Endocrinology (2) Flashcards
Define multiple endocrine neoplasia
An autosomal dominant inherited syndrome characterised by tumours of the endocrine organs.
Summarise the aetiology of multiple endocrine neoplasia
Genetically inherited autosomal dominant
MEN1 gene mutation - mutation of tumour supressor gene
Causes MEN type 1
RET gene mutation - mutation of proto-oncogene
Causes MEN type 2A and 2B
MEN 1: Parathyroid adenoma Pituitary adenoma Pancreatic cancer - most often gastrinoma Facial angiofibromas and collagenomas
MEN 2A:
Thyroid medullary cancer
Phaeochromocytoma
Parathyroid adenoma
MEN 2B: Thyroid medullary cancer Phaechromocytoma Multiple neuromas Marfanoid habitus
Summarise the epidemiology of multiple endocrine neoplasia
Very rare
MEN 1 diagnosis usually made in 4th decade of life, however tumours develop in teenage years
What are the presenting symptoms and signs on physical examination of multiple endocrine neoplasia?
MEN1: Parathyroid adenoma - hypercalcaemia Abdominal pain and tenderness Constipation Confusion Symptoms of nephrolithiasis - loin to groin pain
Pancreatic gastrinoma - Zollinger-Ellison syndrome: Abdominal pain Dysphagia Gastro-oesophageal reflux Vomiting
Pancreatic insulinoma - hypoglycaemia - dizziness, hunger
Pancreatic glucagonoma - hyperglycaemia
Prolactinoma - galactorrhoea, gynaecomastia, amenorrhoea, headaches, bilateral hemianopia
Hypersomtatotrophinaemia - acromegaly, headaches, bilateral hemianopia
MEN 2A:
Thyroid medullary cancer - hoarseness, coughing, trouble swallowing, sweating, hypertension, pruritic skin lesions, lump in the neck, diarrhoea, palpable thyroid nodules
Phaeochromocytoma - hypertension, sweating, tremor, tachycardia, palpitations, headaches
Parathyroid adenoma
MEN 2B: Thyroid medullary cancer Phaechromocytoma Multiple neuroma Marfanoid habitus - long limbs, long fingers, high arched palate
What are the appropriate investigations for multiple endocrine neoplasia?
MEN 1: Hormone hypersecretion blood tests - PTH, gastrin, insulin, glucagon, prolactin, GH, IGF-1 Serum calcium DNA testing for genetic abnormality MRI head to look for pituitary adenoma
MEN 2:
24hr urine metanephrines for phaechromocytoma
MRI/CT adrenals
Serum calcitonin - elevated in Medullary thyroid cancer
FNA of thyroid nodules
Thyroid ultrasound
Parathyroid adenoma - elevated calcium and PTH
Define primary hyperaldosteronism
Increased autonomous production of aldosterone by the adrenal glands due to a problem with the adrenals, resulting in suppression of plasma renin activity.
Summarise the aetiology of primary hyperaldosteronism
Conn’s syndrome - adrenal adenoma secreting aldosterone (most common - 70%)
Adrenal carcinoma - RARE
Adrenal cortex hyperplasia - 30% of cases
Familial hyperaldosteronism - dominant inheritance,
Idiopathic
Summarise the epidemiology of primary hyperaldosteronism
1-2% of hypertensive patients
Conn’s syndrome is more common in WOMEN and YOUNG patients
Bilateral adrenal hyperplasia is more common in MEN and presents at an older age
What are the presenting symptoms of primary hyperaldosteronism?
Usually asymptomatic and found incidentally on bloods
Hypertension symptoms:
Headaches
Flushing
Hypokalaemia symptoms: Polydipsia and polyuria (due to nephrogenic DI) Nocturia Constipation Weakness Fatigue Numbness Tingling Tetany
What are the signs on physical examination of primary hyperaldosteronism?
Hypertension
Complications of hypertension eg hypertensive retinopathy
What are the appropriate investigations for pulmonary hyperaldosteronism?
