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Endocrine Diseases Flashcards

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1
Q

what is the most common endocrine condition in cats?

A

hyperthyroidism

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2
Q

where in the world is hyperthyroidism seen?

A

everywhere

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3
Q

why is feline hyperthyroidism being recognised much more commonly now?

A

awareness is better
older cats that are living longer
may be becoming more common

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4
Q

is there evidence that feline hyperthyroidism is auto-immune?

A

no, unlike in humans

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5
Q

what are 95% of feline hyperthyroidism cases caused by?

A

benign adenomatous hyperplasia

adenoma pf thyroid tissues

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6
Q

what does benign adenomatous hyperplasia / adenoma of thyroid tissues cause?

A

spontaneous secretion of thyroid hormones

escaping control of hypothalamus and pituitary gland

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7
Q

what are <5% of feline hyperthyroidism cases caused by?

A

adenocarcinoma (malignant)

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8
Q

is feline hyperthyroidism more commonly bilateral or unilateral?

A

2/3 bilateral

1/3 unilateral

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9
Q

where is ectopic thyroid tissue most commonly seen?

A

mediasteinum

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10
Q

how many cases of feline hyperthyroidism have ectopic thyroid tissue?

A

5%

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11
Q

what are the potential causes of feline hyperthyroidism?

A

nutritional factors
environmental factors
genetic factors
circulating factors

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12
Q

what are the nutritional factors which cause feline hyperthyroidism?

A

high levels of iodine in diet

presence of goitrogens

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13
Q

what cats are much less likely to have feline hyperthyroidism?

A

siamese or himalayan (10x less likely)

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14
Q

what circulating factors can increase the risk of feline hyperthyroidism?

A

thyroid growth stimulating immunoglobulins in the blood stream

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15
Q

what are the risk factors for feline hyperthyroidism?

A

regular use of flea sprays or powders
indoor cats
reported exposure to lawn herbicides, fertilisers and pesticides
cats fed mainly canned foods

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16
Q

what is the signalment of feline hyperthyroidism?

A

middle aged to elderly cats (10-13 years)

no sex predeliction

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17
Q

what does the severity of signs of feline hyperthyroidism depend on?

A

duration of disease

presence of concurrent diseases

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18
Q

what are the effects on the body of raised thyroid hormones?

A 
increased: 
metabolic rate
cardiac output
HR
BP
GI motility
CNS activity

decreased:
sleep
body weight

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19
Q

what does increased GI motility due to increased thyroid hormone mean for feline hyperthyroidism patients?

A

may have vomiting and diarrhoea

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20
Q

what are the major clinical signs of feline hyperthyroidism?

A 
palpable enlarged lymph nodes
weight loss
polyphagia
hyperactive for their age
PUPD
tachycardia
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21
Q

what are the minor clinical signs of feline hyperthyroidism?

A 
lethargy
intermittent anorexia
voice changes
muscle weakness / tremors
CHF
heat intolerance
mild pyrexia
dyspnoea / tachypnoea
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22
Q

what is apathetic feline hyperthyroidism?

A

type of hyperthyroidism seen in a small number of patients (<10%) who likely have underlying comorbidity

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23
Q

in how may patients is apathetic feline hyperthyroidism seen?

A

<10%%

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24
Q

what are the signs of apathetic feline hyperthyroidism?

A

lethargy
inappetance
weight loss
obtundation

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25
Q

what is apathetic feline hyperthyroidism likely reflecting?

A

underlying comorbidity

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26
Q

what abnormalities are often present in patients with apathetic feline hyperthyroidism?

A

cardiac

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27
Q

what effect can thyroid hormones have on cardiac disease?

A

often worsen

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28
Q

how should feline hyperthyroidism patients be handled?

A

cat friendly
hands off
should be allowed to acclimatise and settle

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29
Q

what parameters should be closely monitored in feline hyperthyroidism patients?

A

RR

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30
Q

what may be provided to feline hyperthyroidism patients on arrival to veterinary practice?

A

O2 therapy if tachypnoeic

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31
Q

why are feline hyperthyroidism patients often stressed?

A

high thyroid hormones cause agitation

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32
Q

what can feline hyperthyroidism patients be given before travel to calm them?

A

50mg Gabapentin 2 hours before travel

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33
Q

how is feline hyperthyroidism diagnosed?

A

compatible clinical signs
screening tests
confirmatory diagnostic tests

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34
Q

how can thyroid glands be palpated?

A

lift head with one hand and extend neck

use other hand thumb and index finger to feel all the way from the larynx to the thoracic inlet

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35
Q

what are screening tests used for when diagnosing feline hyperthyroidism?

A

baseline health

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36
Q

what screening tests are used during feline hyperthyroidism diagnosis?

A

haematology
biochemistry
urinalysis
BP

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37
Q

what is often seen on biochemistry in a cat with feline hyperthyroidism?

A

elevated liver enzymes (mild to moderate)

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38
Q

what can be shown by biochemistry when testing for feline hyperthyroidism?

A

CKD

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39
Q

what will urinalysis show in a feline hyperthyroidism patient?

A

if concurrent CKD

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40
Q

what sudden issue can severe feline hyperthyroidism patients get?

A

sudden blindness due to hypertension

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41
Q

what is the gold standard confirmatory diagnostic test for feline hyperthyroidism?

A

serum total thyroxine (T4) - TT4

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42
Q

how elevated is total T4 in most hyperthyroid cases?

A

> 50-60 nmol/L

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43
Q

what total T4 level may be seen in some feline hyperthyroidism patients?

A

fluctuating

high normal

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44
Q

why may high normal total T4 levels be seen in some feline hyperthyroidism patients?

A

early disease

presence of non-thyroidal illness that lowers T4 prodution

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45
Q

what are the 4 main treatment options for feline hyperthyroidism?

A

medical management with antithyroid drugs
iodine restricted diet
thyroidectomy
radioactive iodine treatment

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46
Q

which of the treatment options for feline hyperthyroidism are curative?

A

thyroidectomy

radioactive iodine treatment

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47
Q

what should be tried first to treat feline hyperthyroidism?

A

medical management

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48
Q

what should be assessed before undertaking any irreversible feline hyperthyroidism treatment?

A

renal function when patient is euthyroid

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49
Q

what must be done before any surgery/GA if the patient has feline hyperthyroidism?

A

patient should be stabilised

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50
Q

what is the purpose of anti-thyroid drugs?

A

block thyroid production

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51
Q

what is the main drug used to treat feline hyperthyroidism?

A

methimazole

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52
Q

how often should Methimazole be given?

A

BID

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53
Q

in what form can Methimazole be given?

A

tablets
transdermal gel
oral liquid

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54
Q

where is transdermal Methimazole applied?

A

pinna

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55
Q

what tablets are available to treat feline hyperthyroidism that can be given once a day?

A

slow-release carbimazole tablets

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56
Q

what is the role of slow release anti-thyroid tablets?

A

converted in the body to methimazole which is then utilised

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57
Q

who should be careful when handling anti-thyroid drugs?

A

pregnant women

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58
Q

when is a feline hyperthyroidism patient normally euthyroid after anti-thyroid drugs?

A

<2-3 weeks

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59
Q

when should total T4 be checked following anti-thyroid treatment?

A

2-3 weeks

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60
Q

what tests should be run in the first 1-3 months following anti-thyroid drugs?

A

CBC and biochem

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61
Q

what is the purpose of CBC and biochem tests in the first 3 months after beginning treatment for feline hyperthyroidism?

A

monitor for side effects

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62
Q

what may anti-thyroid drugs be used for in the short term?

A

stabilisation prior to more curative therapy

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63
Q

what are the advantages of anti-thyroid drugs?

