GENERAL MEDICINE ASSINGMENT - MAY 2021

Yogita Ailani

Roll no: 149

31st MAY 2021

I have been given the following cases to solve in an attempt to understand the topic of "Patient clinical data analysis" to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations, and diagnosis, and come up with a treatment plan.

The link given below contains questions asked regarding the cases:

http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1

Below are my answers to the Medicine Assignment based on my comprehension of the cases. 

1] PULMONOLOGY:

A)  A 55 year old female patient, with the chief complaints of shortness of breath, pedal edema and facial puffiness.

Link to patient details:

https://soumyanadella128eloggm.blogspot.com/2021/05/a-55-year-old-female-with-shortness-of.html

Questions:

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

Ans:  

EVOLUTION OF SYMPTOMS: 

• 1st episode of sob - 20 yr back
• 2nd episode of sob - 12 yr back
• From then she has been having yearly episodes from the past 12 yrs 
• Diagnosed with diabetes - 8yrs back
• Anemia and  took iron injections  - 5yr ago
• Generalised weakness  - 1 month back 
• Diagnosed with hypertension  - 20 days back
• Pedal edema - 15 days back
• Facial puffiness- 15 yrs back

ANATOMICAL LOCATION:

• LUNGS - Bronchi and Bronchioles.
• This led to increased blood pressure in the pulmonary artery which resulted in RIGHT HEART FAILURE.

ETIOLOGY:

•   As the patient works in a paddy field  

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:

Non-Pharmacological Interventions:

1. Head end 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. 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.
4. 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.
5. 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).
6. O2 Inhalation: It is used to 

• manage the condition of hypoxia
• maintain o2 tension in blood plasma
• increase oxy haemoglobin in RBC
• maintain ability of cells to carry out normal metabolic function
• reduce the risk of complications. 

Pharmacological Interventions:-

• Tab.Augmentin
• Tab.Azithromycin
• Inj.Lasix
• Tab.Pantop
• Inj.Hydrocortisone
• Tab.Pulmoclear
• Neb with budecort
• Neb with Ipravent
• inj.HAI
• Inj.Thiamine

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

Ans: There can be two causes - due to infection 

                                                   or environment pollutants.

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

Ans: YES we can see that ATT affects her symptoms. 

Reason:Rifampicin and Isoniazid both cause nephrotoxicity because of which there is a elevation in Renal function tests.

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

Ans: There are two causes which cause electrolyte imbalnce

• Hyponatremia:Worsening of Hypoxia
                        Respiratory acidosis
                        Right heart failure
   
• Hypochloremia:Respiratory acidosis with metabolic alkalosis

2] NEUROLOGY

A) A 40 year old male presented to the hospital with the chief complaints of irrelevant talking and decreased food intake since 9 days. 

Link to patient details:

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

Questions:

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

Ans: 

EVOLUTION OF SYMPTOMS:

• Started drinking alcohol:2009 (12 years ago).
• Diagnosed with Diabetes Mellitus, prescribed oral hypoglycemic:2019 (2 years ago).
• Has an episode of seizures (most likely GTCS):2020 (1 year ago)
• Has another seizure episode (most likely GTCS)- following cessation of alcohol for 24 hours. Starts drinking again after seizure subsides:January 2021 (4months ago).
• Last alcohol intake, around 1 bottle. Starts having general body pains at night:Monday, May 10, 2021.
• Decreased food intake. Starts talking and laughing to himself. Unable to lift himself off the bed, help required:Tuesday, May 11, 2021.
• Conscious, but non coherent. Disoriented to time, person, place.Goes to an RMP the same day- is prescribed IV fluids and asked to visit a hospital
• Admitted to a tertiary care hospital for alcohol withdrawal symptoms, and is treated for the same:Saturday, May 15, 2021.

ANATOMICAL LOCATION: 

• The most probable location in the brain is the hippocampus and frontal lobe.

ETIOLOGY: Consumption of ALCOHOL since 12 years.

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

IVF NS and RL @150ml/hr

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

3. Inj. Lorazepam

4. T. Pregabalin 75mg/PO/ BD

5. Inj. HAI S.C.- premeal

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

7. Lactulose 30ml/PO/BD

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

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

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

Ans:  A possible cause for this is due to a phenomenon known as kindling. 

4) What is the reason for giving thiamine in this patient?

