Ebook Davidsons essentials of medicine (2/E): Part 2

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Ebook Davidsons essentials of medicine (2/E): Part 2

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(BQ) Part 2 book Davidson''s essentials of medicine has contents: Gastrointestinal and nutritional disorders, liver and biliary tract disease, blood disease, neurological disease, skin disease, laboratory reference ranges, interpreting key investigations,... and other contents.

Gastrointestinal and nutritional disorders 12   Diseases of the GI tract are a major cause of morbidity and mortality Approximately 10% of all GP consultations in the UK are for indigestion, and in 14 is for diarrhoea Infective diarrhoea and malabsorption are responsible for much ill health and many deaths in the developing world PRESENTING PROBLEMS IN GASTROINTESTINAL DISEASE Dysphagia Dysphagia means difficulty in swallowing, as distinct from globus sensation (a ‘lump’ in the throat without organic cause) and odynophagia (pain during swallowing) Oropharyngeal dysphagia results from neuromuscular dysfunction that affects swallowing, causing choking, nasal regurgitation or tracheal aspiration Drooling, dysarthria, hoarseness and other neurological signs may be present Oesophageal causes include benign or malignant strictures and oesophageal dysmotility Patients complain of food ‘sticking’ after swallowing, although swallowing of liquids is normal until stric­ tures become extreme Endoscopy is preferred to facilitate biopsy and dilatation of stric­ tures Videofluoroscopic barium swallow will detect most motility disorders Oesophageal manometry is occasionally required Dyspepsia Dyspepsia (‘indigestion’) may arise from within or outside the gut (Box 12.1) Heartburn and other ‘reflux’ symptoms are separate and are considered elsewhere Although symptoms correlate poorly with diagnosis, careful history may reveal classical symptoms of peptic ulcer, ‘alarm’ features requiring urgent investigation (Box 12.2) or symptoms of other disorders Dyspepsia affects up to 80% of the population at some time, often with no abnormality on inves­ tigation, especially in younger patients Examination may reveal anaemia, weight loss, lymphadenopathy, abdominal masses or liver disease Patients with ‘alarm’ symptoms, G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 CLINICAL EXAMINATION OF THE GASTROINTESTINAL TRACT Head and neck Pallor Jaundice Angular stomatitis Glossitis Parotid enlargement Mouth ulcers Dentition Lymphadenopathy Abdominal examination Observe Distension Respiratory movements Scars Colour Virchow’s gland Palpate Tender/guarding Masses Viscera Liver (Ch 13) Kidneys (Ch 7) Spleen Percuss Ascites Viscera Auscultate Bowel sounds Bruits Atrophic glossitis Angular stomatitis Hands Clubbing Koilonychia Signs of liver disease (Ch 13) Groin Hernias Lymph nodes Perineum/rectal Fistulae Skin tags Haemorrhoids Masses Clubbing Skin and nutritional status Muscle bulk Signs of weight loss Observation Pyoderma gangrenosum 414 • Distressed/in pain? • Fever? • Dehydrated? • Habitus • Skin Haemorrhoids   12.1  Causes of dyspepsia • • • • • • • • Peptic ulcer disease Acute gastritis Gallstones Motility disorders, e.g oesophageal spasm Colonic carcinoma ‘Functional’ (non-ulcer dyspepsia and irritable bowel syndrome) Pancreatic disease (cancer, chronic pancreatitis) Hepatic disease (hepatitis, metastases) Systemic disease • Renal failure • Hypercalcaemia Drugs • • • • NSAIDs Iron and potassium supplements Corticosteroids Digoxin Others • Psychological, e.g anxiety, depression • Alcohol   • • • • • • 12.2  ‘Alarm’ features in dyspepsia Weight loss Anaemia Vomiting Haematemesis and/or melaena Dysphagia Palpable abdominal mass G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 GI disorders and those > 55 with new dyspepsia require prompt endoscopy Younger patients should be tested for Helicobacter pylori; if symptoms persist after treatment, these patients should have endoscopy Vomiting Vomiting is a complex reflex involving contraction of the diaphragm and intercostal and abdominal muscles, and simultaneous relaxa­ tion of the lower oesophageal sphincter, causing forcible ejection of gastric contents The history should reveal associated abdominal pain, fever, diar­ rhoea, relationship to food, drugs, headache, vertigo and weight 415 G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12   416 • • • • • • • 12.3  Common causes of acute upper GI haemorrhage Oesophagitis (10%) Mallory–Weiss tear (5%) Varices (2–9%) Peptic ulcer (H pylori or NSAID) (35–50%) Gastric erosions (NSAID or alcohol) (10–20%) Vascular malformation (5%) Carcinoma of stomach or oesophagus (2%) loss Pregnancy, alcoholism or bulimia should be considered Examination may reveal: ● Dehydration ● Fever ● Abdominal masses ● Peritonitis or intes­ tinal obstruction ● Papilloedema ● Nystagmus ● Photophobia ● Neck stiffness The diagnostic approach will be dictated by the history and examination GI bleeding Acute upper GI haemorrhage This is the most common GI emergency, accounting for 