I have been given the following cases to solve in an attmept 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.
Name :- Chenna Bhavana
Roll No :- 20
This is the link of the Questions asked regarding the Cases:-
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the Medicine Assignment based on my Comprehension of cases :-
1) Pulmonology :-
A 55 Year Old Female with Shortness of Breath, pedal Edema and Facial Puffiness.
Link to the Patient Details :-
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1)what is the evolution of symptomatology in
this patient in terms of an event timeline and
Where is the anatomical localization for the
Problem and what is the primary etiology of
Patient's problem?
A :- Timeline of Symptomatology in this Patient :-
20 years Ago ( January,2001) :- She had Shortness of breath which lasted for 1 week during which time she was working in a paddy field. This First episode was relieved upon taking Medication.
For the next Eight years (2002-2009) :- She had suffered from similar episodes of SOB every year which lasted for 1 week and occuring around January when she worked at paddy fields. All these episodes were relieved upon taking Medication.
12 years Ago (2009) :- She had another episode of SOB which lasted for 20 days and had to be Hospitalized.
From the past 12 years (2009-2021) :- She has been having an yearly episodes which have lasted for month again around January, which are of Grade 2.
8 years Ago (2013) :- She was diagnosed with Diabetes when she had seeked help for her Polyuria and is being treated for it ever since.
5 years Ago (2016) :- She was treated for Anaemia with Iron injections.
1 month Ago ( April,2021) :- she had Generalized Weakness for which she was administered IV fluids
(3 pints in 2 days) by a local RMP.
30 days Ago (17/04/2021) :- She had latest episode od SOB.
20 days Ago (27/04/2021) :- Due to the ongoing COVID 19 pandemic, she had an HRCT done outside which showed the signs of Bronchiectasis.
20 days Ago (27/04/2021) :- She was diagnosed with Hypertension and is being treated for the same.
Since 15 days (02/05/2021) :- She has pedal edema upto the level of ankle which is of Pitting type.
Since 15 days (02/05/2021) :- She developed Facial puffiness.
Since 2 days (15/05/2021) :- She started having SOB even at rest ( Grade 4) which not relieved with nebulizers. She also has Drowsiness and Decreased Urine output.
Anatomical Localization :- It is the Lungs, Particularly the Bronchioles.
Primary Etiology :- Exposure to the environmental pollutants, in the paddy fields.
2) What are mechanism of action, indication
and efficacy over placebo of each of the
pharmacological and non pharmacological
interventions used for this patient?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
1 . Head End Elevation :
Mechanism of Action :- The Head of the Mechanically Ventilated patients should be maintained between 30° and 45° to reduce the risk of Aspiration and mechanical Ventilation associated Pneumonia by improving the End expiratory Lung volume.
• In addition to promoting a reduction in the
risk of developing pneumonia, some postural positions can increase the possibility of more Homogeneous Alveolar Ventilation and possibly reduce the risk of Lung injury caused by mechanical ventilation.
2. O2 Inhalation to maintain SPO2 above
92% :
3. Intermittent BiPAP for 2 hours :
Mechanism of action :- Bilevel positive airway pressure involves both IPAP and EPAP.
• IPAP (Higher Pressure) gives inspiratory Support to augment the tidal volume which assists CO2 clearance.
• EPAP ( Lower Pressure) prevents alveoli closure at expiratory phase which Increases the Lung volume and Functional Residual Capacity, Improves alveolar exchange and Oxygenation.
• EPAP = CPAP = PEEP.
Indications :-
• Chronic obstructive pulmonary disorder (COPD)
• Obstructive sleep apnea
• Obesity hypoventilation syndrome
• Pneumonia
• Asthma flare-up
• Poor breathing after an operation
• Neurological disease that disturbs breathing
4. Injection. AUGMENTIN 1.2 gm IV BD
( Amoxicillin and Potassium clavulanate) :
Mechanism of Action :- Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis.
• Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.
Indications :-
• Middle ear (Acute Otitis Media) nad and Sinus infections.
• Respiratory tract Infections (Bronchitis).
• Urinary tract Infections.
• Skin and Soft tissue Infections.
• Bone and joint Infections
5. TAB. AZITHROMYCIN 500mg OD :
Mechanism of Action :- Azithromycin is a Macrolide Antibacterial Drug.
• It works by decreasing the production of protein, thereby stopping bacterial growth.
Indications :-
• Prevention and treatment of acute bacterial exacerbations of chronic obstructive pulmonary disease due to H. influenzae, M. catarrhalis, or
S. pneumoniae.
• Community-acquired pneumonia due to C. pneumoniae, H. influenzae, M. pneumoniae, or S. pneumoniae.
• Uncomplicated skin infections due to S. aureus, S. pyogenes, or S. agalactiae.
• Urethritis and cervicitis due to C. trachomatis or N. gonorrhoeae.
• Trachoma due to C. trachomatis.
• Genital ulcer disease (chancroid) in men due to H. ducrey.
• Acute bacterial sinusitis due to H. influenzae, M. catarrhalis, or S. pneumoniae.
• Acute otitis media caused by H. influenzae, M. catarrhalis or S. pneumoniae.
• Pharyngitis or tonsillitis caused by S. pyogenes as an alternative to first-line therapy in individuals who cannot use first-line therapy.
6. Injection. LASIX IV BD if SBP greater than 110 mmHg :
Mechanism of Action :-Furosemide, like other loop diuretics, acts by inhibiting the luminal Na - K - Cl co-transporter in the thick ascending limb of Loop of henle, by binding to the chloride transport channel, thus causing sodium, chloride and Potassium loss in urine .
• It also abolishes the cortico - medullary osmotic gradient and blocks negative as well as positive free water clearance. Because of the large NaCl absorptive capacity of the loop of Henle, diuresis is not limited by development of acidosis, as it is with the carbonic anhydrase inhibitors.
• Additionally, Furosemide is a noncompetitive subtype-specific blocker of GABA-A receptors.
•Furosemide has been reported to reversibly antagonize GABA-evoked currents of α6β2γ2 receptors at μM concentrations, but not α1β2γ2 receptors. During development, the α6β2γ2 receptor increases in expression in cerebellar granule neurons, corresponding to increased sensitivity to furosemide.
Indications :-
• Treatment of Hypertensive emergency
• Treatment of Edema
7. TAB. PANTOP 40 mg PO OD :
Mechanism of Action :- It inhibits the final step in gastric acid production.
• In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
• The covalent binding prevents acid secretion for up to 24 hours and longer.
Indications :-
• For heartburn and chest pain due to stomach acid reflux disease in which acidic content from stomach comes up to food pipe and mouth.
• For the treatment of ulcers of stomach and intestine and inflammation and erosion of food pipe due to stomach acid.
• Gastro- esophageal reflux disease.
8. Injection. HYDROCORTISONE 100 mg IV :
Mechanism of Action :- Hydrocortisone injection belongs to class of drugs called glucocorticoids, or steroid hormones.
• Hydrcortisone injection works by reducing inflammation ( Irritation and Swelling ) in the body.
Indications :-
• Arthritis
• Severe Allergies
• Blood diseases
• Breathing Problems
• Certain Cancers
• Eye diseases
• Intestinal disorders
• Skin diseases
9. Nebulizer with IPRAVENT, BUDECORT
6 Hourly :
Mechanism of Action :-
BUDECORT is a potent topical anti-inflammatory agent.
• It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT).
• This budesonide-CBP (HAT) receptor complex prevents the production of inflammatory genes (inhibition of gene transcription) that might cause bronchoconstriction.
IPRAVENT is an acetylcholine antagonist via blockade of muscarinic cholinergic receptors.
• Blocking cholinergic receptors decreases the production of cyclic guanosine monophosphate (cGMP).
• This decrease in the lung airways will lead to decreased contraction of the smooth muscles.
• The actions of intranasal ipratropium mimic the action of atropine by inhibiting salivary and mucous glands secretions as well as dilating bronchial smooth muscle.
Indications :-
• Chronic Obstructive pulmonary disease (COPD).
• Asthma
10. TAB. PULMOCLEAR 100 mg PO OD
Mechanism of Action :-
• Acebrophylline works by relaxing the smooth muscles of airways and induces the release of pulmonary surfactants which helps in the clearance of congestion.
• Acetylcysteine breaks down and loosens thick phlegm, making it runny and easy to cough up and clears the airway.
Indications :-
• COPD
11. Chest Physiotherapy :
Mechanism of Action :- Manual chest Physiotherapy (MCP) involves external manipulation of the thorax using Percussion and vibration techniques.
• Their purpose of these is to intermittently to apply kinetic energy to the chest wall to dislodge bronchial secretions.
• The Patient then clears these secretions with an expiratory manoeuvre such as forced expiration technique (FET).
Indications :-
• Cystic fibrosis
• Bronchiectasis
• Atelctasis
• Lung abscess
• Neuromuscular diseases
• Pneumonias in dependent lung regions
12. Injection HAI SC (8pm-2pm-8pm) :
• Insulin is crucial to allow the entry of blood glucose into each cell of the body.
• In type 1 diabetes mellitus, the body fails to produce adequate insulin.
