MEDICINE BLENDED ASSIGNMENT (MAY)
Online blended bimonthly assignment toward summative assessment for the month of May 2021.
I have been given the following cases to solve in an attempt to understand the topic of 'Patient clinical data analysis' to develop my competency in reading and comprehending clinical data including history, clinical findings, investigations and diagnosis and come up with a treatment plan.
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.
CASE A.
A 55 Year Old Female with Shortness of Breath, pedal Edema and Facial Puffiness.
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?
ANSWER:
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:
1.primary etiology could be in lungs,(occupational pathology-working in paddy fields)
Working in paddy fields
⬇️
⬇️
Allergen leading to increased mucus secretion
⬇️
⬇️
Secondary bacterial infection
⬇️
⬇️
Bronchiectasis
⬇️
⬇️
SOB,, increased work load on heart
⬇️
⬇️
Right heart failure
⬇️
⬇️
Fluid over load
↙️ ↘️
Kidney stress. Edema
QUESTION 2:
what are the mechanism of action indication and efficacy over placebo of each of the phramacological and nonphramacological interventions used for this patient?
ANSWER :
1. HEAD END ELEVATION:
MECHANISM OF ACTION:
✓Improves oxygenation.
✓ Decreases incidence VAP
✓ Increase hemodynamic performance ✓Increase end expiratory Lung volume
✓ Decrease incidence of aspiration
INDICATIONS:
Meningitis, Head injury, Pneumonia
2. OXYGEN INHALATION TO MAINTAIN SPO2 ABOVE 92%
3.BiPAP : assist ventilation by delivering positive expiratory and inspiratory pressure with out need for ET incubation9
4.AUGMENTIN (Amoxicillin,clavulinic acid)
Mechanism of Action
Amoxicillin binds to penicillin-binding proteins within the bacterial cell wall and inhibits bacterial cell wall synthesis. Clavulanic acid is a β-lactam, structurally related to penicillin, that may inactivate certain β-lactamase enzymes.5. AZITHROMYCIN
Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit.
6.LASIX( FUROSEMIDE)
Furosemide works by blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine.
7.HYDROCORTISONE.
Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes.
8.IPRAVENT:
Ipravent belongs to a group of medicines known as anticholinergic bronchodilators. Anticholinergic bronchodilators work by relaxing the bronchial tubes (air passages) that carry air in and out of your lungs. This makes breathing less difficult.
9.PANTOP (PANTAPRAZOLE)
pantoprazole inhibit the final step in gastric acid production. In the gastric parietal cell of the stomach, pantoprazole covalently binds to the H+/K+ ATP pump to inhibit gastric acid and basal acid secretion.
QUESTION 3:
WHAT COULD BE THE CAUSES OF HER SUDDEN EXACERBATION?
ANSWER :
As the lungs tend to be vulnerable organs due to their exposure to harmful particles in the air, several things can cause an acute exacerbation of COPD:
Respiratory infection, being responsible for approximately half of COPD exacerbations. Approximately half of these are due to viral infections and another half appears to be caused by bacterial infections.[6] Common bacterial pathogens of acute exacerbations include Haemophilus influenzae, Streptococcus pneumoniae and Moraxella catarrhalis.[7] Less common bacterial pathogens include Chlamydia pneumoniae and MRSA.[7] Pathogens seen more frequently in patients with impaired lung function (FEV<35% of predicted) include Haemophilus parainfluenzae (after repeated use of antibiotics), Mycoplasma pneumoniae and gram-negative, opportunistic pathogens like Pseudomonas aeruginosa and Klebsiella pneumoniae.[7]
Allergens, e.g., pollens, wood or cigarette smoke, pollution[5]
Toxins, including a variety of different chemicals[5]
Air pollution[citation needed]
Failing to follow a drug therapy program, e.g. improper use of an inhaler[citation needed]
In one-third of all COPD exacerbation cases, the cause cannot be identified.[citation needed]
QUESTION 4:
Could the ATT have affected her symptoms? If so how?
ANSWER:
Yes ATT affected her symptoms
Isoniazid and rifampcin -nephrotoxic - raised RFT was seen.
QUESTION 5:
What could be the causes for her electrolyte imbalance?
ANSWER:
Imbalance in serum electrolytes has been proved in patients with COPD, in both acute exacerbation and during stable disease
Hyponatremia in patients with COPD developed secondary to many reasons, such as development or worsening of hypoxia, hypercapnia, and respiratory acidosis, and right-side heart failure with development of lower limb edema, renal insufficiency, use of diuretics, Syndrome of Inappropriate Antidiuretic Hormone Synthesis, malnutrition, and poor intake during acute exacerbations are common contributing factors in such patients. Activation of the renin-angiotensin-aldosterone system and inappropriately elevated plasma arginine vasopressin in COPD may aggravate the electrolyte imbalance during acute exacerbation of COPD .
2.NEUROLOGY.
CASE A:
A 40year old male presented with chief complaints of irrelevant talking and decreased food intake since 9days.
QUESTION 1:
what is the evolution of the symptomology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
ANSWER:
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.
QUESTION 2:
what are the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
ANSWER:
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.
QUESTION 3:
why have neurological symptoms appeared this time, that were absent during withdrawal earlier ? what could be a possible cause for this time?
ANSWER:
Due to excess thiamine deficiency and excess toxins accumulation due to renal disease caused by excess alcohol addiction.
QUESTION 4:
what is the reason for giving thiamine in this patient?
ANSWER:
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.
QUESTION 5:
what is the probable cause for kidney injury in this patient?
ANSWER:
The kidneys have an important job as a filter for harmful substances .alcohol causes changes in the function of the kidneys and makes them less able to filter the blood .alcohol also affects the ability to regulate fluid and electrolytes in the body. In addition, alcohol can disrupt hormones that disrupt hormones that affect kidney function .people who drink too much are more likely to have high blood pressure. High blood pressure is a common cause of kidney disease.
QUESTION 6:
what is the probable cause for the normocytic anaemia?
ANSWER:
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 .
QUESTION 7:
could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
ANSWER:
yes,As the patient is diabetic the chance of ulcer formation increases .in a patient of chronic alcoholic theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
CASE B:
A 52 year old male with cerebellar Ataxia.
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?
ANSWER:
No 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.
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?
ANSWER:
1.TAB VERTIN:
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.
2.TAB ZOFER (Ondanseteron)
MOA: Anti emetic 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.
3.TAB ECOSPIRIN ( ASPIRIN)
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.
4.TAB ATORVOSTATIN ( 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.
5.CLOPIDOGREL( ANTI PLATELET)
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.
6.THIAMINE
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.
7.TAB MVT ( methyl cobalamine)
Mainly given in this case for vitamin B12 deficiency.
QUESTION 3:
Did the patients history of denovo HTN contribute to his current condition?
ANSWER:
A cerebellar infarct is usually caused by a blood clot obstructing blood flow to the cerebellum. High blood pressure that is seen in hypertension (especially if left untreated) can be a major risk factor for the formation of cerebellar infarcts.
Increased shear stress is caused on the blood vessels. The usual adaptive responses are impaired in this case, thus leading to endothelial dysfunction in this case. High BP can also promote cerebral small vessel disease. All these factors contribute to eventually lead to stroke.
QUESTION 4:
Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
ANSWER:
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.
