Module 17 Week 2 Flashcards

1
Q

(Investigation of PUPD)

What should be you basic approach to a PUPD patient?

A
  • History
  • Clinical examination
  • Urinalysis
  • Routine Biochem
  • Routine Haematology
  • Daignostic imagaing - radio +US
  • Support the patient
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2
Q

What is osmolality?

A

The number of particles in solution

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3
Q

What is the specific gravity?

A

The number and size of the particles ina solution

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4
Q

What is the concentration of urine when the patient is hyposthenuria?

A

1.000-1.008

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5
Q

What is range of concentration of urine of a isothenuria patient?

A

1.008-1.012

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6
Q

What is the range of urine concentration of urine that is minamally concentrated?

A

1.013 to 1.030

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7
Q

What is the range of urine concentration from a patient that is hyposthenuria?

A

1.030-1.055

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8
Q

What are the causes of PUPD in the dog?

A
  1. Diabetes mellitus
  2. Renal failure
  3. Hyperadrenocorticism
  4. Hypercalcaemia
  5. Neoplasia
  6. Liver failure
  7. Pyogenic foci
  8. Diabetes insipidus
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9
Q

What are the causes of PUPD in the cat?

A
  1. Renal failure
  2. Hyperthyroidism
  3. Diabetes mellitus
  4. Pyogenic foci (CBA)
  5. Liver failure
  6. Neoplasia
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10
Q

What will the clinical history be like of a polydipsia patient?

A
  • changes are as importnat as absolute qunatities = 80ml/kg/day?
  • Dietary and environmental influences
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11
Q

What will the clinical history be like of a polyuria patient?

A
  • Increases in both frequency and volume
  • may lead to urinary incont
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12
Q

What are things to focus on in history if a PUPD patient?

A
  • Behaviour - lethargy, episodic collapse
  • Appetite
  • Skin chnages - alopecia, comedomes
  • GI - vomiting/diarrhoea
  • Discharge
  • medical history such as drugs/urinary obstruction
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13
Q

On clinical examination what should you pay close attention too on a patient that is presenting PUPD?

A
  • Lymph nodes
  • Dermatological
  • Purulent discharges – vulva + prepuce
  • Abdominal palpation – intraabdominal masses
  • Rectal examination – rectal adenocarcinomas can cause PUPD
  • Thyroid palpation (cats) – hyperthyroidism common cause in cats
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14
Q

What does the specific gravity need to be greater than to excludes PUPD?

A

1.035

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15
Q

What does the specific gravity need to be between to excludes diabetes insipidus?

A

1.008 – 1.035

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16
Q

When doing biochem of a patient with PUPD what might mild hyperglycemia be caused by?

A

Stress

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17
Q

When doing biochem of a patient with PUPD what might severe hyperglycemia be caused by?

A

Diabetes mellitus or stress in cats cause why not

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18
Q

When doing biochem of a patient with PUPD what might hypercalcaemia be caused by?

A

lymphomas, anal sac carcinomas causing an increase in para thyroid hormones

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19
Q

When doing biochem of a patient with PUPD what might hypocalcaemia be caused by?

A

This is much more rare but mainly always causes by parathyroid damage

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20
Q

If urea and creatinine are normal, does it rule out renal failure as the cause of PUPD

A

yes

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21
Q

When looking at heam of PUPD patient what does neutrophilia indicate?

A

inflammatory process

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22
Q

When looking at heam of PUPD patient what does neutrophilia with a left shift indicate?

A

pyogenic focus

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23
Q

When looking at heam of PUPD patient what does neutrophilia and lymphopenia indicate?

A

stress leuckogram, hyperadrenocortcicism

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24
Q

What organs should youe xamine in PUPD patient on US?

A

liver, kidneys, spleen, bladder, uterus

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25
Q

What is central cause of primary diabetes insipidus?

A

It is a rare disorder caused by inadequate ADH production due to damage to the posterior pituitary gland.

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26
Q

What things can cause damage to the pituatary gland do cause primary diabetes insipidus?

A
  • Neoplasia
  • Congenital
  • Trauma
  • Inflammation
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27
Q

What is the the nephrogenic cause of primary diabetes insipidus?

