Medicine Case Discussion

 Online Blended Bimonthly assignment towards summative assessment for the month of May 2021

Pulmonolgy

1) A 55yr old female with Shortness of breath,pedal edema and facial puffiness. 

A) 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:At the month of january that year during which time she was working in a paddy field. For the next 8 years the patient has suffered from similar episodes of SOB every year each lasting aproximately 1 week For the past 12 years she has been having an yearly episodes now lasting around a month again around january. Until her latest episode the SOB was of grade II Her latest episode of shortness of breath started 30 days ago, her SOB was insidious in onset and gradual in progression. Initially the SOB occurred on exertion and was relieved upon rest. From 2 days ago she started having SOB even at rest (grade IV) Pedal edema since 15 days upto the level ankle and pitting type OTHER SYMPTOMS Facial puffiness since 15 days. She hkas drowsiness since 2 days She has decreased urine output for the past 2 days. ANATOMICAL LOCATION; LUNG ALVEOLI PRIMARY ETIOLOGY

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

ANS 

A] Head end elevation

B] O2 inhalation to maintain SPO2 above 92%

C] Intermittent BiPAP for 2hrs

   

D] Inj. AUGUMENTIN 1.2gm IV BO

    MECHANISM OF ACTION;

         THIS BLOCKS THE ACTION OF 𝜷 -LACTAMASE 

POTASSIUM CLAVULANTA CAN BE INCORPORATED WITH AMOXICILLIN TO FORM AUGUMENTIN

INDICATIONS;

1)lower respiratory tract infection

2)acute bacterial otitis media

3)sinusitis

4)skin and skin structure infections

5)urinary track infections

E] TAB. AZITHROMYCIN 500mg OD

  mechanism of action;

 Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit

INDICATIONS;

Azithromycin is an antibiotic. It's widely used to treat chest infections such as pneumonia, infections of the nose and throat such as sinus infection (sinusitis), skin infections, Lyme disease, and some sexually transmitted infections.

F]INJ.LASIX IV BO if SBP GREATER THAN 110 mmHg

 mechanism of action;

Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours

INDICATIONS;Furosemide is a type of medicine called a diuretic. It's used to treat high blood pressure, heart failure and oedema (a build up of fluid in the body). It's also sometimes used to help you pee when your kidneys aren't working properly. Diuretics are sometimes called "water pills/tablets" because they make you pee more.

G] TAB PANTOP 40mg PO OD

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.

INDICATIONS;

 It is commonly used for the diagnosis or treatment of Gastro-esophageal reflux disease, Heartburn, oesophagus inflammation, Stomach ulcers. It has some side effects such as Loss of balance, Increased bone fractures, Skin itching, Diarrhea.

H] INJ. HYDROCORTISONE 100 mg

MECHANISM OF ACTION;

Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes

INDICATIONS;

Hydrocortisone is approved by the U.S. Food and Drug Administration as a prescription steroid medication that is indicated to treat inflammation, status asthmaticus, acute and chronic adrenal insufficiency, and as physiologic replacement in pediatric use.

I] IV NEB. with IPRAVENT, BUDECORT 6 hrly

 J]TAB PULMOCLEAR 100 mg PO OD

MECHANISM OF ACTION;

They belong to the class of bronchodilators and mucolytics, respectively. Pulmoclear works by relaxing the airways and loosening the cough, thus making the expulsion of cough easy.

INDICATION;

Pulmoclear Tablet is used for relieving the symptoms of coughing, wheezing, congestion and blockage in the airways in a condition called chronic obstructive pulmonary disease (COPD

K] chest physiotherapy

Chest PT, or CPT expands the lungs, strengthens breathing muscles, and loosens and improves drainage of thick lung secretions. Chest PT helps treat such diseases as cystic fibrosis and COPD (chronic obstructive pulmonary disease).

L] GRBS 6 hrly

M] INJ. HAI SC ( 8 am- 2pm- 8pm) Temp, BP, PR, SPO2 monitoring I/O charting

N] INJ. THIAMINE 1 amp in 100 ml of NS )

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

INDICATIONS;

Thiamine is taken for conditions related to low levels of thiamine, including beriberi and inflammation of the nerves (neuritis) associated with pellagra or pregnancy. Thiamine is also used for digestive problems including poor appetite, ulcerative colitis, and ongoing diarrhea.

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

ANS; The most common cause of an exacerbation is infection in the lungs or airways (breathing tubes). This infection is often from a virus, but it may also be caused by bacteria or less common types of organisms. 

D) Could the ATT have affected her symptoms? If so how?