CASE C:
A 45 YEARS OLD FEMALE PATIENT WITH PALPITATIONS, PEDAL EDEMA, CHEST PAIN,CHEST HEAVINESS,RADIATING PAIN ALONG LEFT UPPER LIMB
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?
ANSWER:
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 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.
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.
QUESTION 2:
What are the reasons for recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
ANSWER:
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
QUESTION 3:
What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ANSWER:
Earliest change :decreased T-wave amplitude, ST depression, Twave - and inversion or flat;prolonged PR interval;presence of Uwaves
SYMPTOMS OF HYPOKALEMIA:
Weakness & fatigue, palpitations, muscle cramps & pain, anxiety, psychosis, depression, delirium.
CASE D:
55years old patient with seizures.
QUESTION 1:
Is there any relationship between occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
ANSWER:
If you've had a stroke, you have an increased risk for having a seizure. A stroke causes your brain to become injured. The injury to your brain results in the formation of scar tissue, which affects the electrical activity in your brain. Disrupting the electrical activity can cause you to have a 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?
ANSWER:
Abnormal increased activity in fronto-parietal association cortex and related subcortical structures is associated with loss of consciousness in generalized seizures. Abnormal decreased activity in these same networks may cause loss of consciousness in complex partial seizures.
CASE E:
A 48 YEAR OLD MALE WITH SEIZURES AND ALTERED SENSORIUM.
QUESTION 1:
What could have been the reason for this patient to develop ataxia in the past 1 year?
ANSWER:
Firstly,
✓Addicted to alcohol for the past 3 years. According to the attendant he used to drink "a few bottles per day". Drinks both bottled liquor and toddy.
✓History of multiple falls when inebriated and history of minor head injuries that were left unattended.
✓History of change in gait since 1 year
✓The CT scan showed an acute cerebral hemorrhage of the frontal, parietal and temporal lobes with a 13mm midline shift.
So, Alcohol might be responsible for his present condition.
QUESTION 2:
What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
ANSWER:
Alcohol-induced impairment of the
blood-clotting and/or fibrinolytic
systems can have serious medical
consequences. Most significantly,
clinical epidemiological data suggest
that a recent bout of heavy drinking
increases the drinker’s risk of suffer-
ing a hemorrhagic or ischemic stroke.
During a hemorrhagic stroke, the
blood flow to a brain area is impaired
due to a ruptured blood vessel that
results in bleeding in the brain. If the
blood flow is interrupted because a
blood vessel is blocked by a blood
clot.
CASE F:
A 30 YR OLD MALE PATIENT WITH WEAKNESS OF RIGHT UPPER LIMB AND LOWERLIMB.
QUESTION 1:
Does the patient's history of road traffic accident have any role in his present condition?
ANSWER:
1. YES, I think there is a role of patient's RTA for his present condition because
According to history
•He is not a K/C/O Diabetes and Hypertension
• Not a chronic alcoholic. ( In chronic alcoholic they may fell down more frequently due to drowsiness.
• he is also not on any medications.
So most possibly RTA might be responsible for his present condition.
QUESTION 2:
What are warning signs of CVA?
ANSWER:
QUESTION 3:
What is the drug rationale in CVA?
ANSWER:
Aspirin -antiplatlet drug prevents stroke
Atorvostatin - decreases LDL cholesterol to prevent recurrent attacks of stroke.
QUESTION 4:
Does alcohol has any role in his attack?
ANSWER:
Liver damage due to too much alcohol can stop the liver from making substances that help your blood to clot. This can increase your risk of having a stroke caused by bleeding in your brain.
QUESTION 5:
Does his lipid profile has any role for his attack??
ANSWER:
Studies have demonstrated a trend toward a higher risk of stroke with lower HDL-C and support HDL-C as an important modifiable stroke risk factor. In patients with recent stroke or transient ischemic attack and no coronary heart disease, only lower baseline HDL-C predicted the risk of recurrent stroke.
CASE G:
A 50 YEAR OLD PATIENT WITH CERVICAL MYELOPATHY.
QUESTION 1:
What is myelopathy hand ?
QUESTION 2:
What is finger escape ?
What is Hoffman’s reflex?
CASE H:
A 17 YEAR OLD FEMALE WITH SEIZURES.
QUESTION 1:
What can be the cause of her condition ?
ANSWER:
According to MRI cortical vein thrombosis might be the cause of her seizures.
QUESTION 2:
What are the risk factors for cortical vein thrombosis?
ANSWERS:
QUESTION 3
There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why
ANSWER:
Seizures are resolved and seizure free period got achieved after medical intervention but sudden episode of seizure was may be due to any persistence of excitable foci by abnormal firing of neurons.
QUESTION 4
What drug was used in suspicion of cortical venous sinus thrombosis?
ANSWER:
It has now been conclusively shown that intravenous heparin is the first-line treatment for cerebral venous sinus thrombosis because of its efficacy, safety and feasability.
Clexane is an anticoagulant that belongs to a group of medicines called Low Molecular Weight Heparin (LMWH). These medicines help to prevent clots from getting bigger and stopping new clots from forming
CARDIOLOGY
CASE A:
A 78YEAR OLD MALE WITH SHORTNESS OF BREATH, CHEST PAIN, B/L PEDAL EDEMA AND FACIAL PUFFINESS.
QUESTION 1:
What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
ANSWER:
Ejection fraction (EF) is a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction. An ejection fraction of 60 percent means that 60 percent of the total amount of blood in the left ventricle is pushed out with each heartbeat.
This indication of how well your heart is pumping out blood can help to diagnose and track heart failure.
Preserved ejection fraction– also referred to as diastolic heart failure. The heart muscle contracts normally but the ventricles do not relax as they should during ventricular filling (or when the ventricles relax).
Reduced ejection fraction- also referred to as systolic heart failure. The heart muscle does not contract effectively, and therefore less oxygen-rich blood is pumped out to the body.
QUESTION 2:
Why haven't we done pericardiocenetis in this pateint?
ANSWER:
Pericardiocentesis is a procedure performed to remove pericardial fluid from the pericardial sac that surrounds the myocardium. It is often performed in the setting of pericardial tamponade to correct the hypotension caused by decreased stroke volume, which is a result of the extrinsic compression of the chambers of the heart by the pericardial fluid.
2.07cms effusion at the time of admission -1.4mm at the time of discharge).Pericardiocentesis is an invasive procedure. In our patient we were able to decrease the effusion with conservative therapy.
QUESTION 3:
What are the risk factors for development of heart failure in the patient?
ANSWER:
Depending on how quickly pericardial effusion develops, the pericardium can stretch somewhat to accommodate the excess fluid. However, too much fluid causes the pericardium to put pressure on the heart, which prevents the chambers from filling completely.
This condition, called tamponade (tam-pon-AYD), results in poor blood flow and a lack of oxygen to the body.
The pressure prevents the heart’s ventricles from expanding fully and keeps your heart from functioning properly. Your heart can’t pump enough blood to the rest of your body when this happens. This can lead to organ failure.
QUESTION 4:
What could be the cause for hypotension in this patient?
ANSWER:
CASE B:
A 73 YEAR OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS OF BREATH AND DECREASED URINE OUTPUT
QUESTION 1:
What are the possible causes for heart failure in this patient?
