GENERAL MEDICINE ASSIGNMENT- MAY 2021
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
PULMONOLOGY
CASE-1:
Q1) 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?
A1) Timespan of patients symptomology:
20 years ago: First episode which lasted for 1 week and relieved upon taking medications.
Similar episodes of SOB every year each lasting 1 week duration which were relieved upon medication.
12 years ago: Another episode of SOB which lasted FOR 20 days and relieved upon treatment in the hospital.
8 years ago: She was diagnosed with DM.
5 years ago: She was treated for anemia with iron injections.
30 days ago: Latest episode of SOB which is insidious in onset and gradual in progression.
20 days ago: Diagnosed with HYPERTENSION and HRCT reports showed signs of bronchiectasis.
15 days ago: Pedal edema upto the level of the ankle and pitting type.
On 30/04/21: Sputum examination which tested negative for AFB
On 04/05/21: She was started on empirical ATT which resulted in generalized weakness. A few days later she started developing pedal edema and facial puffiness.
On 16/05/21: ATT was stopped on advice of pulmonologist.
From past 2 days: Drowsiness , decreased urine output and shortness of breath which is not relieved by medication.
Anatomical location of the problem is at the bronchioles.
Primary etiology of the patients problem may be due to the exposure of dust in paddy fields.
Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
A2)Head end elevation: Head angle affected the respiratory mechanics of mechanically ventilated patients. It can reduce the risk of mechanical ventilated- associated pneumonia. In addition, it can increase the possibility of more homogeneous alveolar ventilation and possibly reduce the risk of lung injury.
O2 inhalation to maintain spO2 above 92%
BiPAP: It is a non invasive method. It assists ventilation by delivering positive expiratory and inspiratory pressure without the need of ET incubation.
Inj. Augmentin: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.
Tab. Azithromycin: Prevents bacteria from growing by interfering with their protein synthesis. It binds to the 50S subunit of the bacterial ribosome, thus inhibiting translation of mRNA.
Inj. Lasix: Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours.
Tab. Pantop: inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
Inj. Hydrocortisone: Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.
Tab. Pulmoclear: works by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.
Inj. Thiamine: 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.
Q3) What could be the cause for her current acute exacerbation?
A3) Acute exacerbation can be due to generalized weakness or due to any infection.
Q4) Could the ATT have affected her symptoms? If so how?
A4) ATT might have affected her symptoms due to nephrotoxicity.
Q5) What could be cause of electrolyte imbalance?
A5) Hyponatremia can occur in COPD patients as a manifestation of secondary water retention in comorbidities such as heart or renal failure.
NEUROLOGY
CASE 1:
Q1) 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?
A1) Timespan of patients symptomology:
2 years ago: DM type 2 and antibiotic treatment
1 year ago: Seizures
4 months ago: seizures following cessation of alcohol
10 days ago: General body pains
9 days ago: Patient started talking to himself and laughing. Sudden onset. Decreased food intake. Short term memory loss.
15 May: Admitted.
Primary etiology of the patient: GABA system and glutamate systems are affected in the brain by alcohol consumption.
GABA system: GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.
Glutamate system: The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
Pathophysiology: Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum. The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis .The deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.
Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
A2) Inj. Thiamine: Alcoholic are at high risk of B1 deficiency. Thiamine is used to form thiamine pyrophosphate which is am essential co-factor used by several cellular enzymes.
Inj. Lorazepam: It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cells.
Tab. Pregablin: 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.
Inj. HAI S.C.: Hepatic Arterial Infusion (HAI) is a medical procedure that delivers chemotherapy directly to the liver. The procedure, mostly used in combination with systemic chemotherapy, plays a role in the treatment of liver metastases in patients with colorectal cancer.
Syp Potchlor: Helps to maintain K+ balance in the body if the patient is hypokalemic.
Q3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
A3) Due to excess thiamine deficiency and excess accumulation due to renal disease caused by excess alcohol addiction.
Q4) What is the reason for giving thiamine in this patient?
A4) Due to excess alcohol consumption there will be deficiency of thiamine in the body which is compensated by giving thiamine in quantities.
Q5) What is the probable reason for the kidney injury in this patient?
A5) Alcohol may cause changes in the functions of kidney and effects the ability to regulate the water electrolyte balance in the body. It also effects the hormones acing on kidney. This may be the reason for kidney damage in this patient.
