Bimonthly internal assesment

BIMONTHLY INTERNAL ASSESSMENT FOR MONTH OF  NOVEMBER

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 3 days



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. 

Pain in the epigastric region:

Cardiac : Inferion wall MI

Biliary: cholecystitis, cholangitis

              Pancreatitis

Vascular :abdominal aortic aneurysm

GI :gastritis,  early appendicitis


    2)  Decreased urine output-pre renal Aki secondary to volume loss(oliguric)

3rd space loss due to pancreatitis

Sepsis induced aki

3)abdominal distention with constipation and nausea secondary to paralytic ileus

4) sob may be due to metabolic acidosis or  lung involvement as pt is chronic smoker (? Copd) 

https://photos.app.goo.gl/jDcfft4XgUU9x5Aq8

Outcomes:

1)Pancreatis may resolve or may even leads to chronic changes or may also leads to morbidity


2) AKI (resolve/ or land in CKD) 

In this patient earlier his kidneys shows normal echotecture but further usg scan shows RPD changes and landed in MHD

3) sepsis has been controlled with antibiotics



. 





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? 




https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886461/



A)Fluid management for 3 rd space fluid loss due to pancreatitis and hypotension

Increased vascular permeability in acute pancreatitis causes the loss of intravenous fluid and reduces plasma volume. In severe cases, in patients with massive ascites, pleural effusion, and retroperitoneal and mesenteric edema, circulating plasma volume decreases markedly. Hypovolemia may lead to shock and acute renal failure, and, because hypovolemic shock may impair the pancreatic microcirculation and promote pancreatic ischemia and necrosis, restoration and maintenance of plasma volume is crucial in severe acute pancreatitis.

2) antibiotics

On the other hand, a placebo-controlled, double-blind trial of ciprofloxacin  +  metronidazole in patients with predicted severe acute pancreatitis showed that prophylactic administration of these antibiotics did not prevent pancreatic infection (Level 1b).

3)analgesics inj tremadol to relieve pain abdomen) 

4) nebulization in view of b/l wheeze

5)diuretics for decreased urine output due to renal failure


Non pharmacological interventions

1)nill per mouth

https://pubmed.ncbi.nlm.nih.gov/27107634/

2)ryles tube catheterisation: to prevent the further inflammation of pancreas

3)oxygenation :As  pt is in acidotic breathing and to maintain the saturation 



Question 2:

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

1)bone marrow and bones : hypercellilar marror and pancytopenia

2)kidneys : proteinuria

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3205153/

The pathophysiology of renal failure in multiple myeloma is often multifactorial but is mostly due to the high excretion of immunoglobulin free light chains. When the light chains combine with Tamm-Horsfall proteins, they form obstructing casts (5). Chemotherapy should therefore be initiated rapidly to decrease light chain production. Intravenous fluids can be given to treat volume depletion, hypercalcemia, or hyperuricemia.

3)lungs(infection-incrsead susceptibility)

https://www.cancer.org/cancer/multiple-myeloma/causes-risks-prevention/what-causes.html

 Plasma cell tumors have important abnormalities in other bone marrow cells and that these abnormalities may also cause excess plasma cell growth. Certain cells in the bone marrow called dendritic cells release a hormone called interleukin-6 (IL-6), which stimulates normal plasma cells to grow. Excessive production of IL-6 by these cells appears to be an important factor in development of plasma cell tumors.

Outcome: Need an oncologist opinion for further management


2) what are pharmacological and non pharmacological interventions given and efficay of each of them? 

