This document discusses how drugs are eliminated by the kidneys and the mechanisms of renal injury caused by various drugs. It notes that many drugs can injure the kidneys through a few common mechanisms, such as altering renal blood flow or causing direct tubular toxicity. It provides examples of specific drugs that can cause these types of renal injuries. The document also discusses factors that influence drug dosing in patients with renal impairment and principles for safely prescribing drugs in such patients.
Drug induced Kidney Injury in the ICU. Presentation by Dr Sandra Kane Gill , President Society of Critical Care Medicine (SCCM) , USA at the Egyptian Critical care Summit 2022 conference , organized by the Egyptian College of Critical care Physicians (ECCCP) , Egypt
Drug induced Kidney Injury in the ICU. Presentation by Dr Sandra Kane Gill , President Society of Critical Care Medicine (SCCM) , USA at the Egyptian Critical care Summit 2022 conference , organized by the Egyptian College of Critical care Physicians (ECCCP) , Egypt
Dose Adjustment in Renal Failure ...Practical Approach for Clinical Pharmacists to help them perfectly adjust doses for medications according to best evidence to date
Detailed mechanisms of certain antimicrobials that cause renal failure
ANTIMICROBIALS CAUSING RENAL FAILURE
Aminoglycosides
Amphotericin – B
Trimethoprim
B – lactam antibiotics
Fluoroquinolones
Vancomycin
Acyclovir
Tetracycline
Many medicines can cause acute kidney injury (which used to be called acute renal failure), such as:
Antibiotics. These include aminoglycosides, cephalosporins, amphotericin B, bacitracin, and vancomycin.
Antihypertensive: ACE inhibitors, such as lisinopril and ramipril; Angiotensin receptor blockers, such as candesartan and valsartan.
Anticancer drugs (chemotherapy): Examples are cisplatin, carboplatin, and methotrexate.
Dyes (contrast media):These are used in medical imaging tests.
Illegal drugs: Examples are heroin and methamphetamine.
Antiviral drugs: Examples are indinavir and ritonavir, acyclovir
Non-steroidal anti-inflammatory drugs: These include ibuprofen, ketoprofen, and naproxen.
Anti Ulcer medicines: One example is cimetidine.
The kidney maintains the vital functions of clearing excess body fluid and removing metabolic and exogenous toxins from the blood
The kidney is particularly vulnerable to drugs and other agents that cause renal damage
The heart pumps approximately 25% of cardiac output into the kidneys
Any drug in the blood will eventually reach the highly vascularized kidneys
It may potentially cause drug induced renal failure
If the drug is primarily cleared by the kidney, the drug will become increasingly concentrated as it moves from the renal artery into the smaller vasculature of the kidney
The drug may be filtered or secreted into the lumen of the renal tubules
The concentrated drug exposes the kidney tissue to far greater drug concentration per surface area
Drug-induced kidney disease or nephrotoxicity (DIN) is a relatively common complication of several diagnostic and therapeutic agents.
Drug-induced kidney disease or nephrotoxicity (DIN) is a relatively common complication of several diagnostic and therapeutic agents.
Any drug in the blood will eventually reach the highly vascularized kidneys
It may potentially cause drug induced renal failure
If the drug is primarily cleared by the kidney, the drug will become increasingly concentrated as it moves from the renal artery into the smaller vasculature of the kidney
The drug may be filtered or secreted into the lumen of the renal tubules
The concentrated drug exposes the kidney tissue to far greater drug concentration per surface area
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
5. Because of 2 reasons
the first one
is that we are all prescribing
drugs all the time
6. The second one is more
important
Which is that every body
usually has 2 kidneys
7. Many drugs can injure the kidneys,
but they cause renal injury via only
. a few common mechanisms
Many patients who develop renal
injury after drug exposure have
identifiable risk factors that could be
???. modified
8. Renal elimination of drugs
Drugs may be eliminated via the kidneys by
two main mechanisms:
Glomerular filtration: a passive process
such drugs will be water-soluble.
