Online blended bimonthly assignment toward summative assessment for the month of May 2021
GENERAL MEDICINE case study of may
NAME: B.AISHWARYALAXMI
ROLL NO: 152
SEMESTER: 8th
I have been given the following cases to solve in an attmept to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and coem up with a treatment plan.
This is the link of the questions asked regarding the cases:
medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1)PULMONOLOGY
First case :
A 55 Year Old Female with Shortness of Breath, pedal Edema and Facial puffiness.
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?
Answer:
History:- I) Shortness of breath since 20years
• Her first episode 20 years ago lasted for 1 week and occured in the month of January while working in a paddy field and relieved upon taking medication.
•For the next 8 years the patient has suffered from similar episodes every year each lasting aproximately 1 week and occurring around January (when she worked at the paddy fields) and relieved upon taking medication.
•12 years ago she had another episode which lasts for 20 days and relieved upon medication during hospitalisation.
•Her latest episode of SOB which is grade-II started 30days ago, SOB was insidious in onset and gradual in progression which was relieved upon rest and from 2days ago she is having SOB even at rest of grade-IV which was not relieved by nebulisers.
II) 20days ago she showed signs of bronchiectasis by HRCT
III) She was diagnosed with hypertension 20days back
IV) Pedal edema and Facial puffiness since 15days.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1)Head end elevation
2)O2 inhalation to maintain SPO2 above 92%
3)Intermittent BiPAP for 2hrs
4)Inj. AUGUMENTIN 1.2gm IV BO
Composition:1 g amoxicillin (as amoxicillin sodium) and 200 mg clavulanic acid (as potassium clavulanate)
Mechanism of action: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.
5)TAB. AZITHROMYCIN 500mg OD
Mechanism of action: Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit
6) INJ. LASIX IV BO if SBP greater than 110 mmHg
Mechanism of action: Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours.
7)TAB PANTOP 40mg PO OD
Mechanism of action: To inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.
8)INJ. HYDROCORTISONE 100 mg IV
Mechanism of action: Binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.
9)NEB. with IPRAVENT, BUDECORT 6 hrly
Mechanism of action: Ipravent belongs to a group of medicines known as anticholinergic bronchodilators. Anticholinergic bronchodilators work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.
• Budesonide is a potent topical anti-inflammatory agent. It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT).
10)TAB PULMOCLEAR 100 mg PO OD
Mechanism of action: They belong to the class of bronchodilators and mucolytics, respectively. Pulmoclearworks by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.
11)chest physiotherapy
12)GRBS 6 hrly
13)INJ. HAI SC ( 8 am- 2pm- 8pm)
14)Temp, BP, PR, SPO2 monitoring
15)I/O charting
16)INJ. THIAMINE 1 amp in 100 ml of NS
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
3) What could be the causes for her current acute exacerbation?
Answer: Infection of her lungs or airways by Allergens (paddy field)
4. Could the ATT have affected her symptoms? If so how?
Answer: Yes it can affect as on 30/4/21 she had a sputum examination which was negative (-) for AFB. On 4/5/21 she was started on empirical ATT. This resulted in generalized weakness. A few days after ATT she started developing pedal edema and facial puffiness.
5.What could be the causes for her electrolyte imbalance?
Answer: Activation of the Renin-angiotensin-aldosterone-system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the ELECTROLYTE IMBALANCE during acute exacerbation of COPD.
NEUROLOGY:
1) FIRST CASE: Altered sensorium in 40Y/O Male.
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?
Answer:
•The patient was apparently asymptomatic 9 days ago, when he started talking, as well as laughing to himself, which was sudden in onset.It was associated with a decrease in food intake since 9 days.
•He also had short term memory loss since 9 days
•Previously, he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago.
•The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors.
•Diagnosed with diabetes 2years ago.
PRIMARY ETIOLOGY: Alcohol withdrawal
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1. IVF NS and RL @150ml/hr
2. Inj. 1amp THIAMINE in 100ml NS, TID
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
3. Inj. Lorazepam
Indication : altered sensorium
Mechanism of action: Lorazepam binds to the GABA Receptor at different allotsteric sites which facilitates the GABA action which increase the opening of calcium channels leads to membrane hyper polarisation and CNS depression.
