MEDICINE MONTHLY ASSESSMENT (MAY 2021)

SNEHA CHAUHAN 

ROLL NO. 126

8th SEMESTER

2017 BATCH

MBBS

Medicine Bimonthly Assessment (May 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 to come up with treatment plan. 

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

http://medicinedepartment.blogspot.com

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

Question no 1) Pulmonology

1. Link to patient’s details: 55 yr old female with shortness of breath, pedal edema, and facial puffiness.

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.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’s the primary etiology of the patient’s problem?

• From patient’s history, we have 

• Shortness of breath since 20 years- her first episode lasted a week and occurred in the month of January while working in a paddy field and relieved upon medication.
• For next 8 years, patient suffered from similar episodes every year lasting approximately 1 week occurring around January 
• Her latest episode of SOB started 30 days ago, of grade 2 

• Diagnosed with hypertension 20 days back

• 20 days back she showed signs of bronchiectasis through HRCT scan

• Pedal edema and facial puffiness 15 days ago.

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

• Oxygen inhalation to maintain saturation above 90%
• Head elevation
• Intermittent BiPAP for 2 hrs
• Inj AUGMENTIN 1.2g IV- mechanism of action is that the amoxicillin binds to penicillin binding proteins in the bacterial cell wall and inhibits it’s synthesis. Clavulinic acid is a beta lactam, structural similar to penicillin, is said to inactivate certain beta lactamase enzymes.

• Tab AZITHROMYCIN 500mg OD- binds to 23S rRNA of bacterial subunit. Stops bacterial protein synthesis by inhibiting translocation process of protein synthesis 

• Tab PANTOP 40mg OD- Inihibits gastric acid production by binding to ATP pump to inhibit gastric acid secretions

• Inj HYDROCORTISONE 100mg IV- Binds to glucocorticoid receptor leading to downstream effects such as inhibition of phospholipids A2 etc.

• Nebuliser BUDEFORT 6hrly- potent anti inflammatory agent which binds and activates glucocorticoid receptors in the effector cells aka lung cytoplasm. 

• Chest physiotherapy

• Inj HAI S.C.

• GRBS 6th hrly

• Temp, BP, RR, PR monitoring 

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

• Apart from infections owing to the worsening of cough, and SOB due to increased volume purulence and sputum therefore causing acute exacerbation,
• In this case, it could be stress/pollution/ smoke especially since she’s been using an indoor Chulha cooking stoves (for past 20 yrs) which produces a large amount of smoke hence causing suffocation.
• Allergens whilst working on fields.

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

• Yes it could have affected the patient
• As after getting tested negative for AFB, empirical ATT was started for her on 4/5/2021, after which she may have developed 
• Generalised weakness
• Pedal edema
• Facial puffiness 

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

• According to the patient’s serum electrolyte levels, she has decreased sodium levels (hyponatremia) and decrease chloride levels (hypochloraemia)
• Possible causes of hyponatremia -- being a hypertensive, she is prescribed Tab TELMA 40 OD (Generic name- Telmisartan), which is an angiotensin 2 receptor blocker class of anti hypertensive drugs.
• In some patients especially with co morbid conditions such as diabetes Mellitus, telmisartan may cause both Hyperkalemia and hyponatremia as well as generalised weakness.
• Possible cause of hypochloraemia- can occur as a result of chronic hypercapnia in COPD due to respiratory acidosis with metabolic alkalosis (due to renal compensation). 

Question no 2) Neurology 

1. Link to patient’s details- Altered sensorium in 40 year old male. 

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’s the primary etiology of the patient’s problem?

Evolution of symptoms from history 

• A year ago- patient developed an episode of seizures for the first time 
• 4 months back- last episode of seizures 
• On 9/5/2021- was talking to himself, laughing to himself, but was oriented to time, place and and person occasionally.
• He was unable to get up from bed, had decreased food intake from the past 9 days and short term memory loss.
• 15/5/2021- was admitted to tertiary care hospital.

