Medicine blended assignment

 

I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.

This is the link to the questions asked regarding the cases:


http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1


Below are my answers to the Medicine Assignment based on my comprehension of the cases. 


Question number.1: PULMONOLOGY 

A)Link to patient details :

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

Questions:

i)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?

Answer: 

•Evolution of Symptomatology:

Pt had shortness of breath for past 20 years .

20 years ago - pt had her 1st episode which lasted for a week-grade II SOB-relieved on taking medication 

For next 8 years she had an episode every year (around the same time i.e,January)-gradeII SOB-relieved on taking medication      

12 years back -pt had a severe episode which lasted for about 20 days -grade II SOB -pt was hospitalised and SOB relieved on taking medication. (From then she’s having yearly episodes which last for about a month,which is again in January)-grade II SOB-relieved on taking medication

30 days back-her latest episode of SOB has started 

  ( SOB is insidious in onset and gradually    progressive.Initially-SOB occurred only on exertion and relieved my taking rest )

Pedal edema since 15 days 

Facial puffiness since 15 days 

From 2 days -she started having SOB at rest -grade IV-not relieved on medication .

From 2days- drowsiness 

From 2days -decreased urine output

   

Anatomical localization of problem: 

   Is in LUNGS(bronchi and bronchioles)

•  Primary Etiology of patient’s problem : 

Since she’s a farmer and she’s been having these episodes while working in paddy fields the etiological factor could be OCCUPATIONAL EXPOSURE to rice dust which is more common in Agricultural workers.

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

Answer:


Pharmological and non pharmacological interventions used in this patient ,their mechanism of action ,indication and efficacy over placebo are as follows:

 Head end elevation Bed head elevation was defined as the angle of the head of the bed and was expressed in degrees of elevation above horizontal.

Mechanism of action :

Increases oxygenation ,has also been shown hemodynamic performance. 

and associated with a decreased incidence of aspiration and ventilator-associated pneumonia (VAP)

Indication:

        Head injury ,

        Ventilator assosciated pneumonia ,

        Meningitis

oxygen inhalation:

 Why is it done?

              Long-term oxygen therapy is used for COPD if you have low levels of oxygen in your blood (hypoxia). It is used mostly to slow or prevent right-sided heart failure. It can help you live longer.

Oxygen may be given in a hospital if you have a rapid, sometimes sudden, increased shortness of breath (COPD exacerbation). Oxygen can also be used at home if the oxygen level in your blood is too low for long periods.

Long-term oxygen therapy should be used for at least 15 hours a day with as few interruptions as possible. Regular use can reduce the risk of death from low oxygen levels.

To get the most benefit from oxygen, you use it 24 hours a day. 

Oxygen therapy has good short-term and long-term effects in people who have COPD.

Using oxygen may also improve confusion and memory problems. It may improve impaired kidney function caused by low oxygen levels.


Indications:


Chronic conditions:

A common use of supplementary oxygen is in people with chronic obstructive pulmonary disease (COPD), the occurrence of chronic bronchitis or emphysema, a common long-term effect of smoking, who may require additional oxygen to breathe either during a temporary worsening of their condition, or throughout the day and night.

Oxygen is often prescribed for people with breathlessness, in the setting of end-stage cardiac or respiratory failure, advanced cancer or neurodegenerative disease, despite having relatively normal blood oxygen levels. 


Acute conditions:

Oxygen is widely used in emergency medicine, both in hospital and by emergency medical services or those giving advanced first aid.

Intermitteny BiPAP :

    BiPAP stands for bi-level positive airway pressure. It is one type of PAP, or positive airway pressure machine, that is used to maintain a consistent breathing pattern at night or during symptom flare-ups in people with COPD.

     The machine pressurizes the air to a higher level than the air in the room, and so it helps a person to take in oxygen and exhale carbon dioxide. This helps them to breathe more easily, either while sleeping or when experiencing a flare-up of symptoms.

Inj.Augumentin:

Amoxicillin/clavulanic acid is a combination penicillin-type antibiotic used to treat a wide variety of bacterial infections. It works by stopping the growth of bacteria.

binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis.  

Indications:

        Amoxicillin/clavulanic acid is a combination penicillin-type antibiotic used to treat a wide variety of bacterial infections.


Azithromycin:

Mechanism of action :

Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit .This results in the control of various bacterial infections        


https://www.pediatriconcall.com/drugs/azithromycin/300


Indications:  

  • Community-acquired Pneumonia. 
  • Pharyngitis or Tonsillitis. 
  • Uncomplicated skin/skin structure. 
  • Acute bacterial exacerbations of chronic obstructive pulmonary disease. 
  • Acute bacterial sinusitis. 
  • Genital Ulcer Disease (Chancroid) 
  • Nongonococcal or Gonococcal Urethritis and Cervicitis.
  • Pelvic Inflammatory Disease



Inj Lasix

(Furosemide)

 MOA: works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine 

Indications:

 LASIX is indicated in adults and pediatric patients for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome


Tab .Pantop :

     The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazolecovalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. 

Indications: 

  • Gastro-esophageal reflux disease (GERD)
  • Esophageal gastric varices bleeding prophylaxis, erosive esophagitis.
  • Acid peptic disease.
  • Helicobacter pylori eradication.


