Tiffany Test 3 Flashcards

1
Q

AIDS

A
  • Most common secondary immune deficiency disease in the world
  • Identified in 1981
  • Serious worldwide epidemic
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2
Q

Laboratory Assessment of HIV

A
  • Lymphocyte counts
  • CD4+ T-cell and CD8+ T-cell count
  • Antibody tests
  • ELISA - first
  • Western blot- if elisa is positive then do this
  • Home tests (e.g., OraQuick In-Home HIV test)
  • Viral load testing
  • Blood chemistries, CBC, stool testing, biopsies
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3
Q

Viral load

A

amount of virus present in blood/other body fluids

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4
Q

Window Period

A

risk of transmission due to negative test during certain time frame

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5
Q

Drug Therapy for HIV

A
  • Antiretroviral drugs – Multiple drugs used together in combinations (HAART)
  • NRTIs
  • NNRTIs
  • PIs
  • Integrase inhibitors
  • Fusion inhibitors
  • Entry inhibitors
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6
Q

liver produces __ and _____

A

prothrombin and vitamin k

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7
Q

what is the result of a hematologic disorder?

A

impaired gas exchange and tissue perfusion

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8
Q

what are the diagnostic tests for hematologic disorders?

A
  • peripheral blood smear: quick analysis of size and shape of RBC
  • CBC: reb wbc count, h and h
  • reticulocyte count- blood marrow function
  • hemoglobin electrophoresis: detects abnormal forms of hemoglobin
  • coombs: looking for blood typing
  • serum ferritin, transferrin, and TIBC: measure iron levels
  • PT: prothrombin time-measure bleeding and coagulation
  • INR: measure bleeding and coagulation
  • PTT: measure bleeding and coagulation
  • anti-factor Xa test: heparin
  • platelet aggregation: when using aspirin
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9
Q

what is anemia?

A

Reduction in number of RBCs, Hgb, or Hct

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10
Q

what are some causes of anemia?

A

impaired function, decreased production, increased destruction

∙ dietary problems   		∙ genetic disorders
∙ bone marrow disease	∙ excessive bleeding
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11
Q

Systemic Manifestations of Anemia

A

▪ Integumentary
-pallor, cool to touch, brittle nails, intolerance to cold

▪ Cardiovascular
-tachycardia at rest and increases with activity, orthostatic hypotension, murmurs or gallops (when severe)

▪ Respiratory
-dyspnea on exertion, decreased O2 sats

▪ Neurological
-increased fatigue, decreased LOC, headache

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12
Q

Vaso-occlusive event (VOE)

A

-repeated episodes can cause organ damage and infarction

Etiology –

∙ HbS cells sensitive to ↓O2 conditions
∙ Sickle shaped RBC’s adhere to each other and 	vascular endothelium

∙ compromises circulation → pain → edema → tissue 	hypoxia → infarction

Causes – 
∙ low/high temps    hypoxia	∙ dehydration
∙ physical exertion	venous stasis    ∙ stress
∙ pregnancy	        alcohol		∙infection
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13
Q

Sickle Cell Anemia manifestations

A
  • Cardiovascular- low BP, slow cap refill
  • Skin- pallor, cyanosis, ulcers
  • Abdominal- damage to spleen and liver, look for pain, -enlargement of spleen or liver
  • Kidney- poor kidney perfusion, chronic kidney disease, hyperkalemia, fluid volume overload
  • Musculoskeletal- arms and legs are sites of blood cell occlusion, move all joints? look for swelling
  • Neuro- during crisis at risk for stroke, and hypoxia, check LOC
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14
Q

Diagnosis of sickle cell anemia

A

∙ early diagnosis critical – all States mandate
newborn screening

Lab assessment:

  • Percentage of HbgS
  • CBC: anemia
  • WBC: elevated

Diagnostic test:
-Based on complications: ie; EKG to r/o MI

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15
Q

Sickle Cell Crisis Interventions

A

1 priority is managing pain

Managing pain:

- IV analgesics: Opiods
- IV hydration
- Hydroxyurea
- Complimentary therapies

Preventing sepsis:

- role of the spleen: immunizations
- antibiotics
- assessments
- lab data

Perfusion:

- Remove restrictive clothing
- Keep room > 72 degrees F
- Keep extremities extended
- Oxygen
- Transfusion

reduce condition that is causing the sickling
IV opioids is the best way to manage pain, PCA
IV hydration- normal saline
IV fluids will hopefully reduce the clumping of the sickle cells
most patients who come in are dehydrated in sickle cell crisis so blood is hypertonic so give NS or hypotonic solution. BP will tell how hydrated they are
Hydroxyurea - medication that can help with sickle cell crisis
oral, reduce number of sickling events
comfortable in bed, extremities extended: get blood flow back, restricted clothing: can encourage clot formation, do not move knees above bed, keep temp above 72: cold causes vasoconstriction, elevated HOB no more than 30 degrees
decreases immune function can lead to sepsis
spleen can not function with our immunity response- get flu vaccine and pneumococcal
o2 given during crisis
transfusion with RBC will dilute hemoglobin s levels and will provide RBC when pt is anemic
*teaching prevention of sickle cell crisis, and when to come in for treatment: early is better!

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16
Q

DKA

A
  • Uncontrolled hyperglycemia, metabolic acidosis, ketones
  • Results from insulin deficiency and increase in counterregulatory hormone release
  • Infection is the most common precipitating factor
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17
Q

DI

A
Water metabolism problem caused by an ADH deficiency (either decrease in ADH synthesis or inability of kidneys to respond to ADH)
Classifications
Kidneys:
Do not conserve fluid
Do not reabsorb water
Put out large amounts of dilute urine
Risk for dehydration!
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18
Q

Assessment findings in DI

A

think about dehydration due to massive water loss
skin- dry, cracked, poor skin turgor

lab values- hypernatremia due to loss of water

GU-Increased UOP, dilute, low specific gravity
Cardio-Hypotension, tachy, weak pulses, hemoconcentation (risk for hypernatremia)
Neuro-Great thirst, Decreased LOC (with dehydration)

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19
Q

Management of DI:

A

I/Os, IVF, weights, urine specific gravity
Oral chlorpropamide
Desmopressin acetate
Early detection of dehydration and maintenance of adequate hydration
Lifelong vasopressin therapy with permanent condition
Teach patients to weigh themselves daily to identify weight gain

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20
Q

SIADH Interventions

A
  • Fluid restriction - patient is retaining water
  • Drug therapy: diuretics, hypertonic saline (3% saline IV), Vasopressin antagonists
  • Monitor for fluid overload
  • Monitor labs
  • Safe environment - Risk for seizure due to Sodium levels
  • Neurologic assessment - Decreased serum sodium levels can lead to CNS/LOC changes
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21
Q

Posted care for hypophysectomy:

A

managing ICP and anything that will delay healing

Monitor neurologic response- change in LOC, vision, mental status, strength in extremities

Assess for post nasal drip- csf leak due to “digging around in brain” (clear drainage, positive for glucose, severe headache)

Elevate HOB- promote drainage to release any ICP

Assess nasal drainage- color, clarity, odor

Avoid coughing soon after surgery- can increase ICP

Assess for meningitis- sx in brain increases risk for meningitis. monitor temp, vitals, change in LOC, headache, neucoregidity

Hormone replacement- lifelong HRT

Avoid bending- decrease ICP

Avoid straining at stool- to decrease ICP

Avoid tooth brushing- can introduce foreign particles, and infection and can cause delay in healing in sx site

Numbness in the area of the incision

Decreased sense of smell

Vasopressin- at risk for DI

Monitor fluid balance- i/o’s, cardiovascular status

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22
Q

Adrenal Medulla

A

Catecholamine secretion
Epinephrine
Norepinephrine

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23
Q

Adrenal cortex

A
  • sex hormones: androgen and estrogen
  • sugar: glucocorticoids (cortisol): response to stress, protein, carb, fat metabolism. immune function, na+ and water balance, emotional stability, prevents - hypoglycemia - increases liver gluconeogenesis, maintains responsiveness of cardiac muscles
  • salt - mineralcorticoids aldosterone- maintain ECF volume, promotes na and water reabsorption, potassium excretions
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24
Q

