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127 Cards in this Set
- Front
- Back
2 features of the hepatic artery:
|
1. high Pressure
2. low Volume (25%) - vice versa for portal vein |
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the portal vein brings in 75% of the liver's blood supply; components of this supply:
(3) |
1. DEoxygenated blood (that's why portal vein is low P)
2. nutrients for the liver 3. waste products/toxins from the intestines/spleen |
|
PA's / triads contain:
(3) |
1. portal venules (no SM)
2. hepatic arterioles 3. interlobular bile ducts |
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2 consequences of cirrhosis, at the lvl of the sinusoids:
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1. loss of fenestrations (=> no holes)
2. deposition of BM (=> blockage of transfers from blood) |
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what are Kupfer cells and what do they do?
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macrophages WITHIN sinusoids that attach to endo
- remove bact . coming in from the gut |
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what is the Space of Disse and why is it important?
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space between hepatocytes and sinusoids
- full of stellate cells, which normally produce Vit. A, but during cirrhosis, synthesize fibrous CT => dec. liver function |
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2 markers of hepatocellular injury:
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ALT,
AST |
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***3 markers of cholestasis:***
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1. AP
2. GGT 3. total Bilirubin |
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cholestasis =
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little or no bile secretion
|
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3 markers of hepatic synthesis function:
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1. PT
2. Albumin (produced exclusively in the liver) 3. (bilirubin) |
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PT is an *excellent* measure of liver function b/c:
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clotting factors have a very short half-life => change in liver function will be noticed almost immediately
|
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Bilirubin pathway: RBC's metabolized in the spleen => heme catabolized into:
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UNconjugated bili (Bu)
|
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***3 features of Bu:***
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1. INSOLUBLE in blood
2. MUST be (non-covalently) bound to albumin for transport to the liver 3. ***NEVER found in the urine*** |
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what does the liver do to Bu?
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conjugates it to glucuronic acid
=> Bc |
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4 features of Bc:
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1. SOLUBLE
2. excreted into bile 3. CAN be filtered through kidneys => urine 4. NOT NORMAL to be in the urine - indicates disease state |
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from the liver, Bc is excreted into bile and then goes to:
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the GI tract if needed or to the gallbladder for storage
|
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**from the GI tract, Bc of bile is:**
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*metabolized by bact. of the gut,*
into **urobilinogens** |
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5 features of urobilinogens:
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1. mostly eliminated in the *feces* as stercobilin
2. => brown color 3. small amount is recycled in the liver 4. should NOT show up in the kidneys 5. (its breakdown product, urobilin, does - gives urine a yellow color) |
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when Bc is HIGH for an extended period of time, it becomes:
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COVALENTLY bound to albumin
t1/2 becomes 20 days (that of albumin) => called Bd |
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when the cause of high lvls of bilirubin are removed, the high lvls of Bu and Bc quickly drop to normal, but:
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Bd only *gradually* decreases (due to long half-life)
- responsible for persistent bilirubinemia |
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You should NOT see Bd in:
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the urine
- it's bound to albumin |
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total Bilirubin =
(3) |
Bu + Bc + Bd
|
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direct Bilirubin =
(2) |
Bc + Bd
- in most cases, Bd is so low that in can be ignored, and direct Bilirubin IS Bc |
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indirect Bilirubin =
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Bu
|
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hyperbilirubinemia occurs in 3 ways:
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1. pre-hepatic
2 hepatocellular 3. post-hepatic/obstructive |
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pre-hepatic hyperbilirubinemia/jaundice is a result of:
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TOO MUCH Bu
|
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2 potential causes of pre-hepatic hyperbili:
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1. hemolysis
2. overproduction of Bili |
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does urine change color in pre-hepatic hyperbili?
