Online blended bimonthly assignment toward summative assessment for the month of May 2021
May 31,2021
Navya Rathlavath,
Roll no:112,8th sem.
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.
*Primary etiology of patient:
(4)What is the reason for giving thiamine in this patient?
(5)What is the probable reason for kidney injury in this patient?
(2)What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
*Chronic NSAIDs use has also been related to hepatotoxicity.
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.
[1]PULMONOLOGY:
A.LINK TO PATIENT DETAILS:
(1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of the symptoms:
> 1st episode of sob - 20 yr back
> 2nd episode of sob - 12 yr back
> From then she has been having yearly episodes from the past 12 yrs
> Diagnosed with diabetes - 8yrs back
> Anemia and took iron injections - 5yr ago
> Generalised weakness - 1 month back
> Diagnosed with hypertension - 20 days back
> Pedal edema - 15 days back
> Facial puffiness- 15 yrs back
*Anatomical localisation of the problem:
LUNGS-Bronchi and Bronchioles:- lead to increased blood pressure in the pulmonary artery which resulted in RIGHT HEART FAILURE.
*The symptoms are probably due to the inhalation of Paddy dust.
> Paddy dust is biologically composed of
plant material fungi: of genus epicocum, fusarium
*Usage of chulha since 20 yrs -cooking fumes may also be responsible.
(2)what r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
-Ans:
*Non-Pharmacological Interventions:-
1.Head end Elevation:
Significantly increases global and regional end-expiratory lung volume. It has also been shown to improve oxygenation and hemodynamic performance.
2.BiPAP Intermittent:
By having a custom air pressure for when you inhale and a second custom air pressure when you exhale, the machine is able to provide relief to your overworked lungs and chest wall muscles.
3.Chest physiotherapy:
It is a term used for a group of treatments designed to improve respiratory efficiency, promote expansion of the lungs, strengthen respiratory muscles, and eliminate secretions from the respiratory system.It includes postural drainage, chest percussion, chest vibration, turning, deep breathing exercises, and coughing.
4.Vitals Charting:
This allow for continuous monitoring of a patient, with medical staff being continuously informed of the changes in general condition of a patient.
5.I/O chart:
Urine input/output chart
This chart (also known as a frequency-volume chart or bladder diary) is used to assess how much fluid you drink, to measure your urine volume, to record how often you pass urine over 24 hours and to show any episodes of incontinence (leakage)
6.O2 Inhalation:
It is used to
a) manage the condition of hypoxia
b)maintain o2 tension in blood plasma
c)increase oxy haemoglobin in RBC
d) maintain ability of cells to carry out normal metabolic function
e)reduce the risk of complications
*Pharmacological Interventions:-
9.inj.HAI
10.Inj.Thiamine
(3)What could be the causes for current acute excerbation?
-Ans:
*It could be due any infection or environment pollutants.
(4)could the ATT affected her symptoms if so how?
-Ans:
*Yes ATT affected her symptoms
*Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
(5)What could be the causes for her electrolyte imbalance?
-Ans:
*Hyponatremia:
> Worsening of Hypoxia
> Respiratory acidosis
> Right heart failure
*Hypochloremia:
> Respiratory acidosis with metabolic alkalosis.
[2]NEUROLOGY:
A.LINK TO PATIENT DETAILS:
(1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of the symptoms:
> 2009 (12 years ago): Started drinking alcohol
> 2019 (2 years ago): Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemics
> 2020 (1 year ago): Has an episode of seizures (most likely GTCS)
> January 2021 (4months ago): Has another seizure episode (most likely GTCS)- following cessation of alcohol for 24 hours. Starts drinking again after seizure subsides
> Monday, May 10, 2021: Last alcohol intake, around 1 bottle. Starts having general body pains at night.
> Tuesday, May 11, 2021: Decreased food intake. Starts talking and laughing to himself. Unable to lift himself off the bed, help required.
-Conscious, but non coherent. Disoriented to time, person, place.Goes to an RMP the same day- is prescribed IV fluids and asked to visit a hospital
> Saturday, May 15, 2021: Is admitted to a tertiary care hospital for alcohol withdrawal symptoms, and is treated for the same.
*Anatomical localisation of the problem:
The most probable location in the brain is the hippocampus and frontal lobe.
*Primary etiology of the patient's problem:
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?
-Ans:
*Pharmacological interventions:-
1.Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency
2.Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
3.pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
4.Lactulose is used in preventing and treating clinical portal-systemic encephalopathy.its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
5.Potchlor liquid is used to treat low levels of potassium in the body.
