Endocrine System
3/6/2014 9:45:00 AM
Diabetes Mellitus
-normal Blood glucose 70-110mg/dl
-chronic systemic disorder of metabolism of carbs, proteins, & fat due to absolute or relative
deficiency of insulin
-7% of population, (20.8 million); 41 million pre-diabetes
-black, Hispanic, native Americans 3x more likely, >60years
-90% are Type II
-Type I: Insulin dependant (juvenile onset)
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hyperglycemia due to deficiency of insulin production & secretion by beta cells
ketoacidosis common: acidic blood due to ketones (breakdown of fat)

Management: require exogenous insulin to maintain life; dependent on age, level of
compliance & severity
 cell mediated autoimmune destruction of beta cells
 Risk factors: hereditary
-Type II: Non-insulin dependent/adult onset

cellular resistance to insulin action or abnormal insulin secretory response or relative
insulin deficiency
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control with diet, exercise, oral hypoglycemic agents
Risk factors: family hx, ethnicity, obesity, history of gestational DM, HTN 140/90, DL
<35
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Management: proper diet & regular daily exercise; oral medication if necessary
o Diet: foods for fast & slow glucose conversion, weight reduction
o Exercise: begin when sugar under control (100<x<300mg/dl); aerobic (Karovonen’s
formula) & resistance to promote weight loss, relaxation, decrease stress, improve
insulin receptor sensitivity, decrease risks for heart & PVD
 ECG necessary if pt. has Type II> 10 yrs, Cad risk factors, complications, PVD
 Precautions: hypoglycemia b/c exercise will lower blood sugar, duration, work
out with friend, have immediate glucose sources available

Contraindications
 Alcohol ingestion <3hrs prior
 Hypoglycemia <70mg: shakiness, pale, dizzy, seating, clumsy, hunger,
seizure, h/z
 Hyperglycemia >300mg with ketones: SOB, nausea, vomiting
-Gestational DM: glucose intolerance recognized with onset of pregnancy, b/c hormones for fetal
development block insulin; return to normal
-Acute complications: caused by immediate lack of insulin in hyperglycemic individual

polydipsia, polyuria, weight loss, fatigue, poor wound healing, blurred vision, vaginitis,
diabetic ketoacidosis
-Pathogenesis

insulin function impaired when glucose in circulation not taken up to
metabolizeaccumulates in blood
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affects mm. and fat cells requiring insulin as carrier for glucose
3 problems
o 1. Decreased utilization of glucose: glucose doesn’t get to liverliver synthesizes
more glucoseeven higher blood glucose level
o 2. Increased fat mobilization: formation of ketones when fat use for energy b/c sugar
not availablepH falls and get ketoacidosis
 lipid level rises to 5x normalatherosclerosis, clots, CV complications
o 3. Impaired protein utilization: no insulin to transport amino acids into cellsinc
protein catabolism protein loss and dec inflammatory process & wound healing

to restore glucose levels: kidney excretes excess glucose glucosuria; ketones
excretedfluid loss with sodiumfurther acidosis

Microangiopathy: long standing diabetesglycosylation of proteins in the basement
membranethick/leaky BVsexudation & ischemiaend organ damage
(retinopathy/neuropathy)
-Cardinal signs & symptoms:
 polyuria, polydipsia, polyphagia
 weight loss
 fatigue, weakness
 ketoacidosis
Medical Management
-Screening

Metabolic Syndrome: characteristics that place an individual at risk (elevated waist
circumference, triglycerides >150 mg/dl, DL, HTN with SBP and DBP, elevated fasting
blood glucose
-Diagnosis: blood glucose, fasting blood sugar, glucose tolerance test, glycosylated hemoglobin
(<7%)
-Long Term effects/precautions

Blindness: diabetic retinopathy is leading cause of new blindness; avoid increasing
pressure

Diabetic nephropathy: 10-10% of diabetics will develop, most common cause of end
stage renal disease (dialysis)

Heart disease: 2-4x more likely and suffer a stroke b/c of high cholesterol, blood sugar,
and obesity

Nerve disease & amputations: nerve damage due to sugar embedded in nerveslose
senselimb amputations especially in foot due to peripheral neuropathy (stocking/glove
distribution)
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Impotenance: blood vessel blockage or neuropathy
Neuromusculoskeletal: hands, shoulders, spine, feet
o Sensory, motor & ANSjoint destruction from repeated un-noticed trauma
o Chronic progressive degeneration: stress-bearing part of a joint has neuropathic
arthropathy of proprioceptors

