Online blended bimonthly assignment for the month of May 2021
I have been given the following cases to solve
in an attempt to understand the topic of 'Patient clinical data analysis'
to develop my competency in reading and comprehending clinical data including
history, clinical findings, investigations and diagnosis and come up with a
treatment plan.
This is the link of the questions asked
regarding the cases:
Below are my answers to the Medicine
Assignment based on my comprehension of the cases.
1) Pulmonology
(10 Marks)
A)
" A
55 Year Old Female with Shortness of Breath, pedal Edema and Facial
Puffiness."
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
Questions:
1) What is the
evolution of the symptomatology in this patient in terms of an event timeline
and where is the anatomical localization for the problem and what is the
primary etiology of the patient's problem?
Ans: EVOLUTION
OF SYMPTOMATOLOGY
1st episode of SOB --20 years back
2nd episode of SOB --12 years back
From then she has been having yearly episodes for past 12 years
Then she diagnosed with diabetes 8 years back
she is anemic and took IM injections 5 years back
generalized weakness since 1 month
diagnosed with hypertension 20 days back
pedal edema 15 days back
facial puffiness 15 days back
ANATOMICAL LOCATION OF PROBLEM
Lungs
PRIMARY ETIOLOGY OF PATIENT PROBLEM
Usage of chulha since 20 years
Might be due to chronic dosage
2) What are mechanism
of action, indication and efficacy over placebo of each of the pharmacological
and non pharmacological interventions used for this patient?
Ans: Head end
elevation:
MOA-improves oxygenation
decreases incidence of VAP
increases hemodynamic
performance
increases end expiratory
lung volume
decreases incidence of
aspiration
INDICATIONS-head injury
meningitis
pneumonia
O2 inhalation to maintain spo2
Bipap : non invasive method
MOA- Assist ventilation by delivering positive expiratory and
inspiratory pressure with out need of ET
intubation
3) What could be the
causes for her current acute exacerbation?
Ans: may be due to any
infection
4. Could the ATT have
affected her symptoms? If so how?
Ans :YES,
ATT affected her symptoms .Isoniazid and Rifampcin which are
nephrotoxic which causes raised RFT
5.What could be the
causes for her electrolyte imbalance?
Ans: ATT could have
caused renal damage which lead to her electrolyte imbalance
2) Neurology (10
Marks)
A)
" A
40 Year Old Male with Complaints of Irrelevant Talking"
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.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?
Ans
: EVOLUTION OF SYMPTOMATOLOGY
2009 (12 years ago):
Started drinking alcohol
2019 (2 years ago):
Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemics
2020 (1 year ago): Has
an episode of seizures (most likely GTCS)
January 2021 (4months
ago): Has another seizure episode (most likely GTCS)- following cessation of
alcohol for 24 hours. Starts drinking again after seizure subsides
Monday, May 10, 2021:
Last alcohol intake, around 1 bottle. Starts having general body pains at
night.
Tuesday, May 11, 2021:
Decreased food intake. Starts talking and laughing to himself. Unable to lift
himself off the bed, help required.
Conscious, but
non coherent. Disoriented to time, person, place.
Goes to an RMP
the same day- is prescribed IV fluids and asked to visit a hospital
Saturday, May 15,
2021: Is admitted to a tertiary care hospital for alcohol withdrawal symptoms,
and is treated for the same.
ANATOMICAL LOCATION OF
PROBLEM: The most
probable location in the brain is the hippocampus and frontal lobe.
PRIMARY ETIOLOGY OF
PATIENT 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?
A randomized, double-blind, placebo-controlled trial was conducted on 120 non-treatment seeking, actively drinking, alcohol dependent men and women volunteers (mean age=47 years) from the Kansas City area who met DSM-IV-TR criteria current alcohol dependence. Subjects were randomized to receive 600 mg benfotiamine or placebo (PL) once daily by mouth for 24 weeks with 6 follow-up assessments scheduled at 4 week intervals. Side effects and daily alcohol consumption were recorded. Results Seventy (58%) subjects completed 24 weeks of study (N=21 women; N=49 men) with overall completion rates of 55% (N=33) for PL and 63% (N=37) for BF groups. No significant adverse events were noted and alcohol consumption decreased significantly for both treatment groups. Alcohol consumption decreased from baseline levels for 9 of 10 BF treated women after 1 month of treatment compared with 2 of 11 on PL. Reductions in total alcohol consumption over 6 months were significantly greater for BF treated women (BF: N=10, −611±380 Std. Dev; PL: N=11, −159±562 Std. Dev, p-value=0.02). ConclusionsBF supplementation of actively drinking alcohol dependent men and women was well-tolerated and may discourage alcohol consumption among women. The results do support expanded studies of BF treatment in alcoholism.
