Basic must know things about Anti Hypertensive drugs including the recent JNC-8 classification and protocols for treating Hypertension with various co-morbid condition.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
EFFECTS OF EXCESS SALT DIET ON ANGITENSINOGEN SECRETIONS IN THE KIDNEY OVER TIMEchiehyin
Abstract
Background: Salt is an important component for normal function of cells. However, we consume more than 10 times the salt that is required. This high salt content affects the renin–angiotensin–aldosterone system (RAAS) that regulates blood pressure (BP) and water content of our body. Angiotensinogen is an oligopeptide hormone precursor serving as a substrate for renin in the formation of angiotensin I. Angiotensin I is converted to angiotensin II that causes vasoconstriction and a subsequent increase in BP. We hypothesized that angiotensinogen secretions increases in the kidney and urine with intake of high salt diet.
Methods: Dahl salt sensitive (SS) and salt resistant (SR) male rats (8 weeks old) were fed with high salt (HS) and low salt (LS) diet along with or without aldosterone (ALDO); aldosterone antagonist, eplerenone (EPL); and NADPH oxidase inhibitor, apocynin (APC) for 21 days. Urine samples and kidney were collected; total proteins isolated, and quantified using the microassay procedure and analyzed by western blot for angiotensinogen.
Results: Angiotensinogen was detected in the kidney samples of Dahl SS rat when fed either low or high salt diet, whereas angiotensinogen was detected in kidney samples of Dahl SR rats when fed with high salt diets. Angiotensinogen was not detected in urine samples.
Conclusions: In conclusion, consuming a high salt diet increases Angiotensinogen that lead to an increase in angiotensin II which may cause an increase in BP.
Acknowledgements: Vivien Thomas Summer Research Program, Morehouse School of Medicine, Atlanta, GA, USA.
Diuretics
Pharmacology
Katzung
Abnormalities in fluid volume and electrolyte composition are common and important clinical disorders. Drugs that block specific transport functions of the renal tubules are valuable clinical tools in the treatment of these disorders. Although various agents that increase urine volume (diuretics) have been described since antiquity, it was not until 1937 that carbonic anhydrase inhibitors were first described and not until 1957 that a much more useful and powerful diuretic agent (chlorothiazide) became available. Technically, a “diuretic” is an agent that increases urine volume, whereas a “natriuretic” causes an increase in renal sodium excretion and an “aquaretic” increases excretion of solute-free water. Because natriuretics almost always also increase water excretion, they are usually called diuretics. Osmotic diuretics and antidiuretic hormone antagonists (see Agents That Alter Water Excretion) are aquaretics that are not directly natriuretic.
Individualized Webcam facilitated and e-Classroom USMLE Step 1 Tutorials with Dr. Cray. 1 BMS Unit is 4 hr. General Principles and some Organ System require multiple units to complete in preparation for the USMLE Step 1 A HIGH YIELD FOCUS IN Biochemistry / Cell Biology, Microbiology / Immunology and the 4 P’s-Phiso, Pathophys, Path and Pharm. Webcam Facilitated USMLE Step 2 Clinical Knowledge and Clinical Skills diadactic tutorials /1 Unit is 4 hours, individualized one-on-one and group sessions, Including all Internal Medicine sub-sub-specitialities. For questions or more information.. drcray@imhotepvirtualmedsch.com
EFFECTS OF EXCESS SALT DIET ON ANGITENSINOGEN SECRETIONS IN THE KIDNEY OVER TIMEchiehyin
Abstract
Background: Salt is an important component for normal function of cells. However, we consume more than 10 times the salt that is required. This high salt content affects the renin–angiotensin–aldosterone system (RAAS) that regulates blood pressure (BP) and water content of our body. Angiotensinogen is an oligopeptide hormone precursor serving as a substrate for renin in the formation of angiotensin I. Angiotensin I is converted to angiotensin II that causes vasoconstriction and a subsequent increase in BP. We hypothesized that angiotensinogen secretions increases in the kidney and urine with intake of high salt diet.