Charcot: tarsal & MT joints have collapsed bone and ‘rocker bottom foot’ with
cuboid now the WB bone

Syndrome of Limited Joint Mobility: painless stiffness of finger joints (type I), flexion
contractures & tenosynovitis
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Adhesive capsulitis: loss of motion in abd & hyperextension due to capsular thickening
Spine: Diffuse idiopathic skeletal hyperostosis (DISH)- osteophytes & bony spurs in
thoracic spine; spurs in calcaneus & olecranon
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Osteoporosis: w/in 5 years of Type Irisk of fxs from galls & loss of sensation
Foot Ulcers: improper glucose metabolismdec vascular perfusion to nerve
tissuedevelop ulcers b/c of altered pressures & gait
o Skin is insensitive and shear forces cause breakdownpoor wound healing b/c skin
stiff

Chronic Regional Pain Syndrome: severe pain, swelling, trophy skin
changespermanent loss of function

Neuropathy
o CNS, PNS, ANS: polyneruopahty of hands and feet; avoid weight lifting, high
intensity aerobic exercise, don’t want SBP >180
o Motor: bilateral, asymmetrical proximal weakness/deformity (claw toes, flatfoot,
collapse of longitudinal arch, Charcot’s)
o Peripheral: CTS due to neuropathy & compression
Prevention
-Foot/skin care
 skin changescan lead to bacteria entering
 calluses on bottom of footincreased pressureulcer
-recognize symptoms early: lowered skin temp of feet, dec sensation, loss of deep tendon
reflexes, weak feet, eye evaluations
ENDOCRINE
-Cells: glandular secretory cells into the extracellular fluidcan affect local/adjacent cells or
over a distance
-Functions
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1. Differentiation: reproductive & CNS of fetus
2. Coordination: male & female reproductive systems
3. Stimulation of sequential growth: growth & development during childhood &
adolescence
 4. Maintenance: keep optimal internal environment
 5. Initiation: corrective/adaptive responses in emergency
-Hypothalamus: controls function of endocrine organs through neural & hormonal pathways

Control by:
o Secretion of regulatory hormones form Ant/Post pituitary
o Control sympathetic output of adrenal medulla
o Produce Ne & epinephrine
-Pituitary Gland (hypothysis)

Anterior (adenohypophysis): Hypophyseal portal system that releases tropic (stimulating)
hormone release down short axis
o Tropic: ACTH, TSH, LH, FSH
o Effector: GH, PRL

Posterior (neurohypophysis): axons of hypothalamus; long axis
o Neural stimulation to provoke secretion of 2 effectors: ADH Oxytocin
o ADH (vasopressin): water retention, BV constrictionraise BP
 Stimulus: rise in osmolarity of blood/fall in blood vol/P
 Controls body fluid concentration by dec water loss in kidneys & water absorbed
in gut
-Thyroid gland secretes T3 & T4 (T3 more effective)

For normal growth & development: inc O2/energy consumption, HR/contractility,
sensitivity to sympathetic stimulation, accelerate turnover of mineral in bone, inc cellular
metabolism & cellular respiration
-Parathyroid gland secretes PTH
 regulate Ca & phosphate metabolism
 Ca re-absorption & phosphate from bone
 Ca reabsoprtion from kidneys; excretion of phosphates
-Pancreas
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alpha cells: glucagon breaks down glycogen to inc blood sugar
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beta cells: insulinglucose transport, storage, protein synthesis & fatty acid uptake
o deficiencyDM
-Adrenal Cortex

Mineralcorticoids: Aldosterone stimulated by angiotensin II to regulate Na+ reabsoption
& K+ secretionregulate BP

Glucocorticoids: Cortisol inc rate of glucose synthesis & glycogen formation
o Anti-inflammatory effects
o Addisons: hypoactive
o Cushings: hyperactivecan cause muscle/bone atrophy
-Adrenal Medulla

Epinephrine/NE to mobilize glycogen reserves in muscle & breakdown glucose
o Breakdown stored fats & glycogen in liver
o Inc HR & contractility (Beta 1 heart cells) (Beta 2 lung cells in bronchodilation
ENDOCRINE DISORDERS
-Pituitary gland

