December online assessment

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:Problem statement

Rights monoplegia of upperlimb-which is sudden onset

with rt sided focal seizures with progression to secondary generalisation which was refractory to medical treatment for 2 days 

uncontrolled sugars

anatomical localisation of right sided focal seizures with secondary generalisation

https://www.epilepsy.com/living-epilepsy/epilepsy-and/professional-health-care-providers/co-existing-disorders/brain-tumors-1

Anatomic location and General characteristics of seizures:

Frontal lobe :  Usuallyoccur several times per day, short in duration, during sleep. Complex gestural automatisms common at onset. Tonic/postural manifestations prominent.

Occipital lobe:Usually simple partial and secondarily generalized seizures. Initial signs can include tonic/clonic contraversion of eyes, head, or both; palpebral jerks; and forced closure of eyelids.Most commonly, but not always, include visual symptoms that are contralateral to cortex: Positive visual manifestations include sparks, flashes, and phosphenes (more common). Negative visual manifestations include scotoma, hemianopsia, and amaurosis.

Parietal lobe : mostly partial but can secondarily generalize.In the dominant parietal lobe, language is often involved. Most frequently involve hand, arm, and face with predominantly sensory features:Positive symptoms include tingling and electric feeling. Negative symptoms include numbness, absent body part, and asomatognosia.

Temporal lobe: Simple partial seizures: autonomic/psychic symptoms and sensory phenomena: olfactory, auditory, and (most commonly) rising epigastric sensation. Complex partial seizures: alteration in consciousness with behavioral arrest, often followed by oroalimentary or hand automatisms. Postictal confusion is usually followed by amnesia of the event.

https://www.google.com/url?sa=t&source=web&rct=j&url=https://academic.oup.com/brain/article-pdf/119/1/17/967046/119-1-17.pdf&ved=2ahUKEwjijPHxodTtAhXmzjgGHTzoDKYQFjALegQIBhAB&usg=AOvVaw0_uvXB0bS_LsjG6x7vyNlJ

After the focal seizure, the area of cortex that is most involved can have postictal depression of function lasting from minutes to hours. This can result in paralysis ("Todd paralysis") if the motor cortex is involved. Patients can have the appearance of focal deficit during this period and it may be difficult to distinguish from a patient with stroke. The history of seizure and the gradual recovery of function is critical to this differentiation.

If the focal seizure is not contained by normal inhibitory processes in the brain, it can spread to involve both hemispheres via the corpus callosum and/or the reticular formation of the mesodiencephalon and a generalized motor clinical seizure results. This may be tonic, tonic-clonic or just clonic in nature and is termed a "secondarily generalized seizure".

Anatomical localisation of rt upperlimb hemiparesis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844548/

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

These infarcts were classified as large subcortical, small deep, or cortical. Large subcortical infarcts were diagnosed if they were located in the basal ganglia, internal capsule, or corona radiata, with a diameter between 15 and 40 mm. Small deep infarcts were defined according to the same locations but with a diameter of <15 mm. Cortical infarcts were defined as wedge-shaped, superficial ischemic lesions in the territory of one of the large major cerebral arteries or lesions in a border zone; the underlying white matter might be involved as well.

https://www.ahajournals.org/doi/10.1161/01.STR.0000226993.88307.ff

In addition to the changes in the infarct itself, the infarct lesion will cut off the nutritional supply and synaptic connection between the inferior nerve fibers and the upper cortex, leading to Wallerian degeneration of the inferior nerve fibers, which causes axonal and myelin sheath disintegration and nerve fiber atrophy.

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

https://onlinelibrary.wiley.com/doi/abs/10.1111/epi.13965

 4. What is your take on the ecg? 

And do you agree with the treating team on starting the patient on Enoxaparin?

Ecg 

https://www.aafp.org/afp/2009/0401/p560.html

Objectives: To determine the effect of heparins (UFH and LMWH) compared with placebo for the treatment of patients with acute coronary syndrome.

Search Strategy: The authors searched the Cochrane Central Register of Controlled Trials on The Cochrane Library (Issue 4, 2002), Medline (1966 to May 2002), EMBASE (1980 to May 2002), and CINAHL (1982 to May 2002). Authors of included studies and pharmaceutical industry representatives were contacted to determine if unpublished studies that met the inclusion criteria were available.

Selection Criteria: Randomized controlled trials of parenteral UFH or LMWH versus placebo in persons with acute coronary syndrome (unstable angina or NSTEMI).