2.lorazepam and pregabalin are given for the neurological symptoms. Benzodiazepines
Benzodiazepines (BZD) are the mainstay of treatment in alcohol withdrawal. Benzodiazepines are safe, effective and the preferred treatment for AWS. Benzodiazepines are cross-tolerant with alcohol and modulate anxiolysis by stimulating GABA-A receptors During withdrawal from one agent, the other may serve as a substitute. They are proven to reduce withdrawal severity and incidence of both seizures and delirium tremens (DT)
The ideal drug for alcohol withdrawal should have a rapid onset and a long duration of action, a wide margin of safety, a metabolism not dependent on liver function, and absence of abuse potential Various BZDs offer many of these advantages. BZDs have been found effective in: 1) preventing agitation and alcohol withdrawal seizures; 2) preventing delirium tremens; and 3) as cross-tolerant agents with ethanol. BZDs, owing to their wide margin of safety and low potential to produce physical dependence and tolerance in short-course therapy, are therefore very, effective in the treatment of alcohol-withdrawal syndrome. They are the drugs of choice for alcohol withdrawal
3.PREGABALIN
Mechanism of action:it is analog of neurotransmitter GABA
Indications:-peripheral neuropathic paint like diabetic neuropathy and post hermetic neuropathy
- adjuvant treatment of partial seizures
- management of fibromyalgia
Efficacy of pregabalin
3) Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
Ans:
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.
eg, in this
patient
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?
Ans:
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?
Ans:
As the urea levels are
very high, it denotes an acute onset- Acute Renal Failure.
As high serum
creatinine, and urea levels are present, denotes that reabsorption from tubules
is taking place- therefore the primary cause is prerenal, most probably due to
generalised dehydration.
A slightly high FENa
level also denotes that tubular necrosis is occurring to some degree, hence the
Prerenal AKI (mostly due to dehydration) is in turn leading to Acute Tubular
Necrosis (ATN)
6). What is the
probable cause for the normocytic anemia?
Ans :
Possible causes:
a. Increased oxidative
stress and inflammation, leading to hemolysis of the RBCs
b. Decreased bone
marrow production of RBCs, due to EPO deficiency owing to kidney failure
c. Loss of blood
through chronic foot ulcer
7) Could chronic
alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Ans :
Yes, as alcoholism
itself can cause peripheral neuropathy (alcoholic neuropathy), which along with
Diabetic neuropathy, can lead to a non-healing foot ulcer.
B)
A 52 year old male with Cerebellar Ataxia
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
Questions-
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?
2) What are mechanism of action,
indication and efficacy over placebo of each of the pharmacological and non
pharmacological interventions used for this patient?
3) Did the patients history of
denovo HTN contribute to his current condition?
4) Does the patients history of
alcoholism make him more susceptible to ischaemic or haemorrhagic type of
stroke?
C)
A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB
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?
2) What are the reasons for
recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
3) What are the changes seen in ECG
in case of hypokalemia and associated symptoms?
D
55years old patient with seizures
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
QUESTIONS:
1. Is there any relationship between
occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
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?
E)
A 48 year old male with seizures and altered sensorium
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Questions: 1) What could have been
the reason for this patient to develop ataxia in the past 1 year?
Damage from alcohol is a common cause of cerebellar ataxia. In patients with alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech.So alcohol may be reason for his ataxia
.https://publicdocuments.sth.nhs.uk/pil3307.pdf
2) What was the reason for his IC
bleed? Does Alcoholism contribute to bleeding diatheses ?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1341444/#:~:text=The%20impaired%20platelet%20function%2C%20together,associated%20with%20excessive%20alcohol%20intake.
F)
" A
30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND
LOWERLIMB"
Questions
1.Does the patient's history
of road traffic accident have any role in his present condition?
Ans: yes
after trauma
there may be tear in the head or neck blood vessels that leads to brain which
can be source of bloodclots that
may cause stroke
2.What are warning signs of CVA?
Ans ;
Sudden numbness
or weakness in the face, arm, or leg, especially on one side of the body.
Sudden
confusion, trouble speaking, or difficulty understanding speech.
