Medicine Blended Assignment (May 2021)
Anigani Kavya
roll number- 06
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.
This is the link of the questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1) Pulmonology:
A) Link to patient details:
Question 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:
- 1st episode of SOB- 20years back
- 2nd episode- 12years back (from then she has been having yearly episodes for the past 12years)
- 15years back- Facial puffiness
- 8years back- Diagnosed with diabetes
- 5years ago- Diagnosed with anemia and took iron injections
- 1month back- Generalized weakness
- 20days back- Diagnosed with hypertension
- 15days back- Pedal edema
Anatomical Location of problem-Lungs- Bronchi and bronchioles
Primary etiology- Usage of chulha since 20years
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
- HEAD END ELEVATION:
Indications:
- Head injury
- Meningitis
- Pneumonia
- oxygen inhalation to maintain SpO2
Mechanism of action- It assists ventilation by delivering positive expiratory and inspiratory pressure without need of endotracheal intubation
Indications:
- COPD
- Obstructive sleep apnea
- Pneumonia
Question 3: What could be the causes for her current acute exacerbation?
Answer: Cause due to current acute exacerbation is due to infection (bacterial, viral)
Question 4: Could the ATT have affected her symptoms? If so how?
Answer: Isoniazid and Rifampicin are nephrotoxic. Raised RFT was seen in this patient
RFT: Urea- 48mg/dl ; Creatinine- 1.9mg/dl
Question 5: What could be the causes for her electrolyte imbalance?
Answer:
- Arises out of disease process
- Respiratory acidosis and
metabolic alkalosis
- Long standing steroid therapy (example- use of beta-2 agonist like salbutamol contribute to hypokalemia in patients with COPD)
Case 1
A) Link to patient details:
Question 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: Evalution of symptoms-
- 1year ago- he had 2-3 episodes of seizure
- 4months ago- he developed seizures following cessation of alcohol for 24hrs, which was associated with restlessness, sweating and tremors
- since 9days- he started talking and laughing to himself, which is sudden in onset, he was unable to lift himself from the bed and move around, it was associated with decrease in food intake and memory loss
Etiology- the deficiency of thiamine is due to chronic alcohol consumption which causes impaired absorption of thiamine from intestine, and increase in levels of toxins due to renal disease is primary etiology
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1. Thiamine- helps the body cells change carbohydrates into energy. It has been used as supplement
2.Lorazepam
3.Pregablin
4. Lactulose- decreases intestinal production and absorption of ammonia
5. Potchlor liquid- used to treat low levels of potassium in body
Question 3: Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Answer: Due to excess thiamine deficiency and excess toxins accumulation and due to renal disease caused by excess alcohol addiction.
Question 4: What is the reason for giving thiamine in this patient?
Answer:
- Chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism.
- This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation.
- Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate.
- This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.
Answer:
- The kidneys have an important job as a filter for harmful substances, alcohol causes changes in the function of the kidneys and makes them less able to filter the blood.
- Alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function.
- People who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.
Answer:
- Alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e, bonemarrow and the metabolism of iron.
- Alcohol causes a affect on progenitor cells of blood causing decreased WBC and RBC.alochol decreases iron absorption from intestine.
Answer: Yes, as the patient is diabetic the chance of ulcer formation increases. In a patient who is chronic alcoholic the immune system is weak due to the affect on blood cells formation and iron absorption. Thus Healing of an ulcer dampens.
Case 2
B) Link to patient details:
Question 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: 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). Conditions causing ataxia are:
- Head trauma
- Alcohol abuse
- Stroke
- Tumours
- Cerebral palsy
- Cerebral palsy
- 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.
Answer:
1. Tab Vertin 8mg
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
2. Tab Zofer 4mg
Indications- Used to control the episodes of vomiting and nausea in this patient.
3. Tab Ecosprin 75mg
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
4. Tab Atorvostatin 40mg-
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
5. 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
6.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.
7. Tab MVT- This is methylcobalmin. Mainly given in vItamin b12 defficency
Question 3: Did the patients history of denovo HTN contribute to his current condition?
Answer:
- 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.
