ONLINE BLENDED BIMONTHLY ASSIGNMENT
GOLI HARSHITHA
8th SEMESTER
ROLL NO 3
I have been given the following cases to solve in an attempt to understand the topic of ‘patient clinical data analysis’ to develop my competency in reading and comprehending the clinical data including history, clinical findings, investigations, and diagnosis, and come up with a treatment plan.
This is the link of questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the assignment based on my comprehension of the cases.
CASE 1-
55 year old patient with seizures
1. Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
Seizures after stroke
You’re more likely to have a seizure if you had a haemorrhagic stroke (bleed on the brain). Seizures can also be more likely if you had a severe stroke, or a stroke in the cerebral cortex, the large outer layer of the brain where vital functions like movement, thinking, vision and emotion take place.
Some people will have repeated seizures, and be diagnosed with epilepsy. The chances of this happening may depend on where the stroke happens in the brain and the size of the stroke.
WHAT IS A SEIZURE?
The cells in brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal bursts of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.
A seizure can affect you in many different ways such as changes to vision, smell and taste,loss of consciousness and jerking movements.
MECHANISM BEHIND IT:
There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury ,(particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.14 In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.
2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
Initially the early seizures are of focal motor type, hence no loss of consciousness. But the late post stroke seizures are of GTCS and complex partial type which include loss of consciousness.
Also the history of seizures leads to organic lesions in the brain which causes progressively more severe symptoms which could explain the loss of consciousness.
CASE 2-
67 year old patient with acute coronary syndrome
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?
TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest
Anatomical localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause
- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Pharmacological interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). Beta blockers also help open up your veins and arteries to improve blood flow.
Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .
EFFICACY STUDIES.
Patients were randomized to one of four treatment arms: placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.
Results: mean baseline BP was 132/78 +/- 9/9 mmHg. Following 4 weeks of treatment, mean changes in sitting BP were: placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9 mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg. Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.
Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
3) What are the indications and contraindications for PCI?
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?
Although PCI is generally a safe procedure , it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
Because of all these complications it is better to avoid PCI in patients who do not require it.
⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.
⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.
Harms to patients
. Performing screening tests in patients with who at low risk for the disease which is being screened.
For example:Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.
.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations.
Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained irrelevant - OVERDIAGNOSIS.
Also the adverse effects due to this are more when compared to the benefits.
.Overdiagnosis through overtesting can psychologically harm the patient.
Hospitalizations[41] for those with chronic conditions who could be treated as outpatients[ can lead to economic burden and a feeling of isolation.
Harms to health care systems
The use of expensive technologies and machineries are causing burden on health care systems.
CASE 3-
A 40 Year Old Male with Complaints of Irrelevant Talking
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
1) what is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
EVOLUTION OF SYMPTOMATOLOGY:
12 YEARS AGO
- Addicted to alcohol, drinks about 3-4 quarters per day
2 YEARS AGO
- Diagnosed with type 2 Diabetes (irregular medication; once in 2 or 3 days)
1 YEAR AGO
- 1-2 episodes of seizures (mostly due to alcohol consumption)
4 MONTHS AGO
- Developed a seizure (mostly GTCS)
- Cessation of alcohol for 24 hours assosiated with symptoms of restlessness, sweating, and tremors.
10 DAYS AGO
- General body pains
9 DAYS AGO
- Started talking and laughing to himself (sudden onset)
- Decreased food intake
- Required assistance to move around
- Short term memory loss (couldn't recognise family members)
ANATOMICAL LOCALISATION
PRIMARY ETIOLOGY
- Wernicke's encephalopathy: thiamine deficiency secondary to alcohol dependence
- Uremic encephalopathy:
- Altered sensorium: alcohol withdrawal syndrome
2)what are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Ans: I) Thiamine helps the body cells change carbohydrates into energy. It has been used
as a supplement to cope with thiamine deficiency
ii)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
iii)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
iv)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy .its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
v)Potchlor 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 time?
Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.
4)what is the reason for giving thiamine in this patient?
chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.
5)what is the probable cause for kidney injury in this patient?
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.
6)what is the probable cause for the normocytic anaemia?
alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .
7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
CASE 4-
A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension
1) What is the most probable diagnosis in this patient?
Differential Diagnosis:
· Ruptured Liver Abscess.
