Medicine blended assingment
MEDICINE BLENDED ASSIGNMENT(MAY)
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
MAY29,2021
I have been given the following cases to solove in an attempt to understand the topic of "patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history,clincal findings,investigations and diagnosis and coem up with a treatment plan.
This is the link of the questions asked regarding the cases.
medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment
Below are my answers to the medicine assignment based on my comprehension of the cases.
case-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
Question 1:what is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer:
History:
I) Shortness of breath since 20years
• Her first episode 20 years ago lasted for 1 week and occured in the month of January while working in a paddy field and relieved upon taking medication.
•For the next 8 years the patient has suffered from similar episodes every year each lasting aproximately 1 week and occurring around January (when she worked at the paddy fields) and relieved upon taking medication.
•12 years ago she had another episode which lasts for 20 days and relieved upon medication during hospitalisation.
•Her latest episode of SOB which is grade-II started 30days ago, SOB was insidious in onset and gradual in progression which was relieved upon rest and from 2days ago she is having SOB even at rest of grade-IV which was not relieved by nebulisers.
II) 20days ago she showed signs of bronchiectasis by HRCT
III) She was diagnosed with hypertension 20days back
IV) Pedal edema and Facial puffiness since 15 days.
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1)Head end elevation
2)O2 inhalation to maintain SPO2 above 92%
3)Intermittent BiPAP for 2hrs
4)Inj. AUGUMENTIN 1.2gm IV BO
Composition:1 g amoxicillin (as amoxicillin sodium) and 200 mg clavulanic acid (as potassium clavulanate).
Mechanism of action: Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.
5)TAB. AZITHROMYCIN 500mg OD
Mechanism of action: Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit.
6)INJ.LASIX IV BO if SBP greater than 110mmhg.
Mechanism of action: Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours.
7)TAB PANTOP 40 mg PO OD
Mechanism of action: 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.
8)INJ. HYDROCORTISONE 100 mg IV
Mechanism of action: Binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.
9)NEB. with IPRAVENT, BUDECORT 6 hrly
Mechanism of action: Ipravent belongs to a group of medicines known as anticholinergic bronchodilators. Anticholinergic bronchodilators work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.
• Budesonide is a potent topical anti-inflammatory agent. It binds and activates glucocorticoid receptors (GR) in the effector cell (e.g., bronchial) cytoplasm that allows the translocation of this budesonide-GR complex in the bronchi nucleus, which binds to both HDCA2 and CBP (HAT).
10)TAB PULMOCLEAR 100 mg PO OD
Mechanism of action: They belong to the class of bronchodilators and mucolytics, respectively. Pulmoclearworks by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.
11)Chest physiotherapy.
12)GRBS 6 hrly
13)INJ. HAI SC ( 8 am- 2pm- 8pm)
14)Temp, BP, PR, SPO2 monitoring
15)I/O charting
16)INJ. THIAMINE 1 amp in 100 ml of NS
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
Question 3: What could be the causes for her current acute exacerbation?
Answer: Infection of her lungs or airways by Allergens (paddy field).
Question 4: Could the ATT have affected her symptoms? If so how?
Answer: Yes it can affect as on 30/4/21 she had a sputum examination which was negative (-) for AFB. On 4/5/21 she was started on empirical ATT. This resulted in generalized weakness. A few days after ATT she started developing pedal edema and facial puffiness.
Question 5:What could be the causes for her electrolyte imbalance?
Answer: Activation of the Renin-angiotensin-aldosterone-system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the ELECTROLYTE IMBALANCE during acute exacerbation of COPD.
CASE 2:
A 40 YEAR OLD MALE WITH COMPLAINTS OF IRRELEVANT TALKING.
Question 1:what is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer:
symptomatology in terms of an event timeline:
1) 2-3 episodes of seizures- 1 year ago.
2)Another episode 4 months ago.
3)Recent episode 9 days ago,he started takling and laughing to himself,sudden on onset.he was unable to lift himself off the bed and move around ,associated with decrease of food intake with cessation of alcohol on the same day.short term memory loss since 9 days.
Anatomical location:
Brain stem lesions may include cranial nerves 3,4,6,7 nuclei,the medial thalamic nuclei,and the dorsal nucleus of the vagus nerve.
oedema may be found in the regions surrounding the third ventricle, and fourth ventricle,also appearing petechiae and small hemorrhages.
