Medicine Bimonthly Assessment May-2021


Sarbesh Mishra

THIS IS THE BLOG MADE IN RESPONSE TO THE FOLLOWING QUESTIONS.This is the link of 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) Link to patient details


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

Ans)EVOLUTION OF SYMPTOMATOLOGY
  • 1st episode of sob - 20 yr back
  • 2nd episode of sob - 12 yr back
  • From then she has been having yearly episodes for the past 12 yrs 
  • Diagnosed with diabetes - 8 yrs back
  • Anemia and  took iron injections  - 5 yrs  ago
  • Generalized weakness  - 1 month back 
  • Diagnosed with hypertension  - 20 days back
  • Pedal edema - 15 days back
  • Facial puffiness- 15 yrs back
  • Anatomical location of problem - lungs
  • Primary etiology of patient- usage  of chulha since 20 yrs might be due to chronic usage 

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

Ans) 1) Head end elevation :# MOA;
  • improves oxygenation 
  • decreases incidence VAP
  • increases hemodynamic performance 
  • increases end expiratory lung volume
  • decreases incidence of aspiration 
     # Indication: .head injury
  • meningitis 
  • pneumonia 
        2) Oxygen inhalation to maintain spo2

        3) Bipap: non invasive method
     
     # MOA :assist ventilation  by delivering positive expiratory and inspiratory pressure with out need          for ET incubation

3) Cause for current acute excerbation ?

Ans)  It could be due any infection or environmental pollutants   
 

4) Could the ATT affected her symptoms if so how?

Ans) Yes ATT affected her symptoms
        Isoniazid and rifampcin -nephrotoxic - raised RFT was seen


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

Ans) Possible causes are

          #  Hyponatrimia :

·         Right heart failure

·         Respiratory acidosis

·         Worsening hypoxia

          # Hypochloremia : Compensated respiratory acidosis 



2) NEUROLOGY

Case A) 

Link to patient details

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

 

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

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

  • He had 2-3 episodes of seizures, one being 1 year ago and the most recent being 4 months ago. The most recent time, (4 months ago), he had developed seizures (most probably GTCS) following cessation of alcohol for 24 hours, which was associated with restlessness, sweating, and tremors. Following this episode, he started drinking again.
  • He was unable to lift himself off the bed and move around, and had to be assisted. It was associated with a decrease in food intake since 9 days
  • He also had short term memory loss since 9 days
  • The primary etiology of the patient's problem

ALOCHOL INTAKE

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

Ans) 1. IVF NS and RL @150ml/hr.

# Mechanism of action:

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

# Indication:

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

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

Thiamine; MOA

# Mechanism of Action: 

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

# Indications and Usage:

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

3. Inj. Lorazepam

# Mechanism of action:

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

# Indication:

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

4. T. Pregabalin 75mg/PO/ BD

# Mechanism of action:

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

# Indication:

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

5. Inj. HAI S.C.-  premeal

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

7. Lactulose 30ml/PO/BD

# Mechanism of action:

Lactulose is used in preventing and treating clinical portal-systemic encephalopathy. Its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia. It has also gained popularity as a potential therapeutic agent for the management of subacute clinical encephalopathy

# Indication:

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

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

# Mechanism of action:

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

# Indication:

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

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

# Mode of Action:

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

 

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

Ans)  Altered sensorium due to alcohol withdrawal syndrome, DECREASE LEVEL OF THIAMINE LEADS TO THE SYMPTOMS

 

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

Ans) Thiamine is a key vitamin in the maintenance of membrane integrity and osmotic gradients across cell membranes and is stored in body tissues predominantly as thiamine diphosphate (TDP). TDP participates in energy production as an essential cofactor for several enzymes in the TCA cycle and pentose phosphate pathways

Thiamine deficiency causes depletion of intracellular TDP, leading to a decreased activity of the TCA cycle and pentose phosphate pathways. Consequently, cellular energy (ATP) depletion and reduction of DNA/RNA and NADPH synthesis ensues, which results in low resistance to oxidative stress. Moreover, there is an accumulation of toxic intermediate metabolic products such as lactate, alanine and glutamate, reduced cellular pH in cells, and disruption of the homeostasis of cellular electrolytes, which results in cytotoxic edema.



