OSCE Clinical Conditions Flashcards
AKI Pathophysiology
It is an abrupt loss of kidney function, that develops within 7 days.
Pre renal – due to decreased renal perfusion. This could be due to decreased ECF volume, so hypovolaemia (blood loss or fluid loss), systemic vasodilation (sepsis, cirrhosis or anaphylaxis) or cardiac failure. It may be due to impaired renal autoregulation, which usually maintains normal perfusion. Pre glomerular vasoconstriction can be due to: sepsis, hypercalcaemia, hepatorenal syndrome or drugs (eg NSAIDs).
Post glomerular vasodilation can be due to: ACE inhibitors or angiotensin II antagonists. Post renal – due to obstruction of urine flow once it has left the tubules, so may be in ureters, bladder or urethra. This obstruction can be caused by: calculi (kidney stones), blood clot, papillary necrosis or a tumour. There may be pressure from the outside causing obstruction – prostatic hypertrophy, malignancy, aortic aneurysm, diverticulitis or accidental ligation of the ureter in surgery.
Intrinsic – this is direct injury to the kidney. Acute tubular necrosis can occur if pre renal AKI is not treated quickly – it will cause severe acute ischaemia. In toxic acute tubular necrosis, the damage is caused by nephrotoxins. They damage the epithelial cells which line the tubules, causing cell death and shedding into the lumen. Nephrotoxins can be endogenous (myoglobin, urate and bilirubin) or exogenous (drugs – gentamicin, ACE inhibitors, NSAIDs and angiotensin receptor blockers). Acute glomerulonephritis occurs due to immune disease attacking the kidney. This may be primary (only affecting the kidney) or secondary (kidneys involved as part of something affecting the whole body). Acute tubulo-interstitial nephritis is inflammation of the kidney interstitium. This can be caused by infection (acute pyelonephritis – ascending UTI) or nephrotoxins.
AKI Symptoms and signs
The clinical picture is usually due to the underlying cause.
Disturbances in kidney function can lead to electrolyte imbalances which can cause a variety of symptoms: fatigue, loss of appetite, headache, nausea and vomiting.
Increase in potassium levels in the blood can lead to abnormal heart rhythms.
Kidneys may be unable to produces sufficient amounts of urine, leading to oliguria or anuria. If the AKI is caused by inflammation there may be flank pain
AKI Investigations and outcomes
Serum biochemistry – increased urea and creatinine in all forms of AKI
Urine dipstick – blood and protein present on glomerulonephritis
Urine microscopy - hyaline cast if pre renal cause, muddy brown cast in ATN, red blood cell cast in glomerulonephritis
Soluble immunological tests – circulating antibodies present if immune disorder
Imaging – ultrasound to check renal size and presence of obstruction
Biopsy – this is carried out if pre renal and post renal are ruled out, and a diagnosis of ATN cannot be confidently made
AKI Progression
If the cause of pre renal AKI is not recognised and treated quickly, this can develop to ischaemic acute tubular necrosis (ATN).
Reduced kidney function means electrolyte imbalances could occur, leading to dangerous complications – hyperkalaemia and metabolic acidosis.
The risk of developing chronic kidney failure is increased.
AKI Treatment
The treatment of AKI depends on its cause.
Pre renal – volume correction. If it caused by hypovolaemia, there will be fluid replacement and if it caused by heart failure (fluid overload) a diuretic will be used (furesomide).
Post renal – urological intervention to re establish urine flow
Intrinsic – maintaining good kidney perfusion and avoiding nephrotoxins (come of nephrotoxic drugs), supportive treatment Some patients may require dialysis if kidney function deteriorates further.
Alcoholic liver disease Pathophysiology
The first stage of alcoholic liver disease is fatty liver or steatosis. This is due to the metabolism of alcohol, which produces NADH from NAD+. Increased NADH means that there is an increase in fatty acid synthesis, and decreased NAD+ means there is less oxidation of fatty acids. The increased fatty acids are converted to triacylglycerides, which accumulate in the liver, resulting in a fatty liver.
The next stage of alcoholic liver disease is alcoholic hepatitis, which is inflammation of the hepatocytes. At these two stages, alcoholic liver disease is reversible.
