GIT, pancreas, liver and biliary tract Flashcards
Conjugated hyperbilirubinaemia results from which of the following options?
A Gilbert’s syndrome
B Excess production of bilirubin
C Cholestasis
D Decreased hepatic uptake
C
Explanation
Conditions which lead to an obstruction of the biliary ducts, both intra-hepatic and extra-hepatic, and a decrease in excretion of bilirubin glucuoronides will lead to conjugated hyperbilirubinaemia. Hereditary conjugated hyperbilirubinaemia syndromes include Dubin Johnson and Rotor syndrome
In relation to jaundice, which of the following statements is correct?
A In unconjugated hyperbilirubinaemia, bilirubin is tightly bound to albumin
B Unconjugated bilirubin does not colour the sclera
C Unconjugated bilirubin produces bilirubin in the urine
D Conjugated bilirubin produces kernicterus in adults
A
Explanation
Unconjugated bilirubin is insoluble and tightly bound to albumin. It cannot be excreted in the urine but is deposited in tissues giving rise to the yellow discolouration of the skin and sclera. Haemolytic disease of the newborn may lead to the accumulation of unconjugated bilirubin in the brain, which can cause severe neurological damage called kernicterus. Conjugated bilirubin is soluble and loosely bound to albumin
Which is the most common route of Hepatitis C transmission?
A Multiple sex partners
B IVDU
C Employment in medical or dental fields
D Having surgery within the last six months
B
Explanation
IVDU drug abuse 54%
Multiple sex partners 36%
Having surgery within the last six months 16%
Needle stick injury 10%
Multiple contacts with a HCV infected person 10%
Employment in medical or dental fields 1.5%
Unknown 32%
Which of the following statements is correct regarding hepatic failure?
A It has a mortality of <10%
B It is not associated with ascites
C It occurs with loss of functional liver capacity of approximately 60%
D Encephalopathy is a result of decreased ammonia breakdown
D
Explanation
Whatever the cause, 80-90% of hepatic function must be eroded before hepatic failure ensues. Overall mortality from hepatic failure is 70-95% (Current textbook says 80% mortality). Clinical features include jaundice, cerebral compromise due to hyperammonaemia as a result of impaired liver function and of shunting blood around the liver (muscle wasting-a common feature in liver disease patients can also contribute to increased levels of ammonia as muscle is an important site for the extrahepatic removal of ammonia), foetor hepaticus, ascites, palmar erythema, spider angiomata, gynaecomastia and hypogonadism
Note: Ammonia formation is not increased in liver failure. Encephalopathy is due to decreased hepatic breakdown of ammonia
Regarding liver failure, which of the following statements is correct?
A Has a 20-40% mortality
B Can be caused by tetracyclines
C Is not associated with ascites
D Rarely results from cirrhosis
B
Explanation
Whatever the cause, 80-90% of hepatic function must be eroded before hepatic failure ensues. Overall mortality from hepatic failure is 70-95%. Clinical features include jaundice, cerebral compromise due to hyperammonaemia as a result of low albumin levels, foetor hepaticus, ascites, palmar erythema, spider angiomata, gynaecomastia and hypogonadism. The ultimate mechanism of most cirrhotic deaths is progressive liver failure. Tetracyclines can produce idiosyncratic reactions including liver failure.
With regard to jaundice, which of the following options is correct?
A Unconjugated hyperbilirubinaemia will result in bilirubin in the urine
B Conjugated bilirubin is tightly bound to albumin
C Unconjugated bilirubin is tightly bound to albumin
D Unconjugated bilirubin does not colour the sclera
C
Explanation
Unconjugated bilirubin is insoluble and tightly bound to albumin. It cannot be excreted in the urine but is deposited in tissues giving rise to the yellow discolouration of the skin and sclera. Haemolytic disease of the newborn may lead to the accumulation of unconjugated bilirubin in the brain, which can cause severe neurological damage called kernicterus. Conjugated bilirubin is soluble and loosely bound to albumin
Which of the following does not cause fatty liver?
A Smoking
B Obesity
C Protein malnutrition
D Alcohol
A
Explanation
Alcohol, obesity, vitamin A deficiency, starvation, diatetes mellitus (DM), corticosteroids, poisons (carbon tetrachloride and yellow phosphorus), Cushing’s syndrome, and hyperlipidaemia are some of the cause of fatty liver. Microvesicular fatty liver may be caused by valproic acid toxicity, high-dose tetracycline or during pregnancy.
