GENERAL MEDICINE BLENDED ASSIGNMENT FOR THE MONTH OF MAY 2021
May 25,2021
SIGNET RING SIGN
Indications-
CARDIOLOGY
I am G MEGHANA , R.NO:161 FROM 8 TH SEMESTER
I have created a log regarding my learning, comprehension and clinical understanding of various cases
This would help me to improve my competency in reading, and comprehending clinical data of patients which would be suCcessful with precise knowledge of history taking, examination, clinical investigations analysis which i have improved during the course of creating my log
THIS IS THE LINK TO VARIOUS CASES :
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers
case 1 :
"A 55 yr old female with shortness of breath,pedal edema and facial puffiness"
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
1) What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem ?
ANS)The evolution of symptoms in the patient in a event timeline is as follows:
- The first episode of shortness of breath (Grade 2) , occurred 20 yrs ago in the month of January which lasted for a week
- Similar episodes of SOB over the next 8 yrs , occurred around the month of Jan lasting for about a week, relieved on medication
- 12 yrs ago, episode of SOB (grade 2) lasted for a period of 20 days
- latest episode of SOB occurred 30 days ago on exertion , progressed to Grade 4 2 days ago ( not relieved on nebulization)
- Pedal edema since 15 days (upto ankle, pitting type)
- Facial puffiness since 15 days
- drowsiness and ↓urine output since 2 days .
Anatomical localization for the problem :
- When the investigations were carried out , the HRCT SCAN reveals "SIGNET RING SIGN "
Indicative of BRONCHIECTASIS
primary etiology for the patient's problem :
- It could be occupational exposure to paddy ,as she faces the episodes while working in the field
2)what are mechanism of action , indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used in this patient ?
ANS )Non pharmacological interventions:
1. head end elevation : Indication : COPD Mechanism of action : Eases the symptoms like shortness of breath and buildup of mucus in the lung
2. chest phsyiotherapy /Airway clearance technique :
Indication : Bronchiectasis
mechanism of action : helps to drain the built up secretions in the lungs and
loosen the mucus
3. Intermittent BiPaP: Indication : hypoventilating patients
Mechanism of Action : augments lung expansion , delivers aerosol medication
Pharmacological interventions :
1. Inj.Augmentin IV BD :
Indication : acute exacerbation in bronchiectasis
mechanism of action : reduce bacterial load in the lung , treat infection
2. tab azithromycin 500 mg OD :
same as above
3. INJ Lasix IV BO :
Indication : fluid build up, edema
Mechanism of action : furosemide : Blocks absorption of Na, Cl in kidney (diuretic)
4.INJ Hydrocortisone 100 mg IV :
INDICATION : Inflammation
MOA : Anti inflammatory effect , reduce amount of sputum production
5. Nebulisation with Ipravent budecort :
INDICATION : COPD
MOA : reduces symptoms like shortness of breath , wheezing
facilitates breathing
6. tab.pulmoclear 100 mg OD :
INDICATION : COPD
MOA :reduces wheezing , congestion , blockage in airways
7. INJ HAI SC :
INDICATION : Diabetes mellitus
MOA : Regulate blood glucose levels
3. what could be the causes of her acute exacerbation ?
ANS ) Evident electrolyte imbalance possibly due to kidney injury caused due to ATT
4) Could the ATT have affected her symptoms , if so how ?
Ans) The patient was on ATT for 12 days
The ATT Drugs Isoniazid and rifampicin are nephrotoxic ,possibly they caused Acute kidney injury leading to the symptoms
5) what could be the causes of her electrolyte imbalance ?
ans) two possible reasons :
ACTIVATION OF RAAS , and inappropriate increase in plasma arginine vasopressin in COPD
This aggravated electrolyte imbalance in acute exacerbation of COPD
2)kidney injury
pulmonology
case 2 :
link to patient details :
1)hat What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS ) Evolution of symptoms in the patient in an event timeline is as follows :
- Previously, he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol associated with " tremors , restlessness and sweating ". He started drinking again and when he discontinued ,
Talking as well as laughing to himself
- decreased food intake and short term memory loss since 9 days anatomical localisation of the problem :Brain
2) What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non- pharmacological interventions used for this patient ?
