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Thyroid Gland and Disease of Thyroid GlandRanadhi Das
The thyroid gland is one of the largest endocrine glands.
The thyroid gland is located immediately below the larynx and anterior to the upper part of the trachea. It weighs about 15-20g.
It consists of 2 lateral lobes connected by a narrow band of thyroid tissue called the isthmus.
The isthmus usually overlies the region from the 2nd to 4th tracheal cartilage.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
Thyroid Gland and Disease of Thyroid GlandRanadhi Das
The thyroid gland is one of the largest endocrine glands.
The thyroid gland is located immediately below the larynx and anterior to the upper part of the trachea. It weighs about 15-20g.
It consists of 2 lateral lobes connected by a narrow band of thyroid tissue called the isthmus.
The isthmus usually overlies the region from the 2nd to 4th tracheal cartilage.
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused primarily by Salmonella enterica, subspecies enterica serovar typhi and, to a lesser extent, related serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated, typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or permanent neuropsychiatric complications.
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female sexual dysfunction
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acute leukemia
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Introduction to toxicology gases and metalsNITISH SHAH
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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
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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
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.
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.
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
- 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
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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
2. Hypothyroidism
■ Hypothyroidism is a clinical syndrome resulting from a
deficiency of thyroid hormones.
■ There is a generalized slowing down of metabolic
processes.
■ In newborn infants – Cretinism
■ In adolescents – short stature, mental retardation,
precocious puberty
■ In adults – symptoms largely reversible after therapy
3.
4. Interpretation for Thyroid Function Test
High T4 Normal T4 Low T4
High
TSH
In vivo or in vitro artefact
Pituitary hyperthyroidism
Thyroid hormone resistance
Subclinical hypothyroidism Primary hypothyroidism
Normal
TSH
As above
Sampling within 6 h of
thyroxine dose
Normal
Pituitary or hypothalamic
hypothyroidism
Severe non-thyroidal illness
Low TSH Hyperthyroidism
Subclinical hyperthyroidism
Subtle thyroxine
overreplacement
Autonomous functioning
thyroid nodule
Non-thyroidal illness
Pituitary or hypothalamic
hypothyroidism
Severe non-thyroidal illness
5. Etiology of Hypothyroidism
■ Primary – thyroid failure
■ Secondary – pituitary TSH deficit (Hypopituitarism due to
pituitary adenoma, apoplexy, infiltrative disease-sarcoidosis)
■ Tertiary – hypothalamic deficiency of TRH (rare)
■ Peripheral resistance to the action of thyroid
hormone
6.
7. Hashimoto’s Thyroiditis
■ Chronic lymphocytic thyroiditis
■ Probably the most common cause of hypothyroidism
■ With (younger patients) or without goiter (older patients – atrophy
gland after destruction by immunologic process)
■ High titer of autoantibodies to thyroidal antigens
(Thyroglobulin Ab, Thyroperoxidase Ab = TPO Ab =
Antimicrosomal Ab = AMA)
8. Pathogenesis of Hypothyroidism
■ Characteristic finding: accumulation of
glycosaminoglycans – mostly hyaluronic acid – in
interstitial tissues
■ The accumalation is due not to excessive synthesis but
to decreased destruction of glycosaminoglycans.
■ Accumulation of this hydrophilic substance and
increased capillary permeability to albumin account for
this interstitial edema that is particularly evident in the
skin, heart muscle, and striated muscle.
9. Clinical Manifestations of
Hypothyroidism
■ Symptoms and signs vary in relation to the magnitude of
the thyroid hormone deficiency, and the acuteness with
which the deficiency develops.
❖ Less prominent clinically and better tolerated when
gradual loss of thyroid function (as in most cases of
primary hypothyroidism)
❖ Symptoms develop acutely after thyroidectomy or
abrupt withdrawal of exogenous thyroid hormone
10.
11. Clinical Manifestations of Hypothyroidism -- Skin
■ Cool and pale skin blood flow
■ Dry roughness of skin the epidermis has an
atrophied cellular layer and hyperkeratosis
■ Decreased sweating calorigenesis and acinar gland
secretion
■ Generalized nonpitting edema (myxedema) in severe
hypothyroidism infiltration of the skin with
glycosaminoglycans and associated water retention
12. Clinical Manifestations of Hypothyroidism -- Eyes
■ Periorbital edema -- as a manifestation of generalized
nonpitting edema or Graves' ophthalmopathy.
■ Graves' ophthalmopathy may persist or worsen when
hypothyroidism develops after treatment of Graves'
hyperthyroidism. Patients will have variable degrees of
stare, protrusion of the eyes, and extraocular muscle
weakness.
13. Clinical Manifestations of Hypothyroidism --
Cardiovascular System
■ Bradycardia reductions in heart rate
■ Impaired muscular contractility
■ Reduced cardiac output decreased exercise capacity and
shortness of breath during exercise
■ ECG: low voltage of QRS complexes and P and T waves
■ CXR: cardiomegaly interstitial edema, myofibrillary
swelling, LV dilatation, pericardial effusion
14. Clinical Manifestations of Hypothyroidism --
Cardiovascular System
■ Myxedema induces coronary artery disease ??
■ CAD more common in p’ts with hypothyroidism
■ Symptoms and signs of congestive heart failure are
usually absent in patients who have no other cardiac
disease
■ Congestive heart failure or angina may worsen when
hypothyroidism develops in patients with heart disease
15. Clinical Manifestations of Hypothyroidism --
Cardiovascular System
■ Hypertension peripheral vascular resistance
❖ In normotensive patients, BP increases are small
(<150/100 mmHg).
