BIMONTHLY TEST NOV.

 Question 1

1) "55 year old male patient  came with the complaints of 

Chest pain since 3 days

Abdominal distension since 3 days

Abdominal pain since 3 days and decreased urine output since 3days and not passed stools since 3days 

https://sreejaboga.blogspot.com/2020/11/is-online-e-log-book-to-discuss-our.html?m=1

Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? 

Q ) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? 

I localise patients problem to Abdomen ( pancreas ) which is involving other organs systems such as KIDNEY and LUNG.

Etiological possibilities: 

1] Gall bladder calculus/ polyps

2) Hypertriglyceridemia. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040532/ )

3) DKA inducing Hypertriglyceridemia causing Acute pancreatitis ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4206354/ )

KIDNEY INVOLVEMENT (AKI) 

May be due to Severe pancreatitis causing AKI ( https://cjasn.asnjournals.org/content/14/7/1106  ) which may be further aggravated by nephrotoxic drugs like Piptaz.

AKI causing Metabolic acidosis with High anion gap other differentials for High anion gap in this Pt may be UREMIA, DKA, Starvation ketoacidosis, PCM intake.

LUNG INVOLVEMENT:

May be due to severe pancreatitis causing plural effusion, secondary infections, ARDS, atelectasis. Pathogenesis is not clear assumed to be due to cytokine mediated injury ( https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4087768/ )

Q ) Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

https://cjasn.asnjournals.org/content/14/7/1106

EXPECTED OUTCOMES AFTER REVIEW OF SOME ARTICLES :

Pt AKI may worsen and land up in CKD.

AKI May resolve ( less likely)

Pancreatitis resolves in due course with current medical management.

a comprehensive, retrospective, observational study utilizing the National Inpatient Sample, Devani et al. reported an overall AKI prevalence of 7.9% among 3,466,493 patients hospitalized with acute pancreatitis (3). The mortality rate among AKI subgroup was significantly higher (8.8% in AKI group versus 0.7% in non-AKI; P<0.01). Prospective studies clearly needed to determine the actual incidence and prognosis of AKI in acute pancreatitis.

The mortality rate of patients with AKI and acute pancreatitis varied between 25% and 75% (5,7). However, Devani et al. found a three-fold fall in mortality rate among patients with AKI over the past decade (3).

https://cjasn.asnjournals.org/content/14/7/1106

NON PHARMACOLOGICAL interventions

1.NBM:

2.Ryles tube:If nutritional support is supplemented by the enteral route, then it is usually delivered by tube feeding. There is a controversy about nasogastric versus nasojejunal feeding. But there is not much evidence to support any one over the other. Though traditionally nasojejunal feedings (to be delivered distal to the ligament of Treitz) have been preferred with the concept of less stimulation of the exocrine pancreas, cholecystokinin (CCK) cells that are present in the distal third part of the duodenum get stimulated when food passing through duodenum. It releases CCK that stimulates the pancreas and increased volume of pancreatic enzymes and bicarbonate secretion. This may worsen the course of the disease. Nasogastric tube feedings have now been shown to as safe as the jejunal feeding. Nasogastric insertion can be at bedside. Fluoroscopy endoscopic (endoscopically placed guide wire) and specialist help is not needed. With the Nasogastric (NG) feeding, the standard precautions of aspiration like elevation of head end of bed should be followed.

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management 

3:Oxygen support:Patients with acute severe pancreatitis should be monitored closely for early detection of failure. Respiratory support usually initiated by supplemental oxygen and mechanical ventilation is often required depending on the severity of respiratory dysfunction. Nasogastric decompression will decrease the distension and improve the compliance and prevent aspiration. Non-invasive ventilation is poorly tolerated in most of the patients because of abdominal distension and reduced functional residual capacity, careful selection of patient is warranted. Non-invasive ventilation is good choice to start with as it may avoid endotracheal intubation. Acute lung injury and Acute respiratory distress syndrome (ARDS) secondary to acute severe pancreatitis is similar to any other condition using lung protective strategies. Pleural effusion may need ultrasound-guided drainage. Good analgesia will help in chest physiotherapy, early physiotherapy will prevent atelectasis and related complications 

