Medicine blended assignment

Name: k.shirisha

rollno: 60

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

First case:

Pulmonology;

A 55 year old female with" shortness of breath,pedal edema and facial puffiness

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

Questions:

1)What is the evolution of the symptomatology in this patient in terms of an event time line and wher is the anatomical localization for the problem and what is primary etiology of the patients problem.

Ans: Symptomatology:

The patient has following features:

* shortness of breath since 20 years ( on and off) lasted for 1 week and relieved on medication

latest episode of her sob started 30 days ago which was grade 4

*pedal edema: upto the level ankle

Type: pitting since 15 days

* facial puffiness: since 15 days

* she is known case of diabetes since 8years

* Hypertension is diagnosed 20 days ago treated for the same

* 5 years ago she was treated for anemia with iron injections

on 30/4/2021 she had sputum examination which was negative for Afb.on 4/5/2021 she was started on empirical ATT. this resulted in generalized weakness.a few days after ATT she started developing pedal edema and facial puffiness.

The ATT was stopped 16/5/21 on advice of pulmonologist

drowsiness since 2 days

decreased urine out put since 2 days

Surgical history:

Operated for intestinal perforation 20 years ago

Om investigations:

HRCT imaging: signet ring sign

Anatomical localisation for problem;

Lungs bronchial tube

Primary etiological agent:

* Biomass combustion with poor ventilation used for cooking

2) what are MOA,indication and efficacy are placebo of each of pharmacological and non pharmacological interventions used for this patient

Ans;

Pharmacological interventions:

1) injection Augmentin:(amoxycillin,clavulinic acid potassium).

MOA; Amoxicillin- binds to penicillin binding proteins within in the bacterial cell wall and inhibits cell wall synthesis

clavulinic acid:

B lactam structurally related to penicillin,that may inactivate certain Blactamase enzymes

indications:

copd, lower respiratory tract infections

efficacy: 87.2%

placebo

Tab: azithromycin 500mg

moa:

Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit

indication: respiratory tract infections

efficacy; 82.9%

3)inj lasix:

moa:

Furosemide, like other loop diuretics, acts by inhibiting the luminal Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.

indication: heart failure

efficacy:

4)Tab: pantop40mg po od,

moa:

indication: For heartburn and chest pain due to stomach acid reflux disease in which acidic content from stomach comes up to food pipe and mouth.

efficacy:

5) inj hydrocortisone100mg iv:

moa: Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.

indication: Anti infammatory effect;

Acute exacerbation of COPD

efficacy:

6) neb with ipravent,budecort 6hourly

7) pulmoclear 100mg po od

Moa;

Pulmoclear works by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.

Pulmoclear Tablet is used for relieving the symptoms of coughing, wheezing, congestion and blockage in the airways in a condition called chronic obstructive pulmonary disease (COPD).09-Apr-2021

8)injHAISc(8am-2pm-8pm)

It works by helping move sugar from the blood into other body tissues where it is used for energy. It also stops the liver from producing more sugar. All of the types of insulin that are available work in this way

9) inj Thiamine 1amp in 100ml of ns:

Non pharmacological interventions:

Head end elevation

O2 inhalation to maintain spo2 above 92%

Intermittent Bipap for 2hrs

Chest physiotherapy

Grbs 6th hrly

Temp,bp,pr,spo2monitering

I/O charting

3)What could be causes for her current acute exacerbation?

ans:

In this patient current exacerbation is bronchiectasis,heart failure

4. Could the ATT have affected her symptoms? If so how?

Ans

5.What could be the causes for her electrolyte imbalance?

Ans

Bronchiectasis, heart failure , copd

2) second case:

Neurology;

A) 40 year old male presented to old with chief complaints of irrevalent talking and decreased food intake since 9 days

https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html

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: symptomatology;

Irrevalent talking, decreased food intake 9days

Laughing himself,

He was chronic alcoholic since 12 years

Previously, he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again.

He is known case of diabetic

He also had short term memory loss since 9 days, where he could not recognize family members from time to time.

2x2cm chronic ulcer on heel of R foot with sloping edges

Pale granulation tissue present

Surrounding tissues normal

Peripheral pulses present

Sensation near normal

Investigtions

Smear findings: Normocytic normochromic anemia, leukocytosis

Serum electrolytes

-K: 2.9 mEq/L (decreased)

-Cl: 112 mEq/L (increased)

LFT:

Albumin: 3.3g/dL (decreased

RFT

-Urea: 248mg/dL (increased)

-Creatinine: 3.8 mg/dL (increased)

-Uric Acid: 18mg/dL (increased)

Consistent with prerenal AKI.

9.RBS

-215mg/dL (increased)

2D ECHO

-Mild LV hypertrophy

USG abdomen

-Bilateral Grade1 RPD

-Echogenic intramural foci noted in gallbladder

Anatomical localisation; brain, kidneys , foot ulcer on right leg

Primary etiological agent: chronic alcohol abuse

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:IVF NS and RL @150ml/hr

2. Inj. 1amp THIAMINE in 100ml NS, TID

3. Inj. Lorazepam

4. T. Pregabalin 75mg/PO/ BD

5. Inj. HAI S.C.- premeal

6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am

7. Lactulose 30ml/PO/BD

Used for constipation or washout toxins in encephalopathy

8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours

9. Syp Potchlor 10ml in one glass water/PO/BD

For the ulcer:

1. Daily dressing

2. Megaheal ointment

3. Avoid pressure over ulcer

3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

Ans: Because these symptoms are not due to alcohol withdrawal.

Possible cause is uremic encephalopathy due to excessive toxins that are accumulated in brain caused encephalopathy signs

4) What is the reason for giving thiamine in this patient?

It is a B1 supplement used to treat thiamine deficiency

In chronic alcoholic s there will be deficiency of thiamine and also to treat ecephalopathy wernickes

5) What is the probable reason for kidney injury in this patient?

Ans:diabetes

Azotemia_ increased urea levels ,creatinine levels increased , hyperuricemia,

6). What is the probable cause for the normocytic anemia?

Ans: increased blood loss

Chronic kidney diseaae

7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Ans: no,it is an diabetic foot open wound ulcer

Heals slowly , individuals with diabetes have poor circulation of blood

People with diabetes have slow healing process and heals slowly

B)A 52 year old male with cerebellar ataxia

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

Questions;

Symptomatology; slurring of speech, deviation of mouth since 2 days and

Giddiness associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.

vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.

H/o postural instability- he is unable to walk without presence of supports, swaying is present and he has tendency to fall while walking

Medical History- Patient was found to have denovo HTN, and he did not continue taking medication regularly.

He is a chronic alcoholic, been consuming alcohol since 30 years, consumes 90-180 ml daily

Ataxic gait

NYSTAGMUS- Bilateral horizontal nystagmus, vertical upbeat nystagmus, more on right lateral position with a fast component to the left.

RFT:

Urea- 28 mg/dl

Creatinine- 0.9 mg/dl

Uric acid- 7.4 mg/dl

Calcium- 9.8 mg/dl

Phosphorous- 1.3 mg/dl

Sodium- 140 mEq/L

Potassium- 3.5 mEq/L

LIVER FUNCTION TESTS:

Total Bilirubin- 2.00 mg/dl

Direct bilirubin- 0.55 mg/dl

SGOT (AST)- 17 IU/L

SGPT (ALT)- 18 IU/L

Alkaline phosphatase- 187 IU/L

Total proteins- 7.2 g/dl

Albumin- 4.5 g/dl

A/G Ratio- 1.72

CT SCAN- Computed tomography scan of the brain was done, which revealed a cerebellar infarct.

2D ECHO- Diastolic Dysfunction present

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Tab Veratin 8 mg PO TID; it is a antihistamine ( betahisine)

MOA;

Betahistine has two mechanisms of action. Primarily, it is a weak agonist on the H₁ receptors located on blood vessels in the inner ear. This gives rise to local vasodilation

and increased permeability, which helps to reverse the underlying problem of endolymphatic hydrops.