Anterior Lobe (GH)
o Hyperpituitarism (tumors)
 Gigantism (children)-overgrowth of long bones
 Acromegaly (adults)-increased bone thickness
o Hypopituitarism (pahyhypopituitarism)
 Short stature, delayed growth & puberty, ACTH deficiency from adrenal glands,
hypothyroidism, sexual/reproductive disorders
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Posterior lobe
o Hypersecretion- inappropriate ADH levelsexcessive releasewater intoxication
from fluid retention, Hyponatremia, CNS dysfunction & brain swelling
 Monitor weight gain and BP
o Hyposecretion- Diabetes Insipidus (ADH deficiency)
 Kidneys fail to reabsorb waterpolyuria of dilute urine, polydipsia, dehydration
-Thyroid gland

Hyperthyroidism-excessive thyroid hormone
o Thyrotoxicosis(Graves T4): tachycardia, excitable, weight loss, exophthalmoses,
goiter
o Monitor exercise intolerance & vitals

Hypothyroidism- deficiency of thyroid hormone
o Congenital (cretinism)- abnormal growth development @ birth
o Myxedema (adults)- slow metabolism, lethargy, swelling, bradycardia
o Monitor for activity intolerance skin tears
-Parathyroid gland

Hyperparathyroidism: bone damage due to inc bone resorption, hypercalcemia, kidney
damage
o Monitor: skeletal, articular, neuromuscular fx, weight bearing

Hypoparathyroidism: decreased bone resorption, hypocalcemia, muscle twitching
o Monitor: chronic client with muscle twitching
-Adrenal cortex

Addison’s Disease: hypofunctiondec cortisol (dec gluconeogenesis) and dec
aldosterone (inc Na secretion)
o Weakness, dehydration, exhaustion, hypotension, decreased cardiac output

Cushing’s disease: hyperfunction, extra cortisolbreakdown of protein & lipids,
impaired glucose metabolism (cortisone shots)
o Weakness, buffalo hump, round face, osteoporosis, hairiness
o Monitor: infection, inflammation, muscle atrophy
Metabolic System
3/6/2014 9:45:00 AM
-Metabolism: physical & chemical processes allowing cells to utilize food, rebuild body cells,
transform food to energy
 anabolism (tissue-building)
 catabolism (energy-producing)
 rate increased by exercise, after food ingestion, hormones, elevated body temp
-Homeostasis: maintain body’s chemical and physical balance
 fluids preserve osmotic pressure, pH, electrolytes
-Osteoporosis: group of bone disorders which result in a reduction of bone mass/unit of bone
volume

incidence: most common metabolic bone disease
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
females>males, mostly Caucasian >45yrs old
risk: heredity, hormonal status, physical inactivity, medications, smoking, ethnicity,
ETOH, diet, nutrition, depression
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Primary: postmenopausal (most common), senile/involutional, idiopathic
Secondary: caused by other disorders (Malabsorption, steroids)
Clinical: low back pain & wedge fx, hip fx, thoracic kyphosis
Diagnosis: radiographsosteopenia in vertebral bodies, ribs, radius, femur
o affects cortical and trabecular bone
o >30% bone density loss

Treatment: prevention, develop quality peak bone mass <30yrs
o Regular exercise with walking/jogging
o Supplements: estrogen, androgens, Ca, Vit D, calcitonin, bisphosphates
-Osteomalacia: bone condition with insufficient mineralization



softening of bone without loss
deficiency of Ca and phosphate due to potential lack of Vit D
Causes
o Insufficient intestinal Ca absorption
o Increased renal phosphorus loss (renal tubular defects, antacids, hyperparathyroidism)

Risk factors: age, cold geographic area, Vit D deficiency, intestinal malabsorption, longterm use of medications

Pathogenesis:
o Low Ca & phosphate concentrationimproper ossification
o Vit D deficiencydisrupts mineralization
o Pseudofx on concave side of long bones, ischial/pubic rami, ribs, scapula
o Mechanical stress pointstrue fractures

Clinically: general aching/fatigue, proximal myopathypoor gait, bone pain
o Postural deformities (thoracic kyphosis, heart pelvis, bowing of femur & tibia)
Muscular weaknesswaddling gait, difficult to sit/stand, out of bed

Diagnosis: radiographs, bone scan, labs: Slipped capital femoral epiphysis (SCFE)-fx
through the bone plate

