NSG 3040: GI Alterations | 81 questions with complete verified solutions | 100% Accuracy

PUD

stress related erosive syndrome

esophageal varices

what are examples of causes of acute upper GI bleeds?

Primary factor is H. pylori, ingestion of ASA, NSAIDs, smoking (erodes stomach lining), prolonged antibiotic/PPI/H2 blocker use

causes of PUD:

Decreased perfusion of stomach mucosa, related to physiologic stress

- increased gastric acid (especially when stressed with no food)

causes of stress-related erosive syndrome:

Collateral circulation as a result of portal hypertension, rising pressure causes tortuous distended veins or varices

causes of esophageal varices:

diverticulosis

angiodysplasia/AV malfunction

IBD

causes of acute lower GI bleeds:

Sac-like protrusions in the colon; arteries are prone to injury.

Risk factors: diet low in fiber, ASA/NSAIDs, advanced age, and constipation

- pts should avoid popcorn, etc. - seeds get caught and cause perforation

definition and causes of diverticulosis:

Dilated, tortuous submucosal veins, small AV communications, or enlarged arteries (fragile, may burst)

Occurs anywhere in the colon and can be venous or arterial bleed

definition and causes of angiodysplasia/AV malfunction:

(irritable bowel disease)

- chron's

- ulcerative colitis (inflammatory)

causes of IBD:

mouth to opening of pylorus (after stomach)

where does the upper GI tract stretch from?

opening of pylorus to rectum

where does the lower GI tract stretch from?

- hx (food habits)

- physical exam

- History of PUD, dyspepsia, alcohol, smoking, vomiting/retching, NSAIDs or ASA

- Hemodynamic stability, VS, orthostatics, tissue perfusion, LOC

- abdominal /rectal exam (we will not perform rectal exam, assist - pt lying on left side)

what are things that should be included in the upper GI tract assessment?

- hx

- physical exam

- Peptic ulcer disease, inflammatory bowel disease, renal/liver disease (72 hour dietary recall and present symptoms)

- Medication, color and consistency of stool, abdominal pain, fever, rectal urgency, weight loss (smell, color, size)

- changes in bowel habits

- VS (esp BP), palpable mass, rectal exam

what are things that should be included in the lower GI tract assessment?

Low H & H

Mild leukocytosis and hyperglycemia

High BUN (inadequate kidney perfusion)

Hypernatremia, hypokalemia (diarrhea/vomiting, loss of water)

Prolonged PT/PTT

Thrombocytopenia (decreased platelets, increased bleeding)

Hypoxemia

CBC

Electrolytes

BUN and creatinine

PT/PTT

Type and cross-match

what are examples of GI lab studies?

Presentation depends on the amount of blood loss.

Slight anemia to shock

Orthostatic changes imply volume depletion of 15% or more.

Hallmark of GIB is hematemesis, hematochezia, and melena.

- changes in RBC, rectal bleeding, blood in stool

Upper GIB—hematemesis, "coffee ground," melena

- irregular coagulation with blood

what is the clinical presentation of a pt with an upper GI bleed?

Hemodynamic instability and hematochezia

Diverticular bleeding is often painless, may complain of cramping.

Angiodysplasia presents with painless hematochezia.

Chronic lower GIB presents with iron deficiency anemia.

- black tarry stool, stool coated/mixed with bright red

Hemorrhoids can present with massive bleeding from rectal varices from portal hypertension.

esophageal varices - MEDICAL EMERGENCY

what is the clinical presentation of a pt with a lower GI bleed?

Volume resuscitation with IVF or blood products, vasopressors

Oxygen, central line

NPO, NGT

Electrolyte repletion

Acid-suppressive therapy—PPIs or H2 antagonistic drugs (pepcid, etc)

- associated with PU, h.pylori

Pharmacotherapy for decreasing portal hypertension (Vasopressin, octreotide [IV meds, clamps down vessels to stop internal bleeding] , somatostatin, beta blocker [reduce vascular pressure to decrease bleeding])

no alcohol

management of upper GI bleeds:

Fluid resuscitation, NGT

Colonoscopy for diagnosis and treatment

Upper endoscopy distinguishes the source.

