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GI must knows Flashcards

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1
Q

Risk factor pnemonic for Esophageal cancer

A

AABCDEFFGH

Alcohol- Squamous (upper and Middle Esophagus)
Achalasia
Barrett's- Adeno
Cigarretes- both
Diverticula- Squamous
Esophageal web- Squamous
Familial- 
Fat- 
GERD- Adeno
H- Hot liquids- Squamous
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2
Q

Carcinoid Tumor is made up of what type of cell

A

neuroendocrine cells

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3
Q

Chromogranin positive tumor…think what?

A

Carcinoid Tumor

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4
Q

Carcinoid tumors often secrete what?

A

Serotonin

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5
Q

How does Carcinoid syndrome develop?

A

Carcinoid tumors release serotonin. As long as the tumor is somewhere in the GI that is not the liver, this serotonin is secreted into the portal circulation which brings it to the liver where it is metabolized by MAO into 5-HIAA. If the tumor mets to the liver however, it can secrete serotonin into the hepatic vein which can bypass liver metabolism and cause serotonin to enter the systemic circulation causing bronchospasm, diarrhea, and skin flushing. May also cause Carcinoid heart disease which is right sided valvular fibrosis (not left side because there is MAO in the lungs).

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6
Q

Most common location of gastric ulcer

A

Antrum of the stomach (lesser curvature I think)

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7
Q

Black gallstones indicate

A

hemolysis

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8
Q

What makes the black gallstones black?

A

High Billirubin content

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9
Q

Acute Gastritis is or is not related to H. Pylori?

A 
NOT
Acute Gastritis risk factors include:
-Curling Ulcer (Burn- leads to hypovolemia which leads to decreased blood supply to the stomach. Normally the stomach is aided by blood supply which picks up leaked acid)
- Cushing ulcer- increased vagal nerve stimulation from increased intracranial pressure
- NSAIDS
- ALcohol
- Chemo
- Shock
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10
Q

Chronic Gastritis causes

A
  • Autoimmune

- H Pylori

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11
Q

What does a Urea breath test test for?

A

H Pylori…remember they give off urease

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12
Q

Chronic Autoimmune gastritis, whats the best way to test for it?

A
  • Test for antibodies against parietal cells and intrinsic factor.
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13
Q

Know Ulcerative Colitis vs Crohns

A

ok

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14
Q

The inflammation and hemorrhage of the pancreas during acute pancreatitis is due most generally to what?

A

autodigestion of the pancrease by inappropriately activated pancreatic enzymes

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15
Q

What enzyme is responsible for activating all other pancreatic enzymes?

A

Trypsin! MUST KNOW THAT

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16
Q

two causes of acute pancreatitis

A

alcohol and gallstones

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17
Q

Which pancreatic enzyme is more specific for acute pancreatitis

A

serum lipase

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18
Q

What truly characterizes chronic pancreatitis?

A

Fibrosis of the pancreatic parenchyma

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19
Q

Clinical features of chronic pancreatitis

A

Pain that radiates to the back, steatorrhea, fat soluble vitamin deficiency, diabetes mellitus secondary to the destruction of islets, increased risk for pancreatic cancer

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20
Q

Peutz Jeghers Syndrome

A

Hamartomatous polyps throughout GI and freckle like spots on lips, oral mucosa.
Increased risk for colorectal, breast, and Gynecologic cancer

So, Polyps and Freckles…high cancer risk

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21
Q

Hyperplastic polyps most commonly found where

A

Left colon

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22
Q

What findings = bad prognosis with adenomatous polyp

A

Greater than 2cm, Sessile growth, villous histology

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23
Q

FAP?

A

Familial Adenomatous Polyposis Syndrome
This is an inherited APC (Adenomatous polyposis coli) mutation.
Colon and rectum removed prophylactically.

