general medicine may assignment
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General medicine assignment for may
30/5/2021
Name: Palle Lokesh Reddy
Roll no:103
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 coem up with a treatment plan.
This is the link of the questions asked regarding the cases:http://medicinedepartment.blogspot.com/021/05/online-blended-bimonthly-assignment.html
Below are my answers to the Medicine Assignment based on my comprehension of the case
Pulmonology
A) Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem? ans;History
a]few years back that is almost 20 years back-shortness of breath was seen as this is the 1st episode
in the month of january .that was releveied by taking medication and it was lasted about one week during working in the paddy feilds .[this continued about seven years in the same period]
12 years ago she had shortness of breath which has lasted about 20 days and continued same pattern for 30days.
Latest episode; it lasts for about 30 days and it does not releive by medication.
Other sympyoms; amnesia - 5 yrs ago,generalised weakness [one month ago], Hypotension,Pitting type pedal edema and facial puffiness.
ANATOMICAL LOCALISATION OF PROBLEM;
bronchi and bronchioles of the lung
PRIMARY ETIOLOGY;
The symptoms are probably due to the inhalation of paddy dust,and ongoing causative exposure,and abnormal inflamatory responce of the lung.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS; 1] Head and elevation; It improves end expiratory lung volumes.and also shown to improve the oxygenattion and hypodynemic performance.
2] B2.Bipap intermittent: By having a custom air pressure for when you inhale and a second custom air pressure when you exhale, the machine is able to provide relief to your overworked lungs and chest wall muscles.
3.inj.Augmentin
Augmentin is a prescription antibiotic medication. It’s used to treat infections caused by bacteria. Augmentin belongs to the penicillin class of antibiotics.Augmentin contains two drugs: amoxicillin and clavulanic acid. This combination makes Augmentin work against more types of bacteria than antibiotics that contain amoxicillin alone.Augmentin is effective for treating infections caused by many different types of bacteria. These include bacteria that cause:
pneumonia, ear infections, sinus infections,skin infections,urinary tract infections
4. Tab Azithromycin antibiotic
It's widely used to treat chest infections such as pneumonia, infections of the nose and throat such as sinus infection (sinusitis), skin infections, Lyme disease, and some sexually transmitted infections.
5. Inj lasix
Furosemide is used to reduce extra fluid in the body (edema) caused by conditions such as heart failure, liver disease, and kidney disease. This can lessen symptoms such as shortness of breath and swelling in your arms, legs, and abdomen.This drug is also used to treat high blood pressure.
6.Tab pantop
It is commonly used for the diagnosis or treatment of Gastro-esophageal reflux disease, Heartburn, Esophagus inflammation, Stomach ulcers.
7.Inj.Hydrocortisone
It is used to treat disorders of the skin, hormones, stomach, blood, nerves, eyes, kidneys, or lungs. They also include rheumatic disorders, allergic problems, certain cancers, or problems with the intestines such as ulcerative colitis.
8.Nebuliser with
A) ipravent: It is an anticholinergic bronchodilator. It is used in the Treatment of COPD and prevention of asthma
B)budecort: It is a corticosteroid and acts as an anti-asthmatic agent. It helps in controlling daily symptoms such as shortness of breath, wheezing and chest pain and prevents the worsening of these symptoms. Budecort should always be administered with the help of nebulisers. Nebuliser is a machine that forms a mist of medicine so that it can reach the lungs2.Bipap intermittent: By having a custom air pressure for when you inhale and a second custom air pressure when you exhale, the machine is able to provide relief to your overworked lungs and chest wall muscles.
3.inj.Augmentin
Augmentin is a prescription antibiotic medication. It’s used to treat infections caused by bacteria. Augmentin belongs to the penicillin class of antibiotics. Augmentin contains two drugs: amoxicillin and clavulanic acid. This combination makes Augmentin work against more types of bacteria than antibiotics that contain amoxicillin alone. Augmentin is effective for treating infections caused by many different types of bacteria. These include bacteria that cause:
pneumonia, ear infections, sinus infections ,skin infections, urinary tract infections
4. Tab Azithromycin antibiotic
It's widely used to treat chest infections such as pneumonia, infections of the nose and throat such as sinus infection (sinusitis), skin infections, Lyme disease, and some sexually transmitted infections.