Serum aldosterone - high
Serum renin - low
Serum potassium - may be hypokalaemic
Serum sodium - may be hypernatraemic
Serum magnesium - may be hypomagnesiumaemic
Urine potassium - high
Aldosterone:renin activity ratio: elevated
CT adrenals - may show adrenal adenoma or carcinoma
Genetic testing for familial hyperaldosteronism
Confirmatory Tests
Salt Loading: failure of aldosterone suppression following salt load confirms Conn’s
Postural Test: Measure plasma aldosterone, renin activity and cortisol when patient lies down at 8am, and measure again after 4 hours of the patient being upright.
Aldosterone-producing adenoma: aldosterone secretion decreases between 8am and noon
Bilateral adrenal hyperplasia: adrenals respond causing increase renin leading to increased aldosterone
What is the management of primary hyperaldosteronism?
Bilateral Adrenal Hyperplasia:
Spironolactone (aldosterone receptor antagonist)
Eplerenone if spironolactone side-effects are intolerable
Amiloride (potassium-sparing diuretic)
Monitor serum K+, creatinine and BP
ACE inhibitors and CCBs may also be added
Aldosterone Producing Adenomas: Adrenalectomy
Adrenal Carcinoma: Surgery and post-operative mitotane (antineoplastic)
What are the possible complications of primary hyperaldosteronism?
Hypokalaemia Metabolic alkalosis Hypertension Stroke MI AF Heart failure Impaired renal function Complications of hypertension
Summarise the prognosis of primary hyperaldosteronism
Surgery may cure the hypertension or make the hypertension easier to manage
Hypertension improved by management in all forms
Define osteoporosis
A metabolic bone disorder characterised by a decrease in bone mineral density and altered bone architecture, resulting in increased bone fragility and susceptibility to fracture. Bone mineralisation is normal
Summarise the aetiology of osteoporosis
Mainly post-menopausal or senile osteoporosis
Secondarily seen with drugs or systemic conditions
Other causes:
Low oestrogen eg postmenopausal leading to loss of bone matrix
Age related - osteoblast senescense
Iatrogenic - glucocorticoids, heparin, L-thyroxine
Malignancy – myeloma, metastatic carcinoma
Rheumatological – rheumatoid arthritis, ankylosing spondylitis
Gastrointestinal – malabsorption, liver disease, anorexia
Hypogonadism (in young men and women) – sex hormones inhibit bone resorption
Endocrine - Cushing’s, hyperthyroidism, primary hyperthyroidism
What are the risk factors of osteoporosis?
Post-menopause Age Family history Low BMI Low calcium intake/serum calcium Smoking Lack of physical exercise Low exposure to sunlight Alcohol abuse Late menarche Early menopause Hypogonadism Glucocorticoid use
Summarise the epidemiology of osteoporosis
Predominently white post-menopausal women
Can affect any sex, age and ethnicity
In the UK, osteoporosis causes fractures in 50% of women and 20% of men aged >50 years
What are the presenting symptoms of osteoporosis
Asymptomatic until a pathologic fracture occurs
Most often vertebral fracture which results in back pain, height loss and hunched posture
Can also have distal radius and femoral neck fractures often in post-menopausal
What are the signs on physical examination of osteoporosis?
There are often no signs until complications develop
When vertebral fractures occur:
Tenderness on percussion
Thoracic kyphosis (due to multiple vertebral fractures)
Neck of femur fracture:
Severe pain when hip flexed and externally rotated
What are the appropriate investigations for osteoporosis?
DEXA Scan - compares bone density to that of normal individual to develop t-score. T score compares to healthy 25 year old female at peak bone mass.
T score -1 is normal
Quantitative ultrasound/CT scan/x-ray of the heel to detect reduced bone mineral density
X-rays to diagnose fractures
Biochemical markers of bone resorption and formation (urinary deoxypyridinoline)
Serum albumin - may be decreased
Serum alkaline phosphatase - normal, osteomalacia if raised
Serum calcium - normal. If low, osteomalacia. If high, hyperparathyroidism.
