Week 10: Metabolic & Endocrine Disorders Flashcards

1
Q

Endocrine System

A

-Network of glands in the body that make hormones

Regulate:
-Mood
-G&D
-Organ functions
-Metabolism
-Reproduction

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2
Q

Endocrine Glands

A

-Ductless glands that secrete hormones directly into the blood
-Distributed throughout the body
-Each gland secretes different hormones

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3
Q

Hormones: Communication & Coordination

A

-Each hormone has a different function and works on a specific organ or cell
-Binds to receptors of specific tissue or organ: “target tissue” to cause an effect
(lock and key mechanism)

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4
Q

Hypothalamus & Pituitary (connectors)
Endocrine System:

A

-Chemical system
-Hormones via blood
-Slower response
-Long term effects

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5
Q

Hypothalamus & Pituitary (connectors)
Nervous System:

A

-Electrical system
-Nerve impulses
-Rapid response
-Short term effects

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6
Q

Hypothalamus

A

-A structure that is part nervous system and part endocrine system
-Connects nervous & endocrine systems to coordinate control & regulation of body
-Receives information from receptors throughout the body via the nervous system
-Regulates body’s reaction via the endocrine system, specifically the pituitary gland

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7
Q

Hormones- Regulation (Feedback Loops)

A

-Keeps hormone levels within a set normal range (self-regulating)
-Negative–↑or↓ secretion of hormone (think thermostat)
-Positive – ↑ the target organ action beyond normal (think oxytocin & labor)

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8
Q

Hormones- Regulation (Biorhythms)

A

-Rhythmic alterations in a hormone’s rate of secretion
-Circadian rhythm: 24h rhythm, repeats once per day (sleep- wake cycle)
-Monthly rhythm: repeats once per month (menstrual cycle)

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9
Q

Hormones- Regulation (Central Nervous System)

A

-Helps control the secretion of hormones in 2 ways:
ACTIVATION: of the hypothalamus
STIMULATION: of the sympathetic nervous system
-Emotional centre: impacts endocrine system

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10
Q

Anterior Pituitary Hormones

A

Thyroid-stimulating hormone TSH:
-stimulates the thyroid gland

Adrenocorticotropic hormone (ACTH):
-stimulates the adrenal glands

Gonadotropins: FSH / LH
* Follicle stimulating hormone
* Luteinizing hormone
-Stimulates the ovaries & testes

Growth hormone GH:
-Acts on bones, muscles, and cells to promote growth of body tissues

Prolactin PRL:
-Acts on mammary glands to stimulate milk production

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11
Q

Posterior Pituitary Hormones

A

Antidiuretic Hormone ADH:
-Prevents kidneys from excreting excessive amounts of water

Oxytocin:
-Causes the uterine muscles to contract during childbirth

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12
Q

Thyroid and Parathyroid Glands

A

Thyroid:
-regulates all phases of metabolism

T3 & T4:
-Affects nervous system and G&D

Calcitonin:
-Inhibits loss of calcium from bone

Parathyroid Hormone (PTH):
-Regulates the blood level of calcium
-Renal conversion of vitamin D to its most active form

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13
Q

Adrenal Glands

A

Adrenal Medulla
-Stimulated by the sympathetic nervous system “fight or flight”
-Emergency/stress situations:
Epinephrine (adrenaline)
Norepinephrine (noradrenaline)

Adrenal Cortex
-Steroids essential for life
Cortisol: regulates blood glucose concentration by stimulating gluconeogenesis
Aldosterone: salt-retaining hormone
Sex Hormones: onset of puberty

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14
Q

Glands- Gonads & Hormones

A

-Produce hormones needed for the development of sexual characteristics & maintenance of reproductive organs

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15
Q

Pancreas- Regulation of Blood Glucose

A

Islets of Langerhans- hormone secreting cells

Insulin:
-Breaks down glucose for energy
-Transports glucose into cells
-Stabilizes blood glucose range 4-6 mmol/L

Glucagon:
-Ensures a supply of glucose for busy cells
Converts:
-Glycogen into glucose in the liver & releases into the bloodstream
-Proteins into glucose

