Diabetes and Endocrinology Flashcards
State the normal fasting glucose range for non-diabetics (in mmol/L)
4 to 6 mmol/L
State fasting glucose level for which diabetes is suspected (in mmol/L)
Above 7 mmol/L
State random glucose level for which diabetes is suspected (in mmol/L)
Above 11 mmol/L
State HbA1C level for which diabetes is suspected (in mmol/L and %)
Above 48 mmol/L or 6.5%
Outline the symptoms and average age of onset of T1DM
Triad:
- Polyuria
- Polydipsia
- Weight loss
plus
- Tiredness
- Weakness
May also present in DKA
- Nausea and vomiting
- Pear drop breath
- Hypotension (from dehydration)
- Altered consciousness
Average age of diagnosis of 13 years
Outline the symptoms of T2DM
Triad:
- Polyuria
- Polydipsia
- Weight loss
plus
- Fatigue
- Opportunistic infections
- Slow healing
- Glucosuria
Average age of diagnosis is much later in life compared to T1DM
State the investigations for suspected T1DM (how you many you need to be able to diagnose diabetes)
- HbA1C (> 6.5% or 48 mmol/L)
- Fasting blood glucose (above 7mM)
- Oral glucose tolerance test
Symptomatic + 1 abnormal test
Asymptomatic + 2 abnormal tests
Tests need to be 1 week apart
State the investigations for suspected T2DM
- HbA1C (> 6.5% or 48 mmol/L)
- Fasting blood glucose (above 7mM)
- Random blood glucose (above 11mM)
- Oral glucose tolerance test (above 11mmol/L)
Symptomatic + 1 abnormal test
Asymptomatic + 2 abnormal tests
Tests need to be 1 week apart
State the management for T1DM
- Insulin!! Basal-bolus regimen
- Patient education
- Monitor carbohydrate intake
- Monitor blood sugars 3 times a day
- Monitor development of any complications
State the management for T2DM, including:
- Lifestyle modifications
- Regular monitoring required
- Medication hierarchy
Lifestyle modifications:
- Reduce glucose intake and increase fibre intake
- Potentially low carbohydrate (but not mainstream advice)
- Reduce other lifestyle risks e.g. stop smoking, increase exercise and weight loss
- Control other co-morbidities e.g. hypertension, hyperlipidaemia
Monitor for long term complications:
- Diabetic foot reviews
- Kidney disease checks
- Eye checks for retinopathy
Medications:
- Metformin (1st line)
- Sulphonylurea
- Pioglitazone
- Incretin mimetics
- SGLT-2 inhibitors
- Insulins
List short term and long term (microvascular and macrovascular) complications of T1DM
Also list some infection related complications
Short term:
- Hypoglycaemia
- Hyperglycaemia
Long term - macrovascular:
- Coronary artery disease
- Peripheral ischaemia
- Stroke
- Hypertension
Long term - microvascular:
- Peripheral neuropathy
- Nephropathy
- Retinopathy
Infection related complications:
- UTIs
- Thrush and other fungal infections
- Pneumonia
- Soft tissue / skin infections
List long term complications of T2DM (microvascular and macrovascular)
Macrovascular:
- Coronary artery disease
- Peripheral ischaemia
- Stroke
- Hypertension
Microvascular:
- Peripheral neuropathy
- Nephropathy
- Retinopathy
List risk factors for T2DM
Non-modifiable:
- Increased age
- Ethnicity (black, chinese, south asian)
- Family history
Modifiable:
- Obesity
- Sedentary lifestyle
- HIgh carbohydrate intake
Describe how the Oral Glucose Tolerance Test is performed
Performed first thing before breakfast (fasting plasma glucose)
- Measure fasting plasma glucose
- Give 75g glucose drink
- Measure plasma glucose 2 hours post-drink
Assesses ability of the body to cope with carbohydrate
Explain ways of monitoring T1DM (longer term)
HbA1C - reflects glucose control over the past 3 months
Capillary blood glucose (CBG) or libre devices (flash glucose monitoring of glucose level in interstitial fluid)
Describe some ways in which ensure that insulin is prescribed safely
- Check brand name (some are similar)
- Check device.
- Check dose
- NEVER abbreviate “units” to “u” or “iu” due to risk of 10x overdose.