Serum creatinine, phosphate, vitamin D
Thyroid function tests and serum parathyroid hormone
Define polycystic ovarian syndrome
A condition characterised by 2 of the three:
Hyperandrogenism
Oligo/anovulation
Polycystic ovaries on USS
It also shows oligo/amenorrhoea, hirsuitism, obesity, insulin resistance and can be associated with diabetes mellitus and dyslipidaemia.
Summarise the aetiology of polycystic ovarian syndrome
Increased secretion of LH by the anterior pituitary gland
Aetiology is unknown
Environmental factors
Genetic variants
Hyperinsulinaemia results in increased ovarian androgen synthesis and reduced hepatic sex hormone binding globulin (SHBG) synthesis - causes increase in free androgens (which gives rise to the symptoms)
Summarise the epidemiology of polycystic ovarian syndrome
Most common endocrine disorder of females of reproductive age
Accounts for 80-90% of causes of hyperandrogenism in women
Affects 6-8% of women
Most common cause of infertility in women
What are the presenting symptoms of polycystic ovarian syndrome?
Symptoms of hyperandrogenism:
Acne on face, back, chest
Hisutism - facial hair on chin, upper lip chest and back
Male pattern hair loss
Obesity
Oligomenorrhoea or amenorrhoea
Dysfunctional uterine bleeding
Infertility
What are the signs on physical examination of polycystic ovarian syndrome?
Hirsutism Acne Obesity Male pattern hair loss Ancanthosis nigricans - dark velvety thickened, hyperpigmented patches in creases on neck, groin, underarm - sign of insulin resistance
What are the appropriate investigations for polycystic ovarian syndrome?
Bloods: LH - elevated LH:FSH - elevated >3:1 Elevated androgens - testosterone, androstenedione, DHEA Low FSH and sex hormone binding globulin
USS pelvis - may show follicles on ovaries and increase in ovarian volume
Rule out: Hyperprolactinaemia Hypo/hyperthyroidism Cushing’s syndrome Congenital adrenal hyperplasia (check 17OH-progesterone levels)
Look for impaired glucose tolerance/T2DM: Fasting blood glucose, HbA1c
Fasting lipid profile
Define Paget’s disease of bone
A chronic bone remodelling disorder characterised by excessive osteoclastic breakdown and excessive osteoblastic formation, resulting in abnormal mosaic organised, weak bone
Summarise the aetiology of Paget’s disease of bone
Aetiology is unknown
Genetic component - may be autosomal dominant pattern. SQSTM1 mutation
Prior virus infection eg measles
Environmental component
Summarise the epidemiology of Paget’s disease of bone
2nd most common chronic bone remodelling disorder after osteoporosis
More common in men
Mean age of onset is 55 years old
Polyostotic in 75% of cases
Paget’s disease prevalence is highest in the UK, North America, Australia and New Zealand.
What are the presenting symptoms of Paget’s disease of bone?
Can often be asymptomatic Bone pain, particularly deep hip pain - insidious onset, aggravated by weight bearing and movement Bowing of the legs Increasing shoe or hat size Hearing loss as bone growth compresses auditory nerve Visual loss Lion face Lower limb muscle weakness Arthritis Microfractures Headaches Radiculopathy due to nerve compression
What are the signs on physical examination of Paget’s disease of bone?
Skull, thoracolumbar spine, pelvis, femur and tibia most commonly affected
Arthritis
Bone pain and deformity (enlarged skull, sabre tibia)
Increasing skull size
Bitemporal skull enlargement with frontal bossing (prominent, protruding forehead)
Sensorineural deafness (due to compression of vestibulocochlear nerve)
Increased local temperature
Tibial, femur or forearm bowing
Pathological fractures
Leontiasis
Kyphosis
What are the appropriate investigations for Paget’s disease of bone?
