MEDICINE CASE BASED LEARNING || Online assignment for the month of MAY 2021

 

I have been given the following cases to solve in an attmept 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 coem up with a treatment plan.

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

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

1) Pulmonology (10 Marks) 

A) Link to patient details:

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

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 

Indication: Presence of Dyspnea 

Efficacy: The high dynamic compliance value was observed with head end elevation 

Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4738820/

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

Case A) Link to patient details:

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

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:

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

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:

MOA: Aspirin exerts direct neuroprotective effects according to recent studies

Indication: Patient has Cerebellar infarction

efficacy: At the acute phase of cerebral infarction, two recent large studies found that the use of aspirin reduces both mortality and the risk of the recurrence of stroke.

reference:https://www.researchgate.net/publication/262926658_Aspirin_and_cerebral_infarction#:~:text=At%20the%20acute%20phase%20of,not%20reduce%20that%20of%20stroke

Atorvastatin:

MOA: Reduces cholesterol synthesis by inhibiting HMG-CoA reductase

Indication: The cerebellar infarct could be a cause if ischemic stroke due to Atherosclerosis

Efficacy: In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events

Reference Link: https://www.nejm.org/doi/10.1056/NEJMoa061894#:~:text=In%20patients%20with%20recent%20stroke,the%20incidence%20of%20hemorrhagic%20stroke.

Clopidogrel

MOA: Inhibits P2Y-12 receptors on platelets in-turn inhibiting their aggregation

Indication: Patient has a possible Ischemic Stroke

Efficacy: Combination antiplatelet therapy with clopidogrel and aspirin may reduce the rate of recurrent stroke during the first 3 months after a minor ischemic stroke or transient ischemic attack

Reference link: https://www.nejm.org/doi/full/10.1056/nejmoa1800410#:~:text=Combination%20antiplatelet%20therapy%20with%20clopidogrel,the%20risk%20of%20recurrent%20stroke.

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:

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

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:

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

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:

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

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:

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

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:

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

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.

H)Link to patient details:

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                  

  

Possible questions: 

              

1) What can be  the cause of her condition ?             

• Cortical vein thrombosis.

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

• Clotting disorders

• Sickle cell anemia

• Chronic hemolytic anemia

• Beta-thalassemia major

• Heart disease — either congenital or acquired .

• Iron deficiency

• Dehydration

• Head injury

• Pregnancy

• Perperium

• Oral Contraceptive pills

3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?             

• There may be some edema that was not resolved and was excitable,that might have lead to further seizure reccurence.

              

             

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

• Clexane was used which is an anticoagulant.

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.

 

B) Link to patient details:

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

Questions:

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

· As the patient is known case of hypertension since 19 years it is a major risk factor for heart failure it  

· Sclerotic aortic valve need more work done by the left ventricle which can lead to dialated left ventricle and heart failure

· Diabetes is a risk factor for heart failure as it leads to hypertension and elevated lipid levels both of which may cause atherosclerosis which is a cause of heart failure  

· The chronic anemia present in the patient may be a risk factor as total volume of blood is less and heart needs to work harder to supply to all organs

· The chronic kidney disease is one of the causes of heart failure as it releases more renin to increase blood supply to kidneys it leads to more work load on heart resulting in heart failure  

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

· Due to chronic kidney disease, the kidneys fail to produce erythropoietin that is needed for rbc production this is the reason for chronic anemia in this case

3. What is the reason for blebs and nonhealing ulcer in legs of Patient?

· The patient already has diabetes which is risk factor for non healing ulcer and due to heart failure ,the rate of perfusion and oxygenation to extremities is reduced and can delay healing

4. What sequence of stages of diabetes has been noted in this patient?  

· Diagnosed with type 2 diabetes 30 years ago  

· Diabetic retinopathy causing blurring of vision since 4 years (vascular complication)  

· Diabetic nephropathy  

·  

Reference :

        https://www.heart.org/en/health-topics/heart-failure/causes-and-risks-for-heart-failure/causes-of-heart-failure

https://www.kidneyfund.org/kidney-disease/chronic-kidney-disease-ckd/complications/heart-disease/

https://www.diabetes.co.uk/news/2018/dec/four-stages-of-type-2-diabetes-identified-by-us-doctors-99311412.html#:~:text=The%20statement's%20four%20stages%20of,%2C%20or%2C%20related%20microvascular%20events

Case C)

Link to patient details:

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

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: 

MOA: Blocking Na-K-Cl co transporter in loop of Henle > loss of K, Na and Cl in urine

Indication:The patient has Congestive Cardiac Failure 

Efficacy:Torasemide is a lipophilic anilinopyridine sulphonylurea derivative that acts as a high ceiling loop diuretic and has been used for the treatment of both acute and chronic congestive heart failure (CHF) and hypertension 

Reference link: https://pubmed.ncbi.nlm.nih.gov/8852525/#:~:text=Torasemide%20is%20a%20lipophilic%20anilinopyridine,failure%20(CHF)%20and%20hypertension. 

