Bimonthly Assignment

 ) A 55 year old man with Recurrent Focal Seizures


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

A 55 year old male , with Type 2 Diabetes mellitus who is a chronic alcoholic & smoker came with c/o weakness of right upper limb with involuntary movements of both right upper and lower limbs .
The anatomical site of lesion may be internal capsule(left sided) as it is the most common site for lacunar infarcts,also presents as hemiparesis.

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

subcortical infarcts are more common as the penetrating artery supplying this region are prone to occlusion because of its small diameter.They usually arise 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?



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 is present
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 Type 2 Diabetes mellitus and Hypertension since 10 years came with c/o 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? 

It may probably be Drug induced hypoglycemia because kidney failure (increased duration of action of OHA due to decreased excretion)
Factitious (or factitial) hypoglycemia occurs secondary to the surreptitious use of insulin or insulin secretagogues (sulfonylureas, meglitinides). 

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

DYSPNEA:

There is blunting of coastophrenic angle,suggestive of Collection of fluid(pleural effusion,left sided)
Also the pt is obese suppresing the movements of chest wall
Collection of ascitic fluid in the abdomen may also push the diaphragm upwards,reducing the volume of thoracic cavity.
He may also be having metabolic acidosis,leading to hyper ventilation.
Hypoalbuminemia may be because of renal excretion of albumin .Spot protein creatinine ratio > 1 --- albuminuria .
4. What is the pathogenesis involved in hypoglycemia ?

Hypoglycemia in diabetes patients





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)
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

1.What are your differentials for this patient and how would you evaluate?

-Post transfusion delayed hemolytic reaction

Evaluation:

ABO and Rh incompatability
Non ABO,Rh incompatibility
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 crepitations and wheezing
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

1. What is the problem representation of this patient?

A 60 year old female with T2DM & HTN since 2 years 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?




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
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)
Organ damage(liver) due to sepsis leading to decreased albumin production
Approach to hypoalbuminemia:



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

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?
Treatment for acute hepatitis B infection
If   hepatitis B infection is acute —  rest, proper nutrition and plenty of fluids is recommended while your body fights the infection. In severe cases, antiviral drugs or a hospital stay is needed to prevent complications.

Treatment for chronic hepatitis B infection
Most people diagnosed with chronic hepatitis B infection need treatment for the rest of their lives. Treatment helps reduce the risk of liver disease and prevents you from passing the infection to others. Treatment for chronic hepatitis B may include:

Antiviral medications. Several antiviral medications — including entecavir (Baraclude), tenofovir (Viread), lamivudine (Epivir), adefovir (Hepsera) and telbivudine (Tyzeka) — can help fight the virus and slow its ability to damage your liver. These drugs are taken by mouth. 
Interferon injections. Interferon alfa-2b (Intron A) is a man-made version of a substance produced by the body to fight infection. It's used mainly for young people with hepatitis B who wish to avoid long-term treatment or women who might want to get pregnant within a few years, after completing a finite course of therapy. Interferon should not be used during pregnancy. Side effects may include nausea, vomiting, difficulty breathing and depression.
Liver transplant is a final resort.

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.

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).
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

1. What is the problem representation of this patient?

A 58 year old weaver occasional alcoholic with complaints of 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?
these are some of the questionnaires for evaluation of dementia



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

Yes 

NeuroImaging of a pt with multi infarct dementia


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



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

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 who is a 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 Upper and lower limbs with LOC for 5 min1 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?

Metastasis
Abcess
Glioblastoma
Infarct subacute
Contusion
Demyelination
Radiation necrosis


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.

How to interpret an ABG and ECG
I learned about the antihypertensives and antidiabetic a commonly used in clinical settings and their dosages
Transfusion reactions


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