Indication ; meniere's disease

Inj Zofer 4 mg IV/TID

Indication ; vomiting

Tab Ecosprin 75 mg PO/OD

Indication: anti-inflammatory, infracts

Tab Atorvostatin 40 mg PO/HS

Indication ; used to lower high blood pressure to treat strokes,lowers cholesterol synthesis

BP monitoring- 4rth hourly

Tab Clopidogrel 75 mg PO/OD

Anti patelet

Inj Thiamine 1 AMP in 100 ml NSPO/BD

MOA;

Indication ; used to treat B1 deficiency in chronic alcoholics

3) Did the patients history of denovo HTN contribute to his current condition?

Yes

4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?

Hypertension

C) A 45 years old female ,house wife by occupation came to opd with chief complaints of palpitations,chest heaviness,pedal edema,chest pain,radiating pain along her left upper limb

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Questions:

Palpitations since 5 days

Pain along her left upper limb associated with tingling and numbness-6 days

*Chestpain -since5 days

*Difficulty in breathing-5 days

*Swelling over the legs(bilateral)-8 months

bilateral pedal edema which is gradually progressing and it is present both in sitting and standing position and relieved on taking medication.

Palpitations: since 5days which are sudden in onset,more during night time and aggregated by lifting weights, speaking continuously and it is relieved by drinking more water, medication

*dyspnoea during palpitations (NYHA-CLASS-3)-since5 days

*Pain:since 6days radiating along the left upper limb which is dragging in nature, aggrevated during palpitations and relieved by taking medication for palpitations.

*Chest pain associated with chest heaviness

right and left)paresis due to hypokalemia 1year back

2 months back came to KIMS NARKETPALLY for treatment of neck pain for which she received medication:

10 yrs back had the episode of paralysis of both upper and lowerlimbs(rt and left)

2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

Cervical spondylosis, due to intrinsic muscle wasting Hypokalemia occurs

Risk factors;

Cervical spondylosis

Paresis

3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Disappearance T wave

Progressive increase in amplitude of u wave

First and second degree AV

ST segment depression

Symptoms; palpitations, chest pain, neck pain, bilateral pedal edema pitting type

D) 55years old patient with seizures.

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

Questions;

1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

Yes,

2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?

Ans; Because it get severed on left side onlyBut in recent it get severed all over the body

This disturbance is caused by electrical signals spreading through the brain inappropriately. Often this will result in signals being sent to your muscles, nerves, or glands. The spread of these signals in your brain can make you lose consciousness and have severe muscle contractions

Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures.

A 48 year old male with seizures and altered sensorium

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions;

Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?

Minor head injury or neurological deficit

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Head trauma,alcoholism

Seizures contribute to bleeding diathesis

F) A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWERLIMB

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?

Yes

2.What are warning signs of CVA?

Ans;. There may be no warning signs of stroke until it occurs

It is why high blood pressure one of risk factors for stroke - silent killer

3.What is the drug rationale in CVA?

4. Does alcohol has any role in his attack?

Yes

5.Does his lipid profile has any role for his attack??

Yes

A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

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

2)What is finger escape ?

Described by Ono as a one of the signs in cervical cord damage
Deficient adduction and or extension of the ulnar 2-3 digits
Differentiating it from other similar looking signs affecting the little finger

3)What is Hoffman’s reflex?

H) A 17 year old female with seizures

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1

Questions:

1) What can be the cause of her condition ? Metabolic causes; hypokalemia

Systemic; dehydration

2) What are the risk factors for cortical vein thrombosis?

Iron deficiency anemia

Dehydration

Seizures( focal or generalized)

Headache

3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?

4) What drug was used in suspicion of cortical venous sinus thrombosis?

Treat infection with antibiotics

Anticoagulants are indicated( low molecular weight heparin orUFH)

Adequate dehydration

Antiedema measures if needed

3) Cardiology (10 Marks)

A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html

Questions;

1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.

2.Why haven't we done pericardiocenetis in this pateint?

It is resolving with antibiotics or it cause ruputre to lungs

3.What are the risk factors for development of heart failure in the patient?

Ans:

Age, hypertension, obesity, diabetes

4.What could be the cause for hypotension in this patient?

Pericardial effusion

Acute pericarditis

A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html

Questions;

1.What are the possible causes for heart failure in this patient?

Obesity, hypertension, Diabetes, chronic kidney disease

2.what is the reason for anaemia in this case?

Chronic kidney disease

Heart failure with preserved ejection fraction

Diabetic retinopathy

Hypoxia-

3.What is the reason for blebs and non healing ulcer in the legs of this patient?

Reason for bleb infection by environmental agents or organisms

Prolonged pressure on feet,circulatory problems

Kidney failure

Diabetes

High cholesterol

High blood pressure

These conditions impair the circulation and damages nerves leads to non healing ulcer

4. What sequence of stages of diabetes has been noted in this patient?

sequence of stages of diabete s in this patient are diabetes are insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.

C)Atrial fibrillation and bilateral thrombus in a 52 year old male

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

Questions

decreased urine output and shortness of breath at rest since one day.

Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital.
Patient also complains of decreased urine output since 2 days and Anuria since morning.
CBP;

* Hemoglobin - 12.8 gm/dl

* Neutrophils - 87%

* Platelets - 88000

Renal function test

* Urea - 198mg/dl

* Creatinine - 5.4mg/dl

* Uric acid - 11.9mg/dl

* Phosphorus - 5.6mg

Blood Urea - 122mg/

* Serum Creatinine - 3.2mg/dl

Liver function test

* Total Bilirubin - 2.96mg/dl

* Direct Bilirubin - 1.93mg/dl

* SGOT - 476 IU/L

* SGPT - 551 IU/L

* Alkaline Phosphate - 172 IU/L

CT pulmonary angiogram

* Dilated Main Pulmonary Artery and Left Pulmonary Arteries.

* No evidence of Pulmonary Arterial Embolism.

*Thrombi noted in Left Atrial Appendages and Left atrium

9. 2D Echo

* Dilated All chambers

* Global Hypokinesia

* Severe LV dysfunction (EF = 28) (Moderate to severe eccentric TRF positive)

* IVC dilated 2.15 cms

Anatomical localisation ; heart, lungs

Primary etiologic agent; chronic alcoholic, hypertension diabetes

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;

the day of admission -

* INJ. Dobutamine 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg.

On Day 3 -

* ECG showed Irregular rhythm and he was started on TAB. Digoxin 0.25mg OD 5/7 and INJ. Unfractionated Heparin 5000 IU TID.

* As patient's D DIMER was high, Anti coagulants were started and planned for CPTA.

On Day 4 -

* Patient was started on TAB. Carvediol 3.125mg BD

On Day 5 -

* Patient's Serum Creatinine and Serum Urea were increased after CPTA.

* Nephrology opinion was taken in view of Contrast Induced Nephropathy.

On Day 6 -

* Patient was started on INJ. Unfractionated Heparin Infusion @5ml/hr and TAB. Acetyl cysteine 600mg PO TID.

* Daily monitoring of APTT, PT, INR and RFT was done.

On Day 7 -

* TAB. Acitrom 2mg OD was started.

On Day 8 -

* The Infusion of Heparin was increased to 7ml/hr and it was stopped after attaining the APTT of >70secs, PT of 23secs and INR of 2.3.

Other medications used during the course in hospital -

1. TAB. Cardivas3.125mg PO/BD

Moa

Carvedilol reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevents a response to the sympathetic nervous system, leading to decreased heart rate and contractility.

Indication; CCF,left ventricular dysfunction, high blood pressure

2. TAB. Dytor 10mg PO/OD

Dytor 10 Tablet works by increasing the amount of urine produced. This helps your body get rid of extra water thereby relieving symptoms such as shortness of breath and swelling in your arms, legs, or abdomen. This will help you go about your daily activities more easily and make you more confident about being active.

Indication; treats high blood pressure, excessive accumulation of water in body

3. TAB Pan D 40mg PO/OD

4. TAB. Taxim 200mg PO/OD

Taxim Injection works by inhibiting the formation and growth of bacterial cell wall which eventually leads to the death of the bacteria responsible for causing infection

5. INJ. Thiamine 100mg in 50ml NS IV/TID

6. INJ. HAI S.C 8U-8U-6U

Used to control blood sugar levels

3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?

Type-4 cardiorenal syndrome

4) What are the risk factors for atherosclerosis in this patient?

Hypertension, CCF ,left ventricular dysfunction,

Diabetes ,old age

5) Why was the patient asked to get those APTT, INR tests for review?

