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153 Cards in this Set

  • Front
  • Back
Definition of Type 1 DM
A disease of insulin insufficiency due to autoantibody destruction of the pancreatic beta islet cells
Acute presentation of Type 1 DM
DKA - patient is unwell, hyperventilating, ketones (sweet smell) on breath, polyuria, polydispia, fatigue
Definition of Type 2 DM
Disease of decreased insulin secretion and increased insulin resistance
Symptoms of hyperglycemia
polyuria, polydipsia, unexplained weight loss, visual blurring, thrush, lethargy
Diagnosis of DM
Fasting blood glucose > 7 mmol/L, random blood glucose > 11.1 mmol/L, Hba1c > 6.7% after an OGTT
Potential causes of DM to keep in mind
Acromegaly, phaeochromocytoma, hyperthyroidism, pregnancy
Definition of impaired glucose tolerance
OGTT 7.8-11.1 mmol/L
Consequences of gestational diabetes
Increased birthweight, neonatal hypoglycemia, sacral agenesis
Metabolic syndrome
Central obesity, hypertension, hyperglycaemia, dyslipidaemia (increased triglycerides, decreased HDL)
Treatment of type 2 DM
1. Lifestyle measures, 2. BP control, 3. Metformin (a biguanide - SFX include diarrhoea, abdo pain), 4. If Hba1c > 7% 16 weeks later add gliclazide (a sulfonylurea - SFX hypoglycaemia), 5. If Hba1c > 7.4% 6 months later add insulin or glitazone
Common complication of injection
Injection site lipohypertrophy
Diabetic nephropathy
urine albumin:creatinine ratio > 3 reflects early renal damage. Inhibition of RA system via candesartan will protect kidneys
Background retinopathy
Microaneurysms, haemorrhages and hard exudates (dots, blots and lipid deposits)
Pre-proliferative retinopathy
Cotton wool spots (infarcts), haemorrhages and venous beading
Proliferative retinopathy
Formation of new vessels. Urgent referral needed.
Decreased acuity
Osmotic changes in the lens induced in acute hyperglycaemia reverse on normoglycaemia
Rubeosis iridis
New vessels occur on iris, occurs late and may lead to glaucoma
Treatment of hyperthyroidism
Beta blockers for rapid symptom control and until carbimazole takes effect (10-20 days due to long half life of T4). If relapse on suspension of treatment - radioiodine therapy and surgery. Radioiodine therapy is contra-indicated in pregnant women as it is teratogenic.
Signs of hypothyroidism
BRADYCARDIC - Bradycardic, Reflexes relax slowly, Akinesia, Dry skin/hair, Yawning/drowsy, Cold peripheries, Ascites, Round face, Depressed, Immobile, Congestive cardiac failure
Causes of primary hyperparathyroidism
80% solitary adenoma, 20% hyperplasia of all glands, <0.5% parathyroid cancer
Presentation of hyperparathyroidism
Relate to hypercalcaemia - Stones, moans, bones and groans. Weak, tired, depressed, thirsty, dehyrated but polyuric, fractures, osteoporosis
IVx hyperparathyroidism
Raised Ca and PTH. Decreased phosphate. Raised alk phos (bone activity). Pepper-pot skull.
Secondary hyperparathyroidism
Low Ca, high PTH. Caused by decreased vitamin D intake and chronic renal failure. Correct with phosphate binders.
Tertiary hyperparathyroidism
High Ca, very high PTH. Occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously having undergone hyperplastic or adenomatous change.
Failure of target cell response to PTH. Signs include short metacarpals, round face, short stature, calcified basal ganglia.
Definition of Cushing's syndrome
Clinical state produced by chronic glucocorticoid excess + loss of normal feedback mechanisms of hypothalamic-pituitary-adrenal axis + loss of circadian rhythm of cortisol secretion
Causes of Cushing's
Majority are iatrogenic (steroids). Endogenous causes are rare but most often increased ACTH via pituitary adenoma (Cushing's disease)
Ectopic ACTH production
Due to small cell lung cancers and carcinoid tumours. Special features include pigmentation, hypokalaemic metabolic alkalosis, weight loss and hyperglycaemia. Even a high dose dexamethasone suppression test fails to suppress cortisol production
Signs and symptoms of Cushing's
Signs - central obesity, moon face, buffalo hump, skin and muscle atrophy, bruises, purple striae on abdo, osteoporosis, infection prone. Symptoms reflect heavy steroid use - increased weight, mood changes, proximal weakness, gonadal dysfunction, acne, recurrent Achilles tendon rupture
Cushing's investigation
No cortisol suppression on high dose dexamethasone suppression test. May also see impaired glucose tolerance and hypokalaemia. Severe hirsuitism suggests an adrenal tumour.
Definition of Addison's
Destruction of the adrenal cortex leading to glucocorticoid and mineralocoritcoid deficiency
Causes of Addison's
80% autoimmunity, others include TB, metastases (lung, breast, renal), lymphoma
Signs and symptoms of Addison's
Lean, tanned, tired, tearful, weak, anorexic, dizzy, faints, myalgias/arthralgia, nausea, vomiting, abdo pain, diarrhoea. Pigmented palmar creases and buccal mucosa
Addison's investigations
Low Na, high K and Ca. High urea. Bloods show anaemia and eosinophilia. Low serum cortisol. Short ACTH stimulation test (tetracosactide)
Hypopituitarism - order of affect
GH, FSH, LH, Prolactin, TSH, ACTH.
Signs and symptoms of hyperprolactinaemia
Amenorrhoea or oligomenorrhoea, infertility, galactorrhoea, decreased libido, increased weight, dry vagina, erectile dysfunction
Signs and symptoms of acromegaly
Spade-like hands and feet, big tongue and facial features, excessive sweating, headaches, decreased libido, arthralgia, finding that rings/clothes become too small, weight gain.
Diabetes medication
Metformin = a biguanide
Gliclazide = a suphonylurea
Rosglitazone = thiazolidinedione
All of the above increase insulin sensitivity