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 

MOA: Na-K ATPase inhibition causing intracellular Ca and hence the contractility 

Indication: Patient is suffering from CHF and Atrial fibrillations and therefore has incomplete contractions

Efficacy: Digoxin, also called digitalis, helps an injured or weakened heart pump more efficiently. It strengthens the force of the heart muscle's contractions, helps restore a normal, steady heart rhythm, and improves blood circulation.

Reference link: https://www.webmd.com/heart-disease/heart-failure/heart-failure-treating-digoxin#:~:text=Digoxin%2C%20also%20called%20digitalis%2C%20helps,the%20symptoms%20of%20heart%20failure.

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:

MOA: Vitamin K antagonist, produces anticoagulant effect

Indication: oral anticoagulant given as prophylaxis for biatrial thrombus   

Efficacy: Efficacy of acenocoumarol has been evaluated in atrial fibrillation.  Acenocoumarol is effective and safe in all age groups.

Reference link: https://pubmed.ncbi.nlm.nih.gov/27730796/#:~:text=Efficacy%20and%20safety%20of%20acenocoumarol,safe%20in%20all%20age%20groups.

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.

 

D) Link to patient details:

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

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?

· The following is the event timeline of symptoms occurrences in the patient:

· She had heartburn like episodes which subsided without medication since 1year

· She was diagnosed with tuberculosis 7 months ago for which she has completed the course of medication  

· She was diagnosed with diabetes 12 years back and with hypertension 6 months back

· She had the first episode of SOB half an hour ago  

· ECG taken then upon admission showed NSTEMI(coronary syndrome) and she was given TAB MET XL 25 MG/STAT.

· She was advised to get PCI but she didn’t get it and symptoms subsided and she is doing fine now

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 pharmacological and non pharmacological interventions provided include:

· TAB MET XL 25MG/STAT (Metoprolol)  

MOA:by blocking beta-1-adrenergic receptors on the cardiac cells

Indication : ECG was suggestive of NSTEMI

Efficacy : The use of early β-blocker therapy in acute MI reduces the risks of reinfarction and ventricular fibrillation, but increases the risk of cardiogenic shock, especially during the first day or so after admission.  

Reference : https://scholar.google.co.in/scholar?q=efficacy+of+Metoprolol+over+placebo&hl=en&as_sdt=0&as_vis=1&oi=scholart#d=gs_qabs&u=%23p%3DeD1C5YL5F2wJ

· PCI

MOA : PCI is a non surgical minimally invasive technique in which the balloon catheter widens the coronary artery and a stent is placedtwith the help of angiography

Indication : NSTEMI

           Efficacy : in immediate invasive strategy (<2hours) indicated in very-high-risk NSTEMI criteria, immediate coronary angiography along with PCI is effective  

Reference: https://academic.oup.com/eurheartjsupp/article/20/suppl_B/B10/4944485

3) What are the indications and contraindications for PCI?

 

Clinical Indications and Contraindications to PCI

Indications

· Acute ST elevation myocardial infarction (STEMI)

· Non ST elevation acute coronary syndrome

· Stable angina

· Anginal equivalent (eg, dyspnea, arrhythmia, dizziness/syncope)

· Asymptomatic or mildly symptomatic patients with objective evidence of a moderate to large area of viable myocardium or moderate to severe ischemia on noninvasive testing

Contraindications

· Significant comorbidities (relative contraindication)

Angiographic Indications and Contraindications to PCI

Indications

· Hemodynamically significant lesion in a vessel serving viable myocardium (vessel diameter >1.5 mm)

Relative contraindications

· Left main stenosis in a patient who is a surgical candidate

· Diffusely diseased small-caliber artery or vein graft

· Other coronary anatomy not amenable to percutaneous intervention

Reference : https://medicalcriteria.com/web/carpci/  

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?

· There are often risks associated with PCI like blood clots, renarrowing of the coronary artery, bleeding from the site of catheterization .We may push the patient into these risks when the procedure is performed in patients who may not need it or when it can be managed by medication .

· Harms of overtretment are psychological stressors, morbidity, unnecessary surgical complications as seen after small renal masses resection surgeries  

· Research on overtesing and overtretment is important because there are downfalls to overtesing and overtretment .

· Huge amount of healthcare money is wasted on unnecessary treatment and testing and more testing and treatment is not linked to better outcome and may become worse sometimes  

Reference :

 https://onlinelibrary.wiley.com/doi/full/10.1111/acem.12820

https://pubmed.ncbi.nlm.nih.gov/30905599/#:~:text=The%20harms%20of%20overdiagnosis%20and%20overtreatment%20are%20numerous%2C%20including%20psychosocial,addition%20to%20unnecessary%20surgical%20complications

https://www.mayoclinic.org/tests-procedures/coronary-angioplasty/about/pac-20384761

E) Link to patient details:

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

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?

A) Evolution of symptomatology

Patient developed hypertension few years ago.

Dragging type of retrosternal chest pain on the right side, 3 days back. 