- Check dose time
- Correctly write on both charts (drug/EPMA and green chart)
Diabetic Ketoacidosis - state the following:
- Pathophysiology
- 3 biochemical disturbances that occur (most consequential effects of DKA)
- Presentation
- How it is diagnosed
Pathophysiology:
- Occurs in T1DM
- When there is insufficient exogenous insulin
- Occurs because the body doesn’t have enough insulin to process glucose
3 biochemical disturbances:
These 3 are the most consequential effects of DKA and can KILL the patient!!
1. Ketoacidosis - ketogenesis is used in order to generate alternative fuel source
2. Dehydration
3. Potassium imbalance
Presentation:
- Nausea and vomiting
- Acetone (pear drop) breath
- Polydipsia (hyperglycaemia)
- Polyuria (hyperglycaemia)
- Hypotension and dehydration
- Altered consciousness
- History / evidence of reduced insulin or illness
How it is diagnosed (HKA):
1. Hyperglycaemia - blood glucose >11mmol/L
2. Ketosis - blood ketones > 3mmol/L
3. Acidosis - pH < 7.3
Hyperosmolar hyperglycaemia syndrome - state the following:
- Pathophysiology
- Presentation
- Are there normally ketones in the urine?
- Diagnosis
- Management
Pathophysiology:
- Occurs in T2DM
- Results from prolonged high blood glucose levels (over weeks)
- High glucose levels usually caused by acute illness (e.g. infection)
- Glucose can rise as a result of hormones the body produces during illness e.g. cortisol
- High glucose causes osmotic diuretics and dehydration
- Can be the first presentation of T2DM
Presentation:
- Polyuria
- Polydipsia
- Nausea
- Hypotension
- Tachycardia
- Dry skin
- Disorientation, drowsiness and altered consciousness
Ketones in the urine?
- No, ketones develop in DKA due to lack of insulin (no glucose into cells)
- T2DM may still be producing some insulin, ketones may not be created
- However it is still possible to get DKA with T2DM (just less common)
Diagnosis:
- Blood glucose (often very high)
- Blood pH and ketones (often low)
Management:
- Transfer to acute care bay or ICU if required
- Fluid resuscitation
- Potassium infusion if required
- Only start insulin infusion if there are raised ketones (otherwise don’t start)
Explain why ketoacidosis occurs in DKA
- Lack of insulin results in lack of glucose WITHIN cells
- Body uses ketogenesis to produce ketone bodies as fuel for brain
- Ketone levels increase which raises the blood pH
- Bicarbonate is produced at the kidneys to reduce acidity
- At point at which there can no longer be compensation then ketoacidosis occurs
Explain why dehydration occurs in DKA
Dehydration occurs because of the hyperglycaemia
- Hyperglycaemia overwhelms kidneys so glucose is filtered into urine (osmotic diuresis)
- Polyuria occurs leading to dehydration
Patient will also have polydipsia as a compensatory mechanism
Explain why potassium imbalance occurs in DKA
- Insulin usually causes potassium to be taken up into the cells
- Without normal insulin levels, serum potassium can be normal (kidney compensation) or rise
- HOWEVER body’s cellular potassium levels are low
- Therefore caution when starting insulin treatment as severe hypokalaemia can ensue
Outline the acute management steps for DKA (acronym)
FIG PICK
Fluids!! - 1L stat of 0.9% saline, then 4L with potassium over next 12 hrs
Insulin - IV Actrapid infusion
Glucose - closely monitor and use Dextrose fluid infusion if low glucose
Potassium - closely monitor and correct as required
Infection - check/treat any underlying infection
Chart - fluid balance
Ketones - monitor ketones closely
Once stable, resume patient on normal subcutaneous insulin regimen
Explain how the following chronic DM complications are managed:
- Diabetic foot ulcer
- Retinopathy
- Nephropathy
- Peripheral neuropathy (painful)
For all complications, control of glucose levels are mainstay of management
Diabetic foot ulcer:
- Offloading (non-weight bearing)
- Debridement
- Wound dressing / negative pressure therapy
- Regular monitoring
Retinopathy:
- Eye test at time of diagnosis
- Regular eyesight/screening tests thereafter
Nephropathy:
- Aim to reduce blood pressure <140/90 mmHg
- Antihypertensives e.g. ACE inhibitor, can reduce proteinuria or preservation GFR, or both
- Cholesterol lowering drugs e.g. statins
- Regular monitoring of UandEs e.g. eGFR, Albumin:Creatinine
Peripheral neuropathy (painful):
- Initial neuropathic drugs: Amitriptyline, Duloxetine, Gabapentin or Pregabalin
Outline some medications used to treat peripheral neuropathy (painful)
Gabapentin or Pregabalin
Amitriptyline
Duloxetine
- Consider additional topical capsaicin cream
How does chronic hyperglycaemia in DM cause retinopathy? What are the 3 main stages?
