BIMONTHLY EXAM FOR THE MONTH OF DECEMBER 2020
Questions:1) A 55 year old man with Recurrent Focal Seizures
Detailed patient case report here:
1. What is the problem representation of this patient and what could be the anatomical site of lesion ?
A:
A 55 year old male maestri(who builds houses)with Type 2 Diabetes Mellitus who is a chronic alcoholic & smoker came with c/o weakness of right upper limb with involuntary movements of both right upper limb and lower limb.
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
A: Subcortical infarcts are caused because of the minute branches of main arteries supplying the subcortex rather than cortical area which is supplied by major artery
3. What is the pathogenesis involved in cerebral infarct related seizures?
A: Infarct causes hypoxia which causes imbalanced electrical activity in the brain which leads to seizures.
4. What is your take on the ecg? And do you agree with the treating team on starting the patient on Enoxaparin?
A: ECG: There is RBBB with LEFT AXIS DEVIATION seen in the Ecg.
Sinus tachycardia noted in the intital Ecg.
Poor R wave progression can be seen.
Yes I agree with the treating team on starting the patient on Enoxaparin.
Because Enoxoparin is given post stroke to prevent the emboli from travelling to the heart or lungs and thus helps in preventing cardiac arrest or pulmonary embolism.
5. Which AED would you prefer?
A: I would prefer carbamazepine.
If so why?
Because it is drug of choice for focal seizures.
Carbamazepine and phenytoin are drugs of choice in initial monotherapy for adult partial and secondarily generalized tonic-clonic seizures. These designations reflect the results of the Veterans Administration Epilepsy Cooperative Study Group of 1985. An earlier comparative study of carbamazepine and phenytoin by Ramsay and associates found both drugs equally effective in controlling new-onset seizures. Among the advantages of carbamazepine is that it causes relatively few cognitive and dysmorphic side effects. Its disadvantages are its unavailability in parenteral formulation and its metabolic autoinduction. The latter must be compensated for by planned dosage increases to maintain therapeutic plasma steady-state levels during the first 2 or 3 months of treatment.
Question 2) 55 year old man with Recurrent hypoglycemia
1. What is the problem representation for this patient?
A: A 55 year old male with Type 2 Diabetes mellitus with c/o dyspnea on exertion and cough since 3 days and sudden onset of giddiness and profuse sweating secondary to Oral hypoglycemic agents induced hypoglycemia.
2. What is the cause for his recurrent hypoglycemia? And how would you evaluate?
A: The oral hypoglycemic agent (glimiperide ) isn't getting excreted due to decreased functioning of the kidney. Hence it's prolonged effect is causing recurrent hypoglycemia.
Evaluation
3. What is the cause for his Dyspnea? What is the reason for his albumin loss?
A: There seems to be presence of haziness in the lung fields in the chest xray of the patient which might be consolidation due to any respiratory Infection and thus the patient might be feeling dyspnoeic. And also the chest xray shows cardiomegaly which might also be a factor for his SOB.
4. What is the pathogenesis involved in hypoglycemia ?
A: The hormone insulin lowers blood sugar levels when blood sugar is too high. If you have type 1 or type 2 diabetes and need insulin to control your blood sugar, taking more insulin than you need can cause your blood sugar level to drop too low and result in hypoglycemia.
5. Do you agree with the treating team on starting the patient on antibiotics? And why? Mention the efficacies for the treatment given.
A: Yes i agree with the treating team starting the patient on antibiotics as his renal parameters are deranged. So it might help the recovery of the kidney.
Question 3)A
41 year old man with Polyarthralgia
Case details here: https://mahathireddybandari.blogspot.com/2020/11/41m-with-chest-pain-and-joint-pains.html?m=1
1. How would you evaluate further this patient with Polyarthralgia?
2. What is the pathogenesis involved in RA?
3. What are the treatment regimens for a patient with RA and their efficacies?
A: Pharmacological Strategies
NSAIDs
Corticosteroids
Methotrexate
Hydroxychloroquine
Sulfasalazine
Leflunomide
Tumor Necrosis Factor Inhibitors— etanercept, adalimumab , and infliximab
T-cell Costimulatory Blocking Agents—abatacept
B cell Depleting Agents—rituximab
Interleukin-1 Receptor Antagonist Therapy—anakinra
Other Immunomodulatory and Cytotoxic agents— azathioprine , cyclophosphamide and cyclosporine A
Reduction of joint stress
Surgical approaches
Synovectomy is sometimes appropriate for patients with rheumatoid arthritis, though in many patients the relief is only transient.
Question 3)B
75 year old woman with post operative hepatitis following blood transfusion
Case details here:
1.What are your differentials for this patient and how would you evaluate?
A: Post transfusion hemolytic reaction
Evaluation by following..
