MEDICINE BIMONTHLY ASSIGNMENT - 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 to the assignment questions:

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are the answers to my  medicine assignment based on my understanding of the cases: 

1) PULMONOLOGY:

A) A 55 year old female patient, with the chief complaints of shortness of breath, pedal edema and facial puffiness.

Patient details: https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

Questions:

1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

ANSWER:

Timeline:

Shortness of breath- 20years ago

(lasting for 1week)

1 episode per year for next 8years

🠋

Shortness of breath- 12years ago

(lasting for 20 days and hospitalized)

1 episode per year

🠋

Generalized weakness - 1month ago

(IV fluids- 3pints in 2days)

🠋

Shortness of breath- 30days ago

(grade 2 SOB)

🠋

Pedal edema- since 15 days

( level: ankle, pitting type)

🠋

Facial puffiness- since 15days

🠋

shortness of breath- since 2days

(grade 4 SOB)

🠋

Drowsiness- since 2days

The patient has a history of working in paddy fields and using indoor chulha since 20years. 

The anatomical  lesions are generalized to the entire lung bilaterally.  

Bilaterally generalized honey comb lesions.
 
Signet ring sign.

ETIOLOGY: 
The etiology of the patient is the history of working in paddy fields and using of indoor chulha without proper ventilation.

The general etiology for COPD is:
  • tobacco smoking
  • air pollution
  • indoor burning of biomass fuels
  • occupational exposure to dusts, chemical agents
  • alpha 1 antitrypsin deficiency 

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANSWER:

Head end elevation:

The positioning of a patient in bed can directly affect respiratory function in mechanically ventilated patients.
Benefits: 
  • Facilitate diaphragmatic performance.
  • Reduce the risk of mechanical ventilation-associated pneumonia.
  • Increase the possibility of more homogeneous alveolar ventilation.
  • Reduce the risk of lung injury caused by mechanical ventilation 
Drawbacks:
  • May increase the mechanical load against the respiratory system airflow.
The current recommendation is that the head of MV patients should be maintained between 30° and 45° because of the high risk of Broncho aspiration . The highest dynamic compliance value was observed at the 30º position relative to the other angles, and the driving pressure was increased at head angles of 45º and 60º.

Indication:
  • Mechanically ventilated patients
  • Meningitis
  • Head trauma
  • increased intracranial pressure



O2 inhalation:

Nasal high-flow oxygen therapy (HFOT) is a novel treatment option for patients suffering from acute or chronic respiratory failure.
Benefits:
  • Relieving the hypoxia associated with COPD
  • Reduces symptoms of dyspnea 
  • Improved dyspnea and endurance during exercise in COPD patients
  • Cardiac output was also increased.
  • Hypoxic pulmonary vasoconstriction improved
  • Pulmonary hemodynamics may also be improved
  • Increased systemic oxygen delivery 
  • Improved respiratory muscle function
  • Stimulate upper airway and facial receptors
Drawbacks:
  • It does not benefit patients with mild to less severe COPD.
The correct use of supplemental oxygen therapy during exacerbations of COPD is an important factor that can strongly influence outcomes.

Indications:
  • Documented hypoxemia 
  • respiratory distress
  • Increased metabolic demand (burns, multiple injuries, severe sepsis)
  • Cardiac failure or myocardial infarction
  • Short term therapy (post anesthesia recovery)

Intermittent BiPAP:

Augmentin:

Patients with exacerbations of mild to moderate COPD have a higher rate of cure when given amoxicillin/clavulanate compared with placebo.
"Approximately 75 percent of patients treated with antibiotics were cured, compared with 60 percent of those treated with placebo (number needed to treat = 8; 95% confidence interval, 5 to 27). Additionally, patients taking antibiotics had a longer time to the next exacerbation compared with patients taking placebo (233 versus 160 days)"

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:

Antibiotics should only be started or continued in patients with signs and symptoms of a bacterial infection that include the following:  

  1. Increased dyspnea, increased purulence of sputum, and increased volume of sputum. 
  2. Ventilator support (invasive or non-invasive) for AECOPD.

Patients with a PCT <0.1 ng/mL are unlikely to benefit from antibiotic administration.

Study:  


Azithromycin:

Azithromycin decreased the frequency of exacerbations and improved quality of life but caused hearing decrements in a small percentage of subjects compared to placebo.
"The frequency of exacerbations was 1.48 exacerbations per patient-year in the azithromycin group, as compared with 1.83 per patient-year in the placebo group (P=0.01), and the hazard ratio for having an acute exacerbation of COPD per patient-year in the azithromycin group was 0.73 (95% CI, 0.63 to 0.84; P<0.001)"

 


Mechanism of action: 

 Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit.

Indications:

Antibiotics should only be started or continued in patients with signs and symptoms of a bacterial infection that include the following:  

  1. Increased dyspnea, increased purulence of sputum, and increased volume of sputum. 
  2. Ventilator support (invasive or non-invasive) for AECOPD.

Patients with a PCT <0.1 ng/mL are unlikely to benefit from antibiotic administration.

Study:

Inj Lasix:

Furosemide decreases peripheral edema and  decreases PaCO2 and also increases FEV1 scores when discontinued in patients with COPD as compared to the placebo.

"Ventilation increased from 10.4 L/min (range, 6.7 to 15.4 L/min) at baseline to 11.6 L/min (range, 8.7 to 14.0 L/min) after discontinuation of furosemide (p < 0.05). PaCO(2) decreased from 45 mm Hg (range, 35 to 64 mm Hg) to 41 mm Hg (range, 32 to 61 mm Hg; p < 0.01)"

 

Mean VAS scores during constant work rate exercise testing (open squares = after placebo; closed squares = after furosemide)

Mechanism of action:

Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis).

Indication:

 patients with stable COPD who satisfied the following criteria:

  • Moderate to severe COPD (FEV1 < 70% predicted) with a clinical course consistent with chronic bronchitis and/or emphysema 
  • Moderate to severe chronic breathlessness (Medical Research Council Dyspnea Scale Grades 4 and 5)
  • Age 50 years or older
Study:

In comparison to placebo, systemic corticosteroids improve airflow, decrease the rate of treatment failure and risk of relapse, and may improve symptoms and decrease the length of hospital stay.
"Compared with placebo, systemic corticosteroids reduced treatment failure by 46% (95% confidence interval [CI], 0.41 to 0.71), length of hospital stay by 1.4 days (95% CI, 0.7 to 2.2), and improved FEV1 by 0.13 L after 3 days of therapy (95% CI, 0.04 to 0.21). Meanwhile, the risk of hyperglycemia significantly increased (relative risk, 5.88; 95% CI, 2.40 to 14.41)"


Mechanism of action:

Decreases in inflammatory cytokines, C-reactive protein, and inflammatory cells have been observed with corticosteroid use, suggesting a possible mechanism for a therapeutic benefit of steroids. 

Indication:
  • Exacerbations in patients with moderate to severe COPD.
  • Should be avoided in stable COPD patients.
Study:

Ipravent with Budecort:

Budesonide and ipratropium bromide have shown improved lung function and measures of dyspnea when compared with placebo or either individual component
"Combined treatment improved QOL and decreased the rate of exacerbation, particularly in patients with an FEV1 of less than 50% predicted (). Patients with severe COPD may show particular benefit to combined ICS and LABAs as when compared with LABAs alone because patients with an FEV1 of less than 50% predicted had a 35% reduction in moderate and severe COPD exacerbations over a 44-week study period" 

Mechanism of action: 

Decreases in inflammatory cytokines, C-reactive protein, and inflammatory cells have been observed with corticosteroid use, suggesting a possible mechanism for a therapeutic benefit of steroids.

Indications:

  • Acute exacerbation of moderate to severe COPD.
  • Stable COPD

Study:


Inj HAI: given to control diabetes mellitus.

Inj Thiamine:

The administration of a single dose of thiamine was associated with a trend toward increase in V.o2 in critically ill patients compared to placebo.
"In patients with preserved CI (>2.4 L/min/m2) there was an increase of 21.4 ml/min (P = 0.027) (Table 2). There was no increase in V.o2 in patients with mean CI below the group mean. In contrast, patients with a mean CI above the group mean of 3 L/min/m2 showed an average increase of 70.9 ml/min in V.o2 (P < 0.0001)"

 



Mechanism of action:

Thiamine deficiency impairs production of adenosine triphosphate (ATP), leading to accumulation of adenosine. This increase causes reduction in systemic vascular resistance via direct vasomotor depression, leading to a compensatory high-output state with increased blood volume.

Study:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4298978/


3. What could be the causes for her current acute exacerbation?

ANSWER: The cause for her exacerbation can be:
  • Viral or bacterial infection 
  • Inhalation of smoke
  • Allergy
4. Could the ATT have affected her symptoms? If so how?

ANSWER: They might have been the reason for the development of generalized weakness.

5. What could be the causes for her electrolyte imbalance?

ANSWER: Patients with COPD present with a number of metabolic changes owing to disease process or because of the treatment instituted, like hyponatremia, hypokalemia, hyperbilirubinemia, elevated transaminases, elevated blood urea, and elevated serum creatinine .


The systemic response to hypercapnia has the effect of reducing the renal blood flow and, as a result, increasing water and sodium retention with the final effect of edema and hyponatremia. This hyponatremia can cause potassium ion imbalance leading to hypokalemia.


2) NEUROLOGY

A) A 40 year old male presented to hospital  with chief complaints of irrelevant talking and decreased food intake.


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?