The third stage is cirrhosis. There is necrosis of liver cells, followed by regeneration in nodules surrounded by bands of fibrosis (collagen). There is reduction in liver function at this stage. There is increased resistance to blood flow, which causes portal hypertension.
Alcoholic liver disease Symptoms and signs
Symptoms are not usually seen until the liver becomes badly damaged. Early symptoms are generally vague: abdominal pain, loss of appetite and fatigue.
As the liver becomes more damaged, more obvious symptoms and signs are present. Jaundice is present (mixed unconjugated and conjugated hyperbilirubinaemia). Easy bruising and bleeding due to reduced clotting factors. Oedema and ascites due to reduced oncotic pressure (the liver makes proteins). Palmar erythema (red blotchy palms), clubbing of the nails and Dupuytren’s contracture are all seen in the hands. Hepatosplenomegaly (enlarged liver and spleen) may also be present.
If there is portal hypertension, there may be oesophageal varices, rectal varices (haemorrhoids) and caput medusae. If there are varices present, there will be signs and symptoms of anaemia due to blood loss.
Alcoholic liver disease Investigations
Early alcoholic liver disease is usually discovered by a liver function test in a routine health check, and there will be raised liver enzymes – ALT and AST.
A blood test will pick up low levels of serum albumin, high levels of bilirubin and deranged clotting.
Imaging and a biopsy may be done if the blood tests suggest more advanced alcoholic liver disease (hepatitis and cirrhosis).
Alcoholic liver disease Progression
There are the three stages of alcoholic liver disease fatty liver disease, alcoholic hepatitis and cirrhosis.
If the patient does not stop drinking alcohol at the early stages, they’re more likely to progress to the next. However, not all alcoholics develop cirrhosis. Fatty liver disease and alcoholic hepatitis are both reversible, but cirrhosis is not. However, if the patient stops drinking alcohol at this stage their liver function can be maintained and prevented from getting worse and developing further complications.
The complications of alcoholic liver disease are complete liver failure, hepatocellular carcinoma, Wernicke-Korsakoff syndrome (thiamine deficiency), encephalopathy (due to increased toxins), dementia and epilepsy. There are also the complications due to portal hypertension
Alcoholic liver disease treatment
The most important advice to give the patient is abstinence from alcohol.
If they have been diagnosed at the fatty liver stage, then they can begin drinking alcohol again after a few weeks (if they stick to the NHS guidelines). However, with alcoholic hepatitis and cirrhosis lifelong abstinence is advised.
If the patient is dependent on alcohol, then they may experience withdrawal symptoms, so they may need to gradually reduce alcohol intake. They may need to be inpatients in rehabilitation clinics, depending on level of dependence. It is important to advice the patient of any help in the community that may be available to them, like support groups or online forums. There are medications that help prevent relapse – like disulfarim.
Malnutrition is also common in people who have alcoholic liver disease, so they may need dietary advice.
Liver damage may mean it is unable to store glycogen, which mean there may need to be changes to the diet.
Corticosteroids can be given for alcoholic hepatitis, and liver transplant may be considered if liver failure occurs once the patient has stopped drinking alcohol.
Anaemia Pathophysiology
Anaemia is reduced haemoglobin concentration in the blood. This can be due to a variety of reasons:
Problems making haemoglobin – gene mutations (thalassaemias and sickle cell disease), lack of iron (blood loss, dietary, chronic disease) and deficiency in building blocks for DNA synthesis (vitamin D or folate/B12 – diet, pernicious anaemia), problems with red cell membrane (hereditary spherocytosis and elliptocytosis), There may be reduced production of red cells due to bone marrow failure – but this would also reduced white cell and platelet count.
May be due to destruction of red cells, which can be immune (transfusion, haemolytic disease of the newborn, autoimmune) or mechanical (heart valves, MAHA).problems with red cell metabolism – G6PD deficiency and Pyruvate kinase deficiency and increased red cell removal – enlarged spleen.
Kidney failure can also cause anaemia because they will be unable to produce erythropoietin to stimulate erythropoiesis.
