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

Exam 2 (213 cards)

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
What is the most common cause of gallstones?
High concentration of cholesterol in the bile (most common)
26
Why does a high level of cholesterol in bile lead to gallstones?
Bile cannot dissolve the excessive level of cholesterol. Excessive cholesterol forms a mass or calculi.
27
What else other than excess cholesterol lead to gallstone formation?
Excessive bilirubin contributes to gallstone formation.
28
Other than bile and bilirubin, what can lead to gallstones?
Gallbladder does not empty completely Gallbladder empties infrequently or incompletely. Stagnant bile becomes more concentrated --> formation of gallstones.
29
Why would a gallstone not empty properly?
Gallbladder does not empty completely Gallbladder empties infrequently or incompletely.
30
What are the five F's that can lead to increase in gallstone formations?
Fair Female Forty and up Fat Fertile
31
What are the big risk factors to gallstone formation?
Big risk factors: 5fs, rapid weight loss, pregnancy
32
What are symptoms of gallstones:
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
33
How may abdominal cramping and pain occur with gallstones?
RUQ abdominal cramping & pain worsens after fatty meals, may radiate to back or right shoulder,
34
What is the primary roles of the liver?
Storage, excretion, metabolism, 1st pass, glucose regulation, detoxification
35
What does the liver store?
Stores blood (~ 450mL), Stores Fe, Stores fat-soluble vitamins (A, D, E,K), B12, glycogen.
36
What does the liver synthesize?
Synthesis of clotting factors (prothrombin) and albumin Lipoprotein synthesis -LDL, HDL
37
What does the liver do to hemogobin?
Degrades hgb --> globin and amino acids to be re-used in the synthesis of more hgb
38
What is the role of the liver with blood?
Stores blood and Filtration/detox of blood
39
What cells of the liver remove bacteria?
Phagocytic cells, Kupffer cells, remove bacteria
40
What does the liver metabolize?
Metabolism of CHO, protein, fat, drugs
41
The liver is a source of what?
Heat
42
What does the liver do when RBC breakdown occurs in the blood?
Conjugates bilirubin when RBC breakdown in blood
43
What is a by product of protein metabolism?
Ammonia (NH3)
44
What is ammonia converted into by the liver?
Urea
45
Common Labs of Hepatic Function assess what?
Liver enzymes (Liver function tests, LFTs)
46
Liver enzymes (Liver function tests, LFTs) include?
AST (aspartate aminotransferase) & ALT (alanine aminotransferase) ALP (alkaline phosphatase) Bilirubin
47
Labs to measure hepatic function and liver disease also include
Albumin Prothrombin time Blood Urea Nitrogen (BUN) Ammonia (NH3)
48
AST (aspartate aminotransferase) & ALT (alanine aminotransferase) What are they involved in? Where are they mainly present?
Involved in metabolic reactions, present mainly in liver cells
49
AST (aspartate aminotransferase) & ALT (alanine aminotransferase) When are they released?
Released into circulation in liver disease, hepatocellular injury, necrosis
50
AST (aspartate aminotransferase) & ALT (alanine aminotransferase) What are they markers for? How do they present in liver disease and injury?
Markers of injury, elevated in liver disease, liver injury released into circulation
51
ALP (alkaline phosphatase) Where is it mainly?
Mainly in bile ducts
52
ALP (alkaline phosphatase) How are ALP in biliary obstruction?
Increases with biliary obstruction
53
ALP (alkaline phosphatase) When biliary tree obstruction occurs? What happens?
When biliary tree obstructed, bile duct cells release ALP (elevation)
54
What is a component of bile?
Bilirubin Breakdown of RBCs????
55
Bilirubin is a measure of what?
Measure of liver’s ability to perform enzymatic/metabolic functions
56
How is bilirubin presented in liver disease?
Elevated in liver disease
57
Albumins
Serum protein synthesized by liver
58
What does Albumin measure?
