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 ? 

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.

3. What is the pathogenesis involved in cerebral infarct related seizures

Poststroke seizures can occur soon after the onset of ischemia or can be delayed. Many clinical studies make a distinction between early and late seizures based on differences in their presumed pathophysiology. Early poststroke seizures are thought to result from cellular biochemical dysfunction leading to electrically irritable tissue.2,3Acute ischemia leads to increased extracellular concentrations of glutamate, an excitatory neurotransmitter that has been associated with secondary neuronal injury.2,4 Recurrent epileptiform-type neuronal discharges can occur in neural networks of surviving neurons exposed to glutamate.5 In addition, transient peri-infarct depolarizations have been observed in the penumbra after experimental occlusion of the middle cerebral artery.6,7 Other investigators failed to confirm this phenomenon in humans.8 There is a correlation between the number and the total duration of depolarizing events and infarct volume in the setting of ischemia,9 perhaps due to reductions in capillary perfusion leading to more profound ischemia in penumbral tissue.10 Experimental data also suggest that epileptogenesis is enhanced by hyperglycemia at the time of ischemia.11

In contrast to early-onset seizures, late-onset seizures are thought to be caused by gliosis and the development of a meningocerebral cicatrix.12Changes in membrane properties, deafferentation, selective neuronal loss, and collateral sprouting may result in hyperexcitability and neuronal synchrony sufficient to cause seizures.13,14 Pronounced neocortical neuronal hyperexcitability was found in primary somatosensory neurons of rats 10 to 17 months after transient forebrain ischemia.13,15,16

Experimental studies in laboratory animals suggest that repeated seizure-like activity in the setting of cerebral ischemia significantly increases infarct size and can impair functional recovery, an effect that can be ameliorated with the administration of certain neuroprotective agents.17–19 Although frequent repeated seizures are undoubtedly harmful, it is not entirely clear that infrequent seizures worsen the outcome after experimental brain injury.20 In fact, isolated seizures after experimental cortical contusion were found to accelerate behavioral recovery in rats.21



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
NSTEMI

Yes , i agree with the treating team on starting the patient on Enoxaparin.

5. Which AED would you prefer?
If so why?
Please provide studies on  efficacies of each of the treatment given to this patient.

As it is focal seizure i would prefer carbamazepine
And lorazepam / diazepam to prevent the conversion of focal seizure to GTCS





Patient details in the intern logged online case report here: http://manojkumar1008.blogspot.com/2020/12/shortness-of-breath-with-high-sugars.html

Questions:
1. What is the problem representation for this patient? 

A 55 year old male with T2DM 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? 

Drug induced hypoglycemia because kidney failure (increased duration of action of OHA due to decreased excretion)






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).



HYPOALBUMINEMIA:
Spot protein creatinine ratio > 1 --- albuminuria secondary to ? diabetic nephropathy

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)

1. How would you evaluate further this patient with Polyarthralgia?

 Arthralgias are joint pains without obvious inflammation; whereas, arthritis is associated with demonstrable features of inflammation like joint swelling and tenderness. Raised temperature and visible redness are usually not seen in chronic arthritides like rheumatoid arthritis (RA) or spondarthritides (SpA). These are more a feature of conditions like acute gout or septic arthritis. Arthralgias are non-specific and seen in several non-MSK conditions, e.g. haematological diseases, post-viral fever, metabolic arthropathy like hypothyroidism, etc. A drug history may be important because some commonly used drugs like statins can cause MSK symptoms. Nature of Disease (Inflammatory or Non-Inflammatory?) One of the fundamental concepts in rheumatology is to differentiate inflammatory rheumatic diseases like RA, SpA, lupus, etc. from non-inflammatory disorders like osteoarthritis (OA) since the management is radically different. Inflamed joints stiffen or ‘gel’ after periods of inactivity and tend to loosen with use. In contrast,  non-inflammatory or mechanical joint pain improves with rest and is typically associated with use related pain. Table 2 outlines the points that help in clinical differentiation. It has to be borne in mind that even patients with inflammatory joint disease can develop mechanical symptoms, for example, secondary OA of knees in a patient with RA.

Joints of both upper and lower limbs are involved in RA, SLE and psoriasis. Predominant involvement of lower limbs is seen in gout, SpA and erythema nodosum, whereas, haemochromatosis preferentially affects joints of upper limbs. Type of Joints Affected Small versus large RA typically affects both small and large joints.

2. What is the pathogenesis involved in rheumatoid arthritis?


The pathogenesis of RA is not completely understood. An external trigger (eg, cigarette smoking, infection, or trauma) that sets off an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals.

Synovial cell hyperplasia and endothelial cell activation are early events in the pathologic process that progresses to uncontrolled inflammation and consequent cartilage and bone destruction. Genetic factors and immune system abnormalities contribute to disease propagation.