ApTT - To check time at which clots are formed

INR- To moniter blood thinning medication

67 year old patient with acute coronary syndrome

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

Questions

shortness of breath (SOB) since 1/2 hour.

She had H/O heartburn like episodes since a year. They were relived without use of any medication.

She has H/O TB diagnosed 7 months ago for which she completed the course of medication a month ago.

Patient was apparently asymptomatic till 9pm on that day (27/4/21). She apparently ate dinner and slept. When she woke up at night for washroom she developed sweating on exertion and shortness of breath even at rest.

K/C/O of DM2 since 12 years and is on Rx GLIMI M2 PO/BD

K/C/O of hypertension since 6 months and is on Rx TELMA 20 mg PO/OD

H/O pulmonary TB 7 months ago when she had cough, chest pain. Completed the course for TB a month ago. Currently negative for TB.

INVESTIGATIONS-

1) An ECG was done upon admission. The ECG shows NSTEMI ( acute coronary syndrome)

ECG will show the following characteristics for an NSTEMI:

depressed ST wave or T-wave inversion
no progression to Q wave
partial blockage of the coronary

Anatomical localisation ; heart, coronary arteries

Primry etiological agent;

Causes:

Atherosclerosis – Also known as coronary artery disease, this condition is the most common cause of heart attacks and occurs when the buildup of fat, cholesterol, and other substances forms plaque on the walls of the coronary arteries
Coronary artery spasm – A rare cause of blockage, spasms of the coronary arteries can cause them to become temporarily constricted.
Coronary artery tear – Also known as a spontaneous coronary artery dissection, a tear in a coronary artery can prevent blood from reaching the heart and cause a heart attack.

Risk factors:

High cholesterol
Hypertension
Smoking
Illicit drug abuse
Obesity
Stress
Type 1 DM
Family history

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Upon seeing the ECG, the patient was given TAB MET XL 25 MG/STAT.

Met XL 25 tablet works by relaxing the blood vessels, slowing down the heart rate. By doing this, it reduces the workload on the heart of pumping the blood effectively

Non pharmacological interventions ; per cutaneous intervention

Indication; used to treat high blood pressure mainly, along with certain heart conditions such as angina (chest pain) and heart failure. Decreased blood pressure helps prevent other conditions like kidney problems, stroke, heart attack and migraine

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?

Common complications of pci;

Hematoma, bleeding ,pseudoaneurysm at access site

Absolute Contraindications:

Noncompliance with the procedure and inability to take dual antiplatelet therapy.
High bleeding risk (thrombocytopenia, peptic ulcer, severe coagulopathy)
Multiple percutaneous coronary intervention restenosis

Relative 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
Stenosis of <50%

Harms of overtreatment ;

More than 80% of stable patients with STEMI who underwent PCI were treated in the ICU after the procedure although the risk for developing a complication was 16%,.

cardiac arrest (4.1%), death (4.1%), stroke (1%), shock (9.8%), respiratory failure (6.4%) and high-grade atrioventricular block requiring treatment (4.6%).

So overtreatment is important in current health care system.

E) A 60year old Male patient, resident of xxxxxxxx, came to the OPD with the Chief complaint of chest pain since 3 days and giddiness and profuse sweating since morning

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

Questions

chest pain since 3 days and giddiness and profuse sweating since morning.

Patient was apparently asymptomatic 3 days back and then he developed mild chest pain in the right side of the chest. The pain was insidious in onset and gradually progressive. The pain was of dragging type and was radiating to the back (retrosternal pain).

The patient is a known case of hypertension and type 2 diabetes.

GRBS: 626mg/dl

On evaluation his GRBS was very high. He was immediately given 6U oh HAI iv and then his GRBS was checked which showed 506mg/dl so he was administered 16U of Actrapid

BLOOD SUGAR- FASTING:

The patient was immediately treated for high blood sugar by giving 20U of actrapid

LIVER FUNCTION TESTS:

INTERPRETATION: high total bilirubin, hypoalbuminemia.

Renal function tests;

INTERPRETATION: increased urea, creatinine, uric acid and hyponatremia.

ECG;

INTERPRETATION: elevations in lead 2 and lead 3 and AVF.

Anatomical localisation ; Heart- inferior wall

Primary etiological agent; ischemia

Causes:

Atherosclerosis – Also known as coronary artery disease, this condition is the most common cause of heart attacks and occurs when the buildup of fat, cholesterol, and other substances forms plaque on the walls of the coronary arteries
Coronary artery spasm – A rare cause of blockage, spasms of the coronary arteries can cause them to become temporarily constricted.
Coronary artery tear – Also known as a spontaneous coronary artery dissection, a tear in a coronary artery can prevent blood from reaching the heart and cause a heart attack.

Risk factors:

High cholesterol
Hypertension
Smoking
Illicit drug abuse
Obesity
Stress
Type 1 DM
Family history

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans: TAB. ASPIRIN 325 mg PO/STAT

Moa;

Indication ; myocardial infraction to prevent clot formation

TAB ATORVAS 80mg PO/STAT

Indication ; To lower cholesterol synthesis, high blood pressure

TAB CLOPIBB 300mg PO/STAT

It is an antiplatelet medicine or blood thinner helps to prevent formation of blood in your blood vessels

This helps to lower the chances of you getting heart attack or stroke

It is widely used medicine for heart protection

INJ HAI 6U/IV STAT

Used to correct blood glucose levels

Blood pressure monitoring

3) Did the secondary PTCA do any good to the patient or was it unnecessary?

Repeat coronary angioplasty has become the standard approach to a first restenosis. However, the long-term outcome of such a strategy is not well defined. In the present study, 465 patients (mean age 58 years [range 27 to 79], 53% with multivessel disease) underwent a second angioplasty procedure at the same site. The procedure was successful in 96.8% with a 1.5% rate of in-hospital bypass surgery, a 0.9% incidence rate of myocardial infarction and no procedural deaths. Four hundred sixty-three patients (99.6%) were followed up for a mean of 40.5 months. Forty-nine patients (10.6%) underwent a third angioplasty procedure at the same site, 55 (11.8%) had coronary bypass surgery and 33 (7.1%) underwent angioplasty at a different site. During follow-up, 12 patients (2.6%) sustained a myocardial infarction and 21 (4.5%) died including 13 (2.8%) with cardiac death. Of the 442 surviving patients, 88% experienced sustained functional improvement and 78% were free of angina. The actuarial 5-year cardiac survival rate was 96% and the rate of freedom from cardiac death and myocardial infarction was 92%. For the subgroup of 49 patients who had a third angioplasty procedure at the same site, the success rate was 93.9% with a 2% incidence rate of myocardial infarction. There were no in-hospital deaths or coronary artery bypass operations. The mean follow-up interval for this subgroup was 30.5 months with a 22.4% cross-over rate to coronary bypass surgery, a 4.1% incidence rate of myocardial infarction and a 2% cardiac mortality rate. At last follow-up, 89% of patients had sustained functional improvement and 76% were free of angina. The combined angiographic and clinical restenosis rate was 48%. Repeat angioplasty as treatment for restenosis is an effective approach associated with a high success rate, low incidence of procedural complications, and sustained functional improvement in combination with an acceptable rate of bypass surgery. However, there is a trend toward diminished angioplasty efficacy after a second restenosis. Thus, decisions for further revascularization should be made after careful review of available options.

https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h

Questions:

1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

2. What is the rationale of using torsemide in this patient?

Uses ;

Torsemide is a diuretic used to reduce edema (swelling) from multiple causes such as heart failure,

3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Ceftriaxone is used to treat bacterial infections

Yes

4) Gastroenterology (& Pulmonology) 10

A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

Questions;

Abdominal pain, vomiting since 1 week

Constipation burning micturition,fever since 4

Days

abdominal pain in umbilical, left hypochondriac, left lumbar and hypogastric regions.

Since 20 days he is taking heavy alcohol.

Abdominal pain was incresed after food intake.

* Pain is throbbing type and radiating to back and is associated with nausea and vomiting( 1 episode) , which is non bilious, non projectile and also has food particles and water content 1 week.

* Fever was high grade, continuous and associated with chills and rigors.

Then he developed constipation since 4 days and passing flatus.

