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
What is the goal of treating IBS?
Symptom management
26
What lifestyle modifications can be used to treat IBS?
Stress reduction Sleep Exercise Dietary restrictions - identifying triggering foods
27
What drugs are used to manage IBS-C?
Fiber Polyethylene-glycol Lubriprostone
28
What drugs are used to manage IBS-D?
Alosetron - seratonin antagonist Rifaximin - non absorbable antibiotic Eluxadoline - acts on opioid receptors and decreases colonic motility
29
How do antidepressants treat IBS?
Increase seratonin levels Improves intestinal transit times and abdominal discomfort
30
How do anti-spasmodics treat IBS?
Manage abdominal pain - drug of choice Dicyclomine (Bentyl)
31
What kind of drug is Dicyclomine?
GI anti-cholinergic
32
What is dicyclomine used for?
IBS
33
What form is dicyclomine available in?
PO IM
34
Nursing implications for dicyclomine
Ask patient to void before taking
35
MOA of GI anti-cholinergics
Blocks the effects of acetylcholine Results in GI smooth muscle relaxation
36
Adverse effects of dicyclomine
Blurred vision Dry mouth Altered taste perception Urinary retention
37
What is the appendix?
Narrow, worm-like organ attached to the cecum Fills with the products of digestion and empties into the cecum
38
Why is the appendix prone to obstruction and vulnerable to infection?
Empties inefficiently and the lumen is small
39
Pathophysiology of appendicitis
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
40
Clinical manifestations of appendicitis
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
41
What is the Rovsing sign?
Sign of appendicitis Pain felt in RLQ after LLQ has been palpated
42
Where is McBurney's point?
Between umbilicus and anterior superior iliac spine
43
Treatments for appendicitis
Appendectomy Antibiotics Analgesic pain meds Cole therapy - heat not recommended, can cause rupture
44
What is diverticulitis?
Inflammation of diverticula
45
Where is diverticulitis most common and why?
Sigmoid colon Narrowest part of the colon
46
Risk factors for diverticulitis
Obesity Aging Smoking Low fiber diet
47
Pathophysiology of diverticulitis
Colon herniates, herniations fill with waste and become infected/inflamed
48
Complications of diverticulitis
Perforation Abscesses Fistula Bowel obstruction Peritonitis Bleeding
49
Clinical manifestations of diverticulities
Can be asymptomatic Chronic constipation LLQ pain Nausea Fever Bleeding Fistulas
50
What are the two surgical methods to manage diverticulitis?
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
51
How is diverticulitis managed?
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
52
What treatment should not be used for diverticulitis?
Enema
53
What is a mechanical intestinal obstruction?
There is a detectable reason for the obstruction Tumors, adhestions, hernia, volvulus, intussception
54
What is a non mechanical intestinal obstruction?
Suspension of peristalsis, parayltic ileus Amyloidosis, diabetes, parkinson's, after surgery, hypokalemia
55
Pathophysiology of intestinal obstructions
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
56
Clinical manifestations of intestinal obstruction
Negativ BM and flatus N/V Metabolic alkalosis Electrolyte depletion Crampy and wavelike abdominal pain Abdomen feels like a rock
57
Management of intestinal obstruction
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
58
Risk factors for colorectal cancer
Smoking Alcohol Low fiber diet and high intake of beef Aging Obesity H/O IBD and diabetes H/O genital cancer Family history
59
What is FAP and its characteristics?
Familial ademonatous polyposis 100+ polyps Single gene mutation
60
What is Lynch syndrome and its characteristics?
No polyps Several gene mutations
61
Common symptoms of colorectal cancer
Change in bowel habit Blood in stool Anemia Weight loss Fatigue
62
Pathophysiology of colorectal cancer
Adenocarcinoma - starts as benign polyp and destroys normal cells
63
Signs of right sided colon cancer
Abdominal pain Melena
64
Signs of left sided colon cancer
Abdominal pain Constipation and distension Passage of fresh blood from rectum
65
Signs of rectal cancer
Rectal pain Bloody stool Alternating between diarrhea and constipation
66
Pathophysiology of IBD
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
67
What are the two kinds of IBD?
