Assignment
Answer all questions
Max Marks: 100 (10 marks for each first seven questions and 30 marks for the last question)
Submit by:
Date: 16/12/2020 9:00 AM
Questions:
Please go through the patient data in the links below and answer the following questions:
1) A 55 year old man with Recurrent Focal Seizures
Detailed patient case report here: http://ushaindurthi.
blogspot.com/2020/11/55-year- old-male-with-complaints-of. html 1. What is the problem representation of this patient and what could be the anatomical site of lesion ?
Ans:Problem Representation:
-c/o weakness in right upper limb,recurrent episodes of seizures .His seizures were sudden in onset, tonic clonic in type ,lasting for 2 minutes with more (8) episodes of focal seizures with a 2 mins of gap between each episode,associated with uprolling of eyes.Late Postictal confusion lasting for 40 minutes.
- An alcoholic since 30 yrs daily whiskey 180ml/day and his last intake was 5 days ago,occasional beedi smoker since 35 yrs.K/c/o Type2 diabetic 5 years back.
?right temporal lobe epileptogenic focus.
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
Ans:subcortical infarcts are caused by occlusion of a Single,penetrating artery ,most commonly from the Circle of Willis. These penetrating arteries arise at sharp angles from major vessels and are thus, anatomically prone to constriction and occlusion.
So subcortical infarcts are more common than cortical infarcts.3. What is the pathogenesis involved in cerebral infarct related seizures?
4. What is your take on the ecg? And do you agree with the treating team on starting the patient on Enoxaparin?
Ans:ST depressions noted in leads V1 to V6 NSTEMI.
Yes , I agree as it has better efficacy and improves clinical outcome in clinical trials of people with NSTEMI.
5. Which AED would you prefer?
If so why?
Please provide studies on efficacies of each of the treatment given to this patient.
Ans:
As it is focal seizure i would prefer carbamazepine And lorazepam / diazepam to prevent the conversion of focal seizure to GTCS
Antiepileptics https://pubmed.ncbi.nlm.nih.gov/28661008/
Question 2) 55 year old man with Recurrent hypoglycemia
Questions:
1. What is the problem representation for this patient?
Ans:A 55 year old male with T2DM & HTN since 10 years c/o exertional dyspnea and cough since 3 days and sudden onset giddiness and profuse sweating secondary to OHA induced hypoglycemia.2. What is the cause for his recurrent hypoglycemia? And how would you evaluate?
Ans:Drug induced hypoglycemia.
He is using glimiperide which increases the secretions of insulin
3. What is the cause for his Dyspnea? What is the reason for his albumin loss?
Ans:Increased anaerobic pathway due to accumulation lactic acid and obesity is the cause for dyspnea.
-Prolonged hypoglycemia state lead to breakdown of protein,so it may have decreased albumin in the body.
4. What is the pathogenesis involved 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.
Ans: yes,I agree with the treating team starting with as the patient improved.
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?
B.
75 year old woman with post operative hepatitis following blood transfusion
Case details here: https://
bandaru17jyothsna.blogspot. com/2020/11/this-is-online-e- log-book-to-discuss.html 1.What are your differentials for this patient and how would you evaluate?
Ans:Post transfusion delayed hemolytic reactionDifferentials:-Transfusion related acute hepatic injury (TRAHI)-Post transfusion hepatitis-Ischemic hepatitisEvaluation:ABO and Rh compatability
coombs testing
antibody panel testing2. What would be your treatment approach? Do you agree with the treatment provided by the treating team and why? What are their efficacies?
Ans:Symptomatic management
I agree with the treatment provided by the treating teamLasix & Nebulization : For wheezing and creptsLactulose : To prevent hepatic encephalopathy https://pubmed.ncbi.nlm.nih.gov/27089005/Zofer : For vomitingsPantop : To prevent gastritis4) 60 year woman with Uncontrolled sugars4) 60 year woman with Uncontrolled sugars
http://manojkumar1008.
blogspot.com/2020/12/60-yr- old-female-with-uncontrolled. html 1. What is the problem representation of this patient?
A 60 year old female with T2DM & HTN since 2 years c/o pricking type of chest pain since 4 days ---uncontrolled sugars secondary to ? right upper lobe pneumonic consolidation with sepsis
2. What are the factors contributing to her uncontrolled blood sugars?
3. What are the chest xray findings?
Plain radiograph of chest in PA view showing-Trachea shifted towards right
-Hyperdense area noted in the right upper lobe(consolidation)4. What do you think is the cause for her hypoalbuminaemia? How would you approach it?
Ans-Inflammation (acute phase reactant)-Malnutrition-Albuminuria-Approach to hypoalbuminemia5. Comment on the treatment given along with each of their efficacies with supportive evidence.