Sudden trouble
seeing in one or both eyes.
Sudden trouble
walking, dizziness, loss of balance, or lack of coordination.
3.What is the drug rationale in CVA?
Ans:
Aspirin
-antiplatlet drug prevents stroke
Atorvostatin -
decreases LDL cholesterol to prevent recurrent attacks of stroke
4. Does alcohol has any role in his
attack?
Ans:
Excessive alcohol consumption has
been associated with a wide range of medical conditions. Moderate alcohol
consumption is linked to a lower risk of stroke than abstinence, whereas heavy
alcohol consumption has been associated with an increased risk of stroke and
stroke mortality. In addition to alcohol consumption, the most important risk
factors for stroke are hypertension, coronary artery disease, cardiac
insufficiency, atrial fibrillation, type 2 diabetes, smoking, overweight,
asymptomatic carotid artery stenosis and elevated levels of cholesterol.
5.Does his lipid profile has any
role for his attack??
Ans:
Yes increased LDL causes
atherosclerosis -Blood vessels - ischemia leads to - stroke
G)
"A
50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY"
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
__*Questions*_
1)What is myelopathy hand ?
Ans :
There is loss of power
of adduction and extension of ulnar 2/3 fingers and inability to grip
and release rapidity
with these fingers is called myelopathy hand
right hand -
myelopathy hand
2)What is finger escape ?
Ans :
Wartenberg's sign is a
neurological sign consisting of involuntary abduction of the fifth (little)
finger, caused by unopposed action of the extensor digiti minimi. ... This
finding of weak finger adduction in cervical myelopathy is also called the
"finger escape sign".
3)What is Hoffman’s reflex?
Ans ;
Hoffman's sign or
reflex is a test that doctors use to examine the reflexes of the upper
extremities. This test is a quick, equipment-free way to test for the possible
existence of spinal cord compression from a lesion on the spinal cord or
another underlying nerve condition
A positive Hoffman sign
indicates an upper motor neuron lesion and corticospinal pathway dysfunction
likely due to cervical cord compression. However, up to 3% of the population
has been found to have a positive Hoffman without cord compression or upper
motor neuron disease
H)
"A 17 year old female with seizures "
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
questions:
1) What can be the cause of
her condition ?
Ans :
According to MRI
,
cortical vein thrombosis might be the cause of her seizures
2) What are the risk factors for
cortical vein thrombosis?
Ans :
Infections:
Meningitis, otitis,mastoiditis
Prothrombotic states:
Pregnancy, puerperium,antithrombin
deficiency proteinc and protein s deficiency,Hormone replacement therapy.
Mechanical:
Head trauma,lumbar puncture
Inflammatory:
SLE,sarcoidosis,Inflammatory bowel
disease.
Malignancy.
Dehydration
Nephrotic syndrome
Drugs:
Oral
contraceptives,steroids,Inhibitors of angiogenesis
Chemotherapy:Cyclosporine and l
asparginase
Hematological:
Myeloproliferative Malignancies
Primary and secondary polycythemia
Intracranial :
Dural fistula,
Vasculitis:
Behcets disease wegeners
granulomatosis
3)There was seizure free period in
between but again sudden episode of GTCS why?resolved spontaneously why?
Ans :
Seizures are resolved and
seizure free period got achieved after medical intervention but sudden episode
of seizure was may be due to any persistence of excitable foci by abnormal
firing of neurons.
4) What drug was used in suspicion
of cortical venous sinus thrombosis?
Ans :
Anticoagulants are used
for the prevention of harmful blood clots.
Clexane ( enoxaparin)
low molecular weight heparin binds and potentiates antithrombin three a serine
protease Inhibitor to form complex and irreversibly inactivates factor
xa.
3) Cardiology (10
Marks)
A) Link to patient
details:
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?
3.What are the risk
factors for development of heart failure in the patient?
4.What could be the
cause for hypotension in this patient?
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?
2.what is the reason
for anaemia in this case?
3.What is the reason
for blebs and non healing ulcer in the legs of this patient?
4. What sequence of
stages of diabetes has been noted in this patient?
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?
2) What are mechanism
of action, indication and efficacy over placebo of each of the pharmacological
and non pharmacological interventions used for this patient?
3) What is the
pathogenesis of renal involvement due to heart failure (cardio renal syndrome)?
Which type of cardio renal syndrome is this patient?
- TYPE 4 CRS is seen in this patient.
4) What are the risk
factors for atherosclerosis in this patient?
