General Medicine assignment - I (May)

MEDICINE BLENDED Assignment

M. NAGA VARSHA , 8TH SEM,

ROLL. NO: 76

MAY 18,2021

I've been given this case to solve in an attempt to understand the topic of "patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and come up with diagnosis and treatment plan. 

This the link of questions asked regarding the case :

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are my answers to the Medicine Assignment based on my comprehension


CARDIOLOGY 


Case A

A 78 yr old male  patient, resident of kattangur and shepherd by occupation came to the Opd  on 14 /5/2021 with chief complaints of :

SHORTNESS OF BREATH ,SINCE 20 DAYS
CHEST PAIN ,SINCE 20 DAYS
B/L PEDAL EDEMA , SINCE 4 DAYS
FACIAL PUFFINESS , SINCE 4 DAYS

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html

1. What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?

Heart failure (HF) is a complex clinical syndrome arising from deficient cardiac output that is unable to meet the metabolic needs of the organs and tissues in the body. HF evolves from systolic and/or diastolic contractile dysfunction caused by progressive structural and functional alterations of the heart.

Preserved ejection fraction– also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). Reduced ejection fraction also referred to as systolic heart failure.




Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952981/



2.Why haven't we done pericardiocenetis in this patient


Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the heart (pericardium). It's done using a needle and small catheter to drain excess fluid.
In this case, to keep a check if Pt. is having cardiac tamponade , review of ECHO is being done.



Report suggests that there is no development of cardiac tamponade.

As there is no development of cardiac tamponade, therapeutic procedure pericardiocentesis is not done in this case.

reference : https://emedicine.medscape.com/article/80602-overview



3.What are the risk factors for development of heart failure in the patient?

The risk factors for development of heart failure in this patient are

  i) hypertension since 1 year
 ii) diabetes since 1 year 
iii) chronic smoker since 30 years
 iv) chronic alcoholic since 30 years
 v) People age 65 and older are much more likely than younger people to suffer a heart attack, to have a stroke, or to develop coronary heart diseases and heart failure.


4.What could be the cause for hypotension in this patient?

i) pericardial effusion impairs cardiac filling, leading to low cardiac output and sometimes shock and death. If fluid (usually blood) accumulates rapidly, even small amounts (eg, 150 mL) as the pericardium cannot stretch quickly enough to accommodate it.

ii) irregular heart beat is a rare complication of tablet telma.

reference : https://www.mayoclinic.org/diseases-conditions/pericardial-effusion/symptoms-causes/syc-20353720
                   https://pharmeasy.in/online-medicine-order/telma-40mg-strip-of-15-tablets-11848
             

CASE B

A 73 yr male patient teacher by occupation, resident of  .............. presented to Opd with  chief complaints of :

  • PEDAL EDEMA ,SINCE 15 DAYS
  • SHORTNESS OF BREATH, SINCE 4 DAYS
  • DECREASED URINE OUTPUT ,SINCE 2 DAYS

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html

1.What are the possible causes for heart failure in this patient?

The risk factors for development of heart failure in this patient are

  i) hypertension since 19 years
 ii) type 2 diabetes since 30 years
 iii) chronic alcoholic since 40 years
 iv) People age 65 and older are much more likely than younger people to suffer a heart attack, to have a stroke, or to develop coronary heart diseases and heart failure.


2.What is the reason for anemia in this case?

The most important factors leading to anemia in heart failure are inadequate erythropoietin production resulting from renal failure in this case as patient has grade 1 renal parenchymal disease
Also in chronic heart failure (CHF) patients a low hematocrit may result from an increased plasma volume (hemodilution) or from reduced red blood cell volume (true anemia).


3.What is the reason for blebs and non healing ulcer in the legs of this patient?

In this case, patient is diagnosed by type 2 diabetes mellitus 30 years back (chronic diabetes) . In the chronic cases of diabetes as there is abnormally high levels of sugar in blood there will be delay in healing process. Therefore, bleb or blisters  and non healing ulcers are formed.

4. What sequence of stages of diabetes has been noted in this patient?
  • stage 1 : obesity
  • stage 2 : impaired glucose tolerance 
  • stage 3 : diabetes mellitus 
  • stage 4 : diabetic triopathy
  • stage 5 : micro vascular changes 
  
                         

                                                                                                                              

CASE C

 

A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest since one day.

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html


1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology

3 years ago:
Pain at surgical site of inguinal hernia (surgery took place 10 years ago)
Facial puffiness : on and off

1 year ago:
Shortness of breath : Grade II
Hypertension diagnosed

2 days back:
Decrease in urine output

Since morning:
Anuria

Anatomical localization 
 
Dilated Main Pulmonary Artery and Left Pulmonary Arteries.
Thrombi noted in Left Atrial Appendages and Left atrium

 Dilated All chambers

          * Global Hypokinesia

          * Severe LV dysfunction

          * IVC dilated 2.15 cms

Atrial fibrillation with rapid ventricular response (RVR)
Cardio Renal Syndrome 4

primary etiology
Elderly people and those with pre-existing heart conditions are more likely to suffer heart damage or strokes from NSAIDs.

In AFib, these signals don't go out correctly. Instead of contracting, the atria quiver. The flutters are too weak to send enough blood into the ventricles. In AFib with rapid ventricular response, the ventricles also beat too fast. These beats are too weak to push enough blood out of the heart to your lungs and body.

One of the most important comorbidities in heart failure is renal dysfunction. Diminished estimated glomerular filtration rate is a potent predictor of cardiovascular mortality and complications. On the other hand, worsening heart failure or acute decompensated heart failure can accelerate worsening of renal function

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

*DRUG NAME  :   dobutamine
MOADobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.
INDICATION: Indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures.
EEFFICACY OVER DOBUTAMIN
  • P- 673 participants
  • I - dobutamine
  • c - out of 673 participants random number of patients are given placebo
  • o - dobutamine is not associated with improved mortality in patients with heart failure, and there is a suggestion of increased mortality associated with its use
       
https://go.drugbank.com/drugs/DB00841
https://link.springer.com/article/10.1007/s00134-011-2435-6

*DRUG NAME : carvedilol
MOACarvedilol inhibits exercise induce tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure.
INDICATION Carvedilol is indicated to treat mild to severe heart failure, left ventricular dysfunction after myocardial infarction with ventricular ejection fraction or hypertension.
EFFICACY OVER CARVIDILOL :
  • p : 131
  • i : carvedilol
  • c : out of 131 participants random number of patients are given placebo
  • o : The beta-blocker carvedilol can be safely employed in patients with severe heart failure. Improved left ventricular function
https://go.drugbank.com/drugs/DB01136
https://pubmed.ncbi.nlm.nih.gov/9330125/

