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64 Cards in this Set

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What is the primary route of excretion of corticosteroids in cats and dogs
Dogs- Urinary
Cats- Biliary
What are 3 main fxns of glucocorticoids
Affects metabolism
Helps cope with stress
Increases renal excretion of H2O
What are four ways in which glucocorticoids affect metabolism
Increase liver gluconeogen.
Decrease peripheral glucose utilization
Protein catabolism
Increase lipolysis
What causes ACTH release from pituitary
CRH from hypothalamus
True/False: Cortisol has negative feedback on hypothalamus and pituitary
True
What are some fxns of Aldosterone
Maintain electrolyte balance
Maintain EC H2O volume
Increase renal Na retention
Increase renal K excretion
Increase renal tubular H+ secretion
Minor increase in intestinal Na resorption
What stimulates secretion of Aldosterone
High plasma [K+]
Low BP via RAAS
Reduced plasma Na via RAAS
Which catecholamine is most prevalent in bloodstream
Epinephrine
What are the actions of catecholamines
Vasoconstriction
Increased HR and strength
Inhibits GI activity
Mydriasis
Increased metabolic rate
What are 2 causes of naturally occurring cases of hyperadrenocorticism
PDH (80-85%)
ADH
What is PDH hyperadrenocorticism
Pituitary dependent
Excess ACTH is made by the pituitary
What is the typical signalment of a dodg w/ hyperadrenocorticism
7-9yrs
male= female for PDH
female > male for ADH

PDH-
Mini poodles
Dachshunds
Bostons
Silkies

ADH-
No real breed predilection, but most are >20kg
True/False: The basal cortisol concentration is often normal in cases of hyperadrenocorticism
True
There is just lack of normal fluctuation of cortisol
What percentage of PDH cases have an indentifiable, fxnl pituitary mass
85-90%
What is the difference in the pathophysiology as it relates to the adrenal glands b/t ADH and PDH
PDH- blateral adrenal cortical hyperplasia

ADH- Tumor on one side (usually AC) and atrophy of the contralateral adrenal gland
Are most cases of ADH unilateral or bilateral; benign or malignant
Unilateral
Malignant (only 40% adenomas, the rest AC)
What are three mechanisms of excessive cortisol's ability to cause diuresis and polyuria
Inhibits ADH
Enhances natriuretic factor
Increases GFR
What causes the pot belly commonly seen with Cushing's
Protein catabolism induced muscle wasting
What are the effects of excess cortisol on metabolism
Breakdown more protein and fat

Increase gluconeogenesis
(and cause peripheral insulin resistance)

Store more glycogen in liver
What is the most common sign seen in Cushing's patients
PU/PD
What are 4 reasons for the pendulous abdomen seen with Cushing's
Large liver
Full bladder
More fat there
Decreased muscle tone
True/False: Only Cushing's patients will have abnormally high adrenal fxn tests
False
Other illnesses can cause stress and increase cortisol
What are the common CBC changes seen in hyperadrenocorticism
Stress Leukogram
(mature neutrophilia, eosinopenia, lymphopenia)

Erythrocytosis
Why do you see increased liver enzymes in Cushing's
ALP- steroid induced
ALT- hepatocytes packed w/ glycogen
True/False: Concentrated urine is not compatible w/ a dx of Cushing's
False
(esp. if in hospital and not drinking much)
Why may you see vulva enlargement in hyperadrenocorticism
Because of weak sex hormones made by the adrenal cortex
What are some UA findings in hyperadrenocorticism
Proteinuria (67%)
Bacteriuria (often w/o pyuria or clinical signs)
USG < 1.035 often
What are three uses for U/S in the dx of Cushings
Helps tell PDH from ADH if see adrenal tumor (usually)

Identifies which gland is affected

Also demonstrates invasiveness
What are three main other dzs that can cause adrenal test abnormalities
Uncontrolled DM
Liver dz
Renal failure
What is a pro and con for ACTH Stim
PRO: Most specific (fewest false +s)

