Year 3 revision - chapter 2 Flashcards
What are the features of diverticular bleeding?
A diverticular bleed is abrupt and of significant volume, but settles in 80% of cases.
What antibiotics would you use for diverticulitis?
NotesRecent trials have suggested that antibiotic therapy may not be required for patients with mild abdominal pain and tenderness who do not have significant systemic signs or symptoms.Antibiotics should be considered in patients with signs of diverticulitis who have markers of systemic involvement (eg fever, elevated white cell count), or in patients who have failed to respond to conservative management.Remember that Tazocin and Timentin cover G+, G-, enterococci and anaerobes
How common are diverticula?
50% of people over age 50
What symptoms would make you worry/further investigate a patient with diagnosed irritable bowel syndrome?
Pain associated with anorexia, malnutrition, or weight loss.Pain that is progressive, awakens the patient from sleep, or prevents sleep.
What is the difference between a gastric erosion and a gastric ulcer?
PUD is classified as a break in the mucosal lining of the stomach or duodenum > 5mm in depth* involving the SUBMUCOSA.(* note that erosions differ from ulcers in that they are
What are the 2 most important causes of peptic ulcer disease?
Helicobactor pylori infectionNon-steroidal Antiinflammatory drugs (NSAIDs)
What are the features of pain caused by gastric/duodenal ulcers?
Chronic/recurrent abdominal pain or discomfort around epigastriumDuodenal ulcers: abdominal pain may be severe and radiate to the back as a result of penetration of the ulcer posteriorly into the pancreas..The “classic” pain of duodenal ulcers (DU) occurs when acid is secreted in the absence of a food buffer. Food is usually well emptied by two to three hours after meals, but food-stimulated acid secretion persists for three to five hours; thus, classic DU symptoms occur two to five hours after meals. Symptoms also classically occur at night, between about 11 PM and 2 AM, when the circadian stimulation of acid secretion is maximal.Painwhich is worse between meals or in the middle of the night, and eased by eating (= duodenal ulcer)Pain which is aggravated by eating (= gastric ulcer)
What investigations are appropriate for peptic ulcer disease?
FBELook for anaemiaEndoscopy (+/- Biopsy)Do if ‘red flag’ symptoms –>upper GI cancerWeight loss/bleeding/anaemia/vomiting/early satiety/dysphagiaBiopsy the edge of the ulcer to DDx between simple ulcer and gastric adenocarcinomaH pylori testingIn the absence of ‘red flag symptoms’H pylori breath/stool antigen testsH Pylori serologyTests may give FALSE NEGATIVE results in patients taking PPI’s, bismuth or other medications.Switch to H2 antagonists before test
What is Zollinger-Ellison syndrome?
A rare disorder caused by a gastrin-secreting tumor found in either the islet cells of the pancreas or in the duodenal wall. The release of gastrin stimulates the production of large quantities of HCL in the gastric antrum leading to predominant distal (duodenum) ulceration.
What are the causes of haematemesis?
Very common * gastric ulcer/erosion * duodenal ulcer/erosion Common: * Mallory Weiss tear * ulcerative oesophagitis * oesophageal varices -->emergency Uncommon : * AVM (arteriovenous malformations) * Cancer * GIST * Aorto-enteric fistula
What is the epidemiological relationship between cirrhosis, varices and death?
30% of cirrhotics have varices30% of varices haemorrhageVariceal haemorrhage has up to 30% mortality (depends on severity of liver disease)
What are the causes of haematochezia?
Under 40 years Common * Haemorrohoids * Anal fissure * IBD Less common * Polyps * Infective colitis * Meckels diverticulum * Intussusception Rare * Colorectal cancer Over 40 years age * Haemorrhoids * Anal fissures * Colorectal cancer * Colorectal polyps (mostly adenomatous) * Angiodysplasia * Diverticular disease * Inflammatory bowel disease * Colitis – ischaemic, infective, post-radiation
What are the causes of acute hepatitis?
Bacterial * Q fever * Typhoid * Syphilis Viral * Hepatitis A, B, C * Cytomegalovirus (CMV) * EBV * HSV Autoimmune * SLE * Autoimmune hepatitis Drugs (include but not limited to) * Amoxicillin-Calvulanic Acid (Augmentin) * Paracetemol (AST often rises above 5000) * Anti-Tuberculosis medications * Trimethoprim-sulfamethoxazole (Bactrim) * Minocycline * Nitrofurantoin
Who does auto-immune hepatitis usually affect?
females in second and third decade of life
What is the clinical picture of autoimmune hepatitis?
Onset may be insidious or acute. Can be anywhere from asymptomatic to fulminant hepatic failure.Symptoms are non-specific but may include:
* Fatigue/Malaise
* Nausea / Anorexia
* Abdo pain
* Jaundice/pruritis
* Signs of chronic liver disease, especially spider naevi and hepatospenomegaly
* Amenorrhea
* Rheumatological or thyroid complaints
Exam findings can range from a normal to the presence of hepatomegaly, splenomegaly, stigmata of chronic liver disease, and/or deep jaundice (rare).At the far end of the spectrum are those patients who present with an acute, sometimes fulminant picture characterized by profound jaundice, an elevated prothrombin time, and aminotransferase values in the thousands.