ANS; The most common cause of an exacerbation is infection in the lungs or airways (breathing tubes). This infection is often from a virus, but it may also be caused by bacteria or less common types of organisms

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

ANS; RIFAMPICIN [DAILY OR INTERMITTENT] CAN CAUSES EDEMA BY IMMUNOALLERGIC MECHANISM EDEMA OF LOWER LIMB ARE A POTENTIAL SIGNAL IN PHARMACOVIGILANCE REQUERING MORE INVESTIGATION TO ARGUE WITH THE RELATION OF CAUSE AND EFFECT AND TO FIND RISK FACTOR TO MANAGE AND AVOID THESE EFFECT

5.What could be the causes for her electrolyte imbalance?

ANS; RISK FACTORS 

                         🡻 

            ACTIVATION OF RAS [RENIN+

                          🡻 

AGGREVATES ELECTROLYTE IMBALANCE

COMMON FACTORS;

                                          1.RENAL INSUFFICIENCY 

                                            2.HYPOXIA

                                             3.HYPERCAPNIA

                                               4.RESPIRATORY ACIDOSIS

                                                  5.RIGHT SIDED HEART FAILURE WITH DEVELOPMENT OF 

                                                       LOWER LIMB EDEMA

                                                      6.MALNOURISHED ETC.....

 

MOST COMMON ELECTROLYTE IS SODIUM ION DECREASES IN COPD

 

HYPOKALEMIA IS DEU TO TO INDEPENDENTLY OR COMBINED WITH HYPONATREMIA

LOWER LEVEL OF ELECTROLYTE LEADS TO ;

1) DECREASE OF pH

2) DECREASE OF paO2

3) DECREASE OF O2 SATURATION 

4) INCREASE OF paCO2

Neurology

Case:1

40years old male complaining of irrelevant talking.

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

 A) 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 the symptomatology in this patient in terms of an event timeline;

, he had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again. 

He was unable to lift himself off the bed and move around, and had to be assisted. It was associated with a decrease in food intake since 9 days

He also had short term memory loss since 9 days

* the primary etiology of the patient's problem

~ Alcohol intake

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

1. IVF NS and RL @150ml/hr

mechanism of action;

   Sodium Chloride is source of water and electrolytes. It is capable of inducing diuresis depending on the clinical condition of the patient. It is a crystalloid given intravenously in case of shock, dehydration, and diarrhoea to increase the plasma volume.

indication;

The following are primary indications for the use of normal saline infusion that have been approved by the FDA: Extracellular fluid replacement (e.g., dehydration, hypovolemia, hemorrhage, sepsis) Treatment of metabolic alkalosis in the presence of fluid loss. Mild sodium depletion

2. Inj. 1amp THIAMINE in 100ml NS, TID

Thiamine MOA

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

Indications and Usage

Thiamine hydrochloride injection should be used where rapid restoration of thiamine is necessary, as in Wernicke's encephalopathy, infantile beriberi with acute collapse, cardiovascular disease due to thiamine deficiency, or neuritis of pregnancy if vomiting is severe.tion;

3. Inj. Lorazepam

mechanism of action;

Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system (CNS). It enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell

indication;

ATIVAN Injection is indicated in adult patients for preanesthetic medication, producing sedation (sleepiness or drowsiness), relief of anxiety, and a decreased ability to recall events related to the day of surgery.

4. T. Pregabalin 75mg/PO/ BD

MECHANISM OF ACTION;

Pregabalin has demonstrated anticonvulsant, analgesic, and anxiolytic properties in preclinical models. The drug's exact mechanism of action is unclear, but it may reduce excitatory neurotransmitter release by binding to the α2-δ protein subunit of voltage-gated calcium channels 

INDICATION;

Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures in patients 1 month of age and older

5. Inj. HAI S.C.- premeal

6. GRBS 6th hourly, premeal: 8am, 2pm, 8pm,2am

7. Lactulose 30ml/PO/BD

MECHANISM OF ACTION;

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. It has also gained popularity as a potential therapeutic agent for the management of subacute clinical encephalopathy

INDICATION;Lactulose is a prescription drug used by mouth or rectally to treat or prevent complications of liver disease (hepatic encephalopathy). It does not cure the problem, but may help to improve mental status. Lactulose is a colonic acidifier that works by decreasing the amount of ammonia in the blood.

8. Inj 2 ampoule KCl (40mEq) in 10 NS over 4 hours

MECHANISM OF ACTION;

Potassium ions participate in a number of essential physiological processes, including the maintenance of intracellular tonicity; the transmission of nerve impulses; the contraction of cardiac, skeletal, and smooth muscle; and the maintenance of normal renal function.

