MEDICINE BLENDED ASSIGNMENT
May 24,2021
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, investigation, and diagnosis, and come up with the treatment plan.
This is the link of questions asked regarding the cases:
http://medicinedepartment.blogspot.com/2021/05/online-blended-bimonthly-assignment.html?m=1
Below are my answers to the medicine assignment based on my comprehension of the cases.
PULMONOLOGY CASE
A 55-YEAR-OLD FEMALE WITH SHORTNESS OF BREATH
Name B. sowjanya
Roll no.:129
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 problem?
1Ans)Evolution of symptomatology
1st episode of sob - 20 yr back
2nd episode of sob - 12 yr back
From then she has been having yearly episodes for the past 12 yrs
Diagnosed with diabetes - 8yrs back
Anemia and took iron injections - 5yr ago
Generalized weakness - 1 month back
Diagnosed with hypertension - 20 days back
Pedal edema - 15 days back
Facial puffiness- 15 yrs back
Anatomical location of the problem - lungs
Primary etiology of patient- usage of chulha since 20 yrs might be due to chronic usage
2Q)what r the mechanism of action indication and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
2Ans)~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
Bipap: a noninvasive method
#MOA: assist ventilation by delivering positive expiratory and inspiratory pressure without the need for ET incubation9
3. Cause for current acute exacerbation - it could be due to any infection
4.could the ATT affected her symptoms if so how?
Yes ATT affected her symptoms
Isoniazid and rifampicin -nephrotoxic - raised RFT was seen
NEUROLOGY:
CASE: A
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.
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?
Ans: 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?
Ans: 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 normocytic anemia?
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 theimmune system is weak due to the affect on blood cells formation and iron absorption.due to this healing of an ulcer dampens.
NEUROLOGY CASE:B
A 52-YEAR-OLD MALE WITH CEREBELLAR ATAXIA
Name :B.sowjanya
Roll no.:129
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?
ANS. The timeline of the patient is as follows-
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- The 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, nonbilious 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 coordination 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 coordination)
Many conditions cause cerebellar ataxia- Head trauma, Alcohol abuse, certain medications eg. Barbituates, stroke, tumors, 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 blockage 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 is the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
ANS.
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 patient's history of giddiness and balance issues.
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.
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 antiplatelet medications and in this case used to prevent the formation of blood clots in blood vessels and prevent stroke.
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 the 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 the primary prevention of stroke.
E) Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP-mediated platelet aggregation by blocking the P2Y12 receptor on the platelets.
Indications- In this case, it decreases the risk of heart disease and stroke by preventing clotting
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 Wernicke's encephalopathy- which can lead to confusion, ataxia and ophthalmoplegia.
G) Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.
3) Did the patient's history of denovo hypertension contribute to his current condition?
ANS. 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 patient's history of alcoholism make him more susceptible to ischaemic or hemorrhagic stroke?
ANS. Meta-analysis of the relation between alcohol consumption and increased risk of stroke has mainly weighed into the formation of two types- ischaemic and hemorrhagic 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
Hemorrhagic stroke- occurs when an aneurysm bursts or when a weakened blood vessel leaks, thus causing cerebral hemorrhage
According to a Cambridge study, heavy drinkers have 1.6 more chance of intracerebral hemorrhage and a 1.8 increased chance of subarachnoid hemorrhage. The adverse effect on BP that is seen due to increased drinking is a major stroke risk factor and increases 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.
NEUROLOGY CASE:C
A 45-YEAR-OLD FEMALE PATIENT WITH PALPITATIONS,PEDAL EDEMA ,RADIATING PAIN ALONG LEFT UPPER LIMB
Name:B.sowjanya
Roll no.: 129
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?
10 years back-Paralysis of both upper and lower limbs bilateral
1-year back-Right and left paresis due to hypokalemia
8 months back swelling over legs
7 months back - blood infection
2 months back- neck pain
6 days back- pain along left upper limb
5 days back- chest pain, Difficulty in breathing and was able to feel her own heart beat
Anatomical localization: Cervical spine
degenerative changes that occur in the cervical spine with age.
Dehydrated disks. Disks act like cushions between the vertebrae of your spine. By the age of 40, most people's spinal disks begin drying out and shrinking, which allows more bone-on-bone contact between the vertebrae.
Bone spurs. Disk degeneration often results in the spine producing extra amounts of bone in a misguided effort to strengthen the spine. These bone spurs can sometimes pinch the spinal cord and nerve roots.
Herniated disks. Age also affects the exterior of your spinal disks. Cracks often appear, leading to bulging (herniated) disks — which sometimes can press on the spinal cord and nerve roots.
Stiff ligaments. Ligaments are cords of tissue that connect bone to bone. Spinal ligaments can stiffen with age, making your neck less flexible.
2) What are the reasons for the recurrence of hypokalemia in her? Important risk factors for her hypokalemia?
