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Ettinger > Endocrine Disease > Flashcards

Endocrine Disease Flashcards

1
Q

When do cats typically present with congenital hyposomatotropism?

A

2 months of age. Initial postnatal growth genetically determined, second phase growth hormone dependent

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2
Q

What are the typical clinical findings of feline congenital hyposomatotropism?

A

Proportional dwarfism, retained deciduous teeth, dry and dull haircoat, general weakness and lethargy

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3
Q

What % of cats with DM have acromegaly?

A

26%

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4
Q

Is there a sex predisposition in acromegalic cats?

A

70% neutered male

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5
Q

What non-diabetic clinical signs are often reported in cats with acromegaly?

A

Polyphagia, respiratory stertor, snoring, prognathia inferior, enlarged distal limbs, organomegaly, heart murmur, CNS signs

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6
Q

How is acromegaly screened for, what is the PPV of this test?

A

IFG-1 >1000 = PPC 95%

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7
Q

When can a false negative IGF be seen in acromegalic cats?

A

9% untreated diabetic cats (IGF-1 production dependent on portal insulin)

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8
Q

Can IGF-I levels be used as a marker of treatment success in cats with Hypersomatotropism treated with surgery or radiation?

A

Surgery - yes
Radiation - no

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9
Q

What alternative markers of Hypersomatotropism in cats have been explored?

A

Serum type III pro collagen peptide - marker of collagen turnover, 5x higher in FeHS DM than DM
Gherkin - lower in FeHS than controls but not diabetics. Increases post radiation

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10
Q

What % of FeHS cases experience diabetic remission following hypophysectomy?

A

85%

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11
Q

What medical management do cats need following hypophysectomy?

A

Hydrocortisone and T4 (life)
DDAVP - can be discontinued in most

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12
Q

What options for medical management of FeHS have been described?

A

Pasireotide - SST analogue - remission in 25% on long acting form
Cabergoline

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13
Q

What is the response to radiation treatment for FeHS?

A

Unpredictable

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14
Q

Describe GH secretion in dogs. What regulates it’s secretion?

A

From anterior pituitary, pulsatile
GHRH +
Somatostatin -
Ghrelin +
IGF directly inhibits and stimulates somatostatin release
From mammary - progestogen, non-pulsatile, not controlled by SS, GHRH or ghrelin

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15
Q

When is canine mammary GH production increased?

A

Dioestrus

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16
Q

What are the physiological effects of GH in dogs?

A

Rapid - insulin antagonism - ^lipolysis, gluconeogenesis, reduced glucose transport and hyperglycaemia
Slow - IGF growth factors - growth-promotion

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17
Q

What can cause excess GH in dogs?

A

Endogenous/exogenous progesterone
GH-producing mammary tumour
Hypothyroidism associated with increased GH and IGF-1
Pituitary somatotropin adenoma (RARE)

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18
Q

What are the clinical signs of GH hyper secretion in dogs?

A

Soft tissue swelling of head, neck, abdomen, snoring, stertor, joint issues (articular cartilage proliferation), PU, PP, increased organ size

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19
Q

How is CaHS diagnosed?

A

GHRH stimulation or SS suppression tests
IGF-1

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20
Q

What should be tested in a dog with GH excess, not receiving progestogens?

A

T4/TSH

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21
Q

How can dogs with somatotroph adenomas causing CaHS be treated medically?

A

Octreotide/lanreotide

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22
Q

What are the typical endocrine findings in GSD with pituitary dwarfism?

A

GH, TSH and prolactin deficiency
Normal ACTH

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23
Q

What mutation is associated with congenital pituitary dwarfism?

A

LHX3

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24
Q

What are the clinical manifestations of pituitary dwarfism in dogs?

A

Proportionate dwarfism, retained secondary hairs, lack of primary hairs, truncal alopecia, pointed muzzle, cryptorchidism/ovulation failure. Lethargy develops at 2-3 years due to secondary hypothyroidism

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25
Q

What are the findings on biochem for canine pituitary dwarfs?

A

High creatinine - GH needed for normal glomerular development

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26
Q

How is pituitary dwarfism diagnosed in dogs?

