BIMONTHLY INTERNAL ASSESSMENT FOR THE MONTH OF MAY 2021
"This is my submission for the Bimonthly internal assessment for the month of May."
Most of the information here have been collected from different reference sites, the links to which have been mentioned. The points copy pasted have been put in quotes.
The questions to the cases being discussed can be viewed from the link below 👇
'http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1'
1) Pulmonology (10 Marks)
A) Link to patient details:
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?
A 55 year old woman, farmer by occupation with a history of on and off episodes of Shortness of breath since the past 20 years, a known diabetic since the past 8 years and a known hypertensive since the past 20 days presented with the complaints of Shortness of breath since 15 days
Bilateral pedal edema since 15 days
Facial puffiness since 15 says
Problem List:
COPD
Right heart failure
A known diabetic since 8 years
A known hypertensive since 20 days
Anatomical localization for her problem:
The localization of her problem is in the heart and the Lungs. She has right heart failure which has exacerbated her COPD. Her HRCT chest reveals brochiectatic changes.
Primary Etiology to the patients problem:
Primary Etiology of the recent exacerbation is because of right heart failure on the pre existing COPD.
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 comparing Azithromycin or placebo in patients with COPD (AECOPD)
P - 301 patients with COPD, had a smoking history of ≥10 pack-years and one or more exacerbations in the previous year were randomized (1:1) within 48 hours of hospital admission
I - Azithromycin (n = 147). The drug (500 mg/d for 3 d) was administered on top of a standardized acute treatment of systemic corticosteroids and antibiotics, and subsequently continued for 3 months (250 mg/2 d).
C - Placebo (n = 154)
O - The TF rate within 3 months was 49% in the azithromycin group and 60% in the placebo group ( P = 0.0526). Treatment intensification, step-up in hospital care, and mortality rates within 3 months were 47% versus 60% (P = 0.0272), 13% versus 28% (P = 0.0024), and 2% versus 4% (P = 0.5075) in the azithromycin and placebo groups, respectively.
Three months of azithromycin for an infectious AECOPD requiring hospitalization may significantly reduce TF during the highest-risk period. Prolonged treatment seems to be necessary to maintain clinical benefits.
A multicenter, double-blind, randomized, placebo-controlled trial, the efficacy of nebulized budesonide, oral prednisolone, and placebo
P - 199 patients with acute exacerbations of COPD requiring hospitalization.
I - 2 mg of budesonide every 6 h (n = 71)
I- 30 mg of oral prednisolone every 12 h (n = 62), C - Placebo (n = 66)
O - The mean change (95% confidence interval) in postbronchodilator FEV(1) from H(0) to H(72) was greater with active treatments than with placebo: budesonide versus placebo, 0.10 L (0.02 to 0.18 L); prednisolone versus placebo, 0.16 L (0.08 to 0.24 L). The difference in FEV(1) between budesonide and prednisolone was not significant, -0.06 L (-0.14 to 0.02 L). The occurrence of serious adverse events was similar for all groups. Budesonide had less systemic activity than prednisolone as indicated by a higher incidence of hyperglycemia observed with prednisolone. Both budesonide and prednisolone improved airflow in COPD patients with acute exacerbations when compared with placebo.
3. What was the cause for the exacerbation?
COPD has been exacerbated secondary to right heart failure
4. Could the ATT have affected her symptoms? If so how?
Yes
Facial puffiness and pedal edema could be due to the renal or hepatic dysfunction caused secondary to the use of ATT medications.
Rifampicin among the ATT drugs is most commonly associated to cause AKI followed by isonizid and ethambutol
Hepatic dysfunction is most common with Pyrazinamide followed by Isonizide, Rifampicin, Rthambutol.
5.What could be the causes for her electrolyte imbalance?
Hyponatremia in patients with right heart failure is primarily caused by increased activity of arginine vasopressin (AVP). AVP increases free-water reabsorption in the renal collecting ducts, increasing blood volume and diluting plasma sodium concentrations.
2) Neurology (10 Marks)
A) Link to patient details:
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?