- Piptaz & clarithromycin : for his right upper lobe pneumonic consolidation and sepsis
- Egg white & protien powder : for hypoalbuminemia
- Lactulose : for constipation
- Actrapid / Mixtard : for hyperglycemia
- Tramadol : for pain management
- Pantop : to prevent gastritis
- Zofer : to prevent vomitings
5) 56 year old man with Decompensated liver disease
Case report here: https://appalaaishwaryareddy.
blogspot.com/2020/11/56year- old-male-with-decompensated. html 1. What is the anatomical and pathological localization of the problem?
Liver : Chronic liver disease (cirrhosis) secondary to HBVKidney : AKI on CKD (Hepatorenal syndrome) , HyperkalemiaGI : GAVE , portal hypertensive gastropathyLung : pneumonia , pleural effusion2. How do you approach and evaluate this patient with Hepatitis B?
3. What is the pathogenesis of the illness due to Hepatitis B?
4. Is it necessary to have a separate haemodialysis set up for hepatits B patients and why?
Ans-
Yes , separate machines must be used for patients known to be infected with HBV (or at high risk of new HBV infection). A machine that has been used for patients infected with HBV can be used again for non-infected patients only after it has been decontaminated using a regime deemed effective against HBV because of increased risk of transmission due to contamination.
5. What are the efficacies of each treatment given to this patient? Describe the efficacies with supportive RCT evidence.
- Lactulose : for prevention and treatment of hepatic encephalopathy. https://pubmed.ncbi.nlm.nih.gov/27089005/
- Tenofovir : for HBV
- Lasix : for fluid overload (AKI on CKD) https://www.ncbi.nlm.nih.gov/books/NBK499921/#:~:text=The%20Food%20and%20Drug%20Administration,failure%20including%20the%20nephrotic%20syndrome.
- Vitamin -k : for ? Deranged coagulation profile (PT , INR & APTT reports not available)
- Pantop : for gastritis
- Zofer : to prevent vomitings
- Monocef (ceftriaxone) : for AKI (? renal)
6) 58 year old man with Dementia
Case report details: http://
jabeenahmed300.blogspot.com/ 2020/12/this-is-online-e-log- book-to-discuss.html 1. What is the problem representation of this patient?
58/M weaver by occupation with1) 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.2)He has delayed response to commands.Dysphagia to both solids and liquids since 10 days.3)Urinary urge incontinence since 6 months.4)Forgetfulness since 3 months.He has delayed response to commands.Dysphagia to both solids and liquids since 10 days.K/c/o 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?
3. Do you think his dementia could be explained by chronic infarcts?
4. What is the likely pathogenesis of this patient's dementia?
Post stroke dementiapost-stroke dementia may be the direct consequence of vascular lesions in the brain
- post-stroke dementia could be the result of pre-existing neuropathological effects AD's related
- recurrent stroke that is cause by vessel damages and by white matter lesions that may lead to cognitive decline and contribute to post-stroke dementia;
One of the mechanism involved in ischemic VaD is under the control of large vessels disease (atherosclerosis, and other arteriopathies), however, impaired cerebral flow in the absence of infarct as consequence of arterial stenosis has been documented, although its clinical consequences remain to be fully investigated. It is also unclear whether and to what degree large vessel disease contributes to the white matter pathology and lacunes associated with the subcortical type of VaD. Statistical association suggests it may have additive effects to small vessel pathology.
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?
PHARMACOLOGIC:Cholinesterase inhibitors:DonepezilRivastigmineGalantamineNMDA antagonist:MemantineNON PHARMACOLOGIC:Counselling the patient and care giversGeriatric careCognitive / emotion oriented interventionsSensory stimulation interventionsBehaviour management techniques7) 22 year old man with seizures
Case report here http://geethagugloth.
blogspot.com/2020/12/a-22- year-old-with-seizures.html 1. What is the problem representation of this patient ? What is the anatomic and pathologic localization in view of the clinical and radiological findings?
22 /M delivery boy by occupation with1) involuntary stiffness of both upper and lower limbs2) Headache3) involuntary weight loss in past 6 months4) Chronic alcoholic and tobacco chewerBrain - multiple ring enhancing lesions in right cerebellum ? TuberculomaRVD positive2. What the your differentials to his ring enhancing lesions?
3. What is "immune reconstitution inflammatory syndrome IRIS and how was this patient's treatment modified to avoid the possibility of his developing it?
Ans-A paradoxical clinical worsening of a known condition or the appearance of a new condition after initiating anti retroviral therapy (ART) therapy in HIV-infected patients resulting from restored immunity to specific infectious or non-infectious antigens is defined as immune reconstitution inflammatory syndrome (IRIS).As his CD4 count is > 50 /mm3 consider delayed initiation of ART ideally after 8 weeks of starting ATT to reduce the chances of developing IRIS8) Please mention your individual learning experiences from this month.
-Transfusion reactions
-Importance of detailed history taking events wise.- Antihypertensives and antidiabetic drugs commonly used in clinical settings and their dosages.-counselling a RVD+ patient.-ECG Interpretation.-LFT Interpretation-Managing uncontrolled sugars conditioned patient-have seen IgG related disease case.-how to manage a patient in seizure.
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