MEDICINE CASE DISCUSSION - NON COVID CASES

 Online blended bimonthly assignment toward summative assessment for May 2021 

Name: Sreshta

Roll no: 48

May 31 2021

I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.

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

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

Below are my answers to the Medicine Assignment based on my comprehension of the cases.

1. PULMONOLOGY

1. what is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary aetiology of the patient problem?

-Evolution of symptomatology

• 1st episode of sob - 20 yr back
• 2nd episode of sob - 12 yr back
• From then she has been having yearly episodes for the past 12 yrs 
• Diagnosed with diabetes - 8yrs back
• Anaemia and  took iron injections-5yr ago
• Generalised weakness  - 1 month back
• Diagnosed with hypertension  - 20 days back
• Pedal oedema - 15 days back
• Facial puffiness- 15 yrs back
• Anatomical location of the problem - lungs
• Primary aetiology of patient- usage  of chulha since 20 yrs might be due to chronic usage 

2Q)what r the mechanism of action indication and efficacy over placebo of each of the pharmacological and non-pharmacological interventions used for this patient?

-Head end elevation :# MOA;

• .improves oxygenation 
• .decreases incidence VAP
• .increases hemodynamic performance 
• .increases end expiratory lung volume
• .decreases incidence of aspiration 
• #Indication: .head injury,.meningitis, pneumonia 

-oxygen inhalation to maintain spo2

-Bipap: a non-invasive method

• #MOA: assist ventilation  by delivering positive expiratory and inspiratory pressure without the need for ET incubation9

3. Cause for current acute exacerbation - it could be due to any infection

4.could the ATT affected her symptoms if so how?

• Yes ATT affected her symptoms
• Isoniazid and rifampicin -nephrotoxic - raised RFT was seen.

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

• Renal insufficiency
• Hypoxia
• Hypercapnia
• Respiratory acidosis.

2. NEUROLOGY

2A) link to pt details: https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

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

 -evolution of the symptomatology in this patient in terms of an event timeline;

• , he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again. 
• He was unable to lift himself off the bed and move around and had to be assisted. It was associated with a decrease in food intake since 9 days
• He also had short term memory loss for 9 days. the primary aetiology of the patient's problem-ALCOHOL INTAKE

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

1. IVF NS and RL @150ml/hr

mechanism of action;

•    Sodium Chloride is the source of water and electrolytes. It is capable of inducing diuresis depending on the clinical condition of the patient. It is a crystalloid given intravenously in case of shock, dehydration, and diarrhoea to increase the plasma volume.

indication;

• The following are primary indications for the use of normal saline infusion that have been approved by the FDA: Extracellular fluid replacement (e.g., dehydration, hypovolemia, haemorrhage, sepsis) Treatment of metabolic alkalosis in the presence of fluid loss. Mild sodium depletion

2. Inj. 1amp THIAMINE in 100ml NS, TID

Thiamine MOA

• Mechanism of Action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.

Indications and Usage

• Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, as in Wernicke's encephalopathy, infantile beriberi with acute collapse, cardiovascular disease due to thiamine deficiency, or neuritis of pregnancy if vomiting is severe. to;

3. Inj. Lorazepam

mechanism of action;

• Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell

indication;

• ATIVAN Injection is indicated in adult patients for preanesthetic medication, producing sedation (sleepiness or drowsiness), relief of anxiety, and a decreased ability to recall events related to the day of surgery.

4. T. Pregabalin 75mg/PO/ BD

MECHANISM OF ACTION;

• Pregabalin has demonstrated anticonvulsant, analgesic, and anxiolytic properties in preclinical models. The drug's exact mechanism of action is unclear, but it may reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels 

INDICATION;

• Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures in patients 1 month of age and older

5. Inj. HAI S.C.- premeal
6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am
7. Lactulose 30ml/PO/BD

MECHANISM OF ACTION;

• Lactulose is used in preventing and treating clinical portal-systemic encephalopathy. Its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia. It has also gained popularity as a potential therapeutic agent for the management of subacute clinical encephalopathy

INDICATION;

• Lactulose is a prescription drug used by mouth or rectally to treat or prevent complications of liver disease (hepatic encephalopathy). It does not cure the problem but may help to improve mental status. Lactulose is a colonic acidifier that works by decreasing the amount of ammonia in the blood.

