General medicine assignment


 I Pranay kumar, roll no.32 of 8th semester 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 :


PULMONOLOGY


https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

1) What is the evolution of the symptomatology in this patient interms 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 :- Evolution of symptomatology

     • 1st episode of sob - 20 yrs back

     • 2nd episode of sob - 12 yrs back

Then onwards, she has been having yearly episodes of sob for the past 12 yrs.

》Diagnosed with diabetes - 8yrs back

》Anemia and  took iron injections  - 5yr ago

》Generalised weakness  - 1 month back 

》Diagnosed with hypertension(HTN) - 20 days back

》Pedal edema - 15 days back

》Facial puffiness- 15 yrs back

~ Anatomical location of problem - Lungs

~ Primary etiology of patient- usage of chulha for prolonged period  (20 yrs)


2) What are the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions  used for this patient?

Ans :- Head end elevation : MOA;

  • Improves oxygenation 

  • Decreases the incidence of VAP

  • Increases hemodynamic performance 

  • Increases end expiratory lung volume

  • Decreases incidence of aspiration 

》Indication: head injury

 meningitis 

 pneumonia 

•oxygen inhalation to maintain spo2

•Bipap : Non invasive method (bipap is bilevel positive airway pressure)

》MOA : Assist ventilation  by delivering positive expiratory and inspiratory pressure with out the need for ET incubation.


3) Cause for current acute excerbation 

Ans :- It could be any infection.


4) Could the ATT affected her symptoms if so how?

Ans : Yes! ATT (Anti tubercular treatment) affected her symptoms. 

Isoniazid and rifampicin are nephrotoxic drugs. Urea and creatinine levels( RFT) are elevated.


NEUROLOGY


 CASE A

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.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:  Evolution of symptomatology 

    Irrelevant talking and laughing - since 9 days

    Decreased food intake - since 9 days 

    short term memory loss - since 9 days

The above symptoms may occur due thiamine deficiency...Thiamine deficiency occurs either due to..

1) Decreased absorption from intestine ( Hereditary condition)

2) Inadequate nutrition etc..

 He had developed seizures following stoppage of alcohol intake for 24hours which is due to this reason:- Alcohol affects the way in which nerve cells communicate. receptors are some specialized proteins on the surface of nerve cells which receive chemical signals from one another. Due to long-term alcohol intake, receptors affected by alcohol undergo adaptive changes to maintain normal function.

The two important brain communication systems affected by alcohol involve the neurotransmitters: gamma-aminobutyric acid and glutamate.

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 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.


2) What are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?

Ans: I) Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency

ii)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)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.


3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?

Ans : Excess thiamine deficiency and excess toxins accumulation which occcured due to renal disease caused by excess alcohol addiction.


4) What is the reason for giving thiamine in this patient?

Ans : Chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,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. 


 5) What is the probable cause for kidney injury in this patient?

Ans: 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.


6) What is the probable cause for the normocytic anaemia?

Ans : 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 ?

Ans : 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 - B

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 localisation for the problem and what is the primary etiology of the patient's problem?

Ans : 7 days back : Giddiness associated with one     episode of vomiting

Then asymptomatic for 3 days he consumed a small amount of alcohol 

Then he developed : giddiness associated with aural fullness ,bilateral hearing loss,tinnitus,2 to 3 episodes of vomiting's

DENOVO hypertension

LOCALISATION OF LESION: Presence of Infract in the Inferior Cerebellar hemisphere of the Brain

PRIMARY ETIOLOGY: Ataxia is the loss of muscle control or coordination of Voluntary movements such as, Walking or Picking up of objects.

In this case, Patient is a known case of denovo hypertension. For this he has not taken medication.

Stroke is due to infract can be caused by blockage or bleeding in the brain, due to which brain is deprevied of Nutrients and Oxygen. This may lead to infract formation.


