December exam

This is my submission to online exam of December month .

1- A 55 year old female patient with recurrent focal seizures 

http://ushaindurthi.blogspot.com/2020/11/55-year-old-male-with-complaints-of.html

Patient is a chronic alcoholic and a diabetic now presented for the first time with right side focal seizures and unable to lift right upper limb 

1. What is the problem representation of this patient and what could be the anatomical site of lesion ?

Problem representation : 

1- right upper limb weakness 

2- recurrent focal seizures 

3-ventricular premature complexes

4- diabetes and alcohol 

Anatomical site of lesion :

1-Weakness of right upper limb -Weakness could be due to central or peripheral nervous system involvement.

Acute onset monoplegia affecting upper limb can be caused by the following conditions: 

1. Stroke, affecting superior division of contralateral middle cerebral artery territory, affecting parietal lobe, or unpaired anterior cerebral artery.

2. Head injury, with contusion in the parietal lobe.

3. Trauma to the brachial plexus.

4. Injury to multiple cervical nerve roots.

5. Functional or psychogenic.

nature of weakness was sudden in onset and progressed to static state  ,without history of trauma indicating -acute vascular event -could be ischemic or hemorrhagic.

And the MRI shows evidence of ischemic infarct in left frontal and parietal lobe .

2-Right side focal seizures indicates  lesion  in left cerebral hemisphere -

The most common cause of seizures in elderly population is cerebrovascular disease.

Incidence and prevalence of which increases with age and other comorbidities

2-

3- pathogenesis of seizures in post stroke patient 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585721/

There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies.

In ischaemic strokes; the severity of the initial neurological deficit, the severity of persistent disability after the stroke, the involvement of multiple sites or a larger lesion, cortical damage, and hippocampus involvement are factors that predict the likelihood of developing post‐stroke seizures.Another recognised risk for early post‐stroke seizures is embolic stroke.

https://www.neurologyindia.com/article.asp?issn=0028-3886;year=2018;volume=66;issue=4;spage=949;epage=951;aulast=Ranganathan  

ECG - 

• Normal standardization 
• Rate approximately 150/min 
• Irregular rhythm -VPC present 
• Left axis deviation -axis -30 degree 
• P wave ,PR interval ,QRS duration appears to be normal 
• St t changes in leads 1,avl,and chest leads 

  As we do not have the patients previous ecg -its difficult to comment whether they ecg findings are new changes due to post stroke cardiac abnormalities or previously existing cardiac pathology . 

The regular ecg tracing showed resolution of ST T changes indicating most likely to be post CVA cardiac abnormality .

Given the data it appears less likely to be embolic stroke ,and cardiac chambers appears to be normal on echo.

I wouldn’t agree starting of heparin in this patient because of 

• The risk of hemorrhagic transformation 
• Age ,alcoholism ,multiple chronic infarcts all these factors need to be consider                           

5- post stroke seizure management :

Hemorrhagic ,cortical involvement ,severity of initial neurological deficit,younger age ,family history of seizures ,genetic factors are few high risk factors for development of pss 

No available data exists on which anti epileptic is efficacious and more potent in PSS 

So using an AED in PSS - particularly in elderly population with addictions like alcohol needs to be individualized -depending on cost of the AED ,altered liver function , side effects and tolerability 

 Here I quote a study which showed Levetriactem is better tolerated and found to have lesser adverse effects  than carbamazepine ,although the seizure free period ,efficacy is same for all three drugs

 

Results

Of 361 randomized patients, 359 were included (CR‐CBZ n = 121, LTG n = 117, LEV n = 122) in the modified intent‐to‐treat population (mean age [range] 71.4 [60–95] years). At week 58, the retention rate for LEV was significantly higher than for CR‐CBZ (61.5% vs. 45.8%, p = 0.02), and similar to LTG (55.6%). Seizure freedom rates at weeks 30 and 58 were not different across the groups. Twice as many patients receiving CR‐CBZ discontinued due to adverse events or death compared to those in the LEV group (32.2% vs. 17.2%; odds ratio 2.28, 95% confidence interval [CI] 1.25–4.19, p = 0.007), whereas discontinuation was intermediate for LTG (26.3%). 

