RACHANA GANGULA

8TH SEMESTER

ROLL NO 110

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 of 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.

SECTION I- Pulmonology

A) “A 55 year old female patient, a resident of Miryalaguda and farmer by occupation ,chief complaints of shortness of breath, pedal edema and facial puffiness.”

Link to patient details:

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

EVOLUTION OF SYMPTOMATOLOGY

ANATOMICAL LOCATISATION-

LUNGS- COPD and Bronchiectasis

(which subsequently lead to Cardiac involvement and heart failure)

ETIOLOGY-

· The various reasons that could have contributed to the etiology in this patient are-

· OCCUPATION- Patient was a farmer by occupation. Hence, the inhalation of allergens like mold hay spores, dust from other grains, tobacco, or some pesticides. Could also be exposure to various other bacteria and fungi.

· Prolonged exposure of fumes from ‘chulha’ . Patient has been using ‘chulha’ for the past 20 years.

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?

-Head elevation

- increases hemodynamic performance and increases end expiratory lung volume

- Indications- .head injury, meningitis,pneumonia

-Antibiotics

- INDICATIONS- severe exacerbations of COPD leading to hospitalization

- TAB. AUGUMENTIN - broad-spectrum antibacterial

- Formulation of Amoxicillin and Clavulanate Potassium

- TAB. AZITHROMYCIN - macrolide-type antibiotic

-Diuretics

- INJ. LASIX IV – Furosemide

§ Loop Diuretic

§ Used to maintain blood pressure

-Corticosteroids

INJ. HYDROCORTISONE

Relieve inflammation and decrease bronchospasm

-Nebulization

NEB. with IPRAVENT

- Ipratropium Bromide – Bronchodilator

- Blocking cholinergic receptors

- decreases the production of cyclic guanosine monophosphate (cGMP)

- leading to relaxation of smooth muscles, and hence Bronchodilation

NEB. With BUDECORT

– Budesonide- corticosteroid

- Used to control inflammation leading to bronchodilation

-Other Bronchodilators

TAB PULMOCLEAR - Acebrophylline and Acetylcysteine

- Airway mucus regulation and anti-inflammatory action causing bronchodilation

Question 3

What could be the causes for her current acute exacerbation?

The probable causes for current acute exacerbation-

- Triggered by an allergen during occupational work (agriculture)

- Triggered by environmental pollutants

- Underlying conditions such as DM and HTN could have caused worsening of shortness of breath in latest episode

- Past history of multiple episodes of shortness of breath which have become more frequent points to the progression of COPD which could explain the current acute exacerbation of the patient.

- Improper use of inhalational medication can also be a cause of acute exacerbation

Question 4

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

The various antitubercular drugs that are used in the ATT are Isoniazid, Rifampicin, Pyrazinamide, Ethambutol, Streptomycin.

Out of these , the drugs that are known to be nephrotoxic are-

§ Rifampicin

§ Ethambutol

§ Isoniazid

They are frequently responsible for the causation of Acute Kidney Injury.

Renal Function Tests show increased values of both Urea as well as creatinine which points to kidney damage.

o Urea: 48 mg/dl

o Creatinine: 1.9 mg/dl

Symptoms like – Facial Puffiness and Pedal Edema could have been affected by the Acute Injury to Kidney. Na+ and water retention is seen, leading to fluid and volume overload, explaining the above symptoms of the patient.

Question 5

What could be the causes for her electrolyte imbalance?

Heart Failure in this patient causes decreased cardiac output which is probably the main reason behind her electrolyte imbalance.

Hyponatremia is seen in this patient.

The association between heart failure and hyponatremia is-

Hence, to sum up, the electrolyte imbalances in this patient are due to the following factors-

Decreased GFR
Vasopressin- Anti-Diuretic effect
Impairment of renal water excretion by angiotensin II

SECTION 2- Neurology

NEUROLOGY-A

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

Link to this case - https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

Question 1

EVOLUTION OF SYMPTOMATOLOGY

ANATOMICAL LOCALISATION

The anatomical localization of the patient's problem is associated with Central Nervous System(CNS).

ETIOLOGY

Chronic alcohol intake in this patient is the main causative factor.

Chronic alcohol intake leads to thiamine deficiency following the interference of many cellular processes which in-turn leads brain disorders like Wernicke-Korsakoff syndrome, Uremic Encephalopathy, etc.

A brief episode of alcoholic withdrawal was the cause of an episode of seizure that occurred 4 months ago. ( Alcohol withdrawal syndrome)

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?

1)Drug name: PREGABALIN

MOA: - presynaptic binding of pregabalin to voltage-gated calcium channels

- anti-seizure and antinociceptive effects

Indication: Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures

Efficacy of Pregabalin:

A Randomized, Double-blind, Placebo-controlled, Dose–Response Study in Adults with Partial Seizures to study efficacy of Pregabalin (PGB)

Study conducted on patients with refractory partial seizures
96 patients received placebo (n = 96)
99 patients received PGB, 150 mg/day (n = 99)
92 patients received PGB 600 mg/day (n = 92); given 3 times a day
Results: PGB, 150 mg/day and 600 mg/day, were both significantly more effective than placebo in reducing the RRatio ( which correspond to seizure-frequency reductions)
Conclusions: PGB, 150 mg/day and 600 mg/day, is highly effective and well-tolerated add-on therapy in patients with partial seizures.

https://onlinelibrary.wiley.com/doi/full/10.1111/j.0013-9580.2004.31203.x

2) Drug name: LORAZEPAM

MOA: binds on the benzodiazepine receptors in the post-synaptic GABA ligand-gated chloride channel in the central nervous system (CNS)

eads to increase on the GABA inhibitory effects causing hyperpolarization .

