Usmle Fa Gi Flashcards

Front 1

Name major pancreatic enzymes

Back 1

Alpha-amylase—starch digestion, secreted in active form.
enzymes Lipase, phospholipase A, colipase—fat digestion.
Proteases (trypsin, chymotrypsin, elastase, carboxypeptidases)—protein digestion,
secreted as proenzymes also known as “zymogens.”
Trypsinogen—converted to active enzyme trypsin by enterokinase/enteropeptidase, an
enzyme secreted from duodenal mucosa. Trypsin activates other proenzymes and more
trypsinogen (positive feedback loop).

Front 2

Achalasia

Back 2

Failure of relaxation of lower esophageal sphincter (LES) due to loss of myenteric (Auerbach’s) plexus. High LES opening pressure and uncoordinated peristalsis lead to progressive dysphagia. Barium swallow shows dilated esophagus with an area of distal stenosis (bird's bick appearance)

Front 3

What risk is achalasia associated with?

Back 3

Increased risk of esophageal carcinoma

Front 4

Name two otther conditions, outside of Aerbach's Plexus absence that will lead to achalasia

Back 4

1. Chagas Disease - caused by Trypanosoma cruzi (Kissing bag)
2. Schleroderma (CREST Syndrome - five main features:
Calcinosis, Raynaud's syndrome, Esophageal dysmotility, Sclerodactyly
Telangiectasia)

Front 5

Back 5

Cleft palate:Due to failure of fusion of the facial processes in the embryonic period. (Gi200)

Front 6

Back 6

Herpes simplex
Note the vesicular lesions above the vermilion border of the lip. The virus remains dormant in the cranial sensory ganglia. (Gi201)

Front 7

Back 7

Reflux Esophagitis:
This is the most common type of esophagitis. There is acid chemical damage to the mucosa of the esophagus, owing to relaxation of the LES. Barrett's esophagus is a complication of GERD and predisposes to distal adenocarcinoma. (Gi017)

Front 8

Patient: executive under great stress, severe epigastric pain, shooting down the left shoulder: workup?

Back 8

Flat Plate of the abdomen: an X-ray of the abdomen, without use of contrast media and obtained while the patient is recumbent.
The ulcer perforates, acid irritates diaphragm becomes irritated (phrenic nerve)--> referred pain to the shoulder because this is the same dermatome.

Front 9

Name the main causes of panctreatic insufficiency

Back 9

Chronic pancreatitis: usually due to alcoholism in adults and cystic fibrosis in children. Leads to maldigestion of fats, fat-soluble minerals, carbs and proteins

Front 10

Back 10

Councilman hyaline body is an eosinophilic globule often found in the liver in viral hepatitis, yellow fever, or other viral syndrome. It represents a hepatocyte that is undergoing apoptosis.

Front 11

Back 11

Duodenal Atresia: radiograph of the abdomen demonstrates the double bubble sign: an enlarged stomach (S) and proximal duodenum (D) in a neonate with duodenal atresia. Note the absence of distal gas.
Symptoms: obstruction - vomiting and abdominal distension, biliary vomit.

Front 12

3 week old male infant with recurrent projectile, nonbilious vomiting. No signs of illness (fever, diarrhea etc). Physical exam shows an olive shaped mass in the epigastric region

Back 12

Pyloric sphincter stenosis

Front 13

Name three main congenital mechanical disorders of the esophagus

Back 13

1. Tracheoesophageal fistula
2. Esophageal webs
3. Achalasia

Front 14

Esophageal webs/rings
Associated sydromes

Back 14

Weblike protrusions of the esophageal mucosa into the lumen.
Presentation: dysphasia
Epidemiology: women in 40s
Risk factors: GERD
Consequences: Fe deff anemia, increased risk of carcinoma
Seen in Plummer-Vilson Syndrome
Think of middle aged unmarried women purposely putting webs in their pipes esophagus) to lure in a cute plummer.

