Exam 4 Flashcards
hematopoiesis
- blood cell production
- occurs within the bone marrow: produces RBCs, WBCs, and platelets
what are nondifferentiated immature blood cells in the bone marrow called?
stem cells
why might the body make more RBCs?
loss of blood, anemia, need more O2
how much of our blood does plasma constitute?
55% of blood
what is plasma composed of?
primarily of water but also contains proteins, electrolytes, gases, nutrients, and waster products
serum plasma
refers to plasma minus its clotting factors ~ has everything to do with hydration
how much of our blood do blood cells constitute?
45%
erythrocytes
RBCs ~ oxygen transportation
leukocytes
WBCs ~ protection from infection
thrombocytes
platelets ~ promote coagulation
normal platelet count
150-450
what does hematocrit show?
hydration status
if you give fluids, what will H&H be like?
low
erythropoiesis
- making RBCs
- stimulated by hypoxia
- controlled by erythropoietin (created by kidneys)
what do reticulocytes do?
mature into RBCs and are a good indication of production rates
what does hemolysis do?
removes abnormal, defective, damaged, and old RBCs from circulation
if someone is in kidney failure, what can we expect?
them to be anemia
two types of leukocytes
- granulocytes
- agranulocytes (have to do with immunity)
types of granulocytes
- neutrophils (most common)
- eosinophils
- basophils
types of agranulocytes
- lymphocytes
- monocytes
why would neutrophils be increased?
due to bacterial infection
neutrophils
- primary function is phagocytosis
- primary phagocytic cells involved in acute inflammatory response
- mature neutrophil is segmented (“seg”)
- immature neutrophils are called bands
- first site of infection
an increase in percent of bands is called what?
a shift to the left, meaning bone marrow is releasing less-mature cells into circulation in response to a site of injury (increased in acute infection and inflammation)
life-span of neutrophils
2-14 days
eosinophils
- have a reduced ability for phagocytosis compared with neutrophils
- granules contain histamine
- engulf antigen-antibody complexes formed during an allergic response
- defend against parasites
- found in large numbers in lungs and GI tract
basophils
- limited role in phagocytosis
- have cytoplasmic granules that contain heparin, serotonin, and histamine
lymphocytes
form the basis of cellular and humoral immune response
two subtypes of lymphocytes
B cells and T cells
if there is a dysfunction in B and T cells, what can that mean?
lost ability of immune system
monocytes
- potent phagocytic cells
- second type of cell to arrive at site of injury ~ try to clean things up
- when they migrate into tissue, they become macrophages
macrophages
monocytes that have migrated to tissue
where are macrophages stores?
- in spleen, lymph nodes, tonsils, and liver
- when damage, infection, or injury triggers a response, the monocytes leave their primary location and travel through blood stream to enter other tissues and organs
what would happen if we removed someone’s spleen?
they would be immunocompromised
what are thrombocytes regulated by?
thrombopoietin
hemostasis
the arrest of bleeding
vascular response of hemostasis
- immediate local vasoconstrictive response of injured blood vessels
- reduces leakage of blood
- gives time for platelet response and plasma clotting factors to be triggered
platelet plug formation of hemostasis
- activated by exposure to interstitial collagen from the injured blood vessel
plasma clotting factors of hemostasis
- form a visible fibrin clot on the platelet plug ~ scab
- always present in circulation in inactive forms
two pathways of clotting
- intrinsic pathway is activated by collagen exposure
- extrinsic pathway is initiated when tissue factor or tissue thromboplastin is released from injured tissue
thrombin
most powerful enzyme in the coagulation process because it converts fibrinogen to fibrin
lysis of clot
anticoagulation, the reverse of clotting, helps keep blood fluid
what two means does anticoagulation occur by?
- antithrombins: interfere with thrombin
- fibrinolysis: process that results in dissolution of the fibrin clot
function of the speeln
- filtration
- immunologic
- storage
what does lymph system help with?
- F/E movement
- protein and fat from the GI tract and certain hormones are returned to circulatory system
- returns excess interstitial fluid to the blood to prevent or reduce edema
what does too much interstitial fluid or reduced absorption lead to?
lymphedema
what do lymph nodes indicate?
infection
primary function of lymph nodes
filtration of pathogens and foreign particles carried by lymph fluid
what does the liver do for the lymph system?
