General medicine assignment
I M.Vasitha , roll no.170 of 8th semester 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 clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
1)Pulmonology;
A)
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 ?
Ans :Evolution of symptomatology ;
1st episode of SOB - 20 yr back lasted 1week approximately
2nd episode of SOB - 12 yr back lasted for 20 days
From then she has been having yearly episodes for the past 12 yrs lasting around a month
8 years ago she was diagnosed with diabetes
Anemia 5 years ago
Generalisedweakness - 1 month back
Diagnosedwith hypertension - 20 days back
pedaledema - 15 days back
Facialpuffiness- 15 days back
Anatomical location of problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs
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
decreasesincidence VAP
increaseshemodynamic performance
Increasesend 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 -infection
4.could the ATT affected her symptoms if so how?
Yes,
Isoniazidand rifampcin -nephrotoxic - raised RFT was seen
NEUROLOGY
CASE 2A
A 40year old male presented with chief complaints of irrelevant talking and decreased food intake since 9days.
He was conscious but oriented to time, person and place only from time to time.
He also had short term memory loss since 9days, where he couldn't recognize family members from time to time
Previously, he had 2-3episodes of seizures, one being one year ago and the most recent being 4months ago. The most recent one, he had developed seizures following cessation of alcohol for 24hours.
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?
Ans: 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.

The GABA system:
GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects. During withdrawal, brain GABA levels fall below normal and GABA activity declines. The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol. In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.
The glutamate system:
The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures. Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans. As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect. Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
The symptom: irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.
THE PATHOPHYSIOLOGY:
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. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.
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. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis.
the deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.
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 2B
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 patients problem?
ANS. Timeline of the patient is as follows-
7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.
Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)


Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.
In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.
2) What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
ANS.
A) Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
B) Tab Zofer 4mg- This is ondanseteron- It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications- Used to control the episodes of vomiting and nausea in this patient.
C) Tab Ecosprin 75mg- This is aspirin. It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
D) Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
F) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patients history of denovo hypertension contribute to his current condition?
ANS. A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.
Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.
Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.
CASE 2D
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)
CASE 2C
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
10 years back-Paralysis of both upper and lower limbs bilateral
1 year back-Right and left paresis due to hypokalemia
8 months backSwelling over legs
7 months back - blood infection
2 months back- neck pain
6 days back- pain along left upper limb
5 days back- chest pain, Difficulty in breathing and was able to feel her own heart beat
Anatomical localization: Cervical spine
degenerative changes that occur in the cervical spine with age.
Dehydrated disks. Disks act like cushions between the vertebrae of your spine. By the age of 40, most people's spinal disks begin drying out and shrinking, which allows more bone-on-bone contact between the vertebrae.
Bone spurs. Disk degeneration often results in the spine producing extra amounts of bone in a misguided effort to strengthen the spine. These bone spurs can sometimes pinch the spinal cord and nerve roots.
Herniated disks. Age also affects the exterior of your spinal disks. Cracks often appear, leading to bulging (herniated) disks — which sometimes can press on the spinal cord and nerve roots.
Stiff ligaments. Ligaments are cords of tissue that connect bone to bone. Spinal ligaments can stiffen with age, making your neck less flexible.
2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Reasons for recurrence
The primary hypokalemic periodic paralysis is autosomal dominant and is exacerbated by strenuous exercise, high carbohydrate diet, cold and excitement, which was not found in this case. secondary periodic hypokalemic paralysis have been reported in association with gastroenteritis, diuretic abuse, renal tubular acidosis, Bartter syndrome, villous adenoma of colon, and hyperthyroidism.
Risk factors

Female [1] [2]
Medications like diuretics
Heart failure
Hypertension
Low BMI [3]
Eating disorder and alcoholism: low intake of potassium
Diarrhea, cushing syndrome, a
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalemia.


CASE 2E

1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans: the reason for patient to develop ataxia in past one year is ALCOHOL
The toxic effects of alcohol are diverse. Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia(ALCOHOL INDUCED TOXIC ATAXIA).
The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death

2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Ans: the reason for IC bleed is
CHRONIC ALCOHOL CONSUMPTION
↓
ALCOHOL INDUCED TOXIC ATAXIA
↓
REPEATED FALLS
↓
IC BLEEDING
* The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.
CASE 2F
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?

