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Patho > GI/Liver > Flashcards

GI/Liver Flashcards

1
Q

Type of cells lining the esophagus

A

Stratified squamous cells. This type of epithelium is well suited to areas of the body subjected to constant abrasion, such as the mouth, esophagus, and vagina. Your mom, for example, has a thick layer of stratified squamous epithelium.

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2
Q

The fluid leaving the stomach must have the same ________ as blood

A

Tonicity

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3
Q

Once fluid enters the small intestine, the pH need to be raised from _______ to about _____.

A

1.5 to 8

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4
Q

Area of the GI tract where B and T cells might hang around to find their antigen

A

Appendix

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5
Q

Nutrients absorbed in the stomach

A

Water and alcohol

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6
Q

Nutrients absorbed by the duodenum

A 
Water
Fats
Sugars
Proteins
Vitamins
Calcium
Sodium
Mag
Iron
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7
Q

Nutrients absorbed by the Jejunum

A

Sugars and proteins. Most absorption occurs in the jejunum.

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8
Q

Nutrients absorbed by the ileum

A

B12
Bile Salts
Chloride

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9
Q

Nutrients absorbed by the large intestine

A

Water and electrolytes

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10
Q

Barrett’s Esophagus involves replacing this type of tissue with this type of tissue

A

Stratified squamous with metaplastic columnar epithelium with goblet cells (which secrete mucus)

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11
Q

Barrett’s esophagus can lead to

A

Adenocarcinoma, which is cancer of the epithelium.

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12
Q

Types of esophageal cancer

A

1) Squamous cell
- Arises from normal esophageal tissue
- Caused by tobacco/ETOH, achalasia (from increased irritation and mitotic turnover), and very hot tea (>65C)

2) Adenocarcinoma
- Arises of metaplastic tissue associated with Barrett’s Esophagus

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13
Q

Symptoms of esophageal cancer

A

Obstruction leading to dysphagia

However, this occurs late in cancer progression.

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14
Q

Chronic gastritis can lead to

A

Peptic ulcers

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15
Q

Acute gastritis can lead to

A

Acute gastric ulceration

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16
Q

Layers of muscle in the stomach

A

Longitudinal, circular, and oblique

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17
Q

Purposes of the duodenum

A

Raises the pH of chyme and controls the rate of gastric emptying. It also absorbs a bunch of shit.

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18
Q

Chief cells produce ______

Parietal cells produce _____

A 
Chief = the enzymes of gastric juice
Parietal = stomach acid
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19
Q

How do we deal with the excess bicarb production as a result of acid production?

A

The bicarb generated gets dumped into the lumen of the duodenum, preventing the blood from becoming alkalotic and raising the pH of chyme in the duodenum.

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20
Q

Why are NSAIDs damaging to the stomach?

A

The inhibit prostaglandins, which normally stimulate the production of mucus. Decreased mucus production subjects the gastric mucosa to damage.

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21
Q

Basic difference between acute and chronic gastritis

A

Chronic gastritis is due to an H. pylori infection or chronic NSAID use. It is usually asymptomatic, but may cause upper abdominal discomfort, N/V, and peptic ulcers.

Acute gastritis is general injury to the body (not specifically the stomach), such as heavy NSAID use, smoking, ETOH, chemo, systemic infection, severe stress, etc. This can cause epigastric pain with N/V, and hematemesis and/or melena.

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22
Q

Treatment for acute gastritis

A

Remove the cause of stress to the body

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23
Q

__-__% of people with H pylori get ulcers, but H pylori is present in ___% of those with gastric and duodenal ulcers

A

10-20%

70%

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24
Q

These things can aggravate peptic ulcers

A 
NSAIDS
Smoking
ETOH
Corticosteroids
High-stress personality
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25
Q

Treatment for peptic ulcer

A

We can give antibiotics because most cases are caused by H pylori

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26
Q

Complications of peptic ulcers

A

Epigastric pain
N/V
Perforation and hemorrhage

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27
Q

Do peptic ulcers progress to cancer?

A

No.

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28
Q

Causes of acute gastritis

A 
Acute mucosal inflammation due to systemic things like:
Heavy NSAID use (like ASA)
Excessive ETOH
Heavy smoking
Chemo
Uremia
Systemic infection
Severe stress (trauma, burns, surgery)
Ischemia and shock
Ingestion of caustic agents
Mechanical trauma (nasogastric tube placement)
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29
Q

S/S of acute gastritic

A

The same as chronic gastritis.

Epigastric pain, N/V, hematemesis and/or melena

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30
Q

Treatment for acute gastric ulcer (stress ulcer)

A

Remove the cause of stress to the body

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31
Q

2 Types of stomach cancer

A

1) Intestinal Adenocarcinoma (decreased in frequency)
- Caused by nitrates, smoked food, pickled/salted food, low fruit and veggie consumption, chronic gastritis, and H pylori

2) Diffuse carcinoma
- Risk factors poorly understood
- Incidence hasn’t decreased, but was never very prominent anyway

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32
Q

It takes ___ hours to get from the mouth to the cecum, and ___ hours to get from the cecum to the anum

A

2-4

20-22

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33
Q

Causes of ischemic bowel disease

A

Arterial or venous thromboembolism
Non-occlusive ischemia (shock, dehydration, vasoactive drugs)
Mechanical obstruction (volvulus, stricture, herniation, etc

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34
Q

Complications of ischemic bowel disease

A

Mild infarction ok because it may only kill mucosal cells, which we replace frequently.