ANS) INJ . 1 amp THIAMINE in 100 ml
Indication : thiamine deficiency
mechanism of action : helps the body to convert carbohydrates to energy . as a supplement in thiamine deficiency
INJ LORAZEPAM :
INDICATION : seizures
MOA : 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
TAB. PREGABALIN 75 mg OD :
INDICATION :Seizures
MOA :Subtly reduces the synaptic release of several neuro transmitters.
binds to alpha 2 delta subunits
actions invivo to neuron excitability and seizures
LACTULOSE 30 ml PO BD :
INDICATION : Portal systemic encephalopathy
MOA : Decreases the intestinal production and absorption of ammonia
POTCHLOR LIQUID :
INDICATION : Hypokalemia
MOA : Maintains potassium balance in the body , restores normal levels
3 ) why have neurological symptoms applied this time , that were absent earlier , what could be the possible cause for this ?
ANS ) Due to Chronic alcoholism , excess thiamine deficiency gave rise to WERNICKE'S ENCEPHALOPATHY and symptoms like tremors, restlessness, delirium
Added to it , is excess toxins accumulation due to kidney damage
4 )what is the reason for giving thiamine in this patient ?
Ans ) we observe neurological symptoms indicative of wernicke's encephalopathy , characterised by biochemical lesions in the brain , due to exhaustion of biochemical reserves of vit b esp vit b 1 ( thiamine ) , caused by alcohol misuse
Therefore , we give thiamine to the patient
5) what is the probable reason for kidney injury in this patient ?
ANS ) 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 affect kidney function.
Chronic Alcoholics are more likely to have high blood pressure.
High blood pressure is a common cause of kidney disease.
6)what is the probable cause for normocytic anemia ?
ANS ) Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e, bone marrow and the metabolism of iron
Alcohol causes a affect on progenitor cells of blood causing decreased WBC and RBC
Alcohol decreases iron absorption from intestine.
the above are the causes for normocytic anemia in the patient
7) could chronic alcoholism might have aggravated the foot ulcer formation in the patient , if yes how and why ?
ANS ) Yes , chronic alcoholism has aggravated the foot ulcer formation in the patient
The patient is a known case of type 2 diabetes mellitus and chronic alcoholism since 12 yrs
This has increased the chances of ulcer formation within the patient ,
Excess alcohol is detrimental to wound healing
There is increased risk of wound infection due to body's decreased resistance to bacteria
case 3 :
link to patient details :
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
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 ) 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 in 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 localization to the problem :
There is a presence of an the infarct in the inferior cerebellar hemisphere of brain.
primary etiology :Ata
ATAXIA is a result of DAMAGE TO CEREBELLUM
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 ) ) Tab Vertin 8mg-
This is betahistine, which is an anti- vertigo medication
MOA- 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.
B)Tab Zofer 4mg-
This is ondanseteron( ANTIEMETIC )
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block emetic receptors even in the CTZ and solitary tract nucleus
INDICATION : Nausea, vomiting
C) Tab Ecosprin 75mg:
This is aspirin. It is an NSAID
MOA- 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.
D) Tab Atorvostatin 40mg-
This is a statin
MOA: It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis.
It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
E) Clopidogrel 75mg-
It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptors on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
.F) Thiamine-
It is vitamin B1
to prevent Wernicke"s encephalopathy that can lead to confusion, ataxia and opthalmoplegia
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) 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 and eventually lead to stroke
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic 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
heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subarachnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke
.However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
case 4 :
link to patient details :
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS ) EVOLUTION OF THE SYMPTOMOLOGY IN THE PATIENT :
8months back She complains that she could feel her own heartbeat since 5 days and it is more rapid since yesterday night
*Pain along her left upper limb associated with tingling and numbness-6 dayS
*Chestpain -since 5 days
*Difficulty in breathing- since 5 days
dyspnoea during palpitations (NYHA-CLASS-3)-since5 days
ANATOMICAL LOCALISATION OF THE PROBLEM :
Blood , kidney
PRIMARY ETIOLOGY :electrolyte imbalance
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Ans ) diuretics usage, Other risk factors :-
A) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo-corticoid excess, renal tubular acidosis, hypomagnesenemia
B) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
D) psuedohypokalemia: delayed sample analysis, significant leukocytosis
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS )
Earliest change :decreased T-wave amplitude, ST depression, T wave - and inversion or flat;
prolonged PR interval; presence of U waves
In Severe cases :ventricular fibrillation, rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
CASE 5 :
LINK TO PATIENT DETAILS:
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANS )
seizures after ischaemic strokes.: An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury
Seizures after haemorrhagic strokes are thought to be attributable to irritation due to hemosiderin Deposits caused by products of blood metabolism
Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
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 )
progression of simple partial seizures into generalized tonic clinic seizures night be the cause of unconsciousness.
