1) Pulmonology (10 Marks)
A) Link to
patient details:
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 timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Symptomatology in this patient in terms of an event
timeline:
- 20 years ago: the patient had an episode of SOB (grade
II) during the month of January while working on the paddy fields which
decreased on taking inhalers. It
eepeated every year.
- 12 years ago: she had a severe episode of SOB that
required hospitalization after which her symptoms reduced.
- 8
years ago: she was diagnosed with diabetes.
- 5
years ago: patient was treated for anemia with iron injections
- 1
month ago: patient started experiencing generalized weakness.
- 30
days ago: patient had her latest
episode of SOB.
- 20
days ago: patient had an HRCT done due to suspicion of COVID.
- 15
days ago: patient developed pedal
edema.
- 15
days ago: patient developed facial puffiness.
- 2
days ago: patient had reduced urine output .
The anatomical localization
of the disease is at the lungs
The primary aetiology of her problem is COPD that has led to right heart failure. The COPD is most probably
a consequence of using an indoor stove (choolha)
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:
- Augumentin
- MOA:
Amoxicillin is a beta lactam antibiotic that acts by preventing the cross
linking of bacterial cell wall. Clavulanic acid acts by protecting Amoxicillin
from being inactivated by beta lactamases.
- Indication:
lower respiratory tract infections, otitis media, skin infections, UTI,
sinusitis, etc
- Efficacy:
highly effective against sensitive strains of: staphylococci, E. Coli,
klebsiella, Proteus as compared to placebo or ampicillin.
2. Azithromycin:
- MOA:
prevents bacterial protein synthesis by preventing the translocation step
by binding to 50s su8bunit.
- Indication:
Community acquired pneumonia, tonsillitis, acute exacerbation of COPD, PID
- Efficacy:
effective against staphylococci, streptococcus and moroxella along with
many other gram8 positive and negative bacteria
3. Lasix
- MOA:
it is furosemide that is a loop diuretic that acts by blocking the
Na+k+cl- transport channel in the loop of Henle
- Indications:
heart failure, liver cirrhosis, kidney disease
- Efficacy:
highly effective diuretic
4.Pantop
- MOA: it is a
proton pump blocker that decreases gastric acid secretion
- Indications:
acidity
- Efficacy:
highly effective
5.Hydrocortisone
- MOA: it is a
steroid drug that decreases inflammation
- Indication:
asthama, COPD, thyroiditis,Rheumatoid arthritis, adrenocortical
insufficiency
- Efficacy:
highly effective
6. Ipravent2
- MOA: An anti
cholinergic that causes bronchodilation
- Indications:
bronchial asthama , COPD
- Efficacy:
highly effective
7. Budecort
- MOA;beta 2
agonist that causes bronchodilation.
- Indications:
asthama, COPD, COVID
- Efficacy:
highly effective
8. Pulmoclear
- MOA:
acebrophylline:acts by bronchodilation, anti inflammatory action and as a
mucolytic. Acetylcysteine: has mucolytic action.
- Indications:
COPD
- Efficacy:
highly effective
9. thiamine
- MOA:
thiamine diphosphate is a coenzyme in carbohydrate metabolism
- Indications:
deficiency, wernicke's encephalopathy, beri beri
Non-Pharmacological
interventions:
1. O2 supplementation
- MOA: Acts by
increasing alveolar oxygen partial pressure
- Indications:
decreased SPO2
2.Chest physiotherapy
- MOA: expands
lungs' strengthen s respiratory muscles, improves drainage of mucus.
- Indications:
COPD, bronchiectasis, cystic fibrosis
3) What could be the causes for her current acute exacerbation?
- Allergens: like pollen, wood smoke (choola)
- Respiratory infections: responsible for half of all
acute exacerbations. Commonly due to H. Influenzae, S. Pneumoniae,
Moraxella catarrhalis.
- Air pollution
- Toxins
4. Could the ATT have affected her symptoms? If so how?
Yes, ATT could have affected her
symptoms.
According to the history the patient
started d2eveloping pedal edema and facial puffiness a few days after starting
ATT. As these both are signs of re2nal dysfunction it is possible that
some of her symptoms are due AKI as a consequence of adverse reaction to ATT.
5.What could be the causes for her electrolyte imbalance?
The patient has hypochloremia and hyponatremia.
hypochloraemia could have been a consequence of heart failure in addition to her treatment
with diuretics such as Lasix (furosemide).
The
hyponatremia can be a consequence of AKI. In AKI there is a loss of renal function
thus compromising its ability to reabsorb sodium leading to excess urinary
sodium loss. Hence the hyponatremia.
2) Neurology (10 Marks)
A) Link to
patient details:
h2ttps://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?
Ev2olution of the symptomatology:
20029 (12 years ago): the patient Started drinking alcohol
2019 (2 years ago): the patient was Diagnosed
with Diabetes Mellitus, prescribed oral hypoglycemics
2020 (1 year ago): the patient had an episode of seizures (most likely GTCS)
January 2021 (4months ago): the patient Has another seizure episode (most likely GTCS)-
following cessation of alcohol for 24 hours. Starts drinking again after
seizure subsides
Monday, May 10, 2021: the patient had his Last alcohol intake, around 1 bottle. Starts
having general body pains at night.