Radionucleotide imaging—locates the site of bleed

Angiography—for diagnosis and embolization

Surgical intervention (Exploratory lap, segmental bowel resection, total colectomy)

no alcohol

management of lower GI bleeds:

-iliostomy: reversible, watery stool (fluid loss, K)

stoma site red at first, then pink

- colostomy: more formed, still fluid intake (we dont want stool to be too solid and block)

stool and ostomy placement:

Endoscopy within 12 to 24 hours to identify the site

Can be done at bedside

Angiography—locates the site or abnormal vasculature, insensitive in venous bleeding

Barium studies are often inconclusive, and risk of retained barium

definitive diagnosis of GI bleeds:

Endoscopy—hemostasis 90% of cases but 25% of high-risk sites may rebleed (can locally apply vasopressor, balloon tamponade, diversion, etc)

Angiography

Balloon tamponade—with esophageal varices

Transjugular intrahepatic portosystemic shunt (TIPS)

Surgery (uncontrolled variceal hemorrhage that doesnt respond to endoscopic/medical treatment)

- Rarely indicated; severe hemorrhage unresponsive to initial resuscitation, unavailable/failed endoscopy, perforation, obstruction, malignancy

Hypovolemic shock: mod. trendelenburg, vasopressor

therapeutic intervetnion GI bleeds:

pancreatic duct becomes obstructed, and enzymes back up, causing autodigestion and inflammation of the pancreas

- pancreas dissolves itself, autodigestion

- smelling food and eating food makes it worse - increased pancreatic juices and increased pain

acute pancreatitis:

progressive inflammatory disorder with destruction of the pancreas; cells are replaced by fibrous tissue; pressure within the pancreas increases, obstructing the pancreatic and common bile ducts

- too much alcohol, bad diet, scar tissue formation, etc

- abdominal pain, back pain - occurs after a heavy meal, distention

HIGH AMYLASE / LIPASE - upper abdominal pain

chronic pancreatitis:

- acute pain

- ineffective breathing pattern (atelectasis, painful to take big deep breaths, inflammatory chemicals secreted -> ARDS)

- imbalanced nutrition (NPO -> TPN to bypass GI tract, avoid pancreas)

- impaired skin integrity, can barely move

- potential kidney failure

acute pancreatitis:

Fluid and electrolyte disturbances

Necrosis of the pancreas

Shock - fluid shifts -> hypovolemic shock -> MODS, DIC

Multiple organ dysfunction syndrome

DIC

chronic pancreatitis: DM, malabsorption, pseudocyst, etc

potential complications for pancreatitis:

whipple procedure

pancreatoduodenectomy

- takes out large portion of the duodenum

- removes head of pancreas, first part of small intestine (duodenum), gallbladder, and bile duct

- primarily for pancreatic cancer

- massive invasive procedure

- prevents metastis, more palliative to cancer pts

whipple procedure:

carries bile, helps digest fat/protein, hormones to manage blood sugar

pancreas fxn:

- complications: hemorrhage, FV imbalance, ventilation issues

- TPN, NG (salem sump)-suction air frequently

- lack of B12 absorption

- watch for dumping syndrome

- NPO until peristalsis

- small, frequent meals- no water until after meal

- sit upright for 20-30 minutes after meals

care for a pt with a whipple:

PNS - stomach dumps food to small intestine too fast

- hypotension, bradycardia, syncope

dumping syndrome:

NOTE DRAINAGE:

- over 200 ml bloody drianage: notify surgeon

- some bleeding expected

NG TUBE

- pulls out excess air, gastric juices

- preserved mucosal lining

- blood -> pink serosanginous -> serous (no RBCs)

care for multiple sumps after pancreatic surgery:

Liver failure occurs when large parts of the liver become damaged beyond repair and the liver is no longer able to function (has regenernative properties)

Liver failure is a life-threatening condition that demands urgent medical care.

