Endocrinology Flashcards
Acromegaly
Hypersecretion of GH caused most often by GH-secreting PITUITARY tumour.
Features: Very slow progression of features Increased hand and feet size Headaches Visual field loss (peripheral due to bitemporal hemianopia) Carpal tunnel syndrome Face (prognathism)
Investigate: GH levels, Glucose tolerance test (Failure to suppress GH after 75g oral glucose dose), IGF-1 (raised- GH stimulates liver IGF1 secretion)
MRI of brain
Treatment:
Surgery (trans-sphenoidal) resection
radiotherapy and medical (octreotide - somastatin analogue) and dopamine agonist
Adrenal Insufficiency
Addisons
deficiency of adrenal cortical hormones (mineralocorticoids, glucocorticoids, androgens)
- Autoimmune (UK)
- TB (world)
Symptoms: weight loss, weakness, lethargy, anorexia, diarrhea, vomiting, depression
Acute presentation: Addisonian crisis (Major hemodynamic collapse often precipitated by stress) Tachycardia, hypotensive shock
Signs: Postural hypotension, Increased pigmentation
Investigate:
9 am serum cortisol low, acth high
Short synacthen test (give 250ug synachten IM->measure cortisol response)
Adrenal antibodies
Treatment:
crisis-> dextose fluid and hydrocortisone
Mineralo -> fludrocortisone
Glucco -> hydrocortisone
steroid warning card
carcinoid syndrome
Occurs when a rare cancerous tumour secretes chemicals into your blood stream causing a variety of symptoms.
Majority found in small bowel and rectum.
Symptoms appear once liver metastasised.
Facial flushing, diarrhea, wheeze, sweating, carcinoid crisis (bronchospasm, tachycardia), RS heart murmur
Investigate: MEN-1 (present in 10%) 5-hiaa metabolite of serotonin in urine ct or mi localise tumour
Cushings syndrome
Syndrome associated with chronic inappropriate elevation of free circulating cortisol.
1) ACTH - dependent (80%)
- Cushings disease: Pituitary adenoma secreting excess ACTH
- Ectopic ACTH source (lung tumours)
2) Independent of ACTH (20%)
- excess cortisol secreted from benign adrenal adenoma or adrenal carcinoma
Symptoms: Increasing weight and fatigue. Muscle weakness. thin skin. easy bruising. poor wound healing. hirsutism. acne.
Signs: Facial fullness and plethora, inter-scapular fat pad, PROXIMAL Muscle weakness, central obesity, pink/purple striae on abdomen, bruises
Diabetes insipidus
Passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption by the kidney because of decreased secretion of ADH from the posterior pituitary (cranial DI) or impaired response of the kidney to ADH (nephrogenic DI).
Polyuria, nocturia, polydipsia
Few signs if patient drinks appropriately
urine output >3L/24 hours
If fluid intake is less than fluid output signs of dehydration may be present (dry mucous membranes, postural hypotension, reduced tissue turgor)
Test: water deprivation (diagnosis urine is dilute)
Management:
Cranial DI: desmopressin
Nephrogenic: Na and K restriction may help polyuria thiazide diuretics to stimulate RAS
Complications: hypernatraemia dehydration
Adrenocortical failure causes
1) Adrenal gland destroyed
TB Addison’s
Autoimmune Addison’s
2)Enzymes in synthetic pathway not working
Congenital adrenal hyperplasia
Adrenocortical failure presentation
Fall in blood pressure Loss of salt in urine High plasma potassium anorexia, fatigue, lethargy hyperpigmetation Fall in glucose due to glucocorticoid deficiency Eventual death due to severe hypotension
Congenital Adrenal Hyperplasia
Inherited (autosomal recessive) disorder of adrenal steroid synthesis.