Reasons for recurrence
The primary hypokalemic periodic paralysis is autosomal dominant and is exacerbated by strenuous exercise, a high carbohydrate diet, cold, and excitement, which was not found in this case. secondary periodic hypokalemic paralysis has been reported in association with gastroenteritis, diuretic abuse, renal tubular acidosis, Bartter syndrome, villous adenoma of the colon, and hyperthyroidism.
Risk factors
Female [1] [2]
Medications like diuretics
Heart failure
Hypertension
Low BMI [3]
Eating disorder and alcoholism: low intake of potassium
Diarrhea, Cushing syndrome,
3) What are the changes seen in ECG in case of hypokalemia and associated symptoms?
ECG changes include flattening and inversion of T waves in mild hypokalemia, followed by Q-T interval prolongation, visible U wave and mild ST depression4 in more severe hypokalemia.
NEUROLOGY CASE :D
A 55-YEAR-OLD PATIENT WITH SEIZURES
Name :B.sowjanya
Roll no.:129
1.Is there any relationship between the occurrence of seizure to brain stroke. If yes what is the mechanism behind it?
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 hemorrhagic strokes are thought to be attributable to irritation due to (hemosiderin. Deposits)caused by-products of blood metabolism
Late-onset seizures are associated with persistent changes in neuronal excitability and gliotic scarring is most probably the underlying cause.
2. In the previous episodes of seizures, the patient didn't lose 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)
NEUROLOGY CASE :E
A 48-YEAR-OLD MALE WITH SEIZURES
Name:B.sowjanya
Roll no.:129
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
Ans: the reason for a patient develop ataxia in past year is ALCOHOL
The toxic effects of alcohol are diverse. Alcohol-related cerebellar degeneration is one of the commonest causes of acquired cerebellar ataxia(ALCOHOL INDUCED TOXIC ATAXIA).
The pathophysiology remains unclear but proposed mechanisms include excitotoxicity, dietary factors, oxidative stress, compromised energy production and cell death
2) What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses?
Ans: the reason for IC bleed is
CHRONIC ALCOHOL CONSUMPTION
↓
ALCOHOL-INDUCED TOXIC ATAXIA
↓
REPEATED FALLS
↓
IC BLEEDING
* The impaired platelet function, together with the reduced platelet count, may contribute to the bleeding diathesis associated with chronic alcoholism and to the increased incidence and recurrence of gastrointestinal hemorrhage associated with excessive alcohol intake.
NEUROLOGY CASE: F
A 30 yr old male patient with weakness of right upper limb and lower limb
name: B. sowjanya
roll no.:129
A 30-year-old male patient lorry driver by occupation came to the opd with chief complaints of
1) weakness of right upper limb and lower limb
2)deviation of the mouth towards left since one day
1) does the patient's history of road traffic accidents have any role in his present situation?
Ans: The patient has an ischemic cerebrovascular accident which is caused due to his stressful conditions and the lipid profile which has high LDL levels and low HDL levels--leading to narrowing of the middle cerebral artery. the history of the accident has no role in his present situation.
2)what are the warning signs of a cerebrovascular accident?
1) sudden numbness or weakness of the face, arm leg, especially on one side of the body
2)sudden confusion, trouble speaking or understanding
3)sudden trouble seeing
4)sudden trouble walking, dizziness, loss of balance
5)sudden, severe headache with no known cause.
3)what is the drug rationale in CVA?
Ans :Mannitol: osmotic diuretic, decreases the intracranial pressure
phenytoin: antiepileptic
monocef: antibiotic
amlodipine: AntiHTN
citicoline:neuroprotective
aspirin: antiplatelet
Atorvastatin: antihyperlipidemic
4)Does alcohol has any role in his attack?
Ans: As the patient is daily drinker alcohol has a synergistic effect on worsening the ischemia due to liver damage, which decreases the production of substances that reduce the effect.
5)does his lipid profile have any role in his attack?
Ans: the patient has high LDL levels and low HDL levels which have to lead to narrowing middle cerebral artery.
NEUROLOGY CASE: G
A 50-year-old patient with cervical myelopathy
A 50-year-old male patient presented to the hospital with complaints of weakness of all four limbs since 8pm.
No h/o slurring of speech.
No h/o fever.
1)what is myelopathy hand?
Ans: The loss of power of adduction and extension of ulnar two or three fingers and an inability to grip and release with these fingers.
2)what is finger escape?
Ans: hold fingers adducted and extended.
Small and ring fingers fall into flexion abduction, usually within 30 seconds.
3) what is Hoffman's reflex?
Ans: Hoffman's reflex is a neurological examination finding elicited by a reflex test that can help verify the presence or absence of issues arising from the corticospinal tract.
Procedure: it involves loosely holding the middle finger and flicking the fingernail downward, allowing the middle finger to flick upward reflexively. A positive response is seen when there is flexion and adduction of the thumb on the same hand.