* patient also had burning micturition since 4 days, which is associated with suprapubic pain, increased frequency and urgency

* No history of blood or mucus in stools.

* No other complaints.

Past history ; 5years ago similar complaints for which he stopped alcohol after 3 years again started taking alcohol

khaini : 1 per day since 5 yrs.

3) Ghutka: 5 per day since 6 months

On palpation;

Tenderness present over umbilical, left hypochondriac, left lumbar, hypogastric and suprapubic region.

* Guarding and rigidity : present

On auscultation; sluggish bowel sounds are heard

1) CE CT ( Contrast Enhanced CT):

* Showing pseudocyst and infective fluid collections

2)Chest x ray:

* 1 st image showing pleural effusion and basal atelectasis and 2 nd image shows pneumothorax ( collapsed lung ) which developed in the course of hospital.

CBP showed LEUCOCYTOSIS.

* LFT showed Increased ALP and decreased ALBUMIN.

* Pleural fluid was EXUDATIVE in nature according to lights criteria and pleural fluid amylase being: 469 mg/dl.

* CE CT abdomen shows ; LARGE PSEUDOCYST COMPRESSING STOMACH (Dimensions: 15*9*10 cms ) & MULTIPLE INFECTIVE FLUID COLLECTION IN MIDLINE ALONG ANTERIOR ABDOMINAL WALL AND SUB HEPATIC REGION; WHICH ARE CONTINUOUS AND LOCULATED ASCITIS.

Chest x ray showed; MODERATE PLEURAL EFFUSION , BASAL ATELECTASIS IN LEFT LUNG

LEFT PNEUMOTHORAX SECONDARY TO BRONCHO PULMONARY FISTULA

Anatomical localisation; pancreas,(pseudocyst compresses the stomach) , lungs (left side)

Primary etiological agent; chronic alcohol abuse

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) ING. MEROPENAM ; TID for 7 days

Meropenam broad spectrum antibiotic used to treat abdominal infections caused by bacteria

cure rates with meropenem were 86.2% and 73.1%,

2) ING. METROGYL 500 mg IV TID for 5 days

Inj metrogyl ha metronidazole an antibiotic

Metronidazole is effective for the management of anaerobic infections, such as intra-abdominal infections, respiratory tract infections

3) ING. AMIKACIN 500 mg IV BD for 5days

Aminoglycoside antibiotic used to treat intra abdominal ,lung infections

## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as 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

* Fluids are given to vein , it provides most of the nutrients body needs.

* TPN has proteins, carbohydrates, fats, vitamins, minerals.

5) IV NS / RL at the rate 12l ml per

Given for fluid replacement ie., 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

## After 4 days of this treatment; there is no improvement in patient and infact he is deteriorating clinically !!!

Non pharmacological interventions;

The pseudocyst was drained per cutaneously per abdominally under local anaesthesia with USG guided malecot drain placed inside and pus was drained.

Also , two other USG guided drains were placed in peri- pancreatic collections are drained per cutaneously per abdominally.

* Following day after the placement of the drain, patient was dramatically improved with reduced fever spikes and TLC dropped from 30,000 to 18,000. AKI and SVT also subsided.

Approch to patient;

Clinical findings ; Abdominal pain ,vomitings fever ,stools , constipation, burning micturition

Investigations ;CBP - increased leucocytosis, Liver fun tests, urine analysis, serum amylase levels

Chest x ray

CE- CT scan

Any complications like ; pseudocyst SIRS ( leucocytosis,fever, tachycardia,tachypnoea)

Management conservative ,medical, dirainage of exudative material.

B);

CASE OF 52 YEAR OLD MAN, WITH SEVERE EPIGASTRIC PAIN

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

Questions

1) What is causing the patient's dyspnea? How is it related to pancreatitis?

Hypoxia- acute respiratory distress syndrome due to microthrombi in pulmonary vessels

With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs. Causes sob

2) Name possible reasons why the patient has developed a state of hyperglycemia.

Due to altered hypoecohic head of pancreas

Disruption of islets of Langerhans with altered insulin or glucagon release

3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

Grade- 1 fatty liver

Specific marker AST,ALT for alcoholic fatty liver diseade

4) What is the line of treatment in this patient?

• IVF: 125 mL/hr

• Inj PAN 40mg i.v

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

A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

Questions

1) what is the most probable diagnosis in this patient?

Ruptured liver abscess

2) What was the cause of her death?

Post operative sepsis

3) Does her NSAID abuse have something to do with her condition? How?

5) Nephrology (and Urology) 10 Marks

Post TURP

with non oliguria ATN

Diabetic Nephropathy

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

Questions;

1. What could be the reason for his SOB ?

Ans;

High serum creatinine levels, electrolyte imbalance .

Due to less water intake , bilateral hydroureteronephrosis

2. Why does he have intermittent episodes of drowsiness ?

Ans; Hyponatremia

Electrolytes imbalance

3. Why did he complaint of fleshy mass like passage in his urine?

Due to Urinary tract infection.

4. What are the complications of TURP that he may have had?

TURP syndrome ;

Hyponatremia,

Bacteremia causes sepsis( ureo sepsis)

An Eight year old with Frequent Urination

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

Questions

1.Why is the child excessively hyperactive without much of social etiquettes ?

Anxiety

2. Why doesn't the child have the excessive urge of urination at night time ?

Since the child does not get the urgency to urinate when he is asleep, there can be a chance of the manifestation being psychosomatic, or as a result of an undiagnosed anxiety disorder , or a stressor triggering this manifestation.

3. How would you want to manage the patient to relieve him of his symptoms?

Ans,;

Reassurance, muscle relaxation

The medication oxybutynin is used to control such problems as urgent, uncontrolled, or frequent urination

and other conditions that affect the bladder muscles. Oxybutynin works by relaxing the bladder muscles to prevent urinary problems.

6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks

A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html

Questions

1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

Dysphagia ( diffulty in swallowing while taking foods and drinks)

Respiratory distress

Hoarseness of voice

Physical findings; laryngeal crepitus- positive,

Wheeze

2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?

Iris;

Most common chances ; opportunistic infections

In this patient has disseminated tb which occured after start of HAART after 2 months

7) Infectious disease and Hepatology:

LIVER ABSCESS

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

Questions

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, the reason of locally made alcohol is for this association between local alcohol beverages and ALA could be multifactorial. Factors influencing the association could be related to the pathogen, contents of beverages, status of the liver, and the immunity of the host. They are more vulnerable perhaps due to the large infective dose of Entamoeba histolytica and other bacterial pathogens ingested with the unhygienically brewed beverage. Associated nutritional status of the population and poor sanitation could also play a vital role

Cause in this patient ; locally made alcohol which get infected with Entamoeba histolytica

Methicillin sensitive staphylococcus aureus

2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)

Ans ;

Etiopathogenesis of liver abscess in a chronic alcoholic patient;

Liver abscess may result from a variety of pathogenic organisms including bacteria, fungus, protozoa, and parasites. It is a common clinical entity encountered by physicians throughout the world

2. Amoebic Liver Abscess and Alcohol

A close relationship between the consumption of indigenously brewed alcohol beverages and the occurrence of ALA in the tropics has been established over a period of time by several large-population studies [3, 4, 5]

Reasons for this association between local alcohol beverages and ALA could be multifactorial. Factors influencing the association could be related to the pathogen, contents of beverages, status of the liver, and the immunity of the host. They are more vulnerable perhaps due to the large infective dose of Entamoeba histolytica and other bacterial pathogens ingested with the unhygienically brewed beverage. Associated nutritional status of the population and poor sanitation could also play a pivotal role. Hai et al. stated that alcohol-induced hepatic dysfunction and possible suppression of amoebistatic immune mechanisms by substances in the beverages could also be attributed in the mechanism [6].

Mukhopadhyay et al. [5] have suggested that “alcohol can predispose to ALA through a multitude of mechanisms, including hepatic damage by alcohol, lowered body resistance and suppression of liver function due to poor nutritional status of habitual consumers of alcohol, increased presence of amoebae in the liquor prepared locally with poor regard to aseptic procedures, and depression of immune mechanisms in chronic alcoholics.” A study conducted in India in 2011 [4] showed that 67.5% of patients with amoebic liver abscess are from the low socioeconomic class and 72% were alcoholics. It was also noted that alcoholics had larger abscesses, a greater frequency of complications, and delayed resolution of the abscesses.