5. Inj lasix
Furosemide is used to reduce extra fluid in the body (edema) caused by conditions such as heart failure, liver disease, and kidney disease. This can lessen symptoms such as shortness of breath and swelling in your arms, legs, and abdomen.This drug is also used to treat high blood pressure.
6.Tab pantop
It is commonly used for the diagnosis or treatment of Gastro-esophageal reflux disease, Heartburn, Esophagus inflammation, Stomach ulcers.
7.Inj.Hydrocortisone
It is used to treat disorders of the skin, hormones, stomach, blood, nerves, eyes, kidneys, or lungs. They also include rheumatic disorders, allergic problems, certain cancers, or problems with the intestines such as ulcerative colitis.
8.Nebuliser with
A) ipravent: It is an anticholinergic bronchodilator. It is used in the Treatment of COPD and prevention of asthma
B)budecort: It is a corticosteroid and acts as an anti-asthmatic agent. It helps in controlling daily symptoms such as shortness of breath, wheezing and chest pain and prevents the worsening of these symptoms. Budecort should always be administered with the help of nebulisers. Nebuliser is a machine that forms a mist of medicine so that it can reach the lungs
9. Chest physcio therapy
10. GRBS 6hrly
11. vitals charting
12; inj thiamine ;to treat or prevent thiamine insufficiancy.
13. O2 inhalation
It is used to
A) manage the condition of hypoxia
B)maintain o2 tension in blood plasma
C)increase oxy haemoglobin in RBC
D) maintain ability of cells to carry out normal metabolic function
E)reduce the risk of complication
3) What could be the causes for her current acute exacerbation?
Ans; respiratory infectiionbeing responcibleb for the approx half of the COPD exacerbations.as the infection by allergens
4. Could the ATT have affected her symptoms? If so how?
Ans;yes, it can affect There are some case reports about interstitial lung disease (ILD) such as pneumonitis caused by isoniazid (INH), rifampin (RFP), ethambutol (EMB). Therefore The causative drug was discontinued permanently or re-administrated after desensitization therapy.
5.What could be the causes for her electrolyte imbalance?
Ans; Activatyion of the renin angiotensin -aldosterone system and appropriately elevated vplasma arginine vasopressin in COPD may aggrevate the Electrolyte imbalance durind active accerbation of COPD.
2) Neurology
A) Link to patient details: A 40 year old male presented the hospital from Yadagirigutta withb the cheif complaints of
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans ; as the patient is chronic alchoholic,he drinks about 3-4 quarters per day.
Evolution of symptomology;
1 year ago-2 to 3 episodes of seizures
4 months ago-Following cessation of alcohol he developed seizures probably GTCS
9 days back-The patient started talking and laughing to himself
withdrawal seizures are triggered by neuronal networks in the brainstem, including the inferior colliculus.
Ethanol is the primary alcohol ingested by chronic users. It is a central nervous system (CNS) depressant that the body becomes reliant on with extended exposure to ethanol. It does this by inhibiting the excitatory portion (glutamate receptors) of the CNS and enhancing the inhibitory portions (GABA receptors) of the CNS. When the depressant is stopped, the central nervous system becomes overexcited as the inhibition is taken away. Thus, the body gets an excitatory overload, which results in the symptoms of withdrawal.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ans; as the aim of lowering the alcohol levels and its metabolites ,its neuro deppresive effects
and making patients spnding less in the ED
THIAMINE -
mechanism of action ;combines with adenisine tri phosphate in the liver. and it has no effect onthe symptoms and signs of the alcohol withdrawl .or on the incidence of the seizuers . routine use of the thiamine is recomended because the development of Wernicke encephalopathy or Wernicke-Korsakoff syndrome is disastrous in these patients and can remain unrecognized. Because orally administered thiamine may have poor enteral absorption in individuals with alcoholism, high-risk patients should receive parenteral thiamine at 100-250 mg once daily for several days.
LORAZEPAM; it was by the rehab facilities across the nations to help patients overcome the AUD
As the mechanism of action it binds to the benzodizepam receptors on the post synaptic GABA ligand gated channels.
the indications are active seizures ,severe anxiety.