NEUROLOGY CASE: H
A 17-year-old female with seizures
Name B.sowjanya
roll no.:129
1)what can be the cause of the condition?
Ans: It is due to iron deficiency anemia.As iron is an important regulator of of thrombopoiesis, low iron levels disinhibit megakaryocyte activity ,which provokes secondary thrombocytosis,thus leading to a hypercoagulable state .in addition,microcytosis alters red cells deformability ,which increases viscosity and possibly the risk of venous thrombosis.
2)What are the risk factors for CVT?
Ans:Inherited risk factors:factor v leiden mutation ,prothrombin gene mutation ,protein c deficiency,antithrombin deficiency ,homocysteniemia,dysfibrogenemia.
acquired disorders:malignancy ,surgery, trauma ,iron deficiency anemia,pregnancy ,OCP'S,CHF,nephrotic syndrome,HIV ,HRT ,APLA,PNH.
3)There was a seizure-free period in between but again suddenly an episode of GTCS why? resolved spontaneously why?
Ans: there was a seizure-free period due to the administration of antiepileptic drugs as the effect of drugs weans off the seizures appear again followed by administration of phenobarbitone leading to spontaneous resolution of the seizures.
4)What drug was used in suspicion of CVST?
Ans: A diagnosis of a drug (norethisterone enanthate)- induced CVST was considered.
3) CARDIOLOGY
CASE: A
A 78-YEAR-OLD MALE WITH SHORTNESS OF BREATH,CHEST PAIN ,B/L PEDAL EDEMA AND FACIAL PUFFINESS
Name : B.sowjanya
Roll no. :129
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
Ans: Preserved ejection fraction (HFpEF) – 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 (HFrEF) – also referred to as systolic heart failure
HFpEF is preceded by chronic comorbidities, such as hypertension, type 2 diabetes mellitus (T2DM), obesity, and renal insufficiency, whereas HFrEF is often preceded by the acute or chronic loss of cardiomyocytes due to ischemia, a genetic mutation, myocarditis, or valvular disease
2.Why haven't we done pericardiocentesis in this patient?
Ans: Pericardiocentesis is not done here Because the effusion was self-healing, It reduced from 2.4cm to 1.9 cm.
3.What are the risk factors for the development of heart failure in the patient?
Ans: risk factors for the development of heart failure in this patent
Alcohol abuse increases the risk of atrial fibrillation, heart attack, and congestive heart failure
high blood pressure
Smoking
Diabetes
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
Ans: visceral pericardium may have thickened which is restricting the heart to expand causing hypotension
(Maybe secondary to TB)
CARDIOLOGY CASE:B
A 73-YEAR-OLD MALE PATIENT WITH PEDAL EDEMA, SHORTNESS BREATH, AND DECREASED URINE OUTPUT
Name :B .sowjanya
Roll no.:129
1) What are the possible causes of heart failure in this patient?
the patient has various comorbidities which could have led to a heart failure
1. The patient was diagnosed with type 2 diabetes mellitus 30 years ago and has been taking human mix trad insulin daily and was also diagnosed with diabetic triopathy indicating uncontrolled diabetes which is a major risk factor for heart failure
2. The patient has also diagnosed with hypertension 19 yrs. ago which is also a risk factor for heart failure
3. He is a chronic alcoholic since 40 years which is a risk factor for heart failure
The findings in this article provide longitudinal evidence that moderate and heavy alcohol consumption are associated with decreased LVEF and trend towards a higher risk of incident LV systolic dysfunction, compared to light drinkers.
4. The patient has elevated creatinine and AST/ALT ratios is >2 and was diagnosed with chronic kidney disease stage IV. CKD is also one of the risk factors for heart failure
2) what is the reason for anemia in this case?
The patient has normocytic normochromic anemia. it could be anemia of chronic disease as the patient is diagnosed with CKD stage IV.
Chronic kidney disease results in decreased production of erythropoietin which in turn decreases the production of red blood cells from the bone marrow.
Patient’s with anemia and CKD also tend to have a deficiency in nutrients like iron, vitamin B12, and folic acid essential in making healthy red blood cells
3) What is the reason for blebs and non-healing ulcers in the legs of this patient?
The most common cause for blebs and non-healing ulcers in this patient is diabetes mellitus. CKD is also known to cause a delay in the healing of wounds along with poorly controlled diabetes. Anemia can also slow down the process of healing due to low oxygen levels.
4) What sequence of stages of diabetes has been noted in this patient?
There are 4 stages in type 2 diabetes- insulin resistance, prediabetes, type 2 diabetes, and type 2 diabetes and vascular complications, including retinopathy, nephropathy or neuropathy, and, or, related microvascular events.
