Q.509.. Define “subfulminant” hepatic failure?
Fulminant Hepatic Failure
Revise please the abbreviation list on:
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Q.508. Define FHF.?
A. Hepatic
failure: [acute,
frequently fatal process é severe metabolic abnormalities, neurologic
complications & MODS Liver Dialysis].: Ac. hepatocyte dysfunction Dcr. protein level,
clotting f. & global odema.
FHF: [Severe Ac. liver failure in a ptn. without pre-existing liver dis., ence-phalopathy
dev. é two w., fr. 1st
manifestation of liver dis. (us Jaundice)].
Q.509.. Define “subfulminant”
hepatic failure?
A. “Subfulminant”
hepatic failure: occ. >
2-3 w. fr. Jaundice.
Q.510.. What is the most
common cause of hepatic encephalopathy (H.E.)?
A. Acetaminophen overdose, is
the most
common cause
of H.E.
- Aceta.:
matabolite8 to NAD QI (N-acetyl-P-benzoquinone
imine), wch. normally neutralized by Glutathione, but if the amount of aceta. overwhelm
Gluta. ”Hepatic Encephalopathy”
occ. by this (NAD QI)
toxic metabolite.
Q.511.Which cause has the best
prognosis?
A. HAV.
hs the best prognosis (No progression to ch. hepatitis, Dgx. by HAV anti-Ig M
A.B.), 2nd best Drug-induced, Acetaminophen, é rate of onset indicative of dis.
prognosis, with the most
rapid onset the best prognosis.
Q.512.Which patient is more
susceptible?
A. “Glutathione”-depleted
ptn. are more susceptible, us. due to:
1) Alcoholism.
2) Malnourishment.
3) P450-inducing drugs,
e.g. Rimactane.
- A single dose of 10 g.
aceta.➤
F.H.F., but a therapeutic
dose of same drug F.H.F in
alcoholics.
Q.513.What about anesthetic agents?
A. HalothaneF.H.F., but not used now,..[Enflurane,
Isoflurane, Methoxy Flurane] much less hepatotoxic.
Q.514.Mention
the other causes?
A. Other causes:
1) Sulfonamides, NSAID, Phenacetin, amiodarone, Valproic a., propyl
thiouracil & ecstasy= MDMA (3,4-methylenedioxymethamphetamine).
2) Mushroom: [Amnita Phalleides]rare, but recognized as a cause of FHF 8 Hepatic, renal, pancreatic, cerebral damage can
occur due to [Toxin a-amantin] 8 Profuse watery Drr. & abdominal pain last 1-6 d. prior to liver failure.
3) Wilson’s Syndrome: hemolytic
anemia 2ndry to massive copper release
fr. liver, Kayser-Fleischer ring é slit lamp, low
ceruloplasmin, unless liver T.X.,100% Fatal.
Q.515.What
is the clinical picture?
A.{N. & V.,
jaundice, Encephalopathy, Hypo.(Na, K, Gluc.),
Metabolic acidosis, cerebral edema, uncal or cerebral herniation}… Rapid rise
in brain water occ. due to incr. permeability of blood-brain
barrier brain water in face of solid cranium
I.C.T. &
cerebral perfusion. Decerbrate
pattern, brain stem pattern cn be also observed.
Q.516. What
is the clue of cerebral edema?
A. Cerebral edema is manifested by:
1) Bradycardia.
2) Systolic Hypertension.
3) Abnormal pupillary reflexes.
- I.C.P. cn be measured by
[subdural transducer]
risk of bleeding
& infc.,
so, only used é ventilated &
sedated ptn.s. I.C.P. monitoring
is advised in G. III/IV. Encephalopathy,
as recovery cn occ., but permanent
dge cn occ.
Q.517. Describe
the full picture of other systemic organs & metabolic status?
A. All ptn.s. hv. circulatory compromise & hypotension
is common due to:
Circulating
endotoxin.
TNF. effect.
- Microthrombi ➤🠟 vital organ perfusion,
both Hpt.
& microthrombi
+ Defective delivery & uptake of O2 ➤Anaerobic
metabolisma Lactc
acidosis & MODS.
Q.518.What
is effect on blood picture?
A. Thrombocytopenia occur due to:
1) Consumption.
2) Splenomegaly.
3) Low production by B.M.
Q.519.What
is the effects on coagulation profile?
A. Liver compromise production of: factor
I, II,..V, VII, IX, X. P.T.& P.T.T.
- .
reduced rapidly, as it has short ½ life, So, the {level of f.V.} often used as a measure of dis. progression
& considered independent
prognostic factor.
- Hge. is not common, but if occur G.I. is the most
common.
Q.520.What
coagulopathy is candidate to occur?
A. DIC occur due to:
1) Release of thromboblastic material fr. necrotic
hepatocyte.
2) Platelet activating F. & circulating bacterial non-hepatic endotoxin.
3) Expression of tissue factor on active endothelial cells Coagulation cascade.
Q.521.What
about immunological status & liability for infection?
A. Immunocompromised status
arise Bacterial & fungus (Candida,
aspergilla) infection is expected due to:
1. Complement deficiency.
2. Diminished Opsonin
activity.
3. Impaired
leucocytic
function.
Q.522.What about kidney function?
A. Renal dysfunction occur é 55% of
cases due to:
1. H.R.S.
2. Circulation: compromised R.B.F.
3. Direct toxin of :
I.
Aceta overdose.
II.
A.B. use.
III.
Radiocontrast.
Q.523. Which
modality of dialysis is suitable for those patients?
A. CRRT is the 1st choice, even é hemodynamically stable ptn., do
NOT use IRRT (Intermittent Renal Replacement Therapy) ICT , but no rise in CRRT.
