medicine bimonthly assessment
Name : Sakilam Lasya
Roll num
: 117
Batch : 2017
MEDICINE BIMONTHLY
ASSESSMENT
I
have been given the following cases to solve in an attempt 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 to come up with treatment plan
This is link of questions asked regarding the case :
medicinedepartment.blogspot.com/2020/09/medicine-paper-for-october-2020-first.html?m=1
1.PULMONOLOGY
A.Acute exacerbation of COPD
Link to patient
details:
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
Question – 1 :
What is the evolution of the symptomatology in
this patient in terms of an event timeline and where is the anatomical
localization for the problem and what is the primary etiology of the patient's
problem?
Evolution of symptomatology :
Ø
In 2001 : SOB
[ 1 week in the month of January ]
Intestinal
perforation surgery
Ø
In 2013 : diagnosed with diabetes
Ø
In 2016 : anemia
Ø
april 2021 : latest episode of SOB
generalized
weakness
Ø
28 th april 2021 : bronchiectasis
Diagnosed
with HTN
Ø
3 rd may 2021 : pedal
edema
Facial
puffiness
Ø
15 th may 2021 : drowsiness
Decreased
urine output
Anatomical localization :
Ø
Bronchioles and alveoli
Primary etiology :
Ø
Allergens : to paddy [ since the
episodes coincide with paddy crop]
Chula usage [ from 20 yrs ]
Question
-2 :
What are mechanism of action, indication and
efficacy over placebo of each of the pharmacological and non pharmacological
interventions used for this patient?
|
Treatment
|
Mode
of action |
Indications
|
Efficacy
|
|
Inj Augmentin |
Inhibits bacteriak cell wall
synthesis Penicillin antibiotic |
Bronchiectasis |
|
|
Tab Azithromycin |
Interferes with bacterial protein
synthesis Macrolide antibiotic |
Bronchiectasis |
|
|
Inj Lasix |
Increase urine output Loop diuretic |
Pedal edema Facial puffiness Decrease urine output |
|
|
Tab Pantop |
Proton pump inhibitor |
Prescribed with antibiotics |
|
|
Inj hydrocortisone |
Reduces inflammation |
COPD |
|
|
Neb ipravert , budecort |
Bronchodilators |
COPD |
|
|
Tab Pulmoclear |
Bronchodilator and mucolytic |
COPD |
|
|
Inj HAI |
Peripheral utilization of glucose Fast acting insulin |
Raised blood glucose |
|
|
Inj Thiamine |
Supplements vit B 1 |
Vitamin B1 deficiency |
|
|
Head end elevation |
Increases expiratory lung volume
and oxygenation |
SOB |
|
|
O2 inhalation |
Supplements o2 |
Hypoxia |
|
|
Intermittent BiPAP |
Creates positive pressure to push
air into lungs |
COPD |
|
|
Chest physiotherapy |
Strenghthens muscles and increase
lung capacity |
Chronic lung disease |
|
|
Vitals monitoring |
Measures important body functions |
|
|
|
GRBS 6 hrly |
To check glucose levels |
DM |
|
Question
– 3 :
What could be the causes for her current acute
exacerbation?
Ø
Bronchiectasis : HRCT shows evidence
of bronchiectasis 20 days ago
Ø
Bronchiectasis is one of the risk
factor for the acute exacerbation of COPD
Question
– 4 :
Could the ATT have affected her symptoms? If
so how?
Ø
The possible reason for her weakness
could be ATT
Ø
Some of the 1 st line drugs eg .
Isoniazid and Rifampicin cause damage to kidney which might have caused pedal
edema , facial puffiness and decreased urine output
Question
-5 :
What could be the causes
for her electrolyte imbalance?
Ø
Hyponatremia : Right heart failure
Respiratory acidosis
Hypoxia
Ø
Hypochloremia :
compensated respiratory acidosis
2.NEUROLOGY
:
A.Altered sensorium :
Link to patient details:
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
Question-1:
What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Evolution
of symptomatology:
Ø 1
year back : an episode of SEIZURES for first time
Ø 4
months back : last episode of SEIZURES
Ø On
9th may 2021 : Laughing and talking to self
Oriented to time ,place ,person only from time to time
Unable to get up from bed
Decreased food
intake
Short term memory loss
Ø On
15th may 2021 : admitted to tertiary care hospital
Anatomical
localization :
Ø Thalamus
and hypothalamus
Ø Wernickes
Encephalopathy due to excess alchohol
Primary
etiology :
Ø Vitamin
B 1 deficiency due to excess alcohol consumption
Ø Increased
serum urea ,creatinine due to kidney failure
Question
-2 :
What are
mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non pharmacological interventions used for this patient?