(3)Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
-Ans:
*A possible cause for this is due to a phenomenon known as kindling.
-Ans:
*One of the differential diagnoses for altered sensorium following chronic alcoholism is Wernicke-Korsakoff Syndrome, caused by deficiency of thiamine (B1). To either treat or rule this differential out, thiamine is given.
*Thiamine is necessary to provide energy to the CNS, helps in conduction of nerve signals.
Hence, deficiency leads to confusion and ataxia, both of which are present in this patient.
-Ans:
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 prerenal, most probably due to generalised dehydration.
A slightly high FENa level also denotes that tubular necrosis is occurring to some degree, hence the Prerenal AKI (mostly due to dehydration) is in turn leading to Acute Tubular Necrosis (ATN).
(6)What is the probable cause for the normocytic anemia?
-Ans:
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?
-Ans:
*Yes, as alcoholism itself can cause peripheral neuropathy (alcoholic neuropathy), which along with Diabetic neuropathy, can lead to a non-healing foot ulcer.
B.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patients problem?
-Ans:
*Evolution of symptoms:
> 7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
> 4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
> H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
> Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
> Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
*Anatomical localisation of the problem:
There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.
*Primary etiology:
-Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)
-Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.
In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.
-Ans:
*Pharmacological interventions:
A) Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
B) Tab Zofer 4mg- This is ondanseteron- It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications- Used to control the episodes of vomiting and nausea in this patient.
C)Tab Ecosprin 75mg- This is aspirin. It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
D)Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F)Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G)Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
(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.
C.LINK TO PATIENT DETAILS:
*Answers:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> patient was normal 8 months back then developed bilateral pedal oedema which gradually progressed.
Aggerevated in sitting and standing position, relived on taking medication
> palpitations since 5days, sudden in onset which is more during night
Aggerevated by lifting heavy weights, speaking continuously
> Dyspnoea during palpitations (NYHA-3) since 5 days
> Pain since 6days, radiating along left upper limb, more during palpitations and relived on medication.
> chest pain associated with chest heaviness since 5 days
*Anatomical localisation:
Cervical spondylosis is the most common progressive disorder in the aging cervical spine. It results from the process of degeneration of the intervertebral discs and facet joints of the cervical spine.
*Primary Etiology:
*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?
-Ans:
Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
*Other risk factors:-
A) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
B) transcellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
D) psuedohypokalemia:delayed sample analysis, significant leukocytosis
(3)What are the changes seen in ECG in case of hypokalemia and associated symptoms?
-Ans:
changes seen in ECG :
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves
In Severe cases :ventricular fibrillation, rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D.LINK TO PATIENT DETAILS:
*Answers:
(1)Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
-Ans:
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
(2)In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
-Ans:
Normally the “consciousness system”—a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness. Diverse seizure types including absence, generalized tonic-clonic and complex partial seizures converge on the same set of anatomical structures through different mechanisms to disrupt consciousness.
E.LINK TO PATIENT DETAILS:
(1)What could have been the reason for this patient to develop ataxia in the past 1 year?
-Ans:
The patient has minor unattended head injuries in the past 1 yr.Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal lobe ataxia.
(2)What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
-Ans:
*The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own.
*But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobe.
F.LINK TO PATIENT DETAILS:
*Answers:
(1)Does the patient's history of road traffic accident have any role in his present condition?
-Ans:
*No it was alcohol drinking and emotional disturbance of the patient that led to his current situation. Road traffic accident only lead to dislocation of shoulder,zygomatic and mandibular process.
"Research shows that drinking large amounts of alcohol can greatly increase your risk of having a stroke"
(2)What are warning signs of CVA?
-Ans:
*WARNING SIGNS OF CEREBROVASCULAR ACCIDENT
1.Difficulty walking.
2.dizziness
3.loss of balance and coordination.
4.difficulty speaking or understanding others who are speaking.
5.numbness or paralysis in the face, leg, or arm, most likely on just one side of the body.
6.blurred or darkened vision.
(3)What is the drug rationale in CVA?
-Ans:
*DRUG RATIONALE FOR STROKE:
(4)Does alcohol has any role in his attack?
-Ans:
Yes alcohol has a role in his attack..Patient was occasionally alcoholic who used to drink 500ml of alcohol (whiskey) once in a week.
(5)Does his lipid profile has any role for his attack??
-Ans:
The inverse relationship between serum HDL-C and stroke risk . When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.
G.LINK TO PATIENT DETAILS:
(1)what is myelopathy hand?
