Pituitary Gland and Its Disorders Flashcards
(29 cards)
1
Q
What are the clinical signs and symptoms of pituitary tumours?
A
- Hormone hypersecretion
- Space occupying lesion
- Headaches
- Visual loss (field defect)
- Cavernous sinus invasion
- Hormone deficiency states
- Interference with surrounding normal pituitary
2
Q
What can excess LH/FSH be a sign of?
A
Non-functioning pituitary tumour
3
Q
What may cause excess PRL?
A
Prolactinomas
- Common
- PRL different control to all other anterior pituitary hormones - Tonic release of dopamine inhibits PRL release
- Positive feedback
4
Q
What are the direct and indirect actions of GH?
A
Direct:
- Increase gluocose transport, lipolysis, amino acid transport, protein synthesis, fibroblast differentiation
Indirect:
- Increase linear growth, collagen synthesis, bone remodelling, somatic cell growth
5
Q
What are some stimulating factors for GH?
A
- GHRH - From hypothalmic parvocellular neuronendocrine cells
- Ghrelin - From epsilon cells
- Hypoglycemia
- Decreased fatty acids
- Fasting
- Exercise
- Sleep
- Stress
6
Q
What are some inhibitory factors for GH?
A
- Somatostatin (GHIH) - From hypothalmic parvocellular neuroendocrine cells
- GH in circulation
- Hyperglycemia
- Increased fatty acids
- IGF-1 - Released by liver in response to GH
7
Q
What are the features of non-functioning tumours?
A
- 30% of all pituitary tumours
- No syndrome of hormone excess produced
- Cause symptoms due to space occupation
- Headache
- Visual field defects
- Nerve palsies
- Interfere with rest of pituitary function - deficiency of hormones
- Treatment:
- Surgery (transsphenoidal approach) +/- radiotherapy
- No effective medical treatment
8
Q
How are pituitary adenomas treated?
A
- Surgery
- Transsphenoidal
- Adrenalectomy - Nelson’s syndrome
- Radiotherapy
- Slow
- Drugs
- Block hormone production
- Stop hormone release
9
Q
What is Acromegaly?
A
GH excess
Test - Oral glucose tolerance test
10
Q
Describe the systemic effects of GH/IGF-I excess
A
- Acral enlargement - Space like hands, rings too small, increase shoe size, macroglossia, carpal tunnel syndroe
- Increased skin thickness
- Increased sweating
- Skin tags and acanthosis nigricans
- Inter-dental spacing
- Visceral enlargement
Other effects:
- Cardiomyopathy
- Hypertension
- Bowel polyps, colon cancer
- Multinodular goiter, hypogonadism
- Arthropathy, OSA
11
Q
What are underproduction GH syndromes?
A
- Dwarfism (Laron’s)
- Adult GH deficiency
- Pituitary Destruction
Test:
- Insulin Tolerance test
- Glucagon Test
12
Q
What is Cushing’s disease?
A
ACTH excess
13
Q
Describe the consequences of Cushing’s disease?
A
- Changes in protein and fat metabolism:
- Change in body shape
- Central obesity
- Moon face
- Buffalo hump
- Thin skin, easy bruising
- Osteoporosis (brittle bones
- Diabetes
- Changes in sex hormones:
- Excess hair growth
- Irregular periods
- Problems conceiving
- Impotence
- Salt and water retention:
- High BP
- Fluid retention
14
Q
What is Secondary thyrotoxicosis?
A
Excess TSH
15
Q
Describe the features and treatment of prolactinomas
A
Many drugs interfere with DA and PRL secretion:
- Antiemetics
- Antipsychotics
- OCP/HRT (contraceptive pill)
Features of PRL excess (hypogonadism):
- Infertility
- Amenorrhoea
- Reduced libido
- Oligoamenorrhoea - Periods stop
- Galactorrhoea
- Erectile dysfunction
Treatment: Dopamine agonists
- Broocriptine
- Cabergoline
16
Q
What are causes of pituitary failure?
A
- Tumour (benign or malignant)
- Trauma
- Infection
- Inflammation - Sarcoidosis, histiocytosis
- Latrogenic
17
Q
Describe the effects of hypopituitarism
A
- Thyroid
- Bradycardia
- Weight gain
- Cold intolerance
- Hypothermia
- Constipation
- Sex steroids
- Oligomenorrhoea
- Reduced libido
- Hot flushes
- Reduced body hair
- Reduced cortisol
- Tiredness
- Weakness
- Anorexia
- Postural hypotension
- Myalgia
- Reduced GH
- Tired
- Central weight gain
18
Q
How is hypopitutarism treated?
