NOVEMBER BIMONTHLY EXAM

 

CASE 1

Question 1) pain in the epigastric region differentials

Gastric ulcers

Inferior wall MI

Acute pancreatitis (Boaring kind of pain)

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

Treatment

1) Antibiotics

 imipenem, ciprofloxacin, ofloxacin, ceftriaxone, cefotaxime, ceftizoxime, cefotiam, piperacillin, mezlozillin, metronidazole and tazobactam were detected in pancreatic tissue at concentrations exceeding the MICs of most of the relevant bacteria

A first controlled clinical study with prophylactic imipenem in patients with severe acute pancreatitis showed a reduction in the rate of sepsis

https://www.karger.com/Article/PDF/172465#:~:text=According%20to%20efficacy%20factor%20analysis,in%20the%20rate%20of%20sepsis.

2)analgesics for pain

3)diuretics for decreased urine output due to renal failure

4) Fluid replacement.

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 ( prevent aspiration of bile fluid) 

CASE 2

1)bone marrow and bones

2)kidneys

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.

A) pharmacological interventions

Antibiotics

Antibiotic prophylaxis for a finite duration can decrease the overall incidence of infection within the first 3 months following diagnosis. This does not lead to a decrease in mortality. Further data on antibiotic resistance patterns, toxicity, healthcare expenditures, and the impact of antibiotics on subsequent therapies can assist providers in helping make decisions on prophylactic antibiotics with their patients.

Blood transfusion in severe casses

B)non pharmacological

Pleural fluid analysis

Imaging -xray skull, hrct chest

Serum electrophoresis,sputum culture

CASE 3

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.

CASE 4

1)heart(rt and left)

Mention has been made of the coexistence

of beriberi with other organic types of heart

disease. In a patient with heart failure of

known etiology, particularly when there is a

history or evidence of an inadequate diet,

when signs and symptoms of failure fail to re-

spond to the usual therapeutic regime, an

additional factor of thiamine deficiency should

be strongly considered.

www.ahajournals.org › doi › pdf

Beriberi Heart Disease - AHA Journals

pharmacological interventions

Diuretics

Thiamine

Specific therapy for beriberi heart disease

consists in the administration of thiamine

chloride. Milder cases require 10 to 30 mg.

3 times a day, whereas the more severe cases

may require 100 mg. thrice daily. Intrave￾nous or subcutaneous administration should

be used when associated gastrointestinal or

liver disorders may interfere with the ab￾sorption of thiamine. In markedly edematous

or severely dyspneic patients digitalis, oxy￾gen, salt restriction, and diuretics should be

used. As Blankenhorn and co-workers9 have

pointed out, there is considerable doubt re￾garding the dictum that digitalis is without

value and that if the heart responds well to

this drug the diagnosis of beriberi is elimin￾ated. In the acutely ill patient, therapy

should be immediate and no time should be

lost with diagnostic studies or test thiamine￾deficient diets, since some patients may

2)non pharmacological interventions

Salt and fluid restriction