Ans: By seeing the history of patient we can say that he has altered sensorium and is even a chronic alcoholic. Both of these can lead to a differential diagnosis of Wernicke-Korsakoff Syndrome, caused by deficiency of thiamine (B1). To either treat or rule this differential out, thiamine is given.

Thiamine is necessary to provide energy to the CNS, helps in conduction of nerve signals.

Hence, deficiency leads to confusion and ataxia, both of which are present in this patient.

5) What is the probable reason for kidney injury in this patient? 

Ans:

• As the urea levels are very high, it denotes an acute onset- Acute Renal Failure.
• As high serum creatinine, and urea levels are present, denotes that reabsorption from tubules is taking place- therefore the primary cause is prerenal, most probably due to generalised dehydration.
• A slightly high FENa level also denotes that tubular necrosis is occurring to some degree, hence the Prerenal AKI (mostly due to dehydration) is in turn leading to Acute Tubular Necrosis (ATN).

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

Ans: Possible causes are:

• Alcohol causes iron deficiency by causing defect in cell production.
• Loss of blood through chronic foot ulcer
• Decreased bone marrow production of RBCs, due to EPO deficiency owing to kidney failure

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

Ans: 

Yes, as alcoholism can cause peripheral neuropathy which along with Diabetic neuropathy leads to a non-healing foot ulcer.

B) A 52 YEAR OLD MALE WITH CEREBELLAR ATAXIA

Link to patient details:

https://kausalyavarma.blogspot.com/2021/05/a-52-year-old-male-with-cerebellar.html?m=1

Questions:

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

Ans:

EVOLUTION OF SYMPTOMS :

• 13/5/2021 – Giddiness and vomiting (1 epidsode)
• 15/5/2021-Giddiness(increased),Bilateral hearing loss, aural fullness, tinnitus, Vomitings, Postural instability

ANATOMICAL LOCATION : right inferior cerebellar hemisphere

ETIOLOGY: : high cholesterol levels  -> embolization -> infarct -> ataxia

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: 

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
H/O postural instability- falls while walking
Associated with bilateral hearing loss, aural fullness, presence of tinnitus
Associated vomiting- 2-3 episodes per day
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 

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

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.

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

Ans: 

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

Ans:

C) A 45 years old female ,house wife by occupation came to opd with chief complaints of palpitations,chest heaviness,pedal edema,chest pain,radiating pain along her left upper limb , generalized body weakness.

Link to patient details:

http://bejugamomnivasguptha.blogspot.com/2021/05/a-45-years-old-female-patient-with.html

Questions:

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

Ans:

EVOLUTION OF SYMPTOMS:

• August 2019 – Bipedal edema (pitting type)
• 12/5/2021 – pain in left arm
• 13/5/2021 – Chest pain
• 13/5/2021 – Difficulty in breathing (NYHA-CLASS-3)
• 13/5/2021 – Palpitations (more at night, increased since last night)

ANATOMICAL LOCATION: 

• Vertebral discs between C2, C3 and C4 vertebral bodies-in relation to Cervical spondylosis.
• Palpitations felt in chest

ETIOLOGY:  

• Electrolyte imbalance (hypokalemia) causes manifestations like palpitations, chest heaviness, generalised body weakness.
• Radiating pain along her left upper limb due to cervical spondylosis.

2) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?

Ans: 

REASON:Recurrent hypokalemic periodic paralysis 

 

Current risk factor - Use of diuretics

Other risk factors -

• Abnormal loses:
  Medications-diuretics, laxatives, enema, corticosteriods
  Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia.
• Trance cellular shift : alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis.
• Inadequate intake: anorexia, dementia, stareation, total parental nutrition
• Psuedohypokalemia:delayed sample analysis, significant leukocytosis

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

Ans:

Changes seen in ECG -

• Earliest change - decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves 
• In Severe cases - ventricular fibrillation, rarely AV block

Symptoms of Hypokalemia

D) A 55year old male patient came to opd with c/o altered sensorium and involuntary movements from 11pm and recurrent episodes of seizures since 5yrs.

Link to patient details:

https://rishikoundinya.blogspot.com/2021/05/55years-old-patient-with-seizures.html

QUESTIONS:

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

Ans:

Occurrence of seizure due to brain stroke:

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.

Mechanism of seizure activity:

You’re more likely to have a seizure if you had a haemorrhagic stroke . Seizures can also be more likely if you had a severe stroke .

