Endocrinology Flashcards

Question

Describe the anatomy of the endocrine pancreas?

Answer 1

the pancreas lies in close association with the lesser curvature of the stomach and the duodenum. The exocrine component accounts for more than 90% of the total pancreatic mass, whereas the endocrine pancreas accounts for less than 10% and consists of several hundred thousand clusters of cells called the islets of langerhans. alpha cells - approx 25% of cells secrete glucagon. Beta cells - approx 60% - secrete insulin. Delta cells - approx 10% - secrete somatostatin. F cells - secrete Pancreatic polypeptide cells Beta cells occupy the centre of the islets while alpha and delta cells are situated at the periphery. Both glucagon and insulin are polypeptide hormones and they are responsible for maintaining blood glucose levels within a narrow range.

Answer 2

The metabolism of glucose to provide energy as ATP

Answer 3

the breakdown of glycogen to yield glucose

Answer 4

The formation of glucose from protein and fats.

Answer 5

The formation of glycogen from glucose.

Answer 6

A small protein, consisting of an A andB petide chain held together by disulfide bonds. if the chains are split apart it loses its biological activity. porcine and canine insulins are identical while bovine differs from canine insulin by several amino acids. feline insulin is most closely related to bovine insulin. Insulin is produced in response to elevated blod glucose. the overall action of insulin is to promote nutrient uptake, utilisation and storage by tissues and thus lower the concentration of glucose in the circulation. Increased glucose uptake by peripheral cells; especially muscle, liver, fat, synthesis of glycogen in liver for storage, inhibition of glycoenolsys & gluconeogenesis (liver).

Answer 7

Glucagon has a major role in maintaining blood glucose levels by increasing the concentration i.e exactly the opposite of insulin. production is increased by low blood glucose or Excercise which results in initiating hepatic glycogenolysis, stimulating hepatic gluconeogenesis, stimulating breakdown of triglycerides in fat to provide fatty acids for fuel.

Answer 8

Insulin deficiency diabetes. associated with a total loss of beta cell function as occurs due to immune mediated disease, pancreatitis or irreversible beta cell exhaustion. This is the most common form of DM seen in dogs. affected animals have high resting blood glucose levels, low resting insulin and fail to secrete insulin in the presence of hyeprglycaemia. they are insulin dependent diabetics. almost all dogs diagnosed with DM will require insulin treatment for life. immune mediated disease is the usual cause of type I dm in humans. may occur in dogs.

Answer 9

Insulin resistance diabetes. patients have high resting blood glucose and normal/high levels of insulin, but this is insufficient for demand. most cases occur because of insulin resistance due to excess diabetogenic hormones or obesity. (progestagens, glucocorticoids, growth hormone, glucagon, adrenaline). PEripheral cell insulin receptors are less responsive to insulin, meaning ever higher insulin levels are required. initially as insulin secretion rises this keeps blood glucose levels normal. If the cause of insulin resistance is not removed, beta cell exhaustion results in a relative or lack of insulin. blood glucose rises and patients become type 1 insulin dependent diabetics. this is most common type of DM seen in cats. Associated with amyloid deposits around the islet cells in up to 90% of cases.

Answer 10

Can occur in any breed. DM seen most freqently in middle aged dogs. Entire females are at increased risk due to prolonged high levels of progesterone during dioestrus. DM in keeshund puppies due to congenital aplasia of beta cells has been reorted. Twice as many males are affected as females in cats. usually middle age 10-13years. Burmese at increased risk.

Answer 11

Obesity, Progesterone, DM is more common in entire female dogs due to action of progesterone - growth hormone is stimulated from the mammary gland during dioestrus which induces insulin resistance. Glucocorticoids - inflammatory processes elevate glucocorticoids and inflammatory factors which will antagonise insulin. Growth hormone from pituitary adenomas, excessive catecholamines from pheochromocytomas of adrenal medulla and glucagon from glucagonomas of the islet alpha cells will antagonise insulin. Pancreatitis - chronic pancreatitis may lead to sufficient loss of endocrine tissue to result in DM.

Answer 12

Insulin deficiency results in a failure of glucose uptake by peripheral tissues leading to hyperglycaemia. the normal balance between insulin and glucagon is lost. predominance of glucagon permits uncontrolled glycogenolysis and gluconeogenesis, further increasing blood levels. Once the renal threshold for glucose is reached, hyperglycaemia induces glucosuria and osmotic diuresis, hence polyuria and compensatory polydipsia. Blood glucose cannot be taken up and used by cells for energy and remains in the circulation. the body mobilises proteins and adipose stores to release amino acids and fatty acids for gluconeogenesis. this leads to cachexia and weight loss. fatty acids from the circulation are oxidised to the ketones acetyle co A acetoacetate and beta hydrooxybutyrate in the liver. ketones are not used efficiently due to the lack of insulin and accumulate in the circulation leading to ketoacidosis. ketoacidosis has negative physiological effects including vomiting, anorexia, further osmotic diuresis, further electrolyte disturbances, dehydration and hypovolaemia. Polyphagia, polyuria, polydipsia, to weight loss, lethargy, anorexic, vomiting dehydrated and collapsed patient.

Answer 13

Well or uncomplicated diabetes - polyphagia, polyuria and polydipsia. bright and active. Ketoacidotic diabetics - depression, anorexia, vomiting, dehydration. PUPD for some time previous presentation. Initially animals are obese but most patients lose weight as condition advances. clinical signs often observed following a recent oestrus and the history may indicate transient pupd following previous oestrous. early signs of pdpu and polyphagia often go unnoticed in outdoor cats. may also exhibit a plantigrade stance due to peripheral neuropathy. ddx - diabetes insipidus, psychogenic polydipsia, hyperadrenocorticism, hypoadrenocorticism, CRF, pyometra, hyperthyroidism.

Answer 14

Documenting appropriate clinical signs, persistent fasting blood glucose of greater than 14mmmol with glucosuria. hyperglycaemia can be as high as 35mmol. presence of ketones in urine also supports diagnosis. Moderate hyperglycaemia of up to around 16mmol can occur rapidly due to stress. Recheck in 4 hours or the following day if hospitalised.

Answer 15

Fructosamine is produced by the irreversible glycosylation of albumin iin proportion to the surrounding glucose levels. its half life is around 1-2 weeks so levels give an indication of the average blood glucose level over that time span. Levels are used to primarily monitor diabetic control in response to treatment in both dogs and cats and also to aid differentiation of stress hyperglycaemia from DM in cats.

Answer 16

produced in a similar manner to fructosamine but the half life is considerably longer. not routinely used as veterinary assays not commercially available. most common complication of DM is bacterial cystitis due to glucosuria and an impaired immune system. This may be missed due to the PUPD and a lack of an adequate inflammatory immune response. Every newly diagnosed diabetic should have a urine sediment exam and culture performed in addition to routine analysis.

Answer 17

bacterial cystitis Formation of cataracts retinopathy peripheral neuropathy - weakness and plantigrade stance Recurrent bacterial infections - urinary tract, skin, dental) Life threatening diabetic ketoacidosis.

Answer 18

Twice daily insulin to stabilise adequately. once daily insulin regimes can be tried if it is impossible for the owner to give twice daily injections. May be necessary to use a longer acting insulin if caninsulin fails to stabilise the patient due to its short duration of action. Caninsulin is given at 12 hourly intervals. A meal should be fed at the time of each injection, contanining 30-50% of the daily requirement. some patients need additional small meals between injections to avoid hypglycaemic episodes. providing dry food free choice for non greedy eaters will help avoid this. feed the same amount at the same times every day and avoid titbits. Reduce weight. water must always be freely available. Patients monitored by checking blood glucose. glucometers readily available and cheap to buy. At revisit carry out blood glucose curve and adjust insulin dose accordingly. Aim to maintain blood glucose between 5-11 however many diabetics will remain well with good quality of life despite not achieving this level of control. Intact bitches should be spayed during anoestrus.