Efficacy; it is used to treat all the seizuers
PREGABALIN; It was the high α2δ voltage gated channel subunit ligand and acounting for there actions invivo to reduce neuronal excitability and seizures
Potchlor Potklor liquid is used to treat low levels of potassium in the body
3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Ans; due to the excess thalamine deficiency and excess toxins accumalation and due to renal disease caused by excess alcohol addiction.
4) What is the reason for giving thiamine in this patient?
Ans; chronic alcohol cosumption causes thalamine deficiency due to impaired absorbstion of thalamine from the intestine A number of mechanisms may be involved in the pathogenesis of thiamin deficiency in the alcoholic population. An important cause is inadequate intake of thiamin. Moreover, there may be decreased conversation of thiamine to the active coenzyme, reduced hepatic storage of the vitamin in patients with fatty metamorphosis, ethanol inhibition of intestinal thiamine transport, and impaired thiamine absorption secondary to other states of nutritional defi
5) What is the probable reason for kidney injury in this patient?
Ans; Mechanical ventilation was an important treatment for patients with AECOPD.13 On the contrary, mechanical ventilation was also an independent risk factor for AKI.
6). What is the probable cause for the normocytic anemia
Anemia of chronic disease (ACD) is probably the most common type of anemia associated with COPD. ACD is driven by COPD-mediated systemic inflammation. Anemia in COPD is associated with greater healthcare resource utilization, impaired quality of life, decreased survival, and a greater likelihood of hospitalization. Anemia was normocytic and normochromic in nature. The exact cause of anemia of chronic disease may vary. Anemia can be caused by a slight shortening of normal red blood cell survival. the production of red blood cells (erythropoiesis) or erythropoietin (a hormone that stimulates red blood cell production) may be impaired.
7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Oxygen is important for cell metabolism and is critical for all wound-healing processes Inhibits wound healing by reducing the quantity and quality of oxygen to the wound site.
B) Link to patient details:
Questions-
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans; 7 days back- Giddiness and 1 episode of vomiting
Asymptotic for 3 days
4 days back-Giddiness (sudden continuous and gradually progressive)
Bilateral hearing loss with aural fullness and tinnitus
Vomitings 2-3 episodes per day(non projectile non bilious with food particles
Postural instability Unable to walk without support and is swaying with tendency to fall while walking
Anatomical localisation
Cerebellum which is responsible for postural stability ,ocular movements and vertigo(central)
usually results from damage to the part of your brain that controls muscle coordination (cerebellum). conditions can cause ataxia, including alcohol misuse, certain medication, stroke, tumor, cerebral palsy, brain degeneration and multiple sclerosis.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans; Vertin Tablet is employed to stop and treat a disorder of the internal ear referred to as disease. The symptoms include dizziness (vertigo), ringing within the ears (tinnitus), and loss of hearing, probably caused by fluid within the ear. This medicine helps relieve the symptoms by reducing the number of fluid.
Zofer anti-emetics' primarily utilized in the prevention of vomiting (being sick) and nausea (feeling sick) that typically occur after cancer chemotherapy, radiation treatment or surgery.
Ecosporin commonly used for the diagnosis or treatment of Headache, migraine, fever, pharyngitis, neuralgia
Atorvostatin
Statins are effective in reducing both first-ever and recurrent stroke, and this effect seems driven by the extent of LDL-C lowering
Clopidogrel could be a variety of medicine called an antiplatelet: it reduces the danger of blood clots forming within your vascular system or blood vessels.
Mvt Methylcobalamin is employed in cyanocobalamin deficiency.
Methylcobalamin could be a kind of vitamin B that restores its level within the body thereby helping in treating certain anemias and nerve problems.
3) Did the patients history of denovo HTN contribute to his current condition?
