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PATHO/PHARM II > Mod 3 Lecture 2: Conditions Effecting the Gastrointestinal System and Pharmacotherapy > Flashcards

Mod 3 Lecture 2: Conditions Effecting the Gastrointestinal System and Pharmacotherapy Flashcards

Exam 2

1
Q

Location of the Liver

A

Upper right quadrant (URQ) of the abdomen, under the diaphragm

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2
Q

What is the structure of the liver?

A

Large fibrous capsule divided by falciform ligament into right and left lobes

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3
Q

Where are the liver ducts located and what do they do?

A

Has right and left hepatic ducts and a common hepatic duct; drains bile

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4
Q

What are the functional units of the liver?

A

Hepatocytes

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5
Q

Hepatocytes

A

liver cells; arranged in lobules, can regenerate, up to a point

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6
Q

What is involved in the liver’s blood supply?

A

Hepatic artery

Hepatic Portal vein

Hepatic vein

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7
Q

Hepatic artery

A

brings oxygenated blood from general circulation to liver

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8
Q

How much blood does the hepatic artery bring to the liver?

A

400-500ml/min

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9
Q

Hepatic artery supplies how much blood to the liver?

A

Supplies 25% of blood, dependent on cardiac output

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10
Q

Hepatic portal vein does what?

A

Receives deoxygenated blood from stomach, pancreas, spleen, small & large intestines to the liver

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11
Q

How much blood does the hepatic portal vein deliver to the liver?

A

1,000-1500 mL/min

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12
Q

The hepatic portal vein carries what else to the liver?

A

The hepatic portal vein, which carries 75% of the blood to the liver, is rich in nutrients that have been absorbed from the intestinal tract

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13
Q

Hepatic vein

A

Empties into the inferior cava

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14
Q

Bile is made up of what?

A

Bile is an alkaline, bitter-tasting, yellowish green fluid that contains bile salts (conjugated bile acids), cholesterol, bilirubin (a pigment), electrolytes, and water.

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15
Q

What do electrolytes in the bile do?

A

Electrolytes ~ HCO3
Neutralizes acidic gastric contents
Promotes actions of intestinal & pancreatic enzymes

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16
Q

What is bile produced from?

A

Produced by hepatocytes

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17
Q

How much bile is secreted by the liver a day?

A

700-1200 ml/day

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18
Q

How does bile exit the liver?

A

Exits from liver via hepatic duct system 

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19
Q

Where is bile stored?

A

Gallbladder ~ storage

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20
Q

Bile drains from _____to ______

A

Common Bile Duct to Duodenum

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21
Q

What is bile salts/acids made from?

A

Formed from cholesterol

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22
Q

What does bile do to fats

A

Emulsification of fats and facilitates absorption via small intestine of fat-soluble vitamins ~ A, D, E, K for digestion

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23
Q

What are the fat soluble vitamins?

A

A, D, E, K for digestion

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24
Q

What lipid-lowering agents did we discuss last semester that decreases cholesterol absorption in the small intestine and block bile from being reabsorbed so more passes out of stool?

A

Cholesterol absorption inhibitors - Ezetimibe (zetia)

Bile-Acid Sequestrants (colesevelam)
Flaxseed

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25
Q

What is the most common cause of gallstones?

A

High concentration of cholesterol in the bile (most common)

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26
Q

Why does a high level of cholesterol in bile lead to gallstones?

A

Bile cannot dissolve the excessive level of cholesterol.

Excessive cholesterol forms a mass or calculi.

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27
Q

What else other than excess cholesterol lead to gallstone formation?

A

Excessive bilirubin contributes to gallstone formation.

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28
Q

Other than bile and bilirubin, what can lead to gallstones?

A

Gallbladder does not empty completely

Gallbladder empties infrequently or incompletely.

Stagnant bile becomes more concentrated –> formation of gallstones.

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29
Q

Why would a gallstone not empty properly?