Acarbose = alpha glucosidase inhibitor, decreases sugar absorption
Fasting and 2 hr post glucose for normal pts, IFG, IGT, DM

Normal = < 6
IFG = 6.1-6.9
DM = > 7

2hr post glucose

Normal = <7.8
IGT = 7.8-11
DM = > 11.1
The DM2 equivalent of DKA. Features raised sodium and increased osmolality. Mortality of 20-40%.
Anterior pituitary hormones
GH, TSH, FSH, LH, Prolactin, ACTH, melanocyte stimulating hormone
Posterior pituitary hormones
Oxytocin, ADH (vasopressin)
Growth hormone and gonadotrophins are effected first. Typically, there will be hyPER prolactinaemia due to loss of inhibitory control via dopamine.

Gold standard ivx is insulin tolerance test. Steroid and thyroid hormones given for life.
Thyroid cancer + hypercalcaemia?
Cancer is medullary cell
Anaplastic thyroid cancer
No treatment apart from surgery. If surgery is no good, palliative.
Syndrome of inappropriate antidiuretic hormone
Retention of water and hyponatraemia. Presentation is vague - confusion, irritability. No oedema, hypokalaemia or hypotension. Normal renal, adrenal and thyroid function.

Causes include neoplasms, lung disease, CNS causes, alcohol withdrawal, cytotoxic agents.

Treat with fluid restriction, demeclocycline and, if severe, hypertonic saline.
Diabetes insipidus
Deficiency of vasopressin leading to polyuria, nocturia and compensatory polydipsia. Leads to dehydration. Typically follows hypothalamic-pituitary surgery.

Biochem shows high plasma osmolality with low urine osmolality. Results in high plasma sodium.

