General Medicine

Pulmonology :

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

Ans: Evolution of symptomology:

20 yrs back-First episode of shortness of breath(lasted for 1 week during January)and continued in the same pattern for 7 years

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12 years back-Episode lasted for 20 days and continued in the same pattern till 30 days back

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Latest episode- lasted for 30 days and not getting relieved on medication

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Other symptoms

5 yrs ago-Anaemia

1 month back-Generalised weakness

20 days ago- Hypertension 

15 days ago- pitting type of pedal edema and facial puffiness

Anatomical localization of the problem:

Bronchi and bronchioles of the lung 

Primary etiology :

The symptoms are probably due to the inhalation of Paddy dust

Paddy dust is biologically composed of 

plant material

fungi: of genus epicocum, fusarium

parts of insects: House dust mites and storage mites

bacteria

soil

Rice dust enters human airway(extrinsic antigen)

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It triggers and stimulate the plasma cells and lymphoid tissue to produce IgE

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IgE bind to mast cell and release Histamine and Bradykinin

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These narrow the respirator tract and increase of mucus production 

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

1.Head and elevation: Significantly increases global and regional end-expiratory lung volume. It has also been shown to improve oxygenation and hemodynamic performance.

2.Bipap intermittent: By having a custom air pressure for when you inhale and a second custom air pressure when you exhale, the machine is able to provide relief to your overworked lungs and chest wall muscles.

3.inj.Augmentin 

Augmentin is a prescription antibiotic medication. It’s used to treat infections caused by bacteria. Augmentin belongs to the penicillin class of antibiotics.Augmentin contains two drugs: amoxicillin and clavulanic acid. This combination makes Augmentin work against more types of bacteria than antibiotics that contain amoxicillin alone.Augmentin is effective for treating infections caused by many different types of bacteria. These include bacteria that cause:

pneumonia, ear infections, sinus infections,skin infections,urinary tract infections

4. Tab Azithromycin 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.

5. Inj lasix 

Furosemide is used to reduce extra fluid in the body (edema) caused by conditions such as heart failure, liver disease, and kidney disease. This can lessen symptoms such as shortness of breath and swelling in your arms, legs, and abdomen.This drug is also used to treat high blood pressure. 

6.Tab pantop

 It is commonly used for the diagnosis or treatment of Gastro-esophageal reflux disease, Heartburn, Euophagus inflammation, Stomach ulcers.

7.Inj.Hydrocortisone 

It is used to treat disorders of the skin, hormones, stomach, blood, nerves, eyes, kidneys, or lungs. They also include rheumatic disorders, allergic problems, certain cancers, or problems with the intestines such as ulcerative colitis.

8.Nebuliser with 

A) ipravent: It is an anticholinergic bronchodilator. It is used in the Treatment of COPD and prevention of asthma 

B)budecort: It is a corticosteroid and acts as an anti-asthmatic agent. It helps in controlling daily symptoms such as shortness of breath, wheezing and chest pain and prevents the worsening of these symptoms. Budecort should always be administered with the help of nebulisers. Nebuliser is a machine that forms a mist of medicine so that it can reach the lungs easily. Your doctor or pharmacist will guide you on how to use nebulisers properly. You should take Budecort regularly as advised by your doctor for effective control of your asthma

9. Tab pulmoclear 

It contains a combination of two medicines, Acebrophylline and Acetylcysteine. They belong to the class of bronchodilators and mucolytics, respectively. It is used for relieving the symptoms of coughing, wheezing, congestion and blockage in the airways in a condition called chronic obstructive pulmonary disease (COPD).

10) Chest physiotherapy 

It is a term used for a group of treatments designed to improve respiratory efficiency, promote expansion of the lungs, strengthen respiratory muscles, and eliminate secretions from the respiratory system.It includes postural drainage, chest percussion, chest vibration, turning, deep breathing exercises, and coughing.

11)Inj HAI SC 

Human Actrapid 40IU/ml Solution for Injection is a short-acting insulin used to treat type 1 and type 2 diabetes mellitus. It is used together with a healthy diet and regular exercise to control blood sugar levels after meals. This helps to prevent serious complications of diabetes like kidney damage and blindness.

12) Inj thiamine

To treat or prevent thiamine(B1) insufficiency 

13)Vitals charting

This allow for continuous monitoring of a patient, with medical staff being continuously informed of the changes in general condition of a patient.

14)I/O chart

Urine input/output chart

This chart (also known as a frequency-volume chart or bladder diary) is used to assess how much fluid you drink, to measure your urine volume, to record how often you pass urine over 24 hours and to show any episodes of incontinence (leakage)

15) O2 inhalation 

It is used to 

A) manage the condition of hypoxia

B)maintain o2 tension in blood plasma

C)increase oxy haemoglobin in RBC

D) maintain ability of cells to carry out normal metabolic function 

E)reduce the risk of complications 

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

Respiratory infection, being responsible for approximately half of COPD exacerbations. Common bacterial pathogens of acute exacerbations include Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis.[7]Less common bacterial pathogens include Chlamydia pneumoniae and MRSA.

