ONLINE BLENDED ASSESSMENT FOR THE MONTH OF MAY 2021
May 2021
M.Abhignya ,8thsem ,Roll.No. 71
I have been given the following cases to solve in an attmept 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 coem up with a treatment plan.
This is the link of the questions asked regarding the cases:
Below are my answers to the Medicine Assignment based on my comprehension of the cases.
1) Pulmonology
A) Link to patient details:
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?
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 diabetis - 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 of problem - lungs
* Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage
as it causes several lung diseases like asthma, ch.bronchitis....due the smoke released from it
2Q)what r the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patien
*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
~ oxygen inhalation to maintain spo2
Efficacy over placebo
~Bipap:non invasive method
#MOA
:Assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation
Efficacy over placebo
3. Cause for current acute excerbation -
it could be due any infection or right heart failure
4.could the ATT affected her symptoms if so how?
*Yes ATT affected her symptoms
* Isoniazid and rifampcin ---.>nephrotoxic -- > raised RFT was seen in this pt sugest the effect of ATT
5.What could be the causes for her electrolyte imbalance?
*Renal function disturbances due to ATT therapy side effects mainly Hyopnatremia and hypochloremia
*here is the link showing electrolyte imbalances as side effects of using ATT
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3614323/
2) Neurology
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 localization for the problem and what is the primary etiology of the patient's problem?
symptomatology
A 40year old male presented with chief complaints of irrelevant talking and decreased food intake since 9days.
He was conscious but oriented to time, person and place only from time to time.
He also had short term memory loss since 9days, where he couldn't recognize family members from time to time
Previously, he had 2-3episodes of seizures, one being one year ago and the most recent being 4months ago. The most recent one, he had developed seizures following cessation of alcohol for 24hours.
* anatomical location ....effects the brain mainly the THALAMUS AND HYPOTHALAMUS
*the primary etiology is chronic alcoholism
*: The patient is a chronic alcoholic, he drinks about 3-4quarters/day.he had developed seizures following the cessation of alcohol for 24hours it is due to the following reason:-alcohol affects the way in which nerve cells communicate. receptors are specialized proteins on the surface of nerve cells that receive chemical signals from one another. With long-term alcohol consumption, receptors affected by alcohol undergo adaptive changes in an attempt to maintain normal function.
Two important brain communication systems affected by alcohol involve the neurotransmitters:gamma-aminobutyric acid and glutamate.
The GABA system:
*GABA is an inhibitory neurotransmitter that helps to regulate brain function by rendering nerve cells less sensitive to further signaling. single doses of alcohol facilitate the inhibitory function of the GABA receptor, contributing to alcohol intoxicating effects.
* During withdrawal, brain GABA levels fall below normal and GABA activity declines.
The combination of reduced brain GABA levels and GABAa receptor sensitivity may be contributed an adaptation to the presence of alcohol.
* In the absence of alcohol, the resulting decrease in inhibitory function may contribute to Symptoms of nervous system hyperactivity associated with both acute and protracted AW.
The glutamate system
*The major excitatory neurotransmitter in the brain is glutamate, which communicates with three major subtypes of glutamate receptors. Among these, the N-methyl-D-aspartate (NMDA) receptor plays a role in memory, learning, and the generation of seizures.
*Alcohol inhibits the excitatory function of the NMDA receptor in laboratory studies at concentrations associated with mild to moderate alcohol intoxication in humans.
*As with the increased inhibitory function of the GABAA receptor, the decreased excitatory function of the NMDA receptor is consistent with alcohol’s general sedative effect.
* Long-term alcohol administration produces an adaptive increase in the function of NMDA receptors. *Acute AW activates glutamate systems. In turn, AW seizures are associated with increased NMDA receptor function. Persistent alterations in NMDA receptor function may potentiate the neurotoxic and seizure-inducing effects of increased glutamate release during withdrawal.
*The symptom: irrelevant talking, decreased food intake, tremors, sleep disturbance is due to the following reason: chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver and other nutritional deficiencies.
THE PATHOPHYSIOLOGY:
*Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism.
*This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation.
*Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. *Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate.
*This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease. The increase in levels of urea, creatinine, uric acid leads to uraemic encephalopathy. which causes asterixis.
the deficiency of thiamine and increase in levels of toxins in the body due to renal disease is the primary etiology of the patient's problem.
