Cushings/Addisons Flashcards

1
Q

Know the different divisions of the adrenal cortex and what is produced there.

A

Zona Glomerulosa - aldosterone.
Zona Fasciculata - cortisol
Zona Reticularis - 17-ketosteroids and cortisol.

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2
Q

Breed and age incidence of cushing’s

A

Toy and mini breeds, poodle and dachshunds have increased incidence.
Age 3-13 years (8y avg).

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3
Q

What is exogenous/iatrogenic cushing’s?

A

Caused by giving large doses of glucocorticoids. Tx is slowly weaning off of the meds and giving the adrenals time to start producing again.

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4
Q

Physical features of cushing’s

A

Pot bellied
Thin skin, esp on abdomen
Truncal, bilateral, symmetrical alopecia.
Occ, calcinosis cutis.

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5
Q

Cushing’s functional adrenal tumor incidence and pathophys-

A

15-20% of cases.
Tumor causes excessive amounts of cortisol to be produced/released. This DOES feed back to the pituitary and cause a decrease in ACTH.

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6
Q

Pituitary-dependent cushing’s incidence and pathophysiology

A

80-85% of cases.

Feedback loop is damaged by tumor and ACTH continues to be released despite high cortisol levels.

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7
Q

Clinical signs of cushing’s disease

A

PU/PD, polyphagia, weight gain, weakness/lethargy, hyperpigmentation of skin and hair, testicular atrophy, and hepatomegaly. Physical appearance changes.

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8
Q

Cushinoid dogs are ____coagulable.

A

Hypercoagulable.

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9
Q

Lab findings for cushing’s

A

Stress leukogram (lymphopenia, eosinopenia, neutrophilia and monocytosis).
^Chol, ALP, ALT.
Proteinuria, +/- UTI.

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10
Q

Endocrine dx of cushing’s

A
ACTH stim test
LDDT
HDDT
Plasma ACTH
Urine cortisol/Cr ratio
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11
Q

ACTH stimulation test evaluation

A

Elevated - cushing’s
Depressed - addison’s

Abdominal U/S could then be done to see if adrenal tumor present for cushinoid animals.

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12
Q

OPDDD (AKA - lysogren, mitotane)

A

Used in dogs only. Cat rapidly metabolize so ineffective. Phenobarb makes ineffective as well b/c of P450.

  • Cytotoxic to all layers of adrenal cortex.
  • If ACTH >10 reload dose.
  • drug tox - depression, weakness, v/d, anorexia. Stop med until signs abate then restart on lower dose.
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13
Q

Trilostane

A

Used in dogs and cats. Most popular drug used for PDH.

1-2 mg/kg BID, titrate to effect (as high as 3mg/kg BID)

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14
Q

Cushinoid cat

A

Etiology similar to dogs. Many diabetic, testing is the same but interpretation difficult.

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15
Q

LDDST interpretation

A
  • Failure of suppression by atleast 50% base cortisol level by 4-8hrs is diagnostic for cushing’s disease — either PDH or ADH.
  • 30% of PDH patients will have suppression of cortisol by 4 hrs and increase by 8 hrs.
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16
Q

HDDST interpretation

A

Used to differientiate PDH from ADH.

*PDH - cortisol level <50% baseline at 4-8hrs post-dex..

17
Q

ACTH stimulation test interpretation

A

Measures response to synthetic ACTH.

  • If pre and post <2 ug/dl - hypoadrenocorticism.
  • If post is >18 patient is cushinoid but a HDDST or abdominal ultrasound needs to be done to deterine if PDH or ADH.
18
Q

Incidence of addison’s

A

Not common, but frequently undiagnosed.
No known sex predilection.
Most common in young dogs <5yr.

19
Q

Causes of adrenal insuffiency

A
Iatrogenic
Infiltrative - dz, cancer, mycosis.
Infartion
Pituitary insufficiency
OPDDD induced
Idiopathic
Autoimmune destruction
20
Q

Electrolyte abnormalities associated with hypoaldosteronism

A

Decreased Na and Cl

Increased K

21
Q

S/S of acute addisonian crisis

A

Hx of wt loss, lethargy, anorexia, +/- GI signs.
Dog presents weak or lateral recumbent.
Mentally dull.
Bradycardia, weak femoral pulses.

22
Q

Lab findings with acute addison’s crisis

A
► ± ↓ Neuts
► ± ↑ Eos
► ± ↑ Lymphs
^^^Insensitive
► ↑ K+
► ↓ Na
► ↑ BUN
► ↓ Glu (rare)
► ↓ HCO3
23
Q

Other causes of decreased Na and increased K - pseudoaddison’s

A

renal disease
GI disease
DKA, HNKD,
Chylothorax

24
Q

Dx of addisons

A

Gold standard is ACTH stim test.

Na/K <20

25
Q

Plasma aldosterone

A

Low in most addisonian dogs.
Low blood levels are independent of serum Na and K levels…. sometimes Na and K can be normal despite low aldosterone due to independent compensatory mechanisms.

26
Q

A patient presents in what you believe is an addisonian crisis. How do you treat and Dx at the same time?

A

Begin IV NaCl. Collect resting serum cortisol blood.
Give Cortrosyn IV.
Give dexamethasone IV.
Collect 2nd serum cortisol at 1 hr.

27
Q

Goals of treating addisonian crisis

A
Restore volume.
Provided glucocorticoid.
        Pred Na succinate or dexamethasone.
Provide mineralcorticoid.
        Florinef or DOCP
Reverse marked hyperkalemia.
28
Q

Maintenance tx for addison’s

A

Florinef or DOCP
+/- Prednisone
Periodic Na/K eval.

29
Q

What is DOCP?

A

Percorten-C. Tx for addison’s.
Contains only mineralocorticoid. Need to give pred with.
*OD = hypokalemic myopathy. Tx w/ KCl in fluids.

30
Q

What is Florinef?

A

Treatment for addison’s. Has both glucocorticoid and mineralcorticoid activity. Occ need to supplement with pred.

31
Q

Atypical addision’s

A

Chronic lethargy, weakness, poor appetite, wt loss.

Normal Na/K despite low aldosterone. Absent to minimal ACTH-induced cortisol response.

32
Q

Tx of atypical addison’s

A

If lytes normal: Pred

If lytes ABnormal: Pred w/ florinef (DOCP) OR percorten-V.

33
Q

What is important to remember when managing an addisonian patient?

A

Any medical or surgical stress will warrent the use of significant supplemental doses of glucocorticoids.

34
Q

Comparison between typically and atypical addison’s

A
Typical |Atypical
Na+            ↓      N or ↓
K+              ↑      N or ↑
Cl-              ↓       N or ↓
BUN           ↑       N
Cortisol       ↓        ↓
Glucose  N, ↓ ↑   N or ↓