 CASE B) Cerebellar Ataxia 

Link to the case:

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

Question 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 symptomatology :

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

# Anatomical localization : right inferior cerebellar hemisphere

# Primary etiology : high cholesterol levels  -> embolization -> infarct -> ataxia


Question 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)

 

MOA

INDICATIONS

EFFICACY

Tab Veratin

Histamine analogue

Vertigo; Tinnitus

 

Inj Zofer

Serotonin inhibitors

Gastric problems

 

Tab Ecosprin

Inhibits formation of thromboxane A2

Presence of blood clot(infarct)

 

Tab Atorvostatin

Inhibits HMG-COA reductase

High cholesterol

 

Tab Clopidogrel

Inhibits ADP mediated glycoprotein activation

-

 

Inj Thiamine

-

Vitamin B1 deficiency

 

Tab MVT

-

Vitamin b12 deficiency

 

BP Monitoring

-

-

 

 

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

Ans) NO. (other way round is possible).

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

 Ans) Yes – hemorrhagic type –liver 


CASE C: Cervical spondylosis and recurrent hypokalemic paralysis.

Link to the case:

Question 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 symptomatology:
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 localization: vertebral discs between C2, C3 and C4 vertebral bodies

# Primary etiology :  Spondylosis : aging
                          Hypokalemia : genetic


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

Ans)  Hypokalemic periodic paralysis – a genetic disorder is a possible reason for recurrence of the hypokalemia.


Question 3:
What are the changes seen in ECG in case of hypokalemia and associated symptoms?
Ans)
  • Flattening and inversion of t-wave. QT interval prolongation and St depression in severe cases.
  • Associated symptoms: weakness, fatigue, muscle cramps, worsening of diabetes, palpitations.

CASE D: Seizures.

Link to the case:

Question 1:

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

Ans) Yes  (patient has most likely suffered ischemic stroke)

+ Seizure is defined as sudden alteration of behavior due to a temporary change in the electrical functioning of the brain.

+ Stroke is defined as damage to the brain from interruption of its blood supply.

# Mechanism :

A stroke - brain is injured

Scar tissue formed in area of injury

Affects the electrical activity in brain

Disrupting the electrical activity

Seizure.

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?

Ans) There is a possibility that over time the infarct grew in size, causing increased pressure over surrounding area, leading to unconsciousness in the latest episode of seizure.


CASE E: Seizures ans altered sensorium.


Link to the case:

Question 1:

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

Ans) Possibly an untreated and thus an unregistered fall leading to head injury a year ago, led to intracranial hemorrhage – causing pressure on brain areas and ataxia.


Question 2:

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

Ans)

  • In the new study, drinking alcohol causes liver damage  - leading to decreased clumping  of clotting cells in the blood.  
  • The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism.
  • Considering the episode of binge drinking approximately 3 hours ago, the excessive amout of metabolized alcohol might have led to IC bleed followed by seizures.


CASE F: Right sided CVA.

Link to the case:

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

Ans) Yes, there may be an association between the two events.
An unidentified injury at that time might have developed over 4 years into a clot now leading to infarct.

Question 2:
What are warning signs of CVA?

Ans) Warning signs of CVA include :
• Sudden onset of weakness or numbness on one side of the body.
 Sudden speech difficulty or confusion.
 Sudden difficulty seeing in one or both eyes.
 Sudden onset of dizziness, trouble walking or loss of balance.
 Sudden, severe headache with no known cause
 

Question 3:
What is the drug rationale in CVA?
Ans)
  • Mannitol The role of mannitol therapy in acute stroke is controversial. 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.
  • Ecosprin-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. The effects of aspirin on prostacyclin are dose related.
  • Atorvastatin belongs to a group of medicines called statins. It's used to lower cholesterol if you've been diagnosed with high blood cholesterol. It's also taken to prevent heart disease, including heart attacks and strokes.
 
Question 4:
 Does alcohol has any role in his attack?

Ans) I would like to highlight 2 points here:
  • Normally, excessive alcohol ( most studies define excessive as more than 2 glasses each day) may lead to liver dysfunction. This causes reduced production of substances that aid in blood clotting, increasing the risk of stroke.
  • On the other hand, over a long period of time, alcohol consumption may lead to increased risk of hypertension wich inturn is a risk for infarct typr of stroke.
Considering he is an occasional drinker and has no history of hypertension, in this case the role of alcohol in stroke seems insignificant.