Primary etiology:
Alcohol associated thiamine deficiency,as the patient is alcohol addict since 12 years.
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1. IVF NS and RL @150ml/hr
2. Inj. 1amp THIAMINE in 100ml NS, TID
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
3. Inj. Lorazepam
Indication : altered sensorium
Mechanism of action: Lorazepam binds to the GABA Receptor at different allotsteric sites which facilitates the GABA action which increase the opening of calcium channels leads to membrane hyper polarisation and CNS depression.
4. T. Pregabalin 75mg /PO/BD
Mechanism of action:Pregabalin site of action is alpha 2- delta channels and reduces the synaptic release of several neurotransmitter apparently by binding to alpha2-delta subunits and possibly accounting to its actions to reduce neuronal excitability.
5. Inj. HAI S.C.- premeal
Mechanism of action:
Regular insulin is a short acting form of the synthetic hormone.it helps to move glucose from the blood into body’s cells.The cells then use this glucose for energy regular insulin typically starts to work within 30 mins to 1 hour of an injection
6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am
7. Lactulose 30ml/PO/BD
Indication : Liver disesase
Mechanism of action: The lactulose converts the ammonia in the colon is Ionised to ammonium ions that are incapable of being absorbed back into the circulation this facilitates the excretion of excess amount of ammonia.
8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours
Indication: to correct the electrolyte imbalance.
9. Syp Potchlor 10ml in one glass water/PO/BD
Indication: used for treating low potassium levels in the blood.
Question 3: Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?
Answer: It is due to kindling. Kindling refers to the phenomenon of increasingly severe withdrawal symptoms, including an increased risk of seizures, that occurs as a result of repeated withdrawal from alcohol or other sedative–hypnotics with related modes of action.
Question 4: What is the reason for giving thiamine in this patient?
Answer:Thamine is the main treatment modality in this case.As thiamine blood levels fall,thiamine dependent enzymes involved in prevention of cellular damage become impaired and metabolic demands increase,which can result in selective brain lesions correlated with wernicke's encephalopathy and korsakoff's syndrome.
Question 5: What is the probable reason for kidney injury in this patient?
Answer:As the patient is chronic alcoholic, due to alcoholism kidney tissue gets injury.
Question 6: What is the probable cause for the normocytic anemia?
Answer: ↓ synthesis of erythropoietin →↓ stimulation of RBC production → normocytic, normochromic anemia. When patient have kidney disease, kidneys cannot make enough EPO. Low EPO levels cause red blood cell count to drop and anemia to develop. Most people with kidney disease will develop anemia. Anemia can happen early in the course of kidney disease and grow worse as kidneys fail and can no longer make .
Question 7:Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?
Answer: Excessive alcohol can cause nutritional deficiencies and alcohol toxicity. These in turn can cause poor nutrition leading to poor wound healing and problems with the nerves (neuropathy). When the sensory nerves in the foot stop working, the foot can get injured and this leads to foot ulcers.
CASE 3:
A 52 YEAR OLD MALE WITH CEREBELLAR ATAXIA.
Question 1:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer:
History:- Patient has giddiness 7 days back and associated with 1 episode of vomiting on the same day.
•Patient was asymptomatic for 3 days, after which he consumed a small amount of alcohol He then developed giddiness, that was sudden in onset, continuous and gradually progressive.
•This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.
•He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.
•Patient has H/o postural instability.
Question 2: What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
1)Tab Veratin 8 mg PO TID
Mechanism of action: Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but strong effect on H3 receptors.
2)Inj Zofer 4 mg IV/TID
Mechanism of action: Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.
3)Tab Ecosprin 75 mg PO/OD
Mechanism of action: Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.
4)Tab Atorvostatin 40 mg PO/HS
Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
5)BP monitoring- 4rth hourly
6)Tab Clopidogrel 75 mg PO/OD
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.
7)Inj Thiamine 1 AMP in 100 ml NSPO/BD
Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
8)Tab MVT PO/OD.
Question 3:
Did the patient history of denovo HTN contribute to his current condition?
Answer:YES,Hypertension alters the structure of cerebral blood vessels and disruptes intricate vasoregulatory mechanisms that assure an adequate blood supply to the brain.these alterations threaten the cerebral blood supply and increase the suseptibility of the brain to ischemic injury.
Question 4:Does the patient history of alcoholism make him susceptible to ischemia or hemmorhagic type of stroke?
Answer:The patient's history of alcoholism makes him more susceptible to hemmorhagic type of stroke.
