Manaswini rollno 153 medicine bi-monthly assignment

                                                                         1st case

 https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.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?

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

                                                                     2ndcase

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

 

1) What is the most probable diagnosis in this patient?

àDifferential 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

àThe 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?

àAfter 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? 

àNSAID-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. 

 

                                                                  3rdcase

D) Link to patient details:

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

QUESTIONS:

1.Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?

seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury 

Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism

Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. 

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 patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)

                                                              4thcase

E) Link to patient details:

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions: 1) What could have been the reason for this patient to develop ataxia in the past 1 year?

The patient has minor unattended head injuries in the past 1 yr. Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal love ataxia

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes

            

                                                                  5thcase

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions

1.Does the patient's  history of road traffic accident have any role in his present condition?

The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition

2.What are warning signs of CVA?

Weakness or numbness of the face, arm or leg, usually on one side of the body

Trouble speaking or understanding

Problems with vision, such as dimness or loss of vision in one or both eyes

Dizziness or problems with balance or coordination

Problems with movement or walking

Fainting or seizure

Severe headaches with no known cause, especially if they happen suddenly

3.What is the drug rationale in CVA?

Mannitol- Because of its osmotic effect, mannitol is assumed to decrease cerebral edema. Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant. 

Ecospirin 

For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.

Atrovas-Atorva 40 Tablet belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases. Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.

Rt feed RT feed is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely. 

4. Does alcohol has any role in his attack?

When the patient met with an accident there might be cranial damage which was unnoticed.

If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition

But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.

Therefore it cannot be evaluated without further details

5.Does his lipid profile has any role for his attack??

The inverse relationship between serum HDL-C and stroke risk . When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.

                                                          Case6

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

Questions

1.Why is the child excessively hyperactive without much of social etiquettes ?

Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age

For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).

2. Why doesn't the child have the excessive urge of urination at night time ?

Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition 

1. Psychosomatic disorder

2. Undiagnosed anxiety disorder 

3. How would you want to manage the patient to relieve him of his symptoms?

bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.

If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder

To treat attention deficit hyperactivity disorder:

For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents.  Schools can be part of the treatment as well. 

Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.

Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.

                                                           Case7

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html

1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

Ans:Preserved ejection fraction (HFpEF) – also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax). 

Reduced ejection fraction (HFrEF) – also referred to as systolic heart failure

                                    

HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease  

2.Why haven't we done pericardiocenetis in this pateint?

        

Ans: Pericardiocentesis is not done here  Because the effusion was self healing ,It reduced from 2.4cm to 1.9 cm.

        

3.What are the risk factors for development of heart failure in the patient?

Ans: risk factors for development of heart faliure in this patent

Alcohol abuse increases the risk of atrial fibrillation, heart attack and congestive heart failure 

high blood pressure

Smoking

Diabetes

AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.

wosening of pericardial effusion leaing to cardiac tamponade.

4.What could be the cause for hypotension in this

Ans : visceral pericardium may have  thickened which is restricting the heart to expand causing hypotension 

(May be secondary to TB)

     

                                                              Case8

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans: *the anatomical site is BLOOD VESSELS;

* ETIOLOGY: 

The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.

The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

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 INTERVENTIONS

1. TAB. Dytor

mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

2. TAB. Acitrom 

mechanism: 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

3. TAB. Cardivas 

mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.

4. INJ. HAI S/C

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.TAB. Digoxin 

mechanism:

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.

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient? 

Ans: *cardiorenal syndrome type 4 is seen in this patient.

4) What are the risk factors for atherosclerosis in this patient?

Ans: effect of hypertention

 They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.

5) Why was the patient asked to get those APTT, INR tests for review?

Ans: APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule.

                                                               Case9

https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h

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.

                                         Case10   

                                                               https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.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?

With the evidence of exposure to dust from paddy field and other pollen material over the years besides winter season,SOB could have been triggered and progression of airway damage over the years evident with increasing severity over the years.

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

efficacy of every other intervention is far better than placebo because placebo is something which is of zero efficiency.

Intervention-MOA-indication.

.head end elevation-positional elevation eases sob and mucous buildup-COPD

.chest physiotherapy-loosen mucus and clear airway- bronchiectasis

.BiPaP-augumented lung expansion- hypoventilation

.Augmentin.inj-reduce lung bacterial load-acute exacerbation in bronchiectasis

. Azithromycin- reduce lung bacterial load- acute exacerbation in bronchiectasis

.lasix- (furosemide)Na , cl absorption blockage in kidneys-fluid buildup and edema.

. hydrocortisone-anti inflammatory-any inflamation

.Nebulization with ipravent budecort- facilities breathing-COPD

.pulmoclear-reduces congestion in airways- COPD

. insulin- recudes blood glucose levels- diabetes mellitus.

3) What could be the causes for her current acute exacerbation?

evident electrolyte imbalance possibly due to kidney injury caused byATT.

4. Could the ATT have affected her symptoms? If so how?

ATT drugs isoniazid and rifampicin are nephrotoxic, possible acute kidney injury leading to her symptoms.

5.What could be the causes for her electrolyte imbalance 

electrolyte loss due Kidney injury 

 https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.ht

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?

2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

3) Why have neurological symptoms appeared this time, that were absent during withdrawal earlier? What could be a possible cause for this?

4) What is the reason for giving thiamine in this patient?

5) What is the probable reason for kidney injury in this patient? 

6). What is the probable cause for the normocytic anemia?

7) Could chronic alcoholism have aggravated the foot ulcer formation? If yes, how and why?

Answers:

1stans: 

The patient is a chronic alcoholic, he drinks about 3-4quarters/day.he had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.

Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.

ANATOMICAL localisation: Brain.

Primary etiology: thiamine deficiency.

2nd 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.

3rd ans:

Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.

4th ans:

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.

5th ans:

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.

6th ans:

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.

7th ans:

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.