Less haemoglobin means that our bodies are unable to carry as much oxygen. The body’s physiological response to this is increase cardiac output, increased heart rate, increased 2-3 BPG and increased erythropoietin in the kidneys.
Anaemia Symptoms and signs
Symptoms – dyspnoea, weakness, lethargy (TATT), palpitations and headaches
Signs – Pallor (check conjunctiva and palmar creases), tachycardia, koilonychia (iron deficiency), glossitis and angular stomatitis (iron deficiency), jaundice (haemolytic
Anaemia investigations and outcomes
Haemoglobin conc - <13.5g/dl adult men <11.5g/dl adult women
Reticulocyte count – reticulocytosis (making new red blood cells) should be increased due to low haemoglobin, if it is not increased this suggest that red blood cells are not being produced appropriately
Mean cell volume – microcytic/macrocytic/normocytic
Mean cell haemoglobin – hypochronic/hyperchronic/normochronic
Ferritin levels – only useful if LOW (confirms iron deficiency), because it is an acute phase protein so can be normal/raised for many reasons
Serum iron – low in iron deficiency
Folate levels – low in folate deficiency
Serum vitamin B12 – low in B12 deficiency
Direct Coombes Test – positive if autoimmune Bone marrow exa
Anaemia Progression
The progression and complication depend on the underlying cause of the anaemia.
However, all types of anaemia have increased risk of tachycardia and heart failure as the heart increases its workload to try to get enough oxygen around the body.
Anaemia treatment
Treatment of anaemia depends on the type and underlying cause.
For example, patients with anaemia caused by deficiencies may be given dietary advice so they will no longer have these deficiencies. They may also be given supplements (iron tablets).
If the anaemia is caused by a GI bleed, the cause of the GI bleed must be established and this will be treated.
For example, if NSAIDs are causing the bleed, the patient will be taken off NSAIDs and put on an alternative medication.
If the anaemia is being caused by blood loss due to menorrhagia the patient may be put on the COCP to try and stop the periods being so heavy.
In an emergency, patients with anameia may be given a blood transfusion (does not happen commonly).
Asthma Pathophysiology
Asthma is a chronic disorder characterised by airway wall inflammation and remodelling. There is the early and late phase responses.
The early phase response is the initial response to an allergen, due to its interaction with mast cell fixed IgE. This causes release of histamine and other spasmogens, causing immediate bronchospasm.
The late phase response causes: epithelial damage, thickening of the basement membrane and mucus production due to leucocytes. Remodelling of the airways is due to loss of cilia, hyperplasia of smooth muscle and collagen deposition in the basement membrane.
Asthma is a reversible airflow obstruction. Triggers cause the airway smooth muscle to contract, narrowing airway radius, increasing resistance and therefore reducing airflow.
Asthma Symptoms and signs
Symptoms – dry cough – worse at night (lack of sleep), exercise induced (less participation in activities), wheeze – polyphonic, high pitched, expiratory, breathlessness, chest tightness and variable airflow obstruction
Signs – hyperexpansion of the chest (barrel chest), hyper resonant on percussion and a polyphonic wheeze on expiration It is associated with other conditions like eczema and hay fever.
Asthma Investigations and outcomes
Spirometry – low PEFR, low FEV1/FVC ratio, >12% increase in FEV1 after salbutamol (reversible airflow obstruction)
Allergy testing – testing for triggers of asthma (dogs/cats)
Chest xray – this is done to exclude any other conditions
The diagnosis of asthma is a clinical one, there is no definition of symptoms or findings on investigation.
Asthma Progression
If asthma is left untreated, the chronic inflammation can lead to irreversible obstruction due to airway remodelling. Patients asthma will become more severe if they are not complying with their treatment.
Severe, acute episodes of asthma require hospitalisation and can be life threatening. Severe acute asthma is defined as any one of: unable to complete sentences, pulse >110 bpm, respiration rate > 25 per minute or peak expiratory flow 33-50% of predicted. This becomes life threatening if there are any of the following features: PEF <33%, PaO2 < 8kPa, PaCO2 > 4.5kPa, silent chest, feeble respiratory effort, hypotension, bradycardia, arrhythmia, exhaustion, confusion or coma.
