Medicine B Flashcards
How should pyrexia in the returning traveller be investigated?
When assessing a fever in the returning traveller: T – Time of onset R – Room and board A – activities V – Vaccination E – exposure L – location
Pyrexia of Unknown Origin has multiple aetiologies including infective, inflammatory, autoimmune, neoplastic and miscellaneous. All patients with a PUO should have a HIV test and non-infective causes should be considered early on. Do not give empirical antibiotics or steroid trials and consider PET CT scanning.
What are the precipitating factors for DKA?
Precipitating factors include infections/sepsis, cardiovascular disease (Stroke or MI), discontinuation of insulin, inadequate insulin, new diagnosis of diabetes and medication induced such as when SGLT2 inhibitors are used.
What is the pathophysiology of DKA?
The pathophysiology is that the body has secreted no insulin at all so there is a dramatically reduced glucose uptake peripherally. Glucagon is secreted as the cells have no glucose. This causes uninhibited gluconeogenesis and glycogenolysis which increases the hyperglycaemic state. When there is too much glucose in the blood it is excreted by the kidneys which is known as glycosuria. Osmotic diuresis brings water with the glycosuria which causes severe dehydration.
Lipolysis also occurs in response to glucagon release and lack of glucose in target cells. Beta oxidation is the metabolic action which produces acetyl co-A and energy for cells. Acetyl coA goes into ketogenesis and produces ketone bodies which dissociate in the blood and cause metabolic acidosis.
What are the symptoms of DKA?
Polydipsia (extreme thirst), polyuria, weakness, weight loss, abdominal pain, nausea and vomiting, confusion and coma. Signs include acetone breath, kussmaul respiration (laboured deep breathing seen in metabolic acidosis), dry mucous membranes, dehydration, hypotension and tachycardia
How should DKA be investigated and treated?
Investigations include capillary blood glucose meter, ketone meter, urine dipstick and venous gas. Other investigations include FBC, U&E, CRP, ECG, CXR, urinalysis and blood cultures.
On presentation the management includes an ABCDE approach, IV insulin, IV fluids with potassium, anticoagulation, treating underlying causes such as infection, monitor fluid balances, repeat CBG, ketones, U&Es and venous HCO3. Escalate to critical care if severe.
What is a hyperosmolar hyperglycaemic state?
Hyperosmolar Hyperglycaemic State is defined as a serious complication of diabetes mellitus characterised by marked hyperglycaemia without ketonaemia or acidosis and hypervolaemia or hyperosmolarity. This usually occurs in T2DM and has a 15-20% mortality rate but occurs in less than 1% of T2DM patients.
What is the pathophysiology of HHS?
Precipitating factors include infection/sepsis, acute illnesses (MI, stroke, surgery or trauma), dehydration and a new diagnosis of T2DM. The pathophysiology is due to relative insulin deficiency. There is not enough insulin to allow glucose uptake in the peripheries but there is enough to prevent lipolysis and ketogenesis. Counter regulatory hormones are activated which causes gluconeogenesis and glycolysis and hence hyperglycaemia ensues. The patient will also have glycosuria with osmotic diuresis and dehydration with increased thirst. Hyperosmolarity leads to renal failure.
What are the clinical features of HHS?
Clinical features include fatigue, weight loss, polyuria, polydipsia, dehydration, tachycardia, hypotension, shock and an altered mental status such as confusion or coma. It is diagnosed on the bases of hypovolemia, marked hyperglycaemia (above 30mmol/l) without ketonaemia or acidosis and with hyperosmolarity (>320).
How should HHS be investigated and treated?
Investigations include CBG, venous gas, ketone meter, FBC, U&E, CRP, ECG, CXR, urinalysis, blood cultures and input/output chart. Management is with ABCDE assessment, intravenous insulin, potassium in IV fluids, anticoagulation, treating underlying causes, repeating CBG, osmolarity and UE and involving critical care if needed.
Describe the pathophysiology of hypoglycaemia
This is defined as a reduction in plasma glucose levels which is low enough to result in signs and symptoms. Generally, this is levels less than 4mmol/L. It is always important to assess why this has happened.
Hypoglycaemia can be caused by excessive insulin dosing, sulphonylureas, exercize, insufficient food intake, missed meals, impaired awareness, alcohol inhibition of glycogenolysis and reduced renal clearance of insulin which occurs in elderly patients. Non-diabetic causes include post prandial hypoglycaemia, post gastrectomy, critical illness (hepatic, renal or cardiac failure and sepsis), prolonged fasting, malnutrition, hormone deficiencies and islet cell tumours.
What are the symptoms of hypoglycaemia?
