- increased type 2 diabetes

-elevated blood cholesterol/lipid levels

-increased BP

-musculoskeletal problems

-psychological problems

-increased intake of high fat and high carb. foods

-decreased physical activity 

-high BMI with significant abdominal mass

-changes in glucose metabolism

-changes in lipoprotein metabolism

-HTN

-type 2 diabetes

-coronary artery disease

-stroke

-kidney failure

-shortened life expectancy 

"hunchback"

-increase in the convexity of the thoracic spine

-postural

-uneqaul growth of spinal muscles

--developmental or genetic

-can interfere with lung expansion and ventilation (cardiopulmonary)

-GI problems

Surgery - rods

External brace

physical therapy

"swayback"

-exaggerated concave lumbar curvature

-unequal growth of muscles 

-genetic factors

-females > males (5:1)

-Congenital  (with associated urinary tract abnormalities)

-degenerative (older adults with osteoporosis)

etiology of functional (non-structural) scoliosis

-lateral curvature of the spine affecting thoracic or lumbar area or both

-may compress the heart, lungs or both

-surgery - rods

-external brace

-physical therapy

Staphylococcus aureus (most common pathogen)

Salmonella (common in sickle cell patients)

Metaphysis (area between end and shaft of long bone) is most common site

-Hematogenous (spreading by blood)

-Contiguous spread (actual contact)

-direct trauma

-infection generates inflammatory response (Exudate formation)

-pain due to chemicals , pressure, and stretching of periosteum

-new bone growth around infection/necorsis which walls off area and makes harder to treat

-pressure of exudate may tear periosteum which can lead to even more spread to adjacent tissues

-possible joint involvement

-involvement of epiphysis (epiphyseal plate usually prevents this)

-local s/s of inflammation

-system signs of inflammation (fever, leukocytosis, malaise, irritability)

IV antibiotics

and

debridement of necrotic bone

-group of autoimmune diseases with onset prior to age 16

-chronic inflammation in connective tissues - joints

-unclear

-genetic, preceding infection

-inflammation of synovial membrane (effusion, swelling, pain, limitation of movement)

-damage to joint with adhesions and permanent deformity

-joint swelling or discomfort lasting more than 6 weeks

-general signs of inflammation

-NSAIDS

-glucocorticoids (for severe inflammation)

-Disease modifying antirheumatic drugs (DMARD's) 

(Methotrexate)

-Pauciarticular (oligoarticular)

-Polyarticular 

- systemic ("still's disease")

-affects large joints more commonly

-asymmetrical involvement (one side)

- positive anti-nuclear antibody (ANA)

-greatest risk for eye involement (uveitis)

-Girls affected more than boys (5:1)

-smaller joints more commonly affected

-symmetrical involvement (both sides)

-negative ANA

-girls > boys (3:1)

-systemic onsent with fever, rash, arthritis, and spleen enlargement

-(fever is recurrent same time each day, rash is transient with salmon pink macules)

-large and small joints affected equally

-affects girls and boys equally 

-extreme loss of weight due to self-starvation

-may demonstrate purging

-perfectionists and high achievers

-overbearing mothers, passive fathers

-seek control

-fear of fatness

-altered body image

effects of anorexia

-amenorrhea

-low body temp (cold intolerance)

-Low BP and slow HR

-dry skin and brittle nails

-find body hair

-low calcium intake

-dehydration

-electrolyte imbalances (cardiac arrhythmias and arrest)

-outpatient or inpatient

-long term psychotherapy 

-binge eating, followed by purging

-compulsive exercise

-bulimina and anorexia may overlap

-occurs more frequently in older adolescents

-poor self image

-frequent dieting

-often maintains normal weight

-may result in anemia

-menstrual irregularities

-f/e imblances

(cardiac arrhythmias, tetany, severe abdominal pain)

-erosion of tooth enamel

-tears and ulcers in oral mucosa

-esophagitis

-swollen parotid glands

-common skin infection in adolescence

-involve sebaceous glands and assoicated hair follicles on the face, neck and upper trunk

-can be mild or severe

-if severe there is permanent scarring

-comedones (whiteheads or blackheads - non-inflammatory collection of sebum)