Anatomical localization

• Thalamus 
• Hypothalamus 
• Wernickes encephalopathy due to chronic alcohol intake 

Primary etiology

• Vitamin B1 deficiency due to excess alcohol consumption
• Increased serum urea and creatinine accounting for kidney failure. 

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

• Thiamine-

• Indication: Thiamine deficiency due to chronic alcohol consumption in this case.

• Mode of action: To increase thiamine in the body

• Lorazepam-

• Indication: reduce stress and anxiety 

• Mode of action: Increasing GABA levels

• Pregabalin-

• Indication: for seizures

• Mode of action: similar to GABA, mimics it and binds to alpha 2 delta receptors 

• HI injection-

• Indication: increased blood sugar levels on RBS

• Mode of action: Increases peripheral uptake of glucose therefore reduces blood sugar levels.

• Lactulose-

• Indication: for cognitive function in hepatic encephalopathy 

• Mode of action: improves mental status 

• KCl injection-

• Indication: for hypokalemia

• Mode of action: acts as a potassium supplement

• Potchlor-

• Indication: hypokalemia

• Mode of action: potassium supplement

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

• May be due to significant damage to the brain caused from
• - excessive alcohol and 
• - decreased food intake since 9 days (despite withdrawal) hence no adequate nutrition to the body. 

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

• Excessive alcohol intake brings about inflammation to stomach lining which then interfere’s with the body’s ability to absorb essential vitamins from food.
• This may typically result in vitamin B1 (thiamine) deficiency which is essential for breaking down glucose hence essential for proper brain functioning as it acts as an essential coenzyme to TCA cycle and pentose phosphate shunt.
• Lack of vitamin B1 leads to brain damage.
• Other causes of Thiamine deficiency would be malabsorption.

5. Probable cause of kidney injury in this patient?

• Increase in creatinine levels have been speculated to cause Uraemic encephalopathy 
• Along with that other reasons could be—
• Free amino acid changes
• Damage of degeneration of blood brain barrier
• Decrease in brain energy demand. 

6. Probable cause for normocytic anemia?

• Chronic kidney disease
• Increase hemato-toxicity of both 
• Alcohol (as they enter cell membrane and alter the lipid components of it)
• And it’s metabolite (ie acetaldehyde)
• Malabsorption 
• Chronic alcoholism

7. Could chronic alcoholism have aggravated the foot ulcer formation

• Yes, Chronic alcoholism as stated previously leads to various nutritional deficiency due to inflammation of stomach hence interfering with the proper absorption of essential nutrients.
• Poor nutrition leads to poor wound healing and interference with normal bodily functions.
• Typically vitamin B1 is a vitamin required by the brain for breakdown of glucose. Excessive alcohol decreases the stomach’s absorption of thiamine hence leading to significant brain damage.
• This then leads to decrease of sensory nerve function of foot, leading to tingling and burning sensation hence when foot gets injured, ulcers form if not retreated adequately if persists for more than 3-6 months.

B) Link the patient’s details- 52 year old male with cerebellar ataxia. 

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

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

Evolution of symptomatology 

• On 13/5/2021- Giddiness and vomiting 
• On 16/5/2021- Giddiness: sudden onset, gradual progression bilateral hearing loss, aural fullness, tinnitus. Vomiting of 2 episodes per day non bilious 
• On 18/5/2021- slurring of speech, deviation of mouth

Anatomical localization 

• Right inferior cerebellar hemisphere 

Primary etiology 

Alcohol intake and persistent not properly treated hypertension 

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

• Tab Vertin

Mode of action- Histamine analogue 

Indication- Dizziness

• Inj Zofer

Mode of action- Inhibits serotonin by blinding to serotonin receptors

Indication- Nausea and vomitting

• Tab Ecosporin

Mode of action- antiplatelet action by inhibiting formation of thromboxane A2

Indications- infarct in brain

• Tab Atorvostatin

Mode of action- HMG CoA reductase inhibitor

Indications- High serum cholesterol 

• Tab Clopidogrel

Mode of action- inhibits platelet aggregation

Indications- infarct in brain

• Inj Thiamine

Mode of action- thiamine supplement 

Indications- thiamine deficiency 

• Tab MVT

Mode of action- supplements cobalamin (vitamin B12)