Answer: 
    
a) Symptomatology in the patient in terms of an event timeline : 


 History of 2-3 episodes of seizures 1 year back
 🠋
1 episode of seizure (most probably a GTCS)
Associated with restlessness, sweating, tremors-10 days back
🠋
Generalized body pains- 9 days back 
🠋
Altered sensorium - 9 days back 
[Started talking to himself and laughing to himself (sudden onset) , Conscious , but oriented to time, place and person only from time to time. Unable to lift himself from bed and move around. Decrease in food intake Short term memory loss and unable to identify family members from time to time]
🠋
Taken to a local RMP, given I.V fluids and referred to a higher care facility
🠋
Admitted to tertiary care hospital on 15th may

b) Anatomical localization of the problem :
 
  •  Acute symmetrical lesions in thalamus , mamillary bodies , tectal plates , periaqueductal area , floor of 4rth ventricle (includes oculomotor and vestibular nuclei and cerebellar vermis)
  • Lesions in the form of vascular congestion, microglial perforation and petechial hemorrhages.

c) Primary etiology for the patient's condition:

- Primary etiology for the patient's conditions are:
  •  chronic alcoholism and dependence
  • This lead to a chronic thiamine deficiency leading to Wernicke's encephalopathy
  • Alcohol dependence lead to symptoms of sweating , restlessness, and seizures as withdrawal symptoms on stoppage of alcohol.

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANSWER:

Inj. 1amp Thiamine in 100ml NS,TID 

Thiamine deficiency leads to Wernicke's encephalopathy and the administration of thiamine has been recommended as one of the first treatment modalities in Wernicke's.
'Patients with suspected WE were treated with ≥500 mg intravenous thiamine for a median of 3 days with 73% of patients (eight out of eleven) displaying symptom resolution or improvement after treatment.'
Benefits:
•Reversing the induced biochemical changes in the brain
•Preventing the development of structural lesions

Drawbacks:
•Reports of rare anaphylactoid reactions have led to a dramatic reduction in the usage of thiamine in Wernicke's encephalopathy.

Indications:
Thiamine has been recommended to be used to Wernicke's to combat the deficiency of thiamine in the patient presenting with Wernicke's

References : 
 Inj. Lorazepam 

Mechanism of action:

Seizure prophylaxis with lorazepam injection is a commonly followed intervention in alcohol withdrawal seizures. Lorazepam binds to benzodiazepine receptors in post synaptic GABA-A chloride channels and increases the conduction of chloride ions thereby enhancing the inhibitory actions of GABA.

Indications: 
Lorazepam is used in alcohol withdrawal in cases of:
  •  patients with severe liver dysfunction.
  •  patients who are at high risk of experiencing serious        medical consequences following sedation
  •  people with severe lung disease
  •  elderly patients


T. Pregabalin

Pregabalin is a novel GABA-analogue approved for the treatment of alcohol withdrawal, partial onset seizures, neuropathic pain, and general anxiety disorder compared to placebo.
'Alcohol withdrawal symptoms and craving for alcohol resulted significantly reduced (p < 0.001) over time after pregabalin treatment. Pregabalin also resulted in a favourable improvement in psychiatric symptoms and quality of life (p < 0.001).'

 


Indications:
  • Associated psychiatric symptoms in patients with alcohol withdrawal symptoms
  • Seizure prone patients of alcohol withdrawal
  • Anxiety, hostility and psychoticism in patients of alcohol withdrawal


Inj. HAI s.c - premeal and GRBS

Mechanism of action:

HAI is a short-acting insulin. It works by helping blood sugar (glucose) get into cells so your body can use it for energy. GRBS stands for General Random Blood Sugar. Due to the deficiency of Vit.B1 patients of Wernicke's encephalopathy cannot utilize the glucose in their body and hence require short term insulin to be administered in the presentation to hospital.

Indications:
  • Chronic alcoholics presenting with diabetic ketoacidosis
  • Chronic alcoholics presenting in the comatose state


Lactulose 30ml/PO/BD 

Compared with placebo or no intervention, lactulose significantly reduced the risk of no improvement in neuropsychological tests .

Compared with placebo or no intervention, lactulose significantly reduced the risk of no improvement in neuropsychological tests (RR: 0.52, 95% CI: 0.44–0.62, P<0.00001), the time required for the completion of the number connection test-A (WMD: −26.95, 95% CI: −37.81 to −16.10, P<0.00001), and the mean number of abnormal neuropsychological tests (WMD: −1.76, 95% CI: −1.96 to −1.56, P<0.00001). Furthermore, the meta-analysis also showed that lactulose prevented the progression to overt hepatic encephalopathy (RR: 0.17, 95% CI: 0.06–0.52, P=0.002), reduced blood ammonia levels (WMD: −9.89 µmol/l, 95% CI: −11.01 to −8.77 µmol/l, P<0.00001), and improve health-related quality of life (WMD: −6.05, 95% CI: −6.30 to −5.20, P<0.00001). However, no significant difference was observed in the mortality of patients with MHE (RR: 0.75, 95% CI: 0.21–2.72, P=0.66), and lactulose significantly increased the incidence of diarrhea (RR: 4.38, 95% CI: 1.35–14.25, P=0.01).
Mechanism of action: 

Lactulose is nonabsorbable disaccharide stimulates the passage of ammonia from tissues into the gut lumen and inhibits intestinal ammonia production.

Indications: 
•Acute onset of severe encephalopathy symptoms 
•Minimal hepatic encephalopathy
•chronic alcoholism

References: 


Inj. 2 amp of KCl 

KCl is given to treat the hypokalemia present in the patient compared to placebo.

In a patient with hypertension due to hypokalemia given with KCl therapy caused an average rise in the serum potassium concentration of 0.56 mmol per liter, the mean blood pressure fell by an average of 5.5 mm Hg (P = 0.004), with at least a 4 mm Hg fall observed in 9 of the 16 patients. The fall in blood pressure correlated with a fall in plasma renin activity (r = 0.568, P = 0.043) but not with changes in plasma aldosterone levels or other variables.

Indications:
•hypokalemia
•uremia
•metabolic acidosis
•insulin therapy given
•intermittent iv infusions
 

3)Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

The previous episodes of seizures in the patient were of simple partial type. But the seizures which occurred recently are complex partial seizures. These complex seizures are generally associated with loss of consciousness.

This loss of consciousness occurs due to the seizures which spread to both the hemispheres of the brain.

4) What is the reason for giving thiamine in this patient?

Answer:

Chronic alcoholics have high incidence of vitamin B1(thiamine) deficiency and this is the main reason for the Wernicke's encephalopathy in this patient case a lot of neurological symptoms in the patient. Thiamine is thus given as a prophylactic and treatment therapy of Wernicke's encephalopathy.

5) What is the probable reason for kidney injury in this patient?

Answer: 
  • Alcohol affects the ability of the  kidneys to maintain water balance. When alcohol dehydrates  the body, the drying effect can affect the normal function of cells and organs, including the kidneys.
  • Too much alcohol can also affect  blood pressure.  High blood pressure is a common cause of kidney disease. More than two drinks a day can increase your chance of having high blood pressure.
  • Chronic drinking can also cause liver disease. This adds to the kidney's job. The rate of blood flow to your kidneys is usually kept at a certain level, so that your kidneys can filter your blood well. Liver disease impairs this important balancing act. 



6) What is the probable cause for the normocytic anemia?

Answer:

Normocytic anemia  develops  as a result of another cause, such as a disease. This is known as anemia of chronic disease (ACD) or anemia of inflammation, because the diseases that can lead to normocytic anemia cause inflammation in certain parts of the body or throughout the body. 

The patient has chronic alcoholism which lead to a chronic kidney disease which might have been the cause for normocytic anemia.

The patient is also malnourished due to his chronic alcoholism and hence may also be the reason for normocytic anemia


7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Answer:

Chronic alcoholism is a main cause of peripheral neuropathy which may be a main cause for the development of repeated ulcers on the foot.

Alcoholic neuropathy is one of the most common consequences of heavy alcohol use. People with a long history of alcohol misuse might experience pain, tingling, weakness, numbness, or loss of balance as a result of alcoholic neuropathy. This neuropathy might be the main cause for the formation in foot ulcer in the patient.


B) A 52 year old male came to the hospital 2 days back presenting with slurring of speech and deviation of mouth that lasted for 1 day and resolved on the same day. 



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?

Answer:

a) Symptomatology in the patient in terms of an event timeline: 
Giddiness- 7days back
(1 episode)
🠋
vomitings- 7days back
(1 episode)
🠋
dizziness- 3days back
(associated with bilateral hearing loss, tinnitus, aural fullness)

Patient has a history of postural instability.


b) Anatomical localization : 

Cerebellar infarct revealed on the CT Scan images. 


c) Primary etiology in causing the disease : 

 The primary etiology in causation of the disease in the patient may be:
  • Hypertension
  • 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?

Answer : 

Tab Veratin 8 mg PO TID 

Several clinical trials have demonstrated that betahistine is effective in reducing the frequency and severity of vertigo, and improving vertigo-associated symptoms, including nausea and vomiting
Cochrane Review of randomized controlled trials of betahistine versus placebo in patients with symptoms of vertigo suggested that betahistine may have a positive effect in terms of reduction in vertigo symptoms
Mechanism of action : Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action: 
  •  agonist of H1 receptors and 
  •  antagonist of H3 receptors. 
It has a weak effect on H1 receptors but strong effect on H3 receptors. Betahistine is thought to work by increasing the blood flow around the inner ear. This reduces the amount of fluid in the inner ear and prevents symptoms from developing.