ANSWER:
QUESTION 2:
what is the reason for anaemia in this case?
ANSWER:
QUESTION 3:
What is the reason for blebs and non healing ulcer in the legs of this patient?
ANSWER:
✓ Peripheral vascular disease — Diabetes also affects the flow of blood. Without good blood flow, it takes longer for a sore or cut to heal. Poor blood flow in the arms and legs is called peripheral vascular disease.
✓If you have an infection that will not heal because of poor blood flow, you are at risk for developing gangrene, which is the death of tissue due to a lack of blood
✓ This is reason for non healing ulcer
✓People with diabetes might occasionally experience blisters on their skin. These are known as diabetic blisters, bullosis diabeticorum, or diabetic bullae
✓ Diabetic blisters most often develop in people who do not control their diabetes correctly for several years
✓ People who are not controlling blood sugar levels effectively.
Those with diabetic neuropathy, a type of nerve damage that occurs due to prolonged high blood sugar.
Individuals with peripheral artery disease.
QUESTION 4:
What sequence of stages of diabetes has been noted in this patient?
ANSWER:
Here patient developed
1. Diabetes mellitus type 2
2. after few years, even after taking anti hyperglycaemic drugs were unable to control diabetes. So, insulin therapy
3 then diabetic retinopathy.
4 peripheral vascular disease.
CASE C:
A-Fib and Biatrial Thrombus in a 52yr old Male.
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?
ANSWER:
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.
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?
ANSWER:
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.
QUESTION 3:
What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
ANSWER:
cardiorenal syndrome type 4 is seen in this patient.
QUESTION 4:
4) What are the risk factors for atherosclerosis in this patient?
ANSWER:
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.
QUESTION 5:
Why was the patient asked to get those APTT, INR tests for review?
ANSWER:
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.
CASE D:
67 year old patient with acute coronary syndrome
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?
ANSWER:
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 localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic , both these conditions can cause
- Atherosclerosis: there is build up of fatty and fibrous material inside the wall of arteries.(PLAQUE)
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?
ANSWER:
Pharmacological interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine, also known as adrenaline. Beta blockers cause your heart to beat more slowly( negative chronotropic effect)
and with less force( negative inotropic effect). 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 +/- 9/9 mmHg. Following 4 weeks of treatment, mean 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).
QUESTION 3:
What are the indications and contraindications for PCI?
ANSWER:
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)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
QUESTION 4:
What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
ANSWER:
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 used
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.
CASE E:
CASE DISCUSSION ON ACUTE MYOCARDIAL INFARCTION
QUESTION 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?
ANSWER:
Ans: *the anatomical location ofetiology is BLOOD VESSELS.
*myocardial infarction is usually due to thrombotic occlusion of a coronary vessel caused by rupture of a vulnerable plaque. Ischemia induces profound metabolic and ionic perturbations in the affected myocardium and causes rapid depression of systolic function
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?
ANSWER:
Ans: PHARMACOLOGICAL INNTERVENTION
1.TAB. ASPIRIN
mechanism:Aspirin inhibits platelet function through irreversible inhibition of cyclooxygenase (COX) activity. Until recently, aspirin has been mainly used for primary and secondary prevention of arterial antithrombotic events.
2.TAB ATORVAS
mechanism:Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
3.TAB CLOPIBB
mechanism:The active metabolite of clopidogrel selectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
4.INJ HAI
mechanism:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.ANGIOPLASTY
mechanism:Angioplasty, also known as balloon angioplasty and percutaneous transluminal angioplasty (PTA), is a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
QUESTION 3:
Did the secondary PTCA do any good to the patient or was it unnecessary?
ANSWER:
Ans:the second PCI was NOT necessary in this patient.
PCI performed from 3 to 28 days after MI does not decrease the incidence of death, reinfarction or New York Heart Association (NYHA) class IV heart failure but it is associated with higher rates of both procedure-related and true ST elevation reinfarction.3 A retrospective analysis of the clinical data revealed The Thrombolysis in Myocardial Infarction (TIMI) Risk Score of 4 predicting a 30-day mortality of 7.3% in this patient. Late PCI leads to the increased risks of periprocedural complications, long-term bleeding, and stent thrombosis.
The high incidence of CAD and the increasing need for PCI provides an opportunity to evaluate its appropriate use and highlight potential overuse. PCI is frequently reported to be overused and inappropriately recommended. Behnke et al defined overuse as ‘use of unnecessary care when alternatives may produce similar outcomes, resulting in a higher cost without increased value’.8Overuse causes a heavy financial burden on people living in countries, where fee-for-service and ill-regulated private healthcare provides much of the patient care. As a result, cost of healthcare increases and causes potential harm to the patients.
CASE F:
A CASE OF CARDIOGENIC SHOCK.
QUESTION 1:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
ANSWER:
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.
QUESTION 2:
2. What is the rationale of using torsemide in this patient?
ANSWER:
Torsemide used to relieve abdominal distension
.
QUESTION 3:
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
ANSWER:
IT IS THE TREATMENT FOR UTI
Rationale- Used for any bacterial infection.
4.GASTROENTEROLOGY:
CASE A:
A 33 YEAR OLD MAN WITH PANCREATITIS, PSEUDOCYST AND LEFT BRONCHO-PLEURAL FISTULA.
QUESTION 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?
ANSWER:
Evolution of symptomatology
H5 years back-1st episode of pain abdomen and vomitings
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
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.
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?
ANSWER:
1) ING. MEROPENAM ; TID for 7 days
* Meropenem ( broad spectrum Carbepenem ) an antibiotic.
2) ING. METROGYL 500 mg IV TID for 5 days
* inj. Metrogyl has METRONIDAZOLE
( Nitroimidazole drug ) an antibiotic
3) ING. 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.
CASE B:
CASE DISCUSSION ON 25 YEAR OLD MALE WITH EPIGASTRIC PAIN.
QUESTION 1:
What is causing the patient's dyspnea? How is it related to pancreatitis?
ANSWER:
the cause of dyspnea might be PLEURAL EFFUSION.
QUESTION 2:
Name possible reasons why the patient has developed a state of hyperglycemia.
ANSWER:
*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells
* elevated levels of catecholamines and cortisol.
QUESTION 3:
What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
ANSWER:
LFT are increased due to hepatocyte injury
*If the liver is damaged or not functioning properly, ALT can be released into the blood. This causes ALT levels to increase. A higher than normal result on this test can be a sign of liver damage.
*elevated alanine transaminase (ALT) and aspartate transaminase (AST), usually one to four times the upper limits of normal in alcoholic fatty liver.
The reasons for a classical 2:1 excess of serum AST activity compared to serum ALT activity in alcoholic hepatitis have been attributed to
(i) decreased ALT activity most likely due to B6 depletion in the livers of alcoholics
(ii) mitochondrial damage leading to increased release of mAST in serum.
QUESTION 4:
What is the line of treatment in this patient?
ANSWER:
Plan of action and Treatment:
Investigations:
✓ 24 hour urinary protein
✓ Fasting and Post prandial Blood glucose
✓ HbA1c
✓ USG guided pleural tapping
Treatment:
• IVF: 125 mL/hr
• Inj PAN 40mg i.v OD
• Inj ZOFER 4mg i.v sos
• Inj Tramadol 1 amp in 100 mL NS, i.v sos
• Tab Dolo 650mg sos
• GRBS charting 6th hourly
• BP charting 8th hourly.