Methods: Dahl salt sensitive (SS) and salt resistant (SR) male rats (8 weeks old) were fed with high salt (HS) and low salt (LS) diet along with or without aldosterone (ALDO); aldosterone antagonist, eplerenone (EPL); and NADPH oxidase inhibitor, apocynin (APC) for 21 days. Urine samples and kidney were collected; total proteins isolated, and quantified using the microassay procedure and analyzed by western blot for angiotensinogen.
Results: Angiotensinogen was detected in the kidney samples of Dahl SS rat when fed either low or high salt diet, whereas angiotensinogen was detected in kidney samples of Dahl SR rats when fed with high salt diets. Angiotensinogen was not detected in urine samples.
Conclusions: In conclusion, consuming a high salt diet increases Angiotensinogen that lead to an increase in angiotensin II which may cause an increase in BP.
Acknowledgements: Vivien Thomas Summer Research Program, Morehouse School of Medicine, Atlanta, GA, USA.
A review of the existing evidence that supports the current practice in perioperative medicine regarding Renin-angiotensin-aldosterone system antagonists, mainly ACE inhibitors and Angiotensin type 1 receptor blockers (ARB's).
Presented as the Cleveland Clinic Hospital Medicine Grand Rounds on April 1, 2009. CME AMA Category 1 - 1 hour.
Vk gmailcomcom and care Educate the ‘at the hell is not known meaning in 12 hindi meaning of the positive thought ke liye liye mana kiya hai maine us se baat karunga to delay ho gya h kya mere se baat
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of 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 leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
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. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
2. BLOOD PRESSURE
• Measure of pressure exerted on the lateral
wall of the blood vessels by a flowing column
of blood
• Has two components
– Systolic
– Diastolic
• Normal- 120/80 mm of Hg
3. FACTORS INFLUENCING BP
• Blood pressure = Cardiac output (CO)* Total
peripheral resistance(TPR)
• Cardiac output = Heart rate * Stroke volume
• Stroke volume in turn depends upon the
venous return and blood volume
• TPR depends upon the size of the blood
vessels mainly under the control of ANS
• RAAS System
6. How Anti Hypertensives work?
• By reducing blood volume and sodium
concentration
• By abolition of the sympathetic activity
• By dilating the blood vessels
• By inhibiting the RAAS system
8. DIURETICS
• THIAZIDE-1st line drug in Management.
– Hydrochlorthiazide- 12.5 to 50 mg
– Chlorthaidone- 12.5 to 25mg
– Indapamide- 1.25 to 5 mg . Longer acting
• LOOP DIURETICS
– Furosemide: 20 to 80 mg twice daily
– Torsemide: 10 to 40 mg
• POTASSIUM SPARING
– Amiloride: 5 to 10 mg
– Spiranolactone: 25 to 50 mg
– Triamterene : 100 mg
9. • Initial and prolonged effect?
– Initailly: Both CO and TPR reduces
– Later: CO comes to normal and TPR remains low
• ADR:
– Hypokalemia*
– Hyperglycemia* (What to do in diabetics?)
– Hyperuricemia *(What to do in GOUT?)
12. CENTRAL SYMPATHETIC OUTFLOW
INHIBITORS
• CLONIDINE (0.1 to 0.2 mg twice daily) and ALPHA
METHYL DOPA (250 to 500 mg twice daily)
• Alpha 2 receptor agonists in brain
• ADR:
– Clonidine- Rebound Hypertension
– Alpha Methyl Dopa- Hemolytic anemia
• Moxonidine and Rilmenidine- Imidazoline receptors
that modulate the activity of alpha 2 recpetors in brain
• Better to add diuretics in prolonged use due to their
sodium and water retention activity on prolonged use.