Indications : 
•Meniere's syndrome
•vertigo
•tinnitus
•hearing loss and
•nausea


Inj. Zofer 4mg IV/TID 

Ondansetron is a better antiemetic in patients compared to placebo.
"For every 100 patients receiving an adequate dose of ondansetron 20 patients will not vomit who would have vomited had they received placebo. The antinausea effect is less pronounced. Of these 100, three will have elevated liver enzymes and three will have a headache who would not have had these adverse effects without the drug"

Mechanism of action: 

Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea 

Indications : 
•Nausea and vomiting due to certain medical conditions like stomach upset
•Nausea and vomiting caused due to any surgery, cancer drug therapy or radiotherapy.


Tab. Ecosprin 75mg PO/OD 

Aspirin prevented more number of strokes due to its antiplatelet action as compared to placebo.
There was a significant 14% (SD 7) proportional reduction in mortality during the scheduled treatment period (343 [3·3%] deaths among aspirin-allocated patients vs 398 [3·9%] deaths among placebo-allocated patients; 2p=0·04). There were significantly fewer recurrent ischaemic strokes in the aspirin-allocated than in the placebo-allocated group (167 [1·6%] vs 215 [2·1%]; 2p=0·01) but slightly more hemorrhagic strokes (115 [1·1%] vs 93 [0·9%]; 2p>0·1). For the combined in-hospital endpoint of death or non-fatal stroke at 4 weeks, there was a 12% (6) proportional risk reduction with aspirin (545 [5·3%] vs 614 [5·9%]; 2p=0·03), an absolute difference of 6·8 (3·2) fewer cases per 1000. At discharge, 3153 (30·5%) aspirin-allocated patients and 3266 (31·6%) placebo-allocated patients were dead or dependent, corresponding to 11·4 (6·4) fewer per 1000 in favour of aspirin (2p=0·08).

 


Mechanism of action : 

Ecosprin provides the antiplatelet action by irreversibly inhibiting the formation of thromboxane A2, via acetylation of platelet cyclooxygenase. 

Indications: 

•For prevention of blood clot formation in individuals with a high risk of clotting in blood vessels. 
•For prevention of heart attack. 
•For prevention of cerebellar infarct due to a clot formation. 
•For treatment of an Cardiovascular infarct/Stroke


Tab. Atorvastatin 40mg PO/HS 

The efficacy of standard and intensive statin treatment in the secondary prevention of major cardiovascular and cerebrovascular events is better than placebo.
"Compared with placebo, standard-dose statin treatment resulted in a significant relative risk (RR) reduction of 15% in the occurrence of any major cardiovascular or cerebrovascular event (RR 0.85, 95% CI 0.79–0.91). Compared with standard-dose statin treatment, intensive-dose statin treatment resulted in an additional 9% relative risk reduction (RR 0.91, 95% CI 0.84–0.98)."


Mechanism of action: 

Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver

Indications :  

Adults without a history of CVD are given statins when all of the following criteria are met:
  •  They are aged 40 to 75 years; 
  • They have 1 or more CVD risk factors (i.e., dyslipidemia, diabetes, hypertension, or smoking);
  • They have a calculated 10-year risk of a cardiovascular event of 7.5% to 10% 

Tab. Clopidogrel 75mg PO/OD 

Clopidogrel has proved to be a potent antiplatelet used in stroke or other hypercoagulable conditions over placebo.
The CREDO trial, PCI-CURE subset analysis, and ISAR studies support the benefit of early treatment with clopidogrel before PCI. The combined analysis of these studies clearly indicates that adequate inhibition of platelet function with clopidogrel and aspirin alone can be achieved in troponin-negative patients without a need for a Gp IIb/IIIa inhibitor on board.


Mechanism of action: The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. 

Indications : FDA-approved indications for clopidogrel include:

Use during a percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) and stable ischemic heart disease.
  • Primary prevention of thromboembolism atrial fibrillation
  • Symptomatic carotid artery stenosis
  • Secondary prevention post-coronary artery bypass grafting
  • Peripheral artery percutaneous angioplasty in •peripheral artery bypass grafting



Inj. Thiamine 1 amp in 100ml NS PO/BD :

Thiamine is commonly used for the treatment of Wernicke's encephalopathy and has also been recommended as the first drug to be administered in all the complications due to alcoholism in chronic alcoholics.

Mechanism of action : 

Thiamine is useful in chronic alcoholics in preventing Wernicke encephalopathy in , an acute disorder due to thiamine deficiency manifested by confusion, ataxia, and ophthalmoplegia, as well as the chronic Korsakoff syndrome, which is manifested by memory impairment and amnesia.

Indications : 

  • In conditions of thiamine deficiency commonly noticed in chronic alcoholics with presenting symptoms of Beri Beri and Wernicke's encephalopathy
  • In malabsorption disorder caused due to chronic alcoholism
  • In patients with chronic alcoholism and associated psychiatric symptoms.


3) Did the patients history of denovo HTN contribute to his current condition?

Answer :  Yes the patients history of Hypertension may have contributed to his present condition. High blood pressure causes blood clots to form in the arteries leading to brain, blocking blood flow and potentially causing a stroke.

 

"The crude incidence of stroke was 289/100000 person-year in controlled hypertensive subjects and 705/100000 person-year in treated hypertensive subjects with BP 140/90 mm Hg. It was estimated that 45% of all strokes among subjects with treatment for hypertension might be attributed to uncontrolled BP. HTN is a major risk factor associated with 67%(70.104) of patients with AIS. Multivariate analysis suggests higher odds of 4.088(95%Cl, 0.721–23.179) and 2.437(95%Cl, 0.721–23.179) for 12 and 18 months outcome in patients with AIS and HTN, respectively." 




4) Does the patients history of alcoholism make him more susceptible to ischaemic or hemorrhagic type of stroke?

Answer : 
The patient's history of alcoholism is a major risk factor for ishaemic stroke. 
Heavy drinking should be considered as one of the risk factors for hemorrhagic stroke. In contrast to the protective effect of mild-to-moderate alcohol use against ischemic strokes, moderate drinking might result in an increased risk of hemorrhagic strokes

"Most case-control and cohort studies either reported only on total strokes or on a combined group of hemorrhagic strokes including intracerebral as well as subarachnoid hemorrhages. There was a consensus among reports that heavy alcohol consumption was associated with a higher risk of hemorrhagic strokes. Controversy remains regarding the effect of mild-to-moderate alcohol consumption: while some studies reported a protective effect, others found a dose-dependent linear relationship between the amount of alcohol consumed and the risk of hemorrhagic stroke."


C) A 45 years old female , came to OPD with chief complaints of palpitations, chest heaviness, pedal edema, chest pain, radiating pain along her left upper limb


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?

Answer : 

 Bilateral pedal edema - 8 months back  
 (present on both sitting and standing positions)
🡳
Pain radiating along left upper limb-  6 days back
🡳
Chest pain - 6 days back
(associated with chest heaviness)
🡳
Palpitations -  5 days back
( sudden in onset, more during night time )
🡳
Dyspnea (NYHA-CLASS-3) - 5 days back




b) Anatomical localization :  The localization of the condition is cervical spine, as cervical spondylosis is the reason causing for the symptoms occurring due to compression of nerve roots.

c) Primary etiology in the problem : 
 
The main etiology in the patient is:
  • Old age
  • Overhead work 
  • Stress


2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

ANSWER:  

Hypokalemic periodic paralysis is an inherited condition . hence the paralysis occurs as episodes.

Risk factors of this condition are:
  • medications like diuretics, enema
  • inadequate intake of potassium
  • transcellular shift of potassium
  • renal causes like osmotic diuresis, RTA
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Answer : 

a)ECG findings :
•3-3.5 meq/L : Flattening of T wave , Prominent U wave and Prominent QT interval
•2.5-3 meq/L : Sagging or depression of ST segment 
• <2.5 meq/L : QRS widening , increased risk of arrhythmia , PR prolongation.

b) Symptoms of hypokalemia : 

•Weakness
•Fatigue
•Muscle cramps or twitching
•Constipation
•Arrhythmia
•Worsening diabetes control or polyuria.
•Palpitations.
•Psychological symptoms (eg, psychosis, delirium, hallucinations, depression)


D) A 55year old male patient came to OPD with c/o altered sensorium and involuntary movements and recurrent episodes of seizures .


QUESTIONS: 

1) Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it? 

Answer : 

Relationship Between Seizure and Stroke
 
Strokes can damage the brain in many ways, and these negative effects take different forms depending on the person and their stroke. But in general, strokes can influence emotions, mobility, verbal communication, behavior, and memory. One problem caused by stroke that’s harder to notice is the increased risk of seizures.

Seizures are actually more common after stroke. Statistics show that seizures afflict 22 percent of people who suffer from strokes. They are important to watch out for as they indicate malfunctions in brain activity and cause an altered state of awareness for a stretch of time. 

There are several causes for early onset seizures after ischemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarization, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury (particularly after carotid end atherectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after hemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Hemosiderin deposits are thought to cause irritability after a hemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.

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? 

ANSWER: 

The patient in previous seizure episodes she had simple partial seizure but in the recent episodes she had a complex partial seizure which resulted in tonic clonic seizure which lead to loss of consciousness. Complex seizures spread to both sides of the brain leading to loss of consciousness.

E) A 48-year-old gentleman ,came to the hospital with the chief complaints of unresponsiveness  and 3 intermittent episodes of seizures .



QUESTIONS : 

1) What could have been the reason for this patient to develop ataxia in the past 1 year?