 2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient

A) VERTIN TAB: It is an anti histamine, as the patient is suffering from bi-lateral hearing loss, aural-fullness, tinnitus (Simulating meinieres disease)

It acts as a agonist on H1 receptors

B) ZOFER: Ondensetron to treat nausea and vomiting

    ▪ acts antagonist of 5H3 receptors on vagal afferents in gut and even block receptors in  CTZ and solitary tractus nucleus

C) Tab ECOSPRIN : aspirin  it is anti platelet reduces the platelet adhesiveness and aggregation and there by preventing clot formation

D) Tab ATORVOSTATIN:  acts as a HMG Co A  reductase inhibitor rate limiting step in cholesterol biosynthesis thus decreasing blood LDL and VLDL   so, used for primary prevention of stroke

E) CLOPIDOGREL: it is antiplatelet drug thereby preventing clot formation

F)THIAMINE: as the patient is alcoholic there may be chance of Wernickes encephalopathy

 so, to prevent it thiamine is given

G) Tab : MVT : it is methylcobalamine given in case of vitamin B12 deficiency


3) Did the patient's history of denovo hypertension contribute to this current condition?

Ans : Cerebellar infract is usually caused by blood clot obstructing blood flow to Cerebellum.

High blood pressure is a risk factor for the formation of Cerebellar infracts.

Increased shear stress caused on blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelal dis-function in this case. Hign BP can also promote cerebral small vessel disease. All these factors contribute to the stroke.


4) Does the patient's history if Alcoholism make him more susceptible to Ischaemic or Haemorrhagic stroke?

Ans : Light to Moderate consumption of Alcohol lower's the risk of Ischaemic stroke but it had no impact on the risk of developing Haemorrhagic stroke.

Alcohol consumption lowers the level of fibrinogen, a protein helps in formation of clot. So, there by decreases chance if Ischaemic stroke.

However heavy alcohol consumption increases the chance of Haemorrhagic stroke.

Heavy drinker's have 1.6 times more chance of intra cerebral Haemorrhage and 1.8 times increased chance subaracnoid Haemorrhage.

However heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP & Heart rate. So, in this case, history of alcoholism coupled with his hyper-tension could be a cause of stroke.


CASE - C

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?

A) *Evolution of symptoms :patient was normal 8 months back then developed b/l pedal edema which gradually progressed.

Aggerevated in sitting and standing position, relived on taking medication

Palpitations :since 5days, sudden in onset which is more during night

Aggravated by lifting heavy weights, speaking continuously

Dyspnoea during palpitations (NYHA-3) since 5 days

pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.

Chest pain associated with chest heaviness since 5 days

Palpitations





Dysnoea



Chest pain

Radiating pain along her left upper limb


Etiological agent :
*By localization, electrolyte imbalance (hypokalemia) causing the her   manifestations like palpitations, chest heaviness, generalised body weak   ness
*radiating pain along her left upper limb due to cervical spondylosis 

2Q) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia? 

A) Reason: recurrent hypokalemic periodic paralysis 
Current risk factor:due to use of diuretics
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?
A) changes seen in ECG : 
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves 
In Severe cases :ventricular fibrillation, rarely AV block 


Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium. 



CASE - D


1Q)Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

Ans : Occurrence of seizure due to brain stroke
Cells in the brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.
A seizure can affect you in many different ways such as changes to vision, smell and taste, loss of consciousness and jerking movements.

Mechanism of seizure activity
You’re more likely to have a seizure if you had a haemorrhagic stroke (bleed on the brain). Seizures can also be more likely if you had a severe stroke, or a stroke in the cerebral cortex, the large outer layer of the brain where vital functions like movement, thinking, vision and emotion take place.
Some people will have repeated seizures, and be diagnosed with epilepsy. The chances of this happening may depend on where the stroke happens in the brain and the size of the stroke. 

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. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.

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 :Normally the “consciousness system”—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 - E


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:- Liver damage due to too much alcohol can stop the liver from synthesis of coagulants. Some of the epidemiological studies show that there is increased risk for intracranial bleeding in alcoholics. 


CASE - F


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.


