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Nurs332 > Medicine P1 > Flashcards

Medicine P1 Flashcards

1
Q

what are the functions of the liver?

A
  • metabolizes carbohydrates, fats, and proteins
  • detoxifying blood
  • converting ammonia to urea for excretion
  • Synthesizing plasma proteins, nonessential amino acids, Vit A and essential nutrients such as iron, Vit D, B12
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2
Q

if lipids are decreased, what does the liver break down fatty acids into?

A

ketones

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3
Q

the liver excretes bilirubin from breakdown of what? where is it eliminated?

A

hemoglobin

excreted in bile

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4
Q

what does the liver secrete to help with digestion? what does that do?

A

bile.
it is a greenish fluid that helps to digest fats and absorb aides, cholesterol and other lipids. it also gives stool its color

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5
Q

how does the liver protect itself? can the leftt lobe take over for the right?

A

it regenerates itself by repairing or replacing injured tissue.

yes

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6
Q

would the liver be tender for recent or chronic enlargement?

A

recent

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7
Q

how can hepatitis be acquired?

A

virus, inherited disorder or medications or toxins such as alcohol and drugs

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8
Q

what is cirrhosis?

A

it is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis, scar tissue and regenerative nodules that leads to loss of liver function

diffuse scarring of liver- follows hepatocellular necrosis of hepatitis

inflm- healing with fibrosis- regeneration of remaining hepatocytes from regenerating nodules

common end of chronic liver disorders

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9
Q

what is liver disease?

A

hepatitis
cirrhosis
tumors
others

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10
Q

defn of non viral hepatitis?

cause?

A

inflm of liver usually from chemical/drugs. most recover from non-viral hepatitis although some develop cirrhosis

cause: hepatotoxic chemicals such as carbon tetrachloride, trichloroethylene, vinyl chloride

hepatotoxic drugs such as tylenol

poisonous mushrooms

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11
Q

what is the non viral hepatitis treatment?

A

remove causative agent by lavage (irrigating or washing out), catharsis (causing diarrhea) or hyperventilation

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12
Q

what is the defn of viral hep

A

acute inflm of liver marked by liver cell destruction, necrosis and autolysis. in most patients hepatic cells eventually regenerate w little or no damage

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13
Q

when is prognosis poor in viral hepatitis?

A

presence of deem and hepatic encephopathy

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14
Q

how can you acquire hep A?

A

eating infected food or water.. food is affected by a virus called HAV (hepatitis A virus)

Anal-oral contact during sex can be a cause

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15
Q

what is the chance of recovery in hep A?

A

nearly everyone makes a full recovery- does not lead to chronic disease

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16
Q

how can you acquire hep B?

A

STD. contact with blood, semen, and other body fluids. can be thru

unprotected sexual intercourse
skin perforated with unsterilized needles,

being bitten by someone infected

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17
Q

can hep B turn into cancer?

A

yes

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18
Q

how is hep C transmitted/

A

through direct contact with the blood of a person ho has the disease.

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19
Q

can hep C turn into cancer?

A

liver cancer is a risk only increased in people with cirrhosis (only 20% of ppl with hep C)

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20
Q

how can misuse of anesthesia cause hep c?

A

can result in the transmission of hepatitis B and hepatitis C viruses, The cause of infection tends to be from anesthesia contamination, and not endoscopy contamination. Experts say that more effort is needed to better educate the health care community about the importance of strict sterile techniques when using any type of anesthesia.

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21
Q

which types of hepatitis are blood transfusions tested for?

A

B and C

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22
Q

which hepatitis accounts for approx 20% of all viral hepatitis? related to IV drug use and blood transfusions?

A

hep C

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23
Q

T or F: you can get hep C from contact with feces

A

F

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24
Q

which hepatitis can be transmitted through contact with someone else razor who has this type?

A

hep B

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25
Q

what hepatitis are you at risk of transmitting at a day-care?

A

hep A

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26
Q

what are GI signs and symptoms of liver failure?

A

anorexia, malnourished, indigestion, nausea and vomiting, constipation or diarrhoea, dull abdominal ache, GI bleed, clay coloured stools

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27
Q

what are respiratory symp of liver failure?

A

pleural effusion, limited thoracic expansion, dyspnea, hypoxia

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28
Q

what are hematological S&S of liver failure?

A

bleeding tendencies. anemia, DIC, Thrombocytopenia,  WBCs, Hypokalemia , Hypocalcemia, Hypo/Hypernatremia, Hypomagnesia

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29
Q

what are endocrine S&S of liver failure?

