Week 11: Gastrointestinal + Hepatobiliary Disorders Flashcards
1
Q
What are some gastrointestinal infections?
A
Appendicitis, Peritonitis
2
Q
What are some gastrointestinal disorders related to cancer and inflammation?
A
Colon cancer, Ulcerative colitis, Crohn’s disease
3
Q
What are common gastrointestinal diseases related to acid?
A
GERD, PUD
4
Q
What are the types of viral and alcoholic liver diseases?
A
Viral hepatitis, Alcoholic liver disease (Fatty Liver)
5
Q
What is a type of liver cancer?
A
Hepatocellular carcinoma
6
Q
What are common issues related to the gallbladder?
A
Gall stones
7
Q
What is gastroenteritis?
A
Often used broadly to describe acute infectious disease of the digestive tract, though stomach infection is usually not a major feature.
8
Q
What is enteritis?
A
Strictly, inflammation of the small intestine, whether infectious or not.
9
Q
What is colitis?
A
Inflammation of the large intestine.
10
Q
What is enterocolitis?
A
Inflammation of both the small and large intestines.
11
Q
What is diarrhea?
A
Diarrhea is defined as a disruption in bowel habits where feces become more fluid and are passed more frequently than usual.
12
Q
What is acute diarrhea?
A
Acute diarrhea refers to most cases lasting a few days and are self-limiting. During recovery, damaged epithelium regenerates rapidly.
13
Q
What is prolonged diarrhea?
A
Prolonged diarrhea lasts more than two to three days and can lead to significant fluid loss, which can be life-threatening, especially in young children.
14
Q
What is chronic diarrhea?
A
Chronic diarrhea lasts more than a few weeks, usually not caused by infection, and may indicate a chronic condition like cancer or inflammatory bowel disease.
15
Q
What pathogens are responsible for acute infectious diarrhea?
A
Pathogens responsible for acute infectious diarrhea include bacteria, viruses, and protozoa, usually acquired via fecal-oral routes, through contaminated water, food, or hands.
16
Q
Can some viruses causing diarrhea be transmitted through the air?
A
Yes, some viruses can be contracted through airborne transmission.
17
Q
What do viruses infect in viral diarrhea?
A
Viruses infect enterocytes (epithelial cells) of the small intestine.
18
Q
What type of diarrhea is most commonly associated with viral infections?
A
In most cases, viral diarrhea is watery and termed ‘non-inflammatory’.
19
Q
What are the common symptoms of viral diarrhea?
A
Symptoms include vomiting, fever, and abdominal pain alongside diarrhea.
20
Q
Which viral pathogen is the most common among children?
A
Rotavirus is the most common viral pathogen among children.
21
Q
Which virus is more common in adults?
A
Norovirus (Norwalk virus) is more common in adults.
22
Q
What are the most common pathogens responsible for bacterial diarrhea?
A
Salmonella, Campylobacter, Shigella, Yersinia, and Escherichia coli (gram-negative)
In poorer countries and disaster areas, Vibrio cholerae is the cause of cholera epidemics.
23
Q
What is the pathogenesis of bacterial diarrhea?
A
Bacteria invade the intestinal epithelium, usually of the large intestine, damaging it, which results in an acute inflammatory response.
24
Q
What are the effects of the acute inflammatory response in bacterial diarrhea?
A
It reduces the absorptive capacity of the epithelium and stimulates the secretion of water and mucus, resulting in inflammatory diarrhea.
25
What are the characteristics of feces in inflammatory diarrhea?
Feces will contain mucus, blood, or both, along with neutrophils and protein from inflammatory exudate.
26
What is markedly bloody diarrhea sometimes called?
Dysentery, particularly when the pathogen is Shigella or the protozoan Entamoeba.
27
What is Hemolytic Uremic Syndrome (HUS)?
HUS is a condition caused by infection with certain invasive toxigenic strains of E. coli, notably serotype O157:H7.
## Footnote
HUS occurs most often in children and can be life-threatening.
28
What toxin is associated with HUS?
HUS is caused by a shiga-like toxin (verotoxin), similar to that produced by Shigella dysenteriae.
29
What is the pathogenesis of HUS?
The shiga-like toxin is absorbed into the bloodstream and targets the vascular endothelium, especially in the glomerular capillaries of the kidney.