Major transmural infarction causes wall weakness that can lead to rupture, sepsis, and peritonitis. 90% mortality.

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35
Q

Common causes of hemorrhoids

A

Straining on defecation
Portal HTN
Pregnancy (pressure on IVC shunts blood to the portal system)

Caused by increase venous pressure in the hemorrhoidal plexus.

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36
Q

Secretory diarrhea

A

Ex- Cholera

Epithelial cells secrete Cl- into the lumen. Sodium and water follow, causing high volume, watery diarrhea. Occurs in places without clean drinking water.

37
Q

Osmotic Diarrhea

A

Ex- GoLYTELY (PEG)

PEG isn’t absorbed, so it holds water in the GI tract

38
Q

Exudative Diarrhea

A

An infectious agent (Shigella, salmonella, etc) kills mucosal cells, causing them to slough off and act as an osmotic diuretic.

39
Q

This form of IBD has deep fissures that go through the mucosal layer and can even cause fistulas from the lumen of the intestine to the abdominal space

A

Crohn’s Disease

40
Q

Why does hookworm work?

A

In order for the hookworm to survive in the gut, it turns off the immune system and alleviates some of the symptoms associated with Crohn’s and asthma.

41
Q

This form of IBD has pseudopolyps

A

Ulcerative colitis

42
Q

Why do you get left sided abd pain with diverticulitis?

A

Because stool is more solid here

43
Q

Treatment of diverticulosis/itis

A

Eat more fiber! And avoid eating small seeds.

44
Q

Complications of diverticulosis/itis

A

Bleeding, perforation, and fistula formation

45
Q

4 types of mechanical bowel obstruction

A

Hernia
Volvulus
Intussusception
Adhesions

46
Q

3 causes of pseudo-bowel obstructions

A

Paralytic ileus
Bowel infarction
Myopathy/neuropathy (Hirschsprung)

47
Q

What does it mean for a tumor to be sessile?

A

It doesn’t have a stalk.

48
Q

What is an adenoma?

A

Neoplastic polyp from epithelial cells

49
Q

What is an adenocarcinoma?

A

Cancer arising from adenomatous polyps (98% of colorectal cancers)

50
Q

A colon tumor is considered invasive once it penetrates the

A

Muscularis layer and enters the submucosal layer

51
Q

Common symptoms of colorectal cancer

A

Pain
Obstruction
Changes in bowel habit
Remains asymptomatic for years

52
Q

Liver and lymph

A

The liver makes about half of our lymph each day. It has a higher protein content than lymph elsewhere in the body

53
Q

The portal vein gives ___% of the liver’s blood supply and the hepatic artery supplies the remaining ___%

A

80%

20%

54
Q

The liver releases albumin as

A

Pro-albumin. The liver makes protein as it needs it.

55
Q

Enterohepatic circulation of bile salts

A

Hepatocytes make primary bile acids which get added to the bile acid pool. Amino acids are added to bile acids, forming bile salts. These bile salts then go to the gallbladder or directly to the duodenum. At the terminal ileum, the salts are either actively transported across the intestinal lumen or are degraded by bacteria into secondary bile salts that diffuse passively across the lumen. These enter the portal system back to the bile acid pool. 10% of the bile salts in the terminal ileum are lost in the feces.

56
Q

Basic cause of liver fibrosis and cirrhosis

A

Chronic inflammation causes macrophages (Kupffer cells) to activate, stimulating fibroblasts to lay down colagen. This fibrosis obstruction of channels causing jaundice and portal HTN.

Fibrosis is irreversible damage and has lasting consequences on patterns of blood flow and perfusion of hepatocytes.

Activated Kupffer cells release TGF-Beta, which activate stellate cells to lay a dense extracellular matrix.

57
Q

Labs that measure hepatocyte integrity

A

AST (SGOT)

ALT (SGPT)

58
Q

Labs that measure biliary tract integrity

A

Serum alkaline phosphatase (AP, ALP, ALKP)
- remember that this one is also a marker of bone breakdown
Serum gamma-glutamyltransferase (GGT)

59
Q

Measures of bilirubin

A

Direct (Conjugated)

Total (conjugated + unconjugated)

60
Q

Measures of hepatocyte function

A 
Serum albumin (compared with total protein)
PT (will increase without clotting factors)
Serum ammonia (we don't want ammonia- it should be converted to urea by the liver)
61
Q

Consequences of liver disease

A 
Jaundice and cholestasis
Hypoalbuminemia
Hyperammonia
Fasting hypoglycemia
Fetor hepaticus
Gypogonadism
Gynecomastia
Palmar erythema
Spider angiomas (estrogen opens the precapillary sphincters)
Weight loss
Muscle wasting
62
Q

Life threatening consequences of liver disease

A 
Multiple organ failure
Coagulopathy
Esophageal varices rupture
Hepatorenal syndrome
Hepatic encephalopathy (mostly due to ammonia crossing the BBB)
Hepatocellular carcinoma
63
Q

Causes of excess unconjugated bilirubin in the blood

A

Excess bilirubin production (increased RBC destruction)
Reduced hepatic uptake
Impaired conjugation

Unconjugated is tightly bound to albumin and insoluble in water (can’t be excreted by the kidney).
The form that is not bound to albumin can cause toxic injury, enter the brain, and cause severe neurological damage.

