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Endocrinology > Lect. 7 - Hypoadrenocorticism in dogs > Flashcards

Lect. 7 - Hypoadrenocorticism in dogs Flashcards

1
Q

Addison’s disease =

A

Primary hypoadrenocorticism

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2
Q

another name for Hypoadrenocorticism

A

Adrenocortical insufficiency

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3
Q

what hormone regulates arterial blood pressure

A

renin

in response to reduced renal perfusion pressure

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4
Q

the most active vasopeptide/vasoconstrictor is considered to be

A

angiotensin II in plasma

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5
Q

name 4 effects of angiotensin II

A

increases the sensation of thirst
increases ADH
increases arteriolar constriction
increases aldosterone release

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6
Q

aldosterone increases what exactly?

A

renal reabsorption of Na+

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7
Q

where is aldosterone secreted from?

A

the zona glomerulosa of the adrenal cortex

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8
Q

The two main regulators of aldosterone secretion are

A

RAAS and potassium (K+) ions

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9
Q

how do potassium ions affect aldosterone?

A

hyperkalemia stimulates aldosterone secretion by depolarization of the zona glomerulosa cells, hypokalemia inhibits by repolarization of the same membranes

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10
Q

Why does Addison’s cause hypovolemia?

A

A lack of aldosterone results in the loss of sodium, chloride, and water. One result is hypovolemia, which in turn reduces cardiac output and contributes to hypotension.

In Addison’s disease, hyponatremia results from aldosterone deficiency (leading to renal sodium loss).

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11
Q

How does Addisons disease cause hyperkalemia?

A

Hyperkalemia in Addison’s disease is mediated mainly by hypoaldosteronism, and thus a deficiency of aldosterone will result in potassium retention, through its inability to excrete potassium in the urine.

aldosterone mediates K+ excretion

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12
Q

2-3 functions of Aldosterone

A

Balance of water and electrolytes.

Conservation of Na+ & H20. (deficiency causes hyponatremia)

Excretion of K+ (deficiency causes hyperkalemia)

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13
Q

Aldosterone is Stimulated by (2)

A

hypovolemia and hyperkalemia

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14
Q

3 things Deficiency of aldosterone will cause

A

Dehydration/hypovolemia

Hyponatremia

Hyperkalemia

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15
Q

2 clinical manifestations of Hyperkalemia due to aldosterone deficiency

A
  • Weakness
  • Cardiac arrhythmias
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16
Q

clinical manifestations of Hyponatremia due to aldosterone deficiency

A
  • PD/PU
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17
Q

clinical manifestations of Hypovolemia due to aldosterone deficiency

A
  • Hypovolemic shock
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18
Q

Glucocorticoids broad functions (5)

A
  • Glucose metabolism and
    gluconeogenesis
  • Immune system
  • Inflammatory response
  • Integrity of GI* mucosa
  • Stress tolerance
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19
Q

broad Classification of Hypoadrenocorticism

A

primary and secondary

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20
Q

Primary Hypoadrenocorticism involves

A

Destruction of adrenal glands (>90%)

Deficiencies of mineralocorticoids and glucocorticoids

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21
Q

secondary Hypoadrenocorticism involves

A

Decreased ACTH secretion

or e.g. iatrogenic due to glucocorticoid use and sudden withdrawal of exogenous glucocorticoids

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22
Q

causes of Primary Hypoadrenocorticism (3)

A
  • Immune-mediated destruction of adrenal cortex (most common), Addison’s disease.
  • Iatrogenic: drug induced adrenocortical lysis.
  • Neoplasia, infection, or infarction of the adrenal glands
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23
Q

causes of secondary Hypoadrenocorticism (2)

A
  • Iatrogenic: Exogenous glucocorticoid administration which Inhibits the release of ACTH through negative feedback. OR Drug-induced adrenocorticolysis due to Drugs used to treat hypERadrenocorticism.
  • Pituitary lesions
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24
Q

What is „ Atypical“ hypoadrenocorticism?

A

Isolated Deficiency of glucocorticoids without deficiency of mineralcorticoids = no electrolyte imbalance.

so the zona fasciculata is destroyed but the zona glomerulosa is preserved.