Serum calcium - normal
Serum PTH - normal
Serum phosphate - normal
Serum ALP - isolated large increase
X-Ray:
Lytic lesions early on
Late: thickened cortical bone, sclerotic changes
Osteoporosis circumscripta
Trabeculae are coarsened inside (particularly at femoral head/neck)
Bone is bent
Enlarged, deformed bones
Skull changes: cotton wool appearance, enlargement of frontal and occipital areas
Bone biopsy - abnormal disorganised bone with mosaic pattern of lamellar bone, osteoclasts with multiple nuclei, wide canaliculi with disorganised matrix
Bone scan: areas of dense uptake in Paget’s bone
Raised serum alkaline phosphatase, urinary hydroxyproline, pyridinoline cross-links
Define thyroid nodules
Abnormal growth of the thyroid cells, forming a lump in the thyroid gland.
Summarise the aetiology of thyroid nodules
The vast majority of thyroid nodules are BENIGN, but a small proportion can lead to thyroid cancer
Most thyroid nodules are adenomatous, and most are multiple
The nodules are usually non-functioning
Summarise the epidemiology of thyroid nodules
40% of the general population have a single nodule or multiple nodules
More common in WOMEN
Very small proportion of thyroid nodules will be malignant
What are the presenting symptoms of thyroid nodules?
Most are ASYMPTOMATIC - usually found on self-examination or clinical examination
Lump on thyroid gland
A single isolated nodule is more likely to be malignant
They can sometimes cause pain and will rarely compress the trachea or cause dysphagia
Usually non-functional, if functional there will be symptoms of hyperthyroidism
What are the signs on physical examination of a thyroid nodule?
Lump in the neck
Moves up and down neck when swallowing
Check for lymphadenopathy - indicative of malignancy
If functional, will find signs on hyperthyroidism
What are the appropriate investigations of thyroid nodules?
TFTs - usually non-functioning, therefore normal. If functioning, high T3/4, low TSH
USS thyroid - visualise nodules
Radioiodine isotope scan - if functional, shows hot nodule and if non-functional, cold nodule
FNA of nodule
Define osteomalacia
A metabolic bone disease in which there is decreased mineralisation of newly formed osteoid bone in adults (after fusion of the epiphyseal plates), often due to vitamin D deficiency, leading to soft bones which are prone to fracture.
Summarise the aetiology of osteomalacia
The main cause is vitamin D deficiency Inadequate exposure to sunlight Inadequate intake Malabsorption Chronic kidney disease or liver failure: decreased activation of vit D
Hypophosphataemia - acquired and X linked hypophosphataemia
Long term use of anticonvulsants eg phenytoin
Mesenchymal tumours
Summarise the epidemiology of osteomalacia
Incidence decreasing in Western world due to fortification on food with vitamin D
What are the presenting symptoms and signs on physical examination of osteomalacia?
Early, mild osteomalacia - asymptomatic Bone pain Muscle weakness Soft bones Increased fractures from low impact Joint pain Spjnal tenderness to percussion Muscle pasms - hands and feet Waddling gait Fatiguability and malaise Proximal myopathy Bone tenderness
What are the appropriate investigations for osteomalacia?
Bloods: Vitamin D - low Calcium - low Phosphate - low PTH - elevated ALP - elevated Serum urea and creatinine - elevated if due to CKD
X-ray:
Osteopenia
Looser zones (psuedofractures, transverse lucency with sclerotic margins)
Bone biopsy:
Increased unmineralised osteoid volume, increased width of osteoid seam, no new bone mineralisation
Tetracycline labelling:
Tetracycline antibiotic can detect and examine bone mineralisation in the living patient. The tetracycline is related to a fluorescent stain.
Contraindicated in children
What is the management of osteomalacia?
