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70 Cards in this Set
- Front
- Back
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Functions of the liver |
Carbohydrate and fat metabolism, protein synthesis, protein catabolism, bile synthesis, storage and dotoxification of drugs and hormones. |
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Responses of the liver to injury |
Fatty change, hepatocyte necrosis, cholestasis, inflammation, fibrosis, regeneration, cirrhosis and neoplasia. |
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Jaundice |
Yellowing of the skin and eyes due to high levels of bilirubin in the blood. Cholestasis is where bile plugs in canaliculi causing alkaline phosphatase to be elevated. There are pre-hepatic, hepatic and post-hepatic causes. |
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Pre-hepatic causes of jaundice |
Unconjugated bilirubin usually due to increased red blood cell destruction. Red blood cell membrane problem which can be genetic e.g.spherocytosis or acquired e.g. autoimmune haemolytic anaemia or blood group incompatability. RBC cytoplams problem can be genetic e.g.sickle cell or thalassemia or acquired e.g. malaria. |
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Hepatic causes of jaundice |
Conjugated plus unconjugated bilirubin due to abnormality in the liver. Congenital such as immaturity of liver enzymes due to prematurity or enzyme defects in processing of bilirubin. Acquired such as viral hepatitis or alcohol. |
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Post-hepatic causes |
Conjugated bilirubin due to obstruction to bile flow. Congenital e.g. biliary atresia. Acquired e.g. bile duct problem which may be in the lumen such as gall stone, tumour or worn, in the wall e.g tumour or outside the wall e.g. calcified head of the pancreas. |
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Acute liver failure |
Damage to the majority of hepatocytes which occurs due to acute liver damage and decompensation in chronic liver disease. Acute decline in stable chronic liver disease occurs due to an exacerbating factor. |
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Causes of acute liver damage |
Toxins, viruses or ischaemia which cause massive liver cell necrosis. Specific causes include alcoholic liver disease, parcetamol overdose, viral hepatitis, acute fatty liver of pregnancy and idiosyncratic reactions to medications |
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Consequences of acute liver failure |
There is release of transaminases which show up on a lab test, failure of bilirubin metabolism resulting in build up and failure to detoxify nitrogenous compounds which causes encephalopathy. There is also failure to synthesise factors 2,7,9 and 10 which causes bleeding and hepatorenal syndrome resulting in renal failure. |
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Treatment of acute renal failure |
There is no good way to take over the liver functions and there is high mortality with only 40% survival. Transplantation is now frequently used, treatment is only supportive and to manage the complications. If a patient does survive, the liver may regenerate and return to normal or develop post-necrotic cirrhosis. |
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Chronic hepatitis |
Inflammation of the liver persisting for more than 6 months. It may progress to cirrhosis which is nodules of regeneration separated by fibrosis. It is classified according to the causation e.g. hepatitis B,C and D, autoimmune, drugs and metabolic disease. It is generally stable and asymptomatic. |
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Liver hepatitis |
Liver cell necrosis and inflammation occurs of the portal tracts and periportal hepatocytes. There is bridging between portal tracts. Fibrosis results in portal expansion, periportal and bridges between portal tracts. Severity of necrosis and inflammation give the grade and extent of fibrosis gives the stage. |
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Alcohol (cause of liver disease) |
There is a dose response relationship but this varies between individuals. Acute alcoholic hepatitis has a high mortality rte and alcohol can result in cirrhosis and hepatocellular carcinoma. It results in fatty liver (steatosis) or fatty liver with inflammation (steatohepatitis). |
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Non-alcoholic fatty liver disease |
Very common. Related to obesity and metabolic syndrome and is pathologically similar to alcoholic liver disease. It progresses slowly and there is simple steatosis with no cell damage and NASH which includes ballooning, fibrosis and inflammation. The fibrosis pattern is pericellular. |
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Consequences of cirrhosis |
Reduced hepatocyte function. Portal hypertension: back pressure in the portal venous system and causes splenomegaly, ascites and porto-systemic anastamoses. Varices occur which are large veins shunting blood past the liver to systemic circulation. Causes variceal haemorrhage, spontaneoud bacterial peritonitis, hepatic encephalopathy, chronic liver failure and hepatocellular carcinoma. |
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Primary biliary cirrhosis |
Usually diagnosed by serology (AMA). It involves portal inflammation, damage to bile ducts and granulomas. |
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Primary sclerosing cholangitis |
Best diagnosed by imaging (MRI or ERCP) and it's pathology is patchy but there is portal inflammation with periductal sclerosis. |
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Respiratory failure |