3.What is the drug rationale in CVA?
3ans
Aspirin -antiplatlet drug prevents stroke
Atorvostatin - decreases LDL cholesterol to prevent recurrent attacks of stroke
4. Does alcohol has any role in his attack?
ans : 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??
5ans
Yes increased LDL causes atherosclerosis -Blood vessels - ischemia leads to - stroke

CASE 2G
a)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.

b)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".

c)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 2H
1) What can be the cause of her condition ?
the cause of her condiion could be IRON DEFICENCY ANEMIA.

2) What are the risk factors for cortical vein thrombosis?
Ans: Risk factors for children and infants include:
Problems with the way their blood forms clots
Sickle cell anemia
Chronic hemolytic anemia
Beta-thalassemia major
Heart disease — either congenital (you're born with it) or acquired (you develop it)
Iron deficiency
Certain infections
Dehydration
Head injury
For newborns, a mother who had certain infections or a history of infertility
Risk factors for adults include:
Pregnancy and the first few weeks after delivery
Problems with blood clotting; for example, antiphospholipid syndrome, protein C and S deficiency, antithrombin III deficiency, lupus anticoagulant, or factor V Leiden mutation
Cancer
Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
Obesity
Low blood pressure in the brain (intracranial hypotension)
Inflammatory bowel disease like Crohn’s disease or ulcerative colitis
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
Ans: there was a sezuire free period due to administration of antiepileptic drugs as the effect of drugs weans off the sezures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the sezuires.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
Ans: heparin as CLEXANE was given to relive clot in suspicion of CVS
1)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans:- Heart failure with preserved ejection fraction occurs in conditions where there is diastolic dysfunction of the ventricles like hypertrophic cardiomyopathy and restrictive cardiomyopathy. The ventricles are unable to relax completely , but they contract adequately , there by maintaining the ejection fraction.
Heart failure with reduced ejection fraction occurs in intrinsic heart diseases like DILATED CARDIOMYOPATHY. The ventricles are dilated and their wall is thinned out in this condition. There will be systolic dysfunction of the ventricles leading to reduced ejection fraction.
2)Why haven't we done pericardiocentesis in this patient?
Ans:- Pericardiocentesis is indicated when there is considerable pericardial effusion causing compression over the heart chambers. In this condition, there is no need for pericardiocentesis as it is resolving.
3)What are the risk factors for development of heart failure in the patient?
Ans:- Hypertension, CAD, DM, MEDICATIONs.
4)What could be the cause for hypotension in this patient?
Ans:- Systemic venous return to the heart is reduced which in turn reduces the pulmonary venous return. This causes decrease in the end diastolic volume and finally reduced cardiac output.
CASE - B
Ans:- Chronic hypertension can be the cause of heart failure in this patient.
2)What is the reason for anemia in this case?
Ans:- Anemia is considered to be frequent comorbidity of heart failure.
3)What is the reason for blebs and non-healing ulcer in the legs of this patient?
Ans:- The cause for nonhealing ulcer is diabetes (hyperglycemia impairs the healing process)
4)What sequence of stages of diabetes has been noted in this patient?
Ans:- Diabetes leading to macrovascular complication in the form of foot ulcer.
Ans:- The patient presented with short ness of breath which progressed from grade 2 to grade 4. Patient also complained of oliguria since two days and anuria since morning.
2)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non-pharmacological interventions used for this patient?
Ans:-
1.DOBUTAMINE
Mechanism of action: It is an inotropic drug.
Indications: cardiogenic shock, severe congestive cardiac failure, hypoperfusion if associated with increased peripheral vascular resistance.
Efficacy: https://www.uptodate.com/contents/inotropic-agents-in-heart-failure-with-reduced-ejection-fraction
2.UNFRACTIONED HEPARIN
Mechanism of action: it inactivates thrombin and factor X through an antithrombin dependent mechanism.
Indications: Atrial fibrillation with embolization, treatment of acute and chronic consumptive coagulopathies like DIC, prophylaxis and treatment of venous thromboembolism, prevention of clotting in arterial and cardiac surgery.
Mechanism of action: it is a non-selective adrenergic blocker.
Indication: heart failure with reduced ejection fraction, hypertension, left ventricular dysfunction following MI.
Mechanism of action: It increases the synthesis of glutathione in liver, glutathione acts as an antioxidant.
