Fundamentals of Endocrinology Flashcards
What are the consequences of diabetes?
- Atherosclerosis
- Diabetic retinopathy
- Renal failure
- Ulcers- gangrene
- Erectile dysfunction
What are the symptoms and signs of Cushing’s Syndrome?
- High blood pressure
- Diabetes
- High blood cholesterol
- Central (visceral) obesity
- Stretch marks
- Bruising
- Osteoporosis
- Muscle weakness
- Infertility
- Depression
- Memory loss
Pituitary tumour= to much ACTH so cortisol from adrenal glands
*Curable= remove tumour
What is a hormone?
Circulating factors which act on remote target organs
=endocrine, paracrine (local), autocrine (own self), neurotransmission (dopamine)
What are the classical endocrine glands?
- Thyroid
- Adrenal
- Ovary
- Testis
- Pancreas
- Parathyroids
- Pituitary
- Most other organs make or metabolise hormones (liver, kidney, brain, bone, adipose, skin, gut, heart)
What hormones does the pituitary gland secrete?
- ACTH
- LH
- FSH
- GH
- PRL
- TSH
- AVP
What hormones does the thyroid secrete?
- Thyroxine
- Calcitonin
What hormones does the parathyroid secrete?
-PTH
What hormones does the pancreas secrete?
- Insulin
- Glucagon
What hormones does the adrenal cortex secrete?
- Cortisol
- Aldosterone
- DHEA
What hormones does the adrenal medulla secrete?
- Adrenaline
- Noradrenaline
What hormones does the ovary secrete?
- Oestrogen
- Inhibin
What hormones does the testis secrete?
-Testosterone
What hormones does the adipose tissue secrete?
- Leptin (hunger cessation- resistance in obesity)
- Adiponectin
- Resistin
- TNFa
- IL6
- Cortisol
- Angiotensinogen
- PAI-1
What are the different types of hormone structure?
-Peptides (gene products) =Growth hormone =Insulin =Thyroxine -Amines (modified AAs) =Adrenaline =Noradrenaline -Steroids (from cholesterol) =Oestrogen =Androgen =Glucocorticoids (metabolism and stress) =Vitamin D
Describe the receptors for hormones
-Peptides and amines
=Surface receptors
=Second messengers
=Multiple cellular effects
-Steroids and thyroid hormones
=Nuclear receptors
=Via transcription/ translation
=Many target genes
What is unicoid?
-Small testis= less to no testosterone
=Long limbs as plates did not fuse (require sex steroids to stop growing)
=No puberty
Describe the anatomy of the pituitary fossa
-Gland lies beneath pituitary stalk (blood and nerves) from hypothalamus
-Optic chiasm above pituitary gland
-Low intensity microadenoma= pituitary tumour
=Bigger tumours= acromegaly (stretches and damages optic chiasm- loss of outer field of vision)
How is growth hormone regulated?
-Regulated by GHRH (growth hormone releasing hormone) from hypothalamus
-Stimulates pituitary gland directly to produce GH
=complex cascade
-insulin growth factor type 1 created in liver
What lead to an excess of growth hormone?
- Acromegaly/ gigantism
- Genetics (Gs alpha mutations= inside GH producing cell so always active)
- Immune- antibodies stimulate GH
- Pituitary tumours, or those producing IFG1 or related IGF2
- GHRH hypersecretion
- Factitious use by body builders
What are the causes of hypothyroidism?
-Source gland damage =Genetic/ developmental failure (thyroid synthetic enzyme defects) =Autoimmune (Hashimoto's) =Tumours/ infiltrations (rare) =Iatrogenic (carbimazole, radio-iodine) =Surgery (thyroidectomy)
-Target organ resistance
=Pre-receptor defects (monodeiodinase defects)
=Receptor mutations (thyroid resistance syndrome)
=Post-receptor
Generally, how can we make a diagnosis in endocrinology?
- If hormone deficient= show it can be stimulated normally
- If excess hormone= show it can be suppressed normally
- Sometimes just basal levels of the hormone or regulators are sufficient for diagnoses
Describe endocrine therapy
-If hormone deficient, replace it
=Diurnal rhythms
=Stress or illness and requirements may alter
-If excess hormone, suppress/ remove
=Often better to remove all and replace back to physiology
-Monitor replacement if possible (TSH for thyroxine)
Describe glucocorticoid remedial hyperaldosteronism
-Curable hypertension
-Genetic endocrine disease
-Aldosterone synthase (controlled by renin and Angiotensin 2) and cortisol synthase (11-hydroylase, controlled by ACTH)= highly homologous
=Promoter regions similar
=Unequal lining up of chromosomes= regulatory regions mixed up so more aldosterone made (chimeric gene) under ACTH control
How can you treat glucocorticoid remedial hyperaldosteronism?
- Suppress ACTH
- Give glucocorticoid- turns off ACTH production so ectopic aldosterone synthesis stopped