• This medicine lowers blood sugars by stimulating glucose uptake by cells, tissue and muscles, especially by skeletal muscles and fat and by inhibiting glucose production by the
liver.
Indications :-
• Diabetes Mellitus
13. TEMP, BP, PR, SPO2 Monitoring
14. I/O Charting
15. Injection THIAMINE 1 Amp in 100 ml of
NS :
Mechanism of Action :- Thiamine combines
with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate.
• Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
Indications :-
• Beri Beri and inflammation of the Nerves
Neuritis associated with Pellagra or Pregnency.
• Thiamine is also used for digestive problems including Poor appetite, Ulcerative Colitis and Ongoing diarrhoea.
• Thiamine is also used for AIDS and Boosting the immune system, Diabetic Pain, Heart disease, alcoholism, Aging, Cerebellar syndrome, Canker sores, Cataracts and Glaucoma, Motion sickness and improving Athletic performance.
• Other uses include preventing cervical cancer and progression of kidney disease in patients with type 2 diabetes.
• We can also give thiamine shots for a Memory disorder called Wernicke's Encephalopathy syndrome, other thiamine deficiency syndromes in Critically ill people, Alcohol withdrawal amd coma.
16. GRBS 6 Hourly
3) What could be the causes for her current
Acute exacerbation?
A :- The most common cause of an exacerbation is infection in the lungs or airways (breathing tubes).
• This infection is often from a virus, but it may also be caused by bacteria or less common types of organisms.
• In this Patient, it could be the bacterial Infection which was responsible for her Acute Exacerbation of COPD
( Mycobacterium tuberculosis )
4) Could the ATT have affected her symptoms?
If so how?
A :- Yes, ATT may be the cause for her Generalized weakness. Patient also had pedal edema and facial puffiness after 1 week of therapy which indicates that follo up care and early intervention for COPD may be necessary for TB Patients.
"our results showed that a history of TB caused more hospitalizations, reduced respiratory functions and increased PaCO2. It was found that, despite similarity of the overall mortality, COPD diagnosis and death occurred 5 years earlier in patients with past TB. We conclude that history of TB has an important role in the natural course of COPD."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5261555/#:~:text=Conclusion,in%20patients%20with%20past%20TB.
5) What could be the causes for her electrolyte
imbalance?
A:- Chronic hypoxia and hypercapnia secondary to the underlying pulmonary illness, heart failure or renal insufficiency, use of diuretics, SIADH, hypokalemia attributed to steroids bronchodilators, malnutrition, and poor intake
of food during acute exacerbations are common contributing factors for Hyponatremia in Chronic Obstructive pulmonary disease.
• Respiratory Acidosis occurs when breathing out does not get rid of enough CO2. The increased CO2 that remains results in an acidic state. This can occur as a result of respiratory problems, such as COPD.
• Respiratory acidosis with metabolic alkalosis (due to renal compensation) in AECOPD patients with chronic hypercapnia is the usual cause of Hypochloremia in these patients.
2) Neurology :-
A) A 40 Year Old Male with Complaints of Irrelevant Talking.
Link to the Patient Details :-
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
12 years Ago (2009) :-He started drinking Alcohol.
2 years Ago (2019) :- He was diagnosed with Type 2 Diabetes mellitus for which he was prescribed Oral Hypoglycemics.
1 year Ago (2020) :- He had an episode of Seizures.
4 months Ago (January) :- He had another episode of seizures (Most probably GTCS) following Cessation of Alcohol for 24 hours which was associated with restlessness, Sweating and Tremors, and started drinking Alcohol again after the seizures subsided.
Since 9 days (06/05/2021) :- Irrelevant Talking where he started talking as well as laughing to himself and was unable to lift himself off the bed and move around, so had to be assisted.
Since 9 days (06/05/2021) :- Decrease in Food intake for which he was taken to local RMP and given IV fluids
Since 9 days (06/05/2021) :- He also had Short term memory loss where he couldn't recognise his family members.
10/05/2021, Monday :- On this day, He had his Last alcohol intake when he drank around
1 bottle.
15/05/2021 :- He was admitted to Tertiary care Hospital.
Anatomical Localization :- Thalamus and hypothalamus are most commonly affected in Wernicke's Encephalopathy.
Primary Etiology :- Chronic Alcoholism.
2) What are the Mechanism of action, indication
and efficacy over placebo of each of the
pharmacological and non pharmacological
interventions used for this patient?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
1. IVF NS and RL 150ml/hr :
Mechanism of Action :- Administer intravenous (IV) fluids such as Normal saline (NS) and Ringer Lactate (RL) for rehydration, as and when necessary.
• Most patients with severe alcohol withdrawal are significantly dehydrated, and their fluid requirements range from 4-10 L in the first 24 hours.
• Because hypoglycemia is common in these patients due to depleted glycogen stores, a 5% dextrose solution (in 0.90% or 0.45% saline) should be used to prevent hypoglycemia
2. Injection.1 amp THIAMINE in 100ml NS
TID :
Mechanism of Action :-It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1 (thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome, cerebellar degeneration, and cardiovascular dysfunction.
• If the thiamine deficiency is left untreated, these complications can result in irreversible damage to several parts of the central nervous system (CNS).
Indications :-
• Beri Beri and inflammation of the Nerves
Neuritis associated with Pellagra or Pregnency.
• Thiamine is also used for digestive problems including Poor appetite, Ulcerative Colitis and Ongoing diarrhoea.
• Thiamine is also used for AIDS and Boosting the immune system, Diabetic Pain, Heart disease, alcoholism, Aging, Cerebellar syndrome, Canker sores, Cataracts and Glaucoma, Motion sickness and improving Athletic performance.
• Other uses include preventing cervical cancer and progression of kidney disease in patients with type 2 diabetes.
• We can also give thiamine shots for a Memory disorder called Wernicke's Encephalopathy syndrome, other thiamine deficiency syndromes in Critically ill people, Alcohol withdrawal amd coma
.
3. Inj. LORAZEPAM
Mechanism of Action :- It involves enhancing
the effects of the neurotransmitter gamma-amino butyric acid (GABA) in the brain.
• This slows down nerve impulses throughout the entire body and drastically reduces the brain’s output of other neurotransmitters such as Norepinephrine, Serotonin, acetyl choline and dopamine.
• These neurotransmitters are necessary for alertness, memory, muscle tone and coordination, emotional responses, endocrine gland secretions, heart rate, and blood pressure.
• The use of benzodiazepines impairs all of these functions which results in a relaxed state.
Indications :-
• Anxiety
• Psychosomatic Disorders
• Premedication
• Status epilepticus
• Insomnia due to anxiety
• Acute Panic attacks
4.TAB. PREGABALIN 75mg PO BD
Mechanism of Action :- Pregabalin is structurally related to the antiepileptic drug, gabapentin and the site of action of both drugs is similar, the Alpha 2 - delta protein, an Auxiliary subunit of voltage - gated calcium channels.
• Pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha 2 - delta subunits, and possibly accounting for its actions in vivo to reduce neuronal excitability and seizures.
Indications :-
• Neuropathic pain
• Epilepsy/Seizures
• Fibromyalgia
5. Injection HAI SC - Premeal
Mechanism of Action :- Insulin is crucial to allow the entry of blood glucose into each cell of the body.
• In type 1 diabetes mellitus, the body fails to produce adequate insulin.
• This medicine lowers blood sugars by stimulating glucose uptake by cells, tissue and muscles, especially by skeletal muscles and fat and by inhibiting glucose production by the
liver.
Indications :-
• Diabetes Mellitus
6. GRBS 6th hourly, Premeal - 8am, 2pm, 8pm, 2am
7. LACTULOSE 30ml PO BD
Mechanism of Action :- To treat or prevent complications of liver disease (hepatic encephalopathy).
• It does not cure the problem, but may help to improve mental status.
• Lactulose is a colonic acidifier that works by decreasing the amount of ammonia in the blood. It is a man-made sugar solution.
Indications :-
• Constipation
• Portal systemic Encephalopathy
8. Injection 2 ampoule KCl ( 40mEq ) in 10 NS
over 4 hours :
Mechanism of Action :-
Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.09
Indications :-
• Treatment of severe hypokalaemia (arrhythmia, marked muscular weakness, rhabdomyolysis or serum potassium level ≤ 2.5 mmol/litre).
9. SYP. POTCHLOR 10ml in one glass water
PO BD :
Mechanism of Action :- Potchlor liquid contains potassium chloride which is an essential component for many important functions of the body like muscle contraction, nerve transmission, proper functioning of kidney etc.
• It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium.
Indications :-
• Hypokalemia
This medicine is used for the prevention or treatment of low potassium levels in the blood.
For the ulcer:
1. Daily dressing
2. Megaheal ointment :
Mechanism of Action :- Megaheal gel contains colloidal silver. Colloidal silver is an anti-microbial agent and kills the bacteria by destroying the cell wall of the bacteria.
Indications :- For wound care on burns, cuts, minor skin injuries and skin tears.
3. Avoid pressure over ulcer
3) Why have neurological symptoms appeared
this time, that were absent during withdrawal
earlier? What could be a possible cause for this?
A :- When a person struggling with alcohol addiction quits and then relapses several times, they are at risk of developing Kindling .
