GENERAL MEDICINE ASSIGNMENT FOR MAY 2021
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:
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
PULMONOLOGY
CASE-1:
Q1) 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?
A1) Timespan of patients symptomology:
20 YEARS BACK -- first episode of SOB
15 YEARS BACK -- facial puffiness
12 YEARS BACK --second episode of SOB
yearly episodes from the past 12 years
8 YEARS BACK -- diagnosed with diabetes
5 YEARS BACK -- anemia and took Fe injections
1 MONTH BACK-- Genrealized weakness
15 DAYS BACK-- Pedal edema
ANATOMICAL LOCALIZATION ---
LUNGS-Bronchi and bronchioles -
Primary etiology of the patients problem may be due to the exposure of dust in paddy fields.
Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
A2)Head end elevation: Head angle affected the respiratory mechanics of mechanically ventilated patients. It can reduce the risk of mechanical ventilated- associated pneumonia. In addition, it can increase the possibility of more homogeneous alveolar ventilation and possibly reduce the risk of lung injury.
O2 inhalation to maintain spO2 above 92%
BiPAP: It is a non invasive method. It assists ventilation by delivering positive expiratory and inspiratory pressure without the need of ET incubation.
Inj. Augmentin: 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.
Tab. Azithromycin: Prevents bacteria from growing by interfering with their protein synthesis. It binds to the 50S subunit of the bacterial ribosome, thus inhibiting translation of mRNA.
Inj. Lasix: 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.
Tab. Pantop: 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.
Inj. Hydrocortisone: Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.
Tab. Pulmoclear: works by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.
Inj. Thiamine: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
Q3) What could be the cause for her current acute exacerbation?
A) It could be due to any infection or environmental pollution
4. Could the ATT have affected her symptoms? If so how?
A) YES
as isoniazide and rifampacin are nephrotoxic raised RFT was seen
5.What could be the causes for her electrolyte imbalance?
1)hytponatremia
2)worsening of hypoxia
3)respiratory acidosis
4)right heart failure
5) hypochloremia
NEUROLOGY
CASE 2 : https://143vibhahegde.
Q1 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?
TIME LINE OF PATIENT SYMPTOMATOLOGY
12 YEARS BACK -- started drinking alcohol
2 YEARS BACK -- Diagnosed with Diabetes Mellitus
1 YEAR BACK--Has an episode of seizures(GTCS)
4 MONTHS BACK-- Has another episode of seizure following cessation of alcohol for 24 hours.
starts drinking again after seizure subsides(jan 2021)
ON MAY 10,2021--Last alcohol intake(1 bottle),general body pains at night
ON MAY 11,2021--Decreased food intake. started talking and laughing to himself. unable to getup by himself from bed
he is conscious but not coherent. disoriented to time, person,place. Goes to an RMP the same day is prescribed iv fluids and asked to visit a hospital
ON MAY 15 2021-- Is admitted to a tertiary care hospital foe alcohol withdrawal symptoms, and is treated for the same
ANATOMICAL LOCALIZATION :
HIPPOCAMPUS AND FRONTAL LOBE
HIPPOCAMPUS
FRONTAL LOBE
ETIOLOGY:
CHRONIC ALCOHOLISM
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
MOA :
PLACEBO is an inert substance that it doesn't create any effect
these mechanisms are discussed from the psychological and neurobiological points
PSYCOLOGICAL MECHANISM:
expectations, conditioning,learning,memory,motivation,somaticfocus,reward and reduction of anxiety
NEUROBIOLOGICAL MECHANISMS:
Research into the neurobiology of responsiveness to placebo has addressed placebo analgesia; accordingly, the neurobiology of placebo effects is commonly considered in terms of opioid and non-opioid mechanisms.[9,10] Several studies have demonstrated that placebo effects can be completely or partially reversed by the opioid antagonist naloxone, supporting the involvement of endogenous opioids in some analgesic effects of placebo.[11–14] Furthermore, analgesic effects of placebo are likely to be inhibited by the peptide cholecystokinin (CCK) for they are potentiated when a CCK antagonist is administered. Considered together, these studies de,16]
INDICATIONS:
PAIN
INSOMNIA
ANXIETY
RISK OF SUBSTANCE ABUSE
EFFICACY:
The efficacy of placebo was clear, and varied not only between the five indication groups but also within them. Whereas placebo, unlike active treatment, produced hardly any improvement in symptoms in patients with severe stroke, it was as effective as active treatment in patients with mild neurological deficits, producing an improvement of about 50%. In patients with angina pectoris, placebo produced an increase in exercise tolerance (treadmill walking time to onset of ST-segment depression and angina attacks) of about 10% on average, compared with about 22% under active treatment (nisoldipine). In diabetes therapy, placebo produced no improvement in fasting and postprandial blood glucose levels compared with active treatment (acarbose), and also had no effect on HbA1C values.
