Medicine online blended bimonthly assignment.
Online blended bimonthly assignment toward summative assessment for the month of May 2021
125 S.Neeraja Reddy. 8th sem
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
1) Pulmonology (10 Marks)
A) Link to patient details:
Case 1
1Q) what is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
Ans)Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs
Diagnosed with diabetis - 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 location of problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage
2Q)what r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
Ans)~Head end elevation :# MOA;
.improves oxygenation
.decreases incidence VAP
.increases hemodynamic performance
.increases end expiratory lung volume
.decreases incidence of aspiration
#Indication: .head injury
.meningitis
.pneumonia
~ oxygen inhalation to maintain spo2
~Bipap:non invasive method
#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation9
3. Cause for current acute excerbation.?
Ans - it could be due any infection
4.could the ATT affected her symptoms if so how?
Yes ATT affected her symptoms
Isoniazid and rifampcin ➡➡nephrotoxic - raised RFT was seen
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898246/
Att leading to acute kidney disease
5.What could be the causes for her electrolyte imbalance?
Ans:hypoventilation may be the cause of her electrolyte imbalance.
2) Neurology (10 Marks)
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:Timeline of symptoms:
- 1 year ago 2 to 3 episodes of seizures
- 4 months ago 1 episode followed by cessation of alcohol for 24hrs associated with sweating tremors restlessness
- Started taking alcohol.
- General body pains a day before main symptoms.
- Main complaints
- 9 days ago irrelevant talking and decreased food intake
- Given iv fluids by RMP
- STOPPED DRINKING ALCOHOL
- Again resumed drinking alcohol
- also short term memory loss 9 days ago.
- Patient experienced tremors, sleep disturbances, sweating when he does not consume alcohol.
- -Patient told wife that he saw his brother (who expired recently) and was talking to him.
- -H/O multiple involuntary movements associated with rolling of eyes, frothing, tongue bite, loss of consciousness.
Anatomical localization:Brain
Primary etiology:
Wernicke encephalopathy caused due to chronic alcoholism
https://www.ninds.nih.gov/Disorders/All-Disorders/Wernicke-Korsakoff-Syndrome-Information-Page#:~:text=Wernicke's%20encephalopathy%20is%20a%20degenerative,the%20brain's%20thalamus%20and%20hypothalamus.
ò2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
1. IVF NS and RL @150ml/hr
Indication: For fluid and electrolyte replenishment
2. Inj. 1amp THIAMINE in 100ml NS, TID
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.
3. Inj. Lorazepam
MOA:Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
:Indication:Management of anxiety
4. T. Pregabalin 75mg/PO/ BD
Moa:
Indication:Management of neuropathic pain,postherpetic Neuralgia,adjunctive therapy foradult patients with partial-onset seizures.
Management of fibromyalgia
5. Inj. HAI S.C.- premeal
Mechanism of action: facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver
Indication :for the treatment of Diabetes mellitus
6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am
7. Lactulose 30ml/PO/BD
Mechanism of action lactulose is a disaccharide that is not absorbed the intestine and causes retention of of water through Osmosis leading to softening of stools
Indication :constipation
8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours
9. Syp Potchlor 10ml in one glass water for low levels s of potassium. Alcohol
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Ans.: Due to kindling phenomenon
4) What is the reason for giving thiamine in this patient?
Answer:For the management of thiamine deficiency manifested by confusion in this patient.
5) What is the probable reason for kidney injury in this patient?
Answer:Alcohol can affect the ability of kidney to regulate fluid and electrolyte balance
Hypertension and alcohol can be the causes.
6). What is the probable cause for the normocytic anemia? Answer answer:haemolysis of RBC due to oxidative stress
Blood loss due to foot ulcer.
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Chronic alcoholism is the major risk factor for ulcer formation. Yes chronic alcoholism and aggravated the ulcer by delaying the ulcers healing and can cause more pain in the ulcer
Questions-
NEUROLOGY
1) What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patients problem?
- ANS. Timeline of the patient is as follows-
- 7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
- 4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
- H/O postural instability- falls while walking
- Associated with bilateral hearing loss, aural fullness, presence of tinnitus
- Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
- Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.
Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)
Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.
In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.
2) What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS.
A) Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
B) Tab Zofer 4mg- This is ondanseteron- It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications- Used to control the episodes of vomiting and nausea in this patient.
C) Tab Ecosprin 75mg- This is aspirin. It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
D) Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
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
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:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A) *Evolution of symptoms :patient was normal 8 months back then developed b/l pedal edema which gradually progressed.
Aggerevated in sitting and standing position, relived on taking medication
*Palpitations :since 5days, sudden in onset which is more during night
Aggerevated by lifting heavy weights, speaking continuously
*Dyspnoea during palpitations (NYHA-3) since 5 days
*pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.
