This review provides insights into diabetes mellitus, including the causes of hyperglycemia and diabetic ketoacidosis. It also discusses the physiological responses to hypoglycemia and strategies to reduce hypoglycemia events and unawareness in the context of a case study. The review aims to enhance understanding of diabetes management.
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Diabetes Educator Review 1
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Contents Introduction......................................................................................................................................3 Main Body.......................................................................................................................................3 1. Why insulin deficiency for Jen leads to profound hyperglycaemia, and the pathophysiology of hyperglycaemia leading to Diabetic ketoacidosis...................................................................3 2. Physiologic responses to hypoglycaemia and hypo-unawareness...........................................4 3.Justification of the information provided to Jen to reduce her hypoglycaemia events and reduce hypo-unawareness in the context of her life....................................................................6 Conclusion.......................................................................................................................................7 REFERENCES................................................................................................................................8 3
Introduction Diabetes mellitus is a metabolic disease which cause high level of blood sugar. Insulin hormone moves sugar from blood to cells to be used for energy (Mitchell, and et. al., (2020). It is a chronic condition which occurs due to insufficient production or absence of insulin or body's inability to properly utilise it. This report is based on the case study of Jen who was suffering from type 1 diabetes. This report includes some questions based on the case study which are answered in it. Main Body 1. Why insulin deficiency for Jen leads to profound hyperglycaemia, and the pathophysiology of hyperglycaemia leading to Diabetic ketoacidosis Jen is a 29 years old lady who is suffering from diabetes ketoacidosis secondary to insulin omission. She is experiencing variations in glycaemic control and the reason behind that was not taking proper care of her. Apart from this, she was self adjusting her insulin doses. For the proper management of type 1 diabetes, ongoing patient education, coordinated guidance or directions from multi-disciplinary teams and access to proper treatment is required. Omission of insulin is the main risk factor due to which Jen leads to diabetes ketoacidosis.Omission of insulin is the precipitants of diabetes ketoacidosis. Increased concentration of counter regulatory hormones and decreased insulin concentrations leads to ketosis and hyperglycemia(Buse, and et. al., (2020). It develops as an outcome of three processes, accelerated glycogenolysis, maximized gluconeogenesis and impaired utilization of glucose by the peripheral tissue. The deficiency of insulin leads to profound hyperglycemia. In normal state, insulin make sure the storage of glucose in liver as glycogen. Deficiency of insulin leads to increase in production of hepatic glucose by increased gluconeogenesis and glycogenolysis and decrease the use of glucose. This resulted into hyperglycemia. Hyperglycemia is a situation which occurs when the sugar levels in blood are too high. If the diabetes of people is not treated appropriately, then hyperglycemia develops. When the body cannot utilize insulin properly or has too little insulin, then hyperglycemia occurs.Its symptoms involve high blood sugar, increased thirst, frequent urination and high sugar level in urine (Drucker, (2020).When body produce high level of ketones, then the condition is referred as diabetic ketoacidosis. It is a serious complication associated with diabetes and occurs when body 4
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cannot produce required insulin. The disease is usually triggered through illness and issue with insulin therapy. The other possible triggers include heart attack, alcohol or drug abuse, emotional and physical trauma inserting medications like diuretics and corticosteroids. In case of Jen, her level of Ketones in body is high, i.e., 6 due to which she faces may face the issue of Diabetes Ketoacidosis. Pathophysiology of hyperglycemia leading to diabetes ketoacidosis: Hyperglycemia is the outcome of immunologic, environmental and genetic factors which leads to destruction of beta cells in pancreas and insulin deficiency. Increased insulin counter regulatory hormones like growth hormone, glucagon, catecholamines and cortisol, peripheral insulinresistanceandinsulindeficiencyleadtodehydration,electrolyteimbalance, hyperglycemia and ketosis which underline pathophysiology of diabetes ketoacidosis(Flatt, and et. al., (2020). Hyperglycemia of diabetes ketoacidosis evolves by accelerated glycogenolysis, gluconeogenesis and decreased utilization of glucose - all because of deficiency of absolute insulin. Of note, the patient with diabetes