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24
Q

Gardner Syndrome

A

FAP + Fibromatosis + Osteomas

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25
Turcot Syndrome?
FAP with CNS tumors
26
2 pathways that lead to CRC?
1) Adenoma - Carcinoma pathway | 2) Microsatellite Instability Pathway
27
Tumor marker for pancreatic cancer
CA19-9
28
Major signs/symptoms for pancreatic adenocarcinoma in the head of the pancreas?
Obstructive Jaundice, Pale stools. Palpable gallbladder,
29
Major signs and symtpoms with pancreatic adenocarcinoma that arises in the tail or body?
Secondary diabetes Mellitus
30
Jaundice Bilirubin level?
Over 2.5 mg/dl
31
The fibrosis seen during liver cirrhosis is mediated by what?
Stellate cell ( relelase TGF- beta)
32
Periductal onion skin fibrosis
Primary sclerosing cholangitis
33
Ulcerative colitis associated with what other diseases?
Primary sclerosing cholangitis and p-ANCA positivity
34
Crohns associated with?
Ankylosing spondylitis, sacroilitis, migratory polyarteritis, erythema nodosum, uveitis
35
Achlorhydria seen when?
Chronic atrophic gastritis. | Not seen in PUD because you must have acid and pepsin present for ulceration to occur.
36
Oral contraceptives and the liver
Hepatic adenoma
37
Angiosarcoma and the liver
vinyl chloride
38
Corneal Kayser Fleischer rings
Wilson's Disease
39
What the F is Wilson's disease?
Inadequate hepatic copper excretion and failure of copper to enter the circulation as ceruloplasmin.
40
Where does copper accumulate>
Liver, Brain, Cornea, Kidneys, Joints
41
Lab findings in Wilson's disease?
Low Ceruloplasmin, high urinary copper
42
Wilson's disease follows what type of inheritance pattern and what gene is affected?
Auto Recessive. ATP7B gene (this gene codes for the ATP powered copper transporting ATPase which genenreally excretes copper into the bile where it can be incorporated into ceruloplasmin. Without this copper ATPase, copper builds up in the liver, leaks into the serum, and deposits in tissues.
43
Wilson's disease generally presents when? How
Childhood. Cirrhosis of the liver Behavioral changes like parkinsonian symptoms due to basal ganglia degeneration Asterixis- Tremor of the hand Dementia, Dyskinesia, Dysarthria
44
Bridging necrosis most commonly related to what?
Viral hepatitis (chronic)
45
Pancreatic psuedocyst is a complication of what?
Chronic pancreatitis most often secondary to chronic alcoholism.
46
In hemochromatosis, what organs are most commonly affected?
heart, pancreas , liver.
47
Prussian blue stain turns what color with Hemochromatosis
Blue
48
Hemochromatosis follows what inheritance pattern?
Autosomal recessive.
49
Necrosis of hepatocytes at the interface between the portal tracts and liver lobule =
Chronic Hepatitis....this eventually leads to bridging necrosis and then cirrhosis with portal bridging fibrosis and nodular regeneration.
50
Concentric bile duct fibrosis is associated with what?
Sclerosing cholangitis
51
Microvesicular steatosis
acute fatty liver of pregnancy and Reye Syndrome in children
52
Limiting plate inflammation, or inflammation around the portal triads?
Chronic viral hep...think HCV or potentially HBV
53
Obesity and cholesterol
Obesity leads to high levels of HMG CoA reductase which means acetate is converted to free cholesterol
54
Estrogen and cholesterol
Estrogen = increased cholesterol uptake pretty much...increased uptake of serum lipoproteins.
55
Progesterone
Decreased cholesterol ester stores and increased free cholesterol
56
Biliary Colic
Stone blocking the cystic duct - Pain for a short period of time then goes away. Nausea and vomitting present - NO fever, chills, jaundice
57
After Biliary colic, what is the next in the line of severity
Cholecystitis- Stone blocking the cystic duct but it has been there for a longer period of time. Associated with inflammation of the gallbladder walls. Pain, fever, chills, nausea and vomitting. NO Jaundice Probably needs gallbladder removed
58
After cholecystits, what is next most severe
Choledocholithiasis- stone has moved into common bile duct and bile backs up into both gallbladder and liver. pt presents with pain, nausea, vomitting, JAUNDICE
59
After choledocholithiasis
Cholangitis- Infloammation of the bile ducts in the liver...NOT GOOD NEWS AT ALL