Regarding cirrhosis of the liver, which of the following statements is correct?
A The left lobe of the liver is most affected
B The Ito cell is a major source of excess collagen
C Fibrosis is confined to the delicate bands around central veins
D Vascular architecture is preserved
B
Explanation
Cirrhosis is defined by three characteristics: fibrous septa (collagen depostion), parenchymal nodules and disruption of the architecture of the liver. Vascular architecture is reorganised by the parenchymal damage and scaring. The major source of excess collagen in cirrhosis appears to be perisinusoidal hepatic stellate cells (Ito cells). The right lobe is bigger and thus more affected.
Which of the following statements is correct regarding oesophageal varices?
A Lie primarily in the middle portion of the oesophagus
B Additional instances of haemorrhage occur in over 50% within one year
C Occur in approximately one third of all patients with cirrhosis
D Are most often associated with cirrhosis due to hepatitis C
B
Explanation
Current TB
Oesophageal varices are present in nearly half of patients with cirrhosis and 25-40% of these develop variceal bleeding. Approximately 12% of previously asymptomatic varices bleed each year. Despite any intervention, 30% or more patients with variceal haemorrhage die as a direct consequence of haemorrhage. Furthermore, 50% of patients who survive the first variceal bleed will have another one within a year and this carries a mortality rate similar to the first bleed
Older edition
Oesophageal varices occur in 90% of cirrhotic patients (GIT chapter), especially when the condition is due to alcohol. Varices account for less than half of the cases of haematemesis. Hepatitis C bears a small association as some cases develop cirrhosis. The varices lie primarily in the lower portion of the oesophagus. Among those patients who survive (first rupture), additional instances of haemorrhage occur in over 50% within one year
Note: in the liver and biliary chapter, there is mention of oesophageal varices that appear in 40% of patients with advanced cirrhosis of the liver and cause massive haematemesis and death in about half of them. (Go figure). Also note the information in the new TB above. I have however left the question as is
Which of the following may occur in acute pancreatitis?
A Serum levels of lipase increase before levels of amylase
B Metabolic alkalosis
C Hypercalcaemia
D Glycosuria in 10% of cases
D
Explanation
Acute pancreatitis is a relatively common condition with an incidence rate of 20 per 100000 cases in the western world. 80% of cases are associated with 2 conditions; biliary tract disease and alcoholism. Gallstones are present in 35-60% of cases of pancreatitis, and about 5% of patients with gallstones develop pancreatitis.
Male to female ratio 1:3.
Alcohol as a cause differs depending on country; USA up to 65% of cases and in Sweden 20%. Other causes include: infection, drugs, hypercalcaemic states, hyperparathyroidism and acute ischaemia. 10-20% of cases are idiopathic.
Laboratory findings include a metabolic acidosis. Serum lipase elevations occur earlier and last longer than elevations in amylase and are therefore useful in patients who present after 24hrs. Serum lipase is also more sensitive as compared with amylase in pancreatitis secondary to alcohol. Hypocalcaemia may arise from precipitation of calcium soaps in the fat necrosis. Glycosuria occurs in 10% of cases. Pancreatitis results from autodigestion of the pancreas by activated pancreatic enzymes. The mechanisms by which activation of pancreatic enzymes is initiated are: pancreatic duct obstruction, primary acinar cell injury and defective intracellular transport of proenzymes within acinar cells.
One of the major exocrine enzymes produced by the pancreas is trypsin. It can activate other proenzymes and converts prekallikrein to its activated form, initiating the kinen system.
NOTE: S-lipase rises within 4 to 8 hours of the onset of symptoms, peak at 24hrs, and return to normal within 8-14days. S-amylase rises within 6-12hours of the onset of acute pancreatitis. Amylase has a short half-life of 10hrs and in uncomplicated pancreatitis, returns to normal levels within 3-5days.
The current text states that there is a marked elevation of serum amylase levels during the first 24hrs, followed within 72-96hrs by a rising serum lipase.
Extra:
One of the stems states: Serum levels of lipase increase before levels of amylase This is also found in the explanation. But if you notice in the explanation, I have added that the The current text states that there is a marked elevation of serum amylase levels during the first 24hrs, followed within 72-96hrs by a rising serum lipase. Therefore the earlier statement of Serum levels of lipase increase before levels of amylase may be incorrect. I have left the question and answer as is, because I am not sure of the correct response needed, this way you can at least have all the information
Regarding acute pancreatitis, which of the following statements is true?
