BI- WEEKLY

 1) pain in the epigastric region differentials

Inferior wall MI(normal ecg and echo)

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

Perforated peptic ulcer 

Causes of acute pancreatitis-harrison pg no 2348


Gall stones :https://gi.org/topics/gallstone-pancreatitis/

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



2) pharmacological interventions

https://link.springer.com/article/10.1007/s00534-005-1050-8

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

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

2)ryles tube catheterisation

3)oxygenation



Question 2:(55M)

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

1)bone marrow and bones


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

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)

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

Blood transfusion


B)non pharmacological

Pleural fluid analysis

Imaging -xray skull, hrct chest

Serum electrophoresis,sputum culture



Question 3)

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

1)pedal edema with abdominal distention with 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. 

2 )Pharmacological interventions

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

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

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

1)heart(rt and left)

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

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.

https://www.medindia.net/patients/patientinfo/beriberi-disease.htm

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



Comments

Post a Comment

Popular posts from this blog

PRE FINAL PRACTICAL (45 year old male with giddiness) LONG CASE

Image
Presenting complaints :  45 year old male who is a resident of Narketpalli driver by occupation , came to the casuality who studied till degree came with complaints  of : Giddiness since yesterday afternoon    vomiting’s 4 episodes  since afternoon  shivering since afternoon which lasted till he was brought to the hospital subsided on medication .  HOPI & PAST HISTORY :  He’s the last child in his family . Mother and father expired at 20 years    , mother expired because of paralysis . Father expired because of ? Renal issues .  Marriage : consanguinity ( first degree ) at 20 years survived with 2 kids (2sons ) one son is intern completed and other is working in hyd in a laboratory.  20 years back he worked in an pharmacy for 3-4 years , then he owned his own auto and drove for 3-4 years , later he brought his car gave it for trips ,and he worked    a private driver , and also used to drive hens to chicken shop , He’s an night driver , he used to leave home at 7:30 pm and come bac
Read more

MARCH EXAM

  Internal assesment to the questions asked in the above blog spot. 1) Please go through the patient data in the links below and answer the following questions: https://ashakiran923.blogspot.com/2021/03/60-years-old-male-fever-under-evaluation.html?m=1 a). What is the problem representation of this patient and what is the anatomical localization for his current problem based on the clinical findings?How specific is his dilated superficial Abdominal vein in making diagnosis? Abdominal distension with clinical Image of umbilicus everted : Ascitis  Decreased urine output with burning micturition : renal pathology But is GI pathology causing renal or renal causing git or is that both are independent entities is we are not sure off. b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? What is the cause of his hypoalbuminemia?Why is the SAAG low? Etiology : GIT ascitis pathology would be known by doing SAAG and his pain abdo
Read more

Jan 2021 Bi-weekly exam

Image
  1.26 year old woman with complaints of altered sensorium since day,headache since 8 days,fever and vomitings since 4 days  https://harikachindam7.blogspot.com/2020/12/26-year-old-female-with-complaints-of.html a). What is the problem representation of this patient and what is the anatomical localization for her current problem based on the clinical findings? A 28 year old woman with the complaints of Headache since 8 days Fever since 4 days Vomitings since 4 days Altered sensorium since 1 day 28 year old woman with 1. Hyponatremia secondary to SIADH 2. Tubercular meningitis 3. Acute infarct in the left thalamic region 4. SLE with multiple joint pains  b) What is the etiology of the current problem and how would you as a member of the treating team arrive at a diagnosis? Please chart out the sequence of events timeline between the manifestations of each of her problems and current outcomes.  2. Tubercular meningitis: Patient presenting in altered sensorium with Fever, vomitings, neck
Read more