2)what are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
: i) Thiamine helps the body cells change carbohydrates into energy. It has been used
as a supplement to cope with thiamine deficiency
ii)Lorazepam binds to benzodiazepine receptors on the postsynaptic GABA-A ligand-gated chloride channel neuron at several sites within the central nervous system.it enhances the inhibitory effects of GABA, which increases the conductance of chloride ions into the cell
iii)pregabalin subtly reduces the synaptic release of several neurotransmitters, apparently by binding to alpha2-delta subunits, and possibly accounting for its actions invivo to reduce neuronal excitability and seizures.
iv)Lactulose is used in preventing and treating clinical portal-systemic encephalopathy .its chief mechanism of action is by decreasing the intestinal production and absorption of ammonia.
v)Potchlor liquid is used to treat low levels of potassium in the body.
3)why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?
Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.
4)what is the reason for giving thiamine in this patient?
*chronic alcohol consumption causes thiamine deficiency due to impaired absorption of thiamine from the intestine,Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism.
*This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles.
*Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine, and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death.
5)what is the probable cause for kidney injury in this patient?
*The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure.
*High blood pressure is a common cause of kidney disease.
6)what is the probable cause for the normocytic anaemia?
alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .
7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
yes ...,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic the immune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
B) Link to patient details:
Questions-
1) What is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patients problem?
Symptomotology
**7 days back- Patient gave a history of giddiness that started around 7 in the morning; subsided upon taking rest; associated with one episode of vomiting
⬇⬇
*4 days back- Patient consumed alcohol; He developed giddiness that was sudden onset, continuous and gradually progressive. It increased on standing and while walking.
*H/O postural instability- falls while walking
*Associated with bilateral hearing loss, aural fullness, presence of tinnitus
*Associated vomiting- 2-3 episodes per day, non projectile, non bilious without food particles
*Present day of admission- Slurring of speech, deviation of mouth that got resolved the same day
Anatomical location- There is a presence of an infarct in the inferior cerebellar hemisphere of the brain.
Etiology-
* Ataxia is the lack of muscle control or co-ordination of voluntary movements, such as walking or picking up objects. This is usually a result of damage to the cerebellum (part of the brain that controls muscle co-ordination)
*Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. *Barbituates, stroke, tumours, cerebral palsy, brain degeneration etc.
*In this case, the patient has hypertension for which he has been prescribed medication that he has not taken. Stroke due to an infarct can be caused by blockade or bleeding in the brain due to which blood supply to the brain is decreased, depriving it of essential oxygen and nutrients. This process could’ve caused the infarct formation in the cerebellar region of the brain, thus causing cerebellar ataxia.
2) What are the mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient
.
A) Tab Vertin 8mg
This is betahistine, which is an anti- vertigo medication
MOA- It is a weak agonist on H1 receptors located on blood vessels of the inner ear. This leads to local vasodilation and increased vessel permeability. This can reverse the underlying problem.
Indications- Prescribed for balance disorders. In this case it is used due to patients history of giddiness and balance issues.
over placebo
B) Tab Zofer 4mg-
This is ondanseteron- It is an anti emetic
MOA- It is a 5H3 receptor antagonist on vagal afferents in the gut and they block receptors even in the CTZ and solitary tract nucleus.
Indications-
Used to control the episodes of vomiting and nausea in this patient.
over placebo
C) Tab Ecosprin 75mg-
This is aspirin. It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
over placebo
D) Tab Atorvostatin 40mg- This is a statin
MOA-
It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications-
Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
over placebo
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
over placebo
F) Thiamine- It is vitamin B1
It is naturally found in many foods in the human diet
. In this case, the patient consumes excess alcohol- so he may get thiamine deficiency due to poor nutrition and lack of essential vitamins due to impaired ability of the body to absorb these vitamins.
Indications
- Given to this patient mainly to prevent Wernickes encephalopathy- that can lead to confusion, ataxia and opthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patients history of denovo hypertension contribute to his current condition?
* A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum
* High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.
*Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic stroke?
* Meta analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed in to the formation of two types- ischaemic and haemorrhagic stroke.
*Ischaemic stroke- this is more common. This Is caused by a blood clot blocking the flow of blood and preventing oxygen from reaching the brain
*Haemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral haemorrhage
*According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral haemorrhage and a 1.8 increased chance of subaracnoid haemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increase the risk of heart stroke.
