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Dr. Bernhard Arianto Purba, M.Kes., AIFO
ANATOMI DAN FISIOLOGIHIPOFISE DAN PANKREAS
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Textbooks
Guyton, A.C & Hall, J.E. 2006. Textbook of Medical Physiology. The11th edition. Philadelphia: Elsevier-Saunders: 918-930, 961-977.
Brooks, G.A. & Fahey, T.D. 1985. Exercise Physiology. HumanBioenergetics and Sts Aplications. New York : Mac Millan PublishingCompany: 122-143.
Foss, M.L. & Keteyian, S.J. 1998. Foxs Physiological Basis forExercise and Sport. 4th ed. New York : W.B. Saunders Company:471-491.
Astrand, P.O. and Rodahl, K. 1986. Textbook of Work Pysiology,Physiological Bases of Exercise. New York : McGrawHill.
Braunwald, Pauci, et al.2008. Harrison's PRINCIPLES OFINTERNAL MEDICINE. Seventeenth Edition. New York : McGrawHill: Chapter 332, 333, 338.
Kronenberg, and Melmed. 2008. WILLIAMS TEXTBOOK OFENDOCRINOLOGY. The 11th edition . Philadelphia: Elsevier-Saunders: 155-235, 1329-1407.
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General Features of theEndocrine System
1. Endocrine glands are ductless
2. Endocrine glands have a rich supply of blood.
3. Hormones, produced by the endocrine glands aresecreted into the bloodstream.
4. Hormones travel in the blood to target cells closeby or far away from point of secretion.
5. Hormones receptors are specific binding sites onthe target cell.
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Important Definitions
What are hormones?
Hormones are organic chemical messengers producedand secreted by endocrine cells into the bloodstream.
Hormones regulate, integrate and control a wide rangeof physiologic functions.
Silverthorn, Human Physiology, 3rd
edition Figure 6-1&2
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What are endocrine glands?
Endocrine glands are ductless glands comprised of endocrinecells. This means that these glands do not have ducts that lead tothe outside of the body. For example, sweat glands are NOTendocrine glands (they are instead exocrine glands) becausesweat glands have ducts that lead to the outside surface of yourskin (thats how the sweat gets out). The fact that endocrineglands are ductless means that these glands secrete hormones
directly into the blood stream (instead of to the outside of yourbody).
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What are target cells?
Target cells refer to cells that contain specific
receptors (binding sites) for a particular hormone.Once a hormone binds to receptors on a target cell, aseries of cellular events unfold that eventually impactgene expression and protein synthesis.
Silverthorn, Human Physiology, 3rd
edition Figure 6-1&2
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What are hormone receptors?
Hormone receptors are binding sites on the target cell (eitheron the surface or in the cytoplasm or nucleus of the target cell)that are activated only when specific hormones bind to them. Ifa hormone does not/cannot bind to its receptor, then nophysiologic effect results.
See next slide for a picture of a hormone bound to its receptor
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Growth hormone regulates cell growth
by binding to growth hormone
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Steps in Signal Communication
1. Synthesis2. Release3. Transport to target cell4. Signal detection by specific receptor
5. Change in cellular metabolism6. Signal removal termination cellular response
f
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Hypofunction Hyperfunction
Gland
ProH
Hormon
Response
Effector
Receptor
Degraded Degraded
Destruction
Block
Tumor
Antibodies
Block
Block
Hyperplasia
Stimulation
Iatrogenic
Ectopic production
Antibodiesantagonist
Tissue damage Tissue damage
Stimulation
Defect
Target cell
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Clinical Application
1111
Growth Hormone Ups and Downs
Gigantism - hypersecretion of GH in childrenAcromegaly hypersecretion of GH in adultsDwarfism hyposecretion of GH in children
Figure shows oversecretion of GH in adulthood as changes occur in thesame person at ages (a) nine, (b) sixteen, (c) thirty-three, and (4) fifty-two
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Master control
Master integrator
HYPOTHALAMUS
PITUITARY GLAND
AKA = hypophysis
1 cm in diameter
0,5-1 gr in weight
InfundibulumHypophysis stalk
Sella turcica
hypothalamus
infundibulum
pituitary gland
