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125 Cards in this Set
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Liver function
-How does the liver control carbohydrate metabolism through glyconeogenesis? |
-The liver can convert certain amino acids and lactic acid to glucose, and it can convert other sugars such as fructose and galactose into glucose for energy
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Liver function
-How does the liver regulate glucose levels if they are low? |
-The liver is important in maintaining a normal blood glucose level. When blood glucose is low, the liver can break down glycogen to glucose and release glucose into the bloodstream
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Liver function
-How does the liver regulate glucose levels if they are high? |
When blood glucose is high, as occurs just after eating a meal, the liver converts the glucose to glycogen and triglycerides for storage
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CM seen with a dysfunctional liver with carbohydrate metabolism?
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hypoglycemia
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Liver function
-How does it regulate ammonia conversion? |
The ammonia is removed from the intestine through portal circulation and then goes to the liver where it is broken down. Ammonia is toxic to the body
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Liver function
-CM with liver dysfunction and it can't regulate ammonia conversion? |
hepatic encephalopathy, (ammonia accumulates in the brain)
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How does the liver play a role in protein metabolism?
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-The liver synthesizes protein & clotting factors
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What CM will you see if the liver can't metabolize protein?
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pts with liver problems bruise easily and have clotting/bleeding problems
-bruising: the liver can’t metabolize the clotting factors |
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What CM will you see if the liver can't metabolize protein (why is albumin so important)?
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albumin is necessary to keep fluid in the vascular space, if there is a lack of this, fluid does not stay in the vascular space and can leak into the abdominal cavity causing ascites
-lack of protein metabolism: muscle wasting, you can’t heal. -They will have thin extremities but a large abdomen because of the ascites |
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How does the liver regulate fat metabolism?
-breaks down what? -produces what 2 things? |
-Break down of fatty acids for energy
-produces ketones for energy when glucose is not available -synthesis of cholesterol/lipids -the liver produces the bile which breaks down fat |
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-Liver dysfunction
What is seen if fat metabolism is impaired? (2) |
-Lipids may accumulate in liver → fatty liver
-Stearorrhea (presence of excess fat in feces) |
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-the liver is the prime storage site for vitamins and minerals which are released from the liver when needed elsewhere in the body, What are the vitamins and minerals stored?
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(fat soluble vitamins)
A D E K, B12, copper & iron |
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Vit A: |
-A: dry (xerosis), scaly skin, anorexa ↑ risk for infection, eye irritation, blindness,
keratinization of respiratory and GI tract, anemia, renal stones, G&D delay |
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
B12: |
-B12: anemia, inadequate myelin sheath synthesis, anorexia, glossitis,sore mouth and tongue, pallor, neurologic problems, (depression and dizziness, weight loss
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Iron: |
iron deficiency anemia
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Copper: |
anemia, weakness, impaired respiration, impaired growth, poor use of iron
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Vitamin K |
defective blood coagulation
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Vitamin E |
neurological deficits
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CM seen with a dysfunctional liver related to the inability to store vitamins and minerals
Vitamin D |
muscular weakness, ↑ sweating, diarrhea, GI disturbance, rickets, bone pain, ostermalacia (bone softening)
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The liver is significant for the metabolism of various drugs, such as:
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-most drugs are metabolized in the liver
Ex: barbiturates, opioids, sedative, anesthetics, amphetamines |
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CM seen with a dysfunctional liver that can't metabolize drugs?
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-Overdose
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How does the liver regulate steroid metabolism?
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Inactivates and excretes aldosterone, glucocorticoids, estrogen, progesterone, testosterone
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CM seen with a dysfunctional liver that can not regulate steroid metabolism?
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-increased ADH and aldosterone (edema)
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What is the function of the liver in respect to bile?
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Liver makes bile
Bile collected and stored in the gallbladder → released into duodenum Bile salts needed for fat digestion |
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CM seen with a dysfunctional liver that can't make bile?
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-impaired fat breakdown, steatorrhea
-the bile is not being produced so it can be released in the presence of fat so it can break down the fat in the food we |
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The liver is involved in bilirubin excretion
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bilirubin is derived from the breakdown of RBCs and is absorbed by the liver from the blood and secreted into bile.
