Bimonthly medicine assignment

ROLL NO : 50

NAME: K.LASYA MITHRA

GASTRENTROLOGY

 

CASE:1

QUESTION 1 :

 Evolution of symptomology:

·        5 yrs back patient had pain abdomen & vomitings - was taken to a local hospital and treated conservatively.

·       
He stopped taking alcohol - advised by the physician and was symptom free for nearly 3 yrs.

      ·        again started alcohol consumption following which he had recurrent episodes of                pain abdomen & vomiting 

·        Last year he had almost 5-6 episodes and got treated by a local RMP.

      ·        past 20 days – he consumed increased amount of  alcohol (5 bottles of toddy per              day) 

 ·        last alcohol - 1 week back following which he again had pain abdomen & vomiting from 1 week and fever from 4 days.

      ·        Presently patient complained of pain in umbilical, left hypochondriac, left                        lumbar and hypogastric region.

·        Pain – throbbing type and radiating to back and associated with nausea and vomiting - 1 episode , which is non bilious, non projectile and also has food particles and water content since 1 week. pain increased after taking food.

·        Fever was high grade, continuous and associated with chills and rigors.

·        Then patient developed constipation since 4 days and passing flatus. 

·        Patient also complained of burning micturition since 4 days, which is associated with suprapubic pain, increased frequency and urgency.

Anatomical localization: Pancreas

Primary etiology: consumption of alcohol

     QUESTION 2:

      Efficacy of drugs

1)   

Injection. MEROPENAM ; TID for 7 days

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

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

             These are antibiotics given for control of infection. They also help in reducing the septic complications of pancreatitis. 

4) TPN (Total Parenteral Nutrition)

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

Dehydration seen in pancreatitis due to fluid loss. Hence these patients are given plenty of fluids.

6) ING. OCTREOTIDE 100 mg SC – BD

            Used to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.

7) ING. PANTOP 40 mg IV – OD

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

               Patient is chronic alcoholic. Alcohol causes thiamine deficiency (given prophylactically) and long fasting and TPN may lead to B1 deficiency.

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

            Opioid analgesic, given to relieve pain.

 

 

CASE 2 :

QUESTION 1

·        Pancreatitis sometimes associated with pulmonary complications.

·        Pulmonary complications seen due to pancreatic enzymes reaching lung through hematogenous route. As these are active enzymes, they cause damage to the lung tissue causing symptoms of lung damage like dyspnoea.

QUESTION 2

·        Hyperglycemia is seen because in acute pancreatitis there occurs release of pancreatic enzymes with the pancreatic substance. This leads to damage to the pancreas including the beta cells of pancreas.

·        Beta cells release insulin hormone. Due to damage insulin is not released into blood. This leads to high glucose levels causing hyperglycaemia.

·        Hyperglycemia can also occur due to inflammation in the body cused by pancreatitis( sepsis like state).

QUESTION 3

·        Elevated LFT’s : may be due to alcohol causing liver damage.

·        GGT- Gamma Glutamyl Transferase is most specific marker for alcoholic liver disease.

QUESTION 4

LINE OF TREATMENT

·        Intravenous fluids – 125 ml/hr

§  Given to treat dehydrated state as seen in acute pancreatitis.

·        INJ PAN : 40mg IV – OD

·        INJ ZOFER : 4 mg IV – SOS

                             Antiemetic, given for vomiting.

·        INJ TRAMADOL: 1 amp in 100ml NS, IV, SOS

               Opoiod analgesic, given for pain control.

·        Tab Dolo : 650 mg SOS

·        GRBS charting- 6^th hrly

·        BP charting- 8^th hrly

 

CASE 3

QUESTION 1

 Most probable diagnosis

The most probable diagnosis  is abdominal hemorrhage. This might be the reason for findings seen in patient like abdominal distension, rigitidity and guarding in clinical examination etc.

 Differential Diagnosis:

·        Ruptured Liver Abscess.

·        Organized collection secondary to Hollow viscous Perforation.

·        Organized Intraperitoneal Hematoma.

·        Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.

·        Grade 3 RPD of right Kidney.

 QUESTION 2

 Cause of her death

·        Patient was referred to other hospital where she underwent an emergency exploratory laparotomy. The patient passes away the next day. May be the cause of her death is due to complications of surgery like bleeding, infection etc,

 QUESTION 3

 NSAID abuse have something to do with her condition?