Crohn's Disease Ulcerative colities
68
What are the inflammatory cytokines involved in IBD?
CRP - C reactive protein IL - interleukins TNFA - tumor necrosis factor alpha
69
What part of the intestinal tract can Crohn's disease affect?
Any part - mouth to anus
70
Which layers of the GI tract are involved in Crohn's disease?
All 4 - mucosa, submucosa, muscular layer, and serosa
71
Complications of Crohn's disease
Fistula Intestinal obstruction Abscesses
72
What happens in the GI tract in Crohn's disease?
Microscopic or crypt inflammation Ulcers that look like cobblestones Skip lesions Thickening and fibrosis of bowel wall, narrowing of bowel lumen
73
What part of the GI tract does UC occur in?
Colon and rectum
74
What layers of the GI tract does UC effect?
Superficial layers - mucosa and submucosa
75
How do ulcers appear in UC?
Continous
76
Clinical manifestations of UC
Profound bleeding Bloody diarrhea 10-12x/day Severe abdominal cramps
77
Complications of UC
Perforated bowel Toxic megacolon
78
Clinical manifestations of IBD
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
What drugs are used to treat mild IBD?
Topical corticosteroids Antibiotics 5-ASAs
80
What drugs are used to treat moderate IBD?
Immunomodulators Oral corticosteroids
81
What is used to treat severe IBD?
Surgery Biologics
82
What drugs are 5-ASAs?
Sulfasalazine Mesalamine
83
MOA of 5-ASAs
Reduce inflammation locally in the lining of the intestine
84
Sulfasalazine route of administration
PO
85
Mesalamine route of administration
PO, PR
86
Adverse effects of sulfasalazine
Decreased sperm production SJS
87
Adverse effects of mesalamine
Pancreatitis
88
What is the main difference between sulfasalazine and mesalamine?
Sulfasalazine has sulfa, mesalamine does not
89
MOA of corticosteroids
Fast acting inflammatory effect
90
Use of corticosteroids
Short term treatment for acute IBD
91
Corticosteroids routes of administration
PO IV Foam Liquid enemas
92
Adverse effects of corticosteroids
Immunosuppression Bone loss Weight gain Mood swings Hypertension Hypergylcemia
93
Do corticosteroids have a specific target on the immune system?
No
94
MOA of immunomodulators
Modify the body's immune system so that it can't cause ongoing inflammation
95
Immunomodulators routes of administration
PO IV
96
Use of immunomodulators
Maintain remission in those who haven't responded to other therapies Decreases the long term need for steroids
97
Adverse effects of immunomodulators
GI Hepatotoxicity Nephrotoxicity Infections Lymphoma
98
Patient education for immunomodulators
Get regular vaccines Avoid live vaccines Get liver and renal systems monitored regularly Report ant fever, chills, or sore throat
99
How long do immunomodulators take to work?
6-8 weeks
100
Which drugs are corticosteroids?
Budesonide Prednisone
101
Which drugs are immunomodulators?
Azathioprine Mercapropurine Methotrexate Cyclosporine
102
Which drugs are biologics?
Infliximab Adalimumab Cerolizumab
103
MOA of biologics
Inhibit pro-inflammatory cytokines and repress inflammatory response
104
Patient education for biologics
Get all annual vaccines Get evaluated for TB annually Report fever, new cough, or signs and symptoms of infection
105
Biologics route of administraton
IV SQ
106
Adverse effects of biologics
Infusion reaction Immunosuppression Increased risj of cancer
107
How do you assess the therapeutic effects of IBD medication?
Check CBC, CRP, electrolytes, WBC, nutritional labs, and platelets
108
Clinical manifestations of hepatitis
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
What happens in hepatitis?