INDICATIONS;

Potassium chloride is used to prevent or to treat low blood levels of potassium (hypokalemia). Potassium levels can be low as a result of a disease or from taking certain medicines, or after a prolonged illness with diarrhea or vomiting.

9. Syp Potchlor 10ml in one glass water/PO/BD

Mode of Action ;It helps to maintain potassium balance in the body by restoring normal potassium levels in patients with a low level of potassium...

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

Ans: The neurological symptoms which were before was due to the sudden alcohol withdrawal as diagnosed. The reason for the absence of those neurological symptoms could be due to the Wernicke's encephalopathy which is due to the thiamine deficiency.

d. What is the reason for giving thiamine in this patient?

Ans: Thiamine is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. It acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway. It's deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.

   

       "There is some evidence that thiamine treatment can improve the confusional state, quick resolution of ataxia, ophthalmoplegia, and nystagmus".

e. What is the probable reason for kidney injury in this patient? 

Ans: There is direct and indirect evidence for several possible mechanisms. These changes are caused either by alcohol itself or by excessive amounts of the products formed when cells break down (or metabolize) alcohol, including acetaldehyde, NADH, and free radicals. These alcohol-related pathophysiologic changes in cells have been linked to damage in many organs and may play a role in kidney damage.

F)What is the probable cause for the normocytic anemia?

Ans: The probable cause is kidney failure and the reasons for the anemia is

                1) a moderately reduced red cell life span,

                2)blood loss, and

                3) an inadequate increase in erythropoiesis relative to the fall in hemoglobin (Hb).

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

Ans: Excessive alcohol can cause nutritional deficiency and alcohol toxicity these in turn can cause poor nutrition leading to poor wound healing and problems with nerves (neuropathy) when sensory nerves in the foot stops working the foot can get injured and this leads to foot ulcers .

Case :2

52 YEAR OLD MALE WITH CEREBELLAR ATAXIA. 

a. 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: Anatomical localization: The localization lies in the cerebral blood vessels where there is the either rupture of blood vessels or blockage of blood vessels.

           

Primary Etiology: The etiology would be the combined effects of DENOVO HYPERTENSION, SMOKING AND ALCOHOLISM.

b. 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 VERATIN- It works as a histamine analogue through 2 modes of action(1) agonist of H1 receptors and (2) antagonist of H3 receptors. It improves the microcirclation of the ear.

INJ. ZOFER- It's a serotonin antagonist, meaning its mechanism of action is blocking the serotonin receptors in the CTZ. It reduces the simulation of the vomiting centre and prevents nausea and vomiting.

TAB. ECOSPIRIN: It acts as an antiplatelet drug which prevents the aggregation of platelets, thus preventing formation of blood clots.

TAB ATORVOSTATIN: It is an HMG-CoA reductase inhibitors which reduces the production of cholesterol in the body. Thus preventing the building of cholesterol in the wall of arteries which contribute to the hypertension.

TAB. CLOPIDOGREL: It is an antiplatelet medicine or a blood thinner that helps to prevent the formation of harmful blood clots in your blood vessels.

INJ. THIAMINE

c. Did the patients history of denovo HTN contribute to his current condition?

Ans: Hypertension causes alterations in cerebral artery structure and function that can impair blood flow, particularly during an ischemic insult or during periods of low arterial pressure. Hypertensive artery remodeling results in reduction in the lumen diameter and an increase in the wall-to-lumen ratio in most cerebral arteries; this is linked to reduced blood flow postischemia and increased ischemic damage. Hypertension causes blood-brain barrier breakdown by mechanisms involving inflammation, oxidative stress, and vasoactive circulating molecules. This exposes neurons to cytotoxic molecules, leading to neuronal loss, cognitive decline, and impaired recovery from ischemia.

d. Does the patients history of alcoholism make him more susceptible to ischemic or hemorrhagic type of stroke?

 Ans: Previous research has found an association between alcohol consumption and lower levels of fibrinogen – a protein in the body which helps the formation of blood clots. This may explain the association between light to moderate alcohol consumption and lower ischemic stroke risk.

However, drinking may, in fact, increase the risk of hemorrhagic stroke. This is more apparent when looking at the heavy drinking category.

The adverse effect of alcohol consumption on blood pressure – a major risk factor for stroke – may increase the risk of hemorrhagic stroke and outweigh any potential benefit.

