AI generated questions -Hepatic encephalopathy Flashcards
(44 cards)
2 main ways ammonia is generated in the GI
- enterocyte glutamine metabolism. 2. microbiome (urease producing bacteria -cleavage urea to ammonia)
Kidney, why they produce ammonia?
in order to make bicarbonate- glutamine in metabolized in the kidneys (to NH4+ and bicarbonate)
which cells are the common ones in the CNS?
The astrocytes. They contribute up to 50% of brain volume. contain glutamate synthetase and mitigate increasing ammonia by converting glutamate to glutamine and consuming 1 ammonia molecule
: What is the role of ammonia in the pathogenesis of hepatic
encephalopathy (HE)?
Central role in HE pathogenesis
○ Generated in GI tract through enterocyte metabolism and intestinal
microbiome activity
○ Complex interplay with triggers allows HE to occur even with modest or
normal ammonia levels
How is ammonia generated and removed in the body relating to HE?
Generated in the GI tract by enterocytes by metabolism of glutamine
and by urease producing bacteria and by kidney metabolism of
glutamine (in the kidneys to produce bicarbonate)
○ Removed by kidneys through urea excretion and by muscle and CNS
activity (astrocytes, both by synthesize glutamine)
: What role do skeletal muscles play in ammonia metabolism in HE?
Produce glutamine that consume ammonia, later upon catabolism of
glutamine– ammonia will be generated
○ Acts as an ammonia buffer when systemic concentrations rise
How does the CNS contribute to managing increased ammonia levels in
HE?
Astrocytes convert glutamate to glutamine, consuming ammonia
○ Key in mitigating increasing ammonia concentrations
How is inflammation related to HE in dogs with cPSS?
○ Dogs with cPSS and HE have higher CRP levels than dogs without HE
○ Both ammonia and systemic inflammation predictive of HE
○ pro inflammatory cytokines alter the cerebral endothelial permeability to
neurotoxins and potentiate ammonia toxicity. cytokines cross the BBB,
and activate microglia that produce local cytokines, causing cerebral
vasodilatation and hyperemia due to loss of cerebral autoregulation.
○ hepatic necrosis releases pro inflammatory cytokines. the cytokines alter the
permeability of the cerebral endothel- increase permeability of neurotoxins
and potentiate ammonia toxicity. cytokines cross the BBB, activating
microglia- that release local cytokines. all this causes cerebral vasodilatation
and htperemia- secondary to loss of cerebral autoregulation.
What is the significance of manganese (Mn) in HE?
Essential trace element but can be neurotoxic
○ can be Extremely increased concentrations in blood of dogs and cats
with PSS
How do non-absorbable disaccharides manage HE?
Metabolized by colonic bacteria into SCFAs, decreasing systemic
ammonia
○ Acidify colonic content to trap ammonia
○ Act as osmotic laxatives for ammonia removal
What dietary management is proposed for high-grade HE?
○ Initial Short-Term protein restriction necessary
○ Increase protein intake gradually once stabilized, considering life-stage
requirements
: What is the starting dose protocol for lactulose in HE management?
0.5 mL/kg orally, every 8-12 hours, titrated for 2-3 soft stools per day
How is a lactulose enema administered for HE?
○ 1 part lactulose to 3 parts warm water, 10 mL/kg via Foley catheter,
retain 30-60 mins, repeat as required
: What is the protocol for using lactose in managing HE?
Empirical dosing to effect 2-3 soft stools per day
○ Consider protein content; suggested in cats
: What is the dosing protocol for neomycin in HE, and what are its risks?
○ 20 mg/kg orally every 12h
○ Risk of oto- and nephrotoxicosis if absorbed systemically
What is rifaximin’s role in HE treatment, and what limits its use?
Dosed at 5 mg/kg orally every 12-24 hours
○ Nonabsorbable antibiotic; expense and limited anecdotal use restrict its
application in dogs
What dietary consideration is given to pets with cPSS in HE management?
○ Prefer high-quality standard life-stage diets over expensive,
protein-restricted “hepatic diets”
What is hepatic encephalopathy (HE)?
● Neuropsychiatric syndrome involving neurologic abnormalities.
● Occurs with >70% loss of liver function or portal blood bypassing the liver
What role does ammonia play in the pathogenesis of hepatic encephalopathy?
Ammonia has a central role.
● Generated in the GI tract via enterocyte glutamine metabolism and intestinal
microbiome.
● Kidneys excrete urea, contributing to acid/base balance.
● Skeletal muscles release glutamine, potentially contributing to ammonia
levels.
· what role play the astrocytes in hepatic encephalopathy?
● Contain glutamine synthetase, converting glutamate to glutamine.
● Mitigates increasing ammonia concentrations.
● Consumes ammonia in the process.
What role does inflammation play in hepatic encephalopathy?
Pro-inflammatory cytokines released following hepatic necrosis.
● Alter cerebral endothelial permeability to neurotoxinsPotentiate ammonia toxicity.
What is the management approach for hepatic encephalopathy?
● Non-absorbable disaccharides (lactulose, lactitol).
● short term Protein restriction in high-grade HE.
● Antibiotics to reduce bacterial numbers in the intestinal microbiota.
· What is portal hypertension?
● ↑ Portal pressure due to altered hepatic resistance and capacitance.
● Can be pre-hepatic, hepatic (pre-sinuoidal, sinusoidal, post-sinuoidal), or
post-hepatic.
How does hepatic sinusoidal portal hypertension develop?
Inflammatory/fibrotic hepatopathies lead to endothelial changes secondary to
oxidation, inflammatory mediators and physical changes to sinusoidal
endothelium.
● SECs become less able to compensate for ↑ in portal blood flow. producing
less vasodilators and more vascoconstrictirs (endothilin 1 , Ag II)
● local Vasodilators release causes splanchnic arteries to dilate, exacerbating
hypertension.
