Medicine blended assignment

Medicine Assignment -May 30, 2021

May 30, 2021

I G vishal (roll no :- 42)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.

Pulmonology 

 A)55 Year Old Female with Shortness of Breath, pedal Edema and Facial Puffiness.

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

Questions

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  problem ?

1A)Evolution of symptomatology

 1st episode of sob - 20 yr back

2nd episode of sob - 12 yr back

From then she has been having yearly episodes for the past 12 yrs 

Diagnosed with diabetis - 8yrs back

Anemia and  took iron injections  - 5yr ago

Generalised weakness  - 1 month back 

Diagnosed with hypertension  - 20 days back

Pedal edema - 15 days back

Facial puffiness- 15 yrs back

Anatomical location of problem - lungs

Primary etiology of patient- usage  of chulha since 20 yrs might be due to chronic usage 

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

2A:- Head end elevation :# MOA;

.improves oxygenation 

.decreases incidence VAP

.increases hemodynamic performance 

.increases end expiratory lung volume

.decreases incidence of aspiration 

Indications: 1.head injury

                    2.meningitis 

                    3.pneumonia 

~ oxygen inhalation to maintain spo2

~Bipap:non invasive method

*MOA :-assist ventilation  by delivering positive expiratory and inspiratory pressure with out need for ET incubation9

3)~Cause for current acute excerbation 

3A:-It can be due to any infection

I 

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

4A:- Yes ATT affected her symptoms

Isoniazid and rifampcin -nephrotoxic - raised RFT was seen

Neurology

A)A 40 Year Old Male with Complaints of Irrelevant Talkinng

Patient details:-https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

Questions

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?

A) evolution of symptamatology: The patient is a chronic alcoholic, he drinks about 3-4quarters/day.He had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.

Anatomical location:Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.

1)The GABA system :- 

GABA is an amino acid which acts as a neurotransmitter in the central nervous system. GABA's natural function is to reduce the activity of the neurons to which it binds. It inhibits nerve transmission in the brain, calming nervous activity.

2)The glutamate:- 

The glutamate system is a fast-signaling system that is very important for information processing in neuronal networks of the neocortex and hippocampus in particular. Glutamate is very much involved in the process of long-term potentiation, which is a neuronal model of memory.

The symptom: irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.

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?

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

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

A:- 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?

A:- 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?

A:- 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 alcohlism have aggravated the foot ulcer formation ?if yes and why ?

A:- 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)A 52 year old male with Cerebellar Ataxia

Patient details:- https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

Questions

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient's problem?

A:-evolution of symptomatology

~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:-

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

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 denova hypertension contribute to this current condition?

A:- 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?

A:- 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 that helps in formation of clot. So, there by decreases chance of 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.

C)A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB

Patient details:-http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Questions

1Q)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

~Aggerevated 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

Anatomical localisation :

Palpitations

Dyspnoea(NYHA-3)

Pedal edema

Radiating pain along her left upper limb

Etiological agent :

~By localization, electrolyte imbalance (hypokalemia) causing the her   manifestations like palpitations, chest heaviness, generalised body weakness

~radiating pain along her left upper limb due to cervical 

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,

                               • T wave - 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. 

D)55years old patient with seizures.

Patient details:-https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

Questions

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

A:- Relation b/w seizure and 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 occur 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.

•Causes for the early onset of seizures after ischaemic strokes:-

1.An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation

2. glutamate excitotoxicity, hypoxia, metabolic dysfunction, global  hypo perfusion and hyper perfusion injury ,(particularly after carotid end arterectomy)

 have all been considered 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.

2Q). 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?

A:- 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.

E)A 48-year-old gentleman hailing from a small town in Telangana presented to the casualty ward on 25th April 2021 at 7:40am with the chief complaints of unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the past 3 hours

Patient details:-https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions

Question no 1:-What could have been the reason for this patient to develop ataxia in the past 1 year?