Most often, chronic liver failure occurs gradually and over many years.

- alcohol, hep, >4g tylenol consistently, etc

However, a more rare condition known as acute liver failure occurs rapidly (in as little as 48 hours) and can be difficult to detect initially.

when does liver failure occur?

Acetaminophen (Tylenol) overdose.

Viruses including hepatitis A, B, and C (especially in children).

Reactions to certain prescription and herbal medications.

Ingestion of poisonous wild mushrooms.

etiology of acute liver failure:

Hepatitis B

Hepatitis C

Long term alcohol consumption

Cirrhosis

Hemochromatosis (an inherited disorder that causes the body to absorb and store too much iron)

Malnutrition

etiology of chronic liver failure:

Jaundice

Nutritional deficiencies

Nausea

Loss of appetite

Fatigue

Diarrhea

Ascites

Sleepiness

urgent (but not fatal) manifestations of liver failure:

Portal hypertension

Esophageal varies

Increase propensity for bleeding

- liver is a dense, bloody, solid organ that helps produce clotting factors

Hepatic encephalopathy

- caused by a buildup of toxins (ammonia)

Coma

life threatening manifestations of liver failure:

Clotting factors

Serum alkaline phosphatase

Serum ammonia

Lipids

Serum aminotransferase: AST, ALT, GGT, GGTP, LDH

Serum protein studies (liver metabolizes protein)

Direct and indirect serum bilirubin, urine bilirubin, and urine bilirubin and urobilinogen

liver function studies:

Liver biopsy ( at risk for bleeding -> watch for abdominal girth growth -PRONE POSITION)

Ultrasonography

CT

MRI

Other

additional diagnostic studies for liver failure:

- hepatic encelopathy

- brain edema

- IC HTN

- immunoparesis

- neutrophil dysfunction

- systemic inflammatory response

- muscle catabolism

- renal dysfunction

- adrenal insufficiency

- pancreatitis

- portal HTN

- ileus

- endothelial dysfunction

- cardiovascular collapse

- acute lung injury

- ARDS

systemic manifestations of acute liver failure:

Focus: onset of symptoms, history of precipitating factors

Alcohol use or abuse

Drug use and sexual history

Dietary intake and nutritional status

Exposure to toxic agents and drugs

Assess changes in mental status, ADL and IADLs, job and social relationships

Monitor signs and symptoms related to bleeding; changes in fluid volume and laboratory data

hepatic failure assessment:

Activity intolerance

Imbalanced nutrition

Impaired skin integrity

Risk for injury

Risk for bleeding

hepatic failure diagnosis:

Goals may include

increased participation in activities

improvement of nutritional status

improvement of skin integrity (may be inhibited by uremic frost: flakey itchy skin, leaking of toxins through the pores)

- nail care

- tepid baths

decreased potential for injury

improvement of mental status

absence of complications

planning and goals for hepatic failure:

ammonia to brain -> coma, fights, unable to follow commands, lethargic (seems drunk)

- lactulose (only given through GI tract )

- induces diarrhea to rid body of ammonia

- electrolyte labs Q4H

improvement of mental status for hepatic failure pts:

Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes.

A and E: fecal-oral route

B and C: bloodborne

D: only people with hepatitis B are at risk

Hepatitis G and GB virus-C

Nonviral hepatitis: toxic and drug induced

hepatitis types:

Spread by poor hand hygiene; fecal-oral

Illness may last 4 to 8 weeks

Mortality rate is 0.5% for those younger than age 40 years and 1% to 2% for those older than age 40 years

Manifestations: mild flulike symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen

what is hepatitis A?

