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N352 > GI Tract Disorders and Drugs > Flashcards

GI Tract Disorders and Drugs Flashcards

1
Q

What are esophageal varices?

A

Enlarged tortuous veins in the lower part of the esophagus
Veins are very fragile - rupture causes massive hemorrhage and is a medical emergency

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2
Q

What are two main symptoms of esophageal varices?

A

Coffee ground emesis
Melena - black tarry stools

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3
Q

Pathophysiology of esophageal varices

A

Damaged liver causes obstruction of the portal venal circulation, which increases pressure in portal circulation
Increased pressure causes venous blood from intestinal tract to seek alternative paths b/c the portal vein can’t accommodate all the blood
Venous blood goes to other veins like esophageal and gastric veins that aren’t meant to hold large amounts of blood
Increased amount of blood in esophageal veins results in enlarged tortuous veins

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4
Q

What is normal venous pressure?

A

5-10mm Hg

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5
Q

What is portal hypertension level?

A

over 10mm Hg

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6
Q

What factors can contribute to hemorrhage from esophageal varices?

A

Lifting heavy objects
Straining at stool
Sneezing, coughing
Irritation of blood vessels by poorly chewed food
Reflex of stomach contents
Alcohol

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7
Q

Medical management of bleeding esophageal varices

A

ICU admission
Fluid resuscitation - IV
Octreotide - causes selective splanchnic vasoconstriction
Vasopressin - constricts distal esophageal veins

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8
Q

Prevention of bleeding esophageal varices

A

Patient education on aggravating factors
Beta blockers I.e. Propranolol
Nitrates I.e. isosorbide - decrease risk of bleeding when used with propranolol

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9
Q

Symptoms of an upper GI bleed

A

Hematemesis
Melena

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10
Q

Where do upper GI bleeds occur?

A

Above the jejunum

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11
Q

Where do lower GI bleeds occur?

A

Jejunum and below

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12
Q

Causes of upper GI bleeds

A

PUD
Varices
Aspirin
NSAIDs
Corticosteroids
Gastric cancer

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13
Q

Causes of lower GI bleeds

A

Diverticula
Colon cancer
IBD
Hemorrhoids
Fissures

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14
Q

Symptoms of a lower GI bleed

A

Melena
Hematochezia

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15
Q

Symptoms of chronic GI bleed

A

Occult or microscopic without visible blood
+ Fecal occult blood test

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16
Q

Causes of chronic GI bleed

A

Cancer
Ulcers

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17
Q

Complications of GI bleed

A

Anemia
Hypovolemic shock

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18
Q

What is irritable bowel syndrome?

A

Functional disorder of intestinal motility - no structural abnormalities

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19
Q

What are the two types of IBS?

A

IBS-D: diarrhea is main symptom, increased levels of seratonin
IBS-C: constipation is main symptoms, decreased levels of seratonin

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20
Q

Causes of IBS

A

Exact causes unknown
Genetics
Environmental factors
Psychosocial factors
Food sensitivities
Alterations in intestinal micro-flora

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21
Q

Symptoms of IBS

A

Chronic abdominal pain
Altered bowel habits
Diarrhea
Constipation
Bloating
Abdominal distension

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22
Q

Pathophysiology of IBS

A

Alteration of serotonin signaling causes dysmotility of the intestine at particular segments, which alters the intensity of the forward movement of feces
Abnormal contractions and dysmotility cause abdominal pains

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23
Q

What are the ROME criteria?

A

Used to diagnose IBS
Recurrent abdominal pain one day a week with 2+ of the following for 3 months
Abdominal pain related to defecation
Abdominal pain associated with a change in frequency of stool
Abdominal pain associated with a change in form/appearance of stool

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24
Q

How do probiotics help with IBS?

A

Less abdominal pain
Management of diarrhea and constipation
Decrease abdominal bloating and gas

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25
Q

What is the goal of treating IBS?

A

Symptom management

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26
Q

What lifestyle modifications can be used to treat IBS?

A

Stress reduction
Sleep
Exercise
Dietary restrictions - identifying triggering foods

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27
Q

What drugs are used to manage IBS-C?

A

Fiber
Polyethylene-glycol
Lubriprostone

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28
Q

What drugs are used to manage IBS-D?

