Liver: hepatitis and cirrhosis Flashcards
1
Q
What are the 4 major types of unconjugated hyperbilirubinemia?
A
physiologic jaundice (50%) breastfeeding-associated jaundice (10-25%) breastmilk jaundice (2-3%) hemolytic disease (pathologic)
2
Q
Describe the cause, onset, and treatment for breastfeeding-associated jaundice
A
Cause - poor milk intake related to fewer calories and fluid consumed by infant before mother's milk is established Onset - 4-7 days after birth Treatment - Frequent breastfeeding - Caloric supplements e.g. formula - phototherapy for bililrubin > 275 mcmol/L
3
Q
Describe the cause, onset, and treatment for breast milk jaundice
A
Cause
- Possible factors in breast milk that prevent bilirubin breakdown to water soluble form and/or decreased excretion of bilirubin
- less frequent stooling
Onset
- 4-7 days after birth
Treatment
- temporary discontinuation of breastfeeding for up to 24h to identify causes; as bilirubin levels decrease, resume breastfeeding
- may include home phototherapy with uninterrupted breastfeeding
4
Q
Describe the cause, onset, and treatment for jaundice caused by hemolytic disease
A
Cause
- Rh incompatibility –> RBC hemolysis
- liver unable to conjugate and excrete excess bilirubin from breakdown
Onset
- DURING 1st 24h
Treatment
- postnatal phototherapy; if severe, exchange transfusion
- prenatal transfusion (fetus)
- prenatal prevent Rh incompatibility of Rh negative mother with RhoGAM
5
Q
What are some potential complications of hyperbilirubinemia?
A
- Bilirubin encephalopathy d/t toxicity of unconjugated bilirubin to neurons (kernicterus)
- Physiologic jaundice
6
Q
Bilirubin is damaging to neurons when toxic blood levels are reached. What factors would contribute to this?
A
Metabolic acidosis
decreased levels of albumin
abrupt increases in BP
drugs such as salicylates or sulfonamides that compete for the attachment of proteins
any condition that increases demand for oxygen or glucose will increase the risk of brain damage despite lower levels of bilirubin: fever, hypoxia, hypothermia, hypoglycemia
7
Q
Explain how phototherapy and early/frequent breastfeeding work as treatment for hyperbilirubinemia.
A
Phototherapy: fluorescent lights cause photoisomerization i.e. alters structure of bilirubin to souble form (lumirubin) for easier excretion
Breastfeeding promotes intestinal motility, decreased reabsorption of unconjugated bilirubin, and establishes normal flora to effectively enhance the excretion of unconjugated bilirubin
8
Q
What are some side effects of phototherapy?
A
- Loose green stools, transient skin rashes, hyperthermia, increased metabolic rate, dehydration, and skin breakdown
- Bronze baby syndrome: serum, urine, and skin turn grey-brown when under bili lights d/t retention of converted bili-lite bilirubin (clears spontaneously)
9
Q
Describe the anatomy and location of the liver
A
heavy and red organ due to vascular supply
gritty due to storage of minerals
smooth due to storage of fat
largest gland in body
on right side of body below diaphragm
blood supply is largely venous - bring nutrients from GIT: 70% portal vein and 30% hepatic artery
Kuppfer’s cells - part of reticuloendothelial system in immune function
10
Q
Liver has 500+ functions, but name and briefly describe the main ones
A
Vascular: blood storage and filtration
- hold ~13% of body’s blood
Metabolic: carbohydrate metabolism - stores ~ 4 hours of glycogen, broken down under the influence of EP (glycogenolysis), and formation of glucose from amino and fatty acids (GNG)
- fat storage and metabolism, production of lipoproteins, cholesterol (for bile, steroid hormones), phospholipids (cell membranes)
- protein metabolism: synthesis of serum proteins e.g. albumin, fibrinogen, alpha and beta transport globulins
Coagulation: synthesis of clotting components (all except factor VIII) and heparin
Biotransformation: removal of activated clotting factors from circulation
Detoxification and biotransformation of hormones, drugs, and other substances
Secretory function: bilirubin production
Storage function: fat soluble vitamins, blood, glucose, fat, minerals (iron, magnesium)
11
Q
What is the normal albumin:globulin ratio
A
Albumin 2: Globulin 1
12
Q
Where is albumin produced? Where are gamma globulins produced?