A Gall stones are present in 80% of cases
B 35% of patients with gall stones develop pancreatitis
C Trypsin activates prekallikrein to its active form
D Less than 5% are idiopathic
C
Explanation
Acute pancreatitis is a relatively common condition with an incidence rate of 20 per 100000 cases in the western world. 80% of cases are associated with 2 conditions; biliary tract disease and alcoholism. Gallstones are present in 35-60% of cases of pancreatitis, and about 5% of patients with gallstones develop pancreatitis. Male to female ratio 1:3 for biliary disease and 6:1 for alcoholism. Alcohol as a cause differs depending on country; USA up to 65% of cases and in Sweden 20%. Other causes include: infection, drugs, hypercalcaemic states, hyperparathyroidism and acute ischaemia. 10-20% of cases are idiopathic. Laboratory findings include a metabolic acidosis, a marked elevation of serum amylase and lipase level in the first 24hrs followed by a further rise in lipase over 72-96hrs. Hypocalcaemia may arise from precipitation of calcium soaps in the fat necrosis. Glycosuria occurs in 10% of cases. Pancreatitis results from autodigestion of the pancreas by activated pancreatic enzymes. The mechanisms by which activation of pancreatic enzymes is initiated are: pancreatic duct obstruction, primary acinar cell injury and defective intracellular transport of proenzymes within acinar cells.
One of the major exocrine enzymes produced by the pancreas is trypsin. It can activate other proenzymes and converts prekallikrein to its activated form, initiating the kinen system.
Which of the following is a result of chronic pancreatitis?
A Hypoglycaemia
B Steatorrhoea
C Hypercalcaemia
D Hypermagnesaemia
B
Explanation
Chronic pancreatitis is defined as inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis and at a later stage destruction of endocrine parenchyma. Patients with chronic pancreatitis usually present with persistent abdominal pain or steatorrhoea. Steatorrhoea is due to the malabsorption of fats. The development of steatorrhoea occurs late in the disease process and is a manifestation of severe exocrine deficiency. Diabetes is a common complication of chronic pancreatitis. Pseudocyts are also common. Note that hypercalcaemia and hyperlipidaemia can both cause chronic pancreatitis
Regarding acute pancreatitis, which of the following statements is correct?
A Intraductal activation of enzymes is an important aetiology
B Backflow of bile is a significant risk factor
C It affects intraperitoneal fat only
D Alcohol and gallstones cause 60%
A
Explanation
Acute pancreatitis is a relatively common condition with an incidence rate of 20 per 100000 cases in the western world. 80% of cases are associated with 2 conditions; biliary tract disease and alcoholism. Gallstones are present in 35-60% of cases of pancreatitis, and about 5% of patients with gallstones develop pancreatitis. Male to female ratio 1:3. Alcohol as a cause differs depending on country; USA up to 65% of cases and in Sweden 20%. Other causes include: infection, drugs, hypercalcaemic states, hyperparathyroidism and acute ischaemia. 10-20% of cases are idiopathic. Laboratory findings include a metabolic acidosis, a marked elevation of serum amylase and lipase level in the first 24hrs followed by a further rise in lipase over 72-96hrs. Hypocalcaemia may arise from precipitation of calcium soaps in the fat necrosis. Glycosuria occurs in 10% of cases. Pancreatitis results from autodigestion of the pancreas by activated pancreatic enzymes. The mechanisms by which activation of pancreatic enzymes is initiated are: pancreatic duct obstruction, primary acinar cell injury and defective intracellular transport of proenzymes within acinar cells.
The TB refers to the activation of pancreatic enzymes via three potential unclear mechanisms. Pancreatic duct obstruction is one way, but the explanation refers to enzyme rich interstitial fluid and lipase which is already active. I do not feel that this mechanism is well explained
One of the major exocrine enzymes produced by the pancreas is trypsin. It can activate other proenzymes and converts prekallikrein to its activated form, initiating the kinen system.
Regarding acute pancreatitis, which of the following options is correct?