Answer 19

By having the owner feed and inject their dog at home as per their normal routine and then bringing them straight to the surgery. A period of 5-7 days should be allowed before assessing the response to a change in insulin. Some dogs may always have an erratic response when hospitalised.

Answer 20

Diabetics should be encouraged to exercise regularly and there is no reason to restrict it. however consistency is important. large fluctuations in amount of exercise from day to day may result in instability of blood glucose levels or hypoglycaemic episodes. Advise owners to take a sugary snack or oral glucose gel with them on walks.

Answer 21

Many cats have reversible DM. All cats will require twice daily insulin if caninsulin is used. the shorter duration of action means that often even this is inadequate and three times dosing or longer acting preparation is required. Cats should retain their usual feeding schedule if possible. should be allowed free choice food if not overweight. weight reduction is vital if overweight. Blood glucose curves difficult due to stress hyperglycaemia. Moitor carefully for remission of DM and taper dose gradually. Glipizide is a sulphonylurea which stimulates insulin secretion and therefore its action depends ont he presence of functioning beta cells. this added strain on beta cells will decrease chances of achieving remission of DM. Acarbose impairs glucose absorption from the nitestine but must be given with food.

Answer 22

History is usually short onset, diagnosis can be confirmed by presence of ketonuria or ketonaemia. consider the placement of an IV line. A baseline electrolyte panel, total proteiin, blood gases, haematology and urinalysis should be obtained. Asess degree of dehydration. calculate fluid deficit - give fluids. monitor urine output. start insulin therapy. Adjust potassium in IV fluids as necessary. Hypophosphataemia coon following treatment of DKA and can cause haemolytic anaemia. Patients may be hyper or hyponatraemic at presentation. IV sodium bicarbonate to correct acidosis should be used with great caution and only if blood gas analysis is available. Once blood glucose level has been maintained between 10 and 15 mmol for at least 12 hours the ketone levels are falling and electrolyte levels are normalised, patient should be much brighter and keen to et.

Answer 23

The most frequent complication is hypoglycaemic crisis. Signs of hypoglycaemia include anxiety, muscle tremors, ataxia, collapse, convulsions, coma and death. IF these signs occur and the patient is conscious then feed a high glucose food/drink/gel. The majoirity of problems are not due to complex hormonal interactions but the failures in the routine home management.

Answer 24

Somogyi effect, rapid decline in blood gucose followed by rebound hyperglycaemia due to counter regulatory response. these animals willl be hyperglycaemic most of the day and the hypoglycaemia may be very transient so patients apear as if they have insulin resistance unless a very detailed blood glucose curve is examined. Suspect this if control was initially good but has deteriorated despite increasing blood glucose level.

Answer 25

avoid semi moist foods which are high in sugars. the aim is to ensure food is available or in digestive tract during periods of high insulin concentrations. if dogs are not greedy eaters providing dry food free choice will help avoid hypoglycaemic episodes. some clinicians prefer giving insulin before food, some after food and some at the same time. Giving insulin after the dog has eaten is the safetst option to avoid risk of hypoglycaemia should the dog not eat. Some dogs will not eat well until insulin is given and blood glucose falls to stimulate appetite. For dogs on once daily insulin provide 25-30% of daily ration at time of injection and the remainder at peak of insulin action 6-8 hours later. For dogs on twice daily provide 50% at each injection. Some dogs may need a snack 6-8 hours after each injection to alleviate hunger.

Answer 26

Allow cats to adhere to their usual feeding schedule whenever possible most cats eat small frequent meals and having free choice food available will help avoid hypoglycaemic episodes. otherwise feed the ration split to as many meals as is practicable and at leas two meals given at the time of the insulin injections. Automatic feeders may be useful.

Answer 27

The diet should not contain large amounts of simple sugars which will cause post prandial surges in blood glucose levels. calories should be provided by complex carbohydrates (Starch) and high quality protein. in dogs, rice based diets may result in higher postprandial glucose than those with sorghum or barley. in cats, high protein diets more closely mimc the natural diet than high carbohydrate does. thus diets with increased protein content and restricted quantities of fat and especially carbohydrate decreases postprandial hyperglycaemia and may improve insulin sensitivity even to the point where diabetic remission occurs.

Answer 28

Diabetic diets often have high fibre but evidence from studies have shown a marked individual variation in the glycaemic responses of dogs to increased fibre i.e not a consistent improvement in postprandial hyperglycaemia. high fibre diets are not suitable for thin diabetic dogs. In cats only very high glucose diets produce post prandial hyperglycaemia ad so fibre would appear to be even less important.

Answer 29

Fats only need to be specifically restricted in dogs which are overweight or those with a history of chronic pancreatitis. diabetes may occur secondary to chronic pancreatitis and diabetes may be a risk factor for pancreatitis so evaluate patients for pancreatic disease and restrict fat content of diet when appropriate.

Answer 30

Carnitine plays a key role in fatty acid metabolism. supplemental carnitine promotes fatty acid oxidation over protein catabolism for energy mobilisation and so may protect against muscle wastage in diabetic dogs and cats. carnitine may be beneficial in cats undergoing weight loss due to protection against hepatic lipidosis. it has also been shown to promote weight loss in cats undergoing caloric restriction.

Answer 31

Genetics and breeds - labs, golden retrievers, pugs, chihuahuas, spaniels. Neutering and age - unnetured cats and dogs generally weigh less. Neutering appears to result in a decrease in metablic rate. Oestrogen also inhibits lipogenesis (fat production) and this decreases in female animals after spaying. with spaying - lean body mass declines causing a decrease in total daily energy expenditure. Diet and feeding - highly palatable diets most important exogenous factor influencing obesity in companion animals. Feeding of table scraps and treats. Hypothyroidism lowers metabolic rate and orthoaedic disease impairs ability to excercise, decreasing energy expenditure.

Answer 32

A balanced proprietary diet should be fed, these are generally low fat and high fibre with moderate carbohydrate levels. Carnitine, supplementary vitamins etc are likely to be added. Calculate energy requirement based on ideal body weight and feed 60-65% of this for weight loss. Wet diets may give higher satiety than dry diets. n diabetic animals monitor insulin dosage carefully as the requirement may drop with weight reduction. Talk to owners about eliminating or reducing treats. Advise what to use as low calorie treat. Advise on weight loss exercise programme.

Answer 33

Do not over restrict food to encourage rapid weight loss in cats as they are prone to developing hepatic lipidosis if severely energy restricted. A low carbohydrate balanced proprietary diet will be most effective and most likely to reduce insulin requirement in diabetic animals. Calculate energy requirements based on ideal body weight and feed 70% of this amount for weight loss. wet diets may give higher satiety than dry diets. monitor insulin dosage carefully as requirement may drop quickly and significantly. advise on how to increase the cats activity levels. If this fails after several months consider switching to a more calorie restricted diet which will have higher carbohydrate and higher fibre content

Answer 34

Insulinomas are functional tumours of the beta cells secreting insulin. they are rare in dogs and extremely rare in cats. they occur more often in ferrets. high insulin levels are responsible for profound hypoglycaemia which causes the clinical signs. More often reported in larger breeds such as GSD, irish setter, boxer, poodles, collies. Middle age dogs. During normal fasting blood glucose is maintained by glycogenolysis for approx 24 hours. therafter hepatic glucogenesis is required. Excessive insulin from an insulinoma promotes rapid uptake of circulating glucose by tissues and inhibits glycogenolysis and Gluconeogenesis and so hypoglycaemia develops. An attempt is made by counter regulatory hormones including GH, cortisol and catecholamines to reverse the fall in blood glucose but is not efective.