A

Alosetron - seratonin antagonist
Rifaximin - non absorbable antibiotic
Eluxadoline - acts on opioid receptors and decreases colonic motility

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29
Q

How do antidepressants treat IBS?

A

Increase seratonin levels
Improves intestinal transit times and abdominal discomfort

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30
Q

How do anti-spasmodics treat IBS?

A

Manage abdominal pain - drug of choice
Dicyclomine (Bentyl)

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31
Q

What kind of drug is Dicyclomine?

A

GI anti-cholinergic

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32
Q

What is dicyclomine used for?

A

IBS

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33
Q

What form is dicyclomine available in?

A

PO
IM

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34
Q

Nursing implications for dicyclomine

A

Ask patient to void before taking

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35
Q

MOA of GI anti-cholinergics

A

Blocks the effects of acetylcholine
Results in GI smooth muscle relaxation

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36
Q

Adverse effects of dicyclomine

A

Blurred vision
Dry mouth
Altered taste perception
Urinary retention

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37
Q

What is the appendix?

A

Narrow, worm-like organ attached to the cecum
Fills with the products of digestion and empties into the cecum

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38
Q

Why is the appendix prone to obstruction and vulnerable to infection?

A

Empties inefficiently and the lumen is small

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39
Q

Pathophysiology of appendicitis

A

Appendix becomes occluded or kinked, causing it to become inflamed
Intraluminal pressure is increased, worsening obstruction and causing ischemia and bacterial overgrowth, eventually leading to perforation

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40
Q

Clinical manifestations of appendicitis

A

RLQ pain
Nausea
Low grade fever
Local tenderness at McBurney’s points
Rebound tenderness
Rovsing’s sign
Increased WBC count
Rupture - diffuse abdominal pain and distension

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41
Q

What is the Rovsing sign?

A

Sign of appendicitis
Pain felt in RLQ after LLQ has been palpated

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42
Q

Where is McBurney’s point?

A

Between umbilicus and anterior superior iliac spine

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43
Q

Treatments for appendicitis

A

Appendectomy
Antibiotics
Analgesic pain meds
Cole therapy - heat not recommended, can cause rupture

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44
Q

What is diverticulitis?

A

Inflammation of diverticula

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45
Q

Where is diverticulitis most common and why?

A

Sigmoid colon
Narrowest part of the colon

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46
Q

Risk factors for diverticulitis

A

Obesity
Aging
Smoking
Low fiber diet

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47
Q

Pathophysiology of diverticulitis

A

Colon herniates, herniations fill with waste and become infected/inflamed

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48
Q

Complications of diverticulitis

A

Perforation
Abscesses
Fistula
Bowel obstruction
Peritonitis
Bleeding

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49
Q

Clinical manifestations of diverticulities

A

Can be asymptomatic
Chronic constipation
LLQ pain
Nausea
Fever
Bleeding
Fistulas

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50
Q

What are the two surgical methods to manage diverticulitis?

A

One stage - remove inflamed area and connect healthy areas
Two stage - remove damaged area, place temporary ostomy, give time to heal damaged areas and fistula, reverse the ostomy 2-3 months later

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51
Q

How is diverticulitis managed?

A

Pain relief - analgesics
Manage constipation - increase oral fluids to 2L/day, high fiber diet, increase physical activity, bulk forming laxative
Antibiotics
Surgery - for complicated cases

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52
Q

What treatment should not be used for diverticulitis?

A

Enema

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53
Q

What is a mechanical intestinal obstruction?

A

There is a detectable reason for the obstruction
Tumors, adhestions, hernia, volvulus, intussception

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54
Q

What is a non mechanical intestinal obstruction?