Antagonistic Hormones: opposite

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16
Q

Assessment

A

Hormones affect every tissue and system in the body, causing great diversity in manifestations of endocrine dysfunction
-Endocrine disorders generally result from too much or too little of a specific hormone
-The onset of symptoms is often gradual
-Pts may also present with acute symptoms that are life-threatening

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17
Q

Assessment- Subjective Data

A

Past health Hx:
-Usually c/o a group of S&S
-Fatigue
-Weakness
-Menstrual irregularities
-Weight changes

Family Hx:
-1st degree relatives with:
-diabetes
-thyroid probs
-endocrine gland cancers
-goitre

Meds
-Rx
-OTC
-Hormone replacement:
insulin, thyroid, prednisone

Surgery or other Tx
-Hospitalizations
-Surgery
-Chemotherapy
-Radiation, esp of the neck

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18
Q

Assessment- Objective Data

A

Physical Exam:
-Body temp: varies r/t thyroid
-Height & Weight
-Alertness & emotional state
-Hair, skin, nails
-Facial features & eyes
-Neck

Auscultate:
-Heart rate
-Blood pressure

Palpate:
-Extremities for edema
-Skin for texture & temp
-Neck for thyroid size & shape

Diagnostics:
-Blood & urine testing
- K+, Na+
-Glucose & A1C
-Thyroid studies (TSH)
-Ultrasound, x-ray, CT,MRI

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19
Q

Posterior Pituitary Disorders

A

Posterior Pituitary Gland: antidiuretic hormone (ADH)

-Syndrome of inappropriate antidiuretic hormone (SIADH) (overproduction of ADH)

-Diabetes insipidus (deficiency of ADH)

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20
Q

Syndrome of Inappropriate ADH (SIADH)

A

-Increased antidiuretic hormone
-Increased water reabsorption in renal tubules
-Increased intravascular fluid volume
-Dilutional hyponatremia and decreased serum osmolality

Most Common Cause in Lung Cancer:
-Head trauma, psychosis, meds, metabolic disease

S&S:
-N&V, abdominal cramps, muscle twitching, seizure

Decreased plasma osmolality & decreased Na+:
-Cerebral edema, low urine output, increase weight

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21
Q

SIADH- Nursing Care

A

Goal:
restore normal fluid volume and serum osmolality
If Severe:
-IV hypertonic saline solution 3-5%
If chronic:
-Water restriction 800-1000 ml/d

Frequent Measurement:
-Daily weight
-I&O
-Urine specific gravity
-VS
-Lung sounds
-LOC
-S&S of hyponatremia

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22
Q

Diabetes Insipidus

A

Occurs suddenly:
-Increased thirst, nocturia
-Polyuria: 5-20 L/day
-Fatigue & weakness

Fluid Deficit Results In:
-Wt loss
-Constipation
-Poor skin turgor
-Hypotension
-Tachycardia
-Shock
-CNS S&S

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23
Q

Decreased Antidiuretic Hormone

A

-Decreased water reabsorption in renal tubules
-Decreased intravascular fluid volume
1.)increased serum osmolality (hypernatremia)
2.)excessive urine output

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24
Q

Diabetes Insipidus- Nursing Care

A

Goal: maintenance of fluid & electrolyte balance
-Fluid & hormone replacement is cornerstone of tx
-Acute
* hypotonic saline – IV 0.45% NS
* Desmopressin acetate (ADH replacement)
-Long term
* Desmopressin acetate

Monitoring:
-daily weight
-I&O
-Urine specific gravity
-VS
-LOC
-S&S of dehydration

