This document summarizes a grand rounds presentation on hypothyroidism. Dr. Samir Abdi moderated while Dr. Abdirisak Jacda presented on the case of a 20-year-old woman with a known history of recurrent ascites who was experiencing worsening body swelling. On examination, she displayed signs of profound anasarca. Laboratory tests found low T3 and T4 levels with a low TSH, consistent with hypothyroidism. The presentation reviewed the classification, pathogenesis, signs and symptoms, complications, and treatment of hypothyroidism.
Cushing syndrome and Addison disease-Dr.Hamisi MkindiMkindi Mkindi
#Cushing syndrome #Addison Disease #Adrenal Insufficiency #Adrenal Excess #Hyperaldosteronism #Nelson Syndrome #Dr.Hamisi Mkindi #Samuel Kalluvya
Adrenal insufficiency can be caused by diseases of the adrenal gland (primary),
Interference with corticotropin (ACTH) secretion by the pituitary gland (secondary)
Interference with
corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary)
Etiology:
Primary = adrenocortical disease = Addison’s disease
1.Autoimmune: isolated or in assoc w/ APS
2.Infection: TB, CMV, histoplasmosis, paracoccidioidomycosis,syphillis
3.Vascular: hemorrhage (usually in setting of sepsis Eg:Warerhouse-Friderichson), adrenal vein thrombosis, HIT, trauma
4.Metastatic disease: (90% of adrenals must be destroyed to cause insufficiency)
5.Deposition diseases: hemochromatosis, amyloidosis, sarcoidosis
6.Drugs: azole antifungals, etomidate (even after single dose), rifampin, anticonvulsants
Nelson syndrome
Secondary = pituitary failure of ACTH secretion
But aldosterone intact b/c RAA axis
Any cause of primary or secondary hypopituitarism
-Hypophysitis
Glucocorticoid therapy (can occur after ≤2 wk of “suppressive doses”; dose effect variable; even <10 mg of prednisone daily chronically can be suppressive
Megestrol (a progestin with some glucocorticoid activity)
Early a.m. serum cortisol: <3 µg/dL virtually diagnostic; ≥18 µg/dL generally consistent with intact adrenal function
Standard (250 µg) cosyntropin stimulation test (testing ability of ACTH → ↑ cortisol)
Normal = 60-min (or 30-min) post-ACTH cortisol ≥18 µg/dL
Abnormal in primary b/c adrenal gland diseased and unable to give adequate output
Abnormal in chronic secondary b/c adrenals atrophied and unable to respond (very rarely, may be normal in acute pituitary injury b/c adrenals still able to respond→ use early a.m. cortisol instead)
All glucocorticoids (incl creams, inh. & drops) affect test. Must know exposure to interpret.
Other tests : renin, aldosterone, insulin-induced hypoglycemia (measure serum cortisol response)
Metyrapone (blocks cortisol synthesis and therefore stimulates ACTH, measure plasma 11-deoxycortisol and urinary 17-hydroxycorticosteroid levels)
ACTH: ↑ in 1°, ↓ or low-normal in 2°
Imaging studies to consider pituitary MRI to detect anatomical abnormalities
Adrenal CT: small, noncalcified adrenals in autoimmune, enlarged in metastatic disease, hemorrhage, infection or deposition (although they may be normal-appearing)
Cushing's syndrome may be either corticotropin (ACTH) dependent or independent.
80 percent of endogenous Cushing's syndrome cases are ACTH dependent, and approximately 20 percent are ACTH independent
Primary (adrenal disorders, renin-independent increase in aldosterone)
Adrenal hyperplasia (60–70%), adenoma (Conn’s syndrome, 30–40%), glucocorticoid-remediable aldosteronism (GRA; ACTH-dep. rearranged promoter)
Secondary (extra-adrenal disorders, ↑ aldosterone is renin-dependent)
-Primary reninism:
How to approach a case of proteinuria and differential diagnosis of proteinuria, how to assess protein loss in the kidney
Dr. Abdel Rahman Mansy, Beni-Suef University, internal medicine department, nephrology unit
Cushing syndrome and Addison disease-Dr.Hamisi MkindiMkindi Mkindi
#Cushing syndrome #Addison Disease #Adrenal Insufficiency #Adrenal Excess #Hyperaldosteronism #Nelson Syndrome #Dr.Hamisi Mkindi #Samuel Kalluvya
Adrenal insufficiency can be caused by diseases of the adrenal gland (primary),
Interference with corticotropin (ACTH) secretion by the pituitary gland (secondary)
Interference with
corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary)
Etiology:
Primary = adrenocortical disease = Addison’s disease
1.Autoimmune: isolated or in assoc w/ APS
2.Infection: TB, CMV, histoplasmosis, paracoccidioidomycosis,syphillis
3.Vascular: hemorrhage (usually in setting of sepsis Eg:Warerhouse-Friderichson), adrenal vein thrombosis, HIT, trauma
4.Metastatic disease: (90% of adrenals must be destroyed to cause insufficiency)
5.Deposition diseases: hemochromatosis, amyloidosis, sarcoidosis
6.Drugs: azole antifungals, etomidate (even after single dose), rifampin, anticonvulsants
Nelson syndrome
Secondary = pituitary failure of ACTH secretion
But aldosterone intact b/c RAA axis
Any cause of primary or secondary hypopituitarism
-Hypophysitis
Glucocorticoid therapy (can occur after ≤2 wk of “suppressive doses”; dose effect variable; even <10 mg of prednisone daily chronically can be suppressive
Megestrol (a progestin with some glucocorticoid activity)
Early a.m. serum cortisol: <3 µg/dL virtually diagnostic; ≥18 µg/dL generally consistent with intact adrenal function
Standard (250 µg) cosyntropin stimulation test (testing ability of ACTH → ↑ cortisol)
Normal = 60-min (or 30-min) post-ACTH cortisol ≥18 µg/dL
Abnormal in primary b/c adrenal gland diseased and unable to give adequate output
Abnormal in chronic secondary b/c adrenals atrophied and unable to respond (very rarely, may be normal in acute pituitary injury b/c adrenals still able to respond→ use early a.m. cortisol instead)
All glucocorticoids (incl creams, inh. & drops) affect test. Must know exposure to interpret.
Other tests : renin, aldosterone, insulin-induced hypoglycemia (measure serum cortisol response)
Metyrapone (blocks cortisol synthesis and therefore stimulates ACTH, measure plasma 11-deoxycortisol and urinary 17-hydroxycorticosteroid levels)
ACTH: ↑ in 1°, ↓ or low-normal in 2°
Imaging studies to consider pituitary MRI to detect anatomical abnormalities
Adrenal CT: small, noncalcified adrenals in autoimmune, enlarged in metastatic disease, hemorrhage, infection or deposition (although they may be normal-appearing)
Cushing's syndrome may be either corticotropin (ACTH) dependent or independent.
80 percent of endogenous Cushing's syndrome cases are ACTH dependent, and approximately 20 percent are ACTH independent
Primary (adrenal disorders, renin-independent increase in aldosterone)
Adrenal hyperplasia (60–70%), adenoma (Conn’s syndrome, 30–40%), glucocorticoid-remediable aldosteronism (GRA; ACTH-dep. rearranged promoter)
Secondary (extra-adrenal disorders, ↑ aldosterone is renin-dependent)
-Primary reninism:
How to approach a case of proteinuria and differential diagnosis of proteinuria, how to assess protein loss in the kidney
Dr. Abdel Rahman Mansy, Beni-Suef University, internal medicine department, nephrology unit
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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.
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
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.
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
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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
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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
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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Summary
Hx 20 yrs. old woman with known history of recurrent ascites
CC.. Worsened body swelling last 2 months
HPI she was having recurrent ascites body swelling for last 2 years but
worsened last two 2months the swelling spread from abdomen to
extremities then lastly to her face,
ROS
respiratory SOB orthopnea Cough
Neuro headache dizziness and
Cardiac palpitation anasarca
GU freq, urgency, burning, dysuria with flank pain
GI epigastric pain nausea constipation
General fatigue loss of appetite but no fever or night sweet
3. Summary
Past obhx two previous NSVD with later one with PPH
Pmhx two paracentesis one therapeutic and one diagnostic
Fmhx no similar case
Social hx:- near baki district
Drug hx frusemide 40mg od po Paracetamol 500mg po PRN
4. Phsyicals
Vitals BP 120/75 P. 117 O2 stat 96% T 36.5 RR 26
Day 2 vitals
BP 140/90 P. 96 O2stat 88% T 37.4 RR 22
RBG 207 FBS 124
Generally, young aged woman looking sick with profound
anasarca
HEENT, severe pallor on congictiva nails and palms
neck, painless diffuse goiter mobile with swallowing
5. Cardiac:- unremarkable
Lungs:- orthopnea in day one bilateral basilar crackles with
dullnes on percussion
Abdomen non-tender, distended due to gravidarum. Have also
shifting dullnes with active bowel sounds
Neuro GCS of 15/15
Periphery bilateral biting edema
6. Date Before admission Day 1 on admission Day 6 on admission
HGB 8.6 7.7 9.1
MCV 89 86 87
PLT 361 Normal Normal doen to rule out
preecalpsia
Cr 1.2 0.8 0.6
BUN 49 38 32
UA
WBC
LE
Protein
Serum
albumi
n
Numerous
+++
++++
20g/L or 2mg/dL
TSH 0.54 Recheck 0.48
T3 0.5
T4 37.5
HbsAg Positive
12. Assessments
1. UTI
2. Hypothyroidism
3. AKI
4. Nephrotic syndrome
5. Chronic HBV infection
PLAN
• Two Units of blood given
superheema 1 ampule BID
• Augmentin 625mg BID
• Tramadol 50mg IM PRN
• Omeprazole 20mg po od
• Levothyroxine 100mg po od
• Dexamethasone 6mg IM BID
14. For nephrotic syndrome
Protein loss from kidney
3-4 gram per dipstick
Anasarca
Hypoalbuminemia
Against
Hypothyroid sx
15. NEPHROTIC GNs
less inflammation (proliferation) than the nephritic GNs
“nephrotic” urine:
see less hematuria, more proteinuria
azotemia less common, or at least less rapid
hypertension not as common
16. NEPHROTIC SYNDROME
Is a syndrome, not a disease
collection of symptoms and signs due to a common pathology
Can be caused by a variety of diseases
Must look for the specific disease
17. DEFINITION
Syndrome consisting of the following:
proteinuria > 3.5 grams/24 hrs
hypoalbuminemia
hyperlipidemia and lipiduria
peripheral edema
19. HYPOALBUMINEMIA
due to losses in urine
liver attempts to compensate by albumin synthesis (up to 50-
60%)
probably in response to plasma oncotic pressure
general correlation between urine losses and serum levels
20. MECHANISM
glomerular abnormality “nephrotic” range
proteinuria is initial insult
generally > 3.5 grams/24 hrs
hypoalbuminemia
hyperlipidemia/lipiduria
21. HYPERLIPIDEMIA
see triglycerides, VLDL, LDL, Lp(a) in serum
see lipid in urine in form of:
free fat droplets
fatty casts
oval fat bodies
22.
23. HYPERLIPIDEMIA
vascular risk likely the same as for non-
nephrotics
nephrotic pts may have 5.5x greater risk for MI
HMG CoA reductase inhibitors (“statins”)
are drugs of choice
24. MECHANISM
glomerular abnormality “nephrotic” range
proteinuria is initial insult
generally > 3.5 grams/24 hrs
hyperlipidemia/lipiduria
hypoalbuminemia
peripheral edema
(+ renal salt retention)
25. Glomerulopathy
Primary
Secondary
some glomerulopathy
can present as more than one syndrome at different times
26. The Spectrum of Glomerular
Pathology
The Nephritic-Nephrotic Spectrum
a clinical picture anywhere on a spectrum with
pure nephritic and pure nephrotic syndromes
at the extremes
29. EDEMA
HEART LIVER KIDNEY CAP LEAK
urinalysis
nephrotic nephritic
MCD
MGN
FSGS
DMN
IgAN
IgAN
SLE
antiGBM
IC
ANCA
(quantitate proteinuria)
LYMPH/VEINS
30. OTHER COMPLICATIONS
progression to ESRF
EDEMA
infection
hypercoagulation
risk of complication correlates with degree of proteinuria
reduction of proteinuria leads to reduction in risk
if proteinuria cannot be reduced, then risk must be addressed
hyperlipidemia
34. PATHOGENESIS
MCD and FSGS
T cells produce abnormal cytokine that leads to
glomerular epithelial cell damage
retraction of podocytes due to ?interaction with anchoring
proteins
b-dystroglycan
a3-b1 integrin
Membranous
due to immune complex deposition
35. PATHOGENESIS
Causes
most commonly idiopathic (“primary”)
90% of cases
may be secondary to:
drugs..(NSAIDs, lithium, gold)
malignancy
infections..(HIV, hepatitis B+C)
36. PRESENTATION
Symptoms
usually present with
edema
facial, lower limb,
arms/hands
often quite abrupt
with MCD
otherwise well. .don’t look
sick
may complain of foamy
Signs
pitting edema in
dependent areas
usually not much else
37. INVESTIGATIONS
Urine
dipstick strongly (+) for protein, little
blood
usually more than 3.0g/24 hr on
collection
microscopy shows lipiduria
free fat droplets
oval fat bodies
fatty casts
Blood
hypoalbuminemia
hyperlipidemia
creatinine usually normal or mildly
elevated
40. PROGNOSIS
MCD MGN FSGS
Persistent
proteinuria
60-70% remit or
stabilize
persistent
proteinuria
Renal failure
usually NOT a
concern
30% chance of
progression to ESRF
over 15 yrs
5 yr renal
survival 60-90%
10 yr renal
survival 30-50%
41. TREATMENT
MCD
corticosteroids the drug of choice
in children, biopsy usually not done straight to steroids with nephrotic
syndrome
in adults, biopsy usually done for diagnosis first
1 mg/kg daily usual dose
may require 4-8 wks. before response is seen
42. TREATMENT
MGN
all pts should receive angiotensin converting
enzyme inhibitors (ACEi) or angiotensin receptor
blocking agents (ARBs)
2nd line treatment reserved for those pts at risk of
progression
elevated creatinine at presentation
normal GFR after 3 yrs is good sign
proteinuria > 10g/24 hrs
esp if > 6 months duration
43. TREATMENT
FSGS
corticosteroids the drug of choice
2 mg/kg alternate days is usual dose
may require 3 months before response is seen (often 6-9 months for full
response)
50% remission rate
44. TREATMENT
3 main 2nd line agents include
corticosteroids
variable results when used alone
best used in combination with another agent
cyclophosphamide
probably more effective than steroids alone but
higher toxicity
cyclosporine
may also be useful as first line…usually less toxicity
45. MGN and FSGS
Recommendations
asymptomatic, protein < 3.5 g/day ACEi/ARB
asymptomatic, protein > 3.5 g/day and no risk factors
ACEi/ARB
symptomatic, protein > 3.5 g/day ACEi/ARB + 2nd line
agent
asymptomatic, protein > 3.5 g/day + risk factors
ACEi/ARB + 2nd line agent
47. TAKE HOME MESSAGE
some glomerular diseases present with a
“nephrotic” picture
proteinuria, edema, hyperlipidemia,
hypoalbuminemia
thrombosis, infection
these diseases may progress to ESRF but
usually very slowly
renal Bx is usually the only way to make a
firm diagnosis
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Disease Burden
1. 5% of the general population are Sub-clinically Hypothyroid
2. 15 % of all women > 65 yrs. are hypothyroid
3. Detecting sub-clinical hypothyroidism in pregnancy is highly essential
– order for TSH and FT4 routinely in all pregnant women at the
beginning of each trimester
4. All persons aged above 60 years – Order for TSH
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Multi system effects - Hypothyroidism
General
•Lethargy, Somnalence
•Weight gain, Goitre
•Cold Intolerence
Cardiovascular
•Bradycardia, Angina
•CHF, Pericardial Effusion
•HyperlipIdemia,
Xanthelsma
Haematological
Iron def. Anaemia,
Normo cytic /chromic
Anaemia
Reproductive system
•Infertility, Menorrhagia
•Impotence, Inc. Prolactin
Neuromuscular
•Aches and pains
•Muscle stiffness
•Carpel tunnel syndrome
•Deafness, Hoarseness
•Cerebellar ataxia
•Delayed DTR, Myotonia
•Depression, Psychosis
Gastro-intestinal
•Constipation, Ileus,
Ascites
Dermatological
•Dry flaky skin and hair
•Myxoedema, Malar
flushes
•Vitiligo, Carotenimia,
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Clinical Signs of Hypothyroidism
Coarse Hair; Dry cool and pale skin
Goitre (not in all cases), Hoarseness of voice
Non-pitting oedema (myxoedema)
Puffiness of eyes and face
Delayed relaxation of DTR
Slow hoarse speech and slow movements
Thinning of lateral 1/3 of eye brows
Bradycardia, pericardial effusion
56. What the mind knows the eyes see !!
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Psychiatric patients
Elderly women / men
Patients of OSA
Hypercholesterolemia
Lithium, Amiodarone
Postpartum women
Other Autoimmune disease
Rx. Grave’s Ophthalmopathy
Family H/o thyroid disease
Neck irradiation therapy
Previous Rx for thyrotoxicosis
Autoimmune Thyroiditis
Order for TSH alone as a screen
70. Many Causes, One Treatment
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Normalize TSH level regardless of cause of hypothyroidism
Once daily dosing with Levothyroxine sodium (1.6µg/kg/day) this
comes to 100 mcg per day
Monitor TSH level at 6 to 8 weeks, after initiation of therapy or
dosage change
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• Treatment of choice is levothyroxin
• Branded thyroxine recommended
• No divided doses - illogical
• Not recommended for use :
Desiccated thyroid extract
Combination of thyroid hormones
T3 replacement except in Myxedema coma
Many Causes, One Treatment
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Age (in elderly start with half dose)
Severity and duration of hypothyroidism (↑ dose)
Weight (0.5µg/kg/day ↑ upto 3.0µg/kg/day)
Malabsorption (requires ↑ dose)
Concomitant drug therapy (only on empty stomach)
Pregnancy ( 25% ↑ in dose), safe in lactating mother
Presence of cardiac disease (start alternate day Rx)
Dosage Adjustments
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Goal : normalize TSH level – 25, 50 and 100 mcg tablets avail.
Starting dose for healthy patients < 50 years at 1.0 µg/kg/day
Starting dose for healthy patients > 50 years should be < 50 µg/day. Dose ↑
by 25 µg, if needed, at 6 to 8 weeks intervals.
Starting dose for patients with heart disease should be 12.5 to 25 µg/day and
increase by 12.5 to 25 µg/day, if needed, at 6 to 8 weeks intervals
Start Low and Go Slow
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How the patient improves
Feels better in 2 – 3 weeks
Reduction in weight is the first improvement
???????????????????
Facial puffiness then starts coming down
Skin changes, hair changes take long time to regress
TSH starts showing decrements from the high values
TSH returns to normal eventually
76. 76
The Commandments
Highly suspect
hypothyroidism
Growth and pubertal delay
Unexplained depression
TSH is the test in Hypothy.
TSH, FT4 to confirm Dx.
Nine square magic
Test cord blood for TSH
All obese patients TSH a must
For all pregnant -test TSH,
FT4
Postmenopausal 15%
Hypothy
Start low and go slow
Use Levothyroxine only
Always on empty stomach
Thyroxine - avoid empirical
use
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• Case Report
• A 60years old male patient presented with symptoms of
insidious onset, painless, progressive abdominal
distension since 2 months and progressive swelling of
both lower limbs since 1 month.
• He also had constipation and progressive hoarseness
of voice for 2 months.
• He had no history of chest pain, shortness of breath,
orthopnea, paroxysmal nocturnal dyspnea, jaundice,
abdominal pain, hematemesis, melena, urinary symptoms,
anorexia or weight loss.
• He was a chronic smoker for last 25 years and non-
alcoholic.
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• Examination revealed mild periorbital and facial puffiness along
with bilateral pitting pedal edema.
• His skin was dry and coarse.
• Neurological examination revealed delayed relaxation of ankle
jerks.
• The patient was afebrile with a pulse rate of 75/min, blood pressure
130/80 mm of Hg and elevated jugular venous pressure.
• On cardiopulmonary examination there was muffled heart sounds
with absent breath sounds.
• Chest radiograph showed massive cardiomegaly with bilateral
pleural effusion.
• Ultrasonography abdomen showed moderate ascites and computed
tomography chest and abdomen revealed massive pericardial
effusion, bilateral pleural effusion and moderate ascites.
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• Electrocardiogram showed low voltage QRS complexes .
• 2D Echocardiogram done subsequently showed a large
circumferential echo free space consistent with massive pericardial
effusion and evidence of cardiac tamponade (diastolic collapse of
right atrium and right ventricle free wall) with preserved left
ventricular systolic function, ejection fraction 55%.
• Viral serology for both hepatitis B and C were negative,
• UGI endoscopy and colour doppler of abdomen were done to
rule out portal hypertension and both were normal.
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Ascitic fluid study showed total cells of 100/ cumm with 98%
lymphocytes, high protein (3.24 gm%) and high serum ascitic
albumin gradient (SAAG - 1.91) and normal adenosine
deaminase level (ADA - 6.8 U/L) .
Pleural fluid examination showed total cells of 200 / cumm
with 90% lymphocytes, high protein (3 . 97 gm%), normal
sugar and normal ADA level (8.1 U/L).
Cytology of both the fluids were negative for malignancy.
In view of cardiac tamponade, pericardiocentesis was done with
aspiration of about 1500 ml straw colour fluid.
Analysis of fluid showed total cells of 10 /cumm with high protein
(5.3 gm%), normal ADA level (8.3 U/L), and cytology revealed
mainly lymphoid and degenerated cells but no malignant
cells.
Culture of the pericardial fluid was negative for bacteria and acid
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Thyroid function tests showed TSH 137.8 mIU/ml (normal
range 0.4 – 4), free T4 0.45 ng/dl (normal range 0.89
– 1.76), and free T3 0.63 pg/ml (normal range 0.92 – 2.78).
Ultrasonography revealed atrophic changes in both thyroid
lobes. TPO antibody was negative.
Subsequent hospital course was uncomplicated and he was
discharged with gradually escalating dose of levothyroxine
from 50 to 100 microgram daily.
On 4 weeks follow up he was in good health and had
abatement of ascites, pleural effusion and tissue edema
and only minimal pericardial effusion left.
His TSH was 30.1m IU/ ml and he continued on a
maintenance dose of 100 microgram with regular follow up.
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The recent studies, however, conclude that PE is extremely
infrequent in hypothyroidism, with an incidence of 3% to 6%.
The mainstay of treatment for thyroid PE is simple thyroxine
replacement, except in those patients w i t h pericardial
tamponade or impending tamponade, this condition mandates
urgent pericardiocentesis.
Pleural effusion per se due to hypothyroidism is rare and
requires careful exclusion of other associated conditions.
Effusions solely due to hypothyroidism have borderline
characteristics between exudates and transudates and show
little evidence of inflammation.
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In conclusion hypothyroidism can have rare modes of
presentations
.
It can present with either isolated effusion or in
combination of multiple body cavity effusions along with
tissue edema.
High index of clinical suspicion is required to diagnose
such cases.
The treatment is simple and gratifying with almost
complete regression of findings after thyroid hormone
85. For pre-eclampsia
Proteinuria
Generalized edema
Hypo-albuminemia
Against
Goiter
Normotensive
Normal liver enzymes
Normal platelet count
Editor's Notes
Spectrum of glomerular diseases. At one extreme, specific injury to podocytes or structural alteration of the glomerulus affectingpodocyte function (for example, by scarring or deposition of excess matrix or other material) causes proteinuria and nephrotic syndrome (see Box 17.11 ,p. 475). The histology to the left shows diabetic nephropathy. At the other end of the spectrum, inflmmation leads to cell damage and proliferation,breaks form in the GBM and blood leaks into urine. In its extreme form, with acute sodium retention and hypertension, such disease is labelled nephriticsyndrome. The histology to the right shows a glomerulus with many extra nuclei from proliferating intrinsic cells, and inflx of inflmmatory cells showscrescent formation (arrows) in response to severe post-infectious glomerulonephritis. (FSGS = focal and segmental glomerulosclerosis; MCGN =mesangiocapillary glomerulonephritis)