Normally caused by a virus Diffuse liver inflammation causes necrosis Altered liver function
110
Hepatitis A
Fecal-oral route Vaccine available Mild severity No progression to chronic conditions
111
Hepatitis B
Blood-borne, sexual, parenteral, and maternal-neonatal transmission Vaccine available Increased risk of cirrhosis and hepatic cancer
112
Hepatitis C
Blood-borne, sexual, parenteral, maternal-neonatal transmission No vaccine available Increased risk of cirrhosis and hepatic cancer
113
Hepatitis D
Parenteral, sexual transmission Increased risk of cirrhosis No vaccine available
114
Hepatitis E
Fecal oral transmission Does not result in chronic condition No vaccine available
115
Goals of hepatitis treatment
Minimize infectivity Minimize liver inflammation Decrease symptoms
116
What drugs are used to treat hepatitis?
Interferon Oral nucleoside analogues Polymerase inhibitors
117
MOA of interferon
Protein with antiviral, anti proliferative, and immune regulating activity
118
Use of interferon
Chronic Hepatitis B and C
119
Interferon route of administration
SQ
120
Adverse effects of interferon
Flu like symptoms Bone marrow suppression - neutropenia, anemia, thrombocytopenia
121
Interferon nursing considerations
Rotate injection site
122
What drugs are oral nucleoside analogues?
Lamivudine Entecavir Ledipasvir-sofobuvir
123
MOA of lamivudine
Antiretroviral - disrupts viral DNA chain
124
Lamivudine route of administration
PO with or without food
125
Adverse effects of lamivudine
Pancreatitis Neuropathy GI upset Neutropenia
126
Lamivudine nursing considerations
Monitor AST and ALT for therapeutic effects
127
Entecavir MOA
Inhibits hep B viral DNA synthesis
128
Entecavir route of administration
PO on empty stomach
129
Adverse effects of entecavir
Hepatomegaly Lactic acidosis
130
Ledipasvir-sofobuvir MOA
Polymerase inhibitor that inhibits viral replication
131
Adverse effects of ledipasvir-sofobuvir
MSK weakness Myalgia GI upset Hep B reactivation
132
What is the drug of choice for Hep C?
Ledipasvir-sofobuvir
133
Risk factors for non-alcoholic fatty liver disease
Obesity High cholesterol Diabetes Sedentary lifestyle
134
Treatments for NAFLD
Vitamin E - can prevent progression Pioglitazone - improves insulin sensitivity
135
Pathophysiology of liver cirrhosis
Regeneration disturbances of liver Health liver tissue replaced with scar tissue
136
Causes of liver cirrhosis
Alcohol consumption Hepatits B and C Fatty liver Chemicals Medications
137
Clinical manifestations of liver inflammation
Abdominal pain Indigestion Change in bowel habits
138
Compensated vs decompensated liver cirrhosis
Compensated is early and mild - damaged liver is still able to perform normal functions Decompensated is late stage
139
Clinical manifestations of liver necrosis
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
Clinical manifestations of severe liver fibrosis and scarring
Portal hypertension Ascites Edema Splenomegaly Hepatomegaly Epistaxis Muscle wasting Varices Mental status changes Fetor hepaticus - sweet, acetone, or rotten egg breath
141
Complications of cirrhosis
Portal hypertension with esophageal varices Ascites Hepatic encephalopathy Peritonitis Present of these complications means patient is in decompensated stage of cirrhosis
142
Clinical manifestations of portal hypertension
Splenomegaly Varices Ascites - accumulation of serous fluid in the peritoneal cavity
143
What causes portal hypertension?
Obstruction of blood flow through damaged liver
144
What can happen because of ascites?
Spontaneous bacterial peritonitis
145
What is hepatic encephalopathy?
Neuropsychiatric disorder Potentially reversible
146
Why does hepatic encephalopathy occur?