A

The ADH is produeced but there are no receptors in the kidneys

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28
Q

What are the indications to perform a water deprivation test?

A
  • Severe PU/PD
  • Normal renal function
  • Not hypercalcaemic
  • Not hyperglycaemia
  • Not hypercortisolaemic
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29
Q

Describe method1 of water deprivation?

A

Phase 1 - water restriction
- 2 x maintenance for one day ?
Phase 2 – water deprivation
- Empty bladder and weigh every 2 hours
- Check urea and creatinine every 2 hours
- Preserve urine and plasma samples

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30
Q

Describe mathod 2 od water deprivation?

A

Phase 1 - water restriction
- 2 x maintenance for one day ?

Phase 2 – water deprivation
- Empty bladder and weigh every 2 hours
- Check urea and creatinine every 2 hours
- Preserve urine and plasma samples

Stop
- Urine S.G. greater than 1.025
- 5% body weight loss
- dog becomes azotaemic or appears depressed

Phase 3 – DDAVP response – synthetic ADH
- 2 – 4 mg DDAVP IV
- monitor urine S.G for 2 – 4 hours
- gradually re-introduce water

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31
Q

If you dehydrate the dog and give it the synthetic ADH and specific gravity doesn’t increase what does this indicate?

A

Indicates a lack of receptors – so nephrogenic and could do a kidney biopsy

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32
Q

If you dehydrate the dog and give it the synthetic ADH and specific increases what does this indicate?

A

This indicates the dogs is not producing its own ADH– so central and could do a MRI

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33
Q

(Approach to the Patient with Suspected Diabetes Mellitus)

Does diabetes affect all aspects of metabolism?

A

Yes

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34
Q

In dogs what dogs are more likely to be seen with diabetes mellitus?

A

Older pancreatic dogs

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35
Q

What things cause resistance to insulin in dogs?

A
  • Cortisol as it fights against the production of insulin
  • obesity
  • progesterone
  • inflammation
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36
Q

How does in a increase in glucose affect insulin?

A

An in crease in glucose causes a decrease in insulin receptors meaning insulin that is there doesnt work.

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37
Q

If glucose levels are reduced for a period of time in the diabetic patient what will happen to insulin receptors?

A

The insulin recepetors may regenerated without increasesing the insulin levels

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38
Q

Describe the signalment of an uncomplicated diabetes mellitus patient

A
  • Any age but more commoner in older animals
  • Can be either sex but females more common in countires that dont neuter
  • any breed but for dogs terriers are common and for cats burmeses
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39
Q

Describe the history you might be presented with for a pateient with uncomplicated diabetes mellitus

A
  • PUPD
  • weight loss
  • Polyphagia
  • excercise intolerance
  • blindness
  • severe hindlimb weakness
  • recent oeastrus in dogs
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40
Q

what are clinical signs of uncomplicated diabetes mellitus

A
  • BAR
  • Thin
  • cataracts
  • neuropathies
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41
Q

How do you confirm diagnosis of uncomplicated diabetes mellitus

A
  • Urinalysis
  • serum biochem
  • glycated blood proteins
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42
Q

How should you treat dogs that have uncompicated diabetes mellitus?

A

They dont have insulin so give insulin (only route injection)

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43
Q

How should you treat cats that have uncompicated diabetes mellitus?

A

Cats may have some insulin, so either give them oral hypoglycaemics (SGLT2 inhibitors) or insulin injections

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44
Q

What are the two requirements for treatment of diabetes mellitus?

A

Owner compliance and veterinary support

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45
Q

What should a daily routine that you make for client include for a patient with diabetes mellitus?

A
  • feeding time
  • Feeding amounts
  • Type of food
  • insulin amount
  • Timing of insulin injections
  • Exercise
  • Enviroment
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46
Q

For obese diabetes mellitus animals what is the energy requirements?

A

70% of the calculated requirement for a target weight

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47
Q

For thin diabetes mellitus animals what is the energy requirements?

A

100% requirement for optimal weight

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48
Q

For normal weight diabetes mellitus animals what is the energy requirements?