 
Question 5:
Does his lipid profile has any role for his attack??

Ans) Yes it is does have a role.
Patient’s lipid profile shows low levels of HDL and normal levels of LDL – thus suggesting increased cholesterol levels in the body, associating with increased risk of plaque formation in the vessels.

Increased cholesterol levels
Increased risk of plaque formation
Possible embolization
Infarct.


Note: Cervical Mylopathy – a degenerative condition caused due to pressure on spinal cord. It is characterized by clumsiness in hands and gait imbalance.



Question 1:
What is myelopathy hand ?

Ans) It is a condition associated with Cervical Myelopathy . 

Question 2:
What is finger escape ?

Ans) It is also seen in Cervical Myelopathy. Also known as  

Question 3:
What is Hoffman’s reflex?

Ans)
  • It is a test that doctors use to examine the reflexes of the upper extremities.
  • This test is a quick, equipment-free way to test for the possible existence of spinal cord compression from a lesion on the spinal cord or another underlying nerve condition.
# Procedure:

The Hoffmann's reflex test itself involves loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. A positive response is seen when there is flexion and adduction of the thumb on the same hand.

# Interpretations:
  • A positive Hoffmann’s reflex and finger jerks suggest -  hypertonia, but can occur in healthy individuals, and are not useful signs in isolation. In cerebellar diseases, the reflexes may be pendular, and muscle contraction and relaxation tend to be slow, but these are not sensitive or specific to cerebellar signs
  • Absent Hoffman’s  reflexes are characteristic of acute inflammatory demyelinating polyneuropathy (Guillain–Barré syndrome). This loss of H reflexes occurs early and may be an isolated finding in patients studied within several days after onset of illness

CASE H:.Seizures


Link to the case:


Cerebral venous sinus thrombosis (CVST) occurs when a blood clot forms in the brain’s venous sinuses. This  prevents blood from draining out of the brain. As a result, blood cells may break and leak blood into the brain tissues, forming a hemorrhage.

This chain of events is part of a stroke that can occur in adults and children. It can occur even in newborns and babies in the womb. A stroke can damage the brain and central nervous system. A stroke is serious and requires immediate medical attention.
This condition may also be called cerebral sinovenous thrombosis.
 

Question 1:
What can be  the cause of her condition ? 

Ans) The causes of seizures in this patient can be
•Electrolyte imbalance(hypomagnesimia)
•Iron deficiency anemia(mainly in endemic area of malaria)
•hypogylcemia 
 

Question2:
What are the risk factors for cortical vein thrombosis?

Ans) Also known as superficial cerebral vein infarct, its risk factors in general include :
  • Excessive blood clot formation.
  • Sickle cell anemia.
  • Chronic hemolytic anemia.
  • Beta-thalassemia major.
  • Heart disease — either congenital (you're born with it) or acquired (you develop it)
  • Iron deficiency.
  • Dehydration
 
# In addition, the risk factors for adults include :
  • Pregnancy and the first few weeks after delivery
  • Problems with blood clotting- for example, antiphospholipid syndrome
  • Cancer
  • Collagen vascular diseases like lupus, Wegener’s granulomatosis, and Behcet syndrome
  • Obesity
  • Low blood pressure in the brain (intracranial hypotension)
  • Inflammatory bowel disease like Crohn’s disease or ulcerative colitis
 
Question 3 :
There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously  why?   

Ans) Normally, When the disturbed neuronal signals stops, the person's condition is reversed to normal.
 
 
Question 4:
What drug was used in suspicion of cortical venous sinus thrombosis?

Ans)  Acitrom tablet is an oral anticoagulant medicine that is used for the treatment and prevention of the formation of abnormal blood clots (thrombus) in blood vessels and disease associated with it affect.



3) CARDIOLOGY

A) Link to patient details:

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


Q1) What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?

Ans) The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). A normal EF is usually around 55 to 70 percent, but it can be lessened in some forms of heart failure.

People with heart failure with reduced ejection fraction (HFrEF) have an EF that is 40 to 50 percent or lower. This is also called systolic heart failure. People with heart failure with preserved ejection fraction (HFpEF) do not have much of a change in their ejection fraction. This is often called diastolic heart failure.

HFrEF were often diagnosed earlier in life and right after a heart attack.