A:- Ataxia is the term used for group of disorders that effect co-ordination,speech and balance

 

Any part of the body can be effected but people with ataxia have problems like:- 

                      1.balance and walking

                      2.speaking

                      3.swalloing

                      4.tasks with high degree of control like writing&eating

                    5.vision

Ataxia usually results from damage to the part of brain called cerebellum but can also be caused by damage to other parts of nervous system.This damage can be part of ms or can be caused by head injury, lack of oxygen supply to brain and longterm alcohol consumption.

Types of ataxia :- 1.acquired ataxia 

                             2.heridetary ataxia

                             3.idiopathic late onset cerebellar ataxia

~Some induviduals can develop ataxia due to prolong exposure to alcohol(aquired ataxia)-cerebellar ataxia

   

~in patients with alcohol ataxia symptoms effect gait(walking) and lowerlimbs more than arms and speech.it can also cause peripheral neuropathy 

Mechanism:-

1. Inside the brain alcohol directly damages the cells within cerebellum and rest of the brain and for those who drink excessively over a long period of time it can cause particularly severe and often permanent damage

 

2.patients who drink excessively are prone to nutritional deficiencies(thiamine,vit e) due to poor diet or damage to the gut lining ,preventing the absorption of vitamins

Question no 2:-What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Reason for IC Bleed: 

~Heavy drinkers have about  1.6 times more risk to suffer from intracerebral hemorrhage and 1.8 times more likely to suffer from subarachnoid 

~Chronic alcohol abuse tends to elevates blood pressure, resulting in increased occurrence of HICH and exaggerated HICH-contributed brain injury.(vasoconstriction induced bleed)

 

F)A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWER LIMB

 Patient details:-http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions

Question no 1 : Does the patient's  history of road traffic accident have any role in his present condition?

A:-Road traffic accident occured 4 years ago and might not have any role in this present situation.

Rta mostly causes Hemorrhagic stroke but our patient has ischemic stroke due to narrowing of blood vessels.

Question no : 2 What are warning signs of CVA?

The five warning signs of stroke are:-

1.Sudden onset of weakness or numbness on one side of the body

2. Sudden speech difficulty or confusion.

3. Sudden difficulty seeing in one or both eyes.

4. Sudden onset of dizziness, trouble walking or loss of balance.

5. Sudden, severe headache with no known cause                

QUESTION NO : 4  Does alcohol has any role in his attack?

A:-Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.

QUESTION NO : 5 Does his lipid profile has any role for his attack??

A:-In this case patient has LOW HDL Levels .

Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor. In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke.

G)A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY

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

Questions

Question no 1:-what is mylopathy hand?

A:-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. 

Question no 2:-what is finger escape

A:-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".

Question no 3:-What is hoffmans reflex?

A:-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)17 year old female with seizures

Patient details:-https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1

Questions

 Question no 1:-What can be the cause of her condition ?  

A:-Cotical vein thrombosis have caused her repeated seizures by increased venous capillary pressure

Question no 2:- What are the risk factors for cortical vein thrombosis?

A:- Genetic prothrombin states :-  antithrombin deficiency,prothrombin mutation, resistance to activated protein c

 ~  Haematology:-  polycythemia,thrombotic      thrombocytopenic purpura

~  Activated prothrombotic states:- pregnancy, nephrotic syndrome,homocysteinemia.

~  Drugs:- oral contraceptives, sumatropin , intravenous immunoglobulin, steroids,lithium androgens.

~ Infection:-  mastoditis, AIDS, meningitis, systemic infections, sinusitis.

~Other causes :-dehydration,throtoxicosis, head trauma, congenital heart disease

Question no 3:- There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?

 A:- seizure free period occurs due use of medication and, which relived it

Sudden episodes of GTCS occurs due to abnormal firing of neurons. 

Question no 4:- What drug was used in suspicion of cortical venous sinus thrombosis?

A:- Heparin should be considered seriously in the management of cerebral venous thrombosis (CVT), with subsequent conversion to warfarin as maintenance therapy suggested. Subcutaneous low ̶ molecular-weight heparin (Lovenox) also has been used in patients with venous sinus thrombosis.

Cardiology

A) A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS

Pateint details :-https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html

Questions

1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

A:-The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). 