*Many studies show that with mild and moderate drinking . the risk of ischaemic stroke decreases due to decreased level of fibrinogen which helps in the formation of blood clots. However, heavy alcohol intake is associated with impaired fibrinolysis, increased platelet activation and increased BP and heart rate.
*So In this case, his history of alcoholism, coupled with his hypertension definitely could be a causative factor of his current condition.
C) Link to patient details:
Questions:
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?
*Evolution of symptoms
:patient was normal 8 months back then developed b/l pedal edema which gradually progressed.
Aggerevated in sitting and standing position, relived on taking medication
*Palpitations :since 5days, sudden in onset which is more during night
Aggerevated by lifting heavy weights, speaking continuously
*Dyspnoea during palpitations (NYHA-3) since 5 days
*pain:since 6days, radiating along left upper limb, more during palpitations and relived on medication.
Chest pain associated with chest heaviness since 5 days
Anatomical localisation : BRAIN
Etiological agent :
*By localization, electrolyte imbalance (hypokalemia) causing the her manifestations like palpitations, chest heaviness, generalised body weak ness
*radiating pain along her left upper limb due to cervical spondylosis
2Q) What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
A) Reason:
recurrent hypokalemic periodic paralysis
Current risk factor:due to use of diuretics
Other risk factors
A) Abnormal loses:
Medications-diuretics, laxatives, enema, corticosteriods
Real causes- osmotic diuresis, mineralo corticoid excess, renal tubular acidosis, hypomagnesenemia
B) trance cellular shift :
alkalosis, thyrotoxicosis, delirium tremans, head injury, Myocardial, ischemia, recurrent hypokalemic periodic paralysis
C) Inadequate intake:
anorexia, dementia, stareation, total parental nutrition
D) psuedohypokalemia:
delayed sample analysis, significant leukocytosis
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
A) changes seen in ECG :
Earliest change :
* ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves
*In Severe cases :ventricular fibrillation, rarely AV block
Symptoms of hypokalemia :
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
D) Link to patient details:
QUESTIONS:
1.Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
What is a seizure?
*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 cons
Seizures after stroke
*You’re more likely to have a seizure if you had a haemorrhagic stroke (bleed on the brain). Seizures can also be more likely if you had a severe stroke, or a stroke in the cerebral cortex, the large outer layer of the brain where vital functions like movement, thinking, vision and emotion take place.
Some people will have repeated seizures, and be diagnosed with epilepsy. The chances of this happening may depend on where the stroke happens in the brain and the size of the stroke.
*A seizure can affect you in many different ways such as changes to vision, smell and taste, loss of consciousness and jerking movements.
seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypoperfusion, and hyperperfusion injury
Seizures after haemorrhagic strokes are thought to be attributable to irritation due to (hemosideri. Deposits)caused by products of blood metabolism
Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
Pathogenesis
There are several causes for early onset seizures after ischaemic strokes. An increase in intracellular Ca2+ and Na+ with a resultant lower threshold for depolarisation, glutamate excitotoxicity, hypoxia, metabolic dysfunction, global hypo perfusion and hyper perfusion injury ,(particularly after carotid end arterectomy) have all been postulated as putative neurofunctional aetiologies. Seizures after haemorrhagic strokes are thought to be attributable to irritation caused by products of blood metabolism. The exact pathophysiology is unclear, but an associated ischaemic area secondary to haemorrhage is thought to play a part. Late onset seizures are associated with the persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause. Haemosiderin deposits are thought to cause irritability after a haemorrhagic stroke.14 In childhood, post‐stroke seizures can occur as part of perinatal birth trauma.
2. In the previous episodes of seizures, patient didn't loose his consciousness but in the recent episode he lost his consciousness what might be the reason?
Initially the patient might have had Simple partial seizures (no loss of consciousness) and might have progressed to Generalised Tonic Clonic seizures (loss of consciousness)
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) Link to patient details:
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
The patient has minor unattended head injuries in the past 1 yr. Accoding to the CT scan, the patient has cerebral haemorrhage in the frontal lobe causing probably for the occurrence of Frontal love ataxia
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
The patient has minor unattended head injuries. During the course of time the minor hemorrhages if present should have been cured on their own. But the patient is a chronic alcholic. This might have hindered the process of healing or might have stopped the healing rendering it to grow further more into 13 mm sized hemorrhages occupying Frontal Parietal and Temporal lobes
F) Link to patient details:
Questions
1.Does the patient's history of road traffic accident have any role in his present condition?
*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?