2-55/M with recurrent hypoglycemia

http://manojkumar1008.blogspot.com/2020/12/shortness-of-breath-with-high-sugars.html

Problem representation :

1- shortness of breath 

2— recurrent hypoglycemia 

3-renal failure 

4-morbid obesity ,Diabetes 

Hypoglycmia is defined as Blood glucose less than 54 mg/dL according to ADA 

Blood glucose less than 70 is a hypoglycemic alert value.

Causes of hypoglycemia :

1- overdose of oral hypoglycemic agents or insulin 

2-skipping meals after taking insulin or OHA 

3- Decreased elimination of drug in renal failure if the mode of excretion is through the kidneys 

The cause of hypoglycemia in this patient appears to be decreased elimination of drugs due to renal failure.

And also dual drug therapy - long acting insulin and sulfonylurea -increased risk of recurrent hypoglycemia in the background of renal failure .

Most of the oral hypoglycemic agents are predominantly excreted through the kidneys,hence renal failure leads to decreased GFR and thus increasing serum levels of OHA and Insulin .

Cause of Dyspnea : 

Probable causes of dyspnea in this patient appears to be 

• Hypoglycemia causes release of excess of catecholeamines and thus increases workload on                              previously diseased heart
• OSA secondary to obesity 
• Pedal edema ,shortness of breath—right heart failure -Pulmonary HTN Secondary to OSA
• HFPEF  

Cause of albuminuria - 

Diabetic nephropathy 

Pathogenesis of hypoglycemia 

https://www.ncbi.nlm.nih.gov/books/NBK279100/

Normal physiological defenses against hypoglycemia-GLUCOSE COUNTER REGUGULATORY MECHANISM  in normal individuals : 

As soon as blood glucose level falls there will be following actions :

1-Decrease in insulin secretion 

2-increase in epinephrine release ,increase in renal and hepatic glucose production 

3-decreased uptake of glucose by fat and muscle cells 

4-stimulation of neurohumoral response - for hypoglycemic awarness - cholinergic symptoms - sweating ,hunger ,paraestheisa 

Adrenergic symptoms are -palpitations,tremors ,anxiety,arousal 

All these mechanisms are compromised in diabetes 

Pathogenesis of hypoglycemia -

A) Excess therapeutic insulin with normal counter regulatory mechanisms -which is rare 

B) Increase in therapeutic insulin,with impaired counter regulatory mechanisms 

C) Hypoglycemia associated autonomic failure -causing recurrent hypoglycemia

Diabetic nephropathy 

 3 -A. 41 year old man with Polyarthralgia

    https://mahathireddybandari.blogspot.com/2020/11/41m-with-chest-pain-and-joint-pains.html?m=1

  

Problem Representation: 

 

patient presented with loss of appetite,dyspnea ,fatigue since 6 months 

Weight loss since 2 months 

Multiple joint pains since 1 month  

Cough ,chest pain since 15 days 

Examination findings revealed symmetric poly arthritis with piano key sign,radial and ulnar deviation indicating a chronic erosive arthritis 

Even ESR is found to be high 

1- Evaluation begins with  clinical history ,physical examination ,plain x ray of musculoskeletal system 

It’s important to  to distinguish between inflammatory and  degenerative arthritis 

Common symptoms of inflammatory arthritis are joint pain,swelling,early Ming stiffness longer than 0.5-1 hr and radiological evidence of bone lesion .

Approach to poly arthritis : 

Role of ultrasound in identifying and differentiating patients with early inflammatory arthritis .

