Week 8 Alterations In Endocrine Function Student PDF

Alterations in Endocrine Function SLIDES BY KARA SEALOCK EdD MEd BN RN CNCC(C) CCNE OCTOBER 2024  Topics for this Lecture: Structure and Function of the Pancreas Acute Pancreatic Dysfunction  Acute Pancreatitis Acute Endocrine Dysfunction  Diabetes  Diabetic Ketoacidosis (DKA)  Hy...

Alterations in Endocrine Function SLIDES BY KARA SEALOCK EdD MEd BN RN CNCC(C) CCNE OCTOBER 2024  Topics for this Lecture: Structure and Function of the Pancreas Acute Pancreatic Dysfunction  Acute Pancreatitis Acute Endocrine Dysfunction  Diabetes  Diabetic Ketoacidosis (DKA)  Hyperglycemia Hyperosmolar State (HHS) By the End of this Lecture You Will: Critically reflect upon the overall anatomy and physiology of the endocrine system and how dysfunction leads to significant changes systemically Explain pathophysiology and effects on the body related to:  Acute Pancreatitis  Diabetes DKA and HHS Begin to prioritize patient conditions related to nursing assessment and clinical manifestations based on lecture material and how it relates to other systems Objectives for this lecture: You will be able to identify at least two causes for pancreatitis and how this affects the body You will be able to verbalize the pathophysiology of diabetes; type 1 and type 2 You will be able to differentiate between diabetic ketoacidosis and hyperglycemia hyperosmolar syndrome Pancreatic Dysfunction  Pancreas: Structure and Function  Has both endocrine and exocrine functions Endocrine: secretes hormones such as insulin, glucagon, somatostatin and pancreatic polypeptide Exocrine: acinar cells secret enzymes and networks of ducts that secret alkaline fluids important for digestive functions  Aqueous secretions contain potassium, sodium, bicarbonate and chloride  Alkaline pancreatic juice neutralizes the acidic chime that enters the duodenum from the stomach and provides the medium for actions of digestive enzymes and intestinal absorption of fat.  Pancreatic enzymes hydrolyze proteins (proteases), carbohydrates (amylases), and fats (lipases)  Secretion of pancreatic juice is controlled by hormonal and vagal stimuli  Secretin stimulates the acinar and duct cells to secrete the bicarbonate rich fluid that neutralizes chime and prepares for digestion  Enzymatic secretion follows and stimulated by cholecystokinin and acetylcholine  Acute Pancreatitis  Risk factors include: obstructive biliary tract disease (particularly cholelithiasis), alcoholism, obesity, peptic ulcers, trauma, hyperlipidemia, hypercalcemia, smoking, certain drugs and genetic factors Pathophysiology:  Usually mild but can lead to necrotizing or hemorrhagic  Develops due to an obstruction of the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction (i.e.: gallstones)  Leads to autodigestion of pancreatic cells  vascular damage, coagulation necrosis, fat necrosis and edema  ETOH  acinar cell metabolizes ethanol with toxic metabolites which in turn injure pancreatic acinar cells, causing a release of activated enzymes  Chronic ETOH use causes formation of protein plugs in pancreatic ducts and spasm of the sphincter of Oddi, resulting in obstruction release of activated enzymes, inflammation and pancreatitis  Acute Pancreatitis Pathophysiology (con’t):  Severe acute pancreatitis, proinflammatory cytokines activate leukocytes, cause injury the vessel walls and abnormal coagulation in the lungs and kidneys paralytic ileus and GIB can occur bacteria in the bloodstream may cause peritonitis or sepsis vasoactive peptides cause vasodilation, hypotension, and shock ARDS, renal failure and Systemic inflammatory Response syndrome (SIRS) EMERGENCY! Clinical Manifestations:  Mid-epigastric or LUQ pain, nausea and vomiting (paralytic ileus), jaundice, fever and leukocytosis, abdominal distention, hypovolemia, hypotension, tachycardia, myocardial insufficiency and shock.  