A

testicular atrophy, menstrual irregularities, gynecomastia, loss of chest and axillary hair

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30
Q

what are hepatic S&S of liver failure?

A

jaundice, hepatomegaly, ascites, edema of the legs

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31
Q

will a patient with liver failure have a temperature?

A

yes

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32
Q

why does a patient with liver failure have musty breath?

A

inc ammonia levels

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33
Q

what is the treatment for hepatitis?

A

time to rest

small meals high in calories and protein

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34
Q

what is the treatment for chronic hep b?

A

interferon alfa-2b for 16 weeks -monitoring blood counts is essential

lamivudine therapy to dec viral load of hep B (antiretroviral med used to prevent HIV/AIDS and used to treat chronic hep B0

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35
Q

treatment for hep C?

A

interferon and ribavirin therapy

decisions regarding tx made after labs and biopsy results confirm inflm early cirrhosis. tx lasts 6-18 months

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36
Q

does alcohol interfere with tx?

A

no

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37
Q

what effect does the cirrhotic liver have on proteins?

A

it causes the body to breakdown proteins at a fast rate, quickly depleting stores and increasing body needs.this can cause inc in ammonia bc it is a by-product of protein metb

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38
Q

why might you restrict protein in the diet of someone with cirrhosis?

A

because in a cirrhotic liver , ammonia is the byproduct of protein metb…many adverse effects of this

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39
Q

what kind of liver failure would have inc protein intake?

A

hepatitis not cirrhosis

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40
Q

is malnutrition common or uncommon in cirrhosis? why or why not?

A

common

due to poor appetite and intake, malabsorption of nutrients and impaired nutrient metabolism.

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41
Q

if your patient is receiving bowel protocol what is the best form? why?

A

lactulose because it binds with ammonia and helps to excrete it

42
Q

what are the patterns of alcohlic liver disease?

A

fatty changes
acute hepatitis
chronic hepatitis and portal fibrosis
cirrhosis and chronic liver failure

43
Q

which types of liver disease are reversible?

A

fatty changes
acute hepatitis
chronic hepatitis and portal fibrosis (maybe)
chronic liver failure

44
Q

what are some neurological signs and symptoms? for alcoholic liver disease i think?

A 
asterixis (flapping of hand)
dec LOC
behavioural changes
paraesthesias
sensory disturbances
cognitive changes
45
Q

what are some integumentary signs and symptoms? for alcoholic liver disease i think?

A 
spider angiomas
jaundice
dec hair production
inc pigmentation
white nails
palmar erythema
pruitis
caput medusa
bruising
46
Q

when giving lactulose, how many stools/day is the goal?

A

2-4. requires electrolyte monitoring

47
Q

why is ammonia elevated in liver disease?

A

GI bacterial action and inc protein (byproduct of metb)

48
Q

what medication might you give to dec the amount of bacteria subsequently, ammonia?

A

metronidazole

49
Q

what cause of liver disease has a high correlation with esophageal varices?

A

alcohol

50
Q

what is caput medusa?

A

tangle of little varices around the umbilicus

51
Q

why does gynaecomastia occur in cirrhosis?

A

because the liver is unable to metabolize hormones

52
Q

what is jaundice?

A

yellow discolouration of skin and sclera due to excess serum bilirubin

53
Q

does jaundice always mean liver disease?

A

no

54
Q

what is the urine like with jaundice?

A

tea lik rusty yellow

55
Q

what are the common causes of jaundice?

A

hemolytic

hepatocellular

post hepatic (obstuctive)

hereditary hyperbilirubinemia

56
Q

what is hemolytic jaundice?

A

increased destruction of RBC, liver is flooded with plasma with bilirubin so rapidly that the liver is unable to excrete bilirubin and hemolytic transfusion reactions and hemolytic disorders

57
Q

what is hepatocellular jaundice?

A

the liver is unable to clear bilirubin from liver due to damage. can be due to infection, toxins, meds, alcohol, obesity (fatty liver disease)
serum bilirubin and urobilinogen may be elevated
AST and ALT levels may increase- indicating cellular necrosis
Headache chills, fever if infectious cause.
May be reversible unless cirrhosis develops and then little reversal.

58
Q

what is obstructive jaundice?

A

biliary atresia; biliary disease or blockage due to inflammation; gall stones; cholestatic medications can cause internal blockage of ducts;
Bile cannot flow into the intestines but backs up into liver, blood, staining skin, sclera, urine bright orange and frothy. Stool clay colored, skin itchy
Intolerance of fatty foods, fatty stools
If not reversed can damage liver.
AST and ALT and GGT rise moderately but blood bilirubin levels and alkaline phosphatase levels are elevated.

