Nursing 311 Exam 3

What is Diabetes Mellitus?
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What are the etiologies of DM?Both are probably multifactorialWhat is the Pathophysiology of DM I?Most widely accepted theory is that the Beta Cells are destroyed by an inappropriate autoimmune response. This Theory supported by the presence of islet cell antibodies in 85% of newly Dx IDDM clients. Inherited Susceptibility Viruses possibly either trigger the immune response or cause inflammation which leads to Beta Cell destruction. End result is little or no production of endogenous insulin.What is the Pathophysiology of DM - Type 2?Resistance to insulin in the cell membrane receptors, or a decrease or a decrease in the number of receptors. Can result in normal or increased production of endogenous insulin. Age, Obesity and Heredity.Body Weight at onset of DM?Type I - Thin or IBW Type 2 - ObeseClinical Manifestations of Type 1 DM:Polyuria - increased urine output Polydipsia - increased thirst (Hypothalamus) Polyphagia - Increased Hunger Weight Loss - Fats and Proteins broken down and used for energy Weakness/Fatigue - Poor use of food productsClinical Manifestations of Type 2 DM:Polyuria, Polydipsia, Polyphagia, Weakness, Fatigue, but may be asymptomatic.Management of Type 1 DM:Exogenous Insulin, Diet, Exercise, Acute complications are more common, Chronic complications usually occur at an earlier age.Management of Type 2 DM:Diet, Exercise, Oral Hypoglycemic medication, Insulin possiblyControl of DM Type 1 and Type 2:type 1 - more difficult, wide fluctuations in BS type 2 - usually easily controlled if adhere to diet.What are the criteria for Dx of DM?1. FBS > 126 mg/dl 2. Presence of islet cell antibodies 3. Glycosylated hemoglobin > 5.5% 4. Glucose tolerance testCriteria for Good Control:1. Maintain optimal weight and in good health 2. Glycosylated hgb < 7% 3. FBS under 140 mg/dl 4. Postprandial BS no higher than 180 mg/dlWhat are acute complications of DM?1. Diabetic Ketoacidosis 2. HypoglycemiaDiabetic KetoacidosisExtreme Hyperglycemia of 300-800 mg/dl with ketonuria. Caused by: Not enough insulin, illnesses, psychologic stressPathophysiology of Diabetic Ketoacidosis- Marked decrease in insulin -> Decreased glucose transport into the cells - The body senses this lack of cellular fuel (but still high in blood stream) --> Glycogenolysis (breakdown of glycogen stores and gives us more glucose, the body thinks its helping) and Gluconeogenesis (creation of new glucose from fats and proteins) -- both of these processes make things worse, they increase the blood sugar levels within the body, the body needs insulin not more sugar. - The high BS -> Exerts an Osmotic Diuresis (Pulls fluid into the vasculature, which is filtered out of the bloodstream by the kidneys and increases urine output) --> Dehydration results (can be extreme) (and also remember osmotic action leads to polyuria and polydipsia) - Increased lipolysis --> Ketone Production and Ketone Accumulation --> Ketonuria (Ketones in the urine) and acidosis, Excretion of ketone acids by the lungs (breathe hard, deep, and fast). - Acidosis --> Hyperkalemia (REVIEW UNIT #1 Hyperkalemia Manifestations). - Increased proteolysis and Lipolysis --> Increase in gluconeogenesisClinical Manifestations of Diabetic KetoacidosisHyperglycemia Ketonuria Polyuria, Polydipsia, Polyphagia Nausea/Vomiting, Abdominal Pain Kussmaul's Respirations (fast, hard, deep) Can lead to hypotension, tachycardia, shock, cardiac arrhythmias.Management of Diabetic KetoacidosisA. Shift from fat catabolism to CHO catabolism - by giving insulin B. Correct fluid and electrolyte imbalances C. Correct the causeWhat is hypoglycemia (insulin reaction)?Definition: BS level less than 60 mg/dl - often called "insulin