Dizziness present 

 Anatomical localization:

Inferior ventricular wall of the myocardium.

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

A) 

TAB. ASPIRIN 325 mg:

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. Odds ratios (ORs) ranged from 0.85 (95% CI 0.79–0.92) to 0.90 (95% CI 0.85–0.96).

 

TAB ATORVASTATIN 80mg:

MOA: .It is a competitive inhibitor of the enzyme HMG-CoA reductase, which is an enzyme involved in cholesterol systhesis. 

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%.

TAB CLOPIDOGREL 300mg PO/STAT

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: 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: 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)

INJ HAI 6U/IV STAT ( Human ACTRAPID Injection)

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 thscase 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 hyperglycaemia (blood glucose above 10 mmol/L) in 204 diabetic and 1344 non-diabetic patients undergoing major surgery showed that normoglycaemia (blood glucose 4.4 - 6.1 mmol/L) induced by intravenous Actrapid reduced mortality by 42%

3) Did the secondary PTCA do any good to the patient or was it unnecessary?

A)  Immediate PTCA after thrombolytic surgery has been beneficial in many cases, but there are HIGH chances of REOCCLUSION and REINFARCTION. Therefore, this secondary PTCA could be helpful only if these complication are well prevented and taken care of.

https://www.ahajournals.org/doi/full/10.1161/01.CIR.91.2.476

F) Link to patient details:

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?

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

• Torsemide was used because patient had cardiogenic pulmonary edema which caused shortness of breath in him.

• Torsemide decreases fluid volume(pulmonary oedema) as it is a diuretic .

• It blocks the sodium pottasium channels in ascending loop of henle and thus blocking their absorption leading to exrcretion in urine.

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

• May be prophylactic use because the patient did not have UTI symptoms like urgency or dysuria.

4) GASTROENTEROLOGY & PULMONOLOGY: 

A) Link to patient details: 

CASE I: 

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

 

QUESTIONS & ANSWERS: 

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?

 A.) EVOLUTION OF SYMPTOMATOLOGY:

 

1) 5yrs ago patient developed abdominal pain along with vomiting, which subsided on treatment in a local hospital.

 

2) Patient stopped consuming alcohol for 3 years on physician’s advice.

 

3) Resumed consumption after 3 years due to which he had recurrent episodes of pain abdomen and vomiting.

 

4) 5-6 episodes in past 1 year, treated by local RMP.

 

5) He increased consumption of alcohol from past 20 days @ 5 bottles of toddy/day.

 

6) Binge drinking 1 week back, due to which symptoms of pain abdomen and vomitings arose.     

 

7) Abdominal pain after food intake

 

8) Following this pain, there was nausea and vomiting (1 episode)

 

9) Patient became Febrile, ( high grade & continuous with chills and rigors )

 

10) Patient was constipated for 4 days, with flatus.

 

11) Patient had burning micturition for 4 days with suprapubic pain.

 

12) Urinary frequency & urgency increased.

 

ANATOMICAL LOCALIZATION :

1. Body of the pancreas.

2. Left basal lung.

3. Sub-hepatic region

4. Stomach 

 

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?

 

A.  1) ING. MEROPENAM 

MEROPENEM is carbapenem antibiotic approved by the US FDA, for the treatment of complicated intra abdominal infections. Like other carbapenems, meropenem is stable against chromosomal and extended-spectrum beta-lactamases. In patients with moderate to severe intra-abdominal infections, empirical monotherapy with meropenem achieved clinical response rates ranging from 91 to 100% in 7 randomised comparative trials.   

https://www.researchgate.net/publication/12294847

 

2) ING. METROGYL 

 Eight studies comparing metronidazole combination therapies and carbapenem were included. No difference was found between combined therapy with metronidazole and carbapenem regarding clinical success (odds ratio [OR] = 1.31; 95% confidence interval [CI], .75-2.31), bacteriological eradication (OR = 1.27; 95% CI, .84-1.91), all-cause mortality (OR = 0.61; 95% CI, .37-1.00), or drug-related adverse events (OR = 0.58; 95% CI, .18-1.88). Sensitivity analyses found similar results.

 Combined therapy with metronidazole is as effective and safe as carbapenem in treatment of cIAI. Therefore, combined therapy with metronidazole offers an effective alternative to carbapenem with low risk of drug resistance.

https://pubmed.ncbi.nlm.nih.gov/27704002/

 

3) ING. AMIKACIN

Administration of amikacin in intra abdominal sepsis has become increasingly widely used because of the appropriate efficacy of this agent against the invasive gram negative pathogens as well as the lack of existing antibiotics.

4) ING. OCTREOTIDE

Octreotide being the long-acting analogue of somatostatin, inhibits exocrine secretions of pancreas. It also has direct anti inflammatory and cytoprotective effects.

The overall efficiency of observation group was significantly higher than that of control group (83.3% vs 65.0%, P < 0.05).