Answer 35

The brain is dependent on glucose and very sensitive to hypoglycaemia. this results in a neuroglycopaenic response: trembling, anxiety, weakness, ataxia, disorientation, seizures, coma and death. Clinical signs vary due to degree of hypoglycaemia and the speed with which it develops. Signs may be episodic and are most frequent during fasting and improve on feeding. Typically patients will exhibit weakness, excercise intolerance, behavioural changes, ataxia followed by collapse and seizures. Most patients are polyphagic.

Answer 36

hunting dog, toy dog or neonatal hypoglycaemia, prolonged starvation, infections, glycogen storage diseases, hepatic insufficiency, hypoadrenocorticism, sepsis, toxins, extrahepatic producing tumours, panhypopituitarism. Tumours usually difficult to detect even with imaging. Diagnosis relies on laboratory testing. normal fasted insulin levels are less than 20uU/ml but resting values alone are not a reliable indicator of insulinoma. simultaneous glucose and insulin levels are required. In practice this means hospitalising the patient for fasting and serial blood glucose estimations 2 hourly under close observation. The aim is to document hyperinsulinaemia in the presence of hypoglycaemia. This is the diagnosis for insulinoma.

Answer 37

Surgery. unfortunately the tumour has usually metastasised at the time of diagnosis so usually only gives remission for several months or even a few years but the prognosis remains guared. prior to surgery feed several small meals daily and give prednisolone to antagonise insulin. During surgery administer IV glucose saline and closely monitor blood glucose. Palpate and remove all detectable pancreatic nodules.

Answer 38

small frequent meals throughout the day to reduce risk of hypoglycaemic episodes. Avoid simple sugars which may provoke insulin release and provide calories with complex carbohydates protein and fat. Prednisolone good for management. Diazocide increase slowly from smallest dose to satisfactory response. this drug inhibits insulin secretion by blocking calcium entry into beta cells. It also increases hepatic gluconeogenesis, glycogenolysis and peripheral uptake of glucose b y tissue cells. Ocreotide - only work where there are somatostatin receptrs expressed on the neoplastic cells.

Answer 39

A rare neuroendocrine gastrin secreting tuour in the pancreas reported in middle aged dogs and cats. Clinical signs relate to overproduction of gastric acid, with vomiting anorexia, diarrhoea, gastroduodenal and oesophageal ulceration and perforation, haematemesis, haematology and serum biochemistry abnormalities. Diagnosis based on demonstrating elevated fasting gastrin levels and diagnostic imaging of the pancreas for insulinoma. Treament is surgical removing any pancreatic nodules, debulking metastases and repairing and gastrointestinal ulcers.Medical treatment with antacids and gastroprotectants, omeprazle, sucralfate, misoprostol, ocreotide. Poor prognosis.

Answer 40

A rare neuroendocringe glucagon secreting tumour of the islet alpha cells only. only around 20 cases reported. clinical signs - inappetance, lethargy, lymphadenopathy and diarrhoea, skin lesiosn with erythema, crusting and ulceration and secondary skin infections, most dogs have hyperglycaemia and often overt diabetis mellitus. glucagon assays are not readily available so premortem diagnosis is based on clinical sgns. diagnostic imaging of the pancreas. Surgical removal for treatment or for medical treatment; insulin therapy, amino acid suupplementation, antibiotics for skin infection.

Answer 41

The adrenal glands are paired with one at the cranial pole of each kidney and embedded in an island of fat, they are retroperitoneal. Each is composed of cortex and medulla. The cortex surrounds the medulla and produces aldosterone from zona glomerulosa, cortisol from the zona fasciculata and zona reticularis and sex hormones from the zona reticularis. The adrenal medulla secretes adrenaline and noradrenaline from chromaffin cells.

Answer 42

By the hypothalamic pituitary adrenal axis. Stress and illness override this normal negative feedback control which normally maintains plasma ACTH and cortisol levels and high concentrations of these hormones result.

Answer 43

During stress or starvation cortisol increases and thus maintains normal blood glucose concentration via mobilisation of amino acids from muscle and fatty acids from adipose tissue for energy substrates and hepatic gluconeogenesis and inhibition of glucose and amino acid uptake in muscle and adipose tissue by antagonism of insulin action.

Answer 44

Glucocorticoids have potent anti inflammatory and immunosuppresive properties especially on lymphocyte and antibody production. Cortisol decreases release of inflammatory mediators from damaged cells and migration of neutrophils from the general circulation into tissues. Cortisol stimulates production of RBC and platelets from the bone marrow.

Answer 45

Excess cortisol can result in hypertension and hypervolaemia. Connective tissue cortisol impairs fibroblast function leading to poor wound healing and thinning of the skin. Increased fragility of skin and blood vessels leads to easy bruisiing.

Answer 46

Cortisol promotes bone resorption, decreases bone matrix synthesis, decreases calcium absorption from the intestine and promotes calcium excretion in the urine.

Answer 47

Cortisol antagonises the actions of AVP resulting in an inability to concentrate urine and increased urination and thirst.

Answer 48

By the renin angiotensin system and increased potassium in the extracellular fluid. Sodium ions in the ECF and AVP inhibit secretion. ACTH is necessary for secretion but does not control the rate.

Answer 49

Aldosterone plays a critical role in regulating extracellular electrolyte concentrations particularly sodium and potassium. It acts through the mineralocorticoid receptor in those tissues controling salt metabolism, primarily the kidney but also the sweat glands, salivary glands and colonic epithelial cells. Absence of aldosterone leads rapidly to life threatening abnormalities in electrolyte and fluid balance and death within just a few days. aldosterone stimulates exchange of sodium and potassium in the renal tubular epithelial cells resulting in increased sodium resorption - less excreted in urine, increased renal excretion of potassium, increased water resorption - an osmotic effect directly related to the increased resorption of sodium and resulting in expansion of the extracellular fluid volume and increase in arterial pressure. Thus aldosterone protects against hypovolaemia, hypotension and Pottassium intoxication.

Answer 50

Caused by excessive production or administration of glucocorticoids. Pituitary dependent HAC - accounts for 85-90% of cases of naturally occuring. Autonomous excessive ACTH secretion from a pituitary neoplasm results in bilateral adrenocortical hyperplasia and excessive cortisol secretion. Adrenal dependent HAC accounts for the remaining cases and results from adrenocortical neoplasia which may be benign or malignant. They result in decreased ACTH secretion and atrophy of contralateral adrenal cortex. IAtrogenic HAc is most common and results from systemic or topical glucocorticoid use.

Answer 51

symptoms of HAC will usually have an insidious onset and owners may fail to notice them until they are well advanced or may attribute them to ageing. polyphagia may be taken as a sign of good health. in dogs with adrenocortical carcinoma signs may develop and progress rapidly and therefore common dermatological signs of the disease may be mild or absent. Dogs usually show abnormalities of may organ systems due to the wide ranging effects of glucocorticoids. Polyuria, polydipsia, polyphagia, pendulous or enlarged abdomen/obesity, hepatomegaly, excessive panting, muscle atrophy, lethargy, skin changes, alopecia, anoestrus/testicular atrophy, calcinosis cutis, neurological signs, hypertensive retinopathy.

Answer 52

Stress leucogram, leukocytosis with neutrophilia, eosinopaenia, lymphopaenia and monocytosis, high normal values for RBC parameters due to cortisol stimulating bone marrow, raised SAP due to glucocorticoid induction of a specific hepatic isoenzyme of AP, elevations of SISAP, Raised ALT, bile acids concentrations may be normal or marginally elevated, hypercholesterolaemia, hypertriglyceridaemia, high normal glucose, low thyroxine. A dog with a normal leucogram and a referance range SAP concentration is unlikely to have hyperadrenocorticism

Answer 53

Specific gravity is usually sub normal. Dogs can usually concentrate urine if water is withheld unless a pituitary macroadenoma is compressing the hypothalamas and interfering with ADH release. bacteriuria is common. often urine sediment is inactive due to immunosuppresion. always assess HAC cases for urinary tract infection with culture from cystocetesis sample. mild proteinuria is common. Hepatomegaly and good intraabdominal contrast due to fat tissue, m ineralisation, osteoporosis, distended bladder, cystic calculi, pulmonary metastasis possible, abdominal ultrasonography to determine adrenal size, MRI to assess pituitary tumours.