CON: Less sensitive then LDDST
Why is Dexamethasone used to try to suppress Cortisol in LDDST and HDDST
It doesn't interfere with the assay being used to tell amount of Cortisol
What is LDDST's utility
Good as a screening test
Good sensitivity, but poor specificity (lots of false positives)
What signifies a positive LDDST
Failure to suppress cortisol concentrations to <1 ug/dL at 8 hours
Why would one do a Urine Cortisol:Creatinine Test
Good for screening, but not done well enough in this country to stand alone as a way to confirm diagnosis
What are 4 ways to tell PDH from ADH
HDDST
Endogenous ACTH
U/S Abd
LDDST (for ~50% cases)
How can a LDDST help tell b/t ADH and PDH (in 50% cases)
If cortisol has been suppressed to less than 1/2 of baseline after 3-4 hours, it is likely PDH
Will you see any suppression on HDDST if the hyperadrenocorticism is due to ADH
NO
How often will cortisol suppress in PDH patients during a HDDST
75-85% of the time
What is more helpful when interpreting HDDST:
suppression or no suppression
Suppression!
Failure to suppress does not tell for sure b/t ADH and PDH (there are rare cases of ADH that don't suppress), but suppression can only mean PDH
Why is it impt to tell b/t ADH and PDH
Changes tx plan
ADH might be able to be treated surgically, but PDH can only be treated medically
Increased cortisol w/ high endogenous ACTH means what
Likely PDH
Pituitary doesn't care that it is getting negative feedback-- it wants to keep doing its own thing and making ACTH
Increased cortisol w/ low endogenous ACTH means what
Suggests ADH
Pituitary recognizes that it doesn't need to ask adrenals to make more cortisol, but adrenal(s) are fxning autonomously
What is the tx for PDH
Mitotane- kills adrenal cortex
OR
Trilostane- inhibits enzymes used to make Cortisol (fewer SEs than Mitotane)
What is the first step of tx for ADH
Medical tx should be attempted first to replace corticosteroids before removing the tumor (since other adrenal gland will be turned off)

Can use:
Mitotane
Ketoconazole (helps 80% cases)
Trilostane (works well but does not shrink mass)
What are some SEs encountered w/ Ketoconazole used as a medical tx for ADH
Hepatotoxicity and Anorexia
How does the prognosis differ b/t PDH dogs treated w/ Mitotane vs/ Trilostane
About the same
What percentage of ADH cases w/ AC have inoperable tumors
1/2 of the 60% of cases w/ AC cannot be operated b/c invade vena cava or phrenicoabdominal vein
True/False: The goal of tx for Cushing's is to cure
False
What is primary hypoadrenocorticism most commonly caused by
Immune destruction of the adrenal cortices
How common in secondary hypoadrenocorticism and what is its cause
Rare
Pituitary failure causing loss of ACTh production
What deficiency(ies) is/are caused by primary hypoadrenocorticism vs. secondary
Primary- mineralo and gluco
Secondary- gluco only
What is the typical signalment of Addison's
Young adult dogs (4-4.5yr avg)
More commonly female, esp. intact females
See more in NM than M
What are the two main signs of glucocorticoid deficiency
Inability to deal w/ stress
Hypoglycemia

(weakness and lethargy)
What are the 5 main signs of mineralocorticoid deficiency
Severe Na loss
Hypovolemia
K retention leading to hyperK+
Decreased excretion of H+ by kidneys leading to acidosis
Excess colonic Na & H2O loss
What does hyperkalemia cause
Negative inotrope
Arrhythmias
Usually bradycardia
AV Block (first degree progressing to complete)
What is the usefulness of a basal cortisol concentration for dx of hypoadrenocorticism
Won't rule it in, but can rule it out

Also useful, is the ACTH Stim which will show failure of cortisol to increase
What are 4 main disturbances you expect to see on chem of Addison's patient
Na:K <27:1
Hyperkalemia
Increased BUN (Pre-renal b/c of hypovolemia)
Hyponatremia
Why might Addison's be, on the surface, hard to tell from renal failure
May see increased BUN and Creat, but isosthenuria

USG is variable in Addison's
What are hypovolemia's effects on thoracic rads in Addison's patients
Small heart and great vessels b/c of hypovolemia
If the basal cortisol level is low, then what
Do ACTH Stim b/c some normal dogs have low basal cortisol test
But, Sp 98% for <1 ug/dL basal cortisol
Explain the therapy for an acute Addisonian crisis
Correct hypovolemia
Correct electrolytes
ACTH Stim
Replace gluco and mineralo
NPO 24hrs (since many v+)

Start tx before get definitive dx
What are two drugs used to replace mineralocorticoids long term
Fludrocortisone PO
Injectable DOCP
What is used to replace glucocorticoids long term
Oral Prednisolone

Can withdraw Pred in many on Fludrocortisone b/c it, too, has gluco activity

But, those on DOCP must stay on Pred b/c DOCP has no gluco activity
What is the px for hypoadrenocorticism
Excellent
Normal life span

But, must give meds and can be very expensive for lg dogs