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25
Q

name 2 Iatrogenic causes of hypoadrenocorticism:

A

Exogenous glucocorticoid administration which Inhibits the release of ACTH through negative feedback (this is secondary hypoadrenocorticism)

OR Drug-induced adrenocorticolysis due to Drugs used to treat hypERadrenocorticism (e.g. mitotane). (this is primary disease)

26
Q

Which is more common Cushings or Addisons

A

Cushings/hypERadrenocorticism

27
Q

Primary hypoadrenocorticism in cats

A

Very rare in cats

Fewer than 40 cases described as either case reports/series or in textbooks

28
Q

typical signalment for Canine hypoadrenocorticism

A
  • Young to middle aged (2 - 5y) female dogs RR* 1.85

– Breed predisposition
– Genetic predisposition

29
Q

clinical signs of Canine hypoadrenocorticism

A
  • Nonspecific clinical signs: lethargy, anorexia, weight loss
  • Gastrointestinal signs: vomiting, diarrhoea (or constipation!)

PU/PD

  • May present in hypovolemic shock, collapse, bradycardia
30
Q

define/describe Addisonian crisis

A

Adrenal crisis is a potentially life-threatening medical condition requiring immediate emergency treatment.

It is a constellation of symptoms (caused by insufficient levels of the hormone cortisol) that indicate severe adrenal insufficiency.

severe electrolyte imbalance, hypovolemic shock, syncope, possible convulsions

31
Q

≈30% of dogs with acute hypoadrenocorticism are in what clinicial state?

A

hypovolemic shock (adrenocortical/addisonian crisis)

32
Q

What is meant by „Relative bradycardia“ ?

A

Although hypovolemic shock is usually characterized by tachycardia (>160 bpm), dogs presenting with addisonian crisis may be tachycardia-free
animals (due to hyperkalemia) which is termed „Relative bradycardia“.

+ a weak pulse, pale mucous membranes, CRT increased.

33
Q

First steps for treatment of addisonian crisis.

A

immediate treatment if suspicion of crisis is strong, need not wait for lab results.

main aims: correct hypovolemia, restore Na+ with appropriate fluid therapy (often by jugular venous access)

corticosteroid restoration with appropriate preparations.

blood and urine collection in conjunction with catheter placement before administration of therapies.

34
Q

clinical signs of Atypical hypoadrenocorticism

A

The same nonspecific signs as typical hypoadrenocorticism

– lethargy, weight loss, anorexia
Gastrointestinal signs
– Vomiting, diarrhoea; megaoesophagus

35
Q

Absence of a stress leukogram in a dog presenting with possible (atypical) hypoadrenocorticism =

A

seriously ill animal!

36
Q

possible hematologic findings in a dog presenting with possible atypical hypoadrenocorticism

A
  • Eosinophilia
  • Lymphocytosis
  • Mild normocytic normochromic anemia but Hypovolemia masks anemia.
37
Q

possible biochemical findings in a dog presenting with possible hypoadrenocorticism

A
  • Hyponatremia
  • Hyperkalemia
  • Hypochloremia
    (Cl- content usually correlates to Na+)

Prerenal azotemia (is caused by a decrease in blood flow (hypoperfusion) to the kidneys)

38
Q

possible urinanalytical findings in a dog presenting with possible hypoadrenocorticism

A
  • Specific gravity is usually low. May be
    isosthenuric.
    – Unexpected finding in a dehydrated patient
  • Difficult to differentiate from renal diseases
39
Q

possible thoracic imaging findings in a dog presenting with possible hypoadrenocorticism

A

– Microcardia
– Small caudal vena cava
(both due to hypovolemia)

– Megaoesophagus (rare)

40
Q

what % possibility hypothyroidism + hypoadrenocorticism occuring

A

20% possibility hypothyroidism + hypoadrenocorticism (polyglandular disease)

Note: that high cTSH levels and low TT4 levels can create false diagnosis of
hypothyroidism in hypoadrenocorticism cases.

41
Q

The diagnosis of hypoadrenocorticism is confirmed by

A

ACTH stimulation test.

42
Q

The criteria for confirmation of diagnosis of hypoadrenocorticism are

A

a pre- and post ACTH stimulation test cortisol concentration less than the ref. range for basal cortisol.

43
Q

What are some causes for a borderline response to ACTH stimulation? (middle line) (4)

A

prior glucocorticoid administration

treatment with certain drugs such as mitotane, trilostane, ketoconazole

ACTH-stim product loss of potency or error in administration or sample collection etc.

rarely, sex hormone secreting adrenal tumors

Critical illness related corticosteroid insufficiency (CIRCI) (relative adrenal insufficiency)

44
Q

Interpretation of ACTH-stimulation test Cortisol concentration after the stimulation.

post-stimulation cortisol should be how much for Hypoadrenocorticism?

