S.p. Exam #2 - G.i. & Hepatobiliary

Front 1

5 layer structure of the GIT

Back 1

1. Mucosa: Innermost layer; absorptive layer
2. Lamina propria + muscularis mucosa
3. Submucosa: No muscle; transport layer
Nerves, blood vessels, lymphatics that feed the inner layer
4. Muscularis propria: inner circular m. + out longitudinal m. (pathologically count as one layer)
5. Serosa (for the most of the GI tract) or Adventitia (for esophagus): Outer protective layer
CT layer functions as a barrier, lubricant

Front 2

main signs/symptoms of GI problems

Back 2

Pain
Bleeding
Emesis – dysmotility going upward
Diarrhea – dysmotility going downward
Anorexia

Front 3

place of most common GI complaint

Back 3

esophagus

Front 4

the most common disease of the GIT

Back 4

GERD

-Caused by dysfx of the lower esophageal sphincter
-Simple motility disorder
-The anatomy of the sphincter would look normal but the function is abnormal

Front 5

Hyatus hernia

Back 5

-Helps lower esophageal sphincter dysfunction to occur more readily (predisposing factor of )
-Attachment of the crura has loosened and the upward portion of the stomach is pulled through the hiatus (next slide)
-Crura cannot bend the esophagus
-Only the intrinsic lower esophageal sphincter in the wall of the esophagus can prevent upward flow of the acid

--> much more likely to get acid reflux

Front 6

Lower esophageal sphincter dysfunction

Back 6

inappropriate relaxation of the sphincter
(Aka reflux aka heartburn)

It is not the excess acid that causes the heart burn; it is the inappropriate opening or prolonged opening that causes acid reflux

Front 7

Complications of Esophagitis

Back 7

Complications
-Ulceration + inflammations – acid burns through the SQ mucosa
-Barrett’s esophagus
-Stricture – repeated inflammation leading to fibrosis (scar tissue)
--> Narrowing of the esophagus
-Cancer: repeated injury leads to mutation in dividing cells

Front 8

Barrett’s Esophagus

Back 8

Specialized Intestinal Metaplasia of Esophagus is a precursor to adenocarcinoma

--> SQ to Col metaplasia (pre-neoplastic)

Growth of intestinal tissues in the esophagus
-Goblet cells – producer of mucin
-Gland formation

Front 9

Metaplastic esophageal intestinal tissue

Back 9

Metaplastic esophageal intestinal tissue is a precursor of adenocarcinoma

Metaplasia --> Dysplasia(crowding of the glands + nuclei not near the basal membrane ) --> adenocarcinoma(more abnormal nuclei + differently shaped + mitotic figures)
Gross analysis of intestinal metaplasia – pink tissue formation (color of the s. intestine) that travel upward

Front 10

the most common type of esophageal cancer

Back 10

Adenocarcinoma: the most common type of esophageal cancer (since the 1980s)

- From dysplastic change in the esophagus (columnar esophagus)
- From Barrett’s esophagus
- Occurs most frequently at the Barrett’s region (lower esophagus)
- Risk factor: smoking, overweight, middle age men, refluxers

Front 11

SQ cell cancer

Back 11

associated with excess alcohol, tobacco (same as oral SQ cancer)
More in low SES populations
Can occur in upper esophagus, middle esophagus, lower esophagus because SQ tissue cover the entire length of the esophagus
#1: middle esophagus, #2: lower esophagus , #3: upper esophagus
Dysplasia: pre-malignant
Thcikening of the cell
Dark nuclei
Enlarged nuclei
Not well organized cells

Front 12

common cancer of overweight middle-aged men

Back 12

Adenocarcinoma: the most common type of esophageal cancer (since the 1980s)

- From dysplastic change in the esophagus (columnar esophagus)
- From Barrett’s esophagus
- Occurs most frequently at the Barrett’s region (lower esophagus)
- Risk factor: smoking, overweight, middle age men, refluxers

Front 13

in TNM staging.... T refers to

Back 13

T: depend on how deep the cancer goes (most focus on this)

In the GIT, T staging is the most important prognosticator in the staging of the disease***

Front 14

in TNM staging.... N refers to

Back 14

N: depends on how to define N is (no detail given)

Front 15

in TNM staging.... M refers to

Back 15

M - presence or absence of metastasis

Front 16

In the GIT, T___staging is the most important prognosticator in the staging of the disease***

Back 16

In the GIT, T___staging is the most important prognosticator in the staging of the disease***

Front 17

Peptic ulcer disease

Back 17

the most common gastric disease

- Disorder of mucosal breakdown
- PEPTIC ulcer: a special type of ulcer associated with acid and pepsin (enzyme)
- Ulcer can occur in any part of the stomach:
the most common place of peptic ulcer = lower portion of the stomach or the duodenal bulb
--> PEPTIC ulcers RARELY cause cancer (unlike peptic esophagitis that frequently causes cancer)***
- Ulcers in unusual spots = suspect cancer

Front 18

the most common place of peptic ulcer

Back 18

lower portion of the stomach or the duodenal bulb

Front 19

H. pylori

Back 19

THE MOST IMPORTANT ETIOLOGIC FACTOR FOR CAUSING FAILURE OF THE DEFENSE MECHANISM

- Feco-oral transmission
- Inhibits the ability to make mucin
- Inhibit the process of making mucin basic
- Not all ulcers are due to H. pylori

Front 20

Aspirin + NSAIDs

Back 20

Inhibitors of prostaglandins
- PG is a growth factor in the stomach that induce gastric cells to produce bicarbonate and mucin

Front 21

Gastritis

Back 21

it is a specific diagnosis with histological change
inflammation of the gastric mucosa

There MUST be inflammatory infiltrations:
- lymphocytic infiltrations, Nphil infiltration, Ephil infiltration

“IT IS NOT JUST AN IRRITATION” – irritation of the stomach is called gastropathy

Front 22

Type A Gastritis

Back 22

2 types of gastritis depending on the location of the inflammation – but both are caused by H. pylori (there are other causes of gastritis such as allergy, causing E. phallic gastritis, but not major)

Type A: Proximal stomach (body)
- Tend to lead to atrophy of the thickness of the gastric wall
- Consequences
--- Failure of parietal cells to produce Intrinsic factors – necessary for absorption of B12; result in pernicious anemia
--- Failure of parietal cells to produce HCl
--> Parietal cells in the body of stomach produce HCl when stimulated by gastrin from G-cells in antrum
--> H. pylori infection causes the state of low acid by causing atrophy of the parietal cells

Type B: Distal stomach (antrum)

Front 23

Type B gastritis

Back 23

2 types of gastritis depending on the location of the inflammation – but both are caused by H. pylori (there are other causes of gastritis such as allergy, causing E. phallic gastritis, but not major)

Type A: Proximal stomach (body)
- Tend to lead to atrophy of the thickness of the gastric wall
- Consequences
--- Failure of parietal cells to produce Intrinsic factors – necessary for absorption of B12; result in pernicious anemia
--- Failure of parietal cells to produce HCl
--> Parietal cells in the body of stomach produce HCl when stimulated by gastrin from G-cells in antrum
--> H. pylori infection causes the state of low acid by causing atrophy of the parietal cells

Type B: Distal stomach (antrum)

Front 24

H. pylori and cancer

Back 24

H. pylori = major carcinogen

- There are other causes of cancer
- H. pylori is the major risk factor for gastric cancer, which is most often found in the upper portion of the stomach

Front 25

What is the major risk factor for gastric cancer, which is most often found in the upper portion of the stomach

Back 25

H. pylori = major carcinogen

- There are other causes of cancer
- H. pylori is the major risk factor for gastric cancer, which is most often found in the upper portion of the stomach

Front 26

what type of caner is gastric cancer?

Back 26

Mostly adenocarcinoma (like the barrett’s cancer)***
- Has the propensity to invade into the CT
- Low cure rate
- Frequently migrate to LN – micro-metastasis often occur by the time of diagnosis
-
Risk factors of gastric cancer:
- Nitrosamines (preservative) and other pro-oxidants found in under-refrigerated foods
- H. pylori
- Smoking

Typical presentation of gastric cancer
- Pain
- Bleeding – as the cancer erodes the wall (like in - peptic ulcer)
- Wt loss

Front 27

Gastric cancer

Back 27

Mostly adenocarcinoma (like the barrett’s cancer)***
- Has the propensity to invade into the CT
- Low cure rate
- Frequently migrate to LN – micro-metastasis often occur by the time of diagnosis
-
Risk factors of gastric cancer:
- Nitrosamines (preservative) and other pro-oxidants found in under-refrigerated foods
- H. pylori
- Smoking

Typical presentation of gastric cancer
- Pain
- Bleeding – as the cancer erodes the wall (like in - peptic ulcer)
- Wt loss

Front 28

risk factors for gastric cancer

Back 28

Mostly adenocarcinoma (like the barrett’s cancer)***
- Has the propensity to invade into the CT
- Low cure rate
- Frequently migrate to LN – micro-metastasis often occur by the time of diagnosis
-
Risk factors of gastric cancer:
- Nitrosamines (preservative) and other pro-oxidants found in under-refrigerated foods
- H. pylori
- Smoking

Typical presentation of gastric cancer
- Pain
- Bleeding – as the cancer erodes the wall (like in - peptic ulcer)
- Wt loss

Front 29

pattern of spread of gastric cancer vs. esophageal cancer

Back 29

2 Patterns of the spread of gastric cancer (unlike just one pattern of spread in the esophageal cancer, which only travels deeply downwards)

1. burrows towards the muscle layers
- Once it hits mucosa/submucosa, it can invade into the LN

2. Lateral spread***
- First burrows into a layer and then travel ALONG the layer
- Eg. Spread along the wall through the submucosal layer
- Linitis Plastica***: Wall itself becomes rigid due to subsurface spread of cancer (unique in gastric cancer)

Front 30

Linitis Plastica

Back 30

Gastric adenocarcinoma

when there are large areas of inflammation, diffuse rugal flattening and a rigid, thickened wall may impart a leather bottle appearance termed linitis plastica

. Breast and lung cancers that metastasize to the stomach may also create a linitis plastica–like appearance.

Front 31

GI Staging - T1

Back 31

T1: mucosal or submucosal
T2: into muscularis
T3: through muscularis
T4: into important adjacent structures

Front 32

GI Staging - T2

Back 32

T1: mucosal or submucosal
T2: into muscularis
T3: through muscularis
T4: into important adjacent structures

Front 33

GI Staging - T3

Back 33

T1: mucosal or submucosal
T2: into muscularis
T3: through muscularis
T4: into important adjacent structures

Front 34

GI Staging - T4

Back 34

T1: mucosal or submucosal
T2: into muscularis
T3: through muscularis
T4: into important adjacent structures

Front 35

why is it that esophageal cancers are harder to cure?

Back 35

- esophagus has extremely thin advintitia (not thick serosa like in GI tract)

Front 36

primary function of the small intestines

Back 36

absorption

Front 37

Serosa

Back 37

1. Mucosa: Innermost layer; absorptive layer
2. Lamina propria + muscularis mucosa
3. Submucosa: No muscle; transport layer
Nerves, blood vessels, lymphatics that feed the inner layer
4. Muscularis propria: inner circular m. + out longitudinal m. (pathologically count as one layer)
5. Serosa (for the most of the GI tract) or Adventitia (for esophagus): Outer protective layer
CT layer functions as a barrier, lubricant

Front 38

Submucosa

Back 38

1. Mucosa: Innermost layer; absorptive layer
2. Lamina propria + muscularis mucosa
3. Submucosa: No muscle; transport layer
Nerves, blood vessels, lymphatics that feed the inner layer
4. Muscularis propria: inner circular m. + out longitudinal m. (pathologically count as one layer)
5. Serosa (for the most of the GI tract) or Adventitia (for esophagus): Outer protective layer
CT layer functions as a barrier, lubricant

Front 39

Mucosa

Back 39

1. Mucosa: Innermost layer; absorptive layer
2. Lamina propria + muscularis mucosa
3. Submucosa: No muscle; transport layer
Nerves, blood vessels, lymphatics that feed the inner layer
4. Muscularis propria: inner circular m. + out longitudinal m. (pathologically count as one layer)
5. Serosa (for the most of the GI tract) or Adventitia (for esophagus): Outer protective layer
CT layer functions as a barrier, lubricant

Front 40

lamina propria

Back 40

1. Mucosa: Innermost layer; absorptive layer
2. Lamina propria + muscularis mucosa
3. Submucosa: No muscle; transport layer
Nerves, blood vessels, lymphatics that feed the inner layer
4. Muscularis propria: inner circular m. + out longitudinal m. (pathologically count as one layer)
5. Serosa (for the most of the GI tract) or Adventitia (for esophagus): Outer protective layer
CT layer functions as a barrier, lubricant

Front 41

3 primary diseases of the small intestine

Back 41

Infection** (very common)
Inflammation
Obstruction

Front 42

main disease of the esophagus

Back 42

dysmotility (reflux)