HFpEF were diagnosed later in life and first experienced symptoms of heart failure between the ages of 65 and 69. Many of those with HFpEF also shared that they have other health problems that led to their diagnosis. Many of them also live with additional health conditions, including acid reflux (GERD), high blood pressure, kidney disease, and sleep disorders.

HFrEF shared that they feel depressed and/or anxious about their heart failure diagnosis. Risk factors for those in this group include genetics or a family history of heart failure.

HFpEF shared that they are still able to do the things they enjoyed before their heart failure diagnosis.risk factors, including:

  • Sedentary lifestyle
  • High blood pressure
  • Sleep apnea
  • Other heart conditions

HFrEF are more likely to have had surgery, including surgery to implant a pacemaker or other heart rhythm control device.HFrEF shared that they currently use a combination therapy to treat their heart failure.

HFpEF have never had surgery to treat their heart failure or had a device implanted.

HFrEF are men who live in rural areas.

However, most respondents with HFpEF are women who live in urban areas.

 

Q2) Why haven't we done pericardiocenetis in this pateint?       

Ans) Pericardiocentesis is done when the pericardial effusion is not resolving on its own . Here the pericardial fluid which has accumulated was resolving on itw own , at the time of admission it was 2.4mm and when discharged it was 1.9 mm . Therefore we did not do pericardiocentesis in this pt.            

Q3) What are the risk factors for development of heart failure in the patient?

Ans) IN THIS PATIENT:

NON MODIFICABLE:

  • age
  • gender

MODIFIABLE:

  • hypertension
  • smoking
  • type 2 diabetes .
  • kidney disease.

 

Q4)What could be the cause for hypotension in this patient?

Ans) The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension.



B) Link to patient details:


Q1) What are the possible causes for heart failure in this patient?

Ans) 

  • obesity
  • alcohol
  • diabetes
  • hypertension


Q2) what is the reason for anemia in this case?

Ans) Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections.

 

Q3) What is the reason for blebs and non healing ulcer in the legs of this patient?

Ans) 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. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases.

In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.

There are many risk factors that may lead to foot ulcers at the end:

  • Poor quality or fitting of the footwear.
  • Unhygienic appearance of foot.
  • Improper care of the nails of the toe.
  • Heavy intake of alcohols and tobacco.
  • Obesity and Weight-related
  • Complication arising from Diabetes like eye problems, kidney problems and more.
  • Although aging or old age can also be counted among them.

 

Q4) What sequence of stages of diabetes has been noted in this patient?

Ans) 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.



C) Link to patient details:


Q1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?

Ans) the anatomical site is BLOOD VESSELS;

# ETIOLOGY: 

The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.

 The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.

 

Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans) PHARMACOLOGICAL INTERVENTIONS

 1. TAB. Dytor

#Mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.

 2. TAB. Acitrom 

#Mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting

 3. TAB. Cardivas 

#Mechanism: Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.

4. INJ. HAI S/C

#Mechanism: Regulates glucose metabolism

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

5.TAB. Digoxin 

#Mechanism: Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:

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

6. Hypoglycemia symptoms explained

7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.

8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

 

Q3) 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.

 

Q4) What are the risk factors for atherosclerosis in this patient?

Ans) effect of hypertention

They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.

 

Q5) Why was the patient asked to get those APTT, INR tests for review?

Ans) APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.

Here, an INR of 3-4.5 is recommended. Warfarin should be started in conjunction with heparin or low molecular weight heparin when the diagnosis of venous thromboembolism is confirmed, although local protocols may vary in their starting doses and titration schedule




Q1) What is the evolution of symptomatology in the patient in terms of an event timeline and where is the anatomical localization for the problem and what is the  primary etiology of the patients problem ?

Ans) TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently               sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath since half an hour-SOB even at rest
 Anatomical localization : Cardiovascular system

# Etiology:  The patient is both Hypertensive and diabetic , both these conditions can lead to Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)


Q2) 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:
TAB MET XL 25 MG/STAT-contains  Metoprolol as active ingredient

#MOA: METOPROLOL is a cardio-selective beta blocker .
  - Beta blockers work by blocking the effects of the hormone epinephrine  also known as adrenaline.
  - Beta blockers cause your heart to beat    more slowly( negative chronotropic effect) and with less            force( negative inotropic effect). Beta blockers also help open up your veins and arteries to                      improve blood flow.