-inflammatory (hair follicle sweels and ruptures, organisms invade and create pustule)

direct contact with infected saliva, airborne droplets, or blood

"kissing disease"

acute strep throat

(significant number of people treated with amoxicillin/ampicillin will develop rash)

-sore throat, HA

-fever

-fatigue, malaise

-enlarged lymph nodes and spleen

-rash on the trunk

-increase in lymphoctyes and monocytes in blood

-atypical T-lymphocytes

-hepatomegaly and splenomeagaly (restricts participation in sports0

-hepatitis

-ruptured spleen

-meningitis

-extra X chromosome in males (XXY)

-mental retardation

-fialure of secondary sex charc. to develop

- 1 monsomy X is missing in females (XO)

-failure of development of secondary sex charac. 

-lack of menstruation 

-treat with hormone replacement

-uncommon prior to age 20

usually malignant 

-delayed menarche

-absence of menstruation after age 17

-athlete triad

-pain associated with menstrual cycles

-varying degrees during 1-2 day of menstruation

-due to increased secretion of prostaglandins

-nausea, vomiting, diarrhea

-fainting

-genetic makeup

-lifestyle

-health status

-cardiovascular fitness

-those that cannot regenerate effectively

-CNS

-skeletal muscle

-cardiac muscle

-kidney

Theories of aging

-aoptosis (genetically programmed)

-"wear and tear" (accumulated wastes, altered proteins, altered lipids, changes in collagen)

-random errors during mitosis

-latent viruses

-increased autoimmune reactions

-environmental agents

-"free radicals"

-peroxides

-less organized cell arrangement in tissues

-decline in cell function (decrease in fiber production such as collagen and elastin)

-decline in mitosis

--hormonal changes

-number of tissue receptors decrease

-speed of hormonal response may diminish

Women:

-menopause leading to thinning of skin and mucosa, decreased vaginal secretions, decrease in breast tissue, hot flashes, HA's, irritability, insomnia

Men:

-decline in testosterone production

-decrease in testes size, and sperm production

-BPH (common prob. resulting in urinary obstruction)

-many based on exposure to sun and weather

-skin and mucous membranes become thinner and easily damaged

-dermis thinning and SQ tissue diminished

-number of specilaized structures declines (sweat glands, receptors)

-skin dry

-wrinkles

-slower wound healing (less vascular)

-lesions (skin tags, keratoses, lentigines (liver spots)

-gray hair

-thinning of hair

-cardiac muslce fibers decrease in size and number

-fatty tissue and collagen fibers accumulate which leads to reduced strength of cardiac contraction

-valves thicken and become less flexible

-cardiac reserve is diminshed 

hardening of arteries

- can be due to old age

- loss of elasticity and collagen accumulation in wall predisposes one to this

-skeletal muscle mass declines with age

-coordination and balance reduced

-decreased mineral content of bone

-cartilage in joint deteriorates

effects of aginin on respiratory system

-ventilation is limited by the elasticity in lung tissue reducing, costal cartilage calcifies, intercostal muscles weaken

-expiration is reduced, residual volume is increased and decreased expansion for deep breathing and coughing which increases risk of pneumonia

-vascular changes (decreased perfusion and reduced gas exchange in alveoli)

-natural reduction of neurons

-loss of myelin

-decreased response to neurotransmitters

-slower response time

-lens of eye becomes less flexible (reduced accommodation- presbyopia)

-lens tends to yellow, cataracts develop

-glaucoma

-night and color vision is reduced

-hearing loss

-sense of taste reduced

-sense of smell and ability to discriminate diminished which may impair appetite and nutrition 

-periodontal disease

-xerostomia

- slower transit time and emptying of stomach

-atrophy of mucosa and glands (reduces digestive secretion, impaired absorption of B12, calcium and iron)

-constipation

-hemorrhoids

-increased risk of malignances of GI tract

-kidney function reduced (diminished ability to adapt to f/e changes and acid/base changes)

-reduced capacity to secrete drugs

-nocturia

-frequency

-incontinence

-delayed healing (reduced rate of mitosis)

