Week 128 General Endocrine Flashcards
Describe the signs and symptoms of Hypoadrenalism (adrenal insufficiency)
Profound Hypotension (especially postural) Vomiting Diarrhoea Abdo pain/salt craving Increased skin pigmentation
Describe the signs and symptoms of Cushing’s syndrome.
Prolonged and inappropriate elevation of free corticosteroid levels.
Central Obesity & Moon Face, Plethora & Acne, menstrual Irregularity
Hirsutism, Hypertension, Diabetes,
Muscle wasting and weakness
Osteoporosis
What are the initial investigations of Cushing’s syndrome?
Full Blood count, U&E, LFT, Bone profile Thyroid stimulating hormone Urinary free cortisol Low dose dexamethasone suppression test (Initial screen is positive if cushings)
Describe the investigations you would use for a patient with Addison’s disease.
ACTH = < Free cortisol = > ACTH stimulation Test (Failure to rise) U&E: >Na+, normal or < K+, < Urea < Plasma renin & >Aldosterone
Whats is a rare cause of Addison’s often coming up in an EMQ?
Haemochromatosis
List common causes of Hypercalcaemia.
Primary Hyperparathyroidism (proliferation of cells secreting parathyroid hormone) accounts for about 90% of cases.
Malignancy 30-70% in hospital.
Excess vitamin D may cause Hypercalcaemia.
List the common causes of Hypocalcaemia.
Hypocalcaemia with high PTH = Chronic kidney disease (reduced hydroxylation of 25-hydroxy-vitamin D; Vitamin D Deficiency (decreased 25-hydroxylation in the liver)
Hypocalcaemia with low PTH = Hypoparathyroidism after neck surgery, acute pancreatitis, severe hypomagnesia, sepsis/major illness.
What happens to PTH and CA2+ in primary hyperparathyroidism?
Elevated both.
What happens to serum PTH and CA2+ in secondary hyperparathyroidism?
Increased PTH
Normal or LOW serum calcium
Describe the initial investigations you would conduct for a patient with hypercalcaemia.
Serum calcium - corrected for serum albumin
Above 2.65 mmol/L
ECG - look for shortened QT intervals,
Describe the initial investigations of a patient with hypocalcaemia.
Calcium (adjusted for albumin) Serum PTH (low = check magnesium) (high = check urea/creatnine) Magnesium = low = magnesium deficiency Urea/Creatinine = High = renal failure Vitamin D = Low = Vitamin D deficiency
What are the clinical signs of hyperparathyroidism?
Renal Stones Corneal calcification Muscle weakness Tiredness Polydypsia/Polyuria
What is the most common cause
of hypothyroidism?
Hasimoto’s throiditis
Autoimmune
F:M 12:1
What are the common causes of male Primary hypogonadism?
Androgen deficiency.
Klinefelter’s syndrome.
Surgical castration or trauma
Infections - orchitis ; age ; Chronic liver and kidney disease
Drugs, alcohol, chemotherapy, radiotherapy; androgen resistance
Name the typical causes of secondary hypogonadism in men.
Constitutional delayed puberty
CUSHINGS SYNDROME
drugs, opiates, anabolic steroids
Chronic disease, liver, kidney, HIV, diabetes
Ageing; obesity; Hypopituitarism; Hyperprolactinaemia
Clinical signs of Klinefelter’s?
Small firm testes
Gynaecomastia, eunuchoid
Infertile, hyalinised seminiferous tubules
Elevated gonadotrophin and low testosterone levels
Two or more X chromosomes; learning disabilities
Clinical symptoms of Kallmann’s syndrome (2ndary Hypogonadism)
Low testosterone
Abscent facial hair, infertility, gynaecomastia, poor musculature.
Pubertal deficiency, eunochoid body proportions span 5cm >height
Bilateral small testis
Anosmia, colour blindness
What are the causes of Gynaecomastia?
Deficient testosterone sythesis
< oestrogen production
Drug induced
What is a typical cause of gonadal dysfunction in women?
Drugs
Noonan’s syndrome (46xx)
Turners Syndrome (45XO)
Disorders of hypothalamo-pituitary function or hyperprolactinaemia
Ovarian dysfunction, <androgen production (PCOS and Adr.Hyperpla.)
Describe symptoms and signs of hypogonadism in men AND women
Amenhorrea/Weight loss Gynaecomastia/Hirsuiitism/Small hard testis Infertility Poor muculature Span <5cm than height
Describe initial investigations of Hypogonadism in men and women.
Testosterone, LH, FSH, Free T4, TSH, U&Es, LFTs
Prolactin
Oestradiol, Gnrh (gonadotrophin regulating hormone)
How do you differentiate primary from secondary hypogonadism?