|
DRUG |
MODE OF ACTION |
INDICATION |
EFFICACY |
|
NS
and RS |
Fluid
and electrolyte replenishment |
Fluid
and electrolyte imbalance |
|
|
Thiamine
|
Thiamine
stores are replenished |
Thiamine
deficiency due to alcohol consumption |
|
|
Lorazepam
|
Increases
levels of GABA |
Reduce
stress and anxiety |
|
|
Pregabalin
|
Mimics
GABA , Binds to alpha 2 delta receptors |
For
seizures |
|
|
HI
injection |
Reduces
blood sugar by peripheral glucose uptake |
Increased
blood sugar on RBS |
|
|
Lactulose |
Improves
mental status |
Improves
cognitive function in hepatic encephalopathy |
|
|
KCl
injection |
Potassium
supplement |
Decreased
serum k+ |
|
|
Potchlor |
Potassium supplement |
Decreased serum k+ |
|
|
GRBS 6 th hourly |
To monitor blood glucose levels |
k/c/o diabetes with increased blood
sugars |
|
Question
-3 :
Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
Ø Chronic alcohol intake has worsened condition of patient
over time
Question
-4 :
What is the reason for giving thiamine in this patient?
Ø The
effects are seen in this patient as memory loss , confusion , etc
Ø Thiamine
deficiency occurs in chronic alcoholism
Ø So
we are giving thiamine to supplement the deficiency
Question
– 5 :
What
is the probable reason for kidney injury in this patient?
Ø 2D
Echo shows left ventricular hypertrophy , which is one of the cause of pre
renal acute kidney injury
Ø Alchoholic
cirrhosis can also lead to acute kidney injury [since the patient is alchohol
addicted
Question
-6 :
What is the probable
cause for the normocytic anemia?
Ø Alchohol
decreases number of precursors of rbc s in bone marrow
Ø Further
alchohol induced malnutrition leads to iron and folic acid deficiency anemias
Question
-7 :
Could chronic
alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Ø Alcohol
leads to malnutrition which decreases the ability of wound healing and causes
neuropathy
Ø The
combined effect of diabetes and alchoholism has lead to foot ulcer in this
patient
B.Cerebellar ataxia :
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
Question
-1 :
What is the evolution
of the symptomatology in this patient in terms of an event timeline and where
is the anatomical localization for the problem and what is the primary etiology
of the patient's problem?
Evolution
of symptomatology :
Ø on
13 th May 2021 : Gidddiness
and vomiting
Ø on
16 th May 2021 : Giddiness – sudden onset, continuous ,
gradual progression
bilateral
hearing loss , aural fullness , tinnitus
vomitings
– 2 episodes / day , non projectile ,
non bilious
Ø on
18 th May 2021 :
slurring of speech
deviation
of mouth
Anatomical
localisatiion :
Ø Right
inferior cerebellar hemisphere
Primary
etiology :
Ø Increased serum
cholesterol leads to formation of embolus which causes infarct and stroke
Question
– 2 :
What are mechanism of action, indication and efficacy over
placebo of each of the pharmacological and non pharmacological interventions
used for this patient?
|
Treatment |
Mode of action |
Indication |
Efficacy |
|
Tab
. Vertin |
Histamine
analogue |
Dizziness
|
|
|
Inj
. Zofer |
Inhibits
serotonin by binding to 5HT3 receptor |
Nausea
, vomiting |
|
|
Tab . Ecosporin |
Antiplatelet
action by inhibiting formation of thromboxane A2 |
Infarct
in brain |
|
|
Tab
:. Atorvostatin |
HMG
CoA reductase inhibitor , decrease cholesterol |
High
serum cholesterol |
|
|
Tab
. Clopidogrel |
Inhibits
platelet aggregation |
Infarct
in brain |
|
|
Inj
. Thiamine |
Supplements
vitamin B1 |
Vitamin
B1 deficiency |
|
|
Tab
. MVT |
Supplements
vitamin B12 |
Vitamin
B 12 deficiency |
|
Question
– 3:
Did the patients
history of denovo HTN contribute to his current condition?
Ø Yes
, hypertension can cause stroke
Ø Hypertension
> damage to blood vessels >blood clot >infarct >stroke
Ø But
in this patient since the hypertension is recent , it might not be the cause of
stroke
Question
– 4 :
Does the patients history of alcoholism make
him more susceptible to ishcaemic or haemorrhagic type of stroke?