Eight studies (3,318 participants) were included in this review. We found no evidence for difference in overall mortality between the groups treated with heparin and placebo (relative risk [RR] = 0.84; 95% confidence interval [CI], 0.36 to 1.98). Heparins reduced the occurrence of myocardial infarction (RR = 0.40; 95% CI, 0.25 to 0.63; number needed to treat = 33), and increased the incidence of minor bleeds (RR = 6.80; 95% CI, 1.23 to 37.49; number needed to harm = 17).

. 5.Which AED would you prefer? If so why?

AED of choice for acute presentation is bzd agonists

Focal seizure -carbamazepine,oxcarbazepine.

Secondary genererlisation-sodium valproate,levitiracetem

 Please provide studies on efficacies of each of the treatment given to this patient.

leviteracetam

https://pubmed.ncbi.nlm.nih.gov/10908898/

Of 294 patients randomized, 268 completed the study. Partial seizure frequency during the entire evaluation period (primary efficacy variable) was lower with levetiracetam compared to placebo (p /=10%), mostly mild to moderate in severity, with incidences higher than placebo were asthenia, dizziness, flu syndrome, headache, infection, rhinitis, and somnolence.

Conclusion: Adjunctive therapy with levetiracetam was effective and well tolerated in controlling partial seizures.

carbamazepine vs sodium valproate for partial seizures and secondary generalisation

https://pubmed.ncbi.nlm.nih.gov/1298221/

For the control of secondarily generalized tonic-clonic seizures, carbamazepine and valproate were comparably effective (in 136 patients and 138 patients, respectively). For complex partial seizures, four of five outcome measures favored carbamazepine (100 patients) over valproate (106 patients): the total number of seizures (2.7 vs. 7.6, P = 0.05), the number of seizures per month (0.9 vs. 2.2, P = 0.01), the time to the first seizure (P less than 0.02), and the seizure-rating score (P = 0.04). Carbamazepine was also superior according to a composite score that combined scores for the control of seizures and for adverse effects (P less than 0.001). Valproate was associated more frequently than carbamazepine with a weight gain of more than 5.5 kg (12 lb) (20 percent vs. 8 percent, P less than 0.001), with hair loss or change in texture (12 percent vs. 6 percent, P = 0.02), and with tremor (45 percent vs. 22 percent, P less than 0.001). Rash was more often associated with carbamazepine (11 percent vs. 1 percent, P less than 0.001).

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?  

Sob since three days progresseive

symptoms of hypoglycemia refractory to dextrose infusion for 2 days

secondary to aki ?renal -acute tubular necrosis (non oliguric)

cough 

2. What is the cause for his recurrent hypoglycemia? And how would you evaluate? 

 cause for recurrent hypoglycemia

is oha (glimiperide 1mg)

creatinine clearance 33ml/min

egfr is 26.2ml/min/1.73m2

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4732385/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4470208/

Sulfonylureas. 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 creatinine

ultrasound-size of the kidneys and rpd changes

cue-albuminuria

24hour urinary protein-quantification of proteinuria

Gylcemic control:

Fbs,plbs,hba1c

aprroach to pt with hypoglycemia

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

reason for albumin loss

spot urine protein creat ratio >1 , albuminuria

?diabetic nephropathy

https://www.aafp.org/afp/2000/0915/p1333.html

Pic

Approach to proteinuria from the above link.

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.

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?

approach to polyarthragia

MSK.rheumatology

2. What is the pathogenesis involved in RA?

pathogenesis of RA

https://academic.oup.com/rheumatology/article/51/suppl_5/v3/1787104

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?

https://www.hopkinsarthritis.org/arthritis-info/rheumatoid-arthritis/ra-treatment.

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?

https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/delayed-hemolytic-transfusion-reaction

Delayed hemolytic transfusion reactions (DHTRs) occur 3–10 days after the transfusion of RBC products that appear to be serologically compatible. These reactions occur in patients who have been alloimmunized to minor RBC antigens during previous transfusions and/or pregnancies; pretransfusion testing fails to detect these alloantibodies due to their low titer. After reexposure to antigen-positive RBCs, an anamnestic response occurs, with a rapid rise in antibody titer. Decreased survival of the transfused RBCs may result, primarily due to extravascular hemolysis. In the majority of cases, however, anamnestic antibody production does not cause detectable hemolysis. The term delayed serologic transfusion reaction (DSTR) defines reactions in which an anamnestic antibody is identified serologically, in the absence of clinical evidence of accelerated RBC destruction. Antigens implicated most often in DHTRs and DSTRs are in the Kidd, Duffy, Kell, and MNS systems, in order of decreasing frequency.