Answer:
- Meta analysis of the relation bewteen alcohol consumption and increased risk of stroke has mainly weighed into the formation of two types of 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.
- 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:
Question 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:
- 1year ago- history of paresis due to hypokalemia and an episode of paralysis of both upper and lower limbs(right and left).
- 8months back- he developed b/l pedal edema which gradually progressed
- since 5days- palpitations and dyspnoea (NYHA-3) which was more sudden in onset and more during night
- Chest pain associacted with heaviness since 5days
- since 6days- pain radiating along left upper limb, more during palpitations
- Palpitations, chest pain- CVS
- paralysis of limbs-skeletal muscles
- pedal edema- renal
- Hypokalemia leading to palpitationa ,chest pain and pedal edema.
- Radiating pain along her left upper limb due to cervical spondylosis
Answer:
Reason- Recurrent hypokalemic periodic paralysis
Risk factors-
- Current risk factor- usage of diuretics
- Other risk factors- Osmatic diuresis, renal tubular acidosis
- Trance cellular shift- alkalosis, thyrotoxicosis, head injury
- Anorexia, dementia
- Pseudohypokalemia- delayed sample analysis
Answer: ECG changes
- Decreased T wave amplitude
- ST depression
- Prolonged P-R interval
- Presence of U-waves
Case 4
D) Link to patient details:
Question 1: Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Answer:
Occurrence of seizure due to brain stroke
- Cells in the brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.
Mechanism of seizure activity:
- Seizures after ischaemic strokes.-An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate toxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury
- Seizures after haemorrhagic strokes are thought to be attributable to irritation due to hemosiderin deposits caused by products of blood metabolism.
Answer: Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousnes
Case 5
E) Link to patient details:
Question 1:What could have been the reason for this patient to develop ataxia in the past 1 year?
Answer: The patient has minor unattended head injuries in the past 1 yr. According to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal love ataxia.
Question 2: What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Answer:
- 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 alcoholic
- 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.
F) Link to patient details:
Question 1: Does the patient's history of road traffic accident have any role in his present condition?
Answer: The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition
Question 2: What are warning signs of CVA?
Answer:
- 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
Answer:
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.
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- 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.
Question 4: Does alcohol has any role in his attack?
Answer: 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 which were healing and might have caused this condition.
Question 5: Does his lipid profile has any role for his attack??
Answer: 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.
Case 7
G) Link to patient details:
Question 1: What is myelopathy hand ?
Answer: 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.
Question 2: What is finger escape ?
Answer: Presence of weak finger adduction in cervical myelopathy is called - FINGER ESCAPE SIGN
Answer: It is a 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 nerves
H-REFLEX- is expression of of monosynaptic reflex, which runs in afferents from the muscle and back again through efferents of same muscles
Case 8
H) Link to patient details:
Question 1: What can be the cause of her condition ?
Answer: According to MRI cortical vein thrombosis might be the cause of her seizures.
Question 2: What are the risk factors for cortical vein thrombosis?
Answer:
- 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
Answer: 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.
Question 4: What drug was used in suspicion of cortical venous sinus thrombosis?
Answer: 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
Case 1
A) Link to patient details:
Question 1: What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Answer: 
Question 2: Why haven't we done pericardiocenetis in this pateint?
Answer:Pericardiocentesis is not done here, because the effusion was self healing ,it reduced from 2.4cm to 1.9cm.
Question 3: .What are the risk factors for development of heart failure in the patient?
Answer: Risk factors for development of heart faliure in this patient
- 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.
- Worsening of pericardial effusion leading to cardiac tamponade.
Answer: Visceral pericardium may have thickened which is restricting the heart to expand causing hypotension (May be secondary to TB)
Case 2
B) Link to patient details:
Question 1: What are the possible causes for heart failure in this patient?
Answer: Patient has diabetes since 30yrs back and also having diabetic triopathy(neuropathy-retinopathy - nephropathy), so there is an increased risk for heart failure
- Hypertension since 19yrs - important risk factor
- Chronic alcoholic since 40yrs, leads to decreased LVEF and causes LV dysfunction
- Patient has elevated creatinine, chronic kidney disease, AST/ALT greater than 2,all of this are important risk factors for heart failure
Question 2: what is the reason for anaemia in this case?