who develop diabetes ketoacidosis when treated with SGLT-2inhibitorscanexistwithouthyperglycemia,thatis,witheuglycemicdiabetes ketoacidosis. Because of decreased lipogenesis and maximize lipolysis, abundant free fatty acids are transform to ketone bodies including acetone, acetoacetate and beta hydroxy butyrate. The hyperglycemia induced osmotic diuresis when not accompanied through adequate intake of oral fluid, leads to dehydration, electrolyte loss, hyperosmolarity as well as subsequent decline in glomerular filtration(PATHOPHYSIOLOGY OF HYPERGLYCEMIA, 2018). The glycosuria diminishes with decrease in renal function and hyperosmolarity / hyperglycemia worsens. With hyperosmolarity as well as impaired insulin action, the use of potassium through skeletal muscle is diminished which leads to intracellular potassium depletion. Apart from this, potassium is also lost through osmotic diuresiswhich cause profound deficiency of total body potassium.Thus,thepatientwithdiabetesketoacidosiscanpresentwithwiderangeof concentrationsofserumpotassium.Nevertheless,normallevelofplasmapotassium concentration may depict that potassium is a store in the body of patient are diminished severely andthecorrectionofhyperglycemiaandinstitutionofinsulintherapyleadstofuture hypokalemia(Fanelli, and et. al., (2020). 2. Physiologic responses to hypoglycaemia and hypo-unawareness Physiological responses to hypoglycemia: 5
With the intact of counter regulatory components, a drop in plasma glucose outcomes in mainphysiologicaldefensesagainstdecliningconcentrationsofplasmaglucose:risein pancreatic Alpha cell glucagon secretion, decline in pancreatic beta cell insulin secretion and rise in secretion of adrenomedullary epinephrine. It also outcomes in hypoglycemic symptoms perception which are highly sympathetic neutral as well as that prompt ingestion of carbohydrate (PHYSIOLOGICAL RESPONSES TO HYPOGLYCEMIA, 2011). Glucagon and insulin:the initial response to declining levels of glucose is decreased secretion of insulin. As plasma glucose falls continuously, glucagon is released by incompletely understoodmechanism.Similartobetacells,AlphacellsexpressKATPchannelsand glucokinase so low glucose concentrations can sense directly. Sympathoadrenal response:normally, 3.6 - 3.9 mmol/L of plasma glucose level increasescatecholaminemediatedaswellasacetylcholinemediatedneurotransmissionin peripheral autonomic nervous system and central nervous system. The level of glucose at which catecholamine responses activation occur in child has been depicted to be high in comparison to adult and differs with glycemic control level(Pratley, and et. al., (2020). The sympathoadrenal response involves adrenal medulla activation to secrete norepinephrine and epinephrine along withactivationofsympatheticnervoussysteminordertoreleaseacetylcholineand norepinephrine. Gluconeogenic precursors co-infusion with epinephrine and glucagon further augmented this rise in production of hepatic glucose through maximizing gluconeogenesis after 60 minutes’ issues that gluconeogenic precursors peripheral production is limiting element in hepatic gluconeogenesis induced through epinephrine and glucagon. Cortisol and growth hormone:contrasting to rapid effects of epinephrine and glucagon on regulation of glucose, the effect of cortisol and growth hormone at the time of hypoglycemia are delayed. In selective replacement through pancreatic adrenocortical pituitary clamp along with subcutaneous insulin infusion and pharmacologically induced suppression of glucose counter regulatory hormones in people, lack of cortisol increase outcomes in low rate of production of glucose and increased rate of use of glucose after 6 hours when growth hormone, insulin and glucagon were infused in order to maintain similar plasma concentrations(Fabris, and et. al., (2020). Physiological responses to hypoglycemia unawareness: 6
Hypoglycemia unawareness is referred as the beginning of neuroglycopenia previous the autonomic warning symptoms appearance. In patients with diabetes mellitus like Jen, recurrent hypoglycemia has been depicted to decline the level of glucose that precipitates counter regulatory response required to restore euglycemia at the time of subsequent hypoglycemia episode.The key risk factors for hypoglycemia unawareness development includes duration of disease as well asenhanced metaboliccontrol(Lacy, and et. al., (2020). Hypoglycemia unawareness severity is related to longer duration of diabetes and history of frequent lower level of glycemic. Whereas, but blood glucose decreasing rate and aging, which declines from near level of blood glucose are risk of severe hypoglycemia unawareness. Aberrant glucose counter regulation hypoglycemia unawareness are the elements of hypoglycemia related autonomic failure in the patients of diabetes. It is often caused due to recurrent or recent iatrogenic hypoglycemia, as well as in death hypoglycemia related autonomic failure is maintained through recurrent hypoglycemia. Patients with type 1 diabetes have been constrained through adverse impactsofinsulininducedhypoglycemia(Chow,&Seaquist,(2020).Hypoglycemia unawareness is related to diminished response of brain to mild hypoglycemia. In addition to this, the pattern of brain responses loss appears to include fronto-parietal and cortico-striatal neuro circuits which play a significant role in regulating goal-directed behavior and motivation and attention, thus are possibly to have implications for understanding the reason people with hypoglycemia unawareness are failed to appropriately respond to falling levels of blood glucose. 