3.What is the drug rationale in CVA?
Mannitol-
*Because of its osmotic effect, mannitol is assumed to decrease cerebral edema.
*Mannitol might improve cerebral perfusion by decreasing viscosity, and as a free-radical scavenger, it might act as a neuroprotectant.
Ecospirin
For the prevention of heart attack, stroke, heart conditions such as stable or unstable angina (chest pain) due to a blood clot.
Atrovas-Atorva 40 Tablet
*belongs to a group of medicines called statins. It is used to lower cholesterol and to reduce the risk of heart diseases.
* Cholesterol is a fatty substance that builds up in your blood vessels and causes narrowing, which may lead to a heart attack or stroke.
Rt feed RT feed
is a nursing procedure to provide nutrition to those people who are either unable to obtain nutrition by mouth or are not in a state to swallow the food safely.
4. Does alcohol has any role in his attack?
When the patient met with an accident there might be cranial damage which was unnoticed.
If so his occasional drinking may or may not have hindered the process of the minor hemorrhages getting healed and might have caused this condition
But since the patient is not a chronic alcoholic and so Alcohol might not have played any role.
Therefore it cannot be evaluated without further details
5.Does his lipid profile has any role for his attack??
*The inverse relationship between serum HDL-C and stroke risk .
*When taken together it seems clear that higher baseline levels of serum HDL-C lower the risk of subsequent ischemic stroke.
G) Link to patient details:
__*Questions*_
1)What is myelopathy hand ?
There is loss of power of adduction and extension of the ulnar two or three fingers and an inability to grip and release rapidly with these fingers. These changes have been termed "myelopathy hand" and appear to be due to pyramidal tract involvement.
2)What is finger escape ?
Wartenberg's sign is a neurological sign consisting of involuntary abduction of the fifth (little) finger, caused by unopposed action of the extensor digiti minimi. ... This finding of weak finger adduction in cervical myelopathy is also called the "finger escape sign".
3)What is Hoffman’s reflex?
The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down. The reflexive pathway causes the thumb to flex and adduct quickly.
https://youtu.be/jW7H76sO_Lo
H) Link to patient details:
Possible questions:
1) What can be the cause of her condition ?
According to MRI cortical vein thrombosis might be the cause of her seizures.
2) What are the risk factors for cortical vein thrombosis?
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
*Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis
Anticoagulants are used for the prevention of harmful blood clots
.
Clexane ( enoxaparin) low molecular weight heparin binds and potentiates antithrombin three a serine protease Inhibitor to form complex and irreversibly inactivates factor xa.
3) Cardiology
A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
* preserved ejection fraction - diastolic heart failure(Muscle contracts but ventricles donot relax)
*Reduced ejection fraction - systolic heart failure(Muscle doesnot contract effectively)
2.Why haven't we done pericardiocenetis in this pateint?
* In this pt. the pericardial effusion was self limiting ,so there is no need to do pericardiocentesis and aslo
* : The patient diagnosed as heart failure and suspected to be
*POST MI so it might be CONTRAINDICATION OF PERICARDIOCENTESIS due to risk of scarring and injury.
3.What are the risk factors for development of heart failure in the patient?
* Chronic alcoholism --leads to risk of AFIB, heartattack,,,,,,,,,,,,,,,,, CHF
*Smoking
*Hypertension,
*T2DM
*1ST degree AV block can be associated with severe bradycardia and hemodynamic instability. It has a greater risk of progressing to third-degree (complete) heart block or asystole.
*wosening of pericardial effusion leaing to cardiac tamponade
4.What could be the cause for hypotension in this patient?
*Due to thickening of pericardium it led to restriction of movement of heart
*Hypotension may be due to
DIASTOLIC DYSFUNCTION and LV COLLAPSE.
B) Link to patient details:
Questions:
1.What are the possible causes for heart failure in this patient
causes-
* patient has stage 4 CKD- has pedal edema ( increased preload)
* Hypertension since 19 yrs
2.what is the reason for anaemia in this case?
Cause-
* chronic kidney disease leads to kidney damage →decrease erythropoietin production from kidney →erythropoietin is low→RBC count drops →ANEMIA develops.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
Type 2 diabetes is reason for non healing ulcer and bleb formation
4. What sequence of stages of diabetes has been noted in this patient?
*For 26 yrs: diabetes (controlled by tablets)
↓
* Since 4yrs: on insulin
↓
*Stage 4 DBCD with vascular malformations with retinopathy
C) 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 localization for the problem and what is the primary etiology of the patient's problem?
