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122 Cards in this Set
- Front
- Back
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Paracentesis- what is it
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draining of ascites fluid
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benefits of paracentesis (4)
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Therapeutic relief of abdominal pressure
can be used to guide diagnostics look to see if portal htn present see if SBP (infected fluid) |
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paracentesis dx: how to tell if portal htn is present (like what kind of ascites?)
(2) |
Albumin concentration blood and compare to peritoneal fluid- Serum ascites albumin gradient (SAAG)
if albumin >1.1 mg/dL diagnostic for hypertension in 97% of cases (transudate) look this up... |
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how to use paracentesis to dx SBP (3)
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WBC with differential
Total protein concentration Peritoneal cultures |
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how paracentesis offers therapeutics relief (2)
but you have to be careful, why? |
Take of 1-5 L (or more) of fluid
Albumin replacement (see next slide) ... what's this have to do with paracentesis- i guess it's used to calc how much albumin to add watch for hypotension |
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Pro and con of albumin replacement in ascites
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Pro: Prevent intravascular volume depletion and renal impairment (helps to keep the heart and kidneys perfused!)
Con: Play no role in long term morbidity and mortality |
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in practice, albumin replacement is commonly done (due to liver not making it) because it is thought to prevent what? (2)
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Thought to prevent hepatorenal syndrome and hyponatremia and makes them feel better
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how much albumin to replace? (typical rate based on paracentesis)
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replace albumin via 8 grams for each liter of ascites withdrawn
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endogenous albumin (bodies normal albumin)- synthed where?
controls what? |
Synthesized by hepatocytes
controls oncotic pressure in extravascular hepatic space |
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distribution half life/rate of endogenous albumin
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Distribution t1/2 15 hours (~4 g/hour)
if you give this (can you give this??) it takes a while to reach where it's supposed to go |
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half life of endogenous albumin
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Elimination t1/2 18 days
pt will feel better for a while |
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endogenous albumin - distribution (2 areas and conc. of albumin there)
accounts for what % of total protein in plasma? |
Interstitium 2 g/dL
Plasma 4 g/dL higher in plasma Accounts for 50-70% of total protein in plasma (70% of oncotic pressure) |
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when you give exogenous albumin as treatment...vs endogenous
duration of volume expansion and half life |
gives equivalent expansion of plasma volume vs interstitial
Duration of volume expansion 12-24 hours (much shorter) Plasma t1/2 16-24 hours |
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exogenous albumin- wtf- osmolarity (normal osmolarity of blood?); how much oncotic pressure it adds? I have no idea he didn't talk about this in class
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290 mOsm/L
20-30 mmHg oncotic pressure |
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know albumin replacement calculations on test
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4 sizes/conc. that albumin comes in
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25% (50 mL)
25% (100 mL) 5% (250 mL) 5% (500 mL) |
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cirrhosis and hepatic circulation- % of blood flow that actually reaches hepatic veins?
what happens to the rest of blood? most dangerous collaterals (2) |
10% of blood flow reaches the hepatic veins and the rest circumvents the liver via the collateral circulation
Gastro/esophageal collaterals (“varices”) are the most dangerous |
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most common presenting
feature of portal hypertension |
GI hemorrhage from varices (GI varices)
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Are all collateral systems dangerous?
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clinically benign
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Diagnosis of Portal Hypertension methods (4) indicate best method
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endoscopy is best method
Ultrasound, MRI, Venography |
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in an endoscopy, what do varix show up as?
what color is assoc. with higher risk of bleed (and what is the name for this color/sign) |
Varix appear white or bluish, cherry red spots indicate higher risk of bleed (wale sign- red streak)
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Probability to bleed corresponds with (5) risk factors basically
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size of varices, wale sign,
continued EtOH, GERD, Child’s score with ascites |
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grade I esophageal varices
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Dilated veins (< 5mm) still at the level of the surrounding tissue
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grade II esophageal varices
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dilated, straight veins (>5 mm) protruding into esophageal lumen but not obstructing it
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grade III esophageal varices
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large, tense and winding vens already obstructing esophageal lumen considerably
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grade IV esophageal varices
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near complete obstruction of lumen with impending danger of hemorrhage (cherry red spots)
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why is it really important to prevent hemorrhage of esophageal varices?