CASE - G

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

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:-  Hoffmann’s 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 - H


 1)What can be the cause of her condition?                            
  Ans:- According to MRI, Cortical Vein Thrombosis might be the cause of her seizures.

 2) What are the risk factors for cortical vein thrombosis?

Ans:-

Infections: Meningitis, otitis, mastoiditis.

Prothrombotic states: Pregnancy, puerperium, antithrombin deficiency proteinic and protein s deficiency, Hormone replacement therapy.

Mechanical: Head trauma, lumbar puncture.

Inflammatory: SLE, sarcoidosis, Inflammatory bowel disease, Malignancy, Dehydration, Nephrotic syndrome.

Drugs: Oral contraceptives, steroids, Inhibitors of angiogenesis.

Chemotherapy: Cyclosporine and l asparaginase.

Hematological: Myeloproliferative Malignancies, Primary and Secondary polycythemia.

Intracranial: Dural fistula

Vasculitis: Bechet’s disease, Wegener’s granulomatosis.

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.


CARDIOLOGY



CASE - A




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 maintaining 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 in turn reduces the pulmonary venous return. This causes decrease in the end diastolic volume and finally reduced cardiac output.


CASE - B


1)What are the possible causes for heart failure in this patient?

Ans:- Chronic hypertension can be the cause of heart failure in this patient.

2)What is the reason for anemia in this case?

Ans:- Anemia is considered to be frequent comorbidity of heart failure.

3)What is the reason for blebs and non-healing ulcer in the legs of this patient?

Ans:- The cause for nonhealing ulcer is diabetes (hyperglycemia impairs the healing process)

 4)What sequence of stages of diabetes has been noted in this patient?

Ans:- Diabetes leading to macrovascular complication in the form of foot ulcer.


CASE - C



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 presented with short ness of breath which progressed from grade 2 to grade 4. Patient also complained of oliguria since two days and anuria since morning.

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:-

1.DOBUTAMINE 

Mechanism of action: It is an inotropic drug.

Indications: cardiogenic shock, severe congestive cardiac failure, hypoperfusion if associated with increased peripheral vascular resistance.

Efficacy:  https://www.uptodate.com/contents/inotropic-agents-in-heart-failure-with-reduced-ejection-fraction

2.UNFRACTIONED HEPARIN 

Mechanism of action: it inactivates thrombin and factor X through an antithrombin dependent mechanism. 

Indications: Atrial fibrillation with embolization, treatment of acute and chronic consumptive coagulopathies like DIC, prophylaxis and treatment of venous thromboembolism, prevention of clotting in arterial and cardiac surgery. 

Efficacy 

3.CARVEDILOL 

Mechanism of action: it is a non-selective adrenergic blocker.

Indication: heart failure with reduced ejection fraction, hypertension, left ventricular dysfunction following MI.

Efficacy 

4.ACETYLE CYSTEIN 

Mechanism of action: It increases the synthesis of glutathione in liver, glutathione acts as an antioxidant.

Indication: It is used in paracetamol overdosing, to relive chest congestion due to thickened mucous in cystic fibrosis, asthma, bronchitis.

Efficacy 


3)What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?

Ans:- 


In this patient Type 4 is seen.


4) What are the risk factors for atherosclerosis in this patient?

Ans:- Risk factors are Abnormal lipid profile, DM, Hypertension, High saturated fats in diet, Obesity.

5) 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 - D



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 SYMTOMATOLOGY

》Diabetes for 12 years

》Heart burn like episodes for 1 year but it relieved 

》Pulmonary TB 7 months back - treatment took now she is sputum negative. 

》Hypertension for 6 months - on medications

》Day of admission to hospital:- SOB since half an hour  

•ANATOMICAL LOCATION OF PROBLEM: Cardiovascular system

•PRIMARY ETIOLOGY:- Atherosclerosis - Plague formation [hypertension + 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:-   

~TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient.

▪︎Mechanism of action:- METOPROLOL is a cardio selective beta blocker. 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.

Efficacy studies:-  Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients. 