Ans; Raised blood pressure (BP) is common after stroke but its causes, effects, and management still remain uncertain.It exists in more than three quarters of patients, of which about half have a history of hypertension [1], and it declines spontaneously in two-thirds of cases returning to prestroke levels over the first week. Its decrease usually occurs 4–10 days after stroke, but in a significant percentage of patients it falls by about 25–30% just within the first 24 hours; particularly when they are moved to a quiet room, they are allowed to rest and their bladder is empty
4) Does the patients history of alcoholisM make him more susceptible to ischaemic or haemorrhagic type of stroke?Ans; Yes, Atrial fibrillation and alcohol Drinking excessive amounts of alcohol can trigger atrial fibrillation – a type of irregulaR heartbeat. Atrial fibrillation increases your risk of stroke by five times, because it can cause blood clots to form in the heart. If these clots move up into the brain, it can lead to stroke.
C) Link to patient details http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html
Questions:1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
10 years back-Paralysis of both upper and lower limbs bilateral 1 year back-Right anD left paresis due to hypokalemia8 months backSwelling over legs 7 months back - blood infection 2 months back- neck pain6 days back- pain along left upper limb5 days back- chest pain, Difficulty in breathing and was able to feel her own heart bAnatomical localization: Cervical spinE degenerative changes that occur in the cervical spine with age.Dehydrated disks. Disks act like cushions between the vertebrae of your spine. By the age of 40, most people's spinal disks begin drying out and shrinking, which allows more bone-on-bone contact between the vertebrae.Bone spurs. Disk degeneration often results in the spine producing extra amounts of bone in a misguided effort to strengthen the spine. These bone spurs can sometimes pinch the spinal cord and nerve roots.Herniated disks. Age also affects the exterior of your spinal disks. Cracks often appear, leading to bulging (herniated) disks — which sometimes can press on the spinal cord and nerve roots.Stiff ligaments. Ligaments are cords of tissue that connect bone to bone. Spinal ligaments can stiffen with age, making your neck less flexible.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia
Ans; Reasons for recurrence The primary hypokalemic periodic paralysis is autosomal dominant and is exacerbated by strenuous exercise, high carbohydrate diet, cold and excitement, which was not found in this case. secondary periodic hypokalemic paralysis have been reported in association with gastroenteritis, diuretic abuse, renal tubular acidosis, Bartter syndrome, villous adenoma of colon, and hyperthyroidism
Risk factors
Female [1]
[2]Medications like diureticsHeart failure
HypertensionLow BMI [3]Eating disorder and alcoholism: low intake of potassiumDiarrhea, cushing syndrome,
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?Ans; ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalemia. Severe hypokalemia can also result in arrhythmias such as Torsades de points and ventricular tachycardia.
Associated symptoms:
Weakness and fatigue (most common)
Muscle cramps and pain (severe cases)
Worsening diabetes control or polyuria.
Palpitations.
Psychological symptoms
D) Link to patient details:
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Ans; The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition
2.What are warning signs of CVA
Ans;Normally the “consciousness system”—a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness These functions involve a group of brainstem and forebrain areas that form the consciousness system and include the reticular formation of the brainstem, hypothalamus, basal forebrain, thalamus, and cerebral cortex.
Mechanism: Although many cognitive and behavioral processes occur without awareness, consciousness plays a critical role in cognitive mechanisms and forms the basis of our experience. An improved understanding of conscious mechanisms will provide insights into a variety of neurological disorders and new therapeutic approaches.
E) Link to patient details:
Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans; By the history, Patient is an alcoholic and he has change in his gait since a year are the findings which leads to cause of ataxia.
Mechanism:Damage from alcohol is a common cause ofcerebellar ataxia. In patients with alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech. It can also cause associated signs of peripheral neuropathy. Peripheral neuropathy is damage to the body's peripheral nervous system.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
Ans; Patient has a history of binge drinking for 3 hours before the day of admission.
Heavy drinkers were about 1.6 times more likely to suffer from intracerebral hemorrhage and 1.8 times more likely to suffer from subarachnoid hemorrhage. The association between heavy alcohol consumption and these two types of stroke was stronger than that for ischemic stroke. Yes alchol could have increased IC bleeding.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.
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition
Ans; Yes
2.What are warning signs of CVA?
Answer: The five warning signs of stroke are:
•Sudden onset of weakness or numbness on one side of the body.
Sudden speech difficulty or confusion.
Sudden difficulty seeing in one or both eyes.
Sudden onset of dizziness, trouble walking or loss of balance.
Sudden, severe headache with no known cause.
3.What is the drug rationale in CVA?
