Medicine blended assignment (M)
1. Pulmonology
Case 1.
1)A 55-year-old female with shortness of breath ,pedal Edema ,and facial puffiness.
https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html
- the anatomical localization of the problem is at the bronchioles.
- etiology-its is due exposue of dust /allergens in paddy feilds or indoor burning coal kitchens
b. Pharmacological interventions
- head end elevation
- BiPAP
- Agumentin(amoxicillin+calvulanic acid)
- Azithromycin
- inj.lasix
- tab.Pantop
- inj. hydrocortisone
- Neb. with ipravent ,budecortisone
- tab.pulmoclear
- chest physiotherapy
- inj.thiamine
- BP,PR,SPO2,Temp
- I/O charting
C.
The acute exacerbation could be due to the infection of upper respiratory tract or it could be due to the smoke from the continuous usage of indoor chulha.
D.
ATT could have effected the patient’s condition by causing generalised weakness.
ATT has affected her symptoms. Rifampicin has a side effect of nephrotoxicity causing pedal edema and facial puffiness.
https://www.ncbi.nlm.nih.gov/
E.
Hyponatraemia in COPD develops due to many reasons such as worsening of hypoxia, hypercapnia ,respiratory acidosis and right-sided heart failure with development of lower limb oedema ,it could also be due to renal insufficiency.
2. Neurology
Alcohol produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N-methyl-D-aspartate (NMDA) receptors; at higher concentrations, it leads to acute intoxication by potentiation of the gamma-aminobutyric acid (GABA) effects, particularly in receptors with delta subunits. The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol.
Continued excessive alcohol consumption can lead to the development of dependence. For some people the fear of withdrawal symptoms may help perpetuate alcohol abuse.Many neurobiological and environmental factors influence motivation to drink.
Primary etiology- When an alcohol-dependent individual abruptly terminates or substantially reduces his or her alcohol consumption, a characteristic withdrawal syndrome ensues.
Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate-mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures. The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.
Primary etiology- Alcohol causes deficiency of vitamin b1 called thiamine. There may be decreased conversion of thiamin to the active coenzyme, reduced hepatic storage of the vitamin in patients with fatty metamorphosis, ethanol inhibition of intestinal thiamin transport, and impaired thiamin absorption secondary to other states of nutritional deficiency.
Wernicke encephalopathy. This condition presents in well-defined steps starting with nausea and vomiting, followed by horizontal nystagmus, ocular nerve palsy, fever, ataxia, and progressive mental impairment, eventually leading to the korsakoff syndrome.
B. Pharmacological interventions
1.INJ. THIAMINE- As chronic alcoholics are more prone for development of thiamine deficiency, thiamine is administered to improve the condition of Wernicke's encephalopathy to prevent the progression towards korsakoff's syndrome
How thiamine work in the brain?
Thiamin (vitamin B1) helps the body's cells change carbohydrates into energy. The main role of carbohydrates is to provide energy for the body, especially the brain and nervous system. Thiamin also plays a role in muscle contraction and conduction of nerve signals. Thiamin is essential for the metabolism of pyruvate acting through thiamine pyrophosphate.Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
E.
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.
F.
The probable cause is kidney failure and the reasons for the anemia is
1) a moderately reduced red cell life span,
2)blood loss, and
3) an inadequate increase in erythropoiesis relative to the fall in hemoglobin (Hb).
7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
aa) Tab Vertin 8mg- This is betahistine; It is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
b) Tab Zofer 4mg- This is ondanseteron; It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications- Used to control the episodes of vomiting and nausea in this patient.
c) Tab Ecosprin 75mg- This is aspirin; It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
D) d) Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) e) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F) f) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) g) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
C. c. Did the patients history of denovo HTN contribute to his current condition?
Q4. Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subarachnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.
Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition
CASE 3
http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Q1. 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 symptomology
1) 10 years back – episode of right and left upper limb paralysis
2) 1 year back- right and left paresis due to hypokalemia
3) 8 months ago- bilateral pedal edema, gradually progressing, present in both sitting and standing position, relieved on taking medication
4) 7 months ago – diagnosed with infection in the blood
5) 2 months ago – visited our hospital for neck pain and received medication
6) 6 days ago – pain in the left upper limb, radiating along the upper limb, dragging type, nocturnal increase in the pain, aggravated during palpitations and relieved on medication
7) 5 days ago –
i) Palpitations, sudden in onset, more during night time, aggravated by lifting weights and speaking continuously, relieved by drinking more water, medication
ii) Dyspnoea during palpitation ( NYHA class 3)
iii) Chest pain associated with chest heaviness
Anatomical location- Cervical spine
Etiology- The patient experienced episodes of palpitations, paresis, paralysis and edema because of hypokalemia
Neck pain is due to cervical spondylosis
Q2. What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANS. Since the patient complains of edema, the drugs used to relieve it such as diuretics can cause hypokalaemia.