CASE:3

A 45years old female patient with palpitations, pedal edema, chest pain, chest heaviness, radiating pain along left upper limb

a. 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: Anatomical localization: The localization would be the electrolyte imbalance.

        Primary etiology: The etiology could be electrolyte imbalance causing palpitations, generalized weakness.

b. What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

Ans: Recurrent hypokalemic periodic paralysis

        Risk Factors: Usage of diuretics, laxatives, corticosteroids

                                renal tubercular acidosis, hypomagnesemia

                                thyrotoxicosis, head injury, myocardial ischemia

                                anorexia, inadequate intake

c. What are the changes seen in ECG in case of hypokalemia and associated symptoms?

Ans: Changes in ECG in hypokalemia: As the serum potassium levels fall,

                        T waves become flattened and may disappear.

                        U wave becomes more prominent as the hypokalemia worsens.

                        Shortening of QT interval.

                        ST segment depression.

            Symptoms of hypokalemia: fatigue and weakness

                                                    Muscle cramps,

                                                    Palpitations,

                                                    Anxiety, Pyschosis, Depression.

CASE :4

A 55 years old male patient with seizures.

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

Ans: Cells in the brain send electrical signals to one another. The electrical signals pass along your nerves to all parts of the body. A sudden abnormal burst of electrical activity in the brain can lead to the signals to the nerves being disrupted, causing a seizure. This electrical disturbance can happen because of stroke damage in the brain.

A seizure can affect you in many different ways such as changes to vision, smell and taste, loss of consciousness and jerking movements.

Seizures after stroke

You’re more likely to have a seizure if you had a hemorrhagic stroke (bleed on the brain). Seizures can also be more likely if you had a severe stroke, or a stroke in the cerebral cortex, the large outer layer of the brain where vital functions like movement, thinking, vision and emotion take place.

Some people will have repeated seizures, and be diagnosed with epilepsy. The chances of this happening may depend on where the stroke happens in the brain and the size of the stroke.

Pathogenesis 

There are several causes for early onset seizures after ischemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarization, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury ,(particularly after carotid end arteriotomy) have all been postulated as putative neurofunctional etiologies. Seizures after hemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischemic area secondary to hemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Hemosiderin deposits are thought to cause irritability after a hemorrhagic stroke. In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.

b. 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?

Ans: Normally the “consciousness system”—a specialized set of cortical-subcortical structures—maintains alertness, attention and awareness. Diverse seizure types including absence, generalized tonic-clonic and complex partial seizures converge on the same set of anatomical structures through different mechanisms to disrupt consciousness.

CASE 5

A 48 years old male with seizures and altered sensorium

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

Ans: Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia. The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death

"Some argue that the direct toxic effects of alcohol on cerebellar cells is responsible, whilst others report that nutritional factors particularly thiamine deficiency are required to drive the underlying process."

b. What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?

Ans: Alcohol may cause the person to fall multiple times due to gait instability(alcohol induced toxic ataxia) which causes IC bleeding.

CASE 6

A 30year old male patient with weakness of right upper limb and lower limb.

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

Ans: The patient's present condition could be due to the road accident. However, there are risk factors such as negative energy, emotional disturbances, anger, heavy drinking.

 "Research shows that drinking large amounts of alcohol can greatly increase your risk of having a stroke"

"It shows that seven possible risk factors: negative and positive emotions, anger, heavy eating, heavy physical exertion, sudden body position changes due to a startling event (such as standing up suddenly at a loud noise or a grandchild's cry), and sudden temperature change that can cause stroke"

b. What are warning signs of CVA?

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

Trouble speaking or understanding

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

Dizziness or problems with balance or coordination

Problems with movement or walking

Fainting or seizure

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

C.What is the drug rationale in CVA?

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

Ecospirin 

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

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

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

D) Does alcohol has any role in his attack?

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

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

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

Therefore it cannot be evaluated without further details

E) Does his lipid profile has any role for his attack??

ANS;

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

CASE 7

A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY

a. What is myelopathy hand ?

Ans: 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 ?

Ans: 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 reflex?

Ans: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 8

A 17year old female with seizures

a. What can be the cause of her condition ?

Ans: According to MRI cortical vein thrombosis might be the cause of her seizures.

b. What are the risk factors for cortical vein thrombosis?

Ans: Infections:

Meningitis, otitis, mastoiditis

Prothrombotic states:

Pregnancy, puerperium, antithrombin deficiency proteins and protein s deficiency, Hormone replacement therapy.

Mechanical:

Head trauma, lumbar puncture

Inflammatory:

SLE sarcoidosis, Inflammatory bowel disease. 

Malignancy.