4. T. Pregabalin 75mg /PO/BD
Mechanism of action:Pregabalin site of action is alpha 2- delta channels and reduces the synaptic release of several neurotransmitter apparently by binding to alpha2-delta subunits and possibly accounting to its actions to reduce neuronal excitability.
5. Inj. HAI S.C.- premeal
Mechanism of action:
Regular insulin is a short acting form of the synthetic hormone.it helps to move glucose from the blood into body’s cells.The cells then use this glucose for energy regular insulin typically starts to work within 30 mins to 1 hour of an injection
6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am
7. Lactulose 30ml/PO/BD
Indication : Liver disesase
Mechanism of action: The lactulose converts the ammonia in the colon is Ionised to ammonium ions that are incapable of being absorbed back into the circulation this facilitates the excretion of excess amount of ammonia.
8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours
Indication: to correct the electrolyte imbalance.
9. Syp Potchlor 10ml in one glass water/PO/BD
Indication: used for treating low potassium levels in the blood.
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Answer: It is due to kindling. Kindling refers to the phenomenon of increasingly severe withdrawal symptoms, including an increased risk of seizures, that occurs as a result of repeated withdrawal from alcohol or other sedative–hypnotics with related modes of action.
4) What is the reason for giving thiamine in this patient?
Answer: Thiamine replacement is the primary treatment for WKS in order to reverse mental status changes and prevent further disease progression. Parenteral thiamine is used in the acute treatment of Wernicke's since intestinal absorption of thiamine may be impaired, as in the case of alcoholics.
5) What is the probable reason for kidney injury in this patient?
Answer:As the patient is chronic alcoholic, due to alcoholism kidney tissue gets injured.
6). What is the probable cause for the normocytic anemia?
Answer: ↓ synthesis of
erythropoietin
→↓ stimulation of RBC production → normocytic, normochromic anemia. When patient have kidney disease, kidneys cannot make enough EPO. Low EPO levels cause red blood cell count to drop and anemia to develop. Most people with kidney disease will develop anemia. Anemia can happen early in the course of kidney disease and grow worse as kidneys fail and can no longer make EPO.7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Answer: Excessive alcohol can cause nutritional deficiencies and alcohol toxicity. These in turn can cause poor nutrition leading to poor wound healing and problems with the nerves (neuropathy). When the sensory nerves in the foot stop working, the foot can get injured and this leads to foot ulcers.
2) SECOND CASE: A 52 year old male with Cerebellar Ataxia.
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?
Answer:
History:- Patient has giddiness 7 days back and associated with 1 episode of vomiting on the same day.
•Patient was asymptomatic for 3 days, after which he consumed a small amount of alcohol He then developed giddiness, that was sudden in onset, continuous and gradually progressive.
•This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.
•He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.
•Patient has H/o postural instability
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1)Tab Veratin 8 mg PO TID
Mechanism of action: Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but strong effect on H3 receptors.
2)Inj Zofer 4 mg IV/TID
Mechanism of action: Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.
3)Tab Ecosprin 75 mg PO/OD
Mechanism of action: Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.
4)Tab Atorvostatin 40 mg PO/HS
Mechanism of action: 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.
5)BP monitoring- 4rth hourly
6)Tab Clopidogrel 75 mg PO/OD
Mechanism of action: The active metabolite of clopidogrelselectively 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.
7)Inj Thiamine 1 AMP in 100 ml NSPO/BD
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
8)Tab MVT PO/OD
3) Did the patients history of denovo HTN contribute to his current condition?
Answer: No
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Answer: Yes, Atrial fibrillation and alcohol Drinking excessive amounts of alcohol can trigger atrial fibrillation – a type of irregular heartbeat. Atrial fibrillation increases your risk of stroke by five times, because it can cause blood clots to form in the heart. If these clots move up into the brain, it can lead to stroke.
3)THIRD CASE: A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB
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?
