Defense & Barriers 2: (4) Endocrine Diseases of the Adrenal Gland Flashcards
2 classifications for HYPOADRENOCORTICISM?
PRIMARY adrenocortical failure = failure of the ADRENAL GLANDS
SECONDARY adrenocortical failure = failure of the PITUITARY OR HYPOTHALAMUS (not enough ACTH or CRH produced)
PRIMARY adrenocortical failure…
occurs when…
how can dogs COMPENSATE?
characterized by what 2 things?
5 possible causes?
occurs when…
= >90% of adrenocortical cells are LOST BEFORE CLINICAL SIGNS ARE APPARENT
compensation?
–> dogs can physiologically COMPENSATE for the loss BEFORE 90% LOST
characterized by…
1. DECREASED GCC SECRETION
2. DECREASED MINERALOCORTICOID SECRETION
possible causes?
1. Immune-mediated destruction of ADRENALS
2. Genetic
3. Granulomatous disease (mycobacterium)
4. Trauma
5. Iatrogenic (lysodren, ketoconazole); Medications that decrease cortisol & can CAUSE ADDISON’S
IMMUNE-MEDIATED destruction of ADRENALS…
this is classified as WHAT?
dogs with ____ had MORE ____-____ than when compared to NORMAL dogs
but when the ____ ____ is COMPLETELY ____….
classification = PRIMARY adrenocortical failure
DOGS WITH HYPOADRENOCORTICISM had MORE AUTO-ANTIBODIES than when compared to NORMAL dogs
but when the ADRENAL GLAND is COMPLETELY ATROPHIED, then NEGATIVE for auto-antibodies because NO ENZYMES/PROTEINS present to elicit immune response
LYMPHOCYTIC ADRENALITIS…
can be a cause of WHAT?
tend to see…
can be a cause of PRIMARY adrenocortical failure/HYPOADRENOCORTICISM, also causes HYPOTHYROIDISM
tend to see an ABUNDANCE of CD4 T CELLS (> CD8 T cells)
BREEDS that commonly can get PRIMARY ADRENOCORTICAL FAILURE
- Great Danes
- Leonburger
- Pomeranian
- Bearded collies
- Springer spaniels
- Cocker spaniels
- Nova Scotia Duck Tolling Retriever
- Laborador Retriever
- West Highland Terrier
- Portuguese Water Dog –> may be INFLUCNED BY A SINGLE LOCUS or AUTOSOMAL RECESSIVE
- Poodles –> may be INFLUENCED BY A SINGLE LOCUS or AUTOSOMAL RECESSIVE
SECONDARY adrenocortical failure
commonality?
characterized by WHAT 2 things? why for the second one?
2 possible causes?
commonality? = RARE
characterized by…
1. DECREASED GCC secretion
2. NORMAL MINERALOCORTICOIDS; Mineralocorticoid secretion REGULATED BY RENIN & ANGIOTENSIN IN KIDNEY, so they’re NORMAL
2 possible causes?
1. NEOPLASIA, INFLAMMATION or TRAUMA in PITUITARY or HYPOTHALAMUS
2. IATROGENIC from abrupt DISCONTINUATION of CHRONIC PREDNISONE TREATMENT
isolated HYPERALDOSTERONISM…
commonality?
EFFECTS of LACK OF ALDOSTERONE? (6)
VERY RARE
effects of LACK of ALDOSTERONE?
1. Hyponatremia
2. Hypochloremia
3. REDUCED extracellular volume (hypotension)
4. DILUTE URINE despite DEHYDRATION; Sodium is being lost in urine so BRINGING WATER WITH IT
5. Hyperkalemia
6. Acidosis
effects from LACK of GCCs? (8)
Start with what GCCs NORMALLY act like
Normally GCCs act like a PROTECTIVE ASPECT OF GI MUCOSAL BARRIER, so when NOT present…
- Anorexia
- Vomiting
- Abdominal pain
- Weight loss
- Hypoglycemia
- Lethargy
- Impaired intolerance to stress
- Increased risk for GDV
DIAGNOSIS of HYPOADRENOCORTICISM…
what 3 things should we initially start with?