And abdominal pain relief time, decompression time, surgical intervention rate, length of stay and mortality rate of observation group (1.9 ± 0.9 d, 6.3 ± 2.2 d, 1.7%, 11.8 ± 0.5 d, 5%) were significantly lower than those of control group (3.6 ± 0.7 d, 10.4 ± 3.1 d, 8.3%, 23.7 ± 2.1 d, 15.0%) (P < 0.05).

After treatment, the levels of blood amylase, white blood cell (WBC), C-reactive protein (CRP) and interleukin 6 (IL-6) of observation group were significantly lower than those of control group (P < 0.05).

And the incidences of such complications as acute respiratory distress syndrome (ARDS), acute renal failure and shock of observation group (10.0%, 5.0%, 13.3%) were significantly lower than those of control group (36.7%, 21.7%, 33.3%) (P < 0.05).

https://pubmed.ncbi.nlm.nih.gov/26178495/

CASE II:

B) Link to patient details:

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?

A)   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.

https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227

 

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

A) Some pancreatic tissue dies during acute pancreatitis episodes, which increase the risks for developing diabetes. This might be the reason for the development of the hyperglycemia in this patient.

 

  https://www.mayoclinic.org/diseases-conditions/pancreatitis/symptoms-causes/syc-20360227/

 

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

A.)  Elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels reflect nonspecific hepatocellular damage. In NAFLD/NASH, aminotransferase levels may be elevated two to four times over the upper limit of normal , with ALT being higher than AST, in contrast to alcoholic steatohepatitis. However, in the absence of advanced disease, routine liver function tests are either normal or typically show only mild elevations in aminotransferase levels, with alkaline phosphatase and gamma-glutamyl transferase (GGT) 1.5 to three times the upper limit of normal.

Several studies involving hepatology clinic patients undergoing liver biopsy and morbidly obese individuals undergoing bariatric surgery have found ALT levels to be higher in the presence of NASH than in those with simple steatosis, although this has not been universally observed.

Therefore, Alanine aminotransferase (ALT) could be the specific marker for alcoholic liver disease, but extensive reasearch into this topic is very much needed.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277175/

 

 

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

A. Here, the patient is being given symptomatic treatment, with IV fluids and basic drugs like Paracetamol, Ondansetron, and Tramadol.

No surgical intervention is needed in this patient as of now. But pleural tapping is being done so as to assess the pleural effusion fluid biochemically.

 

CASE III: 

C) Link to patient details:

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

1.)  What is the most probable diagnosis in this patient?

A.  A.) It most probably looks like hollow viscus perforation, attributed to intestinal obstruction following which patient must have gone int shock, causing multiple organ failure , even though in the starting stage.

               INTESTINAL OBSTRUCTION  ----> HOLLOW VISCUS PERFORATION  

              ---->  SHOCK  ---->  MULTIORGAN FAILURE                                                                                                             

                                                                                                                            

2) What was the cause of her death?

A) The probable cause of her death could be lung atelectasis, as it was the Day 1 of postoperation.  

3) Does her NSAID abuse have  something to do with her condition? How? 

A) NSAID abuse could have caused this condition: 

     NSAID ABUSE (for 4 years)   ---->  ULCER IN GIT ----> PERFORATION

       ----> INTERNAL HAEMMORHAGE ( hence haemorraghic aspirate) ---->

     SHOCK ----> MULTIORGAN  FAILURE.

5)Nephrology and urology 

A) Link to patient details:

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

Questions:

1.what could be the reason for his SOB? 

1 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.2 Absorption of the irrigation fluid (2000 ml or more) may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnoea, 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. 

Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4543890/

2.why does he have intermittent episodes of drowsiness ?

It might be due to uremic encephalopathy

Reference : https://www.ncbi.nlm.nih.gov/books/NBK564327/

3.why does he complain of fleshy mass like thing passing in the urine? 

It might be the blood clot or the scab falling off the prostate during healing after the turp surgery 

https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate-turp/recovery/ 

 

4 what are the complications of turp he may have had? 

Urinary tract infection 

Passing of  blood clots in urine 

TURP syndrome 

https://www.medicalnewstoday.com/articles/321190#complications

B) Link to patient details:

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

Questions

1.Why is the child excessively hyperactive without much of social etiquettes ?

 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

 

2. Why doesn't the child have the excessive urge of urination at night time? 

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 

  

3. How would you want to manage the patient to relieve him of his symptoms?

Urinating on schedule and gradually lengthening the time between bathroom visits

Medication. Drugs that relax bladder like botox injection 

                            Anti anxiety drugs 

Nerve stimulation. This includes some of the latest treatment options for OAB. They sometimes may help when there is no improvement with medications 

Reference : https://www.webmd.com/urinary-incontinence-oab/causes-overative-bladder

https://www.healthgrades.com/right-care/overactive-bladder/mind-over-bladder-mental-tricks-for-managing-oab#:~:text=It%20involves%20urinating%20on%20a,urge%20until%20it%20goes%20away.

6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)  10 Marks 

A) Link to patient details:

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

Questions:

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

• Cough on taking food and liquid.

• Difficulty in swallowing.

• Weight loss of 10kg.