A
Albumin - liver
Gamma globulin - B lymphocytes
13
Q
Which 2 organs work together to break down insulin?
A
Liver and kidney
14
Q
What are the fat-soluble vitamins and what are their main functions?
A
A - vision and skin
D - antioxidant, assist calcium absorption
* must be converted from D1–>D2 (by liver) then kidneys convert from D2 –> D3
E - antioxidant
K - clotting
15
Q
Explain the process of deamination of proteins in the liver
A
Proteins –> amino acids –> amine group = NH2 broken off amino acid so that ketoacids can go to kreb’s cycle to be used for energy
amine group converted to insoluble ammonia (NH3) by GIT bacterial flora –> ammonia to be converted into urea by liver requires potassium –> urea is water soluble –> excreted by kidneys
16
Q
Blood leaves the liver and enters the inferior vena cava through the
a. heptatic artery
b. hepatic vein
c. portal artery
d. portal vein
A
B) hepatic vein
17
Q
The liver plays a major role in glucose metabolism by
a. producing ketone bodies
b. synthesizing albumin
c. participating in gluconeogenesis
d. all of the above
A
C) participating in gluconeogenesis
18
Q
The liver synthesizes prothrombin only if there is enough vitamin
a. A
b. B12
c. D
d. K
A
D) K
19
Q
The substance necessary for the manufacture of bile salts by hepatocytes is
a. albumin
b. bilirubin
c. cholesterol
d. vitamin D
A
C) cholesterol
20
Q
The main function of the bile salts is
a. albumin synthesis
b. fat emulisification in the intestines
c. lipid manufacture for the transport of proteins
d. urea synthesis from ammonia
A
B) fat emulsification in the intestines
21
Q
Hepatocellular dysfunction will result in all of the following except:
a. decreased serum albumin
b. elevated serum bilirubin
c. increased blood ammonia levels
d. increased levels of urea
A
D) increased levels of urea
22
Q
A person who consumes contaminated shellfish would probably develop hepatitis
a) A virus
b) B virus
c) non-A, non-B virus
d) C virus
A
A) A virus
23
Q
Immune serum globulin provides passive immunity to type A hepatitis if administered 2-7 days after exposure. Immunity is effective for about
a. 1 month
b. 2 months
c. 3 months
d. 4 months
A
B) 2 months
24
Q
Choose the correct statement about hepatitis B vaccine
a. All persons at risk should receive active immunization
b. Evidence suggests that the HIV may be harbored in the vaccine
c. It should be given only once because of its potency
d. One dose in the dorsogluteal muscle is recommended
A
A) All persons at risk should receive active immunization
25
Indications for post exposure vaccination with hepatitis B immune globulin include
a. accidental exposure to HBsAg-positive blood
b. perinatal exposure
c. sexual contact with those who are positive for HbsAg
d. all of the above
D) all of the above
26
Late presentations of hepatic cirrhosis include all of the following except
a. edema
b. hypoalbuminemia
c. hypokalemia
d. hypercalcemia
D) hypercalcemia
27
Cirrhosis results in shunting of the portal system blood into collateral blood vessels in the GIT. The most common site is
a. esophagus
b. lower rectum
c. stomach
d. a combination of all of the above
D) a combination of all of the above
28
Indicator of probable esophageal varices is:
a. hematemesis
b. anemia
c. melena
d. all of the above
D) all of the above
29
Bleeding esophageal varices result in decrease in
a. nitrogen load from bleeding
b. renal perfusion
c. serum ammonia
d. all of the above
B) renal perfusion
30
Before a liver biopsy the nurse should check to see 3 things
1. blood cross-matched
2. hemostasis tests
3. vital signs
31
The nurse begins preparing for the biopsy assisting the client into the correct position which is
a. Trendelenburg with the exposure of the thoracic region
b. recumbent with the right upper abdomen exposed
c. lying on the right side with the left upper thoracic area exposed
d. supine with the left lateral chest wall exposed
B) recumbent with the RUQ exposed
32
Immediately before needle insertion, the client needs to be instructed to
a. breathe slowly and deply so that the rib cage expansion will be minimized during needle insertion
b. inhale and exhale deeply and then hold her breath at the end of expiration until the needle is inserted
