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CVNT2 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is the most common endocrine condition in cats?

A

feline hyperthyroidism

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2
Q

why is feline hyperthyroidism recognised with increasing frequency?

A

awareness of the disease
cats living longer
becoming more common?

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3
Q

what is the aetiology of feline hyperthyroidism?

A

no evidence of autoimmune disease

mostly benign adenomatous hyperplasia/adenoma of thyroid tissues

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4
Q

is feline hyperthyroidism usually bilateral or unilateral?

A

2/3rds bilateral

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5
Q

what is ectopic thyroid tissue?

A

functional thyroid tissue found elsewhere - usually mediastinum

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6
Q

what are the potential factors contributing to feline hyperthyroidism?

A

nutritional factors (iodine levels, goitrogens)

environmental factors (flea sprays, garden pesticides)

genetic factors (some breed dispositions)

circulating factors (thyroid growth stimulating immunoglobulins)

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7
Q

what are the risk factors for developing feline hyperthyroidism?

A

regular use of flea sprays/powders

indoor cats

primarily canned food diet

exposure to lawn herbicides/fertilisers/pesticides

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8
Q

what signalment more commonly presents with feline hyperthyroidism?

A

middle aged-elderly cats (10-23 years)

no sex predilection

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9
Q

what is increased in the body due to feline hyperthyroidism?

A 
metabolic rate 
cardiac output 
heart rate 
blood pressure 
GI motility 
CNS activity
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10
Q

what is reduced due to feline hyperthyroidism?

A

sleep

body weight

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11
Q

what are the major clinical signs of feline hyperthyroidism?

A 
palpable enlarged thyroid glands 
weight loss 
polyphagia 
hyperactivity 
PUPD 
tachycardia
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12
Q

what are the minor clinical signs of feline hyperthyroidism?

A 
lethargy 
intermittent anorexia 
voice changes 
muscle weakness/tremors 
congestive heart failure 
heat intolerance 
mild pyrexia 
dyspnoea/tachhypnoea
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13
Q

what are the signs of apathetic hyperthyroidism?

A

lethargy, inappetence, weight loss, obtundation

small percentage, likely reflecting an underlying comorbidity

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14
Q

which comorbidity often accompanies apathetic hyperthyroidism?

A

severe cardiac abnormalities

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15
Q

how should cats with feline hyperthyroidism be handled?

A

cat-friendly, hands-off approach

put in quiet room to calm

oxygen therapy, sedation (gabapentin) if required

acclimatisation period

monitor RR

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16
Q

what is required for diagnosis of feline hyperthyroidism?

A

compatible clinical signs
positive screening tests
serum total thyroxine test

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17
Q

how do we feel for enlargement of the thyroid gland?

A

feel the neck up to the larynx from the level of the thoracic inlet

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18
Q

what screening tests are used for diagnosis of feline hyperthyroidism?

A

haematology

biochemistry (elevated liver enzymes, concurrent disease?)

urinalysis (CKD?)

blood pressure measurement

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19
Q

what ocular feature can accompany severe feline hyperthyroidism?

A

retinal detachment due to acute hypertensive crisis

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20
Q

what is the gold standard test for feline hyperthyroidism?

A

serum total thyroxine (TT4) test - elevated in most hyperthyroid cats but may fluctuate

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21
Q

what TT4 value is considered feline hyperthyroidism?

A

> 50-60nmol/L

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22
Q

why might TT4 present as high-normal in feline hyperthyroidism?

A

early disease

non-thyroidal illness can affect T4

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23
Q

what are the treatment options for feline hyperthyroidism?

A

anti-thyroid drugs
iodine-restricted diet
thyroidectomy
radioactive iodine treatment

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24
Q

why should medical management be tried for feline hyperthyroidism first?

A

to assess renal function when patient is euthyroid before undertaking irreversible treatment

to stabilise the patient prior to anaesthesia if surgery is planned

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25
Q

how do anti-thyroid drugs work?

A

block production of T4 by the thyroid gland

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26
Q

what anti-thyroid drugs are available?

A

methimazole - BID tablets/transdermal gel/oral liquid

slow-release carbimazole tablets SID (rapidly converted to methimazole)

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27
Q

how long does it take for antithyroid drugs to work?

A

normally euthyroid in <2-3 weeks - recheck TT4 2-3 weeks after starting treatment

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28
Q

what are the advantages of anti-thyroid drugs?

A 
readily available 
rapidly effective 
inexpensive 
practical 
no GA/hospitalisation
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29
Q

what are the drawbacks of anti-thyroid drugs?

A

life-long
long-term resistance
must be good compliance
side effects

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30
Q

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

A

vomiting
anorexia
lethargy

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31
Q

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

A

persistent GI signs

blood dyscrasias (severe leukopenia/anaemia/thrombocytopenia)

dermatitis (facial excoriation)

hepatopathy

lymphadenomegaly

myasthenia gravis

stop treatment if any of these occur!

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32
Q

what diet is available for managing feline hyperthyroidism?