·        NSAID’s are group of drugs usually given for pain.

·        These drugs on long-term use can cause many complications like renal dysfunction causing decreased glomerular filtration rate, acute kidney injury etc.

·        They also cause damage to liver ranging from elevated serum aminotransferase to fulminant liver failure.

·       NSAIDS also cause damage to gastrointestinal mucosa leading to ulcer formation.

 

NEPHROLOGY

 

CASE 1

 

QUESTION 1

  Reason for shortness of breathe

·                   Can be due to acidosis caused by diuretics

 QUESTION 2

Reason for Intermittent Episodes of drowsiness

·                          Drowsiness is due to hyponatremia in this patient.

QUESTION 3

Fleshy mass like passage in urine

·               plenty of pus cells in his urine passage  appeared as fleshy mass like passage to him.

QUESTION 4

 Complications of TURP

·        Difficulty micturition

·        Electrolyte imbalances

·        Infection

CASE 2

QUESTION 1

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

One possible Provisional diagnosis of this patient is ADHD (Attention deficit/Hyperactive disorder).

Symptoms may start before the age of 12 and include inattention , hyper active and impulsive behaviour

ADHD patients generally have following symptoms.

·        Have problems sustaining attention in tasks or play

·        Have problems organizing tasks and activities, such as doing tasks in sequence

       Become easily distracted by unrelated thoughts or stimuli

·        Avoid or dislike tasks that require sustained mental effort, such as schoolwork or homework

  Hyper active impulsive -

·        Have difficulty sitting in one place and are always on the run.

·        Fidget with their hands or legs.

·        Talk too much 

·        Have difficulty waiting for their turn.

Academic difficulties are frequent as are problems with relationships. 

QUESTION 2

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

        It maybe Psychosomatic. The child has the urge to urinate in the morning due to stress or mental conflict. During sleep, the kid is free of stress and may not have the urge to urinate excessively.

QUESTION 3

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

The only management is reassurance to the kid and his relaxation by reducing stress. The problem will resolve overtime (most commonly by the time he reaches 10yrs).

There are other approaches like counselling by psychologists and psychiatrists, psychotherapy, cognitive-behavior therapy, support groups, parent training, meditation, and social skills training. 

CARDIOLOGY

CASE 1

QUESTION 1

 difference between heart failure with preserved ejection fraction and with reduced ejection fraction

·        The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). A normal range is usually around 55 to 70 percent.

 

HEART FAILURE WITH REDUCED EJECTION FRACTION ( HFrEF)	HEART FAILURE WITH PRESERVED EJECTION FRACTION(HFpEF)
Also called as systolic heart failure and are people with heart failure with reduced ejection fraction < 40 to 50%.	Also called as diastolic heart failure and are people with heart failure with preserved ejection fraction (same ejection fraction seen)
Usually diagnosed early in life almost at the time of presentation of heart attack in patient	Diagnosed later in life that is patient will have complains of heart attack initially. HEpEF is also associated with other health problems like GERD.
Risk factors: family history of heart failure	Risk factors: sedentary life style, hypertension , other heart diseases
Patients usually have history of surgery for heart failure eg: pacemaker implantation	Patient usually have no history of surgery for heart failure.
Cardiac cell death is seen.	Cardiac cell death not seen.
Cardiomyocyte hypertrophy is eccentric due to remodeling of heart.	Cardiomyocte hypertrophy is concentric.

QUESTION 2

 pericardiocenetis

Pericardiocentesis : It is a procedure done to remove excess pericardial fluid from pericardial sac. It is usually done if the accumulated fluid is causing hemodynamics in patient.in this patient the pericardial fluid which has accumulated was resolving on its own .Hence pericardiocentesis is not done in this patient.            

QUESTION 3

 risk factors for development of heart failure in the patient

Risk factors in this patient

 

Non modifiable                   and                                  modifiable

Age                                                                      hypertension

gender                                                                  Smoking

                                                                             diabetes

                                                                             Kidney disease

QUESTION 4

 cause for hypotension in this patient

        Patient had anemia with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension.

 

CASE 2

QUESTION 1

 possible causes for heart failure in this patient

·        obesity

·        alcohol

·        diabetes

·        hypertension

QUESTION 2

 reason for anemia in this case

·        patient is an alcoholic. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia.