Retina supplied by small blood vessels which can be damaged by hypergylcaemia over time
3 main stages:
- Bulges in blood vessels - may bleed slightly but don’t usually affect your vision (background retinopathy)
- More significant changes - significant bleeding into the eye (pre-proliferative retinopathy)
- Scar tissue and angiogensis (bleed easily), develop on the retina (proliferative retinopathy) - can result in some loss of vision
State how nephropathy is diagnosed in DM
Measure urine albumin
- persistent albuminuria (severely increased)
- Co-existing retinopathy
- No evidence of alternative kidney disease
Hyperglycaemia
- Definition
- Symptoms
- Investigations
- Management
Hyperglycaemia:
- Elevated plasma glucose, generally > 11.1 mmol/L (random fasting glucose)
Symptoms:
- Polydipsia
- Polyuria
- Weight loss
- Blurred vision
- Fatigue
Investigations:
- Investigate further to look for the cause e.g. T1DM / T2DM, sepsis, incorrect dose of oral hypoglycaemics
- Check ketones (be aware of DKA / HSS)
Management:
- Depends on cause (whether acute or chronic)
- Treat underlying cause
Hypoglycaemia
- Definition
- Symptoms
- Investigations
- Management
Hypoglycaemia:
- Low plasma glucose, generally < 4 mmol/L (random fasting glucose)
Symptoms:
- General malaise
- Headache
- Nausea
- Autonomic – pallor, sweating, tremor, tachycardia
- Neuroglycopaenic – loss of concentration, behavioural changes, fits, reduced level of consciousness
Investigations:
- Check diabetic status including whether medications have been correctly given recently
- Investigate any other cause e.g. post gastric surgery or anorexia
Management:
- Use ‘Hypo boxes’ on the wards
- Give oral easy release glucose e.g. Glucojuice (up to 3 doses)
- If unsuccessful, give IV Dextrose infusion or IM Glucagon
- If severe hypoglycaemia/NMB then give IV glucose
Hyponatraemia - state the following:
- Pathophysiology
- Causes
- Presentation
- Management
Pathophysiology:
- Serum sodium concentration of < 135 mmol/L (mild, moderate or severe)
Causes:
- Medications (most commonly thiazide diuretics).
- SIADH
- Underlying medical conditions (such as heart failure, kidney disease, and liver disease)
Presentation:
- Nausea and vomiting
- Headache
- Drowsiness, seizures, coma
Management:
- Understand the underlying cause
- Hypertonic saline to serum sodium concentration (prevent cerebral oedema)
Hypernatraemia - state the following:
- Pathophysiology
- Causes
- Presentation
- Management
Pathophysiology:
- Serum sodium concentration of > 145 mmol/L (hypovolaemic, euvolaemic, hypervolaemic)
Causes:
Hypovolaemic
- Sweating, vomiting / diarrhoea, diuretics, kidney disease
Euvolaemic
- Fever, diabetes insipidus, lithium
Hypervolaemic
- Hyperaldosteronism, excessive IV saline, increased salt ingestion
Presentation:
- Confusion
- Muscle twitching or spasm
- Impaired consciousness
Management:
- Oral water or Dextrose infusions (needs to be done slowly)
- Treat underlying cause if known
Adrenal crisis - state the following:
- Pathophysiology
- Causes
- Symptoms
- Blood results seen
- Investigations
- Management
Pathophysiology:
- Crisis resulting from inadequate production of cortisol
Causes:
- Sudden steroid withdrawal
- Failure to double steroid dose during acute illness/stress
- Addison’s disease
- CAH (Congenital Adrenal Hyperplasia)
- Hypopituitarism
Symptoms:
- Nausea & vomiting
- Weakness / lethargy
- Weight loss
- Dizziness / low BP
Blood results seen:
- Hyponatraemia
- Hyperkalaemia (only IF Addison’s)
- Hypoglycaemia
- Metabolic acidosis
- Evidence of AKI
Investigations:
Unstable patient - skip straight to management
Stable patient:
- CBG
- ABG
- Bloods FBC, U&E, LFT and glucose
- Free T4 & TSH
Management:
Unstable/unconscious patient:
- Hydrocortisone (IV or IM) 100mg stat
- IV fluids
- Maintenance IV Hydrocortisone 50mg qds