-less rapid immune responses

-higher cumulative exposure to carcinogens

-autoimmune diseases more common

-degenerative diseases become more apparent

symmetrical paralysis in any area of the body

cerebral palsy is the most common cause involving the legs

-loss of bone mass

-elevated serum calcium due to reduced osteoblastic activity and continued osteoclastic activity 

-risk of osteopenia and osteoporosis 

-impaired circulation to skin

-ischemia

-necrosis

-ulcers

-ischial tuberosities

-sacrum

-greater trochanters

-heels

-elbows

other contributing factors to skin breakdown r/t immobility

-anemia and edema

-lack of SQ tissue for cushioning

-lack of sensation

-mechanical irritation/trauma

-excessive moisture

-poor hygiene 

-poor nutrition/hydration

-orthostatic hypotension (acutely see increase in venous return, but with prolonged immobility skeletal muscle inactivity and atrophy impedes venous return)

-blood stasis leading too DVT, emboli, ulcers

-slows BMR (decreased demand of tissues for oxygen)

-restriction of functional chest volume and expansion resulting in decreased ventiliation which is due to weakness of respiration muscles and complicated by drugs and pain

-increased pooling of secretions

-atelectasis (collapse of part of the lung leading to poor gas exchange)

-slowed transit time through GI tract (delayed gastic emptying resulting in early satiety)

-slower passage of material through large intestine (constipation can result and is major problem)

-decreased appetite (may lead to negative nitrogen balance which promotes breakdown of muscle fibers)

-infection (risk is increased if pt. has catheter)

-renal calculi (risk is incrased by hypercalcemia seen with immobility)

a state of affairs that arises when a person relates to situations in certain ways

-individuals experience stress when demands exceed the individuals coping mechanisms 

-disturbed cognition, emotion and behavior

-adverse effect on well being

-maladaptive responses (smoking, overeating, over consumption of alcohol)

pain, exposure to environmental extremes, trauma, illness

-can be physical or psychological (anxiety, fear, excitement)

-appropriate coping mechanisms are in place

-stressor is not overwhelming

-stressor is not coinciding with other factors that would interfere with an appropriate response

-physiologic response to stress is basically the same regardless of the stressor and can result in a decline in health

-individual's perception of a stressor will vary and invidiuals ability to adapt to a stressor will vary

-body's ability to adapt to stressor depends on individual factors as well as the number and intensity of the stressors

-alarm stage

-stage of resistance or adaptation

-stage of exhaustion 

-activation of the hypothalamus, pituitary gland, sympathetic nervous system and adrenal gland

-mobilization of fight or flight

-CRH (corticotropin releasing hormone)

-ACTH (adrenocorticotropic hormone)

-epinephrine and norepinephrine

-hormone levels are elevated

-body responses are at optimal functioning

-continuation of fight or flight

-body is unable to respond further (have depleted resources)

-body systems become disrupted and maladaptive response may be seen (loss of homeostasis)

-may see either resolution of response, onset of disease or possibly death "diseases of adaptation"

corticotropin releasing hormone (or factor)

-released by hypothalamus

-causes release of ACTH and beta-endorphins from anterior pituitary 

adrenocorticotropic hormone

-released by anterior pituitary

-stimulates adrenal cortex to release cortisol and aldosterone

-stimulates gluconeogenesis 

-chronically suppresses the immune response, WBC, inflammation, allergic response and delays healing

-increases gastric secretions (development of ulcers maybe)

-makes heart more responsive to catecholamines and stimulates the CNS

-increases urinary excretion of calcium 

-released by adrenal cortex

-sodium retention, increases blood volume and BP

anti-diuretic hormone

-released by posterior pituitary folloing stimulation from hypothalamus

-water retention, increases blood volume and BP

Catecholamines: norepinephrine and epinephrine

(released how and by)

-SNS releases NE following activation by hypothalamus

-adrenal medulla releases NE (20%) and Epi (80%) following direct stimulation by SNS

-dilates blood vessles to heart, brain, skeletal muscles, and increases blood flow to these organs

-constricts arterioles in viscera and skin (pallor, decreases Glomerular filtration rate, urinary output drops, decreases blood flow to GI

-dilates pupils

-hyperglycemia due to glycogenolysis and gluconeogenesis

-increases cholesterol levels due to lipolysis

-dilates airways (increases O2 delivery to blood)