Hence, stabilization of the cellular plasma membrane.

Indication: -short-term relief of symptoms related to anxiety disorders.

- anesthesia premedication in adults( reduce anxiety/ produce sedation/amnesia )

-the treatment of status epilepticus.

Efficacy of lorazepam:

randomized, double-blind trial evaluate intravenous benzodiazepines.
Population- Adults with prolonged (lasting five minutes or more) or repetitive generalized convulsive seizures.
Total Population- 205 patients- 66 received lorazepam, 68 received diazepam, and 71 received placebo.
Results-status epilepticus had been terminated on arrival at the emergency department in more patients treated with lorazepam (59.1 percent) or diazepam (42.6 percent) than patients given placebo (21.1 percent)
Conclusion- Efficacy of Lorazepam in treatement of status epilepticus is higher than both diazepam and the placebo.

3) Drug name: KCl

MOA: For use as an electrolyte replenisher

Indication: treatment of hypokalemia.

4) Drug name: SYP POTKLOR

MOA: It increases the potassium levels

Indication: Hypokalemia

Question 3

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

A possible cause for the occurrence of neurological symptoms in this episode, which were not present during the previous episodes could probably be explained by the phenomenon called- 'Kindling'.

Kindling refers to the progressive intensification of of neurological symptoms following repeated alcoholic withdrawal episodes mainly seen in chronic alcoholics that have a history of binge drinking.

The main cause is due to long-term changes in NMDA and GABA receptor functioning.

The two neurological symptoms seen in this patient were

1) Seizures

2) Memory loss

While the seizures can be explained by the phenomenon of 'Kindling', while the memory loss could be attributed to the direct toxicity of alcohol on the brain.

Question4

What is the reason for giving thiamine in this patient?

Thiamine deficiency is usually seen in chronic alcoholics mainly due to intestinal malabsorption.
This deficiency of thiamine leads to anaerobic glucose metabolism as it is an important cofactor in various biochemical reactions.
The lactic acid that is formed from anaerobic glycosylation leads to various pathological effects.
It mainly affects the CNS, usually causing a presentation of characteristic symptoms of Nystagmus, Ataxia and Mental Confusion. This triad of symptoms is called Wernicke's Encephalopathywhich is commonly seen in chronic alcoholics.

Hence, Thiamine is given to prevent this kind of encephalopathy in the patient.

Question5

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

Chronic alcohol consumption might have lead to kidney injury in this patient. The various effects that alcohol can have on the kidney are-

Endotoxin - induced inflammation : caused by increased gut permeability and inflammation of liver
Myoglobin - induced tubular toxicity : due to alcoholic myopathy
Hypoxic Tissue Injury- Decreased Renal Blood Flow : due to alcoholic cardiomyopathy.
Hepato-Renal Syndrome in in patients with Alcoholic liver cirrhosis.
Oxidative Stress can also lead to tissue injury of the kidneys.

Question 6

What is the probable cause for the normocytic anemia?

In this patient, the Renal Function Test shows the following values

Urea: 248mg/dL (increased)
Creatinine: 3.8 mg/dL (increased)
Uric Acid: 18mg/dL (increased)

Hence, from the above values we can say that there has been Kidney damage in this patient.

The cause of normocytic anemia is most probably due to the Kidney damage present in this patient.

Question 7

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

Yes, excessive alcohol can cause nutritional deficiencies and subsequent damage to the liver.
These in turn can lead to decreased formation of procoagulants by the liver and alterations in the function of platelets leading to poor wound healing
Long term excessive alcohol consumption may also lead to peripheral neuropathies which could lead to sensory nerve impairment in the foot resulting in delayed responses and cause aggravation of the ulcer.

Neurology-B

(B)" A 52 year old male with Cerebellar Ataxia"

Link to patient details:

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

Question 1

-Evolution of Symptomatology

7 days Ago - Patient complained of giddiness. (subsided briefly; associated with one episode of vomiting)
4 days ago- complained of giddiness- sudden in onset, continuous and gradually progressive. It increased in severity upon getting up from the bed and while walking. Associated with bilateral healing loss and aural fullness and tinnitus.

-Anatomical localisation

Cerebellum- (infract in right inferior cerebellar hemisphere)

-Etiology

Mainly due to acute Cerebro-Vascular Accident (CVA)

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?

Question 3

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

Yes, Hemorrhagic stroke can be caused by prolonged hypertension like de novo hypertension in this patient and not using medication. By treating hypertension, we can reduce the symptoms of cerebellar infarct like giddiness, nausea and headache

Question 4

Does the patients history of alcoholism make him more susceptible to ischemic or hemorrhagic type of stroke?

Moderate and high intakes of alcohol have been documented to have deleterious physiological effects like impaired fibrinolysis and increased platelet activation,

blood pressure and heart rate. Hence making him more susceptible to ischemic stroke.