30
What effect does the toxin have on endothelial cells?
The toxin inhibits protein synthesis in endothelial cells, leading to their death and triggering the blood clotting cascade.
31
What are the consequences of HUS?
Consequences of HUS include thrombosis of small blood vessels, damage to erythrocytes (hemolysis), thrombocytopenia (due to platelet aggregation), and fatal acute renal failure.
32
What is the nature of bacterial toxin byproduct that causes diarrhea?
This is considered intoxication rather than infection.
33
Which types of bacteria are known to produce toxins that lead to diarrhea?
Staphylococcus aureus, Bacillus cereus, and Clostridium botulinum.
34
What type of toxins do Staphylococcus aureus and Bacillus cereus produce?
They can produce heat-stable toxins if they grow on food.
35
Where do the toxic byproducts of S. aureus and B. cereus act?
They act in the small intestine.
36
What symptoms are caused by the toxins from S. aureus and B. cereus?
Rapid onset of symptoms including nausea, abdominal pain, vomiting, and diarrhea.
37
What is the effect of the toxin from C. botulinum?
It is absorbed and blocks transmission at neuromuscular junctions.
38
What is the consequence of botulinum toxin affecting the neuromuscular junctions?
It causes paralysis of the respiratory muscles and is fatal if the patient isn’t ventilated.
39
What causes acute appendicitis?
Acute appendicitis develops due to obstruction of the lumen of the appendix, often by a fecalith (hard mass of feces).
40
What other factors can cause obstruction in acute appendicitis?
Obstruction can also be caused by increased activity and swelling of subepithelial lymphoid tissue due to earlier infection.
41
What are the typical symptoms of acute appendicitis?
Patients typically complain of periumbilical or right lower quadrant (RLQ) pain.
42
How does the pain in acute appendicitis progress?
The pain is initially mild but intensifies as the inflamed appendix puts pressure on the parietal peritoneum.
43
What physical examination signs are suggestive of appendicitis?
Rebound tenderness is highly suggestive of appendicitis, and guarding and rigidity are common.
44
What may occur as the pain worsens in acute appendicitis?
Vomiting may occur as the pain worsens.
45
What is peritonitis?
Inflammation of the normally sterile peritoneum.
46
How does peritonitis occur?
Occurs when bacteria or chemical irritants (bile, stomach acid, pancreatic juice) are introduced into the peritoneal cavity.
47
What are the etiologies of peritonitis?
Can develop internally due to perforation of the digestive tract or externally from trauma or surgical procedures. May also arise from infection of female reproductive organs (especially fallopian tubes) or rupture of a ureter.
48
What type of infections are usually associated with peritonitis?
Such infections are usually polymicrobial.
49
What are common symptoms of peritonitis?
Symptoms include acute pain originating mainly from the parietal peritoneum and vomiting. Can present as a life-threatening systemic inflammatory response.
50
Where are the majority of colon cancers located?
The majority (70%) are located in the rectum and sigmoid colon.
51
What type of tumours are most colon cancers?
Almost all malignant tumours are adenocarcinomas, originating in the epithelium.
52
How do most colon cancers develop?
Most develop from adenomas (benign tumours of glandular epithelial tissue).
53
What is a minority of colon cancers derived from?
A minority arise from normal epithelium.
54
What are some risk factors for colon cancer?
Risk factors include age, presence of large numbers of adenomas, inherited HNPCC genes, and ulcerative colitis.
55
What is the peak incidence age for colon cancer?
The peak incidence is between 60-70 years.
56
What are common symptoms of colon cancer?
Symptoms often include abdominal discomfort, change in bowel habits, and pain.
57
What symptoms can advanced colon cancer cause?
Advanced tumours can cause fatigue, anorexia, and weight loss.
58
What acute symptoms may occur due to colon cancer?
Acute symptoms include nausea, vomiting, pain, and fever due to obstruction or perforation.
59
What is Ulcerative Colitis?
Ulcerative Colitis is an abnormal activation of immune processes leading to inflammation of the epithelium of the large intestine.
60
Where does Ulcerative Colitis usually begin?
It usually begins in the rectum and progresses proximally.
61
Which tissue layers are typically affected by Ulcerative Colitis?
