exam 4 Flashcards

1
Q

Can affect people of all ages
Most cancers occur in people > 65 years of age
More than 1.5 million people are diagnosed with CA each year
Leading cause of death among cancers:
-Lung
-Prostate
-Colorectal
Combination of managing illness and psychosocial factors
Determine which crisis the patients want to treat and which ones they don’t (risk/benefit ration)
Which treatments can be suspended?
Patho
-Cancer is characterized by the presence of the following:
–Cellular or genetic changes within the body
–Abnormal cell proliferation or growth
–Unchecked local growth and invasion of surrounding tissue
–Ability to metastasize to distant organs
-Hallmark: cells no longer resemble what they originally were (now they’re foreign)
-Lymph carries blood, so close to this spreads faster

A

cancer

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2
Q

Neoplasms – a new and abnormal growth of tissue in some part of the body
Malignant cells have abnormal regulation of growth (worse)
-Cancer cells continue to grow even at expense of the host
-Follows no physiological demand
-Uncontrolled growth
Benign – not harmful in effect (of a tumor) (could be in a bad area and obstruct ducts, etc)
-Not malignant
-Does not invade surrounding tissue

Benign neoplasms
-well differentiated, resemble cells in the tissue of origin
-usually encapsulated
-progressive and slow
-doesn’t spread
Malignant neoplasms
-cells are undifferentiated, bear little resemblance to cells in tissue of origin
-grows by invasion
-variable rate of growth - can be rapid
-gains access to blood and lymph channels to metastasize

A

cancer 2

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3
Q

Diagnosis
-Complete H&P: unexpected changes, bleeding, pain
-Diagnostic tests determined on s/s of patient: if lump, take picture (1. size/extent of tumor/location 2. metastasized? 3. effects on where it’s at like pancreas = pancreatitis 4. biopsy for grading)
-Tumor Staging and Grading
–Staging – determines the size of the tumor and extent of the disease
—TNM system
–Grading – refers to the classification of the tumor cells
—Find the tissue from where the CA originated
Management
-Surgery
–Diagnostic surgery: check location - cut out piece/whole thing; send down to frozen section, keep removing as need
–Surgery as primary treatment
–Prophylactic surgery: remove r/t high probability of cancer - like breast cancer
–Palliative surgery: removed without ability to cure (if it’s blocking blood flow, etc)
-Multidisciplinary approach
-Other combined treatment methods – radiation & chemotherapy

A

cancer 3

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4
Q

Ionizing radiation is used to interrupt cellular growth
Palliative radiation – relieves symptoms of metastatic disease
*Cells that undergo cell division are most sensitive
-Bone marrow, lymphatic tissue, epithelium of GI tract, hair cells, gonads
External & internal radiation (brachytherapy) (insert radiation into cancer)
NM
-Safety Precautions with implanted radiation
-Limit visitors and time with patients
–30 minute daily max, stand 6 feet away from radiation source
-Private rooms
-Posting radiation safety precautions: shows exposure of radiation
-Staff members wear dosing monitors
-No pregnant women or children r/t they have lots of growing cells
-Education on radiation source – external vs. internal
-Protecting skin
–Avoid lotions, ointments, and powders on treated area
–Gently cleanse skin with mild soap with fingertips & gently pat dry
–No emollients (even approved) 4 hours prior to radiation treatment
-Protecting oral mucosa
–Provide gentle oral hygiene & use daily fluoride
–Use bland mouth rinse before and after meals
Radiation therapy safety
1. time
2. distance
3. shielding

A

radiation therapy in cancer

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5
Q

Antineoplastic agents are used to destroy tumor cells by interfering with cellular functions (replication) through meds
Used to treat systemic disease and not localized lesions
Often combined with surgery and radiation (or both)
Chemotherapeutic agents are characterized by their relationship to the cell cycle
Administered PO, IV, IM, SQ, arterial, intracavitary, intrathecal, topical
NM
-Monitor for extravasation with IV vesicants
-Indications:
–CVC = pain in upper arm, upper back, chest, neck, or jaw (port, triple lumen - Huber needle placed wrong –> flow under skin –> extravasation of vesicant)
–Absence of blood return from IV catheter (in wrong place)
–Resistance to flow of IV fluid (in wrong place)
–Swelling, pain, or redness at the site (in wrong place)
-If occurs - Stop infusion immediately
-Then aspirate any residual drug in the line (take empty siring and pull back as much as possible - warm cloth isn’t enough)
-Administer the antidote
Don’t want absorption into the skin
-GI System – nausea and vomiting most common side effect (premediate with Zofran)
-Hematopoietic System – myelosuppression
–Leukopenia: low WBC
–Anemia: low RBC
–Thrombocytopenia: low platelets
(all those s/e of chemo)
-Reproductive System – possible sterility
-Alopecia

