Medicine Assignment - 2021
I/Sai Jignesh (roll no. 57) of 8th semester 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.
LINK TO QUESTIONS REGARDING CASES :
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Neurology:
CASE A:- Wernicke's Encephalopathy patient
Wernicke's-encephalopathy
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:- Timeline of Symptomatology for this Patient
1 year ago:- History of 2-3 episodes of seizures
4 months ago:- Recent episode of seizures occurred after cessation of alcohol
intake for 24 hours.
9 days ago:- Patient started to talk and laugh to himself and there is
decreased food intake and also he was unable to move himself off the bed and
move around. There was also short term memory loss.
2 years ago:- He was detected with type
2 diabetes mellitus and not taking regular medication.
Primary Etiology is related to alcohol withdrawal.
Anatomical Localization:- CNS (brain)
The symptomatology suggests that patient is
having withdrawal symptoms.
Q2)What
are mechanism of action, indication and efficacy over placebo of each of the
pharmacological and non-pharmacological interventions used for this patient?
Ans:- Pharmacological intervention:
1. 1)Thiamine:-
Mechanism of action: Thiamine prevents occurrence of Wernicke encephalopathy
which occurs due to deficiency of thiamine
Indications:
treatment of Beri Beri, Neuritis, Ulcerative colitis, to prevent Wernicke
encephalopathy
Efficacy: Background - Alcohol dependence is associated with severe
nutritional and vitamin deficiency. Vitamin B1 (thiamine) deficiency
erodes neurological pathways that may influence the ability to drink in
moderation. The present study examines tolerability of supplementation using
the high-potency thiamine analogue, benfotiamine (BF), and BF’s effects on
alcohol consumption in severely affected, self-identified, alcohol dependent
subjects.
Methods: 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). Conclusions BF 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.
Mechanism of action: 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.
BZDs have been found effective in: 1) preventing agitation and alcohol withdrawal seizures
2) preventing delirium tremens
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: https://pubmed.ncbi.nlm.nih.gov/18553183/
3) Why have
neurological symptoms appeared this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
Ans:- The reason can be thiamine, during previous withdrawal the
body might have enough thiamine which prevented the occurrence of neurological
symptoms. During this withdrawal due to thiamine deficiency the neurological
symptoms have occurred.
4) What is the reason
for giving thiamine in this patient?
Ans:- Thiamine is useful in preventing WERNICKE ENCEPHALOPATHY. It is an
acute disorder due to thiamine deficiency manifested by confusion, ataxia,
ophthalmoplegia, impaired memory and amnesia.
5) What is the
probable reason for kidney injury in this patient?
Ans:- Chronic alcoholism can cause acute kidney injury.
6)What is the probable
cause for the normocytic anemia?
Ans:- Anemia is common in alcoholics, the person who takes excess
alcohol won’t eat properly so they will be nutritionally deprived.
7) Could chronic
alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Ans:- As mentioned above excess alcohol intake can cause
nutritional deficiencies which results in poor wound healing but per se alcohol
does not cause foot ulcer alcohol is associated with duodenal and gastric
ulcers.
CASE B:- A 52 year old male with cerebellar
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:- COURSE OF SYMPTOMATOLOGY:
DAY 1:- The patient had an episode of giddiness at around 7 am while
doing his routine work which later on subsided upon taking rest. He also had an
episode of vomiting on the same day.
DAY 2:- Asymptomatic.
DAY 3:- Asymptomatic
DAY 4:- Asymptomatic.
DAY 5:- an episode of giddiness which is sudden onset after taking
alcohol. There is bilateral hearing loss, aural fullness and tinnitus. 2 to 3
episodes of vomiting and postural instability was also present.
DAY 6 - 7:- All the symptoms were aggravated with accompanying postural
instability.
ANATOMICAL LOCALISATION:- cerebellum.
MAJOR ETIOLOGY:- Long standing undiagnosed hypertension. Chronic alcoholism led to CVA as suggested in CT scan.
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:- Placebo has no physiological and pharmacological actions.
DRUG THERAPY:-
VERTIN:- Anti vertigo drug. Its composition is betahistine. Acts as
H1 receptor agonist and H3 receptor antagonist. It is indicated in
endolymphatic hydrops.