reaction" or "insulin shock" Results from: Overdose of insulin Inadequate food intake Increased amounts of exerciseWhat are the two types of Clinical Manifestations of hypoglycemia?1. Neurogenic reaction when the hypothalamus senses decreased glucose levels: Increased HR, RR, - Diaphoresis, pallor, tremors, cool skin. 2. Cellular Malnutrition: Headache, Dizziness, irritability, confusion, fatigue, vision changes, hunger, seizures, and coma.Management of Hypoglycemia:Give Glucose Correct fluid and electrolyte imbalances Correct the causeWhat are chronic complications of DM?1. Macrovascular Degenerative Changes. 2. Microvascular Disease (Degenerative Changes) 3) Neuropathy 4) Infection/Poor Wound HealingMacrovascular Degenerative is probably related to:Lipolysis --> Hyperlipidemia --> Atherosclerosis --> CAD, PVD, CVA (Stroke)Microvascular Disease:1) Glycosylation of proteins (attaching glucose to proteins, overtime)--> Formation and deposits of AGE's (Advanced Glycosylation End Products) in vessel walls. (irreversible) 2) Protein Kinase C (enzyme) is activated (inappropriately) by high BS So then 1 and 2 above lead to vascular cell proliferation ---> --> Thickens the basement membrane --> decreased perfusion --> hypoxia, ischemia to those affected areas. Major places affected Retina (Diabetic Retinopathy) Kidney (nephropathy, renal failure) Also affects extremities - (feet and lower legs)Neuropathy:Etiology: Related to the microvascular disease Vascular Ischemia --> Nerve endings are destroyed in the ischemic areas. - Peripheral: Pain and tingling in extremities, Decreased sensation, - Autonomic Nervous System: gastroparesis (Decreased GI movement of feces), neurogenic bladder (Decreased emptying of bladder), sexual dysfunction, CV - no HR variability.Infection/Poor Wound Healing related to DM- Glucose is a good media for growth - Decreased sensation, decreases possible prevention. - Hypoxia/Ischemia causes poor wound healingPurines:Adenine (bonds with Thymine) Guanine (bonds with Cytosine)Pyrimidines:Thymine (bonds with Adenine) Cytosine (bonds with Guanine)Characteristics - Autosomal dominant:1. Males = females 2. No skipping of generations 3. Affected heterozygous individuals have a 50% chance to transmit the trait to each offspring.Characteristics - Autosomal recessive:1. Males = females 2. Usually skips a generation 3. Both parents of an affected child are carriersCharacteristics - X-Linked dominant:1. Males = females 2. On males, traits either dominant or recessive are expressed as phenotype 3. Usually, affected dads have unaffected sons, but affected daughters 4. Heterozygous moms have a 50% chance of transmitting the trait to each daughter or son.Characteristics - X-Linked recessive:1. Males > females 2. Affected dads cannot transmit to sons, but transmit to all daughters 3. Sons of mom carriers have a 50% chance of being affected carriers. 4.Daughters of mom carriers have a 50% chance being carriers.Compare and Contrast Veins and ArteriesArteries - Elastic (Constrict and Dilate), Maintain BP and perfusion (Deliver O2 and nutrients). Veins - can stretch but not as elastic, Adequate "venous return" requires valves and muscles that contract.FACTORS AFFECTING BLOOD FLOWPressure - "if you have low BP you will not have good blood flow." Resistance - Obstruction, constrictions, dilation Viscosity - "thickness"Types of ObstructionsThrombus- a clot. Thrombosis- when a thrombus occludes a vessel. Embolus- any foreign object, usually a thrombus, that circulates.Which Obstructive Diseases are acute?Arterial Thromboembolism Venous Thrombosis ThrombophlebitisWhich Obstructive Diseases are CHRONIC?Arterial Atherosclerotic Occlusive Disease Venous Insufficiency and Venous StasisArterial Thromboembolism EtiologyEtiologies: -Atherosclerotic