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. 

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?

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.

E) A 48-year-old man presented to the casualty ward on 25th April 2021 with the chief complaints of unresponsiveness for 7 hours and 3 intermittent episodes of seizures in the past 3 hours.

Link to patient details:

https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1

Questions: 

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

Ans: The CT scan done in the patient shows cerebral haemorrhage in frontal lobe which is caused by minor head injuries.  

This can lead to development of Frontal lobe ataxia.

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

Ans: Generally After minor head injuries the haemorrhage gets cured on itself if present.

But in this case as we know that the patient is a chronic alcoholic which might have stopped the process of healing or may have lead to increase in the size of haemorrhage. .

F) A 30 YEAR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPERLIMB AND LOWERLIMB ,DEVIATION OF MOUTH  TOWARDS  LEFT

Link to patient details:

http://shivanireddymedicalcasediscussion.blogspot.com/2021/05/a-30-yr-old-male-patient-with-weakness.html

Questions:

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

Ans:  YES

There is a role of road traffic accident in his present condition which was unidentified.

The closeness of facial bones to the cranium would suggest that there are chances of cranial injuries. 

Since the Zygomatic arch and Mandibular process is very close to the cranium, this might play a role in the patient's present condition.

 

2) What are warning signs of CVA?

Ans: There are mainly 5 warning signs

1. Sudden loss of eye sight in one or both the eyes.
2. Sudden headache without any known cause.
3. Sudden dizziness, loss of balance and confusion.
4. Sudden weakness or numbness in arms, legs and face especially on one side.
5. Sudden trouble in walking, speaking and understanding speech.

3) What is the drug rationale in CVA?

Ans:

Ecospirin-Aspirin(antiplatelet drug)

Aspirin irreversibly inhibits cyclooxygenase, which prevents the conversion of arachidonic acid to thromboxane A2 (TXA2). Thromboxane A2 is a vasoconstrictor and stimulator of platelet aggregration. Platelets are inhibited for their full life cycle (5–7 days) after exposure to aspirin. Aspirin also inhibits prostacyclin activity and this inhibits platelet aggregration. 

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.

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.

4) Does alcohol has any role in his attack?

Ans: 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.

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

Ans: YES! 

According to the study  below there might be a relation with lipid profile in the patient.

Few studies have compared serum HDL-C against serum LDL-C to determine relative contributions to stroke risk. In one study of the very old (aged ≥85 years) low serum HDL-C was associated with an increased risk of stroke, cardiovascular disease, and mortality whereas LDL-C and total cholesterol had no association. On the other side of the age spectrum, a study of young stroke patients demonstrated that low HDL-C was the only serum lipid index associated with an increased risk of stroke.  Low HDL-C was associated with a significant increase in carotid plaque volume by ultrasound. The association of low HDL with increased plaque volume was strengthened when patients on cholesterol-lowering agents were excluded and may indicate an independent effect of HDL-C.

G) A 50 YEAR OLD MALE WITH CERVICAL MYELOPATHY 

Link to patient details:

https://amishajaiswal03eloggm.blogspot.com/2021/05/a-50-year-old-patient-with-cervical.html

Questions:

1)What is myelopathy hand ?

Ans: Cervical myelopathy - common degenerative condition caused by compression on the spinal cord that is characterized by clumsiness in hands and gait imbalance.

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.

Aetiology-

• Degenerative cervical  spondylosis 
• Congenital stenosis 
• Epidural abscess 
• tumour

Treatment is typically operative as the condition is progressive. 

2)What is finger escape ?

Ans: Also known as the WARTENBERG'S SIGN in cervical myelopathy.

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

A method of surgical correction is described for Wartenberg's sign, or persistent abduction of the little finger, using a slip of the extensor digitorum communis of the ring finger. The transferred component can be either the central slip, or the ulnar slip extended by the connexus intertendineus to the little finger.

3)What is Hoffman’s reflex?

Ans: It is reflectory reaction of muscles after electrical stimulation of type 1a sensory fibres(primary afferent fibres which constantly monitor the how fast a muscle stretch CHANGES) in their innervation nerves 

H-REFLEX- is expression of of monosynaptic reflex, which runs in afferents from the muscle and back again through efferents of same muscles.

H) A 17 year old female student by occupation presented to causality with

Chief complaints of Involuntary movements of both upper and lower limbs.

