GIT management and diagnosis Flashcards

Question

Comparison of SBO and paralytic Ileus

Answer 1

Both conditions cannot promote bowel contents (impaired motility) Both show distended loops of small intestine detected by XR or CT OBSTRUCTION physically blocks the contents: the lumen is closed ILEUS: the paralysis of the intestinal wall muscles makes contents stagnant: the lumen in open, this is a FUNCTIONAL obstruction Ileus has no hyper-secretion and therefore no colic usually Bowel sounds are absent/diminished in ileus but are hyperactive in SBO Ileus is temporary motility disorder, reversed by correction of the cause

Answer 2

Dilatation of a loop(s) of small bowel called sentinel loops are seen on AXR Results from abdominal pathology causing focal inflammation of the small bowel ``` Causes: Cholecystitis Pancreatitis Appendicitis Diverticulitis Ureteral stones ```

Answer 3

Most often post operative Involves the entire bowel, large and small Cause of generalised function ileus: operations, infection and inflammation, electrolyte imbalances, drugs Abdominal surgery Infection: sepsis, intra-abdominal abscess, peritonitis, pneumonia, electrolyte abnormalities (hypokalaemia, hypomagnesemia, hypermagnesemia, hyponatremia) Medication: anticholinergics, opiates, phenothiazines, CCB, tricyclic antidepressants Hypothyroidism Retroperitoneal haemorrhage Spinal cord injury Myocardial infarction Mesenteric ischaemia

Answer 4

Inability to tolerate liquids or solids by mouth Nausea Lack of flatus or bowel movements Vomiting and abdominal distension MAY occur

Answer 5

Far less common than small bowel (20% bowel obstructions) Causes: Malignancies Diverticular disease Colonic volvulus

Answer 6

``` Nausea and vomiting Abdominal colics Abdominal distension Lack of wind/gas passage ie constipation or obstipation Loss of lots of fluid: hypovolemic ``` Upper obstruction (small intestine): Vomiting occurs earlier on Distance between colics are SHORTER Abdominal distension and constipation are LATE presenting ``` Lower obstruction (large intestine): Abdominal distension and constipation occur earlier on Distance between colics is longer Vomiting occurs later on *in complete obstruction, symptoms are complete, but in partial obstruction symptoms are more mild usually and they may also develop diarrhoea (hyper-secretion)* ```

Answer 7

``` SBO: Central gas shadows No gas in large bowel Mucosal folds (valvulae conniventes) completely cross lumen May show fecal impact sign ``` LBO: Peripheral gas shadows Dilation >6 cm Gas proximal to blockage but not in rectum (unless PR exam done beforehand) Mucosal folds (haustra) do NOT cross all lumen width

Answer 8

ALL bowel obstructions need fluid resuscitation and correction of electrolyte imbalances Conservative: usually successful secondary to adhesions, Ileus and partial obstructions - Monitor patient regularly, regular examinations and imaging to monitor progress, NBM, if signs of strangulation, ischaemia, peritonitis or toxaemia then ready for emergency surgery Surgical intervention: strangulation, frank perforations, peritonitis, LBO all need immediate surgical intervention

Answer 9

Two large IV lines administer saline or hartmann Bloods: FBC (Hb, WCC), U+Es (Na, K), CRP, amylase, lipase, group and save NBM, NG tube insertion Catheterise Fluid balance chart ABG needed if in shock, suspected ischaemic bowel or pancreatitis

Answer 10

Appendix is attached to cecum found in left inguinal fossa (RIF) Most common acute abdomen complaint Highest incidence between 10-20 years but can occur at any age Very wide range of presentations

Answer 11

Causes: Fecalith (poop rock) Undigested seeds Pinworm infection Pathophysiology: Obstruction blocks the blind ending lumen The appendix continues secreting fluid and becomes oedematous Causing inflammation of the appendix and leading to compression of afferent visceral nerves nearby causing pain Can lead to gangrene if the obstruction of blood vessels supplying the organ persists

Answer 12

Epigastric or periumbilical pain that moves to the right inguinal fossa (RIF) Gradual pain onset, constant and moderate-severe Peritonism: Shows guarding and rebound tenderness or percussion tenderness in RIF Tachycardia Fever Anorexia Nausea may be present but vomiting is rare Constipation in adults, diarrhoea in children Rovsing’s sign (pain greater in RIF than LIF when LIF pressed) Psoas sign (pain on flexion and internal rotation of right hip if appendix close relation to obturator internus)

Answer 13

``` Perforation: if faecolith present and diagnosis delayed can cause generalised peritonitis Gangrenous appendix Appendix abscess (usually treat with drainage or antibiotics) Appendix mass (inflamed and covered with omentum) diagnosed with US/CT, early surgery or conservative NBM and antibiotics treatment used +/- delayed appendectomy ```

Answer 14

Bloods: neutrophil leucocytosis, elevated CRP CT scan has high diagnostic accuracy!! Mcburney's point +ve

Answer 15

Mild: rest GI and antibiotics for inflammation Appendectomy +/- antibiotics Laparoscopic appendicectomy (esp. Good for women and obese with suspected gangrenous perforation)

Answer 16

Outpouching of the lower part of the small intestine It is a remnant of the vitello-intestinal duct (leftover umbilical cord should obliterate during fifth week foetal development) Most common congenital defect of the GIT (2-3% population) Usually asymptomatic The majority of symptomatic pts begin presenting before age 2 Meckel's diverticulitis occurs in 20% patients who become symptomatic, it is clinically indistinguishable from appendicitis

Answer 17

2% people have this 2:1 M:F ratio 2 inches in length usually 2 more common ectopic tissues: pancreas and stomach 2 complications other than diverticulitis: obstruction, bleeding 2 mechanisms of obstruction: secondary intussusception (inverted diverticulum acts as lead point), volvulus (loops around band between diverticulum and umbilicus)

Answer 18

Presentation: GI bleeding Obstructive symptoms Diagnosis: technetium -99m pertechnetate scan (Meckel's scan) Management: Asymptomatic - no treatment needed Symptomatic - monitoring Meckel's diverticulitis - laparoscopic surgery

Answer 19

Inflammation of the peritoneum Generally secondary generalised bacterial infection Common complication of many abdominal pathologies Classification: Chemical, viral, bacterial (primary or secondary) Local peritonitis - localised tenderness Generalised peritonitis - generalised tenderness

Answer 20

Post-surgical eg anastomotic leak, enteric injury (30%) Acute perforated appendicitis (most common esp <45 yrs (20%) Acute diverticulitis (most common in elderly) Peptic ulcer perforation - 10% (or other upper GI perforation) Perforated acute cholecystitis Perforated tumours (colonic or gastric) Perforated ischaemic bowel (eg acute mesenteric ischaemia) Acute pancreatitis Peritoneal dialysis-related

Answer 21

Widespread absorption of toxins from large, inflamed surface (peritoneum) Paralytic ileus with loss of fluid, electrolytes and protein Gross abdominal distension with elevation of diaphragm, increases susceptibility to lung collapse and pneumonia Primary (rare): monomicrobial, typically streptococcal. Probable port of entry via the bloodstream Secondary (common): polymicrobial, gram - and +ve and anaerobes. Portal of entry from intra-abdominal organs (secondary to perforation, ischaemia or infection of other organs etc) Usually shows mixed faecal flora (E.coli, strep facalis, pseudomonas)

Answer 22

Anorexia Fever Severe generalised abdominal pain, radiating to shoulder and back Abdo pain worse with movement, coughing, sneezing Alleviated when lying still Tachycardia Generalised abdominal tenderness, rebound tenderness, guarding and rigidity Max tenderness may indicate underlying cause if in one particular area May be abdominal mass present ``` Advanced stages: Distended abdomen and tympanic on percussion Increasingly toxin and ill Feculent vomit Sunken eyes (severe dehydration) Rapid, febril pulse (shock) Moist, cold, cyanosed skin (shock) drowsy/confused (shock) ```

Answer 23

ABCDE assessment and act accordingly Analgesia Find cause: Bloods show infection markers, Abdo CT scan confirms or excludes acute pancreatitis or locates probably source of pathology Laparoscopy Prep patient for possible surgery: most causes of peritonitis need surgery, however, acute pancreatitis is contraindicated for surgery!

Answer 24

Early: IV antibiotics (wide coverage) eg metronidazole 500mg IV tds + Cefuroxime 750mg IV tds Oxygen therapy, serum therapy (IVI), correction of electrolyte abnormalities Definite specific management should then be based on diagnosis of cause: surgery, medications ect.] *if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy* Bacteroides fragilis - antibiotics in peritonitis needs to cover this bacteria (common gut flora causing abdo infections)

Answer 25

Diverticulitis Cholecystitis Salpingitis Appendicitis

Answer 26

Presentation: Localised tenderness/rebound tenderness Presentation of cause ``` Investigations: Bloods CT US CXR AXR *if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy* ```

Answer 27

(adults) An infection of the GIT, nonspecific term to describe a condition with a combination of nausea, vomiting, diarrhoea and abdominal pain About 20% of the UK develops every year Viral infections cause 30-40% of gastroenteritis in adults (higher in children) Management is not usually dependent on cause as it is never isolated and the responsible agent never diagnosed (children): Infective gastroenteritis in young children by the sudden onset of diarrhoea with/without vomiting Mostly due to viral infection but can be from bacterial or protozoal infections. Usually resolves within days but can cause severe dehydration and become life threatening

Answer 28

children: Retrovirus most common (56%), campylobacter spp., salmonella spp., norovirus, E.coli Cause never isolated and responsible agent never diagnosed adults: A variety of viral (norovirus, rotavirus, adenovirus), bacterial (E. coli, salmonella, staph.aureus toxins) and parasitic pathogens

Answer 29

Poor hygiene, lack of sanitation Compromised immunity Achlorhydria: lack of HCL in digestive juices (especially for salmonella and campylobacter) can result from acid-suppressing drugs Poorly cooked food, cooked food left too long, insufficient reheating etc

Answer 30

History of eating mispreppared food (incubation usually around 24-36 hours for virus’, few hours to 4 days for bacillary dysentery and 7-10 days for parasites) or may have recently been to exotic location Vomiting and nausea Abdominal pain Diarrhoea (bloody diarrhoea may indicate bacterial infection especially E. coli) Pyrexia (in adults can indicate invasive organism)

Answer 31

Dehydration and electrolyte disturbance Haemolytic uraemic syndrome (HUS): AKI, haemolytic anaemia and thrombocytopenia Reactive complications such as urticaria, reactive arthritis, erythema nodosum etc. IBS

Answer 32

Vitals: temp, BP, pulse, HR, respiratory rate Abdominal examination to exclude other diagnoses (appendicitis) Assess for dehydration Stool microscopy, culture and sensitivity if there is blood/mucus in stool or the patient is immunocompromised or the patient has been abroad to anywhere other than western europe, north america, australia or NZ recently, if diarrhoea has not improved by day 7 or uncertain diagnosis. Unwell patients may need FBC, renal function and electrolytes

Answer 33

Prevention: Good hand hygiene Good food hygiene and preparations (cooking) Management: All dysentery and food poisoning are notifiable diseases Hospital admission if unable to retain oral fluids, features of shock or severe dehydration Assess the extent of dehydration and manage accordingly, patient education of infection prevention, advising small light meals, avoiding spice or heavy food while ill. Oral rehydration salt (ORS) can be used in frail elderly patients Advise exclusion from work or other settings until at least 48 hours after being free from diarrhoea and vomiting Can advise antimotility drugs if these will enable quicker resolution to essential activities in those with mild to moderate diarrhoea (loperamide 1st line). AVOID if blood or mucus in stool or high fever present CHILDREN Encourage fluid intake and normal breastfeeding etc. but avoid solid foods if during rehydration therapy Offer oral rehydration salts to those at increased risk of dehydration Racecadotril can be used with oral rehydration in infants over 3 months Monitor vitals very well.

Answer 34

``` Appears unwell or deteriorating Altered responsiveness Sunken eyes Tachycardia Tachypnoea Reduced skin turgor ```

Answer 35

``` Decreased level of consciousness Pale or mottled skin Cold extremities Decreased level of consciousness Tachycardia Tachypnoea Weak peripheral pulses Prolonged capillary refill Hypotension ```

Answer 36

Mild: lassitude (weak, lacks energy), anorexia, nausea, light-headed, postural hypotension Moderate: apathy (lack of interest or concern), tiredness, dizzy, muscle cramps, dry tongue, sunken eyes, reduced skin elasticity, postural hypotension, tachycardia, oliguria Severe: profound apathy, weakness, confusion, shock, tachycardia, marked peripheral vasoconstriction, hypovolemia, oliguria or anuria

Answer 37

70% patients with gallstones are asymptomatic and have no issues Can cause acute or chronic cholecystitis, biliary colic, pancreatitis or obstructive jaundice Biliary colic is most common, caused by gallstone impacting in the cystic duct or the ampulla of Vater, blocking the tubes. Second most common is acute cholecystitis, caused by gallbladder distension and subsequent necrosis and ischemia of mucosal wall

Answer 38

Bile is formed of cholesterol, phospholipids and bile pigments, stored in the gallbladder before passing into the duodenum the cystic duct travels from the GB, joins the common hepatic duct to form the common bile duct, joined by the pancreatic duct close to the duodenum to form the hepatopancreatic ampulla of Vater which deposits bile into the duodenum. Gallstones form as a result of supersaturation of bile

Answer 39

Cholesterol stones: composed purely of cholesterol from excess cholesterol production. Highly linked to poor diet and obesity. Pigment stones: composed purely of bile pigments from excess bile pigments production. Commonly seen in those with haemolytic anaemia Mixed stones: mixture of both

Answer 40

5 Fs: Fat, forty, fertile, female, family history Increasing age Positive family history Female Loss of bile salts (after obesity surgery) Diabetics (metabolic syndrome) Oral contraception, particularly in young women

Answer 41

Case by case basis: very small risk of complications so mostly a ‘watch and wait’ policy Younger patients are more likely to develop complications more frequently due to having gallstones for longer - monitor more frequently Modify risk factors if possible

Answer 42

Occurs when the gallbladder neck becomes impacted by a gallstone. No inflammatory response, but the contraction of the gallbladder against the occluded neck will cause pain Over 50% symptomatic pts with gallstones will present with biliary colic

Answer 43

Sudden, dull pain Colicky Focussed often in the RUQ, although may radiate to epigastrium and/or the back Pain may be precipitated by consumption of fatty foods (stimulates CCK release from duodenum, causing contraction of GB) Nausea/vomiting Often relieved quickly with pain relief

Answer 44

Inflamed gallbladder Most often caused by gallstones More common in women 25% pts with cholelithias will present with acute cholecystitis

Answer 45

Most individuals with gallstones are asymptomatic, the gallstones mostly stay within the gallbladder and cause no harm Cholecystitis is usually caused when a gallstone seemingly becomes stuck in the cystic duct Bile then builds up in the gallbladder, which becomes distended and the walls of the gallbladder consequently become inflamed or may even become infected Infection is more prone to complications Repeated attacks of acute cholecystitis leads to chronic cholecystitis; the walls of the gallbladder become thickened and scarred and the gallbladder becomes shrivelled

Answer 46

5 Fs: fat, fertile, female, forty, family history ``` Gallstones or biliary sludge Hospitalisation for trauma or acute biliary illness Female Increasing age Obesity Rapid weight loss Pregnancy Crohn's disease Hyperlipidaemia ```

Answer 47

Upper abdomen pain, usually worse on the right side under the ribs (RUQ) continuous epigastric pain May radiate to the back or to the right shoulder and tends to last several hours Nausea and vomiting Fever, lethargy +ve Murphy’s sign May have previous history of cholecystitis *Murphy’s sign positive: increased pain when placing hand under the ribs on the right hand sign and asking patient to take deep breath, putting pressure on the gallbladder*

Answer 48

Vitals: BP, temperature, pulses, urine output Abdominal examination including Murphy's sign Ultrasound: thickened GB walls (>3mm), gallstones Bloods: WWC raised, mildly abnormal liver enzymes CT of abdomen if indicated Magnetic resonance cholangiopancreatography (MRCP): shows potential defects in biliary tree with almost 100% sensitivity *trans-abdominal US is most sensitive!! = FIRST LINE*

Answer 49

Acute cholecystitis: Opioid (morphine or pethidine) given parenterally and/or diclofenac by suppository - overcomes absorption difficulties due to vomiting. Pain lasting >24 hours with fever needs hospital admission IV antibiotics (coamoxiclav + metronidazole) Open cholecystectomy surgery to remove stones in emergency - very rarely perform cholecystectomy for acute cases Sepsis 6 if septic

Answer 50

``` Laparoscopic cholecystectomy preferred Percutaneous cholecystostomy (surgical drainage) is useful for those not fit for cholecystectomy *Post op complications are rare but include bile duct injury, fat intolerance and post-cholecystectomy syndrome (abdominal pain, jaundice or dyspeptic symptoms* ``` *Prognosis is good however there is a high chance they may experience more bouts of cholecystitis which is why usual treatment is to remove the gallbladder entirely*

Answer 51

Infection of the biliary tract Associated with high morbidity and mortality if untreated Cause: Biliary outflow obstruction Gallstones ERCP (iatrogenic) Cholangiocarcinoma Most common organisms are E. coli, Klebsiella and enterococcus Pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy and parasitic infections (rare)

Answer 52

Pathophysiology: During obstruction the stasis of fluid combined with elevated intraluminal pressure allows bacterial colonisation of the biliary tree to become pathological Risk factors: Oral contraceptive Fibrates Lipid-rich diet

Answer 53

Charcot's triad: jaundice, fever, RUQ pain ``` RUQ pain Fever Jaundice (when bilirubin >50 umol/L) Pruritus (as result of bile accumulation) Pale stool Dark urine Pyrexic Rigors Confusion Hypotension, tachycardia May have history of cholelithias, recent biliary tract procedure (ERCP/cholecystectomy) or previous history of cholangitis ```

Answer 54

Bloods: FBC (Hb and WCC) shows leukocytosis, LFTs (raised ALP and GGT) Blood cultures Biliary tract USS shows bile duct dilation >6mm and may indicate underlying cause GOLD STANDARD: ERCP is diagnostic and therapeutic