Measure liver’s capacity for protein synthesis
59
How are albumin levels in liver disease? Why?
Decreased in liver disease because liver cannot produce plasma proteins.
60
Prothrombin Time?
Measures function of clotting cascade
61
?????? Liver clotting
Liver synthesizes most coagulation factors Liver decreases production of vitamin K and prothrombin.
62
What happens to prothrombin time in liver disease? What causes this?
Deficient clotting & elevated prothrombin time
63
Having to do with Blood Urea Nitrogen (BUN), what is made in the liver?
Urea is made in the liver
64
In liver disease, what happens to BUN?
Decreased BUN (ammonia not being converted to urea) This leads to high levels of ammonia
65
Ammonia is a by product of what process?
By-product of protein metabolism
66
Where is most ammonia absorbed? And what is it converted to?
Most is absorbed into portal circulation & converted to urea
67
What can liver NOT do with ammonia?
Liver cannot convert ammonia to urea for excretion.
68
How are ammonia levels in liver disease?
Elevated in liver disease
69
What is hepatitis?
Inflammation of the liver
70
How is hepatitis viewed?
Treatable/Manageable with drugs, self-limiting
71
What are the two causes/types of hepatitis?
1. Infections, contagious 2. Nonviral, noncontagious
72
Infections, contagious hepatitis are often what/.
Viral
73
What are the five types of viral hepatitis?
A, B, C, D, E,
74
What are the most common types of viral hepatitis?
A, B, C most common
75
How is recovery of viral hepatitis?
Can recover in time but advanced age & comorbidities - ↑’d risk of liver failure, liver ca, cirrhosis
76
What are non-viral, non contagious causes of hepatitis?
EtOH Meds ~ APAP, antiseizure meds, ABX Autoimmune DX
77
Types of meds that would lead to non viral noncontagious hepatitis?
APAP, antiseizure meds, ABX
78
How is recovery of nonviral, non-contagious hepatitis?
Usually recover
79
What maynonviral, non-contagious hepatitis develop into?
May develop liver failure, liver cancer, or cirrhosis
80
Nonviral and viral hepatitis can result in what?
Both types can result in liver cell destruction, necrosis, autolysis, hyperplasia & scarring
81
What are the two forms of hepatitis? (Different from types)
1. Acute 2. Chronic 3. Fulminant
82
How does acute hepatitis occur?
Proceeds through phases – prodromal/pre-icteric, icteric, recovery
83
What are the phases of acute hepatitis?
prodromal/pre-icteric, icteric, recovery
84
What is considered chronic hepatitis?
Cont’d disease lasting > 6 months
85
What types of hepatitis can become chronic? Which ones primarily?
Only types B, C, D - Primarily B & C
86
Severity and disease progression of chronic hepatitis depends on what?
Severity & disease progression depends on extent of liver damage
87
How can someone live with chronic hepatitis?
Can live with it for years, but health deteriorates as liver function declines --> fibrosis, obstruction, cirrhosis, failure, liver ca
88
What are the effects of deteriorating liver function due to living with chronic hepatitis for years?
Can live with it for years, but health deteriorates as liver function declines  fibrosis, obstruction, cirrhosis, failure, liver ca
89
Fulminant
Fulminant ~ liver failure sudden?
90
Patho of Hepatitis Viral Hepatitis: How does hepatitis infection start?
One of the 5 Virus strains targets the hepatocytes
91
Patho of Hepatitis Viral Hepatitis: Why does hepatocyte damage occur in viral hepatitis?
Virus attacks the hepatocytes
92
Patho of Hepatitis Viral Hepatitis: What occurs after virus attack the hepatocytes?
Cell-mediated immune responses to the virus
93
Patho of Hepatitis Viral Hepatitis: What are the Cell-mediated immune responses to the virus?
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
Patho of Hepatitis Viral Hepatitis Pathologic lesions of chronic hepatitis include:
necrosis, scarring, Kupfer cell hyperplasia, phagocyte infiltration
95
Patho of Hepatitis Viral Hepatitis Swelling and necrosis in the liver cells. This can lead to ?
