GENERAL MEDICINE ASSIGNMENT

Name: K.ROHITH DHARMA

Roll no : 165 

Semester: 8 

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 clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.

1) PULMONOLOGY

CASE: 1

A)Link to the patient details : 

 :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 - it could be due any infection

4.could the ATT affected her symptoms if so how?

Yes ATT affected her symptoms

Isoniazid and rifampcin -nephrotoxic - raised RFT was seen 

2) 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.

2) CASE :2b

QUESTIONS:

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

Answer:

History:- Patient has giddiness 7 days back and associated with 1 episode of vomiting on the same day.

•Patient was asymptomatic for 3 days, after which he consumed a small amount of alcohol He then developed giddiness, that was sudden in onset, continuous and gradually progressive.

•This was associated with Bilateral Hearing loss, aural fullness and presence of tinnitus.

•He has associated vomiting- 2-3 episodes per day, non projectile, non bilious containing food particles.

•Patient has H/o postural instability

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

Answer:

1)Tab Veratin 8 mg PO TID

   Mechanism of action: Betahistine is one of the few drugs known which is said to improve the microcirculation of the inner ear. It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It has a weak effect on H1 receptors but strong effect on H3 receptors.

2)Inj Zofer 4 mg IV/TID

   Mechanism of action: Zofer Tablet works by inhibiting the action of a chemical substance named serotonin, which is responsible for inducing nausea and vomiting. Ondansetron binds to a receptor known as 5-HT₃, thus inhibits the binding of serotonin to it and prevents vomiting and nausea.

3)Tab Ecosprin 75 mg PO/OD

   Mechanism of action: Ecosprin is an antiplatelet medicine. It works by inhibiting the action of an enzyme, which makes platelets aggregate together to form a blood clot.

4)Tab Atorvostatin 40 mg PO/HS

   Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.

5)BP monitoring- 4rth hourly

6)Tab Clopidogrel 75 mg PO/OD

    Mechanism of action: The active metabolite of clopidogrelselectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.

7)Inj Thiamine 1 AMP in 100 ml NSPO/BD

    Mechanism of action: Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiaminediphosphate. Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.

8)Tab MVT PO/OD

2) 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.

2) 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)

2) CASE: 2e

Questions: 

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

Answer: By the history, Patient is an alcoholic and he has change in his gait since a year are the findings which leads to cause of ataxia.

Mechanism:Damage from alcohol is a common cause ofcerebellar ataxia. In patients with alcohol related ataxia, the symptoms affect gait (walking) and lower limbs more than arms and speech. It can also cause associated signs of peripheral neuropathy. Peripheral neuropathy is damage to the body's peripheral nervous system.

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

Answer: Hemoglobin and its metabolites can exert deleterious effects on brain tissue through NO depletion and vasospasm, ROS production, stimulation of inflammatory response, inhibition of DNA repair, and glutamate release.

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.

2) CASE: 2f

Questions

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

Answer: Yes

2.What are warning signs of CVA?

Answer: The five warning signs of stroke are:

   •Sudden onset of weakness or numbness on one side of the body.

Sudden speech difficulty or confusion.

Sudden difficulty seeing in one or both eyes.

Sudden onset of dizziness, trouble walking or loss of balance.

Sudden, severe headache with no known cause.

3.What is the drug rationale in CVA?

Answer: 1.Injection Mannitol 100ml/IV/TD 

2.TAB Ecospirin 75 mg po/OD

3.TAB ATORVAS 40mg po/HS

4.BP/PR/TEMP/SP02 MONITORING (4th hourly)

5.RT FEEDS-100ml milk with protein powder(2nd hourly)

2) 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. 

D    

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

2) 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 suspission of CVST

3) CARDIOLOGY

CASE: 3a

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)

 

3) CASE: 3b

QUESTION: What are the possible causes for heart failure in this patient?

the patient has various comorbidities which could have led to a heart failure

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

3) CASE :3c

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.

3) CASE : 3d

 

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.  

3) CASE:3e

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

Ans: *the anatomical location ofetiology is BLOOD VESSELS.

*myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function

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

 Ans: PHARMACOLOGICAL INNTERVENTION

1.TAB. ASPIRIN

mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.

 

2.TAB ATORVAS 

mechanism:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.

3.TAB CLOPIBB 

mechanism:The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.

4.INJ HAI

mechanism:Regulates glucose metabolism

Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue

5.ANGIOPLASTY

mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.

3) Did the secondary PTCA do any good to the patient or was it unnecessary?

Ans:the second PCI was NOT necessary in this patient.

PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.

The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as ‘use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value’.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm to the patient

4) GASTROENTEROLOGY

CASE :4a

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: *antomical location of etiology is pancreas(ductal obstruction,acinar cell injury,defective intracellular transport)

*The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport and by an activation of pancreatic enzymes Attributed to alcohol

2) What is the efficacy of drugs used along with other non pharmacological  treatment modalities and how would  you approach this patient as a treating physician?

PHARMACOLOGICAL INTERVENTIONS

1) ING. MEROPENAM 

mechanism:Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactams, it is highly resistant to degradation by β-lactamases or cephalosporinases.

2) ING. METROGYL 

mechanism:Metronidazole diffuses into the organism, inhibits protein synthesis 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 

mechanism:he primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.

4) TPN ( Total Parenteral Nutrition )

mechanism: the 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 

mechanism:

Like somatostatin, octreotide also 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 

mechanism:The mechanism of action of pantoprazole is to inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion. The covalent binding prevents acid secretion for up to 24 hours and longer.

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 

mechanism:Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.

 4)CASE :4b

1)what could be the cause for his SOB

Ans- His sob was is due to Acidosis which was caused by Diuretics

2. Reason for Intermittent Episodes of drowsiness

 Ans-Hyponatremia was the cause for his drowsiness 

3.why did he complaint of fleshy mass like passage inurine

Ans-plenty of pus cells in his urine passage  appeared as

 fleshy mass like passage to him

4. What are the complicat ions of TURP that he may have had

Ans- 

       Difficulty micturition

        Electrolyte imbalances

         Infection

1) What is causing the patient's dyspnea? How is it related to pancreatitis

1ans:the cause of dyspnea might be PLEURAL EFFUSION

2) Name possible reasons why the patient has developed a state of hyperglycemia

2 ans:

*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress

* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells 

* elevated levels of catecholamines and cortisol

3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?

A: LFT are increased due to hepatocyte injury

*If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.

*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.

The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to

 (i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics

 (ii) mitochondrial damage leading to increased release of mAST in serum.

4) What is the line of treatment in this patient?

For the master chart to the "pancreatitis thesis project" please get in touch with Dr Shashikala PGY1 and Dr Divya PGY2 and share their insights into the above project problem they are working on. 

A: Plan of action and Treatment:

Investigations:

✓ 24 hour urinary protein 

✓ Fasting and Post prandial Blood glucose 

✓ HbA1c 

✓ USG guided pleural tapping 

Treatment:

• IVF: 125 mL/hr 

• Inj PAN 40mg i.v OD 

• Inj ZOFER 4mg i.v sos 

• Inj Tramadol 1 amp in 100 mL NS, i.v sos

• Tab Dolo 650mg sos 

• GRBS charting 6th hourly 

• BP charting 8th hourly

 4) CASE :4c

 

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. 

5)NEPHROLOGY

CASE :5a

1.what could be the cause for his SOB

Ans- His sob was is due to Acidosis which was caused by Diuretics

2. Reason for Intermittent Episodes of drowsiness

 Ans-Hyponatremia was the cause for his drowsiness 

3.why did he complaint of fleshy mass like passage inurine

Ans-plenty of pus cells in his urine passage  appeared as

 fleshy mass like passage to him

4. What are the complicat ions of TURP that he may have had

Ans- 

       Difficulty micturition

        Electrolyte imbalances

         Infection

5) CASE 5b

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

1ans* 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 ?

