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GUMC SMP > APP GI and LIver > Flashcards

APP GI and LIver Flashcards

1
Q

List the risk factors associated with GERD

A
  1. Obesity
  2. Pregnancy
  3. Nervous system injury
  4. Alcohol/Smoking
  5. Delayed gastric emptying
  6. Hiatal hernia
  7. Physiological GERD: eating a big meal, reclining, etc.
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2
Q

What is hiatal hernia?

A

when your stomach is up in your throax - the LES is surrounded by the diaphragm, which partly helps it maintain its tone. If the LES is pushed up into the thorax, you aren’t going to get as much constriction of the sphincter

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3
Q

List the 4 complications associated with GERD

A
  1. Ulceration
  2. Esophagitis
  3. Barrett Esophagus
  4. Stricture
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4
Q

Which patients need an endoscopy to check for GERD?

A

Patients with multiple risk factors for Barret’s/Cancer: white male, >50 years old, chronic GERD, obesity, etc.

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5
Q

Describe how the loss of neurons can result in Achalasia

A
  1. There are two types of neurons in the plexus that controls the smooth muscle: inhibitory neurons (inhibit the muscle - muscle relaxes) and stimulatory neurons (cause the muscle to constrict)
  2. Preferential loss of inhibitory neurons in the myenteric plexus
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6
Q

What do we see with the Manometry study that proves it is Achalasia?

A

the resting tone is elevated - the tone doesn’t decrease with swallow

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7
Q

What is a key indicator of Pyloric Stenosis?

A

non-bilious because of the obstruction

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8
Q

Explain how blood travels through the liver

A
  1. The blood that is coming in from your portal vein and hepatic vein are going to come in to these outside artery and vein branches on each of the lobules and they will then send branches through the lobules to that central blood vessel
  2. As these blood vessels send blood through these canals, they are going to be lined by hepatocytes (where a lot of the liver filtration system is happening)
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9
Q

List the functions of the liver

A
  1. Regulation of carbohydrate, lipid, and protein metabolism
  2. Regulation of cholesterol production
  3. Beta-oxidation of fatty acids - breakdown of fats
  4. Endocrine - make angiotensin, albumin, insulin-like growth factor, metabolizing hormones in the liver, etc.
  5. Detoxification
  6. Vitamin and iron storage
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10
Q

What type of hormone do we mainly metabolize in the liver?

A

Steroid-based

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11
Q

List the 3 key things you expect to see in the blood of patients with liver failure

A
  1. Anemia
  2. Thrombocytopenia
  3. Coagulation defects
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12
Q

Why do you expect to see anemia in patients with liver failure?

A

Because we lose our iron stores - prevents us from making new blood cells

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13
Q

What is thrombocytopenia?

A

low platelet count; thrombopoietin is a hormone made in the liver that tells bone marrow to produce platelets

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14
Q

Why do we see gonadal disturbances with liver failure?

A

the liver is responsible for metabolism of steroid hormones

With liver failure there are high levels of testosterone and estrogen

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15
Q

What happens when there is a decrease in aldosterone metabolism?

A

Increased salt and water retention, hypokalemia

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16
Q

List the skin disorders that are associated with liver failure

A
  1. Jaundice
  2. Vascular spiders
  3. Palmar erythema
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17
Q

What are vascular spiders and what causes them?

A
  1. Vascular Spiders: on the skin, there is an arteriole that dilates and all of the arterioles and venules coming around it will also dilate –> it looks like a circle with these “little legs coming off of it”
  2. Caused by high levels of estrogen
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18
Q

When do we see Hepatorenal Syndrome?

A

acute renal failure that is commonly seen during the terminal stages of liver failure

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19
Q

What causes Hepatorenal Syndrome?

A
  1. The cause of this is not changes to the kidney itself - the kidney is actually totally functioning
  2. In the end stages of liver failure, the liver begins to change the patterns of blood flow in the body –> causes a significant decrease in blood flow to the kidneys
  3. The kidneys are suddenly getting hyperperfused, resulting in acute renal failure –> this is the prerenal renal failure
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20
Q

How do you characterize hepatorenal syndrome?

