medicine assignment

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 ?

55 yr old male who is k/c/o diabetic and chronic alcoholic with right upper limb weakness and involuntry movements of right upper and lower limbs,

Internal capsule:

pure motor strokes, ataxic hemiparesis, and clumsy hand-dysarthria. 

Frontal lobe:

urinary incontinence, and head and eye deviatiation

Temporal lobe:

It is preceeded by aura. Aura could be  sensory, emotional, cognitive, or autonomic features prior to onset of impaired awareness. Postictal confusion typically occurs.



2. Why are subcortical internal capsular infarcts more common that cortical infarcts?

 Subcortical areas are supplied by penetrating branches,Occlusion of these penetrating arteries result in subcortical infarcts. 

They are common because perforating arteries that supply the region are predisposed to occlusion or rupture due to their small diameter

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?

ST depressions noted in precordial leads V1 to V6.Sinus Rhythm with LAD,NSTEMI in septal .

Yes I agree,

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994029/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994029/

5. Which AED would you prefer?

Carbamazepine



If so why?

pubmed.ncbi.nlm.nih.gov ›


Please provide studies on  efficacies of each of the treatment given to this patient.

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.hindawi.com/journals/ert/2015/415082/&ved=2ahUKEwjjuZK7_9ftAhWjxDgGHU0dCvsQFjAKegQIGhAB&usg=AOvVaw27c1fo_X7FrtboiREUJdRi

Question 2) 55 year old man with Recurrent hypoglycemia

Patient details in the intern logged online case report here: http://manojkumar1008.blogspot.com/2020/12/shortness-of-breath-with-high-sugars.html 
1. What is the problem representation for this patient? 
55 yr old man k/c/o type 2 DM  since 10 yrs,HTN,with c/o sob,cough, giddiness and sweating 
2. What is the cause for his recurrent hypoglycemia? And how would you evaluate? 

In this pt he has elevated Serum Creatinine and Significant loss of proteins in his urine signifying a Renal Failure. 
Other causes:

3. What is the cause for his Dyspnea? What is the reason for his albumin loss?

Fluid overload due to Aki causes dyspnoea


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.

No,as I think there is no features of infection.


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?

https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348345/%23:~:text%3DAmerican%2520College%2520of%2520Rheumatology%252020%2525%252C%252050%2525%252C%2520and%252070,endpoints%2520were%2520ACR70%2520and%2520remission.&ved=2ahUKEwjdtsGQi9jtAhXGyTgGHbqpCCAQFjACegQIDBAE&usg=AOvVaw2uRIxS4pTeXHctoN68ypNY


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?



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

I agree with the treatment provided by the treating team 

Lasix & Nebulization : For wheezing and crepts

Lactulose : To prevent hepatic encephalopathy 

Zofer : For vomitings

Pantop : To prevent gastritis


4) 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?

60yr old woman who is a k/c/o diabetes since 2yrs with c/o chest pain since 4 days and burning type of pain in epigastric region.


2. What are the factors contributing to her uncontrolled blood sugars?

Due to irregular usage of OHA's as mentioned in the history

3. What are the chest xray findings?

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

4. What do you think is the cause for her hypoalbuminaemia? How would you approach it?

It is decreased to acute inflammatory condition

5. 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?

jaundice with abdominal distention-liver

sob with abdominal distention-heart failure, renal failure 

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?


HBV attaches to the host hepatocyte cell membrane through its envelope proteins. When the viral membrane fuses with the cell membrane, it will result in releasing the viral genome into the cell cytoplasm. After the viral genome reaches the nucleus, the viral polymerase enzyme will convert the partially double-stranded DNA genome into cccDNA. This is followed by transcription and nuclear export of all viral mRNA to the cytoplasm for translation. The surface protein enveloping process occurs in the endoplasmic reticulum and then assembled in the cytoplasm. These proteins are transported to the post-endoplasmic reticulum and Golgi compartments for the budding of the nucleocapsid. The different viral components will assemble into new virions that will be released out of the host and infect new hepatocyte.

4. Is it necessary to have a separate haemodialysis set up for hepatits B patients and why?

Yes,it is necessary to have separate haemodialysis set for hepatitis B patients to prevent spread of infection to other patients

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.

Tenofovir : for HBV

Octreotide : for upper GI bleed. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750992/#:~:text=In%20a%20meta-analysis%2C%20somatostatin,(mostly%20caused%20by%20gastritis).

Lasix : for fluid overload (AKI on CKD) 

Vitamin -k : for Deranged coagulation profile (PT , INR & APTT reports not available)

Pantop : for gastritis

Zofer : to prevent vomitings

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?

58yr old man with c/o Slurring of speech since 6 months , deviation of mouth to right side associated with
Drooling of saliva from left angle of mouth, food particles and water predominantly from left angle of mouth and smacking of lips

Urinary incontinence since 6 months, dribbling of urine while rushing to bathroom.

Forgetfulness since 3 months, able to remember his name and close relatives. Patient often forgets path to his own home, forgets wearing chappals, patient also wanders sometimes, self hygiene is maintained.
He has delayed response to commands.
Dysphagia to both solids and liquids since 10 days.


2. How would you evaluate further this  patient with Dementia?




3. Do you think his dementia could be explained by chronic infarcts?

Multi-infarct dementia is the most common form of vascular dementia, which describes a loss of cognitive function from damaged blood vessels in the brain. "Multi-infarct" means that multiple areas of the brain have been injured due to a lack of blood from a series of small strokes.

Blockages in the arteries of the brain usually cause a stroke (infarction), but sometimes there are no stroke symptoms. These "silent" strokes increase a person's risk of vascular dementia. If there are a number of small strokes experienced over time, multi-infarct dementia may result.



4. What is the likely pathogenesis of this patient's dementia?

Several mechanisms may explain why patients affected by stroke are prone to develop dementia

- post-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?

https://pubmed.ncbi.nlm.nih.gov/20395618/

7) 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 year old man with complaints of headache since 2 months and involuntary stiffness of bilateral upper and lower limbs since 1 week along with Loss of consciousness.

Anatomical localisation - Brain

Involving both the upper limbs and lower limbs

Could be due to multiple infarcts

Ring enhancing lesions as he is RVD positive 


2. 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?

Immune reconstitution inflammatory syndrome (IRIS) is a condition seen in some cases of AIDS or immunosuppression, in which the immune system begins to recover, but then responds to a previously acquired opportunistic infection with an overwhelming inflammatory response that paradoxically makes the symptoms of infection worse

WHO recommends that all HIV-infected TB patients should be commenced on ART irrespective of their CD4 count. This has the potential to reduce mortality. ART should be given within 8 weeks of initiation of antituberculosis treatment and based on the CAMELIA, SAPIT and STRIDE trials, in TB patients with a CD4 count of less than 50cells/mm3, ART should be started within 2 weeks after the onset of antituberculosis treatment.

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 IRIS

8) Please mention your individual learning experiences from this month.
1.ABG interpretation and how to differentiate respiratory acidosis from metabolic acidosis
2.ecg interpretation
3.MI case management
4.NTG tapering in Hypertensive emergency case
5.Drug induced Hypoglycemia
6.Acute pancreatitis case management
7.LFT interpretation and ruling out the causes.
8.MRI changes in parkinsonism and parkinsonism plus syndrome





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