Ø Alcohol
> liver damage >decrease clotting factors > Hemorrhagic stroke
C. Recurrent hypokalemic paralysis :
C) Link to patient details:
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Question
-1:
What is the evolution
of the symptomatology in this patient in terms of an event timeline and where
is the anatomical localization for the problem and what is the primary etiology
of the patient's problem?
Evolution
of symptomatology :
Ø October
2020 : pedal edema
Ø April
2021 : neck pain
Ø 6
days back : pain radiating to left arm
Ø 5
days back : palpitations
Dyspnoea
Chest pain with
heaviness
Anatomical localization :
Ø Cervical
spondylosis : at the level of C 2,3,4
veretebrae
Ø Hypokalemic
paralysis : serum
Primary
etiology :
Ø Cervical
spondylosis : aging
Ø Recurrent
hypokalemic paralysis : genetic mutation
Question
– 2 :
What are the reasons
for recurrence of hypokalemia in her? Important risk factors for her
hypokalemia?
Ø Reason
for recurrent hypokalemia : genetic mutation in CACNA1S or SCN4A gene
Question- 3 :
What are the changes seen in ECG in case of
hypokalemia and associated symptom
Ø ECG changes in hypokalemia :
1) Increased
P wave amplitude
2) Prolonged PR interval
3) Widespread
ST segment depression and T wave flattening
4) Prominent
U waves [ most common seen in V2-V3 leads ]
D . Seizures :
Link to patient details:
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
Question
-1 :
Is there any
relationship between occurrence of seizure to brain stroke. If yes what is the
mechanism behind it?
Ø Yes
, there is association between seizure and brain stroke
Ø 
Injury to brain
Scar tissue
Disrupts electrical activity of brain
Seizures
Question
– 2:
In the previous episodes of seizures, patient
didn't loose his consciousness but in the recent episode he did . Is there any
relationship between occurrence of seizure to brain stroke. If yes what is the
mechanism behind it?
Ø The
1 st episode of seizure was 5 yrs back , immediately following head trauma
Ø Over
the time the infarct must have grown in size
Ø This
may be the reason for the unconsciousness in the latest episode
E. Ataxia :
Link to patient details:
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Question
-1 :
What could have been
the reason for this patient to develop ataxia in the past 1 year?
Ø The
multiple unattended head injuries are maybe the reason for ataxia in the past
year
Question
-2 :
What was the reason
for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Ø Yes
, alcohol contributed to bleeding diathesis
Ø 
Alcohol liver damage decreases clotting factors bleeding
Ø Since
the patient gave the H / O binge of alcohol 3 hrs prior to attack , it must
have triggered the sudden bleeding
F. CVA :
Link to patient details:
Question
– 1 :
Does the patient's
history of road traffic accident have any role in his present condition?
Ø Yes,
head trauma has lead to cerebrovascular accident in this case
Question
– 2 :
What are warning signs
of CVA?
Ø Warning signs of CVA :
1.
BALANCE : sudden dizziness , loss
of balance or coordination
2.
EYES : sudden trouble seeing in one
/ both eyes
3.
FACE : facial weakness
4.
ARM : weakness , unable to raise
both arms equally
5.
SPEECH : impaired , slurred
Question
– 3 :
What are warning signs
of CVA?
Ø Drug rationale in CVA :
1. MANNITOL
: lowers intracranial pressure
2. ECOSPORIN
: Antiplatelet action
3. ATORVASTATIN
: Decreases cholesterol levels
Question
– 4 :
Does alcohol has any
role in his attack?
Ø Yes
, alcohol damages liver function
Ø This
reduces production of clotting factors leading to bleeding
Ø This
can cause stroke
Question
– 5 :
Does his lipid profile
has any role for his attack??
Ø Yes
, lipid profile has a role in development of stroke
Ø This
patient shows decrease in HDL cholesterol levels
Ø An
increase LDL and decreased HDL can cause large artery atherosclerosis leading
to stroke
Ø However , small artery occlusion due to
dyslipidemia is rare
G . Cervical myelopathy :
Link to patient details:
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
sQuestion
– 1 :
What is myelopathy
hand ?
Ø MYELOPATHY HAND : Loss
of power of abduction and extension of the ulnar two to three fingers and
inability to grip and release rapidly with these fingers
Ø This
occus due to pyramidal tract involvement
Question
– 2 :
What is finger escape
?
Ø FINGER ESCAPE : also
known as Wartenberg sign
Ø This
is involuntary abduction of little finger caused by unopposed action of
extensor digiti minimi
Question
– 3:
What is Hoffman’s
reflex?