CASE C:
A 45 year old Female patient with Fever, Pain abdomen, Decreased Urine output and Abdominal distension.
QUESTION 1:
What is the most probable diagnosis in this patient?
ANSWER:
(Differential Diagnosis:
Ruptured Liver Abscess.
Organized collection secondary to Hollow viscous Perforation.
Organized Intraperitoneal Hematoma.
Free fluid with internal echoes in Bilateral in the Subdiaphragmatic space.
Grade 3 RPD of right Kidney
(The most probably diagnosis is there is abdominal hemorrhage. This will give reasoning to the abdominal distention, and the blood which is aspirated.
QUESTION 2:
2) What was the cause of her death?
ANSWER:
(After 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.
QUESTION 3:
3) Does her NSAID abuse have something to do with her condition? How?
ANSWER:
(NSAID-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.
CASE A:
POST TURP WITH NON OLIGURIC ATN.
QUESTION 1:
What could be the reason for his SOB ?
ANSWER:
Reasons for sob:hypotension nd Bradycardia which are complications of the turp.....the blood loss which is more because the size of the gland is 60grams.....all these factors hyvolemia nd Bradycarfia all these culminate nd results in SOB
QUESTION 2:
Why does he have intermittent episodes of drowsiness ?
ANSWER:
He has intermittent episodes of drowsiness because of increased levels of creatinine in the body...
When the creatinine quantity decreased to normal level the patient the patient become allright....
But again when the creatinine levels raises the patient becomes drowsy.
QUESTION 3:
Why did he complaint of fleshy mass like passage in his urine?
ANSWER:
3A). He complains of fleshy mass in urine because of patient feels thick urine coming out of his body...the reason behind is the patient had urosepsis.....the culture and sensitivity showed the E.Coli infection...it is the most common cause of UTI....because these infection many pus cells has formed...and these pus cells increase the cloudyness of the urine ..so the patient feels fleshy mass like urine.
QUESTION 4:
What are the complications of TURP that he may have had?
ANSWER:
INTRA-OPERATIVE COMPLICATIONS 1-Hypotension 2-TURP syndrome 3-Haemorrhage 4-Perforation of bladder/prostatic capsule 5-Hypothermia 6-Bacteremia and sepsis 7-Complications of positioning 8-Erection.
CASE B:
An Eight year old with Frequent Urination
QUESTION 1:
1.Why is the child excessively hyperactive without much of social etiquettes ?
ANSWER:
Attention deficit hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by inattention, or excessive activity and impulsivity, which are otherwise not appropriate for a person's age
For a diagnosis, the symptoms have to be present for more than six months, and cause problems in at least two settings (such as school, home, work, or recreational activities).
QUESTION 2:
2. Why doesn't the child have the excessive urge of urination at night time ?
ANSWER:
Since the child doesn’t have excessive urge of urination at night but at day there might be a psychiatry related condition
1. Psychosomatic disorder
2. Undiagnosed anxiety disorder
QUESTION 3:
3. How would you want to manage the patient to relieve him of his symptoms?
ANSWER:
Bacterial kidney infection, the typical course of treatment is antibiotic and painkiller therapy.
If the cause is an overactive bladder, a medication known as an anticholinergic may be used. These prevent abnormal involuntary detrusor muscle contractions from occurring in the wall of the bladder
To treat attention deficit hyperactivity disorder:
For children 6 years of age and older, the recommendations include medication and behavior therapy together — parent training in behavior management for children up to age 12 and other types of behavior therapy and training for adolescents. Schools can be part of the treatment as well.
Methylphenidate A stimulant and a medication used to treat Attention Deficit Hyperactivity Disorder. It can make you feel very ‘up’, awake, excited, alert and energised, but they can also make you feel agitated and aggressive. They may also stop you from feeling hungry.
Amphetamine belongs to a class of drugs known as stimulants. It can help increase your ability to pay attention, stay focused on an activity, and control behavior problems. It may also help you to organize your tasks and improve listening skills.
INFECTIOUS DISEASE:
CASE A:
A 40 YEAR OLD LADY WITH DYSPHAGIA,FEVER AND COUGH.
QUESTION 1:
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula?
ANSWER:
Cough since 2 months on taking food and liquids
•difficulty in swallowing since 2 month . It was initially difficult only with solids but then followed by liquids also.
•laryngeal crepitus- positive
These favour for tracheo esophageal.fistula
QUESTION 2:
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent it?
ANSWER:
Immune reconstitution inflammatory syndrome (IRIS) represents the worsening of a recognized (paradoxical IRIS) or unrecognized (unmasking IRIS) pre-existing infection in the setting of improved immunologic function.
The most effective prevention of IRIS would involve initiation of ART before the development of advanced immunosuppression. IRIS is uncommon in individuals who initiate antiretroviral treatment with a CD4+ T-cell count greater than 100 cells/uL.
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
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 ?
ANSWER:
1. A retrospective study was conducted on 108 patients to know the role of alcoholism in liver abscess
Conclusion:From our study it was undoubtedly proved that 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 an etiological factor for the formation of liver abscess.
QUESTION 2:
What is the etiopathogenesis of liver abscess in a chronic alcoholic patient ? ( since 30 years - 1 bottle per day)
ANSWER:
Pathophysiology
Infection can reach the liver in several ways (Box 22.43). Pyogenic
abscesses are most common in older patients and usually result
from ascending infection due to biliary obstruction (cholangitis) or
contiguous spread from an empyema of the gallbladder. They can
also complicate dental sepsis or colonic pathology, e.g. cancer,
diverticulitis or inflammatory bowel disease causing portal pyaemia.
QUESTION 3.
Is liver abscess more common in right lobe ?
ANSWER:
QUESTION 4:
What are the indications for ultrasound guided aspiration of liver abscess ?
ANSWER:
INDICATIONS OF LIVER ABSCESS DRAINAGE:
1) If the abscess is large ( 5cm or more) because it has more chances to rupture.
2) If the abscess is present in left lobe as it may increase the chance of peritoneal leak and pericardial leak.
3) If the abscess is not responding to the drugs for 7 or more days.
CASE B:
CASE DISCUSSION ON LIVER ABSCESS.
QUESTION 1:
Cause of liver abcess in this patient ?
ANSWER:
QUESTION 2:
How do you approach this patient ?
ANSWER:
QUESTION 3:
Why do we treat here ; both amoebic and pyogenic liver abcess?
ANSWER:
QUESTION 4:
Is there a way to confirmthe definitive diagnosis in this patient?
ANSWER:
Here in this patient there may be any associated secondary bacterial infections,so we will give antibiotics in this patient.
8. INFECTIOUS DISEASE (MUCORMYCOSIS).
CASE A:
50/Male came with altered sensorium.
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 aetiology of the patient's problem?
