December bimonthly internal assesment
https://medicinedepartment.blogspot.com/2020/11/blended-bimonthly-assessment-oct-nov.html?m=0
Internal assesment to the questions asked in the above blog spot.
First 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 ?
This 55 year old man has right upper limb and lower limbs weakness suggestive of left cortical or subcortical infarct .
Its an early onset post stroke seizures( within first 24 hours of Stroke) progressing to post stroke epilepsy.
Anatomical site: Brain - left side cortex /sub cortical but patient has post stroke seizures giving a clue of large epileptogenic focus in the brain likey cortex.
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
Subcortical internal capsular infarcts are known as lacunar infarcts.
Lacunar syndromes are clinical manifestations of lacunar infarctions. Lacunar infarctions are defined as small subcortical lesions with a size of less than 15 mm in diameter 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.
an occlusive disease in these penetrating arteries causes a small infarct in the territory that the small vessel supplies. Since collateral circulation in these distant pontine and subcortical areas is so limited, and multiple penetrating vessels are likely affected in these patients,areas of infarct coalesce to form lake-like areas of infarcted/edematous brain tissue.
3. What is the pathogenesis involved in cerebral infarct related seizures?
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.
Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585721/
4. What is your take on the ecg? And do you agree with the treating team on starting the patient on Enoxaparin?
Does he have any chest pain or heart failure? I am not sure of NSTEMI ecg and one of the ecg showed irregular rhythm responsible for ?cardio embolic stroke ( one of the predictable factor of post stroke seizures)
5. Which AED would you prefer?
Carbamazepine is the drug i would prefer as it covers focal and generalised tonic clonic seizures post stroke.
Antiepileptic drugs (AED) remain the mainstay of epilepsy management in all age groups.29,30 Single therapy controls the seizures (in 88% of cases). For both focal (with or without generalised tonic‐clonic) seizures and generalised seizures, the recommended first line AEDs include carbamazepine, lamotrigine, sodium valproate, and toppiramate.30 For carbamazepine there has been shown to be a good correlation between the dose and the plasma concentration. Alternative monotherapy includes phenytoin, Phenobarbital, and clonazepam. Phenytoin is the most commonly used alternative, particularly in older patients.
Question 2) 55 year old man with Recurrent hypoglycemia
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?
Hypoglycemia
Deranged RFT (? ATN urinary sodium 190 and FENA>1%)
Medication history
2. What is the cause for his recurrent hypoglycemia? And how would you evaluate?
Recurrent hypoglycemia secondary to insulin dose with skipped meals
OHA with reduced excretion (increased bioavailability of the drug) secondary to deranged RFT.
Elicit the drug history
Medicated Individual
1. Drugs
Insulin or insulin secretagogue Alcohol
Others
2. Critical illness
Hepatic, renal or cardiac failure Sepsis
Inanition
3. Hormone deficiency Cortisol
Growth hormone
Glucagon and epinephrine (in insulin-deficient diabetes)
4. Non–islet cell tumor (e.g., Mesenchymal tumors)
3. What is the cause for his Dyspnea? What is the reason for his albumin loss?
Albumin loss secondary to proteinuria ? Diabetic nephropathy or HTN causing proteinuria which may also be responsible for dyspnoea
4. What is the pathogenesis involved in hypoglycemia ?
Sulfonylure failure :Clinical factors, such as declining β-cell function, long-standing diabetes, high baseline glucose levels and a high degree of insulin resistance are known to predispose patients to sulfonylurea failure. Along the same lines, sulfonylurea-induced hypoglycemia may result from the duration of sulfonylurea action (e.g., the incidence of hypoglycemia is higher with chlorpropamide and glyburide), mild baseline hyperglycemia, irregular eating patterns, excessive alcohol intake and age.
In terms of drug-metabolizing enzyme polymorphisms, CYP2C9*3(Ile359Leu) and to a lesser extent CYP2C9*2(Arg144Cys), influence the pharmacokinetics of many sulfonylureas [14]. Oral clearance of tolbutamide, glyburide (glibenclamide), glipizide and glimepiride is reduced in patients carrying a CYP2C9*3allele, resulting in decreased clearance and increased plasma drug exposure of most of these agents.
5. Do you agree with the treating team on starting the patient on antibiotics? And why? Mention the efficacies for the treatment given.
Clinically patient has no fever tachycardia
So would have waited to start any antibiotic as TLC counts are also just on upper limit as focus of infection isnt still known.
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?
