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Failure to grow/GH Flashcards

1
Q

Endocrine causes of failure to grow (9)

A 
GH deficiency
Juvenile diabetes mellitus (insulin deficency)
Juvenile hypothyroidism
Glucocorticoid excess
Gonadal hormone excess
Primary hypoadrenocorticism
IGF-1 deficiency
Hypoparathryoidism
Disorders of vitamin D metabolism
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2
Q

Non-endocrine causes of failure to grow (9)

A 
Reduced dietary intake
Insufficient nutrient intake (parasites, poor quality diet, V+/D+)
Maldigestion (EPI)
Malabsoprtion
Renal/hepatic disease
Anaemia (impaired oxygen delivery)
Severe chronic disease (incl infection)
Cardiac disease (shunt)
Chrondrosytrophy (abnormal bone growth)
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3
Q

Cause of disproportionate dwarfism (2)

A

Hypothyroidism, chrondrodystrophy

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4
Q

Cause of proportionate dwarfism

A

Pituritary dwarfism

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5
Q

GH secretion pattern in dogs (2)

A

1) Pulsatile from pituritary

2) Non-pulsatile by progestagens

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6
Q

Where may endogenous progestagens arise from in the dog

A

Mammary gland

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7
Q

Are progestagens sensitive to GHRH/ somatostatin

A

no

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8
Q

Stimulation of GH secreation (3)

A

GHRH
Progestagens
Ghrelin

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9
Q

Inhibition of GH

A

somatostatin

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10
Q

Direct metabolic effects of GH (4)

A

Insulin antagnosism
Lipolysis
Protein synthesis
Epiphyseal growth

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11
Q

Clinical manifestations of GH excess in the dog (5)

A

slow, inspiratory dyspnoea, pu/pd, thickening of the skin, excessive skin flods along head and neck

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12
Q

Conditions associated with GH excess in the dog (4)

A

1) Pituritary neoplasia
2) Endogenous progestagens - middle aged/older bitches in diestrus (luteal phase), mammary tumour
3) Exogenous progestagens - for oestrus prevention/BPH
4) Hypothroidism - increase GH and IGF-1

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13
Q

Laboratory changes associated with GH excess (4)

A

Hyperglycaemia (insulin antagonism), increased cholesteol and ALP, +/- raised progesterone

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14
Q

Diagnostics GH excess in the dog (3)

A

GH (pulsatile, need 305 samples)
Somatostatin supression test
IGF-1

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15
Q

Treatment of GH excess in the dog (5)

A

1) OHE is dioestrus associated
2) Discontinue exogenous progestagens
3) Resection of mammary tumours
4) Hypophysectomy/radiation of pituritary tumour
5) Progesterone receptor blocker (aglepristone)
6) Treat hypothryoidism

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16
Q

Two causes of GH deficiency in the dog (3)

A

1) Trauma (e.g. surgical - following hypophysectomy)
2) Neoplasia - Pituritary gland
3) Primary hypophysitis

Overall - diseases causing destruction of the somatotrophic cells in the pituritary gland

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17
Q

Pathogenesis of pituritary dwarfism dog

A

Pressure atrophy of the anterior

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18
Q

How does GH exert effects on metabolism indirectly

A

through IGF-1

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19
Q

Metabolic effects of IGF-1

A

Insulin like activity
Inhibit lipolysis
Protein synthesis
Epiphyseal growth

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20
Q

Condition requried for stimulation of IGF-1

A

Stiimulated by GH when nutrient intake is sufficient and insulin concentration in the portal vein is high.

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21
Q

Does GH or IGF-1 parallel body size

A

IGF-1

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22
Q

Breed and mutation associated with congenital hyposomatropism in the dog

A

GSD

Autosomal recessive inheritance of LHX3 mutation (genetic test available)

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23
Q

Pathophysiology of congenital hyposomatropism (2)

A 
Pressure atrophy secondary to cysts 
Pituritary hypoplasia (failure oropharyngeal ectoderm  of Rathe pouch to differentiate into normal trophic hormone secreting cells)
24
Q