A 
readily available
rapidly effective
inexpensive
practical
no GA or hospitalisation
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64
Q

what are the disadvantages of anti-thyroid drugs?

A

lifelong
long term resistance
compliance is crucial
side-effects

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65
Q

what are the minor, common, transient side effects of anti-thyroid drugs?

A

vomiting
anorexia
lethargy

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66
Q

what are the major, rare and persistent side effects of anti-thyroid drugs?

A 
persistent GI signs
blood dyscrasias (leukopenia, anaemia and thrombocytopenia)
dermatitis 
hepatopathy
lymphadenomegaly
myasthenia gravis
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67
Q

what sort of dermatitis is commonly seen as a major side effect of anti-thyroid drugs?

A

facial excoriation

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68
Q

what is lymphadenomegaly?

A

enlarged lymph nodes

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69
Q

what should happen if major side effects of anti-thyroid drugs are seen?

A

stop treatment

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70
Q

how can diet be used to control feline hyperthyroidism?

A

iodine restricted diet fed to reduce T4 production

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71
Q

what iodine restricted food is available?

A

Hills y/d

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72
Q

what can be fed alongside and iodine restricted diet?

A

must be fed as sole food - no treats

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73
Q

how quickly can feline hyperthyroidism patients be euthyroid when fed an iodine restricted diet?

A

within 3 weeks

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74
Q

how long must be feline hyperthyroidism patient be on the iodine restricted diet for?

A

lifelong

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75
Q

when is an iodine restricted diet less effective / unsuitable?

A

for severe hyperthyroid cats

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76
Q

what are the main pre-surgical considerations for treatment of feline hyperthyroidism?

A

systemic effects of feline hyperthyroidism
cardiac disease
hypertension
other diseases

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77
Q

what should happen to a feline hyperthyroidism patient prior to surgery?

A

stabilisation

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78
Q

what is removed during thyroidectomy?

A

one or both of the thyroid glands

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79
Q

what must be preserved during a thyroidectomy?

A

parathyroid tissue

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80
Q

why must the parathyroid tissue be preserved in thyroidectomy?

A

to avoid post op complications such as hypocalcaemia

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81
Q

why could hypocalcaemia occur following thyroidectomy?

A

PTH is essential for calcium homeostasis

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82
Q

in what % of patients does thyroidectomy achieve euthyroidism?

A

> 90%

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83
Q

when is euthyroidism achieved following thyroidectomy?

A

24-48 hours

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84
Q

what structures must you be careful of when performing thyroidectomy?

A

parathyroid

vagus nerves

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85
Q

is is possible to save the parathyroid gland if feline hyperthyroidism is advanced?

A

not usually due to enlargement of glands

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86
Q

what are the advantages of thyroidectomy?

A

curative
rapidly effective
short hospitalisation period

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87
Q

what are the disadvantages of thyroidectomy?

A 
GA
skill required to save parathyroid
location
recurrance
cost
complications
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88
Q

what are the complications associated with thyroidectomy?

A

damage or removal of parathyroid tissue leading to post op hypoparathyroidism
damage to recurrent laryngeal nerve
damage to sympathetic trunk
possible recurrence of feline hyperthyroidism if only unilateral thyroidectomy

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89
Q

is laryngeal paralysis a common complication of thyroidectomy?

A

no

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90
Q

what is a condition that can be caused by damage to the sympathetic trunk during thyroidectomy?

A

Horner’s syndrome - nictating membrane prolapse and myosis

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91
Q

when does iatrogenic hypoparathyroidism occur?

A

usually after bilateral thyroidectomy

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92
Q

how long does iatrogenic hypoparathyroidism last for?

A

usually transient

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93
Q

what will cause resolution of iatrogenic hypoparathyroidism?

A

recovery of glands/restored function of ectopic tissues

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94
Q

how long does it take to recover from iatrogenic hypoparathyroidism?

A

weks to months

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95
Q

when are clinical signs of iatrogenic hypoparathyroidism seen?

A

withi 2-3 days

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96
Q

what are the signs of iatrogenic hypoparathyroidism?

A 
due to hypocalcaemia
inappetance
weakness 
tremors
ptyalism
pawing at face
progression to tetany
seizures
coma
death
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97
Q

what should be monitored if concerned about iatrogenic hypoparathyroidism or there has been bilateral thyroidectomy?

A

serum calcium twice a day

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98
Q

how should iatrogenic hypoparathyroidism be treated?

A

IV 10% calcium gluconate slowly (10-20 mins)

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99
Q

what is the initial bolus of calcium gluconate to treat iatrogenic hypoparathyroidism followed by?

A

CRI

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100
Q

what fluids should be avoided when giving calcium gluconate?

A

bicarbonate, lactate or phosphate containing fluids as will precipitate calcium
not Hartmann’s

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101
Q

can calcium gluconate be given SC?

A

no

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102
Q

why can calcium gluconate not be given SC?

A

skin sloughs

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103
Q

what should patients receiving calcium gluconate be monitored for?

A

ECG for arrhythmia and bradycardia

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104
Q

what should happen once the patient with iatrogenic hypoparathyroidism is stabilised on IV calcium gluconate?

A

oral therapy ASAP of calcium and vitamin D

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105
Q

how is the patient switched from IV calcium gluconate to oral therapy?

A

elemental calcium in divided doses to wean off IV

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106
Q

how are iatrogenic hypoparathyroidism cats managed orally once IV calcium gluconate has stopped?

A

oral vitamin D only

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107
Q

can iatrogenic hypoparathyroidism patients be weaned off all treatment?

A

yes - eventually

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108
Q

how long does oral therapy for iatrogenic hypoparathyroidism take to work?

A

1-3 days

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109
Q

what is the gold standard treatment for feline hyperthyroidism?

A

radioiodine treatment

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110
Q

how is radioiodine treatment administered?

A

systemically

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111
Q

where does radioiodine therapy target?

A

excessive T4 producing cells in the thyroid

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112
Q

what do beta particles of radioiodine cause?

A

cell death

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113
Q

how long must the cat be isolated for following radioiodine treatment?

A

1-2 weeks post injection

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114
Q

why does the cat need to be isolated for 1-2 weeks following radioiodine injection?

A

gamma rays they emit are dangerous

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115
Q

how many centres are available for radioiodine treatment in the UK?

A

15 (including Bris)

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116
Q

what are he advantages of radioactive iodine treatment for feline hyperthyroidism?

A 
gold standard
curative
simple procedure
higher dose to treat adrenocarcinoma
no GA
cost
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117
Q

what are the disadvantages of radioactive iodine treatment?

A 
limited availability
isolation period
irreversible 
may take some time to achieve euthyroid
very rarely iatrogenic hypothyroidism
cost
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118
Q

what is the risk associated with feline hyperthyroidism and CKD?

A

hyperthyroidism may mask CKD and so treatment may unmask it

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119
Q

how much can treatment of feline hyperthyroidism change CKD level?

A

maximum of one IRIS stage

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120
Q

what must be considered about feline hyperthyroidism and CKD?

A

medical management of feline hyperthyroidism before curative treatment to see effect on kidneys
reassess once euthyroid

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121
Q

what may not prevent definitive feline hyperthyroidism treatment relating to CKD?

A

unmasking of mild azotemia through thyroid medical management

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122
Q

when should feline hyperthyroidism patients be monitored irrespective of treatment regime?

A

6 monthly check ups if stable

soone if not

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123
Q

what are you monitoring for when having feline hyperthyroidism check ups?

A

recurrence
hypertension
CKD (urea, creatinine, BP, urinalysis)

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124
Q

what is the prognosis of feline hyperthyroidism dependent on?

A

severity / presence of concurrent disease (especially heart disease)

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125
Q

what cats have excellent feline hyperthyroidism prognosis?

