Monthly assignment
Radiating pain along her left upper limb
- difficulty walking.
- dizziness.
- loss of balance and coordination.
- difficulty speaking or understanding others who are speaking.
- numbness or paralysis in the face, leg, or arm, most likely on just one side of the body.
- blurred or darkened vision
3Q What is the drug rationale in CVA?
4. Does alcohol has any role in his attack?
- Stroke
- Malformation of the cerebellum.
- Multiple sclerosis.
- Migraine or vertigo.
- Genetic or metabolic disorders.
- Brain tumor.
- Alcohol use disorder.
- Certain medications(barbiturates, such as phenobarbital; sedatives, such as benzodiazepines; antiepileptic drugs such as phenytoin; and some types of chemotherapy. Vitamin B-6 toxicity also may cause ataxia.
A) * Tab vertin8mg- This is betahistine; It 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.
Uses:used to prevent and treat nausea, vomiting, and dizziness caused by motion sickness. It may also be used to reduce dizziness and loss of balance (vertigo) caused by inner ear problems.
* 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.
* Tab Ecosprin 75mg- This is aspirin; It is an NSAID
MOA- They inhibit COX-1 and COX-2 thus decreasing the prostaglandin level and thromboxane synthesis
Indications- They are anti platelet medications and in this case used to prevent formation of blood clots in blood vessels and prevent stroke.
* Tab Atorvostatin 40mg- This is a statin
MOA- It is an HMG CoA reductase inhibitor and thus inhibits the rate limiting step in cholesterol biosynthesis. It decreases blood LDL and VLDL, decreases cholesterol synthesis, thus increasing LDL receptors in liver and increasing LDL uptake and degeneration. Hence plasma LDL level decreases.
Indications- Used to treat primary hyperlipidemias. In this case it is used for primary prevention of stroke.
* Clopidogrel 75mg- It is an antiplatelet medication
MOA- It inhibits ADP mediated platelet aggregation by blocking P2Y12 receptor on the platelets.
Indications- In this case it decreases the risk of heart disease and stroke by preventing clotting
* Thiamine- It is vitamin B1,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.
* Tab MVT- This is methylcobalamin
Mainly given in this case for vitamin B12 deficiency.D
2)Did the patients history of denovo HTN contribute to his current condition?
A) Although it is well established that hypertension is the main risk factor for stroke, the complexity of cerebrovascular problems related to hypertension is not generally appreciated.
Hypertension can cause stroke through many mechanisms:.
* A high intraluminal pressure will lead to extensive alteration in endothelium and smooth muscle function in intracerebral arteries.
* The increased stress on the endothelium can increase permeability over the blood-brain barrier and local or multifocal brain oedema.
* Endothelial damage and altered blood cell-endothelium interaction can lead to local thrombi formation and ischaemic lesions.
* Fibrinoid necrosis can cause lacunar infarcts through focal stenosis and occlusions. Degenerative changes in smooth muscle cells and endothelium predisposes for intracerebral haemorrhages.
* Furthermore, hypertension accelerates the arteriosclerotic process, thus increasing the likelihood for cerebral lesions related to stenosis and embolism originating from large extracranial vessels, the aortic arch and from the heart.
* Adaptive structural changes in the resistance vessels, while having the positive effect of reducing the vessel wall tension, have the negative consequence of increased peripheral vascular resistance that may compromise the collateral circulation and enhance the risk for ischaemic events in connection with episodes of hypotension or distal to a stenosis.
Hypertension is clearly a risk factor for vascular dementia. All the mechanisms referred to above may be important.
4) Does the patients history of alcoholism make him more susceptible to ischaemic or haemorrhagic type of stroke?
Regular heavy alcohol consumption increases the risk for ischemic stroke, whereas frequent light to moderate alcohol intake may decrease the risk.
Alcohol has been reported to precipitate vasoconstriction and rupture of small cerebral arteries in experimental animals.
Alcohol-induced neck trauma has been shown to precipitate traumatic strokes, and alcohol-induced cardiac arrhythmias have been observed in patients with embolic brain infarction
The effects of alcohol on hemostasis, fibrinolysis and blood clotting are variable and could either prevent or promote the occurrence of strokes
The antiatherogenic effects of regular light-to-moderate alcohol consumption could be mediated by inhibition of low-density lipoprotein oxidation, and by elevated estrogen levels.
Hemorrhagic Stoke occurs when there is an ruptured aneurysm which is visible on scan
CASE-6
https://neerajareddysingur.blogspot.com/2021/05/general-medicine-case-discussion.html?m=1
1Q) What can be the cause of her condition ?
Cotical vein thrombosis have caused her repeated seizures by increased venous capillary pressure
2) What are the risk factors for cortical vein thrombosis?