A

Gallbladder does not empty completely

Gallbladder empties infrequently or incompletely.

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30
Q

What are the five F’s that can lead to increase in gallstone formations?

A

Fair

Female

Forty and up

Fat

Fertile

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31
Q

What are the big risk factors to gallstone formation?

A

Big risk factors: 5fs, rapid weight loss, pregnancy

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32
Q

What are symptoms of gallstones:

A

Sx:

Biliary colic, RUQ abdominal cramping & pain worsens after fatty meals, may radiate to back or right shoulder, abdominal distension, n/v, jaundice, clay-colored stools, fever, leukocytosis, inflammation and infection

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33
Q

How may abdominal cramping and pain occur with gallstones?

A

RUQ abdominal cramping & pain worsens after fatty meals, may radiate to back or right shoulder,

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34
Q

What is the primary roles of the liver?

A

Storage,
excretion,
metabolism,
1st pass,
glucose regulation,
detoxification

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35
Q

What does the liver store?

A

Stores blood (~ 450mL),

Stores Fe,

Stores fat-soluble vitamins (A, D, E,K), B12, glycogen.

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36
Q

What does the liver synthesize?

A

Synthesis of clotting factors (prothrombin) and albumin

Lipoprotein synthesis -LDL, HDL

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37
Q

What does the liver do to hemogobin?

A

Degrades hgb –> globin and amino acids to be re-used in the synthesis of more hgb

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38
Q

What is the role of the liver with blood?

A

Stores blood and

Filtration/detox of blood

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39
Q

What cells of the liver remove bacteria?

A

Phagocytic cells, Kupffer cells, remove bacteria

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40
Q

What does the liver metabolize?

A

Metabolism of CHO, protein, fat, drugs

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41
Q

The liver is a source of what?

A

Heat

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42
Q

What does the liver do when RBC breakdown occurs in the blood?

A

Conjugates bilirubin when RBC breakdown in blood

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43
Q

What is a by product of protein metabolism?

A

Ammonia (NH3)

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44
Q

What is ammonia converted into by the liver?

A

Urea

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45
Q

Common Labs of Hepatic Function assess what?

A

Liver enzymes (Liver function tests, LFTs)

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46
Q

Liver enzymes (Liver function tests, LFTs) include?

A

AST (aspartate aminotransferase) & ALT (alanine aminotransferase)

ALP (alkaline phosphatase)

Bilirubin

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47
Q

Labs to measure hepatic function and liver disease also include

A

Albumin

Prothrombin time

Blood Urea Nitrogen (BUN)

Ammonia (NH3)

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48
Q

AST (aspartate aminotransferase) & ALT (alanine aminotransferase)

What are they involved in? Where are they mainly present?

A

Involved in metabolic reactions, present mainly in liver cells

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49
Q

AST (aspartate aminotransferase) & ALT (alanine aminotransferase)

When are they released?

A

Released into circulation in liver disease, hepatocellular injury, necrosis

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50
Q

AST (aspartate aminotransferase) & ALT (alanine aminotransferase)

What are they markers for? How do they present in liver disease and injury?

A

Markers of injury, elevated in liver disease, liver injury released into circulation

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51
Q

ALP (alkaline phosphatase)
Where is it mainly?

A

Mainly in bile ducts

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52
Q

ALP (alkaline phosphatase)
How are ALP in biliary obstruction?

A

Increases with biliary obstruction

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53
Q

ALP (alkaline phosphatase)
When biliary tree obstruction occurs? What happens?

A

When biliary tree obstructed, bile duct cells release ALP (elevation)

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54
Q

What is a component of bile?

A

Bilirubin

Breakdown of RBCs????

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55
Q

Bilirubin is a measure of what?

A

Measure of liver’s ability to perform enzymatic/metabolic functions

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56
Q

How is bilirubin presented in liver disease?

A

Elevated in liver disease

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57
Q

Albumins

A

Serum protein synthesized by liver

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58
Q

What does Albumin measure?