3. Is liver abscess more common in right lobe ?

Ans; yes

4.What are the indications for ultrasound guided aspiration of liver abscess ?

INDICATIONS OF LIVER ABCESS DRAINAGE:

1) If the abcess is large ( 5cm or more) because it has more chances to rupture.

2) If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

3) If the abcess is not responding to the drugs for 7 or more days

Method of abcess drainage:* Aspiration using needle or catheter under imaging

B) liver abscess

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

Questions

1) Cause of liver abcess in this patient ?

* Organisms reaching the liver via portal vein by hematogenous spread eg ; Entamoeba histolytica ( intra abdominal infections)

2) How do you approach this patient ?

Clinical findings;

Abdominal pain is most common symptom, in right upper quadrant,

Fever, enlarged and tender liver , loose stools

Mild jaundice may present becoming severe if large abscess causes biliary obstruction

Investigations;

Liver imaging- 90% or more of symptomatic abscess

Needle aspiration under USG guidance confirm s the diagnosis and provide pus for culture

Leucocytosis is frequently found

Plasma Alp is increased,

Serum albumin low

Chest xray- raised right diaphragm and lung collapse or effusion at the base of right lung

Management;

Based on results of pus andblood culture sensitivity report should be commenced with antibiotics such as Ampicillin, gentamicin, metronidazole

If abscess is large- or doesn't respond to antibiotics - Aspiration or drainage with catheter is placed in the abscess under USG guidance

3) Why do we treat here ; both amoebic and pyogenic liver abcess?

Because we don't know the particular source of the condition

4) Is there a way to confirmthe definitive diagnosis in this patient?

Stool or any exudate should undergo prompt microscopic examination for motile trophozites containing red blood cells

Movements cease rapidly as stool preparation cools

8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks

50/Male came with altered sensorium

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

Ans;

Fever associated with chills and rigors, high grade since 10days

Facial puffiness and periorbital edema since 4 days

Weakness of right upper limb and lower limb since 4 days

Altered sensorium since 2 days

On examination of face -blackish discoloration on medial canthus, swollen eye lids( periorbital edema), bloody discharge from left eye,

On examination of oralcavity;. Foul smelling blackish eschar extending hardpalate towards upper lip.

ABG: acidosis diagnosed with diabetic ketoacidosis

Past history; known case of hypertension Since 3 years

CT imaging with brain and orbit done;

Preseptal cellulitis

acute infarcts in frontal and temporal lobe

CT brain showing soft tissue swelling in maxillary sinus

CT brain showing mucosal thickenings of sinus

KOH mount showing hyphae confirming the diagnosis of Acute rhino oro cerebral mucormycosisis

Anatomical localisation for problem;

Sinuses - orbit - brain

Primary etiology of patient problem;

Mucormycosis (previously called zygomycosis) is a serious but rare fungal infection caused by a group of molds called mucormycetes. These molds live throughout the environment.

Dust air, bread molds

Mode of transmission ; inhalation of infected dust in environment.

Diabetic ketoacidosis- risk factor

2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?

Ans: pharmacological interventions :

Deoxycholate amphotericin-b,liposomal amphotericin-b, posconazole, ivermectin(200mg given for correction of creatinine levels).

Efficacy:

Efficacy of ivermectin;

Efficacy of posconazole; reduces risk factors

Non pharmacological interventions; Surgery is done

Approch to mucormycosis patient as physician

Clinical findings: fever, weakness of right upper limb and lower limb,facial puffines,periorbital oedema,

On examination of face -blackish discoloration on medial canthus, swollen eye lids( periorbital edema), bloody discharge from left eye,

On examination of oralcavity;. Foul smelling blackish eschar extending hardpalate towards upper lip.

CBP, electrolytes, blood sugar, wetKOH mount

CT- imaging

Pharmacological intervention; amphotericin-b ( liposomal), itraconazole,posconazole

Correct risk factors

Non pharmacological interventions; surgical debridement

Risk factors: diabetic ketoacidosis, uncontrolled DM, steroids, neutropenia, immunosuppressant therapy ,high levels of free iron level( Desferroximetherapy)

3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?

Ans;

Download PDF

Invited Mini Review
Published: 28 January 2019

Fungal Rhinosinusitis: Unravelling the Disease Spectrum

Virendra Singh

Journal of Maxillofacial and Oral Surgery volume 18, pages164–179 (2019)Cite this article

1877 Accesses
11 Citations
Metricsdetails

Abstract

Fungal rhinosinusitis (FRS), once considered a rare disease, has seen a steep rise in incidence in recent times. This global rise in the burden of fungal disease is a consequence of an increment in the population with weakened immune systems. Increased life expectancy with rise in conditions like diabetes mellitus, medical advancements with invasive interventions, use of immunosuppressive drugs and chemo-radiotherapy all lead to unique risk situations. The situation becomes more alarming with the fact that there has been a significant rise in cases in immune-competent hosts with no predisposing factors. FRS represents a wide spectrum of disease ranging from the mild form of superficial colonization, allergic manifestations to life threatening extensive invasive disease. The categorization of disease into acute and chronic and invasive or noninvasive is important factor with implications in disease management and prognosis and this has been emphasized greatly in recent years. Diagnosis of FRS has been a challenge as the presenting clinical signs and symptoms and radiographic manifestations are often nonspecific. Definitive diagnosis requires direct fungi identification and hence culture and microscopic examination remain the gold standard. Availability of advanced and rapid diagnostic techniques is rare in majority of developing nations. Therapeutic dilemmas are another aspect of the management of FRS as in spite of the availability of new antifungal drugs, treatment is often empirical due to non-availability of early diagnosis, rapid disease progression and high costs of antifungal drugs. A description of the different types of FRS, their diagnosis and management has been presented in this review

Key words; fungal rhinosinuitis, mucormycosis, invasive fungal sinusitis

Covid19 cases

Name; k.shirisha

Rollno:60

9) Question:

1) Covid 19 with co morbidity (Pulmonology/Rheumatology)

Covid pneumonia in a pre existing case of interstitial lung disease

A 58-year-old female presented with the chief complaints of fever for 6 days, and shortness of breath for 2 days.

https://nikhilasampathkumar.blogspot.com/2021/05/covid-pneumonia-in-pre-existing-case-of.html

1) How does the pre-existing ILD determine the prognosis of this patient?

The prognosis of COVID‐19 patients with per‐existing ILD is significantly worse than that of non‐ILD patients. And more, aggravated inflammatory responses and coagulation dysfunction appear to be the critical mechanisms in the COVID‐19 patients with ILD.

2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism?

There is no clear connection so far between autoimmunity and COVID-19. Autoimmunity is different from immunodeficiency (in which the immune system is too weak to fight off infections). If anything, autoimmunity makes the immune system relatively over-active, often causing it to attack the body. That doesn’t mean an autoimmune patient is necessarily better at fighting infections. An over-active immune system could help fight off the virus, but it also could cause unneeded inflammation.

3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?

The triggering of post-COVID-19 autoimmunity phenomena could be associated with both transient immunosuppression and an inappropriate form of immune reconstitution in susceptible individuals

4) Why was she prescribed clexane (enoxaparin)?

Prophylactic dose r standard recommended for patients

To relieve inflammation , Thrombosis

2) Covid 19 with Diabetes ;

A 50 year old female with Viral Pneumonia secondary to Covid-19

https://nehapradeep99.blogspot.com/2021/05/a-50-year-old-female-with-viral.html

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 plausible reasons being that the SARS-CoV-2 causes injury of pancreatic beta cells and impaired insulin secretion, which may contribute to the development of DKA. Thus, this virus affects the pancreas. The interaction between the SARS-CoV-2 virus and the renin-angiotensin-aldosterone system might offer insight into the pathophysiology ofDKA in these patients

The other cause of this COVID induced dysglycemia can be the use of steroids in COVID patients with respiratory failure

2) Did the patient's diabetic condition influence the progression of her pneumonia?

Yes

3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?

D-dimer is commonly elevated in patients with COVID-19. D-dimer levels correlate with disease severity and are a reliable prognostic marker for in-hospital mortality in patients admitted for COVID-19.