Answer: The patient has normocytic normochromic anemia, it could be anaemia of chronic disease as the patient is diagnosed with CKD stage IV.
- CKD results in decreased production of erythropoietin which in turn decreases the production of RBCs from bone marrow
- Patients with anaemia and CKD also have definciency in nutrients like iron, vitamin B12 and folic acid which are essential in making healthy red blood cells
Answer: The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.
Question 4: What sequence of stages of diabetes has been noted in this patient?
Answer:
Stages of Type 2 diabetes
The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy
Case 3
C) Link to patient details:
Question 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:
- Since 3years- On and off pain at surgical site (surgery for inguinal hernia was done 10yrs ago)
- Since 2years- On and off facial puffiness
- 1year ago- SOB (Grade-2) on exertion
- Since 1year- Hypertensive
- Since 2days- SOB (Grade-2) on exertion which progressed to Grade-4 at rest and decrease in urine output and anuria
Etiology- Physical stress of hypertension on arterial walls leads to aggravation and acceleration of atherosclerosis
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
PHARMACOLOGICAL INTERVENTIONS:
1.TAB. Dytor- 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- 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- 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
5.TAB. Digoxin-
NON PHARMACOLOGICAL INTERVENTIONS
- Hypoglycemia symptoms explained
- Watch for any bleeding manifestations like Petechiae, Bleeding gums.
- 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.
Answer: Cardiorenal syndrome type 4 is seen in this patient
Question 4: What are the risk factors for atherosclerosis in this patient?
Answer:Risk factors for atherosclerosis in this patient is hypertention
Question 5: Why was the patient asked to get those APTT, INR tests for review?
Answer:
- 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.
Case 4
D) Link to patient details:
Question 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: 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)
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
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
Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
EFFICACY STUDIES
Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.
Results: mean baseline BP was 132/78 +/- 9/9 mmHg. Following 4 weeks of treatment, mean changes in sitting BP were: placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9 mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg. Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.
Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
Question 3: What are the indications and contraindications for PCI?
Answer:
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
Question 4: What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
Answer: 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
Case 5
E) Link to patient details:
Question 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:
- 3days back- he developed mild chest pain on right side
- Dizziness was not increasing or decreasing with change of position
- He is known case of HTN and type 2 diabetes
Anatomical location- BLOOD VESSELS
Etiology- Myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
PHARMACOLOGICAL INNTERVENTIONS
1. TAB ASPIRIN
2.TAB ATORVAS
3. TAB CLOPIBB
4.INJ HAI
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.
Question 3: Did the secondary PTCA do any good to the patient or was it unnecessary?
Answer: 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.3 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:
Question 1: How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Answer: Because of the fluid loss occurred to the patient there is decreased preload- so, SOB occurred due to decreased CO2
IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.
Question 2: What is the rationale of using torsemide in this patient?
Answer: Torsemide used to relieve abdominal distension.
Question 3: Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Answer: IT IS THE TREATMENT FOR UTI
Rationale- Used for any bacterial infection.
4) Gastroenterology:
Case 1
A) Link to patient details:
Question 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: 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: Pancreas and left lung
Etiology-
- Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury.
- Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation.
- Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
Answer- approach to treat the patient
Antibiotics given to combact infection
TNP preferred because of the gastrointestinal symptoms of the patient.
Pleural effusion should be drained
Case 2-
B) Link to patient details:
Question 1- What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer- the cause of dyspnea might be PLEURAL EFFUSION
Question 2- Name possible reasons why the patient has developed a state of hyperglycemia.
Answer: 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 results in elevated levels of catecholamines and cortisol
Question 3- What is the line of treatment in this patient?
Answer- 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.
Question 4- What is the line of treatment in this patient?
Answer- 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
Case 3
C) Link to patient details:
Question 1: what is the most probable diagnosis in this patient?
Answer-
Question 2- What was the cause of her death?
Answer- On the next day of surgery, Patient had severe cough and Shortness of breath eventually resulting in Abnormal Vital signs.
• This suggests that her cause of death may be due to- Sepsis or Acute respiratory distress syndrome.