Tissue layers other than the epithelium are typically not affected.
62
What are the consequences of the inflammatory process in Ulcerative Colitis?
The inflammatory process leads to abscesses, erosions, and ulcers in the epithelium, with considerable blood loss possible.
63
What are pseudopolyps in the context of Ulcerative Colitis?
Pseudopolyps are surviving patches of epithelium that remain after large areas are destroyed.
64
What are signs and symptoms of a systemic inflammatory response in Ulcerative Colitis?
Signs and symptoms include fever, tachycardia, hypotension, and leukocytosis.
65
What is a life-threatening condition that may occur in severe acute cases of Ulcerative Colitis?
Toxic megacolon is a life-threatening condition that may occur due to dilation of the large intestine.
66
What is the long-term risk associated with Ulcerative Colitis?
The likelihood of cancer increases in the damaged area over the long term.
67
What are other common signs and symptoms of Ulcerative Colitis?
Other signs and symptoms include rectal bleeding, diarrhea, tenesmus, and cramping.
68
How might nicotine in tobacco smoke affect Ulcerative Colitis?
Nicotine may suppress the immune system, decrease inflammation, increase mucus production, and release nitric oxide, potentially having a protective effect against ulcerative colitis.
69
What is Crohn’s Disease?
A chronic inflammatory condition affecting the digestive tract, characterized by inflammation in all four layers of the intestinal wall.
70
Where can Crohn’s Disease occur?
It can occur in any part of the digestive tract from mouth to anus, but is most common in the ileum (last part of the small intestine).
## Footnote
Also known as regional ileitis or regional enteritis.
71
What is the pathogenesis of Crohn’s Disease?
The epithelium develops ulcers that extend as fissures, giving a 'cobblestone' appearance to the luminal surface.
72
What complications can arise from Crohn’s Disease?
Fissures can deepen, causing perforations or forming fistulas with nearby organs or skin. Abscesses may form around the anus (perianal abscesses).
73
What happens to the other layers of the intestinal wall in Crohn’s Disease?
The subepithelium, muscularis, and serosa become edematous and then fibrotic (scarred).
74
What histological features are seen in inflamed tissues?
Inflamed tissues show infiltrates of lymphocytes and often granulomas, indicating chronic cell-mediated immune processes.
75
What changes occur in the affected regions of the intestine?
Affected regions become thickened, narrow, and rigid, often separated by healthy areas ('skip lesions').
76
What are the symptoms of Crohn’s Disease?
Symptoms are highly variable and include general malaise, lethargy, anorexia, abdominal pain, fever, malabsorption, nutritional deficiency, diarrhea, bowel obstruction, and abscesses and fistulas.
77
What is the pattern of Crohn’s Disease?
It is characterized by a typical pattern of remission and relapse, with the disease present for a lifetime.
78
What is the distribution of Crohn's Disease?
Crohn's affects both the small and large bowel.
79
What is the distribution of Ulcerative Colitis?
Ulcerative colitis affects only the large bowel.
80
How does endoscopy findings differ between Crohn's Disease and Ulcerative Colitis?
In Crohn's, the rectum is frequently spared, inflammation is not continuous, and the bowel wall is thickened and cobblestoned. In Ulcerative colitis, the rectum is always affected, inflammation is uniform, and the bowel wall is thin with loss of vascular pattern.
81
What histological features are associated with Crohn's Disease?
Granulomas are often present, inflammation extends through the mucosa and muscle of the bowel, and it is predominantly lymphocytes.
82
What histological features are associated with Ulcerative Colitis?
Granulomas and inflammation are usually confined to the mucosa, with polymorphs present.
83
How does diet affect Crohn's Disease?
Remission is achievable with enteral feed.
84
How does diet affect Ulcerative Colitis?
Ulcerative colitis is unaffected by diet.
85
What is the clinical appearance of Crohn's patients?
Crohn's patients are often thin and malnourished, with bloody diarrhea and abdominal masses.
86
What is the clinical appearance of Ulcerative Colitis patients?
Ulcerative colitis patients may have weight loss related to disease severity and often have bloody diarrhea; abdominal masses are not common.
87
How does smoking affect Crohn's Disease?
Smoking is strongly associated with a worse course in Crohn's.
88
How does smoking affect Ulcerative Colitis?