Neurology-C

(c)"A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB"

Link to this e-log- https://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Question 1

EVOLUTION OF SYMPTOMATOLOGY

ANATOMICAL LOCALISATION

The main localization for the patients problem is - Cervical spine.

ETIOLOGY

The etiology of the patients symptoms can be attributed to the following causes

hypokalemia (leading to palpitation)
cervical spondylitis (causing pain the patient)

Question 2

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

Question 3

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

Various ECG changes seen in hypokalemia are-

decrease in T wave amplitude (earliest ECG manifestation )
Increased P wave amplitude
Prolongation of PR interval
Widespread ST depression and T wave flattening/inversion
Prominent U waves
Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia (seen on worsening of hypokalemia)

Associated symptoms of hypokalemia are-

weakness and fatigue
muscle cramps and pain
palpitations
neurological symptoms- psychosis, delirium, depression

Neurology-D

(D)"A 55year old male patient came to opd with c/o altered sensorium and involuntary movements "

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?

The occurrence of seizure is closely linked to a brain stoke in numerous patients, mainly the elderly population.

In the elderly, stroke is one of the most common causes of seizures and seizures are among the most common neurologic sequelae of stroke, according to many population studies.

So, YES, I agree that there is a relationship between occurrence of seizure to brain stroke.

Seizures may occur as 1) Early onset Seizures (or)

2)Late Onset Seizures,

according to their timing of occurrence after brain ischemia

The following shows the various pathophysiological mechanisms behind the occurrence of Early and Late seizures following Cerebro-Vascular Accidents.

QUESTION2

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?

The general occurrence of types of seizures following Stroke in relation to their timing of occurrence after brain stroke.

*EARLY SEIZURES- [ Focal Seizures] Usually are not associated with the loss of consciousness as they are localized to one area of the cerebral hemisphere and their onset is localized.

*LATE SEIZURES- [Generalised tonic-clonic Seizures AND Complex Partial Seizures] Usually association with the loss of consciousness. These type of seizures disrupt the upper brainstem/medial diencephalon, medial and lateral fronto-parietal association cortex, which constitutes the consciousness system, hence impairing it.

Hence, the previous episodes of seizures could have been Focal Motor Seizures as they were associated with folding of fist, Tremors in leg, frothing, tongue biting, eye rolling without the impairment of consciousness

Whereas, the most recent episode being a Generalised Tonic-Clonic seizure leading to the loss of consciousness in this episode.

Another theory as to why the patient has loss of consciousness in the most recent episode of seizure is –

Neurology-E

(e)"A 48 year old male with seizures and altered sensorium"

link to this case -

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?

- The main reason for the patient to develop ataxia could be the effect of chronic alcohol intake on the cerebellum.

- Direct toxicity by alcohol can lead to cerebellar degeneration and atrophy leading to ataxia.

- The history of chronic alcoholism and development of ataxia point to –

WERNIKE ENCEPHALOPATHY

A triad of symptoms of 1) Mental Confusion 2) Nystagmus 3) Cerebellar Ataxia are seen

Caused mainly in chronic alcoholics due to thiamine deficiency

Pathology of Wernicke’s Encephalopathy

QUESTION 2

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

History of Chronic alcohol intake leads to impaired platelet function and reduced platelet count which is a major cause for Intracranial Bleeding.
Multiple head injuries due to possible minor trauma from frequent falls and no subsequent check-up can also contribute as a cause for his intracranial bleeding.

Contribution of alcohol to bleeding diathesis

Neurology-F

(f) "A 30 YEAR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPERLIMB AND LOWERLIMB "

QUESTION 1

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

Axonal shearing may be caused during trauma to the head
This could aggravate the stoke
So, yes, the history of road trauma does play a role in the condition of this patient

QUESTION 2

What are the warning signs of CVA?

Sudden confusion, trouble speaking, or difficulty understanding speech.
Sudden numbness or weakness, especially on one side of the body.
Sudden changes in vision
Sudden loss of balance
Sudden headache.

QUESTION 3

What is the drug rationale in CVA?

Aspirin, antiplatelet- prevention of stroke again, to prevent other thrombotic event
Mannitol, osmotic agent- to decrease cerebral edema, increase cerebral perfusion

QUESTION 4

Does alcohol has any role in his attack?

Alcohol exhibits an acute inhibitory effect on lipoprotein lipase activity which leads do decreased breakdown of lipids.
Alcohol, hence, causes hyperlipidemia which increase in triglycerides and LDL levels.
This inturn leads to atherosclerosis and ischemia of cerebal vessels leading to stroke

QUESTION 5

Does his lipid profile has any role in his attack?

Association of lipid profile-

Neurology-G

(G)"A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY"

Link to patient details:

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

QUESTION 1

What is myelopathy hand ?

Myelopathy of hand- The changes in the hands observed in various cervical spinal disorders when there is involvement of the spinal cord.
The main clinical features are localized wasting and weakness of the extrinsic and intrinsic hand muscles,
Usually, there is 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.

QUESTION 1

What is finger escape ?

It is a neurological sign of weak finger adduction, usually found in cervical myelopathy patients.
It consists of involuntary abduction of the fifth (little) finger
This is caused by unopposed action of the extensor digiti minimi.