- functions as a filter
- produces all procoagulants essential to hemostasis and blood coagulation
- stores excess iron
thrombocytopenia
- reduction of platelets
- results in abnormal hemostasis = prolonged or spontaneous bleeding
causes of thrombocytopenia
- inherited
- acquired
acquired types of thrombocytopenia
- immune thrombocytopenia purpura (ITP)
- thrombotic thrombocytopenia purpura (TTP)
- heparin-induced thrombocytopenia (HIT)
most common acquired thrombocytopenia
ITP
ITP
- syndrome of abnormal destruction of circulating platelets
- autoimmune disease
manifestations of ITP
- chronic in adults
- gradual onset with transient remissions
TTP
- an uncommon syndrome with a variety of features that are not always present
- associated with enhanced aggregation of platelets that form into microthrombi ~ like in DIC
- caused by plasma enzyme deficiency
- idiopathic or from drug toxicities
- medical emergency! bleeding and clotting occur simultaneously
HIT
- associated with increased use of heparin ~ creates positive feedback loop which can result in clots
- life-threatening
- platelet destruction and vascular endothelial injury
- develops 5-10 days after heparin therapy is started
- clots while on heparin
major clinical problems with HIT
- venous thrombosis
- arterial thrombosis
- DVT and PE
clinical manifestations of thrombocytopenia
- patients are often asymptomatic
- most common symptoms is mucosal or cutaneous bleeding - think GUMS and HANG-NAIL
- petechiae (microhemorrhages)
- purpura (bruise form numerous petichiae)
- ecchymoses (larger lesions from hemorrhage)
- prolonged bleeding after routine procedures
- hemorrhage
how will platelet counts look in thrombocytopenia?
- prolonged bleeding < 50,000
- hemorrhage < 20,000
what kind of drug should pts. avoid with thrombocytopenia?
aspirin and other medications that affect platelet function or production
in ITP, when is therapy initiated?
if platelets are < 30,000
how do we treat ITP?
- corticosteroids
- high dose of IVIG and anti-Rh (competes with antiplatelet antibodies for macrophage receptors in the spleen
- rituximab
- splenectomy (an enlarged spleen sequesters and destroys platelets, resulting in less available in circulation
- platelet transfusions (indicated for platelet counts < 10,000 or if bleeding is anticipated before a procedure
how do we treat TTP?
- first treat underlying disorder or remove cause
- plasmapheresis is used to aggressively reverse platelet consumption
- rituximab
- other immunosuppressants
- splenectomy
how do we treat HIT?
- permanently stop all heparin including heparin flushes
- start pt. on direct thrombin inhibitor
- start coumadin
causes of anemia
- deficiency in the number of erythrocytes (RBCs)
- quantity of Hgb
- volume of packs RBCs (Hct)
what is used to determine the severity of anemia?
Hgb levels
normal Hgb levels in men and women
men: 13.8 - 17.2
women: 12.1 to 15.1
clinical manifestations of anemia
- pallor
- jaundice
- pruritus
- tachycardia due to CO being maintained by increasing the HR and SV
- fatigue
- imbalanced nutrition
- ineffective self-health management
goal of anemia therapy
correcting the cause
acute interventions for anemia
- blood or blood product transfusions
- drug therapy such as erythropoietin and vitamins
- volume replacement
- dietary and lifestyle changes
- O2 therapy
- prevent falls and injuries
what is common in older adults with anemia?
nutritional deficiencies ~ S/S may go unrecognized or may be mistaken for normal aging changes
what do we always give blood with?
NS
life span of RBC
120 days
iron-deficiency anemia
- one of the most common chronic hematologic disorders
- iron is present in all RBCs as heme in hemoglobin
where does iron absorption occur?
in the duodenum ~ diseases of surgery that alter, destroy, or remove the absorption surface can cause anemia
where does blood loss most commonly occur in iron-deficiency anemia?
GI and GU systems
what else contributes to iron-deficiency anemia?
pregnancy
clinical manifestations of iron-deficiency anemia
- pallor is most common
- glossitis
- cheilitis
how do we treat iron-deficiency anemia?