A Trypsin plays a central role in the activation of the kinin system
B Gallstones are present in 80% of cases
C Less than 5% of cases are idiopathic
D 35% of patients with gallstones develop pancreatitis
A
Explanation
Acute pancreatitis is a relatively common condition with an incidence rate of 20 per 100000 cases in the western world. 80% of cases are associated with 2 conditions; biliary tract disease and alcoholism. Gallstones are present in 35-60% of cases of pancreatitis, and about 5% of patients with gallstones develop pancreatitis. Male to female ratio 1:3. Alcohol as a cause differs depending on country; USA up to 65% of cases and in Sweden 20%. Other causes include: infection, drugs, hypercalcaemic states, hyperparathyroidism and acute ischaemia. 10-20% of cases are idiopathic. Laboratory findings include a metabolic acidosis, a marked elevation of serum amylase and lipase level in the first 24hrs followed by a further rise in lipase over 72-96hrs. Hypocalcaemia may arise from precipitation of calcium soaps in the fat necrosis. Glycosuria occurs in 10% of cases. Pancreatitis results from autodigestion of the pancreas by activated pancreatic enzymes. The mechanisms by which activation of pancreatic enzymes is initiated are: pancreatic duct obstruction, primary acinar cell injury and defective intracellular transport of proenzymes within acinar cells.
One of the major exocrine enzymes produced by the pancreas is trypsin. It can activate other proenzymes and converts prekallikrein to its activated form, initiating the kinen system.
Complications of alcoholic chronic pancreatitis include the following except?
A There is a 20-25 year mortality rate of 50%
B Pancreatic cancer is common
C About 10% of patients develop pseudocysts
D Severe chronic pain can be the dominant problem
B
Explanation
While patients with hereditary pancreatitis have a 40% lifetime risk of developing pancreatic cancer, the degree to which other forms of pancreatitis predispose to the development of pancreatic cancer is unclear. There is only a modest increased risk of pancreatic carcinoma in patients with pancreatitis, due to the risks of smoking and alcohol consumption rather than a casual role of chronic pancreatitis per se
All of the following are acute effects relating to acute pancreatitis, with the exception of?
A DIC
B Acute respiratory distress syndrome (ARDS)
C Diabetes mellitus
D Renal failure
C
Explanation
Diabetes mellitus is not an acute effect of pancreatitis but rather the result of chronic pancreatic inflammation. Glycosuria occurs early in acute pancreatitis
Note: psudocysts can develop as a result of an acute pancreatitis episode. It takes about 4 weeks to develop. They are not solely a result of chronic pancreatitis
Extra:
Many of the systemic features of severe acute pancreatitis can be attributed to release of toxic enzymes, cytokines, and other mediators into the circulation and explosive activation of a systemic inflammatory response, resulting in leukocytosis, disseminated intravascular coagulation, edema, and acute respiratory distress syndrome. Shock, due to the systemic inflammatory response syndrome, and acute renal tubular necrosis may occur
Which of the following statements is correct in relation to pancreatitis?
A Duct obstruction is not the causal mechanism in acute alcoholic pancreatitis
B The chronic form is usually due to gallstones
C The second most common cause is infectious agents
D Trypsin is implicated as an activator of the kinin system
D
Explanation
Acute pancreatitis is a relatively common condition with an incidence rate of 20 per 100000 cases in the western world. 80% of cases are associated with 2 conditions; biliary tract disease and alcoholism. Gallstones are present in 35-60% of cases of pancreatitis, and about 5% of patients with gallstones develop pancreatitis. Male to female ratio 1:3. Alcohol as a cause differs depending on country; USA up to 65% of cases and in Sweden 20%. Other causes include: infection, drugs, hypercalcaemic states, hyperparathyroidism and acute ischaemia. 10-20% of cases are idiopathic. Laboratory findings include a metabolic acidosis, a marked elevation of serum amylase and lipase level in the first 24hrs followed by a further rise in lipase over 72-96hrs. Hypocalcaemia may arise from precipitation of calcium soaps in the fat necrosis. Glycosuria occurs in 10% of cases. Pancreatitis results from autodigestion of the pancreas by activated pancreatic enzymes. The mechanisms by which activation of pancreatic enzymes is initiated are: pancreatic duct obstruction, primary acinar cell injury and defective intracellular transport of proenzymes within acinar cells.
One of the major exocrine enzymes produced by the pancreas is trypsin. It can activate other proenzymes and converts prekallikrein to its activated form, initiating the kinin system.