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.

https://www.ijbcp.com/index.php/ijbcp/article/view/64

Background: Data on clinical spectrum and etiology of chronic cholestatic liver disease (CCLD) in Indian patients is limited. This prospective, observational real-world study aimed to profile patients with CCLD being recommended Udiliv®, determine reasons for recommendation along with its safety and effectiveness.

Methods: CCLD patients (18-65 years) scheduled to receive Udiliv® as part of routine clinical practice were enrolled. Healthcare utilizations, clinical manifestations (jaundice, pruritus, fatigue) and liver biochemistry were assessed over 12 weeks. Reasons for recommending Udiliv® were recorded at the initiation of therapy.

Results: The intent-to-treat analysis population included 248 patients. The mean (±SD) age was 44.1(11.8) years and 78.23% were males. Majority (89.1%) were classified as intrahepatic cholestasis (IHC). Most common etiologies of IHC were alcoholic liver disease (ALD) (39.92%) and viral hepatitis (24.60%) followed by non-alcoholic fatty liver disease (NAFLD) (22.18%), which is less well known. Udiliv®, 300 mg twice daily was preferred dose due to known efficacy (73.39%), as standard of care (62.5%) and good tolerability (45.56%). There was reduction in healthcare visits, inpatient hospitalization and days off work, within 4 weeks of treatment initiation (P<0.0001). There was improvement in clinical presentation (P<0.0001) and reduction in biochemical markers over 12 weeks. The treatment was well-tolerated.

Question 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?

chest pain -radiating to epigastrium and back

uncontrolled sugars 

leucocytosis secondary to ?community acquired pneumonia

?lung abscess

no further history mentioned in terms of fever , cough, sob

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

2)reason for uncontrolled sugars

sepsis

poor glycemic control prior to hospital administration with hba1c 8, (history not clear about compliance)

https://www.semanticscholar.org/paper/Stress-hyperglycemia%2C-insulin-and-immunomodulation-Marik-Raghavan/24f1499f7360fc0564d7f66cee5cfa7953c73616

Changes in whole-body glucose uptake and glucose oxidation in sepsis are complex and may depend on the severity of illness and the stage of the disease. Wholebody glucose uptake and glucose oxidation may be increased in the early stages of sepsis and endotoxemia [25, 26]. This may be the result of cytokine-induced increase in non-insulin mediated glucose uptake by tissues rich in mononuclear phagocytes, including the liver, spleen, ileum, and lung [27, 28]. Enhanced noninsulin mediated glucose uptake appears to result from an increase in the synthesis, concentration or activity of the GLUT1 transporter [29, 30]. With the development of insulin resistance glucose utilization and oxidation may decrease [25, 31, 32]. Exogenous insulin increases glucose utilization and oxidation; however, nonoxidative disposal (storage) remains impaired [25, 31

3. What are the chest xray findings?

the xray findings in this pt are

p/a view ,adequate exposure with opacities in right upper lobe ,

with air bronchogram, with bulging fissure sign suggestive of lobar consolidation

4. What do you think is the cause for her hypoalbuminaemia? How would you approach it?

4) hypoalbunemia 

https://www.dvm360.com/view/approach-hypoalbuminemia-proceedings

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

https://onlinelibrary.wiley.com/doi/10.1002/jpen.1451

Inflammation increases capillary permeability and escape of serum albumin, leading to expansion of interstitial space and increasing the distribution volume of albumin. The half‐life of albumin has been shown to shorten, decreasing total albumin mass. These 2 factors lead to hypoalbuminemia despite increased fractional synthesis rates in plasma. 

5. Comment on the treatment given along with each of their efficacies with supportive evidence.

treatment efficacies

piperacillin tazobactum

https://pubmed.ncbi.nlm.nih.gov/9721959/

A favorable clinical response was observed in 90% of the piperacillin/ tazobactam group and in 84% of the co-amoxiclav/aminoglycoside group (not significant). The bacteriological efficacy was comparable in both groups

clarithromycin

https://journal.chestnet.org/article/S0012-3692(15)42279-2/abstract

This randomized, double-blind multicenter study compared clarithromycin and cefixime as treatment for patients with community-acquired lower respiratory tract infections (n=213). Patients had bacterial pneumonia (clarithromycin, 19 percent; cefixime, 21 percent) or acute bacterial exacerbation of chronic bronchitis or asthmatic bronchitis (clarithromycin, 81 percent; cefixime, 79 percent). Patients received 500 mg of clarithromycin twice daily (n = 103) or 400 mg of cefixime once daily (n = 110) for 7 to 14 days.