Answer 55

Vitals: check for sepsis, manage as needed Gain IV access for fluid resus Routine bloods and blood cultures taken early Broad spectrum antibiotics therapy (co amoxiclav + metronidazole) Definitive management given via endoscopic biliary decompression (ERCP +/- sphincterotomy and stenting) PTC percutaneous transhepatic cholangiography 2nd line In long term may need cholecystectomy if gallstones are underlying cause

Answer 56

Sudden inflammation of the pancreas Typically caused by hypersecretion of backflow (obstruction) of exocrine digestive enzymes, resulting in autodigestion of the pancreas Can be mild or life threatening With effective treatment has good prognosis

Answer 57

Occurs when digestive enzymes are activated before release into the duodenum and so attack the pancreas If the enzymes enter the bloodstream other organs can become affected which can lead to life threatening shock symptoms Pancreatic damage can be classified into two major categories: interstitial oedematous (most common, better prognosis) and necrotising (5-10% cases, more severe) The damage is potentially reversible whereas chronic pancreatitis results in irreversible damage from ongoing inflammation

Answer 58

I GET SMASHED ``` Iatrogenic Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune disease Scorpion sting Hypercholesterolaemia/hypertriglyceridaemia ERCP Drugs: thiazides, septrin, tetracyclines, azathioprine ```

Answer 59

``` Male Increasing age Obesity Smoking Family history ```

Answer 60

Severe, sudden epigastric pain Sharp, stabbing pain, may radiate to sides or back if cholecystitis present too Vomiting Pain rapidly crescendos, duration likely 1 day May have history of biliary colic, recent surgery or illness Exacerbated by movement, alleviated partially by leaning forward or adopting foetal position Tetany may occur from hypocalcemia (secondary to fat necrosis)

Answer 61

Abdominal examination: epigastric tenderness, abdominal distension Cullen’s sign: periumbilical bruising (LATE sign of retroperitoneal haemorrhage) Grey-Turner’s sign: flank bruising (LATE sign of retroperitoneal haemorrhage) Bloods: FBC, CRP, U+Es, LFTs, Lipase, serum amylase, VBG, ABG, Beta-hCG (rule out pregnancy and permit safe investigation of XR and CT) ECG to ensure no MI Urinalysis CXR to look for free gas under diaphragm (pneumoperitoneum) USS - abdominal ultrasound CT of abdomen and pelvis glasgow-Imrie scale

Answer 62

two of three criteria Abdominal pain + history suggestive of acute pancreatitis Serum amylase/lipase of over 3 times upper limit of normal Imaging characteristic of acute pancreatitis

Answer 63

Mild: most common, no organ dysfunction/complications, resolves within 1 week Moderate: initially some evidence of organ failure which improves within 48 hours Severe: persistent organ dysfunction >48 hours with local or systemic complications

Answer 64

PANCREAS: Perfusion: fluid resus and oxygenation Analgesia Nutrition: enteral feeding <48 hours Clinical: APACHE II or APACHE I scores to assess need to transfer to HDU Radiology: USS for gallstones, choledocholithias and local complications. CECT after 48-72 hours pain onset to determine degree and extent of necrosis. Percutaneous catheter drainage USS guided helpful to manage necrosis ERCP: within 72 hours if cholangitis or severe acute pancreatitis with persistent obstruction Antibiotics: empirical ABs if infection suspected Surgery: multiorgan failure with necrosis not responding to conservative management Predict severity using the glasgow-Imrie scale, predict mortality using APACHE II scoring Once diagnosis is confirmed, largely supportive management: fluid resuscitation, analgesia (IV paracetamol and opioids) Nil-by-mouth until initial pain improves - gradual feeding re-introduced via oral feeding or nasojejunal feeding Antiemetics: IV ondansetron Calcium derangement corrected Control glucose Antibiotics for prophylaxis PRN Infected necrotic tissue needs to be removed via: percutaneous drainage or surgical necrosectomy Gallstone pancreatitis: Obstructed bile duct needs ERCP to relieve obstruction with/without sphincterotomy to dilate the sphincter of Oddi to allow removal of ductal stones, biliary sludge etc. Cholecystectomy for all patients with gallstone pancreatitis during same admission of acute episode Alcoholic pancreatitis: Benzodiazepines for withdrawal agitation and seizures Thiamine, folate and B12 replacement

Answer 65

``` PaO2 <7.9 Age >55 Neutrophils/WCC >15 Calcium <2 Renal function/ urea >16mmol Enzymes (LDH >60) Albumin <32 g/l Sugar >10mmol ``` *if CRP >150mg/l likely to be severe

Answer 66

Chronic inflammation resulting in progressive and irreversible damage to the pancreas parenchyma Male to female ratio 4:1 ``` Cause: Chronic alcohol abuse (60%) Idiopathic (30%) Hyperlipidaemia Infection (viral and bacterial) Hereditary (CF) Autoimmune ```

Answer 67

Chronic pain, complicated by recurring attacks of acute pancreatitis (acute-on-chronic pain) Typically in epigastrium and back Nausea and vomiting Endocrine insufficiency (secondary to islet of langerhans damage) Exocrine insufficiency (secondary to acinar cell damage causing malabsorption - weight loss, diarrhoea, steatorrhoea) Abdo examination: soft abdomen but tender epigastrium, may have signs of cachexia and malabsorption

Answer 68

Urine dip Bloods: FBC, CRP, serum amylase/lipase (often not raised in established disease), BLOOD GLUCOSE, LFTs (obstructive jaundice) Faecal elastase level will be low

Answer 69

Treat underlying cause (alcohol cessation, statin therapy for hyperlipidaemia) Analgesia (opioid or neuropathic analgesics) Enzyme replacement for malabsorption Vitamins A, D, E and K (fat soluble) Regularly check for endocrine insufficiency, (HbA1c annually) treat as needed, also screen bone density regularly

Answer 70

Cholesterol gallstones often appear yellow and are the most common type of gallstone. Scientists believe that cholesterol stones are caused by bile that contains: too much cholesterol too much bilirubin not enough bile salts The cause of pigment stones is not known. They seem to occur in people who have: cirrhosis of the liver biliary tract infections hereditary blood disorders in which the liver makes too much bilirubin

Answer 71

(also called bile duct stones or gallstones in the bile duct) is the presence of a gallstone in the common bile duct.

Answer 72

abdominal pain in the RUQ or epigastric region fever jaundice (yellowing of the skin and eyes) loss of appetite nausea and vomiting clay-colored stools Pain severity can vary throughout, can be sporadic or can linger

Answer 73

Cholangitis Biliary cirrhosis pancreatitis

Answer 74

transabdominal ultrasound (TUS) abdominal CT scan endoscopic ultrasound (EUS) endoscopic retrograde cholangiography (ERCP) magnetic resonance cholangiopancreatography (MRCP) percutaneous transhepatic cholangiogram (PTCA) complete blood count bilirubin pancreatic enzymes liver function tests

Answer 75

stone extraction via biliary endoscopic sphincterotomy (BES) using balloon/basket device fragmenting stones (lithotripsy) surgery to remove the gallbladder and stones (cholecystectomy) surgery that makes a cut into the common bile duct to remove stones or help them pass (sphincterotomy) biliary stenting

Answer 76

Common in infants 3-12 months Boys:girls 3:1 ratio Usually occurs in the ileocecal region (usually ileum telescoping into cecum) Primary: 95% in infants and children, most often due to lymphoid hyperplasia from peyer's patches Secondary: adults mostly, much less common, lead point/apex is a polyp, tumour or inverted Meckel’s diverticulum etc. Low mortality within 24 hours, but very high in irreducible or gangrenous cases Pathophysiology: Telescoping of portion of the intestine Mesentery is dragged alongside proximal bowel wall into the distal lumen, obstructing venous return Causes Oedema, mucosal bleeding and increased pressure If arterial flow is compromised then causes ischaemia, necrosis and perforation can result

Answer 77

classic triad: sudden severe paroxysmal colicky pain, bilious vomiting, red currant jelly stools ``` Colicky abdominal pain and guarding Leg flexing Fever (if septic) Lethargy Vomiting Blood in stool: red currant jelly stool Poor feeding Dance’s sign: empty RIF + sausage shaped mass in mid/RUQ Abdominal distension Signs of shock in late presentation ```

Answer 78

``` USS if stable may show bullseye sign, doughnut sign or crescent in doughnut Diagnostic enema (CI if peritonitis, shock, perforation or pt unstable) shows meniscus sign/coiled spring sign ```

Answer 79

Acute: clinically stable, no CI to contrast enema reduction: NBM, nasogastric tube, Fluid resus and contrast enema reduction Broad spectrum antibiotics IF sign of infection/ischaemia Clinically unstable or CI contrast enema Fluid resus and surgical reduction Broad spectrum antibiotics IF sign of infection/ischaemia

Answer 80

Rare disorder of the oesophagus making it difficult to swallow food or drink Motility disorder of the lower oesophageal or cardiac sphincter This layer of muscle has impaired peristalsis and failure of relaxation causing functional stenosis or stricture Exact cause is unknown but can occur secondary to other conditions such as oesophageal cancer Tends to present in adult life, children is very rare

Answer 81

Muscle tone and activity are controlled by a balance of excitatory transmitters such as ACh and substance P and inhibitory transmitters such as NO and Vasoactive intestinal peptide (VIP) The interstitial cells of Cajal (cells within the intestinal wall which provide the pacemaker function of the musculature) are thought to be involved in the condition Autoimmune reactions to viral infections and genetic factors have also been implicated to trigger the condition

Answer 82

Dysphagia Food bolus impaction Regurgitation (may also induce regurgitation to reduce pain) Retrosternal chest pain in some pts, after eating Heartburn also common and can be aggravated by treatment Weight loss Nocturnal cough (later sign of disease) Inhalation of refluxed contents - inhalation pneumonia incidences! (later sign)

Answer 83

Examinations are unlikely to reveal anything!! Sometimes high incidences of inhalation pneumonia may indicate CXR may show signs of inhalation or may show dilated oesophagus behind the heart (rare to see in practice) Barium swallow (contrast material) to rule out malignancy Endoscopy Manometry GOLD STANDARD: detects up to 9-% cases, high resting pressure in cardiac sphincter, incomplete relaxation on swallowing and absent peristalsis. If this shows normal results but there are symptoms of achalasia then pseudoachalasia might be present Lower oesophageal pH monitoring to exclude GORD

Answer 84

CCB and nitrates may reduce pressure in lower oesophageal sphincter but only effective in 10% pts. Heller myotomy is considered best treatment if pts are fit, performed by laparoscope (success rate 85-95%, low complication rate) For older pts can use pneumatic dilatation: insert balloon and inflate to rupture muscle while leaving mucosa intact (multiple dilations over months or years has better success rates) Endoscopic injection of botulinum toxin Peroral endoscopic myotomy and endoscopic stent

Answer 85

Nocturnal inhalation Aspiration pneumonia GORD (from treatments) Oesophageal cancers

Answer 86

``` Indegestion Complex of upper GI symptoms present for typically more than four weeks Includes abdominal pain or discomfort Heartburn Acid reflux Nausea Vomiting ```

Answer 87

``` Epigastric discomfort Fullness and bloating Excessive flatus Nausea Fatty food intolerance ``` Red flags: Weight loss Recurrent vomiting Dysphagia Evidence of GI bleeding (blood in stool etc) *Urgent 2WW referral for chronic GI bleeding or for >55 years with weight loss*

Answer 88

Abdominal exam: always check for masses Bloods: FBC for iron deficiencies Test for helicobacter pylori Endoscopy (considered in >55 years who are treatment resistant, raised platelet count, nausea or vomiting, previous Barrett's oesophagus)

Answer 89

Uninvestigated without alarm features: Review medications: NSAIDs, steroids, Ca antagonists, nitrates, theophyllines, bisphosphonates Lifestyle advice: smoking cessation, regular meals, cease excessive alcohol consumption, avoid triggering foods, reduce stress, anxiety and depression if needed Antacids for occasional symptom relief Test for H.pylori and treat if positive Empirical acid suppression (with proton pump inhibitors) for 1 month with full dose, continue long term either PPI, H2RA on lowest effective dose (eg ranitidine) Investigate to find underlying cause and treat best as possible Review at end of treatment course to confirm outcome

Answer 90

Lansoprazole 30 mg, omeprazole 20–40 mg, esomeprazole 20 mg, pantoprazole 40 mg, or rabeprazole 20 mg. 7-day triple therapy regimen of: PPI twice-daily and amoxicillin 1 g twice-daily and Either clarithromycin 500 mg twice-daily or metronidazole 400 mg twice-daily. PENICILLIN ALLERGY: 7-day triple therapy regimen of: A PPI twice-daily and clarithromycin 500 mg twice-daily and metronidazole 400 mg twice-daily. If the person is allergic to penicillin and has had previous exposure to clarithromycin, offer a 7–10 day triple therapy regimen of: A PPI twice-daily and metronidazole 400 mg twice-daily and levofloxacin 250 mg twice-daily. If re-testing is indicated, wait at least 4 weeks (ideally 8) after initial eradication therapy

Answer 91

Inflammation of the oesophagus lining, mostly due to reflux of stomach contents leading to chronic irritation ``` Presentation: Heartburn Upper chest and abdomen pain Nausea Bloating Dyspepsia (indigestion) Tend to be related to meal intake Persistent cough particularly at night Mouth and gum problems, bad breath ```

Answer 92

Stage 1: Single of multiple erosions on single fold. May be exudative or erythematous Stage 2: Multiple erosions on multiple folds. May be confluent Stage 3: Multiple circumferential erosions Stage 4: Ulcer, stenosis or oesophageal shortening Stage 5: Barrett’s epithelium. Columnar metaplasia in form of circular or non-circular extensions (Islands or tongues) OR A - one or more mucosal breaks <5mm none extending to tops of mucosal folds B - one or more mucosal breaks >5mm none extending between tops of two mucosal folds C - mucosal breaks extending between tops of two or more mucosal folds, involving <75% mucosal circumference D - mucosal breaks involving >75% mucosal circumference

Answer 93

Acid from stomach leaks up into oesophagus, usually as result of cardia sphincter weakening 2-3 x more common in men 25% adults experience heartburn 5% have daily symptoms Spectrum of disorders ranging from the most common endoscopy negative GORD to oesophageal mucosal damage, which can progress to ulceration, stricture (although only 8% will have mod-severe oesophagitis)

Answer 94

Gastro-oesophageal reflux is a natural protective mechanism of the lower oesophagus If reflux is prolonged or excessive it can cause breakdown of protection with inflammation of the oesophagus (oesophagitis) Abnormalities of the lower oesophageal sphincter may facilitate excessive reflux of the gastric and sometimes bile contents into the oesophagus Reflux of duodenal contents (bile) is more severe

Answer 95

``` Increased intra-abdominal pressure Weak cardiac sphincter Smoking Alcohol Fat Coffee Pregnancy Obesity Tight clothes Large meals Surgery in achalasia of the cardia Systemic sclerosis Hiatus hernia Drugs: tricyclic antidepressants, NSAIDs, anticholinergics, nitrates, CCBs ``` *most of these factors increase intra-abdominal pressure

Answer 96

Heartburn, related to eating, lying down, stooping, straining Relieved by antacids Retrosternal discomfort Acid brash (regurgitation of acid or bile) Water brash (excessive salivation) Odynophagia (pain on swallowing) can indicate stricture or severe oesophagitis Atypical symptoms: found in up to 50% cases Chest pain Epigastric pain Bloating

Answer 97

ENDOSCOPY - gold standard Bloods: FBC to exclude anaemia Barium swallow Oesophageal pH monitoring (24 naso-oesophageal study or wireless pH capsule)

Answer 98

Dysphagia Dyspepsia with weight loss, proven anaemia or vomiting Dyspepsia >55 years with <1 onset or continuous symptoms since onset Dyspepsia with at least 3 risk factors

Answer 99

Lifestyle: reduce weight, smoking cessation, decreased alcohol consumption, raise head of bed at night, small regular meals, avoid hot drinks and eating <3 hours before going to bed, avoid triggering drugs (nitrates, NSAIDs, anticholinergics, antidepressants) PPI full dose for one month (two months if severe oesophagitis), can add H2RA (ranitidine) at bedtime, or switch entirely to H2RA if needed with confirmed oesophagitis H. pylori eradication if indicated Long term acid suppression for recurring symptoms after initial management (healing dose for one-two months then taper to lowest dose providing symptom relief) Referral for endoscopy Surgery: laparoscopic insertion of magnetic bead band Review patients annually if on long term treatments or as needed

Answer 100

Break in inner lining of stomach, duodenum or lower oesophagus Gastric ulcers in stomach, duodenal ulcers, oesophageal ulcers Helicobacter pylori infection associated with 95% duodenal ulcers and 80% gastric ulcers Pathophysiology: Stomach mucosa is prone to ulceration from: breakdown of protective layer of the stomach and duodenum and an increase in stomach acid (stress, excessive caffeine, smoking, spicy foods etc) ``` Cause: H pylori NSAIDs Pepsin Smoking Alcohol Bile acids Steroids Stress Changes in gastric mucin consistency (genetically determined) ```

Answer 101

very nonspecific presentation sometimes Epigastric pain usually 1-3 hours postprandial, may sometimes wake patient in night Relieved by food (DUODENAL ulcer) Worsened by food (GASTRIC ULCER) Nausea and vomiting Oral flatulence Bloating, distension and intolerance of fatty foods Heartburn (sometimes) Posterior ulcer may cause pain radiating to back Symptoms relieved by antacids Epigastric tenderness Succussion splash (if gastric emptying is slow) Melaena Haematemesis Dyspepsia Iron deficiency anaemias

Answer 102

can present with unheralded perforation or bleeding ``` Increasing age Male sex Smoking H pylori infection Absence of atrophic gastritis ```

Answer 103

Bloods: FBC for iron deficiencies H pylori testing Endoscopy

Answer 104

Lifestyle: avoid triggering medications, smoking cessation H pylori +ve = eradication treatment, follow up for proof of eradication PPIs or H2RA for H pylori -ve Exclude rare conditions (if not caused by common eg infection or NSAIDs) such as Zollinger-Ellison syndrome - take samples from ulcer and mucosa Treat bleeding ulcers PRN (correct fluid loss, transfusions, surgical interventions) Annual reviews for regular intermittent treatments

Answer 105

``` Abdominal pain Nausea and vomiting Change in bowel motions, constipation, diarrhea, incontinence Blood in stool Anorectal pain, masses or sensation of incomplete emptying (tenesmus) Weight change Jaundice Dysphagia Dyspepsia ```

Answer 106

``` Common GI disorders: GORD Peptic ulcer disease IBD; Crohn’s, ulcerative colitis Coeliac disease Diverticular disease Anorectal disease; fissures, fistulas, ulcers, haemorrhoids Hernia; inguinal, femoral, umbilical ventral IBS ``` ``` Hepatobiliary disease: Liver cirrhosis Alcoholic liver disease Non-alcoholic fatty liver disease Hepatitis B or C Chronic pancreatitis ``` also ask about procedural history!