Link to patient details:

https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1                  

Questions: 

1) What can be  the cause of her condition ?                             

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

Other causes of seizures in this patient can be

• Electrolyte imbalance(hypomagnesimia)

• Iron deficiency anemia(mainly in endemic area of malaria)

• hypogylcemia

2) What are the risk factors for cortical vein thrombosis?

Ans: 

A) Infections:

Meningitis, otitis,mastoiditis

Prothrombotic states:

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

B) Mechanical:

Head trauma

lumbar puncture

C) Inflammatory:

SLE,sarcoidosis,Inflammatory bowel disease. 

Malignancy.

Dehydration 

Nephrotic syndrome 

D) Drugs:

Oral contraceptives,steroids,Inhibitors of angiogenesis

Chemotherapy:Cyclosporine and l asparginase

E) Hematological:

Myeloproliferative Malignancies

Primary and secondary polycythemia

F) Intracranial :

Dural fistula, 

venous anomalies

 

G) Vasculitis:

Behcets disease wegeners granulomatosis

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

Ans: 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.            

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

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

In this patient we are giving -  Inj.Clexane 0.4ml given subcutaneously twice a day.

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

3] CARDIOLOGY 

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

 

Link to patient details:

https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html.

Questions:

1) What is the difference between heart failure with preserved ejection fraction and with reduced ejection fraction?

Ans: 

Preserved ejection fraction: 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: referred to as systolic heart failure.

2) Why haven't we done pericardiocenetis in this pateint?        

Ans: PERICARDIOCENTEIS is indicated in the following cases-cardiac tamponate  , large or symtomatic pericardial effusion  , highly suspected TB ,purulent or neoplastic etiology

In our patient - As the effusion was self healing, we don't need to do pericardiocentesis.

3) What are the risk factors for development of heart failure in the patient?

Ans: 

4) What could be the cause for hypotension in this patient?

Ans:  Cardiac tamponade happens if too much fluid collects in the sac, putting pressure on the heart. This prevents the heart from properly filling with blood, so less blood leaves the heart, causing a sharp drop in blood pressure.

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

Link to patient details:

https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html. 

Questions:

1) What are the possible causes for heart failure in this patient?

Ans:  Major causes - 

• Chronic alcoholic - Since 40 years 
• Diagnosed with type 2 DM - 30 years ago. Patient also diagnosed with diabetic triopahy indicating uncontrolled diabetes.
• Hypertension - 19 years ago.
• Elevated creatinine and AST/ASL ratio >2 and with chronic kidney disease IV

2) What is the reason for anaemia in this case?

Ans: 

The most common reason-

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.

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

Ans:  Reason for blebs and non healing ulcer is DIABETES MELLITUS.

Delay in healing of wounds along with poorly controlled diabetes caused by CKD.

Anaemia can also slow down the process of healing due to low oxygen levels.

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 
• Vascular complications, including retinopathy, nephropathy or neuropathy and     related microvascular events.

In our patient we can observe:

• Diabetes mellitus-30 yrs 
• Ckd-4 yrs 
• Diabetic retinopathy-4 yrs 
• Skin changes-bleps and diabetic ulcer-2 months 
• Cardiac disorder-atrial fibrillation-diagnosed on ecg in hospital

C) A 52yr old male came to the OPD with the chief complaints of decreased urine output and shortness of breath

 

Link to patient details:

https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html

Questions:

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

Ans: 

EVOLUTION OF SYMPTOMS:

• Shortness of breath - 2 days ago
• Decreased urine output - 2 days ago
• Anuria - since morning

ANATOMICAL LOCATION: BLOOD VESSELS

 

ETIOLOGY:
The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, of the coronary and cerebral vessels. Hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
The cause of arterial thrombosis is artery damage due to atherosclerosis.

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 - 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
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:

a) Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
b) An enzyme that controls the movement of ions into the heart.

6. Hypoglycemia symptoms

7. Bleeding manifestations - 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 hypertension - 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. hypertension appears to increase the susceptibility of the small and large arteries to 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.

D) A 67 year old patient with acute coronary syndrome

 

Link to patient details:

https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1

Questions:

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

Ans:

EVOLUTION OF SYMPTOMS:

• She developed sweating on exertion and shortness of breath even at rest – 13/05/2021 
• SOB half an hour before coming to the hospital– 14/05/2021.