*DRUG NAME :  unfractioned heparin
MOAAdministered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.
INDICATION:  it is used to prevent embolisms in patients with atrial fibrillation and as an adjunct antithrombin therapy in patients with unstable angina and/or non-Q wave myocardial infarctions 
EFFICACY OVER UNFRACTIONED HEPARIN:
  • p : 1473
  • i : unfractioned heparin
  • c :  out of 1473 participants random number of patients are given placebo
  • o :  decrase in thromoembolism
https://clinicaltrials.gov/ct2/show/NCT00432796
https://go.drugbank.com/drugs/DB01109

*DRUG NAME  tab dytor
MOA : torasemide is known to have an effect in the renin-angiotensin-aldosterone system by inhibiting the downstream cascade after the activation of angiotensin II. This inhibition will produce a secondary effect marked by the reduction of the expression of aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the aldosterone receptor binding.
INDICATION Torasemide is indicated for the treatment of edema associated with congestive heart failure, renal or hepatic diseases.
EFFICACY OVER DYTOR:
  • p : 68
  • i : torsemide
  • c : 34
  • o : improvement in peripheral edema
https://pubmed.ncbi.nlm.nih.gov/11862232/

*DRUG NAME  : tab taxim
MOA : The bactericidal activity of cefotaxime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefotaxime shows high affinity for penicillin-binding proteins in the cell wall including PBP Ib and PBP III.
INDICATION Used to treat gonorrhoea, meningitis, and severe infections including infections of the kidney (pyelonephritis) and urinary system. Also used before an operation to prevent infection after surgery
EFFICACY OVER  TAXIM:
  • p : 60
  • i : taxim
  • c : out of 60 participants random number of patients are given placebo
  • o :  the results indicate that cefixime twice daily is comparable in safety 
https://go.drugbank.com/drugs/DB00493
https://pubmed.ncbi.nlm.nih.gov/2663735/


*DRUG NAME :  inj thiamine
MOA : It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions.
INDICATION For the treatment of thiamine and niacin deficiency states, Korsakov's alcoholic psychosis, Wernicke-Korsakov syndrome, delirium, and peripheral neuritis.
EFFICACY OVER THAMINE :
  • P : 50
  • I : thiamine
  • C : 25
  • O : Thiamine was not associated to a significant reduction in vasopressor-free days over 7-days in comparison to placebo in patients with septic shock
https://go.drugbank.com/drugs/DB00152
https://bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-020-01195-4



3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 
Cardiorenal syndrome encompasses a spectrum of disorders involving both the heart and kidneys in which acute or chronic dysfunction in 1 organ may induce acute or chronic dysfunction in the other organ. It represents the confluence of heart-kidney interactions across several interfaces. These include the hemodynamic cross-talk between the failing heart and the response of the kidneys and vice versa, as well as alterations in neurohormonal markers and inflammatory molecular signatures characteristic of its clinical phenotypes.



reference : https://www.nature.com/articles/nrneph.2013.250

This patient had type 4 cardio renal syndrome that is chronic renocardiac syndrome in which progressive kidney disease resulting in deceased or worsening cardiac functions.

4) What are the risk factors for atherosclerosis in this patient?

The risk factors for atherosclerosis in this case is hypertension and age of the patient.

5) Why was the patient asked to get those APTT, INR tests for review?
.
As the patient is on unfractioned heparin medication laboratory monitoring is widely recommended to measure the anticoagulant effect of unfractionated heparin and to adjust the dose to maintain levels in the target therapeutic range. 

reference : https://pubmed.ncbi.nlm.nih.gov/17080209/



CASE D

67 year old patient with acute coronary syndrome.



https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Evolution of symptomatology

12 years agol
Diabetes mellitus  2

1 year ago :
Heatburn like episodes :  relived without use of any medication.


7 months ago:
Pulmonary tuberculosis : diagnosed 7 months ago for which she completed the course of medication a month ago with cough, chest pain.Currently negative for TB.


30 minutes ago:
Shortness of breath

Anatomical localization 
Acute coronary syndrome



primary etiology

The increasing population in older age will lead to greater numbers of them presenting with acute coronary syndromes (ACS).he elderly are a high risk group with more significant treatment benefits than younger ACS. Nevertheless, age related inequalities in ACS care are recognised and persist. 


2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
*DRUG NAME  : tab met
MOA : Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization
INDICATION Metformin is indicated as an adjunct to diet and exercise to increase glycemic control in adults and pediatric patients 10 years of age and older diagnosed with type 2 diabetes mellitus
EFFICACY OVER TAB MET :
  • p : 451
  • i : metformin
  • c : out of 451 participants random number of patients are given placebo
  • o : Metformin improved glucose variables as compared with placebo. 
https://go.drugbank.com/drugs/DB00331
https://pubmed.ncbi.nlm.nih.gov/9428832/


3) What are the indications and contraindications for PCI?

Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multivessel coronary artery disease (CAD)


INDICATIONS:

  • Acute ST-elevation myocardial infarction (STEMI)
  • Non–ST-elevation acute coronary syndrome (NSTE-ACS)
  • Unstable angina.
  • Stable angina.
  • Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
  • High risk stress test findings.      
  •   
    CONTRAINDICATIONS:
  • Intolerance for oral antiplatelets long-term.
  • Absence of cardiac surgery backup.
  • Hypercoagulable state.
  • High-grade chronic kidney disease.
  • Chronic total occlusion of SVG.
  • An artery with a diameter of <1.5 mm.


  • 4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?

    Is PCI is performed in a patient who doesn't need it then one of the following may occur:

    • -Injury to the heart arteries, including tears or rupture
    • -Infection, bleeding, or bruising at the catheter site
    • -Allergic reaction to the dye or contrast used
    • -Kidney damage from the dye or contrast
    • -Blood clots that can lead to stroke or heart attack
    • -Bleeding into the abdomen (retroperitoneal bleeding)

    Harms of overtreatment:

    Over-testing is at the root of many of our problems. Ordering, reviewing, and interpreting tests, explaining results, and follow-up testing consume valuable time.When a test isn’t necessary, time can be more appropriately spent counseling patients, listening to them, and redoubling efforts to follow well-supporte preventive guidelines .

    There are at least 5 reasons why clinicians over-test: 

    1) Belief that ordering many tests will help detect subclinical disease 
    2) Defensive medicine
     3) Lack of knowledge or confidence 
    4) Patients’ expectations 
    5) Profit
    Individual clinicians should consider implementing 4 actions to help avoid over-testing: 
    1) Refrain from ordering “baseline” or “screening” tests on patients who otherwise have no medical indication. 
    2) Refrain from ordering preoperative tests that do not make medical sense. Advocating for your patients means helping them avoid unnecessary blood draws, worry, expense, and radiation.
     3) Become familiar with evidence-based guidelines and use them to guide testing. 
     4) Share with your patients your reasons for avoiding over-testing



    CASE E



    A 60year old Male patient, resident of xxxxxxxx, came to the OPD with the  Chief complaint of chest pain since 3 days and giddiness and profuse sweating since morning.   


    https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    Known case of hypertension and diabetes 

    3 days ago:
    Mild chest pain - right side 
                                     insidious in onset and gradually progressive
                                     dragging type and was radiating to the back 

    Drowsiness - not increasing or decreasing with change of position.


