Medicine Blended Assignment - May 2021

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 Medicine Blended Assignment - May 2021

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

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

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



1) Pulmonology (10 Marks) 

A) Link to patient details:

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

Questions:

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

Ans- Evolution of symptomatology in this patient is as follows-

  • 20 years ago – 1st episode of shortness of breath
  • Next  8 years – similar episodes 1/year ,lasting a week
  • 12 years ago – a more severe episode of shortness of breath – hospitalized
  • Next 12 years  - similar episodes 1/year 
  • 8 years ago – diagnosed with diabetes
  • 5 years ago – diagnosed with anemia 
  • 1 month ago – generalized weakness
  • 20 days ago - diagnosed with hypertension
  • 15 days ago -  pedal edema and facial puffiness

Anatomical localization : LUNGS (bronchi and bronchioles) – lesions here led to increased pulmonary blood pressure thus causing Right Heart Failure.

 Primary etiology : 

• This condition is seen to reccur every year around the same time and area of work, thus suggesting that it is an allergic reaction to Paddy dust. 

• Apart from that there is a history of use of CHULHA for years – which might have aggrevated the condition in following years.

Primary etiology of patient-  Usage  of chulha since 20 yrs might be due to chronic usage .

2) What r the mechanism of action indication(MOA) and efficacy over placebo of each of the phramacological and nonphramacological interventions  used for this patient?

Ans- Nonphramacological interventions-

1)     Head end elevation-

MOA- Improves oxygenation, decreases incidence VAP, increases hemodynamic performance, increases end expiratory lung volume, decreases incidence of aspiration.

Indication- Head injury, meningitis, pneumonia.

2)     O2 inhalation to maintain SPO2 above 92%-

3)     Intermittent BiPAP for 2hrs

MOA- Assist ventilation  by delivering positive expiratory and inspiratory pressure with out need for ET incubation

         Phramacological interventions-

1)     Inj. AUGUMENTIN 1.2gm IV BO

MOA-  THIS BLOCKS THE ACTION OF 𝜷 -LACTAMASE , POTASSIUM CLAVULANTA CAN BE INCORPORATED WITH AMOXICILLIN TO FORM AUGUMENTIN.

INDICATIONS-

1)lower respiratory tract infection

2)acute bacterial otitis media

3)sinusitis

2)TAB. AZITHROMYCIN 500mg OD

MOA-  Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit

Indication- chest infections such as pneumonia, infections of the nose and throat such as sinus infection (sinusitis), skin infections, Lyme disease, and some sexually transmitted infections.

 


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

Ans- The most common cause of an exacerbation is infection in the lungs or airways (breathing tubes). This infection is often from a virus, but it may also be caused by bacteria or less common types of organisms.

4) Could the ATT have affected her symptoms, if so how?

Ans- Yes ATT affected her symptoms

Isoniazid and rifampcin can be nephrotoxic – Thus, raised RFT was seen.

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

Ans-


RISK FACTORS


ACTIVATION OF RAS [RENIN ANGIOTENSIN-ALDOSTERON SYSTEM]

ELEVATED PLASMA ARGININE VASOPRESSIN

AGGREVATES ELECTROLYTE IMBALANCE

Common causes-             1.RENAL INSUFFICIENCY

                                            2.HYPOXIA

                                            3.HYPERCAPNIA

                                            4.RESPIRATORY ACIDOSIS

                                            5.RIGHT SIDED HEART FAILURE

                                            6.MALNOURISHED

 

2) Neurology (10 Marks) -

A) Link to patient details:

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

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

Ans- Evolution of the symptomatology in this patient in terms of an event timeline-

1-He had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago.

2-The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again.

3-He was unable to lift himself off the bed and move around, and had to be assisted. It was associated with a decrease in food intake since 9 days

4-He also had short term memory loss since 9 days

The primary etiology of the patient's problem-  ALOCHOL INTAKE

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

Ans- 1. IVF NS and RL @150ml/hr

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

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

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

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

Indications and Usage-

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

3. Inj. Lorazepam

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

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

4. T. Pregabalin 75mg/PO/ BD

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

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

5. Inj. HAI S.C.- premeal

6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am

7. Lactulose 30ml/PO/BD

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

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

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

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

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

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

Ans- Altered sensorium due to alcohol withdrawal syndrome,

Decreased levels of Thiamine lead to the symptoms.

