General Medicine Internal assessment.
Detailedpatientca report here: http://ushaindurthi.
1. What is the problem representation of this patient and what could be the anatomical site of lesion ?
A 55 year old male construction worker with T2DM who is a chronic alcoholic & smoker came with c/o weakness of right upper limb with involuntary movements of both right UL & LL secondary to ? right temporal lobe epileptogenic focus.
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
subcortical infarcts are caused by occlusion of a penetrating artery from a large cerebral 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.
https://www.ncbi.nlm.nih.gov/books/NBK534206/#:~:text=Lacunar%20syndromes%20are%20clinical%20manifestations,from%20the%20Circle%20of%20Willis.
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?
Ventricular ectopics seen
Left axis deviation +
ST depressions noted in precordial leads V1 to V6
NSTEMI
Yes , i agree with the treating team on starting the patient on Enoxaparin.
https://www.google.co.in/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwia7d_Ci-btAhX4_XMBHaZNAkYQFjACegQIAhAC&url=https%3A%2F%2Fpubmed.ncbi.nlm.nih.gov%2F12644342%2F&usg=AOvVaw1BufP2z_JTKG4a8aLVV9o8
5. Which AED would you prefer?
As it is focal seizure i would prefer carbamazepine
And lorazepam / diazepam to prevent the conversion of focal seizure to GTCS
Please provide studies on efficacies of each of the treatment given to this patient.
Antiepileptics https://pubmed.ncbi.nlm.nih.gov/28661008/
Atorvastatin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036014/
Aspirin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6206448/
Enoxaparin https://www.sciencedirect.com/science/article/pii/S0735109702029017
Patient details in the intern logged online case report here: http://manojkumar1008.
Questions:
1. What is the problem representation for this patient?
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?
3. What is the cause for his Dyspnea? What is the reason for his albumin loss?
DYSPNEA:
Obesity increases the work of breathing because of the reductions in both chest wall compliance and respiratory muscle strength.
Excess metabolically active adipose tissue plus increased workload on supportive respiratory muscle leads to increased CO2 production (hypercapnia) and increased O2 consumption (hypoxia).
Pulmonary function abnormalities resulting from obesity
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.
Yes i agree with the treating team starting antibiotics as his renal parameters are deranged and he may be having AKI (?renal)
CUE / urine cultures / USG abdomen are not available to support it as renal cause of AKI
Spot urine sodium is high may be secondary to ATN
3)
A. 41 year old man with Polyarthralgia
Case details here: https://
1. How would you evaluate further this patient with Polyarthralgia?
2. What is the pathogenesis involved in RA?
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.hopkinsarthritis.org/arthritis-info/rheumatoid-arthritis/ra-pathophysiology-2/&ved=2ahUKEwjI-J_ZrObtAhWF7nMBHYHDCy4QFjAXegQIKRAB&usg=AOvVaw27b8Rt0lo57Q6Rpp6UjASB&cshid=1608803720629
3. What are the treatment regimens for a patient with RA and their efficacies?
Treatment options include medications, reduction of joint stress, physical and occupational therapy, and surgical intervention
Pharmacological Strategies
There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal anti-inflammatory agents (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARDs)
Non-steroidal Anti-inflammatory Agents (NSAIDs)
The major effect of these agents is to reduce acute inflammation thereby decreasing pain and improving function
Newer "second-line" drugs (DMARDs)
75 year old woman with post operative hepatitis following blood transfusion
Case details here: https://
1.What are your differentials for this patient and how would you evaluate?
Post transfusion delayed hemolytic reaction
Evaluation:
ABO and Rh compatability
coombs testing
antibody panel testing
https://www.learnhaem.com/courses/frcpath-transfusion/lessons/antibody-screening-and-identification/topic/antigrams/
-Transfusion related acute hepatic injury (TRAHI)
-Post transfusion hepatitis
-Ischemic 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?
Symptomatic management
4) 60 year woman with Uncontrolled sugars
http://manojkumar1008.