8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours

MECHANISM OF ACTION;

• Potassium ions participate in several essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.

INDICATIONS;

• Potassium chloride is used to prevent or treat low blood levels of potassium (hypokalemia). Potassium levels can be low as a result of a disease or from taking certain medicines, or after a prolonged illness with diarrhoea or vomiting.

9. Syp Potchlor 10ml in one glass water/PO/BD

• Mode of Action; It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium...

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

• Altered sensorium due to alcohol withdrawal syndrome, DECREASE LEVEL OF THIAMINE LEADS TO THE SYMPTOMS

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

• Thiamine is a key vitamin in the maintenance of membrane integrity and osmotic gradients across cell membranes and is stored in body tissues predominantly as thiamine diphosphate (TDP). TDP participates in energy production as an essential cofactor for several enzymes in the TCA cycle and pentose phosphate pathways
• Thiamine deficiency causes depletion of intracellular TDP, leading to a decreased activity of the TCA cycle and pentose phosphate pathways. Consequently, cellular energy (ATP) depletion and reduction of DNA/RNA and NADPH synthesis ensue, which results in low resistance to oxidative stress. Moreover, there is an accumulation of toxic intermediate metabolic products such as lactate, alanine and glutamate, reduced cellular pH in cells, and disruption of the homeostasis of cellular electrolytes, which results in cytotoxic oedema.

2B)  Link to pt details:

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

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

- the evolution of the symptomatology in this patient in terms of an event timeline

• -history of giddiness
•  This was associated with 1 episode of vomiting on the same day.
• from the bed and while walking.
• - This was associated with Bilateral Hearing loss, aural fullness and the presence of tinnitus.
• - He has associated vomiting- 2-3 episodes per day, non-projectile, non-bilious containing food particles.

• - Patient has H/o postural instability- he is unable to walk without the presence of supports, swaying is present and he has a tendency to fall while walking 

PRIMARY ETIOLOGY;

•  obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia. Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anaesthesia with contralateral hemibody sensory loss of pain and temperature. Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting. However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts.

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

Tab Veratin 8 mg PO TID

MECHANISM OF ACTION;

• Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but a strong effect on H3 receptors.

INDICATIONS;

• Vertin Tablet is used to prevent and treat a disorder of the inner ear known as Ménière's disease. The symptoms include dizziness (vertigo), ringing in the ears (tinnitus), and loss of hearing, probably caused by fluid in the ear.

Inj Zofer 4 mg IV/TID

Mode of Action of Zofer 

• Zofer Injection works by inhibiting the action of a chemical substance known as serotonin. Serotonin is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.

Tab Ecosprin 75 mg PO/OD

MECHANISM OF ACTION;

• Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot

INDICATION;

•  This tablet is also used to prevent heart attacks, stroke and heart-related chest pain (angina)

Tab Atorvostatin 40 mg PO/HS

Mechanism of Action

• Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver

INDICATIONS;

• Reduce the risk of non-fatal myocardial infarction.
• Reduce the risk of fatal and non-fatal stroke.
• Reduce the risk for revascularization procedures.
• Reduce the risk of hospitalization for CHF.
• Reduce the risk of angina.

BP monitoring- 4rth hourly

Tab Clopidogrel 75 mg PO/OD

MECHANISM OF ACTION;

• The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.

INDICATIONS;

• FDA-approved indications for clopidogrel include: Use during a percutaneous coronary intervention (PCI) for the acute coronary syndrome (ACS) and stable ischemic heart disease.  Primary prevention of thromboembolism atrial fibrillation

Inj Thiamine 1 AMP in 100 ml NSPO/BD

Tab MVT PO/OD

3) Did the patients history of denovo HTN contribute to his current condition?

