Exam 3: Hepatic Fxn and Transplant Flashcards

1
Q

Liver

A

largest GLAND in the boyd at 3-4 pounds

highly vascular wiht 4 different lobes

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2
Q

Where is the liver located

A

beneath the diaphragm and right upper quadrant

this is important since it is close to the GI tract where it gets nutrients and plays a key role in whether these are stored or not

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3
Q

About how much blood circulates in the liver and how much is stored in the liver

A

1.5 L circulate within the liver with 200-400 mL of blood being stored by it

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4
Q

Portal Vein

A

75% of blood to the liver goes through the portal vein which is NUTRIENT RICH OXYGEN POOR blood from the spleen, intestines, etc

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5
Q

Hepatic Artery

A

25% of blood to the liver is goes through the hepatic artery from the heart and is NUTRIENT POOR OXYGEN RICH

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6
Q

What happens to the blood entering the liver lobules from the portal vein and hepatic artery

A

The blood mixes in the liver lobules –> through the hepatic veins –> inferior vena cava –> heart

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7
Q

Functions of the Liver

A
  1. Glucose Metabolism
  2. Ammonia Conversion
  3. Protein Metabolism
  4. Fat Metabolism
  5. Vitamin and Iron Storage
  6. Bile Formation
  7. Bilirubin Excretion
  8. Drug Metabolism
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8
Q

How does the liver do glucose metabolism

A

it helps maintain a stable blood glucose by storing glucose as glycogen and then converting it to glucose when needed

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9
Q

What is the ammonia conversion function of the liver

A

ammonia is what is left over after protein breakdown

liver takes ammonia and converts it to urea for excretion

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10
Q

Why are ammonia levels super important

A

ammonia can be toxic so levels are important to look at with hepatic disorders

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11
Q

What is the protein metabolism of the liver like

A

the liver makes proteins needed for clotting (so liver issues can lead to bleeding issues)

This means Vitamin K intake is important as it is needed to make factors in the liver

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12
Q

What does the liver do to fat

A

it stores fat and breaks it down to be used as energy, but too much can cause a fatty liver

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13
Q

What sort of vitamins adn minerals are stored in the liver

A

Vitamin A, B, D, Iron and Copper

Vitamin K is used a lot to make clotting factors here as well

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14
Q

Bile

A

a substance made and released in the liver to the gallbladder (storage)

when needing to digest fats the bile can emulsify them to help move them out of the body

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15
Q

Bilirubin

A

what is left once RBCs die and break down

it is carried into intestines and excreted in stool to cause the brown coloring

can be excreted in urine but the liver is working to get rid of the RBCs as they die and dispose of it in a timely manner

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16
Q

The liver is basically a ___ of the body

A

gatekeeper (think first pass)

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17
Q

More than ___% of the liver can be damaged before changes become abnormal

A

70

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18
Q

What sort of Liver Lab studies are done and seen with abnormal livers

A

CEA - presence can indicate cancer

PT increase - prolonged clotting = more bleeding

Protein Studies - Low levels means liver isnt making them

ALT, AST = Liver damage and enzymes release into blood

Bilirubin, Cholesterol (decreased in liver disease), and Ammonia (damage means higher as it usually becomes urea)

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19
Q

Liver Biopsy

A

Needle aspiration through the abdominal wall for analysis

A transvenous version can be done with fluoroscopy for real time rays guiding through the hepatic vein to the liver

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20
Q

Complications of a Liver Biopsy

A

bleeding

potential for bile peritonitis if gall bladder damaged

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21
Q

What needs to be done prior to a liver biopsy

A

coagulation studies since risk for bleeding is so high

we may even want to wait until pt is clear with meds to prevent bleeding

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22
Q

Blind Needle Aspiration

A

a version of liver biopsy where they are ultrasound guided or done laproscopically

used with severe ascites or abnormal anticoagulation studies

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23
Q

What needs to be done after a liver biopsy

A

Pt lay on right side for several hours to push liver against the costal margin for compression (can use a pillow)