-increases mental alertness and anxiety

-increases BP by vasoconstriction and constricts blood vessels of viscera and skin which shunts blood to organs involved in stress response

-decreases gastric secretion and motility

-dilates pupils

-dilates airways

-stimulates sweat glands and piloerection (goosebumps)

-HA

-chronic infections and diseases flare with stress

-necrosis due to prolonged vasoconstriction 

-stress ulcers 

-stomatitis

-necrotizing periodontal disease

-can precipitate acute renal failure

-infection

-unhealthy behaviors

-slowed healing

post traumatic stress disorder

-usually occurs within 3 months of event

-characterized by 3 categories of symptoms 

(revisiting/reliving the event, avoidance of certain activities and lack of emotional response, and dissociative state where the person is unresponsive)

-high risk for developing dependence on drugs and/or alcohol

-level of stimulation required to stimulate nerve endings and elicit a pain response

-usually does not vary between individuals

-the ability to withstand or cope with pain

-culturally related

-varies between individuals

-degree of pain, intensity or duration which is endured before an individual takes action to decrease pain

-may be increased by endorphin release

-may be reduced to fatigue or stress

-inflammation

-infection

-ischmia and necrosis

-streching of tissue

-streching of tendons, ligaments, joint capsule

-chemicals

-burns

-muscle spasms

-somatic pain

-visceral pain

-pain receptors

-stimulated by:

thermal means

chemical

physical

-myelinated A delta fibers

(rapid transmission, acute pain that is sudden, sharp and localized)

-unmyelinated C fibers

(slow transmission, Chronic pain that is diffuse, dull, burning or aching)

-area of skin innervated by specific spinal nerve

-are "mapped" to area of somatosensory cortex and corresponds to source of painful stimuli

-fast impulses

-acute pain

-slow impulses

-chronic/dull pain

-stress reponse

-houses emotional factors

-communication with other regions of the brain to integrate responses

-gates open = pain impulses transmitted from periphery to brain

-gates closed = reduces or modifies the passage of pain impluses which is due to either competing stimuli or inhibitory messages from higher brain centers

-release of endorphins from interneurons (stimulated by serotonin)

-blocked activity of substance P

-location of pain

-quality of pain (descriptive terms)

-associated symtpoms i.e., N/V, fainting, dizziness, anxiety and fear

-timing of pain

-duration of pain

-physical evidence of pain (pallor and sweating, high BP, tachycardia, clenched fists or rigid face, restlessness or constant motion, guarding

physiologically

(tachycardia, increased BP, facial expressions)

referred pain

-source of pain is identified at a site different from the actual source

(characteristic of visceral damage in abdominal organs, heart attack or ischemia in the heart, pain is perceived as coming from surface of the body)

-usually in adults

-more common if chronic pain has occurred

-following an amputation

-usually does not respond to common pain therapies

-may resolve within weeks to months

-indicates tissue damage

-usually sudden and severe, short term

-localized or generalized

-initates a physiologic stress response (increase in BP, HR, cool, pale, moist skin, increased RR, increased muscle tension

-vomiting may occur

-strong emotional response may occur

chronic pain

-occurs over extending time, may be recurrent

-usually more difficult to treat than acute pain

-often perceived to be generalized

-sleep disturbances are common

-specific cause may be less apparent

-appetite may be affected

-frequently affects daily activities

-periods of acute pain may accompany chronic pain

-usually reduces tolerance to additional pain

-removing cause asap

-analgesic medications

-sedatives and anti-anxiety drugs

-increasing dosages or adding new drugs when tolerance develops

-PCA pump

-cannot be controlled with medication

-surgical intervention is choice

(Rhixotomy - selectively destroys problematic nerve roots in the spinal cord, Cordotomy - disables selected pain-conducting tracts in the spinal cord, injections)

neuroleptanesthesia

-patient can respond to commands

-relatively unaware of procedure, no discomfort 

cell counts with percentage of different types of WBC

Hct, Hgb

blood smear gives morphology of RBC and platelets

mean corpuscular volume (mean volume of each RBC)

