Endocrine Disorders | My Assignment Tutor

1RMIT Classification: Trusted—Pathophysiology of EndocrineDisorders2RMIT Classification: TrustedLearning objectivesDescribe and contrast pathophysiology of type 1 and 2 diabetes mellitus.Describe the acute and chronic complications of diabetes mellitus.Describe the causes and symptoms, and explain the pathophysiologyassociated with hyposecretion and hypersecretion of the thyroidhormones.Describe the causes and symptoms, and explain the pathophysiologyassociated with hyposecretion and hypersecretion of the hormones of theadrenal gland.Essential Readings: Craft, Gordon, Huether, McCance and Brashers, Chapter 11Alterations in Endocrine function across lifespan, Understanding Pathophysiology 3rdEdition, 20183RMIT Classification: TrustedDiabetesIs the most common chronic disorder ofthe endocrine system1.2 million Australia are affected byDiabetesAbnormal secretion of insulin and/oraction of insulinType 1 :Decreased insulin →hyperglycaemiaType 2: Obesity → insulin resistance →hyperglycaemiaType I DiabetesNormalType II Diabetes4RMIT Classification: TrustedControl of blood glucoseInsulin is secreted by Betacells of pancreasGlucagon is secreted byAlpha cells in pancreas5RMIT Classification: TrustedControl of blood glucoseGlucagonSecreted due to low bloodglucose levelsGlycogenolysis Breakdownof glycogen to glucoseGluconeogenesis –Synthesis of glucose fromlactic acid, fatty acids andamino acids6RMIT Classification: TrustedControl of blood glucoseInsulinCarbohydrate metabolismGlucose uptake by the cellsGlycogen synthesis (liver, muscle)GlycogenolysisGlycolysisGluconeogenesis7RMIT Classification: TrustedControl of blood glucoseInsulinLipid metabolismTriglyceride synthesisProtein metabolismAmino acid uptake by cellsProtein synthesisProtein catabolism8RMIT Classification: TrustedMetabolic actions of insulin in striatedmuscle, adipose tissue, and liver9RMIT Classification: TrustedDiabetes1.2 million Australians have DiabetesApproximately 280 Australians develop diabetes every day. That’sone person every five minutes!Diabetes is recognised as the world’s fastest growing chronicconditionApproximately 415 millions adults have diabetes globally( approx.one in 11 adults)10RMIT Classification: TrustedTypes of DiabetesType I (IDDM; insulin-dependent)JuvenilesAbrupt onset of symptomsType II (NIDDM, non-insulin-dependent)AdultsComplex, multi-factorialDecrease insulin, insulin resistance, decrease insulin uptake,increase secretion of glucagon11RMIT Classification: TrustedTypes of DiabetesGestational DiabetesOccurs during pregnancyMother: can develop nephropathy and retinopathy andcomplicationsFetus: can major congenital defects (eg. absence of brain, spinemalformations, kidney & heart abnormalities)increases risk of spontaneous abortion and stillbirth and newborndeathsMost women will not have diabetes after the baby is born12RMIT Classification: TrustedType I Diabetes MellitusCausesAutoimmune disease (body’s immune system attacks the insulinproducing cells of the pancreas – β cells)Genetic ie loss of self tolerance leads to autoreactive CTLsEnvironmental ie virusExtensive damage to pancreatic beta cells which synthesiseinsulin13RMIT Classification: TrustedType I Diabetes MellitusCan occur at any age, although it mostly occurs in children andyoung adultsReferred to as juvenile onset diabetes or insulin dependentdiabetes.Peak onset: FRequire lifelong insulin injections for survival14RMIT Classification: TrustedType II Diabetes MellitusNon-insulin dependent diabetes (NIDDM)85-90% of diabetesAssociated with hereditary factors and lifestyle risk factors → poordiet, insufficient physical activity and being overweight or obeseMay manage their condition through lifestyle changesHowever, diabetes medications or insulin injections