59
Q

what is Hereditary Hyperbilirubinemia?

A

inc serum bilirubin and jaundice.
gilberts syndrome is a familial disorder characterized by an inc level of unconjugated bilirubin that causes jaundice

dubin-johnson syndrome (chronic idiopathic jaundice w pigment in the liver)

Rosters syndrome (chronic familiar conjugated hyperbilirubinemia)

60
Q

why does portal htn occur?

2 major consequences?

A

results from circulatory changes within the diseases liver and producing severe GI hemorrhages and marked Na and h20 retention

  • inc p throughout the portal venous system that results from obstr of blood through the damaged liver
  • associated with hepatic cirrhosis, noncirchotic liver disease
  • two major consequnces: ascites and varices
61
Q

why does ascites occur?

A

inc in cap p and obstr of venous blood flow through the damaged liver and vasodilation that occurs in the splanchnic circulation (arterial supply and venous drainage og GI system from distal esophagus to the midrectum including liver n spleen)

liver can’t metb aldosterone- inc Na and water retention which inc intravascular fluid vol and dec synthesis of albumin. fluid then moves from vascular to peritneal space.

62
Q

mints of ascites?

A 
inc abd and weight gain
SOB
striae and distended veins
umbilical hernias
fluid and lyts imbal
63
Q

why is ascites a self-perpetuating problem?

A

Liver unable to metabolize Aldosterone increasing Na and water retention, that increases intravascular fld volume and decreases synthesis of albumin. Fluid then moved from the vascular system to the peritoneal space. – it then draws more Na causing a self perpetuating problem

64
Q

how many L of albumin rich fluid can accumulate in abd?

A

15l

65
Q

what is the treatment for ascites?

A

dietary modification - low sodium diet
Diuretics and sodium restriction
Bedrest
Paracentesis- comfort
Trans jugular intrahepatic portosystemic shunt
albumin admin to shift from interstitial to vascular space
spiralnocolactone (k+ sparing diuretic and aldosterone blocking agent) and lasix (loop diuretic)

66
Q

what is transjugular intrahepatic portosystemic shunt (TIPS)?

A

cannula treated into portal vein by transjugular route

to reduce portal htn, stent inserted to serve as an intrahepatic shunt between the portal circulation and hepatic vein

dec Na retention, improves renal respose to diuretic therapy, and preventing reoccurence of fluid accumulation

67
Q

what are the 3 common areas you’ll find varices?

A

esophageal, legs and hemorrhoids

68
Q

why might you have pitting edema?

A

because you have hypoalbuminemia due to decreased hepatic production of albumin, (therefore no osmotic pressure pulling fluid in?)

69
Q

what should all patients with alcoholism be given in regards to nutritional def?

A

thiamine and multivitamins to prevent koraskoff’s dementia

70
Q

what is korsakoff syndrome?

A

s a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1- which affects the brain and nervous system). Korsakoff syndrome is most commonly caused by alcohol misuse, but certain other conditions also can cause the syndrome

71
Q

why are alcoholics thiamine deficient?

A

poor eating habits
alcohol can interfere with he coversion of thiamine into the active form of the vitamin

alcohol inflames the stomach lining and can causing frequent vomiting

alcohol also makes it hard to store vitamins in the liver

72
Q

why are nutritional deficiencies a concern with liver failure?
what can this lead to?

A

Inability of the damaged liver cells to metabolize certain vitamins leading to:
Impaired functioning of the central and peripheral nervous systems.
Abnormal bleeding tendencies.

73
Q

what is marasmus?

A

universal starvation and kwashiorkor (protein deficiency)

74
Q

how might you present with nutritional deficiency with liver diseases?

A

wrinkled face due to lack of skin proteins
hepatomegaly with fatty liver. deficient haemopoesis and impaired Immune defence

ascites

growth failure

hunger edema- lack of plasma protein

75
Q

what is hepatic encephalopathy?

A

accumulation of ammonia in the serum due to impaired protein metabolism

76
Q

what are esophageal varices?

why does this occur

A

dilated, Tortuous veins in the submucosa of the lower esophagus but can be in higher esophagus or extend into the stomach.
due to portal htn.- Increased opbstruction of the portal vein so venous bld seek alt route back to right atrium resulting in increased pressure in the vessels in the submucosal layer of the lower esophagus and upper part of the stomach

• In turn there is an inc serum ammonia level, inc risk of encephalopathy

77
Q

mnfts of esophageal varices/

A

• Hematemesis, melena, or general deterioriation in mental or physical status and often have a hz of alcohol abuse
• S&S of shock
- can lead to dec cerebral, hepatic, and renal perfusion if bleeding

78
Q

what are some liver function tests?