Dehydration 

Nephrotic syndrome 

Drugs:

Oral contraceptives, steroids, Inhibitors of angiogenesis

Chemotherapy: Cyclosporine and asparginase

Hematological:

Myeloproliferative Malignancies

Primary and secondary polycythemia

Intracranial :

Dural fistula, 

 venous anomalies 

Vasculitis:

C) There was seizure free period in between but again sudden episode of GTCS why? Resolved spontaneously why? 

Ans: There was a seizure free period due to administration of antiepileptic drugs as the effect of drugs weans off the seizures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the seizures

d. What drug was used in suspicion of cortical venous sinus thrombosis?

Ans: Anticoagulants are used for the prevention of harmful blood clots.

Clexane (enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.

CARDIOLOGY

CASE 1

A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS

a.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  

b. Why haven't we done pericardiocentesis in this patient?

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

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

Ans: Risk factors for development of heart failure in this patient:

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.

worsening of pericardial effusion leading to cardiac tamponade.

d.What could be the cause for hypotension in this patient?

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

CASE:2

A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT.

a. What are the possible causes for heart failure in this patient?

Ans: The possible causes are: 

 high blood sugar can damage blood vessels and the nerves that control your heart. People with diabetes are also more likely to have other conditions that raise the risk for heart disease: High blood pressure increases the force of blood through your arteries and can damage artery walls

High blood pressure: Damaged kidneys may release too much of an enzyme called renin, which helps to control blood pressure. This increases the risk for heart attack, congestive heart failure and stroke.

 The narrowing and blocking of blood vessels caused by high blood pressure (HBP or hypertension) increases your risk of developing heart failure

as a complicaion of COVID

b.what is the reason for anaemia in this case?

Ans: Diabetes in this patient may have caused kidney damage. The damaged kidneys do not produce enough erythropoietin and cause anemia.

    Alcohol also cause reduction in red blood cells by reducing the precursor cells in bone marrow.

c. What is the reason for blebs and non healing ulcer in the legs of this patient?

Ans: STAGE 1: insulin resistance

    STAGE 2: prediabetes

    STAGE 3:diabetes type 2

    STAGE4: microvascular complications

CASE:3

A-Fib and Biatrial Thrombus in a 52yr old Male

A. 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;

        Primary etiology: The hypertension causes acceleration of atherosclerosis in both coronary and cerebral vessels. Hypertension causes the development of plaques formation in the vessels and cause the increase susceptibility to the formation of arterial thrombus which is the primary etiology in this case

b. 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 DYTOR- It antagonizes the action of the aldosterone and inhibits the exchange of sodium and potassium ions. Thus it decreases the loss of potassium ions.

TAB. ACITRON- It is the vitamin k epoxide reductase inhibitor which is used to regenrate the vit k for blood clotting.

TAB CARDIVAS- 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.

INJ HAI SC- It regulates glucose metabolism and enhances protein synthesis, inhibits lipolysis and proteolysis.

TAB. DIGOXIN-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.

Hypoglycemia symptoms explained

Watch for any bleeding manifestations like Petechiae, Bleeding gums.

 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.

d. 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.

e. 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.

CASE 4

67 year old patient with acute coronary syndrome 

A. 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:

diabetes since 12 years hypertension since 6 months.          

  pathophysiology- MI occurs due to decreased myocardial oxygen supply due to severe coronary artery narrowing or acute atherosclerotic plaque rupture/erosion and superimposed thrombus formation.                                                                                                 

  Due to decrease in myocardial oxygen supply there is heartburn Due to heart muscle damage there is decrease in the pump function of left ventricle causing decrease in pulmonary circulation which leads to shortness of breathe (dyspnea). It occurs due to partial occlusion of a major vessel or a complete occlusion of a minor vessel (subendocardial).                                 

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

Ans:

 MET XL - Tablet belongs to a group of medicines called long-acting beta-blocker. Met XL Tablet works by blocking the effects of some chemicals on your heart and blood vessels. It slows down your heart rate and helps it to beat with less force

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) 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, a condition known as atherosclerosis.

c. What are the indications and contraindications for PCI?

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

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

d.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?

Ans: Factors responsible for percutaneous coronary intervention (PCI) overuse

        Provider-related factors

Inappropriate PCI recommendation without coronary artery bypass grafting (CABG) facility availability.

PCI and diagnostic catheterisation performed during the same session (ad hoc PCI).

Lack of shared decision making.

Medico-legal concerns related to risks from failed medical intervention.

Poorly regulated, privatisation and fee-for-service in healthcare.