Treat with desmopressin.
Fluid replacement in DKA
NaCl 0.9% at a rate of 1L/hr for 2 hours
500 mls/hr in hours 3 and 4

If K <5.5 mmol/L give pre-prepared back of 40 mmol/L
Insulin prescribing in DKA
50 units act rapid in 50mls 0.9% NaCl. Infuse at a fixed rate of 6 units/hr
When to discuss DKA with ITU/HDU
If blood glucose >33
GCS < 15
Pulse >100 or <60
SBP <90
pH <7.1
HCO3 <5
Lactate >2
Subsequent management of DKA (hour 5 onwards)
Give 10% glucose infusion at 100 mls/hr in conjunction with sodium chloride 0.9%
Convert to S/C insulin when stable and eating
Stop IV fluids and insulin 1 hr after first dose of S/C insulin
Definition of hypoglycaemia
4 mmol/L or less
Definition and management of mild hypoglycaemia
4 mmol/L

Trembling, sweating, hungry, tingling, headache, anxiety, palpitations, nausea

Give 4 gluco tabs or 1 bottle of glucojuice or 100 mls lucozade or 200 mls fruit juice

If NBM, give 100 mls 10% glucose IV
Definition and management of moderate hypoglycaemia
3 mmol or 2 mmol/L

Difficulty concentrating and speaking. Confusion. Weakness and giddiness. Drowsy. Unsteady. Headache.

Same as mild if cooperative. If uncooperative, give 2 tubes of glucogel
Definition and management of severe hypoglycaemia
1 mmol/L

Patient unconscious and unable to swallow. Potentially fitting.

ABC. Fast bleep doctor.
100 mls of 10% glucose or 1 mg glucagon im. Repeat if no improvement.
Transfer to ITU.
If patient was on a sulphonylurea, consider octreotide 50 mcg 12 hourly.
What do coeliac disease and DM1 have in common? (genotype)
Heredity in diabetes
Type 1 = HLA DR3-DQ2 or DR4-DQ8
No HLA links in Type 2
Complications of diabetes that may be the presenting feature
Staphylococcal skin infections
Erectile dysfunction
Arterial disease
HbA1c level diagnostic of diabetes
>6.5 (48 mmol/mol)
What type of medication is metformin?
A biguanide
Management of type 1 DM
Basal bolus insulin + pre meal insulin correction dose + amylin analogue (pramlintide)

2nd line - fixed dose insulin if trouble managing basal bolus regimen
Management of type 2 DM
BP control + lipid control + lifestyle changes + smoking cessation + glycaemic management + antiplatelet management (primary = aspirin, secondary = clopidogrel)
Management of type 2 DM if marked hyperglycaemia (FG > 16.6 or RG >19.4)
Straight on to basal bolus insulin + metformin
DVLA rules for diabetes
BCL = bus/coach/lorry drivers

If managed by diet, no need to tell DVLA

If treated by tablets or non-insulin injections, only BCL.

If on insulin, all need to tell DVLA
What is an insulinoma?
Pancreatic islet cell tumours. 95% are benign.
What is Whipple's triad?
Diagnostic criteria for an insulin secreting tumour.

Symptoms associated with fasting or exercise
Symptoms relieved by glucose

Additional criteria includes inappropriately high insulin levels
Diagnosis of insulinoma
Measurement of overnight fasting glucose and insulin on three occasions
Management of insulinoma
Surgical excision. If malignant, give diazoxide. If tumour can't be located, give a somatostatin analogue such as octreotide or lanreotide
Hypothalamic-pituitary-thyroid axis
Hypothalamus secretes thyrotropin releasing hormone to anterior pituitary, which secretes TSH.
Gender ratio of hyperthyroidism
5:1 F:M
Pathogenesis of Graves
Serum IgG bind to TSH receptors, stimulating thyroid hormone production. These are called TSHR-Ab and are specific for Graves disease.
Three most common causes of hyperthyroidism
Graves disease, toxic multinodular goitre, soltary toxic nodule
What is de Quervain's thyroiditis?
Transient hyperthyroidism from an acute inflammatory process. Usually fever, malaise and pain in the neck. TFTs show hyperthyroidism, raised ESR. May be followed by transient hypothyroidism.
Which drug commonly causes thyrotoxicosis?
Two types of amiodarone induced thyrotoxicosis
Type 1 = pre-existing Graves' disease or multinodular goitre