Answer 54

HAC and diabetes mellitus are found concurrently in some dogs. diabetic dogs with signs of HAC and or insulin resistance should always be tested for HAC. this should be delayed until the diabetes has been stabilised as the stress of diabetes may produce false results.

Answer 55

Episodic secretion of ACTH in HAC results in fluctuating cortisol concentrations that will at times be within the reference range. the basal cortisol concentration should not be used in the diagnosis of hyperadrenocorticism.

Answer 56

It investigates the capacity of the adrenal cortex to produce cortisol. the enlarged adrenal cortex in naturally occuring HAC respponds to ACTH or its synthetic analogues with excessive cortisol production.

Answer 57

Low doses of exogenous glucocorticoids suppress blood cortisol concentrations of healthy dogs by negative feedback but are less effective in dogs with naturally occuring HAC. The test is of no value in the diagnosis of iatrogenic HAC. In healthy dogs, this low dose of dexamethasone consistently suppresses blood cortisol concentrations. dogs with PDH and ADH are resistant to this dose.

Answer 58

Cortisol is excreted in the urine and so the urinary cortisol:creatinine ratio provides a reliable estimate of cortisol release over the previous few hours. a morning urine is collected, a normal result eliminates HAC, however test has low specificity as an increase in the cortisol:creatinine ratio occurs in non adrenal illness.

Answer 59

In PDH, both adrenal glands are mildly to moderately enlarged and normal architecture, in ADH one gland is enlarged and the other is atrophied, in iatrogenic HAC both glands are atrophied. 30% of dogs with PDH show suppressed blood cortisol concs at 4 hours with escape from suppresion at 8 hours. ACTH is low in dogs with hyper functional adrenocortical tumours due to normal negative feedback.ACTH is within the high referance range in dogs with PDH, indicating autonomous secretion in the face of raised circulating cortisol concentrations. Dogs with iatrogenic HAC show subnormal responses to ACTH.

Answer 60

Trilostaine is the only licensed product to treat canine HAC in the uK. It is a competitive and reversible inhibitor of 3Bhydroxysteroid dehydrogenase and so blocks the adrenal steroid biosynthesis pathway. However at therapeutic dosages it has little to no effect on serum sodium and potassium concentrations. Its effects are reversible. Mitotane is cytotoxic and therapeutic dosages destroy the zona fasiculata and reticularis of the adrenal gland while leaving the zona glomerulosa mostly intact. Not used unless trilostaine fails to control the condition. Pituitary irradiation is indicated where there is a macroadenoa associated with clinical signs. Hypophysectomy removes the cause but requires very skilled surgeon and has significant mortality. Bilateral adrenoelectomy removes end organ response. MAnagement is difficult not recommended.

Answer 61

Surgical management - dogs with ADH have the best prognosis if their adrenal tumour can be removed surgically. Trilostaine has been reported to be effective. Mitotane is relatively effective in adrenocortical neoplasia as it is cytotoxic.

Answer 62

some dogs with typical clinical and clinicopathological features of HAC have normal ACTH response and LDDS test results. if the clinial suspicion remains high, 17a hydroxyprogesterone ca be measured along side cortisol. Management is as above. the ACTH response rest cannot be used for monitoring response to treatmetnw ith trilostane as the block in corticosteroid metabolism occurs downstream from 17-a hydroxyprogesterone.

Answer 63

Most of the clinical signs seen in dogs can occur in cats but general presentation differs significantly; diabetes mellitus - antagonism of AVP by cortisol does not sem to occur in cats which are more prone to developiing diabetes mellitus due to insulin antagonism. Extreme skin fragility - skin will tear easily even with normal handling and lage areas denude. Weight loss - due to poorly controlled diabetes usually. normally severe hyperglycaemia and glycosuria. urine SG usually remains above 1.020. Increases in liver enzymes may be seen in cats due to hepatic lipidosis. A glucocorticoid induced isoenzyme of SAP does not exist in cats. Hypercholesterolaemia occurs in 25-30% of cats.

Answer 64

LDDS test is recommended. a higher dose must be used in cats. ACTH response test is not recommended due to low sensitivity in cats. Discriminatory tests - high dose dexamethasone supression test. ACTH - low plasma ACTH indicates ADH r iatrogenic HAC.

Answer 65

Trilostane - not licensed. bilateral adrenalectomy with subsequent mineralocorticoid and glucocorticoid replacement therapy. Mortality far less than in dogs. Unilateral adrenalectomy used for ADH. radiotherapy may be attempted for PDH. Iatrogenic hyperadrenocorticism - treat as for dogs.

Answer 66

Primary HOC - Usually arises from idiopathic bilateral adrenocortical atrophy which is thought to be an immune mediated process. There are other rare causes. clinical signs result from deficiency of both mineralocorticoids and glucocorticoids once more than 95% of the adrenal cortex has been destroyed. Secondary HOC results from deficiency of glucocorticoids alone - caused by reduced ACTH production and release following abrupt cessation of long term glucocorticoid administration. Iatrogenic HOC can arise from treatment with o,p'-DDD.

Answer 67

Standard poodles and bearded collies are predisposed. Portugese water spaniels, Great Danes, Nova Scotia duck tolling retrievers, rotweilers, wheaten terriers and WHWT. 75% cases are female. Most cases occur in young to middle aged dogs. 2-4 yrs.

Answer 68

May be acute or chronic in presentation. the signs may be vague non specific and wax and wane, often associated with stress. History - inappetance, anorexia, depression, lethargy, weakness, vomiting, diarrhoea, weight loss, shivering, muscle tremors, stiffness, pu/pd, collapse, dehydration in almost all cases, bradycardia and weak pulse, hypotension, hypothermia, abdominal pain, muscle weakness. Reverse stress leucogram: eosinophilia, lymphocytosis, low neutrophils or neutrophilia, normochromic anaemia due to lack of cortisol stimulating bone marrow. Increased excretion of sodium accompanied by chloride, bicarbonate and water and retention of potassium lead to hyperkalaemia, hyponatraemia, hypochloraeia, reduced plasma sodium:potassium ratio. Pre renal azotaemia. Metablic acidosis. urine may be dilute for degree of dehydration. Hyperkalaemia leads ti impaired cardiac action potential conduction and bradycardia. - spikig of t wave, shortening of q-t interval, prolonged P-r interval, reduced P wave amplitude, as hyperkalaemia worsens the P waves may dissapear, severe bradycardia, ventricular fibrillation and cardiac arrest may result. Radiographiic changes directly reflect hypovolaemia.

Answer 69

Impaired adrenal steroid production must be confirmed to make a diagnosis of HOC. a basal cortisol level of >60nmcan be used to exclude a diagnosis of HOC. A subnormal to absent post ACTH cortisol response confirms the diagnosis. in severe hypotension the IV route should be used, as absorption from an IM injection may be poor. The three most important criteria for the diagnosis of primary hypoadrenocorticism are demonstration of hyponatraemia, hyperkalaemia and a poor response in the ACTH response test.

Answer 70

Hyperkalaemia can be life threatening. Provide fluid therapy and corticosteroid replacement, emergency measures to lower potassium are almost never required. Administer isotonic saline IV. this raises sodium levels, reduces potassium levels, corrects hypovolaemia. Over rapid correction of hypoatraemia can result in neurological damage. Glucocorticoids should be given immediately after the ACTH stimulation test has been completed. the drug of choice is hydrotortisone sodium succinate. Monitor sodium and potassium concentrations hourly. once these are in the normal range and the dog is eating and drinking, maintenance therapy with oral medications can be commenced.