A

GHRH/clonidine/xylazine stimulation test. GH should increase 2-4x
Ghrelin suppression test can be used to exclude

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27
Q

What are the typical imaging findings in pituitary dwarfism in dogs?

A

Pituitary cysts +/- hypoplasia

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28
Q

How is canine pituitary dwarfism treated?

A

Porcine GH
Progestogens described

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29
Q

What is the prognosis for canine pituitary dwarfism?

A

Poor without treatment, guarded with
Loss of pituitary function, expansion of pituitary cysts renal failure

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30
Q

Describe vasopressin secretion?

A

AVP formed in the magnocellular neurons in the hypothalamus and transported to the posterior pituitary

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31
Q

What stimulates AVP release?

A

Increased plasma osmolality and Na content
Angiotensin II

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32
Q

What inhibits AVP release?

A

Baroreceptor stimulation
BNP

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33
Q

How does AVP act?

A

Binds V2 receptors, increase cAMP, activates protein-kinase A - causes expression of aquaporin 2

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34
Q

In addition to AVP release, what are the effects of AVP binding V2 receptors?

A

VWF release
TPA release
ANP release
NO synthesis
FVIII release

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35
Q

What are the most common causes of CDI in dogs and cats?

A

Dogs - neoplasia
Cats - trauma

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36
Q

What are the causes of NDI?

A

HAC, pyometra, hyperCa++, pyelonephritis, liver disease, primary

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37
Q

What % of dogs with CDI develop neuro signs within a year?

A

~40%

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38
Q

What treatment options are described for NDI?

A

Thiazide diuretics - decrease Na+ absorption, reduce delivery to distal tubules
Low Na diet

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39
Q

What are the actions of the V1a and V1b receptors?

A

V1a - vascular SM, glucogenolysis, platelet activation
V1b - stimulates ACTH, catecholamine and insulin secretion

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40
Q

How is glargine insulin modified to increase its duration of action?

A

Structure modified to make soluble at pH 4 and relatively insoluble at physiological pH

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41
Q

How is detemir insulin modified to increase its duration of action?

A

Structure modified so reversibly binds albumin

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42
Q

How does the potency of detemir in dogs differ from other species?

A

4x as potent

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43
Q

If spaying isn’t possible in a recently diagnosed FE diabetic what is an alternative?

A

Aglepristone

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44
Q

What is fructosamine?

A

Glycated protein formed by irreversible non-enzymatic reaction between glucose and plasma proteins

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45
Q

What non-diabetic factors can alter fructosamine?

A

Hypothyroidism and multiple myeloma associated with increase

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46
Q

Where is the calcium-sensing receptor found?

A

Parathyroid, kidneys, bone, cartilage

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47
Q

How is circulating calcium found?

A

50% ionised
40% protein bound
10% bound to anions

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48
Q

What factors can falsely alter TCa/iCa measurement?

A

Haemolysis, lipaemia increase TCa
Hypoproteinaemia decreases TCa
Storage - RBC produce lactic acid, pH decreases, iCa increases
Air exposure - CO2 lost, pH rises, iCa decreases

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49
Q

What 4 hormones regulate calcium?

A

PTH
PTHrP
Vit D
Calcitonin

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50
Q

How is PTH production regulated?

A

CaSR activated by hypercalcaemia and reduced PTH production

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51
Q

Describe the anatomy of the parathyroid glands

A

4 glands, cranial pair external, caudal internal

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52
Q

How does PTH act?

A

Increases Ca, decreases PO4 by action in bone, kidneys and GIT

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53
Q

How do vitamin D and phosphate affect PTH production?

A

^Vit D = v PTH
^PO4 = ^ PTH

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54
Q

What is PTHrP

A

Integral in the foetus, undetectable after birth
Same physiological effects as PTH
Causes humoral hypercalcaemia of malignancy

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55
Q

Describe vitamin D metabolism

A

Cholecalciferol, hydroxylated in the liver to produce 25-OH calciferol (calcidiol) - inactive and unregulated
Activated to 1,25-OH-vit D (calcitriol) in kidney
Increased by PTH
Suppressed by PO4
Can also be catabolised to 24-OH and excreted

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56
Q

What is calcitonin

A

Produced in thyroid gland C-cells
Reduces serum Ca
Limits post prandial hypercalcaemia

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57
Q

What breed is predisposed to PHPT?