QUESTION 1

What is Hoffman’s reflex?

It is a marker for cervical compression of spinal cord.
Procedure- Performed by tapping or flicking the nail of the middle finger and observe the response of this action on the thumb and middle finger
Reflex flexion of thumb and index finger are signs of a positive test.

Neurology-H

"A 17 year old female with seizures"

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

Question1

What can be the cause of her condition ?

MRI Impression in this patient- "Acute cortical vein thrombosis with hemorrhagic venous infarction involving Right posterior temporal lobe with midline shift to left by 4mm"
Hence, cortical vein thrombosis might be the cause of her seizures.

Question 2

What are the risk factors for cortical vein thrombosis?

Infections- Meningitis, otitis ,mastoiditis
Prothrombotic states- Pregnancy, antithrombin deficiency, Hormone replacement therapy.
Mechanical Injury- Head trauma, lumbar puncture
Inflammatory- SLE, sarcoidosis, Inflammatory bowel disease.
Nephrotic syndrome
Drugs-Oral contraceptives, steroids, Inhibitors of angiogenesis
Chemotherapy-Cyclosporine and l-asparginase
Hematological-Myeloproliferative Malignancies, Primary and secondary polycythemia
Intracranial -Dural fistula, venous anomalies

Question 3

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

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

Question 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.

SECTION 3- Cardiology

Cardiology-A

(A)"A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS"

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?

Heart Failure with Preserved Ejection Fraction	Heart Failure with decreased ejection fraction
Cause- Thickened Ventricles	Cause- Enlarged Ventricles
Also called Diastolic Heart Failure	Also called Systolic Heart Failure
The left ventricle does not relax properly, resulting in impaired filling.	This is caused by reduced contraction of the left ventricle.
Results in increased pressure in left atria and ventricle Causing pressure build up in the lungs.	As a result, not enough blood is supplied to organs.

Question 2

Why haven't we done pericardiocenetis in this patient?

Indication for doing pericardiocentesis- when pericardial effusion does not resolve on its own
In this patient- at the time of admission pericardial fluid was 2.4mm and at the time of discharge it was 1.9 mm .
Hence, it is showing self resolution.
Therefore we did not do pericardiocentesis in this pt.

Question 3

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

NON MODIFICABLE RISK FACTORS in this patient

age- old age
gender- male

MODIFIABLE RISK FACTORS in this patient

hypertension
smoking
type 2 diabetes
kidney disease

Question 4

What could be the cause for hypotension in this patient?

Cardiology-B

B)"A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT"

Link to patient details:

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

Question 1

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

The probable causes for heart failure in this patient are:

Chronic alcohol abuse
Long standing case of hypertension (19 years)
Stage 4 Chronic Kidney disease

Question 2

what is the reason for anaemia in this case?

The cause of anemia in this case could be due to chronic history of alcohol intake.

Alcohol causes anemia by-

↓Erythropoietin (EPO) production by kidney due to kidney damage
↑ Hepcidin as a result of hepatoxicity
Suppression of erythropoiesis as a result of circulating inflammatory cytokines released due to alcohol intake
Hepcidin mediated decreased iron absorption from gut

Question 3

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

The underlying causes for leg and foot ulcers in this patient who is a diabetic are-

venous insufficiency
peripheral neuropathy
peripheral arterial occlusive disease

Question 4

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

Cardiology-C

(c)"A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest since"

Link to patient details:

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

Question 1

EVOLUTION OF SYMPTOMATOLOGY

10 YEARS AGO

Surgery for inguinal hernia

3 YEARS AGO

Aggravated on and off pain at the site of surgery
On and off facial puffiness

1 YEAR AGO

Grade II shortness of breath - diagnosed for HTN (on medication)

2 DAYS AGO

Shortness of breath Grade II (on exertion)
Decreased urine output
Constipation

ONE DAY AGO

Shortness of breath Grade IV (at rest)

DAY OF ADMISSION

Anuria

ANATOMICAL LOCALISATION-

The pateint seems to have a problem in the cardiac musculature

ETIOLOGY-

The main cause of the patients problem is Congestive heart failure, which is a chronic progressive condition.

Loss of atrial contraction and left atrial dilation in this case cause stasis of blood in the left atrium and may lead to thrombus formation in the left atrial appendage

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?

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?

-Any acute or chronic problem in the heart or kidneys could result in an acute or chronic problem of the other, this is the cardio-renal syndrome.

-There is immediate stress on the kidney through pathophysiological connections when CHF develops. The regulation by the sympathetic nervous system and RAAS leads to continuous stress on the nephron.

-An important source of renal stress is increased cardiac preload. The kidneys receive 25% of blood flow, where the majority goes to the cortex, which also has the greatest neural innervations to regulate changes acutely. The medulla receives only 10% of the blood supply. The renal microvascular bed however is continuous throughout. Disease in any glomeruli could have implications when placed under stress from SNS or RAAS and matched with early disease in vascular endothelium.

-Compensation to ensure adequate GFR includes increased renal blood flow (afferent arteriolar vasodilatation), filtration pressure (via efferent arteriolar vasoconstriction) and glomerular hypertrophy, and hyperfiltration (leads to scarring).