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50% mortality rate from first bleeding event
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how do you prevent EV? indicate drug type of choice
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Prevent or control portal hypertension
Nonselective beta-blockers – Drug of Choice |
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dosing of 2 types of drugs for EV prevention
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Propranolol 10 mg PO TID or 20 mg BID
Nadolol 40 mg PO QD |
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what do non specific beta blockers do for EV prevention? (2) indicate receptors involved
end result |
Reduce cardiac output
decrease splanchnic blood flow (via b2 receptor vasoconstriction) Significant reduction in initial bleeding, improve mortality |
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goals of therapy with beta blockers in EV (3)
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Start low and go slow
Increase to produce 20-25% decrease in heart rate or target heart rate of 50-60 bpm |
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Acute variceal hemorrhage presents as (2)
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hematemesis or
melena |
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risk factors for varices hemorrhage (3)
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Active alcohol abuse (binge amounts)
NSAIDs Previous hemorrhage risks for bleeds |
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goals of treatment for varices/hemorrhage (5)
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Adequate fluid resuscitation
Correction of coagulopathy and thrombocytopenia Control of bleeding Prevention of rebleeding Preservation of liver function |
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key to bleeding varices treatment: 3 things to do
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Stabilize bleed with EGD (Electrogastroduodenoscopy)
via sclerotherapy or band ligation Fluid resuscitation with colloids (blood) and/or cystalloids Vasoactive drug therapy to stop or slow bleeding |
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benefits of using blood products (colloid) for fluid resusc. (2)
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liver dysfunction/splenic dysfunction - not enough blood products (clotting factor, low platelets from spleen etc)
also bleeding = losing blood |
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3 blood products you can use for fluid resusc.
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Packed red blood cells (PRBC)
Fresh frozen plasma (FFP) Platelets |
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3 drugs used to stop bleeding in EV
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Somatostatin
Octreotide Terlipressin |
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examples of colloids (3)
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Albumin
Starches Blood products |
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colloid use for EV- freq of use
benefits downside |
-colloids are more commonly done but more expensive
-good because they stay in vascular space, you get best fluid replacement- but riskier -if you give a liter most of it will stay in intervascular space? Inter? or intra? |
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fluid distribution in body
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60% intracellular fluid
40% extracellular fluid (intravascular/interstitial) (or 2/3 + 1/3) |
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intravascular definition
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within blood vessel
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examples of crystalloids (3)
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Normal saline (0.9%
NaCl) Lactated ringers (LR) D5W |
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distribution of crystalloid in body (2) (excluding D5W)
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if you give 1L of crystalloid-
3/4 (750 mL) will go into interstitial and only a quarter of it will stay in blood vessel |
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distribution of D5W in body
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initially will perform like other crystalloids but it is very quickly metabolized to free water
thus, for 1 liter you'd get like 600 mL into INTRACELLULAR, then only 100 mL in intravascular, and 300 mL as interstitial (least amount in intravascular) |
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choosing fluid for FR in EV (3) like what do you pick and what's not appropriate
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crystalloids quickly and easily available
occasionally will move to colloids D5W not appropriate unless that's all you have |
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AE for using albumin (colloid) (2)
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allergic rxn
infections |
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AE for using NaCl
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Hyperchloremic
metabolic acidosis |
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idk look at stpuid comparison chart of crystalloid vs. colloid (albumin)
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25% albumin vs. 5% albumin vs. NaCl - which gets you the most bang for your buck? why?
