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My DEMS I > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

Cirrhosis

A

Late stage of progressive hepatic fibrosis
Characterized histologically by regenerative nodules surrounded by fibrous tissue
Generally irreversible
two types:
Compensated (no complications)
Decompensated (complications)

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2
Q

ex of complications of cirrhosis

A

variceal hemorrhage
ascites
encephalopathy
jaundice

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3
Q

suspect cirrhosis in

A

Any patient with chronic liver disease
Chronic abnormal aminotransferases (ALT) and/or alkaline phosphatase (alk phos)

Liver insufficiency
Low albumin ( 1.3)
High bilirubin (> 1.5 mg/dL)
Portal hypertension
Low platelet count (
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4
Q

Etiologies of cirrhosis

A

Viral:
Hepatitis C*
Hepatitis B

Alcoholic liver disease*

Autoimmune:
Primary biliary cirrhosis
Primary sclerosing cholangitis
Autoimmune hepatitis

Metabolic:
Hemochromatosis (iron)
Wilson Disease (copper)
Alpha-1 Antitrypsin deficiency

Vascular:
Budd-Chiari syndrome
Congestive heart failure

Non-alcoholic fatty liver disease

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5
Q

signs of cirrhosis

A 
scleral icterus
jaundice
spider angioma
pectoral alopecia
enlarged left lobe
caput medusae
umbilical hernia
white nails/clubbing
femal escutcheon
edema
muscle wasting
gynecomastia
splenomegaly
ascites
testicular atrophy
palmar erythema/Dupuytren's contracture
purpura/petechiae
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6
Q

prehepatic portal htn

A

Prehaptic portal htn:

  • portal vein thrombosis
  • schistosomiasis (eggs get stuck before sinusoids–> portal htn)
  • cirrhosis
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7
Q

Post sinusoidal htn

A

post-sin obstructive syndrome:

obstruce of small veins after sinusoids

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8
Q

Liver biopsy and cirrhosis

A

not necessary:
Decompensated cirrhosis (variceal hemorrhage, ascites, encephalopathy)
CT scan diagnostic of cirrhosis

not needed for pretransplant eval

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9
Q

Way to assess mortality in cirrhosis

A

Child-Turcotte-Pugh Score (CTP)

MELD score
Mathematical survival model created from data on patients undergoing TIPS
MELD score estimates risk of 3-month mortality
Uses 3 laboratory values
- Serum total bilirubin
- Serum creatinine
- INR

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10
Q

Calculating MELD score

A

normal 6

  1. 4 + 9.8 x log (INR) +
  2. 2 x log (Cr) +
  3. 8 x log (Bilirubin)
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11
Q

Organ allocation for liver transplant

A

Fulminant hepatic failure has highest priority
MELD score determines priority in cirrhosis
Amongst patients with same blood type, highest MELD score determines priority
Waiting time used only to break ties with identical MELD scores
MELD scores are updated at regular intervals

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12
Q

Mech of portal htn

A

P=RxF (pressure, resistance, flow)

Portal hypertension can result from:
increase in resistance to portal flow and/or
increase in portal venous inflow

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13
Q

mech leading to portal htn in cirrhosis

A

Increased intrahepatic resistance
is the initial mechanism leading to portal hypertension

-distorted sinusoidal architecture leads to increased resistance in cirrhosis

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14
Q

causes of portal htn

A
  • cirrhosis (sinusoidal site)
  • prehepatic :portal or splenic v thrombosis, schistosomiasis

-post sinusoidal: veno-occlusive disease
post hepatic: Budd Chiari syndrome (hepatic v thrombosis

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15
Q

Intrahepatic resistance in cirrhosis

A

structural (sinusoidal fibrosis and regenerative nodules) but also functional (active vasoconstriction)

  • in cirrhosis Nitric oxide activity is reduced and vasoconstrictors are increased
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16
Q

Splanchnic vasodilation in portal htn

A

results from increase in NO
(shear stress in splanchnic vasculature increases NO, as does bacterial translocation from ascites)–> splnachnic vasodil, increase in portal inflow

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17
Q

MEch of portal htn in sirrhosis

A

Increased intrahepatic resistance
Structural (fibrosis, regenerative nodules)
Active vasoconstriction (decreased nitric oxide, increased vasoconstrictors)
Increased portal venous inflow
Splanchnic vasodilation (increased nitric oxide)

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18
Q

Safest method for measuring portal pressure

A

measurement of the hepatic venous pressure gradient (HVPG)

subtracting the free hepatic venous pressure (FHVP) from the wedged hepatic venous pressure (WHVP):

HVPG= WHVP-FHVP

FHVP is “internal zero” (correct for extravascular, intraabdominal pressure increases)

Normal HVPG: 3-5 mmHg

Will be NORMAL in presinusoidal portal htn and post-hepatic portal htn; increased in sinusoidal portal htn, post-sinusoidal.