A

chemotherapy

chemo is poison

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6
Q

Obstruction of the superior vena cava (SVC)
Blockage-> pleural effusion-> facial (see 1st), chest, arm, and neck edema-> impaired cardiac filling r/t not draining properly
SVC collects blood that drains from the
head and neck and upper thoracic cavity
Treatment
-Diagnostics: spiral CT with contrast
-Radiation therapy to shrink to decrease compression
-Chemo, if the tumor is responsive
-Antifibrinolytics or anticoagulants (if hypercoagulability is cause)
-Stent placement (issue = device can clog like others)
-Steroids (decrease swelling and obstruction)
NM
-Avoid chest and neck catheter placement
-AIRWAY
–Avoid lying flat
–Short term intubation
–O2 therapy
-Medications
-Avoid Valsalva (close mouth, breather/pressure)
-Elevation of arms to get excess fluid drained
-Assess for complications:
–fluid = excess edema, fluid -> HF
–pressure on SVC can rupture vessel
–excess fluid in lungs -> pneumonia

A

superior vena cava syndrome

oncologic emergencies

Tumor/clot -> compression/obstruction of SVC -> collects excess fluid

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7
Q

Risks:
-chest, neck or epigastric tumor (more likely to compress SVC)
-devices in the SVC (has fibrin clot on it) (especially triple lumen r/t more lumens = higher risk r/t tube/catheter is bigger)
-hypercoagulability syndromes
S/S
-Periorbital and conjunctival edema 1st
-Facial swelling 1st
-Stoke’s sign (collar shirt is tightening)
-Visual disturbances, headaches, Altered LOC (fluid going to brain -> cerebral edema)
-Distention of veins in the thorax (late) trachea –>
-Dysphagia, dyspnea, cough, hoarseness
-Tachypnea (compensate for narrow airway)
-Pleural effusions
-More prominent in am r/t less movement and decreases throughout day

A

superior vena cava syndrome 2

oncologic emergencies

Tumor/clot -> compression/obstruction of SVC -> collects excess fluid

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8
Q

Tumor cells or vertebrae put pressure on spinal cord or broken vertebrae from bone metastasis
What (pathophysiolocally) will happen to these patients? - compression of tumor -> pressure on cord -> decrease circulation -> ischemia/neuro issues
For long term survival you need…
-Favorable diagnosis (treatable/responsive to treatment)
-No visceral metastases
-Long course radiation therapy schedule
S/S
-Pain
-Early = Sensory changes
-Elimination changes (emergency)
-Cauda equine “horse’s tail”: loss of bladder function (emergency)
-hypotension, bradycardia, temperature fluctuation r/t spinal column is compressed
-Autonomic dysfunction
-What might you hear patient’s say? slipped disc = numbness/tingling down back, cold skin, don’t feel light touch

A

spinal cord compression

oncologic emergencies

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9
Q
Treatment
-Diagnostics
-Corticosteroids
-Radiation therapy
-Laminectomy and decompression: remove tumor/pick out bone fragment to decrease pain on spinal column 
-Vertebroplasty: use cement to bind broken bokes (falls can sever spinal column)
-Chemo (if chemo sensitive)
NM
-Good Assessments/documentation (5 P's)
-Treat the patient’s symptoms
--Pain meds
--Bedrest
careful transfers (halo traction)
--ROM
--Bowel retraining
--Urinary Catheterization
--Skin integrity
A

spinal cord compression

oncologic emergencies

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10
Q

Metabolic com plication- serum calcium > 11 mg/dL
Most common emergency r/t metastasis of bone
Most common cause:
-Bone with metastasis release more calcium into the extracellular fluid than can be filtered by the kidneys and excreted in the urine
High Risk Cancers:
-Bone metastases
-breast cancer
-Lung
-GI
-Hematological
-Renal: issue r/t kidneys pull out calcium
-Thyroid: r/t parathyroid hormone regulates calcium
-Other risk factors: immobility, renal insufficiency, head/neck radiation with N/V/A -> malnourished/dehydration