Chest pain associated with chest heaviness since 5 days
Anatomical localisation :Brain.
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
2Q) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
A) Reason: recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
Other risk factors
A) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
B) trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C) Inadequate intake: anorexia, dementia, stareation, total parental nutrition
D) psuedohypokalemia:delayed sample analysis, significant leukocytosis
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

Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D) Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury
Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism
Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585721/
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?
Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)
E) Link to patient details:
Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?
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 ?
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 lobes
https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2585721/&ved=2ahUKEwj51oDIqvLwAhUalEsFHYmQCzIQFjALegQIDRAC&usg=AOvVaw3w7C6B9jUuaBqu-y__jzW7&cshid=1622409606090
F) Link to patient details:
http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
No Road traffic accident doesn’t have any role foror for his condition.
2.What are warning signs of CVA?
Weakness or numbness of the face, arm or leg, usually on one side of the body
Trouble speaking or understanding
Problems with vision, such as dimness or loss of vision in one or both eyes
Dizziness or problems with balance or coordination
Problems with movement or walking
Fainting or seizure
Severe headaches with no known cause, especially if they happen suddenly
3.What is the drug rationale in CVA?
Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
Ecospirin
For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.
Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.
Rt feed RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.
4. Does alcohol has any role in his attack?
When the patient met with an accident there might be cranial damage which was unnoticed.
If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition
Low and moderate self reported alcohol intake was associated with reduced risk of stroke.
5.Does his lipid profile has any role for his attack??
No his lipid profile has no
role for his attack .
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1127514/
According to this article stroke has direct relationship with triglycerides and inverse relationship with HDL
G) Link to patient details:
__*Questions*_
1)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. 
2)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".
3)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
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
According to MRI cortical vein thrombosis might be the cause of her seizures.
2) 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 inactivates factor xa.
3) Cardiology (10 Marks)
A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans:Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle cocts normally but the ventricles do not relax as they should during ventricular filling (or when the ventriclelax).
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 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.
https://www.ncbi.nlm.nih.gov/books/NBK470347/
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
Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure
high blood pressure
Smoking
Diabetes
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.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809680/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2878263/
4.What could be the cause for hypotension in this patient?
acute, rapid accumulation of fluid in the pericardium causes signs of acute hemodynamic compromise in cardiac tamponade. Patients with this condition develop tachycardia, hypotension, pulsus paradoxus, and distended neck veins
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
Answers: Chronic alcoholism, obesity, hypertension and obesity are possible causes
Patient was diagnosed with type 2 diabetes 30 years ago and was taking mixtrad insulin daily lead to trio neuropathy nephropathy and retinopathy.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494155/
Hypertension since 19 years
Chronic alcoholism since 40 years
https://www.nmcd-journal.com/article/S0939-4753(19)30360
2.what is the reason for anaemia in this case?
Reason: Chronic alcoholism
Chronic alcoholism leads to anaemia. megaloblastic and sideroblastic changes in bone marrow . Potential cause may be low Hematocrit.
Decreased rbc production in bone marrow
https://pubmed.ncbi.nlm.nih.gov/15131790/
According to this article consumption of more than 2 drinks per day is associated with significant elevation of iron overload.
https://www.medscape.com/viewarticle/562546_2
One more cause may be due to chronic kidney disease 
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Answer:As the patient is known case of diabetes and chronic alcoholic it will lead to non healing of ulcers and wound healing is impaired.
4. What sequence of stages of diabetes has been noted in this patient?
Patient was diagnosed with type 2 diabetes mellitus 30 years back
On medication Tab Glicazid 80mg BD and since 4years 15u-0-8u daily human mixtard insulin.
Since 4 years Blurring of vision(diabetic retinopathy)
Bleb and non healing ulcer formation in left leg followed by RTA 10 days back
Diabetic nephropathy.
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: *the anatomical site is BLOOD VESSELS;
* ETIOLOGY:
The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans: PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
mechanism:
Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
an enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans: *cardiorenal syndrome type 4 is seen in this patient.
4) What are the risk factors for atherosclerosis in this patient?
Ans: effect of hypertention
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
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?
TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest
Anatomical localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause
- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Pharmacological interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline.
Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). .
Non pharmacological intervention : PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
3) What are the indications and contraindications for PCI?
INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
Although PCI is generally a safe procedure , it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
.
Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant - OVERDIAGNOSIS.
Also the adverse effects due to this are more when compared to the benefits.
.Overdiagnosis through overtesting can psychologically harm the patient.
Hospitalizations for those with chronic conditions who could be treated as outpatients can lead to economic burden and a feeling of isolation.
E) Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer:symptomatology ➡➡ Mild chest pain 3 days ago
Insidious in onset gradually progressive, dragging type and radiating to back.
Known case of hypertension and type 2 diabetes
Vaccinated for covid 19 5 days back
Primary etiology:Blood vessels (coronary)
Myocardial infarction occurs due to thrombosis occlusion of coronary vessels. There will be rupture of vulnerable plaque and ischemia of a
ffected myocardium causes systolic function defect.
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.tablet aspirin
mechanism: irreversible inhibition of cox activities
For prevention of antithrombotic events of arteries
2.TAB ATORVOSTATIN
Mechanism: competitively inhibits HMG-COA reductase
To reduce cholesterol production in liver
3.TAB CLOPIDOGREL
Mechanism:Selectively inhibits binding of ADP TO P2Y12 RECEPTOR
inhibits platelet aggregation
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
5.ANGIOPLASTY
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
➡
Ans:the second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with
➡higher rates of both procedure-related and true ST elevation reinfarction.
A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient.
Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended.
F)
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.
4.Gastroenterology
Gastroenterology (& Pulmonology)
A) Link to patient details:
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Symptomatology:
Developed pain abdomen and vomiting 5yrs ago
Treatment was given conservatively
Stopped alcohol 3 yrs back
In past 1year 5 to 6 episodes of pain abdomen and vomitings
20 days back increased intake of alcohol
1 week back developed pain abdomen vomiting
constipation, burning micturition, fever since 4 days.
Anatomical location:pancreas
Etiology:increased alcohol consumption 20days back might aggrevated the previous symptoms.
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
1.Inj.Meropenam
#Carbapenem type antibiotic for infections
2.Inj Metrogyl
Is an antibiotic
Nitromimidazole drug
3) ING. AMIKACIN 500 mg IV BD for 5days
* It is an Aminoglycoside antibiotic
antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.
4) TPN ( Total Parenteral Nutrition )
* Method of feeding that by passes gastrointestinal tract
* TPN has proteins, carbohydrates, fats, vitamins, minerals.
5) IV NS / RL at the rate 12l ml per hour
treat dehydration
6) ING. OCTREOTIDE 100 mg SC , BD
* It is a Somatostatin long acting analogue.
* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.
7) ING. PANTOP 40 mg IV , OD
* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
* It is B1 supplement.
* It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
* Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
9) ING. TRAMADOL in 100 ml NS IV , OD
* It is an opioid analgesic, given to releive pain
Non pharmacological:IcD and màlacot drain
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer:a.PLEURAL EFFUSION
In patients with pleural effusion associated with acute pancreatitis
Dyspnea is the symptom.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Elevated cortisol
Damaged pancreatic beta cells leading to downregulation of insulin
Elevated levels of corticosteroids.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
A
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
4) What is the line of treatment in this patient?
Plan of action and Treatment:
Investigations:
✓ 24 hour urinary protein
✓ Fasting and Post prandial Blood glucose
✓ HbA1c
✓ USG guided pleural tapping
Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly
C) Link to patient details:
Possible Questions :-
1) what is the most probable diagnosis in this patient?
Answer: Abdominal hemorrhage
Differential diagnosis
Ruptured liver abscess
Intraperitoneal hematoma
Free fluid in sub diaphragmatic space
2) What was the cause of her death?
After leaving hospital
She undergone laporomy surgery .May be patient died due to complications of surgery like hemorrhage or infection.
3) Does her NSAID abuse have something to do with her condition? How?
Yes
NSAID may caused hepatotoxicity
It might have lead to renal dysfunction like decreased gfr, and acute renal failure,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809680/
5) Nephrology (and Urology) 10 Marks
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 inurine
Ans-plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him
4. What are the complicat ions of TURP that he may have had
Ans-
Difficulty micturition
Electrolyte imbalances
Infection
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
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 ?
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?
antibiotic and painkiller therapy for infection and PAIN relief
For overreactive. Bladder anticholinergic to prevent abnormal involuntary muscle contractions of detrusor muscle.
To treat attention deficit hyperactivity disorder
METHYLPHENIDATE stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
Amphetamine belongs to a class of drugs known as stimulants.
It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems.
It may also help you to organize your tasks and improve listening skills.
Questions
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
Ans
Patient has cough and difficulty in swallowing since 2 months
Laryngeal crepitus present
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent.
