ONLINE BLENDED BIMONTHLY ASSIGNMENT (May 2021)

Meesum Abbas 

Roll no: 82

I have been given the following cases 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 diagnosis and come up with a treatment plan.

Below is the link of the questions asked regarding the cases:





1)Pulmonology 

A) Link to patient details:

Questions 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?
Answer: 
The following is the event timeline of symptom occurrences in the patient: 
  • 1st episode of SOB 20 years ago was of Grade 2. Lasted one week. Relieved on medication 
  • Next 8 years, similar events every January which lasted 1 week, grade 2 severity. Relieved on medication 
  • Was diagnosed with Diabetes 18 years ago 
  • 2nd severe episode of SOB 12 years ago and was of grade 2 type. Lasted 20 days. Relieved on hospitalization and treatment
  • Next 12 years, each SOB incident started every January and lasted 30 days
  • Latest episode started one month ago in April, is persistent since 30 days with grade 3 dyspnea. 
  • 20 days ago, She was diagnosed with Hypertension
  • 15 days ago she started developing pedal edema and facial puffiness 
  • Since 2 days ago, severity of breathlessness went up to grade 4 dyspnea (SOB at rest) not relieved on Nebulization along with decreased urine output and drowsiness.
Anatomical localization: 
  • Right paracardiac localization of COPD
The possible etiological factors could be the following: 
  • Exposure to allergens which could make it a possible occupational hazard 
  • Infections by Moraxella, H. influenzae or Pneumococcus
  • Dust or pesticides exposure
Question 2 : 
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: 
The pharmacological and non pharmacological intervention provided include the following: 

Furosemide :
  • MOA: Blocking Na-K-Cl co transporter in loop of Henle > loss of K, Na and Cl in urine
  • Indication: 2D Echo was suggestive of potential development of Right Heart failure 
  • Efficacy: Furosemide is the Ideal for the loop diuretic therapy in Heart failure 
  • Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4038646/
 Budisonide 
  • MOA: Inhibit inflammatory cytokine production
  • Indication: The dyspnea that was suggestive of COPD
  • Efficacy : Budesonide/formoterol reduced the mean number of severe exacerbations per patient per year by 24% versus placebo and 23% versus formoterol.
  • Reference link: https://erj.ersjournals.com/content/21/1/74
Ipratropium Bromide
  • MOA: bronchodilation and inhibition of mucous secretions
  • Indication: The dyspnea that was suggestive of COPD
  • Efficacy : Ipratropium controls the acute Exacerbation of COPD
  • reference link: https://pubmed.ncbi.nlm.nih.gov/2977109/
 Amoxicillin/clavulanic acid
  • MOA: bacteriostatic + Beta-Lactamase inhibition
  • Indication: Possibility of an infectious etiology for acute exacerbation of COPD
Human Actrapid insulin
  • MOA: Inhibition of glucose output by liver with simultaneous glucose uptake via the muscles 
  • Indication: known case of Diabetes Mellitus
Head end elevation 
O2 inhalation 
Question 3: 
What could be the causes for her current acute exacerbation?
Answer:
The possible causes of her acute exacerbation can be due to the following: 
  • Exposure to allergens which could make it a possible occupational hazard 
  • Infections by Moraxella, H. influenzae or Pneumococcus (Bacterial), Influenza, Rhinovirus, Coronavirus (Viral)
  • Dust or pesticides exposure


Question 4: 
Could the ATT have affected her symptoms? If so how?
Answer: 
The ATT could have been the reason for generalized weakness 

Question 5: 
What could be the causes for her electrolyte imbalance?
Answer: 
The cause of Hyponatraemia and Hypochloremia can be due vigorous high ceiling diuretic therapy in order to control right heart failure. 

2) Neurology Gastroenterology (& Pulmonology)

Case A) Link to patient details:
Question 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?
Answer:
The following is the event timeline of symptom occurrences in the patient: 
  • An episode of seizure (GTCS) one year ago
  • Latest episode of Seizure 4 months ago associated with restlessness, sweating, and tremors following cessation of alcohol
  • 9 days ago, patient developed Altered mental state with discontinuous spatial and temporal orientation, loss of appetite, weakness 
  • After admission, tremors, sleep disturbances, sweating
  • Involuntary rolling of eyes, tongue biting, frothing, loss of consciousness
Anatomical localisation: 

  • Wernicke’s encephalopathy is normally localised to frontal lobe, thalamus and hypothalamus. 

  • Uremic encephalopathy is usually confined to basal ganglia, thalamus and midbrain
The possible etiological factors could be the following: 
  • Alcohol use disorder in addition to poor appetite leading to Vit. B1 (Thiamine) deficiency 
  • Uremia could be secondary to prerenal acute kidney injury 
Question 2: 
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: 

The pharmacological and non pharmacological intervention provided include the following: 

Thiamine

  • MOA: Replenishment of the thiamine lost reserves of Thiamine 
  • Indication: Chronic Alcoholism could be a potential cause of Thiamine deficiency 
  • Efficacy: For the treatment of acute Wernicke’s encephalopathy, the case series given below demonstrates that IV thiamine appears efficacious and safe for use
  • Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354137/

Lorazepam

  • MOA: Acts on GABA-A receptors produces an increase in the frequency of opening of the chloride ion channel
  • Indication: Alcohol withdrawal syndrome and Seizure activity
  • Efficacy: Oral benzodiazepines are the best studied and most effective drugs for preventing a severe alcohol withdrawal syndrome
  • Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4606320/

Pregabalin
  • MOA: Crosses the BBB and enhances the release of GABA but does not act as an agonist on the GABA-a receptor
  • Indications: Alcohol withdrawal syndrome and Seizure activity
  • Efficacy: Separate analyses of the pregabalin and the placebo group showed a significant reduction in diazepam use from Day 2 to 6 (pregabalin: Z = −2.842, P = 0.004; placebo: Z = −2.916, P = 0.004). 
  • Reference link: https://academic.oup.com/alcalc/article/47/2/149/187301

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

It is possible that the patient developed higher dependence with time when compared his previous attempts to cease alcohol consumption.




Question 4: 
What is the reason for giving thiamine in this patient?
Answer:

As the patient is a chronic alcoholic, there is a possibility that he has developed Thiamine deficiency. If the thiamine deficiency is left untreated, these complications can result in irreversible damage to several parts of the CNS and develop Wernike’s Encephalopathy. Hence in order to prevent any irreversible damage, thiamine has been administered. 





Question 5: 
What is the probable reason for kidney injury in this patient? 
Answer:
Elevated levels of urea and creatinine are suggestive of Prerenal Azotemia being the most likely cause of kidney injury in this patient. This can be a result of decreased blood flow to the kidneys possibly due to dehydration secondary to Alcoholism.

Question 6: 
What is the probable cause for the normocytic anemia?
Answer:

The possible causes of anemia can be the following:

  • Chronic alcohol dependence causing decreased erythropoiesis as there is a direct toxic effect of alcohol on the bone marrow
  • Anemia can be secondary to poor nutrition and malabsorption syndrome 
  • Alcoholic gastritis that could have caused a hemorrhage in the stomach leading to loss of blood
  • Possibility of liver cirrhosis that could have caused sequestration of RBCs in spleen

Question 7: 
Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Answer:

Alcoholic polyneuropathy could be the most probable cause of ulcer formation. The patient is also a known case of diabetes since two years. So it is also likely for the uncontrolled diabetes to have caused diabetic neuropathy and lead to diabetic foot ulcer. 