2-3 hours of this

avoid coughing or straining

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24
Q

How often should you check VS after a liver biopsy

A

every 10-15 min for the first hour then every 30 minutes for the next 1-2 hours

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25
Q

Things neede after a liver biopsy

A

right side, pillow, dressing, 2-3 hours

avoid coughing and straining

VS protocol

avoid heavy lifting for a week

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26
Q

General CAUSES of Liver Dysfunction

A

Acetaminophen Overdose / Prescription Meds like NSAIDS, antibiotics, anticonvulsants

Herbal supplements (Skull cap, penny roal)

Hepatitis and other viruses like CMV, Herpes, and Epstein Barr

ETOH and Toxins

Autoimmune Diseases

Diseases of the veins in the liver

Metabolic Disease

Cancer

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27
Q

What are some general s/s of liver dysfunction

A

pallor

jaundice

muscle atrophy

edema

vitamin deficiencies

skin excoriation r/t itching

petechiae

ecchymotic areas

spider angiomas

palmar erythema

neuro changes

male specific changes

unstable blood glucose

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28
Q

What causes jaundice?

A

When the body cannot excrete bilirubin it will leek into the dermal layers causing the coloring

Also since it seeps onto the peripheral nerves it causes scratching and itching

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29
Q

Why does liver dysfunction cause muscle atrophy

A

because there is decreased ability to make protein

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30
Q

Why does edema occur from liver dysfunction

A

because of low protiein levels

proteins hold water in the bloodstream and prevent it from leaking out, but if these levels are low then water will begin third spacing

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31
Q

Why does petechiae occur with liver disease

A

broken capillaries

its because there is a low platelet count associated with it

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32
Q

What causes the ecchymosis seen with liver dysfunction

A

the increased clotting time since the lvier cannot make the clotting factors

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33
Q

Spider Angiomas

A

abnormal collection of blood vessels near the surface of the skin

the liver cannot metabolize the circulating estrogen causing dilation of the vessels and causing this to form

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34
Q

What about liver dysfunction causes the palmar erythema

A

red itchy hands

due to estrogen which is dilating the vessels

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35
Q

What sort of changes occur in males as a result of liver dysfunction

A

gynecomastia

testicular hypertrophy

(all due to hormone metabolism being improper)

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36
Q

What sort of neuro changes occur with liver dysfunction and why?

A

cognition issues, tremors, asterixis, weakness, slurred speech

It occurs because large amounts of ammonia build up and seep into the neuro system

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37
Q

Asterixis

A

s/s of hepatic encephalopathy/cirrhosis

the patient will hold the hand out and dorsiflex for a few seconds. If the patients hand begins flopping down and up it is a sign

“flapping tremor”

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38
Q

Child-pugh Classification

A

scale used to predict the outcomes of patients with liver disease

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39
Q

What is the total child-pugh score based on

A

5 Parameters:

Ascites

Bilirubin

Albumin

PT

Encephalopathy Stage

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40
Q

The ____ the child-pugh score the ___ the prognosis

A

higher; poorer

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41
Q

What are the points like in the child-pugh classification

A

Grade A = score of 1-6

Grade B = Score of 7-9

Grade C = Score of 10-15

Each category is 1,2, or 3 points from absent, slight to moderate

The higher the score the worse

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42
Q

What is the most common type of jaundice with liver disease

A

hepatocellular/ OBSTRUCTIVE jaundice

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43
Q

4 types of Jaundice

A

Hemolytic

Hepatocellular

Obstructive

hereditary

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44
Q

Hemolytic Jaundice

A

Increased destruction of RBCs - maybe liver is fxning but bilirubin isnt secreted as fast as breakdown is

could be from a hemolytic transfusion rxn with a high level fo free/unconjugated bilirubin

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45
Q

At what level of bilirubin is the CNS beginning to have effects on it

A

20-25 mg/dL

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46
Q

Hepatocellular Jaundice

A

Liver cells are damaged so bilirubin cannot be cleared

Can occur with cirrhosis, hepatitis, and other dx of damaged liver

underlying pathology - so there may be anorexia, fatigue, malaise, weakness, weight loss