A

Keeshonden

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58
Q

How does hypercalcaemia cause PUPD

A

Ca antagonises AVP
Ca inhibits tubular uptake of Na and Cl

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59
Q

What are the clinical signs of PHPT?

A

PUPD (mild), lethargy, urolithiasis, muscle wastage, weakness

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60
Q

In dogs with PHPT how is the risk of urolithiasis increased?

A

Increased renal excretion of Ca
Increased PO4 excretion
GI absorption of oxalate increased when calcium absorption increased
Therefore urine supersaturated with Ca, PO4 and oxalate

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61
Q

What medications can be used to lower serum calcium, what is their MOA?

A

Steroids - increase renal loss, decrease intestinal absorption, decrease bone resorption
Bisphosphanates - inhibit osteoclast activity and increase apoptosis
Calcitonin - inhibits osteoclast activity and inhibits renal reabsorption
Cinacalcet - calcimemetic - interacts with the CaSR directly

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62
Q

How do the post operative outcomes for ethanol ablation, heat ablation and surgery in PHPT

A

Ethanol - 72-90%
Heat - 90%
Surgery - 94%

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63
Q

What oral vitamin D formulations are available. What is the active ingredient?

A

Calcitriol - 1,25-(OH)2
Alfacalcidol - needs 25-hydroxylation, rapid and unregulated - no significant difference in time to become effective

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64
Q

What should be monitored for on the ECG when administering IV calcium

A

ST elevation
QT shortening
Arryhmias

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65
Q

What are the clinical signs of PHPT in cats?

A

Vomiting, PUPD, weight loss, cervical mass

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66
Q

What are the effects of hypoparathyroidism?

A

vCa
^PO4

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67
Q

What is the most common cause of hypoparathyroidism

A

Idiopathic
Evidence to support IM aetiology

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68
Q

What are the predispositions to hypoparathyroidism?

A

Females, miniature Schnauzers, Poodles, GSD, Terriers

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69
Q

What are the clinical signs of hypoparathyroidism?

A

Seizures, muscle tremors, stiff gait, inappetence, vomiting, lethargy, tacchycarrythmias

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70
Q

What eye change is described with hypoparathyroidism?

A

Lenticular cataract formation

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71
Q

What routine blood testing changes are found in hypoparathyroidism?

A

v Ca
^ PO4
Elevated CK

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72
Q

What are the ddx for hypocalcaemia?

A

Hypomagnesemia
AKI
CKD
Pancreatitis
DM
Eclampsia
Malabsorption
Urinary obstruction
Phosphate-containing enema

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73
Q

What ECG changes are described with hypoclacaemia?

A

ST and QT prolongation

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74
Q

In what forms (and relative quantities) is thyroid hormone found?

A

60% - thyroxine-binding globulin
17% - transthyretin
12% - albumin
11% - lipoprotein fractions

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75
Q

How does the potency of T3/T4 compare?

A

T3 3-5x more potent

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76
Q

How is T3 produced?

A

40% in thyroid
60% by peripheral outer ring monodeodination of T4

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77
Q

How is T3/4 secretion regulated

A

TRH (hypothalamus)
TSH (anterior pituitary)

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78
Q

What is rT3

A

Reverse T3 - metabolically inactive

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79
Q

How do thyroid hormones work?

A

Modify gene expression

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80
Q

In which dog breeds have congenital thyroid dyshormogenesis been described?

A

Toy Fox and Rat terriers

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81
Q

What are the common histopathological findings in primary acquired hypothyroidism?

A

Lymphocytic thyroiditis
Thyroid atrophy

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82
Q

What % of hypothyroid dogs have TgAAs?

A

50%

83
Q

What breeds have a higher risk of developing TgAAs?

A

English Setter, Golden Retriever, Rhodesian Ridgeback, Cocker Spaniel, Boxer

84
Q

What cardiac changes are associated with hypothyroidism in dogs and how often are they reported?

A

15%
Asymptomatic bradycardia
Low voltage R waves, inverted T, 1st/2nd degree AV block
Reduced FS

85
Q

What neurological changes have been described in hypothyroid dogs?

