Esophagus /certified fixed orthodontic courses by Indian dental academy

Esophagus



Normal esophageal mucosa appears white to tan
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


Esophageal mucosa is lined by non-keratinized stratified
squamous epithelium
Gastric mucosa is lined by columnar glandular epithelium

Selected disorders of the esophagus









Motor disorders: Achalasia
Mechanical injury: Lacerations (Mallory-Weiss
syndrome)
Varices
Esophagitis: Reflux, infections, drugs,
irradiation
Barrett’s esophagus
Malignant neoplasms

Achalasia (failure to relax)










Incomplete relaxation of lower sphincter during
swallowing leading to functional obstruction and proximal
dilatation
Aperistalsis, incomplete relaxation, increased resting tone
Ganglion cells of the myenteric plexus are diminished or
absent
Loss of inhibitory innervation to the sphincter
Clinical picture: dysphagia, regurgitation and aspiration
Histology: Inflammation in the area of M. plexus
Hypotheses: autoimmune, viral infections
May occur secondary to Trypanosoma cruzi infection
(Chagas disease)
5% develop squamous cell carcinoma, at younger age

Esophageal lacerations (MalloryWeiss syndrome)








Longitudinal tears at the gastroesophageal junction
Clinical setting: chronic alcoholics after a bout of severe
vomiting
Tear may be superficial or deep affecting all layers
Clinical picture: Pain, bleeding, superimposed infection
Hiatal hernia is found in 75% of patients
Most often bleeding stops w/o intervention, but lifethreatening hematemesis may occur.
Supportive therapy and balloon tamponade. Healing is
prompt with minimal or no residue

Hiatal hernia
Dilatation of the space between the diaphragmatic muscles which permits a
dilated segment of the stomach to protrude above the diaphragm.
95%

5%

1-20% of adult subjects; only 9% of those affected suffer from heartburn
and reflux esophagitis; complications may include ulceration and bleeding

Esophagitis








Reflux esophagitis
Infections
Crohn disease, acute graft versus host disease
Prolonged gastric intubation
Ingestion of irritant substance
Chemotherapy and irradiation

Reflux esophagitis






Reflux of gastric contents
into esophagus
Possible etiologies:
inadequate function of
lower sphincter; sliding
hiatal hernia
CP: “heart burn”
Complications:
ulceration, bleeding,
stricture, Barrett
esophagus

Infection-induced esophagitis





More common in patients with impaired immunity
Fungal : Candida
Viruses: Herpes and Cytomegalovirus

Barrett esophagus






A complication of long standing reflux esophagitis
Replacement of squamous epithelium by columnar
epithelium with goblet cells
30- to 40-fold greater risk to develop adenocarcinoma

Esophageal varices



Tortuous dilated veins in the submucosa of distal
esophagus

Esophageal varices







Etiology: portal hypertension secondary to liver cirrhosis
Asymptomatic until they rupture leading to massive
hemorrhage
50% subsides spontaneously
20-30% die during the first episode
Rebleeding occurs in 70% of cases within one year

Esophageal carcinoma



Squamous cell carcinoma





More prevalent worldwide
Risk factors: long-standing
esophagitis, achalasia,
smoking, alcohol, diet (low
vitamins and zinc), genetics
50% in middle 1/3



Adenocarcinoma





More common in USA
Occurs on top of Barrett
esophagus
More in distal 1/3


Stomach
2
1
3





1) Cardia
2) Body: Parietal and Chief cells
3) Antrum: Mucin secretion and Gcells that secrete gastrin

Selected disorders of the stomach




Gastritis
Peptic ulcers
Gastric cancer


Chronic Gastritis



Infiltration of the mucosa by chronic inflammatory cells
(lymphocytes and plasma cells)
Causes:






Helicobacter pylori: G-ve bacilli; Noble prize in Medicine
2005, for Barry Marshal & Robin Warren
Autoimmune: rare in USA, autoantibodies to parietal cells
(decreased acid and intrinsic factor)

Helicobacter pylori is present in 70-90% of patients
with gastric and duodenal ulcers, respectively
Look for intestinal (goblet cell) metaplasia as a
precancerous lesion