Fear of missing the ‘widow-maker’.

        Patient related factors

Patient preference for minimally invasive PCI over CABG.

Lack of health literacy among patients.

Fear, anxiety, misperceptions and misbeliefs among patients about PCI benefits over optimal medical therapy and lifestyle modification.

CASE 5

a. 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: 3 days ago developed pain on right side of the chest.

        the anatomical location of etiology 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

B. 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. ASPIRIN- 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.

TAB ATORVAS -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.

TAB CLOPIBB -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.

INJ HAI- 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.

ANGIOPLASTY: 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.

c. Did the secondary PTCA do any good to the patient or was it unnecessary?

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

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

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

CASE 6

A case of cardiogenic shock 

a. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

Ans: Because of the fluid loss occurred to the patient

there is decreased preload- so, SOB occurred due to decreased CO

IV fluids administered- there is increased preload- SOB decreased due to better of cardiac output.

b. What is the rationale of using torsemide in this patient?

Ans: Torsemide used to relieve abdominal distension.

c. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Ans: IT IS THE TREATMENT FOR UTI

 Rationale- Used for any bacterial infection

Gastroenterology (& Pulmonology)

CASE 1: 

A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA

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

Evolution of symptomatology 

H5 years back-1st episode of pain abdomen and vomitings 

Stopped taking alcohol for 3 years

1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again 

20 days back increased consumption of toddy intake

Since 1 week pain abdomen and vomiting

Since 4 days fever constipation and burning micturition

Anatomical localisation: Pancreas and left lung

Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis

B )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?

1) ING. MEROPENAM ; TID for 7 days 

* Meropenem ( broad spectrum Carbepenem ) an antibiotic.

2) ING. METROGYL 500 mg IV TID for 5 days

* inj. Metrogyl has METRONIDAZOLE

( Nitroimidazole drug ) an antibiotic

3) ING. AMIKACIN 500 mg IV BD for 5days

* It is an Aminoglycoside antibiotic 

## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.

4) TPN ( Total Parenteral Nutrition )

* Method of feeding that by passes gastrointestinal tract

* Fluids are given to vein , it provides most of the nutrients body needs.

* TPN has proteins, carbohydrates, fats, vitamins, minerals.

5) IV NS / RL at the rate 12l ml per hour

* Given for fluid replacement ie., treat dehydration 

6) ING. OCTREOTIDE 100 mg SC , BD

* It is a Somatostatin long acting analogue.

* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.

7) ING. PANTOP 40 mg IV , OD

* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.

8) ING. THIAMINE 100 mg in 100 ml NS IV , TID

* It is B1 supplement. 

* It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency 

* Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.

9) ING. TRAMADOL in 100 ml NS IV , OD

* It is an opioid analgesic, given to releive pain

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

ANS]

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

2. The patient was also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure

3. He is a chronic alcoholic since 40 years which is a risk factor towards heart failure

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

2.QUESTION: what is the reason for anaemia in this case?

ANS]

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

 

4) What sequence of stages of diabetes has been noted in this patient?

ANS]

There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy and, or, related microvascular events.

The patient is diagnosed with diabetic triopathy exhibiting sequence of neuropathy, retinopathy and nephropathy

The patient has been diagnosed with diabetic retinopathy, CKD stage IV and shows signs of diabetic neuropathy such as numbness

CASE 2

CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN 

a.What is causing the patient's dyspnea? How is it related to pancreatitis?

Ans the cause of dyspnea might be PLEURAL EFFUSION

b. Name possible reasons why the patient has developed a state of hyperglycemia.

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

Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia.

c. 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

        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.

d. What is the line of treatment in this patient

Ans: Plan of action and Treatment:

            Investigations:

24 hour urinary protein 

 Fasting and Post prandial Blood glucose 

 HbA1c 

 USG guided pleural tapping 

            Treatment:

IVF: 125 mL/hr 

Inj PAN 40mg i.v OD 

Inj ZOFER 4mg i.v sos 

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

Tab Dolo 650mg sos 

GRBS charting 6th hourly 

BP charting 8th hourly.

CASE 3

A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension

A. what is the most probable diagnosis in this patient?

Ans: haemoperitonium might be the probable diagnosis

b. What was the cause of her death?

Ans: its possible for the blood to accumulate in the cavity extremly quickly.this could have caused her to go in shock from blood loss become unresponsive and may have resulted in death

c. Does her NSAID abuse have something to do with her condition? How? 

Ans: NSAID abuse may have been the reason behind her hepatomegaly as they are known to cause drug induced hepatitis which inturn leads to cirrhosis.