CASE 4:A 45 YEAR OLD FEMALE PATIENT WITH PALPITATIONS,PEDAL EDEMA,CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB.
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?
Answer: Evolution of symptoms: Patient was apparently normal 8 months back then developed pedal edema (pitting type)which gradually progressed.
chest pain radiating along left upper limb since 5 days.
palpitations since 5 days, sudden in onset aggravated on lifting weight ,speaking continuously and night time.
Difficulty in breathing since 5 days.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Answer: risk factors:
1)Abnormal loses:Medications:Diuretics, laxatives,enemas ,corticosteroids
2)Renal causes:Oswmotic diuretics,renal tubular acidosis,excess mineralocorticoids.
3)transcellular shifts: head injury, myocardial ischemia, thyrotoxicosis
4) inadequate intake: anorexia, dementia, starvation,TPN
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Answer: earliest change in ECG: decreased T wave amplitude,ST depression, T wave inversion, flat prolonger PR interval
symptoms:weakness, fatigue, muscle cramps, pain , palpitations, psychosis, delerium, depression.
CASE 5:55 YEAR OLD PATIENT WITH SEIZURES.
QUESTIONS:
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Answer:. Due to brain stroke there will be change in the electric impulse transmission in the brain..so this cuases the seizures.
2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
Answer: It is may be due any scar formation or any hemorrhages which shows more severity in the symptoms.so, there is loss of consciousness in the recent attack. A
CASE 6: A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATY.
Questions
1)What is myelopathy hand ?
Answer: 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 ?
Answer: Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. This finding of weak finger adduction in cervical myelopathy is also called finger escape sign.
3)What is Hoffman’s reflex?
Answer: Hoffman's reflex is a neurological examination finding elicited by reflex test which can help verify the presence or absence of issues arising from corticospinal tract.
CASE 7:A 45 YEAR OLD FEMALE PATIENT WITH FEVER, PAIN IN ABDOMEN, DECREASED URINE OUTPUT AND ABDOMINAL DISTENSION.
Questions :-
1) what is the most probable diagnosis in this patient?
Answer:Ruptured liver abcsess.
2) What was the cause of her death?
Answer:Sepsis.
3) Does her NSAID abuse have something to do with her condition? How?
Answer:She had grade-3 RPDchanges in the rignt kidney.
She may be having underlying CKD which is secondary to her NSAID abuse(Analgesic nephropathy).
CASE 8:A 17 YEAR OLD FEMALE WITH SEIZURES.
QUESTIONS :
1) What can be the cause of her condition ?
According to MRI cortical vein thrombosis might be the cause of her seizures.
2) What are the risk factors for cortical vein thrombosis?
Infections:
Meningitis, otitis, mastoiditis
Prothrombotic states:
Pregnancy, puerperium, antithrombin deficiency proteinc and protein s deficiency ,Hormone replacement therapy.
Mechanical:
Head trauma,lumbar puncture
Inflammatory:
SLE, sarcoidosis, Inflammatory bowel disease.
Malignancy.
Dehydration
Nephrotic syndrome
Drugs:
Oral contraceptives ,steroids, Inhibitors of angiogenesis
Chemotherapy: Cyclosporine and l asparginase
Hematological:
Myeloproliferative Malignancies
Primary and secondary polycythemia
Intracranial :
Dural fistula,
venous anomalies
vasculitis :Behcets disease Wegener's granulomatosis.
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
Answer: Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Answer: Anticoagulants are used for the prevention of harmful blood clots.
Clexane ( enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.
CASE 9:A 78 YEAR OLD MALE WITH SHORTNESS OF BREATH,CHEST PAIN,B/L PEDAL EDEMA AND FACIAL PUFFINESS.
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Answer:-The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). A normal EF is usually around 55 to 70 percent, but it can be lessened in some forms of heart failure.
-People with heart failure with reduced ejection fraction (HFrEF) have an EF that is 40 to 50 percent or lower. This is also called systolic heart failure. People with heart failure with preserved ejection fraction (HFpEF) do not have much of a change in their ejection fraction. This is often called diastolic heart failure.
-HFrEF were often diagnosed earlier in life and right after a heart attack.
HFpEF were diagnosed later in life and first experienced symptoms of heart failure between the ages of 65 and 69. Many of those with HFpEF also shared that they have other health problems that led to their diagnosis. Many of them also live with additional health conditions, including acid reflux (GERD), high blood pressure, kidney disease, and sleep disorders.