Once patient is stable:
- Identify & treat precipitating factors
- IV dextrose if hypoglycaemia
- Perform short synacthen test if cause is unclear
- Eventually switch back to oral steroids (from IV)
Addison’s disease - state the following:
- Pathophysiology
- Causes
- Symptoms
- Blood results seen
- Investigations
- Management
Pathophysiology:
- Destruction of the adrenal glands leading to reduced endogenous aldosterone, cortisol and testosterone production
Causes:
- Autoimmunity (90% in developed world)
- CAH (congenital adrenal hyperplasia)
- TB and other infection
Symptoms:
- Nausea & vomiting
- Fatigue / weakness / lethargy
- Polydipsia / polyuria
- Weight loss
- Dizziness / low BP
Blood results seen:
- Hyponatraemia
- Hyperkalaemia
- Hypoglycaemia
- Metabolic acidosis
- Evidence of AKI
Investigations:
- Bloods checking ATCH level, will be high in primary adrenal failure
- Short synacthen test
Management:
If in adrenal crisis - see previous flashcard!
- Hydrocortisone as life-long cortisol (steroid) replacement
- Fludrocortisone as life-long mineralocorticoid (aldosterone) replacement
State how the short synacthen test is conducted
- Performed in the morning (adrenal glands are most responsive)
- Give synacthen (synthetic ACTH)
- Measure plasma cortisol at 30 minutes and 60 minutes
If normal:
- This will cause a rise in cortisol to more than DOUBLE baseline
If primary adrenal insufficiency:
- Cortisol doesn’t rise significantly (lack of response to synthetic ACTH)
Cushing’s disease - state the following:
- Pathophysiology
- Symptom
- Signs
- Blood results
- Investigations
- Management
Pathophysiology:
- Subset of Cushing’s syndrome which is chronic high levels of cortisol
- Specifically where there is a pituitary adenoma leading to increased cortisol production
Symptoms:
- Weakness
- Weight gain
- Low mood
- Polydipsia / polyuria
- Headaches
- Visual field defects
- Increased frequency of infections
Signs:
- Melon on a stick appearance
- Striae
- Buffalo hump
- Rounded face
- Hypertension
Blood results:
- Raised WCC due to effects of raised glucocorticoid
- Hypernatraemia
- Hypokalemia
Investigations:
- Dexamethasone suppression test (low dose followed by high dose)
Management:
Treat underlying cause!
- Transsphenoidal removal of pituitary adenoma
Explain how the Dexamethasone suppression test is completed (low dose and high dose)
Low dose suppression test:
- (10pm) give low 1mg dose of Dexamethasone (synthetic cortisol)
- (9am next morning) measure cortisol and ACTH levels
Normal: Cortisol = suppressed (and ACTH = suppressed)
Abnormal: Cortisol = NOT suppressed (Cushing’s syndrome)
High dose suppression test:
- Completed if low dose gave abnormal results
- Give high dose 8mg Dexamethasone
Cushing’s disease: cortisol suppressed
Adrenal cushing’s: cortisol normal, ACTH low
Ectopic ACTH: cortisol normal, ACTH normal
Explain how the Dexamethasone suppression test is completed (low dose and high dose)
Low dose suppression test:
- (10pm) give low 1mg dose of Dexamethasone (synthetic cortisol)
- (9am next morning) measure cortisol and ACTH levels
Normal: Cortisol = suppressed (and ACTH = suppressed)
Abnormal: Cortisol = NOT suppressed (Cushing’s syndrome)
High dose suppression test:
- Completed if low dose gave abnormal results
- Give high dose 8mg Dexamethasone
Cushing’s disease: cortisol suppressed
Adrenal cushing’s: cortisol normal, ACTH low
Ectopic ACTH:Hy cortisol normal, ACTH normal
Hypothyroidism - state the following:
- Pathophysiology
- Symptoms
- Investigations / TFT results
- Management
Pathophysiology
- Reduced production of thyroid hormones (T3 and T4) by thyroid glands
Causes:
- Autoimmune Hashimoto’s thyroiditis
- Post-pregnancy
- Over-treatment for hyperthyroidism
- Iodine deficiency (developing world)
- Medications e.g. Lithium and Amiodarone