50–170 hos­ pital admissions per 100 000 each year in the UK Haematemesis may be red with clots when bleeding is profuse, or black (‘coffee grounds’) when less severe Syncope may occur with rapid bleeding Anaemia suggests chronic bleeding Melaena is the passage of black, tarry stools containing altered blood This is usually due to upper GI bleeding, although the ascending colon is occasionally responsible Severe acute upper GI bleeding occasion­ ally causes maroon or bright red stool Causes of acute upper GI haemorrhage are shown in Box 12.3 Management IV access: Access should be secured with a large-bore cannula Clinical assessment: Risk of complications is related to circulatory status (tachycardia, hypotension and oliguria indicating severe bleeding), liver disease (jaundice, cutaneous stigmata, hepato­ splenomegaly and ascites) and comorbidity (cardiorespiratory, cer­ ebrovascular or renal disease, which increase the hazards of endoscopy and surgery) Blood tests: These should include FBC (slow bleeding causes anaemia; haemoglobin may be normal after sudden, major bleed­ ing); cross-matching of at least 2 U of blood; U&Es (shock may cause renal failure; the urea also rises as the luminal blood is digested); LFTs and prothrombin time, if there is clinical suggestion of liver disease or in anticoagulated patients Resuscitation: Oxygen is given to patients in shock IV crystalloid infusion restores BP, and blood transfusion is indicated if there is shock and active bleeding Antibiotics are given in chronic liver Lower GI bleeding This may be due to haemorrhage from the small bowel, colon or anal canal Severe acute lower GI bleeding Diverticular disease: This is the most common cause Patients present with profuse, red or maroon diarrhoea and shock Bleeding almost always stops spontaneously, but if not, the diseased segment is located by angiography or colonoscopy and resected Angiodysplasia: Vascular malformations in the proximal colon of elderly patients cause bleeding, which usually stops spontaneously but commonly recurs Treatment is by colonoscopic thermal abla­ tion, or resection if bleeding continues Ischaemia due to inferior mesenteric artery occlusion: Presents with abdominal colic and rectal bleeding It occurs in elderly patients with atherosclerosis and is diagnosed by colonoscopy Resection is required only if peritonitis develops Meckel’s diverticulum: May erode into a major artery and cause profuse lower GI bleeding in children or adolescents The diagnosis is commonly made only by resection at laparotomy G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 disease CVP monitoring helps to reveal rebleeding and guide fluid replacement, particularly in patients with cardiac disease Endoscopy: After resuscitation, this will reveal a diagnosis in 80% of cases Patients with spurting haemorrhage or a visible vessel can be treated by thermal probe, adrenaline (epinephrine) injection or metal clips This may stop bleeding and, combined with IV proton pump inhibitor (PPI) therapy, prevent rebleeding, thus avoiding surgery Monitoring: Hourly pulse, BP and urine output should be monitored Surgery: This is indicated when endoscopic haemostasis fails to stop the bleeding, or rebleeding occurs once in an elderly or frail patient/twice in younger, fitter patients Following successful surgery for ulcer bleeding, all patients should be treated with H pylori eradication therapy if positive, and should avoid NSAIDs Subacute or chronic lower GI bleeding This is extremely common and is usually due to haemorrhoids or anal fissure Proctoscopy reveals the diagnosis but if there is altered bowel habit and in all patients presenting at age 40 and over, colon­ oscopy is necessary to exclude colorectal cancer Obscure major GI bleeding If upper endoscopy and colonoscopy are inconclusive, mesenteric angiography usually identifies the site and embolisation can be used to stop the bleeding If angiography is negative, double balloon enteroscopy or wireless capsule endoscopy can be employed to identify a bleeding source in the small intestine When all else fails, laparotomy with on-table endoscopy is indicated 417 G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 Occult GI bleeding Occult bleeding (no visible blood) may reach 200 mL/day, cause iron deficiency anaemia and signify serious disease The most important cause is colorectal cancer, which may have no GI symp­ toms GI investigations should be considered in any patient with unexplained iron deficiency anaemia A negative faecal occult blood (FOB) test does not exclude important GI disease FOB is now only used in population screening for bowel cancer Diarrhoea Diarrhoea is defined as the passage of > 200 g of stool daily, com­ monly with increased frequency and loose or watery stools In severe cases, urgency of defecation and faecal incontinence occur Acute diarrhoea Infective diarrhoea is usually due to faecal–oral transmission of bacteria, viruses or parasites, and is normally short-lived Diar­ rhoea lasting > 10 days is rarely caused by infection Drugs, includ­ ing