CASE 6 :
LINK TO PATIENT DETAILS :
https://n1ikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
ANS ) Cerebral hemorrhage into the frontal lobe, due to unattended head injury one year ago could Have caused it.
2) ) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANS )lAlcohol abuse can make blood vessels non healable and also have narrowing effect which is the main reason for non healing haemorrhage which from frontal extended into parietal and temporal lobes.
case-7 :
link to patient details :
http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html
1 ) .Does the patient's history of road traffic accident have any role in his present condition?
Ans ) The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries.
Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition
2.What are warning signs of CVA?
ANS ) Weakness or numbness of the face, arm or leg, usually on one side of the body
Trouble speaking or understanding Problems with vision, such as dimness or loss of vision in one or both eyes , Dizziness or problems with balance or coordination
Problems with movement or walking, Fainting or seizure
Severe headaches with no known cause, especially if they happen suddenly
3.What is the drug rationale in CVA?
ANS ) Mannitol-
Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
Ecospirin:
For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot. Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins.
It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke
.Rt feed :
RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.
4. Does alcohol has any role in his attack?
ANS )
When the patient met with an accident there might be cranial damage which was unnoticed.
If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition
But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.
Therefore it cannot be evaluated without further details
5.Does his lipid profile has any role for his attack?
ANS) There is inverse relationship between serum HDL-C and stroke risk. When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.
case 8 :
link to patient details :
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
1)What is myelopathy hand ?
ans )
loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly ,occurring due to pyramidal track involvement
2) What is finger escape ?
ans ) Presence of weak finger adduction in cervical myelopathy is called - FINGER ESCAPE SIGN
3))What is Hoffman’s reflex?
ans )Reflectory reaction of muscles after electrical stimulation of type 1a sensory fibres in their innervation nerve
CASE 9:
LINK TO PATIENT DETAILS :
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
1) 1) What can be the cause of her condition ?
ANS ) cortical vein thrombosis
2) What are the risk factors for cortical vein thrombosis?
ANS ) 
3) )There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
ANS ) Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
ANS ) Anticoagulants are used for the prevention of harmful blood clots..
Clexane (enoxaparin) low molecular weight heparin binds and potentiates antithrombin three, a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.
CASE 10 :
Link to patient details :
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
1) .What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Preserved ejection fraction (HFPEF) - also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
Reduced ejection fraction (HFrEF) - also referred to as systolic heart failure HFPEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease
2) .Why haven't we done pericardiocenetis in this pateint?
ans) No , because the effusion was self healing.
3) .WHAT ARE THE RISK FACTORS FOR THE DEVELOPMENT OF CARDIAC FAILURE IN THIS PATIENT?
ans )
iRIsk factors for development of heart faliure in this pATIENT :
Alcohol 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.
worsening of pericardial effusion leading to cardiac tamponade.
4) WHAT COULD THE CAUSE OF HYPOTENSION IN THIS PATIENT ?
ANS ) secondary to tuberculosis ,or maybe due to thickened visceral peritoneum.
Case 11 :
)patient details:https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
1)What are the possible causes for heart failure in this patient?
ans ) metabolism syndrome would be the best possible diagnosis
2)what is the reason for anaemia in this case?
Ans )Alcoholism, chronic kidney disease
3).What is the reason for blebs and non healing ulcer in the legs of this patient?
ANS ) diabetes and alcoholism
4) What sequence of stages of diabetes has been noted in this patient?
ANS ) chronic alcoholism leading to diabetes has led patient into tripathy- neuropathy -retinopathy and nephropathy.