The risk factors include-
- Excess Alcohol use
- Chronic kidney disease
- Diabetic ketoacidosis
- Diarrhoea
- 5. Diuretics
- Excessive laxative use
- Folic acid deficiency
- Vomiting
Q3. What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANS. The earliest electrocardiogram (ECG) change associated with hypokalemia is a decrease in the T-wave amplitude. As potassium levels decline further, ST-segment depression and T-wave inversions are seen, while the PR interval can be prolonged along with an increase in the amplitude of the P wave. The U wave is described as a positive deflection after the T wave, often best seen in the mid-precordial leads.
CASE 5
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
Q1. What could have been the reason for the patient for developing ataxia in the past 1 year?
ANS. This patient has a history of alcohol abuse for the past three years. Excessive alcohol consumption can be a major risk factor for development of cerebellar dysfunction or cerebellar ataxia.
A potential mechanism for this is alteration in GABA-A receptor dependent neurotransmission. Ethanol is shown to disrupt molecular events at the mossy fibre-granule cell-golgi cell synaptic site and the granule cell fibre-Purkinje cell synaptic site, which is mainly responsible for ethanol induced cerebellar ataxia.
Another mechanism is the relation between age related effect of ethanol on the endoplasmic reticulum of purkinje cells of dendrite causing dendritic regression, and the effect of ethanol withdrawal that causes mitochondrial damage in the cerebellum.
Ethanol also causes neuroinflammation and neurotoxicity in the cerebellum.
These can all affect the cerebellum, which is the motor coordination centre of the central nervous system, and also involved in cognitive processing and sensory discrimination. These can all result in altered hand movements, impaired postural stability and balance, loss of fine movements etc.
ANS. This patient has a history of excessive alcohol consumption for the past three years. According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subarachnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke. Heavy drinking is a major cause of the acute cerebral hemorrhage of frontal, parietal and temporal lobes in this patient.
Bleeding diathesis is an unusual susceptibility to bleed (hemorrhage) mainly due to hypercoagulability. Heavy drinking can cause thrombocytopenia, as well as impact shape and functions of platelets. Impaired platelet function, together with reduced platelet count, can contribute to this condition associated with chronic alcoholism. This can also cause an increased incidence and recurrence of gastrointestinal hemorrhage associated with excessive alcohol intake.
Q1. Does the patient’s history of road traffic accident have any role in his present condition?
ANS. https://www.ahajournals.org/doi/pdf/10.1161/01.STR.14.4.617
The above study is similar to the case discussed where an accident occurring years ago has eventually led to an infarct. Similarly, the accident that occurred in our patient 4 years ago can be the reason for his present condition.
Q2. What are warning signs of CVA?
ANS.
- Sudden numbness or weakness in the face, arm, or leg, especially on one side of the body.
- Sudden confusion, trouble speaking, or difficulty understanding speech.
- Sudden trouble seeing in one or both eyes.
- Sudden trouble walking, dizziness, loss of balance, or lack of coordination.
- Sudden severe headache with no known cause.
Q3. What is the drug rationale in CVA?
ANS. 1) Thrombolytics- Thrombolytics restore cerebral blood flow in some patients with acute ischaemic stroke and may lead to improvement or resolution of neurologic deficits.
2) Antiplatelet therapy- Due to the thrombotic origin of AIS and the involvement of platelet aggregation in the development of said thrombus, antiplatelet drugs are indicated. The most commonly used one is aspirin (NSAID).
3) Anticoagulant therapy- Anticoagulants are a heterogeneous group of pharmacological agents that by interacting with the coagulation cascade disrupt the formation of the fibrin mesh that forms the scaffold of the clot, thus preventing the formation of a blood clot in situ, or thrombus, inside the blood vessels.
Q4. Does alcohol has any role in his attack?
ANS. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007300/
According to the above study, patients who consume 1-21 drinks a week, have a lower chance of developing ischemic or hemorrhagic stroke than those who are heavy drinkers. The patient is an occasional alcohol drinker, so the chances of alcohol affecting his attack is improbable. In heavy drinkers, alcohol can increase the chances of both types of strokes.
Q5.Does his lipid profile has any role for his attack?
ANS. The patient has an overall normal lipid profile except for the HDL count. The HDL is 33mg/dl which is lower than the normal range (40-60 mg/dl).
HDL is known as the good cholesterol. Any decrease in the count is an indicator that there can be a cardiovascular disorder.
Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C. Some see 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.
CASE 7
Q1.What is myelopathy hand?
ANS. A characteristic dysfunction of the hand observed in various cervical spinal disorders, 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.
CASE 8
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
Q1. What can be the cause of her condition?
ANS. The patient’s GTCS episodes can be due to acute cortical vein thrombosis as seen in her MRI. Seizures are the most common symptoms of CVT.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771304/
This case report illustrates that CVT can occur in the setting of anaemia and thrombocytopenia.