Tuesday, May 11, 2021: the patient food intake decreased. He Started talking and laughing to
himself. He was unable to lift himself off the bed, help was required.
He was Conscious, but non coherent.
Disoriented to time, person, place. He was taken to an RMP the same day-
is prescribed IV fluids and asked to visit a hospital.
Saturday, May 15, 2021: he was admitted to a tertiary care hospital for alcohol withdrawal
symptoms, and is treated for the same.
Anatomical localisation of problem: the brain -hippocampus and frontal lobe.
Primary etiology of patient's problem: Chronic Alcoholism
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
1. Inj. 1amp THIAMINE in
100ml NS, TID
MOA: Thiamine is necessary to provide energy to the
CNS, helps in conduction of nerve signals.
Hence, deficiency leads to
confusion and ataxia, both of which are present in this patient.
Indication: Since Wernicke syndrome (deficiency of B1 vitamin) is
a differential diagnosis.
Efficacy: Highly effective in treating B1 deficiency
2. Inj. Lorazepam
MOA: Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A
ligand-gated chloride channel neuron at several sites within the central
nervous system (CNS). It enhances the inhibitory effects of GABA, which
increases the conductance of chloride ions into the cell.
Indication: Used to sedate patient
Efficacy: High efficacy
3. T. Pregabalin 75mg/PO/
BD
MOA: Acts by releasing GABA
Indications: in seizures
Efficacy: Newer antiepileptic, good efficacy with fewer side effects
4. Inj. HAI S.C.- premeal
MOA: Short- acting insulin
Indications: Diabetes Mellitus
Efficacy: Effective for short periods of time
5. Lactulose 30ml/PO/BD
Given for same reason as
Ringer's lactate
6. Inj 2 ampoule KCl
(40mEq) in 10 NS over 4 hours
7. Syp Potchlor 10ml in one
glass water/PO/BD
MOA: Potassium to increase serum K levels
Indications: in hypokalemia
Efficacy: Highly effective
3) Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
A possible cause for this is due to a
phenomenon known as kindling. In kindling, repeated attempted
alcohol detoxification leads to an increased severity of the withdrawal
syndrome. Patients with previous withdrawal symptoms are more likely to have
more medically complicated withdrawal symptoms with time.
Chronic alcohol use and kindling together
leads to permanent alteration in GABA receptors, leading to downregulation of
GABA. This in turn leads to inhibition of inhibitory neurotransmitter GABA,
hence leading to seizures (hyperactivity).
4) What is the
reason for giving thiamine in this patient?
One of the differential diagnoses for altered
sensorium following chronic alcoholism is Wernicke-Korsakoff Syndrome, caused
by deficiency of thiamine (B1). To either treat or rule this differential out,
thiamine is given. Thiamine is necessary to provide energy to the CNS, helps in
conduction of nerve signals.
Hence, deficiency leads to confusion and
ataxia, both of which are present in this patient.
5) What is the
probable reason for kidney injury in this patient?
The most probable reason for kidney injury in this patient is generalised dehydration.
6). What is
the probable cause for the normocytic anemia?
Probable causes of
normocytic anaemia are:
·
Increased oxidative stress and inflammation,
leading to hemolysis of the RBCs
·
Decreased bone marrow production of RBCs, due
to EPO deficiency owing to kidney failure
·
Loss
of blood through chronic foot ulcer
7) Could
chronic alcoholism have aggravated the foot ulcer formation? If yes, how and
why?
Yes, as chronic alcoholism itself can cause
peripheral neuropathy (alcoholic neuropathy), which along with Diabetic
neuropathy, can lead to a non-healing foot ulcer.
B) Link to patient
details:
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
Questions-
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Evolution of the
symptomatology
Since 1991(30 years ago):
Patient has been drinking alcohol, 90-180ml per day
May 13, 2021: he Felt
giddy, which subsided after a while. He had one episode of vomiting
May 13-16: patient
stopped consumption of alcohol
May 16, 2021: he
Consumed alcohol again.
May 17, 2021: he had
Another bout of giddiness which was associated with Bilateral hearing loss,
aural fullness, tinnitus, nystagmus, 2-3 episodes of vomiting per day.
May 18, 2021: he was Admitted
to a tertiary care hospital.
Anatomical location: Infarct in the right inferior cerebellar
hemisphere
Primary etiology: Cerebellar infarction, most probable cause:
Primary HTN
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
1.
Inj Zofer 4 mg IV/TID
MOA: 5-HT receptor antagonist
Indication: Ondansetron, used as an anti emetic
Efficacy: Effective
2.
Tab Ecosprin 75 mg PO/OD
MOA: Aspirin, Cyclo-oxygenase inhibitor
Indication: To prevent strokes
Efficacy: Used as a preventive measure
3.