-Ans:
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.
(2)what is finger escape?
-Ans:
Involuntary abduction of fifth finger caused due to unopposed action of extensor digiti MINIMI-WARTENBERG'S SIGN
Presence of weak finger adduction in cervical myelopathy is called - FINGER ESCAPE SIGN
(3)What is Hoffman's reflex?
-Ans:
HOFFMANS REFLEX:It is reflectory reaction of muscles after electrical stimulation of type 1a sensory fibres(primary afferent fibres which constantly monitor the how fast a muscle stretch CHANGES) in their innervation nerve.
H-REFLEX- is expression of of monosynaptic reflex, which runs in afferents from the muscle and back again through efferents of same muscles.
H.LINK TO PATIENT DETAILS:
(1)What can be the cause of her condition ?
-Ans:
According to MRI cortical vein thrombosis might be the cause of her seizures.
(2)What are the risk factors for cortical vein thrombosis?
-Ans:
(3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
-Ans:
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?
-Ans:
*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 inactivates factor xa.
[3]CARDIOLOGY:
A.LINK TO PATIENT DETAILS:
(1)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
-Ans:
*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
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?
-Ans:
Pericardiocentesis is not done here Because the effusion was self healing ,It reduced from 2.4cm to 1.9 cm.
(3)What are the risk factors for development of heart failure in the patient?
-Ans:
*Risk factors for development of heart faliure in this patent:-
1.Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure
2.high blood pressure
3.Smoking
4.Diabetes
5.AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.
wosening of pericardial effusion leaing to cardiac tamponade.
(4)What could be the cause for hypotension in this?
-Ans:
*visceral pericardium may have thickened which is restricting the heart to expand causing hypotension (May be secondary to TB)
B.LINK TO PATIENT DETAILS:
(1)What are the possible causes for heart failure in this patient?
-Ans:
1.atient has diabetes since 30yrs back and also having diabetic triopathy(NEUROPATHY-RETINOPATHY-NEPHROPATHY)so there is an increased risk for heart failure.
2.Hypertension since 19yrs - important risk factor.
3.Chronic alcoholic since 40yrs, leads to decreased LVEF and causes LV dysfunction.
4.atient 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?
-Ans:
*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?
-Ans:
*As patient was diabetic, which impairs healing process leading to development of non healing ulcers
*Due to chronic alcoholism leading to decreased production of proteins and clotting factors required for wound healing
C.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> Shortness of breath (Grade II i.e SOB on exertion) 1yr ago for which he visited the local hospital and was diagnosed to be Hypertensive (On medication)
> HTN since 1yr
> Facial puffiness On and Off since 2 yrs
> 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 localisation of the problem: Heart and blood vessels
*Primary etiology:
(2)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
-Ans:
*Pharmacological interventions:
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
mechanism:
Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
an enzyme that controls the movement of ions into the heart.
*Non pharmacological interventions:
1.Hypoglycemia symptoms explained
2.Watch for any bleeding manifestations like Petechiae, Bleeding gums.
3.APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
(3)What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
-Ans:
*Pathogenesis of cardiorenal syndrome:
*cardiorenal syndrome type 4 is seen in this patient.
(4)What are the risk factors for atherosclerosis in this patient?
-Ans:
1.Hypertension
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
(5)Why was the patient asked to get those APTT, INR tests for review?
-Ans:
*APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
*Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.
D.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> Diabetes since 12 years - on medication
> Heart burn like episodes since an year- relieved without medication
> Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
> Hypertension since 6 months - on medication
> Shortness of breath since half an hour-SOB even at rest
*Anatomical localisation of the problem:coronary artery
*Primary Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause - Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
(2)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
-Ans:
*Pharmacological Interventions:
*TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredientingredient
*MOA: METOPROLOL is a cardioselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.
*Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
*EFFICACY STUDIES:
*Non pharmacological Interventions:
•PERCUTANEOUS CORONARY INTERVENTION:
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
(3)What are the indications and contraindications for PCI?
-Ans:
*INDICATIONS:
1.Acute ST-elevation myocardial infarction(STEMI)
2.Non–ST-elevation acute coronary syndrome (NSTE-ACS)
3.Unstable angina.
4.stable angina.
5.Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
6.High risk stress test findings.
*CONTRAINDICATIONS:
1.Intolerance for oral antiplatelets long-term.
2.absence of cardiac surgery backup.
3.Hypercoagulable state.
4.High-grade chronic kidney disease.
5.Chronic total occlusion of SVG.
6.An artery with a diameter of <1.5 mm.
