4.Gastroenterology (& Pulmonology) M.SRI SAI PAVAN ROLL NO :79 8TH SEM

 A.LINK TO PATIENT DETAILS:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

QUESTIONS: 

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology 

H5 years back-1st episode of pain abdomen and vomitings 

Stopped taking alcohol for 3 years

1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 

20 days back increased consumption of toddy intake

Since 1 week pain abdomen and vomiting

Since 4 days fever constipation and burning micturition

Anatomical localisation: Pancreas and left lung

Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

A) * Non pharmacological interventions : drains ( malecot & icd )

* Even i as a treating physician will follow the same approach

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

B) Link to patient details:

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

1) What is causing the patient's dyspnea? How is it related to pancreatitis?

*pleural effusion is cause for patients dyspnea.

*pleural effusion may occur due to  pancreaticopleural fistulae secondary to leak and disruption of pancreatic duct .

2) Name possible reasons why the patient has developed a state of hyperglycemia.

* Hyperglycemia is developed due to abnormalities in insulin secretion , increase in counter regulatory hormone release ,decreased utilization of glucose by peripheral tissue.

Exocrine pancreatic dysfunction impairs the endocrine pancreas.

3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

*

4) What is the line of treatment in this patient?

* iv fluids and colloids to maintain normal intravascular volume.

*Nil orally

*Analgesics for pain relief

*Nasogastric suction -to decrease gastrin release from stomach

* Monitor 

-BP, pulse,blood sugars ,serum amylase, serum lipase ,urine output.

* laparotomy and debridement of hemorrhagic pancreatic tissue.

* antibiotic therapy like ciprofloxacin , ofloxacin, imipenem

C) Link to patient details:

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

1) What is the most probable diagnosis in this patient?

àDifferential Diagnosis: 

·        Ruptured Liver Abscess.

·        Organized collection secondary to Hollow viscous Perforation.

·        Organized Intraperitoneal Hematoma.

·        Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.

·        Grade 3 RPD of right Kidney

àThe most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated. 

  

2) What was the cause of her death?

àAfter leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs. 

3) Does her NSAID abuse have something to do with her condition? How? 

àNSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death