CASE 12:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient
4) What are the risk factors for atherosclerosis in this patient?
5) Why was the patient asked to get those APTT, INR tests for review?
Answers:
1st ans:
Hypertension- arteriosclerosis- arterial thrombosis .
ANATOMICAL localisation: Blood vessels.
Primary Etiology: hypertension.
2nd ans:
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
.TAB. Digoxin
mechanism:Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive lonotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,an enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3rd ans
cardiorenal syndrome type 4
4th ans)
Hypertension
5th ans: )
APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.
case 13 :
D)patient details:https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) What are the indications and contraindications for PCI?
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?
answers :
1st ans:
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 localisation - Cardiovascular system Etiology: The patient is both Hypertensive and diabetic, both these conditions can cause
Primary Etiology- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
2nd ans:
MOA: METOPROLOL is a cardioselective betablocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow. Indications: it is used to treat Angina, High blood pressure and to lower the risk of heart attacks.
3rd ans:
INDICATIONS:
cute 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. An artery with a diameter of <1.5 mm
4th ans:
Although PCI is generally a safe procedure, it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting.
Because of all these complications it is better to avoid PCI in patients who do not require it
case 14 :
patient details:
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Answers:
1st ans:
rupture of vulnerable plaque-coronary vessel occlusion- thrombosis-infraction.
Anatomical localisation: blood vessels.
Primary etiology: infraction leading to decrease is systolic function.
2ans)
1.TAB. ASPIRIN
mechanism: 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.
2. TAB ATORVAS
mechanism: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3. TAB CLOPIBB
mechanism: 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/Illa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
mechanism: Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
mechanism: 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.
3rd ans
the second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.
A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient.
Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse.
PCI is frequently reported to be overused and inappropriately recommended.
Behnke et al defined overuse as 'use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value'
.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care.
As a result, cost of healthcare increases and causes potential harm the patients.
case 15 :
F)patient details:https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
Questions:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
2. What is the rationale of using torsemide in this patient?
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Answers:
1st ans:
better cardiac output, Possible correction of hypotensive crisis .
2nd ans:
reduce retention of fluid in body tissues. abdominal distension
3rd ans:
treatment of UTI, if it was prophylactic then the treating physician is exploiting it and even can cause resistance in near future.
gastroenterology and pulmonology :
case 16 :
A)patient details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
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?
1st ans:)
Evolution of symptomatology
5 years back-1st episode of pain abdomen and vomitings
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung.
Primary etiology: Auto digestion of pancreas.
2nd ans:
compared to placebo(efficacy:0) efficacy of drugs used are good, I would use the same treatment approach if I were the treating physician.
case 17 :
)patient details:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
Questions:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
2) Name possible reasons why the patient has developed a state of hyperglycemia.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
4) What is the line of treatment in this patient?
Answers:
1st ans:
pleural effusion, pancreatic insult leading to pleural effusion.
2nd ans:
*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic B-cells
* elevated levels of catecholamines and cortisol
3rd ans:
LFT is 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.
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.
4th ans:
Plan of action and Treatment:
Investigations:
✓24 hour urinary protein
✓ Fasting and Post prandial Blood glucose
✓ HbA1c
✓ USG guided pleural tapping
Treatment:
• 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 18 :
C)patient details:https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Questions :-
1) what is the most probable diagnosis in this patient?
2) What was the cause of her death?
3) Does her NSAID abuse have something to do with her condition? How?
Answers:
1st ans:
ruptured liver abscess with fluid accumulation and internal hemorrhage
2nd ans:
complications to surgery, hypotension, cardiopulmonary arrest, only if the description and case taking was clear, there would have been a definitive way to diagnose.
3rd ans:
NSAID abuse could have possible liver and kidney injury causing wide spectrum of problems within the body.
nephrology and urology
A)patient details:https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Questions:
1. What could be the reason for his SOB ?
2. Why does he have intermittent episodes of drowsiness ?
3. Why did he complaint of fleshy mass like passage in his urine?
4. What are the complications of TURP that he may have had?
ANSWERS:
1st ans:
use of diuretics leading to acidosis could cause sob.