A

Facial nerve paralysis
Laryngeal paralysis
Megaoesophagus
Peripheral/central vestibular
Lower motor neurone dysfunction
Crichopharyngeal achalasia

86
Q

What ophthalmological changes have been described in hypothyroid dogs?

A

Arcus lipoides
KCS?

87
Q

What are the 5 most common clinicopathological abnormalities in hypothyroid dogs?

A

Anaemia
Hypercholesterolaemia
Hypertriglyceridaemia
Increased CK
Increased fructosamine

88
Q

What medications interfere with T4 measurement? Which affect TSH?

A

Pred (vTSH)
Phb
TMPS (^TSH)
Aspirin
Clomipramine
NSAIDs
Toceranib (^TSH)

89
Q

What is the value in measuring TT3 when hypothyroidism is suspected?

A

Limited
Maintained in normal range in 90%
May be useful in greyhounds

90
Q

What is the value in measuring TT4 when hypothyroidism is suspected?

A

High sensitivity
T4AA may falsely increase

91
Q

What is the value in measuring fT4 when hypothyroidism is suspected?

A

Most specific test

92
Q

What is the value in measuring cTSH when hypothyroidism is suspected?

A

Moderate sensitivity
WNLs in significant proportion of hypothyroid dogs

93
Q

What is the value in measuring TgAAs when hypothyroidism is suspected?

A

May be elevated before clinical hypothyroidism
No information on thyroid function

94
Q

What is the value in performing TSH stimulation when hypothyroidism is suspected? How is it interpreted?

A

Gold standard
Euthyroid expect >1.5x increase
Absolute level >30nmol/l

95
Q

What imaging modality is the most accurate for differentiating hypothyroidism and NTI? When is it not reliable?

A

T-99
Steroids

96
Q

How does feeding affect the bioavailability of T4?

A

Halves it

97
Q

What are the clinical signs of hypothyroidism in cats?

A

Inappetence, mental dullness
Dull, dry, unkempt haircoat

98
Q

Is FT4 useful to diagnose hypothyroidism in cats?

A

Not known

99
Q

Is TSH useful to diagnose hypothyroidism in cats?

A

Feline specific assay not available. Use of canine assay described

100
Q

In hyperthyroid cats, is disease most often uni- or bilateral?

A

2/3 bilateral

101
Q

What is the most common CBC change in hyperthyroidism?

A

Erythrocytosis - 50%

102
Q

What biochem changes are commonly seen in hyperthyroid cats?

A

^ALT - 80%
^ALKP - 50%
Azotaemia - 25%

103
Q

If FT4 useful for diagnosing hyperthyroidism?

A

No - sensitivity 98%
However, elevated in !2% cats with NTI

104
Q

What suppression test can be used to diagnose hyperthyroidism in cats? How is it performed/interpreted?

A

T3 suppression test
Baseline blood collected. T3 administered for 2 days. Resampled. Both sampled assayed for TT4 and TT3
TT4 should be suppressed

105
Q

What stimulation test can be used to diagnose hyperthyroidism in cats? How is it performed/interpreted? What are it’s limitations

A

TRH stimulation test
TT4 concentration increases <50% in hyperthyroid cats
Cost, limited accuracy if concurrent illness, risk of cholinergic/CNS reactions

106
Q

What imaging test can be used to diagnose hyperthyroidism in cats? How is it performed/interpreted?

A

Scintigraphy
Thyroid:salivary >1.5 - hyperT
<1 normal

107
Q

What side effects are reported with anti-thyroid medications in cats?

A

Agranulocytosis, thrombocytopenia, hepatopathy, bleeding

108
Q

What medications are used to manage hyperthyroidism in cats? What is their MOA?

A

Methimazole and carbimazole (prodrug)
Thioureylenes - inhibit thyroid follicular cell peroxides, inhibit iodination of tyrosyl residues

109
Q

What is the expected behaviour of canine thyroid tumours?

A

Malignant

110
Q

What are the common canine thyroid tumours?