A

Suspension of peristalsis, parayltic ileus
Amyloidosis, diabetes, parkinson’s, after surgery, hypokalemia

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55
Q

Pathophysiology of intestinal obstructions

A

Part of bowel collapses, causing fluid, gas, and intestinal contents to accumulate
This causes fluid retention because they can’t be absorbed back into circulation, which distends the bowel and increases pressure in the bowel
Capillary permeability increases and fluids seep into the peritoneal cavity
Circulating blood volume decreases, causing hypovolemic shock

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56
Q

Clinical manifestations of intestinal obstruction

A

Negativ BM and flatus
N/V
Metabolic alkalosis
Electrolyte depletion
Crampy and wavelike abdominal pain
Abdomen feels like a rock

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57
Q

Management of intestinal obstruction

A

NPO
Decompress stomach - insert NG tube to drain fluid
Fluid and electrolyte replacement
Antiemetics, analgesics
Stress ulcer management - H2RA or PPI
Surgical management for hernia or adhesions

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58
Q

Risk factors for colorectal cancer

A

Smoking
Alcohol
Low fiber diet and high intake of beef
Aging
Obesity
H/O IBD and diabetes
H/O genital cancer
Family history

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59
Q

What is FAP and its characteristics?

A

Familial ademonatous polyposis
100+ polyps
Single gene mutation

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60
Q

What is Lynch syndrome and its characteristics?

A

No polyps
Several gene mutations

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61
Q

Common symptoms of colorectal cancer

A

Change in bowel habit
Blood in stool
Anemia
Weight loss
Fatigue

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62
Q

Pathophysiology of colorectal cancer

A

Adenocarcinoma - starts as benign polyp and destroys normal cells

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63
Q

Signs of right sided colon cancer

A

Abdominal pain
Melena

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64
Q

Signs of left sided colon cancer

A

Abdominal pain
Constipation and distension
Passage of fresh blood from rectum

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65
Q

Signs of rectal cancer

A

Rectal pain
Bloody stool
Alternating between diarrhea and constipation

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66
Q

Pathophysiology of IBD

A

Genetic predisposition
Environmental factors like exposure to air pollutants, food, and tobacco
Alterations in intestinal microbiota
All can trigger autoimmune response that results in inflammation of the intestinal tract and proliferation of inflammatory cytokines

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67
Q

What are the two kinds of IBD?

A

Crohn’s Disease
Ulcerative colities

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68
Q

What are the inflammatory cytokines involved in IBD?

A

CRP - C reactive protein
IL - interleukins
TNFA - tumor necrosis factor alpha

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69
Q

What part of the intestinal tract can Crohn’s disease affect?

A

Any part - mouth to anus

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70
Q

Which layers of the GI tract are involved in Crohn’s disease?

A

All 4 - mucosa, submucosa, muscular layer, and serosa

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71
Q

Complications of Crohn’s disease

A

Fistula
Intestinal obstruction
Abscesses

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72
Q

What happens in the GI tract in Crohn’s disease?

A

Microscopic or crypt inflammation
Ulcers that look like cobblestones
Skip lesions
Thickening and fibrosis of bowel wall, narrowing of bowel lumen

73
Q

What part of the GI tract does UC occur in?

A

Colon and rectum

74
Q

What layers of the GI tract does UC effect?

A

Superficial layers - mucosa and submucosa

75
Q

How do ulcers appear in UC?

A

Continous

76
Q

Clinical manifestations of UC

A

Profound bleeding
Bloody diarrhea 10-12x/day
Severe abdominal cramps

77
Q

Complications of UC

A

Perforated bowel
Toxic megacolon

78
Q

Clinical manifestations of IBD

A

Diarrhea
Crampy abdominal pain
Rectal bleeding
Bowel urgency
Sensation of incomplete evacuation
Loss of appetite
Weight loss
Anemia
Fatigue
Anxiety and depression
Arthritis and osteoporosis
Skin lesions
Ocular disoreders
Liver disorders

79
Q

What drugs are used to treat mild IBD?

A

Topical corticosteroids
Antibiotics
5-ASAs

80
Q

What drugs are used to treat moderate IBD?

A

Immunomodulators
Oral corticosteroids

81
Q

What is used to treat severe IBD?

A

Surgery
Biologics

82
Q

What drugs are 5-ASAs?

A

Sulfasalazine
Mesalamine

83
Q

MOA of 5-ASAs

A

Reduce inflammation locally in the lining of the intestine

84
Q

Sulfasalazine route of administration

A

PO

85
Q

Mesalamine route of administration

A

PO, PR

86
Q

Adverse effects of sulfasalazine

A

Decreased sperm production
SJS

87
Q

Adverse effects of mesalamine

A

Pancreatitis

88
Q

What is the main difference between sulfasalazine and mesalamine?