ANSWER:
3 years ago- diagnosed with hypertension
21 days ago- received vaccination at local PHC which was followed by fever associated with chills and rigors, high grade fever, no diurnal variation which was relieved on medication
18 days ago- complained of similar events and went to the the local hospital, it was not subsided upon taking medication(antipyretics)
11 days ago - c/o Generalized weakness and facial puffiness and periorbital oedema. Patient was in a drowsy state
4 days ago-
patient presented to casualty in altered state with facial puffiness and periorbital oedema and weakness of right upper limb and lower limb
towards the evening patient periorbital oedema progressed
serous discharge from the left eye that was blood tinged
was diagnosed with diabetes mellitus
patient was referred to a government general hospital
patient died 2 days ago
patient was diagnosed with diabetic ketoacidosis and was unaware that he was diabetic until then. This resulted in poorly controlled blood sugar levels. The patient was diagnosed with acute oro rhino orbital mucormycosis . rhino cerebral mucormycosis is the most common form of this fungus that occurs in people with uncontrolled diabetes https://www.cdc.gov/fungal/diseases/mucormycosis/definition.html the fungus enters the sinuses from the environment and then the brain.
The patient was also diagnosed with acute infarct in the left frontal and temporal lobe. Mucormycosis is associated with the occurrence of CVA https://journal.chestnet.org/article/S0012-3692(19)33482-8/fulltext#:~:text=There%20are%20few%20incidences%20reported,to%20better%20morbidity%2Fmortality%20outcomes
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?
ANSWER:
The proposed management of the patient was –
inj. Liposomal amphotericin B according to creatinine clearance
200mg Iitraconazole was given as it was the only available drug which was adjusted to his creatinine clearance
Deoxycholate was the required drug which was unavailable
this article talks about the efficacy and toxicity of different formulations of amphotericin B
along with the above mentioned treatment for the patient managing others symptoms is also done by-
Management of diabetic ketoacidosis –
Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in blood.
Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. Patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, patient will receive insulin therapy
QUESTION 3:
What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point of time?
ANSWER:
Mucormycosis is may be being triggered by the use of steroids, a life-saving treatment for severe and critically ill Covid-19 patients. Steroids reduce inflammation in the lungs for Covid-19 and appear to help stop some of the damage that can happen when the body's immune system goes into overdrive to fight off coronavirus. But they also reduce immunity and push up blood sugar levels in both diabetics and non-diabetic Covid-19 patients.
With the COVID-19 cases rising in India the rate of occurrence of mucormycosis in these patients is increasing.
9.INFECTIOUS DISEASES COVID -19.
Case 9-1.
1) Covid 19 with co morbidity (Pulmonology/Rheumatology)
Questions:
1) How does the pre-existing ILD determine the prognosis of this patient?
The pre-existing ILD significantly worsens the prognosis of this covid patient.
Interstitial lung disease is characterized by dyspnea, decreased pulmonary diffusing capacity, decreased FVC and TLC. The SpO2 of these patients is usually decreased due to increased A-a gradient
A superimposed covid-19 infection in these cases can cause an acute exacerbation of symptoms such as dyspnea, decreasing levels of SpO2 further and faster than in Covid-19 patients without interstitial lung disease.
Radiology (HRCT) usually shows the development of new pulmonary opacities and fibrosis.
Patient factors:
Since this patient already had a reduced SpO2 of 90-92% (compared to the normal range of >96%) she is more susceptible to worsening of hypoxia and dyspnea unless immediate ventilator support is provided
The patient reportedly did not have dyspnea prior to the covid infection but developed a grade 2 SOB
ILD by itself makes the patient much more susceptible to acquiring Covid-19 infection.
Prognosis: Poor
2) Why was she prescribed clexane (enoxaparin)?
The main pathogenesis of systemic inflammation caused by Covid-19 is by inducing a cytokine storm that causes epithelial cell necrosis, increased vascular permeability, dysfunctional humoral and CMI which all collectively lead to acute lung injury and ARDS
Of these cytokines, IL-6 is one that is the most important in determining the prognosis. IL-6 levels are highly elevated in patients with severe disease
Enoxaparin is said to relieve and prevent inflammation produced by IL-6 by inactivating it by binding it with its non-anticoagulant fraction, especially in pulmonary epithelial cells.
Moreover, patients with Covid-19 are more susceptible to the development of venous thromboembolism, which can be prevented by Enoxaparin (LMWH).
CASE 9-2: COVID-19 SEVERE
QUESTIONS:
1) Since patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause the indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausible?
The patient may have already had slight hyperglycemia, owing to high HbA1c levels (7.1%), which may have aggravated due to COVID-19. The possible biochemical pathways include: [6]
2) Did the patient's diabetic condition influence the progression of her pneumonia?
Yes, with DM or hypergycemia in patients leads to an increase in COVID-19 severity. Also, poor glycaemic control predicts an increased need for medications and hospitalizations, and increased mortality.
In monocytes: elevated glucose levels increase SARS-CoV-2 replication, and glycolysis sustains SARS-CoV-2 replication via the production of mitochondrial reactive oxygen species and activation of hypoxia-inducible factor 1α. Therefore, hyperglycaemia supports viral proliferation.
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
D- Dimer levels indicate the severity of COVID-19, pertaining to possible thrombotic complications- as D Dimer is formed post- fibrinolysis.
D- Dimer does change the management, as D-Dimer levels above 2000ng/dl were found to have a direct link with increasing severity of COVID-19 [7]. Moreover, D- dimer levels would be helpful in fast diagnosis and prevention of thrombotic complications
CASE 9-3 (COVID-19 SEVERE)
QUESTIONS:
1. Why was this patient given noradrenaline?
Following kidney failure, the patient had sudden and persistent hypotension. To combat this, the patient was given noradrenaline, a potent vasoconstrictor.
2. What is the reason behind testing for LDH levels in this patient?
LDH (Lactate Dehydrogenase) catalyzes the conversion of lactate to pyruvate and back. Hence, an increase in LDH denotes some form of tissue damage. In this patient, an increase in LDH levels would denote inflammation, and a high increase would denote Multi-Organ Failure.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
Although BiPaP is a positive pressure system, unlike tracheal intubation, it does not send the air to the trachea and depends on the patient's ability to respire. In this patient, as SpO2 levels were dropping to 30% despite BiPAP, a more invasive method was required to push the air directly into the lungs- hence intubation was preferred.
CASE 9-4 (COVID-19 MILD)
QUESTIONS:
1. Is the elevated esr due to covid related inflammation?
Yes, as ESR is an important indicator of immunological loss, and owing to an increased inflammation and immunological dysfunction in COVID, elevated ESR is most likely dur to COVID related inflammation.
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and harms of hospitalization?
Hospitalisation was due to Grade 3 Shortness of Breath (SOB), and long duration of COVID-19 infection.
Challenges of home isolation-
Physical challenges- Many patients may find it hard to cut themselves from the outside world and confine themselves to a room for long periods of time
Emotional challenges- Sitting in a small room all day leads to stress, anxiety and even depression, with an increase in mental health issues being reported during the pandemic
Social challenges- Members of society who cannot care for themselves on their own (eg, patients with disability, geriatric patients etc) are at a major loss
Economic challenges- Some patients, such as daily wage labourers, cannot afford to home isolate as they need to earn on a daily basis to keep their family going
Harms of hospitalisation-
Infection- Members visiting may get COVID from exposure to the hospital ward alone
Cost- PAtient may not be able to bear the brunt of high costs
Overtesting- Hospitals may ask the patients to stay overnight despite the conditions being mild, based on preliminary test results
Economic- Working patients may have to take a leave of absence, hence affecting both their work and decreasing their salary, on top of spending money on hospitalisation
CASE 9-5 (COVID-19 SEVERE)
QUESTIONS:
1) What was the reason for coma in this patient?