Inj.Hydrocortisone:

MOA: Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.


https://go.drugbank.com/drugs/DB00741


Indications:

  • Collagen diseases. Systemic lupus erythematosus.
  • Dermatological diseases. Severe erythema multiforme (Stevens-Johnson syndrome)
  • Allergic states.
  • Gastro-intestinal diseases.
  • Respiratory diseases.


Neb Ipravet:

MOA: Ipratropium acts as an antagonist of the muscarinic acetylcholine receptor.This effect produces the inhibition of the parasympathetic nervous system in the airways and hence, inhibit their function. The function of the parasympathetic system in the airway is to generate bronchial secretions and constriction and hence, the inhibition of this action can lead to bronchodilation and fewer secretions.


https://go.drugbank.com/drugs/DB00332


Indications:

 Ipravent is used to relieve the symptomsof lung disease such as asthma or chronic obstructive bronchitis. It may be used in other conditions where breathing is difficult, such as after surgery or during assisted ventilation.

•Neb .Budecort:

MOA: 

Budesonide is a potent topical anti-inflammatory agent. It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT). This budesonide-CBP (HAT) receptor complex prevents the production of inflammatory genes (inhibition of gene transcription) that might cause bronchoconstriction. Also, the budesonide-receptor complex activates the HDCA2 increasing the gene expression, which results in the reduction of formation of the cytokines such as ILs and TNF.

It also inhibits the activation of the eosinophils by increasing apoptosis and suppresses the activation of the inflammatory cells such as mast cells, neutrophils, T-lymphocytes, macrophages, and dendritic cells. The result of the overall inhibition of ILs and TNF leads to reduced airway inflammation and hyperreactivity, causing inhibition of the bronchospasm, wheezing, and coughing. 


https://www.ncbi.nlm.nih.gov/books/NBK563201/


Indications:

  • Bronchial asthma.
  • Bronchopulmonary dysplasia.
  • Croup.
  • Allergic rhinitis.

Tab pulmoclear:

    Pulmoclear Tablet is a combination of two medicines that helps the airways in your lungs stay open. It works by relaxing the muscles of these airways. This makes it easier for air to get in and out. This medicine also loosens thick mucus, making it easier to cough out.


Inj.Thiamine :

 Mechanism of ActionThiaminecombines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.


https://m.pdr.net/Mobile/Pages/drug-summary/Thiamine-thiamine-hydrochloride-2546


  INDICATIONS AND USAGE:

Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, as in Wernicke's encephalopathy, infantile beriberi with acute collapse, cardiovascular disease due to thiaminedeficiency, or neuritis of pregnancy if vomiting is severe.


(iii) What could be the causes for her current acute exacerbation?
Answer
    Does hypertension has any association with this acute exacerbation?


(iv) Could the ATT have affected her symptoms? If so how?
 Answer:
Since Rifampicin and Isoniazid are nephrotoxic and they can cause AKI (acute kidney injury) and it is possible for ATT to affect her symptoms in this case as we can see increased RFT.
    

(v)  What could be the causes for her electrolyte imbalance?
Answer:
    It may be due to inadequate absorption in kidneys that might have occurred due to ATT use resulting in AKI 

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Question .number :2 : NEUROLOGY
 
Link to patient details:

Questions:
(i) 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?

Answer:



Evolution of symptomatology:


•one year ago: 2-3 episodes of seizures (mostly due to alcohol) 

•4months ago: another seizure episode (most probably GTCS)

•9days back: started Sudden talking and laughing to himself 

(Disability in lifting himself off the bed move around is seen.Later, short-term memory loss associated with not being able to recognize family members from time to time was observed.)


Anatomical localization :

Thalamus and hypothalamus.


Primary etiology :


Wernicke's encephalopathy is a degenerative brain disorder caused by the lack of thiamine (vitamin B1). It may result from alcohol abuse, dietary deficiencies, prolonged vomiting, eating disorders, or the effects of chemotherapy. B1 deficiency causes damage to the brain's thalamus and hypothalamus.


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.



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

Answer:


 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.



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

Answer: Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.


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

Answer: 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. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5354137/

(v) What is the probable reason for kidney injury in this patient? 

Answer: 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.

(vi) What is the probable cause for the normocytic anemia?

Answer: 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 .

(vii) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Answer:


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.


__________________________________________


B)Link to patient details:

(i)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?
Answer: Timeline of the patient is as follows-

•7 days back- Patient had giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting

•4 days back- Patient consumed alcohol; He developed giddiness( that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.)

H/O postural instability- falls while walking

Associated with bilateral hearing loss, aural fullness, presence of tinnitus

Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles

Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day


Anatomical localization of the problem :

 There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.


Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)

Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.

In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.




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

Answer: 
A)     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- It is an anti emetic

MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.

Indications- Used to control the episodes of vomiting and nausea in this patient.

 

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.

Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.

E)      Clopidogrel 75mg- It is an antiplatelet medication

MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.

Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting

F)      Thiamine- It is vitamin B1

It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.

Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.

G)     Tab MVT- This is methylcobalamin

Mainly given in this case for vitamin B12 deficiency.