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volume expansion- 25% albumin gets more bang for your buck in terms of volume (most effective)
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Correction of Coagulopathy and
Thrombocytopenia (INR) options (2) |
FFP (blood products) is good cuz it replaces all the factors
Vitamin K- poor quality data in hepatic insufficiency |
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Vitamin K in correcting coagulopathy in cirrhosis- does it make sense?
risky? |
doesn't make a lot of sense because there's a lot more factors involved in clotting and you may not even be vitamin K deficit- the issue is...you don't have factors
not a lot of risk though so often given |
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vit K routes (3)
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IV, PO, SQ route available
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vit K routes- which one is not recommended?
which one has a black box warning (and for what)? |
SQ – erratic absorption, not recommended for use
IV has black box warning for anaphylaxis (3/10,000 patients- rare) |
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IV vs. PO vit K onset
when does one become significantly better than the other? |
IV to PO have same onset (>24 hours), although IV is significantly better than PO at 3 days
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Dosing for Vit K: IV, PO and SQ dose ranges
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IV: 1-10 mg (dilute in 50 mL)
PO: 1.25-10 mg SQ: 5 mg (no dilution) <-- idk why we even have to know this since it's not recommended |
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5 goals of treatment for coagulopathy (wtf is this for bleeding from varices still?)
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Adequate fluid resuscitation
Correction of coagulopathy and thrombocytopenia Control of bleeding Prevention of rebleeding Preservation of liver function |
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Adequate fluid resuscitation and correction of coagulopathy and thrombocytopenia- how you do this?
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combination of giving blood
products and fluid resuscitation |
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Control Bleeding- how to do this (for coagulopathy/varices)
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vasoactive therapy
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vasoactive therapy for coagulopathy/bleeding varices- what does it do? (2)
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Reduce portal blood flow and portal pressure (vasoconstricts blood flow there)
Causes splanchnic vasoconstriction which reduces bloodflow to splanchnic organs |
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vasopressin as vasoactive therapy (3) used much? why or why not (3)? acts on what receptors
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Not first line and rarely used
acts via V1 receptors Powerful, nonselective (unwanted) effects on blood pressure 30-65% complication rate Efficacy is unknown |
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most used drug for vasoactive therapy
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Octreotide
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octreotide- MoA
efficacy vs. vasopressin |
it is a synthetic splanchnic vasoconstriction – reduces portal flow and pressure without systemic effects
Effectiveness equivalent to vasopressin with better safety |
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dosing for IV/SQ octreotide (which route preferred)
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25-50 mcg IV bolus, continuous IV infusion of 25-50 mcg/hr
Note the doses for SQ administration and IV administration look similar- but IV is most used |
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If you administer octreotide IV what MUST you do?
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dilute it
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octreotide AE (4)
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bradycardia, dizziness, GI side effects, cholelithiasis
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Other Management for bleeding varices
reasoning for this |
PPI- for acid irritation/etc/protection/reduce risk of bleeds- many pt have GERD
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PPI- which one?
dosing regimen (3) |
Proton pump inhibitor infusion to rule out
upper GI bleed Protonix 8 mg/hr x 72 hours (pantoprazole) Then 40 mg PO twice daily not sure if this is any better than IV push twice daily |
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Control of Bleeding and 2° Prevention for EV options (3)
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Endoscopic therapy: sclerotherapy and banding
Balloon tamponade – temporary hemostasis by direct compression of varices (rarely used) Beta blockers +/- nitrate...i'm not sure i'm clear when to give BB... |
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endoscopic therapy (banding/sclerotherapy- injects substance into varices that causes it to shrink) properties (2) gold standard for what ?treatment of choice for what?
