VANDANA REDDY

 

December 2020

 1.55 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. Patient presented with right sided hemiparesis with multiple episodes of focal seizure involving right upper limb and lower limb with up rolling of eyes followed by gtcs,lesion might be in left parietal area(cerebral cortex) and seizures due to infarct. 


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

Sub cortical internal capsule infarcts 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 these infarcts are more common than cortical infarcts. 


3.What is the pathogenesis involved in cerebral infarct related seizures?
First few weeks after a stroke, some survivors have seizures — a sign of brain injury caused by sudden disorganized electrical activity.
electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causinga seizure. This electrical disturbance can happen because of stroke damage in the brain.

4. What is your take on the ecg? And do you agree with the treating team on starting the patient on Enoxaparin?

Ventricular ectopics seen
Left axis deviation +
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





2.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? 

A 55 year old male with T2DM & HTN since 10 years 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).


Pulmonary function abnormalities resulting from obesity



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

Question 3

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

In this patient as eular criteria score is 7 for further evauation anticcp antibodies can be send in diff RA from other polyarticular devices as it is ass vth other chronic inflammatory conditions..
it is more specific than RAfactor in diagnosing and may predict erosive disease more effectively.

Radiography of joints : intial finding in RA is PERIARTICULAR OSTEOPENIA. others include symmetric joint space loss,subchondral erosions(mostly seen in wrists and hands).In advanced stages 
signs of sev destruction vth joint sublaxation and collapse..



2. What is the pathogenesis involved in RA?

The complex interaction of immune modulators is responsible for the joint damage that begins at the synovial membrane and covers most IA structures (Fig. 1) [12]. Synovitis is caused by the influx or local activation, or both, of mononuclear cells (including T cells, B cells, plasma cells, dendritic cells, macrophages and mast cells) and by angiogenesis [12]. The synovial lining then becomes hyperplastic, and the synovial membrane expands and forms villi [12]. The osteoclast-rich portion of the synovial membrane, or pannus, destroys bone, whereas enzymes secreted by neutrophils, synoviocytes and chondrocytes degrade cartilage 


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

the intial treatment was conservative and NSAIDS for pain relief for several yrs and only progressing to DMARDS when the dis was not Controlled.
DMARDs possess a slow onset of action, and response to treatment is usually expect- ed between 4-6months.
Sulfasalazine and methotrexate are gener- ally regarded as first line therapies due to their improved efficacy profile (approxi- mately 40 per cent response rates) and high continuation rates compared to the other DMARDs.
Steroids: Systemic corticosteroids have long been used in the management of RA and were the first drugs to result in reversibility of the disease. 
Oral prednisolone can be used to provide temporary relief until a DMARD becomes effective, or in patients with aggressive disease who cannot be ade- quately controlled with a combination of DMARDs (“step-up” or “step-down” approach). 
TNF blockade : at the present time, agents for TNF blockade are only used in patients that are resistant to, or fail conventional disease- modifying treatment 

Question 3b

75 year old woman with post operative hepatitis following blood transfusion
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 hepatitis

As pt is having febrile reaction during 1st transfusion ( feverspikes were present ) repeat lft was not available to rule out whether there is any acute hemolytic reaction.
later during 2nd transfusion post op pt had another febrile reaction vth elevated bilirubin and sr ldh levels.   this could be delayed hemolytic reaction ( indirect coombs test- positive) vth mixed hyperbilirubinemia
pt could be having ischemic hepatitis ( as there is intraop hypotension episode and post op too).
Evaluation:

ABO and Rh compatability
coombs testing 
antibody panel testing

2. What would be your treatment approach? Do you agree with the treatment provided by the treating team and why? What are their efficacies?

Treatment is only supportive management with no role of udiliv as the cause for hepatitis is self resolving with increased about of bilirubin due to destruction of rbc as  substrate for hepatitis.

Lasix & Nebulization : For wheezing and crepts

Lactulose : To prevent hepatic encephalopathy 

Zofer : to stop vomitings

Pantop : To prevent gastritis


Question 4
4) 60 year woman with Uncontrolled sugars

1. What is the problem representation of this patient?
60 yrs woman who is k/c/o htn and diabetic presented vth complaints of chestpain acute onset, location?, radiating, pricking type vth no h/o fever cough cold sob palpitations sweatings. could be due to? lung pathology,? cardiac prob..
 as the xray shows rt upper lobe consolidationit could be due to pulmonary prob.(? rt upper lobe pneumonia).

pt is having uncontrolled sugars diabetis can cause gastroparesis which can affect the normal spontaneous movement of the stomach muscles could be the reason for her constipation.

pt having ?acute renal injury.

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

causes of uncontolled sugars:not using diabetic medications 
                                                    not following diabetic eating plan
                                                    being inactive
                                                    using certain medications ( ex-steroids)
                                                    infections(pneumonia,uti,sepsis,gastroenteritis)
in this patient could be due to infection (?pneumonia)

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?

The potential causes of hypoalbuminemia are many, and include:

Hepatic failure (failure of albumin synthesis)

Gastrointestinal protein loss (protein-losing enteropathy)

 Renal protein loss (protein-losing nephropathies)

Other external losses in exudate or hemorrhage

  Hyperglobulinemia (with a 'compensatory' decrease in albumin production)

  Starvation/protein malnutrition

 Chronic illness

Hypoadrenocorticism

  Laboratory error

the cause in this patient can be attributes to malnutrition or albumin as acute phase reactant


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 preventvomitings - 
  • Question 5
  • 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?

    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?







    3. What is the pathogenesis of the illness due to Hepatitis B?


    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. 

    • 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)
    • Question 6

    • 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) Forgetfulness since 3 months impairing his daily activitiesDeviation of mouth ,leading to slurring of speech and unable to swallow since one month which increased 

      Altered sensorium (delirium) with intact awareness , fluctuations .

      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.


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

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

      Vascular dementia symptoms vary, depending on the part of your brain where blood flow is impaired. Symptoms often overlap with those of other types of dementia, especially Alzheimer's disease dementia.

      Vascular dementia signs and symptoms include:

      • Confusion
      • Trouble paying attention and concentrating
      • Reduced ability to organize thoughts or actions
      • Decline in ability to analyze a situation, develop an effective plan and communicate that plan to others
      • Difficulty deciding what to do next
      • Problems with memory
      • Restlessness and agitation
      • Unsteady gait
      • Sudden or frequent urge to urinate or inability to control passing urine
      • Depression or apathy
      • Sometimes a characteristic pattern of vascular dementia symptoms follows a series of strokes or ministrokes. Changes in your thought processes occur in noticeable steps downward from your previous level of function, unlike the gradual, steady decline that typically occurs in Alzheimer's disease dementia.
      • Multi-Infarct Dementia Information Page | National Institute of ...www.ninds.nih.gov › Disorders › All-Disorders › Multi-I...

      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?
      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
      • Question7

      • 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?

        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
        • Cardiorenal association in different ways
        • Intradialytic hypoglycemia
        • Temporal lobe epilepsy
        • Recurrent CVA and efficacy of carotid artery stunting / end arterectomy as a mode of treatment
        • HFpEF secondary to wet beriberi
        • CKD with HFpEF unresponsive to LASIX - ceiling doses of lasix usage with risk of hearing loss
        • 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
        • Hypertensive urgency management
        • Status epilepticus management
        • Ballismus & chorea
        • Alcohol withdrawal seizures
        • ASD & VSD in 2D ECHO
        • Phenytoin toxicity
        • Essential tremors

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