PHARMACOLOGICAL interventions

1.Iv fluids:Hypotension is one of the most common presentations with acute pancreatitis. It is a sign of impending organ dysfunction. The hypotension is due to the third space loss secondary to the inflammatory response, this contributes to hypoperfusion and end organ perfusion dysfunction. Aggressive fluid resuscitation and rapid restoration of intravascular volume are the main stay of the treatment. It requires several liters of fluids. Both crystalloids and colloids can be used as resuscitation fluids

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

2.Diuretics:for decreased urine output and renal failure

3.Antibiotics:

Role of antibiotic prophylaxis in severe acute pancreatitis

Prophylactic antibiotics in severe acute pancreatitis have been a topic of debate in the last 4–5 decades. Pancreatic necrosis more than 30% increases the chances of infection. The right choice of antibiotics is very important, those which have high penetration into pancreatic tissue. Carbapenems are both broad spectrum and excellent pancreatic penetration properties. Other antibiotics, which penetrate well in the pancreatic tissue, are cephalosporin, ureidopenicillins, fluoroquinolones, metronidazole and imipenem. Aminoglycosides have a poor penetration ability. Patients with mild pancreatitis do not benefit

from antibiotics. In a meta-analysis by Sharma et al. [16], use of prophylactic antibiotics has shown mortality benefit in patients with Acute necrotizing pancreatitis (ANP) confirmed by contrast-enhanced CT (21–12.3%). Ref. [15, 16] prophylactic antibiotics use has not shown to decrease the need for interventional and surgical management but no effect on mortality.

https://www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

4.ANALGESIA:Pain is one of the symptoms of acute severe pancreatitis. It causes discomfort and heightened sympathetic activity, impairment of oxygenation due to restriction of abdominal wall movement. Effective analgesia can be provided by the use of opioids and parenteral route, i.e. intravenous route is the preferred route. Analgesia may improve pulmonary dysfunction. In the past, morphine was supposed to exacerbate acute pancreatitis by promoting contraction of the sphincter of Oddi and increase pressure in the sphincter of Oddi dysfunction, but there is no good supportive evidence. Another modality of pain management is use of drugs like local anaesthetics through in epidural route 

https//www.intechopen.com/books/intensive-care/severe-acute-pancreatitis-and-its-management

CASE2 

2) A 55 year old male, shepherd by occupation, presented to the OPD with the chief complaints of fever (on and off), loss of appetite, headache, body pains, generalized weakness since 2 months, cough since 2 weeks and vomitings and pain abdomen since 2 days. 

https://aakansharaj.blogspot.com/2020/11/55-year-old-male-with-anemia.html?m=1

a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

1.Pt has Anemia 

2.Acute renal failure

3.lytic bony leisons ,

4.cxr and sputum reports  showing pneumonia.

Anemia with low retic count

Total proteins (12.4 g/dl) 

 albumin (1.84 g/dl)

 high gamma gap

Possible differential : Multiple myeloma

Multiple myeloma is a plasma cell dyscrasia ,where there are clone of plasma cells causing excessive production of immunoglobulins ,but these immunoglobulins are defective hence confer no immunity and these people are prone for more infections .

Multiple myeloma (MM) is a clonal plasma cell proliferative disorder characterized by the abnormal increase of monoclonal paraprotein leading to evidence of specific end-organ damage. 

Anatomical locations of problems and their etiologies:

Image:archith baloor textbook of medicine pg 587

1) Bone marrow - due to marrow infiltration anemia,leucopenia,thrombocytopenia

2)lytic bone lesions pepper pot skull

3)renal failure - Excess monoclonal immunoglobulin can cause hyperviscosity, platelet dysfunction and renal tubular damage, leading respectively to neurologic derangement, bleeding, and renal failure.

excess production of monoclonal light chains (light- chain cast nephropathy), deposition of intact light chains causing nephrotic syndrome, light chain amyloidosis, hypercalcemia, hyperuricemia, dehydration.