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CM seen with a dysfunctional liver if there is a problem with bilirubin excretion (3)
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-impaired fat breakdown
-steatorrhea -dark colored urine |
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Bilirubin metabolism
-what's the difference between conjugated and unconjagated bilirubin? |
Unconjaged bilirum circulates in the plasma, when it gets to the liver it now mixes with glucuronic acid and now becomes conjugated bilirubin. Then it goes to the small intestine and is excreted in the urine and feces.
-unconjagated bilirubin has not reached the liver yet (means liver is not functioning) |
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The liver has a phagocytic function:
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The liver contains “Kupffer’s” cells have a phagocytic action of removing bacteria and debris from blood
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Cirrhosis
-2 most common causes are: |
-most common causes are alcoholism and hepatitis C
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Cirrhosis is a chronic progressive disease with extensive degeneration and destruction of the liver.
-It refers to the extensive: |
-refers to extensive scarring of the liver caused by necrotic injury or a chronic reaction to inflammation over a prolonged period of time. Normal liver tissue is replaced with fibrotic tissue that lacks function.
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what is the major CM of liver dysfunction
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Jaundice is the major CM of liver dysfunction
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Cirrhosis - Hemolytic (prehepatic): increased lysis of RBC
what are 3 examples? what lab value will you see? |
blood transfusions, sickle cell crisis, hemolytic anemia
-you will have an increase in the unconjugated (indirect) bilirubin |
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Cirrhosis
Hepatocellular (hepatic) –Causes: hepatocellular disease |
liver’s altered ability to take up bilirubin from blood
(the problem is with the liver itself. The liver can not take the bilirubin from the blood and conjugate it) |
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Cirrhosis
-Obstructive (posthepatic): impeded or obstructed bile flow through liver or biliary duct system What are some examples: |
obstructions, liver fibrosis, stones, (gall bladder disease, tumor – something that is obstructing the flow of bile from the liver)
-bilirubin is making it to the liver and it is being conjugated (direct) but it can’t be passed down out of the liver |
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How does alcoholism cause Cirrhosis (Hepatic Failure)
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causes an accumulation of fat in the liver; if don’t stop drinking à scar tissue and fibrosis infiltrate the liver as a result of cellular necrosis (most common cause)
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-Cardiac: right side heart failure, cor pulmonale, constrictive pericarditis, tricuspid insufficiency can cause cirrhosis.
-how might CHF cause it? |
-CHF causes enlargement of the organs and the blood and plasma gets stagnant and his difficulty flowing and backs up into the organs, causing organ dysfunction
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Cirrhosis - Diagnosis
Increased Liver enzymes: |
-Alkaline phosphate
-AST -SGOT -ALT -SGPT -GGT (they are letters of the alphabet whereas pancreatic enzymes end in “ase”) |
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Cirrhosis - Labs
-Cholesterol? |
increased cholesterol - fat metabolism impaired
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Cirrhosis - Labs
-Impaired protein metabolism: (because this is a function of the liver) 3 |
decreased total protein
decreased albumin increased globulin levels -this is a result of decrease synthesis by the liver |
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Cirrhosis - Labs
What happens to PT? |
-PT is prolonged because the liver decreases the production of prothrombin
-(INR is prolonged too, Iggy) -the liver metabolizes the clotting factors, if there is impairment of the liver you will see prolonged bleeding times.. patients easily bruise |
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Cirrhosis - Labs
Platelets? |
-the platelet count is low (less than 150,000)
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Cirrhosis - Diagnosis
-Liver biopsy What is a complication? |
they go in between the ribs.
- Complication of this? Hemothorax & Pneumothorax (hits the lung) and hemorrhage. So what do we do to control the bleeding? INTERVENTION: Know their PT, have the person lie on the right side to tamponade the area to apply direct pressure… |
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Cirrhosis - Diagnosis
-CBC (shows what??) -Liver Ultrasound is most common -CT -EGD (esophagogastroduodenoscopy) |
anemia, WBC is low
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Cirrhosis - Diagnosis
-Electrolyte panel (what level elevated?) -stool occult blood may be done, why? |
-Electrolyte panel (ammonia levels are elevated)
-stool occult blood to see if there is any internal bleeding |
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Cirrhosis - Diagnosis
Bilirubin metabolism impaired –Serum bilirubin is increased (what happens to unconjugated & conjugated levels) |
-Unconjugated increased (because of the inability of the
failing liver to excrete bilirubin) -Conjugated increased or decreased |
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Clinical Manifestations seen with Liver Dysfunction
-most CM are a result of what? |
high ammonia levels
-early CM are vague (nausea, anorexia, weakness, wt loss) |
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-Ascites occurs with liver dysfunction, why?