2Nd ans hyponatremia
3rd ans:
large amount of pus cells could have been interpreted as fleshy mass.
4th ans:
difficulty in micturition,Infection and electrolyte imbalance.
CASE 20 :
B)patient details :https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
Questions:
1.Why is the child excessively hyperactive without much of social etiquettes ?
2. Why doesn't the child have the excessive urge of urination at night time ?
3. How would you want to manage the patient to relieve him of his symptoms?
Answers:
1st ans:
why not we blame the innocence of childhood and merry ways children being active which seems to be mischievous to is and hyper active!
2nd ans:
seems to a psychological feeling patient has developed to urinate over and over then awake.
3rd ans:
proper counsellling and therapy without destroying the patients activeness has to be done.
case 21 : Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology).
atient details:https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Answers:
1st ans:
difficulty in swallowing, barium swallow, endoscopic findings.
2nd ans:
in view of the patient condition patient is likely to develop immune reconstitution inflammatory syndrome. IRIS prevention can be effectively done by initiation of ART before development of advanced immunosuppression.
infectious disease and hepatology :
CASE 22
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
uestions:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
3. Is liver abscess more common in right lobe ?
4.What are the indications for ultrasound guided aspiration of liver abscess ?
Answers:
1st ans:
possible, can be due to contaminated toddy.
2nd ans:
according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3rd ans:
yes right lobe involvEment due to highblood flow.
4th ansI:ndications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs
CASE 23
)patient details:https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:
1) Cause of liver abScess in this patient ?
2) How do you approach this patient ?
3) Why do we treat here ; both amoebic and pyogenic liver abScess?
4) Is there a way to confirm the definitive diagnosis of this patient?
1 st ans:
poor personal hygiene, malnutrition, eating contaminated food and drinking contaminated water .
2nd ans:
as the patient is responding with liquefaction of mass there seems to me no more narrowing so patient is treated for both bacterial and amoebic causes.
3rd ans:
Since there is no definitive way of knowing without risking patient's health ,we cannot take risk , we should treat for both.
4th ans:
abscess aspiration can give a defInitive diagnosis.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology).
A)patient details:http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions :
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
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?
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Answers:
1st ans: Fever since 10 days
Facial puffiness and periorbital edema since 4 days
Weakness of right upper limb and lower limb since 4 days
Altered sensorium since 2 days
ANATOMICAL localisation: periorbital region.
Primary etiology: mucormycosis.
2nd ans:
Compared to placebo the efficacy of the drugs used is good. Amphotericin B is the drug of choice in the patient, IF I was a physician I would have given the same .
3rd ans:
unnecessary prophylatic steroid usage, unhygienic masks, sedentary life style leading to metabolic syndrome leading to easy susceptability to infections.
infectious disease : COVID 19
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension
Answers:
https://kimselogs.blogspot.com/2021/05/covid-19.html?m=1
10) Medical Education:
this is my experience of learning the subject general medicine in the month of may during my stay at home
though we as students were apprehensive initially , if we would fall behind in experiential and clinical learning due to lockdown, thanks to Rakesh Biswas sir , for showing great enthusiasm in keeping us updated about the cases day to day
in the first week of may :
i went through the elogs daily
studied in detail about the pharmacological therapy and treatment being given to covid patients
made myself enlightened with various drugs and their mechanism of action ,
read about heart stroke and viral pneumonia in detail
attended the case discussions between 2-4 , 4 days a week
WEEK 2 :
i went through the cases in the e log
i read about wernickes encephalopathy and alcohol misuses and its effects in detail
i tried to learn to analyse chest x rays from the images available on the log group and with online sources
i read about brochiectasis in detail
attended 2-4 sessions
WEEK 3 :
I have tried to learn analyse a ct scan and ecg though not fully succes ful yet
from the sources available , i learnt basic normal range values of various biochemical parameters
improved my understanding about myocardial infarction, cerebro vascular stroke through seeing patients reports and images and videos
WEEK 4 :
read about the various effects of steriods on covid patients, remedesvir action, and about d glucose
studied about asthma and copd
studied and observed a case of mucormycosis
rea about renal failure and its clinical presentation, pathology
complications of diabetes
i would like to pace up more and learn more things through online e log and submit my elog soon.
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