The above case is similar to our patient. Though neurological manifestations are not common in iron deficiency anaemia our patient presented with CVT. Also, our patient had thrombocytopenia which one would have expected to cause a bleeding tendency but paradoxically could have contributed to the development of the venous thrombosis as explained in the article above.
The associated symptoms such as headache and vomiting can be explained by the midline shift.
Q2. What are the risk factors for cortical vein thrombosis?
ANS.
- Birth control or excess oestrogen use.
- Dehydration.
- Ear, face, or neck infection.
- Protein deficiencie
- Head trauma or injury.
- Obesity
Q3. There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously why?
ANS. The patient developed high grade fever (the patient had thrombophlebitis) with could have been the cause of the seizures. The decrease in the fever could have resolved the seizures.
Q4. What drug was used in suspicion of cortical venous sinus thrombosis?
ANS. The approach to treatment includes anticoagulation (intravenous heparin or subcutaneous low molecular weight heparin), thrombolytics (systemic or local), and symptomatic treatment (including antiepileptic therapy, lowering intracranial pressure, decompressive craniotomy).
Cardiology
CASE 1
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
Q1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
ANS. Ejection fraction (EF) is a measurement of how much blood the left ventricle pumps out with each contraction.
- HF with preserved ejection fraction (HFpEF) is also known as diastolic HF. In this, muscles of the heart contract normally and the heart may seem to pump a normal proportion of the blood that enters it. However, heart muscle thickening may cause the ventricle to hold an abnormally small volume of blood (chamber hypertrophy)
Therefore, although the heart’s output may still appear to be in the normal range, its limited capacity is inadequate to meet the body’s requirements.
Causes- Coronary artery disease, Aortic stenosis, High blood pressure
- HF with reduced ejection fraction (HFrEF) is also known as systolic HF. In this, the heart muscle is not able to contract adequately(chamber dilatation) and, therefore, expels less oxygen-rich blood into the body. Patients with this form of the disease will have lower-than-normal left ventricular ejection fraction on an echocardiogram.
Causes- Diabetes, Hypertension, valvular heart disease
Q2.Why haven't we done pericardiocenetis in this patient?
ANS. Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the heart (pericardium).
It's done using a needle and small catheter to drain excess fluid.
There are 3 approaches for needle entry - left parasternal, subxyphiod approach, left apical approach. All these require a lot of precision as they might damage the surrounding pleura, diaphragm , liver.
Pericardial effusion is mild - moderate in this patient , so symptomatic treatment was given rather than opting for an invasive procedure like pericardiocentesis which requires a lot of precision.
Risks of pericardiocentesis include- Puncturing the heart, which may require surgery to repair, Puncturing the liver, Excess bleeding, which might compress the heart and affect its normal function, Air in the chest cavity, Infection etc. if the procedure is not done properly
Also this patient has pleural effusion, this might make fluid extraction difficult without inflicting and damage as the needle is inserted very close to the lungs.
Q3.What are the risk factors for development of heart failure in the patient?
ANS.
A) Cigarette smoking
The patient is a chronic smoker (30years), which is a habit known to increase the risk of heart failure.
Mechanism- Cigarette smoking leads to impaired endothelial function via decreased nitric oxide production, pro-thrombotic state, increased oxidative stress, and activated inflammatory pathways.
Smoking, via increased oxidative stress and inflammation, directly effects on the myocardium leading to systolic and diastolic dysfunction.
It also promotes other heart failure (HF) risk factors including blood pressure, increased heart rate, diabetes, and atherosclerosis.
B) Chronic alcohol consumption
Patient consumes 90ml per day for the past 30 years
Heavy alcohol consumption is associated with alcoholic cardiomyopathy, characterized by left ventricular dilation, increased left ventricular mass, and reduced or normal left ventricular wall thickness among patients with a long-term history of heavy alcohol consumption.
Based on studies alcoholic patients with symptomatic HF had 10 years or more of exposure to heavy drinking .
C) Hypertension and Diabetes
Diabetes results in changes in myocardial structure and function by causing disproportionate left ventricular hypertrophy and perivascular and interstitial fibrosis
These changes result in diastolic and systolic dysfunction and increase risk of heart failure.
Hypertension increases work load on the heart and a result there is left ventricular hypertrophy — risk of heart failure
D) ECG reports of the patient indicate first degree AV block.
This is associated with an increased risk of heart failure.
Among patients with heart failure, first-degree atrioventricular block is present in anywhere between 15% and 51%.
E) 2D ECHO of the patient shows pericardial effusion
This increases pressure on the heart and if left untreated will lead to heart failure.
Q4.What could be the cause for hypotension in this patient?
ANS. Hypotension in this patient could be due to combination of pericardial effusion and use of diuretic LASIX (furosemide).