A

uncomplicated with curative treatment

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126
Q

what are the main types of canine thyroid neoplasia?

A

carcinomas more common

adenomas usually incidental

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127
Q

what sort of masses are canine thyroid neoplasia?

A

large, solid, palapabel

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128
Q

what type of tumor is canine thyroid neoplasia?

A

locally invasive

some metastatic

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129
Q

what are most canine thyroid neoplasia patients thyroid levels like?

A

most euthyroid or hypothyroid

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130
Q

what percentage of canine thyroid neoplasia patients are hyperthyroid?

A

10%

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131
Q

what is the signalment of canine thyroid neoplasia?

A

10 years

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132
Q

what are the signs of canine thyroid neoplasia?

A

mass in ventral neck

may have cough or dyspnoea due to pressure on trachea

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133
Q

how is canine thyroid neoplasia diagnosed?

A

histopathology of mass
FNA
surgery usually needed to confirm

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134
Q

why must care be taken when gaining histopathology of a mass to diagnose canine thyroid neoplasia?

A

very vasular area

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135
Q

what is the issue with FNA of canine thyroid neoplasia?

A

often blood contaminated sample

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136
Q

how is canine thyroid neoplasia treated?

A

surgical removal

chemotherapy or radiation to follow

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137
Q

why is radioactive iodine treatment for canine thyroid neoplasia not often performed?

A

high doses required

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138
Q

what does the prognosis of canine thyroid neoplasia depend on?

A

size
local invasion
functional status
histological diagnosis of carcinoma or adenoma

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139
Q

what is the prognosis for dogs with large, invasive canine thyroid neoplasia masses?

A

guarded to poor

6-24 months if aggressive treatment

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140
Q

when is the prognosis for canine thyroid neoplasia excellent?

A

surgical removal of adenomas

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141
Q

when is the prognosis for canine thyroid neoplasia good?

A

removal of small, well circumcised carcinomas

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142
Q

what is the most common endocrine disorder in dogs?

A

canine hypothyroidism

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143
Q

why is canine hypothyroidism likely to be over-diagnosed?

A

due to tests used

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144
Q

where are the thyroid glands located?

A

lateral to the proximal tracheal rings

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145
Q

what hormones are produced by the thyroid?

A

thyroxine - T4

triiodythyronine - T3

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146
Q

what are thyroid hormones formed from?

A

tyrosine amino acids

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147
Q

what enzyme causes the oxidation of iodine?

A

thyroid peroxidase

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148
Q

what is the main thyroid hormone that is secreted?

A

T4

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149
Q

where is 99% of T4 found in circulation?

A

bound to proteins

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150
Q

what is the role of unbound T4 (fT4)?

A

biologically active and exerts a negative feedback on TSH production

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151
Q

what happens to fT4 within the cell?

A

diodinated to form either T3 or reverse T3

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152
Q

what does T3 bind to in the cell?

A

nuclear receptor

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153
Q

how does the HPA control T4 and T3 release?

A

hypothalamus releases TRH
causes pituitary gland to release TSH
this stimulates the thyroid glands to release T4, T3 and rT3

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154
Q

how is T4, T3 release controlled?

A

T4 and T3 negatively feedback on hypothalamus and pituitary to stop TRH and TSH release

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155
Q

where does primary hypothyroidism occur?

A

at the level of the thyroid gland

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156
Q

what is the most common type of canine hypothyroidism?

A

primary

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157
Q

what are the 2 causes of primary canine hypothyroidism?

A

lymphocytic thyroiditis

thyroid atrophy

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158
Q

what is lymphocytic thyroiditis caused by?

A

immune mediated destructive process
infiltration of lymphocytes and other WBC
thyroid tissue is replaced by fibrous connective tissue

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159
Q

when do clinical signs of lymphocytic thyroiditis occur?

A

when 75% of gland is destroyed

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160
Q

what causes thyroid atrophy?

A

degenerative process
progressive replacement of thyroid tissue with adipose and connective tissue
possibly due to end stage lymphocytic thyroiditis

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161
Q

what are the causes of secondary hypothyroidism?

A

pituitary hypoplasia - congenital (disproportionate dwarfism) or dysfunction (neoplasia)

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162
Q

is secondary canine hypothyroidism common?

A

rare

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163
Q

what is the most common cause of secondary hypothyroidism?

A

suppression of TSH secretion by exogenous glucocorticoid administration (steroids) and hyperadrenocorticism (cushings)

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164
Q

what is the mean age of diagnosis of canine hypothyroidism?

A

7 years

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165
Q

what animals tend to develop canine hypothyroidism sooner?

A

those breeds predisposed to lymphocytic thyroiditis

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166
Q

what breeds are predisposed to lymphocytic thyroiditis?

A

english setter
golden retriever
cocker spaniel
boxer

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167
Q

what are the areas of the body which may exhibit signs of canine hypothyroidism?

A 
decreased metabolic rate
dermatologic
repro
cardiac
neuromuscular
occular
GI
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168
Q

what are the clinical signs of canine hypothyroidism linked to decreased metabolic rate?

A

weight gain
lethargy
inactivity

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169
Q

what are the clinical signs of canine hypothyroidism linked to dermatologic signs?

A

endocrine alopecia
rat tail
tragic facial expression hair in telogen phase
mixoedema

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170
Q

what is endocrine alopecia?

A

symmetrical hair loss

non puretic

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171
Q

what is mixodema?

A

thickened skin

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172
Q

what are the clinical signs of canine hypothyroidism linked to the reproductive system?

A 
persistent anoestrus
weak/silent oestrus
prolonged oestral bleeding
inappropriate lactation
no effect on males
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173
Q

what are the clinical signs of canine hypothyroidism linked to the CVS?

A

bradycardia
association with atrial fibrilation
some reports of atrial thromboembolysm

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174
Q

what cardiac condition may canine hypothyroidism be linked to?

A

DCM

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175
Q

what is the mechanism of neuromuscular disease linked to canine hypothyroidism?

A

accumulation of mucopolysaccharides leading to impaired transport along axons and arthrosclerosis

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176
Q

what are the clinical signs of canine hypothyroidism linked to neuromuscular diseases?

A

megaoesophagus
laryngeal paralysis
peripheral vestibular syndrome (head tilt)
facial nerve paralysis

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177
Q

are neuromuscular diseases usually linked to canine hypothyroidism?

A

more likely concurrent disorders than causal effect of hypothyroidism

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178
Q

what is myxoedema coma?

A

life threatening potential consequence of hypothyroidism

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179
Q

what are the signs of myxoedema coma?

A 
profound mental dullness
weakness
hypothermia
bradycardia
hypotension
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180
Q

what usually leads to a hypothyroid patient developing myxoedema coma?

A

precipitating factor e.g. surgery, heart failure or sepsis

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181
Q

what are the clinical signs of canine hypothyroidism linked to the eyes?

A

corneal lipid deposits due do hyperlipidaemia
ulcreation
uveitis

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182
Q

what are the clinical signs of canine hypothyroidism linked to the GI tract?

A

diarrhoea due to bacterial overgrowth

constipation due to reduced peristalsis

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183
Q

how is canine hypothyroidism diagnosed?

A

appropriate history and clinical signs
haematology and biochemistry
specific thyroid testing

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184
Q

what signs are typically seen on the biochemistry and haematology of a canine hypothyroidism patient?

A

mild non-regenerative anaemia (normocytic and normochromic)
hypercholesterolaemia
hypertriglycerideaemia

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185
Q

what effect do thyroid hormones have on lipids?

A

stimulate synthesis, mobilisation and degradation (no T4 no degradation of lipids)

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186
Q

what thyroid abnormalities do you expect in a canine hypothyroidism patient?

A 
low T4
high TSH (no inhibition)
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187
Q

what is total T4 useful for in canine hypothyroidism?