Outcome:-  Mean baseline BP was 132/78 +/- 9/9 mmHg. Following 4 weeks of treatment, mean changes in sitting BP were: placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9 mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg. Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.

 Non-pharmacological intervention:

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).

3) What are the indications and contraindications for PCI?

Ans:-

Indications:

>Acute ST Elevation MI

>Acute non-ST elevation acute coronary syndrome

>Angina equivalent

>Stable and unstable angina

>Critical coronary artery stenosis

Absolute contraindications:-

~Noncompliance with the procedure and inability to take the dual antiplatelet therapy.

~Multiple percutaneous interventions re stenosis

~High bleeding risk

Relative contraindications:-

• 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 over testing and overtreatment important to current healthcare systems?

Ans:- Although PCI is generally a safe procedure, it might cause serious certain complications like:

▪︎ Bleeding 
▪︎ Blood vessel damage
▪︎ Allergic reaction to the contrast dye used
▪︎ Arrhythmias
▪︎ 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 - E

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.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 : - EVOLUTION OF SYMTOMATOLOGY:

• Diabetic since 8 years
• Hypertension since 8 years
• First dose of COVISHIELD vaccine 5 days back before admission to hospital
• Chest pain in right side of chest
• Giddiness and profuse sweating on day of the admission

》ANATOMICAL LOCATION: Cardiovascular system

》PRIMARY ETIOLOGY: As she is diabetic for 8 years that might cause atherosclerosis due to accumulation of fatty and fibrinous material in the walls

 
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:-  Pharmacological interventions:

a) tab. ASPIRIN 325 mg 

Mechanism of action: inhibits platelet aggregation by interfering with thromboxane in platelets caused by COX 1 inhibition.

Indications: To reduce the cardiovascular deaths in suspected case of MI

Efficacy: Low dose aspirin each day for atleast10 years lower the risk of cvd by 10% and odds ratio from 0.85 to 0.90

b) tab. ATORVASTATIN 80 mg

Mechanism of action: Competitive inhibitor of enzyme HMG CO A reductase

Indication: To prevent CV events in patients who are at risk used as preventive agent 

Efficacy: studies shown that it decreases LDL cholesterol concentration by61% and triglycerides by 46%

c) tab. Clopidogrel 300 mg 

Mechanism of action: Inhibitor of platelet aggregation by binding one of the ADP receptors on platelets

Indications: ACS recent MI, recent stroke, peripheral arterial disease.

Placebo has no pharmacological and physiological actions.


3)Did the secondary PTCA do any good to the patient or was it unnecessary?

Ans:- Yes it is good to patient, stent was placed and the patient is doing good.



CASE - F




1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

Ans : 
           As i.v fluids are administered in order to increase the ability of heart to pump blood,it might have relieved the hypotension there by relieving the symptoms


2. What is the rationale of using torsemide in this patient?

Ans : Torsemide is used to treat abdominal                            distension.

3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

ANS : 
            As the patient has dribbling of urine with oliguria and a previous history of TURP they might have suspected UTI and empirically ceftriaxone was given.


GASTROENTEROLOGY 


CASE - A


https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-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:- COURSE OF THE SYMPTOMS-

• Pain abdomen and vomiting was treated conservatively 5yrs ago.

• Pain abdomen and vomiting for 1 week.

• Constipation, burning micturition, fever for 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 no physiological and pharmacological actions.

• DRUG THERAPY:-

Amikacin, Metronidazole and Meropenem 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 in order 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 supplementation is necessary.

• Inj. TRAMADOL -

It is an opioid analgesic which is given to relieve pain.



CASE - B


https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html



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 pseudocyst 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 pancreatic beta cells secondary to pancreatitis. 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 also 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 - C


https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html



1) What is the most probable diagnosis in this patient?


Ans:- The patient is suffering from ruptured liver abscess which led to intraperitoneal hematoma. Patient also has intraparenchymal renal disease.

 2) What was the cause of her death?

