This patient presented with multiple symptoms including loose motions, blisters, cough, shortness of breath, abdominal fullness, and limb swelling. Laboratory tests found hypothyroidism, hypokalemia, anemia, and leukocytosis. Sputum culture grew Klebsiella pneumoniae and Acinetobacter species. The patient was diagnosed with Addison's disease, hypothyroidism, acute gastroenteritis caused by Giardia, iatrogenic Cushing's syndrome and pneumonia. The patient has a history of taking hydrocortisone, fludrocortisone, thyroxine, and prednisone for Addison's disease and hypothyroidism treatment, but developed Cushing's
Case study - suspicion of Cushing Syndrome (undiagnosed)Robert Ferris
Anonymised patient case with elder female, multiple metabolic comorbidities, no definitive diagnosis made at time of presentation. Slides mainly focus on differentials and appropriate management in absence final Dx.
By Robert Ferris and Philip Aigner, as part of medical school studies.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
Case study - suspicion of Cushing Syndrome (undiagnosed)Robert Ferris
Anonymised patient case with elder female, multiple metabolic comorbidities, no definitive diagnosis made at time of presentation. Slides mainly focus on differentials and appropriate management in absence final Dx.
By Robert Ferris and Philip Aigner, as part of medical school studies.
Sources for all imagery and sources listed in references section where possible. I do not claim ownership of any images or graphics. Slides for educational purposes only, and should not replace clinical judgement. No monetary gain was made for this work.
Dental Management of Patient With Adrenal Cortex Disorder Tarek Zaid
a presentation describe the physiology of adrenal gland and focuses on line of treatment and dental management of patient with adrenal cortex problems as over and under production of adrenal secretions
Addison Disease
By Dr Usama Ragab Youssif
The term ‘adrenal insufficiency’ (AI) refers to failure of the adrenal cortex to secrete enough glucocorticoids, mineralocorticoids, or both. AI can be divided into two general categories:
lack of adequate hormone secretion by the adrenals (primary AI)
inadequate ACTH or CRH secretion (secondary AI).
Dental Management of Patient With Adrenal Cortex Disorder Tarek Zaid
a presentation describe the physiology of adrenal gland and focuses on line of treatment and dental management of patient with adrenal cortex problems as over and under production of adrenal secretions
Addison Disease
By Dr Usama Ragab Youssif
The term ‘adrenal insufficiency’ (AI) refers to failure of the adrenal cortex to secrete enough glucocorticoids, mineralocorticoids, or both. AI can be divided into two general categories:
lack of adequate hormone secretion by the adrenals (primary AI)
inadequate ACTH or CRH secretion (secondary AI).
a brief on thyroid gland covering following titles:
Introduction
Anatomy and physiology of thyroid gland
Synthesis of thyroid hormones
Regulation
Mechanism of action
Biological function
MI is one of the CVS complication leading to mortality whose diagnosis is mainly dependent on clinical presentation and other supportive investigation. clinical laboratory plays crucial role in its diagnosis, prognosis and monitoring therapy.
introduction of Purine and Pyrimidine metabolism, biosynthesis and degradation of nucleotides, biological functions and metabolic disorders, chemical analogues and therapeutic drugs, uric acid metabolism
Triacylglycerol and compound lipid metabolismDipesh Tamrakar
Biosynthesis and metabolic regulation of triglyceride and other compound lipids: glycerophospholipids, sphingophospholipids, ether glycerolipids and glycolipids
Methionine metabolism
Activation of methionine and transmethylation
Conversion of methionine to cysteine
Degradation of cysteine.
Cysteine metabolism
Formation
Metabolic Function
Metabolism Disorders of Sulfur containing amino acid
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.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
- 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
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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263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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.
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
2. Case history
• A 50 years old woman from Rautahat presented to TUTH with chief
complaints of :
• Multiple episodes of loose motions (6-7 episodes)
• 1 ½ mths back, multiple blisters seen
• Cough and insidious shortness of breath gradually progressive serous
sputum
• Interference with sleep and orthopnea (+)
• Abdominal fullness and limb swelling
2
3. History of:
• Increased weakness and low BP for 2 mths followed by frequent falls
• Hyperpigmented patches over right leg, chest and upper back for 2
mths
• Multiple subcutaneous swellings for 3 yrs and removed 1 yr back
• Whitish patches over tongue for 10 days causing difficulty eating and
increased dryness of tongue
• Diuretic intake for 8 days
• Hypovolemic shock 4 yrs back
3
4. General physical examination
• GC: conscious, oriented to time, place and person
• Ill-looking
• Negative for Pallor & icterus
• B/L limb swelling and fatigue
• BP: 90/60 mmHg,
• Pulse: 66 bpm
• Temp: 97.9 0F
• RR: 22/min
• SpO2: 90%
4
5. • Chest: Bronchial / Breath sounds
• Rt. Supraclavicular, interscapular, supra-mammary and mammary
(Cavitation on Rt. Upper Zone)
• Lt. suprascapular
• CVS: S1S2M0
• P/A: soft, non distended, non tender, no organomegaly
• CNS: grossly intact
5
11. Peripheral Blood Smear
• RBC: Normocytic Normochromic
• WBC: Leukocytosis with neutrophilia, no atypical or blast cells seen
• Platelets: Adequate in number
• No malarial or filarial parasites seen
11
13. Microbiology investigations
• Sputum sample:
• Gram’s Stain: presence of GPC and GNB
• AFB stain: No AFB seen but few fungal stains
• Culture: Klebsiella pneumonie and Acinetobacter sps
• Gene Xpert: Negative
• Stool RE/ME:
• Cyst of G. lamblia
• Urine RE/ME:
• NAD
13
17. Adrenal gland
Anatomy
• are orange-colored glands that sit on
top of the kidneys near the spine,
just underneath the last rib and
extending down about an inch.
• Supra-renal glands.
• Shape: pyramidal ( usually right
adrenal is pyramidal, whereas the
left is shaped more like a half moon)
• Size: 2- 3 cm wide, 4- 6 cm long, and
about 1 cm thick.
• Weight: 6-10 g.
17
18. THE ADRENAL CORTEX
•The cortex is divided into 3 regions:
•Zona Glomerulosa
•Zona Fasciculata
•Zona Reticularis
•These secrete different hormones that carry out
specific functions throughout body
•Hormones produced by the adrenal cortex are
referred to as corticosteroids.
•These comprise mineralocorticoids, glucocorticoids
and androgens.
18
19. ADRENALS
Zona Reticularis
Sex steroids (androgens)
Zona Fasciculata
Glucocorticoids (Cortisol)
Glucose homeostasis
Zona Glomerulosa
Mineralocorticoids (Aldosterone)
Na+, K+ and water homeostasis
Medulla: “Catecholamines”
Epinephrine, Norepinephrine
CORTEX
19
20. ADDISON’S DISEASE
• Thomas Addison, 1st reported hypofunction of the adrenal cortex in
1855
• Primary adrenocortical deficiency causing combined
mineralocorticoid and glucocorticoid deficiency
• Rare disorder with a prevalence of only 4-11 cases per 100,000
• If untreated, adrenal insufficiency can be fetal
• “general languor and debility, feebleness of the heart’s action,
irritability of the stomach, and a peculiar change of the color of the
skin”-summarizes the dominant clinical features
• Advanced cases are usually easy to diagnose, but recognition of the
early phases can be a real challenge
20
21. Etiology and Pathogenesis
• Results from progressive destruction or dysfunction of the adrenals
which must involve >90% of the glands before adrenal insufficiency
appears
• In early series, tuberculosis was responsible for 70-90% cases but the
most frequent cause now is IDIOPATHIC atrophy and autoimmune
mechanism
• Autoimmune destruction exact mechanism still unknown but some
antibodies (like Ab against enzyme 21-hydroxylase) causes adrenal
insufficiency by blocking the binding of ACTH to its receptors
• Autoimmune polyendocrine syndrome (APS type 1 or 2) may also
involve thyroid and pancreas.
21
26. Laboratory findings & Diagnosis
• In early phase of gradual adrenal destruction, no demonstrable
abnormalities in the routine lab parameters
• Initially adrenal reserve is decreased
• In advanced stages of adrenal destruction, serum sodium, chloride
and bicarbonate levels are reduced
• The hyponatremia is due to both to loss of Na+ into urine ( due to
aldosterone deficiency) and to movement into the intracellular
compartment
• This extravascular Na+ loss depletes extracellular fluid volume and
accentuates hypotension
26
27. • The ECG may show nonspecific changes and the EEG exhibits a
generalized reduction and slowing
• There may be a normocytic anaemia, a relative lymphocytosis and
moderate eosinophilia
• Diagnosis of adrenal insufficiency should be made only with ACTH
stimulation testing to assess adrenal reserve capacity for steroid
production
• Measurement of basal ACTH and cortisol conc along with the ACTH
stimulation test is recommended if primary adrenal insufficiency is
suspected.
• Basal plasma ACTH conc >150 pg/ml and serum cortisol conc <10 g/dl
are diagnostic of adrenal insufficiency
• A subnormal cortisol response in the ACTH stimulation test supports
the diagnosis of primary adrenal insufficiency
27
29. • The best screening test is the cortisol response 60 min after 250 ug of
Cosyntropin given IM/IV
• Cortisol levels should exceed 495 nmol/L (18 g/dL)
• If the response is abnormal, then primary and secondary adrenal
insufficiency can be distinguished by measuring aldosterone levels from
the same blood samples.
• In secondary adrenal insufficiency, the aldosterone increment will be
normal (5 ng/dL)
• Single-Dose Metyrapone Stimulation Test is not recommended in cases
of suspected Addison disease for fear that suppression of cortisol
production might precipitate an Addisonian crisis.
• That being said, patients with Addison disease have an inadequate rise in
11-desoxycortisol in response to metyrapone.
29
32. Differential Diagnosis
• Common signs and symptoms may be difficult to make diagnosis so it is
mandatory to perform ACTH stimulation testing to rule out adrenal
insufficiency, particularly before steroid treatment is begun
• Weight loss is useful in evaluating the significance of weakness and
malaise
• Racial pigmentation may be a problem but a recent and progressive
increase in pigmentation is usually reported by the patient with gradual
adrenal destruction
• Hyperpigmentation is usually absent when adrenal destruction is rapid,
as in bilateral adrenal hemorrhage
• When doubt exists, measurement of ACTH levels and testing of adrenal
reserve with the infusion of ACTH provide clear cut differentiation
32
35. Treatment
• Requires specific hormone replacement therapy
• It should correct both glucocorticoid and mineralocorticoid
deficiencies
• Hydrocortisone (cortisol) is the main stay of treatment
• Since the replacement dosage of hydrocortisone does not replace the
mineralocorticoid component of the adrenal hormones,
mineralocorticoid supplementation is usually needed: fludrocortisone
• The adequacy of mineralocorticoid therapy can be assessed by
measurement of BP and serum electrolytes
35
36. Iatrogenic Cushing’s Syndrome
• In 1912 Harvey Cushing 1st described the polyglandular syndrome
with pituitary involvement.
• Cushing’s syndrome is the result of autonomous, excessive
production of cortisol leading to classic symptoms characteristic of
this disorder
• Frequently the cause is iatrogenic; excessive exogenous steroid
therapy
• In the form of Cushing’s syndrome associated with primary adrenal
disease s/a adrenocortical adenoma, increased secretion of cortisol
suppresses both CRH synthesis and ACTH secretion
36