GI Tract Disorders and Drugs Flashcards
What are esophageal varices?
Enlarged tortuous veins in the lower part of the esophagus
Veins are very fragile - rupture causes massive hemorrhage and is a medical emergency
What are two main symptoms of esophageal varices?
Coffee ground emesis
Melena - black tarry stools
Pathophysiology of esophageal varices
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
What is normal venous pressure?
5-10mm Hg
What is portal hypertension level?
over 10mm Hg
What factors can contribute to hemorrhage from esophageal varices?
Lifting heavy objects
Straining at stool
Sneezing, coughing
Irritation of blood vessels by poorly chewed food
Reflex of stomach contents
Alcohol
Medical management of bleeding esophageal varices
ICU admission
Fluid resuscitation - IV
Octreotide - causes selective splanchnic vasoconstriction
Vasopressin - constricts distal esophageal veins
Prevention of bleeding esophageal varices
Patient education on aggravating factors
Beta blockers I.e. Propranolol
Nitrates I.e. isosorbide - decrease risk of bleeding when used with propranolol
Symptoms of an upper GI bleed
Hematemesis
Melena
Where do upper GI bleeds occur?
Above the jejunum
Where do lower GI bleeds occur?
Jejunum and below
Causes of upper GI bleeds
PUD
Varices
Aspirin
NSAIDs
Corticosteroids
Gastric cancer
Causes of lower GI bleeds
Diverticula
Colon cancer
IBD
Hemorrhoids
Fissures
Symptoms of a lower GI bleed
Melena
Hematochezia
Symptoms of chronic GI bleed
Occult or microscopic without visible blood
+ Fecal occult blood test
Causes of chronic GI bleed
Cancer
Ulcers
Complications of GI bleed
Anemia
Hypovolemic shock
What is irritable bowel syndrome?
Functional disorder of intestinal motility - no structural abnormalities
What are the two types of IBS?
IBS-D: diarrhea is main symptom, increased levels of seratonin
IBS-C: constipation is main symptoms, decreased levels of seratonin
Causes of IBS
Exact causes unknown
Genetics
Environmental factors
Psychosocial factors
Food sensitivities
Alterations in intestinal micro-flora
Symptoms of IBS
Chronic abdominal pain
Altered bowel habits
Diarrhea
Constipation
Bloating
Abdominal distension
Pathophysiology of IBS
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
What are the ROME criteria?
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
How do probiotics help with IBS?
Less abdominal pain
Management of diarrhea and constipation
Decrease abdominal bloating and gas
What is the goal of treating IBS?
Symptom management
What lifestyle modifications can be used to treat IBS?
Stress reduction
Sleep
Exercise
Dietary restrictions - identifying triggering foods
What drugs are used to manage IBS-C?
Fiber
Polyethylene-glycol
Lubriprostone
What drugs are used to manage IBS-D?
Alosetron - seratonin antagonist
Rifaximin - non absorbable antibiotic
Eluxadoline - acts on opioid receptors and decreases colonic motility
How do antidepressants treat IBS?
Increase seratonin levels
Improves intestinal transit times and abdominal discomfort
How do anti-spasmodics treat IBS?
Manage abdominal pain - drug of choice
Dicyclomine (Bentyl)
What kind of drug is Dicyclomine?
GI anti-cholinergic
What is dicyclomine used for?
IBS
What form is dicyclomine available in?
PO
IM
Nursing implications for dicyclomine
Ask patient to void before taking
MOA of GI anti-cholinergics
Blocks the effects of acetylcholine
Results in GI smooth muscle relaxation
Adverse effects of dicyclomine
Blurred vision
Dry mouth
Altered taste perception
Urinary retention
What is the appendix?
Narrow, worm-like organ attached to the cecum
Fills with the products of digestion and empties into the cecum
Why is the appendix prone to obstruction and vulnerable to infection?
Empties inefficiently and the lumen is small
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
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
What is the Rovsing sign?
Sign of appendicitis
Pain felt in RLQ after LLQ has been palpated
Where is McBurney’s point?