disease -Stimulation of Coagulation System - Irritation - Trauma - Inflammation - Stasis (immobility, atrial fib(Cardiac Rhythm Problem) ) - lack of blood flowClinical Manifestations of Arterial Thromboembolism - Acute- R/T Ischemia (Not Enough O2) Pain - Described as Cramping and Squeezing Pain - During or after exercise - Relieved by rest Diminished Pulses - distal to blockage Pallor, Cyanosis Cool Extremities Tissue Death - only if not enough O2 gets to tissue distal to blockage.More Thrombosis occur because?More Venous Thrombosis because of lower pressure, less flow compared to arterial pressure and flow.Venous Thrombosis - ACUTE-Thrombi range from partial to complete occlusion -Emboli may develop, loosen, and circulate Etiology: Inflammation/Infection Trauma Stasis (Immobility, atrial fibrillation) Hypercoagulability Incompetent Valves Poor Muscle Contraction (Aging) Severity of venous thrombosis is related to two things: 1) Degree of obstruction (can be partial or complete) 2) Degree that collateral circulation can compensate.When there is inadequate Collateral Circulation:1) Increased venous pressure in distal veins. 2) Distension of veins 3) Congestion/pressure changes 4) EDEMA/Damage VenulesThrombophlebitis - ACUTEit is venous thrombosis with inflammation - Symptoms can occur hours after thrombus, and usually persist 1-3 weeks - Inflammatory cells accumulate & cause congestion of capillaries/venulesVenous Thrombosis is on a Continuum:Thrombosis Little Inflammation......................................Thrombosis Severe InflammationClinical Manifestations of Venous Thrombosis/Thrombophlebitis:R/T Swelling / Congestion / Inflammation - Pain - Localized Tenderness - Redness/Warmth - EDEMAComplications of Thrombosis/Thrombophlebitis if a clot breaks loose:Clots forming in the heart (with atrial fib) travel to the: - BRAIN Venous Clot travel to the: - LUNGS - Pulmonary EmbolismVenous Insufficiency and Venous Stasis - CHRONICThis one is CHRONIC!! Inadequate venous return over time: - Lead to stasis (Over time causes problems on both the venous and arterial sides) - Especially involves iliofemoral veins Mechanisms that Fail: -Muscles (Calf) -Elastic Veins -Valves -Mechanisms Fail ---> Venous HTN (distal to the process) --> Upsets Capillary fluid exchange ---> Congestion and Edema ---> StasisClinical Manifestations of Venous Insufficiency and Venous Stasis:Pain - describes as a DULL ACHE - Worse with legs in a dependent position or standing still - Relieved with walking or leg elevation - Brawny Edema - hard feel to skin - Dermatitis and Hyperpigmentation r/t poor nutrition - Poor Circulation - effect arterial side as well - may loose hair and legs appear shiny - Stasis Ulcers - r/t ischemia and poor nutritionARTERIAL ATHEROSCLEROTIC OCCLUSIVE DISEASE - CHRONICCommon sites: Coronary Arteries Abdominal aorta Iliac/Femoral Arteries Carotid Arteries - Arteriosclerosis: Thickening and Hardening of the arteries - Atherosclerosis = arteriosclerosis due to fatty and fibrin deposits.Clinical Manifestations of Arterial Atherosclerotic Occlusive Disease:R/T Ischemia: Occlusion --> Decreased Blood Flow --> Decreased perfusion 1)Pain - cramping, squeezing, during or after exercise, relieved by rest. 2)Diminished Pulses - distal to the blockages 3)Pallor, cyanosis 4)Cool Extremities 5)Tissue Death 6)Prolonged Capillary Refill/Loss of Hair 7)Slowed Nail Growth/Muscle WeaknessThree Factors in the Maintenance of Arterial Blood Pressure:1) Blood Volume 2) Peripheral (Systemic) vascular resistance (PVR or SVR) Vasoconstrict and Vasodilation 3) Cardiac Output (Heart Rate * Stroke Volume)Neural Control of Blood Pressure:Autonomic Nervous System: - PSNS but not much Mostly the Sympathetic System:Cardiovascular Control Center:Receives information about bp