Symptoms of hypoglycaemia include autonomic symptoms (<3.2 mmol/L) of sweating, nausea, palpitations, hunger, tremors and anxiety. At less than 2.5 mmol/L there can be cognitive dysfunction, visual changes, incoordination, confusion, aggression, seizures and coma.
What is Whipple’s Triad?
Signs and symptoms consistent with the diagnosis of hypoglycaemia, low plasma glucose and resolution of the symptoms once glucose is administered
How is hypoglycaemia classified?
- Mild: Plasma glucose between 3-3.9 mmol/L
- Moderate: Plasma glucose <3mmol activating a neuroglycopenic response
- Severe: Having low blood glucose affecting the mental or physical state and thus requiring 3rd party assistance
How should hypoglycaemia be managed?
Management is dependent on the GCS score as this determines how much glucose they need. Glucose levels should be rechecked 15-20 mins later.
What is Charcot foot?
Charcot Foot presents as a red, warm, painless swollen foot. It is often mistaken for cellulitis and osteomyelitis. Progressive pathological fractures and joint dislocation causes the Charcot formation and management is with emergency bed rest and total contact casting or removable walker.
The bony changes cause the shape of the foot to change to a “Rocker-Bottom” foot where the arch has collapsed, the foot is broadened, and the plantar aspect has a prominent midfoot. Recurrent ulceration is very common.
What are the causes and symptoms of hypothyroidism?
Causes of hypothyroidism include autoimmune conditions (Hashimoto’s), radioactive iodine, surgery, and drugs such as lithium and sulfonamides.
Symptoms include weight gain, lethargy, depression, hair loss, bradycardia, diastolic hypertension, constipation, menstrual disorders, cognitive impairment, voice changes, dry skin and goitre.
What are the causes and symptoms of hyperthyroidism?
Causes of hyperthyroidism include Graves (autoimmune), thyroiditis and thyroid nodules. The excess thyroid hormone causes increased metabolic rate and hence signs include anxiety, tremor, proximal muscle weakness, goitre, heat intolerance, exopthalmous, weight loss, hair loss, hypertension, widened pulse pressure, palpitations, tachycardia, AF and amenorrhoea or oligomenorrhoea.
How is hypothyroidism treated?
Levothyroxine
How is hyperthyroidism treated?
Hyperthyroidism is treated with anti-thyroid drugs such as Carbimazole and propylthoouracil. Symptomatic relief is provided with beta blockers. Permanent treatment is with radioiodine therapy or surgery.
What is coeliac disease?
Coeliac disease is a small bowel enteropathy in response to an immune mediated attack after gluten exposure. Symptoms include abdominal pain, lethargy, diarrhoea, bloating and weight loss.
What are the risk factors for coeliac disease?
Downs and Turner’s syndrome increases the risk of coeliac and Type 1 diabetes also increases the risk.
What are the extra-intestinal manifestations of coeliac disease?
Extra-intestinal manifestations include dermatitis herpetiformis which occurs in 15% of coeliac patients. This is treated with dapsone and topical steroids. Neuropathy and osteoporosis may also occur.
How is coeliac diagnosed?
Diagnosis is based on serology. Anti-IgA transglutaminase or endomysial antibodies are very accurate for diagnosis. Panel testing is not useful. Patients have to be eating gluten for 6 weeks prior to a TTG test. Biopsy of the duodenum can see scalloping and can be confirmed on histology. Diagnosis requires positive blood test and positive biopsy.
The histology is proven based on the March classification. Type 0 is normal, 1-2 is supportive but not diagnostic and 3 is suggestive of disease. HLA DQ5 and 8 genes are also required for coeliac disease (it is a genetic disease) and can be tested for in patients who refuse OGD.
Investigations include blood tests: Calcium, Vitamin D, TSH, HbA1c, FBC and LFTs. Also perform a DEXA scan if there are concerns about osteoporosis. Patients are also prone to pneumococcal infections and so may need vaccinations.
How is hyponatraemia subdivided?
Mild (130-134mmol/L)
Moderate (125-129mmol/L)
Severe (<125mmol/L).
What are the causes and symptoms of hyponatraemia?
Causes include medication, reduced blood volume, SIADH, renal salt wasting, Liver heart or renal failure, primary polydipsia or pseudohyponatraemia. Symptoms include nausea, vomiting, confusion, reduced GCS, headache and seizures.
How should hyponatraemia be investigated?
Always assess severity of symptoms, fluid status, signs of hypoaldosteronism (check cortisol), thyroid dysfunction and urine output. Always order a urine and serum osmolarity, urine U+Es, cortisol, TFTs and blood glucose. Pseudohyponatraemia can be caused by blood glucose and blood lipids.