• This condition is a worsening of withdrawal symptoms each time the individual attempts to quit alcohol again.
• The body becomes increasingly sensitive to changes in neurotransmitters, as GABA floods the brain during periods of drinking too much and is suddenly stopped during periods of abstinence.
• Over a few cycles, the risk of developing delirium tremens, seizures, and other health problems associated with unsupervised alcohol withdrawal dramatically increases.
4) What is the reason for giving thiamine in this
patient?
A :- Thiamine is useful in preventing Wernicke's Encephalopathy, 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.
5) What is the probable reason for kidney injury
in this patient?
A :- The sudden removal of alcohol can also cause kidney failure. Alcohol has to be broken down and cleared from the body as urine. This needs water, as the products of the breakdown have to be in solution.
• Alcohol also inhibits the production of an anti-diuretic hormone, so large quantities of alcohol make you urinate a lot and become dehydrated.
• Electrolytes in the body, such as sodium, magnesium, calcium and potassium, are usually in solution (water) and excessive amounts of alcohol can cause an imbalance in these electrolytes as well as an acid-base imbalance. These imbalances can eventually lead to acute kidney failure.
6). What is the probable cause for the
normocytic anemia?
A :- When you have kidney disease, your kidneys cannot make enough EPO. Low EPO levels cause your red blood cell count to drop and anemia to develop. Most people with kidney disease will develop anemia.
7) Could chronic alcoholism have aggravated
the foot ulcer formation? If yes, how and why?
A:- Excessive alcohol can cause Nutritional deficiencies and Alcohol toxicity.
• These in turn can cause Poor Nutrition leading to Poor wound Healing and problem with the nerves(Neuropathy).
• When the sensory nerves in the Foot stops working, the foot can get injured and this leads to Foot ulcers.
B) A 52 year Old male with Cerebellar Ataxia
Link to the Patient Details :-
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
Questions-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
1991 (Since 30 years) :- He has been consuming Alcohol which is approximately
90-180 ml daily.
13 / 05 / 2021 (7 days back) :- Patient had Giddiness which was subsided on taking rest and it was also associated with one episode of Vomiting.
13 / 05 / 2021 - 16 / 05 / 2021 ( For 3 days ) :- Stopped consumption of alcohol due to which he was asymptomatic for 3 days.
16 / 05 / 2021 :- starts consuming alcohol again.
17 / 05 / 2021 :- Developed Giddiness again which was associated with Bilateral Hearing loss, Aural fullness, Tinnitus and 2 to 3 episodes of Vomiting in a day and also postural instability.
18 / 05 / 2021 :- Admitted to Hospital.
Anatomical Localization :- Infarct in the right inferior Cerebellar Hemisphere.
Primary Etiology :- Long standing Undiagnosed Hypertension and Chronic alcoholism.
2) What are mechanism of action, indication
and efficacy over placebo of each of the
pharmacological and non pharmacological
interventions used for this patient?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
1. TAB VERATIN 8 mg PO TID
Mechanism of Action :-The active ingredient of Betahistine is Betahistine hydrochloride or Betahistinedemesytate.
• It works as a histamine analogue through 2 modes of action :
(1) Agonist of H1 receptors
(2) Antagonist of H3 receptors
• It has a weak effect on H1 receptors but strong effect on H3 receptors.
• It causes vasodilatattion in the inner ear and also acts as vestibular suppressant by acting on neurotransmitters which are responsible for carrying signals from primary neurons.
Indications :- Anti - Vertigo agent prescribed for Vertigo in those who have meniere's disease.
2. Injection ZOFER 4 mg IV TID
Mechanism of Action :- ZOFER Injection works by inhibiting the action of a chemical substance known as serotonin.
• Serotonin is responsible for inducing nauea 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 :-
• An antiemetic medicine commonly used to control nausea and vomiting due to certain medical conditions like stomach upset.
• It is also used to prevent nausea and vomiting caused due to any surgery, cancer drug therapy or radiotherapy.
3. TAB ECOSPRIN 75 mg PO OD
Mechanism of Action :- Ecosprin is an antiplatelet medicine.
• It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.
• When clot formation occurs in blood vessels, blood flow is obstructed or blocked, which can be dangerous in cases of heart attack and could lead to stroke or chest pain (angina).
Indications :-
• For the prevention of heart attack, stroke,
heart conditions such as stable or unstable angina (chest pain) due to a blood clot.
• Treatment of acute heart attack and blood clot formation after heart surgery.
• As a preventive measure in patients with a history of stroke due to blood clots or risk of vascular thrombosis (blood clot obstructing blood flow in a vein).
4. TAB ATORVASTATIN 40 mg PO HS
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.
•Atorvastatin also increases the number of LDL receptors on the surface of hepatic cells.
Indications :- Atorvastatin is also used to treat to lower the risk of stroke, heart attack, or other heart complications in people with type 2 diabetes, coronary heart disease, or other risk factors.
5. BP monitoring - 4th hourly
6. TAB CLOPIDOGREL 75 mg PO OD
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
• Symptomatic carotid artery stenosis
• Secondary prevention post-coronary artery bypass grafting
•Peripheral artery percutaneous angioplasty in peripheral artery bypass grafting
7. Injection THIAMINE 1 AMP in 100 ml NS PO BD :
Mechanism of Action :-It is well known that chronic alcoholics are at high risk for being deficient in vitamin B1 (thiamine), which is known to put the patient at an increased risk for Wernicke-Korsakoff Syndrome, cerebellar degeneration, and cardiovascular dysfunction.
• If the thiamine deficiency is left untreated, these complications can result in irreversible damage to several parts of the central nervous system (CNS).
Indications :-
• Beri Beri and inflammation of the Nerves
Neuritis associated with Pellagra or Pregnency.
• Thiamine is also used for digestive problems including Poor appetite, Ulcerative Colitis and Ongoing diarrhoea.
• Thiamine is also used for AIDS and Boosting the immune system, Diabetic Pain, Heart disease, alcoholism, Aging, Cerebellar syndrome, Canker sores, Cataracts and Glaucoma, Motion sickness and improving Athletic performance.
• Other uses include preventing cervical cancer and progression of kidney disease in patients with type 2 diabetes.
• We can also give thiamine shots for a Memory disorder called Wernicke's Encephalopathy syndrome, other thiamine deficiency syndromes in Critically ill people, Alcohol withdrawal amd coma
8. TAB MVT PO OD
Mechanism of Action :- Methylcobalamin is a form of vitamin B12 that restores its level in the body thereby helping in treating certain anemias and nerve problems.
Indications :- This medication is a multivitamin product used to treat or prevent vitamin deficiency due to poor diet, certain illnesses, or during pregnancy.
• Vitamins are important building blocks of the body and help keep you in good health.
Advice on Discharge :
1. TAB VERTIN 8 mg PO TID - 1 week
2. TAB ZOFER 4 mg IV TID - 1 week
3. TAB ECOSPRIN 75 mg PO OD - 1 week
4. TAB ATORVASTATIN 40 mg PO HS - 1 week
5. TAB CLOPIDOGREL 75 mg PO OD - 1 week
6. TAB MVT PO OD - 1 week
3) Did the patients history of denovo HTN
contribute to his current condition?
A :- Hypertension can cause stroke through :-
• A high intraluminal pressure will lead to extensive alteration in endothelium and smooth muscle function in intracerebral arteries.
• The increased stress on the endothelium can increase permeability over the blood-brain barrier and local or multifocal brain oedema.
• Endothelial damage and altered blood cell-endothelium interaction can lead to local thrombi formation and ischaemic lesions.
4) Does the patients history of alcoholism make
him more susceptible to ischaemic or
haemorrhagic type of stroke?
A :- Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain, Haemorrhagic Stroke.
C) A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS, RADIATING PAIN ALONG LEFT UPPER LIMB
Link to the Patient Details :-
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Questions:
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
2011 ( 10 years Ago ) :- She had one episode of Quadriplegic paralysis.
2020 ( 1 year Ago ) :- Right and Left Paresis due to Hypokalaemia.
October, 2020 ( Since 8 Months ) :- She developed Swelling over the Legs bilaterally which is of Pitting type.
March, 2020 ( 2 Months Ago ) :- Came to Hospital fot the Treatment of Neck pain for which she was advised Medication.
09 / 05 2021 ( 6 days Ago ) :- Pain along her Left upper limb which is in association with Tingling and Numbness.
10 / 05 / 2021 ( 5 days Ago ) :- Palpitations, Difficulty in Breathing ( NYHA - Grade 3 ), Chest Pain and Chest Heaviness
15 / 05 / 2021 :- Admitted into the Hospital.
Anatomical Localization :- Cervical spine
Primary Etiology :- Hypokalaemia, Old age
2) What are the reasons for recurrence of
hypokalemia in her? Important risk factors for
her hypokalemia?
A :- The following Risk factors are known to be associated with increased risk of Hypokalaemia :-
• Female
• Medications like diuretics
• Heart failure
• Hypertension
• Low BMI [3]
• Eating disorder and alcoholism
• Diarrhoea
• Cushing syndrome
3) What are the changes seen in ECG in case of
hypokalemia and associated symptoms?