Case B) Link to patient details:

Question 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?
Answer:
The following is the event timeline of symptomatology in the patient: 
  • Chronic alcohol consumption since past 30 years (90-180 ml/daily)
  • 7 days before admission, had a brief episode of giddiness and one episode of vomiting 
  • 4 days ago, consumed alcohol and developed giddiness associated with Bilateral Hearing loss, aural fullness tinnitus and 2-3 episodes of vomiting per day.
  • Presented to the OPD with Slurring of speech and deviation of mouth
Anatomical Localisation:
  • Infarction in the Right inferior Cerebellar Hemisphere 
Primary Etiology:
  • Untreated Hypertension 
  • Chronic Smoking
Question 2:
 What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient? 
Answer:
Ondansetron:
  • MOA: Blocks 5-HT action on Vagal afferents in GIT
  • Indication: Patient had non-projectile vomiting 
Aspirin:
Atorvastatin:
Clopidogrel
Question 3:
Did the patients history of de novo HTN contribute to his current condition?
Answer:
Yes, Hypertension is the most likely cause of this patient’s cerebellar infarct. 
Uncontrolled Hypertension leads to endothelial dysfunction and injury. This in-turn could have caused a stroke leading to Infarction. 




Question 4:
Does the patients history of alcoholism make him more susceptible to ischemic or hemorrhagic type of stroke?
Answer:
Hemorrhagic Stroke
Chronic Alcoholism leads to liver damage which is the source of blood clotting factors that include fibrinogen and factors II, V, VII, IX, X, XI, and XII. Scarcity of these factors makes the brain more susceptible to bleeding and can be a contributing factor to a Hemorrhagic Stroke. 



Case C) Link to patient details:


Question 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?
Answer:
The following is the event timeline of symptom occurrences in the patient:
  • 10 years back, had an episode of Quadriplegia 
  • Quadriparesis since 1 year
  • Bilateral Pedal Edema (pitting) since 8 months
  • Since 6 days, radiating pain in the left upper limb 
  • 5 days ago, developed chest pain along with grade 3 dyspnea associated with palpitations
Anatomical localisation: 
  • Dorsal nerve roots of Cervical Vertebrae
Possible Primary Etiology 
  • Age > 40 years
  • Female who has likely attained menopause may have Osteoporosis
  • Degenerative Disc Disease



Question 2:
What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Answer:
The patient is likely suffering from Hypokalemic Periodic Paralysis which is a Genetic disorder and is a possible reason for recurrence of the hypokalemia.  

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

Answer:
The ECG changes in Hypokalemia include:
  • Slightly prolonged PR interval
  • Flattening and Inversion of T-wave 
  • Q-T interval prolongation
  • Visible U wave 
  • Mild ST depression 

Case D) Link to patient details:

Question 1:
Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Answer:
If a patient has history of occurrences of stroke then he/she pose an increased risk of as there is injury to the brain which can lead to formation of scar tissue that might disrupt the electrical impulses, hence inducing a seizure. 
A patient is more likely to develop a seizure after an episode of Hemorrhagic type of stroke and only 5% are likely to develop it within a few weeks of the stroke episode.

Question 2:
In the previous episodes of seizures, patient didn't lose his consciousness but in the recent episode he lost his consciousness what might be the reason?
Answer:
Simple Partial Seizures with Secondary Generalization:
  • The patient's seizures were secondary to trauma
  • Initial episodes of seizures had unilateral clonal jerking and patient retained consciousness. This is evident of a Simple Partial Seizure
  • Recent episode had loss of consciousness. This indicates there the simple partial seizure had evolved into a Generalized Tonic-Clonic Seizure





Case E) Link to patient details:

Question 1:
What could have been the reason for this patient to develop ataxia in the past 1 year?
Answer:
  • The minor incidents of falls could have caused concussions in the brain and hence Ataxia
  • Alcohol consumption could also have caused cerebellar dysfunction and resulted in ataxia


Question 2:
What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Answer:
The reasons for IC bleed could be the following:
  • The patient has history of multiple episodes of fall which had lead to minor head injuries
  • Cirrhosis of liver, leading to sequestration of platelets causing thrompocytopenia and hence increased intracranial bleeding tendencies.


F) Link to patient details:

Question 1:
Does the patient's  history of road traffic accident have any role in his present condition?
Answer:
No. If the accident had caused this condition then the patient's MRI reports would have been positive for hematoma or hemorrhage. But as the MRI showed Infarcts, it is not a consequence of the road traffic accident.

Question 2:
2.What are warning signs of CVA?
Answer:
These include the following:
  • Loss if Balance, headache and dizziness
  • Sudden loss of vision in one or both eyes
  • Facial drooping
  • Arm or leg weakness
  • Slurring of speech

Question 3:
3.What is the drug rationale in CVA?
Answer:
  • Mannitol
  • Ecosprin
  • Atorvastatin 
Question 4:
4. Does alcohol has any role in his attack?
Answer:
As there is Infarction, there was probably ischemic Stroke. Chronic alcohol consumption can lead to hemorrhagic stroke but not ischemic. Hence alcohol does not have role in this CVA.

Question 5:
Does his lipid profile has any role for his attack??
Answer:
Probably not. As Cholesterol and Triglycerides are normal, The thrombosis was probably not a result of an atherosclerotic plaque. Low HDL can cause it, but the incidences are rare.
 

Case G) Link to patient details:

Question1 :
What is myelopathy hand ?
Answer:
Loss of power of adduction and extension of ulnar two or three fingers and inability to grip and release easily with these fingers is termed as Myelopathy hand. This condition appears when there is involvement of pyramidal tracts. Seen in cervical Myelopathy. 

Question 2:
What is finger escape ?
Answer:
Also known as Wartenberg’s sign is a neurological sign where involuntary abduction of the 5th finger caused by unopposed action of extensor digiti minimi. 
It is seen in the following conditions: 
  • Ulnar nerve neuropathy 
  • Cervical myelopathy 
  • Upper motor neuron disorders
Question 3:
What is Hoffman’s reflex?
Answer:
Also known as digital reflex or snapping reflex. Grasp the middle finger and flick the distal phalangeal joint. The test is considered positive if the Thumb shows adduction and index finger shows flexion. This is to test for pathological upper motor neuron reflexes seen in Cervical Myelopathy. 


Case H) Link to patient details:

Question 1:
 What can be  the cause of her condition ?                             
Answer:
Seeing that the patient is a young female, the possible causes could include the following:
  • Trauma
  • Estroprogestative therapy ( oral contraceptives)
  • Iron deficiency anemia 
Question 2:
What are the risk factors for cortical vein thrombosis?
Answer:
The risk factors include the following:
  • Congenial or acquired heart diseases
  • Underlying Infection
  • Birth control pills use
  • Dehydration
  • Cancer
Question 3:
There was seizure free period in between but again sudden episode of GTCS. why? IT resolved spontaneously. why?                           
Answer: 
 Underlying unresolved edema is the probable cause for the recurrent precipitation of seizures. So when the edema resolved, the seizure resolved spontaneously.
  
Question 4:
What drug was used in suspicion of cortical venous sinus thrombosis?
Answer:
Injection Clexane was used to resolve the thrombosis and Mannitol infusion was given to bring down cerebral edema.

3) Cardiology

Case A) Link to patient details:

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


Question 1:

What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

Answer:

Ejection fraction is the percentage of blood that has been pumped out with that contraction i.e. it compares the amount of blood pumped out to the amount of blood in the chamber before contracting.

Normal ejection fraction is when anything between 50-70% blood is pumped out

Borderline ejection fraction when 41-49% blood is pumped out with each contraction 

In reduced ejection fraction, less that 40% of the blood is pumped out



Heart failure with reduced ejection fraction could be caused by: 

  • Coronary Artery Disease 
  • Non-ischemic dilated Cardiomyopathy 
  • COPD/Cor pulmonale 
  • Valvular heart diseases
  • Chronic brady or tachy arrhythmias

Heart failure with preserved ejection fraction can be caused by:

  • Hypertension 
  • Restrictive Cardiomyopathy 
  • Chronic constructive pericarditis 
  • Hypertrophic cardiomyopathy 

Question 2:

Why haven't we done Pericardiocentesis in this pateint?

Answer:

As cardiac tamponade was ruled out, pericardiocentesis for pericardial effusion was not necessary because it was mild and the Diuretics are sufficient to help subside it. 