Esophageal rings (Chatzki rings for Polish housewives) are very similar, but circumferential and thicker. They include mucosa, submucosa and muscularis propria

Front 15

Achalasia

Back 15

Failure of the LES to relax with swallowing
Etiology: mostly unknown - loss of distal esophageal inhibitory neurons that release NO and VIP. In South America - Chagas disease that causes destruction of myenteric plexus.
Presentation: progressive dysphagia
Gross: esophageal dilation proximal to the LES
Barium swallow: "Bird's Beak sign"
Micro: loss of ganglion cells in myenteric plexus.
Treatment: LES balloon dilation or myotomy.
Increased

Front 16

Describe treatments for achalasia

Back 16

- Laparascopic myotomy
- Balloon dilation
- Botulinum toxin (botox) injection to inhibit LES cholinergic neurons

Front 17

What is achalasia putting one at an increased risk for?

Back 17

Esophgeal carcinoma because food is roating in the dilated portion of the esophagus above strictured LES.

Front 18

Mallory - Weiss Tears

Back 18

- Longitudinal linear tears in the esophagus near gastroesophageal junction.
- Associated with severe retching or vomiting secondary to acute alcohol intoxication.
Mechanism: relaxation of LES fails with prolonged vomiting - refluxing gastric contnents overwhelm and stretch and tear esophageal wall.
10% of upper esophageal bleeds are due to esophageal lacerations.
Treatment: generally heal by themselves.

Front 19

Name the condition and its etiology

Back 19

Esophageal achalasia - hypertonia of the lower esophageal sphincter produces the characteristic "birds beak" deformity.
Etiology: 1ry achalasia - caused by failure of distal esophageal inhibitory neurons.
2ry: Chagas disease, diabetic autonomic neuropathy

Front 20

Name the condition and describe its possible etiology

Back 20

Esophageal stricture - concentric fibrosis of the submucosa produces
a long narrowed esophagus. This could be caused by chronic GERD, scarring or irradiation.
The dysphagia associated with stenosis is usually progressive.

Front 21

What pathology is seen on this gross image?

Back 21

At the lower end of the esophagus (which has been turned inside out at autopsy) are linear dark blue submucosal dilated veins known as varices. In patients with portal hypertension (usually micronodular cirrhosis from chronic alcoholism), the submucosal esophageal veins become dilated (form varices). These varices are prone to bleed.
Esophageal varices DEVELOP IN 90% OF CIRRHOTIC PATIENTS, most commonly in association with alcoholic liver disease.
Presentation: asymptomatic, with massive hematemesis when ruptured --> potentially fatal hemorrhage.
TreatmentL surgical: band ligation

Front 22

Pathophysiology of GERD

Back 22

GERD is most common in adults over 40.<BR>Clinical symptoms: heartburn, dysphagia, sometimes regurgitation of sour-tasting gastric contents.<BR>Reflux of gastric juices leads to the development of mucosal injury in GERD.<BR>Barrett's Esophagus is a common complication of GERD characterized by intestinal metaplasia within the esophageal squamous mucosa. On the image we see patches of red, velvety columnar gastric mucosa rwith intestinal goblet cells eplacing pale, smooth esophageal squamous mucosa.<BR>Diagnosis requires histologic presence of gastric columnar mucosa with goblet cells above esophageal junction.<BR>Complications of GERD: bleeding, stricture formation, Barrett's esophagus

Front 23

Describe two most common complications of Barretts esophagus

Back 23

1. Ulceration with stricture formation (most common)
2. Glandular dysphasia with increased risk for distal adenocarcinoma (seen on image)

Front 24

Barrett's Esophagus

Back 24

Metaplasia of the squamous esophageal mucosa to a more protective columnar type because of chronic exposure to gastric secretions.
Incidence is increasing.
Gross: iregular GE junction with tongues of red granular mucosa extending up into the esophagus.
Increased risk of dysphasia and esophageal carcinoma.