Syndrome where oxygenation or carbon dioxide elimination or both fail. It is defined as a PaO2 less than 8MPk or PaCO2 more than 6.7KPa. Investigations done should include physical examination, chest imaging, arterial blood gas analysis, bradycardia and hypotension. |
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The lungs |
They supply the body with oxygen and remove CO2. It has three mechanisms: ventilation to delier air to the alveoli, diffusion of gas across the capillary and alveolar walls and circulation so oxygen is carried to it's site of use. |
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Signs of respiratory depression |
Respiratory compensation including tachypnoea, use of accessory muscles, nasal flaring and intercostal, suprasternal or supraclavicular recession. Increased sympathetic tone including tachycardia, hypertension and sweating. End-organ hypoxia causes altered mental state (confusion and disorientation), bradycardia and hypertension. Haemoglobin desaturation. |
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V/Q mismatch (ventilation/perfusion mismatch) |
If ventilated alveoli are not perfused or perfused alveoli are not ventilated then there is V/Q mismatch. It is the most common cause of hypoxaemia. Hypoxaemia increases respiratory rate by chemoreceptor stimulation the nthe PaCO2 level is generally not affected. |
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V/Q units |
They vary from low to high ratios in the presence of disease process. The low V/Q units contribute to hypoxaemia and hypercapnia in contrast to high V/Q units which waste ventilation but do not affect gas exchange unless it is quite severe. Administration of 100% oxygen eliminates all low V/Q units correcting hypoxaemia. |
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Diffusion problems |
Occurs if there is physical separation of gas and blood e.g. in diffuse interstitial lung disease due to scarring of the alveolar walls. Also occurs if there is shortened transit time of red blood cells through the capillaries as in pulmonary emphysema with loss of the capillary bed. |
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Shunting |
The persistence of hypoxaemia despite 100% oxygen inhalation. Deoxygenated blood bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through alveoli, consequently leading to a reduction in arterial blood content. Occurs in pneumonia, lung collapse and severe pulmonary oedema. Hypercapnia generally doesn't occur. |
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Type 1 (hypoxaemia) respiratory failure |
PaO2 less than 8kPa with normal or low PaCO2. Can be associated with virtually all acute disease of the lung which generally involve fluid filling or collapse of alveolar units. Causes include chronic bronchitis and emphysema (COPD), pneumonia, pulmonary fibrosis/oedema/embolism, asthma, pneumothorax, pneumoconiosis, bronchiectasis and adult respiratory distress syndrome. |
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Emphysema |
Permanent dilatation of the air spaces distal to the terminal bronchiole with destruction of their walls, in the absence of scarring. There is a protease - antiprotease hypothesis for causation. |
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Chronic bronchitis |
Excessive bronchial mucus with a productive cough for 3 months or more over two consecutive years without any other disease that could account for these symptoms. May be caused by hyperplasia of mucous glands in the bronchial wall or smooth wall hyperplasia and it predisposes to bacterial infections, acute bronchitis and pneumonia. |
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Chronic obstructive pulmonary disease |
Reduced maximal expiratory flow and slow forced emptying of the lungs. There features don't change markedly over several months and the limitation in air flow is only minimally reversible with bronchodilators. May be caused by emphysema or chronic bronchitis. |
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Pneumoconiosis |
Caused by inhalation of non-organic mineral dusts which lead to inflammatory reaction and lung scarring. Examples include coal workers pneumoconiosis, asbestosis and silicosis. |
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Extrinsic allergic alveolitis |
The inhalation of organic dusts with local allergic reaction in the lungs. Inflammation leads to fibrosis in the lungs e.g. farmers lung or bird fancier's lung. |
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Type 2 (hypercapnic) respiratory failure |
PaCO2 more than 6.7KPa. Hypoxemia is common in those who are breathing room air. The blood pH depends on bicarbonate and duration of hypercapnia. Caused by COPD, pulmonary oedema, asthma, drug overdose, poisoning, neuropathies, primary muscle disorders, head and cervical cord injury, primary alveolar hypoventilation and obesity hypoventilation syndrome. |
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Comparisons of acute and chronic respiratory failure |
Takes minutes to hours with no compensatory changes in acid base balance. Chronic takes place in days to weeks and if it is hypercapnic there is compensation with high bicarbonate and if it hypoxic there is compensation with increased haemoglobin and pulmonary hypertension. |
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Pulmonary hypertension |
Frequently present in chronic respiratory failure. Alveolar hypoxemia potentiated by hypercapnia causes pulmonary alveolar constriction. If chronic this is accompanied by hypertrophy and hyperplasia of the pulmonary arterial smooth muscles and narrowing of the arterial bed. Increased vascular resistance increases afterload on right ventricle which may induce RVF. This causes enlargement of the liver and peripheral oedema. |
