1) The document discusses the effects of thyroid hormones on cardiovascular function and how thyroid diseases can impact the cardiovascular system.
2) It describes the cellular mechanisms of thyroid hormone action on the heart and blood vessels as well as changes in thyroid hormone levels that can occur due to conditions like heart attack or heart failure.
3) Both hyperthyroidism and hypothyroidism are associated with changes in cardiovascular hemodynamics and can manifest as various heart conditions or symptoms. Successful treatment of the underlying thyroid abnormality can help reverse many of these cardiovascular impacts.
Study material for Doctor of pharmacy and other medical students. Hypertension is a condition in which the force of the blood against the artery walls is too high. Approximately one billion adults or ~22% of the population of the world have hypertension. It is slightly more frequent in men, in those of low socioeconomic status, and prevalence increases with age. So it is more important to manage it as early, this includes Pharmacological as well as Non-pharmacological Management.
Thyroid Hormones and Cardiovascular Function and Diseasesmagdy elmasry
Thyroid hormone system.
Thyroid hormone action on the CVS.
Thyroid hormones and cardioprotection.
How does thyroid disease affect the heart?
- Thyroid disease and CV risk factors.
- Thyroid dysfunction and CVD.
Thyroid hormones : a future therapeutic option?
New recommendations for a thyroid and CVD.
Thyroid and CV drugs.
Study material for Doctor of pharmacy and other medical students. Hypertension is a condition in which the force of the blood against the artery walls is too high. Approximately one billion adults or ~22% of the population of the world have hypertension. It is slightly more frequent in men, in those of low socioeconomic status, and prevalence increases with age. So it is more important to manage it as early, this includes Pharmacological as well as Non-pharmacological Management.
Thyroid Hormones and Cardiovascular Function and Diseasesmagdy elmasry
Thyroid hormone system.
Thyroid hormone action on the CVS.
Thyroid hormones and cardioprotection.
How does thyroid disease affect the heart?
- Thyroid disease and CV risk factors.
- Thyroid dysfunction and CVD.
Thyroid hormones : a future therapeutic option?
New recommendations for a thyroid and CVD.
Thyroid and CV drugs.
The third presentation in my ACEM Fellowship Summary series. Focuses on the aetiology, diagnosis and management of acute heart failure in its many forms.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- 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
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
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
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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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.
3. Cellular mechanisms of thyroid hormone action
Effects of thyroid hormone on cardiovascular
hemodynamics
Clinical manifestations of thyroid diseases from a
cardiovascular perspective
Changes in thyroid hormone metabolism that arise
from acute MI and chronic congestive heart failure
4. Classic “feedback” loop mechanism: T4 & T3 regulate
pituitary synthesis and release of TSH
A highly sensitive TSH assay- initial test
Suggestion about narrowing TSH reference range
especially upper limit at which hypothyroidism may be
present
TSH>20 mIU/L: overt hypothyroidism
TSH 3-20 mIU/L: milder or subclinical hypothyroidism
Suppressed TSH <0.1 mIU/L: hyperthyroidism
6. Thyroid gland secrets mainly (≈85%) T4 which is converted to T3 by
5´-monodeiodinase in various tissues
No significant myocyte intracellular deiodinase activity- the heart
relies mainly on serum T3
T3 binds to thyroid hormone nuclear receptors (TRs), belongs to
superfamily of steroid hormone receptors
TRs bind to thyroid hormone response elements (TREs) in the
promoter region of positively regulated genes → mediate induction
of transcription
TRs bind to TREs in the absence as well as in the presence of
ligand
While bound to T3, TRs induce transcription, and in the
absence of T3 they repress the transcription
7. Occur rapidly, do not involve TRE-mediated transcriptional
events
Changes in various membrane ion channels for Na, K & Ca
Effects on:
Actin polymerization
Adenine nucleotide translocator 1 in mitochondrial
membrane
Variety of intracellular signaling pathways in heart &
vascular smooth muscle
11. Expression of both structural & regulatory genes in cardiac
myocyte
↑ T3 → cardiac hypertrophy, mainly due to ↑ hemodynamic load
Hyperthyroidism resembles hyperadrenergic state: no evidence to
suggest ↑TH enhance cardiac sensitivity to adrenergic stimulation
Serum catecholamines low or normal
Several components of cardiac myocyte β adrenergic system are
regulated by thyroid hormones:
β1 adrenergic receptors are positively regulated
Guanine nucleotide regulatory proteins
Adenylate cyclase
12. TRα1 receptors are negatively regulated