 A normal EF is usually around 55 to 70 percent, but it can be lessened in some forms of heart failure.

a) People with heart failure with reduced ejection fraction (HFrEF) have an EF that is 40 to 50 percent or lower. This is also called systolic heart failure. 

b) People with heart failure with preserved ejection fraction (HFpEF) do not have much of a change in their ejection fraction. This is often called diastolic heart failure.

 -HFrEF were often diagnosed earlier in life and right after a heart attack. 

 HFpEF were diagnosed later in life and first experienced symptoms of heart failure between the ages of 65 and 69. 

-HFrEF shared that they feel depressed and/or anxious about their heart failure diagnosis. Risk factors for those in this group include genetics or a family history of heart failure.

-HFpEF shared that they are still able to do the things they enjoyed before their heart failure diagnosis.                          risk factors including:-

1.Sedentary lifestyle

2.High blood pressure

3.Sleep apnea

4.Other heart conditions

-HFrEF are more likely to have had surgery, including surgery to implant a pacemaker or other heart rhythm control device.HFrEF shared that they currently use a combination therapy to treat their heart failure.

HFpEF have never had surgery to treat their heart failure or had a device implanted.

 -HFrEF are men who live in rural areas.

 However, most respondents with HFpEF are women who live in urban areas.

2.Why haven't we done pericardiocenetis in this pateint?

        

A:-Pericardiocentesis is done when the pericardial effusion is not resolving on its own . Here the pericardial fluid which has accumulated was resolving on its own , at the time of admission it was 2.4mm and when discharged it was 1.9 mm . Therefore we did not do pericardiocentesis in this pt. 

            

3.What are the risk factors for development of heart failure in the patient?

A:-   IN THIS PATIENT:

NON MODIFICABLE:

-age

-gender

MODIFIABLE:

-hypertension

-smoking

-type 2 diabetes .

-kidney disease.

IN GENERAL RISK FACTORS:

4.What could be the cause for hypotension in this patient?

A:- The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension.

B)A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT

Pateint details:- https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html

Questions

Question no 1:-What are the possible causes for heart failure in this patient?

A:-   1.obesity 

        2.alcohol

        3.diabetes

        4.hypertension

Question no 2:-what is the reason for anemia in this case?

A:- Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections.

Question no 3:-What is the reason for blebs and non healing ulcer in the legs of this patient?

A:- The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type-2 diabetes mellitus.

Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases. 

In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.

There are many risk factors that may lead to foot ulcers at the end.

Poor quality or fitting of the footwear.

Unhygienic appearance of foot.

Improper care of the nails of the toe.

Heavy intake of alcohols and tobacco.

Obesity and Weight-related

Complication arising from Diabetes like eye problems, kidney problems and more.

Although aging or old age can also be counted among them.

Question no 4:-What sequence of stages of diabetes has been noted in this patient?

A:- alcohol------obesity------impaired glucose tolerance------diabetes mellitus------microvascular complications like triopathy and diabetic foot ulcer-------macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease.

C)A-Fib and Biatrial Thrombus in a 52yr old Male

 

Patient detials:- https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

Questions

Question no 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:- anatomical location:- BLOOD VESSELS;

* ETIOLOGY: 

The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.

The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

Question no 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:- PHARMACOLOGICAL INTERVENTIONS

1. 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.

2. 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

3. 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.

4. 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

5.TAB. Digoxin 

Moa:-

Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:

 Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,

 an enzyme that controls the movement of ions into the heart.

6. Hypoglycemia symptoms explained

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

Question no 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: cardiorenal syndrome type 4 is seen in this patient.

Question no 4:-What are the risk factors for atherosclerosis in this patient?

A:-effect of hypertention

 They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.

Question no 5:-  Why was the patient asked to get those APTT, INR tests for review?

Ans: APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.

D)67 year old patient with acute coronary syndrome

Patient details:- https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

Questions 

Question no 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 sympomatology:-

~ 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)

Question no 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:- Pharmacological interventions:

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

 MOA: METOPROLOL is a cardiselective 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 hear 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.

Results:  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. 

Non pharmacological intervention:- advised to this patient is: 

  ~PERCUTANEOUS CORONARY INTERVENTION.

