This document discusses the role of beta blockers in the treatment of hypertension. It covers the pharmacodynamics and pharmacokinetics of beta blockers, specific agents used, their adverse effects, history of use, and concerns regarding their use. While beta blockers were previously considered first-line treatment for hypertension, more recent trials have shown other agents may provide better outcomes. However, beta blockers are still important treatment options, especially newer vasodilating agents like nebivolol and carvedilol which have shown benefits over older non-vasodilating beta blockers.
heparin in detail : mechanism of action, pharmacokinetics, clinical uses, adverse effect and contraindication of heparin and low molecular heparin.
for undergraduates.
Sulfonyl ureas pharmacology Presented by arjumandPARUL UNIVERSITY
Sulfonylureas are most commonly used Oral Hypoglycemic drugs helpful in treating Diabetes Mellitus .
They show their effects on beta cells of the pancreas to release insulin which maintains the blood sugar level.
They are also called as ATP sensitive Potassium[K] channel blockers
This presentation deals with the beta blockers commonly used in day-to-day practice alongwith some interesting mnemonics to remember their names & site of action
heparin in detail : mechanism of action, pharmacokinetics, clinical uses, adverse effect and contraindication of heparin and low molecular heparin.
for undergraduates.
Sulfonyl ureas pharmacology Presented by arjumandPARUL UNIVERSITY
Sulfonylureas are most commonly used Oral Hypoglycemic drugs helpful in treating Diabetes Mellitus .
They show their effects on beta cells of the pancreas to release insulin which maintains the blood sugar level.
They are also called as ATP sensitive Potassium[K] channel blockers
This presentation deals with the beta blockers commonly used in day-to-day practice alongwith some interesting mnemonics to remember their names & site of action
E BOOK SLIDES CONTAINING QUESTIONS WITH BRIEF ANSWERS AND MNEUMONICS AND IMAGES TO HELP ALL PG ASPIRANTS-DR MANJUNATH DIRECTOR DOCTORS ACADEMY DAVANAGERE
India has a large pool of diabetic patients
ICMR-INDIAB study – extrapolated estimations suggest 62.4 million people with diabetes and 77.2 million are prediabetic
Estimates show ~ 85.5% men and 97.8% women who are diabetic in India have concomitant dyslipidemia
Medicinal Chemistry of Antihypertensive agents pptxSameena Ramzan
introduction of Hypertension, Pharmacological classification of antihypertensives, Chemical classification, Drug synthesis profile (including every class), Mechanism of Action(including every class), Uses, Adverse Effects, Structure Activity Relationship(including every class)
A presentation hypertension
(what blood pressure is, what is hypertension, what are the risk factors of hypertension, how is it managed?) and other related knowledge on hypertension
Pharmacology of Hypertension.
Pulmonary Hypertension.
Regulation of blood pressure.
Classification of Anti-Hypertensive drugs.
Treatment of Hypertension.
Diuretics.
Pharmacotherapy of congestive heart faliure Rahulvaish13
This PPT covers the pathophysiology, treatment protocol and details of individual drugs used and those drugs failed in clinical trials; taken from standard text books and articles as reference. This will be extremely useful for undergraduates ( MBBS, BDS,) and postgraduates (MD,MDS ,Phd).
Similar to Beta blockers: Role in Hypertension (20)
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
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
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
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
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
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
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
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.
2. TABLE OF CONTENT
Introduction
Pharmacodynamics & Pharmacokinetics
Specific Agents
Adverse Effects
Clinical Use
History
Concerns
End of the Road?
Indications for use in Hypertension
Conclusion
3. INTRODUCTION
Beta Blockers are competitive antagonists that block the receptor site for
endogenous catecholamines on the adrenergic beta receptors.
Some are partial agonists while most are pure antagonists.
Beta blockers differ in their relative affinity for β1 and b2 receptors.
4. ADRENERGIC BETA RECEPTORS
β1 RECEPTORS
Located mainly in the heart and the kidneys.
Stimulates viscous, amylase-filled secretions from salivary glands.
