This presentation covers different thyroid and parathyroid disorder, their aetiology, clinical manifestation, signs, symptoms, treatments and case studies.
Endocrinology is a specialty of medicine; some would say a sub-specialty of internal medicine, which deals with the diagnosis and treatment of diseases related to hormones. Endocrinology covers such human functions as the coordination of metabolism, respiration, reproduction, sensory perception, and movement
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
Proteins, peptides and amino acid derivatives
Proteins are large molecules made of many amino acids
Peptides are smaller molecules typically made of a few amino acids
Amino acid derivatives are molecules derived from a single amino acid
This presentation covers different thyroid and parathyroid disorder, their aetiology, clinical manifestation, signs, symptoms, treatments and case studies.
Endocrinology is a specialty of medicine; some would say a sub-specialty of internal medicine, which deals with the diagnosis and treatment of diseases related to hormones. Endocrinology covers such human functions as the coordination of metabolism, respiration, reproduction, sensory perception, and movement
Hyperthyroidism (overactive thyroid) occurs when your thyroid gland produces too much of the hormone thyroxine. Hyperthyroidism can accelerate your body's metabolism, causing unintentional weight loss and a rapid or irregular heartbeat
Hypothyroidism (underactive thyroid) is a condition in which your thyroid gland doesn't produce enough of certain crucial hormones.
Proteins, peptides and amino acid derivatives
Proteins are large molecules made of many amino acids
Peptides are smaller molecules typically made of a few amino acids
Amino acid derivatives are molecules derived from a single amino acid
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
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.
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
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.
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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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
8. Thyroid
Follicular cells—excretion of triiodothyronine (T3)
and thyroxine (T4)—Increase BMR, increase bone and
calcium turnover, increase response to catecholamines,
need for fetal G&D
Thyroid C cells—calcitonin. Lowers blood calcium
and phosphate levels
10. Pancreatic Islet cells
Insulin
Glucagon—stimulates glycogenolysis and
glyconeogenesis
Somatostatin—decreases intestinal absorption of
glucose
11. Kidney
1, 25 dihydroxyvitamin D—stimulates calcium
absorption from the intestine
Renin—activates the RAAS
Erythropoietin—Increases red blood cell production
17. Assessment
Health history—energy level, hand and foot size
changes, headaches, urinary changes, heat and cold
intolerance, changes in sexual characteristics,
personality changes, others
Physical assessment—appearance including hair
distribution, fat distribution, quality of skin,
appearance of eyes, size of feet and hands, peripheral
edema, facial puffiness, vital signs
18. Diagnostic Evaluation
Serum levels of hormones
Detection of antibodies against certain hormones
Urinary tests to measure by-products (norepinephrine,
metanephrines, dopamine)
Stimulation tests—determine how an endocrine gland
responds to stimulating hormone. If the hormone
responds, then the problem lies w/hypothalmus or
pituitary
Suppression tests—tests negative feedback systems
that control secretion of hormones from the
hypothalamus or pituitary.
19. Disorders of the Pituitary
Pituitary Tumors
Eosinophilic tumors may result in gigantism or in
acromegaly. May suffer from severe headaches, visual
disturbances, decalcification of the bone, endocrine
disturbances
Basophilic tumors may cause Cushing’s syndrome
w/features of hyperadrenalism, truncal obesity,
amenorrhea, osteoporosis
Chromophobic tumors—90% of pituitary tumors.
Present with lowered BMR, obesity, somnolence, scant
hair, low body temp, headaches, visual changes
20. Growth hormone deficiency in childhood will result in
primary dwarfism.
22. Diabetes Insipidus
Deficiency of ADH
Excessive thirst, large volumes of dilute urine
Can occur secondary to brain tumors, head
trauma, infections of the CNS, and surgical
ablation or radiation
Nephrogenic DI—relates to failure of the renal tubules
to respond to ADH. Can be related to hypokalemia,
hypercalcemia and to medications (lithium
demeocycline)
24. Assessment and Diagnostic Findings
Fluid deprivation test—withhold fluids for 8-12 hours.
Weigh patient frequently. Inability to slow down the
urinary output and fail to concentrate urine are
diagnostic. Stop test if patient is tachycardic or
hypotensive
Trial of desmopressin and IV hypertonic saline
Monitor serum and urine osmolality and ADH levels
25. Pharmacologic Tx and Nursing
Management
DDAVP—intranasal bid
Can be given IM if necessary. Every 24-96h. Can
cause lipodystrophy.