Ø HOFFMAN’S REFLEX :
also known as finger flexor reflex
Ø Verifies
presence / absence of issues arising from corticospinal tract
Ø Positive
reflex – flexion and abduction of thumb
Ø Positive
reflex suggests hypertonia , but also seen in healthy individuals
H . Seizures :
Link to patient details:
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Question – 1 :
What can be the
cause of her condition ?
Acute cotical venous sinus thrombosis [ CVST ] with
hemorrhagic venous infarction involving right posterior temporal lobe
Question
– 2 :
What are the risk
factors for cortical vein thrombosis?
Ø RISK FACTORS FOR CVST :
a) Hepatitis
C infection
b) Problem
with blood clotting eg . antiphospholipid syndrome , protein c or s deficiency
c) Sickle
cell anemia , chronic hemolytic anemia
d) Collagen vascular diseases
e) Cancer
, obesity
Question
– 3:
What drug was used in
suspicion of cortical venous sinus thrombosis?
Ø CLEXANE
: contains enoxaparin
Ø It
is anticoagulant which is used here to treat CVST
3
. CARDIOLOGY:
A. Pericardial Effusion :
Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
Question
– 1:
What is the difference
btw heart failure with preserved ejection fraction and with reduced ejection
fraction?
Ø Left
Heart failure :
|
With reduced ejection fraction |
With preserved ejection fraction |
|
Also
known as systolic heart failure |
Also
known as diastolic heart failure |
|
Inability
of heart to contract enough to provide blood flow forward |
Inability
of left ventricle to relax normally resulting in fluid backup in lungs |
|
Enlarged
left ventricle , cardiomegaly seen |
Normal
/ slightly enlarged ventricle , pulmonary congestion seen |
Question
-2 :
Why haven't we done
pericardiocenetis in this pateint?
Ø Patient
has pericardial effusion , which was mild at beginning and progressed to
moderate level later
Ø The
patient is responding well with conservative treatment [ effusion size
decreased from 2.07 cm to 1.4 mm ]
Ø Because
of the above reason and complications associated with pericardiocentesis , we
have not done pericardioccentesis in this patient
Question
– 3:
.What are the risk
factors for development of heart failure in the patient?
Ø Risk factors :
1. smoking
2. alcohol
3.diabetes mellitus
4. Hypertension
Question
-4 :
What could be the
cause for hypotension in this patient?
Ø Cause of hypotension :
Pericardial fluid
accumulation in pericardial sac
Decreases maximum size of
ventricles
Lowers end diastolic volume
Decrease stroke volume [
determinant of SBP ]
HYPOTENSION
B . Diastolic heart failure :
Link to patient details:
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html.
Question
-1 :
What are the possible
causes for heart failure in this patient?
Ø Cause of heart failure :
a) AGEING
: causes stiffening of heart muscle
b) CHRONIC
HYPERTENSION : leads to left
ventricular hypertrophy and increase connective tissue content
Question
-2 :
what is the reason for
anaemia in this case?
Ø Cause of anemia :
a) Elderly
patient
b) Chronic
Alcohol consumption leads to malnutrition and anemia
c) CHRONIC
KIDNEY DIEASE : leads to erythropoietin
deficiency and then anemia
d) Associated
comorbidities : diabetes
Question-
3 :
What is the reason for
blebs and non healing ulcer in the legs of this patient?
Ø
Ø The
reason for ulcers in this patient is poor wound healing due to diabetes
Question
-4:
. What sequence of
stages of diabetes has been noted in this patient?
Diabetes mellitus [ 30 yrs ago ]
Diabetic retinopathy [ 4 yrs ]
Diabetic nephropathy i. e . CKD [ at present ]
Diabetic neuropathy i. e reduced sensation leading to foot ulcer [ at
present ]
C. CCF with atrial fibrillation :
Link to patient details:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
Question
– 1 :
What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Evolution
of symptomatology :
Ø 10
yrs back : inguinal hernia surgery
Ø 3
yrs back : on and off pain at surgical site
On and off facial puffiness
Ø 1
yr back : SOB
Developed
hypertension
Ø 2
days ago : decreased urine output
SOB
Anatomical
localization :
Ø Atria
Primary
etiology :
Ø Hypertension
Question
– 2 :
What are mechanism of
action, indication and efficacy over placebo of each of the pharmacological and
non pharmacological interventions used for this patient?