Front 43

Infection in small intestine

Back 43

Main characteristics of S. int infection
- Villi fail to function which results in failure of absorption, which in turn leads to passage of fluids down the GIT
- Characteristic of S. int infection as compared to infections in other parts of the GI:
-- S. int infection produces a large volume diarrhea (not bloody)*
-- L. int infection is associated with small volume diarrhea and bleeding
- Vomiting
-- Downward motility is disrupted during infection; bolus reverses back out upwards
- Summary: Clinical characteristics of s. int infection = large volume diarrhea without bleeding and vomiting

Front 44

the most common pathogens of the small intestines are

Back 44

viral

- The most common pathogen of the s. int is viral pathogen
- Pathogens of the small int are almost always transmitted in feco-oral routes
- Transmission of the disease is easier in crowded areas, poor sanitation
-- Eg. Cruise ship, military base, daycare
- The most common viral agent: rotavirus , Norwalk agent, adenovirus
-- Rotavirus is commonly associated with children
-- Adenovirus is associated with elderly
-- Norwalk agent is associated with cruise-ship
- The virus does not induce any substantial injury to the organ although it invades into the mucosa

Front 45

describe viral infections on the small intestines

Back 45

The virus does not induce any substantial injury to the organ although it invades into the mucosa

- Majority of the damage comes from inflammatory infiltration of lymphocytes in response to acute infection
- The absorptive mechanism is disrupted with the failure of the cAMP mechanism that drives in ions across the S. int
- Osmotic state occurs where ions remain in the lumen and water follows the ions via passive diffusion, resulting in diarrhea (passive secretion of fluids due to failure of active absorption)
- Failure of the secretion of enzymes (that cleave sugars) into the lumen causes malabosorption; the remaining sugars in the lumen also attract water
- Biopsy of such intestine would show normal tissues; but the tissues are ACTING abnormally

- Immune response results in febrile reaction
--> Death may occur in children – death is always from dehydration

Front 46

bacterial infections in small intestine

Back 46

- Common agents include toxogenic E. coli, campylobacter
- Most important pathogenic agent in S. int = cholera
- Cholera
-- Extremely transmissible via fecooral route
Infection can occur at any ages
-- Very high death rate
-- Toxin producing bacteria; it does not invade (resides in the intervilli spaces) and does not cause the cells to look abnormal
--> CTX –affects the cAMP mechanism and causes excess ion presence in the lumen. Causes dehydrating diarrhea
--> Dehydrating diarrhea due to cholera is more dangerous than virally induced diarrhea because bacterial diarrhea involves active transmission of ions across the membrane
--> Still non-bloody diarrhea
- toxogenic E. coli, campylobacter
-- Traveller’s diarrhea
-- Also causes colitis
-- Summary: therefore, these agents cause both S. int infection and L.int infection

Front 47

Cholera infections in small intestine

Back 47

- Cholera
-- Extremely transmissible via fecooral route
Infection can occur at any ages
-- Very high death rate
-- Toxin producing bacteria; it does not invade (resides in the intervilli spaces) and does not cause the cells to look abnormal
--> CTX –affects the cAMP mechanism and causes excess ion presence in the lumen. Causes dehydrating diarrhea
--> Dehydrating diarrhea due to cholera is more dangerous than virally induced diarrhea because bacterial diarrhea involves active transmission of ions across the membrane
--> Still non-bloody diarrhea

Front 48

parasitic infections of small intestines

Back 48

Parasitic infections
- High risk of parasitic infections with HIV because it makes people immunodeficient
- Common agents: cryptosporidium
- Causes non-bloody diarrhea

Front 49

Clinical sequelae of infections of the small intestine

Back 49

- Depends on how well the affected person is supported
- Rehydration by IV prevents death from dehydration
- The disease is self-limiting when the pathogens are cleared

Front 50

Causes of obstruction of small intestines

Back 50

Twist:
--> Frequently occur because the loops of small intestine are mobile
Post operational development of scar tissues called adhesions. Intestine slips in but it cannot slip back out because the substance in the lumen fills the inside.

Cancer

Inflammatory diseases

Front 51

Pathophysiology of obstruction

Back 51

- Obstruction make complete absorption of the material impossible
- Remaining materials in the lumen increases the internal pressure at the point before the obstruction
- Pressure build up causes intestinal distention
- Pressure build up also thins the intestinal wall
-- Compressed villi and submucosal fat, lymphatics, and blood vessels
-- Compression of the blood vessels cause intestinal ischemia, which results in gangrene
-- Severe gangrene leads to perforation
- The disease is time-dependent; early treatment to REDUCE THE PRESSURE will prevent the damage.
- Treatment: suck the fluids out

Front 52

what sensations can you feel in the small intestines

Back 52

PRESSURE !!!

--> if you were to go and do a clean cut, you wouldn't feel it

Front 53

3 classic inflammatory diseases of the intestine

Back 53

Rheumatoid arthritis
Crohn’s disease
Ulcerative colitis

Front 54

Crohn’s disease

Back 54

Inflammatory disease
- A form of autoimmune disease because it is a disorder of the function of the lymphocytes; lymphocytes are attacking the intestinal lining

Can occur in all parts of the GI, but most commonly associated with the small intestine and proximal colon

Classic area of the Crohn's disease: terminal ileum

The disease is multifactorial: associated with abnormal cytokines, lymphocyte activities, NK Cells, Mphages, leakiness between the cells
- Primarily a disorder of T-helper cell overacrivity (?

First described as an inflammation at the terminal ileum that resembled tuberculosis

Front 55

Pathology of Crohn's Disease

Back 55

Inflammation with granuloma ***

- Thickening and Creeping of the mesenteric fat around the intestine
- Deep ulcers: Ulcerations on the mucosal surface that skips spaces (cobblestoning of the intestine)
- Shallow ulcers: Apthous ulcerations in the intestine, lip, mouth

IMPORTANT POINT: Crohn's disease is a TRANSMURAL INFLAMMATION:
- The disease affects the inner-lining (cobblestoning)
- Fistuli develop because the inflammation spreads from the lumen through the muscle layer to the adjacent organ
--> The fistuli can develop through the skin, to another loop, to bladder, to vagina

Front 56

what kind of inflammation is present in crohn's disease?

Back 56

Inflammation with granuloma ***

- Thickening and Creeping of the mesenteric fat around the intestine
- Deep ulcers: Ulcerations on the mucosal surface that skips spaces (cobblestoning of the intestine)
- Shallow ulcers: Apthous ulcerations in the intestine, lip, mouth

IMPORTANT POINT: Crohn's disease is a TRANSMURAL INFLAMMATION:
- The disease affects the inner-lining (cobblestoning)
- Fistuli develop because the inflammation spreads from the lumen through the muscle layer to the adjacent organ
--> The fistuli can develop through the skin, to another loop, to bladder, to vagina

Front 57

Clinical features of Crohn's disease

Back 57

Diarrhea – because the cobblestoning inhibits efficient absorption (reduced absorptive surface)

Pain from intestinal wall breakdown

Small intestinal obstruction – narrowing of the lumen due to thickened wall

Front 58

Gluten

Back 58

- Protein common in wheat and other grains
- Not harmful unless you have celiac disease
- People with celiac disease are allergic to gluten

Front 59

Pathology of Celiac Spure (gluten enteropathy)

Back 59

Genetic predisposition

Gluten allergy is topically expressed allergy: Ppl w/ celiac disease produce IgA against gluten; When gluten contacts the villi, IgA binds gluten & elicits inflammatory response. Plasma cells &lymphocytes infiltrate into subepithelial space and cause low grade inflammation

Result of the inflam.
- Villi changes OVER-TIME (no acute symptoms like rash, wheeze)
- In celiac disease, villi are blunted/absent; subepithelial space is expanded
- This causes reduced absorptive capacity (malabsorption)
--Less villi + thicker space for the nutrient to travel through (due to subEp expansion)
- Loss of protein, mineral, vit D3, loss of weight,
osteopenia(due to vit D deficiency)
- Removal of gluten from diet reverses the pathology
- Assoc. disorders w/ celiac disease
--> Celiac disease is a risk factor for lymphoma
--> Dermatitis Herpatiformus: Chroinc disruption of normal skin (looks like hepatitis rash); may develop into malignancy (mantle cell lympoma)

Front 60

Clinical features of Celiac Sprue(gluten enteropathy)

Back 60

Malnutrition, osteopenia, loss of weight

No Acute allergic symptoms: rash, wheezing

Front 61

Typical features of colonic infections

Back 61

- More invasive infection than small intestine infections
- Low volume diarrhea (because secretion and absorption in the colon is less than small intestine – less fluid flow in the lumen )
- Bleeding : disruption of the vasculature
- Pus formation from Nphil infiltration (acute inflammation)

Front 62

if you see pus formation..... infection is in (small intestines / colon)

Back 62

COLON !!!!!

Front 63

The most common colonic infections

Back 63

E. coli, EHEC (Enterohemorrhagic E. coli),

Salmonella (common in poorly cooked poultry)

Shigella (fecooral route of TM; the organism is so infectious that 10 organisms can cause gastroenteritis; Shigella toxin causes small intestinal diarrhea AND colonic diarrhea by upregulating the secretion via cAMP mechanism )

campylobacter (traveler’s diarrhea – frequent, small volume diarrhea)

C. difficile – ABX related
- TM via healthcare setting
- Loss of the normal flora that suppresses the growth of C. deficile
- C. difficile produces toxin and invade into the lining
- Bloody diarrhea or Non-bloody diarrhea with pus formation (pseudomembrane formation)

Front 64

Pathology of colon infection

Back 64

Nphil infiltration

Abscesses in the gland (krypt abscess – classical feature of acute diarrhea)

Breakdown of the surface of the normal colonic lining

Front 65

most important difference between ulcerative colitis and crohn's disease

Back 65

ulcerative colitis ONLY AFFECTS THE COLON

also.... ulcerative colitis is NOT A TRANSMURAL DISEASE

Front 66

where does ulcerative colitis start ?

Back 66

- only affect the colon
- ALWAYS starts from anal-rectal region of the GI and spreads upward (proximally). It can move an inch or cover the entire colon.
- The disease is not Transmural; no matter how developed the disease is, it does not penetrate into the musculature, no fistula, no spread.
- The first medications used to treat the disease: salicylate and amino-salicylate (aspirin)

Other extraintestinal manifestations
- Primary sclerosing colengitis: biliary tract disease
- Arthritis (common in both UC and CD)
- Pyoderma gangrenosum (ulcerating skin lesion of the lower extremities associatd with UC and CD)

- Not a Recurring disease: Excising the area affected with UC and suturing back will cure the disease ***
- UC resembles apthous ulcers throughout the colon

Krypt abscess formation**
UC affecting a glandular structure
Pus infiltration; exudate of fibrin and pus)

Front 67

Ulcerative colitis

Back 67

- only affect the colon
- ALWAYS starts from anal-rectal region of the GI and spreads upward (proximally). It can move an inch or cover the entire colon.
- The disease is not Transmural; no matter how developed the disease is, it does not penetrate into the musculature, no fistula, no spread.
- The first medications used to treat the disease: salicylate and amino-salicylate (aspirin)

Other extraintestinal manifestations
- Primary sclerosing colengitis: biliary tract disease
- Arthritis (common in both UC and CD)
- Pyoderma gangrenosum (ulcerating skin lesion of the lower extremities associatd with UC and CD)

- Not a Recurring disease: Excising the area affected with UC and suturing back will cure the disease ***
- UC resembles apthous ulcers throughout the colon

Krypt abscess formation**
UC affecting a glandular structure
Pus infiltration; exudate of fibrin and pus)

Front 68

skip lesions

Back 68

Crohn’s disease
- Skipped disease: the lesion may be present at the ileum and some part of the jejunum (but inbetween area are healthy)
- Granulomatous lesion formation (not always seen in biopsy but common)
- Recurring disease: Excising the area affected with CD and suturing back will not cure the disease because CD will occur at the same site (where the suture is) few years later***

SO CD IS NOT CURABLE WITH SURGERY

Front 69

ulcerative colitis vs. crohn's disease

Back 69

Front 70

Colon neoplasms

Back 70

Polyps: Precursor lesion to colon cancer

Most polyps that lead to colon cancers are ADENOMAS*

Front 71

Most polyps that lead to colon cancers are _____

Back 71

Polyps: Precursor lesion to colon cancer

Most polyps that lead to colon cancers are ADENOMAS*

Front 72

Natural history of polyps

Back 72

Starts from normal tissues --> Mutation --> Growth in controlled pattern --> subsequent mutations --> metaplasia and dysplasia --> Cancers

Slow growth: Most takes ~10 years from the development of polyp basis to cancer formation

Result in
-Bleeding
-Colon obstruction
-Metastatic disease

Colon cancer has a fair cure rate because of its thick serosa and muscular wall that keeps the cells from spreading as quickly