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Obstructive airways disease |
FEV1/FVC ratio is less than 0.75 and it normally exceeds this. It could be acute such as astham or chronic such as obstructive airways disease, chronic bronchitis and emphysema. |
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Restrictive lung disease |
FEV/FVC ratio is normal but may be reduced forced vital capacity. It is caused by fibrosis in the lungs, inflammation and fibrosis, autoimmune disease, pneumoconiosis amd extrinsic allergic alveolitis. |
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Kidneys |
The kidney excretes nitrogenous waste, secretes renin and erythropoietin and is important in slat, ion and water homeostasis. The functioning unit is the nephron, the golumerulus excretes, the tubules selectively excrete and reabsorb and the collecting system maintains water homeostasis. |
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Bownan's capsule function |
Collection of glomerular filtrate. |
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Proximal convoluted and straight tubule |
Reabsorption of water, proteins, amino acids, glucose and carbohydrates. |
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Loop of henle |
Creation of hypertonicity gradient between collecting ducts and interstitium. |
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Distal straight and convoluted tubule |
Acid-base and water balance, absorption of water, sodium and bicarbonate and excretion of potassium and hydrogen ions. |
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Collecting tubule and collecting ducts |
Controlled reabsorption of water under the influence of ADH. |
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Acute kidney injury |
The abrupt deterioration of renal function. Occurs in 7% of hospital in patients and 25% of those in critical care. Mortality is greater than 50% in the context of multi-organ failure. Cause rapidly rising blood urea and creatine, electrolyte inbalance and oliguria leading to anuria (failure to produce urine in 24 hours). |
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Diagnosis of acute kidney injury |
If serum creatine rises by 26mmol/litre fromthe baseline value within 48 hours. If serum creatine rises 1.5 fold within a week. If urine output is less than 0.5ml/kg/hour for more than 6 hours. |
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Pre-renal causes of AKI |
Occurs in response to reduced renal perfusion which causes the kidneys to attempt to retain sodium and water so the renal excretory capacity is impaired. Occurs due to shock, bleeding, burns or sepsis or cardiac failure. Treated by increasing perfusion pressure by blood transfusion or intravenous infusion of fluids. |
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Acute tubular necrosis |
Occurs when central perfusion failure means less oxygenated blood is getting through so tubular epithelial cells die. Tubular epithelial function ceases; there is no ion, salt and water pumping so the kidneys swell. It can be reversed if the necrotic tubules are eliminated. Tubules become repopulated with epithelial cells from stem cells and normal function resumes. |
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Glomerular disease (glomerulonephritis) |
An intrinsic cause of AKI. It is inflammation of the glomerulus and nephrons. It can be due to immunecomplex-mediated disease where an allergic reaction causes attacking of tissue by auto-antibodies. Some cases are post-infective or linked to vasculitis. |
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Vasculitis |
Immune-mediated inflammation and destruction of small vessels which may lead to malignant (sustained) hypertension and disseminated intravascular coagulation (DIC). If blood pressure rises rapidly there is hypertrophy of the vessel walls which stops blood getting through as the lumen is diminished. |
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Tubulo interstitial disease |
Can be immune-mediated or caused by nephrotoxins (including drugs). If the tubule is lost the whole nephron is lost. Autoimmune disease varies in whether it affects mainly the glomerulus or tubule. |
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Post-renal causes of AKI |
Caused by obstruction of the lower urinary tract which may be caused by the prostate, ureters, a stone in the lumen, tumour or inflammation of the wall or obstruction may be due to an extrinsic mass like a tumour. |
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Chronic kidney disease |
Can progress to end-stage kidney disease which requires dialysis and/or renal transplantation. It is slow progressing and there is irreversible loss of renal function due to loss of large amounts of nephrons. Gradual deterioration over years due to large reserve capacity of nephrons. |
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Symptoms of chronic kidney disease |
Polyuria, malaise, lethargy, increased uraemia, confusion, electrolyte imbalance, sodium and water retention, hypertension and eventual coma. |
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Initiating factors of chronic kidney disease |
Age, family history, primary renal disease, nephrotoxins, diabetes mellitus, urinary infection, obstruction and cardiovascular disease. |
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Perpetuating factors of chronic kidney disease |