These patients can also have bleeding manifestations due to thrombocytopenia and anitbody coated platelets which are defective.

5) Head ache ,paresthesia and blurring of vision- are features of hyper viscosity.

6) Lungs : showing Moderate to gross right pleural effusion and  Multilobar consolidations of the right lung, involving upper and middle lobes  With Passive collapse of basal segments of right lower lobe .

Pneumonia is because of immunodeficiency state ,as the immunoglobulins produced are defective.

Pleural fluid analysis showing exudative picture suggesting parapneumonic effusion.

SEQUENCE OF EVENTS

OUTCOMES

Median survival for newly diagnosed MM is about 44.8 months . MM cannot be cured , but new drugs are available to manage patients with MM.

https://www.hindawi.com/journals/bmri/2016/6848902/

CASE 3

3) 51 Year old man with complaints of B/L pitting pedal edema from 5 to 6months,abdominal distension from 2 to 3 days,SOB from 3days.

nithishaavula.blogspot.com/2020/11/51-yr-old-male-with-hfref.html?m=1

a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

1.Diabetes and hypertension causing macrovasuclar and microvascular dysfunction

2.Heart failure with reduced ejection fraction

LVF due to hypertension

Leading to PAH

PAH causing right heart failure

3.Atrial fibrillation :heart failure ,diabetic and hypertension are also risk factors for AF.

4) Due to AF - there is formation and dislodgement of thrombus , leading to stroke in this patient.

5.seizures in this patient is again due to stroke .

(Infarct in right frontal lobe ).

SEQUENCE OF EVENTS

b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them? 

Preload reducing agents - Diuretics (only if symptomatic)

Afterload reducing agents - vaso dilators ,ace inhibitors and arb 

Beta blockers for preventing cardiac remodeling and reduce mortality.

https://pmj.bmj.com/content/79/937/634

Antiepileptics ( known case of epilepsy)

Insulin for glycemic control in diabetes.

Non pharmacological interventions

Salt and fluid restriction

https://pubmed.ncbi.nlm.nih.gov/23787719/

Individualized salt and fluid restriction can improve signs and symptoms of CHF 

 

Case 4

31 yr old man with B/L pedal edema with scrotal and penile swelling since 2 months

https://nairaditya97.blogspot.com/2020/11/31-yr-old-male-with-bl-pedal-edema-with.html?m=1

a) Where are the different anatomical locations of the patient's problems and what are the different etiologic possibilities for them? Please chart out the sequence of events timeline between the manifestations of each of these problems and current outcomes. 

1.Patient is a chronic alcoholic which causes wet beri beri(heart failure due to thiamine deficiency)

2.peripheral neuropathy due to thiamine deficiency

Wet beriberi is one of the clinical syndromes associated with thiamine deficiency. Thiamine, in its phosphorylated form thiamine pyrophosphate (TPP), is the precursor for the cofactor of both pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, which are both key enzymes of the Krebs cycle. The Krebs cycle is an essential part of aerobic glucose metabolism. A decrease in the activity of these 2 enzymes due to thiamine deficiency may lead to the tissue accumulation of pyruvate and lactate.[1] Moreover, the accumulation of pyruvate and lactate decreases peripheral resistance and increases venous blood flow, increasing the cardiac preload. Increased preload and myocardial dysfunction ultimately leads to congestive heart failure.[2,3] Wet beriberi mainly triggers right heart failure.[4–6] The moderate pulmonary hypertension is common for wet beriberi patient.[3,4,7

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5851725/

SEQUENCE OF EVENTS 

b) What are the pharmacological and non pharmacological interventions used in the management of this patient and what are the efficacy of each one of them? 

Thiamine 

Pantoprozole.

Lasix

Salt restriction

Fluid restriction