Medicine blended Assignment (May)
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
This is the link of the questions asked regarding the cases:
Preity Yarlagadda
Roll no - 145
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1. PULMONOLOGY :
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 and Event timeline -
Past-
- 20 Years ago - SOB Grade I lasted for a week. Occurred every year for the same duration.
- 20 years ago - Operated for Intestinal obstruction.
- 18 Years ago - Polyuria and was diagnosed with DM.
- 12 Years ago - SOB Grade I lasted for 20 days.
- 5 years ago - Given injections for Anemia.
- 1 Month ago - Weakness, was giving IV
- 30 days ago - SOB (latest episode) gradually progressive.
- 20 days ago - HRCT showed Bronchiectasis.
- 20 days ago - Diagnosed with Hypertension.
- On 30-04, Sputum sample was taken and AFB -ve. She was given ATT and used it for 12 days.
- 15 days ago - Pedal edema and Facial puffiness.
- 2 days ago - SOB Grade IV, drowsiness and decreased urine output.
Primary etiology - Rice dust exposure as patient is a farmer working in Paddy fields.
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: Augmentin - Amoxicillin + Clavulanic acid
MOA- Amoxicillin binds to penicillin- binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam that inactivates certain β-lactamase enzymes.
Indications - COPD, Lower respiratory infections, skin infections, bacterial sinusitis.
Azithromycin - It is a Macrolide.
MOA- It binds to 23S rRNA of 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit.
Indications - Pneumonia, infections of nose and throat, skin infections
Pantop - It is a Proton pump inhibitor
MOA - Inhibits the final step in gastric acid production. In the gastric parietal cell of stomach, it binds to H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
Indications - Heavy bloating, gas, heart burn, indigestion, GERD.
Hydrocortisone - It is a steroid
MOA - The steroid diffuses across cell membrane and binds to the glucocorticoid receptor and causes a conformational change in it. It leads to inhibition of Phospholipase A2, and other inflammatory enzymes.
Indications - Allergic conditions, breathing disorders, arthritis, lupus
Budecort - It is a steroid
MOA - The steroid diffuses across cell membrane and binds to the glucocorticoid receptor and causes a conformational change in it. It leads to inhibition of Phospholipase A2, and other inflammatory enzymes.
Indications - Mainly used for asthma
Lasix - It is a diuretic
MOA - Acts by inhibiting Na-K-Cl cotransporter in the thick ascending limb of loop of henle, by binding to the chloride transport channel, thus Na+, Cl- and K+ are lost in the urine.
Indications - Congestive heart failure, liver disease and edema.
Pulmoclear - It is a combination of bronchodilators and mucolytics.
MOA - It relaxes the airways and loosens the cough, thus making the expulsion of cough easy.
Indications - COPD, Asthma.
Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
Inj. HAI - It is a short acting insulin.
3. What could be the causes for her current acute exacerbation?
Ans- In spite of her being AFB -ve, the patient was given ATT. The acute exacerbation may have been due to the lowered immunity or due to the ATT drug side effects.
Could there have been a relapse of TB in the patient as her X-rays showed evidence of previous TB?
4. Could the ATT have affected her symptoms? If so how?
Ans- The ATT received by the patient could have affected her symptoms. One possible explanation could be Paradoxical TB- Immune reconstitution inflammatory syndrome. The ATT drugs mainly Rifampicin may lead to immune problems in the patient.
5. What could be the causes for her electrolyte imbalance?
Ans- Activation of the renin-angiotensin-aldosterone system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the electrolyte imbalance during acute exacerbation of COPD
2. NEUROLOGY :
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 and event timeline -
Past-
- Alcoholic since 12 years.
- 2 years ago - Diagnosed with DM-2 and is using medication irregularly.
- 1 year ago - Seizure episode.
- 4 months ago - Seizure episode.
- 9 days ago - Irrelevant talking, laughing, short term memory loss and decreased appetite.
- Referred to psychiatry - was diagnosed with Alcohol dependence syndrome
- Referred to surgery - Chronic foot ulcer was treated.