Answer: Patient was normal 8 months back then developed b/l pedal edema which gradually progressed.
• 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
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Answer: Reason: recurrent hypokalemic periodic paralysis
•Risk factors: Risk factors associated with a low serum potassium levels (hypokalemia) include female gender, intake of medication (diuretics), heart failure, hypertension, low body mass index (BMI), eating disorder, alcoholism, diarrhea, Cushing's syndrome.
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Answer: ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalemia. Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.
Associated symptoms:
- Weakness and fatigue (most common)
- Muscle cramps and pain (severe cases)
- Worsening diabetes control or polyuria.
- Palpitations.
- Psychological symptoms (eg, psychosis, delirium, hallucinations, depression)
FOURTH CASE: 55years old patient with seizures.
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?
Answer: Occurrence of seizure due to brain stroke
Cells in the brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.
A seizure can affect you in many different ways such as changes to vision, smell and taste, loss of consciousness and jerking movements.
Mechanism: Seizure initiation is characterized by two concurrent events: 1) high-frequency bursts of action potentials, and 2) hypersynchronization of a neuronal population. The synchronized bursts from a sufficient number of neurons result in a so-called spike discharge on the EEG.
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?
Answer: Normally the “consciousness system”—a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness These functions involve a group of brainstem and forebrain areas that form the consciousness system and include the reticular formation of the brainstem, hypothalamus, basal forebrain, thalamus, and cerebral cortex.
Mechanism: Although many cognitive and behavioral processes occur without awareness, consciousness plays a critical role in cognitive mechanisms and forms the basis of our experience. An improved understanding of conscious mechanisms will provide insights into a variety of neurological disorders and new therapeutic approaches.
FIFTH CASE: A 48 year old male with seizures and altered sensorium.
E) Link to patient details:
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Answer: By the history, Patient is an alcoholic and he has change in his gait since a year are the findings which leads to cause of ataxia.
Mechanism:Damage from alcohol is a common cause ofcerebellar ataxia. In patients with alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech. It can also cause associated signs of peripheral neuropathy. Peripheral neuropathy is damage to the body's peripheral nervous system.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
Answer: Hemoglobin and its metabolites can exert deleterious effects on brain tissue through NO depletion and vasospasm, ROS production, stimulation of inflammatory response, inhibition of DNA repair, and glutamate release.
The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.
SIXTH CASE:
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
Answer: Yes
2.What are warning signs of CVA?
Answer: 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?
Answer: 1.Injection Mannitol 100ml/IV/TD
2.TAB Ecospirin 75 mg po/OD
3.TAB ATORVAS 40mg po/HS
4.BP/PR/TEMP/SP02 MONITORING (4th hourly)
5.RT FEEDS-100ml milk with protein powder(2nd hourly)
4. Does alcohol has any role in his attack?
Answer: 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??
Answer:His HDL cholesterol levels are low
low serum HDL-C was associated with an increased risk of stroke.
SEVENTH CASE:
A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY
G) Link to patient details:
Questions:
1)What is myelopathy hand ?
Answer: There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
Answer: 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".
3)What is Hoffman’s reflex?
Answer: Hoffman's sign or reflex is a test that doctors use to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.
EIGHTH CASE: A 17year old female with seizures
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
Answer:Iron deficiency anemia
2) What are the risk factors for cortical vein thrombosis?
- Answer: 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?
Answer: Causes: 1) micro vessel embolism
2)Might be increased area of haemorrhagic infarct that can cause compression of other areas and get seizure
3)There may be edema around infarct that can also compress surrounding to cause new seizure attack
4)might be midline shift increased and can cause seizure
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Answer: Heparin should be considered seriously in the management of cerebral venous thrombosis(CVT), with subsequent conversion to warfarin as maintenance therapy suggested. Subcutaneous low ̶ molecular-weight heparin (Lovenox) also has been used in patients with venous sinus thrombosis.
3) Cardiology (10 Marks)
A) Link to patient details:
A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Answer: Preserved ejection fraction(HFpEF) – also referred to as diastolic heart failure. The heartmuscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure.
HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease
2.Why haven't we done pericardiocenetis in this pateint?
Answer: It’s resolving : 2.07cms effusion at the time of admission -1.4mm at the time of discharge)
DM type 2 (since 1month)
So, No need of pericardiocentis.
3.What are the risk factors for development of heart failure in the patient?
Answer: Risk factors
- High blood pressure.
- Coronary artery disease
- Diabetes.
- Some diabetic and hypertensive medications.
• age
4.What could be the cause for hypotension in this patient?
Answer: Decreased venous return cause decreased cardiac output which results in hypotension.
B) Link to patient details:
A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT
Questions:
1.What are the possible causes for heart failure in this patient?
Answer: patient has diabetes since 30yrs back and also having diabetic triopathy(neuropathy-retinopathy - nephropathy), so there is an increased risk for heart failure
* Hypertension since 19yrs - important risk factor
* Chronic alcoholic since 40yrs, leads to decreased LVEFand causes LV dysfunction
* patient has elevated creatinine, chronic kidney disease, AST/ALT greater than 2,all of this are important risk factors for heart failure
2.what is the reason for anaemia in this case?
Answer: As he was chronic alcoholic, which impairs the production of precursors of RBC in bone marrow, also causes change in shape and functions of cells
Due to chronic kidney disease
Impaired renal clearance leading to decreased erythropoetin production-impaired production of rbc
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Answer: As he is diabetic, Leg and foot ulcers in diabetic patients have three common underlying causes: venousinsufficiency, peripheral neuropathy (neurotrophic ulcers), or peripheral arterial occlusive disease.
And he is alcoholic, Drinking alcohol (including wine or beer) can make your ulcer more painful, both from the stomach acid that may be produced and from the alcohol coming into contact with the ulcer itself.
4. What sequence of stages of diabetes has been noted in this patient?
Answer: four stages of type 2 diabetes are insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.
C) Link to patient details:
A-Fib and Biatrial Thrombus in a 52yr old Male
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?
Answer:Patient was apparently asymptomatic 2 days ago when he developed Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital.Patient also complains of decreased urine output since 2 days and Anuria since morning.
Anatomical localization is heart
Primary etiology is atrial fibrillation
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1) INJ. Dobutamine 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg.
Mechanism of action: Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine.
2) TAB. Digoxin 0.25mg OD 5/7 and INJ. Unfractionated Heparin 5000 IU TID.
Mechanism of action: 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.
3) TAB. Carvediol 3.125mg BD
Mechanism of action: Carvedilol reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevents a response to the sympathetic nervous system, leading to decreased heart rate and contractility.
4) INJ. Unfractionated Heparin Infusion @5ml/hr
Mechanism of action: It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. ... By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.
5)TAB. Acetyl cysteine 600mg PO TID.
Mechanism of action: Acetylcysteine is a sulfhydryl compound and acts to increase synthesis of glutathione in the liver. Glutathione subsequently acts as an antioxidant and facilitates conjugation to toxic metabolites, particularly the toxic metabolites of acetaminophen.
6)TAB. Acitrom 2mg OD
Mechanism of action: 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
Other medications used during the course in hospital -
1. TAB. Cardivas3.125mg PO/BD
2. TAB. Dytor 10mg PO/OD
3. TAB Pan D 40mg PO/OD
4. TAB. Taxim 200mg PO/OD
5. INJ. Thiamine 100mg in 50ml NS IV/TID
6. INJ. HAI S.C 8U-8U-6U
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Answer: The pathophysiology of CRS can be attributed to two broad categories of "hemodynamic factors" such as low cardiac output, elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors or "cardiorenal connectors" such as neurohormonal and inflammatory activation.[5] It was previously believed that low cardiac output in heart failure patients result in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of these patients will result in hypovolemia and pre-renal azotemia.
In addition, CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.[3]Therefore, there must be additional mechanisms involved in the progression of CRS. Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to worsening kidney function.[3]
In addition, many neurohormonal and inflammatory agents are implicated in the progression of CRS. These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which can result in myocardial hypertrophy and necrosis.