A

100% of calculated requiremeny of current weight

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49
Q

What is the current recomentadtion for canine diabetes mellitus?

A

energy = 50-55%
fat = restricted
protein = moderate
carbohydrates = no simple sugars

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50
Q

What are the current recommadations for feline diabetes mellitus?

A

Protein = 50-55%
carbs = no simple and reduced complec CHOs, limited availability to digest starches

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51
Q

What is the stabilisation method for cats with diabetes mellitus?

A
  • Velagliflozin once daily and feed twice daily
  • wait 7 days
  • Then give fructosamines
  • adjust dose after 7 days
  • repeat this till stable
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52
Q

Describe the untreated diabetic cat?

A
  • Glucose toxicity due to no insulin
  • high levels go to glumoerous to kidney tubule
  • most reabsorbed but still enough to go into urine
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53
Q

Which cats should not be selected for SGLT2?

A
  • Previous DKA
  • anorexic, lethargic and dehydration
  • baseline labe works showing evidence of DKA, pancreatitis, liver disease, blood ketones greater than 2.5mmol/L
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54
Q

What are possible adverse reactions to the SGLT2?

A
  • Acute diarrhoea = common, generally short-lasting and self-limiting + Urinary tract infections
  • Weight loss
  • PUPD
  • Mild dehydration
  • Hypersalivation
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55
Q

What are the 4 types of insulin?

A
  • soluble
  • isophane
  • Lente
  • P21
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56
Q

Qhat is the blood glucose stabilisation method for dogs?

A

0.3iu/kg lente insulin q12hr
Feed twice daily
!!wait 3 days!!
Then adjust glucose on basis of average morning urine test
!!repaeat this until stable or more than 2iu/kg!!

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57
Q

If there is no glucose after 3days of 0.3iu/kg lente insulin what should you do to the insulin?

A

Reduce by 5%

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58
Q

If there is less than 1% glucose after 3days of 0.3iu/kg lente insulin what should you do to the insulin?

A

No change

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59
Q

If there is more than 2% glucose after 3days of 0.3iu/kg lente insulin what should you do to the insulin?

A

increase by 5%

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60
Q

What is stable in a diabetic patient?

A

Control of clinical signs and glucose in urine at least once every 5 days

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61
Q

What does more than 2iu/kg suggest about the pateient?

A

They are insulin resistant and should increase dose anyways but further investigate.

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62
Q

What is the second stabilisation method for diabetic dogs and cats?

A

0.3-0.5 iu/kg lente insulin q12hrs
Feed and inject twice daily
!!wait 3 days!!
take a blood glucose curve and adjust dose
!!wait 3 days!!
repeat until stale

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63
Q

Describe how you manage a diabetic patient in surgery.

A

On the day of surgery
= 1/2 insulin dose and no food
= operate early in the day
= dextrose infusion IV
= Feed 1/2 normal food as soon as able too
= monitor blood glucose

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64
Q

What are complications of diabetes?

A
  • failure to stabilise
  • cataracts in dogs
  • ketoacidosis
  • hypoglycaemia
  • neuropathies in cats
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65
Q

(Hyperadrenocorticism in dogs and cats)

What are the two different stypes of spontaneous causes of hyperadrenocorticism?

A
  • Pituitary dependent = This is likely to be a pituatary tumour that causes high levels of cortisol that may flucuate, leading to a big overlap in cortisol concentration, which leads to inhibition of insulin action so glusise rises along with lipid metabolism, protein metabolism, retention of water, and increasing in ADH
  • Adrenal dependent = adrenal tumour
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66
Q

How do you diagnose a patient with hyperadrenocorticism?

A
  • Clinical signs
  • Screening tests
  • Specific tests to confirm and identify the cause
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67
Q

Qhat are the clinical signs of hyperadrenocorticism?

A
  • PUPD
  • Derm changes - symmetrical alopecia
  • abdominal distension
  • polyphagia
  • lethargy
  • resp signs
  • muscle weakness
  • obesity
  • Haemostatic abnormalities
  • reproductive problems
  • neuro signs
  • mytonia
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68
Q

Why might a a dog or cat get abdominal distension as clinical sign of hyperadrenocorticism?