Commonest cause is 21-hydroxylase deficiency
- Complete (aldosterone and cortisol totally absent) -> can survive less than 24 hours
Sex steroids and testosterone in excess
Presentation is at birth with a salt losing Addisonian crisis - Partial (Low levels of cortisol and aldosterone) high levels of sex steroids and testosterone. Will present at any age as partial, with hirsutism and virilisation girls and precocious puberty in boys
11B hydroxylase deficiency
hypertension and hypokalaemia
17A hydroxylase deficiency
Hypertension, hypokalaemia
No androgens
Cushings Investigations
- 24 hour urinary free cortisol collection
- Blood diurnal cortisol levels ( Cortisol is highest at 9am and lowest at midnight)
- Low dose dexamethasone suppression test (0.5mg 6 hourly for 48 hours)
Normals will suppress cortisol to 0
Any cause of cushings will fail to suppress
Diagnosis:
Basal 9 am cortisol 800 nM
End of LDDST: 680nM
To determine cause: Plasma ACTH levels and HDDST
Cushings Management
Iatrogenic -> switch to steroid sparing alternative or lower dose
Medical: Metyrapone or ketoconazole
Surgical:Pituitary transsphenoidal
removal or adrenalectomy
Complications of Cushings
diabetes, osteoporosis, hypertension
5 year survival in 50% if not treated
Cranial DI
no vasopressin
idiopathic (50%)
Nephrogenic DI
vasopressin is present but tissue insensitivity
inherited, drugs (lithium, demeclocycline)
Diabetes values
Fasting blood glucose greater or equal to 7 mmol/L
Random blood glucose greater or equal to 11 mmol/L
HbA1c -> estimates overall blood glucose levels in the past 2-3 months
FBC: MCV, reticulocytes (increase in erythrocytes causes misleading hbA1c levels)
Urine: glycosuria, ketones
Type 1 DM
absolute insufficiency in pancreatic insulin production
Pt prone to ketoacidosis and weight loss
associated with other autoimmune conditions (HLA dr3 and 4)
treatment: Insulin
Also address vascular risk factors, structured eduction programme, offer lifestyle advice and smoking cessation help, give statin, control BP, give foot care.
Diet changes.
Diabetic ketoacidosis
Nausea Vomiting polyuria polydipsia kussmaul breathing ketotic breath confusion coma signs of dehydration
Type 2 DM
Multifactorial aetiology (genetic and environmental) -> more geenetic than type 1
Obesity, lack of exercise, calorie and alcohol excess
Cause: impaired insulin srecetion, increased insulin resistance
Features: polyuria, night, polydipsia, unexplained weight loss, visual blurring, genital thrush
Maturity onset diabetes of the young (MODY)
rare
autosomal dominant
form of type 2 DM
affects young people with family history
Latent autoimmune diabetes of adults (LADA)
form of type 1 DM
slower progression to insulin dependance later in life
Type 2 Diabetes Mellitus:
Assess vascular risk factors, give statin, BP control, and foot care, structured education programme, lifestyle advice and smoking cessation programme.
Diet increased in complex carbs and decreased in sat fats and sugars.
- Initially try and control with diet and exercise
- Metformin (Increases insulin sensitivity and helps weight loss - side effects are nausea, vomiting, diarrhea, abdo. pain)
- sulphonyureas (gliclazide, glimeprazide) - increases insulin secretion - side effects - hypoglaecaemia and increased weight
- INSULIN
- Thiozolidinediones (pioglitazone) increases insulin sensitivity (replace with metformin or sulphonyurea) side effects: hypos, fractures, fluid retention, increased LFTs
- GLP 1 analogue (exenatide) increases action of incretins which lower blood glucose levels
- DPP4 inhibitors (sitagliptin) -> to prevent breakdown of GLP 1
- alpha glycosidase inhibitors (acarbose) breakdown of starch to sugar - side effects abdominal pain, distension, wind, diarrhoa
Complications of Diabetes M.
Microvascular:
Neuropathy, nephropathy, retinopathy
Macrovascular: IHD, peripheral vascular disease, TIA/Stroke
Diabetic foot
Both ischaemic (macro) and neuropathic (micro) signs
Leads to dry skin, ulceration, gangrene, reduced subcutaneous tissue
Chargot’s arthropathy
Loss of sensation or pain
SIADH
Continued secretion of ADH, despite the absence of normal stimuli for secretion (Increased serum osmolality, decreased blood volume)
Cause of hyponatraemia
diagnosis requires: 1. Concentrated urine 2. Hyponatraemia 3. Low plasma osmolality In absence of hypovolaemia, oedema, diuretics
Causes: Malignancy: small- cell lung Cns disorers: abscess, stoke Chest: TB Drugs; opiates
Hyponatraemia is the most common electrolyte imbalance seen in hospital <50% of all severe hyponatraemia are due to SIADH
Hyponatraemia is dilutional from increased water not decreased sodium.
Mild hyponatraemia: asymptomatic as it gets more severe:
Headache, nausea, vomiting, muscle cramps and weakness, irritability, confusion, drowsiness, convulsions and coma
mild h. -> no signs
Severe h. -> decreased reflexes
Cognitive impairment -> memory loss, confusion, disorientation
Seizures
Brainstem herniation in severe, acute case
SIADH MANAGEMENT
- Water restriction (0.5-1 L per day) -> if infective give demeclocycline -> decreases responsiveness of renal tubule cells to ADH
- Vasopressin antagonist (tolvaptan)
- in severe cases ->seizures and decreased consciousness -> give slow IV hypertonic saline 3% -> change in concentration of sodium should be less than 10 mmol/L otherwise can lead to central pontine myelinolysis
