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NUR 326 > liver > Flashcards

liver Flashcards

1
Q

major functions of liver

A

Metabolism &/or storage of: Fat, CHO, PRO, vitamins and minerals
Blood volume reservoir: Distends/compresses to alter circulating blood volume
Blood filter: Helps purify blood
Blood clotting factors: Including prothrombin & fibrinogen
Drug metabolism and detoxification

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2
Q

Is the liver the largest organ in the body?

A

YES, it weighs lbs.

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3
Q

where does the liver lie?

A

the right epigastric region

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4
Q

where is most of the liver enclosed?

A

in the peritoneum

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5
Q

what type of capsule divides the liver into a left & right low?

A

fibrous capsule

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6
Q

what the the functional parts of the liver

A

the lobules

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7
Q

fill in the blank: each lobule has rows of hepatic cells (_) arranged around a central vein

A

hepatocytes

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8
Q

fill in the blank: The _ (capillaries) are in between the hepatocytes and are lined with Kupffer cells

A

sinusoids

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9
Q

Fill in the blank: _ _ remove bacteria and toxins from
the blood

A

Kupffer cells

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10
Q

portal circulation

A

The portal circulatory system brings blood to the liver from the stomach, intestines, spleen, and pancreas
The blood enters the liver through the portal vein.
The absorbed products of digestion come directly to the liver, and are sent to the lobules.
This is the “first pass effect”

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11
Q

The functions of the liver are numerous and
can be summarized into 4 main categories:

A

digestive
endocrine
hematologic
excretory

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12
Q

digestive function

A

Bile secretion (helps with fat digestion).
Processing and storage of fats, carbs, proteins, and minerals.

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13
Q

endocrine funtion

A

Metabolism of glucocorticoids, mineralcorticoids, and sex hormones.
Regulation of carb, fat, and protein metabolism.

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14
Q

hematologic function

A

Temporary storage of blood.
Removal of bilirubin (broken down hgb) from bloodstream.
Synthesis of blood clotting factors.

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15
Q

excretory function

A

Excretion of bile pigment & cholesterol.
Synthesis of urea
Detoxification of drugs and other foreign substances

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16
Q

typically when talking about LFTs we are talking about which labs?

A

ALT, AST, & Alk Phos.

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17
Q

thinking of all liver tests which increase and which decrease when the liver is not working?

A

ALT, AST, & Alk Phos = increase.
bilirubin= increase
serum ammonia= increase
serum protein= decrease
serum albumin= decrease
prothrombin time = increase.

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18
Q

jaundice [icterus]: what is it and whats the cause?

A

Yellowish discoloration of skin and deep tissues.
Caused by increased level of bilirubin in the bloodstream.
Usually causes problems and is noticeable with total bilirubin is greater than 2-2.5mg/dl.
Look at conjugated versus unconjugated to determine possible cause.

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19
Q

3 classifications of jaundice

A

Hemolytic: increased breakdown of RBCs
Hepatocellular: liver unable to take up bilirubin from blood or unable to conjugate it
Obstructive: decreased or obstructed flow of bile

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20
Q

bilirubin

A

By product of heme breakdown, mainly hemoglobin

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21
Q

Elevations of INDIRECT (unconjugated) bilirubin =

A

bilirubin overproduction OR impaired liver functioning
overproduction ex: hemolysis, ineffective erythropoiesis.

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22
Q

Elevations of DIRECT (conjugated) bilirubin =

A

liver working, but can’t get the bilirubin out
EX. bile duct obstruction, gall stones.

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23
Q

Jaundice: Clinical Manifestations

A

Urine = darker
Liver enzymes = elevated
Stools = Normal or clay colored, d/t liver infection that reduces bile production or flow.
Pruritis d/t bilirubin build up; specifically on palms of hands & soles of feet or generalized.

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24
Q

define viral hepatits

A

Inflammation of the liver.
systemic virus that affects the liver.

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25
Q

what are the different types of hepatitis?

A

HAV, HBV, HCV
Other viruses that cause hepatitis: Epstein-Barr, cytomegalovirus.

26
Q

can hepatitis occur from other causes?

A

yes, from Alcohol abuse, drugs, chemicals, and bacteria.

27
Q

which Hepatitis is most dangerous in pregnancy?

A

Hep E

28
Q

patho of viral hepatitis

A

1.Viral infection
2.Immune response: inflammatory mediators
3.Lysis of infected cells
4.Edema and swelling of tissue
5.Tissue hypoxia
6.Hepatocyte death!

29
Q

describe the prodromal phase

A

2 weeks after exposure.
s/s: Fatigue, anorexia, malaise, nausea, vomiting, HA hyperalgesia, cough, low-grade fever.
HIGHLY transmissible

30
Q

describe the icteric phase

A

Begins with jaundice, usually occurs 1-2 weeks after prodromal stage & lasts 2-6 weeks.
s/s: Jaundice, dark urine, clay-colored stools.
Liver enlarged and may be painful to palpation
Fatigue, abdominal pain persists or increases in severity.
can develop to chronic hep B or C.

31
Q

describe the recovery phase

A

Resolution of jaundice
6-8 weeks after exposure, symptoms diminish
Liver remains enlarged/tender
LFT & enzymes return to normal 2-12 weeks after onset of jaundice.
can happen with hep A, B or C.

32
Q

Viral Hepatitis: Complications

A

Chronic hepatitis
Liver cirrhosis
Liver cancer
Fulminant viral hepatitis – acute liver failure

33
Q

Hepatitis A

A

considered food borne illness r/t unclean sanitation practices.
Transmission: fecal-oral, parental, sexual.
Acute onset with fever.
Usually mild severity
Does NOT lead to chronic hepatitis.
Usually affects children and adult.
prevention: Hand hygiene, Hep A vaccine.