During plasma coagulation, soluble fibrin is generated. D-Dimers are released as characteristic degeneration products of cross-linked fibrin. Low D-Dimer concentrations can be used to exclude venous thrombic events (VTE) such as deep vein thrombosis of the leg (DVT) and pulmonary embolism (PE). On the other hand, increased D-Dimer levels indicate the activation of coagulation and following fibrinolytic processes demanding for further diagnostic and therapeutic approaches.

Yes it can change the management

3) Covid 19 Severe

A 26 Year Old Female with Fever and Shortness of Breath

https://143vibhahegde.blogspot.com/2021/05/covid-in-26-yo-female.html

1. Why was this patient given noradrenaline?

Hypotension or acute kidney injury

2. What is the reason behind testing for LDH levels in this patient?

LDH is an important enzyme in anaerobic metabolism in almost all living organisms (3). Several studies suggested that serum LDH was elevated in severe COVID-19 patients (4,5). Consistently, we show that patients infected by SARS-CoV-2 with high levels of LDH on admission are more likely to develop ARDS.

Research has shown that SARS-CoV-2 as a positive-sense RNA virus may activate inflammasomes, leading to cellular pyroptosis and aggressive symptoms (9). This may partly explain the association of LDH with ARDS in COVID-19 patients. However, we found that the best threshold for predicting ARDS was 273 U/L. LDH level was independently associated with ARDS, and could strongly predict the incidence of ARDS.

3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?

If you have trouble breathing, a BiPap machine can help push air into your lungs. You wear a mask or nasal plugs that are connected to the ventilator. The machine supplies pressurized air into your airways. It is called “positive pressure ventilation” because the device helps open your lungs with this air pressure

If her oxygen saturation levels are low then on emergency we can put on mechanical ventilation

Ventilator Effectiveness

Outcomes can vary according to medical circumstances, but historical data provide some insight. The most comprehensive evaluation of prolonged (generally >14 days) mechanical ventilation is a 2015 meta-analysis of 124 observational studies, which found that 57% of patients suffering from various conditions were liberated from mechanical ventilation and 38% were alive at 1 year.

But most80% people died on mechanical ventilation

4) Covid 19 Mild

29 year old male patient with viral pneumonia secondary to COVID-19

https://gsuhithagnaneswar.blogspot.com/2021/05/29-year-old-male-patient-with-viral.html?m=1

1. Is the elevated esr due to covid related inflammation?

The sustained high level of ESR possibly brings a negative effect on COVID-19 patients' prognosis, since high ESR could damage the joint and thus leads to joint diseases such as osteoarthritis[11,12]. Furthermore, it may be a precursor of hepatic and renal 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?

Because he was taken some treatment and home isolation might be the reason

Challenges in home isolation

Centre issues fresh guidelines for home isolation ... for home isolation of mild and asymptomatic COVID-19 cases. ... and hospital is a prerequisite for the entire duration of home ...

5) Covid 19 and comorbidity (Altered sensorium, azotemia, hypokalemia)

45 Y/O MALE WITH COVID-19 AND COMORBIDITIES (ALTERED SENSORIUM, AZOTEMIA, HYPOKALEMIA.)

https://anuragreddy72.blogspot.com/2021/05/case-discussion-on-hypokalemic-periodic.html

1) What was the reason for coma in this patient?

Hypokalemia, azotemia, altered sensorium

Hypoxia or metabolic abnormalities can lead to severe neurological manifestations like altered sensorium, delirium, and coma.

Approximately 3.2% of patients infected with COVID-19 require invasive ventilation during the course of the illness. Within this population, 25% of patients are affected with neurological manifestations. Among those who are affected by severe neurological manifestations, some may have acute cerebrovascular complications (5%), impaired consciousness (15%) or exhibit skeletal muscle hypokinesis (20%). The cause of the severe cognitive impairment and hypokinesis is unknown at this time.

Potential causes include COVID-19 viral encephalopathy, toxic metabolic encephalopathy, post-intensive care unit syndrome and cerebrovascular pathology.

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?

Hypoxia-, ,muscle weakness and paralysis of all limbs

Yes hypokalemia is coma related

3) How may covid 19 cause coma?

with coronavirus disease 2019 (COVID-19) who are admitted to the intensive care unit (ICU) for respiratory distress, an encephalopathy, most notably in the form of delirium, occurs in up to 84%.¹ Brain MRI studies in patients in the ICU with COVID-19, including those with prolonged comatose state, reported varying degrees of MRI abnormalities, although few to no details were reported on the clinical picture, course, and prognosis of prolonged unconsciousness in such patients.² Here, we report a case series of patients withCOVID-19 admitted to the ICU for respiratory failure who, after cessation of sedatives, remained unconscious for longer than expected periods

6) Severe Covid 19 with altered sensorium

65 YEARS OLD MALE WITH VIRAL PNEUMONIA SECONDARY TO COVID-19.

https://vijaykumarkasturi.blogspot.com/2021/05/65-years-old-male-with-viral-pneumonia.html

1. What was the cause of his altered sensorium?

2. What was the cause of death in this patient?

Due to coma or severity of infections

7) Covid 19 Moderate with ICU psychosis

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

What is the grade of pneumonia in her?

Moderate

What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?

To start after 1week

What all could be the factors that led to psychosis in her ?

Hypothyroidism

Severe inflammatory response , vascular changes .neurototoxins contribute inflammatory response

In what ways shall the two drugs prescribed to her for psychosis help ?

Neuroprotective

What all are the other means to manage such a case of psychosis?

Counselling the patient

What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharge

What precautions should a recently-recovered COVID-19 patient take? Find out

'After the acute phase of COVID-19 is over, patients may return to hospitals with symptoms such as lethargy, body aches and itchy throats, even four to six weeks later,' says Dr Md Shakeel of Hiranandani Hospital, Vashi

By: Lifestyle Desk | New Delhi |
Updated: September 22, 2020 2:10:17 pm

COVID-19, symptoms of COVID-19, post COVID-19 care, COVID-19 treatment, post discharge assessment of COVID-19, health, indian express news

'Now that the infection has been in the country for over five months, we need to start looking at post-COVID-19 rehabilitation.' (Source: Pixabay)

It has been a while now since the COVID-19 pandemic, and people are slowly learning of many different ways to deal with it — both in terms of recovery and prevention. It is a known fact that the virus, once it is inside the body, does not isolate and attack the respiratory system alone, but instead makes its way to many other organs.

Dr Md Shakeel, Head-Emergency & Trauma, Hiranandani Hospital, Vashi — a Fortis Network Hospital — says a study conducted in Italy showed that 87.4 per cent of patients, who had recovered from COVID-19, reportedly felt some kind of fatigue and dyspnoea (laboured breathing). This was reported even after two months of being discharged from the hospital.

“Some patients who had recovered had to be rushed back with low oxygen saturation levels, just a day after discharge. These patients were admitted to the hospital for at least 10 more days, and were discharged only after they started doing well. These patients returned to the hospital with a whole spectrum of lung diseases – from fibrosis (formation of hard fibrous tissues as the lung heals from an injury) to secondary infections and pneumonia. It was also noted that after recovering from COVID-19, some patients came back with reduced heart function, heart attack or even stroke,” he says.

ALSO READ | Home-based care for COVID-19 infection; here are some dos and don’ts

Dr Shakeel goes on to say that the virus — which is known to attack the endothelial cells that line the blood vessels — causes excessive blood clotting in the body. And now that the infection has been in the country for over five months, we need to start looking at post-COVID-19 rehabilitation.