Morning LH and FSH.
Testosterone
PRIMARY = >Testosterone, High/normal FSH & LH
SECONDARY = Low testosterone, high normal to high levels of LH and FSH.
You can use testosterone replacement therapy to treat WHICH clinical signs?
Loss of libido, erectile dysfunction, diminished intellect, depression
Lethargy, osteoporosis, loss of secondary sexual characteristics, loss of muscle and strength
Causes of PRIMARY Hypogonadism?
Noonan syndrome, Turner syndrome, Klinefelter syndrome, XY females with SRY gene immunity.
Causes of secondary hypogonadism?
Polycystic ovary syndrome
Kallmann syndrome
Haemochromatosis
Diabetes M
Turner syndrome is in ____ and Klinefelter is in ____.
Females = Turner Males = Klinefelter
How would you treat Hypogonadism?
Testosterone therapy.
Gonadotrophin therapy stimulates sperm production in secondary hypogonadism
Type 5 phosphodiesterase inhibitor (Sildenafil, alprostadil)
Treatment for Infertility?
Intracytoplasmic sperm injection (ICSI) after genetic assessment
Vasectomy reversal
Gonadotrophin-releasing hormone receptor - for secondary hypogonadism.
Foetal androgen deficiency is caused by a deficiency in _____.
5 alpha reductase.
Treatment for foetal androgen deficiency?
Pre-pubertal orchidectomy (testicle removal)
Oestrogen replacement.
turners syndrome will present with ____.
Primary amenorrhea.
PCOS presents with….?
Irregular bleeding from menarche, hirsuitism.
Ovarian/Adrenal tumour presents with…..?
Hirsuitism/virilisation
Congenital adrenal hyperplasia presents with…?
Progressive hirsuitism from menarche.
Prolactinoma presents with …?
Secondary amenorrhoea
Galactorrhea
Precocious puberty is defined as _____.
Oestrogen secretion or cyclical ovarian activity before 7-8 years in girls.
Androgen secretion and spermatogenesis before 9-10 years in boys.
Causes of central precocious puberty?
Idiopathic
Hypothalamic hamartoma
Pineal gland tumour
Hypothyroidism
Investigations for central precocious puberty?
LHRH/LH, FSH test, MRI pituitary, Oestradiol, Ovarian ultrasound, Free T4, bone age.
What causes pseudo precocious puberty?
Adrenal and gonadal disease, HCG secreting tumours.
Investigations for pseudo precocious puberty?
DHEAS
17 alpha oh –> Progesterone, HCG
In precocious puberty, what happens to LH and FSH levels?
ELEVATED.
What are the signs of premature ovarian failure?
Hypergonadotrophic amenorrhoea in women 6 months, vaginal dryness, menopausal flushes
Serum FSH >40 Mu/l
which key investigation would you do for premature ovarian failure?
Serum FSH
Clinical signs of Turners syndrome?
Short stature Lymphoedema Webbed short neck Wide nipples, short 4th metacarpal absent 2ndary sexual characteristics, amenorrhea.
What investigations would you conduct if you suspected turners syndrome?
FSH (<)
Bone age (delayed)
GH
FT4 TSH
What are the biochemical abnormalities in Polycystic ovaries?
< prolactin
< testosterone
< LH/FSH ratio
Lowered sex hormone binding globulin Raised urinary oxosteroid excretion
Investigations in polycystic ovaries?
Elevated LH:FSH ratio testosterone Prolactin Free T4 and TSH 17 alpha hydroxyprogesterone
What are the clinical signs of an ovarian tumour?
Increased facial and body hair
Centrally plethoric
Cliteromegaly
what investigations would you consider if you suspected an ovarian tumour?
Cortisol
Prgesterone
Dexamethasone suppression test.
CT scan abdo and pelvis.
With androgen deficiency and or impaired sperm production in male hypogonadism, what do you treat with?
Testosterone replacement
Occasionally infertility treatment
Gonadotrophins
Phosophodiesterase Type V inhibitors
What are the three clinical types of male hypogonadism?
Adult Deficiency
Pubertal Deficiency = eunochoid
Foetal deficiency = phenotypically female
What are causes of androgen excess?
PCOS
Congenital adrenal hyperplasia
drugs
Adrenal and ovarian tumours
What do you use Cyproterone acetate to treat?
ANDROGEN EXCESS
WHAT ARE THE PRINCIPAL FUNCTIONS OF THE ENDOCRINE SYSTEM?