# Indications: it is used to treat Angina, High blood pressure and to lower the risk of hear attacks .

# EFFICACY STUDIES:
Patients were randomized to one of four treatment arms: Placebo or ER metoprolol (0.2 mg/kg, 1.0 mg/kg, or 2.0 mg/kg). Data were analyzed on 140 intent-to-treat patients.

# RESULTS : 
- Mean baseline BP was 132/78 +/-9 mmHg                                                   
- Following 4 weeks of treatment, changes in sitting BP were:
   Placebo = -1.9/-2.1 mmHg; ER metoprolol 0.2 mg/kg = -5.2/-3.1 mmHg; 1.0 mg/kg = -7.7/-4.9     mmHg; 2.0 mg/kg = -6.3/-7.5 mmHg.
- Compared with placebo, ER metoprolol significantly reduced systolic blood pressure (SBP) at       the 1.0 and 2.0 mg/kg dose (P = .027 and P = .049, respectively), reduced diastolic blood pressure (DBP) at the 2.0 mg/kg dose (P = .017), and showed a statistically significant dose response relationship for the placebo-corrected change in DBP from baseline. There were no serious adverse events or adverse events requiring study drug discontinuation among patients receiving active therapy.

 - Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY  

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

Q3) 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 (eg, dyspnea, arrhythmia, or dizziness or syncope)
           
# CONTRAINDICATIONS:
 - Intolerance for oral anti-platelets 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.

Q4) 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 overt  esting and overtreatment important to current healthcare systems?

Ans) Although PCI is generally a safe procedure, it might cause serious  certain complications like :

A)Bleeding 

B) Blood vessel damage

C) Allergic reaction to the contrast dye use

D) Arrhythmias

E) Need for emergency coronary artery bypass grafting .

Because of all these complications it is better to avoid PCI in patients who do not require it.

⁃ OVER TESTING AND OVER TRAETMENT HAVE BECOME COMMMIN IN TODAY’S MEDICAL PRACTICE.

⁃ Research on overtesting and overtreatment is important as they are more harmful than useful.

Harms to patients

.Performing screening tests in patients with who at low risk for the disease which is being screened.

For example: Breast Cancer Screenings Can Cause More Harm Than Good in Women Who Are at Low Risk. A harmless lump or bump could incorrectly come up as cancer during routine breast screenings. This means that some women undergo surgery, chemotherapy or radiation for cancer that was never there in the first place.

.Overuse of imaging techniques such as X- RAYS AND CT SCANS as a part of routine investigations. 

.Overuse of imaging can lead to a diagnosis of a condition that would have otherwise remained  irrelevant 

- OVERDIAGNOSIS.

-Also the adverse effects due to this are more when compared to the benefits.

-Overdiagnosis through overtesting can psychologically harm the patient.

-Hospitalizations[41] for those with chronic conditions who could be treated as outpatients[ can lead to   economic burden and a feeling of isolation.

-Harms to health care systems

-The use of expensive technologies and machineries are causing burden on health care systems.


E) Link to patient details:




Q1) 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 symptomatology:
Uncontrolled DM2 since 8 years

3 days back Mild chest pain dragging type and retrosternal pain(radiated)

# Anatomical localisation: Inferior wall of heart

# Primary etiology: Diabetes type 2 (uncontrolled)

High blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels

 

Q2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?

Ans) TAB. ASPIRIN 325 mg PO/STAT

# Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.

TAB ATORVAS 80mg PO/STAT

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

TAB CLOPIBB 300mg PO/STAT

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

  

Q3) Did the secondary PTCA do any good to the patient or was it unnecessary?

Ans) Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty.

Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times



F) Link to patient details:


Q1) How did the patient get  relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?

Ans) Because of the  fluid loss occurred to the patient

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

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

 

Q2) What is the rationale of using torsemide in this patient?

Ans) Torsemide used to relieve abdominal distension.

 

Q3) Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?

Ans) IT IS THE TREATMENT FOR UTI 

Rationale- Used for any bacterial infection.