Ans;Mannitol- 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.
Ecospirin
For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.
Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.
Rt feed RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.
4. Does alcohol has any role in his attack?
Ans; When the patient met with an accident there might be cranial damage which was unnoticed.
If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition
But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.Therefore it cannot be evaluated without further details
5.Does his lipid profile has any role for his attack??
Ans; The inverse relationship between serum HDL-C and stroke risk . When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.
G) Link to patient details:
__*Questions*_
1)What is myelopathy hand ?
Ans; A characteristic dysfunction of the hand has been observed in various cervical spinal disorders when there is involvement of the spinal cord. There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
2)What is finger escape ?
Ans; Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi.
This commonly results from weakness of some of the ulnar nerve innervated intrinsic hand muscles -in particular the palmar interosseous muscle to the little finger- caused by damage to their nerve supply (denervation)
3)What is Hoffman’s reflex?
Ans ; The Hoffmann's reflex test itself involves loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. A positive response is seen when there is flexion and adduction of the thumb on the same hand
which can help verify the presence or absence of issues arising from the corticospinal tract.
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
Ans; Presence of cortical vein thrombosis with hemorrhagic venous infarction in right posterior temporal lobe and also Iron deficiency anaemia
2) What are the risk factors for cortical vein thrombosis?
Ans; For children and infants Problems with the way their blood forms clots
Sickle cell anemia
Chronic hemolytic anemia
Beta-thalassemia major
Heart disease — either congenital (you're born with it) or acquired (you develop it)
Iron deficiency
Certain infections
Dehydration
Head injury
For newborns, a mother who had certain infections or a history of infertility
For adults
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?
Ans Missed medication
Lack of sleep
Stress
Menstruation About half of women of childbearing age with epilepsy have increased seizures around their period. This is most likely due to hormonal changes that occur during your monthly cycle.
Herbal medications — as well as the herbs that go into many dietary supplements — can actually cause seizures or worsen side effects of seizure medication. The same goes with essential oils. Certain ones, such as juniper and umbrella plant, have been known to induce seizures.
Vitamin B6 (pyridoxine) deficiency is the only type of vitamin deficiency that’s been proven to potentially cause or worsen seizures
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Ans ; Inj sodium valproate and Inj phenytoin have anti platlet activity
3) Cardiology (10 Marks)
A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans; Preserved ejection fraction(HFpEF) – also referred to as diastolic heart failure. The heartmuscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure.
HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease
2.Why haven't we done pericardiocenetis in this pateint?
Ans It’s resolving : 2.07cms effusion at the time of admission -1.4mm at the time of discharge)
DM type 2 (since 1month)
So, No need of pericardiocentis.
3.What are the risk factors for development of heart failure in the patient?
Answer: Risk factors
High blood pressure.
Coronary artery disease
Diabetes.
Some diabetic and hypertensive medications.
• age
4.What could be the cause for hypotension in this patient?
Answer: Decreased venous return cause decreased cardiac output which results in hypotension.
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient?
Ans;l Alcoholic cardiomyopathy is a form of heart disease caused by alcohol abuse. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
High blood pressure can strain your heart, damage blood vessels, and increase your risk of heart attack
Diseases in the kidneys can affect the heart. It is common for people with chronic kidney disease or end-stage kidney disease to develop heart disease, including heart attack or heart failure.
2.what is the reason for anaemia in this case?
Ans; In the general elderly population, anemia is caused by nutritional deficiencies (primarily iron), chronic inflammation/CKD, or unexplained anemia of the elderly (a hypoproliferative anemia with blunted erythropoietin response)
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Ans; When high blood sugar destroys nerves, they do not regenerate; thus many patients with diabetes are increasingly less sensitive to pain in their limbs. With this loss of sensation, patients don't feel developing blisters, infections, or existing wound changes. That means that wound healing is complicated not only by the fact that patients don't feel wounds as they occur, but they also have no pain to alert them that a wound is getting worse or infected.
4. What sequence of stages of diabetes has been noted in this patient?
Ans; stage 1: defined as DCBD (dysglycemia-based chronic disease )insulin resistance;
stage 2: defined as DCBD prediabetes;
stage 3: defined as DCBD type 2 diabetes; and
stage 4: defined as DCBD vascular complications, including retinopathy, nephropathy or neuropathy, and/or type 2 diabetes-related microvascular events.
