endocrine system hormonal feed back mechanism

Endocrine SystemEndocrine System

Hormonal feed back Hormonal feed back mechanismmechanism

Endocrine GlandsEndocrine Glands Controls many body functionsControls many body functions

• exerts control by releasing special exerts control by releasing special chemical substances into the blood chemical substances into the blood called called hormoneshormones

• Hormones Hormones affect other endocrine glands affect other endocrine glands or body systemsor body systems

Ductless glandsDuctless glands Secrete hormones directly into Secrete hormones directly into

bloodstreambloodstream• Hormones are quickly distributed by Hormones are quickly distributed by

bloodstream throughout the bodybloodstream throughout the body

Hormones= substance released from Hormones= substance released from cells that circulates and affect cells that circulates and affect distant organsdistant organs

Physiologic functions of hormones:Physiologic functions of hormones: - growth- growth - maintenance of homeostasis- maintenance of homeostasis - reproductionreproduction

HormonesHormones Chemicals produced by endocrine Chemicals produced by endocrine

glandsglands Act on target organs elsewhere in Act on target organs elsewhere in

bodybody Control/coordinate widespread Control/coordinate widespread

processes: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 Polypeptides (amino acid

derivatives)derivatives)• Lipids (fatty acid derivatives or Lipids (fatty acid derivatives or

steroids)steroids)

HormonesHormones Amount of hormone reaching target Amount of hormone reaching target

tissue directly correlates with tissue directly correlates with concentration of hormone in blood.concentration of 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 Consists of several glands located in

various parts of the bodyvarious parts of the body Specific GlandsSpecific Glands

• HypothalamusHypothalamus• PituitaryPituitary• ThyroidThyroid• ParathyroidParathyroid• AdrenalAdrenal• KidneysKidneys• Pancreatic IsletsPancreatic Islets• OvariesOvaries• TestesTestes

Pituitary GlandPituitary Gland

Small gland located on stalk hanging Small gland located on stalk hanging from base of brain - from base of brain - AKAAKA

““The Master Gland” The Master Gland” • Primary function is to control other Primary function is to control other

glands.glands.• Produces many hormones.Produces many hormones.• Secretion is controlled by Secretion is controlled by

hypothalamus in base of brain.hypothalamus in base of brain.

Pituitary gland Anterior lobe -ACTH-ACTH -growth hormone-growth hormone -follicular st hormone-follicular st hormone -lactinogenic hormone-lactinogenic hormone -thyroid stimulating H-thyroid stimulating H -melanocyte -melanocyte

stimulating Hormonestimulating Hormone -interstitial -interstitial

stimulating Hormonestimulating Hormone

Posterior lobe -antidiuretic -antidiuretic

hormone:hormone: regulate flow of regulate flow of

water through the water through the kidneykidney

-oxytocin: contract -oxytocin: contract uterusuterus

Pituitary GlandPituitary Gland Two areasTwo areas

• Anterior PituitaryAnterior Pituitary• Posterior PituitaryPosterior Pituitary

Structurally, functionally differentStructurally, functionally different

Pituitary GlandPituitary Gland Anterior PituitaryAnterior Pituitary

• Thyroid-Stimulating Hormone (TSH)Thyroid-Stimulating Hormone (TSH) stimulates release of hormones from stimulates release of hormones from

ThyroidThyroid– 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 stimulates growth of all organs and

increases blood glucose increases blood glucose concentrationconcentration

– decreases glucose usage– increases consumption of fats as an energy

source

• Adreno-Corticotrophic Hormone (ACTH)Adreno-Corticotrophic Hormone (ACTH) stimulates the release of adrenal stimulates the release of adrenal

cortex hormonescortex hormones


• Follicle Stimulating Hormone (FSH)Follicle Stimulating Hormone (FSH) females - stimulates maturation of females - stimulates maturation of

ova; release of estrogenova; release of estrogen males - stimulates testes to grow; males - stimulates testes to grow;

produce spermproduce sperm• Luteinizing Hormone (LH)Luteinizing Hormone (LH)

females - stimulates ovulation; females - stimulates ovulation; growth of corpus luteumgrowth of corpus luteum

males - stimulates testes to secrete males - stimulates testes to secrete testosteronetestosterone


• ProlactinProlactin stimulates breast development stimulates breast development

during pregnancy; milk production during pregnancy; milk production after deliveryafter delivery

• Melanocyte Stimulating Hormone Melanocyte Stimulating Hormone (MSH)(MSH)

stimulates synthesis, dispersion of stimulates synthesis, dispersion of melanin pigment in skinmelanin pigment in skin

Pituitary GlandPituitary Gland Posterior PituitaryPosterior Pituitary

• Stores, releases two hormones Stores, releases two hormones produced in hypothalamusproduced in hypothalamus