A

iodine-restricted

Hills y/d

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33
Q

what are the drawbacks of feeding an iodine-restricted diet?

A

must be fed as sole food (strictly)
life-long
less effective and not suitable for severely hyperthyroid cats

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34
Q

what are the pre-surgical considerations for feline hyperthyroidism?

A

systemic effects of hyperthyroidism
cardiac disease
hypertension
other disease

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35
Q

what is a thyroidectomy?

A

removal of one/both thyroid glands

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36
Q

what must great care be taken during thyroidectomy surgery?

A

preservation of parathyroid tissue to avoid post-operative complications (hypocalcaemia)

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37
Q

how long does thyroidectomy take to work?

A

typically achieves euthyroidism in >90% patients in 24-48 hours

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38
Q

what are the advantages of thyroidectomy?

A

curative
rapidly effective
short hospitalisation period

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39
Q

what are the drawback of thyroidectomy?

A 
GA and great skill required 
location 
recurrence 
cost 
complications
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40
Q

what are the complications associated with thyroidectomy surgery?

A

damage to/removal of parathyroid tissue (post-operative hypoparathyroidism)

damage to the recurrent laryngeal nerve

damage to sympathetic trunk (horners syndrome)

possible recurrence of disease (if unilateral)

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41
Q

what condition commonly occurs due to bilateral thyroidectomy?

A

iatrogenic hypoparathyroidism - usually transient, weeks-months to recover

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42
Q

what are the clinical signs of iatrogenic hypoparathyroidism?

A 
inappetence
weakness 
tremors 
ptyalism 
pawing at face

progressing to tetany, seizures, death

monitor serum calcium twice a day of bilateral surgery or if concerned

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43
Q

what is the treatment for iatrogenic hypoparathyroidism?

A

IV 1-% calcium gluconate slowly (10-20 mins)

oral therapy ASAP - elemental calcium in divided doses while weaning off IV drip PLUS oral vitamin D long-term

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44
Q

how should you monitor patients during hypoparathyroidism treatment?

A

monitor with ECG for arrhythmia and bradycardia

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45
Q

what fluids should be avoided when administering IV calcium for hypoparathyroidism?

A

bicarbonate, lactate or phosphate-containing fluids –> precipitate calcium

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46
Q

why can’t calcium gluconate be administered subcut?

A

can cause skin sloughs

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47
Q

what is the gold standard for treating feline hyperthyroidism?

A

radioiodine treatment

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48
Q

how is radioiodine treatment carried out?

A

administered systemically but concentrated in thyroid

cat isolated for 1-2 weeks - gamma rays dangerous

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49
Q

what are the advantages of radioactive iodine treatment?

A

gold standard

curative

simple procedure

higher doses can treat adenocarcinoma

no GA

lower cost (compared to lifelong antithyroid drugs)

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50
Q

what are the drawbacks of radioactive iodine treatment?

A

cost

limited availability

isolation period

irreversible

may take some time to achieve euthyroid

iatrogenic hypothyroidism (rare)

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51
Q

how are feline hyperthyroidism and CKD linked?

A

feline hyperthyroidism may mask underlying CKD –> treatment may unmask CKD

usually only change by maximum one IRIS stage

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52
Q

how often should we monitor cats with feline hyperthyroidism? what are we monitoring for?

A

6-monthly check-ups once stabilised, regardless of treatment regime

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

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53
Q

what is the prognosis for feline hyperthyroidism?

A

largely dependent on severity/presence of concurrent disease (especially heart disease)

uncomplicated hyperthyroid cats have an excellent prognosis following curative treatment

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54
Q

what are the characteristics of canine thyroid neoplasia?

A

carcinomas common, adenomas usually incidental findings

usually large, solid, palpable mass at level of thyroid gland

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55
Q

does canine thyroid neoplasia result in hyperthyroidism?

A

no - usually euthyroid or hypothyroid

10% hyperthyroid

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56
Q

what are the clinical signs of canine thyroid neoplasia?

A

average age 10 years
mass in ventral region of neck
+/- cough/dyspnoea

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57
Q

how is canine thyroid neoplasia diagnosed?

A

histopathology of the mass - FNA often blood contaminated but may confirm thyroid origin

care as very vascular

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58
Q

what treatments are available for canine thyroid neoplasia?

A

surgical removal followed by chemotherapy/radiation therapy

radioactive iodine treatment (high doses required)

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59
Q

what is the prognosis for canine thyroid neoplasia?

A

depends on size, local invasion, functional status and histological diagnosis (adenoma vs carcinoma)

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60
Q

what does thy thyroid gland produce?

A

active thyroid hormones
thyroxine (T4)
triiodothyronine (T3)

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61
Q

what are the thyroid hormones produced from?

A

from tyrosine amino acids and action of thyroid peroxidase (TPO) - oxidation of iodine

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62
Q

which thyroid hormone is secreted in higher amounts

A

mostly T4, small amount of T3

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63
Q

how much T4 is bound to proteins?