The patient is diagnosed with diabetic triopathy exhibiting a sequence of neuropathy, retinopathy, and nephropathy
The patient has been diagnosed with diabetic retinopathy, CKD stage IV, and shows signs of diabetic neuropathy such as numbness
CARDIOLOGY CASE:C
AFIB AND BIATRIAL THROMBUS IN A 52-YEAR-OLD MALE
Name:B.sowjanya
Roll no.:129
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: *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 the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Ans: PHARMACOLOGICAL INTERVENTIONS
1. TAB. Dytor
mechanism: Through its action in antagonizing the effect of aldosterone, spironolactone inhibits the exchange of sodium for potassium in the distal renal tubule and helps to prevent potassium loss.
2. TAB. Acitrom
mechanism: Acenocoumarol inhibits the action of an enzyme Vitamin K-epoxide reductase which is required for regeneration and maintaining levels of vitamin K required for blood clotting
3. TAB. Cardivas
mechanism:Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol belongs to a class of drugs known as alpha and beta-blockers.
4. INJ. HAI S/C
MECHANISM:Regulates glucose metabolism
Insulin and its analogues lower blood glucose by stimulating peripheral glucose uptake, especially by skeletal muscle and fat, and by inhibiting hepatic glucose production; insulin inhibits lipolysis and proteolysis and enhances protein synthesis; targets include skeletal muscle, liver, and adipose tissue
5.TAB. Digoxin
mechanism:
Digoxin has two principal mechanisms of action which are selectively employed depending on the indication:
Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump,
an enzyme that controls the movement of ions into the heart.
6. Hypoglycemia symptoms explained
7. Watch for any bleeding manifestations like Petechiae, Bleeding gums.
8. APTT and INR are ordered on a regular basis when a person is taking the anticoagulant drug warfarin to make sure that the drug is producing the desired effect.
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans: *cardiorenal syndrome type 4 is seen in this patient.
CARDIOLOGY CASE :D
A 67 old patient with acute coronary syndrome
Name B. sowjanya
ROll no.:129
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?
TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heartburn like episodes since a year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed a full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Shortness of breath for half an hour-SOB even at rest
Anatomical localization - 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)
2) What is the mechanism of action, indication, and efficacy over placebo of each of the pharmacological and nonpharmacological interventions used for this patient?
Pharmacological interventions:
TAB MET XL 25 MG/STAT contains Metoprolol as the 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).
3) What are the indications and contraindications for PCI?
INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
High risk stress test findings.
CONTRAINDICATIONS:
Intolerance for oral antiplatelets long-term.
Absence of cardiac surgery backup.
Hypercoagulable state.
High-grade chronic kidney disease.
Chronic total occlusion of SVG.
An artery with a diameter of <1.5 mm.
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
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.
CARDIOLOGY CASE:E
ACUTE MYOCARDIAL INFARCTION
Name : B . sowjanya
Roll no. :129
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans: *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
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 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.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
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.
4)GASTROENTEROLOGY CASE:A
A 33 YEAR OLD MAN WITH PANCREATITIS ,PSEUDOCYST AND LEFT BRONCHO PLEURAL FISTULA
Name :B. Sowjanya
Roll no.:129
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?
A: *anatomical location of etiology is pancreas(ductal obstruction, acinar cell injury, defective intracellular transport)
*The pathophysiology of acute pancreatitis is characterized by a loss of intracellular and extracellular compartmentation, by an obstruction of pancreatic secretory transport, and by activation of pancreatic enzymes Attributed to alcohol
2) What is the efficacy of drugs used along with other nonpharmacological treatment modalities and how would you approach this patient as a treating physician?
PHARMACOLOGICAL INTERVENTIONS
1) ING. MEROPENEM
mechanism:Meropenem is bactericidal except against Listeria monocytogenes, where it is bacteriostatic. It inhibits bacterial cell wall synthesis like other β-lactam antibiotics. In contrast to other beta-lactam, it is highly resistant to degradation by β-lactamases or cephalosporinases.
2) ING. METROGYL
mechanism: Metronidazole diffuses into the organism, inhibits protein synthesis by interacting with DNA, and causing a loss of helical DNA structure and strand breakage. Therefore, it causes cell death in susceptible organisms.
3) ING. AMIKACIN
mechanism: the primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth.
4) TPN ( Total Parenteral Nutrition )
mechanism: the early administration of enteral nutrition must be the standard therapeutic approach in patients with severe acute pancreatitis it decreases the risk of infection; TPN is only required in a few patients.
5) IV NS / RL
mechanism: Patients with acute pancreatitis lose a large number of fluids to third spacing into the retroperitoneum and intra-abdominal areas. Accordingly, they require prompt intravenous (IV) hydration within the first 24 hours. Especially in the early phase of the illness, aggressive fluid resuscitation is critically important.
6) ING. OCTREOTIDE
mechanism:
Like somatostatin, octreotide also decreases the release of growth-stimulating hormones, decreases blood flow to the digestive organs, and inhibits the release of digestive hormones such as serotonin, gastrin, vasoactive intestinal peptide, secretin, motilin, and pancreatic polypeptide.