|
Treatment |
Mode of action |
Indication |
Efficacy |
|
Inj
Dobutamine |
Ionotropic
action Weak
chronotropic action |
Atrial
fibrillation Congestive
cardiac failure |
|
|
Tab
Digoxin |
Ionotropic
action |
Atrial
fibrillation Congestive
cardiac failure |
|
|
Inj
unfractionated heparin |
Inactivates
thrombin and activated factor 10 A |
Atrial
thrombus |
|
|
Tab
Carvediol |
Beta
blocker |
Atrial
fibrillation |
|
|
Tab
Acetyl cysteine |
Mucolytic
|
|
|
|
Tab
Acitrom |
Anticoagulant
|
Atrial
thrombus |
|
|
|
|
|
|
|
Tab
Dytor |
Loop
diuretic |
Cardiorenal
syndrome |
|
|
Tab
pan D |
Proton
pump inhibitor |
Gastric
irritation |
|
|
Tab
Taxim |
Antibiotic
|
Infection
|
|
|
Inj
thiamine |
Vit
b1 supplement |
Vit
B 1 deficiency |
|
|
Inj
HAI |
Peripheral
utilization of glucose |
Increased
blood sugar |
|
Question
– 3 :
What is the
pathogenesis of renal involvement due to heart failure (cardio renal syndrome)?
Which type of cardio renal syndrome is this patient?
Ø Cardio renal syndrome :
Heart failure
Decreased cardiac output
Renal hypoperfusion
 |
Renal dysfunction
 |
Cardiorenal syndrome
Ø type
4 cardiorenal syndrome : chronic nephrocardiac
Question
– 4 :
What are the risk factors for atherosclerosis
in this patient?
Ø Risk factors for atherosclerosis :
1. Diabetes
mellitus
2. Hypertension
3. Age
; 52 yr
Question
– 5 :
Why
was the patient asked to get those APTT, INR tests for review?
Ø APTT
and INR were asked for review because – patient is prescribed anticoagulant
medicine whose most common side effect is BLEEDING
D. Acute coronary syndrome :
Link to patient
details:
Question
– 1:
What is the evolution
of the symptomatology in this patient in terms of an event timeline and where
is the anatomical localization for the problem and what is the primary etiology
of the patient's problem?
Evolution
of symptomatology :
Ø 12
yrs back : type 2 DM
Ø 1
yr back : heartburn
Ø 7
months back : diagnosed with TB
Ø 6
months back : hypertension
Ø Half
an hour ago : SOB
Anatomical
localization :
Ø Coronary
arteries
Primary
etiology :
Ø age
: 67 yrs
Ø H/O
DM 2 since 12 yrs
Ø H/O
hypertension
Question
– 2 :
What are mechanism of
action, indication and efficacy over placebo of each of the pharmacological and
non pharmacological interventions used for this patient?
|
Treatment |
Mode of action
|
Indications |
Efficacy |
|
Tab . Metaprolol |
Beta blocker |
NSTEMI |
|
|
PCI |
Surgery for coronary artery
blockage |
NSTEMI |
|
Question
– 3 :
What are the
indications and contraindications for PCI?
Ø Indications of PCI :
1. STEMI
2. NSTEMI
3. Unstable
angina
4. Stable
angina
5. Angina
equivalent [ dyspnoea , arrhythmia ]
Ø Contraindications of PCI :
1. Hypercoagulable
state
2. Intolerance
to oral antiplatelets
3. Abvsence
of cardiac surgery backup
4. High
grade CKD
Question
-4 :
What happens if a PCI
is performed in a patient who does not need it? What are the harms of
overtreatment and why is research on overtesting and overtreatment important to
current healthcare systems?
Ø If
unnecessary PCI is performed it leads to certain complications such as
1. Injury
to heart arteries
2. Infection
at the catheter site
3. Bleeding
4. Allergic
reactions and kidney damage due to dye used
5. Blood
clots leading to heart attack
E. Acute MI :
LINK TO PATIENT DETAILS :
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Question
– 1 :
What is the evolution of the symptomatology in
this patient in terms of an event timeline and where is the anatomical
localization for the problem and what is the primary etiology of the patient's
problem?
Evolution of symptomatology :
Ø On 12 may 2021 : chest pain
Ø On 14 may 2021 : giddiness and profuse sweating
Anatomical localization :
Ø Right coronary artery [ inferior
wall MI ]
Primary etiology :
Ø Atherosclerosis due to DM ,HTN
Question - 2 :
What are mechanism of
action, indication and efficacy over placebo of each of the
pharmacological and
non pharmacological interventions used for this patient
|
Treatment |
mode of action |
Indications |
Efficacy |
|
Tab
aspirin |
Antiplatelet
action by inhibiting PG synthesis |
Right
coronary artery blockage |
|
|
Tab
Atorvastatin |
Inhibits
HMG CoA reductase and decrease cholesterol production |
Coronary
blockage |
|
|
Tab
Clopidogrel |
Aqntiplatelet
action |
Coronary
blockage |
|
|
Inj
HAI |
Fast
acting insulin |
Increased
blood glucose |
|
Question
– 3 :
Did the secondary PTCA do any good to the
patient or was it unnecessary?