The pumping ability of the heart in this patient is compromised already. Along with this he is on a loop diuretic (causing sodium, potassium and chloride loss in the urine) and is on anti hypertensive medication (Telma 40 mg), along with fluid restriction. All these factors might result in Hypovolemia and thereby Hypotension
- high blood sugar can damage blood vessels and the nerves that control your heart. People with diabetes are also more likely to have other conditions that raise the risk for heart disease: High blood pressure increases the force of blood through your arteries and can damage artery walls
- High blood pressure: Damaged kidneys may release too much of an enzyme called renin, which helps to control blood pressure. This increases the risk for heart attack, congestive heart failure and stroke.
- The narrowing and blocking of blood vessels caused by high blood pressure (HBP or hypertension) increases your risk of developing heart failure
- as a complicaion of COVID
- shoes that do not fit correctly
- reduced circulation
- Candida albicans, a fungal infection
- other injury or irritation in the feet or hand.
CASE 3
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
Q1. What is the evolution of the symptomology 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 patients problem?
ANS. Timeline of the patient is as follows-
· 1 year ago- History of shortness of breath (Grade II- SOB on exertion); He visited the hospital where he was diagnosed to be hypertensive (on medication)
· 2 days ago- Patient was apparently asymptomatic 2 days ago when he developed Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital. Patient also complains of decreased urine output since 2 days.
· Present day- Patient came to the hospital with SOB grade IV (on rest) and anuria for the past one day.
Anatomical Location- Patient has an issue that was localized as an issue in the cardiac region.
Etiology- Congestive heart failure is a chronic progressive condition that affects the pumping power of the cardiac muscle. It occurs if the heart cannot pump (systolic) or fill (diastolic) adequately. Loss of atrial contraction and left atrial dilation in this case cause stasis of blood in the left atrium and may lead to thrombus formation in the left atrial appendage. This predisposes to stroke and other forms of systemic embolism.
2) Q2. What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS.
a) INJ. Dobutamine-
MOA- It is a synthetic catecholamine, that acts on B1, B2 and alpha 1 receptors.
Indications- It is a potent inotropic agent but only causes a slight increase in heart rate. It is given to patients with acute heart failure as iv infusion. 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg in this case.
b) TAB. Digoxin-
MOA- It acts on the digitalis receptor and inhibits NA-K-ATPase, thus increasing cardiac output.
Indications- Digitalis is used in patients with low output failure especially when associated with atrial fibrillation, as indicated in this case.
c) INJ. Unfractionated Heparin 5000-
MOA- At low concentration, heparin selectively inhibits the conversion of prothrombin to thrombin, thus preventing thrombus formation. High dose heparin has antiplatelet action and prolongs bleeding time.
Indications- Patient had a biatrial thrombus and in this case it was used to prevent further thrombus formation.
d) TAB. Carvediol 3.125mg BD
MOA- It blocks B1, B2, Alpha 1 adrenergic receptors and no intrinsic sympathomimetic activity.
Indications- Used as a long term drug to reduce mortality in patients with congestive heart failure.
e) TAB. Acetyl cysteine 600mg PO TID
f) TAB. Acitrom 2mg OD
MOA- It is an anticoagulant that functions as a vitamin K antagonist.
Indications- oral anticoagulant which helps to prevent formation of harmful blood clots in the legs, lungs, brain and heart. It is used for deep vein thrombosis, pulmonary embolism and stroke prevention.
g) TAB. Cardivas 3.125mg PO/BD
MOA- It is carvediol. It blocks B1, B2, Alpha 1 adrenergic receptors and no intrinsic sympathomimetic activity.
Indications- Used as a long term drug to reduce mortality in patients with congestive heart failure.
h) TAB. Dytor 10mg PO/OD
MOA- It is torsemide, a loop high ceiling diuretic. It acts on the thick ascending limb of the loop of henle, increases Na, K and Cl excretion in the urine.
Indications- preferred in cases of hypertension associated with CCF and renal failure.
i) TAB Pan D 40mg PO/OD
MOA- It is a combination of domperidone and pantaprazol. It is a proton pump inhibitor and helps decrease acid production in the stomach.
Indications- used to treat gastroesophageal reflux disease (Acid reflux) and peptic ulcer disease by relieving the symptoms of acidity such as indigestion, heartburn, stomach pain, or irritation.
j) TAB. Taxim 200mg PO/OD
MOA- It is cefixime. They are beta-lactam antibiotics that inhibit synthesis of bacterial cell wall and produce a bactericidal effect.
Indications- Given mainly to prevent development of bacterial infections.
k) INJ. Thiamine 100mg in 50ml NS IV/TID
It is vitamin B1. It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
l) INJ. HAI S.C 8U-8U-6U
Insulin given in this case to treat the patients denovo diabetes mellitus.