Activetubular secretion: drugs act as
substrates for secretory processes that
are designed to eliminate endogenous
molecules. ???
9. When renal disease leads to a
reduction in nephron, the kidney’s
ability to eliminate drugs declines
in proportion to the decline in
glomerular filtration rate. As renal
failure progresses, drugs filtered or
secreted by the kidney can
accumulate , potentially resulting
in toxicity.
10. Renal injury can present as acute
renal failure, Nephrotic syndrome,
renal tubular dysfunction, or chronic
renal failure
11.
12. Drug nephrotoxicity
Drugs can lead to renal damage in a
number of different ways :
1. Alteration of renal blood flow
NSAIDs:alteration in prostaglandin
metabolism can lead to critical
reduction in glumerular perfusion,
interstitial nephritis can also result
from NSAIDs
ACE inhibitors and ARBs: ARF or
renal impairment ????
13. Occurring in patients who are critically
dependant upon RAA system.
Cyclosporine A
2. Direct tubular toxicity
Aminoglycosides :disturbance of renal
function is seen in up to a third of patients
receiving aminoglycosides.
14. Cisplatin : selectively toxic to proximal
tubules by inhibiting nuclear DNA
synthesis
Amophotercin:
3.glumerulonephritis
Gold :
Is believed to induce an immune
complex GN
Penicillamine :
It is dose related
15. 4. Other nephrotoxic effects of drugs:
Interstitial nephritis
Retropertoneal fibrosis
Drug induced SLE
Nephrogenic DI
16.
17. Drugs which accumulate and cause
toxicity in patients with sever renal
failure include:
1.Pencillins and cephalosporins high dose.
2.digoxin
3. Erythromycin
Nephrotoxic drugs may lead to an acute
deterioration of renal function in patients
with CRF and they can severely excerbates
renal damage in ARF.
18. Absorption of some drugs may be altered in
uremia as a consequence of
edema of the gastrointestinal tract coupled
with uremic nausea ,vomiting or
gastroparesis. Alteration in the distribution
of drugs vary depending on the agents .
Acidic drugs will have a higher free fraction
in the plasma of uremic patients as a
consequence of decrease protein binding.
19. How nephrotoxic are the
NSAIDs ?
PG have relatively little effect on the
normal kidney in the euvolemic person
However in renal insufficiency or
hypovolemic states PG are important in
maintaining adequate glomerular flow and
pressure by VD of renal arteries , ↑ Na loss
and ↑ rennin release
20. nephrotoxic effects of NSAIDs
↑ Na retention and blood volume (CHF)
Papillary necrosis
↑ K
Acute allergic interstitial nephritis ass with
fenoprofen
ATN
Interstitial nephritis with aspirin
,caffeine ???
21. Diabetic drugs and the kidney
Glucophage
Insulin
TZDs
Acarboses
DPP-IV Inhibitors
sulphonylureas
22. Insulin in renal patients
Insulin resistance
Insulin catabolism
23. Liver diseases and
the kidney
Which organ you should be more
careful about?
HRS
Electrolyte disturbance
Renal impairment in HCV
24. Heart failure and the kidney
■ Diuretics
■ digitalis
■ B-blocker in HD patients
25. Radio-contrast nephropathy
Mild renal dysfunction may complicate up to
10% of angiographic procedures and
IVUs. Radio-contrast nephropathy is
manifest by non oliguric ARF, typically
occurring 1-5 days after the procedure.
Intra- renal vasoconstriction, mediated
largely by endothelin, and tubular cell
toxicity (with ATN) are important in the
pathogenesis . The ARF is fully reversible.
26. Risk factors for radio- contrast nephropathy
High contrast load
Hypovolaemia
Myeloma , Hyperuricaemia
Age
High iodine content of contrast
Diabetes
Hypercalcaemia
Pre-existing CRF
27.
