Diabetes and Endocrinology Flashcards

Question

How does chronic hyperglycaemia in DM cause retinopathy? What are the 3 main stages?

Answer 1

Retina supplied by small blood vessels which can be damaged by hypergylcaemia over time 3 main stages: 1. Bulges in blood vessels - may bleed slightly but don’t usually affect your vision (background retinopathy) 2. More significant changes - significant bleeding into the eye (pre-proliferative retinopathy) 3. Scar tissue and angiogensis (bleed easily), develop on the retina (proliferative retinopathy) - can result in some loss of vision

Answer 2

Measure urine albumin - persistent albuminuria (severely increased) - Co-existing retinopathy - No evidence of alternative kidney disease

Answer 3

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

Answer 4

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

Answer 5

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)

Answer 6

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

Answer 7

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)

Answer 8

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

Answer 9

- 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)

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

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)

Answer 14

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)

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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)

Answer 20

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

Answer 21

1. Primary hyperparathyroidism Cause: parathyroid gland tumour PTH level: high Calcium level: high 2. Secondary hyperparathyroidism Cause: vitamin D deficiency or chronic renal failure PTH level: high Calcium level: low/normal 3. Tertiary hyperparathyroidism Cause: chronic secondary hyperparathyroidism (failure to resolve to normal after treatment) PTH level: high Calcium level: high

Answer 22

1. Rapid acting e.g. NovoRapid 2. Short acting e.g. Actrapid 3. Intermediate acting e.g. Insuman Basal 4. Long acting e.g. Lantus

Answer 23

- Addison's disease and other conditions affecting cortisol levels - Anorexia - Chronic liver disease - Reactive hypoglycaemia - Insulinoma (increased insulin production)

Answer 24

- DKA - Hypoglycaemia (especially if driving) - Hypokalaemia and arrhythmias - Anaphylaxis (reaction to insulin)

Answer 25

- Long QT syndrome - Seizures - Laryngospasm - Coma - Heart failure

Answer 26

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

Answer 27

Bisphosphonates Denosumab Both work by inhibiting osteoclasts

Answer 28

1. Papillary thyroid cancer (70%) 2. Follicular thyroid cancer 3. Medullary thyroid cancer 4. Anaplastic thyroid cancer

Answer 29

- Infection - Medicine non-compliance - Drugs e.g. steroids or diuretics - Trauma - Stroke / MI

Answer 30

- 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)

Answer 31

Gram-positive organisms: - Staphylococcus aureus - Enterococcus Gram-negative organisms: - Pseudomonas aeruginosa - E coli

Answer 32

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

Answer 33

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

Answer 34

- 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

Answer 35

Women > 65 Men > 75 Plus men and women > 50 if they have any of the risk factors above

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

Hashimoto's: TPO (thyroid peroxidase) Graves: TSH-receptor stimulating

Answer 40

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)

Answer 41

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

Answer 42

J (Osborn) waves (also seen in hypercalcaemia and intracranial bleeds)

Answer 43

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

Answer 44

- Frostbite - Arrythmias - Hypotension - Respiratory depression / aspiration pneumonia - Pulmonary oedema - Pancreatitis - Acute tubular necrosis - Cardiac arrest / death

Answer 45

- 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

Answer 46

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

Answer 47

Calculate BMI and take waist circumference (central obesity) Cardiovascular risk profile: - BP and HR - Lipid profile - LFTs (NAFLD) - TFTs (hypothyroidism) - Fasting plasma glucose / HbA1c

Answer 48

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