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25
Thyroid Disorder: Goitre
-Abnormal growth of thyroid gland -Manifestation of thyroid disorders
26
Thyroid Disorder: Thyroiditis
-Viral, bacterial or fungal infection -Autoimmune (Hashimoto’s)
27
Thyroid Disorders: Hyperthyroidism
-↑ thyroid hormone -Grave's disease
28
Thyroid Disorders: Hypothyroidism
-↓ thyroid hormone -Tx with Synthroid
29
Thyroiditis
Acute: -thyroid gland is tender & enlarged -Neck pain & fatigue Chronic Autoimmune: -Hashimoto’s thyroiditis -Most common in women -Can lead to hypothyroidism and goitre Treatment: -Depends on type -Salicylates & NSAIDs -corticosteroids
30
Hyperthyroidism – Graves’ Disease
Autoimmune disease of unknown etiology marked by diffuse thyroid enlargement and excessive thyroid hormone secretion -Thyrotoxicosis Signs & Symptoms -Heat intolerance & excessive sweating -Tachycardia -Weight loss -Tremors -Goitre -Exophthalmos Exophthalmos Impaired venous drainage Increased fat deposits & edema behind the eyeball Eyeballs are forced outward & protrude
31
Grave's Disease: Collaborative Care
Goal is to block the adverse effects of thyroid hormones and stop their oversecretion Diagnostics: -Bloodwork -TSH levels * free T4 -24h radioactive iodine uptake (RAIU) test Therapies: -Radioactive iodine -Subtotal thyroidectomy – 90% -Nutritional: frequent, high- calorie, high- protein Medication: -Antithyroid -Tapazole -Propyl-Thyracil -Iodine -Inderal
32
Grave's Disease- Thyroidectomy
Indicated When: -A large goitre causes tracheal compression -Condition does not respond to antithyroid therapy -The pt has thyroid cancer Post OP: monitor q2h x 24h -Hemorrhage or tracheal compression -Vital signs -Signs of hypocalcemia & tetany -Check for Trousseau’s & Chvostek’s signs x72h -Pain and nausea control Hypocalcemia is a major post-op complication r/t 2o hypo- parathyroidism following damage to one or more parathyroid glands during surgery.
33
Hypothyroidism
High serum levels of TSH and insufficient free circulating T4 hormone Causes: -Iodine deficiency (worldwide) -Canada: atrophy of thyroid gland -Hashimoto’s, Graves’ -Thyroidectomy -Radioactive iodine therapy
34
Hypothyroidism: Signs and Symptoms
-Insidious and nonspecific slowing of body processes -Neurological, cardiovascular, GI, reproductive, & hematological systems -Fatigued & lethargic -↓ cardiac output * SOB -Anemia -Personality & mental changes -Impaired memory -Slowed speech -↓ initiative & somnolence; may appear depressed -↓ GI motility & constipation -Myxedema -Menorrhagia
35
Hypothyroidism: Collaborative Care
Goal is restoration of normal thyroid function as safely & rapidly as possible with hormone replacement therapy Diagnostics -Blood Work -TSH levels -free T4 -Cholesterol -Triglycerides -Anemia Therapies -Monitor thyroid hormone levels -Nutritional: promote weight loss -Pt & caregiver teaching -Thyroid hormone replacement Medication -Levothyroxine (Synthroid): lifelong Most individuals with hypothyroidism do not require acute nursing care. Myxedema coma does require acute nursing care, often in a critical care setting. Mortality 30-50% With treatment, striking transformations occur in both appearance & mental function. In most adults, both return to normal.
36
Hyperparathyroidism
Over Secretion of parathyroid hormone (PTH): -osteoclast activity Ca2+ leached from bones: -↓ Bone density Hypercalcemia & hypophosphatemia: -Renal calculi -Tx goal: relieve the symptoms & prevent complications caused by excessive PTH -Parathyroidectomy – partial or complete via endoscopy (outpatient) -Autotransplantation in forearm -Tetany r/t sudden ↓ in Ca2+ -Unpleasant tingling sensation of the hands and around the mouth -Monitor I&O -Assess Chvostek’s & Trousseau’s signs -Encourage mobility to promote bone calcification
37
Cushing's Syndrome
-A metabolic disorder that occurs when the body makes too much cortisol over a long period ~85% of cases result from an ACTH-secreting Most common among pituitary tumour -Most common among women aged 20-40
38
Cushing’s Syndrome: Clinical Manifestations