Asthma Treatment
The first step in management of asthma is patient education, so they know how to recognise their symptoms, use their medication appropriately and use services available.
In terms of primary prevention, the patient is advised to stop smoking, get fresh air, reduce exposure to triggers and lose weight.
In terms of pharmacological management there are five steps. The first step is an inhaled short acting B2 agonist (eg salbutamol). The next step is the addition of a regular preventative therapy – a corticosteroid (eg beclametasone). The third step is the addition of a long acting B2 agonist (eg salmeterol). Step 4 is the addition of a trial therapy, such as: muscarinic antagonist (eg ipatropium bromide), leukotriene receptor antagonist (eg montelukast) or a methylxanthine (eg theophylline). The final step is frequent use of oral steroids (eg prednisolone). If the patient’s asthma is under control, there will be a stepwise reduction of treatment.
Atrial fibrillation Pathophysiology
This is the most common arrhythmia. The normal, regular impulses from the SAN are overwhelmed by disorganised electrical impulses. This causes irregular conduction of ventricular impulses.
Atrial fibrillation can be caused by hypertension, heart valve disease, thyrotoxicosis and excess alcohol consumption. However, in many patients no underlying cause can be found.
Atrial fibrillation Investigations and outcomes
Irregular pulse on examination
ECG – there will be no visible P waves and an irregularly irregular QRS comple
Atrial fibrillation Progression
Having atrial fibrillation increases the risk of stroke. Lack of organised contraction can lead to stagnant blood, therefore increasing the risk of thrombus formation. The thrombus can be carried in the blood stream – becoming an embolus. It can reach the cerebral vessels, causing an ischaemic stroke or a TIA.
The risk of a patient with atrial fibrillation having a stroke depends on other risk factors, such as hypertension, diabetes and a history of blood clots.
In extreme cases of atrial fibrillation, heart failure can occur as the heart is unable to pump blood around the body.
Atrial fibrillation Treatment:
If there is an underlying cause (such as hyperthyroidism) then the underlying cause is treated.
Anti coagulation is given to reduce the risk of stroke – warfarin is often used.
Rate control is considered first, usually with a beta blocker or a calcium channel blocker (verapamil). If rate control is not sufficient, then drugs are given for rhythm control (amiodarone or a beta blocker).
Atrial fibrillation Symptoms and signs:
Symptoms – palpitations, tiredness, breathlessness, dizziness and feeling faint
Signs – irregular pulse Many patients will not have any symptoms.
Cerebrovascular disease Pathophysiology
This includes any vascular disease of the cerebral circulation: TIA, stroke and vascular dementia.
Ischaemic strokes (cerebral infarct) are caused by a blockage of a blood vessel of the brain by either a thrombus or an embolism (cardiac embolism due to atrial fibrillation), which causes part of the brain to have insufficient blood supply. These account for 85% of strokes. Heamorrhagic strokes (intracerebral haemorrhage) are caused by rupture of cerebral blood vessels and are caused by: hypertension, aneurysm, anticoagulation, thrombocytopenia, thrombolysis, drugs (cocaine/ amphetamines) and tumours. These account for 15% of strokes.
TIA is a transient ischaemic attack. It is a sudden onset, focal disturbance of brain function. To be defined as a TIA rather than a stroke, it will completely resolve within 24 hours.
Vascular dementia is generalised intellectual loss seen due to multiple infarcts. Mood changes are prominent in this type of dementia.
Cerebrovascular disease Symptoms and signs:
The presentation of a patient who has had a stroke depends on the location of the cerebrovascular accident.
Frontal lobe symptoms – motor, speech output, incontinence, personality changes
Parietal lobe symptoms – sensory, inferior homonymous quadrantanopia
Temporal lobe symptoms – taste and smell, hearing and balance, speech input, memory, superior homonymous quadrantanopia
Occipital lobe symptoms – homonymous hemianopia
There is a sudden onset of symptoms. If it is a haemorrhagic stroke the patient may also have had a headache
Cerebrovascular disease Investigations and outcomes
Check blood glucose as a differential is hypoglycaemia
ECG – check if the patient has atrial fibrillation
Brain imaging – CT scan will immediately show if haemorrhage, MRI will show infarct
Cerebrovascular disease Progression
Once a patient has had a TIA they are at a much higher risk of having a stroke in the future.