Indications- Vitamin B12 deficiency 

3. Did the patient’s history of de novo HTN contribute to his current condition?

• Yes, the patient’s condition can be attributed to not only these habits posing as potential risk factors (mainly chronic alcohol intake in this case), but also long standing or persistent HTN for which he wasn’t consistent with treating it using medication.
• This sort of cause leads to haemorrhagic type of stroke that directly damages brain tissue or obstructs vascular flow through local elevated pressure. 

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

• The patient’s alcoholism makes him more susceptible to haemorrhagic type of stroke also paired with the patient’s HTN being an even bigger risk factor.
• Alcohol is said to decrease the levels of liver produced coagulation factors and brings about platelet abnormalities all of which predispose to haemorrhagic strokes. 

C) Link to patient’s details- 45 year old female patient with palpitations, pedal edema, radiating pain along the left upper limb. 

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-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’s the primary etiology of the patient’s problem?

Evolution of symptoms 

• Patient developed edema pitting type which gradually progressed 
• Chest pain radiating along left upper limb since 5 days aggravated on lifting weight 
• Difficulty breathing since 5 days .

Primary etiology

• Main cause is the patient’s hypokalemia leading to symptoms of dyspnea and palpitations
• The radiating pain along her upper limb can be due to her cervical spondylosis 

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

Reasons for recurrence of hypokalemia could be due to 

• Abnormal loss from diuretics, laxatives, hypomagnesemia, osmotic diuretics etc
• Inadequate nutrition or intake
• Alkalosis shift, head injuries etc.

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

• ECG changes in 

• Mild hypokalemia:- Flattening of T waves 
• Severe hypokalemia:- followed by, Q-T interval prolongation, visible U wave, and mild ST depression. 

• Symptoms of hypokalemia are-

• Weakness 
• Fatigue
• Muscle cramps
• Palpitations
• Psychosis 
• Delirium 
• Depression
• Muscle pain

D) Link to patient’s details- 55 year old patient with seizures.

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

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

• Yes, a stroke patient might experience frequent seizures which could indicate epilepsy (diagnosed if seizures become regular and are not associated with a specific cause)
• How ever frequent and seizure attacks is somewhat indicative of the former
• At times, if signs of are not clear of a stroke, a seizure may be evident enough for it if he had suffered a stroke in the past.

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

• Repeated seizures may indicate epilepsy. Usually epilepsy type of seizures cause dynamic changes and abnormal increase in activity in brain function which typically leads to loss of consciousness. 

E) Link to patient’s details- 48 yr old male with seizures and altered sensorium. 

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

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

• Multiple unattended head injuries may be the reason which could account to ataxia in this patient.

2. What was the reason for his IC bleed? Does alcoholism contribute to bleeding diatheses?

• The main reason in this case would be alcohol.
• Alcohol brings about liver damage, which decreases production of liver produced clotting factors hence causes bleeding 
• Since patient has is a known alcoholic, it may have been a contributing factor to which diathesis may have occurred all of a sudden. 