Ø The PTCA procedure was necessary here to restore blood flow
because patient was starting to develop symptoms of cardiogenic shock
F. Cardiogenic shock :
LINK TO PATIENT DETAILS :
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html
Question – 1 :
How did the patient get relieved from
his shortness of breath after i.v fluids administration by rural medical
practitioner?
Ø The patient has cardiogenic shock
Ø In this case fluid resuscitation corrected the hypovolemia
and thus provided temperory relief to patient
Question
– 2 :
What is the rationale of using torsemide in
this patient?
Ø
Patient has high serum urea and
creatinine levels and electrolyte imbalance due to cardiorenal syndrome
Ø
Torsemide is a loop diuretic
Ø
It help in clearance of accumulated
metabolites and restores electrolyte balance
Question
– 3 :
Was the rationale for administration of
ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ø
There is no evidence suggestive of
UTI
Ø
So it might be prophylactic for UTI
4. GIT :
A. Pancreatitis
Link to patient details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
Question
-1 :
What is the evolution of the symptomatology in
this patient in terms of an event timeline and where is the anatomical
localization for the problem and what is the primary etiology of the patient's
problem
Evolution
of symptomatology
Ø 5
yrs back : fever and vomiting
Ø 6
th May 2021 : pain abdomen and vomitings from this
day
Ø 9
th May 2021 : constipation
Burning
micturition
Fever
Anatomical
localization :
Ø Abdomen
Primary
etiology :
Ø Alcohol
consumption
Question
-2 :
What is the efficacy of drugs used along with
other non pharmacological treatment modalities and how would you
approach this patient as a treating physician?
|
Treatment
|
Mode
of action |
Indication
|
Efficacy
|
|
Inj meropenem |
Inhibits synthesis of bviral cell
wall components Broad spectrum antibiotic |
Prophylaxis [complications of acute pancreatitis ] |
|
|
Inj Metrogyl |
Inhibits protein synthesis antibiotic |
Prophylaxis |
|
|
Inj Amikacin |
Inhibits bacterial protein
synthesis Aminoglycoside antibiotic |
Prophylaxis |
|
|
IV NS/RL |
Fluid and electrolyte replacement |
Dehydration |
|
|
Inj Octreotide |
Somatostatin analogue |
Excess pancreatic secetion |
|
|
Inj Pantop |
Proton pump inhibitors |
Reduces pancreatic secretions |
|
|
Inj Thiamine |
Supplements vit B1 |
Vitamin B1 deficiency |
|
|
Inj Tramadol |
Opioid analgesic |
Pain |
|
B. epigastric pain
Link to patient details:
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
question
-1 :
What is causing the
patient's dyspnea? How is it related to pancreatitis?
Ø The dyspnoea is most probably due to pancreatitis
Ø Pancreatitis leads to multiorgan failure
Ø The most common organ involved is lung leading to pulmonary
complications
Ø These are divided into 3 stages
Ø STAGE 1 : no radiological changes , but pulmonary
complications seen
Ø STAGE 2 : Radiologial changes seen
Ø STAGE 3 : ARDS
Ø According to reports the patient is in stage 2 , xray
showing pleural effusion which is the cause of dyspnoea
Question
– 2 :
Name possible reasons
why the patient has developed a state of hyperglycemia.
Ø RISK FACTORS :
1.
Age
2.
Insulin resistence
3.
Chronic alcohol consumption
4.
Pancreas damaged : source of insulin
gone
Question
– 3 :
What is the reason for
his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver
disease?
Ø Inflammation of gall bladder due to gall stones ;lead to
increased LFT s
Ø Both AST and ALT are non specific indicators for liver disease
Ø But in case of alcoholic fatty liver AST > ALT
Question
-4 :
What is the line of
treatment in this patient?
Ø IVF : maintains fluid level
Ø Inj Pan D : reduces gastric irritation
Ø Inj Zofer : reduces nausea ,vomiting
Ø Inj tramadol : opioid analgesic
Ø GRBS : to monitor blood glucode
Ø Tab Dolo : analgesic and antipyretic
Ø Bp monitoring
C. Abdominal pain;
Link to patient
details:
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Question – 1 :
what is the most probable diagnosis in this patient?