3.Justification of the information provided to Jen to reduce her hypoglycaemia events and reduce hypo-unawareness in the context of her life The hypoglycemia unawareness happens when someone does not perceive or experience hypoglycemia symptoms which typically happen when the level of blood sugar declines below 54 mg/dl. It has been depicted by the study that people with hypoglycemia unawareness are at high risk of experience severe hypoglycemia as they are less possibly to identify early alert signs like hunger, sweating or shakiness. Another symptoms involves neuroglycopenic symptoms that outcomes from impaired function of brain because of low level of blood sugar and non-specific symptoms. Some of the factors which are associated with hypoglycemic unawareness includes exercise as the possibility of hypoglycemia is maximized after and during the exercise. While exercising, the tissues of body are more sensitive to insulin(Kwan, and et. al., (2020). Another factor is going low while sleeping as many individuals develop hypoglycemia when they are 7
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asleep as well as not able to perceive symptoms. Frequent occurrence of this can influence capability to detect warnings of hyperglycemia symptoms while awake. Another factor is having diabetes for long time. It has been found in the study that around 50% of individuals who had utilised insulin for more than 20 years had high chances to develop impaired hypoglycemia awareness. Whereas, around 20% among those who are on insulin for less than 10 years feel this issue(Misra-Hebert, and et. al., (2020). The individuals who are suffering from diabetes for longer time have high chances to being exposed to multiple hypoglycemia episodes which contributes to hypoglycemia unawareness. Apart from all these factors, age, consuming alcohol and certain prescription drugs are also the factors which contribute to hypoglycemia unawareness.In order tominimize the hypoglycaemia, Jen needs to acknowledge the issue, taken into consideration each risk factor as well as executing relevant intensive glycaemic therapy principles(Hoogwerf, (2020). These principles involvesutilizing more physiological insulin regimens when insulin is indicated; make sure that users are confident in self-management; taken into consideration the insulin treatment technologies like continuous glucose monitoring (CGM), continuous subcutaneous insulin infusion (CSII), and CSII with CGM(Satin, Butler, Ha, & Sherman, (2015).Proper knowledge and awareness of all these factors will help Jen in minimising her hypoglycemia events and declining the hypo unawareness in relation to her life. In addition to this, most frequent measurement of blood glucose, continuous monitoring of glucose and work with healthcare provider in order to fine tune insulin regimen will also assist Jen in addressing the issue properly and minimising the hyperglycaemia level(Lontchi-Yimagou, and et. al., (2020). Physiology of endogenous insulin secretion in comparison to exogenous (injections) insulin therapy: Endogenous insulin is defined as the insulin which pancreas secrete and exogenous is insulin which people inject through insulin pump. In patients with type 1 diabetes, exogenous insulin therapy is used to supplement deficient insurance generation in pancreatic beta cells. It is injected and acts same as the endogenous counterpart which assist in normalising the levels of glucose and metabolism (Tarchick, and et. al., (2019).The main goal of insulin therapy is to mimic endogenous insulin release.For the proper management of type 1 diabetes, insulin therapy is crucial induced increasingly to accomplish optimal glycaemic control. Individuals with type 1 diabeteshaveinabilitytodisposeofcarbohydratesproperlyandthushaveuncontrolled 8
fluctuations in the glucose in blood. Severe but reversible impairment causes by hyper glycaemia in impairment of beta cells as well as promote the complications of diabetes. Significantly, there are two ways or methods to dampen harmful extrusions of glucose: i) moderate glucose intake or ii)andenhancedisposalofglucoseeitherthroughindependentlyorinsulinsystem (EXOGENOUS AND ENDOGENOUS INSULIN IN TYPE 1 DIABETES, 2018). When insulin isadministeredthroughslowintravenousinfusioninawaywhichreduceorprevent hypoglycaemia as well as its counter regulatory response, a decrease in hepatic glucose output ensured. On the other side, insulin is given through rapid intravenous injection, the output of hepatic glucose either increased or remain unchanged. The basal bolus insulin therapy includes taking a form of insulin which is long acting in order to keep the level of blood glucose stable by fasting period as well as separate injections of short acting insulin in order to prevent increase in level of blood glucose resulting from meals. The main role of basal insulin is to keep the level of blood