A
  • Due to dogs undergoing fat redistribution which will go into abdominal cavity
  • can be secondary to muscle weakness
  • Hepataic lipidosis
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69
Q

What haemostatic abnormalities can be seen clinically with a patient with hyperadrenocorticism?

A
  • Bruising due to no elastic recoil in the vessels
  • Poor wound healing due to thin skin
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70
Q

What reproductive problems might you see as a clinical sign of hyperadrenocortiscism?

A
  • Females won’t have seasons due to glucocorticoids
  • males will have small soft testicles, penis gets smaller due to glucocorticoids
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71
Q

On serum biochem of a patient with hyperadrenocorticism, what would the results look like?

A
  • Increased AP
  • Increased cholesterol
  • Increased triglycerides
  • Increased glucose
  • Increased ALT, GGT, AST
  • Increased bile salts
  • Decreased urea and creatinine
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72
Q

On the haematology of a patient with hyperadrenocorticism, what would the results look like?

A

Stress leucogram
- neutrophilia
- lymphopenia
- eosinopenia
- monocytosis
- erythrocytosis

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73
Q

On the urinalysis of a patient with hyperadrenocorticism, what would the results look like?

A
  • Low SG
  • Proteinuria
  • Urinary tract infection
  • Glucosuria – over into diabetes melitus
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74
Q

What changes do you expect to see on radiographs of a hyperadrenocorticism patient?

A
  • adrenal masses
  • thoracic masses
  • intercurrent disease
  • large liver
  • fat
  • pot belly
  • bladder still full after urinating
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75
Q

What is the priniciple of the ACTH stimulation test?

A

ACTH stimulates adrenal cortex to maximally secrete cortisol

76
Q

What is the method of the ACTH stimulation test?

A
  • Take blood sample for basal cortisol
  • administer 0.2mg CTH IV or IM
  • Take a second blood sample 0.5-2hr later
77
Q

What are problems with ACTH stim test?

A
  • Only 50% of dogs with AD-HAC will be indentified
  • Only 85% of dogs with PD-HAC will be identified
78
Q

What is the principle of the low dose Dexamethasone suppression test?

A
  • DXM suppresses ACTH secretion
  • rapid recovery or failure to suppress in HAC
79
Q

What is the method of the the low dose DXM suppression test?

A
  • Take blood sample for basal cortisol
  • Administer 0.015mg/kg DXM IV
  • take blood smaples 3 and 8 hrs later
80
Q

What are the problems with the low DXM suppression test?

A
  • Its time consuming
  • Stress-induced cortisol interferes
81
Q

Should the low DXM suppression test be you 1st or 2nd choice test?

A

“nd as it really rules out cushings rather than ruling it in due to its high sensitivity but becuase of this sensitivity compared to the ACTH it can give a lot more false positives

82
Q

What is the difference in ACTH assay results for pituatary or adrenal Hydroadrenalcortiscism?

A
  • PD - HAC results in increased ACTH concentrations
  • AD - HAC results in suppression of ACTH secretion
83
Q

What is the normal diameter of the adrenal gland?

A

less than 7mm

84
Q

What are the treatment options for Pituatary dervived Hyperadrenocorticism?

A

Trilostane (steriod enzyme inhibitor)

Others
- Mitotane (adrenolytic)
- Ketoconazole (steroid enzyme inhibitor)
- l-Deprenyl (MAO-type B inhibitor)

Hypophysectomy (specialist neurosurgeon)

85
Q

What are the treatment options for canine adrenal dervived hyperadrenocortiscism?

A
  • Trilostane
  • Mitotane
  • Unilateral adrenalectomy (ICU)
86
Q

What is the effect of trilostane?

A

Get a block in steroid synthesis

87
Q

What do you have to be careful with when using trilostane?

A

Even though the steroid synthesis block is temporary, it affects other steroids, so if you overdose, you can get aldosterone deficiency as well as cortisol.

88
Q

What should the initial dose of trilostane be?