Answer : 
The main reason for the patient to develop ataxia is due to chronic alcoholism.

Alcohol induced cerebellar degeneration is the commonest type of acquired toxic ataxia.  Permanent cerebellar deficits are observed among alcoholics, and they persist even with alcoholic abstinence.

"A total of 78 chronic alcoholics were examined neurologically as well as by electroneurography, myography and posturography. Clinical signs of peripheral neuropathy were detected in 45% of these patients, with electromyographic and neurographic abnormality in 67% and 55% respectively. Clinical signs of cerebellar ataxia were found in 33% of our patients, whereas posturographic measurements of increased sway were recorded in 69%. The posturographic characteristics of cerebellar anterior lobe atrophy were observed in two-thirds of the latter patients. The severity of cerebellar-ataxia did not correlate with the degree of neuropathy. This lack of correlation is interpreted as an indication of different pathogenetic mechanisms acting on peripheral nerves and cerebellum."


2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Answer : 

The most probable reason for the Intracranial bleed in the patient might be chronic alcoholism. Chronic alcoholism has been equated to increased risk and chances of causing intracranial bleeding may be due to the fact that alcohol thins your blood. This could increase the risk of hemorrhagic stroke, in which a blood vessel breaks inside the brain.
"Heavy alcohol consumption demonstrated a strong association with increased nonlobar ICH risk (OR 2.04, p = 0.0003). Heavy alcohol consumption was associated with significant increase in nonlobar ICH risk in black (OR 2.34, p = 0.0140) and Hispanic participants (OR 12.32, p < 0.0001)." 



F) A 30 year old male patient with weakness of right upperlimb and lowerlimb, deviation of mouth towards left.


QUESTIONS : 

1) Does the patient's  history of road traffic accident have any role in his present condition?

Answer : 

The patient's MRI indicated the presence of 'Altered signal intensity areas involving left caudate nucleus, left frontal and temporal regions, that is hyperintense on T2/FLAIR with evidence of diffuse restrictions and loss of grey white matter differentiation 

These findings are indicative of Acute infarct in the Middle Cerebral Artery territory without any evidence of hemorrhages.

These infarcts might be consistent with the finding in the history of the patient which has a road traffic accident mentioned as Post-traumatic cerebral infarction (PTCI) is one of the most severe secondary insults after traumatic brain injury (TBI), and is known to be associated with poor outcome and high mortality rate.
Of the 986 patients with TBI in this study, cerebral infarction was observed in 21 patients (2.1%) within 3 months after trauma. In one retrospective cohort study, the prevalence of cerebral infarction was 1.9%.12) Other studies revealed that prevalence of PTCI was up to 10.4%.19,21,22) These studies included only moderate or severe brain trauma patients. However, patients with TBI of all grades of severity were enrolled in this investigation. Therefore, our result showed low incidence of PTCI compared to other studies. When excluding patient with GCS score of 12 to 15, incidence of PTCI was 6.9%.


2)What are warning signs of CVA ?

Answer:

The five warning signs of CVA/Stroke are:

•Sudden onset of weakness or numbness on one side of the body
•Sudden speech difficulty or confusion
•Sudden difficulty seeing in one or both eyes
•Sudden onset of dizziness, trouble walking or loss of balance
•Sudden, severe headache with no known cause

3)What is the drug rationale in CVA?
 
Answer:

The Role of Medications in General Supportive Care:

•Oxygenation
Maintaining adequate tissue oxygenation is important during periods of acute cerebral ischemia in order to prevent hypoxia and potential worsening of the neurologic injury. 

•Antihypertensives
In the setting of AIS, many patients will have elevated blood pressure for the first 24–48 hours. Although severe hypertension is a contraindication for thrombolytic therapy, there are no data to define the levels of arterial hypertension that mandate emergent management.

•Insulin
Hypoglycemia can cause focal neurologic signs that mimic stroke and can itself lead to brain injury. Additionally, several clinical studies have associated hyperglycemia with poor outcomes.[7,8] Therefore, prompt measurement and normalization of serum glucose concentration is important. 

•Antipyretics
Increased body temperature in the setting of acute ischemic stroke has been associated with poor neurologic outcome, possibly due to increased metabolic demands, enhanced release of neurotransmitters, and increased free radical production.

Rationale of drugs in the treatment of Acute Ischemic Stroke:

•Thrombolysis
Intravenous administration of alteplase is the only FDA-approved medical therapy for treatment of patients with acute ischemic stroke. Its use is associated with improved outcomes for a broad group of patients. Recent trials have shown the therapeutic window may be extended out to 4.5 hours in selected patients. 

•Device Therapies
Mechanical thrombectomy delivered endovascularly is another option for clot removal, either as an adjunct to thrombolysis or for patients who are ineligible for IV alteplase.

•Anticoagulants
Data suggest that urgent anticoagulation in unselected acute ischemic stroke patients leads to symptomatic intracranial hemorrhage that outweighs any potential benefit. Heparin UFH has its anticoagulant effects by inactivating thrombin and activated factor X. 

•Antiplatelet Agents
Aspirin irreversibly inhibits cyclooxygenase, which prevents the conversion of arachidonic acid to thromboxane A2 (TXA2). Thromboxane A2 is a vasoconstrictor and stimulator of platelet aggregation.

Clopidogrel irreversibly blocks ADP receptors on platelets and thus prevents the cascade resulting in activation of GP IIb/IIIa receptor. 

The CAPRIE (Clopidogrel versus Aspirin in Patients at Risk of Ischaemic Events) trial tested clopidogrel 75 mg daily versus aspirin 325 mg daily in the prevention of cardiovascular and cerebrovascular events.

•Mannitol is an osmotic diuretic, typically used at 0.25–0.5 g/kg IV administered over 15 minutes. It lowers intracranial pressure, and can be given every 6 hours.[76] The usual maximal dose is 2 g/kg. Its effect in patients with ischemic brain swelling is still unknown, but it is often used as a temporizing measure before patients undergo decompressive craniectomy.


4)Does alcohol has any role in his attack?

Answer : 

Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase the risk of having a stroke caused by bleeding in the brain. It is also debated that alcohol may exhibit a protective effect on ischemic strokes. 

But in the patient history it has been described that the patient is an occasional alcohol consumer and also he had not consumed any alcohol prior to the attack indicates that alcohol might not have any role to play in the causation of this disease.

5)Does his lipid profile has any role for his attack??

Answer : 

The patient has lower levels of HDL in his body while the other parameters of lipid profile are normal.  Lower levels of HDL is a potential risk factor for stroke.

Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor. In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke


G)50-year-old male patient presented to hospital with complaints of weakness of all four limbs since 8 PM yesterday.


QUESTIONS : 

1)What is myelopathy hand ?

Answer : 

A characteristic dysfunction of the hand observed in various cervical spinal disorders when there is involvement of the spinal cord. There is 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. The characteristic nature of the signs permit the distinction between myelopathy and changes due to nerve root or peripheral nerve disorder.  
The main clinical features are localized wasting and weakness of the extrinsic and intrinsic hand muscles, but not accompanied by either sensory loss or spastic quadriparesis. For an accurate diagnosis, attention should be paid to the narrow anteroposterior (AP) canal diameter of the cervical spine (less than 13mm), multisegmental spondylosis in C5-6 and C6-7 disc levels and a reduced transactional area of the spinal cord at the C7, C8, or T1 spinal cord segments. 


2)What is finger escape ?

Answer:

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.

It may be due to : 
  • Ulnar nerve neuropathy ,
  • Cervical myelopathy, 
  • Upper motor neuron disorders of the cerebral cortex (such as mild hemiplegic stroke or hemiplegic migraine where the same clinical finding has been called the "digiti quinti sign")

This commonly results from weakness of some of the ulnar nerve innervated intrinsic hand muscles -in particular the palmar interosseous muscle to the little finger- caused by damage to their nerve supply (denervation).

3)What is Hoffman's sign? 

Answer:

The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down. The reflexive pathway causes the thumb to flex and adduct quickly. A positive Hoffman sign indicates an upper motor neuron lesion and corticospinal pathway dysfunction likely due to cervical cord compression. 

H) A 17 year old female student by occupation presented to causality with complaints of involuntary movements of both upper and lower limbs


QUESTIONS : 

1) What can be the cause of her condition ? 

Answer : The main cause for the patient's condition are:
  • Iron deficiency anemia
As the MRI indicates the patient has Acute cortical vein thrombosis with hemorrhagic venous infarction involving Right posterior temporal lobe with midline shift to left by 4mm.

The patient is also suffering from severe iron deficiency anemia which can increase the number of platelets in blood, which is linked with a hypercoagulable state. Erythropoietin which stimulates megakaryocytes is also increased during the iron deficiency. Under conditions of stress or infections, the metabolic demand at the tissue level rises which can create anemic hypoxia and can predispose to venous thrombosis.

2)What are the risk factors for cortical vein thrombosis?

Answer:

Risk factors for children and infants include:

•Problems with the way their blood forms clots
•Sickle cell anemia
•Chronic hemolytic anemia
•Beta-thalassemia major
•Heart disease — either congenital  or acquired 
•Iron deficiency
•Certain infections
•Dehydration
•Head injury
•For newborns, a mother who had certain infections or a history of infertility

Risk factors for adults include:

•Pregnancy and the first few weeks after delivery
•Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
•Cancer
•Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
•Obesity
•Low blood pressure in the brain (intracranial hypotension)
•Inflammatory bowel disease like Crohn’s disease or ulcerative colitis

3)There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously  why?  