What antibodies are associated with type 1 and type 2 autoimmune hepatitis?
Type 1 * antinuclear antibodies (ANA) * anti-smooth muscle antibodies (ASMA) Type 2 * anti-liver-kidney microsome-1 antibodies (ALKM-1) and * anti-liver cytosol antibody-1 (ALC-1)
What is the management and prognosis of autoimmune hepatitis?
Management
* Patients have 45% chance of progression to cirrhosis
* The benefit of corticosteroids in asymptomatic patients with only histologic features is not clear (relatively few studies have elucidated the natural history of AIH in such patients) If decide to treat
* High-dose prednisolone (30-50mg/day for 6 weeks then titrate down)
* Add azathioprine as a steroid sparing agent to reduce AEs of steroids
* As a general rule, treatment should be continued until remission, treatment failure, or the development of drug toxicity
* Following steroid withdrawal, 75% of patients relapse.
Prognosis
* Can be severe: 40% mortality at 6 months without treatment.
* Appropriate management can improve quality of life, prolong survival, and delay the need for liver transplantation.
* The life-expectancy of treated patients is similar to age- and gender-matched controls in patients who have been followed for up to 20 years
How contagious is Hep A?Who becomes symptomatic?
Highly infectiousFaecal-oral routeMost infections in adults are symptomatic, whereas 70% of infections in children younger than 6 years, who are also the key reservoir for transmission, are asymptomatic
What test do you use for Hep A?
Anti HAV IgM and IgG (positive for 5-10days before symptoms)
What is the management and prognosis of Hep A?
ManagementUnvaccinated people with recent exposure to hepatitis A (Symptomatic patients = Supportive care + bed restRarely, hospitalisation may become necessary for volume depletion, coagulopathy, encephalopathy, or severe prostration. This is particularly important in patients with co-infection with hepatitis B virus, hepatitis C virus, or cirrhosis of any cause, as acute hepatitis A virus (HAV) infection in these conditions has a higher risk for severe disease.In Prompt referral to centres experienced in liver transplantation is warranted in such cases.Prognosis≈85% have full clinical and biochemical recovery within 3-monthsnearly all individuals recover within 6 months10% to 20% of symptomatic patients –>prolonged and relapsing course lasting several months with persistent fever, pruritus, diarrhoea, jaundice, weight loss, and malabsorptionReported case fatality is 0.6% - 1.5% depending on age.
How is Hep B transmitted?
Body fluidsNeedlstick/sharing needlesSTI (semen)Mother to baby
What is the natural history of Hep B?
Most healthy adults (90%) who are infected will recover and develop antibodies against future hepatitis B infections. 5-10% will be unable to get rid of the virus and will develop chronic infections.This is not true for infants and young children – 90% of infants and up to 50% of young children infected with hepatitis B will develop chronic infections. Therefore, vaccination is essential to protect infants and children.Approximately 70% of patients with acute HBV infection are asymptomatic.About 30% of adults with acute HBV may have symptomatic icteric hepatitis.Patients who develop chronic HBV have a 10% to 30% risk of developing cirrhosis
What tests constitute Hep B serology and how do you interpret them?
What is the management of Hep B infection?
Acute = supportive careChronic
- Treatment is recommended in patients who are HBeAg-positive, with HBV DNA levels >20,000(IU)/mL
- Give pegylated interferon or antiviral monotherapy (tenofovir)
- The endpoint of treatment is seroconversion from HBeAg positive to HBeAg negative, with production of HBeAb.
How is Hep C spread?
Transmission is blood born only (very low risk of transmission from sexual activity.) In rare occasions can spread from mother to baby.
What is the natural history of Hep C?
What tests can you order for Hep C?
Anti-HCV antibodies(However this doesnt tell you if you’re in the lucky 15% who cleared the infection)Active infection is confirmed by the presence of serum hepatitis C RNA in anyone who is antibody-positive
When is US usually diagnosed?When is Crohn’s usually diagnosed?
UCMost patients are aged 20 to 40 years at diagnosis. Another peak occurs at age 60.CrohnsThe peak age of onset is between 15 and 40 years, and there is a smaller second peak between 60 and 80.
What are the causes of jaundice?
What tumour marker can be used for pancreatic cancer?
CA19-9
What are the causes of pancreatitis?
Explain the significance of calcium in pancreatitis?
The lipase released in pancreatitis breaks down the fat laden mesentery (ommentum), to form fatty acids. Fatty acids then combine with calcium (a ubiquitous component in the intercellular fluid) to form a chalky/soapy pancreas (fat necrosis, fat saponification). This process –>hypocalcaemia.
What is the clinical picture of pancreatitis?
Severe, constant upper abdominal pain that radiates to the back in 65% of cases builds up over 15-60 minutes.The pt will be learning forward in attempt to alleviate retroperitoneal pain.Nausea, vomiting, anorexia and tachycardia are common.