5) Why was the patient
asked to get those APTT, INR tests for review?
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?
Diabetes since 12 years
heart burn like episodes since 1 year but it relieved
pulmonary TB 7 months back --treatment took now she is sputum negative
hypertension since 6 months --on medications
SOB since half an hour on day of admission to hospital
ANATOMICAL LOCATION OF PROBLEM: Cardio vascular system
PRIMARY ETIOLOGY OF PATIENT PROBLEM: atherosclerosis --plague formation [hypertension+ diabetes]
2) What are mechanism
of action, indication and efficacy over placebo of each of the pharmacological
and non pharmacological interventions used for this patient?
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA:
METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.
Indications:
it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
EFFICACY STUDIES:
Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.
Outcome :
mean baseline BP was 132/78 +/- 9/9 mmHg. Following 4 weeks of treatment, mean changes in sitting BP were: placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9 mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg. Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.
Non pharmacological intervention :
PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
3) What are the
indications and contraindications for PCI?
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
4) What happens if a
PCI is performed in a patient who does not need it? What are the harms of
overtreatment and why is research on overtesting and overtreatment important to
current healthcare systems?
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it.
OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
Following are harms to patients:
. Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations.
Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant -
OVERDIAGNOSIS.
Also the adverse effects due to this are more when compared to the benefits.
.Overdiagnosis through overtesting can psychologically harm the patient.
Hospitalizations for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.
Harms to health care systems:
The use of expensive technologies and machineries are causing burden on health care systems.
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?
diabetic since 8 years
hypertension since 8 years
took first dose of COVISHIELD vaccine 5 days back before admn to hospital
chest pain in right side of chest
giddiness and profuse sweating on day of the admission
ANATOMICAL LOCATION OF PROBLEM: cardio vascular system
PRIMARY ETIOLOGY OF PATIENT PROBLEM: as she is diabetic since 8 years that might cause atherosclerosis due to accumulation of fatty and fibrinous material in the walls
2) What are mechanism
of action, indication and efficacy over placebo of each of the pharmacological
and non pharmacological interventions used for this patient?
tab ASPIRIN 325 mg
MOA: inhibits platelet aggregation by interfering with thromboxane in platelets caused by COX 1 inhibition
indications :
to reduce the cardio vascular deaths in suspected case of MI
efficacy:
low dose aspirin each day for atlaest 10 years lower the risk of cvd by 10% and odds ratio from 0.85 to 0.90
tab ATORVASTATIN 80 mg
MOA :competitive inhibitor of enzyme HMG CO A reductase
indication:
to prevent CV events in patients who are at risk used as preventive agent
efficacy:
studies shown that it decrease LDL cholestrol concentration by61% and triglycerides by 46%
tab clopidegrel 300 mg
MOA : Inhibitor of platelet aggregation by binding one of the ADP receptors on platelets
indications:
ACS
recent MI ,recent stroke ,peripheral arterial disease
3) Did the secondary
PTCA do any good to the patient or was it unnecessary?
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?
2. What is the
rationale of using torsemide in this patient?
3. Was the rationale
for administration of ceftriaxone? Was it prophylactic or for the treatment of
UTI?
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 symptomatology
H5 years back-1st episode of pain abdomen and vomitings
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung
Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
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?
Mechanism of action:antibacterial
Indications: used to treat severe and serious bacterial infections such as respiratory tract infection, urinary tract infection, skin and soft tissue infection, joint and bone infection
2.inj METROGYL
Mechanism of action:anti bacterial and anti parasitic
Indications used to treat diarrhoea or dysentery due to parasitic infections such as amoebiasis. It is used to prevent sexually transmitted infections such as urogenital trichomoniasis or giardiasis. It is also used to treat infections of the gums, teeth and skin due to various infective microorganisms
3.ULTRACET
Mechanism of action: centrally acting analgesic
Indications moderate to severe pain
Approach to treat the patient
Antibiotics given to combact infection
TNP preferred because of the gastrointestinal symptoms of the patient.
Pleural effusion should be drained
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?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4087768/
2) Name possible
reasons why the patient has developed a state of hyperglycemia.
3) What is the reason
for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver
disease?
An ALT to AST ratio over 2 is highly suggestive of alcohol liver disease.
4) What is the line of
treatment in this patient?
Line of treatment;
i)manage hyperglycemia and monitor GRBS
ii)ask the patient to stop alcohol consumption.
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?
2) What was the cause
of her death?