may also berequired to control blood sugar levelsOccurs mostly in people aged over 40 years old, however, thedisease is also becoming increasingly prevalent in younger agegroups15RMIT Classification: TrustedType II Diabetes MellitusPathophysiology of Type II DiabetesDevelops over a number of yearsInsulin resistance occursInsulin is less able to facilitate entry ofglucose into the liver, skeletal muscles andadipose tissuesPancreas increases production of insulinand this can lead to loss of insulinproducing cells16RMIT Classification: TrustedType II Diabetes MellitusGenetic susceptibilityFamily historyEthnicity ( increased risk in south Asians or Africans)Environmental factorsObesity – single most important risk factorIncreased intra-abdominal obesity10x risk with severe obesityPhysical inactivityDiet17RMIT Classification: TrustedSymptoms Diabetes MellitusPolyuriaHighblood glucoselevelsGlucoseexceeds renalthresholdcausingGlucosuriaGlucose is anosmoticdiuretic↑water loss inurinePolydipsiaHigh bloodglucoselevelsWaterosmoticallyattracted frombody cells intobloodIntracellulardehydrationStimulationof thirst18RMIT Classification: TrustedSymptoms Diabetes MellitusPolyphagiaGlucose isunable toenter cells↑ breakdowncellular storesofcarbohydrates,fats, proteinsIncreasedhunger andweightlossRecurrentinfections↑ GlucoselevelsDecreasedimmunefunction↑ Growth ofmicroorganismseg fungalgrowth causesgenital pruritis19RMIT Classification: TrustedSymptoms of Diabetes MellitusSlow healingsores↑ GlucoselevelsDamagedblood vesselsanddecreasedimmunefunctionDecreasedblood flowand slowhealingBlurred vision↑ GlucoselevelsGlucose ismetabolisedto sorbitaland then tofructoseIncreasedosmosiscauses lens inthe eye toswell,damage toblood vesselsand retina20RMIT Classification: TrustedAcute Complications of Diabetes MellitusHyperglycaemiaDue to high blood glucose levels, fluid is drawn out of the cells intothe blood streamCells become dehydratedCan result in non-Ketotic Hyperosmolar Coma (Neurologicaldamage, slurred speech, paralysis, loss of sensory function),seizures and death21RMIT Classification: TrustedAcute Complications of Diabetes MellitusKetoacidosisPeripheral tissue becomesstarved(insulin-dependent)Breakdown of fatty acids ( lipolysis)produces ketone bodies ( ketogenesis)Ketones are acidicAcidosis can occur when excessketones levels overwhelm body’sbuffering capacityBreath have a fruity odour22RMIT Classification: TrustedAcute Complications of DiabetesMellitusHypoglycaemiaImbalance between:EatingActivity levelsDose of drugsBrain function affected → activation SNS → headaches, irritability, finetremors, skin becomes cold and clammy23RMIT Classification: TrustedChronic Complications of DiabetesMellitusGlycationBinding of glucose to protein and formation of advanced glycation endproducts. The result is changes in structure and functionDiabetic RetinopathyHigh glucose levels can damage blood vessels in the retina. It can lead tohaemorrhage and swelling.Cerebrovascular and Heart diseaseHigh blood glucose levels can cause endothelial dysfunction, inflammationdeposition of plaque ( due to high plasma LDL) and narrowing of arteriesand subsequent stroke and heart diseasePeripheral artery diseaseHigh blood glucose can lead to damage to the blood vessels and thedeposition of plaque. The narrowing of the arteries will affect blood supply tothe organs24RMIT Classification: TrustedChronic Complications of DiabetesMellitusDiabetic NeuropathyHigh blood glucose can damage nerves. It commonly occurs inlegs and feet but can affect any nerveDiabetic NephropathyHigh blood glucose can damage the delicate glomeruli of thekidney and cause renal failure25RMIT Classification: TrustedQuestion 11. The most common cause of Type 1 Diabetes isA. ObesityA. Autoimmune mediated destruction of beta