Tab Atorvostatin 40 mg PO/HS
MOA: Statin, HMG CoA reductase inhibitor
3) Did the
patients history of denovo HTN contribute to his current condition?
Yes, as a cerebellar
infarct is a type of ischaemic stroke, which occurs due to infarction following
decreased blood supply to that area.Since HTN causes hyaline arteriosclerosis,
and eventually rupture, HTN is a cause for stroke and in turn, cerebellar infarcts.
4) Does the
patients history of alcoholism make him more susceptible to ischaemic or
haemorrhagic type of stroke?
Binge drinking causes hyperlipidemia with an
increase in LDL, which in turn leads to atherosclerosis. Atherosclerosis of the
vessels to the brain leads to ischaemia, hence causing ischaemic stroke.
C) Link to patient
details:
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Questions:
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Evolution of the
symptomatology
2011, 10 years ago: The
patient had One episode of quadriplegic paralysis
October 2020: The
patient developed bilateral pedal edema, pitting type
May 10, 2021: The
patient ecperienced Pain along the left upper limb, dragging in nature
May 11, 2021: The patient
complained of palpitations, sudden in onset, associated with dyspnoea (grade
3), Chest pain with chest heaviness.
Anatomical localisation: Skeletal muscle, Neuromuscular junction
Primary etiology: Hypokalemia (decreased serum potassium)
2) What are the
reasons for recurrence of hypokalemia in her? Important risk factors for her
hypokalemia?
the reasons for recurrence of
hypokalemia is Possibly inherited or idiopathic causes for
hypokalemia.
Risk factors of
hypokalemia:
- Female
- Medications
(diuretics)
- Heart
failure
- Hypertension
- low
BMI
- Alcoholism
- Diarhhoea/
severe vomiting
- Cushing
syndrome
3) What are
the changes seen in ECG in case of hypokalemia and associated symptoms?
Changes seen include a
shallow or inverted T wave, QT prolongation in mild hypokalemia, and
Visible U wave, mild ST
depression in severe hypokalemia.
D) Link to patient
details:
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, there is. Post-stroke seizures occur more often after hemorrhagic
stroke, and are more likely to be recurrent when they are late onset seizures.
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?
After effects of stroke
include scar formation, leading to gliotic scarring as seen in this patient.
Increased scarring may have led to worsening of symptoms, hence causing loss of
consciousness in the recent episode.
E) Link to patient
details:
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Questions: 1) What could
have been the reason for this patient to develop ataxia in the past 1 year?
- The
patient was a chronic alcoholic who started drinking 3 years ago. He
represents a classic case of cerebellar ataxia due to
toxic damage by alcohol.
2) What was the
reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
The reason for his IC bleed
may be:
- This
patient has a history of an alcohol binge a few hours prior to the onset
of symptoms.
- He
has a history of repeated falls and head trauma over the past 2-3 years
that went undetected and were medically unattended.
- He
has no history of hypertension but was reported to be hypertensive after
the development of intracranial bleeding (BP: 150/90)
Yes, Alcoholism contribute to
bleeding diatheses
F) Link to patient
details:
Questions
1.Does the
patient's history of road traffic accident have any role in his present
condition?
Yes, Trauma to the head in an RTA may cause axonal
shearing as well as microthrombi formation, both of which can aggravate a
stroke.
2.What are
warning signs of CVA?
3.What is the
drug rationale in CVA?
- Mannitol, osmotic agent- to decrease cerebral edema,
increase cerebral perfusion
- Aspirin, antiplatelet- prevention of stroke again, to
prevent other thrombotic events
- Atorvastatin, to decrease LDL- prevention of another stroke
4. Does
alcohol has any role in his attack?
Alcohol causes hyperlipidemia with an
increase in LDL, which in turn leads to atherosclerosis. Atherosclerosis of the
vessels to the brain leads to ischaemia, hence causing a stroke.
5.Does his
lipid profile has any role for his attack?
Yes,
an increase in LDL with time leads to atherosclerosis. Atherosclerosis of the
vessels of the brain leads to ischaemia, causing a stroke.
G) Link to patient
details:
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
__*Questions*_
1)What is
myelopathy hand?
It is characterised by loss of adduction
and extension of the ulnar 2-3 fingers. Inability to rapidly grip and
release with these fingers is also seen. There is weakness and wasting of
the muscles but no sensory involvement.
This is due to pyramidal tract
involvement. It is seen in various cervical spine disorders with spinal cord
involvement.
2)What is
finger escape ?
Finger escape is elicited by asking the patient to hold their fingers in extension and
abduction. The little and ring fingers slowly fall into flexion and adduction
within 30 seconds. This happens because of poorly innervated palmar
interosseous muscle between the fourth and fifth metacarpals susceptible
in myelopathy.
It is a sign of cervical spinal cord
problems like cervical myelopathy.
3)What is
Hoffman’s reflex?
Hoffman’s reflex is performed by loosely holding the middle finger and flicking the
fingernail downward, allowing the middle finger to flick upward
reflexively.
Positive response: flexion and adduction of the thumb and flexion of the index finger.