A :- ECG changes seen in Hypokalaemia :-
• Increased P wave amplitude
• Prolongation of PR interval
• Widespread ST depression and T wave flattening/inversion
• Prominent U waves (best seen in the
precordial leads V2-V3)
• Apparent long QT interval due to fusion of T and U waves (= long QU interval)
D) 55years old patient with seizures.
Link to the Patient Details :-
https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1. Is there any relationship between occurrence
of seizure to brain stroke. If yes what is the
mechanism behind it?
A :- Yes, there is a relationship between the occurrence of seizures following Stroke.
Mechanism :-
Acute ischemic injury
↓
Accumulation of intracellular calcium and sodium
↓
Depolarization of transmembrane potential and other calcium mediated effects
(Local ionic shifts)
↓
Increased Excitability
↓
Lowering of Seizure threshold
• 2,12 Glutamate excito-toxicity is a well-established mechanism of cell death in the experimental stroke model.
• In the setting of large regions of ischemic hypoxia, high levels of excito-toxic neurotransmitters may be released extracellularly.
• Hypoxic-ischemic encephalopathy is one of the most common causes of status epilepticus and carries a poor prognosis.
• Particularly vulnerable to ischemic insult is
the hippocampus, which is an especially epileptogenic area.
• A gliotic scarring has been implicated as the nidus for late-onset seizures, just as the meningocerebral cicatrix may be responsible for late-onset post-traumatic epilepsy.
• Cortical location is among the most reliable risk factors for post-stroke seizures.
• Post-stroke seizures were more likely to develop in patients with larger lesions involving multiple lobes of the brain than in those with single lobar involvement.
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?
A :- Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures.
• Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures.
E) A 48 year Old male with seizures and altered sensorium
Link to the Patient Details :-
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Questions: -
( Referral links for the Answers
mentioned at the end of the Blog )
1) What could have been the reason
for this patient to develop ataxia in the past 1
year?
A :- The reason for this Patient to develop Ataxia in the past 1 year is Alcohol.
• The alteration in GABA receptor-dependent neurotransmission is a potential mechanism
for ethanol-induced cerebellar dysfunction.
• Ethanol-induced increases in GABA release are not only seen in Purkinje cells (PCs), but also in molecular layer interneurons and granule cells.
• Ethanol is shown to disrupt the molecular events at the mossy fiber – granule cell – Golgi cell (MGG) synaptic site and granule cell parallel fibers – PCs (GPP) synaptic site, which may be responsible for ethanol-induced cerebellar ataxia.
2) What was the reason for his IC bleed? Does
Alcoholism contribute to bleeding diathesis ?
A :- Reason for Intracranial Bleeding :-
• Chronic alcoholics
have decreased concentrations of liver-produced coagulation factors and platelet abnormalities that
predispose them to hemorrhagic stroke.
• The reduced
number of platelets and impaired platelet function would weaken the blood vessel wall, and combined with impaired coagulation factors, this predisposes alcoholics to ICH.
• In alcoholics with
hepatic damage, there may be decreased concentrations of clotting factors, increased fibrinolysis, and laboratory evidence of disseminated intravascular coagulation.
YES, Alcoholism contributes to the Bleeding diathesis.
F) A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWER LIMB.
Link to the Patient Details :-
http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1.Does the patient's history of road traffic
accident have any role in his present condition?
A :- There are 3 Main causes of stroke following a Car Accident :-
• The most common injury that car accident victims face is whiplash. This is caused by a collision with another car that severely and suddenly jerks your head and neck forward, resulting in the shredding of smooth muscle tissues. When the lining of arteries in your neck tears, it creates a large pressure of pooling blood that eventually gets trapped and forms a clot.
• Hemorrhagic strokes, on the other hand, can occur from less severe trauma. These types of strokes happen when blood from arteries seeps into the brain, usually a consequence of weakened blood vessels that rupture. These usually occur in people living with high blood pressure, but head injury from an automobile collision can also cause brain hemorrhage and induces a stroke.
• Depending on the type of collision that had occurred, a disruption of blood supply could trigger a stroke. If a car accident prevents a victim from being able to receive ample oxygen to the brain, and if the person has an underlying health issue, the narrowing of the arteries could be so severe that the stroke arises immediately.
2.What are warning signs of CVA?
A :- Warning Signs of Stroke :-
• 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?
A :- Drug Rationale in stroke :-
1. Injection MANNITOL 100ml IV TD :- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema.
•Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
2. TAB. ECOSPRIN 75 mg po OD :- Aspirin, which thins the blood and thereby prevents clots, is currently used to reduce the long-term risks of a second stroke in patients who've had an ischemic stroke.
• But giving aspirin to patients who've had a hemorrhagic stroke is considered dangerous, as it can cause more bleeding and more damage.
3. TAB ATORVAS 40mg po HS :- Statins, inhibitors of HMG-CoA reductase, are widely used cholesterol-lowering drugs and reduce the incidence of myocardial infarctions and stroke.
4. Does alcohol has any role in his attack?
A :- In this case, Alcohol may not have any role in his Stroke as he drinks Alcohol occasionally like once in a week.
5.Does his lipid profile has any role for his
attack??
A :- Patient has Decreased levels of HDL cholesterol.
• HDL cholesterol is inversely associated with the risk of Ischemic stroke, which means that decreased levels of HDL cholesterol increases the risk of Ischemic stroke.
G) A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY
Link to the Patient Details :-
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1)What is myelopathy hand ?
A :- Myelopathy Hand :-
• A characteristic Dysfunction of the Hand has been observed in several 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 as ”Myelopathy Hand".
• It appears 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.
2) What is finger escape ?
A:- Finger escape Sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi.
• This sign is also called as Wartenberg's sign.
Differential Diagnosis :-
- Cervical Myelopathy
- Ulnar Neuropathy
3)What is Hoffman’s reflex?
A :- Hoffmann's reflex is a 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.
Procedure :-
The Following steps should be followed while performing thi test :-
• Position the subject’s relaxed hand ensuring dorsiflexion at the wrist and partial flexion of the fingers.
• Hold the subject's partially extended middle finger between your index and middle finger, ensuring you stabilize the proximal IP joint.
Perform a sharp and forceful flick of your
thumb, making contact with the nail of the subject’s middle finger.
• The subject's finger will flex immediately followed by relaxation.
• The presence of Hoffmann's sign is characterized by flexion and adduction of the thumb and flexion of the index finger.
Interpretation :-
• A positive Hoffmann's sign is suggestive of corticospinal tract dysfunction localized to the cervical segments of the spinal cord.
• Conditions such as Multiple Sclerosis, Hyperthyroidism and Anxiety will also result
in positive sign.
• While the solitary presence of Hoffmann's sign is inconclusive for the diagnosis of cervical myelopathy,
unilateral positive sign is more specific and a bilateral positive finding is highly sensitive for confirmation of the same.
• Nevertheless, MRI remains the gold standard for diagnosing cervical myelopathies.
H) A 17 year Old female with Seizures.
Link to the Patient Details :-
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Questions: -
( Referral links for the Answers
mentioned at the end of the Blog )
1) What can be the cause of her condition ?
A :- The Cause of her condition could be Iron Deficiency Anaemia.
Iron deficiency and iron deficiency anemia may play an important role in inducing seizures
from the following mechanisms : -
1. Decrease of GABA inhibitory neurotransmitter due to change in its metabolism;
2. Change in neuron metabolism;
3. Reduction of enzymes such as monoamine and aldehyde oxidases ; and,
4. Impairment in oxygenation and energy metabolism of the brain
2) What are the risk factors for cortical vein
thrombosis?
A :- 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 anaemia
• 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?
A :-
4) What drug was used in suspicion of cortical
venous sinus thrombosis?
A :- Injection CLEXANE 0.4 ml SC which is a Low molecular weight HEPARIN, an Anticoagulant drug.
3) Cardiology :-
A) A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS
Link to the Patient Details :-
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1.What is the difference btw heart failure with
preserved ejection fraction and with reduced
ejection fraction?
A:-Heart Failure with Reduced Ejection Fraction :-
Biological Processes :-
• Regulation of Sequence - Specific DNA binding Transcription
• Smooth muscle cell proliferation
• Nitric oxide biosynthesis
Specific Markers :-
• AMP - dependant Transcription factor activating Transcription factor 2
• N - terminal pro - B - type natriuretic peptide
• Growth differentiation factor - 15 ( GDF - 15 )
• Interlukin 1 receptor - like 1
Heart Failure with Preserved Ejection Fraction :-
Biological Processes :-
• Cell adhesion
• Leucocyte Migration
• Inflammatory response
• Neutrophil degranulation
• Integrin mediated signalling pathways
• Extracellular matrix organisation
Specific Markers :-
• Integrin subunit Beta 2
• Catenin Beta 1
2.Why haven't we done pericardiocentesis in this
patient?
A :- Pericardiocentesis was not done in this Patient because 2.07 cm of Effusion at the time of admission waa reduced to 1.4 mm at the time of discharge which means that the Pericardial Effusion is Self resolving.
3.What are the risk factors for development of
heart failure in the patient?
A :- Risk factors for Heart Failure :-
• High blood pressure
• Diabetes
• Smoking
• Alcohol - Drinking too much alcohol can weaken heart muscle and lead to heart failure.