-Truncal or general obesity -Moon face with facial swelling & redness -Purplish red striae on the abdomen, the breasts, or the buttocks -Hirsutism in women -Amenorrhea, erectile dysfunction, ↓ libido -Hypertension -Unexplained hypokalemia
39
Cushing’s Syndrome: Collaborative Care
Tx goal: normalize hormone secretion * If pituitary tumour: surgical removal * If adrenal tumour: bilateral laparoscopic adrenalectomy -Nursing care -VS, daily wt, glucose level -Pre-op & post-op care -↑ risk for hemorrhage -Fluid & electrolyte balance
40
Cushing's Syndrome: Meds
-Mitotane (Lysodren) -Ketoconazole
41
Addison's Disease
Adrenocortical insufficiency: -Glucocorticoids/ Mineralocorticoids/ Androgens Most often among patients < 60 years ↑ antibodies that destroy adrenal tissue Treatment: -Replacement therapy with hydrocortisone -Increased salt in the diet S&S not usually evident until 90% of adrenal cortex is destroyed (very slow onset): -Progressive weakness; fatigue -Wt loss; anorexia -Skin hyperpigmentation over joints Hypotension -Hyponatremia -Hyperkalemia -N&V -Diarrhea -Irritability -Depression
42
Addison's Disease: Complication
Adrenal Crisis -Refers to acute adrenal insufficiency, a life-threatening emergency caused by insufficient adrenocortical hormones Triggered By: -Stress: infection, surgery, trauma, hemorrhage, or psychological distress -Sudden withdrawal of corticosteroid hormone therapy -Adrenal surgery; or sudden pituitary gland destruction -Hypotension: shock: circulatory collapse Collaborative Care: -Tx focused on shock mgmt, and high-dose IV hydrocortisone replacement -IV 0.9% NS
43
Diabetes Mellitus (Epidemiology)
-11.7 million Canadians are currently living with diabetes or prediabetes -Approximately 65% to 80% of people with DM will die as a result of heart disease or stroke -DM is a contributing factor in the deaths of approximately 41,500 Canadians each year -Adults with DM are twice as likely to die prematurely as people without DM
44
Diabetes Mellitus: Definition
- Diabetes mellitus is primarily a disorder of glucose metabolism The body either can’t: * produce insulin, * or properly use the insulin it produces Most common endocrine-system disorder -In diabetes, sugar cannot move into the cells: sugar level increases in blood Two Types: Type 1 / 2 Other Types: gestational / prediabetes
45
Diabetes: Type 1
-Autoimmune disease: body attacks the pancreas with antibodies; not preventable -Develops in childhood – young adulthood; <30yrs -10% of clients with diabetes have Type 1 -The pancreas is left damaged and does not make insulin -Without the insulin “keys” for the cell receptors, glucose is unable to enter the “doors” into the cell -Without glucose, cells are starved for energy and cannot perform their functions -Meanwhile, glucose levels rise in the blood: severe hyperglycemia
46
Type 1- Symptoms
Sudden onset: within weeks -Increased thirst -Increased urination -Increased hunger -Blurred vision -Tiredness/fatigue -Unexplained weight loss Manifestations of type 1 DM develop when the person's pancreas can no longer produce insulin The patient presents to the ER with ketoacidosis (LIFE THREATENING CONDITION)
47
Type 1: Treatment
Insulin injections/pumps -replace insulin not produced by the pancreas Blood Glucose Monitoring -to keep blood glucose within target range -pumps do this automatically
48
Diabetes: Type 2
-Body can’t produce enough insulin or is unable to use what it produces effectively -Develops in adulthood; >30yrs -Most common form of diabetes: 90% of clients with diabetes -With fewer insulin “keys” for the cell receptors, glucose is less able to enter the “doors” into the cell -With less glucose, cells receive less energy and their performance is compromised -Meanwhile, glucose levels rise in the blood: hyperglycemia
49
Type 2 Contributing Factors
-Age 30+ -Overweight: poor diet -Family history -Inactivity -History of gestational diabetes
50
Type 2 Manifestations
Slow Onset: over many years -Increased thirst -Increased urination -Increased hunger -Blurred vision -Tiredness/fatigue -Numbness, tingling in hands, feet -Sores/wounds that take longer to heal -Weight changes
51
Type 2 Treatment