Octreotide is useful in overdose management of sulfonylurea-type hypoglycemic medications, when recurrent or refractory to parenteral dextrose. The mechanism of action is the suppression of insulin secretion.
7) ING. PANTOP
mechanism: The mechanism of action of pantoprazole is to 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. The covalent binding prevents acid secretion for up to 24 hours and longer.
8) ING. THIAMINE
mechanism: Vitamin B1 (thiamin) is indispensable for the normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining a normal cellular redox state.
9) ING. TRAMADOL
mechanism: Tramadol is a centrally acting analgesic with a multimode of action. It acts on serotonergic and noradrenergic nociception, while its metabolite O-desmethyl tramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one-tenth that of morphine
GASTROENTEROLOGY CASE:B.
A CASE OF 25 YEAR OLD MAN WITH SEVERE EPIGASTRIC PAIN
Name :B.sowjanya
Roll no.:129
1) What is causing the patient's dyspnea? How is it related to pancreatitis
1ans: the cause of dyspnea might be PLEURAL EFFUSION
2) Name possible reasons why the patient has developed a state of hyperglycemia
2 and:*This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress
* the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells
* elevated levels of catecholamines and cortisol
3) What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
A: 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.
4) What is the line of treatment in this patient?
For the master chart to the "pancreatitis thesis project" please get in touch with Dr Shashikala PGY1 and Dr Divya PGY2 and share their insights into the above project problem they are working on.
A: 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
GASTROENTEROLOGY CASE:C
A 45 YEAR OLD FEMALE PATIENT WITH FEVER ,PAIN ,ABDOMEN ,DECRESED URINE OUTPUT AND ABDOMINAL EXTENSION
Name:B.sowjanya
Roll no.:129
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
NEPHROLOGY CASE:A
POST TURP WITH NON OLIGURIA ATN CASE
NAME :B.SOWJANYA 8SEM
ROLL NO. :129
A 52 yr old male patient who is a farmer by occupation . Presented to hospital with chief complaints of :
sob since 4 days
burning micturition since 4 days.
fever sine 2 days .
QUESTIONS :
1)WHAT COULD BE THE REASON OF HIS SOB?
ANS:i)The high levels of creatinine and low levels of sodium levels indicate the kidney failure due to hydroureteronephrosis.
ii)the acute kidney failure alters the homeostasis fluid balance ,acid base balance and vascular tone .
iii)This leads to increasing pulmonary vascular permeability
iv)which causes pilmonary edema,it causes shortness of breath.
2)WHY DOES HE HAVE INTERMITTENT EPISODES OF DROWSINESS?
ANS:The hyponatremia is caused due to the absortion of irrigants, glycine,sorbitol,or mannitol contained in nonconducting flushing solutions used for the transurethral resection of the prostrate .the symptoms of hyponatremia is drowsiness and lethargy .
3)WHY DID HE COMPLAINTS OF FLESHYMASS LIKE PASSAGE IN URINE?
ANS:On bilateral incomplete obstruction of urinary tract leads to polyuria insted of anuria caused in a case of complete obstrction .As the patient is aknown case of diabetic and undergone transurethral resection of prostrate . The surgery of prostrate have caused thickening of walls of urinary bladder as a complication which lead to obstruction of flow of urine .due to forced backflow of urine causes pressure destruction of renal parenchyma leading to enlargement of renal pelvis and calcus and atropy of renal cortex.As the obstruction is incomplete the fleshymass is the destructed renal parenchyma due to diabetic nephropathy and hydroureternephrosis.
4)what are the complications of turp that he may had?
ANS :i)urinary tract infection:which lead to burning micturition and high grade fever.
ii)hyponatremia
iii)obstruction to the flow of urine.
NEPHROLOGY CASE:B
AN 8-YEAR-OLD BOY WITH FREQUENT URINATION
Name B.sowjanya
Roll no.:129
The informant is the mother, who complained that her son urinates frequently i.e, about 25 times /day.
1) why is the child excessively hyperactive without much social etiquette?
Ans: From the history of excessive hyperactivity, impulsiveness, lacking attentivity,a thought goes towards attention deficit hyperactivity and in association urination disorders.
2)Why doesn't the child have excessive urination at night time?
Ans: since the child does not get the urge to urinate when he is asleep, there can be a chance of manifestation being psychosomatic, or as a result of an undiagnosed anxiety disorder.
3)How would you want to manage the patient to relieve him of his symptoms?
Ans: daytime overactive bladder is a common pediatric problem that usually resolves over time which usually resolves over time with reassurance and relaxation and behavioral therapy.