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

Ans- Thiamine is a key vitamin in the maintenance of membrane integrity and osmotic gradients across cell membranes and is stored in body tissues predominantly as thiamine diphosphate (TDP). TDP participates in energy production as an essential cofactor for several enzymes in the TCA cycle and pentose phosphate pathways

Thiamine deficiency causes depletion of intracellular TDP, leading to a decreased activity of the TCA cycle and pentose phosphate pathways. Consequently, cellular energy (ATP) depletion and reduction of DNA/RNA and NADPH synthesis ensues, which results in low resistance to oxidative stress. Moreover, there is an accumulation of toxic intermediate metabolic products such as lactate, alanine and glutamate, reduced cellular pH in cells, and disruption of the homeostasis of cellular electrolytes, which results in cytotoxic edema.

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

Ans- Elevated levels of urea and creatinine are suggestive of Prerenal Azotemia being the most likely cause of kidney injury in this patient. This can be a result of decreased blood flow to the kidneys possibly due to dehydration secondary to Alcoholism.

6) What is the probable cause for the normocytic anemia?

 Ans- The possible causes of anemia can be the following:

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

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

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


B) Link to patient details:

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

Questions-

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

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

1.History of giddiness associated with 1 episode of vomiting on the same day.

2.This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.

3.He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.

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

Primary Etiology-

Obstruction of the posterior inferior cerebellar artery (PICA, also the most frequent location for a cerebellar infarct) leads to a headache and less commonly vomiting, vertigo, horizontal ipsilateral nystagmus, and truncal ataxia.

Anterior inferior cerebellar artery (AICA) territory infarction more often leads to dysmetria, Horner's syndrome, unilateral hearing loss and ipsilateral facial paralysis or anesthesia with contralateral hemibody sensory loss of pain and temperature.

Finally, obstruction of the superior cerebellar artery (SCA, located most rostral) tends to produce more ataxia, dysarthria, and nystagmus, with less vertigo, headache, and vomiting.

However, presentations can often be atypical or overlap, in particular for hemorrhagic infarcts.


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

Ans- Pharmacological interventions-

1. Tab Veratin 8 mg PO TID

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

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

2. Inj Zofer 4 mg IV/TID

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

3. Tab Ecosprin 75 mg PO/OD

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

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

4.Tab Atorvostatin 40 mg PO/HS

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

Indication- Reduce the risk of non-fatal myocardial infarction.

Reduce the risk of fatal and non-fatal stroke.

Reduce the risk for revascularization procedures.

Reduce the risk of hospitalization for CHF.

Reduce the risk of angina.

5. Tab Clopidogrel 75 mg PO/OD

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

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

Non-Pharmacological interventions-

1. BP monitoring- 4rth hourly

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

Ans- Yes

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

Ans- Yes, the patient has H/O chronic alcoholism and is susceptible to ischaemic type of stroke.

 

C) Link to patient details:

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

Ans- Evolution of symptoms-

1.Patient was normal 8 months back then developed b/l pedal edema which gradually progressed. (Aggerevated in sitting and standing position, relived on taking medication)

2.Palpitations : since 5days, sudden in onset which is more during night

(Aggerevated by lifting heavy weights, speaking continuously)

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

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

5.Chest pain associated with chest heaviness since 5 days

Etiological agent -Electrolyte imbalance (hypokalemia) causing the her  manifestations like palpitations, chest heaviness, generalised body weakness.

Radiating pain along her left upper limb due to cervical spondylosis.

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

Ans- Reason: recurrent hypokalemic periodic paralysis

Current risk factor:due to use of diuretics

Other risk factors

A) Medications-diuretics, laxatives, enema, corticosteroids causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia

B) Trans-cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis

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

D) Psuedohypokalemia: delayed sample analysis, significant leukocytosis.