Helicobacter pylori and associated
disorders

H. pylori




Gastric ulcer

Gastritis (chronic and acute), peptic (gastric
and duodenal) ulcers
Gastric adenocarcinoma, intestinal type
Gastric lymphoma

Mechanisms of H. pylori-induced
pathology





Although the organism is not invasive, it induces
intense inflammatory and immune response:
cytokines and B-cell activation
Enhances gastric acid secretion
Bacterial products such as urease, lipases and
proteases that induce epithelial injury


Acute gastritis “gastropathy”



Injury to the gastric mucosa (erosions) with no
significant participation of inflammatory cells
Causes include:
Non-steroidal antiinflammatory drugs
 Alcohol
 Hypovolemia
 Shock
 Stress
 Uremia
 Enterogastric reflux



Peptic ulcer







Location: stomach or first portion of duodenum
Life time risk is 10% in the USA
More frequent in patients with alcoholic
cirrhosis, chronic obstructive pulmonary disease,
chronic renal failure and hyperparathyroidism.
Causes include: H. pylori and causes of acute
gastritis (especially NSAID)
Clinical features: Epigastric pain (worse at night
and relieved by food), bleeding (30%) and
perforation (5%; accounts for 2/3 of deaths).

Gastric cancer


Intestinal-type:









Risk factors: diet (nitrites,
smoked food, increased
salt), chronic gastritis (H.
pylori), altered anatomy
after resection
On top of intestinal
metaplasia
Decreasing in incidence
Glandular morphology

Diffuse-type:
Undefined risk factors
( no known relation to H.
pylori)
 Signet cell morphology



Macroscopic growth patterns of gastric adenocarcinoma
Mass

Ulcer

Lintis plastica

Clinical picture:
asymptomatic or abdominal
discomfort, weight loss,
anemia

Small and large bowel




Developmental: Meckel diverticulum
Vascular
Diarrheal disease:
Infections: viruses, bacteria, protozoa
 Idiopathic inflammatory bowel disease
 Malabsorption





Diverticular disease
Tumors

Meckel diverticulum
Meckel
diverticulum





A blind pouch located in distal small bowel
The most common congenital anomaly of the small intestine; results
from failure of the involution of the omphalomesenteric (vitelline)
duct
The rule of 2’s:




2% of the population, 2 inches in length, 2 feet proximal to the ileocecal valve,
2 types of heterotopic tissue (pancreas and stomach); 2% are symptomatic.

Symptoms are rare:



Overgrowth of bacteria that depletes vitamin B12 leading to anemia
“Peptic” ulcer and bleeding

Types and causes of diarrheal illness


Secretory diarrhea: loss of intestinal fluid that is
isotonic with plasma and persists during fasting
Viruses: rotavirus: destroy the absorptive surface
children 6-24 M of age, 130 million cases per year,
fecal oral mode of transmission.
 Toxin-mediated: Vibrio cholera, E.coli (need time)
 Preformed toxin: Stapylococcus aureus (immediate
effect)
 Excessive laxatives



Types and causes of diarrheal illness, continued


Osmotic diarrhea: secondary to intraluminal
fluids with high osmolarity; it abates with
fasting.


Specific therapies:
Lactulose therapy: used for constipation and hepatic
encephalopathy
 Gut lavage before endoscopy
 Antacids





Exudative diarrhea: pruluent bloody stool
(inflammation of the mucosa and/or
hemorrhage)
Infections causing tissue damage: Shigella,
Salmonella, Entamoeba histolytica
 Infections causing both tissue damage and toxins:
Clostridium difficile; with antibiotic therapy, leading
to pseudomembranous colitis
 Idiopathic inflammatory bowel disease



Parasites








Entamoeba histolytica: Invasive, amebic colitis
and amebic liver abscesses
Giardia lamblia: noninvasive, duodenum and
jejunum, diarrhea and malabsorption
Cryptosporidium: self-limited diarrhea in
immunocompetent individuals; long course in
AIDS patients
Worms: uncommon in USA

Pseudomembranous colitis




Membranes made of neutrophils and fibrin
Seen in Cl. Difficile infection and in ischemia

Idiopathic inflammatory bowel disease
Crohn disease







Small bowel and colon
(mostly right side)
Patchy involvement
Transmural inflammation,
fistulas, strictures, serositis
Non-caseating granulomas
Poor response to surgery
Increased risk for cancer

Ulcerative colitis







Colon only
Continuous involvement
Superficial inflammation
No granulomas
Good response to surgery
Increased risk for cancer




Malabsorption diarrhea (steatorrhea):
voluminous bulky stool with increased
osmolarity resulting from unabsorbed nutrients
and excess fat; usually abates on fasting.