Chronic pancreatitis is caused by alcohol in most cases
Alcohol has a direct toxic effect on pancreatic acinar cells and also increases oxidative stress. Alcohol can also result in functional obstruction by (1) contracting the sphincter at the ampulla of vater, (2) direct toxic effect on the aciner cells, including induction of oxidative stress in acinar cells, which lead to membrane damage (3) increasing pancreatic protein secretion, leading to inspissated protein plugs that block small ducts (Chronic alcoholism)
Which of the following hepatitis infections does not cause chronic liver disease?
A Hepatitis D
B Hepatitis C
C Hepatitis A
D Hepatitis B
C
Explanation
Hepatits infections
Frequency of chronic liver disease (hepatitis)
A: NEVER
B: 10%
C: about 80%
D: 5% (co-infection), <70% for superinfection.
E: NEVER
Regarding peptic ulcer disease (PUD), which is FALSE?
A H. pylori induced ulcers occur more in the duodenum than in the stomach
B PUD is most often associated with H.pylori-induced hyperchlorhydric chronic gastritis
C PUD may occur in any portion of the GIT exposed to gastric juices
D The ulcer in PUD has normal gastric mucosa adjacent to it, as opposed to stress ulcer which has abnormal mucosa adjacent to it
D
Explanation
Peptic ulcer disease (PUD) is most often associated with H.pylori-induced hyperchlorhydric chronic gastritis, which is present in 85% to 100%of individuals with duodenal ulcers and in 65% with gastric ulcers. The presence of chronic gastritis can help to distinguish PUD form acute erosive gastritis or stress ulcers, since the mucosa adjacent to the ulcer is generally normal in the latter two conditions. PUD may occur in any portion of the GIT exposed to gastric juices, but is more common in the gastric antrum and the first portion of the duodenum. PUD may occur in the oesophagus as a result of GORD (gastro-oesophageal reflux disease) or acid secretion by ectopic gastric mucosa. Gastric mucosa within a Meckel diverticulum can result in peptic ulceration of adjacent mucosa
An elderly patient presents to the emergency department complaining of severe abdominal pain, vomiting, and bloody diarrhoea, absent bowel sounds. What is the most likely diagnosis?
A Appendicitis
B Bowel obstruction
C Gastroenteritis
D Ischaemic bowel disease
D
Explanation
Ischaemic bowel disease tends to occur in older patients with coexisting cardiac disease and vascular disease. Acute transmural infarction typically presents with the above clinical picture and may progress rapidly to shock and vascular collapse within hours. Due to these physical signs overlapping with other GIT disorders including perforated gastric ulcer, cholecystitis appendicitis, delay in diagnosis can occur. The pathogenesis occurs in two phases. The initial hypoxic phase occurs at the onset of the vascular compromise. While some damage occurs at this stage, the epithelial cell lining of the intestine is relatively resistant tot transient hypoxia. The second phase, reperfusion injury, is initiated by restoration of blood flow and it is at this time that the GREATEST damage occurs. (Mechanism: free radicals, neutrophil infiltration, and inflammatory mediators)
Which of the following viruses is more commonly associated with intussusception?
A Adenovirus
B Rotavirus
C Coronavirus
D Parvovirus
B
Explanation
Robbins: Intusseption is the commonest cause of intestinal obstruction in children <2yrs. Often the cause is idiopathic. Cases have been associated with viral infection and rotavirus vaccine, perhaps due to reactive hyperplasia of Peyer’s patches and other mucosa associated lymphoid tissue which can act as a leading edge of the intussuscipiens.
Note: Robbin’s mentions rota virus vaccines in the text. However Uptodate mentions adenovirus. I have kept the answer according to Robbin’s
Influence of viral factors — An increasing body of evidence suggests that viral triggers may play a role in some cases, as illustrated by the following observations:
●The incidence of intussusception has a seasonal variation, with peaks coinciding with seasonal viral gastroenteritis in some populations
●Intussusception has been associated with some forms of rotavirus vaccine. An early form of the vaccine (RRV-TV: Rotashield) was removed from the market because of a 22-fold increase in intussusception among vaccinated infants.
●Approximately 30 percent of patients experience viral illness (upper respiratory tract infection, otitis media, flu-like symptoms) before the onset of intussusception.