· Organized collection secondary to Hollow viscous Perforation.
· Organized Intraperitoneal Hematoma.
· Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
· Grade 3 RPD of right Kidney
-The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
2) What was the cause of her death?
-After leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
3) Does her NSAID abuse have something to do with her condition? How?
-NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.
CASE 5-
Case: A 60year old Male patient, resident of xxxxxxxx, came to the OPD with the Chief complaint of chest pain since 3 days and giddiness and profuse sweating since morning.
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
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 patients.
CASE 6-
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
1Q) what is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
1Ans)Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs
Diagnosed with diabetis - 8yrs back
Anemia and took iron injections - 5yr ago
Generalised weakness - 1 month back
Diagnosed with hypertension - 20 days back
Pedal edema - 15 days back
Facial puffiness- 15 yrs back
Anatomical location of problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage
2Q)what r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
2Ans)~Head end elevation :# MOA;
.improves oxygenation
.decreases incidence VAP
.increases hemodynamic performance
.increases end expiratory lung volume
.decreases incidence of aspiration
#Indication: .head injury
.meningitis
.pneumonia
~ oxygen inhalation to maintain spo2
~Bipap:non invasive method
#MOA :assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation9
3. Cause for current acute excerbation -
4.could the ATT affected her symptoms if so how?
Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen
CASE 7-
A SEVENTEEN YEAR OLD FEMALE WITH SEIZURES
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
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 wegeners granulomatosis
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
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?
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 8-
A 52 YEAR OLD MALE WITH CEREBELLAR ATAXIA
https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
7 days before hospitalization he had giddiness and an episode of vomiting on the same day
After 3 days of being asymptomatic, he again had giddiness which was sudden in onset and continuous
Severity of giddiness increased upon getting up from bed and while walking
Bilateral hearing loss, aural fullness, tinnitus was associated with this
Also had 2-3 episodes of vomiting per day
Anatomical localization of the problem – infarct in the right inferior cerebellar hemisphere
A cerebellar infarct is a type cerebrovascular event involving posterior cranial fossa involving mainly cerebellum.it results in impaired perfusion which reduces oxygen delivery and causes deficits in motor and balance control
Etiology
Cerebellar infarcts are divided into two types ischemic and hemorrhagic events
Ischemic strokes are caused by arterial obstruction that impair blood and oxygen delivery directly.
These can be further subdivided into source of obstruction in the blood vessel
-migration from heart /directly at the vasculature
Thrombotic phenomenon can occur in small or large vessels and can travel from large to small vessels. These can be due to atherosclerosis or other vasculopathies. Emboli that occur from heart are either due to pump failure or due to irregular heart rhythm that disrupts smooth blood transit as in atrial flutter or fibrillation. Cerebral venous thrombosis can cause obstructed venous outflow resulting in infarction or hemorrhage
In contrast to ischemic strokes, hemorrhagic strokes are usually caused by arterial bleeding that directly damages brain tissue and obstructs vascular flow by elevated local pressure. these usually occur spontaneously especially inpatients with long standing hypertension or long-term anticoagulant or antiplatelet therapy. Secondary hemorrhagic conversion can also occur from ischemic infarcts, damaged tissue due to tumor or trauma
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 -
Ecosprin+clopidogrel – antiplatelet drugs
Ecosprin or aspirin is a thromboxane synthesis inhibitor that acetylates and irreversibly inactivates COX 1 and TX synthase. TXA2 is the main arachidonic acid product produced by platelets that change the shape of platelets and help in aggregation and adhesion this is inhibited
Clopidogrel is a P2Y12 receptor blocker that blocks the function i.e., when the receptor gets activated through ADP it in turn activates platelets
DAPT (dual antiplatelet therapy) is beneficial only in short term therapy, whereas in long term therapy it may cause hemorrhage
Veratin – antihistamine drug
It is used as an antivertigo it reduces the symptom of the patient by causing CNS depression
Zofer inj. – antiemetic
used to treat symptoms of nausea and vomiting
It blocks the depolarization action of 5-HT through 5-HT3 receptors on vagal afferents in git as well as in NTZ and CTZ
atrovostatin – hypolipidemic drug
used to decrease LDL and cholesterol
3) Did the patients history of denovo HTN contribute to his current condition?