F) Link to patient’s details- 30 year old male with weakness of right upper limb and lower limb

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

1. Does patient’s history of road traffic accident have any role in this present condition?

• Yes, patient’s history of road traffic accident has a role in patient’s current condition, usually ischemic type of stroke as indicated by the presence of infarct in MRI scan

2. What are the warning signs of CVA?

• Sudden numbness or weakness in face, upper limbs, lower limbs, usually on one side of the body
• Confusion
• Trouble speaking
• Loss of balance
• Loss of coordination 
• Severe headache with no known origin
• Trouble walking
• Trouble seeing with one or both eyes

3. What is the drug rationale in CVA?

• Alteplase- thrombolytic drug usually given for ischemic stroke, 0.9mg/kg IV
• Anti-platelet drugs- Aspirin 

4. Does alcohol have any role in this attack?

• Moderate alcohol consumption is said to have decreased platelet aggregation, increase fibrinolysis and decrease levels of clotting factors. 
• Heavy consumption however always leads to I’ll effects due to increase in risks such as hypertension, nutritional imbalance etc. 
• But alcohol is said to have increased the risk of haemorrhagic stroke.
• studies based on relation of alcohol and stroke are unclear though.

G) Link to patient’s details- A 50 yr old patient with cervical myelopathy.

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

1. What is myelopathy hand?

• When there’s loss of power in both adduction and extension of ulnar 2/3 fingers supplied by it,
• Along with Inability to grip and release rapidly with these 2 fingers
• Is termed as “Myelopathy hand” due to pyramidal tract involvement.

2. What is finger escape?

• It’s a neurological sign involving abduction of the 5th finger (little pinky finger), caused by unopposed action of extensor digiti minimi due to weakness of ulnar nerve.
• This is called “finger escape sign” or “Wartenberg’s sign”

3. What is Hoffman’s reflex?

• Hoffmann’s sign or reflex is a test used to examine the upper extremities reflexes
• It is easy, requires no equipment
• And is convenient to test for any possible existing spinal cord compression.
• It is said to be positive for upper motor neuron lesion and corticospinal tract dysfunction, leading to spinal cord compression. 

H) Link to patient’s details: 17 yr old female with seizures.

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

1. What can be the cause of her condition?

• Iron deficiency anemia
• Problems related to blood clot formation
• Infections
• Beta thalassemia major
• Chronic haemolytic anemia
• Head injuries
• Dehydration

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

• Neoplasms
• Pregnancy
• Systemic diseases such as hypertension 
• Dehydration 
• Intracranial tumors
• Oral contraceptives 
• Coagulopathies
• May be Associated with- head injuries, surgery, A-V malformations etc.

3. What drug was used in suspicion of cortical venous sinus thrombosis?

• Tab ACITROM 2mg/po/OD

Question 3) Cardiology

1. Link to patient’s details- 78 year old male with shortness of breath, chest pain, bilateral pedal edema, and facial puffiness.

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

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

• Heart failure with preserved ejection fraction, also known as diastolic heart failure, is where the cardiac muscle contracts normally but the ventricles do not relax as they should when there’s ventricular filling. 

• Heart failure with reduced ejection fraction, also known as systolic heart failure, cardiac muscle does not contract effectively, therefore there’s decreased oxygen rich blood being supplied to the rest of the body. 

2. Why haven’t we done pericardiocenetis in this patient?

• It is contraindicated in this patient due to potential risk of myocardial rupture through rapid pericardial decompression.

• Another risk factor may also be excessive excessive bleeding that may occur, which is a risk considering he’s a hypertensive.

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

• Most of them are modifiable risk factors in this patient which are-

Chronic alcohol consumption since 30 yrs 

Smoking since 30 yrs

Hypertension- diagnosed a year ago 

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

• Due to considerable hemodynamic changes that occur, which brings about systolic blood pressure to fall by 10mmHg or more on inspiration termed “Pulsus paradoxicus”, a classic hallmark of cardiac tamponade (usually detectable in 70-80% of patient’s suffering from this) and in about one third of patients suffering from acute pericarditis. 

• In constrictive pericarditis, no forward flow from superior Vena cava and inferior vena cava during inspiration, Kussmaul’s sign, which is swelling of vein necks as of to right side of heart. 

B) Link to patient’s details- 73 year old male patient with pedal edema, Shortness of breath, and decreased urine output.