Swelling and severe inflammation of the liver can produce biliary stasis
96
Patho of Hepatitis Viral Hepatitis: How is recovery?
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
Patho of Hepatitis Viral Hepatitis: How do/can carriers spread?
Carriers can still spread hepatitis even if they are asymptomatic.
98
Patho of Hepatitis Viral Hepatitis: "Hepatitis double punches hepatocytes" What does that mean?
Hepatocytes get attacked (virus) AND lysed (by body’s defense mechanisms).
99
Here is a trick to their mode of transmission of different hepatitis strains: Hepatitis A
Hepatitis A = Anal for mouth-fecal route
100
Here is a trick to their mode of transmission of different hepatitis strains: Hepatitis B
Hepatitis B = Blood and body fluids
101
Here is a trick to their mode of transmission of different hepatitis strains: Hepatitis C
Hepatitis C = Circulation, for blood and IV use
102
Here is a trick to their mode of transmission of different hepatitis strains: Hepatitis A and E
Hepatitis A and E = Vowels and bowels for fecal route
103
Clinical Presentation of Hepatitis Stages?
1. Preicteric (prodromal) 2. Icteric 3. Posticteric/Recovery
104
Clinical Presentation of Hepatitis Preicteric (prodromal) occurs when?
2 weeks post exposure
105
Clinical Presentation of Hepatitis Icteric Phase occurs when? How long does it last?
1-2 weeks after prodromal phase Lasts 2-6 weeks
106
Clinical Presentation of Hepatitis Posticteric/Recovery Phase- when does it occur?
6-8 weeks after exposure
107
Clinical Presentation of Hepatitis Preicteric (prodromal) phase Manifestations?
Fatigue, malaise, anorexia, nausea, general muscle aches, fever, headache, mild upper RQ discomfort
108
Clinical Presentation of Hepatitis Preicteric (prodromal) phase Explanation of Manifestations? Is it transmissible?
Hepatocytes are infected by the virus causing pain to liver (RUQ) as well as liver inflammation and swelling Infection transmissible
109
Clinical Presentation of Hepatitis: When is the actual phase of illness?
Icteric Phase
110
Clinical Presentation of Hepatitis Icteric phase Manifestations?
Jaundice, light-colored stools, dark urine, pruritic skin, tender and enlarged liver, mild aching pain, clotting problem
111
Clinical Presentation of Hepatitis Icteric phase Explanation of Manifestations?
Hepatocytes malfunction, altering bilirubin metabolism, which causes an increase in serum bilirubin (jaundice) and dark urine
112
Clinical Presentation of Hepatitis Icteric phase Explanation of Manifestations? What does inflammation lead to?
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
Clinical Presentation of Hepatitis Posticteric/Recovery phase Manifestations?
Manifestations fade, may take several weeks to return to normalcy
114
Clinical Presentation of Hepatitis Posticteric/Recovery phase Explanation of Manifestations?
Hepatocytes recover Symptoms diminish but liver still large and tender
115
The Hepatitis B Panel Includes The Following Three Tests:
1. Hep B Surface Antigen 2. Hep B Surface Antibody 3. Hep B Core Antibody
116
SLIDE 20
Read/study
117
Prevention/Treatment of Hepatitis With Strains of Hepatitis have a vaccine
Hep A and Hep B
118
Prevention/Treatment of Hepatitis With Strains of Hepatitis DO NOT have a vaccine?
Hep C, D, E
119
Prevention/Treatment of Hepatitis When is the Hep A vaccine administered and to who?
All children @ 1yo Immune serum globulin?????
120
Prevention/Treatment of Hepatitis Why would the Hep A vaccine be administered?
Non-domestic traveling MSM IV abusers Long-term liver disease Frequent blood transfusions, hemophilia Exposure, living w/ someone who is hep A (+)
121
Prevention/Treatment of Hepatitis Why is it important to get the Hep A virus?