    Anatomical localization 





    primary etiology

    In this patient age and hypertension are the primary etiology.


    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
    *DRUG NAME  : aspirin
    MOA : blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation
    INDICATION : Due to its ability to inhibit platelet aggregation.

    Reducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI)

    EFFICACY OVER  :

    • p: 157 248
    • i : aspirin
    • c : out of 157248 participants random number of patients are given placebo
    • o : Aspirin was associated with a lower incidence of myocardial infarction. associated with an increased incidence of major bleeding

    https://academic.oup.com/eurheartj/article/40/7/607/5250614
    https://go.drugbank.com/drugs/DB00945

    *DRUG NAME  : tab atrovas
    MOAAtorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.
    INDICATION : Atorvastatin is indicated, in combination with dietary modifications, to prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles.2

    Atorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.

    EFFICACY OVER  ATROVAS :
    • p : 60
    • i:  atrovastin
    • c : 42
    • o : Atorvastatin lowered LDL-C, apoB, and atherogenic lipoprotein subparticles in children with T1D and elevated LDL-C without worsening insulin resistance. The drug was well tolerated and safe. Long-term studies would provide better insight on the impact of these interventions in the development of cardiovascular disease in children with diabetes.
    https://go.drugbank.com/drugs/DB01076
    https://pubmed.ncbi.nlm.nih.gov/25418907/

    *DRUG NAME  :tab clopib (active metabolite of clopidogrel)
    MOA : Clopidogrel is metabolized to its active form by carboxylesterase-1. The active form is a platelet inhibitor that irreversibly binds to P2Y12 ADP receptors on platelets. This binding prevents ADP binding to P2Y12 receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.
    INDICATION : Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease
    EFFICACY OVER  TAB CLOPIB
    • p : 79,613
    • i : clopidogrel
    • c :  out of 79613 subject placebo is given to random subjects
    • o :clopidogrel was associated with a highly significant 14% proportional reduction in the risk of cardiovascular events
    https://go.drugbank.com/drugs/DB00758
    https://pubmed.ncbi.nlm.nih.gov/19909874/



    3) Did the secondary PTCA do any good to the patient or was it unnecessary?
    Percutaneous transluminal coronary angioplasty (ANGIOPLASTY) is a surgical treatment to reopen a blocked coronary artery to restore blood flow. It is a type of percutaneous (through-the-skin) coronary intervention (PCI). When performed on patients with acute myocardial infarction (MI), it is called primary angioplasty.
    After the secondary PTCA the patient was doing better so it was necessary to do.





    CASE F

    An 87 year old male patient has presented with the complaints of shortness of breath since 3 days constipation since 3 days decreased urine output since 2 days

    https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html

    1. How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

    In this case one of the possibility is that patient might have received placebo.

    2. What is the rationale of using torsemide in this patient?

    Torsemide is used to reduce extra fluid in the body (edema) caused by conditions such as heart failure, liver disease, and kidney disease. This can lessen symptoms such as shortness of breath and swelling in your arms, legs, and abdomen. This drug is also used to treat high blood pressure.

    https://www.webmd.com/drugs/2/drug-5237/torsemide-oral/details

    3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

    Ceftriaxone is a 3rd generation cephalosporins which is commonly used for bacterial infections. So in this case ceftriaxone is used for tratement of UTI.


    GASTROENTEROLOGY 



    CASE A

    A case discussion on pancreatitis, pseudocyst and and left broncho pleural fistula.

    https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    5 years ago:
    Abdominal pain and vomiting

    1 year ago:
    As resumed consumption of alcohol - abdominal pain and vomiting 

    1 week ago:
    abdominal pain : in umbilical, left hypochondriac, left lumbar and hypo-gastric                                      regions
                                     throbbing type and radiating to back
                                      associated with nausea and vomiting
    vomiting : non bilious, non projectile,contains food particles v and water content


    Since 4 days:
    Consumption of alcohol - abdominal pain and vomitings
    fever
    burning micturation
    constipation

    During hospital stay:
    Developed progressive pneumothorax

    Anatomical localization

    Chronic pancreatitis with pseudocyst

    Acute infective peri pancreatic fluid collections


    Left pleural effusion with basal atelectasis in left lung


    Left pneumothorax with secondary to broncho pleural fistula



    primary etiology

    The patient is a chronic alcoholic. This might be the cause of pancreatitis.


    2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

    *DRUG NAME  : tab metrogyl
    MOA : The exact mechanism of action of metronidazole has not been fully established, however, it is possible that an intermediate in the reduction of metronidazole which is only made by anaerobic bacteria and protozoa, binds deoxyribonucleic acid and electron-transport proteins of organisms, blocking nucleic acid synthesis.
    INDICATION  infections treated by metronidazole are Bacteroides species infections, Clostridium infections, and Fusobacterium infections, as well as Peptococcus and Peptostreptococcus infections.
    EFFICACY OVER METROGYL :
    • p :44
    • i : metrogyl
    • c : 22
    • o : Oral administration of metronidazole is effective in pain management
    https://go.drugbank.com/drugs/DB00916
    https://pubmed.ncbi.nlm.nih.gov/26541658/

    *DRUG NAME  : octreoride
    MOA : Octreotide's suppression of luteinizing hormone (LH), reduction in splanchnic blood flow, and inhibition of serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide provide relief for the gastrointestinal and flushing symptoms of carcinoid and/or VIPoma tumors.
    INDICATION : Octreotide by injection is used for the treatment of acromegaly and the reduction of flushing and diarrhea symptoms related to carcinoid tumors and/or vasoactive intestinal peptide (VIPoma) tumors.
    EFFICACY OVER 
    • p : 1902
    • i : octreotide
    • c : out of 1902 subjects placebo is given to random number of subjects
    • o :  better efficacy in preventing fluid collection and postoperative pancreatitis.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5521901/
    https://go.drugbank.com/drugs/DB00104


    *DRUG NAME  : pantrop
    MOA : Proton pump inhibitors such as pantoprazole are substituted benzimidazole derivatives, weak bases, which accumulate in the acidic space of the parietal cell before being converted in the canaliculi (small canal) of the gastric parietal cell, an acidic environment, to active sulfenamide derivatives. This active form then makes disulfide bonds with important cysteines on the gastric acid pump, inhibiting its function. Specifically, pantoprazole binds to the sulfhydryl group of H+, K+-ATPase, which is an enzyme implicated in accelerating the final step in the acid secretion pathway. The enzyme is inactivated, inhibiting gastric acid secretion
    INDICATION Treatment of gastroesophageal reflux disease associated with a history of erosive esophagitis
    EFFICACY OVER PANTROP
    • p :174
    • i : pantoprazole
    • c : out of 174 subjects placebo is given to random number of subjects 
    • o :  PPZ possesses anti-inflammatory in vivo properties and attenuates the course of AP.
    https://go.drugbank.com/drugs/DB00213
    https://clinicaltrials.gov/ct2/show/NCT02274961