CBC? (5)
Chem screen? (8, include Na, K, glucose, cholesterol, Ca, pH, albumin, kidneys)
urinalysis? (1)
urine culture & sensitivity? (2, only performed if WHAT)
fecal PARASITIC EXAMINATION (2)
abdominal RADS? (3)
thoracic rads? (2)
abdominal US? (1)
ECG? (4)
what 3 things should we initially start with?
1. history
2. clinical signs
3. PE
CBC
1. CAN be normal
2. RBC can be LOW if EPO NOT WORKING PROPERLY
3. WBC usually NORMAL
4. Can see EOSINOPHILIA/LYMPHOCYTOSIS (>1,000 lymphs)
5. Tend to have LOWER neutrophil count because UNABLE TO MOUNT STRESS LEUKOGRAM
chem screen
1. Azotemia
–> Check for KIDNEY FUNCTION
–> When lacking aldosterone, Na and water EXCRETED, so AZOTEMIA COMMON
2. Hyponatremia
3. Hyperkalemia
4. Mild metabolic acidosis
5. Hypercalcemia
6. Hypoglycemia
7. Hypoalbuminemia
8. Hypercholesterolemia
urinalysis
–> ISOSTHENURIA in face of dehydration
= concentration of URINE is NO GREATER THAN PLASMA CONCENTRATION
Urine culture & sensitivity
1. Performed ONLY IF THERE ARE CLINICAL SIGNS OF UTI, such as PU/PD
2. NO GROWTH EXPECTED IN HYPOADRENOCORTICISM
Fecal parasitic examination
1. ALWAYS performed in dogs with VOMITING OR DIARRHEA
2. NORMAL results expected with hypoadrenocorticism
Abdominal rads
1. (GI foreign body?)
2. ALWAYS perform in dogs with VOMITING
3. NORMAL results expected with hypoadrenocorticism
THORACIC RADS…
1. MICROCARDIA from DEHYDRATION
2. MEGAESOPHAGUS from auto-antibodies
Abdominal US
1. SHRUNKEN, SHRIVELED adrenals
ECG
1. BRADYCARDIA (from hyperkalemia
2. PROLONGED P-R interval
3. WIDENED and SHORT QRS
4. ** POSSIBLE ventricular FIBRILLATION
why are CLINICOPATHOLOGIC findings so important in DIAGNOSING HYPOADRENOCORTICISM? (3)
- CLINICOPATHOLOGIC FINDINGS are NECESSARY BEFORE ADRENAL AXIS TESTING!!
- Adrenal axis testing IS VERY HELPFUL, can CONFIRM YES OR NO
- BUT screen carefully because ACTH STIM IS EXPENSIVE!
Na:K ratio in dogs with HYPOADRENOCORTICISM (3)
- Na:K ratio often LOW
- > 27 in NORMAL DOGS
- <27 in dogs with ADDISON’S
what is EOSINOPHILIA usually due to? & is a symptom of WHAT ENDOCRINE DZ?
what OTHER DIFFERENTIALS can it be due to? (6)
USUALLY due to PARASITISM, but is a symptom of HYPOADRENOCORTICISM
OTHER DDxs…
1. Nonparasitic skin disese
2. Mast cell tumor
3. Eosinophilic myositis, pneumonitis, enterocolitis
4. Hypereosinophilic syndrome
5. Eosinophilic leukemia
6. Eosinophilic granuloma complex
differentials for HYPONATREMIA/HYPERKALEMIA? (7)
what ENDOCRINE DZ is this a symptom of?
HYPOADRENOCORTICISM!
DDXs….
1. PSEUDO-Addison’s disease
2. SEVERE GI disease like parvo or gastroenteritis
3. SEVERE liver disease
4. Urethral obstruction
5. ACUTE renal failure
6. CHF
7. Pleural effusion
PSEUDO-Addison’s disease…
age?
clinical signs? (6)
seen in YOUNG DOGS
clinical signs?
1. VOMITING
2. D+
3. EOSINOPHILIA
4. LARGE Na:K RATIO
5. HYPONATREMIA/HYPERKALEMIA
6. NORMAL ACTH STIM
differentials for HYPOGLYCEMIA? (8)
what ENDOCRINE DZ is this a symptom of?