Other cardiorenal connectors include renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, inflammatory factors and abnormal activation of the sympathetic nervous system, which can cause structural and functional abnormalities in both heart and/or the kidney. There is a close interaction within these cardiorenal connectors as well as between these factors and the hemodynamic factors which makes the study of CRS pathophysiology complicated.
4) What are the risk factors for atherosclerosis in this patient?
Answer:
- High cholesterol and triglyceride levels.
- High blood pressure.
- Smoking.
- Type 1 diabetes.
- Obesity.
- Physical inactivity.
- High saturated fat diet.
5) Why was the patient asked to get those APTT, INR tests for review?
Answer: Standard coagulation screening tests such as activated partial thromboplastin time (APTT), prothrombin time (PT), and the international normalized ratio (INR) are important constituents of basic examinations in clinical laboratories. APTT can be used as an indicator of intrinsic coagulation pathway activity, and a short APTT is linked to increased thrombin generation and increased risk for thrombosis.
D) Link to patient details:
67 year old patient with acute coronary syndrome
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?
Answer: History:- She had H/O heartburn like episodes since a year. They were relived without use of any medication.
She has H/O TB diagnosed 7 months ago for which she completed the course of medication a month ago.
shortness of breath (SOB) since 1/2 hour.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: TAB MET XL 25 MG/STAT.
Mechanism of action: Met XL 50 Tablet works by blocking the effects of some chemicals on your heart and blood vessels. It slows down your heart rate and helps it to beat with less force.
3) What are the indications and contraindications for PCI?
Answer: Clinical indications for PCI include the following:
- 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 to Percutaneous Coronary Interventions
- Lack of cardiac surgical support.
- Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
- Coagulopathy.
- Hypercoagulable states.
- Diffusely diseased vessels without focal stenoses.
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?
Answer: Medical therapy with high dose statins is preferred over balloon angioplasty in patients with mild anginal symptoms.
PCI is preferred over medical therapy has:
1) severe symptoms
2) failed medical therapy
3) high risk coronary anatomy
4) worsening LV function
OVERTREATMENT: The main and worst consequences of overdiagnosis is overtreatment if an incident lesion or disease which is unlikely to have benefits for the patient. At the same time the likely interventions like surgery, radiation and chemotherapy can have side effects resulting in significant morbidity and fatalities can occur. As over diagnosis is some non neoplastic conditions leads to over prescription and over medicalisation , and resulting in many undesirable and sometimes dangerous side effects.
C) Link to patient details:
A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension
Possible Questions :-
1) what is the most probable diagnosis in this patient?
Answer: Ruptured liver abcess
Grade 3 RPD in right kidney
2) What was the cause of her death?
Answer: Her cause of death might be due to sepsis
3) Does her NSAID abuse have something to do with her condition? How?
Answer:she had grade-3 RPD changes in right kidney
She may be having underlying CKD which is secondary to her NSAID abuse (Analgesic nephropathy)
5) Nephrology (and Urology)
A) Link to patient details:
1.what could be the cause for his SOB
Answer:His sob is due to Acidosis which was caused by Diuretics
2. Reason for Intermittent Episodes of drowsiness
Answer: Hyponatremia was the cause for his drowsiness
3.why did he complaint of fleshy mass like passage inurine
Answer:plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him
4. What are the complicat ions of TURP that he may have had
Answer: Difficulty micturition
Electrolyte imbalances
Infection
B) Link to patient details:
An Eight year old with Frequent Urination
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
Answer:
This might be because of :
There is no association with
Flank pain
Lower abdominal pain
Burning sensation while micturating
Fever
Malaise
2. Why doesn't the child have the excessive urge of urination at night time ?
Answer:Since the child does not get the urgency to urinate when he is asleep, there can be a chance of the manifestation being psychosomatic, or as a result of an undiagnosed anxiety disorder , or a stressor triggering this manifestation.
3. How would you want to manage the patient to relieve him of his symptoms?
Answer:The child need counselling sand therapies
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient details:
A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Answer: Tracheoesophageal fistula is suggested by copious salivation associated with choking, coughing, vomiting, and cyanosiscoincident. Esophageal atresia and the subsequent inability to swallow typically cause polyhydramnios in utero.