Clinical cure or improvement occurred in 86 percent of the clarithromycin-treated patients and 88 percent of the cefixime-treated patients.

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?

1) anatomical and pathological localisation

as per the symptoms

jaundice with abdominal distention-liver

sob with abdominal distention-heart failure, renal failure 

examination- ecchymosis and petechiae-bleeding manifestations in uraemia, ?liver failure(no reports of coagulation profile)

chronic mild elevations with AST>ALT (2:1) are suggestive of alcohol related liver injury or cirrhosiscompared to the chronic viral hepatitis due to hepatitis B.

Hepatorenal failure type 1 , with increase in serum creatinine

2. How do you approach and evaluate this patient with Hepatitis B?

Pic aprroach to a patient with hepatitis b with cirrhosis

reference from pg 200,api textbook of medicine

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?

https://www.hepatitisbannual.org/article.asp?issn=0972-9747;year=2006;volume=3;issue=1;spage=76;epage=105;aulast=Wong

https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5005a1.htm

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

5.hat are the efficacies of each treatment given to this patient? Describe the efficacies with supportive RCT evidence. 

efficacy of tenofovir

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220271/#:~:text=Among%20HBeAg%2Dpositive%20patients%2C%20rates,na%C3%AFve%20and%20treatment%2Dexperienced%20patients.

Ninety-two patients were identified who fulfilled the enrolment criteria. Median follow-up was 26 mo (range 3-114). Mean age was 46 (24-78) years, 64 (70%) were male and 77 (84%) were of Asian origin. 55 (60%) patients were treatment-naïve and 62 patients (67%) were HBeAg-negative. Complete virological suppression was achieved by 45/65 (71%) patients at 12 mo, 37/46 (80%) at 24 mo and 25/28 (89%) at 36 mo. Partial virological response (HBV DNA 20-2000 IU/mL) was achieved by 89/92 (96.7%) of patients. Multivariate analysis showed a significant relationship between virological suppression at end of follow-up and baseline HBV DNA level (OR = 0.897, 95%CI: 0.833-0.967, P = 0.0046) and HBeAg positive status (OR = 0.373, 95%CI: 0.183-0.762, P = 0.0069

aldactone

https://pubmed.ncbi.nlm.nih.gov/6339312/#:~:text=These%20results%20indicate%20that%20(a,and%20spironolactone%20in%20these%20patients

Group 1 contained 21 patients treated with furosemide; group 2 contained 19 patients treated with spironolactone. The initial doses were 80 and 150 mg/day, respectively. These doses were increased to 160 and 300 mg/day, respectively, if there was no response. Cases not responding to furosemide and spironolactone were later treated with spironolactone and furosemide, respectively. In group 1, 11 of the 21 patients responded to furosemide, while in group 2, 18 of the 19 patients responded to spironolactone (p less than 0.01).

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 

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

An approach to the patient with dementia includes

History, cognitive assessment, general neurological assessment , laboratory investigations and neuro imaging

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2553866/

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

https://documentcloud.adobe.com/link/review?uri=urn:aaid:scds:US:e999cbad-a49f-4d17-ae4d-7b64e30a99e7

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.35"

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

 

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?

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? 

complaints of  pure tonic seizures with loc 

headache since two months, but not enough to cause caessation of activities

on further questioning he had history of insignificant weightloss , with lowgrade fever

anatomic localisation:

brain- with no focal onset and other fnd, 

radiologically-ring enhancing lesion in rt. cerebellum

(epileptogenic focus)with perilesional edema which can be attributed to the reason for headache and seizures.

no meningeal enhancement

with no clinical manifestations of cerebellar dysfunction

general examination:patient was thin built and not well nourished with temporal muscle wasting

2. What the your differentials to his ring enhancing lesions?

https://www.jpgmonline.com/article.asp?issn=0022-3859;year=2010;volume=56;issue=4;spage=307;epage=316;aulast=Garg

The pattern of ring enhancement had two differentials, tuberculoma and toxoplasma in this patient, but the cd4 count being more than 200, the lesion not in basal ganglia are and cbnaat positive, favoured tuberculoma over toxoplasma

3. What is "immune reconstitution inflammatory syndrome IRIS and how was this patient's treatment modified to avoid the possibility of his developing it?

IRIS-immune reconstitution inflammatory syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3221202/

since the cd4 count is above 300,

the patient is currently started on att for 6 months and then planned for art

8) learning points for this month

The efficacious use of antibiotics

Treating pt with hypoglycemia