·        patient was diagnosed with chronic kidney disease . patients with kidney disease have anemia due to decreased erythropoietin levels .

 QUESTION 3.

reason for blebs and non healing ulcer in the legs of this patient

·        The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to diabetes mellitus. Diabetic foot ulcers generally arise as a result of poor circulation in the foot region.High blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers.

·        Infection of wounds can also occur at the injury site due to high sugar levels (more growth of infectious organisms) and further nerve damage in diabetics leads to decreased perception of sensation when injury occurs.

·        Many associated risk factors :

§       Alcohol consumtion and smoking

§       Obesity, age

§       Poor quality or fitting of the footwear.

§       Unhygienic appearance of foot.

§        Improper care of the nails of the toe.

§       Complication arising from Diabetes like eye problems, kidney problems and more.

QUESTION 4.

  sequence of stages of diabetes in this is patient

§    alcohol , obesity     -    impaired glucose tolerance        -    diabetes mellitus - 

    microvascular complications like triopathy and diabetic foot ulcer - 

 macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease.

CASE 3

Evolution of symptomology:

·       Patient has underwent a surgery for inguinal hernia 10 years back. He was after the surgery but developed on and off pain at the surgical site from last 3 years for which patient was using NSAID’s.

·       Patient gives a history of facial puffiness from 2 to 3 years which is on and off.

·       Patient had complaint of shortness of breathe 1 year back for which he was treated at local hospital and was also diagnosed with hypertension.

·       Presently patient is complaining of shortness of breathe from 2 days which is initially grade 2 (on exercise) later progressed to grade 4 (at rest)

·       Patient also had decreased urine output from 2 days and anuria since morning(day of presentation to hospital).

·       Patient also has constipation from 2 days.

 anatomical site  BLOOD VESSELS;

Etiology: Hypertension

 QUESTION 2

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

Ans: PHARMACOLOGICAL INTERVENTION

1. TAB. Dytor: It is a diuretic.It is given to treat the volume overload which occurs due to renal dysfunction.

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 : It is an anticoagulant

mechanism: Acitrom 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 :It is a beta blocker

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.

4. INJ. HAI S/C it is insulin given to maintain his glucose levels.

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:

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. Watch for any bleeding manifestations like Bleeding gums.

7. 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.

QUESTION 3

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

Cardiorenal syndrome : It is an entity in which damage to heart causes damage to kidney and viceversa.

Pathogenesis: cardiac dysfunction leads to fluid overload in the body. Fluid overload causes increase in venous pressures. These increased pressures are transmitted back to efferent arterioles causing renal injury.

cardiorenal syndrome type 4 is seen in this patient.

QUESTION 4

 risk factors for atherosclerosis in this patient

 hypertension: It is one of the main risk factor involved.

Changes in smooth muscles of blood vessel causes impairment in relaxation of blood vessels also leads to atherosclerosis.

QUESTION 5:

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

Patient is on drug Warfarrin.to monitor the drug APTT and INR are ordered on a regular basis. 

 CASE 4

QUESTION 1

Evolution of symptomology

•                       Diabetes since 12 years - on medication

•                       Heart burn like episodes from 1 year and are relieved without any  medication

•                       Diagnosed with pulmonary TB 7 months back and completed full course of treatment.

•                       Hypertension from 6 months and on medication

•                       Shortness of breath since half an hour-SOB even at rest

Anatomical localisation - Cardiovascular system

Etiology:  Hypertensive and diabeties. These conditions can lead to atherosclerosis.

QUESTION 2

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

Pharmacological interventions:

TAB MET XL 25 MG/STAT-contains Metoprolol . It is an cardioselective beta blocker

 Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers decrease the conductivity and contractility of heart. They also help in increasing the blood flow to heart

Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.

Percutaneous Coronary Intervention  is a non-surgical procedure that uses a dye to view the block in the coronary vessels flowed by passing a catheter to place a stent that helps in opening of the blood vessels which are narrowed.

QUESTION 3

 indications and contraindications for PCI

     INDICATIONS:

·        Acute ST-elevation myocardial infarction (STEMI)

·        Non–ST-elevation acute coronary syndrome (NSTE-ACS)

·        Unstable angina.

·        Stable angina.

·        Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)

   CONTRAINDICATIONS:

·        Intolerance for longterm oral antiplatelets.

·        Hypercoagulable state.