28. KDIGO 2012
Consider alternative imaging methods in patients at
increased risk for CI-AKI. (Not Graded)
Use the lowest possible dose of contrast medium in
patients at risk for CI-AKI. (Not Graded)
We recommend using either iso-osmolar or low-
osmolar iodinated contrast media, rather than high-
osmolar iodinated contrast media in patients at
increased risk of CI-AKI. (1B)
We recommend i.v. volume expansion with either
isotonic sodium chloride or sodium bicarbonate
solutions, rather than no i.v. volume expansion, in
patients at increased risk for CI-AKI. (1A)
29. We recommend not using oral fluids alone in patients
at increased risk of CI-AKI. (1C)
We suggest using oral NAC, together with i.v.
isotonic crystalloids, in patients at increased risk of
CI-AKI. (2D)
Wesuggest not using theophylline to prevent CI-
AKI. (2C)
Werecommend not using fenoldopam to prevent CI-
AKI. (1B)
We suggest not using prophylactic intermittent
hemodialysis (IHD) or hemofiltration (HF) for
contrast-media removal in patients at increased risk
for CI-AKI. (2C)
30. The objective is to
obtain a therapeutic
drug concentration-
time profile that is
therapeutic and not
toxic.
31. GENERAL PRINCIPLES
Be vigilant. Adverse renal effects of drugs are
largely silent in the early stages
. Identify patients at risk
.Take precautions
Manage the renal failure
32. When in doubt about the
cause of renal failure, hold
all potentially offending
drugs
33. A careful history and physical
examination are always the first steps
in clinical evaluation of patients with
renal disease. Particularly important for
this purpose is the history of previous
drug allergy or toxicity and the use of
concurrent medications.
34. Physical assessment should include
An estimate of the extracellular fluid volume.
Oh ??
Edema or ascites increases the distribution
volume of many drugs, while dehydration
contracts this volume. Evidence of impaired
function of other excretory organs should
be sought. Stigmata of liver disease are clue
that the drug dose may need to be altered.
35. II. Measurement of renal function
the rate of elimination of drugs excreted by the
kidneys is proportional to the glomerular
filtration rate. The serum creatinine , creatinine
clearance is needed to determine renal function
before prescribing many drugs . The Cockcroft
and Gault equation is useful for this purpose, as
shown in the following formula:
CrCl (ml/min)= (140-age)x (BW in kg)(x0.85if female)
72x Scr(mg/dl)
36. The Scr reflects muscle mass as well as
glomerular filtration rate. Scr
measurement within the normal range
are frequently used to establish normal
renal function. This may cause serious
over- dose and resultant toxic drugs
accumulation in elderly or debilitated
patients with decreased muscle mass.
37. ?Do we have another option
Cystatin –C is a good indicator of
renal function specially in children
and elderly patients
Estimated GFR is the best way to
assess progression of kidney
disease in chronic renal patients
38.
39. Pretreatment hydration can reduce
the nephrotoxic potential of many
drugs.
So ,it is very simple steps by which
you can avoid getting yourself and
your patient in a big problem.
40. What are special concerns regarding the
use of antimicrobial agents in patients with
renal failure?
The majority of antimicrobial agents are
excreted at least partially by the kidney so
that dose reductions often are apporpiate
in patients with glumerular filtration rates
less than 50% of normal. Gastrointestinal
absorption of tetracycline and
ciprofloxacin may me decreased if
41. How should antibiotic doses be adjusted in patients
with renal failure?
Several antibiotics need dosage modification in the
presence of renal failure, most cephalosporins,
many penicillin's and vancomycin. The
adjustments can be made by :
1. maintaining the usual dose and varying the
dosing interval,
2. maintaining the dosing interval and varying the
dose,
3. or a combination of the two.
42. they are taken with phosphate-binding
antacids. Decreased protein binding may
contribute to increased neurotoxicity of
betalactam antibiotics in patients with
renal failure.
Nephrotoxicity of antimicrobial agents is a
major concern in patients with impaired
renal function and limited renal reserve.
The majority offenders are the
aminoglycosides and Amophotercin.
43. The catabolic effects of tetracycline may
results in a rise in blood urea nitrogen and
therefore its use should be avoided in
patients with advanced renal insufficiency.