(iii)Did the patients history of denovo HTN contribute to his current condition?
Answer:


A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts. 

Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke. 


(iv)Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Answer:


•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


• risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate. 

•In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition. 


_____________________________________


C) Link to patient details:


(i)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?
Answer:


10 years back-Paralysis of both upper and lower limbs bilateral

1 year back-Right and left paresis due to hypokalemia

8 months backSwelling over legs 

7 months back - blood infection 

2 months back- neck pain

6 days back- pain along left upper limb

5 days back- chest pain, Difficulty in breathing and was able to feel her own heart beat


Anatomical localization: Cervical spine

Intervertebral discs of cervical vertebrae .



(ii)What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

Answer:


Reasons for recurrence of hypokalemia in this patient is :

    Due to Diuretics administration 



Other risk factors 


Female 

Heart failure

Hypertension

Low BMI

Eating disorder and alcoholism: low intake of potassium

Diarrhea, cushing syndrome


(iii)What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Answer:


ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression in more severe hypokalemia.


_____________________________________



D) Link to patient details:





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

Answer: Yes,there is relationship between occurance of. Seizure Due to brain stroke ,there will be change in the electric impulse transmission in the brain..so this cuases the seizures.

Pathogenesis:

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 hypoperfusion, and hyperperfusion 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.


(ii)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?


Answer: It is may be due any scar formation or any hemorrhages which shows more severity in the symptoms.so, there is loss of consciousness in the recent attack


_____________________________________


E) Link to patient details:




(i)What could have been the reason for this patient to develop ataxia in the past 1 year?
Answer:


the reason for patient to develop ataxia in past one year is ALCOHOL

The toxic effects of alcohol are diverse. Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia(ALCOHOL INDUCED TOXIC ATAXIA). 

 The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death


(ii)What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Answer:


  • Reason  for IC bleed could be because of Chronic ALCOHOL CONSUMPTION  resulting in ALCOHOL INDUCED Toxic ataxia .Beacuse of which patient is having Repeated falls leading to IC BLEEDING

  • The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.


_____________________________________


F) Link to patient details:





(i)Does the patient's  history of road traffic accident have any role in his present condition?
Answer:
No, patient’s h/o RTA has no role in his condition .
It could be due to alcohol consumption and his emotionally disturbed status .


(ii)What are warning signs of CVA?

Answer:

  • Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
  • Sudden confusion, trouble speaking, or difficulty understanding speech.
  • Sudden trouble seeing in one or both eyes.
  • Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
  • Sudden severe headache with no known cause.
(iii)What is the drug rationale in CVA?
Answer: 

Alteplase, an intravenously administered form of recombinant tissue plasminogen activator (rt-PA), remains the only US FDA-approved thrombolytic treatment for acute ischemic stroke within 3 h of symptom onset.

Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema,lowers intra cranial pressure.


Ecospirin :

Inhibits cyclooxygenase irreversibly and prevents formation of thromboxane A2 ,Since thromboxane A2 is responsible for platelet aggregation .Using ecospirin will inhibit platelet aggregation .


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. 

(iv)Does alcohol has any role in his attack?
Answer: 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

(v)Does his lipid profile has any role for his attack??

Answer: The 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.


__________________________________________



G) Link to patient details:






(i)What is myelopathy hand ?
Answer:


There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 


(ii)What is finger escape ?
Answer: 
Finger escape

Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".


(iii)What is Hoffman’s reflex?
Answer: 
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition


_____________________________________





H) Link to patient details:


           
(i)What can be  the cause of her condition ?                             
Answer:

It could  be due to Iron deficiency anemia .


Iron deficiency and iron deficiency anemia may play an important role in inducing seizures from the following mechanisms:

1. Decrease of GABA inhibitory neurotransmitter due to change in its metabolism;

2. Change in neuron metabolism;

3. Reduction of enzymes such as monoamine and aldehyde oxidases; and,

4. Impairment in oxygenation and energy metabolism of the brain


(ii) What are the risk factors for cortical vein thrombosis?
Answer:


Risk factors for CVT in children and infants include:



Problems with the way their blood forms clots


Sickle cell anemia


Chronic hemolytic anemia


Beta-thalassemia major


Heart disease — either congenital (you're born with it) or acquired (you develop it)


Iron deficiency


Certain infections


Dehydration


Head injury


For newborns, a mother who had certain infections or a history of infertility


Risk factors for CVT in adults include:



Pregnancy and the first few weeks after delivery


Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation


Cancer


Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome


Obesity


Low blood pressure in the brain (intracranial hypotension)


Inflammatory bowel disease like Crohn’s disease or ulcerative colitis


(iii)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?                           
 Answer:        there was a sezuire free period due to administration of antiepileptic drugs as the effect of drugs weans off the sezures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the sezuires.
(iv)What drug was used in suspicion of cortical venous sinus thrombosis?
Answer:


CLEXANE (LMWH)was given to relive clot in suspission of CVST


_____________________________________


Question number :3 cardiology 

A) Link to patient details:



(i)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Answer:


  • 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


  • Heart failure with preserved ejection fraction:

 Heart failure with preserved ejection fraction (HFpEF), also referred to as diastolic heart failure, is characterized by signs and symptoms of heart failure and a left ventricular ejection fraction (LVEF) greater than 50%. Heart failure associated with intermediate reductions in LVEF (40% to 49%) is also commonly grouped into this category.


