DO SIXTH Week Two: Hypoadrenocorticism/Addisons

Hypoadrenocorticism is the

inadequate production of glucocorticoids by the adrenal glands

Hypoadrenocorticism is usually accompanied by

mineralocorticoid deficiency

T/F Hypoadrenocorticism is overall uncommon but also underdiagnosed

T

T/f Hypoadrenocorticism is not as common as Cushing's

T

etiology of primary Hypoadrenocorticism

majority are idiopathic

a majority of primary Hypoadrenocorticism are idiopathic and it is likely

immune mediated, slowly destroys the adrenal gland

most animals with Hypoadrenocorticism dont become symptomatic until

the adrenal gland is nearly entirely destroyed

Hypoadrenocorticism is truly a

adrenal gland disease

95% of dogs with Hypoadrenocorticism have

primary adrenal gland failure

T/F a secondary Hypoadrenocorticism is very very rare

T

T/F we can create iatrogenic Hypoadrenocorticism

T

age of dogs with Hypoadrenocorticism

young to middle age (3-5 years)

why do we see young to middle age dogs with Hypoadrenocorticism

because most animals with immune mediated diseases are young to middle age

breed of dogs with Hypoadrenocorticism

many but standard poodle, nova scotia, bearded collie, poruguese water dog

T/F there is a slight female predisposition for Hypoadrenocorticism

T

many ____ breed dogs are poster child for Hypoadrenocorticism

large

breed that is an outlier and has a very very high prevelance of Hypoadrenocorticism

westies

T/F we can see Hypoadrenocorticism at any age, any breed, both sexes

T

functions of aldosterone

Na absorption/K excretion

water retention

Na/H exchange

regulation of aldosterone

Plasma K

RAAS

if dogs lack cortisol they can develop _____ signs

GI

lack of cortisol can lead to a number of

cardiovascular complications

dogs with Hypoadrenocorticism often present with clinical signs that relate to one of what three body systems

GI

Urinary

CV

what GI signs do we see with Hypoadrenocorticism

vomiting

anorexia

diarrhea

urinary signs in dogs with Hypoadrenocorticism

polyuric and polydypsic

azotemia

_______ are exceedingly common in dogs with Hypoadrenocorticism

lethargy and weakness

what two distinct categories do we think of for Hypoadrenocorticism

acute manifestation

chronic manifestation

T/F the acute manifestation of Hypoadrenocorticism the dogs are extremely ill

T

often in acute manifestations dogs are in a state of

hypovolemic shock

dogs in acute phase of Hypoadrenocorticism generally have clincal features of both _____ and ______

cortisol and aldosterone deficiency

T/F often the illness if life threatening in acute stage

T

this manifestation is a population of dogs that have clinical signs that wax and wane over time

chronic manifestation

in the chronic manifestation what are the clinical signs

vague and nonspecific lethargy and intermittent GI signs

T/F in the chronic manifestation aldosterone deficiency is not always apparent

T

one of the big CBC features in these dogs is they will often have

hemoconcentration, volume depleted

on CBC in dogs with addisons we often see a lack of

stress leukogram (80% of dogs)

What USG do addison dogs have and why

low due to no aldosterone, cant concentrate urine

in terms of Na and K what do they show up as on bloodwork with addisons

hyponatremic and hyperkalemic

why is chloride low on addison BW

it follows Na

what clinical feature in addions dog may contribute to low chloride

vomiting

what acid base disturbance can addisons dogs have

metabolic acidosis, no more H exchange

30% of dogs with addisons have _____ due to combined cortisol and aldosterone deficiency

mild hypercalcemia

what happens to glucose on bloodwork with addisons

hypoglycemia, no more cortisol (30-50%)

T/F we see a low albumin in 20-40% of cases mainly due to GI losses from cortisol deficiency

T

T/F in 30-50% of cases the cholesterol is low

T

T/F we can see mild liver enzymes increased due to hypoperfusion

T

this finding is found in 25% of chronic addison dogs

low level anemia

why do we see low level anemia

cortisol potentiates effects of erythropoietin

GI losses from cortisol deficiency

in 10-20% of dogs instead of a stress leukogram they can have a

reverse leukogram

addisons disease is call the great

imitator

why do they call it the great imitator

there are a lot of other diseases that can look similar to addisons

what is the problem with measuring Na:K ratio for addisons

other disease can cause really severe electrolyte disturbances and 20% of dogs with addisons dont have electrolyte abnormality