A

initial screeing test

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188
Q

why is total T4 not used as a definitive canine hypothyroidism diagnosis?

A

thyroglobulin antibodies can falsely increase TT4

TT4 decreases with age, breed, non thyroidal illnesses and drug therapy (steroids)

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189
Q

when are thyroglobulin antibodies produced?

A

in lymphocytic thyroiditis

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190
Q

what other tests apart from TT4 can be used to diagnose canine hypothyroidism?

A

canine TSH

anti-thyroglobulin antibodies

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191
Q

why is TSH increased in canine hypothyroidism cases?

A

lack of negative feedback

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192
Q

why does the canine TSH test have moderate sensitivity?

A

low TSH in central hypothyroidism (pituitary cause)

low TSH if there is corticosteroid therapy

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193
Q

what is canine TSH level not affected by?

A

largely unaffected by non-thyroidial illness or drugs

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194
Q

when may TSH be elevated in euthyroid dogs?

A

if recovering from NTI

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195
Q

what is a positive anti-thyroglobulin antibody test indicative of?

A

lymphocytic thyroiditis

196
Q

what does anti-thyroglobulin antibodies give no information about?

A

thyroid function

197
Q

when can anti-thyroglobulin antibodies be present?

A

long before hypothyroidism

198
Q

how us canine hypothyroidism treated?

A

synthetic T4 - prohormone for active T3

199
Q

what is the main drug given for canine hypothyroidism?

A

sodium levothyroxine

200
Q

how often is sodium levothyroxine given?

A

SID or divided BID

201
Q

what effect does food have on bioavailability of sodium levothyroxine?

A

halves bioavailability

202
Q

what is crucial when giving sodium levothyroxine to treat hypothyroidism?

A

consistency with dosing times and monitoring times

203
Q

how should dogs with cardiac disease, DM or hypoadrenocorticism be dosed with sodium levothyroxine?

A

start with 25% of dose and titrate up

204
Q

when should sodium levothyroxine effect on hypothyroidism be evaluated?

A

6-8 weeks after first administration

205
Q

when is peak sodium levothyroxine concentration?

A

3-5 hours post pill

206
Q

what is the half life of sodium levothyroxine?

A

9-15 hours

207
Q

why does dose and timing need to be tailored to the dog when giving sodium levothyroxine?

A

absorption and metabolism vary between dogs

208
Q

what are the formulations of sodium levothyroxine available?

A

Soloxine - tablets
Thyroforon - flavored tablets
Leventa - liquid

209
Q

what should be observed when monitoring the canine hypothyroid patient?

A

clinical response
TT4
fT4
cTSH

210
Q

when should monitoring blood tests for canine hypothyroidism be carried out

A

6-8 weeks after starting treatment

2-4 weeks after dose altered

211
Q

when should TT4 be measured when monitoring canine hypothyroidism that is being treated?

A

6 hours post pill SID

4-6 hours BID

212
Q

when should fT4 be measured during canine hypothyroidism monitoring?

A

if chronic prednisolone admin

213
Q

what is the aim for T4 and TSH values in canine hypothyroidism patients when receiving treatment

A

TT4 upper half of reference

TSH normal

214
Q

does hyperthyroidism often occur after treatment for canine hypothyroidism?

A

rare

215
Q

what are the complications of canine hypothyroidism treatment?

A

thyrotoxicosis

myxoedema coma

216
Q

what is thyrotoxicosis secondary to?

A

drug overdose

217
Q

what are the clinical signs of thyrotoxicosis?

A 
panting
anxiety/aggression
PUPD
weight loss
polyphagia 
(signs of hyperthyroidism)
218
Q

how is myxoedema coma treated?

A 
supportive care of other conditions
IV levothyroxine (hard to get hold of)
219
Q

what is the prognosis for canine hypothyroidism?

A

good - adult dogs with primary

guarded if seocndary

220
Q

what are the 3 areas of the adrenal cortex?

A

zona glomerulosa
zone fasiculata
zona reticularis

221
Q

what is produced in the zona glomerulosa?

A

mineralocorticoids

222
Q

what is produced in the zona fasiculata and zone reticularis?

A

glucocorticoids and sex hormones

223
Q

what is produced in the adrenal medulla?

A

catecholamines

224
Q

what is the main mineralocorticoid produced?

A

aldosterone

225
Q

where is the major site of aldosterone action?

A

cells in distal convoluted tubule and collecting duct (renal tubules)

226
Q

what is the action of aldosterone?

A

resorption of H2O and NaCl

secretion of K+ and H+

227
Q

what electrolyte is aldosterone more important for regulating?

A

K+ more than Na+

228
Q

what is the most important stimuli of aldosterone production?

A

hyperkalaemia

increased angiotensin II

229
Q

how does the HPA axis stimulate secretion of cortisol and aldosterone?

A

hypothalamus produces CRH
pituitary gland is then stimulated to produce ACTH
stimulates adrenal glands to produce cortisol and aldosterone

230
Q

what organ is affected by primary hypoadrenocorticism?

A

adrenal glands

231
Q

what is caused by primary hypoadrenocorticism?

A

addison’s disease

lack of cortisol and aldosterone

232
Q

what is caused by secondary hypoadrenocorticism?

A

lack of cortisol

233
Q

what organ is affected by secondary hypoadrenocorticism?

A

pituitary gland

234
Q

what is the most common type of hypoadrenocorticism?

A

primary

235
Q

what happens as a result of primary hypoadrenocorticism?

A

lack of glucocorticoids and minuralocorticoids

236
Q

what happens in atypical hypoadrenocorticism?

A

lack of glucocorticoids but normal mineralocorticoids

237
Q

what is the suspected cause of primary hypoadrenocorticism?

A

immune mediated destruction of the adrenal cortex

238
Q

what is the cause of secondary hypoadrenocorticism?

A

pituitary gland is cause

neoplasia, inflammation, infection, infarct, iatrogenic (hypophysectomy)

239
Q

what deficiency does secondary hypoadrenocorticism cause?

A

glucocorticoid only as aldosterone is regulated by RAAS as well and so will still be released

240
Q

why may there be neurological signs with secondary hypoadrenocorticism?

A

brain lesion present

241
Q

what are the typical dogs that get hypoadrenocorticism?

A

young/middle aged

female

242
Q

what breeds are predisposed to hypoadrenocorticism?

A

standard poodles
bearded collie
novia scotia duck toller
great dane

243
Q

what are the clinical signs of hypoadrenocorticism?

A

vague waxing and waning history

244
Q

what are the signs caused by lack of cortisol?

A

weakness
vomiting
diarrhoea
anorexia

245
Q

when are signs of lack of cortisol due to hypoadrenocorticism exacerbated?

A

at times of stress

246
Q

what are the signs of lack of aldosterone?

A

PUPD to to low Na

not in atypical hypoadrenocorticism

247
Q

what is a severe complication of hypoadrenocorticism?

A

Addisonian crisis - emergancy

248
Q

what are the signs of Addisonian crisis?

A 
collapse
severe dehydration
hypovolaemia (low sodium)
pre-renal azotemia (dehydration)
cardiac arrhythmias (hyperkalaemia - bradycardia)
249
Q

how is hypoadrenocorticism diagnosed?

A 
compatible history and clinical signs
haematology
biochemistry
urinalysis
basal cortisol
250
Q

what is found on the haematology results of a patient with hypoadrenocorticism?

A

non-regenerative anaemia

absence of stress leukogram (which should be seen in a sick patient)

251
Q

what will the leukogram of a hypoadrenocorticism patient show?

A

decreased neutrophils
increased lymphocytes
increased eosinophils

252
Q

what is seen on the biochemistry results of hypoadrenocorticism patients?

