My experiences with general cellular and neural cellular pathology in a case based blended learning ecosystem's CBBLE

 Hello,

This is Nitish Dampuru, a medical undergraduate studying in India.
I'd like to share some of the interesting cases that helped me to learn more about medicine.
I'd also like to thank my seniors and my professors for guiding, teaching me, enhancing my respect for the art of medicine and finally make me better as a person.

NOTE: THIS IS AN ONLINE E LOGBOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS/HER GUARDIAN'S SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR INDIVIDUAL PATIENT'S PROBLEMS THROUGH A SERIES OF INPUTS FROM THE AVAILABLE GLOBAL ONLINE COMMUNITY OF EXPERTS INTENDING TO SOLVE THOSE CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE-BASED INPUT.



What is the greatest achievement for a doctor?

To be the reason for their patient's smile. Isn't it ??

Alright let's get to the details of my first encounter with a patient. She was a 45 year old daily wage worker whose chief complaints were vomiting (4-5 episodes per day for 2 days).
I took her history where I came to know that  she had undergone simple right nephrectomy for pyelonephritis and examined her thoroughly.
Then we have sent a sample for checking her single kidney functioning
And to our surprise her urea and Sr. Creatinine levels were elevated.
Well, that piqued my interest
'How would a gastroenteritis lead to acute kidney injury'

https://nitishdampuru33.blogspot.com/2022/06/45-yr-old-female-patient-with.html


Then I started searching for it and came across this article that cleared my doubts

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8284204/

This blog report  is a short compilation of few of the cases involving the neural cellular pathology that I have seen during my MBBS and ongoing Internship.

Case 1:-
I came across a 27 yr old male patient who came to our hospital in a vegetative state since 1 year, whose attenders came to seek medical advise for removal of tracheostomy tube. 
The sequence of events are depicted in the flow chart in the case report (link is mentioned below )

Where I came to know the importance of door to doctor time benchmark, which unfortunately lead to the current condition of the patient

For further details :

https://nitishdampuru33.blogspot.com/2023/03/1801006030-long-case.html?m=1

Case 2:-
This is a case of 65 years old female came to casualty with
C/C of headache since 4 hours
Involuntary movements in right upper and lower limbs since 3 hours, that I came across during my internship.
She was alright 4 hours back  then she developed  headache in frontal region, sudden in onset, took seizure medication levipil 500 mg. Involuntary movements in right upper and lower limbs since 3 hours, 2 episode every 5 mins, each episode lasted for 2-3 mins.
Associated with uprolling of eyeballs, frothing from the mouth, involuntary defection and is unresponsive since 3 hours
We had to crash intubate her as she went into respiratory failure.
For further details:

https://nitishdampuru33.blogspot.com/2023/05/65-year-old-male-with-involuntary.html?m=1

Case discussion:-

[08/05, 21:13] Rakesh Biswas Sir GM HOD: ABG repeated? 

Sedation rate? Share the complete details of ventilation settings and current pharmacological dose and drip rate

[10/05, 21:33] Ajay Sir Pg GM: https://pubmed.ncbi.nlm.nih.gov/20581136/

[10/05, 21:36] Rakesh Biswas Sir GM HOD: So with this information what does your patient fit into?

[10/05, 21:36] Ajay Sir Pg GM: https://go.gale.com/ps/i.do?p=AONE&u=googlescholar&id=GALE|A128075131&v=2.1&it=r&sid=AONE&asid=7d1af1d7

[10/05, 21:37] Ajay Sir Pg GM: Source

[10/05, 21:40] Ajay Sir Pg GM: The patient fits mostly into true seizures sir 

The patient doesn't have any intention to do pseudoseizures as per the history provided by the attenders and patient , 

There is rigidity f/b jerking, 

There is involuntary defecation and micturition

[10/05, 22:50] Rakesh Biswas Sir GM HOD: Any review of literature around respiratory and metabolic acidosis in seizures similar to what our patient had?