The immune reconstitution inflammatory syndrome (IRIS) is a frequent early complication of antiretroviral therapy (ART) in patients with advanced HIV. Because there is no confirmatory diagnostic test, the diagnosis is based on clinical presentation and exclusion of alternative causes for deterioration, such as antimicrobial drug resistance. Opportunistic infection treatment should be optimized. Mild cases may require symptomatic therapy alone or nonsteroidal anti-inflammatory drugs. Corticosteroids have been used to treat more severe cases of IRIS associated with mycobacterial and fungal infections. There is evidence from a randomized controlled trial that prednisone reduces morbidity and improves symptoms in paradoxical tuberculosis (TB)-IRIS. Neurological TB-IRIS is potentially life-threatening; high-dose corticosteroids are indicated and ART interruption should be considered if level of consciousness is depressed. When considering corticosteroid treatment clinicians should be aware of their side effects and only use them when the diagnosis of IRIS is certain. In viral forms of IRIS corticosteroids are generally avoided.
7) Infectious disease and Hepatology:
A)Link to patient details:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors
present in it ?
What could be the cause in this patient ?
Ans: yes could be due to the consumption of toddy.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
Ans:Conclusion:From our study it was undoubtedly proved that alcoholism, mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/
3. Is liver abscess more common in right lobe ?
Ans : Yes right lobe receives more blood supply from superior mesenteric and portal veins.
4.What are the indications for ultrasound guided aspiration of liver abscess ?
Ans : ➡➡caudate lobe abcess
➡Left lobe abcess
➡abcess which is not responding to drugs
➡abcess more than 6cms
B) Link to patient details:
QUESTIONS:
1) Cause of liver abcess in this patient ?
A) 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.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/
2) How do you approach this patient ?
A) * The patient is well managed by treating team ; even me will follow the same approach.
3) Why do we treat here ; both amoebic and pyogenic liver abscess?
A) * Considering the following factors:
1) Age and gender of patient: 21 years ( young ) and 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:
1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.
2) Sometimes ; it has thin thinwall which may rupture if u aspirate.
3) Sometimes ; it is unliquefied.
## There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.
https://academic.oup.com/bmb/article/132/1/45/567714
4) Is there a way to confirmthe definitive diagnosis in this patient?
A) * Yes in a high resource setting cause of liver abscess is usually determined using multiple diagnostic strategies , including blood cultures , entamoeba serology , liver abscess aspirate for culture and molecular and antigen testing.
https://academic.oup.com/bmb/article/132/1/45/5677141
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) Link to patient details:
Questions :
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer:
3 years back diagnosed by hypertension
21 days back received vaccination followed by fever chills and rigor
High grade fever relieved by medication.
18 days ago experienced same symptoms but not relieved by medication
11days sago generalized weakness and facial puffiness and periorbital edema
4 days ago :diagnosed by diabetes ,
bloodtinged serous discharge from left eye,
periorbital edema and weakness of right upper Limb and right lower Limb
Patient died 2 days ago.
Patient was diagnosed with acute infarct in left frontal and temporal lobe
and acute oro rhino orbital 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: Inj Liposomal amphotericin B according to creatinine clearance.
https://pubmed.ncbi.nlm.nih.gov/14579660/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2947016/
200mg itraconazole which was adjusted to creatinine clearance
Deoxycholate drug not available.
Posaconazole not affordable
Diabetic ketoacidosis management :
1. fluid and electrolyte replacement :
The lost fluids and electrolyte replenishment and for diluting the excess sugar in blood.
2.Insulin therapy:
It also helps in reversal of diabetic ketoacidosis.
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Answer: Mucormycosis is triggered by the use of steroids in covid 19 patients . Incidence is on rise due to increased use of Chemotherapy and steroids .
The steroids are life saving by reducing inflammation in lungs but also reduce s immunity an increases the blood sugar levels in both diabetic and non diabetic covid patients .
9 Questions1) 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).
Master chart
10.Medical education
Elog making helped me alot in learning new cases and questions and discussions are very much helpful. Through e blogging which very new my best experience where we can correlate with very first symptom her progression and final investigation of the patient.Thank you so much sir making patient centered learning
1) Covid 19 with co morbidity (Pulmonology/Rheumatology)
Possible questions:
1) How does the pre-existing ILD determine the prognosis of this patient?
9) Infectious Disease (Covid 19)
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
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).
1) Covid 19 with co morbidity (Pulmonology/Rheumatology)
Questions:
1) How does the pre-existing ILD determine the prognosis of this patient?
The pre-existing ILD significantly worsens the prognosis of this covid patient.
Interstitial lung disease is characterized by dyspnea, decreased pulmonary diffusing capacity, decreased FVC and TL
Radiology (HRCT) usually shows the development of new pulmonary opacities and fibrosis.
.
Prognosis: Poor
2) Why was she prescribed clexane (enoxaparin)?