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portal hypertension occurs (the liver is congested so the blood can’t dump into the liver) so it backs up into portal circulation. It is an increase in the blood volume in portal circulation. The volume has to go somewhere so it moves into the capillary network, which then backs up and leaks into the abdominal cavity and that’s how ascites occurs. You do not have the metabolism of proteins (missing albumin) which holds fluid in the vascular space.
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Ascites with liver dysfunction
-what CM can you see -what can this also cause problems with? |
-may have fluid wave: lay on their side and you can see the fluid shift. Can put pressure on the diaphragm and cause respiratory problems.
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Neurological findings seen with liver dysfunction
7 |
1) Asterixis: flapping tremor
characterized by rapid extension and flexion of the wrist and fingers 2) Paresthesias of feet 3) Peripheral nerve degeneration 4) Reversal of sleep-wake pattern 5) Sensory disturbances (also related to deficiency of Vitamin B12 |
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Neurological findings seen with liver dysfunction are related to what?
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These CM are related to high ammonia levels. The ammonia can’t be broken down in the liver. Ammonia is toxic to the body!
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Renal findings seen with liver dysfunction:
(2) |
-Hepatorenal syndrome (nephrons become occluded)
-Increased urine bilirubin |
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Endocrine findings seen with liver dysfunction (4 things are elevated)
-what changes do you see in men and women? |
-Increased aldosterone
-Increased antidiuretic hormone -Increased circulating estrogens -Increased glucocorticoids The liver can’t metabolize them! -Gynecomastia, impotence, testicular atrophy in men -Menstrual irregularities and amenorrhea in women |
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Gastrointestinal findings seen with liver dysfunction?
13 |
1) Abdominal pain
2) Anorexia 3) Ascites 4) Clay-colored stools (due to no bile. Not released from liver to break down fat) 5) Diarrhea 6) Esophageal varices – vessels at the end of the esophagus become enlarged and fragile 7) Fetor hepaticus (breath odor that is fruit and musty due to high ammonia levels) 8) Gallstones (supersaturation of bile) 9) Gastritis 10) GI bleeding 11) Hepatomegaly (organ digestion – dullness upon assessment) 12) Malnutrition 13) Nausea 14) Vomiting |
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Gastrointestinal findings seen with liver dysfunction are a result of what?
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These CM are related to high ammonia levels which is irritating to the GI tract. We give neomycin
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Immune System Disturbances is seen with liver dysfunction (2)
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-Increased susceptibility to infection (b/c proteins are not available to make leukocytes)
-Leukopenia |
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Cardiovascular findings seen with liver dysfunction
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-cardiac dysrhythmias
-development of collateral circulation -fatigue -peripheal edema -portal hypertension -spider angiomas (superficial fine veins on the body due to collateral circulation) |
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Cardiovascular findings seen with liver dysfunction are a result of what
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These CM are due to fluid volume excess and because electrolytes are impaired. Plasma proteins maintain osmotic pressure and without them, fluid leaks out.
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Dermatologic findings seen with liver dysfunction:
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-axillary and pubic hair changes (because adrenal hormones are not metabolized)
-Caput medusa (angiomas or spider veins around one’s belly button) -increased skin pigmentation & jaundice -palmar erythema (red palms) -pruritus (itching from jaundice) |
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Fluid and Electrolyte Disturbances seen with liver dysfunction:
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-decreased blood volume
-hypocalcemia -hypokalemia -peripheral edema -water retention |
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Hematologic findings seen with liver dysfunction:
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-anemia
-DIC -impaired coagulation -splenomegaly -thrombocytopenia (platelets less than 150,000 – the spleen isn’t working |
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Pulmonary findings seen with liver dysfunction:
These CM are due to what? |
-Dyspnea
-Hydrothorax -Hyperventilation -Hypoxemia These CM are due to fluid accumulation putting pressure on the diaphragm |
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Complications of Cirrhosis
Portal hypertension is what? |
- an increase in the blood pressure within a system of veins called the portal venous system.
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Complications of Cirrhosis
Portal hypertension results from what |
-results from increased blockage or resistance of blood flow through the portal vein and its branches.
-blood then seeks out alternative way to get around the high pressured area |
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Complications of Cirrhosis
Portal hypertension -blood backs into where? -what happens to the veins? |
-blood backs into the spleen, causing splenomegaly.
