Showing posts with label Endocrinology. Show all posts
Showing posts with label Endocrinology. Show all posts

18 March 2012

Assessment and Management of Patients with Diabetes Mellitus



Clinical Case Presentation Diabetes Mellitus Type 2
Prof. A. Vernillo
Case Presentation Diabetes Mellitus.ppt

Diabetes Mellitus Overview and Treatments
Andrew P. Vogt
Diabetes Mellitus Overview and Treatments.ppt

Renal Failure - Assessment of Renal Function
Michele Ritter, M.D.
Renal_Failure.ppt

Understanding and Managing Type 1 Diabetes Mellitus
Jason F. Lopez, Ali Cinar, Ph.D.
Understanding and Managing...ppt

Study on HT & DM
HT & DM.ppt

Chronic Disease Management: Diabetes Mellitus
Rachel Waite
Management: Diabetes Mellitus.ppt

Assessment and Management of Patients With Biliary Disorders
Miss: Iman Shaweesh
Patients With Biliary Disorders .ppt

Diabetes Mellitus
Nursingcareofptwithdiabetes.ppt

Management of Patients with Renal Disorders
Patients with Renal Disorders.ppt

Assessment and Management of Patients with Eye and Vision Disorders
Assessment and Management of Patients....ppt

Assessment and Management of Patients with Diabetes Mellitus
by Linda Self
Assessment_and_Management_of_Patients_with_Diabetes_Mellitus.ppt

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06 March 2012

Pituitary Disorders



Adrenal and Pituitary
Dr. Kathleen Ethridge
http://faculty.ntcc.edu/

Endocrine Disorders
http://www.mac.edu/

Disorders of the Hypothalamic – Pituitary Axis
K. Dionne Posey,  MD, MPH
http://www.med.wayne.edu/

Disorders  of the Pituitary Gland
http://www.d.umn.edu/

Hypothalamus  and Pituitary
http://www.uic.edu/

Pituitary Gland - Anterior Pituitary (adenohypophysis)
http://www.austincc.edu/

Endocrine Dysfunction: Adrenal & Pituitary
http://www.austincc.edu

Pituitary  Disorders
Jo  Choudhry, M.D.
http://wichita.kumc.edu/

Reproductive Endocrinology Female Reproductive System
Ricki Otten, MT(ASCP)SC
http://webmedia.unmc.edu

Is my child too short?
http://sfghdean.ucsf.edu/

Common Inpatient Endocrine Consults
William E. Clutter, M.D.
http://endo.wustl.edu/
Pituitary Disorder in PDF format

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27 February 2012

Ketoacidosis Ppt and published articles



Diabetic  Ketoacidosis
http://elearning.najah.edu/OldData/pdfs/6709Diabetic%20Ketoacidosis.ppt

Diabetic Emergencies 
by Andjela Drincic M.D.
DiabeticEmergenciesNew.ppt

Endocrine  Emergencies
by Bobby Oakes
Endocrine Emergencies.ppt

Diabetic  Ketoacidosis - DKA
by Amy Creel, MD
DKA2010.ppt

Diabetic Ketoacidosis in Children
by Arleta Rewers MD, PhD, Robert Slover MD
Ketoacidosis in Children.ppt

Diabetic  Ketoacidosis
by Abdelaziz  Elamin
Diabetic Ketoacidosis 43651.ppt

Diabetic Ketoacidosis
by Michele Ritter, M.D.
DKA.ppt

Diabetic  Ketoacidosis & Hyperosmolar  Hyperglycemic State- Inpatient  management
by Susan  Schayes M.D
Hyperosmolar Hyperglycemic DKA HONK.ppt

Diabetic Ketoacidosis
by Gary David Goulin, MD
DKA.ppt

Alcoholic Ketoacidosis
by Eric  Niederhoffer
Alcoholic_ketoacidosis.ppt

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Thyroid Ppts



Benign  Thyroid Diseases
by Alan  Cowan, MD, Shawn  Newlands, MD, PhD
Thyroid-benign-slides.ppt
Hypothyroidism
by Kommerien  Daling, MD
thyroid_disease.ppt

Interpreting  Thyroid Function Tests
by Rozina Mithani
Thyroid Function Tests .ppt

Basic Thyroid Function
Thyroid.ppt

Drugs  to Treat Autoimmune Diseases
by Chelsea  Wells
AutoimmuneDisorders_ChelseaWells.ppt

Assessment  and Management of Patients with Endocrine  Disorders
By  Linda Self
Patients_with_Endocrine_Disorders.ppt

Thyroid  Disease
Thyroid Dz.ppt

Subacute  (de Quervain’s) Thyroiditis
by Lauren Galpin,  MD
Thyroiditis.ppt

ubclinical Hypothyroidism
by D. Allen Brantley, M.D.
http://intmedweb.wfubmc.edu/download/subclinical.ppt

Benign  Thyroid Disease
by Sarah  Rodriguez, MD, Francis  Quinn, MD
Thyroid-benign.ppt

Evaluation  of Thyroid Nodules
by Eric  Oliver
Radiology Thyroid.ppt

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24 February 2012

Medullary Thyroid Cancer Ppts and Recently published articles



Medullary Thyroid Cancer
by Travis Baggett
http://www.bcm.edu/sims/Files/vignette2.ppt

Surgical Treatment  of Medullary Carcinoma of the Thyroid 
by Jacques Peltier  MD, Francis B. Quinn,  MD
CA-thyroid-slides-070120.ppt

Pediatric  Thyroid Malignancies
by Kristen Boyle,  MD
ModificationDate=1264544885803

Evaluation of a Thyroid Nodule
by Michael E. Decherd, MD, Matthew W. Ryan, MD
http://med.mui.ac.ir/clinical/ent/Thyroid-Nodule-2002-01-slides.ppsx

Update in the Management of Thyroid Neoplasms
by David R. Byrd, MD
http://depts.washington.edu/surgstus/Clerkship/Lectures/print/Thyroid_Byrd.ppt

Medullary Thyroid Cancer
by David  M. Gleinser, MD, Susan  D. McCammon, MD
Thyroid-ca-slides-101027.ppt

Thyroid Cancer
by Christopher Muller
ThyroidCA-9810.ppt

Evaluation  of Thyroid Nodules
by Eric  Oliver
RadiologyThyroid.ppt

Evaluation of the Effects of Low Dose Radiation-dose reconstruction
by Lynn  R. Anspaugh, Ph.D
Anspaugh-Radiation_Dose_Reconstruction.ppt

Evaluation of Thyroid Nodules
by Michael L. Tuggy, MD
Thyroid nodules.ppt

Pathology of the Thyroid Gland
by Prof. Dipak Shah
Thyroiddiseases.ppt

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23 February 2012

Pituitary Disorders Ppts and Publications




Hypothalamus  and Pituitary
http://www.calstatela.edu/faculty/mchen/439Lectures/439EnHypoPIT9.ppt

Pituitary  Apoplexy
by Kyla  Lokitz
http://www.med.unc.edu/medicine/web/Pituitary%20Apoplexy2005-6.ppt

Pituitary Gigantism
by Dan Chandler, Matt Packard & Spencer P.S
http://academics.hamilton.edu/courses/soph222/projects/group5_files/group5.ppt

Pituitary  Disorders
by Jo  Choudhry, M.D.
http://wichita.kumc.edu/obgyn/slides/choudhry05.ppt

Pituitary  Adenomas
by Chien  Wei OMS IV
PituitaryAdenomas_ohsu_9_06.ppt

Pituitary Gland
Endocrine/endocrine orientation.ppt

Hypothalamus  and Pituitary
Hypothalamus and Pituitary.ppt

Pituitary and Adrenal Stressors
by Prof.  Borrero
Adrenal Stressorst.ppt

Posterior Pituitary
http://open.umich.edu/sites/default/files/2434/022709.RGrekin.ADH.WaterBalance_1.ppt

Endocrine Dysfunction: Adrenal & Pituitary
http://www.austincc.edu/nursmods/online/online_lev4/rnsg_2432/documents/Module18PituitaryPTT2010.ppt

Hypothalamic  & Pituitary hormones
by Eric  Lazartigues, Ph.D.
http://www.medschool.lsuhsc.edu/pharmacology/docs/HPA%20hormones%20lecture-students.ppt

The Neuroendocrinology of the Hypothalamo-Pituitary Adrenal Axis
http://gpilsinside.umaryland.edu/Courses/GPLS613/Old%20Lecture%20Files/HPA.ppt

Phayrngeal  Region Endocrine Glands
http://faculty.uncfsu.edu/ssalek/Biol%20610%20Endocrinology%20online/online%2011.ppt

Pituitary Gland
http://www.austincc.edu/nursmods/cec/cec_lev4/rnsg_2432/documents/Module18PituitaryPowerptF11StudentVersion.ppt

The Anterior  Pituitary and Hypothalamus
http://www.sci.tamucc.edu/~wiki/uploads/PALS-RThomas/4335%20Chapter%206.ppt

Endocrine  Hypothalamus and Anterior Pituitary
http://www.clt.astate.edu/agrippo/Endocrine%20Hypothalamus%20and%20Anterior%20Pituitary.ppt

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04 February 2012

Cholestasis ppts and Latest 50 published articles



Cholestasis: Cholestasis is any condition in which the flow of bile from the liver is blocked.

Intrahepatic  Cholestasis of Pregnancy
http://ihcs.msu.edu/powerpoint/Group4SlidesPMafterBreak.ppt

cholestatic Liver Disease
http://www.medicine.nevada.edu/residency/lasvegas/internalmed/documents/CholestaticLiverDiseasejaundicewithCholangiocarcinomafocus.ppt

Primary  Biliary Cirrhosis (PBC)
by Thomas  W. Faust, M.D., M.B.E.
http://www.med.upenn.edu/gastro/documents/PBCgrandroundsMay2010.ppt

Tests  for Detecting Cholestasis
http://elearning.najah.edu/OldData/pdfs/5508Liver_2.ppt

Medical Nutrition Therapy for Liver, Biliary System, and Exocrine Pancreas Disorders
http://www.uwgb.edu/laceyk/NutSci486/Chapter31.Liver.ppt

Liver  Disease in Pregnancy
by Britt  B. Drake, M.D.
http://gastro.dom.uab.edu/Fellow_Articles/PowerPoint/PPT%20Presentations/PPT%20Presentations/Liver%20Disease%20in%20Pregnancy.ppt

Approach  to the Jaundiced Patient
Internal  Medicine Survivor Series
by Joel  Bruggen, MD
http://intmedweb.wfubmc.edu/download/jaundiced.ppt

Laboratory Assessment a Method of Monitoring Liver, Coagulation, & Endocrine
ftp://math.auburn.edu/pub/departments/pharmacy/pypp5320/liver_coag_endocrine.ppt

Hepatitis  A
http://ihcs.msu.edu/powerpoint/Group3SlidesPM.ppt

Clinical  Pathology Conference: A 39 y.o. male with jaundice
http://www.uab.edu/gim/education/conferences/Previous%20Noon%20Conference/2009-2010/10-20-09%20CPC.ppt

Diseases of  the Liver & Biliary Tract
http://nhscience.lonestar.edu/biol/durham/docs/biol2305/16%20Diseases%20of%20the%20Liver%20&%20Biliary%20Tract.ppt
Latest 50 articles

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15 December 2011

Hypercalcemia, Hypercalcemia and Renal Sarcoid,Hypercalcemia and Multiple Myeloma, Milk-Alkali Syndrome and Evaluation of Hypercalcemia, Approach to Hypercalcemia, Disorders of Calcium and Phosphate Metabolism, Calcium homeostasis, Case Studies in Calcium Metabolism, Endocrine Emergencies ppt



Hypercalcemia
By: Ayesha Shaikh
Emory Family  Medicine Residency Program
http://www.fpm.emory.edu/Family/didactics/powerpint/Hypercalcemia.ppt

Hypercalcemia  secondary to Primary Hyperparathyroidism
by - Emily  Kingsley, MD
https://medicine.med.unc.edu/education/internal-medicine-residency-program/files/ppt/1.11.10%20Kingsley%20Hypercalcemia.ppt

Hypercalcemia  and Renal Sarcoid
by Jason  McClune
http://www.med.unc.edu/medicine/web/9.23.08.%20McClune.%20HyperCa,%20Sarcoidosis.ppt

Hypercalcemia  and Multiple Myeloma
http://www.med.unc.edu/medicine/web/7.16.08%20Rometo.%20MM.ppt

Milk-Alkali  Syndrome and Evaluation of Hypercalcemia
by: TJ O’Neill
https://medicine.med.unc.edu/education/internal-medicine-residency-program/files/ppt/8.17.09%20ONeill%20Hypercalcemia.ppt

Approach to  Hypercalcemia
by Elizabeth  George M.D.
University  of Wisconsin-Madison
http://www2.medicine.wisc.edu/home/files/domfiles/genintmed/George-5-4-05-Hypercalcemia.ppt

Hypercalcemia
http://www.medicine.nevada.edu/residency/lasvegas/internalmed/documents/calciumdisorders.ppt

Disorders  of Calcium and Phosphate Metabolism
http://medresidents.stanford.edu/

Calcium  homeostasis
http://www.uic.edu/classes/phyb/phyb402dbh/lecture5.ppt

Case Studies in Calcium Metabolism
http://www.hsc.unt.edu/tcom2006/endoQuiz2.ppt

Endocrine Emergencies
William E. Clutter, M.D
http://endo.wustl.edu/conferences/PDFs/Thur-noon-conf/STAT%20Consults_Clutter.ppt

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18 November 2011

Thyroid, Parathyroid, Adrenal, Endocrine and Hepatic Disorders, Hormonal Regulation, Renal Failure ppts



Thyroid Disorders - Hyperthyroidism
http://www.mccc.edu/~martinl/documents/EndocrineDysfunctionTHYROIDandParathyroidDISORDERSs2009student.ppt

Thyroid, Parathyroid, and Adrenal
http://academicdepartments.musc.edu/surgery/education/basic_science/2009-10/Thyroid_Parathyroid_and_Adrenal.pps

Nutrition and Metabolism Dysfunction: Thyroid and Adrenal Disorders
http://employees.csbsju.edu/mbyrne/322/ThyroidAdrenalSummary.ppt

Renal Failure and Treatment
http://www.austincc.edu/nursmods/cec/cec_lev4/rnsg_2432/documents/CRDstudentversionKelleHowardlecture_001.ppt

Endocrine Disorders
http://faculty.mccneb.edu/DBlum3/NURS2150/Endocrine_and_Hepatic_Disorders1.ppt

Endocrine and Hepatic Disorders
by: Kimberley McComb-Meisinger RN-BC MSN
http://faculty.mccneb.edu/DBlum3/NURS2150/Endocrine_and_Hepatic_Disorders.ppt

Alterations of Hormonal Regulation
http://faculty.felician.edu/Goldbergb/Classes/Spring%202009/Pathophysiology/Powerpoint%20Pathophysiology/Chapter18.ppt

Introduction to the Endocrine System
http://faculty.spokanefalls.edu/InetShare/AutoWebs/GaryB/AP%20243/Unit%204/Endocrine%20System.ppt

Endocrine and Nervous Systems
http://faculty.ccri.edu/jgluck/MEDL-Endocrine%20and%20Nervous%20Systems.ppt

Renal Failure and  Treatment
http://www.austincc.edu/cmorse/2410/renal/renal_lecture/Renal_Failure_Treatment.ppt

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15 July 2011

Hyperlipidemia 12 Presentations



Hyperlipidemia 12 Presentations
Hyperlipidemia, Hypertension, and Diabetes
http://www.longwood.edu/staff/roycj/Hyperlipidemia.ppt


Hyperlipidemia by Michele Ritter, M.D
http://www9.georgetown.edu/faculty/wheltosa/Shelly_Hyperlipidemia.ppt


Hypertension, Hyperlipidemia: Are our children safe? by Patrick R
http://www9.georgetown.edu/faculty/wheltosa/Saleeb-HTN,_Lipids_(ATP_III).ppt

New Nutritional Approaches for the Treatment of Hyperlipidemia by Laura S. Kinzel, M.S., R.D
http://www.pitt.edu/~super7/PC/pc0041.ppt

Thyroid Disorders and Hyperlipidemia by Uzma Khan M.D.
http://imed.missouri.edu/immse/Y3/conference_handouts/management/M3lip-thyroid907.ppt

Hyper(dys)lipidemias: Disorders of Lipoprotein Metabolism by Michael J. Caplan
http://www.musc.edu/comyear2/BLOCK4/ASF/26-Hyperlipidemia%5B1%5D_MJC_modified_11-23-10.ppt

Lipid Transport: Lipoprotein Structure, Function, and Metabolism
http://www.cwu.edu/~geed/543/Lipid%20Transport.ppt

Primary Care Approach to Dyslipidemia by David Thom, MD, PhD
http://sfghdean.ucsf.edu/barnett/FCM/PGY1/0502_Hyperlipidemia.ppt

Dyslipidemia and Atherosclerosis by Eliot A. Brinton, M.D.
http://umed.med.utah.edu/ms2008/Vault/Cardio/OSLecture8-12-7-05.ppt

Antihyperlipidemic Drugs
http://www.coastalbend.edu/Occu/Nursing/olma/pharmacology/spring%202010/Ch%2035.ppt

Drugs for Lipid Disorders
http://www.mac.edu/faculty/ChristineStaake/Nursing%20311/Web%20Drugs%20for%20Lipid%20Disorders.ppt

Dyslipidemia
http://www.longwood.edu/staff/roycj/EIDdyslipidemia.ppt

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21 April 2010

Sphingolipid Disorders



Sphingolipid Disorders
by:Eric Niederhoffer
SIU-SOM

Sphingolipids (phospho- or glycolipids)

General Structure
Gangliosidoses
Generalized gangliosidosis
Tay-Sachs disease
Niemann-Pick disease
Metachromatic leukodystrophy
Krabbe’s disease
Gaucher’s disease
b-galactosidase
b-hexosaminidase A
GM2 activator
neuraminidase
(sialidase)
SAP-B
b-galactosidase
SAP-B, SAP-C
b-glucosylceramidase
SAP-C
b-hexosaminidase A&B
a-galactosidase A
SAP-B
sphingomyelinase
arylsulfatase A
SAP-B
b-galactosylceramidase
SAP-A, SAP-C
Cerezyme
Targeting of Lysosomal Enzymes to Lysosomes
Addition of M6P to lysosomal enzymes
Recognition by MPRs
M6P independent pathways

Review Questions

* How do you interpret ganglioside names (G, D, M, 1, 2, 3)?
* What do the different lysosomal enzyme names mean in the context of removing saccharides?
* Where does ganglioside degradation occur?

Sphingolipid Disorders

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06 October 2009

Hyponatremia



Hyponatremia
By :
James Yost, MD, MS, MBA
Emory Family Medicine

Hyponatremia
* Definition
* Epidemiology
* Physiology
* Pathophysiology
* Types
* Clinical Manifestations
* Diagnosis
* Treatment

Hyponatremia
* Definition:
o Commonly defined as a serum sodium concentration 135 meq/L
o Hyponatremia represents a relative excess of water in relation to sodium.
* Epidemiology:
o Frequency
+ Hyponatremia is the most common electrolyte disorder
+ incidence of approximately 1%
+ prevalence of approximately 2.5%
+ surgical ward, approximately 4.4%
+ 30% of patients treated in the intensive care unit
o Mortality/Morbidity
+ Acute hyponatremia (developing over 48 h or less) are subject to more severe degrees of cerebral edema
# sodium level is less than 105 mEq/L, the mortality is over 50%
+ Chronic hyponatremia (developing over more than 48 h) experience milder degrees of cerebral edema
# Brainstem herniation has not been observed in patients with chronic hyponatremia
o Age
+ Infants
# fed tap water in an effort to treat symptoms of gastroenteritis
# Infants fed dilute formula in attempt to ration
+ Elderly patients with diminished sense of thirst, especially when physical infirmity limits independent access to food and drink
* Physiology
o Serum sodium concentration regulation:
+ stimulation of thirst
+ secretion of ADH
+ feedback mechanisms of the renin-angiotensin-aldosterone system
+ renal handling of filtered sodium
o Stimulation of thirst
+ Osmolality increases
# Main driving force
# Only requires an increase of 2% - 3%
+ Blood volume or pressure is reduced
# Requires a decrease of 10% - 15%
+ Thirst center is located in the anteriolateral center of the hypothalamus
# Respond to NaCL and angiotensin II
o Secretion of ADH
+ Synthesized by the neuroendocrine cells in the supraoptic and paraventricular nuclei of the hypothalamus
+ Triggeres:
# Osmolality of body fluids
* A change of about 1%
# Volume and pressure of the vascular system
+ Increases the permeability of the collecting duct to water and urea
o renin-angiotensin-aldosterone
+ Renin
# Stemuli are perfusion pressure, sympathetic activity, and NaCl delivery to the macula densa
# Increase in NaCl delivery to the macula decreases the GFR by decrease in the renin secretion
+ Aldosterone
# Reduces NaCl excretion by stimulating it’s resorption
* Ascending loop of Henle
* Distal tubule
* Collecting duct
o extracellular-fluid and intracellular-fluid compartments make up 40 percent and 60 percent of total body water
o renal handling of water is sufficient to excrete as much as 15-20 L of free water per day
o sodium is the predominant osmole in the extracellular fluid (ECF) compartment and serum

* Pathophysiology
o hyponatremia can only occur when some condition impairs normal free water excretion
o acute drop in the serum osmolality:
+ neuronal cell swelling occurs due to the water shift from the extracellular space to the intracellular space
+ Swelling of the brain cells elicits 2 responses for osmoregulation, as follows:
# It inhibits ADH secretion and hypothalamic thirst center
# immediate cellular adaptation
* Types
o Hypovolemic hyponatremia
o Euvolemic hyponatremia
o Hypervolemic hyponatremia
o Redistributive hyponatremia
o Pseudohyponatremia
Hypovolemic hyponatremia
* develops as sodium and free water are lost and/or replaced by inappropriately hypotonic fluids
* Sodium can be lost through renal or non-renal routes
* Nonrenal loss
o GI losses
+ Vomiting, Diarrhea, fistulas, pancreatitis
o Excessive sweating
o Third spacing of fluids
+ ascites, peritonitis, pancreatitis, and burns
o Cerebral salt-wasting syndrome
+ traumatic brain injury, aneurysmal subarachnoid hemorrhage, and intracranial surgery
+ Must distinguish from SIADH
* Renal Loss
o Acute or chronic renal insufficiency
o Diuretics

Euvolemic hyponatremia
* Normal sodium stores and a total body excess of free water
o Psychogenic polydipsia, often in psychiatric patients
o Administration of hypotonic intravenous or irrigation fluids in the immediate postoperative period
o administration of hypotonic maintenance intravenous fluids
o Infants who may have been given inappropriate amounts of free water
o bowel preparation before colonoscopy or colorectal surgery
* SIADH
o downward resetting of the osmostat
o Pulmonary Disease
+ Small cell, pneumonia, TB, sarcoidosis
o Cerebral Diseases
+ CVA, Temporal arteritis, meningitis, encephalitis
o Medications
+ SSRI, Antipsychotics, Opiates, Depakote, Tegratol

* Total body sodium increases, and TBW increases to a greater extent.
* Can be renal or non-renal
o acute or chronic renal failure
+ dysfunctional kidneys are unable to excrete the ingested sodium load
o cirrhosis, congestive heart failure, or nephrotic syndrome

Redistributive hyponatremia
o Water shifts from the intracellular to the extracellular compartment, with a resultant dilution of sodium. The TBW and total body sodium are unchanged.
+ This condition occurs with hyperglycemia
+ Administration of mannitol
* Pseudohyponatremia
o The aqueous phase is diluted by excessive proteins or lipids. The TBW and total body sodium are unchanged.
+ hypertriglyceridemia
+ multiple myeloma
* Clinical Manifestations
o most patients with a serum sodium concentration exceeding 125 mEq/L are asymptomatic
o Patients with acutely developing hyponatremia are typically symptomatic at a level of approximately 120 mEq/L
o Most abnormal findings on physical examination are characteristically neurologic in origin
o patients may exhibit signs of hypovolemia or hypervolemia
* Diagnosis
o CT head, EKG, CXR if symptomatic
o Repeat Na level
o Correct for hyperglycemia
o Laboratory tests provide important initial information in the differential diagnosis of hyponatremia
+ Plasma osmolality
+ Urine osmolality
+ Urine sodium concentration
+ Uric acid level
+ FeNa
o Plasma osmolality
+ normally ranges from 275 to 290 mosmol/kg
+ If >290 mosmol/kg :
# Hyperglycemia or administration of mannitol
+ If 275 – 290 mosmol/kg :
# hyperlipidemia or hyperproteinemia
+ If <275 mosmol/kg :
# Eval volume status
o Plasma osmolality < 275 mosmol/kg
+ Increased volume:
# CHF, cirrhosis, nephrotic syndrome
+ Euvolemic
# SIADH, hypothyroidism, psychogenic polydipsia, beer potomania, postoperative states
+ Decreased volume
# GI loss, skin, 3rd spacing, diuretics
o Urine osmolality
+ Normal value is > 100 mosmol/kg
+ Normal to high:
# Hyperlipidemia, hyperproteinemia, hyperglycemia, SIADH
+ < 100 mosmol/kg
# hypoosmolar hyponatremia
* Excessive sweating
* Burns
* Vomiting
* Diarrhea
* Urinary loss
o Urine Sodium
+ >20 mEq/L
# SIADH, diuretics
+ <20 mEq/L
# cirrhosis, nephrosis, congestive heart failure, GI loss, skin, 3rd spacing, psychogenic polydipsya
o Uric Acid Level
+ < 4 mg/dl consider SIADH
o FeNa
+ Help to determine pre-renal from renal causes
* Treatment
o four issues must be addressed
+ Asyptomatic vs. symptomatic
+ acute (within 48 hours)
+ chronic (>48 hours)
+ Volume status
o 1st step is to calculate the total body water
+ total body water (TBW) = 0.6 × body weight
o next decide what our desired correction rate should be
o Symptomatic
+ immediate increase in serum Na level by 8 to 10 meq/L in 4 to 6 hours with hypertonic saline is recommended
o acute hyponatremia
+ more rapid correction may be possible
# 8 to 10 meq/L in 4 to 8 hours
o chronic hyponatremia
+ slower rates of correction
# 12 meq/L in 24 hours

* Symptomatic or Acute
o Treatment Cont. - Here comes the Math!!!
+ estimate SNa change on the basis of the amount of Na in the infusate
+ ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
# ΔSNa is a change in SNa
# [Na + K]inf is infusate Na and K concentration in 1 liter of solution
o OH MY GOD, what did he just say!!!!!!!!!!!!!!!!!!

* IV Fluids
o One liter of Lactated Ringer's Solution contains:
+ 130 mEq of sodium ion = 130 mmol/L
+ 109 mEq of chloride ion = 109 mmol/L
+ 28 mEq of lactate = 28 mmol/L
+ 4 mEq of potassium ion = 4 mmol/L
+ 3 mEq of calcium ion = 1.5 mmol/L
o One liter of Normal Saline contains:
+ 154 mEq/L of Na+ and Cl−
o One liter of 3% saline contains:
+ 514 mEq/L of Na+ and Cl−

* Example:
o a 60 kg women with a plasma sodium of 110 meq/L
o Formula:
+ ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
o What is the TBW?
o How high will 1 liter of normal saline raise the plasma sodium?
* Answer:
o TBW is 30 L
o Serum sodium will increase by approximately 1.4 meq/L for a total SNa of 111.4 meq/L

* Example:
o a 90 kg man with a plasma sodium of 110 meq/L
o Formula:
+ ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
o What is the TBW?
o How high will 1 liter of 3% saline raise the plasma sodium?
* Answer:
o TBW is 54 L
o Serum sodium will increase by approximately 7.3 meq/L for a total SNa of 117.3 meq/L

* Asymptomatic or Chronic
o SIADH
+ response to isotonic saline is different in the SIADH
+ In hypovolemia both the sodium and water are retained
+ sodium handling is intact in SIADH
+ administered sodium will be excreted in the urine, while some of the water may be retained
# possible worsening the hyponatremia

Hyponatremia

* Asypmtomatic or Chronic
o SIADH
+ Water restriction
# 0.5-1 liter/day
+ Salt tablets
+ Demeclocycline
# Inhibits the effects of ADH
# Onset of action may require up to one week

* Example:
+ 85 y/o male with weakness and head ache
+ SNa is 118 mEq/L
+ Plasma osmolality is 254 mosmol/kg
+ Urine osmolality is 130 mosmol/kg
+ Urine sodium >20 mEq/L
+ Uric acid is 3mg/dl
o What type of hyponatremia does this patient have?
o What additional labs/studies would you want?

* Example Cont.:
o Noncontrast CT Head:
* Tx
o Call Neurology and neurosurgery
o Free water restriction

* Example:
o 63 y/o female at 75 Kg with N/V/D for 4 days
o SNa is 108 mEq/L
o She has had one seizure in the ambulance
# Plasma osmolality is 251 mosmol/kg
# Urine osmolality is 47 mosmol/kg
# Uric acid is 6mg/dl
o What type of hyponatremia does this patient have?
o What additional labs/studies would you want?
* How will you Tx her?
o Calculate the total body water
+ 0.5 x weight = 37.5 L
o What rate of correction do you want?
+ 8 to 10 mEq/L in 6 to 8 hours
o What fluid will you use?
+ 3% Saline
o How will you calculate the amount of sodium to give her?
+ ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
o How will her sodium increase after 1 liter of 3% saline?
+ By 10.8 mEq/L to 118.8 mEq/L

* What other medication will she need?
o Lasix and a foley
* Her sodium increases to 118.8 mEq/L over the next 8-10 hours. How will you continue to correct her hyponatremia?
o ΔSNa = {[Na + K]inf − SNa} ÷ (TBW + 1)
o ΔSNa = 154mEq/L – 118.8mEq/L ÷ 38.5L = 0.9 mEq/L
* So 2 liters of normal saline over the next 14 hours

Hyponatremia.ppt

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Fluid, Electrolyte & Acid-Base Balance



Fluid, Electrolyte & Acid-Base Balance

Body Fluids
* Your body is 66% water
* Not evenly distributed – separated into compartments
* Able to move back and forth thru the cell membranes to maintain an equilibrium

Fluid Compartments
* Intracellular fluid – fluid inside cells [ICF]
* Extracellular fluid – fluid outside cells and all other body fluids --- ž is plasma [intravascular fluid], remaining Å« is interstitial fluid. Small amount is localized as CSF, serous fluid, synovial fluid, humors of eye & endo/perilymph of ears

Edema
* Condition in which fluid accumulates in the interstitial compartment. Sometimes due to blockage of lymphatic vessels or by a lack of plasma proteins or sodium retention

Fluid Balance
* Amount in = amount out
* Average daily intake is 2500 ml [ fluids, food and metabolic water]
* Average daily output is 2500 ml [ urine, feces, perspiration, insensible perspiration]
* What can throw off these numbers?

Electrolyte Balance
* Def: - concentration of individual electrolytes in the body fluid compartments is normal and remains relatively constant.
* Electrolytes are dissolved in body fluids
* Sodium predominant extracellular cation, and chloride is predominant extracellular anion. Bicarbonate also in extracellular spaces
* Potassium is the predominant intracellular cation and phosphates are the predominant intracellular anion
* Cations are actively reabsorbed, anions passively follow by electrochemical attraction
* Aldosterone works at kidney tubules to regulate sodium & potassium levels
* Because of sodium and potassium influence, water will move between compartments
* Example: if high [sodium], then water will move from intracellular space to extracellular space due to osmotic pressure

Balance of other Electrolytes
* Calcium – hypercalcemia / hypocalcemia
* Magnesium – hypermagnesemia/ hypomagnesemia
* Phosphate – hyperphosphatemia/ hypophosphatemia
* Chloride – hyperchloremia/ hypochloremia
Acid - Base Balance
* Blood - normal pH of 7.2 – 7.45
* < 7.2 = acidosis > 7.45 = alkalosis
* 3 buffer systems to maintain normal blood pH
* Buffers
* Removal of CO2 by lungs
* Removal of H+ ions by kidneys
Buffers
* Protein Buffer Systems
* Amino Acid buffers
* Hemoglobin buffers
* Plasma Protein buffers
* Phosphate Buffer Systems
* Carbonic Acid – Bicarbonate Buffer System
Maintenance of Acid-Base Balance
* Respiratory System: removal of CO2 by lungs – stabilizes the ECF, has direct effect on Carbonic Acid – Bicarbonate Buffer System

* Urinary System: removal of H+ ions by kidneys

Disturbances to Acid-Base Balance
* Respiratory Acidosis
* Respiratory Alkalosis
* Metabolic Acidosis [ lactic acidosis, ketoacidosis]
* Metabolic Alkalosis

Fluid, Electrolyte & Acid-Base Balance.ppt

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01 July 2009

Endocrine Emergencies



Endocrine Emergencies
By:Bobby Oakes


Endocrine Emergencies
* Diabetic Ketoacidosis
* Thyroid Storm
* Adrenal Insufficiency
Diabetic Ketoacidosis (DKA)
Physiology
* Hyperglycemia
* Ketoacidemia
* Fluid and Electrolyte Depletion
Diabetic Ketoacidosis General Considerations
Diabetic Ketoacidosis
* Essentials of Diagnosis
Diabetic Ketoacidosis Clinical Findings
* Symptoms:
* Signs:
Diabetic Ketoacidosis Laboratory Findings
Diabetic Ketoacidosis Treatment
* Insulin Replacement
* Fluid Replacement
DKA vs HHS
* Diabetic Ketoacidosis
* Hyperglycemic Hyperosmolar State
Thyroid Storm
Thyroid Storm Treatment
Acute Adrenal Insufficiency
Acute Adrenal Insufficiency General Presentations
Adrenal Insufficiency Diagnosis
Adrenal Insufficiency Treatment

Endocrine Emergencies.ppt

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15 June 2009

Male Hypogonadism



Male Hypogonadism
By: Michael Jakoby, MD/MA
Clinical Associate Professor of Medicine
Chief, Division of Endocrinology

Case study:
Definition

Decrease in one or both of the two major functions of the testes.
Gonadotrope failure
Secondary
Elevated
Testicular failure
Primary
Sperm count
Testosterone
Gonadotropins
Pathology
Hypogonadism
Gonadal Axis
Male Gonadal Function
Male Puberty
Clinical Features
Postpuberty
* Incomplete puberty
* Eunichoidal body habitus*
Prepuberty
Micropenis
3rd trimester
Incomplete virilization
1st trimester
Effects
Age
Screening for Androgen Deficiency
* Infertility
* Sellar mass, radiation, or surgery
* Osteoporosis or low trauma fracture
* HIV-associated weight loss
* ESRD
* COPD (moderate to severe)
* Type 2 diabetes mellitus
* Medications that effect testosterone production
o Glucocorticoids
o Opiates
o Ketoconazle

The Endocrine Society recommends against screening for androgen deficiency in the general population
History
* Symptoms onset
* Testicular size
* Breast enlargement
* Behavioral abnormalities
* Chemotherapy or radiation therapy
* Alcoholism
* Visual field defects
* Medications
Examination
* Testicular size
* Pubic hair
* Gynecomastia
* Muscle mass
* Body proportions
* Fundoscopy & visual fields screening

Laboratory Testing
Secondary hypogonadism
Primary hypogonadism
Elevated
Diagnosis
Gonadotropins (LH/FSH)
Semen analysis
Testosterone

Testosterone Measurements
* Total testosterone (free + protein bound) is almost always an accurate measure of testosterone secretion
* Free testosterone should be measured by equilibrium dialysis; analog methods commonly available give results proportionate to SHBG levels (Vermeulin A JCEM 84:3666)
* Testosterone should be measured in the morning (~ 8 AM) due to diurnal variations in testosterone levels, especially in young men
* Conditions that predispose to low SHBG levels:
o Obesity (BMI > 40)
o Senescence
o Nephrotic syndrome
o Cirrhosis
o Anticonvulsants

Testosterone in Obese Men
Testosterone Secretion: Comparison of Young and Elderly Men
Standard Semen Analysis
* Typically ordered for infertility w/u only
* Normal specimen:
o > 40 million sperm/ejaculate
o > 50% motile; > 25% rapidly motile
o > 50% normal morphology
DDx: Primary Hypogonadism
* Klinefelter’s syndrome
* Gonadotropin receptor mutations
* Cryptorchidism
* Androgen biosynthesis disorders
* Varicocele
* Congenital anorchia
* Mumps orchitis
* Radiation
* Antineoplastic drugs
* Ketoconazole
* Glucocorticoid excess
* Trauma
* Testicular torsion
* Autoimmune orchitis
* Cirrhosis
* Chronic renal failure
* HIV infection
* Idiopathic

Congenital
Acquired

DDx: Secondary Hypogonadism
* Isolated hypogonadotropic hypogonadism
* Kallman’s syndrome
* DAX1 mutation
* GPR 54 mutation
* Leptin or leptin receptor mutations
* Gonadotrope receptor mutations
* Hypopituitarism
* Hyperprolactinemia
* Androgen therapy
* GnRH analog therapy
* Glucocorticoid therapy
* Critical illness
* Chronic illness
* Diabetes mellitus
* Opiates
* Pituitary mass lesions
* Infiltrative diseases
* Sellar surgery
* Sellar radiation

DDx: Primary Hypogonadism
* Klinefelter’s syndrome
* Gonadotropin receptor mutations
* Cryptorchidism
* Androgen biosynthesis disorders
* Varicocele
* Congenital anorchia
* Mumps orchitis
* Radiation
* Antineoplastic drugs
* Ketoconazole
* Glucocorticoid excess
* Trauma
* Testicular torsion
* Autoimmune orchitis
* Cirrhosis
* Chronic renal failure
* HIV infection
* Idiopathic

Evaluation of Men with Androgen Deficiency
Confirmed low testosterone
Check LH+FSH (SA if infertility)
High gonadotropins – 1o
Low/low nl gonadotropins – 2o
Karyotype
Prolactin, other pituitary hormones, iron studies, sella MRI
What is the initial diagnosis?
Primary hypogonadism
What is the next step in work up?
Karyotype: 47 XXY
Klinefelter’s Syndrome
Gonadal Manifestations of Klinefelter’s Syndrome
Decreased penis length
Decreased axillary hair
Gynecomastia
Decreased sexual function
Increased gonadotropins
Decreased facial hair
Low testosterone
Azoospermia
Decreased testicular length
Abnormal testicular histology
Frequency (%)
Abnormality
Testosterone Replacement
* Primary goal is to restore testosterone levels to the laboratory reference range
* Prescribe only for patients with confirmed hypogonadism
* Role in “treating” decline in testosterone levels with aging uncertain
* Multiple preparations
o Oral
o Intramuscular
o Transdermal
o Buccal
Oral Testosterone Preparations
* Alkylated testosterone more slowly metabolized by liver than native testosterone
* May not induce virilization in adolescents
* Untoward effects
+ Cholestatic jaundice
+ Peliosis hepatis
+ Hepatocellular carcinoma
Intramuscular Testosterone
* Enanthate and cypionat
Serum testosterone levels after a single 200 mg IM dose of testosterone enanthate.
Transdermal Testosterone
* Patch (Androderm)
* Gels (Androgel, Testim)
Desirable Effects of Testosterone Therapy
Untoward Effects of Testosterone Therapy
* Pain at injection site (IM preparations)
* Contact dermatitis (patch >> gel)
* Acne or oily skin
* Gynecomastia
* Aggressive behavior (adolescents)
* Short stature (adolescents)
* Increased prostate volume/PSA
* Urinary retention (BPH exacerbation)
* Sleep apnea
* Erythrocytosis

Contraindications to Testosterone Therapy
* Very high risk of adverse outcomes
o Prostate cancer
o Breast cancer
* High risk of adverse outcomes
o Undiagnosed prostate nodule
o Unexplained PSA elevation
o BPH with severe urinary retention
o Erythrocytosis
o NYHA Class III or IV heart failure

Pre-treatment Screening
* Digital rectal exam
* History of urinary retention (urodynamic studies, bladder US PRN)
* History of sleep apnea symptoms (polysomnography PRN)
* PSA (urology referral if > 4 ng/mL)
* CBC

Treatment Monitoring
* Serum testosterone
* Prostate
* Red cell mass
Summary

* Signs and symptoms of hypogonadism depend on when the condition occurs in development
* Initial evaluation focuses on distinguishing between primary and secondary hypogonadism
o Primary: LH elevated, testosterone low
o Secondary: LH low, testosterone low
* Goal of testosterone replacement is physiological testosterone levels and preservation of testosterone-dependent physiological functions

Male Hypogonadism.ppt

Read more...

13 June 2009

Current Obesity Management in Primary Care



Current Obesity Management in Primary Care
By:Eileen L. Seeholzer, M.D., M.S.

Obesity Defined

· Traditionally defined as a weight 20% greater than ideal body weight
· Severe obesity or morbid obesity is defined traditionally defined as a weight 100% greater than ideal body weight

Fat Distribution
Upper-body obesity or abdominal obesity or androgenic obesity: An independent risk factor for diabetes mellitus, cardiovascular disease, hypertension, arthritis, menstrual irregularities and gallbladder disease
(Diabetes mellitus is thirty times higher in highest waist-to-hip ratio (whr)compared to lowest quartile whr)
Clinical Guidelines on the Identification, Evaluation and Treatment of overweight and Obesity in Adults

Body Mass Index Chart
Scope of the problem in the U.S.
Increased Risk for Adult Obesity
* Gender/Ethnicity: Women, blacks, Hispanics and Native Americans
* Family History
* Childhood Obesity
* In lower socioeconomic status
* Sedentary lifestyle
* Increased time-spent watching TV
Local Public Health Data
Associated Medical Problems
Renal: Proteinuria/glomerulosclerosis, CRF
Dermatologic: intertrigo, venous stasis, cellulitis, hidradenitis suppurativa, acanthosis nigricans
Psychiatric: depression, binge eating disorder, night eating syndrome
GU: stress incontinence, PCOS, infertility, pregnancy risk
Rheumatologic: DJD- knee, hip, low back pain
General: fatigue, pain, disability, lower socio- economic status, poorer quality of life
Obesity associated Increased Risks in Pregnancy
* Gestational Diabetes
* Hypertension
* Disordered breathing/Obstructive Sleep Apnea
* Cesarean section rate (RR1.5-1.8)
* Congenital heart defects (OR 1.4-2.0)
* Spina Bifida (OR 3.5)
* Omphalocele (OR 3.3)
* Increased levels of leptin, crp and tnf-alpha

Birth Weight and Obesity
* LBW and (<2000gm)OR2.16 and high birth weight (>4000gm)OR 1.53 increased gestational DM risk
* LBW associated with increased overweight adolescence
* Prolonged breast feeding associated with lower rates of adult obesity
Metabolic Syndrome
Three or more of the following present:
* Abdominal obesity(>102cm M/88cm F)
* Elevated triglycerides (>150mg/dl)
* Low HDL (<40 for men mg/dl; <50 for mg/dl for women)
* Hypertension
* High fasting blood sugar
Neuroendocrine Environment
* Leptin/Leptin receptor resistance (at VMH)
* TNF-α, IL-6, adiponectin (aconitase theory – decreased cellular ATP,increased FFA and glucose, Wlodek, et. Al. 2003)
* CRP
* Dopamine, serotonin, norepinephrine
* Low growth hormone levels observed
* Higher cortisol levels sometimes seen
Ghrelin and Peptide YY
Impact of Weight Loss on Risk Factors
Obesity Treatment Pyramid
Diet
Physical Activity
Lifestyle Modification
Pharmacotherapy
Surgery
Non-Pharmacologic Treatments
Components of Basic Program
* Diet Recommendations
* Exercise Recommendations
* Behavior Therapy
* Regular f/u in maintenance phase
Behavior therapy
Combined therapy
Time (mo)
Assessing Weight Loss Readiness
* Motivation:
* Stress level:
* Psychiatric issues:
* Time availability:
Patient seeks weight reduction
Results from Non-pharmacologic Programs
Pharmacologic Treatments
Other Agents
Experimental Agents - Phase 3
Medications That May Promote Weight Gain
* Antipsychotics: risperidone, clonazepine, olanzepin
* Antidepressants: Tri-cyclics, SSRI
* Antiepileptics: valproic acid, gabapentin, carbemazepine
* Lithium
* DM treatments: Sulfonylureas, insulin
* Progestin steroids
* Cortisone
* Antihistamines
* Beta blockers
Surgical Treatment
Surgical Outcomes
Improvement in Comorbid Conditions s/p Gastric Bypass
Common longer-term Complications after Gastric Bypass
Screening For Obesity in Adults
Weight Management Clinic
Obesity Treatment Guidelines

Current Obesity Management in Primary Care.ppt

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27 May 2009

Hormone Replacement Therapy



Hormone Replacement Therapy… and other options
By:Marc Childress, MD


Risks vs. Benefits in a post-WHI world
* Cancer Risk
* Osteoporosis
* Dementia
* Vasomotor Symptoms
* Urogenital Symptoms
* Cardiovascular Disease

Breast Cancer
* Mixed Results
* Excess risk approx ½ of anticipated
* Question of prognosis, timeframe of concern

Gratuitous Perspective Slide
* Increased risk of breast CA with 10% weight gain (2 add’l cases per 1000 pt-years)
* Increased risk of breast CA with combined tx (0.8 add’l cases per 1000 pt-years)

Endometrial Cancer
* Known increase in risk with unopposed estrogen
* WHI showed no signif risk of CA with combined tx

Ovarian Cancer
* No overt correlation b/w combined HRT and ovarian CA risk
* There IS a signif risk reduction associated with OCPs

Colorectal Cancer
* Signif Risk Reduction of Colon CA with combined Est/Pro
* While less cases, trend toward worse prognosis (nodal spread)
* No risk reduction observed with estrogen alone

Osteoporosis
* Well established
* Risk reduced at hip, vertebrae, and wrist over placebo
* Similar numbers for estrogen alone vs combined tx.

Dementia
* Presumed correlation with long-term estrogen and cognitive fxn
* WHIMS (memory study)

Vasomotor Symptoms
* Signif Reduction in hot flashes
* Mod improvement in sleep
* Well-known and unchanged

Urogenital Symptoms
* Can preclude occurrence of atrophic vaginitis
* Thought to prevent urinary incontinence, contradicted by WHI and HERS

Cardiovascular Disease
* Counter to previous belief, very small increase in risk of CV events with combined tx
* Estrogen alone did not show increase in risk of CV events,
* Stroke
* Venous Thromboembolism

* Which one of the following would be accurate advice regarding these risks and benefits?
* The incidence of stroke is decreased
* The incidence of myocardial infarction is decreased
* The incidence of pulmonary embolism is decreased
* The risk of breast cancer is increased
* The incidence of colorectal cancer is increased

Overview
* Current indications (brief? Tx)
o Vasomotor sxs
o Sleep disturbance
o Urogenital changes
* Additional benefits
o Osteoporosis prevention
* Risks include
o Increase in ischemic stroke
o Increase in DVT, PE
o Mild increase in breast CA risk for combined tx
o Increase in inconclusive mammograms
o Increase in GB dz with combined tx

Osteoporosis
Vasomotor Symptoms
* Pharmacologic Therapies
Vasomotor Symptoms
* Pharmacologic Therapies
Herbal Options
Vasomotor Symptoms
* Herbal/Complementary Compounds
Vasomotor Symptoms
* Not Helpful
Urogenital Symptoms

Hormone Replacement Therapy.ppt

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Thyroid Disease Facts



Thyroid Disease Facts
By:Jeffrey Medland
Lt Col, USAF, MC, SFS
Chief, Endocrinology
MGMC, Andrews AFB, MD
Capital Conference-June 2007

Outline
* Thyroid Testing
* Hypothyroidism
o Causes
o Signs/symptoms
o Treatment
* Hyperthyroidism
o Causes
o Signs/symptoms
o Treatment
* Thyroid Nodules/ Cancer
* Thyroid Disease and Pregnancy
o Hypothyroidism
o Hyperthyroidism (Hyperemesis Gravidarum, Graves’)
o Thyroiditis
* Factors affecting Thyroid function, LT4

Thyroid
Colloid
Apical Membrane
Basal Membrane
Thyroid Peroxidase (TPO)
“Iodination Reaction”
“Coupling Reaction”

Thyroid Testing
* TSH
o Best test for screening for thyroid dysfunction!
o Log/linear response w/ FT4
+ A 2-fold change in FT4 produces a 100-fold change in TSH
o Not specific for a particular thyroid disease.
+ Don’t use TSH alone for diagnosis!
o Also useful in
+ Assessing LT4 tx in 1° hypothyroidism
+ Monitoring TSH-suppressive tx in thyroid Ca
* FT4
o Testing methods:
+ Equilibrium dialysis
+ Analog assays
o Abnormal TSH check this next
o Indications:
+ In conjunction w/ TSH for diagnosing hyperthyroidism or hypothyroidism.
+ Monitoring LT4 replacement in central hypothyroidism (TSH not helpful)
+ Assessing response to tx following 131-RAIA (Graves, toxic nodules)
+ Monitoring ATD tx in pregnant females
* FT3
o Abnormal TSH + normal FT4, then check this (T3 Thyrotoxicosis)

Pituitary Hypothyroidism
Subclinical Hyperthyroidism, Autonomous nodules
Thyrotoxicosis, Thyroiditis (stage 1)
Pituitary Hyperthyroidism
Subclinical Hypothyroidism
Primary Hypothyroidism, Thyroiditis (stage 3)
Clinical Status
FT4
Overview of Thyroid Function Tests
* Thyroid Antibodies (TPO, Tg, TSI, TRAb)
* Thyroglobulin (Tg)
* Radioactive Iodine Uptake and Scan (RAIU/Scan)
* Tc99m-Pertechnetate Scan
* Fine Needle Aspiration (FNA)
* Ultrasound
* Calcitonin

Hypothyroidism
Thyroiditis
Hypothyroidism (Treatment)
Hypothyroidism (treatment in general)
Indications for LT4 replacement
Hypothyroidism + surgery
Hypothyroidism + elderly
Combined LT4/LT3 tx
Hyperthyroid Eye Disease
Does131-RAIA worse ophthalmopathy?
Graves’ Dermopathy Thyroid Dermopathy
Thyroid Acropachy
RAIU/Scan
Increased RAIU
Decreased RAIU
Surgery (sub-total thyroidectomy)
Apathetic Hyperthyroidism
Thyroid Storm
Subclinical Hyperthyroidism
Thyroid Nodules
Red Flags concerning for Cancer
FNA Results:
Thyroid Nodules “Mimickers”
Thyroid Cancer
MTC
Thyroid Disease in Pregnancy
Four factors alter thyroid function in pregnancy
1) Transient ↑ in hCG, during the 1st trimester can stimulate the TSH-R
2) E2-induced ↑ in TBG during the 1st trimester, which is sustained during pregnancy.
3) Alterations in immune function leading to onset, exacerbation, or amelioration of an underlying autoimmune thyroid disease.
4) urinary iodide excretion, which can cause impaired thyroid hormone production in areas of marginal iodine deficiency (<50 µg/d).
Known Hypothyroidism already on LT4
Stage 1 to 4
Hyperemesis Gravidarum (HG)
Hyperemesis Gravidarum vs. Graves’
Causes of Increased LT4 requirement
Drugs Affecting Thyroid Function
Somatostatin, Glucocorticoids
Dopamine
Amiodarone Effect on Thyroid Function
Amiodarone and the Thyroid
Iodine Effect
Direct Toxic Effect
* Thyroiditis (AIT type 2)
“Innocent Changes”
Jod-Basedow phenomenon (Historical)
* Definition- Hyperthyroidism induced by excess Iodine.
* Coindet (French physician) in 1821 published his cases about Hyperthyroidism.
* In the English speaking world this became known as Graves’ disease (1835), and in the German speaking world as von Basedow’s disease (1840).
* Coindet’s cases of hyperthyroidism were actually Iodine-induced, hence it came to be known as the Iodine-Basedow phenom.
* Jod is German for Iodine, hence the Jod-Basedow phenom!
* Coindet was deprived of credit for not only describing Hyper- thyroidism, but also the variant of hyperthyroidism caused by excess Iodine
* The credit was given to Dr “Jod” who never existed!

Conditions affecting Thyroid Function
Autoimmune Polyglandular Syndromes 2
Hypokalemic Periodic Paralysis
Hyperthyroid Eye Disease
Cutis Aplasia
Cutis Aplasia Keloid
Cutis Aplasia
Thyroid Binding Globulin (TBG)
Increased TBG
Decreased TBG
Thyroid Regulation
Amiodarone the Thyroid
Amiodarone Effects on Thyroid
Thyroid Hormone
* There is no absorption from the stomach. Absorption occurs in the small bowel.
* The main absorptive sites appear to be the proximal and mid-jejunum.
* Progressively decreasing degrees of absorption occur along the distal bowel and proximal colon.
* Hypothyroidism can lead to a slight increase in absorption.

Thyroid Disease Facts.ppt

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Diabetes: The 2007 Guidelines



Diabetes: The 2007 Guidelines
By:Kevin E. Moore, M.D.
LTC, MC
Residency Director
NCC-DACH Family Medicine Residency


ADA 2007 Clinical Practice Recommendations

* Why is this important?
* Current screening guidelines
* 6 cornerstones of diabetes
* New developments


Medical Management Can Change All of the Above
Screening
Risk Factors
* Family History
* Obesity (BMI > 25)
* Race/Ethnicity (African-American, Hispanic-American, Native Americans, Asian Americans, Pacific Islanders)
* Age > 45
* Hypertension (> 140/90)
* HDL Cholesterol < 35
* Triglycerides > 250
* History of GDM
* History of Macrosomia
* Polycystic Ovarian Disease
* Previous Abnormal Screening
* Physically Inactive
* Vascular Disease

Screening Recommendations
Repeat and Confirm all Screening Tests in 24 Hours!
Screening Tests
Cornerstones of Diabetes Management?
* Glycemic Control
* Hypertension
* Hyperlipidemia
* Nephropathy
* Retinopathy
* Foot Care
Drug Therapy
Nutrition Therapy
Screening Tests for Albuminuria
Screening Test Results
Annual Foot Exam
Risk Factors for Foot Disease
New Developments - Prevention
New Developments - Children

Diabetes: The 2007 Guidelines.ppt

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14 May 2009

15 Pancreas Presentations



Pancreas Gland with Double Duties

The Pancreas

Physiology of The Pancreas

The Pancreas

Pancreatic disease seminar.pdf

Acute Pancreatitis

Disorders of the Liver and Pancreas.pdf

The Endocrine Pancreas

Liver, Pancreas, and Gallbladder Anatomy-Histology Correlate

Acute Pancreatitis

The Endocrine Pancreas

Pancreas

Cystic Fibrosis and The Effects on the Pancreas

FUNCTION /DYSFUNCTION OF ENDOCRINE PANCREAS

The Artificial Pancreas Project

Read more...
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