Physical findings suggestive of tracheooesophageal fistula:

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

The suppression of CD4 T cells by HIV causes a decrease in the body's normal response to certain infection.

 If the CD4 count rapidly increases (due to effective treatment of HIV, or removal of other causes of immunosuppression), a sudden increase in the inflammatory response produces nonspecific symptoms such as fever, and in some cases a worsening of damage to the infected tissue. 

There are two common IRIS scenarios. The first is the “unmasking” of an occult opportunistic infection. The second is the “paradoxical” symptomatic relapse of a prior infection despite microbiologic treatment success. Often in paradoxical IRIS, microbiologic cultures are sterile. In either scenario, there is hypothesized reconstitution of antigen-specific T cell-mediated immunity with activation of the immune system following HIV therapy against persisting antigen, whether present as intact organisms, dead organisms, or debris. 

To prevent IRIS , ART treatment is given before CD4 cells count go down below 100cells/ul.

We should prevent advanced immunosuppression.

 https://en.m.wikipedia.org/wiki/Immune_reconstitution_inflammatory_syndrome#:~:text=Immune%20reconstitution%20inflammatory%20syndrome%20(IRIS,paradoxically%20makes%20the%20symptoms%20of

https://www.infectiousdiseaseadvisor.com/home/decision-support-in-medicine/infectious-diseases/immune-reconstitution-inflammatory-syndrome/#:~:text=How%20can%20immune%20reconstitution%20inflammatory,greater%20than%20100%20cells%2FuL.

7) Infectious disease and Hepatology:

 CASE I:

Link to patient details:

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

 

Q&A:

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 ?

A. In this case, LOCALLY-BREWED ALCOHOL can be the possible cause of liver abscess because alcoholism, mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver.  Following alcoholism, poor economic status & malnutrition also plays a vital role as predisposing factors in the formation of liver abscess. Among alcoholism also, consuming locally prepared alcohol plays a vital role, but the reason is still been unknown.

 

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

A. 1.] Factors influencing the association could be related to the:

 Pathogen

 Contents of beverages

 Status of the liver

 Immunity of the host.

 Large infective dose of Entamoeba histolytica or Other bacterial pathogens ingested with the unhygienically brewed beverage.

 Nutritional status of the population 

 Poor sanitation

 Alcohol-induced hepatic dysfunction 

 Possible suppression of amoebistatic immune mechanisms by substances in   the beverages could also be attributed in the mechanism.

2.] Mechanisms responsible:

Hepatic damage by alcohol,

Lowered body resistance and

Suppression of liver function due to poor nutritional status of habitual consumers of alcohol,

Increased presence of amoebae in the liquor prepared locally with poor regard to aseptic procedures, and

Depression of immune mechanisms in chronic alcoholics.

3. Is liver abscess more common in right lobe ?

A. Liver abscess is more common in right lobe because of more blood supply to the right lobe relatively. Due to this fact pathogens are carried in increased proportions to the right  lobe.

    

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

A.  INDICATIONS OF LIVER ABCESS DRAINAGE:

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 

 

CASE II

B) Link to patient details:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

 

Q&A: 

1) Cause of liver abcess in this patient ?

A)  Most amoebic infections are caused by Entamoeba histolytica. The pyogenic abscesses are usually polymicrobial, but some organisms are seen more commonly in them, such as 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).

          The right lobe is more commonly affected lobe. 

 

2) How do you approach this patient ?

A.Treatment along with rationale:  

INJ. ZOSTUM 1.5mg IV (twice daily):

 Zostum is a  combination of  drugs - SULBACTUM (pencillin) &  CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause ( since we can’t take the risk relying on only anti amoebic therapy) 

INJ. METROGYL 500mg IV TID  

Metrogyl has the drug called METRONIDAZOLE [Antibiotic]: For amoebic cause 

INJ. OPTINEURIN 1amp in 100ml NS IV OD: 

Optineurin is a multivitamin drug {A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement 

TAB. ULTRACET 1/2 QID: 

Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever 

TAB. DOLO 650mg  sos,  given for fever and pain 

* Here ; due to medical therapy his symptoms subsided and clearly we can see it in usg reports ( liquefaction has occured) meaning abcess responded to our medical therapy. 

* We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.

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

A. Empirical antibiotic coverage is essential when the organism is unknown. The antibiotics should cover Enterobacteriaceae, anaerobes, streptococci, enterococci, and Entamoeba histolytica. Such antibiotic regimens include cephalosporins plus metronidazole, Beta-lactam Beta-Lactamase inhibitor plus metronidazole, or synthetic penicillins plus aminoglycosides and metronidazole.

Metronidazole should cover Entamoeba histolytica. The duration of treatment varies but is usually from two to six weeks. After initial intravenous treatment, the oral route can be used safely in most cases to complete the course.

 

4) Is there a way to confirm the definitive diagnosis in this patient?

A. As the condition subsided with empirical treatment in this patient, there is no need of a definitive diagnosis in this patient.