Question 3- Does her NSAID abuse have something to do with her condition? How?
Answer- Patient's USG report shows that She had Grade 3 RPD changes of Right kidney.
• It highly suggests that she may have underlying CKD (Chronic Kidney Disease),which is secondary to her NSAID abuse (Analgesic Nephropathy)
5) Nephrology (and Urology)
A) Link to patient details:
Question 1- What could be the reason for his SOB ?
Answer- reason for his sob can be POST TURP SYNDROME: it occurs because of irrigation of absorption of large volumes of irrigation fluid during turp which can cause HYPONATREMIA,CARDIORESPIRATORY depression.
Question 2- Why does he have intermittent episodes of drowsiness ?
Answer- the hyponatremia which occurs as a part of post turp syndrome-low levels of sodium in the body can cause lethargy,fatigue and sleep.
Question 3- Why did he complaint of fleshy mass like passage in his urine?
Answer- passing of fleshy like mass which is foamy can be because of infection where pus cells are more.
Question 4- What are the complications of TURP that he may have had?
Answer- complications of turp can be bladder injury,bleeding,hematuria,dysuria,infection. in this patient it can be infection as pus cells are seen .
B) Link to patient details:
Question 1- Why is the child excessively hyperactive without much of social etiquettes ?
Answer- 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).
Question2- Why doesn't the child have the excessive urge of urination at night time ?
Answer-
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
Question3- How would you want to manage the patient to relieve him of his symptoms?
Answer- For 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, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.
- Methylphenidate A 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.
.6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
A) Link to patient details:
Question1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANSWER:
- Cough since 2 months on taking food and liquid difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
- laryngeal crepitus- positive.These favour for tracheo esophageal.fistula
QUESTION 2:
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANSWER:
- 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 disease and Hepatology:
Link to patient details:
Question 1- Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?
Answer- yes, it could be due to intake of contaminated toddy
Question 2-What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
Answer- 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.
Question 3- Is liver abscess more common in right lobe ?
Answer- yes right lobe is involved due to its more blood supply
Question 4- What are the indications for ultrasound guided aspiration of liver abscess ?
Answer- Indications for USG guided aspiration of liver abscess
- amoebic liver abscess
-Large abscess more than 6cms
- Left lobe abscess
-Caudate lobe abscess
-Abscess which is not responding to drugs
-seronegative abscess
B) Link to patient details:
Question 1- Cause of liver abcess in this patient ?
Answer-The patient is occasional toddy drinker which has high amount of Entamoeba histolytica. This causes liver abscess by suppressing the function of Kuffper cells.Therefore Toddy is most probable cause of Liver abscess in this patient
Question 2- How do you approach this patient ?
Answer-
Hematology:
- Common hematological finding being LEUCOCYTOSIS , indicating inflammation or infection.
- Anemia may be present , or not.
Biochemistry:
- Elevated liver enzymes such as AST,ALP are noted .
Question 3- Why do we treat here ; both amoebic and pyogenic liver abcess?
Answer-
INJECTION. ZOSTUM 1.5 gm IV BD (twice daily)
Zostum is a combination of drugs - SULBACTUM (pencillin) & CEFOPERAZONE(cephalosporin) [Antibiotic]: It is used here to treat if any bacterial cause ( since we can’t take the risk relying on only anti amoebic therapy)
* INJECTION. METROGYL 500mg IV TID ( thrice daily )
Metrogyl has the drug called METRONIDAZOLE[Antibiotic]: For amoebic cause
* INJECTION. OPTINEURIN 1amp in 100 ml NS( Nor
mal Saline) IV OD ( once daily)
Optineurin is a multivitamin drug { A combination of B1,B2, B3, B5,B6, B12 } given here as a supplement
* TAB. ULTRACET 1/2 QID( four times a day)
Ultracet is a combination of drugs - TRAMADOL(opiod analgesic) and ACETAMINOPHEN (analgesic and antipyretic) : Given for pain and fever
* TAB. DOLO 650 mg SOS (if needed) given for fever and pain
* Here ; due to medical therapy his symptoms subsided and clearly we can see it in usg reports ( liquefaction) meaning abcess responded to our medical therapy.