Front 25

Squamous Cell Carcinoma
("Second Class Citizen" carcinoma)

Back 25

Squamous Cell Carcinoma
- arises most commonly
in the upper and middle esophagus.
Epidemiology: most common esophageal cancer in the world. Males>females, African Americans x 6>Caucasians.
Risk factors:
- Smoking
- Alcohol
- POVERTY
- Plummer-Vinson syndrome
- Achalasia
Presentation: often asymptomatic until late in the course. Progressive dysphasia. Weight loss and anorexia. Bleeding.
Histo: Squamous cell carcinoma is composed of nests of malignant cells that partially recapitulate the organization of squamous epithelium.
Treatment: Surgery
Prognosis: poor

Front 26

What type of esophgeal carcinoma this is more likely to be? Why? Describe pathophysiology

Back 26

Squamous cell carcinoma is composed of nests of malignant cells that partially recapitulate the organization of squamous epithelium.

Front 27

Adenocarcinoma of the esophagus

Back 27

Adenocarcinoma arising in Barrett's Metaplasia -
the presence of a nodular mass in a field of Barrett's metaplasia
is highly suspicious for adenocarcinoma.
Adenocarcinoma of esophagus is the most common in Western countries and US.
Caucasians>Africans
Arises in DISTAL esophagus.
Associated with Barrett's esophagus and dysphasia - presumably due to accumulationof mutations during progression to dysphasia and ivasive carcinoma.
Histo: esophageal adenocarcinoma is organized into back-to-back glands.

Front 28

Esophageal cancer: how to distinguish between adenocarcinoma and squamous cell carcinoma?

Back 28

- Adenocarcinoma usually occurs distally and often involves gastric cardia. Initially appears as flat or raised pathes in otherwise intact mucosa. Adenocarcinomas frequently produce musin and form glands.
Squamous cell carcinoma - are most frequently found in mid esophagus, where it is commonly causes strictures.

Front 29

Pyloric stenosis

Back 29

Congential form is due to hyperthrophy of pyloric sphincter resulting in gastric outlet obstruction.
Males>females
Associated with Turner and Edwards syndrome.
Presentation: onset of regurgitation and vomiting in the second week of life.
Waves of peristalsis are visible in the abdomen plus a firm, ovoid abdominal mass.

Acquired pyloric stenosis: in adults as a result of antral gastritis or peptic ulcers close to pylorus.

Front 30

Diaphragmatic hernia

Back 30

Congenital defect in the diaphragm resulting in hurniation of the abdominal organs into the thoracic cavity.
The stomach is the most common hurniated organ.
Often associated with intestinal malrotation
Complications: respiratory compromise - underdeveloped lungs

Front 31

What is the pathology?

Back 31

Menetrier disease Think of a Man becoming Tree-Like.
Menetrier disease is a disorder characterized by increased secretion of Transforming Growth Factor (TGF-alpha).
As a result: diffuse hyperplasia of the foveolar mucous-secreting epithelium of the body and fundus and hypoprotenemia. Replacement of parietal and chief cells-> decreases HCl production
Increased risk of gastric adenocarcinoma.
Treatment: supportive
Histo: can see elongated cork-screw like foveolar glands.

Front 32

What is the pathology?

Back 32

Menetrier disease Think of a Man becoming Tree-Like.
Menetrier disease is a disorder characterized by increased secretion of Transforming Growth Factor (TGF-alpha).
As a result: diffuse hyperplasia of the foveolar mucous-secreting epithelium of the body and fundus and hypoptotenemia. Replacement of parietal and chief cells-> decreases HCl production
Increased risk of gastric adenocarcinoma.
Treatment: supportive
Histo: can see elongated cork-screw like foveolar glands.

Front 33

Describe the pathophysiology of Zollinger-Ellison Syndrome

Back 33

Caused by gastrin secreting tumors, gastrinomas, usually found in the pancreas or small intestine.
Gross: enlarged rugal folds because Gastrin induces hyperplasia of parietal cells (5X increase) and mucous producing cells-> Increased acid secretion.
Presentation: multiple intractable peptic ulcers.
Treatment: goal 1: blockage of acid hypersecretion by PPI or high dose H2 histamine receptor agonists.
goal 2: identification and resection of gastrinomas. Most are solitary tumors and are easily resected. 25% have multiple neoplasia type I.