A

> 99%

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64
Q

which type of T4 is biologically active?

A

unbound/free t4 is biologically active and exerts a negative feedback on TSH production

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65
Q

what is the most common form of hypothyroidism?

A

primary hypothyroidism

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66
Q

what are the 2 causes of primary hypothyroidism in dogs?

A

lymphocytic thyroiditis

thyroid atrophy

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67
Q

what is lymphocytic thyroiditis?

A

destructive immune-mediated process - infiltration of lymphocytes, macrophages and plasma cells and replacement by fibrous connective tissue

clinical signs occur when 75% of the gland is destroyed

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68
Q

what is thyroid atrophy?

A

degenerative process with limited inflammation

progressive replacement by adipose and connective tissue

possibly end-stage lymphocytic thyroiditis

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69
Q

what is secondary hypothyroidism?

A

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

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70
Q

what signalment predisposes hypothyroidism?

A

mean age at diagnosis is 7y

breed dispositions: english setter, golden retriever, rhodesian ridgeback, cocker spaniel, boxer

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71
Q

what are the metabolic signs of hypothyroidism?

A

decreased metabolic rate - weight gain, lethargy, inactivity

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72
Q

what are the dermatologic signs of hypothyroidism in dogs?

A

endocrine alopecia (symmetrical, non-pruritic)

rat-tail (hair loss at tail tip)

tragic facial expression due to myxoedema

hair in telogen phase - poor hair growth after clipping

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73
Q

what are the reproductive signs of hypothyroidism?

A

persistent anoestrus
weak/silent oestrus
prolonged oestral bleeding
inappropriate lactation

no effect on male reproductive system

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74
Q

what are the cardiac signs of hypothyroidism?

A

bradycardia

association with atrial fibrillation and DCM

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75
Q

what are the neuromuscular signs of hypothyroidism?

A

megaoesophagus

laryngeal paralysis
facial nerve paralysis

peripheral vestibular syndrome

(more likely concurrent disorders than causal effect)

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76
Q

what is the association between hypothyroidism and myxoedema coma?

what are the symptoms of a myxoedema coma?

A

life-threatening consequence of hypothyroidism

profound mental dullness, weakness, hypothermia, bradycardia and hypotension

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77
Q

what are the ocular signs of hypothyroidism?

A

corneal lipid deposits (via hyperlipidaemia), ulceration, uveitis

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78
Q

what are the GI signs of hypothyroidism?

A

diarrhoea due to SIBO

constipation due to decreased peristalsis

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79
Q

how is hypothyroidism diagnosed?

A

appropriate history and clinical signs

haematology and biochemistry markers

specific thyroid testing

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80
Q

what haematology/biochemistry abnormalities are used in diagnosis of hypothyroidism?

A

mild non-regenerative anaemia (normocytic and normochromic)

hypercholesterolaemia

hypertriglyceridaemia

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81
Q

what hormone abnormalities would you expect to see in a hypothyroid dog?

A

low T4
high TSH
(low T4 = no negative feedback on pituitary gland production of TSH)

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82
Q

which thyroid tests are performed in diagnosing hypothyroidism?

A 
total T4 (TT4) 
canine TSH (cTSH)
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83
Q

why is total T4 a useful screening test for hypothyroidism?

A

has excellent sensitivity

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84
Q

what are the limitations of using TT4 as a diagnostic test?

A

thyroglobulin antibodies can falsely increase TT4

poor specificity - TT4 decreases naturally with ages/breed/non-thyroidal illness and drug therapy

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85
Q

how sensitive is the canine TSH test?

A

moderate sensitivity - low cTSH in central hypothyroidism or corticosteroid therapy

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86
Q

how specific is the canine TSH test?

A

Good specificity - largely non affected by NTI or drugs

will be elevated in euthyroid dogs in recovery from NTI

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87
Q

how is hypothyroidism treated?

A 
synthetic T4 (physiologic prohormone for active T3) 
in the form of sodium levothyroxine SID or divided BID
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88
Q

how does pairing with food affect the bioavailability of sodium levothyroxine?

A

halved with food

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89
Q

how should you dose sodium levothyroxine in dogs with cardiac disease, diabetes mellitus, or hypoadrenocorticism?

A

start with 25% of dose and titrate up

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90
Q

how long should Sodium levothyroxine be given before evaluating its effect?

A

6-8 weeks

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91
Q

how long does it take Sodium levothyroxine to reach peak concentration?

A

3-5 hours post-pill

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92
Q

what is the half-life of Sodium levothyroxine?

A

9-15 hours (affects dosing intervals)

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93
Q

what products are available to administer sodium levothyroxine?

A

soloxine - tablets
thyforon - flavoured tablets
leventa - liquid formulation

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94
Q

how often should you monitor dogs with hypothyroidism?

A

6-8 weeks after starting treatment or 2-4 weeks after altering dose

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95
Q

what are the aims of hypothyroidism treatment?