A

30% adenoma
70% carcinoma
Carcinomas - 70% follicular cell, 30% medullary (also called parafollicular or C-cell)

111
Q

What has been shown to be a risk factor for the development of thyroid tumours in dogs?

A

Chronic exposure to excess TSH

112
Q

What is the average age and sex predilection for thyroid carcinoma in dogs?

A

9-11
No sec predilection

113
Q

Which tests have the highest sensitivity and specificity for diagnosing thyroid carcinoma?

A

CT - 100% spec
MRI - 93% sens

114
Q

Is scintigraphy useful for screening for metastasis of thyroid carcinoma?

A

No

115
Q

What effect does diagnosis of a malignant thyroid carcinoma have on prognosis?

A

None

116
Q

What is the MST for dogs following removal of a unilateral thyroid carcinoma?

A

3 years

117
Q

What is the median PFI following radiation therapy of thyroid carcinoma in dogs?

A

45 months

118
Q

What are the treatment options for thyroid carcinoma in dogs?

A

Surgery
Radiation
I131
Chemotherapy - doxorubicin/cisplatin/mitoxantrone
Medical

119
Q

What chemotherapy drug has been shown to be most effective in treating thyroid carcinoma in dogs and what is the MST?

A

Cisplatin
11 months

120
Q

What proportion of thyroid carcinoma are functional?

A

10%

121
Q

How is normal insulin secretion regulated?

A

Glucose enters beta cells
Metabolised to ATP
Closes ATP-sensitive K channels
Reduced K efflux, depolarisation
Ca channels open
Insulin exocytosis

122
Q

What are the counter regulatory hormones secreted in hypoglycaemia?

A

Glucagon
Catecholamines
GH
Glucocorticoids

123
Q

What unusual neurological clinical signs are recognised in insulinoma?

A

Peripheral polyneuropathy - posterior paresis/tetraparesis

124
Q

Ddx - hypoglycaemis

A

Insulinoma
Extrapancreatic tumour - gastric, hepatic, intestinal
Beta cell hyperplasia
Hypoadrenocorticism
Hypopituitarism
Hepatic insufficiency
Glycogen storage disease
Sepsis
Hunting dogs
Oral hypoglycaemic, beta blockers, ethanol, ACE-i, lidocaine OD, lithium

125
Q

What % dogs with insulinoma have a mass identifiable on US?

A

56%

126
Q

Other than IV glucose, what treatment has been described for acute hypoglycaemia associated with an insulinoma? What is the MOA? What is a drawback of this treatment?

A

IV glucagon CRI
Promoted glycogenolysis and gluconeogenesis
Increases insulin secretion

127
Q

What medical treatments of insulinoma have been described? What is their MOA?

A

Streptozocin - nitrosurea antibiotic, destroys beta cells. Risk of DM, nephrotoxic
Red - increases gluconeogenesis and glucose-6-phosphatase activity. Decreases glucose uptake into tissue. Stimulated glucagon secretion.
Diazoxide - inhibits closure of beta cell ATP-dependent K channels. GI se’s
Octreotide - SSA, inhibits insulin secretion but also glucagon and GH - varied response

128
Q

What factors influence prognosis of insulinoma?

A

Tumour size
Ki67 index

129
Q

What % of cats diagnosed with DM have pancreatitis at the time of diagnosis?

A

60%

130
Q

Which cat breed has an association with DM?

A

Burmese

131
Q

What are the processes responsible for the development of DM in cats?

A

Insulin resistance
Reduced insulin secretion
Deposition of amylin and islet amyloid polypeptide
Oxidative damage - glucose/lipotoxicity

132
Q

What % of obese cats >8yo are glucose intolerant?

A

20%

133
Q

What % of cats in diabetic remission relapse? How many of these can achieve a 2nd remission?

A

25-30%
25%

134
Q

What is the recommended CHO content of a diet for a diabetic cat?

A

12%

135
Q

What oral hypoglycaemic are available for use in cats? What are their MOA?

A

Sulfonylureas - stimulate insulin secretion by binding ATPases - close K+ and open Ca channels
Meglitinides - bind ATPases (different site)
Biguanides - insulin sensitiser
Thiazolidinedione - bind in nucleus and alter gene expression, improve insulin sensitivity in adipose, muscle and liver
Alpha glucosidase inhibitors - inhibit action of membrane-bound brush border disaccharides - slow glucose absorption
Glucagon-like peptides - enhance beta cell survival

136
Q

What % of cats with HAC have DM at diagnosis?

