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path 375 > 8 - GI Tract, Liver, Biliary Tract and Pancreas > Flashcards

8 - GI Tract, Liver, Biliary Tract and Pancreas Flashcards

1
Q

What is the most common craniofacial malformation of the newborn?

A

Cleft lip and/or palate

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2
Q

The etiology of cleft lip is multifactorial. What can contribute to it?

A
  1. Genetic factors
  2. Environmental factors
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3
Q

What is the most well-known cleft lip/palate syndrome? What causes it?

A

DiGeorge Syndrome
22q11 deletion

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4
Q

5 Risk factors of dental carries?

A
  1. poor oral hygiene
  2. anything that promotes plaque formation
  3. sugar
  4. lack of saliva
  5. possibly genetics
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5
Q

What is pulpitis

A

Painful cavities because erosion is so bad it reaches the pulp, which is the innermost layer of the tooth where the nerves are

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6
Q

What is periodontitis and what three things does it cause

A

Severe gingivitis

  1. tooth falls out
  2. bad breath
  3. infections spreads to jaw bone
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7
Q

What is stomatitis?

A

Inflamed/sore mouth

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8
Q

What is the difference between aphthous stomatitis and infectious stomatitis?

A

Aphthous = canker sores
- unknown cause

Infectious = herpes “cold sore”
- cause = candida fungus

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9
Q

Name two immune system diseases that can result from stomatitis

A

Behcet syndrome
Inflammatory Bowel disease

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10
Q

What is the main type of oral cavity neoplasm? What are the two main causes? What are 3 other causes?

A

Squamous cell carcinoma/squamous dysplasia

  1. alcohol and tobacco
  2. HPV
  3. therapeutic radiation
  4. immunosuppression
  5. UV exposure on lips
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11
Q

What is the term for persistent white patch and persistent red patch? What are they both associated with etiologically?

A

leukoplakia
erythroplakia

alcohol and tobacco

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12
Q

Treatment of oral cavity neoplasms?

A

surgical resectioning and radiation therapy

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13
Q

What are two infectious and three non-infectious causes of sialadenitis?

A

Infectious:
1. bacteria (S. aureus)
2. virus (mumps)

Non-infectious:
1. autoimmune (Sjogren syndrome)
2. stones in salivary glands (Sialolithiasis)
3. therapeutic radiation

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14
Q

Name a benign and malignant oral sialadenitis neoplasm

A

Benign: pleomorphic adenoma
Malignant: mucoepidermoid carcinoma

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15
Q

What is a hiatus hernia? What is a sliding hernia and paraesophageal hernia?

A

Hiatus: when part of stomach protrudes out from diaphragm. Two exampels are sliding and paraesophageal hernia

Sliding: ‘sliding’ of gastroesophageal junction and cardia out of the stomach

Paraesophageal: part of stomach protrudes upwards and forms a pocket besides the esophagus

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16
Q

What is achalasia?

A

degeneration of ganglion cells in myenteric plexus causes LES to contract, leading to dysphagia (difficulty swallowing) and food build up in esophagus

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17
Q

Primary and secondary causes of achalasia?

A

Primary: unknown

Secondary: parasitic infections (T. cruzi aka Chagas disease), or diseases that infiltrate esophagus (amyloidosis, sarcoidosis)

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18
Q

What is varicies? Common cause? Treatment?

A

Varicies: dilation of submuscoal veinsin the esophagus -> rupture -> life-threatening bleeding

Common cause: hepatic cirrhosis (portal HTN)

Treatment: banding, medications, liver transplant

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19
Q

What is one main example of esophagitis? What are some risk factors?

A

Gastroesophageal Reflux Disease (GERD)
- reflux of gastric contents into esophagus
- due to pressure buildup in stomach and insufficient LES tone
- risk factors: alcohol, drugs, pregnant, obese, xs caffeine

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20
Q

What are 4 other causes of esophagitis besides GERD?

A
  1. infectious: virus (HSV), candida
  2. ingestion of irritating substance
  3. allergies and inflammation
  4. autoimmune diseases
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21
Q

What exactly is Barrett esophagus and how can it go from bad to worse?