sella turcica insphenoid bone
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Anterior pituitary
(adenohypophysis)
PITUITARY GLAND (HYPOPHYSIS)
derived from Rathkespouch
Invagination of pharyngeal
epitheliumconnected tohypothalamus by
hypophyseal portalsystem
Posterior pituitary(neurohypophysis)
A neural tissue outgrowth ofhypothalamusconnected to hypothalamus
by
nerve tract
contains pituicytes
neurohypophyseal budfrom hypothalamus
infundibulum
bud from roof of mouthcalled Rathkes pouch
loses connectionwith mouth cavity
neurohypophysis
adenohypophysis
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Hypophysis or Pituitary Gland
D = pars distalis, I= pars intermediN = pars nervosa, S = stem or stalT = pars tuberalis
Posterior lobe Anterior lobe
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Pars distalis or anterior lobe
Pars nervosaor posterior lobe
Intermedia between black lines
uitary gland or Hypophysis
Adenohypophysis
eurohypophysis
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Hormones of the PituitaryGland
1818
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Hypothalamic
Hormones
1919
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Tissues can be targeted by multiple hormones
Hormones can act synergistically, permissively, orantagonistically
Synergistic effects ofhormones on bloodglucose concentration
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Neuroendocrineorigins of
signals
First target
Seconds targets
Ultimate targets
Sensory input from environment
Central nervous system
Hypothalamus
Hypothalamic hormones(releasing factors)
Anterior pituitary
Corticotropin(ACTH)
Mr4,500
Adrenalcortex
Cortisol
corticosterone,aldosterone
Manytissues
ThyrotropinMr28,000
Thyroid
Thyroxine
(T4), triiodothyronine (T3)
Muscles,liver
Folicle-stimulating
hormoneMr24,000
Ovaries/testes
Progesterone,
extradiol
Reproductive organs
Luteinizinghormone
Mr20,500
Testosterone
Somatotropin(growth hormone)
Mr21,500
Liver,bone
ProlactinMr22,000
Mammaryglands
Posterior pituitary
OxytocinMr1,007
Smoothmuscle,
mammaryglands
Vasopressin(antidiuretic
hormone)Mr1,040
Arterioles
Bloodglucose
level
Islet cells ofpancreas
Insulin,
glucogen,somatostatin
Liver,muscles
Adrenalmedulla
Epinephrine
Liver,muscles,
heart
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POSTERIOR PITUITARY GLAND HORMONESOxytocin and Vasopressin are manufactured in the hypothalamus(magnocellular neurons), but released in the posterior pituitary.
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sa
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Hypothalamic centersSupraoptic nucleus
Paraventricularnucleus
Axonal Transport
Pituicytes function
ParsNerv
osa
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Neurohormones
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Pituitary-HypothalamicRelationships:
Anterior LobeThere is a vascular connection, thehypophyseal portal system, consistingof:
The primary capillary plexus
The hypophyseal portal veins
The secondary capillary plexus
InterActive Physiology: Endocrine System: The Hypothalamic-PituitaryAxis
ANTERIOR PITUITARY GLAND
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Releasing vs. inhibiting factors
Hypophyseal portal system
ANTERIOR PITUITARY GLAND
arterial supply
primary plexus ofcapillaries
hypophyseal veins
second plexus ofcapillaries
anterior hypophyseal veins
hypothalamicneurons
releasing factor
primary plexushypophysealveins
secondary plexus
hormone
anteriorhypophysealvein
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Note PituitaryPortal System!!
RELEASING HORMONES stimulate release of anteriorpituitary hormones.
INHIBITING HORMONES inhibit release of anteriorpituitary hormones.
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Hypothalamus
Anterior Pituitary Posterior Pituitary
Target Organs Target Organs
RF
SH
Hormone
Hormone
RF = Releasing Factor SH = Stimulating
Hormone
Pituitary & all Hormones are Underthe Control of the Hypothalamus
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Two Important Points:
Hormones released from the posteriorpituitary are synthesized in the
hypothalamus.
Hormones released from the anteriorpituitary are dormant unless directed to
be released by the hypothalamus via
Releasing Factors.
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Hypothalamic Hormones:
Gondotropin RF Corticotropin RF
(CRF)
Thyrotropin RF Growth HorRF
Prolactin RF
Pituitary Hormones:
Follicle SH &
Lutenizing Hor.
