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Critical Care Exam 3 > Hepatic > Flashcards

Hepatic Flashcards

1
Q

if not good blood flow to the gut –

A

perliticiteus* – gut quits performing role, its just sitting there and anything in gut doesn’t move forward, body doesn’t get fed, leads to translocation of bacteria* – sets up for sepsis

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2
Q

Portal vein takes whatever you’ve eaten to

A

the liver hepatic first pass – detoxification by the way of the hepatic vein feds into the heart

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3
Q

If gall stones in the common bile duct will have problems with

A

pancreas

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4
Q

Hematemesis:

A

vomiting bright or dark red blood or vomiting old digested blood (which looks like coffee grounds); will see hematemesis from stomach, esophageal sources and in 90% of bleeding duodenal ulcers

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5
Q

Hematochezia:

A

red blood or mahogany-colored stool due to lower GI bleeding from colon, rectum, or anus

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6
Q

Melena:

A

passage of black or tarry stools; occurs from digestion of blood from an upper GI bleed.

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7
Q

upper GI bleeding

A

Bleeding above the duodenojejunal junction

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8
Q

Reasons for GI tract bleeding

A
  • Gastric, duodenal ulcers
  • Erosive gastritis or esophagitis
  • Angiomas of the stomach or small intestine
  • Aortoenteric fistulas – opening between arota and gut
  • Lower bleeds: GI cancer, inflammatory bowel disease (chrons disease), bowel perforation, NSAIDs, anticoagulation therapy
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9
Q

Mallory-Weiss Tear: **

A

occurs in mucosal barrier at esophageal-cardiac sphincter due to wretching & vomiting;
o Occurs right were esopoghas goes into stomach from hard vomiting

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10
Q

Esophageal Varices: *

A

“ large dilated veins in the submucosa of the stomach and lower esophagus”

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11
Q

portal hypertension: *

A

an increase in portal venous pressure in the liver (greater than 12 mm Hg

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12
Q

Effects of Alcohol

A
  • Alcohol is oxidized to aldehyde by the liver resulting in damage to cells
  • Chronic consumption of alcohol causes increase of smooth endoplasmic reticulum in liver cells, increases production of cholesterol that accumulates in the mitochondria
  • Over time mitochondria swell, leading to increased inflammation, fibrosis, necrosis of liver’s cells
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13
Q

How Portal Hypertension Results **

A
  • Fibrosis and scarring leads to distorted vessels in liver
  • Eventually blood flow through liver is impaired
  • Venous blood from GI tract has nowhere to go
  • There is a “Back-up” into a very low pressured venous system- Esophageal Varices
  • Veins eventually rupture leading to Gastrointestinal Bleed
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14
Q

Effects of Bleeding

A
  • BP: orthostatic changes- BP 86/40 sitting up;96/60 lying flat – heart working hard
  • HR 132/minute
  • RR 22 breaths/minute, dyspnea – not getting O2 to tissues
  • Look also for restlessness, dizziness, anxiety
  • All of these are indicators of HYPOVOLEMIA secondary to blood loss
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15
Q

Blood Loss

A
  • < 500 mls: no change in vital signs
  • 500 to 1000 mls: sympathetic response: thirst, tachycardia, drop in BP
  • > 1000 mls: shocklike symptoms, typically if BP drops more than 10 mm Hg with change of position and HR is 20 beats higher than normal, then there is usually close to 1000 mls blood loss.
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16
Q

HCT and Hgb with blood loss

A

• Initial Hgb and Hct values will not match the degree of blood loss so these do not tell us how severe or rapid the blood loss has been
o It will be behind
o So pt might look good when in trouble
• Part of the decrease may be due to IV fluid resuscitation, a hemodilution effect
o With Hct and Hgb think about how many fluids are given – fluids can dilute

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17
Q

Albumin if liver damage

A
  • Liver unable to synthesize albumin; leads to “leaky” capillary membranes, ascites
  • Liver also makes proteins needed for production of fibrinogen, prothrombin, and other clotting factors: Implication? More bleeding if no clotting factors
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18
Q