ZOFER:- An anti-emetic drug. Acts
as serotonin receptor antagonist
CLOPIDOGREL:- An antiplatelet drug used in impending stroke.
ATORVASTATIN:- It is a HMG - CoA inhibitor and is used to lower the blood
cholesterol levels.
ASPIRIN:- It is a NSAID which acts by inhibiting cyclooxygenase
enzyme. It is used in patients with heart diseases.
MULTI VITAMIN TABLETS:- These are used to prevent vitamin deficits
and also help to replenish the stores of fat soluble vitamins.
3) Did the patients history of denovo HTN contribute to his current condition?
Ans:- Based on the history and the fact that long standing hypertension might be the cause of CVA. Moreover alcoholism acts as an independent risk factor for CVA which supports the presumptions.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Ans:- Yes because even alcohol is also a risk factor for stroke.
CASE C:- A 45 years old female patient with pedal edema
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:-
8 Months ago:- Patient developed bilateral pedal edema which is
present in both sitting and standing position
6 Days ago:- Pain radiating to left
limb which was dragging in nature.
5 Days ago:- She had Palpitations, chest
pain and heaviness is also present.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Ans:- As the patient do not have diarrhea or vomiting may be inadequate dietary intake or excess loss through kidney can cause recurrent hypokalemia. the patient also has pedal edema which can be suggestive of kidney malfunctioning.
3)What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Ans:- ECG changes in hypokalemia include inversion of T wave, QT interval prolongation, visible U wave and mild ST depression .if there is severe hypokalemia arrhythmias like Torsade’s de points and ventricular tachycardia.
CASE D:- 55 yr old patient with seizures
A 55 years old patient with seizures
1) Is
there any relationship between occurrence of seizure to brain stroke. If yes
what is the mechanism behind it?
Ans:- Evidences suggest that increased attacks of brain stroke may
cause increase occurrence of seizures. It is believed that brain stroke causes
injury to the brain tissue. The damaged brain tissue heals by forming a scar.
The scar tissue cannot conduct the electrical activities. This disruption of
the electrical activity may cause the occurrence of 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?
Ans:- Abnormal increased activity in frontal -parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of conscious-ness in complex partial seizures. Thus, abnormally increased or decreased activity in the same networks can cause loss of consciousness. Information flow during normal conscious processing may require a dynamic balance between these two extremes of excitation and inhibition.
CASE E:- 48 yr male with seizures
A 48-year old male with seizures
1) What
could have been the reason for this patient to develop ataxia in the past 1
year?
Ans:- Cause could be ALCOHOLISM.
Alcohol induced cerebellar damage is the major
cause of cerebellar ataxia in alcoholics. In alcohol induced ataxia , the
patients have gait and lowerlimb abnormalities more than upper limb and speech
abnormalties.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Ans:- Liver damage due to too much alcohol can stop the liver from
synthesis of coagulants. Some of the epidemiological studies show that
there is increased risk for intracranial bleeding in alcoholics.
CASE F:- 30 yr male patient with weakness
A 30-yr old male patient with weakness
1)Does
the patient's history of road traffic accident have any role in his
present condition?
Ans:- NO.
2) What are warning signs of CVA?
Ans:-
- ·
Sudden headache with no
known cause.
- ·
Sudden onset of
confusion, trouble speaking and understanding the speech.
- ·
Sudden onset of
giddiness,
- · Sudden onset of weakness
or numbness in the arms and legs with difficulty in walking.
3) What is the drug rationale in CVA?
Ans:- Thrombolytic drugs along with neuroprotective agents are given.
4) Does alcohol has any role in his attack?
Ans:- Patient is a chronic alcoholic. Alcoholics generally have
increased risk for vascular pathologies like atherosclerosis. Alcoholism could
have been the underlying cause but the sudden attack might be precipitated by other
risk factor.
5) Does his lipid profile has any role for his attack?
Ans:- YES. Patient's lipid profile shows high triglyceride levels and high cholesterol levels. Long term abnormalities in lipid profile could have been the etiology of the attack.
CASE G:- A 50 YEAR OLD MALE WITH CERVICAL MYELOPATHY
A 50-year old patient with cervical myelopathy
1)What is
myelopathy hand?