Type 2 = no previous thyroid disease. Associated with a high T4:T3 ratio.
How long does it take before thyroid drugs take effect and why?
10-20 days due to long half life of T4. In the mean time, gain symptomatic control via propanolol
Which thyroid treatment regimen is contraindicated in pregnancy?
Block and replace
Major side effect of drug therapy in thyroid disease
Should only be performed in euthyroid patients. Conventional practice is stop antithyroid drugs 10-14 days before operation and give potassium iodide.
What is a thyroid storm and how would you manage it? And what is mortality?
Hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure and liver dysfunction.

Managed with full dose propanolol with potassium iodide, antithyroid drugs, corticosteroids and supportive measures.
Mortality is 10%
5 types of thyroid malignancy
Papillary (most common) - typically occurs in young people, normally local spread w/ occasional lung/bone metastases. Manage surgically. Prognosis is good.

Follicular (second most common) - more common in women. Metastasises to lung and bone. Manage surgically. Prognosis is good if tumour is resectable.

Anaplastic (uncommon) - aggressive and locally invasive. Prognosis is very poor

Medullary cell (uncommon) - Often familial. Prognosis is poor with indolent course

Lymphoma (rare) - variable behaviour and spread. Responds to radiotherapy.
Role of parathyroid gland
Regulates calcium and phosphate levels. Secretes PTH as calcium levels fall. Calcium levels are then raised by osteoclastic resorption of bone, intestinal absorption of calcium, synthesis of 125-(OH)2D3, increased renal reabsorption, increased excretion of phosphate.
Causes of hypercalcaemia
Hyperparathyroidism, ectopic PTH secretion, myeloma, bone mets, vitamin D excess, granulomatous disease (TB, sarcoidosis, lymphoma), excessive intake, thiazides, lithium use, Addison's, thyrotoxicosis, immobility.
What is secondary hyperparathyroidism?
Compensatory hypertrophy of parathyroid glands due to chronic hypocalcaemia, typically due to CKD or vit D deficiency
What is tertiary hyperparathyroidism?
Permanently raised parathyroid hormone production after longstanding secondary hyperparathyroidism. Parathyroidectomy is necessary.
Symptoms of hypercalcaemia
Bones (pain), stones (renal), moans (depression) and groans (abdo pain).
Hallmark of primary hyperparathyroidism
Hypercalcaemia and hypophophataemia with raised PTH
Presentation of acute hypercalcaemia
Dehydration, N&V, nocturia and polyuria, drowsiness, altered consciousness.
Management of severe hypercalcaemia
Rehydration, IV bisphosphonates.