Treatment: correct disease of malabsorption or increase dietary intake of calcium, vit D,
and phosphates
Vascular
3/6/2014 9:45:00 AM
-S&S of Cardiovascular Disease:

Chest/neck, arm, jaw pain
o Angina, MI, pericarditis, endocarditis, valve prolapse, aneurysm, anemia, nausea,
vomiting, dyspnea, fatigue
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Palpitations: irregular heartbeats
Dyspnea (SOB): with exertion, Paroxysmal Nocturnal (CHF), Orthopnea (with positional
changes)
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Syncope: b/c reduced O2 to the brain; also due to anxiety/stress
Fatigue with minimal exertion
Cough: pulmonary conditions L ventricular dysfunction due to pulmonary edema
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Cyanosis: blue lips/nailbeds/toes/fingers and mucous membranes
Peripheral Edema: R ventricular failure with dependency
o RUQ pain, ascites, abdominal distension, jugular venous distension
 Claudication with activity: leg pain/cramping, PVD/CAD, pitting edema
-Aging of the heart

Dec in # of myocytes, cardiac fibrosis, dec Ca transportchange in contractility, dec in
response to adrenergic stimulation of SNS, impaired ANS reflex control of HR
 Advanced aging: thickened LV wall due to overwork, inc left atrial size
-Aging of Vasculature

stiffened walls, inc change of aneurism, inc arteriosclerosis, Ca deposition with
elastin/collagen changes, dec in functional capacity with exercise (O2 uptake, HR, CO)
Diseases
-Coronary Artery (Ischemic Heart): ¼ deaths in US, most common type

involves coronary arteries carrying O2 to myocardium becoming
narrowed/blockedmuscle becomes ischemic, injured & possible infarction

Arteriosclerosis: group of diseases of thickening/hardening and loss of elasticity of
arterial walls
o Atherosclerosis: Plaques of fatty deposits form in INTIMA
o Monckeberg’s Arteriosclerosis: destruction of muscle & elastic fibers with formation
of Ca deposits in middle layer
o Arteriolosclerosis: thickening of walls of arterioles
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
Treatment: lifelong management of changing habits, medications, and sometimes sx
Etiology/Risk factors
o Major: cigarettes, hyperlipidemia, hypertension, physical inactivity
o Minor non-modifiable: age, male, family hx, race
o Minor modifiable: obesity response to stress, personality type, diabetes, alcohol,
hormonal status

Pathogenesis: Injury to endothelial lininginfiltration of macromolecules (cholesterol)
from blood to SMnaked collagen place for platelets to aggregate and plug
woundrelease chemicals altering structure of wallobstructs flow through BV & can
have formation of thrombosis
o Normal arteryfatty streaksatheromafibrous plaqueocclusion

Dx Test
o Stress test: ECG before, during, after exercise of different workloads
o Nuclear Scanning: show damaged areas of heart to expose problems with pumping
action
o Angiography: explore coronary arteries using catheter

Angina: chest pain felt as squeezing/crushing pressure that can radiate
o Triggers: exertion, emotional stress, exposure to cold/wind, large meal
o Chronic Stable: exertional that occurs predictably; stop with rest or nitroglycerin
o Unstable: unpredictable/not related to usual demand for myocardial O2
o Prinzmetal’s/Vasospastic: coronary artery spasm during the morning; relieved with
minor activity

MI: 3 zones of damage
o Zone of Infarction: area of myocardium completely deprived of O2cell death
o Zone of Hypoxic injury: next level, will recover if BF restore quickly
o Zone of Ischemia: outer layer, usually reversible damage
o Healing: 18-24hrs anti-inflammatory response2-4days necrosis, debris
removed4-10 days debris cleared, collagen matrix laid10-14 days weak/fibrotic
scar revascularized6 weeks touch, inelastic scar placed b/c heart tissue cannot
regenerate
o Complications; arrhythmias, pericarditis, extension of infarction, CHF, sudden death
o Medications: Beta-blocker (dec workload & recurrence of heart attack), Nitrates
(vasodilate peripheral vessels), Ca-channel blockers (relax arteries), Aspirin (reduce
clot formation), ACE inhibitors (impaired pump function)
o Revascularization Sx to restore normal BF to heart
 CABG: Traditional using heart-lung machine & Mid for more minor procedures
 Percutatneous transluminal coronary angioplasty (PTCA), Artherectomy

