Hypoadrenocorticism Flashcards
(32 cards)
1
Q
OBJ: Understand adrenal gland functional anatomy and regulation
A
- see picture
2
Q
OBJ: Understand the pathological bases for Hypoadrenocorticism
A
- Destruction of adrenal cortex
- immune-mediate adrenalitis/adrenal atrophy (most common)
- lowers GC and MC production
- Infiltrative diseases (granuloma, amyloidosis
- same size /bigger gland but decreased functional ability
- immune-mediate adrenalitis/adrenal atrophy (most common)
- Adrenal suppression by exogenous GC’s
- Iatrogenic
- adrenal gland can shrink due to disuse
3
Q
OBJ: Know the clinical signs and laboratory findings of Hypoadrenocorticism
A
- Waxing and waning illness
- Loss of appetite - weight loss
- lethargy/depression
- Vomiting/diarrhea
- PU
- weakness
- Regurgitation/abdominal pain
- Mild anemia
- lack of stress leukogram
- Azotemia
- Electrolyte abnormalities
- usually hyponatremia and hyperkalemia
- Na+/K+ ratio <27:1
- usually hyponatremia and hyperkalemia
- dilute USG
4
Q
OBJ: Understand the diagnostic approach to Hypoadrenocorticism
A
- ACTH stimulation test
- synthetic ACTH used
- Dogs with Addisons show no increase in cortisol after admin
- their adrenal gland does not work so there is no response to the extra ACTH
5
Q
OBJ: Know and understand the treatment of a patient with Hypoadrenocorticism
A
- Fix crisis
- glucocorticoid, mineralocorticoid both injectable
- Maintain healthy
- can move to long lasting oral glucocorticoid and mineralocorticoid
- Monitor for life:
- electrolyte balance
- clinical signs
6
Q
Which hormones are released from the adrenal gland? give specific areas and examples
A
7
Q
How is cortisol secretion regulated?
A
- ACTH secretion is pulsatile
- ACTH secretion influenced by:
- feeding
- Physiologic / environmental stress
- pain, trauma, hypoxia, pyrogens, cold exposure, surgery
- HYPERadrenocorticism - excess cortisol
- HYPOadrenocorticism - cortisol and aldosterone deficiency
8
Q
What are the two types of hypoadrenocorticism? how are they different?
A
9
Q
What are causes of adrenal cortex destructuion?
A
- Immune-mediated adrenalitis / adrenal atrophy
- most common - possibly genetic?
- Infiltrative diseases (ex granuloma, amyloidosis)
10
Q
What are the results of adrenal suppression by exogenous Glucocorticoids?
A
Usually GC deficiency, sometimes aldosterone deficiency
11
Q
What are the consequences of Adrenal Failure?
A
- See signs at 85% loss
-
Cortisol deficiency - multisystemic
- inappetence, weight loss, lethargy, GI signs, hypoglycemia, hypercalcemia
-
Aldosterone deficiency - salt and water
- Electrolyte disturbances
- hypoNa, HypoCl, HyperK
- Decreased plasma volume
- Polyuria and inc water loss
- Electrolyte disturbances
12
Q
What affects does a cortisol deficiency have on the body?
A
- Multisystemic
- Inappetence
- Weight loss
- Lethargy
- GI signs
- hypoglycemia
- Hypercalcemia
13
Q
What affects does aldosterone deficiency have on the body?
A
- Salt and water affects:
- Electrolyte disturbances
- Hyponatremia, hypocloremia, hyperkalemia
- Decreased plasma volume
- Polyuria and increased water loss
- Electrolyte disturbances
14
Q
What are the patient factors that can play a role in hypoadrenocorticism?
A
- “young dog” disease
- mean age 4.5yo @ diagnosis
- Genetic influences based on:
- breed susceptibility, pedigree analysis, genomic studies
- In early stages - basal hormone secretion is sufficient unless stressed
- may be “ill” with non-specific signs
- “waxing and waning”
15
Q
What are the most common signs of hypoadrenocorticism?
A
- Loss of appetite
- Lethargy/depression
- vomiting / diarrhea
- Polyuria
- Weakness
- Weight loss
- Regurgitation / abdominal pain
16
Q
What is an “Addisonian crisis”
A
- Severe hypoadrenocorticism
- Progression of disease
- Severe signs caused be electrolyte distrubances and volume depletion
- Bradycardia
- Weak pulses
- Poor perfusion
- Hypothermia
- Shock
- Melena
- Collapse
- Seizure
17
Q
What changes are seen on a CBC of a patient with hypoadrenocorticism?
A
- Mild anemia
- Lack of a ‘stress leukogram’
- important observation in a ‘critical’ patient
18
Q
What changes are seen on serum chemistry of a patient with hypoadrenocorticism
A
- Azotemia - elevated BUN and creatinine
- Electrolyte abnormalities
- Hyponatremia and hypochloremia - aldosterone deficiency
- Hyperkalemia - aldosterone deficiency and acidosis
- Addison’s usually causes both!
- Na+/k+ ration (normal > 27:1)
- < 27:1 is suspicious; < 20:1 strongly suspicious
- Other: hypoglycemia, hypercalcemia, hypoalbuminemia, acidosis
19
Q
What changes on a urinalysis are seen in a patient with hypoadrenocorticism? Why?
A
- USG often dilute (<1.030) despite dehydration
- Aldosterone deficiency - Sodium and Chloride losses cannot take place without concurrent loss of water
20
Q
What is hypoadrenocorticism commonly misdiagnosed as? why?
