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Module 17 > Approach to Metabolic Collapse & Hypoadrenocorticism > Flashcards

Approach to Metabolic Collapse & Hypoadrenocorticism Flashcards

1
Q

what is the etiology of hypoadrenocorticism

A

Deficiency of mineralocorticoids (aldosterone), glucocorticoids (cortisol) or both

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2
Q

what is the most common cause of hypoadrenocorticism

A

Primary adrenocortical insufficiency (Addison’s) with a deficiency of mineralocorticoid and glucocorticoid secretion is the most common

Usually idiopathic —> the cause is not known

Immune-mediated destruction of adrenal cortices is believed to occur in most dogs with idiopathic adrenal insufficiency

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3
Q

what does aldosterone controlled

A

Loss of aldosterone secretion results in impaired renal conservation of sodium and chloride and excretion of potassium, leading to development of hyponatremia, hypochloremia and hyperkalemia

Inability to retain sodium and chloride reduces extracellular volume, leading to progressive development of hypovolemia, hypotension, reduced cardiac output and decreased perfusion of the kidneys and other tissues

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4
Q

what is the hallmark sign of hypoadrenocorticism

A

Hallmark sign of hypocortisolism are impaired tolerance to stress and clinical signs often become more pronounced when the animal is placed in stressful situations

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5
Q

what are the breeds that are predisposed to immune mediated hypoadrenocorticism

A

Young to middle aged dogs, often female

Standard poodles, bearded collies, Rottweilers, west highland white terriers

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6
Q

how does mitotate/trilostane cause hypoadrenocorticism

A

Adrenal necrosis/suppression

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7
Q

what are other causes of hypoadrenocorticism

A

Hemorrhage, infarction, infection, tumour

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8
Q

what is the signalment of hypoadrenocorticism

A

Young to middle aged female dogs with a median age of onset for all breeds of 4 years

Dogs with glucocorticoid deficient hypoadrenocorticism tend to be older at the time of diagnosis than dogs with mineralocorticoid hypoadrenocorticism

Inherited as an autosomal recessive trait in Portuguese water spaniels, nova scotia duck tolling retrievers, standard poodles and bearded collies

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9
Q

what are the clinical signs of hypoadrenocorticism in dogs

A

Lethargy

Anorexia

Vomiting

Weakness

Diarrhea

Weight loss

Shivering/shaking

Polyuria, polydipsia

Abdominal pain

Most have a long history of unwell, not quite right, poor doer

Wax and wane of symptoms

May look like other diseases (ex IBD, kidney failure, etc)

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10
Q

what are the clinical signs of hypoadrenocorticism in cats

A

Lethargy

Anorexia

Weight loss

Vomiting

Polyuria, polydipsia

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11
Q

what is the history of hypoadrenocorticism patients

A
  1. chronic, vague: often respond to non-specific therapy
  2. neurological: depression, weakness
  3. GI signs: inappetance, vomiting, diarrhea
  4. metabolic: failure to thrive, PUPD
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12
Q

what are the clinical findings of acute hAC (6)

A
  1. severe dehydration
  2. anorexia
  3. vomiting
  4. collapsed
  5. bradycardia
  6. hemorrhagic gastroenteritis
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13
Q

what are complications of acute hAC (5)

A
  1. acute renal failure
  2. GI hemorrhage
  3. pancreatitis
  4. pulmonary thromboembolism
  5. disseminated intravascular coagulation
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14
Q

what are examples of ddx of hypoadrenocorticism (8)

A
  1. Hemorrhagic gastroenteritis (HGE): parvovirus
  2. Bradycardia: atrioventricular block
  3. Episodic collapse: myasthenia gravis
  4. Lethargy: congestive heart failure
  5. Vomiting/diarrhea: inflammatory bowel disease
  6. Polyuria/polydipsia: renal failure
  7. Weight loss: neoplasia
  8. Abdominal pain: pancreatitis
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15
Q

what is seen on hematology with hAC (2)

A
  1. anemia: GI losses, bone marrow suppression, IMHA

dehydration masks severity: 70% of cases are anemic

  1. white blood cells: ‘reverse stress leukogram’ (low WBC, neutropenia, lymphocytosis, eosinophilia)
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16
Q

what is seen on biochem with hAC (8)

A
  1. serum electrolytes: sodium, potassium
  2. renal parameters: urea/creatinine increased 80%, minimally concentrated urine
  3. calcium increased 30%
  4. decreased glucose
  5. hypoalbuminemia
  6. hypocholestermia
  7. liver function decreased
  8. decreased pH
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17
Q

what do these abnormalities indicate

A

hypoadrenocorticism

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18
Q

what are the causes of hypokalemia (3)

A

red blood cell lysis

failure of excretion

others –> rhabdomyolysis

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19
Q

what are the causes of hyponatremia (3)

A
  1. excessive loss
  2. overhydration
  3. others – lab error, lipemia
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20
Q

what would the sodium:potassium ratio be in hAC

A

Normal: 27:1 and 40:1

Values are often less than 27 and may be less than 20 in animals with primary adrenal insufficiency

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21
Q

what are the similarities of hAC and renal failure (4)

A

1. History:

Acute episode after period of illness

2. Clinical examination:

Thin, dehydrated, may be or have collapsed

3. Renal azotemia:

Increased urea and creatinine

Effect of GI hemorrhage

Urine specific gravity 1.007 to 1.030

4. Electrolyte abnormalities:

High potassium:

Acute renal failure and urinary obstruction

Low sodium:

Polyuric phase of acute renal failure

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22
Q
A
23
Q

how would you diagnose hypoadrenocorticism

A

ACTH stimulation test

but cannot distinguish primary hAC from iatrogenic HAC or recent steroid adminstration