Answer 71

oral mineralocorticoid therapy using fludrocortisone acetate should begin as soon as possible. starting dose is 10ug/kg/day and the dosage is adjusted according to the plasma sodium and potassium concentrations. Initially serum electrolytes should be checked weekly. It is common for dose to require increase with time. as fludrocortisone has significant glucocorticoid activity, many dogs will not require daily glucocorticoid replacement. Desoxycortiosterone pivalate DOCP is administered by IM every 25 days - pure mineralocorticoid so dogs require additional glucocorticoid. Once stable check every 3-6 months for sodium potassium and urea/creatinine concentrations.

Answer 72

Some dogs may present with typical clinical and clinicopathological features of glucocorticoid insufficiency b ut normal serum electrolyte concentrations and no clinical signs related to these. They show a subnormal response to the ACTH response test but have no history of glucocorticoid administration.

Answer 73

Naturally occurring very rare in cats. traumatic destruction and lymphoma infiltration of the adrenal cortex can also occur. bradycardia less common. diagnosis - h yperkalaema, hyponatraemia, subnormal ACTH response, intravenous glucocorticoids, fludrocortisoone, prednisolone. Iatrogenic secondary hypoadrenocorticism due to glucocorticoid or progestagen administration much more common. Clinical signs due to glucocorticoid defiency.

Answer 74

Uncommon. Autonomous excessive secretion of aldosterone leads to excessive sodium retention and excessive potassium scretion. usually this is due to a unilateral adrenal tumour. adenomas and carcinomas occur with equal frequency. no breed or sex predisposition. miiddle aged to old cats. features; hypokalaemia, muscle weakness and ataxia, cervical ventroflexion, retinopathy intraocular haemrrhage, acute onset blindness. Diagnosis: elevated plasma aldosterone with concurrent low plasma renin levels. Eliminate other causes of raised plasma aldosterone concentration including congestive heart failure or renal disease. Treatment: adrenalectomy, medical stabilisation first. medical control of hypokalaemia and hypertension.

Answer 75

functional tumour of the chromaffin cells of the adrenal medulla. uncommon. usually unilateral. 35% malignant. older animals. Excessive production of catecholamines - episodic so clinical signs are typically intermittent which can make diagnosis challenging, weakness and lethargy, collapse, restlesness and panting, tachycardia, hypertension, pupd, local nvasion in caudal vena cava where tumour thrombus may form, non traumatic rupture leading to life threatening or fatal haemorrhage. Detection of adrenal mass on ultrasound, CT or MRI examination. surgical removal of affected adrenal is treatment of choice - mitotane and trilostane are ineffective.

Answer 76

Dogs and cats usually have four parathyroid glands (two parathyroid glands associated iwth each thyroid lobe) the principal role of the parathyroid glands is to secrete parathyroid hormone which alongside 1,25 dihydroxyvitamin D and calcitonin, tightly controls plasma calcium concentrations.

Answer 77

Parathyroid hormone is secreted by the chief cells int he parathyroid glands and leads to an increase in plasma calcium concentrations through a variety of mechanisms including mobilising calcium from bones and increasing calcium reabsorption in the distal tubule of the nephron. Bitamin D is first metabolisted in the liver to 25hydroxyvitamin D which is then metabolised to the metaboilcally more acive 1,25 (OH)2D in the kidneys (calcitriol). Which increases serum calcium concentrations by increasing intestinal absorption of calcium, mobilising calcium from bone and causing calcium reabsorption in the kidney. Calcitonin is secreted by C cells in the thyroid gland, which reduces calcium resorption from the bones thereby lowering calcium concentrations.

Answer 78

It play san important role in calcium metabolism, particularly in malignant conditions such as lymphoma and anal sac adenocarcinoma. PTHrp has a similar structure and function as PTH

Answer 79

Physiologically active ionised calcium 50% Chelated form complexed with lactate, citrate and bicarbonate 10% Protein bound form 40% Since 40% of calcium is bound to protein, an animals calcium concentration should always be interpreted alongside the albumin concentration. hypoalbuminaemia can result in low total calcium concentrations but as the ionised calcium concentration may be within the reference range clinical signs of hypocalcaemia are unlikely to develop.

Answer 80

Total calcium is routinely measured in standard serum or plasma biochemistry profiles. ionised calcium can be measured by ion specific electrodes which can be performed in diagnostic labs or patient side analysers. Both PTH and PTHrp can be measured by two site immunoradiometric assays. usually the sample needs to be harvested in eDTA blood collection tubes. the sample needs to be centrifuged immediately after collection. 25 oHD and 1,25 oH2D can be measured in serum although these assays are not widely available in veterinary clinical practice.

Answer 81

Malignancy, lymphoma, anal sac adenocarcinoma, multiple myeloma, carcinoma eg squamous cell, pulmonary, mammary, nasal, miscellaneous eg thymoma, malignant melanoma, osteosarcomas, hypadrenocorticism, chronic renal failure, primary hyperparathyroidism, hypervitaminosis D, granulomatous disease, idiopathic (cats only), young animal. Many tumours will produce PTHrp which cause hypercalcaemia and in cases of hypervitaminosis D the consumptiion of excessive amounts of vitamin D causes hypercalcaemia.

Answer 82

Most commonly associated with a solitary adenoma of the parathyroid gland resulting in atrophy of the other three glands. Tumour does not respond to usual feedback control so high PTH secretion continues despite high calcium concentrations.

Answer 83

Uncommon disease in older dogs, rare disease in cats, breed predisposition in keeshond, clinical signs typical of hypercalcaemia which include PU/PD, listlessness, weakness, exercise intolerance, inappetance, muscle wasting, urinary tract signs such as dysuria, haematuria due to UTI or uroliths, vomiting, constipation, shivering, stiff gait. Clinical signs of PU PD develop as a result of impaired renal tubular response to anti diuretic hormone and altered renal tubular handling of sodium and chloride. This results in increased production of relatively dilute urine causing compensatory polydipsia. Physical examination paying particular attention to the palpation of all peripheral lymph nodes and the anal sac glands.

Answer 84

By finding the persistently increased calcium concentrations in the presence of an inappropriately increased plasma PTH concentration. Serum phosphate concentrations tend to be below the reference range or normal which means that the risk of soft tissue mieralisation is low. Most parathyroid adenomas can be detected by ultrasound. The diagnosis of primary hyperparahtyroidism may be complicated when the prolonged hypercalcaemia has caused renal damage resulting in an increase in phosphate, urea and creatinine, these biochemical findings are similar to those detected in some cases of CRF. in this scenario, measurement of ionised calcium is advisable since it tends to be normal in CRF but increased in primary hyperparthyroidism.

Answer 85

IV Fluid therapy is advisable in patients with symptomatic hypercalcaemia pending a definitive diagnosis and treatment. Close monitoring of calcium and potassium concs is advisable. The patients should be carefully monitored to allow early detection of adverse effects. Surgical removal of parathyroid mass is advisable in all s ymptomatic cases. The hypercalcaemia typically resolves between 1-3 days post surgery. The unaffected parathyroid glands will be atrophied due to suppression by the autonomous parathyroid adenoma so dogs with primary hyperparathyroidism are at risk of developing hypocalcaemia post surgery.

Answer 86

The vast majority of dogs and cats with CRF have secondary hyperparathyroidism. The pathogenesis of secondary hyperparathyroidism in CRF is multifactorial. progressive renal disease reduces excretion of phosphorous resulting in Hyperphosphataemia and a reciprocal reduction in serum calcium. Hyperphosphataemia and CRF results in reduced production of 1,25 (OH)2D. together these factors drive an increate in PTH secretion. Typical dogs and cats with CRF will have either normal or low total calcium and only a small minority develop hypercalcaemia. Patients may have bone pain, pathological fractures, rubber jaw, facial swelling.