Other complications of decreased blood flow to the liver

A
  • As pressure in the liver increases resistance to blood flow, liver less able to detoxify wastes or transport nutrients – so accumulation of wastes in blood
  • As blood flow through liver decreases, less protein if filtered by liver into the lymphatic system
  • The increased pressure causes protein to “sweat” through the liver capsule into the peritoneal cavity
  • Intravascular protein diminishes severely, abdomen becomes very distended, increasing third spacing occurs
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19
Q

increase LFT’s

A

Over 70% of parenchyma (tissue of liver) may be damaged before see an increase LFT’s

20
Q

Enzymes and end products are released into the blood with the

A

destruction of liver cells

21
Q

Alanine aminotransferase (ALT):

A

most specific indicator of hepatocellular damage; produced predominantly in liver

22
Q

Aspartane aminotransferase (AST):

A

increases with liver and other organ damage

23
Q

Ammonia

A

( normal: 35- 65 mcg/dL)
• Liver converts ammonia (NH3), a byproduct of protein metabolism into urea, which is excreted by the kidneys.
• When liver is damaged, toxic levels of ammonia accumulate in blood.

24
Q

Will see a drop in the BUN as the ammonia level rises. Why a drop and not a rise?

A

Because the liver is not making urea

25
Q

Hepatic Encepalopathy

A

manifested by a spectrum of disturbances in consciousness, ranging from subtle behavioral abnormalities to marked confusion and stupor to deep coma and death…associated fluctuating neurologic signs include rigidity, hyperreflexia, and particularly asterixis: nonrhythmic, rapid extension-flexion movements of the head and extermities, best seen when the arms are held in extension with dorsiflexed wrists…
• Hand writing can deteriorate

26
Q

Lactulose**

A

• MOA: increases H2O content & softens stool; lowers pH of colon which inhibits diffusion of ammonia (NH4) from colon into blood- LOWERS ammonia levels
o Won’t let ammonia go back in bc creating acute environment so can evacuate ammonia in stool
• Adverse Effects: belching, cramps, flatulence, diarrhea
o Will need bedside commode ready
• Should not be used with other laxatives
• Monitor NH4 levels, BG levels “lose” form of sugar
• Administer with 8 oz. water or juice; better to give on empty stomach for full absorption

27
Q

How would you evaluate that the Lactulose was effective?

A

o Decreased level of confusion
o Improved mental status
o Should be cleaning up stool

28
Q

Bilirubin

A

(normal: 0.5 mg/dl) may be 15 –20 mg in severe liver failure
• Derived from breakdown of hemoglobin and red cells
• Is fat soluble, binds to albumin for transport to liver
• Liver CONJUGATES bilirubin making it water soluble so it can be excreted by kidney
• If liver is working bilirubin will remain unconjugated and will see higher levels of unconjucated bilirubin

If high levels unconjugated bilirubin – liver not working
If high levels of conjugated – working liver, blockage in common bile duct
• Can have both is bad liver failure

29
Q

Increased “Conjugated” Bilirubin or Direct Bilirubin

A
  • Usually due to a blockage in the hepatic duct, bile duct, or collecting channels of liver
  • A degree of liver “functioning” still present – liver still conjugates (makes water soluble) bilirubin but the massage is blocked
30
Q

Increase in “Unconjugated” or “Indirect” Bilirubin

A
  • Liver no longer able to function and can no longer change “fat soluble” form of bilirubin into a “water soluble” form
  • As bilirubin accumulates in body, patient will become more and more jaundiced
  • As liver failure progresses will see an increase in both conjugated and unconjugated bilirubin
31
Q

Liver synthesizes all clotting factors except

A

VIII

• Will see prolonged bleeding times if liver unable to function

32
Q

Vitamin K

A
  • Necessary for making clotting factors, insufficient Vitamin K will lead to decreased prothrombin production (prothrombin time will become increased)
  • In obstructive biliary disease, bile cannot move from gallbladder to duodenum, nor can liver make bile
  • Must have bile to absorb fat from small intestine
  • Fat soluble vitamins can no longer be absorbed (Vitamins A, D, E, and K)
33
Q

Obstructive Disorder or True Liver Failure?