Primary etiology - Alcohol
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- Lorazepam - It is a benzodiazepine.
MOA - It binds to BZD receptors on the postsynaptic GABA-A ligand gated chloride channel within the CNS. It enhances the inhibitory effects of GABA which increases the inflow of Chloride ions.
Indications - It is indicated to reduce anxiety and its symptoms, for seizures and depressive symptoms.
Efficacy - It is effective over placebo in inducing and maintaining sleep.
Reference -
Pregabalin - It is an anti epileptic.
MOA - It may reduce excitatory neurotransmitter release by binding to the subunit of voltage-gated calcium channels. Exact mechanism is unknown.
Indications - Partial seizures, partial diabetic neuropathy and post herpetic neuralgia.
Efficacy - It is effective over placebo.
Lactulose - It is a synthetic derivative of lactose.
MOA - Lactulose (galactose+fructose) is acted upon by saccharolytic bacteria and broken down into lactic acid + formic acid + acetic acid. These acids, acidify the contents of colon and contribute to treatment of encephalopathy.
Indications - It is used commonly as a laxative and as an adjunct therapy in treating postal systemic encephalopathy.
Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
Inj. HAI - It is a short acting insulin.
Potchlor - It is Potassium chloride electrolyte given through I.V
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Ans- Wernicke encephalopathy is the presence of neurological symptoms caused by biochemical lesions of the CNS after exhaustion of Vit-B reserves, particularly Thiamine. In this patient, the neurological symptoms might have developed due to the exhausation of Vit B reserves, the reserves may have not been exhausted during the previous withdrawal episodes.
4) What is the reason for giving thiamine in this patient?
Ans- Mechanisms involved in the pathogenesis of thiamine deficiency in alcoholics-
- Inadequate intake of thiamine.
- Decreased conversion of thiamine to the active coenzyme.
- Reduced hepatic storage of the vitamin
- Ethanol inhibition of intestinal Thiamine transport
- Impaired Thiamine absorption
5) What is the probable reason for kidney injury in this patient?
Ans- Chronic Alcoholism might be the probable reason for kidney injury in this patient. Raised alcohol levels can cause a sudden drop in kidney function which is also known as Acute kidney injury. Dialysis will be needed in this case, until the patient returns to normal.
6). What is the probable cause for the normocytic anemia?
Ans- Reduced RBC life span, blood loss and inadequate increase in erythropoiesis relative to fall in HB are the probable causes of Normocytic anemia. It regularly develops in chronic renal failure and is also known as Renal anemia.
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Ans- Chronic alcoholism --> Nutritional deficiency --> Reduced immunodeficiency, Poor wound healing, neuropathy.
So yes, Chronic alcoholism could have aggravated the foot ulcer formation.
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 and event timeline -
Past-
- Alcoholic since 30 years.
- 7 days ago - Episode of giddiness and vomiting.
- 4 days ago - Episode of giddiness, vomiting, aural fullness, Bilateral hearing loss and tinnitus. He also had postural instability.
- CT scan was done which showed cerebellar infarcts.
Primary etiology - Ataxia is mainly caused by damage to the cerebellum. In this case, damage to the cerebellum is due to stroke. The patient does not take his medication for hypertension regularly which could have caused a blood clot --> infract --> stroke.
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- Vertin - It is an anti-vertigo medication.
MOA - It is a weak H1 agonist. It leads to local vasodilatation and increases vessel permeability.
Indications - It is used for balance disorders.
Zofer - It is an anti emetic.
MOA - It is a 5H3 antagonist.
Indications - It is used to control nausea and vomiting.
Ecosprin - It is an NSAID.
MOA - It inhibits COX-1 and COX-2 to decrease the Prostaglandin and thromboxane synthesis.
Indications - They are used as anti platelet drugs to prevent clot formation and stroke.
Atorvostatin - It is a statin.