- treat underlying disease causing reduced intake or absorption of iron
- replace iron
how is iron best absorbed?
as ferrous sulfate in an acidic environment
side effects of taking iron?
heartburn, constipation, diarrhea, black stools
why would we give parenteral iron?
- indicated for malabsorption, oral iron intolerance, need for iron beyond normal limits, poor patient compliance
- IV or IM ~ IM may stain skin
- hospital or infusion center
when do we check iron levels are starting therapy and how long until it returns to normal levels?
check again in 1 month, won’t return to normal for 3 months
thalassemia
- a group of diseases involving inadequate production of normal Hgb ~ decreased erythrocyte production
- common in ethnic groups near the mediterranean sea and equatorial or near-equatorial regions
- genetic problem with globulin protein
megaloblastic anemia
- group of disorders caused by impaired DNA synthesis
- presence of megaloblasts
- majority result from deficiency in cobalamin (vit. B12) and folic acid
what is required for cobalamin absorption?
intrinsic factor (IF)
what is cobalamin deficiency most commonly caused by?
pernicious anemia which is caused by an absence of IF
clinical manifestations of cobalamin deficiency
- sore tongue
- anorexia
- N/V and abdominal pain
- weakness
- paresthesias of feet and hands
- decreased vibratory and position senses
- ataxia
- muscle weakness
- impaired though process
how do we treat cobalamin deficiency?
parenteral or intranasal administration
how does folic acid deficiency differ from cobalamin deficiency?
clinical manifestations are similar, but absence of neurologic problems
normal serum folate levels
3-25 mg/mL
how do we treat folic acid deficiency?
- replacement therapy ~ 1 mg per day PO
- eating foods with large amounts of folic acid
aplastic anemia
- pancytopenia ~ decrease in all blood cell types
- hypocellular bone marrow
- bone marrow made out of plastic, not working
2 major types of aplastic anemia
- congenital: chromosomal alterations
- acquired: results from exposure to ionizing radiation, chemical agents, viral and bacterial infection
clinical manifestations of aplastic anemia
- symptoms caused by suppression of any or all bone marrow elements
- fatigue, dyspnea
- cardiovascular and cerebral responses
- neutropenia
how do we treat aplastic anemia?
- identify and remove all causative agents
- provide supportive care
- prevent infection
- prevent hemorrhage
anemia caused by blood loss
- acute blood loss occurs as a result of sudden hemorrhage
- the sources of chronic blood loss are similar to those of iron-deficiency anemia
clinical manifestation of acute blood loss
- caused by body’s attempts to maintain adequate blood volume and meet oxygen requirements
- tired, falls, tachycardia
how do diagnostic studies look with acute blood loss?
- since it is sudden, values may seem normal or high for 2-3 days
- once plasma volume is replaced, low RBC concentrations become evident
how do we treat acute blood loss?
- replace BV to prevent shock
- identifying source of hemorrhage and stopping blood loss
- providing supplemental iron
chronic blood loss sources
- bleeding ulcer
- hemorrhoids
- menstrual and postmenopausal blood loss
how do we manage chronic blood loss?
- identify the source
- stopping the bleeding
- providing supplemental iron
hemolytic anemia
destruction of hemolysis of RBCs at a rate that exceeds production
manifestations of hemolytic anemia
- general manifestations of anemia
- jaundice
- enlargement of spleen and liver
major focus of treatment in hemolytic anemia
maintenance of renal function is a major focus of treatment
sickle cell disease
- group of inherited, autosomal recessive disorders
- characterized by the presence of an abnormal form of Hgb in the RBC
- predominant in african americans
- severe, painful, acute exacerbation of sickling causes a vaso-occlusive crisis
how do we unstick sickle cells?
give more fluids
in sickle cell disease, what can severe capillary hypoxia lead to?
tissue necrosis
in sickle cell disease, what can be a result of severe O2 depletion?
life-threatening shock
clinical manifestations of sickle cell disease
- typical patient is asymptomatic except during sickling episodes
- pain from tissue hypoxia and damage
- pallor of mucous membranes
- jaundice from hemolysis ~ prone to gallstones
major complication of sickle cell disease
infection since the function of the spleen becomes compromised from sickled RBCs, pneumococcal pneumonia is most common
what can severe infection in sickle cell crisis lead to?
aplastic crisis which can lead to shutdown of RBC production
what do we want to teach pts. in sickle cell disease?