A positive
Hoffmann's sign is suggestive of corticospinal tract dysfunction
localized to the cervical segments of the spinal cord.
H) Link to patient
details:
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Possible
questions:
1) What can be
the cause of her condition ?
·
The patient was
suffering from acute cortical vein thrombosis which led to a haemorrhagic
venous infarction. In cortical vein thrombosis due to the
close contact of cortical veins to the cerebral cortex, local alterations are
of the blood–brain barrier are produced which also trigger seizures.
·
In addition, occlusion of the superior
sagittal sinus and cortical veins, which drain venous blood from motor and
sensory cortices could increase the risk of seizures due to damage to the motor
cortex.
·
If haemorrhage occurs, focal cortical
irritation caused by blood metabolites could also predispose acute seizures.
3) What are the
risk factors for cortical vein thrombosis?
Risk factors for cortical vein
thrombosis in adults:
- Clotting disorders such as: antiphospholipid syndrome,
protein C and S deficiency, antithrombin III deficiency
- Pregnancy
- Cancer
- Obesity
- Collagen
vascular disorders like : wagner's granulomatosis, behecet syndrome .
- Intracranial
hypotension.
- Inflammatory
bowel diseases like crohn's disease and ulcerative colitis.
3)There was
seizure free period in between but again sudden episode of GTCS why?resolved
spontaneously why?
Seizures after CVA tend to be of two
types:
·
Early
·
Late.
Early seizures are usually seen within
24 days of the incident and the late seizures occur 1-2 weeks after the
incident. The patient’s seizures on 1/5/21 can be case of early onset seizures
and on 10/5/21 can be late onset.
4) What drug was
used in suspicion of cortical venous sinus thrombosis?
·
Clexane (Enoxaparin) an anticoagulant
·
mannitol (to decrease the intracranial
pressure)
3) Cardiology (10 Marks)
A) Link to patient
details:
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
1.What is the
difference btw heart failure with preserved ejection fraction and with reduced
ejection fraction?
2.Why haven't
we done pericardiocenetis in this pateint?
Pericardiocentesis was not done in the
patient as he was hemodynamically stable and his pericardial effusion was
improving with medical treatment. It had come down to 1.9 cm from an initial
value of 2.4 cm
3.What are the
risk factors for development of heart failure in the patient?
- Advanced age
- Diabetes
- Hypertension
- Smoking
- Alcohol consumption
- Anaemia
- Renal disorders
4.What could
be the cause for hypotension in this patient?
·
Diastolic dysfunction could be the reason for the hypotension.
·
Diastolic dysfunction can lead to
hypovolemia which in turn can lead to hypotension.
·
The patient was also on Lasix which
can again lead to hypovolemia.
·
Anaemia can also be a contributing factor to the hypotension.
B) Link to patient
details:
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?
Possible risk
factors for heart failure in this patient include:
- Advanced age
- Diabetes
- Alcohol consumption
- Anemia
- Renal disorders
- Obesity
2.what is the
reason for anaemia in this case?
·
Erythropoietin (hormone responsible
for erythropoiesis) is produced by interstitial fibroblasts of kidney.
·
In kidney diseases like CKD,
the erythropoietin production decreases due to damage to the kidneys thus
leading to anaemia.
·
Another proposed mechanism
for anaemia in CKD is the inhibition of erythropoiesis by uremic induced
inhibitors.
3.What is the
reason for blebs and non-healing ulcer in the legs of this patient?
Bleb which were formed on
the toe could be due to the tight fitting of the footwear. As they fit too
tight, they rub against the skin. This causes friction as a result of
which fluid builds up underneath the upper layer of skin. This is often
seen in patients with long standing diabetes due to loss of sensation as a
result of peripheral neuropathy.
Peripheral neuropathy caused by diabetes could
be a contributing factor. In addition diabetes causes peripheral arterial
disease that leads to decreased peripheral blood flow which delays the healing.
Diabetes is a common cause for non-healing ulcers.
4. What sequence
of stages of diabetes has been noted in this patient?
The patient’s obesity
is likely to have caused insulin resistance (stage 1).
This later developed into frank diabetes.
(stage 3).
As the patient shows signs of vascular complications
such as diabetic retinopathy, nephropathy and peripheral neuropathy which are
complications of diabetes, it could be said that the patient has stage 4
diabetes mellitus.
C) Link to
patient details:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.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?
Evolution of symptomatology:
- 2-3 years ago: patient had episodic facial
puffiness
- 1 year ago: patient developed grade 2 SOB
- 1 year ago: patient was diagnosed with hypertension
- 2 days before admission: patient’s SOB grade 2
progressed to grade 4
- 2 days before admission: patient’s urine output
decreased.