MAINTENANCE OF INTERNAL ENVIRONMENT IN THE BODY
INTEGRATION AND REGULATION OF GROWTH AND DEVELOPMENT
CONTROL MAINTENANCE AND INSTIGATION OF SEXUAL REPRODUCTION
HOW DO ENDOCRINE HORMONES TRAVEL
BLOODSTREAM
HOW DO AUTOCRINE HORMONES TRAVEL?
SECRETED AND ACT ON CELL THAT SECRETED THEM
WHAT DO PARACRINE HORMONES ACT ON?
NEIGHBOURING CELLS
HOW DO NEUROHORMONES TRAVEL?
SYNAPSES –> THEN TRAVEL VIA BLOODSTREAM
WHAT GROUP OF HORMONES DO GH PROLACTIN, INSULIN, ACTH, LH AND FSH BELONG TO?
PEPTIDE HORMONES
NAME FOUR STEROID HORMONES
CORTISOL
ALDOSTERONE
TESTOSTERONE
OESTROGEN
NAME AN AMINO ACID DERIVATIVE HORMONE
THYROID HORMONE
THE HYPOTHALAMUS SECRETES WHICH HORMONES?
GNRH TRH CRH GHRH SOMATOSTATIN
POSTERIOR PITUITARY SECRETES…?
VASOPRESSIN
OXYTOCIN
ANTERIOR PITUITARY SECRETES?
FSH LH; ACTH; MSH; ENDORPHINS; LIPOTROPIN; GH TSH CGA PROLACTIN
PLACENTA PRODUCES WHICH HORMONE?
hCG
PANCREAS SECRETES?
GLUCAGON
INSULIN
SOMATOSTATIN
THYNUS SECRETES WHAT?
THYMOSIN
THYMOPOIETIN
THYMULIN
WHAT DO GLUCOCORTICOIDS DO?
CONTROL CARB METABOLISM
MODERATE INFLAMMATORY RESPONSE
RESPOND TO STRESS
WHAT DO MINERALCORTICOIDS DO? (IE ALDOSTERONE)
CONTROL SALT BALANCE AND BP
NAME THE DIFFERENCE BETWEEN WATER SOLUBLE AN LIPID SOLUBLE HORMONES
WATER: BIND TO RECEPTOR ON CELL MEMBRANE, FAST ACTING
LIPID: DIFFUSE THROUGH CELL MEMBRANE, BIND TO NUCLEAR RECEPTORS, SLOW ACTING
GNRH ACTS ON THE ___.
PITUITARY
FSH AND LH ACT ON THE ____.
OVARIES
IF IT’S FEEDBACK CONTROLLED, ITS PROBABLY A ______ HORMONE.
PITUITARY
WHAT IS THE FUNCTION OF THYROID HORMONES?
T3 AND T4: METABOLISM REGULATIN
CALCITONIN: DECREASE BLOOD CALCIUM AND BLOOD PHOSPHATE LEVELS
T3 AND T4 ARE CONTROLLED BY ____.
ANTERIOR PITUITARY LOBE TSH/
CALCITONIN IS CONTROLLED BY ______.
BLOOD CALCIUM LEVELS AND DIGESTIVE CHEMICALS.
WHAT DOES ALDOSTERONE DO?
REGULATES MINERAL ELECTROLYTE LEVELS (BLOOD PLASMA ION CONCENTRATIONS)
THE OVERALL EFFECT OF CORTISOL IS TO:
KEEP BLOODY GLUCOSE LEVELS BETWEEN NORMAL LEVELS BETWEEN MEALS
CUSHINGS SYNDROME CAN LEAD TO HYPO____
KALAEMIA
CUSHINGS IS CONFIRMED BY WHICH TEST?
DEXAMETHASONE SUPPRESSION
FREE CORTISOL
ANY RAISED 17 HYDROXYPROGESTERONE LEVELS SHOULD LED YOU TO THINK OF WHICH CONDITION?
CONGENITAL ADRENAL HYPERPLASIA
WHICH FORM OF CUSHINGS SYNDROME IS CORTISOL NOT RAISED IN?
ECTOPIC ACTH
IF TESTOSTERONE IS RAISED, AND SO IS GH/FSH RATION IT IS LIKELY _____ (IN WOMEN)
POLYCYSTIC OVARY SYNDROME
HYPERPIGMENTATION, RAISED ACTH AND LOW CORTISOL EQUALS WHAT?
ADDISONS!
ACHONDROPLASIA IS ASSOCIATED WITH WHAT?
DISPROPORTIONATE SHORT STATURE.
PROPORTIONAL SHORT STATURE WITH CENTRAL OBESITY IS ASSOCIATED WITH WHICH OF THE FOLLOWING?
GROWTH HORMONE DEFICIENCY