A

hypercalcemia
oncologic emergency
serious diagnosis

sometimes find this before cancer diagnosis

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11
Q
S/S
-Nausea
-Constipations
-Polyuria
-Mental status changes
--Somnolence
--Combativeness
--Confusion
Treatment 
-lab work 
-ECG/telemetry may show bradycardia and prolonged PR, QRS, QT if symptomatic
-IV fluids: dilute it out and make it less concentrated (if renal issue this is harder)
-Dialysis 
NM
-Watch for constipation
-Careful I&O with increased fluids: ensure what goes in comes out
-K+ supplementation
-Increase oral fluids
-Eat salty foods
-Remain physically active
-Limit dairy and Vit D foods
A

hypercalcemia
oncologic emergency
serious diagnosis

sometimes find this before cancer diagnosis

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12
Q

Results from rapid destruction of a large number of tumor cells
-Fast growing and chemo sensitive
Occurs within 24-48 hours after chemotherapy
Can lead to renal failure MODS – Death
S/S
-Hallmark manifestations (and 3 causes of tumor lysis)
–Hyperkalemia (>6)
–Hyperuricemia (>10)
–Hyperphosphatemia (>10)
–Hypocalcemia (<6)
-Uremia due to renal failure
-Possible fluid volume overload
Treatment
-Treat electrolyte imbalances
–Potassium: kayxelate to decrease K - immediate = insulin
–Phosphate
—Calcium carbonate
—Calcium acetate
—Sevelamer – phosphate binder
–Control of hyperuricemia
—Allopurinol: can give ahead of time PRN
–Adequate hydration
NM
-Cardiac Monitoring/telemetry
-Force fluids
-Monitor labs/electrolytes
-Monitor for infections: bone marrow suppression -> decrease WBC/Platelets/etc. so can’t fight infection
-Monitor for bleeding – thrombocytopenia
-Assess and manage stomatitis: sensitive to radiation - can inflame - keep dry/moist
-Manage nausea and vomiting with Zofran
-Maintain skin integrity
-Improve nutritional status: small frequent high calorie
-Relieve pain: light/music therapy, acupuncture, narcotics (risk for tolerance/constipation)
-Promote self-care activities at home to give patient back power

A

tumor lysis syndrome
oncologic emergencies

metabolic
can predict - fight cancer with chemo/radiation, kill it, release to blood -> tumor lysis syndrome

Risks = damage to kidneys

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13
Q

Hypothalamus: regulates hunger, thirst sleep, body tempt
Pituitary Gland – posterior and anterior: controls other endocrine glands, influences growth, metabolism and regeneration
Thyroid Glands – thyroid hormones & calcitonin: regulates energy, metabolism
Parathyroid Glands – PTH: secretes hormones necessary for calcium absorption
Pancreas: digestion of protein, fats, carbs, produces insulin/control BS
Adrenal Glands: secretes cortisone, adrenaline, regulates metabolic process

A

endocrine system is made of up this

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14
Q
Produce the following:
-Thyroxine (T4) &amp; Triiodothyronine (T3): metabolism, growth/development, metabolic rate 
-- too much/overproduce = hyperthyroidism and graves disease
-- too little = hypothyroidism 
-Calcitonin
Gland produces too much hormone
-Hyperthyroidism
-Grave’s disease
Gland does not produce enough hormone
-Hypothyroidism

2nd most prevalent endocrine disorder
Increased thyroid hormone production
-Results in overproduction of T3 &/or T4
These patients have a significantly increased metabolic rate
Causes:
-Graves disease, thyroiditis, overmedication, thyroid nodules r/t tumor produces too much