A

Measure liver’s capacity for protein synthesis

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59
Q

How are albumin levels in liver disease? Why?

A

Decreased in liver disease because liver cannot produce plasma proteins.

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60
Q

Prothrombin Time?

A

Measures function of clotting cascade

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61
Q

?????? Liver clotting

A

Liver synthesizes most coagulation factors

Liver decreases production of vitamin K and prothrombin.

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62
Q

What happens to prothrombin time in liver disease? What causes this?

A

Deficient clotting & elevated prothrombin time

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63
Q

Having to do with Blood Urea Nitrogen (BUN), what is made in the liver?

A

Urea is made in the liver

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64
Q

In liver disease, what happens to BUN?

A

Decreased BUN (ammonia not being converted to urea)

This leads to high levels of ammonia

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65
Q

Ammonia is a by product of what process?

A

By-product of protein metabolism

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66
Q

Where is most ammonia absorbed? And what is it converted to?

A

Most is absorbed into portal circulation & converted to urea

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67
Q

What can liver NOT do with ammonia?

A

Liver cannot convert ammonia to urea for excretion.

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68
Q

How are ammonia levels in liver disease?

A

Elevated in liver disease

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69
Q

What is hepatitis?

A

Inflammation of the liver

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70
Q

How is hepatitis viewed?

A

Treatable/Manageable with drugs, self-limiting

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71
Q

What are the two causes/types of hepatitis?

A
  1. Infections, contagious
  2. Nonviral, noncontagious
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72
Q

Infections, contagious hepatitis are often what/.

A

Viral

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73
Q

What are the five types of viral hepatitis?

A

A, B, C, D, E,

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74
Q

What are the most common types of viral hepatitis?

A

A, B, C most common

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75
Q

How is recovery of viral hepatitis?

A

Can recover in time but advanced age & comorbidities - ↑’d risk of liver failure, liver ca, cirrhosis

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76
Q

What are non-viral, non contagious causes of hepatitis?

A

EtOH
Meds ~ APAP, antiseizure meds, ABX
Autoimmune DX

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77
Q

Types of meds that would lead to non viral noncontagious hepatitis?

A

APAP, antiseizure meds, ABX

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78
Q

How is recovery of nonviral, non-contagious hepatitis?

A

Usually recover

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79
Q

What maynonviral, non-contagious hepatitis develop into?

A

May develop liver failure, liver cancer, or cirrhosis

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80
Q

Nonviral and viral hepatitis can result in what?

A

Both types can result in liver cell destruction, necrosis, autolysis, hyperplasia & scarring

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81
Q

What are the two forms of hepatitis? (Different from types)

A
  1. Acute
  2. Chronic
  3. Fulminant
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82
Q

How does acute hepatitis occur?

A

Proceeds through phases – prodromal/pre-icteric, icteric, recovery

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83
Q

What are the phases of acute hepatitis?

A

prodromal/pre-icteric,
icteric,
recovery

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84
Q

What is considered chronic hepatitis?

A

Cont’d disease lasting > 6 months

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85
Q

What types of hepatitis can become chronic? Which ones primarily?

A

Only types B, C, D - Primarily B & C

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86
Q

Severity and disease progression of chronic hepatitis depends on what?

A

Severity & disease progression depends on extent of liver damage

87
Q

How can someone live with chronic hepatitis?

A

Can live with it for years, but health deteriorates as liver function declines –> fibrosis, obstruction, cirrhosis, failure, liver ca

88
Q

What are the effects of deteriorating liver function due to living with chronic hepatitis for years?

A

Can live with it for years, but health deteriorates as liver function declines  fibrosis, obstruction, cirrhosis, failure, liver ca

89
Q

Fulminant

A

Fulminant ~ liver failure

sudden?

90
Q

Patho of Hepatitis Viral Hepatitis:

How does hepatitis infection start?