2- pathogenesis involved in RA :

•       Risk factors include : 
• Genetics - HLA DRB 1*01,HLA‐DRB1*04, which are significantly associated with the risk of developing RA
• SEX- Females are 2-3 fold more likely to develop RA ,attributed to stimulatory effect of estrogen on immune system 
• Smoking 
• Dust inhalation - silica,textile dust           

 DISEASE COURSE :  The course of RA is divided into three phases 

1. Pre clinical RA 
2. Early RA 
3. Established RA 

 Pre clinical RA - RA disease activity begins years before development of clinical symptoms .All the genetic factors,environmental play a role and initiate post translation modifications  producing altered peptides that bind to MHC leading to antigen presentation to T cells that stimulate B cells to produce antibodies against self proteins 

presence of ACPAs alone is not suffi- cient to cause synovitis; an additional hit (for example, immune complex formation, complement activation or microvascular insult) is likely required to initiate clinical synovitis characterized by increased vascular permeability and influx of inflammatory cells into the  synovium 

Early and Established RA : 

Early RA is characterized by synovial inflammation -macrophages ,CD4 T cell and stromal cell activation       

Most data suggest that pathogenetic pathways in the synovium are established early and remain remarkably stable over the ensuing years, although some differences have been reported; early RA is sometimes described as a ‘window of opportunity’ for these reasons.

role of macrophages and fibroblasts in per- petuating synovitis is more prominent in established disease.

PATHOGENESIS:

Rheumatoid arthritis (RA) is a chronic, inflammatory joint disease of autoimmune nature characterized by autoantibodies to immunoglobulin G (IgG; that is, rheumatoid factor (RF)) and citrullinated proteins (that is, anti-citrullinated protein antibodies (ACPAs))

    

1- SYNOVIUM :

Two key pathogenetic changes in the synovium are evident in RA 

First, the intimal lining greatly expands owing to an increase and activation of both synoviocyte types, which are a prominent source of cytokines and proteases. The macrophage-like synovio cytes produce a variety of pro-inflammatory cytokines, including IL-1, IL-6, tumour necrosis factor (TNF) and others. Although FLS express IL-6, their most promin- ent feature is the production of prodigious amounts of MMPs and small-molecule mediators such as prosta- glandins and leukotrienes .

The second change associated with RA is infiltration of adaptive immune cells into the synovial sublining

2- JOINT DAMAGE - 

Damage to cartilage and bone due to synovial invasion into adjacent articular structures is a cardinal sign of RA.

The pathways involved in damage are likely heterogeneous and include distinct mechanisms between individuals who are ACPA pos- itive and those who are ACPA negative and perhaps even those who have other autoantibodies..

Macro- phages, neutrophils (particularly in the synovial fluid space) and mast cells contribute to joint damage via release of cytokines and MMPs. However, the domin- ant destructive cell type for cartilage are considered the cadherin-11-positive FLS-which produce pro- teases, most notably MMPs, such as collagenases and stromelysins 

Bone erosions are most likely due to maturation and activation of osteoclasts 

TREATMENT REGIMENS FOR RA : 

| Disease-modifying antirheumatic drugs for RA

Disease-modifying antirheumatic drugs (DMARDs) are listed per target.

Synthetic DMARDs

Conventional synthetic DMARDs

• Unknown target: methotrexate, sulfasalazine, chloroquine, hydroxychloroquine and gold salts

• Known target: that is, dihydroorotate-dehydrogenase for leflunomide Targeted synthetic DMARDs

• Janus kinase 1 (JAK1) and JAK2: baricitinib • JAK1, JAK2 and JAK3: tofacitinib

Biological DMARDs

Biological originator DMARDs

• Tumour necrosis factor: adalimumab, certolizumab, etanercept, golimumab and infliximab

• IL-6 receptor: tocilizumab and sarilumab

• IL-6a: clazakizumab, olokizumab and sirukumab

• CD80 and CD86 (involved in T cell co-stimulation): abatacept

• CD20 (expressed by B cells): rituximab

Biosimilar DMARDs

B- 75/F with post operative hepatitis following blood transfusion 

1- Given the history patient had a mild allergic reaction - with chills and fever with first transfusion which subsided with avil and hydrocortisone 

Second transfusion reaction was uneventful 

With the 3rd transfusion  patient developed -  non fatal hemolytic transfusion reaction .