A

Sulfasalazine has sulfa, mesalamine does not

89
Q

MOA of corticosteroids

A

Fast acting inflammatory effect

90
Q

Use of corticosteroids

A

Short term treatment for acute IBD

91
Q

Corticosteroids routes of administration

A

PO
IV
Foam
Liquid enemas

92
Q

Adverse effects of corticosteroids

A

Immunosuppression
Bone loss
Weight gain
Mood swings
Hypertension
Hypergylcemia

93
Q

Do corticosteroids have a specific target on the immune system?

A

No

94
Q

MOA of immunomodulators

A

Modify the body’s immune system so that it can’t cause ongoing inflammation

95
Q

Immunomodulators routes of administration

A

PO
IV

96
Q

Use of immunomodulators

A

Maintain remission in those who haven’t responded to other therapies
Decreases the long term need for steroids

97
Q

Adverse effects of immunomodulators

A

GI
Hepatotoxicity
Nephrotoxicity
Infections
Lymphoma

98
Q

Patient education for immunomodulators

A

Get regular vaccines
Avoid live vaccines
Get liver and renal systems monitored regularly
Report ant fever, chills, or sore throat

99
Q

How long do immunomodulators take to work?

A

6-8 weeks

100
Q

Which drugs are corticosteroids?

A

Budesonide
Prednisone

101
Q

Which drugs are immunomodulators?

A

Azathioprine
Mercapropurine
Methotrexate
Cyclosporine

102
Q

Which drugs are biologics?

A

Infliximab
Adalimumab
Cerolizumab

103
Q

MOA of biologics

A

Inhibit pro-inflammatory cytokines and repress inflammatory response

104
Q

Patient education for biologics

A

Get all annual vaccines
Get evaluated for TB annually
Report fever, new cough, or signs and symptoms of infection

105
Q

Biologics route of administraton

A

IV
SQ

106
Q

Adverse effects of biologics

A

Infusion reaction
Immunosuppression
Increased risj of cancer

107
Q

How do you assess the therapeutic effects of IBD medication?

A

Check CBC, CRP, electrolytes, WBC, nutritional labs, and platelets

108
Q

Clinical manifestations of hepatitis

A

Anorexia
Weight loss
Jaundice - bilirubin diffuses into tissues
Dark urine - bilirubin excreted by the kidneys
Light or clay colored stools - bilirubin excreted in feces
Pruritis - accumulation of bile salts below the skin
Increased liver enzymes - ALT and AST

109
Q

What happens in hepatitis?

A

Normally caused by a virus
Diffuse liver inflammation causes necrosis
Altered liver function

110
Q

Hepatitis A

A

Fecal-oral route
Vaccine available
Mild severity
No progression to chronic conditions

111
Q

Hepatitis B

A

Blood-borne, sexual, parenteral, and maternal-neonatal transmission
Vaccine available
Increased risk of cirrhosis and hepatic cancer

112
Q

Hepatitis C

A

Blood-borne, sexual, parenteral, maternal-neonatal transmission
No vaccine available
Increased risk of cirrhosis and hepatic cancer

113
Q

Hepatitis D

A

Parenteral, sexual transmission
Increased risk of cirrhosis
No vaccine available

114
Q

Hepatitis E

A

Fecal oral transmission
Does not result in chronic condition
No vaccine available

115
Q

Goals of hepatitis treatment

A

Minimize infectivity
Minimize liver inflammation
Decrease symptoms

116
Q

What drugs are used to treat hepatitis?

A

Interferon
Oral nucleoside analogues
Polymerase inhibitors

117
Q

MOA of interferon

A

Protein with antiviral, anti proliferative, and immune regulating activity

118
Q

Use of interferon

A

Chronic Hepatitis B and C

119
Q

Interferon route of administration

A

SQ

120
Q

Adverse effects of interferon

A

Flu like symptoms
Bone marrow suppression - neutropenia, anemia, thrombocytopenia

121
Q

Interferon nursing considerations

A

Rotate injection site

122
Q

What drugs are oral nucleoside analogues?