3)There was seizure free period in between but again sudden episode of GTCS why?resolved spontaneously why?
A) seizure free period occurs due use of medication and, which relived it
Sudden episodes of GTCS occurs due to abnormal firing of neurons.
4) What drug was used in suspicion of cortical venous sinus thrombosis?
A) Heparin should be considered seriously in the management of cerebral venous thrombosis (CVT), with subsequent conversion to warfarin as maintenance therapy suggested. Subcutaneous low ̶ molecular-weight heparin (Lovenox) also has been used in patients with venous sinus thrombosis.
CASE-7
https://nikhilasampathkumar.blogspot.com/2021/05/a-48-year-old-male-with-seizures-and.html?m=1
1) What could have been the reason for this patient to develop ataxia in the past 1 year?
A) chronic alcoholism would lead to development of chronic cerebellar syndrome, characterised by weakness, incoordination, unsteadiness of gait(ataxia)
Later minor incoordination and tremors in arms, dysarthria, intermittent diplopia
2Q)What was the reason for his IC bleed? Does Alcoholism contribute to bleeding diatheses ?
Reason for IC Bleed:
heavy drinkers were about 1.6 times more likely to suffer from intracerebral hemorrhage and 1.8 times more likely to suffer from subarachnoid hemorrhage.
The association between heavy alcohol consumption and these two types of stroke was stronger than that for ischemic stroke.
Chronic alcohol abuse tends to elevates blood pressure, resulting in increased occurrence of HICH and exaggerated HICH-contributed brain injury.(vasoconstriction induced bleed)
CASE-8
https://143vibhahegde.blogspot.com/2021/05/wernickes-encephalopathy.html
1Q What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
A 40year old male presented with chief complaints of irrelevant talking and decreased food intake since 9days.
Hewas 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 24hour
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.
GABA PATHWAY
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.
GLUTAMATE PATHWAY
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 the normocytic anaemia?
alcohol causes iron deficiency or iron overload due its affect on production of new blood cells organs i.e,bonemarrow and the metabolism of iron .alocohol causes a affect on progenitor cells of blood causing decreased WBC .RBC.alochol decreases iron absorption from intestine .
7)could chronic alcohlism have aggravated the foot ulcer formation ?if yes and why ?
yesAs 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.
CARDIOLOGY
CASE-1
https://muskaangoyal.blogspot.com/2021/05/a-73-year-old-male-patient-with-pedal.html
1Q) .What are the possible causes for heart failure in this patient?
A) patient has diabetes since 30yrs back and also having diabetic triopathy(neuropathy-retinopathy - nephropathy), so there is an increased risk for heart failure
* Hypertension since 19yrs - important risk factor
* Chronic alcoholic since 40yrs, leads to decreased LVEF and causes LV dysfunction
* patient has elevated creatinine, chronic kidney disease, AST/ALT greater than 2,all of this are important risk factors for heart failure
2Q)what is the reason for anaemia in this case?
As he was chronic alcoholic, which impairs the production of precursors of RBC in bone marrow, also causes change in shape and functions of cells
Due to chronic kidney disease
Impaired renal clearance leading to decreased erythropoetin production-impaired production of rbc
3Q).What is the reason for blebs and non healing ulcer in the legs of this patient?
As patient was diabetic, which impairs healing process leading to development of non healing ulcers
Due to chronic alcoholism leading to decreased production of proteins and clotting factors required for wound healing
4Q). What sequence of stages of diabetes has been noted in this patient?
Stages include:
CASE - 2
https://muskaangoyal.blogspot.com/2021/05/a-78year-old-male-with-shortness-of.html
1Q)What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
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
2.Why haven't we done pericardiocentesis in this pateint?
Pericardiocentesis is a procedure done to remove fluid that has built up in the sac around the heart (pericardium). It's done using a needle and small catheter to drain excess fluid. A fibrous sac known as the pericardium surrounds the heart.
As we suspect that the patient having 1st degree AV block which is an contraindication for pericardiocentesis, due to increased risk of rupture of Wall of heart.
3Q)What are the risk factors for development of heart failure in the patient?
A) Cigarette smoking
The patient is a chronic smoker (30years), which is a habit known to increase the risk of heart failure.
Mechanism- Cigarette smoking leads to impaired endothelial function via decreased nitric oxide production, pro-thrombotic state, increased oxidative stress, and activated inflammatory pathways.
Smoking, via increased oxidative stress and inflammation, directly effects on the myocardium leading to systolic and diastolic dysfunction.
It also promotes other heart failure (HF) risk factors including blood pressure, increased heart rate, diabetes, and atherosclerosis.