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NO
- Bu is NOT excreted in the urine |
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hepatocellular jaundice results from damage to or within the liver, as with:
(2) |
1. drug toxicity
2. viral hepatitis |
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(remember, damage to liver results in decrease of:
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uptake, conjugation, and excretion of bilirubin/bile)
|
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**result of hepatocellular jaundice ** =
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MIX of Bu and Bc, depending on where the damage is
=> urine MAY be darkly pigmented, if enough Bc is being excreted by the kidneys |
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when Bc is high in the urine, it's color will be:
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DARK
|
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obstruective/post-hepatic jaundice essentially equals:
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choledocholithiasis,
obstruction of the CBD (usually due to gallstones) |
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if the CBD is completely obstructed, bile reach severely-high lvls; at this point, the bilirubin seen will be:
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almost entirely Bc, and Bd if it persists for several days
|
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respective color of urine and stool in obstructive hyperbilirubinemia:
(2) |
1. urine will be VERY dark
2. stool will be PALE/CLAY-colored, due to LACK of Bc in the intestines => no conversion of Bc into urobilinogens => no stercobilin |
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AST is NOT liver-specific; it's also found in:
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brain, kidney, etc.
|
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the height of ALT lvls roughly estimates:
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severity of liver parenchymal damage
|
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nl aminotransferases lvls do NOT exclude:
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liver disease
e.g. advanced cirrhosis => LOWER lvls than nl, while Hep C ~~ fluctuating lvls |
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Alkaline Phosphatase is also found in:
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*bone and placenta*
=> raised in bone disease, late-stage pregnancy |
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if it IS liver-related, increased AP indicates:
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cholestasis
|
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cholestasis =
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little or no bile secreted
|
|
GGT helps to confirm:
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***hepatic origin of AP***
|
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2 other features of GGT:
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1. nonspecific if by itself
2. induced by alcohol, meds as well as liver damage |
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low lvls of albumin suggest:
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**decompensation**
- ascites, edema, etc. |
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*hemolysis =>
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MODerate inc's in tBili
|
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a therapeutic dose of Tylenol may be fatal in someone with:
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cirrhosis
|
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2 detox roles of the liver:
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1. converts ammonia to urea
2. metabolizes EtOH |
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Phase I drug metabolism is achieved via:
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Cytochrome P450 family
|
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cirrhosis is a plumbing problem; there is too much:
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R
|
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activation of Kufer cells following liver injury contributes to:
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the activation of stellate cells
|
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****7 clinical signs of cirrhosis:****
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1. ascites
2. peripheral edema 3. palmar erythema 4. asterexis (hand pulses when extended) 5. jaundice 6. caput/varices 7. spider naevi on arm |
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SBP ~~ bact from:
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GUT get into peritoneal fluid
|
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portal HTN is defined as:
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>10-12 mmHg (when clinical symptoms start)
*normal = 5* |
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Pressure =
(equation) |
Flow x R
|
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portal Pressure =
(equation) |
[in]flow x R [to outflow]
|
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"portal R to outflow" is a function of the R of:
(3) |
1. portal vein
2. hepatic sinusoids 3. hepatic vein |
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collateral vessels become:
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the sites of varices if portal Outflow is obstructed
|
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increased inflow to mesenteric arterioles contrbutes to portal HTN; this increased inflow is a result of:
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inc. CO and vasodilation, which occur as a result of cirrhosis in the first place
|
|
fluoroscopy ~~
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barium
|
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**"decompensated" = **
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has developed ANY complication of cirrhosis
(see Sheet schematic) |
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**what is the most devastating complication of cirrhosis?**
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*varices*
- high mortality |
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most effective approach to varices =
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PREVENTION
-screen e/o with cirrhosis or portal HTN with endoscope |
|
gastric or esophageal varices are the most common; one problem with them:
|
TOO BIG to tie
- need to use BORTO (balloon obliteration) => inject sclerotherapy (irritant that causes coagulation and narrowing of the vessel wall) |
|
3 causes of ascites:
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1. cirrhosis (75%)
2. malignancy 3. many other etiologies |
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**what determines ascites etiology?**