Answer 87

A nutritional disorder that occurs in puppies and kittens which have been fed diets that contain an excessive amount of phosphate and insufficient amounts of calcium. Affected animals have usually been fed mainly meat diets. The lack of dietary calcium leads to increased PTH concentrations which promotes ineral resorption from bone resulting in progressive skeletal demineralisation. clinical signs typically lameness, reulctance to walk. Costochondral junctions and metaphyses may appear swollen. RAdiographs reveal thin cortices, normal growth plates but relatively radio opaque zones in the adjacent metaphyses.

Answer 88

PTH concentrations are typically elevated in dogs with hyperadrenocorticism. However this does not usually leda to significant alterations in plasma calcium concentrations.

Answer 89

Primary hypoparathyroidism, eclampsia, acute pancreatitis, hypoalbuminaemia, acute or chronic renal failure, nutritional secondary hyperparathyroidis, protein loosing enteropathies, ethylene glycol toxicity, miscellaneous eg phosphate containing enemas, overzealous phosphate supplementation.

Answer 90

A rare condition in dos and cats which can occur following immune mediated destruction of the parathyroid glands. Hypoparathyroidism can also develop following removal or damage of parathyroid lands during the surgical treatment of hyperthyroidism in cats. the absence of PTH production leads to a decrease in plasma calcium concentrations and an increase in phosphate concentration.

Answer 91

Female predisposition in immune mediated primary hypothyroidism. breeds most commonly affected are poodles, min schauzers, retrievers, GSDS. typical age of onset is 5 years although condition is recognised in puppies and can develop in much older dogs. Clinical signs tend to be related to sudden onset of neuromuscular or neurological disturbances which may be worsened or initiated by Exercise or excitement. Including nervousness, behavioural changes, focal muscle twitching, facial rubbing, muscle cramps, stiff gait, pyrexia, tetany, seizures.

Answer 92

should be suspected in a dog or cat with persistent hypocalcaemia, hyperphosphtaemia and normal renal function. the diagnosis is confirmed by identifying low plasma PTh concentration with concurrent hypocalcaemia in which other causes of hypocalcaemia have been eliminated. As the PTH protein is liable it is important to ensure transported to the lab frozen.

Answer 93

Involves administation of vitamin D and calcium supplements which is typically divided into acute and chronic treatment phases. the acute phase treatment of patients with hypocalcaemic tetany involves the administration of calcium until clinical signs are controlled. Heart rate should be closely monitored and if bradycardia is observed, iv infusion should be discontinued. response tend to be rapid and tetany usually quickly controlled, once this occurs administration of IV calcium gluconate continued at a lower rate. Once stable - chronic phase of oral treatment should be initatied consisting of oral vitamin D and calcium supplementation. ORal calcium can be administered as calcium gluconate, calcium lactate or calcium carbonate. Monitor calcium concentrations weekly.

Answer 94

The thyroid gland consists of two lobes in dogs and cats. the metabolically active thyroid hormones are L thyroxine (T4) and L triiodothyronine (T3). All circulating T4 is produced by the thyroid gland. only 30% of T3 is produced by the thyroid gland. the majority of T3 is derived from extra thyroidal enzymatic de iodination of T4. More than 99% of T4 or T3 are bound to plasma proteins. Only the non protein bound free hormone is metabolically active and can enter cells to produce a biological effect. Thyroid hormone synthesis and secretion is tightly controlled by pituitary and hypothalamas through the effects of thyrotropin and thyrotropin releasing hormone (TRH). Thyroid hormones are metabolised by progressive deiodination which can convert T4 to T3 and also to biologically inactive reverse T3. Thyroid hormones have a wide range of biological effects. they can increase metabolic rate and in most tissues have positive inotropic and chronotropic effects on the heart. they also have catabolic effects on muscle, stimulate erythropoiesis and regulate cholesterol synthesis and degradation.

Answer 95

lymphocytic thyroiditis and idiopathic follicular atrophy cause almost all cases of primary hypothyroidism in dogs. lymphocytic thyroditis is an immune mediated disorder which results in progressive destruction of the thyroid gland by infiltrating lymphocytes, plasma cells and macrophages, the thyroid follicles are ultimately replaced with fibrous connective tissue. in idiopathic follicular atrophy there is a loss of thyroid parenchyma and replacement by adipose connective tissue. it is unclear if idiopathic follicular atrophy is a separate disease or simply end stage lymphocytic thyroiditis.

Answer 96

Inadequate production of TSH, which causes reduced thyroid hormone production, is an unusual cause of hypothyroidism in dogs. this may be congenital or acquired as a result of pituitary trauma or neoplasia. Tertiary hypothyroidism is extremely rare.

Answer 97

Reduction in metabolic rate, lethargy, weight gain, Exercise intolerance, cold intolerance, alopecia which can be bilaterally symmetrical or patchy, thinning of hair on tail, skin may also bruise more easily, predisposed to bacterial infections of skin, myxoedema a rare dermatological manifestation, reproductive changes include irregular oestrous cycles and anoestrus, galactorrhoea may also occur, low libido, testicular atrophy, myopathy and neuropathy, severe cerebral dysfunction may occur in hypothyroid dogs due to myxoedema coma. SInus brady cardia and weak apex beat, reduced ventricular function, occular changes including corneal lipidosis, uveitis and keratoconjunctivitis sicca.

Answer 98

routine biochemistry and haematology can be helpful screening tests. A mild non regenerative anaemia occurs in 30% of hypothyroid dogs. Fasting hypercholesterolaemia and hypertriglyceridaemia occurs in around 75% of dogs with hypothyroidism.

Answer 99

TT4 bound and free T4 is a very good screening test for thyroid function. A normal T4 concentration demonstrates that dog is euthyroid unless anti T4 antibodies cause a spurious increase in TT4 concentration. A low T4 does not confirm diagnosis of hypothyroidism. Decreased T4 may occur due to a non thyroidal illness. Some drugs can also lower TT4 concentrations, notably trimethoprim potentiated sulphonamides, glucocorticoids and phenobarbitone. Sight hounds eg greyhounds whippets and irish wolfhounds have lower T4 concentrations.

Answer 100

Protein bound hormone acts as a reservoir to maintain concentrations of free hormone in plasma. Since FT4 is not affected by changes in protein concentrations and only free hormones can enter cells, the measurement of FT4 should give a more accurate measurement of thyroid function. FT4 does not always remain in reference range in dogs with sick euthyroid syndrome.

Answer 101

In primary hypothyroidism, negative feedback should result in TSH concentrations increasing above the reference range. Many dogs with hypothyroidism have a TSH concentration within the reference range. In dogs with clinical signs consistent with hypothyroidism low TT4 and high TSH concentrations is highly suggestive of primary hypothryoidism.

Answer 102

Measurement of TT4 before and after TSH administration is a test of thyroid function reserve and is considered to be the most accurate test for the diagnosis of hypothyroidism. Human TSH is most widely used and dogs with primary hypothyroidism will not have a significant increase in TT4 post TSH stimulation. TRH stimulates synthesis and release of TSH which causes production of T4 by the thyroid but is regarded to be less reliable than TSH stimulation test to diagnose hypothyroidism.

Answer 103

Anti thyroglobulin antibodies are found in approximately half of dogs with primary hyptothyroidism. A positive ATA is not diagnostic of abnormal thyroid function because subclinical thyroiditis may be present for a long period of time before clinical hypothyroidism is present.

Answer 104

thyroid ultrasonography -- t ypically smaller and less echogenic in dogs with hypothyroidism, however unhelpful in functional assessment of thyroid gland so is rarely performed unless thyroid neoplasia is a differential diagnosis. Scintigraphy - quantitative measurement of thyroidal uptake of radioactive pertechnetate has high discriminatory power in differentiating hypothyroid and euthyroid dogs. Thyroid biopsy - allow primary causes of hypothyroidism to be distinguished however histological appearance is difficult to correlate to biochemical function and so thyroid biopsies are rarely helpful.