Ulcerative colitis is associated with non-smokers or ex-smokers and appears protective.
89
What is Gastro Esophageal Reflux Disease (GERD)?
GERD is a condition diagnosed when reflux symptoms (heartburn and regurgitation) impair quality of life or pose a risk of complications.
90
What is considered normal reflux?
Transient involuntary reflux of gastric juices into the esophagus is considered normal.
91
What causes GERD?
A key factor is lower esophageal sphincter (LES) dysfunction, including failure of tonic contraction, leading to incompetence and regurgitation.
92
What can exposure of gastric contents lead to?
Exposure of gastric contents can lead to mucosal damage (esophagitis).
93
What is esophagitis?
Esophagitis is inflammation of the esophageal mucosa, leading to pain and discomfort, and can cause narrowing of the esophageal lumen and strictures.
94
What are potential complications of esophagitis?
Esophagitis can lead to Barrett's esophagus (metaplasia of lining) and esophageal cancer.
95
What is NERD?
When reflux does not cause mucosal damage, it is called NERD (non-erosive reflux disease).
96
What contributes to prolonged clearance of contents from the esophagus?
Altered neuromuscular control of the LES and GI motility contribute to prolonged clearance of contents from the esophagus.
97
What factors contribute to the development of GERD?
Factors include gastric and abdominal distension, delayed gastric emptying, increased pro-inflammatory mediators, increased intra-gastric and abdominal pressure, poor posture, level of physical activity, smoking, and a possible genetic link.
98
What are serious complications of GERD in adults?
Serious complications include esophagitis, esophageal strictures, Barrett's esophagus, and esophageal cancer.
99
What are common signs and symptoms of GERD?
Signs and symptoms include heartburn, epigastric or chest pain, nausea, flatulence, chronic cough, hoarseness, and earache.
100
How do infants typically present with GERD?
Infants commonly show regurgitation and occasional projectile vomiting.
101
What is Peptic Ulcer Disease (PUD)?
A term for stomach (gastric) and duodenal ulcers characterized by a mucosal erosion of 5 mm or more in-depth.
102
What causes mucosal damage in PUD?
Mucosal damage is associated with the aggressive action of gastric juices (acid and pepsin) and weakened mucosal protection.
103
What are the two strong links to PUD development?
1. Chronic use of non-steroidal anti-inflammatory drugs (NSAIDs)
2. Helicobacter pylori (H. pylori) infection.
104
What is the synergistic effect in PUD?
NSAID use combined with H. pylori has a synergistic effect, working together to produce a greater effect than they would individually.
105
What is the prevalence of H. pylori in ulcer patients?
Present in 90% of duodenal and 70-90% of gastric ulcer patients.
106
How does H. pylori survive in the stomach?
By releasing urease to alkalinize its environment.
107
How does H. pylori damage the mucosa?
By inducing chronic inflammation and breaking down mucosal defenses.
108
What effect does H. pylori have on gastric acid secretion?
Causes hypersecretion of gastric acid due to inflammation and increased parietal cell mass.
109
What is the role of NSAIDs in PUD?
They reduce prostaglandin (PG) synthesis by inhibiting cyclo-oxygenase (COX), which maintains the mucosal barrier.
110
What are the complications of PUD?
GI bleeding and perforation.
111
What occurs during perforation in PUD?
Continued erosion through the GI wall leads to peritonitis.
112
How can GI bleeding manifest?
As anemia, hematemesis (vomiting blood), or melena (dark red or black tarry stools).
113
What are common signs and symptoms of PUD?
Pain, nausea, vomiting, bloating, weight loss, and loss of appetite.
114
What type of pain is typically associated with PUD?
Epigastric, burning pain that occurs when the stomach is empty (before meals and overnight).
115
What does peritonitis from perforation cause?
Sudden and severe abdominal pain.
116
Where are gastric ulcers located?
Gastric ulcers are located in the stomach.
117
Where are duodenal ulcers located?
Duodenal ulcers are located in the duodenum.
118
When does gastric pain occur?
Gastric pain occurs during or 30 minutes to 2 hours after eating.
119
When does duodenal pain occur?
Duodenal pain occurs 3-4 hours after eating and is aggravated by hunger.
120
Is gastric pain relieved by eating?