A
  1. Progressive azotemia
  2. Increased serum creatinine levels
  3. Oliguria
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21
Q

Describe Hepatic Encephalopathy

A
  1. You make ammonia all over your body: the gut makes ammonia, the muscles make ammonia, etc. as part of the metabolism
    1a. That ammonia all goes to the liver, and through the urea cycle that ammonia is converted to urea
    1b. Urea is a non-toxic substance that gets excreted in the urine
  2. In liver failure, the hepatocytes aren’t functioning so the ammonia is not converted into urea –> ammonia levels rise
    2a. That ammonia is converted in the CNS and muscles to glutamine
    2b. Glutamine is a potent neurotransmitter –> there is inappropriate firing of neurons when glutamine is present
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22
Q

Hepatopulmonary Syndrome

A

Syndrome of shortness of breath and hypoxemia caused by vasodilation of the lungs of patients with liver disease

Mechanism unknown but increased NO production by the lungs is a key mediator

23
Q

What are the 4 causes of jaundice?

A

Abnormally high accumulation of bilirubin in the blood

  1. Excessive destruction of RBC
  2. Impaired uptake of bilirubin
  3. Decreased conjugation of bilirubin
  4. Obstruction of bile flow
24
Q

Describe the breakdown of red blood cells into bilirubin

A
  1. Our blood cells come into the Reticuloendothelial System and are broken down into globin and heme
    1a. Globin is just a protein so it is broken down into amino acids and recycled back to the body
    1b. Heme is broken down by heme oxidase into biliverdin
  2. Biliverdin is reduced by biliverdin reductase into bilirubin
    2a. Bilirubin will be released into the bloodstream - because it is insoluble, it is carried by albumin to the liver
  3. Once bilirubin gets to the liver, it is conjugated with glucuronic acid to form bile, which is sent to the small intestine
25
Q

What happens once bile is in the small intestine?

A
  1. Some of it gets unconjugated by bacterial beta-glucuronidases
  2. Some of it gets turned into urobilinogen –> the kidneys are able to secrete this form into the urine
  3. Some of it is sent out in the feces
  4. Some of it gets sent to the blood stream
26
Q

Describe the causes of pre-hepatic hemolysis

A

the result of excess hemolysis

  1. Hemolytic blood transfusion - when you are transfused with the wrong blood type
  2. Sickle cell anemia - lyse the sickle cells
  3. Hemolytic disease of a newborn - extremely common in newborns: part of it is that the lifespan of red blood cells is shorter for them (turned over quicker, higher amount of hemolysis)
  4. Autoimmune hemolytic anemia: you are going to lyse the sickle cells
  5. Dyserythropoiesis: when you make bad red blood cells - your body recognized them as sucky and attacks them
27
Q

Intrahepatic Jaundice

A

Disorders that directly affect the ability of the liver to remove bilirubin from the blood or conjugate it so it can be eliminated in the bile

28
Q

What does intrahepatic jaundice usually present with?

A

Hypoalbuminemia

29
Q

What are the common causes of intrahepatic jaundice?

A
  1. Hepatitis
  2. Cirrhosis = fibrosis
  3. Cancer of the liver
30
Q

What is post-hepatic jaundice?

A

bile flow is obstructed between the liver and the intestine

31
Q

What causes post-hepatic jaundice?

A
  1. Strictures of the bile duct
  2. Gallstones
  3. Tumors of the bile duct
32
Q

List the symptoms of Cholestasis?

A
  1. Pruritus = itching
  2. Skin xanthomas = accumulation of cholesterol under the skin
  3. Nutritional deficiency of fat soluble vitamins: A, D, K
33
Q

What is the problem with unbound unconjugated bilirubin?

A

it may diffuse into tissues and produce toxic injuries

34
Q

Where is Kernicterus usually found?

A

The basal ganglia, hippocampus, thalamus, hypothalamus, corpus traitum, medulla and pons

35
Q

What 3 things do you see with portal hypertension?

A
  1. Ascites (intrahepatic portal hypertension
  2. Splenomegaly
  3. Portosystemic Shunts
36
Q

Ascites

A

edema of the abdomen: there is fluid moving out of the portal system and moving into the abdomen itself

37
Q

What are the causes of cirrhosis?