A

TT4 upper half of the reference value

TSH normal value

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96
Q

how common is iatrogenic thyrotoxicosis?

A

rarely cause hyperthyroidism with treatment for hypothyroidism

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97
Q

what are the potential complications of hypothyroidism treatment?

A 
thyrotoxicosis (rare) - secondary to drug overdose 
myxoedema coma (rare)
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98
Q

what are the clinical signs of thyrotoxicosis?

A 
panting 
anxiety/aggression 
PUPD 
weight loss 
polyphagia
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99
Q

what is the treatment for thyrotoxicosis?

A

reduce dose/discontinuation of treatment

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100
Q

what is the treatment for a myxoedema coma?

A

supportive care
IV levothyroxine
antibiotics if sepsis

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101
Q

what is the prognosis for hypothyroidism?

A

good for adult dogs with primary hypothyroidism

guarded for secondary hypothyroidism

102
Q

what are the main 2 parts of the adrenal glands? what does each produce?

A

medulla (catecholamines)

cortex (mineralocorticoids/glucocorticoids/sex hormones)

103
Q

what type of molecule is aldosterone?

A

mineralocorticoid (steroid hormone)

104
Q

where is aldosterone produced?

A

adrenal cortex

105
Q

where is the major renal tubular site of aldosterone action?

A

principal cells in the last distal tubule and collecting tubule

106
Q

what is the action(s) of aldosterone?

A

reabsorption of NaCl and H2O
secretion of K+ and H+

more important for K+ regulation than Na+ regulation

107
Q

what are the most important stimuli for aldosterone production?

A

hyperkalaemia

increased angiotensin II

108
Q

what other name is given to primary hypoadrenocorticism?

A

addison’s disease

109
Q

what happens in primary hypoadrenocorticism?

A

lack of aldosterone secretion by the adrenal cortex, resulting in hyperkalaemia, hyponatremia and hypocalcaemia

110
Q

what is secondary hypoadrenocorticism?

A

Secondary hypoadrenocorticism refers to a central (anterior pituitary) deficiency of ACTH, resulting in isolated glucocorticoid insufficiency

111
Q

what is atypical hypoadrenocorticism?

A

lack of glucocorticoids but normal mineralocorticoids

112
Q

what causes primary hypoadrenocorticism?

A

suspected immune-mediated destruction of the adrenal cortex

113
Q

what causes secondary hypoadrenocorticism?

A

central (anterior pituitary) cause - neoplasia, inflammation, infection, infarct, iatrogenic

114
Q

what secretion is affected in secondary hypoadrenocorticism?

A

only glucocorticoid deficiency as aldosterone secretion is regulated by RAAS

115
Q

what secretion is affected in primary hypoadrenocorticism?

A

lack of glucocorticoids and mineralocorticoids

116
Q

which dogs are more prone to developing hypoadrenocorticism?

A

typically young/middle-aged female dogs

breeds: standard poodles, bearded collie, nova scotia duck toller, great dane

117
Q

what are the symptoms of a lack of cortisol in hypoadrenocorticism?

A

weakness, vomiting, diarrhoea, anorexia

especially at times of stress

118
Q

what are the symptoms of lack of aldosterone?

A

polyuria and polydipsia (due to low Na)

119
Q

what type of molecule is cortisol?

A

glucocorticoid (steroid hormone)

120
Q

what are the symptoms of an addisonian crisis?

A

collapse
severe dehydration and hypovolaemia
pre-renal azotemia
cardiac arrhythmias due to hyperkalaemia (bradycardia)

121
Q

how do you diagnose primary hypoadrenocorticism?

A

compatible history and clinical signs
compatible haematology and biochemistry results
basal cortisol to exclude the disease
ACTH to confirm

122
Q

what haematology results suggest hypoadrenocorticism?

A

non-regenerative anaemia

absent stress leukogram (especially in a sick patient)

123
Q

what biochemistry results indicate primary hypoadrenocorticism?

A

hyperkalaemia
hyponatraemia and hypocalcaemia

pre-renal azotemia due to hypovolaemia and dehydration

acidaemia

hypoglycaemia due to lack of glucocorticoids

increased liver enzymes due to poor perfusion

decreased albumin and cholesterol due to GI insult (lack of GC)

124
Q

what basal cortisol result suggests hypoadrenocorticism is unlikely?

A

> 55nmol/l

125
Q

what basal cortisol result suggests hypoadrenocorticism is likely?

A

<55nmol/L

126
Q

which test can be used to confirm hypoadrenocorticism?

A

ACTH stimulation test - usually both pre- and post-ACTH cortisol concentrations below 20nmol/l with HOA

127
Q

what is the protocol for an ACTH stimulation test?

A

collect serum for basal cortisol concentration

inject 5mcg/kg ACTH IV

collect second serum sample 60 min after

128
Q

what happens to serum cortisol in a ACTH stimulation test if the dog has hypoadrenocorticism?

A

remains at same level (increases in normal dog)

129
Q

how is an addisonian crisis treated?