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47
Q

Hereditary Jaundice

A

Result of several inherited disorders characterized by an increase in unconjugated bilirubin

hereditary in nature

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48
Q

Obstructive Jaundice

A

bile duct occlusion from gall stones, tumors, or inflammation

bile backs up in intestines

intolerance to fatt foods, voiding orange foamy urine and clay colored stool

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49
Q

What are some interventions for Jaundice

A

soothing baths for itchiness

keeping naisl as short as possible

other ways of providing good skin care to the patient

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50
Q

Signs/Symptoms of Hepatocellular Jaundice

A

mild or severely ill

lack of appetite, NV, weight loss

malaise, fatigue, weakness

HA, chills, fever, infection

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51
Q

S/S of Obstructive Jaundice

A

dark orange brown urine

clay colored stools

dyspepsia and intolerance of fatsand impaired digestion

pruritis

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52
Q

General Consequences of Liver Dysfunction

A

ascites

esophageal varices

hepatic encephalopathy

hepatic coma

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53
Q

Portal HTN

A

associated with cirrhosis

increased pressure in the portal venous system from obstruction of blood flow into and through the damaged liver

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54
Q

Major consequences of portal HTN are __ and __

A

ascites and varices

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55
Q

Why can splenomegaly and thrombocytopenia occur with portal HTN

A

blood back up increases platelet pooling in the spleen increasing the size

this pooling also accounts for the worsening thrombocytopenia

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56
Q

Ascites

A

Shifting of fluid into the peritoneal cavity

manifests as distention and pressure can lead to an umbilical hernia

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57
Q

Why does ascites occur

A

combination of portal HTN and obstruction of blood flow through the damaged liver cells which causes SODIUM and WATER RETENTION leading to hypovolemia

Basically, if liver not working no proteins are broken down –> albumin synthesis and osmotic pressure decreases –> fluid shifts into peritoneal cavity

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58
Q

Diagnostic Findings for Ascites

A

SHIFTING DULLNESS - on percussion

Flank Edema

Fluid Wave

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59
Q

Shifting Dullness

A

percussion sound of ascites

the area of dullness changes moving supine to side lying

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60
Q

Abdominal Fluid Wave

A

a way to assess for ascites

place hands on the sides of the patients flank and strike one side of the flank

this will detect a wave with the other hand on the opposite side

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61
Q

What is the major complication of ascites

A

spontaneous bacterial peritonitis (SBP)

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62
Q

Spontaneous Bacterial Peritonitis

A

ascites fluid in the peritoneal cavity gets infected

there may be no clinical signs of this but if they do show it is worsening liver fnx, malaise, and fever

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63
Q

What is needed to diagnose spontaneous bacterial peritonitis

A

a pericentesis

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64
Q

What is the treatment for SBP

A

antibiotics and prophylactic antibiotics to prevent recurrence

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65
Q

Hepatorenal syndrome

A

a potential complication coming from SBP

if the SBP is untreated or v aggressive this syndrome can occur which is renal failure without any pathological changes to the kidney

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66
Q

Medical management of Ascites

A
  1. Low Sodium Diet
  2. Diuretics
  3. Bed Rest (Lay Down)
  4. Paracentesis
  5. TIPS
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67
Q

What is the salt limitation maximum with ascites

A

500 mg-2 G a day

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68
Q

What is important to teach about the low salt diet with ascites the patient may not realize

A

to avoid salt substitutes because they can have ammonia in them and if the liver is damaged it cannot get rid of them

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69
Q

Paracentesis

A

removal of fluid from the peritoneal cavity via a puncture or small incision to the abdominal wall under sterile conditions

no longer routine tx, but just dx and examination of fluid or for large ascites

done via ultrasound

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70
Q

What position should a patient be in during paracentesis

A

Upright to keep the fluid near the abdominal wall and promote easier puncture and removal of peritoneal fluid

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71
Q

Risk of paracentesis

A

risk of infection

risk for bleeding (esp with a compromised liver)

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72
Q

Pre-Op Paracentesis

A

Check Consent

Have Patient Void (comfort and prevent injury)

Monitor VS

Obtain weight and abdominal girth

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73
Q

Intra-Op Paracentesis

A

position as upright as possible

monitor VS

monitor for s/s of hypovolemia (pallor, tachycardia, hypotension)