  • Heart failure with reduced ejection fraction:

Heart failure with reduced ejection fraction happens when the muscle of the left ventricle is not pumping as well as normal. The ejection fraction is 40% or less. The amount of blood being pumped out of the heart is less than the body needs.


                                    



(ii)Why haven't we done pericardiocenetis in this pateint?       

  Answer:        
Pericardiocentesis(PCC) aka pericardial tap ,is a medical procedure where fluid is aspirated from pericardium .
Pericardiocentesis can be used to diagnose and treat cardiac tamponade.Cardiac tamponade is a medical emergency in which excessive accumulation of fluid within the pericardium (pericardial effusion ) creates increased pressure.

  Pericardiocentesis is not done here  Because the effusion was self healing ,It reduced from 2.4cm to 1.9 cm.

(iii)What are the risk factors for development of heart failure in the patient?
Answer: 

Risk factors for development of heart faliure in this patent


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.


(iv)What could be the cause for hypotension in this patient?


Answer:

        Visceral pericardium may have  thickened which is restricting the heart to expand causing hypotension 


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B) Link to patient details:





(i)What are the possible causes for heart failure in this patient?
Answer: Possible factors for heart failure :
Underlying comorbidities are the possible causes ,,they are 

•   The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mixtrad insulin daily and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is major risk factor for heart failure.

•   The patient was also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure

•   He is a chronic alcoholic since 40 years which is a risk factor towards heart failure


•   The patient was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure


(ii)what is the reason for anaemia in this case?
Answer: 
The patient has normocytic normochromic anaemia. it could be anaemia of a chronic disease as the patient is diagnosed with CKD stage IV.

Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.

Patient’s with anaemia and CKD also tend to have deficiency in nutrients like iron, vitamin B12 and folic acid essential in making healthy red blood cells

(iii)What is the reason for blebs and non healing ulcer in the legs of this patient?
Answer:


The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.


(iv)What sequence of stages of diabetes has been noted in this patient?
Answer:

The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy

The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness



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C) Link to patient details:
 


(i)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?
Answer:


Evolution of symptomatology:

•10 years back -underwent inguinal hernia surgery(still has on and off pain) 

  [pain is aggravated since 3 years]

•Since 2-3 years: facial puffiness (on and off )

•Since 1 year-Hypertension 

•2 days back : SOB initially grade 2 

Later progressed to grade 4 and anuria 


the anatomical localization of problem is in BLOOD VESSELS;


Primary ETIOLOGY: 


•Physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels.

•Hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.


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

Answer: 
PHARMACOLOGICAL INTERVENTIONS


•Inj.dobutamine:

Dobutamine injection is indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of adults with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures.


•Tab .Digoxin:

Digoxin is a type cardiac glycoside. It's used to control irregular heartbeats (arrhythmias) including atrial fibrillation. It can also help to manage the symptoms of heart failure, usually with other medicines. 


•Inj.unfractionated heparin:

unfractionated heparin (UFH), is a medication and naturally occurring glycosaminoglycan. As a medication it is used as an anticoagulant. Specifically it is also used in the treatment of heart attacks and unstable angina.


•Tab.Carvediol:

Carvedilol is used alone or together with other medicines to treat high blood pressure (hypertension).


•TAB. Dytor

MOA: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.



•TAB. Acitrom 

MOA: 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


• TAB. Cardivas 

MOA: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.


• INJ. HAI S/C

MOA: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




Non pharmacological interventions:


• Watch for any bleeding manifestations like Petechiae, Bleeding gums.



•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.


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

Since the patient is known case of hypertension , patient is at risk of developing cardiorenal syndrome .

Risk factors include hypertension, diabetes, elderly age, and prior history of heart or renal failure. The pathophysiology of the cardiorenal syndrome involves intrarenal hemodynamics, transrenal perfusion pressure and systemic neurohormonal factors.

cardiorenal syndrome type 4 is seen in this patient.

(iv)What are the risk factors for atherosclerosis in this patient?
Answer: 
Risk factor for atherosclerosis in this patient is hypertension 


(v)Why was the patient asked to get those APTT, INR tests for review?

Answer: 
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.


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D) Link to patient details:



(i) 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?
Answer:
Evolution of symptomatology:
 • 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
                  - Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)

(ii)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
Pharmacological interventions:
•Tab Met Xl 25 MG Tablet is a beta-blocker that works on the heart and blood vessels. It is used to treat high blood pressure and chest pain. It slows down the activity of your heart allowing your heart to beat slower and less forcefully. As a result Met Xl 25 MG Tablet helps to prevent abnormally fast heartbeats. It also reduces the pressure at which blood is pumped out of the heart and around the body.

•Glimi.M2 This medicine is used to treat Type 2. It contains a combination of glimepiride and metformin as active ingredients.