c. pant deeply and continue panting during needle insertion so pain perception will be minimized
d. take a deep inspiration and not breathe for 30 seconds so the needle insertion site can be determined then resume normal breathing for the rest of the procedure
B) inhale and exhale deeply and hold her breath at the end of expiration until the needle is inserted
33
After the biopsy the nurse assists the client to
a. high Fowler's position in which the client can effectively deep breathe and cough
b. ambulate with splinting her incision
c. assume the Trendelenburg position to prevent post biopsy shock
d. the right side lying position with a pillow placed under the right costal margin
D) right side lying position with a pillow placed under the right costal margin
34
After a paracentesis a client should be observed for signs of vascular collapse which include the following except:
a. bradycardia
b. hypotension
c. oliguria
d. pallor
e. pyrexia
A) bradycardia and
| E) pyrexia
35
The alterations in liver function that occur in cirrhosis relate to
a. formation of bands of fibrous tissue that replace normal hepatic cells and distort the architecture of the liver
b. excessive accumulation of fat within hepatocytes and biliary ducts
c. localized injury to biliary ducts in the liver
d. abnormal deposition of minerals within hepatic cells and biliary ducts
A) formation of bands of fibrous tissue that replace normal hepatic cells and distort the architecture of the liver
36
In cirrhosis, an increased blood ammonia level is related to impaired liver function as it relates to
a. gluconeogenesis
b. prothrombin production
c. production of ketones
d. urea synthesis
D) urea synthesis
37
The encephalopathies or alterations in CNS function which appear late in the course of cirrhosis are associated with
a. impaired blood flow to the brain resulting from portal vein obstruction
b. failure of the liver to remove ammonia and metabolic wastes from the blood
c. elevated levels of blood urea nitrogen
d. elevated blood sugar levels
B) failure of the liver to remove ammonia and metabolic wastes from the blood
38
Asterixis is best described as
a. small reddened pinopint center from which tiny capillaries extend
b. an intention hand tremor
c. noticeable uncontrolled bobbing of extended hands
d. distended tortuous veins radiating from the umbilicus
e. inability to replicate basic figures from a drawing
C) noticeable uncontrolled bobbing of extended hands
39
T/F: Factors that contribute to the formation of ascites include decreased aldosterone levels, portal HTN, hypernatremia, hypoalbuminemia
False: there are increased aldosterone levels in liver cirrhosis
40
From the following list, select clinical manifestations that are common to cirrhosis and renal failure. Explain the pathophysiology for those manifestations.
a. cardiac dysrhythmias
b. ascites
c. hypotension
d. osteoporosis
e. anemia
f. GI bleeding
g. oliguria
h. yellow skin discolouration
i. altered LOC
j. ankle edema
A. cardiac dysrhythmias in renal failure due to increased potassium retention; in liver failure due to bleeding/hemolysis causing increased serum potassium
D. osteoporosis in renal failure due to lack of calcium absorption (with low vitamin D2->3 conversion); in liver failure due to lack of calcium absorption (low vitamin D1->2 conversion)
E. anemia in renal failure due to lack of EPO and RBC production; in liver failure due to bleeding, decreased sythesis of clotting factors with decreased absorption of vitamin K, decreased synthesis of proteins (Hgb), low iron (for heme) and vitamin B12 storage (for maturation of RBC)
F. GI bleeding in renal and liver failure due to low calcium; liver failure due to decreased sythesis of clotting factors
G. oliguria due to hypoperfusion; in renal failure due to low GFR; in liver failure due to hypoalbuminemia and decreased blood volume (bleeding) = hepatorenal syndrome
I. altered LOC in renal failure due to metabolic acidosis; in liver failure due to buildup of ammonia --> encephalopathy
J. ankle edema in renal failure due to fluid overload and shifting into interstitial spaces; in liver failure due to portal HTN, hyperaldosteronism, hypoalbuminemia, ascites blocks venous return
41
Which of the following is NOT a metabolic function of the liver?