1. What is the problem representation of this patient?
60 year old female with T2DM & HTN since 2 years 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?
3. What are the chest xray findings?
Plain radiograph of chest , frontal view
Trachea shifted towards right
Hyperdense area noted in the right upper lobe
(consolidation)
Peripheral pulmonary vasculature is normal
Heart is central in position
Cardiac size normal
The domes of diaphragm are normal in position and smooth outline
Visualized bones and soft tissue appear normal.
Approach to hypoalbuminemia
5) 56 year old man with Decompensated liver disease
Case report here: https://appalaaishwaryareddy.
1. What is the anatomical and pathological localization of the problem?
Liver : Chronic liver disease (cirrhosis) secondary to HBV
Kidney : AKI on CKD (Hepatorenal syndrome) , Hyperkalemia
GI : GAVE , portal hypertensive gastropathy
Lung : pneumonia , pleural effusion
2. 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?
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.
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.
6) 58 year old man with Dementia
Case report details: http://
1. What is the problem representation of this patient?
A 58 year old weaver occasional alcoholic 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.
K/c/o CVA 3 years back and now he was diagnosed as neuro degenerative disease - Alzheimer's (? Vascular - post stroke sequale.
2. How would you evaluate further this patient with Dementia?
3. Do you think his dementia could be explained by chronic infarcts?
Yes
ABBREVIATIONS
AD : Alzheimer’s disease
CH : cerebral haemorrhage
CVD : cerebrovascular disease
MI : myocardial infarction
MID : multi-infarct dementia
LVD : large vessel disease
SIVD : subcortical ischaemic vascular dementia
SVD : small vessel disease
VCI : vascular cognitive impairment
VaD : vascular dementia
4. What is the likely pathogenesis of this patient's dementia?
Aβ plaque formation are key hallmarks of the AD brain. Specialized pro-resolving mediators and strategies aimed at boosting resolution such as using omega-3 polyunsaturated fatty acid exert differential effects on these targets and provide anti-inflammatory and pro-cognitive effects in neuroinflammation/degeneration
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:
1. What is the problem representation of this patient and what could be the anatomical site of lesion ?
A 55 year old male construction worker with T2DM who is a chronic alcoholic & smoker came with c/o weakness of right upper limb with involuntary movements of both right UL & LL secondary to ? right temporal lobe epileptogenic focus.
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
subcortical infarcts are caused by occlusion of a penetrating artery from a large cerebral 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.
https://www.ncbi.nlm.nih.gov/books/NBK534206/#:~:text=Lacunar%20syndromes%20are%20clinical%20manifestations,from%20the%20Circle%20of%20Willis.
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?
Ventricular ectopics seen
Left axis deviation +
ST depressions noted in precordial leads V1 to V6
NSTEMI
Yes , i agree with the treating team on starting the patient on Enoxaparin.
https://www.google.co.in/url?sa=t&rct=j&q=&esrc=s&source=web&cd=&ved=2ahUKEwia7d_Ci-btAhX4_XMBHaZNAkYQFjACegQIAhAC&url=https%3A%2F%2Fpubmed.ncbi.nlm.nih.gov%2F12644342%2F&usg=AOvVaw1BufP2z_JTKG4a8aLVV9o8
5. Which AED would you prefer?
As it is focal seizure i would prefer carbamazepine
And lorazepam / diazepam to prevent the conversion of focal seizure to GTCS
Please provide studies on efficacies of each of the treatment given to this patient.
Antiepileptics https://pubmed.ncbi.nlm.nih.gov/28661008/
Atorvastatin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036014/
Aspirin https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6206448/
Enoxaparin https://www.sciencedirect.com/science/article/pii/S0735109702029017
Patient details in the intern logged online case report here: http://manojkumar1008.
Questions:
1. What is the problem representation for this patient?
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?
3. What is the cause for his Dyspnea? What is the reason for his albumin loss?
DYSPNEA:
Obesity increases the work of breathing because of the reductions in both chest wall compliance and respiratory muscle strength.