Many of the penicillins are prepared with
sodium or pottasium. High doses of such
agents may be problematiac in renal
patients with volume overload of
hyperkalemia.
44. Dosing of antimicrobial drugs in renal
patients
Antimicrobial and antiprotozoal drugs
Drug Half-life Dosage for severe renal failure
Normal/ESRD
(h)
Amoxycillin 0.09-2.3/5-20 Maximum 500 mgq 8h
Amoxycillin Amoxycillin Maximum 375 mg q12 h
Clavulanic acid PO 0.9-2.3/5-20
Clavulanic
acid1/3-4
ampicillin 0.8-1.5/7-20 250-500 mg q6h
Cefotaxime IV 1/15 1g loading dose then 50% standard
dose
45. Drug Half-life Dosage for severe renal failure
Normal/ESRD
(h)
Ceftazidime IV 1.2/13-25 0.5-1 g q24h
Ceftriaxone IV 7-9/12-24 1-2 g q24h
Cefuroxime IV 1.2/17 750 mg q12h
Cefuroxime PO 1.2/17 Standard dose
Cephalexin 0.7/16 250-500 mg q12h
Chloroquiine 7-14 days/5- 50 days Treatment:50% standard
dose
Ciprofloxacin IV/PO 3-6/6-9 50% standard dose q12h
Calrithromycin 2.3-6.0/- 250 mg q12h
Cotrimoxazole Sulphamethoxazole PCP treatment:Standard dose
IV/PO 10/20-50 q48h
Sulphamethoxazole/ Trimethoprime PCP prophylaxis
Trimethoprime 9-13/20-49 25% Standard dose q48-72h
Erythromycin IV/PO 1.4/5-6 50-75% Standard dose
Max 1.5g in 24h
46. Drug Half-life Dosage for severe renal failure
Normal/ESRD
(h)
Flucloxacillin 0.8-1/3 Max PO 500 mg q6hIV 1g q 6 h
Gentamicin IV 1.8/20-60 Titrate to levels
Impenem/ cilastin IV Impenem ¼ 250 mg or 3.5 mg/kg q12 h
Cilastin1/15-24
Meropenem IV 1.1/6-8 50% standard dose q24h
Penoxymethyl-pencillin 0.6/4.1 Standard dose
Piperacillin IV 0.8-1.8/3.3-5.1 4 g q12 h
Piperacillin/dihydrochloride IV Piperacillin 0.18-0.3/3.3-5.1 4.5 g q12 h
Dihydrochloride 1/7
Quinine difydrochloride IV 9 healthy,18 malaria/ Treat,emt 5-10 mg/kg q24h
unchanged
Trimethoprim 9-13/20-49 50% standard dose
Vancomycin IV 6-8/200-250 Titrate to levels
47. Dosing of common drugs in renal patients
Allopurinol-GFR 30 ml/min use
100mg,60ml/min use 200mg,90ml/min use
300mg
Corticosteroids-no need to change the dose
NSAIDs :-most are metabolized in the
liver , aspirin is a good choice in renal
impairment,
- In ESRD patients ,no need for dose
adjustment
48. In patients with low urine output avoid
sulindac owing to renal stone formation.
Reduce dose of ketoprofen
Penicillamine ,avoid if GFR less than
50ml/min
Cyclosporine, no dose adjustment in renal
insufficiency, however use of Cyclosporine
can worsen renal insufficiency
Gold , if GFR 50-75ml/min use 50% of
usual dose ,if less than 50% avoid gold
49. Methotrexate ,take care from hematologic
toxicity
Tacrolimus (FK506,prograf)….Gout
Sulfasalasine ,no change in dose.
Mycophenylate mofetil (cellcept) ,mainly
hepatic metabolism ,but if GFR less than 25
ml/min reduce dose by 25%.
Tramadol , give dose every 12 h instead of
every 6h
Narcotics, avoid using Darvon and
Mepiridine, for others if GFR less than
10ml/min cut 50% of the dose ,if GFR 10-
50ml/min use 75% of the dose
50. You are what you repeatedly
do; then excellence is not an
art but just a habit
Aristo