• Age
• Pericardial Effusion leading to Cardiac Tamponade - When fluid accumulates in the pericardial space, the intrapericardial pressure increases. This leads to a compression of the right heart, increasing the right heart pressure.
- The pressure prevents the heart's ventricles from expanding fully and keeps your heart from functioning properly. Your heart can't pump enough blood to the rest of your body when this happens. This can lead to Heart Failure.
• AV Block can be associated with severe bradycardia and hemodynamic instability. It
has a greater risk of progressing to third-degree (complete) heart block or asystole.
4.What could be the cause for hypotension in
this patient?
• If the fluid builds up quickly, it can cause
cardiac tamponade. This is a sudden build-up
of fluid in between the layers of the pericardium that keeps your heart from working like it should and can cause your blood pressure to drop.
B) A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT
Link to the Patient Details :-
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
Questions:-
( Referral links for the Answers
mentioned at the end of the Blog )
1.What are the possible causes for heart failure
in this patient?
A :- Possible Causes of Heart Failure :-
1) Hypertension
- When blood pressure is high, your heart has to pump harder to move blood to the body. This can cause the left ventricle to become thick or stiff, and you can develop HF-pEF.
- High blood pressure can also cause your coronary arteries to become narrow and lead to coronary artery disease.
2) Diabetes
3) Myocarditis
- Myocarditis is an inflammation of the heart muscle.
- It's most commonly caused by a virus, including COVID-19, and can lead to left-sided heart failure.
4) Obesity
- Obesity can cause the heart to work much harder than for a non-obese person.
- Being obese is also a cause of sleep apnea and can cause cardiomyopathy.
- When there aren't enough red blood cells to carry oxygen, the heart tries to move the small number of cells at a faster heart rate.
- It can become overtaxed from the effort.
6) Heart Muscle Disease ( Dilated cardiomyopathy, Hypertrophic Cardiomyopathy )
- Any damage to the heart muscle–whether because of drug or alcohol use, viral infections or unknown reasons–increases the risk of Heart failure.
7) Causes of acute heart failure include viruses that attack the heart muscle, severe infections, allergic reactions, blood clots in the lungs, the use of certain medications or any illness that affects the whole body.
2.what is the reason for anaemia in this case?
A :- Diabetes often leads to Kidney Damage , and failing kidneys can cause anemia. Healthy kidneys know when your body needs new red blood cells. They release a hormone called erythropoietin (EPO), which signals your bone marrow to make more. Damaged kidneys won't send out enough to cope up with out with your needs.
•Alcohol can impact red blood cell production as it decreases the number of precursor cells in the bone marrow, resulting in fewer mature blood cells to be made. In addition to this, alcohol can also impact red blood cell maturation, causing abnormality (shapes) or dysfunction of the cells. When enlarged red blood cells (due to alcohol) are produced, as a complication, they are likely to be destroyed faster than normal cells.
3.What is the reason for blebs and non healing
ulcer in the legs of this patient?
A :- Reason for non healing Ulcers in the Legs :-
• Circulation of blood at the wound site is critical for wound healing.
• As a result of narrowed blood vessels, diabetic wound healing is impaired because less oxygen can reach
the wound and the tissues do not heal as quickly.
• In addition, elevated glucose levels decrease the functioning of red blood cells carrying nutrients to the injured area and limit the effectiveness of white blood cells fighting infections.
Reason for Blebs :-
* The exact cause of diabetic blisters is unclear, but several factors might play a role in their development.
* The blisters may result from:
- Shoes that do not fit correctly
- Reduced circulation
- Candida albicans, a fungal infection
- Other injury or irritation in the feet or hands
4. What sequence of stages of diabetes has been
noted in this patient?
A :- Stages of Diabetes :-
• Stage 1 - Insulin resistance
• Stage 2 - Pre-diabetes
• Stage 3 - Type 2 Diabetes
• Stage 4 - Type 2 Diabetes and vascular complications like Retinopathy, Nephropathy and Neuropathy and Related Microvascular events.
C) A-Fib and Biatrial Thrombus in a 52yr Old Male.
Link to the Patient Details :-
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
2011 ( 10 years ago ) :- Surgery for inguinal Hernia but he had on and off pain at surgical site which was aggravated since 3 years.
Since 3 years :- NSAID abuse.
Since 2-3 Years :- He was having Facial Puffiness on and off.
2020 ( 1 year ago ) :- He had similar episode of Shortness of Breath on Exertion (Grade 2)
2020 ( Since 1 year ) :- He was diagnosed with Hypertension.
01 / 04 / 2021 :- He had Decreased Urine output, Constipation and Shortness of Breath on Exertion ( Grade 2).
02 / 04 / 2021 :- He developed Shortness of Breath even at rest for which he was referred by local RMP to Higher Centre.
03 / 04 / 2021 :- He was admitted to Hospital.
Anatomical Localization :- Upper chambers of the heart, Right and Left atrium.
Primary Etiology :- 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?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
On the Day of Admission in Hospital :-
1. Injection DOBUTAMINE 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg :
On Day 3 :-
1. TAB. DIGOXIN 0.25mg OD 5/7 :
2. Injection Unfractionated HEPARIN 5000 IU TID :
* As patient's D DIMER was high, Anti coagulants were started and planned for CPTA.
On Day 4 :-
1. TAB. CARVEDIOL 3.125mg BD :
On Day 6 :-
1. Injection Unfractionated HEPARIN Infusion 5ml/hr :
2. TAB. ACETYLCYSTEINE 600mg PO TID :
3. Daily monitoring of APTT, PT, INR and RFT was done.
On Day 7 :-
1. TAB. ACITROM 2mg OD :
On Day 8 -
1. The Infusion of Heparin was increased to 7ml/hr and it was stopped after attaining the APTT of >70secs, PT of 23secs and INR of 2.3.
Other Medications used during the Course in Hospital :-
1. TAB. CARDIVAS 3.125mg PO BD :
2. TAB. DYTOR 10mg PO OD :
3. TAB PAN D 40mg PO OD :
4. TAB. TAXIM 200mg PO OD :
5. Injection THIAMINE 100mg in 50ml NS IV TID :
6. INJ. HAI S.C 8U-8U-6U :
** As patient symptomatically improved during stay in the hospital, he was Discharged on request, on 12-4-21.**
Advice at Discharge :-
1. TAB. DYTOR 10mg PO OD :
2. TAB. ACITROM 2mg PO OD :
3. TAB. CARDIVAS 3.125mg PO BD :
4. Injection HAI SC 6U-6U-4U :
5. TAB. DIGOXIN 0.25mg OD 5/7 except Saturday and Sunday :
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. PT, INR, APTT after 15 days & Review SOS.
3) What is the pathogenesis of renal
involvement due to heart failure (cardio renal
syndrome)? Which type of cardio renal
syndrome is this patient?
A :- Pathogenesis of Cardio-Renal Syndrome :-
• When you have heart Failure, your heart may not pump blood in the right way. Your heart
may become too full of blood. This causes pressure to build in the main vein connected to your kidneys, which may lead to a blockage and a reduced supply of oxygen rich blood to the kidneys. This can lead to kidney disease.
• Inability of the failing heart to generate forward flow, thus resulting in prerenal hypoperfusion. 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.
4) What are the risk factors for atherosclerosis
in this patient ?
A :- Risk factors for Atherosclerosis include:-
• High cholesterol and triglyceride levels.
• High blood pressure.
• Type 1 diabetes.
• Obesity.
• Physical inactivity.
• High saturated fat diet
5) Why was the patient asked to get those APTT,
INR tests for review?
A :- Patient has Biatrial Thrombus which is in turn a complication of Atrial fibrillation.
• The aPTT test measures the length of time (in seconds) that it takes for clotting to occur.
• The aPTT is used to evaluate the coagulation factors.
• An INR test measures the time for the blood to clot. It is also known as prothrombin time. It is used to monitor blood-thinning medicines, which are also known as anticoagulants.
• Both of these tests are used to find out whether the thrombus is dissolved or not.
D) 67 year Old patient with acute coronary syndrome.
Link to the Patient Details :-
https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
Questions-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
Since 2009 ( Since 12 years ) :- She is a known case of Type 2 Diabetes Mellitus for which she was taking Medication. ( TAb. Glimiperide )
Since 1 year (2020) :- She had HeartBurn like episodes which were relieved without taking any Medication.
October, 2020 (7 Months Ago) :- She was diagnosed with Tuberculosis for which she completed entire course of Antitubercular therapy.
November, 2020 (Since 6 Months) :- She is a known case of Hypertension for which she was taking Medication. ( TAB. Telmisartan )
At 9pm on 27 / 04 / 2021 :- She developed Sweating on Exertion and Shortness of Breath even at rest.
At 9.30pm on 27 / 04 / 2021 :- She was admitted to Hospital.
Anatomical Localization :- Myocardium
Primary Etiology :- Diabetes Mellitus, Hypertension and Old age.
2) What are mechanism of action, indication
and efficacy over placebo of each of the
pharmacological and non pharmacological
interventions used for this patient?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
1. TAB MET XL 25 MG/STAT :
Mechanism of Action :- This works by relaxing the blood vessels, slowing down the heart rate. By doing this, it reduces the workload on the heart of pumping the blood effectively.