4) Does the patient's history of alcoholism make him more susceptible to an ischaemic or haemorrhagic type of stroke?

• yes, the pt has h/o chronic alcoholism and is susceptible to the ischemic type of stroke.

2C) link to pt details:

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

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 aetiology of the patient's problem?

A) *Evolution of symptoms: the patient was normal 8 months back then developed b/l pedal oedema which gradually progressed.

Aggravated in sitting and standing position relived on taking medication

*Palpitations: since 5days, sudden in onset which is more during the night

Aggravated by lifting heavy weights, speaking continuously

*Dyspnoea during palpitations (NYHA-3) since 5 days

*pain: since 6days, radiating along left upper limb, more during palpitations and relived on medication.

Chest pain associated with chest heaviness for 5 days

Etiological agent :

*By localization, electrolyte imbalance (hypokalemia) causing her   manifestations like palpitations, chest heaviness, generalised body weakness

*radiating pain along her left upper limb due to cervical spondylosis 

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

A) Reason: recurrent hypokalemic periodic paralysis 

Current risk factor: due to the use of diuretics

Other risk factors 

A) Abnormal losses:

Medications-diuretics, laxatives, enema, corticosteroids

Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia 

B) trance cellular shift: alkalosis, thyrotoxicosis, delirium remains, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis

C) Inadequate intake: anorexia, dementia, starvation, total parental nutrition

D) psuedohypokalemia: delayed sample analysis, significant leukocytosis

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

A) changes seen in ECG : 

• Earliest change: decreased T-wave amplitude, ST depression, T-wave - and inversion or flat; prolonged PR interval; the presence of U waves 
• In Severe cases: ventricular fibrillation, rarely AV block 

Symptoms of hypokalemia :

• Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium. 

2D)Link to patient details:

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

QUESTIONS:

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

• Seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury 
• Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosiderin. Deposits)caused by-products of blood metabolism.

• Late-onset seizures are associated with persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. 

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

• Initially, the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic-Clonic seizures (loss of consciousness)

2E) Link to patient details:

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

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

• The patient has minor unattended head injuries in the past 1 yr. According to the CT scan, the patient has a cerebral haemorrhage in the frontal lobe causing probably the occurrence of Frontal love ataxia

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

• The patient has minor unattended head injuries. With time the minor haemorrhages if present should have been cured on their own. But the patient is a chronic alcoholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow furthermore into 13 mm sized haemorrhages occupying Frontal Parietal and Temporal lobes

2F) Link to patient details:

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

Questions

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

• The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition

2.What are the warning signs of CVA?

• Weakness or numbness of the face, arm or leg, usually on one side of the body
• Trouble speaking or understanding
• Problems with vision, such as dimness or loss of vision in one or both eyes
• Dizziness or problems with balance or coordination
• Problems with movement or walking
• Fainting or seizure
• Severe headaches with no known cause, especially if they happen suddenly

3.What is the drug rationale in CVA?

• Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral oedema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant. 
• Ecospirin 

• For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.
• Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.

• Rt feed is a nursing procedure to provide nutrition to those who can either not obtain nutrition by mouth or are not in a state to swallow the food safely. 

4. Does alcohol has any role in his attack?

• When the patient met with an accident there might be cranial damage that was unnoticed.
• If so his occasional drinking may or may not have hindered the process of the minor haemorrhages getting healed and might have caused this condition
• 
  
• But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.
• 
  
• Therefore it cannot be evaluated without further details.

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

• The inverse relationship between serum HDL-C and stroke risk. When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.

2G) 

link  to pt details: 

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

a)what is myelopathy hand?

• There is a loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 

b)what is finger escape?

• Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digit minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".

c)what is Hoffman's sign?

• Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition

2H) Link to pt details: 

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

1) What can be the cause of her condition?     

•    According to MRI  cortical vein thrombosis might be the cause of her seizures

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

• Infections: Meningitis, otitis, mastoiditis
• Prothrombotic states: Pregnancy, puerperium, antithrombin deficiency protein and protein s deficiency, Hormone replacement therapy.
• Mechanical: Head trauma, lumbar puncture
• Inflammatory: SLE,sarcoidosis,Inflammatory bowel disease. 
• Malignancy.
• Dehydration 
• Nephrotic syndrome 
• Drugs: Oral contraceptives, steroids, Inhibitors of angiogenesis
• Chemotherapy: Cyclosporine and l asparaginase
• Haematological: Myeloproliferative Malignancies, Primary and secondary polycythemia
• Intracranial : Dural fistula, 
•  venous anomalies 
• Vasculitis:
• Behcets disease Wegener's granulomatosis

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

• Seizures are resolved and a seizure-free period got achieved after medical intervention but the sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.

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

• Anticoagulants are used for the prevention of harmful blood clots.
• Clexane  ( enoxaparin)  low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor Xa.

3. CARDIOLOGY

3A) Link to pt details:

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

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

• Ans: Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). 
• Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure
• HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease.

2.Why haven't we done pericardiocentesis in this patient?

• Ans: Pericardiocentesis is not done here  Because the effusion was self-healing, It reduced from 2.4cm to 1.9 cm.

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

• Ans: risk factors for the development of heart failure in this patent
• Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure 
• high blood pressure
• Smoking
• Diabetes
• AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.
• wosening of pericardial effusion leaing to cardiac tamponade.

4.What could be the cause for hypotension in this

• Ans: visceral pericardium may have  thickened which is restricting the heart to expand causing hypotension (May be secondary to TB)

3B) Link to pt details: 

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

QUESTION: What are the possible causes of heart failure in this patient?

the patient has various comorbidities which could have led to a heart failure

• 1.       The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mix trad insulin daily and was also diagnosed with diabetic arteriopathy indicating uncontrolled diabetes which is a major risk factor for heart failure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494155/ 
• 2.       The patient has also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure. https://pubmed.ncbi.nlm.nih.gov/31472888/ 
• 3.       He is a chronic alcoholic for 40 years which is a risk factor for heart failure. https://www.nmcd-journal.com/article/S0939-4753(19)30360-6/fulltext
• The findings in this article provide longitudinal evidence that moderate and heavy alcohol consumption is associated with decreased LVEF and trend towards a higher risk of incident LV systolic dysfunction, compared to light drinkers.
• 4.       The patient has elevated creatinine and AST/ALT ratios is >2 and were diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900793/ 

 

QUESTION: what is the reason for anaemia in this case?

• The patient has normocytic normochromic anaemia. it could be anaemia of chronic disease as the patient is diagnosed with CKD stage IV.
• Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.
• Patient’s with anaemia and CKD also tend to have a deficiency in nutrients like iron, vitamin B12 and folic acid essential in making healthy red blood cells

 

QUESTION: What is the reason for blebs and non-healing ulcer in the legs of this patient?

• The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause a delay in the healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.

                                         

QUESTION: What sequence of stages of diabetes has been noted in this patient?

• There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.
• The patient is diagnosed with diabetic arteriopathy exhibiting a sequence of neuropathy, retinopathy and nephropathy
• The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness.

3C)

Link to pt details:

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

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

Ans: *the anatomical site is BLOOD VESSELS;

* ETIOLOGY: 

• The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
• The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

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

Ans: PHARMACOLOGICAL INTERVENTIONS

1. TAB. Dytor

• mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

2. TAB. Acitrom 

• mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting

3. TAB. Cardiovasc 

• mechanism: Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.

4. INJ. HAI S/C

• MECHANISM: Regulates glucose metabolism
• Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue

5.TAB. Digoxin 

• mechanism: Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
•  Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart.