Question 3:

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

Answer: 

Possible Risk factors for development of heart failure in the patient include:

  • Diabetes  
  • Hypertension 
  • Older age
  • Male patient 
  • Smoker
  • Alcohol consumption 


Question 4:

What could be the cause for hypotension in this patient?

Answer: 

  • The most likely cause of the hypotension can be Drug induced as the patient is on antihypertensive therapy that include furosamide and telmisartan. 
  • The other possible causes could also include Viral myocarditis or Extensive Myocardial Infarction. 
  • Cardiac tamponade is also a possible but it was ruled out in the 2D echo.


Case B) Link to patient details:

Question 1:
1.What are the possible causes for heart failure in this patient?
Answer:
  • The most probable cause of heart failure in this patient is Alcoholic Cardiomyopathy
  • The contributing factors could also include Hypertensive state and Diabetes.

Question 2:
What is the reason for anemia in this case?
Answer:
  • Chronic Kidney Disease along with Alcoholism together contribute to reduced production of erythropoietin hence the anemia
  • It could also be due to poor nutrition to the body because of Malabsorption syndrome secondary to chronic alcoholism.
Question 3:
What is the reason for blebs and non healing ulcer in the legs of this patient?
Answer:
Diabetic foot ulcer (non healing type) was secondary to ischemia of the foot and diabetic neuropathy due to uncontrolled diabetes mellitus.

Question 4:
What sequence of stages of diabetes has been noted in this patient?
Answer:


The following are the stages of Diabetes noted in the patient:
  • Stage 1: Normal Glucose tolerance 
  • Stage 2: Pre-diabetes 
  • Stage 3: Clinical diabetes
  • Stage 4: Stage of complication (This occurred in the following order: Diabetic Retinopathy, nephropathy, Neuropathy and Cardiomyopathy)


Case C) Link to patient details:

Question 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?
Answer:
Following is the timeline of patient's symptomatology:
  • Inguinal hernia 10 years ago. Got surgery
  • First episode of grade 2 dyspnea one year ago
  • Facial edema on and off since 2-3 years
  • hypertensive since 1 year
  • Decreased urine output since 2 days
  • Grade 2 dyspnea which progressed to grade 4 since 1 day
  • Anuria since the morning of admission
Anatomical localisation:
  • Atrial Septum
primary etiology: 
  • Atrial Septal defect leading to Atrial Fibrillation
  • Atrial fibrillation caused stagnation of blood and hence thrombus formation
  • Atrial septal defect also caused shunting from left to right atrium causing pulmonary hypertension
  • Pulmonary Hypertension caused reversal of shunting and hence increased stagnated pool of blood contributing to thrombus formation and Congestive Cardiac failure


 
Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
The following are the pharmacological and non pharmacological interventions used in the patient:
Torsemide: 
Dobutamine:
  • MOA: Acts on alpha-1, beta-1 and beta-2 adrenergic receptors. In the heart, the stimulation of these receptors produces a relatively strong, additive inotropic effect and a relatively weak chronotropic effect
  • Indication: To increase contractility of heart in CCF patients 
  • Efficacy: Dobutamine is a cardiac inotrope useful in the acute treatment of congestive heart failure. Dobutamine improves cardiac output, decreases pulmonary wedge pressure, and decreases total systemic vascular resistance with little effect on heart rate or systemic arterial pressure
  • Reference link: https://pubmed.ncbi.nlm.nih.gov/3545732/#:~:text=Dobutamine%20is%20a%20cardiac%20inotrope,rate%20or%20systemic%20arterial%20pressure.
Digoxin 
Heparin:
  • MOA: Produces an anticoagulant effect by inhibiting activated factor X and thrombin and hence prevents fibrin formation 
  • Indication: The patient had thrombi in left atrium and left appendages 
Acenocoumarol:

Question 3:
What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 
Answer:
The renal involvement was due to ischemia which happened due to:
  • LV dysfunction which developed due pulmonary hypertension which was a cause of Atrial fibrillation
  • The Atrial Septal Defect caused shunting of blood, and when pulmonary hypertension developed due to this, that resulted in reversal of shunt causing deoxygenated blood to reach the left atrium which was pumped to the rest of the body

Question 4:
What are the risk factors for atherosclerosis in this patient?
Answer:
The risk factors specific to patient include:
  • Hypertension
  • NSAID abuse
  • Older age (52 years)
  • Male gender


Question 5:
Why was the patient asked to get those APTT, INR tests for review?
Answer:
As the patient was started of Acenocoumarol, an oral anticoagulant, monitoring of aPTT and Pt-INR is necessary to aim achieve the therapeutic effect and reduce any chances of bleeding. 



Case D) Link to patient details:

Question 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?
Answer:
Event timeline: 
  • Heartburn since 1 year
  • Tuberculosis 7 months ago
  • Shortness of breath since 30 minutes
Anatomical localisation:Coronary vessels

Primary etiology: 
  • Type 2 diabetes mellitus
  • Hypertension

Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: 
The treatment modality used in this patient is
Metoprolol:
  • MOA: Acts of beta receptor, creates negative chronotropic and ionotropic effect
  • Indication: Patient is hypertensive with LV dysfunction.

Question 3:
What are the indications and contraindications for PCI?
Answer: 
The indications of PCI include the following:
  1. Acute ST-elevation myocardial infarction (STEMI)
  2. Non–ST-elevation acute coronary syndrome (NSTE-ACS)
  3. Unstable angina.
  4. Stable angina.
  5. Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
  6. High risk stress test findings
  • Contraindications of PCI include:
  1.  Lack of cardiac surgical support.
  2. Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
  3. Coagulopathy.
  4. Hypercoagulable states.
  5. Diffusely diseased vessels without focal stenosis.



Question 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 over-testing and overtreatment important to current healthcare systems?
Answer: 
The 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines for the management of STEMI consider primary PCI as a class I indication in STEMI patients within 12 hours’ of initial symptom onset.2 Beyond this timeframe PCI does not show benefit, as shown in the occluded artery trial which evaluated PCI benefit among stable, high-risk patients with persistent total coronary occlusion after MI.


Case E) Link to patient details:


Question 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?
Answer:
The evolution of symptomatology is as follows:
  • Diabetic and Hypertensive
  • Developed right sided chest pain 3 days back
  • Giddiness and profuse sweating since the morning of admission

Question 2:
What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
Pharmacological interventions used in this patient include:
Aspirin
  • MOA: Aspirin inhibits platelet aggregation by interfering with thromboxane A2 in platelets, caused by COX-1 inhibition. Thromboxane A2 is an important lipid responsible for platelet aggregation, which can lead to clot formation and future risk of heart attack or stroke
  • Indication: Reducing the risk of cardiovascular death in suspected cases of myocardial infarction (MI)
  • Efficacy: a low-dose aspirin each day for at least 10 years can lower your risk of cardiovascular disease by as much as 10%.  A significant decrease in the risk of serious cardiovascular events, including nonfatal myocardial infarction, stroke, or cardiovascular death, was seen with use of aspirin
Atorvastatin:
  • MOA: It is a competitive inhibitor of the enzyme HMG-CoA reductase, which is an enzyme involved in cholesterol synthesis.
  • Indication: To prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles. Its used as a preventive agent for non-fatal myocardial infarction, fatal and non-fatal stroke, revascularization procedures, hospitalization for congestive heart failure and angina in patients with coronary heart disease.
  • Efficacy: Clinical studies with this agent have shown that LDL cholesterol concentrations may be decreased by up to 61% at doses of 80 mg, and triglycerides may be reduced by 46%.