Malabsorption syndromes


Malabsorption syndromes








Defective intraluminal digestion:
 pancreatic insufficiency
 Defective bile secretion
Mucosal abnormalities:
 Disaccharide deficiency (lactose intolerance)
Reduced surface area
 Gluten-sensitive enteropathy (Celiac disease)
 Surgical resection
Infections: Tropical sprue, whipple disease

Selected malabsorption syndromes






Gluten-sensitive enteropathy (celiac disease): 1:300
persons are affected, hypersensitivity to gliadin, a
component of gluten (present in wheat flour) leading to
blunted villi and increased intraepithelial lymphocytes.
Increased risk for lymphoma.
Tropical sprue: malabsorption and diarrhea after a visit
to the tropics. Infectious etiology, responds to
antibiotics.
Whipple disease: systemic disease that affects GIT,
nervous system and joints. Caused by T. whippelii
(gram-positive actinomycete).

Clinical features of malabsorption
syndromes


Hematopietic system:





Musculoskeletal system:




Amenorrhea, impotence, infertility

Skin:





Osteopenia: calcium and vitamin D deficiency

Endocrine system:




Anemia: iron, folate and B12 deficiency
Bleeding: vitamin K deficiency

Purpura: vitamin K deficiency
Dermatitis: vitamin A deficiency

Nervous system:


Peripheral neuropathy: folate and B12 deficiency.

Diverticulosis








Herniation of the mucosa and submucosa
through the muscle wall
50% after age 50
Related to low-fiber diet, increased intraluminal
pressure and focal defects in muscular layer
Mostly in sigmoid colon
Asymptomatic unless infected

Tumors of the large bowel




Hyperplastic polyps: not precancerous
Adenomatous polyps: precancerous
Familial polyposis syndrome: Autosomal
dominant; 500-2500 polyps, 100% risk for
developing cancer; mutations in APC gene


Colonic adenocarcinoma:







Almost always arises from adenomatous polyp
Risk factors: low fiber, high fat, decreased vit A,
C, E, idiopathic inflammatory bowel disease,
familial adenomatous polyposis
Several hits to different genes: APC, k-ras, p53;
or DNA mismatch repair genes
Survival depends on stage (depth of invasion
and node metastasis)

Colonic adenocarcinoma
Exophytic tumor
leading to partial
obstruction



Clinical picture: Asymptomatic or fatigue, weakness
and iron deficiency anemia in tumors of right side.
Left sided tumors may produce bleeding, change in
bowel habits and crampy pain






Course: tumor invades bowel wall and
lymphatics/blood vessels with metastasis to
lymph nodes, liver, lungs, and bones. 25% of
patients have metastatic disease at presentation
Diagnosis is based on endoscopy and biopsy
Prognosis depends on stage (depth of invasion,
nodal and distant metastasis), and 5-year survival
varies from >90% in stage I, to 4% with distant
metastasis.



A 47-year-old man has a history of drinking 1 to 2 liters of
whisky per day for the past 20 years. He has had numerous
episodes of nausea and vomiting in the past 5 years. He
experiences a bout of prolonged vomiting, followed by
massive hematemesis. On physical examination in the
emergency room, he has vital signs with T 36.8 C, P 110, RR
22, and BP 80/40 mm Hg. His heart has a regular rate and
rhythm with no murmurs and his lungs are clear to
auscultation. There is no abdominal tenderness or distension
and bowel sounds are present. His stool is negative for
occult blood. Which of the following is the most likely
diagnosis?
1.
2.
3.
4.
5.

Barrett’s esophagus
Esophageal stricture
Esophageal lacerations (Mallory Weiss syndrome)
Esophageal squamous cell carcinoma
Achalasia



All these statements about Barrett’s esophagus
are true, except:
1.