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

Ans- Changes seen in ECG-

Earliest change- Decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves

In Severe cases- ventricular fibrillation, rarely AV block

Symptoms of hypokalemia-

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

 

D) Link to patient details:

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

QUESTIONS:

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

Ans- Yes. Seizures after haemorrhagic strokes are thought to be attributable to irritation due to Hemosiderin deposits caused by products of blood metabolism.

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

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

 

E) Link to patient details:

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

Questions:

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

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

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

Ans- The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes.

 

F) Link to patient details:

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

Questions:

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

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


2) What are warning signs of CVA?

Ans- Weakness or numbness of the face, arm or leg, usually on one side of the body

Trouble speaking or understanding

Problems with vision, such as dimness or loss of vision in one or both eyes

Dizziness or problems with balance or coordination

Problems with movement or walking

Fainting or seizure

Severe headaches with no known cause, especially if they happen suddenly


3) What is the drug rationale in CVA?

Ans- 1.Mannitol-

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

2.Ecospirin-

For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.

3.Atrovastin- Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.

4.RT feed- RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.


4) Does alcohol has any role in his attack?

Ans- When the patient met with an accident there might be cranial damage which was unnoticed.

If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition

But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.

Therefore it cannot be evaluated without further details.

 

5) Does his lipid profile has any role for his attack?

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

 

G) Link to patient details:

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

QUESTIONS:

1)What is myelopathy hand ?

Ans- 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. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.

 

2)What is finger escape ?

Ans- Finger escape sign or Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi.

This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign"

 

3)What is Hoffman’s reflex?

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

 

H) Link to patient details:

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

Questions-

1) What can be  the cause of her condition ?

Ans-  Seeing that the patient is a young female, the possible causes could include the following:

·        Trauma

·        Estroprogestative therapy ( oral contraceptives)

·        Iron deficiency anemia 

·         

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

Ans-  The risk factors include the following:

·        Congenial or acquired heart diseases

·        Underlying Infection

·        Birth control pills use

·        Dehydration

·        Cancer


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

Ans-  Underlying unresolved edema is the probable cause for the recurrent precipitation of seizures. So when the edema resolved, the seizure resolved spontaneously.

     

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

Ans- Injection Clexane was used to resolve the thrombosis and Mannitol infusion was given to bring down cerebral edema.

 

3) Cardiology (10 Marks) 

A) Link to patient details:

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

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

Ans- Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). 

Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure

HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease.  

 

2)Why haven't we done pericardiocenetis in this pateint?        

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

             

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

Ans- Risk factors here are-

1.Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure 

2.High blood pressure

3.Smoking

4.Diabetes

5.AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.

 

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

Ans- Visceral pericardium may have  thickened which is restricting the heart to expand causing hypotension (May be secondary to TB).

 

B) Link to patient details:

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

Questions:

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

Ans- The patient has various comorbidities which could have led to a heart failure

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

 

2.what is the reason for anaemia in this case?

Ans- Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections which may lead to anemia.

 

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

Ans- The patient had recurrent blebs and ulcer on lower limbs (foot). This is due to Type-2 diabetes mellitus.

Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases.

In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.

There are many risk factors that may lead to foot ulcers at the end-

  • 1.     Poor quality or fitting of the footwear.
  • 2.     Unhygienic appearance of foot.
  • 3.     Improper care of the nails of the toe.
  • 4.     Heavy intake of alcohols and tobacco.
  • 5.     Obesity and Weight-related
  • 6.     Complication arising from Diabetes like eye problems, kidney problems and more.
  • 7.     Although aging or old age can also be counted among them.

 

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

Ans- Sequence of stages here is-

  • 1.     Alcohol abuse
  • 2.     Obesity
  • 3.     impaired glucose tolerance
  • 4.     diabetes mellitus
  • 5.     microvascular complications like triopathy and diabetic foot ulcer
  • 6.     macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease.