Indications :-
• Hypertension
• Angina
• Arrhythmia
• Prevention of Heart attack
• Prevention of Migraine
2. The patient was then advised to shift to a HC for Percutaneous Coronary Intervention (PCI) upon explaining to the patient’s attender about the patient’s condition.
3. The patient was then taken to another hospital, for further treatment but PCI was not done as there were no vacancies in hospitals at that time.
4. The patient was discharged after that and is currently doing fine.
3) What are the indications and
contraindications for PCI?
A :- Indications of Percutaneous Coronary Intervention :-
• 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 Percutaneous Coronary Intervention :-
• Intolerance for oral antiplatelets long-term.
• Absence of cardiac surgery backup.
• Hypercoagulable state.
• High-grade chronic kidney disease.
• Chronic total occlusion of SVG.
• An artery with a diameter of <1.5 mm
4) What happens if a PCI is performed in a
patient who does not need it? What are the
harms of overtreatment and why is research on
overtesting and overtreatment important to
current healthcare systems?
A :- Percutaneous Coronary Intervention is preferred over Medical therapy if the patient
has :-
- Severe symptoms
- Failed Medical therapy
- High risk Coronary Anatomy
- Worsening LV function
If PCI is performed in a Patient who doesn't need it, it is an Unnecessary procedure done in the Patient with so many risks associated with the procedure with no benefit from it.
Factors associated with the Increased rates of Complications from PCI :-
- Advanced age
- Diabetes
- Chronic Kidney Disease
- Acute coronary syndrome
- Heart failure
- Multi-vessel Coronary artery disease
Femoral vascular Complications occur in about 2 - 6% overall which are mostly related to vascular access and may include :-
- Access site hematoma
- Pseudoaneurysm
- Arteriovenous Fistula
- Arterial dissection and/or Occlusion
- Retroperitoneal Hematoma
Complications from the Radial access may include :-
- Loss of Radial pulse reported in ≤5 % of procedures
- Radial artery spasm
- Compartment syndrome
- Pseudoaneurysm
- Sterile abscess ( with previous generation hydrophilic sheaths )
Overtreatment :-
• The worst consequence of overdiagnosis is Overtreatment of an indolent lesion or disease which is unlikely to have any benefit for the Patient.
• At the same time, Interventions like Surgery, Radiation and Chemotherapy can have side effects resulting in Significant Morbidity and rarely even Fatalities can occur.
• As over diagnosis in some Non - Neoplastic conditions leads to Over Prescription and Over Medicalisation, resulting in many undesirable and some dangerous side effects.
• It can also contribute to the release of the pharmaceuticals into the environment as, for example, in case of over and misuse of Antibiotics thus contributing to the proliferation of Antimicrobial Resistance.
E) CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION.
Link to the Patient Details :-
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Questions:-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
Since 8 years :- He is a known case of Hypertension.
5 days back :- He took First dose of COVISHIELD vaccine against COVID 19.
Since 3 days :- He was suffering from Mild Chest pain on the right side of the chest, which was associated with reduced sleep due to the discomfort.
Since Morning :- He has Giddiness and Profuse Sweating.
Anatomical Localization :- Inferior Wall of the Heart
Primary Etiology :- Diabetes Mellitus type 2 and 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?
A :- Pharmacological and Non Pharmacological interventions used for this Patient :-
1. TAB. ASPIRIN 325 mg PO/STAT :
Mechanism of Action :- Aspirin may disaggregate platelet microthrombi and may reduce the size of a developing thrombus.
• Effects of aspirin other than on platelets have also been suggested and these include an increase in the permeability of a fibrin clot and an enhancement of clot lysis.
Indications :-
• Angina pectoris
• Ankylosing spondylitis
• Cardiovascular risk reduction
• Colorectal cancer
• Ischemic stroke
• Myocardial infarction
• Osteoarthritis
• Revascularization procedures: Prophylaxis
• Rheumatoid arthritis
• Systemic lupus erythematosus
2. TAB ATORVAS 80mg PO/STAT :
Mechanism of Action :- Cholesterol is produced by an enzyme known as HMG-CoA reductase.
• It inhibits the activity of this enzyme, thus lowering the bad cholesterol (LDL) levels.
• It also increases the good cholesterol levels which is also known as high-density
lipoprotein (HDL).
Indications :-
• High Cholesterol
• Prevention of Heart attack
3. TAB CLOPIBTAB 300mg PO/STAT :
Mechanism of Action :- Clopidogrel belongs to a class of drugs called platelet inhibitors or thienopyridine class inhibitors of P2Y12 ADP platelet receptors. A class of drugs is a group of medications that work in a similar way. These drugs are often used to treat similar conditions.
• Platelets are blood cells that help your blood clot normally. Clopidogrel helps prevent platelets from sticking together. This stops
them from forming blood clots.
Indications :- Prevent blood clots in conditions such as:-
• Atherosclerosis
• Unstable angina or myocardial infarction
• Atrial fibrillation
4. Injection HAI 6U/IV STAT :
Mechanism of Action :- It lowers blood sugars by stimulating glucose uptake by cells, tissue and muscles, especially by skeletal muscles and fat and by inhibiting glucose production by the liver.
Indications :- Diabetes Mellitus
5. Vitals Monitoring
The patient was shifted to a higher center where he underwent angioplasty and a stent was placed. He was later discharged.
The patient is currently doing fine.
3) Did the secondary PTCA do any good to the
patient or was it unnecessary?
A :- The secondary PTCA is not necessary in
this patient as he already crossed the Window period of 12 hours and is currently doing fine.
F) A case of Cardiogenic Shock.
Link to the Patient Details :-
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1. How did the patient get relieved from his
shortness of breath after i.v fluids
administration by rural medical practitioner?
A :- His shortness of Breath may be due to the Hypovolemia. It is because of this reason his dyspnoea got relieved after administration of iV fluids.
2. What is the rationale of using torsemide in
this patient?
A :- Torsemide is used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance.
3. Was the rationale for administration of
ceftriaxone? Was it prophylactic or for the
treatment of UTI?
A :- History of white discharge in urine (cloudy urine) is due to the presence of pus cells in the urine, which in turn indicates the presence of any Urinary Tract Infection. Rationale for the administration of Ceftriaxone was for treatment of Urinary Tract Infection.
4)Gastroenterology & Pulmonology :-
A) A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA.
Link to the Patient Details :-
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
QUESTIONS: -
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
9 years Ago (2012) :- Started drinking Alcohol where he consumed 3 Sara bottle per day.
5 years Ago (2016) :- He had Pain Abdomen and Vomiting for which he was admitted in local hospital and treated conservatively.
5 years Ago (2016) :- Following Treatment, He stopped drinking alcohol as advised by the physician and was symptom free for nearly 3 years.
1 year Ago (2020) :- He started drinking Alcohol again.
1 year Ago (2020) :- Following this, He had recurrent episodes of pain abdomen and Vomiting ( 5-6 episodes in the past 1 year) which were treated by local RMP.
6 months Ago (October,2020) :- Started having Ghutka 5 per day.
From Past 20 days (10/04/2021) :- He had increased amount of alcohol consumption around 5 bottles per day.
1 week back (23/04/2021) :- Last binge of Alcohol following which he again had Vomiting and Pain abdomen which was increased after food intake.
Since 4 days (26/04/2021) :- He developed Fever, Constipation and Burning Micturition which is associated with Suprapubic pain.
30/04/2021 :- Admitted to Hospital.
Anatomical Localization :- Pancreas
Primary Etiology :- Chronic Alcoholism
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?
A :- 1) ING. MEROPENAM ; TID for 7 days
* Meropenem ( broad spectrum Carbepenem )
an antibiotic.
2) ING. METROGYL 500 mg IV TID for 5 days
* inj. Metrogyl has METRONIDAZOLE
( Nitroimidazole drug ) an antibiotic
3) ING. AMIKACIN 500 mg IV BD for 5days
* It is an Aminoglycoside antibiotic
## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.
4) TPN ( Total Parenteral Nutrition )
* Method of feeding that by passes gastrointestinal tract
* Fluids are given to vein , it provides most of the nutrients body needs.
* TPN has proteins, carbohydrates, fats, vitamins, minerals.
5) IV NS / RL at the rate 12l ml per hour
* Given for fluid replacement ie., treat dehydration
6) ING. OCTREOTIDE 100 mg SC , BD
* It is a Somatostatin long acting analogue.
* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.
7) ING. PANTOP 40 mg IV , OD
* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
* It is B1 supplement.
* It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
* Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
9) ING. TRAMADOL in 100 ml NS IV , OD
* It is an opioid analgesic, given to releive pain
## After 4 days of this treatment; there is no improvement in patient and infact he is deteriorating clinically !!!
* So USG GUIDED MALECOT DRAIN - PLACED INSIDE AND PSEUDOCYST WAS DRAINED
* TWO OTHER USG GUIDED DRAINS ARE PLACED TO DRAIN THE PERI-PANCREATIC COLLECTIONS
## After this patient was dramatically improved but in the mean time he developed PNEUMOTHORAX IN LEFT LUNG !!!
* Oxygen supply for mild hypoxia
* And ICD ( Inter Coastal Drain ) was placed.
B) CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN.
Link to the Patient Details :-
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is causing the patient's dyspnea? How
is it related to pancreatitis?
A :- Patient's dyspnoea is due to Pleural Effusion.
Two main causes of Pleural Effusion in Pancreatitis are :-
• Transdiaphragmatic lymphatic blockage
• Pancreaticopleural fistulae secondary to leak and disruption of the pancreatic duct or pseudocyst caused by an episode of acute pancreatitis.
- The leak or disruption is more likely to lead to a pleural effusion if the duct disruption is posteriorly into the retroperitoneum.
- The pancreatic enzymes can track up into the mediastinum and then rupture into the pleural cavity either left side or bilaterally and so create a connection between the pancreatic duct and the pleural cavity.
2) Name possible reasons why the patient has
developed a state of hyperglycemia.
A :- Acute Pancreatitis
↓
Damage to the Pancreatic
Beta cells
↓
Decreased Synthesis and release
of Insulin
↓
Increased Glucagon stores
↓
Hyperglycemia
3) What is the reason for his elevated LFTs? Is
there a specific marker for Alcoholic Fatty Liver
disease?
A :- Patient was a Chronic Alcoholic due to which he has Grade 1 Fatty Liver which in turn is evident by Elevated LFTs.
• AST / ALT Ratio ( De Ritis Ratio ) is > 2 in Alcoholic Fatty Liver disease.
4) What is the line of treatment in this patient?
C) A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension.
Link to the Patient Details :-
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1) what is the most probable diagnosis in this
patient?
A :- As the Patient had Elevated levels of Alkaline Phosphatase, Hyperbilirubinemia, Hypoalbuminemia and Hepatomegaly, the most probable diagnosis in this Patient could be
Ruptured Liver Abscess.
2) What was the cause of her death?
A :- On the next day of surgery, Patient had severe cough and Shortness of breath eventually resulting in Abnormal Vital signs.
• This suggests that her cause death may be
Sepsis or Acute respiratory distress syndrome.
3) Does her NSAID abuse have something to do
with her condition? And How?
A :- Patient's USG report shows that She had
Grade 3 RPD changes of Right kidney.
• It highly suggests that she may had
underlying CKD (Chronic Kidney Disease),
Which is secondary to her NSAID abuse.
(Analgesic Nephropathy)
5. Nephrology and Urology :-
A) Post TURP with non oliguric ATN
Link to the Patient Details :-
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1. What could be the reason for his SOB ?
A :- It may be due to Acidosis caused by Acute Kidney Injury secondary to the Urosepsis with Hydrouretonephrosis.
2. Why does he have intermittent episodes of
drowsiness
A :- The reason for intermittent episodes of Drowsiness may be Hyponatremia which is
111 mEq/L. (Normal Sodium levels → 136-145 mEq/L)
3. Why did he complaint of fleshy mass like
passage in his urine?
A :- The Patient has Acute tubular necrosis which is a kidney disorder involving the death of tubular epithelial cells that forms the renal tubules of kidneys which further can lead to acute renal failure.
• This results in the excretion of this dead tubular epithelial cells in the form of Granular,
Muddy brown casts in the urine sediment which is highly suggestive of ATN.
4. What are the complications of TURP that he
may have had?
A :- Complications include :-
• Urinary incontinence
• Urethral strictures
• Others include -
* Bleeding – in around 2% of cases there may be persistent bleeding during or after the operation that means a blood transfusion is required.
* Urinary tract infection (UTI) – in around 5% of cases, a UTI could develop after surgery; UTIs can usually be successfully treated with antibiotics.
* Urinary retention – in around 2% of cases, the muscles that control the bladder may be temporarily damaged, which can lead to problems fully emptying the bladder; in some cases, the bladder muscles regain their normal function within a few weeks.
* Prostate becoming enlarged again – about 10% of men need to have a TURP again within 10 years.
• TURP syndrome :-
* A rare but potentially serious risk associated with a TURP is known as TURP syndrome. This occurs when too much of the fluid used to wash the area around the prostate during the procedure is absorbed into the bloodstream.
* Initial symptoms of TURP syndrome include:
• Feeling or being sick
• Disorientation
• Dizziness
• Headache
• Swelling of your tummy
• Slow heartbeat (bradycardia)
Left untreated, life-threatening problems can develop, such as seizures (fits), shortness of breath, blue skin (cyanosis) and coma.
B) An Eight year old with Frequent Urination.
Link to the Patient Details :-
https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
Questions:-
( Referral links for the Answers
mentioned at the end of the Blog )
1.Why is the child excessively hyperactive
without much of social etiquettes ?
A :- Child is excessively Hyperactive without much of Social etiquettes may be due to the Attention Deficit Hyperactivity Disorder (ADHD).
• ADHD includes a combination of persistent problems, such as difficulty sustaining attention, hyperactivity and impulsive behavior.
• The primary features of ADHD include inattention and hyperactive-impulsive behavior. ADHD symptoms start before age 12.
2. Why doesn't the child have the excessive urge
of urination at night time ?
A :- Child doesn't have excessive Urge of Urination at night time may be due his manifestation being Psychosomatic or some Stressers triggering the manifestation.
3. How would you want to manage the patient to
relieve him of his symptoms?
A :- This Patient can be managed by Behavioural Therapy, Psychotherapy, Social skills training and certain medications like Amphetamines etc.
6) Infectious Diseases( HI Virus, Tuberculosis, Gastroenterology and Pulmonology):-
A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH.
Link to the Patient Details :-
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
Questions:-
( Referral links for the Answers
mentioned at the end of the Blog )
1.Which clinical history and physical findings
are characteristic of tracheoesophageal fistula?
A :- Clinical History and Physical Findings that precipitated the appropriate diagnostic study includes :-
* Cough since 2 months on taking food and liquids which was initially non productive and then associated with sputum which is white in color , moderate in quantity and non foul smelling
* Difficulty in swallowing since 2 months which was initially difficult only with solids but then followed by liquids also.
* Fever since 2 months which is sudden in onset, high grade and intermittent on and off associated with chills and rigors.
* Weight loss of 10 kgs since 2 moths.
A Chronic cough aggravated by heavy meals and recurrent chest infections are the common presenting symptoms.
Bouts of coughing when swallowing liquids are pathognomonic of this condition.
2) What are the chances of this patient
developing immune reconstitution
inflammatory syndrome? Can we prevent it?
A :- A paradoxical clinical worsening of a known condition or the appearance of a new condition after initiating antiretroviral therapy (ART) therapy in HIV-infected patients resulting from restored immunity to specific infectious or non-infectious antigens is defined as immune reconstitution inflammatory syndrome (IRIS).
Pathogenesis of Syndrome involves Combination of :-
1. Underlying antigenic burden
2. Degree of immune restoration following Highly active antiretroviral therapy (HAART)
3. Host genetic susceptibility.
Diagnostic Criteria of IRIS :-
Major Criteria :-
• Atypical presentation of “opportunistic infections or tumors” in patients responding to antiretroviral therapy.
• Decrease in plasma HIV RNA level by at least 1 log10copies/mL.
Minor Criteria :-
• Increased blood CD4+ T-cell count after HAART.
• Increase in immune response specific to the relevant pathogen, e.g. DTH response to mycobacterial antigens.
• Spontaneous resolution of disease without specific antimicrobial therapy or tumor chemotherapy with continuation of antiretroviral therapy.
7) Infectious Diseases & Hepatology :-
A) Case Discussion On Liver Abscess.
Link to the Patient Details :-
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
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 ?
A :- Yes
" A study has found that alcohol increases virulence of Streptococcus pneumonia by upregulating its alcohol dehydrogenase.In a similar manner,it could increase the virulence of EH. Moreover,EHADH2 is an ‘iron‐activated’ enzyme,and experimental studies have demonstrated that the iron promotes growth and in‐vivo invasiveness of Entamoeba histolytica "
" Alcohol suppresses the function of Kupffer cells in the liver, which has the important role of clearing the amoeba. Thus, the mechanism involved in the increasing virulence of EH seems to be related to both the alcoholic and nonalcoholic contents of toddy "
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6586571/
2. What is the etiopathogenesis of liver abscess
in a chronic alcoholic patient ? ( since 30 years -
1 bottle per day)
3. Is liver abscess more common in right lobe ?
A :-The right hepatic lobe is affected more often than the left hepatic lobe by a factor of 2:1.
The predilection for the right hepatic lobe can be attributed to :-
• The right hepatic lobe receives blood from both the superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior mesenteric and splenic drainage
• It also contains a denser network of biliary canaliculi and, overall, accounts for more hepatic mass
• Studies have suggested that a streaming effect in the portal circulation is causative.
4.What are the indications for ultrasound
guided aspiration of Liver Abscess?
A :- The specific indications for intervention were :-
• To differentiate pyogenic from amebic abscess
• Pain and imminent rupture
• Poor response to medical therapy
• False-negative results of serologic tests
• Noncompliance with medical treatment
• Left lobe abscess
• Pregnancy.
B)CASE DISCUSSION ON LIVER ABSCESS.