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Gold standard for acute variceal hemorrhage
Treatment of choice for secondary prophylaxis |
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what is TIPS?
used for what? (2) |
Transjugular Intrahepatic Portosystemic Shunts (TIPS) - last ditch effort that shunts blood to bypass liver altogether
Mainstay of treatment for refractory variceal hemorrhage Bridge to liver transplant |
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what does TIPs do, physiologically? (2)
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Creates a pathway through liver parenchyma for blood to
flow from hepatic vein to portal vein |
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TIPS- risk and benefit for survival
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Increase the risk of
hepatic encephalopathy and has no benefit on survival |
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HE (hepatic encephalopathy)- pathophys (2) what chemical is primary cause
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Liver is responsible for detoxification of toxic products of intestinal metabolism and digestion
Ammonia is thought to be primary cause of HE |
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sx of HE (3)
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confusion, lethargy, coma
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how does ammonia cause obtundation/other sx of HE? (direct effect on what 2 things?)
acts like what type of agent? |
Pass blood brain barrier and exert direct effect on cortical neurons and/or postsynaptic inhibitory potentials
Act like a GABA-nergic agent like benzodiazpines |
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incidence of HE in cirrhosis
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Incidence is 50-80% with cirrhosis
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grading system for HE- how to interpret score
usually based on what? (3) |
0= minimal to 4=worst
Family/spouse/children comments Serial 7’s - make them subtract backwards from 100 (part of MMSE) presence of asterixis (liver flap) |
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8 precipitating factors of HE
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constipation
high protein intake electrolyte/water imbalance stemming from paracentesis, diuretics infection (SBP) drugs hypotension hypoxia hypoglycemia |
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drugs that can precipitate HE (3)
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hypnotics, sedative, alcohol
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3 main things you need to do to manage HE
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Remove or treat precipitating factor
Decrease ammonia production Increase clearance of ammonia |
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ways to decrease ammonia production (3)
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Limit protein intake
Intestinal acidifiers – lactulose- turns NH3 into NH4+ so it can't cross intestine and poop it out Antibiotics |
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ways to Increase clearance of ammonia
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cathartics (like lactulose)
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how does lactulose clear ammonia? (2)
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acidifies colon and prevents conversion of NH4+ (ammonium) to NH3 (ammonia) so it can't cross colon wall
cathartic |
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properties of lactulose - what is it?
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Non-absorbable disaccharide
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MoA of lactulose lowering pH in gut
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Colonic bacteria ferments lactulose producing organic acids
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Dosing of lactulose- 2 routes and the dosing titration regimen (same for both)
target of therapy |
PO or PR
20-30 grams (30-45 mL) every hour until catharsis begins Decrease to 10-30 grams every 8-12 hours to have 2-3 soft stools/daily |
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how does using abx decrease ammonia in blood? (2)
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Inhibit the activity of urease-producing strains (make ammonia) of colonic bacteria
Urease splits urea to ammonia and CO2 |
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abx use for HE- how is it used
which abx (most commonly used, then 4 others) |
Not first line or monotherapy- added to lactulose
Rifaximin neomycin, metronidazole, PO vancomycin, PO quinolones |
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rifaximin properties (2) absorption, FDA status
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orphan status- rarely used
not absorbed at all |
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rifaximin dosing (2 dosing regimens)
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400 mg TID **more used for traveler's diarrhea OR 550 mg BID (more recently approved dose for HE specifically)
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AE of rifaximin (2)
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peripheral edema (15%) and dizziness (13%)
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what is SBP? how did it occur? (2) spontaneous bacterial peritonitis
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Spontaneous infection of ascitic fluid presumably resulting
from altered gut permeability i.e. Direct access of enteric organisms into bloodstream via portosystemic collaterals + decreased immune system WHY- but exact mechanism is controversial absence of primary source (no obvious other infection) |
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most common bacteria in SBP (5)
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Enterobacteriaceae (E.coli, Enterbacter,
K.pneumonia) and non-enteric Streptococcus and Stapholococcus (skin) |
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prevalence if SBP in ascites patients (%)
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Prevalence 10-25% of patients with ascites
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who should received broad spectrum antibiotics (suspected SBP --> empirical treatment) (3)
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hit on any of these:
Patients with documented SBP positive ascitic fluid cultures ascitic fluid polymorphonuclear leukocyte (PMN) count ≥250 cell/mm3 usually will als ohave sx of infection (elevated wbc, fever) |
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other risk factor for SBP?? (not related to bacteria)
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Serum bilirubin (Tbili) > 2.5 mg/dL also a risk factor
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abx options for SBP (4)
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3rd gen cephalosporins- more commonly used (cefotaxime, ceftriaxone**most common, cefpodoxime)
fluoroquinolones (cipro) -equally effective for gram -/+ |
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Initial studies for fluoroquinolones on SBP were using what? (2)
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norfloxacin and ofloxacin
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cefotaxime dosing
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Cefotaxime 2 g IV q8-12 hours
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ceftriaxone dosing
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Ceftriaxone 1-2 g IV q12 hours
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cefpodoxime dosing
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Cefpodoxime 100 mg PO q12 hours
wtf its PO |
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ciprofloxacin dosing
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400 mg IV q12 hours or 500 mg PO q12 hours
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how long do you continue abx for SBP?