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Answer: There are chances that patient may develop IRIS. The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
Link to patient details: LIVER ABSCESS
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 ?
Answer: Yes it can cause as he is drinking toddy since 30years. Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy is a local alcoholic beverage consisting of fermented palm juice.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
Answer: proved that alcoholism, mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver.
3. Is liver abscess more common in right lobe ?
Answer: 50% of solitary liver abscesses occur 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 ?
Answer: The indications for drainage of amebic liver abscessinclude the following:
- Presence of a left-lobe abscess more than 10 cm in diameter.
- Impending rupture and abscess that does not respond to medical therapy within 3-5 days.
B) Link to patient details:LIVER ABSCESS
QUESTIONS:
1) Cause of liver abcess in this patient ?
Answer: Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy is a local alcoholic beverage consisting of fermented palm juice.
2) How do you approach this patient ?
Answer: Based on right hypochondriac and epigastric pain , fever and USG findings
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
Answer: Amoebic liver abscess: The first line treatment in uncomplicated amebic abscess should be amebicidial drugs. Metronidazole is the drug of choice and has replaced the use of emetine and chloroquine. Metronidazole is effective against both the intestinal and hepatic phase. 750 mg three times a day for 7–10 days is recommended.
Payogenic liver abscess: Treatment usually consists of placing a tube through the skin into the liver to drain the abscess. Less often, surgery is needed. You will also receive antibiotics for about 4 to 6 weeks. Sometimes, antibiotics alone can cure the infection.
4) Is there a way to confirmthe definitive diagnosis in this patient?
Answer: Analysis of reports and diagnosis:
*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 LIVERABCESS.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 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?
Answer:18/04/21 He went to local PHC for COVID 19 vaccination.. Since that night patient is complaining of Fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication...
No c/o cold and cough
Followed by patient is having similar complaints after three days and he visited local hospital which is not subsided by medication ( Antipyretics) ( not taken medication such as steroids, oxygen therapy, anti virals)
On 28/04/21 , c/o Generalized weakness and facial puffiness and periorbital edema.. And also patient is in drowsy state..
On 04/05/21, patient presented to casualty In altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb...
primary etiology: Diabetes can lead to mucormycosis
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?
Answer: Proposed management -
Inj. Liposomal amphotericin B according to creatinine clearence
Loading dose 30mg/IV over 2-6 hrs
Maintenance dose 60mg / IV once a day
Treatment modalities:
The successful treatment of mucormycosis requires four steps: 1) early diagnosis; 2) reversal of underlying predisposing risk factors, if possible; 3) surgical debridement where applicable; and 4) prompt antifungal therapy
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Answer:Thus far, this surge has been attributed to the improper use of steroids to treat Covid-19 patients, coupled with poorly managed diabetes. But steroids in themselves are not the villains.
“Systemic (oral and intravenous) corticosteroids have been proven to reduce mortality in Covid-19,” Lancelot Pinto, consultant pulmonologist at Mumbai’s Hinduja Hospital, told Quartz. “The largest trial, Recovery, which proved this beyond a reasonable doubt among individuals who had low oxygen levels, used them in a dose of 6 milligrams Dexa per day for up to 10 days.”
Not only in Covid-19, but steroids are also widely used in orthopaedic and pulmonary diseases. In India, the problem lies not in the drug but in how it is prescribed. “Most of us who work in India will agree that prescribing practices more often than not tend towards higher doses for longer periods of time, which is a clear risk factor for invasive fungal infections
Medicines used in treating Covid-19 tend to bring down the count of lymphocytes. Lymphocytes are one of the three types of white blood cells whose job is to defend our body against disease-causing pathogens such as bacteria, viruses, and parasites. The reduced count of lymphocytes leads to a medical condition called lymphopenia, making way for opportunistic fungal infection in Covid-19 patients.