    *DRUG NAME  : tramadol
    MOA : Tramadol exists as a racemic mixture consisting of two pharmacologically active enantiomers that both contribute to its analgesic property through different mechanisms: (+)-tramadol and its primary metabolite (+)-O-desmethyl-tramadol (M1) are agonists of the μ opioid receptor while (+)-tramadol inhibits serotonin reuptake and (-)-tramadol inhibits norepinephrine reuptake. These pathways are complementary and synergistic, improving tramadol's ability to modulate the perception of and response to pain.
    INDICATION : Tramadol is approved for the management of moderate to severe pain in adults
    EFFICACY OVER TRAMADOL
    • P :46
    •  : TRAMADOL
    • C :23
    • o : tramadol are equally effective in controlling pain in AP with similar safety profile.
    https://go.drugbank.com/drugs/DB00193
    https://onlinelibrary.wiley.com/doi/abs/10.1002/ejp.1515





    CASE B

    https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html


    1) What is causing the patient's dyspnea? How is it related to pancreatitis?

    With pancreatitis there are a lot of inflammartory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs. As a result, a person may experience shortness of breath as  affecting your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.

    https://www.uchicagomedicine.org/forefront/gastrointestinal-articles/what-you-need-to-know-about-pancreatitis

    2) Name possible reasons why the patient has developed a state of hyperglycemia.

    Pancreatitis damages the Alpha cells (A cells) and Beta cells (B cells) that produce glucagon and insulin which are the hormones that control the amount of sugar in the .blood This can lead to an increase in blood sugar levels causing hyperglycemia.









    3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?





    According to the report patiet have grade I fatty liver. This might be the cause of elevation on LFT's.

     Alcohol abuse is a major cause of abnormal liver function throughout the world. While measurements of liver enzyme activities (GGT, ALT, AST) are important screening tools for detecting liver disease, due to lack of ethanol-specificity and inconsistencies regarding the definitions of significant alcohol consumption, several other blood tests such as mean corpuscular volume (MCV) and carbohydrate-deficient transferrin (CDT)[82-84] are usually needed to exclude competing and co-existing causes of abnormal liver function. An AST to ALT ratio over 2 is highly suggestive of ALD[85,86].

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155359/

    4) What is the line of treatment in this patient?

    The line of treatment of this patient is:

    • IVF: 125 mL/hr 

    • Inj PAN 40mg i.v OD 

    • Inj ZOFER 4mg i.v sos 

    • Inj Tramadol 1 amp in 100 mL NS, i.v sos

    • Tab Dolo 650mg sos 

    • GRBS charting 6th hourly 

    • BP charting 8th hourly 



    CASE C

    A 45 year old female patient with fever, pain abdomen, decreased urine output and abdominal distension.


    https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html


    1) What is the most probable diagnosis in this patient?
    The most probable diagnosis in this patient is RUPTURED LIVER ABCESS


    2) What was the cause of her death?
    In this patient cause of death maybe due to sepsis.


    3) Does her NSAID abuse have  something to do with her condition? How? 
    The patient had grade 3 RPD changes in right kidney. she maybe having underlying CKD which is secondary to her NSAID abuse


    NEPHROLOGY

    CASE A

    Post TURP with non oliguria ATN, Diabetic Nephropathy



    https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html


    1. What could be the reason for his SOB ?
     
    Absorption of large volumes of irrigation fluid during transurethral resection of the prostate (TURP) can produce hyponatremia, coma, blindness, and cardiorespiratory depression. This has been termed the "post-TURP syndrome." 


    2. Why does he have intermittent episodes of  drowsiness ?


    Patient has low sodium levels that is hyponatrimia. This might have cause episodes of drowsiness.


    https://www.medicalnewstoday.com/articles/323831

    3. Why did he complaint of fleshy mass like passage in his urine?
     Fleshy mass like passage in his urine is because of pyuria.  Pus cells in the urine appear as fleshy mass.



    4. What are the complications of TURP that he may have had?
    •      
    •          Complications of TURP are:
    • i)Bladder injury.
    • ii) bleeding
    • iii)Blood in the urine after surgery.
    • iv)Electrolyte abnormalities.
    • v)Infection.
    • vi)Painful or difficult urination.

    https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/transurethral-resection-of-the-prostate-turp


    CASE B


    An Eight year old with Frequent Urination


    https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html


    1.Why is the child excessively hyperactive without much of social etiquettes ?
    The child seems to be psycho somatic, hence the behaviour.

    2. Why doesn't the child have the excessive urge of urination at night time ?
    The child has excessive urge to urinate during the daytime even though the bladder isn't full because of his psychological impulse to urinate. During the night time he wouldn't have the compulsion to do so since he's asleep.

    3. How would you want to manage the patient to relieve him of his symptoms?
    I wouldn't recommend any medicines as such because all the reports, clinical findings seem normal. He could be counselled mentally and go to therapy to overcome his psychological compulsion to urinate excessive amount of times even when he doesn't need to. A placebo might be of help.



    INFECTIOUS DISEASES 


    CASE A

    A 40 year old lady who works in cotton fields came to the hospital with the chief complaints of :
    • DIFFICULT IN SWALLOWING,FEVER AND COUGH, SINCE 2 MONTHS

    https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html


    1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

    Characteristic clinical history of tracheoesophageal fistula are :
         cough
         difficulty in swallowing
         loss of weight
         shortness of breath
    Characteristic physical findings of tracheoesophageal fistula are:
       Fistulous communication between left main bronchus and mid thoracic oesophagus.








     

    2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

    As patient is TB positive, during or after completion of anti-TB therapy, there is a chance of developing tuberculosis immune reconstitution inflammatory syndrome.
    The most effective prevention of immune reconstitution inflammatory syndrome would involve initiation of ART before the development of advanced immunosuppression.



    https://www.sciencedirect.com/science/article/pii/S2405579415300097



    HEPATOLOGY

    CASE A

    A 55 year old male patient who is a palm tree climber by Occupation 

    came on 17th April 2021 with the chief Complaints of  

    PAIN ABDOMEN SINCE ONE WEEK 

    DECREASE APPETITE SINCE ONE WEEK

     FEVER SINCE 2 DAYS



    https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html



    1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?

    As mentioned patient is chronic alcoholic and smoker. In 50% of the liver abcess cases these ae the predisposing factors.