Prevention

Good handwashing, safe water, and proper sewage disposal

Vaccine

Immunoglobulin for contacts to provide passive immunity

Bed rest during acute stage

Nutritional support

- should dissipate in 4-8 weeks, but can cause liver failure

treatment for hepatitis A:

Transmitted through blood, saliva, semen, and vaginal secretions; sexually transmitted; transmitted to infant at the time of birth

A major worldwide cause of cirrhosis and liver cancer

Manifestations: insidious and variable; similar to hepatitis A

what is hepatitis B?

Medications for chronic hepatitis type B include alpha interferon and antiviral agents: lamivudine (Epivir), adefovir (Hepsera)

Bed rest and nutritional support

Vaccine: for persons at high risk, routine vaccination of infants

Passive immunization for those exposed

Standard precautions and infection control measures

Screening of blood and blood products

- prevention: vaccine

treatment for hepatitis B:

Transmitted by blood and sexual contract, including needle sticks and sharing of needles

The most common bloodborne infection

A cause of one third of cases of liver cancer and the most common reason for liver transplant

Symptoms are usually mild

Chronic carrier state frequently occurs

- at greater risk for HIV

- most likely form of hepatitis to cause liver failure

what is hepatitis C?

Antiviral medications: interferon, ribavirin (Rebetol)

Measures to reduce spread of infection as with hepatitis B

Alcohol potentiates disease; medications that effect the liver should be avoided

Prevention: public health programs to decrease needle sharing among drug users

Screening of blood supply

Safety needles for health care workers

treatment for hepatitis C:

Only persons with hepatitis B are at risk

Blood and sexual contact transmission

Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis

hepatitis D:

Transmitted by fecal-oral route,

Resembles hepatitis A; self-limiting, abrupt onset, not chronic

hepatitis E:

- alcoholic

- postnecrotic

- biliary

what are the three types of hepatic cirrhosis?

secondary to tissue breakdown associated with pancreatitis

- or secondary to liver shock (sepsis)

postnecrotic hepatic cirrhosis:

gallbladder issues -> acidic foods that cause inflammation

biliary hepatic cirrhosis:

liver enlargement, portal obstruction (leads to portal vein HTN), ascites, GI varices, edema, vitamin deficiency, anemia (can be associated with hepatic cirrhosis), mental deterioration from ammonia

manifestations of hepatic cirrhosis:

Yellow- or green-tinged sclera and skin caused by increased serum bilirubin levels in bloodstream

jaundice:

Distended, almost pregnant belly

Portal hypertension resulting in increased capillary pressure and obstruction of venous blood flow

Vasodilatation of splanchnic circulation (blood flow to the major abdominal organs)

Changes in the ability to metabolize aldosterone, increasing fluid retention (RAAS)

Decreased synthesis of albumin, decreasing serum osmotic pressure

Movement of albumin into the peritoneal cavity

- when the liver fails, it leaks protein into the peritoneal space

- water from other parts of the body drawn to space

what is ascites?

fluid leave -> dry vasculature -> RAAS system slowed -> fluid dumping to peritoneal space

how does ascites change the ability of thwe RAAS system to function?

Record abdominal girth and weight daily (most accurate indicator of fluid volume, measure 1x per shift)

Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave

Monitor for potential fluid and electrolyte imbalances

3% saline

Low-sodium diet

Diuretics

Bed rest

Paracentesis

Administration of salt-poor albumin

Transjugular intrahepatic portosystemic shunt (TIPS)

treatment for fluid in the peritoneal cavity?

moves fluid back into vasculature and out through kidneys

how do diuretics aid with ascites?

needle aspiration only really done for difficulty breathing

when is paracentesis done?

- to reduce portal HTN

- vascular surgery, places a bypass graft, takes pressure off of the liver

how does TIPS procedure help decrease the presence of ascites?