A

Complication of GERD

Squamous mucosa -> columnar mucosa (intestinal metaplasia) -> dysplasia -> esophageal adenocarcinoma

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22
Q

4 signs and symptoms of malignant esophageal neoplasms?

A
  1. occult GI bleeding (anemia)
  2. Unintentional weight loss
  3. dysphagia (difficulty swallowing)
  4. odynophagia (painful swallowing)
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23
Q

What is gastropathy?

A

Injury to stomach lining without inflammation, but can be severe enough to cause stomach lining erosion or ulceration

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24
Q

3 causes of gastropathy?

A

Causes:
- chemical injury (alcohol, NSAIDs)
- vascular injury (ischemia, portal HTN)
- physiological injury: trauma, burn, sepsis

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25
Q

Difference btwn acute and chronic gastritis? Talk about type of WBC present and causes.

A

Acute
- neutrophils present
- drugs, alcohol, severe physiologic stress

Chronic
- lymphocytes present
- autoimmune conditions, H. pylori

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26
Q

What is peptic ulcer diseaes?

A

ulceration of gastric or duodenal mucosal lining from either acute or chronic gastritis

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27
Q

3 risk factors of peptic ulcer disease? 4 complications?

A

Risk Factors:
1. H. pylori
2. reduced mucosal barrier
3. drugs

Complications:
1. hemorrhaging
2. perforation -> peritonitis
3. penetration into the pancreas
4. scarring

28
Q

How does H. pylori cause gastritis? What are some symptoms of helicobacter gastritis? What happens if left untreated?

A

Gram-neg bacteria hides in mucosal lining to avoid stomach acid and releases urease

Usually asymptomatic but can cause abdominal discomfort (dyspepsia)

Can lead to MALT lymphoma, mucosal atrophy, and intestinal metaplasia

29
Q

What are the functions of parietal, chief, and G cells in normal gastric function?

A

Parietal: releases HCl for stomach acid and intrinsic factors for B12 absorption

Chief: release pepsinogen which digests protein

G: releases gastrin which tells parietal to make more HCl

30
Q

What happens to the three gastric function cells during autoimmune gastritis?

A

Parietal cells and chief cells get destroyed. Lack of HCl causes G cells to produce more gastrin.

31
Q

What are the three consequences to autoimmune gastritis and solutions to each?

A
  1. Inability to absorb B12
    - parietal cells dead so no IF and thus no absorption of B12
    - leads to megaloblatic anemia and possible chronic nerve dmg
    SOLUTION: early detection and lifelong injection of B12
  2. Increased risk of gastric adenocarcinoma
    - due to G cells making too much gastrin
    - longstanding chronic inflammation, atropy, and intestinal metaplasia
    SOLUTION: early detection and biopsy screening
  3. Increased risk of gastric well-differentiated neuroendocrine tumor
    - due to G cells making too much gastrin
    - leads to endocrine cell proliferation which can end up as a tumor
    SOLUTION: endoscopic screening and resectioning
32
Q

Name two stomach neoplasms

A

Gastric adenocarcinoma
Lymphoma (MALT)

33
Q

Gastric adenocarcinoma: What are some of its risk factors? Why does it have such a poor prognosis?

A

H. pylori gastritis, autoimmune gastritis

Poor prognosis due to metasis to lymph nodes (Virchow supraclavicular lymph node) and ovaries (Krukenberg tumor)

34
Q

MALT lymphoma: main characteristic (e.g. grade and progressive speed), major cause, and treatments

A

Main characteristic: slow-progressing, low-grade lymphoma

Major cause: H. pylori infection

Treatment: treat H. pylori, but if it still persists even when bacteria is gone, radiation or chemotherapy

35
Q

What is Meckel’s diverticulum? What is the rule of 2?

A

Developmental disorder involving the persistene of vitelline duct staying partially open even after birth

  • 2% of population
  • 2% develop symptoms
  • presents after 2 yo
  • 2 ft proximity to ileocecal valve
  • 2 in long
  • 2 types of ectopic tissue (gastric, pancreatic)
36
Q

Three mechanisms of malabsorption (small bowel pathology)?