3) Does her NSAID
abuse have something to do with her condition? How?
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 ?
2. Why does he have
intermittent episodes of drowsiness ?
3. Why did he
complaint of fleshy mass like passage in his urine?
fleshy mass like passage to him
4. What are the
complications of TURP that he may have had?
Electrolyte imbalances
Infection
B) Link to patient
details:
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
Questions
1.Why is the child
excessively hyperactive without much of social etiquettes ?
2. Why doesn't the
child have the excessive urge of urination at night time ?
3. How would you want
to manage the patient to relieve him of his symptoms?
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?
Cough since 2 months on taking food and liquids
difficulty in swallowing since 2 month
H/O weight loss of 10 Kgs since 2 months, hoarseness of voice
Incapable of food intake
Oropharygeal regurgitation
2) What are the
chances of this patient developing immune reconstitution inflammatory syndrome?
Can we prevent it?
: REVENTION :
The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
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
?
2. What is the
etiopathogenesis of liver abscess in a chronic alcoholic patient ? (
since 30 years - 1 bottle per day)
3. Is liver abscess
more common in right lobe ?
4.What are the
indications for ultrasound guided aspiration of liver abscess ?
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs
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 ?
* Amoebic liver abcess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
## Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
2) How do you approach
this patient ?
3) Why do we treat
here ; both amoebic and pyogenic liver abcess?
1) Age and gender of patient: 21 years ( young ) and male.
2) Single abcess.
3) Right lobe involvement.
## The abcess is most likely AMOEBIC LIVER ABSCESS …
** But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.
# And considering the risk factors associated with aspiration for pus culture:
1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.
2) Sometimes ; it has thin thinwall which may rupture if u aspirate.
3) Sometimes ; it is unliquefied.
## There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.
4) Is there a way to confirmthe
definitive diagnosis in this patient?
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?
3 years ago- diagnosed with hypertension
2.
21
days ago- received vaccination at local PHC which was followed by fever
associated with chills and rigors, high grade fever, no diurnal variation which
was relieved on medication
3.
18
days ago- complained of similar events and went to the the local hospital, it
was not subsided upon taking medication(antipyretics)
4.
11
days ago - c/o Generalized weakness
and facial puffiness and periorbital oedema. Patient was in a drowsy state
5.
4
days ago-
a.
patient
presented to casualty in altered state with facial puffiness and periorbital oedema
and weakness of right upper limb and lower limb
b.
towards
the evening patient periorbital oedema progressed
c.
serous
discharge from the left eye that was blood tinged
d.
was
diagnosed with diabetes mellitus
6.
patient
was referred to a government general hospital
7.
patient
died 2 days ago
patient was diagnosed with
diabetic ketoacidosis and was unaware that he was diabetic until then. This
resulted in poorly controlled blood sugar levels. The patient was diagnosed
with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the
most common form of this fungus that occurs in people with uncontrolled
diabetes ( https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html ) the fungus enters the
sinuses from the environment and then the brain.
The patient was also
diagnosed with acute infarct in the left frontal and temporal lobe.
Mucormycosis is associated with the occurrence of CVA ( https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes. )
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 proposed management of the patient was –
1.
inj.
Liposomal amphotericin B according to creatinine clearance
2.
200mg
Iitraconazole was given as it was the only available drug which was adjusted to
his creatinine clearance
3.
Deoxycholate
was the required drug which was unavailable
https://pubmed.ncbi.nlm.nih.gov/23729001/ this article talks about
the efficacy and toxicity of different formulations of amphotericin B
along with the above mentioned
treatment for the patient managing others symptoms is also done by-
I.
Management
of diabetic ketoacidosis –
(a)
Fluid
replacement- The fluids will replace those lost
through excessive urination, as well as help dilute the excess sugar in blood.
(b)
Electrolyte
replacement-The absence of insulin can lower the level of
several electrolytes in blood. Patient will receive electrolytes through a vein
to help keep the heart, muscles and nerve cells functioning normally.
(c) Insulin
therapy- Insulin reverses the processes that cause
diabetic ketoacidosis. In addition to fluids and electrolytes, patient will
receive insulin therapy
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 may be being triggered by the use of
steroids, a life-saving treatment for severe and critically ill Covid-19
patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to
help stop some of the damage that can happen when the body's immune system goes
into overdrive to fight off coronavirus. But they also reduce immunity and push
up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of
occurrence of mucormycosis in these patients is increasing
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