CHF: heart unable to pump sufficient blood supply to body’s needs due to poor
musculature or valvular problems
o Etiology/Risks: pre-existing heart diseases, conditions exacerbating stress on a
diseased heart: MI, CHD, pericarditis, infection, anemia
o Left failure: CHF
o Progresses to R heart failure
 Dyspnea (3 Types), pulmonary edema, spasmodic cough, fatigue, muscle atrophy,
Nocturia, Oliguria (Na & H20 retained, adds to the loadkidney release of rennin
o Right failure: Cor Pulmonale
 Cyanosis, engorgement of jugular veins, hepatomegaly, ascites, dependent edema,
inc venous P, anorexia, anxiety
 Pressure receptors in body detect dec volumekidney retains fluid to inc BV to
peripheral tissues (compounding problem)fluid accumulatesdependent edema
possibly backing up into lungs & venous system00>JVD Hepatomagaly
o Begins in L unable to pump blood into systemic circulationbody compensates by:
inc HR, dilate ventricles, ventricular hypertrophy, SNS response, kidney response to
change BP
o Compensated-combined efforts of compensatory mechanism achieve normal CO;
Decompensated- when the measures are not effective
o Medical DX: ECG, cardiac catheritization, angiography, arterial blood gasses, liver
enzymes
o Tx: diet, medications, exercise (strengthening, peak O2 consumption) and begin &
low intensity, short duration
 Acute: hospitalization get diuretics, vasodilators, ionotropics
 Angiotensin converting enzyme…ACE inhibitors: block renin agiotensisn
aldosterone to prevent retention of sodium & fluid
 Vasodilators
 Surgical: CABG, valve reconstruction, venoarterial bypass
-Cardiac Muscle

Myocarditis: inflammatory condition of muscular wall of heart usually due to
bacterial/viral infection or inflammation; membranes affectedinc HR, abnormal
contractions, weakened heart mm
o Endocarditis: damage to chordae tendonae & valvescomplications of blood clots
o Clinical manifestations: chest pain, soreness in GI, palpitations, fatigue, dyspnea
o Complications: CHF, arrhythmias, congestive cardiomyopathy, sudden death
o Prognosis: resolves with tx; if active, contraindicates exercise

Cardiomyopathy: progressive, irreversible degeneration of myocardium affecting heart
mm so systole & diastole impaired
o Dilated (fatigue/weakness with normal-low BP), Hypertrophic (asymptomatic with
sudden death), and Restricted (decreased CO high intraventricular P)
o TX: determined by cause (physical, dietary, radiography, ECG, pharmacological,
transplantation
o 75% with idiopathic Dilated, die <5years
-Heart Valve Disorders: Mitral Valve Prolapse

slight variation in shape/structure of mitral valveleaflets billow/bulge backward into L
atrium during ventricular contraction


most common cardiac problem; women>men & family hx
symptoms: irregular heart beat, tachycardia, fatigue/weakness, panic attack anxiety,
mitral click/murmur
VASCULATURE
-Aneurysm: abnormal stretching/dilation of the wall of an artery/vein expansionweak and
thin wall @ risk for rupturehematoma
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due to: ATHEROCLEROSIS, trauma, congential malformation, disease, infection
manifestations depend on size, location and effect on adjacent organs
common sites: thoracic & abdominal
Incidence: inc with age, men>women, HTN, arteriosclerosis

Types: Saccular (one-sided), Fusiform (bilateral), Dissecting (intima layer torn away with
blood btwn layers = medical emergency), False (wall ruptures and clot formation)

S&S of Abdominal aortic aneurysm
o Chest pain with palpable pulsating mass, abnormal heart beat, dull ache in low back,
weakness
o Ruptured: severe chest pain w/ tearing sensation, systolic BP <100mmHG,
lightheadedness & nausea
Peripheral Vascular Disease
-Inflammatory Disorders:
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
inflammation/damage to large & small vesselsend-stage organ damage
Vasculitis: necrotizing inflammation of arteries & veins of all sizes
o Affects PNS or CNS
o Hypersensitivity: small vessels; from an upper respiratory infection in those with
allergy issues
 Triad of purpura (bruising & petechiae under skin), arthritis, abdominal pain
o Kawasaki: medium & small vessels; mucocutaneous lymph node syndrome
 Young Asian children seasonally; possible infectious cause