Front 73

Risk factors for colon cancer

Back 73

- Genetic predisposition
--> If have a first degree relative with colon cancer: - 3-7x fold chance of having the cancer
- Cigarette smoking
- Western diet (meat, fat, preserved food)
- UC and CD

Front 74

Polyp syndromes

Back 74

FAP-Familial adenomatous polyposis
- Most common;
- Autosomal dominant pattern of transmission
- Fatal due to colon cancer if not treated
- Gozillion polyps are present in the intestine – the polyps are all adenomatous and develop into colon cancer
- Diagnosis is made by looking into the intestine; if a 12 yr old does not have multiple polyps, he does not have FAP
- Treatment: colon removal

HNPCC –Hereditary Non-Polyposis colon cancer
- Not as severe as FAP
- Genetic abnormality – genetic predisposition
- Have gozillions of polyps – but not as many as FAP
- High risk for colon cancers
- Treatment: remove polyps if there are limited number
- Adenomatous polyps

Lynch Syndrome
- Some patients with HNPCC get additional neoplasms can get the lynch syndrome
- Lynch syndrome: uterine cancer + breast cancer + blader cancer

Front 75

FAP-Familial adenomatous polyposis

Back 75

FAP-Familial adenomatous polyposis
- Most common;
- Autosomal dominant pattern of transmission
- Fatal due to colon cancer if not treated
- Gozillion polyps are present in the intestine – the polyps are all adenomatous and develop into colon cancer
- Diagnosis is made by looking into the intestine; if a 12 yr old does not have multiple polyps, he does not have FAP
- Treatment: colon removal

HNPCC –Hereditary Non-Polyposis colon cancer
- Not as severe as FAP
- Genetic abnormality – genetic predisposition
- Have gozillions of polyps – but not as many as FAP
- High risk for colon cancers
- Treatment: remove polyps if there are limited number
- Adenomatous polyps

Lynch Syndrome
- Some patients with HNPCC get additional neoplasms can get the lynch syndrome
- Lynch syndrome: uterine cancer + breast cancer + blader cancer

Front 76

HNPCC –Hereditary Non-Polyposis colon cancer

Back 76

FAP-Familial adenomatous polyposis
- Most common;
- Autosomal dominant pattern of transmission
- Fatal due to colon cancer if not treated
- Gozillion polyps are present in the intestine – the polyps are all adenomatous and develop into colon cancer
- Diagnosis is made by looking into the intestine; if a 12 yr old does not have multiple polyps, he does not have FAP
- Treatment: colon removal

HNPCC –Hereditary Non-Polyposis colon cancer
- Not as severe as FAP
- Genetic abnormality – genetic predisposition
- Have gozillions of polyps – but not as many as FAP
- High risk for colon cancers
- Treatment: remove polyps if there are limited number
- Adenomatous polyps

Lynch Syndrome
- Some patients with HNPCC get additional neoplasms can get the lynch syndrome
- Lynch syndrome: uterine cancer + breast cancer + blader cancer

Front 77

Lynch Syndrome

Back 77

FAP-Familial adenomatous polyposis
- Most common;
- Autosomal dominant pattern of transmission
- Fatal due to colon cancer if not treated
- Gozillion polyps are present in the intestine – the polyps are all adenomatous and develop into colon cancer
- Diagnosis is made by looking into the intestine; if a 12 yr old does not have multiple polyps, he does not have FAP
- Treatment: colon removal

HNPCC –Hereditary Non-Polyposis colon cancer
- Not as severe as FAP
- Genetic abnormality – genetic predisposition
- Have gozillions of polyps – but not as many as FAP
- High risk for colon cancers
- Treatment: remove polyps if there are limited number
- Adenomatous polyps

Lynch Syndrome
- Some patients with HNPCC get additional neoplasms can get the lynch syndrome
- Lynch syndrome: uterine cancer + breast cancer + blader cancer

Front 78

Most common colon polyp syndrome

Back 78

FAP-Familial adenomatous polyposis
- Most common;
- Autosomal dominant pattern of transmission
- Fatal due to colon cancer if not treated
- Gozillion polyps are present in the intestine – the polyps are all adenomatous and develop into colon cancer
- Diagnosis is made by looking into the intestine; if a 12 yr old does not have multiple polyps, he does not have FAP
- Treatment: colon removal

HNPCC –Hereditary Non-Polyposis colon cancer
- Not as severe as FAP
- Genetic abnormality – genetic predisposition
- Have gozillions of polyps – but not as many as FAP
- High risk for colon cancers
- Treatment: remove polyps if there are limited number
- Adenomatous polyps

Lynch Syndrome
- Some patients with HNPCC get additional neoplasms can get the lynch syndrome
- Lynch syndrome: uterine cancer + breast cancer + blader cancer

Front 79

Adenomatous colon polyps

Back 79

Overgrowth of glands

The nuclei are nicely organized – not a dysplastic cancer

Precancerous tubularadenoma

Front 80

Villil tubuer adenoma

Back 80

Some surfaces of the polyps are covered with villi

More precancerous than simple tubueradenoma

If the majority of the structure is covered with villi, it is called the villous adenoma, which is the most precancerous

Front 81

staging of colon cancer

Back 81

T1: on the surface; little bit intomucosa
T2: deeply into the mucosa; touching the muscle
T3: through the muscle
T4: metastatic disease

Stage 1 = T1 + no lymphn node spread
Stage 2 = T2
Stage 3 = T3 + lymph node spread

Front 82

Diverticular disease

Back 82

Diverticulum: pocket in the wall

Front 83

Diverticulosis of the colon is a true/false diverticula

Back 83

Diverticulosis of the colon is a false diverticula
--> Not a true pocketing with the entire intestinal lining because the pocket lacks the other layers such as muscles; it is just the mucosa + submucosa +serosa

Front 84

Diverticular disease in colon

Back 84

The pocket forms along the penetration points where big blood vessels become small blood vessels and enter into the colon (these are the weak points)

The outpouching is caused by pressure – due to constipation
- The pocket most often occurs in the sigmoid colon, which is where most activity of the colon occurs.
- Contraction, relaxation of sigmoid colon = most intense pressure = most likely to develop pockets

Front 85

diverticulosis vs. diverticulitis

Back 85

diverticulosis = makign the outpouchings

diverticulitis = when one of them get infected

Front 86

Appendicitis

Back 86

- Obstruction leads to pressure build up in the appendix
- Wall gets thinner and blood vessels are compressed
- Gangrene and perforation occurs – similar to small bowel obstruction


**Appendectomy is successful when appendectomy occurs before perforation and gangrenous spillage occur

Front 87

dysphagia

Back 87

difficulty in swallowing

Front 88

what do the cells look like in iron deficiency anemia?

Back 88

microcytic and hypochromic

Front 89

esophagitis

Back 89

- chemical & infectious
- alcohol, corrosive acids, or alkalais, or pill-induced
- infectious viral (CMV) or fungal (Candida)
- reflux esophagitis
- GERD and its complications

Front 90

complications of esophagitis

Back 90

- ulcerations
- fibrosis
- strictures
- dysphagia
- leukoplakia
- metaplasia
- malignancy

Front 91

etiology of GERD

Back 91

- Decreased efficacy of esophageal
anti-reflux mechanism: age, alcohol, tobacco, fatty foods, central nervous systems depressants, obesity, smoking
- Sliding hiatal hernia
- Decreased efficiency of LES
- Delayed gastric emptying

Front 92

Achalasia

Back 92

- if someone tried to swallow food, they would NOT be able to swallow easily bc lower esophagus is coming to a point like a bird's beak (OBSTRUCTION); can't get food past this
-- lower esophagus is constricted (obstruction)
-- Attributed to problems with neurons, idiopathic, or neurological disease, i.e. Parkinson's
--> Motor neuron impairment disease
--> Inhibition of motor neurons: peristalsis is obstructed
- Limited amount of food will make it through the narrowed area

***If you're obstructing food at the lower esophagus, can aspirate the food back up into lung → chemical type of pneumonia
- chemical-type of pneumonia associated

Increased risk for SCC (only slight increase)

Front 93

bird's beak esophagus

Back 93

Achalasia

- if someone tried to swallow food, they would NOT be able to swallow easily bc lower esophagus is coming to a point like a bird's beak (OBSTRUCTION); can't get food past this
-- lower esophagus is constricted (obstruction)
-- Attributed to problems with neurons, idiopathic, or neurological disease, i.e. Parkinson's
--> Motor neuron impairment disease
--> Inhibition of motor neurons: peristalsis is obstructed
- Limited amount of food will make it through the narrowed area

***If you're obstructing food at the lower esophagus, can aspirate the food back up into lung → chemical type of pneumonia
- chemical-type of pneumonia associated

Increased risk for SCC (only slight increase)

Front 94

90% of cases of chronic gastritis are caused by___

Back 94

h. pylori

(other 10% pericious anemia)

Front 95

most common cause of acute gastritis

Back 95

NSAIDs !!

Front 96

what is the 2nd most popular cause of chronic gastritis?

Back 96

pernicious anemia

(90% is from h pylori)

Front 97

melena

Back 97

blood loss into the stool --> turns dark tarry brown due to clotted blood

--> bleeding in the UPPER GI TRACT

Front 98

bleeding at the end of the GI tract

Back 98

hematochezia --> bright red bleeding in the stool

- usually associated with hemmorhoids, but can also be a tumor

Front 99

bright red bleeding in the stool

Back 99

hematochezia

- usually associated with hemmorhoids, but can also be a tumor

Front 100

do you get bleeding in gastritis?

Back 100

YES

even though its only an erosion (DID NOT CROSS THE BASEMENT MEMBRANE AKA LAMINA PROPRIA)

Front 101

coffee-ground

Back 101

acute gastritis

Front 102

how are acute ulerative gastritis different from peptic ulcers?

Back 102

ACG is NOT caused by h pylori .. however... ulceration caused by h pylori is seen as peptic ulers in CHRONIC gastritis

in peptic ulcers... there wil be scarring b/c it is a chronic disease

Front 103

peptic ulcers can be found in (chronic/acute) gastritis

Back 103

CHRONIC !!!!!!!
- caused by h pylori

Front 104

H. Pylori and autoimmune gastritis are associated with an increased incidence of __

Back 104

gastric cancer

Front 105

Etiology of Peptic Ulcer Disease (PUD)

Back 105

- H. pylori and NSAIDs are the primary underlying causes of PUD
- Co-factors include smoking, high dose steroid therapy
- Imbalance of mucosal and damaging forces; require the action of gastric acid for PUD
- H. pylori in 85 % to 100 % with duodenal PUD; 65 % with gastric ulcers (PUD)**
- PUD develops on a background of chronic gastritis
- Malignant transformation of PUD is rare

Front 106

the the case of chronic gastritis... do peptic ulcers cause cancer?

Back 106

NOOO

they just happen to co-exist

Front 107

most common anemia in western world

Back 107

iron deficiency anemia
--> most common cause is due to bleeding

Front 108

most common cause of iron deficiency anemia

Back 108

bleeding !!

Front 109

#1 cause of cancer death in US

Back 109

#1 - lung
#2 - reproductive (prostate / men)
#3 - colon
#4 - pancreatic

Front 110

top causes of cancer in US

Back 110

#1 - lung
#2 - reproductive (prostate / men)
#3 - colon
#4 - pancreatic

Front 111

why might someone have prepandial (pre-meal) pain?

Back 111

peptic ulcer --> sensitive to stomach acid

Front 112

etiology and incidnce of crohn's disease

Back 112

Etiology: bacterial, viral, dietary factors

Peak incidence: teens and twenties; can be present at any age

Front 113

what are only times you would see a liver enzyme >1000

Back 113

- ischemic hepatitis
- tylenol toxicity
- acute viral hepatitis (usually B)
- flare of hep B

Front 114

where does crohn disease occur?

Back 114

almost anywhere....

40% in small bowel
30% large bowel
30% large & small bowel together
Oral cavity: uncommonly

Front 115

what kind of inflammation is in crohn disease?

Back 115

non-caseating, non-necrotizing granulmatous

Front 116

function of small intstine

Back 116

absorption of fat-soluble vitamins
--> A, D, E, K

Front 117

what does the colon (large intestine) absorb?

Back 117

WATER !!!

not fat soluble vitamins like small intestine

Front 118

unlike crohn disease... ulcerative colitis affects the ___

Back 118

mucosa !!!!! (sometimes the submucosa...but does NOT go thru the wall)

Front 119

how would you end up infarcting small intestine if you have thrombolitic disease?