2.
3.
4.

5.

It is associated with 30- to 40-fold greater risk to
develop adenocarcinoma
It appears as salmon-pink mucosa on endoscopy
It is associated with high risk for esophageal bleeding
It represents replacement of the stratified squamous
epithelium by columnar epithelium with goblet cells
It could be a complication of long-standing reflux
esophagitis



All these statement about Helicobacter pylori
are correct except:
1.
2.

3.
4.

5.

H. pylori organisms are Gram negative bacilli
It is associated with intestinal-type gastric
adenocarcinoma
It is associated with gastric lymphoma
It is associated with diffuse-type gastric
adenocarcinoma
It is associated with peptic ulcer




1.
2.
3.
4.

A 20-year-old man has noted cramping abdominal
pain for the past week associated with fever and lowvolume diarrhea. On physical examination, there is
right lower quadrant tenderness. Bowel sounds are
present. His stool is positive for occult blood. A
colonoscopy reveals mucosal edema and ulceration in
the ascending colon, but the transverse and
descending portions of the colon are not affected.
Which of the following microscopic findings is most
likely to be present in biopsies from his colon
Entamoeba histolytica organisms
Adenocarcinoma
Non-caseating granulomas
Diverticulosis



1.
2.
3.
4.
5.

A 35-year-old woman has a 10 year history of
intermittent, bloody diarrhea. She has no other major
medical problems. On physical examination there are no
lesions palpable on digital rectal examination, but a stool
sample is positive for occult blood. Colonoscopy reveals
a friable, erythematous mucosa with focal ulceration that
extends from the rectum to the mid-transverse colon.
Biopsies are taken and all reveal mucosal acute and
chronic inflammation with crypt distortion, occasional
crypt abscesses, and superficial mucosal ulceration. This
patient is at risk for development of which of the
following conditions?
Diverticulitis
Acute pancreatitis
Peri-rectal fistula
Appendicitis



1.
2.
3.
4.
5.

A 25-year-old man complains of a low volume but
chronic, foul smelling diarrhea for the past year. He has
no nausea or vomiting. On physical examination there
is no abdominal pain or masses and bowel sounds are
present. His stool is negative for occult blood.
Laboratory studies include a quantitative stool fat of 10
g/day. Upper GI endoscopy is performed with biopsies
of the duodenum. The biopsies reveal the absence of
villi, and increased surface intraepithelial lymphocytes.
Which of the following therapies is most likely to be
useful for this man?
Antibiotics
Anti-Entamoeba therapy
Corticosteroids
Gluten-free diet
Surgical resection

Diseases of the liver

Sherif Tawfic, MD, Ph.D.
Surgical Pathology
Fairview University Medical Center, and University of Minnesota
tawfi001@umn.edu


Liver
Normal liver has smooth
brown surface
Weight: 1200-1600 g



Maintaining body metabolic homeostasis:







Lipid and carbohydrate metabolism: production and secretion of
glucose
Protein synthesis: albumin, coagulation factors
Detoxification and drug metabolism
Conjugation and excretion of bilirubin
Synthesis and excretion of bile salts

Liver anatomy and
histology


Patterns of hepatic injury







Inflammation
Steatosis: accumulation of fat droplets within
hepatocytes
Cell death: those cells closer to the central vein are
more susceptible to ischemia, toxins and drugs leading
to “centrilobular” necrosis
Fibrosis: Irreversible, affect blood flow and hepatocyte
function
Cirrhosis: End stage liver disease with diffuse fibrosis
and regenerating nodules

Steatosis
Alcohol
Obesity
Diabetes
Hyperlipidemia

Clinical picture:
Silent, or fatigue,
malaise, right upper
quadrant discomfort

Liver cirrhosis


Definition: bridging fibrous septa and parenchymal
nodules with disruption of architecture. End stage for
many diseases affecting the liver

Mechanism: cell death, regeneration and fibrosis

Clinical consequences of liver
disease (life-threatening complications are in yellow)


Hepatic dysfunction:


Decrease synthesis capacity leading to :






Decrease detoxification capacity leading to:






Hypoalbuminemia: edema, ascitis, muscle wasting, weight loss
Hypoglycemia: weakness and syncope
Coagulation factor deficiency: bleeding
Hyperammonemia and increase toxic metabolites:
Encephalopathy (altered behavior and disturbances in
consciousness that may lead to deep coma and death)
Injury to other organs by active toxins

Hepatorenal syndrome:


Renal failure without intrinsic or functional causes of renal
failure. ? Altered blood flow to the kidney.