A

2mg/kg q 24hr orally

89
Q

What adjustments can be made to the dose of trilostane?

A

Can be put up to twice daily

90
Q

What are mild complications of trilostane?

A
  • electrolyte abnormalities
  • diarrhoea, lethargy, anorexia and vomiting
91
Q

What are the serious complications of trilostane?

A
  • Hypoadrenocorticism
  • some can die
92
Q

(Approach to patient and hypoadrenocorticism)

What are the causes of metabolic collapse?

A
  • Diabetic ketoacidosis
  • Hypoglycaemia
  • Hyper/hypokalaemia
  • Hyper/hypocalcaemia
  • Hyper/hyponatraemia
  • Hepatic encephalopathy
  • Pheochromocytoma
  • Hyperviscocosity syndrome
  • Thyrotoxicosis
  • Myxoedema coma
93
Q

What should your initial lab tests be for a collapsed patient?

A
  • glucose
  • calcium
  • electrolytes
94
Q

What is fainting called?

A

syncope and it is an acute apisodic flaccid collapse relating to the cardiovascular system

95
Q

What is a fit called?

A

seizure and it is an acute, central, tonic colinic collapse relating to the neurological system

96
Q

What clinical signs can collapsed patients present with?

A
  • pallor
  • cyanosis
  • dyspnoea
  • distended veins
  • resp - noises/crackles, arrhythmias, muffled thoracic sounds
97
Q

If normal clinical exam should you do labs?

98
Q

What is the most common thing to see on biochem of a patient that has collapsed?

A

Hypokalaemia = less than 3 mmol/l

99
Q

What is hypokalaemia a very common cause off?

A
  • intestinal loss - vomiting, diarrhoea
  • CRF (cats)
  • CHronic diuresis
100
Q

What are complications of metabolic collapse?

A
  • pacreatitis
  • Acute renal failure
  • UTI
  • Bacteraemia/Septicaemia
  • GI haemorrhage
  • Pulmonary thromboembolism
  • disseminated intravascular coagulation
101
Q

Describe how hypoadrenocorticism (addisons disease) works

A

Hypoadrenocorticism (Addison’s disease) results from adrenal gland failure, leading to deficient cortisol and often aldosterone production. This disrupts glucose metabolism, vascular tone, and stress response due to cortisol deficiency, while aldosterone loss causes sodium wasting, hyperkalemia, dehydration, and hypotension.

102
Q

What are the causes of hypoadrenocorticism?

A
  • Immune mediated destruction
  • Mitotane/trilostane induced
  • Haemorrhage
  • Infarction
  • Infection
  • Tumour
103
Q

What are the clinical findings for acute hypoadrenocoticism?

A
  • severe dehydration
  • anorexia
  • vomiting
  • collaspe
  • bradycardia
  • haemorrhagic gastroenteritis
104
Q

What are complications of acute hypoadrenocorticism?

A
  • Acute renal failure
  • GI haemorrhage
  • Pancreatitis
  • Pulmonary thromboembolism
  • Disemmenated intravacular coagulation
105
Q

To diagnose Addisons what should your red cell haematology loook like?

A

Anaemia for GI losses, Bone marroe suppresion and IMHA

106
Q

What can mask the anaemia in addison patients?

A

Dehydration can mask the severity of the anaemia

107
Q

To diagnose Addisons what can your white cell haematology loook like?

A

Reverse stress leucogram’ = low WBC, neutropenia, lymphocytosis, eosinophilia BUT most dogs normal

108
Q

When diagnosing using your serum biochem what might you see in an addisons patient?

A
  • Na and potassium effected
  • Urea and creatinine increased by 80%
  • Ca increased by 30%
  • can also be effected = glucose, albumin, cholesterol, liver enzymes, PH decreased 10-30%
109
Q

What causes hyperkalaemia?

A
  • red blood cell lysis
  • failure of excretion
  • rhabdomyolysis
110
Q

What causes hyponatraemia (low Na)?

A
  • excessive loss
  • overhydration
  • lab errors, lipaemia
111
Q

When taking a patients history what is a similarity between hAC and Renal failure?