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74
Q

Post-Op Paracentesis

A

Monitor for s/s of hypovolemia

obtain weight and abdominal firth

measure, describe, document fluid collected

assess puncture site for drainage (pressure dressing may be applied)

check and monitor neuro status

limit activity

fluid/lyte replacement (albumin) (to correct ineffective blood volume that can lead to sodium retention)

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75
Q

TIPS stands for

A

Transjugular Intrahepatic Portosystemic Shunt (Procedure)

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76
Q

Purpose of TIPS

A

decrease portal HTN which can contribute to ascites

done for refractory ascites (ascites not responsive to Na restriction or diuretics) and after several rounds of paracentesis

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77
Q

Big Risk of TIPS

A

considerable risk for encephalopathy

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78
Q

What happens during TIPS

A

cannula goes into a portal vein and an expandable stent is placed to serve as a shunt between portal circulation and the hepatic vein

this decreases sodium retention and improves renal response to diuretic therapy as a result

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79
Q

What are some of the procedures to treat ascites

A

Paracentesis

Diet and Diuretic

TIPS

Peritoneovenous Shunts (Denver, LeVeen)

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80
Q

Peritoneovenous Shunts

A

Drains or catheters permanently placed if patients have frequent ascites hx and dont need to keep getting paracentesis

prevents incisions and constant procedures needed

can also drain lung fluid

shunts fluid from the peritoneal cavity into systemic circulation (through the internal jugular vein or superior vena cava)

81
Q

What is the issue with peritoneovenous shunts

A

they are hard to maintain long term

a liver transplant may ultimately be considered

82
Q

Education for those with Ascites

A

defintion of ascites

rationale for low sodium diet, bed rest

medications (diuretics)

major complication (spontaneous bacterial peritonitis

paracentesis and TIPS

83
Q

Things to monitor with ascites

A

abdominal girth q shift

daily weight

strict I&Os

fluid and electrolyte balances

respiratory status

s/s of encephalopathy

84
Q

Most common cause of Ascites

A

cirrhosis

85
Q

Main contributor to why ascites occurs

A

portal HTN

exact patho is unknown but sodium retention related to portal HTN is the key

86
Q

What is the pathway of treatment for ascites

A

1st line: Sodium restriction diet and aldactone K sparing diuretic

2nd: may add loop diuretic like lasix

3rd - paracentesis

4th - TIPS / P Shunt

5 - liver transplantation

87
Q

Varices

A

Another complication from liver disorders

Portal HTN occurs so the veins drain into the portal system and are subject to high pressure from the liver

this makes the veins distended, tortuous, and varicosities develop

can occur in the esophagus and stomach

88
Q

More than 50% of ___ patients will develop varcies

A

cirrhosis

89
Q

Why is a varicosity rupture a medical emergency

A

the patient can bleed out fast

plus with liver issues theres coagulation issues so its even faster than normal

90
Q

What sort of things can cause a varices rupture/bleeding

A

heavy lifting

sneezing

coughing

vomtiting

reflux

straining

ASA

91
Q

What are some of the manifestations of varices

A

hematemesis

melena

general deterioration of physical and mental status

s/s of shock - develop fast

92
Q

What can happen if the s/s of shock from varices does not occur

A

then renal perfusion may be decreasing leading to ammonia levels rising high and leaving them at risk for encephalopathy

93
Q

What diagnosis presence of varices bleeding

A

ENDOSCOPY

Also: CT, Barium Swallow, Angiography

94
Q

What are some of the interventions for bleeding varices

A

ICU admission and transfer:

Balloon tamponade

vasopressin

sclerotherapy

banding

TIPS

95
Q

How does a balloon tamponade help bleeding varices

A

a gastric balloon entered through the nsoe will inflate and sit in the stomach to compress varices in the esophagus

but it will need frequent suctioning

96
Q

Why should there always be scissors bedside with a balloon tamponade

A

in case the tube slips or move you need to be able to cut the tube fast to prevent asphyxiation

97
Q

Why is cardiac monitoring important with a balloon tamponade

A

the placement of the tube can stimulate the vagal nerve so it could cause bradycardia and we need to monitor for thatq