ANATOMICAL LOCATION: HEART

ETIOLOGY:

• Known c/o DM Type-2 since 12 years
• Known c/o Hypertension since 6 months

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

Ans:

Pharmacological interventions:

A)TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient

 MOA - METOPROLOL is a cardiselective beta blocker

Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect) and with less force( negative inotropic effect).

 

B) Beta blockers also help open up your veins and arteries to improve blood flow.
Indications - it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .

 

Non pharmacological intervention:

 

PERCUTANEOUS CORONARY INTERVENTION. 

It is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).

3) What are the indications and contraindications for PCI?

Ans:

INDICATIONS:

• Acute ST-elevation myocardial infarction (STEMI)
• Non–ST-elevation acute coronary syndrome (NSTE-ACS)
• Unstable angina.
• Stable angina.
• Anginal equivalent (e.g., dyspnea, arrhythmia, or dizziness or syncope).
• High risk stress test findings.      

CONTRAINDICATIONS:

• Intolerance for oral antiplatelets long-term.
• Absence of cardiac surgery backup.
• Hypercoagulable state.
• High-grade chronic kidney disease.
• Chronic total occlusion of SVG.
• An artery with a diameter of <1.5 mm.

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

Ans:

COMPLICATIONS:

• Injury to the heart arteries, including tears or rupture
• Infection, bleeding, or bruising at the catheter site
• Allergic reaction to the dye or contrast used
• Kidney damage from the dye or contrast
• Blood clots that can lead to stroke or heart attack
• Bleeding into the abdomen (retroperitoneal bleeding

HARMS OF OVERTREATMENT AND OVERDIAGNOSIS:

 The harms of over diagnosis and overtreatment are numerous Including psychosocial stressors, Renal morbidity, Unnecessary surgical complications. 

E)  A 60year old Male patient, came to the OPD with the Chief complaint of chest pain since 3 days and giddiness and profuse sweating. 

  

Link to patient details:

https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1

Questions:

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

Ans:

EVOLUTION OF SYMPTOMS:

• chest pain since 3 days from 11/o5/2021 
• giddiness and profuse sweating on the day of admission – 14/05/2021

ANATOMICAL LOCATIONS: HEART coronary artery block rt coronary or left circumflex artery

§  ETIOLOGY: RISK FACTORS -hypertension and type 2 diabetes.

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

Ans:

PHARMACOLOGICAL INTERVENTION:
 

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

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

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

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

 

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

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

Ans:

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.

F) An 87 year old male patient has presented with the complaints of shortness of breath, constipation, decreased urine output.

Link to patient details:

https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.html

Questions:

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

Ans:

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.

2) What is the rationale of using torsemide in this patient?

Ans: §  As the patient has decreased urine output so we need to give TORSEMIDE as it is a diuretic.

MOA of Diuretics:

Diuretics are relatively ineffective in patients with cardiogenic shock, but can be used in case of fluid overload once the cardiac output has increased.

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

Ans: §  Ceftriaxone is used to treat a wide variety of bacterial infections.

It was mainly for the prophylactic use as the patient has CARDIORENAL SYNDROME.

4] GASTROENTEROLOGY & PULMONOLOGY

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

 

Link to patient details:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html

QUESTIONS: 

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

Ans:

EVOLUTION OF SYMPTOMS:

• Episode of fever and vomiting 5yrs back 
• Pain abdomen (in umbilical, left hypochondriac, left lumbar and hypo gastric region) & vomiting since 1 week – 6/05/2021.
• Constipation, burning micturition, fever since 4 days – 9/05/2021.

ANATOMICAL LOCATION: Pancreas and Left lung

ETIOLOGY: Consumption of ALCOHOL

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

Ans: Non pharmacological interventions : drains ( malecot & icd )

I as a treating physician will follow the same approach.

B) A 25 YEAR OLD MAN, WITH SEVERE EPIGASTRIC PAIN 

Link to patient details:

https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html

Questions:

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

Ans: DYSPNEA is caused because of pleural effusion in this patient.