- Secondary hypothyroidism (pituitary gland affected by infection, radiation etc)
Symptoms:
- Dry skin and hair
- Constipation / reduced bowel movements
- Fatigue
- Intolerance to cold
- Weight gain
- Fluid retention
Investigations / TFT results:
- Thyroid function tests: low fT4, high TSH
(if secondary hypothyroidism, then both low fT4 and low TSH)
Management:
- Levothyroxine (synthetic T4 replacement)
Hyperthyroidism - state the following:
- Pathophysiology
- Symptoms (including specific Graves symptoms)
- Investigations / TFT results
- Management
Pathophysiology
- Increased production of thyroid hormones (T3 and T4) by thyroid glands
Causes:
- Autoimmune Graves’ disease
- Thyroid nodules (single or multiple)
- Post-pregnancy
- Overtreatment of hypothyroidism with Levothyroxine
- Medications that contain iodine e.g. Amiodarone
- Viral infection e.g. De Quervain’s thyroiditis
- Inflammation (thyroiditis)
- Pituitary adenoma
- Thyroid cancer
Symptoms:
- Sweating
- Anxiety / agitation
- Intolerance to heat
- Weight loss
- Tachycardia
- Frequent loose stools
(Graves specifically)
- Exophthalmos / Graves eye disease
- Pretibial myxoedema
- Goitre
Investigations / TFT results:
- Thyroid function tests: high fT4, low TSH
(if secondary hyperthyroidism, then both high fT4 and high TSH)
- Test for autoantibodies
- Doppler ultrasound to look for thyroid nodules
Management:
- Medications: Carbimazole (1st line) and Propylthiouracil (2nd line)
- Radioactive iodine
- Surgery (specific nodules or whole thyroid)
- Beta blockers e.g. Propranolol (symptom control)
Hypokalaemia - state the following:
- Pathophysiology
- Causes
- Symptoms
- Investigations (plus results)
- Management
Pathophysiology:
- Low serum potassium, less than 4mmol/L
Causes:
- Generally gastrointestinal or urinary losses
- Medications e.g. insulin, beta agonists (Salbutamol or Adrenaline)
Symptoms:
- Fatigue / weakness
- Leg cramps
- Constipation
Investigations:
Blood test - serum K < 4mmol/L
Mild (3-4, no arrhythmia)
Moderate (2.5-3.5 with
arrhythmia)
Severe (less than 2.5)
ECG - ST segment depression, small T waves, large U waves, (slightly) prolonged PR interval
Management:
Mild (3-4, no arrhythmia): oral potassium with Sando K or IV potassium with saline/dextrose through cannula
Moderate (2.5-3.5 with arrhythmia): IV potassium with saline/dextrose through cannula
Severe (less than 2.5): IV potassium with saline/dextrose through central venous catheter
Hourly monitoring of K levels until resolved
Hyperkalaemia - state the following:
- Pathophysiology
- Symptoms
- Investigations (plus results)
- Management
Pathophysiology:
- High serum potassium, more than 5.5mmol/L
- Commonly associated with CKD and can occur in DKA
Symptoms:
- Can be asymptomatic
- Cardiac arrhythmias
- Muscle weakness
- Paralysis
Investigations:
- Blood test - serum K > 5.5mmol/L
ECG - flattened P waves, broad QRS, peaked T waves
Management:
Immediately give calcium gluconate 10% 30ml over 5-10 mins and check ECG (if no improvement, administer calcium gluconate again)
Then:
- Give sodium zirconium cyclosilicate 10g
- Give nebulised Salbutamol 20mg
- Give Insulin (Actrapid) 10 units with IV Glucose 25g
- Give fluids if needed
Outline how calcium gluconate and calcium resonium work in their use in treatment of hyperkalaemia and which one is given first
Calcium gluconate = given immediately
- Works to stabilise the cardiac membrane / myocytes
- Cardioprotective immediately
Calcium resonium = given later on
- Stops the absorption of potassium in the bowel
- Helps to decrease plasma potassium over time, much slower than calcium gluconate
Hypocalcaemia - state the following:
- Pathophysiology
- Common causes
- Symptoms
- ECG changes
- Investigations
- Management
Pathophysiology:
- Low calcium, less than 2.1 mmol/L
Common causes:
- Most commonly following a thyroidectomy