A) Pharmacological interventions antibiotics (?aytpical pneumonia-azithromycin)

https://www.intechopen.com/books/update-on-multiple-myeloma/infections-in-patients-with-multiple-myeloma-in-the-era-of-novel-agents-and-stem-cell-therapies

However, the infections encountered in patients with MM include: (1) bacterial infections, predominantly involving respiratory and urinary tract, caused by Streptococcus pneumonia, Staphylococcus aureus, Haemophilus influenzae, Klebsiella pneumonia, Escherichia coli, Pseudomonas aeruginosa, and Enterobacteriaceae; (2) viral infections caused by herpes simplex virus (HSV), VZV, and cytomegalovirus (CMV); (3) fungal infections caused by Candida species and Aspergillus species; and (4) Pneumocystis jiroveci pneumonia

2)Blood transfusion :  I/v/0f pancytopenia


B)non pharmacological

Pleural fluid analysis: Exudative picture 

imaging -xray skull: Lytic lesions

hrct chest: pleural effusion, consolidatiom

Serum electrophoresis

sputum culture : klebsiella species



Question 3)

http://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 ?

https://www.cfrjournal.com/articles/Right-Ventricular-Failure

A) Pedal edema with abdominal distension and sob suggestive of right heart failure or renal failure

B)etilogy of rt heart failure

https://www.ncbi.nlm.nih.gov/books/NBK459381/

chronic conditions of pressure overload may lead to RVF. These include:
  • Primary pulmonary arterial hypertension (PAH) and secondary pulmonary hypertension (PH) as seen in chronic-obstructive pulmonary disease (COPD) or pulmonary fibrosis)
  • Congenital heart disease (pulmonic stenosis, right ventricular outflow tract obstruction, or a systemic RV).
The following conditions result in volume overload causing RVF:
  • Valvular insufficiency (tricuspid or pulmonic) 
  • Congenital heart disease with a shunt (atrial septal defect (ASD) or anomalous pulmonary venous return (APVR)).
Another important mechanism that leads to RVF is intrinsic RV myocardial disease. This includes:
  • RV ischemia or infarct
  • Infiltrative diseases such as amyloidosis or sarcoidosis
  • Arrhythmogenic right ventricular dysplasia (ARVD)
  • Cardiomyopathy
  • Microvascular disease.
Lastly, RVF may be caused by impaired filling which is seen in the following conditions:
  • Constrictive pericarditis
  • Tricuspid stenosis
  • Systemic vasodilatory shock
  • Cardiac tamponade
  • Superior vena cava syndrome
  • Hypovolemia.
Diabetes (since 7 yrs) 
Hypertension( since 5 yrs) 
Chronic infarct and seizures( 3 yrs back) 
AF with HFrEF (since 3 yrs) 
   Hypertension and diabetics are risk for AF
    AF risk factor for thromboembolic events like stroke and MI
These are lines taken from harrison


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? 

A) Pharmacological interventions

https://heart.bmj.com/content/104/5/407(meta analysis with each class of drugs)

Preload reducers

Diuretics should be used only occasionally if pt is symptomatic

 Afterload reducers-ace inhibitors

Rate controlling agents-beta blockers


Antiepileptics for 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 with no negative effects on thirst, appetite, or QoL in patients with moderate to severe CHF and previous signs of fluid retention.


Question 4

4) 31 yr old man with B/L pedal edema with scrotal and penile swelling since 2 months



https://photos.app.goo.gl/5a5TwqsXz7Lvuidy9 



Wet beri beri 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.

https://www.healthline.com/health/beriberi#symptoms

Other conditions cause beriberi include:

  • Excessive alcohol usage, which results in inadequate intake in the diet as well as prevents the body from absorbing and storing vitamin B1.
  • Genetic beriberi, which is an inherited condition where people lose the ability to absorb thiamine from foods. Symptoms usually present during adulthood.
  • Pregnancy; pregnant women often present with vitamin B1 deficiency. Breastfeeding infants can suffer from vitamin B1 deficiency if the mother is deficient.
  • People with endocrine disorders like hyperthyroidism who require extra vitamin B1.
  • Chronic liver disease, which prevents the body from absorbing sufficient vitamin B1.
  • Kidney dialysis, which leads to a loss of vitamin B1.
  • A prolonged bout of diarrhea, which also  to a loss of vitamin 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? 



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

Pharmacological interventions:

Diuretics to decrese the preload

Thiamine to replinish the stores which were lost due to chronic alcoholism

2)non pharmacological interventions

Salt and fluid restriction to decrease the fluid overload





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