A

Acute episode after peiod of illness

112
Q

When performing a clinial exam what is a similar finding between hAC and Renal failure?

A

Thin, dehydrated and may or may not have collapsed

113
Q

When looking at a patients lab results what is a similarity between hAC and Renal failure?

A

Renal azotaemia
- Increased urea and creatinine = effect of GI haemorrhage
- Urine specific gravity 1.007 to 1.030

Electrolyte abnormalities
- High potassium = acute ARF and urinary obstruction
- Low sodium = Polyuric phase of acute ARF

114
Q

What are the key issues in an acute Addisonian crisis?

A

Hypovolaemia, sodium deficit, hyperkalaemia.

115
Q

What IV fluid is used to treat hypovolaemia and sodium deficit in an Addisonian crisis?

A

0.9% saline.

116
Q

What glucocorticoid is given in an acute Addisonian crisis?

A

IV hydrocortisone 100 mg bolus, followed by continuous infusion or 50 mg IV every 6 hours.

117
Q

How is hyperkalaemia managed in an Addisonian crisis?

A

Calcium gluconate, insulin-dextrose infusion, or sodium bicarbonate (if severe).

118
Q

What are the key components of chronic Addison’s disease treatment?

A

Mineralocorticoid replacement, glucocorticoid replacement, dietary changes.

119
Q

What medication is used for mineralocorticoid replacement in chronic Addison’s disease?

A

Fludrocortisone.

120
Q

What dietary changes are recommended for chronic Addison’s disease?

A

Increased salt intake, adequate hydration, and monitoring for hypoglycaemi

121
Q

(small animla obesity)

What are consequences of obesity?

A
  1. predisposition of other diseases
  2. decreased quality of life
  3. effect on lifespan
  4. deceased physical activity
122
Q

Is the lifespan od a dogs life effected by obesity?

A

Yes shortened

123
Q

What are the dietary risk factors for obesity?

A
  • number of meals and snacks
  • table scraps and fresh meat
  • present when owners preparing food
  • feeding ad lib
124
Q

what things about the animal itself are risk factors for obesity?

A
  • breed - labs, CKC, Spaniel, beagle
  • middle age
  • neutered
  • female dogs
  • male cats
125
Q

What are the behavioiral risk factors for obesity?

A
  • over-humanisation
  • feeding behaviour
  • Owner not interested in prevention
  • Close owner-pet relationship
  • Misperception
  • Lack of education about BCS and BW
  • Lack of education about pet food labels
  • Imprecision when feeding
126
Q

What lifecycles factor poses risk for obesity in dogs?

A
  • indoor lifestyle
  • inactivity
127
Q

What owner factors pose risk of dogs developing obesity?

A
  • older owners
  • human obesity
  • female gender
  • lower income
  • close owner-pet relationship
128
Q

What endocrine factors pose risk on dogs developing obesity?

A
  • hypothyroidism
  • hyperadrencorticism
129
Q

How can obesity be prevented?

A
  • Discussion of proper feeding and BCS with owners
  • Quantify and measure food for pets
  • Achieve ideal BCS
  • Discussion at time of spay/neutering
  • Lifelong weight management and obesity prevention
  • Yearly wellness visits, noting BCS and BW
130
Q

What are the 6 treatments for obesity?

A
  1. Appropriate caloric restriction
  2. Diet selection
  3. Exercise
  4. Modification of owner behaviour
  5. Continued monitoring
  6. Pharmaceutical therapy
131
Q

How do you work out the maintenance energy requirement for dogs?

A

95 x bodyweight (to the power of 0.75)

132
Q

How do you work out the maintenance energy requirement for cats?

A

Maintenance energy requirement = 77.6 x bodyweight0.711

133
Q

What is the energy requirement for weight loss in cats

A

Energy requirement for weight loss = 42 x ideal bodyweight0.711

134
Q

Describe why you should use a purpose-formulated diet for obses patients?

A
  • Restricted in fat and caloric density
  • Supplemented in protein and micronutrients
  • High in fibre and protein thats best
135
Q

What do dirlotapide/miratapide do?

