hepatic disorders Flashcards

1
Q

largest gland

A

liver

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2
Q

blood supply to liver

A

portal vein, and it’s unoxygenated. gets oxygenated blood from hepatic artery.

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3
Q

functions of the liver

A

Bile production and excretion
Excretion of bilirubin, cholesterol, hormones, and drugs
Metabolism of fats, proteins, and carbohydrates
Enzyme activation
Storage of glycogen, vitamins, and minerals
Synthesis of plasma proteins, such as albumin, and clotting factors
Blood detoxification and purification

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4
Q

fats break down into

A

ketones

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5
Q

albumin

A

without it leaking

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6
Q

ammonia?

A

ammonia conversion to urea

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7
Q

liver can store how much blood?

A

1 liter

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8
Q

liver Storages what vitamins?

A

Storage-fat-soluble vitamins (A,D, E, K) and minerals

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9
Q

Synthesis of

A

Synthesis-serum proteins, phospholipids, cholesterol, clotting factors

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10
Q

liver immunity (my kupffer is immune to my liver)

A

filters blood via Kupffer cells

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11
Q

increased resistance within the portal venous system results in

A

decreased blood flow through and out of the liver. Collateral circulation develops to help relieve pressure. doesn’t help splanchnic (digestive) circulation.

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12
Q

blood backed up in the livers backs up in

A

splenic vein and collaterals

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13
Q

portal HTN will cause (varicose)

A

varices in GI tract and rectum (hemorrhoids)

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14
Q

portal HTN - symptoms (just if the liver doesn’t work) and what do ppl look like?

A

Hepatomegaly, splenomegaly
Esophageal, gastric, rectal varices (hemorrhoids)
Alterations in
Production & secretion of bile
can’t process CHO, protein, lipid fat (skinny arms and legs, big belly) metabolism
can’t clear Hormones
Detoxification

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15
Q

liver labs

A

if liver problems - Enzyme elevation
ALT, AST, alkaline phosphatase
Bilirubin elevations
Total , indirect, direct, urine bilirubin
Protein reduced
Serum albumin, total protein low
Ammonia elevated
Coagulation prolonged PT, PTT, INR

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16
Q

liver diagnostics (tips for the liver)

A

Liver biopsy
TIPS (rerouting)
Paracentesis
CT
MRI
PET (for liver cancer)

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17
Q

gall bladder diagnostics (Erp is a good gal)

A

MRCP
ERCP
Ultrasonography
Cholesintigraphy
Cholangiography (dye into ducts to view biliary tract)

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18
Q

liver problems - exam for resp CV renal

A

fluid volume deficit (3rd spacing) - flat neck veins - fluid leaks out
Edema (crackles)
Adventitious BS
BP low, pulse - high and weak
BUN, Cr, urine sodium, UO, and I & O (hepatorenal syndrome, low survival rate and can’t get a transplant)
put them in reverse trendelenberg

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19
Q

liver disease - neurologic

A

GCS (hepatic encephalopathy) aspiration
MS
Coordination
Reflexes
Movement
Seizures

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20
Q

liver disease - GI assessment

A

N, V, anorexia
Diarrhea or constipation, color of stool, volume, consistency
Lactulose?
Ascites- enlarging abd girth, abd fluid wave, ***if fluid it will be dullness on percussion, protruding umbilicus, assess BS, visible collateral veins on abdominal wall
Bleeding esophageal varices, CBC, hematemesis, melena
Hepatic tenderness and enlargement

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21
Q

liver problems - integumentary system (liver spiders and medusa)

A

Jaundice
Pruritus
Spider angioma (red and purple marks)
Edema
Dry, flaky skin
Poor skin turgor
Caput medusa (circulation around belly button)
Poor wound healing, ecchymosis, petechiae, bleeding gums

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22
Q

NAFLD (non-alcholic fatty liver disease)

A

Steatohepatitis (fatty hepatitis)
Accumulation of fat in liver causes scarring and damage leading to liver failure

