MEDICINE BLENDED 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.
LINK TO QUESTIONS REGARDING CASES.
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html
M. VARUN SAI
ROLL NO.: 73
8th Semester.
PULMONOLOGY
Link to patient details:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?
Ans... Course of the symptomatology in the patient :
* Acute episode of SOB 20yrs back .
* Then repeated episodes of SOB every year usually in the month of january . Each episode duration of 1 week.
* An acute exacerbation of chronic SOB 12 yrs back for which the patient was hospitalised for 20 days.
* Similar episodes of acute SOB every year till her current episode.
* Current episode details : duration of episode from 30 days. Dyspnea on exertion and relieved on rest initially. From past 2 days , dyspnea even on rest.
CAUSE OF THE ATTACKS : it is possible that the patient is sensitive to the cold climate and pollens. Repeated attacks may be triggered by the exposure to the cold climate as acute exacerbation is seen in january . Chronic exposure to the allergens , there may be repeated damage to the airway . This might be the reason for the progression of disease and patient experiencing repeated attacks of SOB.
Anatomical location : CT scans of the patient suggest the pathology in the lower airways.
Main Etiology : chronic exposure to cold climate and allergens like pollen.
Other symptoms :
- Pedal edema extending upto ankle since 15 days.
- Facial puffiness since 15 days.
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 ... Placebo has no physiological and pharmacological actions in the body.
1. HEAD END ELEVATION : to improve the ventilaton in the patient.
2. O2 inhalation : to improve the spO2 of the patient so that tissues get enough oxygen perfusion.
3. INTERMITTENT BiPAP : to maintain normal breathing pattern of the patient .
DRUG THERAPY :
1. AUGMENTIN : antibiotic drug with combination of penicillin and clavulanic acid. Penicillin acts efficiently against gram positive organisms and clavulanic acid enhances the action of penicillin by inhibiting penicillinase enzyme produced by resistant bacteria.
2. AZITHROMYCIN : antibiotic drug given to resolve bacterial infections. Given to this patient in suspicion
of any underlying bacterial infection.
3. LASIX :: it is a diuretic ( Furosemide ) . This is used to relieve pedal edema and facial puffiness.
4. HYDROCORTISONE : steroid drug with its anti inflammatory and anti fibrotic action , reduces the severity and further progression of the disease.
5. NEBULIZATION WITH BRONCHODILATORS :
Bronchodilators like budecort ( steroid drug ) is used to relieve the edema and inflammation in the trache-bronchial tree . They provide immediate reilief during acute attacks of dyspnea.
6. GRBS charting : to monitor the blood sugar levels of the patient as he is diabetic.
7. TEMPERATURE , B.P. & spO2 MONITORING.
8. I/O charting : indicated in diabetic and hypertensive patients.
9. THIAMINE : to prevent its deficiency , which may lead to neurological and cardiological defects.
3) What could be the causes for her current acute exacerbation?
Ans... * Acute secondary bacterial infection.
* Exposure to the allergens ( pollen ).
* Underlying heart disease as suggested by echocardiogram findings.
4. Could the ATT have affected her symptoms? If so how?
Ans ...NO
5.What could be the causes for her electrolyte imbalance?
Ans... It could be due to drug induced hyponatremia. Antihypertensive drugs like telmisartan might be the reason for electrolyte imbalance.
NEUROLOGY
CASE 1 ::
Link to patient details:
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 .. COURSE OF SYMPTOMATOLOGY :
DAY 1 : The patient had an episode of giddiness at around 7 am while doing his routine work which later on subsided upon taking rest. He also had an episode of vomiting on the same day.
DAY 2 : Asymptomatic.
DAY 3 : Asymptomatic
DAY 4 : Asymptomatic.
DAY 5 : an episode of giddiness which is sudden onset after taking alcohol. There is bilateral hearing loss , aural fullness and tinnitus . 2 to 3 episodes of vomiting and postural instability was also present.
DAY 6 -7 : All the symptoms were aggaravated with accompanying postural instability.
ANATOMICAL LOCALISATION : cerebellum.
MAJOR ETIOLOGY : Long standing undiagnosed hypertension. Chronic alcoholism led to CVA as suggested in CT scan .
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.... Placebo has no physiological and pharmacological actions.
DRUG THERAPY :
* VERTIN : anti vertigo drug. Its composition is betahistine. Acts as H1 receptor agonist and H3 receptor antagonist. It is indicated in endolymphatic hydrops.
* ZOFER : an anti emetic drug. Acts as serotonin receptor antagonist
* CLOPIDOGREL : an antiplatelet drug used in impending stroke .