98
Q

What is used to minimize ballooon tamponade displacement

A

traction

99
Q

Why use vasopressin for bleeding varices

A

Causes vaso constriction to decrease portal pressure

BUT contraindicated for those with CAD (can cause MI)

Caution: has diuretic effect so monitor lytes, Na, and K levels

100
Q

Why use beta blockers for bleeding varices

A

decrease portal pressure and can be used as prophylaxis for bleeding

101
Q

Sclerotherapy

A

endoscope

sclerosing agent injected into a varices to shrink it

you then monitor for esophagus perforation, aspiration pneumonia, and strictures

102
Q

Varices Banding

A

using an endoscope, a tube with rubber bands goes in and suctions and then bands a bleeding varices until it necroses and falls off

103
Q

Hepatic Encephalopathy

A

(Portosystemic Encephalopathy (PSE))

The FINAL consequence of hepatic dysfunction

Life Threatening

Profound liver failure causing neuropsychiatric (not physical) manifestations

104
Q

How fast is the presence or onset of hepatic encephalopathy

A

can be gradual OR sudden

105
Q

What are some s/s of Hepatic Encephalopathy

A

sleep and behavioral changes

patient is confused and unkempt

alterations in mood or sleep patterns

106
Q

What are the 2 explanations for Hepatic Encephalopathy

A
  1. Ammonia
  2. Portosystemic Shunting
107
Q

Ammonia explanation of hepatic encephalopathy

A

The liver is unable to detoxify these ammonia byproducts, so levels build up to neuropsych conditions by saturating the CNS

108
Q

Portosystemic Shunting explanation of hepatic encephalopathy

A

Since the liver is not working, the blood if shunted through with toxic substances to collateral vessels

These substances end up in systemic circulaton causing the neuropsych symptoms

109
Q

What are some things that can precipitate encephalopathy when there is liver dysfunction

A

things increasing ammonia levels!!!:

GI bleeding (HgB breakdown stimulating ammonia increase)

high protein diets

bacterial infections

hypercatabolic state (excessive breakdown of body tissue or substances)

renal failure leading to inability to clear ammonia

110
Q

How many stages of hepatic encephalopathy are there

A

4 stages

111
Q

Stages of Hepatic Encephalopathy S/S

A

1: LOC nL, lethargy, euphroai, up at night sleep during day, normal EEG, inability to draw line figures, asterixis

2: drowsy, disoriented, mood swings, abnormal EEG

3: Stupour, hard to rouse, sleeps a lot, confusion, increased DTRs, rigid extremities

4: Comatose, absence of DTR and asterixis, flaccid extremities, seizures

112
Q

Nursing Dx for Hepatic Encephalopathy

A

1: Activity intolerance, self care deficit

2: impaired social interaction, ineffective role performance, risk for injury, confusion

3: Imbalanced nutrition, impaired mobility, impaired verbal communication

4: risk for aspiration, impaired gas exchange, impaired tissue integrity

113
Q

Constructional Apraxia

A

a symptom of hepatic encephalopathy

graphic evidence of hep. enceph.

Progresses from not being able to produce a simple figure in 2 or 3 dimensions and gets worse

114
Q

Medical Management of Hepatic Encephalopathy focuses on what

A

eliminating precipitating factors

115
Q

What are some of the nursing care ways for patients with hepatic encephalopathy

A

ammonia lowering therapy - medicine, fruit juice po, NG or enema

IV glc - record I&O, monitor sugar, explain meds

Vit/Lyte - explain reason and monitor

antibiotic - explain and report s/s infection

prevent worsening and consider liver transplant - VS q 4 hours, neuro check, daily weight, etc

home care teaching like diet

116
Q

Why is lactulose given to hepatic encephalopathy patients

A

it works to remove ammonia by trapping it and allowing for it to be expelled in feces

117
Q

Why is IV glucose given to someone with hepatic encephalopathy

A

to minimize protein breakdown and reduce the amount of free ammonia floating around in the body

118
Q

When is a protein restricted diet used for hepatic encephalopathy

A

only if lactulose does not work

it only is used short term because longer restrictions do more damage than good

vegetable proteins are tolerated better and high protein diet is contraindicated because of ammonia production