Q6) What is the probable cause for the normocytic anaemia?
A6) Alcohol causes iron deficiency due to its effects on production of new blood cell organs. It also decreases the iron absorption from the intestine.
Q7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes and why?
A7) Yes, as the patient is diabetic, there is a chance of formation of ulcers. Due to low immune system the healing of the ulcers dampens.
CASE 2:
Q1) 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?
A1) Timespan of patients symptomology:
7 days back: History of giddiness that started around 7 in the morning and subsided upon taking rest with one episode of vomiting.
4 days back: Developed giddiness which is sudden in onset, gradually progressive and continuous. He developed these signs after consumption of alcohol. Associated bilateral hearing loss. vomiting 2-3 per day. History of postural instability.
Anatomical location of the problem: Infarct in the cerebral blood vessels.
Etiology: Hypertension can cause ataxia by causing decreased blood supply to the brain.
Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
A2) Tab. Vertin: 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.
Tab. Zofer: is an antiemetic medication. It works by blocking the action of a chemical messenger (serotonin) in the brain that may cause nausea and vomiting during anti-cancer treatment (chemotherapy) or after surgery.
Tab. Ecosprin: aspirin and other non-steroid anti-inflammatory drugs (NSAIDs) inhibit the activity of the enzyme now called cyclooxygenase (COX) which leads to the formation of prostaglandins (PGs) that cause inflammation, swelling, pain and fever.
Tab. Atorvastin: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conver
sion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
Tab. Clopidogrel: he 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.
Q3) Did the patients history of denovo HTN contribute to his current condition?
A3) High blood pressure can have risk of developing cerebral infarcts. High blood pressure causes impaired endothelial dysfunction.
Q4) Does the patients history of alcoholism make him more susceptible to ischaemic or hemorrhagic type of stroke?
A4) 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.
CASE: 3
Q1) 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?
A1) Timespan of symptomology:
10 years ago: She had a episode of paralysis of both upper and lower limb.
8 months back: She developed pedal edema which is gradually progressing.
7 months back: Blood infection.
Since 6 days: Radiating pain along the upper limb which is dragging in nature.
Since 5 days: palpitations which are sudden in onset and more during the night time. Dyspnoea during palpitations.
Q2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
A2) Use if diuretics, laxatives, corticosteroids, mineralocorticosteroids excess acidosis, familial hypokalemia may be cause of recurrent hypokalemia in her.
Q3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
A3) Earliest change in ECG: Decreased T-wave amplitude, ST depression, T-wave inversion, prolonged PR interval.
Severe cases: Ventricular fibrillation, rarely AV block.
CASE-4:
Q1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
A1) There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarization, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after hemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to hemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a hemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.
Q2) 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?
A2) Scar formation due to previous episode of seizures will worsen the symptoms on subsequent attack of another episode of seizure.
CASE-5:
Q1) What could have been the reason for this patient to develop ataxia in the past 1 year?
A1) Alcohol may be the reason for this patient to develop ataxia in the past 1 year. Damage from alcohol is a common cause of cerebellar ataxia. In patients with alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech. It can also cause associated signs of peripheral neuropathy.
Q2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
A2) Heavy alcohol consumption was associated with increased ICH risk.
CASE-6:
Q1) Does the patient's history of road traffic accident have any role in his present condition?
A1) Cerebrovascular accidents can be caused by moderate to severe trauma ( traffic accident ). Large blows causes high pressure of blood pooling that gets trapped and forms a clot.
Q2) What are warning signs of CVA?
A2) One side of the face is drooping
Arm weakness
Speech difficulty
Blurred vision
Loss of balance, headache, dizziness.
Q3) What is the drug rationale in CVA?
A3) Tab. Ecospirin
Inj. Mannitol
Tab. Atorvastatin
Q4) Does alcohol has any role in his attack?
A4) As he consumes alcohol occasionally, alcohol may not have a role in his attack.
Q5) Does his lipid profile has any role for his attack?
A5) Lipid profile of the patient seems to be normal. So lipid profile of this patient doesn't have any role for his attack.
CASE-7:
Q1) What is myelopathy hand?
A1) 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.
Q2) What is finger escape?
A2) 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 commonly results from weakness of some of the ulnar nerve innervated intrinsic hand muscles -in particular the palmar interosseous muscle to the little finger- caused by damage to their nerve supply (denervation).