- Severe vitamin D deficiency
- CKD
- Pancreatitis
- Hypomagnesaemia
Symptoms:
- Early symptoms: peri-oral and digital paraesthesia and carpopedal spasm
- Severe symptoms: arrhythmias, seizures and acute laryngospasm
ECG changes:
- Prolonged QT interval
- Arrhythmias
Investigations:
- Bloods (see above)
- ECG (see above)
Management:
Correct underlying cause
- Post-thryoidectomy: oral calcium supplements
- Vitamin D deficiency: supplements
- Hypomagnesaemia: stop offending drugs, IV magnesium if needed
If severe (medical emergency):
- Administer 10mls 10% calcium gluconate in 50mls 5% dextrose over 10 minutes
- Repeat until patient asymptomatic
- In post-surgical hypoparathyroidism, start 1-alfacalcidol 0.25-0.5mcg/day
Hypercalcaemia - state the following:
- Pathophysiology
- Common causes
- Symptoms
- Investigations
- Management
Pathophysiology:
- Increased serum calcium, greater than 2.6 mmol/L (symptoms apparent above 3.5 mmol/L)
Common causes:
- Primary hyperparathyroidism
- Malignancy
- Sarcoidosis / TB
- Paget’s disease
Symptoms:
- Fatigue
- Nausea
- Weakness
- Polydipsia / polyuria
- Constipation
- Abdominal pain
- Confusion
- Loss of concentration
(same as hyperparathyroidism)
Investigations:
Investigate underlying cause
? Primary hyperparathyroidism
? Malignancy
? Paget disease
? Medications e.g. Thiazide diuretics
Management:
Mild: Restrict dietary calcium, discontinue thiazide diuretics / vitamin D / calcium supplements and repeat checks in 2 weeks
Moderate / severe: Rapid IV saline infusion (4-6 L / day) and Bisphosphonates e.g. Zoledronate (inhibits osteoclasts)
Hyperparathyroidism - state the following:
- Pathophysiology
- Causes
- Symptoms
- Investigations
- Management
Pathophysiology:
- Increased production of PTH at the parathyroid glands (within thyroid gland) in response to low calcium levels
- Overall effect it to raise calcium levels
Causes:
Primary
- Parathyroid gland tumour
Secondary
- Insufficient vitamin D
- Chronic renal failure
Tertiary (from chronic secondary parathyroidism, and doesn’t resolve upon resolving initial cause)
Symptoms (symptoms of hypocalcaemia):
- Fatigue
- Nausea
- Weakness
- Polydipsia / polyuria
- Constipation
- Abdominal pain
- Confusion
- Loss of concentration
Investigations:
- Blood tests looking at PTH and Ca levels
Management:
Treat underlying cause!
Primary - removal of tumour
Secondonary - vitamin D supplements or manage chronic renal failure
Tertiary - removal of part of parathyroid gland
List the causes and blood test results for the following regarding Calcium and PTH levels
1. Primary hyperparathyroidism
2. Secondary hyperparathyroidism
3. Tertiary hyperparathyroidism
- Primary hyperparathyroidism
Cause: parathyroid gland tumour
PTH level: high
Calcium level: high - Secondary hyperparathyroidism
Cause: vitamin D deficiency or chronic renal failure
PTH level: high
Calcium level: low/normal - Tertiary hyperparathyroidism
Cause: chronic secondary hyperparathyroidism (failure to resolve to normal after treatment)
PTH level: high
Calcium level: high
What are the 4 types of insulin and give some examples
- Rapid acting e.g. NovoRapid
- Short acting e.g. Actrapid
- Intermediate acting e.g. Insuman Basal
- Long acting e.g. Lantus
List some non-diabetic causes of hypoglycaemia
- Addison’s disease and other conditions affecting cortisol levels
- Anorexia
- Chronic liver disease
- Reactive hypoglycaemia
- Insulinoma (increased insulin production)
List some potential dangers of giving insulin
- DKA
- Hypoglycaemia (especially if driving)
- Hypokalaemia and arrhythmias
- Anaphylaxis (reaction to insulin)
List some severe potential complications of acute hypo-calcaemia
- Long QT syndrome
- Seizures
- Laryngospasm
- Coma
- Heart failure
What malignancies tend to cause hypercalcaemia and what are the mechanisms behind this?