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19
Q

Cirrhosis and varices

A

increased resistance to portal flow–> increased portal pressure–> varices, variceal growth

varices increase in diameter progressively (none to small to large at rates of 7-8% per year)

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20
Q

Predictors of variceal HEMORRHAGE

A

variceal size
red signs
child b/c

2 year probability of first bleed: small 7%, large 30%

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21
Q

major determinant of variceal rupture

A

variceal wall tension (T)

T=tpx r/w

tp: transmural pressure
r: radius
w: wall thickness

22
Q

What can decrease risk of variceal bleeding

A

decrease in HVPG to a level below 12 mmHg essentially eliminates the risk of recurrent variceal hemorrhage, while a reduction of at least 20% from baseline reduces this risk significantly (7-13%)

23
Q

Endoscopic variceal band ligations

A 
Bleeding controlled in 90%
Rebleeding rate 30%
Compared with sclerotherapy:
Less rebleeding
Lower mortality
Fewer complications
Fewer treatment sessions
24
Q

Therapy for varices/hem

A

three types of therapy for varices and variceal hemorrhage (pharmacotherapy, endoscopic therapy, shunt therapy)

Combining a vasoconstrictor with a venodilator will have a combined effect reducing both flow and resistance

Shunt therapy, by bypassing the liver (the site of increased resistance) maximally reduces resistance, leading to normalization of portal pressure. However, by bypassing the liver this therapy can lead to other complications such as encephalopathy and liver failure

25
Q

Octeotride

A

vasoconstrictor that decreases splanchnic flow**

26
Q

Most common complication of cirrhosis for portal htn and vasodilation

A

development of ascites
(Extreme: hepatorenal syndrome)

SLIDE 71

27
Q

Most common cause of ascites

A

cirrhosis 80%

28
Q

Portal htn progression to hepatorenal syndrome

A 
Portal htn w/o ascites *HVPG 10, mod vasodil)
refractory ascites (>10 sever vasodil)
hepatorenal syndrome (>10, extreme vasodil)
29
Q

Work up of ascites

A

diagnostic paracentesis
routine:
PMN count, culture
Protein, albumin

Optional
Glucose LDH
amylase
cytology
RBC count
TB smear/culture
cytology
triglycerides
30
Q

Indications of paracentesis

A 
New-onset ascites
Admission to hospital
Symptoms/signs of SBP
Renal dysfunction
Unexplained encephalopathy

contraindic: none

31
Q

***serum ascites albumin gradient

A

SAAG Calculation: serum albumin minus ascites albumin

SAAG 1.1 g/dLcorrelates to pressure of 11 mmHg (HVPG)

The cutoffs for SAAG and ascites protein levels are 1.1 g/dL and 2.5 g/dL respectively. Cirrhotic ascites is typically high SAAG and low protein; cardiac ascites is high SAAG and high protein; and ascites secondary to peritoneal malignancy is typically low SAAG and high protein.

SLIDE 81

32
Q

Diuretics

A

tell kidneys to get rid of salt, water follows, and will get rid of fluid out of body

33
Q

Portal htn,no ascites

A

no specific therapy ?salt restriction

34
Q

uncomplicated ascites tx

A

1) Salt restriction + diuretics

2) Large volume paracentesis (LVP) with tense ascites

35
Q

refractory ascites tx

A

1) LVP + albumin

2) TIPS (only if they have LOW MELD score)

36
Q

refractory ascites

A

Occurs in ~10% of cirrhotic patients
-worse survival than diuretic responsive

Diuretic-intractable ascites (80%)
Therapeutic doses of diuretics cannot be achieved because of diuretic-induced complications

Diuretic-resistant ascites (20%)
No response to maximal diuretic therapy (400 mg spironolactone + 160 mg furosemide/day)