A

They reduce appeitie and fat absorption in dogs by reducing dietary lipids

136
Q

What side effects are there of dirlotapide/miratapide?

A

vomiting, loose stools, lethargy and anorexia

137
Q

(Hypothyroidism)

What effects do thyroid hormones have?

A
  • They increase the metabolic rate
  • They can cause cretinism in infant growth
  • They activate anagen for hair growth
138
Q

Describe the synthesis of thyroid hormones

A
  • There is two big storage areas and a conversion phase before you get any activity
  • T4 release iscontrolled by TSH release from pituitary
  • As TSH goes up T4 goes down and opposite way (neg feedback)
  • T3 is detructed T4 thats not functional. T3 is produced when you dont been T4
139
Q

What are some physiological aspects that influence thyroid hormone levels?

A
  • age
  • breed
  • sex
  • time of day
  • time of year
  • obesity
  • stavation
140
Q

What are some therapeutics that influence the levels/production of thyroid hormones?

A
  • steroids
  • potential sulphonamides
  • diuretics
  • sedatives/anaesthetics
141
Q

What are primary causes of hypothyroidism?

A
  • lymphocytic thyroiditis
  • idiopathic atrophy
  • congenitial but rare
142
Q

What are secondary causes of hypothyroidism?

A
  • TSH failure (eg pituatary tumour)
143
Q

Wha breeds can have congenital hypothyroidism?

A

Boxer, gaint schnauzer

144
Q

What are signs od congenital hypothyroidism?

A
  • Dysproportionate Dwarfism
  • Cretinism
  • Hypothyroidism
145
Q

What breeds, age and sexes are more likely to suffer with primary hypothyroidsism?

A
  • Dysproportionate dwarfism
  • Cretinism
  • Hypothyroidism
146
Q

What is a common marker of lymphocytic thyroiditis?

A

thyroglobulin autoantibodies

147
Q

What are clinical signs of hypothyroidism?

A

lethargy
obesity
cold intolerance
hypothermia

148
Q

What Deermatalogical clinical signs does hypothyroidism cause?

A
  • symmetrical, non-purtitic alopecia
  • seborrhea
  • hyperpigmentation
  • myxoeadema
149
Q

Does hypothyroidsism cause Bradycardia?

A

Yes - small ORS complexes, weak apex beats

150
Q

Why might a hypothyroid patient have pale mm?

A

non-regenatibe normochromic anaemia

151
Q

What female repro abnormalities may be seen in the hypothyroid patient?

A
  • infertility, abortion
  • inappropriate galactorrhoea
152
Q

What neurological abnormalitites may be seen in the hypothyroidism patient?

A
  • LMN disease
  • peripheral vestibular syndrome
  • Laryngeal paralysis
  • megaoesophagus
153
Q

What ocular abnormalities might you see in the hypothyroid patient

A
  • lipid effusion into aqueous humour
  • cornal lipidosis
  • chronic uveitis
  • glaucoma
  • keratoconjunctivitis sicca
154
Q

What clinical pthology helps confirm hypothyroidism as the diagnosis?

A
  • cholesterol - most will have high
  • triglycerides
  • PCV
  • CK
155
Q

What is the normal level of T4?

A

more than 35 nmol/l

156
Q

What T4 level indicates hypothyroid or sick euthhyroid?

A

0-14nmol/l

157
Q

Will TSH go up or down with hypothydroidism?

A

up as T4 supressed

158
Q

Is TSH or TRH stimulation test gold standard?

A

TSH is as TRH is less reliable

159
Q

Is thyrogobulin antibodies precenec a good indicator that dog has hypothyroidism?

A

Yes its common to see them, they are not identifies in other diseases and rare in healthy dogs

160
Q

So overall what is the clinical diagnosis of canine hypothyroidism?

A

low T4 and high TSH
obesity, alopecia

161
Q

Decribe the therapy for hypothyroidism?

A

Sodium levothyroxine at 0.02mg/kg once daily or 0.01mg/kg twice daily

162
Q

(Hyperthyroidism)

What are the causes of hyperthyroidism?