NEPHROLOGY

CASE 1

POST TURP WITH NON OLIGURIC ANT DIABETIC NEPHROPATHY

a. What could be the reason for his SOB ?

Ans: he reason for SOB was- metabolic acidosis

b. Why does he have intermittent episodes of drowsiness ?

Ans: Acidosis has also been suggested to decrease muscle performance during fatigue by inhibiting Ca2+ release from the SR. Such inhibition will decrease the degree of activation of the contractile machinery and hence lead to decreased force production.

        Another mechanism by which intracellular acidosis may induce fatigue is by inhibition of energy metabolism. Key enzymes in glycogenolysis and glycolysis are phosphorylase and phosphofructokinase, respectively.

c. Why did he complaint of fleshy mass like passage in his urine?

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

 fleshy mass like passage to him

d. What are the complications of TURP that he may have had?

Ans: Difficulty micturition

        Electrolyte imbalances

         Infection

CASE 2

An Eight year old with Frequent Urination

a. 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.

b. 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 psychosomatic disorder.

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

Ans: The diagnosis of the child is psychosomatic overactive bladder, which can be triggered by various stressors or the possibility of the child having undiagnosed ADHD.

The most common treatment options include bladder retraining and pelvic floor exercises.

Bladder retraining involves putting the child on a “voiding schedule” where they go to the restroom to urinate on a schedule. This helps to slowly train the bladder to hold more and more urine, as it is designed to. Pelvic floor exercises provide a way to strengthen the muscles that are used to slow and stop the flow of urine and prevent wetting.

If these techniques do not work or seem to have no effect on the overactive bladder, there are some medications that can be used to calm the overactive bladder. Drugs like oxybutynin can help in controlling an overactive bladder. 

Along with these, certain lifestyle measures can be adopted to help with an overactive bladder.

Children with ADHD welcome easily accessible distractions. By decreasing time with electronics and increasing time doing engaging activities outside the home, your child will have an outlet for built-up energy. Get regular, daily physical activity and exercise. This can help manage the stressors that can trigger an overactive bladder in children.

 

INFECTIOUS DISEASES(HI VIRUS, MYCOBACTERIA, GASTROENTEROLOGY, PULMONOLOGY)

CASE1

A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH

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

Ans: the 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).

b. What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it

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.

Infectious disease and Hepatology

CASE 1

a. Do you think drinking locally made alcohol caused liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient ?

Ans: Local indigenously prepared alcohol do cause the liver abscess mostly contributing to the amoebic liver abscess than the pyogenic liver abscess due to the harmful effects of alcohol on liver.

c.Is liver abscess more common in right lobe ?

Ans: Yes, it is common in right lobe due to more vascular supply.

d. What are the indications for ultrasound guided aspiration of liver abscess ?

Ans:

 If the abcess is large ( 5cm or more) because it has more chances to rupture.

If the abcess is not responding to the drugs for 7 or more days 

 If the abcess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.

CASE 2

CASE DISCUSSION ON LIVER ABCESS

a. Cause of liver abcess in this patient ?

Ans: The cause of the liver abscess id due to ENTAMOEBA HISTOLYTICA.

c. Why do we treat here ; both amoebic and pyogenic liver abscess? 

Ans: we treat the patient for both amoebic and pyogenic abscess so that we don't rely only on anti-amebic therapy and insure complete treatment of the cause

d: Is there a way to confirm the definitive diagnosis in this patient?

Ans: The confirmatory test for amoebic abscess 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:

  a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess, clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder), 

 enlarged and/or tender liver, usually without jaundice, 

 raised right dome of the diaphragm on chest radiograph, and 

improvement after treatment with ant amebic drugs (e.g., metronidazole). 

INFECTIOUS DISEASES(Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)

CASE 1

50/Male came with altered sensorium

a. 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:

. 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 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

3)QUESTION: What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?

Ans; 

 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 DISEASE (COVID-19)

1) What is the reason for hypoalbuminemia in the patient?

Answer:

It may be due to pulmonary capillary leakage in lungs , in response to epithelial endothelial damage due to covid infection. 

Question 2:

What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?

Ans:

Yes, what the patient is experiencing is known as viral exanthem which is one of the cutaneous manifestation of COVID-19. 

Question 3:

What is the reason for Cardiomegaly?

Answer:

The most probable cause of that appearance is AP view of the chest. When an anteroposterior view is taken, most times the CXR shows false cardiomegaly. To confirm the cardiomegaly a PA view of chest must be taken. 