•Telma20 Telma 20 tablet is an antihypertensive medicine that is used to treat high blood pressure and can also help in reducing other heart problems. It contains telmisartan as its active ingredient.

(iii)What are the indications and contraindications for PCI?
Answer
INDICATIONS:
        Acute ST-elevation myocardial infarction (STEMI)
         Non–ST-elevation acute coronary syndrome (NSTE-ACS)
         Unstable angina.
         Stable angina.
         Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
         High risk stress test findings.      
  
 CONTRAINDICATIONS:
     Intolerance for oral antiplatelets long-term.
     Absence of cardiac surgery backup.
      Hypercoagulable state.
      High-grade chronic kidney disease.
      Chronic total occlusion of SVG.
      An artery with a diameter of <1.5 mm.

(iv)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?
Answer: 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.
OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
. Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations. 
 Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant - OVERDIAGNOSIS.
Also the adverse effects due to this are more when compared to the benefits.
.Overdiagnosis through overtesting can psychologically harm the patient.
Hospitalizations for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.
Harms to health care systems
The use of expensive technologies and machineries are causing burden on health care systems.

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E) Link to patient details:


(i)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?
Answer: the anatomical location of etiology is BLOOD VESSELS.

•myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function


(ii)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:


PHARMACOLOGICAL INTERVENTION



•TAB. ASPIRIN

MOA:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.


•TAB ATORVAS 

MOA:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.


•TAB CLOPIBB 

MOA:The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.


•INJ HAI

MOA: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


•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.


(iii) Did the secondary PTCA do any good to the patient or was it unnecessary?
Answer:

Yes,because PTCA, or percutaneous transluminal coronary angioplasty, is a minimally invasive procedure that opens blocked coronary arteries to improve blood flow to the heart muscle.


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F) Link to patient details:


(i)How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Answer:
      IV fluids are administered in cardiogenic shock to increase heart’s pumping ability .
      Thus,following IV fluid administration his shortness of breath was relieved due to corrected blood pressure .
   
(ii)What is the rationale of using torsemide in this patient?
Answer:

Torsemide is a loop diuretic 

Torsemide is used to help treat fluid retention (edema) and swelling that is caused by congestive heart failure, liver disease, kidney disease

It is also helpful to treat Hyperkalemia .


(iii)Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Answer:

    Considering decreased urine output and history of Trans Urethral Resection of Prostate(TURP) patient is at high risk of developing UTI .

   Therefore, ceftriaxone is administered prophylactically in this patient.


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Question number :4 
Gastroenterology (& Pulmonology) 

A) Link to patient details:



(i)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?
Answer
Evolution of symptomatology ;

* Patient was apparently asymptomatic 5 yrs back when he had painabdomen & vomitings for which he was taken to a local hospital and treated conservatively.
(Following that he stopped taking alcohol.Later he again started taking alcohol following which he had recurrent episodes of pain abdomen & vomiting )
* (5-6 episodes in the past 1 year) which were treated by a local RMP.
* From 20 days he had increased amount alcohol consumption (5 bottles of toddy per day) 
*Last binge of  alcohol 1 week back following which he again had pain abdomen & vomiting from 1 week and fever from 4 days.
(* abdominal pain in umbilical, left hypochondriac, left lumbar and hypogastric regions,Abdominal pain was incresed after food intake.)
* Pain is throbbing type and radiating to backand is associated with nausea and vomiting( 1 episode) , which is non bilious, non projectile and also has food particles and water content 1 week.
* Fever was high grade, continuous  and associated with chills and rigors.
* Not associated with loose stools.
* since 4 days  , he developed constipation and passing flatus. 
* patient also had burning micturition since 4 days, which is associated with suprapubic pain, increased frequency and urgency

 •antomical location of etiology is pancreas(ductal obstruction,acinar cell injury,defective intracellular transport)

•The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes Attributed to alcohol


(ii)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?
Answer:

PHARMACOLOGICAL INTERVENTIONS
 •INJ MEROPENAM 
MOA:
   Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics.

 •INJ. METROGYL 
MOA:
      Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.


•INJ AMIKACIN 
MOA:
    It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.

 •TPN ( Total Parenteral Nutrition )
MOA:
      the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.

•IV NS / RL 
MOA:
      Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal areas,they require prompt intravenous (IV) hydration within the first 24 hours.


•INJ OCTREOTIDE 
MOA:
Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.

•INJ. PANTOP 
MOA:
      The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.

•INJ. THIAMINE
MOA:
     Vitamin B1 (thiamine) is indispensable for normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining normal cellular redox state.

•INJ TRAMADOL 
MOA:
      Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.