The main pathogenesis of systemic inflammation caused by Covid-19 is by inducing a cytokine storm that causes epithelial cell necrosis, increased vascular permeability, dysfunctional humoral and CMI which all collectively lead to acute lung injury and ARDS
Of these cytokines, IL-6 is one that is the most important in determining the prognosis. IL-6 levels are highly elevated in patients with severe disease
CASE 9-2: COVID-19 SEVERE
QUESTIONS:
1) Since patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause the indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausibl
The patient had slight hyperglycemia, high HbA1c levels (7.1%), which may have aggravated due to COVID-19.
2) Did the patient's diabetic condition influence the progression of her pneumonia?
Yes, with DM or hypergycemia in patients leads to an increase in COVID-19 severity.
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
D- Dimer levels indicate the severity of COVID-19, pertaining to possible thrombotic compliicatons- as D Dimer is formed post- fibrinolysis.
D- Dimer does change the management, as D-Dimer levels above 2000ng/dl were found to have a direct link with increasing severity of COVID-19
CASE 9-3 (COVID-19 SEVERE)
QUESTIONS:
1. Why was this patient given noradrenaline?
Following kidney failure, the patient had sudden and persistent hypotension.
2. What is the reason behind testing for LDH levels in this patient?
LDH (Lactate Dehydrogenase) catalyzes the conversion of lactate to pyruvate and back. Hence, an increase in LDH denotes some form of tissue damage. In this patient, an increase in LDH levels would denote inflammation, and a high increase would denote Multi-Organ Failure.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
Although BiPaP is a positive pressure system, unlike tracheal intubation, it does not send the air to the trachea and depends on the patient's ability to respire. In this patient, as SpO2 levels were dropping to 30% so switched to mechanical ventilation
CASE 9-4 (COVID-19 MILD)
https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1
QUESTIONS:
1. Is the elevated esr due to covid related inflammation?
Yes, as ESR is an important indicator of immunological loss and immunological dysfunction.
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
Hospitalisation was due to Grade 3 Shortness of Breath (SOB), and long duration of COVID-19 infection.
Challenges of home isolation-
Physical emotional and social challenges
Harms of hospitalisation-infection cost and overtesting
CASE 9-5 (COVID-19 SEVERE)
https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html
QUESTIONS:
1) What was the reason for coma in this patient?
Severe hypoxia and low spo2 leading to coma
2) What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related?
The main competency gap was in the lack of testing for serum electrolytes, as the hypokalemia had caused weakness and fatigue in this patient.
Hospital 2 make a diagnosis of hypokalemic periodic paralysis based on the fact that the patient had generalised weakness before becoming comatose, along with tingling and symptoms of paralysis. On testing serum electrolytes, his potassium levels were found to be 2.3 mEq/L (normal-3.5-5)
3) How may covid 19 cause coma?
Yes, as the brain is extremely sensitive to oxygen, oxygen deprivation due to COVID-19 can lead to a comatose state.
Spo2 levels (20%), which may have caused the coma.
CASE 9-6 (COVID-19 WITH ALTERED SENSORIUM)
https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html
QUESTIONS:
1. What was the cause of his altered sensorium?
Probable causes include
Hypoxia and increased urea levels leading to uraemic encephalopathy
2. what is the cause of death in this patient?
The cause of death in this patients was due to complications of COVID-19, most probably Acute Kidney Failure (AKI) due to increased urea and creatinine levels.
:
7) A 67 year old lady in the ICU with COVID induced Viral Pneumonia .
https://drsaranyaroshni.blogspot.com/2021/05/a-67-year-old-lady-in-icu-with-covid.html
Q1. What is the grade of pneumonia in her?
A. Moderate based her ct severity score.
Q2. What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?
A. It isbest to start dexamethasone before cytokine storm onset
Q3. What all could be the factors that led to psychosis in her ?
A. The following can lead to ICU psychosis
Sleep deprivation
Stress
Continuous monitoring
Lack of orientation
Dehydration
Q4. In what ways shall the two drugs prescribed to her for psychosis help ?
A. Pirecetam improves memory and causes cognitive enhancement
Resperidone acts by decreasing the dopaminergic pathways in the brain
Q5. What all are the other means to manage such a case of psychosis?
A. The icu psychosis can be managed by sleep deprivation correction
Haloperidol drug is used for managing icu psychosis.
Anti-psychotics.
Q6. What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharged ?
A. The patient is supposed to self isolate after they are discharged for next 7 days
Look for danger signs like breathlessnes and bluish discolouration
Continue o2 monitoring.
Q7. What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge?
Elevated levels of D Dimer and CRP and persistence of cough,fever and breathlessnes
8) 35YR/M WITH VIRAL PNEUMONIA SECONDARY TO COVID 19 INFECTION
https://bhavaniv.blogspot.com/2021/05/35yrm-with-viral-pneumonia-secondary-to.html?m=1
Q1. Can psoriasis be a risk factor for severe form of COVID?