All these stages have been noted in this case
C) Link to patient details:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: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 and Anuria since morning.
Anatomical localization is heart
Primary etiology is atrial fibrillation
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans; 1) INJ. Dobutamine 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg.
Mechanism of action: Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine
2) TAB. Digoxin 0.25mg OD 5/7 and INJ. Unfractionated Heparin 5000 IU TID.
Mechanism of action: Digoxin has two principal mechanisms of action which are selectively employed depending on the indication: Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the hear.
3[INJ. Unfractionated Heparin Infusion @5ml/hr
Mechanism of action: It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. ... By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.Other medications used during the course in hospital -
1. TAB. Cardivas3.125mg PO/BD
2. TAB. Dytor 10mg PO/OD
3. TAB Pan D 40mg PO/OD
4. TAB. Taxim 200mg PO/OD
5. INJ. Thiamine 100mg in 50ml NS IV/TID
6. INJ. HAI S.C 8U-8U-6U
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans; The pathophysiology of CRS can be attributed to two broad categories of "hemodynamic factors" such as low cardiac output, elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors or "cardiorenal connectors" such as neurohormonal and inflammatory activation.[5] It was previously believed that low cardiac output in heart failure patients result in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of these patients will result in hypovolemia and pre-renal azotemia.
In addition, CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.[3]Therefore, there must be additional mechanisms involved in the progression of CRS. Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to worsening kidney function.[3]
In addition, many neurohormonal and inflammatory agents are implicated in the progression of CRS. These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which can result in myocardial hyprtrophy and necrosis.
Other cardiorenal connectors include renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, inflammatory factors and abnormal activation of the sympathetic nervous system, which can cause structural and functional abnormalities in both heart and/or the kidney. There is a close interaction within these cardiorenal connectors as well as between these factors and the hemodynamic factors which makes the study of CRS pathophysiology complicated.
4) What are the risk factors for atherosclerosis in this patien
Ans; High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet.t?
5) Why was the patient asked to get those APTT, INR tests for review?
Ans; Standard coagulation screening tests such as activated partial thromboplastin time (APTT), prothrombin time (PT), and the international normalized ratio (INR) are important constituents of basic examinations in clinical laboratories. APTT can be used as an indicator of intrinsic coagulation pathway activity, and a short APTT is linked to increased thrombin generation and increased risk for thrombosis.
D) Link to patient details:
Questions-
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans; Evolution of symptomatology
12 years ago- DM2
1year back Heart burn like episodes(relieved without medication)
7 months back pulmonary TB (completed the course one month back)
6 months back Hypertension
1/2 hour ago- SOB
Anatomical localisation: Heart muscle
Primary etiology
Coronary artery disease:involves the reduction of blood flow to the heart muscle due to build-up of plaque (atherosclerosis) in the arteries of the heart
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans;Met XL 25 tablet is used to lower the raised blood pressure and various other heart-related conditions such as angina (chest pain), heart failure, preventing further complications.
Glimiprime M 2 Forte Tablet is a combination of two medicines: Glimepiride and Metformin. This medicine is used in the treatment of type 2 diabetes mellitus (DM). It improves blood glucose levels in adults when taken along with proper diet and regular exercise
Telma 20 tablet is an antihypertensive medicine that is used to treat high blood pressure and can also help in reducing other heart problems It acts by relaxing the blood vessels and leads to lower blood pressure
3) 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)
High risk stress test findings.
CONTRAINDICATIONS:
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?
Ans ;people suffer complications including bleeding, blood clots, infection, heart rhythm disturbances and even death from heart attack if PCI is performed in a patient who doesnot need it.
associated with substantial morbidity and mortality given the large amount of subtended myocardium at risk
) Link to patient details:
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans ;Evolution of symptomatology:
Uncontrolled DM2 since 8 years
3 days back Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical localisation: Inferior wall of heart
Primary etiology: Diabetes type 2 (uncontrolled)
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans;TAB. ASPIRIN 325 mg PO/STAT
Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.
TAB ATORVAS 80mg PO/STAT
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.