throughout - which increases inhibition or decreases inhibition of SNSSNS Impulses does two things- Releases Norephinephrine and epinephrine which excites: Alpha Receptors and Excites Beta1 Receptors (heart)When Alpha Receptors are excited they:Cause vasoconstriction and Increases blood pressureWhen Beta 1 Receptors are excited:Increase HR and Increase force of cardiac contraction which increases blood pressureWhat are the two main types of baroreceptors that respond to changes in BP?1)Arterial Pressoreceptors 2)Atrial Receptors (Volume)Arterial Pressoreceptors:- Located immediately off of the left ventricle. - Sense changes in "pressure" in the major arteries - Send impulses to the CV control center to either increase or decrease SNS inhibition. ****CV control center works by inhibiting the SNS If BP Low, CV will reduce inhibition to promote more SNS activity BP increases If BP High, CV inhibits SNS Activity, BP decreases,Atrial Receptors:- Located on Venous Side, Vena Cava and Right Atrium - Sense Tension (Volume) in Large VeinsHow do Kidneys affect BP?through the Renin-Angiotensin-Aldosterne System, which is separate from Neural Control. REVIEW THIS DIAGRAM!Hypertension is known as?The Silent Killer Types: 1. Essential (90%) - Primary - No Known Cause 2. Secondary (10%) - Due to a known cause - cause can be found andHypotheses of Primary HTN:1)Increase in Blood Volume 2)Overstimulation of the SNS 3)H2O and Na+ retention by the kidneys.Pathophysiology of Chronic HTN:1)High Bp, over time, vascular cellular proliferation and damages arterial walls. 2) Thickening of the basement membrane of arteries 3) Permanent narrowing and poor perfusion out of capillaries.Clinical Manifestations of Mild to Moderate HTN:May be asymptomatic or vagueClinical Manifestations of Advanced HTN:- Related to increased pressure in arterial system and in fragile capillaries: - Headache, epistaxis (nose bleed) - Dizziness, unsteadiness, blurred vision - Retinopathy - CAD - leads to a hardening of the arteries - HTN is a definite risk factor for early contraction of CAD. - Renal Insufficiency (Kidneys are extremely vascular and susceptible to damage.What are the organs most acutely affected and what are the Tx of HTN:- Heart, Brain, Eyes, Kidneys - Drug Therapy, Exercise, Diet, Low Na +Orthostatic Hypotension- Decrease in BP upon standing - Poor Reflex Vasoconstriction Related Symptoms: Dizziness, Blurred Vision, FaintingShock is?Overall or generalized reduction of adequate blood flow and O2 delivery to the tissues.Hypovolemic Shock:Results from loss of circulating blood volume. Etiology: Hemorrhage, Dehydration, Burns/Tissue TraumaCM of Hypovolemic Shock:R/T to decreased perfusion and related to compensatory mechanisms. - Hypotension - Low BP - Tachycardia - Blood is shunted away from Skin and Kidney to the Brain, Heart and Lungs - Oliguria - decreased urine output - Cool/Pale Skin - Restlessness and altered LOCWhat are the three stages of Shock?1. Non-Progessive 2. Progressive 3. IrreversibleNon-progressiveInitial or early phase Compensatory mechanisms are activated This maintains adequate perfusion to the tissues.ProgressiveCompensatory mechanisms are STILL activated, but unable to restore BP and perfusion, due to not enough volume. Start to see effects of hypoperfusion to the tissues.IrreversibleInadequate compensation Ischemic cell death occurs Multi-organ dysfunctionPathophysiology of Physical Inactivity:Skeletal Muscles down-regulate their capacity to burn fuel: - Decreases capillary Density - Increases Insulin resistance - Decreases glucose transportWith Regular Exercise:Decreased: -LDL, VLDL -BP -Insulin Resistance -CRP - an inflammatory marker -Platelet aggregation -Myocardial O2 demand Increased: -HDL -Cardiovascular function -Coronary blood flow