The pathology of RA is characterized by the infiltration of several inflammatory cells into both the pannus and the joint fluid and by subsequent tissue destruction. Chemokines, as well as other inflammatory mediators, play key roles in the pathogenesis of RA, and the coordinated production of chemokines and proinflammatory cytokines is important in the orchestration of the inflammatory responses observed in patients with RA. Imbalance between pro- and anti-inflammatory cytokine activities favors the induction of autoimmunity, chronic inflammation, and thereby joint damage. Monocytes that are attracted to the RA joint differentiate into macrophages and become activated. These macrophages play a pivotal role in RA because they are numerous in the inflamed synovial membrane and at the cartilage-pannus junction. They activate MHC Class-II (Major Histocompatibility Complex Class-II) molecules and secrete proinflammatory or regulatory cytokines and growth factors like IL-1, IL-2, IL-6, IL-10, IL-13, IL-15, IL-17, IL-18, TNF-Alpha (Tumor Necrosis Factor), GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor), chemokines and chemoattractants
3. What are the treatment regimens for a patient with RA and their efficacies?
Pharmacological Strategies
There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal anti-inflammatory agents (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARDs). NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect. DMARDs include methotrexate, sulfasalazine, leflunomide (Arava®), etanercept (Enbrel®), infliximab (Remicade®), adalimumab (Humira®), certolizumab pegol (Cimzia®), golimumab (Simponi®), abatacept (Orencia®), rituximab (Rituxan®), tocilizumab (Actemra®), anakinra (Kineret®), antimalarials (e.g. Plaquenil®)
Surgical approachSynovectomy is sometimes appropriate for patients with rheumatoid arthritis, though in many patients the relief is only transient. However, an exception is synovectomy of the wrist, which is recommended if intense synovitis is persistent despite medical treatment over 6 to 12 months. Persistent synovitis involving the dorsal compartments of the wrist can lead to extensor tendon sheath rupture resulting in severe disability of hand function.
Total joint arthroplasties, particularly of the knee, hip, wrist, and elbow, are highly successful.
https://www.hopkinsarthritis.org/arthritis-info/rheumatoid-arthritis/ra-treatment/
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?
Hemolytic reaction ( Post transfusion)
DIC secondary to hemolytic transfusion reaction
Ischaemic hepatitis
Flank pain fever tachycardia and Serum LDH raise in indirect bilirubin
fall in hb followed by transfusion suggests a hemolytic reaction
Thrombocytepenia deranged coagulation profile gives a clue of DIC
Post op raise in AST ALT followed by hypotension gives a clue of ishchaemic hepatitis
2. What would be your treatment approach? Do you agree with the treatment provided by the treating team and why? What are their efficacies?
IVF for treating hypovolemia.
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?
Uncontrolled sugars with diabetes
Hypertension
Right upper lobe pneumonia
Acute kidney injury
2. What are the factors contributing to her uncontrolled blood sugars?
The factors being The ongoing infection in the upper lobe of lung , the drug dosage and food intake and increased serum creatinine.
3. What are the chest xray findings?
Homogenous opacity of the right upper lobe : Right upper lobar consolidation ( treacheal displacement , fissural displacement) increased space between the ribs with overinflation of the other hemithorax.
4. What do you think is the cause for her hypoalbuminaemia? How would you approach it?
One of the causes of hypoalbuminemia is the ongoing proteinuria secondary to hypertesnion and diabetes
And albumin being a negative phase reactant there was hypoalbuminemia secondary to ongoing infection.
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?
Anatomical localisation is Liver hepatocytes which undergo inflammation secondary to chronic undergoing HBV infection and on top of that alcohol acts as a contributive factor for further fastening of the inflammation.
Pathological localisation is due to the ineffective adaptive and humoral immunity causing for further progression of the disease.
2. How do you approach and evaluate this patient with Hepatitis B?
Laboratory tests on the initial visit
should include a chemistry panel of serum enzymes, direct and total bilirubin, albumin, total protein and creatinine, complete blood count, coagulation tests and alpha-fetoprotein. HBV markers including HBsAg, hepatitis B e antigen (HBeAg) and antibody (anti-HBe) and HBV DNA will confirm the diagnosis and help determine the phase of disease
HBV DNA levels are very important to know the replicative phase of the disease.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881483/
3. What is the pathogenesis of the illness due to Hepatitis B?
The pathogenetic and antiviral potential of the cytotoxic T lymphocyte (CTL) response to HBV has been proven by the induction of a severe necroinflammatory liver disease following the adoptive transfer of HBsAg specific CTL into HBV transgenic mice. Remarkably, the CTLs also purge HBV replicative intermediates from the liver by secreting type 1 inflammatory cytokines thereby limiting virus spread to uninfected cells and reducing the degree of immunopathology required to terminate the infection.
Persistent HBV infection is characterized by a weak adaptive immune response, thought to be due to inefficient CD4+ T cell priming early in the infection and subsequent development of a quantitatively and qualitatively ineffective CD8+ T cell response. Other factors that could contribute to viral persistence are immunological tolerance, mutational epitope inactivation, T cell receptor antagonism, incomplete down-regulation of viral replication and infection of immunologically privileged tissues. However, these pathways become apparent only in the setting of an ineffective immune response which is, therefore, the fundamental underlying cause. Persistent infection is characterized by chronic liver cell injury, regeneration, inflammation, widespread DNA damage, and insertional deregulation of cellular growth control genes which, collectively, lead to cirrhosis of the liver and hepatocellular carcinoma.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2888709/
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
Therefore as per this study, the patients are segregated due to the shortcomings of proper maintenance in our setup
https://www.hepatitisbannual.org/article.asp?issn=0972-9747;year=2006;volume=3;issue=1;spage=76;epage=105;aulast=Wong
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?