* ATORVASTATIN : it is a HMG - coA inhibitor and is used to lower the blood cholesterol levels.
* ASPIRIN : it is a NSAID which acts by inhibiting cyclooxygenase enzyme. It is used in patients with heart diseases .
* MULTI VITAMIN TABLETS : These are used to prevent vitamin deficits and also help to replenish the stores of fat soluble vitamins.
3) Did the patients history of denovo HTN contribute to his current condition?
Ans... Based on the history and the fact that , long standing hypertension might be the cause of CVA. Moreover alcoholism acts as an independent risk factor for CVA which supports the presumptions.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ans... YES.
CASE 2 ::
Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans ....The patient has palpitations,pedal edema ,chest pain and heaviness , dragging type of pain radiating to the left upper limb all suggestive of a underlying heart disease.
Previous history of hypokalemic paralysis suggestive of recurrent hypokalemic episodes might be present.
This might lead to auto compensation by kidney leading to reabsorption of the potassium along with water excessively which might lead to pedal edema.
Further the hypokalemia is known to cause physiological heart defects and ECG changes which could Be the cause for palpitations and left upper limbs paralysis.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Ans... RISK FACTORS FOR HYPOKALEMIA :
* ABNORMAL LOSS :
- Medications:enema,diuretics,laxatives,steroids
- renal causes: mineralocorticoid excess,osmotic diuresis,renal tubular acidosis,hypomagnesemia.
* TRANSCELLULAR SHIFTS :
- alkalosis
- thyrotoxicosis
- delirium tremens
- head injury
- hypokalemic periodic paralysis
* INADEQUATE INTAKE.
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Ans...ECG changes in a case of hypokalemia are
- Earliest change in ECG: Decreased T- wave amplitude
- ST depression and T wave inversions
- Prolonged PR interval.
- U wave
- Pseudo prolonged QT interval which actually is QU interval.
CASE 3 ::
Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Ans ... Evidences suggest that increased attacks of brain stroke may cause increase occurence of seizures. It is believed that brain stroke causes injury to the brain tissue. The damaged brain tissue heals by forming a scar. The scar tissue cannot conduct the electrical activities. This disruption of the electrical activity may cause the occurence of seizures.
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...Abnormal increased activity in frontal -parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of conscious-ness in complex partial seizures. Thus, abnormally increased or decreased activity in the same networks can cause loss of consciousness. Information flow during normal conscious processing may require a dynamic balance between these two extremes of excitation and inhibition.
CASE 4 ::
Link to patient details:
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans... Cause could be ALCOHOLISM.
Alcohol induced cerebellar damage is the major cause of cerebellar ataxia in alcoholics. In alcohol induced ataxia , the patients have gait and lowerlimb abnormalities more than upper limb and speech abnormalties.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Ans .. some of the epidemiological studies show that there is increased risk for intracranial bleeding in alcoholics.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5440244/#:~:text=Heavy%20alcohol%20consumption%20demonstrated%20a,12.32%2C%20p%20%3C%200.0001).
CASE 5 ::
Link to patient details:
__*Questions*_
1)What is myelopathy hand ?
Ans ...
In many of the cervical spinal cord disorders,the ulnar 2-3 fingers lose their ability to grasp ,and rapidly release objects and also there is an impairment of adduction and extension in these fingers. it is called as myelopathy hand.
2)What is finger escape ?
Ans...
It is also called as WARTENBERG SIGN
It is an involuntary abduction of little finger due to unopposed action of EXTENSOR DIGITI MINIMI
DIFFERENTIAL DIAGNOSIS: ULNAR NERVE PALSY, CERVICAL MYELOPATHY
3)What is Hoffman’s reflex?
Ans...
Hoffmanns reflex
When The investigator flicks the fingernail of middle finger down , there is an involuntary Flexion of thumb or index finger
This is called as positive Hoffman's reflex
It is seen in UMN lesions and corticospinal tract lesions.
CASE 6 ::
Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
Ans ...THROMBOSIS AND INFARCTION.
2) What are the risk factors for cortical vein thrombosis
?
Ans...RISK FACTORS FOR CORTICAL VEIN THROMBOSIS :
- BETA THALASSEMIA
- HEMOLYTIC ANEMIA
- HEAD TRAUMA
- IRON DEFICIENCY
- CANCER
- INTRACRANIAL HYPOTENSION
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
Ans....The seizure free period between each episode is called post ictal period. It is characterized by altered state of consciousness. Generally post ictal period lasts for about 5 min to 30min depending on the severity of the seizures and neurological lesion. Other symptoms include drowsiness , nausea , vomiting and disorientation.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Ans... Anti coagulants are used. They prevent further progression of the thrombosis. They donot have any effect on already formed thrombus.