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered regularly when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

3) What is the pathogenesis of renal involvement due to heart failure (cardiorenal syndrome)? Which type of cardiorenal syndrome is this patient? 

• Ans: *cardiorenal syndrome type 4 is seen in this patient.

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

• Ans: effect of hypertention
•  They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.

5) Why was the patient asked to get that APTT, INR tests for review?

• Ans: APTT and INR are ordered regularly when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
• Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.

3D) Link to pt details:

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

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

Aetiology: 

• female sex  
• age -  67 years
• diabetes since 12 years
• hypertension since 6 months

Pathophysiology:

• MI occurs due to decreased myocardial oxygen supply due to severe coronary artery narrowing or acute atherosclerotic plaque rupture/ erosion and superimposed thrombus formation
• Due to a decrease in myocardial oxygen supply, there is heartburn
• due to heart muscle damage there is a decrease in pump function of the left ventricle causing a decrease in pulmonary circulation which leads to SOB. It occurs due to partial occlusion of a major vessel or a complete occlusion of a minor vessel.                                                                                     

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

Analgesic-                                                                                                                                        

• to relieve distress
•  to lower adrenergic drive and reduce vascular resistance, BP, infarct size, susceptibility to ventricular arrhythmias

Antiplatelet therapy - aspirin + ticagrelor

• aspirin improves survival, reduces the risk of mortality, MI, stroke
• ticagrelor reduces recurrent ischemic events

Glycoprotein 2b/ 3a receptor antagonists

• tirofiban & abciximab block the common pathway of platelet aggregation and are potent inhibitors of platelet rich-thrombus formation.

Anticoagulants

• heparin reduces the risk of thromboembolic complications and prevents reinfarction

Angioplasty and coronary artery bypass surgery

• these are non-pharmacological interventions and their outcome is determined by the no. of diseased vessels, the severity of cardiac dysfunction and no. of concomitant diseases as much as age itself.

3) What are the indications and contraindications for PCI?

Indications-                

• STEMI     
• atypical chest pain
• stable angina
• unstable angina
• non STEMI
• positive stress test                                                                                                                               

Contraindications-  

• lack of cardiac support
• coagulopathy
• hypercoagulable state
• a diffusely diseased vessel without focal stenosis                                                                                                                                             

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?

Complications-              

• occlusion of target vessels or a side branch by thrombus or a loose flap of the intima and consequent myocardial damage
• Re-stenosis

3E) Link to pt details:

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

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

• ; Evolution of symptomatology:
• Uncontrolled DM2 for 8 years
• 3 days back Mild chest pain dragging type and retrosternal pain(radiated)
• Anatomical localisation: Inferior wall of the heart
• Primary aetiology: Diabetes type 2 (uncontrolled)
• 
  
• high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels

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

TAB. ASPIRIN 325 mg PO/STAT

•  Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.

TAB ATORVAS 80mg PO/STAT

• Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.

TAB CLOPIBB 300mg PO/STAT

• Mechanism of action: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible. 

INJ HAI 6U/IV STAT

VITAL MONITORING.

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

• Ans; Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percentage of patients with the documented long-term success of angioplasty
• Over testing and overtreatment can raise a person’s risk of cardiovascular death by as much as four times.

3F) Link to pt details:

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

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

• Because of the  fluid loss that occurred to the patient
• there is decreased preload- so, SOB occurred due to decreased CO
• IV fluids administered- there is increased preload- SOB decreased due to better cardiac output.

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

• Torsemide used to relieve abdominal distension.

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

• IT IS THE TREATMENT FOR UTI
•  Rationale- Used for any bacterial infection.