A
  1. inadequate intraluminal digestion
  2. primary mucosal absorptive defect
  3. impeded transport of nutrients
37
Q

What is celiac disease? Pathogenesis of it? Treatment?

A

What it is: gluten allergy HSR IV

Pathogenesis: breakdown of gluten triggers immune sys and causes small bowel disease. Malabsorption also causes dmg

Treatment: lifelong gluten-free diet

38
Q

What is intraepithelial lymphocytosis? Anti-tissue transglutaminase?

A

Too many lymphocytes in epithelium, result of malabsorption of gluten in small bowel

Antibodies produced when malabsorption of gluten in small bowel

39
Q

What are 6 similarities between CD and UC?

A
  1. both affect young ppl
  2. more common in caucasians and has familial predisposition
  3. similar extra-intestinal manisfestations (arthritis, skin lesions, liver involvement)
  4. affects upper GI (more common in CD)
  5. predisposes to dysplasia and carcinoma (more so in UC)
  6. treated with anti-inflammatory drugs
40
Q

What is Hirschsprung’s disease and how is it treated

A

Congenital absence of colonic ganglion cells = no peristalsis and thus remains in permanent spasm (creating obstruction)

Treated by resecting the agangliaonic segment

41
Q

What is diverticular disease? What’s an example?

A

Acquired disease involving formation of tiny pouches especially on the sigmoid colon

Meckel Diverticulum

42
Q

Difference between diverticulosis and diverticulitis (what it is and treatment)?

A

Diverticulosis: many diverticula
- wall of bowl is thin and can easily bleed
- treat with colonscopy or resection

Diverticulitis: inflammation of diverticula
- if uncomplicated, treat with antibiotics
- if complicated, pouches are obstructure and are very painful because it becomes trapped with bacteria
- treate with surgical resection

43
Q

What causes hemorrhoids? Possible treatments (6)?

A

Dilation of veins in submucosa of anorectal area, caused by increased venous pressure in area (obesity, pregnancy), can be painful and bleed

High fiber diet, stool softener, steroid cream, band ligation, sclerotherapy, local resection

44
Q

What are the three types of serrated polyps

A

hyperplastic polyp
sessile serrated lesion
traditional serrated adenoma

45
Q

What exactly are adenomatous polyps?

A

Polyps that protrude and thus are easier to detect and completely remove

46
Q

What is familial adenomatous polyposis (FAP)?Why can’t you simply resect it

A

Autosomal dominant hereditary tumor syndrome with so many adenomatous polyps that cannot resect; requires total colectomy

47
Q

What are hamartomatous polyps? Example of a disease characterized by these?

A

Usually low to no malignant potential and involves benign disorganized growth of polyps

Peutz-Jeghers syndrome, an autosomal dom diseaese with hamartomatous colon polyps

48
Q

What is colorectal adenocarcinoma? Whys is it considered one of the top killer cancers in both men and women? How is it diagnosed?

A

The most common form of colon cancer, often associated with IBD or genetics (Lynch, FAP) but risk factors can come into play.

Metastasizes via lymphatics and bloodstream

Screening of fecal occult blood, goal is to find colon polyps

49
Q

What causes appendicitis? What do symptoms look like? How can it be treated?

A

Acute bacterial infection of appendix secondary to luminal obstruction

Symptoms: Abdominal pain, nausea/vomit/anorexia, elevated WBC, can rupture and lead to peritonitis/sepsis

Treatment: resection or antibiotics (similar to diverticulitis)

50
Q

What causes jaundice?

A

hyperbilirubinemia, which is buildup of bilirubin, a breakdown product of hemoglobin

51
Q

What are the three classifications of jaundice/hyperbilirubinemia

A

Pre-hepatic: e.g. hemolysis of RBC

Hepatic: e.g. severe hepatitis or cirrhosis

Post-hepatic: e.g. cancer at pancreas head

52
Q

What is glucuronide?