A 
hyperkalaemia and hypernatraemia
hypercalcaemia
pre-renal azotemia
acidaemia (vomiting)
hypoglycaemia
increased liver enzymes
decreased albumin and cholesterol
253
Q

what sodium / potassium ratio indicates hypoadrenocorticism?

A

<27 - due to lack of mineralocorticoids

254
Q

what is pre-renal azotemia in hypoadrenocorticism due to?

A

hypovolaemia and dehydration

255
Q

what is hypoglycaemia in hypoadrenocorticism due to?

A

lack of glucocorticoids

256
Q

why does hypoadrenocorticism lead to increased liver enzymes?

A

poor perfusion

257
Q

why is decreased albumin and cholesterol seen in hypoadrenocorticism?

A

GI insult from lack of glucocorticoids affecting vascular flow to tract

258
Q

what are the urinalysis findings of a patient with hypoadrenocorticism?

A

variable USG due to low Na and high Ca2+

could be dilute due to low Na or concentrated due to dehydration

259
Q

what is basal cortisol used to test?

A

exclusion of hypoadrenocorticism

260
Q

what basal cortisol level indicates hypoadrenocorticism is unlikely?

A

> 55 nmol/L - cortisol is being stored

261
Q

what basal cortisol level indicates an ACTH stim is necessary?

A

<55 nmol/L

262
Q

what is used to confirm the hypoadrenocorticism diagnosis?

A

ACTH stim

263
Q

what are the levels of pre and post ACTH cortisol in hypoadrenocorticism patients?

A

both below 20 nmol/L

264
Q

what can affect the results of ACTH stim?

A

exogenous glucocorticoid will cross react and be measured

previous glucocorticoid treatment will suppress adrenal cortisol production

265
Q

how is an ACTH stim performed?

A

cortisol level tested before and 1hr after ACTH administration
collect serum for basal cortisol level
inject 5 mg/kg of ACTH IV
collect second sample 1 hr later

266
Q

when is cortisol measured in an ACTH stim?

A

before and 1 hour after ACTH admin

267
Q

what will the results of an ACTH stim be in a hypoadrenocorticism patient?

A

pre and post ACTH cortisol will be the same rather than increasing

268
Q

how is an Addisonian crisis treated?

A

IV 0.9% NaCl at shock dose (60-90ml/kg)
hydrocortisone or dexmathasone IV (or CRI)
correction of hypernatraemia
treatment of hypoglycaemia and hyperkalaemia as needed

269
Q

what si the shock does of 0.9% NaCl required for Addisonian crisis?

A

60-90 ml/kg

270
Q

what are hydrocortisone and dexmathasone used for?

A

replacement glucocorticoids and mineralocorticoids

271
Q

why must hypernatraemia be treated?

A

can cause brain oedema

272
Q

how should hyponatraemia be treated?

A

slowly

273
Q

how can hypoglycaemia and hyperkalaemia be treated?

A

glucose and/or insulin

calcium gluconate to protect myocytes

274
Q

what is the most commonly used long term glucocorticoid therapy for hypoadrenocorticism?

A

prednisolone

275
Q

what is the dose of prednisolone required to treat hypoadrenocorticism?

A

0.5 mg/kg PO q12hrs initially

then 0.1 or 0.2 mg/kg PO q12-24hr

276
Q

what must the dose of prednisolone be tailored to do?

A

limit clinical signs of polyphagia, PUPD and weight gain

277
Q

when should glucocorticoid dose be increased?

A

if signs of lethargy, vomiting and diarrhoea

double dose if stressful event expected

278
Q

what drug is used as mineralocorticoid long term therapy?

A

desoxycortone pivalate

279
Q

what is the benefit of Zycortal mineralocorticoid therapy?

A

able to manage GC need separately from MC

280
Q

what is the starting dose for Zycortal (MC)?

A

1.5 mg/kg SQ

281
Q

how can glucocorticoid levels be monitored?

A

ask for evidence of lethargy, vomiting, diarrhoea which would prompt increase in dose as indicate low levels

282
Q

how are mineralocorticoid levels tested?

A

blood test to measure Na/K ration 10-14 days after DOCP admin to see peak effect
then measure Na/K 25/30 days after DOCP admin to see duration of
DOCP

283
Q

what will the measurement of peak DOCP effect determine?

A

next mg/kg dose

284
Q

what Na/K ratio will lead to dose increase of mineralocorticoids?

A

> 32 or K below reference range = 10% dose increase

285
Q

what should happen if Na/K ratio is below 32 or K is in the lower half of the reference ranges 25-30 days after DOCP administration?

A

delay injection by 5 days and repeat the same process

286
Q

what was the drug used preciously to treat hypoadrenocorticism?

A

fludrocortisone

287
Q

why is fludrocortisone less commonly used?

A

required check of Na/K weekly initially

dose requirements would often increase

288
Q

what is the prognosis of hypoadrenocorticism?

A

good if well managed on lifelong medication

289
Q

what should dogs with atypical Addison’s be monitored for?

A

development of mineralocorticoid deficiency which may develop in the future

290
Q

what is canine hyperadrenocorticism also known as?

A

Cushing’s disease

291
Q

what does hyperadrenocorticism occur due to?

A

excessive production of cortisol as a consequence of pituitary or adrenal tumors

292
Q

how is cortisol produced?

A

hypothalamus releases CRH
pituitary releases ACTH
adrenal glands release cortisol
cortisol provides negative feedback to hypothalamus and pituitary

293
Q

what are the 3 types of hyperadrenocorticism?

A

pituitary dependent
adrenal dependent
iatrogenic- admin of glucocorticoids

294
Q

what is the most common type of hyperadrenocorticism?

A

pituitary dependant (secondary)

295
Q

what is caused by pituitary dependent hyperadrenocorticism (PDH)?

A

overproduction of ACTH due to adenoma of pars distalis
loss of negative feedback from cortisol leading to bilateral adrenal hyperplasia
macroadenoma in some leading to CNS signs

296
Q

what animals are predisposed to hyperadrenocorticism?

A

daschunds, poodles, small terriers
no sex predisposition
middle/old aged dogs

297
Q

what is adrenal dependent hyperadrenocorticism caused by?

A

adenomas / carcinomas leading to the production of excess cortisol which suppresses ACTH production
leads to atrophy of other gland

298
Q

in what breed / type is adrenal dependent hyperadrenocorticism more common?

A

female

large breeds

299
Q

what is iatrogenic hyperadrenocorticism caused by?

A

suppression of CRH and ACTH production due to excessive glucocorticoids
bilateral adrenal atrophy

300
Q

what are the major clinical signs of hyperadrenocorticism?

A 
abdominal distension
hepatomegaly
lethargy and exercise intolerance
panting
PUPD (nocturia and incontinence as a result)
polyphagia
skin changes (thinning and erythema)
alopecia (symmetrical and non-pruretic)
301
Q

how is polydipsia defined in dogs?

A

> 100ml/kg/day

302
Q

how is polyuria defined in dogs?

A

> 50 ml/kg/day

303
Q

what are the complications associated with hyperadrenocorticism?

A

progression of major signs
DM from insulin resistance due to excess cortisol
pulmonary thromboembolism
neurologic signs - obtunded, blindness and seizure
pancreatitis due to poor fat management
secondary infections as immune system suppressed
hypertension
glomerulopathy and proteinuria - direct effect of cortisol in kidney

304
Q

what are the main initial general screening tests used for hyperadrenocorticism?

A

haematology
biochemistry
urinalysis

305
Q

what are the screening tests used for the HPA axis?

A

ACTH stim
low-dose dexamethasone suppression test
urine cortisol:creatinine ratio

306
Q

is there a single test for hyperadrenocorticism that is 100% accurate?