64
Q

Causes of excess conjugated bilirubin in the blood

A

Obstruction of bile flow
Decreased hepatocellular secretion

This type is weakly bound to bilirubin and will be excreted by the kidney.

65
Q

What are reticular fibers?

A

Connective tissues of our solid organs that keep them together

66
Q

Why are fat alcoholic men at risk for developing breast cancer?

A

The liver can’t clear estrogen. Estrogen builds up causing gynecomastia on top of their already-existant man boobs. Fat is able to convert testosterone to estrogen, causing further increase in estrogen levels.

67
Q

What is colestasis?

A

Bile unable to move due to an obstruction. Bile builds up into the canaliculi, causing damage to hepatocytes.

Ex- Biliary atresia in kids can lead to liver failure

68
Q

We can lose ____-____% of liver function before we get liver failure

A

80-90%

69
Q

What is hepatic failure?

A

Sudden and massive hepatic destruction. This is life-threatening

70
Q

Does cirrhosis cause hepatomegaly?

A

No, impaired blood flow out of the liver causes hepatomegaly.

71
Q

These types of hepatitis do not cause chronic hepatitis or cancer

A

A&E

72
Q

We have vaccines for these types of hepatitis

A

A&B

73
Q

Characteristics of hepatitis B, C, & D

A

Can cause a carrier state, chronic hepatitis, and cancer.

Transmitted via parenteral transmission

74
Q

Why does alcoholic fatty liver disease develop?

A

The alcoholic damage liver takes up fatty acids normally but is unable to turn them into lipoproteins to export them.

Remember that each time the liver “heals” it lays down collagen, cause it’s a total bitch like that.

75
Q

Hemochromatosis

A

Uncontrolled uptake of iron. Iron overload causes damage.

76
Q

Types of hemochromatosis

A

1) Primary
- Autosomal recessive disease
- More often in males (b/c ladies do their menstruation thing)
- Treatment is blood-letting
- Another type of primary is Bantu Siderosis (basically the same thing, but less common and exists in Africa)

2) Secondary
- Excessive tranfusions
- Ineffective erythropoiesis (Beta-thalassemia and siderblastic anemia)

77
Q

Each blood transfusion has ___g of iron

A

.25g

78
Q

Primary biliary cirrhosis

A

Autoimmune disease of unknown etiology.

Intrahepatic bile ducts are destroyed (will see elevates AP and cholesterol).
Hallmark is antimitochondrial antibodies (AMA)
Hyperbilirubinemia present late in disease.
Often fatal

79
Q

Secondary biliary cirrhosis

A

Biliary tract is obstructed due to gall stones, tumors, biliary atresia, or strictures from surgery.

80
Q

Primary sclerosis cholangitis

A

Very similar to primary biliary cirrhosis.
Differences: affects intrahepatic AND extrahepatic bile ducts.
AMA not present.
Associated with ulcerative colitis.

81
Q

4 Circulatory disorders

A

1) Obstruction
- Right heart failure (more common)
- IVC thrombus
2) Impaired intrahepatic blood flow
- Due to cirrhosis
- Will get splenomegaly, but not hepatomegaly
3) Impaired flow into liver
- Portal vein obstructed by thrombosis or tumor
4) Impaired hepatic artery flow
- Complication of transplant

82
Q

Hepatocellular carcinoma arises from

A

hepatocytes

83
Q

Causes of HCC

A 
HBV
Chronic liver disease (HCV and alcohol)
Aflotoxin (toxin produced by mold)
Tyrosinemia
Cirrhosis
84
Q

Risk factors for cholesterol stones (80%)

A 
Fair
Fat
Forty
Female
Fertile
Gallbladder stasis
Hyperlipidemia
85
Q

Risk factors for pigment stones (20%)

A

Chronic hemolytic syndromes
Biliary infection
GI disorders (Crohn’s)
Asian > western

86
Q

What is choledocholithiasis?

A

Bile stones in the biliary tree

87
Q

Complications of choledocholithiasis

A

Biliary obstruction
Pancreatitis
Cholangitis (infection of the common bile duct) -> hepatic abcess
Chronic liver disease with biliary cirrhosis
Acute calculous cholecystitis

88
Q

Causes of pancreatitis

A 
Idiopathic
Gallstones
ETOH
Trauma
Steroids

Patho (14 decks)

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