a. detoxifying chemicals
b. synthesizing and storing glycogen
c. breaking down RBC and WBC
d. synthesizing and secreting bile
C) breaking down RBC and WBC
| - most occurs in the spleen
42
When caring for a patient with cirrhosis, you'd want to remain alert for spontaneous bleeding caused by the
a. rupture of esophageal varices
b. decreased synthesis of blood-clotting factors by the liver
c. failure of the gut to absorb water-soluble vitamins needed to promote coagulation
d. decreased venous pressures as well as slow blood flow
B) decreased synthesis of blood-clotting factors by the liver
43
Which of the following would NOT contribute to ascites in a patient with cirrhosis?
a. portal HTN, venous dilation, and stasis
b. hypoproteinemia
c. decreased blood volume with increased total body fluid
d. increased blood volume causing increased blood hydyrostatic pressures in the capillary bed
D) increased blood volume causing increased blood hydyrostatic pressures in the capillary bed
- blood volume DECREASES due to hypoalbuminemia
44
Mr. Swenson has viral hepatitis. His anemia would result from
a. increased RBC fragility from folic acid deficiencies, which have been caused by inadequate dietary intake
b. decreased efficiency of Kupffer's cells in the liver
c. increased blood ammonia levels
d. decreased amino acid breakdown and synthesis
A) increased RBC fragility from folic acid deficiencies, which have been caused by inadequate dietary intake
45
Mr. Swenson is put on a moderate protein, high carbohydrate, high calorie, low salt diet. What is the best rationale for his diet?
a. the liver may not be able to detoxify proteins, so carbohydrates are substituted to meet metabolic and nutritional needs
b. Enough protein is given to facilitate tissue repair. A high-carb diet prevents further weight loss and spares proteins from energy metabolism. The sodium restriction helps manage fluid imbalances
c. High-protein foods are harder to digest than low protein foods and have a high sodium content. Carbohydrates are more palatable and will correct the weight loss more quickly
d. High-carb diets, particularly if they contain adequate fiber, are more likely to decrease dyspepsia and diarrhea. Sodium is always restricted when a patient is edematous.
B) Enough protein is given to facilitate tissue repair. A high-carb diet prevents further weight loss and spares proteins from energy metabolism. The sodium restriction helps manage fluid imbalances
46
Which of the following would help Mr. Swenson comply with his diet?
a. sitting with him until he's eaten his entire meal
b. giving his wife the responsibility of seeing that he eats properly
c. feeding him yourself
d. offering him frequent small meals instead of 3 large ones
D
47
Paracentesis is a minor surgical procedure done to remove ascitic fluid. After you explain the procedure to Mr. Swenson, your next action would be to
a. position him in a chair or the high Fowler's position
b. tell him to void
c. take his vital signs
d. drape his abdomen with sterile towels
B) voiding before the procedure prevents accidentally nicking or perforating the bladder during paracentesis
48
Because ascitic fluid is rich in serum proteins, during the procedure you'd observe the patient for
a. disequilibrium
b. hypotension
c. hypoalbuminuria
d. paralytic ileus
B) hypotension or shock may occur during or after paracentesis
49
How much ascitic fluid would you expect to be removed?
a. 500 ml
b. 1,000 ml
c. 2,000 ml
d. 3,000 ml
B) to minimize risk of hypotension and shock, the maximum withdrawn is 1 litre
50
4 days after admission, Mr. Swenson starts to bleed from esophageal varices. The earliest indications of this would include
a. tachycardia, restlessness, and pallor
b. tachycardia, lethargy, and flushing
c. a sudden drop in BP of 10 mmHg or more
d. increasing combativeness and widening pulse pressure
A) tachycardia, restlessness and pallor are all caused by vasoconstriction, which is a compensatory mechanism to maintain venous return and CO
51
Initially, Mr. Swenson's bleeding is controlled with a saline lavage. Later a Sengstaken-Blakemore tube is inserted to
a. prevent bleeding by applying pressure to the esphageal varices
b. prevent blood accumulation in the GIT, which could lead to hepatic coma
c. stop bleeding by applying pressure to the cardiac portion of the stomach and against the esophageal varices
d. reduce transfusion requirements
C
52
Which of the following is NOT related to the increased level of circulating estrogens?
a. gynecomastia
b. decreased chest and body hair
c. impotence
d. increased libido
D
53
Mr. Carter complains of itchiness and scratches himself, even when he's sleeping. Which abnormality is the itching related to?
a. folic acid deficiency
b. prolonged prothrombin time
c. increased bilirubin levels
d. hypokalemia
C
54
Mr. Carter has a history of cirrhosis related to chronic alcoholism.