Antidiuretic hormone (ADH)Antidiuretic hormone (ADH) OxytocinOxytocin

Pituitary GlandPituitary Gland egnancy (Pitocin®); release of milk from breastegnancy (Pitocin®); release of milk from breast

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 Stimulates contraction of uterus at end of

prpr

hyperpituitrismhyperpituitrismIN CHILDREN : GIGANTISM

-Before closure of epiphysis(before puberty)

-Increase bone length,width proportionally

-Patient have monstrous size

IN ADULT: ACROMEGALLY

-After closure of epiphesis (after puberty)

-Periosteal overgrowth,cortical thikening

-hands and fingers enlargement

-increase size of cranium

-symptoms of arthralgia,headacke

ORALLY: -overgrowth of mandible, prognathism=lantern jaw

-accelerated dental development

-marked thikening of cranium

-sinus enlargement

-lips and nose enlarged

-in acromegaly , there is classIII malocclusion

-flattened palate

-enlarged tongue with identation on lateral borders

-spacing of teeth

- Dental radiograph =large pulp chamber( taurodontism)

TREATMENT:

surgery and radiotherapy

hypofunctionhypofunctionA-IN CHILDREN

leads to dwarfism

-growth retard ration ,most patient have normal birth length,weight

-growth retard ration not noticed until 2,3 years

-hypoglycemia and lack of cortisol

-delayed puberty,with normal body proportion

ORAL FEATURES:

-mandible under developed

-severe malocclusion,crowding of teeth

-delayed teeth eruption

-over retard ration of primary teeth

-incomplete oxcification of permanent teeth

TREATMENT:

-use of growth hormone

B-IN ADULTS:

-usually 2ry to tumors or disease of pituitary gland

-treated by surgery or radiotherapy

HypothalamusHypothalamus Also responsible for:Also responsible for:

• Regulation of water balanceRegulation of water balance• Esophageal swallowingEsophageal swallowing• Body temperature regulation Body temperature regulation

(shivering)(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

Thyroid glandThyroid gland

ThyroidThyroid Located below larynx and Located below larynx and

low in necklow in neck• Not over the thyroid Not over the thyroid

cartilagecartilage Thyroxine (TThyroxine (T44) and ) and

Triiodothyronine (TTriiodothyronine (T33))• Stimulate metabolism of all Stimulate metabolism of all

cellscells CalcitoninCalcitonin

• Decreases blood calcium Decreases blood calcium concentration by inhibiting concentration by inhibiting breakdown of bonebreakdown of bone

ParathyroidsParathyroids Located on posterior Located on posterior

surface of thyroidsurface of thyroid Frequently damaged Frequently damaged

during thyroid surgeryduring thyroid surgery Parathyroid hormone Parathyroid hormone

(PTH)(PTH)• Stimulates CaStimulates Ca2+2+ release from release from

bonebone• Promotes intestinal Promotes intestinal

absorption and renal tubular absorption and renal tubular reabsorption of calciumreabsorption of calcium

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 Bones, stones, hypertones, abdominal moansmoans””

Thymus GlandThymus Gland

Located in anterior chest Located in anterior chest Normally absent by ~ age 4Normally absent by ~ age 4 Promotes development of Promotes development of

immune-system cells (T-immune-system cells (T-lymphocytes)lymphocytes)

Adrenal GlandsAdrenal Glands

Small glands Small glands located near located near (ad) the kidneys (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 the Adrenal Medulla secretes the catecholamine hormones catecholamine hormones norepinephrinenorepinephrine and and epinephrineepinephrine

• Epinephrine and NorepinephrineEpinephrine and Norepinephrine Prolong and intensify the sympathetic nervous Prolong and intensify the sympathetic nervous

system response during stresssystem response during stress

Adrenal GlandsAdrenal Glands Adrenal CortexAdrenal Cortex

• Aldosterone (Mineralocorticoid)Aldosterone (Mineralocorticoid) Regulates electrolyte (potassium, sodium) Regulates electrolyte (potassium, sodium)

and fluid homeostasisand fluid homeostasis

• Cortisol (Glucocorticoids)Cortisol (Glucocorticoids) Antiinflammatory, anti-immunity, and Antiinflammatory, anti-immunity, and

anti-allergy effects.anti-allergy effects. Increases blood glucose Increases blood glucose

concentrationsconcentrations• 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 accounts for 95% of adrenal cortex hormone productionhormone production

the level of glucose in the bloodthe level of glucose in the blood Released in response to stress, Released in response to stress,

injury, or serious infection - like the injury, or serious infection - like the hormones from the adrenal medullahormones from the adrenal medulla


Adrenal CortexAdrenal Cortex• MineralcorticoidsMineralcorticoids

work to regulate the concentration work to regulate the concentration of potassium and sodium in the bodyof potassium and sodium in the body

OvariesOvaries Located in the abdominal cavity Located in the abdominal cavity

adjacent to the uterusadjacent to the uterus Under the control of LH and FSH Under the control of LH and FSH

from the anterior pituitaryfrom the anterior pituitary Produce eggs for reproductionProduce eggs for reproduction Produce hormonesProduce hormones

• estrogenestrogen• progesteroneprogesterone• Functions include sexual development Functions include sexual development

and preparation of the uterus for and preparation of the uterus for implantation of the eggimplantation of the egg

OvariesOvaries EstrogenEstrogen

• Development of female secondary Development of female secondary sexual characteristicssexual characteristics

• Development of endometriumDevelopment of endometrium ProgesteroneProgesterone

• Promotes conditions required for Promotes conditions required for pregnancypregnancy

• Stabilization of endometriumStabilization of endometrium

TestesTestes Located in the scrotumLocated in the scrotum Controlled by anterior pituitary Controlled by anterior pituitary

hormones FSH and LHhormones FSH and LH Produce sperm for reproductionProduce sperm for reproduction Produce testosterone -Produce testosterone -

• promotes male growth and promotes male growth and masculinizationmasculinization

• promotes development and maintenance promotes development and maintenance of male sexual characteristicsof male sexual characteristics

PancreasPancreas Located in retroperitoneal space between Located in retroperitoneal space between

duodenum and spleenduodenum and spleen Has both endocrine and exocrine Has both endocrine and exocrine

functionsfunctions• 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 Disorders of the Endocrine SystemEndocrine System

Thyroid glandThyroid gland

Thyroid functionThyroid function

Thyroid hormone important for:

-normal growth,maturation

-affect O2 consumption

-protein synthesis in the body

Toxic goitreToxic goitre

Etiology:

-severe emotional trauma or infection

-immunologic cause

- or circulating thyroid stimulator in pt serum called long acting thyroid stimulator which act as antibody,

-affects middle-aged women

-characterized by a syndro

1)nodular thyroid enlargemen 2)exophthalmos 3)peritibial myxedema

CLINICAL FEATURE:

-exophthalmoses producing vision problem -peritibial myxoedema -if untreated lead to thyroid storm:

-this condition is precipitated by infection,trauma,dental surgery under local anesthesia

-rapid onset of muscle ,weakness ,fatigue ,fever , nausea, vomiting, abdominal pain,profuse swatting ,marked tachycardia, congestive heart failure,cardiac arrhythmias, hypotension may develop and can cause death

ORALLY: -no pathologic changes

DENTAL CONSIDERATION:

-it is contraindicated to use local anesthesia with epinephrine

Abnormal Thyroid Abnormal Thyroid FunctionFunction HypothyroidismHypothyroidism

•Too little thyroid hormoneToo little thyroid hormone HyperthyroidismHyperthyroidism

(Thyrotoxicosis / Thyroid (Thyrotoxicosis / Thyroid Storm)Storm)•Too much thyroid hormoneToo much thyroid hormone

HypothyroidismHypothyroidism Thyroid hormone deficiency causing Thyroid hormone deficiency causing

a decrease in the basal metabolic a decrease in the basal metabolic raterate• 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 Hashimoto’s thyroiditis - autoimmune

destructiondestruction

hypothyroidismhypothyroidism

In children=cretinism

In adult=Myxedema

1)young juvenile myxedema

2)adult myxodema

cretinismcretinism

-Result from not enough iodine in mother’s diet

-or congenital partial absence of thyroid tissue

CLINICAL FEATURE:

-lack of normal physical development and activity

-delayed mental development

-child has facial expression ,head to large for

the rest of the body

-skin dry and wrinkly

-thickened lip

-increases size of the tongue leading to open mouth

-voice is coarse and hoarse

ORALLY:

-Malocclusion

-widening of dental arch with spacing of teeth

-extensive gingival enlargement

-enlarged tongue,tendency to early periodontal disaese

myxedemamyxedema

1) JUVENILE

-there is loss of concentration

-there is no permanent retard ration of mental development as cretinism

-tissues have pseudo edematous appearance not pit on pressure

-general retard ration of osseous development and marked change of body structure

ORALLY:

-retard ration of tooth eruption

-teeth are poorly formed and susceptible to carries

-faulty jaw development leading to overlapping of teeth, malocclusion, facial disharmony

ADULT MYXEDEMA:

-occur mainly in women at menopause

-pt easily fatigued

-lack of attention to surrounding

-general mental inactivity

-pt has poor appetite but put on weight

-there is non pitting oedema especially in face

-skin dry and scaly,brittle thin hair

-blood pressure and pulse are low

-low basal metabolic rate

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 Non-pitting peripheral

edemaedema DepressionDepression Facial edema, loss of hairFacial edema, loss of hair Dry, coarse skinDry, coarse skin

Appearance of Myxedema

hypothyroidism

In children=cretinism

In adult=Myxedema

1)young juvenile myxedema

2)adult myxodema

HypothyroidismHypothyroidism Myxedema ComaMyxedema Coma

• Severe hypothyroidism that can be Severe hypothyroidism that can be fatalfatal

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 Excessive levels of thyroid levels

cause hypermetabolic statecause hypermetabolic state• Person is “sped up”.Person is “sped up”.

Causes of HyperthyroidismCauses of Hyperthyroidism• Overmedication with levothyroxine Overmedication with levothyroxine

(Synthroid®) - Fad diets(Synthroid®) - Fad diets• Goiter (enlarged, hyperactive thyroid Goiter (enlarged, hyperactive thyroid

gland)gland)• Graves DiseaseGraves Disease

HyperthyroidismHyperthyroidism Nervousness, irritable, Nervousness, irritable,

tremors, paranoidtremors, paranoid Warm, flushed skinWarm, flushed skin Heat intolerantHeat intolerant Tachycardia - High output Tachycardia - High output

CHFCHF HypertensionHypertension TachypneaTachypnea DiarrheaDiarrhea Weight lossWeight loss ExophthalmosExophthalmos GoiterGoiter

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 Usually short-term use prior to more definitive treatmentdefinitive treatment

• SSKI® (potassium iodide)SSKI® (potassium iodide)

Thyroid Thyroid Storm/ThyrotoxicosisStorm/Thyrotoxicosis

Severe form of hyperthyroidism Severe form of hyperthyroidism that can be fatalthat can be fatal• Acute life-threatening hyperthyroidismAcute life-threatening hyperthyroidism

CauseCause• Increased physiological stress in Increased physiological stress in

hyperthyroid patientshyperthyroid patients


Severe tachycardiaSevere tachycardia Heart FailureHeart Failure DysrhythmiasDysrhythmias ShockShock HyperthermiaHyperthermia Abdominal painAbdominal pain Restlessness, Agitation, Delirium, Restlessness, Agitation, Delirium,

ComaComa


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)

The parathyroid glandsThe parathyroid glands

This gland control the calcium metabolism by mobilysing this substance from the bones into the blood stream and maintaining the normal Ca level of 9-11.5 mg\100ml blood

Normal shape

Abnormal shape

Parathyroid gland

HyperparathyroidismHyperparathyroidism“Osteitis fibrosa cystica”

1-Due to hyperplasia or neoplasm of parathyro 2-more in female over 40y

3-there is increased osteoclastic activity cause:

*osteoporosis ,fibrous degeneration, cyst formation

4 -there is bone pain,pathologic fracture

5-renal calculi,back pain

6-urinary tract infection

oral radiograohic changes:

1-there is decalcification or cyst unrelated to the apices of the teeth

2-the skull have a ground glass,mouth eaten or sa paper appearance

3-there is loss of lamina dura and indisti pattern of alveolus ,mandible

4-there is drifting and looseness of teeth formation

5 -single or multiple radioluscencies or cyst formathe jaws

hypoparathyroidismhypoparathyroidismCause metabolic disturbance leads to

hypocalcaemia and increase neuromuscular excitability

hypoparathyroidismhypoparathyroidism

1)Digeorge 1)Digeorge syndromesyndrome

Congenital Congenital absence of absence of parathyroid,thyrparathyroid,thyroid gland,aortic oid gland,aortic arch arch anomalies,congeanomalies,congenital heart nital heart defectdefect

2)Idiopathic2)Idiopathic Unknown Unknown

etiology,may be etiology,may be congenitalcongenital

hypoparathyroidismhypoparathyroidism

3)Postoperative3)Postoperative RemoRemoval or val or

injury of injury of parathyroid parathyroid gland during gland during surgicalsurgical removal of removal of thyroidthyroid

4)pseudohypotyr4)pseudohypotyroidioidimm

-genetic effect-genetic effect -normal -normal

parathyroid gland parathyroid gland but defect exist but defect exist in the target in the target organ(bone,kidneorgan(bone,kidneyy))

Clinical featureClinical feature

1 -hypocalcaemia present give tetany, parasthesia of

lip ,tongue ,fingers

2 -twitching of facial muscles (chvostek’sign)

3-tapping of facial nerve

4-carpopedal spasm (trouseau’s sign)

5-muscle weakness, cramps, heart palpitation

6-abnormalities of hair,skin,teeth

7-annorexia,nausia,vomiting,peptic ulcer

8-hypercalcemia in bone may cause:

* muscle wekness, fatigue, weight loss

and cardia irregularities

ORALLY: -enamel hypoplasia, abnormal

dentine formation

DIAGNOSIS: -serum calcium decreased below

7mg\100ml

-serum phosphorous elevated

Adrenal glandAdrenal gland

Adrenal Adrenal medullamedulla

1)epinephrine1)epinephrine 2)norepinephrin2)norepinephrin

ee

Adrenal cortexAdrenal cortex 1)glucocorticoid1)glucocorticoid

ss (cortisol)(cortisol) 2)mineralocortic2)mineralocortic

oidsoids

(aldosterone)(aldosterone) 3)sex hormone3)sex hormone

Abnormal Adrenal Abnormal Adrenal Function Function

HyperadrenalismHyperadrenalism• Excess activity of the adrenal glandExcess activity of the adrenal gland• Cushing’s Syndrome & DiseaseCushing’s Syndrome & Disease• PheochromocytomaPheochromocytoma

Hypoadrenalism (adrenal Hypoadrenalism (adrenal insufficiency)insufficiency)• Inadequate activity of the adrenal Inadequate activity of the adrenal

glandgland• Addison’s diseaseAddison’s disease

HyperadrenalismHyperadrenalism

Primary Aldosteronism Primary Aldosteronism • Excessive secretion of aldosterone by Excessive secretion of aldosterone by

adrenal cortexadrenal 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 especially those with androgenic or estrogenic effectsestrogenic 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 Results from increased adrenocortical secretion of cortisolsecretion of cortisol

• 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 excess secretion of ACTH by a neoplasm

within the adrenal cortexwithin the adrenal cortex excess secretion of ACTH by a malignant excess secretion of ACTH by a malignant

growth outside the adrenal glandgrowth outside the adrenal gland excessive or prolonged administration of excessive or prolonged administration of

steroidssteroids

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 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 Assess for cardiovascular event

requiring treatmentrequiring treatment– severe hypertension– myocardial ischemia


PheochromocytomaPheochromocytoma• Catecholamine secreting tumor of Catecholamine secreting tumor of

adrenal medullaadrenal medulla• PresentationPresentation

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


PheochromocytomaPheochromocytoma• ManagementManagement

Supportive care based upon Supportive care based upon presentationpresentation

Airway/Ventilation/OxygenAirway/Ventilation/Oxygen Calm/ReassureCalm/Reassure Assess blood glucose Assess blood glucose Consider beta blocking agent - Consider beta blocking agent -

LabetalolLabetalol Consider benzodiazepinesConsider benzodiazepines

HypoadrenalismHypoadrenalism

Adrenal InsufficiencyAdrenal Insufficiency• decrease production of glucocorticoids, decrease production of glucocorticoids,

mineralcorticoids and androgensmineralcorticoids and androgens CausesCauses

• Primary adrenal failure Primary adrenal failure (Addison’s (Addison’s Disease)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, areas exposed to sun, pressure points, joints and creasesjoints 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 Assess blood glucose - D50 if

hypoglycemichypoglycemic• Steroids Steroids

hydrocortisone or dexamethasonehydrocortisone or dexamethasone florinef (mineralcorticoid)florinef (mineralcorticoid)

• Vasopressors if unresponsive to IV fluidsVasopressors if unresponsive to IV fluids

Side effect of Side effect of corticosteroid therapycorticosteroid therapy

1-Interferance with the immunological defence mechanism

2-long term use cause suppression and atrophy of adrenal cortex

3-Osteoporosis occur

4-Congestive heart failure and hypertensive 5__cardiovascular disaese may occur

DiabetesDiabetes

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 ) cells of the

islets of Langerhans in the pancreas, AND/ORislets of 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 The other 3 major food sources for

glucose areglucose are• carbohydratescarbohydrates• proteinsproteins• fatsfats

Most sugars in the human diet are Most sugars in the human diet are complex and must be broken down complex and must be broken down into simple sugars: glucose, into simple sugars: glucose, galactose and fructose - before usegalactose 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, If not “burned” immediately by body,

stored in liver and skeletal muscle as stored in liver and skeletal muscle as glycogen (short-term energy) or as glycogen (short-term energy) or as fat (long-term energy needs)fat (long-term energy needs)

• After normal meal, approximately After normal meal, approximately 60% of the glucose is stored in liver 60% of the glucose is stored in liver as glycogenas glycogen

Regulation of GlucoseRegulation of Glucose

FatsFats• Broken down into fatty acids and Broken down into fatty acids and

glycerol by enzymesglycerol by enzymes• Excess fat stored in liver or in fat Excess fat stored in liver or in fat

cells (under the skin)cells (under the skin)


Pancreatic hormones are required Pancreatic hormones are required to regulate blood glucose levelto regulate blood 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 to

control blood glucose levelcontrol blood glucose level• When blood glucose levels fall, When blood glucose levels fall, cells cells

the amount of glucagon in the blood the amount of glucagon in the blood• The surge of glucagon stimulates liver The surge of glucagon stimulates liver

to release glucose stores by the to release glucose stores by the breakdown of glycogen into glucose breakdown of glycogen into glucose (glycogenolysis)(glycogenolysis)

• Also, glucagon stimulates the liver to Also, glucagon stimulates the liver to produce glucose (gluconeogenesis)produce glucose (gluconeogenesis)

Regulation of GlucoseRegulation of Glucose Beta Cells Beta Cells (() ) release release insulin insulin

(antagonistic to glucagon) to (antagonistic to glucagon) to control blood glucose levelcontrol blood glucose level• Insulin Insulin the rate at which various body the rate at which various body

cells take up glucose cells take up glucose insulin lowers insulin lowers the blood glucose level the blood glucose level

• Promotes glycogenesis - storage of Promotes glycogenesis - storage of glycogen in the liverglycogen in the liver

• Insulin is rapidly broken down by the Insulin is rapidly broken down by the liver and must be secreted constantlyliver and must be secreted constantly

Regulation of GlucoseRegulation of Glucose Delta Cells (Delta Cells () produce ) produce

somatostatin, somatostatin, which inhibits both which inhibits both glucagon and insulinglucagon and insulin• inhibits insulin and glucagon secretion inhibits insulin and glucagon secretion

by the pancreasby the pancreas• inhibits digestion by inhibiting inhibits digestion by inhibiting

secretion of digestive enzymessecretion of digestive enzymes• inhibits gastric motilityinhibits gastric motility• inhibits absorption of glucose in the inhibits absorption of glucose in the

intestineintestine

Regulation of GlucoseRegulation of Glucose Breakdown of sugars carried out by Breakdown of sugars carried out by

enzymes in the GI systemenzymes in the GI system• As simple sugars, they are absorbed As simple sugars, they are absorbed

from the GI system into the bodyfrom the GI system into the body To be converted into energy, To be converted into energy,

glucose must first be transmitted glucose must first be transmitted through the cell membranethrough the cell membrane• Glucose molecule is too large and does Glucose molecule is too large and does

not readily diffusenot readily diffuse

Regulation of GlucoseRegulation of Glucose Glucose must pass into the cell by Glucose must pass into the cell by

binding to a special carrier protein on binding to a special carrier protein on the cell’s surface. the cell’s surface. • Facilitated diffusion - Facilitated diffusion - carrier protein binds carrier protein binds

with the glucose and carries it into the cell.with the glucose and carries it into the cell. The rate at which glucose can enter The rate at which glucose can enter

the cell is dependent upon insulin the cell is dependent upon insulin levelslevels• Insulin serves as the messenger - travels Insulin serves as the messenger - travels

via blood to target tissuesvia blood to target tissues• Combines with specific insulin receptors on Combines with specific insulin receptors on

the surface of the cell membranethe surface of the cell membrane


Body strives to maintain blood Body strives to maintain blood glucose between 60 mg/dl and 120 glucose between 60 mg/dl and 120 mg/dl.mg/dl.

GlucoseGlucose• brain is the biggest user of glucose in brain is the biggest user of glucose in

the bodythe body• sole energy source for brainsole energy source for brain• brain does not require insulin to utilize brain does not require insulin to utilize

glucoseglucose


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 Decreasing blood glucose

concentrationconcentration

• Acts primarily on liver to increase Acts primarily on liver to increase rate of glycogen breakdownrate of glycogen breakdown

• Increasing blood glucose levels Increasing blood glucose levels have inhibitory effect on have inhibitory effect on glucagon secretionglucagon 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 Acts on cell membranes to increase glucose uptake from blood streamglucose uptake from blood stream

• Promotes facilitated diffusion of Promotes facilitated diffusion of glucose into cellsglucose into cells

Diabetes MellitusDiabetes Mellitus 2 Types historically based on age of 2 Types historically based on age of

onset (NOT insulin vs. non-insulin)onset (NOT 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 Types of Diabetes MellitusMellitus

Type IType I Type IIType II SecondarySecondary GestationalGestational

Pathophysiology of Pathophysiology of Type I Diabetes MellitusType I Diabetes Mellitus

Characterized by inadequate or absent Characterized by inadequate or absent production of insulin by pancreasproduction of 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 body destroys own insulin-producing cells in pancreaspancreas

• 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 Onset usually after age 25 in overweight adultsadults• Some morbidly obese children develop Type II Some morbidly obese children develop Type II

diabetesdiabetes 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 Secondary Diabetes MellitusMellitus

Pre-existing condition affects Pre-existing condition affects pancreaspancreas• PancreatitisPancreatitis• TraumaTrauma

Gestational Diabetes Gestational Diabetes MellitusMellitus

Occurs during pregnancyOccurs during pregnancy• Usually resolves after deliveryUsually resolves after delivery

Occurs rarely in non-pregnant Occurs rarely in non-pregnant women on BCPswomen on BCPs

Increased estrogen, progesterone Increased estrogen, progesterone antagonize insulinantagonize insulin

Presentation of New Presentation of New Onset Diabetes MellitusOnset Diabetes Mellitus 3 Ps3 Ps

• PolyuriaPolyuria• PolydipsiaPolydipsia• PolyphagiaPolyphagia

Blurred vision, dizziness, altered Blurred vision, dizziness, altered mental statusmental 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 Currently genetic engineering has lead to

human insulin (Humulin) human insulin (Humulin)

Long Term Treatment ofLong Term Treatment ofDiabetes MellitusDiabetes Mellitus

InsulinInsulin• Available in various forms distinguished Available in various forms distinguished

on onset and duration of actionon onset and duration 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 Must be given by injection as insulin is

protein which would be digested if protein which would be digested if given orallygiven orally

extremely compliant patients may extremely compliant patients may use an insulin pump which provides use an insulin pump which provides a continuous dosea continuous dose

current research studying inhaled current research studying inhaled insulin forminsulin form

Long Term Treatment of Long Term Treatment of Diabetes MellitusDiabetes Mellitus

Oral Hypoglycemic AgentsOral Hypoglycemic Agents• Stimulate the release of insulin from Stimulate the release of insulin from

the pancreas, thus patient must still the pancreas, thus patient must still have intact have intact betabeta cells in the pancreas. cells in the pancreas.

• Common agents includeCommon agents include:: Glucotrol® (glipizide)Glucotrol® (glipizide) Micronase® or Diabeta® Micronase® or Diabeta® (glyburide)(glyburide)

Glucophage® (metformin) [Not Glucophage® (metformin) [Not a sulfonylurea]a sulfonylurea]

Emergencies Emergencies Associated Blood Associated Blood

Glucose LevelGlucose Level HyperglycemiaHyperglycemia

• Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA)• Hyperglycemic Hyperosmolar Hyperglycemic Hyperosmolar

Nonketotic Coma (HHNC)Nonketotic Coma (HHNC) Hypoglycemia Hypoglycemia

• ““Insulin Shock”Insulin Shock”

HyperglycemiaHyperglycemia Defined as blood glucose > 200 Defined as blood glucose > 200

mg/dl 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 Two hyperglycemic diabetic

states may occurstates may occur• Diabetic Ketoacidosis (DKA)Diabetic Ketoacidosis (DKA)• Hyperglycemic Hyperosmolar Hyperglycemic Hyperosmolar

Non-ketotic Coma (HHNC)Non-ketotic Coma (HHNC)

Diabetic Ketoacidosis Diabetic Ketoacidosis (DKA)(DKA)

Occurs in Type I diabetics (insulin Occurs in Type I diabetics (insulin dependency)dependency)

UsuallyUsually associated with blood associated with blood glucose level in the range of 200 - glucose level in the range of 200 - 600 mg/dl600 mg/dl

No insulin availability results in No insulin availability results in ketoacidosisketoacidosis


PathophysiologyPathophysiology• Results from absence of insulinResults from absence of insulin

prevents glucose from entering the prevents glucose from entering the cellscells

leads to glucose accumulation in the leads to glucose accumulation in the bloodblood

• Cells become starved for glucose and Cells become starved for glucose and begin to use other energy sources begin to use other energy sources (primarily fats)(primarily fats)

Fat metabolism generates fatty acidsFat metabolism generates fatty acids Further metabolized into ketoacids Further metabolized into ketoacids

(ketone bodies)(ketone bodies)


Pathophysiology (cont)Pathophysiology (cont)• Blood sugar rises above renal threshold Blood sugar rises above renal threshold

for reabsorption (blood glucose > 180 for reabsorption (blood glucose > 180 mg/dl)mg/dl)

glucose “spills” into the urineglucose “spills” into the urine Loss of glucose in urine causes Loss of glucose in urine causes

osmotic diuresisosmotic 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 NRB Airway/Ventilation/Oxygen NRB

maskmask 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 Hyperosmolar Hyperglycemic Hyperglycemic

Nonketotic Coma Nonketotic Coma (HHNC)(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 Hyperosmolar Hyperglycemic Hyperglycemic

Nonketotic Coma Nonketotic Coma (HHNC)(HHNC)

PathophysiologyPathophysiology• Some minimal insulin productionSome minimal insulin production

enough insulin available to allow glucose enough insulin available to allow glucose to enter the cells and prevent ketogenesisto enter the cells and prevent ketogenesis

not enough to decrease gluconeogenesis not enough to decrease gluconeogenesis by liverby liver

no ketosisno ketosis• Extreme hyperglycemia produces Extreme hyperglycemia produces

hyperosmolar state causinghyperosmolar state causing 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 Bicarbonate (severe cases documented by

ABG)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 therapy is startedonce therapy 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 block glucose synthesis in liver (gluconeogenesis)(gluconeogenesis)

Hypoglycemia causes impaired functioning Hypoglycemia causes impaired functioning of brain which relies on constant supply of of brain which relies on constant supply of glucoseglucose

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 Decreased dietary intake (took insulin and

missed meal)missed meal)• Vigorous physical activityVigorous physical activity

PathophysiologyPathophysiology• Inadequate blood glucose available to brain Inadequate blood glucose available to brain

and other cells resulting from one of the and other cells resulting from one of the above causesabove 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: Hypoglycemia: PathophysiologyPathophysiology

Blood Glucose Falls

Brain Lacks Glucose SNSResponse

Altered LOCSeizures

HeadacheDizzinessBizarre

BehaviorWeakness

AnxietyPallor

TachycardiaDiaphoresis

NauseaDilated Pupils

HypoglycemiaHypoglycemia

Beta Blockers may mask symptoms by

inhibiting sympathetic

response

Management of Management of Hypoglycemia 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 Management of HypoglycemiaHypoglycemia

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, ) 25gms IV in patent,

free-flowing vein, may repeatfree-flowing vein, may repeat

• Children: Dextrose 25% (DChildren: Dextrose 25% (D2525) @ 2 - 4 cc/kg (0.5 - ) @ 2 - 4 cc/kg (0.5 - 1 gm/kg) [Infants - may choose Dextrose 10% 1 gm/kg) [Infants - may choose Dextrose 10% @ 0.5 - 1 gm/kg or 5 - 10 cc/kg@ 0.5 - 1 gm/kg or 5 - 10 cc/kg]]

Management of Management of HypoglycemiaHypoglycemia

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 Management of Hypoglycemia 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 Unknown, atypical or untreated cause of

hypoglycemiahypoglycemia

Long-term Long-term Complications of Complications of Diabetes MellitusDiabetes Mellitus BlindnessBlindness

• Retinal hemorrhagesRetinal hemorrhages Renal DiseaseRenal Disease Peripheral NeuropathyPeripheral Neuropathy

• Numbness in “stocking glove” Numbness in “stocking glove” distribution (hands and feet)distribution (hands and feet)

Heart Disease and StrokeHeart Disease and Stroke• Chronic state of Hyperglycemia leads Chronic state of Hyperglycemia leads

to early atherosclerosisto early atherosclerosis Complications in PregnancyComplications in Pregnancy

Long-term Long-term Complications of Complications of Diabetes MellitusDiabetes Mellitus Diffuse Diffuse

AtheroscleroisAtherosclerois• AMIAMI• CVACVA• PVDPVD

HypertensionHypertension• Renal failureRenal failure• Diabetic Diabetic

retinopathy/blindneretinopathy/blindnessss

• 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 Long-term Complications of Complications of Diabetes MellitusDiabetes Mellitus

Long-term Long-term Complications of 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 diSuspect MI in any diabetic with MI abetic with MI signs/symptoms with or without CPsigns/symptoms with or without CP

Diabetes in PregnancyDiabetes in Pregnancy Early pregnancy (<24 Early pregnancy (<24

weeks)weeks)•Rapid embryo growthRapid embryo growth•Decrease in maternal blood Decrease in maternal blood

glucoseglucose•Episodes of hypoglycemiaEpisodes of hypoglycemia

Diabetes in PregnancyDiabetes in Pregnancy Late pregnancy (>24 Late pregnancy (>24

weeks)weeks)• Increased resistance to Increased resistance to

insulin effectsinsulin effects• Increased blood glucoseIncreased blood glucose•KetoacidosisKetoacidosis

Diabetes in PregnancyDiabetes in Pregnancy Increased maternal risk for:Increased maternal risk for:

•Pregnancy-induced Pregnancy-induced hypertensionhypertension

• 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-Liver dysfunction-

hyperbilirubinemiahyperbilirubinemia•Hypocalcemia Hypocalcemia

Assessment of the Assessment of the Diabetic PatientDiabetic Patient

Maintain high-degree of suspicionMaintain high-degree of suspicion Assess blood glucose level in all Assess blood glucose level in all

patients withpatients with• seizure, neurologic S/S, altered mental seizure, neurologic S/S, altered mental

statusstatus• vague history or chief complaintvague history or chief complaint

Blood glucose assessment IS NOT Blood glucose assessment IS NOT necessary in all patients with necessary in all patients with diabetes mellitus!!diabetes mellitus!!

Assessment of the Assessment of the Diabetic PatientDiabetic Patient

History and Physical Exam includesHistory and Physical Exam includes• Look for insulin syringes, medical alert Look for insulin syringes, medical alert

tag, glucometer, or insulin (usually tag, glucometer, or insulin (usually kept in refrigerator)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 Blood Glucose AssessmentAssessment

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

END OF DIABETESEND OF DIABETES

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?

endocrine system hormonal feed back mechanism

Documents

hormone fshfemales

concentration of hormone

growth hormonefollicular

growth maintenance

endocrine glandsact

tsh releasehypothyroidism

target organs

base of brain