[11/05, 08:35] Dr. Navya Ma’am PG GM: https://www.ncbi.nlm.nih.gov/books/NBK441871/

Treatment of PNES may be difficult, but it is clear that anti-epileptic drugs (AEDs) are of no benefit. In addition to unnecessary costs and the potential side effects of AEDs for these patients, life-threatening side effects such as respiratory depression may occur if psychogenic nonepileptic status epilepticus is treated with large dosages of benzodiazepines.

[11/05, 09:19] Ajay Sir Pg GM: https://linkinghub.elsevier.com/retrieve/pii/S0007-0912(17)47615-X

[11/05, 09:25] Ajay Sir Pg GM: https://pubmed.ncbi.nlm.nih.gov/1191463/

[11/05, 11:57] Rakesh Biswas Sir GM HOD: Share the images of encephalomalacia from this patient's MRI as well as the previous patient with migraine and visual loss asap @⁨Dr. Navya Ma’am PG GM⁩

[14/05, 08:54] Rakesh Biswas Sir GM HOD: 👆MRI images of encephalomalacia ? @⁨Dr. Deepika Ch GM PG Ma'am⁩

[15/05, 23:59] Dr. Deepika Ch GM PG Ma'am: Age, number of lesion sites, size of encephalomalacia, and seizure frequency were independent risk factors for the prognosis of patients with REAE (OR > 1, P < 0.05). Surgical treatment was an independent protective factor associated with the prognosis of patients with REAE

variety of causes can lead to liquefaction and necrosis of brain tissue and the formation of encephalomalacia [9]. These causes include trauma, cerebrovascular disease, and intracranial infection [10]. The pathological manifestations of brain soft focus ranged from early neuronal necrosis to neuronal disappearance and then to glial cell proliferation. There are no nerve cells in the brain softening focus, which does not cause epileptic discharge. The real pathological site of epileptic discharge is the peripheral nerve tissue [11]. The traction of fibrous scar tissue in the brain can embed the remaining normal neurons cause abnormal discharge and disrupt the function of intertwined proliferative cells. It affects the electrical activity of normal neurons, resulting in seizures. A study suggested that glial cells can lead to epileptic seizures through mechanisms such as increasing the excitability of normal neurons, neuronal cluster discharge, and failure to inhibit the excitability of neurons

[15/05, 23:59] Dr. Deepika Ch GM PG Ma'am: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9273423/

[16/05, 00:00] Dr. Deepika Ch GM PG Ma'am: The predictive efficacy of encephalomalacia size on the prognosis of patients with refractory epilepsy secondary to encephalomalacia. AUC: area under the curve; CI: confidence interval.

[16/05, 00:00] Dr. Deepika Ch GM PG Ma'am: Efficacy of seizure frequency in predicting prognosis in patients with refractory epilepsy secondary to encephalomalacia. AUC: area un

[16/05, 00:02] Dr. Deepika Ch GM PG Ma'am: refractory epilepsy associated with encephalomalacia (REAE).

[16/05, 06:47] Rakesh Biswas Sir GM HOD: For the AJND article :

Can encephalomalacia be a form of neurodegeneration?

[16/05, 10:39] Dr. Deepika Ch GM PG Ma'am: Encephalomalacia also known as cerebromalacia, is the softening of brain tissue. It can be caused either by vascular insufficiency, and thus insufficient blood flow to the brain, or by degeneration. Encephalomalacia can be the formation of necrosis, or dead tissue, in a portion of the brain due to a partial complete blockage of blood flow to the area, which in turn can be caused by a natural condition or by infection or trauma (TBI). The term encephalomalacia is also used at times to refer more generally to degenerative conditions affecting the brain. If the condition affects the white matter of the brain, it is called leukoencephalomalacia. If it affects the gray matter, it is known as polioencephalomalacia.