-HFrEF shared that they feel depressed and/or anxious about their heart failure diagnosis. Risk factors for those in this group include genetics or a family history of heart failure.
HFpEF shared that they are still able to do the things they enjoyed before their heart failure diagnosis.risk factors, including:
Sedentary lifestyle
High blood pressure
Sleep apnea
Other heart conditions
-HFrEF are more likely to have had surgery, including surgery to implant a pacemaker or other heart rhythm control device. HFrEF shared that they currently use a combination therapy to treat their heart failure.
HFpEF have never had surgery to treat their heart failure or had a device implanted.
-HFrEF are men who live in rural areas.
However, most respondents with HFpEF are women who live in urban areas.
2.Why haven't we done pericardiocenetis in this pateint?
Answer : Pericardiocenetis is normally done when pericardial effusion is not resolved on its own.but in this case thhe pericardial fluid that was accumulated resolved on its own.
At the time of admission it was 2.4mm and during discharge it was 1.9.Therefore we din't do pericardiocenetis in this patient.
3.What are the risk factors for development of heart failure in the patient?
Answer: IN THIS PATIENT:
NON MODIFICABLE:
age
gender
MODIFIABLE:
hypertension
smoking
type 2 diabetes .
kidney disease.
4.What could be the cause for hypotension in this patient?
Answer:
The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further it causes hypotension.
CASE 10:A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA,SHORTNESS OF BREATH AND DECREASED URINE OUTPUT.
QUESTIONS:
1.What are the possible causes for heart failure in this patient?
Answer: obesity
alcohol
diabetes
hypertension
2.what is the reason for anemia in this case?
Answer:
Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Answer:
The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to diabetes mellitus.
Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases.
In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.
There are many risk factors that may lead to foot ulcers at the end.
Poor quality or fitting of the footwear.
Unhygienic appearance of foot.
Improper care of the nails of the toe.
Heavy intake of alcohols and tobacco.
Obesity and Weight-related
Complication arising from Diabetes like eye problems, kidney problems and more.
Although aging or old age can also be counted among them.
4. What sequence of stages of diabetes has been noted in this patient?
ANS: alcohol------obesity------impaired glucose tolerance------diabetes mellitus------microvascular complications like triopathy and diabetic foot ulcer-------macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease.
CASE 11:A 33 YEAR OLD MAN WITH PANCREATITIS,PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-
pancreatitis-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?
Evolution of symptomatology
H5 years back-1st episode of pain abdomen and vomitings
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung
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.
.
2) What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
A) * Non pharmacological interventions : drains ( malecot & icd )
* Even i as a treating physician will follow the same approach.
CASE 12: A 21 YEAR MALE STUDENT WITH ABDOMINAL PAIN SINCE 20 DAYS AND FEVER SINCE 18 DAYS.
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html
QUESTIONS;
1) Cause of liver abcess in this patient ?
A) Here ; the cause of liver abcess is :
* Amoebic liver abcess (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 extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
2) How do you approach this patient ?
A) The patient is well managed by treating team ; even me will follow the same approach.
3) Why do we treat here ; both amoebic and pyogenic liver abscess?
A) Considering the following factors:
1) Age and gender of patient: 21 years ( young ) and male.
2) Single abscess.
3) Right lobe involvement.
The abscess is most likely AMOEBIC LIVER ABSCESS …
But most of the patients with amoebic liver abscess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.
And considering the risk factors associated with aspiration for pus culture:
1) Sometimes ; abscess is not accessible for aspiration if it is in posterior aspect or so.
2) Sometimes ; it has thin wall which may rupture if u aspirate.
3) Sometimes ; it is unliquefied.
There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.
4) Is there a way to confirm the definitive diagnosis in this patient?
A) Yes in a high resource setting cause of liver abscess is usually determined using multiple diagnostic strategies , including blood cultures , entamoeba serology , liver abscess aspirate for culture and molecular and antigen testing.
CASE 13:A 48 YEAR OLD MALE WITH SEIZURES AND ALTERED SENSORIUM.
Questions:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Answer :Multiple attended head injuries may be the reason for ataxia in this patient.
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Answer: The main reason in this case would be alcohol.
Alcohol brings about liver damage, which decreases production of liver produced clotting factors hence causes bleeding.
Since patient has is a known alcoholic, it may have been a contributing factor to which diathesis may have occured all of a sudden.
CASE 14: A-FIB AND BIATRIAL THROMBUS IN A 52 YEAR OLD MALE.
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Answer: 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
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer:
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 heart
3) TAB. Carvediol 3.125mg BD
Mechanism of action: Carvedilol reversibly binds to beta adrenergic receptors on cardiac myocytes. Inhibition of these receptors prevents a response to the sympathetic nervous system, leading to decreased heart rate and contractility.
4) 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 factor 7
5)TAB. Acetyl cysteine 600mg PO TID.
Mechanism of action: Acetylcysteine is a sulfhydryl compound and acts to increase synthesis of glutathione in the liver. Glutathione subsequently acts as an antioxidant and facilitates conjugation to toxic metabolites, particularly the toxic metabolites of acetaminophen.
6)TAB. Acitrom 2mg OD
Mechanism of action: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
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?
Answer: 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…
4) What are the risk factors for atherosclerosis in this patient?
Answer:
High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet.
5) Why was the patient asked to get those APTT, INR tests for review?
Answer: 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.
CASE 15 : 67 YEAR OLD PATIENT WITH ACUTE CORONARY SYNDROME.
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem
Answer: History:- She had H/O heartburn like episodes since a year. They were relived without use of any medication.
She has H/O TB diagnosed 7 months ago for which she completed the course of medication a month ago.
shortness of breath (SOB) since 1/2 hour.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Answer: TAB MET XL 25 MG/STAT.
Mechanism of action: Met XL 50 Tablet works by blocking the effects of some chemicals on your heart and blood vessels. It slows down your heart rate and helps it to beat with less force.
3) What are the indications and contraindications for PCI?
Answer: Clinical indications for PCI include the following:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
Contraindications to Percutaneous Coronary Interventions
Lack of cardiac surgical support.
Critical left main coronary stenosis without collateral flow from a native vessel or previous bypass graft to the left anterior descending artery.
Coagulopathy.
Hypercoagulable states.
Diffusely diseased vessels without focal stenoses.
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?
Answer: Medical therapy with high dose statins is preferred over balloon angioplasty in patients with mild anginal symptoms.
PCI is preferred over medical therapy has:
1) severe symptoms
2) failed medical therapy
3) high risk coronary anatomy
4) worsening LV function
OVERTREATMENT: The main and worst consequences of overdiagnosis is overtreatment if an incident lesion or disease which is unlikely to have benefits for the patient. At the same time the likely interventions like surgery, radiation and chemotherapy can have side effects resulting in significant morbidity and fatalities can occur. As over diagnosis is some non neoplastic conditions leads to over prescription and over medicalisation , and resulting in many undesirable and sometimes dangerous side effects.
CASE 16 : A CASE OF CARDIOGENIC SHOCK.
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
QUESTIONS:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Because of the fluid loss occurred to the patient
there is decreased preload- so, SOB occurred due to decreased CO
IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.
2. What is the rationale of using torsemide in this patient?
Torsemide used to relieve abdominal distension.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
IT IS THE TREATMENT FOR UTI
Rationale- Used for any bacterial infection.
CASE 17 : AN EIGHT YEAR OLD WITH FREQUENT URINATION.
QUESTIONS:
1.Why is the child excessively hyperactive without much of social etiquettes ?
Answer: The exact pathophysiology of Attention Deficit Hyperactivity Disorder (ADHD) is not clear. With this said, several mechanisms have been proposed as factors associated with the condition. These include abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.
* Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.
* Depressed dopamine activity has been associated with the condition,
2. Why doesn't the child have the excessive urge of urination at night time ?
Answer: the child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder .
3. How would you want to manage the patient to relieve him of his symptoms?
Answer: Management includes boyh investigations and treatment:
A)INVESTIGATIOS include:
Ultrasonography abdomen,
routine investigations such as CBP,CUE.
B)TREATMENT:
OXYBUTIN to decrease urgency and frequency of urination.
CASE 18: A 30 YEAR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWER LIMB.
QUESTIONS:
1.Does the patient's history of road traffic accident have any role in his present condition?
A:One cause of stroke after trauma is a tear in the head or neck blood vessels that lead to the brain, which can be a source of blood clots that cause a stroke. If a tear in these arteries can be diagnosed at the time of the trauma, a patient could be treated with an anti-clotting medicine to help prevent stroke
2.What are warning signs of CVA?difficulty walking.