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

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

• Chronic alcoholic since 40 years
• Hypertension since 19 years
• Heavy build of this patient 

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

• Chronic alcohol drinking can lead to anemia due to disturbance in iron absorption for its storage in the body. 

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

• Diabetes 

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

C) Link to this patient’s details- A-fib and biatrial thrombus in a 52 yr old male.

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

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

Evolution of symptoms-

• Shortness of breath- since 1 yr, but aggravated 2 days back, and progressed from grade 2 to grade 4 
• Since 2 days- decreased urine output and Anuria on the day of examination. 

Anatomical localization- Atrium

Primary etiology - Hypertension

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

Inj DOBUTAMINE 

• Mechanism of action- acts in beta 1 adrenergic receptors to increase heart contraction, therefore to increase Cardiac output.

• Indications- Cardiogenic shock 

Tab DIGOXIN

• Mechanism of action- positive ionotropic effect by increasing force of contraction by reverse inhibition of myocardial Na K ATPase pump

• Indications- Heart failure and Chronic Atrial Fibrillation

Inj Unfractionated HEPARIN

• Mechanism of action- is an Anticoagulant, inactivated thrombin and activates Factor Xa and inhibits thrombin induced act of platelets and of Factor V and VII 

• Indications- Pulmonary embolism, Deep Vein Thrombosis and Atrial Fibrillation. 

Tab CARVEDILOL

• Mechanism of action- is a non selective adrenergic blocker, therefore decreases blood pressure.

• Indications- Reduced ejection fraction heart failure, and Left ventricular dysfunction following Myocardial infarction.

Tab ACITROM

• Indications- Deep vein thrombosis and pulmonary embolism 

Inj THIAMINE- Vitamin B1 supplementation

Inj HAI

Tab TAXIM

• Mechanism of action- Inhibits bacterial cell wall growth

• Indications- Bacterial infections such as in meningitis, lower respiratory tract infection, and meningitis.

Tab PAN D- anti reflux action

Tab Dytor

• Mechanism of action- aldosterone antagonist 

• Indications- high blood pressure 

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

• Type 4- Chronic nephrocardiac 

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

• Alcohol consumption 
• NSAID abuse- causing cardiovascular symptoms 

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

• APTT (Activated Partial Thromboplastin Time)- is done to investigate the cause of blood clots/bleeding, A-fib increases risk of blood clot formation in heart which can lead to stroke. 

• INR (International Normalised Ratio)- is done to assess the risk of excessive bleeding against risk of thrombosis. 

D) Link to patient’s details- 67 year old patient with acute coronary syndrome.

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

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

Evolution of symptoms-

• Heart burn- 1 yr back
• Diagnosed for Tuberculosis- 7 months back
• Hypertension- 6 months back
• Shortness of breath on the day of admission

Anatomical localization- Coronary arteries 

Primary etiology- 

• Hypertension 
• Age ( 67 years old)

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

Tab MET XL

• Mechanism of action- it is a long acting beta blocker to help decrease pulse rate

• Indications- high blood pressure and heart conditions such as heart failure etc 

3. What are the indications and contradictions for PCI?

Percutaneous Coronary Intervention (PCI)

Indications 

• Acute ST Elevation myocardial infarction (STEMI)
• Non ST Elevation acute coronary syndrome
• Unstable angina

Contraindications 

• Long term antiplatelet therapy 
• Coagulopathy
• Any significant comorbid conditions 

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

E) Link to patient’s details- Case discussion on acute myocardial infarction 

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

1. What is the evolution of 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?

• Mild chest pain since 3 days radiating to the back (retrosternal pain)
• Is a known case of Type 2 Diabetes Mellitus and Hypertension 

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

Tab ASPIRIN 

• Mechanism of action: inhibits COX-1

• Indications: Angina pectoris, Fever and Ischemic Stroke etc 

Tab ATORVAS

• Mechanism of action: competitively inhibits HMG-CoA reductase, therefore decreases cholesterol.