Q3. What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
ANS. Cardio renal syndrome is basically defined as “any acute or chronic problem in the heart or kidneys that could result in an acute or chronic problem of the other.”
The leading cause of CHF includes ischemic heart diseases and myocardial infarction, diabetes mellitus (DM), the metabolic syndrome and hypertension. CHF evolves due to a single cause, such as myocardial infarction or a cumulative process of multiple minor effects. Often one entity is poorly controlled and causes significant system stress. There is immediate stress on the kidney through pathophysiological connections when CHF develops. The connectivity of the vascular bed, and its regulation by the sympathetic nervous system (SNS) and renin-angiotension-aldosternone system (RAAS), continues the stress on the nephron. The long-term process results in scarring and fibrosis to both organs.
CHF as a syndrome occurs due to the over expression of biologically active molecules that are capable of deleterious effects. The cells such as the myocardial myocytes, are capable of producing these potentially toxic effectors within close vicinity of the injury with the capacity for ongoing autocrine and paracrine activity. The spill over of this toxic milieu reaches the kidney, which has to regulate salt and water retention to compensate for loss of cardiac output. Finally, an important source of renal stress is increased cardiac preload.
The kidneys receive 25% of blood flow, where the majority goes to the cortex, which also has the greatest neural innervations to regulate changes acutely. The medulla receives only 10% of the blood supply. The renal microvascular bed however is continuous throughout. Thus, disease in any glomeruli could have implications when placed under supraphysiological stress from SNS or RAAS and matched with early disease in vascular endothelium and nitric oxide systems.
( Reference- https://www.ncbi.nlm.nih.gov/books/NBK542305/ )
In this case the patient has Type 4 cardiorenal syndrome: a chronic decline in kidney function that results in chronic cardiac dysfunction.
4) Q4. What are the risk factors for atherosclerosis in this patient?
ANS. In this case, the risk factors for the development of atherosclerosis include:
a) Patient has Diabetes mellitus type 2, which can accelerate atherosclerosis by driving inflammation and slowing down blood flow.
b) Patient has history of alcohol abuse that can lead to atherosclerosis and increase the risk of stroke.
c) Patient has a history of NSAID abuse, which can change the vessels ability to relax and also stimulate growth of smooth muscle cells inside the arteries, thus leading to the clogging of the arteries.
d) Patient also has a history of hypertension- effect on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
5) Q5. Why was the patient asked to get those APTT, INR tests for review?
ANS. APTT- Activated partial thromboplastin time; this is a blood test that characterizes coagulation of blood. The patient has a propensity for thrombus formation, which needs to be monitored by keeping check on the aPTT levels which is an indicator for the coagulability of the blood.
INR- It is international normalized ratio; it is also a measure of the ability of the blood to clot. This is an important test for patients who are on blood thinners (ie) anticoagulants. The patient in this case was taking heparin, so everyday reports of his INR value were needed.
67 year old patient with acute coronary syndrome
Timeline of events-
- 12 years ago- Diagnosed with type 2 diabetes mellitus (on medication)
- Last 1 year- Heart burn like episodes since, relieved without medication
- 7 months ago- Diagnosed with pulmonary TB; Completed full course of treatment; presently sputum negative.
- Past 6 months - Hypertension diagnosis (on medication)
- Since half an hour- Shortness of breath, Grade IV (SOB even at rest)
Anatomical localisation - Cardiovascular system
Etiology- The patient is both Hypertensive and diabetic, both these conditions can cause atherosclerosis (there is build up of fatty and fibrous material inside the wall of arteries)
Q2. What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS. Pharmacological interventions:
a) TAB MET XL 25 MG/STAT
Contains Metoprolol as active ingredient
MOA: Metoprolol is a cardioselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect) and with less force (negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.
Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
Efficacy studies- Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.
Non pharmacological interventions - Advised to this patient is PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup (atherosclerosis).
Q3. What are the indications and contraindications for PCI?
ANS. Indications:
- 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)
Contraindications:
- Intolerance for oral antiplatelets long-term.
- Absence of cardiac surgery backup.
- Hypercoagulable state.
- High-grade chronic kidney disease.
- An artery with a diameter of <1.5 mm
Q4. 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?
ANS. Although PCI is generally a safe procedure , it might cause serious certain complications like
- Bleeding
- Blood vessel damage
- Allergic reaction to the contrast dye used
- Arrhythmias
- Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it. Research on over-testing and over-treatment is important as they are more harmful than useful.
Harm to patients
- Performing screening tests in patients with who at low risk for the disease which is being screened.
- For example: Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
- Overuse of imaging techniques such as X-rays and CT Scans as a part of routine investigations.
- Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant
- Over-diagnosis through overtesting can psychologically harm the patient.
- Hospitalisations for those with chronic conditions who could be treated as outpatients can lead to economic burden and a feeling of isolation.
- The use of expensive technologies and machineries are causing economic burden on health care systems.
CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION
- TAB. ASPIRIN- Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
- TAB ATORVAS -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.
- TAB CLOPIBB -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.
- INJ HAI- Regulates glucose metabolism. Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue.
- ANGIOPLASTY: Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
CASE 6
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
ANS. The patient presented with rapid breathing, which is an indicator of cardiogenic shock, if the patient also presents along with other signs such as cold, clammy extremities.
In cardiogenic shock, there is hypovolemia, which causes reduced perfusion to major organs in the body. When there is decreased perfusion, the body slows starts shutting down. To halt this process, iv fluids are given rapidly to continue the perfusion of fluids at the normal rate. Fluid resuscitation helps restore lost blood volume, regain tissue perfusion, and reduce mortality.
When this patient was given fluids, the perfusion returns to normal which helps abate the shortness of breath.
Q2. What is the rationale of using torsemide in this patient?
ANS. In patients who have cardiorenal syndrome, there is a renal dysfunction along with cardiac abnormalities. In such patients there is a volume overload and heart failure, the combination of which causes increased pulmonary artery or central venous pressure with low systemic pressure that may lead to a severe compromise of the net renal perfusion pressure.
Furosemide is a commonly used diuretic to treat volume overload state in heart failure, yet it is particularly prone to the problem of diuretic resistance because of its particular pharmacokinetics. Alternatives to furosemide, such as torsemide, have been shown to have a slight advantage in selected studies because of somewhat more favourable pharmacokinetics, such as longer half life and increased bioavailability of the drug.
Q3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
ANS. Patients with cardiorenal syndrome are known to have systemic inflammation which can be drawn parallel to end stage kidney disease. Here there is an inflammation of monocytes and other inflammatory cells. This puts the patient in a immune suppressive state.
Due to this state, to reduce the chances of infection, as a prophylactic measure, ceftriaxone might have been started.
4) GASTROENTEROLOGY (& Pulmonology)
CASE A
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
Q1. What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANS. Timeline of events-
5 years ago- An episode of pain abdomen and vomiting, treated conservatively at a local hospital.
Stopped alcohol consumption.
Symptom free for almost 3 years
2 years ago- Patient started consuming alcohol, this lead to recurrent episodes of pain abdomen and vomiting.
1 year ago- 5-6 episodes of pain abdomen and vomitings
Treated by a RMP.
1 week ago- Binge of alcohol
Since 1 week- Following this he had pain abdomen and vomiting
Since 4 days- High grade fever with chills and rigors, Developed constipation, burning micturition associated with subrapubic pain, increased frequency and urgency.
Anatomical localisation- Pancreas and left lung
Etiology- The patient is a chronic alcoholic, episodes of abdominal pain and vomiting are following alcohol consumption. Therefore it is heavy drinking that has led to the above condition in the patient.
Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
B.pharmacological interventions
- ING. MEROPENAM: Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
- ING. METROGYL :Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.
- ING. AMIKACIN The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
- TPN ( Total Parenteral Nutrition ): the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
- IV NS / RL Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal areas. Accordingly, they require prompt intravenous (IV) hydration within the first 24 hours. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important.
- ING. OCTREOTIDE Like somatostatin, octreotide also decreases the release of growth stimulating hormones, decreases blood flow to the digestive organs, and inhibits the release of digestive hormones such as serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.
- ING. PANTOP The mechanism of action of pantoprazole is to inhibit 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.
- ING. THIAMINE Vitamin B1 (thiamin) is indispensable for normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining normal cellular redox state.
- ING. TRAMADOL Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
CASE B
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
Q1. What is causing the patient's dyspnoea? How is it related to pancreatitis?
ANS. Pancreatitis is associated with shortness of breath. Acute pancreatitis can cause chemical changes in your body that affect your lung function, causing the level of oxygen in your blood to fall to dangerously low levels.
Acute pancreatitis is associated with release of inflammatory factors which the lungs, fluid accumulation which is also associated with pancreatitis (the patient was diagnosed pleural effusion) results in shortness of breath.
Q2. Name possible reasons why the patient has developed a state of hyperglycaemia.
ANS. Hyperglycemia in the early phase of AP may arise from mechanisms such as uncontrolled pre-existing DM, damage to the endocrine pancreas due to severe attack of AP, and metabolic stress associated with critical illness
1. Pancreatitis damages cells that produce insulin and glucagon which are hormones that control the levels of blood sugar. Insufficiency of these hormones can lead to hyperglycaemia.
2. Patient is a known alcoholic with increased consumption since 2 months (2 litres of toddy everyday) which could also be a cause of diabetes in the patient. But the patient was never tested before he came to our OPD and did not recall any notable signs.
Q3. What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
ANS. Excess alcohol consumption is known to elevate LFT’s.