A

The thing bilirubin binds to when conjugated in the liver before being excreted into bile

53
Q

What are the 4 main classifications of liver disease?

A
  1. Hepatitis
  2. Drug-induced liver disease
  3. Autoimmune diseaes
  4. Metabolic diseases (fatty liver disease, hemochromatosis, Wilson’s disease, Alpha-1 antitrypsin deficiency)
54
Q

What are the three main metabolic liver diseases and how do they harm the body?

A

Hemochromatosis
- AR disorder preventing liver from regulating iron in body
- results in iron buildup leading to scarring/cirrhosis, possibly to hepatocellular carcinoma

Wilson’s disease
- AR disorder preventing liver from excreting xs copper into bile
- results in liver cirrhosis and other abnormalities

Alpha-1 antitrypsin
- AR disorder causing misfolding of alpha-1 antitrypsin
- misfolded protein accmulation in hepatocytes causes scarring/cirrhosis
- lack of the protein in blood can cause problems with inflammation

55
Q

What are two drugs/toxins that can induce hepatitis

A

Acetaminophen (Tylenol) and alcohol

56
Q

What are five other liver diseases caused by microorganisms?

A

Hepatic Abscess (bacteria or amoeba)

Hydatid disease (echinococcus spp; parasite-filled cysts)

Schistosomiasis (schistosoma spp; lays eggs in your veins, may cause portal HTN)

Ascariasis (Ascaris lumbricoides; obstruction of bile ducts, looks like earth worms)

Fascioliasis (Fasciola hepatica or gigantica; liver flukes that lead to inflammation and scarring)

57
Q

What are three immunologic disorders related to biliary pathology (Hint: APP)?

A

Autoimmune hepatitis (AIH)
- causes chronic hepatitis

Primary biliary cholangitis (PBC)
- disease of unknown etiology characterized by destruction of SMALL intra-hepatic bile ducts

Primary sclerosing cholangitis (PSC)
- disease of unknown etiology characterized by destruction of LARGE intra-hepatic bile ducts

58
Q

What are two examples of benign liver neoplasms? Three malignant neoplasms?

A

Benign:
Cavernous hemangioma (endothelium)
Hepatocellular adenoma (neoplasm of hepatocytes)

Malignant:
Hepatocellular carcinoma (HCC)
Metastatic malignancy
Cholangiocarcinoma (adenocarcinoma of the bile ducts)

59
Q

How would you treat hepatocellular carcinoma (HCC)? (3)

A

Embolization, direct thermal ablation, resection

60
Q

What are the three types of stones in gallstones (cholelithiasis)

A
  1. cholesterol (caused by xs cholesterol secretion by liver)
  2. pigment stones
  3. mixed stones
61
Q

What is cholelithiasis

A

Gallstones

62
Q

What are 4 complications with cholelithiasis

A
  1. cholecystitis
  2. choledocholithiasis (stones block bile duct) => obstructive jaundice, ascending cholangitis
  3. gallstone ileus (obstruction of bowel)
  4. risk factor for gallbladder cancer
63
Q

Difference btwn acute (2) and chronic (4) pancreatitis?

A

Acute:
- due to release of pancreatic enzymes
- alcohol and gallstones primarily responsible

Chronic:
- persistence of infection even after causative agent removed
- CF is an imporant factor, alcohol too
- progressive and irrev fibrosis
- may result in exocrine/endocrine insufficiency

64
Q

6 complications of acute pancreatitis?

A
  1. abscess
  2. pseudocyst
  3. peritonitis
  4. chronic pancreatitis
  5. diabetes
  6. high mortality
65
Q

Differences btwn PDAC (2) and WDNETs (3)

A

Pancreatic ductal adenocarcinoma:
- poor prognosis
- difficult to detect early cuz asymptomatic, when detect already metastasized

Pancreatic Well-differentiated neuroendocrine tumors
- arises from endocrine cells of pancreatic islets
- much better prognosis than PDAC but still can metastasize and kill
- treatment: surgical removal

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