Ans:- In many of the cervical spinal cord disorders, the ulnar 2-3
fingers lose their ability to grasp ,and rapidly release objects
and also there is an impairment of adduction and extension in these fingers. it
is called as myelopathy hand.
Ans:- It is also called
as WARTENBERG SIGN. It is an involuntary abduction of little finger due
to unopposed action of EXTENSOR DIGITI MINIMI.
Differential Diagnosis: Ulnar Nerve Palsy, Cervical
Myelopathy
3)What is
Hoffman’s reflex?
Ans:- Hoffmann’s reflex – When
the investigator flicks the fingernail of middle finger down, there is an
involuntary Flexion of thumb or index finger. This is called as positive
Hoffman's reflex. It is seen in UMN lesions and corticospinal tract
lesions.
CASE H:- A 17 year old female with seizures
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 proteinic
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 asparaginase.
Hematological: Myeloproliferative Malignancies, Primary and Secondary polycythemia.
Intracranial: Dural fistula
Vasculitis: Bechet’s disease, Wegener’s 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.
Cardiology:
Case A:- A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS.
1)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans:- Heart failure with preserved ejection fraction occurs in conditions where there is diastolic dysfunction of the ventricles like hypertrophic cardiomyopathy and restrictive cardiomyopathy. The ventricles are unable to relax completely , but they contract adequately , there by maintaining the ejection fraction.
Heart failure with reduced ejection fraction
occurs in intrinsic heart diseases like DILATED CARDIOMYOPATHY. The
ventricles are dilated and their wall is thinned out in this condition. There will
be systolic dysfunction of the ventricles leading to reduced ejection fraction.
2)Why haven't we done pericardiocentesis in this patient?
Ans:- Pericardiocentesis is indicated when there is
considerable pericardial effusion causing compression over the heart chambers.
In this condition, there is no need for pericardiocentesis as it is resolving.
3)What are the risk factors for development of heart failure in the patient?
Ans:- Hypertension, CAD, DM, MEDICATIONs.
4)What could be the cause for hypotension in this patient?
Ans:- Systemic venous return to the heart is reduced which in turn reduces the pulmonary venous return. This causes decrease in the end diastolic volume and finally reduced cardiac output.
Case B:- A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT.
1)What are the possible
causes for heart failure in this patient?
Ans:- Chronic hypertension can be the cause of heart failure in this
patient.
2)What is the reason for anemia in this case?
Ans:- Anemia is considered to be frequent comorbidity of heart failure.
3)What is the reason for blebs and non-healing ulcer in the legs of this patient?
Ans:- The cause for nonhealing ulcer is diabetes (hyperglycemia impairs the healing process)
4)What sequence of stages of diabetes has been noted in this patient?
Ans:- Diabetes leading to macrovascular complication in the form of foot
ulcer.
CASE C:- Biatrial Thrombus in 52 yr patient
Biatrial thrombus in 52yr old patient.
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:- The patient presented with short ness of breath which progressed from grade 2 to grade 4. Patient also complained of oliguria since two days and anuria since morning.
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:-
1.DOBUTAMINE
Mechanism of action: It is an inotropic drug.
Indications: cardiogenic shock, severe congestive cardiac failure,
hypoperfusion if associated with increased peripheral vascular resistance.
Efficacy: https://www.uptodate.com/contents/inotropic-agents-in-heart-failure-with-reduced-ejection-fraction
2.UNFRACTIONED HEPARIN
Mechanism of action: it inactivates thrombin and factor X through an
antithrombin dependent mechanism.
Indications: Atrial fibrillation with embolization, treatment of acute and
chronic consumptive coagulopathies like DIC, prophylaxis and treatment of venous
thromboembolism, prevention of clotting in arterial and cardiac surgery.
Efficacy: https://pubmed.ncbi.nlm.nih.gov/18425889/
3.CARVEDILOL
Mechanism of action: it is a non-selective adrenergic blocker.
Indication: heart failure with reduced ejection fraction, hypertension, left
ventricular dysfunction following MI.
Efficacy over placebo: https://pubmed.ncbi.nlm.nih.gov/7664433/
4.ACETYLE CYSTEIN
Mechanism of action: It increases the synthesis of glutathione in
liver, glutathione acts as an antioxidant.