“These long and short-term impacts are called ‘post-COVID syndrome’. This means, after the acute phase of COVID-19 is over, patients come back to hospitals with symptoms such as lethargy, body aches and itchy throats, even four to six weeks later. Patients are also seen to have had some psychological stress, leading to anxiety and depression. It is of utmost importance to monitor such cases, and a proper post-discharge rehabilitation plan be put in place, to monitor the patient’s health, so timely intervention can be done,” he explain

The doctor says that there are some things that COVID survivors should assess:

* Their daily check of oxygen saturation, it should be maintained at >94% in room air.
* They must watch for respiratory symptoms like persistence or worsening of cough and breathlessness.
* Check for persistent rise of body temperature above 100F.
* Watch out for signs of lethargy, drowsiness, and altered sensorium.
* Regular monitoring of blood sugar in known diabetic patients. COVID infection (as any other infection) alters blood sugar levels of the body. Strict monitoring once in three days and regular consultation with your doctor is required.
* Regular blood pressure monitoring in known hypertensive patients is required to avoid accelerated hypertension-related complications. Weekly blood pressure monitoring in case of controlled hypertension, or more frequently in case of abnormal readings, is required.
* Follow up consultation with the doctor within seven days of discharge.
* Blood investigations like CBC, CRP at first follow up, and subsequent follow-ups, if advised by a physician.
* Repeat CT scan of chest after three months to look at the extent of lung recovery post-infection.

What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge?

8) Covid 19 Moderate

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

1. Can psoriasis be a risk factor for severe form of COVID?

Yes

What do we know about psoriasis that is relevant to the COVID-19 pandemic? First, psoriasis is an autoimmune disease in which the risk for hypertension, diabetes, cardiovascular disease, chronic lung disease and premature mortality increases with increasing severity of skin disease. Thus, as a population, patients with psoriasis, particularly those with more severe disease, are at risk for worse outcomes from COVID-19. Second, most of our treatments, aside from perhaps acitretin and phototherapy, are “immunosuppressive” and typically have warnings for infection in FDA prescribing information

One model about COVID-19 is that and at risk for progression of infection with SARS-CoV-2, but immunosuppression may be helpful later in the course of the illness by suppressing the dysregulated immune response in the lungs that leads to acute respiratory distress syndrome and death.

2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?

Yes

3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?

Yes

9) Covid with de novo Diabetes

New onset of DM in Covid-19:

Similar to SARS-CoV which caused an epidemic in 2002- 03, the novel coronavirus enters cell hosts through Angiotensin II Converting Enzyme receptor (ACE2). This receptor is found throughout the body and its pulmonary distribution explains, not only the respiratory clinical features, but also the acute respiratory distress syndrome that leads to severity of the disease.
ACE2 receptor is found in the pancreas, both on exocrine cells and in the endocrine cells, that constitute pancreatic islets. Interestingly, its expression is also relevant in the endothelial cells of the microvasculature supplying beta-cells that produce insulin.
As it has been postulated, upon the 2003-SARS pandemic, coronavirus spike protein enters the cells using the ACE2 receptor, initiating an inflammatory response that leads to apoptosis. Previous studies attempting to understand the pathophysiology of the SARS-CoV-2 infection over different organs and systems, have su- ggested that, following viral entrance and cell infection, ACE2 receptor is downregulated in lung tissue, which subsequently may trigger an inflammatory response.

Although SARS-CoV-2 could directly impair insulin production of beta-cells, diminishing its function and disturb glucose metabolism, would that be enough to com- promise insulin production in a long-term manner and induce type 1 diabetes? Is there any immune mediated process? Or is ACE2 downregulation the factor at stake?
One hypothesis could be that the cytokine storm - caused by the severe inflammatory response taking place in the lungs also targets the pancreas possibly causing diabetes .

Other hypothesis is related to the role of the renin-angiotensin system (RAS) and its counterbalancing arm, the ACE2-Ang(1-7)-Mas axis on the development of diabetes. It has been shown previously how ACE2 decreased activity is detrimental for the development of acute respiratory distress syndrome (ARDS), verified both during the SARS-CoV epidemic as well during the current pandemic of COVID-19.

In recent years, it has also been proposed that stimulation of the ACE2-Ang(1-7)-Mas axis could be protective against deleterious effects of diabetic nephropathy, hypertension and diabetic retinopathy and that patients with diabetes have lower Angiotensin-(1-7) levels and lower activity of ACE2. These findings are consistent with the clinical features of patients infected by SARS- -CoV-2: that develop de novo hyperglycemia with difficult metabolic control, since there is downregulation of the ACE2 receptor which is internalized.

A 45 year old female with viral pneumonia secondary to Covid-19

https://vidya36.blogspot.com/2021/05/a-45-year-old-female-with-viral.html

•What is the type of DM the patient has developed ?(is it the incidental finding of type 2 DM or virus induced type 1DM )?

Virus induced type 1 Dm

•Could it be steroid induced Diabetes in this patient?

10) Comparing two covid patients with variable recovery

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

What are the known factors driving early recovery in covid?

Ans;

The benefits of immunisation, and other possible factors, but they ... and intensive measures to drive down the reproduction number ...

11) Covid moderate with first time detected diabetes:

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?

Factors; Hypertension , obesity

Obsructive sleep apnea

Pre existing microvascular and macro vascular condition s

2) Why couldn't the treating team start her on oral hypoglycemics earlier?

Because it denovo diabetes which is new onset in Covid patient

For good prognosis they have first started insulin

12) Moderate to severe covid with prolonged hospital stay:

42 YEARS FEMALE PATIENT WITH VIRAL PNEUMONIA SECONDARY TO COVID-19https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html

1) What are the potential bioclinical markers in this patient that may have predicted the prolonged course of her illness?

D- dimers , serumLDH,crp,

Diabetesdenovo,

Hypothyroidism

13) Severe covid with first diabetes

58 years female patient with viral pneumonia secondary to covid-19

https://vignatha45.blogspot.com/2021/05/58-years-female-patient-with-viral.html

What are the consequences of uncontrolled hyperglycemia in covid patients?

Does the significant rise in LDH suggests multiple organ failure?

What is the cause of death in this case?

Due to uncontrolled hyperglycemia or use of steroids,

14) Long covid with sleep deprivation and ICU psychosis

COVID with ICU psychosis

https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html

1)Which subtype of ICU psychosis did the patient land into according to his symptoms?

2)What are the risk factors in the patient that has driven this case more towards ICU pyschosis?

Elevated d dimers ,

CvA

Family (and lack of visitation)

Clotting problems

Oxygenation issues

Virus itself

Immobilization

Drugs (eg, benzodiazepines)

3)The patient is sleep deprived during his hospital stay..Which do u think might be the most propable condition?

A) Sleep deprivation causing ICU pyschosis

B) ICU psychosis causing sleep deprivation

4) What are the drivers toward current persistent hypoxia and long covid in this patient?

15) Moderate Covid with comorbidity (Trunkal obesity and recent hyperglycemia)

A 42YR OLD MALE WITH FEVER AND COUGH.

https://meghanaraomuddada.blogspot.com/2021/05/case-1-2021-42yr-old-male-with-fever.html

1. As the patient is a non- diabetic, can the use of steroids cause transient rise in blood glucose?

Yes

2. If yes, can this transient rise lead to long term complication of New-onset diabetes mellitus?

Yes

3. How can this adversely affect the prognosis of the patient?

If new on set of diabetes present it can cause inflammatory response leads to delayed recovery

4. How can this transient hyperglycemia be treated to avoid complications and bad prognosis?

First glucose levels are replaced by insulin

5. What is thrombophlebitis fever?

The redness and tenderness may follow the course of the vein under the skin. Low grade fever may accompany superficial and deep phlebitis. High fever or drainage of pus from the site of thrombophlebitis may suggest an infection of the thrombophlebitis (referred to as septic thrombophlebitis).

Cause s; insertion intravenous catheters

6. Should the infusion be stopped inorder to control the infusion thrombophlebitis? What are the alternatives?

Yes

16) Mild to moderate covid with hyperglycemia

A 35 Y/O Male with Viral Pneumonia Secondary to COVID-19

https://vaishnavimaguluri138.blogspot.com/2021/05/viral-pneumonia-secondary-to-covid-19.html

1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?

Inflammatory response

Alcoholic

Stress,anxiety , depression

2. What is the frequency of this phenomenon of New Onset Diabetes in Covid Patients and is it classical type 1 or type 2 or a new type?

New type

3. How is the prognosis in such patients?

4. Do the alterations in glucose metabolism that occur with a sudden onset in severe Covid-19 persist or remit when the infection resolves?

Resolves slowly

Proper glucose control increases recovery and survival

5) Why didn't we start him on Oral hypoglycemic agents earlier?