Front 34

36 yo male patient presents with burning epigastric pain accompanied by nausea and vomiting. Melena is present in his stool. Patient is a chronic NSAIDs user and smoker of 15 years. The physical examination findings are often normal with occasional mild epigastric tenderness. What is the most likely diagnosis?

Back 34

Acute Hemorrhagic Gastritis
Definition: acute inflammation, erosion, hemorrhage of gastric mucosa due to a breakdown of mucosal barrier and acid-induced injury.
Etiology:
- Chronic aspirin/NSAID use
- Alcohol use
- Smoking
- Postsurgery
- Burns
- Ischemia
- Stress
Presentation: epigatstric abdominal pain. Gastric hemorrhage, hematomesis, melena.

Front 35

36 yo male patient presents with burning epigastric pain accompanied by nausea and vomiting. Melena is present in his stool. Patient is a chronic NSAIDs user and smoker of 15 years. The physical examination findings are often normal with occasional mild epigastric tenderness. What is the most likely diagnosis?

Back 35

Acute Hemorrhagic Gastritis
Definition: acute inflammation, erosion, hemorrhage of gastric mucosa due to a breakdown of mucosal barrier and acid-induced injury.
Etiology:
- Chronic aspirin/NSAID use
- Alcohol use
- Smoking
- Postsurgery
- Burns
- Ischemia
- Stress
Presentation: epigatstric abdominal pain. Gastric hemorrhage, hematomesis, melena.

Front 36

Describe the pathophysiology of gastric stress ulcers

Back 36

Gross: multiple, small, round, superficial ulcers of the stomach and duodenum.
Etiology: NSAIDs use, severe stress, sepsis, shock, severe burns or trauma (Curling ulcers), elevated intracranial pressure (Cushing ulcers)
HIGH INCIDENCE AMONG ICU PATIENTS
Complication: bleeding.

Front 37

Describe the pathophysiology of chronic gastritis

Back 37

Chronic inflammation of the gastric mucosa eventually leading to athrophy.
Two main types:
- Fundic/Body type - Autoimmune gastritis (Abs are produced to parietal cells and intrinsic factor)
- Antral type - medicated by Helicobactor Pylori. Most common in the US. Associated with duodenal and gastric ulcers. Foci of acute inflammation. chronic inflammation with lymphoid follicles.

Front 38

Describe the pathophysiology of autoimmune gastritis

Back 38

- Fundic/Body type of gastritis
- Abs are produced to parietal cells and intrinsic factor
- Loss of patietal cells
- Decreased acid secretion
- Increased serum gastrin (G cell hyperplasia)
- Pernicious anemia
Gross: loss of rugal folds
Histo: mucosal athrophy with loss of glands and patietal cells
Increased risk of gastric carcinoma

Front 39

In a newborn, projectile vomiting after feeding and an olive-shaped mass palpable within the andomen is indicative of what congenital abnormality of the GI tract?

Back 39

Pyloric stenosis - when the muscle of the pyloric sphincter is too hyperthropied to allow adequate passage of chyme from the stomach into duadenum.

Front 40

Describe pathogenesis of Hepatic adenoma

Back 40

See slides

Front 41

What are the main risk factors for the development of malignancy from hepatic adenoma?

Back 41

Beta – Catenin mutation

Glycogen storage disease

Front 42

Describe the pathogenesis of Focal Nodular Hyperplasia

Back 42

Regenerative nodule formation due to abnormal vascular supply

Front 43

Name four main types of primary hepatic tumors

Back 43

Hepatocellular carcinoma
Angiosarcoma
Hepatoblastoma
Cholangiocarcinoma

Front 44

Name four major etiologic factors associated with hepatocellular carcinoma

Back 44

- Chronic viral infections (HBV, HCV)
- chronic alcoholism
- non-alcoholic steatohepatitis (NASH)
- food contominanst (mainly afilatoxin - binds to DNA and messes with p53)
Plus some others (glycogen storage disease, hereditary hemochromatosis, alpha-1 antitrypsin deficiency)

Front 45

Is there a difference in etiologic factors between Asia and Western countries?