Increases cardiac output:
(+) Chronotropic effect.
(+) Inotropic effect.
(+) Dromotropic effect.
(+) Bathmotropic effect.
Renin release from juxtaglomerular cells.
Lipolysis in adipose tissue.
Relaxation of urinary bladder.
5. ADRENERGIC BETA RECEPTORS
b2 RECEPTORS
Located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular
smooth muscle and skeletal muscle.
Muscular system:
Smooth muscle relaxation – Delay in digestion and micturition, inhibition of
labour & facilitation of respiration.
Blood vessels – Dilates arteries increasing perfusion.
Circulatory system:
Increases cardiac output.
Eye: Increases intraocular pressure.
GI: Glycogenolysis and gluconeogenesis with Insulin secretion.
Lung: Bronchiole dilatation.
6. ADRENERGIC BETA RECEPTORS
β3 RECEPTORS
Located mainly in the adipose tissues.
Enhancement of lipolysis.
Thermogenesis in skeletal muscles.
7. PHARMACODYNAMICS &
PHARMACOKINETICS
PHARMACOKINETICS:
Most of the drugs are absorbed well orally, peak concentrations occur 1-3
hours after ingestion.
Bioavailability of most β-blockers is limited.
Rapidly distributed.
Some like Propranolol and Pindolol are lipophilic and readily cross the
blood-brain barrier.
Most of them have half-lives in the range of 3-10 hours.
8. PHARMACODYNAMICS
The effects of β-blockers are due to occupation and blockade of β
receptors.
Some actions may be due to partial agonist activity and local anesthetic
action.
CARDIOVASCULAR SYSTEM:
β-blockers lower the blood pressure in patients with hypertension.
Mechanism is not fully understood; but probably include suppression of
renin release and effects in the CNS.
Prominent effect on the heart and valuable in the treatment of angina,
chronic heart failure and following myocardial infarction.
Negative chronotropic, inotropic, dromotropic & bathmotropic effect.
9. PHARMACODYNAMICS
Oppose β2 mediated vasodilation which may acutely lead to rise in
peripheral vascular resistance from unopposed a receptor mediated
effects in the sympathetic nervous system.
RESPIRATORY TRACT:
Increase in airway resistance, especially asthmatics.
Selective β-blockers are advantageous over non-selective ones, however
none of them are sufficiently specific to completely avoid β2 -receptors.
EYE:
Reduce intraocular pressure by decreasing aqueous humor production,
especially in Glaucoma.
10. PHARMACODYNAMICS
METABOLIC & ENDOCRINE EFFECTS:
Inhibit lipolysis via sympathetic system.
Glycogenolysis is partially inhibited in the liver by b2 blockade.
Impairment of recovery from hypoglycaemia although b1 selective
antagonism may be less prone to it.
Increased concentration of VLDL and decreased concentration of HDL,
although this is less prone in partial agonists.
EFFECTS NOT RELATED TO b BLOCKADE:
Intrinsic sympathomimetic activity.
Membrane-stabilizing activity.
11. SPECIFIC AGENTS
PROPRANOLOL:
Prototypical non-selective b Blocker.
METOPROLOL AND ATENOLOL:
β1-selective group.
Preferred in COPD, Asthma (caution), Diabetes and PVD over non-
selective β-Blockers.
NEBIVOLOL:
Most highly selective β1-Blocker.
Causes vasodilation.
Increases insulin sensitivity and does not have adverse effect on lipid
metabolism.
12. SPECIFIC AGENTS
PARTIAL AGONISTS:
Pindolol, Acebutolol, Cartelol, Penbutolol, etc.
Likely to cause less rest bradycardia, less reduction in cardiac output,
abnormalities in plasma lipids and may produce vasodilation with
increased arterial compliance.
LABETALOL:
Reversible a1 and b blocker with partial agonist activity.
Decreases BP with having little effect over HR and CO.
CARVEDILOL:
Non-selective b-Blocker with a1 adrenoreceptor blocking capacity.
Decreased peripheral vascular resistance by causing vasodilation.
SOTALOL:
Class III Anti-arrhythmic agent.
13. ADVERSE EFFECTS
CARDIAC EFFECTS:
Exacerbation of acute heart failure.
Negative chronotropic effect.
b-Blocker withdrawal.
EXTRA-CARDIAC EFFECTS:
Increased airway resistance.
Exacerbation of peripheral artery disease.
Facilitation of hypoglycaemia.
Hyperkalemia.
Depression, fatigue, sexual dysfunction.
Lipid metabolism and weight gain.
15. HISTORY
In the 1960s, Dr. James Black, a Scottish pharmacologist and his
associates started working on β-Blockers for treatment of angina.
Pronethalol was released in 1963 but marketed only for life-threatening
conditions because of its side effects.
Propranolol was launched in 1965 as ‘Inderal’. It quickly became a best-
selling drug , used to treat a wide range of cardiovascular diseases such
as angina, arrhythmia, hypertension and hypertrophic cardiomyopathy.
In 1976, Atenolol was launched as ‘the ideal β-Blocker’ and soon replaced
Propranolol as the best selling heart drug.
Metoprolol was made in 1969 and launched in the U.S in 1978.
Bisoprolol and Carvedilol was released in 1986 and 1995 respectively.
Dr. James Black was awarded the Nobel Prize in Medicine in 1988.
16. HISTORY
In ancient Indian Ayurvedic and Chinese medicine, a hard pulse felt on
palpation qualified as hypertension.
Dr. Akbar Mahomed, an Irish-Indian, was the first physician to describe
essential hypertension in the late 19th century.
The modern quantitative concept of hypertension came along after the
discovery of the sphygmomanometer in the early 20th century.
Even then, Hypertension was not considered a disease.
Veterans Administration Co-operative Research Study published in 1967
and 1970 was a landmark achievement in Medicine that established that
treating essential hypertension leads to lower incidence of CHF and
Stroke.
18. TRIALS
MRC Trial (1985): Use of Propranolol & Thiazide diuretic to treat mild
hypertension. Found decreased risk of Stroke in comparison to placebo.
HAPPHY & MAPHY (1987): Use of Atenolol & Metoprolol in comparison to
Thiazide diuretics. No significant difference in end-points.
STOP – Hypertension (1991): Use of Atenolol, Pindolol, Metoprolol &
Hydrochlorothiazide. No significant difference observed.
SHEP (1991): Use of Atenolol or Hydrochlorothiazide. Benefits of treating
isolated systolic hypertension.
TOMHS (1993): Use of Acebutolol. To compare BP lowering effects of six
treatment regimen. All six had sizeable BP reduction.
UKPDS (1998): Use of Atenolol. To compare outcomes in hypertension
management among diabetics with Captopril. Equally effective outcomes.
19. TRIALS
AASK (2002): Use of Metoprolol. To determine a suitable drug regimen in
hypertension control to prevent renal failure (Ramipril, Amlodipine).
Superiority of Ramipril over Metoprolol was only marginal.
LIFE (2002): Use of Atenolol and Losartan in patients with hypertension
and LVH. Greater reduction in cardiovascular and cerebral end-points with
Losartan.
INVEST (2003): Comparison of CCB with Atenolol for patients with
Hypertension and Coronary Artery Disease. Equally effective.
CONVINCE (2003): Use of CCB and Atenolol. No significant difference in
risk of MI.
21. CONCERNS
ALLHAT (2002): Brought Thiazide diuretics to the forefront. Showed
reduced HF rates in hypertensives and dyslipidemics.
Lancet Meta-Analysis (2004): Suggested that Atenolol did worse than
other antihypertensives in reducing stroke [Lindholm et al].
Lancet Meta-Analysis (2005): In comparison with other antihypertensive
drugs, the effect of β blockers is less than optimum, with a raised risk of
stroke [Lindholm L et al].
Cochrane Meta-Analysis (2012): Beta blockers were inferior to other
antihypertensive drugs in reduction of cardiovascular disease [Wiysonge
et al].
ASCOT-BPLA (2005): CCB and ACEI are better than β blocker and
Thiazide diuretics [Dahlof B et al].
CAFE (2006): Amlodipine reduced central aortic pressure more than
Atenolol [Williams B et al].
22. CONCERNS
Based on the mounting evidence, β blockers were relegated to the
second-line in JNC-8 guidelines.
Several theories have been proposed to explain the observed risk of
stroke:
Pulse wave dyssynchrony leading to increased central aortic pressure.
Less effective lowering of blood pressure.
Visit-to-visit blood pressure instability (Peak-trough ratio).
Unfavourable metabolic effects.
24. END OF THE ROAD?
A CJC Meta-Analysis in 2014 revealed all β blockers were effective in reducing
cardiovascular end-points in young adults. Increased incidence of Stroke with
Atenolol in older population [Kuyper & Khan].
A CMAJ Meta-Analysis in 2007 revealed that most of the previously observed
stroke risk was confounded by older populations [Khan & McAlister].
Most of the analysis on cardiovascular outcomes are derived from studies
using Atenolol.
Vasodilatory β blockers may be safer!
Many recent studies have shown that Nebivolol, Labetalol and Carvedilol
significantly reduce central aortic pressure.
HJ (2011): Nebivolol vs Metoprolol.
JCH (2013): Nebivolol, Carvedilol, Metoprolol.
Nature (2014): Losartan vs Carvedilol.
HJ (2016): Meta-analysis comparing vasodilating β blockers and non-vasodilating β
blockers.
25. INDICATIONS FOR USE IN
HYPERTENSION
DIABETES:
The adverse metabolic and lipid consequences of traditional β blockers
raises some concerns.
There seems to be a increased risk of new-onset diabetes with use of
Atenolol and Propranolol.
Nebivolol and Carvedilol have shown neutral or beneficial effects on
metabolic parameters.
GEMINI Trial.
YESTONO Study.
26. INDICATIONS FOR USE IN
HYPERTENSION
CORONARY ARTERY DISEASE:
β blockers not only reduce blood pressure but decrease the myocardial
oxygen demand.
Effects of nonvasodilating β blockers on hyperemic coronary blood flow
are variable.
Because of amelioration of rest and hyperemic coronary blood flow,
vasodilatory β blockers may be a better option than traditional β blockers in
patients with high coronary artery disease risk.
27. INDICATIONS FOR USE IN
HYPERTENSION
POST MYOCARDIAL INFARCTION:
Recommended in the AHA guidelines.
The value of β blockers in patients after MI has been established in BHAT
and CAPRICORN.
Only Carvedilol is recommended among the vasodilatory β blockers.
28. INDICATIONS FOR USE IN
HYPERTENSION
HEART FAILURE:
It is a serious natural progression of uncontrolled hypertension.
3 β blockers are found to improve outcomes in patients with systolic heart
failure by inhibiting the negative effects associated with sympathetic
nervous system.
Carvedilol: COPERNICUS (2001)
Metoprolol: MERIT HF (1999)
Bisoprolol: CIBIS (1999)
Their benefits include reducing the risk of death and reducing symptoms,
improving clinical status and improving the overall well-being of the patient.
Risk of mortality and rehospitalization are significantly lower with their use.
29. CONCLUSION
β blockers may no longer be the undisputed leader in management of
hypertension.
They still hold a special place in the treatment of cardiovascular diseases
including hypertension due to their cost-effectiveness and a reasonable
adverse effect profile.
The reality of modern hypertension treatment is that most patients will
require multiple drugs. In patients with comorbidities, combination therapy
will be essential.
Third generation vasodilating β blockers have many advantages over their
predecessors and should be preferred whenever possible.
30. REFERENCES
Harrison’s Principles of Internal Medicine
Katzung’s Basic & Clinical Pharmacology
The Lancet
The Cochrane Library
www.uptodate.com
www.medscape.com
www.ncbi.nlm.nih.com
www.aha.com
www.ajconline.org
31. “I wish I had my beta blockers handy”
- Dr. James Whyte Black (on being told that he had won the Nobel Prize)
THANK YOU