Graves disease: cause of hyperthyroidism

  • Autoimmune disease of the thyroid gland
  • Antibodies bind to TSH causing the overproduction of hormones
  • Symptoms may appear after an emotional shock, stress, or infection – relationship not understood
  • Overproduction of TSH by pituitary gland and TSH is what makes T3/T4
A

hyperthyroidism

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15
Q

S/S
-Weight loss with increased appetite
-Heat intolerance – excessive sweating
-Flushed skin
-buldging eyes
-Nervousness: can’t sit still, overly active
-Palpitations: sinus tachy or a fib
-Frequent bowel movements
-Muscular weakness and fatigued easily
Untreated = delirium, heart failure
Nursing assessment
-Palpation of enlarged thyroid gland: note any tenderness, pain, pulsations, bruie?
-Assess for respiratory distress: thyroid could block trachea/compress airway
-Monitor cardiac function – telemetry
-Body temperature: risk for hyperthermia so cool bath/clothes (don’t want pt to shiver r/t that increases metabolic rate)*

A

hyperthyroidism

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16
Q

Diagnosis:
-Look at both manifestations and laboratory/diagnostic data
Total T4 (thyroxine): increase in hyper, decrease in hypo
–Free T3 & free T4 – will be elevated r/t excess amount being produces already
–TSH – extremely low levels
–Radioactive Iodine Uptake
Fine Needle Biopsy: check nodule for malignancy, 1st for nodule
–US: check structure for cysts, nodules, etc.
–ECG
Treatment
-Anti-thyroid medications
–Propylthiouracil (PTU) & Methimazole (Tapazole)
-Iodine solutions – Na+ iodide or K+ iodide
-Glucocorticoids: inhibit thyroid release
-Radioisotope Iodine 131 Therapy (usually cured in 1 dose)
–Goal is to destroy overactive thyroid cells
-Thyroidectomy – Surgical removal of most of the thyroid gland: post op concern is airway*
-Beta blockers – Propanolol (Inderal): decrease HR, BP, and work on heart
NM
-Treat precipitating factors
-Administer IV fluids as ordered
-Monitor airway: trach tray at bedside* be prepared to lose airway (intubation is hard)
-Give extra O2 r/t body increase metabolic demand so want to increase tissue oxygenation
-Monitor cardiovascular – assess BP, HR, and rhythm
-Monitor neurological status
-Monitor for hyperthermia – give antipyretics, cooling
-Nutritional support: increase metabolic demand r/t it uses up calories/diarrhea

A

hyperthyroidism 2

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17
Q

Severe form of hyperthyroidism – medical emergency
Abrupt onset - associated with physiological and psychological stress
Often referred to as thyroid storm
Sudden release of thyroid hormones causes hypermetabolic state
Stimulates sympathetic nervous system
Risk Factors:
-Infection, trauma, stress, medical illness, pregnancy, exposure to cold
Admitted to ICU for supportive measures
-Antithyroid meds, steroids, continuous nursing care
Manifestations:
-Delirium
-N/V
-Hyperpyrexia (102 – 106) High fever*
-Tachycardia (>130 bpm) & hypertension
-Mental status changes & psychosis
-Multisystem organ failure
Untreated = heart failure, MI, total cardiovascular collapse, coma, death

A

thyroid crisis
with hyperthyroidism

like hyperthyroidism on crack

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18
Q

Have decreased thyroid hormone production
-T3 & T4
Slow onset – 10 times more common in women
Severe hypothyroidism
-Myxedema = non - pitting edema throughout the body
Can be primary or secondary
Patho
-1. Primary hypothyroidism (thyroid is the issue) – thyroid gland unable to produce the amount of hormones the pituitary gland is requesting
–Thyroid gland is the problem
-Possible causes:
-Hashimoto’s Thyroiditis
-Congenital defects
-Loss of thyroid tissue post treatment or thyroidectomy
-Iodine deficiency
-Medications - Amiodorone (Cordarone) therapy – contains iodine
-2. Secondary hypothyroidism (pituitary is the issue)– the pituitary gland is not stimulating the thyroid to produce hormones
–Pituitary gland is the problem
-May result from:
–Pituitary TSH deficiency
–Peripheral resistance to thyroid hormones

A

hypothyroidism

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19
Q

Hashimotos Thyroiditis

  • Most common cause of goiter and primary hypothyroidism
  • Autoimmune disorder, antibodies develop that destroy the thyroid tissue
  • Goiter in early stages due to TH deficiency