USEFULLNESS:
The use of placebo is not equivalent to the absence of treatment, for example, placebo could be used in addition to standard care. In all cases, its use should be associated with measures to minimize exposure and avoid irreversible harm, especially in serious or rapidly evolving diseases. As appropriate, rescue treatment and escape procedures should be set up.
Other situations where the use of placebo should be scrutinized and challenged include run-in periods where a protocol requires active treatment to be withheld.
Situations in which placebo may be considered as a comparator, for example, might be when there is no commonly accepted therapy for the condition and the investigational medicinal product is the first one that may modify the course of the disease process.
It is useful when the commonly used therapy for the condition is of questionable efficacy or carries with it a high frequency of undesirable adverse reactions and the risks may be significantly greater than the benefits.[24]
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
KINDLING ALCOHOL WITHDRAWL
4) What is the reason for giving thiamine in this patient?
Deficiency of thiamine (vit- B1) leads to WERNICKEKORSAKOFF SYNDROME
To treat or rule this differential out thiamine is given
5) What is the probable reason for kidney injury in this patient?
As the urea levels are very high, it denotes an acute onset -- ACUTE RENAL FAILURE
As high serum creatinine and urea levels are present, denotes that reabsorption from tubules is taking place
therefore the primary cause is perenal, most probably due to generalised dehydration
A slightly high FENa level also denotes that tubular necrosis is occuring to some degree, hence the PerenalAKI is in turn leading to Acute Tubular Necrosis(ATN)
6). What is the probable cause for the normocytic anemia?
Possible causes:
a)Alcohol causes iron deficiency by causing defect in cell production
b)Decreased bone marrow production of RBCs, due to EPO deficiency owing to kidney failure
c)Loss of blood through chronic foot ulcer
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Yes , as alcoholism itself can cause peripheral neuropathy (alcoholic neuropathy), which along with Diabetic neuropathy, can lead to a non-healing foot ulcer
CASE:2 https://kausalyavarma.
Q1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A) TIME LINE OF THE PAITIENT SYMPTAMOLOGY
7 DAYS BACK-- Pt has giddiness that started around 7 in the morning , subsided upon taking the rest
associated with one episode of vomiting
4 DAYS BACK--Pt consumed alcohol ; he developed giddiness that was sudden in onset ,continuous and gradually progressive. it increased on standing and while walking
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- he is unable to walk without presence of supports, swaying is present and he has tendency to fall while walking
- No diplopia, dysphagia, dysarthria
- No H/o any seizure like activity.