A

Lamivudine
Entecavir
Ledipasvir-sofobuvir

123
Q

MOA of lamivudine

A

Antiretroviral - disrupts viral DNA chain

124
Q

Lamivudine route of administration

A

PO with or without food

125
Q

Adverse effects of lamivudine

A

Pancreatitis
Neuropathy
GI upset
Neutropenia

126
Q

Lamivudine nursing considerations

A

Monitor AST and ALT for therapeutic effects

127
Q

Entecavir MOA

A

Inhibits hep B viral DNA synthesis

128
Q

Entecavir route of administration

A

PO on empty stomach

129
Q

Adverse effects of entecavir

A

Hepatomegaly
Lactic acidosis

130
Q

Ledipasvir-sofobuvir MOA

A

Polymerase inhibitor that inhibits viral replication

131
Q

Adverse effects of ledipasvir-sofobuvir

A

MSK weakness
Myalgia
GI upset
Hep B reactivation

132
Q

What is the drug of choice for Hep C?

A

Ledipasvir-sofobuvir

133
Q

Risk factors for non-alcoholic fatty liver disease

A

Obesity
High cholesterol
Diabetes
Sedentary lifestyle

134
Q

Treatments for NAFLD

A

Vitamin E - can prevent progression
Pioglitazone - improves insulin sensitivity

135
Q

Pathophysiology of liver cirrhosis

A

Regeneration disturbances of liver
Health liver tissue replaced with scar tissue

136
Q

Causes of liver cirrhosis

A

Alcohol consumption
Hepatits B and C
Fatty liver
Chemicals
Medications

137
Q

Clinical manifestations of liver inflammation

A

Abdominal pain
Indigestion
Change in bowel habits

138
Q

Compensated vs decompensated liver cirrhosis

A

Compensated is early and mild - damaged liver is still able to perform normal functions
Decompensated is late stage

139
Q

Clinical manifestations of liver necrosis

A

Jaundice, light colored stools, dark urine - bilirubin
Imbalance of testosterone and estrogen - menstrual abnormalities, gynecomastia, edema
Spider angiomas
Palmar erythema
Increased liver enzymes
Hypoglycemia

140
Q

Clinical manifestations of severe liver fibrosis and scarring

A

Portal hypertension
Ascites
Edema
Splenomegaly
Hepatomegaly
Epistaxis
Muscle wasting
Varices
Mental status changes
Fetor hepaticus - sweet, acetone, or rotten egg breath

141
Q

Complications of cirrhosis

A

Portal hypertension with esophageal varices
Ascites
Hepatic encephalopathy
Peritonitis
Present of these complications means patient is in decompensated stage of cirrhosis

142
Q

Clinical manifestations of portal hypertension

A

Splenomegaly
Varices
Ascites - accumulation of serous fluid in the peritoneal cavity

143
Q

What causes portal hypertension?

A

Obstruction of blood flow through damaged liver

144
Q

What can happen because of ascites?

A

Spontaneous bacterial peritonitis

145
Q

What is hepatic encephalopathy?

A

Neuropsychiatric disorder
Potentially reversible

146
Q

Why does hepatic encephalopathy occur?

A

Liver is unable to detoxify ammonia and it accumulates
Excess ammonia causes digestion of blood proteins and dietary proteins
Ammonia enters the brain and stimulates GABA neurotransmission, which is an inhibitory NT

147
Q

Clinical manifestations of hepatic encephalopathy

A

Day time sleepiness
Awake during night
Confusion
Disorientation
Apraxia
Asterixis
Hyperactive DTRs, then hypoactive and absent

148
Q

Treatment for ascites

A

Low sodium diet
Diuretics
Monitor electrolytes and I/Os
Fluid restriction
Paracentesis

149
Q

Treatment of portal hypertension

A

Avoid NSAIDs, aspirin, and irritating foods
URI treated promptly and coughs controlled
Beta blockers

150
Q

Treatment for hepatic encephalopathy

A

Decrease ammonia
Lactulose
Avoid constipation
Control GI bleed

151
Q

Lactulose MOA

A

Split into lactic acid and acetic acid
Acidic environment decreases bacteria and lactulose expels ammonia through feces

152
Q

Lactulose routes of administration

A

PO
NG
Enema

153
Q

How do you assess the therapeutic effect of lactulose?