Between umbilicus and anterior superior iliac spine
Treatments for appendicitis
Appendectomy
Antibiotics
Analgesic pain meds
Cole therapy - heat not recommended, can cause rupture
What is diverticulitis?
Inflammation of diverticula
Where is diverticulitis most common and why?
Sigmoid colon
Narrowest part of the colon
Risk factors for diverticulitis
Obesity
Aging
Smoking
Low fiber diet
Pathophysiology of diverticulitis
Colon herniates, herniations fill with waste and become infected/inflamed
Complications of diverticulitis
Perforation
Abscesses
Fistula
Bowel obstruction
Peritonitis
Bleeding
Clinical manifestations of diverticulities
Can be asymptomatic
Chronic constipation
LLQ pain
Nausea
Fever
Bleeding
Fistulas
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
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
What treatment should not be used for diverticulitis?
Enema
What is a mechanical intestinal obstruction?
There is a detectable reason for the obstruction
Tumors, adhestions, hernia, volvulus, intussception
What is a non mechanical intestinal obstruction?
Suspension of peristalsis, parayltic ileus
Amyloidosis, diabetes, parkinson’s, after surgery, hypokalemia
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
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
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
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
What is FAP and its characteristics?
Familial ademonatous polyposis
100+ polyps
Single gene mutation
What is Lynch syndrome and its characteristics?
No polyps
Several gene mutations
Common symptoms of colorectal cancer
Change in bowel habit
Blood in stool
Anemia
Weight loss
Fatigue
Pathophysiology of colorectal cancer
Adenocarcinoma - starts as benign polyp and destroys normal cells
Signs of right sided colon cancer
Abdominal pain
Melena
Signs of left sided colon cancer
Abdominal pain
Constipation and distension
Passage of fresh blood from rectum
Signs of rectal cancer
Rectal pain
Bloody stool
Alternating between diarrhea and constipation
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
What are the two kinds of IBD?
Crohn’s Disease
Ulcerative colities
What are the inflammatory cytokines involved in IBD?
CRP - C reactive protein
IL - interleukins
TNFA - tumor necrosis factor alpha
What part of the intestinal tract can Crohn’s disease affect?
Any part - mouth to anus
Which layers of the GI tract are involved in Crohn’s disease?
All 4 - mucosa, submucosa, muscular layer, and serosa
Complications of Crohn’s disease
Fistula
Intestinal obstruction
Abscesses
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
What part of the GI tract does UC occur in?
Colon and rectum
What layers of the GI tract does UC effect?
Superficial layers - mucosa and submucosa
How do ulcers appear in UC?
Continous
Clinical manifestations of UC
Profound bleeding
Bloody diarrhea 10-12x/day
Severe abdominal cramps
Complications of UC
Perforated bowel
Toxic megacolon
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
What drugs are used to treat mild IBD?
Topical corticosteroids
Antibiotics
5-ASAs
What drugs are used to treat moderate IBD?
Immunomodulators
Oral corticosteroids
What is used to treat severe IBD?
Surgery
Biologics
What drugs are 5-ASAs?
Sulfasalazine
Mesalamine
MOA of 5-ASAs
Reduce inflammation locally in the lining of the intestine
Sulfasalazine route of administration
PO
Mesalamine route of administration
PO, PR
Adverse effects of sulfasalazine
Decreased sperm production
SJS
Adverse effects of mesalamine
Pancreatitis
What is the main difference between sulfasalazine and mesalamine?
Sulfasalazine has sulfa, mesalamine does not
MOA of corticosteroids
Fast acting inflammatory effect
Use of corticosteroids
Short term treatment for acute IBD
Corticosteroids routes of administration
PO
IV
Foam
Liquid enemas
Adverse effects of corticosteroids
Immunosuppression
Bone loss
Weight gain
Mood swings
Hypertension
Hypergylcemia
Do corticosteroids have a specific target on the immune system?