Another possible cause can be Direct Myocardial Cell Injury. The interaction of SARS-CoV-2 with ACE2 can cause changes to the ACE2 pathways, leading to acute injury of the lung, heart, and endothelial cells. A small number of case reports have indicated that SARS-CoV2 might directly infect the myocardium, causing viral myocarditis. However, in most cases, myocardial damage appeared to be caused by increased cardiometabolic demand associated with the systemic infection and ongoing hypoxia caused by severe pneumonia or ARDS

Question 4:

What other differential diagnoses could be drawn if the patient tested negative for covid infection?

Answer:

Possible alternative diagnoses may include:

• Influenza

• Mycoplasma pneumonia

• Parainfluenza

• Respiratory syncytial virus

• Streptococcus pneumonia

• Other viral or bacterial pneumonia.

5)Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

Answer:

It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar haemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.

• D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)

5) Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?

It is well known that D-dimer are produced during fibrin breakdown and serve as a marker of fibrinolytic activity. A relationship between proinflammatory cytokines and markers of activation of the coagulation cascade, including D-dimer, has been demonstrated in critical patients or patients with sepsis .There is also evidence that under inflammatory conditions, the alveolar haemostatic balance is shifted towards a predominance of prothrombotic activity .In addition, pro-inflammatory cytokines may be involved in endothelial injury, and may activate coagulation and inhibit fibrinolysis in patients with severe sepsis.

• D-dimer can be elevated such as in pregnancy, inflammation, malignancy, trauma, liver disease (decreased clearance), heart disease, sepsis or as a result of hemodialysis, CPR or recent surgery)

D;Questions:

1. Is the elevated esr due to covid related inflammation? 

Ans:Erythrocyte sedimentation rate (ESR) is a blood test. It measures how quickly erythrocytes, or red blood cells, separate from a blood sample that has been treated so the blood will not clot.

The sustained high level of ESR possibly brings a negative effect on COVID-19 patients' prognosis

However the elevation in esr cannot be explained based on the present knowledge on Covid

2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization? 

Ans;

after 14 days of isolation he got tested again for COVID-19 which was positive . He then developed fever since 4 days, cough which was productive since 4 days and shortness of breath grade 3 since 2 days. He also had fatigue.He lost the sense of taste and smell. 

Since the patient has SOB of grade 3. This poses a challenge for home isolation.

Patients with COVID-19 had almost 19 times the risk for acute respiratory distress syndrome (ARDS) than did patients with influenza, (adjusted risk ratio [aRR] = 18.60; 95% confidence interval [CI] = 12.40–28.00), and more than twice the risk for myocarditis (2.56; 1.17–5.59), deep vein thrombosis (2.81; 2.04–3.87), pulmonary embolism (2.10; 1.53–2.89), intracranial hemorrhage (2.85; 1.35–6.03), acute hepatitis/liver failure (3.13; 1.92–5.10), bacteremia (2.46; 1.91–3.18), and pressure ulcers (2.65; 2.14–3.27). The risks for exacerbations of asthma (0.27; 0.16–0.44) and chronic obstructive pulmonary disease (COPD) (0.37; 0.32–0.42) were lower among patients with COVID-19 than among those with influenza. The percentage of COVID-19 patients who died while hospitalized (21.0%) was more than five times that of influenza patients (3.8%), and the duration of hospitalization was almost three times longer for COVID-19 patients. 

E Questions:

1) What was the reason for coma in this patient? 

Ans:The patient has an spo2 of 20%. This might have lead to cerebral hypoxia thus leading to coma.

Also, low blood potassium can make you short of breath, as it can cause the heart to beat abnormally. This means less blood is pumped from your heart to the rest of your body

Thus low spo2 and thus coma

2) What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related? 

Ans;

Hospital 1 might not have correlated Severe weakness of 4 limbs with low values of potassium which hospital 2 has diagnosed.

Yes, coma is related to Hypokalemia periodic paralysis as it might have caused cerebral hypoxia.

3) How may covid 19 cause coma? 

Ans;

After cessation of sedatives, the described cases all showed a prolonged comatose state. 

unconsciousness after prolonged periods of mechanical ventilation in the ICU.

Question F

1.What was the cause of his altered sensorium?

Can be any of the following reasons

An altered state is any mental state(s), induced by various physiological( increased hospital stay) , psychological( mental depression due to isolation), or pharmacological maneuvers or agents( drugs of COVID)

2. What was the cause of death in this patient?

Ans:

This patient is an elderly chronic alcoholic and smoker.

This might have delayed his healing process thus causing death

Also he had elevation LFT and RFT values