BIMONTHLY INTERNAL ASSIGNMENT--- DECEMBER 2020

 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:

• weakness of right upper limb with involuntary movements of both right Upper Limb & Lower Limb 
• secondary to ? right temporal lobe epileptogenic focus. 
• he is chronic smoker and alcoholic with type 2 diabetes 
• anatomical site :Temporal lobe 

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

ANS:

• Large subcortical infarctions may be due to cerebral embolism and cause cortical signs more frequently than small subcortical infarctions, which usually result from small-vessel disease and are not associated with cortical findings. 
• some studies  evaluated 51 consecutive patients with a subcortical infarct on CT that was 1.5 cm or larger for a potential carotid or cardiac source of embolism and determined how frequently aphasia, hemineglect, or gaze paresis occurred. 
• A carotid or cardiac embolic source was identified in 63% of the total population with a carotid source occurring in 23% and a cardiac source occurring in 49%. More than one-half of the patients with hypertension or diabetes mellitus had an embolic source, whereas all patients without these risk factors had a possible carotid or cardiac source of embolism. 
• Aphasia or hemineglect occurred in 39% of patients and gaze paresis occurred in 41%. Large subcortical strokes frequently result in a different clinical syndrome and from a different mechanism than small subcortical strokes.
• 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?

patient ecg showing 

• Ventricular ectopics 
• Left axis deviation present
• ST depressions noted in precordial leads V1 to V6
• NSTEMI

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

• Enoxaparin is the only LMWH compound to have demonstrated sustained clinical and economic benefits in comparison with UFH in the management of unstable angina/ non–ST-segment elevation myocardial infarction (NSTEMI). 

https://www.sciencedirect.com/science/article/pii/S0735109702029017

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

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

2)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? 

ANS:

• c/o exertional dyspnea and cough since 3 days and sudden onset giddiness and profuse sweating
• Recurrent hyperglycemia  secondary to  oral hypoglycemic agents(OHA) with morbid obese 
• k/c/o DM T2 and HTN since  10 yr with metabolic syndrome

2. What is the cause for his recurrent hypoglycemia? And how would you evaluate?

ANS: 

• From the reports, he has elevated Serum Creatinine and Significant loss of proteins in his urine signifying a Renal Failure. Apart from that the patient is on OHA's - Glimiperide which is known to cause hypoglycemia.
• Patients with decreased GFR  due to diabetes and CKD have decreased insulin requirement as insulin is cleared by kidneys. 
• In CKD patients the peripheral metabolism of insulin is reduced.
• With decrease in glycogen storage in the patients with CKD and uremia due to suboptimal nutrition anorexia may occur.
• There occurs less renal gluconeogenesis as a result of reduction in renal mass in CKD patients 
•  Most of the medications used for treating diabetes are excreted by kidneys from the body. In CKD incidence of hypoglycaemia increases as a result of accumulation of these drugs and their metabolites.
• 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?

ANS:

• cause for his dyspnea  is obesity

• Pulmonary function abnormalities resulting from obesity
• Obesity causes mechanical compression of the diaphragm, lungs, and chest cavity, which can lead to restrictive pulmonary damage. Furthermore, excess fat decreases total respiratory system compliance, increases pulmonary resistance, and reduces respiratory muscle strength. It is interesting that metabolic syndrome also changes lung function and that the combination of obesity and metabolic syndrome seems to impair lung function

• HYPOALBUMINEMIA: patient albumin is # 2.8 
• Spot protein creatinine ratio > 1 indicates......
• 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.

ANS:

• 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://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?

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/PMC6348345/

3(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?

-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

Evaluation:

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 https://pubmed.ncbi.nlm.nih.gov/27089005/

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?

• 60 year old woman who is a known case of Hypertension and diabetes since 2 years with a history of AKI and septic shock 1 1/2 years back presented with the complaints of chest pain since 4 days, Abdominal pain since 3 days.
•  She doesn’t seem to have tachypnea, tachycardia. And she is a febrile according to the details mentioned in the elog. 
• Her TLC is 18,000 c/cumm on the day of admission. 
• Doesn’t fit into SIRS criteria. 
• Her CUE shows 2 plus urinary sugars loss along with uncontrolled blood sugars.
• She has indirect hyperbilirubinemia with a raised ALP and reduced serum albumin.
•  And a slight elevation in her Serum creatinine 1.5mg/dl  - ?AKI

upper lobe pneumonic consolidation with sepsis

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

• measurement of her average blood sugar levels over the past 3 months (HbA1C) is 8. Her blood sugars have already not been under control owing to her irregular use of OHA'S as it was mentioned in the history.
• Her blood glucose shot through the roof even further after she developed Right lung pneumonia which inturn she would be more susceptible to because of poor blood glucose control.