40 year old man, diabetic since 2 years on irregular medications and regular alcoholic and smoker since 12 years with the history of 2-3 episodes of seizures 1 year back, presented with
Irrelevant talking , forgetfulness and reduced appetite since 9 days.
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, multidose study of thiamin treatment
107 subjects who were detoxifying from alcohol. Five groups of subjects were assessed with the Mini-Mental State Examination and were examined for the presence of neurological signs. Subjects were given different doses of intramuscular thiamin for two consecutive days. The posttreatment performance of these groups then was examined on a test of working memory derived from comparative neuropsychology, namely, the delayed alternation task.
On the posttreatment measure, a superior performance was found in the group that received the highest dose of thiamin, compared with the other four treatment groups.
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
The neurological symptoms are because the patient is in Wernicke's encephalopathy
And the probable other differentials are
Uremic encephalopathy
Alcohol withdrawal
4) What is the reason for giving thiamine in this patient?
Thiamine is present in the body as free thiamine, as well as in several phosphorylated forms: thiamine mono-phosphate (TMP), thiamine diphosphate (TDP), and thiamine triphosphate (TTP). TDP also called thiamine pyrophosphate, is the metabolically active and the most abundant form of thiamine in the body (>80%). Thiamine plays essential coenzyme and non-coenzyme roles in energy transformation, synthesis of pentoses and nicotinamide adenine dinucleotide phosphate(NADPH), and membrane and nerve conduction. In energy transformation, thiamine is a cofactor in multiple enzyme complexes involved in the metabolism of carbohydrates and amino acids, particularly pyruvate dehydrogenase complex (PDH), and a-ketoglutarate dehydrogenase complex (a–KGDH).
Thiamine is an important nutrient required to metabolize glucose used by the brain for energy. The lack of thiamine affects brain functions in the most metabolically active brain regions, including the activity of the hypothalamus which regulates temperature, appetite, emotions and growth. Thiamine deficiency affects the cells of the nervous and cardiovascular systems to a greater degree than the cells of other organ systems.
Alcohol reduces the absorption of thiamine by the body, diminishes stores of thiamine in the liver and hampers the activity of the enzyme that converts thiamine into an active state.
Thiamine is given intravenously because abdominal absorption can be hampered in affected individuals. Mental status changes, vision abnormalities and ataxia all usually improve upon administration of thiamine. Thiamine administration may continue daily for
5) What is the probable reason for kidney injury in this patient?
The probable cause for her kidney injury could be due to alcoholism leading to dehydration, Pre renal AKI
And the long standing history of uncontrolled diabetes makes this patient more prone to kidney diseases
In order to develop a diagnostic approach to the common problem of anemia associated with alcoholism, 121 chronic alcoholics admitted to a general medical service with a low hematocrit were evaluated.
Multiple contributing causes of anemia were present in most patients. Megaloblastic marrow change was found in 33.9% of patients, sideroblastic change in 23.1%, absent iron stores in 13.2%, aggregated macrophage iron in 81.0%, and acute blood loss in 24.8%.
Apart from reduced red blood cell production in the bone marrow there could be loss of blood from ulcer and artificial prosthesis
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
The patient is already a known diabetic and has been on a poor diabetic control.
Diabetes is known to cause peripheral neuropathy, more likelihood of developing wounds and ulcers with a slow healing process.
Alcohol on top of that also is known to cause thiamine deficiency which eventually leads leads peripheral neuropathy
Pathophysiology of alcoholic neuropathy. Alcohol can exert direct and indirect effects on nerve cell function. The direct effects of alcohol result from its metabolism to its toxic byproduct acetaldehyde. Acetaldehyde produced in the liver is transported to the periphery where it can form protein adducts and cause nerve damage. The conversion of alcohol to acetaldehyde also results in the formation of reactive oxygen species, which can exert deleterious effects on peripheral nerve physiology and function. Alcohol enhances protein kinase C e (PKCe) levels and activity in dorsal root ganglia. Administration of PKCe inhibitors reduces ethanol-induced mechanical hyperalgesia. Chronic ethanol exposure can impair both anterograde and retrograde axonal transport. PKCe could also regulate alcohols effects on axonal transport through its interactions with the cytoskeleton. Ethanol impairs Schwann cell proliferation and myelin sheath formation. Alcohol can also mediate indirect effects on nerve cell function by reducing absorption, hepatic storage, and phosphorylation of thiamine. ROS, reactive oxygen species
B) 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?