INFECTIOUS DISEASE (HIV VIRUS ,MYCOBACTERIA,GASTEROENTEROLOGY,PULMONOLOGY) CASE:A
A 40 YEAR OLD LADY WITH DYSPHAGIA ,FEVER AND COUGH
Name :B.sowjanya
Roll no.:129
1.Which clinical history and physical findings are characteristic of tracheo esophageal fistula
1 ans:clinical history and physical finding in this paient that suggest tracheoesophageal fistula is that ,Cough occurs on taking food and liquids
(which was initially non productive then associated with sputum which is white in color , moderate in quantity and non foul smelling)
2) What are the chances of this patient developing immune reconstitution inflammatory syndrome? Can we prevent
2 ans: Immune reconstitution inflammatory syndrome (IRIS) occurs in two forms:
"unmasking" IRIS refers to the flare-up of an underlying, previously undiagnosed infection soon after antiretroviral therapy (ART) is started;
"paradoxical" IRIS refers to the worsening of a previously treated infection after ART is started.
*Patients with mycobacterial disease at the time of initiation of ART are at higher risk of developing IRIS with an approximate risk of 15%. Patients originating from endemic areas for tuberculosis and cryptococcal disease are at higher risk of developing IRIS.
How can immune reconstitution inflammatory syndrome be prevented?
*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.
INFECTIOUS DISEASE AND HEPATOLOGY CASE:A
LIVER ABCESS
Name : B . sowjanya
Roll no.:129
Liver abscess
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?
1ans- yes, it could be due to intake of contaminated toddy
2Q)what is the etiopathogenesis of liver abscess in a chronic alcoholic patient?(since 30 yrs - 1 bottle/day)
2ans - 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?
3ans-yes right lobe is involved due to its moreblood supply
4Q) what are the indications for USG guided aspiration of liver abscess?
4ans- 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
INFECTIOUS DISEASE AND HEPATOLOGYCASE:B
LIVER ABSCESS
Name :B.sowjanya
Roll no.:129
1) Cause of liver abscess in this patient?
1ans: cause of liver abscess in this patient is ENTAMOEBA histolytica
2) How do you approach this patient?
2 and: APPROACH IN THE PATIENT OF AMOEBIC LIVER ABCESS
3) Why do we treat here; both amoebic and pyogenic liver abscess?
3ans: we treat the patient for both amoebic and pyogenic abscess so that we don't rely only on anti-amebic therapy and ensure complete treatment of the cause
4) Is there a way to confirm the definitive diagnosis in this patient?
4 ans: the confirmatory test for an amoebic abscess is
*Serologic testing is the most widely used method of diagnosis for amebic liver abscesses. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).
*The diagnosis of the amebic liver abscess was based on four or more of the following criteria:
(i) a space-occupying lesion in the liver diagnosed by ultrasonography and suggestive of abscess,
(ii) clinical symptoms (fever, pain in the right hypochondrium (often referred to the epigastrium), lower chest, back, or tip of the right shoulder),
(iii) enlarged and/or tender liver, usually without jaundice,
(iv) raised right dome of the diaphragm on chest radiograph, and
(v) improvement after treatment with antiamebic drugs (e.g., metronidazole)
INFECTIOUS DISEASE(MUCORMYCOSIS,OPTHALMOLOGY,OTORHINOLARNGOLOGY,NEUROLOGY) CASE:A
A 50 YEAR OLD MALE CAME WITH ALTERED SENSORIUM
Name:B . sowjanya
Roll no.: 129
QUESTION: 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?
1. 3 years ago- diagnosed with hypertension
2. 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
3. 18 days ago- complained of similar events and went to the local hospital, it was not subsided upon taking medication(antipyretics)
4. 11 days ago - c/o Generalized weakness and facial puffiness and periorbital edema. The patient was in a drowsy state
5. 4 days ago-
a. patient presented to casualty in an altered state with facial puffiness and periorbital edema and weakness of right upper limb and lower limb
b. towards the evening patient periorbital edema progressed
c. serous discharge from the left eye that was blood-tinged
d. was diagnosed with diabetes mellitus
6. patient was referred to a government general hospital
7. patient died 2 days ago
the 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
QUESTION: 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 was –
1. inj. Liposomal amphotericin B according to creatinine clearance
2. 200mg Iitraconazole was given as it was the only available drug that was adjusted to his creatinine clearance
3. Deoxycholate was the required drug which was unavailable
https://pubmed.ncbi.nlm.nih.gov/23729001/ 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-
I. Management of diabetic ketoacidosis –
(a) Fluid replacement- The fluids will replace those lost through excessive urination, as well as help dilute the excess sugar in the blood.
(b) Electrolyte replacement-The absence of insulin can lower the level of several electrolytes in blood. The patient will receive electrolytes through a vein to help keep the heart, muscles and nerve cells functioning normally.
(c) Insulin therapy- Insulin reverses the processes that cause diabetic ketoacidosis. In addition to fluids and electrolytes, the patient will receive insulin therapy
QUESTION: What are the postulated reasons for a sudden apparent rise in the incidence of mucormycosis in India at this point in time?