A
  1. Viral hepatitis
  2. Alcohol
  3. Non-alcoholic steatohepatitis = non-alcoholic fatty liver
  4. Biliary disease
  5. Iron overload
38
Q

What are the 3 things that happen with Cirrhosis?

A
  1. Death of hepatocytes because of viral infection or alcohol abuse
  2. Mass amounts of fibrosis due to the stellate cells - that fibrosis causes reorganization of the vasculature
  3. With vascular reorganization you get resistance within the lobules, which decreases the functionality of the liver
39
Q

What are the 2 factors that result in Cirrhosis?

A

Fatty Liver and Fibrotic Liver

40
Q

Explain alcoholic liver disease

A
  1. Every time you take in alcohol, it is converted to acetaldehyde –> this is going to change your metabolic structure to impede your mitochondrial electron transport system
    1a. change the function of your mitochondria –> results in increased lipid synthesis –> fatty liver
  2. Acetaldehyde is also going to impair the release of lipoproteins that are normally made in the liver –> results in fatty liver
  3. Acetaldehyde is also going to decrease the oxidation of fatty acids, keeping the fatty acids –> results in fatty liver
  4. Acetaldehyde is also going to increase collagen synthesis by stellate cells and other cells in the region –> results in fibrosis and change of structure of the liver
  5. Acetaldehyde also leads to fibrinogenesis which results in fibrotic liver
41
Q

List the components of bile

A
  1. Bile salts
  2. Cholesterol
  3. Bilirubin
  4. Lecithin
  5. Fatty acids
  6. Water
  7. Electrolytes
42
Q

3 factors contribute to the formation of gallstones

A
  1. Abnormalities in the composition of bile
  2. Stasis of bile
  3. Inflammation of the gallbladder
43
Q

List factors of a cholesterol stone (cholelithiasis)

A
  1. Race/Demography - western
  2. Age
  3. Female
  4. Oral contraceptives
  5. Pregnancy
  6. Obesity
  7. Rapid weight reduction
  8. Gall bladder stasis
  9. Disorders of bile/acid metabolism
  10. Hyperlipidemia syndromes
44
Q

List factors of a pigment stone (cholelithiasis)

A
  1. Race/Demography - Asians
  2. Hemolysis syndromes
  3. Biliary Infections
  4. Inflammatory bowel disorders
  5. Ileal resection or bypass
  6. Cystic fibrosis
  7. Chronic pancreatitis
45
Q

What is cholecystitis?

A

Inflammation of the gallbladder as a result of complete or partial obstruction

46
Q

What are signs of cholecystitis?

A
  1. Hyperbilirubinemia - more bile and bilirubin present in blood
  2. There is an increase in the number of cells making bile - causes cell death –> high alkaline phosphatase
47
Q

Why doesn’t the pancreas digest itself when releasing digestive enzymes from the acinar cells?

A

In the granules we have trypsin inhibitors. The enzymes are released as pro-enzymes and are only activated by trypsin

48
Q

List the enzymes found in the acinar cell granules of the pancreas

A
  1. Trypsin
  2. Chymotrypsin
  3. Carboxypolypeptides
  4. Ribonuclease
  5. Pancreatic amylase
  6. Lipases
49
Q

What causes acute and chronic pancreatitis?

A

There is a disconnect somewhere in the pancreas that allows these enzymes to be released and to activate them within the pancreas itself –> results in digestion of the pancreatic tissue

50
Q

What happens when gallstones obstruct flow in the duct of the pancreas?

A
  1. If you obstruct flow, you release the zymogen granules (proenzymes) and they have nowhere to go so they just sit there
  2. Trypsin will eventually activate them, causing breakdown of the tissue
51
Q

How does Alcohol result in pancreatitis?

A
  1. Alcohol increases secretion (normally the exocrine pancreas secretes ~7L)
  2. Results in protein plugs - too many proteins are trying to get through the ducts, blocking the region
  3. The protein plugs obstruct the duct and and any duct that is downstream of there
  4. The duct obstruction will release activated lipase
52
Q

What is the cause of chronic pancreatitis?

A

alcohol

53
Q

What are consequences of chronic pancreatitis as the disease progresses?

A

Diabetes mellitus and malabsorption

GUMC SMP (2 decks)

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