Which of these diets would you encourage Mr. Carter to follow?
a. high-calorie, restricted protein, low sodium
b. bland, low protein, low sodium
c. well balanced normal nutrients, low sodium
d. high protein, high calorie, high potassium
C - protein is not restricted until later stages of liver failure
55
Mr. Carter's wife asks how she can help her husband get better. Which of the following measures would you NOT advise?
a. supplementing his diet with daily multivitamins
b. reinforcing all his efforts to avoid alcohol
c. giving him a sleeping pill at bedtime
d. helping him avoid contact with ill persons when possible
C
56
Mr. Carter has developed ascites over the past 6 months. Ascites results from portal HTN and
a. excess serum sodium and increased aldosterone excretion
b. increased aldosterone excretion and decreased serum albumin
c. decreased colloid osmotic pressure and lymphatic obstruction
d. decreased serum albumin and decreased colloid osmotic pressure
D
57
You'd likely place Mr. Carter in which position due to his ascites?
a. high Fowler's
b. sidelying
c. modified Trendelenburg
d. any position, as long as he changed it often
A - ascites hinders diaphragmatic movement
58
The doctor restricts Mr. Carter's sodium intake to 1 gram daily and orders a diuretic. Which diuretic promotes sodium excretion while conserving potassium?
a. furosemide
b. spironolactone
c. hydrochlorothiazide
d. ethacrynic acid
B
59
Mr.Carter receives 100 ml of 25% serum albumin solution IV. Which development best indicates the albumin is working?
a. increased urine output
b. increased serum albumin levels
c. decreased anorexia and itching
d. easier breathing
A
60
Esophageal varices are primarily related to
a. pronounced abdominal muscles
b. portal HTN
c. chronic arterial HTN
d. elevated central venous pressure
B
61
Mr. Carter receives an IV infusion and oxygen at 4L/minute via nasal cannula. The doctor inserts a Sengstaken-Blakemore tube which
a. has a large diameter for effective gastric lavage
b. applies direct pressure to gastric bleeding sites
c. blocks blood flow to the stomach and esohagus
d. applies direct pressure to the esophagus
D
62
Once the Sengstaken-Blakemore tube is passed for esophageal varices, which nursing intervention would you perform?
a. provide an emesis basin for expectorated secretions
b. get an order for lozenges to counteract dry mouth
c. moisten the internal nares with a petroleum based lubricant
d. get an order fo viscous lidocaine to make swallowing more comfortable
A
63
About 30 minutes after the tube is inserted, Mr. Carter becomes dyspneic. Your first response is to
a. remove the tube
b. deflate the esophageal part of the tube
c. check for airway obstruction
d. raise the HOB and increase oxygen flow rate
C
64
Mr. Carter improves and the doctor removes the Sengstaken-Blakemore tube. He ordrs oral neomycin and a neomycin enema to
a. reduce abdominal pressure and prevent further bleeding
b. prevent straining during bowel movements that could stimulate bleeding
c. remove intestinal contents and block ammonia formation
d. reduce the irritating effect of blood on the intestinal mucosa
C
65
You'd suspect that Mr. Carter has portal systemic encephalopathy if you noted changes in his
a. LOC
b. vital signs
c. urine output
d. respiratory status
A
66
Mr. Carter's serum ammonia rises and the doctor orders lactulose (Cephulac), 30 ml PO daily. Which of the following reactions would you expect?
a. increased urine output
b. improved LOC
c. diarrhea
d. Nausea and vomiting
C - diarrhea initially, then improved LOC
67
Mr. Carter is discharged with a prescription for lactulose. Which statement indicates that Mr. Carter understands what you've told him about lactulose?