But a definitive diagnosis can be achieved if the abscess is aspirated and sent for culture.

8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks 

A) Link to patient details:

 

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

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?

• Evolution of symptomatology:

Day 1-Patient took covid vaccination, on that night patient had high grade fever assosciated with chills and rigor , relieved on medication

Day 4 – Patient had fever assosciated with chills and rigor but not relieved by medication.

Day 11- patient complains of generalised oedema, facial puffiness, periorbital edema.

Day 17- Altered state , facial puffiness, periorbital oedema and weakness of right upper and lower limb.

• Anatomical localization of problem:

Frontal and temporal lobe of brain - infarcts

Orbit 

Oral cavity : eshcar extending from hard palate to lip

Left nasal cavity

• Primary etiology of patients problem

Mucormycosis infection causing rhino-orbito-cerebral mucormycosis.

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?

• Azoles.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 .

•

3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 

• Covid 19 infection among diabetic patients in whom there is lower immunity.

• Increased dose of steroid usage and also because of lower availability of remedesivir , tocilizumab leading to dependance on steroids for treatment. 

• Use of ordinary water instead of sterile water in humidifiers.

• Prolonged ICU stay.

9)

COVID 19 cases:

1)covid 19 with co morbidity (Pulmonology/Rheumatology)

https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html

Possible questions: 

1) How does the pre-existing ILD determine the prognosis of this patient?

• Patients with ILD have diminished pulmonary reserve and impaired gas exchange due injury to alveolar epithelium.

• Prognosis of covid19 patients with preexisting ILD is significantly worse than non ILD patients.

 

2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism? 

• Studies have shown that steroids used for treatment did not worsen the prognosis of rheumatoid arthritis.

• https://www.health.harvard.edu/blog/does-lupus-or-arthritis-affect-your-prognosis-if-you-get-covid-19-2020110921230#:~:text=There%20was%20some%20good%20news,prognosis%20for%20the%20arthritis%20patients.

• Couldn’t find studies,how steroids affect hypothroidism.

3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?

• Not sure about whether this patient has increased risk for post covid autoimmune response.

4) Why was she prescribed clexane (enoxaparin

• 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

covid case 2) Covid 19 with Diabetes 

Link to the patient case report log:

https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html 

Questions:

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?

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 theorised that a coronavirus infection, which affects the ACE2 receptors, might also damage beta cells in the pancreas and hence precipitating diabetes. 

2) Did the patient's diabetic condition influence the progression of her  pneumonia?

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 

3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting? 

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.

covid case 3) Covid 19 Severe 

Link to the complete case report log:

https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html

Questions:

1. Why was this patient given noradrenaline?

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. 

2. What is the reason behind testing for LDH levels in this patient?

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. 

3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?

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.

covid case 4) Covid 19 Mild 

Link to the case report log:

https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1

Questions:

1. Is the elevated esr due to covid related inflammation? 

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. 

2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization? 

 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:

https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html

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. 

It could also have occurred secondary to hypoxic damage due to low O2 saturation which was a result of COVID infection.

 6) Severe Covid 19 with altered sensorium 

Link to the case report log:

https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html

1. What was the cause of his altered sensorium?

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 Hyperglycaemic condition that can cause delirium and even coma might develop. But that would need the evidence of diabetic ketoacidosis. 

2. What was the cause of death in this patient?

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:

https://drsaranyaroshni.blogspot.com/2021/05/a-67-year-old-lady-in-icu-with-covid.html

Questions :

1.What is the grade of pneumonia in her?

A) Grade of pneumonia in this patient is MODERATE. 

2.What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?

A)  Ideal day to start steroids doesnt exist, according to my knowledge, as it depends on the serum markers for covid and reccurance 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.

3.What all could be the factors that led to psychosis in her ?

A) 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

4.In what ways shall the two drugs prescribed to her for psychosis help ?

A)  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.

5.What all are the other means to manage such a case of psychosis?

A) Non pharmacogenic 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

6.What all should the patient and their attendants be careful about ( w.r.t. COVID) after the patient is discharged ?

A) As the patient is in the geriatric age group, gaurdians should take all the precautionary measures  prescribed by the doctors like:

wearing a mask when near them

sanitising all the household items

maintaining personal hygiene

regular drug administration as prescribed by the physician

frequent monitoring of SpO2 levels.

CASE8) Covid 19 Moderate 

Link to the complete case report log 

https://bhavaniv.blogspot.com/2021/05/35yrm-with-viral-pneumonia-secondary-to.html?m=1

Questions:

1. Can psoriasis be a risk factor for severe form of COVID?

a)  Treatment of psoriasis includes few immunosuppresive drugs which can lead to exacerbation of symptoms of covid or increase the risk of disease severity.

So, yes psoriasis can be called as a '' risk factor ".

 

2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?

A) Immunosuppressive drugs can cause various long tern  effects if used for a long time, some of these complications are:

Elevated pressure in the eyes (glaucoma)

Clouding of the lens in one or both eyes (cataracts)

A 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

3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?

