PRE FINAL PRACTICAL (45 year old male with giddiness) LONG CASE

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) 55yr old man, maestri by occupation who is an alcoholic(30yr's),diabetic(5yr's) has GTCS for 2min followed by multiple episodes of Focal seizures of right upper limb and right lower limb with uprolling of eye balls and post ictal confusion

Anatomical site:Left front parietal cortex

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

ANS)The blood supply of the internal capsule is variable but is commonly from small perforating branches of the middle cerebral artery and anterior cerebral artery. These include the lateral lenticulostriate arteries and the recurrent artery of Heubner respectively .

An internal capsule stroke is caused by interruption of blood supply in the middle cerebral artery (MCA) or one of its small branches. ... It may also be caused by a thrombotic blood clot developing within one of the small arteries that supply oxygen-rich blood to the internal capsule.

These penetrating arteries arise at sharp angles from major vessels and are thus, anatomically prone to constriction and occlusion.Bcz of these subcortical internal capsular infarcts more common that cortical infarcts

3.

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

Cerebrovascular diseases, including stroke, are viewed as the most common cause of epilepsy in the elderly population, accounting for 30%-50% of the newly diagnosed cases of epilepsy cases in this age group.

Post-stroke seizures (PSS) have been classified as occurring immediately before, immediately after (24 hours), or of early or late onset. Early-onset seizures are considered to be provoked seizures, which occurred within 1 week  or 2 weeks  after stroke and caused by the acute metabolic and physiological derangement associated with acute infarction. Late-onset seizures after 2 weeks of stroke are considered to be unprovoked seizures that originate from the areas of partially injured brain where neuronal networks have undergone anatomical and physiological alterations, predisposing them to hyperexcitability and synchronization .

ATHOPHYSIOLOGY:

Neurotransmitter amino acids play an important role in the pathogenesis and development of epilepsy [. Increased concentration of the excitatory neurotransmitter glutamate (Glu), the disturbance of electrolyte balance, the destruction of phospholipid membranes, and the secretion of free fatty acids have been documented in the penumbral areas in the acute post-ischemic stroke phase.

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

Left axis deviation +

Ventricular ectopics seen

ST depressions noted in precordial leads V1 to V6

NSTEMI

Enoxheparin usage has variable outcomes and it's use is controversial

5. Which AED would you prefer?

If so why?

 Antiepileptic drugs (AEDs) with fewer adverse effects, including cognitive effects, and AEDs without significant pharmacokinetic drug interactions are needed

6.Question 2) 55 year old man with Recurrent hypoglycemia

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

Questions:

1. What is the problem representation for this patient? 

1)55yrs old man presented vtha) hypoglycemic episodes ? sec to drug induced                                               b)hypoalbunemia ?sec to renal failure (spot protein/creat ratio 3.19) 24hrs urine protein not available? as diabetic nephropathy is leading cause for renal failure.                                                                                   c)anemia(hb 9.7)

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)

Glimepiride is metabolized by the liver to two major metabolites each of which has hypoglycemic activity. In renal disease these metabolites summed. Although the half-life is 5-7 h, the drug can cause severe hypoglycemia that lasts more than 24hrs. along vth insulin clearence is reduced.

Approach to drug induced hypoglycaemia

Practical Approaches to Diagnosing, Treating and Preventing ...www.ncbi.nlm.nih.gov › pmc › articles › PMC5688990

3. What is the cause for his Dyspnea? What is the reason for his albumin loss?

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).

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.

There is no signs of sepsis,  and hence use of antibiotics is not necessary.

        QUESTION-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?

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

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

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 prevent vomitings

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?

according to history anatomical localisation was liver involvement as pt was diagnosed to have 

HEP B since 2yrs. and he is k/c/o alcoholic due to which pt has chronic liver failure leading 

to ascites,portal htn, jaundice, hypoalbunemia, gi bleeds, 

 pt has renal failure could be due to hepb virus infection.