Mucormycosis is maybe 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
INFECTIOUS DISEASE(COVID 19)
COVID CASE 1
1) How does the pre-existing ILD determine the prognosis of this patient?
In patients with preexisting ILD, COVID-19 infection has led to acute exacerbation of underlying ILD. The criteria for ILD exacerbation include subacute worsening of dyspnea and hypoxemia, new pulmonary infiltrates on imaging, and absence of pulmonary emboli, cardiac failure, and other non-pulmonary causes. .Thus it leads to a poor prognosis
2) Given the history of autoimmune disease in the patient, how does the administration of steroids for COVID affect her RA and hypothyroidism?
Corticosteroids are the cornerstone of for managing disease flares and for initial treatment of RA
It is identified glucocorticoids as a significant risk factor for bacterial infections. Glucocorticoid use doubled the rate of serious bacterial infections in a dose-dependent manner as compared with methotrexate
It is concluded that there is no evidence to support its use in COVID-19, and it may in fact lead to more harm than good
3) Would this patient have an increased risk for post covid autoimmune response compared to patients without a history of autoimmune disease?
In Covid, lymphoplasmacytic cell infiltrates are involved (mainly at the lung level), as well as the expression of pro-inflammatory cytokines such as interleukin (IL) IL-1, IL-6, IL-17, and TNF-α, and markers of systemic inflammation such as C-reactive protein or ferritin [34]. Parallelism of events was found with RA, where there are similar infiltrates at the synovial level, with the expression of the same group of proinflammatory cytokines and elevation of acute-phase reactants [35]. However, this route is unlikely, given that there has been no increase in exacerbations of RA patients concomitantly suffering from COVID-19
4) Why was she prescribed clexane (enoxaparin)?
Clexane 60mg Injection is an anticoagulant used to prevent and treat harmful blood clots. It stops the existing clots from getting any bigger and restricts the formation of any new clot. It is also helpful in the prevention of blood clots in veins, a condition called deep vein thrombosis, and pulmonary embolism.
COVID CASE 2
1) Since the patient didn't show any previous characteristic diabetes signs, did the Covid-19 infection aggravate any underlying condition and cause indolent diabetes to express itself? If so what could be the biochemical pathways that make it plausible?
novel coronavirus enters cell hosts through Angiotensin II Converting Enzyme receptor (ACE2).
ACE2 receptor is found in the pancreas, both on exocrine cells and in the endocrine cells, that constitute pancreatic islets. (8) Interestingly, its expression is also relevant in the endothelial cells of the microvasculature supplying beta-cells that produce insulin.
deficiency of this receptor compromises the vasculature in pancreatic islets, thus decreasing its endocrine function.
cytokine storm - caused by the severe inflammatory response taking place in the lungs - also targets the pancreas possibly causing diabetes
2) Did the patient's diabetic condition influence the progression of her pneumonia?
COVID-19 and diabetes, but no other comorbidities (n = 24), were at higher risk for severe pneumonia, the release of tissue injury-related enzymes, excessive uncontrolled inflammation responses, and hypercoagulable state associated with dysregulation of glucose metabolism when compared with patients without diabetes.
3) What is the role of D Dimer in the monitoring of covid? Does it change management or would be considered overtesting?
The D-dimer molecule is a product of the degradation of the fibrin protein. a biomarker-based evaluation that identifies the amount of ongoing coagulation at a given point of time. D-dimer has been shown to be an indicator for cardiac injury in COVID-19 patients in a setting of a prothrombotic state
D-dimer may be able to predict which COVID-19 patients have poorer outcomes.
COVID CASE 3 1. Why was this patient given noradrenaline?
noradrenaline is a medication used to treat people with very low blood pressure. Noradrenaline is a vasoconstrictor that predominantly stimulates α1 receptors to cause peripheral vasoconstriction and increase blood pressure.
It also has some β1 receptor agonist activity that results in a positive inotropic effect on the heart at higher doses.1,2
2. What is the reason behind testing for LDH levels in this patient?
LDH is an intracellular enzyme found in cells in almost all organ systems, which catalyzes the interconversion of pyruvate and lactate, with concomitant interconversion of NADH and NAD+
Lactate dehydrogenase (LDH) is one such biomarker of interest, especially since elevated LDH levels have been associated with worse outcomes in patients with other viral infections in the past
there was a >6-fold increase in odds of severe disease and a >16-fold increase in odds of mortality in patients with elevated LDH.
3. What is the reason for switching from BiPAP to mechanical ventilation with intubation in this patient? What advantages did it provide?
BiPap may not be a good option if your breathing is very poor. It may also not be right for you if you have reduced consciousness or problems swallowing
Therefore patient might have got shifted to Mechanical ventilation
Advantages of Mechanical ventilation:
The patient does not have to work as hard to breathe – their respiratory muscles rest.
The patient's as allowed time to recover in hopes that breathing becomes normal again.
Helps the patient get adequate oxygen and clears carbon dioxide.