(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:
Although PCI is generally a safe procedure , it might cause serious certain complications like:-
Because of all these complications it is better to avoid PCI in patients who do not require it.
⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
*Example of overdiagnosis:(Breast cancer)
E.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> 3 days back - he 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).
*Anatomical localisation of the problem:BLOOD VESSELS.
*Primary etiology:
(2)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
-Ans:
*Pharmacological interventions:
1.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
2.TAB ATORVAS
mechanism:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3.TAB CLOPIBB
mechanism:The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
*Non pharmacological interventions:
*ANGIOPLAST:-
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
(3)Did the secondary PTCA do any good to the patient or was it unnecessary?
-Ans:
*The second PCI was NOT necessary in this patient.
*PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.
*A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient.
*Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
F.LINK TO PATIENT DETAILS:
(1)How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
-Ans:
*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?
-Ans:
*Torsemide used to relieve abdominal distension.
(3)Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
-Ans:
*IT IS THE TREATMENT FOR UTI
*Rationale- Used for any bacterial infection.
[4]GASTROENTEROLOGY AND PULMONOLOGY:
A.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> 5 years back-1st episode of pain abdomen and vomitings
> Stopped taking alcohol for 3 years
> 1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
> 20 days back increased consumption of toddy intake
> Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition
*Anatomical localisation of the problem:
Pancreas and left lung
*Bronchopleural fistula:
*Primary etiology:
Alcohol and its metabolites.
(2)What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
-Ans:
*Pharmacological interventions:
*Non pharmacological interventions:
drains ( malecot & icd )
* Even i as a treating physician will follow the same approach
B.LINK TO PATIENT DETAILS:
(1)What is causing the patient's dyspnea? How is it related to pancreatitis?
-Ans:
*The cause of dyspnea might be PLEURAL EFFUSION
-Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease.
-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%.
(2)Name possible reasons why the patient has developed a state of hyperglycemia.
-Ans:
*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells
* elevated levels of catecholamines and cortisol
(3)What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
-Ans:
LFT are increased due to hepatocyte injury.
*If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
*The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum.
(4)What is the line of treatment in this patient?
Plan of action and Treatment:
-Ans:
*Investigations:
1.24 hour urinary protein
2.asting and Post prandial Blood glucose 3.HbA1c
4.USG guided pleural tapping
*Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly
C.LINK TO PATIENT DETAILS:
(1)What is the most probable diagnosis in this patient?
-Ans:
Differential Diagnosis:
•Ruptured Liver Abscess.
•Organized collection secondary to Hollow viscous Perforation.
•Organized Intraperitoneal Hematoma.
•Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
•Grade 3 RPD of right Kidney
••The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
(2)What was the cause of her death?
-Ans:
After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
(3)Does her NSAID abuse have something to do with her condition? How?
-Ans:
*NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.
NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.
*NSAIDS also cause injury to the gastrointestinal mucosa.
[5]NEPHROLOGY AND UROLOGY:
A.LINK TO PATIENT DETAILS:
(1)what could be the cause for his SOB?
-Ans:
His sob was is due to Acidosis which was caused by Diuretics.
(2)Reason for Intermittent Episodes of drowsiness?
-Ans:
Hyponatremia was the cause for his drowsiness.
(3)why did he complaint of fleshy mass like passage in urine?
-Ans:
plenty of pus cells in his urine passage appeared as fleshy mass like passage to him.
(4)What are the complications of TURP that he may have had?
-Ans:
1.Difficulty micturition
2.Electrolyte imbalances
3.Infection
B.LINK TO PATIENT DETAILS:
(1)Why is the child excessively hyperactive without much of social etiquettes ?
-Ans:
*Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
*For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
(2)Why doesn't the child have the excessive urge of urination at night time ?
-Ans:
Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
(3)How would you want to manage the patient to relieve him of his symptoms?
-Ans:
*bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
*If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
*To treat attention deficit hyperactivity disorder:-
-For children 6 years of age and older: include medications and behavioural therapies.
Stimulants-Amphetamine, Methylphenidate.
[6]INFECTIOUS DISEASES (HIV,Mycobacteria,Gastroenterology,Pulmonology) :
A.LINK TO PATIENT DETAILS:
(1)Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
-Ans:
*clinical history:
•Cough since 2 months on taking food and liquids
•difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
*physical findings:
•laryngeal crepitus- positive
*These favour for tracheo esophageal fistula
(2)What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
-Ans:
*Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.
*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.
*Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
*Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.