MOA - It is a HMG CoA reductase inhibitor and thus inhibits the cholesterol synthesis. It decreases VLDL, LDL in the blood, cholesterol synthesis. It increases LDL receptors in the liver and increases LDL uptake and degeneration. Thus decreasing LDL levels in the plasma.
Indications - Primary hyperlipidemias and prevention of stroke.
Clopidogrel - Antiplatelet medication
MOA - It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications - To decrease risk of heart disease and prevent stroke.
Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
MVT - Methyl cobalamin
MOA - Rapid restoration of B12 levels.
Indications - Vitamin B12 deficiency.
3) Did the patients history of denovo HTN contribute to his current condition?
Ans- Hypertension --> Increased sheer stress on the vessels --> endothelial dysfunction.
It will also promote cerebral small vessel disease.
All these factors together contribute to the stroke so HTN is a major risk factor.
4) Does the patients history of alcoholism make him more susceptible to ischemic or hemorrhagic type of stroke?
Ans-
- Ischemic stroke is due to blood clot blocking the flow of blood to brain and preventing oxygen to reach.
- Hemorrhagic stroke occurs when an aneurysm bursts or blood vessel is weakened.
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 and event timeline -
Past -
- 10 years ago - Paralysis of Right and Left upper and lower limbs.
- 1 year ago - Right and Left paresis due to hypokalemia.
- Since 8 months - Swelling over legs
- 7 months ago - Blood infection
- 2 months ago - Neck pain
- Since 6 days - Pain, tingling and numbness of the Left upper limb.
- Since 5 days - Palpitations, chest pain and difficulty in breathing.
Primary etiology - It may be due to autosomal dominant mutation.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Ans- Risk factors for hypokalemia are female gender, heart failure, hypertension, alcoholism, diarrhea, eating disorders, and low body mass index.
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Ans- ECG changes in Hypokalemia -
- Mild Hypokalemia - Flattening and inversion of T waves.
- Moderate Hypokalemia - QT interval prolongation, visible U wave and mild ST depression.
- Severe Hypokalemia - Arrhythmias such as Torsades de points and ventricular tachycardia.
Questions :
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Ans-
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- The patient might have had simple partial or focal seizures the first time which do not cause impairment of awareness so the patient must have not lost consciousness.
The patient might have had Generalized clonic tonic seizures the second time which can cause impairment of awareness and thus leading to Loss of consciousness.
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans- Could the Ataxia have been due to cerebellar damage in the patient due to one of his falls?
Cerebellar damage is the most common cause of Ataxia. Seeing that the patient has a history of frequent falls. he might have injured his cerebellum during one of his falls.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Ans- Alcohol consumption has always been a consistent risk factor for Intracerebral hemorrhage. Dose dependent relationship is still unknown, but alcohol consumption also contributes to hypertension which is again a risk factor.
Questions -
1.Does the patient's history of road traffic accident have any role in his present condition?
Ans- Is there a possibility that the patient might have suffered a cerebral infarct due to the injury which may have predisposed to this condition?
2.What are warning signs of CVA?
Ans- Warning signs maybe -
- Sudden confusion, trouble speaking, difficulty in understanding speech.
- Sudden trouble seeing in one or both eyes.
- Sudden numbness or weakness in face, arm or leg.
- Sudden trouble walking, dizziness, loss of balance, lack of coordination.
- Sudden severe headache with no known cause.
3.What is the drug rationale in CVA?
Ans-
GENERAL SUPPORTIVE CARE -
a. Oxygenation - In order to prevent hypoxia and worsening of neurological injury during periods of acute cerebral ischemia, maintaining adequate tissue oxygenation is important.
- Supplemental oxygen - if hypoxia or desaturation is present.
- Endotracheal intubation - if there is decreased consciousness.
- I.V - Nicardipine or labetalol for adequate control of BP.
- Oral - Labetalol or lisinopril for more sustained BP lowering.
d. Antipyretics - Increased body temperature has been associated with poor neurologic outcome due to increased metabolic demands, enhanced release of NT and increased free radical production. Maintaining normothermia might improve the prognosis of the patient. It is indicated if Temp > 37.5 C.