Hep A Virus replicates in liver & secreted in feces
122
Prevention/Treatment of Hepatitis When is the Hep B vaccine administered and to who?
All infants @ birth
123
Prevention/Treatment of Hepatitis Who else would be receiving a Hep B vaccine?
Older children not previously vaccinated Adults @ risk Hep B immune globulin???
124
Prevention/Treatment of Hepatitis What adults at risk would be receiving the Hep B vaccine?
Healthcare workers Sexual activity IV abusers
125
Hep B vaccine??? Slide makes no sense (22)
Hep B immune globulin
126
Hep C is screening for what?
Screening of blood donors
127
What is the antiviral therapy for Hep C?
Interferon-alpha or combined with ribavirin (antiviral therapy)
128
What is used to confirm active hep C?
HCV RNA quantification to assess viral load & evaluate antiviral therapy
129
What is used to prevent Hep D?
No specific vaccine Hep B vaccine, only if not already Hep B (+)
130
What can be done to prevent Hep E?
There is no vaccine. Ensure safe drinking water Hygiene
131
In general terms, what is cirrhosis?
Late-stage, irreversible disease, liver scarred
132
In cirrhosis, what leads to disease and liver scarring?
Liver cells swell, fibrosis, hepatomegaly Infiltration of WBCs & inflammatory process
133
In cirrhosis, what do wbcs do?
Infiltration of WBCs & inflammatory process
134
In cirrhosis, what happens to the lobules of the liver?
Lobules of liver covered with fibrous connective tissue and get filled with fat --> obstructed biliary channels & blood flow  jaundice and portal htn
135
In cirrhosis, lobules of liver get covered with fibrous connective tissue and get filled with fat, what does this lead to?
obstructed biliary channels & blood flow causing jaundice and portal hypertension
136
What are causes of cirrhosis? What is the main one? List 4
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
What are causes of cirrhosis? List 2
Long-term exposure to toxic material Storage disorders, such as hemochromatosis, which is a buildup of iron in the body
138
Slide 25???
WWWHHHHHAAAAATTTTTTT
139
What happens to the abdomen during cirrhosis? Why?
Abdominal distension caused by gross ascites.
140
Ascites
Fluid accumulation in peritoneal cavity
141
How does ascites occur in cirrhosis?
Portal HTN pushes fluid back --> abdominal cavity Liver unable to produce sufficient albumin Albumin needed for maintaining colloidal pressure & fluid balance
142
Abdominal distension caused by gross ascites: What does the liver do or not do that leads to ascites during liver cirrhosis?
Liver unable to produce sufficient albumin Albumin needed for maintaining colloidal pressure & fluid balance
143
What is the pharmacological treatment for cirrhosis?
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
Pharmacological Treatment for cirrhosis: What do bile-acid sequestering agents do?
Bile-acid sequestering agents – aid in bile excretion (colesevelam, cholestyramine, colestipol)
145
What are examples of bile sequestering agents used in the pharmacological treatment for cirrhosis?
(colesevelam, cholestyramine, colestipol)
146
Pharmacological Treatment for cirrhosis? What is the treatment for encephalopathy in cirrhosis?
Lactulose ~ rid ammonia via fecal excretion
147
What does lactulose do?
Lactulose ~ rid ammonia via fecal excretion
148
How does lactulose decrease ammonia levels when used for cirrhosis?
Lowers the pH of colon, which inhibits the diffusion of ammonia from colon --> blood, thereby ↓ blood ammonia levels
149
When a patient is given lactulose for cirrhosis, how much will ammonia levels decrease?
Ammonia levels will decrease by 25-50%
150
Other than remove ammonia from the body, what else does lactulose do?
Soft BMs
151
How can lactulose be given? How often are doses given?
Can be given rectally May repeat doses hourly
152
When a patient is given lactulose for cirrhosis, what is the desired outcome?