*And the patient was discharged on 10/5/21.
* We donot aspirate the pus since it is self resolving and aspiration is associated with several other complications.
Question 4- Is there a way to confirm the definitive diagnosis in this patient?
Answer- Apart from serological examination which is positive in 94% of the cases..Further confirmation can be done by using Ultrasonography but these are not commonly used
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
A) Link to patient details:
QUESTION 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?
Answer:
- 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-
- patient presented to casualty in altered state with facial
puffiness and periorbital oedema and weakness of right upper limb and
lower limb
- towards the evening patient periorbital oedema progressed
- serous discharge from the left eye that was blood tinged
- was diagnosed with diabetes mellitus
- patient was referred to a government general hospital
- patient died 2 days ago
The patient was also diagnosed with acute infarct in the
left frontal and temporal lobe. Mucormycosis is associated with the occurrence
of CVA ( https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes.
)
QUESTION 2: What is the efficacy of drugs used along with other
non-pharmacological treatment modalities and how would you approach this
patient as a treating physician?
Answer:
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
https://pubmed.ncbi.nlm.nih.gov/23729001/ this article talks about the efficacy and toxicity of different formulations of amphotericin B along with the above mentioned treatment for the patient managing others symptoms is also done by-
- 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
Question 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 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 increasing
9) Infectious Disease (Covid 19)
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
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).
https://docs.google.com/spreadsheets/d/e/2PACX-1vQuWFPoQm48IiBs1aDOGHPMosE9sylv2WdixecZa7xbmudlxrGMxk1O_1fgKpNxBbNPZLpIy37oQPcy/pubhtml
1) Covid 19 with co morbidity (Pulmonology/Rheumatology)
https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html
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 TLC. The SpO2 of these patients is usually decreased due to increased A-a gradient
A superimposed covid-19 infection in these cases can cause an acute exacerbation of symptoms such as dyspnea, decreasing levels of SpO2 further and faster than in Covid-19 patients without interstitial lung disease.
Radiology (HRCT) usually shows the development of new pulmonary opacities and fibrosis.
Patient factors:
Since this patient already had a reduced SpO2 of 90-92% (compared to the normal range of >96%) she is more susceptible to worsening of hypoxia and dyspnea unless immediate ventilator support is provided
The patient reportedly did not have dyspnea prior to the covid infection but developed a grade 2 SOB
ILD by itself makes the patient much more susceptible to acquiring Covid-19 infection.
Prognosis: Poor
Source: https://ejrnm.springeropen.com/articles/10.1186/s43055-021-00431-2
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
Enoxaparin is said to relieve and prevent inflammation produced by IL-6 by inactivating it by binding it with its non-anticoagulant fraction, especially in pulmonary epithelial cells.
Moreover, patients with Covid-19 are more susceptible to the development of venous thromboembolism, which can be prevented by Enoxaparin (LMWH).
CASE 9-2: COVID-19 SEVERE
https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html
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 plausible?
The patient may have already had slight hyperglycemia, owing to high HbA1c levels (7.1%), which may have aggravated due to COVID-19. The possible biochemical pathways include: [6]
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. Also, poor glycaemic control predicts an increased need for medications and hospitalizations, and increased mortality.
In monocytes: elevated glucose levels increase SARS-CoV-2 replication, and glycolysis sustains SARS-CoV-2 replication via the production of mitochondrial reactive oxygen species and activation of hypoxia-inducible factor 1α. Therefore, hyperglycaemia supports viral proliferation.
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 complications- 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 [7]. Moreover, D- dimer levels would be helpful in fast diagnosis and prevention of thrombotic complications.
CASE 9-3 (COVID-19 SEVERE)
https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html
QUESTIONS:
1. Why was this patient given noradrenaline?
Following kidney failure, the patient had sudden and persistent hypotension. To combat this, the patient was given noradrenaline, a potent vasoconstrictor.
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% despite BiPAP, a more invasive method was required to push the air directly into the lungs- hence intubation was preferred.
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 owing to an increased inflammation and immunological dysfunction in COVID, elevated ESR is most likely dur to COVID related inflammation.