Bone metastasis / primary bone malignancy:
- Increased osteoclast activity (releases Ca)
Ovarian cancer:
- Produces ectopic PTH
- Increased osteoclast activity (releases Ca)
Small cell lung cancer / renal cell carcinoma:
- Produces PTH-related peptide
- Increased osteoclast activity (releases Ca)
Lymphomas:
- Produce vitamin D
List 2 drugs that can help to lower serum calcium?
Bisphosphonates
Denosumab
Both work by inhibiting osteoclasts
Outline the 4 most common types of thyroid cancer (order them in most common first)
- Papillary thyroid cancer (70%)
- Follicular thyroid cancer
- Medullary thyroid cancer
- Anaplastic thyroid cancer
List some factors that can precipitate hyperosmolar hyperglycaemic state (HHS)
- Infection
- Medicine non-compliance
- Drugs e.g. steroids or diuretics
- Trauma
- Stroke / MI
List some factors that can precipitate DKA
- Infection e.g. UTI
- Physiological stress e.g. trauma, surgery
- Non-adherence to insulin treatment
- Co-morbidities e.g. hypothyroidism
- Drug treatments e.g. corticosteroids
- Undiagnosed T1DM (aka untreated T1DM)
What bacterias are commonly found in diabetic foot ulcers?
Gram-positive organisms:
- Staphylococcus aureus
- Enterococcus
Gram-negative organisms:
- Pseudomonas aeruginosa
- E coli
Phaeochromocytoma - state the following:
- Pathophysiology
- Presentation
- Investigations
- Management
Pathophysiology:
- Catecholamine secreting tumour in the adrenal medulla
Presentation:
- Palpitations
- Sweating
- Headaches
- Anxiety
- Weight loss
- Fatigue
- Episodic hypertension
- Flushing
Investigations:
- Plasma metanephrines
- CT Chest Abdomen and Pelvis
Management:
- Definitive management is surgical resection of the tumour
- Can use alpha blockers (phenoxybenzamine) and beta blockers in the meantime before surgery
Hyperaldosteronism - state the following:
- Pathophysiology
- Main causes
- Presentation
- Investigations
- Management
Pathophysiology:
- Hyperaldosteronism can be primary or secondary
- Classically associated with high blood pressure (resistant to BP treatments) and hypokalaemia
Main causes:
- Conn’s Syndrome (adrenal adenoma)
- Bilateral adrenal hyperplasia
- Familial hyperaldosteronism
- Adrenal carcinoma
Presentation:
- Polyuria
- Polydipsia
- Lethargy
- Headaches
Investigations:
- Aldosterone/renin ratio
- CT/MRI to locate adrenal lesions
- Selective adrenal venous sampling = gold standard
Management:
- Identify the underlying cause (using imaging or adrenal venous sampling)
- Surgical removal of affected adrenal gland
- If bilateral adrenal disease, use potassium sparing diuretics e.g. Spironolactone
Outline the risk factors for osteoporosis
- Age (>50 for women and >65 for men)
- Female
SHATTERED Family
S – Steroid use
H – Hyperthyroidism, hyperparathyroidism
A – Alcohol and smoking
T – Thin (BMI < 22)
T – Testosterone deficiency
E – Early menopause
R – Renal/liver failure
E – Erosive/inflammatory bone disease
D – Diabetes
+ Family history
What groups of the population should be investigated for osteoporosis?