Severe acute pancreatitis tachypnea and hypoxemia due to pulmonary edema, atelectasis or pleural effusions, hypovolemia, renal failure (ATN), tetany due to hypocalemia, transient hyperglycemia, multi-system organ failure  Acute Pancreatitis Nursing Assessment:  I-PAP  GI Assessment: bowel sounds, distention, nausea and vomiting, guarding  Respiratory  Cardiovascular  Renal  Hyperlipidemia, hyperglycemia, hypocalcemia  Lab Values: Lipase and Amylase (may be 3x normal), WBC, Bilirubin, Sodium, Potassium, Creatinine, BUN, Lipids (TC, TG, HDL, LDL), Calcium, Troponin, ABG’s Endocrine Dysfunction Regulation of Blood Glucose  Diagnosing Diabetes and Prediabetes Prediabetes is the presence of an impaired fasting glucose and/or impaired glucose tolerance on two separate testing occasions  Types of Diabetes Mellitus Group of metabolic diseases Type 1 Type 2 Other Gestational  Classification of Diabetes Type 1 diabetes∗ encompasses diabetes that is primarily a result of pancreatic beta cell destruction with consequent insulin deficiency, which is prone to ketoacidosis. This form includes cases due to an autoimmune process and those for which the etiology of beta cell destruction is unknown. ∗ Includes latent autoimmune diabetes in adults (LADA); the term used to describe the small number of people with apparent type 2 diabetes who appear to have immune-mediated loss of pancreatic beta cells Type 2 diabetes may range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance. Ketosis is not as common. Gestational diabetes mellitus refers to glucose intolerance with onset or first recognition during pregnancy. Other specific types include a wide variety of relatively uncommon conditions, primarily specific genetically defined forms of diabetes or diabetes associated with other diseases or drug use (see Appendix 2. Etiologic Classification of Diabetes Mellitus).  So… What’s Your Type? TYPE 1 DIABETES TYPE 2 DIABETES Pancreas does not produce Pancreas does not any insulin produce enough insulin or Complete loss of beta cell insulin resistance function Usually diagnosed as an Unknown etiology but may adult but more children be autoimmune or are being diagnosed idiopathic Progressive loss of beta Requires exogenous cell function as the insulin patient gets older Occurs in 10% of Occurs in 90% of population population  So… What’s Your Type? OTHER SPECIFIC TYPES GESTATIONAL DIABETES Genetic defects of beta-cell function Insulin resistance combined Genetic defects in insulin action with inadequate insulin Diseases of exocrine pancreas secretion in relation to hyperglycemia Endocrinopathies Women who are obese, Drug-or-chemical-induced beta cell older than 25 yrs old, family dysfunction hx of DM, history of previous Infections GDM, or of certain ethnic Uncommon forms of immune- groups (Hispanic, mediated DM Indigenous, Asian, or African American) increased risk of Other genetic syndromes associated developing GDM with DM  Etiology - Type 1 DM 10% of patients with diabetes Etiology: Diagnosed in childhood,  Autoimmune adolescence, early adulthood  genetic(HLA) plus environmental trigger absolute lack of insulin autoimmune response - destruction of  cells  years / seasonal  Idiopathic   cell destruction without markers  Etiology – Type 2 DM Accounts for 90% Etiology: DM  genetic  metabolic syndrome  2004: 1:4  Insulin Receptor Canadians >45 yrs Substrate proteins - young adults  Sedentary lifestyle, visceral obesity  Preventable  Gestational DM  Neonate:  Affects 1-2%  macrosomia,  24-28 wks gestation hypoglycemia, placental hormones cause hypocalcemia, insulin resistance ...polycythemia,  50g oral glucose screen hyperbilirubinemia  C-section  disappears in 97% postpartum  20-50% develop type 2  Offspring ↑risk DM & obesity Complications Associated with Diabetes  Complications of Diabetes MACROVASCULAR MICROVASCULAR Cardiac ischemia Retinopathy  CAD/ACS  Angina Neuropathy  MI Nephropathy