Clopidogrel:

  • MOA: The active form of clopidogrel 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: NClopidogrel 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: Clopidogrel had the greatest effect on reducing the rate of an occluded infarct-related artery (18.4% placebo vs 11.7% clopidogrel; 41% odds reduction; 95% CI: 0.28–0.52; p<0.001) and there was a consistent reduction in recurrent MI (3.6% placebo vs 2.5% clopidogrel; 30% odds reduction; p=0.08)

Human Actrapid Insulin:

  • MOA: The blood glucose lowering effect of ACTRAPID (fast - acting insulin) is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver.
  • Indication: For treatment of diabetes mellitus. Its used in this case as it is fast acting and here the patient requires immediate control of hyperglycemia.
  • Efficacy: A clinical trial in a single intensive care unit treating hyperglycemia (blood glucose above 10 mmol/L) in 204 diabetic and 1344 non-diabetic patients undergoing major surgery showed that normal glycaemia (blood glucose 4.4 - 6.1 mmol/L) induced by intravenous Actrapid reduced mortality by 42%



Question 3:
Did the secondary PTCA do any good to the patient or was it unnecessary?
Answer:
Immediate PTCA after thrombolytic surgery has been beneficial in many cases, but there are high chances of re-occlusion and re-infarction. Therefore, this secondary PTCA could be helpful only if these complications are well prevented and taken care of.


Case F) Link to patient details:

Question 1:
How did the patient get  relieved from his shortness of breath after i.v. fluids administration by rural medical practitioner?
Answer:
As the patient was under hypovolemic shock, there was a fall in his fluid levels. To prevent any complications, IV fluids were administered and after fluid restoration, there was relieve from dyspnea.

Question 2:
What is the rationale of using torsemide in this patient?
Answer:
Torsemide is a high efficacy diuretic which works by blocking Na-K-2Cl cotransporter, causing their excretion and hence creating diuresis
It was used in the patient as he was suffering from pulmonary edema and it caused diuresis helping reduce the fluid volume
 
Question 3:
Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Answer:
As there was presence of pus cells in urine, there was a suspicion of UTI. In order to prevent its aggrevation, Ceftriaxine was given for its treatment.


4) Gastroenterology (& Pulmonology)


Case A) Link to patient details:

Question 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?
Answer:
Given below is the timeline of symptom occurrences in the patient:
  • Incident of abdominal pain and vomiting 5 years ago following which there was cessation of alcohol
  • 3 years ago resumed alcohol consumption and had another episode of pain abdomen and vomiting
  • 5-6 episodes of abdominal pain in the past 1 year
  • 20 days ago started binge drinking
  • Abdominal pain and vomiting since 1 week
  • Fever and burning micturition since 4 days
Anatomical localization:
  • Sub-hepatic region
  • Body of the pancreas
  • Left basilar segment of lung
Primary etiology:
  • Chronic alcohol consumption
Question 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?
Answer:
The treatment modalities given to this patient includes:

Meropenem:
Metronidazole:
Amikacin:
  • MOA:  It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and t-RNA acceptor sites, interfering with bacterial growth
  • Indication: prevent septal complications of acute pancreatitis
  • Efficacy: Is being widely used in abdominal sepsis because of appropriate efficacy against invasive gram negative bacteria.
Octreotide: 
  • MOA: It is a long acting analog of somatostatin. It inhibits endocrine secretions of pancreas and also directly acting as an anti inflammatory and showing cyto-protective effects.



Case B) Link to patient details:

Question 1:
What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer:
With severe pancreatitis there are a lot of inflammatory 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 an inflammatory type of reaction in the lungs called ARDS. Specifically, the small air sacs inside the lungs called the alveoli can get inflamed and become filled with fluid causing acute respiratory distress syndrome.
Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.
Question 2:
Name possible reasons why the patient has developed a state of hyperglycemia.
Answer:
It is possible that the patient might have de novo diabetes secondary to pancreatitis. As there is destruction of Beta cells in the islets of Langerhans some patients are susceptible to hyperglycemia.

Question 3:
What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Answer:
As  the patient has been diagnosed with acute cholecystitis, that could be the possible reason for elevated LFT markers. Elevated Lipase and amylase are also considered a diagnostic of acute pancreatitis.
Alanine Aminotransferase is a potential marker for alcoholic fatty liver disease but much is needed in this field.

Question 4:
What is the line of treatment in this patient?
Answer:
Treatment plan of this patient includes the following modalities:
  • Intravenous fluids
  • Pantoprazole
  • Ondansetron
  • Tramadol
  • Paracetamol

Case C) Link to patient details:

Question 1:
What is the most probable diagnosis in this patient?
Answer:
  • The patient had pyogenic liver abscess Rupture
  • Thus led to septicemia 
  • Septicemia caused Multiorgan dysfunction
Question 2:
What was the cause of her death?
Answer:
Septicemia causing multiorgan failure is the most probable cause of her death

Question 3:
Does her NSAID abuse have  something to do with her condition? How? 
Answer:
NSAID abuse could have caused analgesic nephropathy in the patient.

5) Nephrology (and Urology)

Case A) Link to patient details:

Question 1:
What could be the reason for his SOB ?
Answer:
During TURP, the wide plexus of venous sinuses is often opened and the absorption of the irrigation fluid causes a group of symptoms and findings that is called TURP syndrome. Absorption of the irrigation fluid (2000 ml or more) may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnea, arrhythmia, hypotension and seizures and can be fatal if not treated. The symptoms of TURP are generally caused by an excessive fluid load in circulation. 

Question 2:
Why does he have intermittent episodes of  drowsiness ?
Answer: 
Uremic Encephalopathy is the likely cause for the patient's drowsiness.

Question 3:
Why did he complaint of fleshy mass like passage in his urine?
Answer: 
As the patient is healing from the TURP surgery, there might scab or clot formation and is dislodging and flowing out with the urine.
  
Question 4:
What are the complications of TURP that he may have had?
Answer:
The possible risks of TURP include the following:
  • Bladder injury.
  • Bleeding.
  • Blood in the urine after surgery.
  • Electrolyte abnormalities.
  • Infection.
  • Loss of erections.
  • Painful or difficult urination.
  • Retrograde ejaculation




Case B) Link to patient details:

Question 1:
Why is the child excessively hyperactive without much of social etiquettes ?
Answer:
The child might have had attention deficient hyperactive disorder (ADHD) because of which he may be hyperactive and due to his less attention span he may be impulsive and may not be able to interact with others much so he may not have much social etiquettes.

Question 2:
Why doesn't the child have the excessive urge of urination at night time ?
Answer:
The child may be having psychosomatic urge to urinate during the day but this will not be present during sleep as he will not be conscious.

Question 3:
How would you want to manage the patient to relieve him of his symptoms?
Answer:
The ideal management would be urinating on schedule and gradually spacing the time between bathroom visits.
Medications can include Botox injection as it helps bladder relax.
Nerve stimulation: This includes some of the latest treatment options for OAB. They sometimes may help when there is no improvement with medications.



6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 

Case A) Link to patient details:

Question 1:
Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Answer:
The consequential clinical findings in the patient includes Dysphagia and cough. There was Laryngeal crepitus observed in the patient. 




Question 2:
What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 
Answer: 
Immune Reconstitution Inflammatory Syndrome or IRIS is seen patients undergoing ART for RVD. In these patients as there is immunosuppression because of ART, a previous opportunistic infection can reactivate and give an exaggerated response. 
Candida is an opportunistic pathogen hence it is possible for this patient developing IRIS in response to a fresh candida infection
The drug of choice in this infection would be Fluconazole. 

7) Infectious disease and Hepatology

Case A) Link to patient details:

Question 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 ?
Answer:
The primary etiology of patient's condition is probably Alcoholism. The consumption of locally brewed alcohol could be an additional cause as there are high chances of improper filtration being done which could be the cause of amoebic or pyogenic liver abscess. Poor economic conditions lack of sanitation and malnutrition could also play a role as predisposing factors.