A. There is no evidence that patients with moderate-to-severe psoriasis receiving systemic treatments, including biologics, have higher risk of SARS-CoV-2 infection and/or increased hospitalization and death related to COVID-19 compared to the general population.
Q2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?
A. Immunomodulators help COVID 19 patients by suppressing the cytokine storm but they also have thepotentialt to increase the risk of infection (like mucormycosis), traditional clinical signs may be masked with resulting delays in identification and treatment.
Q3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
A. Increasing evidence from experimental and clinical studies suggests that mechanical ventilation, which is necessary for life support in patients with acute respiratory distress syndrome as seen in COVID 19 can cause lung fibrosis, which may significantly contribute to morbidity and mortality. It is believed that ventilator induced lung injury is the cause for the fibroproliferative changes and the resultant lung fibrosis.
9) 45 year old female with viral pneumonia secondary to Covid-19
https://vidya36.blogspot.com/2021/05/comparative-study.html?m=1
Q1. What is the type of DM the patient has developed ?(is it the incidental finding of type 2 DM or virus induced type 1DM)?
A. Incedental type 2 DM can be differentiated from de novo covid induced type 1 DM with the help of the HbAc1 levels.
As HbAc1 levels are indicators of long term blood ssugar levels they are likely to be raised in pre existing DM that was incidentally discovered. But in case ofthe diabetes being de novo in nature then the HbAc1 levels are unlikely to be raised. As the patients HbAc1 levels are not raised we can not at this point determine if the patient has incedental discovered type 2 DM or Covid induced de novo DM.
Q2. Could it be steroid induced Diabetes in this patient?
A. As the patient was given dexamethasone as a part of her treatment regimen it is possible that her elevated glucose levels are a result of steroid induced hyperglycemia.
10) A little difference that altered the entire covid recovery game: a report of two patients with focus on imaging findings.
https://vidya36.blogspot.com/2021/05/comparative-study.html?m=1
Q1. What are the known factors driving early recovery in covid?
A. The following factors can lay a role:
Younger age ggroup
shorter duration of fever
No diabetes
PaO2/FiO2 levels
No comorbidities
11) Viral pneumonia secondary to COVID of a denovo Diabetes Mellitus
https://rishithareddy30.blogspot.com/2021/05/covid-case-report.html
1. How is the diabetes related to the prognosis of COVID patients? What are the factors precipitating diabetes in a patient developing both covid as well as Diabetes for the first time?
A. People suffering from diabetes are like to experience more severe symptoms of the disease than the ones who are not diabetic. Even within the patients that are diabetic the people whose disease is under better control tendtendvbe better diagnosis.
Possible causes for de nov diabetes in COVID19 include:
· The SARS CoV 2 virus enters the cells through the ACE 2 receptors which are present in large numbers in the pancreas and that this damages the pancreatic cells.
· Another theory is that the inflammation caused by the cytokine storm damages the beta cells.
Q2. Why couldn't the treating team start her on oral hypoglycemics earlier?
A. As the insulin is faster acting as compared to oral hypoglycemics and as her blood glucose level was very high it is important to bring it down as fast as possible.
12) Moderate to severe covid with prolonged hospital stay:
https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html
Questions:-
1) What are the potential bio clinical markers in this patient that may have predicted the prolonged course of her illness?
Serum LDH: 571U/L (Normal range=140-280U/L
ALP : 342 U/L (Normal range=44-147U/L)
SpO2: 82% at RA (Normal range= >96%)
HR: 124bpm (Normal range=60-100bpm)
Classically, the bio clinical markers that are predictive of a Covid-19 patient's outcome are
C reactive protein [>57.9mg/dL]
D-Dimer [>1mcg/ml associated with poorer prognosis]
Serum LDH [>248U/L]
IL-6 [2.9 times higher in severe disease compared to mild disease]
SGPT [Isolated rise in SGPT >3 times the normal value]
ESR [high sustained level after recovery from infection]
Albumin
Platelet count
Neutrophil count
NLR: [>5.5]
Urea
Creatinine
High sensitivity Troponin
The patient in question has elevated levels of serum LDH and ALP. Her CRP and D-Dimer levels are not high enough to be considered as a bad prognostic factor.
Sources: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219356/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7194951/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896696/
13) Severe covid with first diabetes
Link to Case report log :
https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html
1) What are the consequences of uncontrolled hyperglycemia in covid patients?
Hyperglycemia can lead to anomalous glycosylation of tissue receptors throughout the body. One of these receptors happens to be ACE2, the same receptor SARS-CoV2 uses to gain entry into the host cell. In fact, glycosylation of ACE2 is necessary for the virus to establish an infection.
