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4th Semester > Cirrhosis And Hepatic Failure/ pancreatitis > Flashcards

Cirrhosis And Hepatic Failure/ pancreatitis Flashcards

1
Q

What is cirrhosis

A

Severe scarring of the liver which in turn alters the function of the liver

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2
Q

How does the function of the liver deteriorate

A

Altered bile duct flow and stasis
Impaired hepatic venous outflow
Decreased blood flow to and through the liver

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3
Q

What are complications of portal hypertension

A

Ascites
Hemmorhage of varices
Hepatic encephalopathy (HE)
Hepato renal syndrome

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4
Q

What is the only feasible treatment for end stage liver cirrhosis

A

Liver transplant

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5
Q

What is albumin

A

A blood protein with a long 1/2 life of 20 days is a late indicator
Of malnutrition

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6
Q

If albumin is decreased what will result

A

Poor wound healing due to decreased zinc levels

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7
Q

Prealbumin

A

1/2 life of 2-3 days

Sensitive indicator of nutritional status with treatments

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8
Q

What deficiency is common in liver disease

A

Thiamine related to poor diet, impaired GI absorption

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9
Q

What is this one needed for

A

This one is needed to maintain cerebral and nerve impulse function

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10
Q

What does alcohol do to the liver

A

Alcohol depletes the liver from gluconeogenesis

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11
Q

What are causes of acute liver failure

A

Toxins, drugs especially acetaminophen
Viral hepatitis
Hypoperfusion / shock due to ischemia

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12
Q

What are ALF signs and symptoms

A 
N/V 
Malaise 
Evidence of coagulopathy ( bruising, bleeding, lab abnormalities, DIC,)
Decreased LOC
HEPATIC ENCEPHALOPATHY
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13
Q

What is collaborative management of ALF

A

Obtain detailed history focused on viral infections, drugs, toxins, direct injury, acetaminophen intake
Prevent cerebral edema and MODS

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14
Q

What are complications of ALF

A 
Respiratory insufficiency/ failure 
Hemodynamic instability 
Infection/ sepsis 
Hypoglycemia 
Electrolyte imbalances
Renal failure 
Malnutrition
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15
Q

Acetaminophen

A 
Readily absorbed from G.I tract 
Primarily metabolized by the liver 
Half life 2-4 hours 
Peaks levels 4 hours after overdose 
90% excreted by the kidneys 
Unintentional poisoning may result from repeated high doses
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16
Q

What exacerbates acetaminophen toxicity

A

Fasting

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17
Q

What is treatment of acetaminophen toxicity

A

If less than 4 hours perform gastric lavage
Draw serum acetaminophen levels between 4 hrs and 24 hrs post ingestion
Promptly administer actetylcysteine I.V in 3 separate infusions over 20-24 hours
Can be given PO
GIVE REGARDLESS OF TIME OF INGESTION based on weight
Can give activated charcoal is ingested within 2 hours

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18
Q

What is considered toxic for acetaminophen

A

INGESTION of 7-10 grams is toxic over 8 hrs or less

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19
Q

What are additional complications of acetaminophen toxicity

A

Seizures that are usually well controlled with benzodiazepines

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20
Q

What are signs and symptoms of hepatic encephalopathy

A

Can start with forgetfulness, mild confusion, poor judgement, wandering, inappropriate behavior or language, poor sleep patterns, worsening handwriting, tremors, slow movement

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21
Q

Can hepatic encephalopathy recur

A

It can recur after treatment due to various triggers

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22
Q

What drug can be used to reduce the risk of recurrence of hepatic encephalopathy

A

Xifaxan-rifaximin

These are drugs that alter the bacterial content of the G.I tract

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23
Q

What is portal hypertension

A

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

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24
Q

What are consequences of portal hypertension

A

Varices in the lower esophagus, stomach, rectum,
Splenomegaly
Ascites
Hepatic encephalopathy

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25
Q

What is hepatic encephalopathy

A

The accumulation of toxins related to liver failure causes disruption of neurotransmission

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26
Q

What are symptoms of hepatic encephalopathy

A

Personality changes
Confusion
Memory loss
Stupor, coma, death

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27
Q

What is hepatorenal syndrome

A

Renal failure demonstrating oliguria, sodium and water retention, hypotension, and peripheral vasodilation due to advanced liver disease

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28
Q

What is a way cirrhosis is caused

A

Biliary channels become obstructed and cause portal hypertension, blood is shunted away from the liver and a hypoxic necrosis develops

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29
Q

What is secondary biliary cirrhosis

A

Obstruction

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30
Q

What is primary biliary cirrhosis

A

Autoimmune

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31
Q

What is pancreatitis

A

Inflammation of the pancreas
Associated with several clinical disorders ( alcohol intake and cholelithiasis, caused by injury or damage to pancreatic cells and ducts causing a leakage of pancreatic enzymes into the pancreatic tissue)

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32
Q

What are manifestations of pancreatitis

A

Epigastric pain radiating to the back
Fever and leukocytosis
Hypotension and hypovolemia
Characterized by a increase in amylase

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33
Q

What is chronic pancreatitis related to

A

Chronic alcohol abuse

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34
Q

What is albumin administered for

A

To expand blood volume
Helps maintain vascular fluid volume
Tells if liver is damaged and if so how much

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35
Q

What are causes of hypoalbuminemia

A

Severe burns

Trauma

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36
Q

What are cause of hyperalbuminemia

A

They are not associated with hepatic disease it is associated with dehydration

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37
Q

What is ammonia

A

Waste product of protein metabolism

The liver converts ammonia to urea. In liver disease the conversion doesn’t take place thus increasing ammonia levels

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38
Q

Hepatic encephalopathy is the result of what

A

High ammonia levels in the brain

The brain is very sensitive to ammonia levels

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39
Q

What is treatment for high ammonia levels

A

Medications ( lactulose, enemas)

Diet (protein intake)

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40
Q

What does lactulose do

A

It eliminates ammonia through the feces, it also causes hypokalemia as k+ is excreted through the stool

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41
Q

Signs and symptoms of hepatic encephalopathy

A

Confusion

Affects fine motor control such as writing

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42
Q

If a patient has liver disease, what happens to bilirubin levels

A

They increase

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43
Q

In liver disease, how does coagulation studies relate

A

PT, INR aPTT will be increased because the liver synthesizes clotting factors 2,7,9,10. The blood will be unable to clot quickly leading to increased risk of bleeding

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44
Q

What are hepatic enzymes

A

ALP, GGT, AST, are enzymes produced mainly in the ,over. These enzymes help identify is the liver is diseased and how badly. The higher the levels the worse the liver prognosis

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45
Q

Manifestations of liver disease

A

Portal HTN
ascites
Hepatic encephalopathy hepatorenal syndrome

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46
Q

What is portal HTN

A

Elevated pressure within the portal system due to resistance to portal blood flow

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47
Q

Varices

A

Develops on stomach, lower part of esophagus, and rectum, due to built up pressure in the portal system. They can be so distended that they rupture. A person can hemmorhage and die before they reach medical treatment

48
Q

What does rectum varices manifest as

A

Hemmorhoids

49
Q

Consequences of portal HTN

A

Splenomegaly
Ascites
Hepatic encephalopathy

50
Q

Symptoms of hepatic encephalopathy

A 
Usually happens over hours to days 
Personality changes 
Confusion 
Hallucinations
Loose fine motor skills 
Memory loss, stupor, coma, death
51
Q

What are signs and symptoms of hepatorenal syndrome

A 
Oliguria
Na and H2O retention 
Hypotension 
Peripheral vasodilation 
Ascites
Peripheral edema
Electrolyte fluid shifts 
Hypovolemia 
Decreased renal blood flow 
Decreased GFR and urine output
52
Q

Cirrhosis

A

Irreversible

Can only manage and prevent further damage

53
Q

Can the liver regenerate itself

A

Yes it can

54
Q

How does jaundice occur

A

Biliary channels are blocked

55
Q

Who is more prone to cirrhosis

A

Woman

56
Q

What is biliary cirrhosis

A

Auto immune

Obstruction in bile duct

57
Q

What is post necrotic cirrhosis

A

Results from chronic disease

58
Q

What is treatment for end stage cirrhosis

A

Liver transplant

59
Q

What lab tells if HRS is developing

A

Creatinine

60
Q

Thiamine deficiency

A

Common in liver disease due to impaired GI absorption

61
Q

What does alcohol do in regards to the liver

A

Alcohol depletes the liver from the ability to provide gluconeogenesis

62
Q

What electrolytes are decreased in cirrhosis and hepatic failure

A

k+, Na, Mg, phosphorus

63
Q

What are causes of ALF

A

Acetaminophen

Viral Hep B

64
Q

What are signs and symptoms of ALF

A

N/V
Malaise
Decreased LOC

65
Q

What’s the toxic range of acetaminophen

A

7-10 gms

66
Q

What’s the antedote to acetaminophen

A

Acetylcysteine

67
Q

For acetaminophen poisoning what should you do

A

Give acetylcysteine regardless of when poisoning occurred
Activated charcoal if ingested within 2 hrs
Gastric lavage if ingested with 4 hrs

68
Q

What are complications of ALF

A 
Respiratory failure 
Cardiac arrest 
Infection/ sepsis
Hypoglycemia 
Renal failure
Hemodynamic instability electrolytes 
Seizures
69
Q

MAT

A

Medication assisted treatment

70
Q

MAT 4 opioids

A

Methadone
Buprenorphine
Naltrexone

71
Q

MAT 4 alcohol use disorder

A

Disulfiram ( Antabuse, makes person violently ill if they try to sneak alcohol)
Acomprosate
Naltrexone

72
Q

When do mild symptoms of alcohol withdrawal occur

A

Within 6-12 hrs of last drink

73
Q

When do peak symptoms of alcohol withdrawals occur

A

They appear in 24-48 hrs

74
Q

What are nutritional needs for alcohol withdrawal

A

Thiamine
Folic SCIs
B12

75
Q

Who is at risk for acute pancreatitis

A

Alcoholics

76
Q

What labs diagnose pancreatitis

A

Increased lipase

Increased calcium

77
Q

What is trypsin

A

It protects cells by preventing avtivation of enzymes until they reach the duodenum. During inflammation trypsin activates enzymes early this basically digesting the pancreas in a process called autodigestion

78
Q

If pancreatitis is left untreated p, what complications can occur

A 
SIRS
MODS
SEPSIS
COAGULOPATHY
DIC
79
Q

What is tx of pancreatitis

A 
Vasopressors 
AGGRESSIVE fluid  rescusitation  
O2
Keep NPO provide enteral TPN feedings, watch for,fluid overload 
IV abx, tele,
80
Q

What are signs and symptoms of acute pancreatitis

A

Severe abdominal pain
Hypovolemia from dehydration
Hypoperfusion

81
Q

What is Cullen’s sign

A

Bluish color Around the umbilicus

Sign of pancreatitis

82
Q

What is turners sign

A

Bluish brownish color around the flank area

83
Q

What is pain mgmt of acute pancreatitis

A

Morphine sulfate
Meperidine decrease spasms of pancreatic duct
Insulin drip( sliding scale isn’t effective, monitor glucose Q2 hrs
Give zofrna for n/v
PPI or H2 antagonist

84
Q

What does PPIs and H2 antagonist do

A

They reduce gastric and pancreatic secretions

85
Q

What is a appropriate diet for pancreatitis

A

High carb
Low fat
Low protein

86
Q

What are complications of pancreatitis

A 
MODS 
HYPOXEMIA 
RESPIRATORY COMPROMISE 
ARDS
EDEMA
PULMONARY  EDEMA 
SIRS esp 7-14 days after dx
87
Q

What are meds for pancreatitis

A

Pancrealipase

88
Q

What is pancrealipase

A

It contains lipase, amylase, and protease which are supplemental enzymes needed for life

89
Q

Pancreatitis leads to an increased risk for what

A

SEPSIS

90
Q

What should a person report while in pancrealipase therapy

A

Report diarrhea, or abdominal cramping

91
Q

What does pancrealipase tend to increase

A

Uric acid levels leading to gout

92
Q

What can pericarditis lead to

A

SEPSIS

93
Q

What are signs and symptoms of endocarditis

A 
Murmurs
Fever
Tachycardia
SOB
fatigue
Dysrthymias
94
Q

What is tx of endocarditis

A

IV abx

May need valves replaced

95
Q

What is dx for endocarditis

A

Echocardiogram

Increased WBC

96
Q

What is serum procalcitonin

A

Early dx of SEPSIS

97
Q

Serum lactate

A

Anaerobic metabolism is taking place now, bc the pt is critically ill, the O2 is depleted and cells go into anaerobic mode. Blood cultures will need to be drawn
The higher the lactate the sicker the patient

98
Q

SIRS is the precursor to what

A

SEPSIS

99
Q

Septic shock

A

The presence of SEPSIS and refractory hypotension

100
Q

What is refractory

A

Not responding to tx

101
Q

D dimer

A

Test that determines if there is a coagulation defect

102
Q

What fluid should be given in a fluid challenge

A

0.9% NS

LR

103
Q

What is given if BP doesn’t rise in SEPSIS after a fluid challenge

A

Vasopressors, the goal is to achieve a MAP of 65 or above
Norepinephrine is the drug of choice
Low dose of dopamine Can be given if the pt is not tachycardic

104
Q

In SEPSIS, how should a fever be treated

A

Alternate between ibuprofen and acetaminophen

105
Q

DIC

A

Can develop clots, bleeding or both, give heparin to dissolve the clots, manage heparin tightly to prevent massive hemmorhaging

106
Q

How is DIC dx

A 
Decrease platelets
Increased D dimer 
Decreased fibrinogen 
Increased PT/ PTT
increased fibrite degradation products
107
Q

Cryoprecipitate

A

Contains clotting factors

108
Q

How is DIC treated

A

Mostly crystalloids
Albumin colloids
PRBCs
Pain relief from ischemia

109
Q

Cardiogenic shock

A

Hemodynamic problem

A problem within the heart itself

110
Q

What are signs and symptoms of cardiogenic shock

A

Decrease CO, leading to decreased BP, LEADING leading to increased SVR

111
Q

What is hypovolemic shock

A

A not enough fluid problem a decreased amount of fluid in the intravascular space

112
Q

What are signs and symptoms of hypovolemic shock

A

Decreased CO, leading to decreased BP, leading to increased HR

113
Q

What is distributive shock

A

Adequate blood flow and fluids, distributed abnormally. Still have decreased CO but not bc of decreased fluids
Fluids won’t help, u must correct the cause

114
Q

What is obstructive shock

A

A type of shock related to the heart, the ventricles don’t feel or empty adequately ( a ventricular problem)

115
Q

What is a disease process that can lead to obstructive shock

A

Cardiac tamponade

116
Q

What is spinal shock

A

Shock resulting form a SCI
there is adequate volume nothing is wrong with the heart
It is a type of distributive shock

117
Q

What are the stages of shock

A

Mild- reversible
Moderate- reversible
Severe- body can’t compensate

4th Semester (18 decks)

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