BIMONTHLY EXAM

                          CASE 1
     This is a case admitted in my unit , so patient is a 57 yr old male with poor lifestyle habits and obesity and chronic alocholic . 
https://swathibogari158.blogspot.com/2020/09/chronic-decompensated-liver-disease.html

1. What is the reason for this patient's ascites? 
 A.  Ascites is defined as the presence of excessive fluid in the peritoneal cavity. 
        Reasons for Ascites: 
     . CHRONIC LIVER DISEASE (ALCOHOL             INDUCED LIVER CIRRHOSIS) 
     .  HYPOALBUMINEMIA
     .  TRUNCAL OBESITY >> METABOLIC                    SYNDROME >> NAFLD >> CIRRHOSIS 
      MECHANISM:
       Portal hypertension ----splanchanic             vasodilation---decreased renal blood flow ----     RAAS system activation------Sodium water.         retention.
 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3860926/#:~:text=Ascites%20is%20defined%20as%20the,resulting%20in%20renal%20sodium%20retention 

2. Why did the patient develop bipedal lymphedema? What was the reason for the recurrent blebs and ulcerations and cellulitis in his lower limbs?  
 A.  Bipedal lymphedema due to FILARIASIS 
       Patients with chronic lymphatic obstruction and venous stasis are at more risk of developing recurrent cellulitis .
 CELLULITIS is an acute diffuse .  inflammation of subcutaneous cellular  tissue usually caused by streptococci or staphylococci.

3. What was the reason for his asterixis and constructional apraxia and what was done by the treating team to address that?  
A.  HEPATIC ENCEPHALOPATHY
    Pathophysiology of hepatic               encephalopathy:
   It is due to accumulation of ammonia.
  1. role of neurotoxins, 

  2.impaired neurotransmission due to  metabolic changes in liver failure, changes in brain energy metabolism, systemic inflammatory response and alterations of the blood brain barrier which produces a wide spectrum of nonspecific neurological and psychiatric manifestations. 

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5SYNDROME

  The only treatment for this was to remove organic waste from bowel ,by giving lactulose syrups and enema , preventing worsening of encephelopathy.
.  SYRUP. HEPAMERZ -It is used for  protecting the liver from harmful chemicals or free radicals. 
. SYRUP. LACTULOSE - Helps to reduce the amount of ammonia in the blood of patients with liver disease. 
TAB.RIFAXIMIN - effective in treating acute HE and is extremely well tolerated.

 
4) What was the efficacy of each treatment intervention used for this patient? Identify the over and under diagnosis and over and under treatment issues in the management of this patient
A.
 1. Air or water bed to prevent pressure bed sores in the dependent areas. 
2. Fluid restriction <1.5litres/day so as to decrease of fluid dissemination into the extra vascular space. 
Salt restriction <2.4gms/day to prevent retention of water.  
3. Inj augmentin 1.2gm IV/BD to prevent secondary bacterial infections.  
4. Inj pan 40 mg IV/OD
5. Inj zofer 4mg IV/BD
6. Tab lasilactone (20/50)mg BD combination of furosemide and aldactone to decrease pedal oedema. 
If SBP <90mmhg - to avoid excessive loss of fluid. 
7. Inj vit k 10mg IM/ STAT ( as vitamin K causes coagulation to further prevent bleeding manifestions. 
8. Syp lactulose 15ml/PO/BD for hepatic encephalopathy. 
9. Tab udiliv 300mg/PO/BD  used to dissolve gallstones. 
10.syp hepameiz 15 ml/PO/OD - It is used for protecting the liver from harmful chemicals or free radicals. L-ornithine- L-aspartate (LOLA), the salt of the natural amino acids ornithine and aspartate acts through the mechanism of substrate activation to detoxify ammonia.
11.IVF 1 NS slowly at 30ml/hr to maintain hydration. 
12. Inj thiamine 100mg in 100mlNS /IV/TID as thiamine deficiency's occur in chronic alcoholics. 
13.strict BP/PR/TEMP/Spo2 CHARTING HOURLY. 
14.strict I/O charting. 
15.GRBS 6th hourly. 
16.protein x powder in glass of milk TID for protein supplementation and muscle wasting.  
17. 2FFP and 1PRBC transfusion to support coagulation pathways.  
18 .ASD DONE for wound infections and ulcer. 
19. High protein diet (2eggs / day) for decreased albumin synthesis. 


                             CASE 2
 A 54 year old male with cough,abdominal tightness,pedal edema and diarrhea.
https://sainiharika469.blogspot.com/2020/09/hello-everyone.html?m=1  

1. Why were his antitubercular therapy stopped soon after his current admission? Was he symptomatic for ATT induced hepatitis? Was the method planned for restarting antitubercular therapy after a gap of few days appropriate? What evidence is this approach supported by?
A.  His ATT was stopped because of ELEVATED LIVER ENZYMES AND LIVER FAILURE (? ATT INDUCED LIVER DAMAGE)

Patient was SYMPTOMATIC 
Starting ATT after few days was appropriate AFTER ACUTE EPISODE OF LIVER FAILURE SUBSIDE.