The reason for coma is due to severe hypoxia, as his SpO2 levels were 20% when he was admitted. Along with this, hypokalemia leads to respiratory muscle paralysis, which may have aggravated his dyspnoea.
2) What were the competency gaps in hospital 1 Team to manage this intubated comatose patient that he had to be sent to hospital 2? Why and how did hospital 2 make a diagnosis of hypokalemic periodic paralysis? Was the coma related?
The main competency gap was in the lack of testing for serum electrolytes, as the hypokalemia had caused weakness and fatigue in this patient.
Hospital 2 make a diagnosis of hypokalemic periodic paralysis based on the fact that the patient had generalised weakness before becoming comatose, along with tingling and symptoms of paralysis. On testing serum electrolytes, his potassium levels were found to be 2.3 mEq/L (normal-3.5-5)
The coma was most probably related, as hypokalemia can cause respiratory muscle paralysis, leading to aggravation of hypoxia, hence causing unconsciousness in the patient.
3) How may covid 19 cause coma?
Yes, as the brain is extremely sensitive to oxygen, oxygen deprivation due to COVID-19 can lead to a comatose state.
This patient had very low SpO2 levels (20%), which may have caused the coma.
CASE 9-6 (COVID-19 WITH ALTERED SENSORIUM)
QUESTIONS:
1. What was the cause of his altered sensorium?
Probable causes include
1. Altered sensorium due to hypoxia, leading to hypercapnic encephalopthy and altered sensorium
2. Increased urea levels leading to uraemic encephalopathy, which causes altered sensorium
2. what is the cause of death in this patient?
The cause of death in this patients was due to complications of COVID-19, most probably Acute Kidney Failure (AKI), as denoted by increased urea and creatinine, and hypoproteinemia. Hypoxia and inflammatory response due to COVID-19 may have triggered the process.
CASE 9-7
7) A 67 year old lady in the ICU with COVID induced Viral Pneumonia .
https://drsaranyaroshni.blogspot.com/2021/05/a-67-year-old-lady-in-icu-with-covid.htmlQ1. What is the grade of pneumonia in her?
A. Based on the CT severity score it can be said that the patients pneumonia is moderate.
Q2. What is the ideal day to start steroids in a patient with mild elevated serum markers for COVID ?
A. It is best to start the treatment with dexamethasone before the onset of cytokine storm.
Q3. What all could be the factors that led to psychosis in her ?
A. The following can lead to ICU psychosis
Sensory deprivation
Sleep deprivation
Stress
Continuous light levels
Continuous monitoring
Lack of orientation
pain
drug reactions
Infections
metabolic disorders
Dehydration
Q4. In what ways shall the two drugs prescribed to her for psychosis help ?
A. Pirecetam improves memory and causes cognitive enhancement and also improves mood.
Resperidone acts by decreasing the dopaminergic and seritonergic pathways in the brain
Q5. What all are the other means to manage such a case of psychosis?
A. The management of ICU psychosis primarily depends on the cause. If it is sleep deprivation then hte patient should be provided a peaceful place to take rest.
If it is due to underlying conditions like heart failure and dehydration then these should first be corrected.
Haloperidol is a medication commonly used to manage ICU psychosis. Other common anti-psychotics can also be used.
Q6. What all should the patient and their attendants be careful about ( w.r.t. COVID )after the patient is discharged ?
A. The patient is supposed to self isolate after they are discharged for another 7 days after discharge. If possible oxygen levels are to be monitored as well for the next 7 days. The patients and the patient's attenders should be on the look out for danger symptoms such as
trouble breathing, chest pain, bluish discolouration of lips, confusion or inability to wake up.
Q7. What are the chances that this patient may go into long covid given that her "D Dimer" didn't come down during discharge?
A. Long COVID is the persistence of symptoms such as cough, breathlessnes, headaches and chest pain weeks to months after discharge. People suffering from long COVID usually have elevated biomarkers such as elevated d dimer and CRP. As this patient has elevated d dimer levels at discharge there is a good chance that she could suffer from long COVID.
8) 35YR/M WITH VIRAL PNEUMONIA SECONDARY TO COVID 19 INFECTION
Q1. Can psoriasis be a risk factor for severe form of COVID?
A. There is no evidence that patients with moderate-to-severe psoriasis receiving systemic treatments, including biologics, have higher risk of SARS-CoV-2 infection and/or increased hospitalization and death related to COVID-19 compared to the general population.
Q2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?
A. Immunomodulators help COVID 19 patients by suppressing the cytokine storm but they also have thepotentialt to increase the risk of infection (like mucormycosis), traditional clinical signs may be masked with resulting delays in identification and treatment.
Q3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
A. Increasing evidence from experimental and clinical studies suggests that mechanical ventilation, which is necessary for life support in patients with acute respiratory distress syndrome as seen in COVID 19 can cause lung fibrosis, which may significantly contribute to morbidity and mortality. It is believed that ventilator induced lung injury is the cause for the fibroproliferative changes and the resultant lung fibrosis.
9) 45 year old female with viral pneumonia secondary to Covid-19
Q1. What is the type of DM the patient has developed ?(is it the incidental finding of type 2 DM or virus induced type 1DM)?
A. Incedental type 2 DM can be differentiated from de novo covid induced type 1 DM with the help of the HbAc1 levels.
As HbAc1 levels are indicators of long term blood ssugar levels they are likely to be raised in pre existing DM that was incidentally discovered. But in case ofthe diabetes being de novo in nature then the HbAc1 levels are unlikely to be raised. As the patients HbAc1 levels are not raised we can not at this point determine if the patient has incedental discovered type 2 DM or Covid induced de novo DM.
Q2. Could it be steroid induced Diabetes in this patient?
A. As the patient was given dexamethasone as a part of her treatment regimen it is possible that her elevated glucose levels are a result of steroid induced hyperglycemia.
10) A little difference that altered the entire covid recovery game: a report of two patients with focus on imaging findings.
Q1. What are the known factors driving early recovery in covid?
A. The following factors can lay a role:
Younger age ggroup
shorter duration of fever
No diabetes
PaO2/FiO2 levels
No comorbidities
11) Viral pneumonia secondary to COVID of a denovo Diabetes Mellitus
How is the diabetes related to the prognosis of COVID patients? What are the factors precipitating diabetes in a patient developing both covid as well as Diabetes for the first time?
A. People suffering from diabetes are like to experience more severe symptoms of the disease than the ones who are not diabetic. Even within the patients that are diabetic the people whose disease is under better control tendtendvbe better diagnosis.
Possible causes for de nov diabetes in COVID19 include:
· The SARS CoV 2 virus enters the cells through the ACE 2 receptors which are present in large numbers in the pancreas and that this damages the pancreatic cells.
· Another theory is that the inflammation caused by the cytokine storm damages the beta cells.
Q2. Why couldn't the treating team start her on oral hypoglycemics earlier?
A. As the insulin is faster acting as compared to oral hypoglycemics and as her blood glucose level was very high it is important to bring it down as fast as possible.
12) Moderate to severe covid with prolonged hospital stay:
Questions:-
1) What are the potential bio clinical markers in this patient that may have predicted the prolonged course of her illness?