Indication: It is used in paracetamol overdosing, to relive chest congestion
due to thickened mucous in cystic fibrosis, asthma, bronchitis.
Efficacy over placebo: http://scholar.google.co.in/scholar_url?url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5535813/&hl=en&sa=X&ei=TeizYNbVD8SLywTO356YCg&scisig=AAGBfm15eOtyydDL6iVQ5hRMLa8FCvXZQA&nossl=1&oi=scholarr
3)What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans:-
Ans:- Risk factors are Abnormal lipid profile, DM, Hypertension, High saturated fats in diet, Obesity.
5) Why was the patient asked to get those APTT, INR tests for review?
Ans:- APTT & INR is indicated in this patient to evaluate the coagulation profile and to assess the thrombotic activities.
CASE D:- Acute Coronary Syndrome Patient
67-year old patient with acute coronary syndrome
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
SYMTOMATOLOGY
Diabetes for 12 years
Heart burn like episodes for 1 year but it
relieved
Pulmonary TB 7 months back - treatment took now
she is sputum negative.
Hypertension for 6 months - on medications
Day of admission to hospital:- SOB since half an
hour
ANATOMICAL LOCATION OF PROBLEM: Cardiovascular system
PRIMARY ETIOLOGY:- 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?
Ans:-
TAB MET XL 25 MG/STAT-contains Metoprolol as
active ingredient.
Mechanism of action: METOPROLOL is a cardio selective 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 heart 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?
Ans:-
- Indications:
- Acute ST Elevation MI
- Acute non-ST elevation acute coronary syndrome
- Angina equivalent
- Stable and unstable angina
- Critical coronary artery stenosis
- Absolute contraindications:-
- Noncompliance with the procedure and inability to take the dual antiplatelet therapy.
- Multiple percutaneous interventions re stenosis
- High bleeding risk
- Relative contraindications:-
- Intolerance for long term antiplatelet therapy
- Short artery less than 1.5 mm
- Hypercoagulable state
- Absence of cardiac surgery backup
- High grade CKD
- Chronic total occlusion of SVG
- Critical left main artery occlusion with no graft or collateral
- Stenosis less than 50%
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 over testing and overtreatment important
to current healthcare systems?
Ans:- Although PCI is
generally a safe procedure, it might cause serious certain complications
like:
- Bleeding
- Blood vessel damage
- Allergic reaction to the contrast dye used
- Arrhythmias
- 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.
CASE E:- Myocardial Infarction Case
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 SYMTOMATOLOGY:
Diabetic since 8 years
Hypertension since 8 years
First dose of COVISHIELD vaccine 5 days back
before admission to hospital
Chest pain in right side of chest
Giddiness and profuse sweating on day of the admission
ANATOMICAL LOCATION: Cardiovascular system
PRIMARY ETIOLOGY: As she is diabetic for 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?
Ans:- Pharmacological interventions:
a) tab. ASPIRIN 325 mg
Mechanism of action: inhibits platelet aggregation by
interfering with thromboxane in platelets caused by COX 1 inhibition.
Indications: To reduce the cardiovascular deaths in suspected case of MI
Efficacy: Low dose aspirin each day for atleast10 years lower the risk
of cvd by 10% and odds ratio from 0.85 to 0.90
b) tab. ATORVASTATIN 80 mg
Mechanism of action: 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 decreases LDL cholesterol concentration
by61% and triglycerides by 46%
c) tab. Clopidogrel 300 mg
Mechanism of action: Inhibitor of platelet aggregation by binding
one of the ADP receptors on platelets
Indications: ACS recent MI, recent stroke, peripheral arterial disease.
Placebo has no pharmacological and physiological actions.
3)Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans:- Yes it is good to patient, stent was placed and the patient is doing good.
CASE F:- Cardiogenic Shock Case
1)How did
the patient get relieved from his shortness of breath after i.v. fluids
administration by rural medical practitioner?
Ans:- The patient experienced SOB because of fluid loss occurred to the patient there is decreased preload - hence SOB occurred due to decreased CO. When IV fluids were administered, there is increased preload - hence SOB decreased due to better of cardiac output.
2)What is the rationale of using torsemide in this patient?
Ans:- Torsemide used to
relieve abdominal distension.