 

C) Link to patient details:

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

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

Ans- Evolution of symptomatology-

  • 1.     Facial puffiness ( since 2 to 3 yrs)
  • 2.     SOB grade 2( 1yr ago)
  • 3.     SOB grade 2( 2days back again)
  • 4.     SOB grade 4
  • 5.     Decreased urine output ( since 2 days)
  • 6.     Anuria (since morning)

Anatomical localisation:- Atrial Septum

Primary etiology:-

  • 1.      Atrial Septal defect leading to Atrial Fibrillation
  • 2.      Atrial fibrillation caused stagnation of blood and hence thrombus formation
  • 3.      Atrial septal defect also caused shunting from left to right atrium causing pulmonary hypertension
  • 4.      Pulmonary Hypertension caused reversal of shunting and hence increased stagnated pool of blood contributing to thrombus formation and Congestive Cardiac failure.

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

Ans- 1.Dobutamine-

MOA: acts on beta 1 receptor

Beta1 ionotropic effect → increases heart contractility → increases cardiac output

Indications- Cardiogenic shock , Reversible heart failure

 

2.Digoxin- 

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

Indications-  Atrial fibrillation ,atrial flutter, Heart failure,Abortion

 

3.Heparin- MOA: Produces an anticoagulant effect by inhibiting activated factor X and thrombin and hence prevents fibrin formation 

Indication: The patient had thrombi in left atrium and left appendages 

 

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

Ans- Pathogenesis of cardiorenal syndrome is described below in the picture:

 


Stage 3 cardio renal syndrome  is seen in this patient.

 

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

Ans- Hypertension is the risk factor for atherosclerosis in this patient.

 

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

Ans- The patient was asked to get those APTT, INR tests for review because of Thrombosis and to check on development of thrombosis.

 

D) Link to patient details:

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

Questions-

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

Ans- Event timeline: 

  • 1.     Heartburn since 1 year
  • 2.     Tuberculosis 7 months ago
  • 3.     Shortness of breath since 30 minutes

Anatomical localisation: Coronary vessels

Primary etiology: 

  • 1.     Type 2 diabetes mellitus
  • 2.     Hypertension

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

Ans- The treatment modality used in this patient is-

Metoprolol:-

MOA: Acts of beta receptor, creates negative chronotropic and ionotropic effect

Indication: Patient is hypertensive with LV dysfunction.

 

3) What are the indications and contraindications for PCI?

Ans- Indications- .

  • 1.ST-elevation myocardial infraction(STEMI)                                                                                                     
  • 2.Atypical chest pain,                                                                                                              
  • 3.Stable angina,                                                                                                                          
  • 4.Unstable angina,                                                                                                                            
  • 5.Positive stress test                                                                                                                           
  • 6.Non ST-elevation myocardial infarction

Contraindications-

  • 1.Lack of cardiac support                                                                                                          
  • 2.Coagulopathy                                                                                                                                   
  • 3.Hypercoagulable states                                                                                                    
  • 4.Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery                                                                             
  • 5.Diffusely diseased vessel without focal stenosis                                                                            
  • 6.A single diseased vessel providing all perfusion to the myocardium                                             
  • 7.Total occlusion of a coronary artery                                                                                               
  • 8.Stenosis <50%

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?

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

 

E) Link to patient details:

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

Questions:

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

Ans- Evolution of symptomatology:

1.     Uncontrolled DM2 since 8 years

2.     3 days back Mild chest pain dragging type and retrosternal pain(radiated)

Anatomical localisation:- Inferior wall of heart

Primary etiology:- Diabetes type 2 (uncontrolled)

High blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels.

 

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

Ans- 1.TAB. ASPIRIN 325 mg PO/STAT

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

 

2.TAB ATORVAS 80mg PO/STAT

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

 

3.TAB CLOPIBB 300mg PO/STAT

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

 

4.VITAL MONITORING.

 

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

Ans- Secondary PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty

Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.

 

F) Link to patient details:

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

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

Ans- Patient got relieved from his SOB due to administration of IV fluids.

Because of the  fluid loss occurred to the patient there is decreased preload- so, SOB occurred due to decreased CO

IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.

 

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

Ans- Torsemide is a high efficacy diuretic which works by blocking Na-K-2Cl cotransporter, causing their excretion and hence creating diuresis.

It was used in the patient as he was suffering from pulmonary edema and it caused diuresis helping reduce the fluid volume

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

Ans-As there was presence of pus cells in urine, there was a suspicion of UTI. In order to prevent its aggrevation, Ceftriaxine was given for its treatment.