Back 45

Asia: mainly due to HBV, aflatoxin, in young patients, cirrhosis uncommon
In Western countries: HCV, alcohol, NASH are main factors
Causes cirrhosis

Front 46

Describe the pathogenesis of Hepatocellular Carcinoma

Back 46

Repeated cycles of cell death and regeneration --> accumulation of mutations --> hepatocellular transformation plus chronic inflammation
In western world: often due to random mutations in Wnt or AKT pathways, KRAS, p53, c-MYC etc
In Asia: due to HBV integration plus aflatoxin's effects

Front 47

Describe clinical presentations of HCC

Back 47

Ill-defined upper abdominal pain
Malaise
Fatigue
weight loss
Sometimes can palpate irregular nodular liver shape

Front 48

Describe the course of clinical progression of HCC

Back 48

Progressive enlargement of the tumor till it seriously disturbs hepatic function or metastasizes, generally to the lungs and then to other sites. Death occurs from either:
a. calcexia
b. GI or esophageal bleeding
c. liver failure with hepatic coma
d. rapture of the tumor with hepatic hemorrhage

Front 49

Is HCC see mainly in males/females or equal in both sexes?

Back 49

3rd most common cause of cancer deaths
Clear predominance of men:
2.4:1

Front 50

Describe the pathogenesis of fibrolamellar carcinoma

Back 50

The etiology unknown. Typically occurs in the absence of underlying liver inflammation or fibrosis. Presents with single large, hard scirrhous tumor with fibrous bands coursing through it.
5% of HCCs, equal in males and females.

Front 51

Comment of Angiosarcoma

Back 51

Rare, aggressive (survival less than 5 months). Uncommon malignant neoplasms characterized by rapidly proliferating, extensively infiltrating anaplastic cells derived from blood vessels and lining irregular blood-filled spaces.
Risk factors:
- vinyl chloride
- arsenic
- thorotrast

Front 52

Comment on main features of Hepatoblastoma

Back 52

The most common liver tumor of young childhood (neonates and infants)
Agrressive
Hepatomegaly, failure to thrive, vomiting
Elevated apha-fetoprotein

Front 53

What is the most common malignant liver tumor?

Back 53

METASTASIS

Front 54

What are the main origination sites of liver metastases?

Back 54

Breast, lung, colon, upper GI, Pancreas, melanoma

Front 55

How do metastatic liver cancers present?

Back 55

Can be asymptomatic despite massive liver involvement.
Liver failure, jaundice, hepatomegaly

Front 56

Define acute cholecystitis

Back 56

Acute inflammation of the gallbladder, precipitated 90% of the time by obstruction of the neck or cystic duct

Front 57

Describe pathogenesis of acute cholecystitis

Back 57

Results from chemical irritation and inflammation of the obstructed gallbladder (mucosal epithelium becomes disrupted by the action of bile salts). Bacterial contamination may also develop.
Acute acalculous cholecystitis is thought to develop from ischemia.

Front 58

Define empyema of the gallbladder

Back 58

Condition where the contents of the gallbladder are almots entirely puss

Front 59

Describe clinical features of acute cholecystitis

Back 59

Progressive RUQ or epigastric pain, frequently associated with mild fever, anorexia, sweating, nausea and vomiting

Front 60

Describe pathogenesis of chronic cholecystitis

Back 60

Typically develop following long-term co-existance of gallstones and low grade inflammation.

Front 61

What are Rokitansky-Aschoff sinuses and in what disease do we see them?

Back 61

In chronic cholecystitis we often see reactive proliferation of mucosa and fusion of the mucosal folds that gives rise to buried crypts of epithelium within the gallbladder wall. These outpouchings are called Rokitansky-Aschoff sinuses (Robbins p.886)

Front 62

What is porcelain gallbladder?

Back 62

Extensive dystrophic calcifications within gallbladder

Front 63

After an extraction of an absessed tooth - sulfur granules in pus, contain gram+ brabching filamentsm anaerone

Back 63

actomyces israeli