3)Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Ans:- IT IS THE TREATMENT FOR
UTI
Rationale- Used for any bacterial infection.
Gastroenterology:
CASE A:- Patient with Pancreatitis, Pseudocyst and Broncho-Pleural Fistula
pancreatitis with pseudocyst and broncho-pleural fistula
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:- COURSE OF THE SYMPTOMS-
Pain abdomen and vomiting was treated
conservatively 5yrs ago.
Pain abdomen and vomiting for 1 week.
Constipation, burning micturition, fever for 4
days.
After admission:-
CT scan - showed Pseudocyst.
Chest X ray - showed left pneumothorax and left
pleural.
ANATOMICAL LOCATION: Pancreas
Primary etiology: Chronic alcohol intake
2) What is the efficacy of drugs used along with other non-pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans:- Placebo has no physiological and pharmacological actions.
DRUG THERAPY:-
Amikacin, Metronidazole and Meropenem are all given to control
infection.
TPN (Total Parenteral Nutrition) - It is given to bed ridden patients.it contains
carbohydrates, proteins, fats vitamins and minerals.
NS/RL - It is given as fluid replacement in order to combat dehydration.
Tab. Pantop - It is a proton pump inhibitor. It is used in this case for its anti-pancreatic
secretory.
Inj. Octreotide –
It is a somatostatin analogue.
It decreases the secretions of pancreas.
It also has anti-inflammatory and cytoprotective
effects.
Inj. Thiamine -
It is B1 supplement.
It is given here because; due to long fasting
& TPN usage, body may develop B1 deficiency.
Wernicke encephalopathy secondary to B1
deficiency may be caused... so a prophylactic B1 supplementation is necessary.
Inj. TRAMADOL -
It is an opioid analgesic which is given to relieve pain.
CASE B:- Male patient with Epigastric Pain
1) What
is causing the patient's dyspnea? How is it related to pancreatitis?
Ans:- Dyspnea in the patient could be due to pleural
effusion. The causes for the development of pleural effusion could be secondary
to pancreaticopleural fistula secondary to the rupture of pseudocyst in
pancreas due to pancreatitis. It could also be due to transdiaphragmatic
lymphatic obstruction.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans:- The causes for the development of hyperglycemia
could be due to damage of pancreatic beta cells secondary to pancreatitis. This
causes low levels of insulin release and could be the reason for hyperglycemia.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans:- History of the patient suggest that he is a
chronic alcoholic. Alcohol induced hepatocyte damage could be the reason for
elevated LFT. Specific markers for alcoholic fatty liver disease are
elevated levels of AST twice more than ALT and also elevated GAMMA GLUTAMYL TRANSFERASE.
4) What is the line of treatment in this patient?
Ans:-
- IVF: 125 mL/hr.
- Inj. PAN 40mg i.v OD.
- Inj. ZOFER 4mg i.v sos.
- Inj. Tramadol 1 amp in 100 mL NS, i.v sos.
- Tab. Dolo 650mg sos.
- GRBS charting 6th hourly.
- BP charting 8th hourly
CASE C:- Patient with Abdominal distension
1) what
is the most probable diagnosis in this patient?
Ans:- The patient is suffering from ruptured liver abscess which led to
intraperitoneal hematoma. Patient also has intraparenchymal renal disease.
2) What was the cause of her death?
Ans:- Cause of her death can be as a complication of
surgery in the form of pneumonia(As symptom just before the death are cough and
sob) as many people who undergo surgery already have weakened immune system and
they are prone to get infections.
3) Does her NSAID abuse have something to do with her condition? How?
Ans:- Long term use of NSAID could be the reason for renal damage.
NSAID use could have lowered the levels of cytoprotective prostaglandins.
Nephrology:
CASE A:- Post TURP with non oliguric ATN
1. What could be the reason for his SOB?
Ans:- Reason for his sob can be POST TURP SYNDROME: it occurs because of irrigation of absorption of
large volumes of irrigation fluid during TURP which can cause HYPONATREMIA, CARDIORESPIRATORY
depression.
2. Why does he have intermittent episodes of drowsiness?
Ans:- Drowsiness indicates that the brain tissue is not getting enough
oxygen supply. This could be due to anemia. Another possibility is due to
electrolyte imbalance in the patient.