Ø
The rise in AST and ALT suggests
liver abscess
Ø
It is the most possible diagnosis
Ø
Other differentials :
1. Organized hematoma : no trauma history
2. Subdiaphragmatic fluid collection : radiological evidence
absent
What was the cause of her death?
Does her NSAID abuse have something to
do with her condition? How?
Ø NSAIDS caused afferent arteriole constriction leading to
increased bp
5.Nephrology :
A.Post TURP
with ATN :
Link to patient
details:
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Question-1 :
.What
could be the reason for his SOB
Ø Acute tubular necrosis leads to retention of
fluid in lungs
Ø Edema in lungs lead to shortness of breath
Question-2:
Why does he have
intermittent episodes of drowsiness ?
Ø Patient shows elevated levels of urea and
creatinine in RFT due to kidney injury
Ø This increased creatinine is the cause of
drowsiness and altered mental state
Question-3 :
Why
did he complaint of fleshy mass like passage in his urine?
Ø During Transurethral resection of the
prostate ( TURP ) surgery ,we do electrocautery to minimise bleeding
Ø This blood may clot and form scab
Ø Clot retention is one of the common
complications of TURP
Ø This scab is passed from urethra following
surgery , which is perceived by patient as passage of mass
Question -4 :
What are the
complications of TURP that he may have had?
Complications
of TURP :
Ø Major:
1.
Clot
retention
2.
Failure
to void
3.
Uncontrolled
acute hematuria
4.
UTI
5.
Chronic
hematuria
Ø Minor:
1.
Bladder
perforation
2.
Sepsis
3.
DIC
B.Frequent
urination :
Link to patient details:
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
Question-1 :
Why is the child
excessively hyperactive without much of social etiquettes ?
Ø The patient is a child with hyperactive
nature, no social etiquettes, doesn’t pay attention at school
Ø The reason for his hyperactivity could be
ADHD (Attention deficit hyperactivity disorder)
Question-2 :
Why doesn't the
child have the excessive urge of urination at night time ?
Ø The child doesn’t show symptoms of nocturnal
enuresis
Ø This points towards psychosomatic origin of
disease i. e . anxiety ,stress etc.
Ø Since there is no probable organic cause ,
excessive urge of urination is absent at night
Question -3 :
How would you
want to manage the patient to relieve him of his symptoms?
1)
Further
investigations to rule out any organic cause . This includes :
Ø Proper USG
Ø Complete blood count
Ø Blood and urine sugars
2)
Diagnosis
of any anxiety disorder if present
3)
In the
absence of organic cause , treatment would be BEHAVIOURAL THERAPY
4)
Ditropan
– to decrease urgency and frequency of urination
5)
Assurance
to mother and child
6 .
Infectious disease
A. Dysphagia ,fever,cough :
Link to patient details:
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
Question -1 :
Which clinical history
and physical findings are characteristic of tracheo esophageal fistula?
v Positive findings of tracheoesophageal
fistula :
History:
1.
C/O
difficulty in swallowing i. e . Dysphagia
2.
C/O
cough on food intake
3.
H/O
retroviral disease
Physical findings:
1.
Laryngeal
crepitus
2.
Endoscopy
showing large opening with proliferative growth in mid esophagus
3.
CECT
: Fistulous communication between left
main bronchus and mid thoracic esophagus
4.
Barium
swallow showing abnormal contrast due to communication between esophagus and
bronchial tree
Question – 2 :
What are the chances
of this patient developing immune reconstitution inflammatory syndrome? Can we
prevent it ?
Ø The chances of development of immune
reconstitution inflammatory syndrome in this patient is high .
Ø The following are the risk factors present in
this patient :
1)
Fever
since 2 months
2)
Diagnosis
of TB after initiation of ART
3)
Lymph
node enlargement in mediastenum
4)
CRP +
ve
7. Infectious disease and hepatology
A.Liver
abscess:
Link to patient details:
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Question – 1 : .
Do
you think drinking locally made alcohol caused liver abscess in this patient
due to predisposing factors present in it ?
Ø Cause of liver abscess in this patient is
consumption of locally brewed toddy
Ø Yes
, locally made alchohol acted as factor for liver abscess in this patient
Question -2 :
What is the
etiopathogenesis of liver abscess in a chronic alcoholic patient ? (
since 30 years - 1 bottle per day)
Ø Liver abscess can be pyogenic ,amoebic or hydatid
Ø Infections are acquired from blood stream (
portal and systemic circulation)
Ø The most common pathophysiology is bowel content leakage and peritonitis . Bacteria travel via portal blood vessels
into liver .