Back 119

superior mesenteric

Front 120

most common cancer of the esophagus

Back 120

squamous cell

Etiology: Alcohol, cigarette smoking, nitrosamines, Plummer-Vinson syndrome (iron deficiency anemia, glossitis, and esophageal dysphagia), chronic esophagitis, achalasia, strictures, diet

Front 121

adenocarcinoma in the esophagus

Back 121

barret esophagus (intestinal metaplasia)

Front 122

keratin pearls

Back 122

squamous cell cancer

Front 123

favored location for carcinoma of the stomach

Back 123

Favored location is the lesser curvature 40%

Front 124

dyspepsia

Back 124

indigestion

Front 125

signet ring cells

Back 125

gastric cancer

Front 126

Intestinal Neoplasms

Back 126

Adenomas (polyps): 2/3 of persons over 65 have at least one

But we concerned about villous adenoma:

Front 127

does hyperplastic polyp have malignant potential ?

Back 127

NO

--> adenoma does

Front 128

Familial Adenomatous Polyposis

Back 128

Genetic adenomas of the colon

Bumps: All polyps (probably malignant cancer will form within one of these if you don't remove them surgically!)

Front 129

Intestinal Neoplasms Malignant
--> Small intestine

Back 129

Uncommon, unless associated with history of regional enteritis (Crohn disease)

Front 130

Intestinal Neoplasms Malignant
--> Large intestine

Back 130

Etiology: Low fiber diet, high fat diet, high anaerobic bacterial content, genetics, age above 50, ulcerative colitis, Crohn disease, Ulcerative Colitis

Pathogenesis: Arise in adenomas, particularly villous

Front 131

guaiac test

Back 131

tests for hemoglobin in stool

Front 132

where does adenocarcinoma of the colon metastize to?

Back 132

liver, lung, brain

Front 133

most common place for diverticuli

Back 133

colon

Front 134

largest solid organ in the abdominal cavity

Back 134

Liver

Front 135

intestinal goblet cells in lower 1/3 of esophagus

Back 135

barret esophagus

Front 136

largest lobe of the liver

Back 136

right lobe

Front 137

Galbladder

Back 137

stores bile (made in the liver) and travels thorugh common bile duct

Front 138

Bile duct drains into

Back 138

duodenum

Front 139

Functions of the Liver

Back 139

Production of bile
- Carry away waste
- Break down fats in the small intestine

Production of plasma proteins

Production of cholesterol and proteins to carry fats through the body

Conversion of excess glucose into glycogen for storage

Regulation of blood levels of amino acids

Front 140

Other functions of the liver

Back 140

Processing of hemoglobin for use of its iron content

Storage of iron

Conversion of ammonia to urea

Clearance of drugs and toxins

Synthesis of clotting factors

Production of immune factors

Removal of bacteria from the blood stream

Front 141

types of Hepatitis

Back 141

Viral: A, B, C, D, E

Autoimmune

Ischemic

Medication induced

Fatty liver disease
- Alcohol liver disease/Alcoholic hepatitis
- Non-alcoholic fatty liver diseases
--> NAFLD/NASH

Front 142

What is hepatitis?

Back 142

Hepatitis = inflammation of the liver

Chronic inflammation can lead to cirrhosis, possible liver failure and/or liver cancer

Severe, acute inflammation can lead to fulminant liver failure

Early damage is reversible but transplant may be necessary for end-stage cirrhosis and cancer

Front 143

Hepatitis A

Back 143

- RNA virus
- Transmitted via fecal-oral route (food-borne)
- Worldwide distribution
- Usually self limited
- Rare cases of fulminant hepatic failure
- Vaccination available
- Diagnosis
-- Liver enzymes (AST, ALT, Alk Phos, Bilirubin)
-- Antibodies to hepatitis A proteins (anti-HAV)

- 30 day incubation period
- Fever, fatigue, nausea, vomiting, anorexia, RUQ pain
- Jaundice may occur
-- Inflammation  biliary obstruction
-- Bilirubin deposition in skin
1% fatality rate > 40 years of age

Front 144

incubation period of hep a

Back 144

- RNA virus
- Transmitted via fecal-oral route (food-borne)
- Worldwide distribution
- Usually self limited
- Rare cases of fulminant hepatic failure
- Vaccination available
- Diagnosis
-- Liver enzymes (AST, ALT, Alk Phos, Bilirubin)
-- Antibodies to hepatitis A proteins (anti-HAV)

- 30 day incubation period
- Fever, fatigue, nausea, vomiting, anorexia, RUQ pain
- Jaundice may occur
-- Inflammation  biliary obstruction
-- Bilirubin deposition in skin
1% fatality rate > 40 years of age

Front 145

Hepatitis E

Back 145

- RNA virus
- Asia, Africa, Middle East, Central America
---> Less common than HAV in US
- Spread
--> Fecally contaminated water
--> Blood transfusion
--> Undercooked wild meat
--> Person to person transmission rare
- Clinical syndrome similar to HAV
--> Incubation 15-60 days
- Fulminant liver failure occurs more often in pregnant patients
--> 15-25% mortality
- Diagnosis: serum antibodies or virus in serum/stool
--> Not commercially available
--> Must contact the CDC

Front 146

spread of hep E

Back 146

- RNA virus
- Asia, Africa, Middle East, Central America
---> Less common than HAV in US
- Spread
--> Fecally contaminated water
--> Blood transfusion
--> Undercooked wild meat
--> Person to person transmission rare
- Clinical syndrome similar to HAV
--> Incubation 15-60 days
- Fulminant liver failure occurs more often in pregnant patients
--> 15-25% mortality
- Diagnosis: serum antibodies or virus in serum/stool
--> Not commercially available
--> Must contact the CDC

Front 147

which hepatitis is caused by a DNA virus ?

Back 147

Hep B

- DNA virus
- Global health problem
--> 350 million infected worldwide
--> 1 million die annually
- Geographic variation
--> 0.1 – 2% US, Canada
--> 10-20% China, SE Asia, SS Africa
- Vaccination available
--> Series of three injections
--> Recommended to start in infancy
--> Booster may be needed
US 1990-2006
- Widespread vaccination
- 81% decline in acute infection

Front 148

Hep B

Back 148

- DNA virus
- Global health problem
--> 350 million infected worldwide
--> 1 million die annually
- Geographic variation
--> 0.1 – 2% US, Canada
--> 10-20% China, SE Asia, SS Africa
- Vaccination available
--> Series of three injections
--> Recommended to start in infancy
--> Booster may be needed
US 1990-2006
- Widespread vaccination
- 81% decline in acute infection

Front 149

modes of transmission of Hep B

Back 149

Perinatal
- Higher risk of chronic infection

Sexual
- Major mode in developed countries
- 39% heterosexual, 24% MSM

IV drug use

Blood transfusion
- Prior to 1975

Needle sticks
- Up to 40% risk

Organ transplantation

Front 150

which Hep is easiest to get thru needle sticks?

Back 150

Hep B

Front 151

Clinical Presentation of Hep B

Back 151

Infection can be chronic or self-limited
- Risk of chronic infection related to age at time of exposure
--> Infants: 90% risk
-- Depends on maternal viral load
-- 95% efficacy with HBIG and vaccination
--> Adults: 15% risk
-- 85% of exposed adults clear the infection

**Only 30% develop jaundice when acutely infected
- Many are unaware they have been exposed

Front 152

jaundice & Hep B

Back 152

**Only 30% develop jaundice when acutely infected
- Many are unaware they have been exposed

Front 153

diagnosis of Hep B

Back 153

Diagnosis
- Serum proteins/antibodies
- DNA viral load
- Liver enzymes (esp ALT)

Types of chronic infection
- Inactive carrier
--> Antibodies present but minimal to zero viral load
--> No evidence of liver damage
- Persistent chronic hepatitis
--> Viral DNA present in bloodstream
--> Chronic liver fibrosis
--> Fibrosis: scarring due to fibrin deposition

Front 154

Inactive carrier vs. Persistent chronic hepatitis B

Back 154

Types of chronic infection
- Inactive carrier
--> Antibodies present but minimal to zero viral load
--> No evidence of liver damage
- Persistent chronic hepatitis
--> Viral DNA present in bloodstream
--> Chronic liver fibrosis
--> Fibrosis: scarring due to fibrin deposition

Front 155

Serologic markers of Hep b

Back 155

Hepatitis B surface antigen

Hepatitis B surface antibody

Hepatitis B core antigen (not detectable in serum)

Hepatitis B core antibody

Hepatitis B e antigen

Hepatitis B e antibody

Hepatitis B viral DNA level

Front 156

which serological marker of Hep b is NOT detectable in serum?

Back 156

Hepatitis B surface antigen

Hepatitis B surface antibody

Hepatitis B core antigen (not detectable in serum)

Hepatitis B core antibody

Hepatitis B e antigen

Hepatitis B e antibody

Hepatitis B viral DNA level

Front 157

Hepatitis B surface antigen (HBsAg)

Back 157

Hepatitis B surface antigen (HBsAg)
- Appears 1-10 weeks after infection
- Undetectable in 4-6 months if patient recovers
- Persistence > 6 months = chronic infection

Hepatitis B surface antibody (anti-HBs)
- Appears after disappearance of HBsAg
- Appears after immunization
- Confers immunity

*HBsAg and anti-HBs present carrier of HBV
*Window period: neither are present

Front 158

(anti-HBs)

Back 158

Hepatitis B surface antigen (HBsAg)
- Appears 1-10 weeks after infection
- Undetectable in 4-6 months if patient recovers
- Persistence > 6 months = chronic infection

Hepatitis B surface antibody (anti-HBs)
- Appears after disappearance of HBsAg
- Appears after immunization
- Confers immunity

*HBsAg and anti-HBs present carrier of HBV
*Window period: neither are present

Front 159

Hepatitis B core antigen (HBcAg)

Back 159

Hepatitis B core antigen (HBcAg)
- Intracellular antigen in infected liver cells
- Not detectable in serum

Hepatitis B core antibody (anti-HBc)
- IgM: Sole marker of HBV infx during window period
- Indication of acute HBV infection but may increase during flares of chronic infection
- IgG: Persists after acute infection
- Isolated anti-HBc
--> Window period
--> Years after recovery when anti-HBs becomes undetectable

Front 160

Hepatitis B core antibody (anti-HBc)

Back 160

Hepatitis B core antigen (HBcAg)
- Intracellular antigen in infected liver cells
- Not detectable in serum

Hepatitis B core antibody (anti-HBc)
- IgM: Sole marker of HBV infx during window period
- Indication of acute HBV infection but may increase during flares of chronic infection
- IgG: Persists after acute infection
- Isolated anti-HBc
--> Window period
--> Years after recovery when anti-HBs becomes undetectable

Front 161

Hepatitis B e antigen (HBeAg)

Back 161

Hepatitis B e antigen (HBeAg)
- Marker of viral replication/infectivity
- Associated with high levels of DNA
- Higher rates of transmission

Hepatitis B e antibody (anti-HBe)
- Presence usually associated with decrease in HBV - DNA and remission of liver disease
- If liver disease persists, viral mutations probably exist

HBV DNA
- Several assays available: PCR technique
- Antiviral therapy indicated if DNA level is high

Front 162

Hepatitis B e antibody (anti-HBe)

Back 162

Hepatitis B e antigen (HBeAg)
- Marker of viral replication/infectivity
- Associated with high levels of DNA
- Higher rates of transmission

Hepatitis B e antibody (anti-HBe)
- Presence usually associated with decrease in HBV - DNA and remission of liver disease
- If liver disease persists, viral mutations probably exist

HBV DNA
- Several assays available: PCR technique
- Antiviral therapy indicated if DNA level is high

Front 163

HBV DNA

Back 163

Hepatitis B e antigen (HBeAg)
- Marker of viral replication/infectivity
- Associated with high levels of DNA
- Higher rates of transmission

Hepatitis B e antibody (anti-HBe)
- Presence usually associated with decrease in HBV - DNA and remission of liver disease
- If liver disease persists, viral mutations probably exist

HBV DNA
- Several assays available: PCR technique
- Antiviral therapy indicated if DNA level is high

Front 164

where would you find Hepatitis B core antigen (HBcAg) ?

Back 164

Hepatitis B core antigen (HBcAg)
- Intracellular antigen in infected liver cells
- Not detectable in serum

Hepatitis B core antibody (anti-HBc)
- IgM: Sole marker of HBV infx during window period
- Indication of acute HBV infection but may increase during flares of chronic infection
- IgG: Persists after acute infection
- Isolated anti-HBc
--> Window period
--> Years after recovery when anti-HBs becomes undetectable

Front 165

what is the Sole marker of HBV infx during window period

Back 165

Hepatitis B core antigen (HBcAg)
- Intracellular antigen in infected liver cells
- Not detectable in serum

Hepatitis B core antibody (anti-HBc)
- IgM: Sole marker of HBV infx during window period
- Indication of acute HBV infection but may increase during flares of chronic infection
- IgG: Persists after acute infection
- Isolated anti-HBc
--> Window period
--> Years after recovery when anti-HBs becomes undetectable

Front 166

Presence usually associated with decrease in HBV DNA and remission of liver disease

Back 166

Hepatitis B e antigen (HBeAg)
- Marker of viral replication/infectivity
- Associated with high levels of DNA
- Higher rates of transmission

Hepatitis B e antibody (anti-HBe)
- Presence usually associated with decrease in HBV - DNA and remission of liver disease
- If liver disease persists, viral mutations probably exist

HBV DNA
- Several assays available: PCR technique
- Antiviral therapy indicated if DNA level is high

Front 167

Marker of viral replication/infectivity of hep B virus

Back 167

Hepatitis B e antigen (HBeAg)
- Marker of viral replication/infectivity
- Associated with high levels of DNA
- Higher rates of transmission

Hepatitis B e antibody (anti-HBe)
- Presence usually associated with decrease in HBV - DNA and remission of liver disease
- If liver disease persists, viral mutations probably exist

HBV DNA
- Several assays available: PCR technique
- Antiviral therapy indicated if DNA level is high

Front 168

Acute HBV Infection

Back 168

Front 169

Chronic HBV Infection

Back 169

Front 170

Hepatitis B core antibody (anti-HBc)
--> acute vs. chronic

Back 170

IgM --> acute

IgG --> chronic (says you've been exposed at one point in the past)

Front 171

first think you see in response to HBV infection?