Pacemaker-related genes, hyperpolarization-activated cyclic
nucleotide-gated channels 2 & 4 are transcriptionally regulated by
thyroid hormones
β-adrenergic receptor stimulation → ↑cAMP → accelerates
diastolic depolarization → ↑ HR
Hyperthyroidism → AF; may be due to combination of genomic &
nongenomic actions on atrial ion channels plus atrial enlargement
β-adrenergic blockade: ↓HR, enhanced diastolic performance is
not altered (indicating that T3 acts directly on the heart to increase
calcium cycling)
13. BP is altered across the entire spectrum of thyroid function
Changes are similar to physiological response to exercise
Hyperthyroidism:
Widened pulse pressure
Increased arterial stiffness
Low SVR →Isolated Systolic HTN
Hypothyroidism:
Endothelial dysfunction
Impaired VSM relaxation → ↑SVR → Diastolic HTN
14. High prevalence of Pulmonary HTN & AV valve regurgitation in
hyperthyroidism
Effect of TH to ↓SVR may not occur in pulmonary vasculature
Primary pulmonary HTN (Pulmonary Artery Pressure >25 mmHg at
rest & >30 mmHg during exercise):
• Often unknown origin
• A link to thyroid disease (both hyper- & hypothyroidism) has
been identified
• Thyroid disease should be considered in DD of Primary
pulmonary HTN
15. ↓ Fractional
clearance of LDL
by liver:
• ↓ No. of LDL
receptors
• ↓ LDL receptor
activity
↓ Catabolism of
cholesterol into
bile
• T3 negatively
regulates liver
specific enzyme
cholesterol 7α-
hydroxylase
Overt
Hypothyroidism:
• Hypercholesterolemia
• Marked ↑ LDL &
Apolipoprotein B
• Changes are also
evident in subclinical
hypothyroidism
90% of hypothyroid patients had hypercholesterolemia
Prevalence of overt hypothyroidism in patients with hypercholesterolemia
is 1.3-2.8%
16. Palpitations Anginal chest pain
Exercise intolerance Atrial fibrillation
Exertional dyspnea Cardiac hypertrophy
Systolic hypertension Peripheral edema
Hyperdynamic circulation Congestive heart failure
Cardiac output increased by 50-300% of normal: combined effect of
increased resting HR, contractility, blood volume & EF with a decrease in
SVR
Cerebrovascular ischemic symptoms has been reported in young patients
with Graves’ disease
Routine TSH in cardiac & cerebral ischemic symptoms
17. Prevalence: 2-20%, ↑ with age (≈15% in patients >70 yrs)
40,628 patients in the Danish National Registry:
• 8.3% developed AF
• Male gender, ischemic or valvular heart disease or CHF
increased risk
Subclinical hyperthyroidism carry same relative risk
In unselected patients who present with AF, <1% were the result
of overt hyperthyroidism
Ability to restore thyrotoxic patients to a euthyroid state & sinus
rhythm justifies TSH testing in new onset AF
18. β-adrenergic blockade: by β1-selective or nonselective agent
Rapid restoration of chemical euthyroid state: ATD or
Radioiodine
Digitalis:
• ↑rate of digitalis clearance, ↓sensitivity of hyperthyroid heart
• Needs higher dose with less predictable response
Calcium channel blockers: sp. parenteral, should be avoided
• Through effects on the smooth muscle cells of the resistance
arterioles, may lead to acute hypotension & CV collapse
19. Risk for systemic embolization is not precisely known
Advancing AGE rather than presence of AF was major risk factor
Review of large series of patients failed to demonstrate a
prevalence of thromboembolic events greater than the risk
reported for major bleeding events from warfarin therapy
In younger patients with hyperthyroidism, in absence of other
independent risk factors for embolization, the benefits of
anticoagulation may be outweighed by the risk
Aspirin reduces risk for embolic events and safe alternative
20. Majority revert to sinus rhythm within 2-3 months of successful
treatment with ATD or RI
Older (>60 yrs) with AF of longer duration less likely to revert
• If AF persists after chemical euthyroidism is achieved,
electrical or pharmacological cardioversion should be
attempted
• Majority can be restored to sinus rhythm & will remain so for a
prolonged period of time
• Addition of Disopyramide (300mg/d) lets such patents to
maintain sinus rhythm
21. Paradoxical finding- ?high-output failure, does not accurately apply
Exaggerated sinus tachycardia or AF can produce LV dysfunction
& HF
Preexistent ischemic or hypertensive heart disease
Mitral valve prolapse: increased incidence, causing LA
enlargement & AF
High prevalence of pulmonary artery HTN: some similar signs
Exercise intolerance & Exertional dyspnea: may be due to
↓pulmonary compliance or ↓respiratory & skeletal muscle function
23. ↓Expression of Sarcoplasmic reticulum Ca2+-ATPase
↑Expression of Phospholamban (inhibitor of SR Ca2+-ATPase)
Slowing of the isovolumic relaxation phase of diastolic function
24. Effect
• Impaired cardiac contractility & diastolic function
• Increased systemic vascular resistance
• Decreased endothelial derived relaxation factor
• Increased serum cholesterol
• Increased C-reactive protein
• Increased homocysteine
Diastolic HTN
• Accelerated atherosclerosis
• Increased risk of CAD