24
Q

how do you interpret ACTH stimulation test

A

The post ACTH serum cortisol concentration is less than 55 nmol/L (2 ug/dL)

A normal dog will produce cortisol greater than this

If there is a dramatic increase it may be due to stress or it may be due to hyperadrenocorticism (but this would have completely different clinical signs)

25
Q

how do you treat acute addisons (3)

A
  1. hypovolemia
  2. sodium deficit
  3. hyperkalemia
26
Q

how do you treat chronic addisons (3)

A
  1. mineralcorticoid replacement
  2. glucocorticoid replacement
  3. dietary changes
27
Q

how would you treat acute hAC with fluids

A

0.9% saline solution if serum sodium concentration less than 130 mEq/L

Isotonic crystalloid solution (ringer’s, ringer’s lactate) if serum sodium is 130 mEq/L or higher

28
Q

what fluid rate would you use to treat addisons

A

Rate: 40-80 ml/kg/24 h IV initially (2-3x maintenance)

20-60ml/kg/hr for 2 hours then 4ml/kg/hr

29
Q

calculate how much fluid you would use to treat a 20kg dog with 10% dehydration

A

2kg = 2 litres

plus 20 x 50ml = 1000ml

total = 2 litres plus any additional losses

30
Q

how do you treat the hyperkalemia

A

corrected by simple dilution and improved renal perfusion even when potassium containing fluids are used

31
Q

how do you correct the sodium deficit

A

Hydrocortisone sodium succinate:

Mineralocorticoid + glucocorticoid

Low potency

Dose: 2-10 mg/kg IV

Repeat every 6-12 hours

Use infusion? 0.5mg/kg/hr

Correct the sodium only —> can damage the brain if you increase too fast

Methylprednisolone

Dexamethasone

32
Q

at what rate should the sodium deficit be corrected

A

Rapid increase in sodium should be avoided in animals with severe hyponatremia, esp if it has been persistent for longer than 24 hours

Should be gradually increased by 10-12 mEq/L per day

33
Q

what should you monitor in acute addisons (5)

A
  1. temp, pulse, resp, mms, CRT, urine output
  2. glucose
  3. calcium
  4. electrolytes
  5. PCV, protein
34
Q

what is the long term treatment of addisons

A

Desoxycortone pivalate (DOCP)

35
Q

what is Desoxycortone pivalate (DOCP)

A

Pure mineralocorticoid

36
Q

how is Pure mineralocorticoid administered and what dose would you start with

A

Monthly injections:

Starting dose 1.5-2.2 mg/kg

Adjust using electrolytes 12-25d after dose:

Usually need lower final dose

37
Q

what should Desoxycortone pivalate (DOCP) be used with

A

Need prednisolone as well:

38
Q

what is the starting dose of prednisolone that you would use with Desoxycortone pivalate (DOCP)

A

Starting dose 0.1-0.2 mg/kg q24h PO

39
Q

what other medication can be used to manage addisons long term

A

Fludrocortisone

40
Q

what is Fludrocortisone

A

75% mineralocorticoid

25% glucocorticoid

41
Q

what dose of Fludrocortisone is administered

A

0.1-0.6 mg/dog PO BID

42
Q

what are causes of metabolic collapse

A

Diabetic ketoacidosis

Hypoglycaemia

Hyper/hypokalemia

Hepatic encephalopathy

Hyper/hypocalcemia

Thyrotoxicosis

Myxedema coma

Hyponatremia

Rare:

Hypernatremia

Pheochromocytoma

Hyper-viscosity syndrome

43
Q

how do you investigate a collapse

A

History

Clinical examination

Vital parameters

Initial laboratory tests

Glucose

Calcium

Electrolytes

44
Q

what is syncope

A

Faint = syncope

Acute episodic flaccid collapse

Cardiovascular

Dogs may struggle, thrash around and disorientated but quickly become orientated again

45
Q

what is a seizure

A

Fit = seizure

Acute, central, tonic-clonic activity

Neurological (primary or secondary to metabolic)

46
Q

what is weakness

A

Falling over = weakness

Generalized

Metabolic, hematological, orthopedic, neurological

47
Q

what should you look for in your clinical exam when investigating a collapse

A

Evidence of cardiac/other disease?

Pallor, cyanosis, dyspnea, distended veins, respiratory noises/crackles, arrhythmias, muffled thoracic sounds

Cause or effect?

If normal (no cardio or resp causes)

Go straight to laboratory tests

48
Q

in what ways can calcium cause collapse

A

decrease: hypoparathyroidism eclampsia
increased: addisons

hypercalcemia

49
Q

in what ways can glucose cause collapse

A

hypoglycemia

ketoacidosis

50
Q

how can electrolytes cause collapse

A

increased sodium

decreased potassium

51
Q

at what amount is it considered hypokalemia

A

<3.0 mmol/l

52
Q

what are the causes of hypokalemia

A

common causes

Intestinal loss — vomiting, diarrhea

CRF (cats)

Chronic diuresis (+/- anorexia)

DKA

Rare causes:

Hyperaldosteronism

Insulin therapy

Hyperadrenocorticism (also myotonia)

53
Q

what are complications of metabolic collapse

A

Pancreatitis (dogs)

Acute renal failure (dog & cat)

Urinary tract infections (less common)

Bacteremia/septicemia

GI hemorrhage (dogs)

Disseminated intravascular coagulation

54
Q

how do you monitor a patient for metabolic collapse (13)

A
  1. temp
  2. pulse
  3. resp
  4. mms
  5. CRT
  6. urine output
  7. glucose
  8. calcium
  9. electrolytes
  10. phosphate
  11. PCV, protein
  12. urea, creatinine
  13. bilirubin

Module 17 (31 decks)

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