[16/05, 10:40] Dr. Deepika Ch GM PG Ma'am: https://www.passenpowell.com/encephalomalacia-brain-injury-children-adults/

[17/05, 07:18] Rakesh Biswas Sir GM HOD: What about microscopic description of the pathology in encephalomalacia?

Also focus on it's association with vascular neurodegeneration 

Also share the MR images of the 35F with CRVO and Vascular migraine and encephalomalacia

[20/05, 13:14] Dr. Deepika Ch GM PG Ma'am: CAA has now been linked with brain atrophy in regions remote from those directly affected by intracerebral hematomas, and with risk for progressive cognitive decline in the absence of new hemorrhagic strokes. Therefore, CAA is associated with features – brain atrophy and progressive cognitive decline – that are typically considered hallmarks of neurodegenerative disease. Although CAA is usually accompanied by some degree of Alzheimer's disease pathology, the profiles of cortical thinning and cognitive impairment do not fully overlap with those seen in Alzheimer's disease, suggesting that there are CAA-specific pathways of neurodegeneration. CAA-related brain ischemia may be an important mechanism that leads to brain injury, cortical disconnection, and cognitive impairment

The terms ‘neurodegeneration’ and ‘neurodegenerative’ are widely used but without a formal definition in the peer-reviewed literature. The terms are frequently used to refer to a group of neurological conditions marked by death of neurons and supporting cells in the neurovascular unit, with accompanying progressive loss of cognitive and motor functions.

Stroke and other forms of monophasic acute brain injury (e.g., because of trauma) are not typically considered to be neurodegenerative disorders. Therefore, CAA is most commonly conceptualized as a cerebrovascular disease associated with risk of lobar ICH, and not as a cause of neurodegeneration. However, accruing evidence suggests that CAA is not so easy to pigeonhole as either a cause of stroke or neurodegeneration, but instead is an important cause of both of these neurological syndromes. To make my case that CAA should be considered a neurodegenerative disease, I focus on associations between CAA and two cardinal features of neurodegenerative diseases: cognitive decline and brain atrophy

Both are a consequence of cleavage of the amyloid precursor protein to form pathogenic Aβ which aggregates into β-amyloid. In the case of AD pathology, the β-amyloid aggregates in the brain parenchyma in the form of neuritic plaques. In the case of CAA, the β-amyloid aggregates in the walls of small arteries and arterioles. Most patients with CAA also have some degree of neuritic plaques, and most patients with AD have some degree of CAA

pattern of cortical thinning in CAA (Fotiadis et al. 2016) overlaps with AD (Dickerson et al. 2009) in some regions (supramarginal gyrus, superior frontal gyrus, and inferior temporal gyrus), but other regions exhibit more thinning in CAA than AD (occipital cortex and medial frontal cortex) or in AD than CAA (precuneus, angular gyrus, and anterior temporal cortex) (Fig. 2). Overall, there are clear differences between the CAA and AD patterns of cortical thinning.

These differences in cognitive profile and regional cortical thinning suggest that neurodegeneration in CAA cannot be solely attributed to the effects of concomitant AD pathology.


Case 3:- 

65 years old male came to OPD with c/o of altered mental status since yesterday night 

History of vomitings 3days back

H/o nausea since 3days

H/o loose stools 2days back

Did not pass stools since 2days

He was apparently alright 3days back then he had vomiting which insidious in onset, non projectile type and had 2episods (which is black coloured) non blood stained and non foul smelling,and had an episode of loose stool 2days back, insidious in onset,which is greenish colour,No aggrevating factors and relieved on medication.

For further details:-

https:/nikithchandrainternrollno4.blogspot.com/2023/05/65m-hypoactive-state-kco-cvalft-side.html?m=1

The one thing is that,this experience had made me realise 

“Where the art of medicine is loved, there is also love for humanity” 

                                             - Hippocrates.

Thankyou hope you enjoed the read.