Clinical consequences of liver
disease, continued





Jaundice: yellow discoloration of skin and sclera due to
accumulation of bilirubin
Cholestasis: systemic accumulation of bilirubin in
addition to bile salts and cholesterol (usually secondary
to obstruction)
Portal hypertension in cirrhosis: increased resistance to
portal blood flow







Esophageal varices
Ascitis
Splenomegaly
Hemorrhoids

Malignancy on top of cirrhosis

Jaundice






Accumulation of bilirubin in tissue leading to
yellow discoloration of skin and sclera (icterus)
Normal serum level: 0.3-1.2 mg/dl; jaundice
appears with levels above 2.0-2.5 mg/dl
Source of bilirubin: the breakdown of senescent red
blood cells in the spleen releases heme that changes
into bilirubin by specific enzymes.


Bilirubin

Conjugation is a function of the liver by
adding glucuronic acid to bilirubin


-

Unconjugated
Albumin bound
Insoluble in
water, toxic


-

-

Conjugated
Loosely bound
to albumin
Water soluble,
non-toxic,
excreted in
urine


Laboratory evaluation of liver disease


Hepatocyte function:






Hepatocyte injury (enzymes normally present inside the
hepatocytes and released with injury):






Serum albumin
Prothrombin time: measuring coagulation factors (II, V, VII, X);
prolonged in liver cirrhosis
Serum ammonia

Serum aspartate aminotransferase (AST)
Serum alanine aminotransferase (ALT)
Serum lactate dehydrogenase

Biliary excretory function:




Serum bilirubin
Serum alkaline phosphatase
Serum gamma-glutamyl transpeptidase

Laboratory evaluation of liver disease


Searching for etiology:
Hepatitis viral antigens and antibodies
 Autoimmune antibodies: for autoimmune hepatitis
 Tissue iron and copper: for hemochromatosis and
Wilson disease



Selected disorders of the liver








Viral hepatitis
Drug-induced hepatitis
Autoimmune hepatitis
Alcoholic hepatitis
Hemochromatosis
Wilson disease
Neoplasms of the liver

Hepatitis A virus
RNA virus
 Mode of transmission: fecal-oral (contaminated water and
food)
 Incubation period: 2-6 weeks
 Virus shedding: 2-3 weeks before and 1 week after
appearance of jaundice
 50% of population above age 50 are seropositive in USA,
no carrier state
 No increase risk for chronic hepatitis, or carcinoma
 Because viremia is transient, no need to screen donated
blood



Hepatitis B virus






dsDNA virus
Mode of transmission: parenteral (blood
products, contaminated needles and IV drug
abuse), and body fluids (including saliva)
Incubation period: 4-26 weeks
Carrier state: yes, 350 million carriers around the
world


Hepatitis B infection: Possible outcomes


Possible outcomes of infection:
Subclinical or acute hepatitis with recovery and
clearance (85%); 1% of those may develop fulminant
hepatitis and death
 Healthy carriers (10%)
 Persistent infection (5%): 80% recover and 20%
develop chronic hepatitis
 20% of chronic hepatitis patients develop cirrhosis
and 10% of those develop hepatocellular carcinoma



Hepatitis C







ssRNA virus
Mode of transmission: parenteral, sexual and vertical,
40% unknown source. It is present in the saliva.
Outcomes of infection:

HCV is the leading
cause for chronic
liver disease

Hepatitis D







Defective RNA virus that needs Hep B capsule
to replicate
Mode of transmission: Parenteral
Coinfection of B and D: mild disease with
recovery in most cases, <5% chronic hepatitis
Superinfection by D after B: accelerated more
severe hepatitis; 80% chronic hepatitis


Hepatitis E







ssRNA virus
Mode of transmission: waterborne
Endemic in certain populations; 40% in Indian
population
Self-limited infection but with higher mortality
in pregnant females

The points to remember
Hepatitis A Hepatitis B

Hepatitis C

Transmission Oral-fecal Parenteral

Parenteral

Carrier state

None

Present

Present

Chronic
hepatitis

None

5-10%

>70%

Fulminant
hepatitis

0.1%

0.1-1.0%

Rare

Carcinoma

No

Yes

Yes


Drug-indued hepatitis







Predictable or unpredictable (idiosyncrasy)
Mechanisms: direct toxicity, conversion of drug
to an active toxin, immune-mediated
A long list of drugs can cause different forms of
injury: hepatitis, fibrosis, granulomas, necrosis,
cholestasis, vascular disorders and neoplasia
Example: Acetaminophen overdose induces
centrilobular necrosis












More in females (70%)
The absence of serologic markers for viral hepatitis
Elevated serum IgG levels
High titers of autoantibodies (antinuclear, anti-smooth
muscle, and anti-microsomal)
Increased frequency of HLA-B8 and DRw3
Associated with other forms of autoimmune disorders
such as rheumatoid arthritis and ulcerative colitis
Risk for cirrhosis is 5%
Respond to immunosuppressive drugs

Alcoholic liver disease




100,000 death annually related to alcohol; 20,000 are
related directly to end-stage liver cirrhosis; the rest is
related to car accidents
Effects on liver:







80% fatty liver (steatosis)
10% alcoholic hepatitis
10% cirrhosis

Short-term ingestion of 80 g (8 beers) of ethanol per day
leads to reversible steatosis
Daily ingestion of 160 g for 10-20 years leads to severe
injury

Hereditary hemochromatosis







Autosomal recessive disease characterized by increased
accumulation of body iron, most of which is deposited
in the liver and pancreas.
Mostly due to increased iron absorption and
accumulation over the years. Normal total body iron is
2-6 g. In hemochromatosis it may reach 50 gm.
Due to mutations in the hemochromatosis gene (HFE);
a gene that regulates iron absorption.
The frequency of being heterozygous is 10% (1 of every
ten persons) and that of being homozygous is 0.45% (1
of every 220 persons)

Hereditary hemochromatosis



Excess iron damages DNA, lipids and stimulates
collagen formation (fibrosis)
Clinical picture:
Males are more affected; 50-60 years old
 Liver cirrhosis, skin pigmentation, diabetes
(pancreatic fibrosis), risk for hepatocellular
carcinoma.
 Diagnosis: elevated serum and tissue iron.
 Early detection and therapy by phlebotomy and iron
chelators lead to normal life expectancy



Wilson disease









Autosomal recessive disorder characterized by
accumulation of copper in liver, brain and eyes, among
other organs
The frequency of being heterozygous is 1:200 (less
common than hemochromatosis)
The mutated gene (ATP7B) is located on chromosome
13; the mutation leads to failure to excrete copper into
bile, and its accumulation in tissue
Clinical picture: neuropsychiatric manifestations, acute
and chronic liver disease and Kayser-Fleisher rings in
the cornea (green to brown deposits)
Diagnosis: Clinical picture, increased hepatic and
urinary copper, and decreased serum ceruloplasmin (a
copper binding protein).

Biliary disease






Secondary biliary cirrhosis: secondary to
extrahepatic bile obstruction by stones, atresia or
tumors
Primary biliary cirrhosis: immune-mediated
destruction of intrahepatic bile ducts, more in
females, presence of anti-mitochondrial
antibodies
Primary sclerosing cholangitis: chronic fibrosis of
intra- and extra-hepatic bile ducts; more in men,
association with ulcerative colitis

Tumor of the liver


Liver cell adenoma


Occurs in women of childbearing age in relation to
oral contraceptives; it regresses on discontinuation
of hormones

Sheets of hepatocytes with no
portal tracts

Well circumscribed mass

Liver cell adenoma


Significance of this benign tumor:
It may be mistaken for carcinoma
 Subcapsular adenomas are at risk for rupture,
especially during pregnancy leading to lifethreatening intraabdominal hemorrhage