ANATOMICAL LOCALIZATION:
THERE IS PRESENCE OF AN INFART IN INFERIOR CEREBELLAR HEMISPHERE OF BRAIN
ETIOLOGY:
Ataxia is the lack of muscle control or co-ordination of voulantary movements
causes of cerebellar ataxia are
1)Head trauma
2)Alcohol abuse
3)Barbiturates
4)Stroke
5)Tumors
6)cerebral palsy
7)brain degeneration
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Tab Vertin 8 mg--- This is betahistine , which is an anti-vertigo medication
MOA:
Vertigo is a disturbing sensation of movement caused by dysfunction of the labyrinth (inner ear), vestibular nerve, cerebellum, brainstem, or Central Nervous System (CNS). Vestibular forms of vertigo are often accompanied by auditory dysfunctions such as hyperacusis, hearing loss, and tinnitus.[A220328] In most cases, adaptive mechanisms of the CNS lead to functional recovery after episodes of vertigo, however, syndromes such as Ménière's disease tend to cause the recurrence of vertigo symptoms. This significantly impacts the quality of life and the ability to carry out daily activities.[A220318] **H1-receptor activity** The mechanism of action of betahistine is multifactorial. Ménière's disease is thought to result from a disruption of endolymphatic fluid homeostasis in the ear.[A220438] Betahistine mainly acts as a histamine H1-receptor agonist. The stimulation of H1-receptors in the inner ear causes a vasodilatory effect leading to increased permeability of blood vessels and a reduction in endolymphatic pressure; this action prevents the rupture of the labyrinth, which can contribute to the hearing loss associated with Ménière's disease. Betahistine is also purported to act by reducing the asymmetrical functioning of sensory vestibular organs and increasing vestibulocochlear blood flow, relieving symptoms of vertigo.[A220433] **H3-receptor activity** In addition to the above mechanisms, betahistine also acts as a histamine H3-receptor antagonist, increasing the turnover of histamine from postsynaptic histaminergic nerve receptors, subsequently leading to an increase in H1-agonist activity. H3-receptor antagonism elevates levels of neurotransmitters including serotonin in the brainstem, inhibiting the activity of vestibular nuclei, thus restoring proper balance and decreasing vertigo symptoms.[A220328]
tab ZOFER 4 mg This is ondanseteron - it is an anti emitic
MOA :
Ondansetron is a selective 5-HT3 serotonin-receptor antagonist used for its antiemetic properties. It is 1 of 4 FDA-approved 5-HT3 serotonin-receptor antagonists used to combat nausea and vomiting, with the others including granisetron, dolasetron, and the second-generation drug, palonosetron. Ondansetron acts both centrally and peripherally to prevent and treat nausea and vomiting. Central effects are mediated by the antagonism of 5HT-3 serotonin receptors in the area postrema. The area postrema, which is located on the floor of the fourth ventricle contains the “chemoreceptor trigger zone.” This zone senses neurotransmitters like serotonin, toxins, and other signals, and plays a role in mediating the sensation of nausea and subsequent vomiting. Ondansetron also has effects peripherally by acting on the vagus nerve. It acts on the 5-HT3 receptors that can be found at the vagus nerve terminals. Within the GI tract, the vagus nerve can sense nausea and vomiting triggers, such as stomach irritants, and it forms synapses within the nucleus tractus solitarius of the brainstem, another region important in vomiting. The peripheral actions of ondansetron are thought to be the predominant mechanism for its antiemetic effects. It is metabolized primarily by the cytochrome P450 system of the liver
TAB ECOSPIRIN 75 mg this is aspirin , it is an NSAID
MOA: They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patients history of denovo hypertension contribute to his current condition?
ANS. A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.
Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid 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.
Many studies show that with mild and moderate drinking . 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
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A) TIME LINE OF THE PAITIENT SYMPTOMATOLOGY:
8 MONTHS BACK--pt developed b/l pedal edema which is gradually progressed ,
aggrevated in sitting and standing position, relieved on taking medication
6 DAYS BACK -- PAIN radiating along left upper limb, more during palpitations and relived on medication.
Chest pain associated with chest heaviness since 5 days
5 DAYS BACK--- PALPITATIONS DEVELOPED, sudden in onset which is more during night, aggrevated by lifting heavy weights, speaking continuously
5 DAYS BACK--Dyspnoea during palpitations
ANATOMICAL LOCALIZATION :
PALPITATION
DYSPNOEA
CHEST PAIN
Etiological agent
*By localization, electrolyte imbalance (hypokalemia) causing the her manifestations like palpitations, chest heaviness, generalised body weak ness
*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?
Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
Other risk factors
2) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
3) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
4) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
5) psuedohypokalemia:delayed sample analysis, significant leukocytosis
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
A) changes seen in ECG :
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves In Severe cases :ventricular fibrillation, rarely AV block
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
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 of seizure activity
You’re more likely to have a seizure if you had a haemorrhagic stroke (bleed on the brain). Seizures can also be more likely if you had a severe stroke, or a stroke in the cerebral cortex, the large outer layer of the brain where vital functions like movement, thinking, vision and emotion take place.
Some people will have repeated seizures, and be diagnosed with epilepsy. The chances of this happening may depend on where the stroke happens in the brain and the size of the stroke.
There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury ,(particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.
2Q). In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
Normally the “consciousness system”—a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness. Diverse seizure types including absence, generalized tonic-clonic and complex partial seizures converge on the same set of anatomical structures through different mechanisms to disrupt consciousness.
CASE 4https://nikhilasampathkumar.
Q1) What could have been the reason for this patient to develop ataxia in the past 1 year ?
Alcohol may be the reason for this oatient to develop ataxia in the past 1 year.Damage from alcohol is a common cause of cerebellar 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.
Q2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
A2) Heavy alcohol consumption was associated with increased ICH risk.
Q1).Does the patient's history of road traffic accident have any role in his present condition?
A) Cerebrovascular accidents can be caused by moderate to severe trauma ( traffic accident ). Large blows causes high pressure of blood pooling that gets trapped and forms a clot.
Q2) What are warning signs of CVA?
A2) One side of the face is drooping
Arm weakness
Speech difficulty
Blurred vision
Loss of balance, headache, dizziness.
Q3) What is the drug rationale in CVA?
A3) Tab. Ecospirin
Inj. Mannitol
Tab. Atorvastatin
4) Does alcohol has any role in his attack?
A4) As he consumes alcohol occasionally, alcohol may have a role in his attack.
Q5) Does his lipid profile has any role for his attack?
A5) Lipid profile of the patient seems to be normal. So lipid profile of this patient doesn't have any role for his attack
Q1)What is myelopathy hand ?
There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
Q2 what is finger escape?
Finger escape
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
Q3)what is Hoffman's sign?
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition
Q1) What can be the cause of her condition ?
According to MRI cortical vein thrombosis might be the cause of her seizures.
Q2) What are the risk factors for cortical vein thrombosis?
Infections:
Meningitis, otitis,mastoiditis
Prothrombotic states:
Pregnancy, puerperium,antithrombin deficiency proteinc and protein s deficiency,Hormone replacement therapy.
Mechanical:
Head trauma,lumbar puncture
Inflammatory:
SLE,sarcoidosis,Inflammatory bowel disease.
Malignancy.
Dehydration
Nephrotic syndrome
Drugs:
Oral contraceptives,steroids,Inhibitors of angiogenesis
Chemotherapy:Cyclosporine and l asparginase
Hematological:
Myeloproliferative Malignancies
Primary and secondary polycythemia
Intracranial :
Dural fistula,
venous anomalies
Vasculitis:
Behcets disease wegeners granulomatosis
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why
Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Anticoagulants are used for the prevention of harmful blood clots.
Clexane ( enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivate FACTOR Xa
CARDIOLOGY:
Q1).What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure.
Q2) Why haven't we done pericardiocenetis in this pateint?
A2) The effusion was already self healing, so pericardiocenetis is not done in this patient.
Q3) What are the risk factors for development of heart failure in the patient?
A) High blood pressure. Your heart works harder than it has to if your blood pressure is high. Coronary artery disease. Narrowed arteries may limit your heart's supply of oxygen-rich blood, resulting in weakened heart muscle. Heart attack. A heart attack is a form of coronary disease that occurs suddenly. Damage to your heart muscle from a heart attack may mean your heart can no longer pump as well as it should. Diabetes. Having diabetes increases your risk of high blood pressure and coronary artery disease. Some diabetes medications. sleep apnea. The inability to breathe properly while you sleep at night results in low blood oxygen levels and increased risk of abnormal heart rhythms. Both of these problems can weaken the heart. Congenital heart defects. Some people who develop heart failure were born with structural heart defects. Valvular heart disease. People with valvular heart disease have a higher risk of heart failure. Viruses. A viral infection may have damaged your heart muscle. Alcohol use. Drinking too much alcohol can weaken heart muscle and lead to heart failure. Tobacco use. Using tobacco can increase your risk of heart failure. Obesity. People who are obese have a higher risk of developing heart failure. Irregular heartbeats. These abnormal rhythms, especially if they are very frequent and fast, can weaken the heart muscle and cause heart failure.