Cardiac system in 3 phases
1. Acute: sudden high fever unresponsive to drugs
2. Subacute: irritability persists, rash on trunk, skin pealing, mucosal
changes
3. Convalescent: 6-8 weeks, symptoms return to normal
 High does antibody to reduce fever
o Takayasu: large and medium vessels
o Localized: peripheral
o Arteritis: involved temporal & cranial arteries with unknown pathology
 Middle layer (tunica media) inflamed in sudden onsetthrobbing headaches in


temporal area
Manage with corticosteroids
Polyarteritis nodosa: multiple sits of inflammation and lesions in arterial system (small
masses of tissue form nodes)
o Small & medium vessels in any organ of body
o Fever, chills, infection, tachycardia
o 50% of cases are with Hep B
o Management: steroid therapy & immunosuppressant

Thromboangiitis obliteran (Buerger’s Disease): thrombotic inflammation from vasculitis
affecting peripheral BVs in extremities, can get thrombus formation
o High incidence in Men<40 who smoke
o Clinically: pain & tenderness, reduced oxygenation, claudication of arch of foot or
palm of hand, edema, hairless skin, absent pulses, possible ulcers & gangrene
o Management: stop smoking!, improve circulation via vasodilators
-Arterial Disorders:

Occlusive Diseases: as a result of atherosclerosis or trauma, thrombus, vascultis,
vasomotor spasms, arterial punctures, polycythemia
o Location dependent: occlusion of brainhemiplegia/weakness/ blurred vision;
intestinesischemic colitis
o S&S: diminished pulses, pain, numbness, cold, sensation change, skin color changes,
venous filling delay, gangrene
o Tx: anticoagulation therapy, embolectomy

PAD (arteriosclerosis obliterans): proliferation of intimaobliteration of lumen of artery
(95%) of occlusive diseases)
o Develops in older ppl w/ DM & smokers
o Bilateral progression w/ intermittent claudication
o
o
o
o
o
Diameter of large & medium BVs is <50%
Distal aortal & iliac arteriess&s in calf, gluteals, quads
Femoral & poplitealcalf & foot
Tibial & common peroneal--.arterial ulcers, skin atrophic
Tx: dietary management, daily walking, prevent skin breakdown, stop smoking

Arterial Thrombosis/Embolism: complication of any vascular condition; may create life
threatening problem if thrombus comes off & carried to heart/lungs as embolism
-Venous Disorders:

Thrombophlebitis: partial/complete occlusion of vein by thrombus with secondary
inflammatory rxn in wall of vein (usually LE) (DVT)
o Common b/c 30% post op pts. Develop DVT
o Caused by venous blood stasis due to absence of calf muscle pump, sugery, obesity,
pregnancy, CHF, prolonged immobility
 Other causes: hypercoagulabilty, malignant neoplasms, oral contraceptives with
smoke, vein wall trauma
o Clinical manifestations: dull ache/tight feeling, unilateral swelling, discoloration
(cyanotic)
o Tx: anticoagulants, heparin, bed rest, elevation, continuous heat, compression with
walking when tenderness &swelling subsided
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
Avoid long standing
Varicose Veins: abnormal dilation of veins (usually saphenous)
o Leads to valve incompetence & thrombosis b/c veins lose elasticity so have blood
flow in both directions
o Associated with high venous pressure due to heavy lifting, prolonged standing, sitting,
pregnancy, obesity, heart failure
o Tx: periodic rest w/ elevation, promote circulation, elastic stockings, vein stripping
o Sclerotharpy: injecting veins with solution to scar & close varicose veins so blood
must reroute
o Ambulatory Phlebotomy: remove smaller varicose veins
o Endoscopic Vein Sx: advanced cases only

Chronic Venous Insufficiency: post phlebitic syndrome/venous stasis; when inadequate
venous return over long period of time
o Damaged veins/valves prevent venous returninc venous P
o Prevents; cellular oxygenation, removal of wastecell death & ulcers, poor wound
healing, impaired immune system
o Tx: compression stockings (tight distal to prox) to promote circulation, exercise,
weight control, avoid heels, elevation through the day
-Vasomotor Disorders:

Raynaud’s: Vasospastic disorder of small artery constriction of extremities (fingers/toes)
o Pallor/cyanosis
o Due to cold or strong emotion hypersensitivity response
o Dec flow of oxygenated bloodischemianumb/painful
o TX: prevent stimuli, Pt. education, stress management, exercise, vasodilators

CRPS/RSD: severe, chronically painful condition of one limb with constant burning pain,
hypersensitive
o Type II: specific nerve is identified
o Type I: no specific nerve
o Pain, ANS overactivity, movement disorders (weakness, tremor, spasm, dystrophy,
atrophy)
o Stage I (acute inflammation): 10 days-3/6 months
 Limb dry, hot, red, painful and more severe, edema
 Good to identify for better prognosis in this stage
o Stage II(paradoxic sympathetic hyperreactivity): >3-6months
 Skin becomes shiny, thin, cool, purplish, swelling, worse pain, brittle nails
o Stage III (Atrophic): 6-12mo
 Skin drawn/dry, shriveled, bones brittle from osteoporosis, skin/muscles/joints
stiffen, less pain possible
o Dx: x-rays, bone scan, electromyography, sympathetic nerve block, burning,
spontaneous pain, hypersensitivity
o Tx: manage pain: corticosteroids, rehab, NSAIDs, analgesics, TENS unit,
biofeedback pain control
S&S of Disorders
-Edema: lymphedema, cerebral, inflammatory, peripheral dependent, pulmonary
 accumulation of fluid w/in interstitial\al tissues/ body cavities
 Lymphedema: chronic swelling of an area due to accumulation of interstitial fluid
o Hematolymphatic disorders: obstruction of lymphatics
o Accumulation of fluidbacterial growth, infection, fibrosis, loss of limb use
-Congestion: accumulation of excess blood w/in vessels of organ/tissue
 localized (venous thrombus, or hands, or lungs)
 generalized (heart failurecongestion in lungs, LE, and abdominal viscera)
-Infarction: localized region of necrosis caused by inadequate arterial perfusion due to
blockage or dec quality (O2 demands of end organ not met)
 commonly: brain, heart, Gi, kidney, spleen
-Clots
 Thrombosis: mass of clotted blood w/in an intact BV that occludes flow (can
result in DVT)
 Embolism: mass of solid/liquid/gas moving w/in a BV and lodges at a site diff
from origin
-Shock: hemodynamic changes diminish arterial blood circulationorgans tissues don’t
receive adequate O2 to meet metabolic needs
 hypovolemic, cardiogenic, obstructive, septic, neurogenic
 Signs: rapid/weak pulse, hypotension (systolic <90mmHg), cool/pale/moist
skincardiovascular collapse
Anemias: disorders of Erythrocytes; reduction in oxygen carrying capacity of the blood
(dec quantity or quality)
-Hemoglobin: <14g/dL M; <13g/dL W
-Hematocrit: <41% M; <37% F
-Most common: Iron deficiency due to dietary lack, GI bleeding, menstrual, genetic
-not a disease but a symptom of other disorders: dietary deficiency, actuate/chronic blood
loss, congenital defects, exposure to toxins, bone marrow, chronic inflammation,
infectious, neoplastic due to chemotherapy
-Causes
 Hemorrhage: post-hemorrhagic anemia from trauma, GI cancer, bleeding peptic
ulcer, hemorrhoids
 Destruction of erythrocytes(hemolytic): mechanical or autoimmune, enzyme
defects, parasites, hereditary
 Dec production of erythrocytes
o Chronic disease: inflammation requires inc demand (TB, HIV)
o Deficiency of B12: Pernicious anemia lacks factor for absorption of Vitamin
B12
o Nutritional deficiency: Folate (erythropoiesis, Iron (Hb production)
o Cellular maturational defects: Aplastic anemia-insufficient RBCs & WBCs &
platelets
o Dec bone marrow stimulation or failure
-common in growing children, low socioeconomic groups, elderly, menstruating/pregnant
women
-Pathogenesis: dependent on cause; mild until hematocrit or hemoglobin <50%
-Clinical Manifestations: weakness, easily fatigue, dyspnea with exercise, tachycardia,
increased angina, spooning nails (koilonychias), pallor/yellowing skin, leg ulcers
 CNS symptoms (75% of those with pernicious anemia)
o Degeneration of spinal cordpyramidal & posterior column defects
(corticospinal tract & DCML)
o Polynueuropathy, mental changes, optic neuropathy
 Severeheart failure, hypoxic damage to liver & kidneys
o Coronary obstruction: low blood O2 levels
-Tx: alleviate/control the cause, relieve symptoms, prevent complications
 B12, folate, iron therapy, O2 therapy, corticosteroids for RBC production, bone
marrow transplant, splenectomy to dec destruction of RBCs
-PT: must know precautions for exercise b/c pt. will have dec exercise tolerance
 recognize underlying cause to identify red flag situations: GI blood loss due to
NSAIDs
 anemia combined with cardiovascular disease
 bleeding under skin due to dec platelet production
Sickle Cell Disease: group of inherited autosomal recessive disorders with the presence
of an abnormal form of hemoglobin (HbS) in the RBC
-Symptoms
 Chronic hemolytic anemia
 Vaso-occlusionischemic injury
-Pathogenesis: sickle cell defect in Hb when valine substituted for glutamine
 transport of O2 normal but once releases O2 Hb molecules stick to each other
& form long rigid rods inside RBCsrods make RBCs take on sickle-shape
o lose ability to deform & squeeze through tiny BVsocclusion of
microcirculationinc hypoxia—more RBCs sickletissue injury
 when O2 reattachessickle assumes normal shape (reversible sickling)
o after repeated action, RBC permanently damaged & maintains sickle
shapeANEMIA
o rupture of RBCspremature release of Hb into plasmadec delivery of O2
to tissues.
o Bone marrow will expand to compensate for RBC hemolysisosteoporosis &
osteosclerosis
-Etiology: developed as selective advantage against malaria
-Clinical manifestations: pain, bone/jt. crises, pulmonary crises, vascular complications,
neurologic complications, renal complications
-Dx: Universal screening of DNA from fetal cells
-Tx: no treatment to cure besides bone marrow transplant
 aggressive re-hydration and transfusion to have HbS <40% level, 2x daily
prophylactic penicillin, medication for musculoskeletal pain
Leukocytes
-Leukocytosis: a normal or abnormal increase in # of circulating WBCs (>10000/mm^3)