Percutaneous Coronary Intervention  is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).

Question no 3:- What are the indications and contraindications for PCI?

 A:-    INDICATIONS:

       1.   Acute ST-elevation myocardial infarction (STEMI)

       2.  Non–ST-elevation acute coronary syndrome 

       3.  Unstable angina.

       4.   Stable angina.

       5. Anginal equivalent (eg, dyspnea, arrhythmia)

       6.  High risk stress test findings.      

  

   CONTRAINDICATIONS:

      1.   Intolerance for oral antiplatelets long-term.

      2.   Absence of cardiac surgery backup.

      3.   Hypercoagulable state.

      4.   High-grade chronic kidney disease.

      5.   Chronic total occlusion of SVG.

      6.   An artery with a diameter of <1.5 mm.

Question no 4:- What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?

A:- 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 .

So, it is better to avoid PCI in patients who do not require it.

⁃ OVER TESTING AND OVER TREATMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.

Harms to patients

.1)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.

.2)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[41] for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.

E)ACUTE MYOCARDIAL INFARCTION

Patient details:- https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

Questions:-

Question no 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 symptomatology:- chest pain since 3 days

      anatomical location is BLOOD VESSELS.

      Primary etiology :-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

Question no 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:-  PHARMACOLOGICAL INTERVENTION

1.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.

 

2.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.

3.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.

4.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

5.ANGIOPLASTY

Moa:- 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.

Question no 3:- Did the secondary PTCA do any good to the patient or was it unnecessary?

A:- The second PCI was NOT necessary in this patient.

PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.

The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse.

F) case of cardiogenic shock 

Patient details:- https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h

Questions

Question no 1:-How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

A:- 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

Question no 2:- What is the rationale of using torsemide in this patient?

A:- 

Question no 3:-Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

A:-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 and pulmonology 

A)A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA

Patient details:- https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

Questions

Question no 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 symptomatology :-

~5 years back-1st episode of pain abdomen and vomitings 

~Stopped taking alcohol for 3 years

~1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 

~20 days back increased consumption of toddy intake

~Since 1 week pain abdomen and vomiting

~Since 4 days fever constipation and burning micturition

Anatomical localisation: Pancreas and left lung

Primary etiology:- Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol its metabolites and by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

Question no 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?

A:

B)CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN

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

Questions

Question no 1:-What is causing the patient's dyspnea? How is it related to pancreatitis?

A:- The cause of dyspnea might be Plueral effusion

~Two main causes of pleural effusion are transdiaphragmatic lymphatic blockage or pancreaticopleural fistulae secondary to leak and disruption of the pancreatic duct or pseudocyst caused by an episode of acute pancreatitis.

Question no 2:-Name possible reasons why the patient has developed a state of hyperglycemia.

A:-This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress

* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 

* elevated levels of catecholamines and cortisol

Question no 3:-What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

A:- 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.

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 is due to:-

 (i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics

 (ii) mitochondrial damage leading to increased release of mAST in serum.

Question no 4:-What is the line of treatment in this patient?

A:- Investigations:

1)24 hour urinary protein 

2)Fasting and Post prandial Blood glucose 

3)HbA1c 

4) USG guided pleural tapping 

Treatment:

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly

C)A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension 

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

Question no 1:-  What is the most probable diagnosis in this patient?

A:- Differential Diagnosis:

• 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. 

 

 

Question no 2:- What was the cause of her death?

A:- After leaving the hospital, the patient went to Hyderabad and underwent emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs. 

 

 

Question no 3:-Does her NSAID abuse have something to do with her condition? How? 

A:- 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.

Nephrology

A)Post TURP with non oliguric

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

Questions

Question no 1:What could be the reason for his SOB ?

A:-During TURP, the wide plexus of venous sinuses is often opened and the absorption of the irrigation fluid causes a group of symptoms and findings that is called TURP syndrome.  This is the cause for the sob in the patient. The symptoms of TURP are generally caused by an excessive fluid load in circulation. 

  

Question no 2:Why does he have intermittent episodes of  drowsiness ?