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the Serum Ascites-Albumin Gradient
SAAG |
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HIGH SAAG:
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>= 1.1
|
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***if the SAAG is HIGH, think:***
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ANATOMICAL etiology:
HF, IVC web, hepatic vein thrombosis, cirrhosis |
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is SAAG is LOW, think:
(3) |
inf's, malignancies, AI disease
|
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2 most common gut pathogens =
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E. coli,
Kleb |
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secondary prophylaxis against SBP =
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STANDING antibiotics, lifelong
|
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HRS =
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acute renal failure due to
cirrhosis or fulminant liver failure ~~ dec'd perfusion to kidneys - an end-stage process |
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3 symptoms for HRS:
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1. oliguric (low urine)
2. hypotensive 3. hyponatremic |
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4 diagnostic criteria for HRS:
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1. cirrhosis with ascites
2. serum creatinine >1.5 3. absence of another cause of renal failure 4. no improvement after 2 days of albumin and no other meds |
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Type I HRS is:
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rapidly fatal
- need transplant ASAP |
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diagnosing Type I HRS:
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serum clearance doubles in <2 weeks
|
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Type II HRS is indolent and usually occurs as a result of:
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diuretic-refractory ascites
|
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prevention is the key to:
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ALL liver problems
|
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HCC is deadly; there is no:
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great therapy apart from transplant
|
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most common cause of HCC in the West =
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HCV and EtOH combined
|
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***special feature of HCC diagnosis:***
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can be achieved WITHOUT biopsy
- use contrast imaging |
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***diagnosing HCC:***
(2) |
1. HCC cells are fed EXCLUSIVELY by hepatic artery
=> will light up FIRST 2. as HCC tumor is getting darker, the REST of the liver lights up via portal vein |
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another way of calling the diagnostic pattern of HCC:
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1. early arterial enhancement
+ 2. portal venous washout |
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TIPS = shunt between:
(effect = ) |
portal vein and hepatic vein,
- *rapidly reduces portal HTN* |
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problems with TIPS:
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*further* loss of flow through portal vein
= further loss of nutrient supply to liver, while gut toxins don't get detoxified |
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3 precipitating factors of hepatic encephalopathy:
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1. **inf's**
2. metabolic imbalance 3. meds |
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hepatic encephalopathy is a diagnosis of:
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exclusion
|
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serum ammonia is a ____ ______ for encephalopathy
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BAD test;
ammount does NOT correspond to severity |
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diagnosis of hepatic encephalopathy depends on:
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clinical symptoms in a "hepatic context"
|
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symptoms of high grade Hep. Enceph. =
(3) |
1. confusion
2. lethargy 3. unable to cooperate |
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which kind of cirrhosis is the best kind to have?
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Child A
~ best survival |
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Child cirrhosis calculations are based on:
(5) |
bile,
albumin, INR, ascites, and encephalopathy |
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3 features of the MELD score:
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1. from 6 to 40
2. determines whether you can get a liver transplant or not 3. higher MELD = gets transplant first |
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MLED is based on:
(3) |
1. bili
2. INR 3. creatinine |
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liver transplants are the ONLY cure for decompensated cirrhosis/HCC, and VERY effective;
|
you must be able to survive
- so HF is out |
|
treatment of variceal bleeding:
(3) |
primary prophylaxis - prevent the first event from happening
1. screen all cirrhosis pts 2. EV Ligation of varices 3. NON-selective B-blockers |
|
2 nonselective B-blockers:
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propranolol,
nadolol |
|
**why do B-blockers have to be NON-selective to treat varices?**
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b/c cardio-selective ones only decrease CO,
whereas NON-selective ones dec. CO AND vasodilate => dec. portal HTN (all titrated to cause HR or 60) |
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EVL might CAUSE:
|
variceal bleeds
|
|
a/o with large varices AUTOMATICALLY gets NON-selective B-blocker treatment, as does anyone with:
|
**with small varix AND decompensated cirrhosis**
- all others get monitored |
|
for ACUTE variceal bleed, focus on:
(ABC's) |
Airway
Breathing Circulation Drugs Endoscopy - in that order |
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***3 drugs for acute variceal bleed***
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1. Octreotide (IV)
2. PPI's 3. antibiotics |
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Octreotide =
|
long-acting analogue of somatostatin
|
|
***what does Octreotide do?***
|
inhibits vasodilatory hormones,
which decreases the inflow into the already- hypertensive portal system, by effectively increasing vasoconstriction of mesenteric arteries **doesn't affect SYSTEMIC vessels/BP** |
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why aren't B-blockers given in an ACUTE variceal bleed?