4)GASTROENTEROLOGY:

CASE A: Pancreatitis with pseudocyst 

Link to the case:

Question 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 symptomatology:
5 years ago - Episode of fever and vomiting
6/5/2021 - Pain abdomen and vomiting (since this day)
9/5/2021 - Constipation
                 burning micturition
                 fever

# Anatomical localization: Abdomen

# Primary etiology: Excessive alcohol consumption


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?
Ans) 

 

MOA

INDICATIONS

EFFICACY

Inj.Meropinam

Broad spectrum antibiotic

Prophylaxis (complications of acute pancreatitis)

 

Inj.Metrogyl

Antibiotic

Prophylaxis as above

 

Inj. Amikacin

Antibiotic

Prophylaxis as above

 

IV NS/RL

Fluid/Electrolyte replacement

Dehydration

 

Inj. Octreotide

Somatostatin analogue

Excessive pancreatic secretion

 

Inj.Pantop

PPI

Reduce pancreatic secretions

 

Inj.Thiamine

Vitamin B1 supplement

Encephalopathy prophylactic

 

Inj. Tramadol

Analgesic

Pain

 




CASE B: Acute Pancreatitis: 

Link to the case:

Question 1:
What is causing the patient's dyspnea? How is it related to pancreatitis?
Ans)
  • The cause of dyspnea in this pateint is probably Pancreatitis.
  • A severe casse of pancreatitis usualy resukts in Multiorgan failure - most importantly pulmonary complications, the pathogenesis of which 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.

Going by the reports (high levels of amylase and protein) and the above classification our patient falls in the 2nd stage as we have found PLEURAL EFFUSION on doing chest x-ray.


Question 2:

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

Ans) Some pointers/risk factors are:

  • Age of patient- due to possible insulin resistance
  • Chronic alcohol consumption- initial dip followed by rise dur to prefered digestion of alcohol to glucose.
  • Affected Pancreas in the patient- source of insulin damaged leading to Hyperglycemia

Question 3:
What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
Ans) 
  • Raised LFT values in patient of acute pancreatitis suggests a inflammation of gall bladder caused by gall-stone . 
  • ALT and AST r nonspecific indicators of liver disease. The AST > ALT in case of alcoholic Fatty Liver Disease (in contrast to Non Alcoholic case).

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

  •  IVF: 125 mL/hr - to maintain body fluid levels and prevent dehydration
  •  Inj PAN - as PPI 
  •  Inj ZOFER - to control infalmatory damage
  •  Inj Tramadol - As analgesic
  •  Tab Dolo - Analgesic
  •  GRBS charting 6th hourly 
  •  BP charting 8th hourly

CASE C: Liver Abscess 

Link to the case:


Question 1:
What is the most probable diagnosis in this patient?

Ans) According to the reports given, the rise in AST and ALT suggest a Liver Abscess.

Other differentials not possible because:
  • Organised intraperitoneal hematoma - no history of trauma of any sort
  • Right kidney RPD - there is no history/ complaint of back pain
  • Subdiaphragmatic fluid collection - radiological evidence deny this possibility.

Question 2:
What was the cause of her death?

Ans) Possible cause of death in this case is 
  • Decreased Diastolic BP - due to septic shock
  • Right lobe atelectasis 

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

Ans) Normally, The efferent arterioles of an organ are seen to be constricted.
But with NSAID abuse, even the afferent vessels are constricted leading to increased blood pressure levels .
...

5) Nephrology and Urology

A) Link to patient details:


Q1) What could be the cause for his SOB?

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

Q2) Reason for Intermittent Episodes of drowsiness

Ans) Hyponatremia was the cause for his drowsiness

 

Q3) Why did he complaint of fleshy mass like passage in urine ?

Ans) plenty of pus cells in his urine passage  appeared as fleshy mass like passage to him

 

Q4) What are the complicat ions of TURP that he may have had?

Ans)

  •  Difficulty micturition 
  • Electrolyte imbalances
  • Infection



B) Link to patient details:


Q1) Why is the child excessively hyperactive without much of social etiquettes ?

Ans) The exact pathophysiology of Attention Deficit Hyperactivity Disorder (ADHD) is not clear. With this said, several mechanisms have been proposed as factors associated with the condition. These include abnormalities in the functioning of neurotransmitters, brain structure and cognitive function.

Due to the efficacy of medications such as psychostimulants and noradrenergic tricyclics in the treatment of ADHD, neurotransmitters such as dopamine and noradrenaline have been suggested as key players in the pathophysiology of ADHD.