Ans:- Cause of her death can be as a complication of surgery in the form of pneumonia(As symptom just before the death are cough and sob) as many people who undergo surgery already have weakened immune system and they are prone to get infections.

 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 - A


https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html



1. What could be the reason for his SOB?

Ans:-  Reason for his sob can be POST TURP SYNDROME: it occurs because of irrigation of absorption of large volumes of irrigation fluid during TURP which can cause HYPONATREMIA, CARDIORESPIRATORY depression.

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 fleshy 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 fluids.

~Hypothermia.




CASE - B


https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html



1)Why is the child excessively hyperactive without much of social etiquettes? 

Ans:- The symptoms of the child point the diagnosis towards ADHD (attention deficit hyperactivity disorder).

2)Why doesn't the child have the excessive urge of urination at nighttime? 

Ans:- As the child do not have bedwetting nor waking up at night to pass urine it can be a case of receptor over activity effected by gravity(neurogenic overactivity bladder) or pollakiuria(idiopathic frequent urination)it can also be psychosomatic as his mother completely restricted him from using smartphone since 4 months before which he is addicted to ,so the child sleeps normally at night.

3)How would you want to manage the patient to relieve him of his symptoms? 

Ans:- First look if any pathology is present in the genitourinary system, then try with the help of psychiatrist find whether it is ADHD or not, if yes do cognitive behaviour therapy.



INFECTIOUS DISEASES ( HI VIRUS, MYCOBACTERIA)



CASE - A


https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html



1)Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

Ans:- Clinical history and physical findings:

> Cough since 2 months on taking food and liquids 

> Difficulty in swallowing since 2 month

> H/O weight loss of 10 Kgs since 2 months, hoarseness of voice

> Incapable of food intake

> Oro pharyngeal regurgitation

2)What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

Ans:- A retrospective analysis examining all forms of IRIS, 33/132 (25%) of patients exhibited one or more disease episodes after initiation of ART. Other cohort analyses examining all manifestations of IRIS estimate that 17–23% of patients initiating ART will develop the syndrome.

INTERVENTION: The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. 




INFECTIOUS DISEASES AND HEPATOLOGY


CASE - A


https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html



1)Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it? What could be the cause in this patient?

Ans:- yes, it could be due to intake of contaminated toddy.

2)What is the etiopathogenesis of liver abscess in a chronic alcoholic patient? (since 30 years - 1 bottle per day)

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.

3)Is liver abscess more common in right lobe?

Ans:- Yes right lobe is involved due to its more blood supply   

4)What are the indications for ultrasound guided aspiration of liver abscess?

Ans:- Indications for USG guided aspiration of liver abscess:

▪︎ Amoebic liver abscess

▪︎ Large abscess more than 6 cms.

▪︎ Left lobe abscess

▪︎ Caudate lobe abscess

▪︎ Abscess which is not responding to drugs

▪︎ seronegative abscess


CASE - B


https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

1)Cause of liver abscess in this patient?

Ans:- Cause may be due to Entamoeba histolytica. the pyogenic abscesses are usually polymicrobial, most seen organisms are E. coli, Klebsiella, streptococcus, staphylococcus, anaerobes.

2)How do you approach this patient?

Ans:- I will approach in the same as given in blog but if abscess rupture emergency laparotomy is to be done.

3)Why do we treat here: both amoebic and pyogenic liver abscess? 

Ans:- Though the probable diagnosis is amoebic liver abscess it’s better to give antibiotics to be safe side.



4)Is there a way to confirm the definitive diagnosis in this patient?

Ans:- USG can be done to see the  site of the abscess. USG guided aspiration can be done to confirm diagnosis, but there is risk of perforation.



INFECTIOUS DISEASES ( MUCORMYCOSIS, OPHTHALMOLOGY, OTORHINOLARYNGOLOGY)


CASE - A

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.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:-  COURSE OF THE SYMPTOMS:

》18 April: post vaccination fever with chills and rigor.

》28 April: facial puffiness, generalized weakness and periorbital edema.

》04 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 drugs. Used instead of 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.

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