Answer 107

Antidopaminergics: - Metoclopramide - Domperidone - Droperidol * Antagonise dopamine D2/3 receptors Serotonin receptor blockers (5-HT): - Ondanstetron * Selectively inhibit serotonin receptors Phenothiazines: - Prochlorperazine * Blocks D2 receptors and alpha adrenoreceptors

Answer 108

H2 receptor antagonists: - Ranitidine * Inhibits histamine H2 receptors, decreasing acid H+ Proton pump inhibitor (PPIs): - Omeprazole - Esomeprazole - Pantoprazole * inhibit H+/K+ ATPase (acid secretion)

Answer 109

Bulking agents: - Psyllium * carbohydrates that retain water Osmotic laxatives: - MgSO4 (epsom salt) - Lactulose - Macrogol 3350 * Osmotically draws water into the GIT Secretory laxatives: - Senna - Sodium picosulphate * Stimulate GI elec. and water secretion Stool softeners: - Docusate sodium * Softens faeces, doesn’t affect motility

Answer 110

Systemic corticosteroids: - Prednisolone - Hydrocortisone * Systemic anti-inflammatory action Aminosalicylates: - Mesalazine - Sulfasalazine * Adenosine release, decreases inflammation Thiopurines: - Azathioprine - Mercaptopurine * Inhibits purine synthesis decreasing DNA synthesis Methotrexate: *Inhibition of IL-1 and other cytokines TNF-Inhibitors: - Infliximab - Adalimumab * Inhibit tumour necrosis factor alpha, decreasing inflammation

Answer 111

``` RUQ pain: Hepatobiliary Hepatic flexure Right renal Right lower lobe pathology Gallbladder pathology ``` ``` RLQ pain: Colonic Appendicitis Gynaecologic Right renal pathology ``` ``` Generalised pain: Bowel obstruction Perforation Bacterial peritonitis IBD ``` ``` Epigastrium: Hepatobiliary Gastric Pancreatic Vascular or cardiac pathology ``` ``` LUQ pain: Gastric Pancreatic Splenic flexure Spleen Left renal Left lower lobe Vascular pathology ``` Umbilical: Gastric Small bowel Vascular pathology LLQ pain: Colonic Gynaecologic Renal pathology Suprapubic: Colonic Gynaecologic Right renal pathology Moving from umbilical to RLQ: Characteristic of appendicitis

Answer 112

Character: Dull, diffuse pain - visceral pain eg from intra-abdominal organs Sharp, localised pain - parietal pain eg from peritoneum Burning pain in epigastrium - suggestive of oesophagitis, gastritis or peptic ulcer disease Radiation: To flank: renal or biliary cause To back: pancreatitis, ruptured AAA, aortic dissection, duodenal ulcer To shoulder: diaphragm irritation eg intra-abdominal gas or blood

Answer 113

Nausea and vomiting Feculent vomiting: bowel obstruction Bloating: gastroparesis Diarrhoea: gastroenteritis Constipation: faecal impaction or bowel obstruction Lack of flatus: bowel obstruction Blood in stool: diverticulitis or ischaemic colitis Frank PR blood: lower GI bleed or massive upper GI bleed Haematemesis or melaena: peptic ulcer Fevers: infection (appendicitis, peritonitis, cholecystitis, diverticulitis, cholangitis etc) RUQ/LUQ pain with cough and fever: pneumonia Heartburn: gastritis, peptic ulcer Dysuria: cystitis, pyelonephritis Haematuria: nephrolithiasis Vaginal discharge: pelvic inflammatory disease Anorexia: appendicitis Weight loss: malignancy

Answer 114

Exacerbating factors: Coughing or movement: peritonitis, perforation, pancreatitis After eating: gastric ulcer, gastritis, cholelithiasis, mesenteric ischaemia Eating fatty foods: cholelithias Alleviating factors: Eating: duodenal ulcer Vomiting: small bowel obstruction Regurgitation: achalasia

Answer 115

Worst in morning: pregnancy, alcohol intake, uraemia, raised intracranial pressure Vomiting 1-2 hours after eating: gastric outlet obstruction Vomiting during meals: anorexia/bulimia Is it affecting daily lifestyle Are they able to keep any solid or fluids down at all Were they in contact with any sick coworkers or family or friends etc.

Answer 116

Lower GI bleed Inflammation: IBD, diverticular disease, infectious colitis, ischaemic colitis Mass: carcinoma, polyp Anorectal disorder: haemorrhoids, fissure, fistula, ulcer, anal SCC Arteriovenous malformation Trauma Massive upper GI bleed: Variceal bleed Peptic ulceration

Answer 117

Blood on toilet paper only: anorectal disorder Blood in stool: colorectal disease Blood in toilet bowl: high volume bleed Heavy bleeding: diverticular bleed or AV malformation Minor bleeding: haemorrhoids, polyp, cancer *RED FLAG* Weight loss: cancer presyncope/syncope: hypovolaemia

Answer 118

Jet black, tarry, sticky, foul-smelling stool Highly suggestive of upper GI bleeding Medications containing iron and bismuth can also cause stools to look similar in appearance CAUSES: Oesophageal: varices, AVM, tumour, oesophagitis, Mallory-Wiess tear Gastric: gastritis, gastric ulcer, gastric carcinoma, hiatus hernia Duodenal: duodenal ulcer, duodenitis

Answer 119

``` peptic ulcer disease, obstruction, IBD, chronic pancreatitis, coeliac disease, gastric bypass surgery ```

Answer 120

When IBD cause the colon to expand, dilate and distend >6cm (toxic colitis with dilated colon = toxic megacolon) The colon is becomes obstipated (no gas or faeces) Is life threatening and may lead to perforations

Answer 121

``` Ulcerative colitis Crohn’s colitis Pseudomembranous colitis Infectious colitis HIV/AIDS immunosuppression Discontinuation of IBD medications Antimotility agents ```

Answer 122

``` Fever/chills Tachycardia Mental status alterations Diarrhoea Abdominal pain and tenderness Hypotension Abdominal distension ```

Answer 123

History of risk factors (IBD, medications) Clinical diagnosis from presentation and history Bloods: FBC, electrolytes, albumin levels, lactic acid, CRP, blood cultures Stool samples CT of abdomen/pelvis Acute AXR series

Answer 124

1st line resus and monitoring Broad spectrum antibiotics Supportive care Nasogastric decompression With suspected severe C difficile colitis: antibiotics With inflammatory colitis: IV corticosteroids No improvement within 72 hours: surgery

Answer 125

Out-pouching of the wall of the gut May be result of smooth muscle over activity Mostly asymptomatic but can cause a wide array of symptoms and complications Diverticulitis is inflammation of a diverticulum and can be caused by infection Classification: Congenital ‘true’ diverticula: all 3 coats of bowel are present in the wall (eg Meckel’s diverticulum) Acquired ‘false’ pulsion diverticula: no muscularis layer, herniation of mucosa and muscularis mucosa through the colonic wall where main blood vessels penetrate the colonic wall (eg sigmoid diverticula, Zenker diverticulum) ``` complications Diverticulitis Segmental colitis Lower GI bleeding Infection Abscess Perforation Peritonitis Fistula formation Obstruction ```

Answer 126

``` Low fibre diet Western diet >50 years BMI >30 NSAID use ```

Answer 127

``` majority asymptomatic found incidentally on colonoscopy History: presence of risk factors LLQ abdominal pain (colicky persisting pain) After eating, relieved by defecation Leukocytosis Fever Guarding in LLQ, tenderness Bloating Constipation, obstipation Diarrhea Anorexia Nausea Flatulence *pain and tenderness on right side as well as if pt is on steroids indicates sigmoid diverticular disease* ```

Answer 128

Asymptomatic: no treatment needed Symptomatic diverticular disease: 1st line: diet modification increase fibre with Oral antibiotics Symptomatic diverticulitis (uncomplicated): 1st line analgesia and oral antibiotics with Low residue diet 2nd line IV antibiotics to cover gram -ve and anaerobes, analgesia and low residue diet ``` Symptomatic diverticulitis (complicated): 1st line with rectal bleeding: endoscopic haemostasis, supportive therapy, low residue diet and analgesia 2nd line surgery plus all above aside from endoscopic haemostasis ``` Unresponsive to IV antibiotics or with >3cm abscess, perforation, fistulae, obstruction: 1st line radiological drainage/surgery, IV antibiotics, analgesia and low residue diet Recurrent diverticulitis: Elective surgery

Answer 129

Group of disorders caused by acute or chronic processes, arising from occlusive or nonocclusive aetiologies resulting in decreased blood flow to the GIT May range from transient to reversible to fulminant (sudden and severe) Classification: Acute mesenteric ischaemia (further split into embolic, thrombotic or venous) Colonic ischaemia (most common with best prognosis) Chronic mesenteric ischaemia

Answer 130

``` Old age Smoking Hypercoagulable states AF MI Structural heart defects Vasculitis history ```

Answer 131

``` Abdominal pain and tenderness (general or specific depending on area of ischaemia) Hematochezia/melaena Diarrhoea Weight loss Abdominal bruit (stenosis of vessel) ```

Answer 132

Bloods: FBC (leukocytosis, anaemia, haemoconcentration), serum lactate, coagulation, ABG Acute abdominal series ECG CT scan Sigmoidoscopy or colonoscopy Mesenteric angiography, duplex US or MRI angiography if indicated

Answer 133

Evidence of infarction, perforation or peritonitis: 1st line fluid resus and supportive measures Empiric antibiotics Exploratory laparotomy or laparoscopy Correct underlying cause (eg embolectomy, heparinization if clot is cause etc) No evidence of infarction, perforation or peritonitis: 1st line supportive measures Empiric antibiotics Correct underlying cause Chronic mesenteric ischaemia: 1st line surgical systemic mesenteric bypass If pt not suitable for surgery: Percutaneous angioplasty and stenting 1st line Non Acute colonic ischaemia: 1st line segmental colectomy OR following chronic stricture as result of healing after an ischaemic event 1st line is endoscopic dilation or segmental resection

Answer 134

uncomplicated diverticulitis: CBC, U+A + culture Abdo and pelvic CT scan Colonoscopy or barium enema (rule out cancer) CT virtual colonoscopy and Ba enema if severely stenotic Complicated diverticulitis: AXR: rule out air perforation or obstruction Colonoscopy rule out cancer CT cystogram rule out colovesicular fistula Barium enema rule out colovaginal fistula Small bowel series to rule out coloenteric fistula

Answer 135

Gram -ve aerobic bacteria Lives in the stomach Causes damage to epithelial lining of stomach resulting in gastritis, ulcers and increased risk of cancer It avoids acidic environment by forcing its way into the gastric mucosa, exposing the underlying epithelial cells to the acid Also produces ammonia to neutralise stomach acid and other chemicals which directly damaged epithelial cells Testing: Must be done >2 weeks without PPI use for accurate result Urea breath test (radio labelled c13) Stool antigen test (now most used) Rapid urease test (performed during endoscopy by taking small biopsy)

Answer 136

Metaplasia from squamous to columnar epithelial cells in the oesophageal lining Typically causes improvements in patients reflux symptoms as the cells are now more protected against the acid Considered a premalignant condition for adenocarcinoma of the oesophagus Treatment is with PPI (omeprazole) Ablation treatment during endoscopy using photodynamic, laser or cryotherapy also used to destroy dysplastic cells allowing healthy squamous ones to regrow

Answer 137

Normal bowel habit is considered to pass stool between 3x per day and 3x per week Constipation is characterised by difficulty emptying bowels with fewer bowel movements than normal for that individual Can also mean: faeces are too hard, it may hurt or they have diarrhoea alternating with constipation Acute <12 weeks, chronic >12 weeks Primary = idiopathic/functional constipation Secondary = organic/due to known cause or condition

Answer 138

``` Diet low in fibre Dehydration Low exercise levels Poor toilet routine Drugs: opioids, antimuscarinics Diabetes IBS Elderly Pregnancy ```

Answer 139

History taking Abdominal exam and PR exam Bloods: FBC, U+E, Ca, TFTs if indicated to look for underlying cause if suspected

Answer 140

Lifestyle: Increase dietary fibre (fruits, veg, whole wheat and bran). Increase exercise regimen Short duration constipation: 1st line: bulk-forming laxative (Ispaghula husk 1 sachet BD) 2nd line: osmotic laxative (Macrogol 1 sachet BD), try lactulose if not tolerated 3rd line: stimulant laxative (Senna, 7.5mg BD) to stimulate peristalsis Opioid induced: Osmotic laxative and stimulant laxative in combination OR docusate (both in one) Titrate dose up until 3x stools per week, then titrate down as needed Chronic As per short term constipation Prucalopride or lubiprostone can be tried if at least two laxatives from different classes are tried at highest tolerance for at least 6 months, only in women. If it is not effective within 4 weeks the benefits v risks should be weighed up Treat as though faecal impaction if this fails

Answer 141

function: Increase faecal mass, stimulating peristalsis Must be taken with plenty of fluid CI: swallowing difficulties, intestinal obstruction, colonic atony, faecal impaction, opioid cause constipation ``` Examples: Bran powder 3.5g 2-3x daily with food Ispaghula husk 1 sachet BD, sit upright for 1 hour after use Methylcellulose Sterculia ```

Answer 142

Side effects can include anal seepage, lipoid pneumonia, malabsorption of fat-soluble vitamins examples: Arachis oil enemas lubricate and soften impacted faeces Liquid paraffin should NOT be used for prolonged period

Answer 143

Increase motility CI for obstruction Avoid prolonged use as may cause colonic atony and hypokalaemia examples: Bisacodyl tablets 5-10mg at night or suppositories 10mg in the morning Senna 2-4 tablets at night (7.5mg BD) Docusate sodium and dantron: associated with colonic and liver tumours. Reserve use for very elderly and terminally ill Glycerol suppositories Sodium picosulfate for rapid bowel evac. For procedures

Answer 144

Retain fluid in bowel examples: Lactulose: discourages growth of ammonia producing organisms. 15ml/12 hour or in hepatic encephalopathy 30-50ml/12 hourly Mg salts rapid bowel evac Macrogels for long term management

Answer 145

Useful additional treatment for constipation examples: Sodium phosphate enemas and glycerin suppositories may be useful Sodium salts should be avoided as they cause sodium and water retention Phosphate enemas rapid bowel evac Excessive use of soapy tap water enemas may lead to water intoxication

Answer 146

The urge to defecate but an impared ability to expel the faecal bolus Symptoms include unsuccessful evacuation, excessive straining, pain, bleeding after defecation and sense of incomplete evacuation Women, especially multiparous women are more likely to present with these symptoms Often associated with structural defects in the retum Managements include diet changes, biofeedback, laxatives, pelvic floor retraining Surgery can also be considered for unresponsive cases

Answer 147

Large hard mass of stool stuck in the colon or rectum, causing obstruction that cannot be pushed out More common in those who already have bowel problems Can be caused by untreated constipation, overuse of laxatives, IBS, colon cancer, ageing, opiates, diverticulitis

Answer 148

``` Liquid diarrhea leaking from rectum Pain or abdominal discomfort Nausea or vomiting Feeling need to push Headache Unintentional weight loss Feeling full/loss of appetite Fever Confusion/irritation Incontinence ```

Answer 149

Clinical history: how often they evacuate bowels and when last time was, how often they’re constipated, how much they have drunk or eaten, if they use laxatives, which medications they take Abdominal and PR exam AXR in some cases

Answer 150

As per constipation but with more rapid dose titration Inadequate response: suppository (Bisacodyl soft stool or bisacodyl with glycerol for hard stools) Mini enema (docusate or sodium citrate) Sodium phosphate or arachis oil retention enema (may need to be repeated)

Answer 151

Defined as 3+ loose or liquid stools per day (or more frequently than normal for that individual) Acute <4 weeks (NICE says <14 days) Persistent diarrhea >14 days Chronic >4 weeks

Answer 152

``` Medications: laxatives, allopurinol, AT2 antagonists, antibiotics (C drugs), metformin, Mg containing antacids, NSAIDs, PPIs, SSRIs C difficile from certain antibiotics Infections such as salmonella, E coli Constipation with ‘overflow’ diarrhea Anxiety Food allergies Acute appendicitis, intestinal ischaemia IBS/IBD ```

Answer 153

Determine frequency, severity, quantity and character of stools Red flag symptoms: blood, recent antibiotic or hospital treatment, persistent vomiting, weight loss, painless, watery, high volume, nocturnal symptoms disturbing sleep Other symptoms: fever, recent travel, contact with sick people, stress, anxiety, clinical presentation of appendicitis etc. Assess for dehydration Consider comorbidities and increased risk of complications Consider rectal exam particularly in >50 years investigations: Stool specimen if pt is unwell, immunocompromised, recently received antibiotics, blood in stool, persistent >7 days, occurs after foreign travel to anywhere other than western EU, north america, NZ or australia Investigations for underlying cause if chronic cause suspected Bloods for ALL chronic cases: FBC, U+E, B12, folate, ferritin, TFTs, ESR, LFTs, CRP, coeliac disease

Answer 154

Oral rehydration therapy (salts to reabsorb water into the body) 1 sachet in 200ml water after every loose motion. Can also add to infant feeds Loperamide, 2x 2mg capsules on onset and one after every loose motion, max 16mg daily (CI if blood or pt is febrile or severe abdominal pain, larger doses increase CV risk, QT prolongation, cardiac arrest). Naloxone used to reverse effects Travellers diarrhoea: ciprofloxacin antibiotic 500mg BD for 3 days Hospital admission needed if vomiting, unable to retain fluids, features of severe dehydration or shock, elderly, blood diarrhea, abdominal pain/tenderness suggestive of cause

Answer 155