Transfusion reactions can be divided into 2 broad categories 

1- Immune mediated —— Immediate and delayed 

2- Non immune mediated —— Immediate and delayed 

Points in favor of hemolytic reaction are 

• Raised bilirubin 
• Increased LDH 
• Fall in hemoglobin 
• Positive Indirect Coombs test 

Treatment approach : 

Main aim is to maintain hemodynamic stability 

Monitor Renal status ,coagulation profile ,LFT 

Main stay of treatment is supportive with Iv fluids 

4-60 year woman with uncontrolled sugars 

http://manojkumar1008.blogspot.com/2020/12/60-yr-old-female-with-uncontrolled.html

Problem representation : 

• Uncontrolled sugars 
• Chest pain 
• AKI 
• RIGHT UPPER LOBE PNEUMONIA 

Factors contributing to her uncontrolled blood sugars 

:

Patient is diagnosed with diabetes 9 months back and used medications for 1 month and stopped .

Non complaince to medications appears to be main cause of her  uncontrolled blood sugars 

 

CXR findings : 

Haziness of right upper zone with air bronchogams 

• consolidation

Approach to hypoalbuminemia : 

It can be due to decreased synthesis —chronic and advanced hepatic cirrhosis 

Increased loss from renal,GIT ,skin,extravascular space 

Increased catabolism 

 

Hypoalbuminemia can either-result from 

1- Acute 

2- chronic disease 

https://www.ncbi.nlm.nih.gov/books/NBK526080/

Albumin is a negative phase reactant -  it’s synthesis is inhibited by pro inflammatory cytokines like IL 6-  

Critical illness causing hypoalbuminemia : 

1- alters the distribution of albumin btw intravascular and extravascular compartments 

2- Affects rate of albumin synthesis ,degradation 

3- rate of synthesis is decreased - due to decreased transcription of albumin mRNA 

Sepsis is associated with increased vascular permeability and capillary leakage resulting  in loss of albumin from the intravascular compartment. Apart from this there is also reduced synthesis and increased catabolism of albumin in the presence of significant sepsis.

Hypoalbuminemia in this patient appears to be multifactorial 

1- due to acute inflammation and ongoing sepsis there is decreased synthesis and increased degradation ,increased vascular permeability leading to loss of albumin into extravascular space 

2- CUE showed albiminuria - With history of uncontrolled sugars - one possibility could be diabetic nephropathy .

5- https://appalaaishwaryareddy.blogspot.com/2020/11/56year-old-male-with-decompensated.html

56 year old man with decompensated liver disease : 

1-1. What is the anatomical and pathological localization of the problem? 

1-Chronic Hepatitis B 

2- Hepatorenal syndrome 

3- refractory hyperklemia 

2- approach and evaluation of patient with Hepatitis B 

Hepatitis B can present as 

1- Acute or 

2- chronic phase

With the given history patient initially had developed acute hepatitis B infection for which he was put on TENOFOVIR and now it progressed to chronic hepatitis 

Risk factors for  progression of  acute to chronic hepatitis 

 Outcomes are related to host (age, male gender, genetic background, immune status) and viral (serum HBV DNA level, HBV genotype, mutation patterns) factors.

Age ,renal failure ,presence of ascites,hyper bilirubin is are corelating independently with survival in patients with HBV related cirrhosis .hence early hepatic decompensation is an indication for antiviral therapy as well as assessment for liver transplanta- tion 

3-Pathogenesis : 

HBV is not a cytopathic virus ,severity of diseased depends n host immune response to virus .

Both cellular and humoral response plays an important role .cellular immunity appears to be principal arm involved in pathogenesis of HBV 

During acute HBV infection, most HBV DNA molecules

are cleared rapidly from the liver via noncytopathic mecha-

nisms mediated by cytokines that are released initially by cells

of the innate immune system and later by liver-infiltrating

HBV-specific CD8+ cells. Cell-mediated immune responses are

efficient in self-limited infection because the responses are

vigorous, multispecific, and oriented toward type 1 helper

T-cell functions. 

Persons with chronic HBV infection, by con-

trast, exhibit infrequent, narrowly focused, and weak HBV-specific T cell functions .In chronic hepatitis most of mononuclear cells infiltrated in liver appears to be non antigenic specific 

Antibody neutralization limits intrahepatic spread of virus during primary infection and serves an important role in preventing reinfection.

natural history of HB infection is divided into 4 phases ; 

Immune tolerance 

Immune clearance 

Inactive carrrier state 

Reactivation 

4- YES there needs to be seggregation of dialysis units for HBV POSITIVE and Negative patients .