A

no

307
Q

define test sensitivity

A

probability of positive result if patient is affected (if high sensitivity and negative result it can be ruled out)

308
Q

define test specificity

A

probability of a negative result if the patient is not affected (high specificity, positive result, rule in)

309
Q

what is seen on the haematology of a patient with hyperadrenocorticism?

A

mid erthyrocytosis and thrombocytosis - effect of cortisol on bone marrow
stress/steroid leukogram - opposite of Addison’s

310
Q

what is seen on the biochemistry screening tests of a patient with hyperadrenocorticism?

A

increased ALKP (5-40x upper end of reference)
increased ALT
hypercholesterolaemia and hypertriglyceraemia due to lipolysis
hyperglycaemia due to insulin antagonism (resistance)
increased bile acids

311
Q

what urine specific gravity is seen in patients with hyperadrenocorticism?

A

variable - <1.015

312
Q

what is found on urinalysis of patients with hyperadrenocorticism?

A 
dilute urine
\+/- proteinuria
\+/- glycosuria
possible UTI
calcium oxalate crystals due to over excretion of calcium
313
Q

what is essential before pursuing diagnosis of hyperadrenocorticism?

A

some historical and clinical signs are apparent

no recent steroid administration

314
Q

what will the ACTH stimulation test of a patient with PDH show?

A

excessive response to administration of ACTH

315
Q

what will the ACTH stimulation show in a normal dog?

A

small cortisol increase

316
Q

what is shown post ACTH stimulation in a patient with iatrogenic hyperadrenocorticism?

A

cortisol remains at pre-admin levels as they are unable to stimulate cortisol release

317
Q

what are the advantages of ACTH stimulation tests to diagnose hyperadrenocorticism?

A

more specific than LDDST and less affected by non-adrenal illness
good first line test (if positive can be confident of illness)
useful for iatrogenic disease
used to monitor treatment response

318
Q

what are the disadvantages of ACTH stimulation tests to diagnose hyperadrenocorticism?

A

less sensitive than LDDST

doesn’t distinguish PDH from ADH

319
Q

how is low dose dexamathasone suppression test (LDDST) performed?

A

collect serum for basal cortisol
inject low dose (may need to dilute for small patients) IV dexamathasone
collect serum sample 4 and 8 hours after injection

320
Q

what is the LDDST result of a patient with ADH and 40% of those with PDH?

A

flat line - no response and cortisol remains high

321
Q

what is the LDDST result in 30% of PDH patients?

A

escape V pattern - cortisol drops at 4 hours but has climbed again by 8

322
Q

what is the response of a normal dog to LDDST?

A

smooth drop in cortisol - lowest at 8 hours

323
Q

what is the advantage of LDDST to test for hyperadrenocorticism?

A

more sensitive that ACTH (excellent sensitivity)

can distinguish PDH from ADH (escape V)

324
Q

what is the disadvantage of LDDST for diagnosis of hyperadrenocorticism?

A

care with false positives
affected by non-adrenal illnesses
should not be used as sole diagnostic test
not useful for iatrogenic disease

325
Q

how is urine cortisol:creatinine ratio test for hyperadrenocorticism performed?

A

urine sample collected at home
2 pooled morning samples
several days following a stressful event

326
Q

what are the advantages of urine cortisol:creatinine ratio to diagnose hyperadrenocorticism?

A

high sensitivity

useful to exclude hyperadrenocorticism (if normal Cushing’s is very unlikely)

327
Q

what is the disadvantage of urine cortisol:creatinine ratio to diagnose hyperadrenocorticism?

A

not very specific - false positives common

328
Q

what tests can be used to differentiate PDH from ADH (adrenal tumors)?

A

LDDST
high dose dexamethasone suppression test (HDDST)
imaging
endogenous ACTH conc

329
Q

what dose of dexamethasone is given for HDDST?

A

0.1mg

330
Q

what will HDDST results look like for a patient with PDH?

A

escape V

331
Q

what will the HDDST results look like for a patient with ADH and 15% with PDH?

A

no suppression of cortisol (flat line)

332
Q

what will HDDST look like in a normal dog?

A

drop smoothly - lowest 8hrs after dex injection

333
Q

what can an abdominal ultrasound be used for in hyperadrenocorticism diagnosis?

A

looking st symmetry and enlargement of adrenal glands

334
Q

what will be seen on abdominal ultrasound of a patient with PDH?

A

symmetrical adrenal glands

enlarged or normal

335
Q

what will be seen on abdominal ultrasound of ADH / AT?

A

asymmetrical adrenal glands

336
Q

what is MRI used for in hyperadrenocorticism diagnosis?

A

evaluation of pituitary gland and adrenal glands

337
Q

what is found in 90% of PD patients?

A

brain mass

338
Q

what types of adenoma can be seen with PDH?

A

microadenoma

macroadenoma

339
Q

what are endogenous ACTH levels like in PDH patients?

A

high (>45 pm/ml)

340
Q

what is endogenous ACTH like in ADH patients?

A

undetectable / low

341
Q

what is the issue with using endogenous (animals own) ACTH to diagnose whether hyperadrenocorticism is PDH or ADH?

A

concentrations of ACTH between 10-45 pg/ml are unhelpful

lab may not be able to manage sample

342
Q

what are the considerations for treatment of hyperadrenocorticism?

A

difficult to diagnose in some cases
progressive disease so could wait and retest if uncertain
treatment is expensive

343
Q

when should hyperadrenocorticism only be treated?

A

if there is a high index of suspicion from history and clinical signs, haematology and biochem and specific tests

344
Q

how is PDH treated?

A

medically with trilostane (Vetoryl)
surgically - hypophesectomy or bilateral adrenalectomy
radiation therapy

345
Q

what does trilostane do?

A

blocks adrenal cortisol production

346
Q

how is trilostane administered?

A

PO with food
SID or dose split to BID
lower dose than formulary suggests given first

347
Q

how is response of patient to trilostane treatment for hyperadrenocorticism monitored?

A

clinical signs and ACTH stim or pre-pill cortisol

348
Q

what are the side effects of trilostane?

A

uncommon but life threatening
GI signs
hypoadrenocorticism
bilateral adrenal necrosis

349
Q

what is involved with hypophysectomy?

A

complete surgical removal of the pituitary gland accessed via the soft palate

350
Q

what is the only potential curative (~75%) option for dogs with PDH?

A

hypophysectomy

351
Q

what is the long term outcome of successful hypophysectomy?

A

3 year survival in 70%

352
Q

what is needed after hypophysectomy?

A

lifelong hormonal supplementation

  • glucocoticoids
  • thyroxine

transient diabetes may insipidus may be seen post op but DDAVP treatment for this can usually be discontinued

353
Q

where is radiation therapy for PDH available?

A

refurral only

354
Q

what is the benefit of radiation therapy for PDH treatment?

A

linear accellerator photon irradiation may be effective in reducing the size of macroadenomas or eliminating neurological signs

355
Q

what concurrent treatment is often required with radiation to treat PDH?

A

trilostane as reduction in ACTH secretion is variable and often not marked

356
Q

what is radiation treatment of PDH particularly useful for?

A

large pituitary macroadenomas where surgery would be contraindicated

357
Q

what is the mean survival time for dogs with PDH treated with radiation therapy?

A

25 months

358
Q

how is ADH treated?

A

adrenalectomy - gold standard

medical therapy

359
Q

what is required before adrenalectomy to treat ADH?

A

work up before operation (assess location/size/infiltration of tumor)

360
Q

what are complications associated with adrenalectomy to treat hyperadrenocorticism?

A 
haemorrhage
hypertension
acute hypocortisolaemia
hypoaldosteronism
wound breakdown
(needs refurral treatment)
361
Q

how effective is trilostane for treatment of ADH?

