BIMONTHLY INTERNAL ASSESSMENT - OCTOBER

CASE 1:

57 year old man with jaundice, pedal edema and abdominal distension

since three years and bleeding gums since three days"

https://swathibogari158.blogspot.com/2020/09/chronic-decompensated-liver-disease.html

1) What is the reason for this patient's ascites?

A) Chronic liver disease (

chronic alcoholic since 40 yes) Truncal obesity leading to fatty liver changes

in echotecture of liver leads to increase hydrostatic pressure and increase

portal hypertension leads to ascitis 

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) Biletral pedal odema is due to decrease

albumin( synthetic activity of liver has affected) leads to decrease oncotic

pressure further causes pitting type of pedal odema blebs and bursting of blebs

and leading to ulceration is due to coagulation activity of liver has affected

i.e explained by increased INR trends leading to bleeding manifestations and

blebs formation self medication with steroids nd unhygienic dressing lead to<b></b>

chronic ulcerations 

3) What was the reason for his asterixis and constructional

apraxia and what was done by the treating team to address that?

A) Asterixis is

myoclonus characterised by muscular inhibition. It's not pathognomic of any

condition but indications the security of disease on examination patient has

flapping tremors seen in liver disease hepatic encephalopathy( WEST HAVEN

criteria )damage occur to brain cells due to impaired metabolism of ammonia

leads to asterixis and impaired neurotransmission due to metabolic changes in

liver failure and alteration of blood brain barrier leads to constrictional

apraxia

They gave lactulose nd rifaximin 550 mg lactulose increases the uptake

of amonia by colonic bacteria lactulose decrease the ph of gut which destroys

urease producing bacteria their by decreasing the production of ammonia

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)High protein diet for low albumin

 2) Air bed to prevent bed sores

3) Fluid restriction due to prevent fluid dissemination into extravascular space

4) Salt restriction ( less than 2.4 gm/day) to prevent retention of water due to osmotic activity of sodium 

4) Inj augmentin 1.2 gm to prevent secondary infections

5)Tab lasilactone 20/50 for fluid diuresis

6)Vit k 10 mg IM causes coagulation to prevent bleeding manifestations

7) syp Lactulose and tab rifaximin to prevent hepatic encephalopathy

8) Tab udiliv 300 mg dissolves gall stones 

9) syp hepamerz 15 ml 

10) IVF 500 ml NS for hydration 

11)Inj thiamine 100 mg in 100 ml NS ( deficiency due to chronic alcoholic)

12 )Proteinex powder I glass of milk TID) as his synthetic activity of liver is decreased and muscle wasting is also seen 

13) 2 FFP and 1 PRBC to support

coagulation pathway

14 ) ASD dressing for ulceration

CASE 2:

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) Lft is deranged Tb raised ALP raised low serum albumin history of watery diarrhoea since 20 days might be due to? Gi infection or Rifampicin induced(pseudomembranous colitis) was noticed although not specific to usage of rifampicin usage of ATT induced hepatotoxicity increased

14-fold in patients with chronic liver disease and liver cirrhosis associated

immune dysfunction syndrome, and case fatality rates are high

If hepatotoxicitydevelops in those with liver cirrhosis,particularly decompensated cirrhosis, the

risk of severe liver failure is markedly increased. currently there are no

established guidelines for ATT in chronic liver disease and liver cirrhosis

Generally in CLD patients ATT should not include more than 2 hepatotoxic drugs

according to chill Turcotte pugh ( CTP less than

7) only 1 hepatotoxic drug with

advanced liver dysfunction CTP:8 to 10) or no hepatotoxic drugs (CTP more than 11)

2) What were the investigational findings confirming the diagnosis of pulmonary

TB in this man? 

A)1) Fever during night time

2) sputum for AFB is positive

3) CXR shows haziness

4) CT chest shows cavity in R lung

3) What was the cause of his ascites? 

A) Chronic decompensated liver disease( ascitic tapping shows

transudative type)

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) INj HAI for diabetic management

2) inj.optineuron for nutrition supplementation 

3) ATT withhold due to hepatotoxicity

4) syp Lactulose 15 ml to prevent hepatic encephalopathy 

5)protein powder and high protein diet for protein supplementation

6) ORS for rehydration due to acute GE 

7)inj vit k to prevent  bleeding manifestations

8)nebulisation for airway clearence

9) inj thiamine 100 mg in 100 ml NS iv for

thiamine deficiency 

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) management should focus on investigating the cause

Primary ( idiopathic ) 

Secondary glomerular pathology 

Primary causes include FSGS

membranous glomerular nephropathy 

minimal change MPGN 

Secondary causes of nephrotic syndrome 1) Diabetes mellitus 

2) Systemic lupus erythematosus 3)Amyloidosis

4) Cancer

5)Myeloma and lymphoma 

Drugs ,Gold ,Antimicrobial agents ,Non-steroidal

anti-inflammatory drugs Penicillamine Captopril Tamoxifen Lithium Infections HIV

Hepatitis B and C, Mycoplasma, Syphilis Malaria, Schistosomiasis, Filariasis, 

Toxoplasmosis, 

Congenital causes like Alport’s syndrome

 

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?

pros : 

gold standard investigation for knowing histopathologiacal diagnosis

cons: 

1)invasive method 

2) post op compications like bleeding infections

3) cost

effective nd non availability of biopsy at every centre( Time consuming?) renal

biopsy report will give the clue whether to start steroids or not in any auto

immune condition