37
Q

LVP vs TIPS and ascites recurrence

A

TIPS assoc with less ascites recurrence, but more encephalopathy

-no difference in survival

38
Q

Hepatorenal failure

A

Renal failure in patients with cirrhosis, advanced liver failure and severe sinusoidal portal hypertension
Absence of significant histological changes in the kidney (“functional” renal failure)
Marked arteriolar vasodilation in the extra-renal circulation
Marked renal vasoconstriction leading to reduced glomerular filtration rate

39
Q

Acitivty in renin/ald in HRS

A

markedly increased

40
Q

Types of hepatorenal syndrome

A

Type 1
Rapidly progressive renal failure (2 weeks)
Doubling of creatinine to >2.5 or halving of creatinine clearance (CrCl) to 1.5 mg/dL or CrCl

41
Q

renal failure in cirrhosis

A

not HRS

vasodilation:
vasodilators
LVP w/o albumin
infection

decreased effective arterial blood vol:
diuretics
diarrhea
hemorrhage

increased renal vasoconstriction:
NSAIDs

42
Q

Major criteria in dx of HRS

A

Advanced hepatic failure and portal hypertension
Creatinine > 1.5 mg/dL or creatinine clearance plasma osmolality
Serum sodium

43
Q

What are always present in HRS?

A

Ascites

Hyponatremia

44
Q

Mgmt of HRS

A

Proven efficacy
Liver transplantation

Under investigation
Vasoconstrictor + albumin
Transjugular intrahepatic portosystemic shunt (TIPS)
Vasoconstrictor (Terlipressin-- IV)
Extracorporeal albumin dialysis (ECAD)

Ineffective
Renal vasodilators (prostaglandin, dopamine)
Hemodialysis

45
Q

What complicates ascites and can lead ot renal dysfunc

A

spontaneous bacterial peritonitis (SBP):

bacterial transloaction is mech: microorg from intestine to mesenteric lymph nodes and other extraintestinal organs/sites

BT doesn’t increase in prehepatic portal htn

mostly gram-negative enteric organisms

46
Q

Mech of bacterial translocation

A
  1. intestinal bacterial overgrowth
  2. intestinal permeability
  3. impaired immunity
47
Q

Dx of SBP

A

diagnostic paracentesis

PMN count >250/mm^3

48
Q

Tx of SBP

A

Recommended antibiotics for initial empiric therapy
i.v. cefotaxime, amoxicillin-clavulanic acid
oral ofloxacin (uncomplicated SBP)

avoid aminoglycosides

Minimum duration: 5 days

Re-evaluation if ascitic fluid PMN count has not decreased by at least 25% after 2 days of treatment

Consider adding albumin: decreases renal dysfun and short term mortality in SBP

49
Q

Hepatic Encephalopathy

A

Neuropsychiatric complication of cirrhosis

Results of both:
Portosystemic shunt (spontaneous, surgical or radiographic)
and
Chronic liver failure

Failure to metabolize neurotoxic substances:
Hyperammonemia results in glutamine accumulation

Alterations of astrocyte morphology and function (Alzheimer type II astrocytosis):
Astrocytes only cells in brain that can metabolize ammonia

***ammonia is thought to be a culprit, poss GABA-R involvement, but ammonia measurement NOT necessary for dx

Dx: 
Clinical findings/hx
(ammonia unreliable)
number connection test
slow dominant rhythm on EEG

Stages 1 (mild confusion) to 4 (coma)

50
Q

Tx of minimal hepatic encephalopathy

A

lactulose or synbiotics may improve condition

Minimal hepatic enceph abnormalities:
Attention and cognitive deficits
Visual-spacial perception impaired
Defects in visual constructive ability
Impaired driving ability
Evoked potentials and spectral electro-encephalography abnormal
51
Q

Hepatic Encephalopathy Precipitants

A 
high protein load
GI bleeding or constipation
infection
overdiuresis
Narcotics and sedatives 
TIPS procedure
52
Q

Tx of hepatic encephalopathy

A 
Identify and treat precipitating factor
Infection
GI hemorrhage
Prerenal azotemia
Sedatives
Constipation

Lactulose (adjust to 2-3 bowel movements/day) (decreases ammonia production in gut, as do abx)

Protein restriction, short-term (if at all– usually not necessary)

Also: ornithine aspartate, benzoate may increase ammonia fixation in liver

My DEMS I (26 decks)

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