Answer 105

Synthetic L-thyroxine (t4). Tablet formations widely used. Response to therapy assessed 4-8 weeks after initiation of treatment by measurement of TT4 4-6 hours post pill. Dose then adjusted. Treatment will need to be continued for life. Dogs who are stable should be re examined every 3-6 months.

Answer 106

Uncommon. Significant changes in thyroid hormones uncommon with dogs with thyroid tumours. most are euthyroid. some develop hypothyroidism (40%) and 5% develop hyperthyroidism. Most canine thyroid tumours are malignant carcinomas which are locally invasive and frequently metastases. Dogs with thyroid tumours often have a palpably enlarged thyroid gland that is typically firm, assymetrical and non mobile. Clinical signs are variable but can include coughing, dyspnoea, dysphagia, dysphoona, local lymphadenopathy. definitive diagnoss requires incisional or excsional biopsy. Surgery is most approprpiate for dogs without metastases. T4 supplementation required after.

Answer 107

Occurs in older cats, no sex or breed predilection, weight loss, polyphagia, polyuria, polydipsia, intermittent vomitting, altered behaviour including irratibility/aggression, lack of or excessive grooming. Poor body condition and muscle score, palpable goitre, tachycardia, gallop rhythmn,cardiac murmur, tachypnoea, plantigrade stance or cervical ventroflexion from muscle weakness, unkempt coat. increased systolic blood pressure. Erythrocytosis/lymphopenia. Elevated liver enzymes and elevated inorganic phosphate, azotaemia and hypokalaemia.

Answer 108

Elevated total T4. Free T4 measured by equilibriuum dialysis, best assessed in tandem with thyroxine. Less susceptible to concurrent illness. Thyroid stimulating hormone suppressed in hyperthyroidis. The canine TSH assay may be used to assess feline TSH but some cats without hyperthyroidism may have a TSH value below the lower limit of detection. T3 suppression test: thyroxine is assayed before and after administration of doses of T3. In normal cat production of T4 is suppressed by T3. In hyperthyroid cat, T4 production is autonomous, administration of T3 does not suppress thyroxine levels. Scintigraphy: subcutaneous injection of radioactive sodium pertechnetate is taken up by the thyroid gland. comparison of activity between salivary gland and thyroid tissue enables demonstration of enlarged and ectopic thyroid tissue.

Answer 109

medical therapies act by inhibiting the enzyme thyroid peroxidase which is involved in a number of steps in the formation of T4 and T3. Medical management may be used before other forms of therapy as it can stabilise the patient prior to surgery and may also enable identification of underlying renal disease previously masked by hyperthyroidism. it is often perceived to be the cheapest option for management however drug and monitoring costs over several years may be cumulatively more expensive than surgery or I131 therapy. It should be borne in mind that medical management will not treat the adenoma. Over time the adenoma and associated thyroxine production may increase.

Answer 110

Thiamazole is the active drug. Side effects associated with its use occur in up to 18% of cats and include GI signs, haematological abnormalities, hepatopathy, facial pruritis, myasthenia gravis. GI side effects may e avoided by use of drug in a transdermal gel which is applied to the inner pinna of the ear.

Answer 111

Carbimazole is metabolised to methimazole to treat hyperthyroidism. a sustained release product is licensed for cats, facilitating owner compliance by allowin once daily dosing Lack of efficacy is anecdotally reported in some cats. Sometimes this drug may be succesful in cases difficult to control with sustained release carbimazole or in cats that are difficult to medicate as the pills are taken m ore readily in the food than other formulations.

Answer 112

The theory is that by severely restricting dietary iodine the thyroid gland is unable to synthesis thyroxine and T3 this diet has been shown to be efficacious in rendering 90% of hyperthyroid cats euthyroid by 8 weeks, provided the cats are fed exclusively on the diet. It is not suitable for cats with outdoor access and is difficult to implement and in multi cat households. Cats can become bored with the diet and the diet will not work if other iodine sources are available e.g water, medications. Concurrent diseases eg CKD may mean the diet is innapropriate. the adenoma will still continue to grow Good for temporary treatment for stabilisation prior to a more definitive treatment such as surgery or radioactive iodine.

Answer 113

radioactive iodine is typically administered by subcutaneous injection then the cat is held in isolation for a period of time specified by the local authority. previously periods of up to 4 weeks isolation were required but not shorter times are allowed at certain sites. Radioactive iodine is not suitable for some patients with concurrent medical problems eg diabetes mellitus that require medication due to the period of isolation.

Answer 114

Ideally patients should be stabilised medically prior to surgery as the hyperthyroid cat is a higher anaesthetic risk due to the potential for cardiac arrhythmias. As approximately 20% of cats have ectopic thyroid tissue, recurrence is likely in up to 1/5 of patients, even where bilateral thyroidectomy is performed.

Answer 115

It lies at the base of the brain below the hypothalamus within a bony recess. the posterior pituitary - neurohypophysis is a neural outgrowth from the hypothalamus. the anterior pituitary - adenohypophysis - derives from the roof of the mouth. the pars intermedia lies between these and derives from the same origin as adenohypophysis. Almost all secretion from the pituitary gland is controlled by signals from the hypothalamus.

Answer 116

Oxytocin, antidiuretic hormone

Answer 117

Adrenocorticotrophic hormone, thyroid stimulating hormone, follicle stimulating hormone, luteinising hormoone, growth hormone, prolactin.

Answer 118

may be non functioning adenoma, adenocarcinoma or carniopharyngioma- may become space occupying and compress dorsal brain structures causing neurological symptoms. functioning adenoma or adenocarcinoma - clinical signs relate to excessive and Innapropriate hormone production, also can become space occupying.

Answer 119

A rare genetic disorder in the GSD and related breeds. it is extremely rare in other breeds and cats. in the GSD, dwarfism is an autosomal recessive trait due to a mutation int he LHX3 transcription. actor gene. genetic testing is available. Defective development of the pituitary gland leadas to GH, TSH and prolactin defiency and impaird release of FSH & LH. ACTH secretion is adequate. Puppies are skeletally stunted, retain their soft woolly puppy coat, retain their puppy bark, retain their deciduous teeth and have fox like facial features, may show cryptorchidism, anoestrus or persistent oestrus. show progressive lethargy and mental dullness. CT or MRI of pituitary may be small and cystic. IGF1 - very low.

Answer 120

GH three times weekly, long term dosage based on plasma IGF-1 levels. Thyroxine supplementation. Medroxyprogesterone acetate at 3 weeks in tervals and longer term at 6 week intervals stimulate GH production from the mammary gland. Guarded to poor prognosis. Effects on body size depend on groth plates of long bones being open when treatment is started.

Answer 121

A result of excess GH activity which results in soft tissue proliferation and insulin antagonism. GH has direct effects and indirect effects mediated via its stimulation of IGF-1 production from the liver. Feline acromegaly is under recognosed, associated with a functional adenoma of the pituitary gland, it should be considered in any cat with DM resistant to insulin. Most > PUPD, polyphagia, weight gain, lethargy, increased interdental spaces, prognathia of manidble, lion head, increased heart size, heart murmur, congestive cardiac failure, increased size of abdomen. Definitive diagnosis is made on documenting grossly elevated serum IGF-1 levels.

Answer 122

Short term prognosis is fair to good. main problem is insulin resistance and control of diabetes. long acting glargine or protamine zinc insulin supplemented with shorter acting insulin at meal times can address this. cats should be fed a low carbohydrate high protein diet. long term prognosis poor , most develop CHF.

Answer 123

Acromegaly in dogs results from progestogen excess, which induces GH production from the mammary gland. this occurs in intact bitches during Dioestrus or due to exogenous progestogen administration to suppress oestrus. it is not due to pituitary adenomas. Clinical signs similar to cats except DM less consistent. history may reveal recent oestrus or administration of medroxyprogesterone acetate. Panting and laryngeal stridor may occur. Elevated serum IGF1 for definitive diagnosis. Withdraw any progestagen therapy otherwise ovariohysterectomy.

