Illnesses

Question 1

pernicious anemia

Answer 1

Pernicious anemia end stage of autoimmune inflammation of the stomach -> stomach cells destroyed by own antibodies. As gastric cells get destroyed, stomach produces less secretions such as acid and intrinsic factor, needing for absorption of B12. Antibodies to intrinsic factor bind to it and further prevent formation of IF-B12 complex that would be absorbed in ileum. So B12 absorption in pernicious anemia is inhibited by - gastric cells destroyed by own antibodies, less intrinsic factor produced - antibodies directly attaching intrinsic factor, preventing it from binding to B12 and forming IF-B12 complex necessary for absorption

Question 2

ERCP

Answer 2

RCP, also known as Endoscopic Retrograde Cholangio Pancreatography, is a procedure to examine the anatomy of the ducts draining the liver and pancreas. This includes the bile ducts, gallbladder, and pancreatic ducts. ERCP is useful in determining whether or not there are gallstones in the bile ducts, cancer involving the bile ducts or pancreas, as well as a number of other conditions. The ERCP endoscope also allows removal of gallstones from the bile ducts, dilating strictures, or placing stents across blocked ducts to hold them open, all without surgery. Stenting a duct may give immediate relief of a malignant obstruction. ERCP is a combined endoscopic and radiologic procedure. A duodenoscope is inserted through the mouth into the upper part of the small intestine to locate the area where the bile ducts and pancreatic ducts drain their contents into the intestine. A catheter or small tube is then fed through the scope and threaded up through the ampulla into the bile ducts and the pancreatic ducts. X-ray contrast is then injected though the catheter filling the ducts. At this point, the x-ray machine is turned on and the ducts filled with contrast show up clearly on the x-ray screen

Question 3

What is malabsorption?

Answer 3

• normal transport, digestion or absorption of various nutrients and minerals interrupted
• results in malnutrition, diarrhea, steatorrhea and weight loss

Question 4

What is assimilation?

Answer 4

process by which indested foods reach body fluids and cells

Question 5

What is malnutrition?

Answer 5

imbalance between supply of nutrients and body’s energy requirement

Question 6

what is maldigestion?

Answer 6

impaired nutrient breakdown (hydrolysis)

Question 7

What are three phases of nutrient digestion and absorption?

Answer 7

• luminal phase
• mucosal phase
• transport phase
• think about the order in which nutrients pass abdo wall - first lumen, then cross mucous lining, then transport to tissues

Question 8

What is Dielafoy’s lesion?

Answer 8

Dieulafoy’s lesion is a medical condition characterized by a large tortuous arteriole in the stomach wall that erodes and bleeds. It can cause gastric hemorrhage but is relatively uncommon. It is thought to cause less than 5% of all gastrointestinal bleeds in adults.

Question 9

Common causes of bloody emesis?

Answer 9

• Mallory-Weiss tear
• peptic ulcer disease
• gastric cancer
• esophageal cancer
• gastric cancer
• gastricl or esophageal varices
• vascular lesions (arteriovenous malformations)
• esophagitis
• Dieulafoy’s lesion (large torturous arteriole in the stomach that breaks)

Question 10

Bloody emesis, patient collapses, BP low. Sample investigations?

Answer 10

• CBC
• renal profile
• coagulation profile (differential!!!)
• lactate test
• liver panel
• type and cross match (for blood transfusions later)
• EKG (b/c of BP)
• chest and abdo X-ray to investigate cause of bleeding

Question 11

What are some physical exam hallmarks of liver disease?

Answer 11

• scleral icterus
• palmar erythema (redness)
• ascites
• leg edema
• spider angiomas (in areas that drain into superior vena cava (head, neck, upper limbs, upper chest; can be normal if <5)
• caput medusa

Question 12

how is octreotide (IV) useful in esophageal varices?

Answer 12

Octreotide is a somatostatin analogue. Beside inhibiting growth hormone, insulin and glucagon, it is also used in the treatment of variceal bleeding. It causes abdominal organ vasoconstriction thereby reducing blood flow in the splanchnic circulation and reduces portal pressure

IV octreotide was used with diagnosis of esophageal varice after injection of sclerosant + variceal band ligation to reduce blood flow to the area

Question 13

Differentials for chronic liver disease?

Answer 13

Viral: Hep B, C etc

Autoimmune: autoimmune hepatitis, primary biliary cirrhosis

Hereditary: hemochromatosis (Fe accumulation), alpha 1 antitrypsin deficiency, Wilson’s disease (Cu accumulation)

Toxin: alcohol

Other: NAFLD (Non Alcoholic Fatty Liver Disease)

Question 14

Treatment of ascites due to liver disease?

Answer 14

• Restrict salt - no added salt in diet <2 g per day (minimize use of 0.9% NaCl in hospital)
• diuretics - furosemide (loop) and spironolactone (aldosterone antagonist) in 40mg: 100 mg with a max dose of 160 mg:400 mg
• monitor K levels and renal function on diuretics!
• if not responsive, can treat with paracentesis or transjugular intrahepatic portosystemic shunt

Question 15

What is asterixis?

Answer 15

Asterixis (also called the flapping tremor, or liver flap) is a tremor of the hand when the wrist is extended, sometimes said to resemble a bird flapping its wings. This motor disorder is characterized by an inability to actively maintain a position, which is demonstrated by jerking movements of the outstretched hands when bent upward at the wrist (usually eyes closed). Asterixis is associated with various encephalopathies, especially hepatic encephalopathy thought due to lack of ammonia metabolization to urea (extra Ns are toxic to brain)

Question 16

Treatment for hepatic encephalopathy?

