PICTURES OF PITUITARY AND TRANS-SPHENOID SURGERY
PICTURES OF PITUITARY AND TRANS-SPHENOID SURGERY
from Otolaryngology Houston
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Showing posts with label Endocrinology. Show all posts
Showing posts with label Endocrinology. Show all posts
13 May 2009
THYROID AND PARATHYROID SURGERY PICTURES
THYROID AND PARATHYROID SURGERY PICTURES, INFORMATION AND IMAGING
from Otolaryngology Houston
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12 May 2009
Endocrine Disruption
♂Endocrine Disruptors♀
Presentation Lecture by:By Sandy Poulos
Endocrine Disruption
* Endocrine System-a complex network of glands that produce and secrete the hormones that regulate all the major body functions.
* Endocrine Disruptor-chemical that interferes with the endocrine system to produce an undesired response, which may affect health, growth, and reproduction.
Mechanisms of Action
* Mimics
* Stimulators
* Blockers
* Endocrine flushers
* Enzyme flushers
* Destructors
EDCs
* Estrogens: any family of steroid hormones that regulate and sustain female sexual development and reproductive function
* Androgen: a class of male sex hormones related to the steroid androstane and produced in the adrenal cortex and the testes
* Substances mimicking feminizing effects are estrogenic and those mimicking masculinizing effects are androgenic
* Also anti-estrogenic and anti-androgenic
Classification
* Pesticides, herbicides, fungicides
* Polyaromatic compounds - PAHs
* Organic oxygen compounds (phthalates, bisphenol A)
* Surfactants
* Drugs
* Metals
* Phytoestrogens
Pesticide-DDT
* 1950’s to 1960’s – DDT
o Estogenic
o Affected reproduction system of birds
o Disrupted the eagle's endocrine system, interfering with calcium metabolism and produced weak egg shells, feminized frogs
o DDT metabolite (DDE) → anti-androgens
* Atrazine & Endosulfan
Bisphenol A & Phthalates
* Bisphenol A
o Used in the manufacture of some clear plastics (e.g. baby feeding bottles), and used in the resin which lines most tin cans
o Potency 4 to 6 times less than 17b-estradiol
+ Weakly estrogenic, anti-androgenic
* Phthalates
o Potency 6 to 7 times less than 17b-estradiol
+ Weakly estrogenic
Phthalates
Surfactants
Drug Example - DES
Sewage Treatment
Metals
Organotins
EDCs in Cosmetics & Toiletries
Parabens?
Dioxin
Phytoestrogens
Isoflavones
Soy-based specialty formula
Lignans
Precocious Puberty
Fertility in Danger ?
EDCs & People
References
Endocrine Disruption.ppt
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Male sex hormones
Male sex hormones
Presentation lecture by:By C.Adithan
Male sex hormones
Androgens
* Synthesis& secretion
* Regulation
* Pharmacological actions
* Pharmacokinetics
* Preparations
* Therapeutic uses
* Adverse effects
Anabolic steroids
* Differ from androgens?
* Preparations
* Therapeutic uses
* Adverse effects
Anti-androgens
* Danazole
* Cyproterone acetate
* Flutamide
* Finasteride
Androgens
* Includes testosterone, DHT & androstenedione
- Testosterone serves as a prohormone for
o Dihydrotestosterone (DHT)
o Oestradiol
Cholesterol
Pregnenolone
Progesterone
17-α- Hydroxy pregnenolone
17- Hydroxy progesterone
Dehydro-epi androsterone
Andro-stenedione
Oestrone
Oestriol
TESTOSTERONE
OESTRADIOL
Regulation of secretion
* Oestrogen – similar to Testosterone
* Inhibin inhibits FSH secretion at A.P level
Testosterone & DHT
+ growth of genitals in a boy
+ production of sperm
+ growth of facial, pubic & axillary hairs
+ muscular development
+ growth of larynx & voice deepens
+ inhibition of bone growth
+ thickening of skin, loss of s.c. fat
+ behavioral changes in men
+ nitrogen retaining effect
+ erythropoietin secretion increased
+ Increased LDL & decreased HDL
Transdermal patches
Orally active preparations:
* Methyl testosterone tab.
* Fluoxymesterone
* Mesterolone
wall of abdomen/thigh
Implants
Testosterone esters:
* Testo. propionate
* Testo. phenylpropionate
* Testo. cypionate
* Testo. enanthoate
Testosterone aq. suspension
Pharmacokinetics
Clinical uses of testosterone
* Testicular failure: Primary & Secondary
* Chronic illness
* Burns
* Osteoporosis
* Long term corticosteroid therapy
* Pituitary dwarfism
* Carcinoma of breast
* Hereditary angioneurotic oedema
* Anaemia (refractory)
* Menopausal syndrome
Adverse effects of testosterone
* Virilization (female)
* Feminizing side effects (male)
* Precocious puberty & stunted growth
* Cholestatic jaundice
* Enlargement of prostate
* Atherosclerosis
* Hepatic carcinoma
* Oedema
Anabolic steroids
Uses of anabolic steroids
o Osteoporosis
o Catabolic states
o Short stature
o Anaemia (refractory)
o Athletic performance
Anti-androgens
* Danazol
* Cyproterone acetate
* Flutamide
* Finasteride
Side effects:
Dose related
Amenorrhea (High doses)
Androgenic side effects
Uses:
* Endometriosis
* Menorrhagia
* Fibrocystic breast disease
* Hereditary angioneurotic
* Gynecomastia
* Infertility
* FSH & LH release in both sexes
* Binding of steroids to receptors
* Enzymes needed for steroid synthesis
* Weak androgenic, anabolic, progestational & glucocorticoid action
Cyproterone acetate
* Block androgen receptors
* secretion of gonadotropins
Uses:
* Acne
* Male pattern of baldness
* hirusitism
* Ca. of prostate
* Virilizing syndrome
* Precocious puberty
* Inappropriate behaviour
Flutamide
* Non-steroidal anti-inflammatory
* Antagonise androgens:
o Accessory sex organs
o Pituitary
Uses:
* Cancer of prostate along with GnRH agonist
* Female hirusitism
Prostate volume
Symptom score
Peak urine flow rate
DHT level in prostate
Side effects: Loss of libido & impotence in 5 % pts.
Also used for prevention of hair loss
Male sex hormones.ppt
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10 May 2009
Insulin Secretion, Beta Cell Biology
Insulin Secretion, Beta Cell Biology and the Pathogenesis of Type 2 Diabetes
Kenneth S. Polonsky
Presentation by:Professor of Medicine, Cell Biology and Physiology
Director Institute of Clinical and Translational Sciences
Washington University School of Medicine
Diabetes:Basic Abnormalities
Islets of Langerhans
GLUCOSE
Pancreas
Muscle
Liver
Fat
INSULIN
* The pancreas does not produce enough insulin
* Muscle, liver and fat tissues don’t respond to insulin-insulin resistance
* Elevated Fatty Acids impair insulin secretion and action
Normal Glucose Tolerance
Genetic susceptibility
Diabetogenic Lifestyle
Normal Glucose Tolerance
Insulin Resistance
Compensatory hypersecretion of insulin
Impaired Glucose Tolerance
Insulin Resistance
β-cell compensation starts to fail
Overt Hyperglycemia
Insulin Resistance
Failed β-cell compensation
Pancreatic beta-cell dysfunction in overt type 2 diabetes
* Abnormal insulin secretion
o Absent first phase response to intravenous glucose
o Delayed and blunted response to a mixed meal
o Abnormal insulin secretory oscillations
o Increased levels of proinsulin and proinsulin breakdown intermediates
* Reduced beta cell mass
Glucose infusion rate (mg/kg/min)
Resistant
Intravenous Glucose Infusion in Insulin resistant subjects
Insulin Secretion and Glucose
Lean Control
Failure of insulin secretion to respond to glucose oscillations in IGT
Decreased Insulin Content in Type 2 Diabetes
T2DM=Type 2 diabetes.
Decrease in Beta-Cell Volume in Type 2 Diabetes
Obese
Lean
Conclusions
* Progressive abnormalities in insulin secretion are consistently present as people progress from NGT to IGT to Diabetes.
* Increases in glucose concentrations within the normal range are associated with progressive reductions in insulin secretion.
* Insulin resistance is consistently present along with defects in insulin secretion and results cannot resolve which factor is playing a primary role.
Classification Based on Genetic Mechanism and Age of Clinical Presentation
Monogenic
* Neonatal diabetes
* Diabetes in older children and young adults (MODY)
* Mitochondrial diabetes
Polygenic
* Type 2 Diabetes in adults
Genome Wide Association Studies
Recent Smaller Genome Wide Association Studies
Transcription factor in Wnt pathway
Polygenic type 2 diabetes genes
Mechanism-Beta cell
Genes that cause or are associated with diabetes
Overall summary and conclusions
* Genetic variation at multiple loci contribute to overall diabetes risk and to date account for <5% of diabetes genetic risk.
* The genes identified affect insulin secretion predominantly.
* Insulin secretion is abnormal at all stages in the evolution of type 2 diabetes and in genetically predisposed individuals with normal glucose.
* The complexity of these results have raised questions regarding the feasibility of personalized medicine and at this stage it is not clear if genetic testing will add to clinical management of the majority of diabetic patients.
Glucose Metabolism
* Glucokinase
* Hnf1α
Glucokinase
* The enzyme that phosphorylates glucose to glucose-6-phosphate allowing further metabolism in the glycolytic pathway
* Expressed in the pancreatic beta cell and liver
* Based on knowledge of physiology, mutations would be predicted to cause
o hyperglycemia associated with
o reduced glucose induced insulin secretion
o reduced liver glycogen
Relationship between Glucose and Insulin Secretion Rate
Changes in Hepatic Glycogen content after meals
Effects of mutations that activate or impair glucokinase activity
Summary
* Subjects with E23K polymorphisms in Kir6.2 who have normal blood glucose levels have reduced insulin secretion.
* At this stage insulin sensitivity is enhanced when compared to matched controls.
* This could be a compensatory response to reduced insulin secretion or an effect of the polymorphism on insulin action.
Beta cell survival and mass
Observations from islet isolation
Questions
Decrease in Beta-Cell Volume in Type 2 Diabetes1
Insulin Secretion.ppt
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MATURITY-ONSET DIABETES OF THE YOUNG
MATURITY-ONSET DIABETES OF THE YOUNG
Presentation by:Stefan S. Fajans, MD
University of Michigan
Definition
* Type-2 diabetes mellitus in the young plus
* Autosomal dominant inheritance
Current Definition of MODY
* A heterogeneous disorder due to heterozygous monogenic mutations in one of at least 6 different genes
* Onset of diabetes early in life: childhood, adolescence, young adulthood
* Autosomal dominant inheritance
* Primary defect in insulin secretion
Heterozygous Gene Mutations Identified in MODY
Homozygous Mutations of MODY-Related Genes
MODY-Related Proteins
Distinguishing Clinical Characteristics of MODY and Type 2 Diabetes (DM2)
MODY1 (HNF-4a Mutation):
Tested and normal
Type 1 diabetes
PVD-A-G
Multiple offspring
MODY1 (HNF-4a Mutation):
Tested and normal
Type 2 diabetes
Phenotypic Expression and Natural History of MODY
MODY1 (HNF-4a Mutation):
Protocol for the Stepped Glucose Infusion Method to Determine Insulin Secretion Rate
MATURITY-ONSET DIABETES OF THE YOUNG.ppt
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09 May 2009
Management of Pancreatic Cystic Lesions
Evaluation and Management of Pancreatic Cystic Lesions with Endoscopic Ultrasound and Fine Needle Aspiration.
Presentation by:Praveen Sateesh, M.D., M.H.S.A.
Georgetown Internal Medicine,
Differential Diagnosis of Pancreatic Cystic Lesion.
* Congenital cysts
* Acquired cysts
* Extrapancreatic cysts
* Cystic Pancreatic Tumors
* Serous Cystadenoma
* Mucinous Cystic Neoplasm
* Intraductal Papillary Mucinous Neoplasm
Role of EUS
* Identify architecture of cystic lesion
* Ease of FNA
* Determine type of CPT and malignant potential
* Examination of pancreatic ducts and parenchyma
* Guide surgery
Cystic Fluid Analysis
* Cytology
* Tumor markers
* Amylase
EUS FNA characteristics of certain pancreatic cystic lesions
Retrospective Study
* Preoperative diagnosis of pancreatic cystic lesions remains difficult and no established guidelines for evaluation and management of these lesions.
* Identify cases of cystic pancreatic lesions identified by CT or MR undergone EUS FNA with fluid sent for amylase, CEA, and cytology
* Evaluate performance of EUS findings and FNA findings (cytology, amylase, CEA) as compared to surgical pathology and/or clinical follow up (final diagnosis)
* Number of cases
* Differentiating cysts based on size, location, and EUS characteristics
* Obtaining data including amylase, CEA, cytology, surgical pathology, and 6 month clinical follow up after EUS FNA.
Management of Pancreatic Cystic Lesions.ppt
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CT Imaging of Acute Pancreatitis
CT Imaging of Acute Pancreatitis
Presentation by:Erin Rikard
Outline
* Definition
* Epidemiology
* Causal Factors
* Pathophysiology
* CT Evaluation and Findings – Normal and abnormal
* Complications
* Management
* Prognosis
Definition
Acute Pancreatitis - Inflammation of pancreas with potential for complete healing
Epidemiology
Causal Factors
Incidence
Cholelithiasis
Trauma/Surgery
Metabolic Disorders
Viral Infection
Pathophysiology
* Pancreatic autodigestion, with activated pancreatic enzymes escaping the ductal system and lysing tissue of pancreas and adjacent structures
* Lack of capsule facilitates spread
Normal CT Findings
Normal Anatomy by CT
* Pancreas arcing anteriorly over spine
* Head adjacent to duodenum
* Tail extending toward spleen
* Splenic vein posterior to body and tail
* Portal vein confluence immediately posterior & left of pancreatic neck
Normal Morphology by CT
Evaluation by CT
Evaluation of Acute Pancreatitis
* Contrast-enhanced CT is imaging modality of choice
* Oral and IV contrast differentiate pancreatic tissue from adjacent blood vessels and duodenum
Recommendations for Contrast-Enhanced CT
* Clinical diagnosis in doubt
* Severe clinical pancreatitis
* Ranson score > 3
* APACHE score > 8
* Failure to rapidly improve within 72 hours of beginning conservative medical therapy
* Initial improvement with later deterioration
Ranson Criteria
Abnormal CT Findings
* Peripancreatic inflammation
* Diffuse or focal pancreatic edema
* Poor definition and heterogeneity of gland
* Fluid collections
* Necrosis
* Thickening of pararenal fascia
Spectrum of Disease
* Mild Cases
* Severe Cases
Peripancreatic Inflammation/ Pancreatic Edema/Fluid Collections
Infection?
Necrosis
Complications
* Pancreatic Pseudocysts
* Abscess
* Hemorrhagic Pancreatitis
* Splenic Artery Pseudoaneurysm formation or rupture/ Splenic Venous Thrombosis
Pancreatic Pseudocyst
* Fluid collection surrounded by fibrous capsule but not lined by epithelium
* Occurs in 10% of cases
* Significant % will not resolve spontaneously
* Seen within pancreas and potential spaces with which gland is continuous (lesser sac and left pararenal space)
Abscess
Hemorrhagic Pancreatitis
Splenic Artery Pseudoaneurysm
Management
Prognosis
Reasons for Reduced Mortality
Resources
CT Imaging of Acute Pancreatitis.ppt
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Recurrent Idiopathic Pancreatitis
Recurrent Idiopathic Pancreatitis
Presentation lecture by:Rebecca Byers, MD
Primary Care Conference
Objectives
* Review the common clinical presentation of chronic pancreatitis.
* Describe the natural course of chronic pancreatitis.
* Discuss the various types of cystic lesions in the pancreas.
* Describe the diagnostic and treatment recommendations
* Disclaimer - I have not received any outside funding in regards to this presentation.
Clinical Cases
Hospitalization
* Stopped Lasix, Lisinopril, Cozaar.
* Renal arteriogram – normal.
* Echo – normal.
* +H. pylori – treated with 2 weeks Biaxin, Flagyl, Prevacid.
* Discharged on Amlodipine and Atenolol.
* BPs never high since.
GI Clinic Follow-up
* Diagnosis of Recurrent Idiopathic Pancreatitis and a mature pancreatic pseudocyst.
* Need to assess for structural abnormality
* Plan for repeat CT in 6 weeks and ERCP and/or endoscopic ultrasound.
* 8/4/03 – Abd CT without change. 4 non-specific pulm nodules, 6-7 mm. Endless f/u.
Surgical Consult
* Diagnosis of acute relapsing pancreatitis.
* Recommendation for resective drainage operation and definitive treatment.
ERPC
* Impression: (1)Recurrent pancreatitis (2) Improved pancreatogram with diffuse pancreatic ductal irregularities less prominent on this exam (3) No definite pancreatic duct stricture(s) visualized (4) s/p 5 mm pancreatic sphincterotomy with prompt drainage of contrast.
Endoscopic Ultrasound
* Impression: 1) Pancreatic tail solid-cystic lesion 2) FNA consistent with a mucinous neoplasm.
* FNA Report - Cytologic Exam: Positive, compatible with a mucinous neoplasm.
Surgery
* Surg Path Report – Predominantly intracystic mucinous adenocarcinoma, with focal infiltrating adenocarcinoma, in a background of chronic pancreatitis.
* Surgical margins were negative for carcinoma.
* Ten out of ten resected lymph nodes were negative for carcinoma. Adrenal gland and spleen also negative for carcinoma.
Surgical Follow-up
* Dilemma – If there was no invasive cancer, her treatment would now be complete; the finding of invasive cancer, along with some previously elevated tumor makers and pulmonary nodules, are concerning.
* Plan – redo all scans and serum markers, discuss at hepatobiliary conference, refer to medical oncologists.
Chronic Pancreatitis
* Chronic pancreatitis is an inflammatory condition that results in permanent structural changes in the pancreas which lead to impairment of exocrine and endocrine function.
* Can be asymptomatic over long periods of time, or can present as recurrent postprandial epigastric pain.
Clinical Features
* The two primary clinical manifestations are abdominal pain and pancreatic insufficiency.
* Pain is typically epigastric, often radiates to the back, often worse 15 to 30 minutes after eating, as the condition progresses, the pain tends to become more continuous.
* Problems digesting food/absorption, fat malabsorption, glucose intolerance/diabetes.
Etiology 1
Etiology 2
Pathogenesis
Diagnosis 1
Diagnosis 2
Complications
* Pseudocysts (10% of patients)
* Mechanical obstruction of the duodenum and common bile duct
* Pancreatic ascites
* Pleural effusion
* Splenic vein thrombosis with portal hypertension
* Pseudoaneurysm formation (e.g., splenic artery)
Cystic Lesions of the Pancreas
* Retention cysts
* Pseudocysts
* Cystic neoplasms.
Pseudocysts
* Result of pancreatic inflammation and necrosis.
* Single or multiple, small or large, located either in or outside of the pancreas.
* Most communicate with pancreatic ductal system, high concentrations of enzymes.
* Walls formed by adjacent structures; fibrous lining; lack an epithelial lining seen in true cystic lesions.
Cystic Neoplasms
* Mucinous cystadenoma/cystadenocarcinoma
* Mucinous duct ectasia (intraductal papillary mucinous neopplasm)
* Serous cystadenoma
* Papillary cystic neoplasm
Mucinous cystadenoma
* Most common cystic neoplasm.
* Typically in middle-aged women.
* Usually a mass lesion composed of one or more macrocystic spaces lined by mucous-secreting cells.
* Most are malignant at time of diagnosis. High potential for malignant change.
Management
Uncertain Etiology
References
Recurrent Idiopathic Pancreatitis.ppt
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Pancreatitis
Pancreatitis
Presentation lecture by:Brad Brough, DO
Acute pancreatitis
* Pathophys- insult leads to leakage of pancreatic enzymes into pancreatic and peripancreatic tissue leading to acute inflammatory reaction
* Etiologies
o Idiopathic
o Gallstones (or other obstructive lesions)
o EtOH
o Trauma
o Steroids
o Mumps (& other viruses: CMV, EBV)
o Autoimmune (SLE, polyarteritis nodosa)
o Scorpion sting
o Hyper Ca, TG
o ERCP (5-10% of pts undergoing procedure)
o Drugs (thiazides, sulfonamides, ACE-I, NSAIDS, azathioprine)
“Less Common” causes
* Pancreas divisum
* Chinese liver fluke
* Ischemia (bypass surgery)
* Cystic fibrosis
Trivia
Signs & Symptoms
* Grey Turner sign
* Cullen’s sign
Differential
* Not all inclusive, but may include:
o Biliary disease
o Intestinal obstruction
o Mesenteric Ischemia
o MI (inferior)
o AAA
o Distal aortic dissection
o PUD
Evaluation
* amylase…Nonspecific
* lipase
* Other inflammatory markers will be elevated
* Depending on severity may see:
Radiographic Evaluation
* AXR - “sentinel loop” or small bowel ileus
* US or CT may show enlarged pancreas with stranding, abscess, fluid collections, hemorrhage, necrosis or pseudocyst
* MRI/MRCP newest “fad”
o Decreased nephrotoxicity from gadolinium
o Better visualization of fluid collections
o MRCP allows visualization of bile ducts for stones
# Does not allow stone extraction or stent insertion
* Endoscopic US (even newer but used less)
o Useful in obese patients
CT Scan of acute pancreatitis
Gall stone pancreatitis by ERCP
Prognosis
Ranson Criteria
CT Severity Index
* CT Grade
* Necrosis score)
* TOTAL SCORE
Therapy
Complications
Prognosis
Chronic pancreatitis
* Pathophys - irreversible parenchymal destruction leading to pancreatic dysfunction
* Persistent, recurrent episodes of severe pain
* Anorexia, nausea
* Constipation, flatulence
* Steatorrhea
* Diabetes
Evaluation
CT - chronic pancreatitis
Complications
Conclusion
References
Pancreatitis.ppt
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05 May 2009
Treatment for Chronic Hepatitis B
Treatment for Chronic Hepatitis B
Screening for Hepatocellular Carcinoma
Presentation by:Mindie H. Nguyen, MD, MAS
Assistant Professor of Medicine
Division of Gastroenterology & Hepatology
Stanford University Medical Center
Chronic Hepatitis B
HBV Disease Burden in Asian-Americans
Hepatitis B Prevalence
Etiology of HCC in Asians
Impact of HBV DNA and ALT Levels on Disease Outcomes
Disease Progression and HCC Risk
Impact of Viral Load
* High viral load:
* Reduction in viral load:
HBV DNA Associated with Increased Risk of HCC
HBV DNA levels and Risk of Cirrhosis and HCC REVEAL-HBV Study
HBV DNA Levels Predict Risk of Developing Cirrhosis
Viral Load Is the Main Predictor of Cirrhosis Regardless of Serum ALT
HBV DNA Levels Predict Risk of Developing HCC
Dose-Response Relationship:
HBV DNA and HCC
HBV DNA Levels are Associated With Clinical Outcomes (HCC)
REVEAL-HBV Study: Cirrhosis Analysis Conclusions
REVEAL-HBV Study: HCC Analysis Conclusions
Impact of Treatment on Disease Progression
Primary Goal of Treatment
Rapid and sustained suppression of HBV to the lowest possible level1,2 Outcomes
Rapid and Profound HBV Suppression: an Important Therapeutic Goal
Lamivudine and Disease Progression and HCC incidence in Advanced HBV (stage III/IV)
HBV DNA Suppression Reduces Cirrhosis Progression
Lamivudine
Placebo
Diagnosis of HCC
HBV DNA Suppression Reduces HCC Incidence Rate
Conclusions
Summary
* HBV DNA is an essential marker for predicting risk for complications
* Viral suppression is associated with improved treatment outcomes in patients with advanced fibrosis.
* Emerging potent antiviral therapies provide the potential for more effective treatment response and prevention of complications of CHB
Screening for Hepatocellular Carcinoma
Screening for HCC Consensus Recommendations
HCC: Screening Tests
Changes in sensitivity and specificity of AFP for diagnosis of HCC using various cut-offs
WHO Principles of Screening
Screening improves survival
HCC Screening: clinical studies
Pseudo-Disease
RCT for HCC Screening
Cost-Effectiveness of Screening: Other Cancers
Cost-Effectiveness of HCC Screening
Real-life studies with cost information:
Screening for HCC: Summary
Treatment for Chronic Hepatitis B.ppt
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03 May 2009
Hypothyroidism Fetal Brain Development
Hypothyroidism Fetal Brain Development
Thyroid Hormone Action
T4 has the highest levels in the body
T3 has the highest affinity for thyroid receptors
T4 can be metabolized into T3
Thyroid receptor sits on promotor in absence of ligand (corepressor complex)
Ligand binding causes recruitment of the coactivator complex and gene transcription
Hypothyroidism and Development
* Fetal and neonatal hypothyroidism has been correlated with neurological deficits
o Severity of deficits are related to severity of hypothyroidism
o Females may be more sensitive to TH and hypothyroidism than males (shown via gene array data, animal models)
* Studies show that TH has different actions in the brain at different developmental times
o Majority of specific neurodevelopmental events affected by TH are poorly understood
Timing of TH Action
* Fetal thyroid gland is not functional until 12th week of gestation
o Fetus dependent entirely on maternal source of thyroid hormone (1st trimester)
o Reduced maternal supply of TH can occur by maternal hypothyroidism or premature birth
* Fetal thyroid gland increases its role in development during gestation
o TH insufficiency late in development by decreased fetal TH production is referred to as congenital hypothyroidism
Maternal Hypothyroidism
* Nearly 3% of pregnant women have low-normal circulating T4
o Most low-normal hypothyroidism is undiagnosed and/or untreated
o Fetuses exposed to thyroid hormone insufficiency as mother does not produce enough T4 for both her and her fetus
o Severity of fetal thyroid hormone insufficiency is dependent on severity of maternal hypothyroidism
* Offspring are often found to have reduced perceptual and motor abilities, short attention spans, developmental delays, variable reaction times to visual stimuli
* Effect of low TH at specific times results in different developmental deficits
o Before 16 weeks: visual attention abilities
o After 16 weeks: fine and graphomotor skills, reading abilities
Premature Birth
* Premature birth causes a loss of TH from maternal sources before fetal gland is operational
o Provide another model of fetal TH insufficiency
o Low-risk premies (50%) show reduced visuospatial and fine motor skills, selective attention and memory abilities, and reduced math competency
Congenital Hypothyroidism
* Takes place later in development than maternal hypothyroidism or premature birth hypothyroidism
o Children exhibit IQ levels 6 points below expectation as well as visuospatial, motor, language, memory and attention deficits
o Newborn screening for congenital hypothyroidism has allowed treatment, reducing severity of deficits
Hypothyroidism and Development
Experimental Evidence
* Hypothyroid rat dams during pregnancy and the effects on their offspring
o General effects
o Effects on oligodendrocytes
o Changes in phosphorylation of protein kinases
o Effects on HDACs, gene repression
Hypothyroidism
* Female rats made hypothyroid (Tx) prior to mating; offspring were cross-fostered to non-hypothyroid dams at birth
o On PND 80:
+ Offspring exhibited learning deficits (via maze learning), “hyperactivity” (increased open-field exploration), less cautious during emotionality testing
+ Gender difference on learning
# Females more sensitive to TH insufficiency than males in terms of learning
Oligodendrocyte Accumulation
* Hypothyroidal animals demonstrate:
o Decreased number of myelinated axons in commissures
o HOWEVER, no difference in the total number of axons; suggests hypothyroidism interferes with myelination of the axons
o Decreased thickness of myelin sheath surrounding those axons that are myelinated
Oligodendrocyte Accumulation
* TH Actions on oligodendrocytes:
o Initiation of oligodendrocyte maturation
+ In absence of TH, precursor O-2A cells proliferate indefinitely; in presence of TH, O-2A cells terminate cell division, mature
o Enhance oligodendrocyte survival
+ Protection from apoptosis (shown in vitro)
o Regulate myelin production in developing oligodendrocyte via MBP (myelin basic protein)
+ MBP levels are reduced in hypothyroid states
Oligodendrocyte Accumulation
* Cortical areas of mammalian brain hemispheres are reciprocally connected via intrahemispheric commissures
o Critical for information transfer in higher brain function
o Arise embryonically in rat and develop post-natally
o TH is required for normal commissure development
Oligodendrocyte Accumulation
* MBP levels are reduced in hypothyroid animals compared to control
* T3 treatment showed no effect on MBP mRNA levels
* Anterior commisure (AC) is reduced in hypothyroid state
* Reduction of cell number
* Similar in Corpus collosum (CC)
Phosphorylation of ERK in Hippocampus
* Congenital hypothyroidism
* Shown previously that ERK phosphorylation and LTP were decreased in the hippocampus of Tx adult rats
o Hypothyroidal neonatal rats were analyzed for ERK phosphorylation in the hippocampus
* Hypothyroidism increased pERK1/2
* Hypothyroidism decreased p38/MAPK
* Changes occurred in the absence of a change in the phosphorylation state of JNK
Phosphorylation of ERK in Hippocampus
* Changes in phosphorylation of ERK and p38 in hypothyroidism may mediate changes in the hippocampus common to hypothyroidism such as:
o synaptic transmission
o migration of dentate granule cells
o decreases in cell number
o Reduction of dendritic arbors of dendrites and pyramidal cells
TH and Hairless
* Hairless (hr) is a direct target of TH in the developing brain
o Originally identified in mice with congenital hair loss
o Analogous phenotype in humans
o Hr mutant mice show altered neuronal morphology, inner ear defects, abnormal retinal cytoarchitecture
o Hr (protein) interacts with unliganded TR to enhance transcriptional repression
+ Binds to TR via two independent domains and has multiple repression domains
+ Known to associate with histone deacetylases (HDACs), suggesting hr and TR form repression complex with HDAC
TH and Hairless
* Hr is able to be co-immunoprecipitated by TR
* Hr co-immunoprecipitates with HDACs
* Hr expression is controlled by TRα
TH and Hairless
* In situ hybridization demonstrates hr and hdac expression overlaps in neonatal rat brain cerebellum forebrain
TH and Hairless
* Expression of hr is regulated during development by TH
* Expression occurs rapidly following treatment with TH
Why do we care?
* PCBs in environment
o Polychlorinated biphenyls bioaccumulate through the food chain and are found in high concentrations in samples of human tissues
o Children exposed to PCBs in utero exhibit neuropsychological deficits such as a lower full-scale IQ, reduced visual recognition memory, attention deficits, and motor deficits
o Developmental deficits overlap with those following developmental TH insufficiency
Activation of HES
* Maternal thyroid status affects the expression of HES1 and HES5 (TH-responsive genes; bHLH regulated by Notch receptor)
o Inhibits neurogenesis while favoring gliogenesis
o Therefore, TH may have role in fate specification of cells in early cortex by enhancing HES activation
o PCBs mimic affects of elevated T4 on HES1/5
o Possible that PCB exposure exerts effects on brain development by interfering with TH action
+ dysregulation of HES expression may be a mediating factor of PCB exposure
ADHD and Hypothyroidism
* Children born to mothers from iodine-deficient area have a higher incidence of ADHD
o Syndrome previously reported to be associated with resistance to TH by receptor mutations
* Study performed in Northeastern Sicily to identify long-term effects of maternal hypothyroxinemia
o Two groups (one normal iodine intake (11#), one low iodine intake (16#)); age-matched mothers and their children
o TSH levels remained normal in mothers, while all 11 identified ADHD children were born to mothers in iodine deficient area
Summary
* TH is required for a number of neuropsychological abilities
o Type of deficit dependent on timing of TH deficiency
* General:
o Prenatal TH loss
+ Visual processing
+ Motor and visuomotor abilities
o Early Neonatal TH loss
+ visuospatial
o Late Neonatal TH loss
+ Sensorimotor
+ Language
o Late Late TH loss
+ Language
+ Fine motor skills
+ Auditory processing
+ Attention
+ Memory skills
What’s Next?
* Though the morphological changes due to hypothyroidism in fetal brain development are well-described, underlying molecular mechanisms have yet to be fully understood
* Potential sex differences in TH action in developing brain may provide insight into some of the mechanisms
* Determine better ways to identify and treat fetal hypothyroidism
* Maternal treatment with either T4 or PCB results in an increase in HES (via in situ hybridization)
Hypothyroidism
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Thyroid Lecture
THYROID PHYSIOLOGY
Presentation lecture by:Jack L. Leonard, Ph.D.
umassmed.edu
THE THYROID GLAND
THYROID GLAND HISTOLOGY
THYROID FOLLICULAR
CELL MORPHOLOGY
THYROID HORMONES
FEEDBACK REGULATION
THE HYPOTHALAMIC-PITUITARY-THYROID AXIS
Hormones derived from the pituitary that regulate the synthesis and/or secretion of other hormones are known as trophic hormones.
Key players for the thyroid include:
TRH - Thyrophin Releasing Hormone
TSH - Thyroid Stimulating Hormone
T4/T3 - Thyroid hormones
PITUITARY-THYROID AXIS
PITUITARY-THYROTROPE CELL
* TSH binds to specific cell surface receptors that stimulate adenylate cyclase to produce cAMP.
* TSH increases metabolic activity that is required to synthesize Thyroglobulin (Tg) and generate peroxide.
* TSH stimulates both I- uptake and iodination of tyrosine resides on Tg.
TSH REGULATION OF THYROID FUNCTION
ION TRANSPORT BY THE THYROID FOLLICULAR CELL
THYROID HORMONE SECRETION BY THE THYROID FOLLICULAR CELL
THYROID HORMONES IN THE BLOOD
THYROID HORMONE METABOLISM
THYROID HORMONE DEIODINASES
* Three deiodinases (D1, D2 & D3) catalyze the generation and/disposal of bioactive thyroid hormone.
* D1 & D2 “bioactivate” thyroid hormone by removing a single “outer-ring” iodine atom.
* D3 “inactivates” thyroid hormone by removing a single “inner-ring”iodine atom.
* All family members contain the novel amino acid selenocysteine (SeC) in their catalytic center.
BASIC ORGANIZATION OF THE SELENODEIODINASES
BASICS OF THYROID HORMONE ACTION IN THE CELL
STEROID/THYROID HORMONE FAMILY OF NUCLEAR RECEPTORS
SPECIFIC ACTIONS OF THYROID HORMONE: METABOLIC
* Regulates of Basal Metabolic Rate (BMR).
* Increases oxygen consumption in most target tissues.
* Permissive actions: TH increases sensitivity of target tissues to catecholamines, thereby elevating lipolysis, glycogenolysis, and gluconeogenesis.
* TH is critical for normal development of the skeletal system and musculature.
* TH is also essential for normal brain development and regulates synaptogenesis, neuronal integration, myelination and cell migration.
* Cretinism is the term for the constellation of defects resulting from untreated neonatal hypothyroidism.
SPECIFIC ACTIONS OF THYROID HORMONE: DEVELOPMENT
EXAMPLES OF THYROID DISEASES
www.hsc.missouri.edu/~daveg/thyroid/thy_dis.html
Congenital Hypothyroidism
Juvenile Hypothyroidism
THYROID Lecture.ppt
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Elevated or Depressed Hormone Levels
Alterations of Hormonal Regulation
Elevated or Depressed Hormone Levels
Presentation by:Dr. Barry Goldberg
Associate Professor of Biology
Felician College
* Failure of feedback systems
* Dysfunction of an endocrine gland
* Secretory cells are unable to produce, obtain, or convert hormone precursors
* The endocrine gland synthesizes or releases excessive amounts of hormone
Elevated or Depressed Hormone Levels
* Increased hormone degradation or inactivation
* Ectopic hormone release
Target Cell Failure
* Cell surface receptor-associated disorders
o Decrease in number of receptors
o Impaired receptor function
o Presence of antibodies against specific receptors
o Antibodies that mimic hormone action
o Unusual expression of receptor function
* Intracellular disorders
* Circulating inhibitors
Hormone Delivery
Alterations of the Hypothalamic-Pituitary System
Diseases of the Posterior Pituitary
* Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
o Hypersecretion of ADH
o For diagnosis, normal adrenal and thyroid function must exist
o Clinical manifestations are related to enhanced renal water retention, hyponatremia, and hypo-osmolality
Diseases of the Posterior Pituitary
* Diabetes insipidus
o Insufficiency of ADH
o Polyuria and polydipsia
o Partial or total inability to concentrate the urine
o Neurogenic
+ Insufficient amounts of ADH
o Nephrogenic
+ Inadequate response to ADH
o Psychogenic
Diseases of the Anterior Pituitary
* Hypopituitarism
o Pituitary infarction
+ Sheehan syndrome
+ Hemorrhage
+ Shock
o Others: head trauma, infections, and tumors
Diseases of the Anterior Pituitary
* Hypopituitarism
o Panhypopituitarism
+ ACTH deficiency
+ TSH deficiency
+ FSH and LH deficiency
+ GH deficiency
o Commonly caused by a benign slow-growing pituitary adenoma
o Manifestations
+ Headache and fatigue
+ Visual changes
+ Hyposecretion of neighboring anterior pituitary hormones
* Hypersecretion of growth hormone (GH)
o Acromegaly
+ Hypersecretion of GH during adulthood
o Gigantism
+ Hypersecretion of GH in children and adolescents
* Hypersecretion of growth hormone (GH)
* Hypersecretion of prolactin
o Caused by prolactinomas
+ In females, increased levels of prolactin cause amenorrhea, galactorrhea, hirsutism, and osteopenia
+ In males, increased levels of prolactin cause hypogonadism, erectile dysfunction, impaired libido, oligospermia, and diminished ejaculate volume
Alterations of Thyroid Function
* Hyperthyroidism
o Thyrotoxicosis
o Graves disease
+ Pretibial myxedema
o Hyperthyroidism resulting from nodular thyroid disease
+ Goiter
o Thyrotoxic crisis
* Hyperthyroidism
Thyrotoxicosis (Graves Disease)
Alterations of Thyroid Function
* Hypothyroidism
o Primary hypothyroidism
+ Subacute thyroiditis
+ Autoimmune thyroiditis (Hashimoto disease)
+ Painless thyroiditis
+ Postpartum thyroiditis
+ Myxedema coma
o Congenital hypothyroidism
o Thyroid carcinoma
Hypothyroidism
Alterations of Parathyroid Function
* Hyperparathyroidism
o Primary hyperparathyroidism
+ Excess secretion of PTH from one or more parathyroid glands
o Secondary hyperparathyroidism
+ Increase in PTH secondary to a chronic disease
o Abnormally low PTH levels
o Usually caused by parathyroid damage in thyroid surgery
Type 1 Diabetes Mellitus
* Demonstrates pancreatic atrophy and specific loss of beta cells
* Macrophages, T- and B-lymphocytes, and natural killer cells are present
* Two types
o Immune
o Nonimmune
* Genetic susceptibility
* Environmental factors
* Immunologically mediated destruction of beta cells
* Manifestations
o Hyperglycemia, polydipsia, polyuria, polyphagia, weight loss, and fatigue
Dysfunction of the Pancreas
* Type 2 diabetes mellitus
o Maturity-onset diabetes of youth (MODY)
o Gestational diabetes mellitus (GDM)
o Common form of diabetes mellitus type 2
+ Insulin resistance
Acute Complications of Diabetes Mellitus
* Hypoglycemia
* Diabetic ketoacidosis
* Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS)
* Somogyi effect
* Dawn phenomenon
Diabetic Ketoacidosis
Chronic Complications of Diabetes Mellitus
* Hyperglycemia and nonenzymatic glycosylation
* Hyperglycemia and the polyol pathway
o Protein kinase C
* Microvascular disease
o Retinopathy
o Diabetic nephropathy
* Macrovascular disease
o Coronary artery disease
o Stroke
o Peripheral arterial disease
* Diabetic neuropathies
* Infection
Alterations of Adrenal Function
* Disorders of the adrenal cortex
o Cushing disease
+ Excessive anterior pituitary secretion of ACTH
o Cushing syndrome
+ Excessive level of cortisol, regardless of cause
Cushing Disease
* Disorders of the adrenal cortex
o Hyperaldosteronism
+ Primary hyperaldosteronism (Conn disease)
+ Secondary hyperaldosteronism
* Disorders of the adrenal cortex
o Adrenocortical hypofunction
+ Primary adrenal insufficiency (Addison disease)
# Idiopathic Addison disease
+ Secondary hypocortisolism
* Disorders of the adrenal cortex
o Hypersecretion of adrenal androgens and estrogens
+ Feminization
+ Virilization
Virilization
* Disorders of the adrenal medulla
o Adrenal medulla hyperfunction
+ Caused by tumors derived from the chromaffin cells of the adrenal medulla
# Pheochromocytomas
+ Secrete catecholamines on a continuous or episodic basis
Elevated or Depressed Hormone Levels.ppt
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Endocrine and Metabolic Disorders
Endocrine and Metabolic Disorders
Presentation Lecture by Jennifer Coleman, Assistant Professor of Nursing
Arkansas Tech University
Background review
* Endocrine glands
o Hypothalamus (brain)
o Pituitary gland (brain)
o Thyroid gland (neck)
o Parathyroid glands (thyroid)
o Adrenal glands (top of kidney)
o Ovaries and testes (reproductive)
o Islets of Langerhans (pancreas)
Hormone functions
* Fetal differentiation of reproductive and CNS
* Growth and development including puberty
* Maintaining homeostasis
* Maintaining optimal levels of hormones
Hypopituitarism (Growth Hormone Deficiency)
* Decreased activity of pituitary gland
* Nl birth wt and length – by 12 months often at or below the 3rd %
* S/Sx
o Hypoglycemic seizures, neonatal jaundice, micropenis, undescended testicles
o Older-overweight, youthful facial features, high pitched voices, delayed dentition, skeletal & sexual maturation, hypoglycemia
Diagnosis and Treatment
* Lab
o IGF (insulin like growth factor)
o Radiographic view of pituitary gland
o Meds given to stimulate GH release
* Treatment
o GH replacement
o Follow-up and monitoring growth
o Educate to treat child by age, not by size
Hyperpituitarism
* Excessive GH secretion, very rare in children
* Pituitary adenoma, Hypothalamus tumor
* Before growth plates fuse – 7-8 feet tall
* After growth plates fuse – overgrowth of facial structure
* Treatment-surgery, radiation, PO meds
Diabetes Insipidus
* Inability to concentrate urine
o Neurogenic (pituitary gland disruption)
o Nephrogenic (insensitive renal tubules to ADH)
* Deficiency in ADH (Vasopressin)-posterior pituitary gland
* Associated with: head injuries, infections, hypopituitarism, familial, tumors, surgery, CVA
* S/S: (abrupt onset) Polyuria, polydipsia, nocturia, enuresis, dehydration, constipation, fever
* Serum sodium concentration increases (hypernatremia)
* Plasma AVP (arginine vasopressin) level is decreased
* Specific gravity <1.010
* U/O > intake (fluid volume deficit)
* Treatment – correct the cause
o IV hypertonic soln, restrict PO fluids
o IV hypertonic soln, inc PO fluids, Desmopressin acetate (DDAVP) IM injections
Negative Feedback – Thyroid
Congenital Hypothyroidism
What you should know:
* Management:
o Early diagnosis and treatment-mental retardation is severe and permanent without treatment
o PO Levothyroxine (Synthroid)
o (Pediatric) Endocrine specialist
o Life long treatment
o Monitor growth and development (mental and physical)
Acquired Hypothyroidism Etiology
* Acquired
* Autoimmune thyroiditis (Hashimoto’s)
* Iodine deficiency
* Radiation/surgery to thyroid
* Drug/substance exposure-lithium
Acquired Hypothyroidism
* Increased risk with family history
* Goiter usually present
* Adverse effects after age 2-3 are reversible with treatment
* Almost 30% Hashimoto’s spontaneously recover (remission)
* S/Sx-
Management
* Elevated TSH & decreased T4
* Treatment: PO Levothyroxine
* Treat the disease not the symptoms
* TSH check at least yearly
* Drug therapy is lifelong
* Reassure and educate parents
Hyperthyroidism
* Thyroid hormone level increased (thyrotoxicosis – inc BMR) high T4 & T3, low TSH
* Graves’ disease most common
o Preschool to teen-highly familial, F>M
o Autoimmune-immunoglobulins stimulate thyroid
o Thyroid hormone-producing tumors (thyroid or pituitary)
o Congenital-prenatally, mother has Graves’
Signs and Symptoms
* Goiter
* Exophthalmos (bulging eyes)
* Tachycardia, sweating, tremors, warm skin
* Nervousness, irritability, mood swings
* Decreasing school performance-decreased concentration
* Increased appetite with weight loss
* Heat intolerance, muscle weakness
* Fine hair, hyperreflexia
* Easily fatigued, unable to sleep
Thyroid - Goiter
Treatment
* Lab-
o TSH, T3, T4
o Thyroid scan
* Drug therapy (side-effects problems)
* Radiation
* Thyroidectomy
* Often not a lifelong disease – tx continued for 6mo-2yrs then individualized to patient
Nursing Management
* Support and educate parents and child
* Caloric intake
* Scheduled rest periods
* Cool, quiet environment – few clothes (layers)
* Medication side effects
* Thyroid storm (surge of thyroid hormone is release) - life threatening
Disorders of the Adrenal Gland
* Cushing's Syndrome
o Glucocorticoid (cortisol) hormone excess
* Congenital Adrenal Hyperplasia (CAH)
o Deficiency of cortisol
* Adrenal Insufficiency
o Acute Adrenocortical Insufficiency
o Chronic Adrenocortical Insufficiency (Addison’s disease)
+ Adrenal gland destruction
Adrenal Gland
* Adrenal cortex
o Glucocorticoids
+ hydrocortisone
+ cortisone
o Mineralocorticoids
+ aldosterone
o Sex steroids
+ androgens
+ estrogens
+ progestins
* Adrenal medulla
o Catecholamines
+ epinephrine
+ norepinephrine
Adrenal Pathway
Anterior
pituitary
ACTH
Adrenal cortex
Cortisol
ACTH: Adrenocorticotropic hormone
*Negative feedback loop
Inhibition
Cushing’s Syndrome
* Adrenocortical hyperfunction
o Excess glucocorticoids (especially cortisol) or ACTH
o Rare in children (mostly F 30-50 yo)
* Etiology
o Primary – Malignant adrenal tumor
o Secondary – Pituitary adenoma (>8yo)
+ adrenocorticotropic hormone (ACTH)
+ Ectopic (nonpituitary) ACTH-secreting tumor
o Iatrogenic – excessive/prolonged steroid therapy (most common cause)
Cushing’s S/Sx
* Alters metabolism: Catabolism of protein, dec. absorption of Ca, inc. appetite, salt-retaining
o Poor wound healing, easily bruised, muscle wasting, demineralization of bone, osteoporosis, fat accumulation (protruding abdomen, “buffalo hump”, “moon face”), striae, edema, HTN, fatigue, hirsutism, acne, impaired glucose tolerance, mood swings, oligomenorrhea/amenorrhea
* Cushingoid appearance reversible with treatment
Cushing’s treatment
* Surgical removal of tumor
o cortisol replacement is then required
o malignant adrenal tumor prognosis is poor
o pituitary tumor cure rate ~25%
* Irradiation
* Pharmacologic
o block steroid synthesis, mainly used with ectopic tumors that can not be resected
* Tapered withdraw of pharmacologically prescribed glucocorticoids
Congenital Adrenal Hyperplasia (CAH)
* Form 1: salt-losing
* Form 2: non-salt-losing (simple virilization)
CAH
* Form 1: salt-losing
o Blockage of cortisol & aldosterone production-excessive salt & fluid excretion
o Adrenal crisis (may be life threatening) recurrent emesis, dehydration, metabolic acidosis, hypotension, hypoglycemia, circulatory collapse
* Form 2: non-salt-losing (simple virilization)
o Overproduce androgen
o Females: Ambiguous genitalia-enlarged clitoris, fused labia, urogenital sinus
o Males: Precocious genital development
* Precocious puberty, tall stature early then short d/t premature epiphyseal closure
CAH Treatment
* PO hydrocotisone (corticosteroid) to suppress ACTH
o given early enough will reverse physical symptoms
o inc. dose required with acute illness, injury, surgery
* Salt-losing:
o aldosterone
o supplementary dietary salt
Acute Adrenal Insufficiency
* Adrenocortical insufficiency (Acute)
* Etiology
o Primary
Addison’s disease (chronic)
Infection/trauma to adrenal gland: TB, AIDS, fulminating infections (meningococcemia, fungal)
o Secondary
Pituitary tumors, surgery, radiation
Exogenous steroids stopped abruptly
Diagnosis
o Based on clinical symptoms
o Confirm: improvement with cortisol therapy
Acute Adrenocortical Insufficiency Clinical Manifestations & Treatment
* Symptoms acute and sudden
* BP drops, minimal pulse, elev temp, severe dehydration & hypoglycemia, seizures, death
* Cortisol replacement
* IV fluids and glucose
* Antibiotic tx for specific infection
* Blood transfusion (hemorrhagic)
Diabetes mellitus (Type I)
* Most common endocrine disorder in childhood
* 1:1500 under 5 yrs
* 1:600 school-aged children
* 1:350 by 16 yrs
* 80 – 95% of children first diagnosed with diabetes have Type I
DMI-Etiology
* Autoimmune disease in which islet cell antibodies lead to the destruction of the pancreatic beta cells (in islets of Langerhans) and eventually to a relative lack of insulin (>90% beta cells are destroyed)
* Disorder of carbohydrate metabolism resulting from the decrease in insulin production
DMI-Etiology
* Influenced by 3 major factors
o Genetic susceptibility to develop - chromosome 6
o Environment - viruses or chemicals in diet may damage beta cells
o Immunologic processes - Increase of circulating antibodies in pancreatic islet cells (inflammatory process) As the beta cells are destroyed, antibodies will decrease
DM-I Onset
* Relatively acute with rapid progression and deterioration of the child
* “Poly-triad”
o Polyuria
o Polydipsia
o Polyphagia
Hyperglycemia
* Poor control/unknown disease
* Symptoms:
o lethargic, sleepy, slowed responses, confusion
o tachypnea, hungry, dehydrated
o weak pulse, flushed, dry skin, thirsty, HA
o abdominal pain, N/V, blurred vision, shock
Hyperglycemia management
* Good insulin control
o Frequent monitoring
o Correct dosing
o Refrigerated, non-expired insulin
o Appropriate diet
o Regular exercise
Ketoacidosis (Metabolic acidosis)
* Etiology
o Glucose unavailable for metabolism-fats used for energy
o Glycerol from fat cells converted by liver to ketone bodies
* Symptoms
o Tachypnea/Kussmaul (deep & rapid) respirations (d/t inc. CO2)
o Dehydration, flushed ears and cheeks
o Sweet “fruity-like” (acetone) breath
o Decreased bowel sounds, abdominal tenderness
o Weight loss, nausea and vomiting, dec. LOC
DKA continued
* Serum glucose – >300 mg/dL
* Serum ketones present
* Acidosis (pH * Glycosuria, ketonuria
* Electrolyte disorder
* Coma: serum osmolality > 350mOsm/kg
o potential for cerebral edema-life threatening
Hypoglycemia
* Causes
o Insulin excess
o Decrease in food intake
o Increased activity
o Alcohol consumption
* Rapid onset of symptoms
Symptoms
* Mild – give 10-15 grams carbohydrate
o Pallor, tachycardia, diaphoresis, shakiness, hunger, fatigue, behavior changes start
* Moderate – give 15-30 grams carbohydrate
o Headache, confusion, poor concentration, irritability, blurred/double vision, slurred speech, shallow breathing, photophobia
* Severe – give glucagon SQ
o Numb lips/mouth, disorientation, combative, loss of consciousness, seizures
Clinical Manifestations
* Hyperglycemia-chronic complications
o Hypertension
o Deceleration in linear growth and maturation
o Dry, rough skin with poor turgor
o Poor wound healing-impaired immune function
o Decreased acuity and blurred vision Retinal vascular changes (diabetic retinopathy)
o Heart disease, renal failure, peripheral vascular disease, neuropathy
o Accelerated atherosclerosis, hepatomegaly
o 30% will develop hypothyroidism
DMI-Management Goals
* Optimal glycemic control
o Medication
o Diet
o Exercise
* Normal growth and development
* Prevention of future complications
* Empowerment of client and family
Medication
* Insulin only one to treat Type I
* Stress, illness, infection, growth spurts and puberty will increase insulin requirements
* Many types of insulin available (short, intermediate and long-acting)
* Generally dosed BID-before breakfast and before evening meal
Insulin Dosing
* 0.5-1.0 U/kg/day
o 2/3 total dose in morning and 1/3 total dose in evening
* Short-acting (regular) Intermediate-acting (NPH) are most common
* Insulin pump - attached via catheter (an implantable device now in trials)
* Inhalation insulin being researched
* More frequent dosing as indicated
* Rotate SQ injection sites
Nutrition
* Ideally designed and monitored by a RD
* Goals:
o Low-saturated fat and low-sodium
o 3 meals with 2 snacks
o Prevention of hyper and hypoglycemia
o Attainment of normal growth & development
o Adequate caloric intake-avoid concentrated sugars
o Lipid levels appropriate for age
o Prevention of obesity
Exercise
* Benefits
o Improved cardiovascular health
o Improved glucose tolerance
o Increased insulin sensitivity
o Reduced hyperinsulinemia
o Reduces overall blood sugar
o Reduced body fat and weight
Exercise precautions
* Plan, ideally 60-90 minutes after a meal
* Consume additional snacks
* Consume snacks before and during strenuous exercise/sports
* Monitor glucose levels closely
* Avoid strenuous exercise in evening or just before going to bed
* Avoid with glucose levels > 240 mg/dl or ketouria present
Monitoring of blood glucose patterns
* Minimum 3-4 times/day
* 0200-0300 glucose check minimum of one time a week
* More frequent monitoring during times of illness, increased activity
* Urine glucose testing of little value
* Test urine for ketones with blood glucose levels > 240 mg/dl; during illness
Sick day rules
* Q 4-6 hour glucose monitoring and urine ketone checks around the clock
* Insulin must be taken even if anorexia, N/V
* Regular insulin supplemented if hyperglycemia and ketonuria are present
* Increased fluids, especially if ketosis, hyperglycemia, or fever present
Contact practitioner for following:
* Treatment of precipitating infection/illness
* Assistance with insulin dosage requirements
* Glucose levels remaining > 240 mg/dl or < 80 mg/dl despite following guidelines for illness
* Presence of ketones
* N/V with inability to tolerate fluids
* Diarrhea present > 5X per day
* Change in mental status
* Labored respirations or dyspnea
Diagnostic criteria
* Many go undiagnosed (~33%) for up to 6 years
* Classic symptoms + >200mg/dL
* No classic symptoms
o 2 fasting plasma glucose levels of >125 mg/dL
o 2 oral glucose tolerance tests with 2-hour plasma glucose levels plus one intervening value >200mg/dL
Laboratory tests
* Plasma glucose
o Normal adult – 80-120 mg/dL
o 1 week to 16 years: 60-105 mg/dl
o >16 years: 70-115 mg/dl
* Hemoglobin A1c (HbA1c)
o Should be performed every 3 months
o 3.9 - 7.7% is normal
o Significantly decrease/delay chronic, long-term complications with tight control
Laboratory
* Fasting lipid profile
o > 2 years old after control of blood sugar obtained
o If values normal, should be assessed every 5 yr.
* Urinalysis
o Glucose (renal threshold for glucose 160 mg/dL), ketones and protein negative
* Serum creatinine
o In children with proteinuria need 24 hr. urine collection
* Thyroid function tests
Diabetes Mellitus Type II
* Non-insulin dependent diabetes mellitus (NIDDM) = insulin resistance + relative insulin deficiency + excess glucose production by the liver
* “Adult onset diabetes” - >40 y.o. and over weight – now known to affect record numbers of adolescents and children – average age of onset in chn/adol is 13
* Risk factors – Obesity, genetic, African-Americans, Hispanics, Native Americans, Japanese, puberty, polycystic ovary syndrome, F>M
DMII
* Most diagnosed after puberty – common to be an “accidental” diagnosis
* Common to have HTN, dyslipidemia, vaginal infection, obesity, family history
* Management
o Diet
o Exercise
o Education, support & counseling
o Oral hypoglycemic drug (Glucophage – only one approved for children)
o Only ~ 20-30% will require any insulin therapy
Hypocalcemia
* Parathyroid Hormone (PTH)
* S/Sx – dry, scaly skin, brittle hair, thin nails, tetany, laryngeal stridor, muscle cramps, twitching, HA, seizures, mood swings, confusion, diarrhea, vomiting
* Treatment – maintaining normal serum calcium, long-term Vit D therapy, PO calcium
Phenylketonuria (PKU)
* Autosomal recessive (1:10,000)
* Absence of liver enzyme to convert phenylalanine (excess phenylalanine – permanent brain damage – MR, seizures)
* Musty/mousy odor to urine and sweat
* Early identification essential – screen at 2 days – Guthrie screening test (heel stick)
* Dietary control – formula Lofenalac
o HIGH – meat, eggs, milk
o LOW – OJ, bananas, potatoes, lettuce, spinach, peas
Maple Syrup Urine Disease
* Rare, autosomal recessive
* Defect in amino acid metabolism (leucine, iso-leucine, valine) – brain damage
* Untreated will die within 2-4 weeks
* Maple syrup/ketoacid odor to urine
* Dietary management – even more difficult than PKU
Galactosemia
* Autosomal recessive (1:40,000)
* Defect in carbohydrate metabolism – high galactose in blood and urine – low glucose – severe brain damage
* Lethargy, hypotonia, diarrhea, vomiting, liver enlarges (cirrhosis), jaundice
* Untreated – dies in 3 days
* Dietary control – free of galactose (lactose free diet)
Glycogen Storage Disease
* Autosomal recessive – group of 13 disorders
* Prevention of glycogen into glucose from liver storage
* Liver enlarges, hypoglycemia, stunted growth, possible brain damage, decreased platelet adhesiveness
* Dietary control – high-carbs, with snacks, NG/GT night feeding, antihypoglycemic drug, liver transplant extends life/does not cure
Tay-Sachs Disease
* Autosomal recessive – Ashkenazi Jewish (Eastern Europe)
* Lacks enzyme to metabolize lipids
* Lipids accumulate on nerves – MR, blindness
* Loss of skills at 6 months, seizures, blindness by 2 yo, death by 3-5 yo
* No cure – no good treatment
Precocious Puberty
* Early onset of Puberty (premature activation of pituitary/hypothalamus)
o Ages for girls: 8-13
o Ages for boys: 9 1/2-14
* Development of secondary sex characteristics and increased rate of growth and bone maturation (initially tall for age, then short d/t early closure of epiphysial plates)
Precocious Puberty
* Test: gonadotropin, LH, FSH, bone study, CT, MRI (often no causative factor is found)
* Treatment:
o none-self resolving (monitor)
o Lupron Depot (synthetic luteinizing hormone releasing factor)
* Education: parents and child, include discussions about sexuality (child is fertile), same-age peers
Endocrine and Metabolic Disorders.ppt
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Care of the Client with Diabetes
Care of the Client with Diabetes
Presentation lecture by:Christie M. Candelaria, MA, RN, CCRN.
DIABETES MELLITUS
* Caused by a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by a lack of response by cells to insulin (insulin resistance)
* Deficient insulin results in abnormal carbohydrate, protein, and fat metabolism due to impaired transport of glucose and amino acids into the cells
Types of Diabetes
* Type I
* Type 2
* Gestational
* Other types include:
o Genetic defect beta cell or insulin
o Disease of exocrine pancreas
o Drug or chemical induced
o Infections
o Others
Pathophysiology: INITIAL STAGE
* Insulin deficit leads to:
o Decreased transportation and use of glucose in many cells of the body
o Blood glucose levels rise (hyperglycemia)
o Excess glucose spills into the urine (glucosuria)
o Glucose in the urine exerts osmotic pressure in the filtrate, resulting in large volume of urine to be excreted (polyuria) with loss of fluids and electrolytes from the body tissues
o Fluid loss through the urine and high blood glucose levels draw water from the cells, resulting in dehydration
o Dehydration causes thirst (polydipsia)
o Lack of nutrients entering the cells stimulates appetite (polyphagia)
PROGRESSIVE EFFECTS
* Lack of glucose in cells results in catabolism of fats and proteins, leading to excessive amounts of fatty acids and their metabolites known as ketones or ketoacids in the blood.
* Some ketoacids are excreted in the urine (ketonuria)
Acute Complications of Diabetes
* Diabetic ketoacidosis
* Hyperglycemic-hyperosmolar-nonketotic syndrome
* Hypoglycemia from too much insulin or too little glucose
Chronic Complications of Diabetes
* Macrovascular complications
o Cardiovascular disease
o Cerebrovascular disease
o Peripheral vascular disease
* Microvascular complications
o Retinopathy (vision) problems
o Diabetic neuropathy
o Diabetic nephropathy
o Male erectile dysfunction
Assessment
* History
* Blood tests
o Fasting blood glucose test: two tests > 126 mg/dL
o Oral glucose tolerance test: blood glucose > 200 mg/dL at 120 minutes
o Glycosylated hemoglobin assays
o Glucosylated serum proteins and albumin
Urine Tests
* Urine testing for ketones
* Urine testing for renal function
* Urine testing for glucose
Drug Therapy
Goal: tight glycemic control
* Drug administration
* Drug selection
* Insulin therapy:
o Insulin analogue
o Short-acting insulin
o Concentrated insulin
o Intermediate
Oral Blood Glucose Lowering Agents
Sulfonylureas
* Appropriate only for clients with pancreatic beta cell function
* Most common serious complication: hypoglycemia
* Side Effects: hematologic reactions
o Allergic skin reactions
o Gastrointestinal effects
Meglitinides
* Repaglinide (Prandin)
* Action and side effects similar to sulfonylureas: hypoglycemia
o GI disturbances
o UR infections
o Arthralgia
o Back pain
o headache
Biguanides
* Metformin (glucophage)
* The only biguanide available in the USA
* Can cause lactic acidosis in clients with renal insufficiency
Alpha-glucosidase inhibitors
* Acarbose (Precose)
* Reduce postprandial hyperglycemia by slowing digestion and absorption of carbohydrate within the intestine
* Side effects: abdominal discomfort related to undigested carbohydrate in the intestinal tract
Thiazolidinedione antidiabetic agents
* Troglitazone
* Enhance insulin action, promoting glucose utilization in peripheral tissues
* Liver function studies should be done at the start of therapy and at regular intervals during therapy
Combination agents
* Combinations from two different classes of medications
* E.g: Glucovance
What’s New
* DDP-4 inhibitors – help lower blood glucose levels by increasing and prolonging the action of GLP-1
o Also called “incretin enhancers”
o How does it work:
When we eat, GLP-1 (glucagonlike peptide-1) is released by the small intestine in response to ingested carbohydrates which
1. helps regulate the synthesis and release of insulin from the pancreatic beta cells
2. initiates neuropeptide reactions that reduce hepatic glucose (glucagon) production after meals
3. induce satiety by crossing the blood-brain barrier to reduce appetite
4. slows down gastric emptying
5. may also play a role in beta-cell regrowth and repair known as its “pancreatic-sparing effect”
* Sitagliptin (Januvia) – first in the market
o Can be used alone or in combination with other oral medications like metformin or thiazolidinediones
o Available in 25 mg, 50 mg, 100 mg tabs.
o Typically administered as a 100-mg dose once daily with or without food; can be titrated down depending on patient’s renal status
o Weight-neutral drug; neither promoting weight loss or weight gain
o Approved only for adults
o Adverse reactions: URTI, nasopharyngitis, diarrhea, headache
* Vildagliptin (Galvus) – in the final stages of FDA approval
Insulin Regimens
* Single daily injection protocol
* Two-dose protocol
* Three-dose protocol
* Four-dose protocol
* Combination therapy
* Intensified therapy regimens
Drug Therapy
o Fixed-combination
o Long-acting
o Buffered insulins
Complications of Insulin Therapy
* Hypoglycemia
* Lipoatrophy
* Dawn phenomenon
* Somogyi's phenomenon
Alternative Methods of Insulin Administration
* Continuous subcutaneous infusion of insulin
* Implanted insulin pumps
* Injection devices
* New technology includes:
o Inhaled insulin
o Transdermal patch (being tested)
Client Education
* Storage and dose preparation
* Syringes
* Blood glucose monitoring
* Interpretation of results
* Frequency of testing
* Blood glucose therapy goals
Diet Therapy
* Goals of diet therapy
* Principles of nutrition in diabetes
o Protein, fats and carbohydrates, fiber, sweeteners, fat replacers
o Alcohol
o Food labeling
o Exchange system, carbohydrate counting
o Special considerations for type 1 and type 2 diabetes
Exercise Therapy
* Benefits of exercise
* Risks related to exercise
* Screening before starting exercise program
* Guidelines for exercise
* Exercise promotion
Whole-Pancreas Transplantation
* Operative procedure
* Rejection management
* Long-term effects
* Complications
* Islet cell transplantation hindered by limited supply of beta cells and problems caused by antirejection drugs
Nursing Diagnoses
Risk for Injury Related to Sensory Alterations
* Interventions and foot care practices:
o Cleanse and inspect the feet daily.
o Wear properly fitting shoes.
o Avoid walking barefoot.
o Trim toenails properly.
o Report nonhealing breaks in the skin.
Wound Care
* Wound environment
* Debridement
* Elimination of pressure on infected area
* Growth factors applied to wounds
Chronic Pain
* Interventions include:
o Maintenance of normal blood glucose levels
o Anticonvulsants
o Antidepressants
o Capsaicin cream
Risk for Injury Related to Disturbed Sensory Perception: Visual
* Interventions include:
o Blood glucose control
o Environmental management
+ Incandescent lamp
+ Coding objects
+ Syringes with magnifiers
+ Use of adaptive devices
Ineffective Tissue Perfusion: Renal
* Interventions include:
o Control of blood glucose levels
o Yearly evaluation of kidney function
o Control of blood pressure levels
o Prompt treatment of UTIs
o Avoidance of nephrotoxic drugs
o Diet therapy
o Fluid and electrolyte management
Potential for Hypoglycemia
* Blood glucose level < 70 mg/dL
* Diet therapy: carbohydrate replacement
* Drug therapy: glucagon, 50% dextrose, diazoxide, octreotide
* Prevention strategies for:
o Insulin excess
o Deficient food intake
o Exercise
o Alcohol
Potential for Diabetic Ketoacidosis
* Interventions include:
o Monitoring for manifestations
o Assessment of airway, level of consciousness, hydration status, blood glucose level
o Management of fluid and electrolytes
o Drug therapy goal: to lower serum glucose by 75 to 150 mg/dL/hr
o Management of acidosis
o Client education and prevention
Potential for Hyperglycemic-Hyperosmolar Nonketotic Syndrome and Coma
* Interventions include:
o Monitoring
o Fluid therapy: to rehydrate the client and restore normal blood glucose levels within 36 to 72 hr
o Continuing therapy with IV regular insulin at 10 units/hr often needed to reduce blood glucose levels
Health Teaching
* Assessing learning needs
* Assessing physical, cognitive, and emotional limitations
* Explaining survival skills
* Counseling
* Psychosocial preparation
* Home care management
* Health care resources
Care of the Client with Diabetes.ppt
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02 May 2009
Male Hypogonadism
Male Hypogonadism
Presentation lecture 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.
Low/low nl
Gonadotrope failure
Secondary
Elevated
Testicular failure
Primary Sperm count
Testosterone
Gonadotropins
Pathology
Hypogonadism
Gonadal Axis
Male Gonadal Function
Male Puberty
Clinical Features
Postpuberty
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
Low sperm ct
Primary hypogonadism
Elevated
Low sperm ct
Low/low nl
Diagnosis
Gonadotropins (LH/FSH)
Semen analysis
Testosterone
Testosterone Measurements
Testosterone in Obese Men
Testosterone Secretion:
Comparison of Young and Elderly Men
Standard Semen Analysis
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
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
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 cypionate esters of testosterone
* Lipophilic, leading to sustained release from muscle depots
* Side effects related to dosing or administration
* Regimens of 100 mg q wk to 300 mg q 3 wks acceptable
* Goal is a mid-cycle level near the middle of the laboratory reference range
Transdermal Testosterone
* Patch (Androderm)
o Apply to skin of upper arms and torso
o Delivers 5 mg testosterone/24 hr in continuous manner
o Approximately 1/3 of patients develop significant contact dermatitis
* Gels (Androgel, Testim)
o Apply to skin of upper arms and torso
o Usually dosed as 5.0 g or 10.0 g of gel to deliver 50 mg or 100 mg testosterone, respectively in a continuous manner
o Reports of contact dermatitis and gel odor uncommon
Desirable Effects of Testosterone Therapy
* Virilization (incompletely virilized men)
* Increased libido and energy
* Improved erectile function?
* Increased muscle mass and strength (8-10 wks)
* Increased bone mass (full effect ~ 24 mo)
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
o IM testosterone: midpoint between injections, level near middle of reference range
o Patch: 3-12 hrs after applying new patch
o Gel: timing not critical
o Buccal pellet: immediately before or after new pellet
* Prostate
o DRE @ 3 months, then annually
o PSA @ 3 months, then annually
o Prostate biopsy if PSA > 4 ng/mL, PSA increases by > 1.4 ng/mL in 12 months, or PSA velocity > 0.4 ng/mL/yr
* Red cell mass
o CBC at 3 months, then annually
o If Hct > 54%, stop therapy, monitor for return to reference range, then resume therapy at a lower dose
Summary
Male Hypogonadism.ppt
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