TAB CLOPIBB 300mg PO/STAT
Mechanism of action: The active metabolite of clopidogrelselectively 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 6U/IV STAT
VITAL MONITORING.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans; Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty
Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.
F) Link to patient details:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
2. What is the rationale of using torsemide in this patient?
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Gastroenterology (& Pulmonology)
A) Link to patient details:
CASE-1:
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
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?
Anbs; Timespan of symptomology
5 years ago: 1st episode of pain abdomen and vomiting
1 year back: 5 to 6 episodes of pain abdomen and vomitings
20 days back: Increased consumption of toddy intake
Since 1 week: Pain abdomen and vomiting
Since 4 weeks: Fever, constipation and burning micturition
Anatomical localization: Pancreas and left lung
Etiology: The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes attributed to alcohol.
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans; Inj. Metrogyl: Metronidazole is of the nitroimidazole class. It inhibits nucleic acid synthesis by forming nitroso radicals, which disrupt the DNA of microbial cells
Inj. 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.
Inj. 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'
TOTAL PARENTAL NUTRITION
Inj. Octerotide: Octreotide suppresses secretion of growth hormone (GH), and in many cases suppresses insulin-like growth hormone-1 (IGF-1) (somatomedin C). Sandostatin works centrally at the site of the tumor and binds to somatostatin receptors to regulate GH secretion and cell growth.
Inj. 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.
Inj. Thiamine: 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.
Inj. 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
B) Link to patient details:
.CASE-2;
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans) Pleural effusion might be the cause of patients dyspnea.
Presence of pleural effusion is currently considered an indication of severe pancreatitis and not just a marker of the disease[24]. Pancreatic ascites and pleural effusion are rare complications of both chronic and acute pancreatitis, and are associated with a mortality rate of 20% to 30%.
2) Name possible reasons why the patient has developed a state of hyperglycemia.
Ans) Hyperglucagonemia secondary to stress could be the result of patient developing hyperglycemia.
Elevated levels of catecholamines and cortisol.
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans) Elevated liver enzymes are a sign that a person has an inflamed or a damaged liver. Many conditions may cause liver inflammation or damage. In this case the probable reason may be due to liver injury. Alanine aminotransferace (ALT) and Asparate aminotransferase (AST) are the specific markers for alcoholic fatty liver disease. Glutamyl transpeptidase (GGT) is another marker of liver injury, and this enzyme is elevated in people who consumes alcohol. Of all the enzyme markers GGT is the most sensitive biomarker of alcohol consumption.
4) What is the line of treatment in this patient?
Ans) IVF: 125 ml/hr
Inj. PAN 40mg i.v.
Inj Zofer 4mg i.v.
Inj. Tramadol 1amp in 100ml i.v.
Tab. Dolo 650mg
GRBS charting 6th hourly
BP charting 8th hourly.
C) Link to patient details:
1) What is the most probable diagnosis in this patient?
Ans) Abdominal Hemorrhage may be the most probable diagnosis in this patient.
2) What was the cause of her death?
Ans) Cause of her death may be due to complications of laparotomy surgery such as hemorrhage, infection, or damage to internl organs.
3) Does her NSAID abuse have something to do with her condition? How?
Ans) NSAIDS are known to cause drug induced hepatitis which may lead to cirrhosis.
5) Nephrology (and Urology)
A) Link to patient details:
1. What could be the reason for his SOB ?
Ans- His sob is due to Acidosis which was caused by Diuretics
2. Why does he have intermittent episodes of drowsiness ?
Ans- His sob is due to Acidosis which was caused by Diuretics
3. Why did he complaint of fleshy mass like passage in his urine?
Ans-plenty of pus cells in his urine passage appeared asfleshy mass like passage to him
4. What are the complications of TURP that he may have had?
Ans;' Difficulty micturition
Electrolyte imbalances
Infection
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
Ans;Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
2. Why doesn't the child have the excessive urge of urination at night time ?
Ans; Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
3. How would you want to manage the patient to relieve him of his symptoms?
Ans; bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
6) Infectious Disease (HI virus, Mycobacteria, Gastroenterology, Pulmonology)
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANS;Tracheoesophageal fistula is suggested by copious salivation associated with choking, coughing, vomiting, and cyanosiscoincident. Esophageal atresia and the subsequent inability to swallow typically cause polyhydramnios in utero.