3. What are the treatment regimens for a patient with RA and their efficacies?



The following abbreviations and nomenclature for disease-modifying antirheumatic drugs (DMARDs) were used in this document:

csDMARD: conventional synthetic disease-modifying antirheumatic drugs - methotrexate, leflunomide, sulfasalazine, and antimalarial drugs (hydroxychloroquine and chloroquine).

tsDMARD: synthetic target-specific disease-modifying antirheumatic drug - tofacitinib.

bDMARD: biological disease-modifying antirheumatic drugs - tumor necrosis factor inhibitors/TNFi (adalimumab, certolizumab, etanercept, golimumab, infliximab), T-lymphocyte co-stimulation modulator (abatacept), anti-CD20 (rituximab), and IL-6 receptor blocker (tocilizumab).

boDMARD: original biological disease-modifying antirheumatic drugs.

bsDMARD: biosimilar biological disease-modifying antirheumatic drugs.

Efficacy and safety of various anti-rheumatic treatments for patients with rheumatoid arthritis:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC63483


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?


-Transfusion related acute hepatic injury (TRAHI)
-Post transfusion hepatitis
-Ischemic


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 

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?


A 60 year old female with T2DM 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?

  • Weight. Being overweight is a main risk factor for type 2 diabetes. ... 
  • Fat distribution. ... 
  • Inactivity. ... 
  • Family history. ... 
  • Race or ethnicity. ... 
  • Age. ..

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


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

  • Inflammation (acute phase reactant)
  • Malnutrition
  • Albuminuria (protein losing nephropathy)

Diagnostic Approach to Hypoalbuminemia

1. Initial diagnostic approach: 

History                         Hematology

Physical examination     Biochemistry (including globulins)

                                    Urine analysis

Serum globulin levels can sometimes provide the clinician with a crude guide as to the potential cause of hypoalbuminemia. Serum globulins tend to be decreased with protein-losing enteropathies, normal with protein-losing nephropathies, and increased with hepatic failure. 

2. Potential further diagnostic testing: 

The above standard investigation will often suggest the likely cause of an animal's hypoalbuminemia. Further testing will be directed by the results of routine investigation, but usually entails specific investigation of urinary, gastrointestinal and hepatic function. Since definitive determination of gastrointestinal protein loss can be difficult and involve invasive testing, potential urinary protein loss and hepatic failure are usually investigated first. 

(i) Protein-Losing Nephropathy (PLN)

Urinary protein levels are initially investigated by protein dipstick or laboratory measurement of protein concentrations. Normal animals have little or no protein in their urine, and such a finding in a hypoalbuminemic patient usually excludes PLN as a diagnosis. When proteinuria is detected in the absence of an active urine sediment (pyuria or hematuria), the magnitude of urinary protein loss can be more accurately quantified using a urine protein:creatinine ratio. 

Protein:creatinine ratio < 1:            Normal 

Protein:creatinine ratio < 2:             Suspicious ('gray' zone) 

Protein:creatinine ratio > 2:             Protein-losing nephropathy 

(ii) Hepatic Failure

Hepatic failure may be suggested by the results of routine serum biochemistry and urinalysis: 

Hypoalbuminemia             Low serum urea

Hyperglobulinemia             Hypoglycemia

Hyperbilirubinemia             Ammonium biurate crystalluria

Elevated SAP and ALT 

Not all patients with hepatic failure, however, will exhibit the classic biochemical changes usually associated with liver dysfunction. Hypoalbuminemia can occasionally be the only real clue to hepatic failure. In such cases, although abdominal radiography and ultrasonography may assist in determining hepatic size and structure, liver function testing is the primary means of establishing the presence of liver failure: 

Resting ammonia and rectal or oral ammonia tolerance testing

Resting and post-prandial serum bile acids

Since ammonia cannot be transported, ammonia can only be measured if an in house chemistry analyzer is available. Such analyzers can produce spuriously high ammonia results, particularly if samples are not tested as soon as collected. Immediate testing has the advantage of providing a rapid diagnosis. Bile acids have the advantage of being stable and easily transportable. 

(iii) Protein-Losing Enteropathy (PLE)

GI signs in a hypoalbuminemic patient with normal renal and hepatic function strongly suggest PLE, particularly if hypoglobulinemia is also present. Some patients with PLE can however have profound hypoalbuminemia and ascites with no history of vomiting or diarrhea. In such patients, PLE is a diagnosis of exclusion that can often only be confirmed by intestinal biopsies. Since collection of biopsies is invasive, PLN and hepatic failure should be excluded first. Infrequently, non-invasive tests such as fecal parasitology and culture, serum TLI, folate and B12 and breathe hydrogen analysis may suggest a cause of PLE. Recently, a fecal test measuring levels of alpha1-protease inhibitor has been developed (Texas A&M GI Laboratory) that may be a useful indirect indicator of the magnitude of fecal protein losses. 



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?

a.liver :chronic liver disease secondary to

b. Kidney : AKI on CKD (Hepatorenal syndrome) 

c.GI : portal hypertensive gastropathy

d.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?


Hepatitis B virus is dangerous because it attacks the liver, thus inhibiting the functions of this vital organ. The virus causes persistent infection, chronic hepatitis, liver cirrhosis, hepatocellular carcinoma, and immune complex disease. 