Symptomatology
Facial puffiness ( since 2 to 3 yrs)
Sob grade 2( 1yr ago)
Sob grade 2( 2days back again)
Sob grade 4
Decreased urine output ( since 2 days)
Anuria (since morning)
*the anatomical site is BLOOD VESSELS;
* ETIOLOGY:
*The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis.
*The most likely cause of arterial thrombosis is artery damage due to atherosclerosis. Atherosclerosis occurs when a person has a buildup of plaque on the walls of their arteries. The arteries then begin to narrow and harden, which increases a person's risk of developing arterial thrombosis.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans: PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor
mechanism:
Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism:
Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
Efficacy over placebo
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-blocker
over placebo
4. INJ. HAI S/C
MECHANISM:
Regulates glucose metabolism
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.
over placebo
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR
are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Pathophysiology of CARDIORENAL SYNDROME
: *cardiorenal syndrome type 4 is seen in this patient.
4) What are the risk factors for atherosclerosis in this patient?
effect of hypertention
They can also impair blood vessels' ability to relax and may stimulate the growth of smooth muscle cells inside arteries. All these changes can contribute to the artery-clogging process known as atherosclerosis.
5) Why was the patient asked to get those APTT, INR tests for review?
*: 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.
D) 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 localization for the problem and what is the primary etiology of the patient's problem?
*Heart burn like episodes ( since 1 yr)
* Tb ( 7 months ago)
* SOB ( half n hr before coming to hospital)
##ANATOMICAL LOCALIZATION- coronary artery
## primary etiology- plaque formation or clot formation , HTN.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
* MOA:
relaxes Bv → decreases load on heart → decreases BP
* INDICATIONS-
over placebo
3) What are the indications and contraindications for PCI?
*percutaneous coronary intervention( PCI)
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
*PCI cause several complications like :
-Severe bleeding
-blood vessel damage
- allergic reactions to the used contrast dye
-arrythmias
TO Avoid these complications we dont do the pci in the patient who doesnot need it.
* Research on overtesting and over treatment is important to current health system:
It increase the economic burden on the health care system due to excess use of machinaries for investigations .
E) link given:
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
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?
*chest pain - since 3 days
* giddiness and profuse sweating - morning after admission
# ANATOMICAL LOCALIZATION- blood vesselsin inferior wall of heart ( ventricle)
# primary etiology - atherosclerosis accelerated by Hypertension and Diabestes
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
MOA:
it is a COX inhibitor → which inhibits prostaglandin formation → prevents inflammation ,swelling, pain
* INDICATIONS-
• Fever
• Relieve mild to moderate pain such as tooth ache ,muscle ache ,common cold
efficacy over placebo
ATORVAS-
*MOA
: It is a HMG Co A reductase inhibitor
It inhibits conversion of HMG Co A ⟶ mevalonic acid .
* INDICATIONS-
• High cholestrol
• lower the risk of heart attack , stroke, any heart complications
• coronary heart disease
over placebo
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Yes ,it does good to the patient
F) link given:
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
*Because of the fluid loss occured to the patient
*There is
*Decreased preload → SOB occured due to decreased cardiac output
*IV fluids administered → there is increase in preload → SOB decreased due to better cardiac output
2. What is the rationale of using torsemide in this patient?
Torsemide is used due to abdominal distension
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Treatment for UTI
Rationale - used for any bacterial infection .
4) Gastroenterology (& Pulmonology)
A) Link to patient details:
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?
Evolution of symptomatology
-1st episode of pain abdomen and vomitings 5 years back
Stopped taking alcohol for 3 years
1 year back 5 to 6 episodes of pain abdomen and vomitings after starting to drink alcohol again
20 days back increased consumption of toddy intake
Since 1 week pain abdomen and vomiting
Since 4 days fever constipation and burning micturition
Anatomical localisation: Pancreas and left lung
Etiology- Alcohol
*Alcohol and its metabolites produce changes in the acinar cells, which may promote premature intracellular digestive enzyme activation thereby predisposing the gland to autodigestive injury. Pancreatic stellate cells (PSCs) are activated directly by alcohol and its metabolites and also by cytokines and growth factors released during alcohol-induced pancreatic necroinflammation. Activated PSCs are the key cells responsible for producing the fibrosis of alcoholic chronic pancreatitis
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?
ii) efficacy of drugs
1) INJ. MEROPENAM ; TID for 7 days
* Meropenem ( broad spectrum Carbepenem ) an antibiotic.