Indication: It is used in paracetamol overdosing, to relive chest congestion due to thickened mucous in cystic fibrosis, asthma, bronchitis.
Ans:-
4) What are the risk factors for atherosclerosis in this patient?
Ans:- Risk factors are Abnormal lipid profile, DM, Hypertension, High saturated fats in diet, Obesity.
5) Why was the patient asked to get those APTT, INR tests for review?
Ans:- APTT & INR is indicated in this patient to evaluate the coagulation profile and to assess the thrombotic activities.
Ans:- EVOLUTION OF SYMTOMATOLOGY
》Diabetes for 12 years
》Heart burn like episodes for 1 year but it relieved
》Pulmonary TB 7 months back - treatment took now she is sputum negative.
》Hypertension for 6 months - on medications
》Day of admission to hospital:- SOB since half an hour
•ANATOMICAL LOCATION OF PROBLEM: Cardiovascular system
•PRIMARY ETIOLOGY:- Atherosclerosis - Plague formation [hypertension + diabetes].
2)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non-pharmacological interventions used for this patient?
Ans:-
~TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient.
▪︎Mechanism of action:- METOPROLOL is a cardio selective 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 heart 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.
Outcome:- 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:
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?
Ans:-
Indications:
>Acute ST Elevation MI
>Acute non-ST elevation acute coronary syndrome
>Angina equivalent
>Stable and unstable angina
>Critical coronary artery stenosis
Absolute contraindications:-
~Noncompliance with the procedure and inability to take the dual antiplatelet therapy.
~Multiple percutaneous interventions re stenosis
~High bleeding risk
Relative contraindications:-
• Intolerance for long term antiplatelet therapy
• Short artery less than 1.5 mm
• Hypercoagulable state
• Absence of cardiac surgery backup
• High grade CKD
• Chronic total occlusion of SVG
• Critical left main artery occlusion with no graft or collateral
• Stenosis less than 50%
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 over testing and overtreatment important to current healthcare systems?
Ans:- Although PCI is generally a safe procedure, it might cause serious certain complications like:
▪︎ Bleeding
▪︎ Blood vessel damage
▪︎ Allergic reaction to the contrast dye used
▪︎ Arrhythmias
▪︎ Need for emergency coronary artery bypass grafting.
Because of all these complications it is better to avoid PCI in patients who do not require it.
1)What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans : - EVOLUTION OF SYMTOMATOLOGY:
• Diabetic since 8 years
• Hypertension since 8 years
• First dose of COVISHIELD vaccine 5 days back before admission to hospital
• Chest pain in right side of chest
• Giddiness and profuse sweating on day of the admission
》ANATOMICAL LOCATION: Cardiovascular system
》PRIMARY ETIOLOGY: As she is diabetic for 8 years that might cause atherosclerosis due to accumulation of fatty and fibrinous material in the walls
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:
a) tab. ASPIRIN 325 mg
Mechanism of action: inhibits platelet aggregation by interfering with thromboxane in platelets caused by COX 1 inhibition.
Indications: To reduce the cardiovascular deaths in suspected case of MI
Efficacy: Low dose aspirin each day for atleast10 years lower the risk of cvd by 10% and odds ratio from 0.85 to 0.90
b) tab. ATORVASTATIN 80 mg
Mechanism of action: Competitive inhibitor of enzyme HMG CO A reductase
Indication: To prevent CV events in patients who are at risk used as preventive agent
Efficacy: studies shown that it decreases LDL cholesterol concentration by61% and triglycerides by 46%
c) tab. Clopidogrel 300 mg
Mechanism of action: Inhibitor of platelet aggregation by binding one of the ADP receptors on platelets
Indications: ACS recent MI, recent stroke, peripheral arterial disease.
Placebo has no pharmacological and physiological actions.
3)Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans:- Yes it is good to patient, stent was placed and the patient is doing good.
Ans :
2. What is the rationale of using torsemide in this patient?
Ans : Torsemide is used to treat abdominal distension.
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
ANS :
As the patient has dribbling of urine with oliguria and a previous history of TURP they might have suspected UTI and empirically ceftriaxone was given
4 A) https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A: Evolution of symptomatology;
One episode of vomiting & pain per abdomen 5years back
5-6episodes of vomiting in past 1 year
Pain per abdomen since 4 days in left hypochondriac,lumber, hypogastric regions
Constipation since 4 days
Burning micturition since 4 days
antomical location of problem is pancreas
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?
PHARMACOLOGICAL INTERVENTIONS
ING. MEROPENEM
Meropenem inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.
2) ING. METROGYL