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23
Q

NAFLD - symptoms (just 3, fatty liver is FAR)

A

Symptoms include RUQ pain, fatigue and anorexia

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24
Q

NAFLD - risk factors (Kel and predinsone make my liver not fat)

A

Gastric bypass surgery, hyperlipidemia, rapid weight loss, obesity, toxic chemicals, medications
Prednisone, amiodarone, tamoxifin, diltiazem, methotrexate

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25
Q

cirrohosis

A

Liver cells are destroyed and replaced by connective/scar tissue that alters circulation/flow within the liver.
Diffuse, fibrotic changes
Destruction of hepatocytes
Congested/obstructed flow
Blood, lymph, bile
Chronic & progressive
All body systems are affected
Can progress to hepatic encephalopathy/coma. only cure is transplant.

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26
Q

general s/sx of cirrohosis - breathing?

A

Firm nodular liver to palpation
Abdominal pain RRQ
Chronic dyspnea,
Change in bowel habits
Anemia/ bruising
SGOT/AST and SGPT/ALT rise

27
Q

early s/sx of cirrhosis (pain in RUQ and gi problems cirrose early in the morning)

A

Generalized weakness, malaise
RUQ pain
Wt. loss, A/N/V, flatulence, GI disturbances, indigestion, change in BM

28
Q

late s/sx of cirrhosis (spiders cirrhose late at night)

A

Change in mental status, memory
Spider angiomas (face, neck, shoulders) , jaundice, esophageal varices, GIB, ascites edema
Coagulopathy, bruising, thrombocytopenia
Splenomegaly, hepatomegaly
Peripheral neuropathy

29
Q

lanecc’s cirrhosis (lance the drinker has cirrhosis)

A

ETOH induced, about 20% of alcoholics develop

30
Q

billiary obstruction cirrhosis

A

Retention of bile/inflammation of ducts-jaundice
Obstruction of common bile duct

31
Q

post necrotic cirrhosis (art has necrosis)

A

hepatic artery is blocked and causes necrosis. shock or trauma.

32
Q

cardiac passive congestion d/t CHF cirrhosis

A

scar tissue forms

33
Q

metabolic cirrhosis (glycogen is metabolic)

A

glycogen storage disease, wilson’s disease (copper)

34
Q

primary cirrhosis (it’s primary autoimmune for cirrhosis)

A

autoimmune disease destroys bile ducts, usually middle-aged women. main complaint is fatigue and they are jaundice.

35
Q

atrophic/hypertrophic cirrhosis (it’s in the name)

A

decrease in size, or connective tissue hyperplasia

36
Q

treatment for cirrhosis - and avoid what meds (bummer if you get cirrohsis)

A

Antacids, vitamins and diuretics (neutralize stomach acid)
NO MORE ALCOHOL
Avoid narcotics
I & O and daily weights
REST
Prevent bleeding
Measure abdominal girth
Monitor jaundice
Good skin care

37
Q

cirrhosis diet (think - too much hurts the brain)

A

Diet
Decrease protein
Low sodium

38
Q

cirrhosis causes (coag in the vein causes cirrhosis)

A

hypercoagulability in the portal vein

39
Q

Esophageal Varicies

A

Most common portal HTN

40
Q

Esophageal Varicies - Pathophysiology

A

Portal HTN >obstruction > collateral circulation in esophagus/venous > increased pressure > ulceration and hemorrhage

41
Q

esophageal varicies - Assessment - what does vomit look like?

A

Hematemesis, melena, hepatic encephalopathy, dilated abdominal veins, ascites
Endoscopy, ultrasound

42
Q

esophageal varicies - treatment

A

Fluid resuscitation, correct coagulopathies, sclerotherapy, banding, Sengstaken-Blakemore tube, vasopressin, TIPS, Warren Shunt, Partial Mesocaval Shunt

43
Q

shunt

A

where it orginates is first word, and where it ends is the last word.