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 challenges- Many patients may find it hard to cut themselves from the outside world and confine themselves to a room for long periods of time
Emotional challenges- Sitting in a small room all day leads to stress, anxiety and even depression, with an increase in mental health issues being reported during the pandemic
Social challenges- Members of society who cannot care for themselves on their own (eg, patients with disability, geriatric patients etc) are at a major loss
Economic challenges- Some patients, such as daily wage labourers, cannot afford to home isolate as they need to earn on a daily basis to keep their family going
Harms of hospitalisation-
Infection- Members visiting may get COVID from exposure to the hospital ward alone
Cost- PAtient may not be able to bear the brunt of high costs
Overtesting- Hospitals may ask the patients to stay overnight despite the conditions being mild, based on preliminary test results
Economic- Working patients may have to take a leave of absence, hence affecting both their work and decreasing their salary, on top of spending money on hospitalisation
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?
The reason for coma is due to severe hypoxia, as his SpO2 levels were 20% when he was admitted. Along with this, hypokalemia leads to respiratory muscle paralysis, which may have aggravated his dyspnoea.
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)
The coma was most probably related, as hypokalemia can cause respiratory muscle paralysis, leading to aggravation of hypoxia, hence causing unconsciousness in the patient.
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.
This patient had very low 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
1. Altered sensorium due to hypoxia, leading to hypercapnic encephalopthy and altered sensorium
2. Increased urea levels leading to uraemic encephalopathy, which causes altered sensorium
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), as denoted by increased urea and creatinine, and hypoproteinemia. Hypoxia and inflammatory response due to COVID-19 may have triggered the process.
Source: https://www.frontiersin.org/articles/10.3389/fphar.2020.579886/full
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. Based on the CT severity score it can be said that the patients pneumonia is moderate.
Q2. What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?
A. It is best to start the treatment with dexamethasone before the onset of cytokine storm.
Q3. What all could be the factors that led to psychosis in her ?
A. The following can lead to ICU psychosis
Sensory deprivation
Sleep deprivation
Stress
Continuous light levels
Continuous monitoring
Lack of orientation
pain
drug reactions
Infections
metabolic disorders
Dehydration
Q4. In what ways shall the two drugs prescribed to her for psychosis help ?
A. Pirecetam improves memory and causes cognitive enhancement and also improves mood.
Resperidone acts by decreasing the dopaminergic and seritonergic pathways in the brain
Q5. What all are the other means to manage such a case of psychosis?
A. The management of ICU psychosis primarily depends on the cause. If it is sleep deprivation then hte patient should be provided a peaceful place to take rest.
If it is due to underlying conditions like heart failure and dehydration then these should first be corrected.
Haloperidol is a medication commonly used to manage ICU psychosis. Other common anti-psychotics can also be used.
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 another 7 days after discharge. If possible oxygen levels are to be monitored as well for the next 7 days. The patients and the patient's attenders should be on the look out for danger symptoms such as
trouble breathing, chest pain, bluish discolouration of lips, confusion or inability to wake up.
Q7. What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge?
A. Long COVID is the persistence of symptoms such as cough, breathlessnes, headaches and chest pain weeks to months after discharge. People suffering from long COVID usually have elevated biomarkers such as elevated d dimer and CRP. As this patient has elevated d dimer levels at discharge there is a good chance that she could suffer from long COVID.
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. Most cases revert to normoglycemia after discontinuation of steroids.
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, infusion thrombophlebitis is not grounds for discontinuation of infusions that are essential for the treatment of the case. Thrombophlebitis can be treated by local compressive dressings, NSAIDs (topical and/or systemic)
16) Mild to moderate covid with hyperglycemia
https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html
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
Stress hyperglycemia due to inflammation-induced insulin resistance
High dose steroid usage
17) Covid 19 with hypertension comorbidity
https://prathyushamulukala666.blogspot.com/2021/05/a-62-year-old-male-patient-with-fever.html
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. It is already known that hypertension is assocatied with a weaker immune system and is seen in older patients which show bad prognosis when dealing with this infection. As there is a high risk of developing cardiovascular events as well as end organ 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
https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html
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( albumin is a negative acute phase reactant that means its level decrease during inflammation)
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 the heart. To compensate this demand, the ventricles undergo remodelling 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
https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html
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 storm. In order to prevent these severe conditions steroids are used.