Oral vitamin D supplements
Calcium replacement
Treat underlying cause
Patients with normal renal function:
Give 25-hydroxycholecalciferol
Patient converts this to 1,25-dihydroxy-vitamin D via 1-alpha hydroxylase (kidney)
Given as ergocalciferol (25-hydroxy vitamin D2) or cholecalciferol (25-hydroxy vitamin D3)
In patients with renal failure:
Can’t activate 25-hydroxy vitamin D preparations
Give alfa calcidiol - 1-alpha hydroxycholecalciferol - this is active vitamin D
What are the possible complications of osteomalacia?
Secondary hyperparathyroidism Insufficiency fractures Hypercalcaemia Hypercalciuria and renal stones Metastatic calcification in renal failure
Summarise the prognosis of osteomalacia
Depends on underlying cause and compliance with therapies
Define hypogonadism
A condition in which there is reduced or absent secretion of hormones, or other physiological activity of the gonads (ovaries in females, testes in males).
Males = decreased testosterone production, sperm production or both.
Females = decreased oestrogen production and impairment of ovarian function
Primary hypogonadism/Hypergonadotropic hypogonadism:
Gonads fail
Loss of negative feedback of sex steroids
Increased secretion of GnRH, FSH and LH
Secondary hypogonadism/Hypogonadotropic hypogonadism:
Hypothalamic or pituitary failure
Deficiency in GnRH or FSH/LH secretion
Hypogonadism entails infertility and an increased risk of developing osteoporosis
Define the aetiology of hypogonadism
Primary hypogonadism:
Radiotherapy
Chemotherapy
Trauma to gonads
Male:
Klinefelter syndrome
Acquired: testicular necrosis (torsion, trauma, radiation), infection
Female:
Turner’s syndrome (45X)
Acquired ovarian failure - premature, ovariectomy, PCOS
Secondary hypogonadism:
Stress, weight loss, excessive exercise, eating disorder
Pituitary tumour
Hypothalamic tumour
Infiltrative disease of pituitary or hypothalamus
Kallmann’s syndrome (isolated GnRH deficiency)
Hyperprolactinaemia (due to a prolactinoma)
Summarise the epidemiology of hypogonadism
Female:
Prevalence increases with age.
Secondary hypogonadism is a more common cause of anovulation and amenorrhoea.
Turner’s syndrome occurs in around 1.5% of conceptions.
Male:
Prevalence increases with age
Primary hypogonadism accounts for 30-40% of male infertility (most common cause is Klinefelter’s syndrome).
Secondary hypogonadism accounts for 1-2%.
What are the presenting symptoms and signs on physical examination of hypogonadism?
Female: Amenorrhoea Absent breast development or breast atrophy Decreased body hair Decreased libido Infertility Short stature Oestrogen deficiency: night sweats, hot flushes, dyspareunia
Turner’s: short stature, wide-spaced nipples, wide carrying angle, low hairline, infertility, high arched palate
Male: Infertility Decreased libido Delayed puberty - small penis, undescended or small testes, high pitched voice Impotence Loss of body hair
Klinefelter’s - decreased IQ, tall, poor muscle tone
If due to pituitary tumour:
Headache
Visual disturbance
Seizures
Kallmann’s syndrome:
Ansomia
What are the appropriate investigations for hypogonadism?
Serum GnRH - high in primary hypogonadism, low in secondary hypogonadism
Serum LSH and FH - high in primary hypogonadism, low in secondary hypogonadism
Serum testosterone - low
Serum oestrogen/estradiol - low
Serum prolactin - elevated if prolactinoma
TFTs - hypothyroidism can cause secondary hypogonadism
MRI head - view pituitary tumour
Karyotyping - assess for genetic condition as a cause
Female:
Pelvic imaging (US/MRI) – check for structural defects (e.g. androgen insensitivity)
Turner’s syndrome: periodic echocardiography, renal ultrasound
Autoimmune oophoritis: check autoimmune adrenal insufficiency
What are the appropriate investigations for hypogonadism?
