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CS endocrinology > Failure to grow/GH > Flashcards

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
Q

Clincal presentation pituritary dwarfism

A

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
Q

Type of dwarfism with low GH and TSH in GSD - why?

A

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
Q

Diagnosis of pituritary dwarfism (3)

A

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
Q 
Treatment of pituritary dwarfism first line
- medication
-dose
-monitoring
Side-effects
A

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
Q

Treatment for pituritary dwarfism in dogs if first line unavailable

  • Drug
  • MOA
  • Adverse effects
A

Progestagin (Medroxyprogesterone acetate)
Induces GH sysnethesis from mammary glands

Known side-effects: pruritic pyoderma, acromegalic appearance
Possible side-effects: DM, mammary tumour

30
Q

Prognosis piturtary dwarfism

A

3-5 years without treatment

Several years if treated with GH, progestins and T4 (if indicated)

31
Q

Causes of low/undetectable IGF-1

A 
GH deficiency
Hepatic dysfunction (location of synthesis)
Lymphoma
Newly diagnomsed DM (lack of insluin)
Renal disease
32
Q

Treatment pituritary dwarfism in cats

A

GH replacement therapy not described and progestins don’t work
Supplement other hormonal deficiencies

33
Q

Prevalence of acromegaly in all cats

A

1 in 800 diabetic and non diabetic cats

34
Q

Prevalence of acromegaly in diabetic cats

A

319/1221 (26.1%) cats in UK had IGF-1 >1000 ng/ml

1 in 5 diabetic cats have acromegaly

35
Q

Presentation of non-diabetic hypersomatropism

A

HCM-like disease, later life onset stertor, CNS disease (e.g. seizures) associted with enlarging pituritary mass.

36
Q

Prevalence hypersomatropism cats with myocardial thickening diagnosed as HCM

A

5-7% (1 in 20)

37
Q

Pituritary pathology associated with acromegaly

A

Most have pituritary somatotroph adenoma

Others - pituritary hyperplasia, carcinoma

38
Q

GH secretion pattern in cats with hypersomatotropism

A

Pulsatile but greater frequency and larger quantities (amplitude) of hormone

39
Q

Pathophysiology DM in acromegaly

A

Insulin resistance associated with GH excess outplays compensatory insulin production

40
Q

Clinical signs diabetic cats with hypersomatotropism (8)

A

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
Q

Pathophysiology of clinical presentation

- heart, hunger, weight, respiratory change, growth, CNS

A

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
Q

Classical clinical presentation of a clinically well non-diabetic acromegalic cat

A

weight gain despite normal appetite

43
Q

Diagnosis of hypersomatropism (cat)

A

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
Q

Gender bias acromegaly

A

71% MN and 26% FN

45
Q

Reason for false negative IGF-1 in acromegalic diabetic cat

Prevalence of false negative

A

9%
Insulin deficiency
Insulin is required for the sunthesis and excretion of IGF-1 by the liver

46
Q

Novel hormonal test for monitoring response to acromegaly treatment in cats

A

Ghrelin
Increases following successful therapy
(not a diagnostic test as concentrations simmilar to uncomplicated diabetics)

47
Q

Treatment of hypersomatotropism in cats (5)

A

Hypophysectomy, radiotherapy, pasireotide, treating consequences of GH excess, cryotherapy

48
Q

Pros of hypophysectomy (5)

A 
Gold standard
85% diabetic remission within 2 months, remainder improved glycaemic control
Predictable success
Normalises IGF-1 
MST 2-3 yr
49
Q

Cons of hypophysectomy (3)

A

Availability, costs, morbdity and mortality (<10%)

50
Q

Pros of radiotherapy (3)

A

Decrease tumour size
Good for larger masses
DM remission 32%

51
Q

Cons of radiotherapy (6)

A

Availability
Cost
Unpredictable effect
Does not normalise GH, IGF-1 - progressive disease
Does not remove tumour - recurrance of signs
Multiple GA

52
Q

What treatment is required post hypophysectomy

A

Temporary DDAVP

Life-long - hydrocortisone and levothyroxine

53
Q

DM Remission rate with pasireotide

A

25%

54
Q

Cons of pasireotide (4)

A

Cost, doe snot normalise hormones, persistent tumour, diarrhoea

55
Q

MOA pasireotide

A

somatostatin receptor angonist with binding affinity for 1, 2, 3 and 5

56
Q

Location of pituritary tumour for hypersomatoropism

A

Pars distalis

57
Q

Possible gene mutation associated with hypersomatoropism in cats

A

polymorphism to AIP-gene

CS endocrinology (4 decks)

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