A

ADH generally more resistant

used pre-surgery to stabilise

362
Q

what are the general considerations when treating any hyperadrenocorticism?

A

may unmask other underlying diseases that have been hidden by high cortisol
reduced cortisol can make pituitary lesions expand leading to CNS signs

363
Q

what is the prognosis of PDH?

A

depends on age, overall health and owner commitment

~30 months survival post diagnosis

364
Q

what is the prognosis of ADH?

A

following successful surgery mean survival is 36 months

metastatic disease leads to death/euthanasia within 12 months

365
Q

is hyperadrenocorticism common in cats?

A

less os

366
Q

what concurrent disease is seen in 80% of cats with hyperadrenocorticism?

A

insulin resistant DM

367
Q

what signs are seen in cats with hyperadrenocorticism?

A

insulin resistant DM
cachexia
fragile skin syndrome (skin may slough off during routine handling so care needed)
alopecia (ventral, symmetrical)

368
Q

what biochemistry signs seen in dogs with hyperadrenocorticism is not seen in cats?

A

increase in ALP

369
Q

how is hyperadrenocorticism in cats diagnosed?

A

HDDST

ACTH stim with post sample at 60 and 90 mins

370
Q

how is hyperadrenocorticism in cats treated?

A

difficult
adrenalectomy if adrenal mass
no reliable medication for PDH - can use trilostane and hypophysectomy is possible

371
Q

what is the prognosis of hyperadrenocorticism in cats?

A

guarded to poor

worse than dogs

372
Q

what type of diabetes mellitus is seen more commonly in dogs?

A

insulin dependent (type 1)

373
Q

what are the possible causes of diabetes mellitus in dogs?

A

destruction of pancreatic beta cells

insulin resistance leading to beta cell exhaustion

374
Q

what causes destruction of pancreatic beta cells?

A

genetics
immune mediate pancreatic damage
pancreatitis
idiopathic

375
Q

what causes insulin resistance leading to beta cell exhaustion?

A

obesity
concurrent disease (e.g. pancreatitis or endocrinopathy)
dioestrus
drugs

376
Q

what is the signalment for canine diabetes mellitus?

A

middle aged/older dogs
female more than male
breed predisposition

377
Q

what are the top 3 dog breeds predisposed to diabetes mellitus?

A

Australian terrier
schnauzer
bichon

378
Q

what are the clinical findings in a dog with diabetes mellitus?

A 
PUPD
polyphagia
weight loss
cataracts
DK
concurrent disease
379
Q

what causes PUPD in diabetes mellitus patients?

A

kidney is unable to process the excess glucose so glycosuria occurs
due to the osmotic pressure of the glucose in the urine more water is drawn out

380
Q

why are polyphagia and weight loss seen in diabetes mellitus?

A

decreased glucose utilisation due to lack of insulin there is a negative calorie balance

381
Q

what are cataracts caused by in diabetes mellitus?

A

altered osmotic relationship in the lens

accumulation of sugars in the lens causing swelling and rupture of lens fibres

382
Q

what are the main signs of diabetic ketoacidosis?

A

vomiting
collapse
dehydration

383
Q

what is necessary to confirm a diabetes mellitus diagnosis?

A

glycosuria

persistent hyperglycaemia

384
Q

what is shown by fructosamine?

A

average of glycaemia over the past 2-3 weeks so give an impression of blood sugar levels over time

385
Q

how does fructosamine measure glycaemia over weeks?

A

glucose binds to proteins (glycated proteins) in an irreversible reaction between glucose and plasma proteins

386
Q

what should fructosamine results be interpreted alongside?

A

clinical signs

387
Q

how is diabetes mellitus treated in dogs?

A 
insulin (in almost all cases)
diet
exercise
consistency
owner commitment
388
Q

what varies between types of insulin?

A

time of onset
time of maximum effect
duration of action

389
Q

what is the most commonly used insulin for dogs?

A

Lente (Caninsulin) - intermediate acting

390
Q

what insulin type is needed to treat DKA?

A

neutral / short acting insulin

391
Q

are oral hypoglycaemic drugs of any use in dogs?

A

no

392
Q

what are the 2 types of long acting insulin?

A

PZI

glargine

393
Q

what is a Caninsulin VetPen used for?

A

small doses

makes administration easy for owners

394
Q

what syringe colour is used for Caninsulin (canine product)?

A

red syringe

395
Q

how many insulin units are within Caninsulin?

A

40 IU/mL

396
Q

how should insulin be handled?

A 
store in fridge / avoid extremes of temperature
replace bottles after 4 weeks
invert to mix gently
use appropriate syringe
vary site of injection
397
Q

how should intact females with diabetes mellitus be managed?

A

spayed 1-3 days after starting insulin especially in dioestrus

398
Q

why do intact females with diabetes mellitus need to be spayed?

A

progesterone is a cause of insulin resistance so makes DM harder to treat as insulin is needed in larger volumes

399
Q

what should be used if it is not possible to spay intact females who have diabetes mellitus?

A

aglepristone

400
Q

what diet should diabetes mellitus patients be fed?

A

diabetic specific food

no simple sugars (reduce glucose spike)

401
Q

in a diabetic diet what should the calories be supplied by?

A

complex carbohydrates and proteins

increased fibre content for overweight dogs

402
Q

what should thin diabetic dogs be fed?

A

calorie dense, low fibre maintenance diet

403
Q

what should picky diabetic dogs be fed?

A

whatever they are used to

404
Q

what is important about the feeding schedule of a diabetes mellitus patient?

A

consistent timing, quantity and type of diet

405
Q

how should patients receiving BID insulin be fed?

A

half daily requirement at time of each injection

406
Q

how should patients receiving SID insulin be fed?

A

1/3-1/2 at time of injection and remainder 8 hours later

407
Q

how long can stabilisation of diabetic patient take?

A

weeks to months

408
Q

how should the first day of insulin administration be managed?

A

start with low dose
avoid hypoglycaemia
check BG several times (q2-3 hours) in the day in practice

409
Q

what are the most important clinical signs to monitor for in the healthy newly diagnosed diabetes dog?

A

PUPD
polyphagia
weight loss

410
Q

what should be checked for if the diabetes patient on insulin no longer has diabetes signs?

A

are there signs of hypoglycaemia

411
Q

what are the signs of hypoglycaemia?

A

lethargy
reluctant to exercise
collapse
seizure

412
Q

when should diabetic dogs on insulin have their first recheck?

A

7-10 days after first dose

413
Q

when should follow up appointments be scheduled for the newly diagnosed diabetic dog?

A

7-10 days post first insulin
14 days later
1 month
then every 3 months if well controlled

414
Q

when is a blood glucose curve important?

A

if there is poor glycaemic control so adjustments can be made to insulin therapy

415
Q

what should a glucose curve be used in conjunction with to make management / insulin changes?

A

clinical signs

416
Q

how is a blood glucose curve performed?

A

serial blood glucose with a glucometer

continuous glucose monitoring

417
Q

how is serial blood glucose taken?

A

in the ear every 2 hours and then every hour close to the nadir

418
Q

how is continuous glucose monitoring performed?

A

measured interstitial blood glucose - device placed on scruff and glucose levels monitored constantly

419
Q

what is the nadir?

A

lowest blood glucose value

420
Q

what parameters should be assessed when doing a blood glucose curve?

A

nadir

duration of action of insulin

421
Q

what is the renal threshold for glucose?

A

point at which glucose will be secreted in the urine as kidneys are no longer able to prevent glucose spilling into urine so PUPD is caused

422
Q

how much glucose will be seen in the urine of a patient with insulin controlled diabetes melitus?

A

mild amount in urine especially before glucose administration

423
Q

what may no glucose in the urine of a patient with insulin controlled diabetes melitus for more than 24 hours indicate?