A

One of the 5 Virus strains targets the hepatocytes

91
Q

Patho of Hepatitis Viral Hepatitis:

Why does hepatocyte damage occur in viral hepatitis?

A

Virus attacks the hepatocytes

92
Q

Patho of Hepatitis Viral Hepatitis:

What occurs after virus attack the hepatocytes?

A

Cell-mediated immune responses to the virus

93
Q

Patho of Hepatitis Viral Hepatitis:

What are the Cell-mediated immune responses to the virus?

A

Cytotoxic cytokines and natural killer cells lyse infected hepatocytes

Injury –> inflammation

Pathologic lesions of chronic hepatitis: necrosis, scarring, Kupfer cell hyperplasia, phagocyte infiltration

Swelling and necrosis in the liver cells.

94
Q

Patho of Hepatitis Viral Hepatitis

Pathologic lesions of chronic hepatitis include:

A

necrosis, scarring, Kupfer cell hyperplasia, phagocyte infiltration

95
Q

Patho of Hepatitis Viral Hepatitis

Swelling and necrosis in the liver cells.

This can lead to ?

A

Swelling and severe inflammation of the liver can produce biliary stasis

96
Q

Patho of Hepatitis Viral Hepatitis:

How is recovery?

A

Recovery possible but can remain as carriers (people with previous chronic low-grade infection, non-active disease).

Carriers can still spread hepatitis even if they are asymptomatic.

97
Q

Patho of Hepatitis Viral Hepatitis:

How do/can carriers spread?

A

Carriers can still spread hepatitis even if they are asymptomatic.

98
Q

Patho of Hepatitis Viral Hepatitis:

“Hepatitis double punches hepatocytes”

What does that mean?

A

Hepatocytes get attacked (virus) AND lysed (by body’s defense mechanisms).

99
Q

Here is a trick to their mode of transmission of different hepatitis strains:

Hepatitis A

A

Hepatitis A = Anal for mouth-fecal route

100
Q

Here is a trick to their mode of transmission of different hepatitis strains:

Hepatitis B

A

Hepatitis B = Blood and body fluids

101
Q

Here is a trick to their mode of transmission of different hepatitis strains:

Hepatitis C

A

Hepatitis C = Circulation, for blood and IV use

102
Q

Here is a trick to their mode of transmission of different hepatitis strains:

Hepatitis A and E

A

Hepatitis A and E = Vowels and bowels for fecal route

103
Q

Clinical Presentation of Hepatitis

Stages?

A
  1. Preicteric (prodromal)
  2. Icteric
  3. Posticteric/Recovery
104
Q

Clinical Presentation of Hepatitis

Preicteric (prodromal) occurs when?

A

2 weeks post exposure

105
Q

Clinical Presentation of Hepatitis

Icteric Phase occurs when? How long does it last?

A

1-2 weeks after prodromal phase

Lasts 2-6 weeks

106
Q

Clinical Presentation of Hepatitis

Posticteric/Recovery Phase- when does it occur?

A

6-8 weeks after exposure

107
Q

Clinical Presentation of Hepatitis

Preicteric (prodromal) phase Manifestations?

A

Fatigue, malaise, anorexia, nausea, general muscle aches, fever, headache, mild upper RQ discomfort

108
Q

Clinical Presentation of Hepatitis

Preicteric (prodromal) phase

Explanation of Manifestations?

Is it transmissible?

A

Hepatocytes are infected by the virus causing pain to liver (RUQ) as well as liver inflammation and swelling

Infection transmissible

109
Q

Clinical Presentation of Hepatitis:

When is the actual phase of illness?

A

Icteric Phase

110
Q

Clinical Presentation of Hepatitis

Icteric phase Manifestations?

A

Jaundice, light-colored stools, dark urine, pruritic skin, tender and enlarged liver, mild aching pain, clotting problem

111
Q

Clinical Presentation of Hepatitis

Icteric phase Explanation of Manifestations?

