1) A 55 year old man with Recurrent Focal Seizures
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) 55 year old man presented with the complaints of Unable to move his right upper limb yesterday recurrent episodes of seizures he suddenly started complaining that he couldn’t move his right upper limb few minutes later he developed a sudden onset, tonic clonic seizures involving his right upper limb and lower limb lasting for 2 minutes following which he had another 8 episodes of focal seizures involving his right upper limb and right lower limb with a 2 minutes of gap between each episode. During these episodes he had uprolling of eyes and wasn’t followed by froth discharge from mouth or tongue bite or any involuntary micturation. He was in postictal confusion lasting for 40 minutes. Recurrent episodes of seizures secondary to ?infarcts chronic alcoholic and smoker with K/c/of DM2
2. Why are subcortical internal capsular infarcts more common that cortical infarcts?
A)The internal capsule, a white matter structure, is a unique location where a large number of motor and sensory fibers travel to and from the cortex. Damage of any kind in this location will cause some relatively unique findings that can allow you to localize the lesions to the internal capule by exam aloneThe internal capsule is one of the subcortical structures of the brain.Subcortical structures: internal capsule, caudate, putamen, globus pallidus, thalamus, brainstemThe anterior limb of the internal capsule separates the caudate nucleus and lenticular nucleus .The posterior limb separates the thalamus and lenticular nucleus.Small lacunar infarctions (between 3 mm and 7 mm) is lipohyalinosis of the small perforating arteries feeding deep subcortical structures. Another mechanism is micro-atheroma formation at the origin of penetrating arteries from major cerebral arteries like the middle cerebral artery, Circle of Willis, or the distal basilar artery. These first two mechanisms are proven pathologically and likely due to chronic hypertension and resulting in small vessel disease.If the size of lacune is larger than 5 to 7 mm, it is often not caused by occlusion of 1 or 2 lenticulostriate arter toial branches but from an atherothrombotic lesion involving the mainstem middle cerebral artery. These infarcts are named striatocapsular infarcts by Bladin and Berkovic.Other proposed mechanisms that have been failed to be proven pathologically include tiny emboli causing obstruction and cerebral arteriolar and capillary endothelial dysfunction leading to small vessel disease as a result of extravasation of blood products.Out of all the causes of Lacunar strokes, hypertension is the most common modifiable risk factor for stroke. For every 10mm hg decrease in blood pressure, there is a 1/3rd lowering of stroke risk in primary prevention. So it is extremely important to control the blood pressure effectively to prevent future strokes. Cigarette smoking doubles stroke risk.
https://www.ncbi.nlm.nih.gov/books/NBK534206/
3. What is the pathogenesis involved in cerebral infarct related seizures
A) https://www.ahajournals.org/doi/full/10.1161/01.str.0000130989.17100.964 .
4)What is your take on the ecg? And do you agree with the treating team on starting the patient on Enoxaparin?
A)ST depressions noted in precordial leads V1 to V6:NSTEMI. Yes I agree with treating team
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1994029/
5.) Which AED would you prefer?
In elderly pts complex partial seziures vthout sec generalization are more common.
Antiepileptic drugs (AEDs) with fewer adverse effects, including cognitive effects, and AEDs without significant pharmacokinetic drug interactions are neede as LEVIPILL has high efficacy,no drug interactions.no cognitive effects,broad spectrum it is useful.pt is having recurrent episodes of focal seziures levipill dose was inc. but dose adjustment has to be made according to renal clearence.pt is still having seziure episode tab carbamazepine was useful high efficacy. as pt gfr was reduced levipill dose has to be tappered and pt to be kept on tab carbamazepine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6706648/.
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
1)Whathat is the problem representation for this patient?
A)sob on exertion since three days progresseive symptoms of hypoglycemia( giddiness , sweating) refractory to dextrose infusion for 2 days secondary to aki ?renal -acute tubular necrosis (non oliguric) with k/c/of HTN(Telma Am 40/2.5) and DM2 (Glimi M1 od and mixtard 30/70 20 units od )since 10 yearsc
cough since 3 days not associated with sputum
2). What is the cause for his recurrent hypoglycemia? And how would you evaluate?
A)cause for recurrent hypoglycemia is due to renal failure failure to excrete the metabolites of glimipride and increases its action of time
creatinine clearance 33ml/mine
egfris 26.2ml/min/1.73m2
https://www.researchgate.net/publication/277355347_Hypoglycemia_in_Patients_with_Diabetes_and_Renal_Disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470208/.
Hypoglycemia risk is increased as a consequence of accumulation of the sulfonylurea and/or its active metabolites and their long duration of action [74]. Glibenclamide (glyburide) and its two active metabolites (M1 and M2) are cleared by the kidneys. Its use is not recommended for people with eGFRs < 60 mL/min/1.73 m2 [65,69,70]. Glimepiride and gliclazide can be used with caution in people with mild-moderate renal insufficiency, and dose reduction is usually necessary especially when eGFR is <30 mL/min/1.73 m2; however, it is recommended to consider alternative agents in people with moderate-severe renal insufficiency specifically when eGFR is <15 mL/min/1.73
evaluating the kidney function
renal function test-urea creatinin
ultrasound-size of the kidneys and rpd change
cue-albuminuria
24hour urinary protein-quantification of proteinuri
gylcemic control:
fbs,plbs,hba1c
joslin's Diabetes mellitus pg no 1163
Q). What is the cause for his Dyspnea? What is the reason for his albumin loss?