• Pancreatitis in its severe form is complicated by multiple organ system dysfunction, most importantly by pulmonary complications which include hypoxia, acute respiratory distress syndrome, atelectasis, and pleural effusion.
• The pathogenesis of some of the above complications is attributed to the production of noxious cytokines.
• Pulmonary complications of PANCREATITIS are divided into three stages.
• Stage 1-pulmonary manifestations without any radiological changes
• Stage 2-Showing radiologic changes
• Stage 3-ARDS.
• According to the above classification our patient falls in the 2^nd stage as we have found PLEURAL EFFUSION on doing chest x-ray.
• Presence of pleural effusion is currently considered an indication of severe pancreatitis.it is characterized by high levels of amylase and protein. As we can see in our patient that his Serum Amylase levels are elevated.
• The pancreatic enzymes can track up into the mediastinum and then rupture into the pleural cavity either left side or bilaterally and so create a connection between the pancreatic duct and the pleural cavity. Pancreatic pleural effusions may be massive and require treatment.
• Treatment of pleural effusion is usually at first con-servative. Pleural effusions which become symptomatic often require thoracentesis, tube thoracotomy, endotracheal intubation, parenteral alimentation, and administration of octreotide. When the intraabdominal etiology is resolved, pleural effusions often resolve as well.

2) 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.

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

Ans:

• LFT are increased due to hepatocyte injury.
• 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.
• Specific marker for Alcoholic Fatty Liver disease - GGT (Gamma-Glutamyl Transferase)

4) 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 

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

 

Link to patient details:

https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html

Questions :

1) What is the most probable diagnosis in this patient?

Ans: Most probable diagnosis - Liver abscess

• As alp and ast elevated

2) What was the cause of her death?

Ans: As the patient was taken for EMERGENCY LAPROTOMY common causes can be

• Post operative complications  like 
• pyrexia (18.2%)  
• nausea and vomiting (12%),
• wound infection (11.4%),
• respiratory tract infection (6.85%),
• urinary tract infection (2.28%)
• gastrointestinal complications (3.71%)
• toxemia and septicaemia (8%).
• Right lobe Atelectasis
• As we can see that patient falls under septic shock which causes low diastolic bp. 

3) Does her NSAID abuse have  something to do with her condition? How? 

Ans:

• NSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure.
• Adverse effects - gastrointestinal mucosa injury. 

5] NEPHROLOGY AND UROLOGY 

A) A 52 yr old male patient with  Chief Complaints of SOB, Burning micturition and Fever.

Link to patient details:

https://kavyasamudrala.blogspot.com/2021/05/medicine-case-discussion-this-is-online.html

1) What could be the reason for his SOB ?

Ans: Reason for his SOB is ACIDOSIS which is caused by diuretics.

2) Why does he have intermittent episodes of  drowsiness ?

Ans: Reason - Hyponatremia

3) Why did he complaint of fleshy mass like passage in his urine?

Ans: We can notice in CUE that the pus cell count is high in this patient.

As these pus cells are passing in urine it appeared to the patient as fleshy masses.

4) What are the complications of TURP that he may have had?

Ans: 

• Difficulty in mictuation
• Electrolytic imbalance
• Infection

B) A 8 year old boy with chief complaints of Frequent micturation.

Link to patient details:

https://drsaranyaroshni.blogspot.com/2021/05/an-eight-year-old-with-frequent.html

Questions:

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

Ans:

• Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity.
• For a diagnosis, the symptoms have to be present for more than six months

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

Ans:

• Psychosomatic disorder
• Undiagnosed anxiety disorder 

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

Ans: Bacterial kidney infection - the typical course of treatment is antibiotic and painkiller therapy.

• If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
• To treat attention deficit hyperactivity disorder
• For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents.  Schools can be part of the treatment as well.
• Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
• Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.

6] INFECTIOUS DISEASE (HI virus, Mycobacteria, Gastroenterology, Pulmonology)

A) A 40 YEAR OLD LADY WITH DYSPHAGIA, FEVER AND COUGH

 

Link to patient details:

https://vyshnavikonakalla.blogspot.com/2021/05/a-40-year-old-lady-with-dysphagia-feer.html

Questions:

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

Ans:

• Cough - since 2 months on taking food and liquids
• Difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
• Laryngeal crepitus- positive
• These favour for tracheo esophageal fistula

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

Ans:

• Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.
• 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.

7] INFECTIOUS DISEASE AND HEPATOLOGY

A) A 55 year old male patient with the chief Complaints of Pain abdomen, decreased appetite and fever.

Link to patient details:

https://kavyasamudrala.blogspot.com/2021/05/liver-abscess.html

Questions:

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 ?