Glucocorticoids

A
Essential for life
Main = cortisol
Metabolism
Response to stress
Immune function
Emotional stability
Prevent hypoglycemia
Catecholamine action = muscle cells
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25
Q

Mineralocorticoids:

A

Fluid and electrolyte balance
Regulated by RAS, K levels, ACTH

Aldosterone:
Regulates Na++ and K+
Promotes sodium and water reabsorption
Promotes potassium excretion

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26
Q

Manifestations Adrenal Insufficiency

A
  • Hyperkalemia
  • Hypoglycemia
  • Hyponatremia
  • Hypovolemia
  • Weakness
  • Anorexia, weight loss, fatigue
  • Hyperpigmentation = Dark pigment on knuckles, knees, elbows
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27
Q

Interventions for addisons

A

-Interventions focus on fluid balance, fluid deficit, and preventing hypoglycemia
Hormone replacement therapy

-Priority: Prevent complications = risk for cardiac dysrhythmias secondary to hyperkalemia

  • Monitor for hypoglycemia and hyperkalemia
  • HRT
  • Diet high in protein, carbs, and normal Na+
  • Avoid stress, illness, and strenuous exercis
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28
Q

Care for a patient with Addisonian crisis

A
  • Prompt intervention needed to prevent hyponatremia, hyperkalemia, and hypotension.
  • # 1 Hormone replacement therapy (IV or IM)
  • IV fluids (NS or something w/ dextrose)
  • Hyperkalemia management (admin iv insulin to shift potassium back into cells)
  • Hypoglycemia management
  • Monitor I/O’s, heart rate, rhythm, EKG (looking for peaked T waves
  • may give Loop diuretics
  • Limit potassium intake
  • Causes: Stress, illness, surgery, withdrawal of steroid meds
29
Q

Nursing management of adrenal crisis:

A
  • Priority is getting pt stable
  • Administer cortisol STAT!
  • Iv fluids
  • Oral glucocorticoids or mineral (replace aldosterone)
  • Monitor glucose, K+ and Na+
  • Prevent infection
30
Q

adrenal cortex:

A

Adrenal cortex: sex hormones
Releases corticosteroids and sex hormones
Steroid hormones: aldosterone and cortisol
Aldosterone: mineralocorticoid, regulates BP via RAAS, retention of Na+ and secretes K+
Cortisol: glucocorticoid, stress hormone, regulates BG, breakdown fats, carbs, and proteins, helps body deal with stress ex: illness, external stress, increases BP

31
Q

S/S of addisons:

A
  • Increased sodium excretion
  • Hypotension
  • Fatigue
  • Appetite loss
  • Sodium and sugar levels will be very low, salt cravings
  • Tired and weak
  • Electrolyte imbalance (K+ and Ca+)
  • Reproductive changes
  • Increased pigmentation (hyperpigmentation of the skin)
  • Diarrhea and nausea, depression
32
Q

Thyroid Secretions:

A
T3 and T4  = Thyroid Hormone
Control of metabolism
Exert effects on HR and contractility
Affect RR and drive
Act as insulin antagonists
Increase RBC production
Calcitonin = helps regulate serum calcium and phosphorus levels
33
Q

Calcitonin

A

Thyroid control Ca and phosphorus levels in blood

Calcitonin decreases serum Ca and phosphorus levels by reducing bone resorption (breakdown)

Serum calcium levels control calcitonin section
Low serum CA, suppress calcitonin
High serum CA, increase secretion
Actions opposite of parathyroid hormone

34
Q

Thyroid Storm:

A

s/s:
increases metabolic rate
key manifestations: fever, tachycardia, HTN
anxious, chest pain, n/v, diarrhea
so hyperstimulated can cause dysrhythmias

35
Q

Management of thyroid storm:

A
Airway
Antithyroid drugs
Blood pressure drugs
Reduce fever
Monitor cardiac, vital signs
Prevent vascular collapse
Glucocorticoids (Hydrocortisone) to treat/prevent shock
36
Q

Parathyroids:

A

4 small glands
Embedded posterior thyroid
Easily removed by accident in thyroid surgery
Secrete Parathyroid hormone (PTH)
Regulate calcium and phosphorus by acting on bone, kidneys and GI tract