TREATMENT -
a. Thrombolysis -
I.V Alteplase is the only FDA approved medical therapy for treatment of patients with acute ischemic stroke. Tenecteplase, steptokinase, desmoteplase are other drugs available.
b. Device therapies - Mechanical thrombectomy delivered endovascularly is another option for clot removal, either as an adjunct to thrombolysis or for patients who are ineligible for IV Alteplase.
c. Anticoagulants -
d. Antiplatelet -
4. Does alcohol has any role in his attack?
Ans- Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.
5.Does his lipid profile has any role for his attack?
Ans- Significant relation between lipid profile and CVA has been identified. LDL was previously considered as a predictor of hemorrhagic stroke. Increased cholesterol and LDL levels are associated with higher risk of developing ischemic stroke.
Questions -
1)What is myelopathy hand ?
Ans-
- Disability - Loss of power of adduction and extension of ulnar two or three fingers and inability to grip and release rapidly with these fingers.
- Cause - Cervical spinal disorders, appears to be pyramidal tract involvement.
2)What is finger escape ?
Ans- Wartenberg's sign in cervical myelopathy is known as 'Finger escape sign'.
Wartenberg's sign- It is a neurological sign consisting of involuntary abduction of the 5th/little finger, caused by unopposed action of the extensor digiti minimi.
3)What is Hoffman’s reflex?
Ans-
- It is used to examine the reflexes of the upper extremities.
- It is a quick and 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.
Questions:
1) What can be the cause of her condition ?
Ans- In this patient, seizures are due to Cortical vein thrombosis which can be seen in the CT.
2) What are the risk factors for cortical vein thrombosis?
Ans- Risk factors may be -
- Mechanical - Head injury, lumbar puncture
- Infections - Meningitis, mastoiditis
- Inflammatory - Nephrotic, IBD, SLE
- Malignancy
- Prothrombotic states - Pregnancy, Hormone replacement therapy.
3)There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously why?
Ans- Due to medical interventions there was resolution of seizures and seizure free period. Persistence of excitable foci due to abnormally firing neurons maybe the reason for sudden episode of seizures.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Ans- Clexane (enoxaparin) is low molecular weight heparin. It is an anticoagulant used to prevent blood clots.
MOA- potentiates Antithrombin III and irreversibly inactivates factor Xa.
3) CARDIOLOGY -
Questions -
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans-
a. In systolic heart failure, patients have reduced ejection fraction which is 40 to 50% lower.
It is diagnosed earlier in life and after a heart attack.
These patients are most likely to have a surgery for pacemaker implantation.
b. In diastolic heart failure, patients do not have much change in their ejection fraction so preserved ejection fraction.
It is diagnosed late in life.
These patients have additional diseases like GERD, kidney disease etc.
2.Why haven't we done pericardiocentesis in this patient?
Ans- The pericardial fluid accumulation has reduced from 2.4mm to 1.9mm. So when there is resolution of the fluid, paracentesis is not required. It is done when there is no resolution.
3.What are the risk factors for development of heart failure in the patient?
Ans- This patient has many risk factors like HTN, DM, smoking, male gender, age.
4.What could be the cause for hypotension in this patient?
Ans- Hypotension is this patient might be as a result of anemia.
Questions:
1.What are the possible causes for heart failure in this patient?
Ans- Predisposing factors like obesity, DM, HTN and alcohol consumption might be the possible causes,
2.what is the reason for anemia in this case?
Ans- Alcoholics have defective Red blood cells which will be destroyed prematurely. This will lead to anemia.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Ans- Diabetic foot ulcer - It occurs as a result of poor circulation in the foot. High blood sugar levels may be an additional risk factor. They take time to heal and develop reduced sensation due to damaged nerves.
4. What sequence of stages of diabetes has been noted in this patient?
Ans- Alcohol, obesity --> Impaired glucose tolerance --> Diabetes mellitus --> microvascular complcations --> macro vascular complications.