HBV infection in itself does not lead to the death of infected hepatocytes.  HBV in a non-cytolytic infection.  Liver damage however, arises from cytolytic effects of the immune system's cytotoxic T lymphocytes (CTL) which attempt to clear infection by killing infected cells.  The strength of the CTL response has been noted to determine the course of the infection. For example, a vigorous CTL response results in clearance and recovery, although often with an episode of jaundice. A weak response results in few symptoms and chronic infection (and hence higher susceptibility for hepatocellular carcinoma). 

The younger a person is when she becomes infected with HBV, the more likely she is to be asymptomatic and become a chronic carrier of the disease. Babies born to infected mothers are at very high risk of to becoming carriers and developing liver pathology.

Vertical is thus one common way that HBV is transmitted, along with transmission through sexual intercourse and mixing of blood products. Vertical transmission can be prevented by administering vaccine the same day of birth. Different modes of transmission are more prevalent in certain areas of the world and among certain high-risk groups, yet all areas of the world see HBV transmission through all of these avenues. About 90% of adults who acquire HBV recover from it completely and become immune to the virus. The other 10% of cases are the people who become chronic carriers.


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. 

  • Tenofovir : for HBV
  • 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?

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 


  2. Cognitive and neuropsychological tests. These tests are used to assess memory, problem solving, language skills, math skills, and other abilities related to mental functioning.
  3. Laboratory tests. ...
  4. Brain scans. ...
  5. Psychiatric evaluation. ...
  6. Genetic tests

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


Multi-infarct dementia (MID) is a type of vascular dementia. It occurs when a series of small strokes causes a loss of brain function. A stroke, or brain infarct, occurs when brain infarct, occurs when the blood flow to any part of the brain is interrupted or blocked


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


1) Neurotoxicity, including dysregulated glutamate and calcium signaling, and neurotransmission imbalance contribute to synaptic dysfunction and neuronal loss


(2) Glia activation, including microglia and astrocytes, interfere with immunological processes in the brain further promoting non-resolving inflammation and neurodegeneration


(3) Tau phosphorylation and neurofibrillary tangle formation; 


(4) 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) The accumulation of Aβ may lead to the microglial accumulation and activation resulting in increases in pro-inflammatory cytokines such as interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha. These cytokine increases in the brain can subsequently lead to tau hyperphosphorylation and a pathological cycle of increased Aβ deposition and persistent microglial activation, ultimately resulting in chronic neuroinflammation and neurodegeneration. 


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:
  • Donepezil
  • Rivastigmine
  • Galantamine

NMDA antagonist:
  • Memantine
NON PHARMACOLOGIC:
  • Counselling the patient and care givers
  • Geriatric care
  • Cognitive / emotion oriented interventions
  • Sensory stimulation interventions
  • Behaviour management techniques

Efficacy:

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? 


A 22 year old delivery boy chronic alcoholic and tobacco chewer 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 UL & LL with 5 min LOC 1 week before the day of admission.

Brain - multiple ring enhancing lesions in right cerebellum ? Tuberculoma
RVD positive

2. What the your differentials to his ring enhancing lesions?

       


Fungal
Actinoimycosis 
Rhodococcosis 
Zygomycosis
Histoplasmosis
Coccidioidomycosis
Aspergillosis
Mucormycosis
Paracoccidioidomycosis
Cryptococcosis
Nocordiosis

Bacterial

Pyogenic abscess
Tuberculoma and tuberculous abscess Mycobacterium avium-intracellulare infection Syphilis


Parasitic
Neurocysticercosis
Toxoplasmosis
Amoebic brain abscess
Echinococcosis
Cerebral sparganosis
Chagas' disease

Neoplastic
Metastases
Primary brain tumor
Primary CNS lymphoma

Inflammatory and demyelinating
Multiple sclerosis
Acute disseminated encephalomyelitis
Sarcoidosis
Neuro-Behcet.s disease
Whipple's disease
Systemic lupus erythematosus


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 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).



 8) Please mention your individual learning experiences from this month.

-ckd

-Neuropathy 

-drugs mechanism and doses :Thidoramide

Calcitriol , warfarin ,ecospirin , sodium bicarbonate ,Anxit 0.25mg(BZD)-to relieve anxiety

HIV-antiretroviral drugs, shelcal ,lasix 40mg.

-Vibration (less than 10-not normal ) for diabetes ,propioception 

-Efgr scoring 

-Chadwag score 

-Reflexes -delayed -hypoalbuminea ,hypothyroid

-SDH(<6mm deviation -no need for decompression)

-EDH 

-Raccoon eyes differential diagnosis

-Vitb12-def-neuronbiotin forte(instant diag-relief on instant treatment )

-Ambulator b.p -best way to checking B.P

-IV fluid management 

-dialysis -indications 

-central line procedure 

—brown tumor 

-hypothyroidism symptoms examination and treatment. 

-hypocalcemia symptoms and treatment 



 





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