Answer:
dizziness.
loss of balance and coordination.
difficulty speaking or understanding others who are speaking.
numbness or paralysis in the face, leg, or arm, most likely on just one side of the body.
blurred or darkened vision.
3.What is the drug rationale in CVA?
Answer:
Aspirin -anti platelet drug prevents stroke
Atorvostatin - decreases LDL cholesterol to prevent recurrent attacks of stroke
4. Does alcohol has any role in his attack?
Answer: Excessive alcohol consumption has been associated with a wide range of medical conditions. Moderate alcohol consumption is linked to a lower risk of stroke than abstinence, whereas heavy alcohol consumption has been associated with an increased risk of stroke and stroke mortality. In addition to alcohol consumption, the most important risk factors for stroke are hypertension, coronary artery disease, cardiac insufficiency, atrial fibrillation, type 2 diabetes, smoking, overweight, asymptomatic carotid artery stenosis and elevated levels of cholesterol.
5.Does his lipid profile has any role for his attack?
Answer:
Yes increased LDL causes atherosclerosis -Blood vessels - ischemia leads to - stroke
CASE 19 : CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION.
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: *the anatomical location ofetiology is BLOOD VESSELS.
*myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function.
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: PHARMACOLOGICAL INNTERVENTION
1.TAB. ASPIRIN
mechanism: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.
2.TAB ATORVAS
mechanism :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.
3.TAB CLOPIBB
mechanism: 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.
4.INJ HAI
mechanism: 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
5.ANGIOPLASTY
mechanism: 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.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans :the second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as ‘use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value’.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm to the patient.
CASE 20: CASE OF 25 YEAR OLD MAN, WITH SEVERE EPIGASTRIC PAIN.
QUESTIONS:
1)1) What is causing the patient's dyspnea? How is it related to pancreatitis?
Answer: cause of dyspnea might be PLEURAL EFFUSION
2)Name possible reasons why the patient has developed a state of hyperglycemia.?
Answer:
*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells
* 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?
Answer: LFT are increased due to hepatocyte injury
*If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum.
4) What is the line of treatment in this patient?
d)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 21:A 52 YEAR OLD MALE PATIENT WITH SOB AND BURNING MICTURATION SINCE 4 DAYS AND FEVER
SINCE 2 DAYS
QUESTIONS:
1)1.what could be the cause for his SOB?
Ans- His sob was is due to Acidosis which was caused by Diuretics
2. Reason for Intermittent Episodes of drowsiness?
Ans-Hyponatremia was the cause for his drowsiness
3.why did he complaint of fleshy mass like passage inurine?
Ans-plenty of pus cells in his urine passage appeared as
fleshy mass like passage to him
4. What are the complicat ions of TURP that he may have had?
Ans-
Difficulty micturition
Electrolyte imbalances
Infection
CASE 22: A 40 YEAR OLD LADY WITH DYSPHAGIA,FEVER AND COUGH.
https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-fever.html
QUESTION 1:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANSWER:
Cough since 2 months on taking food and liquids
•difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
•laryngeal crepitus- positive
These favour for tracheo esophageal.fistula
QUESTION 2:
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANSWER:
Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.
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.
Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.
CASE 23 : A 55 YEAR OLD MALE PATIENT WITH ABDOMEN PAIN SINCE I WEEK AND DECRESED APPETITE SINCE ONE WEEK, FEVER SINCE 2 DAYS.
https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html
1) Cause of liver abscess in this patient ?
A) Here ; the cause of liver abscess is :
* 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 extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
2)How do you approach this patient ?
2 ans:APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS.
3)Why do we treat here ; both amoebic and pyogenic liver abcess
3ans:we treat the paient for both amoebic and pyogenic abcess so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause
4) Is there a way to confirmthe definitive diagnosis in this patient?
4 ans: he confirmatory test for amoebic abcess is
Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
*The diagnosis of amebic liver abscess was based on four or more of the following criteria:
(i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess,
(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder),
(iii) enlarged and/or tender liver, usually without jaundice,
(iv) raised right dome of the diaphragm on chest radiograph, and
(v) improvement after treatment with antiamebic drugs (e.g., metronidazole)
Case 23: 50 year male patient with altered sensorium.
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
Questions:
1) 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?
1. 3 years ago- diagnosed with hypertension
2. 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
3. 18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
4. 11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state
5. 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.