``` AKA inflamed colon/spastic colitis Psychosomatic illness Relapsing functional disorder of the large intestine, characterised by abdominal pain, change of bowel habit, bloating and abdominal distension Almost twice as common in women Peak prevalence ages 20-30 Approx. 10-20% of adults are affected ```

Answer 156

No structural lesion, no single explanation Seems to involve abnormal smooth muscle activity +/- visceral hypersensitivity and abnormal central processing of painful stimulant Associated with increased stress and poor coping strategies Possible disturbed GI motility from abnormal bowel transit time ``` Subclasses: IBS with constipation (IBS-C): loose stools <25% and hard stools >25% of time IBD with diarrhea (IBS-D): loose stools >25% and hard stools <25% time IBS mixed (IBS-M): both hard and soft stools >25% time ```

Answer 157

``` Alternating obstipation and diarrhea, can be continuous or intermittent Flatulence Vertigo Loss of appetite Pressure and bloating with relief on defecation Mild pressure or pain in left lower abdomen, no muscular defense Inconspicuous bowel sounds Excessive mucus in faeces Lethargy Nausea Backache Bladder symptoms ```

Answer 158

Must have at least 6 month history of either: Abdominal pain or discomfort Bloating Change in bowel habit If abdominal pain is either relieved by defecation or associated with bowel frequency or stool form AND at least 2 of the following are present: Altered passage of stool (straining, urgency, incomplete evac) Abdominal bloating, distension or hardness Symptoms aggravated by eating Passage of mucus rectally

Answer 159

Diagnostic criteria Bloods: FBC, ESR, CRP, coeliac screen, faecal calprotectin CA 125 for ovarian cancer If indicated: TFTs, USS, Colonoscopy, faecal occult blood, hydrogen breath tests

Answer 160

Lifestyle: Regular meals, plenty of fluids, reduce alcohol and fizzy drink intake, limiting high fibre foods Avoid sorbitol for diarrhea Flatulence: increase oats and linseeds (1 tablespoon/day) Referral to dietician for those whose diet plays a large role in symptoms CBT for psychosomatic treatment Medications: high rate of placebo effect in IBS Antispasmodics for spasm and abdominal pain (Mebeverine 135mg TDS, Alverine citrate 60-120mg TDS, Peppermint oil 1-2 capsules 3x daily) **CI with obstruction or paralytic ileus** Antimuscarinics (dicycloverine hcl 10-20mg TDS, hyoscine butylbromide 10mg TDS-20mg QDS) **CI obstruction and ileus, angle-closure glaucoma, severe ulcerative colitis, toxic megacolon** side effects CAN’T SEE, CAN’T PEE, CAN’T SHIT, CAN’T SPIT Antimotility (loperamide: 1st line diarrhea choice) Bulk forming laxatives (Ispaghula) Tricyclic Antidepressants (amitriptyline 5-10mg at night) or SSRIs CBT Linaclotide

Answer 161

Umbrella term for two main diseases causing inflammation of the GIT Ulcerative colitis and crohn’s disease Both involve inflammation of the GI walls and are associated with periods of remission and exacerbation

Answer 162

Crohn’s: crows NESTS: No blood or mucus (usually) Entire GIT involved Skip lesions on endoscopy Terminal ileum most affected and Transmural (full thickness) inflammation Smoking is a risk factor (don’t set a nest on fire) *cobblestoning mucosa and aphthous/linear ulcers endoscopic appearance *also associated with weight loss, strictures and fistulas** *Crypt abscesses and granulomas only present in Crohn’s* ``` Ulcerative colitis: U-C- CLOSEUP: Continuous inflammation Limited to colon and rectum only Only superficial mucosa affected Smoking is protective Excrete blood and mucus Use aminosalicylates Primary sclerosing cholangitis *endoscopic appearance is diffuse continuous mucosal involvement* ```

Answer 163

Diarrhea Abdominal pain Passing blood Weight loss Ix: Routine bloods for anaemia, infection, thyroid, kidney and liver function CRP for inflammation and active disease Faecal calprotectin raised (90% sensitive for IBD in adults) Endoscopy with biopsy is diagnostic USS, CT, MRI for complications like fistulas, abscesses, strictures

Answer 164

An IBD characterised by inflammation of the entire GIT (transmural granulomatous inflammation) Likely to have strong family history Associated with excess mortality compared to general population Onset has two age peaks: ages 15-30 is largest and ages 50-70 is second peak Also rapidly increasing in children Usually spares the rectum (less likely GI bleed)

Answer 165

Genetic family history of IBD Smoking increases 3-4 fold risk Intercurrent infections (URTI, enteric infections) NSAIDs

Answer 166

Variable symptoms Diarrhea (may be bloody and become chronic >6weeks) Abdominal pain Weight loss Acute exacerbation periods with remissions or less active disease Malaise Anorexia Fever Children may show poor growth, delayed puberty, malnutrition and bone demineralisation Hypotension, tachycardia, pyrexia in acute exacerbations Anal or perianal lesions Mouth ulcers Finger clubbing, erythema nodosum, pyoderma gangrenosum Large joint arthritis Fatty liver, sclerosing cholangitis (rare) Renal stones Malnutrition Amyloidosis

Answer 167

Bloods: FBC, CRP, U+E, LFTs, *CRP useful for assessing relapse** Stool culture Faecal calprotectin raised Ileocolonoscopy and biopsy to confirm Perianal disease: pelvic MRI gold standard Laparoscopy staging: - CDAI and PCDAI criteria

Answer 168

1st line oral prednisolone, IV hydrocortisone or other glucocorticosteroid for 12 months Immunosuppressant (specialist): azathioprine, mercaptopurine, methotrexate, infliximab, adalimumab Referral for rectal bleeding and abdominal pain, change of bowel habit, weight loss, iron deficiency anaemia Hospital admission if severe pain, tenderness, diarrhea >8x/day, bowel obstruction, fever and systemically unwell

Answer 169

Smoking cessation is vital Tailored to individual based on side effects, preference and nature of disease, may not require medications while well 1st line azathioprine or mercaptopurine Alternatives: methotrexate, infliximab, adalimumab Surgery when disease only affects the distal ileum is possible to resect the area and prevent further disease flares. Can also be used to treat strictures and fistulas secondary to CD

Answer 170

ECG U+E, glucose, anion gap +/- lactate, osmolal gap LFTs, clotting ABG Paracetamol level, salicylates, theophylline, digoxin, lithium, antiepileptics if indicated Urinalysis CXR if pulmonary oedema or aspiration CT scan of brain to exclude other causes of altered conscious

Answer 171

ABCDE assessment and act accordingly History: how much, when, what route of administration, has there been vomiting, past medical history, current medications and allergies, suicide note/suicide risk, third party history for context Cardio, respiratory, abdominal, neurological examinations Vital signs: temperature, pupils, BP, HR Muscle rigidity Skin - cyanosis (methaemoglobinaemia), very pink (carboxyhaemoglobinaemia, cyanide, hydrogen sulphide), blisters (barbiturates, tricyclic antidepressants (TCAs), benzodiazepines), needle tracks, hot/flushed (anticholinergics). Breath - ketones (diabetic/alcoholic ketoacidosis), 'bitter almonds' (cyanide), 'garlic-like' (organophosphates, arsenic), 'rotten eggs' (hydrogen sulphide), organic solvents. Mouth - perioral acneiform lesions (solvent abuse), dry mouth (anticholinergics), hypersalivation (parasympathomimetics)

Answer 172

Single-dose activated charcoal is the preferred method of decontamination in many cases. Patients should have had a significant overdose, be co-operative, without impairment of consciousness and not thought to be likely to fit imminently. Ideally it is used in a 10:1 ratio with the ingested drug - the usual dose is 50 g for an adult (children: 1 g/kg). It may be repeated in one hour if necessary (oral, nasogastric tube). Its large surface area adsorbs many drugs but has its limitations. It may not be be effective if given after the first hour or in cases of poisoning with iron, lithium, boric acid, cyanide, ethanol, ethylene glycol, methanol, malathion, DDT, carbamate, hydrocarbon or strong acids or alkalis.

Answer 173

Presentation: Hepatocellular necrosis (indicated by right subcostal pain and tenderness) Nausea and vomiting Treatment: Acetylcysteine reduced severity of liver damage if given <24 hours ingestion Monitor for signs of liver failure

Answer 174

Presentation: Dry mouth, coma, hypotension, hypothermia, hyperreflexia, extensor plantar responses, convulsions, respiratory failure, cardiac conduction defects, dilated pupils, urinary retention, hallucinations, delirium and confusion ``` treatment: Supportive measures to clear airway IV lorazepam or diazepam for convulsions Activated charcoal <1 hour Correct hypoxia and acidosis Monitor cardiac activity ```

Answer 175

presentation: Nausea, vomiting, agitation, tremor, nystagmus, drowsiness, sinus tachycardia, convulsions treatment: Supportive Activated charcoal <1 hour Convulsions treated with lorazepam, diazepam

Answer 176

presentation: Drowsiness, ataxia, nystagmus, respiratory depression, coma treatment: Flumazenil injection Reverses CNS and respiratory depression. However if person has also taken tricyclic antidepressant or has epilepsy must be cautions as can cause seizures or arrhythmias Activated charcoal <1 hour

Answer 177

Multi Genetic disorder associated with HLA types DQ2 (90%) or DQ8, plus other genetic or environmental factors. Family tendency 10-15% Approx 1 in 100 people in the UK have coeliac disease, however only 10-20% will be diagnosed Highest incidence in ages 50-69

Answer 178

wide variation of signs and symptoms, many cases are asymptomatic Persistent unexplained abdominal or GI symptoms Faltered growth Unexpected weight loss Severe or persistent mouth ulcers Unexplained iron, vit B12 or folate deficiency Type 1 diabetes Autoimmune thyroid disease IBS in adults 1st degree relatives of people with coeliac disease Dermatitis herpetiformis (classic manifestations of CD) Gluten sensitivity

Answer 179

Metabolic bone disorder Unexplained neuro symptoms (ataxia, epilepsy, dementia, depression) Unexplained subfertility or recurrent miscarriage Persistently raised liver enzymes without known cause Dental enamel defects Down’s or Turner syndrome All newly diagnosed type 1 diabetics are screened for coeliac disease*

Answer 180

**only accurate if gluten diet is eaten during diagnostic process** Autoantibodies: total IgA and tTG 1st line. IgA EMAs if weakly positive. For children: total TgA and IgA tTG 1st line. IgG EMA, IgG DGP or tTG if IgA is deficient FBC: anaemia, iron and folate deficiency, B12, ferritin, LFTs (elevated transaminases which should return to normal on gluten free diet), Ca and albumin Small bowel barium studies to exclude other causes of malabsorption Biopsy needed for confirmation by GI endoscopy or suction capsule

Answer 181

Referrals to GI specialist: Young people with +ve serological tests for endoscopic biopsy Children with +ve serology to paediatric specialist for further investigation -Ve serology to gastro specialist if CD still suspected for further investigation ``` Complications: Deficiencies eg vit D and iron Osteoporosis Cancer Ulcerative jejunitis Functional hyposplenism Anxiety, depression Male infertility Poor foetal outcome in UNDIAGNOSED pregnancy women, but not diagnosed ```

Answer 182

Gluten free diet (no wheat, barely, rye, bread, cakes etc) seems to be only effective treatment Refractory CD: consider prednisolone initial management while waiting specialist advice If after GFD excluded but symptoms persist/serology is high for >12 months refer for endoscopic biopsy Annual review to measure weight, height, review symptoms, assess diet and adherence, need for specialist dietitian or nutritional advice Consider DEXA scan, regular bloods for long term complications monitoring

Answer 183

``` Groin Hernias: - Inguinal (direct/indirect) - Femoral hernia Ventral hernias: - Umbilical, para-umbilical hernia - Epigastric hernia Incisional hernia ``` Reducible = can be pushed back into right place Irreducible = implies the hernia sac is not reducible Incarcerated: contents are stuck inside by adhesions without any obstruction or strangulation Obstructed: content is bowel content and is obstructed (typically small or large intestine obstruction). Some obstructed hernias can become strangulated also. Strangulated: content of the hernia is NOT bowel, but there is ischaemia. Patient becomes toxic and needs urgent surgery All these terms describe the condition of the contents of the hernia Usually strangulation happens after obstruction

Answer 184

An inguinal hernia is a protrusion, or movement of abdominal contents, from within the abdominal cavity. This tissue then protrudes, or emerges, at the exit point, the superficial inguinal ring. Location: inguinal hernias are most commonly found superomedial to the pubic tubercle.

Answer 185

Femoral hernias occur just below the inguinal ligament when abdominal contents pass through a naturally occurring weakness in the abdominal wall called the femoral canal. It is important to note that the femoral canal is narrow and is bordered medially by thesharp edge of the lacunar ligament. Therefore, femoral hernias are at higher risk of strangulation and obstruction. more common in women Location: femoral hernias are typically found inferolateral to the pubic tubercle and medial to the femoral pulse.

Answer 186

Umbilical hernias, as the name suggests, occur at the site of the umbilicus and are common. They can be large but are typically low risk for strangulation. Location: umbilical region

Answer 187

Incisional hernias occur at the sites of previous operations where tissue integrity has been compromised. Location: incisional hernias present as a bulge or protrusion at or near the site of a previous surgical incision.

Answer 188

Generally the hernial sac is a protruded part of parietal peritoneum In sliding hernia, the wall of the viscus (caecum, sigmoid etc) forms a portion of the hernial sac. The remainder of the sac being formed by parietal peritoneum Mostly expected to see these hernias as large inguinal hernias Important to classify sliding hernias before surgery to allow dissection of hernia sac from organ forming wall

Answer 189

Aka parietal hernia Abdominal hernia where only a portion of bowel wall is herniated Expect to see this in femoral hernia Likely to present with ischaemia, may end in perforation

Answer 190

``` History: Groin lump, swelling Obstructive symptoms Strangulated symptoms May be reducible or not Cough impulse if irreducible ``` Investigations: Zeimann's technique of palpation (index finger on deep inguinal ring, middle finger on superficial ring, ring finger over saphenous opening after reducing hernia content. patient asked to cough and impulse felt in finger corresponding to hernia) USS CT scan for incisional hernia MRI - good in sports groin with pain Contrast radiology - especially for inguinal hernia Laparoscopy - useful to identity contralateral inguinal hernia

Answer 191

Pain, tenderness and skin colour changes may imply high risk of strangulation Femoral hernia should always be repaired Pts with symptoms or have episodes of irreducibility or bowel obstruction etc should be offered surgical repair Elderly, immobile pts or those with high morbidity if asymptomatic or mild may be observed (watch and wait policy) Groin of truss is of limited symptomatic benefit for these non-surgical pts

Answer 192

indirect: 80% cases, can strangulate, usually young age, often congenital (patent processes vaginalis), lateral to inferior epigastric artery, often descends to scrotum, treatment is herniotomy in infant and open mesh repair/laproscopic repair in adults direct: 20% cases, early reduced, rarely strangulate, more common in older patients, acquired weakness in abdominal wall, medial to inferior epigastric artery, rarely descends to scrotum, treated with open mesh repair or laparoscopic repair femoral hernias: more common in females, frequently strangulate and frequently irreducible

Answer 193

Herniation through defects in the abdominal wall, above or below the inguinal ligament in the groin area Include inguinal (direct and indirect) and femoral hernias Indirect inguinal hernias are most common groin hernia Inguinal hernias are common in male infants due to the patent processus vaginalis Uncommon in female infants: should have androgen insensitivity syndrome tests Women more commonly have femoral hernia Men indirect inguinal Elderly men more commonly direct inguinal hernias ``` causes: Coughing COPD Obesity Straining: constipation or prostatism Pregnancy Low birth weight Family history of hernia Valsalva maneuver Ascites Upright position Congenital connective tissue disorders Defective collagen synthesis Previous RLQ incision Arterial aneurysms Smoking Heavy lifting Physical exertion ```

Answer 194

Always assess both sides of the groin to avoid missing pathology Typical hernia pathology: Single lump in inguinal region +ve cough impulse (unless incarcerated) Soft on palpation Reducible (unless incarcerated) Unable to get above lump during palpation Painless (unless incarcerated) Bowel sounds on auscultation (unless incarcerated) Differentiation of subtypes: Assess relationship to pubic tubercle (inguinal typically above and medial to, femoral typically below and lateral to) Reducibility: can it be flattened out with changing positions (supine) or by applying pressure. Ask pt to lie supine and observe for reduction. If still present, try to reduce with pressure. A hernia that is TENDER and IRREDUCIBLE may be strangulated and needs urgent surgica review If inguinal hernia suspected: determine if direct or indirect Locate deep inguinal ring (midway between ASIS and pubic tubercle), manually reduce hernia with compression towards the deep inguinal ring starting at the inferior aspect. Once reduced, apply pressure over deep inguinal ring and ask patient to cough If it reappears, it’s more likely to be DIRECT, if not, then more likely is INDIRECT (unreliable test - needs further imaging)

Answer 195

Aka piles Abnormally swollen vascular mucosal cushions that are present in the anal canal Pathology: 3 vascular mucosal cushions which help maintain anal continence Typically described as being present at left lateral, right posterior and right anterior positions (varies) When these become enlarged it leads to dilation of the local veins and protrusion into and through the anal canal - haemorrhoids

Answer 196

Depending on origin in relation to the dentate line (situated 2cm from anal verge and marks transition between the upper and lower anal canal) External haemorrhoids originate below the dentate line and are covered by modified squamous epithelium (anoderm) which is richly innervated with pain fibres External can also be more itchy (pruritic) and painful Internal haemorrhoids arise above the dentate line and are covered by columnar epithelium, which have NO pain fibres Therefore are not sensitive to touch, temperature or pain (unless they become strangulated) Internal H are further graded by degree of prolapse (1-4)

Answer 197

