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NUSC 2P14 > Week 10: Metabolic & Endocrine Disorders > Flashcards

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
Q

Thyroid Disorder: Goitre

A

-Abnormal growth of thyroid gland
-Manifestation of thyroid disorders

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26
Q

Thyroid Disorder: Thyroiditis

A

-Viral, bacterial or fungal infection
-Autoimmune (Hashimoto’s)

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27
Q

Thyroid Disorders: Hyperthyroidism

A

-↑ thyroid hormone
-Grave’s disease

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28
Q

Thyroid Disorders: Hypothyroidism

A

-↓ thyroid hormone
-Tx with Synthroid

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29
Q

Thyroiditis

A

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

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30
Q

Hyperthyroidism – Graves’ Disease

A

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

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31
Q

Grave’s Disease: Collaborative Care

A

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

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32
Q

Grave’s Disease- Thyroidectomy

A

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
Q

Hypothyroidism

A

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
Q

Hypothyroidism: Signs and Symptoms

A

-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
Q

Hypothyroidism: Collaborative Care

A

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
Q

Hyperparathyroidism

A

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
Q

Cushing’s Syndrome

A

-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
Q

Cushing’s Syndrome: Clinical Manifestations

A

-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
Q

Cushing’s Syndrome: Collaborative Care

A

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
Q

Cushing’s Syndrome: Meds

A

-Mitotane (Lysodren)
-Ketoconazole

41
Q

Addison’s Disease

A

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
Q

Addison’s Disease: Complication

A

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
Q

Diabetes Mellitus (Epidemiology)

A

-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
Q

Diabetes Mellitus: Definition

A
  • 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
Q

Diabetes: Type 1

A

-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
Q

Type 1- Symptoms

A

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
Q

Type 1: Treatment

A

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
Q

Diabetes: Type 2

A

-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
Q

Type 2 Contributing Factors

A

-Age 30+
-Overweight: poor diet
-Family history
-Inactivity
-History of gestational diabetes

50
Q

Type 2 Manifestations

A

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
Q

Type 2 Treatment

A

-Healthy eating
-Reducing weight
-Exercise
-Monitor blood glucose
-Medication: may include pills and/or insulin injections

52
Q

Prediabetes

A

-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
Q

Gestational Diabetes

A

-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
Q

Diabetes: Diagnostics

A

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
Q

Diabetes: Collaborative Care

A

Goals of Diabetes Management:
-Promote well being
-Decrease symptoms
-Prevent acute complications of hypo- & hyperglycemia
-Delay onset & progression of long-term complications

56
Q

Drug Therapy: Insulin

A

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
Q

Drug Therapy: Insulin Types

A

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
Q

Drug Therapy: Insulin

A

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
Q

Drug Therapy: Insulin Pump

A

-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
Q

Problems With Insulin Therapy

A

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
Q

Drug Therapy: Antihyperglycemic Agents

A

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
Q

Drug Therapy: Antihyperglycemic Agents

A

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
Q

Diabetes- Nutritional Therapy

A

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
Q

Diabetes: Patient teaching

A

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
Q

Nursing Management- Assessment

A

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
Q

Diabetes: Acute Complications

A

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
Q

Diabetic Ketoacidosis (DKA)

A

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
Q

Diabetic Ketoacidosis: Precipitating Factors

A

-Illness/Infection
-Inadequate insulin dosage
-Most likely occurs in type 1
-Poor self management

69
Q

Diabetic Ketoacidosis: Manifestations

A

-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
Q

Diabetic Ketoacidosis: Collaborative Care

A

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
Q

Diabetic Ketoacidosis – Emergency Mgmt

A

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
Q

Hypoglycemia

A

-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
Q

Hypoglycemia – Nursing Care

A

-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
Q

Chronic Complications

A

-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
Q

Macrovascular Chronic Complications

A

-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
Q

Microvascular Chronic Complications

A

-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
Q

Diabetic Retinopathy

A

-microvascular damage to retina
-Reduced vision,
-May result in retinal detachment, potentially leading to blindness

78
Q

Diabetic Nephropathy

A

-microvascular damage to the small blood vessels that supply the glomeruli of the kidney
-Leading cause of end- stage renal disease

NUSC 2P14 (7 decks)

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