Ans:

• Cause of liver abscess in this patient is consumption of locally brewed toddy 
• Yes , locally made alchohol acted as factor for liver abscess in this patient 

2) What is the etiopathogenesis  of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)

Ans:

• Liver abscess can be pyogenic ,amoebic or hydatid 
• Infections are acquired from blood stream ( portal and systemic circulation) 
• The most common pathophysiology is bowel content leakage and peritonitis . Bacteria travel via portal blood vessels into liver .
• In this case , Alcohol consumption specially locally prepared alchohol plays major role in liver abscess ( pyogenic and amoebic ) 
• Alchohol acts as predisposing factor 
• Factors responsible for association between alcohol and liver abcess are as follows: 
• Poor nutritional status due to alchohol consumption 
• Presence of infective organisms in the locally prepared alcohol 
• Immunity of the patient 
• Damage to liver done by alchohol

3) Is liver abscess more common in right lobe ?

Ans:

• Yes ,liver abscess is more common in right lobe compared to left lobe
• Single lesions are more common in right lobe 
• This is attributed to comparatively more blood supply via superior mesenteric vein on right side 

4) 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 present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.
• If the abcess is not responding to the drugs for 7 or more days

B) A 21 yr old male  came with the CHEIF COMPLAINTS: of abdominal pain and fever.

Link to patient details:

https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-liver-abcess.html

Questions:

1) Cause of liver abcess in this patient ?

Ans:

Etiology of liver abscess : 

• Pyogenic liver abscess  
• polymicrobial 
• Staphylococcus 
• E .coli
• Klebsiella
• Streptococcus
• Amoebic liver abscess  
• most commonly caused by Entamoeba hisolytica 
• In this patient, occasional toddy consumption acted as source of pathogens

2) How do you approach this patient ?

Ans:

Treatment of liver abscess : 

• Empirical antibiotics : cover both bacterial and amoebic causes 
• For bacterial cause : penicillin +cephalosporin is given ( zostum 1.5 gm i.v. BD injection) 
• For amoebic cause : metronidazole ( Metrogyl 500mg i.v. TID injection )
• Percutaneous drainage of abscess is not done in this patient because of the response to antibiotic therapy and associated complications of drainage 
• Ultracet to relieve pain 
• Dolo 650 mg for fever 

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

Ans: Based on the following : 

• Age of patient – 21 yr ( young age ) , male gender 
• Single abscess 
• Right lobe involvement 
• Chest x ray showing no involvement  
• The abscess is more likely to be amoebic liver abscess
• Since we cannot take risk we treated patient for both bacterial and amoebic cause 

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

Ans: Yes we can confirm the diagnosis in this patient by : 

• Detection of serum antibodies against Entamoeba 
• Culture and sensitivity report of the aspirate

8] INFECTIOUS DISEASES (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)

A) A 50yr old Male came with altered sensorium.

 

Link to patient details:

http://manikaraovinay.blogspot.com/2021/05/50male-came-in-altered-sensorium.html

Questions :

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

Ans:

EVOLUTION OF SYMPTOMS: 

a) Fever with chills and rigors           :     18 -04-2021

b) Facial puffiness                                :    28-04-2021  

c) Periorbital oedema                         :    28-04-2021

d) Generalised weakness.                   :    28-04-2021

( Right upper & lower limb ) 

e) Altered sensorium                            :     4-05-2021

f) Serous discharge from left eye       :     4-05-2021

g) Oral and nasal cavity involvement :     4-05-2021

ANATOMICAL LOCATION: 

a) Eye 

b) Nasal & sinus mucosa 

c) Oral cavity 

d) Brain 

ETIOLOGY : Rhizopus : fungus 

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

Ans: Drugs that can be used to treat mucormycosis are : 

1) Amphotericin – B 

• Liposomal 

• Deoxycholate 

2) Posaconazole 

Efficacy of drugs :  

• Liposomal AmpB > Deoxycholate AmpB > Posaconazole 
• Deoxycholate AmpB is cheaper compared to Liposomal AmpB 

Approach to patient : 

1. Stabilise the patient 

2. Treat the diabetic ketoacidosis 

3. Treatment with antifungal preferably Liposomal AmpB 

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

Ans:

The reason for recent increase in the cases of mucormycosis is immunocompromised state following recovery from COVID -19 infection.