glucose consistent during fasting period. It is required to keep the level of blood glucose under control and enable cells to get a glucose for energy (Satin, Butler, Ha, & Sherman, (2015).In a person with type 1 diabetes like Jen, it allows her to self-adjust her insulin doses which means that she have the flexibility over the amount of carbohydrate she can take in different meals. Type 1 diabetic patient take rapid acting insulin and long acting insulin. The continuous subcutaneous insulin infusion includes wearing insulin pump that gives a steady insulin steam into body. It allows a patient to take instantaneous action to assist decrease on increased levels of blood glucose (Insulin Pump Therapy, 2019). As Jen was suffering from type 1 diabetes, she can take insulin pump therapy as an intervention to manage her level of blood glucose effectively. It helps her in having better control over diabetes and provide her with the ability to increase or decrease the level of blood glucose on demand. For instance: if Jen has complete knowledge of continuous subcutaneous insulin infusion, then while participated in marathon, she may select to suspend insulin delivery for preventing hypoglycaemia from occurring.Alterationstodeliveryofinsulinwillrequiretobesupportedthroughsound understanding of insulin requirement of body for distinct activities and frequent testing of blood glucose (Szypowska and et. al., (2016). 9
Conclusion As per the above mentioned report, it has been concluded that type 1 diabetes is a serious issue which leads to cause many other complex issues. Omission of insulin increases the risk of diabetes ketoacidosis. Physiological responses to hypoglycemia and hypoglycemic unawareness leads to decline the level of glucose. 10
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REFERENCES Books and Journals Buse, J. B., and et. al., (2020). 2019 update to: management of hyperglycemia in type 2 diabetes, 2018.AconsensusreportbytheAmericanDiabetesAssociation(ADA)andthe European Association for the Study of Diabetes (EASD).Diabetes Care,43(2), 487-493. Drucker, D. J. (2020). Coronavirus infections and type 2 diabetes—shared pathways with therapeutic implications.Endocrine reviews,41(3), bnaa011. Flatt, A. J., and et. al., (2020). Predictors of recurrent severe hypoglycemia in adults with type 1 diabetesandimpairedawarenessofhypoglycemiaduringtheHypoCOMPaSS study.Diabetes care,43(1), 44-52. Fanelli, C. G., and et. al., (2020). Hypoglycemia.Diabetes Complications, Comorbidities and Related Disorders, 615-652. Pratley, R. E., and et. al., (2020). Effect of continuous glucose monitoring on hypoglycemia in older adults with type 1 diabetes: a randomized clinical trial.Jama,323(23), 2397-2406. Fabris, C., and et. al., (2020). The Use of a Smart Bolus Calculator Informed by Real-time InsulinSensitivityAssessmentsReducesPostprandialHypoglycemiaFollowingan Aerobic Exercise Session in Individuals With Type 1 Diabetes.Diabetes Care,43(4), 799-805. Lacy, M. E., and et. al., (2020). Severe Hypoglycemia and Cognitive Function in Older Adults WithType1Diabetes:TheStudyofLongevityinDiabetes(SOLID).Diabetes Care,43(3), 541-548. Chow, L., & Seaquist, E. R. (2020). How Significant Is Severe Hypoglycemia in Older Adults With Diabetes?.Diabetes care,43(3), 512-514. Kwan, T. N., and et. al., (2020). Relative hypoglycemia in diabetic patients with critical illness.Critical Care Medicine,48(3), e233-e240. Misra-Hebert, A. D., and et. al., (2020). Risk prediction for severe hypoglycemia in a type 2 diabetes population with previous non-severe hypoglycemia.Journal of Diabetes and its Complications,34(1), 107490. Hoogwerf, B. J. (2020). Hypoglycemia in Older Patients.Clinics in Geriatric Medicine,36(3), 395-406. Lontchi-Yimagou, E., and et. al., (2020). Plasma Epinephrine Contributes to the Development of Experimental Hypoglycemia-Associated Autonomic Failure.The Journal of Clinical Endocrinology & Metabolism,105(11), dgaa539. Mitchell,S.L.,andet.al.,(2020).Pharmacogeneticsofhypoglycemiaassociatedwith sulfonylurea therapy in usual clinical care.The Pharmacogenomics Journal, 1-9. Szypowska, A. and et. al.,(2016). Insulin pump therapy in children with type 1 diabetes: analysis of data from the SWEET registry. Pediatric diabetes, 17, 38-45. Tarchick, M. J., and et. al., (2019). Endogenous insulin signaling in the RPE contributes to the maintenance of rod photoreceptor function in diabetes. Experimental eye research, 180, 63-74. Satin, L. S., Butler, P. C., Ha, J., & Sherman, A. S. (2015). Pulsatile insulin secretion, impaired glucose tolerance and type 2 diabetes. Molecular aspects of medicine, 42, 61-77. Online 11
PATHOPHYSIOLOGYOFHYPERGLYCEMIA,2018.[Online].Availablethrough: <https://www.ncbi.nlm.nih.gov/books/NBK279146/> PHYSIOLOGICAL RESPONSES TO HYPOGLYCEMIA, 2011.[Online]. Available through: <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3755377/> EXOGENOUSANDENDOGENOUSINSULININTYPE1DIABETES,2018.[Online]. Availablethrough: <https://www.endocrinology.org/endocrinologist/129-autumn18/features/endogenous- insulin-its-role-in-the-initiation-progression-and-management-of-diabetes/> InsulinPumpTherapy,2019.[Online].Availablethrough: <https://www.diabetes.co.uk/insulin/insulin-pump-therapy.html> 12