Answer: 

Levipil is an anti-epileptic drug used to treat epilepsy seizures (fits). It can be used alone or in combination with other medications. It works to avoid seizures as long as you keep taking it. Levipil 500 Tablet works by reducing irregular brain electrical activity

After the stat iv administration of levipil there was a seizure - free period due to the action of the antiepileptic and as soon as the dosage of the drug  worn out the patient started experiencing seizures again.

Then the doctors administered inj.  phenobarbitone 20mg/kg-800 mg iv stat. This cause spontaneous resolution of the seizures due to the rapid action of iv phenobarbitone in the resolution of seizures by decreasing brain activity. 

4) What drug was used in suspicion of cortical venous sinus thrombosis?

Answer : 

Clexane 0.4ml SC BD is the drug given in suspicion of cortical venous sinus thrombosis. 

Clexane is one of a group of medicines called low molecular weight heparins (LMWH). These medicines work by reducing blood clotting activity. 

Heparin anticoagulation is the time-honored treatment, and is advocated in all cases of CVT, irrespective of etiology or presence of hemorrhage


3) CARDIOLOGY:

A) A 78 yr old male patient, came to the OPD with chief complaints of shortness of breath, chest pain, pedal edema and facial puffiness.


Questions:

1. What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

ANSWER:

 Heart failure with preserved ejection fraction (HFpEF) occurs when the lower left chamber (left ventricle) is not able to fill properly with blood during the diastolic (filling) phase. The amount of blood pumped out to the body is less than normal. It is also called diastolic heart failure.

Heart failure with reduced ejection fraction happens when the muscle of the left ventricle is not pumping as well as normal. The ejection fraction is 40% or less. The amount of blood being pumped out of the heart is less than the body needs.




 

          HEART FAILURE WITH PRESERVED EJECTION FRACTION

                HEART FAILURE WITH REDUCED EJECTION FRACTION

Risk factors

Elderly

Females> males

Hypertension

Diabetes mellitus

Obesity

 

Male>female

Dyslipidemia

Smoking

Myocardial necrosis/ inflammation

 

Organ level

Concentric LV remodeling

High LV mass/volume

Eccentric LV remodeling

Low LV mass/volume

Molecular level

Cardiomyocyte  hypertrophy

Collagenolysis

Interstitial fibrosis

Titin isoform shift to N2B( stiff spring)

Cardiomyocyte loss

Replacement fibrosis

Titin isoform shift to N2BA (compliant spring)




2. Why haven't we done pericardiocentesis in this patient?

ANSWER: It is avoided in the patient because:
  • There is no cardiac tamponade in the patient.
  • The pericardial effusion is present as a small pocket .
  • The effusion was noted to be resolving on its own.[ resolved from 2.4cm to 1.9cm]
Indications for pericardiocentesis:
  • Cardiac tamponade is a class I indication for PC according to the European Society of Cardiology guidelines for management of pericardial diseases.
  • A large (>20 mm) pericardial effusion may also be considered for PC (Class IIa recommendation)
  •  PC is not typically performed when an effusion is noted to be resolving on its own or less invasive methods can be used to make the diagnosis and treat the source of the effusion.


3. What are the risk factors for development of heart failure in the patient?

ANSWER: Risk factors are:
  • Diabetes mellitus
  • Old age
  • Diastolic filling impairment
  • Valvular heart disease
  • Collapsing left ventricle
  • Chronic alcoholic
  • Smoking


4. What could be the cause for hypotension in this patient?

ANSWER: It may have been due to thickening of his visceral pericardium secondary to TB , restricting his heart to expand leading to hypotension.


B) A 73 yr male patient presented to OPD with chief complaints of pedal edema, shortness of breath and decreased urine output.


1. What are the possible causes for heart failure in this patient?

ANSWER: The possible causes for HFpEF are:
  • Hypertension
  • Diabetes mellitus
  • Chronic kidney disease
  • Obesity
  • Anemia of chronic disease
2. What is the reason for anemia in this case?

ANSWER: Anemia may have been caused due to:
  • Inadequate erythropoietin due renal failure ( CKD)
  • Nutritional deficiency of iron
  • Decreased RBC production ( Chronic alcoholic since 40years)
Overall the anemia may be due to chronic disease or chronic alcoholism.


3. What is the reason for blebs and non healing ulcer in the legs of this patient?

ANSWER: The blebs may be caused as a complication of diabetes mellitus.

Non healing ulcer is caused due to delayed wounding healing because of:
  • Diabetes mellitus ( narrowing of blood vessels leading to decreased perfusion)
  • Heart failure (due to lower perfusion and oxygenation in the extremities)
  • Anemia ( halt or slow the wound healing stages, which leaves patients more susceptible to other complications such as wound infection.)
4. What sequence of stages of diabetes has been noted in this patient?

ANSWER: stages of diabetes type 2 noted in the patient are:
  • Stage 1: insulin resistance
  • Stage 2: prediabetes
  • Stage 3: diabetes type 2
  • Stage 4: microvascular complications ( retinopathy, nephropathy, neuropathy)

C) A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest and facial puffiness.


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?

ANSWER:
Timeline:
Facial puffiness - since 2-3 years
🡳
Shortness of breath- 1year ago
( grade 2 , diagnosed to be hypertensive)
🡳
Shortness of breath- since 2days
( started as grade 2 and progressed to grade 4)
🡳
Decreased urine output- since 2days
🡳
Anuria- since morning

The patient has a history of surgery for inguinal hernia 10 years ago and pain at surgical site which aggravated since 3years.

The anatomical location of the thrombi are:
  • Left atrial appendages
  • Left atrium
There is presence of dilation of all heart chambers and IVC.







Etiology: The causes of atrial fibrillation with thrombus formation in the patient are:
  • Pulmonary artery hypertension
  • Congestive cardiac failure

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Dobutamine Inj:

 Dobutamine increases contractility, which leads to decreased end-systolic volume and, therefore, increased stroke volume compared to placebo. The larger stroke volume leads to an increase in cardiac output of the heart.

Mechanism of action:

dobutamine is used because of its inotropic effects on the myocardium through binding and activating the beta-1 receptors. 

Indications:

It is indicated in:
  • Temporary intravenous inotropic support until resolution of the acute inducing factors or the patient receives more definitive treatment.
  • Continuous intravenous form for inotropic support to bridge patients with late-stage heart failure, stage D.
  • Short-term for those hospitalized patients with severe systolic dysfunction who present with low blood pressure .
  • Decompensated congestive heart failure because of the sympathomimetic effects.

Digoxin:

Patients with systolic congestive heart failure with normal sinus rhythm, digoxin appears to have a neutral effect on mortality especially if close digoxin level monitoring is employed compared to placebo.
"a trend towards a lower risk of mortality secondary to heart failure with 394 deaths in the digoxin group compared to 449 in the placebo group with a RR of 0.88 (95%CI: 0.77-1.01, P = 0.06). Overall, the number of hospitalizations attributed to worsening heart failure was lower in the digoxin group compared to placebo with a RR of 0.72 (95%CI: 0.66-0.79, P < 0.001)"


Mechanism of action: 

Digoxin’s primary mechanism of action is through inhibition of sodium-potassium adenosine triphosphatase (ATPase). Its role in heart failure patients is based on its inotropic properties, due to inhibition of sodium-potassium ATPase which leads to increased intracellular calcium concentrations through the sodium-calcium exchanger.
digoxin has a parasympathetic effect on the sinoatrial node, by decreasing the automaticity as well as on the atrioventricular conduction system by decreasing conduction and increasing the effective refractory periods.

Indications: 
  • ACC/AHA and ESC guidelines recommendation on the use of digoxin in heart failure with reduced ejection fraction and normal sinus rhythm.
  • Digoxin can be considered in combination with a beta blocker and/or nondihydropyridine calcium channel blocker when the ventricular rate is poorly controlled in patients with underlying left ventricular dysfunction.
  • Use of digoxin in the acute management of patients who present with acute ST elevation myocardial infarction.


Heparin 5000:

The role of heparin for prevention of ischemic stroke and systemic embolism in high-risk patients with nonvalvular AF is better compared to placebo.
"double-blind trial of dose-adjusted IV unfractionated heparin (Class I) in 225 patients with partial stable carotid and vertebrobasilar distribution stroke.7 This trial showed that there was no difference in death at 7 days between patients who were treated with unfractionated heparin (1/112 [0.89%]) and those treated with placebo (2/113 [1.77%]). Functional activity at 7 days, 3 months, and 1 year also was not significantly different between groups. At 6 months, the proportion of patients who were dead or dependent was identical for the group that received unfractionated heparin and the group that avoided heparin (62.9% in each)"

 


Mechanism of action:

 Heparin is a sulfated polysaccharide with a molecular weight range of 3000 to 30 000 Da (mean, 15 000 Da). It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.

Indications:

  • Heparin is used to prevent acute thrombosis after coronary thrombolysis.
  • Heparin represents an effective alternative to warfarin for antithrombotic prophylaxis.

Carvediol:

Beta-blockers have been shown to improve survival in patients with chronic heart failure compared to placebo.

"A significant reduction in mortality was observed in favour of the group treated with carvedilol, with an absolute reduction in mortality of 5.7% over a 5 year follow-up period"


 

Mechanism of action:

Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart.

Indication:
  • Left ventricular dysfunction
  • Hypertension
  • Treatment of mild-to-severe heart failure of ischemic or cardiomyopathic origin


Acitrom:

It has been documented that prolonged oral anticoagulation with proper control of INR significantly reduces the risk of cerebral stroke compared to placebo in patients with atrial fibrillation.