Can also use Diabenese and thiazide diuretics in mild
disease as they potentiate the action of ADH
If renal in origin—thiazide diuretics, NSAIDs
(prostaglandin inhibition) and salt depletion may help
Educate patient about actions of medications, how to
administer meds, wear medic alert bracelet
26. SIADH
Excessive ADH secretion
Retain fluids and develop a dilutional hyponatremia
Often non-endocrine in origin—such as bronchogenic
carcinoma
Causes: Disorders of the CNS like head injury, brain
surgery, tumors, infections or medications like
vincristine, phenothiazines, TCAs or thiazide diuretics
Meds can either affect the pituitary or increase
sensitivity to renal tubules to ADH
Management: eliminate cause, give diuretics (Lasix),
fluid restriction, I&O, daily wt., lab chemistries
27. SIADH
Restoration of electrolytes must be gradual
May use 3% NaCl in conjunction with Lasix
28. Thyroid
T3 and T4
Need iodine for synthesis of hormones—excess will
result in adaptive decline in utilization called the Wolf-
Chaikoff mechanism
Thyroid is controlled by TSH
Cellular metabolism, brain development, normal
growth, affect every organ in the body
T3 is five times as potent as T4
Calcitonin—secreted in response to high levels of
serum calcium, increases deposition in the bone
29. Thyroid
Inspect gland
Observe for goiter
Check TSH, serum T3 and T4
T3 resin uptake test useful in evaluating thyroid
hormone levels in patients who have received
diagnostic or therapeutic dose of iodine. Estrogens,
Dilantin, Tagamet, Heparin, amiodarone, PTU,steroids
and Lithium can cloud the accuracy
T3 more accurate indicator of hyperthyroidism
according to text
30. Thyroid
Antibodies seen in Hashimoto’s, Grave’s and other
auto-immune problems.
Radioactive iodine uptake test measures rate of iodine
uptake. Patients with hyperthyroidism exhibit a high
uptake, hypothyroidism will have low uptake
Thyroid scan—helps determine the location, size,
shape and size of gland. “Hot” areas (increased
function) and “cold” areas (decreased function) can
assist in diagnosis.
31. Nursing Implications
Be aware of meds patient is taking (see list in text) that
can affect accuracy of testing
Also be aware if patient is taking multivitamins and
food supplements
32. Hypothyroidism
Most common cause is Hashimoto’s thyroiditis
Common in those previously treated for hyperthyroidism
Atrophy of gland with aging
Medications like lithium, iodine compounds, antithyroid
meds can cause
Radiation treatments to head and neck
Infiltrative diseases like amyloidosis, scleroderma
Iodine deficiency and excess
Hypothalamic or pituitary abnormality
More common in women, especially over age 50
33. Manifestations
From mild symptoms to myxedema
Myxedema –accumulation of mucopolysaccharides in
sc and interstitial tissues. Is the extreme form of
hypothyroidism. Can progress to shock.
S/S—fatigue, hair loss, dry skin, brittle nails,
numbness and tingling of the fingers, amenorrhea,
weight gain, decreased heart rate and temperature,
lassitude, cognitive changes, elevated cholesterol
levels, constipation, hypotension
34. Pharmacologic Management of
hypothyroidism
Levothyroxine is preferred agent
Dosage is based on TSH
Desiccated thyroid used infrequently due to
inconsistent dosing
Angina can occur when thyroid replacement is
initiated as it enhances effects of cardiovascular
catecholamines (in pt. w/pre-existent CAD). Start at
low dose.
