U4 O2 - Endocrine emergencies Flashcards
What is Isosthenuria?
Production of urine that has the same specific gravity
as the plasma filtrate which passes through the
kidneys i.e. the kidneys are not concentrating or
diluting urine (1.008-1.015).
What is Hyposthenuria?
The production of urine of lower specific gravity than
plasma. Indicates decreased ability to concentrate
urine but normal ability to dilute urine i.e. some
kidney function is present (< 1.008).
What is ketoacidosis?
An uncontrolled break down of fat to produce large
numbers of ketones often leading to a metabolic
acidosis.
What is Paraneoplastic syndrome?
Alterations in physiology due to the production of
biologically active substances by neoplastic (tumour)
cells (tumour).
What is Calciuresis ?
Calcium excretion in urine
What is Pontine myelinolysis ?
Severe damage of the myelin sheath of nerve cells;
in the area of the brainstem known as the pons. This
is a rare condition that has been associated with
rapid correction of hyponatraemia in some patients
What is the most serious presentation of hypoadrenocorticism and why?
The most serious presentation of hypoadrenocorticism is ‘the Addisonian crisis’- this is the life-threatening result of insufficient glucocorticoids and mineralocorticoids. If not promptly recognised and treated the Addisonian crisis can be fatal.
What is primary hypoadrenocorticism usually caused by?
Primary hypoadrenocorticism is usually caused by generally associated with immune-mediated destruction of the adrenal cortex leading to, usually, both mineralocorticoid and corticosteroid deficiency. In some rare cases there may be only mineralocorticoid or glucocorticoid deficiency
What is atypical hypoadrenocorticism caused by?
Atypical hypoadrenocorticism is increasingly recognised- this is the caused by a glucocorticoid deficiency
How does diagnosis of atypical hypoadrenocorticism compare to typical hypoadrenocorticism?
The clinical signs are often like typical
hypoadrenocorticism but as this is a glucocorticoid only deficiency, there are minimal changes in electrolytes as would be caused by a lack of mineralocorticoid. This can make diagnosis more challenging as the hyperkalaemia and hyponatraemia that are usually present with typical hypoadrenocorticism are not likely to be present
What are the cause of secondary hypoadrenocorticism?
There are several causes of secondary hypoadrenocorticism. Hypoadrenocorticism can occur when prednisolone that is being administered to a
patient for medical reasons, is suddenly withdrawn. Iatrogenic hypoadrenocorticism may result secondary to treatment for hyperadrenocorticism with trilostane or mitotane.
What species/breeds is hypoadrenocorticism most common?
Hypoadrenocorticism is often encountered in larger breed, young to middle aged female dogs – although any dog can be affected. It is uncommon in cats.
Certain breeds are more prone to hypoadrenocorticism e.g. Border collies/Bearded
collies and Rough Collies, There may be a history of a recent ‘stressful’ event e.g. kennelling, grooming or recent illness
What is relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI)?
More recently a condition known as relative adrenal insufficiency (RAI) or critical illness-related corticosteroid insufficiency (CIRCI) has been identified in critically ill patients e.g. with sepsis or pancreatitis (Burkitt Creedon, 2015). RAI/ CIRCI is
characterised by lack of an appropriate adrenal response to stress and is most commonly seen in septic animals
Why is hypoadrenocorticism often called the great pretender, what may there be a history of and what clinical signs may be seen?
Hypoadrenocorticism has been called the
‘great pretender’ as it can mimic many other conditions with non-specific clinical signs and waxing and waning illness (Klein and Peterson, 2010). There may be a history of polydipsia and polyuria, or a waxing and waning illness with intermittent GIT signs, weight loss and lethargy. Some patients presenting with acute abdominal pain may be suspected of having acute pancreatitis. Some of the clinical signs can be attributed to a lack of glucocorticoids (cortisol/cortisone) e.g. lethargy and GIT clinical signs; and others due to lack of mineralocorticoid (aldosterone) e.g. sodium loss, dehydration, altered neuromuscular and cardiac function (Mooney, 2015). This is most notable with the resultant hyperkalaemia that can induce bradycardia and other arrhythmias. Remember aldosterone is involved in potassium and hydrogen ion excretion- therefore a lack of aldosterone results in hyperkalaemia and hyponatraemia.
A patient with hypoadrenocorticism may have some or all what following clinical … ?