44
Q

ascites

A

Increase in hydrostatic pressure & lymph formation

45
Q

ascites - 2 main causes (think pressure)

A

portal HTN and decreased colloid osmotic pressure. Then Na retention and the kidneys get involved causing hepatorenal syndrome

46
Q

ascites - s/sx - what about flanks?

A

Bulging flanks, protruding umbilicus, fluid wave, shifting dullness to percussion

47
Q

ascites - treatment

A

Sodium restriction, diuretics, aquaretics (vasopressin V2 receptor agonists), water restriction, administration of albumin/colloids, therapeutic paracentesis, TIPS (transjugular intrahepatic porto systemic shunt, automated low flow pump system (Alfapump)

48
Q

Hepatorenal Syndrome (HRS) - type 1 (#1 dies fast and first)

A

Severe rapidly progressing renal failure with a doubling of creatinine in 2 weeks
Usually follows a precipitating event
Most patient die within 2 weeks of onset

49
Q

Hepatorenal Syndrome (HRS) - type 2 (too (2) slow)

A

Slower, chronic, more progressive increase in creatinine
Patient exhibit signs of liver failure and arterial HTN
Severe ascites refractory to diuretics
Predisposed to developing Type 1

50
Q

hepatorenal syndrome - s/sx (basic renal stuff)

A

Clinical characteristics
Presence of liver failure
Decreased GFR
Reduced urine sodium
Azotemia (high BUN)
Oliguria or anuria
High BUN/creatinine ratio

51
Q

Hepatic Encephalopathy

A

Protein-breaks down to ammonia-liver converts to urea-excreted by kidneys

52
Q

hepatic encephalopathy - s/sx (smell and energy level?)

A

***more and more sleepy over time. reflexes go down. Slow EEG. Foul odor - fetor. AMS, alteration in behavior, LOC changes

53
Q

hepatic encephalopathy - causes

A

Infection, elevated protein intake, worsening hepatic function, constipation, azotemia, GI bleeding, hypovolemia, hypoxia, CNS depressants, overuse of diuretics

54
Q

hepatic encephalopathy - stages 1 - 4 (don’t need to memorize this)

A

1 - mild confusion
2 - lethargy, blindness
3 - incoordination, inactive but arousable
4 - coma, death, unresponsive

55
Q

hepatitis A (A fecal)

A

Transmission through fecal-oral route
High risk groups

56
Q

hepatitis patho

A

Inflammation of the liver caused by a viral infection or toxins
Inflammatory cells/fluid/lymphocytes > congestion > enlargement > distortion of lobular pattern > necrosis
Distortion > increase pressure > portal HTN
Edema of bile channels > increased bilirubin

57
Q

hepatitis B (B sexually active, or virus)

A

DNA virus
Sexually transmitted, perinatal, blood. treatment Interferon, lamivudine

58
Q

Hep C

A

Blood, sexually, perinatal. treatment Interferon, ribavirin

59
Q

need to know this - stages of hepatitis (pre ick, post)

A

Preicteric, Icteric, Posticteric

60
Q

preicteric (P for preicteric, P for prodromal)

A

Prodromal (infection to start of signs and symptoms)
One week
Flu like
Malaise, fatigue, H/A, myalgia
A/N/V, diarrhea, low-grade fever, conjunctivitis, cough
Aversion to odors, avoidance of protein foods
Elevated LFT’s
Severe
Urticaria, rashes, polyarthritis, arthralgia

61
Q

icteric (Ick, you have jaundice for 4 weeks?)

A

starts with jaundice. 4-6 week
Jaundice, dark urine, light colored stools
Tender enlarged liver
Elevated LFT’s
Severe puritis
Preicteric symptoms subside

62
Q

Posticteric - how long? (think of mom at 4)

A

recovery. Up to four months

63
Q

transplant criteria

A

End-stage organ failure
Short life expectancy
Severe functional disability
No other serious health problems
Psychological readiness
Support in place