Serum LDH: 571U/L (Normal range=140-280U/L
ALP : 342 U/L (Normal range=44-147U/L)
SpO2: 82% at RA (Normal range= >96%)
HR: 124bpm (Normal range=60-100bpm)
Classically, the bio clinical markers that are predictive of a Covid-19 patient's outcome are
C reactive protein [>57.9mg/dL]
D-Dimer [>1mcg/ml associated with poorer prognosis]
Serum LDH [>248U/L]
IL-6 [2.9 times higher in severe disease compared to mild disease]
SGPT [Isolated rise in SGPT >3 times the normal value]
ESR [high sustained level after recovery from infection]
Albumin
Platelet count
Neutrophil count
NLR: [>5.5]
Urea
Creatinine
High sensitivity Troponin
The patient in question has elevated levels of serum LDH and ALP. Her CRP and D-Dimer levels are not high enough to be considered as a bad prognostic factor.
13) Severe covid with first diabetes
Link to Case report log :
1) What are the consequences of uncontrolled hyperglycemia in covid patients?
Hyperglycemia can lead to anomalous glycosylation of tissue receptors throughout the body. One of these receptors happens to be ACE2, the same receptor SARS-CoV2 uses to gain entry into the host cell. In fact, glycosylation of ACE2 is necessary for the virus to establish an infection.
Uncontrolled hyperglycemia freely facilitates this glycosylation, making these patients more susceptible to Covid-19 infections and increasing the severity of the infection by helping increase the viral load (by increasing the concentration of glycosylated ACE2)
Control of blood sugar can also decrease the chances of a cytokine storm during the second phase of the infection.
Uncontrolled hyperglycemia hence, suggests a poor prognosis in Covid-19 patients.
2) Does the significant rise in LDH suggests multiple organ failure?
Lactate dehydrogenase has 5 isoenzymes that are present in various tissues such as the heart, RBCs, lungs, liver, kidney, brain, and skeletal muscle.
Since covid-19 primarily causes lung damage, LDH3 is released into the blood giving an elevated titer.
Multi-organ damage that involves the heart (myocarditis) or kidneys (renal failure) can lead to an elevation in respected isoenzymes found in these tissues.
Hence, a significant rise in LDH indicates a poor prognosis and points towards multi-organ damage.
3) What is the cause of death in this case?
This patient was diagnosed with uncontrolled hyperglycemia with severe covid pneumonia.
LFT shows elevated AST, ALT, and ALP with a gross increase in bilirubin titer.
The D-Dimer is elevated (560ng/ml) and the LDH is 835U/L both of which are indicators of a poor prognosis.
The most likely cause of death in this patient seems to be ARDS.
The immediate cause of death: Most probably cardio-pulmonary arrest
Antecedent cause: Severe covid-19 pneumonia
14) Long covid with sleep deprivation and ICU psychosis
Questions:
1)Which subtype of ICU psychosis did the patient land into according to his symptoms?
Hyperactive delirium: Manifests as agitation, restlessness, refusal to cooperate with caregivers, unprovoked mood changes, hallucinations
2)What are the risk factors in the patient that has driven this case more towards ICU psychosis?
Hypertension
History of cerebrovascular accident (makes him more prone to a new one)
Steroid use
Sedative use (Gabapentin)
COPD
3)The patient is sleep-deprived during his hospital stay. Which do you think might be the most probable condition?
A) Sleep deprivation causing ICU psychosis
B) ICU psychosis causing sleep deprivation
4) What are the drivers toward current persistent hypoxia and long covid in this patient?
Elevated bio clinical markers like D-Dimer, LDH, Neutrophils, WBCs(absolute), IL-6, and CRP all contribute to persistent hypoxia and worsen the prognosis. In addition to this, ICU psychosis adds to the prolonged hospital stay.
15) Moderate Covid with comorbidity (Truncal obesity and recent hyperglycemia)
Questions:
1. As the patient is a non-diabetic, can the use of steroids cause a transient rise in blood glucose?
Cortisol stimulates gluconeogenesis in the liver and inhibits glycogen synthesis, increasing blood glucose. Continuous treatment with corticosteroids can lead to elevated blood glucose titers even in non-diabetics.
2. If yes, can this transient rise lead to long-term complications of New-onset diabetes mellitus?
It is still unclear if the alterations brought about by covid-19 in the glucose metabolism are permanent and persist or remit after the resolution of infection. There are ongoing studies that aim to answer these questions.
Steroid diabetes is a term coined to describe diabetes mellitus arising as a result of glucocorticoid use for more than 50 years
3. How can this adversely affect the prognosis of the patient?
Hyperglycemia in general is indicative of a poorer prognosis in a patient compared to covid patients with normal blood glucose levels.
4. How can this transient hyperglycemia be treated to avoid complications and a bad prognosis?
Oral hypoglycemics (such as sulfonylureas) are efficient at controlling blood glucose levels in non-diabetics who develop steroid-induced hyperglycemia. Most cases revert to normoglycemia after discontinuation of steroids.
5. What is thrombophlebitis fever?
Fever in response to thrombophlebitis that is caused due to release of inflammatory mediators
6. Should the infusion be stopped in order to control the infusion thrombophlebitis? What are the alternatives?
No, infusion thrombophlebitis is not grounds for discontinuation of infusions that are essential for the treatment of the case. Thrombophlebitis can be treated by local compressive dressings, NSAIDs (topical and/or systemic)
16) Mild to moderate covid with hyperglycemia
Questions:
1. What could be the possible factors implicated in elevated glycated HB ( HBA1c ) levels in a previously Non-Diabetic covid patient?
The possible factors that could have led to precipitation of diabetes in a covid-19 patient are:
Genetic susceptibility to diabetes
Pre diabetic state
Viral insult to the beta cells of the pancreas
Stress hyperglycemia due to inflammation-induced insulin resistance
High dose steroid usage
17) Covid 19 with hypertension comorbidity
1)Does hypertension have any effect to do with the severity of the covid infection.If it is, Then how?
Yes, hypertensive patients are at a higher risk of COVID 19 severity. It is already known that hypertension is assocatied with a weaker immune system and is seen in older patients which show bad prognosis when dealing with this infection. As there is a high risk of developing cardiovascular events as well as end organ failure.
2)what is the cause for pleural effusion to occur??
Pneumonia caused due to COVID-19 infection lead to increase permeability of microvascular circulation which lead to pleural effusion(exudative type)
18) Covid 19 with mild hypoalbuminemia
QUESTIONS:
1. What is the reason for hypoalbuminemia in the patient?
The reason for hypoalbuminemia in COVID_9 patient is due to increased catabolism of albumin to make amino acids as well as simulataneous decrease in albumin synthesis( albumin is a negative acute phase reactant that means its level decrease during inflammation)
2. What could be the reason for exanthem on arms? Could it be due to covid-19 infection ?
Exanthem is an eruptive skin rash seen in viral infections. Yes, this could be due to COVID-19 infection. The exanthem in COVID-19 resembles that of varicella.
2. What is the reason for Cardiomegaly?
High blood pressure might be the underlying cause for cardiomegaly in this patient.
Uncontrolled high blood pressure leads to increase in work load of the heart. To compensate this demand, the ventricles undergo remodelling leading to cardiomegaly.