-Healthy eating -Reducing weight -Exercise -Monitor blood glucose -Medication: may include pills and/or insulin injections
52
Prediabetes
-Individuals already at risk for diabetes and, if no preventive measures are taken, the condition usually will develop within 10 years -Blood glucose high but not high enough to be diagnosed as having diabetes (6.1–6.9 mmol/L) -Long-term damage already occurring – heart, blood vessels -Usually present with no symptoms
53
Gestational Diabetes
-Develops during pregnancy: detected at 24–28 weeks of gestation -Usually back to normal glucose levels at 6 weeks postpartum -Increased risk for developing Type 2 in 5–10 years -Therapy: first nutritional, then insulin if needed
54
Diabetes: Diagnostics
FOUR METHODS OF DIAGNOSIS Glycated hemoglobin (A1C): ≥ 6.5% determining glycemic levels over time (3-4mos) Fasting plasma glucose (FPG) level ≥7mmol/L Random plasma glucose (RPG) ≥11.1mmol/L Two-hour oral glucose tolerance test (OGTT) ≥11.1mmol/L
55
Diabetes: Collaborative Care
Goals of Diabetes Management: -Promote well being -Decrease symptoms -Prevent acute complications of hypo- & hyperglycemia -Delay onset & progression of long-term complications
56
Drug Therapy: Insulin
Insulin is inactivated by gastric juices, it cannot be taken orally Exogenous (injected) Insulin: -Insulin from an outside source -Required for type 1 diabetes - Prescribed for client with type 2 diabetes who cannot control blood glucose by other means
57
Drug Therapy: Insulin Types
Human Insulin- the only type used today -Different types of insulin may be used for combination therapy Types differ with regard to onset, peak action, and duration: -Rapid-acting -Short-acting -Intermediate-acting -Extended long-acting
58
Drug Therapy: Insulin
Administer S/C: -Fastest absorption from abdomen (preferred site), followed by arm, thigh, & buttock -Rotate injections within one particular site Injection Site -The use of an alcohol swab on the site before self- injection is no longer recommended -Hand washing with soap adequate Insulin Pens -preloaded with insulin -provide consistent & accurate dosing -portable & compact, more discreet
59
Drug Therapy: Insulin Pump
-Continuous subcutaneous infusion of rapid- acting insulin -Battery-operated device that holds & delivers insulin -Connected to a catheter inserted into S/C tissue in abdominal wall -User programs the pump to deliver a bolus of insulin during mealtimes ADVANTAGES: -Reduction of hypoglycemic episodes -Allows for more normal lifestyle DISADVANTAGES: -infection at the insertion site -increased risk for Somogyi effect -cost of the pump & supplies
60
Problems With Insulin Therapy
Somogyi effect: rebound effect in which too much insulin causes hypoglycemia -During hours of sleep, too much insulin -Blood glucose drops -Counter- regulatory hormones released to increase blood glucose -Rebound hyperglycemia and ketosis may occur Dawn phenomenon: hyperglycemia present on awakening in the morning -Growth hormone and/or cortisol possible factors -Release of counterregulatory hormones during predawn hours -Hyperglycemia
61
Drug Therapy: Antihyperglycemic Agents
NOT INSULIN -Work to improve mechanisms by which insulin & glucose are produced and used by the body -Work on three defects of types 2 diabetes: -Insulin resistance -Decreased insulin production -Increased hepatic glucose production
62
Drug Therapy: Antihyperglycemic Agents
Glyburide Repaglinide: -Stimulates insulin release from pancreas Metformin: -Inhibits glucose production in liver Acarbose: -Delays absorption of glucose in GI tract Pioglitazone: -Increases glucose uptake in muscle & fat
63
Diabetes- Nutritional Therapy
Cornerstone of care for person with diabetes & the most challenging for many people. Best to involve the Diabetic Nurse Educator & Registered Dietitian GOAL: Diet & nutritional energy intake balanced with energy output TYPE 1: -Meal plan is based on individual’s usual food intake and is balanced with insulin & exercise patterns -Insulin regimen is managed day to day TYPE 2: -Emphasis is based on achieving glucose, lipid, and blood pressure goals - Calorie reduction: weight loss is recommended for the overweight & obese