``` Constipation Straining Ageing Conditions increasing intra abdominal pressure (pregnancy, labour, ascites, pelvic mass) Chronic cough Heavy lifting Exercising Genetics (congenital weaknesses) Low fibre diet ```

Answer 198

Bright red, painless, rectal bleeding Typically occurs with defecation and seen as streaks of blood on toilet paper (not in stool) Anal itching or irritation Feeling of rectal fullness, discomfort or incomplete evacuation (tenesmus) Soiling due to mucus discharge or impaired continence Pain Strangulated haemorrhoids are extremely painful, acutely thrombosed external haemorrhoids Difficult to palpate internal haemorrhoid as internal mucosal folds also get in the way

Answer 199

Investigations: Digital rectal exam/PR, even though internal haemorrhoids often not palpable Bloods: FBC, ESR/CRP faecal calprotectin test Diagnosis: Clinical history and PR exam May be asymptomatic or can have history of intermittent symptoms lasting from few days to few weeks Can have both internal and external at once

Answer 200

Conservative (lifestyle) Constipation avoidance: good dietary fibre intake, adequate fluids Good toilet habits: clean and dry. Cleanse with moistened towelettes and pat (not rub) dry Advise against stool withholding and undue straining Medications Analgesia: paracetamol (avoid NSAIDs if bleeding), avoid opioids (constipation causing) Topical astringents, lubricants, anaesthetics and corticosteroids for symptom relief Anusol (astringent and emollient) Anacal (heparinoid) Anodesyn (local anaesthetic) Germoloids (lidocaine and astringent) Anusol HC Plus (hydrocortisone and astringent) Proctosedyl (anaesthetic and hydrocortisone) Local anaesthetics can cause anal skin sensitisation Steroids cause thinning of anal skin HOW TO USE: Generally used morning and night and after bowel movements Anaesthetic containing prep should only be used for a few days due to skin sensitisation Corticosteroid containing prep used no longer than 7 days as may lead to skin atrophy, contact dermatitis and skin sensitisation. Avoid excessive application

Answer 201

``` Non-surgical: rubber band ligation injection sclerotherapy infrared coagulation/photocoagulation bipolar diathermy and direct current electrotherapy ``` surgical: haemorrhoidectomy stapled haemorrhoidectomy haemorrhoid artery ligation hospital admission: Strangulated external haemorrhoids <72 hours onset for reduction or excision Internal haemorrhoids that prolapsed or swollen, incarcerated and thrombosed (haemorrhoidectomy may be needed) Perianal sepsis Non-urgent referral: Fourth degree haemorrhoids or third degree haemorrhoids that are too large for non-operative measures (haemorrhoidectomy may be needed). Perianal haematoma (a blue or dark coloured swelling at the anal verge) if symptoms are for less than 24 hours duration for clot evaluation. Combined internal and external haemorrhoids with severe symptoms (surgery may be required). Thrombosed haemorrhoids when bleeding is problematic, or there is chronic irritation or leakage. Large skin tags (surgical excision may be required).

Answer 202

Colorectal and anal cancers Primarily SCC Anal margin tumours are usually well differentiated. More common in men with good prognosis Anal canal tumours are poorly differentiated, more common in women with worse prognosis 2:1 F:M ratio 60% 5 year survival rates

Answer 203

HPV Anal intercourse and high lifetime number of sexual partners (increased HPV risk) Male with male sex HIV/immunosuppression Women with cervical cancer history or cervical intraepithelial neoplasia (CIN) Immune suppression in transplant recipients Smoking

Answer 204

``` Anal pain Tenesmus (incomplete emptying feeling) Rectal bleeding Anal mass or ulceration Rectovaginal fistula (advanced) ```

Answer 205

Diagnosis clinical Proctoscopy and biopsy to confirm Faecal immunology test FIT FBC, LFT, U+E, CRP, ESR Management: 2WW referral Surgical excision + radio or chemotherapy with lymph node excisions depending on severity and spread Red flags for 2WW referral: anal mass or anal ulceration

Answer 206

Mostly adenocarcinomas which evolve from polyps May be present for 10+ years before malignancy develops National screening program for bowel cancer - FIT and scope Bowel cancer is 4th most common cancer in UK

Answer 207

Family history of colorectal neoplasms <60 years old Past history of colorectal neoplasms IBD Polyposis syndromes: Gardner’s syndrome, Turcot’s syndrome etc. Hereditary non-polyposis colorectal cancer (HNPCC) Hormonal factors: nulliparity, late age first pregnancy, early menopause Diet rich in meat and fat, poor fibre, folate and Ca intake Sedentary lifestyle: smoking, high alcohol intake Diabetes Previous irradiation: asbestos exposure etc History of small bowel cancer, endometrial cancer, breast cancer or ovarian cancer

Answer 208

Change of bowel habit: diarrhoea or constipation Rectal bleeding Loss of weight Abdominal pain Tenesmus Iron deficiency anaemia especially in men and postmenopausal women (unexplained = RED FLAG) DVT, abdominal or rectal masses, occult blood in faeces (uncommon)

Answer 209

FIT: detects small amounts of blood in stool samples using antibodies specific to human Hemoglobin FBC, LFTs Colonoscopy and biopsy GOLD STANDARD CT colonography in those unfit for colonoscopy but doesn’t include biopsy

Answer 210

2WW referral Surgery, chemo or radiotherapy or sometimes biological agents such as cetuximab Resection of bowel and stoma may be expected Red flags: 40+, unexplained weight loss and abdominal pain, 50+ unexplained rectal bleeding, 60+ iron deficiency or changes in bowel habit, tests how occult blood in faeces General red flags: abdominal pain, change in bowel habit, weight loss, iron deficiency anaemia

Answer 211

Primary liver cancers Often presents as complication of cirrhosis, usually following chronic viral hepatitis or alcoholic liver disease Most common primary liver cancer is hepatocellular carcinoma Hepatoblastoma more common in children Other includes cholangiocarcinoma

Answer 212

HBV/HCV infection Chronic HBV infection most common cause of HCC in the world HCV most common cause in EU Co infection of both increases HCC risk further Alcoholism Genetic haemochromatosis Primary biliary cirrhosis Metabolic syndrome (HTN, diabetes and obesity) Smoking Saharan africa and asian foods (high concentrations of aflatoxins)

Answer 213

``` RUQ abdominal pain Abnormal LFTs and liver function Hepatomegaly Upper abdominal masses Jaundice Pruritus (from bile build up) Splenomegaly Bleeding oesophageal varices Weight loss Confusion and hepatic encephalopathy Abdominal distension due to ascites ```

Answer 214

Investigations: USS/other imaging Biopsy for confirmation in secondary care Bloods: LFTs, clotting screen, bone profile (albumin) ``` Management: 2WW referral for biopsy in secondary care Surgical resection Thermal ablation Systemic chemotherapy Transarterial chemoembolization Selective internal radiation therapy Red flags: upper abdominal mass consistent with enlarged liver - 2WW USS ```

Answer 215

Pancreatic cancer Categorised into exocrine and endocrine tumours Mostly exocrine tumours Infiltrating ductal adenocarcinomas 90% pancreatic cancers Majority arise from head, neck or uncinate process 90% periampullary malignancies arise from pancreas and remaining 10% from the distal common bile duct, ampulla of Vater and duodenum Metastases most commonly in the liver, peritoneum and lungs Low survival rate 5% 5 years due to patients presenting notoriously late on in disease, only less than one fifth present with localised, potentially curable tumours

Answer 216

``` Smoking High BMI Red meat intake high, low fruit and eg Diabetes High alcohol intake Chronic and hereditary pancreatitis both associated with increased risk Family history Family cancer syndromes: BRCA1 and 2, familial adenomatous polyposis, Peutz-Jegers syndrome, familial melanoma syndromes, Gardner's syndrome IBD Periodontal disease Peptic ulcer disease ```

Answer 217

very late usually Abdominal epigastric pain radiating to back Dull pain worse when supine, eased by leaning forward Loss of appetite Jaundice Weight loss Palpable gallbladder (Courvoisier’s sign, painless jaundice) Nausea and vomiting Endocrine cancer may produce symptoms from secretions of hormonal (diabetes etc)

Answer 218

Investigations: CT scan most sensitive USS Bloods: FBC (anaemia, thrombocytosis), LFTs (raised bilirubin, ALP, GGT), serum glucose (hyperglycaemia) Diagnosis needs biopsy (secondary care often) Management: 2WW referral for biopsy Surgery to remove tumour Red flags: 60+ abdo pain and weight loss, back pain and weight loss, new onset diabetes, change of bowel habit and weight loss, nausea and vomiting with weight loss 40+, jaundice

Answer 219

Mostly SCC or adenocarcinomas M:F 2:1 ratio Risk factors: Male Tobacco and alcohol Barrett’s oesophagus (precursor of adenocarcinoma) Chronic inflammation and stasis from any cause increases risk of SCC eg strictures due to caustic injury or achalasia Tylosis and Paterson-Brown-Kelly syndrome Obesity for AC but reduced risk of SCC Family history of hiatal hernia for AC

Answer 220

``` varies and can overlap with gastric neoplasms Dysphagia Odynophagia Acid reflux Loss of appetite Weight loss Hoarse voice Melaena Retrosternal pain Intractable hiccups Anaemia ```

Answer 221

``` Investigations: Endoscopy GOLD STANDARD Biopsy to confirm Bloods: FBC, U+E, LFTs, glucose, CRP CXR ``` Management: 2WW referral Surgery alone or with chemo or radiation therapy Red flags: dysphagia, haematemesis >55 years with weight loss, upper abdo pain, reflux or dyspepsia Non-urgent referral for >55 years with treatment resistant dyspepsia, upper abdo pain with low Hb levels OR raised platelet count with nausea, vomiting, weight loss, reflux, dyspepsia, upper abdo pain, or nausea and vomiting with, weight loss, reflux, dyspepsia or upper abdo pain

Answer 222

``` Stomach carcinoma Starts anywhere inside stomach or stomach wall 50% involve pylorus 25% less curve 10% cardia 2-8% gastric cancers are lymphomas 5 year survival rate approx 20% Majority of pts present with advanced disease ```

Answer 223

``` Increasing age (95% >55) Male Poor socio-economic status Helicobacter pylori can double risk Diet low in fruit and veg and high in salt and preserved foods Smoking Atrophic gastritis Pernicious anaemia Post-gastrectomy Menetrier’s disease Family history Blood group A Hypogammaglobulinaemia ```

Answer 224

``` Dysphagia Abdominal pain Acid reflux Loss of appetite Weight loss Anaemia ```

Answer 225

Investigations: Endoscopy GOLD STANDARD Biopsy to confirm Bloods: FBC and LFTs Management: 2WW referral Surgery to remove tumours All pts should be screened for nutritional deficiencies and considered for nutritional support Red flags: upper abdo mass consistent with stomach cancer, dysphagia,haematemesis, >55 years with weight loss, upper abdo pain, reflux or dyspepsia Non-urgent referral for >55 years with treatment resistant dyspepsia, upper abdo pain with low Hb levels OR raised platelet count with nausea, vomiting, weight loss, reflux, dyspepsia, upper abdo pain, or nausea and vomiting with, weight loss, reflux, dyspepsia or upper abdo pain

Answer 226

Aspirin, continue taking as normal Warfarin, continue, stop 4 days pre-op and if high risk start LMWH PRN Dipyridamole, continue, stop 24 hours pre-op if high risk Clopidogrel/prasgurel/ticagrelor, continue, stop 7 days pre-op if high risk **switch to aspirin for 7 days if not already taking or CI** Rivaroxaban, stop 24 hours pre-op Dabigatran, stop 1-4 days before op according to eGFR/procedure bleed risk Apixaban, stop 24-48 hours pre-op according to procedure bleed risk ACEi/A2RB, stop on day if BP well controlled (140/80), monitor eGFR Diuretics, stop on day of procedure, confirm electrolyte levels an eGFR NSAID, consider stopping on day and restarting after 3 days, confirm electrolytes and eGFR Lithium and any other medications, do not take within 1 hour bowel cleansing medication to avoid reduced absorption, confirm electrolytes and eGFR

Answer 227

Moviprep sachets 2x2 Citramag SF sachets 2, senna 7.5mg tablets x10 Klean prep sachets 4 ``` CI for bowel prep: GI obstruction, retention, ileus or perforation Severe IBD, ulceration or colitis Toxic megacolon Reduced consciousness level Dysphagia Ileostomy Hypersensitivity to ingredients ```

Answer 228

No solid food should be eaten at least 2 hours before taking bowel cleanse Diarrhea is expected, stay at home close to toilets Drink plenty of clear fluid (water) throughout Side effects: nausea, vomiting, bloating, abdo pain, anal irritation, sleep disturbance Can lead to dehydration, dizziness, headaches, confusion Allergic reaction may include rash, itching, redness and swelling

Answer 229

``` I Normal healthy patient II Mild systemic disease III Severe systemic disease IV Severe systemic disease constant threat to life V Moribund patient not expected to survive without operation VI Declared brain dead - organs being removed for donor purposes ```

Answer 230

Standard criteria measuring how the disease impacts patients daily living 0-5 description 0: fully active, able to carry on all pre-disease performance without restriction 1: restricted in strenuous activity but ambulatory able to carry out work of light nature 2: ambulatory and capable of all selfcare but unable to carry out any work activities, up and about >50% waking hours 3: capable of only limited selfcare, confined to bed or chair >50% waking hours 4: completely disabled, cannot carry out selfcare, totally confined to bed or chair in waking hours 5: dead

Answer 231

Adverse reactions to food, this will be recurring each time the person ingests that food Symptoms depend on the mechanisms of reaction but range from vomiting and diarrhea and skin reactions (eczema, urticaria) to anigio-oedema, severe respiratory distress and anaphylaxis Classification: Immunological reactions (food ALLERGY): IgE and non-IgE mediated (delayed and acute reactions) Non-immunological reactions (food INTOLERANCE) ``` Common foods: Milk Eggs Fish and seafood Peanuts Sesame Tree nuts Soy beans Wheat Kiwi fruit ```

Answer 232

``` Why food allergy suspected What foods are implicated (complete list needed including how it was prepared) Symptoms occurring after eating What age symptoms started How much food needed to cause it Do symptoms occur every time it’s eaten How long do symptoms last Do they follow pattern Frequency of occurrence Worst reaction they had Setting of reaction Personal or family history of allergy Feeding history, age of weaning, formula or breast fed Previous treatments, diet exclusions and results of that Is diet nutritionally adequate ```

Answer 233

Pruritus Erythema Diarrhoea Abdominal pain are all common in both types of reaction IgE mediated: Acute urticaria - localised or generalised Acute angio-oedema, commonly mouth, lips, face, eyes Oral itching, nausea and vomiting Colicky abdominal pain Nasal itching, sneezing, rhinorrhoea, allergic conjunctivitis Cough, shortness of breath, wheezing and bronchospasm (or history of asthma) Other signs of anaphylaxis, feeling of impending doom, CV collapse ``` Non-IgE mediated: Atopic eczema Reflux Infantile colic Stools: loose/frequent/blood/mucus Constipation Perianal redness Pallor and tiredness Faltered growth Food aversion or avoidance ```

Answer 234

Food diary Skin prick tests for specific IgE antibodies to suspected foods Measurement of serum allergen IgE (ELISA) and fluorescent enzyme immunoassay tests Atopy patch testing or oral food challenges Trial elimination diet (2-6 weeks normally) then reintroduce to see if symptoms improve then return

Answer 235

ABCDE assessment High flow oxygen with reservoir mask Lay patient flat, raise legs, in pregnancy use left lateral tilt 15 degrees Adrenaline 0.5micrograms IM adults >12 years old, 0.3 micrograms age 6-12, <6 years 150 micrograms Establish airway UV access and rapid fluid challenge Chlorphenamine after initial resus (dose age dependent) Hydrocortisone (dose age dependent) Continual vitals monitoring

Answer 236

Food avoidance Dietician referral Antihistamines for less severe symptoms Adrenaline for severe anaphylactic reactions Medical emergency bracelet PRN Informing relatives, schools, carer education etc Prognosis: Most children ‘grow out’ of allergy to eggs, milk, wheat and soya. May be due to maturation of gut or immune responses that are responsible for allergy Sensitivity to peanuts, seafood, fish, tree nuts are rarely lost

Answer 237

Tear in the mucosa of the anal canal just inside the anal margin Commonly causes pain on defecation Mostly responds well to topical or conservative management but refractory cases can need surgery Second most common complication after pregnancy (first being haemorrhoids) Acute <6weeks Chronic >6 weeks (uncommon) Primary: no apparent cause Secondary: due to underlying conditions such as constipation, IBD, STI, trauma (surgery, sexual), pregnancy and childbirth or rectal malignancy Aeitology is unclear but thought to be related to increased anal tone.

Answer 238

History of pain with defecation (passing shards of glass) Can persist several hours after passing Fresh blood on toilet paper May have a history of constipation, IBD etc. Investigations: Clinical history PR exam (only external examination if fissures are seen) Abdominal exam

Answer 239

Increase dietary fibre gradually to avoid bloating, shallow warm baths after movements may ease pain Correct anal hygiene, especially in children, keep dry and clean, advise against stool withholding and undue straining during movements which can worsen GTN 0.4% ointment for those with >1 week symptoms without improvement, use twice daily for 6-8 weeks (read CI first) also warn pt if bleeding, that they may bleed slightly more than normal with GTN application before healing. For extreme pain prescribe short course (few days) topical lidocaine 5% ointment used before passing stool, apply 1-2mL PRN Diltiazem ointment (unlicensed) Botulinum toxin injections Oral analgesia PRN for pain, can also prescribe laxatives for constipation, treat underlying condition PRN Referral for children with non-healing <2 weeks, adults with ongoing pain 6-8 weeks, whose symptoms are still present 12-16 weeks after healing, consider earlier referral in elderly Recurrent or chronic cases may need surgery (sphincterotomy) to correct fissure and loosen anal tone follow ups: Primary anal fissure: in children, return if unhealed after 2 weeks or earlier if painful. In adult, review if unhealed after 6-8 weeks or earlier PRN Secondary anal fissue follow ups will depend on underlying cause Advise primary anal fissue when healed they should contiue to keep dietary and lifestyle measures in place to reduce risk of recurrence

Answer 240

Gastric mucosal inflammation Bacterial acute and chronic gastritis are caused by H pylori infection Erosive gastritis may occur in response to NSAID/alcohol long term use, doesnt typically cause inflammation but can lead to bleeding and ulceration in stomach lining Stress gastritis is most commonly related to mucosal ischaemia in critically ill patients, ranging from superficial to deep mucosal damage known as stress ulceration Autoimmune gastritis is diffuse mucosal atrophy characterised by auto-antibodies to parietal cells and intrinsic factor, resulting in inflammatory infiltration and atrophy

Answer 241