Can also use prednisolone if myeloma or sarcoidosis.
Causes of hypocalcaemia
CKD, vit D deficiency, thyroid or parathyroid surgery, idiopathic
What is DiGeorge's syndrome?
Familial hypoparathydoism associated with intellectual impairment, cataracts and calcified basal ganglia
What is pseudohypoparathyroidism?
End organ resistance to PTH. Associated with short stature, short metacarpals, subcutaneous calcification and intellectual impairment.
Clinical features of hypoparathyroidism
Paraesthesiae, circumoral numbness, cramps, anxiety, convulsions, laryngeal stridor, dystonia and psychosis.
What is Chvostek's sign?
Present in hypocalcaemia. Tapping over facial nerve causes twitching of ipsilateral facial muscles
What is Trousseau's sign?
Inflation of sphyg cuff for more than 3 mins causes spasm of fingers and wrist
ECG signs of hypocalcaemia
Prolonged QT interval
Management of hypocalcaemia
With vitamin D deficiency give cholecalciferol, otherwise give alfacalcidol
Causes of hypovolaemic hyponatraemia
Diuretics, Addison's, nephropathy, osmotic diaresis, vomiting, diarrhoea, burns, rhabdomyalosis, pancreatitis, peritonitis
Causes of euvolaemic hyponatraemia
Diuretics, SIADH, CNS disturbances, neoplasms (in particular SCLC), surgery, drugs (SSRI, carbamazepine, cyclophosphamide, opiates, maoi, ecstasy)
Causes of hypervolaemic hyponatraemia
Heart, renal, or liver failure. Hyperglycaemia.
Most common causes of hypokalaemia
Diuretics (thiazides) and hyperaldosteronism. Otherwise, GI losses through vomiting, diarrhoea, bulimia/anorexia, DKA.
Definition of hypokalaemia
Mild = <3.5 mmol/L
Severe = <2.5 mmol/L
Clinical manifestations of hypokalaemia
Muscle weakness, ECG changes, rhabdomyolysis, renal abnormalities, cardiac arrhythmias.
ECG changes in hypokalaemia
ST depression, inverted T waves, large U waves, PR prolongation
Clinical features of hypomagnesaemia
Irritability, tremor, ataxia, carpopedal spasm, hyperreflexia, confusion, hallucination, epileptic convulsions
ECG of hypomagnesaemia
Prolonged QT interval, flattened and broad T waves, ST shortening
Clinical features hypermagnesaemia
Weakness, hyporeflexia, respiratory paralysis
Treatment of hypermagnesaemia
Same as hyperkalaemia
Clinical features of hypophosphataemia
Muscle weakness, left shift of oxyhaemoglobin dissociation curve, confusion, hallucination, convulsions
Causes of hypophasphataemia
What is Addison's?
Destruction of at least 90% of the adrenal cortex leading to reduction of glucocorticoid, mineralocorticoid and sex steroid production. Leads to increased CRH and ACTH production via feedback.
What causes Addison's?
Autoimmune disease, TB, surgical removal of adrenals, infiltration via malignancy/amyloid
Symptoms and signs of Addison's disease
Symptoms - weight loss, anorexia, malaise, weakness, impotence/amenorrhoea, N&V, abdo pain, constipation/diarrhoea

Signs - Pigmentation of new scars and palmer creases, postural hypotension, buccal pigmentation
What is an Addisonian crisis?
Hypotension + hyponatraemia + hyperkalaemia + hypoglycaemia + dehydration. Typically follows infection, infarction, trauma or operation.
Management of Addisonian crisis
1L 0.9% saline. IV bolus hydrocortisone. Supportive.
What is hyperaldosteronism?
A disorder of the adrenal cortex characterised by excess aldosterone production leading to sodium retention, potassium loss, and hypertension.
What causes secondary hyperaldosteronism?
Renal artery stenosis
What causes primary hyperaldosteronism?
Adrenal adenomas (Conn's syndrome, more common in young women), bilateral adrenal hyperplasia (more commen in men >40)
Presentation of hyperaldosteronism
Typically just hypertension. Other symptoms are non specific (weakness, nocturia)
How would you differentiate adenoma from hyperplasia in hyperaldosteronism?
Adrenal CT or MRI.

Also, check plasma aldosterone levels, which rise throughout the day with adenomas and fall with hyperplasia. Also measure 18-OH cortisol levels, which rise in adenoma
Management of hyperaldosteronism
If adenoma, surgical removal. If hyperplasia, spiranolactone.
What is Cushing's syndrome?
The clinical state of increased free ciculating glucocorticoid
What is Cushing's disease?
Pituitary disease leading to Cushing's syndrome
What causes Cushing's syndrome?
Cushing's disease, ectopic ACTH producing tumours, ACTH administration, adrenal adenomas, adrenal carcinomas, steroid use
Signs and symptoms of Cushing's
Pigmentation (if ACTH dependent), impaired glucose tolerance, hypokalaemia, hypertension, pathological fractures, striae, proximal myopathy.