52 year old man, denovo hypertensive and a known alcoholic & smoker since 30 yrs
Giddiness & vomiting 7 days back
Giddinesss , vomiting , bilateral hearing loss , aural fullness , tinnitus , ataxia since 4 days
Deviation of mouth & slurring of speech since 1 day
Anatomical localization:
Brain - Cerebrovascular Accident (CVA) with infarct in the right inferior cerebellar hemisphere
Primary etiology:
Acute infarct in right inferior cerebellar hemisphere with the risk factors being Age, Alcoholism, Smoker, Denovo HTN
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
RCT on aspirin and Clopidogrel in the management of ischaemic stroke
SPARCL - STROKE PREVENTION BY AGGRESSIVE REDUCTION IN CHOLESTEROL LEVELS
* This study was conducted among 4731 patients who had a stroke or TIA within one to six months before study entry, had low-density lipoprotein (LDL) cholesterol levels (100 to 190 mg/dl) , and had no known coronary heart disease
*This was a double-blind prospective study
P- 4731 patients were included
I - 2365 patients received 80 mg of atorvastatin per day
C- 2366 received placebo.
O - During a median follow-up of 4.9 yrs, 265 patients receiving atorvastatin and 311 patients receiving placebo had a fatal or nonfatal stroke. The atorvastatin group had 218 ischemic strokes and 55 hemorrhagic strokes, whereas the placebo group had 274 ischemic strokes and 33 hemorrhagic strokes.
In patients with recent stroke or TIA and without known coronary heart disease, 80 mg of atorvastatin per day reduced the overall incidence of strokes and of cardiovascular events, despite a small increase in the incidence of hemorrhagic stroke.
https://www.ebmconsult.com/articles/sparcl-trial-stroke-prevention-aggressive-reduction-cholesterol-levels
MATCH Trail on Aspirin + Clopidogrel vs Clopidogrel alone in Ischaemic Stroke
7599 high-risk patients with recent ischaemic stroke or transient ischaemic attack and at least one additional vascular risk factor who were already receiving clopidogrel 75 mg/day.
A randomised, double-blind, placebo-controlled trial to compare aspirin (75 mg/day) with placebo.
Duration of treatment and follow-up was 18 months. The primary endpoint was a composite of ischaemic stroke, myocardial infarction, vascular death, or rehospitalisation for acute ischaemia
596 (15.7%) patients reached the primary endpoint in the group receiving aspirin and clopidogrel compared with 636 (16·7%) in the clopidogrel alone group. Life-threatening bleedings were higher in the group receiving aspirin and clopidogrel versus clopidogrel alone.Major bleedings were also increased in the group receiving aspirin and clopidogrel but no difference was recorded in mortality.
Adding aspirin to clopidogrel in high-risk patients with recent ischaemic stroke or transient ischaemic attack is associated with a non-significant difference in reducing major vascular events. However, the risk of life-threatening or major bleeding is increased by the addition of aspirin
TRIAL ON ASPIRIN VS PLACEBO
Patients with ischaemic stroke but not complete paresis were included. Totally, 441 patients (220 aspirin, 221 placebo) completed the trial.
The trial was randomized, double-blind and placebo-controlled.
Tablets Aspirin 325 mg or placebo, water solvable, were administered orally once a day for five consecutive days.
Neurological assessments were carried out three times daily during the treatment period to detect progression of at least two points in the Scandinavian Stroke Supervision Scale.