2) INJ. METROGYL 500 mg IV TID for 5 days
* inj. Metrogyl has METRONIDAZOLE
( Nitroimidazole drug ) an antibiotic
3) INJ AMIKACIN 500 mg IV BD for 5days
* It is an Aminoglycoside antibiotic
## Here all three of these (Inj. Meropenem, Inj. Metrogyl, Inj. Amikacin ) are used as antibiotics to control infection and ; to prevent septic complications of acute pancreatitis.
4) TPN ( Total Parenteral Nutrition )
* Method of feeding that by passes gastrointestinal tract
* Fluids are given to vein , it provides most of the nutrients body needs.
* TPN has proteins, carbohydrates, fats, vitamins, minerals.
5) IV NS / RL at the rate 12l ml per hour
* Given for fluid replacement ie., treat dehydration
6) ING. OCTREOTIDE 100 mg SC , BD
* It is a Somatostatin long acting analogue.
* It is used here to decrease exocrine secretion of pancreas and it also has anti- inflammatory & cytoprotective effects.
7) ING. PANTOP 40 mg IV , OD
* Inj. Pantop has PANTOPRAZOLE ( Proton Pump Inhibitor) used for its anti pancreatic secretory effect.
8) ING. THIAMINE 100 mg in 100 ml NS IV , TID
* It is B1 supplement.
* It is given here because; due to long fasting & TPN usage , body may develop B1 deficiency
* Wernicke encephalopathy secondary to B1 deficiency may be caused... so a prophylactic B1 supplemention is necessary.
9) ING. TRAMADOL in 100 ml NS IV , OD
* It is an opioid analgesic, given to releive pain
* Non pharmacological interventions : drains ( malecot & icd )
* Even i as a treating physician will follow the same approach
And I would like to follow up patient with- CYSTOGASTROSTOMY & MRCP
B) Link to patient details:
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
*pleural effusion is cause for patients dyspnea.
*pleural effusion may occur due to pancreaticopleural fistulae secondary to leak and disruption of pancreatic duct .
2) Name possible reasons why the patient has developed a state of hyperglycemia.
* Hyperglycemia is developed due to abnormalities in insulin secretion , increase in counter regulatory hormone release ,decreased utilization of glucose by peripheral tissue.
Exocrine pancreatic dysfunction impairs the endocrine pancreas.
*Acute pancreatitis is associated with damage to both the endocrine and exocrine pancreas. Glucose intolerance seen with this disease appears to be the result of hyperglucagonemia and relative hypoinsulinemia.
*Although the healing process at 3 wk is associated with return of plasma glucose and glucagon concentrations to normal, the impaired second phase insulin secretion persists.
https://diabetes.diabetesjournals.org/content/29/1/22
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
*
*Elevated liver enzymes in the setting of acute pancreatitis point toward choledocholithiasis as the cause, with an alanine aminotransferase greater than three times the upper limit of normal having a positive predictive value of 95% for gallstone pancreatitis in the nonalcoholic patient.
*Serum alanine aminotransferases (ALT) are released from liver tissue into the circulation in proportion to the degree of hepatocellular damage,33 and their level is thought to be one of the most sensitive markers of liver injury and liver disease progressi
4) What is the line of treatment in this patient?
* iv fluids and colloids to maintain normal intravascular volume.
*Nil orally
*Analgesics for pain relief
*Nasogastric suction -to decrease gastrin release from stomach
* Monitor
-BP, pulse,blood sugars ,serum amylase, serum lipase ,urine output.
* laparotomy and debridement of hemorrhagic pancreatic tissue.
* antibiotic therapy like ciprofloxacin , ofloxacin, imipenem
C) Link to patient details:
Possible Questions :-
1) What is the most probable diagnosis in this patient?
àDifferential Diagnosis:
· Ruptured Liver Abscess.
· Organized collection secondary to Hollow viscous Perforation.
· Organized Intraperitoneal Hematoma.
· Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
· Grade 3 RPD of right Kidney
àThe most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
2) What was the cause of her death?
àAfter leaving the hospital, the patient went to Hyderabad and underwent an emergency laparotomy surgery. The patient passed away the next day. Cause of her death can be due to complications of laparotomy surgery such as, hemorrhage (bleeding), infection, or damage to internal organs.