A

Thyroid tumours - adenomatous hyperplasia/adenomas and adenocarcinomas

163
Q

What can cause these thyroid tumours?

A
  • age
  • If there is long term iodine levels in diet
  • goitrogens
  • genetics
164
Q

On clinical examination of a hyperthyroidism cat how would they present?

A
  • Thin
  • Dehydrated
  • Poor hair coat
  • tachycardic
  • cardiac murmours
  • thyroid nodule
165
Q

What can weight loss be caused by in cats?

A
  • hyperthyroidism
  • chronic renal failure
  • diabetes
  • cardiomyopathy
  • neoplasia
  • inflammatory bowel disease
  • chronic hepatic disease
  • chronic pancreatitis
166
Q

Why might you see behavioural changes in older cats?

A
  • painful diseases
  • metabolic disease
  • neurological diseases
167
Q

T/F if you T4 levels above 60 you have you diagnosis of hyperthyroidism?

168
Q

What should the enviroment be like for a hyperthyroid cat?

A
  • No dogs
  • experienced nurses
  • hiding places
169
Q

What should the diet of a hyperthyroid cats be like?

A

High energy, low fat diet little and often

170
Q

What is the risks with blood sampling hyperthyroid cats?

A

Haematomas

171
Q

When treating the hyperthyroid cat why is a diet with very low iodine suggested?

A

It restricts T4 production analogous to methinmazole

172
Q

What dose of methimazole should be used in the hyperthyroid cat?

A

One tablet (2.5mg) twice a day and can double if needed

173
Q

What dose of carbimazole should be given to the hyperthyroid cat?

A

10-15mg one daily

174
Q

What are mild side effects seen with methimazole and carbimazole?

A

Vomiting and anorexia, and some transient haematological abnormalities

175
Q

What are the severe side effects of methimazole and carbimazole?

A
  • self excoriation
  • hepatotoxicity
  • thrombocytopenia
176
Q

T/F 70% of hyperthyroidism is a bilateral disease and on surgery both need to be removed?

A

Yes if they are both enlarged

177
Q

Shoud you expect recurrence if only one enlarged?

178
Q

What are the complications of thyroid removal surgery?

A
  • haemorrhage
  • hypocalcaemia
  • voice changes
179
Q

Describe the difference between feline hyperthyroidism and canine hypothyroidism

A
  • In Feline hyperthyroidism, they lose weight, whereas in canine hypothyroidism, they gain weight.
  • In feline hyperthyroidism, activity increases, and in canine hypothyroidism, activity is decreased.
  • In feline hyperthyroidism, the coat is starry and in canine hypothyroidism it is alopeciac
  • In feline hyperthyroidism, the heart rate is fast, whereas in canine hypothyroidism, the heart rate is slow.
  • In feline hyperthyroidism GI signs are common and in canine hypothyroidism GI signs are rare.
  • In feline hyperthyroidism the T4 levels are increased whereas in canine hypothyroidism T4 is decreased and TSH increased.
180
Q

(Urinary Tract Problems and PU/PD in the Horse)

Describe the nromal urination process of a the male horse

A
  • stretched lordotic posture
  • elevated tail head
  • penis out of sheath
  • abdominal effort
  • brisk stream (not spray)
  • short bursts at the end
  • may grunt
181
Q

Describe the normal uriniation in the mare

A
  • stretched lordotic posture
  • elevated tail head
  • urine stream clear of legs
  • increased frequency in oestrus
182
Q

How much water per Kg of Bwt per day is required in the horse?

183
Q

how much water is required per kg of dry matter consumed per day in the horse?

184
Q

how much water do polydipsic horses intake per day?

A

more than 100ml/kg per day

185
Q

How muhc urine output should there be in horses?

A

15-30ml/kg/day

186
Q

What is you differentials for PUPD in horses?

A
  • Psychogenic PUPD due to boredom/Change of enviroment/Feed
  • Secondary renal medullary washout which is the inability to concentrate urine due to loss of sodium in renal medulla which is becuase of the increase in water intake which can happen from psychogenic PUPD
  • Cushings syndrome which is a direct inhibition of ADH
  • Chronic renal failure

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