60
After choledocholithiasis with cholangitis?
Biliary Pancreatitis- stone is stuck in the common bile duct below where the pancreatic duct comes in. Pt will have symtoms of cholangitis and pancreatic enzymes will be high. Will develop pancreatitis, Persistent nausea and vomitting
61
ADH2*1
genetic polymorphism in east asians that is associated with higher susceptibility to ALD
62
TNF alpha 238
potential polymorphism in caucasians that is related to ALD
63
Fatty change in alcoholic hepatitis and non-alcoholic macro or micro
Macro
64
Take home for NAFLD and NASH:
Obesity = Inc in FFA synthesis and decrease in FFA oxidation Insulin resistance = Increase in Peripheral lipolysis leading to higher FFA to the liver These two mechanisms lead to increased FFA and increased oxidative stress
65
Most common tumors in the liver are?
Metastatic tumors BY FAR!!! Most common sites of origin = Cancer sometimes penetrates benign liver Colon, stomach, pancreas, breast, lung
66
Most common benign tumor in the liver
Hemangioma...not hepatic adenoma
67
Primary Billiary Cirrhosis associated with what antibodies
anti-mitochondrial
68
Histology of PBC
Dense lymphocyticinfiltrate in and around interlobular bile ducts with granuloma and bile duct destruction
69
PAS positive globules
alpha anti-trypsin
70
Nutmeg liver=
kinda reddish looking. Its a result of Cor Pulmonale----right sided heart failure that is caused by some sort of restrictive lung disease
71
Gastrin tyrosyl residue in what position>
6 position
72
Gastrin tyrosyl in 6 and sulfated
Gastrin II
73
Gastrin Tyrosyl in 6 and desulfated
Gastrin !
74
All of the GI tract is smooth muscle except for?
Upper 1/3 of esophagus and external anal sphincter
75
Vagotomy will lead to lack of peristalsis in what section of the esophagus?
Upper 1/3....because this is skeletal striated muscle and skeletal striated muscle is innervated directly by vagal efferents whereas the myenteric plexus plays a large role in mediating lower 2/3.
76
Salivary amylase is the same as pancreatic amylase
ok
77
Glycerol does not need a micelle to be absporbed
ok
78
Failure to reabsorb bile acids does cause osmotic diarrhea
ok
79
Voluntary contraction of the external anal sphincter and the urge to defecate comes from
sacral region of spinal cordq
80
Where is the H+ pump located in resting/unstimulated parietal cells
membranes of small tubulovesicles, oriented towards the inside.
81
When parietal cells begin to secrete, where do the H+ pump containing tubulovesicles move?
Into the intracellular canaliculus of the secreting cell
82
In the secreting stomach, the pH of venous blood is higher or lower than arterial
Higher, more basic
83
During the stimulation of gastric acid secretion, what happens to the electrical potential difference across the gastric mucosa
Decreases
84
Lymphocytes in myenteric plexus=
Achalasia
85
Enteric nervous system =
Myenteric plexus- B/w inner circular and outer longitudinal layer. Motility Meissner- INSIDE the submucosa...secretion
86
Acute hemorrhagic gastritis =
alcohol, NSAIDS, trauma, sepsis, shock
87
Chronic gastritis
H Pylori or autoimmune
88
Esophageal cancer more common in what sex/ race
men squamous= black adeno= white
89
adenomatous gastric polyps most common where
antrum
90
injury, infxn, genetics ---> gastritis ---> atrophic gastritis ---> Bacterial growth ---> bacterial enzymes like nitrate reductase turn nitrates into nitrites and these lead to mutations
ok
91
Signet ring cell in what type of gastric cancer
Diffuse
92
Drugs associated with constipation, paralytic ileus, or acute megacolon
psychiatric drugs DON't MISS ALso...be careful to watch for C. Dif, IBD
93
FAP
Autosomal dominant... Over 100 adenomatous polyps starting in the 2nd and 3rd decade All will develop CRC unless the colon is removed In FAP, one allele of the mutated APC gene is inherited and another occurs somatically. This is when the problems arise
94
HNPCC
Hereditary Non-polyposis colorectal carcinoma is associated with inherited mutations in DNA mismatch repatin enzymes....also associated with endometrial, ovaria, urinary, and gastric cancer
95
Hyperplastic polyps most commonly arise where?
left colon

Gastrointestinal (58 decks)

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