antibiotics, cytotoxics, PPIs and NSAIDs, may cause acute diarrhoea Chronic or relapsing diarrhoea The most common cause is irritable bowel syndrome, in which diar­ rhoea is most severe before and after breakfast and rarely occurs at night At other times the patient is constipated The stool often contains mucus but never blood, and 24-hr stool volume is  3 kg over 6 mths is significant Previous weight records may be valuable Pathological weight loss can be 418 Clinical features of steatorrhoea • Blood tests (urea and electrolytes, immunoglobulins, Ca2+, Mg2+, full blood count, clotting, albumin, folate, B12, coeliac antibodies) Investigate small intestine • Duodenal biopsy • Barium studies or small bowel MRI • Faecal calprotectin Normal Investigate pancreas • Pancreatic function tests – faecal elastase • Ultrasound scan/CT • MRCP Normal Consider bile salt malabsorption • SeHCAT scan • Serum 7α-hydroxycholestenone Fig 12.1  Investigation for suspected malabsorption due to psychiatric illness, systemic disease, GI causes or advanced disease of any specific organ system G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 ? Malabsorption History and examination ‘Physiological’ weight loss: This should be obvious from the history but may be more difficult to determine in older patients when nutritional history may be unreliable; a dietitian’s opinion is often valuable Psychiatric illness: Features of anorexia nervosa, bulimia and affective disorders may only be apparent after formal psychiatric input Alcoholic patients lose weight through self-neglect and poor diet Systemic diseases: Chronic infections lead to weight loss, and a history of foreign travel, fever, night sweats, rigors, productive cough and dysuria must be sought Sensitive questions regarding lifestyle (promiscuous sexual activity and drug misuse) may suggest HIV infection Weight loss is a late feature of disseminated 419 G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 malignancy (carcinoma, lymphoma or other haematological disor­ ders), which may be revealed on examination GI disease: Dysphagia and gastric outflow obstruction cause defective intake Malignancy may cause weight loss by mechanical obstruction, anorexia or systemic effects Malabsorption from pan­ creas or small bowel causes profound weight loss and nutritional deficiencies Crohn’s disease and ulcerative colitis cause anorexia, fear of eating, and loss of protein, blood and nutrients from the gut Specific diseases of any major organ system: Endocrine disease, including diabetes mellitus, Addison’s disease and thyrotoxicosis, may cause weight loss In patients with disabling end-stage respira­ tory, cardiac or rheumatological diseases, weight loss occurs from a combination of anorexia, physical disability and the systemic effects of their conditions, often compounded by drug effects (e.g digoxin), which may cause nausea, dyspepsia, constipation or depression Investigations ● Urinalysis for glucose, protein and blood ● Blood tests: LFTs, random blood glucose and TFTs; ESR (often raised in infections, connective tissue disorders and malignancy) ● Bone marrow aspira­ tion or liver biopsy: to identify cryptic miliary TB when there is strong clinical suspicion ● Abdominal and pelvic CT: occasionally help, but only after careful history and reweighing Constipation Constipation is the infrequent passage of hard stools, often with straining, a sensation of incomplete evacuation, and perianal or abdominal discomfort It may be the end result of many disorders In the absence of a history suggesting a specific cause (Box 12.4), it is not necessary to investigate every person with constipation Most respond to dietary fibre supplementation and the judicious use of laxatives Middle-aged or elderly patients with a short history or worrying symptoms (rectal bleeding, pain or weight loss) must be   12.4  Causes of constipation GI • Lack of dietary fibre • Altered motility, e.g irritable bowel syndrome • Structural, e.g colonic carcinoma, diverticular disease, Hirschsprung’s disease • Obstructed defecation, e.g anal fissure, Crohn’s disease Non-GI • • • • 420 Drugs, e.g opiates, anticholinergics Neurological, e.g multiple sclerosis, paraplegia Metabolic/endocrine, e.g hypercalcaemia, hypothyroidism Others: any serious illness, especially in the elderly Abdominal pain Abdominal pain may be: ● Visceral: usually midline, due to stretching or torsion of a viscus ● Parietal: usually sharp, lateralised and localised, due to peritoneal irritation ● Referred: e.g gallbladder pain referred to the back or shoulder tip ● Psychogenic: cultural, emotional and psychosocial factors influence the experience of pain In some patients, no organic cause is found despite investigation The acute abdomen This accounts for ~50% of all urgent surgical admissions and is a consequence of one or more pathological processes: Inflammation (e.g appendicitis, pancreatitis, diverticulitis): Diffuse pain develops gradually, over hours If the parietal perito­ neum is involved, pain becomes localised Movement exacerbates it; rigidity