No, gastric pain is not relieved by eating.
121
Is duodenal pain relieved by eating?
Yes, duodenal pain is relieved by eating.
122
What type of vomiting is associated with gastric ulcers?
Gastric ulcers cause hematemesis.
123
What type of vomiting is associated with duodenal ulcers?
Duodenal ulcers cause melena.
124
Is there a special diet for gastric ulcers?
Yes, there is a special diet for gastric ulcers.
125
Is there a special diet for duodenal ulcers?
No, there is no special diet for duodenal ulcers.
126
What is viral hepatitis?
Viral hepatitis is an inflammation of the liver caused by a viral infection.
127
What are the most common types of hepatitis viruses?
The most common types are Hepatitis A (HAV), Hepatitis B (HBV), Hepatitis C (HCV), Hepatitis D (HDV), and Hepatitis E (HEV).
128
How is Hepatitis A (HAV) spread?
Hepatitis A is usually spread through contaminated food or water and often resolves on its own.
129
How is Hepatitis B (HBV) transmitted?
Hepatitis B is transmitted through blood, sexual contact, or from mother to baby; it can become chronic.
130
How is Hepatitis C (HCV) primarily spread?
Hepatitis C is primarily spread through blood, such as sharing needles, and often leads to chronic infection.
131
What is unique about Hepatitis D (HDV)?
Hepatitis D only occurs in people with Hepatitis B and makes the infection more severe.
132
How is Hepatitis E (HEV) usually spread?
Hepatitis E is usually spread through contaminated water and is more common in developing countries.
133
What is fulminant hepatitis?
Fulminant hepatitis is a rapidly developing severe form that can cause total liver failure and death within weeks in a small minority of infected individuals.
134
What are common signs and symptoms of viral hepatitis?
Signs and symptoms include pain, fever, anorexia, nausea and vomiting, and jaundice.
135
How is viral hepatitis diagnosed?
Diagnosis of the specific viral pathogen requires laboratory detection, not just clinical signs.
136
What can chronic infection with HBV or HCV lead to?
Chronic infection can lead to progressive liver damage, including cirrhosis and cancer.
137
What is the proportion of HCV infections that become chronic?
The proportion of HCV infections that become chronic is much higher, possibly up to 70%.
138
What body fluids can HBV be found in?
HBV is viable in blood and other body fluids such as saliva, semen, and vaginal secretions.
139
What percentage of HBV cases develop chronic infection?
Chronic infection develops in about 5-10% of HBV cases.
140
What are the potential outcomes of HBV infection?
Outcomes can range from acute infection with recovery, asymptomatic carrier state, chronic hepatitis, fulminant hepatitis, or hepatocellular carcinoma.
141
How is HCV primarily transmitted?
HCV primarily occurs through percutaneous exposure to blood, such as injecting drug use.
142
What are the outcomes of HCV infection?
Outcomes include acute infection (often asymptomatic), chronic hepatitis (often progressing to cirrhosis), and hepatocellular carcinoma.
143
What is the process by which ethanol is metabolized in hepatocytes?
Ethanol is converted to acetaldehyde and then to acetate (acetyl-CoA).
144
What happens to triglyceride production with excess alcohol consumption?
Excess alcohol leads to increased triglyceride production and decreased fatty acid utilization, causing fatty liver.
145
Is fatty liver reversible?
Yes, fatty liver is reversible.
146
What are the consequences of continued excessive alcohol consumption?
It damages and kills hepatocytes, leading to inflammation.
147
What causes damage to hepatocytes in alcoholic liver disease?
Damage is due to the toxicity of alcohol and, to a greater extent, acetaldehyde.
148
What can extensive hepatocyte damage lead to?
It can lead to cirrhosis and reduced overall liver function.
149
How does increased cell replication among surviving hepatocytes affect cancer risk?
It increases the opportunity for oncogenes to arise, raising the likelihood of malignancy.
150
What are some signs and symptoms of alcoholic liver disease?
Signs and symptoms can be low-grade (GI malaise, mild fever) or more serious (bleeding, alcohol withdrawal symptoms, hepatomegaly, splenomegaly, ascites, encephalopathy).
151
How does fatty liver appear on examination?
Fatty liver appears slightly enlarged and pale yellow.