Link to the Patient Details :-
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS:-
( Referral links for the Answers
mentioned at the end of the Blog )
1) Cause of liver abscess in this patient ?
A :- Amebic liver abscesses are caused by the Entamoeba histolytica.
• This is a protozoan parasite that is acquired via ingestion of food or water contaminated by human feces.
2) How do you approach this patient ?
A :-
3) Why do we treat here ; both amoebic and
pyogenic liver abscess?
• Considering the risk factors associated with the aspiration of pus for culture like :-
1) Some times abscess is not accessible for aspiration if it is in posterior aspect.
2) Sometimes it has thinwall which may
rupture if you try to aspirate resulting in complications.
3) Sometimes it is unliquified.
• For this reason, we treat both PLA and ALA emperically in clinical practice.
• PLA and ALA have many features in common and diagnosis
is often delayed due to vague clinical symptoms resulting in adverse
outcomes.
• Because of the difficulty in differentiating
between these two types of abscesses initially, antiamoebic
therapy is usually recommended in addition to broad-spectrum antibiotics.
• Medical therapy alone is effective in most cases of ALA .
• While some form of intervention is usually needed for PLA.
• Mortality is low with ALA compared with PLA.
4) Is there a way to confirm the definitive
diagnosis in this patient?
A:-On Analysis of Laboratory Reports and the findings that suggests the diagnosis of Liver abscess are :-
• Symptomatology of Right Hypochondriac and Epigastric pain, Fever with chills and rigors
• Hematological findings like Leukocytosis
(Indicates Infection/Inflammation) and
Anaemia
• Biochemical findings like Elevated levels of Alkaline Phosphatase and Hypoalbuminemia
in LFT
• USG finding of Hyperechoic mass in the Right lobe of the liver
Considering the following factors like:-
• Age of the Patient which is 21
• Gender - Male
• Solitary abscess
• Location of abscess which is Segment 8 in the right lobe
*The abscess is most likely to be Amoebic Liver abscess.
This can definitively be confirmed by :-
* Microscopic stool examination is still of little value if the serological and antigen detection tests are not available.
* Stool antigen detection based on Enzyme immunoassay are most common and quite sensitive which facilitates early diagnosis before the antibody response occurs (< 7d) compared to the PCR based methods which is not well standardized and is not widely available.
* Stool culture for amoeba is sensitive but has limited availability.
* Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extra-intestinal disease).
- EIA has now largely replaced indirect hemagglutination (IHA) testing and counter immunoelectrophoresis (CIE) testing which is relatively simple and easy to perform, rapid, inexpensive, and more sensitive which detects antibodies specific for E histolytica in approximately 95% of patients with extra-intestinal amebiasis.
- Entamoeba histolytica galactose lectin antigen is detectable by enzyme-linked immunosorbent assay (ELISA) in at least 75% of serum samples obtained from patients with amebic liver abscess.This test can be used for rapid diagnosis in highly endemic areas, where serology can be misleading, but it is not widely available.
* Aspiration may be performed under computed tomography (CT) scan or sonographic guidance.
• Send the collected specimen for Gram stain and cultures.
• Amoeba rarely are recovered from the aspirate (15%) and, often, they are present only in the peripheral parts of the abscess, invading and destroying adjacent tissue.
• Amoebic liver abscesses only rarely yield positive bacterial cultures following secondary bacterial infection of the abscess cavity.
• Detecting E histolytica antigen in the aspirate is possible and is accomplished as previously described for stool specimens. It is highly specific. The sensitivity was only 20% using enzyme-linked immunosorbent assay (ELISA), but newer polymerase chain reaction (PCR)-based assays have a sensitivity of 83% and a specificity of 100%. [28, 29] However, currently, PCR-based detection is not widely available.
8) Infectious Diseases ( Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology )
50/Male came with altered sensorium.
Link to the Patient Details :-
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions :-
( Referral links for the Answers
mentioned at the end of the Blog )
1) What is the evolution of the symptomatology
in this patient in terms of an event timeline and
where is the anatomical localization for the
problem and what is the primary etiology of the
patient's problem?
A :- Timeline of Symptomatology in this Patient :-
3 years Ago :- He was diathesis with Hypertension and was on regular Medication since then.
18 / 04 / 2021 :- Fever associated with Chills and rigors , No Diurnal variation which was relieved on Medication.
21 / 04 / 2021 :- He had similar complaints and went to Local hospital but was not subsided on Medication ( Only Antipyretics ).
28 / 04 / 2021 :- He had Facial Puffiness, Periorbital edema and Generalized weakness and was also in drowsy State.
Since 4 days :- He had Weakness of Right
upper Limb and Lower Limb.
Since 2 days :- Altered sensorium.
04 / 05 / 2021 :- He was admitted to Hospital.
Anatomical Localization :- Rhino Orbto Cerebral Mucormycosis.
Primary Etiology :-
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?
A :- Injection. Liposomal amphotericin B according to creatinine clearence ,
- Loading dose 30mg/IV over 2-6 hrs
- Maintenance dose 60mg / IV once a day
* He has been given 200mg of itraconazole(only drug currently available) adjusted to his creatinine clearance which is 43 ml / min.
* Deoxycholate amphotericin B requirement is 70mg per day
Affordability issues :-
* Cost of 50mg of Liposomal Amphotericin B is 500to 700rupees
- Where 350mg costs 2400 to 3000 rupees
per day
* Liposomal ampB requirement is 350mg once daily.
* Even the busiest pharmacy in Hyderabad (we called Osmania Medical College pharmacy) doesn't have deoxycholate.
* Liposomal is still available for 30% lesser price. Posaconazole price is 15k starting.
* He was referred to osmania general hospital where he was given one dose of deoxycholate amphotericin B and patient has died On 6th may around 10 am.
3) What are the postulated reasons for a sudden
apparent rise in the incidence of mucormycosis
in India at this point of time?
A :- Reasons for sudden apparent rise in the incidence of Mucormycosis in India :-
• High prevalence of Diabetes in India and Poorly controlled diabetes during COVID
• Indiscriminate use of Steroids ( Oral steroids early in Infection, Higher than required dose or Longer than required duration )
• Use of Immunomodulants ( Eg - Tocilizumab ) with steroids
• Wide use of Antimicrobials that kill normal bacteria ( Eg - Azithromycin, Ivermectin, Doxycycline )
• Feature of B.1.617 variant of SARS - Cov - 2 that suppresses Immunity
• Industrial ( vs Medical Oxygen ) for home oxygen use.
• Overwhelmed hospitals, Lack of hygiene with Masks, Vents, Oxygen systems, Humidifiers among others.
9) Infectious Disease ( COVID 19 ) Master chart :-
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
for this question that contains details of many of our covid 19 patients documented over this month and we would like you to:
1) Sort out these detailed patient case report logs into a single web page as a master chart
2) In the master chart classify the patient case report logs into mild, moderate severe and
3) indicate for each patient, the day of covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe COVID.
Link to the Master Chart :
https://drive.google.com/file/d/1a1MGnNclK8dzlSoSNwXULDXW8hV1nfKn/view?usp=drivesdk
10) Medical Education ( May 2021
E-log) :-
May 10, 2021 :- Discussion on the Main stay treatment of COVID 19 Patients.
May 11, 2021 :- Discussion on the topic of ICU psychosis in COVID 19 Patients.
May 13, 2021 :- Discussion on the case of a Child with frequent urination
May 14, 2021 :- I was allotted a case for the preparation of E - log. I took the patient's history through a phone call and understood the case.
May 15, 2021 :- I read some Books, Articles and journals regarding my case to understand about Liver Abscess
May 16, 2021 :- I prepared the E-log on a case of a 45 year old female Patient with Fever, Pain abdomen and Decreased Urine output.
May 18, 2021 :- I published the E- log and shared it in the group along with possible questions.
May 25, 2021 :- I started working on my Monthly Assignment of May 2021.
- It's a Great opportunity to learn Medicine related Clinical scenarios even in these situations of COVID 19 Pandemic. It helps in improving the way we communicate with a patient through a call. This telemedicine has made us to learn more Medicine related articles and journals than before. It's been a Great experience with the telemedicine so far. Thank you for this Opportunity.
References :
https://pubmed.ncbi.nlm.nih.gov/3818752/#:~:text=There%20is%20loss%20of%20power,due%20to%20pyramidal%20tract%20involvement.
https://pubs.rsna.org/doi/10.1148/radiology.156.3.4023220
https://www.ncbi.nlm.nih.gov/books/NBK519032/
https://www.medscape.com/answers/188802-82179/which-hepatic-lobe-is-more-commonly-affected-by-liver-abscess
https://emedicine.medscape.com/article/183920-workup#c6
https://link.springer.com/chapter/10.1007/978-3-319-98497-1_79
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6586571/
https://emedicine.medscape.com/article/152191-medication
https://www.sharecare.com/health/diabetes-complications/can-drinking-alcohol-effect-a-diabetics-feet#:~:text=Excessive%20alcohol%20can%20cause%20nutritional,this%20leads%20to%20foot%20ulcers.
https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/bipap
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3277043/
https://www.nhs.uk/conditions/transurethral-resection-of-the-prostate-turp/risks/
https://jamanetwork.com/journals/jamaneurology/fullarticle/781335
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