119
Q

Viral Hepatitis

A

systemic infection that can cause necrosis of liver cells

this can then produce a cluster of physical, chemical, and biochemical changes

120
Q

Hepatitis A

A

A viral hepatitis spread by poor hand hygiene

liver infection

121
Q

How is Hep A Spread

A

fecal-oral

122
Q

Hep A mostly infects what population

A

younger children - esp those in daycare

123
Q

Incubation of Hep A

A

2-6 weeks

124
Q

How long does Hep A last

A

4-8 weeks

125
Q

What is the mortality rate of Hep A

A

0.5% for those younger than 40 and 1-2% for those over 40 years old

126
Q

Manifestations of Hep A

A

2 Phases:

  1. Mild flu like symptoms, low grade fever, anorexia
  2. Jaundice, dark urine, indigestion, epigastric distress, enlargement of spleen and liver
127
Q

What is management of Hep A like

A

PREVENTION

Bed rest during the acute phase

Nutritional Support

128
Q

What are some ways to prevent Hep A

A

good handwashing, safe water, proper sewage disposal

vaccination

immunoglobulins for passive immunity

129
Q

When must immunoglobulins be given to prevent Hep A

A

must be administered with 2 weeks of having symptoms, but past that there is less effectiveness

130
Q

Hepatitis B

A

viral liver infection transmitted through blood, saliva, semen, and vaginal secretions

131
Q

How is Hep B transferred

A

sexual transmission

Needle drug use

to infants at time of birth

(blood semen saliva vaginal secretions)

132
Q

Hepatitis ___ is a major worldwide cause of cirrhosis and liver cancer

A

B

133
Q

How long is the incubation period of HepB

A

1-6 months

134
Q

S/S of Hepatitis B

A

Variable and Insidious

Similar s/s to A: loss of appetitive, dyspepsia, abdominal pain, generalized aching, malaise, weakness

Jaundice may or may not be evident unlike in HepA

135
Q

Medications for Chronic Hepatitis Type B

A

alpha interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)

136
Q

Treatment for Hepatitis B

A

Medications

Bed rest and nutritional support

vaccinations

137
Q

What is vaccination like for Hep B

A

for person at high risk

routine vaccination of infants

passive immunization for those exposed

standard precautions and infection control measures

screening of blood and blood products

138
Q

Hepatitis C

A

virla liver infection transmitted by blood and sexual contact including needle sticks and sharing of needles

s/s usually mild

139
Q

Hep _ is the most common bloodborne infection

A

C

140
Q

Hep _ is a cause of one third of cases of liver cancer and most common reason for liver transplant

A

C

141
Q

Incubation period of Hep C

A

variable - 15 to 160 days

wide incubation period

142
Q

What frequently occurs with Hep C

A

chronic carrier state

143
Q

Management Methods of Hep C

A

antiviral meds

avoid alcohol which potentiates the disease and medicines impacting the liver

prevention (programs to decrease needle sharing in drug users)

screening of blood supply

safety needles for healthcare workers

144
Q

Hepatitis D

A

blood and sexual contact transmission viral liver infection

145
Q

Hepatitis D can only occur…

A

in persons with Hepatitis B

146
Q

What are some examples of ways to get Hep D

A

use of IV or injection drugs

patients undergoing hemodialysis

recipients of multiple blood transfusions

147
Q

What is likely to develop because of Hep D

A

fulminant liver failure or chronic active hepatisis and cirrhosis

148
Q

Incubation period of Hep D

A

30-150 days

149
Q

What is the only licensed drug available for Hep D infection

A

interferon alfa

150
Q

Hepatitis E

A

transmitted fecal-oral route through contaminated water

viral liver infection

151
Q

Incubation period of Hep E

A

15-65 days

152
Q

How does Hep E present

A

similar to Hep A

self limiting

abrupt onset

not chronic

153
Q

How to prevent Hep E

A

handwashing

clean water

good hygiene

154
Q

Non-Viral Hepatitis

A

inflammation of the liver r/t hepatotoxins rather than a virus

Can be Toxic Hepatitis or Drug Induced Hepatitis - both are acute events with chronic implications