A)As the patient is morbid obese it may be the cause for his dyspnea
Diabetic nephropathy is the cause of Albunuria and spot protein creatinine ratio more than 1 suggest the renal failure
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
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?
Rheumatoid arthritis
A) (RA) is a chronic systemic inflammatory disease of the connective tissue preferentially involving joints. It is considered an autoimmune disease. Autoantibodies against immunoglobulins, so called rheumatoid factors, are detected in 80% of the patients. The etiology of the disease is unknown. An interesting association to different HLA types is observed. An overview about pathology and pathogenesis of the arthritis is given. After an initial vasculitis the synovial membrane is colonised by T and B cells. Among the more frequent T cells more CD4+ cells than CD8+ cells are found. Additionally activated cytotoxic T cells and NK cells are present. Migration of the lymphocytes is realised by adhesion molecules. By homing of lymphocytes the synovial membrane is structurally transformed an appears morphologically like a secondary immunoorgan. Enhanced pathogenic humoral and cellular immune responses are going on influenced by activated CD4+ cells associated with macrophages via MHC class II molecules. Rheumatoid factors and antibodies against type II collagen are produced, cytotoxic immune complexes are formed. Cellular interactions induce the expression of proinflammatory cytokines and growth factors, the so called pannus is formed. Aggressiveness of the pannus depends on the HLA pattern. T cell rich synovial tissue is positive for HLA-DR4 in 70% of the cases. Only 15% of B cell rich membranes show this HLA type. The T cell rich type shows a high aggressiveness. Pannus destroys articular cartilage and subchondral bone. Cells at the invasion site of the pannus are classified differently. The majority of the investigators characterizes them as macrophages others as activated fibroblasts. The latter opinion is supported by experiments done in SCID mice. RA is characterized by three pathogenic mechanisms: 1. chronic inflammation of the synovial membrane, 2. enhanced pathogenic T and B cell dependent immunoreactions including autoimmune phenomenons, 3. hyperplasia of synovial tissue. Which mechanisms is on the beginning and induces the others consecutively is an open question. Macrophages and CD4+ cells associated via MHC class II molecules play a central role in the pathogenesis of RA.
3. What are the treatment regimens for a patient with RA and their efficacies?
A)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
https://www.pharmaceutical-journal.com/download?ac=1064598&firstPass=false
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678427/
-Post transfusion delayed hemolytic reaction
Evaluation:
ABO and Rh compatability
coombs testing
antibody panel testing
-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
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?
A) Infection and hba1c 8 shows poor sugar control
Q)What are the chest xray findings?
A) R upper lobe shows bulging fissure sign suggestive of consolidation
Q)What do you think is the cause for her hypoalbuminaemia? How would you approach it?
A)She is losing albumin in urine
Decrease synthesis from liver may be due to nutritional cause
Infection and inflammation acts as low albumin production 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
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?
evaluation of hep b:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881483/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2881483/
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.
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).
Lasix : for fluid overload (AKI on CKD) https://www.ncbi.nlm.nih.gov/books/NBK499921/#:~:text=The%20Food%20and%20Drug%20Administration,failure%20including%20the%20nephrotic%20syndrome.
Vitamin -k : for ? Deranged coagulation profile (PT , INR & APTT reports not available)
Pantop : for gastritis
Zofer : to prevent vomitings
Monocef (ceftriaxone)
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?
A 58 year old weaver occasional alcoholic c/o 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?
https://www.aafp.org/afp/2011/1015/p895.html
Risk factors for dementia include age, family history of dementia, apolipoprotein E4 genotype, cardiovascular comorbidities, chronic anticholinergic use, and lower educational level.8–10 The greatest risk factor for dementia is increasing age. In persons 71 to 79 years of age, the prevalence is approximately 5 percent, increasing to 37 percent in persons older than 90 years.5 Having a college education has been shown to delay cognitive dysfunction by two years, compared with having less education.10 The presence of the apolipoprotein E4 genotype can increase the risk of dementia two- to 10-fold, and chronic anticholinergic use is associated with a somewhat increased risk (hazard ratio = 1.65).5,9
When dementia is suspected, physicians should obtain a history from the patient and from a family member or caregiver, because patients with dementia often do not have insight into their deficits. The history should include specifics of cognitive deficit, time of onset, and speed of progression. It is imperative to assess the extent of impairment in instrumental activities of daily living, which include managing money and medications, shopping, housekeeping, cooking, and transportation. In the early stages of dementia, instrumental activities of daily living that require calculation and planning, such as balancing a check-book or filling a pillbox, are often the first to become impaired. Basic activities of daily living, such as dressing, eating, toileting, and grooming, are generally intact in early dementia and do not become impaired until later in the disease progression.