Because it denovo diabetes which is new onset in Covid patient

For good prognosis they have first started insulin

After oral hypoglycemic agents are used

17) Covid 19 with hypertension comorbidity

A 62 YEAR OLD MALE PATIENT WITH FEVER , COUGH AND SHORTNESS OF BREATH

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

2)what is the cause for pleural effusion to occur??

Due toinflammation

18) Covid 19 with mild hypoalbuminemia

A 38 Y/O Male with Viral Pneumonia Secondary to COVID-19

https://meesumabbas82.blogspot.com/2021/05/a-38-yo-male-with-viral-pneumonia.html

1. What is the reason for hypoalbuminemia in the patient?

2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?

Exanthem is the medical name given to a widespread rash that is usually accompanied by systemic symptoms such as fever, malaise and headache. It is usually caused by an infectious condition such as a virus, and represents either a reaction to a toxin produced by the organism, damage to the skin by the organism, or an immune response.

It is due to nonspecific viral exanthem

3. What is the reason for Cardiomegaly?

Creatinine, Urea and CRP levels of patients significantly increased based on cardiovascular disease detection. In contrast, Sodium levels reduced to below the normal in patients with cardiomegaly. Despite respiratory illness as the first symptom of COT

4. What other differential diagnoses could be drawn if the patient tested negative for covid infection?

More common chest imaging characteristics of the confirmed COVID-19 cases by high-resolution computed tomography (HRCT) included ground-glass opacities (GGOs), multiple patchy shadows, and consolidation with bilateral involvement than COVID-19-negative group (82.4% vs 31.4%, P = 0.0002; 41.2% vs 17.6% vs P = 0.048; 76.5% vs 43.1%, P = 0.017; respectively). The rate of clustered infection was higher in COVID-19-positive group than COVID-19-negative group (64.7% vs 7.8%, P = 0.001). Through multiplex PCR nucleic acid testing, 2 cases of influenza A, 3 cases of influenza B, 2 cases of adenovirus, 2 cases of Chlamydia pneumonia, and 7 cases of Mycoplasma pneumoniae were diagnosed in the COVID-19-negative group.

5. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

We demonstrated that in patients diagnosed with COVID-19, D-dimer elevation upon admission was common and was associated with both increased disease severity and in-hospital mortality. D-dimers are one of the fragments produced when plasmin cleaves fibrin to break down clots. The assays are routinely used as part of a diagnostic algorithm to exclude the diagnosis of thrombosis. However, any pathologic or non-pathologic process that increases fibrin production or breakdown also increases plasma D-dimer levels [13]. Examples include deep vein thrombosis/pulmonary embolism, arterial thrombosis, disseminated intravascular coagulation, and conditions such as pregnancy, inflammation, cancer, chronic liver diseases, post trauma and surgery status, and vasculitis. Among adults admitted to the emergency room, infections, instead of VTE/PE, are the most common reason for D-dimer elevation [14].

OtherConditions

recent surgery, trauma, infection, heart attack, and some cancers or conditions in which fibrin is not cleared normally, such as liver disease.

20) Covid 19 with first time diabetes

A 48 year male with viral pneumonia due to COVID

https://srilekha77.blogspot.com/2021/05/a-48-year-male-with-viral-pneumonia-due.html

1)Can usage of steroids in diabetic Covid patients increases death rate because of the adverse effects of steroids???

2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically???

Most of patients are save trough blood thinners are given prophylactically

Some are died due to formation of blood clots

3)Does chronic alcoholism have effect on the out come of Covid infection????

If yes,how??

Yes, chronic alcoholism Increases the risk of acute respiratory distress syndrome which is one of the most severe complication of covid19

21) Severe Covid with Diabetes

A 65 YEAR OLD FEMALE WITH FEVER, SHORTNESS OF BREATH, DRY COUGH AND GENERALISED WEAKNESS

https://sudhamshireddy.blogspot.com/2021/05/a-65-year-old-female-with-fever.html

1. What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non diabetics?

2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?

3. What effect does a history of CVA have on COVID prognosis?

history of stroke was associated with poorer progression of COVID-19. In a cohort of patients from 55 hospitals, history of stroke was twice as frequent among patients classified as having severe COVID-19 than among patients with mild symptoms.

SARS-CoV-2 may cause stroke by several mechanisms: invasion of vessel walls, coagulation disorders, cerebral embolism secondary to myocardial damage, or destabilisation of an existing atheromatous plaque. The virus is able to invade vessel walls because endothelial cells express the ACE2 receptor, which the virus uses to enter cells; SARS-CoV-2 has been detected in the endothelium.²⁷ When it invades vessel walls, it may behave similarly to the varicella zoster virus, the most frequent viral cause of stroke, triggering inflammation and even necrosis of the walls of cerebral

23) Covid 19 with multiple comorbidities:

CASE DISCUSSION ON VIRAL PNEUMONIA SECONDARY TO COVID 19

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?

Brochial , chronic kidney ,diabetes, pulmonary kochs

2) Can you explain why the D dimer levels are increasing in this patient?

3) What were the treatment options taken up with falling oxygen saturation?

First start

o2 supplementation with 15 L/min

Neb with DUOLIN+BUDDCORT 6th hourly inj.

CPAP- continuous pasitive air pressure

Bipap

Mechanical ventilation

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)

Diabetes

10) Medical education

Ans;

Active learning represents a shift away from exposition instruction that has a tendency to render learners bored or passive. Students take responsibility for their learning by engaging in activities or discussion in class. This method emphasizes higher-order thinking and often involves group work.Well-designed AL lessons have been found to be effective for maximizing learning,engagement, peer collaboration, and evidence-based medicine.

medicine online blended assignment

Medicine blended assignment

Anatomical localisation for problem;

Primary etiological agent:

Non pharmacological interventions:

2x2cm chronic ulcer on heel of R foot with sloping edges

D) 55years old patient with seizures.

A 48 year old male with seizures and altered sensorium

F) A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWERLIMB

A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY

A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS

A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT

67 year old patient with acute coronary syndrome

A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA

A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension

Post TURP

with non oliguria ATN

Diabetic Nephropathy

An Eight year old with Frequent Urination

A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH

LIVER ABSCESS

2. Amoebic Liver Abscess and Alcohol

50/Male came with altered sensorium

Abstract

Covid pneumonia in a pre existing case of interstitial lung disease

The triggering of post-COVID-19 autoimmunity phenomena could be associated with both transient immunosuppression and an inappropriate form of immune reconstitution in susceptible individuals

A 50 year old female with Viral Pneumonia secondary to Covid-19

A 26 Year Old Female with Fever and Shortness of Breath

29 year old male patient with viral pneumonia secondary to COVID-19

45 Y/O MALE WITH COVID-19 AND COMORBIDITIES (ALTERED SENSORIUM, AZOTEMIA, HYPOKALEMIA.)

65 YEARS OLD MALE WITH VIRAL PNEUMONIA SECONDARY TO COVID-19.

A 67 year old lady in the ICU with COVID induced Viral Pneumonia .

What precautions should a recently-recovered COVID-19 patient take? Find out

'After the acute phase of COVID-19 is over, patients may return to hospitals with symptoms such as lethargy, body aches and itchy throats, even four to six weeks later,' says Dr Md Shakeel of Hiranandani Hospital, Vashi

35YR/M WITH VIRAL PNEUMONIA SECONDARY TO COVID 19 INFECTION

A 45 year old female with viral pneumonia secondary to Covid-19

A little difference that altered the entire covid recovery game: a report of two patients with focus on imaging findings .

42 YEARS FEMALE PATIENT WITH VIRAL PNEUMONIA SECONDARY TO COVID-19https://93deepanandikonda.blogspot.com/2021/05/42-years-female-patient-with-viral.html

58 years female patient with viral pneumonia secondary to covid-19

COVID with ICU psychosis

A 42YR OLD MALE WITH FEVER AND COUGH.

A 62 YEAR OLD MALE PATIENT WITH FEVER , COUGH AND SHORTNESS OF BREATH

A 38 Y/O Male with Viral Pneumonia Secondary to COVID-19

A 48 year male with viral pneumonia due to COVID

A 65 YEAR OLD FEMALE WITH FEVER, SHORTNESS OF BREATH, DRY COUGH AND GENERALISED WEAKNESS

CASE DISCUSSION ON VIRAL PNEUMONIA SECONDARY TO COVID 19

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