ThyrotropinSH
Adrenocorticoptropin
Hormone (ACTH)
ProlactinGrowth
Hormone
Target Gland or Structure:
Ovaries & Testes
(androgens,
estrogen)
Adrenal Gland
(cortisol)
Cells of bodyThyroid Gland
(thyroxine)
Bones,breasts &cells of body
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Hypothalamus
Adenohypophysis
Endocrine Gland
Target tissues
Control ofAdenohypophysial Hormones
IndirectLoop
ShortLoop
DirectLoop
ReleasingFactor
Trophichormone
Endocrine
hormone
Some loops are negative feedback loops.Increases in the amount of the substances monitored
reduces further secretion of those substances.
eural inputs
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Summary of the Endocrine System
Figure 7-2-1: ANATOMY SUMMARY: Hormones
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Summary of the Endocrine
System
Figure 7-2-2: ANATOMY SUMMARY: Hormones
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Summary of the Endocrine
System
Figure 7-2-3: ANATOMY SUMMARY: Hormones
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Figure 18.1
A Structural Classification of Hormones
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Figure 18.2
A Structural Classification of Hormones
G Proteins and Hormone Activity
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y
Hormone Effects on Gene Activity
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Hormone Effects on Gene Activity
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ySecond level
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Endocrine Gland Stimuli
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Endocrine Gland Stimuli
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PANCREAS
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Pancreas
PANKREAS
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PANKREAS
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En ocr ne Pancreas
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5151
En ocr ne Pancreas
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TYPES OF TISSUES
1.Acini secretes digestive juices
2.Islets of Langerhans- has 3 types of cells namely a. Alpha cells 25% - secrete Glucagon
b.Beta cells 60% - secreteInsulin and Amylinc. Delta cells 10% - secreteSomatostatind. PP cells secretepancreatic polypeptide
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Insulin
Preproinsulin proinsulin insulin + peptide
c peptide: - MW 3000
- 31 aa
- no biologic activity
- released by cell
- not removed by liver
- degraded & excreted by kidney
- T - 12 3 - 4 x insulin
Insulin: 51aa
A chain (21 aa)
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INSULIN Hormone Associated with
Energy Abundance
1. Effect on Carbohydrate Metabolism
A. Promotes Muscle Glucose Uptake and Metabolism-Storage of Glycogen in Muscle
B. Promotes Liver Uptake, Storage and Use of Glucose
Mechanisms: a. inactivates liver phosphorylase
b. causes enhanced uptake of glucose from theblood by the liver cells (by increasing the
activity of the enzymeglucokinase
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C. increases activity of enzyme glycogen synthase , that
promote glycogen synthesis
- Glucose is released from the liver between mealsLack of insulin activatesPhosphorylase , whichcauses splitting of glycogen into glucose phosphate
- Insulin promotes Conversion of Excess Glucoseinto
fatty Acids andInhibits Gluconeogenesis in theliver
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nsu n oun toreceptorsites
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Target
protein
P
Tyr
Translocationof GLUT-4
ATP
ADP
P
Tyr
Tyr
Tyr
Tyr
Tyr
Tyr
P
PTyr
Tyrosinekinase
domains
Carbonil-terminaldomains
P
GLUT-4
P
Tyr
Glicogen
synthesis
Proteinsynthesis
DNA synthesisKinase activation
Transcription factor phosphorilation
Lipid metabolismAmino aciduptake Iontransport
p60
p110 p85
IP3-kinase
IRS-1
P70-kinaseP90-kinase
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
P
Tyr
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C. Lack of Effect of Insulin on Glucose Uptake and Usage
by the Brain
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2. Effect on Fat Metabolism
A.Insulin promotes Fat Synthesis and Storage - Storage of Fat and the Adipose Cells
a. insulin inhibits the action of hormone- sensitive lipase
b. insulin promotes glucose transport throughthe cell membrane into the fat cells
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B. Insulin deficiency Causes Increase Metabolic Useof Fat causing
a. Lipolysis of Storage Fat and Release of FreeFatty Acids
b. Increase Plasma Cholesterol and Phospholipid
c. Excess Usage of Fats during Insulin LackCauses
Ketosis andAcidosis
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3. Effect of Insulin on Protein MetabolismA. INSULIN PROMOTES PROTEIN Synthesis and Storage
a. stimulates transport of amino acids into the cells(valine, leucine, isoleucine, tyrosine, phenylalanine)
b. increases the translation of messenger RNA,
forming new proteinsc. increases the rate of transcription of DNA geneticsequences in cell nuclei
d. inhibits catabolism of proteinse. depresses the rate of gluconeogenesis
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B. Insulin Lack Causes Protein Depletion and IncreasedPlasma Amino Acids
- protein wasting is one of the most serious ofall effects of severe diabetes mellitusC. Insulin and Growth Hormone InteractSynergistically to
Promote Growth
INSULIN PROMOTES PROTEIN FORMATION ANDPREVENTS DEGRADATION OF PROTEINS
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Bloodvessel
Insulin
High bloodglucose
Glucose
Pankreas
1 0 6 05 04 03 02 0
2 0
4 0
6 0
8 0
P e r i o d o f g l u c o s e i n f u s i o n
G l u c o s e
I n s u l i n
0
1 5 0
3 0 0
0
Insulin(ng/mL)
Glucose(ng/mL)
M i n
CONTROL OF INSULIN SECRETION
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CONTROL OF INSULIN SECRETION
1. Increased Blood Glucose Stimulates Insulin secretion
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2. Other Factors That Stimulate Insulin Secretion: a. Amino Acid most potent are arginine and lysine
-potentiates strongly the glucose stimulus for insulin secretion
b. Gastrointestinal Hormones Gastrin, Secretin,
cholecystokinin, Gastric Inhibitory Peptide
c. Other Hormones- Glucagon, Growth Hormone,Cortisol,Progesterone and Estrogen
d. Autonomic Nervous System
-Stimulation of the parasympathetic nerves to the pancreascan increase insulin secretion
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R l f I li i S it hi B t C b h d t
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Role of Insulin in Switching Between Carbohydrateand Lipid Metabolism
GLUCAGON a hormone secreted by the alpha cells of
the isletsof Langerhans when blood glucoseconcentration falls. Its important function is to increaseblood glucose concentration thus is also called the
Hyperglycemic Hormone.