Back 171

HBV DNA

Front 172

most important thing to check for in window period of Hep B

Back 172

Anti-core igM

Front 173

window period of acute HBV Infections

Back 173

imagine if blue line didnt overlap with the red.... BUT the green line would still be ther because that is the core antibody being produced

Front 174

pt coems in with hep.. only thing that is positive is igM anti-HBc

Back 174

window phase

Front 175

positivity informs one is immunized either from exposure or vaccination from HBV

Back 175

Anti-HBS

IF Anti-HBS is the only thing that is positive, this means the individual has been VACCINATED

Front 176

interpretation of HBV serologic panel
--> susceptible to HBV

Back 176

Front 177

interpretation of HBV serologic panel
--> immune due to natural infection

Back 177

Front 178

interpretation of HBV serologic panel
--> immune due to Hep B vaccination

Back 178

Front 179

interpretation of HBV serologic panel
--> acutely infected

Back 179

Front 180

interpretation of HBV serologic panel
--> chronically infected

Back 180

Front 181

interpretation of HBV serologic panel
--> 4 interpretations possible

Back 181

Front 182

Consequences of chronic infection of Hep B

Back 182

Persistent liver inflammation
- Serum tests for liver enzymes
--> AST, ALT, Alk Phos, Bilirubin

Scarring (fibrosis) of hepatocytes
- Severe scarring results in cirrhosis/liver failure
- Increased risk of liver cancer
-- Hepatocellular carcinoma (HCC)
-- High viral load > 1million copies/mL = 15% 10-year risk
-- Cirrhosis is not obligatory to develop cancer
--> Patients must be enrolled in screening program:
--> US and AFP every 6 months to a year

Front 183

what is special about liver cancer from Hep B

Back 183

In HEP B, to develop liver cancer, one does not have to develop cirrhosis

--> HBV virus is just there... but your body lays down scarring fibrosis and respsonse

Front 184

most common liver cancer

Back 184

Hepatocellular carcinoma (HCC)

Front 185

treatment for hep b

Back 185

Interferon
Lamivudine
Adefovir
Entecavir
Telbivudine
Tenofovir

Treatment goals
-Viral load reduction
-Prevention of further fibrosis
-Reversal of liver damage

Front 186

treatment goals for hep b

Back 186

Interferon
Lamivudine
Adefovir
Entecavir
Telbivudine
Tenofovir

Treatment goals
-Viral load reduction
-Prevention of further fibrosis
-Reversal of liver damage

Front 187

can you reverse liver damage from hep b ?

Back 187

YESS !!

Front 188

Hepatitis B and Pregnancy

Back 188

Acute HBV in pregnancy
- Usually not severe
- Possible risk of lower birth weight/prematurity
- Treatment is supportive
--> Antivirals usually unnecessary
--> Lamivudine, telbivudine or tenofovir can be used if acute liver failure or severe hepatitis

Chronic HBV in pregnancy
--> HBsAg (+): can have flares, require bloodwork q3mo
--> Treatment depends on degree of liver disease and serologic markers
--> Patients may elect to stop or switch therapy

Screening for HBV is routine prenatal workup

Front 189

acute HBV in pregnancy

Back 189

Acute HBV in pregnancy
- Usually not severe
- Possible risk of lower birth weight/prematurity
- Treatment is supportive
--> Antivirals usually unnecessary
--> Lamivudine, telbivudine or tenofovir can be used if acute liver failure or severe hepatitis

Chronic HBV in pregnancy
--> HBsAg (+): can have flares, require bloodwork q3mo
--> Treatment depends on degree of liver disease and serologic markers
--> Patients may elect to stop or switch therapy

Screening for HBV is routine prenatal workup

Front 190

chronic HBV in pregnancy

Back 190

Acute HBV in pregnancy
- Usually not severe
- Possible risk of lower birth weight/prematurity
- Treatment is supportive
--> Antivirals usually unnecessary
--> Lamivudine, telbivudine or tenofovir can be used if acute liver failure or severe hepatitis

Chronic HBV in pregnancy
--> HBsAg (+): can have flares, require bloodwork q3mo
--> Treatment depends on degree of liver disease and serologic markers
--> Patients may elect to stop or switch therapy

Screening for HBV is routine prenatal workup

Front 191

Perinatal transmission of Hep B

Back 191

Perinatal transmission:
--> Up to 90% without prophylactic treatment

Transmission can occur in utero, at birth or after birth
- High efficacy of prophylaxis implies most infections occur at time of birth
- Hepatitis B immunoglobulin (HBIG) should be given to infant at birth
- Three-series vaccination in the first 6 months of life
--> Reduced transmission rates to 5-10%
- Breast feeding does not appear to pose a risk
- C-section not clearly found to be protective

Front 192

okay to breast feed with Hep B ?

Back 192

Perinatal transmission:
--> Up to 90% without prophylactic treatment

Transmission can occur in utero, at birth or after birth
- High efficacy of prophylaxis implies most infections occur at time of birth
- Hepatitis B immunoglobulin (HBIG) should be given to infant at birth
- Three-series vaccination in the first 6 months of life
--> Reduced transmission rates to 5-10%
- Breast feeding does not appear to pose a risk
- C-section not clearly found to be protective

Front 193

hep D

Back 193

RNA virus

Rare in US
- Eastern Europe
- Central America
- Mediterranean countries

Defective pathogen
- Requires hepatitis B virus for transmission
- Unable to replicate without machinery from hepatitis B

Similar clinical signs as HBV
- High rate of liver failure among IV drug users

Front 194

Hepatitis C

Back 194

- RNA virus
- Multiple Genotypes
--> 1-4 most common in US

Modes of transmission
- IVDU
- Blood transfusion before 1990
- Rare sexual transmission
--> MSM and “hard sex”
- Organ transplantation
- Perinatal transmission

No vaccination available

Front 195

stats of Hepatitis C

Back 195

4.1 million affected in US
- #1 indication for liver transplantation in US

Acute infection is usually asymptomatic
- <25% of patients acutely infected develop jaundice

85% develop chronic infection with persistent viremia
- Process similar to chronic hepatitis B infection
- Chronic inflammation --> activation of stellate cells --> fibrosis
- 16% of patients develop cirrhosis after 20 years

Most deaths are from end stage liver disease
Increased risk of HCC in cirrhotics: 3% per year
--> Cirrhosis necessary to develop HCC with hepatitis C

Front 196

#1 indication for liver transplantation in US

Back 196

Hepatitis C

Front 197

higher chance to get infection from Hep B or C?

Back 197

C !!!!!

85% develop chronic infection with persistent viremia
(only 15% for hep B)

Front 198

diagnosis for hep c

Back 198

Diagnosis
- Serum antibodies to virus protein (anti-HCV)
- RNA viral load

Treatment
- Currently: Combo of subcutaneous injections and oral meds
- Very difficult to tolerate with multiple side effects
--> Genotype 1-harder to treat: triple regimen
-- PEG-Interferon
-- Ribavirin
-- Sofosbuvir or simeprevir
--> Genotype 2, 3-easier to treat: double regimen, all oral
-- 2: Sofosbuvir/ribavirin x 12 weeks
-- 3: Sofosbuvir/ribavirin x 24 weeks

Front 199

treatment for hep c

Back 199

Diagnosis
- Serum antibodies to virus protein (anti-HCV)
- RNA viral load

Treatment
- Currently: Combo of subcutaneous injections and oral meds
- Very difficult to tolerate with multiple side effects
--> Genotype 1-harder to treat: triple regimen
-- PEG-Interferon
-- Ribavirin
-- Sofosbuvir or simeprevir
--> Genotype 2, 3-easier to treat: double regimen, all oral
-- 2: Sofosbuvir/ribavirin x 12 weeks
-- 3: Sofosbuvir/ribavirin x 24 weeks

Front 200

PEG-interferon

Back 200

pegylated--little molecule on the chemical, inject into arm/l eg pegylation allows diffusion into bloodstream, i.e. will gradually release chemicals

for tx of hep c

Front 201

Ribavirin

Back 201

tc for hep c

take 2x/day,
Side effects: anemia, make tx difficult

Front 202

Sofosbuvir or simeprevir

Back 202

protease inhibitors with good activity against HCV

Front 203

treatment for hep c

Back 203

Decision to treat made on a patient by patient basis
- Very difficult, expensive and many side effects
- Exclusions
*Psychiatric history *Decompensated cirrhosis
*Unreliable patient *Severe anemia

Options changing rapidly

Length of treatment depends on genotype, previous treatment, response to therapy

Transplantation for end stage disease or HCC

Front 204

Autoimmune Hepatitis

Back 204

Chronic hepatitis of unknown etiology

Autoimmune destruction of liver
- Formation of antibodies to specific liver proteins

Two major types
- Type 1: any age affected
- Type 2: girls and young women (less common)

Chronic liver inflammation
- Leads to fibrosis/cirrhosis

Diagnosis
- Serum antibody levels
- Liver biopsy

Front 205

type I autoimmune hepatitis

Back 205

Two major types
- Type 1: any age affected
- Type 2: girls and young women (less common)

Antibody production
- Type 1: Classic
--> Antinuclear antibody (ANA)
--> Anti smooth muscle antibody (ASMA)

- Type 2: less common
--> Anti liver/kidney microsomes (LKM)
--> Anti liver cytosol antigen

Front 206

type II autoimmune hepatitis

Back 206

Two major types
- Type 1: any age affected
- Type 2: girls and young women (less common)

Antibody production
- Type 1: Classic
--> Antinuclear antibody (ANA)
--> Anti smooth muscle antibody (ASMA)

- Type 2: less common
--> Anti liver/kidney microsomes (LKM)
--> Anti liver cytosol antigen

Front 207

antibody production of autoimmune hepatitis

Back 207

Antibody production
- Type 1: Classic
--> Antinuclear antibody (ANA)
--> Anti smooth muscle antibody (ASMA)

- Type 2: less common
--> Anti liver/kidney microsomes (LKM)
--> Anti liver cytosol antigen

Front 208

Anti liver/kidney microsomes (LKM)

Back 208

Type 2 Autoimmune Hep.

Antibody production
- Type 1: Classic
--> Antinuclear antibody (ANA)
--> Anti smooth muscle antibody (ASMA)

- Type 2: less common
--> Anti liver/kidney microsomes (LKM)
--> Anti liver cytosol antigen

Front 209

presentation of autoimmune hepatitis

Back 209

Variable presentation
-Asymptomatic
-Acute hepatitis
-Cirrhosis

Many found incidentally
- Screening for school, work or insurance plans

Front 210

Diagnosis of autoimmune hep

Back 210

Elevated liver function tests (LFTs)
- AST/ALT/Alk Phos/Bilirubin

Detection of serum antibodies
- Not always present

Liver biopsy
- Portal plasma cell infiltrate
- Fibrosis
- Piecemeal necrosis

Front 211

Treatment of autoimmune hep

Back 211

Goal: remission of inflammation to prevent fibrosis and liver failure

Endpoint: LFTs < 2x ULN

Factors
- Severity of illness/symptoms
- Degree of elevation of LFTs
- Histologic activity

Options: antiinflammatory medications
- Steroids alone
- Steroids in combination with azathioprine

Lots of sides effects to treatment
- Weight gain, diabetes, bone marrow suppression, etc

Front 212

Ischemic Hepatitis

Back 212

“Shock Liver”

Diffuse hepatic injury from acute hypoperfusion
- Cardiac arrest
- Sepsis
- Hypovolemic shock (bleeding)
- Disruption of blood flow
- Clotting of hepatic artery or portal vein

- AST/ALT usually > 1000 (ULN = 30-50)
- If patient survives underlying cause, usually no long-term damage to liver
- Treatment is supportive; reverse underlying cause

Front 213

AST/ALT usually > 1000 (ULN = 30-50)

Back 213

Ischemic Hepatitis

Front 214

Pathology findings of ischemic hepatitis

Back 214

Necrosis in zone 3 of hepatocytes
- Most sensitive to oxygen fluctuation

Reversible if circulation restored

LFTs return to normal within 7-10 days

Front 215

what zone of hepatocytes is most susceptible to oxygen fluctuation?