Myxedema Coma
-Life threatening complication of long standing, untreated/uncontrolled hypothyroidism
-Triggered from infection, trauma, med incompliance, stress
-Characterized by:
–Severe metabolic disorders
–Cardiovascular collapse
–Impaired mentation
–Coma or near coma
Treatment
-Maintain airway*, cardiac status, increase body temperature, increase thyroid hormone levels, increase F/E balance

A

hypothyroidism 2

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20
Q
Serum TA
-Hyperthyroidism: increased
-Hypothyroidism: normal
Serum TSH
-Hyperthyroidism: decreased in primary hyperthyroidism 
-Hypothyroidism: increased in primary hypothyroidism
Serum T4
-Hyperthyroidism: increased
-Hypothyroidism: decreased
Serum T3
-Hyperthyroidism: increased
-Hypothyroidism: decreased
T3 uptake
-Hyperthyroidism: increased
-Hypothyroidism: decreased
Thyroid suppression
-Hyperthyroidism: increased RAI uptake and T4 levels
-Hypothyroidism: no change
A

lab values in thyroid disorders

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21
Q

S/S
-Goiter
-Fluid retention and edema r/t slow metabolism with hypothyroidism or slow blood flow and decrease perfusion to kidneys
-Weight gain with anorexia
-Constipation
-Dry skin
-Dyspnea: r/t weak/slow respiratory drive
-Pallor
Treatment
-Levothyroxine (thyroxine, T4) is treatment of choice
-Surgery may be indicated for large goiters
–Respiratory difficulty
–Dysphagia

A

hypothyroidism 3

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22
Q

Parathyroid glands secrete parathyroid hormone (PTH)
Causes an increase in PTH which affects kidneys and bone
*PTH regulates calcium levels
-High PTH levels cause high Ca++
Normal = 8.5-10.5 mg/dL
Patho
-Increased PTH levels cause the following:
-Increased reabsorption of calcium and excretion of phosphate
–Increases risk of renal stones
-Increased bicarbonate excretion, decreased acid excretion
–Results in metabolic acidosis and hypokalemia
-Increased release of calcium and phosphorus from bone
-Deposits of calcium phosphate into soft tissues and kidneys
Types:
1. Primary: occurs with hyperplasia of 1 of the parathyroid glands
2. Secondary: compensatory response to chronic hypocalcemia (increase PTH -> increase Ca levels)
3. Tertiary: results from hyperplasia of parathyroid glands

A

Hyperparathyroidism

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23
Q

S/S:
-Pathologic fractures r/t Ca being pulled from bones
-Muscle weakness and atrophy: increase Ca=neuromuscular depression
-Proximal renal tubule function altered: polyuria and increase thirst
-Metabolic acidosis
-Arrhythmias: acute increase in Ca can lead to cardiac arrest
-Renal calculi formation
-Polyuria
-GI problems: constipation from excess calcium
Treatment
-Diagnosed by excluding all other causes of hypercalcemia
-Treatment geared at decreasing Ca+ levels
–If severe, requires hospitalization and IV fluids
-Meds include:
–pamidronate (Aredia)
–alendronate (Fosamax)
–soledronate (Zometa)
–*Calcitonin: lower plasma levels of calcium by inhibiting bone reabsorption
-Rapid reversal: IV Na+ phosphate or K+ phosphate: give sodium or potassium phosph and make sure they don’t get too low
-Removal of parathyroid glands
NM:
-Provide hydration therapy
–Avoid thiazide diuretics
–At risk for kidney stones so dilute and give >2 L r/t decrease excretion of calcium
-Avoid foods and medications containing Ca++
–These can all increase Ca++ levels
-Encourage activity – bones exposed to stress release less Ca++
-Manage Hypercalcemic Crisis
–Calcium >15 mg/dL result in neurological, cardiac, and renal symptoms that are life threatening

A

hyperparathyroidism

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24
Q

Occurs because of low PTH levels being secreted from parathyroid glands
Without PTH, there is decrease of GI absorption of dietary Ca++
Usually from damage to or removal of parathyroid glands: MC cause
Causes hypocalcemia and hyperphosphatemia
S/S
-Hypocalcemia: neuromuscular excitability
-Peripheral motor and sensory nerve changes
–*Numbness, tingling around mouth, fingertips
–Muscle spasms in hands, feet
–Convulsions
–Laryngeal spasms/tetany: most severe and can cause asthma attack
–Dysrhythmias: prolonged ST wave is MC
-Chrewsvek and Trevesks