Uncontrolled hyperglycemia freely facilitates this glycosylation, making these patients more susceptible to Covid-19 infections and increasing the severity of the infection by helping increase the viral load (by increasing the concentration of glycosylated ACE2)
Control of blood sugar can also decrease the chances of a cytokine storm during the second phase of the infection.
Uncontrolled hyperglycemia hence, suggests a poor prognosis in Covid-19 patients.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7188620/#:~:text=Therefore%2C%20high%20and%20aberrantly%20glycosylated,and%20a%20higher%20disease%20severity.
2) Does the significant rise in LDH suggests multiple organ failure?
Lactate dehydrogenase has 5 isoenzymes that are present in various tissues such as the heart, RBCs, lungs, liver, kidney, brain, and skeletal muscle.
Since covid-19 primarily causes lung damage, LDH3 is released into the blood giving an elevated titer.
Multi-organ damage that involves the heart (myocarditis) or kidneys (renal failure) can lead to an elevation in respected isoenzymes found in these tissues.
Hence, a significant rise in LDH indicates a poor prognosis and points towards multi-organ damage.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7251362/
3) What is the cause of death in this case?
This patient was diagnosed with uncontrolled hyperglycemia with severe covid pneumonia.
LFT shows elevated AST, ALT, and ALP with a gross increase in bilirubin titer.
The D-Dimer is elevated (560ng/ml) and the LDH is 835U/L both of which are indicators of a poor prognosis.
The most likely cause of death in this patient seems to be ARDS.
The immediate cause of death: Most probably cardio-pulmonary arrest
Antecedent cause: Severe covid-19 pneumonia
14) Long covid with sleep deprivation and ICU psychosis
https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html
Questions:
1)Which subtype of ICU psychosis did the patient land into according to his symptoms?
Hyperactive delirium: Manifests as agitation, restlessness, refusal to cooperate with caregivers, unprovoked mood changes, hallucinations
2)What are the risk factors in the patient that has driven this case more towards ICU psychosis?
Hypertension
History of cerebrovascular accident (makes him more prone to a new one)
Steroid use
Sedative use (Gabapentin)
COPD
3)The patient is sleep-deprived during his hospital stay. Which do you think might be the most probable condition?
A) Sleep deprivation causing ICU psychosis
B) ICU psychosis causing sleep deprivation
B) ICU psychosis causing sleep deprivation is more likely in this patient
4) What are the drivers toward current persistent hypoxia and long covid in this patient?
Elevated bio clinical markers like D-Dimer, LDH, Neutrophils, WBCs(absolute), IL-6, and CRP all contribute to persistent hypoxia and worsen the prognosis. In addition to this, ICU psychosis adds to the prolonged hospital stay.
15) Moderate Covid with comorbidity (Truncal obesity and recent hyperglycemia)
https://meghanaraomuddada.blogspot.com/2021/05/case-1-2021-42yr-old-male-with-fever.html
Questions:
1. As the patient is a non-diabetic, can the use of steroids cause a transient rise in blood glucose?
Cortisol stimulates gluconeogenesis in the liver and inhibits glycogen synthesis, increasing blood glucose. Continuous treatment with corticosteroids can lead to elevated blood glucose titers even in non-diabetics.
2. If yes, can this transient rise lead to long-term complications of New-onset diabetes mellitus?
It is still unclear if the alterations brought about by covid-19 in the glucose metabolism are permanent and persist or remit after the resolution of infection. There are ongoing studies that aim to answer these questions.
Steroid diabetes is a term coined to describe diabetes mellitus arising as a result of glucocorticoid use for more than 50 years
3. How can this adversely affect the prognosis of the patient?
Hyperglycemia in general is indicative of a poorer prognosis in a patient compared to covid patients with normal blood glucose levels.
4. How can this transient hyperglycemia be treated to avoid complications and a bad prognosis?
Oral hypoglycemics (such as sulfonylureas) are efficient at controlling blood glucose levels in non-diabetics who develop steroid-induced hyperglycemia.
5. What is thrombophlebitis fever?
Fever in response to thrombophlebitis that is caused due to release of inflammatory mediators
6. Should the infusion be stopped in order to control the infusion thrombophlebitis? What are the alternatives?
No.
Thrombophlebitis can be treated by local compressive dressings, NSAIDs (topical and/or systemic)
16) Mild to moderate covid with hyperglycemia
Questions:
1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?
The possible factors that could have led to precipitation of diabetes in a covid-19 patient are:
Genetic susceptibility to diabetes
Pre diabetic state
Viral insult to the beta cells of the pancreas
High dose steroid usage
17) Covid 19 with hypertension comorbidity
1)Does hypertension have any effect to do with the severity of the covid infection.If it is, Then how?