4. GASTROENTEROLOGY AND PULMONOLOGY

4A) Link to patient details:

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

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

-Evolution of symptomatology 

• H5 years back-1st episode of pain abdomen and vomitings 
• Stopped taking alcohol for 3 years
• 1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 
• 20 days back increased consumption of toddy intake
• Since 1-week pain abdomen and vomiting
• For 4 days fever constipation and burning micturition
• Anatomical localisation: Pancreas and left lung

-Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

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

 

INJ. MEROPENAM ; TID for 7 days 

• Meropenem ( broad spectrum Carbepenem ) an antibiotic.

2) ING. METROGYL 500 mg IV TID for 5 days

• in. Metrogyl has METRONIDAZOLE
• ( Nitroimidazole drug ) an antibiotic

3) ING. AMIKACIN 500 mg IV BD for 5days

•  It is an Aminoglycoside antibiotics 
• Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and; to prevent septic complications of acute pancreatitis.

4) TPN ( Total Parenteral Nutrition )

• * Method of feeding that bypasses the gastrointestinal tract
• * Fluids are given to vein, it provides most of the nutrients body needs.
• * TPN has proteins, carbohydrates, fats, vitamins, minerals.

5) IV NS / RL at the rate of 12l ml per hour

•  Given for fluid replacement ie., treat dehydration 

6) ING. OCTREOTIDE 100 mg SC, BD

• * It is a Somatostatin long-acting analogue.
• * It is used here to decrease exocrine secretion of the pancreas and it also has anti-inflammatory & cytoprotective effects.

7) ING. PANTOP 40 mg IV, OD

• * Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.

8) ING. THIAMINE 100 mg in 100 ml NS  IV , TID

• * It is a B1 supplement. 
• * It is given here because; due to long fasting & TPN  usage, the body may develop B1 deficiency 
• * Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplementation is necessary.

9) ING. TRAMADOL in 100 ml NS  IV , OD

• It is an opioid analgesic, given to relieve pain

4B)  Link to pt 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

• 1ans: the cause of dyspnea might be PLEURAL EFFUSION

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

• This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
• * the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 
• * elevated levels of catecholamines and cortisol

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

• LFT is increased due to hepatocyte injury
• *If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
• *elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
• The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to (i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics (ii) mitochondrial damage leading to increased release of mAST in serum.

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

A: Plan of action and Treatment:

• Investigations:

✓ 24 hour urinary protein 

✓ Fasting and Post prandial Blood glucose 

✓ HbA1c 

✓ USG guided pleural tapping 

• Treatment:

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

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

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly

4C) link to pt details:

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

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

àDifferential Diagnosis: 

• ·        Ruptured Liver Abscess
• ·        Organized collection secondary to Hollow viscous Perforation.
• ·        Organized Intraperitoneal Hematoma.
• ·        Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
• ·        Grade 3 RPD of right Kidney

àThe most probably diagnosis is there is an abdominal haemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated. 

 2) What was the cause of her death?

• àAfter leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. The cause of her death can be due to complications of laparotomy surgery such as haemorrhage (bleeding), infection, or damage to internal organs. 

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

• NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.

5. NEPHROLOGY AND UROLOGY

5A)  Link to pt details:

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

1.what could be the cause for his SOB

• Ans- His sob was is due to Acidosis which was caused by Diuretics

2. Reason for Intermittent Episodes of drowsiness

•  Ans-Hyponatremia was the cause for his drowsiness 

3.why did he complaint of fleshy mass like passage inurine

• Ans-plenty of pus cells in his urine passage  appeared as fleshy mass like a passage to him

4. What are the complications of TURP that he may have had

• Difficulty micturition
• Electrolyte imbalances
• Infection

5B) 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 many social etiquettes?

• Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age.
• For a diagnosis, the symptoms have to be present for more than six months and cause problems in at least two settings (such as school, home, work, or recreational activities).

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

• Since the child doesn’t have the excessive urge of urination at night but at day there might be a psychiatry related condition 
• 1. Psychosomatic disorder
• 2. Undiagnosed anxiety disorder 

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

• bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
• If the cause is an overactive bladder, a medication known as anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
• To treat attention deficit hyperactivity disorder:
• For children 6 years of age and older, the recommendations include medication and behaviour therapy together — parent training in behaviour management for children up to age 12 and other types of behaviour therapy and training for adolescents.  Schools can be part of the treatment as well. 
• Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
• Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behaviour problems. It may also help you to organize your tasks and improve listening skills.