Other notable indicators of dementia include a history of visual hallucinations in patients who have dementia with Lewy bodies, inappropriate disinhibition in patients with frontotemporal dementia, classic symptoms of Parkinson disease in patients with Parkinson-related dementia, and alcohol abuse in patients with alcoholic dementia. Psychoactive drugs, such as benzodiazepines, can cause confusion in older persons. Hypothyroidism and depression commonly cause cognitive impairment, and patients should be screened for signs and symptoms, such as weight change, sleep disturbance, and mood instability. In patients with recent hospitalization or underlying psychiatric disorder, delirium should be considered. Finally, educational level and native language should be assessed, because these can influence scores on several cognitive tests.
Although the physical examination is not usually affected in patients with Alzheimer disease, abnormalities can give clues about less common types of dementia. Focal deficits from a previous stroke are common in patients with vascular dementia. Parkinsonism is seen in patients during the later stages of dementia with Lewy bodies. Table 1 lists key findings from the patient history and physical examination that may accompany cognitive dysfunction, and the suggested diagnose
3. Do you think his dementia could be explained by chronic infarcts?
https://www.ahajournals.org/doi/full/10.1161/01.str.0000130989.17100.96
4. What is the likely pathogenesis of this patient's dementia?
https://www.sciencedirect.com/science/article/pii/S0074774209004085
The pathogenesis of dementia of the Alzheimer's type (DAT) remains elusive. The neurodegeneration occurring in this disease has been traditionally believed to be the result of toxicity caused by the accumulation of insoluble amyloid-beta 42 (AB) aggregates, however recent research questions this thesis and has suggested other more convincing cellular and molecular mechanisms. Dysfunction of amyloid precursor protein metabolism, AB generation/aggregation and/or degredation/clearance, tau metabolism, protein trafficking, signal transduction, heavy metal homeostasis, acetylcholine and cholesterol metabolism, have all been implicated etiologically especially as to production of neurotoxic by-products occurring as a result of a specific process derangement. In this paper, these and other research directions are discussed as well as their implications for future therapies. The relationship of the proposed abnormal molecular and cellular processes to underlying genetic mutations is also scrutinized, all in an attempt to stimulate further insight into the pathogenesis of, and thus therapeutics for this increasingly prevalent disease.
[12/18, 7:40 AM] Cs: (AD) is a genetically complex disease whose pathogenesis is largely influenced by genetic factors. Three decades of intensive research have yielded four established AD genes (APP, PSEN1, PSEN2, APOE), and hundreds of potential susceptibility loci, none of which has been unequivocally shown to modify disease risk using conventional methodologies. The results of genome‐wide association studies (GWAS) are now adding to an already vast and complicated body of data. To facilitate the evaluation and interpretation of these findings, we have recently created a database for genetic association studies in AD (“AlzGene”; available at http://www.alzgene.org). In addition to systematically screening and summarizing the scientific literature for eligible studies, AlzGene provides the results of allele‐based meta‐analyses for all polymorphisms with sufficient genotype data. Currently, these meta‐analyses highlight over 20 different potential AD genes, several of which were originally implicated by a GWAS. First follow‐up analyses in a large collection of over 1300 AD families reveal that—in addition to APOE—genetic variants in ACE, CHRNB2, GAB2, and TF show the most consistent risk effects across a wide range of independent samples and study designs. The chapter highlights these and other promising findings from the recent AD genetics literature and provides an overview of the powerful new tools aiding researchers today to unravel the genetic underpinnings of this devastating disease.
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:
- 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 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?
https://www.ncbi.nlm.nih.gov/pmc/articals/PMC3221202/ A) Major criteria :
1)Atypical presentation of “opportunistic infections (OI) or tumors” in patients responding to antiretroviral therapy.
2)Decrease in plasma HIV RNA level by at least 1 log10copies/mL.
Minor criteria:
1)Increased blood CD4+ T-cell count after HAART.
2)Increase in immune response specific to the relevant pathogen, e.g. DTH response to mycobacterial antigens.
3)Spontaneous resolution of disease without specific antimicrobial therapy or tumor chemotherapy with continuation of antiretroviral therapy.
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 reconstitution2)Types of aphasia
Learning points for December 1) atriall fibrillatio 2)types of aphasia
3 ) IgG4 related disease
4) Efficacy of steroids in IgG4 related disease
5) correction of hyponatremia
6) Pregnancy associated Budd Chiari syndrome
7) Assess the postfrondial sugars and when to start OHA or increase the insulin dose
8)Ring enhancing lesions on MRI
9) Transfusion induced relations
10) Recurrent CVA and efficacy of carotid end arterectomy
11) Approch to patient with massive pulmonary odema with daily dialysis (CRRT)
12) Albumin as negative phase reactant in inflammation
13) Hypoglycemia in renal failure
14) Thiamine action in treatment of wet beri beri
15) Maximum doses and infusion rates of ionotrophs
16). 6 mins walk test
17) cardiac Murmurs inflammatory syndrome (IRIS).
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