result of inflammation/infection (characterizes infectious disease)
also a normal protective response to physiologic stressors (strenuous exercise,
emotional changes)
 S&S: fever, symptoms of infection and inflammation or trauma
 Tx: direct to cause to get rid of infection
-Leukopenia: reduction in # of leukocytes in blood (<5000)
 occurs in bone marrow failure following chemo/radiation, overwhelming
infections, dietary deficiencies, autoimmune diseases
 always negative: @ risk for infection
 S&S: sore throat, cough, fever, chills, sweating, ulcers of mucous membranes,
painful urination, persistent infection
 Tx: elimination of the cause & control infection
-Leukemias: malignant disorder of bone marrow cells
 replacement of bone marrow by malignant clone or lymphocytic/granulocytic cell
 accumulation of dysfunctional cellslose ability to regulate cell division
 uncontrolled proliferation of leukocytes in bone marrowspill into peripheral
circulation prohibiting blood cell production
 Acute: early arrest in cellular development
o Undifferentiated cells due to abrupt onset; if not treated, death within months
 Chronic: gradual onset with mature (well differentiated) cells
o Prolonged/clinical courselonger survival time
-Hemophilia: most common inherited coagulation disorder inherited as a sex-linked
recessive trait; M>F
 Hemophilia A: classic
 Hemophilia B: Christmas
 Classified according to percentage of clotting factor:
o Mild 5-50%
o Mod 1-5%
o Severe <1%
 S&S: slow, persistent bleeding from cuts, excessive bruising, delayed hemorrhage,
severe nosebleeds
o Hemarthrosis: bleeding into joint space; usually synovial jointsrecurrent
leads to chronic synovitis, flex contractures
 Vascular hyperplasia due to attempt to resorb bloodhypertrophy
 Extensive cartilage damage narrowed joint space, erosion at margins,
subchondral cyst formation
 Normal WB impinges furtherchronic pain, severe loss of motion,
muscle atrophy
o Muscle Hemorrhages
 Intramuscular: superficial areapain and limitation of motion
 Peripheral Nerve compression by hematomasevere pain, anesthesia of
innervated part, loss of perfusion
 Tx: no cure, goal is to stop bleeding and infuse missing factors; infusion
recommended if severe

Permanent prophylaxis: use of recombinant factors for severe hemophilia