B) Chronic alcohol consumption
Patient consumes 90ml per day for the past 30 years
Heavy alcohol consumption is associated with alcoholic cardiomyopathy, characterized by left ventricular dilation, increased left ventricular mass, and reduced or normal left ventricular wall thickness among patients with a long-term history of heavy alcohol consumption.
Based on studies alcoholic patients with symptomatic HF had 10 years or more of exposure to heavy drinking .
C) Hypertension and Diabetes
Diabetes results in changes in myocardial structure and function by causing disproportionate left ventricular hypertrophy and perivascular and interstitial fibrosis, these changes result in diastolic and systolic dysfunction and increase risk of heart failure.
Hypertension increases work load on the heart and a result there is left ventricular hypertrophy — risk of heart failure
D) ECG reports of the patient indicate first degree AV block.
This is associated with an increased risk of heart failure.
Among patients with heart failure, first-degree atrioventricular block is present in anywhere between 15% and 51%.
E) 2D ECHO of the patient shows pericardial effusion
This increases pressure on the heart and if left untreated will lead to heart failure.
4Q)What could be the cause for hypotension in this patient?
She already had a compromised heart due AV block causing heart failure, along with this she was taking diuretic which result in more fluid loss both of them lead to devolopment of hypotension.
CASE-3
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
1Q What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) since 2 days,
decreased urine output since 2 days,
Anuria since morning
Facial puffiness On and Off since 2-3yrs.
2Q)What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Paroxysmal Atrial Fibrillation -
Beta-blockers are used as first line therapy since they reduce the ectopic firing that initiates the arrhythmia. They are particularly useful in patients associated with Coronary artery disease, Hypertension and Cardiac failure.
Class 1c drugs :Propafenone, flecainide are also effective.
Ablation for AF is an attractive treatment when drugs are ineffective or poorly tolerated.
Persistent Atrial Fibrillation -
Rhythm control - IV Flecainide can be used for pharmacological cardioversion and will restore sinus rhythm. (IV Amiodarone if any heart disease present)
Rate control - Digoxin, Beta blockers, CCBs like Diltiazem or Verapamil reduce the ventricular rate by slowing AV conduction.
Thromboprophylaxis - Patients undergoing cardioversion to restore sinus rhythm require temporary anticoagulation to reduce the risk of systemic embolus. Warfarin, direct acting anti-coagulants like factor Xa and direct thrombin inhibitors can be used.
3Q)What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
The term cardiorenal syndrome (CRS) refers to a condition in which either renal impairment occurs as a result of cardiac dysfunction, or heart structure and function are negatively affected by renal disorders.
4Q) What are the risk factors for atherosclerosis in this patient?
Patient is known case of hypertension since 1 Yr which is an important risk factor
Other factors:physical inactivity, diabetes, obesity, hyperlipidemia
5Q)Why was the patient asked to get those APTT, INR tests for review?
- The patient was on Anticoagulants,So to predict the occurrence of CVA and ischemic attacks, the patient is advised to get these tests.
CASE-4
https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
She had H/O heartburn like episodes since a year.
She has H/O TB diagnosed 7 months ago
patient had heart burn since a year and then developed SOB an hour ago. The problem is localised to the heart. It could be caused due to risk factors like her age and Hypertension
2Q) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Met XL 25 tablet is used to treat high blood pressure mainly, along with certain heart conditions such as angina (chest pain) and heart failure. belongs to a group of medicines called long-acting beta-blocker. Percutaneous coronary intervention (PCI), also known as coronary angioplasty, is a nonsurgical technique for treating obstructive coronary artery disease, including unstable angina, acute myocardial infarction (MI), and multi vessel coronary artery disease (CAD).
) What are the indications and contraindications for PCI?
Ans:INDICATIONS:
Acute ST-elevation myocardial infarction (STEMI)
Non–ST-elevation acute coronary syndrome (NSTE-ACS)
Unstable angina.
Stable angina.
Anginal equivalent (eg, dyspnea, arrhythmia, or dizziness or syncope)
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 over treatment and why is research on over testing and over treatment important to current healthcare systems?
If PCI is performed in a patient who does not need it, it is an unnecessary procedure done in the patient with many risks associated with the procedure with no benefit from it.
factors associated with increased rates of complications with PCI:
advanced age, diabetes, chronic kidney disease, acute coronary syndrome
heart failure
CASE-5
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
1Q) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Evolution of symptomatology:
Uncontrolled DM2 since 8 years
3 days back Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical localisation: Inferior wall of heart
Primary etiology: Diabetes type 2 (uncontrolled)
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Aspirin - Inhibits Prostaglandins
Atorvastatin - Inhibits HMG Co A reductase there by reduces the Cholesterol Production in the Liver.