HYPOADRENOCORTICISM
- Insulinoma
- Liver disease
- Young animals
- Toy breeds
- Sepsis
- Neoplasia
- Growth hormone deficiency
- Severe polycythemia
why should we perform adrenal axis testing more READILY in addison’s vs. cushing’s?
because if we test it in Cushing’s, results can be LESS DEFINITIVE but STILL LEGAL OBLIGATION TO TREAT
differentials for HYPERCALCEMIA?
(hint = ACRONYM)
H = HYPERPARATHYROIDISM
A = ADDISON’S DZ
R = RENAL DISEASE (acute failure)
D = VITAMIN D TOXICOSIS
O = OSTEOLYTIC DISEASE
N = NEOPLASIA (secretion of PTH-related peptide)
S = SPIRIOUS (idiopathic, more common in cats)
G = GRANULOMATOUS DZ
BABY = YOUNG ANIMALS have more HIGHLY CIRCULATING Ca
ACTH stim in ADDISON’S…
WHEN should it be done?
expected results in a NORMAL dog? (2)
expected results in an ADDISONIAN dog? (2)
why do we NOT measure aldosterone? (1)
when?
= BEFORE ADMINISTRATION OF GCCs, INCLUDING DEXAMETHOSONE
In a NORMAL dog…
1. expect INCREASED CORTSIOL
2. Should be >2 ug/dL
In an ADDISONIAN dog…
1. NO STIMULATION
2. Should have <1 ug/dL PRE- and POST-ACTH administration
Why do we not use ALDOSTERONE levels?
1. If Na:K abnormal, LIKELY ALDOSTERONE ISN’T WORKING WELL EITHER
TREATMENT options for ACUTE ADDISON’S (5)
- FLUID THERAPY + dextrose PRN
- DEXAMETHASONE
- IV GLUCOSE + INSULIN
- BICARBONATE
- DESOXYCORTICOSTERONE PIVALATE (DOCP)
MONITORING of treatment by owner…
signs of ADDISON’S/NOT ENOUGH Tx? (6)
signs of CUSHING’S/TOO MUCH Tx? (3)
Signs of ADDISON’S/NOT ENOUGH TREATMENT?
1. DECREASED…
–> Appetite
–> Water consumption
2. V+
3. D+
4. Lethargy
5. Weakness
6. Ataxia
Signs of CUSHING’S/TOO MUCH TREATMENT?
1. PU/PD
2. Polyphagia
3. Panting
if you DO have to treat an addison’s patient with DEXAMETHASONE, what should you do?
do ACTH STIM MINIMUM of 2 HOURS LATER
DESOXYCORTICOSTERONE PIVALATE (DOCP)
= what is it?
used when?
= SYNTHETIC FORM OF ALDOSTERONE
used when ADDISONIAN patient is PERSISTENTLY HYPERKALEMIC
when can we SUPPLEMENT an ADDISONIAN patient with INSULIN?
can add insulin ONLY AFTER WE’VE MADE THE DOG HYPERGLYCEMIC
DEXAMETHASONE tx for Addison’s…
WHEN should we give this? (2)
action?
WHEN should we give this?
1. usually WAIT to give until AFTER ADRENAL AXIS TEST
2. reserved for LIFE-SAVING situations!
action? = SUPPRESSES ACTH and CRH
FLUID THERAPY (+ dextrose) for ADDISON’S…
in what form of dz is this MOST important?
relation to hyponatremia?
why do we sometimes give DEXTROSE?
MOST important when…
–> FLUIDS are the most important for ACUTE Addisonian crisis!
hyponatremia?
–> Giving SALINE can help resolve HYPONATREMIA
why do we sometimes give DEXTROSE?
1. resolves HYPOGLYCEMIA
2. helps PUSH K BACK INTO CELLS via INSULIN SECRETION if patient is PERSISTENTLY HYPERKALEMIC
MONITORING of ADDISONIAN TREATMENT by VET? (2)
when do we perform next ACTH stim?
- CLINICAL RESPONSE TO THERAPY
- Na:K ratio
** DO NOT PERFORM ANY MORE ACTH STIMS
FELINE hypoadrenocorticism
commonality?
protocol?
treatment & prognosis?
commonality? = RARE
protocol? = ACTH stim test is DIFFERENT
treatment & prognosis (good) are SIMILAR TO DOGS