Desired outcome: clearing of confusion & improved mental status
153
Pancreas A&P: What is the exocrine functions of the immune system?
Responsible for secreting enzymes into the duodenum to facilitate food digestion.
154
Pancreas A&P: What are the enzymes secreted into the duodenum to facilitate food digestion?
Amylase – digestion of starch & glycogen Lipases – digestion of fats Proteases – digestion of proteins Trypsin Chymotrypsin Elastase
155
Amylase
digestion of starch & glycogen
156
Lipases
digestion of fats
157
Proteases
digestion of proteins
158
Pancreas A&P: Exocrine functions Role of electrolytes: What does it result in?
bicarbonate ions – Neutralizes acid to protect enzymes from stomach acid & pepsin The resulting pH elevation inactivates pepsin
159
Pancreas A&P: Exocrine functions Role of water?
Carries enzymes necessary for digestion
160
Pancreas A&P: Exocrine functions Duct system role?
carries these substances (enzymes, electrolytes, h20) to the duodenum to join the chyme
161
Pancreas A&P: What are the endocrine functions of the pancreas?
Hormone production - Insulin, glucagon Maintenance of homeostasis - Blood glucose
162
Pancreas A&P: Endocrine functions of the pancreas: What hormones does it produce?
Insulin Glucagon
163
Pancreas A&P: Endocrine functions of the pancreas: How does it maintain homeostasis
Maintains blood glucose
164
Slide 31?
WWhhaatt
165
What is acute pancreatitis?
Mild to life-threatening inflammation of pancreas Is reversible
166
What causes acute pancreatitis?
*Alcohol Abuse (chronic) *Gallstones and Biliary Tract Disease Viral infections Meds Hypertriglyceridemia
167
How does chronic alcoholism cause acute pancreatitis?
Stimulates increased secretion of pancreatic enzymes Contracts the sphincter of Oddi, blocking flow
168
What does chronic alcoholism cause to happen to the sphincter of Oddi?
Contracts the sphincter of Oddi, blocking flow
169
How does acute pancreatitis feel for someone with chronic alcohol abuse?
severe pain
170
Gallstones and Billiary Tract Disease leads to what?
Obstructs bile flow and pancreatic enzymes
171
When bile flow and pancreatic enzymes are obstructed in gallstones and billiary tract disease, what does this cause?
Causes bile to reflux into the pancreatic ducts
172
What are complications of acute pancreatitis?
Necrosis, abscess, gangrene, hemorrhage, AKI
173
What are more complications of acute pancreatitis?
DM Renal failure Malnutrition Pancreatic cancer
174
Why would the complication of DM occur in acute pancreatitis?
Damage to insulin-producing cells
175
Why would the complication of renal failure occur in acute pancreatitis?
Shock & RAAS activation Decreased renal perfusion
176
Why would malnutrition occur as a complication of acute pancreatitis?
↓ pancreatic enzyme production
177
Why would pancreatic cancer occur as a complication of pancreatitis?
Cellular mutations Long-standing inflammation
178
What is chronic pancreatitis?
Progressive, irreversible destruction
179
What is the main risk factor leads to chronic pancreatitis?
Main risk factor - excessive alcohol consumption.
180
What forms in chronic pancreatitis?
Scar tissue and fibrosis form as pancreas progressively destroyed. Cysts form, walled-off areas of necrosis, pancreatic juice, debris, blood
181
Other than scar tissue formation, what else would occur in chronic pancreatitis? What would this lead to?
Strictures in the ducts and organ failure --> lack of pancreatic enzymes and fat malabsorption.
182
What is not allowed to be given to a patient with chronic pancreatitis?
No alcohol allowed, especially with chronic pancreatitis
183
What are other causes of chronic pancreatitis?
Tumor Pseudocysts Trauma Cystic fibrosis
184
What are pseudocysts?
Walled-off collections of pancreatic secretions
185
What is the prognosis of acute pancreatitis?
Medical emergency 15% mortality rate ~ ↑ with advancing age & comorbidity
186
What are acute complications of acute pancreatitis?