 

4) Gastroenterology (& Pulmonology) 10 Marks

A) Link to patient details:

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

Ans- Given below is the timeline of symptom occurrences in the patient:-

1.     Incident of abdominal pain and vomiting 5 years ago following which there was cessation of alcohol

2.     3 years ago resumed alcohol consumption and had another episode of pain abdomen and vomiting

3.     5-6 episodes of abdominal pain in the past 1 year

4.     20 days ago started binge drinking

5.     Abdominal pain and vomiting since 1 week

6.     Fever and burning micturition since 4 days

Anatomical localization:

1.     Sub-hepatic region

2.     Body of the pancreas

3.     Left basilar segment of lung

Primary etiology:

Chronic alcohol consumption

 

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?

Ans- The treatment modalities given to this patient includes:

1.Meropenem:

MOA: Carbapenems are bactericidal beta-lactam antibiotics that bind to penicillin-binding proteins (PBPs). By binding and inactivating these proteins, carbapenems inhibit the synthesis of the bacterial cell wall, which leads to cell death.

Indication: To prevent septic complications of acute pancreatitis

Efficacy: Preventing septic complications of patients with severe acute pancreatitis.

Reference link: https://pubmed.ncbi.nlm.nih.gov/14576501/#:~:text=Meropenem%20is%20as%20effective%20as,patients%20with%20severe%20acute%20pancreatitis.

2.Metronidazole:

MOA : Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death.

Indication: Preventing septal complications of acute pancreatitis.

Efficacy:  Metronidazole with Carbapenems is successful in treatment of acute pancreatitis. Combination therapy with Metronidazole reduces risk of drug resistance.

Reference link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5047423/#:~:text=Combined%20therapy%20with%20metronidazole%20is,low%20risk%20of%20drug%20resistance.

3.Amikacin:

MOA:  It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and t-RNA acceptor sites, interfering with bacterial growth

Indication: prevent septal complications of acute pancreatitis

Efficacy: Is being widely used in abdominal sepsis because of appropriate efficacy against invasive gram negative bacteria.

 

B) Link to patient details:

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

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

Ans- With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs. As a result, a person may experience an inflammatory type of reaction in the lungs called ARDS. Specifically, the small air sacs inside the lungs called the alveoli can get inflamed and become filled with fluid causing acute respiratory distress syndrome.

Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.

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

 

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

Ans- It is possible that the patient might have de novo diabetes secondary to pancreatitis. As there is destruction of Beta cells in the islets of Langerhans some patients are susceptible to hyperglycemia.

 

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

Ans- As  the patient has been diagnosed with acute cholecystitis, that could be the possible reason for elevated LFT markers. Elevated Lipase and amylase are also considered a diagnostic of acute pancreatitis.

Alanine Aminotransferase is a potential marker for alcoholic fatty liver disease but much is needed in this field.

 

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

Ans- Treatment plan of this patient includes the following modalities:

·        Intravenous fluids

·        Pantoprazole

·        Ondansetron

·        Tramadol

·        Paracetamol

 

C) Link to patient details:

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

Questions :-

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

Ans- The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to 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.

·        Grade 3 RPD of right Kidney

 

2) What was the cause of her death?

Ans- Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.

Or, Septicemia causing multiorgan failure can also be the probable cause of her death.

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

Ans- NSAID abuse should be considered because-

·       NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.

·       Chronic NSAIDs use has also been related to hepatotoxicity.

·       While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known.

·       NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.

 

5) Nephrology (and Urology) 10 Marks 

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 ?

Ans- His SOB was probably due to Acidosis which was caused by Diuretics.

 

2. Why does he have intermittent episodes of  drowsiness ?

Ans- Hyponatremia appears the most probable cause for his drowsiness.

 

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

Ans- Plenty of pus cells in his urine passage  appeared as

fleshy mass like passage to him.

 

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

Ans- The possible risks of TURP include the following:

  • ·       Bladder injury.
  • ·       Bleeding.
  • ·       Blood in the urine after surgery.
  • ·       Electrolyte abnormalities.
  • ·       Infection.
  • ·       Loss of erections.
  • ·       Painful or difficult urination.
  • ·       Retrograde ejaculation

 

B) Link to patient details:

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

Questions-

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

Ans- The exact pathophysiology of Attention Deficit Hyperactivity Disorder (ADHD) is not clear. With this said, several mechanisms have been proposed such as

·       Abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.