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
Clinical manifestations of hepatic encephalopathy
Day time sleepiness Awake during night Confusion Disorientation Apraxia Asterixis Hyperactive DTRs, then hypoactive and absent
148
Treatment for ascites
Low sodium diet Diuretics Monitor electrolytes and I/Os Fluid restriction Paracentesis
149
Treatment of portal hypertension
Avoid NSAIDs, aspirin, and irritating foods URI treated promptly and coughs controlled Beta blockers
150
Treatment for hepatic encephalopathy
Decrease ammonia Lactulose Avoid constipation Control GI bleed
151
Lactulose MOA
Split into lactic acid and acetic acid Acidic environment decreases bacteria and lactulose expels ammonia through feces
152
Lactulose routes of administration
PO NG Enema
153
How do you assess the therapeutic effect of lactulose?
2-3 soft stools per day Less confusion Fever Tremors Decrease in ammonia Decreased liver enzymes
154
Pathophysiology of pancreatitis
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
Causes of pancreatitis
Gall stones Alcohol consumption Smoking Pancreatic cysts or tumors Trauma Medications - corticosteroids, oral contraceptives
156
Clinical manifestations of pancreatitis
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
What is the most common reason patients die from pancreatitis?
Shock
158
Goals of pancreatitis treatment
NPO Maintain circulation Maintain fluid volume Relieve pain Decrease pancreatic secretions Analgesics, antacids, H2RA, antibiotics, insulin
159
Risk factors for pancreatic cancer
Cigarette smoking Exposure to toxins or chemicals Diet high in fat and/or meat Diabetes Chronic pancreatitis Hereditary pancreatitis
160
Clinical manifestations of pancreatic cancer
Progressive and severe pain Pain more severe at night and aggravated by supine position Jaundice Weight loss Insulin deficiency Ascites
161
Management of pancreatic cancer
Surgery - for localized tumors, whipple procedure Chemotherapy Radiation therapy
162
Calculous vs acalculous cholecystitis
Calculous occurs with gall stones, acalculous without
163
Causes of acalculous cholecystitis
Surgery Trauna Burns Bacterial infections Cystic duct obstruction
164
Clinical manifestation of cholecystitis
RUQ pain RUQ tenderness and rigidity Radiating pain to right shoulder or midsternum N/V Fatty foods precipitate symptoms
165
Pathophysiology of cholecystitis
Chemical reaction initiated by obstructed bile Gallbladder sludge Inflammation and edema Gangrene of gallbladder - removal is only option
166
What is cholelithiasis?
Gallbladder stones
167
Pigment stones
Increased bilirubin and bile salts Caused by cirrhosis, hemolysis, and infections Must be removed surgically
168
Cholesterol stones
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
Clinical manifestations of cholelithiasis
Can be silent, mild GI symptoms Vague pain in RUQ precipitated by meal rich in fatty foods Pain with deep inspiration
170
Treatment of cholecystitis and cholelithiasis
Control symptoms - N/V, pain Surgery Dissolution of gall stones Low fat diet Antibiotics Analgesics
171
What med is used to dissolve gallstones?
Ursodeoxycholic acid
172
MOA of ursodeoxycholic acid
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
Ursodeoxycholic acid route of administration
PO for 6-12 months
174
Adverse effects of deoxycholic acid
GI Back pain
175
Contraindications for ursodeoxycholic acid
Don't use with calcified or bile pigment stones
176
Causes of peritonitis
Bacterial infection GI disease Injury or trauma Inflammation from other organs - appendicitis, perforated ulcer, bowel perforation
177
Pathophysiology of peritonitis
Gross soiling of the abdominal cavity Symptoms mimic septic shock Paralytic ileus
178
Clinical manifestations of peritonitis
Fluid in peritoneal cavity Paralytic ileus Diffuse pain Abdominal distention Abdominal tenderness Fever Sepsis