Shock Infection Malnutrition Pseudocyst, abscess
187
Acute complications of acute pancreatitis: Shock- what happens with enzymes? What does this lead to?
Enzymes leak into general circulation Triggered release of chemicals, immune mediators
188
What are acute complications associated with shock that is caused by acute pancreatitis?
inflammatory response, hemorrhage, vasodilation, fluid shifts from the vascular to the peritoneal cavity, and increased capillary permeability.
189
Acute complications of acute pancreatitis: What do enzymes do in infection? What does this lead to? How serious is this?
Enzymes --> peritoneal cavity & destroys tissue Vulnerability to bacteria & infection Serious – require intensive tx
190
Acute complications of acute pancreatitis: Infection: What can happen with bacteria?
Translocation of intestinal bacteria --> bloodstream, pneumonia
191
Acute complications of acute pancreatitis: Malnutrition: What happens with pancreatic enzymes?
↓ pancreatic enzyme production
192
Acute complications of acute pancreatitis: Pseudocysts, abscess? What would a rupture lead to?
Accumulation of pancreatic fluids & necrotic debris Rupturing --> hemorrhaging, infection, peritonitis
193
Clinical Presentation of Pancreatitis: Acute manifestations may vary by what?
symptoms vary and may be precipitated by a large meal or consuming a large quantity of alcohol.
193
Clinical Presentation of Pancreatitis: How do acute manifestations appear?
Sudden & severe onset
194
Clinical Presentation of Pancreatitis: How are serum amylase and lipase levels?
Serum amylase & lipase will be elevated
195
Clinical Presentation of Pancreatitis: Acute manifestations: How does body pain occur?
Upper abdominal pain Radiates to back Worsens after eating
196
What are other changes associated that are acute manifestations of pancreatitis?
N/V Mild jaundice Low-grade fever Blood pressure, pulse, RR △ -----Increased or decreased Hyperglycemia -----Transient
197
What are the chronic manifestations of pancreatitis? List 4
Hyperglycemia Insidious onset Upper abdominal pain heavy, gnawing, or burning and cramp-like. Indigestion
198
What are the chronic manifestations of pancreatitis? List last 4
Unintentional wt loss Steatorrhea ~ oily, fatty, odorous Constipation Flatulence
199
Management of Pancreatitis: What is done?
ICU monitoring Resting for the pancreas Hydration maintenance Meds
200
Chronic manifestations of pancreatitis: How is the upper ab pain?
heavy, gnawing, or burning and cramp-like.
201
Management of Pancreatitis: ICU monitoring includes:
VS (Temp, HR, BP, RR) Intake & output (every hour)
202
Management of Pancreatitis: Resting for the pancreas means?
Fasting TPN --> clear liquids --> low-fat diet Pancreatic enzyme supplements upon diet resuming
203
Management of Pancreatitis: What is hydration maintenance mean?
IVF
204
Management of Pancreatitis: What meds should be given?
Antiemetics, if N/V (+) Antacids & acid-reducing agents (Raise pH ) Narcotics & analgesics ABX, if infection (+) Insulin, for hyperglycemia secondary to Damage TPN
205
Approach to Deficiency of Pancreatic Enzymes: What should be given?
Pancrelipase (Creon)
206
What is pancrelipase?
Mixture Lipases, amylases, proteases
207
What is the MOA of pancrelipase?
Increased digestion of fats, carbs, & proteins in GI tract
208
What is the use of pancrelipase?
Chronic pancreatitis, pancreatectomy, CF, pancreatic cancer
209
What do pancrelipase delayed release capsules do? How are they taken?
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
What are adverse effects of pancrelipase at normal doses?
Abdominal discomfort, flatulence,
211
What are adverse effects of pancrelipase at high doses?
Diarrhea, nausea, cramping
212
What is the efficacy of pancrelipase?
Improved nutritional status Normalization of stools in patients with steatorrhea