- Micro vascular complications - Diabetic foot ulcer, triopathy
- Macro vascular complications - Coronary heart disease, Coronary vascular disease and peripheral vascular disease.
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 and event timeline -
Past-
- 10yrs ago - Operation for Hernia
- Since 2-3 yrs - Facial puffiness
- 1 yr ago - SOB grade II
- 1 yr ago - was diagnosed with Hypertension.
- Since 2 days - SOB which progressed from Grade II to Grade IV.
- Since 2 days - Decreased urine output.
- Since 1 day - Anuria
- CT scan - Showed dilated pulmonary vessels and thrombi in the atria.
- 2D Echo - Showed LV dysfunction.
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- Digoxin - It is a cardiac glycoside
MOA - It increases intracellular sodium that will cause an influx of calcium in the heart and cause an increase in contractility. It is vagomimetic.
Indications - Heart failure and arrhythmias.
Carvediol - It is a beta-blocker.
MOA - It blocks the beta receptors and lowers the heart rate, blood pressure and strain on the heart.
Indications - Hypertension, heart failure, LV dysfunction with MI.
Heparin - It is an anti-coagulant
MOA - It produces its major anticoagulant effect by inactivating thrombin and activated factor X through an antithrombin dependent mechanism. By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin induced activation of platelets and of factors V and VIII.
Indications - Prophylaxis and treatment of venous thromboembolism and pulmonary embolism; Atrial fibrillation with embolization ; chronic consumptive coagulopathies.
Acitrom - It is an Oral anti-coagulant
MOA - It inhibits the reduction of Vitamin K by Vitamin K reductase. This prevents carboxylation of Vitamin K dependent clotting factors, II, VII, IX, X and interferes with coagulation.
Indications - Thromboembolic diseases such as DVT, Coronary occlusion
Cardivas - It is an adrenergic blocker
MOA - Reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevent a response to the sympathetic nervous system, leading to decreased Heart rate and contractility
Indications - Hypertension, Angina and heart failure.
Dytor - It is a diuretic. Contains Torsemide + Spironolactone
MOA - Through its action in antogonizing effect of Aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
Indications - Edema, Hypertension.
Pan D - It is a Proton pump inhibitor
MOA - Inhibits the final step in gastric acid production. In the gastric parietal cell of stomach, it binds to H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
Indications - Heavy bloating, gas, heart burn, indigestion, GERD.
Taxim - It is a cephalosporin antibiotic.
MOA - It is bactericidal through inhibition of cell wall synthesis.
Indications - Treatment of infections of throat, airway and urinary tract ; Typhoid fever.
Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
Inj. HAI - It is a short acting insulin.
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- This patient has Cardiorenal syndrome 4
4) What are the risk factors for atherosclerosis in this patient?
Ans- The risk factors for atherosclerosis are hypertension, high cholesterol and triglyceride, DM-1, obesity, physical inactivity, smoking, high saturated fat diet.
- This patient has Hypertension, physical inactivity and obesity
5) Why was the patient asked to get those APTT, INR tests for review?
Ans- The patient was on Anticoagulants. So to predict the occurrence of CVA and ischemic attacks, the patient is advised to get these tests.
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 and event timeline -
Past -
- 12 yrs ago - Diagnosed with DM 2
- Since 1yr - Heartburn which is relieved with medication
- 7 months ago - Diagnosed with Pulmonary TB, she completed the ATT course.
- 6 months ago - Diagnosed with HTN
- Since half hour - Severe SOB
- ECG showed NSTEMI
Primary Etiology - Ischemia of the heart muscles.
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- Met XL - It is a Beta-blocker
MOA - It blocks Beta receptors and slow down heart rate, and makes pumping more efficient.
Indications - Hypertension, Angina, arrhythmias, migraine.
Telma - It is an Angiotensin receptor blocker.
MOA - It binds to angiotensin II type 1 receptors with high affinity, causing inhibition of action of Angiotensin II on vascular smooth muscle leading to reduction in arterial blood pressure.
Indications - HTN, diabetic nephropathy, CHF.