Q3) What is Hoffman's reflex?
A3) Hoffman's sign or reflex is a test that doctors use 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. The doctor carries out the test procedure by
1)holding the middle finger at the joint closest to the fingernail
2)“flicking” the nail of the person’s middle finger, using their other hand. If there is no movement in the index finger or thumb after this motion, the person has a negative Hoffman’s sign. If the index finger and thumb move, the person has a positive Hoffman’s sign.
CASE-8:
Q1) What can be the cause of her condition ?
A1) Recurrent seizures resolved secondary to cortical vein thrombosis with hemorrhagic venous infarction in right posterior temporal lobe with Iron Deficiency Anemia.
Q2) What are the risk factors for cortical vein thrombosis?
A2) Problems with the way their blood forms clots.
- Sickle cell anemia.
- Chronic hemolytic anemia.
- Beta-thalassemia major.
- Heart disease — either congenital or acquired
- Iron deficiency.
- Certain infections.
- Dehydration.
- Cancer.
- Obesity.
- Inflammatory bowel diseases.
- Q3) There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously why?
- A3) It is due to administration of Antiepileptic drugs as the effect of drugs weans off the seizures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the seizures.\
- Q4) What drug was used in suspicion of cortical venous sinus thrombosis?
- A4) Anticoagulants are used for prevention of blood clots. Ex: Clexane which binds and potentiates anti thrombin to form complex and irreversibly inactivates factor XA.
- CARDIOLOGY
- CASE-1:
- Q1) What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
- A1) 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.
- Q2) Why haven't we done pericardiocenetis in this pateint?
- A2) The effusion was already self healing, so pericardiocenetis is not done in this patient.
- Q3) What are the risk factors for development of heart failure in the patient?
- A3) High blood pressure. Your heart works harder than it has to if your blood pressure is high. Coronary artery disease. Narrowed arteries may limit your heart's supply of oxygen-rich blood, resulting in weakened heart muscle. Heart attack. A heart attack is a form of coronary disease that occurs suddenly. Damage to your heart muscle from a heart attack may mean your heart can no longer pump as well as it should. Diabetes. Having diabetes increases your risk of high blood pressure and coronary artery disease. Some diabetes medications. sleep apnea. The inability to breathe properly while you sleep at night results in low blood oxygen levels and increased risk of abnormal heart rhythms. Both of these problems can weaken the heart. Congenital heart defects. Some people who develop heart failure were born with structural heart defects. Valvular heart disease. People with valvular heart disease have a higher risk of heart failure. Viruses. A viral infection may have damaged your heart muscle. Alcohol use. Drinking too much alcohol can weaken heart muscle and lead to heart failure. Tobacco use. Using tobacco can increase your risk of heart failure. Obesity. People who are obese have a higher risk of developing heart failure. Irregular heartbeats. These abnormal rhythms, especially if they are very frequent and fast, can weaken the heart muscle and cause heart failure. Q4) What could be the cause for hypotension in this patient?
- A4) Hypertension i this case may be due to secondary to Tuberculosis.
- CASE-2:
- Q1) What are the possible causes for heart failure in this patient?
- A1) Patient was diagnosed with diabetes mellitus 30 years ago. Patient was diagnosed with hypertension 19 years ago. Patient is also a chronic alcoholic since 40 years. Above factors are the possible causes for heart failure in this patient.
- Q2) What is the reason for anaemia in this case?
- A2) He is deficit in iron, vitamin B12 and folic acid which may lead to anaemia in this case.
- Q3) What is the reason for blebs and non healing ulcer in the legs of this patient?
- A3) The formation of the bleb and non-healing ulcer may be due to DM, and also CKD is known to delay the healing of this ulcer.
- Q4) What is the reason for blebs and non healing ulcer in the legs of this patient?
- A4) Stage 1: Insulin resistance
- Stage 2: Prediabetes
- Stage 3: DM-2
- Stage 4 : Microvascular complications.
- CASE-3:
- Q1) 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?
- A1) Timeline of symptomology:
- 10 years ago: Surgery for inguinal hernia
- Since 2-3 years: Facial puffiness on and off.
- 1 year ago: Shortness of breath ( Grade-2), Hypertension.
- 2 days ago: Grade-2 to Grade-4 progression of SOB, decreased urine and anuria.
- Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
- A2) Tab. Dytor: It antagonizes the effect of aldosterone, spirolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent K+ loss.
- Tab. Acitrom: Maintains the level of vitamin K required for blood clotting.
- Tab. Cardivas: Carvediol blocks the action of epinephrine on blood vessels and heart, thus lowering the heart rate, blood pressure.
- Tab. Digoxin: It inhibits the action of the myocardial Na-K ATPase pump, this increasing the force of contraction.
- Inj. HAI: Regulates the glucose metabolism.
- Q3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
- A3) Cardiorenal syndrome type-4.
- Q4) What are the risk factors for atherosclerosis in this patient.
- A4) Hypertension impairs the blood vessels ability to relax and may stimulate the growth of smooth muscle cells inside the arteries. All these changes can contribute to the artery clogging process known as atherosclerosis.
- Q5) Why was the patient asked to get those APTT, INR tests for review?
- A5) To ensure that the anticoagulant taken by the patient is producing the desired effect.
- CASE-4:
- Q1) 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?
- A1) Timespan of symptomology:
- Since 12 years: DM and on medication
- Since 1 year: Heart burn like episodes which is relieved with medication.
- 7 months ago: Diagnosed with pulmonary TB with full course of medication.
- Since 6 months: Hypertension and on medication.
- Since half and hour: Shortness of breath even at rest.
- Anatomical localization: Cardiovascular system
- Etiology: hypertension and diabetic etiology
- Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
- A2) Tab. MET XL: Contains Metoprolol. Metoprolol is a beta-1-adrenergic receptor inhibitor specific to cardiac cells with negligible effect on beta-2 receptors. This inhibition decreases cardiac output by producing negative chronotropic and inotropic effects without presenting activity towards membrane stabilization nor intrinsic sympathomimetics.
- Q3) What are the indications and contraindications for PCI?
- A3) Indications:
- Acute ST-elevation myocardial infarction (STEMI)
- Non–ST-elevation acute coronary syndrome (NSTE-ACS)
- Unstable angina.
- Stable angina.
- Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
- High risk stress test findings.
- Contraindications:
- Lack of cardiac surgical support.
- Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
- Coagulopathy.
- Hypercoagulable states.
- Diffusely diseased vessels without focal stenoses.
- Q4) 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?
- A4) If PCI is performed in a patient who doesn't need it may have complications like:
- Bleeding
- Blood vessel damage
- Arrhythmias
- Need for emergency coronary artery surgery.
- Research on overtesting and overtreatment may harm the patient by following ways:
- Overuse of X-rays and CT scan can lead to cancers
- CASE-5:
- Q1) 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?
- A1) Timespan of symptomology:
- Hypertension and DM since long.
- 3 days ago: Chest pain which is insidious in onset with gradual progression and dragging type.
- Morning: Giddiness and Profuse sweating.
- Anatomical localization: Blood vessels.
- Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
- A2) Tab. Aspirin: Aspirin is non-selective and irreversibly inhibits both forms (but is weakly more selective for COX-1). It does so by acetylating the hydroxyl of a serine residue. Normally COX produces prostaglandins, most of which are pro-inflammatory, and thromboxanes, which promote clotting.
- Tab. Atorvast: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
- Tab. Clopibb: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
- Inj. HAI: Regulates glucose metabolism.
- Angioplasty: It is used to widen narrowed and obstructed arteries or veins, typically to treat arterial athersclerosis.
- Q3) Did the secondary PTCA do any good to the patient or was it unnecessary?
- A3) Reasons for a Percutaneous Transluminal Coronary Angioplasty (PTCA) PTCA is performed to restore coronary artery blood flow when the narrowed artery is in a location that can be reached in this manner. Not all coronary artery disease can be treated with PTCA. IN this patient PTCA is not necessary. Late PCTA leads to the increased risk of periprocedural complications, long-term bleeding, and stent thrombosis.
- GASTROENTEROLOGY( & PULMONOLOGY)
- CASE-1:
- Q1) 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?
- A1) Timespan of symptomology:
- 5 years ago: 1st episode of pain abdomen and vomiting
- 1 year back: 5 to 6 episodes of pain abdomen and vomiting
- 20 days back: Increased consumption of toddy intake
- Since 1 week: Pain abdomen and vomiting
- Since 4 weeks: Fever, constipation and burning micturition
- Anatomical localization: Pancreas and left lung
- Etiology: The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes attributed to alcohol.
- Q2) 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?
- A2) Inj. Metrogyl: Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by forming nitroso radicals, which disrupt the DNA of microbial cells.
- Inj. Meropenam: Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
- Inj. Amikacin: The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
- TOTAL PARENTAL NUTRITION
- Inj. Octerotide: Octreotide suppresses secretion of growth hormone (GH), and in many cases suppresses insulin-like growth hormone-1 (IGF-1) (somatomedin C). Sandostatin works centrally at the site of the tumor and binds to somatostatin receptors to regulate GH secretion and cell growth.
- Inj. Pantop: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
- Inj. Thiamine: Mechanism of Action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
- Inj. Tramadol: Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
- CASE-2:
- Q1) What is causing the patient's dyspnea? How is it related to pancreatitis?
- A1) Pleural effusion might be the cause of patients dyspnea.
- Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease[24]. Pancreatic ascites and pleural effusion are rare complications of both chronic and acute pancreatitis, and are associated with a mortality rate of 20% to 30%.
- Q2) Name possible reasons why the patient has developed a state of hyperglycemia.
- A2) Hyperglucagonemia secondary to stress could be the result of patient developing hyperglycemia.
- Elevated levels of catecholamines and cortisol.
- Q3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
- A3) Elevated liver enzymes are a sign that a person has an inflamed or a damaged liver. Many conditions may cause liver inflammation or damage. In this case the probable reason may be due to liver injury. Alanine aminotransferace (ALT) and Asparate aminotransferase (AST) are the specific markers for alcoholic fatty liver disease. Glutamyl transpeptidase (GGT) is another marker of liver injury, and this enzyme is elevated in people who consumes alcohol. Of all the enzyme markers GGT is the most sensitive biomarker of alcohol consumption.
- Q4) What is the line of treatment in this patient?
- A4) IVF: 125 ml/hr
- Inj. PAN 40mg i.v.
- Inj Zofer 4mg i.v.
- Inj. Tramadol 1amp in 100ml i.v.
- Tab. Dolo 650mg
- GRBS charting 6th hourly
- BP charting 8th hourly.
- CASE-3:
- Q1) What is the most probable diagnosis in this patient?
- A1) Abdominal Hemorrhage may be the most probable diagnosis in this patient.
- Q2) What was the cause of her death?
- A2) Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internal organs.
- Q3) Does her NSAID abuse have something to do with her condition? How?
- A3) NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.
- NEPHROLOGY ( AND UROLOGY)
- CASE-1:
- Q1) What could be the reason for his SOB ?
- A1) His shortness of breath may be due to Acidosis which was caused by diuretics.
- Q2) Why does he have intermittent episodes of drowsiness ?
- A2) Hyponatremia was the cause for drowsiness.
- Q3) Why did he complaint of fleshy mass like passage in his urine?
- A3) Pyuria (Many pus cells) are passed in the urine which he observed as fleshy mass like passage.
- Q4) What are the complications of TURP that he may have had?
- A4) Bladder injury.
- Bleeding.
- Blood in the urine after surgery.
- Electrolyte abnormalities.
- Infection.
- Loss of erections.
- Painful or difficult urination.
- CASE-2:
https://drsaranyaroshni.
Q1) Why is the child excessively hyperactive without much of social etiquettes ?
A1) Inattention and hyperactivity/impulsivity are the key behaviors of ADHD. Some people with ADHD only have problems with one of the behaviors, while others have both inattention and hyperactivity-impulsivity. Most children have the combined type of ADHD.In preschool, the most common ADHD symptom is hyperactivity. Due to efficacy of the medications like dopamine and noradrenaline have been suggestive of pathology of ADHD.
Q2) Why doesn't the child have the excessive urge of urination at night time ?
A2)
Q3) How would you want to manage the patient to relieve him of his symptoms?
A3) Antideppresants like Bupropion, trazodone
Antipsychotics like Risperidone, aripiprazole
Mood stabilizers like Carbamazepine are given to the patient to relieve the symptoms of ADHD.
INFECTIOUS DISEASES( HI VIRUS, MYCOBACTERIA, GASTROENTEROLOGY, PULMONOLOGY)
- CASE-1:
Q1) Which clinical history and physical findings are characteristic of tracheo- esophageal fistula?