Depressed dopamine activity has been associated with the condition,

 

Q2) Why doesn't the child have the excessive urge of urination at night time ?

Ans) the child doesn’t have the excessive urge of urination at night time because ADHD is a physcosomatic disorder .


6)INFECTIOUS DISEASES:

CASE A: Patient with fever, dysphagia and cough  

Link to the case:

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

Ans) Positive findings of tracheo-esophageal fistula in above case are:
  • History of difficulty in swallowing
  • History of cough on food intake
  • History of retroviral disease
# Associated physical findings are:
  • Laryngeal crepitus
  • Endoscopy showing proliferative growth in mid esophagus
  • Fistulous communication between - left main bronchus and mid thorasic esophagus
  • Barium swallow showing abnormal contrast
Question 2:
What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it? 

Ans) 
  • Chances are high
  • Risk factors include:
  1. Fever since 2 months
  2. Lymph node enlargement in mediastinum
  3. TB diagnosis after ART
  4. CRP +

7)INFECTIOUS DISEASE AND HEPATOLOGY:


CASE A: Liver abscess  

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 ?

Ans) Yes, i do believe that locally made alcohol caused Liver Abscess in this patient.

# The predisposing factors are :
  • Diabetes.
  • Liver cirrhosis.
  • Immunocompromised state.
  • Male sex.
  • Advanced age.
  • Proton-pump inhibitor use
# The causative factor in this case must have been : Chronic alcoholism


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

Ans) # Etiology :
  • Origin may be : pyogenic ; ameobic ; hydatid cyst; 
  • They are mostly acquired from blood stream 
# Pathology:

  • Most common : Bowel content leakage OR peritonitis - Where bacteria travel via portal vessels.
  • In this case bacteria in locally prepared alcohol played a major role.  
# Factors involved in association between alcohol and abscess:   
  • poor nutritional status - due to alcohol consumption
  • Presence of infective organisms in locally made alcohol
  • Immunity of patient
  • Liver damage
Question 3:
Is liver abscess more common in right lobe ?

Ans) Yes, single lesions of liver abscess are more common in right lobe.
The reason being , comparatively more blood supply the lobe receives from superior mesentric vein.
   

Question 4:   
What are the indications for ultrasound guided aspiration of liver abscess ?       

Ans) Some indications include:
  • Abscess is large - more than 5cm  - chances of rupture Are high.
  • Location is left lobe - more chances of peritoneal leak
  • Not responding to drugs for more than 7 days

CASE B: Liver abscess  

Link to the case:

Question 1:
Cause of liver abcess in this patient ?

Ans) # Etiology:
  • Pyogenic liver abscess – polymicrobial 
  1. Staphylococcus 
  2. E .coli
  3. Klebsiella
  4. Streptococcus
  • Amoebic liver abscess – most commonly caused by Entamoeba hisolytica 
# In this patient, occasional toddy consumption acted as source of pathogens.

Question 2:
How do you approach this patient ?

Ans) Treatment of liver abscess  includes : 
  • Empirical antibiotics : cover both bacterial and amoebic causes -
  1. For bacterial cause : penicillin +cephalosporin is given ( zostum 1.5 gm i.v. BD injection) 
  2. 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 

Question 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.


Question 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:

 CASE AAltered sensorium - mucormycosis case  

Link to the case:

Question 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 symptomatology : 
18 -04-2021 - Fever with chills and rigors          
28-04-2021 - Facial puffiness                               
28-04-2021 - Periorbital oedema                         
28-04-2021 - Generalised weakness.  ( Right upper & lower limb )               
4-05-2021 - Altered sensorium                               
4-05-2021 - Serous discharge from left eye        
4-05-2021 - Oral and nasal cavity involvement    
              
#   Anatomical localisation:
Eye 
Nasal & sinus mucosa 
Oral cavity 
Brain 

#  Primary etiology :  Rhizopus : fungus 


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?

Ans) Drugs that can be used to treat mucormcosis 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 : 

  • Stabilise the patient 
  • Treat the diabetic ketoacidosis 
  • Treatment with antifungal preferably Liposomal AmpB 


 Question – 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
 

Comments

Popular posts from this blog

A 46 YEAR OLD FEMALE WITH AKI WITH UTI AND B/L HIP OSTEOARTHRITIS