2ans: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

3) TREATMENT

6) INFECTIOUS DISEASES (mycobacterium,HIV virus , gastroenterology

 1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula

1 ans: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

2 ans: 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.

 

7)INFECTIOUS DISEASES AND HEPATOLOGY

CASE 7a

Liver abscess

1Q)do u think drinking locally  made alcohol cause liver abscess in this patient due to predisposing fact ors present in it ? What could be the cause in this patient?

1ans- yes, it could be due to intake of contaminated toddy

2Q)what is the etiopathogenesis of liver abscess  in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)

2ans - according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver. It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.

3Q)is liver abscess is more common in right lobe?

 3ans-yes right lobe is involved due to its moreblood supply

4Q) what r the indications  for usg guided aspiration of liver abscess 

4ans- Indications for USG guided aspiration of liver abscess

1. Large abscess more than 6cms

2. Left lobe abscess

3.Caudate lobe abscess

4. Abscess which is not responding to drugs

7)CASE 7b

 1) Cause of liver abcess in this patient ?

1ans:cause of liver abcess in this patient is ENTAMOEBA HISTOLYTICA

2) How do you approach this patient ?

2 ans:APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS

3) Why do we treat here ; both amoebic and pyogenic liver abcess

3ans:we treat the paient for both amoebic and pyogenic abcess  so that we dont rely only on anti-amebic therapy and insure comple treatment of the cause

4) Is there a way to confirmthe definitive diagnosis in this patient?

4 ans: he confirmatory test for amoebic abcess is

*Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).

*The diagnosis of amebic liver abscess was based on four or more of the following criteria:

 (i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, 

(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), 

(iii) enlarged and/or tender liver, usually without jaundice, 

(iv) raised right dome of the diaphragm on chest radiograph, and 

(v) improvement after treatment with antiamebic drugs (e.g., metronidazole). 

8)INFECTIOUS DISEASE(mucormycosis)

CASE 8a

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 ( https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes. )

 

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

 9)INFECTIOUS DISEASES (COVID 19)

 

1) How does the pre-existing ILD determine the prognosis of this patient?

 In patients with preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying ILD. The criteria for ILD exacerbation include subacute worsening of dyspnea and hypoxemia, new pulmonary infiltrates on imaging, and absence of pulmonary emboli, cardiac failure, and other non-pulmonary causes. .Thus it leads to a poor prognosis

2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism? 

Corticosteroids are the cornerstone of for managing disease flares and for initial treatment of RA 

It is identified glucocorticoids as a significant risk factor for bacterial infections. Glucocorticoid use doubled the rate of serious bacterial infections in a dose-dependent manner as compared with methotrexate

It is concluded that there is no evidence to support its use in COVID-19, and it may in fact lead to more harm than good

3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?

In Covid ,lymphoplasmocyte cell infiltrates are involved (mainly at the lung level), as well as the expression of pro-inflammatory cytokines such as interleukin (IL) IL-1, IL-6, IL-17, and TNF-α, and markers of systemic inflammation such as C-reactive protein or ferritin [34]. A parallelism of events was found with RA, where there are similar infiltrates at the synovial level, with expression of the same group of proinflammatory cytokines and elevation of acute-phase reactants [35]. However, this route is unlikely, given that there has been no increase in exacerbations of RA patients concomitantly suffering from COVID-19

4) Why was she prescribed clexane (enoxaparin)?

Clexane 60mg Injection is an anticoagulant used to prevent and treat harmful blood clots. It stops the existing clots from getting any bigger and restricts the formation of any new clot. It is also helpful in the prevention of blood clots in veins, a condition called deep vein thrombosis, and pulmonary embolism.

10) CASE 10

What are the known factors driving early recovery in covid?

These might be the factors responsible for early recovery of Covid:

1. Better immune response of the patient

2. Good food habits prior to And during the Covid period

3. Early detection of symptoms and thus using medication

4. Age related (Elderly have a slow recovery than young)

5. Maintaining hygiene even after Covid infection

6. Mental strength 

7. Health related (patient with Comorbidities have slow recovery)