·        High-grade chronic kidney disease.

·        Chronic total occlusion of SVG.

·        An artery with a diameter of <1.5 mm.

QUESTION 4

 What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?

PCI is a noninvasive and safe procedure , but it can cause some complications like

·        Bleeding

·        Blood vessel damage

·        Allergic reaction to the contrast dye used

·        Arrhythmias.

Hence it can produce some complications when done in patients who dont need it.

 

CASE 5

QUESTION 1

   evolution of the symptomatology:

• Patient was diagnosed with diabetes mellitus 8yrs back.
• 3 days back-He developed chest pain which is radiating to back and dragging type.
• since morning he complained of giddiness and profuse sweating.

Anatomical localization: heart

primary etiology : uncontrolled DM and inferior wall MI

QUESTION 2

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

·        TAB. ASPIRIN 325 mg PO/STAT

·        TAB ATORVAS 80mg PO/STAT

·        TAB CLOPIBB 300mg PO/STAT

·        INJ HAI 6U/IV STAT

QUESTION 3

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

PTCA is a non-invasive procedure done to widened the narrowed blood vessels in heart. PTCA if done in early hours( within12 hrs) is useful. As this patient presented late (3 days after onset of symptoms) it is advisable to not do PTCA.

.

CASE 6

QUESTION 1

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

There was fluid loss which occurred in this patient. This resulted in decreased preload and decreased cardiac output causing SOB.

After administration of IV fluids there was an increase in preload and cardiac output. Hence there were decrease in symptoms.

QUESTION 2

rationale of using torsemide in this patient

It is a diuretic given to treat fluid overload that is causing abdominal distension.

QUESTION 3

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

It is given to treat any bacterial infection causing UTI.

INFECTIOUS DISEASES

QUESTION 1

 clinical history and physical findings are characteristic of Tracheo oesophagal fistula

·        Dysphagia is the common presentation of tracheo oesophagal fistula(TOF)

·        History of weight loss, recurrent chest infections, trauma, malignancy or ingestion of caustic substances, pyrexia of unknown origin

·        Physical findings- Uncontrolled coughing after swallowing, 

·                             Laryngeal crepitus is positive in this patient which can be seen in TOF

QUESTION 2

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

 IRIS (Immune Reconstitution Inflammatory Syndrome) occurs in immunosuprresive conditions likeAIDS where initially there is improvement in immunity but later it deteriorates due to overwhelmimg response to previous opportunistic infection.

It can be prevented by initiating the ART before the development of advanced Immunosuppression i.e; starting the therapy before CD4 cell count decreases more

This patient has  CD4 count of 420 when ART is initiated .So this patient has very less chances of developing IRIS.

 

 

HEPATOLOGY

CASE 1

QUESTION 1

 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 ?

Alcohol is predisposing factor for both amoebic and pyogenic liver abscess. Locally made alcohol is not prepared under aseptic conditions, it could be bacterially contaminated.This could have lead to liver abscess in this patient

QUESTION 2

 etiopathogenesis  of liver abscess in a chronic alcoholic patient ?

 ( since 30 years - 1 bottle per day)

Alcohol is only the predisposing factor of liver abscess but not the true etiological agent. Chronic alcoholism leads to Fatty liver and liver cirrhosis (Alcohol liver disease) which eventually results in liver abscess if liver is infected with entamoeba histolytica or other pathogenic organisms.

Amoebic liver abscess is more common than pyogenic liver abscess.

QUESTION 3

 Is liver abscess more common in right lobe ?

Generally infection to the liver from other abdominal organs spreads through portal vein. Infection arises more commonly in the right lobe, probably due to an unequal distribution of superior and inferior mesenteric vein contents within the portal venous distribution.

QUESTION 4

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

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

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

·        If the abscess is not responding to the drugs for 7 or more days .

 

CASE 2

QUESTION 1

Cause of liver abcess in this patient ?

·        may be due to contamination of food / fluid history of which is not mentioned.

·        malnutrition and poor personal hygiene are also the risk factors of liver abcess..

·        Other associated risk factors are age of the patient, right lobe involvement etc.

·        The cause for abscess in this pt. is infection with amoeba leading to amoebic liver abscess

QUESTION 2

 How do you approach this patient

 we treat both pyogenic and amoebic liver abcess empirically. 

Hence we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.