A patient with hypoadrenocorticism may have some or all the following clinical signs
1. vomiting
2. diarrhoea +/- melaena
3. abdominal pain
4. PUPD
5. inappetence/ anorexia
6. dull/ lethargic
7. weakness
8. collapse
9. hypovolaemia - poor pulse quality, pale mucous membranes, CRT>2 secs
bradycardia which is inappropriate to the presentation (i.e. evidence of hypovolemia)
On occasion an affected dog may present with signs of megaoesophagus.
N.B. some of the clinical signs can be attributed more to glucocorticoid deficiency e.g. lethargy/ dullness; PUPD and GI signs.
What will electrolytes usually demonstrate in a patient with hypoadrenocorticism?
Most cases of typical hypoadrenocorticism have a pronounced hyperkalemia, hyponatraemia and hypochloraemia due to a lack of aldosterone (mineralocorticoid).
The sodium: potassium ratio is typically below 27:1 (often < 23:1). N.B. this finding may not be present in a patient with atypical hypoadrenocorticism that is deficient in glucocorticoid only.
What will biochemistry usually demonstrate in a patient with hypoadrenocorticism?
In addition, there may be hypercalcaemia (~ 30% of cases), hypoglycaemia (~ 33% of cases), hypoalbuminaemia and azotaemia
Why are patients with hypoadrenocorticism usually azotaemic? Why will they have dilute urine?
Patients are often azotaemic due to fluid loss. However, rather than the classic findings of pre-renal azotaemia, these patients will often have dilute urine due to the lack of aldosterone. Consequently, it is important to try to differentiate a patient with kidney disease from a patient with hypoadrenocorticism. Noting bradycardia on a clinical examination of a sick canine patient is significant as this is far less likely to be present in a patient with kidney disease.
What will haematology usually demonstrate in a patient with hypoadrenocorticism?
Haematology
A mild-moderate, non-regenerative anaemia is possible as this is a chronic disease.
However, in a patient with intestinal haemorrhage there may be a more regenerative anaemia. Unusually and significantly for an animal with an acute illness, there will be usually not be a stress leukogram due to the lack of glucocorticoids. Cortisol causes an alteration in the pattern of circulating white blood cells - a stress leukogram is characterised by neutrophilia, lymphopaenia, eosinopaenia and potentially monocytosis. Conversely in a patient with hypoadrenocorticism, there may be neutropaenia, lymphocytosis and eosinophilia instead. Altered Na:K
alongside lymphocytosis could be significant in the investigation of this patient
What will urinalysis usually demonstrate in a patient with hypoadrenocorticism?
Urinalysis
Urine tends to be dilute/ isosthenuric (SG ~ 1.008-1.015) due to the lack of aldosterone (within the kidneys aldosterone normally retains sodium, chloride and water in exchange for potassium and hydrogen ions). This could cause confusion as this finding is also likely with chronic renal failure
What will electrocardiography usually demonstrate in a patient with hypoadrenocorticism?
Electrocardiography may show bradycardia and other changes consistent with hyperkalaemia e.g. spiked T-waves, shortened Q-T interval, prolonged QRS
complex, reduced/ absent P-waves and bradycardia Potassium levels of 7.5 - 8.0mmol/l can be associated with cardiac arrhythmias - higher levels can be fatal
What test is a definitive test for hypoadrenocorticism?
An adrenocorticotrophic hormone (ACTH) stimulation test is the definitive test for hypoadrenocorticism. Base line cortisol levels are measured N.B. the baseline cortisol may be suggestive of hypoadrenocorticism. Generally, when animals are stressed e.g. ill, their baseline cortisol levels will increase as a result of increased release from the adrenal cortex in a ‘stressful’ situation (review the function of cortisol). If the baseline cortisol is low in a sick dog, this can be a significant finding.
What level of baseline/ pre and the post ACTH cortisol would be indicative of hypoadrenocorticism?
Usually in dogs with hypoadrenocorticism both the baseline/ pre and the post ACTH cortisol are below normal (<20nmol/l). A dog with a resting cortisol above 50 nmol/l is unlikely to have hypoadrenocorticism (if cortisol production is affected i.e. the patient has typical hypoadrenocorticism).
What might radiography demonstrate in a patient with hypoadrenocorticism?
Signs consistent with hypovolaemia may be seen on thoracic radiographs e.g. microcardia, decreased liver size, decreased width of vena cava and decreased
pulmonary vasculature. There may be an oesophageal stripe associated with megaoesophagus.