Answer 124

Rare. Central diabetes insipidus - results from a failure in normal synthesis and secretion of ADH by the pituitary gland, can occur congenitally or as an acquired disease. in the latter case it may be due to trauma, inflammation or neoplastic damage to the pituitary gland. Drugs may transiently cause DI. Neprhogenic DI - results from decreased responsiveness of the cells of the renal tubules and collecting ducts to ADH. rarely can be congenital. more commonly due to acquired amage to receptors in the renal cells by tubular necrosis, interstitial nephritis, pyelonephritis, amyloidosis etc.

Answer 125

nephrogenic diabetes insipidus most likely to be secondary to some other underlying disease; hyperadrenocorticism, hyperthyroidism, hypercalcaemia, hypokalaemia, hepatic failure, pyometra, drugs including glucorticoids, vinblastine, amhotericin B. animals with CDI or psychogenic polydipsia are frequently well and show no other signs except PUPD. Those with NDI may show signs of underlying condition.

Answer 126

Full history, routine haematology serum biochem and urinalysis. Hyposthenuria usually detected (SG 1.000-1.006). Assess the unrestricted 24 hour water intake and confirm as >100ml/kg. Modified water deprivation and ADH test - aim is to differentiate between CDI, NDI and PP. In CDI, following DDAVP urine SG will rise and water intake will drop.

Answer 127

Clinical signs are neurologica - weakness, lethargy, seizures, coma. usually brain lesions includig hydrocephalus and neoplasia. Innapropriate secretion of AVP in an animal with unrestricted water intake leads to overhydration, increased extracellular volume and hyponatraemia. Baturesis despite hyponatraemia provides diagnosis, exclude other causes of hyponatraemia and correct the hyponatraemia with fluid restriction. Treatment is moderate water restriction. IF SIADH has developed suddenly and neurological signs are evident emergency management using hypertonic saline may be necessary.

Answer 128

The orbicularis oculi muscle encircles the lid margin and closes the eye. the medial and lateral canthi are stabilised by ligaments. The upper lid is raised centrally by levator palpebrae superioris and medially by levator angularis oculi. a notch in the upper eyelid at the junction of these 2 muslces is common. the upper lid contains mullers muscle. the tarsal glands run at right angles to the lid margins and their openings a re just visible to the naked eye on the lid margin as dots . The dog only has cilia on the upper lid, close to the lid margi. the lids have a good blood supply and numerous mast cells so swell and bleed readily, but heal and resist infections.

Answer 129

Lid margins roll inwards causing hairs or lashes to irritate and potentially abrade the cornea. the pathophysiology involves the relationship between the eyelid and counterpressure from the globe, tone of the orbicularis muscle and size of the palpebral fissure. the commonest site is the lateral lower lid, possibly extending around the lateral canthus to involve the upper lid also. Pain with lacrimation and blepharospasm are always present - assessiing the menace response may trigger an intense blepharospasm. corneal ulceration and pigmentation may also occur.

Answer 130

Excisional correction is not always required in younger patients where there is still considerable anticipated growth, but a temporary procedure is necessary to relieve discomfort - vertical mattress sutures or vertically orientated surgical staples left in place for a few weeks - particularly in sharpei.

Answer 131

Hotz celsus technique - support lid rom inside and make first incision parallel to the lid margin, incision should be only 2-3 mm from the lid margin, leaving just enough room for placement of sutures. start the second incision from one end of the first creating a boat shape with the widest part where the lid is turning in moist and rejoining the other end of the first incision. Close wound edges with simple interrupted sutures.

Answer 132

Loss of tone in the skin of the upper eyelid, combined wth an excessive amount of head skin can result in the lateral upper lid drooping to the extent that hairs and cilia impinge on the cornea, causing discomfort and corneal damage. this is common in ageing cocker spaniels and best treated with a stades procedure as hotz-celsus technique only provides temporary relief.

Answer 133

entropion of the medial lower lid may compress the lower punctum and caniliculis. Caruncular trichiasis and deep medial canthal grooves caused by tight medial cathal ligaments exacerbate the effect of the entropion. common in brachycephalic breeds and toy breeds such as miniature and toy poodle and bichon frise. the cornea is unaffected and the problem is usually cosmetic/

Answer 134

The lower lid turns outward creating a gap between the lid and cornea and exposing the conjunctiva. it is less serious than entropion and usually requires no attention. In severe cases with conjunctivitis or keratitis from chronic exposure, the problem is dealt with by a wedge excision bordering the lateral canthus.

Answer 135

A desirable feature in st bernarnds, newfoundland, clumber spaniels etc in which the lids take ad diamond shape with lateral upper lid entropion and mid lower lid ectropion. Diamond eye is the result of a combination of inadequate support from the lateral canthal ligament, excessive facial skin and abnormally large palpebral fissure. The medial and lateral canthus may not be in the same horizontal plane. these are difficult cases which often require a more elaborate blepharospastic procedure - good candidates for referral.

Answer 136

Some breeds e.g cocker spanie, st bernards, clumber spaniel have excess facial skin that droops downards causing upper lid entropion or extreme ptosis and lower lid ectropion. this can be so severe as to impair vision. in the chow chow and sharpei entropion may be associated with the deposition of subcutaneous fat in the skin folds in entropion in middle age.

Answer 137

macropalpebral fissure with lagopthalmos occurs in brachycephalic breeds, prediposing affected animals to chronic keratitis and progressive pigmentary infiltration. conformational lagopthalmost may be complicated by low tear production, medial canthal entropion or irritation from lacrimal caruncle or nasal fold hairs. Frequent application of ocular lubricants can help but surgical lid shortening provides best longterm solution.

Answer 138

Abnormally positione cilia emerge from the lid margin at or close to the tarsal gland openings. Most dogs with distichiasis show no clinical signs, corneal ulceration has been reported. dogs with convincing evidence of discomfort should be referred for treatment. electrolysis or cryosurgery are commonly performed. the hairs will re grow if plucked.

Answer 139

Usually a single hair emerging through the palpebral conjunctiva a few millimetres from the lid margin at right angles to the cornea. this is a painful condiition. frequently there is a shallow vertically oriented ulcer opposite the emerging cilia. the cilia themselves are hard to see. typically appear a raised pinpoints midway along the lower lid, they occur most often in young dogs. treatment is by excision of a wedge of tissue containing the cilium from the conjunctival surface using a no 11 blade.

Answer 140

Perioccular hairs growing in a normal location may be directed abnormally towards the occular surface, which may cause conjunctivitis and keratitis. trichiasis results from entropion and can be associated with nasal folds, medial canthus and caruncle.

Answer 141

Infection of the meiobomian (Tarsal) glands. unilateral or bilateral, thickening/hyperaemia of the lid margins with swollen and inflamed tarsal glands visible when everting the lid. treat with hot compresses, topical and systemic antibiotics (cefalexin for 2-4 weeks). Culture of expressed gland content may be a useful guide to antibiotic choice in persistent cases.

Answer 142

Glucagon is natural antagonist of insulin. Obesity being an entire female dog, excess progesterone production by luteal cyst, tumour or exogenous progesterone leads to increase GH which leads to diabetes, excess catecholamines, excess oestrogen can antagonize insulin, auto immune disease in dogs, pancreatitis, glucocorticoids, amyloid deposits in cas, sepsis

Answer 143

Hypercholesterolaemia, basal T4 will be low, Thyrotrophin will be high if primary, TSH test will show no increase in thyroid hormone levels in primary condition, antibodies against thyroglobulin.

Answer 144

1) act like space occupying lesion, may have neurological deficits and may interfere with hormone production. 2) pituitary drwarfiism, stunted skeletal growth, retain puppy coat and bark, reproductive failure, retain deciduous teeth. 3) nephrogenic diabetes insipidus - massive PUPD with no ability to concentrate urine. urinate inexcess of >100ml/kg/day.

Endocrinology Flashcards

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