Back 215

zone 3

Front 216

Medication-Induced Hepatitis

Back 216

Acetaminophen
--> ½ of all cases of ALF
--> Safe up to 4g/day in healthy adults

-Statins
-Methotrexate
-Niacin
-Amiodarone
-Vitamins and herbs
-Vitamin A
-Kava Kava

Antibiotics
-Isoniazid
-Sulfonamides
-Augmentin
-Nitrofurantoin

NSAIDs
-Ibuprofen
-Naprosyn

Front 217

most common cause of Medication-Induced Hepatitis

Back 217

acetaminophen

Front 218

Major cause of liver disease in US

Back 218

Alcoholic Liver Disease

Front 219

Alcoholic Liver Disease

Back 219

Major cause of liver disease in US

One alcoholic drink = 10 grams of alcohol
One beer, one glass of wine or one shot

Safe consumption
2 drinks/day for healthy women
3 drinks/day for healthy men

60g/day over 10 years --> liver damage
- Threshold lower in women than in men

Early damage = fatty liver
- Reversible

Chronic exposure --> fibrosis --> cirrhosis

Front 220

safe consumption of alcohol

Back 220

Major cause of liver disease in US

One alcoholic drink = 10 grams of alcohol
One beer, one glass of wine or one shot

Safe consumption
2 drinks/day for healthy women
3 drinks/day for healthy men

60g/day over 10 years --> liver damage
- Threshold lower in women than in men

Early damage = fatty liver
- Reversible

Chronic exposure --> fibrosis --> cirrhosis

Front 221

Alcoholic Hepatitis

Back 221

Acute, symptomatic hepatitis due to excessive alcohol consumption
- Exact amount needed to cause is unknown
- At risk: >100 g/day for >20y
- Recent increased use due to stressors?
- Any type of ETOH

**Usually does not occur until has been heavily drinking for many years
--> Rare in young, college-age individuals to develop alcoholic hepatitis

Front 222

Alcoholic Hepatitis signs/symptoms

Back 222

Signs/symptoms
- Jaundice
- Anorexia
- RUQ pain
- Fever
- Elevated transaminases
--> AST:ALT > 2:1
--> Both <500 units/L

Important to exclude other causes first

Liver biopsy if uncertain

Front 223

Elevated transaminases
--> AST:ALT > 2:1
Both <500 units/L

Back 223

Specific ratio in alcoholic hepatitis

Front 224

mortality rate w/ alcoholic hepatitis

Back 224

High mortality
- Severe cases: 25-35% at one month
- Mild to moderate cases: < 10% at 1-3 months
- Factors associated with increased mortality
*older age *acute kidney inury
*elevated bilirubin *elevated INR
*leukocytosis *ETOH consumption > 120g/d
*infection *encephalopathy
*upper GI bleed *bilirubin:GGT ratio > 1

Front 225

Maddrey discriminant function (DF)

Back 225

DF = (4.6 x [PT (sec) – control PT (sec)]) + (serum bilirubin)

DF > 32 = high short term mortality
>25% at one month
Treatment with steroids is indicated
Prednisolone 40mg daily x 28 days then taper for 2 weeks
Mortality reduction : 34%  20%

Front 226

Model for End Stage Liver Disease (MELD)

Back 226

Three serologic crteria:
- Bilirubin, creatinine, and INR (liver and kidney function measures)

Affords three month mortality statisics:
- IF meld score is low: low chance of mortality
- If >=40: 100% chance mortality unless one has liver transplant

Front 227

Non Alcoholic Fatty Liver Disease (NAFLD)

Back 227

Hepatic steatosis
-Fat deposition in the liver

Risk factors
-Central obesity
-Type II diabetes
-Dyslipidemia

Environmental factors
-High carbohydrate diet
-Sedentary lifestyle
-High intake refined sugars

US: 20% prevalence

Front 228

pathogenesis of Non Alcoholic Fatty Liver Disease (NAFLD)

Back 228

1) insulin resistance
2) increased free fatty acids
3) accumulation in liver

Front 229

Non Alcoholic Steatohepatitis (NASH)

Back 229

Hepatic steatosis with associated inflammation
- Steatohepatitis
- Indistinguishable from alcoholic hepatitis
- Liver biopsy for diagnosis and activity score
- 70% of patients with cryptogenic cirrhosis have risk factors for NAFLD/NASH

Spectrum of disease
- Normal --> NAFLD --> NASH --> Cirrhosis

Front 230

management of NASH

Back 230

- Weight loss
- Vaccinations
--> HAV/HBV
--> Pneumococcus
- Avoid ETOH
- Optimize comorbid conditions
--> HTN, DM, cholesterol
- Vitamin E 400 IU/day with advanced fibrosis
- Screen for liver cancer if cirrhosis

Front 231

provides the oxygenated blood from the aorta to the liver

Back 231

Celiac trunk

Divides into
-Common hepatic
-Left gastric
-Splenic

Blood supply for
-Liver
-Stomach
-Pancreas
-Proximal intestine

Front 232

Celiac trunk

Back 232

provides the oxygenated blood from the aorta to the liver

Divides into
-Common hepatic
-Left gastric
-Splenic

Blood supply for
-Liver
-Stomach
-Pancreas
-Proximal intestine

Front 233

Hepatic Artery

Back 233

Branch of the celiac trunk from the aorta
- 1/3 of blood supply to liver
- 100% of the blood supply to bile ducts
- High oxygen content
- Relatively poor in nutrients compared to portal vein

Front 234

blood supply to the bile ducts

Back 234

Hepatic Artery

Branch of the celiac trunk from the aorta
- 1/3 of blood supply to liver
- 100% of the blood supply to bile ducts
- High oxygen content
- Relatively poor in nutrients compared to portal vein

Front 235

Portal Vein

Back 235

2/3 of blood supply to liver

Deoxygenated blood
- Venous drainage from the intestines

Rich in nutrients
- glucose, amino acids, triglycerides

Front 236

2/3 of blood supply to liver

Deoxygenated blood
- Venous drainage from the intestines

Rich in nutrients
- glucose, amino acids, triglycerides

Back 236

portal vein

Front 237

blood supply to the liver

Back 237

hepatic artery
- 1/3
- high oxygen content
- poor in nutrients

portal vein
- 2/3
- rich in nutrients (glucose, amino acids, triglycerides)

Front 238

Hepatic Veins

Back 238

Drain directly into inferior vena cave

Deoxygenated blood from liver

Returns to the right heart  pulmonary arteries  reoxygenation

Front 239

The Biliary Tree

Back 239

Bile travels through hepatic ducts into the common hepatic duct, eventually into the common bile duct, travels through head of pancreas
-->joins the pancreatic duct
-->Spincter of Oddi controls flow after joining

Front 240

Back 240

biliary tree

Bile travels through hepatic ducts into the common hepatic duct, eventually into the common bile duct, travels through head of pancreas
-->joins the pancreatic duct
-->Spincter of Oddi controls flow after joining

Front 241

The Biliary Tree

Back 241

Intrahepatic bile ducts
-Left and right hepatic ducts
-Interlobular ducts

Extrahepatic bile duct
-Common bile duct
-Common hepatic duct

Gallbladder

Front 242

biliary tree drains where

Back 242

Drains into duodenum at ampulla
-Major papilla
-Common drainage with pancreatic duct
-Sphincter of Oddi
-- Muscle fibers controlling flow from biliary and pancreatic ducts

Front 243

Functions of the Liver

Back 243

Production of bile
- Carry away waste
- Break down fats in the small intestine
Production of plasma proteins

Production of cholesterol and proteins to carry fats through the body

Conversion of excess glucose into glycogen for storage

Regulation of blood levels of amino acids

Front 244

function of biliary tree

Back 244

Biliary tree
-Bile produced in liver
-Transported through the biliary tree to the duodenum
I-ntrahepatics --> common hepatic duct --> common bile duct --> ampulla/Sphincter of Oddi

Gallbladder
-Concentrates and stores bile
-Stimulated during a meal to contract
-Sphincter of Oddi relaxes
-Bile released into the intestine

Front 245

function of gallbladder

Back 245

Biliary tree
-Bile produced in liver
-Transported through the biliary tree to the duodenum
I-ntrahepatics --> common hepatic duct --> common bile duct --> ampulla/Sphincter of Oddi

Gallbladder
-Concentrates and stores bile
-Stimulated during a meal to contract
-Sphincter of Oddi relaxes
-Bile released into the intestine

Front 246

Bilirubin

Back 246

Toxic breakdown product of RBCs (Hemoglobin)

Excreted in bile and urine
-Yellow color of bruises
-Jaundice
-Yellow color of urine (urobilin)
-Brown color of feces (stercobilin)

Two types
- Unconjugated (indirect): has not been processed by liver ;Not water-soluble
- Conjugated (direct): once in the hepatic system, the bilirubin becomes conjugated for water solubility and excretion

Conjugation --> water soluble --> excretion

Front 247

Unconjugated Bilirubin

Back 247

Overproduction
- Hemolysis

Impaired hepatic uptake
- CHF, cirrhosis

Impaired conjugation
- Crigler-Najjar syndrome
- Gilbert’s syndrome

Front 248

Conjugated Bilirubin

Back 248

Inherited disorders
- Dubin Johnson Syndrome
- Rotor Syndrome

Biliary obstruction
- Stones
- Malignancy

Hepatitis
- Viral
- Alcohol/NASH
- Autoimmune/PBC
- Drugs/toxins
- Sepsis
- TPN

Front 249

Enterohepatic Circulation

Back 249

90% of bilirubin is recycled daily

Produced by the liver

Secreted into biliary ducts

Drain into small intestine

Reabsorbed in terminal ileum

10% excreted as waste (urobilin, stercobilin)

Front 250

Classification of both conjugated and unjoguated hyperbilirubinemia

Back 250

Front 251

Cell Types of the Liver

Back 251

Hepatocytes

Kupffer cells

Stellate cells

Immune cells

Front 252

Hepatocyte

Back 252

Hepatocyte is the major cell type of the liver
-Gluconeogenesis
-Fatty acid oxidation
-Synthesis of albumin and plasma proteins
-Metabolism of drugs and toxins
-Synthesis of cholesterol and bile acids

Front 253

-major cell type of the liver
-Gluconeogenesis
-Fatty acid oxidation
-Synthesis of albumin and plasma proteins
-Metabolism of drugs and toxins
-Synthesis of cholesterol and bile acids

Back 253

Hepatocyte

Front 254

Kupffer cells

Back 254

-Live in the lining of the sinusoids
-Phagocytic activity
-Clear endotoxin, bacteria and old blood cells
-Store iron from erythrocytes

Front 255

-Live in the lining of the sinusoids
-Phagocytic activity
-Clear endotoxin, bacteria and old blood cells
-Store iron from erythrocytes

Back 255

Kupffer cells

Front 256

Stellate cells

Back 256

Live in the Space of Disse (space between the hepatocytes and sinusoid)

Store vitamin A

Become activated after liver damage

Deposit collagen --> scarring/fibrosis

Front 257

Live in the Space of Disse (space between the hepatocytes and sinusoid)

Store vitamin A

Become activated after liver damage

Deposit collagen --> scarring/fibrosis

Back 257

Stellate cells

Front 258

Hepatic lobule

Back 258

- Functional unit of the liver
- 1000s of lobules make up the liver

Lobule is a hexagon
- Hepatic vein at center of lobule
- Bounded by 6 peripheral portal triads
--> Hepatic artery branch
--> Portal vein branch
--> Interlobular bile duct

Front 259

portal triads

Back 259

--> Hepatic artery branch
--> Portal vein branch
--> Interlobular bile duct

Front 260

Lobule Zones

Back 260

3 zones

Z3
- Oxygen rich
- Close to portal triad

Z1
- Oxygen poor
- Closest to central vein

Type of injury affects zones differently
--> Z1 handles lack of oxygen better than Z3

Front 261

zone 1 vs zone 3

Back 261

3 zones

Z3
- Oxygen rich
- Close to portal triad

Z1
- Oxygen poor
- Closest to central vein

Type of injury affects zones differently
--> Z1 handles lack of oxygen better than Z3

Front 262

Summary of liver

Back 262

-8 segments to the liver
-Unique blood supply from portal system
-Liver functions in protein synthesis, detoxification and bile production
-Biliary tree drains the liver to duodenum
-Gallbladder stores and concentrates bile
-Hepatocyte is primary cell of liver
-Kupffer cells filter toxins and old blood cells
-Stellate cells responsible for scarring of the liver