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

Dialysis Equipment and BBV infection

• 2.1.
  Machine segregation for patients infected with HBV-We recommend that 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. Healthcare workers dialysing patients with known HBV infection should not dialyse patients without HBV infection at the same time (1A)
• 2.2.
  Precautions for patients with HCV/HIV-We recommend that dedicated machines are not required for patients infected with HCV and HIV, provided cleaning and disinfection procedures are strictly adhered to between patients (KDIGO Hepatitis C guideline 3.1.2) (European Renal Best Practice Guidelines) (1D
• 2.3.
  Utilization of external transducers-We suggest that external transducer protectors on the blood circuit pressure monitoring lines should be inspected by healthcare personnel during and after each dialysis session. If there is evidence of breach by blood or saline then the machine should be taken out of service and machine components that may have come in contact with blood should be replaced or decontaminated by qualified personnel according to a protocol that incorporates the manufacturers’ instructions (2C
• 2.4.
  Disinfection process for dialysis equipment

Rationale

The dialysis process facilitates transmission of BBV due to the considerable potential for exposure to blood. BBV can survive and remain potentially infective on surfaces of clinical equipment through splashes of blood that may not be visible to the naked eye [28, 29]. HCV ribonucleic acid (RNA) has been detected on the hands of nurses dialysing infected patients [30]. Whilst HBV deoxyribonucleic acid (DNA) and HCV RNA have been detected in the dialysate of patients known to have these infections, there is no evidence that the internal fluid pathways offer a viable route for transmission of BBV

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

What is the problem representation of this patient?

1- language difficulty 

2- decline in memory

3- behavioural disturbances 

4-there is also difficulty in executive functions 

5-Dependance on family members 

2- Approach to dementia :

Basic approach is to differentiate between 

1- cortical 

2- subcortical 

3-cortico -subcortical dementia 

The general clinical picture is similar in all primary dementias 

Vital points in diagnosis include :

History taking 

Mode of onset 

Progression 

Fluctuations 

And evolution of disorder 

All cognitive tive -(memor y, language, calculation, perception, spa- tial function and complex executive tasks) and 

behavioral (character change, apathy, disinhibition, mood, hallucinations, delusions, repetitive-stereotypy- ies, obsessive-compulsive behaviours) functions should be explored.

Neurological examination :examination should focus on 

behavior and evaluation of visual attention and orientation, 

myoclonus

, sensory attention and tactile localisation, 

praxis and primitive reflexes 

Neuropsychological Assesment:

Mini mental status examination and MOCA B in this patient shows severe cognitive decline 

The history, neurological signs and patterns of neuropsychological deficits together point to the clin- ical diagnosis in various dementias. The diagnostic process requires pattern recognition and hence famil- iarity with various usual and unusual presentations of the dementias. 

Points in favor for Alzheimer’s disease - based on history ,neuropyschiatric assesment and MRI findings are 

• Earliest symptom was gradual loss of memory -patient was unable to remember his daily activities initially that progressed to inability to remember tools he used for spree weaving,then forgetting his neighbours ,relatives names and their relations 
• Speech difficulty - patient developed slurring of speech -
• On examination comprehension is intact ,but delayed response to commands is observed ,with intact naming, repetition ,impaired fluency 
• Patient is unable to navigate to his own home 
• On examination :there is language impairment  ,visuospatial ,constructional apraxia , lobar examination revealed decline in function of all lobes 
• MRI done 3 months back showed Atrophy of temporal lobe with associated hydrocephalus of temp horn of lateral ventricle .Repeat MRI showed marked cortical atrophy with supratentorial hydrocephalus 

3-

Although patient had chronic ischemic changes -patient never presented with motor deficits or gait disturbances -which would go in favor of Multiinfarct dementia .