Glimi - Glimepiride + Metformin
MOA - The primary mechanism of action of Glimepiride is stimulating release of insulin from functioning pancreatic beta cells. Metformin reduces insulin resistance.
Indications - DM 2
3) What are the indications and contraindications for PCI?
Ans- Indications -
- Stable angina
- Unstable angina
- STEMI
- NSTE - ACS
- Anginal equivalent
- Chronic kidney disease
- Hyper coagulable state
- Intolerance to oral antiplatelet therapy.
- Chronic total occlusion of SVG.
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 over testing and overtreatment important to current healthcare systems?
Ans- PCI being performed in a patient who doesn't need it might lead to unnecessary complications and extra expenditure burden on the patient.
Research on over testing and over treatment is importance in our present health care systems because
- There is development of resistance in the microorganisms to the effective drugs being produced.
- Cost of treatment is increased and it is becoming unaffordable to the common man.
- Over treatment might also make our body's immune system to be dependent on the medication.
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 and event timeline -
Past -
- Since 8 yrs - DM 2
- Known case of HTN
- 5 days ago - received COVISHIELD vaccination
- Since 3 days - Chest pain
- Since morning - Giddiness and Sweating
Primary etiology - Ischemia of the heart muscle.
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- Aspirin - It is an NSAID.
MOA - It inhibits COX-1 and COX-2 to decrease the Prostaglandin and thromboxane synthesis.
Indications - They are used as anti platelet drugs to prevent clot formation and stroke.
Atorvostatin - It is a statin.
MOA - It is a HMG CoA reductase inhibitor and thus inhibits the cholesterol synthesis. It decreases VLDL, LDL in the blood, cholesterol synthesis. It increases LDL receptors in the liver and increases LDL
uptake and degeneration. Thus decreasing LDL levels in the plasma.
Indications - Primary hyperlipidemias and prevention of stroke.
Clopidogrel - Antiplatelet medication
MOA - It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications - To decrease risk of heart disease and prevent stroke.
Inj. HAI - It is a short acting insulin.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans- Ideally, PTCA should be done within 12hrs of the onset of symptoms. In this patient it was done after 3 days of onset of symptoms which can lead to complications. So, secondary PTCA might have been unnecessary in this patient.
4) GASTROENTEROLOGY ( & Pulmonology)
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 and event timeline -
Past -
- 5 years ago - Pain abdomen and vomiting ; was treated conservatively
- Since 1 week - Pain abdomen and vomiting
- Since 4 days- - Constipation, burning micturition, fever
- CT scan - showed pseudocyst
- Chest X ray - showed left pneumothorax and left pleural effusion
Primary etiology - Chronic alcohol intake
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- Pantop - It is a Proton pump inhibitor
MOA - Inhibits the final step in gastric acid production. In the gastric parietal cell of stomach, it binds to H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
Indications - Heavy bloating, gas, heart burn, indigestion, GERD.
Thiamine - It is Vitamin B1.
MOA - Rapid restoration of Thiamine levels
Indications - Wernicke's encephalopathy, infantile beriberi etc.
Metrogyl - It is a nitroimidazole
MOA - It inhibits the protein synthesis by interacting with DNA and causes its breakage. Therefore causes death of the organism
Indications- Bacterial and amoebic infections.
Octrotide - It is a somatostatin.
MOA - It decrease secretion of pancreas and also has an anti-inflammatory and cyto protective effect.
Tramadol - It is an opioid analgesic used for pain relief.
Percutaneous drainage of Pseudocyst.
Intercoastal drainage of Pneumothorax.
QUESTIONS:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans- The inflammation in pancreatitis may encroach onto the lung and cause dyspnea in the patient.
Sudden onset, severe abdominal pain is suggestive of Pancreatitis.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans- Pancreas is the main organ of production of insulin. When this organ gets inflamed, production of insulin is disturbed and results in diabetes. This diabetes caused due to pancreatitis is known as secondary pancreatitis.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans- Liver is the organ which detoxifies the blood and absorbs the toxins like alcohol, so it is the first affected organ due to chronic alcoholism. So in this patient due to liver injury, LFTs are elevated.