●A strong association with adenovirus infection has been shown in a variety of populations. In 30 to 40 percent of cases, there is evidence of recent infection with enteric and non-enteric species of adenovirus. In a prospective case-control study examining a variety of possible infectious triggers for intussusception in Vietnam and Australia, infection with adenovirus, species C emerged as the strongest predictor of intussusception in both populations. In these populations, rotavirus infection and poliovirus vaccine administration were not associated with intussusception.
Viral infections, including enteric adenovirus, can stimulate lymphatic tissue in the intestinal tract, resulting in hypertrophy of Peyer patches in the lymphoid-rich terminal ileum, which may act as a lead point for ileocolic intussusception
Source: UpToDate: intussusception
What volume ascites accumulates before becoming clinically detectable?
A 1000mls
B 750mls
C 250mls
D 500mls
D
Explanation
Ascites becomes clinically detectable when at least 500ml have accumulated.
Rupture of esophageal varices has a mortality of approximately:
A 20%
B 35%
C 10%
D 15%
A
Explanation
Oesophageal varices are the most significant portosystemic shunt. They occur in 50% of patients with cirrhosis, most commonly in association with alcohol-related liver disease. Worldwide, hepatic schistosomiases is the second most common cause of varices
Despite intervention, as many as 20% of patients die from the first bleeding episode, either as direct consequence of haemorrhage or due to hepatic coma triggered by hypovolaemic shock and metabolic disturbance. Among those that survive, additional episodes of haemorrhage, each potentially fatal, occur in as many as 60% of cases.
Source: Robbins Pathology 11edition
Note
Two separate sets of numbers from different places in Robbins. The Liver and Gallbladder chapters says on oesophageal varices: “Each episode of bleeding is associated with ~30% mortality.” While the GIT chapter says: “each episode of variceal hemorrhage confers 20% risk of mortality”
In patients with gastro-esophageal reflux disease, squamous epithelium of the esophagus can change to columnar epithelium. What is this process called?
A Hyperplasia
B Anaplasia
C Metaplasia
D Dysplasia
C
Explanation
Metaplasia is the reversible replacement of one normal cell type with another normal cell type. It can be adaptive or pathological. Examples include columnar epithelium changing to squamous epithelium due to chronic respiratory irritation in smoking, and squamous changing to columnar in Barrett esophagus.
Gallstones are most commonly made up of which substance?
A Calcium pigment
B Calcium Magnesium Phosphate
C Cholesterol
D Calcium oxalate
C
Explanation
There are two main types of stones – cholesterol (most common) and pigment. Cholesterol are due toe supersaturation of bile salts with cholesterol. Pigment stones are due to precipitation of calcium bilirubin salts, usually in the context of chronic haemolytic conditions
What causes acalculous cholecystitis?
A Gall stones
B Ischaemia
C Infection
D Inflammation
B
Explanation
Acalculous cholecystitis occurs due to ischaemia as a result of reduced end-arterial cystic artery circulation, usually in the context of septic shock or multiorgan failure.
Which morphological feature of pancreatitis has the worst prognosis?
A Gray-white parenchymal necrosis
B Interstitial haemorrhage
C Calcium deposits
D Fat necrosis
B
Explanation
In mild forms, there is interstitial oedema and focal areas of fat necrosis in the pancreas and peripancreatic fat. Fat necrosis results from enzymatic destruction of fat cells, the released fatty acids combine with calcium to form insoluble salts that precipitate in situ.
In more severe forms, such as necrotising pancreatitis, the damage also involves acinar and ductal cells, the islets of Langerhans, and blood vessels. Macroscopically, the pancreas exhibits red-black haemorrhagic areas interspersed with foci of yellow-white, chalky fat necrosis.
In the most severe from, haemorrhagic pancreatitis, extensive parenchymal necrosis is accompanied by diffuse haemorrhage within the substance of the gland.
Source: Robbins-basic pathology
A woman presents with her last period 2 months previously, lower abdominal pain, PV bleeding. USS shows an empty uterus. Which of the following conditions is LEAST likely to be associated with this condition?
A Appendicitis
B Salpingitis
C Cystitis
D Endometriosis
C
Explanation
The most important predisposing condition, present in 35% to 50% of patients, is prior pelvic inflammatory disease resulting in intralumenal fallopian tube scarring (chronic salpingitis). The risk of ectopic pregnancy is also increased with peritubal scarring and adhesions, which may be caused by appendicitis, endometriosis, and previous surgery.