-veins in the esophagus, stomach, intestine, abdomen, and rectum become dilated & distended. -this can result in ascites (abdominal fluid, distended veins in the esophagus and abdomen and hemorrhoids |
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Complications of Cirrhosis
Esophageal Varices – as a result of |
portal hypertension
-the blood backs up from the liver and enters the esophageal and gastric veins. |
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Complications of Cirrhosis
Esophageal Varices - these occur when? -what may the patient present with indicating that they have this |
when fragile, thin walled esophageal veins become distended from increased pressure and have the potential to bleed (which is a medical emergency)
may present as hematemesis or melena (black, tarry stools) |
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Complications of Cirrhosis
Ascites is what? |
is the collection of fluid within the peritoneal cavity caused by increased pressure from portal hypertension
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Complications of Cirrhosis
Ascites -the collection of plasma protein in the peritoneal fluid is significant, why? |
the collection of plasma protein in the peritoneal fluid reduces the amount of circulating plasma protein in the blood → when this decrease is combined with the inability of the liver to produce albumin because of the impaired liver cells, the osmotic pressure in the CV system is decreased and results in a fluid shift from the vascular system into the abdomen, a form of third spacing
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Complications of Cirrhosis
Splenomegaly results from what? -what is the CM that appears with this? |
(enlarged spleen)
-results form the backup of blood into the spleen. The enlarged spleen destroys platelets, causing thrombocytopenia (low platelet count, less than 150,000) |
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Complications of Cirrhosis
The pt with cirrhosis has a decreased production of bile in the liver. -this is significant because it prevents the: |
the absorption of fat soluble vitamins (ex: vit K) without Vit K, clotting factors are not produced and the patient is susceptible to bleeding and easily bruising
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Complications of Cirrhosis
Hepatic encephalopathy – affects the function of the brain What are early CM? |
-early CM include sleep disturbance, mood disturbance, metal status changes, and speech problems
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Complications of Cirrhosis
Hepatic encephalopathy – affects the function of the brain -late CM include (3) |
altered LOC, impaired thinking, and neuromuscular problems
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Hepatic encephalopathy - neurological changes that you see as a result of
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elevated ammonia levels which can increase ICP which is seen in end stage cirrhosis, can’t reverse this.
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Hepatic encephalopathy - is seen in stages 0-4. What is the worst stage?
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stage 4
–Not rousable Intellectual function is absent –Decerebrate –May be responsive to painful stimuli |
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Hepatic encephalopathy - what stage?
LOC –Insomnia, sleep disturbance Intellectual function –Slight change in computational skills Neurologic findings –Impaired handwriting, tremor |
0
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Hepatic encephalopathy - what stage?
LOC –Lack of awareness –Personality change Intellectual function –Short attention span –Mild confusion –Depression Neurologic Findings –Uncoordination, asterixis |
1
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Hepatic encephalopathy - what stage?
LOC –Lethargy, drowsiness, inappropriate behavior Intellectual function –Disoriented Neurologic findings –Asterixis, abnormal reflexes |
2
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Hepatic encephalopathy - what stage?
LOC –Asleep, rousable Intellectual function –Loss of meaningful conversation –marked confusion –Incomprehensible speech Neurologic Findings –Asterixis, abnormal reflexes |
3
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Hepatic encephalopathy
-Goal when caring for these patients? -what are we monitoring (3)? -tell me about diet? |
decrease ammonia levels through diet and drugs
–Monitor neuro status, ammonia, pH –Encourage fluids if not restricted –Low protein or no protein diet |
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the most common nursing diagnose for a pt with cirrhosis is
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excess fluid volume related to edema (portal hypertension)
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-if ascites and edema are absent, a high protein diet supplemented with vitamins is prescribed (vitamin A, C, K, folic acid, and thiamine)
(true or false) |
true
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Cirrhosis - Care
•Rest is key!! -teach the pt to do what to help with pruritus |
use cool water with minimal amount of soap and to use lotion
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Diet (Hepatic Failure)
-Tell me bout protein? |
Protein 20 g/day
-Can be increased by 10 g/day as tolerated and without causing signs of hepatic encephalopathy -High biologic value protein |
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Cirrhosis - Care
-Diet: Calories & Carbs? |
High in calories
high carbs |
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Cirrhosis - Care
Diet: Fat and sodium? |
-Low fat - Fat limited only to prevent early satiety (feel full more quickly)
-Na+ and fluid restricted when edema and ascites present |
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Cirrhosis - Care
Ascites treatment: -Sodium? -What drugs are given? -What about fluids? |
–Na+ restriction – 2 g/day --> 250 – 500 g/day
–Diuretics to reduce fluid accumulation and to prevent cardiac and respiratory problems –Fluid restriction for severe ascites |
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Cirrhosis - Care for Ascites treatment:
Paracentesis may be done: -why? -what happens? -what should we be concerned of (2) |
-temporary relief of pressure on diaphragm and abdomen.