Hepatocellular carcinoma (HCC)


Risk factors:
Strongly associated with hepatitis B and C infection.
The carrier state for hepatitis B carries 200-fold
increased risk for HCC
 Chronic liver disease (e.g. alcohol)
 Hepatotoxins (aflatoxin present on moldy peanuts
and grains)



Hepatocellular carcinoma


Clinical picture:
Often patient
already has liver
cirrhosis, with rapid
increase in liver
size, worsening
ascites, fever and
pain; elevated
serum alpha
fetoprotein levels
(>1000 ng/ml)
 Median survival is 7 months (death from bleeding,
liver failure, or profound cachexia)




Metastatic carcinoma




The most common malignant tumors in the liver
Usually multiple lesions
The most common primary sites are colon, lung,
breast, pancreas and stomach


Oral manifestation of liver
dysfunction





Hematoma, gingival bleeding
Jaundiced mucosa
Glossitis (in alcoholic hepatitis)
Reduced healing after surgery




1.
2.
3.
4.

A 48-year-old man has a long history of chronic alcohol
abuse. On physical examination his liver is firm on
palpation of the abdomen, but does not appear to be
enlarged. An abdominal CT scan reveals that the liver
has cirrhosis. He joins a support group for persons with
chronic alcohol abuse and he stops drinking. Despite
his continued abstinence from alcohol, he most likely
remains at risk for development of which of the
following diseases?
Liver cell adenoma
Hepatocellular carcinoma
Gallbladder stones
Lymphoma



1.
2.
3.
4.
5.

A 28-year-old woman with recent onset of depression
ingests an entire bottle (100 capsules, 500 mg each) of a
medication containing acetaminophen. She becomes
progressively obtunded. Which of the following
microscopic findings is most likely to be present in her
liver 3 days following this ingestion?
Normal histology
Steatosis
Centrilobular necrosis
Cirrhosis
Chronic inflammation



1.
2.

3.
4.

Hepatitis C infection is characterized by which
one of the following:
Absence of carrier status
Highest incidence of chronic hepatitis among
other viral hepatitis
No increase risk for hepatocellular carcinoma
It can be transmitted by eating contaminated
food










50 year-old male presented with jaundice and
pruritus. Lab studies show elevated serum
conjugated bilirubin and alkaline phosphatase.
ALT and AST levels were only slightly elevated.
The most likely diagnosis is:
Hepatitis B
Steatosis
Hepatitis C
Extrahepatic bile duct obstruction

The Pancreas


The Pancreas
85% exocrine: enzymes for
digestion
 Acute and chronic
pancreatitis
 Cystic fibrosis
 Tumors

15% endocrine: insulin,
glucagon and others
 Diabetes
 Tumors


Pancreatic exocrine enzymes


Acute pancreatitis


Acute pancreatitis







Clinical presentation:
abdominal pain radiating
to the back, elevated
serum amylase and lipase,
hypocalcemia
Rise in serum lipase is
more specific for
pancreatitis.
Complications: infections,
abscess, pseudocyst
Mortality is high: 20-40%,
from shock, sepsis or
acute respiratory failure,
acute renal failure,
disseminated intravascular
coagulation

Chronic pancreatitis









Progressive destruction of pancreatic parenchyma and
its replacement by fibrosis
Predisposing factors: alcohol, hypercalcemia or
idiopathic
30% of idiopathic cases have been found to have
mutation in CFTR gene
Complications: Pseudocyst, malabsorption, 2ry diabetes
Diagnosis: abdominal pain, malabsorption,
calcifications on X-ray

Pancreatic adenocarcinoma






The 5th most frequent cause of death from
cancer
Risk factors: smoking
CP: symptoms are late; pain and jaundice
Prognosis is poor: 5% survive for 5 years


Islet cell tumors





Rare compared to adenocarcinoma
Insulinomas: secrete insulin ⇒ hypoglycemia ⇒
behavioral changes, confusion and coma. Over
90% are benign
Gastrinomas: secrete gastrin ⇒ increase acid
production ⇒ duodenal and gastric ulcers


Gallbladder


Gallstones (cholelithiasis)