3. Why did he complaint of fleshy mass like passage in his urine?
Ans:- Patient has UTI (pyuria). This was felt like a fleshy white mass by the
patient.
4. What are the complications of TURP that he may have had?
Ans:- COMPLICATIONS OF TURP:
- Bladder perforation
- Coagulopathies
- Bleeding
- Transient bacteremia and septicemia.
- Toxicity due to irrigating fluids.
- Hypothermia.
CASE B:- Attention Deficit Hyperactivity Disorder
1)Why is
the child excessively hyperactive without much of social etiquettes?
Ans:- The symptoms of the child point the diagnosis towards ADHD
(attention deficit hyperactivity disorder).
2)Why
doesn't the child have the excessive urge of urination at nighttime?
Ans:- As the child do not have bedwetting nor waking up at night to
pass urine it can be a case of receptor over activity effected by
gravity(neurogenic overactivity bladder) or pollakiuria(idiopathic frequent
urination)it can also be psychosomatic as his mother completely restricted him
from using smartphone since 4 months before which he is addicted to ,so the
child sleeps normally at night.
3)How would you want to manage the patient to relieve him of his symptoms?
Ans:- First look if any pathology is present in the genitourinary system, then try with the help of psychiatrist find whether it is ADHD or not, if yes do cognitive behaviour therapy.
CASE :- Patient with Dysphagia, Fever and Cough
1)Which
clinical history and physical findings are characteristic of tracheo esophageal
fistula?
Ans:- Clinical history and physical findings:
- 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
- Oro pharyngeal regurgitation
2)What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Ans:-
A retrospective analysis examining all forms of IRIS, 33/132 (25%) of patients exhibited one or more disease episodes after initiation of ART. Other cohort analyses examining all manifestations of IRIS estimate that 17–23% of patients initiating ART will develop the syndrome.
INTERVENTION: The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon inLiver Cases:
CASE A:- Liver Abscess
1)Do you
think drinking locally made alcohol caused liver abscess in this patient due to
predisposing factors present in it? What could be the cause in this patient?
Ans:- yes, it could be due to intake of contaminated toddy.
2)What is the etiopathogenesis of liver abscess in a chronic alcoholic patient? (since 30 years - 1 bottle per day)
Ans:- According to some studies, alcoholism mainly consuming locally
prepared alcohol plays a major role as a predisposing factor for the formation
of liver abscesses that is both amoebic as well as pyogenic liver abscess
because of the adverse effects of alcohol over the Liver.
3)Is liver abscess more common in right lobe?
Ans:- Yes right lobe is involved due to its more blood supply
4)What are the indications for ultrasound guided aspiration of liver abscess?
Ans:- Indications for USG guided aspiration of liver abscess:
- Amoebic liver abscess
- Large abscess more than 6 cms.
- Left lobe abscess
- Caudate lobe abscess
- Abscess which is not responding to drugs
- seronegative abscess
1)Cause
of liver abscess in this patient?
Ans:- Cause may be due to Entamoeba histolytica. the pyogenic abscesses
are usually polymicrobial, most seen organisms are E. coli, Klebsiella,
streptococcus, staphylococcus, anaerobes.
2)How do you approach this patient?
Ans:- I will approach in the same as given in blog but if abscess
rupture emergency laparotomy is to be done.
3)Why do we treat here: both amoebic and pyogenic liver abscess?
Ans:- Though the probable diagnosis is amoebic liver abscess it’s
better to give antibiotics to be safe side.
Ans:- USG can be done to see the site of the abscess. USG guided aspiration can be done to confirm diagnosis, but there is risk of perforation.
CASE :- Patient with Altered Sensorium
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:- COURSE OF THE SYMPTOMS:
18 April: post vaccination fever with chills and rigor.
28 April: facial puffiness, generalized weakness and periorbital edema.
04 May: presented to the OPD with
altered mental state.
ANATOMICAL LOCATION: Rhino-orbito-cerebral disease.
PRIMARY ETOLOGY: Fungal infection with mucor.
2) What is the efficacy of drugs used along with other non-pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans:- Placebo
has no physiological and pharmacological actions.
- LIPOSOMAL AMPHOTERICIN B- potent anti-fungal agent active against mucormycosis.
