57 year old man with a long term alcohol consumption with the symptoms of yellowish discoloration of eyes, abdominal distention, bleeding manifestations along with hypoalbuminaemia, asterixis, constructional apraxia gives a picture of acute decompensation liver failure.
In liver failure with portal hypertension, the patient develops fluid and salt retention because of splanchnic vasodilation which leads to activation of sympathetic system activity, renin angiotensin aldosterone system activation leading to fluid and salt retention which lead to his ascites
2. With long standing fluid and salt retention which lead to his bilateral pedal edema would've lead to venous obstruction and lymphatic obstruction explaining his lymph edema.
Venous stasis and lymphedema for a prolonged duration would've left to cellulitis along with recurrent blebs and ulcers, prone to recurrent infections
3. Asterexis and constructional apraxia are signs of hepatic encephalopathy due to accumulation of ammonia. Since there is an impairment of protein catabolism in liver failure, this leads to accumulation of ammonia along with systemic inflammation, oxidative stress and glutaminase gene alteration are involved in the mechanism of hepatic encephalopathy.
Removal of ammonia along with prevention of more accumulation of ammonia would help for which the treating team has given lactulose which is a laxative.
https://www.sciencedirect.com/science/article/pii/S0168827814006461
Case 2
1. The patient with pulmonary kochs and chronic liver disease was stopped on ATT as isoniazide, rifampicin and pyrazinamide are known for their hepatotoxicity. Reinitiation of ATT with dose adjustments would be helpful.
2. Investigations confirming his pulmonary TB would be the chest xray showing fibrotic changes, sputum being positive for tuberculosis.
Sputum positivity for tuberculosis is the most sensitive investigation for pulmonary kochs. A long standing history convincing of pulmonary kochs would also be sufficient for the physician to start the patient on ATT.
3. The cause for ascites for this patient is because of chronic liver disease and hypoalbuminaemia of 1.6.
4. For his blood sugar control he was put on Inj Human actrapid.
Case 3
3rd Patient
The next go to step in this patient would be a renal biopsy. Renal biopsy helps in diagnosing the cause of the nephrotic syndrome. It could be due to a primary or a secondary cause.
Secondary causes would be
Minimal change disease, focal segmental glomerulosclerosis, igA nephropathy, membranous nephropathy
The next step would be starting the patients on steroids or immunosuppressants or a combination of both the drugs.
If the patient lands up in end stage renal disease then there is a need for haemodialysis.
The last step would be to go for a renal transplant.
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