Anatomical
localization of the problem: the heart; both the atria
Primary etiology of the
patients problem: congestive heart failure
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:
1.Cardivas
- MOA: nonspecific beta blocker with additional alpha 1
blocking properties
- Indication: hypertension, heart failure, post MI
- Efficacy: highly effective
2. Dytor
- MOA:
torsemide: loop diuretic blocks Na+K+Cl- channels. Spironolactone:
aldosterone antagonist blocks Na+k+ channel in DCT
- Indications:
hypertension, heart failure, kidney failure, liver disease
- Efficacy: highly effective
3.Digoxin
- MOA:
causes increased intracellular Na causes increased ca and increased
contractility
- Indications:
heatr failure
- Efficacy: highly effective
4. Taxim:
- MOA:
beta lactam antibioticacts by binding to PBP
- Indications:
broad spectrum acts against many gram + and - bacteria
- Efficacy: highly effective
5.Pan D
- MOA:
it is a proton pump blocker that decreases gastric acid secretion.
Domperidone: D2 receptor antagonist
- Indications:
acidity, GERD
- Efficacy:
highly effective
6. Thiamine:
- MOA:
thiamine diphosphate is a coenzyme in carbohydrate metabolism
- Indications:
deficiency, wernicke's encephalopathy, beri beri.
5) What is the
pathogenesis of renal involvement due to heart failure (cardio renal syndrome)?
Which type of cardio renal syndrome is this patient?
Pathogenesis of cardio renal syndrome:
The patient has type 4 cardio renal syndrome.
6) What are the
risk factors for atherosclerosis in this patient?
The risk factors for
atherosclerosis in this patient include:
·
Hypertension
·
Diabetes mellitus
·
Smoking
·
Obesity
·
Physical inactivity
·
High saturated fat content
in diet.
7) Why was the
patient asked to get those APTT, INR tests for review?
The patient is asked to get these test for review
to ensure that the coagulatory parameters
remain normal, if not, there is a need to modify the treatment in order to
bring them to normal levels.
D) Link to patient
details:
Questions-
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
·
Evolution
of symptomatology in patient: in 2020:the patient has had episodes of chest pain, which were
relieved without medication.
·
2021
:The patient developed shortness of breath and sweating on exertion
·
Anatomical
localization of the problem: coronary artery.
§ Primary aetiology of patient’s problem: Atherosclerosis is the primary
aetiology of the patient’s problem. An acute thrombus which leads to the
obstruction of an atherosclerotic coronary artery causes Acute coronary
syndrome. Which further causes myocardial infarction
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
treatment: The
patient was firstly given MET-XL (beta blocker) as it decreases the oxygen demand of the
heart by reducing heart rate and contractility and thus relieving the symptoms
seen in the patient. It also decreases the risk of ventricular fibrillation and
thus reducing incidences of sudden cardiac death.
·
When compared to the
placebo given, the patients who received metoprolol had significant effect on
ventricular fibrillation but the number of episodes tended to be lower in the
metoprolol treated patients during the later phase.
Source: https://pubmed.ncbi.nlm.nih.gov/2863148/
·
Non- pharmacological
treatment: the patient was advised PCI.
·
PCI: It is a non-surgical
technique used in the treatment of obstructive coronary artery.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC59588/
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.
Source: https://emedicine.medscape.com/article/161446-overview
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?
·
PCI
reduces the cardiovascular events in patients with acute coronary syndrome.
If PCI is performed in a stable patient it might increase the
occurrence/risk of ischemic events due to premature discontinuation of
anti-platelet therapy.
Source: https://pubmed.ncbi.nlm.nih.gov/23459399/
·
Overtreatment continues to be a major contributor to
excessive healthcare spending. When there is over treatment is done it might
not be required and, in some cases, may even cause harmful effects on the
patients rather than relieving the symptoms. Research on over treatment and
over testing is necessary to put an end to unnecessary diagnostic test and
provide appropriate guidelines to approach a particular symptom or disease as a
whole.
E) Link to patient
details:
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Questions:
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
·
Evolution
of symptomatology in patient: the patient has had chest pain since 3 days.
·
Anatomical
localization of the problem: damage to the myocardial muscle(heart) due to obstruction in the
coronary artery.
·
Primary
aetiology of patient’s problem: atherosclerosis is the primary etiology.
2) What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
Pharmacological
interventions:
1)
Asprin:
Mechanism of action: it acts by inhibiting cyclo-oxygenase and thromboxane
synthase. It inhibits platelet function.
indication: anti thrombotic
effect.
Efficacy: High
2)
Atrovastatin:
Mechanism of action: competitive inhibition of HMG Co-A reductase. Helps in lowering
LDL and IDL.
Indication: high LDL levels.
Efficacy: highest LDH-CH lowering efficacy among statins.
3)
Clopidogrel:
Mechanism of action: it alters surface receptors on platelets and inhibits ADP
as well as fibrinogen induced platelet aggregation, it interferes with
activation of platelets.
Indication: in MI
Efficacy:
newer and more potent anti-platelet drug. Synergistic action when used along
with asprin and prevents ischemic episodes.
3) Did the
secondary PTCA do any good to the patient or was it unnecessary?
Percutaneous transluminal coronary
angioplasty, is a minimally invasive procedure that opens blocked coronary
arteries to improve blood flow to the heart muscle.
F) Link to patient
details:
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
1. How did the
patient get relieved from his shortness of breath after i.v fluids
administration by rural medical practitioner?
Administration
of i.v fluids in the early stages of cardiogenic shock can restore circulation
by compensating for the decreased volume and perfusion. But this compensation
is transient.
Inadequate forward blood flow in a right ventricle that's compromised post-MI
can lead to end-organ perfusion deficits.
The patient's
SOB is a compensatory mechanism for the metabolic acidosis brought on by
cardiogenic shock. IV bicarbonate infusion can help reverse this metabolic
acidosis and temporarily alleviate SOB. However, this is not the definitive
treatment as IV fluids alone can cause volume overload states resulting in
edema. They need to be coupled with suitable diuretics, inotropes, ACE
inhibitors/ARBs
Source: https://emedicine.medscape.com/article/152191-treatment
https://www.ahajournals.org/doi/full/10.1161/JAHA.119.011991
https://www.healthline.com/health/metabolic-acidosis-treatment#treatment
2. What is the
rationale of using torsemide in this patient?
Torsemide is a
loop diuretic that acts on the Na+/K+/2Cl- channels in the loop of Henle. One
of the adverse effects of loop diuretics is hypokalemia, which could be the
reason this was chosen as the diuretic for this hyperkalemic patient.
3. Was the
rationale for administration of ceftriaxone? Was it prophylactic or for the
treatment of UTI?
Patients with
cardiogenic shock are extremely susceptible to the development of infections.
Infections that do develop in patients with cardiogenic shock are very
difficult to treat due to low perfusion states.
As severe
stasis and reduced urine output can act as a breeding ground for infectious
pathogens, using prophylactic antibiotics is necessary.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5266423/
4) Gastroenterology (&
Pulmonology) 10 Marks
A) Link to
patient details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
QUESTIONS:
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
·
Evolution of patient’s symptomatology:
·
In 2012: patient started consuming Sara.
·
In 2017: he had pain abdomen and vomiting
following which he stopped consuming sara as advised by the doctor for the next
3 years.
·
In 2020: he started consuming alcohol again,
following which he had similar complaints of vomiting and abdominal pain.(5-6
episodes in the year)
·
20 days ago: increase in the consumption of
alcohol.
·
7 days ago: last binge of alcohol following
which he had vomiting diarrhoea
·
4 days ago: he has had fever, constipation
and burning micturition which was associated with supra pubic region.
·
Anatomical localization of the problem: Pancreas
·
Primary aetiology of the patient’s problem: Chronic alcoholism leading to pancreatitis and
a pseudocyst formation.
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?
The main therapeutic principles for
managing patients with acute pancreatitis relies on supportive care with close
attention to volume status and electrolyte balance, fasting of the patient
(total parenteral nutrition or naso-jejunal feeding tube), and pain management
using narcotic agents(tramadol).
prophylactic broad-spectrum antibiotics are used
to prevent infected pancreatic necrosis.
Octreotide is a
potent inhibitor of exocrine secretion of the pancreas, which plays an
important role in the pathogenesis of acute pancreatitis. Octreotide also has
direct anti-inflammatory and cytoprotective effects. It has therefore been
suggested octreotide be used in the treatment of acute pancreatitis.
Non pharmacological treatment: The development of peri-pancreatic fluid collections
are frequent local complications in acute pancreatitis. These collections are
classified as early (acute peripancreatic fluid collection or acute necrotic
collection) or late (walled-off necrosis or pseudocyst). The majority of
pancreatic fluid collections resolve spontaneously and do not require
intervention. However, in this case as there is an infection it requires
intervention. Interventions may include endoscopic or percutaneous catheter
drainage, or in a next step endoscopic or surgical necrosectomy, minimally
invasive or open.
B) Link to
patient details:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
1) What is
causing the patient's dyspnea? How is it related to pancreatitis?
·
Dyspnoea is caused due to inflammatory
process in the lung.
·
Acute pancreatitis initiates inflammatory
process in the acinar cells which later progresses to generalized systemic
inflammatory response syndrome. Amongst these pulmonary complications is one of
the most serious one.
·
Pancreatic enzymes as well as Inflammatory mediators released
as a result of pancreatic injury play a key role in the pulmonary
complications. The pathophysiology of ARDS is described as increased pulmonary
vasculature leaking protein- rich transudate into the alveolar space and
decreased lung compliance manifested clinically as refractory hypoxemia, and
radiologically as diffuse infiltration in the lungs.
2) Name
possible reasons why the patient has developed a state of hyperglycemia.
·
Acute pancreatitis is associated with damage to both the
endocrine and exocrine pancreas. Glucose intolerance seen with this disease
appears to be the result of hyperglucagonemia and relative
hypoinsulinemia.
·
Hyperglycaemia
can also develop in acute pancreatitis due pancreatic oedema and the inhibitory
effect of trypsin on insulin production
3) What is the
reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty
Liver disease?
As the
patient is an alcoholic, his liver enzymes might be rised. The other reason
would be choledo- cholithiasis.