A

2-3 soft stools per day
Less confusion
Fever
Tremors
Decrease in ammonia
Decreased liver enzymes

154
Q

Pathophysiology of pancreatitis

A

Activation of powerful enzymes within the liver that normally remain inactive
Enzymes digest the pancreas
Activation of the enzymes results in vasodilation, increased vascular permeability, necrosis, and hemorrhage

155
Q

Causes of pancreatitis

A

Gall stones
Alcohol consumption
Smoking
Pancreatic cysts or tumors
Trauma
Medications - corticosteroids, oral contraceptives

156
Q

Clinical manifestations of pancreatitis

A

Pain in the mid epigastrium and can radiate to the back
Pain is aggravated by eating, drinking alcohol, and supine position
Pain relieved by flexing the spine
Pain unrelieved by antacids and vomiting
Abdominal bruising
Ascites
Inflammation of diaphragm
Fever
N/V
Hyperglycemia
Steatorrhea
Jaundice
Dark urine
Hypocalcemia

157
Q

What is the most common reason patients die from pancreatitis?

A

Shock

158
Q

Goals of pancreatitis treatment

A

NPO
Maintain circulation
Maintain fluid volume
Relieve pain
Decrease pancreatic secretions
Analgesics, antacids, H2RA, antibiotics, insulin

159
Q

Risk factors for pancreatic cancer

A

Cigarette smoking
Exposure to toxins or chemicals
Diet high in fat and/or meat
Diabetes
Chronic pancreatitis
Hereditary pancreatitis

160
Q

Clinical manifestations of pancreatic cancer

A

Progressive and severe pain
Pain more severe at night and aggravated by supine position
Jaundice
Weight loss
Insulin deficiency
Ascites

161
Q

Management of pancreatic cancer

A

Surgery - for localized tumors, whipple procedure
Chemotherapy
Radiation therapy

162
Q

Calculous vs acalculous cholecystitis

A

Calculous occurs with gall stones, acalculous without

163
Q

Causes of acalculous cholecystitis

A

Surgery
Trauna
Burns
Bacterial infections
Cystic duct obstruction

164
Q

Clinical manifestation of cholecystitis

A

RUQ pain
RUQ tenderness and rigidity
Radiating pain to right shoulder or midsternum
N/V
Fatty foods precipitate symptoms

165
Q

Pathophysiology of cholecystitis

A

Chemical reaction initiated by obstructed bile
Gallbladder sludge
Inflammation and edema
Gangrene of gallbladder - removal is only option

166
Q

What is cholelithiasis?

A

Gallbladder stones

167
Q

Pigment stones

A

Increased bilirubin and bile salts
Caused by cirrhosis, hemolysis, and infections
Must be removed surgically

168
Q

Cholesterol stones

A

Decreased bile acid synthesis
Increased cholesterol synthesis
Can be dissolved with medications
Caused by being a women over 40, multiparous, and obese, GI disease, diabetes, oral contraceptives, estrogen

169
Q

Clinical manifestations of cholelithiasis

A

Can be silent, mild GI symptoms
Vague pain in RUQ precipitated by meal rich in fatty foods
Pain with deep inspiration

170
Q

Treatment of cholecystitis and cholelithiasis

A

Control symptoms - N/V, pain
Surgery
Dissolution of gall stones
Low fat diet
Antibiotics
Analgesics

171
Q

What med is used to dissolve gallstones?

A

Ursodeoxycholic acid

172
Q

MOA of ursodeoxycholic acid

A

Reduces liver secretion of cholesterol to decrease cholesterol content of bile and bile stones
Medication helps decrease the size of existing stones, dissolve small stones, and prevent formation of new stones

173
Q

Ursodeoxycholic acid route of administration

A

PO for 6-12 months

174
Q

Adverse effects of deoxycholic acid

A

GI
Back pain

175
Q

Contraindications for ursodeoxycholic acid

A

Don’t use with calcified or bile pigment stones

176
Q

Causes of peritonitis

A

Bacterial infection
GI disease
Injury or trauma
Inflammation from other organs - appendicitis, perforated ulcer, bowel perforation

177
Q

Pathophysiology of peritonitis

A

Gross soiling of the abdominal cavity
Symptoms mimic septic shock
Paralytic ileus

178
Q

Clinical manifestations of peritonitis

A

Fluid in peritoneal cavity
Paralytic ileus
Diffuse pain
Abdominal distention
Abdominal tenderness
Fever
Sepsis

N352 (4 decks)

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