γ-Glutamyl transpeptidase is a specific marker for Alcoholic fatty liver. It is considered to be the most sensitive biomarker of alcohol consumption.
4) What is the line of treatment in this patient?
Ans- Abstinence from alcohol consumption is the first thing advised to the patient.
Patient's nutritional status should also be improved.
The patient's blood sugars, hba1c, BP was continuously monitored.
Pan (proton pump inhibitor) ; Zofer (anti emetic) ; Tramadol (opioid analgesic) ; Dolo (PCM) was given to the patient.
Questions :-
1) what is the most probable diagnosis in this patient?
Ans- Ruptured liver abscess and hemoperitoneum might be a possible diagnosis in this patient.
2) What was the cause of her death?
Ans- Hypovolemic shock due to excessive loss of blood.
3) Does her NSAID abuse have something to do with her condition? How?
Ans- Drug induced hepatitis
5) NEPHROLOGY ( AND UROLOGY ) :
Questions-
1. What could be the reason for his SOB ?
Ans- Could the SOB have been due to Pulmonary congestion? Chronic kidney disease in the patient may have led to Diastolic dysfunction and thus to pulmonary congestion.
CKD --> Diastolic dysfunction --> Pulmonary congestion --> SOB
Another cause of the SOB could have been Acidosis resulting from dehydration as a side effect of the Diuretics used in the patient.
Diuretics --> Dehydration --> Acidosis --> SOB
2. Why does he have intermittent episodes of drowsiness ?
Ans- A decrease in the renal clearance of waste nitrogenous products accompanies with their continuous generation leads to diverse uremic retention products such as urea, creatinine, guanidine and homocysteine. Many of these toxins affect functioning of cells and organs, resulting in endothelial vascular injury, neurotoxicity and cognitive dysfunction.
Taken from the following article -
3. Why did he complaint of fleshy mass like passage in his urine?
Ans- The fleshy mass like passage in his urine might be due to excessive pus cells in the urine (according to the reports) and the frothy appearance may be due to the presence of proteins. The urine is pale yellow in colour.
4. What are the complications of TURP that he may have had?
Ans- A complication of TURP that the patient may have had is 'TURP syndrome'.
It is rare but is life threatening.
Cause- It may occur as a consequence of absorption of fluids used to irrigate the bladder during the operation.
Signs and symptoms are due to fluid overload and electrolyte disturbances and hyponatremia.
Questions-
1.Why is the child excessively hyperactive without much of social etiquettes ?
Ans- One possible Provisional diagnosis of this patient is ADHD (Attention deficit/Hyperactive disorder).
Symptoms may start before the age of 12 and include inattention and hyper active impulsive behavior.
Inattention -
- They have trouble to stay focused in tasks or play.
- They appear not to listen even when spoken directly.
- They are easily distracted.
- They avoid or dislike tasks that require mental effort.
- Have difficulty sitting in one place and are always on the run.
- Fidget with their hands or legs.
- Talk too much
- Have difficulty waiting for their turn.
Ans- It maybe Psychosomatic. The child has the urge to urinate in the morning due to stress or mental conflict. During sleep, the kid is free of stress and may not have the urge to urinate excessively.
3. How would you want to manage the patient to relieve him of his symptoms?
Ans- The only management is reassurance to the kid and his relaxation by reducing stress. The problem will resolve overtime (most commonly by the time he reaches 10yrs).
6. INFECTIOUS DISEASE (HI virus, Mycobacteria, Gastroenterology, Pulmonology) :
Questions-
1. Which clinical history and physical findings are characteristic of tracheo-esophageal fistula?
Ans- Clinical history- weight loss, recurrent chest infections, trauma, malignancy or ingestion of caustic substances, pyrexia of unknown origin
Physical findings- Uncontrolled coughing after swallowing, often worse with carbonated drinks (ONO sign).