No
MOA of immunomodulators
Modify the body’s immune system so that it can’t cause ongoing inflammation
Immunomodulators routes of administration
PO
IV
Use of immunomodulators
Maintain remission in those who haven’t responded to other therapies
Decreases the long term need for steroids
Adverse effects of immunomodulators
GI
Hepatotoxicity
Nephrotoxicity
Infections
Lymphoma
Patient education for immunomodulators
Get regular vaccines
Avoid live vaccines
Get liver and renal systems monitored regularly
Report ant fever, chills, or sore throat
How long do immunomodulators take to work?
6-8 weeks
Which drugs are corticosteroids?
Budesonide
Prednisone
Which drugs are immunomodulators?
Azathioprine
Mercapropurine
Methotrexate
Cyclosporine
Which drugs are biologics?
Infliximab
Adalimumab
Cerolizumab
MOA of biologics
Inhibit pro-inflammatory cytokines and repress inflammatory response
Patient education for biologics
Get all annual vaccines
Get evaluated for TB annually
Report fever, new cough, or signs and symptoms of infection
Biologics route of administraton
IV
SQ
Adverse effects of biologics
Infusion reaction
Immunosuppression
Increased risj of cancer
How do you assess the therapeutic effects of IBD medication?
Check CBC, CRP, electrolytes, WBC, nutritional labs, and platelets
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
What happens in hepatitis?
Normally caused by a virus
Diffuse liver inflammation causes necrosis
Altered liver function
Hepatitis A
Fecal-oral route
Vaccine available
Mild severity
No progression to chronic conditions
Hepatitis B
Blood-borne, sexual, parenteral, and maternal-neonatal transmission
Vaccine available
Increased risk of cirrhosis and hepatic cancer
Hepatitis C
Blood-borne, sexual, parenteral, maternal-neonatal transmission
No vaccine available
Increased risk of cirrhosis and hepatic cancer
Hepatitis D
Parenteral, sexual transmission
Increased risk of cirrhosis
No vaccine available
Hepatitis E
Fecal oral transmission
Does not result in chronic condition
No vaccine available
Goals of hepatitis treatment
Minimize infectivity
Minimize liver inflammation
Decrease symptoms
What drugs are used to treat hepatitis?
Interferon
Oral nucleoside analogues
Polymerase inhibitors
MOA of interferon
Protein with antiviral, anti proliferative, and immune regulating activity
Use of interferon
Chronic Hepatitis B and C
Interferon route of administration
SQ
Adverse effects of interferon
Flu like symptoms
Bone marrow suppression - neutropenia, anemia, thrombocytopenia
Interferon nursing considerations
Rotate injection site
What drugs are oral nucleoside analogues?
Lamivudine
Entecavir
Ledipasvir-sofobuvir
MOA of lamivudine
Antiretroviral - disrupts viral DNA chain
Lamivudine route of administration
PO with or without food
Adverse effects of lamivudine
Pancreatitis
Neuropathy
GI upset
Neutropenia
Lamivudine nursing considerations
Monitor AST and ALT for therapeutic effects
Entecavir MOA
Inhibits hep B viral DNA synthesis
Entecavir route of administration
PO on empty stomach
Adverse effects of entecavir
Hepatomegaly
Lactic acidosis
Ledipasvir-sofobuvir MOA
Polymerase inhibitor that inhibits viral replication
Adverse effects of ledipasvir-sofobuvir
MSK weakness
Myalgia
GI upset
Hep B reactivation
What is the drug of choice for Hep C?
Ledipasvir-sofobuvir
Risk factors for non-alcoholic fatty liver disease
Obesity
High cholesterol
Diabetes
Sedentary lifestyle
Treatments for NAFLD
Vitamin E - can prevent progression
Pioglitazone - improves insulin sensitivity
Pathophysiology of liver cirrhosis
Regeneration disturbances of liver
Health liver tissue replaced with scar tissue
Causes of liver cirrhosis
Alcohol consumption
Hepatits B and C
Fatty liver
Chemicals
Medications
Clinical manifestations of liver inflammation
Abdominal pain
Indigestion
Change in bowel habits
Compensated vs decompensated liver cirrhosis
Compensated is early and mild - damaged liver is still able to perform normal functions
Decompensated is late stage
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
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
Complications of cirrhosis
Portal hypertension with esophageal varices
Ascites
Hepatic encephalopathy
Peritonitis
Present of these complications means patient is in decompensated stage of cirrhosis
Clinical manifestations of portal hypertension
Splenomegaly
Varices
Ascites - accumulation of serous fluid in the peritoneal cavity
What causes portal hypertension?