A) NO, disease per say causes the fibroproliferative response. Mechanical ventilation just supports the lungs.

CASE9)

Covid with de novo Diabetes 

Link to Case report log:

https://vidya36.blogspot.com/2021/05/a-45-year-old-female-with-viral.html

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 )?

A)  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. 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445137/#:~:text=A%20possible%20hypothesis%20is%20that,which%20may%20induce%20insulin%20resistance.

2.Could it be steroid induced Diabetes in this patient?

A) 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 maynot 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

Costicosteroids also inhibit the production and secretion of insulin from pancreatic β-cells and induce β-cell failure indirectly by lipotoxicity

 

CASE10) Comparing two covid  patients  with variable recovery 

Case report log: https://vidya36.blogspot.com/2021/05/comparative-study.html?m=1

1.What are the known factors driving early recovery in covid?

A) 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.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7220291/

CASE11) Covid moderate with first time detected diabetes:

Link to Case report log :

https://rishithareddy30.blogspot.com/2021/05/covid-case-report.html 

Questions-

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? 

A) 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.   

2) Why couldn't the treating team start her on oral hypoglycemics earlier? 

A) As the patient didn't have any hyperglycemia before, only when her sugars became uncontrolable she was started on fast acting insulin, ACTRAPID.

12) Moderate to severe covid with prolonged hospital stay:

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

Questions :-

1) What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness? 

• CRP 

Rise in CRP indicate a more severe outcome later and more reliable for early identification of case severity 

• NLR(Neutrophil-to-lymphocyte-ratio) 

High NLR suggest more severe outcome 

• Lactate dehydrogenase

High levels of LDH suggest more necrosis of lung tissue and pneumonia and severe disease that causes prolonged stay

• D-dimer

D-dimer is measure of coagulation and fibrinolysis activity. With increase in D-dimer there is increased risk of mortality and morbidity

Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219356/#!po=20.1220

13) Severe covid with first diabetes 

Link to Case report log :

https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html

1.What are the consequences of uncontrolled hyperglycemia in covid patients?

• Increased hospital stay

• Increased risk of mortality

• Increased risk of complications 

Reference : https://care.diabetesjournals.org/content/43/8/1695#:~:text=A%20retrospective%20study%20of%20451,or%20uncontrolled%20hyperglycemia%20(13).

2. Does the significant rise in LDH suggests multiple organ failure?

 Yes,  Extremely high levels of LDH isoenzymes can indicate multi organ failure 

Reference https://www.healthline.com/health/lactate-dehydrogenase-test#test

3.What is the cause of death in this case?

• 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 

    

14) Long covid with sleep deprivation and  ICU psychosis 

Link to Case report log:

https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html

Questions:

1)Which subtype of ICU psychosis did the patient land into according to his symptoms?

 ICU psychosis can be assessed by Confusion Assessment Method (CAM)-ICU-7 delirium severity scale.

Reference:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5392153/#:~:text=The%20final%20CAM%2DICU%2D7,6%2D7%3A%20severe%20delirium.

 

2)What are the risk factors in the patient that has driven this case more towards ICU pyschosis?

• 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 

3)The patient is sleep deprived during his hospital stay..Which do u think might be the most propable condition?

 A) Sleep deprivation causing ICU pyschosis

 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 

 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 

References : https://link.springer.com/article/10.1007/s12028-019-00795-4

15) Moderate Covid with comorbidity (Trunkal obesity and recent hyperglycemia) 

Link to Case report Log:

https://meghanaraomuddada.blogspot.com/2021/05/case-1-2021-42yr-old-male-with-fever.html

QUESTIONS: 

1. As the patient is a non- diabetic, can the use of steroids cause transient rise in blood glucose?

Yes, due to the use of steroids in non diabetic Covid patient can increase blood sugars transienlty until the usage has stopped 

2. If yes, can this transient rise lead to long term complication of New-onset diabetes mellitus? 

Hyperglycemia in non-diabetic Covid patient can be a risk factor for diabetes but it is still unclear about it 

Reference : https://covidiab.e-dendrite.com/introduction.html

3. can this adversely affect the prognosis of the patient?

• Diabetes is one of the most relevant co-morbidity in worsening the prognosis of COVID-19 [1]. Data is also showing that hyperglycemia, in both people with or without diabetes, is an important risk factor for death in COVID-19

• hyperglycemia in people with diabetes at the time of hospital admission is more relevant as risk factor than the previous glycemic control evaluated by HbA1c 

• hyperglycemia at the admission in hospital seems worsening the prognosis of COVID-19 more in people without diabetes than in people with diabetes 

Reference : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445137/#:~:text=Diabetes%20is%20one%20of%20the,COVID%2D19%2C%2C%2C.

5. How can this transient hyperglycemia be treated to avoid complications and bad prognosis?

Reference : https://www.nature.com/articles/s41574-020-00435-4#Tab2

6. What is thrombophlebitis fever? 

 Phlebitis, if mild, may or may not cause symptoms. Pain, tenderness, redness (erythema), and bulging of the vein are common symptoms of phlebitis. The redness and tenderness may follow the course of the vein under the skin.