A
- Thyroid - Thyroxine
- Sex steroids - Testosterone, oestrogen
- Reduced cortisol - Hydrocortisone
- Reduced GH - Growth hormone
19
Q
Define SIADH and list possible causes
A
- Too much ADH secretion or action
- Brain injury/infection
- Lung cancer/infection asthma IPPV
- Metabolic
- Hypothyroidism
- Addison’s
- Drugs
- Increased release a VP chemotherapy antidepressents (MOA inhibitors)
- Increased receptor sensivity (chlorpropamide clofibrate)
20
Q
How is SIADH diagnosed and treated?
A
- Decrease plasma Na+ (<135mmol/l)
- Decrease plasma osmolality (<285mOsm/kg)
- Increase urine osmolality (>100mOsm/kg)
- Increase urine sodium (>30mmol/l)
Treatment:
- Fluid retention
- Demeclocycline
- ADH antagonist (tolvaptan)
21
Q
Define diabetes insipidus
A
Inability of kidneys to concentrate urine, leading to excessive urine output despite normal blood sugar lvls
22
Q
What is the underlying cause of DI?
A
- Underproduction ADH
- Cranial - Lack of production
- ADH resistance
- Nephrogenic - Receptor resistance or damage to collecting ducts
23
Q
How is DI diagnosed?
A
- Polyuria (>3L)
- Polydipsia
- Increase plasma Na+
- Increase plasma osmolality (>295 mosmol/kg)
- Decrease urine osmolality (<700 mosmol/kg)
- Decrease urine Na+
24
Q
Explain the rationale of the water deprivation test and the steps involved and how this can help determine the cause of DI
A
- Assess how body regulates fluid balance by measuring urine concentration and ADH lvls when fluids restricted
- Typically involves measuring urine output, urine concentration, blood samples to determine how body responds to reduced hydration
- Pre-test:
- Blood + urine samples taken to establish baseline, patient weighed
- Fluid restriction for specific duration (normally 8hrs)
- During test:
- Patients weight, urine ouput, blood + urine samples collected at regular intervals to assess how body is responding to deprivation H2O
- Urine samples analysed to measure osmolality, helps determine kidney ability to concentrate
- Blood samples analysed to measure plasma osmolality
- Post-test:
- If urine osmolality still low despite water deprivation, synthetic ADH (desmopressin) adminstered
- Urine and blood samples then taken to see if kidneys respond to hormone
- Diabetes insipidus:
- Individuals continue to produce dilute urine even after water deprivation as kidneys unable to respond effectively to ADH
- Central DI:
- Administration of synthetic ADH should lead to an increase in urine osmolality, as problem lies with ADH secretion not resistance
- Nephrogenic DI:
- Even after desmopressin administration, urine concentration remains relatively low, as kidneys cannot respond properly to hormone
25
Outline the anatomy of the pituitary gland
- 2 lobes
- Lies below brown in Sella Turcica of sphenoid bone
- Anterior lobe (adenohypohysis) derived from invagination of roof of embryonic oropharynx known as Rathke’s pouch
- Notochordal projection from pituitary stalk, which connects gland to brain and also posterior lobe of pituitary (neurohypophysis)
26
Describe the blood supply to the pituitary gland
- Dual blood supply
- First via long + short pituitary arteries
- Second from hypophyseal portal circulation. Begins as a capillary plexus around Arc
27
What are the pituitary cell types and their hormones?
- Gonadotroph - LH and FSH
- Lactotroph - Prolactin
- Somatotroph - GH
- Corticotroph - ACTH
- Thyrotroph - TSH
28
What do ACTH, TSH, GH, LH/FSH and PRL do?
- ACTH - Regulates adrenal cortex
- TSH - Thyroid hormone regulation
- GH - Growth. Growth and developement (anabolic), couples growth to nutritional status
- LH/FSH - Reproductive control
- PRL - Breast milk production
29
What are the posterior pituitary hormones?
- ADH - Osmoregulation
- Oxytocin - Breast milk expression