    2. What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)




    3. Is liver abscess more common in right lobe ?

    50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.

    https://www.ncbi.nlm.nih.gov/books/NBK538230/

    4.What are the indications for ultrasound guided aspiration of liver abscess?

    Indications
    • complicated diverticular abscess.
    • Crohn's disease related abscess.
    • complicated appendicitis with appendicular abscess.
    • tuboovarian abscess.
    • post-surgical fluid collections.
    • hepatic abscess (e.g. amoebic or post-operative)
    • renal abscess or retroperitoneal abscess.
    • splenic abscess.

    1) If the abcess is large ( 5cm or more) because it has more chances to rupture.

    2) If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

    3) If the abcess is not responding to the drugs for 7 or more days 


    https://radiopaedia.org/articles/ultrasound-guided-percutaneous-drainage





    CASE B

    CASE DISCUSSION ON LIVER ABCESS




    1) Cause of liver abcess in this patient ?

    The most probable cause of liver abcess in this patient is contamination of food or water by microorganisms by bacterial or parasites.

    2) How do you approach this patient ?

    From the given details most likely it is amoebic liver abcess so we will start with antibiotics 


    3) Why do we treat here ; both amoebic and pyogenic liver abcess? 

    • If we dont treate amobic liver abcess there is a chance that one of the following occurs:
    • Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial infection.
    • Direct extension to pleura or pericardium.
    • Dissemination and formation of brain abscess.
    • If we dont treate pyogenic liver abcess there is a chance that one of the following occurs:
    • Sepsis.
    • Empyema resulting from contiguous spread or intrapleural rupture of abscess.
    • Rupture of abscess with resulting peritonitis.
    • Endophthalmitis when an abscess is associated with K pneumoniae bacteremia.

    4) Is there a way to confirm the definitive diagnosis in this patient?
      
    To conform definitive diagnosis of this patient, i would the same investigations as in the given case.


    PULMONOLOGY

    CASE A


    A 55 year old female patient, a resident of Miryalaguda and farmer by occupation came to the hospital on 17/5/21 with the chief complaints of shortness of breath, pedal edema and facial puffiness.




    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    20 years ago:
    Shortness of breath : on of off while working at paddy field
                                           relieved upon taking medication

    12 years ago:
    Episode of SOB : This one lasted 20 days and she had to be hospitalized. The                                          SOB decreased upon treatment at the hospital.(grade II)


    8 years ago
     Similar episodes of SOB every year each lasting approximately 1 week. Relieved upon taking medication

    Diabetes diagnosed
    Polyuria

    5 years ago:
    Anemia treatment with iron injections

    30 days back
    Episode of SOB : insidious in onset and gradual in progression.
                                 occurred on exertion and was relieved upon rest. 
    Generalised weakness

    20 days back:
     HRCT outside which showed bronchiectasis
    Hyperstension diagnosed

    15 days back:
    Pedal edema : upto the level ankle 
                                pitting type.
    Facial puffiness

    2 days back:
    SOB :even at rest (grade IV) 
             not relieved with nebulizers
    Drowsiness

    Anatomical localization 

    Chronic obstructive pulmonary syndrome
    Bronchiectasis





    primary etiology

    COPD is caused by prolonged exposure to harmful particles or gases which may include second-hand smoke, environmental and occupational exposures, and alpha-1 antitrypsin deficiency. In this case patiemt is exposed to paddy frequently.

    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

    • The elevation of the head of bed (HOB) to a semirecumbent position (at least 30 degrees) is associated with a decreased incidence of aspiration and ventilator-associated pneumonia (VAP).
    https://www.ahrq.gov/hai/tools/mvp/modules/technical/head-bed-elevation-lit-review.html

    • During an exacerbation of COPD, give 24% or 28% oxygen via a Venturi facemask to patients with hypercapnia in order to maintain an oxygen saturation > 90%. In patients without hypercapnia, titrate the oxygen concentration upwards to keep the saturation > 90%.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1488761/

    • BiPAP therapy targets these dysfunctional breathing patterns. By having a custom air pressure for when you inhale and a second custom air pressure when you exhale, the machine is able to provide relief to your overworked lungs and chest wall muscles.
    https://www.healthline.com/health/copd/bipap-for-copd#how-it-helps

    *DRUG NAME  : augumentin
    MOA : Amoxicillin competitively inhibits penicillin-binding protein 1 and other high molecular weight penicillin binding proteins. Penicillin bind proteins are responsible for glycosyltransferase and transpeptidase reactions that lead to cross-linking of D-alanine and D-aspartic acid in bacterial cell walls.Without the action of penicillin binding proteins, bacteria upregulate autolytic enzymes and are unable to build and repair the cell wall, leading to bacteriocidal action
    INDICATION : Amoxicillin is given with calvulanic acid to treat acute bacterial sinusitis, community acquired pneumonia, lower respiratory tract infections, acute bacterial otitis media, skin and skin structure infections, and urinary tract infections.
    EFFICACY OVER  AUGUMENTIN :
    • P : 317
    • I : amoxicillin
    • C : 97
    • O : Treatment of ambulatory exacerbations of mild-to-moderate COPD with amoxicillin/clavulanate is more effective and significantly prolongs the time to the next exacerbation compared with placebo.
    https://go.drugbank.com/drugs/DB01060
    https://pubmed.ncbi.nlm.nih.gov/22923662/

    *DRUG NAME  : Azithromycin
    MOA Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit . This results in the control of various bacterial infections . The strong affinity of macrolides, including azithromycin, for bacterial ribosomes, is consistent with their broad‐spectrum antibacterial activities
    INDICATION : Azithromycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria in order to prevent the development antimicrobial resistance and maintain the efficacy of azithromycin
    EFFICACY OVER  AZITHROMYCIN:
    • P 1142 patients
    • I : azithromycin
    • C : random number of patients
    • O : significant reduction in COPD exacerbations
    https://go.drugbank.com/drugs/DB00207
    https://www.amjmed.com/article/S0002-9343(15)00768-8/pdf


    • Chest physiotherapy techniques such as intermittent positive pressure ventilation and positive expiratory pressure may benefit patients with COPD requiring assistance with sputum clearance, while walking programmes may have wider benefits for patients admitted with an exacerbation of COPD.
    https://pubmed.ncbi.nlm.nih.gov/20113757/

    *DRUG NAME  : hydrocortisone
    MOA : The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation.[A187463] Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days
    INDICATION : Hydrocortisone tablets are indicated for certain endocrine, rheumatic, collagen, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, and other conditions
    EFFICACY OVER  HYDROCORTISONE :
    • P  : 83
    • I : hydrocortisone
    • C : random number of patients
    • O : Corticosteroid treatment was associated with a significant reduction in the median duration of mechanical ventilation
    https://go.drugbank.com/drugs/DB00741
    https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1106041



    3) What could be the causes for her current acute exacerbation?

