the endocrine system prof f ammari frcp jusr university

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


• 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


• 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


• 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 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 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


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


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


PheochromocytomaPheochromocytoma• Catecholamine secreting tumor of adrenal medullaCatecholamine secreting tumor of adrenal medulla

• PresentationPresentation AnxietyAnxiety Pallor, diaphoresisPallor, diaphoresis HypertensionHypertension Tachycardia, PalpitationsTachycardia, Palpitations DyspneaDyspnea HyperglycemiaHyperglycemia


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)


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


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


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


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


Increased Blood Sugar

Osmotic Diuresis

Polyuria

PolydipsiaVolume DepletionShock

Inadequate insulin


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


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



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?

the endocrine system prof f ammari frcp jusr university

Documents

hormone fshfemales

concentration of hormone

endocrine systemfigure

endocrine glandsact

tsh releasehypothyroidism

target organs

pituitary glandfigure

base of brain