2. What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Ans-
Prevention- It can be prevented by treating the infection, continuing the ART and administering Steroids.
7) INFECTIOUS DISEASE AND HEPATOLOGY :
Questions-
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- Sufficient evidence has been accumulated by scientists to say that chronic alcohol consumption is one of the predisposing factors for Liver abscess.
2. What is the etio-pathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
Ans- Chronic alcoholism weakens the patient's immunity and also has its own effect on the liver. So it may act as an additional risk factor for a patient with amoebic liver abscess.
3. Is liver abscess more common in right lobe ?
Ans- Yes, liver abscess is more common in right lobe.
4.What are the indications for ultrasound guided aspiration of liver abscess ?
Ans-
- When the abscess has a risk of rupture.
- When the abscess may be large enough to cause compression of adjacent structures.
- When the abscess shows no resolution in spite of medication.
Question :
1. Cause of liver abscess in this patient ?
Ans- The cause of liver abscess in this patient could have been amoebic or pyogenic.
Amoebic - Due to Entamoeba histolytica.
Pyogenic - Due to organisms like E.coli, Klebsiella, Steptococcus.
2. How do you approach this patient ?
Ans- In practice, amoebic and pyogenic liver abscess are treated empirically so antibiotics and anti amoebic drugs are given. Anti pyretic and analgesic are also given along with them.
3. Why do we treat here ; both amoebic and pyogenic liver abscess?
Ans- Amoebic and pyogenic liver abscess clinical presentation is similar and amoebic liver abscess does not have additional GI symptoms. So, both the etiology are treated as it cannot be differentiated.
4. Is there a way to confirm the definitive diagnosis in this patient?
Ans- Liver enzymes and USG help with the diagnosis. Culture of Pus can be used for definitive diagnosis but aspiration of pus is risky so it is avoided.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
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 and evolution of symptomatology-
Past -
- 3 years ago - Diagnosed with hypertension during a regular checkup and is regularly using medication.
- On 18-04, he received COVID-19 vaccination and had fever, chills and rigor.
- 3 days after vaccination, he got fever again but it did not subside even with antipyretics
- Fever since 10 days.
- Since 4 days, Facial puffiness, periorbital edema, weakness of right upper limb and lower limb.
- Since 2 days, Altered sensorium.
- Day 1, Serous discharge from eye which is blood tinged, oral and nasal foul smell, diabetic ketoacidosis diagnosed.
- CT scan was taken - Preseptal cellulitis, Acute infarction in frontal and temporal lobe, soft tissue swelling in the maxillary sinus, mucosal thickening of the sinuses.
- ENT consultation was taken.
Anatomical location - Oral cavity, nose and orbit is affected by the fungus.
Primary etiology - Mucormycosis is caused by fungi Mucormycetes.
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- Amphotericin B - It is a Fungicidal or Fungistatic depending on its concentration.
MOA - It binds to the ergosterol in the fungal cell membrane which leads to the formation of pores, ion leakage and ultimately fungal cell death.
Efficacy - At present, it has the most efficacy and safety in treating Mucormycosis.
Itraconazole - It is an Azole antifungal.
MOA - It acts by inhibiting the fungal enzyme, lanosterol 14-α-demethylase. Inhibition of this enzyme blocks the conversion of lanosterol to ergosterol which disrupts the fungal membrane synthesis.
Efficacy - It is not reliable efficacy against mucormycosis.
Referred from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947016/
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Ans- During this current COVID-19 pandemic, the sudden rise in Mucormycosis may be due to following reasons -
- Immunocompromised state due to the Covid-19 virus
- Improper use of Steroids
- Use of dirty and wet masks.
During these uncertain times due to the pandemic, clinical exposure and learning has been compromised. So to at least have an idea about the patients in the hospital, following their case through admission, investigations and diagnosis is refreshing. Though a hands on experience would be better, these online discussion sessions have been helpful to know the way a clinician should think while dealing with a case. I'm thankful for this opportunity to analyze, discuss and put forth my doubts and suggestions.
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