A

IV fluids at shock doses (60-90ml/kg)

hydrocortisone or dexamethasone IV

treatment of hypoglycaemia and hyperkalaemia if necessary (glucose/insulin and calcium gluconate)

130
Q

what are the considerations for using glucocorticoid therapy for primary hypoadrenocorticism?

A

most commonly prednisolone

trial and error dosage to limit polyphagia/PUPD/weight gain

increase dose if lethargy/V+/D+

double dose if stressful event

131
Q

what is the long-term therapy for primary hypoadrenocorticism?

A

glucocorticoids PO

mineralocorticoids SC

132
Q

what are the considerations for using mineralocorticoid therapy for primary hypoadrenocorticism?

A 
desoxycortone pivalate (zycortal) - able to manage the need for GC separately from MC requirements 
starting dose 1.5mg/kg SC
133
Q

how should we monitor patients with primary hypoadrenocorticism?

A

Ask for evidence of lethargy, V+, D+ - signs that would prompt increase in GC

blood test for mineralocorticoids - measure 10-14 days after DOCP admin for peak effect and 25-30 days after for duration of effect

134
Q

what is the prognosis for hypoadrenocorticism?

A

good if well-managed - life-long medication

may need additional GC at times of stress

monitor dogs with atypical addisons for development of mineralocorticoid deficiency (may develop in future)

135
Q

what are the possible causes of canine diabetes?

A

destruction of pancreatic beta cells
(genetics, immune-mediated pancreatic damage, pancreatitis, idiopathic)

insulin resistance leading to beta cell exhaustion
(obesity, concurrent disease, dioestrus, drugs)

136
Q

which dogs are more prone to developing diabetes?

A

middle aged-older dogs
females more than males
breeds: australian/tibetan/cairn terrier, schnauzers, bichon, samoyed

137
Q

what are the clinical findings with canine diabetes?

A

PUPD (secondary to glycosuria)

polyphagia and weight loss

cataracts

diabetic ketoacidosis (vomiting, collapse, dehydration)

concurrent disease (pyometra, cushings)

138
Q

why do cataracts often form in dogs with diabetes?

A

due to altered osmotic relationship in the lens (due to sugar)
accumulation of sorbitol and galactitol causing swelling and rupture of the lens fibres

139
Q

how is canine diabetes diagnosed?

A

concurrent glycosuria and persistent hyperglycaemia are necessary to confirm a diagnosis

140
Q

what is fructosamine?

A

glycated proteins produced by irreversible non-enzymatic reactions between glucose and plasma proteins

141
Q

why do we test for fructosamine in dogs with suspected diabetes?

A

shows an average of glycaemia of previous 2-3 weeks

142
Q

how is canine diabetes treated?

A

insulin (essential)
diet
exercise
consistency and commitment from owners

143
Q

what is the principle treatment of canine diabetes?

A

insulin supplementation

144
Q

which insulin is most commonly used in treating canine diabetes?

A

Lente - intermediate acting

also need access to neutral insulin for DKA (short acting)

145
Q

can oral hypoglycaemic drugs be used in treatment of canine diabetes?

A

Oral hypoglycaemic drugs are of no value in dogs! they always require insulin

146
Q

which long-acting types of insulin are available?

A

PZI - recombinant human insulin

glargine - synthetic

147
Q

what are the handling considerations for insulin?

A

store in fridge/avoid extremes of temperature

replace bottles after 4 weeks

invert to mix - let foam disperse then gently roll

use appropriate syringes

vary injection site (to avoid fibrosis)

148
Q

why should intact canine females with diabetes be spayed?

A

progesterone is an antagonist of insulin - spaying will make them easier to stabilise

149
Q

how can we alter the diet in patient with canine diabetes?

A

diabetic brands

should not contain simple sugars - calories provided by complex carbohydrates and proteins

increased fibre content in overweight dogs

150
Q

what should the feeding schedule be for dogs with diabetes?

A

consistent quantity/timing/type of diet

if BID injections - feed half daily requirement at time of each injection

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

ad libitum feeding for grazers

151
Q

what is involved in the initial stabilisation of canine diabetes?

A

at home if possible - can take weeks-months

start with low dose

check blood glucose several times over first day in practice (q2-3hrs) - avoid hypoglycaemia

152
Q

how should we monitor a dog with newly diagnosed diabetes?

A

any PUPD, polyphagia, weight loss

hypoglycaemia signs - lethargy, reluctance to exercise, collapse, seizure

153
Q

how is a blood glucose curve performed?

A

either by serial blood glucose with glucometer or continuous glucose monitoring

154
Q

what parameters are important to assess for the blood glucose curve?

A

nadir (lowest blood glucose reading)

duration of action

155
Q

what is the renal threshold?

A

point at which glucose is excreted in the urine (patient presents as polyuric)

156
Q

what might we find in urinalysis of a diabetic dog on treatment?

A

usually a mild amount of glucose in urine, especially before insulin administration

no glucose >24hours may indicate insulin overdose

ketones may indicate poor glycaemic control

157
Q

what are the potential complications of insulin therapy?