Peripheral Arterial Disease CKD Cerebrovascular/Carotid Disease  TIA  Stroke  Hypoglycemia Defined by:  Development of autonomic or neuroglycopenic symptoms  Low plasma glucose level (< 4.0 mmol/L for patients treated with insulin or an insulin secretagogue)  Symptoms responding to the administration of carbohydrate Complications of hypoglycemia:  Prolonged coma associated with paresis, convulsions and encephalopathy  Mild intellectual impairment  Recurrent hypoglycemia impairs the individuals ability to sense hypoglycemia  Symptoms of Hypoglycemia NEUROGENIC (AUTONOMIC) NEUROGLYCOPENIC Trembling Difficulty concentrating Palpitations Confusion Sweating Weakness Anxiety Drowsiness Hunger Vision changes Nausea Difficulty speaking Tingling Headache Dizziness  Severity of Hypoglycemia Mild  Autonomic symptoms are present  The individual is able to self-treat Moderate  Autonomic and neuroglycopenic symptoms are present  The individual is able to self-treat Severe  Individual requires assistance of another person  Unconsciousness may occur  Plasma Glucose is typically < 2.8 mmol/L  Diabetic Ketoacidosis Hyperglycemia  Gluconeogenesis  Glycogenolysis  use of Glucose by the Liver, Muscle and Fat  Serum Glucose Concentration may be > 27.8 mmol/L to 44 mmol/L Anion Gap with Metabolic Acidosis Ketonemia Develops within 1-24 hours  Pathogenesis of DKA Relative Insulin Dehydration Deficiency Ketoacidosis Stress Hormone Fasting/ Excess Starvation  Clinical Presentation of DKA Dehydration Hypotension or shock (systolic < 90 mmHg) Tachycardia (HR > 125 b/min) Kussmaul respiration / tachypnea Fruity breath Altered level of mental status Signs of precipitating cause Dry mouth and thirst Weakness, dehydration, nausea or vomiting  Clinical Presentation of DKA Symptoms Signs Extracellular Fluid Polyuria, polydipsia, Hyperglycemia Volume (ECFV) weakness contraction Air hunger, nausea, vomiting and Precipitating Acidosis abdominal pain condition Altered sensorium See list of conditions in Priorities to be Addressed in the Precipitating Management of condition Patients with Hyperglycemic Emergencies  Am I Missing Anything Else? Glucose CBC with differential Electrolytes to calculate anion gap Serum creatinine Venous (NOT arterial) blood gas for pH Urine for glucose and ketone bodies  Other Considerations Airway Management Cerebral Edema Increase incidence of thrombotic events  Anticoagulation Phosphate Magnesium  Hyperglycemia Hyperosmolar State Hyperglycemia  Serum glucose concentration > 56 mmol/L  Endogenous insulin present but not effective Severe dehydration Hyperosmolarity  Leads to neurologic abnormalities coma Little to no ketosis present More common in elderly Develops over Days*  Priorities to be Addressed in the Management of Adults Presenting with Hyperglycemic Emergencies Metabolic Precipitating Cause Other of DKA of HHS Complications of DKA/HHS  ECFV contraction  New diagnosis of  Hyper/hypokalemia  Potassium deficit diabetes  ECFV and abnormal  Insulin omission overexpansion concentration  Infection  Cerebral edema  Metabolic acidosis  Myocardial  Hypoglycemia  Hyperosmolality infarction  Pulmonary emboli (water deficit  Stroke  Aspiration leading to  ECG changes may  Hypocalcemia (if increased reflect phosphate used) corrected sodium hyperkalemia  Stroke concentration plus  A small increase in  Acute renal failure hyperglycemia) troponin may occur  Deep vein without overt thrombosis ischemia  Thyrotoxicosis  Trauma  Drugs  Key Points to Remember Can you perform a full renal and endocrine assessment and apply anatomy and physiology related to the endocrine system? Explain the “why” associated with endocrine assessment including connections to other systems Identify and apply concepts of normal function of the endocrine system Do you understand the pathophysiology, clinical manifestations and nursing assessment related to :  Acute Pancreatitis  Diabetes DKA and HHS