a. I'll take it with some Maalox
b. I'll mix it with some apple juice
c. I'll take it with a laxative
d. I'll mix the crushed tablets in some gelatin
B
68
In alcoholic liver disease, ethanol in the liver oxidizes into
a. acetaldehyde
b. pyruvic acid
c. dehydrogenase
d. acetic acid
A
69
The accumulation of fluid in the peritoneal cavity is called
a. fatty liver
b. alcoholic cirrhosis
c. ascites
d. portal HTN
C
70
Which of the following is characterized by fibrosis, inflammation, and in some cases, necrosis?
a. hepatic encephalopathy
b. alcoholic cirrhosis
c. hepatorenal syndrome
d. alcoholic hepatitis
D
71
A clinical manifestion of alcoholic liver disease in a patient who is still able to compensate is
a. spider angiomas
b. purpura
c. weight loss
d. jaundice
A
72
A clinical manifestation of alcoholic liver disease in a patient who can no longer compensate is
a. splenomegaly
b. spontaneous bruising
c. ankle edema
d. palmar erythema
B
73
A clinical manifestation typically associated with portal HTN is
a. ascites
b. hepatomegaly
c. epistaxis
d. dyspepsia
A
74
About how many people with cirrhosis develop esophageal varices?
a. 1/10
b. 1/4
c. 1/3
d. 1/2
D
75
About how many people with varices develop variceal hemorrhage?
a. 1/10
b. 1/4
c. 1/3
d. 1/2
C
76
A factor associated with an increased risk of initial variceal hemorrhage is
a. hepatic venous pressures above 8 mmHg
b. moderate portal HTN
c. variceal diameter greater than 2 mm
d. red spots on the varices
D
77
A factor associated with an increased risk of rebleeding is
a. hypotension
b. abdominal pain
c. age above 60 years
d. gonadal atrophy
C
78
Immediate treatment of variceal hemorrhage includes
a. infusing normal saline IV
b. having the patient lie supine
c. raising the HOB to 30 degrees
d. maintaining Hct at 32-34%
A
79
Patients who receive "significant' transfusions are at particular risk for
a. hypermagnesemia
b. hypocalcemia
c. hypernatremia
d. hypokalemia
B
80
The drug of choice for managing acute variceal bleeding is
a. octreotide
b. vasopressin
c. propanolol
d. nitroglycerin
A
81
The preferred definitive treatment for active variceal hemorrhage is
a. balloon tamponade
b. endoscopic injection sclerotherapy
c. transjugular intrahepatic portosystemic shunting
d. endoscopic variceal ligation
D
82
Applying weighted traction during balloon tamponade may increase the risk of
a. liver capsule rupture
b. pleural effusion
c. tube migration
d. bacterial peritonitis
C
83
A long-term complication of transjugular intrahepatic portosystemic shunt (TIPS) placement is
a. hematomas
b. encephalopathy
c. pulmonary edema
d. renal failure
B
84
Explain the pathophysiology behind the emaciation that occurs with cirrhosis
- alterations in carbohydrate, fat and protein metabolism
- glycogenolysis
- gluconeogenesis
- altered storage function of liver
85
Explain the patho behind ascites that occurs with cirrhosis
```
Portal HTN
hypoalbuminemia
congestion of lymph channels
hyperaldosteronism
elevated ADH
prostaglandins
```
86
Explain the patho behind splenomegaly that occurs with cirrhosis
portal HTN
87
Explain the patho behind lower limb edema that occurs with cirrhosis
portal HTN
hyperaldosteronism
hypoalbuminemia
pressure of ascites obstructs venous return from lower limbs
88
Explain the patho behind esophageal varices that occurs with cirrhosis
portal HTN --> collateral veins (anastamoses) that bypass liver to carry blood to superior vena cava via cardiac end of stomach and lower esohagus --> distension of veins
89
Explain the patho behind hemorrhoids that occurs with liver cirrhosis
superior rectal veins dilate with pressure of portal HTN
90
Explain the patho behind caput medusa that occurs with liver cirrhosis
caput medusa = ring of abdominal varices around umbilicus
| - blood flow bypasses fibrosed liver by collateral vessels to SVC (due to portal HTN) --> vessel dilation
91
Describe the process of breakdown of a RBC to excretion of bilirubin
RBC--> globin = protein --> amino acids (recycled for protein synthesis)
--> heme --> iron (stored in liver) + inconjugated bilirubin
unconjugated bilirubin is insoluble and bound to proteins in the blood
- under glucuronyl transferase (produced by liver), unconjugated bilirubin becomes conjugated bilirubin (water soluble) and is recycled many (~18x) times before it becomes inactive --> bacteria in GIT convert bilirubin into stercobilin (excreted in feces) or urobilinogen (excreted in urine)
92
Describe the cause, onset, and treatment for physiologic jaundice
```
Cause
- immature hepatic function
- incread bilirubin load from RBC hemolysis
- sterile GIT
Onset
- AFTER 24 hours
Treatment
- Phototherapy if bilirubin levels increase too rapidly a/o > 300 mcmol/L
```
93
Hyperbilirubinemia occurs when there is an imbalance between RBC destruction and excretion. What factors may upset the balance?
