bimonthly Examination October's exam

Bimonthly Examination

October online exam

October 07,  2020

First Case   

  57/M

1)Reason for ascites:

As per the history and examination: ? A)cirrhosis of the liver secondary to chronic daily alcohol consumption

Hepatosplenomegaly suggestive of portal hypertension

B) hypo albuminemia-serum albumin being 1.6 , suggesting chronic pathology, ?decreased synthesis by the liver, (accompanied by decreased synthesis of vit k dependant clotting factors)

2)Reasons for lymphedema:

Secondary causes as per history and examination are 1)infection:filariasis, cellulitis

2)trauma 3) non obstructive causes of chronic venous insufficiency

https://cervivor.org/armor-know-lymphedema/

https://www.ncbi.nlm.nih.gov/books/NBK537239/

Reason for ulcerations and recurrent blebs

Lymphedema-the stagnation of lymph obstructs the clearance of bacteria

Leading to constant cytokines and other inflammatory mediators release

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804019/

3)asterexis and constructional apraxia

The cause for asterixis is the increased passage of ammonia across the blood brain barrier , absorbed more in the areas of cerebellum and basal ganglia 

Ref from sleisenger (pathophysiology of hepatic encephalopathy, pg 1578)

The treatment included, using non absorbable disachharide (lactulose ) for causing catharsis and lowering intestinal pH to decrease the abdorbtion of ammonia, and use of antibiotics rifaximin for altering intestinal Flora and stool ph.

4) Antibiotics were indicated for the cellulitis and ulcer part ,and also pt was having fever spikes.

Challenge was constant derangement of coagulation profile with aptt and pt greater than 1 min and inr of 3.6 inspite of giving 3-4 FFps per day

. FFP contains all coagulation factors except platelets. FFP contains fibrinogen (400 to 900 mg/unit), albumin, protein C, protein S, antithrombin, tissue factor pathway inhibitor. It is free of erythrocytes and leukocytes. FFP corrects coagulopathy by replacing or supplying plasma proteins in patients who are deficient in or have defective plasma proteins. A standard dose of 10 to 20 mL/kg (4 to 6 units in adults) will raise factor levels by approximately 20%. An increase of roughly 10% of several factors is enough to effect hemostasis.

Even hemoglobin dint increase inspite of 2 prbc transfusion due to constant GI bleed ( manifested as black stools ) and bleeding from ulcers .

Rifaximin is a nonabsorbable antibiotic, which reduces the production of ammonia by gut bacteria and, to some extent, other toxic derivatives from the gut. Clinical trials show that these effects improve episodes of hepatic encephalopathy. A large randomized trial found that rifaximin prevents recurrent episodes of hepatic encephalopathy. Most patients were treated concurrently with lactulose.

Although there is no proven efficacy for it..but giving the drug wouldn't harm the patient much.

HEPAMERZ SYRUP :

Eighty patients were randomized to two treatment groups, L-ornithine-L-aspartate (20 g/d) or placebo, both dissolved in 250 mL of 5% dextrose water and infused intravenously for four hours a day for five consecutive days with 0.5 g/kg dietary protein intake at the end of daily treatment period. Outcome variables were postprandial blood ammonia and mental state grade. Adverse reactions and mortality were also determined.

Results: Both treatment groups were comparable regarding age, gender, etiology of cirrhosis, Child-Pugh class, mental state grade and blood ammonia at baseline. Although, improvement occurred in both groups, there was a greater improvement in L-ornithine-L-aspartate group with regard to both variables. Four patients in the placebo group and 2 in L-ornithine-L-aspartate group died.

https://pubmed.ncbi.nlm.nih.gov/18983791/

Second Case 

Q2)54/M

1) 

https://www.researchgate.net/publication/257434856_A_Guide_to_the_Management_of_Tuberculosis_in_Patients_with_Chronic_Liver_Disease

As per the guidelines suggested here, ATT should be given according to Child PUGH's criteria

<=7 - two potential hepatotoxic drugs , except pyrazinamide can be used

8 to 10 -one hepatotoxic drug

>10 -alternative drugs wid fluroquinolones, tetracycline can be used if renal parameters are normal.

Drugs should be stopped if serum ALT levels rise to 5 times normal,

Or atleast by 3 times if patient has jaundice or symptomatic for hepatitis.

Drug induced hepatitis is usually a diagnosis of exclusion

As the patient is a chronic alcoholic , the baseline levels can be above the normal limit prior to the start of ATT.

His ATT was stopped as his SGOT levels were raised and he showed symptoms like unexplained fatigue, abdominal pain whcih point towards a Drug Induced Liver Injury. He also has risk factors like : above the age of 35, malnutrition and alcoholic. Also monitoring hepatotoxicity post ATT is difficult in patients of Chronic Liver disease.

According to American Thoracic Society,Guidelines for re-introducing ATT are:

1. After AST returns to less than two times the normal upper limit, Rifampicin can be restarted with or without ethambutol.

2. After 3-7 days, Isoniazid maybe added, subsequently after checking AST levels.

3. If symptoms recur, then the last drug added should be stopped.

2)clinical investigations were sputum positive tb

And also with cxr and ct showing consolidation ofright middle lobe and fibrocavitatory changes and pleural thickening secondary to chronic fibrosis .

Pt even had clinical history of low grade fever and weight loss.

3)high saag and low ascitic protein suggestive of cirrhosis is the cause for ascites.

4) Efficacy of treatment :

-Diuretics and lactulose can be treatment modalities for chronic liver disease ,

If pulmonary koch is suspected ,then there would be no requirement for piptaz .

-Insulin would be a choice of treatment for controlling sugars ,as this patient is in sepsis ,sugars wouldn't be that high and glimeperide can cause recurrent hypoglycemia .

Hypoglycemia can also occur due to interaction between isoniazid and glimeperide. Isoniazid is a cytochrome inhibitor so will lead to delayed metabolism of glimeperide and hyper insulinemia.

https://pubmed.ncbi.nlm.nih.gov/23595176/

Third case 

47/M

1)The patient should be started on diuretics and a low sodium diet and owing to his high cholesterol levels he should be started on statins.

A spot urine protein (161) so high indicates renal tubular damage. This is an indication for renal biopsy.

The accepted treatment in most cases of nephrotic syndrome is:

Salt and fluid restriction

Loop diuretics

ACE inhibitors or ARBs

Electron microscopy should be done to determine the type of glomerulopnephritis.

-Drug history should be taken to look for drug induced nephrotic syndrome.

-Antinuclear antibodies and Complement C3 levels should be checked.

2) https://www.kidney-international.org/article/S0085-2538(15)56330-8/fulltext

With respect to the article stated above in relation to advantages and disadvantages of biopsy for the patient

The prognosis can be accertained and response to treatment with spacing interval renal biopsy in case of resistance to treatment .

One of the  case reports for advantage of renal biopsy in nephrotic syndrome with possible corelation with other disease

https://www.ncbi.nlm.nih.gov/pmc/articles/