Patient outcome was followed up at discharge and at 3 months.Aspirin treatment did not significantly reduce the frequency of stroke progression. Amongst aspirin‐treated patients, stroke progression occurred in 15.9% as compared with 16.7% in the placebo group, which is less frequent than expected. The relative risk was 0.95 (95% CI 0.62–1.45) in the treatment group. As regards patient outcome at discharge and after 3 months, aspirin treatment did not show any difference.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Moderate and high intakes of alcohol have been documented to have acute potentially deleterious physiologic effects within hours after consumption, including impaired fibrinolysis and increased platelet activation, blood pressure and heart rate.
The Stroke Onset Study was conducted in three medical centers. This study utilized a case-crossover study design to assess the change in risk of acute ischemic stroke onset during a brief “hazard period” following consumption of alcohol.
390 patients were interviewed between January 2001 and November 2006
The alcohol consumption was associated with a transient increased risk of ischemic stroke in the subsequent hour that was 2.3 times higher than the risk during periods with no alcohol consumption. The risk returned to baseline by three hours and there was a modestly lower risk by 24 hours.
Ethanol intoxication as a risk factor for ischaemic stroke was studied
100 patients (67 men, 33 women) aged from 15-55 with acute ischemic brain infarction were studied.
In 40 cases the onset of symptoms was preceded within 24 hours by ethanol intoxication.
Ethanol intoxication preceding brain infarction was 4-7 times as common in men and 6-15 times as common in women as ethanol intoxication. Nineteen of the patients were heavy drinkers. Heavy drinking was twice as common in men and 5 times as common in women as heavy drinking.
C) 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?
A 45 year old woman, known case of cervical spondylitis with a history of hypokalemia 1 year back presented to us with the complaints of
Bilateral pedal edema since 8 months
Dragging type of pain in left upper limb associated with tingling & numbness
Chest pain , palpitations and Dyspnea grade-III since 5 days
Anatomical localization:
Based on the description of pain which is radiating to her left upper limb, looks like a case with MI
Heart - Coronary Artery Disease
Primary etiology:
Coronary Artery disease
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
From Harrison's principles of Internal Medicine
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
- Increased P wave amplitude
- Prolongation of PR interval
- Widespread ST depression and T wave flattening/inversion
- Prominent U waves (best seen in the precordial leads V2-V3)
- Apparent long QT interval due to fusion of T and U waves
- Frequent supraventricular and ventricular ectopics
- Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
- Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes
D) Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
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?
The patient had a GTCS this time unlike the last time when he had a partial seizure without loss of consciousness.
E) Link to patient details:
Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?
His ataxic gait maybe due to his chronic alcoholism.
Other differentials for an ataxia gait are
Cerebellar stroke, patients with cerebellar stroke are said to walk like a Drunken sailor.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Yes, alcohol are noted to cause strokes especially hemorrhagic infarcts.
Moderate and high intakes of alcohol have been documented to have acute potentially deleterious physiologic effects within hours after consumption, including impaired fibrinolysis and increased platelet activation, blood pressure and heart rate.
The Stroke Onset Study was conducted in three medical centers. This study utilized a case-crossover study design to assess the change in risk of acute ischemic stroke onset during a brief “hazard period” following consumption of alcohol.
390 patients were interviewed between January 2001 and November 2006
The alcohol consumption was associated with a transient increased risk of ischemic stroke in the subsequent hour that was 2.3 times higher than the risk during periods with no alcohol consumption. The risk returned to baseline by three hours and there was a modestly lower risk by 24 hours.
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
No
2.What are warning signs of CVA?
4. Does alcohol has any role in his attack?
Yes, as already discussed earlier, alcohol is known to be associated with increased incidences of CVA. Alcohol causes impaired fibrinolysis and increased platelet activation, blood pressure and heart rate.
5.Does his lipid profile has any role for his attack??
His lipid profile is with in normal limits - no role in his current problem
G) Link to patient details:
*Questions*
1)What is myelopathy hand ?
Loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers.
These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement in various cervical spinal disorders when there is involvement of the spinal cord.
2)What is finger escape ?