In this case the patient has Type 4 cardiorenal syndrome: a chronic decline in kidney function that results in chronic cardiac dysfunction.

Question 4

What are the risk factors for atherosclerosis in this patient?

Hypertension
cholesterol levels not within healthy parameters
Obesity
Diabetes
Lack of physical activity
Age
Smoking

Question 5

Why was the patient asked to get those APTT, INR tests for review?

-APTT: Activated partial thromboplastin time. This is a blood test that characterizes coagulation of blood. The patient has a propensity for thrombus formation, which needs to be monitored by keeping check on the aPTT levels which is an indicator for the coagulability of the blood.

-INR: It is international normalized ratio; it is also a measure of the ability of the blood to clot. This is an important test for patients who are on blood thinners anticoagulants. The patient in this case was taking heparin, so everyday reports of his INR value were needed.

Cardiology-D

(D)"67 year old patient with acute coronary syndrome"

Link to patient details:

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

Question1

TIMELINE OF EVENTS-

• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest

Anatomical localisation

Cardiovascular system

Etiology:

The patient is both Hypertensive and diabetic, both these conditions can cause

- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)

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?

Pharmacological interventions:

TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient

MOA: METOPROLOL is a cardioselective beta blocker

Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)

and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.

Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks

EFFICACY STUDIES.

Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.

Results: mean baseline BP was 132/78 +/- 9/9 mmHg. Following 4 weeks of treatment, mean changes in sitting BP were: placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9 mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg. Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.

Non pharmacological intervention

PERCUTANEOUS CORONARY INTERVENTION.

non-surgical procedure
uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).

Question 3

What are the indications and contraindications for PCI?

INDICATIONS:

Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.

CONTRAINDICATIONS:

Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.

Question 4

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

Although PCI is generally a safe procedure , it might cause serious certain complications like

A)Bleeding

B) Blood vessel damage

C) Allergic reaction to the contrast dye used

D) Arrhythmias

E) Need for emergency coronary artery bypass grafting .

Because of all these complications it is better to avoid PCI in patients who do not require it.

Overtesting and overtreatment are very commonly practiced. Hence, research should be conducted to assess the harms that they pose to the population.

A few examples of the harms caused by overtreatment/testing-

Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations could lead to various pathological maifestations
Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant and could have healed naturally.
Overdiagnosis through overtesting can also psychologically harm the patient.
Hospitalizations or those with chronic conditions who could be treated as outpatients can lead to economic burden and a feeling of isolation.
The use of expensive technologies and machineries can also cause a burden on health care systems.

Cardiology-E

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

Link to patient details:

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

Question 1

EVOLUTION OF SYMPTOMOTOLOGY

3 DAYS AGO

Mild chest pain in the right side of the chest - pain was insidious in onset - gradually progressive - pain was of dragging type - radiating to the back

Dizziness was (not increasing or decreasing with change of position)

Profuse sweating

Disturbed sleep due to discomfort

ANATOMICAL LOCALISATION

The patients problem can be localised to the cardiac musculature.

ETIOLOGY

Myocardial infraction can be caused by a number of factors and associated risk factors as well.

Atherosclerosis
Coronary artery spasm
Coronary artery tear

Question 2

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

1) Drug name: ASPIRIN

MOA: Blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation

Indication: Due to its ability to inhibit platelet aggregation.

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

2) Drug name: TAB ATROVAS

MOA: Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.

INDICATION : Atorvastatin is indicated, in combination with dietary modifications, to prevent cardiovascular events in patients with cardiac risk factors and/or abnormal lipid profiles. Atorvastatin can be used as a preventive agent for myocardial infarction, stroke, revascularization, and angina, in patients without coronary heart disease but with multiple risk factors and in patients with type 2 diabetes without coronary heart disease but multiple risk factors.

3) Drug name: TAB CLOPIB (active metabolite of clopidogrel)

MOA: Clopidogrel is metabolized to its active form by carboxylesterase-1. The active form is a platelet inhibitor that irreversibly binds to P2Y12 ADP receptors on platelets. This binding prevents ADP binding to P2Y12 receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.

Indication: Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease.

Question 3

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

Percutaneous transluminal coronary angioplasty is a surgical treatment to reopen a blocked coronary artery to restore blood flow. It is a type of percutaneous coronary intervention. When performed on patients with acute myocardial infarction, it is called primary angioplasty.

After the secondary PTCA the patient was doing better so it was necessary to do.

Cardiology-F

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

Link to patient details:

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

Question 1

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

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

Question 2

What is the rationale of using torsemide in this patient?

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

Question 3

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

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

SECTION 4-Gastroenterology

Gastro-A

A)"A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA"

Link to patient details:

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

QUESTION1

EVOLUTION OF SYMPTOMATOLOGY

ANATOMICAL LOCALISATION

1. PANCREAS- 1)ACUTE ON CHRONIC PANCREATITIS

2)ACUTE INFECTIVE PERI PANCREATIC FLUID COLLECTIONS

2. LESSER SAC- PSEUDOCYST

3. LEFT LUNG- 1) MODERATE LEFT PLEURAL EFFUSION WITH BASAL ATELECTASIS.

2) LEFT PNEUMOTHORAX SECONDARY TO BRONCHO PLEURAL FISTULA

ETIOLOGY OF DISEASE IN PATIENT

• The main cause of pancreatitis in this patient can be attributed to the chronic intake of alcohol.

