The Endocrine SystemThe Endocrine System
Prof F Ammari FRCPProf F Ammari FRCP
JUSR UniversityJUSR University
Endocrine GlandsEndocrine Glands Controls many body functionsControls many body functions
• exerts control by releasing special chemical exerts control by releasing special chemical substances into the blood called substances into the blood called hormoneshormones
• Hormones Hormones affect other endocrine glands or body affect other endocrine glands or body systemssystems
Ductless glandsDuctless glands Secrete hormones directly into bloodstreamSecrete hormones directly into bloodstream
• Hormones are quickly distributed by bloodstream Hormones are quickly distributed by bloodstream throughout the bodythroughout the body
HormonesHormones
Chemicals produced by endocrine glandsChemicals produced by endocrine glands Act on target organs elsewhere in bodyAct on target organs elsewhere in body Control/coordinate widespread processes:Control/coordinate widespread processes:
• HomeostasisHomeostasis
• ReproductionReproduction
• Growth & DevelopmentGrowth & Development
• MetabolismMetabolism
• Response to stressResponse to stress Overlaps with the Sympathetic Nervous SystemOverlaps with the Sympathetic Nervous System
HormonesHormones
Hormones are classified as:Hormones are classified as:• ProteinsProteins• Polypeptides (amino acid derivatives)Polypeptides (amino acid derivatives)• Lipids (fatty acid derivatives or steroids)Lipids (fatty acid derivatives or steroids)
HormonesHormones
Amount of hormone reaching target tissue Amount of hormone reaching target tissue directly correlates with concentration of directly correlates with concentration of hormone in blood.hormone in blood.• Constant level hormonesConstant level hormones
Thyroid hormonesThyroid hormones
• Variable level hormonesVariable level hormones Epinephrine (adrenaline) releaseEpinephrine (adrenaline) release
• Cyclic level hormonesCyclic level hormones Reproductive hormonesReproductive hormones
The Endocrine SystemThe Endocrine System Consists of several glands located in various parts Consists of several glands located in various parts
of the bodyof the body Specific GlandsSpecific Glands
• HypothalamusHypothalamus• PituitaryPituitary• ThyroidThyroid• ParathyroidParathyroid• AdrenalAdrenal• KidneysKidneys• Pancreatic IsletsPancreatic Islets• OvariesOvaries• TestesTestes
Figure 18.1
Figure 18.1 The Endocrine Figure 18.1 The Endocrine SystemSystem
Pituitary GlandPituitary Gland
Small gland located on stalk hanging from base of Small gland located on stalk hanging from base of brain - brain -
““The Master Gland” The Master Gland” • Primary function is to control other glands.Primary function is to control other glands.
• Produces many hormones.Produces many hormones.
• Secretion is controlled by hypothalamus in base of Secretion is controlled by hypothalamus in base of brain.brain.
Pituitary GlandPituitary Gland Two areasTwo areas
• Anterior PituitaryAnterior Pituitary• Posterior PituitaryPosterior Pituitary
Structurally, functionally differentStructurally, functionally different
Figure 18.6a, b
Figure 18.6 The Anatomy and Figure 18.6 The Anatomy and Orientation of the Pituitary Orientation of the Pituitary
GlandGland
Pituitary GlandPituitary Gland Anterior PituitaryAnterior Pituitary
• Thyroid-Stimulating Hormone (TSH)Thyroid-Stimulating Hormone (TSH) stimulates release of hormones from Thyroidstimulates release of hormones from Thyroid
– thyroxine (T4) and triiodothyronine (T3): stimulate metabolism of all cells
– calcitonin: lowers the amount of calcium in the blood by inhibiting breakdown of bone
released when stimulated by TSH or coldreleased when stimulated by TSH or cold abnormal conditionsabnormal conditions
– hyperthyroidism: too much TSH release
– hypothyroidism: too little TSH release
Pituitary GlandPituitary Gland Anterior PituitaryAnterior Pituitary
• Growth Hormone (GH)Growth Hormone (GH) stimulates growth of all organs and increases stimulates growth of all organs and increases
blood glucose concentrationblood glucose concentration– decreases glucose usage
– increases consumption of fats as an energy source
• Adreno-Corticotrophic Hormone (ACTH)Adreno-Corticotrophic Hormone (ACTH) stimulates the release of adrenal cortex hormonesstimulates the release of adrenal cortex hormones
Pituitary GlandPituitary Gland Anterior PituitaryAnterior Pituitary
• Follicle Stimulating Hormone (FSH)Follicle Stimulating Hormone (FSH) females - stimulates maturation of ova; release of females - stimulates maturation of ova; release of
estrogenestrogen males - stimulates testes to grow; produce spermmales - stimulates testes to grow; produce sperm
• Luteinizing Hormone (LH)Luteinizing Hormone (LH) females - stimulates ovulation; growth of corpus females - stimulates ovulation; growth of corpus
luteumluteum males - stimulates testes to secrete testosteronemales - stimulates testes to secrete testosterone
Pituitary GlandPituitary Gland Anterior PituitaryAnterior Pituitary
• ProlactinProlactin stimulates breast development during stimulates breast development during
pregnancy; milk production after deliverypregnancy; milk production after delivery
• Melanocyte Stimulating Hormone (MSH)Melanocyte Stimulating Hormone (MSH) stimulates synthesis, dispersion of melanin stimulates synthesis, dispersion of melanin
pigment in skinpigment in skin
Pituitary GlandPituitary Gland Posterior PituitaryPosterior Pituitary
• Stores, releases two hormones produced in Stores, releases two hormones produced in hypothalamushypothalamus
Antidiuretic hormone (ADH)Antidiuretic hormone (ADH) OxytocinOxytocin
Pituitary GlandPituitary Gland Posterior PituitaryPosterior Pituitary
• Antidiuretic hormone (ADH)Antidiuretic hormone (ADH) Stimulates water retention by kidneysStimulates water retention by kidneys
– reabsorb sodium and water Abnormal conditionsAbnormal conditions
– Undersecretion: diabetes insipidus (“water diabetes”)
– Oversecretion: Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
• OxytocinOxytocin Stimulates contraction of uterus at end of pregnancy Stimulates contraction of uterus at end of pregnancy
(Pitocin®); release of milk from breast(Pitocin®); release of milk from breast
HypothalamusHypothalamus Produces several releasing and inhibiting Produces several releasing and inhibiting
factors that stimulate or inhibit anterior factors that stimulate or inhibit anterior pituitary’s secretion of hormones.pituitary’s secretion of hormones.
Produces hormones that are stored in and Produces hormones that are stored in and released from posterior pituitaryreleased from posterior pituitary
What are these two hormones?
HypothalamusHypothalamus Also responsible for:Also responsible for:
• Regulation of water balanceRegulation of water balance
• Esophageal swallowingEsophageal swallowing
• Body temperature regulation (shivering)Body temperature regulation (shivering)
• Food/water intake (appetite)Food/water intake (appetite)
• Sleep-wake cycleSleep-wake cycle
• Autonomic functionsAutonomic functions
Pineal GlandPineal Gland Located within the DiencephalonLocated within the Diencephalon MelatoninMelatonin
• Inhibits ovarian hormonesInhibits ovarian hormones
• May regulate the body’s internal clockMay regulate the body’s internal clock
ThyroidThyroid
Located below larynx and low Located below larynx and low in neckin neck• Not over the thyroid cartilageNot over the thyroid cartilage
Thyroxine (TThyroxine (T44) and ) and
Triiodothyronine (TTriiodothyronine (T33))• Stimulate metabolism of all cellsStimulate metabolism of all cells
CalcitoninCalcitonin• Decreases blood calcium Decreases blood calcium
concentration by inhibiting concentration by inhibiting breakdown of bonebreakdown of bone
Figure 18.11 The Thyroid Figure 18.11 The Thyroid GlandGland
Figure 18.11a
ParathyroidsParathyroids Located on posterior surface of Located on posterior surface of
thyroidthyroid Frequently damaged during Frequently damaged during
thyroid surgerythyroid surgery Parathyroid hormone (PTH)Parathyroid hormone (PTH)
• Stimulates CaStimulates Ca2+2+ release from bone release from bone
• Promotes intestinal absorption and Promotes intestinal absorption and renal tubular reabsorption of renal tubular reabsorption of calciumcalcium
ParathyroidsParathyroids UnderactivityUnderactivity
• Decrease serum CaDecrease serum Ca2+2+
Hypocalcemic tetanyHypocalcemic tetany Seizures Seizures LaryngospasmLaryngospasm
ParathyroidsParathyroids
OveractivityOveractivity• Increased serum CaIncreased serum Ca2+2+
Pathological fracturesPathological fractures HypertensionHypertension Renal stonesRenal stones Altered mental statusAltered mental status
• ““Bones, stones, hypertones, abdominal moans”Bones, stones, hypertones, abdominal moans”
Thymus GlandThymus Gland
Located in anterior chest Located in anterior chest Normally absent by ~ age 4Normally absent by ~ age 4 Promotes development of immune-Promotes development of immune-
system cells (T-lymphocytes)system cells (T-lymphocytes)
Adrenal GlandsAdrenal Glands
Small glands located Small glands located near (ad) the kidneys near (ad) the kidneys (renals) (renals)
Consists of:Consists of:• outer cortexouter cortex• inner medullainner medulla
Adrenal GlandsAdrenal Glands Adrenal MedullaAdrenal Medulla
• the Adrenal Medulla secretes the catecholamine the Adrenal Medulla secretes the catecholamine hormones hormones norepinephrinenorepinephrine and and epinephrineepinephrine
• Epinephrine and NorepinephrineEpinephrine and Norepinephrine Prolong and intensify the sympathetic nervous system Prolong and intensify the sympathetic nervous system
response during stressresponse during stress
Adrenal GlandsAdrenal Glands Adrenal CortexAdrenal Cortex
• Aldosterone (Mineralocorticoid)Aldosterone (Mineralocorticoid) Regulates electrolyte (potassium, sodium) and fluid Regulates electrolyte (potassium, sodium) and fluid
homeostasishomeostasis
• Cortisol (Glucocorticoids)Cortisol (Glucocorticoids) Antiinflammatory, anti-immunity, and anti-Antiinflammatory, anti-immunity, and anti-
allergy effects.allergy effects. Increases blood glucose concentrationsIncreases blood glucose concentrations
• Androgens (Sex Hormones)Androgens (Sex Hormones) Stimulate sexual drive in femalesStimulate sexual drive in females
Adrenal GlandsAdrenal Glands
Adrenal CortexAdrenal Cortex• GlucocorticoidsGlucocorticoids
accounts for 95% of adrenal cortex hormone accounts for 95% of adrenal cortex hormone productionproduction
the level of glucose in the bloodthe level of glucose in the blood Released in response to stress, injury, or serious Released in response to stress, injury, or serious
infection - like the hormones from the adrenal infection - like the hormones from the adrenal medullamedulla
Adrenal GlandsAdrenal Glands
Adrenal CortexAdrenal Cortex• MineralcorticoidsMineralcorticoids
work to regulate the concentration of potassium work to regulate the concentration of potassium and sodium in the bodyand sodium in the body
OvariesOvaries Located in the abdominal cavity adjacent to the Located in the abdominal cavity adjacent to the
uterusuterus Under the control of LH and FSH from the Under the control of LH and FSH from the
anterior pituitaryanterior pituitary Produce eggs for reproductionProduce eggs for reproduction Produce hormonesProduce hormones
• estrogenestrogen
• progesteroneprogesterone
• Functions include sexual development and Functions include sexual development and preparation of the uterus for implantation of the eggpreparation of the uterus for implantation of the egg
OvariesOvaries
EstrogenEstrogen• Development of female secondary sexual Development of female secondary sexual
characteristicscharacteristics
• Development of endometriumDevelopment of endometrium ProgesteroneProgesterone
• Promotes conditions required for pregnancyPromotes conditions required for pregnancy
• Stabilization of endometriumStabilization of endometrium
TestesTestes
Located in the scrotumLocated in the scrotum Controlled by anterior pituitary hormones FSH Controlled by anterior pituitary hormones FSH
and LHand LH Produce sperm for reproductionProduce sperm for reproduction Produce testosterone -Produce testosterone -
• promotes male growth and masculinizationpromotes male growth and masculinization
• promotes development and maintenance of male promotes development and maintenance of male sexual characteristicssexual characteristics
PancreasPancreas
Located in retroperitoneal space between Located in retroperitoneal space between duodenum and spleenduodenum and spleen
Has both endocrine and exocrine functionsHas both endocrine and exocrine functions• Exocrine PancreasExocrine Pancreas
Secretes key digestive enzymesSecretes key digestive enzymes
• Endocrine PancreasEndocrine Pancreas Alpha Cells - glucagon productionAlpha Cells - glucagon production Beta Cells - insulin productionBeta Cells - insulin production Delta Cells - somatostatin productionDelta Cells - somatostatin production
PancreasPancreas
Exocrine functionExocrine function• SecretesSecretes
amylaseamylase lipaselipase
PancreasPancreas
AlphaAlpha Cells Cells• GlucagonGlucagon
Raises blood glucose levelsRaises blood glucose levels BetaBeta Cells Cells
• InsulinInsulin Lowers blood glucose levelsLowers blood glucose levels
DeltaDelta Cells Cells• SomatostatinSomatostatin
Suppresses release of growth hormoneSuppresses release of growth hormone
Disorders of the Endocrine Disorders of the Endocrine SystemSystem
Abnormal Thyroid FunctionAbnormal Thyroid Function
HypothyroidismHypothyroidism• Too little thyroid hormoneToo little thyroid hormone
HyperthyroidismHyperthyroidism(Thyrotoxicosis / Thyroid Storm)(Thyrotoxicosis / Thyroid Storm)• Too much thyroid hormoneToo much thyroid hormone
HypothyroidismHypothyroidism
Thyroid hormone deficiency causing a decrease Thyroid hormone deficiency causing a decrease in the basal metabolic ratein the basal metabolic rate• Person is “slowed down”Person is “slowed down”
Causes of HypothyroidismCauses of Hypothyroidism::• Radioactive iodine ablationRadioactive iodine ablation
• Non-compliance with levothyroxineNon-compliance with levothyroxine
• Hashimoto’s thyroiditis - autoimmune destructionHashimoto’s thyroiditis - autoimmune destruction
HypothyroidismHypothyroidism Confusion, drowsiness, comaConfusion, drowsiness, coma Cold intolerantCold intolerant Hypotension, BradycardiaHypotension, Bradycardia Muscle weaknessMuscle weakness Decreased respirationsDecreased respirations Weight gain, ConstipationWeight gain, Constipation Non-pitting peripheral edemaNon-pitting peripheral edema DepressionDepression Facial edema, loss of hairFacial edema, loss of hair Dry, coarse skinDry, coarse skin
Appearance of Myxedema
HypothyroidismHypothyroidism Myxedema ComaMyxedema Coma
• Severe hypothyroidism that can be fatalSevere hypothyroidism that can be fatal Management of Myxedema ComaManagement of Myxedema Coma
• Control airwayControl airway• Support oxygenation, ventilationSupport oxygenation, ventilation• IV fluidsIV fluids• LaterLater
Levothyroxine (Synthroid®)Levothyroxine (Synthroid®) HydrocortisoneHydrocortisone
HyperthyroidismHyperthyroidism Excessive levels of thyroid levels cause Excessive levels of thyroid levels cause
hypermetabolic statehypermetabolic state• Person is “sped up”.Person is “sped up”.
Causes of HyperthyroidismCauses of Hyperthyroidism• Overmedication with levothyroxine (Synthroid®) - Overmedication with levothyroxine (Synthroid®) -
Fad dietsFad diets
• Goiter (enlarged, hyperactive thyroid gland)Goiter (enlarged, hyperactive thyroid gland)
• Graves DiseaseGraves Disease
HyperthyroidismHyperthyroidism Nervousness, irritable, tremors, Nervousness, irritable, tremors,
paranoidparanoid Warm, flushed skinWarm, flushed skin Heat intolerantHeat intolerant Tachycardia - High output CHFTachycardia - High output CHF HypertensionHypertension TachypneaTachypnea DiarrheaDiarrhea Weight lossWeight loss ExophthalmosExophthalmos GoiterGoiter
A 40 year old white female complains of nervousness, fatigue and weight loss which became apparent one year ago. She has lost 14 pounds over this period, but denies anorexia. Recently she has been unable to perform routine household activities because of fatigue, palpitations and exertional dyspnea. She has been extremely uncomfortable this summer, and perspires excessively. She is on oral contraceptives.
THYROID EYE DISEASETHYROID EYE DISEASE
INFILTRATIONINFILTRATION 1. soft tissue 1. soft tissue
involvement :- involvement :- chemosis, chemosis, conjunctival conjunctival injection over the injection over the recti insertions, recti insertions, puffy lids puffy lids
HyperthyroidismHyperthyroidism TreatmentTreatment
• Airway/Ventilation/OxygenAirway/Ventilation/Oxygen
• ECG monitorECG monitor
• IV access - Cautious IV fluidsIV access - Cautious IV fluids
• Acetaminophen for feverAcetaminophen for fever
• BetaBeta-blockers-blockers
• Consider benzodiazepines for anxietyConsider benzodiazepines for anxiety
• PTU (propylthiouracil)PTU (propylthiouracil) Usually short-term use prior to more definitive Usually short-term use prior to more definitive
treatmenttreatment
• SSKI® (potassium iodide)SSKI® (potassium iodide)
Thyroid Storm/ThyrotoxicosisThyroid Storm/Thyrotoxicosis
Severe form of hyperthyroidism that can be Severe form of hyperthyroidism that can be fatalfatal• Acute life-threatening hyperthyroidismAcute life-threatening hyperthyroidism
CauseCause• Increased physiological stress in hyperthyroid Increased physiological stress in hyperthyroid
patientspatients
Thyroid Storm/ThyrotoxicosisThyroid Storm/Thyrotoxicosis
Severe tachycardiaSevere tachycardia Heart FailureHeart Failure DysrhythmiasDysrhythmias ShockShock HyperthermiaHyperthermia Abdominal painAbdominal pain Restlessness, Agitation, Delirium, ComaRestlessness, Agitation, Delirium, Coma
Thyroid Storm/ThyrotoxicosisThyroid Storm/Thyrotoxicosis ManagementManagement
• Airway/Ventilation/OxygenAirway/Ventilation/Oxygen• ECG monitorECG monitor• IV access - cautious IV fluidsIV access - cautious IV fluids• Control hyperthermiaControl hyperthermia
Active coolingActive cooling AcetaminophenAcetaminophen
• Inderal (beta blockers)Inderal (beta blockers)• Consider benzodiazepines for anxietyConsider benzodiazepines for anxiety• Potassium iodide (SSKI®)Potassium iodide (SSKI®)• Propylthiouracil (PTU)Propylthiouracil (PTU)
Abnormal Adrenal Function Abnormal Adrenal Function
HyperadrenalismHyperadrenalism• Excess activity of the adrenal glandExcess activity of the adrenal gland
• Cushing’s Syndrome & DiseaseCushing’s Syndrome & Disease
• PheochromocytomaPheochromocytoma Hypoadrenalism (adrenal insufficiency)Hypoadrenalism (adrenal insufficiency)
• Inadequate activity of the adrenal glandInadequate activity of the adrenal gland
• Addison’s diseaseAddison’s disease
HyperadrenalismHyperadrenalism
Primary Aldosteronism Primary Aldosteronism • Excessive secretion of aldosterone by adrenal cortexExcessive secretion of aldosterone by adrenal cortex
Increased NaIncreased Na++/H/H22OO
• PresentationPresentation headacheheadache nocturia, polyurianocturia, polyuria fatiguefatigue hypertension, hypervolemiahypertension, hypervolemia potassium depletionpotassium depletion
HyperadrenalismHyperadrenalism Adrenogenital syndromeAdrenogenital syndrome
• ““Bearded Lady”Bearded Lady”
• Group of disorders caused by adrenocortical Group of disorders caused by adrenocortical hyperplasia or malignant tumorshyperplasia or malignant tumors
• Excessive secretion of adrenocortical steroids Excessive secretion of adrenocortical steroids especially those with androgenic or estrogenic effectsespecially those with androgenic or estrogenic effects
• Characterized byCharacterized by masculinization of womenmasculinization of women feminization of menfeminization of men premature sexual development of childrenpremature sexual development of children
HyperadrenalismHyperadrenalism Cushing’s SyndromeCushing’s Syndrome
• Results from increased adrenocortical secretion of Results from increased adrenocortical secretion of cortisolcortisol
• Causes include:Causes include: ACTH-secreting tumor of the pituitary ACTH-secreting tumor of the pituitary
(Cushing’s disease)(Cushing’s disease) excess secretion of ACTH by a neoplasm within excess secretion of ACTH by a neoplasm within
the adrenal cortexthe adrenal cortex excess secretion of ACTH by a malignant growth excess secretion of ACTH by a malignant growth
outside the adrenal glandoutside the adrenal gland excessive or prolonged administration of steroidsexcessive or prolonged administration of steroids
HyperadrenalismHyperadrenalism Cushing’s SyndromeCushing’s Syndrome
• Characterized by:Characterized by: truncal obesitytruncal obesity moon facemoon face buffalo humpbuffalo hump acne, hirsutismacne, hirsutism abdominal striaeabdominal striae hypertensionhypertension psychiatric disturbancespsychiatric disturbances osteoporosisosteoporosis amenorrheaamenorrhea
Cushing’s Syndrome
HyperadrenalismHyperadrenalism
Cushing’s DiseaseCushing’s Disease• Too much adrenal hormone productionToo much adrenal hormone production
adrenal hyperplasia caused by an ACTH adrenal hyperplasia caused by an ACTH secreting adenoma of the pituitarysecreting adenoma of the pituitary
• ““Cushingoid features”Cushingoid features” striae on extremities or abdomenstriae on extremities or abdomen moon facemoon face buffalo humpbuffalo hump weight gain with truncal obesityweight gain with truncal obesity personality changes, irritablepersonality changes, irritable
HyperadrenalismHyperadrenalism
Cushing’s SyndromeCushing’s Syndrome• ManagementManagement
Airway/Ventilation/OxygenAirway/Ventilation/Oxygen Supportive careSupportive care Assess for cardiovascular event requiring Assess for cardiovascular event requiring
treatmenttreatment
– severe hypertension
– myocardial ischemia
HyperadrenalismHyperadrenalism
PheochromocytomaPheochromocytoma• Catecholamine secreting tumor of adrenal medullaCatecholamine secreting tumor of adrenal medulla
• PresentationPresentation AnxietyAnxiety Pallor, diaphoresisPallor, diaphoresis HypertensionHypertension Tachycardia, PalpitationsTachycardia, Palpitations DyspneaDyspnea HyperglycemiaHyperglycemia
HyperadrenalismHyperadrenalism
PheochromocytomaPheochromocytoma• ManagementManagement
Supportive care based upon presentationSupportive care based upon presentation Airway/Ventilation/OxygenAirway/Ventilation/Oxygen Calm/ReassureCalm/Reassure Assess blood glucose Assess blood glucose Consider beta blocking agent - LabetalolConsider beta blocking agent - Labetalol Consider benzodiazepinesConsider benzodiazepines
HypoadrenalismHypoadrenalism
Adrenal InsufficiencyAdrenal Insufficiency• decrease production of glucocorticoids, decrease production of glucocorticoids,
mineralcorticoids and androgensmineralcorticoids and androgens CausesCauses
• Primary adrenal failure (Addison’s Disease)Primary adrenal failure (Addison’s Disease)• Infection (TB, fungal, Meningococcal)Infection (TB, fungal, Meningococcal)• AIDSAIDS• Prolonged steroid useProlonged steroid use
HypoadrenalismHypoadrenalism PresentationPresentation
• Hypotension, ShockHypotension, Shock• Hyponatremia, HyperkalemiaHyponatremia, Hyperkalemia• Progressive Muscle weaknessProgressive Muscle weakness• Progressive weight loss and anorexiaProgressive weight loss and anorexia• Skin hyperpigmentationSkin hyperpigmentation
areas exposed to sun, pressure points, joints and creasesareas exposed to sun, pressure points, joints and creases• ArrhythmiasArrhythmias• HypoglycemiaHypoglycemia• N/V/DN/V/D
HypoadrenalismHypoadrenalism
ManagementManagement• Airway/Ventilation/OxygenAirway/Ventilation/Oxygen
• ECG monitorECG monitor
• IV fluidsIV fluids
• Assess blood glucose - D50 if hypoglycemicAssess blood glucose - D50 if hypoglycemic
• Steroids Steroids hydrocortisone or dexamethasonehydrocortisone or dexamethasone florinef (mineralcorticoid)florinef (mineralcorticoid)
• Vasopressors if unresponsive to IV fluidsVasopressors if unresponsive to IV fluids
Diabetes MellitusDiabetes Mellitus
Diabetes MellitusDiabetes Mellitus Chronic metabolic diseaseChronic metabolic disease One of the most common diseases in North One of the most common diseases in North
AmericaAmerica• Affects 5% of USA population (12 million people)Affects 5% of USA population (12 million people)
Results inResults in insulin secretion by the Beta (insulin secretion by the Beta () cells of the islets ) cells of the islets
of Langerhans in the pancreas, AND/ORof Langerhans in the pancreas, AND/OR
• Defects in insulin receptors on cell membranes Defects in insulin receptors on cell membranes leading to cellular resistance to insulinleading to cellular resistance to insulin
Leads to an Leads to an risk for significant risk for significant cardiovascular, renal and ophthalmic diseasecardiovascular, renal and ophthalmic disease
Regulation of GlucoseRegulation of Glucose Dietary IntakeDietary Intake
• Components of foodComponents of food:: CarbohydratesCarbohydrates FatsFats ProteinsProteins VitaminsVitamins MineralsMinerals
Regulation of GlucoseRegulation of Glucose The other 3 major food sources for glucose areThe other 3 major food sources for glucose are
• carbohydratescarbohydrates
• proteinsproteins
• fatsfats Most sugars in the human diet are complex and Most sugars in the human diet are complex and
must be broken down into simple sugars: must be broken down into simple sugars: glucose, galactose and fructose - before useglucose, galactose and fructose - before use
Regulation of Glucose Regulation of Glucose CarbohydratesCarbohydrates
• Found in sugary, starchy foodsFound in sugary, starchy foods• Ready source of near-instant energyReady source of near-instant energy• If not “burned” immediately by body, stored If not “burned” immediately by body, stored
in liver and skeletal muscle as glycogen in liver and skeletal muscle as glycogen (short-term energy) or as fat (long-term (short-term energy) or as fat (long-term energy needs)energy needs)
• After normal meal, approximately 60% of After normal meal, approximately 60% of the glucose is stored in liver as glycogenthe glucose is stored in liver as glycogen
Regulation of GlucoseRegulation of Glucose
FatsFats• Broken down into fatty acids and glycerol by Broken down into fatty acids and glycerol by
enzymesenzymes• Excess fat stored in liver or in fat cells Excess fat stored in liver or in fat cells
(under the skin)(under the skin)
Regulation of GlucoseRegulation of Glucose
Pancreatic hormones are required to regulate Pancreatic hormones are required to regulate blood glucose levelblood glucose level• glucagonglucagon released by Alpha ( released by Alpha () cells) cells
• insulininsulin released by Beta Cells released by Beta Cells (())
• somatostatinsomatostatin released by Delta Cells ( released by Delta Cells ())
Regulation of GlucoseRegulation of Glucose Alpha (Alpha () cells release ) cells release glucagonglucagon to control to control
blood glucose levelblood glucose level• When blood glucose levels fall, When blood glucose levels fall, cells cells the amount the amount
of glucagon in the bloodof glucagon in the blood
• The surge of glucagon stimulates liver to release The surge of glucagon stimulates liver to release glucose stores by the breakdown of glycogen into glucose stores by the breakdown of glycogen into glucose (glycogenolysis)glucose (glycogenolysis)
• Also, glucagon stimulates the liver to produce Also, glucagon stimulates the liver to produce glucose (gluconeogenesis)glucose (gluconeogenesis)
Regulation of GlucoseRegulation of Glucose Beta Cells Beta Cells (() ) release release insulin insulin (antagonistic to (antagonistic to
glucagon) to control blood glucose levelglucagon) to control blood glucose level• Insulin Insulin the rate at which various body cells take up the rate at which various body cells take up
glucose glucose insulin lowers the blood glucose level insulin lowers the blood glucose level
• Promotes glycogenesis - storage of glycogen in the Promotes glycogenesis - storage of glycogen in the liverliver
• Insulin is rapidly broken down by the liver and Insulin is rapidly broken down by the liver and must be secreted constantlymust be secreted constantly
Regulation of GlucoseRegulation of Glucose Delta Cells (Delta Cells () produce ) produce somatostatin, somatostatin, which which
inhibits both glucagon and insulininhibits both glucagon and insulin• inhibits insulin and glucagon secretion by the inhibits insulin and glucagon secretion by the
pancreaspancreas
• inhibits digestion by inhibiting secretion of digestive inhibits digestion by inhibiting secretion of digestive enzymesenzymes
• inhibits gastric motilityinhibits gastric motility
• inhibits absorption of glucose in the intestineinhibits absorption of glucose in the intestine
Regulation of GlucoseRegulation of Glucose Breakdown of sugars carried out by enzymes in Breakdown of sugars carried out by enzymes in
the GI systemthe GI system• As simple sugars, they are absorbed from the GI As simple sugars, they are absorbed from the GI
system into the bodysystem into the body To be converted into energy, glucose must first To be converted into energy, glucose must first
be transmitted through the cell membranebe transmitted through the cell membrane• Glucose molecule is too large and does not readily Glucose molecule is too large and does not readily
diffusediffuse
Regulation of GlucoseRegulation of Glucose Glucose must pass into the cell by binding to a Glucose must pass into the cell by binding to a
special carrier protein on the cell’s surface. special carrier protein on the cell’s surface. • Facilitated diffusion - Facilitated diffusion - carrier protein binds with the carrier protein binds with the
glucose and carries it into the cell.glucose and carries it into the cell. The rate at which glucose can enter the cell is The rate at which glucose can enter the cell is
dependent upon insulin levelsdependent upon insulin levels• Insulin serves as the messenger - travels via blood to Insulin serves as the messenger - travels via blood to
target tissuestarget tissues
• Combines with specific insulin receptors on the Combines with specific insulin receptors on the surface of the cell membranesurface of the cell membrane
Regulation of GlucoseRegulation of Glucose
Body strives to maintain blood glucose between Body strives to maintain blood glucose between 60 mg/dl and 100 mg/dl.60 mg/dl and 100 mg/dl.
GlucoseGlucose• brain is the biggest user of glucose in the bodybrain is the biggest user of glucose in the body
• sole energy source for brainsole energy source for brain
• brain does not require insulin to utilize glucosebrain does not require insulin to utilize glucose
Regulation of GlucoseRegulation of Glucose
Insulin Glucagon
Glucagon and Insulin are opposites (antagonists) of each other.
Regulation of GlucoseRegulation of Glucose GlucagonGlucagon
• Released in response to:Released in response to: Sympathetic stimulationSympathetic stimulation Decreasing blood glucose concentrationDecreasing blood glucose concentration
• Acts primarily on liver to increase rate of Acts primarily on liver to increase rate of glycogen breakdownglycogen breakdown
• Increasing blood glucose levels have Increasing blood glucose levels have inhibitory effect on glucagon secretioninhibitory effect on glucagon secretion
Regulation of GlucoseRegulation of Glucose InsulinInsulin
• Released in response to:Released in response to: Increasing blood glucose concentrationIncreasing blood glucose concentration Parasympathetic innervationParasympathetic innervation
• Acts on cell membranes to increase glucose Acts on cell membranes to increase glucose uptake from blood streamuptake from blood stream
• Promotes facilitated diffusion of glucose into Promotes facilitated diffusion of glucose into cellscells
Diabetes MellitusDiabetes Mellitus 2 Types historically based on age of onset (NOT 2 Types historically based on age of onset (NOT
insulin vs. non-insulin)insulin vs. non-insulin)• Type IType I
juvenile onsetjuvenile onset insulin dependentinsulin dependent
• Type IIType II historically adult onsethistorically adult onset
– now some morbidly obese children are developing Type II diabetes
non-insulin dependentnon-insulin dependent– may progress to insulin dependency
Types of Diabetes MellitusTypes of Diabetes Mellitus
Type IType I Type IIType II SecondarySecondary GestationalGestational
Pathophysiology of Pathophysiology of Type I Diabetes MellitusType I Diabetes Mellitus
Characterized by inadequate or absent production Characterized by inadequate or absent production of insulin by pancreasof insulin by pancreas
Usually presents by age 25Usually presents by age 25 Strong genetic componentStrong genetic component Autoimmune featuresAutoimmune features
• body destroys own insulin-producing cells in pancreasbody destroys own insulin-producing cells in pancreas
• may follow severe viral illness or injurymay follow severe viral illness or injury Requires lifelong treatment with insulin Requires lifelong treatment with insulin
replacementreplacement
Pathophysiology of Pathophysiology of Type II Diabetes MellitusType II Diabetes Mellitus
Pancreas continues to produce some insulin Pancreas continues to produce some insulin however disease results from combination of:however disease results from combination of:• RelativeRelative insulin deficiency insulin deficiency
• Decreased sensitivity of insulin receptorsDecreased sensitivity of insulin receptors Onset usually after age 25 in overweight adultsOnset usually after age 25 in overweight adults
• Some morbidly obese children develop Type II diabetesSome morbidly obese children develop Type II diabetes Familial componentFamilial component Usually controlled with diet, weight loss, oral Usually controlled with diet, weight loss, oral
hypoglycemic agentshypoglycemic agents• Insulin may be needed at some point in lifeInsulin may be needed at some point in life
Secondary Diabetes MellitusSecondary Diabetes Mellitus
Pre-existing condition affects pancreasPre-existing condition affects pancreas• PancreatitisPancreatitis• TraumaTrauma
Gestational Diabetes MellitusGestational Diabetes Mellitus
Occurs during pregnancyOccurs during pregnancy• Usually resolves after deliveryUsually resolves after delivery
Occurs rarely in non-pregnant women on BCPsOccurs rarely in non-pregnant women on BCPs Increased estrogen, progesterone antagonize Increased estrogen, progesterone antagonize
insulininsulin
Presentation of New Onset Presentation of New Onset Diabetes MellitusDiabetes Mellitus
3 Ps3 Ps• PolyuriaPolyuria
• PolydipsiaPolydipsia
• PolyphagiaPolyphagia Blurred vision, dizziness, altered mental statusBlurred vision, dizziness, altered mental status Rapid weight lossRapid weight loss Warm dry skin, Warm dry skin, Weakness, Tachycardia, DehydrationWeakness, Tachycardia, Dehydration
Long Term Treatment of Long Term Treatment of Diabetes MellitusDiabetes Mellitus
Diet regulationDiet regulation• e.ge.g. 1400 calorie ADA diet. 1400 calorie ADA diet
ExerciseExercise• increase patient’s glucose metabolismincrease patient’s glucose metabolism
Oral hypoglycemic agentsOral hypoglycemic agents• SulfonylureasSulfonylureas
InsulinInsulin• Historically produced from pigs (porcine insulin)Historically produced from pigs (porcine insulin)
• Currently genetic engineering has lead to human insulin Currently genetic engineering has lead to human insulin (Humulin) (Humulin)
Long Term Treatment ofLong Term Treatment ofDiabetes MellitusDiabetes Mellitus
InsulinInsulin• Available in various forms distinguished on onset and Available in various forms distinguished on onset and
duration of actionduration of action OnsetOnset
– rapid (Regular, Semilente, Novolin 70/30)
– intermediate (Novolin N, Lente)
– slow (Ultralente) DurationDuration
– short, 5-7 hrs (Regular)
– intermediate, 18-24 hrs (Semilente, Novolin N, Lente, NPH)
– long-acting, 24 - 36+ hrs (Novolin 70/30, Ultralente)
Long Term Treatment ofLong Term Treatment ofDiabetes MellitusDiabetes Mellitus
InsulinInsulin• Must be given by injection as insulin is protein Must be given by injection as insulin is protein
which would be digested if given orallywhich would be digested if given orally extremely compliant patients may use an insulin extremely compliant patients may use an insulin
pump which provides a continuous dosepump which provides a continuous dose current research studying inhaled insulin formcurrent research studying inhaled insulin form
Long Term Treatment of Long Term Treatment of Diabetes MellitusDiabetes Mellitus
Oral Hypoglycemic AgentsOral Hypoglycemic Agents• Stimulate the release of insulin from the pancreas, Stimulate the release of insulin from the pancreas,
thus patient must still have intact thus patient must still have intact betabeta cells in the cells in the pancreas.pancreas.
• Common agents includeCommon agents include:: Glucotrol® (glipizide)Glucotrol® (glipizide) Micronase® or Diabeta® (glyburide)Micronase® or Diabeta® (glyburide) Glucophage® (metformin) [Not a Glucophage® (metformin) [Not a
sulfonylurea]sulfonylurea]
Emergencies Associated Blood Emergencies Associated Blood Glucose LevelGlucose Level
HyperglycemiaHyperglycemia• Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA)• Hyperglycemic Hyperosmolar Nonketotic Hyperglycemic Hyperosmolar Nonketotic
Coma (HHNC)Coma (HHNC) Hypoglycemia Hypoglycemia
• ““Insulin Shock”Insulin Shock”
HyperglycemiaHyperglycemia Defined as blood glucose > 200 mg/dl Defined as blood glucose > 200 mg/dl CausesCauses
• Failure to take Failure to take medicationmedication (insulin) (insulin)• Increased Increased dietarydietary intake intake• StressStress (surgery, MI, CVA, trauma) (surgery, MI, CVA, trauma)• FeverFever• InfectionInfection• PregnancyPregnancy (gestational diabetes) (gestational diabetes)
HyperglycemiaHyperglycemia Two hyperglycemic diabetic states may Two hyperglycemic diabetic states may
occuroccur• Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA)• Hyperglycemic Hyperosmolar Non-ketotic Hyperglycemic Hyperosmolar Non-ketotic
Coma (HHNC)Coma (HHNC)
Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA) Occurs in Type I diabetics (insulin dependency)Occurs in Type I diabetics (insulin dependency) UsuallyUsually associated with blood glucose level in associated with blood glucose level in
the range of 200 - 600 mg/dlthe range of 200 - 600 mg/dl No insulin availability results in ketoacidosisNo insulin availability results in ketoacidosis
Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA) PathophysiologyPathophysiology
• Results from absence of insulinResults from absence of insulin prevents glucose from entering the cellsprevents glucose from entering the cells leads to glucose accumulation in the bloodleads to glucose accumulation in the blood
• Cells become starved for glucose and begin to use Cells become starved for glucose and begin to use other energy sources (primarily fats)other energy sources (primarily fats)
Fat metabolism generates fatty acidsFat metabolism generates fatty acids Further metabolized into ketoacids (ketone Further metabolized into ketoacids (ketone
bodies)bodies)
Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA) Pathophysiology (cont)Pathophysiology (cont)
• Blood sugar rises above renal threshold for Blood sugar rises above renal threshold for reabsorption (blood glucose > 180 mg/dl)reabsorption (blood glucose > 180 mg/dl)
glucose “spills” into the urineglucose “spills” into the urine Loss of glucose in urine causes osmotic diuresisLoss of glucose in urine causes osmotic diuresis
• Results inResults in dehydrationdehydration acidosisacidosis electrolyte imbalances (especially K+)electrolyte imbalances (especially K+)
Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA) PresentationPresentation
• Gradual onset with progressionGradual onset with progression• Warm, pink, dry skin Warm, pink, dry skin • Dry mucous membranes (dehydrated)Dry mucous membranes (dehydrated)• Tachycardia, weak peripheral pulsesTachycardia, weak peripheral pulses• Weight lossWeight loss• Polyuria, polydipsiaPolyuria, polydipsia• Abdominal pain with nausea/vomitingAbdominal pain with nausea/vomiting• Altered mental statusAltered mental status• Kussmaul respirations with acetone (fruity) odorKussmaul respirations with acetone (fruity) odor
Diabetic KetoacidosisDiabetic Ketoacidosis
Increased Blood Sugar
Osmotic Diuresis
Polyuria
PolydipsiaVolume DepletionShock
Cells Can’t Burn Glucose
Cells Burn FatPolyphagia
Ketone Bodies
Metabolic Acidosis
FruityBreath
Kussmaul Breathing
Inadequate insulin
Management of DKAManagement of DKA Airway/Ventilation/Oxygen maskAirway/Ventilation/Oxygen mask Assess blood glucose level & ECGAssess blood glucose level & ECG IV access, large bore NSIV access, large bore NS
• normal saline bolus and reassessnormal saline bolus and reassess
• often requires several litersoften requires several liters Assess for underlying cause of DKAAssess for underlying cause of DKA TransportTransport
How does fluid treat DKA?
Hyperosmolar Hyperglycemic Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Nonketotic Coma (HHNC)
Usually occurs in type II diabeticsUsually occurs in type II diabetics Typically very high blood sugar (>600mg/dl)Typically very high blood sugar (>600mg/dl) Some insulin availableSome insulin available Higher mortality than DKAHigher mortality than DKA
Hyperosmolar Hyperglycemic Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Nonketotic Coma (HHNC)
PathophysiologyPathophysiology• Some minimal insulin productionSome minimal insulin production
enough insulin available to allow glucose to enter enough insulin available to allow glucose to enter the cells and prevent ketogenesisthe cells and prevent ketogenesis
not enough to decrease gluconeogenesis by livernot enough to decrease gluconeogenesis by liver no ketosisno ketosis
• Extreme hyperglycemia produces hyperosmolar state Extreme hyperglycemia produces hyperosmolar state causingcausing
diuresisdiuresis severe dehydrationsevere dehydration electrolyte disturbanceselectrolyte disturbances
Hyperosmolar Hyperglycemic Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Nonketotic Coma (HHNC)
Increased Blood Sugar
Osmotic Diuresis
Polyuria
PolydipsiaVolume DepletionShock
Inadequate insulin
Hyperosmolar Hyperglycemic Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)Nonketotic Coma (HHNC)
PresentationPresentation• Same as DKA but with greater severitySame as DKA but with greater severity
Higher blood glucose levelHigher blood glucose level Non-insulin dependent diabetesNon-insulin dependent diabetes Greater degree of dehydrationGreater degree of dehydration
Management of HHNCManagement of HHNC Secure airway and assess ventilationSecure airway and assess ventilation
• Consider need to assist ventilationConsider need to assist ventilation
• Consider need to intubateConsider need to intubate High concentration oxygenHigh concentration oxygen Assess blood glucose level & ECGAssess blood glucose level & ECG IV access, large bore NSIV access, large bore NS
• normal saline bolus and reassessnormal saline bolus and reassess
• often requires several litersoften requires several liters Assess for underlying cause of HHNCAssess for underlying cause of HHNC TransportTransport
Further Management of Further Management of HyperglycemiaHyperglycemia
Insulin (regular)Insulin (regular)• Correct hyperglycemiaCorrect hyperglycemia
Correction of acid/base imbalancesCorrection of acid/base imbalances• Bicarbonate (severe cases documented by ABG)Bicarbonate (severe cases documented by ABG)
Normalization of electrolyte balanceNormalization of electrolyte balance• DKA may result in DKA may result in hyperkalemiahyperkalemia 2 2o o to acidosisto acidosis
HH++ shifts intracellularly, K shifts intracellularly, K++ moves to moves to extracellular spaceextracellular space
• Urinary KUrinary K+ + losses may lead to losses may lead to hypokalemiahypokalemia once once therapy is startedtherapy is started
HypoglycemiaHypoglycemia True hypoglycemia defined as blood sugar True hypoglycemia defined as blood sugar
< 60 mg/dl< 60 mg/dl ALL hypoglycemia is NOT caused by diabetesALL hypoglycemia is NOT caused by diabetes
• Can occur in non-diabetic patientsCan occur in non-diabetic patients thin young femalesthin young females alcoholics with liver diseasealcoholics with liver disease alcohol consumption on empty stomach will alcohol consumption on empty stomach will
block glucose synthesis in liver (gluconeogenesis)block glucose synthesis in liver (gluconeogenesis) Hypoglycemia causes impaired functioning of Hypoglycemia causes impaired functioning of
brain which relies on constant supply of glucosebrain which relies on constant supply of glucose
HypoglycemiaHypoglycemia CausesCauses of hypoglycemia in diabetics of hypoglycemia in diabetics
• Too much insulinToo much insulin
• Too much oral hypoglycemic agentToo much oral hypoglycemic agent Long half-life requires hospitalizationLong half-life requires hospitalization
• Decreased dietary intake (took insulin and missed Decreased dietary intake (took insulin and missed meal)meal)
• Vigorous physical activityVigorous physical activity PathophysiologyPathophysiology
• Inadequate blood glucose available to brain and Inadequate blood glucose available to brain and other cells resulting from one of the above causesother cells resulting from one of the above causes
HypoglycemiaHypoglycemia PresentationPresentation
• Hunger (initially), HeadacheHunger (initially), Headache• Weakness, Incoordination (Weakness, Incoordination (mimics a strokemimics a stroke))• Confusion, Unusual behaviorConfusion, Unusual behavior
may appear intoxicatedmay appear intoxicated• SeizuresSeizures• ComaComa• Weak, rapid pulseWeak, rapid pulse• Cold, clammy skinCold, clammy skin• Nervousness, trembling, irritabilityNervousness, trembling, irritability
Hypoglycemia: PathophysiologyHypoglycemia: Pathophysiology
Blood Glucose Falls
Brain Lacks Glucose SNSResponse
Altered LOCSeizures
HeadacheDizziness
Bizarre BehaviorWeakness
AnxietyPallor
TachycardiaDiaphoresis
NauseaDilated Pupils
HypoglycemiaHypoglycemia
Beta Blockers may mask symptoms by
inhibiting sympathetic
response
Management of Hypoglycemia Management of Hypoglycemia Secure airway manually Secure airway manually
• suction prnsuction prn
• Ventilate prnVentilate prn High concentration oxygenHigh concentration oxygen Vascular accessVascular access
• Large bore IV catheterLarge bore IV catheter
• Saline lock, DSaline lock, D55W or NSW or NS
• Large proximal vein preferredLarge proximal vein preferred Assess blood glucose levelAssess blood glucose level
Management of HypoglycemiaManagement of Hypoglycemia Oral glucoseOral glucose
• ONLY if intact gag reflex, awake & able to sit upONLY if intact gag reflex, awake & able to sit up• 15gm-30gm of packaged glucose, or15gm-30gm of packaged glucose, or• May use sugar-containing drink or foodMay use sugar-containing drink or food• Oral route often slowerOral route often slower
Intravenous glucoseIntravenous glucose• Adult: Dextrose 50% (DAdult: Dextrose 50% (D5050) 25gms IV in patent, free-flowing ) 25gms IV in patent, free-flowing
vein, may repeatvein, may repeat
• Children: Dextrose 25% (DChildren: Dextrose 25% (D2525) @ 2 - 4 cc/kg (0.5 - 1 gm/kg) ) @ 2 - 4 cc/kg (0.5 - 1 gm/kg)
[Infants - may choose Dextrose 10% @ 0.5 - 1 gm/kg or 5 - 10 [Infants - may choose Dextrose 10% @ 0.5 - 1 gm/kg or 5 - 10 cc/kg]cc/kg]
Management of HypoglycemiaManagement of Hypoglycemia GlucagonGlucagon
• Used if unable to obtain IV accessUsed if unable to obtain IV access
• 1 mg IM1 mg IM
• Requires glycogen storesRequires glycogen stores
• slower onset of action than IV routeslower onset of action than IV route
What persons are likely to have inadequate glycogen stores?
Management of Hypoglycemia Management of Hypoglycemia Have patient eat high-carbohydrate mealHave patient eat high-carbohydrate meal Transport?Transport?
• Patient Refusal PolicyPatient Refusal Policy Contact medical controlContact medical control Leave only with responsible family/friend for 6 hoursLeave only with responsible family/friend for 6 hours Must educate family/friend to hypoglycemic Must educate family/friend to hypoglycemic
signs/symptomssigns/symptoms Advise to contact personal physicianAdvise to contact personal physician
• TransportTransport Hypoglycemic patients on oral agents (long half life)Hypoglycemic patients on oral agents (long half life) Unknown, atypical or untreated cause of hypoglycemiaUnknown, atypical or untreated cause of hypoglycemia
Long-term Complications of Long-term Complications of Diabetes MellitusDiabetes Mellitus
BlindnessBlindness• Retinal hemorrhagesRetinal hemorrhages
Renal DiseaseRenal Disease Peripheral NeuropathyPeripheral Neuropathy
• Numbness in “stocking glove” distribution (hands Numbness in “stocking glove” distribution (hands and feet)and feet)
Heart Disease and StrokeHeart Disease and Stroke• Chronic state of Hyperglycemia leads to early Chronic state of Hyperglycemia leads to early
atherosclerosisatherosclerosis Complications in PregnancyComplications in Pregnancy
Long-term Complications of Long-term Complications of Diabetes MellitusDiabetes Mellitus
Diffuse AtheroscleroisDiffuse Atherosclerois• AMIAMI
• CVACVA
• PVDPVD HypertensionHypertension
• Renal failureRenal failure
• Diabetic Diabetic retinopathy/blindnessretinopathy/blindness
• GangreneGangrene
10% of all diabetics develop renal disease usually resulting in dialysis
Diabetics are up to 4 times more likely to have heart
disease and up to 6 times more likely to have a stroke than a
non-diabetic
Long-term Complications of Long-term Complications of Diabetes MellitusDiabetes Mellitus
Long-term Complications of Long-term Complications of Diabetes MellitusDiabetes Mellitus
Peripheral NeuropathyPeripheral Neuropathy• Silent MISilent MI
Vague, poorly-defined symptom complexVague, poorly-defined symptom complex– Weakness
– Dizziness
– Malaise
– Confusion Suspect MI in any diabetic with MI signs/symptoms Suspect MI in any diabetic with MI signs/symptoms
with or without CPwith or without CP
Diabetes in PregnancyDiabetes in Pregnancy Early pregnancy (<24 weeks)Early pregnancy (<24 weeks)
• Rapid embryo growthRapid embryo growth
• Decrease in maternal blood glucoseDecrease in maternal blood glucose
• Episodes of hypoglycemiaEpisodes of hypoglycemia
Diabetes in PregnancyDiabetes in Pregnancy Late pregnancy (>24 weeks)Late pregnancy (>24 weeks)
• Increased resistance to insulin effectsIncreased resistance to insulin effects
• Increased blood glucoseIncreased blood glucose
• KetoacidosisKetoacidosis
Diabetes in PregnancyDiabetes in Pregnancy Increased maternal risk for:Increased maternal risk for:
• Pregnancy-induced hypertensionPregnancy-induced hypertension
• Infections Infections VaginalVaginal Urinary tractUrinary tract
Diabetes in PregnancyDiabetes in Pregnancy Increased fetal risk for:Increased fetal risk for:
• High birth weightHigh birth weight
• HypoglycemiaHypoglycemia
• Liver dysfunction-hyperbilirubinemiaLiver dysfunction-hyperbilirubinemia
• Hypocalcemia Hypocalcemia
Assessment of the Diabetic Assessment of the Diabetic PatientPatient
Maintain high-degree of suspicionMaintain high-degree of suspicion Assess blood glucose level in all patients withAssess blood glucose level in all patients with
• seizure, neurologic S/S, altered mental statusseizure, neurologic S/S, altered mental status
• vague history or chief complaintvague history or chief complaint Blood glucose assessment IS NOT necessary in Blood glucose assessment IS NOT necessary in
all patients with diabetes mellitus!!all patients with diabetes mellitus!!
Assessment of the Diabetic Assessment of the Diabetic PatientPatient
History and Physical Exam includesHistory and Physical Exam includes• Look for insulin syringes, medical alert tag, Look for insulin syringes, medical alert tag,
glucometer, or insulin (usually kept in refrigerator)glucometer, or insulin (usually kept in refrigerator)
• Last meal and last insulin dose Last meal and last insulin dose
• Missed med or missed meal?Missed med or missed meal?
• Signs of infectionSigns of infection Foot cellulitis / ulcersFoot cellulitis / ulcers
• Recent illness or physiologic stressorsRecent illness or physiologic stressors
Blood Glucose AssessmentBlood Glucose Assessment Capillary vs. venous blood sampleCapillary vs. venous blood sample
• Depends on glucometer modelDepends on glucometer model
• Usually capillary preferredUsually capillary preferred Dextrostick vs GlucometerDextrostick vs Glucometer
• Dextrostick - colorimetric assessment of blood Dextrostick - colorimetric assessment of blood provides glucose estimateprovides glucose estimate
• Glucometer - quantitative glucose measurementGlucometer - quantitative glucose measurement Neonatal bloodNeonatal blood
• Many glucometers are not accurate for neonatesMany glucometers are not accurate for neonates
Case Study #1Case Study #1 You are dispatched to a college residence hall to see a You are dispatched to a college residence hall to see a
20-year-old female complaining of fever and a 20-year-old female complaining of fever and a fluttering in her chest. You find her awake but she fluttering in her chest. You find her awake but she appears very anxious. appears very anxious. • Airway - Open without assistanceAirway - Open without assistance
• Breathing - Slightly increased ventilatory rate; No obvious Breathing - Slightly increased ventilatory rate; No obvious abnormal sounds of breathingabnormal sounds of breathing
• Circulation - Rapid, strong, regular radial pulse; Skin warm Circulation - Rapid, strong, regular radial pulse; Skin warm and pinkand pink
Case Study #1Case Study #1 You direct your partner to assess vital signs while you You direct your partner to assess vital signs while you
place the patient on Oxygen 15 lpm by NRB mask. place the patient on Oxygen 15 lpm by NRB mask. Your physical exam findings are:Your physical exam findings are:• trembling, nervous trembling, nervous
• warm, flushed skinwarm, flushed skin
• clear and equal lung soundsclear and equal lung sounds Your partner relays the following vital signs to you:Your partner relays the following vital signs to you:
• Pulse - 120, regular, strongPulse - 120, regular, strong
• BP - 144/88BP - 144/88
• Ventilatory rate - 20, regular with adequate TVVentilatory rate - 20, regular with adequate TV
• Glucose - 110 mg/dlGlucose - 110 mg/dl
• ECG - Sinus tachycardia with occasional PACsECG - Sinus tachycardia with occasional PACs
What additional information regarding her history would you like to know?
Case Study #1Case Study #1 The patient states this has occurred before but never The patient states this has occurred before but never
lasted this long. She has not been ill lately other than lasted this long. She has not been ill lately other than some recurrent diarrhea and weight loss. She has some recurrent diarrhea and weight loss. She has attributed these to worrying about finals. She has no attributed these to worrying about finals. She has no significant medical history and takes no meds. She significant medical history and takes no meds. She denies use of any drugs. She has no family history of denies use of any drugs. She has no family history of pulmonary disease, diabetes or heart disease. Her pulmonary disease, diabetes or heart disease. Her mother, however, does have a problem with something mother, however, does have a problem with something in her neck for which she takes medication.in her neck for which she takes medication.
What are the two most probable diagnosis for this patient?
Case Study #2Case Study #2 You are dispatched to a residence to see a 44-year-old You are dispatched to a residence to see a 44-year-old
man who has fainted. You arrive to find him semi-man who has fainted. You arrive to find him semi-reclined in bed. He is awake and very wide-eyed but reclined in bed. He is awake and very wide-eyed but appears very tired.appears very tired.• Airway - Maintained without assistanceAirway - Maintained without assistance
• Breathing - No obvious distress; No obvious, unusual soundsBreathing - No obvious distress; No obvious, unusual sounds
• Circulation - Rapid, weak, irregular radial pulseCirculation - Rapid, weak, irregular radial pulse
Case Study #2Case Study #2• Your partner assesses vital signs while you obtain Your partner assesses vital signs while you obtain
the following history:the following history: Hx of Present Illness: For the past month, he has Hx of Present Illness: For the past month, he has
felt very weak and dizzy; He has not felt like felt very weak and dizzy; He has not felt like eating and has been losing weight. He has also eating and has been losing weight. He has also experienced N/V/D on a few days this month.experienced N/V/D on a few days this month.
Past Medical Hx: Has been fairly healthy all of Past Medical Hx: Has been fairly healthy all of his life; Three months ago he became ill with his life; Three months ago he became ill with bacterial meningitis for which he was bacterial meningitis for which he was successfully treated.successfully treated.
Case Study #2Case Study #2• Vital signs are:Vital signs are:
Pulse: 110-126, irregularPulse: 110-126, irregular BP: 92/62BP: 92/62 Ventilatory rate: 20, regularVentilatory rate: 20, regular Skin: cool, clammySkin: cool, clammy ECG: Atrial fibrillationECG: Atrial fibrillation Blood glucose: 74 mg/dlBlood glucose: 74 mg/dl
What should you include in your differential diagnosis?
Case Study #2Case Study #2• Your partner is a brand new, naïve paramedic. He Your partner is a brand new, naïve paramedic. He
comments to the patient, “That is a great tan you comments to the patient, “That is a great tan you have. Have you been on a tropical vacation lately?”have. Have you been on a tropical vacation lately?”
Now, what do you believe is the most likely diagnosis for this patient?
What is your treatment plan for this patient?
Case Study #3Case Study #3 Your last call (you hope) of the shift is to a Your last call (you hope) of the shift is to a
manufacturing plant for a possible drug overdose. manufacturing plant for a possible drug overdose. Your patient is a 24-year-old female. The patient’s Your patient is a 24-year-old female. The patient’s supervisor states the woman seems very jittery and supervisor states the woman seems very jittery and “out of it”. You find the patient to be a very thin “out of it”. You find the patient to be a very thin female who is acting unusual.female who is acting unusual.• Airway - Maintained without assistanceAirway - Maintained without assistance
• Breathing - No distress or unusual soundsBreathing - No distress or unusual sounds
• Circulation - Rapid, strong, regular radial pulse with clammy Circulation - Rapid, strong, regular radial pulse with clammy skinskin
• Disability - Confused and answers questions slowlyDisability - Confused and answers questions slowly
Case Study #3Case Study #3 Your partner quickly assesses the patient’s vital signs Your partner quickly assesses the patient’s vital signs
and relays the following:and relays the following:• Pulse - 110, regular, strongPulse - 110, regular, strong
• BP - 108/76BP - 108/76
• Ventilatory rate - 16 with clear and equal lung soundsVentilatory rate - 16 with clear and equal lung sounds
• Skin - pale, cool, clammySkin - pale, cool, clammy
• Pupils - dilated, equal and reactive to lightPupils - dilated, equal and reactive to light
• ECG - Sinus tachycardia without ectopyECG - Sinus tachycardia without ectopy HistoryHistory
• No significant medical history; No recent illness; No medsNo significant medical history; No recent illness; No meds
What would you like to include in your differential diagnosis for this patient?
Case Study #3Case Study #3 A coworker now tells you that the patient is going A coworker now tells you that the patient is going
through a difficult divorce and has not been eating well through a difficult divorce and has not been eating well latelylately
Your partner now tells you the patient’s blood glucose Your partner now tells you the patient’s blood glucose is 40 mg/dlis 40 mg/dl
Would this patient be a good candidate for Glucagon therapy if an IV can not be established quickly?
What is your specific diagnosis now?