NSG 319 Exam 1

GI and Endocrine Systems

What is ammonia

byproduct of protein digestion and amino acid metabolism

Where is ammonia excreted from

kidneys

What does ammonia convert to in the liver

urea

What is elevated in hepatic encephalopathy due to the livers inability to complete conversion to urea and from accumulation in the bloodstream

ammonia

what is bradykinesia

slowness of movement

what kind of movement can be seen in hepatic encephalopathy

bradykinesia (slowness of movement)

Common term for cholelithiasis

gallstones

where are gallstones formed

in the biliary tract as a result of hypomobility of the gallbladder and impaired metabolism of cholesterol, bilirubin, and bile acids

Erythrocyte (RBCs) normal value

3.5-5.5 million/mm3

Erythropoiesis

production and maturation of RBCs in the bone marrow

Term for development of female secondary sex characteristics that can be present with hepatocellular failure

feminization

Hematemesis

blood vomit

One of the most common manifestations of portal hypertension due to esophageal varices

hematemesis

hemolysis

premature rupture and destruction of RBCs

Premature rupture of blood cells seen in prehepatic jaundice

hemolysis

hepatocytes

functional cells of the liver

purpose of hepatocytes

metabolize nutrients and produce and recycle proteins

Another term for jaundice

icterus

Jaundice is a characteristic sign of

liver disease

melena

black, sticky, tarry, foul-smelling stool

what causes melena

digestion of blood into the GI tract

what condition might we see melena with

grastroesophageal varices

Oliguria

decreased urine output- often seen in hepatorenal syndrome

clinical manifestation often seen in hepatorenal syndrome

oliguria

“itching” often seen in biliary cirrhosis

pruritis

thrombocytopenia

low platelet count/clinical manifestation of portal hypertension

urea

nitrogen-containing waste product formed during protein breakdown in the liver

Responsibilities of the liver

synthesizes glucose, plasma proteins, and blood clotting factors

metabolism of carbs, fats, and proteins

responsible for degradation and elimination of drugs and hormones (biotransformation)

function of endocrine pancreas

supplies insulin and glucagon needed in cell metabolism

functions of the liver

production of bile salts

elimination of bilirubin

metabolism of steroid hormones and drugs

metabolism of carbs, fats, proteins

storage of minerals and vitamins

filtration of blood and removal of bacteria

Portal hypertension manifestations

Gi congestion

Development of: esophageal or gastric varices, hemorrhoids, splenomegaly, ascites

What is portal hypertension

abnormally high blood pressure in the portal venous system due to high resistance to portal blood flow

Portal system

a low pressure system that facilitates blood flow through the liver

Intrahepatic Portal Hypertension causes

Caused by resistance to blood flow within the liver

Most often caused by cirrhosis

Posthepatic Portal Hypertension causes

Caused by resistance to blood flow after blood leaves the liver, but before it reaches the heart

Caused by cardiac disorders that impair right heart pumping

Portal Hypertension complications

Gastroesophageal varices- rupture can lead to deadly hemorrhage

Splenomegaly

ascites

hepatic encephalopathy

Clinical manifestations of splenomegaly

thrombocytopenia

fatigue

dyspnea

cyanosis

clubbing

JVD

ascites

peripheral edema

what is hepatic encephalopathy associated with?

hepatic failure or severe chronic liver disease

hepatic encephalopathy is the buildup of

ammonia due to the inability to convert it to urea

hepatic encephalopathy is charactered by

impaired behavioral, cognitive, and motor function

early symptoms of hepatic encephalopathy

subtle changes in personality, memory loss, irritability, lethargy, disinhibition, and sleep disturbances

later symptoms of hepatic encephalopathy

confusion, disorientation to time and space, asterixis**, slow speech bradykinesia, stupor, convulsions, and coma

correlation between ammonia level and level of encephalopathy

positively correlated

hepatic encephalopathy treatment

Lactulose

Rifamixin

Adequate dietary protein

Peripheral or central IV infusions w vitamins

High-fiber diet

cirrhosis

irreversible, inflammatory, fibrotic liver disease

what happens to the liver durign cirrhosis

it is fibrotic, scarred, and nodular

may be firm with palpation

result of cirrhosis

permanent alteration in hepatic blood flow and liver function

The nurse is reviewing the record for a client with a diagnosis of cirrhosis and notes that there is documentation of the presence of asterixis. How would the nurse assess for its presence?