A 
ALT
AST
GGT
Albumin
PT/INR
Liver Biopsy
CT, MRI, PET, Ultrasound
Laparoscopy
79
Q

which liver function test is not specific to the liver?

A

AST

80
Q

what are high levels of GGT associated with?

A

cholestasis and alcoholic disease

81
Q

what does PT/INR levels indicate?

A

provides an index of livers ability to synthesize it K-dependent clotting factors

82
Q

increased AST and ALT ratio can indicate what?

A

metabolic or drug induced hepatic injury; also best indicators of necrosis and inflm

83
Q

what kind of medications would you give for liver disease?

A

medications to decrease portal htn (beta blockers)
medications that cause selective GI vasoconstriction and slow motility
h2 receptor blockers admin to prevent sterss ulcers and GI bleeding
Ativan- withdrawal symp
lactulose
spironolactone and lasix
metronidazole

84
Q

what do you use endoscopic sclerotherapy for?

A

injection of an agent to promote thrombis and sclerosis. Go in and inject dye and pinpoint bleeder and might give drugs and constrict that area.

85
Q

what might you do for esophageal varices?

A

esophageal banding therapy

balloon tamponade

86
Q

what is esophageal banding therapy?

A

• A modified endoscope laoded with an elastic rubber band is passed through an overtube directly onto the varix to be banded

87
Q

what is balloon tamponade?

A

• Pressure exerted on the cardia (upper orfice of stomach) and against the bleeding carices by a double ballon tamponade

88
Q

what kind of infection could you get from liver disease?

A

spotaneous bacterial peritonitis

89
Q

why would you give lactulose?

A

is administered because it breaks down ammonia (NH3) which is elevated d/t GI bacterial action. The Lactulose breaks down NH3 into components absorbed and excreted in stool. The goal is 2 – 4 stools per day; requires close fluid and electrolyte monitoring. If fluid and electrolyte balance worsens, there is an ↑ risk of hepatorenal failure.

90
Q

why would you give spironolactone?

A

k+ sparing diuretic) and Lasix (loop diuretic)

91
Q

why would you give metronidazole?

A

dec bacteria and subsequently a dec ammonia (bc bacteria produce ammonia)

92
Q

ammonia accumulation converts to what? and causes?

A

urea and causes brain dysfunctions and damage

93
Q

what are signs and symptoms of hepatic encephalopathy and coma

A

Confusion, motor disturbances, mood, altered LOC, cannot copy simple figures (constructional apraxia)
Asterixis (flapping tremor of the hands)
ECG show general slowing of brain waves, fetter hepaticas (sweet, slightly fecal odour to breath)

94
Q

what is hepatic encephalopathy?

A
  • Aka portosystemic encephalopathy (PSE) is life-threatening complic of liver disease that occurs w severe liver failure
  • Hepatic insufficiency may result in encephalopathy d/t inability of liver to detoxify toxic byproducts of metb

toxic byproducts can enter systemic system such as ammonia and can enter the brain and stimulate GABA which depresses the CNS

95
Q

how does lactulose draw out serum ammonia into the stool?

A
  • Ammonia is kept in the ionized state resulting in a fall in colon pH reversing the normal passage of ammonia from the colon to the blood
  • Evacuation of the bowel takes place decreasing and ammonia absorbed from the colon
  • Fecal flora are changed to organisms’ that do not produce ammonia from urea
96
Q

what is non alcoholic fatty liver disease?

A

a condition in which excess fat accumulates in the liver of people who drink little or no alcohol

Is believed to be associated with rising rates of obesity

97
Q

what are the S&S of NAFLD?

A

none

98
Q

what are some contributing factors NAFLD?

A 
Obesity
High Blood Cholesterol
Type Two Diabetes
Malnutrition
Rapid Weight Gain
Medication: steroids, exposure to toxins and
chemicals
99
Q

what is paediatric NAFLD often associated with?

A

obesity

100
Q

treatment of NAFLD?

A

Liver Transplant
No Medication available to treat
Antioxidant vitamins? Studies inconclusive
Ongoing studies with meds designed to increase sensitivity to insulin

101
Q

why would a patient need ventilation for hepatic encephalopathy?

A

because of depressed neuro status because of effect of ammonia stimulating GABA depressing CNS

Nurs332 (12 decks)

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