Ø In
this case , Alcohol consumption specially locally prepared alchohol plays major
role in liver abscess ( pyogenic and amoebic )
Ø Alchohol
acts as predisposing factor
Ø Factors
responsible for association between alcohol and liver abcess are as follows:
a) Poor
nutritional status due to alchohol consumption
b) Presence
of infective organisms in the locally prepared alchohol
c) Immunity
of the patient
d) Damage
to liver done by alchohol
Question -3 :
Is liver abscess more common in right lobe
Ø Yes
,liver abscess is more common in right lobe compared to left lobe
Ø Single
lesions are more common in right lobe
Ø This
is attributed to comparatively more blood supply via superior mesenteric vein
on right side
Question -4 :
What are the
indications for ultrasound guided aspiration of liver abscess ?
Ø 1)
If the abcess is large ( 5cm or more) because it has more chances to rupture.
Ø 2)
If the abcess is present in left lobe as it may increase the chance of
peritoneal leak and pericardial leak.
Ø 3)
If the abcess is not responding to the drugs for 7 or more days
B.Liver
abscess
Link to patient
details:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
Question -1 :
Cause of liver abcess
in this patient ?
Etiology
of liver abscess :
Ø Pyogenic
liver abscess – polymicrobial
·
Staphylococcus
·
E .coli
·
Klebsiella
·
Streptococcus
Ø Amoebic liver abscess– most commonly caused
by Entamoebahisolytica
Ø In this patient, occasional toddy consumption
acted as source of pathogens
Question- 2 :
How do you approach
this patient ?
Treatment
of liver abscess :
Ø Empirical antibiotics : cover both bacterial
and amoebic causes
·
For
bacterial cause : penicillin +cephalosporin is given ( zostum1.5 gm i.v. BD
injection)
·
For
amoebic cause : metronidazole ( Metrogyl 500mg i.v. TID injection )
Ø Percutaneous drainage of abscess is not
done in this patient because of the response to antibiotic therapy and
associated complications of drainage
Ø Ultracet to relieve pain
Ø Dolo 650 mg for fever
Question-3 :
Why do we treat here ;
both amoebic and pyogenic liver abcess?
Ø Based on the following :
Ø Age of patient – 21 yr ( young age ) , male
gender
Ø Single abscess
Ø Right lobe involvement
Ø Chest x ray showing no involvement
The abscess is more likely to be amoebic liver abscess
Since we cannot
take risk we treated patient for both bacterial and amoebic cause
Question- 4 :
Is
there a way to confirmthe definitive diagnosis in this patient
Ø Yes we can confirm the diagnosis in this
patient by :
·
Detection
of serum antibodies against Entamoeba
·
Culture
and sensitivity report of the aspirate
8 . Infectious disease :
A.Mucormycosis:
Link to patient
details:
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Question -1 :
What is the evolution of the symptomatology in this patient in
terms of an event timeline and where is the anatomical localization for the
problem and what is the primary etiology of the patient's problem?
Evolution
of symptomatology :
a)
Fever
with chills and rigors : 18 -04-2021
b)
Facial
puffiness :28-04-2021
c)
Periorbital
oedema : 28-04-2021
d)
Generalised
weakness. : 28-04-2021
( Right upper & lower limb )
e)
Altered
sensorium : 4-05-2021
f)
Serous
discharge from left eye : 4-05-2021
g)
Oral
and nasal cavity involvement :
4-05-2021
Anatomical
localisation:
a)
Eye
b)
Nasal
& sinus mucosa
c)
Oral
cavity
d)
Brain
Primary
etiology :
Ø Rhizopus : fungus
Question – 2 :
What is the efficacy of
drugs used along with other non pharmacological treatment modalities and
how would you approach this patient as a treating physician?
Ø Drugs that can be used to treat mucormycosis
are :
1)
Amphotericin
– B
·
Liposomal
·
Deoxycholate
2)
Posaconazole
Ø Efficacy of drugs :
v Liposomal
AmpB>DeoxycholateAmpB>Posaconazole
Ø DeoxycholateAmpB is cheaper compared to
Liposomal AmpB
Ø Approach to patient :
1.
Stabilise
the patient
2.
Treat
the diabetic ketoacidosis
3.
Treatment
with antifungal preferably Liposomal AmpB
Question – 3 :
What are the
postulated reasons for a sudden apparent rise in the incidence of mucormycosis in
India at this point of time?
Ø The reason for recent increase in the cases
of mucormycosisis immunocompromised state following recovery from COVID -19
infection
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