Excess metabolically active adipose tissue plus increased workload on supportive respiratory muscle leads to increased CO2 production (hypercapnia) and increased O2 consumption (hypoxia).
Pulmonary function abnormalities resulting from obesity
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.
Yes i agree with the treating team starting antibiotics as his renal parameters are deranged and he may be having AKI (?renal)
CUE / urine cultures / USG abdomen are not available to support it as renal cause of AKI
Spot urine sodium is high may be secondary to ATN
3)
A. 41 year old man with Polyarthralgia
Case details here: https://
1. How would you evaluate further this patient with Polyarthralgia?
2. What is the pathogenesis involved in RA?
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.hopkinsarthritis.org/arthritis-info/rheumatoid-arthritis/ra-pathophysiology-2/&ved=2ahUKEwjI-J_ZrObtAhWF7nMBHYHDCy4QFjAXegQIKRAB&usg=AOvVaw27b8Rt0lo57Q6Rpp6UjASB&cshid=1608803720629
3. What are the treatment regimens for a patient with RA and their efficacies?
Treatment options include medications, reduction of joint stress, physical and occupational therapy, and surgical intervention
Pharmacological Strategies
There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal anti-inflammatory agents (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARDs)
Non-steroidal Anti-inflammatory Agents (NSAIDs)
The major effect of these agents is to reduce acute inflammation thereby decreasing pain and improving function
Newer "second-line" drugs (DMARDs)
75 year old woman with post operative hepatitis following blood transfusion
Case details here: https://
1.What are your differentials for this patient and how would you evaluate?
Post transfusion delayed hemolytic reaction
Evaluation:
ABO and Rh compatability
coombs testing
antibody panel testing
https://www.learnhaem.com/courses/frcpath-transfusion/lessons/antibody-screening-and-identification/topic/antigrams/
-Transfusion related acute hepatic injury (TRAHI)
-Post transfusion hepatitis
-Ischemic 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?
Symptomatic management
4) 60 year woman with Uncontrolled sugars
http://manojkumar1008.
1. What is the problem representation of this patient?
60 year old female with T2DM & HTN since 2 years 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?
3. What are the chest xray findings?
Plain radiograph of chest , frontal view
Trachea shifted towards right
Hyperdense area noted in the right upper lobe
(consolidation)
Peripheral pulmonary vasculature is normal
Heart is central in position
Cardiac size normal
The domes of diaphragm are normal in position and smooth outline
Visualized bones and soft tissue appear normal.
Approach to hypoalbuminemia
5) 56 year old man with Decompensated liver disease
Case report here: https://appalaaishwaryareddy.
1. What is the anatomical and pathological localization of the problem?
Liver : Chronic liver disease (cirrhosis) secondary to HBV
Kidney : AKI on CKD (Hepatorenal syndrome) , Hyperkalemia
GI : GAVE , portal hypertensive gastropathy
Lung : pneumonia , pleural effusion
2. 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?
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.
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.
6) 58 year old man with Dementia
Case report details: http://
1. What is the problem representation of this patient?
A 58 year old weaver occasional alcoholic 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.
K/c/o CVA 3 years back and now he was diagnosed as neuro degenerative disease - Alzheimer's (? Vascular - post stroke sequale.
2. How would you evaluate further this patient with Dementia?
3. Do you think his dementia could be explained by chronic infarcts?
Yes
ABBREVIATIONS
AD : Alzheimer’s disease
CH : cerebral haemorrhage
CVD : cerebrovascular disease
MI : myocardial infarction
MID : multi-infarct dementia
LVD : large vessel disease
SIVD : subcortical ischaemic vascular dementia
SVD : small vessel disease
VCI : vascular cognitive impairment
VaD : vascular dementia
4. What is the likely pathogenesis of this patient's dementia?
Aβ plaque formation are key hallmarks of the AD brain. Specialized pro-resolving mediators and strategies aimed at boosting resolution such as using omega-3 polyunsaturated fatty acid exert differential effects on these targets and provide anti-inflammatory and pro-cognitive effects in neuroinflammation/degeneration
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:
