This document discusses different types of antifungals and their mechanisms of action. It covers several classes of antifungals that target the fungal cell membrane or cell wall, such as polyenes like amphotericin B and azoles like fluconazole. It provides details on the spectrum, pharmacokinetics, dosing and side effects of various azoles including fluconazole, ketoconazole and voriconazole. Lipid formulations of amphotericin B are mentioned which are less toxic than conventional amphotericin B. Mechanisms of antifungal resistance and the importance of drug interactions are also summarized.
synthetic antimicrobials having a quinolone structure that are active primarily against gram-negative bacteria, though newer fluorinated compounds also inhibit gram-positive ones.
synthetic antimicrobials having a quinolone structure that are active primarily against gram-negative bacteria, though newer fluorinated compounds also inhibit gram-positive ones.
Anti Tubercular Drugs - Mechanism of Action and Adverse effects Thomas Kurian
A brief outline of the mechanism of action and adverse effects of anti tubercular drugs
Only First line and second line drugs are dealt with.First line drugs may be useful for MBBS students and the rest is directed for postgraduate students.
Hope you find it useful.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Title: Sense of Taste
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 structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
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
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
2. Types of fungal infections - Mycoses
• Superficial mycoses
– Affect the skin, hair and nails
• Subcutaneous mycoses (tropical)
– Affect the muscle and connective tissue immediately below
the skin
• Systemic (invasive) mycoses
– Involve the internal organs
– Primary vs. opportunistic
• Allergic mycoses
– Affect lungs or sinuses
– Patients may have chronic asthma, cystic fibrosis or sinusitis
There is some overlap between these groups
3. What are the targets for antifungal therapy?
Cell membrane
Fungi use principally ergosterol
instead of cholesterol
Cell Wall
Unlike mammalian cells, fungi have a
cell wall
DNA Synthesis
Some compounds may be selectively
activated by fungi, arresting DNA
synthesis.
6. Azoles - Mechanism
In fungi, the cytochrome P450-
enzyme lanosterol 14-a
demethylase is responsible for the
conversion of lanosterol to
ergosterol
Azoles bind to lanosterol 14a-
demethylase inhibiting the
production of ergosterol
Some cross-reactivity is seen with
mammalian cytochrome p450
enzymes
Drug Interactions
Impairment of steroidneogenesis
(ketoconazole, itraconazole)
8. Azoles - Pharmacodynamics
• Concentration-independent fungistatic
agents
– Dosage escalation may be necessary when
faced with more resistant fungal species (e.g.
Candida glabrata)
• Goal of dosing is to maintain AUC:MIC >50
– i.e. maintain concentrations 1-2 x MIC for the
entire dosing interval
9. Ketoconazole
• Spectrum: yeasts and moulds - poor absorption
limits its role for severe infections, generally used
in mucosal infections only
• Pharmacokinetics
– Variable oral absorption, dependent on pH (often given
with cola or fruit juice)
– T1/2 7-10 hours
– Protein binding > 99%
– Hepatic, bile and kidney elimination
10. Ketoconazole - Adverse effects
• Adverse effects
– N&V, worse with higher doses (800 mg/day)
– Hepatoxicity (2-8%), increase in transaminases,
hepatitis
– Dose related inhibition of CYP P450 responsible for
testosterone synthesis
• Gynecomastia, oligosperma, decreased libido
– Dose-related inhibition of CYP P450 responsible for
adrenal cortisol synthesis
11. Ketoconazole - Drug Interactions
• Potent inhibitor of cytochrome P450 3A4
– Rifampin and phenytoin decrease ketoconazole levels
– Ketoconazole increases cyclosporin, warfarin,
astemizole, corticosteroid, and theophylline levels
– Many of these drug interactions are severe
• Drugs that increase gastric pH will decrease blood
levels of ketoconazole
– Antacids, omeprazole, H2 blockers
15. Fluconazole - spectrum
• Good activity against C. albicans and
Cryptococcus neoformans
• Non-albicans Candida species more likely to
exhibit primary resistance
C. krusei > C. glabrata > C. parapsilosis
C. tropicalis
C. kefyr
Always resistant Sometimes resistant
16. Fluconazole - resistance
• Primary resistance (seen in severely ill or
immunocompromised patients)
– Selection of resistant species or subpopulations
– Replacement with more resistant strain
• Secondary resistance (seen in patients with
AIDS who experienced recurrent
orophayrngeal candidiasis and received long-
term fluconazole therapy)
– Genetic mutation
– Upregulation of efflux pumps
17. Mechanisms of antifungal resistance
• Target enzyme
modification
• Ergosterol biosynthetic
pathway
• Efflux pumps
• Drug import
18. Fluconazole - What is not covered
• Candida krusei
• +/- Candida glabrata
• Aspergillus species and other moulds
19. Fluconazole - Pharmacokinetics
• Available as both IV and PO
– Bioavailibility > 90%
• Linear pharmacokinetics
– t 1/2 = ~24 hours
– Cmax (400 mg IV) = 20 µg/ml (steady state)
– Protein binding < 12%
– Vd 0.85 L/kg (widely distributed)
– >90% excreted unchanged through the kidney
20. Fluconazole - adverse effects/monitoring
• N&V, rash:
– More likely with high doses and in AIDS patients
– Asymptomatic increase in LFTs (7%)
• Drug interactions:
– May increase phenytoin, cyclosporin, rifabutin,
warfarin, and zidovudine concentrations
– Rifampin reduced fluconazole levels to half
(even though FLU is not a major substrate)
21. Fluconazole - Dosing
• Mucosal candidiasis
– 100-200 mg/day (150 mg tablet vulvovaginal candidiasis)
• Systemic fungal infections
– 400-800 mg q24h
– > 800 mg q24h in unstable patient, S-DD isolate, or if non-
albicans spp. (except C. krusei)
• Maintenance for cryptococcal meningitis
– 400 mg q24h
22. Key Biopharmaceutical Characteristics of
the Triazole Antifungals
Fluconazole Itraconazole Voriconazole
Spectrum vs.
Candida and
Aspergillus
C. albicans, C.
tropicalis +/-
C. glabrata
No Aspergillus
Similar Candida
coverage as
fluconazole, +
Aspergillus
Broad, includes
most Candida spp.,
Aspergillus,
Fusarium sp. Not
Zygomycoses
Oral formulation
(% bioavailibility)
Tablet (>90%) Capsule (6-25%)
Solution (20-60%)
Tablet (>90%)
Intravenous
formulation
Available, no
solubilizer
Available, cyclodextrin Available,
cyclodextrin
Clearance Renal (80%) Hepatic 3A4 Hepatic 2C19, 3A4
Serum half life (hr) 24 24-30 6-24
CSF penetration Excellent Poor Excellent
CYP 3A4 inhibition Weak Strong Moderate-Strong
Adverse effects N&V, hepatic N&V, diarrhea
(solution), hepatic, CHF
N&V, visual
disturbances,
hepatic, rash
23. Itraconazole Solution - Side Effects
• Taste disturbances
• Nausea and vomiting
• Osmotic diarrhea (especially at doses > 400
mg/day)
– Long-term compliance often difficult
24. Voriconazole - Side Effects
• Visual disturbances (~ 30%)
– Decreased vision, photophobia, altered color perception
and ocular discomfort
– IV > oral
– No evidence of structural damage to retina
• Reversible alterations in function of retinal rods and cones
• Testing 2 weeks after the end of treatment demonstrates a
return to normal function
• Long term effects?..caution against night-time driving
– Effects may be intensified by hallucinations (2-5%)
25. Amphotericin B
• Polyene antibiotic
• Fermentation product of Streptomyces
nodusus
• Binds sterols in fungal cell membrane
• Creates transmembrane channel and
electrolyte leakage.
• Active against most fungi except Aspergillus
terreus, Scedosporium spp.
27. Amphotericin B
• Classic amphotericin B deoxycholate
(Fungizone™) formulation: serious toxic
side effects.
• Less toxic preparations:
1) Liposomal amphotericin B
2) Amphotericin B colloidal dispersion
3) Amphotericin B lipid complex
28. Amphotericin B - Pharmacokinetics
• Absorption from the GI tract is negligible
– Oral solution sometimes used to decontaminate gut;
few side effects
• Only reliable method of administration is IV
• Selective distribution into deep tissue sites, with
slow release of drug
kidney > liver > spleen > lung > heart > skeletal muscle > brain > bone > CSF > eye
LowHigh
29. Amphotericin B - Metabolic elimination
• Metabolic fate is unknown, drug accumulates in
tissues and then is slowly released
– Drug levels can be measured in the kidney, liver, and
spleen up to 1 year after receiving drug
• Dosages of amphotericin B are generally not
altered due to decreased elimination of the drug
in kidney dysfunction
• Hemodialysis does not alter serum drug
concentrations except in hyperlipidemic patients
30. Amphotericin B - Elimination
• Inverse correlation between patient age and
elimination of AmB,
– Age, elimination, side effects
• Paediatric patients often tolerate
amphotericin B better than adults
31. Amphotericin B - Nephrotoxicity
• Most significant delayed toxicity
• Renovascular and tubular mechanisms
– Vascular-decrease in renal blood flow leading to drop
in GFR, azotemia
– Tubular-distal tubular ischemia, wasting of potassium,
sodium, and magnesium
• Enhanced in patients who are volume depleted or
who are on concomitant nephrotoxic agents
32. Amphotericin B - Manoeuvers employed to
blunt nephrotoxicity…
• Sodium loading-> blunt the
vasoconstriction and tubular-glomerular
feedback
– Administration of 500 ml -1000 ml of NaCl
before and after amphotericin B infusion
34. Amphotericin B - Clinical Uses
The drug of choice for:
• Cryptococcal meningitis
• Mucormycosis (zygomycosis)
• Invasive fungal infection, not responding to
other therapy
35. Amphotericin B - Dosing and Administration
• “Test dose” 1.0 mg in 25-100ml 5% dextrose
infused over 10 minutes used to evaluate
possibility of anaphylactic reaction
– No longer recommended, current product has fewer
impurities
– Current recommendation- Start with ~30% of target
dose, infuse for 15 minutes, stop infusion, and monitor
patient for adverse effects before resuming infusion
– Rapidly escalate to full dosages within 48-72 hours
• Delay in giving full dose = worse clinical outcome
38. Flucytosine
• Restricted spectrum of activity.