The biochemical markers for chronic alcohol consumption
that have been most commonly studied are serum GGT, AST, ALT, mean corpuscular
volume (MCV) and carbohydrate-deficient transferrin (CDT). AST to ALT ratio
over 2 is highly suggestive of Alcoholic liver disease.
4) What is the
line of treatment in this patient?
As
mentioned in the previous case, the main course of treatment for acute
pancreatitis is to maintain electrolyte balance and to maintain volume status.
(IVF)
pain
management using narcotic agents(tramadol).
ZOFER is given which is an anti-emetic.
C) Link to patient
details:
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Possible Questions
:-
1) what is the
most probable diagnosis in this patient?
The most
probable diagnosis is an abdominal hemorrhage secondary to a hollow viscus
perforation overlapping with grade 3 renal parenchymal disease.
A ruptured hepatic
abscess could also mimic a hollow viscus perforation and can cause the same
sequelae.
2) What was
the cause of her death?
The most likely
cause of death in this patient is post-operative complications of emergency
laparotomy
3) Does her
NSAID abuse have something to do with her condition? How?
NSAID abuse can
cause nephrotoxicity in a dose-dependent fashion,
decreasing the GFR, causing acute renal failure and tubular necrosis.
NSAIDs have
also been implicated in causing hypertension.
Mechanism: NSAIDs block
renal protective prostaglandin (PGE2) synthesis which causes constriction of
the afferent arteriole and reduces GFR. This may result in acute renal failure
in low renal blood flow states.
This could have
been the reason for her reduced renal compensatory mechanism which led to a low
output state.
Apart from nephrotoxicity, NSAID abuse can also affect the GIT to cause ulcers
and perforation; liver abscess and thromboembolic
events (which could have played a role in her post-operative complication
that led to her death)
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6534025/
5) Nephrology (and Urology) 10
Marks
A) Link to
patient details:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1. What could
be the reason for his SOB ?
The
most possible reason for his SOB is metabolic acidosis, owing to renal
failure. The compensatory response to this would be hyperventilation,
presenting as SOB.
2. Why does he
have intermittent episodes of drowsiness ?
Intermittent
episodes of drowsiness are due to hyponatremia.
3. Why did he
complaint of fleshy mass like passage in his urine?
The
patient has Acute Tubular Necrosis (ATN), which implies necrosis of the renal
tubules.This necrosis leads to the necrosed tubules being excreted in the form
of brown granular casts, which looked like a fleshy mass to the patient.
4. What are
the complications of TURP that he may have had?
Possible
complications in this patient include:
·
Electolyte
abnormalities
·
Pain during
micturition
·
UTI
·
Urinary bladder
thickening
6) Infectious Disease (HI virus,
Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient
details:
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?
clinical
history and physical findings are characteristic of tracheo esophageal fistula
are:
·
RVD positive
- Has had a high-grade fever for 2 months
- Dysphagia for 2 months
- Cough on eating/drinking for 2 months
- Hoarseness of voice
- TB positive
2) What are
the chances of this patient developing immune reconstitution inflammatory
syndrome? Can we prevent it?
Given
that the patient is positive for both HIV and TB and has been compliant with
highly active antiretroviral therapy, there is a chance of her
developing immune reconstitution inflammatory syndrome
TB-IRIS
can be prevented by promptly treating the existing TB and administering
NSAIDs as IRIS is a hyperactive inflammatory immune response.
In
severe cases, systemic corticosteroids can be administered and if
necessary, ART can be discontinued
7) Infectious disease and Hepatology:
Link to patient
details:
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
1. Do you
think drinking locally made alcohol caused liver abscess in this patient due to
predisposing factors present in it ?
The
cause of this patient's abscess might have been due to various factors such as
pre-existing infections, suppressed immunity, toxic injury to the liver that
were all driven by chronic alcoholism, and that toddy, in particular, did not
increase the risk for pyogenic abscess as compared to other forms of alcohol
2. What is the
etiopathogenesis of liver abscess in a chronic alcoholic patient ? (
since 30 years - 1 bottle per day)
- Chronic alcoholism can significantly suppress one's immunity
- Alcohol+smoking both cause injury to normal hepatocytes
- Chronic alcohol use over a period of 10-20 years can consistently
blunt normal liver physiology and histology by bringing about cirrhotic
changes in the liver and cirrhosis, in turn, increases the risk of
developing liver abscesses (even though only 10-15% of alcoholics develop
cirrhosis).
3. Is liver
abscess more common in right lobe ?
Yes,
an abscess of the right lobe is twice as common as the left due to the
anatomical distribution of the blood supply of the liver.
Right hepatic lobe: 1) Right hepatic artery
2) Superior mesenteric vein
3) Portal veins
Left hepatic lobe: 1) Left hepatic artery
2) Inferior mesenteric vein
3) Splenic drainage
It
also accounts for more hepatic mass compared to the left lobe (6:1) and hence
has a larger network for both blood supply and biliary canaliculi
4.What are the
indications for ultrasound guided aspiration of liver abscess ?