3) Does her NSAID abuse have something to do with her condition? How?
àNSAID-induced renal dysfunction has a wide spectrum of negative effects, including decreased glomerular perfusion, decreased glomerular filtration rate, and acute renal failure. Chronic NSAIDs use has also been related to hepatotoxicity. While the major adverse effects of NSAIDs such as gastrointestinal mucosa injury are well known, NSAIDs have also been associated with hepatic side effects ranging from asymptomatic elevations in serum aminotransferase levels and hepatitis with jaundice to fulminant liver failure and death.
5) Nephrology (and Urology)
A) Link to patient details:
1. What could be the reason for his SOB ?
* His is due to acidosis which was caused by using diuretics.
Diuretics help patients to reduce excess fluids that can cause shortness of breath, swollen legs, coughing and weight gain
2. Why does he have intermittent episodes of drowsiness ?
*Hyponatremia was the cause for intermittent episodes of drowsiness.
3. Why did he complaint of fleshy mass like passage in his urine?
*Plenty of pus cells in his urine passage appeared as fleshy mass like passage ,there could be parenchyamal damage.
4. What are the complications of TURP that he may have had?
*Difficulty in micturition
*infection
*Electrolyte imbalances
B) Link to patient details:
Questions
1.Why is the child excessively hyperactive without much of social etiquettes ?
*there could be some Psychological problem underlying in the child like
ADHD or Generalised anxiety disorder
2. Why doesn't the child have the excessive urge of urination at night time ?
* The history and examination suggest that there is no underlying urinary tract pathology for frequent urination(in which frequent urination and bedwetting are commom) in this chiild,,so it could be psychological or idioathic..
3. How would you want to manage the patient to relieve him of his symptoms
*Because all his urine reports and everything came fine..
*And also he doesn't have the complaint at night time
*So it was suspected to be a psychological cause
- Give your child small, fun chores to do so that they can focus on a task.
- Do one of their favorite activities when they feel like they need to urinate a lot, such as reading a book, watching a TV show, or playing a video game.
- Avoid keeping track of how many times your child urinates and telling them about it. Increasing your child’s awareness of how much they urinate can make them feel more anxious and make them urinate more.
6) Infectious Disease (HI virus, Mycobacteria,
Gastroenterology, Pulmonology)
A) Link to patient details:
Questions:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
*Clinical history:
*Cough on taking foods and liquids which was initially non productive then associated with sputum which is white in colour and non foul smelling.
*Difficult in swallowing since 2 months with solids and liquids. Patient is on RT feeding.
*History of weight loss and SOB
*One episode of vomiting
*Fever episodes
Physical finding:
*Thinly built and malnourished
*Respiratory system examination: Wheeze present in bilateral mammary areas.
*Neck examination: laryngeal crepitus- positive
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
* chances of IRIS are less
IRIS:
*The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression.
* IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
*Aggressive efforts should be made to detect asymptomatic mycobacterial or cryptococcal disease prior to the initiation of ART, especially in areas endemic for these pathogens and with CD4 T-cell counts less than 100 cells/uL.
*Two prospective randomized studies are evaluating prednisone and meloxicam for the prevention of paradoxical TB IRIS.
7) Infectious disease and Hepatology:
Link to patient details:
1Q)do u think drinking locally made alcohol cause liver abscess in this patient due to predisposing factors present in it ? What could be the cause in this patient?
* yes, it could be due to intake of contaminated toddyle/day)
* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
## Hence the consumption of locally made alcohol ( toddy ) is the most likely cause of Liver abcess in this patient.
2Q)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - bott
*- according to some studies, alcoholism mainly consuming locally prepared alcohol plays a major role as a predisposing factor for the formation of liver abscesses that is both amoebic as well as pyogenic liver abscess because of the adverse effects of alcohol over the Liver.
* It is also proven that Alcoholism is never an etiological factor for the formation of liver abscess.
3Q)is liver abscess is more common in right lobe?
yes right lobe is involved due to its moreblood supply
left lobe receives blood from --
-inf. mesentric
-spleenic veind
right lobe receives from
-sup mesentric
-portal veins
streaming effect in portal circulation is causative for right lobe abscess
4Q) what r the indications for usg guided aspiration of liver abscess
- Indications for USG guided aspiration of liver abscess
1. Large abscess more than 6cms
2. Left lobe abscess
3.Caudate lobe abscess
4. Abscess which is not responding to drugs
B) Link to patient details:
QUESTIONS:
1) Cause of liver abcess in this patient
the cause of liver abcess is :
* Amoebic liver abcess (ALA )
seen commonly in the tropics is predominantly confined to adult males, especially those who consume locally brewed alcohol, although intestinal amoebiasis occurs in all age groups and in both genders.