Q4) What could be the cause for hypotension in this patient?
A) Hypertension i this case may be due to secondary to Tuberculosis.
Q1)What are the possible causes for heart failure in this patient?
Ans; Alcoholic cardiomyopathy is a form of heart disease caused by alcohol abuse. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
High blood pressure can strain your heart, damage blood vessels, and increase your risk of heart attack
Diseases in the kidneys can affect the heart. It is common for people with chronic kidney disease or end-stage kidney disease to develop heart disease, including heart attack or heart failure.
2.what is the reason for anaemia in this case?
Ans; In the general elderly population, anemia is caused by nutritional deficiencies (primarily iron), chronic inflammation/CKD, or unexplained anemia of the elderly (a hypoproliferative anemia with blunted erythropoietin response)
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Ans; When high blood sugar destroys nerves, they do not regenerate; thus many patients with diabetes are increasingly less sensitive to pain in their limbs. With this loss of sensation, patients don't feel developing blisters, infections, or existing wound changes. That means that wound healing is complicated not only by the fact that patients don't feel wounds as they occur, but they also have no pain to alert them that a wound is getting worse or infected.
4. What sequence of stages of diabetes has been noted in this patient?
Ans;stage 1: defined as DCBD (dysglycemia-based chronic disease )insulin resistance;
stage 2: defined as DCBD prediabetes;
stage 3: defined as DCBD type 2 diabetes; and
stage 4: defined as DCBD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events.
All these stages have been noted in this CASE
Q1) 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: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?
Ans; 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[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.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?
Ans; 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?
Ans; 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?
Ans; 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.
Q1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans; Evolution of symptomatology
12 years ago- DM2
1year back Heart burn like episodes(relieved without medication)
7 months back pulmonary TB (completed the course one month back)
6 months back Hypertension
1/2 hour ago- SOB
Anatomical localisation: Heart muscle
Primary etiology
Coronary artery disease:involves the reduction of blood flow to the heart muscle due to build-up of plaque (atherosclerosis) in the arteries of the heart
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;Met XL 25 tablet is used to lower the raised blood pressure and various other heart-related conditions such as angina (chest pain), heart failure, preventing further complications.
Glimiprime M 2 Forte Tablet is a combination of two medicines: Glimepiride and Metformin. This medicine is used in the treatment of type 2 diabetes mellitus (DM). It improves blood glucose levels in adults when taken along with proper diet and regular exercise …
Telma 20 tablet is an antihypertensive medicine that is used to treat high blood pressure and can also help in reducing other heart problems It acts by relaxing the blood vessels and leads to lower blood pressure
3) What are the indications and contraindications for PCI?
Ans;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?
Ans ;people suffer complications including bleeding, blood clots, infection, heart rhythm disturbances and even death from heart attack if PCI is performed in a patient who doesnot need it.
associated with substantial morbidity and mortality given the large amount of subtended myocardium at risK
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 symptomatology:
Uncontrolled DM2 since 8 years
3 days back Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical localisation: Inferior wall of heart
Primary etiology: Diabetes type 2 (uncontrolled)
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
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;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?
Ans; Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty
Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Because of the fluid loss occurred to the patient
there is decreased preload- so, SOB occurred due to decreased CO
IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.
2. What is the rationale of using torsemide in this patient?
Torsemide used to relieve abdominal distension.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
IT IS THE TREATMENT FOR UTI
Rationale- Used for any bacterial infection.
- GASTROENTEROLOGY( & PULMONOLOGY)
- CASE-1: https://63konakanchihyndavi.
blogspot.com/2021/05/case- discussion-on-pancreatitis- with.html - Q1) 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?