Concurrent hormonal deficiencies in pituritary dwarfism

A

Combined deficiency of TSH and prolactin in GSD

25
Clincal presentation pituritary dwarfism
1) Age - 2-5 month of age 2) Musculoskeletal - Proportionate dwarfism, Delayed dental eruption 3) Dermatologic - Puppy coat (soft, wooly) followed by alopecia 4) Reproductive - often crypthrochid, peristent anestrus 5) Mental dullness/signs of secondary hypothryoidism
26
Type of dwarfism with low GH and TSH in GSD - why?
Proportionate as the clincial manifestations of hypothryoidism are overshadowed by pronounced deficiency of GH. This is in part because a small but significant fraction of thyroid function is idependent of TSH.
27
Diagnosis of pituritary dwarfism (3)
1) genetic testing - LHX3 mutation (GSD) - will have combined pituritary hormone deficiency 2) GH stimulation test using GHRH, clondine, xylazine or ghrelin 3) IGF-1 - but not sole test as can be reduced due to starvation and illness *diagnosis should not be based on piturtary imaging
28
``` Treatment of pituritary dwarfism first line - medication -dose -monitoring Side-effects ```
Drug - Porcine GH (AA sequences dog and pig identical) +/- levothyroxine Dose - 0.1 IU/kg SC three times a week Monitoring - Dosage adjusted according to IGF-1 levels q 4-6 wk and include blood glucose. Side-effects - DM, hypersensitivity reaction
29
Treatment for pituritary dwarfism in dogs if first line unavailable - Drug - MOA - Adverse effects
Progestagin (Medroxyprogesterone acetate) Induces GH sysnethesis from mammary glands Known side-effects: pruritic pyoderma, acromegalic appearance Possible side-effects: DM, mammary tumour
30
Prognosis piturtary dwarfism
3-5 years without treatment | Several years if treated with GH, progestins and T4 (if indicated)
31
Causes of low/undetectable IGF-1
``` GH deficiency Hepatic dysfunction (location of synthesis) Lymphoma Newly diagnomsed DM (lack of insluin) Renal disease ```
32
Treatment pituritary dwarfism in cats
GH replacement therapy not described and progestins don't work Supplement other hormonal deficiencies
33
Prevalence of acromegaly in all cats
1 in 800 diabetic and non diabetic cats
34
Prevalence of acromegaly in diabetic cats
319/1221 (26.1%) cats in UK had IGF-1 >1000 ng/ml | 1 in 5 diabetic cats have acromegaly
35
Presentation of non-diabetic hypersomatropism
HCM-like disease, later life onset stertor, CNS disease (e.g. seizures) associted with enlarging pituritary mass.
36
Prevalence hypersomatropism cats with myocardial thickening diagnosed as HCM
5-7% (1 in 20)
37
Pituritary pathology associated with acromegaly
Most have pituritary somatotroph adenoma | Others - pituritary hyperplasia, carcinoma
38
GH secretion pattern in cats with hypersomatotropism
Pulsatile but greater frequency and larger quantities (amplitude) of hormone
39
Pathophysiology DM in acromegaly
Insulin resistance associated with GH excess outplays compensatory insulin production
40
Clinical signs diabetic cats with hypersomatotropism (8)
1) PU/PD (87%) 2) PP 75% (extreme (20%) 3) Weight gain (17%) - weight loss also possible if impact of DM outweighs anabolic effects of GH excess 4) Stridor (38%) 5) Organomegaly (40%) 6) rognathia inferior (18%) 7) Clubbed paw (13%) 8) Broad facial features (37%)
41
Pathophysiology of clinical presentation | - heart, hunger, weight, respiratory change, growth, CNS
Hypertrophic changes of the myocardium - heart murmur, CHF GH stimulus of hunger centre - PP Anabolic effect of GH - weight gain Growth of tissues - broad facial features, stridor Growth of pituritary mass - CNS signs
42
Classical clinical presentation of a clinically well non-diabetic acromegalic cat
weight gain despite normal appetite
43
Diagnosis of hypersomatropism (cat)
1) IGF-1 >1000 ng/ml (600-1000 grey area) - ppv 95% 2) Procollagen propetide type III (PIIIP) - peripheral indicator of collagen turnover, 5 times higher in HST cats with secondary DM cf uncomplicated DM. Not dependent on insulin availability. 3) Imaging - in conjunction with IGF-1. Pit >4mm consistent with enlargement. MRI more sensitive. (absence does not exclude microadenoma)
44
Gender bias acromegaly
71% MN and 26% FN
45
Reason for false negative IGF-1 in acromegalic diabetic cat Prevalence of false negative
9% Insulin deficiency Insulin is required for the sunthesis and excretion of IGF-1 by the liver
46
Novel hormonal test for monitoring response to acromegaly treatment in cats
Ghrelin Increases following successful therapy (not a diagnostic test as concentrations simmilar to uncomplicated diabetics)
47
Treatment of hypersomatotropism in cats (5)
Hypophysectomy, radiotherapy, pasireotide, treating consequences of GH excess, cryotherapy
48
Pros of hypophysectomy (5)
``` Gold standard 85% diabetic remission within 2 months, remainder improved glycaemic control Predictable success Normalises IGF-1 MST 2-3 yr ```
49
Cons of hypophysectomy (3)
Availability, costs, morbdity and mortality (<10%)
50
Pros of radiotherapy (3)
Decrease tumour size Good for larger masses DM remission 32%
51
Cons of radiotherapy (6)
Availability Cost Unpredictable effect Does not normalise GH, IGF-1 - progressive disease Does not remove tumour - recurrance of signs Multiple GA
52
What treatment is required post hypophysectomy
Temporary DDAVP | Life-long - hydrocortisone and levothyroxine
53
DM Remission rate with pasireotide
25%
54
Cons of pasireotide (4)
Cost, doe snot normalise hormones, persistent tumour, diarrhoea
55
MOA pasireotide
somatostatin receptor angonist with binding affinity for 1, 2, 3 and 5
56
Location of pituritary tumour for hypersomatoropism
Pars distalis
57
Possible gene mutation associated with hypersomatoropism in cats
polymorphism to AIP-gene

CS endocrinology (4 decks)

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