Preserves a stable airway and preventing injury from aspiration.
COVID CASE4
4) Covid 19 Mild
Questions:
1. Is the elevated ESR due to covid related inflammation?
Erythrocyte sedimentation rate (ESR) is a blood test. It measures how quickly erythrocytes, or red blood cells, separate from a blood sample that has been treated so the blood will not clot.
The sustained high level of ESR possibly brings a negative effect on COVID-19 patients' prognosis
However, the elevation in esr cannot be explained based on the present knowledge on Covid
2. What was the reason for this patient's admission with mild covid? What are the challenges in home isolation and the harms of hospitalization?
after 14 days of isolation, he got tested again for COVID-19 which was positive. He then developed fever since 4 days, cough which was productive since 4 days, and shortness of breath grade 3 since 2 days. He also had fatigue. He lost the sense of taste and smell.
Since the patient has an SOB of grade 3. This poses a challenge for home isolation.
Patients with COVID-19 had almost 19 times the risk for acute respiratory distress syndrome (ARDS) than did patients with influenza, (adjusted risk ratio [aRR] = 18.60; 95% confidence interval [CI] = 12.40–28.00), and more than twice the risk for myocarditis (2.56; 1.17–5.59), deep vein thrombosis (2.81; 2.04–3.87), pulmonary embolism (2.10; 1.53–2.89), intracranial hemorrhage (2.85; 1.35–6.03), acute hepatitis/liver failure (3.13; 1.92–5.10), bacteremia (2.46; 1.91–3.18), and pressure ulcers (2.65; 2.14–3.27). The risks for exacerbations of asthma (0.27; 0.16–0.44) and chronic obstructive pulmonary disease (COPD) (0.37; 0.32–0.42) were lower among patients with COVID-19 than among those with influenza. The percentage of COVID-19 patients who died while hospitalized (21.0%) was more than five times that of influenza patients (3.8%), and the duration of hospitalization was almost three times longer for COVID-19 patients.
COVID CASE 5
1) What was the reason for the coma in this patient?
The patient has an spo2 of 20%. This might have lead to cerebral hypoxia thus leading to coma.
Also, low blood potassium can make you short of breath, as it can cause the heart to beat abnormally. This means less blood is pumped from your heart to the rest of your body
Thus low spo2 and thus coma
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?
Hospital 1 might not have correlated Severe weakness of 4 limbs with low values of potassium which hospital 2 has diagnosed.
Yes, coma is related to Hypokalemia periodic paralysis as it might have caused cerebral hypoxia.
3) How may covid 19 cause coma?
After cessation of sedatives, the described cases all showed a prolonged comatose state.
unconsciousness after prolonged periods of mechanical ventilation in the ICU
COVID CASE6
1. What was the cause of his altered sensorium?
Can be any of the following reasons
An altered state is any mental state(s), induced by various physiological( increased hospital stay), psychological( mental depression due to isolation), or pharmacological maneuvers or agents( drugs of COVID)
2. What was the cause of death in this patient?
This patient is an elderly chronic alcoholic and smoker.
This might have delayed his healing process thus causing death
Also, he had elevation LFT and RFT values
COVID CASE 8
1. Can psoriasis be a risk factor for a severe form of COVID?
Elderly psoriasis patients and/or patients using conventional immunosuppressive regimens and biologic agents are at higher risk for infectious diseases.
But the frequency of COVID-19 does not increase in patients using immunosuppressants, including those receiving biological therapy with a diagnosis of psoriasis
2. Can the increased use of immunomodulatory therapies cause further complications in the survivors?
According to the present knowledge on Covid, there is no indication that people taking immunomodulatory drugs for other diagnosed conditions should be concerned that their medication increases their risk for severe COVID-19,"
3. Is mechanical ventilation a risk factor for worsened fibroproliferative response in COVID survivors?
patients of Covid with greater fibrotic changes required more prolonged mechanical ventilation, and this, in turn, was associated with increased severity of systemic organ failure.
Hence Mechanical ventilation is a risk factor
COVID CASE 9
•What is the type of DM the patient has developed? (is it the incidental finding of type 2 DM or virus-induced type 1DM )?
It is most probably the type -1 diabetes, developed due to viral infection and cytokine storm-induced damage to the pancreas might have caused diabetes .!so it could be virus-induced type -1 DM
•Could it be steroid-induced Diabetes in this patient?
There is a chance for steroid-induced diabetes too but it doesn’t seem much significant when compared to virus-induced diabetes.
COVID CASE 10
What are the known factors driving early recovery in covid?
These might be the factors responsible for the early recovery of Covid:
1. Better immune response of the patient
2. Good food habits prior to And during the Covid period
3. Early detection of symptoms and thus using medication
4. Age-related (Elderly have a slow recovery than young)
5. Maintaining hygiene even after Covid infection
6. Mental strength
7. Health-related (patient with Comorbidities have slow recovery)
