Exam 3 - Liver Problems Flashcards
1
Q
portal circulation
A
- brings blood in to the liver from the stomach, intestines, spleen, and pancreas
- blood enters through the portal vein
- after products are absorbed they are sent to the lobules
- this is the first pass effect
2
Q
jaundice
A
- caused by increased level of bilirubin in the bloodstream
- yellowish discoloration of skin and deep tissues
3
Q
another term for jaundice
A
icterus
4
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
5
Q
bilirubin
A
- by product of heme breakdown: mainly hemoglobin
6
Q
elevations of indirect bilirubin
A
- unconjugated
- bilirubin overproduction OR impaired liver functioning
7
Q
elevations of direct bilirubin
A
- conjugated
- liver working but can’t get the bilirubin out
- bile duct obstruction, gall stones
8
Q
clinical manifestations of jaundice
A
- darker urine
- elevated liver enzymes
- normal or clay colored stools
- pruritis
9
Q
viral hepatitis
A
- systemic virus that mainly affects the livers
- inflammation of the liver
10
Q
clinical manifestations of viral hepatitis
A
- similar between all types
- asymptomatic
- causes abnormal elevated LFTs but NOT consistent with cellular damage within the liver
11
Q
prodromal
A
- 2 weeks after exposure
- fatigue, anorexia, malaise, hyperalgesia, low-grade fever
- HIGHLY transmissible
12
Q
icteric
A
- begins with jaundice
- dark urine, clay colored stools
- liver enlarged and may be painful to palpation
- fatigue abdominal pain persists or increases in severity
13
Q
recovery
A
- resolution of jaundice
- 6-8 weeks after exposure, symptoms diminish
- liver remains enlarged/tender
14
Q
complications of viral hepatitis
A
- most recover completely with no complications
- chronic hepatitis
- liver cirrhosis
- liver cancer
- fulminant viral hepatitis - acute liver failure
15
Q
Hepatitis A
A
- transmission: fecal-oral, parental, sexual
- acute onset with fever
- usually mild severity
- does NOT lead to chronic hepatitis
- affects children and adults
- hand hygiene and hep A vaccine
16
Q
Hepatitis B
A
- transmission: parental, sexual
- insidious onset
- severe disease may be prolonged course or develop into chronic
- any age can be affected
- HBV vaccine and safe sex and hygiene
17
Q
Hepatitis C
A
- transmission: parental, sexual
- insidious onset
- mild to severe symptoms
- can develop into chronic hepatitis (80%)
- any age affected
- screening blood, hygiene
- NO VACCINE
18
Q
what can hepatitis C lead to
A
- hepatocellular carcinoma; liver transplant
- new treatment is developing and becoming more widely available
19
Q
Hepatitis A vaccine series
A
- 2 doses 6 months apart
- all children beginning at age 12 months
- special “high risk” populations
20
Q
Hepatitis B vaccine series
A
- 3 doses at least 4 months apart
- recommended in all infants beginning as newborns
21
Q
is there a vaccine for Hepatitis C
A
NO
22
Q
what are the two classes of drugs used for chronic HBV
A
- interferons
- nucleoside analogs
23
Q
who is chronic HBV treatment for
A
- high risk patients
- increased AST levels
- hepatic inflammation
- advanced fibrosis
24
Q
disadvantages of treatment for chronic HBV
A
- prolonged therapy
- costs and adverse effects
- high relapse
25
how is chronic HCV treated
- with direct acting antiviral therapy and interferon-based regiments
- some require treatment along with nucleoside analogue medication
26
who is treatment for HCV recommended
- only recommended for patients with chronic disease
- this is changing with the introduction of newer, effective drugs
- not easily treatable and eliminated in most all patients
27
cirrhosis
- irreversible, inflammatory, fibrotic liver disease
- structural changes from injury and fibrosis
28
what does chaotic fibrosis lead to
- obstructive biliary channels and blood flow -> jaundice and portal hypertension
29
what is liver regeneration disrupted by with cirrhosis
- hypoxia
- necrosis
- atrophy
- liver failure
30
common cirrhosis causes
- hepatitis B and C
- excessive alcohol intake
- idiopathic
- non-alcoholic fatty liver disease
31
alcoholic fatty liver
mildest, asymptomatic
32
alcoholic steatohepatitis
- precursor to cirrhosis
- inflammation, degeneration of hepatocytes
33
alcoholic cirrhosis
fibrosis and scarring alter liver structure
34
what are the stages of liver damage
1. healthy liver
2. fatty liver
3. liver fibrosis
4. cirrhosis
35
early manifestations of cirrhosis
- GI disturbances
- fever, weight loss
- palpable liver
36
late manifestations of cirrhosis
- jaundice
- peripheral edema
- decreased albumin and PT
- ascites
- skin lesions
- hematologic problems
- endocrine problems
- esophageal and anorectal varices
- encephalopathy
37
portal hypertension
- resistant portal blood flow -> leads to varies and ascites
- asymptomatic until complications
38
causes of portal hypertension
- systemic hypotension
- vascular underfilling
- stimulation of vasoactive (RAAS) systems
- plasma volume expansion
- increased cardiac output -> ascites
39
complications of portal hypertension
- vatical hemorrhage
- ascites
- peritonitis
- hepatorenal syndrome
- cardiomyopathy
40
treatment of portal hypertension
- prevent/treat complications
- can't do anything for portal hypertension except liver transplant
41
hepatic encephalopathy
- LOC is the primary driver of diagnosis
- graded by severity
- correlate with liver labs -> mainly ammonia
42
acute liver failure (fulminant)
- edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the liver tissues
- NOT caused by cirrhosis or other types of liver disease
43
what is the most common cause of acute liver failure
acetaminophen overdose
44
indication for lactulose
reduction of ammonia absorption in hepatic encephalopathy
45
MOA of lactulose
reduces blood ammonia levels by converting ammonia to ammonium
46
other considerations for lactulose
- make sure patient is NOT hypokalemic
- can be given to titrate by number of stools or by ammonia levels
47
rifaximin
- second line if lactulose isn't working
- has been associated with increased risk of C diff
48
MOA of rifaximin
- inhibits bacterial RNA synthesis by binding to bacterial DNA
49
side effects of rifaximin
- peripheral edema
- nausea
- ascites
- dizziness
- fatigue
- pruitis
- skin rash
- abdominal pain
- anemia
50
major functions of the liver
- metabolism and storage: fat, CHO, PRO, vitamins and minerals
- blood volume reservoir
- blood filter
- blood clotting factors
- drug metabolism and detoxification