Alcohol is a known hepatotoxin which effects liver functioning and there is no certain linear relation between the amount consumed and the stage of liver damage.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155359/
Sensitivity and specificity of biomarkers in detecting harmful or heavy alcohol consumption
Biomarker | AST | ALT | MCV | CDT | CDT + GGT | CDT + GGT + MCV |
Sensitivity | 47%-68% | 32%-50% | 45%-48% | 63%-84% | 83%-90% | 88% |
Specificity | 80%-95% | 87%-92% | 52%-94% | 92%-98% | 95%-98% | 95% |
AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; MCV: Mean corpuscular volume; CDT: Carbohydrate-deficient transferring; GGT: Gamma-glutamyltranspeptidase
(source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4155359/ )
GGT and CDT are usually taken as specific markers for ALD
Q4. What is the line of treatment in this patient?
ANS. Plan of action and Treatment:
Investigations:
✓ 24 hour urinary protein
✓ Fasting and Post prandial Blood glucose
✓ HbA1c
✓ USG guided pleural tapping
Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly
CASE C
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
Q1) What is the most probable diagnosis in this patient?
ANS. Differential Diagnosis:
- Ruptured Liver Abscess.
- Organized collection secondary to Hollow viscous Perforation.
- Organized Intraperitoneal Hematoma.
- Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
The most probably diagnosis is an abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
Common symptoms include abdominal pain, shortness of breath, chest pain, dizziness, bruising around your navel or on the sides of your abdomen, nausea, vomiting, blood in urine etc.
Q2) What was the cause of her death?
ANS. After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
Q3) Does her NSAID abuse have something to do with her condition? How?
ANS. NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity.
While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.
5)NEPHROLOGY
An Eight year old with Frequent Urination
6.INFECTIOUS DISEASES &(HEPATOLOGY)
CASE A
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
Q1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it? What could be the cause in this patient?
ANS. Patient is toddy drinker since for the past 30 years and by occupation he is a palm tree climber.
Toddy is a locally brewed beverage, which is cultivated from the fruit of the palm tree and left to ferment in clay pots. If the conditions are unhygienic it gets contaminated with bacteria, fungi, parasites.
Of particular contamination with Entamoeba Histolytica is known to cause liver abscess.
Based on his occupation the patient belongs to low socio economic group - so chances of malnutrition is more, which further favours the survival of the parasite.
Q2. What is the etio-pathogenesis of liver abscess in a chronic alcoholic patient ?
ANS. The patient has a history of consumption of alcohol ( 1 bottle per day for the past 30 years). Alcohol causes Amoebic liver abcesses (ALA) through a multitude of mechanisms:
• Alcohol induced hepatic dysfunction
• It lowers body resistance and suppresses immune mechanisms in the habitual consumers.
• Locally prepared alcohol (toddy) when brewed in unhygienic conditions may be contaminated by pathogens (In this case, E Histolytica)
• Toddy has very less alcoholic content (< 5%) - this favours the survival of Entamoeba and promotes the conversion of latent forms to virulent forms resulting in more symptomatic cases.
• Alcohol-induced hepatic dysfunction and possible suppression of amoebistatic immune mechanisms by substances in the beverages could also be attributed in the mechanism [6].
Socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
(Reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/ )
Q3. Is liver abscess more common in right lobe?
ANS. Liver abscess is more common in right lobe than left lobe (The involvement of right lobe to left lobe is in the ratio of 2: 1)
Liver abscess is more common in the right lobe than left lobe because-
• 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 more hepatic mass.
Q4.What are the indications for ultrasound guided aspiration of liver abscess?
ANS. Indications for aspiration of a liver abscess include the following:
• Presence of a left lobe abscess of more than 10cm in diameter.
• Pain and impending rupture.
• Abscess that does not respond to medical treatment within 3-5 days.
CASE B
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
ANS. Amoebic liver abscess (ALA ) seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extra intestinal invasion of the infective protozoan and the subsequent development of ALA. (Ref- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6586571/ , https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/ )
Hence the consumption of locally made alcohol (toddy) is the most likely cause of Liver abscess in this patient.
Q2. How do you approach this patient ?
ANS. When patient presents with chief complaints of abdominal pain, fever -
1. Detailed history regarding each of the symptom should be taken.
2. General examination to know the overall health status should be carried out.
3. Following general examination, systemic examination should be done.
Patient’s symptoms point out to the involvement of Gastrointestinal system, therefore special emphasis should be on per abdominal examination.
4. Through history and examination , we arrive at provisional diagnosis.
5. To confirm the diagnosis, investigations, imaging tests should be taken.
6. For this patient based oh his symptomatology , the following investigations should be done.
CBP, LFT, RFT, Urine analysis
7. Imaging tests- CXR, USG abdomen.
Based on the results of these the diagnosis can be confirmed, treatment can be initiated.
This patient is diagnosed with Liver Abscess (by the above approach).
The following treatment can be given.