- avoid high altitudes
- maintain adequate fluid intake
- treat infection promptly
- avoid crisis
acquired hemolytic anemia
hemolysis of RBCs is caused by four categories of extrinsic factors: macroangiopathic (physical trauma), microangiopathic, antibody reactions, infectious agents and toxins
maroangiopathic destruction
- physical destruction of RBCs results from exertion of extreme force on cells
- hemolysis, extracorporeal circulation used in cardiopulmonary bypass, prosthetic heart valves, abnormal vessels
microangiopathic destruction
- results from fragmentation of the cells as the try to pass by abnormal arterial or venous microcirculation
- RBCs are sheared as they try to pass by excessive platelet aggregation or fibrin polymer formation ~ seen in TTP and DIC
two mechanisms involved in destruction from antibodies
- isoimmune reactions : blood donor reactions
- autoimmune reaction: antibodies develop against own RBCs
how do infectious agents cause hemolysis?
- invade RBCs and destroy its contents
- release hemolytic substances
- generate an antigen-antibody reaction
how do we treat acquired hemolytic anemia?
- supportive care until the causative agent can be eliminated or made less injurious
- emergency preparedness: hydration, electrolyte replacement, corticosteroids, blood products, splenectomy
cancer
- group of diseases characterized by uncontrolled and unregulated growth of cells
- higher incidence in men than women
- second most common cause of death in U.S. after heart disease
- leading cause of death in people 40-79 years of age
two major dysfunctions in the process of cancer development
- defective cell proliferation (growth)
- defective cell differentiation
what happens with cancer cells?
they have no regard for cell boundaries ~ grow on top of one another on top of or between normal cells
bacteriostatic
slows down, stops
two genes that can be affected by mutation
- protooncogenes: regulate normal cellular processes such as promoting growth
- tumor suppressor genes: suppress growth
protooncogenes
- genetic locks that keep cells functioning normally
- mutations that alter their expression can activate them to function as oncogenes
what do mutations do with tumor suppressor genes?
they make them inactive ~ results in loss of suppression of tumor growth
when is screening recommended if a close family member had cancer?
10 years before that family member had it
carcinogens
- cancer-causing agents capable of producing cell alterations
- many are detoxified by protective enzymes and are harmlessly excreted
- failure of protective mechanisms allows them to enter cell’s nucleus and alter DNA
- can be chemical, radiation, or viral
what type of cancer is UV radiation associated with?
melanoma (worst cancer) and squamous and basal (most benign) cell carcinoma ~ sunlight is main source of UV exposure
what is the length of the latent period associated with?
mitotic rate of tissue of origin and environmental factors
what do lymphocytes do in cancer?
continually check cell surface antigens and detect and destroy abnormal cells
what do oncofetal antigens help with?
monitor therapy and look for reoccurance
stages of cancer
o: cancer in situ
I: tumor limited to tissue of origin; localized tumor growth
II: limited local spread
III: extensive local and regional spread
IV: metastasis
TNM cancer classification
T = tumor size and invasiveness
N = spread to lymph nodes
M = metastasis
can stage classification be changed?
no, not once established
osteomyelitis
severe infection of bone, bone marrow, and surrounding soft tissue
how long does acute osteomyelitis last?
infection of < 1 month in duration
clinical manifestations of acute osteomyelitis
- pain that worsens with activity; is unrelieved by rest
- swelling, tenderness, warmth
- restricted movement
- fever, night sweats, chills, restlessness, nausea, malaise, drainage
how long does chronic osteomyelitis last?
infection lasting > 1 month or has failed to respond to initial antibiotic treatment
how does chronic osteomyelitis present and what might the pt. need to be taken home on?
continuous and persistent or process of exacerbations and remissions ~ wound pump to deliver antibiotics
clinical manifestations of chronic osteomyelitis
- systemic manifestations reduced
- local signs are more common: pain, swelling, warmth
how do we care for acute osteomyelitis?
- aggressive, prolonged IV antibiotic therapy
- cultures or bone biopsy
- surgical debridement and decompression
how long are antibiotics given and for how long in acute osteomyelitis?