A

Hepatocytes malfunction, altering bilirubin metabolism, which causes an increase in serum bilirubin (jaundice) and dark urine

112
Q

Clinical Presentation of Hepatitis

Icteric phase Explanation of Manifestations?

What does inflammation lead to?

A

Inflammation occurs, blocking bile production, causing light colored stools, and decreasing the synthesis of blood clotting factors.

Liver inflammation and swelling leads to biliary obstruction

113
Q

Clinical Presentation of Hepatitis

Posticteric/Recovery phase Manifestations?

A

Manifestations fade, may take several weeks to return to normalcy

114
Q

Clinical Presentation of Hepatitis

Posticteric/Recovery phase

Explanation of Manifestations?

A

Hepatocytes recover

Symptoms diminish but liver still large and tender

115
Q

The Hepatitis B Panel Includes The Following Three Tests:

A
  1. Hep B Surface Antigen
  2. Hep B Surface Antibody
  3. Hep B Core Antibody
116
Q

SLIDE 20

A

Read/study

117
Q

Prevention/Treatment of Hepatitis

With Strains of Hepatitis have a vaccine

A

Hep A and Hep B

118
Q

Prevention/Treatment of Hepatitis

With Strains of Hepatitis DO NOT have a vaccine?

A

Hep C, D, E

119
Q

Prevention/Treatment of Hepatitis

When is the Hep A vaccine administered and to who?

A

All children @ 1yo

Immune serum globulin?????

120
Q

Prevention/Treatment of Hepatitis

Why would the Hep A vaccine be administered?

A

Non-domestic traveling
MSM
IV abusers
Long-term liver disease
Frequent blood transfusions, hemophilia
Exposure, living w/ someone who is hep A (+)

121
Q

Prevention/Treatment of Hepatitis

Why is it important to get the Hep A virus?

A

Hep A Virus replicates in liver & secreted in feces

122
Q

Prevention/Treatment of Hepatitis

When is the Hep B vaccine administered and to who?

A

All infants @ birth

123
Q

Prevention/Treatment of Hepatitis

Who else would be receiving a Hep B vaccine?

A

Older children not previously vaccinated

Adults @ risk

Hep B immune globulin???

124
Q

Prevention/Treatment of Hepatitis

What adults at risk would be receiving the Hep B vaccine?

A

Healthcare workers
Sexual activity
IV abusers

125
Q

Hep B vaccine??? Slide makes no sense (22)

A

Hep B immune globulin

126
Q

Hep C is screening for what?

A

Screening of blood donors

127
Q

What is the antiviral therapy for Hep C?

A

Interferon-alpha or combined with ribavirin (antiviral therapy)

128
Q

What is used to confirm active hep C?

A

HCV RNA quantification to assess viral load & evaluate antiviral therapy

129
Q

What is used to prevent Hep D?

A

No specific vaccine

Hep B vaccine, only if not already Hep B (+)

130
Q

What can be done to prevent Hep E?

A

There is no vaccine.

Ensure safe drinking water
Hygiene

131
Q

In general terms, what is cirrhosis?

A

Late-stage, irreversible disease, liver scarred

132
Q

In cirrhosis, what leads to disease and liver scarring?

A

Liver cells swell, fibrosis, hepatomegaly

Infiltration of WBCs & inflammatory process

133
Q

In cirrhosis, what do wbcs do?

A

Infiltration of WBCs & inflammatory process

134
Q

In cirrhosis, what happens to the lobules of the liver?

A

Lobules of liver covered with fibrous connective tissue and get filled with fat –> obstructed biliary channels & blood flow  jaundice and portal htn

135
Q

In cirrhosis, lobules of liver get covered with fibrous connective tissue and get filled with fat,

what does this lead to?

