Gastrointestinal pathology Flashcards
8687 – The disorders of haemostasis seen in cirrhotic liver failure may include
1: disseminated intravascular coagulation
2: hypoprothrombinaemia
3: secondary thrombocytopenia
4: impaired synthesis of several clotting factors
TTTT
Robbins, 6th ed, Ch 14 and Ch 19
15821 – Pathogenetic mechanisms in development of generalised oedema in chronic liver failure include
1: increased microvascular permeability
2: increased renal sodium retention
3: increased renal renin secretion
4: reduced plasma colloid osmotic pressure
FTTT
There is not enough sodium and water aboard the normal individual to produce generalised oedema under any circumstances. When there is sudden loss of fluid from the plasma (without extra being loaded aboard first), the result is shock (anaphylactic, if the loss was due to histamine release, with increased permeability). While the fluid accumulation of ascites in the cirrhotic may or may not involve increased vascular permeability, the generalised oedema does not.
19138 – In severe liver disease, the dose of all of the following drugs should be reduced EXCEPT
A. heparin
B. acyclovir
C. morphine
D. propranolol
E. phenytoin
B
A.C.P. 1996
22129 – When generalised oedema complicates chronic hepatic failure, pathogenetic mechanisms include
1: increased renal sodium retention
2: reduced plasma colloid osmotic pressure
3: increased renal renin secretion
4: increased microvascular permeability
TTTF
Robbins 6th ed. Pages: 113-11
15661 – Fatty change in the liver (hepatic steatosis)
1: is characteristically seen with active hepatitis B infection
2: will cause dangerous derangement of the coagulation profile
3: when due to alcohol abuse, does not regress with abstention
4: is seen in persons suffering from protein malnutrition
FFFT
Fatty change in the liver though common with active hepatitis C, is not part of hepatitis B infection. With simple (uncomplicated) fatty liver, even when quite extensive, significant derangement of function is exceptional. Hepatic fat in the alcoholic usually ‘melts away’ with abstention. The enlarged liver of kwashiorkor and other protein malnutrition states is, paradoxically, due to storage, in the liver, of the (unavailable) calorie source.
15666 – Hepatic steatosis (fatty liver)
1: is the major liver injury resulting acutely from hypovolaemic shock
2: may be due to poorly controlled diabetes mellitus
3: is potentially reversible
4: if discovered in liver biopsy (ie without ‘toxic hepatitis’), has no sinister long term implications for the chronic alcoholic
FTTF
Hypovolaemic shock, when severe, causes hepatic hypoperfusion, with centrilobular degeneration/ necrosis of hepatocytes - this is an acute injury situation. Poorly controlled diabetes mellitus almost always causes prominent fatty liver. If the stimulus to fatty change is reversed, resolution always will occur. However, there is strong evidence that alcoholic fatty liver (even without hepatocyte acute necrosis) of very long standing will stimulate fibrosis (perhaps via activation of the Ito cell) with eventual progression to ‘fatty alcoholic cirrhosis’.
15758 – Hepatic steatosis is commonly seen in
1: chronic congestive heart failure
2: malnutrition
3: chronic hepatitis B carrier state
4: paracetamol (acetaminophen) poisoning
TTFT
Of the viral hepatitides, only hepatitis C is said to be associated with fatty change in the liver - it is quite a common finding on biopsy. I see no reason why someone with alcoholic (or other) steatosis should not contract hepatitis B, but the finding of significant steatosis in active hepatitis B is quite exceptional and off-putting to the histopathologist. It is certainly not a feature of the disease (but is of hepatitis C). The others are ‘givens’.
23039 – Hepatic steatosis (fatty change of the liver) may be caused by
1: chronic venous congestion
2: alcohol excess
3: protein malnutrition
4: alpha-1-antitrypsin in liver cells
TTTF
Robbins 5th ed. Chapter: 1 Page: 25, 27
17768 – Most carcinomas of the gallbladder
1: are squamous or adenosquamous carcinomas
2: present clinically with pain plus an enlarged gallbladder
3: have invaded the liver at the time of operation
4: are always associated with presence of gall bladder calculi
FFTF
Most cancers of the gallbladder are adenocarcinomas. Clinical presentation is typically insidious and indistinguishable from the symptoms and signs of benign gallbladder disease - palpable enlargement of the gallbladder is distinctly unusual. According to Robbins, 60-90% of carcinoma of the gallbladder is associated with gallstones - the point is that there is a very significant incidence of cases occurring without gallstones and the overall incidence of gallbladder carcinoma in patients with gallstones is so low that prophylactic cholecystectomy for gallstones is considered unjustified. By the time these cancers are discovered, most have invaded the liver.