• Indications: heart attack, strokes 

Tab CLOPIBB

• Mechanism of action: severely inhibits ADP binding to platelet receptor therefore irreversibly inhibits platelet aggregation 

• Indications: Thromboembolic atrial fibrillation 

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

F) Link to patient’s details- Case of cardiogenic shock

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

1. How did the patient get relieved from his SOB after IV fluids administration by rural medical practitioner?

• IV fluids are given to correct the hypovolemia and hypotension (unless pulmonary edema is present), that comes with cardiogenic shock
• So there could have been a possibility this that as the cardiogenic symptoms were being treated by IV fluids, one of the major manifestations of cardiogenic shock being Shortness of breath was possibly relieved.

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

• Torsemide belongs to a class of drugs known as Diuretics, specifically loop diuretics which act of the Loops of Henle in the nephron, therefore influencing release of salt and water in urine from kidneys.
• In turn, this reduces the flow in arteries and veins, thereby decreasing blood pressure, and also as a result also increases urine output.

3. What’s  the rationale for administration of ceftriazone? Was it prophylactic or for the treatment of UTI?

• It is more of a prophylactic measure than a treatment modality as it’s known to be very effective in reducing the risk of infection especially amongst UTI and pneumonia cases.

Question no 4) Gastroenterology and Pulmononlogy

1. Link to patient’s details- A 33 yr old man with pancreatitis, pseudo cyst and left broncho-pleural fistula.

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

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

Evolution of symptoms:

• Pain abdomen since 5 years ( patient was treated appropriately)
• Stopped alcohol consumption 3 years back, hence was asymptomatic during this period
• Started alcohol consumption following which he developed recurrent episodes of both pain abdomen and vomiting (non bilious, non projectile)
• 4 days ago from day of admission, developed constipation, flatulence and burning micturition.

Anatomical localization:

• Pancreas
• Lungs

Primary etiology:

• Alcohol consumption being a major precipitating factor for the patient’s condition 

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- given as its a broad spectrum antibiotic
• Inj AMIKACIN- aminoglycoside antibiotic. Antibiotics are given in order to help control the infection spread from sepsis.
• Total parenteral nutrition, to help replenish most of the body’s nutritional needs.
• Inj OCTREOTIDE, anti inflammatory actions
• Inj PANTOP, for controlling pancreatic secretions 
• Inj THIAMINE, for supplementary vitamin B1
• Chest drain
• Surgical intervention may be required.

B) Link to patient’s details- Case of 25 yr old man with severe epigastric pain.

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

1. What is the cause of the patient’s dyspnea? How is it related to pancreatitis?

• Pancreatitis causes chemical changes in the body that affect lung functions 
• This causes oxygen levels in blood to fall to dangerously low levels.

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

• Pancreatitis leads to formation of scar tissue in pancreas if prolonged and goes into chronic stage
• This then leads to a plethora of digestive related problems as well as diabetes Mellitus
• Due to the damage of the alpha and beta cells of the pancreas which produce glucagon and insulin respectively, there is an increase in blood sugar levels.

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

• Elevated liver enzymes in pancreatitis are often linked to cholelithiasis aka gall stones (also noted by distended gall bladder from USG Abdomen)

Specific markers for Alcoholic Fatty Liver Disease-

• AST (Aspartate aminotransferase- increased levels are usually indicative of pancreatitis, hepatitis etc)
• GGT (Gamma Glutamyl Transferase- increased levels usually seen in damage to liver and bile ducts)

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

• IVF- for electrolyte balance
• Inj PANTOP- to help decrease pancreatic secretions 
• Inj ZOFER- to help with nausea and vomiting 
• Inj TRAMADOL- Analgesic 
• Tab Dolo- for fever 

C) Link to patient’s details- 45 year old female patient with fever, pain abdomen, decreased urine output and abdominal distension. 