Answer 16

• put patient on lactulose at 15-30 ml orally up to 4x day until at least 2 soft bowel movements a day
• lactulose is a synthetic sugar used to treat constipation. It is broken down in the colon into products that pull water out from the body and into the colon. This water softens stools (patient had severe constipation with hepatic encephalopathy)
• can be given in the form of enema if poor level of consiousness and cannot do oral intake
• go on low protein diet while encephalopathic, can resume normal diet when hepatic encephalopathy resolves
• antibiotics can be used to kill bacteria in the bowel that produce N

Question 17

What are some diagnostic tests that confirm hepatocellular carcinoma?

Answer 17

• Alpha fetoprotein (AFP) is a tumour marker produced by 70% of HCCs and should be checked everyty 6 months in patients with cirrhosis. In the
• Do imaging: late arterial phase shows hypervascular nodule conssistent with carcinoma (light up); portal venous phase would show hepatocellular carcinoma enhancemnt too (once it lights up, it keeps dye pretty well)

Question 18

How is severity of liver disease determined?

Answer 18

Child-Pugh score, a point system that takes into account total bilirubin, serum albumin, INR, ascites, hepatic encephalopathy and classifies patient into classes (A-C) with predicted 1-year survival (C is worst class to have)

Can then use MELD score to see short-term mortality prognosis (3 months) to see if patient should be on top of the list

Question 20

Hirschprunger’s disease?

Answer 20

Hirschsprung’s disease (HD) is a disorder of the abdomen that occurs when part or all of the large intestine or antecedent parts of the gastrointestinal tract have no ganglion cells and therefore cannot function. During normal fetal development, cells from the neural crest migrate into the large intestine(colon) to form the networks of nerves called Auerbach’s plexus and Meissner’s plexus. In Hirschsprung’s disease, the migration is not complete and part of the colon lacks these nerve bodiesthat regulate the activity of the colon. The affected segment of the colon cannot relax and pass stool through the colon, creating an obstruction. In most affected people, the disorder affects the part of the colon that is nearest the anus. In rare cases, the lack of nerve bodies involves more of the colon. Stomach and esophagus may be affected too. Hirschsprung’s disease is also often called congenital aganglionic megacolon.

Hirschsprung’s disease occurs in about one in 5,000 of Japanese and American children.

Hirschsprung’s disease is a congenital disorder of the colon in which certain nerve cells, known as ganglion cells, are absent, causing chronic constipation. The lack of ganglion cells is in the myenteric plexus (Auerbach’s Plexus), which is responsible for moving food in the intestine. A barium enema is the mainstay of diagnosis of Hirschsprung’s, though a rectal biopsy showing the lack of ganglion cells is the only certain method ofdiagnosis.

Question 21

Colonoscopy screening guidelines?

Answer 21

Screening of individuals at average risk: Individuals over the age of 50 years with a negative family history should undergo screening with one of the following strategies:

FOBT every two years
Flexible Sigmoidoscopy every five years
Flexible Sigmoidoscopy Combined with FOBT every five years
Double contrast barium enema every five years
Colonoscopy every ten years

Screening of Individuals at higher risk: Some groups are at increased risk of colon cancer. Colonoscopy is the recommended screening test for these patients who have:

A first degree relative with the disease diagnosed before age 60 (colonoscopy every 5 years to begin at age 40 or ten years earlier than the youngest diagnosis of polyp or cancer in the family; if diagnosed after the age of 60, then employ average risk screening to begin at age 40),
a family history that suggests a genetic abnormality capable of causing the disease such as HNPCC (Colonoscopy every 1-2 years beginning at age 20 years or ten years younger than the earliest case in the family),
FAP (sigmoidoscopy annually to begin at age 10-12 years) or
long standing colonic inflammatory bowel disease - such as Crohn’s or Ulcerative Colitis (for pancolitis – colitis that involves the entire colon -, begin screening at 8 years after onset of disease, continue with colonoscopy every three years in the second decade, colonoscopy every two years in the third decade and colonoscopy every year in the fourth decade; for left sided colitis, begin screening at 15 years after onset)

Question 22

Cholangitis vs cholecystitis?

Answer 22

Cholangitis - gallbladder inflammation

cholecystitis - bacterial invasion of gallbladder with gallbladder inflammation

Question 23

What is Sjogren’s syndrome?

Answer 23

Sjögren’s syndrome or Sjögren syndrome is a chronic autoimmune disease in which the body’s white blood cells destroy the exocrine glands, specifically the salivary and lacrimal glands, that produce saliva and tears, respectively. The immune-mediated attack on the salivary and lacrimal glands leads to the development of xerostomia (dry mouth) and keratoconjunctivitis sicca (dry eyes), which takes place in association with lymphocytic infiltration of the glands. That inflammatory process eventually severely damages or destroys the glands.

Sjögren’s syndrome is usually classified by a clinician as either ‘primary’ or ‘secondary’. Primary Sjögren’s syndrome occurs by itself and secondary Sjögren’s syndrome occurs when anotherconnective tissue disease is present. However, this classification does not always correlate with the severity of symptoms or complications.

Question 24

How do NSAID ulcers differ from normal ones?

Answer 24

more common in the elderly, more likely to bleed and more likely to be larger.