q

LDDT and HDDT

A

should suppress cortisol to <1.7
If suppresses but not below 1.7, then pituitary cushings.
If does not suppress at all, then adrenal tumor.

20% of PDH will not suppress HDDT

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23
Q

cushing’s treatment?

A
  1. surgical removal of hypothalamus or adrenal gland
  2. medical - OPDDD (dogs) and Trilostane (dogs and cats) suppress cortisol production. Lysodren and Metotane are OPDDD drugs.
  3. Iatrogenic - stop the steroids (taper off)
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24
Q

How to prove iatrogenic cushing’s?

A

hold off pred, do ACTH stim test –> no response

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25
Q

OPDDD drug interactions?

A

It is metabolized in the liver by cytochrome P450 so anything that affects this will affect its metabolism.

Phenobarbital makes OPDDD ineffective because enhances P450 metabolism

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26
Q

OPDDD cytotoxicity?

A

Adrenocorticolytic –> if destroy adrenal cortex, end up with Addison’s.

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27
Q

Lysodren _____ sometimes necessary

A

reloads

28
Q

OPDDD side effects

A

drug toxicity - depression, weakness, vomiting, anorexia, and diarrhea –> stop use —> signs go away –> start again on lower dose
addison’s disease
pituitary tumor growth - nelson’s disease (micro–>macro), pituitary apoplexy (sudden death)

29
Q

Trilostane

A

most popular drug for PDH

adrenal enlargement due to increased intermediate metabolites from steroid synthesis

30
Q

Cushing cat is similar to the dog, but many are ______.

A

Diabetic, may require insulin, thin/friable skin

31
Q

Cushing cat diagnostics are difficult because?

A

ACTH stim not sensitive, HDDT>ACTH stim

32
Q

Most common cause of cushingoid dog?

A

Overtreatment with glucocorticoids

33
Q

Pheochromocytoma incidence?

A

rare

50% benign 50% malignant

34
Q

Pheochromocytoma arises from ____.

A

adrenal medulla

35
Q

Pheochromocytoma signs usually due to _____.

A

catecholamine secretion or postcaval obstruction

36
Q

Pheochromocytoma clinical signs?

A

Paroxysmal (periodic and severe) anxiety, mental depression, restlessness and panting. Also blanching, flushing, weakness and/or collapse.
Tachycardia +/- VPCs, tachyarrythmia or CHF
ascites –> post caval invasion by tumor
hyphema (blood in eye)

37
Q

Pheochromocytoma ddx?

A

hypoglycemia
cardiac disease
cerebral dysfunction
hyperthyroidism

38
Q

Pheochromocytoma dx?

A
history and physical exam!
imaging (rads, U/S, CT)
BP measurements
strong index of suspicion - old dog with unexplained tachyarrhythmia
elevated urinary normetanephrine
39
Q

Pheochromocytoma treatment?

A

surgery

medicine: phenoxybenzamine (alpha blocker), regitine aka phentolamine (alpha blocker), propanolol (beta block)

40
Q

If dog is hypertensive and tachyarrhythmic, do what?

A

ALPHA BLOCK BEFORE YOU BETA BLOCK

41
Q

To increase surgery survival, you should?

A

Start phenoxybenzamine 2 weeks before to stabilize BP

42
Q

Aldosteronoma more common in?

A

Cats&raquo_space; dogs but overall it’s rare

43
Q

Aldosteronoma is neoplasm of the?

A

zona glomerulosa of the adrenal cortex

44
Q

Aldosteronoma clinical signs?

A

XS Na retention –> hypertension –> retinal hemorrhage and blindness
XS K excretion –> hypoK effects
PD/PU

45
Q

Other causes of hypertension in a cat?

A

chronic renal insufficiency

hyperthyroidism

46
Q

Addison’s is also called?

A

Hypoadrenocorticism

47
Q

Cushing’s is also called?

A

Hyperadrenocoticism

48
Q

Addison’s incidence?

A

Not common, mostly in dogs <5 years old

49
Q

Causes of adrenocortical insufficiency?

A
iatrogenic - glucocorticoids induce atrophy
infiltrative - cancer, mycoses
infarction
pituitary insufficiency
OPDDD induced destruction
Idiopathic
Autoimmune destruction
Cosyntropin - really rare
50
Q

Sign that it is autoimmune?

A

adrenal cortex significanly diminished with lymphocytes and plasma cells invading on cytology

51
Q

Relative adrenocortical insufficiency

A

septic patient has cytokines that can decrease glucocorticoid release from adrenals which leaves critically ill and dying patient with no glucs needed to maintain BP and live

52
Q

atrophic zona fasciculata, what happens?

A

decreased cortisol –> decreased gluconeogenesis, decreased sensitivity to catecholamines, decreased water diuresis, decreased appetite, increased eosinophils and lymphocytes, decreased cerebration

53
Q

atrophic zona glomeruloa, what happens?

A

decreased aldosterone –> excrete Na and retain K –> hyperK and low BP

54
Q

Electrolyte markers for addison’s?

A

HyperK and HypoNa (together are really bad for heart)

55
Q

Hypoadrenocorticism dx?

A

history and clinical findings

ECG changes

56
Q

Addisonian crisis signs?

A

history of weight loss, lethargy, decreased appetite, and GI signs
presents weak or in collapse
mentally dull
bradycardia while hypotensive!! (<60 bpm)
weak femoral pulse
may clinically resemble acute uremic state

57
Q

Addisonian crisis lab findings?

A
\+/- netropenia, eosiniphilia, and lymphocytosis
hyperK
hypoNa
high BUN
low bicarb
\+/- hypocholesterolemia
\+/-hypoalbuminemia
\+/- hypercalcemia
highly variable, not reliable for dx
58
Q

Pseudoaddisons?

A

anything that causes low Na and high K

Renal dz
GI dz
DKA, HNKD
Chylothorax

59
Q

Addison’s dx?

A

Na/K <20
ACTH Stim test*** gold standard
Cortisol:ACTH ratio
Aldosterone:Renin ratio

60
Q

Plasma ACTH determination?

A

Primary addisons - ACTH high

Secondary Addison’s - ACTH low

61
Q

When in crisis, need to treat immediately, what is the drug you go to first? Why?

A

Dexamethasone over pred because won’t interfere with cortisol assay

62
Q

Simultaneous treatment and dx for addisonian crisis

A
  1. begin IV NaCl
  2. collect resting serum cortisol
  3. give ACTH
  4. give dex IV
  5. collect 2nd serum cortisol
63
Q

Maintenance treatment for Addison’s

A

Florinef (both mineralocorticoid and glucocorticoid)
Prednisone
DOCP (only mineralocorticoid) - if OD, get hypoK

64
Q

Atypical addison’s

A

chronic lethargy, weakness, poor appetite, weight loss
normal Na and K despite low aldosterone***
absent ACTH stim response

65
Q

atypical Addison’s treatment?

A

because normal electrolyes, just give pred

66
Q

Any medical or surgical stress to an Addisonian will warrant use of significant supplemental doses of ___.

A

glucocorticoids

67
Q

causes of atypical addison’s

A

secondary adrenocortical insufficiency

immune destruction of z. fasciculata or glomerulosa