• Recurrent episodes of pancreatitis has lead to the various complications of Pseudo cyst formation in lesser sac due to pancreatic duct rupture and Broncho Pleural Fistula leading to pneumothorax.( Systemic involvement)

QUESTION 2

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

The mainstay of treatment in this patient includes

• Antibiotics ( Carbapenem, Metronidazole, Amikacin)

• Octreotide- SOMATOSTATIN analogue

• TPN- Total parenteral nutrition

• USG guided Malecot drainage

The various studies critically studying the efficacy of these drugs in the treatment of such patients are given below.

SOMATOSTATIN AND TPN (TOTAL PARENTERAL NUTRITION)

In this study 31 patients with 1st and 2nd degree pancreatitis underwent a prospective RCT.

Aim- to study clinical benefits of parenteral nutrition during acute pancreatitis and therapeutic validity of Somatostatin

Group 1 - Somatostatin (250 micrograms/h for 72-96 h)

Group 2- received total parenteral nutrition with 2,000-2,500 Kal/day through a central vein

Results- In this study the group receiving TPN had shown quicker recovery rate than the group treated with Somatostatin.

Conclusion-The results of the study have indicated the validity of use of BOTH Somatostatin and TPN during the acute phase of pancreatitis.

(reference- https://pubmed.ncbi.nlm.nih.gov/2566958/ )

ANTIBIOTICS

-A prospective RCT in seven Norwegian hospitals with 73 patients of severe pancreatitis was done

- Control group- patients without antibiotics (n=37).

- Imipenem Group- with early antibiotic treatment (imipenem 0.5 g x 3 for 5-7 days) (n=36) or no antibiotics

-Results: The groups were similar in age, cause of pancreatitis, duration of symptoms and APACHE II score. Patients in the imipenem group experienced

1)lower rates of complications (12 versus 22 patients) (p=0.035)

2)lower infection rates (5 versus 16 patients) (p=0.009) than those in the control group.

-Conclusions: The study, although underpowered, supports the use of early prophylactic treatment with imipenem in order to prevent sequalae of complications following acute pancreatitis.

(reference- https://pubmed.ncbi.nlm.nih.gov/17506001/ )

USG GUIDED PERCUTANEOUS MALECOT DRAINAGE

-Single-center retrospective study was performed with acute necrotizing pancreatitis patients from January 2012 to July 2017.

-78 patients with necrotizing pancreatitis and acute necrotic collections (ANC) who were managed with percutaneous catheter drainage (PCD) in early phase of the disease (< 21 days) were under study

-Clinical data and laboratory parameters of the study group were evaluated until discharge from hospital, or mortality.

-Results- Overall survival rate was 73.1%. Forty-two (53.8%) patients survived with PCD alone, while the remaining 15 (19.2%) survivors needed additional necrosectomy.

-Conclusion-An early PCD in clinically deteriorating patients with acute necrotizing pancreatitis, along with aggressive catheter-directed necrosectomy has proved to be of utmost important in the management of much patients and improve outcome.

(reference- https://link.springer.com/article/10.1007/s12664-019-00969-0 )

As a treating physician I would approach this patient in the following manner-

PHYSICAL EXAMINATION

#Various physical examination findings may include - fever, hypotension, tachycardia and/or tachypnea

#Grey turner sign ( bluish discolouration of flanks) and Cullens sign( bluish discolouration of periumbilical area ) are signs of Severe Pancreatitis.

INVESTIGATIONS:

I.LABORATORY INVESTIGATIONS

CBP(Complete Blood Picture ) – Usually demonstrates leukocytosis which points to an inflammatory background
LFT(Liver Function tests )- Mainly alkaline phosphatase, total bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels are monitored.
RFT(Renal Function Test )- blood urea nitrogen (BUN), creatinine, and electrolytes are monitored as their values change in light of third spacing of fluids
Urine analysis- Urine albumins and sugars are monitored mainly to check progression of disease
Serum amylase- significantly elevated serum amylase values are diagnostic for pancreatitis
ABG(Arterial Blood Gas )- Mainly done when patient is in dyspnea, to identify the cause of dyspnea- ARDS or diaphragmatic irritation, etc.
Pleural tapping – Done to assess the nature of pleural fluid as well as culture and sensitivity of the same.

II.RADIOLOGICAL INVESTIGATIONS

CE-CT- Various complications of pancreatitis like interstitial fluid collections, pseudocyst, necrosis etc. can be visualized.
CXR- Done to assess extent of lung involvement.

PHARMACOLOGICAL TREATMENT

1) OPIOD ANALGESICS- TRAMADOL

- To relieve abdominal pain

2) PROPHYLACTIC ANTIBIOTICS

- Carbapenems

- Aminoglycosides

- Metronidazole

- Given mainly to prevent complications.

3) SOMATOSTATIN ANALOGUES

- Somatostatin long-acting analogue.

- decreases exocrine secretion of pancreas.

- also has anti- inflammatory & cytoprotective effects.

4) PROTON PUMP INHIBITOR- PANTORAZOLE

- It has anti pancreatic secretory effect.