A

obstructed biliary channels & blood flow causing jaundice and portal hypertension

136
Q

What are causes of cirrhosis? What is the main one? List 4

A

Alcohol abuse**

Gallstones that obstruct bile flow in the gallbladder

Cystic fibrosis, which causes mucous plugs to form in the bile duct

Chronic hepatitis, particularly HCV

137
Q

What are causes of cirrhosis? List 2

A

Long-term exposure to toxic material

Storage disorders, such as hemochromatosis, which is a buildup of iron in the body

138
Q

Slide 25???

A

WWWHHHHHAAAAATTTTTTT

139
Q

What happens to the abdomen during cirrhosis? Why?

A

Abdominal distension caused by gross ascites.

140
Q

Ascites

A

Fluid accumulation in peritoneal cavity

141
Q

How does ascites occur in cirrhosis?

A

Portal HTN pushes fluid back –> abdominal cavity

Liver unable to produce sufficient albumin

Albumin needed for maintaining colloidal pressure & fluid balance

142
Q

Abdominal distension caused by gross ascites:

What does the liver do or not do that leads to ascites during liver cirrhosis?

A

Liver unable to produce sufficient albumin

Albumin needed for maintaining colloidal pressure & fluid balance

143
Q

What is the pharmacological treatment for cirrhosis?

A

Vitamins (esp Vitamin K)

GI prophylaxis

Ferrous sulfate, folic acid

Bile-acid sequestering agents – aid in bile excretion (colesevelam, cholestyramine, colestipol)

Non-selective Betablocker

TX for encephalopathy

144
Q

Pharmacological Treatment for cirrhosis:

What do bile-acid sequestering agents do?

A

Bile-acid sequestering agents – aid in bile excretion (colesevelam, cholestyramine, colestipol)

145
Q

What are examples of bile sequestering agents used in the pharmacological treatment for cirrhosis?

A

(colesevelam,

cholestyramine,

colestipol)

146
Q

Pharmacological Treatment for cirrhosis?

What is the treatment for encephalopathy in cirrhosis?

A

Lactulose ~ rid ammonia via fecal excretion

147
Q

What does lactulose do?

A

Lactulose ~ rid ammonia via fecal excretion

148
Q

How does lactulose decrease ammonia levels when used for cirrhosis?

A

Lowers the pH of colon, which inhibits the diffusion of ammonia from colon –> blood, thereby ↓ blood ammonia levels

149
Q

When a patient is given lactulose for cirrhosis, how much will ammonia levels decrease?

A

Ammonia levels will decrease by 25-50%

150
Q

Other than remove ammonia from the body, what else does lactulose do?

151
Q

How can lactulose be given? How often are doses given?

A

Can be given rectally
May repeat doses hourly

152
Q

When a patient is given lactulose for cirrhosis, what is the desired outcome?

A

Desired outcome: clearing of confusion & improved mental status

153
Q

Pancreas A&P:

What is the exocrine functions of the immune system?

A

Responsible for secreting enzymes into the duodenum to facilitate food digestion.

154
Q

Pancreas A&P:

What are the enzymes secreted into the duodenum to facilitate food digestion?

A

Amylase – digestion of starch & glycogen

Lipases – digestion of fats

Proteases – digestion of proteins

Trypsin

Chymotrypsin

Elastase

155
Q

Amylase

A

digestion of starch & glycogen

156
Q

Lipases

A

digestion of fats

157
Q

Proteases

A

digestion of proteins

158
Q

Pancreas A&P:

Exocrine functions

Role of electrolytes:

What does it result in?

A

bicarbonate ions – Neutralizes acid to protect enzymes from stomach acid & pepsin

The resulting pH elevation inactivates pepsin

159
Q

Pancreas A&P:

Exocrine functions

Role of water?

A

Carries enzymes necessary for digestion

160
Q

Pancreas A&P:

Exocrine functions

Duct system role?

A

carries these substances (enzymes, electrolytes, h20) to the duodenum to join the chyme

161
Q

Pancreas A&P:

What are the endocrine functions of the pancreas?