"all average monthly INR values were within therapeutic range (2.0-3.0) without differences in the quality of treatment. More than 50% (P = 0.721) as well as >75% (P = 0.714) therapeutic INR values were similar in both groups (Figure 4)."

 

Mechanism of action:

It exerts anticoagulant action by preventing the regeneration of reduced Vit K by interfering with Vit k epoxide reductase.

Dytor: 

Toresamide is superior to placebo for cardioversion of AF, and even though the onset of conversion is delayed, its efficacy is similar at 24 h compared with class Ic drugs.
"significant efficacy was found after 6 to 8 h (relative risk [RR] 1.23, p = 0.022) and at 24 h (RR 1.44, p < 0.001). Efficacy with toresamide was inferior to class Ic drugs for up to 8 h (RR 0.67, p < 0.001) but no difference was seen at 24 h (RR 0.95, p = 0.50)".


Mechanism of action:

Toresamide causes excretion of sodium chloride and water by inhibiting sodium and chloride reabsorption in the ascending loop of Henle and distal collecting tubule. The effect is caused by blocking the chloride-binding site of the Na+/K+/2Cl- cotransport mechanism.

Indications:

  • edema / fluid overload
  • hypertension

3. What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
ANSWER:

Pathogenesis:

The inability of the failing heart to generate forward flow, thus resulting in prerenal hypo perfusion. Inadequate renal afferent flow activates the RAAS axis, the sympathetic nervous system, and arginine vasopressin secretion, leading to fluid retention, increased preload, and worsening pump failure.

This patient has type 4 cardiorenal syndrome.

4. What are the risk factors for atherosclerosis in this patient?

ANSWER:

Risk factors for this patient are:
  • Diabetes type 2
  • Hypertension
  • Age- 52years

5. Why was the patient asked to get those APTT, INR tests for review?

ANSWER:

  • The aPTT used to be the most commonly used method to monitor the effect of UFH therapy. UFH potentiates the activity of antithrombin and covalently neutralizes thrombin and activated factor X (anti-FXa).
  • We regularly monitor the INR of people using anticoagulants in order to balance the risk of excessive bleeding (when the INR is too high, meaning that the blood is too thin) against the risk of clotting or thrombosis (when the INR is too low or the blood is too thick).


D)A 67 year old female patient came to the OPD with C/O shortness of breath (SOB) since 1/2 hour.

Patient details: https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

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?

ANSWER:

Heart burn like episodes- since 1year
🡳
Diagnosed with TB- 7 months ago
🡳
shortness of breath- 30 minutes ago

Etiology:
  • Diabetes mellitus type 2
  • Hypertension
  • High cholesterol diet

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANSWER:

MET- XL:

Beta-blockers have been shown to improve survival in patients with chronic heart failure compared to placebo.

"A significant reduction in mortality was observed in favour of the group treated with metoprolol, with an absolute reduction in mortality of 5.7% over a 5 year follow-up period"

 


Mechanism of action:

Metoprolol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart.

Indications:

  • Left ventricular dysfunction
  • Hypertension
  • Treatment of mild-to-severe heart failure of ischemic or cardiomyopathic origin
  • NSTEMI

3. What are the indications and contraindications for PCI?

ANSWER:

Clinical indications for PCI include the following:

  • 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 of PCI:
  • Lack of cardiac surgical support.
  • Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
  • Coagulopathy.
  • Hypercoagulable states.
  • Diffusely diseased vessels without focal stenosis.
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?

ANSWER: 

The 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines for the management of STEMI consider primary PCI as a class I indication in STEMI patients within 12 hours’ of initial symptom onset.2 Beyond this timeframe PCI does not show benefit, as shown in the occluded artery trial which evaluated PCI benefit among stable, high-risk patients with persistent total coronary occlusion after MI. The study concluded that PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.



E) A 60year old Male patient, came to the OPD with the chief complaint of chest pain , giddiness and profuse sweating .



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?

ANSWER: 
Chest pain- since 3days
🡳
Giddiness - since morning
🡳
Profuse sweating- since morning

Anatomical location of the lesion is inferior wall of the heart.

Etiology: 
  • Smoking
  • Diabetes mellitus
  • Hypertension

2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

ANSWER:

Aspirin:

A lower incidence of nonfatal myocardial infarction in the aspirin group compared with the placebo group.
"The major end point, total mortality, was 10.8% in the aspirin group and 9.7% in the placebo group. There was a nonsignificant trend indicating a lower incidence of nonfatal myocardial infarction in the aspirin group (6.3%) compared with the placebo group (8.1%)"

 

Mechanism of action: 

 Acetylsalicylic acid (ASA) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes . Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation.

Indications: 

  • Reducing the risk of cardiovascular death in suspected cases of myocardial infarction
  • Reducing the risk of a first non-fatal myocardial infarction in patients, and for reducing morbidity and mortality in cases of unstable angina and in those who have  had a prior myocardial infarction  
  • Reducing the risk of transient ischemic attack

Atorvas: 

High-intensity statin therapy might be beneficial in patients with MI compared to placebo.
Mechanism of action: 

Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.

Indications: 
  • Reduce the risk of non-fatal myocardial infarction.
  • Reduce the risk of fatal and non-fatal stroke.
  • Reduce the risk for revascularization procedures.
  • Reduce the risk of hospitalization for CHF.
  • Reduce the risk of angina.
Clopibb: 

Among patients with ST elevation MI, treatment with clopidogrel was associated with a reduction in mortality and in the composite of death, MI, or stroke compared with placebo.
"The primary endpoint of all-cause mortality by hospital discharge was significantly lower in the clopidogrel group (7.5%, n=1,726 vs. 8.1%, n=1,845; p=0.03). Additionally, the co-primary composite endpoint of death, reinfarction, or stroke was lower in the clopidogrel group (9.2%, n=2,121 vs. 10.1%, n=2,310; p=0.002). Reinfarction was lower in the clopidogrel group (2.1% vs. 2.4%, p=0.02), but stroke did not differ by treatment group (0.9% vs 1.1%, p=NS). Any major bleed occurred in 0.58% of the clopidogrel group and 0.55% of the placebo group"

 

Mechanism of action:

The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.

Indications:
  • Use during a percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) and stable ischemic heart disease.
  • Primary prevention of thromboembolism atrial fibrillation
  • STEMI

PTCA:

Clinical indications for PCI include the following:

  • 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

3) Did the secondary PTCA do any good to the patient or was it unnecessary?

ANSWER: The secondary PTCA was unnecessary in the patient as he already crossed the window period of 12 hours and was doing fine without the PTCA.

F) An 87 year old male patient presented to the OPD with chief complaints of shortness of breath, constipation and decreased urine output.


1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

ANSWER: The reason for shortness of breath in the patient may have been hypovolemia which was treated with IV fluids.

2. What is the rationale of using toresamide in this patient?

ANSWER: Loop diuretics such as toresamide improve some hemodynamic parameters and dyspnea due to congestion, i.e., water and salt retention. This may have been the reason behind the use of toresamide in this patient.

3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

ANSWER: ceftriaxone was given as we suspected pyogenic infection because of the presence of pus cells in the urine. It was given as treatment for UTI and not prophylactic.



4) GASTROENTEROLOGY: 

A)A 33 yr old male daily wage labourer from miryalaguda who is a chronic alcoholic and smoker came to hospital on 30/04/2021 with cheif complaints of pain abdomen & vomiting since 1 week and constipation, burning micturition, fever since 4 days.

 

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?

Answer : 

a) Evolution of symptomatology : 
 

 pain abdomen and vomitings - 5years back
🡳
 Pain abdomen and vomitings - 1year back
(5-6 episodes)
🡳
 Pain abdomen and vomitings - 1 week 
🡳
Fever-  since 4 days
🡳
Burning micturition- since 4days
( associated with suprapubic pain, increased frequency and urgency) 
🡳
 Constipation and passing flatulus- since 4days




b) Anatomical localization of the disease : 

•Acute on chronic pancreatitis with pseudocyst & acute infective peri pancreatic fluid collections. The disease is localized to pancreas which lies behind the peritoneum of the posterior abdominal wall and is oblique in its orientation. The head of the pancreas is on the right side and lies within the “C” curve of the duodenum at the second vertebral level


•Moderate left pleural effusion with basal atelectasis with a build-up of fluid between the tissues that line the lungs and the chest.


•Left pneumothorax secondary to broncho pleural fistula. This condition occurs when air leaks into the space between the lungs and chest wall.  


c) Primary etiology of the patient's problem: 

Primary etiology of the patient's main problem that is pancreatitis is:
  •  Chronic and excess consumption of alcohol. 
The pancreatic acinar cells metabolize alcohol into toxic byproducts that damage pancreatic ducts, and enzymes that are normally released into the digestive tract build up and begin to digest the pancreas itself. The damaged pancreatic tissue promotes inflammation, which leads to further damage of the pancreas. 

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?

Answer : 

Meropenem

Meropenem is a better antibiotic at decreasing sepsis than placebo in pancreatitis.

 

There are few randomized clinical trials about the use of antibiotics in AP. Pederzoli et al. in 1993 [16] conducted the first of them, which analyzed 74 patients with SAP in six medical centers in Italy. The patients were randomized in two groups: one control with 33 patients and the treatment group with 41 patients that received Imipenem 3 × 500 mg/day intravenously (i.v.) during 14 days. They observed reduction in pancreatic sepsis in patients that received antibiotics (30.3% vs. 12.2%, p < 0.01). However, they did not find reduction in mortality between the groups (12% vs. 7%, respectively).


Inj. Metrogyl 500mg iv TID 

Metronidazole is a better antibiotic at decreasing  the infection compared to placebo.

It was a prospective randomized double-blind trial that analyzed 114 patients, 58 that received antibiotics (Metronidazole 2 × 500 mg/day i.v.) and 56 that received placebo. It was established that if any patient developed systemic inflammatory response, organic failure, any kind of infection or clinical deterioration, this patient would be discontinued from the protocol with open antibiotic treatment. Their results showed that the use of antibiotics did not reduce pancreatic infection (12% antibiotics vs. 9% placebo, p = n.s.) and mortality (5% antibiotics vs. 7% placebo, p = n.s.). However, 28% of patients in the group that received antibiotics had their protocol opened, versus 46% in the placebo group (p = 0.037). Furthermore, the mean time to open the protocol was 11.5 days in the treatment group and 5 days in the placebo group (Table 2). Based on these data, it is reasonable to suppose that a group of patients had benefits receiving early antibiotics.

ING. AMIKACIN 500 mg IV BD 

Gram negative and Gram positive organisms and fungi may have an important role in infective morbidity and mortality in acute pancreatitis, and selective decontamination with antibiotics like amikacin reduced the incidence of translocation related infections and early mortality in patients with acute necrotizing pancreatitis.

TPN ( Total Parenteral Nutrition )

The experimental data suggests that use of TPN in patients with acute pancreatitis and pancreatic malignancy might result in some clinical benefit by decreasing activity of the pancreas compared to placebo.
Patients with necrotizing pancreatitis suggests that EN may cause complications in  patients  with ductular damage. In the second week, the patients with acute pancreatitis and enteral route of food administration developed >50% pancreatic necrosis, resulting in gastroduodenal obstruction and pain, leading to the use of TPN being a safer and a recommended option.

IV NS / RL 

Fluid resuscitation has emerged as a key therapeutic strategy in patients with acute pancreatitis. It has to be acknowledged that fluid resuscitation in AP is a complex process, with need to take into account the dynamics of fluid sequestration during different stages of the disease. Current knowledge suggests that controlled fluid resuscitation (3.0-4.0 L/24 h) should be started after a bolus infusion of 20 mL/kg (1000 mL over one hour). Among the different fluids, lactated Ringers’ is the one recommended by most guidelines. 



ING. OCTREOTIDE 

The pharmacological inhibition of exocrine pancreatic secretion with the somatostatin analogue octreotide has been advocated as a specific treatment of acute pancreatitis.

The complication rate was lower in the treatment group with regard to sepsis (24% vs 76%, P = 0.0002) and ARDS (28% vs 56%, P = 0.04). The hospital stay was shorter in the treatment group (20.6 vs 33.1 days, P = 0.04). Two patients died in the treatment group and eight in the control group (P < 0.019). These results suggest that octreotide may have a beneficial effect in the treatment of severe acute pancreatitis.

This trial shows that octreotide has no benefit in treatment of acute pancreatitis.


ING. PANTOP 

 Histology showed that PPZ treatment reduced tissue infiltration of inflammatory cells and acinar cell necrosis in severe AP. After PPZ treatment CD62P expression in mild AP and CD31 expression in severe pancreatitis decreased, indicating an inhibition of platelet activation. In mild and severe AP, PPZ significantly decreased amylase, LDH, edema and myeloperoxidase activity. Protein profile of pancreatic juice and serum revealed different spectra and less pancreatic juice proteins in PPZ treated groups indicating less acinar cell leakage.
"Mild AP was induced in rats by caerulein (n = 12). Severe AP was induced by infusion of glycodeoxycholic acid (10 mM) into the pancreatic duct combined with caerulein (n = 12). Both AP models were randomized to PPZ treatment (20 mg/kg at baseline and after 12 h) or placebo. Control animals received Ringer solution (n = 6) without AP induction. After 24 h severity of AP was examined by histology, enzyme levels, edema and inflammatory markers (myeloperoxidase, protein profiling). Furthermore, CD62P and CD31 for leukocyte and platelet activation were investigated"


ING. THIAMINE 

Thiamine is often recommended to patients with chronic alcoholism to prevent the side effects of Wernicke's encephalopathy and other side effects.

ING. TRAMADOL

Tramadol is a better analgesic compared to placebo .
Pain intensities (mean ± SD, 0 = none, 100 = unbearable) before treatment and on day 4 were 75 ± 19 and 8 ± 13 with tramadol (P < 0.001), and 65 ± 21 . On day 4, 67%of patients with tramadol rated their analgesia as excellent (P < 0.001) with mean respective doses of840 mg (range: 80-1920) . OroFecal transit was unchanged after five days of tramadol. Rectal distension threshold pressures increased with tramadol (P < 0.01). It is concluded tramadol is a potent analgesic in severe chronic pancreatitis pain. Tramadol interfered significantly less with gastrointestinal function and was more often rated as an excellent analgesic.



Approach to the patient:


B) A 25 year old man, daily wage worker and tractor driver by occupation, presented with severe abdominal pain since 4 days, One episode of vomiting 2 hours before presenting to hospital, Shortness of breath on walking since 2 hours


QUESTIONS : 

1) What is causing the patient's dyspnea? How is it related to pancreatitis?

Answer : 

The cause of dyspnea is most probably due to acute pancreatitis in the patient. The mechanism of causing dyspnea in pancreatitis patient is : 

With severe pancreatitis there are a lot of inflammatory chemicals that are secreted into the blood stream. These chemicals create inflammation throughout the body, including the lungs

Two different phases in ALI(Acute lung injury) and ARDS (Acute respiratory distress syndrome) have been described. Initially, an exudative phase during the first days with diffuse alveolar damage, microvascular injury, type I pneumocyte necrosis, and influx of inflammatory cells and fluid to the pulmonary interstitium has been seen, followed by a fibro-proliferative phase during days 3-7, during which type II pneumocyte hyperplasia, proliferation of fibroblasts and lung repair occur. As a consequence of a pronounced and complex systemic net pro-inflammatory response, both endothelial and epithelial injury is involved in ALI and ARDS

Thus ALI and ARDS often lead to shortness of breath and present as dyspnea.

2)Name possible reasons why the patient has developed a state of hyperglycemia 

Answer : 

The metabolic response during acute pancreatitis may depend on the one hand on acute stress, which is similar to that seen in other diseases such as sepsis or clinical situations such as surgical interventions, and on the other hand on damage to the Langerhans’s islets related to pancreatic inflammation. Hyperglycemia develops rather often in the early phase of acute pancreatitis, mainly in patients with severe disease . This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 

Hence the two reasons for a hyperglycemic state are :
  •  One is because that sympathetic hyperactivity makes glucagon elevated.
  •  Secondary, microcirculation disorder makes pancreas edema, ischemia and necrosis, affecting secretion and excretion of insulin. In severe acute pancreatitis, there may be ketoacidosis

3)What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

Answer:

The patient is a chronic alcoholic and hence he has elevated liver enzymes and abnormal LFT
Alcohol is known to cause Alcoholic fatty liver and alcoholic hepatitis which eventually lead to elevated liver enzymes in the body

Liver enzymes are typically elevated in chronic alcoholics , and tests of liver function may be abnormal. Up to 35% of heavy drinkers develop alcoholic hepatitis, and of these 55% already have cirrhosis. AH can be mild or severe. 

No laboratory test is diagnostic of Alcoholic fatty liver. Characteristic ultrasonographical findings include a hyperechoic liver with or without hepatomegaly. Computed tomography (CT) and magnetic resonance imaging (MRI) can readily detect cirrhosis. The biochemical markers for chronic alcohol consumption that have been most commonly studied are serum GGT, AST, ALT, mean corpuscular volume (MCV) and carbohydrate-deficient transferrin (CDT). An AST to ALT ratio over 2 is highly suggestive of ALD. 

4) What is the line of treatment in this patient?

ANSWER:
C) A 45 year old female patient came to the OPD with fever, pain abdomen, decreased urine output and abdominal distention.


1. What is the most probable diagnosis in this patient?

ANSWER: Hemoperitoneum may be a possible diagnosis.

2. What was the cause of her death?

ANSWER: It's possible for blood to accumulate in the cavity extremely quickly. This could have caused her to go into shock from blood loss, become unresponsive, and may have resulted in death.

3. Does her NSAID abuse have something to do with her condition? How?

ANSWER: NSAID abuse may have been a reason behind her hepatomegaly as they are known to cause drug induced hepatitis which in turn leads to cirrhosis.



5)  NEPHROLOGY:

A) A 52 yr old male patient , presented to hospital with Chief Complaints of SOB , burning micturition and fever.


1. What could be the reason for his SOB ?

ANSWER:  It may be due to pulmonary renal syndrome caused secondary to AKI or could have been due to TURP syndrome.

2. Why does he have intermittent episodes of drowsiness ?

ANSWER: The patient presented with drowsiness because of the underlying hyponatremia. Mild hyponatremia generally causes extreme lethargy , weakness , drowsiness which are due adaption of brain to decreased osmolality.

3. Why did he complaint of fleshy mass like passage in his urine?

ANSWER: The patient felt that the pus cells to be a mass like thing in his urine bag.

4.What are the complications of TURP that he may have had?

ANSWER: complications caused in the patient post TURP are:
  • Hyponatremia
  • Urinary tract infection
  • TURP syndrome

B) An 8 year old boy was brought to the OPD with the chief complaint of frequent urination.