NON PHARMACOLOGICAL TREATMENT

1) TPN ( Total Parenteral Nutrition)

- Nutrients are given through vein to bypass the GI Tract

2) USG Guided Percutaneous Fluid Drainage

- Drainage of peri-pancreatic fluids and fluids from pseudo cyst in this patient

- Studies have proven this treatment method to be highly effective

3) CYSTOGASTROSTOMY

- Fistula is created between pseudo cyst and stomach/duodenum

- can lead to pancreatic abscess

- infrequently used because of the recovery period

Gastro-B

(B)"CASE OF 25 YEAR OLD MAN, WITH SEVERE EPIGASTRIC PAIN"

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

QUESTION1

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

Pleural Effusion can be visualized on the Chest X-Ray report.
This is causing the difficulty in breathing in the patient.
The cause of Pleural Effusion can be a result of the inflammatory cytokines released in response to acute pancreatitis leading to lung damage and/or SIRS. It can also be due to fluid accumulation at base of lung due to blockage of lymphatic channels.
Persistent dyspnea can be due to formation of sinus tract between pseudo-cyst and pleural space

RELATION BETWEEN ACUTE PANCREATITIS AND DYSPNOEA

QUESTION 2

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

The possible reasons to explain the state of hyperglycemia in this patient could be-

- Intake of large amounts of alcohol could have made the patients body more resistant to insulin, paving the way for Diabetes Mellitus and hence explaining the state of hyperglycemia.

- Surges of blood glucose level are also seen in response to inflammatory states of the body due to production of various inflammatory markers.

- Another theory for hyperglycemic state could be the occurrence of multiple episodes of sub-clinical acute pancreatitis leading to repeated acinar damage. Hence causing pancreatic insufficiency and endocrine/exocrine dysfunction. This is associated with imbalance of blood sugar regulation.

- Initial glucagon level increase associated with defects in insulin secretion are seen in prolonged cases of pancreatitis. This is usually associated with T3Cdm diabetes/ brittle diabetes later in the course of the disease.

QUESTION 3

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

· Patient is a known alcoholic and has a history of alcohol abuse since 4 years before he presented to the hospital.

· While recently, his daily consumption of locally made alcohol has signifanctly increased.

· As alcohol is a known hepatotoxic substance, it is associated with liver injury.

· Hence, elevated LFT’s are a result of hepatocellular injury due to chronic alcohol intake.

The specific markers for Alcoholic Fatty Liver Syndrome are

- GGT (Gamma Glutamyl Transferase)

- CDT (Carbohydrate-deficient transferrin)

QUESTION 4

What is the line of treatment in this patient?

1. Relieve pain in patient

- TRAMADOL

- ACETAMINOPHEN

2. Control Vomiting

- ONDANSETRON

3. Control Pancreatic Secretions

- PANTOPRAZOLE

4. IntraVenous Fluids ( bypass GI Tract)

5. Monitor HyperGlycemia

- Fasting and Post prandial blood glucose

- HbA1c

6. GRBS Charting

7. USG Guided pleural tap to control dyspnea

Gastro-C

QUESTION 1

What is the most probable diagnosis in this patient?

The most probably -abdominal hemorrhage.

This explains the abdominal distention, and the blood which is aspirated.

Differential 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

2) What was the cause of her death?

The most probable cause of death in this patient is due to the complications of laparotomy surgery that she underwent in Hyderabad the next day

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

NSAID-induced renal dysfunction

decreased glomerular perfusion
decreased glomerular filtration rate
acute renal failure.

SECTION 5-Nephrology

A) Link to patient details:

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

1. What could be the reason for his SOB ?

The Patient had renal failure which could lead to metabolic acidosis.

This would explain the shortness of breath in this patient.

2. Why does he have intermittent episodes of drowsiness ?

The intermittent episodes of drowsiness could be due to Hyponatremia

3. Why did he complaint of fleshy mass like passage in his urine?

Fleshy mass like casts in urine are a hallmark feature of Acute Tubular Necrosis, hence the patient passed them in his urine.

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

Electrolyte Imbalances is the most probable complication that this patient developed.

SECTION 6- Infectious Disease

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?

The following finding of the patient points towards treacheo-oesophageal fistula

- Cough occurs on taking food and liquids

- lasted around 2 months

-This is called ONO’S SIGN and is characteristic is most patients with acquired treacheo-oesophageal fistula

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

Immune reconstitution inflammatory syndrome be prevented by-

- initiation of ART before the development of advanced immunosuppression

- to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART

SECTION 7-Hepatology

Hepatology-A

(a) "A 55 year old male patient who is a palm tree climber with PAIN ABDOMEN SINCE ONE WEEK "

Link to this case-

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

QUESTION 1

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 ?

The chronicity of alcohol intake in this patient seems to have a strong association with the occurrence of liver abscess. Socio-economic factors and poor sanitary conditions surrounding the frequent intake of alcohol provide a strong link between alcohol intake and liver abscess as well.

The contents of the locally made alcoholic beverage

QUESTION 2

2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ?

Below is a flowchart summarizing the various factors that are involved in the etiopathogenesis of a liver abscess in a chronic alcoholic

3. Is liver abscess more common in right lobe ?

Yes, Liver abscess is more common in the right lobe due to increased laminar blood flow.