Allergens, e.g., pollens, wood or cigarette smoke, pollution[5]

Toxins, including a variety of different chemicals[5]

Air pollution[citation needed]

Failing to follow a drug therapy program, e.g. improper use of an inhaler

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

There are some case reports about interstitial lung disease (ILD) such as pneumonitis caused by isoniazid (INH), rifampin (RFP), ethambutol (EMB). Therefore The causative drug was discontinued permanently or re-administrated after desensitization therapy. 

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

The distribution of electrolyte disturbances in COPD group (total 58.53%) was found as follows: hypokalemia in 20%, hyponatremia in 13.33%, hypomagnesemia in 6.66%, hypochloremia in 3.33%, and combined disturbances in 15%.

 Activation of the renin-angiotensin-aldosterone system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the electrolyte imbalance during acute exacerbation of COPD

This patient has Hyponatremia and Hypochloremia according to the reports

Hyponatremia in patients with COPD developed secondary to many reasons, such as development or worsening of hypoxia, hypercapnia, and respiratory acidosis, and right-side heart failure with development of lower limb edema, renal insufficiency, use of diuretics

respiratory acidosis with metabolic alkalosis (owing to renal compensation) in patients with COPD with chronic hypercapnia is the usual cause of hypochloremia in those patients.

NEUROLOGY  : case 1

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.

NEUROLOGY : case 2

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

ANS. Timeline of the patient is as follows-

7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting

4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.

H/O postural instability- falls while walking

Associated with bilateral hearing loss, aural fullness, presence of tinnitus

Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles

Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day

Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.

Etiology- Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)

Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.

In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.

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

ANS. 

A)     Tab Vertin 8mg- This is betahistine, which is an anti- vertigo medication

MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem. 

Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.

 

B)     Tab Zofer 4mg- This is ondanseteron- It is an anti emetic

MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.

Indications- Used to control the episodes of vomiting and nausea in this patient.

 

C)      Tab Ecosprin 75mg- This is aspirin. It is an NSAID

MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis

Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.

D)     Tab Atorvostatin 40mg- This is a statin

MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.

Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.

E)      Clopidogrel 75mg- It is an antiplatelet medication

MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.

Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting

F)      Thiamine- It is vitamin B1

It is naturally found in many foods in the human diet. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.

Indications- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.

G)     Tab MVT- This is methylcobalamin

Mainly given in this case for vitamin B12 deficiency.

 

3)      Did the patients history of denovo hypertension contribute to his current condition?

 

ANS. A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts. 

Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke. 

 

4)      Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?

 

ANS. Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.

Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain

Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage

According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.

Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate. 

So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.

NEUROLOGY :case 3

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.

 

NEUROLOGY : case 4

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)

NEUROLOGY : case 5

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

Ans: the reason for patient to develop ataxia in past one year is ALCOHOL

The toxic effects of alcohol are diverse. Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia(ALCOHOL INDUCED TOXIC ATAXIA). 

 The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death

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

Ans: the reason for IC bleed is

       

CHRONIC ALCOHOL CONSUMPTION 

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ALCOHOL INDUCED TOXIC ATAXIA

       ↓       

REPEATED FALLS

       ↓      

IC BLEEDING

* The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal haemorrhage associated with excessive alcohol intake.

NEUROLOGY : case 6

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

A:One cause of stroke after trauma is a tear in the head or neck blood vessels that lead to the brain, which can be a source of blood clots that cause a stroke. If a tear in these arteries can be diagnosed at the time of the trauma, a patient could be treated with an anti-clotting medicine to help prevent stroke

2.What are warning signs of CVA?

3.What is the drug rationale in CVA?

3ans

Aspirin -antiplatlet drug prevents stroke

Atorvostatin - decreases LDL cholesterol to prevent recurrent attacks of stroke

4. Does alcohol has any role in his attack?

ans : Excessive alcohol consumption has been associated with a wide range of medical conditions. Moderate alcohol consumption is linked to a lower risk of stroke than abstinence, whereas heavy alcohol consumption has been associated with an increased risk of stroke and stroke mortality. In addition to alcohol consumption, the most important risk factors for stroke are hypertension, coronary artery disease, cardiac insufficiency, atrial fibrillation, type 2 diabetes, smoking, overweight, asymptomatic carotid artery stenosis and elevated levels of cholesterol.

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

5ans 

Yes increased LDL causes atherosclerosis -Blood vessels - ischemia leads to - stroke

NEUROLOGY : case 7

a) what is myelopathy hand?There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement. 

b)what is finger escape?

Finger escape

Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. . This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".

c)what is Hoffman's sign?

Hoffman's sign or reflex is a test used to examine the reflexes of the upper extremities. This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition

NEUROLOGY : case 8

1) What can be  the cause of her condition ?                             

the cause of her condition 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

CARDIOLOGY : case 1

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)

CARDIOLOGY : case 2

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

CARDIOLOGY :case 3

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.