3. What other differential diagnoses could be drawn if the patient tested negative for covid infection?
· Chicken pox
· Shingles
· Pytriasis
4. Why is there elevated D-Dimer in covid infection? What other conditions show D-dimer elevation?
D-dimer is increased in a COVID-19 patient. It may be related to the viral life cycle. The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels.
20) Covid 19 with first time diabetes
Questions:
1)Can usage of steroids in diabetic Covid patients increases death rate because of the adverse effects of steroids???
COVID-19 infection causes systemic inflammation and cytokine storm. In order to prevent these severe conditions steroids are used.
A well-known adverse effect of steroid usage is the disruption in carbohydrate metabolism. It leads to hyperglycemia. When steroids are given to a diabetic COVID-19 patient utmost care must be taken. The patient should be shifted from oral anti diabetic drugs to s.c. insulin and blood sugars should be closely monitored. If possible, Tocilizumab should be used instead of steroids.
Steroid usage in diabetic patient has shown a increase in death rate as it further decreases the immunity of the patient and make them prone to other opportunistic infections like mucormycosis leadth to inceased death rate.
2)Why many COVID patients are dying because of stroke though blood thinners are given prophylactically?
In COVID-19 infection due to systemic inflammation and cytokine storm even when they are adequately managed, ae leading to damage of inner walls of small blood vessels of the brain. These blood vessels have very little or no collateral blood supply.
Even though the patient is on blood thinners they cannot prevent this damage. When the blood viscocity becomes higher either due to dehydration or high LDL/cholesterol levels, these small blood vessels are blocked leading to stroke.
3)Does chronic alcoholism have effect on the out come of Covid infection?If yes,how?
Yes, chronic alcoholism does worsen the prognosis of COVID-19 patient.
One of the adverse effect of chronic alcoholism is its ill effect on innate as well as adaptive immunity.
Reduced resistance to COVID-19 promotes progression of disease and leading to wrose prognosis
21) Severe Covid with Diabetes
Questions-
1. What can be the causes of early progression and aggressive disease(Covid) among diabetics when compared to non diabetics?
it is observed that there is a early as well as aggressive progression of COVID 19 in diabetics. This is attributed to interactions of several risk factors as well as hyperglycemia which is seen in diabetic patients. It modulates immune response as well as inflammatory responses thus predisposing individuals to lethal course of the disease.
2. In a patient with diabetes and steroid use what treatment regimen would improve the chances of recovery?
methylprednisolone from 40 mg/day to 160 mg/day for 6 days according to the weight and status of the patients. During this course of treatment, blood sugar should be closely monitored and patient should be shifted from oral anti diabetic drugs to insulin.
3. What effect does a history of CVA have on COVID prognosis?
It is established that COVID-19 is associated with coagulopathy. In a patient who has a history of CVA are mostly old and have other co-morbidities which leads to severe course of the disease as well as poor prognosis.
23) Covid 19 with multiple comorbidities:
1) What do you think are the factors in this patient that are contributing to his increased severity of symptoms and infection?
· Old age
· Diabetes mellitus type 2
· Chronic kidney disease
· Bronchial asthama
2) Can you explain why the D dimer levels are increasing in this patient?
It may be related to the viral life cycle. The apoptotic processes target the endothelial cells of the vasculature resulting in triggered coagulopathy and ultimately result in increased d-dimer levels
3) What were the treatment options taken up with falling oxygen saturation?
· Head elevation
· O2 supplementation
4) Can you think of an appropriate explanation as to why the patient has developed CKD, 2 years ago? (Note: Despite being on anti diabetic medication, there was no regular monitoring of blood sugar levels and hence no way to know for sure if it was being controlled or not)
During the early stage diabetes, there is a increase in blood flow to the kidneys, which strains the glomeruli and lessenstheir ability to filter blood. High levels of glucose in the blood leads to accumulation of extra material in glomeruli. It increases the stress of glomeruli inturn leading to gradual and progressive scarring. Eventually leads to the development of CKD
QUESTION 10:
Experiential learning is a very important method of Medical education and while the E logs of the students in the questions above represent partly their and their patient's experiences, reflective logging of one's own experiences is a vital tool toward competency development in medical education and research. A sample answer to this last assignment around sharing your experience log of the month can be seen in the link below but while this is by a student onsite in hospital and not locked down at home we would be very interested to learn about your telemedical learning experiences from our hospital as well as community patients over the last month even while locked down at home: https://onedrive.live.com/view.aspx?resid=4EF578BAE67BA469!4180&ithint=file%2cdocx&authkey=!AOy7BpRTn42DBM
6th may: previous elogs of our senior batch were shared with us. they gave us an idea of how to do elogs
8th may : covid patient updates were shared along with the CT scan and x ray finding and other investigations which were done. the treatment plan was also discussed .
10th may : a case of liver abscess was discussed
21/M student occasional toddy drinker Came with
H/o pain in the epigastrium & right hypochondrium , loss of appetite & fever from 20 days - diagnosed as liver abscess & got treated outside.
In spite of he was having intermittent pain & fever for which he came to our hospital.
O/E:
Pt C/C/C,PR: 82 bpm, BP: 110/70 mmhg
CVS: S1 S2 + , no murmurs,RS: BAE+ , NVBS
P/A: Soft , NT ,CNS: NFND
Dx:
Liver abscess (segment VII of right lobe with 50 to 60% liquefaction)
And our doubts regarding treatment protocols of Covid were clarified, this discussion helped to clear a lot of doubts regarding Covid treatment.
May 11: the following case was discussed in a great detail
67yrs female
Diagnosis-Viral pnemonia secondary to COVID-19, HTN, HYPOTHYROIDISM, CENTRAL OBESITY, CVA
She was having hypersomnolence in the day time during yesterday's morning rounds.
Later her son told me she had phoned them at 3:00 AM yesterday complaining that there was a man here who was threatening to take her away by morning. We checked the CCTV footage during that time yesterday and didn't find anyone near her bed except she did appear to wake up sometime around that time and was on the phone.
With this case I have understood the neuropsychiatric aspects of COVID .
May 12:updates of Covid cases were given
May 13: an interesting case of 8 year old boy with frequent micturition was discussed
May 14 : differential diagnosis for a 78 year old Male with pericardial effusion was discussed
May 15; a case of ICU psychosis with Covid infection has been discussed
https://jahnavichatla.blogspot.com/2021/05/covid-case-discussion.html
May 16: Covid cases updates where given.
May 17: 2 cardiology cases where discussed along with their elogs.
May 18: a case of pericarditis with moderate pericardial effusion and a case of pneumonia secondary to covid infection was discussed.
May 19: A case of DKA with metabolic acidosis with k/c/o Type -1 diabetes and A case of Acute CVA with Acute infarct in right inferior cerebellar hemisphere were discussed
May 20:discussion on few cases of pneumonia secondary to covid.
May 21: a case of cerebellar ataxia and a case of altered sensorium (wernicke's encephalopathy) secondary to alchohol withdrawl delerium were discussed.
May 23: we were allotted few cases and questions as a assignment.
During this week,While reading the cases and understanding the pathology and pharmacological and non pharmacological interventions
It was a whole new experience.
All thanks to Rakesh biswas sir and post graduates ,interns ,medicine department for making us to learn in such a effective and healthy way.