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

1. What is the probable diagnosis in this patient?

• Patient’s USG Abdomen report CBP (which shows both leukocytosis and neutrophilia), these findings are suggestive that the probable diagnosis may be Liver Abscess 

2. What was the cause of her death?

• The liver abscess may have ruptured leading to flow of pus into the eroded vessels which eventually leads to the heart and the lungs. 
• The sudden spread into the small vessels of the lungs may have led to respiratory failure and sudden death.

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

Question 5) NEPHROLOGY AND UROLOGY 

1. Link to patient details- POST TURP WITH NON OLIGURIC ATN

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

1. What is the reason for his shortness of Breath (SOB)?

• Acute Tubular Necrosis (ATN) is often caused by a lack of blood flow and oxygen to the kidney tissues. 
• Other causes may be due to any toxic poisoning etc.
• Typically leads to damage to the internal structure of the kidney, such as to the tubules. 
• Commonly leading to retention of fluid in the lungs due to increase in vascular permeability of lungs resulting in pulmonary edema.  

2. Why does he have intermittent episodes of drowsiness?

• Because of high levels of creatinine and urea that occurs as a result of kidney injury,(normal serum creatinine levels in adult males are : 0.7-1.35 mg/dl), 
• increased creatinine levels is the main cause of intermittent episodes of drowsiness. 

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

• During the surgical procedure (TURP), cauterisation of blood vessels are done to minimise the bleeding. 
• Hence there may be chances of clotting of blood which may later form a scab which may pass through the urethra hence why patient feels a fleshy mass whilst passing urine.

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

Complications of Transurethral Resection of Prostate (TURP) are:

1. Major complications-

• Clot retention
• Acute hematuria
• Urinary Tract infection (UTI)

2. Minor complications-

• Sepsis
• Disseminated Intravascular Coagulation (DIC)

B) Link to patients details-  8 yr old boy with frequent urination. 

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

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

• One of the common causes of excessive hyperactive individuals would be ADHD ( Attention Deficit Hyperactive Disorder) and considering he is still a child of 8 yrs of age, that may account for the lack of social etiquette. 

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

• May be due to a psychosomatic cause such as any stress or fear (considering he is still a child).

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

Management includes both investigations and treatment:-

1. Investigations include-

• Ultrasonography (USG) abdomen 
• Routine investigations such as CBP, CUE 

2. Treatment includes-

• Medication such as Oxybutynin to decrease urgency and frequency of urination. 

C. Others include-

• Anxiety disorder evaluation
• Psychology Therapy for behaviour
• Assurance to both mother and child. 

Question no 6) Infectious Diseases (HI Virus, Mycobacteria, Gastroenterology, Pulmonology)

1. Link to patient’s details- 40 year old lady with dysphagia, fever and cough.

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

1. What clinical findings and physical findings are characteristic for tracheo-esophageal fistula?

• Positive findings of tracheoesophageal fistula are
• C/O of cough whilst eatinG
• Difficulty in swallowing
• History of retro viral disease
• Endoscopy showing large opening with proliferative growth in mid esophagus 
• Barium swallow shows abnormal contrast due to communication between esophagus and bronchial tree
• CECT- Fistulous communication between left main bronchus and mid thoracic esophagus. 

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

• Chances of development of immune reconstitution inflammatory syndrome is high in this individual. 
• The potential risk factors include-
• Diagnosis of tuberculosis after starting antir retro-viral therapy
• Fever since 2 months 
• Lymph node enlargement
• CRP- positive

Question no. 7) Infectious Diseases and Hepatology.

1. Link to patients details- Liver abscess:

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

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

• Yes the locally made alcohol may have been the cause of the liver abscess in this patient.
• Alcohol itself acts as a predisposing factor, as well as:
• Poor nutritional status due to alcohol consumption
• Presence of infective organisms in locally brewed alcohol
• Liver damage
• Immunity of individual.

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

• Liver abscess can be of 3 types—

1. Pyogenic
2. Amoebic
3. And hydatid.

• Most common pathway would be infection usually bacterial through the portal vessels.
• Consumption of locally made alcohol may be of pyogenic or amoebic liver abscess.