The injury to the brain following a stroke can lead to widespread and long lasting problems. Patients will recover from their stroke at different rates. They will go through stroke rehabilitation to help them with their specific needs. They may need help relearning how to carry out day to day tasks. Having a stroke has psychological and physical effects – some patients may become reliant on carers following their stroke.
In terms of vascular dementia, as there is currently no cure and no way to reverse the damage the condition gets worse over time. Some of the more advanced symptoms are: hallucinations, incontinence, personality changes and difficulty walking
Cerebrovascular disease Treatment:
The treatment depends on the type of stroke.
If it has been confirmed that it is an ischaemic stroke then thrombolysis is used to break down the clot (alteplase). This is most effective if it is used as soon as possible after the stroke has occurred. Ischaemic stroke is also an indication for fibrinolytic drugs (streptokinase/recombinant tPAs). Patients are also likely to be given an anti platelet (aspirin) and an anti coagulant (warfarin/heparin). They may be given drugs to lower their risk factors for further ischaemic strokes – anti hypertensives and statins.
For a haemorrhagic stroke, anti hypertensives are often given to reduce the blood pressure of the patient. If they were previously on any anti coagulants they will be given therapy to reverse the effects – vitamin K in the case of warfarin and protamine sulphate in the case of heparin.
After a TIA, although the the symptoms will have completely disappeared, the patient will be counselled on lifestyle changes to reduced their risk of stroke in the future (diet, exercise, smoking and alcohol). They may also be given medication to reduce their risk factors, like anti platelets, anti coagulants and anti hypertensives.
In terms of vascular dementia there is no cure, and the treatment is mainly treating the underlying conditions, so making lifestyle changes and taking the medications mentioned above.
COPD Pathophysiology
COPD is a chronic, slowly progressive disorder characterised by airflow obstruction which does not change markedly over several months.
It is caused by an abnormal inflammatory response of the lung to noxious stimuli like cigarette smoke or pollution. Another, much less common cause of COPD is alpha 1 anti trypsin deficiency, which causes emphysema as well as liver damage.
Chronic bronchitis and emphysema are two forms of COPD. It is a type of type 2 respiratory failure, with increased respiratory rate, increased CO2 and decreased O2.
COPD Symptoms and signs
Symptoms – productive cough (white/clear sputum), wheeze, breathlessness, many years of a smokers cough
Signs – quiet wheezes, accessory muscles of respiration used, pursed lip breathing, hyperventilation in prolonged expiration and hyperinflation of the lungs (barrel chest)
COPD Investigations and outcomes
Chest X-ray – excludes other conditions
MRC dyspnoea scale (history)
Spirometry – low PEFR, low FEV1/FVC ratio
CT (high resolution) – can detect emphysema ABG – high CO2, low O2
COPD Progression:
MRC dyspnoea scale – this has 5 stages.
Stage 1 is not being troubled by breathlessness unless doing strenuous exercise.
Stage 2 is short of breath when hurrying or going up hill.
Stage 3 is walking slower than others when on flat ground and having to stop for breath when walking at own pace.
Stage 4 is stopping for breath after about 100m or walking for a few minutes on the flat.
Stage 5 is being too breathless to leave the house and becoming breathless when getting dressed or undressed.
Acute exacerbations occur, usually due to infection. They are a sudden worsening of symptoms – increased shortness of breath, increased coughing, more sputum production and a change of sputum colour to green or yellow.
COPD Treatment:
The most important part of management of COPD is counselling the patient to stop smoking. Even in advanced disease, stopping smoking can slow the progression.
Drug therapy is used in long term management and short term management of acute exacerbation. Inhaled bronchodilators (beta 2 agonists) and corticosteroids are used. Antibiotics are given as soon as sputum turns yellow, to shorten the length of the exacerbation.
Oxygen therapy is used to increase oxygen saturation – it is a treatment for hypoxia not breathlessness. It is important to realise that giving high flow oxygen to COPD patients can lead to respiratory depression as it removes their respiratory drive.