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
Ans; There are chances that patient may develop IRIS. The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
7) Infectious disease and Hepatology:
Link to patient details:
1. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?
Ans;Yes it can cause as he is drinking toddy since 30years. Amoebic liver abscess (ALA) is the most common manifestation of invasive amoebiasis caused by Entamoeba histolytica (EH). Several studies from India have reported a strong link between consumption of toddy and the occurrences of ALA. Toddy is a local alcoholic beverage consisting of fermented palm juice.
2. What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
ANS;according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3. Is liver abscess more common in right lobe ?
Ans;yes right lobe is involved due to its moreblood supply
4.What are the indications for ultrasound guided aspiration of liver abscess
Ans; Indications for USG guided aspiration of liver abscess
B) Link to patient details:
QUESTIONS:
1) Cause of liver abcess in this patient ?
Ans;:cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA
2) How do you approach this patient ?
Ans;APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS
3) Why do we treat here ; both amoebic and pyogenic liver abcess?
Ans; Amoebic liver abscess: The first line treatment in uncomplicated amebic abscess should be amebicidial drugs. Metronidazole is the drug of choice and has replaced the use of emetine and chloroquine. Metronidazole is effective against both the intestinal and hepatic phase. 750 mg three times a day for 7–10 days is recommended.
Payogenic liver abscess: Treatment usually consists of placing a tube through the skin into the liver to drain the abscess. Less often, surgery is needed. You will also receive antibiotics for about 4 to 6 weeks. Sometimes, antibiotics alone can cure the infection.
4) Is there a way to confirmthe definitive diagnosis in this patient?
Anas;1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs\
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
A) Link to patient details:
Questions :
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans:
18/04/21 He went to local PHC for COVID 19 vaccination.. Since that night patient is complaining of Fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication...
No c/o cold and cough
Followed by patient is having similar complaints after three days and he visited local hospital which is not subsided by medication ( Antipyretics) ( not taken medication such as steroids, oxygen therapy, anti virals)
On 28/04/21 , c/o Generalized weakness and facial puffiness and periorbital edema.. And also patient is in drowsy state..
On 04/05/21, patient presented to casualty In altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb...
primary etiology: Diabetes can lead to mucormycosis
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans;Proposed management -
Inj. Liposomal amphotericin B according to creatinine clearence
Loading dose 30mg/IV over 2-6 hrs
Maintenance dose 60mg / IV once a day
Treatment modalities:
The successful treatment of mucormycosis requires four steps: 1) early diagnosis; 2) reversal of underlying predisposing risk factors, if possible; 3) surgical debridement where applicable; and 4) prompt antifungal therapy [3].
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
ANS;Thus far, this surge has been attributed to the improper use of steroids to treat Covid-19 patients, coupled with poorly managed diabetes. But steroids in themselves are not the villains.
“ Systemic (oral and intravenous) corticosteroids have been proven to reduce mortality in Covid-19,” Lancelot Pinto, consultant pulmonologist at Mumbai’s Hinduja Hospital, told Quartz. “The largest trial, Recovery, which proved this beyond a reasonable doubt among individuals who had low oxygen levels, used them in a dose of 6 milligrams Dexa per day for up to 10 days.”
Not only in Covid-19, but steroids are also widely used in orthopaedic and pulmonary diseases. In India, the problem lies not in the drug but in how it is prescribed. “Most of us who work in India will agree that prescribing practices more often than not tend towards higher doses for longer periods of time, which is a clear risk factor for invasive fungal infections
Medicines used in treating Covid-19 tend to bring down the count of lymphocytes. Lymphocytes are one of the three types of white blood cells whose job is to defend our body against disease-causing pathogens such as bacteria, viruses, and parasites. The reduced count of lymphocytes leads to a medical condition called lymphopenia, making way for opportunistic fungal infection in Covid-19 patients.
There is a higher chance of occurrence of mucormycosis in patients whose immune system is not functioning well, and since Covid-19 treatment tends to suppress the working of the immune system, it places such patients at a higher risk of contracting the black fungus infection
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