Low = microcytic anemia

High = macrocytic anemia

mean corpuscular hemoglobin

content of Hg per each RBC

low = hypochromic anemia

-concentration of Hgb in the RBC

low = hypochromic anemia 

-number of immature non-nucleated RBC circulating in blood

normal ~1%

-bleeding time (not a lab test) - time required to stop bleeding from small puncture wound - indicator of platelet activity

-prothrombin time PT (INR) - measures coagulation by extrinsic pathway

- partial thromboplastin time - PTT or activated PTT = measures coagulation by intrinsic pathway

-used to increase Hb to enhance oxygen carrying capacity of the blood

- 1 unit ~275-400 cc

- 1 unit will increase Hb by 1g/dl and Hct by 3%

-may be washed or filtered to remove traches of platelets, WBC and plasma

fresh frozen plasma

-unconcentrated source of all clotting factors

-does not contain platelets

-used to correct bleeding disorders secondary to factor deficiencies and DIC

-concentrate prepared from fresh frozen plasma (higher amount of clotting factors)

-used to treat hemophilia, Von Willebrand's disease and DIC as well as other disorders

-post exposure prophylaxis for pt's exposed to a variety of infectious diseases 

(Hep A and B, varicella, rabies)

-used to control bleeding in pt's with thrombocytopenia

-1 unit of platelets increases platelet count by ~10,000/uL

-used in immunocompromised individuals

- helps prevent transfusion related GVH disease

-artifical form of erythropoeitin

-before certain surgical procedures

-anemia r/t cancer

-chronic renal failure

anemia hgb levels for males and females

males  <13 g/dl

females < 11.5 g/dl

-fatigue (decreased ATP production)

-Pallor (low Hb-pigment, shunting of blood from skin to vital organs)

-increased RR and depth

-SOB due to air hunger

-increased stroke volume, HR

-impaired healing/thinning of epithelial tissues

- dizziness 

-decline in intellectual functioning

-decline in motor function

-morphological (assessing size and shape of RBC, chemical analysis of hgb)

-etiological (decreased hematopoiesis, increaed destruction of RBC, blood loss)

-normocytic normochromic

-microcytic hypochromic

macrocytic normochromic

-abnormal RBC shape

-normal size/shape of RBC and normal color

-blood loss

-chronic infections where body reserves are depleted and hematopoiesis is affected or RBC are destroyed

-metabolic diseases (adrenal)

-bone marrow failure (aplastic anemia)

-RBC are small and pale

-thalassemia

-iron deficiency 

-large RBC with normal color 

(megalosblasts, non-megaloblasts)

-vit. B12 deficiency

-folic acid deficiency

-chronic liver disease

-hereditary elliptocytosis

-hereditary spherocytosis

-sickle cell anemia

- decreased hematopoiesis

-impaired synethsis of hgb due to lack of iron

-all ages affected

women > men

-more common in pregnancy 

- poor intake of iron

-chronic blood loss

-imapired absorption of iron

(achlorhydia = decrease in HCl acid production in stomach due to protom pump inhibitors and antacids)

-liver disease

-fatigue

-pallor

-increased RR and depth

-SOB

-increased stroke volume and HR

-impaired healing/thinning of epithelial tissues

-dizziness

-decline in intellectual and motor function

-microcytic hypochromic anemia

-low Hb, hct, MCV, MCH

-serium Fe stores will be low

-bone marrow biopsy 

-correct underlying problem

-supplemental iron

(causes GI irritation, nausea, constipation, liquid forms can stain teeth so use a straw)

-decreased hematopoiesis

-imapirment or failure of bone marrow

-see a pancytopenia (decreased number of RBC, WBC and platelets)

-idiopathic (most common type with poor prognosis)

-secondary due to bone marrow supression by cytotoxic drugs, radiation, viral infection

-those seen in anemia

-uncontrollable infections due to leukopenia

-bleeding due to thrombocytopenia

-death is usually due to overwhelming infection

diagnosis of aplastic anemia

-CBC/blood smear (decreased number of RBC, platelets, and WBC)

-anemia is usually normocytic normochromic

-bone marrow biopsy shows depletion of precursor cells and infiltrates of fibroblasts and fat cells

-treat underlying cause

-bone marrow transplant (60% success rate)