A

hypoglycaemia - give small meal or glucose PO/IV

somoygi overswing - rebound hyperglycaemia caused by physiologic response to hypoglycaemia (rebound effect of overdosing insulin)

158
Q

what should you do if the insulin has too short a duration of action?
(PUPD between injections)

A

switch to long acting insulin BID

159
Q

what should you do if the insulin has too long a duration of action? (nadir >10hrs post-injection)

A

risk of hypoglycaemia and somoygi overswing

give SID or switch to short-acting formula

160
Q

what are the long-term complications of diabetes in dogs?

A

cataract formation (common)

diabetic neuropathy (distal) (uncommon) 
diabetic nephropathy (uncommon)

hypertension - mechanism unclear

diabetic ketoacidosis

161
Q

what is the prognosis for canine diabetes?

A

MST 3-5 years

good if well-managed with committed owners

162
Q

what are the risk factors for feline diabetes?

A 
old age 
obesity 
males 
indoor cats 
breeds: burmese, maine coon, russian blue and siamese
163
Q

what is the pathophysiology of feline diabetes?

A

insulin resistance - genetics/obesity?

reduced insulin secretion - inflammation and beta cell damage/death

164
Q

what are the possible causes of insulin resistance?

A

obesity

inflammatory/infectious disease - pancreatitis, UTI, CKD, dental disease, enteropathy

endocrinopathies - hyperthyroidism, acromegaly, hypercortisolism

165
Q

what characterises the pre-diabetic stage in cats?

A

impaired fasting glucose - rarely documented

due to stress hyperglycaemia at vets

BG consistently >6.5 mmol/L

166
Q

what characterises subclinical feline diabetes?

A

BG >10 and <60mmol/L persistently

would benefit from low carb diet, weight loss and possible insulin sensitisers (glipizide)

167
Q

what characterises overt feline diabetes?

A

hyperglycaemia - BG >16mmol/L
increased fructosamine
glycosuria

168
Q

what are the clinical signs of feline diabetes?

A 
PUPD
weight loss 
polyphagia 
DKA 
peripheral neuropathy 
cataracts (rare in cats)
169
Q

how is feline diabetes diagnosed?

A

hyperglycaemia and glycosuria
(be aware of stress hyperglycaemia)
fructosamine test

170
Q

how is feline diabetes treated?

A

insulin
diet
exercise
consistency and commitment

171
Q

what insulin options are available for cats with diabetes?

A

prozinc (recombinant human insulin)

caninsulin (cats unpredictable in their response)

glargine insulin (can only be used under the cascade)

172
Q

how do oral hypoglycaemic drugs work?

A

glipizide - increases insulin secretion, useful if owner decline insulin

used in conjunction with diabetic diet

173
Q

what are the features of a diabetic diet for cats?

A

wet
high protein
low carbohydrate
high fibre less useful than in dogs

must be reliable intake

174
Q

what are the effects of dietary management of diabetes in cats?

A

resolution in 30% of cats

reduction in insulin dose in 50%

175
Q

what is diabetic ketoacidosis?

A

a serious complication of diabetes - concurrent with heart failure/pancreatitis/sepsis

176
Q

what is the pathophysiology of DKA?

A

increased production of glucoregulatory hormones (glucagon/epinephrine/cortisol/GH)

lack of insulin allows the glucogenic effects of these stress hormones to be unopposed in liver/muscle/adipose tissue

leads to excessive free fatty acids breakdown and excessive ketone formation

177
Q

what are the clinical signs of DKA?

A

PUPD, PP, weight loss
lethargy, anorexia and vomiting (with worsening ketosis and acidosis)
strong odour of acetone on breath (pear drops)
severe dehydration and hypovolaemia

178
Q

what is the aim of DKA treatment/management?

A

restore water and electrolyte balance (Na, K, phosphorous)

provide adequate insulin to “switch off” ketone production

correct acidosis

identify any underlying disease

179
Q

what supportive therapies can be given for DKA?

A

analgesia (if concurrent condition causing pain e.g. pancreatitis)

appetite stimulants/anti-nausea drug/NO or O tube

careful monitoring - ketosis can take 48-72hrs to improve

180
Q

what is the prognosis for DKA?

A

25% die or are euthanised, usually due to cost of treatment

with careful treatment, some patients can become healthy happy diabetics

cats can even enter DM remission after DKA

181
Q

why does hyperadrenocorticism occur?

A

due to excessive production of cortisol as a consequence of pituitary or adrenal tumours

182
Q

what effect does cortisol have on the pituitary gland/hypothalamus?

A

negative feedback on ACTH and CRH secretion

183
Q

what are the 3 different types of cushing’s syndrome?

A

pituitary-dependent (PDH)
adrenal-dependent (ADH)
iatrogenic (administration of glucocorticoids)

184
Q

what is the most common type of hyperadrenocorticism in dogs?