·        Inj.Zostum 1.5gmIV BD

             It is a combination of Cephalosporin , Sulbactum.It is an antibiotic to treat if there is any bacterial cause for liver abscess and to prevent secondary infections of liver abscess.

·        Inj Metrogyl 500mg IV TID –

                 It is Metronidazole to treat amoebic cause

·        Inj Optineurin 1amp in 100 ml NS – It is a multivitamin drug.

·        Inj Ultracet ½ QID

            It is a combination of tramadaol (Opiod analgesic) and  acitominophen(analgesic and antipyretic)

·        Tab Dolo 650 mg SOS.

Abcess may get ruptured if untreated and cause peritonitis and shock.

QUESTION 3

 Why do we treat here both amoebic and pyogenic liver abcess? 

we treat both pyogenic and amoebic liver abcess empirically beacuse we cant differentiate whether the abcess is because of bacterial infection or amoebic infecation. So we cover both bacterial causes with broad spectrum antibiotics and also amoebic causes mostly with metronidazole.

QUESTION 4

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

Based on right hypochondriac and epigastric pain , fever

 USG finding of hyperechoic mass in right lobe of liver along with other supportive investigations like leucocytosis (suggestive of infection/inflammation) and ALP ( Alkaline phosphatase ) rise in LFT is a suggestive diagnosis of  LIVER ABCESS.

Serology  and aspiration of fluid and stool examination can be done for definitive diagnosis.

Other factors in favour of diagnosis are age of the patient , right lobe involvement.

 

INFECTIOUS DISEASES

(MUCORMYCOSIS)

 

CASE 1

QUESTION 1

evolution of the symptomatology

• 3yrs ago - Hypertension was diagnosed

·         21 days ago: Received vaccination at PHC which was  followed by high grade fever with chills and rigor which relieved on medication

·         18 days ago:  With similar complaints , patient went to a local hospital and took antipyretics but fever didn’t subside

·         11 days ago:C/O generalized weakness ,facial puffiness and generalized edema.Patient was in a drowsy state.

·         4 days ago: Presented to casuality in altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb.

·         By evening patient developed peri orbital edema. Blood tinged serous discharge from left eye.

·         This patient has uncontrolled blood sugar levels. He has DKA of which he is unaware off.

·         He is diagnosed with Acute oro rhino cerebral mucormycosis which can be commonly seen in patients with incontrolled sugar levels.

·         This fungus, enters sinuses and then go to brain.

·         This patient also has acute ifarct in left frontal and temporal lobe.

Anatomical localization: Oral , Nasal and Eye.

Primary etiology:  Mucormycosis is any fungal infection caused by fungi in the order Mucorales. 

QUESTION 2

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

·                         Itraconazole

• Deoxycholate ampB 
• Inj. Liposomal amphotericin B

QUESTION 3

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

·         Mucormycosis is an fungal infection caused by mucormycetes. It is an opportunistic infection which mainly occurs in immunocompromised states.

·         Increased sugars in blood is also a risk factor for development of this infection.

·         Presently there is an increase in mucormycosis cases due to COVID-19 infection.

  In COVID-19 steroids are given which decreases the immunity of the individual thus predisposing COVID patient to this fungal infection. 

NEUROLOGY

CASE 1

QUESTION 1

evolution of the symptomatology

·        9 days ago – patient suddenly started talking, as well as laughing to himself

·        He was conscious, but oriented to time, person and place only from time to time

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

·        he was taken to a local RMP, given IV fluids, and referred to a higher care hospital

·        patient stopped drinking the same day, citing general body pains the day before

·        he also had short term memory loss since 9 days, where he could not recognize family members from time to time.

·        He had 2 to 3 episodes of seizures 4 months ago folloeing cessation of alcohol which was associated with restlessness, sweating, tremors.after this episode he started drinking again.

Anatomical localization: brain

Primary etiology: chronic alcoholism.

QUESTION 2

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

·        Thiamine helps the body cells change carbohydrates into energy. It has been used as a supplement to cope with thiamine deficiency

·        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.

·        pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions in vivo to reduce neuronal excitability and seizures.

·        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.

·         Potchlor liquid is used to treat low levels of potassium in the body.

 

QUESTION 3

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

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

QUESTION 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, is a coenzyme that is essential for 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. 

QUESTION 5

 probable reason 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.

QUESTION 6
 What is the probable cause for the normocytic anemia?