1. Why is the child excessively hyperactive without much of social etiquettes ?

ANSWER: This presentation in the child may be due to ADHD which may also be the reason for frequent urination owing to associated urination disorders.

2. Why doesn't the child have the excessive urge of urination at night time ?

ANSWER: The child doesn't have excessive nocturnal urination may be due to OCD as in psychosomatic.

3. How would you want to manage the patient to relieve him of his symptoms?

ANSWER: Reassurance and relaxation as of now, since we haven't arrived on a diagnosis and he doesn't have any urological abnormalities.



6) INFECTIOUS DISEASE:

A) A 40 year old female came to the OPD with chief complaints of difficulty in swallowing, fever and cough.


1. Which clinical history and physical findings are characteristic of tracheo esophageal fistula?

ANSWER: The symptoms characteristic to TE fistula are:
  • Dysphagia more to solids initially and later to liquids also
  • Hoarseness of voice
  • Laryngeal crepitus
  • Regurgitation of food
  • Cough on consumption of food or liquids
2. What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?

ANSWER:

An international meta-analysis showed that TB-associated IRIS occurred in 15.7% of patients who were treated for both HIV and TB . Since the patient is being treated for both HIV and Tb there is a greater risk of developing IRIS in her.

Prevention strategies: 

The timing of the start of the ART is crucial in preventing paradoxical IRIS. According to a trial that evaluated starting antiretroviral therapy at three points in TB (SAPiT), ART initiation in TB–HIV patients should be decided based on their CD4 cell counts. If the CD4 counts are <50 cells·mm−3, ART can be started immediately after the initiation of TB treatment. If the CD4+ cell counts are ≥50 cells·mm−3, ART can be delayed.


7) INFECTIOUS DISEASE AND HEPATOLOGY:


A) A 55 year old male patient who is a palm tree climber by occupation came on 17th April 2021 with the chief complaints of  pain abdomen since one week decrease appetite since one week fever since two days 


Patient details : https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html


QUESTIONS : 


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? 


Answer : 


Yes , chronic consumption of locally made alcohol might have caused the liver abscess in this patient. Liver abscess is commonly caused due to organisms such as amoeba and other infections. Locally made alcohol is an important predisposing factor for both pyogenic and amebic liver abscess due to the alcoholic effects on the liver 

From our study 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 


References:  https://www.msjonline.org/index.php/ijrms/article/view/2414#:~:text=Conclusion%3AFrom%20our%20study%20it,of%20alcohol%20over%20the%20Liver.


2) What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)


Answer : 


Reason for the association between local alcohol beverages and ALA could be multifactorial. Factors influencing the association could be related to: 

  •  the pathogen,
  •  contents of beverages, 
  • status of the liver, and 
  • the immunity of the host. 
  • nutritional status of the population
  •  poor sanitation
They are more vulnerable perhaps due to the large infective dose of Entamoeba histolytica and other bacterial pathogens ingested with the unhygienically brewed beverage. Alcohol-induced hepatic dysfunction and possible suppression of amoebistatic immune mechanisms by substances in the beverages could also be attributed in the mechanism .

 "Alcohol can predispose to ALA through a multitude of mechanisms, including hepatic damage by alcohol, lowered body resistance and suppression of liver function due to poor nutritional status of habitual consumers of alcohol, increased presence of amoebae in the liquor prepared locally with poor regard to aseptic procedures, and depression of immune mechanisms in chronic alcoholics.” A study conducted in India in 2011 showed that 67.5% of patients with amoebic liver abscess are from the low socioeconomic class and 72% were alcoholics. It was also noted that alcoholics had larger abscesses, a greater frequency of complications, and delayed resolution of the abscesses.


All these predisposing factors lead to the causation of pyogenic liver abscess due to amebic infection and other infections of the liver.


References : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/


3) Is liver abscess more common in right lobe ?


Answer : Yes , liver abscess is more common in right lobe owing to the fact that it is a more significant part with more blood supply, less commonly in the left liver lobe or caudate lobe. 


The usual pattern of abscess formation is that there is leakage from the bowel in the abdomen that travels to the liver through the portal vein. Many cases have an infected biliary tract that causes an abscess via direct contact.


4) What are the indications for ultrasound guided aspiration of liver abscess ?


Answer : 


USG guided aspiration of liver abscess is required in: 


•Large liver abscess

•Those patients who appear to be superinfected 

•Large abscesses impending rupture/ compression signs 

•Thin rim of liver tissue around the abscess

•Sero negative abscess

•Failure in treatment following non invasive treatment for 4-5 days 



B) A 21 yr old male student, came to the hospital with the chief complaints of abdominal pain and fever .


1. Cause of liver abscess in this patient ?

ANSWER: The cause of liver abscess in the patient maybe infection. This infection may have been acquired from the toddy he drinks occasionally.

2. How do you approach this patient ?

ANSWER:

3. Why do we treat here ; both amoebic and pyogenic liver abcess?

ANSWER:

Considering the following factors:
  • Age and gender of patient: 21 years ( young ) and male.
  • Single abscess.
  • Right lobe involvement. ## The abscess is most likely AMOEBIC LIVER ABSCESS … ** But most of the patients with amoebic liver abscess 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 ; abscess is not accessible for aspiration if it is in posterior aspect or so. 2) Sometimes ; it has thin thin wall which may rupture if u aspirate. 3) Sometimes ; it is uniquified. ## Due to lack of resources , we cannot confirm whether it is pyogenic / amoebic , so we treat them both empirically in clinical practice.
Reference: https://academic.oup.com/bmb/article/132/1/45/5677141


4. Is there a way to confirm the definitive diagnosis in this patient?

ANSWER:

Diagnosis of pyogenic liver abscess
  1. an abdominal ultrasound to locate an abscess.
  2. a CT scan with intravenous contrast, or injected dye, to find and measure the abscess.
  3. blood tests to look for signs of infectious inflammation, such as an increased serum white blood count and neutrophil level.




8) INFECTIOUS DISEASES AND HEPATOLOGY:

A) 50/Male  came with chief complaints of fever since 10 days facial puffiness and periorbital edema ,  weakness of right upper limb and lower limb, altered sensorium.


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?


Answer : 


a) Evolution of symptomatology:




Diagnosed with hypertension- 3 years back: 

 ↓

 COVID vaccination - 16 days ago

[ fevers, chills and rigors, low grade fever, no diurnal, Following this the patient had similar complaints for the next three days ]

↓

Generalized weakness, facial puffiness and periorbital edema - 10days ago

-Patient was in a drowsy state

↓

 Altered state with facial puffiness and periorbital edema- since morning 

 weakness of upper and lower limbs




b) Anatomical localization of the problem:


The patient mainly presented with facial puffiness and periorbital edema localized to the medial eye canthus of the right eye. The patient also had extreme weakness of upper and lower limb. He also complained of generalized weakness of the whole body and altered/drowsy mental state.


c)Primary etiology of the patient’s problem:


The patient was in an immunocompromised state due to his chronic undiagnosed diabetes mellitus of type 2. Hence this caused him to develop mucormycosis leading to the disease.


The patient also had a chronic hypertension due to which there was a cerebrovascular attack leading to an infarct in his left temporal and frontal 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?


Answer : 


The pharmacological modalities used are 


Itraconazole :


 Itraconazole is the only marketed azole drug that has in vitro activity against Mucorales  There are case reports of successful therapy with itraconazole alone. However, itraconazole prophylaxis has been described as a risk factor for breakthrough mucormycosis. Therefore, itraconazole should not be considered a first-line agent against mucormycosis, but its use may be considered as adjunctive therapy in selected situations where highly susceptible fungi have been cultured.


Approach as a physician: 



3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time? 


Answer: 


India is has a high number of diabetics and other immunocompromised patients. During recent times and also in COVID settings the indiscriminate and non judicious use of steroids has increased the number of immunocompromised individuals in the community. This has lead to the vast and sudden increase in the mucormycosis condition in the community which was not a notified disease in the country. This is the main reason for the sudden spike in the cases of mucormycosis in India. 


9) MASTER SHEET- COVID 19


https://drive.google.com/file/d/1rBf7kPbRw2tra-Mum0sQnoGrZu-IO81s/view?usp=sharing



10) MAY 2021 LOG:

10TH MAY: Discussion on the main stay treatment in COVID patients.

11th May: Discussion on a case about ICU psychosis in a COVID patient.

13th May: Discussion on a telemedicine case of a child with frequent urination.

14th May: Discussion on a case of pericardial effusion and it's etiology.
Read about pathophysiology of pericardial effusion and anthrax disease.

15th May: Prepared an ELOG on a case of acute MI with uncontrolled sugars. Read about myocardial infarction and percutaneous interventions.

17th May : Discussion on the overuse of percutaneous intervention in MI and stroke.

18th May: Discussion on a case of  cerebrovascular infarction.

19th May: Prepared an ELOG on a case of viral pneumonia secondary to COVID 19.
Read about pulmonary fibrosis in COVID survivors.

20th May: Discussion on a case of tracheo esophageal fistula. Read about the types of tracheo esophageal fistulas.

24th May : Started working on the monthly assignment. Read about COPD .

This telemedicine has been a great opportunity to learn about various conditions in this current scenario of COVID. This has provided us with a platform to be exposed to various clinical scenarios. The discussions around these cases have given us an outlook on the various differential diagnosis to the symptoms of the patients. Numerous research papers shared on various topics have given us an insight about the logistics and details on the cases.





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