Bimontly GM OCT-7 examination
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?
Ans)In his history after starting of the ATT drugs for 3day's his symptom's of abdominal distension and shortness of breath increased for which he presented to our hospital.On admission his LFT was deranged, icterus was evident so ATT was stopped
The method planned for restarting the ATT was to start with ethambutol then after the other ATT drugs
Once there is evidence of acute hepatitis in a patient receiving ATT, it is essential to immediately stop all potentially hepatotoxic drugs such as INH, RIF, and PZA till complete clinical and biochemical resolution of hepatotoxicity. In the interim period, at least three non-hepatotoxic drugs viz. EMB, streptomycin and quinolones such as ofloxacin, levofloxacin, etc. can be used after checking renal function and visual acuity.54 Most ATD can be safely restarted in a phased manner after complete resolution of transaminitis.
2) What were the investigational findings confirming the diagnosis of pulmonary TB in this man?
Ans)
a)sputum microscopy positive(Confirmed with RNTCP record's)
b)chest X-ray finding's:
Multifocal areas of consolidation in bilateral lung fields with reticulo nodular opacities in right lung and fibrotic bands in bilateral upper zones
3) What was the cause of his ascites?
Pt is a k/c/o of chronic liver disease.Cirrhotic ascites forms as the result of a particular sequence of events. Development of portal hypertension is the first abnormality to occur. As portal hypertension develops, vasodilators are locally released. These vasodilators affect the splanchnic arteries and thereby decrease the effective arterial blood flow and arterial pressures.
Progressive vasodilation leads to the activation of vasoconstrictor and antinatriuretic mechanisms, both in an attempt to restore normal perfusion pressures. Mechanisms involved include the renin-angiotensin system, sympathetic nervous system, and antidiuretic hormone (vasopressin).
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.
Inj Human Actrapid Insulin s/c 8am - 2pm - 8pm--- To Control his sugar's
Inj PAN 40 mg IV/OD---- over treatment
Inj optineuron 1 amp in 100 ml NS Iv/bd-----To supplement B-complex
ATT to be with held----leading to LFT derangement so stopped
Syp lactulose 15ml HS----over treatment as already pt is having episodes of loose stools
Protein powder 3 to 4 scoops in 1 glass of milk or water QID---as his albumin is low
Stop all OHA s
Grbs charting 6th hrly
Strict I/0 charting
High protein diet 4eggs daily
ORS sachets in 1 litre of water--to supplement electrolyte due to diarrhoea
Bp charting hourly
Inj PIPTAZ 4.5gm/IV/bd stat - - --> TID----over treatment, bcz lower antibiotics could have been used
Vit k 10 mg Iv OD for 5 days---to prevent bleeding manifestation's
Temp BP PR monitoring 4th hourly
IVF - 1 DNS @50ml/hr
Nebulisation with salbutamol and mucomist 12th hourly.
Inj thiamine 100 mg in 100 ml NS IV TID.---as he is chronic alcoholic,to replenish thiamine stores
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?
Ans)
a)Chronic alcoholism since 40 years causes portal hypertension increased hydrostatic pressure causing fluid accumulation hence Ascites
2) Why did the patient develop bipedal lymphedema? What was the reason for the recurrent blebs and ulcerations and cellulitis in his lower limbs?
Bilateral pedal oedema which is of pitting type is due to
-Hypoalbuminemia
-Protienuria
-?Filariasis
ulcerations are due his indescriminate use of steroids (self medication) causing ? immune suppression leading to secondary infections hence cellulitis and non healing of wound.
3) What was the reason for his asterixis and constructional apraxia and what was done by the treating team to address that?
Hyperammonemia are the reason’s for asterixis & constructional apraxia
Ammonia is usually produced by bacteria in the gastrointestinal tract from the breakdown product of amino acids and urea followed by metabolism and clearance by the liver. In liver failure there is either a decrease in the number of functioning hepatocytes, portosystemic shunting, or both, resulting in decreased ammonia clearance and hyperammonemia.'
Once ammonia crosses the blood brain barrier, it has multiple neurotoxic effects like asterixis,constructional apraxia
Syp Hepamerz
Syp lactulose
Tab Rifaximine were used for these symptoms
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.
high protein diet (2eggs / day) for decreased albumin synthesis
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 due to osmotic gradient as sodium causes retention
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 contain Ursodeoxycholic acid as an active ingredient. It is used to dissolve gall stones in various liver-related disorders such as cirrhosis
10.syp hepameiz 15 ml/PO/OD
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 which commonly occurs in cirrhosis patients
17. 2FFP and 1PRBC transfusion to support coagulation pathways
18 .ASD DONE for wound infections and ulcer
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?
Causes of nephrotic syndrome are
Primary causes include
FSGS
membranous glomerular nephropathy
Membranoproliferative glomerulo nephritis
Secondary causes
- Diabetes mellitus
- Systemic lupus erythematosus
- Amyloidosis
Cancer
- 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
- Alport’s syndrome
- Congenital nephrotic syndrome of the Finnish type
- Pierson’s syndrome
- Nail-patella syndrome
- Denys-Drash syndrome
Managing the symptoms of the disease such as protein loss, pedal oedema,
A renal biopsy would be helpful in establishing the cause of which type of glomerular pathology is causing the nephrotic 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
renal biopsy would clearly tell what type of nephrotic syndrome i.e FSGS ,MGN ,MPGN
CONS
1.Bleeding
2.Infection
3.Inadequate specimen
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