    Exacerbations of COPD are thought to be caused by complex interactions between the host, bacteria, viruses, and environmental pollution. These factors increase the inflammatory burden in the lower airways, overwhelming the protective anti‐inflammatory defences leading to tissue damage. 
    In this case, patient developed episodes commonly around January, while working in paddy field. dust particles in the paddy field or paddy can be the allergen that is causing the episodes.

    https://www.atsjournals.org/doi/full/10.1513/pats.200701-003FM

    4. Could the ATT have affected her symptoms? If so how?

    Patient has barrel shaped chest.  Usually barrel shaped chest is seen in emphysema. In emphysema there is ATT deficiency.  So deficiency of ATT could have affected her symptoms.










    5.What could be the causes for her electrolyte imbalance?

    Serum electrolyte imbalance such as hyponatremia, hypokalemia, hyperbilirubinemia, and elevated levels of transaminases, blood urea, and serum creatinine are either caused by the disease process or the therapy initiated 

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7544412/


    NEUROLOGY

    CASE A

    A 40 year old male presented to the hospital from Yadagirigutta with the chief complaints of irrelevant talking and decreased food intake since 9 days. 



    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    12 years ago

    • Addicted to alcohol, drinks about 3-4 quarters per day

     2 years ago

    • Diagnosed with type 2 Diabetes (irregular medication; once in 2 or 3 days
    1 year ago
    • 1-2 episodes of seizures (mostly due to alcohol consumption
    4 months ago
    • Developed a seizure (mostly GTCS)
    • Cessation of alcohol for 24 hours assosiated with symptoms of restlessness, sweating, and tremors. 
    10 days back:
    • General body pains

    9 days back:

    • Started talking and laughing to himself (sudden onset)
    • Decreased food intake
    • Required assistance to move around
    • Short term memory loss (couldn't recognize family members)

    Anatomical localization 



    primary etiology

    • Wernicke's encephalopathy: thiamine deficiency secondary to alcohol dependence
    • Uremic encephalopathy: 
    • Altered sensorium: alcohol withdrawal syndrome


    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
    *DRUG NAME  : syp potklor
    MOA It inceases the potassium levels
    INDICATION Hypokalemia
    • This medicine is used for the prevention or treatment of low potassium levels in the blood.

    *DRUG NAME  ; pregabalin
    MOA : Although the mechanism of action has not been fully elucidated, studies involving structurally related drugs suggest that presynaptic binding of pregabalin to voltage-gated calcium channels is key to the antiseizure and antinociceptive effects observed in animal models.
    INDICATION Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures
    EFFICACY OVER PREGABALIN :
    • P : 539
    • I : pregabalin
    • C : 265
    • O :  the most common adverse events were dizziness and somnolence 
    https://go.drugbank.com/drugs/DB00230 
    https://pubmed.ncbi.nlm.nih.gov/30242745/

    • GRBS: general randomized blood sugar
    this test is also called capillary blood glucose assumes recent meals and therefore has higher reference values than fasting blood glucose.

    *DRUG NAME  : KCl
    MOA For use as an electrolyte replenisher and in the treatment of hypokalemia.
    INDICATION For use as an electrolyte replenisher and in the treatment of hypokalemia.
    EFFICACY OVER KCl
    • p : 18
    • i : KCl
    • c : random number of patients
    • o : amiloride might be more effective than potassium chloride in preventing hypokalaemia
    https://go.drugbank.com/drugs/DB00761
    https://pubmed.ncbi.nlm.nih.gov/3911735/

    • INJ NS and RL : Lactated Ringer's is a sterile, nonpyrogenic solution for fluid and electrolyte replenishment and caloric supply in a single dose container for intravenous administration.
    https://www.rxlist.com/lactated-ringers-in-5-dextrose-drug.htm

    *DRUG NAME  : lorazepam
    MOA : Lorazepam allosterically binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane.
    INDICATION : Lorazepam is FDA-approved for the short-term relief of anxiety symptoms related to anxiety disorders and anxiety associated with depressive symptoms such as anxiety-associated insomnia. It is as well used as an anesthesia premedication in adults to relieve anxiety or to produce sedation/amnesia and for the treatment of status epilepticus.
    EFFICACY OVER LORAZEPAM :
    • P : 56
    • I : lorazepam
    • C : 21
    • O : The effect size achieved in the placebo group was not inferior to that of benzodiazepines in general.
    https://go.drugbank.com/drugs/DB00186
    https://pubmed.ncbi.nlm.nih.gov/2575766/




    3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

    Patient had increased symptoms because he relapsed and drank alcohol again. Usually if you stop taking alcohol and start again patient will have severe withdrawal symtoms next time whenn he stops.

    4) What is the reason for giving thiamine in this patient?

     Wernicke’s encephalopathy is an acute neuropsychiatric disorder that occurs as a result of thiamine (vitamin B1) deficiency. Thiamine has been administered to counteract its deficiency.
    https://www.ncbi.nlm.nih.gov/books/NBK470344/

    5) What is the probable reason for kidney injury in this patient? 

    In this case the patient is chronic alcoholic. this might be the portable reason for kidney injury.






    6). What is the probable cause for the normocytic anemia?

    The most common cause of normocytic anemia is a long-term (chronic) disease. In this case, the patient has been suffering from uremic encephalopathy which is an organic brain disorder. It develops in patients with acute or chronic renal failure, usually when the estimated glomerular filtration rate falls and remains below 15 mL/min.
    https://www.ncbi.nlm.nih.gov/books/NBK539871/

    7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
    Yes. Excessive alcohol can cause nutritional deficiencies and alcohol toxicity. These in turn can cause poor nutrition leading to poor wound healing and problems with the nerves (neuropathy). When the sensory nerves in the foot stop working, the foot can get injured and this leads to foot ulcers.
    https://www.therecoveryvillage.com/alcohol-abuse/ulcer-from-drinking/



    CASE B

    A 52 year old male came to the hospital 2 days back presenting with slurring of speech and deviation of mouth that lasted for 1 day and resolved on the same day. 


    https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1




    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    7 days back:

    • Giddiness :
                     i)  it started around 7am 
                      ii) after which it subsided briefly.
                      iii)This was associated with 1 episode of vomiting 

    4 days back:

    • consumed a small amount of alcohol :

                     i) developed giddiness, that was sudden in onset, continuous and                               gradually progressive. It increased in severity upon getting up from the                     bed and while walking.

                     ii) associated with Bilateral Hearing loss, aural fullness and presence of                    tinnitus.

                     iii) associated vomiting- 2-3 episodes per day, non projectile, non                            bilious containing food particles.


    Anatomical localization 

    Cerebellar Ataxia secondary to Acute Cerebrovascular Accident (CVA) with infarct in the right inferior cerebellar hemisphere.




    primary etiology

    The main etiology of this case is acute cerebrovascular accident and age of the patient.