- In practice an empirical treatment is given to treat both amoebic and pyogenic liver abscess
- This includes use of Broad spectrum antibiotics( for pyogenic liver abscess) , Metronidazole ( for amoebic liver abscess)
- Analgesics and anti inflammatory drugs -to relieve pain and fever.
- Multivitamin supplements
- Saline infusion- to maintain fluid levels.
All the above medicines should be given for 7- 10 days.
Following this review the patient and see if there is any improvement.
USG abdomen should be done se if the abscess is resolving.
Investigations ( CBP, LFT , RFT ) should be done to check for the improvement.
If the abscess did not resolve Ultrasound guided aspiration should be done.
Q3. Why do we treat here both amoebic and pyogenic liver Abscess?
ANS. The presentation for both amoebic , pyogenic liver abscess is the same (ie) pain abdomen, fever, constitutional symptoms like nausea and vomiting , loss of appetite, in some cases there may be pulmonary symptoms.
Investigations-
There is leucocytosis, elevated alkaline phosphatase, ALT, AST
USG-a hypo echoic mass for both type of abscess.
Amoebic and pyogenic liver abscess can be differentiated only by culture and sensitivity of the aspirate obtained by USG guided aspiration of abscess.
USG guided aspiration has the following risk factors associated with it:
1) If abscess is thin walled there is a risk of rupture.
2) If abscess is on the posterior aspect of the liver, it will not be accessible.
3) There is also a risk of bleeding.
Blood culture taken prior to the administration of antibiotics is helpful for identifying the causative organism but as this patient had already taken antimicrobials before he came to the hospital, there is severe abdominal pain treatment is started immediately without a blood culture report.
Considering that it is difficult to distinguish amoebic liver abscess from pyogenic liver abscess,
We treat both forms of Liver abscess empirically using-
• Broad spectrum antibiotics- a combination of penicillin , cephalosporin, aminoglycosides
• Metronidazole- has both antibacterial and antiprotozoal activity.
( Reference- https://academic.oup.com/bmb/article/132/1/45/5677141 )
Q4. Is there a way to confirm the definitive diagnosis in this patient?
ANS. Liver abscess can be confirmed by USG Abdomen.
It presents as single/ multiple, round/ oval, hypoechoic- hyper echoic mass more commonly is the right lobe of the liver.
However USG cannot differentiate an amoebic liver abscess from pyogenic liver abscess.
For this
• Blood culture
• USG guided aspiration of the abscess should be done.
This aspirate should be subjected to antigen testing for –
Subjected to microbiological culture and sensitivity to identify pyogenic organisms.
( Reference- https://academic.oup.com/bmb/article/132/1/45/5677141 )
A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
CASE A
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Q1. 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 aetiology of the patient's problem?
ANS.
3 years ago- diagnosed with hypertension
21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication
18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
11 days ago - C/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state
4 days ago-
a. Patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
b. Towards the evening patient periorbital oedema progressed
c. Serous discharge from the left eye that was blood tinged
d. Was diagnosed with diabetes mellitus
6. Patient was referred to a government general hospital
7. Patient died 2 days ago
Patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels.
The patient was diagnosed with acute oro rhino orbital mucormycosis. Rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes. The fungus enters the sinuses from the environment and then the brain.
The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA.
Q2. What is the efficacy of drugs used along with other non-pharmacological treatment modalities and how would you approach this patient as a treating physician?
ANS. The management of the patient was-
1. Inj. Liposomal amphotericin B
2. 200mg Iatraconazole was given as it was the only available drug which was adjusted to his creatinine clearance.
3. Deoxycholate was the required drug which was unavailable
Along with the above mentioned treatment for the patient managing others symptoms is also done by-
I. Management of diabetic ketoacidosis –
(a) Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
(c) Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy
Q3. What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
ANS. Mucormycosis may be being triggered by the use of steroids, which are life-saving drugs for severe and critically ill Covid-19 patients.
Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing.
Reference- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7599039/
9) Infectious Diseases (COVID- 19)
For this question that contains details of many of the hospitals Covid 19 patients documented over this month I have collected information adhering to the following points-
http://medicinedepartment.blogspot.com/2021/05/covid-case-report-logs-from-may-2021.html?m=1
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
3) Indicate for each patient, the day of Covid when their severity changed from moderate to severe or vice versa recognized primarily through increasing or decreasing oxygen requirements
4) Indicate the sequence of specific terminal events for those who died with severe Covid (for example, altered sensorium, hypotension etc).
I have compiled all the data collected in the form of an excel spreadsheet, so as to be able to draw a comparative analysis about the progression of disease and the outcome in various patients.
https://drive.google.com/file/d/1kltJgtrvB1pfk21ebBBGspZ1t_Wn5xHs/view?usp=sharing
10. Medical education
posted by Imama Muhmeen 163 @ May 30, 2021
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