- A1) Timespan of symptomology:
- 5 years ago: 1st episode of pain abdomen and vomiting
- 1 year back: 5 to 6 episodes of pain abdomen and vomiting
- 20 days back: Increased consumption of toddy intake
- Since 1 week: Pain abdomen and vomiting
- Since 4 weeks: Fever, constipation and burning micturition
- Anatomical localization: Pancreas and left lung
- Etiology: The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes attributed to alcohol.
- Q2) 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?
- A2) Inj. Metrogyl: Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by forming nitroso radicals, which disrupt the DNA of microbial cells.
- Inj. Meropenam: Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
- Inj. Amikacin: The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
- TOTAL PARENTAL NUTRITION
- Inj. Octerotide: Octreotide suppresses secretion of growth hormone (GH), and in many cases suppresses insulin-like growth hormone-1 (IGF-1) (somatomedin C). Sandostatin works centrally at the site of the tumor and binds to somatostatin receptors to regulate GH secretion and cell growth.
- Inj. Pantop: The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
- Inj. Thiamine: Mechanism of Action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
- Inj. Tramadol: Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
- CASE-2: https://nehae-logs.blogspot.
com/2021/05/case-discussion- on-25-year-old-male.html - Q1) What is causing the patient's dyspnea? How is it related to pancreatitis?
- A1) Pleural effusion might be the cause of patients dyspnea.
- Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease[24]. Pancreatic ascites and pleural effusion are rare complications of both chronic and acute pancreatitis, and are associated with a mortality rate of 20% to 30%.
- Q2) Name possible reasons why the patient has developed a state of hyperglycemia.
- A2) Hyperglucagonemia secondary to stress could be the result of patient developing hyperglycemia.
- Elevated levels of catecholamines and cortisol.
- Q3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
- A3) Elevated liver enzymes are a sign that a person has an inflamed or a damaged liver. Many conditions may cause liver inflammation or damage. In this case the probable reason may be due to liver injury. Alanine aminotransferace (ALT) and Asparate aminotransferase (AST) are the specific markers for alcoholic fatty liver disease. Glutamyl transpeptidase (GGT) is another marker of liver injury, and this enzyme is elevated in people who consumes alcohol. Of all the enzyme markers GGT is the most sensitive biomarker of alcohol consumption.
- Q4) What is the line of treatment in this patient?
- A4) IVF: 125 ml/hr
- Inj. PAN 40mg i.v.
- Inj Zofer 4mg i.v.
- Inj. Tramadol 1amp in 100ml i.v.
- Tab. Dolo 650mg
- GRBS charting 6th hourly
- BP charting 8th hourly.
- CASE-3: https://chennabhavana.
blogspot.com/2021/05/general- medicine-case-discussion-1. html - Q1) What is the most probable diagnosis in this patient?
- A1) Abdominal Hemorrhage may be the most probable diagnosis in this patient.
- Q2) What was the cause of her death?
- A2) Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internl organs
- .
- Q3) Does her NSAID abuse have something to do with her condition? How?
- A3) NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.
- NEPHROLOGY ( AND UROLOGY)
- Q1) What could be the reason for his SOB ?
- A1) His shortness of breath may be due to Acidodsis which was caused by diuretics.
- Q2) Why does he have intermittent episodes of drowsiness ?
- A2) Hyponatremia was the cause for drowsiness.
- Q3) Why did he complaint of fleshy mass like passage in his urine?
- A3) Pyuria (Many pus cells) are passed in the urine which he observed as fleshy mass like passage.
- Q4) What are the complications of TURP that he may have had?
- A4) Bladder injury.
- Bleeding.
- Blood in the urine after surgery.
- Electrolyte abnormalities.
- Infection.
- Loss of erections.
- Painful or difficult urination.
- CASE-2:https://drsaranyaroshni.
blogspot.com/2021/05/an-eight- year-old-with-frequent.html
Q1) Why is the child excessively hyperactive without much of social etiquettes ?