A

Hormone production
- Insulin, glucagon

Maintenance of homeostasis
- Blood glucose

162
Q

Pancreas A&P:

Endocrine functions of the pancreas:

What hormones does it produce?

A

Insulin

Glucagon

163
Q

Pancreas A&P:

Endocrine functions of the pancreas:

How does it maintain homeostasis

A

Maintains blood glucose

164
Q

Slide 31?

165
Q

What is acute pancreatitis?

A

Mild to life-threatening inflammation of pancreas

Is reversible

166
Q

What causes acute pancreatitis?

A

*Alcohol Abuse (chronic)

*Gallstones and Biliary Tract Disease

Viral infections

Meds

Hypertriglyceridemia

167
Q

How does chronic alcoholism cause acute pancreatitis?

A

Stimulates increased secretion of pancreatic enzymes

Contracts the sphincter of Oddi, blocking flow

168
Q

What does chronic alcoholism cause to happen to the sphincter of Oddi?

A

Contracts the sphincter of Oddi, blocking flow

169
Q

How does acute pancreatitis feel for someone with chronic alcohol abuse?

A

severe pain

170
Q

Gallstones and Billiary Tract Disease leads to what?

A

Obstructs bile flow and pancreatic enzymes

171
Q

When bile flow and pancreatic enzymes are obstructed in gallstones and billiary tract disease, what does this cause?

A

Causes bile to reflux into the pancreatic ducts

172
Q

What are complications of acute pancreatitis?

A

Necrosis, abscess, gangrene, hemorrhage, AKI

173
Q

What are more complications of acute pancreatitis?

A

DM

Renal failure

Malnutrition

Pancreatic cancer

174
Q

Why would the complication of DM occur in acute pancreatitis?

A

Damage to insulin-producing cells

175
Q

Why would the complication of renal failure occur in acute pancreatitis?

A

Shock & RAAS activation
Decreased renal perfusion

176
Q

Why would malnutrition occur as a complication of acute pancreatitis?

A

↓ pancreatic enzyme production

177
Q

Why would pancreatic cancer occur as a complication of pancreatitis?

A

Cellular mutations
Long-standing inflammation

178
Q

What is chronic pancreatitis?

A

Progressive, irreversible destruction

179
Q

What is the main risk factor leads to chronic pancreatitis?

A

Main risk factor - excessive alcohol consumption.

180
Q

What forms in chronic pancreatitis?

A

Scar tissue and fibrosis form as pancreas progressively destroyed.

Cysts form, walled-off areas of necrosis, pancreatic juice, debris, blood

181
Q

Other than scar tissue formation, what else would occur in chronic pancreatitis?

What would this lead to?

A

Strictures in the ducts and organ failure –> lack of pancreatic enzymes and fat malabsorption.

182
Q

What is not allowed to be given to a patient with chronic pancreatitis?

A

No alcohol allowed, especially with chronic pancreatitis

183
Q

What are other causes of chronic pancreatitis?

A

Tumor
Pseudocysts
Trauma
Cystic fibrosis

184
Q

What are pseudocysts?

A

Walled-off collections of pancreatic secretions

185
Q

What is the prognosis of acute pancreatitis?

A

Medical emergency

15% mortality rate ~ ↑ with advancing age & comorbidity

186
Q

What are acute complications of acute pancreatitis?

A

Shock

Infection

Malnutrition

Pseudocyst, abscess

187
Q

Acute complications of acute pancreatitis:

Shock- what happens with enzymes? What does this lead to?

A

Enzymes leak into general circulation

Triggered release of chemicals, immune mediators

188
Q

What are acute complications associated with shock that is caused by acute pancreatitis?

A

inflammatory response, hemorrhage, vasodilation, fluid shifts from the vascular to the peritoneal cavity, and increased capillary permeability.

189
Q

Acute complications of acute pancreatitis:

What do enzymes do in infection? What does this lead to? How serious is this?

