Endocrine Diseases Flashcards
Hyperthyroidism
What is the aetiology?
Functional thyroid tumour
- Usually benign adenomatous hyperplasia (rarely cancerous) of the thyroid gland
May affect one or both lobes (also ectopic tissue)
Hyperthyroidism
What is the pathophysiology?
Affected gland overproduces thyroxine
This leads to a hyper-metabolic state
As thyroxine affects a number of body tissues there are a wide range of clinical signs seen
Complications such as hypertension and hypertrophic cardiomyopathy may occur
Hyperthyroidism
What are the clinical signs?
Polyphagia
Weight loss
Hyperactive/aggressive or restless
Tachycardia
Vomiting and diarrhoea
Poor coat/unkempt
Polydipsia
Hyperthyroidism
What are the diagnostic techniques?
Blood test – serum T4 levels, high levels confirm diagnosis, run in house with rapid results – to show increased thyroid levels
Blood biochem – to check for other conditions like kidney/heart disease
Scintigraphy – imaging using radioisotopes injected into the patient and imaged using a gamma camera. Used to locate thyroid tissue/plan surgery.
Evaluation of cardiac function and measurement of BP advisable – patients can present with high BP and cardiac problems. Can cause retinal detachment and blood clots.
Hyperadrenocorticism
What is the aetiology?
Pituitary tumour – increased production of ACTH (most common)
Adrenal tumour – direct increase of cortisol
Both lead to increased serum cortisol
Hyperadrenocorticism
What is the pathophysiology?
Overactive tissue in pituitary or adrenal gland leads to increased production of cortisol (2 different aetiologies)
High levels of cortisol lead to hyperglycaemia and inhibit ADH – leading to PUPD
High cortisol also causes protein catabolism leading to muscle wasting and poor wound healing
Cortisol affects hair growth and distribution of fat
Hyperadrenocorticism
What are the clinical signs?
Polyuria
Polydipsia
Weight loss
Alopecia (flanks)
Pot bellied
Hepatomegaly
Muscle weakness
Panting
Thinning of the skin
Hyperadrenocorticism
What are the diagnostic techniques?
- History and clinical signs
- ACTH stimulation test – blood at 0 and 1hrs, inj with ACTH after first blood sample - can see an increase in cortisol levels.
- **Low dose dexamethasone suppression test – blood at 0,4 and 8hrs, inj of dexamethasone iv after first b/s – distinguish between types of cushing’s disease **
- Urine cortisol:creatinine ratio (UCCR)
- Endogenous ACTH
- Often diagnosis requires combination of tests
- Imaging
Diabetes Mellitus
What is the aetiology of Type 1?
β cells have been destroyed and can no longer synthesise insulin adequately.
Presumed immune mediated and some breeds predisposed.
- Keeshond and Cairn Terrier thought to be more prevalent.
Damage to the pancreas such as during an episode of pancreatitis may lead to inability to synthesise insulin.
Diabetes Mellitus
What is the aetiology of Type 2?
Reduced ability to respond to insulin.
Due to:
Obesity
Oestrus
Cushing’s disease
Steroids
Acromegaly (cats) - growth hormone disorder causes overgrowth of extremities
Diabetes Mellitus
What is the pathophysiology?
Absolute or relative insulin deficiency
Reduced tissue utilisation of glucose
Leads to hyperglycaemia in bloodstream
And low glucose levels in cells
Renal threshold for glucose exceeded-glycosuria
Eventually fats are broken down as cells can’t access glucose
This can lead to ketosis…
Diabetes Mellitus
What is Ketoacidosis?
An acid state in the body caused by the build up of ketones.
- Gluconeogenesis - synthesis of glucose or glycogen from non-carbohydrate sources
- Utilising fat and protein as energy supply because glucose is unavailable
- By product - acidic Ketone bodies, resulting in anorexia, vomiting and dehydration
Diabetes Mellitus
What are the clinical signs?
Polyphagia
Polyuria
Polydipsia – secondary to polyuria
Glycosuria
Later;
Weight loss
Signs of ketosis – vomiting, depression, dehydration
Development of cataract (Dogs)
Diabetes Mellitus
What are the diagnostic techniques?
History and clinical signs
Blood testing: to check for blood glucose levels
Blood glucose - single test using glucometer or biochem analyser in practice. Quick and cheap. Ideally a fasted sample. Stress can affect results.
Cephalic sample or ear prick.
Glucose curve - serial samples taken at regular intervals over 12-24 hours.
Fructosamine - serum protein produced in response to blood glucose with three weeks lifespan.
Glycosylated haemoglobin - longer term monitoring. Elevated levels of RBC in poorly managed diabetes patients.
Urine testing: to check for glucose and ketones in urine
Dipstick, culture and sensitivity. Used because we can detect both glucose and ketones from a urine sample.