Method followed was:
ETHAMBUTOL followed by RIFAMPICIN followed by PYRAZINAMIDE followed by ISONIAZID.
Each drug should be started with min dosage and increased to max dosage

Currently, there are no established guidelines for anti-tuberculosis therapy (ATT) in CLD and liver cirrhosis hydratiothe need for such guidelines is self-evident. 
1) It is proposed that ATT should include no more than 2 hepatotoxic drugs (RIF and INH) in patients with CLD or liver cirrhosis and stable liver function [Child-Turcotte-Pugh (CTP) ≤7],
2) Only a single hepatotoxic drug (RIF or INH) in those with advanced liver dysfunction (CTP 8–10) and 
3) No hepatotoxic drugs with very advanced liver dysfunction (CTP ≥11). 

2.What were the investigational findings confirming the diagnosis of pulmonary TB in this man? 
A.  Infiltrates in CHEST X-RAY
    Plueral thickening and fibrocavitory .          changes noted in HRCT.
    Sputum positive TB with RIFAMPICIN .        sensitivity. 

3.What was the cause of his ascites? 
A.  ALCOHOLIC CIRRHOSIS OF LIVER >>    PORTAL HYPERTENSION
    LATE BUDD-CHIARI SYNDROME
BCS should be suspected in patients with: 
1) Abrupt onset of ascites and painful hepatomegaly 
2) Massive ascites with relatively preserved liver functions
3) Sinusoidal dilation in liver biopsy without heart disease 
4) Fulminant hepatic failure associated with hepatomegaly and ascites
5) Unexplained chronice liver disease 
6) Liver disease with thrombogenic disorder.
     HYPOALBUMINEMIA 
   
4.What are the efficacy of each intervention mentioned in his treatment plan and identify the over and under diagnosis as well as over and under treatment issues in it. 
A. High protein diet 4eggs daily for protein supplementation 
. ORS sachets in 1 litre of water to compensate electrolytes lost due to diarrhoea 
. Inj PIPTAZ 4.5gm for antibiotic cover
. Vit k 10 mg Iv OD for 5 days to prevent  forthcoming bleeding manifestations as his PT INR APTT are elevated 
. IVF - 1 DNS @50ml/hr for hydration
. Nebulisation with salbutamol and mucomist 12th hourly for cough and crepts
. Inj thiamine 100 mg in 100 ml NS IV TID. for chronic alcoholism. 

                          CASE : 3 
 47 year old man with bipedal edema   since one year and abdominal distension since one month. 
https://sushma29.blogspot.com/2020/09/ascites-secondary-to-nephrotic-syndrome.html?m=1 

1. What will be your further approach toward managing this patient of nephrotic syndrome? How will you establish the cause for his nephrotic syndrome? 
A.Further approach would be first by finding out cause for his nephrotic syndrome ,which could be

A) Primary (idiopathic) forms:
-Minimal change disease - but seen in children so ruled out .
-Focal segmental glomerulosclerosis- seen in adults so a possibility
-Membranous nephropathy - Most commonly seen in adults ,so a possibility.( Anti PLA2R antibodies)

B) Secondary forms :
-Diabetic nephropathy- pt not a known diabetic
-Amyloid nephropathy: can be associated with multiple myeloma (AL amyloidosis) or chronic inflammatory disease such as rheumatoid arthritis (AA amyloidosis) - not seen in our pt.
-Lupus nephritis. - not a possibility 
- Hiv hbsag , were negative . No features of STD .
- Malignancy - lung , adenocarcinoma of colon , stomach , prostate carcinoma ,non hodgkins lymphoma all these are secondary causes of nephrotic syndrome - which could be a possibility in this patient owing to chronic weight loss and muscle wasting and loss of appetite .

So only way to look for diagnosis is :
-First doing a renal biopsy ,
- ANA ,C3,C4 levels would tell us an autoimmune cause - but they are not sensitive and not recommended much . Biopsy would be a better option.
-Can search for primary focus of malignancy ,

By doing HRCT ,Ct abdomen , endoscopy/colonoscopy - All these are very difficult to do in a patient who has financial issues..but sometimes ,it's of benefit to the patient if a malignancy is detected at an early stage . 

2.What are the pros and cons of getting a renal biopsy for him? Will it really meet his actual requirements that can put him on the road to recovery? 
A. PROS:
    getting renal biopsy would clearly tell .      us if it's FSGS ,MGN ,MPGN pattern. 

    CONS:  
  • Bleeding
  • Infection
  • Injury to other organs in the area
  • Inadequate and/or no specimen for interpretation
  • Blood loss sufficient to require either surgery or blood transfusion to stop the bleeding. 

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