A

Enzymes –> peritoneal cavity & destroys tissue

Vulnerability to bacteria & infection

Serious – require intensive tx

190
Q

Acute complications of acute pancreatitis:

Infection: What can happen with bacteria?

A

Translocation of intestinal bacteria –> bloodstream, pneumonia

191
Q

Acute complications of acute pancreatitis:
Malnutrition: What happens with pancreatic enzymes?

A

↓ pancreatic enzyme production

192
Q

Acute complications of acute pancreatitis:

Pseudocysts, abscess?

What would a rupture lead to?

A

Accumulation of pancreatic fluids & necrotic debris

Rupturing –> hemorrhaging, infection, peritonitis

193
Q

Clinical Presentation of Pancreatitis:

Acute manifestations may vary by what?

A

symptoms vary and may be precipitated by a large meal or consuming a large quantity of alcohol.

193
Q

Clinical Presentation of Pancreatitis:
How do acute manifestations appear?

A

Sudden & severe onset

194
Q

Clinical Presentation of Pancreatitis:

How are serum amylase and lipase levels?

A

Serum amylase & lipase will be elevated

195
Q

Clinical Presentation of Pancreatitis:
Acute manifestations: How does body pain occur?

A

Upper abdominal pain
Radiates to back
Worsens after eating

196
Q

What are other changes associated that are acute manifestations of pancreatitis?

A

N/V
Mild jaundice
Low-grade fever
Blood pressure, pulse, RR △
—–Increased or decreased
Hyperglycemia
—–Transient

197
Q

What are the chronic manifestations of pancreatitis? List 4

A

Hyperglycemia
Insidious onset
Upper abdominal pain
heavy, gnawing, or burning and cramp-like.
Indigestion

198
Q

What are the chronic manifestations of pancreatitis? List last 4

A

Unintentional wt loss
Steatorrhea ~ oily, fatty, odorous
Constipation
Flatulence

199
Q

Management of Pancreatitis: What is done?

A

ICU monitoring

Resting for the pancreas

Hydration maintenance

Meds

200
Q

Chronic manifestations of pancreatitis: How is the upper ab pain?

A

heavy, gnawing, or burning and cramp-like.

201
Q

Management of Pancreatitis: ICU monitoring includes:

A

VS (Temp, HR, BP, RR)

Intake & output (every hour)

202
Q

Management of Pancreatitis: Resting for the pancreas means?

A

Fasting
TPN –> clear liquids –> low-fat diet
Pancreatic enzyme supplements upon diet resuming

203
Q

Management of Pancreatitis: What is hydration maintenance mean?

204
Q

Management of Pancreatitis: What meds should be given?

A

Antiemetics, if N/V (+)
Antacids & acid-reducing agents (Raise pH )
Narcotics & analgesics
ABX, if infection (+)
Insulin, for hyperglycemia secondary to Damage
TPN

205
Q

Approach to Deficiency of Pancreatic Enzymes: What should be given?

A

Pancrelipase (Creon)

206
Q

What is pancrelipase?

A

Mixture
Lipases, amylases, proteases

207
Q

What is the MOA of pancrelipase?

A

Increased digestion of fats, carbs, & proteins in GI tract

208
Q

What is the use of pancrelipase?

A

Chronic pancreatitis, pancreatectomy, CF, pancreatic cancer

209
Q

What do pancrelipase delayed release capsules do? How are they taken?

A

Dissolve in duodenum & upper jejunum

Taken with every meal & snack

Do not crush, chew, or retain in mouth – d/t risk of irritating oral mucosa

210
Q

What are adverse effects of pancrelipase at normal doses?

A

Abdominal discomfort, flatulence,

211
Q

What are adverse effects of pancrelipase at high doses?

A

Diarrhea, nausea, cramping

212
Q

What is the efficacy of pancrelipase?

A

Improved nutritional status

Normalization of stools in patients with steatorrhea

PATHO/PHARM II (27 decks)

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