Wartenberg's Sign refers to the slightly greater abduction of the fifth digit, due to paralysis of the abducting palmar interosseous muscle and unopposed action of the radial innervated extensor muscles (digiti minimi, digitorum communis )
3)What is Hoffman’s reflex?
H) Link to patient details:
1) What can be the cause of her condition ?
Acute cortical vein thrombosis with hemorrhagic venous infarction involving right posterior temporal lobe.
2) What are the risk factors for cortical vein thrombosis?
3) What drug was used in suspicion of cortical venous sinus thrombosis?
Anticoagulants- Unfractionated heparin
3) Cardiology (10 Marks)
A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
2.Why haven't we done pericardiocentesis in this patient?
The patient doesn't have cardiac tamponade, there was no need for an invasive pericardiocentesis for this patient
3.What are the risk factors for development of heart failure in the patient?
His Age, Diabetes Mellitus, Hypertension and him being an alcoholic and smoker and a known case of CAD and CKD.
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
His Age, Diabetes Mellitus, Hypertension and him being an alcoholic and smoker and a known case of CAD and CKD
2.what is the reason for anaemia in this case?
Chronic Kidney disease and Heart Failure
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?
Patient has diabetic triopathy - he developed neuropathy first then, diabetic retinitis, and, finally, the nephropathy of diabetes.
Both macro and micrvascular diabetes mellitus complications - Stage 1V
C) Link to patient details:
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?
52 year old man, alcoholic and on regular NSAIDs since 3 yrs, a known hypertensive and Denovo DM presented with the complaints of
Facial Puffiness on & off since 2-3 yrs
SOB grade : II - IV & decreased urine output since 2 days
Anuria since 1 day
Anatomical localization:
Chronic Kidney Disease secondary to Diabetes , Hypertension and NSAID abuse
Heart - DCMP with EF 28%
Bi atrial thrombi with ASD
AF
Metabolic Syndrome
Primary etiology:
Metabolic Syndrome
With type 2 DM and HTN
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Efficacy of Beta blockers in heart failure with Atrial Fibrillation - A meta analysis
18 254 patients were assessed, and of these 13 946 (76%) had sinus rhythm and 3066 (17%) had atrial fibrillation at baseline. Crude death rates over a mean follow-up of 1·5 years were 16% (2237 of 13 945) in patients with sinus rhythm and 21% (633 of 3064) in patients with atrial fibrillation.
β-blocker therapy led to a significant reduction in all-cause mortality in patients with sinus rhythm (p<0·001), but not in patients with atrial fibrillation (p=0·73), with a significant p value for interaction of baseline rhythm (p=0·002).
β blockers didn't improve prognosis in patients with concomitant heart failure and atrial fibrillation.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Our patient is of Type 4 Cardiorenal syndrome
4) What are the risk factors for atherosclerosis in this patient?
Metabolic Syndrome
With type 2 DM and HTN
CKD
Age
5) Why was the patient asked to get those APTT, INR tests for review?
The patient was put on Infusion heparin and Acitrom during his hospital stay and was discharged on Tab Acitrom. It's mandatory to keep reviewing the Aptt, PT, INR levels to adjust the dose and to look for any bleeding manifestations.
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?
Known case of HTN and type 2 DM since 8 yrs
Chest pain since 3 days
Giddiness & profuse sweating since 1 day
Anatomical localization -
Heart : Inferior wall MI
Primary Etiology -
Acute inferior wall MI
Known case of Type 2 DM, HTN
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
A double-blinded RCT comparing clopidogrel to placebo in addition to aspirin in acute ST elevations MI
P - 12,562 patients who had presented within 24 hours after the onset of symptoms
I - clopidogrel (300 mg immediately, followed by 75 mg once daily) (6259 patients) in addition to aspirin for 3 to 12 months.
C - Placebo ( 6303 patients) in addition to aspirin for 3 to 12 months.
O - The first primary outcome — a composite of death from cardiovascular causes, nonfatal myocardial infarction, or stroke — occurred in 9.3 percent of the patients in the clopidogrel group and 11.4 percent of the patients in the placebo group. The second primary outcome — the first primary outcome or refractory ischemia — occurred in 16.5 percent of the patients in the clopidogrel group and 18.8 percent of the patients in the placebo group.
The percentages of patients with in-hospital refractory or severe ischemia, heart failure, and revascularization procedures were also significantly lower with clopidogrel. There were significantly more patients with major bleeding in the clopidogrel group than in the placebo group (3.7 percent vs. 2.7 percent; relative risk, 1.38; P=0.001), but there were not significantly more patients with episodes of life-threatening bleeding (2.1 percent vs. 1.8 percent, P=0.13) or hemorrhagic strokes.
The antiplatelet agent clopidogrel has beneficial effects in patients with acute coronary syndromes without ST-segment elevation. However, the risk of major bleeding is increased among patients treated with clopidogrel.
3) What are the indications and contraindications for PCI?
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
The patient crossed the window period of 12 hours and was doing fine without secondary PTCA.
F) Link to patient details:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
History is unclear as to what was given which releaved his Dyspnea.
2. What is the rationale of using torsemide in this patient?
Torsemide is a loop diuretic and since the patient is in heart failure, it helps in reducing the preload.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
It was not prophylactic.
TLC was 18000 indicating an infection that needed to be localized for which ceftriaxone was given.
4) Gastroenterology (& Pulmonology) 10 Marks
A) 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?
33 year old man, Alcoholic since 9 yrs with history of recurrent episodes of Pain abdomen & vomiting 5 yrs back, stopped consumption of alcohol for 3 years, restarted alcohol consumption, Recurrent episodes (5-6) of pain abdomen & vomiting in last 1 year
Increased alcohol consumption since last 20 days
Pain abdomen & vomiting since 1 week
Fever , burning micturition & constipation since 4 days
Admitted in hospital and treated conservatively
3-4 days later clinical deterioration with tachypnea , SVT , leucocytosis , fever , SOB
Malecot drains were placed for psuedocyst & peripancreatic collections
ICD was placed for left sided hydropneumothorax
Antibiotics & other symptomatic treatment continued
Clinical improvement with resolution of symptoms and was discharged in a stable state 10 days layer
Anatomical localization - Pancreas, Lungs
Primary Etiology -
Alcohol leading to Pancreatitis, Pseudocyst & peri pancreatic collections, Pancreatico pleural fistula, Exudative Pleural effusion, Broncho pleural fistula, eHydropneumothorax
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?
A Randomized, double-blind multicentre trial, efficacy of octreotide in moderate pancreatitis
P- 302 patients with moderate to severe acute pancreatitis within 96 hours of the onset of symptoms
I- Groups 01 (n=98) and 02 (n=101) received 100 and 200 μg of octreotide, respectively, by subcutaneous injection three times daily for seven days
C- 103 patients received placebo
O -No significant differences among treatment groups with respect to mortality , the rate of newly developed complications, the duration of pain, surgical interventions, or the length of the hospital stay.
This trial shows no benefit of octreotide in the treatment of acute pancreatitis.
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
The cause for his dyspnea is pleural effusion, secondary to pancreatitis.
Two main causes of pleural effusion are transdiaphragmatic lymphatic blockage or pancreaticopleural fistulae secondary to leak and disruption of the pancreatic duct or pseudocyst caused by an episode of acute pancreatitis. The leak or disruption is more likely to lead to a pleural effusion if the duct disruption is posteriorly into the retroperitoneum. The pancreatic enzymes can track up into the mediastinum and then rupture into the pleural cavity either left side or bilaterally and so create a connection between the pancreatic duct and the pleural cavity.
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?
4) What is the line of treatment in this patient?
C) Link to patient details:
Questions:
1) what is the most probable diagnosis in this patient?
Ruptured liver abscess, collection secondary to hollow viscus perforation.
2) What was the cause of her death?
SEPSIS with MODS
3) Does her NSAID abuse have something to do with her condition? How?