34
Q

Hepatitis B

A

Transmission: parental, sexual
Insidious onset: has a long incubation period.
Severe disease, may be prolonged course or develop into chronic.
Any age group affected
Prevention: HBV vaccine (children & HCW) and safe sex and hygiene

35
Q

Hepatitis C

A

Transmission: parental, sexual
Insidious onset, Mild to severe symptoms.
Can develop into chronic hepatitis (80%)
Any age is affected
prevention: Screening blood, hygiene; NO vaccine.
Leads to hepatocellular carcinoma, liver transplant.

36
Q

Hep A vaccine

A

2 doses 6 months apart
Recommendations: All children beginning at age 12 months, Special “high risk” populations.

37
Q

Hep B vaccine

A

3 doses at least 4 months apart
Recommendation: All infants beginning as newborns

38
Q

Hep C

A

NO VACCINE.

39
Q

Pharm for HBV: Two classes of drugs are used for chronic HBV….

A

Interferons
Nucleoside analogs

40
Q

Pharm for HBV:
Disadvantages of treatment:

A

Prolonged therapy
Costs and adverse effects
High relapse

41
Q

Pharm for HBV:
Treatment is only for high-risk patients:

A

↑ AST levels
Hepatic inflammation
Advanced fibrosis

42
Q

Pharm for HCV

A

Treatment is only recommended for patients with chronic disease
However this thought process is changing with the introduction of newer, very effective drugs
Now easily treatable and eliminated in most all patients
Treated with direct-acting antiviral therapy and interferon-based regiments
Some require treatment along with a nucleoside analogue medication as well

43
Q

DEFINE Cirrhosis

A

Irreversible, inflammatory, fibrotic liver disease.
Structural changes from injury (alcohol/viruses) & fibrosis.
Chaotic fibrosis leads to obstructive biliary channels and blood flow that cause jaundice and portal hypertension.
Regeneration is disrupted by hypoxia, necrosis, atrophy, and liver failure.

44
Q

Cirrhosis Common Causes

A

Hepatitis B&C
Excessive alcohol intake
Idiopathic
Non-alcoholic fatty liver disease [NASH, NAFLD]

45
Q

name the 1st stage of alcoholic liver disease

A

Alcoholic fatty liver: Mildest, asymptomatic

46
Q

name the 2nd stage of alcoholic liver disease

A

Alcoholic steatohepatitis: Precursor to cirrhosis
increase hepatic fat storage, Inflammation, degeneration of hepatocytes w/ infiltration of WBC that leads to inflammation.
stimulating irreversible fibrosis.
S/S: anorexia, Nausea, Jaundice, edema
very concerning phase.

47
Q

name the 3rd stage of alcoholic liver disease

A

Alcoholic cirrhosis: Fibrosis and scarring alter liver structure.

48
Q

Cirrhosis: patho

A

1.Liver cells destroyed
2.Cells try to regenerate
3.Disorganized process
4.Abnormal growth
5.Poor blood flow and scar tissue
5.Hypoxia
6.Liver failure

49
Q

Cirrhosis: Early Manifestations

A

GI disturbances: N/V, Anorexia, Flatulence, Change in bowel habits.
Fever, weight loss
Palpable liver

50
Q

Cirrhosis: Late Manifestations

A

Jaundice
Peripheral edema
Decreased albumin & PT
Ascites
Skin lesions
Hematologic problems (anemia, bleeding)
Endocrine problems
Esophageal & anorectal varices
Encephalopathy

51
Q

portal hypertension

A

Resistant portal blood flow leads to varices & ascites

52
Q

portal hypertension causes

A

Causes: systemic hypotension, vascular underfilling, stimulation of vasoactive (RAAS system) systems, plasma volume expansion, increased cardiac output = ascites

53
Q

portal hypertension complications

A

asymptomatic until the complications occur.
Variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy

54
Q

portal hypertension treatment

A

prevent/treat complications.
liver transplant

55
Q

Hepatic Encephalopathy

A

30-45% of cirrhosis patients.
LOC is the primary driver of diagnosis.
Correlate with liver labs: mainly ammonia which is primary chemical driver of LOC changes
goes from changes in behaviors to confusion to coma

56
Q

Acute liver failure:

A

Separate liver failure NOT caused by cirrhosis or other type of liver disease.
Can occur 6-8 weeks after a viral hepatitis or metabolic liver disease.
5 days to 8 weeks after an acetaminophen overdose.

57
Q

Acute liver failure patho:

A

edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissue.

58
Q

Acute liver failure: signs & treatment

A

Signs are similar to cirrhosis symptoms.
Treatment: not much, liver transplant

59
Q

Acute liver failure: most common cause

A

acetaminophen overdose

60
Q

acetaminophen antidote

A

acetylcysteine

61
Q

lactulose

A

Class: Hyperosmotic laxative
Indication: reduction of ammonia absorption in hepatic encephalopathy
MOA: reduces blood ammonia levels by converting ammonia to ammonium
Given PO, enema/rectal
Can be given to titrate by # of stools or by ammonia levels.
Not just given for high ammonia levels though– must have signs/symptoms of encephalopathy
Make sure that patient is NOT hypokalemic

62
Q

rifaximin

A

MOA: inhibits bacterial RNA synthesis by binding to bacterial DNA (initially used as an antibiotic for GI infections)
SE: peripheral edema, nausea, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
indication: Second line if lactulose isn’t working.
sometimes given preventive, depends on HCP
Given PO
associated with an increased risk of C diff.

NUR 326 (13 decks)

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