Q.524. How
to evaluate those patients?
A. Full biochemistry,
coagulation profile, ceruloplasmin level, P.T., F.V.
- Swan Ganz catheter, i.v. H2 blocker’s gastric bleeding, liver biopsy é minority of cases, transjugular approach in
case of coagulopathy, due to less risk of bleeding é percutaneous approach.
Q.525. How
to manage?
A. Management:
1) Few cases respond, to [NAC, N-acetyl Cysteine] It enhances
availability of [Glutathione],
if given within 36
h. improved
outcome :
[NAC] mg/kg., oral , foll. by 70 mg/kg./4 h./17 dose.
[NAC] i.v. 150 mg bolus, foll.
by 70 mg. i.v./4h./12 doses.
2) Acyclovir, for
herpes Simplex.
3) Lamivudine for HBV.
4) Acute fatty liver
& HEELP (Hemolysis, Elevated Liver Enzymes, Low
Platelet) Immediate
delivery of
the fetus.
5) Amantia toxin High-dose Penicillin
(300,000-one million U/kg/d.) anta-gonizes muchroom
toxin(Amatoxin & Sylibin) 20-48 mg/kg/d.Block
hepatocyte toxin uptake.
Q.526. How
to do supportive hepatic care?
A. Supportive hepatic care:
1) Fluid
resuscitation for hypotension,
occ. due:
Dcr.
systolic vascular resistance.
Incr.
endothelial permeability.
2) [Albumin& F.F.P.]
1st line
of fluid resuscitation, once it occ., maintain é:
3) Dextrose 5% & ½
N.S. 0.45%, if B.P. still low. (Wedge= 12-14).
4) Noradrenaline, due to its preferential effect on a receptor.
5) Bacteria ammonia, So give lactulose ammonia
absorption.
6) Avoid use
of “ Neomycin”
in H. encephalopathy
Oto/Nephrotoxic.
7) [Flagyl infusion] Bacterial flora & ammonia
production.
8) Antipyretics for fever: as fever I.C.P.
9) Vit.
K+ for coagulopathy, FFP Only
if bleeding occurs.
Q.527. How to deal with brain odema?
A. A common
cause of death, So, ICP.
monitoring + [Romazicon] to keep cerebral brain perfusion pressure
(C.P.P.)>50, If I.C.P>30 & C.P.P< 40 Permanent Neural dge.
Q.528.Which
type of sedation is valid for those patients?
A. Flu ma zenil (Romazicon)رومازيكون a benzodiazepine
antagonist ➤
improve short outcome.
Q.529. Explain,
how can kidney function affect the lines of therapy?
(A) Normal
Renal f.Ø [mannitol] ½ -1 g./kg. I.C.T. a diuresis = twice volume of mannitol shd be expected
within one h., the dose cn be repeated, but ➤ Stop mannitol if Osmolality
reaches :*320* mosmol/kg.
- “Mannitol” cn cause intravascular vol. depletion & AKI.
(B) In R.F.,
mannitol cn
be coupled é hemofiltration, to keep
osmotic effect:
twice
vol. of mannitol given shd be removed by U.F., to ensure this effect.
Q.530.What
are other lines to reduce I.C.P.?
A. Hyperventilation to dcr. PCO2 to “30” used to reduce I.C.P., but some studies showed: PCO2 <24
➤
cerebral V.C. !!
- If the prev. measures fail to keep CPP.>50
➤ use Phenobarbital to
induce coma.
Q.531. What is the role of transplantation in treatment?
A. (1) Liver transplantation:
should be tried EXCEPT in:
ARDS.
Sc vo 2 level.?
Uncontrolled intracranial H.T.
(2) Hepatocyte T.x.
on Splenic bed,
hs bn tried é some success.
Q.532. How can
Liver dialysis help those patients?
A. Liver dialysis uses hemoadsorption = H.DX. é thick suspension of Pulvirized Sorbent, replacing Dzt solution in the Dzr to remove
potential toxins
fr. bld.
- The small size of charcoal particles provide 300,000
m2 of
S.A., much more S.A. of ordinary charcoal column (few thousands).
- Q.B.: 200-250 ml/min., toxins pass directly across Cellulose
membrane, where they bind
the small particles of charcoal or cation
exchange in
sorbent solution,…ttt. of 6 h./d/5 d.
Q.533.What
other sorbent system
can help in management in hepatic failure?
v M.A.R.S.: (Molecule
AdsoRbent Circulatory System)=non-albumin permeable polysulphone DX membrane, used é bld perfused in one side & 20 % albumin on Dzt side,
another sorbent system, dev. for managing
hepatic failure.
v Albumin-bound
substances:[bilirubin- bile salts- tryptophane
& F.A.] cleared across the membrane to the (Dzt albumin), wch’s regenerated by passing thr. (charcoal column), foll.
by (anion exchange resin
column) & finally (Bic-arbonate buffer Dzt)
to remove small toxins e.g. [ammonium
& aromatic a.a.]
- MARS improves survival & impair encephalopathy . Outcome is improved in Ac. on ch. Liver
failure
but not in FHF.
Q.534. What
is the Bioartficial Liver?
A. BAL (Bioartficial Liver) a device in wch Hepatocytes are
inoculated into one side of a semipermeable membrane. Blood
passed into Plasma separator. Plasma warmed, oxygenated, then
passed thr. the device that houses the hepatocytes.
The membrane acts to prevent A.B. fr. entering the cell compartment fr. the
plasma, but allow hepatocyte to extract O2, nutrients & toxins from plasma & allow
metabolites to pass to hepatocytes from the plasma.
- Current BAL use Procine hepatocyte or human immortalized hepatocytes.
- The Heat assisst device hs bn also
evaluated, for further studies.
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
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