A:-Uremic Encephalopathy might have been the cause.

Question no 3:Why did he complaint of fleshy mass like

 passage in his urine?

A:-As the patient is healing from the TURP surgery, it might be a clot formed which is excreted in urine

  

Question no 4:What are the complications of TURP that he may have had?

A:- The possible risks of TURP include the following:

Bleeding.

Electrolyte abnormalities.

Loss of erections.

Retrograde ejaculation

B) An Eight year old with Frequent Urination

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

Questions

Question no 1:- Why is the child excessively hyperactive without much of social etiquettes ?

A:- All these features in the patient's history promote the reason to be around ADHD syndrome and this might be the cause of hyperactivity without social etiquettes

Question no 2:-  Why doesn't the child have the excessive urge of urination at night time ?

A:- The child is supposed to be duffering from OCD and hence he does not urinate during the night

Question no 3:-How would you want to manage the patient to relieve him of his symptoms?

A:- The child has not been tested positive for any renal abnormalities and also he seems to be suffering from ADHD and OCD and hence he is not currently on any treatment but only referred to psychiatric care.

Infectious diseases

A)40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH

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

Questions

 Question no 1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

A:-  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

Question no 2:- What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

A:-   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

A)liver abscess

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

Questions

Question no 1:-  Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factor present in it ? 

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

Question no 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.

Question no 3:- Is liver abscess more common in right lobe ?

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

Question no 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

B)CASE DISCUSSION ON LIVER ABCESS

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

Questions

Question no 1:- Cause of liver abcess in this patient ?

A:-  Here ; the cause of liver abcess is :

* Amoebic liver abcess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.

* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.

* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.

## Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.

Question no 2:-How do you approach this patient ?

A) * The patient is well managed by treating team ; even me will follow the same approach.

Question no 3- Why do we treat here ; both amoebic and pyogenic liver abscess? 

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

Question no 4:- Is there a way to confirmative definitive diagnosis in this patient?

A:-Yes in a high resource setting cause of liver abscess is usually determined using multiple diagnostic strategies , including blood cultures , entamoeba serology , liver abscess aspirate for culture and molecular and antigen testing.

Infectious diseases (Mucormycosis ,ophthalmology, Otorhinolaryngology)

50/Male came with altered sensorium

Patient details :- http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

Questions 

Question no 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:-  COURSE OF THE SYMPTOMS:

1. 3 years ago- diagnosed with hypertension

2.  21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication

3.  18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics) 

4.  11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state

5. 4 days ago-  

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

ii) towards the evening patient periorbital oedema progressed

iii) serous discharge from the left eye that was blood tinged

iv) was diagnosed with diabetes mellitus

6. patient was referred to a government general hospital 

7. patient died 2 days ago

ANATOMICAL LOCATION: Rhino-orbito-cerebral disease.

PRIMARY ETOLOGY: Fungal infection with mucor.

Question no 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?

The proposed management of the patient was : 

1. Inj. Liposomal amphotericin B according to creatinine clearance 

2. 200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance

3. Deoxycholate was the required drug which was unavailable

Along with the above mentioned treatment for the patient managing others symptoms is also done by-

I. Management of diabetic ketoacidosis – 

(a) Fluid replacement-  The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.

(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.

(c) Insulin therapy-  Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy

Question no 3:- What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?

A:-

• Steroid overuse in the covid patients. This led to further immunosuppressive state. COVID causes systemic illness leading to immunosuppression. 
• Mucormycosis is more common among diabetics as thought diabetes is an immunocompromised state. Poor patient hygiene also is a risk factor.

Medical learning;- 

Telemedicine Learning is entirely different concept for me and its actually helping us to stay in touch with patients as well as improve our clinical knowledge.

Such experience is available only in medicine department and its a great step by the hod sir for students.

In such difficult times like with no live patient contact and examination its a little difficult for us but i am very glad that atleast we have this great level of interaction and constant flow of knowledge between faculty and pg's.

By making elogs we are able to learn many new things regarding subject and i am very happy with the process . 

I thank faculty and pg's for always being available to clear doubts and help with making elogs and its a also very interactive .

THANK YOU !!