MOA:Metronidazole inhibits protein synthesis of organism by interacting with DNA and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.
3) ING. AMIKACIN
MOA; aminoglycoside, It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
4) TPN ( Total Parenteral Nutrition )
mechanism: early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
5) IV NS / RL
mechanism:Patients with acute pancreatitis lose a large amount of fluids to third spacing into the retroperitoneum and intra-abdominal areas. Accordingly, they require prompt intravenous (IV) hydration within the first 24 hours. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important.
6) ING. OCTREOTIDE
Octreotide decreases the release of growth stimulating hormones, decreases blood flow to the digestive organs, and inhibits the release of digestive hormones such as serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.
Octreotide is useful in overdose management of sulfonylurea type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. Mechanism of action is the suppression of insulin secretion.
7) ING. PANTOP
MOA; inhibit the 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.
8) ING. THIAMINE
mechanism:Vitamin B1 (thiamin) is indispensable for normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining normal cellular redox state.
9) ING. TRAMADOL
MOA; Analgesic
B) https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
1) What is causing the patient's dyspnea? How is it related to pancreatitis
Ans;The cause of dyspnea might be pleural effusion
2) Name possible reasons why the patient has developed a state of hyperglycemia
Ans:
hyperglycemia could thus be due to hyperglucagonemia secondary to stress
Due to 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?
Ans;
LFT are increased due to hepatocyte injury
increase in ALT levels 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.
4) What is the line of treatment in this patient?
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
C) https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
1) What is the most probable diagnosis in this patient?
As;
The most probable diagnosis is abdominal hemorrhage.
This will give reasoning to the abdominal distention, and the blood which is aspirated.
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
2) What was the cause of her death?
Cause of her death can be due to complications of laparotomy surgery ,
Patient underwent an emergency laparotomy surgery
Complications of emergency laparotomy;
hemorrhage , infection, or injury to internal organs.
3) Does her NSAID abuse have something to do with her condition? How?
NSAID-induced renal dysfunction: decreased glomerular perfusion
decreased glomerular filtration rate
acute renal failure.
Chronic NSAIDs use related to hepatotoxicity.
major adverse effects of NSAIDs ; gastrointestinal mucosa injury, NSAIDs have also been associated with hepatic side effects --hepatitis with jaundice ,fulminant liver failure.
NEPHROLOGY
A) https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html
1.what could be the cause for his SOB
Ans- Due to Acidosis caused by Diuretics
2. Reason for Intermittent Episodes of drowsiness
Ans:Hyponatremia was the cause for intermittent episodes of drowsiness
3.why did he complaint of fleshy mass like passage in urine
Ans-fleshy mass like passage appeared to him bcz plenty of pus cells passes in his urine passage
4. What are the complications of TURP that he may have had
Ans-
1. Difficulty micturition
2. Electrolyte imbalances
3. Infection
B) https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html
1.Why is the child excessively hyperactive without much of social etiquettes ?
ANS;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 ?
Ans: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?
CASE - A
http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.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:- COURSE OF THE SYMPTOMS:
》18 April: post vaccination fever with chills and rigor.
》28 April: facial puffiness, generalized weakness and periorbital edema.
》04 May: presented to the OPD with altered mental state.
• ANATOMICAL LOCATION: Rhino-orbito-cerebral disease.
• PRIMARY ETOLOGY: Fungal infection with mucor.
2) What is the efficacy of drugs used along with other non-pharmacological treatment modalities and how would you approach this patient as a treating physician?
Ans:- Placebo has no physiological and pharmacological actions.
▪︎ LIPOSOMAL AMPHOTERICIN B- potent anti-fungal agent active against mucormycosis.
▪︎ ITRACONAZOLE- Azole group of antifungal drugs. Used instead of amphotericin B.
3) What are the postulated reasons for a sudden apparent rise in the incidence of Mucormycosis in India at this point of time?
Ans:-
Steroid overuse in the covid patients. This led to further immunosuppressive state. COVID causes systemic illness leading to immunosuppression.
Mucormycosis is more common among diabetics as thought diabetes is an immunocompromised state. Poor patient hygiene also is a risk factor.
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