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B) Link to patient details:



(i) What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer
The cause of Dyspnea might be due to 
 PLEURAL EFFUSION
  How is it related to pancreatitis:- Respiratory complications in Acute pancreatitis 
     Severe form of acute pancreatitis is complicated by multiple organ system dysfunctions, of which respiratory complications are the most important one. Amongst all the extra-pancreatic systemic complications, respiratory dysfunctions including acute respiratory distress syndrome (ARDS) is potentially the most serious manifestations of AP.
      Pancreatitis develops in 3 phases of which the initial phase ensues in the first few hours and characterized by activation of intrapancreatic digestive enzyme and acinar cell damage followed by the second phase of an inflammatory reaction with acinar cell necrosis and finally, the last phase is the appearance of extrapancreatic changes where pulmonary damage occurs and ultimately leading to ARDS .
     In the pathogenesis of respiratory complications of AP, Inflammatory mediators released from pancreatic injury and digestive actions of pancreatic enzymes play a key role. The role of active digestive enzymes in circulation, release of multiple pro-inflammatory cytokines, activation and migration of leukocytes/neutrophils, complement mediated injury, and platelet activating factors are primarily involved in development of these complication. A damage to the pulmonary vasculature caused by activated trypsin leads to increased endothelial permeability while the main culprit for pulmonary insufficiency . https://www.longdom.org/open-access/respiratory-complications-in-acute-pancreatitis-2165-7092-1000e149.pdf

(ii) Name possible reasons why the patient has developed a state of hyperglycemia.
Answer:
•Following the damage of pancreatic beta cells ,there is decreased synthesis and release of insulin .
•increased levels of cortisol and catecholamines results in hyperglycemia 
•increased glucagon secondary to stress may be the cause of hyperglycemia 

(iii) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Answer:
 LFT are increased due to hepatocyte injury


•If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.


•elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.


The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to


 —decreased ALT activity most likely due to B6 depletion in the livers of alcoholics


 —mitochondrial damage leading to increased release of mAST in serum.


(iv)What is the line of treatment in this patient?
Answer

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


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C) Link to patient details:



(i)what is the most probable diagnosis in this patient?
Answer:
[Some differentials for this case are :
·        Ruptured Liver Abscess.
·        Organized collection secondary to Hollow viscous Perforation.
·        Organized Intraperitoneal Hematoma.
·        Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
·        Grade 3 RPD of right Kidney]

The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated. 

(ii)What was the cause of her death?
Answer
    Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs. 

(iii)Does her NSAID abuse have  something to do with her condition? How? 
Answer
•NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.
• Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death. 

What would have been the best investigation to diagnose the exact cause???
Why CT was not done in this patient,can we make a precise diagnosis using CT in this patient ??

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Question number .5
Nephrology (and Urology) 

A) Link to patient details:


(i)What could be the reason for his SOB ?
Answer
     SOB in this patient could be due to Acidosis ,which in turn is due to diuretics .
 
Following are some side effects/complications of diuretics:
Loop agents and distal convoluted tubule agents, such as the thiazides produce hypokalemic, hypochloremic, metabolic alkalosis that responds to potassium chloride replacement. Carbonic anhydrase inhibitors produce less hypokalemia and volume depletion but commonly induce metabolic acidosis that is often symptomatic.

(ii)Why does he have intermittent episodes of  drowsiness ?
Answer:
     Intermittent episodes of drowsiness is due to Hyponatremia, which in this patient could be due to Kidney injury and/or Diuretics.

(iii)Why did he complaint of fleshy mass like passage in his urine?
Answer
       Plenty of pus cells in his urine passage appeared as fleshy mass like passage to him .

(iv)What are the complications of TURP that he may have had?
Answer:
The complications of TURP(Trans Urethral Resection of Prostate)in this patient are:
      •Difficulty micturition(painful or difficult urination)
      •Infection 
      •Electrolyte imbalances
    
  _____________________________________

B) Link to patient details:




(i)Why is the child excessively hyperactive without much of social etiquettes ?
Answer:


several factors associated with the ADHD (Attention Deficit Hyperactivity Disorder)condition, include abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.


•Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.


 • Depressed dopamine activity has been associated with the condition,


(ii)Why doesn't the child have the excessive urge of urination at night time ?
Answer: because ADHD is a psychosomatic disorder therefore the child doesn’t have the excessive urge of urination at night time 

(iii)How would you want to manage the patient to relieve him of his symptoms?
Answer:

Treatment strategies for ADHD:

        Therapies:support group , cognitive behavioural therapy,anger management,counselling,applied behavioural analysis.
        Medication:stimulants(amphetamine),
cognition enhancing medication.
                 
Treatment strategies for overactive bladder:
          
Behavioral therapies

Pelvic floor muscle exercises,Biofeedback,Healthy weight
,Scheduled toilet trips,Intermittent catheterization,Bladder training,Absorbent pads.


Medications
Medications that relax the bladder can be helpful for relieving symptoms of overactive bladder and reducing episodes of urge incontinence. These drugs include:
Tolterodine (Detrol)
Oxybutynin, which can be taken as a pill (Ditropan XL) or used as a skin patch (Oxytrol) or gel (Gelnique)
Trospium
Solifenacin
Darifenacin
Fesoterodine 
Mirabegron 

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Question number :6 
Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)  

A) Link to patient details:




(i)Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Answer
Following features are suggestive of tracheo oesophageal fistula in this patient :
  •Cough (on taking food and liquids .)
  •Dysphagia(difficulty in swallowing)
  •Weight loss 
  •Hoarseness of voice 
  •laryngeal crepitus 
  
(ii)What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 
Answer:
  Immune reconstitution inflammatory syndrome:
Risk of developing IRIS:
  Risk of unmasking IRD is directly related to the prevalence of undiagnosed OIs at baseline, which in turn will be related to the degree of immunodeficiency of patients, the methods used to screen for OIs and the prevailing frequency of specific OIs in the geographic location. Additional key risk factors associated with paradoxical IRD (some of which may also contribute to unmasking IRD risk) include the timing of ART during OI treatment, extent of the OI, baseline CD4 count and HIV viral load, and response of CD4 count and HIV viral load to ART.