[7]INFECTIOUS DISEASES AND HEPATOLGY:
A.LINK TO PATIENT DETAILS:
(1)Do u think drinking locally made alcohol cause liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient?
-Ans:
Yes, it could be due to intake of contaminated toddy.
(2)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)
-Ans:
*According to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver.
*It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
(3)is liver abscess is more common in right lobe?
-Ans:
yes right lobe is involved due to its more blood supply
(4)what r the indications for usg guided aspiration of liver abscess
-Ans:
Indications for USG guided aspiration of liver abscess:
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs
B.LINK TO PATIENT DETAILS:
(1)Cause of liver abcess in this patient ?
-Ans:
Here,the cause of liver abcess is :
* Amoebic liver abcess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
••Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
(2)How do you approach this patient ?
-Ans:
-The patient is well managed by treating team,
even me will follow the same approach.
*As mentioned earlier in practice we treat both pyogenic and amoebic liver abcess empirically.
* So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.
* Next we administer patient with analgesic and antipyretic such as tab.dolo 650mg &tab.Ultracet , to releive pain and fever.
**Abcess may get ruptured if untreated and cause peritonitis and shock.
(3)Why do we treat here ; both amoebic and pyogenic liver abscess?
-Ans:
* Considering the following factors:
1.Age and gender of patient:21yrs(young) & male.
2.Single abcess.
3.Right lobe involvement.
••The abcess is most likely AMOEBIC LIVER ABSCESS.
*But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.
••And considering the risk factors associated with aspiration for pus culture:
> Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.
> Sometimes ; it has thin thinwall which may rupture if u aspirate.
> Sometimes ; it is unliquefied.
••There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.
(4)Is there a way to confirm the definitive diagnosis in this patient?
-Ans:
* Yes in a high resource setting cause of liver abscess is usually determined using
1.multiple diagnostic strategies
2.including blood cultures
3.Entamoeba serology
4.liver abscess aspirate for culture
5.molecular and antigen testing.
[8]INFECTIOUS DISEASES (Mucormycosis,Ophthalmology,Otorhinolaryngology, Neurology) :
A.LINK TO PATIENT DETAILS:
(1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary aetiology of the patient's problem?
-Ans:
*Evolution of symptoms:
> 3 years ago- diagnosed with hypertension
> 21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication
> 18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
> 11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state
> 4 days ago-
1.patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
2.towards the evening patient periorbital oedema progressed
3.serous discharge from the left eye that was blood tinged
4.was diagnosed with diabetes mellitus
> patient was referred to a government general hospital
> patient died 2 days ago.
*Anatomical localisation of the problem:the *fungus enters the sinuses from the environment and then the brain.
**The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. [Mucormycosis is associated with the occurrence of CVA]
*Rhinooribtalcerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes.
*Primary etiology:
•patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhinoorbitalcerebral 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?
-Ans:
The proposed management of the patient was:
1.inj. Liposomal amphotericin B according to creatinine clearance
2.200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance
3.Deoxycholate was the required drug which was unavailable
I.Management of diabetic ketoacidosis –
(a)Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
(b)Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
(c)Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy
(3)What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
-Ans:
*Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. *Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
*With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is also increasing.
[9]INFECTIOUS DISEASES (COVID-19) :
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
1.Sort out these detailed patient case report logs into a single web page as a master chart
2.In the master chart classify the patient case report logs into mild, moderate severe and
3.indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4.Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc).
*Link to the master chart:
*Link to the covid cases elogs with answers:
[10]MEDICAL EDUCATION:
*I have learned a lot through this assignment, it was a very great experience to learn through the patient clinical data analysis (Patient centred learning) and during this crisis it is helping us a lot to learn from the patient elogs and every detailed information of the patient's problem is known through them which is very helpful and making me learn the "patient clinical data analysis" including history,diagnosis, investigations and treatment planning.
*I have made a lot of research for every detail which cleared so many doubts about the raised questions which made me learn many concepts through this assignment.
Thankyou Dr.Rakesh biswas sir for orienting towards effective learning through the patient clinical data analysis.
*I have learned the following topics through this assignment:-
1.Bronchiectasis
2.Right heart failure due to copd
3.Augmentin and thiamine
4.Wernicks encephalopathy
5.stroke (cerebrovascular accident)
6.Myelopathy hand
7.Cardio renal syndrome
8.Acute coronary syndrome
9.PCI
10.Cardiogenic shock
11.Pancreatitis
12.Liver abscess
13.IRIS
14.Mucormycosis
15.covid-19 and it's complications
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