Ask the client to extend the arms

Biliary cirrhosis

autoimmune liver disease that mainly affects genetically susceptible middle-aged females

result of biliary cirrhosis

inflammation, destruction, fibrosis, and obstruction of the intrahepatic bile ducts

Alcoholic fatty liver disease (reversible or irreversible) with cessation

reversible

clinical manifestations of alcoholic fatty liver disease

usually mild or asymptomatic

RUQ abdominal discomfort, mild hepatomegaly, portal hypertension

what is alcoholic fatty liver

fat buildup in the hepatocytes

Diagnosis for alcoholic fatty liver

Elevated AST and ALT

Elevated GGT

Hypertriglyceridemia

Abnormal abdominal US or CT

Treatment for alcoholic fatty liver

monitor for signs of alcohol withdrawal

well-balanced nutrition

avoid hepatotoxic agents

Acetaminophen toxicity should be suspected when doses exceed

4-10 grams/day

What happens in acetaminophen overdose

detoxification reaction may be overwhelmed and liver necrosis results (acute liver failure)

Early treatment within (how many) hours is crucial for acetaminophen toxicity (overdose)

8

acetaminophen is usually detoxified rapidly by (what) liver enzymes

glutathione transferase

Clinical manifestations of acetaminophen poisoning

nausea, vomiting, diarrhea, abnormal liver enzyme levels

untreated acetaminophen poisoning can lead to

progressive liver failure with jaundice

encephalopathy

hypoglycemia

coagulopathy

death

Acetaminophen poisoning antiode

N-Acetylcysteine (NAC)

What does NAC do to treat acetaminophen poisoning

stimulates liver production of glutathione to help metabolize toxins

prevents hepatic necrosis and fatal consequences

Most common form of primary liver cancer

Hepatocellular carcinoma (HCC)

Very rare form of liver cancer (primary cancer of bile duct cells)

Cholangiocarcinoma

Cholelithiasis forms as a result of

hypomotility of the gallbladder and impaired metabolism of cholesterol, bilirubin, and bile ducts

Risk factors of Cholelithiasis

4 F’s- female, forty, fat, and fertile

Clinical manifestations of cholelithiasis

RUQ pain radiates to shoulders/upper back, postprandial pain, increased belching, N/V, food intolerance, Murphy’s sign,

most common causes of pancreatitis

cholelithiasis

heavy alcohol consumption

Serotonin receptor agonists are the most effective for

nausea

Ondansetron (Zofran) is a ______

serotonin receptor antagonist

Ondansetron (Zofran) is metabolized through the _____

liver

Ondansetron (Zofran) routes

PO, IV, IM

Ondansetron (Zofran) dose

4-8 mg

Adverse effects of Ondansetron (Zofran)

headache, dizziness, diarrhea, lengthens QT interval, serotonin syndrome

Prochlorperazine (Compazine) class

1st generation (typical) antipsychotic

Indications of Prochlorperazine (Compazine)

Used to treat post-op N/V, chemo-induced nausea, and toxin-induced nausea

Prochlorperazine (Compazine) routes

Oral, rectal, IM, IV

Prochlorperazine (Compazine) dose

5-10 mg

Prochlorperazine (Compazine) adverse effects

extrapyramidal reactions, anticholinergic effects, hypotension, sedation, severe respiratory distress, blood dyscrasias

Contraindicated in children <2

Prochlorperazine (Compazine) Black Box warning

increased mortality rate in elderly patients for patients being treated for dementia-related psychosis

Pseudoparkinsonism signs

Stooped posture

Shuffling gait

Rigidity

Bradykinesia

Tremors at rest

Pill-rolling motion of the hand

Acute dystonia signs

Facial grimacing

Involuntary upward eye movement

Muscle spasms of the tongue, face, neck and back

(back muscle spasms cause trunk to arch forward)

Laryngeal spasms

Akathisia signs

Restlessness

Trouble standing still

Paces the floor

Feet in the constant motion, rocking back and forth

TArdive dyskinesia signs

Protrusion and rolling of the tongue

Sucking and smacking movements of lips

Chewing motion

Facial dyskinesia

Involuntary movements of the body and extremities

Dronabinol (Marinol) class

Cannabinoids

Abuse potential Schedule III

Dronabinol (Marinol) indications

Treatment of N/V

Dronabinol (Marinol) routes

oral

Dronabinol (Marinol) adverse effects

dependency, withdrawal, seizures, depression, hallucinations, tachycardia, hypertension

Dronabinol (Marinol) should use caution with

psych orders

Metoclopramide (Reglan) class

Prokinetic, dopamine antagonist

Metoclopramide (Reglan) indications

Diabetic gastric paresis, GERD, N/V,

Metoclopramide (Reglan) routes

PO, IM, IV

Metoclopramide (Reglan) routes

PO, IM, IV

Metoclopramide (reglan) dose

5-15 mg

Max dose: 60 mg/day

Metoclopramide (Reglan) adverse effects

extrapyramidal symptoms, sedation, diarrhea, tardive dyskinesia, blood dyscrasias, hepatotoxicity

Metoclopramide (Reglan) is contraindicated in

bowel obstruction, perforation, hemorrhage

Antiemetics should be given (before/after) chemotherapy drugs

before

Bulk-forming laxatives MOA

absorbs water, softens and enlarges fecal mass

has actions and effects similar to increasing dietary fiber

Bulk forming laxatives administration

should be given with a full glass of water/juice