Obstruction of blood flow through damaged liver
What can happen because of ascites?
Spontaneous bacterial peritonitis
What is hepatic encephalopathy?
Neuropsychiatric disorder
Potentially reversible
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
Clinical manifestations of hepatic encephalopathy
Day time sleepiness
Awake during night
Confusion
Disorientation
Apraxia
Asterixis
Hyperactive DTRs, then hypoactive and absent
Treatment for ascites
Low sodium diet
Diuretics
Monitor electrolytes and I/Os
Fluid restriction
Paracentesis
Treatment of portal hypertension
Avoid NSAIDs, aspirin, and irritating foods
URI treated promptly and coughs controlled
Beta blockers
Treatment for hepatic encephalopathy
Decrease ammonia
Lactulose
Avoid constipation
Control GI bleed
Lactulose MOA
Split into lactic acid and acetic acid
Acidic environment decreases bacteria and lactulose expels ammonia through feces
Lactulose routes of administration
PO
NG
Enema
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
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
Causes of pancreatitis
Gall stones
Alcohol consumption
Smoking
Pancreatic cysts or tumors
Trauma
Medications - corticosteroids, oral contraceptives
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
What is the most common reason patients die from pancreatitis?
Shock
Goals of pancreatitis treatment
NPO
Maintain circulation
Maintain fluid volume
Relieve pain
Decrease pancreatic secretions
Analgesics, antacids, H2RA, antibiotics, insulin
Risk factors for pancreatic cancer
Cigarette smoking
Exposure to toxins or chemicals
Diet high in fat and/or meat
Diabetes
Chronic pancreatitis
Hereditary pancreatitis
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
Management of pancreatic cancer
Surgery - for localized tumors, whipple procedure
Chemotherapy
Radiation therapy
Calculous vs acalculous cholecystitis
Calculous occurs with gall stones, acalculous without
Causes of acalculous cholecystitis
Surgery
Trauna
Burns
Bacterial infections
Cystic duct obstruction
Clinical manifestation of cholecystitis
RUQ pain
RUQ tenderness and rigidity
Radiating pain to right shoulder or midsternum
N/V
Fatty foods precipitate symptoms
Pathophysiology of cholecystitis
Chemical reaction initiated by obstructed bile
Gallbladder sludge
Inflammation and edema
Gangrene of gallbladder - removal is only option
What is cholelithiasis?
Gallbladder stones
Pigment stones
Increased bilirubin and bile salts
Caused by cirrhosis, hemolysis, and infections
Must be removed surgically
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
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
Treatment of cholecystitis and cholelithiasis
Control symptoms - N/V, pain
Surgery
Dissolution of gall stones
Low fat diet
Antibiotics
Analgesics
What med is used to dissolve gallstones?
Ursodeoxycholic acid
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
Ursodeoxycholic acid route of administration
PO for 6-12 months
Adverse effects of deoxycholic acid
GI
Back pain
Contraindications for ursodeoxycholic acid
Don’t use with calcified or bile pigment stones
Causes of peritonitis
Bacterial infection
GI disease
Injury or trauma
Inflammation from other organs - appendicitis, perforated ulcer, bowel perforation
Pathophysiology of peritonitis
Gross soiling of the abdominal cavity
Symptoms mimic septic shock
Paralytic ileus
Clinical manifestations of peritonitis
Fluid in peritoneal cavity
Paralytic ileus
Diffuse pain
Abdominal distention
Abdominal tenderness
Fever
Sepsis