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they are anti-hypertensive, which is no good when you're bleeding AND hypotensive already
|
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why are PPI's given with acute variceal bleeds?
|
to hedge against possible peptic ulcer bleed
- many cirrhotics have peptic ulcers => you don't know whether the bleed is coming from the ulcer or the varices |
|
why are antibiotics given for acute variceal bleed?
(3) |
1. dec. risk of re-bleeding (due to inflammation)
2. dec. risk of SBP 3. dec. risk of encephalopathy (a little) |
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secondary prophylaxis prevents recurrent variceal bleeds; treatment =
(2) |
combination of band therapy/obliteration
AND life-long B-blockers |
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treatment for ascites:
(3) |
1. low-sodium diet (<2,000 mg/day)
2. diuretics 3. large volume paracentesis if refractory to diuretics |
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**which diuretics are used in ascites, and why?
|
1. Furosemide, for volume reduction
2. Spironolactone, to inhibiti RAA in a 20/50 ratio - watch for hyponatremia |
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treatment for SBP = primary prophylaxis =
|
WEEKLY antibiotics
- ciprofloxacin (a Q) + albumin to protect kidneys |
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primary prophylaxis of SBP is indicated in:
(3) |
1. ascites
2. Child C 3. hyponatremia |
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acute SBP: early therapy saves lives; if you see cirrhosis/ascites with _______(3)__________, start antibiotics
|
cirrhosis/ascites with
1. fever 2. abdominal pain or 3. altered mental status |
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if you DON'T see fever/abd pain/AMS in cirrhosis/ascites pt, wait for:
|
cell count to come back before deciding on antibiotics
|
|
***pertinent cell count for starting early therapy in acute SBP:***
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>250 PMN's/cc
- NEEDS antibiotics |
|
antibiotics for treatment of ACUTE SBP:
|
3rd-gen cephalosporins for 5 days, + albumin
- cefotaxime, ceftriaxone - longer if blood cultures remain positive after 5 days |
|
secondary prophylaxis for SBP =
(2) |
ciprofloxacin or TMP/SMZ
- long-standing |
|
treatment for HRS:
(5) |
1. liver transplant
2. Midodrine + Octreotide + albumin 3. NOR or VP in severe cases 4. dialysis is only a BRIDGE (devastating alone) 5. TIPS doesn't work! |
|
**what do Midodrine and Octreotide do, respectively?**
|
Mido vasoconstircts splanchnic/mesenteric arteries/arterioles;
Octreo inhibits vasodilation |
|
**effect of Mido + Octreo = **
|
blood is shunted back toward the kidneys
|
|
splanchnic means:
|
of the organs
|
|
Terlipressin =
|
analogue of VP
- it too shunts flow back to kidneys, - but also causes cardiac vasoconstriction => MI, a-fib |
|
we can reverse HRS, but can't:
|
cure it
|
|
general treatment of hepatic encephalopathy =
|
reduce Nitrogen load from the gut
|
|
treatment of encephalopathy:
(3) |
1. catharsis/pooping via lactulose
2. antibiotics 3. downsizing/closure of shunts/TIPS |
|
Rifaxamin and metronidazole are used to treat:
|
encephalopathy
|
|
other therapies for encephalopathy (grasping at straws):
(3) |
1. ornithine aspartate
2. zinc 3. short-medium-chain branched FA's |
|
with encephalopathy, do NOT:
|
restrict prot
- just animal prot - bean/veggy prot, is good |