- Physiologic/development of liver related to prematurity
- Association with breastfeeding or breast milk
- Excess production of bilirubin (hemolytic disease, biochemical defects, bruising)
- Disturbed capacity of liver to secrete conjugated bilirubin (enzyme deficiency, bile duct obstruction)
- Combined overproduction and undersecretion e.g. sepsis
- Some disease states like galactosemia (linked to transferase enzyme deficiency)
- Genetic predisposition
94
Explain the patho behind jaundice that occurs with liver cirrhosis
liver inability to conjugate bilirubin
may be obstruction of bile flow due to liver cell dysfunction
excessive RBC destruction with bleeding, early hemolysis of immature RBC
95
Explain the patho behind impaired coagulation that occurs with liver cirrhosis
- impaired absorption of vitamin K (for prothrombin synthesis)
- decreased synthesis of clotting factors fibrinogen, prothrombin, factors V, VII, IX, X
- impaired calcium absorption d/t vitamin D malabsorption
- delayed biotransformation/breakdown of heparin
- thrombocytopenia d/t splenomegaly d/t portal HTN
96
Explain the patho behind anemia that occurs with cirrhosis
- microcytic anemia secondary to GI bleeding and iron deficiency
- macrocytic anemia from folic acid and vitamin B12 deficiency
- splenomegaly causes increased removal of RBC from circulation
- inadequate dietary intake for healthy RBC production
97
Explain the patho behind infection that occurs with cirrhosis
Leukopenia d/t splenomegaly (overactive)
| Kuppfer cells do not phagocytize bacteria in portal circulation that bypass the liver
98
Explain the patho behind -feminization of males/masculinization of females that occurs with cirrhosis
Hyperestrogenism - liver unable to detoxify hormones
99
Explain the patho behind encephalopathy that occurs with cirrhosis
- Shunting of blood around liver causes buildup of toxins that normally are metabolized by the liver
- Ammonia is no longer converted to urea --> toxic to CNS
100
Ammonia toxicity is intensified by ACIDOSIS/ALKALOSIS and HYPERKALEMIA/HYPOKALEMIA
alkalosis
| hypokalemia
101
Which would give a more accurate reading of blood ammonia levels causing encephalopathy, VENOUS or ARTERIAL?
Arterial
102
What is Fetor hepaticus and what is the patho behind it?
- sweet musty odour and client complains of foul tasting mouth
- due to impaired amino acid metabolism
103
Explain the patho behind hypoglycemia that occurs with cirrhosis
- decreased metabolism of carbs, fats, proteins
- direct liver cell damage from ETOH that decreases enzymes necessary for ATP needed for GNG
- impaired liver breakdown of insulin so it remains in circulation longer
104
Explain the patho behind hypotension that occurs with cirrhosis
- changes in liver circulation
| - decreased circulating volume
105
Explain the patho behind hepatorenal syndrome that occurs with cirrhosis
* *Primary cause of death in liver failure**
- damage to kidneys by nephrotoxic substances (liver unable to metabolize)
- decreased renal perfusion