A

80%

137
Q

Describe normal cortisol release regulation?

A

Hypothalamus - CRH
Anterior pituitary - ACTH

138
Q

What stimulates CRH secretion?

A

Cytokines - IL-1/6, TNF-alpha
Leptin
Dopamine
AVP
Ang II

139
Q

What inhibits CRH secretion?

A

Glucocorticoids
Somatostatin

140
Q

What are the 3 regions of the pituitary - what do they secrete?

A

Anterior - ACTH
Intermediate lobe - A cells - alpha-MSH, corticotropin-like intermediate lobe peptide (CLIP)
- B cells - POMC (cleaved to ACTH), beta-LPH
Posterior - oxytocin, prolactin

141
Q

Which regions of the adrenal gland contain 17-alpha-hydroxylase?

A

Fasiculata and reticularis zones

142
Q

What % dogs with HAC have PDH?

A

80-85%

143
Q

Where are tumours found in dogs with PDH?

A

Pars distalis in 70%
Pars intermedia in 30%

144
Q

What features are consistent with adrenal carcinoma?

A

> 2cm
Invasion
Cytology and histo can be unreliable

145
Q

What causes PUPD in HAC?

A

Increased glomerular filtration rates and inhibition of ADH action at renal tubular level

146
Q

How do leptin levels differ in overweight HAC dogs and normal overweight dogs?

A

Higher in HAC

147
Q

What % of HAC dogs have ALP elevation?

A

85-95%

148
Q

How does HAC affect calcium metabolism?

A

Increased urinary calcium, may result in increased PTH and hyperphosphataemia

149
Q

What can be determined from a mineralised adrenal mass?

A

About half adrenal adenomas and carcinomas calcify, does not indicate malignant potential

150
Q

What % of PDH dogs have US normal adrenal glands?

A

25%

151
Q

How do UCCR values differ between dogs with PDH and ADH?

A

Higher in PDH
If >100 probability of PDH >90%

152
Q

What are the sensitivity and specificity of the ACTH stimulation test?

A

Se - 85% (PDH), 60% (ADH)
Sp - 85-90%

153
Q

What test can be used for differentiation of iatrogenic and naturally occurring HAC?

A

ACTH stim

154
Q

What are the sensitivity and specificity of the LDDST? What can affect the specificity?

A

Se - 90-95% (PDH), 100% (ADH)
Sp - 40-50%
Sp affected by NAI

155
Q

When should a LDDST not be performed?

A

Phb treatment

156
Q

How should a V shaped LDDST be interpreted?

A

Likely PDH
30% express this pattern

157
Q

How can a HDDST be used to differentiated PDH from ADH?

A

Suppression to <40 considered diagnostic for PDH
Lack of suppression - could be ADH or PDH

158
Q

In what % of cases that fail to suppress on LDDST does HDDST provide extra information?

A

10%

159
Q

How is a UCCR/HDDST interpreted?

A

UCCR measured on 3 consecutive mornings, 3x dex given after 2nd sample. If 3rd sample <50% baseline, PDH likely

160
Q

How does trilostane work?

A

Inhibits 3-beta-hydroxysteroid dehydrogenase
Prevents conversion of pregnenolone into progesterone

161
Q

How do survival times compare in dogs with ADH treated with trilostane, mitotane and surgery?

A

Similar

162
Q

What proportion of cats with HAC have PD/AD disease?

A

85/15%

163
Q

What are the most common clinical signs observed with feline HAC?

A

DM
PUPD
PP
Abdo distension
Alopecia
Skin fragility
Weight loss
Weakness

164
Q

What proportion of cats with HAC are hypertensive?

A

20%

165
Q

What condition can be associated with a false positive ACTHST in cats?

A

Hyperthyroidism

166
Q

What is the sensitivity of ACTHST for HAC in cats?

A

56-80%

167
Q

What is the screening test of choice for feline HAC?