A1) History findings - Any congenital heart diseases, history of mild respiratory distress, history of recurrent attacks of pneumonia.
Physical findings- drooling, choking, respiratory distress, and feeding inability. Gastric distension is a common complication of a fistula between the trachea and distal esophagus. Reflux of gastric contents through the fistula tract results in aspiration pneumonia and increasing morbidity.
Q2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
A2) The chances of this patient developing immune reconstitution inflammatory syndrome are high as she had a previous infection of TB.
IRIS can be prevented by treating the patient with ATT with as early as possible. Prednisolone and meloxicam are used to prevent further TB IRIS.
INFECTIOUS DISEASES AND HEPATOLOGY
CASE-1:
Q1) Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?
A1) Locally made alcohol like toddy may cause liver abscess if it is contaminated.
Q2) What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day).
A2) All patients of ALA had serum iron values within the normal range but higher than non-ALA cases. In the liver tissue, most patients with ALA had higher (grade II or III) iron deposition, than non-ALA cases (mostly grade I). Thus, patients with ALA, with or without alcohol indulgence, had higher iron levels when compared to the non-ALA cases. It appears that the higher incidence of ALA in alcoholic livers is possibly due to their higher iron content.
Q3) Is liver abscess more common in right lobe ?
A3) Due to more blood supply to the right lobe, liver abscess is more common in right lobe.
Q4) What are the indications for ultrasound guided aspiration of liver abscess ?
A4) Left lobe abscess
Caudate lobe abscess
Large abscess more than 6cms
Abscess which is not responding to drugs.
CASE-2:
Q1) Cause of liver abscess in this patient ?
A1) Entamoeba Histolytica may be the cause of liver abscess in this patient.
Q2) How do you approach this patient ?
A2) 
Q3) Why do we treat here ; both amoebic and pyogenic liver abscess?
A3) Amoebic liver abscess- 
Pyogenic liver abscess:
Third generation cephalosporin with clindamycin or metronidazole.Broad spectrum penicillin with aminoglycosides
Second generation cephalosporin with aminoglycosides.
Q4) Is there a way to confirmthe definitive diagnosis in this patient?
A4) Neutrophils leukocytosis, anemia of chronic disease,
Blood cultures may reveal the diagnosis, imaging studies like Ultrasound , CT scans and hepatic scans are more sensitive and are the confirmatory test for the diagnosis of liver abscess.
INFECTIOUS DISEASES (MUCORMYCOSIS, OPHTHAMALOGY, ENT, NEUROLOGY)
CASE-1:
http://manikaraovinay.
Q1) 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?
A1) Timespan of symptomology:
3 years ago- diagnosed with hypertension
21 days ago- received vaccination at local PHC which was followed by fever, chills, and rigors.
18
days ago- complained of similar events and went to the the local hospital, it
was not subsided upon taking medication(antipyretics).
11
days ago - c/o Generalized weakness and facial
puffiness and periorbital oedema. Patient was in a drowsy state.
4
days ago- (a).
patient
presented to casualty in altered state with facial puffiness and periorbital oedema
and weakness of right upper limb and lower limb (b).
towards
the evening patient periorbital oedema progressed (c).
serous
discharge from the left eye that was blood tinged (d).
was
diagnosed with diabetes mellitus.
2 days ago- died.
the fungus enters the sinuses from the
environment and then the brain.
Q2) 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?
A2) Inj. Amphotericin- B: Amphotericin B is an example of a “polyene” type of antifungal. Polyenes bind to fungal ergosterol (the primary sterol in fungal cell membranes). This alters cell membrane permeability, and intracellular components leak from the cell.
Deoxycholate Amphotericine B: Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years.
Q3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
A3) High steroid usage during COVID 19 treatment causes high blood sugars and suppress the immune system. Due to high population in the state there are easy chances of containmant by the fungus Mucormycosis.
INFECTIOUS DISEASES ( COVID- 19 )
Below is the link to view my Master Sheet on COVID-19 cases.
https://docs.google.com/spreadsheets/d/1gUxSiiufPMSNCuNl45_bdex9lcPzuKXfk2Goee_ROSc/edit?usp=sharing
MEDICAL EDUCATION
This assessment had been really helpful to me
Correlating everything and learning the concepts of different systems and having a study discussion with my friends helped me a lot through this learning process.
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