Serum GnRH - high in primary hypogonadism, low in secondary hypogonadism
Serum LSH and FH - high in primary hypogonadism, low in secondary hypogonadism
Serum testosterone - low
Serum oestrogen/estradiol - low
Serum prolactin - elevated if prolactinoma
TFTs - hypothyroidism can cause secondary hypogonadism
MRI head - view pituitary tumour
Karyotyping - assess for genetic condition as a cause
Female:
Pelvic imaging (US/MRI) – check for structural defects (e.g. androgen insensitivity)
Turner’s syndrome: periodic echocardiography, renal ultrasound
Autoimmune oophoritis: check autoimmune adrenal insufficiency
Define thyroiditis
Autoimmune-mediated lymphocytic inflammation of the thyroid gland leading to a destructive thyroiditis. This causes release of thyroid hormones, leading to a transient hyperthyroidism, followed by hypothyroidism, and finally full recovery.
Summarise the aetiology of thyroiditis
Hashimoto’s thyroiditis: autoimmune condition with autoantibodies against thyroglobulin, thyroid peroxidase and anti-microsomal
The most common cause of hypothyroidism in the UK.
de Quervain’s thyroiditis - following viral upper respiratory tract infection
Postpartum thyroiditis - increased immune system after pregnancy aggravates underlying mild autoimmune thyroiditis
Drug-induced thyroiditis
Acute or infectious thyroiditis
Riedel’s thyroiditis - fibrous tissue replaces
Summarise the epidemiology of thyroiditis
15-20 times more likely in women
Occurs 30-50 years old
Hashimoto’s thyroiditis is most common cause of hypothyroidism in developed world where there are sufficient amounts of iodine
What are the signs and symptoms of thyroiditis?
Hyperthyroid phase: Palpitations Sweating Weight loss Tachycardia Diarrhoea
Hypothyroid phase: Fatigue Constipation Dry skin Weight gain Cold intolerance Menstrual irregularities Depression Hair loss
Enlarged thyroid gland/goitre
Painless mostly, painful in de Quervain’s thyroiditis
Symptoms of compression from goitre - dysphagia, dyspnoea, hoarseness
What are the appropriate investigations for thyroiditis?
TFTs:
Hyperthyroid phase: elevated T3/T4, low TSH
Hypothyroid phase: low T3/T4, elevated TSH
Autoantibodies:
Anti-thyroid peroxidase
Anti-thyroglobulin
Anti-microsomal antibodies
Thyroid ultrasound
Radionuclide isotope scanning (very low radioiodine uptake)
Histology: diffuse lymphocytic and plasma cell infiltration, formation of lymphoid follicles
What is the appropriate management of thyroiditis?
Often self-limiting
1st line - observation and monitoring with beta blockers and CCBs for symptom management
2nd line if non-resolving - oral levothyroxine sodium
If goitre causing symptoms - surgery
What are the possible complications of thyroiditis?
Thyroid hormone over-replacement causing bone loss + tachycardia
Hyperlipidaemia
Hashimoto’s encephalopathy
Myxoedema coma
Define diabetes mellitus
Type 1:
Autoimmune disease characterised by beta cell destruction, leading to hyperglycaemia due to an insulin insufficiency.
Type 2:
Insulin resistance leading to chronic hyperglycaemia which is not ketosis prone and often seen in older obese patients.
Summarise the aetiology of diabetes mellitus
Type 1:
Autoimmune destruction of beta cells in Islets of Langerhans
Due to anti-glutamic acid decarboxylase and anti-islet cell cytoplasmic antibodies
Causes decreased insulin secretion
HLA-DR3 and HLA-DR4 associated with increased risk
Type 2:
Lots of insulin is secreted however the patient is insulin resistant. Eventually the beta cells are exhausted and there is hypothropy and hypoplasia
Obesity
Hypertension
Sedentery lifestyle
Genetics
Summarise the epidemiology of diabetes mellitus
Type 1 accounts for 10% of diabetes. It is more common in younger patients. Most patients present before 30 years old
Type 2 accounts for 90% of cases. More common in those over 40, obese etc. Increasing incidence with increasing obesity incidence
What are the presenting symptoms and signs on physical examination of diabetes mellitus?