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Continue antibiotics until asymptomatic
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why is SBP ppx needed? SBP is big possibility in patients with what?
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25-50% of patient with active GI hemorrhage will develop SBP
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norfloxacin dosing for GI blood SBP ppx
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400 mg PO Q12 hours
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drugs to use for ppx in pt with GI bleed for SBP (2)
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ceftriaxone IV
norfloxacin PO wtf can't use others? |
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who should receive SBP long term ppx?
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Patients who survive SBP should receive long term prophylaxis
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drugs used for SBP ppx (2) and dosing
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Trimethoprim/Sulfamethoxazole 160/800 (high dose) mg PO daily
Norfloxacin 400 mg PO daily |
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No SBP or GI bleed, but positive for cirrhosis and ascites: parameters for dxing this
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Ascitic fluid protein < 1.5 g/dL and one of following:
SCr >1.2 mg/dL, Bun > 25 mg/dL, serum Na < 130 mEq/L or CP score > 9points with Tbili > 3 mg/dL WHAT THE FUCK IS THIS HE DIDNT TALK ABOUT THIS |
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why is liver cirrhosis often assoc. with coagulopathy
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Coagulation factors synthesized by liver
As well as endogenous anti-coagulants proteins C & S |
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Prothrombin time prolongs when what factors are reduced (5)
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I, II, V, VII, X
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Vitamin K Dependent factors (4)
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II, VII, IX, X
(10)972 (1972) |
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Blood product administration for coagulopathies- products to use (2)
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Platelets for thrombocytopenia
Fresh frozen plasma (FFP) for prolongation of PT |
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how to look at INR for hospital patients with cirrhosis and what to do
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INR should not be looked at like warfarin for cirrhosis patients? Just because they have an INR of 2.5 does not mean they are good to go.
So unless pt is bleeding out, usually will give some anticoag. |
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pt at risk for VTE (venous thromboembolism) (6)
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Non-ambulating patients have higher risk (hospital pt)
Cancer, Surgery, Trauma, Obesity, Estrogen |
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why is a 2.5 INR not a good evaluator of whether pt still needs anticoag for cirrhosis pt? (3)
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Only partial picture of coagulation status
Bleeding risk is higher but clot risk still present Patient specific factors should be considered when considering chemical VTE prophylaxis |
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3 other systemic complications of cirrhosis
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hepatorenal dysfunction
hepatopulmonary dysfunction endocrine dysfunction |
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hepatorenal dysfunction- what is it?
incidence in pt with cirrhosis/ascites within 5 years |
Renal failure secondary to vasoconstriction within the renal
vasculature- organ failure dominos Develops in approximately 40% of patients with cirrhosis and ascites within 5 years |
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treatment for hepatorenal dysfunction (3)
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(midodrine, octreotide, albumin) (MOA)
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hepatopulmonary dysfunction from cirrhosis- what is happening?
treatment |
Alterations in lung mechanics caused by edema and ascites, abnormal
ventilation:perfusion ratio, etc Treatment: Control of ascites |
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endocrine dysfunction in cirrhosis- cause
what happens in men? women? |
Perturbs hypothalamic-pituitary axis (HPA)
Men: testosterone levels low, estrogen high (gynecomastia) Women: less well studied |