cells of thepancreasB. Autoimmune destruction of alpha cells of the pancreasC. Insulin resistanceD. Lack of vitamin D26RMIT Classification: TrustedQuestion 11. The most common cause of Type 1 Diabetes isA. ObesityA. Autoimmune mediated destruction of beta cells of thepancreasB. Autoimmune destruction of alpha cells of the pancreasC. Insulin resistanceD. Lack of vitamin D27RMIT Classification: TrustedQuestion 22. Why do diabetics have polyphagia?A. High blood glucose levels cause hungerB. Low blood glucose levels cause hungerC. Glucose is unable to enter cells. There is increasedbreakdown cellular stores of carbohydrates, fats, proteinsD. The loss of glucose in the urine causes hungerE. Acidosis causes hunger28RMIT Classification: TrustedQuestion 22. Why do diabetics have polyphagia?A. High blood glucose levels cause hungerB. Low blood glucose levels cause hungerC. Glucose is unable to enter cells. There is increasedbreakdown cellular stores of carbohydrates, fats, proteinsD. The loss of glucose in the urine causes hungerE. Acidosis causes hunger29RMIT Classification: TrustedThyroidThe thyroid gland plays a crucial role inMetabolism, growth and development.It is located below the larynxIt consists of two lobes connected by anIsthmusCell typesFollicular cells – secrete thyroid hormones:triidothyronine (T3) and thyroxine (T4)Function Regulate basal metabolic rate, heat production, growth,development, blood pressureParafollicular (C) cells – calcitoninFunction decreases calcium levels30RMIT Classification: TrustedActions of thyroid hormoneIncrease basal metabolic rateIncrease heat productionSlight increase in body temp.Tissue growth & developmentNormal skeletal growthNervous system reactivityIncrease Heart rate31RMIT Classification: TrustedRegulation of thyroid hormones Thyroid glandT3T4 Anterior PituitaryThyroid stimulating hormone (TSH) HypothalamusThyroid releasing hormone (TRH) 32RMIT Classification: TrustedHypothyroidismCause: Hyposecretion of the thyroid hormones (T3 & T4)Due to:PrimaryIodine deficiency( non toxic goitre due to increased TSH)Autoimmune destruction of thyroid tissue by circulating thyroidautoantibodies (Hashimoto disease or autoimmune thyroiditis)Congenital defectsThyroidectomy / thyroid ablationSecondaryPituitary dysfunction33RMIT Classification: TrustedIodineDeficiencyNon toxic goitreDue toincreased TSHNon functioning34RMIT Classification: TrustedHashimoto diseaseCauseAutoimmune destruction of thyroid tissue by circulatingautoantibodies (thyroid peroxidase and thyroglobulin)Pathophysiology35RMIT Classification: TrustedHypothyroidismSymptomsDecreased basal metabolic rate leads to cold intolerance,lower body temp, decreased appetite and weight gainDecreased stroke volume, HR and CODecreased protein synthesis leads to dry brittle hair nails anddry and flaky skinDecreased libido, impotence and amenorrhea36RMIT Classification: TrustedHypothyroidismSymptomsMyxedema leads to puffy eyes, hands, feetdeep, hoarse voice and hypoventilationIncreased TSH leads to a goiterNS depression leads to slowed speech &thinking, lethargy, fatigue and confusionSlow reflexes due to stiff, aching muscles &joints and muscle weakness37RMIT Classification: TrustedCretinismCause Congenital defect in infantSymptomsMental retardationStunted skeletal growth that leads to dwarfwith short limbs“Lazy” muscles that leads to protrusion ofabdomen, umbilical hernia(intestine protruding in umbilical region),constipation and lethargy38RMIT Classification: TrustedCretinismSymptomsMyxedema (drying and thickening skin) of oral tissues & vocalcords leads to protruding tongue, difficulty eating & hoarsecryDecreased metabolic rate leads to subnormal bodytemperature, cold coarse skin and bradycardia (heart rate

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