Clopodogrel -Inhibits Platelet Aggregation
3Q) Did the secondary PTCA do any good to the patient or was it unnecessary?Y
es the Patient improved after the secondary PTCA and the patient was discharged from the Secondary Centre.It clears the Obstruction and restores the Blood Supply.
CASE-6
https://kattekolasathwik.blogspot.com/2021/05/a-case-of-cardiogenic-shock.h
1Q) How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
May be the Shortness of Breath was Due to Decreased Cardiac Output.And as The Rural medical Practitioner has given i.v.fluids the Cardiac Output has increased and Shortness of Breath was relieved.
2. What is the rationale of using torsemide in this patient?
Torsemide is used to increase the urine output
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
There was whitish discharge in the Urine.Hence patient was given Ceftriaxone to treat UTI.
GASTROENTEROLOGY
https://nehae-logs.blogspot.com/2021/05/case-discussion-on-25-year-old-male.html
1) What is causing the patient's dyspnea? How is it related to pancreatitis?
May be Pancreatitis is the Cause of Patients Dyspnea.Once Pancreatitis is initiated the inflammatory events within the acinar cells will progress to a generalized systemic inflammatory response syndrome (SIRS). Amongst the systemic complications, pulmonary complications are the most frequent and potentially the most serious.
The most dangerous complication of the pulmonary system is ARDS.
Activated trypsin causes damage to pulmonary vasculature and increases endothelial permeability. Active circulating phospholipase A2 (PLA2) is known to remove fatty acids from phospholipids. One of the main components of surfactant is the phospholipid, dipalmitoylphosphatidylcholine. Many recent studies have assessed the role of platelet activating factor (PAF) which stimulates polymorphonuclear cells (PMNs) regulating the interaction between PMNs and endothelial cells facilitating migration of activated WBC into interstitial spaces.
There are pro-inflammatory cytokines released from the pancreas such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, IL-6, and IL-8. PMNs also contribute to release of cytokines
hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells
3)What is the reason for his elevated LFTs? Is there a specific marker for Alcoholic Fatty Liver disease?
The most common causes of acute pancreatitis are gallstones and alcohol-induced pancreatitis. This patientss liver enzymes (especially ALT) and bilirubin level are elevated, which may suggest choledo- cholithiasis.
Specific marker for alcoholic fatty liver disease:
AST more than ALT, elevated levels of gamma glutmyl transferase
4) What is the line of treatment in this patient?
iv fluids and colloids
NPO (Nill Per Oral)
Analgesics
Nasogastric suction -to decrease gastrin release from stomach
Laparotomy and debridement of hemorrhagic pancreatic tissue.
antibiotic therapy like ciprofloxacin , ofloxacin, imipenem
CASE-2
https://63konakanchihyndavi.blogspot.com/2021/05/case-discussion-on-pancreatitis-with.html
QUESTIONS:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
CHEIF COMPLAINTS of pain abdomen & vomiting since 1 week constipation, burning micturition, fever since 4 days.
asymptomatic 5 yrs back when he had painabdomen & vomitings for which he was taken to a local hospital and treated conservatively
Later he again started taking alcohol following which he had recurrent episodes of pain abdomen & vomiting * (5-6 episodes in the past 1 year) which were treated by a local RMP.
From the past 20 days he had increased amount alcohol consumption (5 bottles of toddy per day)
* Last binge of alcohol 1 week back following which he again had pain abdomen & vomiting from 1 week and fever from 4 days.
Anatomical localisation :pancreas
Etiological agent:chronic alcoholism lead to development of pancreatitis
2)What is the efficacy of drugs used along with other non pharmacological treatment modalities and how would you approach this patient as a treating physician?
1)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-lactams, 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:he 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 amount 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. 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 normal function/health of pancreatic cells due to its critical role in oxidative energy metabolism, ATP production, and in maintaining 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-desmethyltramadol acts on the µ-opioid receptor. Its analgesic potency is claimed to be about one tenth that of morphine.
CASE-3
https://chennabhavana.blogspot.com/2021/05/general-medicine-case-discussion-1.html
1)what is the most probable diagnosis in this patient?
Ruptured Liver Abscess
Patient had Elevated levels of Alkaline Phosphatase, Hyperbilirubinemia, Hypoalbuminemia and Hepatomegaly, the most probable diagnosis is abcess
2) What was the cause of her death?
A :- On the next day of surgery, Patient had severe cough and Shortness of breath eventually resulting in Sepsis, may be this caused her death
3) Does her NSAID abuse have something to do with her condition? And How?
A :- Patient's USG report shows that She had Grade 3 RPD changes of Right kidney.
• It highly suggests that she may had underlying CKD (Chronic Kidney Disease),
Which is secondary to her NSAID abuse. (Analgesic Nephropathy)
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