–The MD inserts a catheter into the abdomen to remove and drain ascitic fluid from the peritoneal cavity -can be done in x-ray or by bedside -concern of hypotension and hypovolemia |
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Cirrhosis - Care for Ascites treatment:
Paracentesis -what do you have the patient do before the procedure? -what are you measuring? |
• Pre - empty bladder prior to procedure to prevent injury to the bladder,
-measure abd girth, weight, VS, done sitting up, limit drainage slowly up to 4 L |
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Cirrhosis - Care for Ascites treatment:
Paracentesis -what are you doing post procedure? -what are you monitoring for? |
VS, sm bandage, measure abdominal girth, wt, VS, monitor for shock because of excessive fluid removal from the abdomen (hypovolemia)
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Cirrhosis – Drugs
Diuretics are used to reduce accumulation and to prevent cardiac and respiratory problems -Spironolactone (aldactone): |
blocks action of aldosterone, K+ sparing
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Cirrhosis – Drugs
Diuretics are used to reduce accumulation and to prevent cardiac and respiratory problems -Amiloride (Midamor): |
inhibits reabsorption of Na+ and secretion of K+
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Cirrhosis – Drugs
Diuretics are used to reduce accumulation and to prevent cardiac and respiratory problems Chlorothiazide (Diuril): |
thiazide that acts on proximal tubule to decrease reabsorption of Na+ and H2O
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Cirrhosis – Drugs
Diuretics are used to reduce accumulation and to prevent cardiac and respiratory problems Furosomide (Lasix): |
rapid action on distal tubule and loop of Henle to prevent reabsorption of Na+ and H2O
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Cirrhosis – Drugs
Magnesium sulfate: why? |
Mg++ replacement; hypomagnesemia occurs with liver dysfunction
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Cirrhosis – Drugs
Vitamin K: why? |
correction of clotting disorders
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Cirrhosis – Drugs
Cimetidine (Tagemet): why? |
decreases gastric acidity
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Cirrhosis – Drugs
Vitamin B12: why? |
deficient with liver disease; needed for hematopopoiesis and CHO metabolism and protein synthesis
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Cirrhosis – Nursing Care
Diet: |
-restrict protein-high biological value
-salt restriction -end stage – let them eat whatever -no fats because of bile issue and cause early satiety (feel more fully quicker) |
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Cirrhosis – Nursing Care
Impaired skin integrity b/c of pruritus from increasing bilirubin, or edema. Skin can be fragile. Bruise easily |
–Alternating air pressure mattresses – reposition Q 2°
–Support abdomen with pillows –Meticulous, gentle skin care -ROM –Scrotal support –Decrease edema – prevent fluid retention –Keep nails short –Antipruritic medications |
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Cirrhosis – Nursing Care
Risk for injury b/c of muscle wasting and bruising easily |
–Assess for decrease sensation
–Avoid restrictive clothing and bed linens –Use heat and cold application carefully –Assist with ambulation |
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Cirrhosis – Nursing Care
Ineffective breathing pattern due to excess fluid volume |
–HOB increased
–Support arm on pillows –Assess lungs, RR |
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Nursing care - Cirrhosis:
Hemorrhage -limit: -monitor for? -tell me about needle use? -toothbrush? |
–Limit physical activity
–Monitor for hemorrhage: epistaxis, purpura, petechiae, easy bruising, gingival bleeding, heavy menstrual bleeding, hematuria, melena –Observe for bleeding from orifices, urine, stool –Use smallest gauge needles – apply prolonged pressure after removal –Soft-bristle toothbrush |
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Nursing care - Cirrhosis:
Hemorrhage -tell them to avoid what: -monitor labs: |
–Avoid irritating food: spicy and rough foods
–Avoid straining at stool causing pressure and can rupture vessels (esophageal varices) –Avoid vigorous blowing nose because it can cause pressure –Observe for bruising on skin, forearms, axillae –Monitor labs – H/H, PT |
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Nursing care for cirrhosis
Teach to avoid the following drugs that are toxic to the liver: Hepatotoxic drugs |
–Acetaminophen
–ASA if bleeding or varices present –ETOH –Straining –Sneezing –Retching and vomiting -NSAIDS (irritate GI tract and contribute to bleeding problems) |
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
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increase ammonia in GI tract (blood breaks down and you have a lot of protein floating around)
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