Hypnotics and sedatives may have profound effects on
sensorium
35. Management in Myxedema
Cautious fluid replacement
Glucose to restore to normal glycemic levels
Avoid rapid overheating due to increased oxygen
demands but keep warm
May give levothyroxine intravenously
With recovery,
Modify activity
High fiber foods
Home health for follow-up
36. Hyperthyroidism
Extreme form is Grave’s disease
Caused by thyroiditis, excessive amount thyroid
hormone, abnormal output by immunoglobulins
Is more common in women
37. Manifestations of hyperthyroidism
Thyrotoxicosis—nervousness, irritable, apprehensive,
palpitations, heat intolerance, skin flushing, tremors,
possibly exophthalmos
Have an increased sensitivity to catecholamines
Can occur after irradiation or presence of a tumor
38. Assessment and Diagnosis
Thyroid thrill and or bruit may be present
Thyroid may be enlarged
Decreased TSH, increased free T4 and an increased
radioactive iodine uptake
39. Management
Reduce thyroid hyperactivity—usually use radioactive
iodine, antithyroid meds or surgery)
Beta blockers
Can be relapse with antithyroid meds
40. Pharmacologic Therapy
Irradiation with administration of radioisotope iodine
131—initially may cause an acute release of thyroid
hormones. Should monitor for thyroid storm
S/S of thyroid storm—high fever. Tachycardia,
delirium, chest pain, dyspnea, palpitations, weight loss,
diarrhea, abdominal pain
Management of thyroid storm—oxygen, IV fluids
with dextrose, hypothermic measures, steroids to treat
shock or adrenal deficiency, iodine to decrease output
of T4, beta blockers, PTU or Tapazole impedes
formation of thyroid hormone and blocks conversion
of T4 to T3
41. Antithyroid Medications
PTU—propylthiouracil—blocks synthesis of hormones
Tapazole (methimazole)—blocks synthesis of
hormones. More toxic than PTU.
Sodium Iodide-suppresses release of thyroid hormone
SSKI (saturated solution of potassium chloride)–
suppresses release of hormones and decreases
vascularity of thyroid. Can stain teeth
Dexamethazone—suppresses release of thyroid
hormones
42. Surgical Management
Reserved for special circumstances, e.g. large goiters,
those who cannot take antithyroid meds, or who need
rapid normalization
Subtotal thyroidectomy
Before surgery, give PTU until s/s of hyperthyroidism
have disappeared
Iodine may be used to decrease vascularity
43. Nursing Management
Reassurance r/t the emotional reactions experienced
May need eye care if has exophthalmos
Maintain normal body temperature
Adequate caloric intake
Managing potential complications such as
dysrhythmias and tachycardias
Educate about potential s/s of hypothyroidism
following any antithyroid tx.
44. Parathyroid Glands
Parathormone maintains sufficient serum calcium
levels
Excess calcium can bind with phosphate and
precipitate in various organs, can cause pancreatitis
Hyperparathyroidism will cause bone decalcification
and development of renal calculi
More common in women
Secondary hyperparathyroidism occurs in those with
chronic renal failure and renal rickets secondary to
excess phosphorus retention (and increased
parathormone secretion)
45. Manifestations of
Hyperparathyroidism
May be asymptomatic
Apathy, fatigue, muscle weakness, nausea, vomiting,
constipation, hypertension and cardiac dysrhythmias
Excess calcium in the brain can lead to psychoses
Renal lithiasis can lead to renal damage and even
failure
Demineralization of bones with back and joint pain,
pain on weight bearing, pathologic fractures
Peptic ulcers and pancreatitis can also occur
46. Assessment and Diagnostic Findings
Persistent elevated calcium levels
Elevated serum parathormone level
Bone studies will reveal decreased density
Double antibody parathyroid hormone test is used to
distinguish between primary hyperparathyroidism and
malignancy
Ultrasound, MRI, thallium scan, fine needle biopsy
also can be used to localize cysts, adenomas, or
hyperplasia
47. Management
Recommended treatment for hyperparathyroidism is
surgical removal
Hydration therapy necessary to prevent renal calculi
Avoid thiazide diuretics as they decrease renal excretion of
calcium
Increase mobility to promote bone retention of calcium
Avoid restricted or excess calcium in the diet
Fluids, prune juice and stool softeners to prevent
constipation
Watch for s/s of tetany postsurgically (numbness, tingling,
carpopedal spasms) as well as cardiac dysrhythmias and
hypotension
48. Hypercalcemic crisis
Seen with levels greater than 15mg/dL
Can result in life-threatening neurologic,
cardiovascular and renal symptoms
Treatments include: hydration, loop diuretics to
promote excretion of calcium, phosphate therapy to
promote calcium deposition in bone and reducing GI
absorption of calcium
Give calcitonin or mithramycin to decrease serum
calcium levels quickly
49. Hypoparathyroidism
Seen most often following removal of thyroid gland,
parathyroid glands or following radical neck surgery
Deficiency of parathormone results in increased bone
phosphate and decreased blood calcium levels
In absence of parathormone, there is decreased
intestinal absorption of dietary calcium and decreased
resorption of calcium from bone and through kidney
tubules
50. Clinical Manifestations of
Hypoparathyroidism
Irritability of neuromuscular system
Tetany—hypertonic muscle contractions , numbnes,
tingling, cramps in extremities, laryngeal spasm,
bronchospasm, carpopedal spasm ( flexion of the
elbows and wrists, dorsiflexion of the feet), seizures
51. Assessment and Diagnostic Findings
Trousseau’s sign—can check with a BP cuff
Chvostek’s sign—tapping over facial nerve causes
spasm of the mouth, nose and eye
Lab studies may reveal calcium levels of 5-6 mg/dL or
lower
Serum phosphate levels will be decreased
52. Management of Hypoparathyroidism
Restore calcium level to 9-10 mg/dL
May need to give IV calcium gluconate for immediate
treatment
Use of parathormone IV reserved for extreme
situations due to the probability of allergic reactions
Monitor calcium levels
May need bronchodilators and even ventilator
assistance
Diet high in calcium and low in phosphorus; thus,
avoid milk products, egg yolk and spinach.