Yes, hypertensive patients are at a higher risk of COVID 19 severity.
They have high risk of developing cardiovascular and endorgan failure
2)what is the cause for pleural effusion to occur??
Pneumonia caused due to COVID-19 infection lead to increase permeability of microvascular circulation which lead to pleural effusion(exudative type)
18) Covid 19 with mild hypoalbuminemia
QUESTIONS:
1. What is the reason for hypoalbuminemia in the patient?
The reason for hypoalbuminemia in COVID_9 patient is due to increased catabolism of albumin to make amino acids as well as simulataneous decrease in albumin synthesis
2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
Exanthem is an eruptive skin rash seen in viral infections. Yes, this could be due to COVID-19 infection. The exanthem in COVID-19 resembles that of varicella.
2. What is the reason for Cardiomegaly?
High blood pressure might be the underlying cause for cardiomegaly in this patient.
Uncontrolled high blood pressure leads to increase in work load of heart leading to cardiomegaly.
3. What other differential diagnoses could be drawn if the patient tested negative for covid infection?
· Chicken pox
· Shingles
· Pytriasis
4. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?
D-dimer is increased in a COVID-19 patient. It may be related to the viral life cycle. The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels.
20) Covid 19 with first time diabetes
Questions:
1)Can usage of steroids in diabetic Covid patients increases death rate because of the adverse effects of steroids???
COVID-19 infection causes systemic inflammation and cytokine leadth to inceased death rate.
In diabetic patient due to disruption of carbohydrates metabolism and leading to hyperglycemia can be the outcome of steroids.
2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically?
In COVID-19 infection due to cytokine storm and inflammation leading to damage of blood vessels. Due to high cholesterol levels it is causing stroke.
3)Does chronic alcoholism have effect on the out come of Covid infection?If yes,how?
Yes, chronic alcoholism does worsen the prognosis of COVID-19 patient.
Chronic alcoholism leads to impaired immune response
21) Severe Covid with Diabetes
Questions-
1. What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non diabetics?
it is observed that there is a early as well as aggressive progression of COVID 19 in diabetics.
Hyperglycemia and low immunity
2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?
methylprednisolone from 40 mg/day to 160 mg/day for 6 days according to the weight and status of the patients.
Continous monitoring of blood sugar levels.
3. What effect does a history of CVA have on COVID prognosis?
History of CVA with coagulopathy leads to poor prognosis
23) Covid 19 with multiple comorbidities:
1) What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection?
· Old age
· Diabetes mellitus type 2
· Chronic kidney disease
· Bronchial asthama
2) Can you explain why the D dimer levels are increasing in this patient?
It may be related to the viral life cycle. The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels
3) What were the treatment options taken up with falling oxygen saturation?
· Head elevation
· O2 supplementation
4) Can you think of an appropriate explanation as to why the patient has developed CKD, 2 years ago? (Note: Despite being on anti diabetic medication, there was no regular monitoring of blood sugar levels and hence no way to know for sure if it was being controlled or not)
During the early stage diabetes, there is a increase in blood flow to the kidneys, which strains the glomeruli and lessenstheir ability to filter blood. High levels of glucose in the blood leads to accumulation of extra material in glomeruli. It increases the stress of glomeruli inturn leading to gradual and progressive scarring. Eventually leads to the development of CKD
Question 10.Medical education
Elog making helpedme alot in learning new cases and questions and discussions are very much helpful. Through e blogging i learnt a lot of things which was very new my best experience where we can correlate with very first symptom her progression and final investigation treatment modality of the patient .Thank you so much sir for making patient centered learning as a best platform for acquiring great clinical knowledge.
Thanks to all the interns and pgs for the guidance.
May 19th 2021
I was alloted a case for eblog making.
May 20 2021
I published the case with possible questions.
Thanks to Dr.Rakesh Biswas sir for this making this e learning interesting with case discussions and blogging.
May 19th 2021
I was alloted a case for eblog making.
May 20 2021
I published the case with possible questions.
Thanks to Dr.Rakesh Biswas sir for this making this e learning interesting with case discussions and blogging.
Elog making helping me alot in learning new cases and questions and discussions are very much helpful. Through e blogging i learnt a lot of things which was very new my best experience where we can correlate with very first symptom her progression and final investigation treatment modality of the patient .Thank you so much sir for making patient centered learning as a best platform for acquiring great clinical knowledge.
Thanks to all the interns and pgs for the guidance.
May 19th 2021
I was alloted a case for eblog making.
May 20 2021
I published the case with possible questions.
Thanks to Dr.Rakesh Biswas sir for this making this e learning interesting with case discussions and blogging
No comments:
Post a Comment