64
Diabetes: Patient teaching
Diet Teaching (Canada's Food Guide) Exercise (regular, consistent physical activity) Monitoring Blood Glucose: -Self-monitoring of blood glucose (SMBG) -Use edges of fingers vs pads -Continuous glucose monitoring -Periphery, around the edges of the fat pad
65
Nursing Management- Assessment
Nursing Diagnoses: -Ineffective health management -Risk for injury -Risk for unstable blood glucose levels -Risk for peripheral neurovascular dysfunction Goals: -Active client participation -Few or no episodes of acute hyperglycemic emergencies or hypoglycemia -Maintain normal blood glucose levels
66
Diabetes: Acute Complications
It is important for the health care provider to be able to distinguish between hyperglycemia and hypoglycemia because hypoglycemia worsens rapidly and constitutes a serious threat if action is not immediately taken
67
Diabetic Ketoacidosis (DKA)
An acute metabolic complication of diabetes occurring when fats are metabolized in the absence of insulin. It is caused by a profound deficiency of insulin and is characterized by: -Hyperglycemia -Ketosis -Acidosis -Dehydration
68
Diabetic Ketoacidosis: Precipitating Factors
-Illness/Infection -Inadequate insulin dosage -Most likely occurs in type 1 -Poor self management
69
Diabetic Ketoacidosis: Manifestations
-Polyuria, polydipsia: S&S of dehydration -Lethargy & weakness -Abdominal pain -N&V -Kussmaul’s respirations -Rapid deep breathing in attempt to reverse metabolic acidosis -Sweet fruity breath due to acetone
70
Diabetic Ketoacidosis: Collaborative Care
Treatment: SERIOUS CONDITION -Must be treated promptly -May or may not need hospitalization -If fluid & electrolyte imbalances are not severe and blood glucose levels can be safely monitored at home
71
Diabetic Ketoacidosis – Emergency Mgmt
Ensure Patent Airway: -O2 administration FLUID RESUSCITATION: -IV fluids until BP is stabilized and urine output (>30-60 ml/h) -IV potassium for hypokalemia -IV sodium bicarbonate if severe acidosis -IV regular insulin drip to allow water & potassium to enter the cell along with glucose MONITOR: -Breath sounds for fluid overload -Serum glucose & potassium, and pH -LOC -Vital signs, cardiac rhythm -O2 sats -Urine output
72
Hypoglycemia
-Low blood glucose occurs when there is too much insulin in proportion to available glucose in the blood -This causes the blood glucose level to drop to less than 4 mmol/L -Once plasma glucose drops to this level, neuroendocrine hormones are released and the autonomic nervous system is activated
73
Hypoglycemia – Nursing Care
-Symptoms may occur when a very high blood glucose level falls too rapidly -Can usually be quickly reversed with effective and rapid treatment -Treated by ingesting 15-20g of a simple (fast-acting) carbohydrate such as: 1.) 3-4 glucose tablets 2.) 175 ml of fruit juice or regular pop 3.) 6 Life Savers candies
74
Chronic Complications
-Are primarily those of end-organ disease that result from damage to the large and small blood vessels (angiopathy) secondary to chronic hyperglycemia -Angiopathy (blood vessel disease) accounts for the majority of deaths among patients with diabetes -These chronic blood vessel dysfunctions are divided into two categories: a.) macrovascular complications, and, b.) microvascular complications
75
Macrovascular Chronic Complications
-Diseases of large & medium-sized blood vessels -Dyslipidemia in contributing to greater risk of cardiovascular disease in clients with diabetes -atherosclerosis -Tight glucose control may delay atherosclerotic process
76
Microvascular Chronic Complications
-Thickening of vessel membranes in capillaries & arterioles -Clinical manifestations usually appear after 10–20 years of diabetes -Areas most noticeably affected * Eyes – retinopathy * Kidneys – nephropathy * Nerves – neuropathy * Skin – dermopathy
77
Diabetic Retinopathy
-microvascular damage to retina -Reduced vision, -May result in retinal detachment, potentially leading to blindness
78
Diabetic Nephropathy
-microvascular damage to the small blood vessels that supply the glomeruli of the kidney -Leading cause of end- stage renal disease