NSAIDS could lead to bowel perforation
NSAID abuse leads to CKD
5) Nephrology (and Urology) 10 Marks
A) Link to patient details:
1. What could be the reason for his SOB ?
Metabolic acidosis
2. Why does he have intermittent episodes of drowsiness ?
Hyponatremia
3. Why did he complaint of fleshy mass like passage in his urine?
Could be tissues of prostate post TURP
4. What are the complications of TURP that he may have had?
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
This is a case of attention deficit hyperactive disorder
2. Why doesn't the child have the excessive urge of urination at night time ?
Child has urge to urinate during day time but during at night he is asleep without an urge to pass urine.
Psychosomatic overactive bladder
3. How would you want to manage the patient to relieve him of his symptoms?
'Treatment has traditionally been that of benign neglect with just an explanation of the condition, perhaps with some directed counseling regarding the putative stressor trigger. This involves reassuring the parents and child and waiting for the condition to self-resolve. Reducing dietary intake of oxalate-rich beverages such as tea and acidic juices such as apple in children who consume large amounts of them, along with liberal intake of water, have been proposed as ancillary approaches while riding the condition out.
A wait-and-see method does work, but it can take quite some time, requiring 1 to 5 months on average for the condition to go away, during which time the pollakiuria can continue to be disruptive to normal routines.
Medication is often tried; this would typically be an anticholinergic drug such as oxybutynin on the assumption that there is a form of bladder dyssynergy taking place. This has usually been reported to be ineffective, which is not surprising given that the problem in pollakiuria is felt to be sensory rather than motoric, and of course it is not without adverse effects such as drowsiness or dry mouth.
Indomethacin has also been proposed as a treatment, but there are no controlled studies looking at its value, and it is again with potential adverse effects. Given this, and the fact that pollakiuria is a benign self-limited condition, there is no role for the use of medication as treatment. Similarly, biofeedback has been advanced as a therapeutic option in an uncontrolled study, with a long response time for effectiveness. Although safe, this is again unproven and can be expensive.
https://www.contemporarypediatrics.com/view/strategy-treat-pollakiuria
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology) 10 Marks
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
The patient complained of regurgitation & cough on taking foods and the barium swallow showed TEF.
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ART should be stopped and ATT needs to be initiated followed by ART initiation 6 weeks later.
7) Infectious disease and Hepatology:
Link to patient details:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ?
Amoebic liver abscess (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.
2. What is the etio-pathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
A retrospective study was conducted on 108 patients to find the role of alcoholism in liver abscess.
'This study was undertaken on patients both male and female admitted in surgical wards of Chennai medical college & hospital. 108 patients were taken up for the study from the surgical wards of the hospital over a period of 1½ year i.e., from January 2013 to June 2014.
Following alcoholism, poor economic status & malnutrition also plays a vital role as predisposing factors in the formation of liver abscess. Among alcoholism also, consuming locally prepared alcohol plays a vital role, but the reason is still been unknown.
It was undoubtedly proved that 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. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess'
3. Is liver abscess more common in right lobe ?
50% of solitary liver abscesses occur in the right lobe of the liver (a more significant part with more blood supply), less commonly in the left liver lobe or caudate lobe.
The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass. Studies have suggested that a streaming effect in the portal circulation is causative.
4.What are the indications for ultrasound guided aspiration of liver abscess ?
- complicated diverticular abscess
- Crohn's disease related abscess
- complicated appendicitis with appendicular abscess
- tuboovarian abscess
- post-surgical fluid collections
- hepatic abscess (e.g. amoebic or post-operative)
- renal abscess or retroperitoneal abscess
- splenic abscess
B) Link to patient details:
QUESTIONS:
1) Cause of liver abcess in this patient ?
Considering the following factors:
Age and gender of the patient
Single abscess.
Right lobe involvement
Socioeconomic status
Consumption of local alcohol
The abscess is most likely to be Amoebic liver abscess
2) How do you approach this patient ?
3) Why do we treat here ; both amoebic and pyogenic liver abscess?
Prior to an invasive procedure, since the causative organism remains unclear, it's better to go with an empirical coverage of antibiotics.
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology) 10 Marks
A) 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?