Heavy alcohol consumption can cause generalized suppression of blood cell production and the production of structurally abnormal blood cell precursors that cannot mature into functional cells. Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia.

QUESTION 7

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

The pt. is already diabetic and therefore chances of formation of foot ulcer is high.In a patient of chronic alcoholic the immune system is weak due to the affect on blood cells formation and iron absorption, therefore , due to this healing of an ulcer decreases.

 

CASE 2

QUESTION 1

 evolution of the symptomatology

·        7days back- H/O giddness with one episode of vomiting

·        4days  back- H/O consumption of alcohol , following giddness and postural instability

·        4days back-Associated with bilateral hearing loss, aural fullness, presence of tinnitus

·        4 days back- associated with vomiting 2-3 episodes.

·        presents with slurring of speech, and deviation of mouth.

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.

QUESTION 2

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

• 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. 

·        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.

·          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.

·        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.

·        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

·        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.

·        Tab MVT- This is methylcobalamin

Mainly given in this case for vitamin B12 deficiency.

QUESTION 3

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

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. 

QUESTION 4

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

Atrial fibrillation and alcohol Drinking excessive amounts of alcohol can trigger atrial fibrillation – a type of irregular heartbeat. Atrial fibrillation increases your risk of stroke by five times, because it can cause blood clots to form in the heart. If these clots move up into the brain, it can lead to stroke

CASE 3 

QUESTION 1

 evolution of the symptomatology

·        10 years ago- had an episode of paralysis attack on all four limbs( due to hypokalemia)

·        8 month ago- B/L pedal edema

·        7months ago- had blood infection

·        2months back- neck pain--diagnosed with cervical spondylosis

·        6days ago- left upper limb pain associated with tingling and numbness

·        5days ago- chest pain , palpitations and SOB

Anatomical localization :Heart.

Primary etiology : HYPOKALEMIA and for radiating pain of left upper limb is CERIVAL SPONDYLOSIS.

QUESTION 2

reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

 pt. is suffering with HYPOKALEMIC PERIODIC PARALYSIS.

Hypokalemic periodic paralysis is characterized by muscle weakness or paralysis when there is a fall in potassium levels in the blood. In individuals with this mutation, attacks sometimes begin in adolescence and most commonly occur with individual triggers such as rest after strenuous exercise (attacks during exercise are rare), high carbohydrate meals, sudden changes in temperature, and flashing lights, cold temperatures and stress etc. Weakness may be mild and limited to certain muscle groups, or more severe full-body paralysis. Attacks may last for a few hours or persist for several days. Recovery is usually sudden when it occurs, due to release of potassium from swollen muscles as they recover. Some patients may fall into an abortive attack or develop chronic muscle weakness later in life.

QUESTION 3

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

The earliest electrocardiogram (ECG) change associated with hypokalemia is a decrease in the T-wave amplitude. As potassium levels decline further, ST-segment depression and T-wave inversions are seen, while the PR interval can be prolonged along with an increase in the amplitude of the P wave.

 

CASE 4

QUESTIONS 1

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

§  epilepsy after hemorrhagic stroke is attributable to irritation casued by products of blood metabolism.

§  Increased concentration of the excitatory neurotransmitter glutamate, the disturbance of electrolyte balance, the destruction of phospholipid membranes can also cause seizures.

§  Repeated seizure-like activity in the setting of cerebral ischemia significantly increases infarct size and can impair functional recovery.

QUESTION 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?
First the pt. did not have loss of consciousness which might mean the pt. has focal seizer which could most commonly can be simple partial or focal seizers without impairment of awareness. Then the pt. has developed generalized tonic clonic seizers which is usually associated with loss of consciousness.

 

CASE 6

QUESTION 1

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

 RTA may have caused an internal brain injury or injury to any vessel which lead to ischemia which was left undiagnosed and in mean time  due to hypoxia turned into infarct.There is also another possibility , that is RTA leading to brain injury which was treated at that time but incompletely, over time edema must have occurred or rupture of vessel due to any pressure effect leading to stroke.

QUESTION 2

What are warning signs of CVA

·         Paralysis or numbness or inability to move parts of the face, arm, or leg - particularly on one side of the body

·         Confusion- including trouble with speaking

·         Headache with vomiting

·         Trouble seeing in one or both eyes

·         Metallic taste in mouth

·         Difficulty in swallowing

·         Trouble in walking (impaired coordination)

·         Dystonia

QUESTION 4

 Does alcohol has any role in his attack?

