MEDICINE Blended Assignment MAY 2021
NAME : ANKITHA
ROLL NO : 67
8th Semester
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
Online blended bimonthly assignment toward summative assessment for the month of May 2021
1) Pulmonology (10Marks)
A) Link to patient details:
A 55 Year Old Female with Shortness of Breath, pedal Edema and Facial Puffiness
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?
* Evolution of symptomology and Event timeline :
- 20 years ago - SOB Grade 1 for a week occured every year for the same duration.
- 18 years ago - Polyuria and was diagnosed with DM
- 12 years ago - SOB Grade 1 for a month
- 1month ago - Weakness was giving IV
- 30 days ago - SOB (latest episode) gradually progressive
- 20 days ago - HRCT showed Bronchiectasis
- 15 days ago - Pedal edema and facial puffiness
- 2 days ago - SOB Grade IV drowsiness and decreased urine output.
* Anatomical location : Bronchioles.
* Primary etiology :
Rice dust exposure as patient is a farmer working in paddy fields.
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?
Augmentin = Amoxicillin + clavulanic acid . Amoxicillin binds to penicillin binding proteins with in the bacterial cell wall and inhibits bacterial cell wall synthesis .Clavulanic acid is a B lactam structurally related to penicillin that may inactivate certain B-lactamase enzymes.
Question no 3 :What could be the causes for her current acute exacerbation?
ANS) Cause for current acute excerbation - it could be due any infection
Question no 4 :Could the ATT have affected her symptoms? If so how?
ANS ) Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
Question no 5 :What could be the causes for her electrolyte imbalance?
A number of things can cause an electrolyte imbalance including :
1. fluid loss from heavy exercise or physical activity
2. medications such as diuretics, antibiotics, and chemotherapy drugs
3. alcoholism and cirrhosis
4. heart failure
5. kidney disease
2) Neurology (10Marks)
A) Link to patient details:
A 40 Year Old Male with Complaints of Irrelevant Talking
Qno 1 : What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS )
The 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: With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.
Two important brain communication systems affected by alcohol involve the neurotransmitters: gamma-aminobutyric acid (GABA )and glutamate.
* The GABA system :
* The glutamate system :
The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures.
Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function.
* SYMPTOMS ETIOLOGY : Irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes Thiamine Deficiency.
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 .
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.
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.
PRIMARY ETIOLOGY : 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.
Question no 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 )
1. Thiamine helps the body cells change carbohydrates into energy. It has been used
as a supplement to cope with thiamine deficiency
2. 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
3. Pregabalin reduces the synaptic release of several neurotransmitters, by binding to alpha2-delta subunits, to reduce neuronal excitability and seizures.
4. Lactulose is used in preventing and treating clinical portal-systemic encephalopathy
MOA : By decreasing the intestinal production and absorption of ammonia.
5. Potchlor liquid is used to treat low levels of potassium in the body.
Question no 3 : Why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?
ANS )
Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.
Question no 4 : What is the reason for giving thiamine in this patient?
ANS )
* Chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine.
* VIT 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.
Question no 5 : What is the probable cause for kidney injury in this patient?
ANS )
* The kidneys have an important job as a filter for harmful substances
Alcohol causes changes in the function of the kidneys and makes them less able to filter the blood alcohol also affects the ability to regulate fluid and electrolytes in the body.
* In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure.
*High blood pressure is a common cause of kidney disease.
Question no 6 : What is the probable cause for the normocytic anaemia?
ANS )
1. Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bone marrow and the metabolism of iron .
2.Alcohol causes a affect on progenitor cells of blood causing decreased WBC , RBC.
3. Alcohol decreases iron absorption from intestine .
Question no 7 : Could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
ANS )
YES . As the patient is diabetic the chance of ulcer formation increases
In a patient of chronic alcoholic the immune 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:
A 52 year old male with Cerebellar Ataxia
Question no 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 patients problem?
ANS )
* Timeline of the patient is as follows-
* 7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
* 4 days back- Patient consumed alcohol; He developed giddiness that was sudden 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 location- 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.
Question no 2 :What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS )
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.
Question no 3 : Did the patients history of denovo hypertension contribute to his current condition?
ANS )
* 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.
Question no 4 : Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS )
* Relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
1. 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
2. Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
*According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral hemorrhage and a 1.8 increased chance of subarachnoid hemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.
Heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
So 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:
A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS,PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS, RADIATING PAIN ALONG LEFT UPPER LIMB
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A) *Evolution of symptoms :Patient was normal 8 months back then developed b/l pedal edema which gradually progressed.
Aggerevated in sitting and standing position, relived on taking medication
*Palpitations :since 5days, sudden in onset which is more during night
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 : Cardiovascular System
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 spondylosis
Question no 2 : 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, mineralocorticoid 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
Question no 3 : What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS ) Changes seen in ECG :
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves
In Severe cases :ventricular fibrillation, rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D) Link to patient details:
55years old patient with seizures
Q1 : Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANS ) Due to brain stroke there will be change in the electric impulse transmission in the brain..so this causes the seizures.
Question no 2 : In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
ANS ) 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:
A 48 year old male with seizures and altered sensorium
Question no 1 : What could have been the reason for this patient to develop ataxia in the past 1 year?
ANS ) History of multiple falls and history of minor head inuries may cause damage to part of brain mainly cerebellum which could have been the reason for this patient to develop gait in the past 1 year .
Question no 2 : What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANS )
Alcohol has numerous adverse effects on the various types of blood cells and their
functions.
1. For example, heavy alcohol consumption can cause generalized
suppression of blood cell production and the production of structurally abnormal
blood cell precursors that cannot mature into functional cells.
2. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia.
3. 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.
4. Alcohol adversely affects the platelets and other components of the blood-clotting system. Heavy alcohol consumption thus may increase the drinker’s risk of suffering a stroke.
F) Link to patient details:
30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWERLIMB
Questions
1) Does the patient's history of road traffic accident have any role in his present condition?
ANS )
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 : 3 What is the drug rationale in CVA?
DRUG RATIONALE :
SUPPORTIVE MEASURES :
1. Oxygenation
2. Anti Hypertensives ( Labetalol 10-20mg IVP or 1-5mg/min CIV (Nicardipin 2.5-15mg/hr )
3. Insulin
4. Antipyretics
SPECIFIC TREATMENT :
1. Thrombolytic agents ( Alteplase 0.9mg/kg i.v )
2. Other Plasminogen Activators ( Streptokinase , Urokinase )
3. Anti Coagulants ( Heparin 5000units 2-3times/day , LMW Heparin , Warfarin 2.5-10mg/day , Dabigatran )
4. Antiplatelets (Aspirin 80-325mg/day PO
Clopidogrel 75mg/day PO )
FOR CEREBRAL EDEMA & INCREASED ICP : Mannitol 0.25-0.5gm/kg i.v over15 mins given 6hrly
IF SEIZURES PRESENT : Antiepileptic Drugs should be given
FOR PREVENTION OF SECONDARY ATTACK : Combination Antiplatelet Therapy
QUESTION NO : 4 Does alcohol has any role in his attack?
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??
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) Link to patient details:
A 50 YEAR OLD MALE WITH CERVICAL MYELOPATHY
Question no 1 : What is myelopathy hand ?
MYELOPATHY HAND :
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.
The main clinical features are localized wasting and weakness of the extrinsic and intrinsic hand muscles, but not accompanied by either sensory loss or spastic quadriparesis.
This Characteristic signs permit the distinction between myelopathy and changes due to nerve root or peripheral nerve disorder.
Question no 2 : What is 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 : HOFFMAN'S REFLEX :
The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down. The reflexive pathway causes the thumb to flex and adduct quickly. This test is 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:
A 17 year old female with seizures
Question no : 1 What can be the cause of her condition ?
Patient has Iron deficiency Anaemia which may have lead to Acute cortical vein thrombosis with hemorrhagic venous infarction which leads to Seizures.
1. Seizures are common consequences of cerebral venous and sinus thrombosis
2. Acute symptomatic seizures frequently associate with focal neurological deficits and supratentorial lesions
Question no 2 : What are the risk factors for cortical vein thrombosis?
ANS:
Risk factors for children and infants include:
Problems with the way their blood forms clots
1. Sickle cell anemia
2 Chronic hemolytic anemia
3 Beta-thalassemia major
4 Heart disease — either congenital (you're born with it) or acquired (you develop it)
5 Iron deficiency
6 Certain infections
7 Dehydration
8 Head injury
For newborns, a mother who had certain infections or a history of infertility
Risk factors for adults include:
1. Pregnancy and the first few weeks after delivery
2. Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
3 Cancer
4 Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
5 Obesity
6 Low blood pressure in the brain (intracranial hypotension)
7 Inflammatory bowel disease like Crohn’s disease or ulcerative colitis.
Question no 3 : There was seizure free period in between but again sudden episode of GTCS why? resolved spontaneously why?
Question no 4 :What drug was used in suspicion of cortical venous sinus thrombosis?
ANS )
Initially Patient was given inj Lorazepam 8mg iv stat Leviteracetam 1gm iv stat,inj sodium valproate 800mg stat started on inj Midazolam 0.2mg/kg/hr and escalated upto 2mg/kg/hr,inj Clexane 0.4ml/sc was started in suspicion of CSVT,inj Mannitol 20gmTID.
CARDIOLOGY
A) Link to patient details:
A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS
Questions
1) What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
ANS ) 
-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.
-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. 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. Many of those with HFpEF also shared that they have other health problems that led to their diagnosis. Many of them also live with additional health conditions, including acid reflux (GERD), high blood pressure, kidney disease, and sleep disorders.
-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.
Question no 2 :Why haven't we done pericardiocenetis in this pateint?
ANS )
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.
Question no 3 : What are the risk factors for development of heart failure in the patient?
ANS )
IN THIS PATIENT:
NON MODIFICABLE:
1. Age
2. Gender
MODIFIABLE:
1.Hypertension
2.Smoking
3.Type 2 diabetes .
4.Kidney disease.
IN GENERAL RISK FACTORS :
Question no 4 : What could be the cause for hypotension in this patient?
ANS:
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) Link to patient details:
A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT
1) What are the possible causes for heart failure in this patient?
ANS:
1. Obesity
2. Alcohol
3. Diabetes
4. Hypertension
Question no 2 : What is the reason for anemia in this case?
ANS:
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?
ANS:
*The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to 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?
ANS:
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) Link to patient details:
A-Fib and Biatrial Thrombus in a 52yr old Male
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?
ANS )
*The anatomical site is 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?
ANS ) PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor
Mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
Mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
Mechanism: Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM: Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
Mechanism:
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.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
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?
ANS ) 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) Link to patient details:
67 year old patient with acute coronary syndrome
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?
ANS )
TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest
Anatomical localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause
- 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?
ANS )
Pharmacological Interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect).
Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks
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?
INDICATIONS:
i) Acute ST-elevation myocardial infarction (STEMI)
ii) Non–ST-elevation acute coronary syndrome (NSTE-ACS)
iii) Unstable angina.
iv) Stable angina.
v ) Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
vi) High risk stress test findings.
CONTRAINDICATIONS:
i) Intolerance for oral antiplatelets long-term.
ii)Absence of cardiac surgery backup.
iii) Hypercoagulable state.
iv) High-grade chronic kidney disease.
v) Chronic total occlusion of SVG.
vi) 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?
Although PCI is generally a safe procedure , it might cause serious certain complications like
1)Bleeding
2) Blood vessel damage
3) Allergic reaction to the contrast dye used
4) Arrhythmias
5) 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.
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[41] 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.
E) Link to patient details:
CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION
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?
ANS ) *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
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?
ANS ) PHARMACOLOGICAL INNTERVENTION :
1.TAB. ASPIRIN
Mechanism : Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
2.TAB ATORVAS
Mechanism : Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3.TAB CLOPIBB
Mechanism: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
Mechanism :Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
Mechanism : Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
Question no 3 : Did the secondary PTCA do any good to the patient or was it unnecessary?
ANS ) The second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.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.
PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as ‘use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value’.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm to the patients.
F) Link to patient details:
Question no 1 : How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Question no 2 : What is the rationale of using torsemide in this patient?
Torsemide was used because patient had cardiogenic pulmonary edema which caused shortness of breath in him.
Torsemide decreases fluid volume ( pulmonary edema ) as it is a diuretic.
It blocks sodium potassium channels in ascending loop of henle and thus blocking their absorption leading to excretion in urine.
Question no 3 : Was the for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
ANS ) May be prophylactic use because the patient did not have UTI symptoms like urgency or dysuria .
4) Gastroenterology (& Pulmonology) 10 Marks
A) Link to patient details:
33 YEAR OLD MAN WITH
PANCREATITIS, PSEUDOCYST
AND LEFT BRONCHO-PLEURAL FISTULA
Question no 1 : ANS ) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS ) *Evolution of symptomatology :
H5 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
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 and its metabolites and also 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?
ANS )
1) ING. MEROPENAM ; TID for 7 days
2) ING. METROGYL 500 mg IV TID for 5 days
3) ING. AMIKACIN 500 mg IV BD for 5days
4) TPN ( Total Parenteral Nutrition )
5) IV NS / RL at the rate 12l ml per hour
6) ING. OCTREOTIDE 100 mg SC , BD
7) ING. PANTOP 40 mg IV , OD
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
9) ING. TRAMADOL in 100 ml NS IV , OD
A) Non pharmacological interventions : Drains
(malecot & icd )
Even i will follow the same approach
B) Link to patient details:
CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN
Questions
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
ANS ) The cause of Dyspnea might be PLEURAL EFFUSION
Question no 2: Name possible reasons why the patient has developed a state of hyperglycemia?
*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?
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
(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?
Plan of action and Treatment :
Investigations:
✓ 24 hour urinary protein
✓ Fasting and Post prandial Blood glucose
✓ HbA1c
✓ USG guided pleural tapping
Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly
C) Link to patient details:
A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension
Question no 1 : What is the most probable diagnosis in this patient?
* Its most probably looks like Hollow viscus perforation though it's not clear on the X ray
Acute history suggests of intestinal obstruction which could have led to perforation and then the patient must have gone into shock
From then on, probably Multiorgan dysfunction.
* Also, past history ask for tuberculosis. One of the extra-pulmonary manifestation of tb can involve the intestine and cause intestinal obstruction. It's more common than we think
Question no 2 : What was the cause of her death?
ANS )
As for the cause of death, Day 1 of post I would suspect Lung Atelectasis.
Question no 3 : Does her NSAID abuse have something to do with her condition? How?
ANS ) NSAID abuse could have also contributed to the kidney injury.
5) Nephrology (and Urology) 10 Marks
A) Link to patient details:
Post TURP with non oliguria ATN
Diabetic Nephropathy
Question no 1 : What could be the reason for his SOB ?
Ans) Due to improper functioning of kidneys in patient there may FLUID OVERLOAD which lead to SOB .
Fluid overload is frequently found in critically ill patients with acute kidney injury (AKI).
Question no 2 : Why does he have intermittent episodes of drowsiness ?
Question no 3 : Why did he complaint of fleshy mass like passage in his urine?
Fleshy mass in urine could be sediment which is often composed of : microscopic particles , various kinds of cells , debris from your urinary tract , mucus .
Also Diabetes affects how you metabolize fat. Ketones, which are a byproduct of this process, can be released in your urine and appear as sediment. Bladder injury.
Question no 4 : What are the complications of TURP that he may have had?
1. Bleeding.
2. Blood in the urine after surgery.
3. Electrolyte abnormalities.
4. Infection.
5. Loss of erections.
6. Painful or difficult urination.
7. Retrograde ejaculation (when ejaculate goes into the bladder and not out the penis)
B) Link to patient details:
An Eight year old with Frequent Urination
Question no 1 : Why is the child excessively hyperactive without much of social etiquettes ?
ANS ) Child may be excessively hyperactive as a result of Attention Deficit Hyperactive disorder. Also children of that age are usually active.
Question no 2 : Why doesn't the child have the excessive urge of urination at night time ?
ANS ) During sleep the hyperactive state of child may be supressed and so he is not having urge for urination.
Question no 3 : How would you want to manage the patient to relieve him of his symptoms?
ANS ) * Reassurance to parents
* Antidiuretic Drugs to reduce urine frequency.
* Refer to pyschology dept. for further treatment of ADHD ( if confirmed )
* If ADHD : Treatment : 1.Behavior therapy, including training for parents
2.Medication ( stimulants or non stimulants )
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
A) Link to patient details:
A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH
Question no 1 : Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANS )
Difficulty in swallowing
Cough on taking foods and liquids
Weight loss
Laryngeal crepitus ?
There is no proper clinical history and physical findings regarding tracheo oesophageal fistula.
Question no 2 : What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANS )
As the patient has low CD4 count and was on ART for the past 2 months and recently diagnosed as TB positive there are chances of patient developing immune reconstitution inflammatory syndrome.
7) Infectious disease and Hepatology
Link to patient details:
LIVER ABSCESS
Question no 1 : Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors
present in it ? What could be the cause in this patient?
ANS )
* 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.
*Though Alcoholism is a predisposing factor, it has no role in the aetiology and the liver function tests also did not show much alteration
Question no 2 : What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
ANS )
* Amoebic liver abscess is more common than pyogenic liver abscess. Commonly occurs in young alcoholic males.
Alcohol is only the predisposing factor of liver abscess but not the true etiological agent. Chronic alcoholism leads to Fatty liver and liver cirrhosis (Alcohol liver disease) which eventually results in liver abscess if liver is infected with entamoeba histolytica or other pathogenic organisms.
Question no 3: Is liver abscess more common in right lobe ?
ANS )
YES ,liver abscesses occur more common in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.
Question no 4 : What are the indications for ultrasound guided aspiration of liver abscess ?
ANS )
Indications for ultrasound guided aspiration of liver abscess are :
Size 5.5 cm or more (in diameter), lesion who appear to be superinfected, large abscess impending to rupture, thin rim of liver tissue surrounding the abscess (less than 10mm) and failure of medical management following noninvasive treatment for 4 to 5 days.
B) Link to patient details:
CASE DISCUSSION ON LIVER ABCESS
Question no 1 : Cause of liver abcess in this patient ?
ANS )
* 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 ?
ANS )
As mentioned earlier in practice we treat both pyogenic and amoebic liver abcess empirically.
* So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
* Next we administer patient with analgesic and antipyretic such as tab.dolo 650mg & tab.Ultracet , to relieve pain and fever.
##Abcess may get ruptured if untreated and cause peritonitis and shock.
Question no 3 : Why do we treat here ; both amoebic and pyogenic liver abcess?
ANS )
We treat both pyogenic and amoebic liver abcess empirically.
So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
Question no 4 : Is there a way to confirm the definitive diagnosis in this patient?
ANS )
Based on right hypochondriac and epigastric pain , fever
USG finding of hyperechoic mass in right lobe of liver along with other supportive investigations like leucocytosis (suggestive of infection/inflammation) and ALP ( Alkaline phosphatase ) rise in LFT is a suggestive diagnosis of LIVER ABCESS.
* Considering the following factors:
1) Age of the patient (21) - young & gender- male
2) Single abcess,
3) Right lobe involvement,
# The abcess is most likely to be AMOEBIC LIVER ABCESS.
We can also do USG guided aspiration to confirm the definitive diagnosis in this patient and also the stool culture.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) Link to patient details:
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 aetiology of the patient's problem?
ANS )
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
Patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhino orbital mucormycosis . The fungus enters the sinuses from the environment and then the brain.
The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is also associated with the occurrence of CVA.
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?
Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients.
Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing
9) Infectious Disease (Covid 19)
for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
1) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc).
10) Medical Education: (10 marks)
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research :
MY EXPERIENCE :
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 !!
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