``` Presentation: Can start suddenly or develop slowly Pain in epigastric or RUQ abdomen Loss of appetite, feeling full in upper abdomen Dyspepsia Bloating Retching Nausea and vomiting ``` Complications: Stomach ulcers Haematemesis

Answer 242

Acute gastritis management: GI bleeding: urgent hospital referral, IV access, fluid resus and stabilisation, urgent OGD if needed. If related to NSAIDs, aspirin, alcohol then bleeding usually resolves quickly, stop aspirin or NSAID and initiate PPI Antacids can reduce irritation and may resolve symptoms Chronic gastritis: H pylori associated: treat with eradication immediately NSAID related gastritis: stop NSAID if possible, if not then after ulcer healing offer long term gastric protection or consider substitution to newer Coc-2 selective NSAID (celecoxib or etoricoxib)

Answer 243

Caused by diffuse hypertrophy and hyperplasia of smooth muscle of antrum and pylorus of stomach Pyloric muscle hypertrophy results in narrowing of the pyloric canal which results in easy obstruction Usually presents in infants aged 2-8 weeks Occurs in 1 in 500 live births More common in males than females (4:1 ratio) Genetically linked, early exposure to erythromycin in first 2 weeks of life

Answer 244

Onset of vomiting around 2-8 weeks of age Non-bilious vomiting for several days often projectile, usually 30-60 minutes after a feed with baby remaining hungry Vomiting increases in intensity over several days Persistent hunger Weight loss Dehydration Lethargy Infrequent of absent bowel movements Stomach wall peristalsis may be visible Enlarged pylorus, described as an ‘olive’ may be palpated in the RUQ or epigastrium at start of feed

Answer 245

Investigations: USS, best test Serum electrolytes to correct imbalances Management: Correct electrolyte imbalances and dehydration Ramstedt’s Pyloromyotomy (can be done laparoscopically) Prognosis is excellent unless diagnosis delayed and patient suffers severe dehydration

Answer 246

Characterised by UGIB from mucosal lacerations in UGIT, usually the gastro-oesophageal junction or gastric cardia Emergency medical condition (mortality 6-13%) Majority are caused by peptic ulcers Common between ages 30-50 Most patients present with single tear, usually just below the gastroesophageal junction on the lesser curve of the stomach, but may be associated with other lesions Cause: Haematemesis usually occurs after prolonged or forceful bout of retching, vomiting, coughing, straining or hiccupping

Answer 247

Repeated/forceful vomiting causes acute increase in intra-abdominal pressure against closed glottis (very sudden and strong valsalva manoeuvre) Sudden forceful contraction of stomach also increases intra-oesophageal pressure Mucosal tear usually occurs at gastro-oesophageal junction/gastric cardia causing arterial bleeding risk factors: Excessive alcohol ingestion Conditions predisposing to retching and vomiting eg gastroenteritis, bulimia, renal disease, raised intracranial pressure, hepatitis, COPD, bronchiectasis, whooping cough, hiatus hernia, NSAIDs

Answer 248

History of haematemesis following bout of retching or vomiting Melaena Dizzy or syncope Abdominal pain and features from initial cause of vomiting investigations: Assess blood loss using rockall scoring system to assess the UGIB Bloods: FBC, coagulation studies Renal function, urea, creatine, electrolyte levels Group and save ECG and cardiac enzymes to rule out MI

Answer 249

ABCDE assessment Resus, maintain airway, high flow oxygen and correcting dehydration and fluid loss Once stable, take history and perform examinations Endoscopy to stop the bleeding (should be performed within 24 hours) Most will stop bleeding spontaneously, few need endoscopic intervention Rockall score calculated post-endoscopy (<3 low risk, >3 needs close observation as high risk) Careful monitoring (urine output, BP and vitals) and those with high risk of rebleeding should be monitored for at least 48 hours

Answer 250

Ask pt to lie comfortably in lateral position and gently part buttocks Acute anal fissures are superficial and well-demercated edges Chronic are wider, deeper, muscle fibres visible in base. Edges often swollen, skin tag may be visible at end of fissure Primary are usually singular, occur in posterior midline of anus, although few cases may be seen in anterior midline (especially in women) Secondary may have irregular outline, be multiple, or occur laterally Anal spasms and pain may prevent full visualisation of fissure. When fissure cannot be seen, pain occurs with gentle pressure on anal margin

Answer 251

Symptoms: Anal pain with defecation Severe and sharp when passing stool, followed with deep burning pain persisting hours afterwards Bleeding may occur with defecation. When present usually seen small quantity of bright red blood on stool or toilet paper Anal spasm and tearing sensation on passing stool commonly reported Duration of symptoms: Acute anal fissures are present <6 weeks Chronic anal fissures present for >6 weeks Features of underlying cause, including: Dietary and bowel habits; constipation, diarrhea, recent changes Previous anorectal trauma; anal surgery and obstetric history Associated symptoms; abdo pain or weight loss Family history of colorectal cancer, IBD etc. STI possibility Recent pregnancy

Answer 252

Thought to be caused by plugging of anal ducts that drain anal glands in anal wall, helping ease passage of faecal matter through mucus secretion ``` ducts: supralevator ischiorectal intersphincteric perianal ```

Answer 253

Pain in perianal region Exacerbated when sitting Localised swelling, itching, discharged Severe abscesses can present with systemic features: fever, rigors, general malaise, septic features Erythematous, fluctuant, tender perianal mass, which may be discharging pus or have surrounding cellulitis Deeper abscesses may not have any obvious external signs, however produce severe tenderness on digital rectal exam, therefore need further examination under anaesthesia for full assessment

Answer 254

Arrange same day incision and drainage (can be performed in primary care if lesion is small and superficial) otherwise refer to colorectal or general surgical unti dependin gon local protocol Paracetamol for pain/fever If response insufficient offer NSAIDs (ibuprofen, naproxen) if not CI Associated cellulitis: oral antibiotics (flucloxacillin mild or co-amoxiclav for severe) Post-drainage advise lifestyle changes to reduce risk of recurrence such as: meticulous peri-anal hygiene, baths, showers, removal of hair

Answer 255

Small tunnel that develops between end of bowel and skin near the anus Usually the result of an infection near the anus causing a collection of pus (abscess) in nearby tissue, eating away a small tunnel in tissue, but can occur without bacterial infection also When pus drains, can leave small channel behind Usually do not get better on their own management same day admission for surgical review

Answer 256

Chronic skin problem found most often in sacrococcygeal region Cleft between buttocks just below base of spine Characterised by one or more sinus tracts; these are cavities with narrow opening on skin surface (pilonidal sinus) Most cases, the cavity is filled with nests of hair - hence pilonidal (means hair nest). Non-inflamed lump known as pilonidal cyst. If the sinus becomes infected a pilonidal abscess may form, pilonidal disease, cysts may be asymptomatic and need no intervention. When abscesses form, always need intervention

Answer 257

Congenital - born with small holes/pits near base of spine (enlarged hair follicles) Follicular occlusion: some people genetically prone to this. May also suffer from hidradenitis suppurativa, acne conglobata and dissecting cellulitis (follicular occlusion syndrome/tetrad) When subjected to friction and motion the follicles are injured and disrupted so hair pokes through wall of follicle into surrounding skin setting up foreign body reaction Neighbouring hairs or free hairs from other parts of body collect in pit and invade small opening created by distorted hair follicles Skin and perineal bacterial (staph. Aureus, bacteroides species etc) invade and cause infection

Answer 258

``` 2-3x more common in men Coarse, curly or crinkly hair Obesity Family predisposition Poor hygiene Prolonged sitting or buttock friction causing increased sweating Repeated local injury Co-existing hidradenitis suppurativa ```

Answer 259

Small painless pit or dimple at base of spine Large painful abscess Progressive tenderness Particularly after prolonged periods of sitting Pain, redness, swelling Small hole or holes draining fluid that may be clear, cloudy or bloody If infected, draining pus may smell foul Fever, malaise, nausea Visible or lumpy tracts 2-5 cm long in chronic or recurrent disease

Answer 260

Asymptomatic: no treatment needed Advice to keep clean, hair free and cyst may self resolve Persistent and inflamed cysts (acute pilonidal abscess) are incised and drained to reduce inflammation Occasionally abscesses need to be cut out completely to remove hair nests and skin debris, this reduces rate of recurrence to about 15% Persistent or complex pilonidal disease can benefit from surgical intervention - consider referral if heavily impacting quality of life, requires packing for several follow ups until complete healing after intervention to ensure proper healing without sinus healing (carried out by nurses/tissue viability)

Answer 261

Very common >50 years Slightly more common in men Can develop single or multiple Exact cause unknown, thought to be by body producing too many cells in lining of the bowel These extra cells then form into a bump (polyp) is a benign tumour ``` Risk factors: Family history of polyp or bowel cancer Condition affecting the gut eg colitis, crohn’s etc Obesity Smoking ```

Answer 262

Asymptomatic Incidental findings on scoping Larger polyps may cause mucus in poo, diarrhea, abdominal pain investigations: Colonoscopy Wire loop can be used during this to cauterise polyp and remove it Rarely some bowel will be removed with the polyp, this is very severe cases where polyp has some cell changes; the polyp is very large or there are lots of polyps

Answer 263

Usually benign Some can be adenomas with increased chance of malignancy if not removed It’s believed most bowel cancers develop from adenoma polyps Very few polyps will turn into cancer but takes many years for this to happen Because of risk of bowel polyps developing into cancer, your dr will always recommend treatment

Answer 264

Bacterial infection commonly affecting those who have recently been on antibiotics Easily spread to others Notifiable condition: must notify authority of all cases once confirmed Normally in the bowel but kept under control by other gut flora Some antibiotics interfere with flora balance and increase risk of c. diff multiplying and producing toxins producing illness Once out of the body the bacteria become spores and can spread to others, can survive for long periods of time so regular disinfecting of all surfaces needed Considered infectious until at least 48 hours after symptoms clear up

Answer 265

Taking broad spectrum antibiotics, several types at once or long term antibiotics Hospital or care home settings >65 years IBD Cancer Kidney disease Immunosuppressed conditions Taking PPI medications (reduced stomach acid) Bowel surgery history *Antibiotics more risky are: fluoroquinolones, cephalosporins, penicillins and clindamycin* ``` the 5 Cs: cephalosporins carbapenems clindamycin ciprofloxacin co-amoxiclav ```

Answer 266

``` Diarrhea several times daily (foul smelling) Fever Loss of appetite Nausea Abdominal pain ``` Management: Hospitalisation for severe infection to correct dehydration and electrolyte imbalances Mild can be treated at home Isolation needed to reduce risk of spreading to others Stopping causative antibiotics 10-14 day course of antibiotics known to kill C. diff, may need to be repeated if symptoms return or persist (vancomycin, fidaxomicin, metronidazole) Rarely, surgery to removal damaged section of bowel

Answer 267

Inflammation of the liver Can be acute or chronic Pathology: Liver cell necrosis and inflammatory cell infiltration in liver Divided into acute or chronic type based on clinical and pathological criteria

Answer 268

``` Acute: Viral Non-viral Alcohol Toxins Drugs Ischaemic Autoimmune Metabolic diseases ``` ``` Chronic: Viral Alcohol Drugs Non-alcoholic steatohepatitis Autoimmune Hereditary ```

Answer 269

``` Can be asymptomatic Fatigue Pruritus Muscle and joint aches Nausea and vomiting Jaundice Fever (viral) ```

Answer 270

liver function tests become deranged with high transaminases (AST / ALT) with proportionally less of a rise in ALP. This is referred to as a “hepatitic picture”. Transaminases are liver enzymes that are released into the blood as a result of inflammation of the liver cells. Bilirubin can also rise as a result of inflammation of the liver cells. High bilirubin causes jaundice.

Answer 271

Five types, A-E Most people commonly affected by A, B and C Management: Have a low threshold for screening patients that are at risk of hepatitis C Screen for other blood born viruses (hepatitis A and B and HIV) and other sexually transmitted diseases Refer to gastroenterology, hepatology or infectious diseases for specialist management Notify Public Health (it is a notifiable disease) Stop smoking and alcohol Education about reducing transmission and informing potential at risk contacts Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma

Answer 272

Most common type of acute viral hepatitis RNA virus Spread by faecal-oral route, ingestion of contaminated foods (shellfish, clams) or water Most infections are in childhood/young patients Incubation 2-6 weeks Presentation: Nonspecific prodromal symptoms (fever, malaise, anorexia, nausea and vomiting, arthralgia) Jaundice (rare in children) Can cause cholestasis, causing dark urine and pale stools Hepatosplenomegaly Adenopathy

Answer 273

Investigations: AST and ALT increased (3-6 weeks post-exposure) Management: Notifiable disease: notify public health Supportive, alcohol cessation, basic analgesia Usually self limiting infection resolves within 3-6 weeks Prevention: good hygiene, avoid risky foods when travelling and vaccinations

Answer 274

DNA virus Spread via blood products, IV drug abusers, sexual partners, direct contact (horizontal transmission) Vertical transmission is from mother to child during parturition is most common means of transmission worldwide Horizontal transmission occurs particularly in children through minor abrasions or close contact with other children Acute hepatitis B: Incubation 1-5 months Pathology: HBV penetrates hepatocytes, in immunocompetent adults will elicit strong cellular immune response and clears the infection 5-10% remain chronic carriers and a risk to others 1% will have fulminant liver failure/fulminant hepatitis

Answer 275

``` Asymptomatic Nonspecific prodromal symptoms (fever, malaise, anorexia, nausea, arthralgia) Jaundice (rare in children) Hepatosplenomegaly Adenopathy ``` Investigations: AST and ALT increased (3-6 weeks post-exposure)

Answer 276

No specific therapy, supportive management if symptomatic Some cases use interferon alfa-2a, Tenofovir, Entecavir Have low threshold for patients at risk, screen for other blood borne diseases (HIV, all hepatitis virals and other STIS) Refer to GI, hepatology or infectious diseases for specialist management Notify public health for all cases Smoking cessation and alcohol Education of reducing transmission and informing potential at risk contacts Test for complications: fibroscan for cirrhosis, USS for hepatocellular carcinoma Antiviral meds can slow progression and reduce infectivity Liver transplant for end-stage liver disease Complications: Short term: 5-10% become carriers, 1% have fulminant hepatitis Long term (in carrier state): cirrhosis, HCC, cholangiocarcinoma

Answer 277

Antigens: HBsAg (active infection) appears in blood 6 weeks- 3 months after acute infection and then disappears HBeAg (viral replication) rises early and usually declines rapidly Persistence of both of these antigens indicates chronic hepatitis Antibodies: Anti-HBs (implies vaccination or past or current infection) appear late and indicates immunity. If all else negative but this is positive, likely immune from vaccination anti-HBc (implies past or current infection) is first to appear and persists for many months. IgM implies active infection, high titre = acute while low titre = chronic infection. IgG indicates past infections when HBsAg is negative anti-HBe appears after anti-HBc and indicates low risk Window period: Diagnosis of viral hepatitis made by finding the antigen or antiviral antibody in serum For HBV, antigens may be detectable after 6 weeks-3 months Early negative result does not exclude acute HBV infection

Answer 278

RNA virus Spread via blood products, IVDU, sexual contact Most common in UK is IV drug users (IVDU) In developing countries is blood products Incubation 2-6 months No vaccination but is now curable with direct acting antiviral meds (1 in 4 make full recovery, 3 in 4 become chronic) ``` Presentation: Early is mild or asymptomatic with only 10% jaundice 85% have silent chronic infection 25% have cirrhosis in 20 years 4% of corrhotic patients develop HCC ```

Answer 279

Most patients are not diagnosed until they present years later, with elevated serum aminotransferase levels (LFTs) found on routine biochemistry or with symptoms and signs of chronic liver disease and cirrhosis LFTs anti-HCV antibodies confirms exposure HCV-PCR confirms ongoing infection Liver biopsy or elastography (if PCR +ve) to assess liver damage and need for treatment. Elastography is assessment of tissue elasticity and stiffness by USS or MRI Window period: Diagnosis made by finding viral antiviral antibody in serum For HCV antibodies are detectable after 8 weeks (2 months)

Answer 280

Alcohol cessation to reduce risk of cirrhosis and HCC All patients with chronic infection need direct acting antiviral therapy (INF-alpha + Ribavirin) over 8-12 weeks Prognosis based on other risk factors (alcohol, HIV, HBV) Prevention is avoiding needle stick injuries, safety measures Liver transplant for end stage liver disease

Answer 281

Incomplete RNA virus, needs HBV present for assembly (attaches to HBsAg) 5% HBV carriers have HDV co-infection, especially in IVDUs Complication: Acute liver failure Cirrhosis Investigations: anti-HDV antibody HBsAg +ve (if +ve request HDV AB also) Management: INF-alpha (limited success) May need liver transplant Prevention: HBV vaccination prevents HDV infection

Answer 282

RNA virus similar to HAV Transmitted by faecal-oral route Common in indo-china More common than HAV in UK Mortality is high in pregnancy Produces only mild illness, virus cleared within 1 month and no treatment is needed Rarely progresses to chronic hepatitis/liver failure, more so in immunocompromised pts Investigation: Anti-HEV antibody Management: Conservative Vaccine available in china

Answer 283

Pathology: Hepatic failure with encephalopathy Acute liver damage from any cause may cause massive liver cell necrosis with encephalopathy Cause: In the UK, viral hepatitis and paracetamol overdose are the most common causes Presentation: Hepatic encephalopathy Severe jaundice Severe coagulation management: Most with need specialist liver unit Emergency liver transplantation usually 80% mortality without transplant

Answer 284

Sustained inflammatory disease of the liver, lasting >6 months Principal cause worldwide is viral hepatitis HBV and HCV Viral hepatitis is also most common cause of cirrhosis and HCC ``` Causes: HBC/HDV HCV Autoimmune Drugs: methyldopa, nitrofurantoin, isoniazid, ketoconazole Hereditary: wilson’s disease IBD Alcohol ```

Answer 285

Persistence of HBsAg in serum for >6 months after acute infection Most patients clear virus after acute infection and only small % progress to chronic Progression depends on several factors: virulence of virus, immunocompetence of patient, age of patent When acquired at birth (vertical transmission) or early childhood, cellular immune response does not occur and chronic infection normally develops Risk of chronic liver disease, cirrhosis, HCC

Answer 286

Antiviral (INF-alpha, lamivudine, adefovir, entecavir, tenofovir) treatment for those with HBV DNA >20,000 IU/ml and elevated ALT Inactive HBV carrier (normal ALT and HBV DNA <2000 IU/ml) are low risk for progressive liver disease and not given antivirals

Answer 287

Rare cause of chronic hepatitis Unknown exact cause but could be genetic predisposition triggered by environment eg viral infection causing T cell mediated response against liver cells Types: Type 1; Occurs in adults. Typically women in late 40-50s. Presents around menopausal time with fatigue, features or liver disease. Takes less acute course than type 2. Type 2; Occurs in children. Teenagers or early 20s present with acute hepatitis with high transaminases and jaundice

Answer 288

Type 1 show antinuclear antibodies (ANA), anti smooth muscle AB (anti-actin), anti soluble liver antigen (anti-SLA/LP) Type 2 show anti-liver kidney microsomes-1 (anti-LKM1) and anti-liver cytosol antigen type 1 (anti-LC1) Diagnosis confirmed with liver biopsy Management: High doses of prednisolone tapered over time while immunosuppressants (particularly azathioprine) are introduced

Answer 289

Chronic inflammation of the liver and damage to liver cells When hepatocytes are damaged, they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver Fibrosis affects the structure and blood flow through the liver, causing increased resistance in vessels, leading to portal HTN Cirrhosis with encephalopathy, ascites or variceal haemorrhage = decompensated cirrhosis Cirrhosis without complications = compensated cirrhosis Pathology: Results from necrosis of liver cells followed by fibrosis and nodule formation Results in impaired hepatocyte function and gross distortion of liver Leading to portal HTN histopathology Micronodular cirrhosis: uniform, small nodules <3mm diameter caused by alcohol damage or biliary tract disease Macronodular cirrhosis: nodules of variable size caused by chronic viral hepatitis

Answer 290