* It has been argued that socioeconomic factors and poor sanitary conditions are the primary culprits that casually link alcohol to ALA.
* However , there has emerged an abundance of data that implicates alcohol in a more causal role in facilitating the extraintestinal invasion of the infective protozoan and the subsequent development of ALA.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6077556/
2) How do you approach this patient ?
A) * The patient is well managed by treating team ; even I will follow the same approach.
3) Why do we treat here ; both amoebic and pyogenic liver abscess?
* Considering the following factors:
1) Age and gender of patient: 21 years ( young ) and male.
2) Single abcess.
3) Right lobe involvement.
## The abcess is most likely AMOEBIC LIVER ABSCESS …
** But most of the patients with amoebic liver abcess have no bowel symptoms, examination of stool for ova and parasite and antigen testing is insensitive and insensitive and not recommended.
# And considering the risk factors associated with aspiration for pus culture:
1) Sometimes ; abcess is not accessible for aspiration if it is in posterior aspect or so.
2) Sometimes ; it has thin thinwall which may rupture if u aspirate.
3) Sometimes ; it is unliquefied.
## There how can u confirm whether it is pyogenic/ amoebic , so we treat them both empirically in clinical practice.
https://academic.oup.com/bmb/article/132/1/45/5677141
4) Is there a way to confirmthe definitive diagnosis in this patient?
* Yes in a high resource setting cause of liver abscess is usually determined using multiple diagnostic strategies ,
- including blood cultures ,
- entamoeba serology
,- liver abscess aspirate for culture
- and molecular and antigen testing.
https://academic.oup.com/bmb/article/132/1/45/5677141
8) Infectious disease (Mucormycosis, Ophthalmology, Otorhinolaryngology, Neurology)
A) Link to patient details:
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?
*3 years ago - diagnosed with hypertension
* 21 days ago recieved vaccination and presented with fever , chills and rigors
* 18 days ago again with similar complaints
*11 days ago - c/o generalised weakness ,facial puffiness and periorbital edema.The patient in drowsy state.
*4 days ago- altered state with facial puffiness and periorbital edema,
* Progressed periorbital edema
*serous discharge from left eye- blood tinged
*diagnosed - diabtes mellitus.
* patient died 2 days ago
#ANATOMICAL LOCALIZATION-eye( Mucormycosis) and infarct in the left temporal lobe.
https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html
#Primary etiology- diabetes
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?
*The proposed management of the patient:
a) inj. liposomal amphotericin
*https://pubmed.ncbi.nlm.nih.gov/23729001/
The article tells us about the efficacy and different formulations of liposomal amphotericin.
b) 200mg itraconazole which was adjusted to his creatin
Management of Diabetic keto acidosis:
- fluid replacement
- insulin therapy
-electrolyte replacement.
3) What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
*Mucormycosis may be triggered by the use of steroids in the covid 19 patients.
*Steroids reduce the inflammation in the covid infected lungs.
*This also rises the blood sugar levels in the steroid using patients and lowers the immunity .
*With covid 19 rising cases there is increase in occurrence of mucormycosis.
9) Infectious Disease (Covid 19)
COVID 19 MASTER SHEET
https://docs.google.com/spreadsheets/d/1LfdH-taUmaotZbaGYL1senVLcoPTohGgKehG-aUu6AM/edit?usp=sharing
*Individual covid case discussions in this link⬇
https://abhignyareddy71.blogspot.com/2021/06/infectious-diseases-covid-19-cases.html
10) Medical Education:
During this pandemic we are really missing out clinical skills but making E -LOGS made us to bridge the gap between it. IN the process of making e-logs I learnt so many new things which would help me in furthuer understanding of cases and case centred learning . And aslo by reading the case e -logs made by friends ,I got to know so many new and rare cases which will enchance a . way of thimking and case solving
Here`s the glimpse if my previous e-Logs
https://abhignyareddy71.blogspot.com/2021/05/51-year-old-female-with-difficulty-in.html
I really want to THANK Rakesh sir
for making us a part of virtual case based learning and PG`s and Interns for helping us through this process
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