T/F the Na:K ratio can be a clue but is not a sensitive or specific indicator for addisons

T

a low Na:K ratio should alert you to

think about addisons

what parasite was the leading cause of pseudo addisons disease

whipworms, live in colon which is responsible for sodium and bicarb

T/F if all you look for on bloodwork with addisons is Na and K issues you may miss a dog that has addisons

T

what is an atypical addisonian

dogs that are addison but have normal electrolytes at time of diagnosis

T/F most of the atypical dogs are also aldosterone deficient

T, no idea why because electrolytes are still normal

T/F some dogs develop electrolyte abnormalities over time

T

unexplained ______ ratio should propmpt testin

Na:K

undiagnosed _____ disease should prompt addisons testing

GI

biochemical signs of _____ deficiency should primpt addisons testing

glucocorticoid

clinical signs like nonspecific _____ and _______ should prompt for addisons testing

lethargy and weakness

gold standard for diagnostic tests of addisons

ACTH stim

what should ACTH stim show in addison dog

pre and post cortisol are less than 55

T/F many exogenous glucocorticoids can cross react with current cortisol assays

T

________ dose not cross react with the cortisol assay

dexamethasone

if we are giving an addison dog a steroid we are going to give _____ as our inital treatment because we dont want to give that dog a steroid that cross reacts wiht our cortisol assay

dexamethasone

if you give a single dose of dexamethasone AFTER BASELINE draw

it will not affect our post ACTH stim cortisol results

T/F if a dog has many dogs of dex it could affect our results

T

T/F if you are dealing with a dog that has had close to five to seven days of steroids their ACTH stim test might look like an addisonian regardless if they are addisonian or not due to HPA axis suppression and adrenal atrophy from prolonged steroids

T

T/F even after you stop steroids it takes at least two weeks for full recovery

T

T/F topical steroids have an effect on the HPA axis as well

T

what are some reasons for borderline results in a small subset of dogs

previous steroid use

loss of potency of ACTH that you use for the stim test

transition phase, becoming addisonian

drug therapy

T/F most dogs with borderline results end up not having addisons

T

most radiographic abnormalities that occur in Addison dogs are the reflection of

hypovolemia

what are some findings on rads due to the hypovolemia

small heart

small vena cava

small liver

in about 1% of Addison dogs _____ dysfunction can occur

esophageal

T/F Addisons should be considered as a differential for esophageal dysfunction

T

acute Addison requires

immediate and aggressive care

chronic Addison needs

generalized and supportive care and management of GI signs

in both acute and chronic what do you have to do

replace hormones, cortisol and aldosterone

T/F just because potassium is higher than 6.5 does not mean they will have hyperkalemia induced ECG changes

T

findings on ecg of addisons

tall tented T waves

blunted P waves

pronlged P-R interval

widen QRS

severe findings on ECG with Addison

absent P wave

sine wave pattern

v fib

death

the mainstay of therapy for volume deficit and hyperkalemia is

IV fluid therapy

fluid of choice for addisons

0.9% sodium chloride

T/F when we give calcium gluconate for hyperkalmeia we are not affecting potassium concentrations

T

when do we give calcium gluconate in an addisonian dog

when they have severe life threatening arrhythmia

T/F the majority of addisonians hyperkalemia can be managed with IV fluid therapy alone

T

what can we give to help treat hypoglycemia and cause insulin release to push K intracellularly

dextrose

what can we give that creates an alkalosis that shift K in cells and H out

bicarb

T/F typically we avoid giving bicarb and usually is not needed in addisonian

T

T/F fluid therapy is the most important life saving measure int he short term

T

what are we going to give in the acute setting to help with cortisol deficiency

dexamethasone

what dose of dex in the acute setting do we give

.1-.2 mg/kg dose

T/F most dogs can be discharged in 2-4 days

T