ABO and Rh compatability
coombs testing
-Post transfusion hepatitis
2. What would be your treatment approach? Do you agree with the treatment provided by the treating team and why? What are their efficacies?
A: Yes i agree with the treatment provided by the treating team
Lasix & Nebulization : For wheezing and crepts
Lactulose : for liver problems
Zofer : to control nausea and vomitings
Pantop : To prevent gastric irritation.
Question 4) 60 year woman with Uncontrolled sugars
1. What is the problem representation of this patient?
A: A 60 year old female with Type 2 Diabetes Mellitus with c/o pricking type of chest pain since 4 days and uncontrolled sugars secondary to ? right upper lobe pneumonic consolidation with sepsis
2. What are the factors contributing to her uncontrolled blood sugars?
A: Too much food, such as a meal or snack with more carbohydrates than usual.
Not being active.
Not enough insulin or oral diabetes medications.
Side effects from other medications, such as steroids or antipsychotic medications.
3. What are the chest xray findings?
A: Trachea shifted towards right
Consolidation is seen in the right upper lobe.
4. What do you think is the cause for her hypoalbuminaemia? How would you approach it?
A: cause :
Malnutrition
Protein loss from urine
Less protein diet
Approach:
5. Comment on the treatment given along with each of their efficacies with supportive evidence.
A: Piptaz & clarithromycin : antibiotics for consolidation
Egg white & protien powder : To replenish protein
Lactulose : to relieve constipation
Actrapid (HAI): to control hyperglycemia
Tramadol : to relieve her pain
Pantop : to prevent gastritis
Zofer : to prevent nausea and vomitings
Question 5) 56 year old man with Decompensated liver disease
Case report here:
1. What is the anatomical and pathological localization of the problem?
A:56 year old male who is a known case of CLD and hepatitis B postive presented with the complaints of abdominal distension since 3months with yellowish discoloration of eyes since 3months and shortness of breath since 2days
Localization of the problem
known case of liver disease with hepatitis B positive with pancytopenia
Kidney injury - With Elevated Serum creatinine and blood urea and refractory hyperkalemia
His ABG shows Metabolic Acidosis
LUNGS - pleural effusion in right side
2. How do you approach and evaluate this patient with Hepatitis B?
A: by evaluating serum hep b antigen and serum markers
3. What is the pathogenesis of the illness due to Hepatitis B?
A:The pathogenesis and clinical manifestations of hepatitis B are due to the interaction of the virus and the host immune system, which leads to liver injury and, potentially, cirrhosis and hepatocellular carcinoma. Patients can have either an acute symptomatic disease or an asymptomatic disease.
4. Is it necessary to have a separate haemodialysis set up for hepatits B patients and why?
A: Not necessarily , because the dialysis machines are well disinfected after every dialysis and it's tubes are also disposable ,so chances of spreading virus through hemodialysis machine are nil to very minimal .. Hence my answer is no
5. What are the efficacies of each treatment given to this patient? Describe the efficacies with supportive RCT evidence.
A:
In the last years, marked progress has been made in the treatment of chronic hepatitis B. The efficacy of lamivudine, the first nucleoside analogue available, is limited by the high incidence of resistance. Adefovir, which was recently approved has a comparable efficacy with a very low frequency of resistance. However, adefovir needs to be indefinitely administered as withdrawal of therapy is generally associated with reactivation and sustained response is uncommon. Recent large randomized controlled trials showed that PEG IFNs induce relatively high sustained response rates both in HBeAg positive and HBeAg negative chronic hepatitis B. So far, the combination of PEG IFN with lamivudine, used simultaneously, is disappointing in terms of short-term efficacy. However, long-term efficacy needs to be assessed and different schedules of combination (for example sequential) need to be evaluated. A number of nucleoside analogues, with favourable toxicity profiles and a promise of increased effectiveness against HBV, are at various stages of clinical development. Results of phase III trials of entecavir and emtricitabine confirmed their efficacy. However, while entecavir is associated with a low incidences of resistance, emtricitabine is associated with a relatively high incidence of resistance which limits its use as a monotherapy. The efficacy and safety of new and more potent drugs like telbivudine and clevudine need to be confirmed. The future of chronic hepatitis B therapy seems to be in the combination of different drugs. Ideally, the optimal drugs to combine would meet the following criteria: they should have different sites of action on HBV DNA replication, a potent antiviral effect, an excellent safety profile and they should induce a sustained response with a limited duration of therapy. Indeed, the concept of combination therapy has been recently developed in order to increase efficacy and to decrease the occurrence of viral resistance. However, so far few combinations have been evaluated. No combination therapy demonstrated a benefit as compared with monotherapy. More potent drugs and new combinations together with the understanding of the mechanisms of resistance to therapy are important challenges to improve the efficacy of treatment and decrease in the future the global burden related to chronic hepatitis B.