Indications for
ultrasound guided aspiration of liver abscess are:
- Abscess of the left lobes: More susceptible to rupture than
abscesses of the right lobe
- To confirm a diagnosis
- Abscesses in uncommon locations
- Large abscesses (>6cm)
- High fever that doesn't respond to antipyretics
- Toxaemia
- Abscesses that don't respond to drug therapy/conservative
treatment
- Expanding abscess
- Complications: Rupture into the peritoneum, pericardial
space, pleural cavity, or through the anterior abdominal wall
B) Link to patient
details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:
1) Cause of
liver abcess in this patient ?
Toddy connsumption
2) How do you
approach this patient ?
Medical
management:
- Antibiotics: Metronidazole, paromomycin, diloxanide furoate+broad
spectrum antibiotics (for secondary infections/ if it's a pyogenic
abscess)
- Analgesics: NSAIDs, opioid analgesics (in cases of severe pain)
- Antipyretics: Paracetamol
- USG guided aspiration: Done in select cases such as abscess>6cm,
refractory to conservative treatment, high-grade fever not responding to
antipyretics or an abscess of the left lobe
Surgical
management:
Surgical
drainage by transperitoneal or posterior transpleural can be done in cases of
thick-walled multiloculated abscesses, failure of previous attempts to drain
via aspiration, peritonitis
3) Why do we
treat here ; both amoebic and pyogenic liver abcess?
As
serological tests were not carried out for this patient, there is no definite
way to diagnose the nature of the abscess. Hence, the patient should be treated
for both pyogenic and amoebic abscess as a part of conservative medical management.
Pyogenic
liver abscesses are usually caused by streptococcus sps, E. coli or Klebsiella
pneumonia, and metronidazole alone does not effectively cover these organisms.
On the other hand, broad-spectrum antibiotics like cephalosporins or quinolones
alone are ineffective against amoebic abscesses. Hence, a combination of the
two will be the most effective in treating the infection.
4) Is there a
way to confirm the definitive diagnosis in this patient?
Yes.
CT
scan is the preferred modality for the detection of a liver abscess.
8) Infectious disease (Mucormycosis,
Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) Link to patient
details:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions :
1) What is the evolution of the symptomatology in this patient in terms
of an event timeline and where is the anatomical localization for the
problem and what is the primary etiology of the patient's problem?
·
Evolution of symptomatology: in 2019: patient
was diagnosed with hypertension
18/04/21 : he took
COVAXIN following which he had fever the same night.
28/04/21: he had generalized weakness and facial puffiness and
periorital edema. 04/05/21: he had altered sensorium and had weakness in right
upper and lower limb.
·
Anatomical localization of
the problem: Orbit, nose, oral cavity, pancreas,
left frontal and temporal lobe
·
Primary aetiology: Diabetic ketoacidosis
promoting infection with mucormycosis.
In the presence of
hyperglycemia and low pH, which is found in patients with diabetic ketoacidosis
(DKA), phagocytes are dysfunctional and have impaired chemotaxis and defective
intracellular killing by both oxidative and nonoxidative mechanisms. This
promotes infection with mucormycosis in the presence of compromised immune
system of the host.
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?
·
Lipid formulations of amphotericin B (LFAB) is the drug of
choice to treat mucormycosis.
·
Adjunctive therapy with recombinant cytokines, hyperbaric
oxygen, and/or granulocyte transfusions can be considered for selected
patients. Early initiation of therapy is critical to maximizing outcomes.
·
Surgical approach:
surgical debridement; “aggressive-conservative” approach- frozen
sections are used to delineate the margins of infected tissues, and uninvolved
tissues are spared from debridement when possible.
Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2809216/
3) What are
the postulated reasons for a sudden apparent rise in the incidence of
mucormycosis in India at this point of time?
Mucormycosis is an
opportunistic fungal infection. That means it infects people who have a weak
immune system, that includes diabetic patients, patients taking
cortico-steroids and other conditions. As there is a recent surge in the
COVID-19 cases, steroids are being used to treat it. This increases the chances
of the patients acquiring mucormycosis post COVID due to the immune-compromised
state caused by usage of steroids. At the same time, it has been noted that
diabetic patients who have contracted COVID have a severe course of disease
leading to usage of steroid for a long time. All such reasons, have led to the
sudden increase in the incidence of mucormycosis in india.
9) Infectious
Disease (Covid 19)
As these
patients are currently taking up more than 50% of our time we decided to make a
separate log link here:
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
for this question
that contains details of many of our covid 19 patients documented over this
month and we would like you to:
1) Sort out these
detailed patient case report logs into a single web page as a master
chart
2) In the master
chart classify the patient case report logs into mild, moderate severe
and
3) indicate for
each patient, the day of covid when their severity changed from moderate to
severe or vice versa recognized primarily through increasing or decreasing
oxygen requirements
4) Indicate the
sequence of specific terminal events for those who died with severe covid (for
example, altered sensorium, hypotension etc).
1) Covid 19 with co morbidity
(Pulmonology/Rheumatology)
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.
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