Which of the following conditions is most likely to be associated with a prehepatic portal hypertension?
A Right sided heart failure
B Constrictive pericarditis
C Sarcoidosis
D Massive splenomegaly
D
Explanation
Prehepatic causes are obstructive thrombosis of portal vein, narrowing of the portal vein before it ramifies within the liver or massive splenomegaly with increased splenic vein blood flow. The main post-hepatic causes are severe right-sided heart failure, constrictive pericarditis, and hepatic vein outflow obstruction. The dominant intrahepatic cause is cirrhosis, accounting for most cases of portal hypertension. Far less frequent intrahepatic causes are schistosomiasis, massive fatty change, diffuse fibrosing granulomatous disease such as sarcoidosis, and diseases affecting the portal microcirculation such as nodular regenerative hyperplasia
A woman presents with toxic megacolon. What is the likely condition that has resulted in this?
A Kaposi’s sarcoma
B Parasitic colitis
C Inflammatory bowel disease
D Pseudomembranous colitis
C
Explanation
Toxic megacolon is total or segmental nonobstructive colonic dilatation that occurs in the context of systemic toxicity. Although toxic megacolon is most commonly considered a complication of inflammatory bowel disease, especially ulcerative colitis and, to a lesser extent, Crohn’s disease, in reality almost any inflammatory or infectious condition of the colon can lead to toxic dilatation
Causes
Inflammatory: Ulcerative and Crohn’s disease.
Infectious:
Bacterial
Clostridiodes difficile-pseudomembranous colitis
Salmonella
Shigella
Campylobacter
Yersinia
Parasitic
Entameba histolytica
Cryptospordium
Viral
CMV colitis
Other
Pseudomembraneous colitis secondary to methotrexate
Kaposi’s sarcoma
Source: uptodate
A patient has diffuse colitis predominantly affecting the mucosa with ulceration. Which condition does this likely reflect?
A Bowel cancer
B Irritable bowel disease
C Ulcerative colitis
D Crohn’s disease
C
Explanation
Crohn’s disease – Skip lesions, thick wall, transmural inflammation, risk of fistulae.
Ulcerative colitis– colon only with diffuse continuous involvement, thin wall, mucosal inflammation only, superficial ulceration. Unlike Crohn’s disease, mural thickening is not present, the serosal surface is normal and strictures do not occur.
What is the most common position of the appendix?
A Pelvic
B Retrocolic
C Retrocaecal
D Retroileal
C
Explanation
The appendix usually lies in the retrocaecal position (64%) in the healthy person, draining to the ileocolic and superior mesenteric lymph nodes. Other appendix positions-
Pelvic appendix-20%. Retroileal-0.5%.
It has its own mesentery - the mesoappendix - through which the appendicular artery runs.
Moore: Most common position is retrocaecal (65%), pelvic (32%), retrocolic, retroileal
A young child presents with blood diarrhoea and blood tests demonstrate anaemia and renal failure. What is the most likely cause?
A Shigella toxin serotype 3
B Salmonella enteritidis
C Escherichia coli
D Campylobacter jejuni
C
Explanation
The term thrombotic microangiopathy encompasses a spectrum of clinical syndromes that includes TTP and HUS. They are caused by insults that lead to excessive activation of platelets, which deposit as thrombi in small blood vessels. “Typical” HUS is strongly associated with infectious gastroenteritis caused by Escherichia coli strain O157:H7, which elaborates a Shiga-like toxin. Haemolytic-uremic syndrome, which is typically associated with enterohemorrhagic E. coli (EHEC), may also occur after infection with S. dysenteriae serotype 1 that secrete Shiga toxin.
What is the most common cause of acute hepatic failure in the developed world?
A Hepatitis E
B Hepatitis B
C Acetaminophen overdose
D Autoimmune hepatitis
C
Explanation
Acute liver failure is caused by massive hepatic necrosis, most often induced by drugs or toxins. Accidental or deliberate ingestion of acetaminophen accounts for almost 50% of cases in the United States, while autoimmune hepatitis, other drugs/toxins, and acute hepatitis A and B infections account for rest of cases.
Extra:
In the USA, it is the cause of about 50%of cases of acute liver failure, with 30% mortality. Intentional overdoses is the most common cause of acetaminophen toxicity in Great Britain, but unintentional overdoses is the most frequent cause in the USA, representing almost 50% of the total intoxication cases.