37
Q

Parathyroid Hormone (PTH)

A

-Kidneys
PTH activates vitamin D, increases absorption of CA and phosphorus
Kidney tubules reabsorb CA and put into serum
Bone
Main storage site of CA
PTH increases bone resorption (from bone to blood), thus increasing serum CA

Serum CA levels determine PTH secretion
PTH secretion decreases when CA levels are high
PTH increases when CA levels are low
Work with calcitonin to maintain balance
Inverse relationship with phosphorus

38
Q

Hyperparathyroidism

A
Common cause benign tumor of parathyroid
Manifestations:
High serum Ca+ and hypophosphatemia
Cardiac dysrhythmias
GI problems
Muscle weakness
Pathological fractures
Skeletal pain
Emotional changes
Kidney stones r/t output of Ca and Phos
39
Q

Nonsurgical and Surgical interventions for hyperparathyroidism

A

furosemide- increase ca+ excretion
Prevent injury/safety: because of loss of ca+ and bones are fragile
calcitonin has opposite effect of parathyroid, also can give other drugs that help or block hypercalcemia and block PTH

40
Q

Hypoparathyroidism

A
S/Sx:
High phosphorus
Low Calcium
S/S of tetany
Tremor and Spasms
Changes in mental status 
Cardiac dysrhythmias

Low Ca with hypoparathyroidism

Trousseau’s sign: carpal spasms with BP cuff 3 minutes

Chvostek’s sign: Tap facial nerve (in front of ear) to produce facial spasms

41
Q

Symptoms of Hypocalcemia

A
  • Neuromuscular changes often occur first in the hands and feet.
  • Paresthesias occur at first, with sensations of tingling and numbness.
  • muscle twitching
  • painful cramps and spasms occur.
  • Tingling may also affect the lips, nose, and ears. (These problems may signal the onset of neuromuscular overstimulation and tetany)
42
Q

Care for patient post thyroidectomy?

A
  • Semi-fowlers position (avoid neck extension)
  • Deep breathing ever 30 min to an hours
  • suction oral and tracheal secretions when necessary
  • Assess for hemorrhage, respiratory distress, parathyroid glad injury (resulting in hypocalcemia) or and tetany)
  • ## Watch for stridor
43
Q

Graves disease and a Goiter are complications or __________

A

Hyperthyroidism

44
Q

What is a thyroid storm (thyrotoxicosis)? What does it result from?

A

A life-threatening, acute, severe, and rare condition that occurs when excessive amounts of thyroid hormones are released into the circulation.

  • Stressors such as infection, trauma, surgery, palpation
45
Q

Interventions when caring for a client with Acute Kidney Failure

A
  • Monitor all drug levels with nephrotoxic side effects
  • Prevent hypotension
  • Observe for early signs of renal failure, and report them immediately to the physician
46
Q

Nusing interventions when caring for a person with Acute Kidney Injury?

A
  • Prevention and Early intervention. Identify and monitor high-risk populations
  • Control exposure to nephrotoxic drugs (mucomyst can be given after cardiac cath to prevent med toxicity)
  • Prevent prolonged periods of hypotension and hypovolemia
  • Monitor I/O’s and electrolyte balance
  • Monitor for infection (leading cause of death in AKI
  • Monitor viatal signs: ART line maybe necessary for accurate MAPs
47
Q

Risk factors for pre-renal failure

A
  • Cardiac Issure (MI)
  • Dehydration
  • Bleeding
  • Burns
48
Q

Lab Results Associated with Renal Failure?

A
  • Increased Serum Creatinine (normal 0.7 - 1.3)
  • Decreases as kidney’s are assaulted GFR (normal 120-125 ml/min)
  • Olguria - decreased urine output. urine will be concentrated (less than 400)
  • Creatinine Clearance
  • Increased BUN (azotemia)
  • ABGs - metabolic acidosis
  • Electrolytes (
49
Q

Viral load

A
  • the amount of virus present in blood and other body fluids, affects transmission. The higher the blood level of HIV (viremia), the greater the risk for sexual and perinatal transmission. Current highly active antiretroviral therapy (HAART) has caused the viral load of some to drop below the detectable levels. Although there is less virus in seminal or vaginal fluids of people receiving HAART, the risk for transmission still exists.
    .
50
Q

Signs and symptoms of HIV

A

Progression of HIV can take months to years. Initially few manifestations (virus/ flu like symptoms) as body is trying to fight off virus. - Then there are no symptoms until the CD4 and T-cell counts get low and opportunistic infections become apparent. Personal factors that can affect progression - stress, poor nutrition, comorbidities, re-exposure to HIV.