Question 2:
 What is the etio-pathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
Answer:
Etiologic factors:
  • Entry of pathogen
  • Content of alcohol
  • Cirrhotic condition of liver 
  • Immune status of the host
  • Nutritional status of the host
  • Sanitary conditions


Pathogenesis:
  • Alcohol induced hepatotoxicity
  • Depression of immune system due to alcoholism
  • Poor nutritional status

Question 3:
Is liver abscess more common in right lobe ?
Answer:
Right hepatic lobe is larger than the left hepatic lobe. Therefore more blood supply to the right lobe and hence more chances of pathogens entering the liver via the right lobe through the hematogenous route. 



Question 4:
What are the indications for ultrasound guided aspiration of liver abscess ?
Answer:

  • If the abscess is large ( 5cm or more) because it has more chances to rupture.
  • If the abscess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.
  • If the abscess is not responding to the drugs for 7 or more days.


Case B) Link to patient details:

Question 1:
Cause of liver abscess in this patient ?
Answer:
  • Most common cause of a liver abscess is amoebic infection are caused by Entamoeba histolytica. 
  • The pyogenic abscesses can also be a potential cause by bacteria that include E.coli, Klebsiella, Streptococcus, Staphylococcus, and anaerobes.
  • While the incidence is low, it is essential to understand the severity of these               abscesses because of the high mortality risk in untreated patients.
  • If the cause is infectious, the majority of liver abscesses can be classified into bacterial (including amebic) and parasitic sources (including hydatiform cyst).

Question 2:
How do you approach this patient ?
Answer:
Treatment approach includes the following:
  • Sulbactam + Cefoperazone
  • Metronidazole
  • Optineurin
  • Tramadol
  • Acetaminophen
  • Paracetamol
Question 3:
Why do we treat here ; both amoebic and pyogenic liver abscess? 
Answer:
The liver abscess is of an unknown etiology. Hence empirical treatment for both the types of liver abscesses is being administered.
Metronidazole is for the amoebic type of abscess and Sulbactam and cefoperazone are broad spectrum antibiotics for the pyogenic liver abscess.  





Question 4:
Is there a way to confirm the definitive diagnosis in this patient?
Answer:
Aspiration and culture of the aspirated fluid can help us draw a definitive diagnosis. It wasn't necessary in this patient as the abscess started subsiding with the empirical treatment.



8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)

Case A) Link to patient details:

Question 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?
Answer:
The evolution if symptomatology is as follows:
  • Diagnosed with hypertension 3 years ago
  • Fever since 10 days
  • Facial puffiness, periorbital edema and Right sided hemiparesis since 4 days
  • Altered sensorium since 2 days 
Anatomical localization: 
  • Infarcts in frontal and temporal lobes of brain
  • Eshcar extending from hard palate to lip
Primary etiology: 
  • Mucormycetes infection causing rhino-orbito-cerebral mucormycosis
Question 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?
Answer:
The treatment modality in this patient includes:
Itraconazole: 
  • MOA: Itraconazole acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-α-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis
  • Indication: Itraconazole is the only marketed azole drug that has in vitro activity against Mucorales. There are case reports of successful therapy with itraconazole alone .However, as mentioned above, itraconazole prophylaxis has been described as a risk factor for breakthrough mucormycosis
Question 3:
What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 
Answer:
The reasons for sudden rise of mucormycosis cases in India include:
  • COVID-19 infection among diabetic patients in whom there is lower immunity.
  • Increased dose of steroid usage and also because of lower availability of remdesivir , tocilizumab leading to dependence on steroids for treatment. 
  • Use of ordinary water instead of sterile water in humidifiers.
  • Prolonged ICU stay

9) Infectious Disease (COVID-19)


Below is the link to the questions of COVID cases:



Link to the COVID cases master chart :




Case 1) COVID-19 with comorbidity (Pulmonology/Rheumatology)
Link to the patient case report log:

Question 1:
How does the pre-existing ILD determine the prognosis of this patient?
Answer:
Patients with ILD have diminished pulmonary reserve and impaired gas exchange due injury to alveolar epithelium.
Prognosis of COVID 19 patients with pre-existing ILD is significantly worse than non ILD patients.
 
Question 2:
Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism? 
Answer:
Studies have shown that steroids used for treatment did not worsen the prognosis of rheumatoid arthritis.

Question 3:
Would this patient have an increased risk for post COVID autoimmune response compared to patients without a history of autoimmune disease?
Answer:
COVID-19 is more severe, with more complications and higher mortality, than influenza among patients with autoimmune disease, according to data published in Rheumatology

Question 4:
Why was she prescribed clexane (enoxaparin)?
Answer:
  • IL6 is involved in cytokine storm, enoxaparin has IL6 binding properties thus preventing cytokine storm.
  • Prevention of infection by decreasing virus cell entry and hence viral load
  • Prevention of activation of coagulation cascade
  • Prevention of venous thromboembolism


Case 2) COVID-19 with Diabetes 
Link to the patient case report log:

Question 1:
Since patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause the indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausible?
Answer:
The exact pathology of new onset diabetes in COVID-19 patients is not known, but this could be a possible explanation. Beta cells in the pancreas contain a significant number of so-called ACE2 receptors. These receptors are believed to be where the spike protein from the coronavirus attaches to cells. Beta cells produce insulin. It is theorized that a coronavirus infection, which affects the ACE2 receptors, might also damage beta cells in the pancreas and hence precipitating diabetes. 



Question 2:
Did the patient's diabetic condition influence the progression of her  pneumonia?
Answer:
Diabetic subjects may have increased susceptibility to pneumonia for several reasons. They are at increased risk of aspiration, hyperglycemia, decreased immunity, impaired lung function, pulmonary microangiopathy, and coexisting morbidity 

Question 3:
What is the role of D Dimer in the monitoring of COVID? Does it change management or would be considered over-testing? 
Answer:
D-dimer is a fibrin degradation product, elevated D-dimer levels have been associated with disease severity and mortality trends. Several studies from Wuhan have shown elevated D-dimer in COVID-19 patients is associated with higher mortality. 
There is not yet a consensus as to how D-dimer levels should be used for management and/or monitoring of COVID-19 patients. Checking D-dimer on initial presentation in the emergency department, urgent care facility or outpatient clinic is appropriate.


Case 3) COVID-19 Severe 
Link to the complete case report log:

Question 1:
Why was this patient given noradrenaline?
Answer:
The patient following AKI along with the viral infection could have gone under septicemic shock. This would create a severe hypotensive state. To correct this, Noradrenaline was administered. 

Question 2:
What is the reason behind testing for LDH levels in this patient?
Answer:
LDH is often used as a marker of tissue breakdown as LDH is abundant in red blood cells and can function as a marker for hemolysis. It can also be used to diagnose renal infarction. So as the patient has both COVID infection and renal complications, LDH works as a diagnostic marker. 

Question 3:
What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
Answer:
As BiPAP is not intended for full ventilatory support and is contraindicated in the patients who are unable to maintain spontaneous breathing, invasive mechanical ventilation provides more support to these patients. Once the patient starts to recover and maintain spontaneous breathing, he can be shifted onto an NIV.


Case 4) COVID-19 Mild 
Link to the case report log:


Question 1:
Is the elevated ESR due to COVID related inflammation? 
Answer:
If there is inflammation following a COVID infection, then elevated ESR can be a possible cause of it. During an inflammatory process, increased levels of fibrinogen is released into the blood, causing them to stick together and form rouleaux. 



Question 2:
What was the reason for this patient's admission with mild COVID? What are the challenges in home isolation and harms of hospitalization? 
 Answer:
The patient was probably admitted as it was a long-standing case of COVID and the patient’s dyspnea had progressed to grade 3 with further exaggeration of his other symptoms also. 
If the patient had opted for home isolation, then an emergency could not have been taken care of. And as the patient’s condition was deteriorating with each following day, hospital admission was advisable
As the steroidal therapy given for COVID could have disrupted his immune system, admission in a hospital makes him more susceptible to the nosocomial infections.




Case 5) COVID-19 and comorbidity (Altered sensorium, azotemia, hypokalemia) 
Link to the case report log:

Question 1:
What was the reason for coma in this patient? 
Answer:
Hypoxic encephalopathy And Viral encephalopathy probably produced the comatose condition of this patient. 