Differentiating features include 

1- In vascular dementia - symptoms present are more localized to area of infarcts and chances of global impairment are less unless if it is a multi infarct dementia

2- more impairment in executive functions than cognitive decline 

3- there are non risk factors such  as DM,HTN ,Atherosclerotic changes,Obesity 

Although there can be some overlap between Vascular and Alzheimer’s 

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

Alzheimer’s disease a chronic degenartive disease .2 proposed mechanism are 

1- amyloid cascade pathway -intracellular depositon of neurofibromas year tangles and extracellular deposition of A beta —disruption of calcium homeostasis ,free radical production ,excitotoxicity and inflammation 

2- cholinergic pathway -reduction in acetyl choline and ACHesterase inhibitor -decline in neurotransmission 

Management of Alzheimer’s include :

1. Educating the patient and care giver -educating them regarding nature of disease,progression,available treatment options.The 3 “R's”—repeat, reassure, and redirect—can help caregivers reduce escalating behaviors and limit the need for pharmacologic management.
2. Caring of the caregiver -if they need any assistance ,physical illness 
3. Reducing excess disability and functional impairement -They include social issues, cultural expectations, environmental factors, sensory deficits (hearing and vision), pain, coexisting disease states (e.g., over- or undercorrection of hypothyroidism, vitamin B12 deficiency, etc.), fear of falling, and lack of motivation. 
4. Counseling - regarding safety issues ,long term care placement 
5. End of life care :

Patients with advanced dementia commonly develop difficulty eating, often when they become bedridden and dependent in all activities of daily living . They may resist or be indifferent to food or fail to manage the food bolus properly once it is in the mouth (oral phase dysphagia). In moderately demented patients, prevention of aspiration and weight loss, if possible, may improve mid-term outcome 

Pharmacotherapy includes :

Cholinesterase inhibitors :Four ChEIs have been approved by the U.S. Food and Drug Administration (FDA) for the treatment of mild to moderate AD. They are tacrine, donepezil, rivastigmine, and galantamine. These compounds increase the concentration of acetylcholine and the duration of its action in synapses by inhibiting the degradation of acetylcholine. These compounds provide symptomatic treatments and may also have disease-modifying effects. 

There is also accumulating evidence that ChEIs may improve behavioral and psychological symptoms of AD, such as psychosis and apathy 

8- 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? 

-recurrent seizures 

-Headache 

-weight loss and low grade fever 

Anatomical localization - ring enhancing lesions in right cerebellum 

Pathological localisation -Trauma,tumor ,abscess ,infection 

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

With the background history of weight loss,headache ,alcoholism 

Chronic infection can be suspected :TUBERCULOMA .

It would have been helpful if we have known Retroviral status  

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 variety of opportunistic pathogens including viruses (human herpesvirus-8 and cytomegalovirus), fungi (Cryptococcus, Pneumocystis and Histoplasma) and bacteria (Mycobacterium) are associated with the development of immune reconstitution inflammatory syndrome (IRIS) after initiation of antiretroviral therapy (ART). IRIS presents as one of two forms, characterised by the timing of IRIS diagnosis in relation to the start of ART [3]. Paradoxical IRIS refers to worsening of symptoms secondary to a known opportunistic infection in the setting of the initiation of ART and treatment of the opportunistic infection. The second form is “unmasked” or ART-associated IRIS, in which infection with an opportunistic pathogen is undiagnosed until the initiation of ART.

Clinical manifestations of TB-IRIS include weight loss, fever, lymphadenopathy and worsening of pulmonary symptoms, including development of abscesses, respiratory failure, acute respiratory distress syndrome and death.

IRIS associated with M. avium complex infection usually presents as either focal or diffuse lymphadenitis, occurring typically within 3 months of initiation of ART, and often with suppuration. M. avium complex related IRIS rarely presents as focal pulmonary disease 

Cryptococcosis manifests frequently as a multiorgan disease process, affecting the brain, lungs and skin; and while cryptococcal IRIS usually involves meningeal disease, pulmonary cryptococcal IRIS may present as a pneumonitis, or as cavitary or nodular lesions

Corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful in the management of IRIS.

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

Evaluated the 58/ M with progressive memory loss -read about dementias 

Reviewed literature around HEP B and HEP C 

Got to see a patient with WPW  syndrome -Discussed and read about it . 

Learnt about dosage and adverse effects of Antiepileptic drugs .