CASE 7 ::
Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
Ans... NO.
2.What are warning signs of CVA?
Ans..
- Sudden headache with no known cause.
- Sudden onset of confusion , trouble speaking and understanding the speech.
- Sudden onset of giddiness ,
- Sudden onset of weakness or numbness in the arms and legs with difficulty in walking.
3.What is the drug rationale in CVA?
Ans.... Thrombolytic drugs along with neuroprotective agents are given.
4. Does alcohol has any role in his attack?
Ans...patient is a chronic alcoholic. Alcoholics generally have increased risk for vascular pathologies like atherosclerosis. Alcoholism could have been the underlying cause but the sudden attack might be precipitated by other risk factor.
5.Does his lipid profile has any role for his attack??
Ans ...YES . Patient's lipid profile shows high triglyceride levels and high cholesterol levels. Long term abnormalities in lipid profile could have been the etiology of the attack.
CARDIOLOGY
CASE 1 ::
Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans... Heart failure with preserved ejection fraction occurs in conditions where there is diastolic dysfunction of the ventricles like hypertrophic cardiomyopathy and restrictive cardiomyopathy. The ventricles are unable to relax completely , but they contract adequately , there by mainataining the ejection fraction.
Heart failure with reduced ejection fraction occurs in intrinsic heart diseases like DILATED CARDIOMYOPATHY. The ventricles are dilated and their wall is thinned out in this condition. There will be systolic dysfunction of the ventricles leading to reduced ejection fraction.
2.Why haven't we done pericardiocentesis in this patient ?
Ans.... Pericardiocentesis is indicated when there is considerable pericardial effusion causing compression over the heart chambers. In this condition , there is no need for pericardiocentesis as it is resolving.
3.What are the risk factors for development of heart failure in the patient?
Ans ..
- hypertension
- CAD
- DM
- MEDICATIONs
4.What could be the cause for hypotension in this patient?
Ans .. systemic venous return to the heart is reduced which inturn reduces the pulmonary venous return. This causes decrease in the end diastolic volume and finally reduced cardiac output.
CASE 2 ::
Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
Ans...
- hypertension
- alcoholic cardiomyopathy
- Cardio- renal syndrome.
2.what is the reason for anaemia in this case?
Ans .. patient also has underlying kidney disease. This can lead to decreased erythropoietin release . This could be the cause for anemia.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Ans ..these might be due to diabetes mellitus.
4. What sequence of stages of diabetes has been noted in this patient?
Ans ..stage 1: defined as DBCD (dysglycemia-based chronic disease )insulin resistance;
stage 2: defined as DBCD prediabetes;stage 3: defined as DBCD type 2 diabetes; and
stage 4: defined as DBCD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events.
All these stages have been noted in this case.
CASE 3 ::
Link to patient details:
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 ... COURSE OF SYMPTOMS :.
* history of facial puffiness since 2 years with on and off episodes.
* History of SOB since 2 days.
2) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans...
Type 1 cardiorenal syndrome occurs when there is acute decompensation of cardiac function leading to a decrease in glomerular filtration. Researchers have previously proposed a decline in cardiac output with decreased renal perfusion as the leading underlying cause for worsening kidney function in cardiorenal syndrome types 1 and 2. However, recent studies have postulated that increased central venous pressures are a more critical factor.[1] When patients develop fluid overload due to worsening cardiac function, venous pressures increase and are transmitted back to the efferent arterioles; this results in a net decrease in the glomerular filtration pressure and renal injury. Other factors involved in the pathogenesis of types 1 and 2 cardiorenal syndromes include elevated intraabdominal pressures, activation of the renin-angiotensin-aldosterone system (RAAS), activation of the sympathetic nervous syndrome and increased inflammatory damage to the kidney related to heart failure.[6][7] Targeting this cycle is the mainstay of therapy for type 1 cardiorenal syndrome. Types 3 and 4 cardiorenal syndromes more likely result from volume overload from renal dysfunction, abnormal cardiac function in the setting of metabolic disturbances (such as acidemia), and neurohormonal changes that accompany renal disease.[8] Patients can develop type 5 cardiorenal syndrome in the setting of sepsis, systemic lupus erythematosus (SLE), diabetes mellitus, decompensated cirrhosis, or amyloidosis; all of these disorders can lead to disease in both the heart and kidney.[9]
SOURCE :
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?
3) What are the risk factors for atherosclerosis in this patient?