A
  • If patient has an obstructive disorder, prothrombin times will return to normal after IM injections of Vitamin K
  • If patient has true liver failure, he/she will not respond to Vitamin K injections because the liver is incapable of making clotting factors
34
Q

Immediate Treatment of GI Bleed Due to Esophageal Varices

A
  • Volume: 2-3 liters of crystalloid, Lactated Ringers or Normal Saline
  • If vital signs remain unstable, then prepare for blood replacement
  • Hgb of less than 10 mg/dl and Hct less than 25% indicate need for blood replacement
  • PRBC’s commonly used because they decrease exposure to antiboldies and the risk of FVE
35
Q

Other Treatment Options for esophageal varices

A
  • Saline Lavage via nasogastric tube: controversial- may resolve accumulation of clots but does not halt bleeding
  • Endoscopic hemostasis via coagulation by cauterizing varices or injecting sclerosing agents
36
Q

Endoscopy

A
  • Patient is medicated with sedative (Versed)
  • A flexible endoscope with a fiber optic light source is swallowed via the esophagus, through the stomach, and into the duodenum
  • The patient is placed on left side with HOB at 30 degrees to prevent aspiration
  • Sclerosing agent such as epinephrine is injected at sites of bleeding, causing vasoconstriction and platelet aggregation
37
Q

Postendoscopy

A
  • Monitor closely for aspiration, monitor respiratory status
  • Test for positive gag reflex
  • Complications: ulceration of the esophagus, esophageal perforation, aspiration pneumonia
38
Q

Endoscopic Band Ligation

A
  • Via the scope, an “O ring” or “band” is placed around the bleeding varice, causing obstruction of the vein; strangulation and necrosis results in scar formation.
  • Ulcer becomes necrotic
  • Success rate of 86% in controlling bleeding
39
Q

Intravenous Vasopressin (Pitressin) **

A
  • Vasopressin: potent vasoconstrictor (will also constrict coronary artery); effective in eliminating the bleed, but side effects such as myocardial infarction, arrhythmias, hypertension are very high
  • Monitor these patients closely post-procedure
  • Concurrent administration of nitroglycerin (IV Tridil) may help decrease side effects)
40
Q

Somatostatin and Octreotide

A
  • As effective in controlling the bleed but have less severe side effects
  • Cause vasoconstriction without cardiac complications
  • Currently the drug of choice
41
Q

TIPS**

A

Transjugular Intrahepatic Portosystemic Shunt **
• May be used when bleeding is not controlled by sclerotherapy or ligation
• Catheterization of the hepatic vein is done through the internal jugular vein starts in jugular until get to hepatic vein
• With fluoroscopy, a needle is directed into the portal vein and a stainless steel stent is placed
• The stent allows a new passage for blood through the liver
• relieving blood pressure in hepatic vein
• like bypass – bypassing clogged liver

42
Q

TIPS procedure

A
  • Risks: puncture site bleeding, hematoma formation, bacteremia, encephalopathy, reaction to contrast media, bile duct trauma, pancreatitis, vascular injury
  • Shunt occlusion occurs in more than 50% of patients following a year.
43
Q

hepatic failure s/s*

A

jaundice, portal hypertension, ascites and varices, nutritional deficiencies, and hepatic enephalogy or coma

44
Q

hepatic failure labs*

A

bilirubin, protein, albumin, PT, serum alkaline phasphate, AST, ALT, Ammonia, cholesterol

45
Q

portal hypertension definition

A

↑ pressure throughout the portal venous system that results from obstruction of blood flow through damaged liver

46
Q

Neomycin **

A

– used to remove or decrease production of nitrogenous wastes in the large intestine; aids in decreasing ammonia
s/e: renal toxicity and hearing impairment

47
Q

Purpose of Sengstaken-Blakemore tube **

A

Mechanical Tamponade
• Pressure on vessels to ↓ bleeding!
• Balloons, gastric and esopheageal balloons, put enough pressure on varices will stop bleeding most concern about – balloon rupture dislodged in throat and airway occlusion

Critical Care Exam 3 (4 decks)

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