A

post-stimulation cortisol < 2 μg/dL (55 nmol/L) → Hypoadrenocorticism

45
Q

ACTH-stimulation test DOES NOT differentiate between

A

primary and secondary Hypoadrenocorticism

46
Q

A post-stimulation ACTH stim cortisol concentration of >2 μg/dL (55 nmol/dL) can be interpreted as?

A

it Eliminates Hypoadrenocorticism as diagnosis in the Majority of cases

47
Q

Previous administration of
glucocorticoids affects the results of the ACTH stim test because of?

A

Cross-reactions.

Stop administration of exogenous glucocosteroids 12-24 h before the testing.

Synthetic glucocorticoids
* Prednisolone and
* Methylprednisolone succinate (stop up to 4 weeks prior)

Note: „Acceptable“ glucocorticoids
* Dexamethasone
* Triamcinolone

48
Q

Chronic administraton of glucocorticoids results in

A

Supression of Hypothalamic-Pituitary-Axis and a weak response to the ACTH stimlulation test.

49
Q

Why would administration of glucocorticoids
before an ACTH test cause false test results?

A

Glucocorticoids provide a negative feedback loop for inhibiting the release of CRH and ACTH from the hypothalamus and anterior pituitary, respectively.

Prior administration of exogenous glucocorticoids can interfere with the ACTH stimulation test by causing abnormally high baseline cortisol levels.

50
Q

What is cosyntropin?

A

synthetic ACTH

51
Q

What alternative test has been investigated for use as a substitute to the ACTH-stimulation test forDiagnosis of Primary Hypoadrenocorticism in Dogs?

A

the Cortisol-to-ACTH Ratio can be used.

52
Q

Treatment of hypoadrenocorticism.

A

lifelong Supportive treatment with
Mineralocorticoids and glucocorticoids

  • IV fluid therapy
53
Q

drug for treatment of mineralocorticoid deficiency

A

DOCP/desoxycorticosterone pivalate (SC, IM administered every 25 days)

  • Acts to retain sodium and chloride ions and excrete potassium and hydrogen ions
    – Requires a functioning kidney

(other drug option is fludrocortisone which has both mineralo- and glucocorticoid activity)

54
Q

drug for treatment of glucocorticoid deficiency

A

Prednisolone

  • Increased dose during periods of excitment or stress

– Some suggestions to use hydrocortisone acetate (Less likely to cause iatrogenic hyperadrenocorticism but more expensive)

55
Q

Treatment of acute HA/ addisonian crisis

A

aggressive Fluid therapy with

  • 0.9% NaCl or
  • Ringer-lactate (better control of acidosis)
  • Check Na+ frequently, must not increase faster than 0.5 mEq/h (12 mEq/day) as this can cause complication myelinolysis among others.
56
Q

Treatment of atypical HA

A

Prednisolone

– Anticipated stress – increase the dose 2-10 x
– Some dogs will develop mineralocorticoid deficiency following initial diagnosis

57
Q

Describe Feline primary
hypoadrenocorticism

A
  • Extremely rare
  • Etiology multifactoral. The majority of cases probably immune-mediated.
  • Caused by a deficiency of glucocorticoids and/or mineralocorticoids.
  • Clinical signs, routine diagnostic test, diagnosis similar to that of dogs.
  • Lifelong treatmentrequired
  • Requires double doses of glucocorticoids per kg of body weight (compared to dogs)
58
Q

the cause of most cases of primary
hypoadrenocorticism (Addison’s disease) is

A

Idiopathic bilateral atrophy of the adrenal glands

59
Q

The three most important clinicopathological findings of hypoadrenocorticism are:

A

hyponatremia,
hyperkalemia and
weak response to ACTH stimulation.

(Next, Prerenal azotemia and low urine specific gravity make it Difficult to differentiate from renal diseses)

60
Q

The most common causes of secondary hypoadrenocorticism in dogs is

A

Iatrogenic causes

61
Q

How to differentiate primary from secondary hypoadrenocorticism?

A

ACTH and/or aldosterone hormone concentrations?

62
Q

Why does hypoadrenocorticism cause anemia?

A

A deficiency of cortisol can result in impaired erythropoiesis.

lifespan of red blood cells and interfering with the normal functioning of the bone marrow.

An imbalance in electrolytes can affect the function of red blood cells

decreased perfusion of the bone marrow, affecting the production of red blood cells.

Endocrinology (16 decks)

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