50 year old man, daily wage laborer, known HTN since 2 yrs, denovo type 2 DM with a history of
COVID-19 vaccination 15 days back presented with the complaints of
Fever since 10 days
Generalized weakness , facial puffiness & peri orbital edema since 1 week
Weakness of right UL & LL since 4 days
Altered sensorium since 2 days
Anatomical localization - Oro rhino orbital mucormycosis - oral cavity, orbits and nasal cavity
Brain - CVA (Acute infarct in left frontal & temporal lobes)
Primary Etiology - Diabetes Mellitus type 2 --> Mucormycosis
HTN - CVA (Acute infarct in left frontal & temporal lobes
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?
'Although amphotericin B deoxycholate (AmB) was the cornerstone of mucormycosis therapy for decades, lipid formulations of AmB are significantly less nephrotoxic and can be safely administered at higher doses for a longer period of time than AmB. Furthermore, treatment of mucormycosis with liposomal amphotericin B (LAmB) was associated with a 67% survival rate, compared to 39% survival when patients were treated with AmB (p = 0.02)'. Multiple other, more recent case series also found initial therapy with LAmB to be substantially more effective than other options.
Available data indicate advantages of LAmB over amphotericin B lipid complex (ABLC) for the treatment of CNS mucormycosis. For example, LAmB levels achieved in rabbit brain were fivefold above ABLC levels . Furthermore, while similarly effective in neutropenic mice, LAmB was markedly superior to ABLC in diabetic ketoacidotic (DKA) mice infected with Rhizopus oryzae, primarily because of superior clearance of fungus from the brain. These animal studies are complemented by a recent, relatively small retrospective case series, in which the outcomes of patients with rhino-orbital-cerebral mucormycosis were found to be worse when ABLC was used as initial therapy versus AmB or LAmB'
Patients with ROCM were studied for the efficacy of polyene- caspofungin therapy
Forty-one patients with biopsy-proven ROCM were identified over 12 years; 23 (56%) of these patients were Hispanic, and 34 (83%) were diabetic. Patients treated with polyene-caspofungin therapy (6 evaluable patients) had superior success (100% vs. 45%; P = .02) and Kaplan-Meier survival time (P = .02), compared with patients treated with polyene monotherapy. Patients treated with amphotericin B lipid complex had inferior success (37% vs. 72%; P = .03) and a higher clinical failure rate (45% vs. 21%; P = .04), compared with patients who received other polyenes. However, patients treated with amphotericin B lipid complex plus caspofungin had superior success (100% vs. 20%; P = .009) and survival time (P = .01), compared with patients who received amphotericin B lipid complex alone. The benefit of combination therapy, compared with monotherapy, was most pronounced in patients with cerebral involvement (success rate, 100% vs. 25%; P = .01). In multivariate analysis, only receipt of combination therapy was significantly associated with improved outcomes (P = .02).'
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Mucormycosis occurs in immunocompromised patients. Recent rise of cases is due to the current covid situation and has been occurring more among diabetic patients, patients who were or are on steroids for covid 19 infection or other reasons, who were previously on oxygen supplementation ( because of improper cleaning of oxygen cylinders).
9) Infectious Disease (Covid 19)
As these patients are currently taking up more than 50% of our time we decided to make a separate log link here:
For this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
1) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) Indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe covid (for example, altered sensorium, hypotension etc).
Please check out the thesis log here for the example of a blogged master chart https://vamsikrishna1996.blogspot.com/2020/10/thesis.html and please get in touch with Dr Sai Charan PGY1 who is liasing between us and the MRD for this project where we hope this data can allow us to get some clues on predicting the factors driving recovery from covid 19.
COVID-19 MASTER CHART:
10) Medical Education: (10 marks)
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.com/view.aspx?resid=4EF578BAE67BA469!4180&ithint=file%2cdocx&authkey=!AOy7BpRTn42DBMo
In the month of May, I was posted in COVID OPD for 2 weeks, apart from taking care of covid patients I was even working on a paper which I'm currently working on along with my other colleagues on Neurodegenerative disorders.
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