• Increased risk of stroke
RESULTS
IN
• Prolongation of QT interval → Ventricular arrhythmias
• Protein rich pericardial and/or pleural effusion
25. Poses some challenge
In young healthy patients: full replacement dose of L-thyroxine of
1.6 µg/kg/d can be initiated at the outset
In older patients: start low (25 to 50 µg/d) and go slow (increase
the dose no more rapidly than every 6 to 8 weeks)
A predictable improvement in thyroid and CV functional measures
Concerns that restoration of the heart to a euthyroid state might
adversely affect underlying ischemic heart disease are largely
unfounded
Patients with atherosclerotic cardiovascular disease more often
improve, rather than worsen, with treatment
26. Low or undetectable serum TSH with normal T4 & T3
May have no clinical signs or symptoms
Prevalence increase with age
Low TSH is associated with increased risk for CV mortality & AF
Treatment is controversial
Older patients with MNG or GD: should be treated especially if
they are deemed to be at risk for cardiovascular disease
27. Affects 7-10% of older women
Frequently asymptomatic but many have symptoms of hypo
↑Cholesterol & CRP
Risk of atherosclerosis, CAD & MI increased
The benefits of the restoration of TSH levels to normal can be
considered to outweigh the risks
28. The low T3 syndrome: a fall in serum T3 accompanied by
normal serum T4 and TSH levels
Results from impaired hepatic conversion of T4 to the biologically
active hormone, T3, by 5´-monodeiodinase
The cardiac myocyte has no appreciable deiodinase activity and
therefore relies on the plasma as the source of T3
In experimental animals the low T3 syndrome leads to the same
changes in cardiac function and gene expression as does
primary hypothyroidism.
Significant similarities exist between the hypothyroid phenotype
and the HF phenotype (↓cardiac contractility & cardiac output, &
an altered gene expression profile)
29. ≈30% of patients with CHF have low T3 levels
Reduction of T3 is proportional to the severity of HF
Reduced serum T3 is a strong predictor of all-cause and CV
mortality and, in fact, is a stronger predictor than age, LV EF, or
dyslipidemia
It has been suggested that T3 therapy might improve cardiac
function in this clinical situation
30. Antiarrhythmic drug with a high iodine content (75mg iodine/200mg)
Can cause either hypothyroidism (5% to 25% of treated patients) or
hyperthyroidism (2% to 10% of treated patients)
Inhibits of 5´-deiodinase activity → Inhibits conversion of T4 to T3
Iodine released from amiodarone metabolism directly inhibit thyroid
gland function, if the effect persists, lead to amiodarone-induced
hypothyroidism
Preexistent thyroid disease and Hashimoto’s thyroiditis ↑ risk
If hypothyroidism develop with a persistent rise in TSH: L-thyroxine
therapy started
31. Type 1 hyperthyroidism:
• iodine-induced excess thyroid hormone synthesis
• underlying thyroid disorder, e.g., nodular goiter or latent GD
• in regions where iodine intake is low
Type 2 hyperthyroidism:
• thyroiditis due to a direct cytotoxic effect of amiodarone →↑release of
thyroid hormones → transient thyrotoxicosis in a previously normal
thyroid gland
Can overlap & difficult to distinguish, RIU is low in both types
Point favors Type 2 hyperthyroidism: Signs of inflammation, elevated ESR
& IL-6, modest increases in thyroid gland size
32. ATDs effective in type 1, ineffective in type 2 thyrotoxicosis.
Prednisolone is beneficial in the type 2 form
Beta blocker should be started
A pragmatic approach is to commence combination therapy with an
ATD and glucocorticoid in patients with significant thyrotoxicosis
A rapid response (within 1–2 weeks) usually indicates a type 2 picture
and permits withdrawal of the antithyroid therapy
A slower response suggests a type 1 picture, when antithyroid drugs
may be continued and prednisolone withdrawn.
Potassium perchlorate can be used to inhibit iodine trapping in thyroid
33. If the cardiac state allows, amiodarone should be discontinued
The course of the disease may last for anywhere between 1 to 3
months
In rare cases, surgical thyroidectomy under local anesthesia has
proven to be effective
To minimize the risk of type 1 thyrotoxicosis, thyroid function should
be measured in all patients prior to commencement of amiodarone
therapy, and amiodarone should be avoided if TSH is suppressed
In general, patients treated with amiodarone should have thyroid
function (specifically TSH) testing periodically throughout therapy
34. Thyroid dysfunction (both hypo & hyper) virtually affects the
whole spectrum of cardiovascular hemodynamics
Thyroid functional abnormality can case a range of
cardiovascular signs-symptoms and cardiovascular
diseases are also associated with derangement of thyroid
functions
Restoration of normal thyroid function most often reverses
the abnormal cardiovascular hemodynamics
35. Prof. Md. Farid Uddin
Chairman, Department of Endocrinology, BSMMU
Prof. M.A. Hasanat
Department of Endocrinology, BSMMU
All the colleagues of my department