A paradoxical clinical worsening of a known condition or the appearance of a new condition after initiating antiretroviral therapy (ART) therapy in HIV-infected patients resulting from restored immunity to specific infectious or non-infectious antigens is defined as immune reconstitution inflammatory syndrome (IRIS).

Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms:
•unmaskingIRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started; 
•paradoxical IRIS refers to the worsening of a previously treated infection after ART is started.
Patients with mycobacterial disease at the time of initiation of ART are at higher risk of developing IRIS with an approximate risk of 15%. Patients originating from endemic areas for tuberculosis and cryptococcal disease are at higher risk of developing IRIS.

Measures to prevent immune reconstitution inflammatory syndrome:

In light of what is known of the risk factors and immunopathogenesis of IRD, it follows that a range of different interventions may reduce the risk and severity of unmasking and paradoxical forms of IRD. These include the initiation of ART much earlier in the course of HIV progression, preventive therapy for OIs prior to ART eligibility, pre-ART screening for OIs, use of optimized treatment for OIs, adjustment of the timing of starting ART during OI treatments, and immunosuppressive and immunomodulatory therapies.

•The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.

•Efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3252684/


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Question number:7 

Infectious disease and Hepatology:

A)Link to patient details:




(i)  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 ?
Answer:
  Yes,I think that drinking locally made alcohol (toddy) caused the liver abscess in this patient 

Some studies suggest that 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. 


There are many studies that suggest the development of liver abscess in people consuming toddy .
To be more specific , chronic consumption of toddy is associated with development of Amoebic Liver Abscess
 
This study states the association  between local alcoholic beverages and amoebic liver abscess.


Since the patient is a chronic toddy consumer for 30 years , why don’t we suspect an amoebic liver abscess in this patient?


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


(iii)Is liver abscess more common in right lobe ?
Answer:
Yes, liver abscesses occur in the right lobe of the liver more commonly  (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.
 Why?
The right hepatic lobe is affected more often than the left hepatic lobe . The predilection for the right hepatic lobe can be attributed to anatomic considerations. The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass. 


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

Answer

•Presence of a left-lobe abscess more than 10 cm in diameter.
•Impending rupture and abscess that does not respond to medical therapy within 3-5 days.
•caudate lobe abscess
 •If the abcess is large ( 5cm or more) because it has more chances to rupture.

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B) Link to patient details:





i) Cause of liver abcess in this patient ?

Answer:

       The cause of liver abscess in this patient is mostly due to TODDY consumption .

       Toddy is believed to be Independent risk factor in developing Liver abscess ,to be more specific Amoebic Liver Abscess .


(ii)How do you approach this patient ?

 Answer:    

  Amoebic liver abscess:

Management:


•The first line treatment in uncomplicated amebic abscess should be amebicidial drugs.       Metronidazole is the drug of choice and has replaced the use of emetine and chloroquine. Metronidazole is effective against both the intestinal and hepatic phase. 750 mg three times a day for 7–10 days is recommended. Abscess smaller than 5 cm in diameter respond better to metronidazole treatment.

AspirationAlthough routine aspiration is not recommended in most cases percutaneous needle aspiration is required for treatment, especially in larger abscesses. 


Surgical open drainage is indicated only for those with complicated amebic abscess, e.g. secondary infection or peritonitis with perforation.


(iii)Why do we treat here ; both amoebic and pyogenic liver abcess? 

Answer:

  Here in this patient there was no confirmatory diagnosis to differentiate if it is amoebic or Pyogenic abscess .It most likely to be amoebic liver abscess ,but not trying not to risk if it is a Pyogenic one which when left untreated ,abscess may rupture causing severe sepsis,which is life threatening  .Therefore we are treating for both the abscesses.

(iv)Is there a way to confirmthe definitive diagnosis in this patient?

   •Cysts of E.histolytica in stools of patients ( in only  15% of hepatic amoebiasis )

   SEROLOGICAL : positive haemagglutination test is quite sensitive and useful for diagnosis of amoebic liver abscess 


The diagnosis of amebic liver abscess was based on four or more of the following criteria:


 (i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, 


(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), 


(iii) enlarged and/or tender liver, usually without jaundice, 


(iv) raised right dome of the diaphragm on chest radiograph, and 


(v) improvement after treatment with antiamebic drugs (e.g., metronidazole). 


______________________________________

Question number : 8
Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 

A) Link to patient details:

 



i)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?