This increases the chances of the organisms to lodge in the right side of the liver via hematological spread of the disease and hence more likely cause abscess in the right lobe of the liver.

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

ANSWER-

USG guided aspiration of liver abscess can be used for both Therapeutic as well as Diagnostic uses.

The Various Indications of USG guided aspiration of Liver Abscess are-

Hepatology-B

Link to patient details:

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

QUESTIONS:

1) Cause of liver abcess in this patient ?

The cause of liver abscess in this patient could be either pyogenic OR Amoebic.

The patient responded well with the medication of metronidazole suggesting that the cause of the abscess is most likely amoebic in origin.

The patient has a history of consuming locally made alcohol called toddy, which could be the cause of the liver abscess.

2) How do you approach this patient ?

Medical management:

To control pain-

Analgesics: NSAIDs, opioid analgesics (in cases of severe pain)

To control fever

Antipyretics: Paracetamol

To control infection

Antibiotics: Metronidazole, paromomycin, diloxanide furoate+ broad spectrum antibiotics

USG guided aspiration: Done if indicated.

Surgical management:

Surgical drainage by transperitoneal approach, mainly in cases of peritonitis

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

To find out the causative organism of the abscess we would have to perform serological tests on the aspirated pus from the abscess, and that is not always indicated as it has various drawbacks and complications.

Hence, treatment for both Amoebic Liver Abscess as well as Pyogenic Liver Abscess is done using a combination therapy of both the drugs- metronidazole and broach spectrum antibiotics

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

The confirmation of Liver Abscess is done by CT Scan.

The Liver abscess can be caused by pyogenic or amoebic organisms, hence to come to a definitive diagnosis between the two, Aspiration of the pus in the Liver Abscess is to be done,.

Amoebic liver abscess aspirates have an anchovy appearance
Pyogenic abscess is usually purulent nature of aspirate . This is not the most reliable test.
Culture of aspirate provides the most accurate diagnosis

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

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 with relation to Anatomical Involvement

Evolution of symptomatology in patient according to timeline

1) ANATOMICAL LOCATION

Anatomical Location in this condition would primarily involve PARANASAL SINUSES

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

§ PARANASAL SINUSES- predominantly, Maxillary and Sphenoid Sinus involvement is seen – Sinusitis

§ ORBITS- Preseptal Cellulitis

§ CEREBRAL CORTEX- infarct around the left corona radiata (front and temporal lobe infarcts) -right hemiparesis

2) Primary Etiology of Patients Problem

The primary etiology surrounding this patient can be strongly linked to a fungal infection caused by a group of opportunistic fungi called- Mucorales.

Hence, Mucromycosis is said to be the primary cause of disease in this patient.

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

The mainstay of treatment in this patient is the use of liposomal Amphotericin B

The main problem regarding the usage of Amphotericin B is the debate of formulation of it – either liposomal or deoxycholate

Liposomal Amphotericin B has better penetration into the CNS as well and mucormycosis being an invasive fungus can cause CNS lesion.

Deoxycholate AmB is nephrotoxic drug and is frequently associated with elevated creatine levels during its use in treatment.

Hence, with liposomal AmB being safer, higher doses can be administered leading to better response from the patient.

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

Immunocompromised state of patients due to impaired neutrophilic responses. As mucormycosis is an opportunistic fungi, these kinds of patients are more at risk. The main causes being-

- Uncontrolled Diabetes

- Aggressive Steroid overuse during the treatment of COVID-19

COVID-19 is known to cause immunological alternation in patients as well ( decreased CD4+ and CD8+ counts)

Mucormycosis may also occur as a secondary infection DURING the treatment of COVID-19 owing to aggressive treatment with Antibiotics and Steroids

References- https://academic.oup.com/jid/article/182/1/274/881972

https://pubmed.ncbi.nlm.nih.gov/26595825/

SECTION 9- COVID19

the following link contains the MATERSHEET FOR COVID-19 cases-

https://docs.google.com/spreadsheets/d/1_7FcWSqHJpY2TxSrjbH-CjDenTpxN_23cbzoAeWNpm0/edit?usp=sharing

SECTION-10

https://docs.google.com/document/d/1NidQsQevk0huozvalMuvX6AtTB2GyR7N0pvCmmND5vU/edit?usp=sharing

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General Medicine Case Discussion

GEN MED BIMONTHLY ASSIGNMENT

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

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

NEUROLOGY-A

Neurology-B

Neurology-C

Neurology-D

Neurology-E

Neurology-F

Neurology-G

Neurology-H

Cardiology-A

Cardiology-B

Cardiology-C

EVOLUTION OF SYMPTOMATOLOGY

10 YEARS AGO

3 YEARS AGO

1 YEAR AGO

2 DAYS AGO

ONE DAY AGO

DAY OF ADMISSION

ANATOMICAL LOCALISATION-

Cardiology-D

(D)"67 year old patient with acute coronary syndrome"

Cardiology-E

Cardiology-F

Gastro-A

Gastro-B

Gastro-C

Hepatology-A

(a) "A 55 year old male patient who is a palm tree climber with PAIN ABDOMEN SINCE ONE WEEK "

Hepatology-B

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