Ans...RISK FACTORS :
- abnormal lipid profile
- DM
- Hypertension
- high saturated fats in diet
- obesity
4 ) Why was the patient asked to get those APTT, INR tests for review?
Ans... APTT & INR is indicated in this patient to evaluate the coagulation profile and to assess the thrombotic activities.
CASE 4 ::
Link to patient details:
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 .. COURSE OF SYMPTOMS :
* Sudden onset sweating on exertion
* Grade 4 shortness of breath at night.
Patient is a case of pulmonary tuberculosis which was treated compeltely . Patient is a known case of hypertension and diabetes.
Blood sugar levels were high at the time of presentation. On examination bilateral crepitations were heard.
ANATOMICAL LOCALISATION :
coronary artery occlusion.
Prime etilogy : chronic hypertension and diabetes mellitus.
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...placebo has no physiological and pharmacological actions.
DRUG THERAPY ::
1. METOPROLOL - a beta blocker drug. It is used in hypertension and also to relieve angina and MI.
3) What are the indications and contraindications for PCI?
Ans...Indications
- Acute STEMI
- Acute non ST elevation acute coronary syndrome
- Angina equivalent
- Stable and unstable angina
- Critical coronary artery stenosis
- Non compliance with the procedure and inability to take the dual antiplatelet therapy
- Multiple percutaneous interventions re stenosis
- High bleeding risk
- Intolerance for long term antiplatelet therapy
- Short artery less than 1.5 mm
- Hypercoagulable state
- Absence of cardiac surgery backup
- High grade CKD
- Chronic total occlusion of SVG
- Critical left main artery occlusion with no graft or collateral
- Stenosis less than 50%
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
Ans... Complications would occur like infection , bleeding , blood clots , sinus rhythm abnormalities and even sudden cardiac death.
CASE 5 ::
Link to patient details:
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... Patient developed right sided chest pain 3 days back which was insidious in onset and gradually progressive. It is also radiating to the back.
ANATOMICAL LOCALIZATION :: inferior wall MI due to ?occlusion in right coronary artery .
PRIMARY ETIOLOGY :: atherosclerotic occlusion secondary to long standing diabetes
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... Placebo has no pharmacological and physiological actions.
DRUG THERAPY ::
1. ASPIRIN : it is a NSAID acts by inhibiting cyclooxygenase enzyme. It is used in cases of impending MI.
2. ATORVASTATIN : indicated in patients with high blood cholesterol levels .
3. CLOPITAB. : Used to prevent MI and further myocardial damage. It has antiplatelet action.
4. INSULIN INJECTION : to control blood sugar levels.
5. VITALS MONITORING.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans... It would be beneficial in this patient as it can remove the occlusion and restore the perfusion.
CASE 6 ::
Link to patient details:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Ans .. administering i.v. fluids had increased the blood volume and there by increasing the cardiac output and systolic blood pressure thereby releieving the symptoms of hypotension.( ? Doubt )
2. What is the rationale of using torsemide in this patient?
Ans... Torsemide is a diuretic agent , that reduces the fluid overload 8. This can reduce the shortness of breath if it is due to pulmonary congestion.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ans...patient gives the history of TURP and also complains of dribbling urine and oliguria. Suspecting underlying UTI , antibiotics like ceftriaxone are helpful in releiveing the disease.
GASTROENTEROLOGY
CASE 1 ::
Link to patient details:
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...COURSE OF THE SYMPTOMS -
* Pain abdomen and vomiting ; was treated conservatively 5 YRS AGO
* Pain abdomen and vomiting Since 1 week
*Constipation, burning micturition, fever Since 4 days.
After admission ::
CT scan - showed pseudocyst
Chest X ray - showed left pneumothorax and left pleural
ANATOMICAL LOCATION - Pancreas
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 ..placebo has bo physiological and pharmacological actions.
DRUG THERAPY ::
# Amikacin, metronidazole and meropenam are all.given to control infection.
# TPN : total parenteral nutrition
It is given to bed ridden patients.it contains carbohydrates,proteins, fats vitamins and minerals
# NS/RL
It is given as fluid replacement inorder to combat dehydration
#. Tab.Pantop
It is a proton pump inhibitor.it is used in this case for its anti pancreatic secretory
# Inj.octreotide
It is a somatostatin analogue
It decreases the secretions of pancreas
It also has anti inflammatory and cytoprotective effects
# Inj.Thiamine
It is B1 supplement.
It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
# Inj.TRAMADOL
It is an opioid analgesic which is given to relieve pain.