    2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
    *DRUG NAME : tab vertin
    MOA Betahistine mainly acts as a histamine H1-receptor agonist. The stimulation of H1-receptors in the inner ear causes a vasodilatory effect leading to increased permeability of blood vessels and a reduction in endolymphatic pressure; this action prevents the rupture of the labyrinth, which can contribute to the hearing loss associated with Ménière's disease. Betahistine is also purported to act by reducing the asymmetrical functioning of sensory vestibular organs and increasing vestibulocochlear blood flow, relieving symptoms of vertigo. subsequently leading to an increase in H1-agonist activity. H3-receptor antagonism elevates levels of neurotransmitters including serotonin in the brainstem, inhibiting the activity of vestibular nuclei, thus restoring proper balance and decreasing vertigo symptoms.
    INDICATION Betahistine is indicated for the reduction of recurrent vertigo episodes associated with Ménière's disease.
    EFFICACY OVER TAB VERTIN:
    • P: 174
    • I : vertin
    • C : 73
    • O : change in quality of life scores, and several observer-reported parameters to assess changes in audiological and vestibular function.
    https://go.drugbank.com/drugs/DB06698

    *DRUG NAME  : tab zofer
    MOA : release of serotonin (5-HT) from enterochromaffin cells of the small intestine, presumably initiating a vomiting reflex through stimulation of 5-HT3 receptors located on vagal afferents . Ondansetron may block the initiation of this reflex. Activation of vagal afferents may also cause a central release of serotonin from the chemoreceptor trigger zone of the area postrema, located on the floor of the fourth ventricle . Thus, the antiemetic effect of ondansetron is probably due to the selective antagonism of 5-HT3 receptors on neurons located in either the peripheral or central nervous systems, or both.
    INDICATION : the prevention of nausea and vomiting
    EFFICACY OVER  TAB ZOFER:
    • P : 60
    • I : tab zofer
    • C : 30
    • O : less frequent rescue therapy as compared with placebo on the first postoperative day.
    https://go.drugbank.com/drugs/DB00904
    https://pubmed.ncbi.nlm.nih.gov/16244017/

    *DRUG NAME  : ecosporin
    MOAblocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation
    INDICATIONindicated to relieve pain, fever, and inflammation associated with many conditions, including the flu, the common cold, neck and back pain, dysmenorrhea, headache, tooth pain, sprains, fractures, myositis, neuralgia, synovitis, arthritis, bursitis, burns, and various injuries. It is also used for symptomatic pain relief after surgical and dental procedures.
    EFFICACY OVER ECOSPORIN
    • P : 485
    • I : ecosporin
    • C : 83
    • O :  well tolerated, and adverse events were not significantly different between groups.
    https://go.drugbank.com/drugs/DB00945
    https://pubmed.ncbi.nlm.nih.gov/15836564/

    *DRUG NAME  : atrovostain
    MOA Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL. Atorvastatin also reduces Very-Low-Density Lipoprotein-Cholesterol (VLDL-C), serum triglycerides (TG) and Intermediate Density Lipoproteins (IDL), as well as the number of apolipoprotein B (apo B) containing particles, but increases High-Density Lipoprotein Cholesterol (HDL-C).
    INDICATION : Atorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.
    EFFICACY OVER ATROVASTATION: 
    • P : 54
    • I : atrovastain
    • C : 28
    • O : Atorvastatin was considered to be well tolerated in this patient cohort.
    https://go.drugbank.com/drugs/DB01076#BE0003848
    https://pubmed.ncbi.nlm.nih.gov/11933922/

    *DRUG NAME  : clopidogrel
    MOA Clopidogrel is metabolized to its active form by carboxylesterase-1.3 The active form is a platelet inhibitor that irreversibly binds to P2Y12 ADP receptors on platelets.9 This binding prevents ADP binding to P2Y12 receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.
    INDICATION : Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease
    EFFICACY OVER CLOPIDOGREL
    • p : 4600
    • i : clopidogrel
    • c : randomized
    • o : death in the placebo given patients
    https://go.drugbank.com/drugs/DB00758
    https://clinicaltrials.gov/ct2/show/NCT00222573



    3) Did the patients history of denovo HTN contribute to his current condition?
     
    The paitent's history of denovo HTN might have been contributed, as long history and irregular medication of denovo HTN can lead to peripheral neuropathy which in case might have lead to cerebral atresia.
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2475602/


    4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?

    Alcohol may increase the risk of hemorrhagic stroke
    It is caused by a blood clot blocking the flow of blood and oxygen from reaching the brain.
    https://pubmed.ncbi.nlm.nih.gov/15330400/





    CASE C



    A 45 years old female ,house wife by occupation came to opd with chief complaints of palpitations, chest heaviness, pedal edema, chest pain, radiating pain along her left upper limb.



    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    10 years ago:

    •  paralysis of both upper and lowerlimbs(rt and left)

    1 year back:

    • (right and left)paresis due to hypokalemia

    8 months back:

    • Bilateral pedal edema        
                                            i) gradually progressing   
                                            ii) present both in sitting and standing position
                                            iii) relieved on taking medication.

    7 months back:

    • Blood infection
       
    8 months back:
    • Swelling over the legs(bilateral)
    2 months back:
    • treatment of neck pain 

    6 days back:

    • Pain : 
                       i)radiating along the left upper limb 
                       ii)dragging in nature, aggrevated during palpitations 
                      iii)relieved by taking medication for palpitations.

    • Chest pain associated with chest heaviness

    5 days back:

    •  could feel her own heartbeat 
    • Chestpain 
    • Difficulty in breathing
    • Palpitation:
                              i)since sudden in onset,more during night time 
                            ii)aggregated by lifting weights, speaking continuously 
                            iii)it is relieved by drinking more water, medication

    • Dyspnoea during palpitations (NYHA-CLASS-3)


    Anatomical localization 

    Palpitations: electrolyte imbalance maybe the cause
    dyspnoea : anxiety maybe the cause



    primary etiology

    The main etiology of this patient in this case is hypokalemia.








    2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

    The main risk factor for recurrence of hypokalemia is due to usage of diuretics. other factors maybe be abnormal loss, trans cellular shift,  recurrent hypokalemic periodic paralysis, psudohypokalemia.



    3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?


    ECG changes include:

    • Flattening and inversion of T waves in mild hypokalemia
    • Q-T interval prolongation
    • Visible U wave and mild ST depression in more severe hypokalemia
    • Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.
    Clinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. 

    The assosiated symptoms are:
    • Muscle weakness (the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis).
    • Fatigue
    • Constipation
    • Muscle twitches
    • Palpitations
    In more severe cases, abnormal rythms may occurs:
    • Atrial or ventricular fibrillation
    • Premature heartbeats
    • Tachycardia
    • Bradycardia






    CASE D

    A 55year old male patient came to OPD with c/o altered sensorium and involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.