3. Is liver abscess more common in right lobe?

• Yes. Liver abscess is more common in the right lobe, mainly due to the fact that the right lobe has more blood supply coming from the superior mesenteric vein on the right side of the liver. 

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

• Usual indications are-
• If abscess is large ie more than 5cm (due to increase risk of rupture)
• If abscess is not responding to medication for 7 or more days 
• If abscess is present on left lobe due to increase chance of peritoneal leak and spread of infection. 

2. Link to patient details-  Liver abscess:

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

1. Causes of liver abscess in this patient?

• In this patient, possible cause would be occasional consumption of toddy. 

• Pyogenic Liver abscess- 
• Staphylococcus 
• Streptococcus

• Escherichia coli

• Amoebic Liver abscess-

• Most commonly caused by Entamoeba histolytica

2. How do you approach this patient?

• For bacterial cause of liver abscess-

• Penicillin and cephalosporin is given ( zostum 1.5g IV BD )

• For amoebic cause of liver abscess-

• Metronidazole ( 500mg IV TID)

• For both bacterial and amoebic causes, empirical antibiotics are given

• Pain medication 

• Paracetamol for fever (650mg Dolo)

• Drainage of abscess is not preferred here in this patient due to complications 

3. Why do we treat here: both amoebic and pyogenic liver abscess?

• Both are treated considering the following which is indicative of amoebic liver abscess but to avoid risk, we treat for both possible causes. 

• Age of patient ie 21 yrs old
• Gender ie male 
• Right lobe involved and as a single abscess
• No spread to lungs 

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

Yes confirmation can be done by-

• Culture and sensitivity report
• Detection of serum antibodies against Entamoeba histolytica

Question number 8) Infectious diseases (Mucormycosis, Otorhinolaryngology, Neurology, Ophthalmology)

1. Link to patient’s details- 50 year old male came with altered sensorium. 

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

1. What is the evolution of 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 symptoms-

1. Fever with chills and rigours: 18/4/2021
2. Facial puffiness: 28/4/2021
3. Periorbital oedema: 28/4/2021
4. Generalised weakness: 28/4/2021
5. Altered sensorium: 4/5/2021
6. Serous discharge from eye: 4/5/2021
7. Oral and nasal cavity involvement: 4/5/2021

• Anatomical localisation-

1. Nasal and sinus mucosa
2. Oral cavity
3. Brain
4. Eye

• Main causative organism- Rhizopus (fungus) 

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

• Main drugs used to treat Mucormycosis are-

1. Posaconazole
2. Amphotericin B (as well as Liposomal and Deooxycholate)

• Liposomal Amphotericin B are said to be the most efficacious followed by Deoxycholate Amphotericin B and lastly Posaconazole. 

• However the more affordable option would be Deoxycholate Amphotericin B.

• Treatment is done by-

• Stabilising patient vitals 
• Treating by giving appropriate anti fungal therapy.
• Treating the diabetic keto acidosis 

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

• There has been increase in cases of Mucormycosis during the Covid-19 pandemic due to increase in immunocompromised state of individuals after recovering from Covid-19 infection. 

Question 9: Infectious Diseases (COVID 19)

https://docs.google.com/document/d/10xqvq7lzos7TB2NKNyliQ7pP73oi_V_waD_-i-jOxvU/edit

Question No. 10

• This Medical E-log is a very practical and useful way to not only help us understand the topic in general as a whole, but also helps us understand the practical aspect of Medicine through Patient Clinical Data Analysis 

• This help’s develop both competency during assessment of cases and comprehension of clinical data. 

• I would like to thank Dr Rakesh Biswas Sir, HOD of General Medicine, for his constant guidance and giving us the opportunity to be able to participate in clinical discussion. 

• I would also like to thank the Professors, Post Graduates and Interns of General Medicine Department for helping us with the information we needed.