A
- Renal failure
- Azotemia + dehydration + dilute urine
21
Q
How can a diagnosis of hypoadrenocorticism be confirmed?
A
- ACTH stimulation test
- Dogs with Addison’s show NO increase in cortisol after administration of exogenous ACTH
- Affected dogs usually have a “flat stim” test
- low baseline cortisol and low cortisol after ACTH
22
Q
are aldosterone levels assessed in Addison’s patients?
A
- NO
- deficiency is inferred by electrolyte abnormalities
23
Q
What are some infrequently used tests for Hypoadrenocorticism?
A
-
Endogenous ACTH
- elevated in primary hypoadrenocorticism but not used for diagnosis
-
Basal (resting) cortisol level
- used to screen suspicious cases for hypocortisolemia
- low result is consistent with hypoadrenocorticism but NOT DIAGNOSTIC
-
Aldosterone concentration
- Not routinely measured; can confirm mineralocorticoid deficiency
- Aldosterone overlaps between normal dogs and dogs with hypoadrenocorticism
- Basal and ACTH-stimulated samples measured
- Occasionally used in elevation of atypical disease
24
Q
What is the treatment for Hypoadrenocorticism?
A
- Initial hormone replacement
- patient is dehydrated, inappetence and in crisis
- Glucocorticoid - usually injectables
- Mineralocorticoid
- Na containing crystalloid - replaces volume
- Improves BP
- Maintenance hormone replacement
- Patient is stable, hydrated, eating
- Glucocorticoid - oral
- Mineralocorticoid supplement
- injectable long-acting product
- Oral Product
- Glucocorticoid replacement:
- Acute therapy - use injectable glucocorticoid
- Dexamethasone 0.05 - 0.1 mg/kg IV
- Prednisolone sodium succinate (alternative)
- Chronic therapy - daily therapy with oral glucocorticoid
- Prednisone - Physiologic dose is 0.2 - 0.4 mg/kg/day
- Increase dose if anticipate stressful event
- Can safely double dose for several days
- Only treatment needed for atypical Addison’s Disease
- Acute therapy - use injectable glucocorticoid
- Mineralocorticoid Replacement
- Administer immediately after diagnosis
- Maintenance therapy for life
- DOCP - Deoxycorticosterone pivalate
- 2.2 mg/kg IM or SC every 21-30 days
- Max dose 50mg/dog/dose
- Slow release of mineralocorticoid
- No GC activity
- Single dose is not harmful if dog does not have Addison’s
- Fludrocortisone (Florinel®)
- Has minor GC activity
- Dose 0.015 - 0.02 mg/kg/day
- Poor absorption
- ~50% of dogs treated with fludrocortisone will not require additional GC
25
What long term monitoring has to be done for patients with hypoadrenocorticism?
* Serial evaluation of electrolytes
* First month after diagnosis; weekly beginning 2-weeks after first DOCP dose
* As needed until the patient's effective dose and interval is determined
* Every 3 - 4 months thereafter
* Adjust mineralocorticoid dose and dosing interval based on electrolyte results
* Serial evaluation of clinical signs
* Owners' observation helpful
* Deficiencies result in subtle manifestations
* If not “ doing quite right” adjust daily GC dose
* MC adjustment if GC adjustment doesn't correct
* No Role for serial ACTH stim tests
26
How can we reduce the cost of treating hypoadrenocorticism patients for owners?
* Get good control
* Reduce hospital costs
* Healthy patient
* Work to find minimal effective dose
* Shop around for best price
* on-line vet pharmacies
* Owner administers DOCP at home
* must be part of long-term monitoring program with veterinarian
27
What is the treatment for an Addisonian Crisis?
* Volume replacement
* death due to vascular collapse and shock
* Restore volume using 0.9% NaCl
* Avoid rapid replacement if Na is \<125 mEq/L
* Hormone replacement after initial fluid bolus
* Glucocorticoid replacement - complete ACTH stim test before GC are given
* Mineralocorticoid replacement
* Treat hyperkalemia if needed
* administer calcium gluconate
* Treat acidosis if needed
* administration of bicarbonate
* rarely needed
28
How is hyperkalemia treated during an Addisonian crisis?
* Specific therapy usually not needed
* often corrects with volume replacement and increased urine production
* Severe or life-threatening hyperkalemia requires immediate treatment
* Signs include bradycardia and arrhythmia
* Options:
* 10% Calcium gluconate
* 0.5 - 1.0 mg/kg IV SLOW over 10 - 20 minutes with continuous ECG monitoring
* 15 - 30 minutes for onset of action
* Cardioprotective effect - protects against K+ but doesn't directly reduce serum K+
* Dextrose + Humulin-R (regular insulin)
* 1 - 2 mls/kg of 50% dextrose IV and 0.125 - 0.5 units regular insulin/kg IV
* follow with glucose CRI
29
What is the prognosis of canine Hypoadrenocorticism?
* Excellent
* if owners are educated
* compliance is excellent
* close follow-up is maintained
30
What is the Etiology of feline Hypoadrenocorticism?
* Primary - rare
* suspected to be immune-mediated
* Secondary
* iatrogenic causes
* adrenal suppresion due to megestrol acetate or glucocorticoids
31
How if Feline Hypoadrenocorticism diagnosed?
* ACTH stimulation test
* 0.125mg/cat
* blood samples taken before, 30 and 60 minutes post injection
32
How are canine and feline Hypoadrenocorticism similar?
* similar clinical signs
* similar laboratory abnormalities
* similar treatments