things like carbon tetrachlorides and meds like acetaminophen cause it

155
Q

Toxic Hepatitis

A

non viral hepatitis but resembles viral hepatitis

ingestion of hepatotoxic chemicals causes this

156
Q

S/S of Toxic Hepatitis

A

fever

extreme physical weakness

hematemesis

vascular collapse

delirium

seizure

coma

157
Q

Drug Induced Hepatitis

A

non viral hepatitis

comes from ingestion of hepatotoxic chemicals in medications

158
Q

S/S of Drug Induced Hepatitis

A

abrupt onset of:

chills, fever, rash

pruritis, arthralgia, anorexia, nausea

jaundice, dark urine, enlarged and tender liver

159
Q

WHy are tx options limited for non viral hepatitis

A

because antidotes are limited

160
Q

What may have to happen if non viral hepatitis is not caught early enough and gets severe

A

liver transplantation will have to be considered
`in the interim fluid and electrolyte balance, blood replacement, and comfort/support measures are the treatment options

161
Q

Fulminant Hepatic Failure

A

a clinical syndrome of sudden and severely impaired liver function

Normally appears in a previously health person - and the patient has gone from being well to jaundice which progresses to encephalopathy quicky within 72 days

162
Q

Most common cause of fulminant hepatic failure

A

viral hepatitis

but it can be caused by drug and toxic hepatitis, and hereditary issues

163
Q

Assessment Findings of Fulminant Hepatic Failure

A

jaundice

profound anorexia

coagulation defects

renal failure

lyte disturbances

cardiovascular abnormalities

infection

hypoglycemia

encephalopathy

cerebral edema

164
Q

Tx of Fulminant Hepatic Failure

A

liver transplant

(however plasma exchange and prostaglandin therapy can be used to treat with less favorable results)

165
Q

What is Plasma Exchange therapy for hepatic failure

A

A correction of coagulation defects where pt blood is separated from plasma and returned with the plasma of a donor

not great results and usualyl they still will need a liver transplant anyways

166
Q

Interventions for Fulminant Hepatic Failure

A

ID root cause

ICU admission and transfer

Antidote

plasma exchanges

prostaglandin therapy

intracranial monitoring

mannitol (cerebral edema)

liver transplant

167
Q

The liver is able to regenerate itself, but what is the point where there is total hepatocyte damage that is irreversible

A

if more than 70% of liver fxn declines

168
Q

Cirrhosis

A

when liver fxn declines more than 70% and hepatocyte cells that are damaged are replaced by scar tissue causing nodules, bumpy appearance of the lvier, and interfere with normal vascular pathways

“Irreversible scarring that disrupts normal function and structure of the liver”

169
Q

Alcoholic Cirrhosis

A

most common cirrhosis

Cirrhosis due to alcoholism, chronic

170
Q

Postnecrotic Cirrhosis

A

second most common cirrhosis type

Cirrhosis commonly caused by viral hepatitis

appears as broad bands of scar tissues

171
Q

Biliary Cirrhosis

A

Least common type of cirrhosis

scarring occurring on bile ducts causing biliart obstruction and infection itself

172
Q

How do we learn of diagnosis and severity of cirrhosis

A

CT

Liver Biopsy

MRI

Radioisotope Liver Scan

173
Q

The two phases of liver cirrhosis are ___ and ___

A

compensated ; decompensated

174
Q

Compensated Cirrhosis

A

first stage of cirrhosis with vague symptoms of the body trying to compensate but can only do so for so long