These viral components will typically get attacked by your antibodies in an attempt to fight the infection. Once this happens, the antibodies will bind with the virus, and the resultant debris will get deposited in the kidney. It can then set off an inflammatory reaction, which could cause kidney damage. 

it could cause either PAN/MPGN/HEPATORENAL SYNDROME

In this pt could be? hepatorenal syndrome( cue not vaialable? to rule out glomerular injury causing albuminuria,hematuria)

2. How do you approach and evaluate this patient with Hepatitis B?Laboratory evaluation of hepatitis B disease generally consists of liver enzyme tests, including levels of alanine aminotransferase (ALT) and/or aspartate aminotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transpeptidase (GGT), as well as liver function tests (LFTs) that include total and direct serum bilirubin, albumin, and the measurement of the international normalized ratio (INR).Hematologic and coagulation studies also include a platelet count and a complete blood count (CBC). Ammonia levels may be obtained, but the results often create diagnostic confusion in clinicians. 

Serologic tests for hepatitis B surface antigen (HBsAg) and hepatitis B core antibody (anti-HBc) immunoglobulin M (IgM) are required for the diagnosis of acute hepatitis B virus (HBV). HBsAg is positive in both acute and chronic HBV infection; however, the presence of IgM anti-HBc is diagnostic of acute or recently acquired infection.Antibody to HBsAg (anti-HBs) is produced after a resolved infection and is the only HBV antibody marker present after vaccination. The presence of HBsAg and total anti-HBc, with a negative test for IgM anti-HBc, indicates chronic HBV infection; the absence of IgM anti-HBc or the persistence of HBsAg for 6 months indicates chronic HBV infection. The presence of anti-HBc alone might indicate acute, resolved, or chronic infection or a false-positive result. 

A positive result suggests not only the likelihood of active hepatitis but also that the disease is much more infectious, as the virus is actively replicating. 

HBV DNA testing is also recommended when occult HBV is suspected (positive anti-HBc and negative antibody to HBsAg [anti-HBs] and HBsAg) or in cases in which all of the serologic tests are negative.

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

The pathogenesis and clinical manifestations of hepatitis B are due to the interaction of the virus and the host immune system, which leads to liver injury and, potentially, cirrhosis and hepatocellular carcinoma.

Hepatitis B: Practice Essentials, Background, Pathophysiologyemedicine.medscape.com › article › 177632-overview

4. Is it necessary to have a separate haemodialysis set up for hepatits B patients and why?

It could remain viable for at least 7 days on environmental surfaces at room temperature.[12] Being a blood handling procedure, hemodialysis, therefore, poses an exceptional risk to dialysis patients as well as clinical staff in terms of nosocomial transmission of HBV. The patients could acquire the infection through injections of contaminated material, having mucosal membrane or breached skin exposed to infective material or being dialyzed with contaminated equipment

HBV DNA had been detected even in the dialysate and ultrafiltrate of those HBsAg positive undergoing high-flux hemodialysis, 

There should be no sharing of supplies, vials, medications, instruments and even ancillary items such as clamps, scissors, blood pressure cuffs and other non-disposable items. Previous studies, indeed, showed that non-separation of infected from non-infected patients was associated with an increased risk of infection while segregation has been shown to be effective

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.

Lasix : for fluid overload (AKI on CKD)

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

QUESTION-7

7) 22 year old man with seizures

Case report  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 antiretroviral therapy in HIV-infected patients is defined as immune reconstitution inflammatory syndrome (IRIS).

BHIVA has issued guidelines[11] for starting the TB treatment with HAART. If CD4+ count is less than 100 cells/μl, both anti-tuberculosis drugs and HAART can be started together. If CD4+ cells are in the range of 100-200; HAART is started 2 months after starting TB treatment. If the CD4+ cells are above 200, HAART is started 6 months after completing TB treatment.