Yes, hemorrhagic stroke can be caused by prolonged hypertension like de novo hypertension in this patient and not using medication. By treating hypertension, we can reduce the symptoms of cerebellar infarcts like giddiness, nausea and headache.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Answer-
Yes, moderate and high intakes of alcohol have been documented to have deleterious physiological effects like impaired fibrinolysis and increased platelet activation ,blood pressure and heart rate which can be a risk for an ischemic stroke
CASE 9-
A 78 yr old male patient, resident of of kattangur and shepherd by occupation came to the OPD on 14 /5/2021 with chief complaints of:
- shortness of breath, since 20 days
- chest pain, since 20 days
- B/L pedal edema, since 4 days
- facial puffiness, since 4 days
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.
Questions:
1.What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?
2.Why haven't we done pericardiocenetis in this pateint?
Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the pericardium. In this case, to keep a check if patient is having cardiac tamponade , review of ECHO has been done. As no cardiac tamponade was seen this procedure wasn't performed.
3.What are the risk factors for development of heart failure in the patient?
The risk factors of heart failure are:
- Hypertension
- Coronary artery disease
- Diabetes
- Certain medication
- Alcohol abuse
- Smoking
- Obesity
- Congenital heart defects
- Sleep apnea
4.What could be the cause for hypotension in this case?
The patient is suffering from acute, rapid accumulation of fluid in the pericardium which causes signs of acute hemodynamic compromise in cardiac tamponade. Patients with this condition develop tachycardia, hypotension and distended neck veins.
CASE 10-
A 73 yr male patient teacher by occupation, presented to OPD with chief complaints of :
- Pedal edema, since 15 days
- Shortness of breath, since 4 days
- Decreased urine output, since 2 days
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html.
Questions:
1.What are the possible causes for heart failure in this patient?
The probable causes for heart failure in this patient are:
- Chronic alcohol abuse
- Long standing case of hypertension (19 years)
- Stage 4 Chronic Kidney disease
2. What is the reason for anaemia in this case?
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Leg and foot ulcers in diabetic patients have three common underlying causes: venous insufficiency, peripheral neuropathy, or peripheral arterial occlusive disease.
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 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath at rest since one day.
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.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
10 YEARS AGO
- Surgery for inguinal hernia
3 YEARS AGO
- Aggravated on and off pain at the site of surgery
- On and off facial puffiness
1 YEAR AGO
- Grade II shortness of breath - diagnosed for HTN (on medication)
2 DAYS AGO
- Shortness of breath Grade II (on exertion)
- Decreased urine output
- Constipation
ONE DAY AGO
- Shortness of breath Grade IV (at rest)
DAY OF ADMISSION
- Anuria
ANATOMICAL LOCALISATION
- HEART: a) Atrial fibrillation with Rapid ventricular response
b) Thrombi noted in Left Atrial Appendages and Left atrium
c) Dilated Main Pulmonary Artery and Left Pulmonary Arteries
d) Severe LV dysfunction
e) IVC dilated
2. KIDNEY: a) Cardiorenal syndrome
ETIOLOGY OF DISEASE IN PATIENT
- Loss of Atrial contraction and Left atrial dilatation causes stasis of blood in the LA and may lead to thrombus formation in the Left Atrial Appendage. This predisposes patients to stroke and other forms of systemic embolism - Bilateral thrombosis
- Cardiorenal syndrome 4 in this patient can be attributed to prior history of heart failure, HTN and age.
- Abnormal heart rhythms, including atrial fibrillation or atrial flutter, affect 50 to 60 percent of all patients over 40 with an ASD.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
1) Drug name: DOBUTAMINE
MOA: Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.
Indication: Indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures.
Efficacy over dobutamine:
- P- 673 participants
- I - dobutamine
- c - out of 673 participants random number of patients are given placebo
- o - dobutamine is not associated with improved mortality in patients with heart failure, and there is a suggestion of increased mortality associated with its use
https://go.drugbank.com/drugs/DB00841
https://link.springer.com/article/10.1007/s00134-011-2435-6
2) Drug name: CARVEDILOL
Mechanism of action: Carvedilol inhibits exercise induce tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure.
Indication: Carvedilol is indicated to treat mild to severe heart failure, left ventricular dysfunction after myocardial infarction with ventricular ejection fraction or hypertension.
