bimonthly assessment

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

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. 

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?  

 ANSWER :

 

1) pain in the epigastric region differentials

a.Inferior wall MI(normal ecg and echo)

Acute pancreatitis(radiation to the back)-usg finding and elevated serum amylase level

b.perforated peptic ulcer 

This occurs at the level of the sphincter of Oddi, a round muscle located at the opening of the bile duct into the small intestine. If a stone from the gallbladder should travel down the common bile duct and get stuck at the sphincter, it blocks outflow of all material from the liver and pancreas. This results in inflammation of the pancreas that can be quite severe.

2)sob- acidosis due to renal failure

         ? Ards secondary to sepsis/pancreatitis

          Pleural effusion due to acute pancreatitis

3)decreased urine output-pre renal Aki secondary to volume loss(oliguric)

3rd space loss due to pancreatitis

Sepsis induced aki

4) abdominal distention with constipation and nausea

Secondary to paralytic ileus

CHARTING OF SEQUENCING OF EVENTS : 

       

2) pharmacological interventions

1.fluid replacement

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

4. nebulization in view of b/l wheeze secondary to ?copd

5.diuretics for decreased urine output due to renal failure

Non pharmacological interventions

1.nill per mouth

2.ryles tube catheterisation

3.oxygenation

QUESTION

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. 

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?    

ANSWER:

1.bone marrow and bones

2.kidneys

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)

Researchers have found that patients with 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.

A) pharmacological interventions

Antibiotics (?aytpical pneumonia-azithromycin)

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

Blood transfusion

B)non pharmacological

Pleural fluid analysis

Imaging -xray skull, hrct chest

Serum electrophoresis,sputum culture  

QUESTION 

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. 

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? 

 

ANSWER:

1)pedal edema with abdominal distention with sob suggestive of right heart failure or renal failure

B)etilogy of rt heart failure

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. 

2 )Pharmacological interventions 

Preload reducers

Diuretics

Afterload reducers-ace inhibitors

Rate controlling agents-beta blockers

Antiepileptics for known case of epilepsy

Insulin for glycemic control in diabetes.

Non pharmacological interventions

1.Salt and fluid restriction

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) 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. 

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? 

 

 ANSWER :

1)heart(rt and left)

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.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 CHF

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 leads to a loss of vitamin B1.

1) pharmacological interventions

Diuretics

Thiamine

2)non pharmacological interventions

Salt and fluid restriction