- 4-6 weeks or longer
- via CVAD
how do we care for chronic osteomyelitis?
- surgical removal
- extended use of antibiotics
- acrylic bead chains containing antibiotics
- intermittent or constant antibiotic irrigation of bone
- casts or braces
- wound vac
- muscle flaps, skin grafts, bone grafts
- amputation
persons at risk for osteomyelitis are usually what?
- immunocompromised
- have diabetes, orthopedic prosthetic devices, vascular insufficiencies
what can lengthy antibiotic therapy cause?
overgrowth of candida albicans and clostridium difficile
osteoporosis
- chronic, progressive metabolic bone disease marked by low bone mass and deterioration of bone tissue
- leads to increased bone fragility
- known as the “silent thief”
why is osteoporosis more common in women?
- lower calcium intake
- less bone mass
- bone resorption begins earlier and becomes more rapid at menopause
- pregnancy and breastfeeding
- longevity
screening guidelines for osteoporosis
- initial bone density test in women over 65
- repeat 15 years if normal
- earlier and more frequent if high risk
how can we best prevent osteoporosis?
- regular weight-bearing exercise
what age do we reach our peak bone mass?
by age 20
osteoblasts
deposit bone
osteoclasts
resorb bone
what happens in osteoporosis with resorption and deposition?
bone resorption exceeds bone deposition
clinical manifestations of osteoporosis
- occurs commonly in spine, hips, and wrists
- back pain
- spontaneous fractures
- gradual loss of height
- kyphosis or “dowager’s hump”
what do T-scores test for?
bone density
t-score between +1 and -1 is
normal bone density
t-score between -1 and -2.5 is
osteopenia
t-score -2.5 or lower is
osteoporosis
recommended calcium intake
- 1,000 mg/day for women ages 19-50 and men ages 19-70
- 1,200 mg/day for women 51 years or older and men 71 years or older
good sources of calcium
milk, yogurt, turnip greens, cottage cheese, ice cream, sardines, spinach
what vitamin is necessary for calcium absorption/function?
vitamin D
radicular pain
irritation of nerve root
referred pain
source of pain is another location
why is back pain common in the lumbar region?
lumbar region:
- bears most of body weight
- contains nerve roots
- has poor biomechanical structure
ideal BMI
18.5-24.9
what should we teach pts. with lower back pain?
- sleep in a side-lying position with knees and hips bent
- sleep on back with a lift under knees and legs or with 10-inch pillow under knees to flex hips and knees
- prevent lower back from straining forward by placing a foot on a step or stool during prolonged standing
- use a lumbar roll or pillow for sitting
- exercise 15 minutes in the morning and evenings regularly
- carry light items close to body
- use local heat and cold application
- maintain appropriate body weight
multiple nerve root (cauda equina) compression
- severe low back pain, weakness
- bowel and bladder incontinence
- medical emergency
when do most pts. heal from intervertebral disc disease?
within 6 months with good back-strengthening exercises
when is surgery indicated in intervertebral disc disease?
- conservative treatment fails
- radiculopathy worsens
- loss of bowel or bladder control
- constant pain
- persistent neurologic deficit
what mechanism can we use after spinal disc surgery?
log rolling, spinal precautions
what can we expect after spinal surgery?
- potential for CSF leakage
- monitor for and report severe headache or leakage of CSF
- clear or slightly yellow drainage on dressing
- for glucose
osteoarthritis
- slowly progressive noninflammatory disorder of the diarthrodial joints
- gradual loss of articular cartilage
- formation of osteophytes ~ bone chunks, extra bone that builds up
risk factors of OA
- age
- decreased estrogen at menopause
- obesity
- anterior cruciate ligament injury
- frequent kneeling and stooping
what can help prevent OA?
regular exercise
is inflammation common in OA?
no, it is just bone broken down and rebuilding
what is the distinction between OA and RA?
systemic manifestations are NOT present in OA
clinical manifestations of OA
- joint pain that worsens with joint use
- pain may be referred to groin, buttock, or outside of thigh or knee
- early morning stiffness usually resolves within 30 minutes
- crepitation
- asymmetrical
- deformity at DIP and PIP joint
what kind of interventions are the basis for OA management?