6A)INFECTIOUS DISEASE

Link to pt details:

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

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

• Cough since 2 months on taking food and liquids
• difficulty in swallowing since 2 months. It was initially difficult only with solids but then followed by liquids also.
• laryngeal crepitus- positive
• These favour tracheoesophageal. fistula

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

• Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.
• The most effective prevention of IRIS would involve the initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
• Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease before the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
• Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.

7. INFECTIOUS DISEASES AND HEPATOLOGY

7A)  Link to pt details:

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

1Q)do u think drinking locally made alcohol cause liver abscess in this patient due to predisposing factors present in it? What could be the cause of this patient?

• 1ans- yes, it could be due to intake of contaminated toddy

2Q)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient? (since 30 yrs - 1 bottle/day)

• 2ans - according to some studies, 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. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.

3Q)is liver abscess is more common in the right lobe?

• 3ans-yes right lobe is involved due to its more blood supply

4Q) what r the indications  for usg guided aspiration of liver abscess 

4ans- Indications for USG guided aspiration of liver abscess

• 1. Large abscess more than 6cms
• 2. Left lobe abscess
• 3.Caudate lobe abscess
• 4. Abscess which is not responding to drugs

7B) Link to pt details:

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

1) Cause of liver abscess in this patient?

• 1ans: cause of liver abscess in this patient is ENTAMOEBA histolytica

2) How do you approach this patient?

• 2 and: APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS

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

• 3ans: we treat the patient for both amoebic and pyogenic abscess  so that we don't rely only on anti-amebic therapy and ensure complete treatment of the cause

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

• 4 ans: the confirmatory test for an amoebic abscess is
• Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
• The diagnosis of the amebic liver abscess was based on four or more of the following criteria:
•  (i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, 
• (ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), 
• (iii) enlarged and/or tender liver, usually without jaundice, 
• (iv) raised right dome of the diaphragm on chest radiograph, and 
• (v) improvement after treatment with antiamebic drugs (e.g., metronidazole). 

8.INFECTIOUS DISEASE

Link to pt details: 

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

QUESTION:  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 aetiology of the patient's problem?

• 1.     3 years ago- diagnosed with hypertension
• 2.     21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigours, high-grade fever, no diurnal variation which was relieved on medication
• 3.     18 days ago- complained of similar events and went to the local hospital, it was not subsided upon taking medication(antipyretics) 
• 4.     11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. The patient was in a drowsy state
• 5.     4 days ago-  
• a.     patient presented to casualty in an altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
• b.     towards the evening patient periorbital oedema progressed
• c.     serous discharge from the left eye that was blood-tinged
• d.     was diagnosed with diabetes mellitus
• 6.     patient was referred to a government general hospital 
• 7.     patient died 2 days ago
• the patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute or rhino orbital mucormycosis. rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes ( https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html ) the fungus enters the sinuses from the environment and then the brain.
• The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA ( https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes. )

QUESTION:  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?

• The proposed management of the patient was – 

1.     inj. Liposomal amphotericin B according to creatinine clearance 

2.     200mg Iitraconazole was given as it was the only available drug that was adjusted to his creatinine clearance

3.     Deoxycholate was the required drug which was unavailable

https://pubmed.ncbi.nlm.nih.gov/23729001/ this article talks about the efficacy and toxicity of different formulations of amphotericin B 

along with the above-mentioned treatment for the patient managing others symptoms is also done by-

       I.          Management of diabetic ketoacidosis – 

• (a)   Fluid replacement-  The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in the blood.
• (b)   Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in the blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
• (c)   Insulin therapy-  Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy

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

•  Mucormycosis is maybe being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients. 
• With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing.