Online blended bimonthly assignment toward summative assessment for the month of May 2021
NAME : M. Tharun Kumar
ROLL NO : 87
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.
1) Pulmonology (10 Marks)
A) Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS :
Evolution of symptomology and Event timeline :
- 20 years ago - SOB Grade I for a week occured every year for the same duration.
- 18 years ago - Polyuria and was diagnosed with DM
- 12 years ago - SOB Grade I 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.
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.
3) What could be the causes for her current acute exacerbation?
Cause for current acute excerbation - it could be due any infection
4. Could the ATT have affected her symptoms? If so how?
Yes ATT affected her symptoms
Isoniazid and rifampcin - nephrotoxic - raised RFT was seen
5.What could be the causes for her electrolyte imbalance?
A number of things can cause an electrolyte imbalance, including:
fluid loss from heavy exercise or physical activity
medications such as diuretics, antibiotics, and chemotherapy drugs
alcoholism and cirrhosis
heart failure
kidney disease
2) Neurology (10 Marks)
A) Link to patient details:
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:-
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.
Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.
The GABA system:
GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling.
The glutamate system:
The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors.
THE PATHOPHYSIOLOGY:
Thiamine, 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.
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 .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. Used as 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.
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?
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?
Chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine. 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?
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?
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.alcohol decreases iron absorption from intestine .
7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
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:
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 patients problem?
ANS.
Timeline of the patient is as follows-
7 days back- Patient gave a history of giddiness 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.
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 beta histine, 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.
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.
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
D) Tab Atorvostatin 40mg- This is a statin
MOA- .
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
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.
G) Tab MVT- This is methylcobalamin.
Mainly given in this case for vitamin B12 deficiency.
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.
.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS.
Ischaemic stroke- more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
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.
The risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
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:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS :
Evolution of symptoms
8 months back bilateral 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 palpitatuons 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.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANS:
A) Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics.
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS:
A) changes seen in ECG :
Earliest change - decreased T-wave amplitude, ST depression, Twave - and inversion or flat , prolonged PR interval; presence of Uwaves
In Severe cases : ventricular fibrillation , rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D) Link to patient details:
QUESTIONS:
1. 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
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:
Questions:
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 .
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. 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. 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. Finally, 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:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
ANS :
Road traffic accident has no role in present patient condition . RTA mainly causes hemorrhagic stoke but where as in this patient he had ischaemic stroke which is mainly due to narrowing of blood vessels supplying brain.
2.What are warning signs of CVA?
ANS :
The five warning signs of stroke are:
Sudden onset of weakness or numbness on one side of the body.
Sudden speech difficulty or confusion.
Sudden difficulty seeing in one or both eyes.
Sudden onset of dizziness, trouble walking or loss of balance.
Sudden, severe headache with no known cause.
3.What is the drug rationale in CVA?
ANS :
GENERAL 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 :
5. 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
4. Does alcohol has any role in his attack?
ANS :
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.
5.Does his lipid profile has any role for his attack??
ANS :
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:
1) what is Myelopathy hand ?
A characteristic dysfunction of the hand has been observed in various cervical spinal disorders when there is involvement of the spinal cord. 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 characteristic nature of the signs permit the distinction between myelopathy and changes due to nerve root peripheral nerve disorder.
2) What is Finger Escape :
- Hold fingers adducted and extended
- Small and Ring fingers fall into flexion and abduction ( usually with in 30 secomds )
3) What is Hoffman's Reflex ?
- Suddenly extend middle finger DIP ( Is done by flicking the nail of middle or ring finger )
- To produce Reflex finger flexion
- When asymmetric indicative spinal cord impingement .
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
ANS :
Patient has Iron deficiency Anaemia which may have lead to Acute cortical vein thrombosis with hemorrhagic venous infarction which leads to Seizures.
Seizures are common consequences of cerebral venous and sinus thrombosis
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
- Sickle cell anemia
- Chronic hemolytic anemia
- Beta-thalassemia major
- Heart disease — either congenital (you're born with it) or acquired (you develop it)
- Iron deficiency
- Certain infections
- Dehydration
- Head injury
- For newborns, a mother who had certain infections or a history of infertility
Risk factors for adults include:
- Pregnancy and the first few weeks after delivery
- Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
- Cancer
- Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
- Obesity
- Low blood pressure in the brain (intracranial hypotension)
- Inflammatory bowel disease like Crohn’s disease or ulcerative colitis.
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
ANS:
Focal seizures where there is no LOC which later turned into general seizures. This is the reason for seizure free period in between but again sudden episode of GTCS.
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.
3) Cardiology (10 Marks)
A) Link to patient details:
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.
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.
RISK FACTORS :
Sedentary lifestyle
High blood pressure
Sleep apnea
Other heart conditions
-HFrEF are more likely to have had surgery, including surgery to implant a pacemaker or other heart rhythm control device.
HFpEF have never had surgery to treat their heart failure or had a device implanted.
2.Why haven't we done pericardiocenetis in this pateint?
ANS :
Pericardiocentesis is a procedure which is done when the pericardial effusion is not 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?
ANS: 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?
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:
1.What are the possible causes for heart failure in this patient?
ANS:
obesity
alcohol
diabetes
hypertension
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.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
ANS:
This is due to Type II 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.
Risk factors that may lead to foot ulcers :
Obesity and Weight-related
Poor quality or fitting of the footwear.
Improper care of the nails of the toe.
Heavy intake of alcohols and tobacco.
4. What sequence of stages of diabetes has been noted in this patient?
ANS:
Alcohol (Intial factor which is responsible)
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:
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:Thee 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.
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.
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.
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.
GENERAL RISK FACTORS INCLUDE :
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 .
D) Link to patient details:
Questions-
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
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)
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
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 .
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).
3) What are the indications and contraindications for PCI?
INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
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
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it.
⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
. Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk.
.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.
E) Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
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
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 INTERVENTION
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:
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.
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. 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.
F) Link to patient details:
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
2. What is the rationale of using torsemide in this patient?
-Because it decreases fluid volume (edema) as it is a diuretic.
-It blocks Na+ K+ channels in ascending loop of henle and blocks absorption leading to excretion of urine.
-It also reduces Cardio pulmonary edema reducing SOB in the patient.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ceftriaxone is cephalosporin for treating the bacterial infections if any.
It is mainly used as prophylactic for UTI and not for the treatment as the patient do not show any symptoms.
4) Gastroenterology (& Pulmonology) 10 Marks
A) Link to patient details:
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Evolution of symptomatology
5 years back-1st episode of pain abdomen and vomiting
Stopped taking alcohol for 3 years
1 year back - 5 to 6 episodes of pain abdomen and vomiting 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
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?
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:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
the cause of dyspnea might be PLEURAL EFFUSION
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
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
These are the non specific markers for alocholic Fatty liver disease.
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:
Possible Questions :-
1) what is the most probable diagnosis in this patient?
It 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.
2) What was the cause of her death?
After leaving the hospital, the patient went to Hyderabad and underwent an 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.
3) Does her NSAID abuse have something to do with her condition? How?
NSAID abuse could have also contributed to the kidney injury.When the kidney is in a salt retaining state or when there is renal vascular damage, NSAIDs can reduce renal blood flow and glomerular filtration rate producing acute renal failure that is reversible upon discontinuation of the drug.
5) Nephrology (and Urology) 10 Marks
A) Link to patient details:
1. What could be the reason for his SOB ?
ANS :
Due to improper functioning of kidneys there may be fluid overload which may be the reason for his SOB.
2. Why does he have intermittent episodes of drowsiness ?
ANS :
3. Why did he complaint of fleshy mass like passage in his urine?
ANS :
Sediment, or particles, in your urine can make it look cloudy.
Sediment is often composed of:
- microscopic particles
- various kinds of cells
- debris from your urinary tract
- mucus
Diabetes affect the metabolism of fat. Ketones which are byproducts of this may appear in the urine as sediment.
4. What are the complications of TURP that he may have had?
ANS :
- Bladder injury.
- Bleeding.
- Blood in the urine after surgery.
- Electrolyte abnormalities.
- Infection.
- Loss of erections.
- Painful or difficult urination.
- Retrograde ejaculation (when ejaculate goes into the bladder and not out the penis)
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
ANS :
The most obvious sign of ADHD (ATTENTION DEFICIT HYPERACTIVE DISORDER) is hyperactivity. While many children are naturally quite active, kids with hyperactive symptoms of attention deficit disorder are always moving.
2. Why doesn't the child have the excessive urge of urination at night time ?
ANS :
During the time of sleep the hyperactive state of the child may be supressed and that could the reason for decreased urge of urination at night time .
It is clearly evident as there is no history of bed wetting.
3. How would you want to manage the patient to relieve him of his symptoms?
ANS :
Types of treatment include :
- Behavior therapy, including training for parents; and reassurance
- Anti diuretics - to decrease the frequency of urination
- Refer to psychology for further treatment for ADHD if confirmed.
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient details:
Questions:
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.
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:
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
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.
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.
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:
QUESTIONS:
1) Cause of liver abcess in this patient ?
ANS :
Cause of liver abcess may be due to contamination of food / fluid history of which is not mentioned.
malnutrition and poor personal hygiene are also the risk factors of liver abcess.
## Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
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.
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.
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.
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.
https://academic.oup.com/bmb/article/132/1/45/5677141
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:
Questions :
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?
3 years ago- diagnosed with hypertension
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
18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema.
4 days ago-
a. patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
b. towards the evening patient periorbital oedema progressed
c. serous discharge from the left eye that was blood tinged
d. 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 patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA
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
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
What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Steroids reduce inflammation in the lungs for Covid-19 .But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients. Sudden apparent rise in covid cases is due to use of steroids for the treatment of covid 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)
As these patients are currently taking up more than 50% of our time we decided to make a separate log link her
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m
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 char
2) In the master chart classify the patient case report logs into mild, moderate severe an
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 requirement
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:
The concept of telemedicine learning is new to us and is appreciated very much. Though it is not much as effective as live learning where we can touch the patients and examine them. But in these difficult times also we are able to take cases and present them and learn new things everyday. Iam very thankful to the whole medicine department who are helping us through this midst times and giving there every minute to us.
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