Pulmonary rehabilitation is a training programme which will improve exercise capacity.
Lung volume reduction surgery is sometimes carried out, in which the damaged parts of the lung are taken out, leaving the relatively well functioning parts of the lung to expand and work more efficiently. This improves the quality of life for some COPD patients. It is also important to treat any comorbidities.
Diabetes Pathophysiology
There are two types of diabetes.
Type 1 diabetes – this is due to the autoimmune destruction of the beta cells of the islets of Langerhans in the pancreas. This means they are unable to produce insulin. Insufficient insulin means that glucose cannot be taken into the cells and used for energy, leading to hyperglycaemia.
Type 2 diabetes – this is due to insulin resistance, and slow progressive loss of beta cells. This resistance to insulin means that cells are unable to take up circulating glucose, leading to hyperglycaemia.
Diabetes Symptoms and signs
The classic picture of type 1 diabetes is a young person with a history of a recent viral infection who is feeling very tired. They appear with a classic triad of symptoms: polyuria – the kidney cannot re absorb all of the extra glucose, so it remains in the tubule, osmotically pulling water into the tubule too and excreted as large amounts of urine, polydipsia – thirst due to excessive water loss, and weight loss as protein and fat are metabolised due to the absence of glucose. Patients with unmanaged type 1 diabetes may present with ketoacidosis – hyperventilation, nausea, vomiting, dehydration and abdominal pain.
Patients will type 2 diabetes may present with the classics triad of symptoms (polyuria, polydipsia and weight loss). However, they are more likely to present with a variety of symptoms: lack of energy, persistent infections (thrush or feet infections), slow healing or visual problems.
Diabetes Investigations and outcomes
Random venous plasma glucose >11.1 mmol/l
Fasting plasma glucose >7 mmol/l
Plasma glucose >11.1 mmol/l 2 hours after 75g anhydrous glucose in an oral glucose tolerance test
HbA1c > 6%
Diabetes Progression
Long term diabetics have a number of micro vascular and macro vascular complications, particularly if their blood glucose is not well controlled.
Macro vascular complications are: increased risk of stroke, increased risk of myocardial infarction and poor circulation to the peripheries (particularly the feet).
Micro vascular complications are: diabetic eye disease, diabetic kidney disease, diabetic neuropathy and diabetic feet. Visual problems can arise due to changes in the lens from osmotic effects – glaucoma, but the more important problem is diabetic retinopathy. This is damage to the blood vessels in the retina that can lead to blindness. Nephropathy is due to damage to the glomeruli, poor blood supply (damage to blood vessels) or damage due to infections of the urinary tract which are more common in diabetics. An early sign of nephropathy is the presence of increased protein in the urine.
Neuropathy is due to damage to the peripheral nerves, causing changes or loss in sensation and changes in the function of the autonomic nervous system. Poor blood supply, damage to nerves and increased risk of infection means that the feet of patients with diabetes are particularly vulnerable. Care is needed to keep feet in good condition, because in the past loss of feet was not uncommon.
Diabetes Treatment
Type 1 – this is treated with the use of insulin analogues which are manufactured using recombinant DNA technology. Different formulations of insulin can be prepared, so rate of uptake following injection varies. This allows for the best control. Examples of rapid acting insulins are: Actrapid, Humulin S and Novorapid. Insulin isophane is intermediate acting and insulin glargine is long acting. There a different regimes the patient can be put on: pre mixed insulin twice a day (less injections) or basal bonus – long acting and fast/short acting with meals (more injections but better control). It is important to educate the patient on the use of their insulin, as too much use leads to hypoglycaemia.
Type 2 – the first line of management is non-pharmacological, involving diet, lifestyle and exercise changes. If this is not sufficient to control the blood glucose, or there is evidence of complications beginning in checks (eg signs of retinopathy on fundoscopy) then a biguanide (metformin) is prescribed. If this is not sufficient to control blood glucose levels then a sulphonylurea is added (eg tolbutamide, gliclazide), and if this is not enough then a third hypoglycaemic agent will be added. The final treatment is insulin therapy