Hypertension, obesity, proteinuria, anaemia, nephrotoxins, cardiovascular disease and smoking. |
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Causes of chronic kidney disease |
Diabetic kidney disease, congenital kidney diseases e.g. polycystic, immunological damage to all glomeruli, chronic kidney reflux and infection such as hep B/C, malaria, TB and HIV. |
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Glomerular disease |
There are many types and some operate by causing thickening of the glomerular basement membrane and mesangium such as diabetic glomerular disease. Membranous glomerulonephritis is an immunologically mediated thickening of the glomerular basement membrane and is less common. |
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Heart failure |
Caused by impairment of the pump function of the heart. Manifested by fluid congestion (backward failure) and inadequate blood flow to tissues (forward failure). Acute failure is rapid and results in forward failure (shock). In chronic failure compensatory mechanisms may be brought into play and back failure dominates (congestions). |
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Compensatory mechanisms in chronic heart failure |
Ventricular chamber enlargement increases the amount of blood the heart ejects but at the cost of fluid retention. Muscle mass increases so heart can eject more but it requires more oxygen for the larger muscle. Sympathetic stimulation also increases heart rate, contractility and increased redistribution and retention of fluid. |
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Fluid congestion in heart failure |
Occurs in response to poor perfusion. Hormonal and neural signals increase water retention by the kidneys. Fluid pressure backed up behind the heart results in excess entering the lungs and other tissue as oedema. Peripheral oedema causes leg swelling and pitting. Pulmonary oedema causes shortness of breath, crepitations and shadowing on CXR. Causes elevated JVP. |
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Structural changes in heart failure |
They aren't positive and mediated by several systems. Hypertrophy occurs in response to increased damands. Adrenergic stimuli, cytokines and angiotensin II mediate effects which are beneficial in increasing cardiac otuput but also cause adverse effects. |
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Adrenergic signals in heart failure |
Benefit by increasing contractility and hypertrophy but cause myocyte apoptosis and toxicity. |
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Angiotensin 2 signals in heart failure |
Benefit by causing hypertrophy but changes expression of contractile proteins. |
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Cytokine signalling in heart failure |
E.g. TNF-alpha. Benefit by causing hypertrophy but causes remodelling of matrix dilation. |
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The new york heart association classification of heart failure |
Class 1: no limitation of physical activity. Class 2: slight limitation of activity (breathlessness/fatigue with moderate exercise) Class 3: marked limitation of activity (breathlessness with minimal activity) Chlass 4: severe limitation of activity (symptoms at rest). |
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The course of left ventricular heart failure |
Raised end diastolic pressure causes raised left atrial pressure which causes raised pulmonary capillary pressure. This leads to increased diffusion barrier for gas exchange and increased interstitial fluid formation (pulmonary oedema) and these both lead to breathlessness. |
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Left ventricular heart failure |
Diagnosis is with a chest X-ray. It is due to insufficient pump power due to a problem with the heart muscle, obstruction of the blood flow outwards due to problem with valves, aorta, arteries or arterioles or obstruction to inflow due to pericardial effusion and constrictive pericarditis. |
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Causes of left ventricular failure |
Acute ventricular dysrhthmias, myocardial infarction and ischaemia heart disease, long standing hypertension, valve disease (aortic and mitral), cardiomyopathies and drugs, congenital heart disease or mitral stenosis (rare). |
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The course of right ventricular failure |
Right ventricular failure causes raised end diastolic pressure then raised right atrial and JVP and then raised central venous pressure. Raised central venous pressure results in liver distension and increased interstitial fluid formation (peripheral oedema). |
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Causes of right ventricular failure |
Failure of the left ventricle is the most common cause. Also caused by massive pulmonary thromboembolism, chronic lung disease, pulmonary hypertension and valve disease (rare). Cor pulmonale may occur doe to emphysema leading loss of lung capillaries and failure of lung ventilation. |
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Congestive heart failure |
A combination of left and right ventricular failure. Usually right follows the left. The commonest cause is ischaemic heart disease. Cardiomyopathies and drugs can also affect both ventricles. |
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High output cardiac failure |
Heart muscle if functional but output can't adequately perfuse tissue. Due to: arterio-venous fistula which cause blood to bypass tissue, septic shock which causes vasodilation, anaemia where oxygen requirements aren't met and thyrotoxicosis where there is increased tissue demand. |