- ITRACONAZOLE- Azole group of antifungal drugs. Used instead of amphotericin B.
3) What are the postulated reasons for a sudden apparent rise in the incidence of Mucormycosis in India at this point of time?
Ans:-
- Steroid overuse in the covid patients. This led to further immunosuppressive state. COVID causes systemic illness leading to immunosuppression.
- Mucormycosis is more common among diabetics as thought diabetes is an immunocompromised state. Poor patient hygiene also is a risk factor.
PULMONOLOGY:
Case :- A 50 year old female with shortness of breath, pedal edema and facial puffiness.
A 55-year old female with shortness of breath
1)what is the evolution of 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 patient's problem?
Ans:- Timeline of Symptomatology for this Patient
20 years ago :- She had shortness of breath which lasted for 1 week during which she worked in a paddy field. It was relieved upon taking medication.
For the next 8 years :- She had suffered from similar episodes of SOB every year which lasted for 1 week and happened in January i.e. when she worked at paddy fields. All these episodes were also relieved upon taking medication.
12 years Ago :- She had another episode of SOB which lasted for 20 days and had to be Hospitalized.
From the past 12 years :- She has been having an yearly episodes which have lasted for month in the usual time of January, which are of Grade 2.
8 years Ago :- She was diagnosed with Diabetes when she had seeked help for her Polyuria and is being treated for it ever since.
5 years Ago :- She was treated for Anaemia with Iron injections.
1 month Ago :- She had Generalized Weakness for which she was administered IV fluids (3 pints in 2 days) by a local RMP.
30 days Ago :- She had latest episode of SOB.
20 days Ago :- Due to the ongoing COVID 19 pandemic, she had an HRCT done outside which showed the signs of Bronchiectasis.
20 days Ago :- She was diagnosed with Hypertension and is being treated for the same.
Since 15 days :- She has pedal edema upto the level of ankle which is of Pitting type.
Since 15 days :- She developed Facial puffiness.
Since 2 days :- She started having SOB even at rest ( Grade 4) which not relieved with nebulizers. She also has Drowsiness and Decreased Urine output.
Anatomical Localization :- At the level of bronchial tubes as evidence of bronchiectasis is present.
Primary Etiology :- Exposure to paddy.
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:- Pharmacological and Non Pharmacological interventions used for this Patient are as following:
1 . Head End Elevation :-
Mechanism of Action :- The Head of the Mechanically Ventilated patients should be maintained between 30° and 45° to reduce the risk of Aspiration and Mechanical Ventilation associated Pneumonia by improving the End expiratory Lung volume.
• In addition to promoting a reduction in the risk of developing pneumonia, some postural positions can increase the possibility of more Homogeneous Alveolar Ventilation and possibly reduce the risk of Lung injury caused by mechanical ventilation.
2. O2 Inhalation to maintain SPO2 above 92% :
Mechanism of Action :-
3. Intermittent BiPAP for 2 hours :
Mechanism of action :- Bilevel positive airway pressure involves both IPAP and EPAP.
• IPAP (Higher Pressure) gives inspiratory support to augment the tidal volume which assists CO2 clearance.
• EPAP ( Lower Pressure) prevents alveoli closure at expiratory phase which increases the Lung volume and Functional Residual Capacity, Improves alveolar exchange and Oxygenation.
• EPAP = CPAP = PEEP.
Indications :-
• Chronic obstructive pulmonary disorder (COPD)
• Obstructive sleep apnea
• Obesity hypoventilation syndrome
• Pneumonia
• Asthma flare-up
• Poor breathing after an operation
• Neurological disease that disturbs breathing
4. Injection. AUGMENTIN 1.2 gm IV BD (Amoxicillin and Potassium clavulanate):
Mechanism of Action :- Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis.
• Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.
Indications :-
• Middle ear (Acute Otitis Media) nad and Sinus infections.
• Respiratory tract Infections (Bronchitis).
• Urinary tract Infections.
• Skin and Soft tissue Infections.
• Bone and joint Infections
5. TAB. AZITHROMYCIN 500mg OD :
Mechanism of Action :- Azithromycin is a Macrolide Antibacterial Drug. It works by decreasing the production of protein, thereby stopping bacterial growth.