A1) Inattention and hyperactivity/impulsivity are the key behaviors of ADHD. Some people with ADHD only have problems with one of the behaviors, while others have both inattention and hyperactivity-impulsivity. Most children have the combined type of ADHD.In preschool, the most common ADHD symptom is hyperactivity. Due to efficacy of the medications like dopamine and noradrenaline have been suggestive of pathology of ADHD
2. Why doesn't the child have the excessive urge of urination at night time ?
A2)
Q3) How would you want to manage the patient to relieve him of his symptoms?
A3) Antideppresants like Bupropion, trazodone
Antipsychotics like Risperidone, aripiprazole
Mood stabilizers like Carbamazepine are given to the patient to relieve the symptoms of ADHD.
INFECTIOUS DISEASES( HI VIRUS, MYCOBACTERIA, GASTROENTEROLOGY, PULMONOLOGY)
Q1) Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
A1) History findings - Any congenital heart diseases, history of mild respiratory distress, history of recurrent attacks of pneumonia.
Physical findings- drooling, choking, respiratory distress, and feeding inability. Gastric distension is a common complication of a fistula between the trachea and distal esophagus. Reflux of gastric contents through the fistula tract results in aspiration pneumonia and increasing morbidity.
Q2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
A2) The chances of this patient developing immune reconstitution inflammatory syndrome are high as she had a previous infection of TB.
IRIS can be prevented by treating the patient with ATT with as early as possible. Prednisolone and meloxicam are used to prevent further TB IRIS.
INFECTIOUS DISEASES AND HEPATOLOGY
Q1) Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?
A1) Locally made alcohol like toddy may cause liver abscess if it is contaminated.
Q2) What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day).
A2) All patients of ALA had serum iron values within the normal range but higher than non-ALA cases. In the liver tissue, most patients with ALA had higher (grade II or III) iron deposition, than non-ALA cases (mostly grade I). Thus, patients with ALA, with or without alcohol indulgence, had higher iron levels when compared to the non-ALA cases. It appears that the higher incidence of ALA in alcoholic livers is possibly due to their higher iron content.
Q3) Is liver abscess more common in right lobe ?
A3) Due to more blood supply to the right lobe, liver abscess is more common in right lobe
.
Q4) What are the indications for ultrasound guided aspiration of liver abscess ?
A4) Left lobe abscess
Caudate lobe abscess
Large abscess more than 6cms
Abscess which is not responding to drugs.
Q1) Cause of liver abscess in this patient ?
A1) Entamoeba Histolytica may be the cause of liver abscess in this patient.
Q2) How do you approach this patient ?
A2) 
Q3) Why do we treat here ; both amoebic and pyogenic liver abscess?
A3) Amoebic liver abscess- 
Pyogenic liver abscess:
Third generation cephalosporin with clindamycin or metronidazole.Broad spectrum penicillin with aminoglycosides
Second generation cephalosporin with aminoglycosides
.
Q4) Is there a way to confirmthe definitive diagnosis in this patient?
A4) Neutrophils leukocytosis, anemia of chronic disease,
Blood cultures may reveal the diagnosis, imaging studies like Ultrasound , CT scans and hepatic scans are more sensitive and are the confirmatory test for the diagnosis of liver abscess.
INFECTIOUS DISEASES (MUCORMYCOSIS, OPHTHAMALOGY, ENT, NEUROLOGY)
CASE-1: http://manikaraovinay.
Q1) 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?
A1) Timespan of symptomology:
3 years ago- diagnosed with hypertension
21 days ago- received vaccination at local PHC which was followed by fever, chills, and rigors.
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. Patient was in a drowsy state.
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.
2 days ago- died.
the fungus enters the sinuses from the environment and then the brain.
Q2) 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?
A2) Inj. Amphotericin- B: Amphotericin B is an example of a “polyene” type of antifungal. Polyenes bind to fungal ergosterol (the primary sterol in fungal cell membranes). This alters cell membrane permeability, and intracellular components leak from the cell.
Deoxycholate Amphotericine B: Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years.
Q3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
A3) High steroid usage during COVID 19 treatment causes high blood sugars and suppress the immune system. Due to high population in the state there are easy chances of containmant by the fungus Mucormycosis