Answer:

Evolution of symptomatology:

 

Pt was asymptomatic 3 years back 

  3 years ago-he was  diagnosed with hypertension       

   21 days back- he received vaccination at local PHC Following which he had fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication

18 days ago- complained of similar events and went to the local hospital, it was not subsided upon taking medication(antipyretics) 

 11 days ago - patient complains of Generalized weakness ,facial puffiness and periorbital oedema. Patient was in a drowsy state

  4 days ago-  

    • patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb

    • the  same evening patient’s  periorbital oedema progressed

   • serous discharge from the left eye that was blood tinged

   •oral and nasal foul smelling was present 

   •was diagnosed with diabetes mellitus associated with DKA (diabetic keto acidosis)

   • On CT :

               Preseptal cellulitis is observed 

               Acute infarcts in frontal and temporal lobes seen 

               Soft tissue swelling in maxillary sinus and mucosal thickenings of sinus seen 

               

 Following Ent referral and KOH mount: 



The patient was diagnosed with acute oro rhino orbital mucormycosis 


  patient was referred to a government general hospital 

       

  patient died 2 days later 



Anatomical localisation of the problem :

      Is the sinuses and the brain 

         • Acute infarcts in frontal and temporal lobes

            •Soft tissue swelling in maxillary sinus and mucosal thickenings of sinus 


Primary etiology of patient’s problem :


  •The factors that are responsible are :

            Mucormycosis and 

           Uncontrolled diabetes associated with diabetic ketoacidosis


      Diabetes mellitus tends to change the normal immunological response of body to any infection in several ways. Hyperglycemia stimulates fungal proliferation and also causes decrease in chemotaxis and phagocytic efficiency which permits the otherwise innocuous organisms to thrive in acid-rich environment. In the diabetic ketoacidosis patient, there is an increased risk of mucormycosis caused by Rhizopus oryzae as these organisms produce the enzyme ketoreductase, which allows them to utilize the patient's ketone bodies.It has been established that diabetic ketoacidosis temporarily disrupts the ability of transferrin to bind iron, and this alteration eliminates a significant host defense mechanism and permits the growth of Rhizopus oryzae

  (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5754995/)



        Why did this condition appear all of a sudden ? Why did he develop this condition following vaccine ? Is it the  post covid vaccine complication in uncontrolled hyperglycaemia associated with DKA?

          It could be due to undiagnosed diabetes associated with DKA ,DKA left untreated might have lead to this condition .



(ii)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?

 Answer:

• Inj. Liposomal amphotericin B according to creatinine clearence :

    MOA: binds to ergosterol in the fungal cell membrane, which leads to the formation of pores, ion leakage and ultimately fungal cell death.

    

• itraconazole  adjusted to his creatinine clearance:


 MOA: Itraconazole acts by inhibiting the fungal cytochrome P-450 dependent enzyme lanosterol 14-α-demethylase. When this enzyme is inhibited it blocks the conversion of lanosterol to ergosterol, which disrupts fungal cell membrane synthesis.



approach to treat this case :


Management of Mucormycosis:

 

  • Intravenous Amphotericin B is the drug of choice for initial therapy
  • Posaconazole or Isavuconazole is tased as stepdown therapy for patients who have responded to Amphotericin B
  • Posaconazole or Isavuconazole can also be used as salvage therapy for patients who don’t respond to or cannot tolerate Amphotericin B
  • Surgery- Aggressive surgical debridement of involved tissues should be considered as soon as the diagnosis of any form of Mucormycosis is suspected.
  • Diabetic ketoacidosis  requires insulin and volume repletion with intravenous fluids.


Management of DKA:


Fluid replacement

At the hospital, your physician will likely give you fluids. If possible, they can give them orally, but you may have to receive fluids through an IV. Fluid replacement helps treat dehydration,which can cause even higher blood sugar levels.

Insulin therapy

Insulin will likely be administered to you intravenously until your blood sugar level falls below 240 mg/dL. When your blood sugar level is within an acceptable range, your doctor will work with you to help you avoid DKA in the future.

Electrolyte replacement

When your insulin levels are too low, your body’s electrolytes can also become abnormally low. Electrolytes are electrically charged minerals that help your body, including the heart and nerves, function properly. Electrolyte replacement is also commonly done through an IV.


   


(iii)What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 

Answer:

Mucormycosis is opportunistic infection that occurs in diabetics,immunocompromised individuals etc,.

 

We know that India has high incidence of Diabetes .

The reason for the increasing incidence in India is being mainly attributed to a continued increase in the patient population with uncontrolled diabetes. 


https://www.researchgate.net/publication/263187827_Epidemiology_of_Mucormycosis_in_India


•it is also due to overuse of steroids in management of covid pneumonia is also the reason .

Steroids being immunosuppressants and favouring the growth of fungus leading to mucormycosis.


_____________________________________________

Question number:9-Infectious Disease (Covid 19)

•My attempt to answer the questions of the topic Covid:




• covid master chart:


  ____________________________________________

Question number 10-Medical Education :


   Preparing elogs and telecommunication with patient’s attendants and subsequent follow up of the patient is helping me to improve my skills and enabling me to learn many things. Researching while preparing blogs is very interesting and it is helping me to build my knowledge in medicine.Initially it seemed difficult,but later this new way of learning medicine seemed a lot more interesting .All thanks to General medicine department and Dr.Rakesh sir for making this possible and helping us to improve our clinical knowledge even when we are locked down at homes.Following is my experiential learning of the month of May-2021:

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