    1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

    Yes, post‐stroke seizure and post‐stroke epilepsy are common causes of hospital admissions, either as a presenting feature or as a complication after a stroke. Also taking into consideration the age of our patient, it is to be noted that stroke is the most common cause of seizures in the elderly population.

    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
    •  Hyperperfusion injury.
    Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.

    https://www.healthline.com/health/stroke/seizure-after-stroke


    2) In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

    The patient might have experienced a grand mal seizure — also known as a generalized tonic-clonic seizure in his last episode.  It is defined as a seizure that has a tonic phase followed by clonic muscle contractions. They are usually associated with impaired awareness or complete loss of consciousness.

    https://www.mayoclinic.org/diseases-conditions/grand-mal-seizure/diagnosis-treatment/drc-20364165




    CASE E

    A 48-year-old gentleman hailing from a small town in Telangana presented to the casualty ward on 25th April 2021 at 7:40am with the chief complaints of unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the past 3 hours.



    1) What could have been the reason for this patient to develop ataxia in the past 1 year?

     Ataxia usually results from damage to a part of the brain called the cerebellum, but it can also be caused by damage to other parts of the nervous system. 

    This damage can be caused by 
    • a head injury
    • lack of oxygen
    •  long-term consumption of alcohol.
    • underlying conditions such as MS
     As the patient has a h/o minor head injuries and addiction to alcohol since 3 years, he might've developed ataxia.

    2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?

    The probable reasons for IC bleed in this case are:
    • Chronic alcohol abuse assosiated to high blood pressure which can cause the thin-walled arteries which supply blood to the brain to rupture, releasing blood into the brain tissue.
    • Untreated head injuries                                                                                    
    Assosiation of alcohol with bleeding disorders:
    • Alcohol has numerous adverse effects on the various types of blood cells and their functions. Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells.
    •  Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. 
    • Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria.
    •  Consequently, alcoholics frequently suffer from bacterial infections. Finally, alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker's risk of suffering a stroke.
    https://www.ahajournals.org/doi/pdf/10.1161/01.STR.19.12.1565



    CASE F

    A 30 year old male patient lorry driver by occupation came to the OPD with chief complaints of weakness of right upper and lower limb since one day and deviation of mouth towards left since one day.

    http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

    1. Does the patient's  history of road traffic accident have any role in his present condition?

    No.


    2. What are warning signs of CVA?

    • Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
    • Sudden confusion, trouble speaking, or difficulty understanding speech.
    • Sudden trouble seeing in one or both eyes.
    • Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
    • Sudden severe headache with no known cause.
    https://www.cdc.gov/stroke/signs_symptoms.htm

    3.What is the drug rationale in CVA?
    • Drug treatment of CVA involves intravenous thrombolysis with alteplase. Intravenous alteplase promotes thrombolysis by hydrolyzing plasminogen to form the proteolytic enzyme plasmin. Plasmin targets the blood clot with limited systemic thrombolytic effects.
    •  Other acute supportive interventions for CVA include maintaining normoglycemia, euthermia and treating severe hypertension. 
    • Urgent antiplatelet use for AIS has limited benefits and should only promptly be initiated if alteplase was not administered, or after 24 hours if alteplase was administered.
    https://www.uspharmacist.com/article/pharmacologic-management-of-stroke

    4. Does alcohol has any role in his attack?

    Liver damage in chronic alcoholics can stop the liver from making substances that help blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.

    5.Does his lipid profile has any role for his attack?

    No.




    CASE G

    50-year-old male patient presented to hospital with complaints of weakness of all four limbs since 8 PM yesterday.




    1) What is myelopathy hand ?

    A characteristic dysfunction of the hand in cervical spinal disorders with loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers.  It appears to be due to pyramidal tract involvement.

    https://journals.lww.com/spinejournal/Abstract/2010/04150/Myelopathy_Hand__New_Evidence_of_the_Classical.17.aspx


    2) What is finger escape ?

    It refers to the slightly greater abduction of the fifth digit, due to paralysis of the abducting palmar interosseous muscle and unopposed action of the radial innervated extensor muscles.

    https://en.wikipedia.org/wiki/Wartenberg%27s_sign

    3) What is Hoffman’s reflex?

    Hoffmann's reflex is a neurological examination finding elicited by a reflex test which can help verify the presence or absence of issues arising from the corticospinal tract. 

    https://en.wikipedia.org/wiki/Hoffmann%27s_reflex




    CASE H

    A 17 year old female student by occupation presented to causality on 1/5/2021 with chief complaints of involuntary movements of both upper and lower limbs a day before.




    1) What can be  the cause of her condition ?  
    Iron deficiency anemia might be the cause of  her condition.

    2) What are the risk factors for cortical vein thrombosis?

    • Risk factors for children and infants include:

    • Beta-thalassemia major
    • Heart disease — either congenital (you're born with it) or acquired (you develop it)
    • Iron deficiency
    • Certain infections
    • Dehydration
    • Head injury
    • Sickle cell anemia
    • For newborns, a mother who had certain infections or a history of infertility

          Risk factors for adults include:

    • Pregnancy and the first few weeks after delivery
    • Problems with blood clotting
    • Collagen vascular diseases
    • Obesity
    • Cancer
    • Inflammatory bowel disease like Crohn's 
    • Low blood pressure in the brain
    https://pubmed.ncbi.nlm.nih.gov/18004052/

    3)There was seizure free period in between but again sudden episode of GTCS, why? Resolved spontaneously, why?   
    3 days after seizure free period  patient was tapered off Midazolam, phenobarbitone. ThIs might be the cause of GTCS.

    4) What drug was used in suspicion of cortical venous sinus thrombosis?

    Clexane 0.4ml/sc was started in suspicion of CSVT



    INFECTIOUS DISEASES

    CASE A

    1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

    Evolution of symptomatology

    i)Fever, generalised weakness

    ii)Facial puffiness, Periorbital edema

    Altered sensorium
    1. Increased progression of periorbital edema
    2. Discharge from eye- blood tinged
    1. Worsening of patients response, drowsy
    2. Blackish discolouration of medial canthus of eye
    Anatomical localization 

    PARANASAL SINUSES.

    Other anatomical parts affected due to spread of disease are ORBITS and CEREBRAL CORTEX.


    primary etiology

    Its likely due to a fungal infection caused by mucorales.

    Hence, mucormycosis is primary cause of disease in the patient.

    2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

    Mucormycosis is a serious infection and needs to be treated with prescription antifungal medicine, usually amphotericin B, posaconazole, or isavuconazole. these medicines are given through IV  or by mouth.

    3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 
    • Uncontrolled diabetes HbA1C > 6.5%
    • Steroid overuse due to COVID 19.
    The above two leads to immunocompromised patients in turn leading to impaired neutrophilic response.
    • Immunological alterations due to COVID 19 ↓CD4+/CD8+
    • Secondary infection due to widespread use of antibiotics and steroids.


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