-decreased/abnormal production

-abnormal hematopoiesis (RBC precursors do not mature normally due to problems with DNA, Large, nucleated RBC are formed (megaloblasts))

-these cells undergo apoptosis and the megaloblasts are destroyed prematurely

-decreased # of RBC results in inadequate oxygen delivery

-pernicious anemia

-B12 deficiency

-folic acid deficiency

pernicious anemia

-most common cause of megaloblastic anemia

-due to lack of intrinsic factor

(antibodies to parietal cells and intrinsic factor, intrinsic factor is required for absorption of B12 in ileum)

-poor intake 

-malabsorption

-folic acid antagonist drugs used in chemotherapy (Methotrexate, flurouracil)
("Leucovorin rescue") 

- same as anemia

-glossitis, stomatitis

-neurological effects with pernicious anemia and B12 deficiency (paresthesias in extremities, ataxia)

-decreased RBC, macrocytic hypersegmented granulocytes

-bone marrow biopsy - increased megaloblasts

-to specifically diagnose pernicious anemia a Schilling's test is used, it uses radioactive B12 to measure absorption

-address underlying cause

-vitamin suplements

-Vit. B12 injection for pernicious anemia

-environmental factors/extrinsic factors (immune reactions, infections (malaria), erythroblastosis fetalis, transfusion reactions, changes in blood osmolatity)

-defect of RBC or hgb

sickle cell disease

-hemolytic anemia

-autosomal rescessive genetic disease

-defect is an abormal hgb (HbS)

-rarely appear before age 12 mo. 

-general s/s of anemia

-gallstones

-splenomegaly in children

-jaundice

-pain

-acute chest syndrome

-hand and foot syndrome

-delayed growth and puberty

-frequent infections

Hgb electrophoresis

-prenatal diagnosis (fetal DNA)

-hydroxyurea 

-dietary supplementaion of folic acid 

-bone marrow transplant

-immunizations in children

-avoid situations that would increase sickling

-hemolytic anemia

-autosomal recessive genetic disease

-higher incidence in areas where malaria is prevalent

-see reduction in hgb and RBC number

-alpha 

-beta

-heteroxygotes

-mild anemia

- often picked up as an incidental finding 

-homozygotes

-severly affected

-Beta Thalassemia Major = Cooley's anemia

-Cooley's anemia

-severe

-destruction of RBC and iron depostion in vital organs

-abnormal Hgb is produced and leads to destruction of RBC and ineffective hematopoiesis

-same as for anemia

-hemosiderosis

-splenomegaly

-hepatomegaly

-CHF

-hyperplasia of the bone marrow (extra medullary RBC production)

-frontal bossing

-Malar prominence

-hpertelorism

-chipmunk faces

-growth retardation with impaired intellectual development

DNA

Hg electrophoreisis

-blood transfusion

-iron chelation therapy

-diasease has high mortality rate in children

-increased production of RBC and other cells in bone marrow

-serum erythropoietin levels are low

-considered a neoplastic disorder of unknown eitiolgy 

-compensation due to high altitudes, chronic lung disease or heart disease

-scondary to erythropoietin secreting tumors (renal cell carcinoma)

-plethoric and cyanosis

-increased blood viscosity slows blood flow

-hepatomegaly, splenomegaly

-increased BP with bounding pulses

-CHF

-elevated uric acid from cell destruction(joint pain)

-dyspnea

-HA

-visual disturbances

-elevated RBC count and hgb, uric acid

-bone marrow - see replacement of yellow marrow with red marrow and hypercellular marrow

-thrombocytopenia (secondary to viarl infection (children) , autoimmune reactions (adults)

-chemotherapy, radiation, cancer

-ESRD - uremia

-ingestion of aspirin or ibuprofen

-Vit. K deficiency

-liver disease

-anticoagulants (coumadin)

-persistent bleeding from gums

-repeated epistaxis

-petechia

-frequent purpura and ecchymosis

-more than normal bleeding in trauma

-bleeding into joint (hemarthrosis)

-hemoptysis

-hematemesis (coarse brown particles)