Accumulation of ammonia and other toxic metabolites in the blood

what is hepatic encephalopathy and coma?

prevention

EEG and changes in LOC to determine brainwave activity

Monitor fluid, electrolyte, and ammonia levels

Lactulose to reduce serum ammonia levels

- ammonia binds to stool, diarrhea to decrease levels

IV glucose to minimize protein catabolism

Protein restriction and sodium restriction

- liver incapable of processing protein

- by-product of protein: ammonia, worsens coma

Reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics

Discontinue sedatives analgesics and tranquilizers

Monitor or treat complications and infections

how do we treat hepatic encephalopathy and coma?

Obstructed blood flow through the liver results in increased pressure throughout the portal venous system

- liver is not functioning properly, over-pressurized fluid, can no longer detoxify blood and assist with the uptake of nutrition (pa

Results in

- Ascites

- Esophageal varices (backup of fluid into portal system, becomes highly pressurized)

what is portal HTN?

Prevention

Treat underlying cause

TIPS procedure (transjugular intrahepatic portosystemic shunt)

Decrease the pressure within the portal system

- high pressurization in GI tract (mouth to rectum)

- creates bypass to offload fluid rom a liver that cannot function properly

treatment for portal HTN:

- hepatic vein

- portal vein

- portal artery

what are the three major vessels going into liver?

takes deoxygenated blood back to cardiopulmonary circuit

hepatic vein:

oxygen-rich blood to liver

hepatic artery:

carries nutrient-rich blood from GI tract into the liver to disseminate and go to body

portal vein:

- veins keep sending blood (dont know that something is wrong)

- ascites, pressure on liver

- pressure builds on portal vein (in inferior section of the liver)

- blood backs up into portal vein

how do the hepatic veins get altered in the presence of liver failure?

over pressurizes entire GI system (mouth to rectum)

- causes bulging veins (varicose veins)\- esophageal varices, hemorrhoids

how does portal HTN affect liver function?

- shunts blood directly to hepatic vein, to offload pressure

- nutrients bypass liver

- only bypasses a small % of flow

stent function:

Occurs in about one third of patients with cirrhosis and varices

First bleeding episode has a mortality rate of 30% to 50% (especially in those where they occur at home)

Manifestations include hematemesis, melena, general deterioration, and shock

Patients with cirrhosis should undergo screening endoscopy every 2 years

Precipitated by portal hypertension

- when esophageal vascular system becomes over-pressurized and leads to portal HTN

- prone to returning, can block esophagus (pt can bleed to death/aspirate on own blood)

- if they rupture -> treat for hypovolemic shock

what is bleeding of esophageal varices?

Treat for shock; administer oxygen

IV fluids, electrolytes, volume expanders, blood and blood products

Vasopressin, somatostatin, octreotide to decease bleeding

Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction

- dilates arteries and supplements vasopressin

Propranolol and nadolol to decrease portal pressure; used in combination with other treatment

- more for active bleeding

Sclerotherapy and Banding

treatment for esophageal varices:

when there is evidence of bleeding

- medication injected into varice that is prone to bleeding/rupture

when is an endoscopic scleropathy done?

- human basal cells

- causes bleeding vein to close up on itself (permanently closed)

- ends of lumen stick together

- done in microvasculature, wont hurt overall blood circulation

what is the medication used in an endoscopic scleropathy made out of?

- when a varicee is bulging and bulbular, but not yet ruptured

- bulb is not oxygenated, cells die and slough off

when is esophageal banding done?

- pt swallows a band, goes through GI, stool

- done in microcirculation

how is esophageal banding done?

major bloody surgery

- pt will have lots of JP drains or T tube ( in gallbladder)

- brown to green to light yellow fluid

- pt will need lifelong immunomodulation therapy

- lifelong recovery and med plan, prevents rejection

liver transplant:

LOW albumin, increase bilirubin

- decreased overall nutritional status

general labs of liver failure and/or liver rejection: