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410 Patho Exam 5 > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

the following flashcards is going to be on the in class recording for cirrhosis

A
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2
Q

what is the function of the liver?
(7 things she mentions in class)

A

metabolizes drugs
( lack of the medication in the body to aid )

produces clotting factors
( bleeding tendencies )

purifies your blood
( focuses on ammonia )

jaundice
( we are not breaking down bilirubin )

amber colored urine

pale colored stool

pruritus - leak out through the skin - bile/salt
- aid with the itching, trim their nails, antihistimaintes for the medication
- oatmeal warm baths

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3
Q

when you have too much ammonia, what happens to our body ?

A

confusion -> encephalopy

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4
Q

what is cirrhosis ?

A

end stage liver disease

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5
Q

what are is the patho behind cirrhosis ?

A

inflammation and necrosis of cells leads to fibrosis
resulting in extensive degeneration and destruction of the liver cells

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6
Q

what are some main/common causes for why patients end up developing cirrhosis ?

A

hepatitis C
NASH
alcohol

other causes include
- extreme dieting
- malabsorption
- obesity
- environmental factors
- genetic predisposition

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7
Q

what is NASH?
nonalcoholic steatohepatitis?

A

a really aggravated fatty liver that can result in patients developing cirrhosis

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8
Q

what is biliary cirrhosis ?

A

associated with blockage of bile ducts or inflammation and obstruction of bile

( gallstones )^

  • can be associated with colitis or crohns disease
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9
Q

what is cardiac cirrhosis?

A

results from long-standing severe right-sided heart failure

  • fluid goes to the peripheral, so the organs will enlarge
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10
Q

how are we going to treat cardiac cirrhosis ?

A

so as she’s talking in the recording, she’s mentioning that we always want to treat the underlying causes, weather the disease is the same for everything.

for cardiac cirrhosis, its our heart that is causing problems to our liver, so we are going to try to treat the right sided heart failure first then treat the resulting pain in the liver after

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11
Q

what are the clinical manifestations you will see in a patient with early stage liver disease?

A

very few to none

but you will see fatigue and an enlarged liver

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12
Q

what are some later clinical manifestation related to liver failure and portal hypertension?

A

jaundice
peripheral edema
ascites
skin lesions
hematologic,endocrine, neurologic disorders

liver becomes smaller and nodular

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13
Q

why do patients with cirrhosis end up having jaundice ?

A

results from decreased ability to conjugate and excrete bilirubin

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14
Q

not only do patients end up with jaundice from the fact that they can’t excrete it, but also from what?

A

the overgrowth of connective tissue in liver compresses bile ducts
- leading to obstruction and increase in bilirubin in vascular system

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15
Q

why do patients develop skin lesions when they have cirrhosis ?

A

due to increase in circulating estrogen due to inability of liver to metabolize steroid hormones

  • this is very itchy
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16
Q

what are the 2 skin lesions patients with cirrhosis have?

A

spider angioma
palmar erythema

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17
Q

why are we concerned for patients with cirrhosis when it comes to developing hematologic disorders ?

A

bone marrow suppression, anemia, and coagulation disorders because the liver can not make clotting factors

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18
Q

why are we concerned for patients with cirrhosis when it comes to developing endocrine disorders ?

describe what happens to men
describe what happens to women

A

gynecomastia - breast
- loss of axillary and pubic hair, testicular atrophy, impotence and loss of libido

women
- amenorrhea or vaginal bleeding

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19
Q

endocrine disorders can lead to something called hyperaldosteronism in both sexes, meaning what two things?

A

sodium and water retention
potassium loss

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20
Q

so we understand that cirrhosis is going to cause the patient to experience a lot of clinical manifestation, but as mentioned in the last flashcard, we are going to have a lot of aldosterone in our body. But due to this high aldosterone, it is going to cause us to have potassium loss.

we know that a patient with cirrhosis is at a very high risk for developing acsitits, so normally we are going to want to use a diuretic to treat it, but we know diuretic are potassium wasting. but what is the name of the diuretic we are going to use to help aid this patient ? and its for two reason too.

A

spirolantone
- potassium sparing
- aids with that aldosterone

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21
Q

why does peripheral neuropathy occur in patients with cirrhosis ?

A

usually due to the dietary deficiencies of thiamine, folic acid, and cobalamin
(vitamin b12)

remember in tb, how to treat peripheral neuropathy, give them b6 ( pyradixe )

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22
Q

what were the clinical manifestation for these patients that we just talked about ? (5)

A

jaundice
skin lesions
hematologic disorders
endocrine disorders
peripheral neuropathy

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23
Q

in compensated cirrhosis, so meaning your body and medication is helping you, what complications can you get?

A

nothing

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24
Q

in decompenstated cirrhosis what are the complications we are going to talk about ? (6)

A

portal hypertesnion
esophageal & gastric varices
peripheral edema
abdominal ascites
hepatic encephalopathy
hepatorenal syndrome

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25
Q

what is portal hypertension?

A

obstruction of normal blood flow in and out of the liver

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26
Q

what does an increase portal hypertension mean?

A

increased venous pressure in portal circulation

splenomegaly - fluid backs up

large collateral veins

ascites

gastric and esophageal varices

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27
Q

what is esophageal varices ?

A

complex of tortuous, enlarged veins at Lower end of esophagus

and bleed easily

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28
Q

esophageal varies is a life threatening complication, why do you think that is ?

think of the example she was using the recording

A

lets say you have an esophageal varies, we understand that this is an outpouching of a large vein at the end of your esophagus.

lets say you get food poisoning, and you start vomiting it out, with that vomit, you can pop the vein and cause life threatening bleeding.

remember you also have cirrhosis, so you dont have the clotting factors that you need to stop it, and not to mention, its hard to stop bleeding, deep inside your mouth.

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29
Q

how do you get peripheral edema?

A

decreased vascular pressure due to decreased albumin production by the liver

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30
Q

how do you get ascites?

A

accumulation of serous fluid in peritoneal or abdominal cavity

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31
Q

what are the 3 main causes or several mechanism on how patients with cirrhosis end up getting ascites?

A

portal hypertension causes proteins to leak into lymph system. the lymph system becomes overwhelmed and leak out.

hypoalbuminemia

hyperaldosteronism

32
Q

patients with severe ascites are at risk for developing what? and what is it?

A

pleural effusion
- accumulation of fluid in the pleural space up near the lungs
- risking patient with aspiration and cardiac tamponade

  • causing short of breathe, pnuemonia risk
33
Q

why do we assess a patients respiratory function when they have ascites?

A

remember think of how the fluid will move in the body.
the lower gi is not that far from your diaphragm and lungs.

so fluid can shift upwards and cause discomfort in your lower respiratory tract, causing your ability to breathe to be alerted and potentially stopped.

34
Q

what are you going to hear when you are percussing on a patients abdomen?

what are you going to see if you push on a patients ascites belly?

A

dullness, its just pure fluid

wave like motion, remember its just free sitting fluid

35
Q

how do patients with cirrhosis end up having hepatic encephalopathy?

A

liver unable to convert increased ammonia to urea

36
Q

why is having an increased ammonia level bad in general?

and describe how patients will behave

A

its neurotoxic because it crosses the blood brain barrier and

results in patients being confused, change in personality, sleep disturbances, and end up imparing their consciousness

37
Q

what are the 3 main hepatic encephalopathy clinical manifestations?

A

asterixis
apraxia
fetor hepaticus

38
Q

what does asterixis mean ?
what does apraxia mean?
what does fetor hepaticus mean?

A

flapping tremors

impairment in writing
( difficulty in moving pen left to right )

musty, sweet odor of patients breath
- from accumulation of digestive by products

39
Q

how do patients with cirrhosis end up developing hepatorenal syndrome ?

A

renal failure with azotemia
( increase nitrogen waste ), oliguria and intractable ascites

acute kidney injury from the fact that your liver in damaged

40
Q

how do you treat hepatoreneal syndrome ?

A

liver transplant

remember its not that your kidneys are messed up, its because your liver is messed up and causing kidney problems

so if we fix your liver, your kidneys will be fixed too

41
Q

what are some diagnostic studies for patients with cirrhosis ?

what is the goal standard?

A

gold standard is a liver biopsy

liver enzyme tests
total protein, albumin levels
serum bilirubin, globulin levels

42
Q

when doing a liver biopsy on a patient who has cirrhosis, what is our main concern after the procedure and why ?

A

bleeding

remember they dont have the clotting factors to stop the bleeding

43
Q

we always want to tell patients that have cirrhosis to rest, however we also want to tell them to avoid ____and what medications (3)?

A

alcohol

medications
1. aspirin
2. acetaminophen
3. nsaids

44
Q

remember patients with cirrhosis are going to have a lot of vitamin deficency, but remember they have peripheral neuropathy, what is that one specific vitmain we are going to encourage these patients to have more of?

A

vitamin b complex

45
Q

what is the scale that we are going to use for patients who drink?

  • we also need to manage their withdrawals symptoms as well
A

CIWA scale

46
Q

patients with cirrhosis are at risk for developing ascites
so we are going to tell them to avoid what? (how much as well)

and what are we going to use to treat their ascites ?

A

avoid sodium for the fluid retention
( 2 grams or less per day)

diuretics - spironolactone
( aldosterone agonist and potassium sparing )

47
Q

why are we going to tell patients with cirrhosis that should consume things with more albumin in it? or receive an albumin infusion?

A

remember, low albumin levels indicate poor nutritional values

typically patients with alcohol or beer consumption, get full off those drugs, so they won’t eat, meaning they will loss weight and put on that beer belly.

we need to make sure they are getting the proper nutritents they need, so we recommend them getting albumin infusion

48
Q

what is the procedure that we can do to help aid patients with ascites?

A

paracentesis

49
Q

if a patient has a high portal hypertension and a lot of ascites, we can do something called ?

and what does it do?

A

TIPS
- transjugular intrahepatic portosystemic shunt

help reduce the portal pressure

50
Q

for esophageal and gastric varies, its is the most lethal complication with patient with cirrhosis.

we must prevent bleeding/hemorrhaging for these patients. so we tell them to avoid what?

how do we know they have this? so like what’s the diagnostic study?

how do we aid these patients to decreases the chances of it bleeding? what medication ?

A

alcohol, aspirin and nsaids.

endoscopy screening

nonselective beta blockers will decrease high portal pressure and decrease bleeding

51
Q

test question

patient with esophageal varies has started on a beta blocker, how do you know the mediation is working?

A

their varies have gotten smaller
or they are not bleeding from their varices

52
Q

this is just additional information that I can’t find on the powerpoint but dr.brooks is mentioning it.

esophageal varies is a medical emergency, remember these patients dont have any clotting factors, so the risk of bleeding becomes extremely high. we need to tell patients to be careful with what they eat, drink and even do because one pop, and they are bleeding to death.

we as a nurse need to recognize that they have this to avoid this.

what doctors can do is put bands behind these varices and make it lose blood supply and then cut it off at the end.

A
53
Q

if bleeding occurs from a esophageal varices, what do we do?

A

stablize patient
manage airway
start iv therapy and blood products

give them beta blockers

54
Q

what are the two therapies we can do to help aid esophageal varices ? (3)

A

endoscopic variceal ligation
( banding )

scleortherpay
- scar the vessels, and close it off - so blood will be redirect to deeper vessels

balloon tamponade
- mechanical compression of varies

55
Q

what are supportive measures for acute bleed with esophageal varices?

dont over think it

A

fresh frozen plasma
packed RBCS
vitamin K
proton pump inhibitors
antibiotics

56
Q

what are the two medications we are going to give these patients with an acute bleed from esopheageal varices?

A

lactulose ( cephulac )
rifaximin ( xifaxan )

57
Q

what does lactulose (cephulac ) do?

biggest side effect?

A

decrease intestinal production and absorption of ammonia

diarrhea

58
Q

breakdown of blood in the gut causes increase ___ so we must take measures to prevent ____ which is result from having this too much

A

ammonia
constipation

59
Q

what is our main concern/goal with patients with hepatic encephalopathy ?

A

reducing the ammonia formation

60
Q

what medication are we going to use to help reduce the ammonia formation in hepatic encephalopathy ?

A

lactulose ( cephulac )
- which traps ammonia in gut

61
Q

what is the diet for patients with cirrhosis ? (4)

A

high calories (3000/day)
high carbohydrate
protein restriction
moderate to low fat

62
Q

nursing assessment notes
Subjective data

Past health history
- Hepatitis
- NASH
- Chronic biliary obstruction and infection
- Severe right-sided heart failure

Medications
- Adverse reactions
- Anticoagulants, aspirin, NSAIDs, acetaminophen

A
63
Q

nursing assessment
Subjective data:

Chronic alcohol use
Weakness, fatigue
Anorexia, weight loss
Dyspepsia
Nausea and vomiting
Gingival bleeding

Dark urine
Decreased output
Light-colored or black stools
Flatulence
Change in bowel habits
Dry, yellow skin
Bruising

RUQ or epigastric pain
Numbness, tingling
Pruritus
Impotence
Amenorrhea

A
64
Q

nursing assessment objective

Fever, cachexia, wasting of extremities
Icteric sclera, jaundice
Petechiae, ecchymoses
Spider angiomas, palmar erythema
Alopecia, loss of axillary and pubic hair
Shallow, rapid respirations
Peripheral edema

Epistaxis
Abdominal distention, ascites
Distended abdominal wall veins
Palpable liver and spleen
Foul breath
Hematemesis; black, tarry stools
Hemorrhoids

Altered mentation
Asterixis
Gynecomastia
Testicular atrophy
Impotence
Loss of libido
Amenorrhea, vaginal bleeding
Anemia, thrombocytopenia, leukopenia

Decreased serum albumin and potassium levels
Abnormal liver function studies
Increased INR
Increased ammonia and bilirubin levels
Abnormal findings on abdominal ultrasonography or MRI

A
65
Q

nursing management
clinical problems

Nutritionally compromised
Ineffective tissue perfusion
Activity intolerance
Fluid imbalance

planning
Overall goals
Relief of discomfort
Minimal to no complications
Return to as normal a lifestyle as possible

A
66
Q

nursing management
Health promotion
Reduce or eliminate risk factors
Treat alcoholism
Maintain adequate nutrition
Identify and treat acute hepatitis
Bariatric surgery for morbidly obese

A
66
Q

nursing management
nutrition
Acute care

Rest needs
Prevent complications
Modify schedule
Nutritional needs
Oral hygiene
Between-meal snacks
Offer preferred foods
Explanation of dietary restrictions

A
67
Q

what is the medication we are going to use help patients with pruritus ?

A

cholestyramine
- watch our for binding affects

68
Q

nursing implementation
Acute care
Monitor color of urine and stools
Accurate I/O recording
Daily weights
Extremities measurement
Abdominal girth measurement

A
69
Q

before a patient gets a paracentesis for their ascites, what do we tell them to do ? and why ?

what position are they going to be in?

what are we monitoring ?

A

void immediately to avoid puncture into the bladder

high fowlers or sitting on the side of the bed

hypovolemia and electrolyte imbalance cause of all the fluid we are laking out

70
Q

nursing implementation
Acute care
Relief of dyspnea
Semi- or high Fowler’s position
Skin care
Special mattress
Turning schedule, at least every 2 hours
ROM exercises
Coughing/deep breathing exercises
Elevate lower extremities/scrotum

Acute care
Monitor for fluid and electrolyte imbalances
Hypokalemia
Water excess (hyponatremia)
Observe for bleeding tendencies
Assess patient’s response to altered body image
Supportive listening

A
71
Q

nursing management
bleeding varices
Close observation for signs of bleeding
Balloon tamponade care
Explanation of procedure
Check for patency
Position of balloon verified by x-ray
Monitor for complications (i.e., aspiration pneumonia)
Scissors at bedside
Semi-Fowler’s position
Oral/nasal care

A
72
Q

nursing management
hepatic encephalopathy
notes

assess neuro status Q 2 hours
Include exact description of behavior
Level of responsiveness
Sensory and motor abnormalities
Fluid/electrolyte imbalances
Acid-base imbalances
Maintain safe environment and minimize injuries
Encourage fluids
Response to treatment measures

A
73
Q

Ambulatory care
Supportive measures
Proper diet
Rest
Avoiding potentially hepatotoxic OTC drugs
Abstinence from alcohol
Caring attitude always

Community support programs
Symptoms of complications
When to seek medical attention
Written instructions with adequate explanations for patient/family
Referral to community or home health nurse

A
74
Q

nursing management evaluation
Maintenance of food/fluid intake to meet nutritional needs
Maintenance of skin integrity
Normalization of fluid and electrolyte balance
Treatment for substance use

A

410 Patho Exam 5 (6 decks)

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