175
Q

S/S of Compensated Cirrhosis

A

intermittent mild fever

spider hemangiomas

palmar erythema

unexplained nosebleed

ankle edema

vague morning indigestion

flatulent dyspepsia r/t malabsorption

abdominal pain

firm and enlarged liver

splenomegaly

176
Q

Decompensated Cirrhosis

A

second stage of cirrhosis

body cannot compensate anymore and signs get much worse and severe

177
Q

S/S of Decompensated Cirrhosis

A

ascited

jaundice

weakness

muscle wasting

weight loss

continuous mild fever

clubbing of fingers r/t hepatopulmonary syndrome

purpura r/t thrombocytopenia

spontaneous bruising

nosebleeds r/t low plts and portal HTN

hypotension

sparse body hair (blood flow drops and albumin level)

white nails

gonadal atrophy

178
Q

What are the 2 main complications from Cirrhosis

A

Hepatorenal Syndrome

Hepatopulmonary Syndrome

179
Q

Hepatorenal Syndrome

A

decrease in renal function related to liver disease/cirrhosis

the kidneys are fine and functionally fine but the blood flow is compromised due to portal HTN causing the renal system to fail

180
Q

Hepatopulmonary Syndrome

A

decrease in lung function related to liver disease/cirrhosis

the lungs are fine and functionally fine but increased portal HTN leads to backflow in the pulmonary system

this can then stress out the heart because it increases CO and decreases peripheral resistance as well

181
Q

Most liver cancer comes form what?

A

Few cancers actually originate in the liver, mostly cancer metastasizes there and the liver is a frequent site of metastatic cancer

182
Q

If cancer does originate in the liver, what is it related to

A

usually associated with hepatitis B and C (hepatocellular carcinoma - HCC)

183
Q

Manifestations of Liver Cancer

A

Dull persistent pain in the RUG, back, or epigastrum

Weight loss, anemia, anorexia, weakness

Jaundice, bile ducts occluded, ascites, or obstructed portal veins

184
Q

What are some early signs and diagnostic findings of liver cancer

A

early signs - liver pain (RUQ, epigastric, back)

weight loss, anorexia, and anemia

enlarged liver (jaundice and ascites)

if cancer is big enough to block portal veins it causes ascites

185
Q

Labs indicative of Liver Cancer

A

Increased serum bilirubin

Increased serum alkaline phosphatase

Increased AST, GGT, Lactic Dehydrogenase

Leukocytosis, erythrocytosis, hypercalcemia, hypoglycemia, hypercholesterolemia

186
Q

Serum Alpha Fetoprotein (AFP)

A

tumor marker elevated in 30-40% of primary liver cancer patients

187
Q

Carcinoembryonic Antigen (CEA)

A

marker of advanced cancer

188
Q

What are some ways to diagnose Liver Cancer

A

AFP

CEA

Imaging - X Ray, MRI, CT, Liver Scan, ultrasound, Arteriography, Laproscopy, PET

Liver Biopsy

189
Q

Medical Management of Liver Cancer

A

Radiation

Chemotherapy

Percutaneous Biliary Drainage

Surgical Management: Lobectomy, Local Ablation, Liver Transplant

190
Q

Percutaneous Biliary Drainage

A

PALLIATIVE NOT CURATIVE

For liver cancer

Catheter is inserted under fluoroscopy to bypass obstructed biliary ducts

191
Q

Liver Transplant

A

total removal of liver and a replacement with a health donor from cadaver, donor, or partial lobe from live donor in same anatomical position is placed

192
Q

When is liver transplant usually used

A

for life threatening and end stage liver disease with no other treatment available

193
Q

Model of End Stage Liver Disease (MELD) Score

A

A score that helps caculate the degree of need for a liver transplant based on bilirubin levels, PT time, INR, creatine, and cause of liver disease

there are some ethicaly questions sometimes for this in regard to alcohol dependent patients

194
Q

Liver Transplant Preoperative Nursing INterventions

A

support, education, and encouragement aare provided to help prepare psychologically for the surgery

195
Q

Liver transplant postoperative nursing interventions

A

monitor for infection, vascular complications, respiratory and liver dysfunction

close constant monitoring

196
Q

Other than the patient what are 2 other concerns for liver transplants

A

caregiver stress

ethical dillemmas

197
Q

Liver transplant success depends on ___

A

immunosuppression

198
Q

What do patients need to understand after a liver transplant

A

they need lifelong immunosuppressant medications

199
Q

Patient Education for LIver Transplants include…

A

education about lifelong measures to promote health

adhere close to therapeutic regimen with emphasis on immunosuppressive agents

education on s/s that indicate problems needing consultation with team

emphasize importance of follow up lab tests and apptments with the team