Front 263

responsible for scarring of the liver

Back 263

-8 segments to the liver
-Unique blood supply from portal system
-Liver functions in protein synthesis, detoxification and bile production
-Biliary tree drains the liver to duodenum
-Gallbladder stores and concentrates bile
-Hepatocyte is primary cell of liver
-Kupffer cells filter toxins and old blood cells
-Stellate cells responsible for scarring of the liver

Front 264

filter toxins and old blood cells

Back 264

-8 segments to the liver
-Unique blood supply from portal system
-Liver functions in protein synthesis, detoxification and bile production
-Biliary tree drains the liver to duodenum
-Gallbladder stores and concentrates bile
-Hepatocyte is primary cell of liver
-Kupffer cells filter toxins and old blood cells
-Stellate cells responsible for scarring of the liver

Front 265

Hemochromatosis

Back 265

Autosomal recessive genetic defect

US Caucasian population
-10% are carriers
-0.5% have disease

HFE gene mutation
-Chromosome 6
-Increases intestinal iron absorption
-Iron deposition causes tissue damage
-Heart, liver, pancreas, skin, pituitary gland

Front 266

clinical manifestations of Hemochromatosis

Back 266

Clinical manifestations
-Liver function abnormalities — 75%
-Weakness and lethargy — 74%
-“Bronze Diabetes”
--> Skin hyperpigmentation — 70 %
--> Diabetes mellitus — 48 %
- Arthralgia — 44 %
- Impotence in males — 45 %
-EKG abnormalities — 31 %

Diagnosis
-Bloodwork
-Liver biopsy for iron content

Front 267

diagnosis of Hemochromatosis

Back 267

Clinical manifestations
-Liver function abnormalities — 75%
-Weakness and lethargy — 74%
-“Bronze Diabetes”
--> Skin hyperpigmentation — 70 %
--> Diabetes mellitus — 48 %
- Arthralgia — 44 %
- Impotence in males — 45 %
-EKG abnormalities — 31 %

Diagnosis
-Bloodwork
-Liver biopsy for iron content

Front 268

Prussian Blue Iron stain

Back 268

detects for iron

Front 269

Treatment for Hemochromatosis

Back 269

Treatment
- Phlebotomy
--> Iron contained in red blood cells
--> Weekly phlebotomy helps normalize hepatic iron level
- Iron chelation
--> Iron binders to prevent absorption
--> Rarely needed due to ease of phlebotomy
- Dietary restriction
--> Limit alcohol consumption
--> Reduce ascorbic acid intake
--> Avoid raw seafood

Prognosis
- Excellent if phlebotomy instituted early
- If cirrhotic --> increased risk of liver failure and hepatocellular carcinoma

Front 270

Prognosis of Hemochromatosis

Back 270

Treatment
- Phlebotomy
--> Iron contained in red blood cells
--> Weekly phlebotomy helps normalize hepatic iron level
- Iron chelation
--> Iron binders to prevent absorption
--> Rarely needed due to ease of phlebotomy
- Dietary restriction
--> Limit alcohol consumption
--> Reduce ascorbic acid intake
--> Avoid raw seafood

Prognosis
- Excellent if phlebotomy instituted early
- If cirrhotic --> increased risk of liver failure and hepatocellular carcinoma

Front 271

Wilson’s Disease

Back 271

Autosomal recessive
- Mutation of ATP7B Gene
- Chromosome 13

Defect in transport of copper
- Ineffective excretion into bile
- Accumulates in the liver
- Excess copper acts as pro-oxidant
- Inflammation and injury to hepatocytes
- Fibrosis --> cirrhosis

Front 272

what is the mutation in wilson's disease?

Back 272

Autosomal recessive
- Mutation of ATP7B Gene
- Chromosome 13

Defect in transport of copper
- Ineffective excretion into bile
- Accumulates in the liver
- Excess copper acts as pro-oxidant
- Inflammation and injury to hepatocytes
- Fibrosis --> cirrhosis

Front 273

diagnosis of wilson's disease

Back 273

Diagnosis
- Disease of young people
--> Almost always before age 30
--> Average age 16
- Keyser Fleisher rings
Dense brown copper deposits around iris
- Neuropsychiatric illness
--> Late symptom
--> Liver damage almost always present

Diagnosis
- Blood ceruloplasmin
- Urinary copper excretion
- Liver biopsy

Front 274

Keyser Fleisher rings

Back 274

Dense brown copper deposits around iris

--> associated with wilson's disease

Front 275

treatment of wilson's disease

Back 275

Treatment
-Chelating agents
-Penicillamine
-Trientine
-Oral zinc
-Ammonium tetrathiomolybdate

Prognosis
- Excellent if early intervention
- Neuropsychiatric symptoms and hepatic damage are reversible
--> Indication: urgent liver transplant

Front 276

prognosis of wilson's disease

Back 276

Treatment
-Chelating agents
-Penicillamine
-Trientine
-Oral zinc
-Ammonium tetrathiomolybdate

Prognosis
- Excellent if early intervention
- Neuropsychiatric symptoms and hepatic damage are reversible
--> Indication: urgent liver transplant

Front 277

Cirrhosis

Back 277

End result of chronic liver disease
- Progressive fibrosis of the liver
- US statistics
--> 25,000 deaths per year
--> 373,000 hospitalizations per year
- Destruction of functional lobules over time
- Non-reversible
--> Controversial: some data support reversal of cirrhosis in hepatitis B with antiviral therapy

Any chronic liver disease can cause
- Hepatitis, alcohol, genetic diseases, fatty liver
- Up to 20% = unknown cause (cryptogenic)

Front 278

is cirrhosis reversible ?

Back 278

NO !!!

End result of chronic liver disease
- Progressive fibrosis of the liver
- US statistics
--> 25,000 deaths per year
--> 373,000 hospitalizations per year
- Destruction of functional lobules over time
- Non-reversible
--> Controversial: some data support reversal of cirrhosis in hepatitis B with antiviral therapy

Any chronic liver disease can cause
- Hepatitis, alcohol, genetic diseases, fatty liver
- Up to 20% = unknown cause (cryptogenic)

Front 279

Cirrhosis: clinical manifestations

Back 279

- Ascites
- Spontaneous bacterial peritonitis
- Hepatorenal syndrome
- Variceal hemorrhage
- Cardiomyopathy
- Encephalopathy
- Portal vein thrombosis
- Hepatocellular carcinoma
- Coagulopathy

Front 280

Ascites

Back 280

fluid within the belly causing a distention

Front 281

Spontaneous bacterial peritonitis

Back 281

cirrhotic patient with ascites in the belly--> manifestations of fever, chills, ab. Pain --> exclude bacterial infection fluid in the abdominal cavity

High mortality risk: requires ABX to prevent overwhelming sepsis and deat

Front 282

Hepatorenal syndrome

Back 282

if liver is damaged and kidneys start showing damage

Can be life-threatening and severe: liver transplant will address both problems

Front 283

Variceal hemorrhage

Back 283

Varicies—dilated BVs that can occur in the esophagus

In cirrhosis of liver, portal system is backed up `--> higher pressureportal HTNvaricies in the esophagus

Front 284

Portal vein thrombosis

Back 284

portal vein reaching liver manifests with low blood flow state --> blood clot formation

If blood clot doesn’t dislodge or move, whole liver failure can occur

TX: anticoagulation to break or reduce further development of clot

Front 285

Hepatocellular carcinoma

Back 285

develops long term in setting of cirrhosis

Front 286

Coagulopathy

Back 286

abnormal coagulation and blood clotting

INR: when high (2-3), one has a higher risk of bleeding

Cirrhotics: naturally anticoagulated because of poor liver function and poor production of clotting proteins (not clinically significant, usually)

Front 287

Cirrhosis: Stages

Back 287

4 stages of fibrosis

0 = no fibrosis
1 = Portal fibrosis without septa
2 = Portal fibrosis with few septa
3 = Portal fibrosis with numerous septa without cirrhosis
4 = cirrhosis

* septa—scarring around portal triads

Front 288

Cirrhosis: Stages

Back 288

4 stages of fibrosis

0 = no fibrosis
1 = Portal fibrosis without septa
2 = Portal fibrosis with few septa
3 = Portal fibrosis with numerous septa without cirrhosis
4 = cirrhosis

* septa—scarring around portal triads

Front 289

Back 289

4 stages of fibrosis

0 = no fibrosis
1 = Portal fibrosis without septa
2 = Portal fibrosis with few septa
3 = Portal fibrosis with numerous septa without cirrhosis
4 = cirrhosis

* septa—scarring around portal triads

Front 290

Most common tumors found in the liver

Back 290

METASTASES from other sites, i.e. colon, breast melanoma, lymphoma

Front 291

Liver Cancer

Back 291

Metastatic lesions
- Most common liver tumors
- Colon, breast, melanoma, lymphoma

Hepatocellular carcinoma
- Primary liver cancer
- Chronic viral hepatitis
- Any cause of cirrhosis

Cholangiocarcinoma
- Cancer of the bile duct

Front 292

Chlangiocrcinoma

Back 292

Rare tumor of biliary tree

5-10% five year survival

Risk factors
-PSC
-Parasitic infections
-Viral hepatitis
-Cholelithiasis (gallstones)
-Diabetes
-Obesity
-HIV

Front 293

Hepatocellular Carcinoma

Back 293

Usually diagnosed at a late stage

Associated with may chronic hepatidities
-Viral hepatitis B, C
-Alcoholic cirrhosis
-Autoimmune hepatitis
-Hemochromatosis
-Cirrhosis of any cause

250,000 to 1 million deaths globally per year

3rd leading cause of cancer death globally

9th leading cause of cancer death in US

Front 294

Hepatocellular Carcinoma --> diagnosis + symptoms

Back 294

Diagnosis
-Ultrasound
-CT scan
-MRI
-Biopsy

Symptoms
-Usually asymptomatic in early stages
-Jaundice
-Weight loss
-RUQ pain

Front 295

prognosis + treatment of Hepatocellular Carcinoma

Back 295

Prognosis
- Medial survival 6-20 months without treatment

Treatment options
- Surgical resection
- Radiofrequency ablation
- Chemoembolization
- Liver transplant
--> Milan criteria
-- One tumor < 5cm
-- Three tumors < 3cm
- Chemotherapy

Front 296

risk factors for Chlangiocrcinoma

Back 296

Rare tumor of biliary tree

5-10% five year survival

Risk factors
-PSC
-Parasitic infections
-Viral hepatitis
-Cholelithiasis (gallstones)
-Diabetes
-Obesity
-HIV

Front 297

Klatskin Tumor

Back 297

pathognomonic tumor such that cholangiocarcinoma occurs at bifurcation of intrahepatic biliary tree as the right and left hepatic ducts join to form the common hepatic duct

Certain tubes annihalated; others remain normal—above point of obstruction

Front 298

Summary of liver carcinomas

Back 298

Genetic liver disorders are rare causes of chronic liver disease

End result of chronic liver disease is cirrhosis
-Reversible to some degree

Hepatocellular carcinoma can result from cirrhosis

Cholangiocarcinoma is a highly lethal cancer of the bile ducts

Front 299

3 bile duct disorders

Back 299

Primary sclerosing cholangitis
Primary biliary cirrhosis
Gallstone disease

Front 300

Primary Sclerosing Cholangitis

Back 300

Chronic progressive disorder of unknown etiology

Inflammation, fibrosis, scarring of bile ducts
- Elevation of liver enzymes
- Jaundice
- Cholangitis
Infection within biliary tree
- Cirrhosis
- Increased risk for cholangiocarcinoma
Cancer of bile duct

90% have underlying ulcerative colitis
- Chronic inflammatory bowel disease

Front 301

treatment & prognosis of Primary Sclerosing Cholangitis

Back 301

Treatment = liver transplant
- Depends on underlying severity and liver function

Prognosis
- 10-12 years after diagnosis without transplant

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“onion skin lesion” around bile duct

Back 302

Primary Sclerosing Cholangitis

Front 303

Primary Biliary Cirrhosis

Back 303

Chronic progressive disorder of unknown etiology

T-cell attack of small bile ducts

Destruction --> stasis of bile
Jaundice and itching

95% are women

Diagnosis
- Antimitochondrial antibody (AMA)
- Serologic hallmark
- Present in 95%

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treatment of Primary Biliary Cirrhosis

Back 304

Treatment
- Ursodeoxycholic acid
- Transplant if cirrhosis

Treatment goals
- Reduction in liver enzymes
- Improvement in symptoms
- Reduction in fibrosis
- Beneficial in early disease

Front 305

“florid bile duct lesion”

Back 305

Primary Biliary Cirrhosis

Front 306

gallstone disease

Back 306

Cholethiasis: gallstones

Cholecystitis: inflammation of the galbladder

Choledocholithiasis: stone in the bile duct

Front 307

Epidemiology of Cholethiasis

Back 307

Very common
- US prevalence (age 20-74)
- Men: 6.3 million
- Women: 14.3 million

Leading cause of hospital admission for biliary disease
- 2000
-260,000 admissions
- 780,000 office visits