14. Ganglion Blockers
• Nn type receptor blockers in Ganglion
• Both sympathetic and parasympathetic system
is blocked
• Hence the side effects like Urinary retention
and dry mouth
• Hexamethonium and Trimethopan
• Not used nowadays except in Aortic dissection
16. ADRENERGIC NEURON BLOCKERS
• Reserpine, Guanethidine and Bretylium
• Reserpine
– Inhibits vesicular uptake of Adrenaline, Serotonin and
Dopamine.
– Serotonin- Depression and Suicidal tendencies
• Guanethidine and Bretylium
– Enters vesicles and displaces the Noradrenaline which
in turn is metabolised
– Active orally
– Orthostatic hypotension – Not a first dose
phenomenon.
18. Alpha Blockers
• NON SELECTIVE:
– Phenoxybenzamine: Pheochromocytoma
– Phentolamine: Clonidine withdrawal
– Tolazoline: Clonidine Withdrawal
– Greater Tachycardia than selective
• SELECTIVE:
– DOC in Hypertension with BPH
– First dose hypotension
– Do not impair metabolism: Can be used in Diabetics, CAD and
Gout
– Prazosin : 0.5 to 20 mg
– Terazosin: 1 to 5 mg
– Doxazosin: 1 to 4 mg
– Usually bed time doses
20. BETA BLOCKERS
• Inhibition of Beta-1 receptors
– Heart
– JG apparatus
– Brain
• Usually Cardioselective drugs are used
• Celiprolol, Oxeprenalol, Pindolol, Alprenolol
and acebutalol
• Esmolol, Atenolol, Nevibolol, Betaxolol and
bisoprolol.
21. • Metoprolol succinate 50-100mg and tartrate 50-
100mg twice daily
• Nebivolol 5-10mg
• Propranolol 40-120mg twice daily
• Carvedilol 6.25-25mg twice daily
• Bisoprolol 5-10mg
• Labetalol 100-300mg twice daily
• Carvedilol and Labetalol is both alpha and beta
blockers
22. • Not first line agents – reserve for post-MI/CHF
• Cause fatigue and decreased heart rate
• Adversely affect glucose metabolism
• Mask hypoglycemic awareness
• Non selective Beta blocker is contra-indiated
in Asthmatics
26. Calcium Channel Blockers
Calcium Channel
Blockers
Phenylalkylamines
Verapamil 80 to
120 mg thrice. ER-
240 to 480 mg
stat
Norverapamil
Benzothiazipines
Diltiazem180 to
360 mg
Dihydropyridines
Nifedipine, 30 to
90mg,Nicardipine,
Amlodipine 5-
10mg etc
27. • Blocks L- type calcium Channels
• Reducing the frequency of opening of the calcium channels and
that results in Smooth muscle relaxation and depression of heart.
• Dihydropyridines are also called as peripheral CCBs- Reflex
tachycardia more common
– Nifedipine
– Amlodipine- Maximum Half life
– Nicardipine- Longest acting
• Parentral
• DOC of hypertensive emergency
– Nimodipine: Cerebroselective
– Clevidipine: Ultrashort acting recently approved for Emergencies
• Verapamil> Diltiazem
33. • Sodium nitroprusside
– Short acting
– Continous i.v infusion in hypertensive emergency
– Accumulation of cyanide and produce toxicity
– Lead to hypothyroidism due to accumulation of
Thiocyanate.
41. Angiotensin Receptor Blockers.
• Candesartan 8-32mg
• Valsartan 80-320mg
• Losartan 50-100mg
– Competetive antagonist of TXA2
• Olmesartan 20-40mg
• Telmisartan 20-80mg
• Side effects are all same as ACE-i Other than
Cough and Angioedema.
46. Lifestyle changes
• Smoking Cessation
• Control blood glucose and lipids
• Diet
Eat healthy (i.e., DASH diet)
Moderate alcohol consumption
Reduce sodium intake to no more than
2,400 mg/day
• Physical activity
Moderate-to-vigorous activity 3-4 days a
week averaging 40 min per session