Central weight gain, thin skin/bruishing, hair growth, acne, back pain, plethora.
Ivx Cushing's
48 hour low dose dexamethasone test - normal result is suppression of plasma cortisol to <50 nmol

24 hour urinary free cortisol measurement

Pronounced circadian variation in cortisol. In Cushing's 09:00 sample of cortisol may be normal, but 00:00 sample will be >100 nmol/L
What causes death in Cushing's?
Complications of hypertension
Management of Cushing's
Depends on cause. Typically surgery (transsphenoidal pituitary adenectomy or adrenalectomy) plus medical management via ketoconazole or mifepristone.
What is congenital adrenal hyperplasia?
Inherited enzyme deficiency that impair normal corticosteroid synthesis by the adrenal cortex - most commonly 21-hydroxylase deficiency.
What is a phaeochromocytoma
A tumour arising from catecholamine producing cells of the adrenal medulla
Clinical features of phaeochromocytoma
Headaches, diaphoresis, palpitations, paroxysmal HTN. Symptoms are episodic and tend to progress as the tumour grows.
IVx of phaeochromocytoma
24 hour urine collection for catecholamines, metanephrines, normatenephrines, and creatinine.
Management of phaeochromocytoma
Anti hypertensive agents + surgery
Hormones secreted by the anterior pituitary
ACTH, TSH, FSH, LH, GH, prolactin, leptin
Hormones secreted by the posterior pituitary
Oxytocin, vasopressin
What does the hypothalamus do?
Essentially links the nervous and endocrine systems via the pituitary gland.
What is pituitary apoplexy?
Bleeding into or impaired blood supply to the pituitary gland, typically due to the presence of a tumour
Clinical features of pituitary apoplexy
Compressive effects of the local region.

i.e. headache, visual field defect (optic chiasm), double vision (third nerve). Followed by symptoms of adrenal insufficiency.

Can present with meningism and decreased level of consciousness.
What causes acromegaly?
Excess GH, typically due to a pituitary adenoma
Signs and symptoms of acromegaly
Change in appearance, increased size of hands/feet, headaches, excessive sweating, visual deterioration, weight gain, deep voice, goitre, pain in hands, polyuria.

Prognathism, interdental separation, large tongue, spade like hands and feet.

May also cause hirsuitism, thick skin, carpal tunnel syndrome, visual field defects, arthropathy.
Ivx of acromegaly
Glucose tolerance test is diagnostic if there is no suppression of GH, or there is a rise.

IGF-1 levels are often raised. MRI for pituitary tumour.
Management of acromegaly
Trans-sphenoidal surgery is first line, followed by radiotherapy.

Also use octreotide, bromocriptine, and pegvisomant.
Definition of a high risk lipid profile
Total cholesterol > 4.0 mmol/L or
LDL > 2.0 mmol/L or
Triglycerides > 4.5 mmol/L
Management of diabetic neuropathy
Duloxetine (amitriptyline if contraindicated)
Second line = amitriptyline or pregabalin or both
Other options include pain management clinic, tramadol, topical lidocaine
Type 2 diabetes blood pressure targets
if no end organ damage < 140/80
If end organ damage <130/80
When to treat subacute hypothyroidism
If TSH>10, thyroid autoantibodies positive, other autoimmune disorder, previous treatment of Graves' disease
Glucocorticoid and mineralocorticoid activity in steroids
Very high mineralocorticoid = fludrocortisone
high mineralocorticoid = hydrocortisone
high glucocorticoid = prednisolone
very high glucocorticoid = dexamethason, betamethasone
Secondary hypothyroidism TFTs
TSH and free T4 both low
Sick euthyroid syndrome TFTs
TSH Low/Normal, T4 low, T3 very low
Subclinical hypothyroidism TFTs
TFT high, T4 normal
Poor compliance with treatment TFTs
TSH high, T4 normal. T4 will normalise before TSH
Steroid therapy TFTs
TSH low, T4 normal