Efficacy over Carvedilol :
- p : 131
- i : carvedilol
- c : out of 131 participants random number of patients are given placebo
- o : The beta-blocker carvedilol can be safely employed in patients with severe heart failure. Improved left ventricular function
https://go.drugbank.com/drugs/DB01136
https://pubmed.ncbi.nlm.nih.gov/9330125/
3) Drug name: UNFRACTIONED HEPARIN
MOA: Administered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.
Indication: It is used to prevent embolisms in patients with atrial fibrillation and as an adjunct antithrombin therapy in patients with unstable angina and/or non-Q wave myocardial infarctions
Efficacy over unfractioned heparin:
- p : 1473
- i : unfractioned heparin
- c : out of 1473 participants random number of patients are given placebo
- o : decrase in thromoembolism
https://clinicaltrials.gov/ct2/show/NCT00432796
https://go.drugbank.com/drugs/DB01109
4) Drug name: TAB. DYTOR
MOA: Torasemide is known to have an effect in the renin-angiotensin-aldosterone system by inhibiting the downstream cascade after the activation of angiotensin II. This inhibition will produce a secondary effect marked by the reduction of the expression of aldosterone synthase, TGF-B1 and thromboxane A2 and a reduction on the aldosterone receptor binding.
Indication: Torasemide is indicated for the treatment of edema associated with congestive heart failure, renal or hepatic diseases.
Efficacy over dytor:
- p : 68
- i : torsemide
- c : 34
- o : improvement in peripheral edema
https://pubmed.ncbi.nlm.nih.gov/11862232/
5) Drug name: TAB. TAXIM
MOA: The bactericidal activity of cefotaxime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefotaxime shows high affinity for penicillin-binding proteins in the cell wall including PBP Ib and PBP III.
Indication: Used to treat gonorrhoea, meningitis, and severe infections including infections of the kidney (pyelonephritis) and urinary system. Also used before an operation to prevent infection after surgery
Efficacy over Taxim:
- p : 60
- i : taxim
- c : out of 60 participants random number of patients are given placebo
- o : the results indicate that cefixime twice daily is comparable in safety
https://go.drugbank.com/drugs/DB00493
https://pubmed.ncbi.nlm.nih.gov/2663735/
6) Drug name: INJ THIAMINE
MOA: It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions.
Indication: For the treatment of thiamine and niacin deficiency states, Korsakov's alcoholic psychosis, Wernicke-Korsakov syndrome, delirium, and peripheral neuritis.
Efficacy over thiamine:
- P : 50
- I : thiamine
- C : 25
- O : Thiamine was not associated to a significant reduction in vasopressor-free days over 7-days in comparison to placebo in patients with septic shock
https://go.drugbank.com/drugs/DB00152
https://bmcanesthesiol.biomedcentral.com/articles/10.1186/s12871-020-01195-4
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Pathogenesis:
The development of CRS mainly focuses on the inability of the failing heart to generate forward flow, thus resulting in prerenal hypoperfusion. Inadequate renal afferent flow activates the RAAS, the sympathetic nervous system, and arginine vasopressin secretion, leading to fluid retention, increased preload, and worsening pump failure.
The patient is suffering from Type 4 CRS in which CKD leads to heart failure.
4) What are the risk factors for atherosclerosis in this patient?
- Hypertension
- Bad cholesterol levels
- Obesity
- Diabetes
- Lack of physical activity
- Age
- Smoking
5) Why was the patient asked to get those APTT, INR tests for review?
The patient was asked to get APTT and INR tests for review as he was prescribed TAB. Acitrom which is a blood thinner and can cause some common side effects such as unusual bleeding from the gums, heavy bleeding from cuts or wounds, unexplained bruising or nosebleeds, heavy periods, abdominal pain, blood vomiting, bloody or black tarry stools.
CASE 12-
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
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula
Clinical history and physical finding in this paient that suggest tracheoesophageal fistula is that ,Cough occurs on taking food and liquids
(which was initially non productive then associated with sputum which is white in color , moderate in quantity and non foul smelling)
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent
Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms:
"unmasking" IRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started;
"paradoxical" IRIS refers to the worsening of a previously treated infection after ART is started.