Indications :-
• Prevention and treatment of acute bacterial exacerbations of chronic obstructive pulmonary disease due to H. influenzae, M. catarrhalis, or S. pneumoniae.
• Community-acquired pneumonia due to C. pneumoniae, H. influenzae, M. pneumoniae, or S. pneumoniae.
• Uncomplicated skin infections due to S. aureus, S. pyogenes, or S. agalactiae.
• Urethritis and cervicitis due to C. trachomatis or N. gonorrhoeae.
• Trachoma due to C. trachomatis.
• Genital ulcer disease (chancroid) in men due to H. ducrey.
• Acute bacterial sinusitis due to H. influenzae, M. catarrhalis, or S. pneumoniae.
• Acute otitis media caused by H. influenzae, M. catarrhalis or S. pneumoniae.
• Pharyngitis or tonsillitis caused by S. pyogenes as an alternative to first-line therapy in individuals who cannot use first-line therapy.
6. Injection. LASIX IV BD if SBP greater than 110 mmHg :
Mechanism of Action :-Furosemide, like other loop diuretics, acts by inhibiting the luminal Na - K - Cl co-transporter in the thick ascending limb of Loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride and Potassium loss in urine .
• It also abolishes the cortico-medullary osmotic gradient and blocks negative as well as positive free water clearance. Because of the large NaCl absorptive capacity of the loop of Henle, diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase inhibitors.
• Additionally, Furosemide is a noncompetitive subtype-specific blocker of GABA-A receptors.
•Furosemide has been reported to reversibly antagonize GABA-evoked currents of α6β2γ2 receptors at μM concentrations, but not α1β2γ2 receptors. During development, the α6β2γ2 receptor increases in expression in cerebellar granule neurons, corresponding to increased sensitivity to furosemide.
Indications :-
• Treatment of Hypertensive emergency
• Treatment of Edema
7. TAB. PANTOP 40 mg PO OD :
Mechanism of Action :- It inhibits the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.
Indications :-
• For heartburn and chest pain due to stomach acid reflux disease in which acidic content from stomach comes up to food pipe and mouth.
• For the treatment of ulcers of stomach and intestine and inflammation and erosion of food pipe due to stomach acid.
• Gastro- esophageal reflux disease.
8. Injection. HYDROCORTISONE 100 mg IV :
Mechanism of Action :- Hydrocortisone injection belongs to class of drugs called glucocorticoids, or steroid hormones. Hydrocortisone injection works by reducing inflammation in the body.
Indications :-
• Arthritis
• Severe Allergies
• Blood diseases
• Breathing Problems
• Certain Cancers
• Eye diseases
• Intestinal disorders
• Skin diseases
9. Nebulizer with IPRAVENT, BUDECORT 6 Hourly :
Mechanism of Action :- BUDECORT is a potent topical anti-inflammatory agent. It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT).
• This budesonide-CBP (HAT) receptor complex prevents the production of inflammatory genes (inhibition of gene transcription) that might cause bronchoconstriction.
IPRAVENT is an acetylcholine antagonist via blockade of muscarinic cholinergic receptors.
• Blocking cholinergic receptors decreases the production of cyclic guanosine monophosphate (cGMP).
• This decrease in the lung airways will lead to decreased contraction of the smooth muscles.
• The actions of intranasal ipratropium mimic the action of atropine by inhibiting salivary and mucous glands secretions as well as dilating bronchial smooth muscle.
Indications :- Chronic Obstructive pulmonary disease (COPD) & Asthma.
Mechanism of Action :- Acebrophylline works by relaxing the smooth muscles of airways and induces the release of pulmonary surfactants which helps in the clearance of congestion & Acetylcysteine breaks down and loosens thick phlegm, making it runny and easy to cough up and clears the airway.
Indications :- COPD
3) What could be the causes for her current acute exacerbation?
Ans:- Current exacerbation can be due the comorbidities like Diabetes, Hypertension, Old age and persistence of an excitable foci.
4) Could the ATT have affected her symptoms? If so how?
Ans:- ATT drugs are known nephrotoxic agents but considering the duration of usage it can be presumed that ATT has no effect on her symptoms.
5) What could be the causes for her electrolyte imbalance?
Ans:- Electrolyte imbalance can be due to kidney dysfunction which is caused by right heart failure.
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