``` most common Alcoholic liver disease Non alcoholic fatty liver disease Hepatitis B Hepatitis C Less common: Autoimmune hepatitis Primary biliary cirrhosis Haemochromatosis Wilson's disease alpha-1 antitrypsin deficiency Cystic fibrosis Drugs: amiodarone, methotrexate, sodium valproate ```

Answer 291

Jaundice from raised bilirubin Hepatomegaly but can shrink if more cirrhotic Splenomegaly from portal HTN Spider naevi Palmar erythema from hyperdynamic circulation Gynaecomastia and testicular atrophy in males from endocrine dysfunction Bruising from abnormal clotting Ascites Caput medusae: distended paraumbilical veins from portal HTN Asterixis Cirrhosis with encephalopathy, ascites or variceal haemorrhage = decompensated cirrhosis Cirrhosis without complications = compensated cirrhosis

Answer 292

Enhances liver fibrosis ELF blood test is first line GOLD STANDARD for non alcoholic fatty liver disease (<7.7 indicates none to mild fibrosis, 7.7-9.8 moderate, >9.8 = severe fibrosis) LFT: normal or slight elevation of ALT, AST FBC: thrombocytopenia Albumin USS to screen for nodularity. Corkscrew arteries may show from compensated reduced portal blood flow Hyponatremia indicates more severe liver disease Test for viral antibodies and antigens to screen for viral hepatitis Alpha-fetoprotein is tumor marker for HCC can check every 6 months screening in patients with cirrhosis along with USS

Answer 293

CP score to determine severity of cirrhosis and prognosis base on bilirubin, albumin, INR, ascites and encephalopathy MELD score: recommended by NICE to be used every 6 months in patients with compensated cirrhosis. Takes into account bilirubin, creatinine, INR and Na and if they need dialysis or not. Gives % estimated 3 month mortality and helps guide referral for liver transplant

Answer 294

Irreversible and progressive, manage only complications such as varices USS and alpha-fetoprotein every 6 months for HCC Endoscopy every 3 years in patients with known varices End stage cirrhosis needs liver transplant High protein, low sodium diet MELD score every 6 months

Answer 295

Malnutrition, muscle wasting Portal HTN, varices and variceal bleeding Ascites, spontaneous bacterial peritonitis Hepato-renal syndrome Hepatic encephalopathy (decline in brain function as result of severe liver disease, due to not being able to remove toxins from blood, leading to brian damage) HCC

Answer 296

occurs in liver cirrhosis. Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys. This leads to hypotension in the kidney and activation of the renin-angiotensin system. This causes renal vasoconstriction, which combined with low circulation volume leads to starvation of blood to the kidney. This leads to rapid deteriorating kidney function. Hepatorenal syndrome is fatal within a week or so unless liver transplant is performed.

Answer 297

also known as portosystemic encephalopathy. It is thought to be caused by the buildup of toxins that affect the brain. One toxin that is particularly worth remembering is ammonia, which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. There are two reasons that ammonia builds up in the blood in patients with cirrhosis: Firstly, the functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products. Secondly, collateral vessels between the portal and systemic circulation mean that the ammonia bypasses the liver altogether and enters the systemic system directly. By giving laxatives we help clear the ammonia from the gut before it is absorbed and by giving antibiotics we reduce the number of bacteria in the gut producing ammonia. Acutely, it presents with reduced consciousness and confusion. It can present in a more chronically with changes to personality, memory and mood.

Answer 298

``` Constipation Electrolyte disturbance Infection GI bleed High protein diet Medications (particularly sedative medications) ``` Management Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially. Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract. Nutritional support. They may need nasogastric feeding.

Answer 299

Usually present as result of portal HTN Most common cause of portal HTN is cirrhosis Presentation: History of alcohol abuse, drug abuse, HBV or liver disease Signs of liver disease: jaundice, telangiectasia, ascites Postural hypotension Dizziness Pallor Signs of shock: cold extremities, drowsiness etc

Answer 300

Approach is usually the same as approach to upper GI bleeding, then later diagnosed as bleeding oesophageal varices ABCDE assessment Management of shock: oxygen, IV infusion, transfusion, ITU Blood transfusion Emergency endoscopy/surgery to locate and fix bleed If stable: IV, bloods, G+S, NBM, IV infusion, clotting corrected: vit K, FFP, platelets For suspected varices: terlipressin (vasopressin) IV 1-2mg/6hr for <3 days g Broad spectrum IV antibiotics eg ciprofloxacin, tazocin (piperacillin/tazobactam) IV 4.5g/8hr Both given before endoscopy: Treated with balloon tamponade (temporary for uncontrolled bleeding) called sengstaken-blakemore tube Band ligation, sclerotherapy, fulguration, laser Danis oesophageal stent TIPS: transjugular intrahepatic portosystemic shunts causes reduction in portal pressure and collapse of varices ** Blakemore not used in MW tear due to more likely being from arterial bleeding - will put pressure on vessels witch is CI for arterial but good for venous bleeds**

Answer 301

Abnormally high pressure in hepatic portal vein Clinically significant portal HTN is defined as hepatic venous pressure >10mmHg Pathology: Portal vein comes from superior mesenteric vein and splenic vein Delivers blood to liver Liver increases resistance increases blood pressure in portal vein, increasing back-pressure in portal system (portal HTN) Causes sites where the portal system anastomoses with the systemic system to dilate and become tortuous (varices) One of these shunts is through the lower oesophageal veins, which if portal HTN is present, will dilate and come to the surface as varices Vulnerable to bleeding ``` Sites varices occur at: Gatro-oesophageal junction Ileocaecal junction Rectum Anterior abdominal wall via umbilical vein (caput medusae) ```

Answer 302

Prehepatic: blockage of vein before liver. Eg Congenital atresia or stenosis, or vein thrombosis Hepatic: cirrhosis (most common cause), chronic hepatitis, idiopathic, nodular, toxins etc Posthepatic: blockage of hepatic veins or venules eg constrictive pericarditis, right heart failure etc

Answer 303

For causes of liver disease: History of jaundice. Alcohol consumption. Blood transfusion, especially abroad; lifestyles that predispose to hepatitis B or hepatitis C. Family history - eg, Wilson's disease or hereditary haemochromatosis. For complications of portal hypertension: Haematemesis or melaena - suggest bleeding varices. Lethargy, irritability and changes in sleep pattern - suggest encephalopathy. Increased abdominal girth, weight gain - suggest ascites. Abdominal pain and fever - suggest spontaneous bacterial peritonitis. Pulmonary involvement is common in patients with portal hypertension

Answer 304

Clinical diagnosis Dilated veins in anterior abdo wall and around umbilicus (caput medusae) Splenomegaly Ascites Bloods: LFT, U+E, FBC, clotting screen USS for organomegaly, portal blood flow, thrombosis CT or MRI for vasculature if inconclusive Endoscopy for varices Indirectly measure portal pressure by hepatic venous pressure gradient (HVPG)

Answer 305

Conservative: salt restriction and diuretics Propranolol reduced portal HTN (non-selective beta blocker) or nitrates and other vasoactive drugs (terlipressin and octreotide) Shunt procedures to create anastomoses between portal and hepatic veins Treat underlying cause Liver transplant

Answer 306

Rare but potentially fatal condition characterised by transmural (complete) tear of the distal oesophageal induced by sudden increase in pressure Diagnosis made by classic triad of vomiting, abdominal pain or chest pain and subcutaneous emphysema but often this does not present Hamman’s sign: crunching sound on auscultation of heart due to pneumomediastinum Treatment can be conservation, surgical or endoscopic

Answer 307

Types: Benign: GORD, corrosives, medication, radiotherapy, endoscopic Tx of varices, post-op, prolonged NGT Malignant Webs: mucosa and submucosa only Rings: mucosa, submucosa and muscle External compression: in neck of mediastinum Schatzki’s ring: Thin circumferential ring in distal oesophagus Only involves mucosa and submucosa (should be named web) Usually appears at proximal part of hiatus hernia Cause uncertain, congenital and acquired factors eg GORD Usually presents in >50 years Chronic intermittent dysphagia to solid food Non-progressive

Answer 308

Peptic: secondary to GORD (most common) Ingestion of corrosives Medications: alendronate, iron, NSAIDs, KCl Radiotherapy Endoscopic treatment of oesophageal varices (sclerotherapy, thermal fulguration etc.) Post-op Prolonged nasogastric tube placement

Answer 309

Dysphagia (progressive worsening from solids to liquids means worsening of stricture) Heartburn Impaction of food Weight loss Chest pain Cough and wheeze from food aspiration or acid Asymptomatic (incidentally found on endoscopy or barium swallow)

Answer 310

Abdominal exam: tenderness, organomegaly, lymphadenopathy Bloods: ferritin, LFTs (ALP increase) CXR Barium swallow + endoscopy GOLD STANDARD CT Endoscopic USS (EUS) for staging or metastasis

Answer 311

``` Benign: long segment concentric and smooth tapering no shouldering no mucosal irregularity ``` ``` Malignant: short segment eccentric, irregular narrowing shouldering is seen usually associated with mucosal irregularity ```

Answer 312

Aspiration pneumonitis Complete obstruction of foods (solid food impaction) Malnutrition Bleeding or perforation from stricture dilatation

Answer 313

Benign stricture or rings: Endoscopic dilatation Endoscopic incisional therapy long term PPI reducing need for number of dilatations Malignant: Surgical excision (oesophagectomy) Radiotherapy Oesophageal stent (palliative)

Answer 314

most common cause of stricture presents with gradually worsening dysphagia treated with endoscopic dilatation and long term PI therapy Chronic GORD may also underlie development of Schatzki ring

Answer 315

ABCDE assessment intervene as needed protect airway, keep NBM insert 2 large bore IV cannula for fluid resus take bloods: FBC, LFT, glucose, clotting screen, G+S rapid IV fluid infusion Blood transfusion PRN continue fluids until stable correct clotting abnormalities (vit K, FFP, platelets) If risk of varices give Terlipressin IV 1-2mg/6hours and broad spectrum antibiotics consider referral to HDU/ICU consider CVP line for fluids (aim for >5cmH2O) catheterise and monitor UO (>30mL/hour aim) notify surgeons of severe bleeds urgent endoscopy for diagnosis and control of bleeding after adequate Jesus (urgent <24 hours, if blood clotting and patient more stable <72 hours)

Answer 316

``` PUD (35-50%) Gastroduodenal erosions 8-15% Oesophagitis 5-15% Mallor-weiss tear 15% Varices 5-15% Upper GI malignancy Vascular malformations Bleeding diathesis Swallowed blood: facial trauma, nose bleed, dental bleed, haemoptysis etc. ```

Answer 317

Haematemesis Altered bowel habit: dark tarry stools (melaena), fresh rectal bleeding Abdominal pain: typically epigastric but can be diffuse Presyncope or syncope: due to hypovolemia and secondary to cerebral hypoperfusion Hypotension/postural hypotension Tachycardia Decreased UO Signs of shock (cyanosis, cool and clammy) **Dark, clotted blood being vomited indicates bleeding is no longer active** can endoscopy within 72 hours (non-emergency) Abdominal tenderness Hematochezia: passage of fresh red blood per rectum, which can occur in context of profuse UGI haemorrhage due to rapid transit of blood through the GIT

Answer 318

``` 60< years Continued bleeding Hemodynamically unstable Liver disease or known varices Significant comorbidity ```

Answer 319

Calculated prior to endoscopy based on lab parameters Used to identify low risk patients who do not need any intervention (blood transfusion, endoscopic therapy or surgery etc.) when presenting with upper GI haemorrhage takes into account: blood urea, haemoglobin (different values men and women), systolic BP, pulse, meleana, syncope, hepatic disease, cardiac failure

Answer 320

Important to identify those at risk of ongoing bleeding and death Post endoscopy score provides most accurate risk assessment With increasing age is increased risk of death Mortality <40 years is negligible Mortality increases to 30% >90 years Patients with evidence of active bleeding and signs of shock have 80% risk of death Those with non-bleeding visible vessel at endoscopy have 50% chance or re-bleeding takes into account age, shock, comorbidities, diagnosis and major surgical history?

Answer 321

``` Alanine transaminase ALT Aspartate aminotransferase AST Alkaline phosphatase ALP Gamma-glutamyltransferase GGT Bilirubin Albumin Prothrombin time PT ``` * ALT, AST, ALP and GGT used to distinguish between hepatocellular damage and cholestasis* * Bilirubin, albumin and PT used to assess livers synthetic function* If ALT has >10 fold increase and ALP has <3 fold increase then suggests hepatocellular injury Vice versa suggests cholestasis Marked raised ALP with raised GGT strongly suggests cholestasis - without suggests non-hepatobiliary cause (bone breakdown increasing ALP instead of liver) Bilirubin >50/60 shows jaundice Unconjugated bilirubin = normal urine colour Conjugated = darker urine colour White stools = post hepatic cause ASTALT = cirrhosis and acute alcoholic hepatitis

Answer 322

ALT acute hepatocellular damage: Very high chronic hepatocellular damage: Normal or high cholestasis Normal or high ALP AHD: Normal or high CHD: Normal or high cholestasis: Very high GGT AHD: normal/high CHD: normal/high cholestasis: very high Bilirubin AHD: high/very high CHD: normal/high cholestasis: very high causes of AHD: Poisoning Infection (HAV, HBV) Liver ischaemia ``` causes of CHD: Alcoholic fatty liver Non-alcoholic fatty liver Chronic infection (HBV, HCV) Primary biliary cirrhosis Alpha-1 antitrypsin deficiency Wilson’s disease Haemochromatosis ```

Answer 323

Prothrombin time 12-13 seconds INR 0.8-1.2 (2-3 if warfarin) APTT 35-45 seconds Thrombin time 10-15 seconds ``` Anticoagulant medications will: Increase PT/INR Increase APTT Antiplatelets (clopidogrel and aspirin): Increase overall bleeding time But won’t affect PT or APTT ```

Answer 324

Hole in wall of GIT May occur anywhere from oesophagus to anorectal junction Delay in resus and definitive surgery can rapidly progress into septic shock, multi-organ dysfunction and death Needs to be first consideration during diagnosis to be excluded with acute abdominal pain Causes: Most commonly peptic ulcers and sigmoid diverticulum Chemical: PUD, foreign body Infection: diverticulitis, cholecystitis, meckel’s diverticulum Ischaemia: mesenteric ischaemia, obstructive lesions (cancers, strangulated hernia etc) resulting in bowel distension, ischaemia and necrosis Colitis: toxic megacolon (C. diff, UC) Iatrogenic: recent surgery, endoscopy, NGT insertion Trauma: high force over small surface area, shear forces from acceleration-deceleration

Answer 325

Abdominal pain Systemic symptoms: vomiting, lethargy, malaise Peritonism Oesophageal perforation: chest/neck pain may radiate to back, pain usually pleuritic, vomiting, respiratory symptoms

Answer 326

CT GOLD STANDARD (XR cannot rule out a perforation) , confirms presence of free air, location of perforation and potentially underlying cause Raised WCC + CRP Lactate Acute AXR series Pneumomediastinum/widened mediastinum if oesophageal perforation

Answer 327

ABCDE, act as needed, bloods, fluid resus etc. Antibiotics prophylaxis Surgical treatment: omental (graham) pouch used to close peptic ulcer perforation, Hartmann’s procedure to resect diverticula and thorough washout Conservative management: elderly or frail or CI for surgery or with localised perforation + peritonism with no evidence of generalised contamination on CT, usually <5mm perforation

Answer 328

Full rupture to oesophagus has mortality 50-80% Full thickness rupture of oesophageal wall If spontaneous (vomiting etc) often called Bperhaave’s syndrome Results in leaking stomach contents into mediastinum and pleural cavity, triggering severe inflammatory response, rapidly overwhelming the body Results in collapse, multi organ failure and death Causes: Two most common causes are iatrogenic (endoscopy etc) or after severe forceful vomiting Rare but mostly occur in patients with otherwise normal oesophagus

Answer 329