What do you find on examination in pancreatitis?
There is marked epigastric tenderness, but in the early stages guarding and rebound tenderness are absent because the inflammation is principally retroperitoneal.Bowel sounds become quiet or absent as paralytic ileus develops.In some cases, the patient becomes hypoxic and develops hypovolaemic shock with oliguria.Oedema and discolouration of the flanks (Grey Turner’s sign), the periumbilical region (Cullen’s sign) or over the inguinal ligament (Fox’s sign) is a feature of pancreatitis with haemorrhage. These are exceptionally rare signs.Abdominal distension is another common feature of pancreatitis.
What are some bedside tests for hypocalcaemia?
What key things do you need to keep in mind when interpreting amylase/lipase results?
- The amylase needs to be 3x the upper limit of normal to be pancreatitis, but it is usually much higher than this.
- Amylase is efficiently excreted by the kidneys, and serum concentrations may return to normal within 24-48hours.
- For diagnosis after this time, Lipase remains raised for 7-10 days.
- Serum amylase does not rise as much in hypertriglyceride pancreatitis.
- A lipase to amylase ratio of greater than 5 favours alcoholic pancreatitis rather than gallstone.
- Levels of serum amylase and lipase does not indicate severity.
- Serum amylase is not specific for pancreatitis, elevations can occur in anyone with small bowel obstruction, mesenteric ischaemia, renal insufficiency or tubo-ovarian disease.
What is the best imaging modality for pancreatitis?
USSMay show pancreatic inflammation, peri-pancreatic stranding, calcifications, or fluid collections. Use limited as bowel gas obstructs the pancreas 25-35% of the time. Sensitivity in detecting pancreatitis is 62% to 95%. Useful when biliary causes are suspected.CTCan be done to exclude other options if diagnosis ambigous. Will not show signs specific to pancreatitis for 72hours because the complications (e.g. necrosis of the tissue) that show on CT take some time to form.
How do we assess the severity of pancreatitis?
What is a dermoid cyst?
A dermoid cyst is a cystic teratoma that contains an array of developmentally mature, solid tissues. It frequently consists of skin, complete with hair follicles, and sweat glands. Other commonly found components include: clumps of long hair, pockets of sebum, blood, fat, bone, nails, teeth, eyes, cartilage, and thyroid tissue.
Where do venous, arterial and neuropathic ulcers typically occur?
Venous- anywhere from maleoli to kneeArterial -Location over prominent osseous areas and other areas where there is a potential for pressure and skin shearing including between the toes, on the tips of toes, over phalangeal heads, at the lateral malleolus, or sites subjected to repetitive trauma such as contact points with footwear.Neuropathic -Location at areas of repeated trauma such as the plantar metatarsal heads or dorsal interphalangeal joints
What is the appearance of arterial vs venous ulcers?
What features are typically associated with venous ulcers?
- Leg is warm, normal pulses
- Varicose veins Haemosiderin staining
- Results from extravasation of blood and deposition of haemosiderin in the tissues due to longstanding ambulatory venous hypertension Atrophie Blanche
- White scarred areas surrounded by tiny red spots (enlarged capillaries) Lipodermatosclerosis
- Inflammation of the subcutaneous fat due to CVI. Characterised by woody induration (hardened), thickened and scaly skin. Venous Eczema
- A collective term for lipodermatosclerosis, haemosiderin deposition and athrophie blanche all caused by CVI
What are some differences between arterial and venous ulcers?
What is this?What is the management?
Seborrhoeic keratoses can easily be removed. The usual reason for removing a seborrhoeic keratosis is your wish to get rid of it.Methods used to remove seborrhoeic keratoses include:
- Cryotherapy(liquid nitrogen) for thinner lesions
- Curettage & cautery
- Laser surgery
- Shave biopsy(shaving off with a scalpel)
What are the gross features of melanoma?
ABCDE Signs and SymptomsAsymmetry (is one half different to the other?)Border (regularity, scalloped, poorly defined?)Colour (what colour? >1 colour?)Diameter (> or Elevation / Evolution (is it raised? Is it evolving?)Firm to touchGrowing progressively over more than a month (evolution)May also bleed and ulcerate.
What are the gross features of basal cell carcinoma?
“If you can see telangiectasia, non-healing chronic wound / scar and a pearly, white colour when stretched, you know it is a BCC”
- slow-growing
- translucent, pearly white when stretched
- telangiecasia
- papule/nodule
- focal ulceration
- raised, rolled edge
- on the face of the elderly
What are the features of a squamous cell carcinoma?
“SCC looks like a red, ulcerated/bleedingor scaly papule, likea non-healing ulcer.”
* Quickly growing (over a few months)
* Painful
* Hyperkeratotic
* Usually nodular
* Crusting, ulceration, scaly, formation of a cutaneous horn
* May be friable and bleed easily and located on sun exposed areas
* Indurated/hard
What margins should be used for different melanomas?
In situ melanoma (level 1, 5mm, just in the epidermis): 5mmMelanoma Melanoma 1-4mm: 1-2cmMelanoma >4mm: 2cm