15671 – Calcification occurring during the acute phase of haemorrhagic pancreatic necrosis
1: occurs predominantly in necrotic pancreatic acinar cells
2: commonly causes severe hypocalcaemia
3: may eventually extensively involve peripancreatic tissues
4: commonly resolves rapidly following recovery from the acute event
FTTF
Calcification is due to reaction of calcium ions with fatty acids formed by lipase action on triglyceride released from cells due to the action of phospholipases released from the necrotic pancreatic parenchymal cells. This commonly results in severe hypocalcaemia and a more or less permanent presence of calcium soaps replacing the retroperitoneal and other fat involved.
23554 – Carcinoma of the extrahepatic bile ducts
1: commonly causes obstructive jaundice
2: causes palpable gallbladder enlargement in most cases
3: is surgically resectable in most instances
4: has a prognostic outlook similar to that of colonic carcinoma
TFFF
Robbins 5th ed. Chapter: 18 Pages: 893
17773 – Carcinoma of the extrahepatic bile ducts
1: in most cases does not cause palpable gallbladder enlargement
2: has a prognostic outlook similar to that of colonic carcinoma
3: is curably resectable in most instances
4: commonly causes obstructive jaundice
TFFT
Only approximately 25% of patients have palpable gallbladder, but obstructive jaundice is the rule, often with stool decolourisation. The majority of ductal cancers are not resectable at the time of diagnosis, despite their small size; mean survival times range from 6 to 18 months, no matter what the treatment given; this is in sharp contrast to the considerably superior survival rates for colonic cancer.
15588 – Adenocarcinoma of the pancreas
1: usually presents at a stage of development when it is incurable
2: commonly presents with secondary diabetes attributable to carcinomatous pancreatic destruction
3: can be reliably predicted in a person presenting with migratory thrombophlebitis
4: most commonly follows a prolonged history of recurrent or ‘chronic’ pancreatitis
TFFF
Refer to Robbins, 6th Ed, Ch 19, page 910-911
893 – Reduction in the mortality of acute pancreatitis is most likely to result from
A. administration of glucagon.
B. administration of aprotinin.
C. early correction of fluid and electrolyte losses.
D. total parenteral nutrition.
E. peritoneal lavage.
C
Acute pancreatitis exhibits a spectrum of severity. Severe acute pancreatitis is accompanied by hypovolaemia with massive sequestration of fluid and electrolytes in the abdomen and retroperitoneum. Early correction of such losses is of major importance in treatment, and is the most likely of the responses to influence mortality (C correct). Aprotinin and glucagon have been widely used in treatment, but have not been demonstrated effective in influencing mortality in clinical trials (A and B incorrect). Parenteral nutrition is helpful in treating the complications of acute pancreatitis such as prolonged ileus and abscess formation, but is not so relevant to early mortality (D incorrect). Peritoneal lavage and dialysis have a role in management of acute pancreatitis (particularly when acute pancreatitis is diagnosed at operation) and in the management of local and systemic complications (pancreatic abscess and renal failure). There is no evidence that they reduce the early mortality (E incorrect).
899 – Which of the following problems does NOT accompany the use of a Sengstaken-Blakemore tube inserted for balloon tamponade of bleeding oesophageal varices?
A. Aspiration.
B. Asphyxia.
C. Oesophageal rupture.
D. Rebleeding upon balloon deflation.
E. Vagal-induced bradycardia.
E
The Sengstaken-Blakemore tube can give effective control of acute bleeding from oesophageal varices. There are a of hazards and complications of its use. Aspiration or asphyxia during insertion, oesophageal pressure necrosis or rupture, and rebleeding after balloon deflation are the most important. The tube should preferably be inserted, and the patient managed, in an intensive-care environment. Vagal-induced bradycardia is not a complication. Stimulation of afferent vagal fibres related to the oesophagus or stomach does not evoke cardio-inhibitory reflexes, whereas hypovolaemic tachycardia is common. E is thus the correct response.