*Patients with mycobacterial disease at the time of initiation of ART are at higher risk of developing IRIS with an approximate risk of 15%. Patients originating from endemic areas for tuberculosis and cryptococcal disease are at higher risk of developing IRIS.
How can immune reconstitution inflammatory syndrome be prevented?
*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 13-
CASE OF 25 YEAR OLD MAN, WITH SEVERE EPIGASTRIC PAIN
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
QUESTION: What are the possible causes for heart failure in this patient?
1. The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mixtrad insulin daily and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is major risk factor for heart failure
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5494155/
2. The patient was also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure
https://pubmed.ncbi.nlm.nih.gov/31472888/
3. He is a chronic alcoholic since 40 years which is a risk factor towards heart failure
https://www.nmcd-journal.com/article/S0939-4753(19)30360-6/fulltext
The findings in this article provide longitudinal evidence that moderate and heavy alcohol consumption are associated with decreased LVEF and trend towards a higher risk of incident LV systolic dysfunction, compared to light drinkers.
4. The patient has elevated creatinine and AST/ALT ratios is >2 and was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2900793/
QUESTION: what is the reason for anaemia in this case?
The patient has normocytic normochromic anaemia. it could be anaemia of a chronic disease as the patient is diagnosed with CKD stage IV.
Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.
Patient’s with anaemia and CKD also tend to have deficiency in nutrients like iron, vitamin B12 and folic acid essential in making healthy red blood cells
QUESTION: What is the reason for blebs and non-healing ulcer in the legs of this patient?
The most common cause for blebs and non-healing ulcer in this patient is diabetes mellitus. CKD is also known to cause delay in healing of wounds along with poorly controlled diabetes. Anaemia can also slow down the process of healing due to low oxygen levels.
QUESTION: What sequence of stages of diabetes has been noted in this patient?
There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.
The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy
The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness
CASE 14-
A 50 YEAR OLD MALE WITH CERVICAL MYELOPATHY
https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html
QUESTION: What is myelopathy hand?
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.
QUESTION: What is finger escape?
Finger escape
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 the "finger escape sign".
QUESTION: What is Hoffman's sign?
Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition
CASE 15-
50/Male came with altered sensorium
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html
QUESTION: What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary aetiology of the patient's problem?
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 that occurs in people with uncontrolled diabetes
( https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html) the fungus enters the sinuses from the environment and then the brain.
The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA
QUESTION: 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?
The proposed management of the patient was –
1. inj. Liposomal amphotericin B according to creatinine clearance
2. 200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance
3. Deoxycholate was the required drug which was unavailable
https://pubmed.ncbi.nlm.nih.gov/23729001/
this article talks about the efficacy and toxicity of different formulations of amphotericin B
along with the above mentioned treatment for the patient managing others symptoms is also done by-
I. Management of diabetic ketoacidosis –
(a) Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
(c) Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy
QUESTION: What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing
CASE 16-
- complicated diverticular abscess.
- Crohn's disease related abscess.
- complicated appendicitis with appendicular abscess.
- tuboovarian abscess.
- post-surgical fluid collections.
- hepatic abscess (e.g. amoebic or post-operative)
- renal abscess or retroperitoneal abscess.
- splenic abscess.
CASE 17-
- If we dont treate amobic liver abcess there is a chance that one of the following occurs:
- a) Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial infection.
- b) Direct extension to pleura or pericardium.
- c) Dissemination and formation of brain abscess.
- If we dont treate pyogenic liver abcess there is a chance that one of the following occurs:
- a) Sepsis.
- b) Empyema resulting from contiguous spread or intrapleural rupture of abscess.
- c) Rupture of abscess with resulting peritonitis.
- d) Endophthalmitis when an abscess is associated with K pneumoniae bacteremia.
CASE 18-
A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA
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?
ANATOMICAL LOCALISATION
ETIOLOGY OF DISEASE IN PATIENT
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?
The various studies critically studying the efficacy of these drugs in the treatment of such patients are given below.
SOMATOSTATIN AND TPN (TOTAL PARENTERAL NUTRITION)
In this study 31 patients with 1st and 2nd degree pancreatitis underwent a prospective RCT.
Aim- to study clinical benefits of parenteral nutrition during acute pancreatitis and therapeutic validity of Somatostatin
Group 1 - Somatostatin (250 micrograms/h for 72-96 h)
Group 2- received total parenteral nutrition with 2,000-2,500 Kal/day through a central vein
Results- In this study the group receiving TPN had shown quicker recovery rate than the group treated with Somatostatin.