nondrug: balance rest and activity, avoid prolonged standing, kneeling, or squatting, assistive devices
what is critical when trying to prevent OA?
weight reduction
rheumatoid arthritis
- chronic, systemic autoimmune disease
- inflammation of connective tissue in diarthrodial (synovial) joints
- periods of remission and exacerbation - SPELLS
- three times as many women as men
- antigen triggers formation of abnormal IgG
- autoantibodies develop against abnormal IgG (rheumatoid factor)
- T helper cells (CD4) are activated
- edges are being shaved off and bones are falling on top of each other
in RA, what can increase the risk in patients who are genetically predisposed?
smoking
stages of RA
- stage I: no joint destruction
- stage II: destruction in joint cartilage
- stage III: extensive cartilage loss and possible deformity
- stage IV: loss of joint function and formation of subcutaneous nodules
clinical manifestations of RA
- insidious
- fatigue, anorexia, weight loss, generalized stiffness
- symptoms occur symmetrically
- often affects small joints, but larger joints and cervical spine may be involved
- joint stiffness after inactivity ~ morning stiffness 60 minutes to several hours long
- MCP and PIP joints swollen
- tenosynovities
- deformity and disability
- walking disability
- sjogren’s syndrome
- felty syndrome
- depression
what laboratory studies are important in RA?
- rheumatoid factor (RF)
- ESR and c-reactive protein (CRP)
- antinuclear antibody (ANA)
- antibodies to citrullinated peptide (anti-CCP)
how long do DMARDs take to have a therapeutic effect?
4-6 weeks; frequent monitoring is required
since BRMs bind with TNFs, what should we check for?
- TB test and chest x-ray
- monitor for infection
- avoid live vaccinations
is prevention possible in RA?
no, early treatment to prevent further joint damage is
what kind of exercises help with RA?
- gentle ROM
- aquatic exercises in warm water
myofascial pain syndrome
- chronic, musculoskeletal pain and tenderness in the chest, neck, shoulders, hips, lower back
- referred pain to buttock, hand, head
- can cause TMJ
- pain within connective tissue of skeletal muscles
- tender points
- vague pain that is deep
how can we treat myofascial pain?
- “spray and stretch method”
- topical patches
- trigger point injections
- massage, acupuncture
fibromyalgia
- chronic central pain syndrome
- widespread, nonarticular musculoskeletal pain and fatigue
- multiple tender points
- might also have nonrestorative sleep, morning stiffness, IBS, anxiety
- disorder involving abnormal CNS processing
clinical manifestations of fibromyalgia
- widespread burning pain
- worsens and improves throughout day
- trouble determining if pain is in muscles, joints, or soft tissues - VAGUE
- head or facial pain
- difficulty concentrating
- feelings of being overwhelmed
- migraine headaches
- fatigue
- paresthesia
- RLS
- depression and anxiety
- stiffness
- nonrefreshing sleep
- IBS
- difficulty swallowing
- frequency of urination
- difficult menstruation
how do we diagnose fibromyalgia?
- difficult to establish a definitive diagnosis
- rule out
it is fibromyalgia if what two criteria are met?
- pain is experienced in 11/18 tender points
- history of widespread pain noted for at least 3 months
what do we want to teach patients in helping with fibromyalgia?
- limit intake of sugar, caffeine, alcohol because they may be muscle irritants
- vitamin and mineral supplements
- relaxation strategies
- psychologic counseling
SEID
- complex, multisystem disease in which exertion of any sort can adversely affect multiple organs
- women more than men
clinical manifestations of SEID
- diagnosis requires three symptoms: profound fatigue lasting 6 months, post-exertional malaise, unrefreshing sleep; plus one of two: cognitive impairment, worsening of symptoms upon standing
- insidious or intermittent episodes that become chronic
- severe fatigue most common
what other disorder is SEID similar to?
fibromyalgia ~ hard to distinguish
how do we diagnose SEID?
rule out, diagnosis of exclusion
what do we want to teach the patient who has SEID?
- avoid total rest
- strenuous exertion can exacerbate exhaustion
- well-balanced diet
- fiber intake
who might we want to refer a pt. with SEID to?
behavioral therapy