• Acquired Resistance.
> result of monotherapy
> rapid onset
Due to:
1) Decreased uptake (permease activity)
2) Altered 5-FC metabolism (cytosine deaminase or
UMP pyrophosphorylase activity)
39. Flucytosine - pharmacokinetics
Oral absorption complete
Plasma half-life 3-6 hrs
Volume of distribution 0.7-1l/kg (low)
Plasma protein binding ~12%
40. Flucytosine - side effects
• Infrequent – include D&V, alterations in liver
function tests and blood disorders.
• Blood concs need monitoring when used in
conjunction with Amphotericin B.
41. Flucytosine – Clinical uses
• Candidiasis
• Cryptococcosis
• ?Aspergillosis
}
In combination with
amphotericin B or
fluconazole.
Monotherapy : now limited
44. Echinocandins - Pharmacology
• Cyclic lipopeptide antibiotics that
interfere with fungal cell wall
synthesis by inhibition of ß-(1,3) D-
glucan synthase
• Loss of cell wall glucan results in
osmotic fragility
Spectrum:
– Candida species including non-
albicans isolates resistant to
fluconazole
– Aspergillus spp. but not activity
against other moulds (Fusarium,
Zygomycosis)
– No coverage of Cryptococcus
neoformansOH
H H
HO
OH
H NH
O
NHH
HO
H2N
HO O
N
H
H3C
HO H
H
O
NH
H
HO OH
H
H NH
NH
O
CH3
OH
H
HO
N
O
H
OH
H
45. Echinocandins - spectrum
Highly active
Candida albicans,
Candida glabrata,
Candida tropicalis,
Candida krusei
Candida kefyr
Pneumocystis carinii
Low MIC ,with
fungicidal activity and
good in-vivo activity.
Very active
Candida parapsilosis
Candida gulliermondii
Aspergillus fumigatus
Aspergillus flavus
Aspergillus terreus
Candida lusitaniae
Low MIC, but without
fungicidal activity in
most instances.
Some activity
Coccidioides immitis
Blastomyces
dermatididis
Scedosporium species
Paecilomyces variotii
Histoplasma
capsulatum
Detectable activity,
which might have
therapeutic potential for
man (in some cases in
combination with other
drugs).
47. Echinocandins-Spectrum vs. Moulds
Staining with antisera
to glucan synthase
subunit (Fks1p)
• Active against Aspergillus
species
– Glucan synthase localized in
apical tips
• Activity against other yeast
and moulds is less well
described or variable
– Mycelial forms of endemic
mycoses?
Aniline blue staining of
β (1-3) glucans –stains
only at apex
48. Caspofungin - Pharmacokinetics
Absorption < 2%
Distribution (Vd) 9.67 L
Protein binding 97% albumin
Major metabolic pathway Peptide hydrolysis, slow
N-acetylation
t 1/2 ß 9-11 hours
CNS penetration
Dosage adjustment
Probably poor
Moderate-severe hepatic dysfunction
Drug-Drug interactions Significant interactions CSA? FK-
506, mycophenolate? Inducers of
3A4?
49. Caspofungin acetate
• IV only
Indication:
– Invasive candidiasis
– Invasive aspergillosis refractory to other therapies
Dosage and administration
– 70 mg day 1, followed by 50 mg daily
• Increase to 70 mg per day in non-responders
• Decrease to 35 mg per day in moderate-severe hepatic
dysfunction (Child-Pugh 7-9)
50. Caspofungin - Adverse effects
• Most common AEs are infusion related:
– Intravenous site irritation (15-20%)
– Mild to moderate infusion-related AE including fever,
headache, flushing, erythema, rash (5-20%)
– Symptoms consistent with histamine release (2%)
• Most AEs were mild and did not require treatment
discontinuation
• Most common laboratory AE
– Asymptomatic elevation of serum transaminases (10-
15%)
• Clinical experience to date suggests that these drugs are
extremely well-tolerated
51. Polyenes
Amphotericin B
deoxycholate
Lipo-AMB (AmBisome)
ABLC (Abelcet)
Amphocil
1 mg/kg/day IV
3 mg/kg/day IV
5 mg/kg/day IV
3 mg/kg/day IV
£7
£554
£246
£380
Triazoles
Fluconazole
Itraconazole
Voriconazole
400/800 mg IV
400 mg IV
4 mg/kg IV
£56/£112
£72
£80
Echinocandins
Caspofungin 50 mg IV x 1 day, £334
Drug Dosage AWP Cost/day for
70kg Patient