A well-known adverse effect of steroid usage is the disruption in carbohydrate metabolism. It leads to hyperglycemia. When steroids are given to a diabetic COVID-19 patient utmost care must be taken. The patient should be shifted from oral anti diabetic drugs to s.c. insulin and blood sugars should be closely monitored. If possible, Tocilizumab should be used instead of steroids.
Steroid usage in diabetic patient has shown a increase in death rate as it further decreases the immunity of the patient and make them prone to other opportunistic infections like mucormycosis leadth to inceased death rate.
2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically?
In COVID-19 infection due to systemic inflammation and cytokine storm even when they are adequately managed, ae leading to damage of inner walls of small blood vessels of the brain. These blood vessels have very little or no collateral blood supply.
Even though the patient is on blood thinners they cannot prevent this damage. When the blood viscocity becomes higher either due to dehydration or high LDL/cholesterol levels, these small blood vessels are blocked leading to 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.
One of the adverse effect of chronic alcoholism is its ill effect on innate as well as adaptive immunity.
Reduced resistance to COVID-19 promotes progression of disease and leading to wrose prognosis
21) Severe Covid with Diabetes
https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html
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. This is attributed to interactions of several risk factors as well as hyperglycemia which is seen in diabetic patients. It modulates immune response as well as inflammatory responses thus predisposing individuals to lethal course of the disease.
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. During this course of treatment, blood sugar should be closely monitored and patient should be shifted from oral anti diabetic drugs to insulin.
3. What effect does a history of CVA have on COVID prognosis?
It is established that COVID-19 is associated with coagulopathy. In a patient who has a history of CVA are mostly old and have other co-morbidities which leads to severe course of the disease as well as poor prognosis.
23) Covid 19 with multiple comorbidities:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-viral-pneumonia.html
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.
10) Medical education-
6th may: elogs of our senior batch were shared with us. they gave us an idea of how to do elogs
8th may : covid patient updates were shared along with the CT scan and x ray finding and other investigations which were done. the treatment plan was also discussed .
10th may : a case of liver abscess was discussed
21/M student occasional toddy drinker Came with
H/o pain in the epigastrium & right hypochondrium , loss of appetite & fever from 20 days - diagnosed as liver abscess & got treated outside.
In spite of he was having intermittent pain & fever for which he came to our hospital.
O/E:
Pt C/C/C,PR: 82 bpm, BP: 110/70 mmhg
CVS: S1 S2 + , no murmurs,RS: BAE+ , NVBS
P/A: Soft , NT ,CNS: NFND
Dx:
Liver abscess (segment VII of right lobe with 50 to 60% liquefaction)
And our doubts regarding treatment protocols of Covid were clarified, this discussion helped to clear a lot of doubts regarding Covid treatment.
May 11: the following case was discussed in a great detail
67yrs female
Diagnosis-Viral pnemonia secondary to COVID-19, HTN, HYPOTHYROIDISM, CENTRAL OBESITY, CVA
She was having hypersomnolence in the day time during yesterday's morning rounds.
Later her son told me she had phoned them at 3:00 AM yesterday complaining that there was a man here who was threatening to take her away by morning. We checked the CCTV footage during that time yesterday and didn't find anyone near her bed except she did appear to wake up sometime around that time and was on the phone.
With this case I have understood the neuropsychiatric aspects of COVID .
May 12:updates of Covid cases were given
May 13: an interesting case of 8 year old boy with frequent micturition was discussed
May 14 : differential diagnosis for a 78 year old Male with pericardial effusion was discussed
May 15; a case of ICU psychosis with Covid infection has been discussed
https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html
May 16: Covid cases updates where given.
May 17: 2 cardiology cases where discussed along with their elogs.
Many more cases were discussed. Learnt many concepts, read many articles on various topics in a short period of time .Thank you Rakesh sir and the whole medicine department for introducing us to this unique way of learning.
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