Women > 65
Men > 75
Plus men and women > 50 if they have any of the risk factors above
Osteoporosis - state the following:
- Investigations
- Management (conservative and pharmacological)
Investigations:
- DEXA scan (Gold standard)
- X-rays if fractures suspected
- MRI spine if vertebral fractures suspected
Management:
Conservative
- Reduce risk factors - eg. stop smoking
- Diet: adequate vitamin D, calcium, protein
- Weight bearing exercises
- Hip protectors (in nursing home patients)
Pharmacological
- Weekly Bisphosphonates = 1st line
- Vitamin D + calcium supplements can also be added if evidence of deficiency
- Denosumab
- Raloxifene
Outline the acid base disturbance seen in Aspirin overdose
Initial respiratory alkalosis (caused by activation of respiratory centres in the brain)
Later metabolic acidosis (causes by wasting of bicarbonate ions due to the ingested acid load) - this is often mixed with the respiratory alkalosis
Paget’s disease - state the following:
- Pathophysiology
- Bones commonly affected
- Common causes
- Symptoms
- Investigations
- Management
Pathophysiology:
- Increased osteoCLAST activity at the start
- This is followed by increased osteoBLAST activity
- Overall, results in disorganised bone breakdown and formation
Bones commonly affected:
- Skull
- Vertebrae
- Pelvis
- Femur
- Tibia
Risk factors:
- Increasing age (normally >40)
- Family history
- Anglo-Saxon descent
Presentation:
- Often asymptomatic (picked up incidentally on x-ray or raised ALP blood test)
- Deep, boring pain over affected bones
- Pathological fractures (often transverse fractures)
- Bony deformities e.g. bowing of femur or tibia
Investigations:
- X-rays
Bloods: raised ALP, normal calcium, normal phosphate
Management:
- Analgesia
- Bisphosphonates e.g. alendronic acid
- Typically treatment lasts 6 months, bone activity may return to normal
- Monitor at regular 6 or 12 month intervals for recurrence
Outline the main antibodies most commonly found in Hashimoto’s and Graves disease
Hashimoto’s:
TPO (thyroid peroxidase)
Graves:
TSH-receptor stimulating
De Quervain’s thyroiditis - state the following:
- Pathophysiology
- Presentation
- Management
Pathophysiology:
Inflammation of the thyroid characterised by a triphasic course of:
1. Transient thyrotoxicosis
2. Hypothyroidism
3. Return to euthyroidism
Presentation:
- Neck swelling/lump that moves on swallowing, but not on tongue protrusion
- Moderate-to-severe pain
- Neck tenderness
- Fever
Management:
- Symptom control (NSAIDs or B-blockers for thyrotoxic phase)
List some symptoms and signs of hypothermia
Symptoms:
- Shivering
- Dizziness
- Slurred speech
- Hunger
- Paradoxical removing of clothes
Signs:
- Low temperature
- Confusion / drowsiness
- Cool peripheries
- Tachycardia / tachypnoea (resp. depression if severe)
- Hypotension
- Ataxia
State the main ECG change seen in hypothermia
J (Osborn) waves
(also seen in hypercalcaemia and intracranial bleeds)
State how you would manage hypothermia
A-E approach
Rewarming - passive e.g. removing wet clothing, covering up with blankets or active e.g. Bair hugger or warmed IV fluids and warmed humidified O2
Require cardiac monitoring
Once stable, investigate and treat the underlying cause if there is one e.g. infection, sepsis
List some potential complications fo hypothermia
- Frostbite
- Arrythmias
- Hypotension
- Respiratory depression / aspiration pneumonia
- Pulmonary oedema
- Pancreatitis
- Acute tubular necrosis
- Cardiac arrest / death
Outline the symptoms and signs of a patient with hyperthermia
- High temperature
- Hot, dry skin and facial flushing
- Dizziness
- N&V
- Headache
- Signs of dehydration
- Confusion
Later stages - multiorgan dysfunction:
- Cardiovascular dysfunction e.g. arrythmias
- Respiratory dysfunction e.g. ARDS
- CNS dysfunction e.g. seizures, coma
- Liver failure and coagulopathy
- Renal failure
- Rhabdomyolysis
Outline management of patients with hyperthermia
A-E approach
Cooling techniques:
- Removal of extra layers
- Fanning
- Cool drinks
- Ice packs in armpits, groin and neck (where there are large blood vessels)
- Consider cool IV fluids
- Consider intravascular cooling catheters
- Consider extracorporal circuits
Regular monitoring of haemodynamics
*Limited evidence that Paracetamol or Dantrolene are effective in heat stroke, may use Diazepam for seizures
State some investigations to consider in someone with obesity
Calculate BMI and take waist circumference (central obesity)
Cardiovascular risk profile:
- BP and HR
- Lipid profile
- LFTs (NAFLD)
- TFTs (hypothyroidism)
- Fasting plasma glucose / HbA1c
Outline the management tiers for obesity treatment
Conservative - lifestyle changes:
- Dietary changes
- Increased exercise and reduce mobility
- CBT and motivational counselling
Medications - only if diet/lifestyle changes unsuccessful:
- GLP-1 medications receptor agonists e.g. liraglutide
- Lipase inhibitor e.g. Orlistat
Surgical - recommended if BMI>35 or significant complications:
- Gastric bypass / sleeve gastrectomy
- Adjustable gastric banding
- Biliopancreatic diversion