CASE 2 ::
Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans.. dyspnea in the patient could be due to pleural effusion. The causes for the development of pleural effusion could be secondary to pancreaticopleural fistula secondary to the rupture of psuedocyst in pancreas due to pancreatitis. It could also be due to transdiaphragmatic lymphatic obstruction.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans.....The causes for the development of hyperglycemia could be due to damage of pancraetic beta cells secondary to pamcreatitis. This causes low levels of insulin release and could be the reason for hyperglycemia.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans....history of the patient suggest that he is a chronic alcoholic . Alcohol induced hepatocyte damage could be the reason for elevated LFT.
Specific markers for alcoholic fatty liver disease are elevated levels of AST twice more than ALT. And alos elevated GAMMA GLUTAMYL TRANSFERASE.
4) What is the line of treatment in this patient?
Ans. ..
- IVF: 125 mL/hr
- Inj PAN 40mg i.v OD
- Inj ZOFER 4mg i.v sos
- Inj Tramadol 1 amp in 100 mL NS, i.v sos
- Tab Dolo 650mg sos
- GRBS charting 6th hourly
- BP charting 8th hourly
CASE 3 ::
Link to patient details:
Possible Questions :-
1) what is the most probable diagnosis in this patient?
Ans... The patient is suffering from ruptured liver absecss which led to intraperitoneal hematoma. Patient also has intraparenchymal renal disease.
2) What was the cause of her death?
Ans...might be due to complications developed post operatively ( ? Due to anaesthesia).
3) Does her NSAID abuse have something to do with her condition? How?
Ans ...long term use of NSAID could be the reason for renal damage . NSAID use could have lowered the levels of cytoprotective prostaglandins .
NEPHROLOGY.
CASE 1 ::
Link to patient details:
1. What could be the reason for his SOB ?
Ans ....SOB could be due to secondary acidosis caused by renal failure and also might be due to low oxygen perfusion to the tissues due to anemia.
2. Why does he have intermittent episodes of drowsiness ?
Ans ...drowsiness indicates that the brain tissue is not getting enough oxygen supply. This could be due to anemia . Another possibility is due to electrolyte imbalance in the patient .
3. Why did he complaint of fleshy mass like passage in his urine?
Ans ...patient has UTI ( pyuria ) . This was felt like a white mass by the patient.
4. What are the complications of TURP that he may have had?
Ans....COMPLICATIONS OF TURP :
* Bladder perforation .
* Coagulopathies .
* Bleeding .
* Transient bacteremia and septicemia.
* Toxicity due to irrigating fluiids.
* Hypothermia.
CASE 2 ::
Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
Ans...It could be due to undiagnosed anxiety disorder which led to this type of behaviour( ?)
2. Why doesn't the child have the excessive urge of urination at night time ?
Ans ... As there is no urgency of urination at night , the patient could be suffering from any psychomotor disorder or undiagnosed anxiety (?).
3. How would you want to manage the patient to relieve him of his symptoms?
Ans... * Antibiotic treatment as prophylatic to UTI. ( more common in pediatric population ).
* Behavioural therapy along with antianxiety medication (. If diagnosed with anxiety disorder ).
INFECTIOUS DISEASES
( MUCORMYCOSIS )
CASE 1 ::
Link to patient details:
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 .. COURSE OF THE SYMPTOMS :
* 18 april -- post vaccination fever with chills and rigor.
* 28 april -- facial puffiness , generalized weakness and periorbital edema .
* 4 may. --- presented to the OPD with altered mental state.
ANATOMICAL LOCATION : Rhino- orbito-cerebral disease.
PRIMARY ETOLOGY : Fungal infection with mucor .
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.....placebo has no physiological and pharmacological actions.
# LIPOSOMAL AMPHOTERICIN B. - potent anti fungal agent active against mucormycosis.
# ITRACONAZOLE - azole group of antifungal drug. Used alternative to amphotericin B.
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Ans ....
* Steroid overuse in the covid patients . This led to further immunosuppressive state .
* COVID causes systemic illness leading to immunosuppression.
* Mucormycosis is more common among diabetics as thought diabetes is an immunocompromised state.
* Poor patient hygiene also is a risk factor.
MEDICAL EDUCATION
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.
Ans ... The effect of covid pandemic has been great on students . We the medical students have been effected more due to lack of adequate clinical exposure. As we continue to learn during these tough times , we need to upgrade and find new methods of learning . One such new comprehensive method is telemedical learning initiated by general medicine department . We are able to learn about all the cases that come to our hospital and gain adequate clinical exposure and knowledge. Thanks to all the staff members who are constantly guiding us even in these difficult times.
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