this presentation is about the acetaminophen or paracetamol as its second name and its overdose reactions and activities. and its toxic effects that may be harmful and cause damages in the people.
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this presentation is about the acetaminophen or paracetamol as its second name and its overdose reactions and activities. and its toxic effects that may be harmful and cause damages in the people.
Liver Function Tests - An Approach for Primary CareJarrod Lee
This presentation is aimed at primary care physicians. It covers the fundamentals of liver function tests, including the basic principles of interpretation, and the key patterns of abnormalities. The focus is on how to approach liver function tests in a primary care setting.
Sean Kelly is an Emergency Physician and Intensivist who's the director at Gosford ICU in New South Wales. He's also the medical director at ICCMU. He gave this great talk at Bedside Critical Care 2012 on Daydream Island. He'll be at SMACC. Check out the ICCMU website.
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Please find the power point on Paracetamol poisoning. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
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2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Study Resources:
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2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
2. PARACETAMOL
Non-steroidal anti-inflammatory drug(NSAID)
Has analgesic and antipyretic effects but weak anti-inflammatory properties
Exerts its effects through the inhibition of cyclo-oxygenase (COX)
COX catalyses the formation of prostaglandins (PGs) and other mediators that
are important in the processing and signaling of pain and control of the
thermoregulatory center of the brain
3. PHARMACOKINETICS
Oral acetaminophen has excellent bioavailability
Peak plasma concentration occur within 30 to 60 minutes
The half-life in plasma is about 2 hours after therapeutic doses
4. METABOLISM
Metabolized in the liver by conjugation with sulfate or glucuronate (90%), and
by CYP2E1 enzymes(5%), and the remainder is secreted unchanged in the
urine(5%)
The CYP2E1 enzyme pathway is the basis for acetaminophen toxicity
5. TOXIC DOSE
More than 7.5 gm (around 15 tablets) – minimal toxicity, severe liver toxicity
if > 15gms (30 tablets)
In adults toxic dose is 150mg/kg
In children under 12 years toxic dose is 200mg/kg
In the presence of chronic liver disease or malnutrition, even 2g of PCM can
be a toxic dose
6. MECHANISM OF TOXICITY
When the dose of paracetamol is high the glucuronide and sulfate conjugation
pathways become saturated, and increasing amounts undergo CYP-mediated
Nhydroxylation to form N-acetyl-para- benzoquinoneminine (NAPQI)
Eliminated rapidly by conjugation with glutathione (GSH) and then further
metabolized to a mercapturic acid and excreted into the urine
In acetaminophen overdose, hepatocellular levels of GSH become depleted.
The highly reactive NAPQI metabolite binds covalently to cell
macromolecules, leading to dysfunction of enzymatic systems and structural
and metabolic disarray
Depletion of intracellular GSH renders the hepatocytes highly susceptible to
oxidative stress and apoptosis.
Binding covalently to cellular proteins, causes cell death
7.
8. STAGES OF INTOXICATION
Stage 1 (time of ingestion to 24 hours) : • Patient typically has anorexia,
nausea, vomiting, and diaphoresis • Results of laboratory tests are usually
normal
Stage 2 (24-72 hours): • Results of laboratory tests begin to be abnormal •
Abnormalities include increases in serum transaminases, bilirubin and PT •
Nephrotoxicity may be evident
Stage 3 (72 to 96 hours):• Also known as hepatic stage • Severe signs of
hepatotoxicity appear
This includes: Plasma ALT and AST levels often >10,000 IU/L, increased in PT or
INR Hypoglycemia Lactic acidosis and A total bilirubin concentration above
70umole/l (primarily indirect)
9. STAGES OF INTOXICATION
Stage 4 (4 days-2 weeks) : •
Is the recovery stage
Patients who survive stage III enter a recovery phase that usually begins by day 4
and is complete by 7 days after overdose
However, transient renal failure may develop 5-7 days after ingestion (Back pain,
proteinuria, hematuria)
Complete hepatic recovery may take 3-6 months.Stage 4 (4 days-2 weeks) : • Is the
recovery stage
Patients who survive stage III enter a recovery phase that usually begins by day 4
and is complete by 7 days after overdose
However, transient renal failure may develop 5-7 days after ingestion (Back pain,
proteinuria, hematuria) • Complete hepatic recovery may take 3-6 months.
10. APPROACH TO THE PATIENT
ABCDE
History
Examination
Investigations
Initial baseline investigations • LFT, PT/INR, blood glucose, platelet count,
electrolyte, urine routine • Plasma paracetamol level • Determined after 4 hours
of ingestion
11. MANAGEMENT
Activated charcoal may be used in patients presenting within 1 hour.
Antidotes for paracetamol poisoning
a. N-acetylcysteine (NAC)
b. Methioinine
Act by replenishing hepatic glutathione
N-acetyl cysteine may also repair oxidation damage caused by NAPQI
12. N-ACETYLCYSTEINE (NAC)
IV is highly efficacious if administered within 8 hours of the overdose
Should not be delayed in patients presenting after 8 hours to await a
paracetamol blood concentration result.
Dose: • 150mg/kg in 200 ml 5% dextrose over 15 minutes • Followed by
50mg/kg in 500 ml 5% dextrose over 4 hours • Followed by 100mg/kg in 1000
ml 5% dextrose over 16 hours
13. METHIONINE
An alternative antidote in paracetamol poisoning
2.5 g orally 4-hourly to a total of four doses
Less effective, especially after delayed presentation
14. SUPPORTIVE MANAGMENT
Give activated charcoal to all patients who present within 1hr post ingestion
Give vitamin K 10mg to all cases of acute ingestion