❖ The BP of patients with established hypertension may
increase further with the development of
hypothyroidism.
16. Clinical Manifestations of Hypothyroidism -- Respiratory
System
■ Fatigue, shortness of breath on exertion, and decreased
exercise capacity impaired respiratory function +
cardiovascular disease
■ Hypoventilation (shallow and slow respirations)
respiratory muscle weakness + reduced pulmonary
responses to hypoxia and hypercapnia
■ Obstructive sleep apnea macroglossia
17. Clinical Manifestations of Hypothyroidism --
Gastrointestinal Disorders
■ Constipation, even ileus gut motility
■ Decreased taste sensation
■ Gastric atrophy presence of antiparietal cell antibodies.
Pernicious anemia occurs in 10% of patients with
hypothyroidism caused by chronic autoimmune thyroiditis.
■ Weight gain decreased metabolic rate + accumulation of
fluid (nonpitting edema) that is rich in glycosaminoglycans
■ Ascites, rare
18. Clinical Manifestations of Hypothyroidism -- Renal
Function
■ Decreased glomerular filtration rate (GFR )
■ Impaired ability to excrete a water load
■ The drug clearance (ex, antiepileptic, anticoagulant,
hypnotic and opioid drugs), is decreased. Drug toxicity
may occur if drug dosage is not reduced.
■ During T4 replacement, drugs that are administered at
effective doses in patients who are hypothyroid may
become less effective.
19. Clinical Manifestations of Hypothyroidism -- Anemia
■ Impaired hemoglobin synthesis thyroxine deficiency
■ Iron deficiency increased iron loss with menorrhagia
+ impaired intestinal absorption of iron
■ Folate deficiency impaired intestinal absorption of
folic acid
■ Pernicious anemia vitamin B12 -deficient
megaloblastic anemia
20. Clinical Manifestations of Hypothyroidism -- Reproductive
Abnormalities
■ Women with hypothyroidism may have either oligo- or
amenorrhea or hypermenorrhea-menorrhagia.
■ Decreased fertility
■ Increased likelihood for early abortion
■ Hyperprolactinemia may occur, and is occasionally
sufficiently severe to cause amenorrhea or galactorrhea
■ The serum sex hormone-binding globulin concentration
may be low in hypothyroidism. This will lower serum total
but not free sex hormone concentrations.
21. Clinical Manifestations of Hypothyroidism -- Neurological
Dysfunction
■ General depression of central nervous system function
■ Sleepiness, inability to concentrate
■ Sluggish thought processes
❖ Respond slowly to questions
❖ Less able to retrieve information from memory
■ Agitated psychosis, rare (“myxedema madness”)
■ PET: 23% reduction in cerebral blood flow and a 12%
reduction in cerebral glucose metabolism
22. Clinical Manifestations of Hypothyroidism --
Neuromuscular Abnormalities
■ A delay in the relaxation phase of deep tendon reflexes
■ Carpal tunnel syndrome
■ Paresthesia
■ Asymptomatic elevation in serum CPK level to muscle
hypertrophy (which may be accompanied by muscle
cramps) to proximal muscle weakness to, in rare cases,
rhabdomyolysis.
23. Clinical Manifestations of Hypothyroidism -- Metabolic
Abnormalities
■ Hyponatremia may result from a reduction in free water
clearance
■ Reversible increases in serum creatinine occur in 20 ~ 90%
of hypothyroid patients
■ lipid clearance may be decreased, resulting in an elevation
in the serum concentrations of free fatty acids and total and
low-density lipoprotein cholesterol
■ Plasma homocysteine concentrations are increased in
some hypothyroid patients,
25. Serum FT4, TSH
Normal FT4, TSH
TSH , FT4 FT4 , TSH normal or
Primary
hypothyroidism
Euthyroid
Secondary hypothyroidism
TRH test
Excessive
response
Normal type
response No response
Pituitary
lesion
Hypothalamic
lesion
Primary
hypothyroidism
26. Treatment of Hypothyroidism
■ Replacement of Triiodothyroxine (T3): unsatisfactory due
to rapid absorption, short half-life, and transient effect
■ Levothyroxine (T4):
❖ Converted to T3 intracellularly
❖ Once daily, half-life: 7 days
❖ Well-absorbed
❖ Easily monitored by following serum TSH and T4
levels
27. Treatment of Hypothyroidism
■ Replacement does of levothyroxine in adults range from
0.05 to 0.2 mg/d. It varies according to the patient’s age
and body weight.
■ In young children: 4-5 ug/kg/d
■ In adults: average 1.7 ug/kg/d
■ In elders, start with lower dose, ex. 0.025mg daily, increase
the dose at 4- to 6-week intervals based on serum FT4 and
TSH levels
■ Dose should be increased about 25% during pregnancy
28. Drugs Potentially Altering Thyroid Hormone Replacement Requirements
Increase replacement requirements
Drugs that reduce thyroid hormone production
Lithium
Iodine-containing medications
Amiodarone (Cordarone)
Drugs that reduce thyroid hormone absorption
Sucralfate (Carafate)
Ferrous sulfate (Slow Fe)
Cholestyramine (Questran)
Colestipol (Colestid)
Aluminum-containing antacids
Calcium products
Drugs that increase metabolism of thyroxine
Rifampin (Rifadin)
Phenobarbital
Carbamazepine (Tegretol)
Warfarin (Coumadin)
Oral hypoglycemic agents
Increase thyroxine availability and may decrease replacement requirements
Drugs that displace thyroid hormone from protein binding
Furosemide (Lasix)
Mefenamic acid (Ponstel)
Salicylates