A

pituitary-dependent hyperadrenocorticism

185
Q

what is the pathogenesis of PDH?

A

adenoma of pars distalis leading to overproduction of ACTH

bilateral adrenal hyperplasia

both leading to a loss of negative feedback on the pituitary gland

186
Q

what dogs are more prone to developing PDH?

A

dachsunds, poodles, small terriers
no sex predisposition
middle aged-old dogs

187
Q

what is macroadenoma?

A

a type of large pituitary tumour which can cause CNS signs (obtundation, seizure)

188
Q

what is the pathogenesis of ADH?

A

adenomas/carcinomas of the adrenal glands, leading to excess cortisol and suppression of ACTH secretion

189
Q

what happens to the contralateral gland with ADH?

A

atrophy of unaffected gland

190
Q

which dogs are more likely to develop ADH?

A

females

>20kg

191
Q

what is iatrogenic hyperadrenocorticism?

A

iatrogenic disease due to chronic administration of glucocorticoids - causes suppression of CRH and ACTH production

192
Q

what can happen to the structure of the adrenal glands with iatrogenic hyperadrenocorticism?

A

bilateral adrenal atrophy

193
Q

what are the major clinical signs of hyperadrenocorticism?

A

polyphagia
abdominal distension

lethargy/exercise intolerance
panting

hepatomegaly

PUPD causing nocturia/incontinence

skin changes/alopecia

194
Q

what are the possible complications of hyperadrenocorticism?

A

progression of major signs

hypertension

DM from insulin resistance

pulmonary thromboembolism

neurological signs (obtundation/blindness/seizure)

pancreatitis

secondary infections (pyoderma/UTI)

glomerulopathy and proteinuria (cortisol-induced)

195
Q

how is hyperadrenocorticism diagnosed?

A

screening tests - haematology, biochemistry, urinalysis

screening tests of HPA axis -
ACTH stimulation test
low-dose dexamethasone suppression test
urine cortisol:creatinine ratio

196
Q

what does sensitivity mean?

A

probability of a positive result if the patient is affected

197
Q

what does specificity mean?

A

probability of a negative result if the patient is not affected

198
Q

what haematology results would you expect to see with hyperadrenocorticism?

A

mild erythrocytosis
mild thrombocytosis

stress/steroid leukogram (increased neutrophils and/or monocytes, decreased eosinophils and/or lymphocytes)

199
Q

what biochemistry results would you expect to see with hyperadrenocorticism?

A

increased ALP and ALT

hypercholesterolaemia and hypertriglycerolaemia due to lipolysis

hyperglycaemia due to insulin antagonism

increased bile acids (cholestasis)

200
Q

what urinalysis results would you expect to see with hyperadrenocorticism?

A

variable specific gravity
dilute urine +/- proteinuria/glycosuria
+/- UTI
urolithiasis (calcium oxalate)

201
Q

what is important to consider when pursuing a diagnosis of HAC via tests of the HPA axis?

A

essential that some historical/clinical signs are apparent first

no recent steroid administration

202
Q

what does the ACTH stimulation test involve?

A

measuring serum cortisol before and 1h post ACTH administration

203
Q

administration of what type of drug will affect the ACTH stimulation test?

A

recent administration of glucocorticoids will affect result

204
Q

what would be expected to happen to cortisol levels in the normal dog in the ACTH stimulation test?

A

small but significant rise

205
Q

what would be expected to happen to cortisol levels in a dog with PDH/ADH in the ACTH stimulation test?

A

dramatic rise >600nmol/L

206
Q

what would be expected to happen to cortisol levels with iatrogenic hyperadrenocorticism in the ACTH stimulation test?

A

levels stay the same - chronic steroid admin means unresponsive to ACTH

207
Q

what are the advantages of performing the ACTH stimulation test?

A

less affected by non-adrenal illness than LDDST

good first-line test

useful for ruling out iatrogenic disease

can be used for monitoring response to treatment

208
Q

what are the drawbacks of the ACTH stimulation test?

A

less sensitive than LDDST - beware of false negatives

doesn’t distinguish PDH from ADH

209
Q

what is involved in the low dose dexamethasone suppression test? (LDDST)

A

comparison of serum cortisol concentration before and 4/8 hours after dexamethasone injection

210
Q

what would be expected to happen to cortisol levels in the normal dog in the LDDST test?

A

cortisol drops significantly after 4 hours and is almost 0 after 8 hours

211
Q

what would be expected to happen to cortisol levels in the ADH dog in the LDDST test?

A

flat line - no change in cortisol levels

212
Q

what would be expected to happen to cortisol levels in the PDH dog in the LDDST test?

A

40% flat line - no change

30% exhibit an escape V pattern - drops at 4 hours but significantly risen again at 8 hours

213
Q

what are the drawbacks of the LDDS test?

A

less specific than ACTH stimulation test - beware false positives
affected by non-adrenal illness

not useful for iatrogenic disease

214
Q

what are the advantages of the LDDS test?