Risk of gallbladder cancer?
- Up to 90% with GB cancer have stones

Front 308

Leading cause of hospital admission for biliary disease

Back 308

Cholethiasis

Front 309

prevalence of gallstones

Back 309

2x prevalence in women
--> Up to 24% of women have gallstones

highest in hispanic females

Front 310

cholesterol stones

Back 310

Most common (up to 70% of cases in US)
- Abnormal ratio of bile constituents  gallstones
--> Cholesterol
--> Phospholipids
--> Bile salts

Three stages
1) Cholesterol solubilization
2) Nucleation
3) Stone growth

Front 311

most common type of gallstones

Back 311

cholesterol stones

Front 312

3 stages of cholesterol stones

Back 312

Most common (up to 70% of cases in US)
- Abnormal ratio of bile constituents  gallstones
--> Cholesterol
--> Phospholipids
--> Bile salts

Three stages
1) Cholesterol solubilization
2) Nucleation
3) Stone growth

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pigmented gallstones

Back 313

NOT cholesterol based

black --> due to RBC breakdown

brown --> due to chronic infection

Front 314

black pigmented stones

Back 314

NOT cholesterol based

black --> due to RBC breakdown

brown --> due to chronic infection

Front 315

brown pigmented stones

Back 315

NOT cholesterol based

black --> due to RBC breakdown

brown --> due to chronic infection

Front 316

Cholecystitis

Back 316

Inflammation of galbladder (not necessarily infection)

Symptoms
RUQ/epigastric abdominal pain
- Lasts > 4-6 hours
- Radiation to right shoulder
- Nausea, vomiting, anorexia

Physical exam
- Fever, tachycardia, avoidance of movement
- Murphy’s sign
--> Cessation of respiration upon inspiration with RUQ palpation
--> May be diminished in the elderly

Front 317

Complications of Complications

Back 317

Gangrene
- Most common complication
- Elderly, diabetics, delay in treatment
- Up to 20% of cases

Perforation
- Usually after onset of gangrene
- 2% of cases
- High mortality

Front 318

Diagnosis of Cholecystitis

Back 318

H&P
- Murphy’s sign (+) most accurate physical finding

Labs
- Leukocytosis
- Elevated LFTs uncommon if uncomplicated
--> Choledocholithiasis (CBD stone)
--> Cholangitis
--> Mirizzi’s syndrome (stone in cystic duct compressing CBD)

Front 319

Mirizzi’s syndrome

Back 319

stone in cystic duct compressing CBD
--> indicative of cholecystitis

Front 320

Cholecystitis: Management

Back 320

Supportive treatment
- Hospitalization, IV hydration, pain control
- Antibiotics or not?
-- Primarily an inflammatory process
--. 22-46% positive cultures
--> E coli > Enterococus > Klebsiella > Enterobacter

Surgical intervention
- Timing of surgery
--Severity
--Surgical risk
--Laparoscopic preferred

Front 321

Choledocholithiasis

Back 321

Gallstones in bile duct

Symptoms are Variable
- Asymptomatic
- Elevated LFTs
- Cholangitis
--> Obstruction of bile duct
--> Infection of biliary tree
--> Life-threatening

Front 322

Diagnosis of Choledocholithiasis

Back 322

Labs
- Elevated LFTs
- Elevated WBC
- CT/MRI

Symptoms
- Charcot’s Triad
--> RUQ pain
--> Fever
--> Jaundice
- Reynold’s Pentad
--> Charcot’s plus:
--> Hypotension
--> Altered mental status

Front 323

Reynold’s Pentad

Back 323

--> Charcot’s plus:
--> Hypotension
--> Altered mental status

Front 324

Charcot’s Triad

Back 324

--> RUQ pain
--> Fever
--> Jaundice

Front 325

Choledocholithiasis treatment

Back 325

Treatment

Mild disease
- ERCP
-- Endoscopic retrograde cholangiopancreatography
- Stone removal

Cholangitis
- Antibiotics
- Emergent ERCP
- Percutaneous drainage

Front 326

summary of gallstones

Back 326

PSC/PBC are chronic inflammatory disorders causing scarring of the bile duct

Gallstones are very common and vary by ethnicity

Cholecystitis is inflammation (possibly infection) of the gallbladder and usually requires surgical treatment

Choledocholithiasis can lead to cholangitis and life-threatening infection of the liver if not removed

Front 327

summary of pancreas disorders

Back 327

Pancreas responsible for production of digestive enzymes and hormones

Pancreatitis can be acute and/or chronic

Gallstones and alcohol most common causes of acute pancreatitis

Alcohol is common cause of chronic pancreatitis

Pancreatic cancer is highly lethal as it is rarely caught early

Front 328

most common causes of acute pancreatitis

Back 328

Gallstones and alcohol

Front 329

Pancreas

Back 329

4-6 inch long

Posterior to the stomach

Connects to CBD at ampulla

Hormone production
- Insulin
- Glucagon
- Somatostatin

Digestive enzyme production
- Amylase
- Lipase

Sodium bicarbonate
-->Neutralizes stomach acid

Front 330

4-6 inch long

Posterior to the stomach

Connects to CBD at ampulla

Hormone production
- Insulin
- Glucagon
- Somatostatin

Digestive enzyme production
- Amylase
- Lipase

Sodium bicarbonate
-->Neutralizes stomach acid

Back 330

pancreas

Front 331

Pancreas Dual Function

Back 331

Exocrine
- Direct release into gut
- 1.5 Liters of digestive enzymes/day
- Digestion of starch, fat and protein
- Secretin hormone controls release

Endocrine
- Release of hormones into the bloodstream
- Islet cells of Langerhans
--> α-cells: Glucagon
--> Β-cells: Insulin

Front 332

exocrine function of pancreas

Back 332

Exocrine
- Direct release into gut
- 1.5 Liters of digestive enzymes/day
- Digestion of starch, fat and protein
- Secretin hormone controls release

Endocrine
- Release of hormones into the bloodstream
- Islet cells of Langerhans
--> α-cells: Glucagon
--> Β-cells: Insulin

Front 333

endocrine function of pancreas

Back 333

Exocrine
- Direct release into gut
- 1.5 Liters of digestive enzymes/day
- Digestion of starch, fat and protein
- Secretin hormone controls release

Endocrine
- Release of hormones into the bloodstream
- Islet cells of Langerhans
--> α-cells: Glucagon
--> Β-cells: Insulin

Front 334

α-cells

Back 334

Islet cells of Langerhans
--> α-cells: Glucagon
--> Β-cells: Insulin

Front 335

Β-cells

Back 335

Islet cells of Langerhans
--> α-cells: Glucagon
--> Β-cells: Insulin

Front 336

Acute Pancreatitis

Back 336

Inflammation of the pancreas

Many causes

Wide range of severity
Up to 30% mortality rate if severe

Symptoms
- Severe abdominal pain
- Nausea, vomiting
- Fevers, chills

Most require hospitalization

Front 337

Causes of Acute Pancreatitis

Back 337

Gallstones**
Alcohol**
Hypertriglyceridemia
Hypercalcemia
Genetic mutations
Medications
Smoking
Congenital anomalies
Trauma
Post-ERCP
Idiopathic

Front 338

Management of Acute Pancreatitis

Back 338

Hospitalization

IV hydration is crucial********
> 250cc normal saline/hr

Pain control

Bowel rest

+/- antibiotics

Remove the cause of the pancreatitis

Front 339

Chronic Pancreatitis

Back 339

Progressive inflammation

Permanent structural damage

Loss of exocrine and/or endocrine function

Symptoms
-Chronic abdominal pain
-Diarrhea
-Weight loss

Front 340

Causes of Chronic Pancreatitis

Back 340

NOT GALLSTONES !!

Causes
-Alcohol
-Smoking
-Hereditary pancreatitis
-Ductal obstruction
-Idiopathic

Treatment
-Pancreas enzyme supplement
-Insulin injections
-Pain control
-Surgical bypass

Front 341

treatment for chronic pancreatitis

Back 341

Causes
-Alcohol
-Smoking
-Hereditary pancreatitis
-Ductal obstruction
-Idiopathic

Treatment
-Pancreas enzyme supplement
-Insulin injections
-Pain control
-Surgical bypass

Front 342

Surgical treatment for chronic pancreatitis

Back 342

Peustow (pancreatico-jejunostomy)

Attach a jejunal limb to pancreatic duct

Pancreas secretion bypasses the duodenum

Front 343

Peustow

Back 343

**Surgical treatment for chronic pancreatitis

dilated pancreatic duct flayed open, attached to small intestine so enzymes from pancreas can flow straight into lumen of jejunum avoiding the obstructed duct
May follow after repeated stenting and pain relief

Front 344

Pancreatic Cancer

Back 344

Types

1) Exocrine pancreas
- Ductal adenocarcinoma (most common-85%)
- Cystic tumors
- Sarcoma

2) Endocrine pancreas
- Neuroendocrine tumors (NETs, PETs)
-- Insulinoma
-- Glucagonoma
-- Gastrinoma
-- Somatostatinoma

3) Lymphoma (very rare)

Front 345

most common pancreatic cancer

Back 345

Ductal adenocarcinoma

Front 346

ancreatic Cancer Endoscopic treatment

Back 346

ERCP
(Endoscopic retrograde cholangiopancreatography)

for palliation but may be necessary (percutaneous drainage also viable)

Stent can be placed across tumor to allow for bile drainage for prevention of cholangitis

--> Stent placement
Different types of stents
-Metal/plastic
Allows for:
- Decompression of biliary tree
- Tissue sampling
- Determination extent of disease

Front 347

in pancreatic cancer... Stent placement to allow for

Back 347

Stent placement to allow for continuity of bile

Metal or plastic: metal preferred to reduce number of future endoscopies

If possible, tissue sampling: BX to conifrm pancreatic cancer

Front 348

treatment of PSC vs. PBC

Back 348

PBS can be treated

Front 349

pima indians have 90% chance of getting

Back 349

gallstones

Front 350

dane particle

Back 350

the whole hepatitis virion

Front 351

Igm refers to acute/chronic infection

Back 351

acute

Front 352

what is the major cell type involved in liver fibrosis

Back 352

stellate cell

Front 353

which is more common... conjugated or unconjugated bilirubin ?

Back 353

unconjugated hyperbilirubinemia is more common

Front 354

why would in a viral hepatitis... liver enzymes would go up 1000-fold?

Back 354

continually activating the liver

Front 355

laboratory tests for hepatic function

Back 355

- serum bilirubin
- AST (aspartate aminotransferase)
- ALT (alanine aminotransferase)
- serum alkaline phosphatate
- serum proteins (albumin, globulin)
- prothrombin time

Front 356

icterus

Back 356

during jaundice... if your eye is also yellow (sclera)

Front 357

ascites happens because...

Back 357

1) lack of albumen b/c cirrhotic liver can't produce enough
2) dripping of lymphs out of the liver

Front 358

hepato-renal syndrome

Back 358

body's response to ascites

---> releases aldosterone.. rening-angiotensin system to increase pressure

Front 359

why would a pt. feel somnolent 9sleepy)

Back 359

increased amount of ammonia in the blood --> hepatic encepholophy

ammonia is toxic to the brain

also causes hand tremor

Front 360

liver flap (aka. asterixis)

Back 360

tremor of your hand due to increased amount of ammonia in the blood --> hepatic encepholophy

ammonia is toxic to the brain

Front 361

bilirubin comes from old/new RBC

Back 361

old --> senescent

Front 362

glucuronides

Back 362

make bilirubin more water-soluble so it can be "conjugated' and better-excreted

--> added into bile where they will travel down common bile duct into intestine @ duodenum

Front 363

urobiligen

Back 363

broekn down into urobilin --> makes urine yellow

Front 364

is feces are gray/white

Back 364

could have a tumor in the head of the pancreas
--> compressing the common bile duct

less bile --> less pigmentation into stool

Front 365

is fatty liver reversible?

Back 365

YES
--> it is an early change

Front 366

mallory body

Back 366

seen in alcoholic hepatitis

Front 367

portal / laenec cirrhosis

Back 367

a disease of the liver in which the normal lobular architecture is lost, with fibrosis and later nodular regeneration

Front 368

varix

Back 368

dilated vein

Front 369

most pancreatic cancers occur where in the gland?

head / body / or tail

Back 369

head

(least in the tail)

Front 370

how much bilirubin do you need to get jaundiced?

Back 370

2-3mg

Front 371

nullyparis

Back 371

no children

Front 372

multiparis

Back 372

multiple children

Front 373

why would the stones be black in the gall bladder?

Back 373

hemolytic anemia (sickle cell... thallasemia etc.)

Front 374

where would you see jaundice in an infant?

Back 374

erythroblastosis fetalis

Front 375

Kernicterus

Back 375

Kernicterus is a rare neurological condition that occurs in some newborns with severe jaundice

unconjugated hyperbilirubinemia in newborn