Conclusion-The results of the study have indicated the validity of use of BOTH Somatostatin and TPN during the acute phase of pancreatitis.
https://pubmed.ncbi.nlm.nih.gov/2566958/
ANTIBIOTICS
-A prospective RCT in seven Norwegian hospitals with 73 patients of severe pancreatitis was done
- Ccontrol group- patients without antibiotics (n=37).
- Imipenem Group- withearly antibiotic treatment (imipenem 0.5 g x 3 for 5-7 days) (n=36) or no antibiotics
-Results: The groups were similar in age, cause of pancreatitis, duration of symptoms and APACHE II score. Patients in the imipenem group experienced
1)lower rates of complications (12 versus 22 patients) (p=0.035)
2)lower infection rates (5 versus 16 patients) (p=0.009) than those in the control group.
-Conclusions: The study, although underpowered, supports the use of early prophylactic treatment with imipenem in order to prevent sequalae of complications following acute pancreatitis.
https://pubmed.ncbi.nlm.nih.gov/17506001/
USG GUIDED PERCUTANEOUS MALECOT DRAINAGE
-Single-center retrospective study was performed with acute necrotizing pancreatitis patients from January 2012 to July 2017.
-78 consecutive patients with necrotizing pancreatitis and acute necrotic collections (ANC) who were managed with percutaneous catheter drainage (PCD) in early phase of the disease (< 21 days) were under study
-Clinical data and laboratory parameters of the study group were evaluated until discharge from hospital, or mortality.
-Results- Overall survival rate was 73.1%. Forty-two (53.8%) patients survived with PCD alone, while the remaining 15 (19.2%) survivors needed additional necrosectomy.
-Conclusion-An early PCD in clinically deteriorating patients with acute necrotizing pancreatitis, along with aggressive catheter-directed necrosectomy has proved to be of utmost important in the management of much patients and improve outcome.
CASE-19
A 48 year old male with seizures and altered sensorium
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
WERNIKE ENCEPHALOPATHY
A triad of symptoms- 1) Mental confusion 2) Nystagmus 3) Cerebellar Ataxia are seen
Caused mainly in chronic alcoholics due to thiamine deficiency
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
1) History of chronic alcohol intake leads to impaired platelet function and reduced platelet count which is a major cause for intracranial bleeding.
2) Multiple head injuries due to possible minor trauma from frequent falls and no subsequent check up can also contribute as a cause for intracranial bleeding.
CASE 20-
A 52 yr old male patient who is a farmer by occupation
Presented to hospital on 17 May 2021 with Chief Complaints of
SOB since 4 days
Burning micturition since 4 days
Fever since 2 days
https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1. What could be the reason for his SOB ?
2. Why does he have intermittent episodes of drowsiness ?
3. Why did he complaint of fleshy mass like passage in his urine?
4. What are the complications of TURP that he may have had?
CASE-21
An Eight year old with Frequent Urination
1.Why is the child excessively hyperactive without much of social etiquettes ?
The child seems to be psycho somatic, hence the behaviour.
2. Why doesn't the child have the excessive urge of urination at night time ?
3. How would you want to manage the patient to relieve him of his symptoms?
CASE 22-
c)"A 45 YEARS 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
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?
EVOLUTION OF SYMPTOMATOLOGY
ANATOMICAL LOCALISATION
The main localization for the patients problem is - Cervical spine.
ETIOLOGY
The etiology of the patients symptoms can be attributed to the following causes
- hypokalemia (leading to palpitation)
- cervical spondylitis (causing pain the patient)
Question 2
What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Question 3
What are the changes seen in ECG in case of hypokalemia and associated symptoms
Various ECG changes seen in hypokalemia are-
- decrease in T wave amplitude (earliest ECG manifestation )
- Increased P wave amplitude
- Prolongation of PR interval
- Widespread ST depression and T wave flattening/inversion
- Prominent U waves
- Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia (seen on worsening of hypokalemia)
Associated symptoms of hypokalemia are-
- weakness and fatigue
- muscle cramps and pain
- palpitations
- neurological symptoms- psychosis, delirium, depression