Alcohol increases the risk of hemorrhagic stroke.

A hemorrhagic stroke ususally occurs when an aneurysm bursts, or a weakened blood vessel leaks. The result is bleeding either inside the brain, causing an intracerebral hemorrhage, or, less commonly, bleeding between the brain and the tissue covering it, causing a so-called subarachnoid hemorrhage.

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

QUESTION 5

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

The lipid profile of the patient is almost normal except HDLP which is little less. This pt. is neither  hypertensive nor diabetic , so lipid profile having any role in attack  is unlikely here.

But in general, Low HDL, High Homocysteine Predicts Poor Stroke Recovery For Diabetics. Patients with diabetes and low levels of HDL cholesterol, and high levels of homocysteine who have had a mild to moderate ischemic stroke were twice as likely as their counterparts without these conditions to have poorer cognitive function and greater disability after a stroke.

 

CASE 7

QUESTION 1

 myelopathy hand ?

It implies the localised wasting and weakness of the extrinsic and intrinsic muscles of the hand as in cervical spondylitis.

QUESTION 2

What is finger escape ?

It is weak finger abduction as seen in cervical myelopathy is also called the "finger escape sign".

QUESTION 3

What is Hoffman’s reflex?
Hoffmann's reflex  is a neurological examination finding elicited by a reflex test which can help verify the presence or absence of issues arising from the corticospinal tract.

 

CASE 8

QUESTION 1   

cause of her condition  

It might be cortical venous thrombosis according to the the results of imaging.

QUESTION 2

What are the risk factors for cortical vein thrombosis?

Infections:

ü Meningitis, otitis, mastoiditis

ü Prothrombotic states

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

Mechanical:

ü Head trauma, lumbar puncture

ü Inflammatory

ü SLE, sarcoidosis, Inflammatory bowel disease. 

ü Malignancy.

ü Dehydration 

ü Nephrotic syndrome 

Drugs:

ü Oral contraceptives, steroids, Inhibitors of angiogenesis

ü Chemotherapy: Cyclosporine and l asparginase

Hematological:

ü Myeloproliferative Malignancies

ü Primary and secondary polycythemia

Intracranial :

ü Dural fistula, 

ü venous anomalies 

Vasculitis:

ü Behcets disease wegeners granulomatosis

QUESTION 3

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

           Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.

QUESTION 4

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

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.

 

PULMONOLOGY 

QUESTION 1

 evolution of the symptomatology

·        20 Years ago - SOB Grade1 for a week , occurred every year for the same duration

·        18 Years ago- Polyuria and was diagnosed with DM

·        12 Years ago - SOB Grade 1 for a month

·        1 Month ago - Weakness was giving IV

·        30 Days ago - SOB ( latest episode) gradually progressive

·        20 Days ago - HRCT showed Bronchiectasis

·        15 Days ago - Pedal edema and facial puffiness

·        2 Days ago - SOB Grade 4 , drowsiness and  decreased urine output. 

Anatomical location :BRONCHIOLES.

Primary etiology : rice dust exposure as patient is a farmer working in paddy fields.

QUESTION 2

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

 Augmentin - Amoxicillin + Clavulanic acid.

It is an antibiotic.

To reduce the development of drug resistant bacteria and maintain the effectiveness of AUGMENTIN.

QUESTION 3

 What could be the causes for her current acute exacerbation?

·        The pt. was started on antitubercular drugs even though she was tested negative for AFB. ATT includes drugs like ISONIAZIDE , RIFAMPACIN , ETHAMBUTOL , PYRAZINAMIDE AND STREPTOMYCIN

·        ISONIAZIDE can cause side effect like hypersensitivity reaction. COPD is a also an allergic which might have exacerbated due to use of isoniazide.

QUESTION 4

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

 YES, some drugs like isoniazide could could acute exacerbation of COPD thereby increasing the symptoms.

QUESTION 5

What could be the causes for her electrolyte imbalance?

D patien

·        Electrolyte imbalance is found among people with COPD, especially for people who are female, 60+ old, take medication Spiriva and have High blood pressure

·        Patients with COPD tend to retain sodium. In addition, serum potassium should be monitored carefully, because diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels.

·        Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.

·        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.