A

LDDST

168
Q

What is the recurrence rate for dogs with PD-HAC undergoing hypophysectomy?

A

25%

169
Q

What is the MOA of trilostane?

A

Competitice inhibitor of 3beta-hydroxysteroid dehydrogenase

170
Q

What tumours have the highest rates of adrenal gland metastasis in dogs?

A

Pulmonary, mammary, prostatic, gastric and pancreatic carcinoma and melanoma

171
Q

What % of primary ATs are adrenocortical or neuroendocrine in origin?

A

75/25%

172
Q

What are the strengths/weaknesses in cytology of adrenal masses?

A

90-100% accuracy in determining cortical vs medullary
Not reliable for distinguishing benign vs malignant

173
Q

What imaging features are suggestive of a AT being malignant?

A

Size >2cm
Invasion

174
Q

What acid-base abnormality is commonly seen with hyperaldosteronism?

A

Metabolic alkalosis (aldosterone-mediated H+ excretion)

175
Q

How is primary hyperaldosteronism diagnosed?

A

PRA and aldosterone concentrations
Fludrocortisone suppression test

176
Q

What are the layers of the adrenal cortex?

A

Out
ZG
ZF
ZR
In

177
Q

Where are glucocorticoids and mineralocorticoids secreted?

A

Glucocorticoids - all 3
Mineralocorticoids - ZG

178
Q

What causes secondary hypoadrenocorticism?

A

Pituitary failure to produce ACTH
or hypothalamus failure to produce CRH

179
Q

What acid-base analysis is common in HA and why?

A

Metabolic acidosis in 60%
Aldosterone facilitates urinary H+ excretion

180
Q

What ECG features are seen with HA?

A

Absent p waves
Wide QRS
Tall T-waves
+/- heart block

181
Q

What is an alternative test to the ACTHst for diagnosis HA ?

A

Cortisol:eACTH

182
Q

Where is secretin produced?

A

S cells (duodenum)

183
Q

Where is glucagon produced?

A

Pancreatic alpha cells

184
Q

What are the main effects of glucagon?

A

Hepatic glycogenolysis and gluconeogenesis

185
Q

Where is gastrin produced?

A

G cells (antrum and duodenum)

186
Q

Where is CCK produced?

A

I cells (duodenum and jejunum)

187
Q

Where is somatostatin produced?

A

Hypothalamus, delta cells (pancreas), enteric nervous system

188
Q

Where is motion produced?

A

GI cells

189
Q

Where is ghrelin produced?

A

Stomach

190
Q

What are the clinical hallmarks of gastrinoma?

A

Antral hypertrophy, hyperacidity and ulceration

191
Q

What are the common clinical signs of gastrinoma?

A

V/D/weight loss

192
Q

What can cause increased blood gastrin levels in dogs?

A

Gastrinoma, gastropathies, hepatopathies, acid blocking medication

193
Q

What diagnostic tests are used to diagnose gastrinoma?

A

Serum gastrin/gastric pH
Secretin/Ca++ stimulation (normally gastrin doesn’t increase)

194
Q

Where are gastrinoma most often found?

A

Right limb/body of pancreas

195
Q

Where are carcinoids found?

A

Neuroendocrine cells of GIT, bronchial tree, biliary epithelium

196
Q

What do carcinoids produce?

A

5-HT (serotonin) or kinins

197
Q

How do carcinoids present?

A

Normally non-functional

198
Q

From which cells to pheochromocytoma arise?

A

Chromaffin cells of adrenal medulla

199
Q

From which amino acid are catecholamines synthesised?

A

Tyrosine

200
Q

Draw the pathway of catecholamine production

A

Ettinger pg 1839

201
Q

What test is most reliable for diagnosing pheochromocytoma in dogs?

A

UMN:crea

202
Q

What medication has the potential to interfere with MN/NMN testing

A

Phenoxybenzamine

203
Q

What test other than MN testing can be used to differentiate pheochromocytoma and HAC in dogs? When is this test not applicable?

A

Serum inhibit - undetectable in pheo
ME/FE dogs

204
Q

MOA phenoxybenzamine?

A

Alpha-adrenergic receptor antagonist
Irreversibly bings a1 and a2

Ettinger (13 decks)

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