·       Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.

 

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

Ans- The child may be having psychosomatic urge to urinate during the day but this will not be present during sleep as he will not be conscious.

 

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

Ans- The ideal management would be-

·       Urinating on schedule and gradually spacing the time between bathroom visits.

·       Medications can include Botox injection as it helps bladder relax.

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

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

 

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

 

A) Link to patient details:

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

Questions:-

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

Ans- The Clinical history and physical findings which are characteristic of tracheo esophageal fistula are-

·       Cough since 2 months on taking food and liquids

·       Difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.

·       Laryngeal crepitus- positive

 

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

Ans- Immune Reconstitution Inflammatory Syndrome or IRIS is seen patients undergoing ART for RVD. In these patients as there is immunosuppression because of ART, a previous opportunistic infection can reactivate and give an exaggerated response. 

Candida is an opportunistic pathogen hence it is possible for this patient developing IRIS in response to a fresh candida infection

The drug of choice in this infection would be Fluconazole. 

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

 

7) Infectious disease and Hepatology:

 

A) Link to patient details:

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 ?

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

 

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

Ans- Etiologic factors:

·       Entry of pathogen

·       Content of alcohol

·       Cirrhotic condition of liver 

·       Immune status of the host

·       Nutritional status of the host

·       Sanitary conditions

Pathogenesis:

·       Alcohol induced hepatotoxicity

·       Depression of immune system due to alcoholism

·       Poor nutritional status



 

3. Is liver abscess more common in right lobe ?

Ans- Right hepatic lobe is larger than the left hepatic lobe. Therefore more blood supply to the right lobe and hence more chances of pathogens entering the liver via the right lobe through the hematogenous route. 

 

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

Ans- Indications for USG guided aspiration of liver abscess

1.     Large abscess more than 6cms

2.     Left lobe abscess

3.     Caudate lobe abscess

4.     Abscess which is not responding to drugs


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 ?

Ans- Most common cause of a liver abscess is amoebic infection are caused by Entamoeba histolytica. 

The pyogenic abscesses can also be a potential cause by bacteria that include E.coli, Klebsiella, Streptococcus, Staphylococcus, and anaerobes.

 

2) How do you approach this patient ?

Ans- Treatment approach includes the following:

  • ·       Sulbactam + Cefoperazone
  • ·       Metronidazole
  • ·       Optineurin
  • ·       Tramadol
  • ·       Acetaminophen
  • ·       Paracetamol

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

Ans- We treat the paient for both amoebic and pyogenic abcess  so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause

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

Ans- Aspiration and culture of the aspirated fluid can help us draw a definitive diagnosis

 

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

A) Link to patient details:

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

Questions :

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

Ans- The evolution if symptomatology is as follows:

  • ·       Diagnosed with hypertension 3 years ago
  • ·       Fever since 10 days
  • ·       Facial puffiness, periorbital edema and Right sided hemiparesis since 4 days

·       Altered sensorium since 2 days 

Anatomical localization:  Infarcts in frontal and temporal lobes of brain

Primary etiology: Mucormycetes infection causing rhino-orbito-cerebral mucormycosis

 

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

Ans- The treatment modality in this patient includes:

1.Itraconazole: 

MOA: Itraconazole acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-α-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis

Indication: Itraconazole is the only marketed azole drug that has in vitro activity against Mucorales. There are case reports of successful therapy with itraconazole alone .However, as mentioned above, itraconazole prophylaxis has been described as a risk factor for breakthrough mucormycosis

 

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

Ans- The reasons for sudden rise of mucormycosis cases in India include:

  • ·       COVID-19 infection among diabetic patients in whom there is lower immunity.
  • ·       Increased dose of steroid usage and also because of lower availability of remdesivir , tocilizumab leading to dependence on steroids for treatment. 
  • ·       Use of ordinary water instead of sterile water in humidifiers.
  • ·       Prolonged ICU stay

 


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