51
Q

Expected lab values in patient with HIV

A

Look at CBC and WBC count.

  • Decreased lymphocytes
  • Expect decrease in WBC (leukopenia).
  • CD4 and T-cell count will decline as disease progresses.
52
Q

Medication used for a client with SIADH

A
  • Vasopressin antagonists - Conivaptan (Vaprisol) and tolvaptan used to increase water diuresis without serum electrolyte loss and may be useful in hypervolemic hyponatremia conditions.
  • Demeclocycline (Declomycin), works in opposition to ADH
  • Diuretics- can give when sodium levels are back to almost normal but you have to be VERY CAREFUL when achieving fluid and electrolyte balance
  • Hypertonic saline (3% saline IV) may be needed for severe hyponatremia (< 118 mEq/ L). Given to replace sodium. MUST BE GIVEN SLOWLY to allow brain to adjust and prevent cerebral edema.
53
Q

The nurse evaluates the treatment plan for a client with SIADH

A
  • fluid restriction (which is usually sufficient to correct the hyponatremia),
  • increased sodium intake, and drug therapy.
  • Preventing fluid overload from becoming worse, so it doesn’t lead to or exacerbate pulmonary edema and heart failure.
  • daily wts, listen to heart and lungs for crackles, JVD, bounding pulses.
  • When serum sodium drops below 120 mEq/L (120 mmol/L), immediate intervention is necessary to prevent severe neurologic dysfunction
  • Monitor labs - Make sure sodium is slowing increasing. Neurologic assessment
54
Q

Symptoms associated with hyper function of the adrenal cortex

A
  • enlarged trunk with thin arms and legs; and a round face (“ moon face”).
  • muscle/Tissue wasting and weakness.
  • Hypertension
  • Hyperglycemia
  • Increased fat deposition (shoulder, neck)
  • Fluid and electrolyte disturbance
  • Immunosuppression
  • Skin and hair abnormalities
  • Emotional disturbance
55
Q

Acromegaly:

A

(form of hyperpituitarism) Overproduction of GH after puberty

  • Acromegaly is Insidious, slow growing and causes overgrowth of all tissues/organs specifically soft tissues such as face, hands, feet, skin.
  • Changes to soft tissues like face, hands, feet, skin are irreversible and Devastating to psychopsypsychoial.
  • Assessment: Early detection important!!! Note changes in shoe size, ring size
  • Diagnose through CT and x-rays of the head.
  • Treatment: revolves around inhibiting growth hormone production using medications such as growth hormone inhibitors drugs such as parlodel. Surgery to remove tumor or Radiation to decrease size.
56
Q

Gigantism-

A

Overproduction of GH before puberty. Pay attention to growth charts.Occurs Before closure of epiphysis and usually r/t tumor. Signs and Symptoms: Large for age, weak, lethargic, visual problems, can cause cardiomegaly, muscle weakness. . Diagnose through CT and x-rays of the head. Treatment: revolves around inhibiting growth hormone production using medications such as growth hormone inhibitors drugs such as parlodel. Surgery to remove tumor or Radiation to decrease size. Related complications: hypertension, congestive heart failure, osteoporosis, delayed sexual development.