Low grade fever may accompany superficial and deep phlebitis. High fever or drainage of pus from the site of thrombophlebitis may suggest an infection of the thrombophlebitis (referred to as septic thrombophlebiti

Reference : https://www.medicinenet.com/phlebitis_and_thrombophlebitis/article.htm#:~:text=The%20redness%20and%20tenderness%20may,referred%20to%20as%20septic%20thrombophlebitis).

7. Should the infusion be stopped inorder to control the infusion thrombophlebitis? What are the alternatives?

• The development of superficial thrombophlebitis frequently complicates the insertion of needles into the veins for catheters to give medication or fluids in hospitalised patients. The best treatment for these blood clots in the hands and arms remains unclear. While local treatment has the potential to improve the painful symptoms and patient discomfort, it may not prevent complications, including infection or the extension or transit of the clot into the deep vein system.

• The evidence about the treatment of acute infusion superficial thrombophlebitis is limited and of low quality. Data appear too preliminary to assess the effectiveness and safety of topical treatments, systemic anticoagulation or oral non‐steroidal anti‐inflammatory drugs.

Reference: https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011015.pub2/full#:~:text=An%20array%20of%20topical%20treatments,reduced%20signs%20and%20symptoms%20intensity.

16) Mild to moderate covid with hyperglycemia 

https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html

QUESTIONS: 

1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?

• 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 [11], [12], and angiotensin converting enzyme 2 (ACE2) as a SARS-CoV-2 receptor has higher expression in pancreatic endocrine tissues than in exocrine tissues

Reference https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7233217/#!po=39.1892

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?

It is still unclear about the type of diabetes following Covid infection 

3. How is the prognosis in such patients? 

Elevated HbA1c  usually leads to severe disease 

4. Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves? 

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. 

https://covidiab.e-dendrite.com/introduction.html

5) Why didn't we start him on Oral hypoglycemic agents earlier? 

Might be because he was non diabetic and they did not suspect diabetes in him

COVID CASE 17

17) Covid 19 with hypertension comorbidity 

https://prathyushamulukala666.blogspot.com/2021/05/a-62-year-old-male-patient-with-fever.html

1)Does hypertension have any effect to do with the severity of the covid infection.If it is, Then how?

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.

2)what is the cause for pleural effusion to occur??

infection causes local inflammatory reaction resulting in increased capillary microvascular permeability and a rapid outpouring of fluid containing inflammatory cells into the pleural space

COVID CASE 18

18) Covid 19 with mild hypoalbuminemia.

https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html

QUESTIONS: 

1.What is the reason for  hypoalbuminemia in the patient?

• It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to covid infection.

•

https://pubmed.ncbi.nlm.nih.gov/33411411/2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?

3. What is the reason for Cardiomegaly?

• 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/

4. What other differential diagnoses could be drawn if the patient tested negative for covid infection?

• Influenza

• Mycoplasma pneumonia

• Parainfluenza

• Respiratory syncytial virus

• Streptococcus pneumonia

• Other viral or bacterial pneumonia.

5. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

• 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 haemostatic 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) 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7286212/#:~:text=It%20has%20been%20reported%20that,patients%20with%20good%20clinical%20prognosis

COVID CASE 19 (20)

19)Covid 19 with first time diabetes .

https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html 

Questions:

1)Can usage of steroids in diabetic Covid patients increases death rate because of the adverse effects of steroids???

There is still no proper studies undertaken , I couldn’t find any results that have been yet published on steroid adverse effect increases death rate among covid patients

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7391982/

2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically???

• 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 occuring even in the tiny blood vessels which is not getting disolved with the normal dose anticoagulants which may increase chances of dying.(MAY BE INCREASING DOSE CAN PREVENT DEATH).

https://www.medicalnewstoday.com/articles/blood-thinners-may-protect-against-covid-19-complications#Several-study-limitations

3)Does chronic alcoholism  have effect on the out come of Covid infection????

If yes,how??

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

COVID CASE 21(21)

21) Severe Covid with Diabetes 

https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html

Questions-

1.What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non diabetics?

• 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, hyperglycaemia might support viral proliferation. In accord with this assumption, hyperglycaemia 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

2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?

• 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.

3. What effect does a history of CVA have on COVID prognosis?

• 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

COVID CASE 23(22)

23) Covid 19 with multiple comorbidities:

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-viral-pneumonia.html

1)What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection? 

• Comorbidities like

• Diabetes mellitus since 7years

• Asthma since 7 years

• History of pulmonary kochs which might have caused some lung damage.

• History of pneumonia might have caused damage in lungs.

• Chronic kidney disease since 2yrs.

2)Can you explain why the D dimer levels are increasing in this patient? 

• 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.

3)What were the treatment options taken up with falling oxygen saturation? 

• 15 litres of oxygen/minute was given

• Patient was intubated when oxygen saturation fell to 30%.

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)

• 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.