A

excellent sensitivity (positive test strongly indicates PDH/ADH)

can distinguish PDH from ADH

215
Q

what is involved in the urine cortisol:creatinine ratio test?

A

urine sample collected at home - 2 pooled morning urine sample
several days following ‘stressful event’ (e.g. vet visit)

216
Q

what is the urine cortisol:creatinine ratio useful for?

A

useful to exclude HAC

i.e. normal results = cushings very unlikely

217
Q

what is hyperadrenocorticism also called?

A

cushing’s disease

218
Q

what is the drawback of the urine cortisol:creatinine ratio test?

A

highly sensitive but not very specific - false positives common

219
Q

what tests are useful in differentiating PDH from an adrenal tumour?

A

low and high-dose dexamethasone suppression tests
imaging
endogenous ACTH concentration

220
Q

what result would be expected from an ADH dog during a HDDS test?

A

flat line - no cortisol change

221
Q

what result would be expected from a PDH dog during a HDDS test?

A

15% show flat line but most exhibit an escape V pattern as for LDDS test

222
Q

what dose rate is given in the HDDS test?

A

0.1mg/kg

223
Q

what would be seen on an abdominal ultrasound of a PDH dog?

A

symmetrical adrenal glands, enlarged or normal

224
Q

what would be seen on an abdominal ultrasound of an AT dog?

A

asymmetrical adrenal glands

225
Q

why might you perform an MRI on a dog with hyperadenocorticism?

A

the evaluate the pituitary gland and adrenal glands - 90% of PDH have a brain mass (microadenoma or macroadenoma)

226
Q

why might an endogenous ACTH test be performed for hyperadrenocorticism?

A

to differentiate between PDH and AT
PDH = ACTH >45pm/ml
AT = undetectable ACTH

227
Q

when should you pursue treatment of HAC?

A

only if very high index of suspicion through history, clinical signs, haem/biochem and specific testing

228
Q

what treatment options are available for for PDH?

A

medical - trilostane

surgical - hypophysectomy, bilateral adrenalectomy

radiation therapy

229
Q

how should trilostane be given?

A

with food, once or twice a day

230
Q

how does trilostane work?

A

blocks production of cortisol at the level of the adrenal glands

231
Q

how should cushings patients be monitored while on trilostane?

A

monitor clinical signs and ACTH stimulation test or pre-pill cortisol

side effects: GI signs, hypoadrenocorticism, adrenal necrosis

232
Q

what is hypophysectomy?

A

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

233
Q

for which type of HAC is hypophysectomy the only potential curative option?

A

PDH

234
Q

what is the prognosis for hypophysectomy?

A

goof long-term outcomes have been reported (3 years)

increasing pituitary tumour size associated with higher mortality and incidence of residual disease and relapse

235
Q

what supportive treatment will hypophysectomy patients require long-term?

A

hormonal supplementation with glucocorticoids and thyroxine

transient diabetes insipidus means that DDAVP administration can often be discontinued

236
Q

what is radiation therapy useful for in PDH?

A

may be effective in reducing the size of macroadenomas or eliminating neurological signs

237
Q

what concurrent treatment is used with radiation therapy for PDH?

A

trilostane - reduction in secretion of ACTH is variable

238
Q

what is the prognosis for treating PDH with radiotherapy?

A

mean survival time of 25 months reported

delayed improvement in clinical signs can occur

239
Q

what type of HAC is adrenalectomy used to treat?

A

ADH

240
Q

what are the complications of adrenalectomy?

A 
haemorrhage
hypertension 
acute hypercortisolaemia 
hyperaldosteronism 
wound breakdown
241
Q

what treatment options are available for ADH?

A 
adrenalectomy 
medical therapy (trilostane)
242
Q

what medical therapy is used for treating ADH?

A

trilostane

generally more resistant to therapy - usually used for management pre-surgery

243
Q

what other general treatment considerations are there for hyperadrenocorticism?

A

treatment may unmask other underlying diseases

reduced cortisol can cause pituitary lesions to expand (CNS signs)

244
Q

what is the prognosis for PDH?

A

depends on age, overall health and owner commitment

mean survival following diagnosis is approx 30 months

245
Q

what is the prognosis for ADH?

A

mean survival following successful surgery is 36 months

dogs with metastatic disease usually die/euthanased within 12 months

246
Q

what most commonly causes hyperadrenocorticism in cats?

A

secondary to insulin-resistant diabetes mellitus

247
Q

what are the signs of hyperadrenocorticism in cats?

A

cachexia
fragile skin syndrome - care with handling
alopecia (symmetrical, non-pruritic)

248
Q

how is hyperadrenocorticism diagnosed in cats?

A

no increase in ALP

HDDS test and ACTH stimulation test (60+90 mins after injection)

249
Q

how is hyperadrenocorticism treated in cats?

A

adrenalectomy if adrenal mass

no reliable treatment for PDH

250
Q

what is the prognosis for hyperadrenocorticism in cats?

A

guarded to poor - worse than in dogs

CVNT2 (47 decks)

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