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

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)

Approach to hypoalbuminemia:

5. Comment on the treatment given along with each of their efficacies with supportive evidence.

ANS:

• 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?

ANS:

• 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?

The initial evaluation of the patient found to have hepatitis B surface antigen (HBsAg) in serum should attempt to establish the diagnosis and assess the grade of the disease.

These phases include 

1. An early, immune-tolerant phase that typically occurs in children and is marked by high levels of HBV DNA, presence of HBeAg, but normal serum aminotransferase levels and absence of disease activity

2. Immune activation phase of chronic hepatitis B, marked by moderate to high levels of HBV replication, continued or fluctuating disease activity and aminotransferase elevations and during which progressive liver damage can occur and 

3. An inactive carrier state, marked by low levels of HBV replication, absence of HBeAg and normal serum aminotransferase levels with inactive liver disease. 

Chronic hepatitis B is a dynamic disease, and patients can pass from one phase to another and back, from disease activity to inactivity. During periods of activity, progressive liver damage can occur, resulting in cirrhosis and its complications, as well as hepatocellular carcinoma (HCC). 

Thus, the presence of HBsAg in serum may have a range of implications, indicating acute or chronic hepatitis B that can be mild or severe and progressive. The goals of the initial evaluation should be to determine the phase of HBV infection, the severity of disease, and the need for monitoring and treatment.

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 , 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.

https://bmcnephrol.biomedcentral.com/articles/10.1186/s12882-019-1529-1

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

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)  0https://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?

ANS:

• 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?

ANS:

• diagnostic criteria for dementia and mild cognitive impairment, introducing the terms major and minor neurocognitive disorders.Major neurocognitive disorder requires demonstration of significant cognitive decline in at least one of the following cognitive domains: complex attention, executive function, language, learning and memory, perceptual-motor, or social cognition. This decline must be based on both subjective and objective findings, and interfere with instrumental activities of daily living. Minor neurocognitive disorder requires only modest cognitive decline that does not interfere with instrumental activities of daily living.

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

Yes 

• Dementia is common  after stroke but we know little of the mechanisms or whether the risk varies with stroke subtype.
•  Stroke risk factors, amounts and regions of the brain affected, and suggested stroke mechanisms all vary with stroke subtype, and could influence the risk of cognitive impairment after stroke. For example, as cortical ischaemic strokes often affect a large area of brain, they may carry a higher risk of cognitive impairment than the smaller, less neurologically severe, lacunar strokes. Alternatively, lacunar strokes may carry a higher risk of cognitive impairment than would be expected on the basis of the lacunar infarct alone as they are part of the spectrum of cerebral small vessel disease (SVD). SVD, which affects the brain diffusely and is the commonest vascular cause of cognitive impairment, could be unmasked by a new lacunar stroke.

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

Post stroke 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:

https://pubmed.ncbi.nlm.nih.gov/9443470/

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?

• Bacterial
• Pyogenic abscess
• Tuberculoma and tuberculous abscess Mycobacterium avium-intracellulare infection Syphilis
• Listeriosis
• Fungal
• Nocardiosis
• Actinoimycosis 
• Rhodococcosis 
• Zygomycosis
• Histoplasmosis
• Coccidioidomycosis
• Aspergillosis
• Mucormycosis
• Paracoccidioidomycosis
• Cryptococcosis
• 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?

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 IRIS

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

• Transfusion reactions
• Hypertensive urgency management
• Status epilepticus management
• Cardiorenal association in different ways
• Temporal lobe epilepsy
• Dialysis on daily basis / CRRT dialysis
• Unexplained delirium due to malnutrition / sepsis
• No rise in Hb after blood transfusion which can be attributed to various factors that lead to RBC destruction during storage
• Role of prophylactic anticoagulant usage in AF
• Management of TB in HIV with minimal risk of IRIS