Constipation: |
increased ammonia from bacterial action on feces (increasing bacteria in GI tract increases ammonia production)
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
Hypokalemia |
K+ needed by brain to metabolize ammonia (b/c electrolytes are not being taken in by the body)
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
Hypovolemia |
increase serum ammonia by causing hepatic hypoxia; impairment of cerebral,
hepatic, and renal function |
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
-Could be a low protein diet (true or false) |
false
a high protein diet would be a factor |
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Infection can contribute to hepatic encephalopathy:
-Increase in catabolism, increase cerebral sensitivity to toxins |
no detoxification by liver (liver can’t break it down)
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Factors Precipitating (things that can contribute to elevation in ammonia levels)
-Metabolic alkalosis: |
increase transport of ammonia across blood-brain barrier, increase in renal production of ammonia
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-Paracentesis for ascites
complications: |
loss of Na+ and K+, decrease blood volume (You can pull out abdominal fluid and fluid from the vascular space if you don’t have the plasma proteins)
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Drugs for high ammonia levels & hepatic encephalopathy
-Lactulose (Cephulac, Lacitol): Why is this given?? |
is prescribed to promote excretion of ammonia in the stool. Can be given PO (liquid), NG, rectally
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Drugs for high ammonia levels & hepatic encephalopathy
-Lactulose (Cephulac, Lacitol): What kind of effect does it have? |
-laxative effect that binds ammonia and then eliminates it (teach them that they will have 4-5 loose stools a day) watch for skin break down
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Drugs for high ammonia levels & hepatic encephalopathy
-Neomycin sulfate or Flagyl is a broad spectrum antibiotic that may be given to act as an intestinal antiseptic. |
It is administered to remove intestinal bacteria, which produces ammonia. It destroys the normal flora in the bowel, diminishing protein breakdown and decreasing the rate of ammonia production. Can be given: po, rectally
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Drugs for high ammonia levels & hepatic encephalopathy
Neomycin sulfate or Flagyl -decreases what? |
it decreases the amount of bacteria in the GI tract which will decrease the ammonia production
-Neomyacin is not absorbed systemically, only has a local effect. Given over Flagyl. |
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Care for hepatic encephalopathy
-Goal to reduce ammonia •Restricted protein why? |
(protein is broken down into ammonia)
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Esophageal varices is seen in what type of disease?
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seen in end stage cirrhosis - located at the base of esophagus. (if pt starts vomiting up blood and they have a history of cirrhosis do not volunteer to put in NG)
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Esophageal varicose are caused by what?
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-are caused by portal hypertension (elevated BP in veins that carry blood from the intestines to the liver is caused by impaired circulation of blood throughout the liver). The blood is re-routed and backs up into the upper stomach and esophagus.
- Varices are fragile and can bleed easily. |
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Esophageal varicose treatment
-drugs that have what effect? -ABCs? -EGD or sclerotherapy çan be done, which is what? |
–Drugs to induce vasoconstriction
ABCs (apply oxygen, raise HOB) –EGD – banding or sclerotherapy -sclerotherapy involves the injection of a sclerosing agent into and around bleeding varices –Balloon tamponode or an NG tube |
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Drugs – Control Bleeding Esophageal Varcies
•Vasopressin (VP) (Pitressin): action: |
problems result because it can affect BP!
-hemostasis, constriction of splanchnic arterial bed, decrease portal blood flow, decrease portal HTN |
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Drugs – Control Bleeding Esophageal Varcies
Propranolol (Inderal): |
decrease portal venous pressure (decreases pressure in vessels)
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Drugs – Control Bleeding Esophageal Varcies
Octreotide (Sandostatin): |
mimicks somatostatin (pancreatic hormone which inhibits insulin and glucagon) by inhibiting serotonin which causes vasoconstriction (dries up the pancreas and causes vasoconstriction)
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Drugs – Control Bleeding Esophageal Varcies
Nitro? |
reduces effects of VP – affects BP → elevated BP
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