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Effects on Glucose
Metabolism
Major Effects
1. breakdown of liver glycogen
(glycogenolysis)
2. increased gluconeogenesis in the liver
Decrease in blood glucose
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Release of
glucagon
Decrease in blood glucose
Glucagon binds to membranereceptor
Activation of adenylate cyclase
Increase in cAMP, activation of cAMP-dependent kinase
Activation of glycogenphosporylase Inhibition of glycogensynthase
Degradation glycogen to glucose, releaseof glucose into blood
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Other Effects (when conc. rises above maximumnormally found in the blood
1. activates adipose cell lipase- increasing fatty acidsavailable to the energy system of the body
2. inhibits storage of triglycerides in the liver
3. enhances the strength of the heart
4. increases blood flow in some tissues, esp. kidneys
5. enhances bile secretion
6. inhibits gastric acid secretion
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Regulation of Glucagon Secretion
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Regulation of Glucagon Secretion
Increased Blood Glucose Inhibits Glucagon Secretion
- the most potent factor that controls glucagonsecretion
- the effect of blood glucose conc. on glucagonsecretion isin exactly the opposite direction from the
effect of glucose oninsulin secretion
b. Increased Blood Amino Acids Stimulate Glucagon
Secretion (especially alanine and arginine)
The Regulation of Blood GlucoseConcentrations
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Concentrations
SOMATOSTATIN INHIBITS GLUCAGON
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SOMATOSTATIN INHIBITS GLUCAGONAND INSULIN SECRETION
Factors Related to Ingestion of Food StimulateSomatostatin Secretion:
1. Increased blood glucose2. Increased amino acids3. increased concentrations of GI hormones4. increased fatty acids
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Inhibitory Effects of Somatostatin:
1. Acts on the islets of Langerhans to depress thesecretion of insulin and glucagon
2. Decreases the motility of the stomach, duodenum andgallbladder
3. Decreases both secretion and absorption in GIT
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The Principal Role of Somatostatinis to
extend the period of time over which thefood nutrients are assimilated into theblood
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SUMMAR Y OF BLOOD GLUCOSE REGULATION Mechanisms:
1. The liver functions as an important blood glucose buffersystem2. Both insulin and glucagon function as important
feedback control systems for maintaining a normal glucoseconcentration3. Severe hypoglycemia stimulates the sympathetic nervoussystem 4. Growth hormone and cortisol are secreted in response to
prolonged hypoglycemia, decreasing the rate of glucoseutilization by most cells
Importance of Blood Glucose Regulation:
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1. Glucose is the only nutrient that normally can be usedby the brain, retina andgerminal epithelium of the
gonads
2. Blood glucose should not too high (reasons)a. glucose exert a large amount of osmotic pressure in
the ECF causing cellular dehydration
b. high levels of blood glucose concentration causes lossof glucose in the urinec. causing osmotic diuresis by the kidneysd. long-term increase in blood glucose cause damage to
many tissues, esp. blood vessels. Vascular injury
leads to heart attack, stroke, end-stage renal failureand blindness
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DIABETES MELLITUS
It is a syndrome of impaired carbohydrate,fat, and protein metabolism caused by eitherinsulin lackor decreased sensitivity ofthetissues to insulin
T f Di b t M llit
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Types of Diabetes Mellitus:
1. Type 1 Diabetes- also called insulin-dependentdiabetesmellitus (IDDM), is caused by lack of insulin secretion.
2.Type II Diabetes also called non-insulin dependentdiabetesmellitus (NIDDM) , is caused by decreased sensitivity of
target tissues to insulin. This reduced sensitivity to insulinis often referred to as insulin resistance
3. Other specific types of diabetes
4. Gestational diabetes mellitus (GDM)
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Type I Diabetes- Lack of InsulinProduction by Beta cells of the Pancreas
CAUSES:
1. Viral Infection or Autoimmune Disease maybe involved in the destruction of the beta cells
2. Heredity
Usual onset of Type I diabetes occurs at about 14years of age thus is often called Juvenile diabetesmellitus
Principal Sequelae:
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Principal Sequelae:
1. Increased blood glucose
2. Increased utilization of fats for
energy and for formation ofcholesterol by the liver
3. Depletion of the bodys proteins
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Blood Glucose Concentration Rises toVery High Levels in Diabetes Mellitus
Increased Blood Glucose Causes Loss of Glucose
in the Urine (>180 mg/100 ml)
Increased Blood Glucose Causes Dehydration Osmotic diuresis, polyuria, intracellular
and extracellular dehydration, increased
thirst(polydipsia)
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Chronic High Glucose ConcentrationCauses Tissue Injury:
Blood vessels function abnormally resulting toinadequate blood supply to tissues leading to riskof
heart attack,stroke,end- stage kidney disease,retinopathy and blindness, and ischemia and
gangrene of the legs
D t ti i i h l h
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Damage to tissues causingperipheral neuropathy(abnormal function of peripheral nerves, and
autonomic nervoussystem dysfunction
Hypertension (secondary to renalinjury) and arteriosclerosis (secondaryto abnormal lipid metabolism)
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Diabetes Mellitus Causes Increase Utilization ofFats and Metabolic Acidosis leading to coma and
death
As a result the patient develops severe metabolic
acidosis leading to coma and death
Arteriosclerosis increased deposition ofcholesterol in the arterial walls
Kussmaul breathing - rapid and deep breathing
physiologic compensation in metabolic acidosis
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Diabetes Causes Depletion of Bodys
proteins
- rapid weight loss and asthenia (lack of
energy) despite of eating large amounts offood (polyphagia)
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Type II Diabetes Resistance to MetabolicEffects of Insulin
more common than type I to 90% of all cases ofdiabetes
Onset occurs after the age of 30, often between 50 to
60 years- referred to asAdult Onset Diabetes- related mainly to the increasing prevalence of
obesity, the most important risk factor for type IIdiabetes in children as well as adults
Obesity, Insulin Resistance and MetabolicSyndrome Usually Precede Development of Type II
Diabetes
Features of Metabolic
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Features of MetabolicSyndrome1. Obesity, especially accumulation
of abdominal fat
2. Insulin resistance
3. Fasting hyperglycemia4. Lipid abnormality such as
increased triglycerides and
decreased blood high densitylipoprotein cholesterol
5. hypertension
Other Factors That cause Insulin
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Resistance and Type II Diabetes
1. Polycystic Ovary Syndrome (PCOS)
2. Excess formation of glucocorticoids(Cushing Syndrome) or growthhormone (acromegaly)
Development of Type II DiabetesDuring Prolonged Insulin Resistance
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Physiologic Diagnosis of Diabetes
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Mellitus
1. Urinary Glucose
2. Fasting Blood Glucose and Insulin Levels
- in the early fasting blood glucose level isnormally 80 to 90 mg/100 ml
-110 mg/100 ml to be the upper limit FBS above this value indicates diabetes mellitus
- type I diabetes plasma insulin levels are verylow or undetectable during fasting and after ameal
type II diabetes plasma insulin concentration is
higher than normal
3. Glucose Tolerance Test
4. Acetone breath
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CONTROL OF HORMONE SECRETIONS
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Negative feedback
time
[glucose]
110 mg%
90 mg%
steady state
hyperglycemia =insulin secretion
hypoglycemia =
glucagon secretion
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TREATMENT OF DIABETES:
A.Type I diabetes administer enough insulin
B. Type II diabetes dieting and exercise drugs
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Insulinoma Hyperinsulinism
- occurs from an adenoma of an islet of Langerhans
- insulin shock and hypoglycemia
- as blood glucose level falls into the range of 50 to70 mg/dl the CNS becomes excitable leading to
hallucinations, extreme nervousness, trembles
all over, breaks out in a sweat
Symptomatic results of insulin deficit(diabetes mellitus)
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(diabetes mellitus)
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TERIMAKASIH
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