-blood in feces

-anemia

-feeling faint and anxious

-low BP

-rapid pulse

-blood clotting disorder

-deficient or inactive clotting factor VIII

-most common inherited clotting factor deficiency

-X linked recessive

-see prolonged bleeding after minor tissue trauma

-varying degrees of severity

-spontaneous bleeds 

-bleeding time and PT normal

PTT, aPTT, coagulation time prolonged

-serum levels of factor VIII are low

-desmopressin (DDAVP)

-replacement therapy for factor VIII

disseminated intravascular coagulation

-uncontrolled activation of clotting factors with widespread thrombi formation, followed by massive hemorrhage

-tissue factors relased from damaged cells activates thrombin and clotting ensues

-process consumes clotting factors and causes occlusion of small blood vessels with clots

-ischemic tissue replaces plaminogen activator which turns on plasmin and result in fibrinolysis

-fibrinolysis reopens occluded vessels

-as blood enters vessesls that were damaged bleeding from vessel occurs

-coagulation

-fibrinolysis (hemorrhage, anemia, shock)

-thrombocytopenia (purpura, ecchymoses)

-clinical picture/senario

-prolonged PT, aPTT, low fibrinogen, elevated FDP (d-dimer), thrombocytopenia, fragmented RBC

-treat underlying problem

-cryoprecipitate, Fresh frozen plasma

-heparin

sudden onset

see large number of immature, non-functional cells in bone marrow and ciruclation

more common in children

-insidious onset

-see more mature, non-functional cells

-pt's are often asymptomatic even though they have abnormal findings

-more common in adults

-better prognosis

acute myelogenous leukemia 

myelognous = affects the granulocytes

chronic myelogenous leukemia

myelogenous = affects the granulocytes

acute lymphocytic leukemia

lymphocytic = affects the lymphocytes (usually B cells)

chronic lymphocytic leukemia

lymphocytic = affects the lymphocytes (usually B cells)

most common form in children

rapid course

w/o therapy death would ensue in 3-6 mo.

with therapy cure is seen in ~2/3 of patients

disease of older adults (most are >50)

CLL cells are indistinguishable from normal lymphocytes 

-cells forget to die

-CLL does not respond well to chemo because the cells are not rapidly dividing 

-most pt's survive 7-10 yrs. from time of diagnosis

-can transform into more agressive lymphoma or leukemia

-many diff. types based on cell markes and cytogenic findings

-most common form of acute leukemia in adults

-very rapid course (w/o therapy death would occur in 6 months)

disease of adults 

three phases (chronic, acclerated, blast)

chemo does not yield good results

bone marrow transplant with radiation gives best results

philadelphia chromosome is a genetic marker for the disease and those without this marker have worse prognosis

-unknown

-adult leukemias are associated with radiation, chemical exposure, viral infections

-chromosomal abnormalities

-anemia, thromocytopenia and lack of normally -functioning WBC

- s/s of anemia

-bleeding

-multiple infections that don't respond to therapy

-bone pain

-hyperkalemia which leads to kidney failure/stones

-weight loss

-anorexia

-enlargement of lymph nodes, spleen and liver due to infiltration with abnormal cells

-CNS infiltration - HA, visual probs., drowsiness, vomiting

CBC/blood smear

bone marrow biopsy

chemo

bone marrow transplant

-onset in 20-40 year old group

-equally affects men and women

-diease beings in lymph nodes

-usual onset is in node above the diaphragm

-enlarged painless lymph node in neck is common

-malignant lymphocytes spread to other nodes and organs

-classic cell is Reed-Sternberg cell

-painless, non-tender lymph node -  usually cervical

0splenomegaly

-lymphadenopathy

-generalized pruritis

-recurrent infection due to nonfunctioning lymphocytes 

-usually presents with multiple nodes and fever

-pattern of spread is less organized and more widespread

-do not see Reed-Sternberg cells

malignant disease of plasma cells with overgrowth of these cells in bone marrow

-production of other blood cells is impaired

- most pt's >45

destruction of bone occurs as cells overgrow in bone marrow

"moth eaten appearence"

-hypercalcemia (destruction of bone, calcium let off into blood)

-immunoglobin secreted by plasma cell is excreted by kidneys (see damage and renal failure)

-progonsis poor with short life-expectancy