Question 6) 58 year old man with Dementia
1. What is the problem representation of this patient?
A: A 58 year old weaver by occupation, alcoholic 20.years back with c/o slurring of speech , deviation of mouth to right side associated with drooling of saliva , food particles and water predominantly from left angle of mouth and smacking of lips since 6 months.
Urinary urge incontinence since 6 months.
Forgetfulness since 3 months.
He has delayed response to commands.
Dysphagia to both solids and liquids since 10 days.
Diagnosed with CVA 3 years back and now he was diagnosed as neuro degenerative disease - Alzheimer's
2. How would you evaluate further this patient with Dementia?
A:
3. Do you think his dementia could be explained by chronic infarcts?
A: Multiinfarct dementia(MID)is caused by a series of small strokes. A stroke, or infarct, is the interruption or blockage of blood flow to any part of the brain. The term “multi-infarct” means many strokes and many areas of damage. If blood flow is stopped for more than a few seconds, brain cells can die from a lack of oxygen. This damage is usually permanent.
A stroke can be silent, which means it affects such a small area of the brain that it goes unnoticed. Over time, many silent strokes can lead to MID. Large strokes that cause noticeable physical and neurological symptoms can also lead to MID.
4. What is the likely pathogenesis of this patient's dementia?
A:
5. Are you aware of pharmacological and non pharmacological interventions to treat such a patient and what are their known efficacies based on RCT evidence?
A: PHARMACOLOGIC:
Cholinesterase inhibitors:
Donepezil
Efficacy of starting of donezepil in early stage Alzheimer's to improve cognitive function.
Rivastigmine
Galantamine
NON PHARMACOLOGIC:
Counselling the patient and care givers
Geriatric care
Question 7) 22 year old man with seizures
Case report here
1. What is the problem representation of this patient ? What is the anatomic and pathologic localization in view of the clinical and radiological findings?
A: A 22 year old delivery boy chronic alcoholic and tobacco chewer with c/o on & off fever since 1 year , involuntary weight loss since 6 months , headache since 2 months , 4 - 5 episodes of involuntary stiffening of both Upperlimb & Lowerlimb with 5 mins of LOC one week before the day of admission.
Brain - multiple ring enhancing lesions in right cerebellum
? Tuberculoma
2. What the your differentials to his ring enhancing lesions?
A: HIV/AIDS
toxoplasmosis
fungal infections such as cryptococcosis or histoplasmosis
primary brain tumors
metastases
brain abscesses
granulomas
resolving hematomas
infarcts
3. What is "immune reconstitution inflammatory syndrome IRIS and how was this patient's treatment modified to avoid the possibility of his developing it?
A: Immune reconstitution inflammatory syndrome (IRIS) describes a collection of inflammatory disorders associated with paradoxical worsening of preexisting infectious processes following the initiation of antiretroviral therapy (ART) in HIV-infected individuals
Awaiting for CD4 count to modify treatment.
8) Please mention your individual learning experiences from this month.
-One day while attending rounds,I have learnt a very interesting and important point that oral hypoglycemic drugs should not be given to a diabetic pt who has renal failure or improper renal function. As the drug won't get excreted, the pt will suffer from hypoglycemia(which is due to prolonged effect of the OHA).
-Also learnt that nor-adrenaline infusion shouldn't be stopped at a time, it should be slowly tapered, else the pt will get collapsed.
-I have learnt ECG basics .Able to identify bundle blocks and st elevations , R wave progression etc
-I have learnt how to diagnose a pt with DKA and also it's management.
-I have learnt that the drugs should be prescribed based on their efficacies in the treatment .
-I have seen many hypertensive patients and their management .
-I have seen heart failure cases and the approach to them.
-I have seen pateints with seizures and the treatment which we give to them.
-I have seen patients with stroke(CVA) , assisted in examining the pts.
-I have tried to identify infarcts in the radiological films.
-I have seen that the resting tremors of parkinsonism can be stopped for a small period of time by deliberately moving the body part.
- I have learnt to read and assess ABG report.
-I have studied abt aphasias especially broca's and wernickie and how the pt will present to the hospital.
-learnt adjustment of Insulin doses according to GRBS levels.
-I gave HAI subcutaneously to a patient.
-Perfomed CPR.
-I have seen a patient with recurrent episodes of seizures and the seizures weren't getting subsided by mutiple doses of antiepileptic drugs and so learnt that the end choice was to intubate the pt and to put on a ventilator for a period of time.
- I have seen 2d echo perfomed on patients and tried to learn the assessment of ventricular contractility and valvular function.
- I have seen endoscopic view of upper GIT in the gastroenterology superspeciality.
-Have studied Neuroanatomy a little.
-I have auscultated and got to know the difference between crepts and wheeze.
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