Question 2:
What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related? 
Answer:
Hypokalemic periodic paralysis diagnostic tests

Question 3:
How may COVID-19 cause coma? 
Answer:
Infarct in the brain could have developed secondary to embolism which could have been the reason for his coma.


Case 6) Severe COVID-19 with altered sensorium 
Link to the case report log:

Question 1:
What was the cause of his altered sensorium?
Answer:
The most probable cause of altered sensorium in this patient can be Hypoxic encephalopathy due to severe fall in SpO2 of the patient. 
It can also be Viral Encephalopathy post covid-19 infection 
Another possibility is the Hyperglycemic condition that can cause delirium and even coma might develop. But that would need the evidence of diabetic ketoacidosis. 



Question 2:
What was the cause of death in this patient?
Answer:
Hypoxic encephalopathy can be the main cause of the Patient’s death after there was ischemic damage done to the neural tissue. 
It could also be due to pulmonary thromboembolism due to COVID infection


Case 7) COVID-19 Moderate with ICU psychosis 
Link to the case report log:

Question 1:
What is the grade of pneumonia in her?
Answer:
Grade of pneumonia in this patient is moderate. 

Question 2:
What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID?
Answer: 
Ideal day to start steroids doesnt exist. It depends on the serum markers for COVID and recurrence of symptoms. Patients are being given steroids starting with a mild dose of 4-8mg if they have even a mild increase of serum markers, so as to prevent the disease from worsening.

Question 3:
What all could be the factors that led to psychosis in her ?
Answer:
There are 3 types of ICU psychosis: 
  • hyperactive
  • hypoactive
  • mixed type
Factors responsible for ICU psychosis:
  • Age
  • Presence of any previous psychological illness
  • Acute or chronic illness
  • Renal disease or impairment
  • Diagnosis of sepsis
  • Smoking
  • Acute respiratory distress
  • COPD
  • Absence of daylight exposure
Question 4:
In what ways shall the two drugs prescribed to her for psychosis help ?
Answer:
PIRACITAM: Piracetam improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes. Furthermore, piracetam may have an effect on NMDA glutamate receptors, which are involved with learning and memory processes.

RISPERIDONE: The primary action of risperidone is to decrease dopaminergic and serotonergic pathway activity in the brain, therefore decreasing symptoms of mood disorders. Risperidone has a high binding affinity for serotonergic 5-HT2A receptors when compared to dopaminergic D2 receptors in the brain.

Question 5:
What all are the other means to manage such a case of psychosis?
Answer:
Non pharmacological treatment:
  • Early mobilization activities
  • Timely removal of catheters and physical restraints
  • Use of eye glasses and magnifying lenses, hearing aids and earwax disimpaction
  • Early correction of dehydration
  • Use of a scheduled pain management protocol
  • Minimization of unnecessary noise/stimuli
  • Other drugs can be prescribed like:
  • Haloperidol
  • Antipsychotics
Question 6:
What all should the patient and their attendants be careful about ( w.r.t. COVID) after the patient is discharged ?
Answer:
As the patient is in the geriatric age group, guardians should take all the precautionary measures  prescribed by the doctors like:
  • Wearing a mask when near them
  • Sanitizing all the household items
  • Maintaining personal hygiene
  • Regular drug administration as prescribed by the physician
  • Frequent monitoring of SpO2 levels.

Case 8) COVID-19 Moderate 
Link to the complete case report log:

Question 1:
Can psoriasis be a risk factor for severe form of COVID?
Answer: 
Psoriasis is a T-cell mediated inflammatory disease which uses extensive topical steroidal therapy along with Vitamin D analogues and sometimes antifungals and rarely systemic steroids. So psoriasis is not a risk factor to increase of severity in COVID as it does not intervene with its pathology.
 
Question 2:
Can the increased use of immunomodulatory therapies cause further complications in the survivors?
Answer:
Immunosuppressive drugs can cause various long term effects if used in excess, some of these complications include:
  • Elevated pressure in the eyes (glaucoma)
  • Clouding of the lens in one or both eyes (cataracts)
  • Round face (moon face)
  • High blood sugar, which can trigger (New onset diabetes) or worsen diabetes
  • Increased risk of infections, especially with common bacterial, viral and fungal (mucormycosis) microorganisms
  • Thinning bones (osteoporosis) and fractures
  • Suppressed adrenal gland hormone production that may result in a variety of signs and symptoms, including severe fatigue, loss of appetite, nausea and muscle weakness
  • Thin skin, bruising and slower wound healing

Question 3:
Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
Answer:
NO, disease per say causes the fibroproliferative response. Mechanical ventilation does not worsen fibroproliferation just acts as a support to the lungs.


Case 9) COVID with de novo Diabetes 
Link to Case report log:

Question 1:
What is the type of DM the patient has developed?(is it the incidental finding of type 2 DM or virus induced type 1DM?
Answer:
A possible hypothesis is that the “Severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2)” may affect the pancreatic β-cells producing a reduction of insulin secretion. At the same time, the infection is also accompanied by a huge production of cytokines, which may induce insulin resistance. Both, reduced insulin secretion and insulin resistance, may hesitate in hyperglycemia. This is therefore Type-2 diabetes. 

Question 2:
Could it be steroid induced Diabetes in this patient?
Answer:
Yes, it is possible for patients to develop steroid induced diabetes, even when treated for a short time, which can result in type 2 DM, which may or may not subside. 

PATHOPHYSIOLOGY: 
  • Increase in insulin resistance with increased glucose production and inhibition of the production and secretion of insulin by pancreatic β-cells
  • Corticosteroids increase endogenous glucose production, increment in gluconeogenesis and antagonizing the metabolic actions of insulin
  • Enhance the effects of other counterregulatory hormones, such as glucagon and epinephrine, which increase the endogenous synthesis of glucose
  • Also been shown that the expression of the nuclear receptor peroxisome proliferator-activated receptor α is necessary for the increment in endogenous glucose production induced by corticosteroids
  • Corticosteroids reduce peripheral glucose uptake at the level of the muscle and adipose tissue
  • Corticosteroids also inhibit the production and secretion of insulin from pancreatic β-cells and induce β-cell failure indirectly by lipotoxicity

Case 10) Comparing two COVID patients with variable recovery 
Case report log: 

Question 1:
What are the known factors driving early recovery in COVID?
Answer: 
Factors responsible for early recovery are:
  • Innate immunity
  • adaptive immunity
Past exposure to any of these endemic viruses (HCoV-229E, HCoV NL-63, HCoV-OC4, HCoV-HKU1)  which show sequence homology of structural proteins in     SAR-Co V and MERS-CoV. Thus, the possibility of a protective cross-immunity in the Indian population against COVID-19 cannot be ignored in explaining a rather mild effect of the current coronavirus pandemic in India in comparison to that in Europe and the USA. 
Malaria endemicity might have a role to play. It is plausible that persons in malaria-endemic zones, which may also be endemic for several tropical pathogens including viruses, have recurrent cytokine fluctuations in response to minor and subclinical infections. These recurrent fluctuations may have a de-sensitizing effect on the body’s immune system, which prevents an uncontrolled and detrimental immune response and thus severe clinical disease in SARS-CoV-2 infection.


Case 11) COVID moderate with first time detected diabetes:
Link to Case report log: 

Question 1:
How is the diabetes related to the prognosis of COVID patients? What are the factors precipitating diabetes in a patient developing both COVID as well as Diabetes for the first time? 
Answer: 
Diabetes can definitely worsen  the prognosis of a COVID patient, as increased sugar levels can help the viruses to thrive for a longer time in the body. 
Factors which can precipitate diabetes in COVID patients can be:
Cytokine storm destroying the pancreatic beta cells, leading to lower levels of insulin.
Virus entering through ACE-2 receptors in the lung tissue, and destroying these receptors which are also present in pancreatic tissue, thereby causing decreased levels of insulin, thereby causing hyperglycemia. 
lets not forget the STEROIDS, which induce hyperglycemia by various mechanisms, not only worsening the condition of already diabetic patient, but also causing New onset diabetes.   