Current problem: forgetfulness since 3 months impairing his daily activities as well
Deviation of mouth ,leading to slurring of speech and unable to swallow since one month which increased
Altered sensorium (delirium) with intact awareness , fluctuations
Slurring of speech since 6 months , deviation of mouth to right side associated with
Drooling of saliva from left angle of mouth, food particles and water predominantly from left angle of mouth and smacking of lips
Urinary incontinence since 6 months, dribbling of urine while rushing to bathroom.
Forgetfulness since 3 months
2. How would you evaluate further this patient with Dementia?
Three major issues should be kept at the forefront: (1) What is the best fit for a clinical diagnosis? (2) What component of the demen-tia syndrome is treatable or reversible? (3) Can the physician help to alleviate the burden on caregivers? A broad overview of the approach to dementia is shown in Table 25-3. The major degenera-tive dementias can usually be distinguished by the initial symptoms; neuropsychological, neuropsychiatric, and neurologic findings; and neuroimaging features (Table 25-4).
PHYSICAL AND NEUROLOGIC EXAMINATIONA thorough general and neurologic examination is essential to doc-ument dementia, to look for other signs of nervous system involve-ment, and to search for clues suggesting a systemic disease that might be responsible for the cognitive disorder. Typical AD spares motor systems until later in the course. In contrast, FTD patients often develop axial rigidity, supranuclear gaze palsy, or a motor neuron disease reminiscent of amyotrophic lateral sclerosis (ALS). In DLB, the initial symptoms may include the new onset of a parkin-sonian syndrome (resting tremor, cogwheel rigidity, bradykinesia, festinating gait), but DLB often starts with visual hallucinations or dementia. Symptoms referable to the lower brainstem (RBD, gastro-intestinal or autonomic problems) may arise years or even decades before parkinsonism or dementia. Corticobasal syndrome (CBS) features asymmetric akinesia and rigidity, dystonia, myoclonus, alien limb phenomena, pyramidal signs, and prefrontal deficits such as nonfluent aphasia with or without motor speech impairment, executive dysfunction, apraxia, or a behavioral disorder. Progressive supranuclear palsy (PSP) is associated with unexplained falls, axial rigidity, dysphagia, and vertical gaze deficits. CJD is suggested by the presence of diffuse rigidity, an akinetic-mute state, and promi-nent, often startle-sensitive myoclonus.
3. Do you think his dementia could be explained by chronic infarcts?
Other concurrent factors, which are not yet fully understood, could be hypothesized as follows: a decrease of blood flow in the white matter of normal elderly subjects,27 the decrease possibly enhanced in patients with vascular risk factors; so-called incomplete white matter infarcts30; the occurrence of subsequent lacunar or large infarcts; the site of the lesion, perhaps of more relevance than its volume1831-34; the degree of cerebral atrophy18; and corticosubcortical disconnections in thalamo- and striato-cortical pathways.
https://documentcloud.adobe.com/link/review?uri=urn:aaid:scds:US:e999cbad-a49f-4d17-ae4d-7b64e30a99e7
4. What is the likely pathogenesis of this patient's dementia?
Pathophysiology depends on the type of dementia presentation as stated below.
(
https://www.researchgate.net/publication/333733171_Dementia_prevalence_and_pathophysiology
The gross pathologic hallmark of FTLD is a focal atrophy of frontal, insular, and/or temporal cortex, which can be visualized with neuroimaging studies (Fig. 424-1) and is often profound at autopsy. Despite the appearance of advanced disease, however, imaging studies suggest that atrophy often begins focally in one hemisphere before spreading to anatomically interconnected cortical and subcortical regions. Loss of cortical serotonergic innervation is seen in many patients. In contrast to AD, the cholinergic system is relatively spared in FTD, which accounts for the poor efficacy of acetylcholinesterase inhibitors in this group. Although early studies suggested that 15–30% of patients with FTD showed underlying AD at autopsy, progressive refinement in clinical diagnosis has improved pathologic prediction accuracy, and most patients diagnosed with FTD at a dementia clinic with expertise in FTD will show underlying FTLD pathology. Microscopic findings seen across all patients with FTLD include gliosis, microvacuolation, and neuronal loss, but the disease is subtyped according to the protein composition of neuronal and glial inclusions, which contain either tau or TDP-43 in ~90% of patients, with the remaining ~10% showing inclusions containing FUS
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
https://pubmed.ncbi.nlm.nih.gov/9443470/
Q. 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?
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).
since the cd4 count is above 300,
the patient is currently started on att for 6 months and then planned for art
Q 8) Please mention your individual learning experiences from this month.
As i am posted in casuality as DMO
I got to see paracetamol poisoing and whole bowel irrigation
Sleeping pills( Tab Alprazolam) poisoning and flumazenil( BZD antidote) administration
RTA with EDH SDH and intraparenchymal haemorrhage
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