There is a higher chance of occurrence of mucormycosis in patients whose immune system is not functioning well, and since Covid-19 treatment tends to suppress the working of the immune system, it places such patients at a higher risk of contracting the black fungus infection
E) Link to patient details:
ACUTE MYOCARDIAL INFARCTION
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?
Answer: 3days back developed mild chest pain in the right side of the chest. The pain was insidious in onset and gradually progressive. The pain was of dragging type and was radiating to the back (retrosternal pain).
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: TAB. ASPIRIN 325 mg PO/STAT
Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.
TAB ATORVAS 80mg PO/STAT
Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
TAB CLOPIBB 300mg PO/STAT
Mechanism of action: The active metabolite of clopidogrelselectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
INJ HAI 6U/IV STAT
VITAL MONITORING.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Answer: Yes PTCA is protective and is needed for good prognosis. It prevents recurrence of MI attack
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?
Answer:1.Symptomatology:- Pain in abdomen since 1wk
Vomiting since 1wk
Fever since 4 days
Constipation since 4days
Burning micturition since 4days
Anatomical localisation:-
The pancreas lies behind the peritoneum of the posterior abdominal wall and is oblique in its orientation. The head of the pancreas is on the right side and lies within the “C” curve of the duodenum at the second vertebral level (L2)
Primary etiology:- Alcoholism
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?
Answer: ING. MEROPENAM ; TID for 7 days
ING. METROGYL 500 mg IV TID for 5 days
ING. AMIKACIN 500 mg IV BD for 5days
TPN ( Total Parenteral Nutrition )
IV NS / RL at the rate 12l ml per hour
ING. OCTREOTIDE 100 mg SC , BD
ING. PANTOP 40 mg IV , OD
ING. THIAMINE 100 mg in 100 ml NS IV , TID
ING. TRAMADOL in 100 ml NS IV , OD
The pseudocyst was drained per cutaneously per abdominally under local anaesthesia with USG guided malecot drain placed inside and pus was drained.
Oxygen supply for mild hypoxia , which was
developed due to pneumothorax ( Spo2: 98% on 6 lts of oxygen )
ICD ( Inter Coastal Drainage ) placed for pneumothorax.
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer:Acute pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion. The pathogenesis of some of the above complications is attributed to the production of noxious cytokines. or may be due to Hepatic hydrothorax in which Abdominal fluid fills the lung (mostly on the right side) and causes SOB
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Answer: The pathogenesis of pancreatogenic diabetes is mainly explained by the development and progression of destructive changes, hypoxic changes in devitalized pancreatic tissues, and endocrine sclerosis.
It is result of primary inflammation of the pancreatic paren-
chyma in ACP which has a linear dependence on the frequency and duration of the disease, and the likelihood of developing diabetes with an exacerbation of the process
during 5-8 years is 17.5%
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Answer: In general, ALD should be suspected in patients with a significant history of alcohol use who present with abnormal serum transaminases, particularly if the level of aspartate aminotransferase (AST) is greater than that of alanine aminotransferase (ALT), hepatomegaly, clinical signs of chronic liver disease, radiographic evidence of hepatic steatosis or fibrosis/cirrhosis, or who have had a liver biopsy showing macrovesicular steatosis or cirrhosis. Patients with ALD may or may not have elevated serum aminotransferase levels. The absolute level of liver enzyme elevation does not correlate well with the severity of ALD, however, the pattern of elevation in
transaminases is helpful in making a diagnosis of liver injury due to alcohol as AST is typically two to three times greater than ALT in alcoholic liver injury. They will also typically have an elevated serum gamma glutamyltranspeptidase (GGT). However, it is important to rule out other etiologies for the patient's liver disease before making a definitive diagnosis of ALD, including chronic viral hepatitis, autoimmune hepatitis, hemochromatosis and drug related hepatotoxicity. In some cases, when the diagnosis is unclear, a liver biopsy may be warranted.
4) What is the line of treatment in this patient?
Answer:Treatment includes a combination of goal-directed fluid therapy, pain control( morphine), antiemetics, electrolyte replacement, early enteral nutrition, alcohol cessation counseling and diuretics for ascites
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