Question 2:
Why couldn't the treating team start her on oral hypoglycemics earlier? 
Answer: 
As the patient didn't have any hyperglycemia before, only when her sugars became uncontrollable she was started on fast acting insulin, Actrapid. 

Case 12) Moderate to severe COVID with prolonged hospital stay

Link to Case report log :

https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html


Question 1:

What are the potential bio-clinical markers in this patient that may have predicted the prolonged course of her illness? 

Answer:

Recent studies have shown that blood levels of C-reactive protein (CRP) and lactic dehydrogenase (LDH) at the time of non-ICU admission for COVID-19 predict likelihood of adverse outcomes, including development of more serious illness, increased oxygen requirements or ICU transfer.

CRP and LDH blood levels can help stratify risk and prioritize resource allocation for non-ICU patients with COVID-19. 


https://www.journalofhospitalmedicine.com/jhospmed/article/229668/hospital-medicine/clinical-characteristics-and-outcomes-non-icu


 
Case 13) Severe COVID with first diabetes 
Link to Case report log :

Question 1:
What are the consequences of uncontrolled hyperglycemia in COVID patients?
Answer:
The consequences of uncontrolled hyperglycemia include:
Question 2:
Does the significant rise in LDH suggests multiple organ failure?
 Answer:
Yes, Extremely high levels of LDH isoenzymes can indicate multi organ failure 

Question 3:
What is the cause of death in this case?
Answer:
The patient has elevated SGPT, SGOT and ALP which indicate there is liver damage
  • SGOT:170 IU/lit
  • SGPT:444 IU/lit
  • ALP:303 IU/lit
  • Serum LDH was very high indicating tissue damage 
  • serum LDH:835 IU/lit
  • CRP is positive 
  • D-dimer level is elevated D-dimer:560ng/ml
  • Blood urea is very high indicating failing kidneys
  • Blood urea:87mg/dl 
So the possible cause of death is due to liver and kidney failure along with coagulation and fibrinolysis or multiple organ failure

Case 14) Long COVID with sleep deprivation and  ICU psychosis 
Link to Case report log:

Question 1:
Which subtype of ICU psychosis did the patient land into according to his symptoms?
Answer:
ICU psychosis can be assessed by Confusion Assessment Method (CAM)-ICU-7 delirium severity scale.
Reference:
 
Question 2:
What are the risk factors in the patient that has driven this case more towards ICU psychosis?
Answer:
  • Prolonged stay at hospital and he has changed 3 different hospitals which might have caused anxiety in him
  • He was isolated environmentally which may be a reason 
Question 3:
The patient is sleep deprived during his hospital stay. Which do u think might be the most probable condition?
Answer:
Sleep deprivation causing ICU psychosis
 B) ICU psychosis causing sleep deprivation 
  • During ICU stay, the lights, machines beeping, waking up to take the medicines may impact the sleep of the patient and this might also be a cause for ICU psychosis and
  • The patient due to ICU psychosis may be in a state of delirium talking to himself not oriented to time which might be the most probable condition 
 Question 4:
What are the drivers toward current persistent hypoxia and long COVID in this patient?
  • Pneumonia secondary to COVID-19 may drive towards persistent hypoxia after being COVID negative 
  • Groundglass appearance of nearly 75% of both lungs
  • Elevated LDH, CRP,D-dimer all are risk factors for prolonged COVID infection 



Case 15) Moderate COVID with comorbidity (Truncal obesity and recent hyperglycemia) 
Link to Case report Log:

Question 1:
As the patient is a non- diabetic, can the use of steroids cause transient rise in blood glucose?
Answer:
YES, steroid use can cause transient hyperglycemia even in a non-diabetic.  COVID itself causes a hyperglycemic state which can be further aggravated by steroid intake.

Question 2:
If yes, can this transient rise lead to long term complication of New-onset diabetes mellitus? 
Answer:
YES again. people who develop transient hyperglycemia here are at an increased risk of developing diabetes in the future so they should be followed up regularly. Though once COVID resolves and steroids are tapered off, sugars will come back to normal.
 
Question 3:
How can this adversely affect the prognosis of the patient?
Answer:
If the monitoring of the sugars is missed, and if the blood sugars rise further, there is a pretty much chance that the patient may go into DKA state and might have a lot of secondary bacterial infections. 

Question 4:
How can this transient hyperglycemia be treated to avoid complications and bad prognosis?
Answer:
Generally, its picked up on time and monitored. usually, a baseline RBS is done before starting the patient on steroids. if the blood sugars cross 200-250 mg/dl, then we start the patient on insulin for a short period of time and once steroids are stopped and sugars normalize, then we stop insulin too and just monitor sugars. 


Question 5:
What is thrombophlebitis fever? 
Answer:
Thrombophlebitis fever, is a low grade fever which develops after superficial and deep phlebitis of the vein. In this case, it is superficial phlebitis, which occurred due to prolonged use of an IV line. 
Sometimes, high fever is present with drainage of pus, from the site of thrombophlebitis, known as Septic thrombophlebitis.  

Question 6:
Should the infusion be stopped in order to control the infusion thrombophlebitis? What are the alternatives? 
Answer:
This condition resolves on its own usually, when the present IV line is changed and a fresh IV line is inserted. Fever is treated with an anti-pyretic like PCM, and a bandage is put over the inflammation site and a warm compress is applied.


Case 16) Mild to moderate covid with hyperglycemia 
Link to patient’s details:

Question 1:
What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic COVID patient?
Answer:
The possible mechanisms of COVID-19 causing abnormal glucose metabolism include islet β cell damage and insulin resistance. Previous studies have reported that some viruses can directly cause pancreatic β-cell damage, and angiotensin converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor has higher expression in pancreatic endocrine tissues than in exocrine tissues

Question 2:
What is the frequency of this phenomenon of New Onset Diabetes in COVID Patients and is it classical type 1 or type 2 or a new type?
Answer:
As there is Beta cells destruction observed in certain COVID patients, we can say that the probable type of diabetes in these patients is Type 2 Diabetes.
 
Question 3
How is the prognosis in such patients? 
Answer:
Elevated HbA1c  usually leads to severe disease and is indicative of a new onset diabetes in non-diabetic COVID positive patients.

Question 4:
Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves? 
 Answer:
It is still unclear if the alterations of glucose metabolism that acutely occur with severe COVID-19 will persist after resolution of COVID-19, or remit when the infection resolves. 


Question 5:
Why didn't we start him on Oral hypoglycemic agents earlier? 
Answer:
He was probable not started on oral hypoglycemic drugs because there was minimal suspicion of patient turning diabetic.


Case 17)  COVID-19 with hypertension comorbidity 
Link to the patient's details:

Question 1:
Does hypertension have any effect to do with the severity of the COVID infection. If it is, Then how?
Answer:
Yes, COVID infection in hypertensives can lead to severe infection.
ACE2 is a modulator of the RAAS. The end product of the RAAS, angiotensin II, is a key vasoactive hormone that binds to angiotensin II receptor type 1 (AT1) located in the heart, lungs, blood vessels, kidneys, and adrenal glands, and it plays a central role in myocardial hypertrophy and fibrosis, inflammation, vascular remodeling, and atherosclerosis , by this binding it increases blood pressure. ACE2 is expressed in many human tissues including the nasal epithelium, heart, kidneys, and lungs, and inactivates angiotensin II diminishing its vasoconstrictive and myoproliferative effects.
SARS-CoV-2 binds to the ACE2 receptor via its spike  protein to allow entry into host cells. This complex is endocytosed leading to down-regulation of ACE2 and resulting in local accumulation of angiotensin II. Severe respiratory illness is a hallmark of COVID-19 and a primary cause of morbidity- and mortality-local activation of the RAAS is proposed as a mechanism for severe lung injury.

