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.
This is the link of the questions asked regarding the cases:
https://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
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?
Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs
Diagnosed with diabetis - 8yrs back
Anemia and took iron injections - 5yr ago
Generalised weakness - 1 month back
Diagnosed with hypertension - 20 days back
Pedal edema - 15 days back
Facial puffiness- 15 yrs back
Anatomical location of problem - lungs
Primary etiology of patient- 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?
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.
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.
Q3) What could be the cause for her current acute exacerbation?
Acute exacerbation can be due to generalized weakness or due to any infection.
Q4) Could the ATT have affected her symptoms? If so how?
ATT might have affected her symptoms due to nephrotoxicity.
Q5) What could be cause of electrolyte imbalance?
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?
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.
Admitted on 15 of May
Primary etiology of the patient: GABA system and glutamate systems are affected in the brain by alcohol consumption.
The 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.
The 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.
The symptom:
Irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.
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?
(i) Inj. Thiamine: Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency
(ii) Inj. Lorazepam: Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
(iii)Tab. Pregablin: Pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
(iv)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.
(v)Potchlor liquid is used to treat low levels of potassium in the body.
Q3)Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
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?
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?
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?
Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine.
7)could chronic alcoholism have aggravated the foot ulcer formation ?if yes and why ?
Yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.Due to this healing of an ulcer 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?
Timeline of the patient is as follows-
7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain..
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?
Tab. Vertin: This is betahistine, which is an anti- vertigo medication.It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
Tab. Zofer: It 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.
Indications- Used to control the episodes of vomiting and nausea in this patient.
Tab. Ecosprin:This is aspirin. It is an NSAID. They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis.
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
Tab. Atorvastin: Atorvastatin competitively yinhibits 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.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
Tab. Clopidogrel: It is an antiplatelet medication.It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
Q3) Did the patients history of denovo HTN contribute to his current condition?
A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts. Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
Q4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
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?
Timeline of the patient is as follows-
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?
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?
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?
There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury ,(particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic 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 haemorrhage 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 haemorrhagic stroke.14 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?
Normally the consciousness system is a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness. Diverse seizure types including absence, generalized tonic-clonic and complex partial seizures converge on the same set of anatomical structures through different mechanisms to disrupt consciousness.
CASE-5:
Q1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Alcohol may be the reason for this oatient 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 ?
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?
One cause of stroke after trauma is a tear in the head or neck blood vessels that lead to the brain, which can be a source of blood clots that cause a stroke. If a tear in these arteries can be diagnosed at the time of the trauma, a patient could be treated with an anti-clotting medicine to help prevent stroke
Q2) What are warning signs of CVA?
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?
Tab. Ecospirin
Inj. Mannitol
Tab. Atorvastatin
Q4) Does alcohol has any role in his attack?
As he consumes alcohol occasionally, alcohol may have a role in his attack.
Q5) Does his lipid profile has any role for his attack?
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:
A)what is myelopathy hand?
Due to involvement of the pyramidal tract, the fingers on ulnar side lose their power of Adduction and Extension and are unable to grip and release the objects rapidly. These changes have been termed as Myelopathy Hand.
B)what is finger escape?
Also known as Wartenberg's sign. It is a neurological sign consisting of involuntary abduction of the little finger, caused by unopposed action of the extensor Digiti Minimi This is a finding of cervical myelopathy.
C)what is Hoffman's sign?
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This is a quick test for assessing any possible existence of spinal cord compression from a lesion on the spinal cord or any other underlying nerve condition.
CASE-8:
Q1) What can be the cause of her condition ?
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?
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?
- There was a sezuire free period 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?
- CLEXANE was given to relive clot in suspission of CVST.
- Clexane 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?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
- Q2) Why haven't we done pericardiocenetis in this pateint?
- 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?
- The risk factors for development of heart faliure in this patient areAlcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure
high blood pressure
Smoking
Diabetes
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.
Q4) What could be the cause for hypotension in this patient?Visceral pericardium may have thickened which is restricting the heart to expand causing hypotension.Hypotension in this case may be due to secondary to Tuberculosis. - CASE-2:
- Q1) What are the possible causes for heart failure in this patient?
- Patient was diagnosed with diabetes mellitus 30 years ago. Patient was also
- diagnosed with hypertension 19 years ago and was a chronic alcoholic since 40 years.These factors are the possible causes for heart failure in the patient.
- The patient has elevated creatinine and AST/ALT ratios >2 and was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure
- Q2) What is the reason for anaemia in this case?
- The patient has normocytic normochromic anaemia. it could be anaemia of a chronic disease as the patient is diagnosed with CKD stage IV. Patient’s with anaemia and CKD also tend to have deficiency in nutrients like iron, vitamin B12 and folic acid.
- Q3) What is the reason for blebs and non healing ulcer in the legs of this patient?
- The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.
- Q4) What sequence of stages of diabetes has been noted in this patient?
- There are 4 stages in type 2 diabetes-
- Stage 1: Insulin resistance
- Stage 2: Prediabetes
- Stage 3: DM-2
- Stage 4 :Microvascular complications including retinopathy, nephropathy or neuropathy.
- CASE-3:
- https://preityarlagadda.
blogspot.com/2021/05/biatrial- thrombus-in-52yr-old-male.html - 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?
- 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?
- 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?
- The patient is Cardiorenal syndrome type-4.
- Q4) What are the risk factors for atherosclerosis in this patient.
- 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?
- 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?
TIMELINE OF EVENTS-
•Diabetes since 12 years - on medication
•Heart burn like episodes since an year- relieved without medication
•Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
•Hypertension since 6 months - on medication
•Shortness of breath since half an hour-SOB even at rest
Anatomical 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?
- TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient. 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.
Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
- Q3) What are the indications and contraindications for PCI?
INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG..
- 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?
- 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.
OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations may lead to cancers.
- CASE-5:
- https://bhavaniv.blogspot.com/
2021/05/case-discussion-on- myocardial-infarction.html?m=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?
- 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?
TAB. ASPIRIN:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events
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: Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
- Q3) Did the secondary PTCA do any good to the patient or was it unnecessary?
- Reasons for a Percutaneous Transluminal Coronary Angioplasty (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?
- 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
- 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?
- 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.
TPN ( Total Parenteral Nutrition ): the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
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:
- https://nehae-logs.blogspot.
com/2021/05/case-discussion- on-25-year-old-male.html - Q1) What is causing the patient's dyspnea? How is it related to pancreatitis?
- 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.
- 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?
LFT are increased due to hepatocyte injury
If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum..
- Q4) What is the line of treatment in this patient?
- 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?
- Abdominal Hemorrhage may be the most probable diagnosis in this patient.
- Q2) What was the cause of her death?
- Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internl organs.
- Q3) Does her NSAID abuse have something to do with her condition? How?
- NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.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.
- NEPHROLOGY ( AND UROLOGY)
- CASE-1:
- Q1) What could be the reason for his SOB ?
- His shortness of breath may be due to Acidodsis which was caused by diuretics.
- Q2) Why does he have intermittent episodes of drowsiness ?
- Hyponatremia was the cause for drowsiness.
- Q3) Why did he complaint of fleshy mass like passage in his urine?
- 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?
- Bladder injury.
- Bleeding.
- Blood in the urine after surgery.
- Electrolyte abnormalities.
- Infection.
- Loss of erections.
- Difficult Micturition
- CASE-2:
https://drsaranyaroshni.
Q1) Why is the child excessively hyperactive without much of social etiquettes ?
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 ?
The child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder
Q3) How would you want to manage the patient to relieve him of his symptoms?
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?
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?
Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms:
"unmasking" IRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started;
"paradoxical" IRIS refers to the worsening of a previously treated infection after ART is started.
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 ?
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).
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 ?
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 ?
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 ?
Entamoeba Histolytica may be the cause of liver abscess in this patient.
Q2) How do you approach this patient ?
Q3) Why do we treat here ; both amoebic and pyogenic liver abscess?
Amoebic liver abscess Treatment is mainly drug therapy with anoebicidal drugs like Metronidazole 750mg orally TID for 5 to 10 days. This acts on both intestinal and hepatic amoebiasis.
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?
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?
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.
The patient died 2 days ago.
The patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was also diagnosed with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes.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?
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.
Q3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19.But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing
INFECTIOUS DISEASES ( COVID- 19 )
Below is the link to view my Master Sheet on COVID-19 cases.
https://docs.google.com/spreadsheets/d/1W5Zwn0rr_C3RUXeN4vzICzH3EnbznG7iyUi0R2TfeVk/edit?usp=sharing
MEDICAL EDUCATION
The development of entrustable professional activities and competency-based learning with identified milestones for achievement have transformed this assessment.This E log experience enhanced many students to profound into their thoughts and helps in gaining clinical knowledge.
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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