Afflict 10% of adult population in
Western countries
Costs of management: $6 billion a
year
20 million patients are estimated
to have gallstones totalling several
tons
Made of cholesterol, bilirubin and
calcium salts with different
concentrations
Two types: cholesterol and
pigmented stones

Gallstones


Cholesterol








Western > others
Advancing age
Female sex
Obesity
Hyperlipidemia and bile
stasis

Pigmented




Asian > Western
Hemolytic anemia
Biliary infection

Complications: empyema, perforation, fistula,
inflammation, obstruction, pancreatitis

Acute cholecystitis




Calculous: acute inflammation of a gallbladder
that has stones. It may represent a medical
emergency; no associated infection initially
Acalculous: no stones, in severely ill patients,
severe trauma, burns and sepsis

Chronic cholecystitis


Almost always associated with gallstones



1.
2.
3.
4.

The risks factors for developing acute
pancreatitis include all of the following except:
Gallstones
Hypocalcemia
Alcoholism
Shock




1.
2.
3.
4.

All of the following statement about
pigmented gallstones are correct except:
Hyperlipidemia is a risk factor
Hemolytic anemias could be a cause
Biliary infections may be present
They are more common in Asians




1.
2.
3.
4.

A 38-year-old woman has experienced episodes of
light-headedness, irritability, and difficulty
concentrating at her work for the past year. On
physical examination there are no abnormal findings.
Laboratory studies show her hemoglobin is 14.2 g/dL.
An abdominal CT scan shows a 1 cm mass in the tail of
the pancreas. Which of the following is the most likely
diagnosis?
Pancreatic pseudo-cyst
Insulinoma



1.
2.
3.
4.

A 50-year-old man gives a history of chronic alcohol
abuse. He has had bouts of abdominal pain in the past
year. For the past month, he has had more frequent
and worsening abdominal pain. Physical examination
reveals right upper and left upper quadrant pain with
guarding. An abdominal plain film radiograph reveals
no free air, but there is extensive peritoneal fluid
collection along with dilated loops of small bowel. An
abdominal CT scan reveals a 7 to 8 cm cystic mass in
the tail of the pancreas. Which of the following is the
most likely diagnosis?
Metastatic carcinoma
Pancreatic pseudocyst
Acute pancreatitis

The Pancreas
Sherif Tawfic, MD, Ph.D.
Surgical Pathology
U of MN
tawfi001@umn.edu

http://www.tc.umn.edu/~tawfi001/


Acute pancreatitis







CP: abdominal pain radiating to the back, elevated serum
and urine amylase, hypocalcemia
Most important causes: Gallstones, alcoholism, shock,
hypercalcemia
Mechanism: Interstitial edema ⇒ impaired blood flow
and ischemia ⇒ acinar cell injury with release and
activation of trypsinogen and lipases ⇒ proteolysis + fat
necrosis + hemorrhage (destruction of blood vessels by
elastases)
Complications: infections, abscess, pseudocyst
Mortality is high: 20-40%, from shock, sepsis or acute
respiratory failure







Progressive destruction of pancreatic parenchyma and
its replacement by fibrosis
Predisposing factors: alcohol, hypercalcemia or
idiopathic
30% of idiopathic cases have been found to have
mutation in CFTR gene
Fibrosis, chronic inflammation and protein plugs within
ducts
Diagnosis: abdominal pain, malabsorption,
calcifications on X-ray







The 5th most frequent cause of death from
cancer
Risk factors: smoking
CP: symptoms are late; pain and jaundice
Prognosis is poor: 5% survive for 5 years

Some of the adverse effects of smoking to remember:
Cancer of the oral cavity, lips, tongue, larynx, lungs, esophagus, pancreas, kidney,
bladder and vulva
Emphysema and chronic bronchitis, atherosclerosis and myocardial infarction

Gallbladder


Gallstones (cholelithiasis)








Afflict 10% of adult population in
Western countries
Costs of management: $6 billion a
year
20 million patients are estimated
to have gallstones totalling several
tons !
Made of cholesterol, bilirubin and
calcium salts with different
concentrations
Two types: cholesterol and
pigmented stones

Thank you
Leader in continuing dental education


Esophagus /certified fixed orthodontic courses by Indian dental academy

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