152
What is Hepatocellular Carcinoma (HCC)?
Hepatocellular Carcinoma (HCC) is the most common type of liver cancer originating from the liver's main cells, called hepatocytes.
153
What chronic liver diseases are often associated with HCC?
HCC is often associated with chronic liver diseases such as Hepatitis B or C infection, Cirrhosis, Non-alcoholic fatty liver disease (NAFLD), and Aflatoxin exposure.
154
What is the most common predisposing factor for HCC?
The most common predisposing factor for HCC is cirrhosis, accounting for approximately 80% of cases.
155
What is the pathophysiology of HCC?
HCC develops in people with chronic HBV or HCV infection or alcoholic liver disease. Increased hepatocyte regeneration in response to cell death may provide scope for mutations, including oncogenes.
156
What are the signs and symptoms of early-stage HCC?
In the early stages, HCC may be asymptomatic.
157
What are the signs and symptoms of later-stage HCC?
Later stages can present with pain in the upper right abdomen, fever, jaundice, ascites, liver enlargement, weakness, nausea, anorexia, and paraneoplastic syndromes.
158
What are gallstones?
Gallstones are solid particles that form in the gallbladder, usually made of cholesterol, bilirubin, or calcium salts.
159
What can happen if gallstones block bile flow?
They can cause pain and complications.
160
What is cholesterol's solubility in water?
Cholesterol is insoluble in water but is emulsified by bile salts for transport in bile.
161
What can cause cholesterol to precipitate as crystals?
Increased cholesterol concentration, decreased bile salt concentration, or prolonged retention of bile in the gallbladder.
162
What are gallstones also known as?
Gallstones are also known as biliary calculi.
163
What symptoms may arise from gallstones?
Symptoms arise when stones block ducts of the biliary system or pancreatic duct.
164
What does blockage of bile ducts cause?
It causes pain in the upper abdomen.
165
What can prolonged blockage of the cystic duct lead to?
It leads to acute inflammation of the gallbladder (cholecystitis), often with secondary bacterial infection.
166
What are the symptoms of acute obstruction from cholelithiasis?
Symptoms include poorly localized severe abdominal pain, nausea, vomiting, tachycardia, hypertension, and diaphoresis.
167
What is pancreatitis?
A condition characterized by the premature activation of the pancreas's own digestive enzymes, leading to self-digestion and inflammation.
168
What are the two forms of pancreatitis?
Acute pancreatitis and chronic pancreatitis.
169
What is acute pancreatitis most often associated with?
Gallstones.
170
What happens in acute pancreatitis?
Gallstones block the pancreatic duct, trapping and activating digestive enzymes within the pancreas, causing destruction.
171
What are the systemic effects of acute pancreatitis?
Fever, shock, kidney failure, and respiratory distress.
172
What are the complications of acute pancreatitis?
Noninfectious peritonitis, infection of necrotic tissue leading to abscesses, exocrine pancreatic insufficiency, and rarely, endocrine dysfunction.
173
What is chronic pancreatitis most often associated with?
Long-term alcohol abuse.
174
What role does smoking play in chronic pancreatitis?
It increases susceptibility to autodigestion and predisposes to CFTR dysfunction.
175
What are the consequences of continued alcohol and smoking in chronic pancreatitis?
Pancreatic fibrosis, calcifications, and disease progression.
176
What percentage of acute pancreatitis survivors develop chronic pancreatitis?
About 20%, especially with recurrent episodes.
177
What happens to normal pancreatic tissues in chronic pancreatitis?
They are replaced by scar tissue, making it progressive and irreversible.
178
What does chronic pancreatitis predispose individuals to?
Pancreatic cancer.
179
What type of cancer is most commonly associated with pancreatic cancer?
Most cases are pancreatic ductal adenocarcinomas.
180
What are the risk factors for pancreatic cancer?
Advancing age, family history (most important), cigarette smoking, male gender, diabetes mellitus, obesity, high-fat diet, chronic pancreatitis, prior gastrectomy.
181
What is the prognosis for pancreatic cancer?
Prognosis is very poor as most cancers are advanced and incurable at diagnosis.
182
What does palliative treatment for pancreatic cancer focus on?
Palliative treatment focuses on pain relief and removal of biliary obstruction.