and guarding occur Perforation (e.g peptic ulcer, ovarian cyst, diverticular disease): Pain starts abruptly, is severe and leads to generalised peritonitis Obstruction (intestinal, biliary or ureteric): Pain is colicky, with spasms causing the patient to writhe around If it does not disappear between spasms, this suggests complicating inflammation If there are signs of peritonitis (i.e guarding and rebound tender­ ness with rigidity), resuscitation with IV fluids, oxygen and antibio­ tics is needed Further investigations should include: ● FBC: may demonstrate leucocytosis ● U&Es: reveal dehydration ● Serum amylase: raised in acute pancreatitis ● Erect CXR: shows air under the diaphragm in perforation; an AXR reveals obstruction ● USS: may help if gallstones, ureteric colic or a soft tissue mass is suspected, and may also reveal free fluid or intra-abdominal abscess ● Contrast studies, by either mouth or anus: useful to evalu­ ate obstruction, and essential to distinguish pseudo-obstruction from mechanical large bowel obstruction ● CT: useful for pancrea­ titis, retroperitoneal collections or masses, and aortic aneurysm ● Angiography or multi-slice CT angiography: used in mesenteric ischaemia ● Diagnostic laparoscopy: may be useful if the cause remains obscure G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 investigated promptly, by either barium enema or colonoscopy Others should be investigated as follows: ● Initially, digital rectal examination, proctoscopy and sigmoidos­ copy, routine biochemistry, including serum calcium and thyroid function, and an FBC ● If normal: a 1-mth trial of dietary fibre and/or laxatives ● If symptoms persist: examination of the colon by barium enema or colonoscopy to look for structural disease Management Perforations are closed, inflammatory conditions are treated with antibiotics or resection, and obstructions are relieved Most but not all patients require surgery The need for, and urgency of, surgical 421 G A S T R O I N T E S T I N A L A N D N U T R I T I O N A L D I S O R D E R S •  12 intervention depend on clinical severity and stability, and the pres­ ence or absence of peritonitis Acute appendicitis: The risk of perforation or recurrence is high with conservative treatment, so surgery is usually advisable Small bowel obstruction: Strangulated hernias require urgent surgery If the cause is adhesions from previous surgery, only patients who not settle within 48 hrs with IV fluids, fasting and nasogastric aspiration, or who develop signs of strangulation (colicky pain becoming constant, peritonitis, tachycardia, fever, leu­ cocytosis) require surgery Large bowel obstruction: Pseudo-obstruction is treated nonoperatively Some patients benefit from colonoscopic decompres­ sion, but mechanical obstruction merits surgery Differentiation between the two is by a water-soluble contrast enema Acute cholecystitis: See page 515 Acute diverticulitis: See page 470 Perforated peptic ulcer: See page 436 Chronic or recurrent abdominal pain A detailed history, including fever, weight loss and mood, is essen­ tial If abdominal and rectal examination is normal, a careful search should be made for disease affecting the vertebral column, spinal cord, lungs and cardiovascular system The choice of investigations depends on the history and examina­ tion (Box 12.5) Persistent symptoms require exclusion of colonic or small bowel disease A history of psychiatric disturbance, repeated negative investigations or vague symptoms not fitting any particular disease or organ pattern may point to a psychological origin Constant abdominal pain Patients with constant abdominal pain usually have features to suggest the underlying diagnosis, e.g malignancy, chronic   422 12.5  Investigation of chronic or recurrent abdominal pain Symptom Probable diagnosis Investigation Epigastric pain; dyspepsia; relationship to food Altered bowel habit; rectal bleeding; features of obstruction Pain provoked by food in widespread atherosclerosis Upper abdominal pain radiating to the back; history of alcohol misuse; weight loss; diarrhoea Recurrent loin or flank pain with urinary symptoms Gastroduodenal or biliary disease Colonic disease Endoscopy and USS Mesenteric ischaemia Chronic pancreatitis or pancreatic cancer Renal or ureteric stones Barium enema and sigmoidoscopy/ colonoscopy Mesenteric angiography USS, CT and pancreatic function tests USS and IV urography ... infrequent passage of hard stools, often with straining, a sensation of incomplete evacuation, and perianal or abdominal discomfort It may be the end result of many disorders In the absence of a history... estimated average global daily supply of food energy per person increased from ~23 50 kcal in the 1960s to ~28 00 kcal in the 1990s Portion sizes, particularly of sugary drinks and high-fat snacks,... adolescence, and 90% of cases are female 428 Diagnostic criteria are: Loss of at least 15% of total body weight ● Avoidance of highcalorie foods ● Distortion of body image ● Amenorrhoea for at least

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