Question 2:
what is the cause for pleural effusion to occur??
Answer:
Infection causes local inflammatory reaction resulting in increased capillary microvascular permeability and a rapid outpouring of fluid containing inflammatory cells into the pleural space.

Case 18) COVID-19 with mild hypoalbuminemia 
Link to the patient's details:

Question 1:
What is the reason for  hypoalbuminemia in the patient?
Answer:
It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to COVID infection.

Question 2:
What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
Answer:
Yes, what the patient is experiencing is known as viral exanthem which is one of the cutaneous manifestation of COVID-19. 

Question 3:
What is the reason for Cardiomegaly?
Answer:
  • The most probable cause of that appearance is AP view of the chest. When an anteroposterior view is taken, most times the CXR shows false cardiomegaly. To confirm the cardiomegaly a PA view of chest must be taken. 
  • Another possible cause can be Direct Myocardial Cell Injury. The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS
  • https://www.ncbi.nlm.nih.gov/books/NBK556152/
Question 4:
What other differential diagnoses could be drawn if the patient tested negative for COVID infection?
Answer:
Possible alternative diagnoses may include:
  • Influenza
  • Mycoplasma pneumonia
  • Parainfluenza
  • Respiratory syncytial virus
  • Streptococcus pneumonia
  • Other viral or bacterial pneumonia.
Question 5:
Why is there elevated D-Dimer in COVID infection? What other conditions show D-dimer elevation?
Answer:
  • It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar hemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.
  • D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)

Case 19) COVID-19 with first time diabetes 
Link to the patient’s details:

Question 1:
Can usage of steroids in diabetic COVID patients increases death rate because of the adverse effects of steroids???
Answer:
There is still no proper studies undertaken, extensive research is still needed on this topic.

Question 2:
Why many COVID patients are dying because of stroke though blood thinners are given prophylactically???
Answer:
In COVID patients, immune system is reacting very strongly to the pneumonia, and the lungs are full of immune cells that produce cytokines. In turn, these cytokines act on liver to make clotting proteins. The inflammatory mechanism leads to what we call a “prothrombotic state.”
  • The main clotting protein in the blood is fibrinogen. It’s soluble, and we have 2–4 grams per liter in your blood.
  • The clotting factors switch soluble fibrinogen to insoluble fibrin, and that is the clot.
  • The level is 2–4 grams per liter in most people. If you are pregnant, or as you get older, the levels get higher. They might go up to 5, 6, or even 7 [grams per liter].
  • But in COVID-19 We are seeing levels of 10, even 14 grams per liter. 
  • And in COVID-19 there is clotting occurring even in the tiny blood vessels which is not getting dissolved with the normal dose anticoagulants which may increase chances of dying.(maybe increasing the dose can prevent death).

Question 3
Does chronic alcoholism  have effect on the out come of COVID infection????
If yes, how??
Answer:
Yes, chronic intake of alcohol alters the body's immune mechanism.

Chronic ethanol abuse almost doubles the risk of developing acute respiratory distress syndrome . Following are the mechanisms: 
Reducing the number of T lymphocytes - by preventing proliferation and by altering cell turnover:
  • Favoring a pro-inflammatory status through an increased level of proinflammatory cytokines, such as tumor necrosis factor alfa (TNF α) and interleukins 1 and 6 (IL-1, IL-6);
  • Decreases the function and number of NK (Natural Killers) cells responsible for removing infected or malignant cells;
  • Disturbance of macrophage functions in the lung alveoli;
  • Damage to the respiratory ciliated cells which plays an essential role in filtering pathogenic microorganisms.
Another important factor is malnutrition secondary to excessive alcohol intake .The harmful effect on the mucosa of the digestive tract consists in decreasing the absorption and metabolism of certain nutrients, including B vitamins (B1, B6 and B9 or folic acid), leading to a slowing of leukocyte proliferation and differentiation . The defense mechanisms of the mucosal immune system are also affected, resulting in a dysfunction of the function of IgA and IgG immunoglobulins, which are responsible for local protection against infectious agents.


Case 21) Severe COVID with Diabetes 
Link to the patient’s details:

Question 1:
What can be the causes of early progression and aggressive disease(COVID) among diabetics when compared to non diabetics?
Answer:
In human monocytes, elevated glucose levels directly increase SARS-CoV-2 replication, and glycolysis sustains SARS-CoV-2 replication via the production of mitochondrial reactive oxygen species and activation of hypoxia-inducible factor 1α.Therefore, hyperglycemia might support viral proliferation. In accord with this assumption, hyperglycemia or a history of T1DM and T2DM were found to be independent predictors of morbidity and mortality in patients with SARS-COV-2.
Also there is altered immune system in diabetics.
https://www.nature.com/articles/s41574-020-00435-4

Question 2:
In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?
Answer:
Two experimental agents (dexamethasone and hydroxychloroquine) have shown some promise as treatment agents.
Combined treatment with these two agents might be more beneficial than either agent alone. However, it should be kept in mind that the efficacy of dexamethasone in treating COVID-19 was proven in well-designed RCTs such as the RECOVERY study , whereas no such compelling RCTs have been performed for hydroxychloroquine.

Question 3:
What effect does a history of CVA have on COVID prognosis?
Answer:
  • In all the case series studied, history of stroke was associated with poorer progression of COVID-19. In a cohort of patients from 55 hospitals, history of stroke was twice as frequent among patients classified as having severe COVID-19 than among patients with mild symptoms. The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke
  • The virus enters the brain parenchyma, endothelium, and heart, and alters coagulation, which may lead to stroke.
  • History of stroke is associated with a three-fold increase in the risk of death due to SARS-CoV-2 infection
Case 23) COVID-19 with multiple comorbidities:
Link to the patient’s details:

Question 1:
What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection? 
Answer:
Comorbidities like
• Diabetes mellitus since 7years
• Asthma since 7 years
• History of pulmonary Koch's which might have caused some lung damage.
• History of pneumonia might have caused damage in lungs.
• Chronic kidney disease since 2yrs.

Question 2:
Can you explain why the D dimer levels are increasing in this patient? 
Answer:
  • D dimer is a product after clot is degraded.
  • In COVID-19 infection, thrombotic events takes place due to release of clotting factors 
  • In response to cytokines release.
  • May be in this patient also, cytokine release led to prothrombotic events and fibrinolytic events which led to increased d dimer levels.

Question 3:
What were the treatment options taken up with falling oxygen saturation? 
Answer:
  • 15 liters of oxygen/minute was given
  • Patient was intubated when oxygen saturation fell to 30%.

Question 4:
Can you think of an appropriate explanation as to why the patient has developed CKD, 2 years ago? (Note: Despite being on anti diabetic medication, there was no regular monitoring of blood sugar levels and hence no way to know for sure if it was being controlled or not)
Answer:
Diabetes might have caused the CKD , Diabetes induces structural changes, including thickening of the glomerular basement membrane, fusion of foot processes, loss of podocytes with denuding of the glomerular basement membrane, and mesangial matrix expansion.




10) MEDICAL EDUCATION


This experience of blogging medicine cases and giving out case opinions and answers to all other patient related questions has been very illuminating and definitely an innovative approach to learning during this pandemic in my opinion. 
During this period, we were given case sheets of the patients to make an attempt and solve them, contact the patient and improve our history taking skills and give our a provisional diagnosis. Along with it we also analyzed others’ cases and the related questions with the case, and made an attempt to solve them. For the above we had to look into various studies conducted and this helped me condition my research skills. 
I would like to thank Dr. Rakesh Biswas sir for this wonderful learning opportunity that he has given us. I would also like to thank Dr. Vamshi sir and Dr. Vilasith sir who helped me with my case and it’s diagnosis. Lastly I would like to thank the medicine department for such a wonderful and wholesome approach to learning in times of crisis.










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