Polyphagia Polydipsia Polyuria Glycosuria Fatigue Nocturia Thrush and other yeast infections
Type 1:
Onset under 30 years old
Weight loss
Often presents as DKA - diffuse abdominal pain, nausea and vomiting, altered mental state, Kussmaul’s respiration, ketotic sweet smelling breath, coma, confusion
Signs of associated autoimmune conditions eg vitiligo, Addison’s, autoimmune thyroiditis
Blurred vision - due to diabetic retinopathy
Type 2:
Infections
Ulcers
Diabetic nephropathy - loss of sensation in stocking and glove distribution
Blurred vision
May present with hyperosmolar hyperglycaemic state - confusion, coma, hyperglycaemia
Overweight
Diabetic foot: dry skin, reduced SC tissue, ulceration, gangrene, Charcot’s arthropathy
Skin changes: necrobiosis lipoidica diabeticorum, granuloma annulare, diabetic dermopathy, acanthosis nigricans
What are the appropriate investigations for diabetes mellitus?
Fasting blood glucose:
5.6-6.9mmol/L = prediabetes
>7mmol/L / >126mg/dL = diabetes
Oral glucose tolerance test - >200mg/dL 2 hours after eating
HbA1c:
5.7 - 6.4% = prediabetes
>6.5% = diabetes
Random plasma glucose: >11.1mmol/L = diabetes
Urinalysis - glycosuria, ketonuria in DKA, proteinuria if diabetic nephropathy, urine albumin:creatinine ratio shows microalbuminuria
Antibodies for T1DM:
Anti-glutamic acid decarboxylase
Anti-islet cell
Insulin antibodies
Fundoscopy - signs of retinopathy - cotton wool spots, microaneurysms, flare haemorrhages
DKA:
ABG - metabolic acidosis, ketonaemia
U+Es - hyperkalaemia
What is the management of diabetes mellitus?
Type 1:
Insulin - short-acting (lispro, aspart, glulisine) insulin analogues 3x daily and long-acting (glargine, determir, degludec) insulin analogues 1x daily
Type 2:
1st line = lifestyle factors - weight loss, exercise, diet, management of hypertension
2nd line = metformin
3rd line = additional anti-diabetics eg sulphonylureas, gliptins etc
If 3 antidiabetics therapy does not work, insulin therapy may be used
DKA = IV fluids, insulin and electrolyte replacement eg potassium
What are the possible complications of diabetes mellitus?
Increased risk of infection
Hypoglycaemia - mood change, fits, confusion, coma, pallor, sweating, tremor, tachycardia
Type 1:
DKA
Type 2:
Hyperosmolar hyperglycaemic state:
Causes severe dehydration, hypernatraemia, high osmolality
Macrovascular complications - MI, stroke, peripheral vascular disease, ischaemic heart disease
Microvascular complications: Neuropathy: Distal symmetrical sensory neuropathy Painful neuropathy Carpal tunnel syndrome Diabetic amyotrophy Mononeuritis Autonomic neuropathy Gastroparesis (abdominal pain, nausea, vomiting) Impotence and urinary retention
Nephropathy: Microalbuminuria and proteinuria Renal failure Prone to UTI Renal papillary necrosis
Retinopathy:
Background leading to pre-proliferative leading to proliferative maculopathy
Prone to glaucoma, cataracts and transient visual loss
Summarise the prognosis of diabetes mellitus
Type 1:
Prognosis depends on early diagnosis, good glycaemic control and compliance with treatment and screening
Vascular disease and renal failure are the main causes of increased morbidity and mortality
Type 2:
Good prognosis with good control