``` Presentation: Mackler's triad: retrosternal chest pain, respiratory distress and subcutaneous emphysema following severe vomiting or retching (actually only seen in 15% patients) Epigastric pain Back pain Dyspnea Shock ``` Investigation: Bloods: routine and G+S also CT chest abdomen pelvis with IV and oral contrast to show air/fluid in mediastinum or pleural cavity CXR evidence of pneumomediastinum or intrathoracic air fluid levels

Answer 330

Often septic and hemodynamically unstable: need septic 6 and IV fluids and blood transfuion PRN Spontaneous perforation needs immediate surgery to control leak and wash out chest (thoracotomy usually performed with on table endoscopy to determine perforation site and site of incision) Decomperess oesophagus via trans- gastric drain or endoscopically placed NGT Nutritional support - feeding jejunostomy Patients need CT scan with contrast 10-14 days before starting oral intake to check for leakage Iatrogenic perforations are often more stable than spontaneous and may be suitable for conservative management: ICU/HDU, antibiotics and antifungal cover, NBM for 1-2 weeks with NGT insertion for drainage Total parenteral nutrition (TPN) or feeding jejunostomy insertion Chest drain

Answer 331

Transmural Oesophageal rupture secondary to forceful vomiting and/or retching Thought to occur due to forceful ejection of gastric contents in unrelaxed oesophagus against closed upper cricopharyngeus Risk factors: Male Alcoholism ``` Presentation: Mackler’s triad: vomiting, chest pain, subcutaneous emphysema (only actually seen in 15% cases) Epigastric pain Back pain Dyspnea Shock ``` Treatment: Surgery gold standard Conservative methods like oesophageal stenting can be used also

Answer 332

``` Can be upper (oesophagus, stomach or duodenum) Or lower (intestines, rectum or anus) All will need PR exam ``` ``` Common causes of upper GI bleeding: Peptic ulcers Oesophageal varices Mallory weiss tears Oesophagitis (most often from GORD) ``` ``` Common causes of LGIB: Diverticular disease IBD Tumours Colon polyps Haemorrhoids Anal fissues Proctitis ```

Answer 333

``` Presentation of UGIB: Haematemesis Coffee ground vomiting Abdominal pain Meleana - black tarry stools Significant blood loss: pale, weak, dizzy, syncope, SoB Raised urea (blood digestion) ``` Investigations: Glasgow-Blatchford score GBS for low and high risk Takes into account, haemoglobin, BUN, systolic BP, sex, HR, meleana, syncope, hepatic disease history and cardiac failure ``` Management: ABCDE IV fluids ad bloods taken Blood transfusion PRN IV PPI pantoprazole 40mg Endoscopy to directly inject medicine, cauterise ulcer or clam/clip off bleeding vessel ```

Answer 334

Rectal bleeding Abdominal pain Significant blood loss: pale, weak, dizzy, SoB ``` management: Based on underlying cause If unknown: CT with contrast/colonoscopy IV fluids to maintain BP Blood transfusion PRN ```

Answer 335

Effects of long term excessive consumption of alcohol on the liver Onset and progression varies May be genetic predisposition to harmful effects of alcohol on the liver Recommended alcohol consumption: 14 units/week (no more than 5 in one day, spread evenly over >3 days) Progression: Alcohol related fatty liver: drinking leading to build up of fat in the liver. If stopped, process is fully reversible within around 2 weeks. Alcoholic hepatitis: alcohol over a long period causes inflammation in the liver. Binge drinking is associated with the same effects. Mild cases are usually reversible with permanent abstinence. Cirrhosis: many hepatocytes replaced with scar tissue. Function impaired, portal HTN likely. Irreversible changes. Drinking cessation can prevent further damage while continuing has very poor prognosis

Answer 336

``` Jaundice Hepatomegaly Spider naevi Palmar erythema Gynaecomastia Bruising Ascites Caput medusae Astrexis ``` ``` Investigations: Bloods: FBC, LFTs, clotting screen, U+Es USS/fibroscan Endoscopy CT and MRI Liver biopsy to confirm ```

Answer 337

Alcohol cessation Detox regimen (benzodiazepine given every 1-4 hours for 5-7 days, IV high dose B vitamins, pabrinex, and low dose oral thiamine after) Nutritional support (thiamine and vitamins) and high protein diet Steroids for short term Treat complications Liver transplant ``` Alcohol withdrawal: 6-12 hours: tremor, sweating, headache, craving, anxiety 12-24 hours: hallucinations 24-48 hours: seizures 24-72 hours: delirium tremens ```

Answer 338

Part of metabolic syndrome group of chronic health conditions relating to increased risk of heart disease, stroke and diabetes Estimated up to 30% adults have this Characterised by fatty deposits in hepatocytes interfering with function Asymptomatic initially but can progress to hepatitis and cirrhosis ``` Stages: Non-alcoholic fatty liver disease Non-alcoholic steatohepatitis Fibrosis Cirrhosis ```

Answer 339

``` Obesity Poor diet and low activity Type 2 diabetes High cholesterol Middle age< Smoking High blood pressure ``` ``` Investigations: USS of liver Hepatitis B and C serology Autoantibodies (ANA, SMA, AMA, LKM-1) Immunoglobulins Caeruloplasmin (wilson’s disease) Alp1 antitrypsin Ferritin and transferrin saturation ```

Answer 340

Weight loss Exercise Smoking cessation Control of diabetes, blood pressure and cholesterol Avoid alcohol Liver fibrosis can refer to specialist for vitamin E or pioglitazone treatment

Answer 341

Excessive accumulation of copper in the body and tissues Caused by mutation in wilson disease protein on chromosome 13 Autosomal recessive disease ``` Presentation: depending on where copper deposition is most predominant: Hepatic problems (40%) Neuro problems (50%) Psychiatric problems (10%) Kayser-fieischer rings in cornea (brown rings around iris) Haemolytic anaemia Renal tubular damage Osteopenia ```

Answer 342

Investigations: Clinical exam: kayser-fleischer rings, physical signs of liver disease etc Gold standard is serum ceruloplasmin - low suggestive of Wilson’s disease (not specific) Liver biopsy 24 hour urine copper assay MRI brain changes Management: With copper chelation using: Penicillamine Trientene

Answer 343

``` Clinical via history taking Abdominal exam/PR exam H pylori testing (antigen, breath) Endoscopy Barium swallow and AXR ```

Answer 344

``` Acute causes: H pylori Alcohol NSAIDs Stress Bile acid reflux (usually post surgical) ``` ``` Chronic: Chronic h pylori infection Crohn’s Sarcoidosis Autoimmune (atophic) ```

Answer 345

Idiopathic chronic inflammation of the colon, follows course of relapse and remission Most common form of inflammatory bowel disease Peak incidence in late adolescence and early adulthood Can be associated with extraintestinal symptoms occasionally More often see GI bleeding Presents with diffuse continuous involvement of mucosa Occurs in 8-15 people per 100,000 Characterised by remissions and exacerbations Likely autoimmune condition triggered by colonic bacteria causing GI inflammation

Answer 346

Distal disease: left sided colitis, colitis confined to the rectum and sigmoid colon More extensive disease includes left sided colitis (up to splenic flexure), extensive colitis (up to hepatic flexure) and pancolitis (affecting whole colon) Patients with pancolitis may have involvment of terminal ileum due to incompetent ileocecal valve

Answer 347

Bloody diarrhea Colicky abdominal pain Urgency or tenesmus (feeling of incomplete emptying of bowels) Disease limited to rectum may present with constipation and rectal bleeding Malaise, fever Weight loss Tachycardia, hypotension, febrile, dehydrated Erythema nodosum Episcleritis Ankylosing spondylitis Primary sclerosing cholangitis

Answer 348

Clinical history Bloods: FBC, renal function, U+Es, LFTs, ESR, CRP, iron studies, B12, folate Faecal calprotectin to differentiate between IBS C difficile testing Colonoscopy and biopsy to confirm CT, MRI Barium fluoroscopy

Answer 349

Disease severity: Subacute: moderately to severe active ulcerqative colitis that would normally be managed in outpatient setting and does not need hospitalisation or urgent surgical intervention Mild: fewer than four stools daily, no more than small amount of blood in stools, no anaemia, pulse rate <90, no fever and normal ESR and CRP Moderate: 4-6 stools daily with more blood in stool. No anaemia, pulse rate <90, no fever, normal ESR and CRP Severe: 6+ stools dailys, visible blood in stools, at least one feature of systemic upset (fever, pulse >90, anaemia, ESR and CRP raised) Indications for hospital referral: Severe colitis Moderate disease fail to respond to steroids within 2 weeks Respond partially to treatment should be seen urgently in outpatient setting treated for refractory colitis Indications for surgery: Severe abdominal pain and fever should raise concern of toxic megacolon or fulminant colitis Haemorrhage Elective surgery for intractability, complications of med therapy, cancinomas

Answer 350

Inducing remission: Mild to mod 1st line aminosalicylate (mesalazine) oral or rectal 2nd line corticosteroids (prednisolone) Severe: 1st line IV corticosteroids (hydrocortisone) 2nd line IV ciclosporin Maintaining remission: Aminosalicylate (mesalazine) oral or rectal Azathioprine Mercaptopurine Panproctocolectomy (removing colon and rectum) and permenant ileostomy or ileo-anal anastomoses (J pouch) where ileum is folded back on itself into larger pouch that functions like a rectum, collecting stools prior to person passing the motion

Answer 351

Herniation of part of abdominal viscera through oesophageal aperture of the diaphragm Vast majority of them only involve herniation of the gastric cardia through hiatal aperture Rarely hernias with a large defect can allow other organs to enter the thoracic cavity, such as the spleen and pancreas Over half peoples with reflux esophagitis have been found to present with hiatus hernia Cause: Widening of oesophageal hiatus Pulling up of stomach due to oesophageal shortening Pushing up of stomach by increased intra-abdominal pressure Acid reflux barrier is lost, the larger then hernia the more impaired the clearance of acid (thereby exacerbates GORD)

Answer 352

Sliding hiatus hernia: gastro-oesophageal junction slides up into thoracic cavity (85-95% cases) Para-oesophageal (rolling) hiatus hernia: gastro-oesophageal junction remains in place, but part of the stomach herniates into chest next to the oesophagus (5-15% cases) Many are mixed presentation Alternative classifications: Type I: sliding; GOJ migrates above diaphragm. Stomach remains in longitudinal alignment and fundus below the GOJ Type II: pre paraesophageal hernias; GOJ remains in normal place, portion of fundus herniates through hiatus Type III: combination of I and II; both GOJ and fundus herniate through hiatus. Fundus superior to GOJ Type IV: structures other than stomach (omentum, colon, small bowel) lie within hernia sac

Answer 353

``` Obesity Pregnancy Ascites Genetic predisposition Previous gastro-oesophageal surgery Trauma to chest or abdomen Skeletal deformities such as scoliosis, kyphosis and pectus excavatum ```

Answer 354

``` Exacerbation of GORD symptoms Volvulus or ischaemia symptoms Retrosternal burning (heartburn) especially on bending or lying down Reflux Dysphagia Can be asymptomatic Chest pain Epigastric pain Excessive fullness Nausea ```

Answer 355

CXR Barium studies Endoscopy Oesophageal manometry Management: Lifestyle: avoid increase in intra-abdominal pressure (tight clothes), raise head of bed at night, avoid eating <3 hours before bed, weight loss, smoking cessation, alcohol avoidance PPIs usually needed long term Surgical: laparoscopic fundoplication or gastropexy

Answer 356

ABCDE assessment and act accordingly History: how much, when, what route of administration, has there been vomiting, past medical history, current medications and allergies, suicide note/suicide risk, third party history for context Cardio, respiratory, abdominal, neurological examinations Vital signs: temperature, pupils, BP, HR Muscle rigidity Skin - cyanosis (methaemoglobinaemia), very pink (carboxyhaemoglobinaemia, cyanide, hydrogen sulphide), blisters (barbiturates, tricyclic antidepressants (TCAs), benzodiazepines), needle tracks, hot/flushed (anticholinergics). Breath - ketones (diabetic/alcoholic ketoacidosis), 'bitter almonds' (cyanide), 'garlic-like' (organophosphates, arsenic), 'rotten eggs' (hydrogen sulphide), organic solvents. Mouth - perioral acneiform lesions (solvent abuse), dry mouth (anticholinergics), hypersalivation (parasympathomimetics)

Answer 357

ABCDE: Eyes (dilated pupils indicate tricyclics, cocaine, amphetamine; pinpoint pupils indicate opiates; nystagmus indicates alcohol, benzodiazepines, phenytoin) Breath (bitter almond smell of cyanide indicates alcohol or organic solvents) burns around mouth (corrosive substances like paraquat, glue) hyperventilation (salicylates) needle marks (recreational drug abuse) Identify substance: if pt is unconscious, third party evidence of what has been taken. Time of ingestion, associated alcohol consumption, past and current medical history (esp if renal or liver disease), symptoms noticed since poisoning (vomiting may have removed some substance already, hematemesis caused by iron overdose, salicylates, alcohol) Elimination: activated charcoal (decontamination) decreases absorption within 1 hr of digestion (preferred), antidote administration, gastric lavage (no longer recommended due to aspiration risk; only indicated in life threatening amount ingested within previous hr and poison cannot be removed via other methods. May be useful for drugs such as lithium and iron which aren’t charcoal absorbed), dialysis (peritoneal, haemodialysis), diuresis (alkaline, acid change urinary pH to increase substance excretion in urine) whole bowel irrigation (when substance would not be absorbed by activated charcoal) Specific and general treatment of pt condition Period of observation Psychiatric assessment

Answer 358

Given for certain poisons which can either prevent poison working or reverse it’s effects Glucagon injection for insulin and beta-blockers N- acetylcysteine for paracetamol Flumazenil for Benzodiazepines Fab fragments for Digoxin Naloxone for opiates Ethyl alcohol for methanol overdoses

Answer 359

Ataxia, dysarthria, nystagmus, and drowsiness, which may progress to coma, with hypotension and acidosis. managed supportively, maintaining clear airway, reduce risk of aspiration of gastric contents, blood glucose monitoring and administration if needed

Answer 360

Hyperventilation, tinnitus, deafness, vasodilation, sweating, coma (very severe) Monitor plasma salicylate, pH and electrolytes Activated charcoal <1hour ingestion if >125mg/kg aspirin taken Replace fluid losses and correct electrolyte imbalances

Answer 361

Coma, respiratory depression and pinpoint pupils, nausea and vomiting Naloxone injection or infusion. Short half life (might only last for 15-20 minutes) so must be monitored for top up or continuous doses if needed Administration of IV used for rapid diagnosis of opiate poisoning. Should show significant improvement in condition within 1-2 mins Monitor for aspiration of vomit, monitor pupils, RR, BP, sepsis, signs of hep B/C or HIV screen if indicated (drug users etc)

Answer 362

``` Hepatocellular necrosis (indicated by right subcostal pain and tenderness) Nausea and vomiting ``` ``` Acetylcysteine reduced severity of liver damage if given <24 hours ingestion Monitor for signs of liver failure Given by IV 150mg/kg initial dose 50mg/kg over next 4 hours 100mg/kg over next 6 hours ``` Side effects: anaphylaxis Hypotension Rash Nausea and vomiting Only given if over paracetamol level threshold due to side effects so must take bloods first 100mg/l at four hours after ingestion is toxic

Answer 363

Tricyclic antidepressants Dry mouth, coma, hypotension, hypothermia, hyperreflexia, extensor plantar responses, convulsions, respiratory failure, cardiac conduction defects, dilated pupils, urinary retention, hallucinations, delirium and confusion ``` Supportive measures to clear airway IV lorazepam or diazepam for convulsions Activated charcoal <1 hour Correct hypoxia and acidosis Monitor cardiac activity ``` SSRIs Nausea, vomiting, agitation, tremor, nystagmus, drowsiness, sinus tachycardia, convulsions, can cause QT prolongation Supportive: guard airway if vomiting, ensure patient safety and take good history of if anything else has been taken Activated charcoal <1 hour Convulsions treated with lorazepam, diazepam

Answer 364

Drowsiness, ataxia, nystagmus, respiratory depression, coma Flumazenil injection Reverses CNS and respiratory depression. However if person has also taken tricyclic antidepressant or has epilepsy must be cautions as can cause seizures or arrhythmias Activated charcoal <1 hour

Answer 365

Bradycardia, hypotension, syncope, heart failure, conduction abnormalities ``` Maintain airway, supportive care Unclear benefit but can give charcoal <1 hour Fluid resuscitation Vasopressors and inotropes Glucagon for severe hypotension Sodium bicarb for metabolic acidosis ```

Answer 366

Nausea, vomiting, dizziness, agitation, confusion, coma, hypotension Charcoal <1 hour Calcium chloride or calcium gluconate injections Atropine sulfate to correct bradycardia

Answer 367

Apathy, restlessness, vomiting, diarrhea, ataxia, weakness, dysarthria, muscle twitching, tremor Gastric lavage <1 hour Whole bowel irrigation considered for significant ingestion Seek advice from national poisons info service

Answer 368

Preventing absorption Renal clearance Hepatic clearance Preventing absorption: Activated charcoal: Repeated doses of charcoal are given after overdose with: Carbamazepine Dapsone Phenobarbital Quinine Theophylline *vomiting may reduce effectiveness *should NOT be used with petroleum distillates, corrosive substances, alcohols, malathion, cyanides and metal salts (Fe and lithium) (not doing anymore) - emesis and gastric lavage Promotion of renal clearance: IV fluids Alkalinisation of urine Administer sodium bicarbonate for salicylates Hemodialysis for ethylene glycol, lithium, methanol, phenobarbital, salicylates, sodium valproate Hepatic elimination: Not generally exploited in overdose management due to the liver being post-intestinal so most substance would be absorbed into the body by then Main strategy is promotion of renal clearance