A

insulin overdose

424
Q

what would ketones in the urine of insulin controlled diabetes melitus patients indicate?

A

poor glycaemic control - not enough insulin

425
Q

what can one off blood glucose monitoring show?

A

good glycaemic control if prior to insulin administration but curve is more useful

426
Q

what are the complications of insulin therapy?

A

hypoglycaemia

somogyi overswing

427
Q

what are the clinical signs of hypoglycaemia?

A

lethargy
weakness
collapse
seizure

428
Q

what blood glucose level indicates hypoglycaemia?

A

<3 mmol/L

429
Q

how should hypoglycaemia be treated?

A

small meal

glucose / sugar solution PO or IV

430
Q

what is somogyi overswing?

A

rebound hyperglycaemia response from other hormones in the body due to physiologic response to hypoglycaemia

431
Q

when may somogyi overswing occur?

A

when blood glucose is <3.6 mmol/L

or quick drop in glucose following insulin

432
Q

how long does lente (caninsulin) work for?

A

8-12 hours

433
Q

how are issues with insulin therapy diagnosed?

A

glucose curve

434
Q

when may short duration of inslin occur?

A

using Lente if duration of action is less than 8 hours

435
Q

how can you tell if patients insulin is too short acting?

A

PUPD between injections

436
Q

how can short duration of insulin be managed?

A

switch to long acting insulin BID

437
Q

when does prolonged duration of insulin occur?

A

when nadir is >10 hours post injection

438
Q

what is the risk of prolonged action of insulin?

A

risk of hypoglycaemia and Somogyi overswing

439
Q

how can prolonged duration of action of insulin be managed?

A

if long acting give SID or switch to short acting

440
Q

what should you do if insulin is having inadequate action?

A

make sure owner is administering the insulin correctly

441
Q

what are the long term complications of diabetes?

A 
hypoglycaemia
cataract formation (inevitable in dogs)
diabetic neuropathy (uncommon in dogs)
diabetic nephropathy (uncommon in dogs)
hypertension
DKA
442
Q

what causes diabetic neuropathy?

A

distal neuropathy due to segmental demylination (patchy breaksdown of myelin sheaths) and axonal degradation

443
Q

what is the prognosis of dogs with diabetes melitus?

A

good if well managed with committed owners (MST - 3 to 5 years)

444
Q

what type of diabetes melitus do cats most often get?

A

non-insulin dependent - type 2

445
Q

what are the risk factors for diabetes melitus in cats?

A

old age
obesity
male
indoor

446
Q

what cat breeds are predisposed to diabetes melitus?

A

burmese
main coon
russian blue
siamese

447
Q

what are the 2 main causes of diabetes melitus in cats?

A

insulin resistance

reduced insulin secretion

448
Q

what can cause insulin resistance in cats?

A

genetically determined

obsetity (antagonises effect of insulin)

449
Q

what element of diabetes can further damage the pancreas in cats?

A

hyperglycaemia

450
Q

how is reduced insulin secretion caused in cats?

A 
amyloid polypeptide (secreted alongside insulin) can become toxic (misfolding of protein) and deposition leads to inflammation and cell death
beta cell damage (some function remains)
451
Q

what can cause insulin resistance in cats?

A

obesity
inflammatory / infectious diseases
endocrinopathies

452
Q

what inflammatory / infectious diseases can cause insulin resistance in cats?

A 
pancreatitis
UTI
CKD
dental disease
enteropathy
453
Q

what endocrinopathies can cause insulin resistance in cats?

A

hyperthyroidism
acromegaly
hypercorticism (iatrogenic steroid use)

454
Q

what are the signs of pre-diabetes melitus in cats?

A

impaired fasting glucose (rarely seen due to stress hyperglycaemia)
BG constantly above >6.5 mmol/L (elevated but not in diabetic range)

455
Q

what is the blood glucose level in subclinical DM in cats?

A

> 10mmol/L and <16mmol/L (renal threshold) persitantly

456
Q

what can be done to manage cats with subclinical DM?

A

low carbohydrate diet
weight loss
insulin sensitisers (glipizide)
try to avoid overt DM

457
Q

what is the BG of a patient with overt DM?

A

> 16 mmol/L

renal threshold is exceeded

458
Q

what are the signs on biochemistry and urinalysis of overt DM cat?

A

hyperglycaemia
increases fructosamine (unaffected by stress hyperglycaemia)
glycosuria

459
Q

what are the clinical signs of DM in cats?

A

as for dogs - weight loss, polyphagia, DKA
peripheral neuropathy
cataracts (rare)

460
Q

how is DM diagnosed in cats?

A

hyperglycaemia and glycosuria

461
Q

what should you be aware of when screening cats for DM?

A

stress hyperglycaemia altering results

462
Q

what does fructosamine show in cats?

A

mean BG in the last week

463
Q

what can be used to differentiate between stress hyperglycaemia and DM?

A

combine fructosamine with history and clinical signs

464
Q

how is DM in cats treated?

A 
insulin
diet
exercise
commitment from owner
consistantcy
465
Q

what insulin is used in cats?

A

longer acting

466
Q

what is the first insulin type that will be tried in cats with DM?

A

Prozinc

467
Q

can Caninsulin be used in cats?

A

yes but response is very unpredictable

468
Q

what is the other insulin type that can be used if prozinc and caninsulin have not worked?

A

Glargine - on cascade as not licenced

469
Q

what do oral hypoglycaemic drugs do?

A

increase insulin secretion to decrease IR

470
Q

when are oral hypoglycaemic drugs useful in cats?

A

if owner declines insulin
with diabetic diet and weight loss
as long as no comorbidities

471
Q

what is a key benefit for management and prevention of DM in cats?

A

diet

472
Q

what should the composition of feline diabetic diets be?

A 
wet
high protein
low carbohydrate
reliable intake
fibre less key than in dogs
473
Q

what can be the result of dietary management and associated weight loss in cats?

A

resolution of DM in 30% of cats

reduction in insulin dose for 50% of cats

474
Q

what is a serious complication of DM?

A

DKA

475
Q

what often caused DKA?

A

DM with serious concurrent disease (e.g. heart failure, pancreatitis or sepsis)

476
Q

how is DKA caused?

A

increased production of glucoregulatory hormones (glucagon, adrenaline, cortisol)
lack of insulin in DM allows the glucogenic effects of the stress hormones to be unopposed in liver, muscle and adipose tissue
leads to excessive breakdown of fatty acids, excessive ketone formation (e.g. acetone) leading to a build up in the body

477
Q

what are the clinical signs of DKA?

A

PUPD
polyphagia
weight loss
systemic signs such as lethargy, anorexia and vomiting which worsen
additional signs of concurrent disease
strong odour of pear drops on breath (acetone) - not everyone can smell it
severe dehydration and hypovolaemia

478
Q

what is the aim of treatment of DKA?

A

restore water and electrolyte balance
provide adequate insulin to ‘switch off’ ketone production
correct acidosis
identify any underlying disease

479
Q

what electrolytes may be altered by DKA?

A

sodium
potassium
phosphorus

480
Q

what insulin is needed to treat DKA?

A

neutral - CRI or IM every hour

481
Q

what supportive therapy is needed for the DKA patient?

A

analgesia (if pancreatitis etc)
feeding to avoid hypoglycaemia (appetite stimulants, mariopitant, feeding tube)
careful monitoring

482
Q

how long does it take for hypoglycaemia to improve?

A

12-24 hours

483
Q

how long does it take for ketosis to improve?

A

48-72 hours

484
Q

what is the prognosis of DKA?

A

challenging to treat
often underlying disease
25% will die or be euthanised

485
Q

what can happen to cats after DKA?

A

DM remission in some cases

X Clinical Veterinary Nursing Theory (70 decks)

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