57
Q

Care for a client who has undergone a hypophysectomy

A
  • PREVENT INCREASED INTRACRANIAL PRESSURE - Avoid bending or straining
  • Monitor neurologic response
  • Monitor for CSF leak and nasal drainage
  • Elevate HOB
  • Avoid coughing soon after surger
  • Assess for meningitis
  • Hormone replacement
  • Avoid brushing teeth
  • Numbness can indicate cranial nerve involvement
  • may have to give vasopressin
58
Q

Cares for a client post thyroidectomy

A
  • Monitor for swelling or hemorrhage b/c it could cause respiratory distress.
  • lifelong hormone therapy in total, subtotal may not need replacement hormones
  • Laryngeal nerve damage can cause voice changes (hopefully these will improve
  • Parathyroid involvement can result in low calcium levels. Monitor for tetany, tingling
  • Watch for thyroid storm
  • Watch suture line to make sure girth of neck isn’t growing
59
Q

What is a complication of hyperthyroidism?

A

Thyroid story: life-threatening condition that can occur in uncontrolled hyperthyroidism or Graves’ disease when a stressful incident, such as this client’s motor vehicle accident, triggers a sudden surge of thyroid hormone.

60
Q

What is Myxedema ?

A

Late clinical signs of hypothyroidism. There is an accumulation of mucus and water in the organs. Fluid shifts into interstitial spaces. This type of edema is NON PITTING. Why do we have this edema? The decreased metabolism causes the heart muscle to become flabby and the chamber size to increase causing decreased cardiac output (no contractility) and decreased perfusion. Myxedema is life threatening. Coma can result.

61
Q

Lab data associated with hypo function of the thyroid gland

A
  • Serum TSH and free thyroxine (FT4) are the most reliable indicators of thyroid function.
  • Serum TSH levels help determine the cause of hypothyroidism. If high, the defect is in the thyroid; if low, it is in the pituitary or hypothalamus.
  • The presence of thyroid antibodies suggests an autoimmune origin of the hypothyroidism.
  • Elevated cholesterol and triglycerides, anemia and increased creatine kinase can occur
62
Q

Manifestations of thyroid storm?

A
  • rapid onset of fever, tachycardia, and elevated blood pressure.
  • The client often feels anxious, tremulous, or restless. Confusion and psychosis can occur, as can seizures and coma. Rapid treatment is necessary.
63
Q

Nurse teaches the client about iron deficiency anemia

A
  • Encourage intake of Red meat, organ meat, green leafy veggies, egg yolk, cook in cast iron skillet, dark molasses
  • Discuss with the patient the need for diagnostic studies to identify the cause of anemia. Reassess the hemoglobin level (Hgb) and RBC counts to evaluate response to therapy.
  • Oral supplements (between meals). Patient needs to take iron therapy for 2 to 3 months after the Hgb level returns to normal.
  • Monitor patients who require lifelong iron supplementation for potential liver problems related to the iron storage.
64
Q

What is AUTOIMMUNE THROMBOCYTOPENIC PURPURA (IDIOPATHIC THROMBOCYTOPENIC PURPURA (ITP) ?

A

Disorder where the number of platelets circulating is reduced when platelet production is normal. This occurs b/c patient makes an antibody that attacks its own platelets Manifestations

65
Q

The nurse recognizes priorities of care for a client with ITP

A
  • Interventions focused on decreased platelet count which puts the patient at risk for bleeding.
  • Interventions: suppress immune function, platelet transfusions, maintaining safety, splenectomy in order to removed spleen in hopes to slow down the destruction of platelets. If spleen is removed patient will need immune function support, VACCInATE!!
66
Q

Interventions for a client with leukemia

A

Reduce risk for infection!

67
Q

Role of the kidneys in RBC formation

A

They release the hormone erythropoietin which is essential for RBC production. Kidneys sense changes in 02 carrying capacity, and then will secrete erythropoietin which then signals the bone marrow to produce more RBC.

68
Q

Client at high risk for folic acid anemia

A
  • Poor nutrition, especially a diet lacking green leafy vegetables, liver, yeast, citrus fruits, dried beans, and nuts, is the most common cause.
  • Malabsorption syndromes, such as Crohn’s disease or anorexia
  • Clients using anticonvulsants and oral contraceptives
  • Alcoholics
  • Pregnant women
  • Infants, teens
69
Q

Complications following renal transplantation secondary to immunosuppressant

A

Transplant recipients may not have the usual manifestations of infection because of the immunosuppressive therapy. Low-grade fevers, mental status changes, and vague reports of discomfort may be the only manifestations before sepsis. INFECTION is a major cause of death in the transplant recipient.