53. Management of Hypoparathyroidism
Keep calcium gluconate at bedside
Ensure has IV access
Cardiac monitoring
Care of postoperative patients who have undergone
thyroid surgery, parathyroidectomy or radical neck
surgery. Be watchful for signs of tetany, seizures, and
respiratory difficulties
54. Adrenals--Pheochromocytoma
Usually benign tumor
Originates from the chromaffin cells of the adrenal
medulla
Any age but usu. Between 40-50 years old
Can be familial
10% are malignant
May be associated with thyroid carcinoma or
parathyroid hyperplasia or tumor
55. Clinical Manifestations
Headache, diaphoresis, palpitations, hypertension
May have hyperglycemia related to excess epinephrine
secretion
Tremors, flushing and anxiety as well
Blurring of vision
Feeling of impending doom
BPs exceeding 250/150 have occurred
56. Assessment and Diagnostic Findings
Associated with the 5 H’s—hypertension, headache,
hyperhidrosis, hypermetabolism and hyperglycemia
Urinary catecholamines and metanephrine are direct and
conclusive tests
Serum epinephrine and norepinephrine levels will be
elevated
Urinary vanillymandelic acid also diagnostic
Must avoid coffee, tea, bananas, chocolate, vanilla and
ASA, nicotine, amphetamines, decongestants before 24h
urine testing
Clonidine suppression test—in normal individual, would
block catecholamine release
Imaging studies
57. Management
Bedrest
Elevated HOB
ICU
Nipride
Calcium channel blockers and Beta blockers
Surgical management (manipulation of the tumor can
cause excessive release of catecholamines)
Steroid therapy if adrenalectomy performed
Hypotension and hypoglycemia can occur post-op
58. Addison’s Disease
Adrenocortical insufficiency
Autoimmune or idiopathic atrophy
Can be caused by inadequate ACTH from pituitary
Therapeutic use of steroids
59. Manifestations
Muscle weakness
Anorexia
Dark pigmentation
Hypotension
Hypoglycemia
Low sodium levels
High potassium levels
Can result in Addisonian crisis
60. Addisonian crisis
Circulatory shock
Pallor, apprehension, weak&rapid pulse, rapid
respirations and low blood pressure
Headache, nausea, abdominal pain and diarrhea
Can be brought on by overexertion, exposure to cold,
acute infection, decrease in salt intake
61. Assessment and Diagnostic Findings
Early morning serum cortisol and plasma ACTH are
performed. Will distinguish between primary and
secondary adrenal insufficiency. In primary, will have
elevated ACTH levels and below normal cortisol
levels.
If the adrenal cortex is not stimulated by the pituitary,
a normal response to doses of exogenous ACTH (see
text)
Blood sugar levels and electrolyte values
62. Management
Restore circulatory status—fluids, steroids
May need antibiotics if infection precipitated crisis
May need lifelong steroid therapy and
mineralocorticoid therapy
May need additional salt intake
Check orthostatics
Daily weights
Aware that stressors can precipitate crises
Medic alert bracelet or similar identification of history
63. Cushing’s Syndrome
Results from excessive adrenocortical activity
May be related to excessive use of corticosteroid
medications or due to hyperplasia of the adrenal cortex
Oversecretion of corticosteroids can also be caused by
pituitary tumor
Can be caused by bronchogenic carcinoma or other
malignancy
65. Assessment and Diagnostic Findings
Overnight dexamethasone suppression test frequently
used for diagnosis
Administered at 11pm and cortisol level checked at
8am
Suppression of cortisol to less than 5mg/dL indicates
normal functioning
Measurement of plasma ACTH (radioimmunoassay) in
conjunction with dexamethasone suppression test helps
distinguish pituitary vs. ectopic sites of ACTH.
MRI, CT and CT also help detect tumors of adrenal or
pituitary
66. Medical Management
If pituitary source, may warrant transphenoidal
hypophysectomy
Radiation of pituitary also appropriate
Adrenalectomy may be needed in case of adrenal
hypertrophy
Temporary replacement therapy with hydrocortisone or
Florinef
Adrenal enzyme reducers may be indicated if source if
ectopic and inoperable. Examples include: ketoconazole,
mitotane and metyrapone.
If cause is r/t excessive steroid therapy, tapering slowly to a
minimum dosage may be appropriate.
67. Primary Aldosteronism or Conn’s
Syndrome
Excessive aldosterone secondary to adrenal tumor
retain sodium and excrete potassium
Results in alkalosis
Hypertension—universal sign of hyperaldosteronism
Inability of kidneys to concentrate the urine
Serum becomes concentrated
Excessive thirst
Hypokalemia interferes with insulin secretion thus will
have glucose intolerance as well
68. Assessment and Diagnostic Findings
High sodium
Low potassium level
High serum aldosterone level
Low renin level
Aldosterone excretion rate after salt loading is
diagnostic for primary aldosteronism
Renin-aldosterone stimulation test
69. Management
Surgical removal of tumor
Correct hypokalemia
Usual postoperative care with abdominal surgery
Administer steroids
Fluids
Monitoring of blood sugar
Control of hypertension with spironolactone
71. Indications
RA
Asthma
MS
COPD exacerbations
Lupus
Other autoimmune disorders
Dermatologic disorders
72. Dosing
Lowest dose
Limited duration
Best time to give dose is in early morning between 7-8
am
Need to taper off med to allow normal return of renal
function
73. Side Effects of Steroids
Hypertension, thrombophlebitis, accelerated
atherosclerosis
Increased risk of infection
Glaucoma and corneal lesions
Muscle wasting, poor wound healing, osteoporosis,
pathologic fractures
Hyperglycemia, steroid withdrawal syndrome
Moon face, weight gain, acne
74. Case Study 1
35 year old male presents with BP of 188/112 at a
yearly physical exam. Previous exams noted blood
pressures of 160/94 and 158/92. On questioning,
patient admits to twice a month episodes of
apprehension, severe headache, perspiration, rapid
heartbeat, and facial pallor. These episodes had an
abrupt onset and lasted 10-15 minutes.
Routine hematology and chemistry studies are wnl and
chest xray and ECG are normal.
What is your impression?
What labs would you draw?
75. Case Study 2
50 year old woman presents with enlargement of left
anterior neck. She has noted increased appetite over
the past month with no weight gain, and more frequent
bowel movements over the same period. Patient feels
jittery at times, experiences palpitations and feels “hot”
a lot recently.
She is 5’8” tall and weighs 150#. Heart rate is 110 and
blood pressure is 110/76.
What might be this patient’s problem?
What lab tests might you draw?
76. Case study 3
48 year old woman with a past history of mental
illness presents with a new onset of bizarre psychotic
behavior. She had been well over the past two years.
She is 5’5” tall and weighs 138#. Her heart rate is 65,
irreg and BP is 130/75. Exam is normal except that she
is confused to place, time and year. Patient c/o joints
aching and of feeling fatigued.
Lab tests reveal serum calcium level of 13.8mg/dL
(reference range is 8.4-10.1)
Phosphorus is 2.4 (reference range is 2.5-4.5)
What is your diagnosis?
77. Case Study 4
40 year old deeply tanned woman presents with a 6
month history of increasing fatigue. For the past three
months she has suffered from recurrent URIs, poor
appetite, abdominal cramps, fatigue and diarrhea. She
has lost 25#. She has noted joint pains, muscle
weakness, and has not menstruated for the past 3
months.
Labs reveal blood glucose of 59, Na+ 130, K+ 6.0.
What disorder do you expect?
78. Case Study #5
27 year old woman presents with depression, insomnia,
increased facial fullness and recent increase in acne. She
had an episode of depression and acute psychosis following
uncomplicated delivery of normal baby boy 9 months
previously. Her menses have been irregular since their
resumption after the birth (she is not breast feeding).
Patient relates has had several vaginal yeast infections
recently.
Heart rate is 90bpm, BP is 146/100. Her face is puffy and
has acne vulgaris. Thin extremities and with truncal obesity.
What are your suspicions?
What labs will you draw?