A

hypoparathyroidism

decrease in calcium r/t decrease PTH levels

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25
Q

Treatment
-IV calcium gluconate: monitor teley when giving clacium
-Supplemental calcium
–TUMS & OsCal
-Vitamin D therapy
–Increases GI absorption of Ca++
-Increased dietary calcium & decreased phosphorus intake: cheese, dark green veggies, oranges, soy beans (whole grains/spinach decrease it)
NM
-Detecting early signs of hypocalcemia
–Patients undergoing thyroidectomy, parathyroidectomy, & radical neck surgeries
-Continuous cardiac monitoring
-Dietary management
–High calcium, low phosphorus
-Patient education: S/S of hypo and hyper calcemia

A

hypoparathyroidism

decrease in calcium r/t decrease PTH levels 2

26
Q

Mineralocorticoids (aldosterone): when aldosterone is unavailable, it causes hyponatremia and weird BP
-Regulates fluid & electrolytes
-Resorption of Na+ & elimination of K+
Glucocorticoids (cortisol)
-Metabolism of CHO, protein, & fat
-Response to stress
-Anti-inflammatory
Androgens (sex hormones): helps with growth spurts
Adrenocorticotropic hormone – ACTH (made in pituitary then travels to adrenal glands and stimulates release of cortisol)
-ACTH regulates cortisol and cortisol is released by adrenal cortex

A

Adrenal glands

in adrenal cortex

27
Q

Mineralocorticoids (aldosterone): when aldosterone is unavailable, it causes hyponatremia and weird BP
-Regulates fluid & electrolytes
-Resorption of Na+ & elimination of K+
Glucocorticoids (cortisol)
-Metabolism of CHO, protein, & fat
-Response to stress
-Anti-inflammatory
Androgens (sex hormones): helps with growth spurts
Adrenocorticotropic hormone – ACTH (made in pituitary then travels to adrenal glands and stimulates release of cortisol)
-ACTH regulates cortisol and cortisol is released by adrenal cortex

Adrenal disorders

  • Cushings
  • Addisons
A

Adrenal glands

in adrenal cortex

28
Q

Excessive amounts of circulating serum cortisol and adrenocorticotropic hormone (ACTH)
AKA Hypercortisolism – high levels of cortisol
Causes:
-People who take long term corticosteroids are at risk (iatrogenic)
-Tumors on pituitary gland that overproduce ACTH (disease)
-Tumors on adrenal glands that overproduce ACTH (syndrome)
Patho
-Cushing’s disease – pituitary produces too much ACTH and stimulates the adrenal cortex to increase its cortisol secretion
-Cushing’s syndrome – adrenal gland involvement – causes ectopic production of ACTH by malignancies causing a release of excess cortisol
-Iatrogenic – synthetic corticosteroid use

A

cushings disease/syndrome
excessive amounts of cortisol

CDP: colleges do pray
CSAP: college students are great

29
Q

Manifestations seen due to oversecretion of glucocorticoids (cortisol) and androgens (sex hormones)

  • Central-type obesity, protruding abdomen, fatty “buffalo hump”
  • “Moon faced” appearance
  • Muscle weakness & wasting with thin extremities
  • Osteoporosis
  • Thin fragile skin, purple striae
  • Emotional lability
  • Peptic ulcers
  • HTN with weight gain r/t retention of sodium and water
  • Hypokalemia-Hypernatremia
  • Hyperglycemia
  • Sleep disturbances
  • Virilization – appearance of masculine traits & recession of feminine
  • excess in androgens -> excess facial hair growth, breast atroph
A

cushings 2

30
Q

Diagnosis
-Plasma cortisol levels
-Plasma ACTH levels: figure out etiology of syndrome
-24 hour urine tests: measure free cortisol/androgens (will be high with cushings and might see ketones)
-Serum Na+ High, K+ Low, Ca+ High, and Glucose High
-ACTH suppression: to identify cause - give cortisol in hopes to suppress ATCH
–if give - issue is enlargement of adrenal cortex
–If go and ATCH isn’t suppressed then its a tumor
Surgery
-When due to an adrenal cortex tumor
–Adrenalectomy
-Result of pituitary disorder
–Pituitary gland is removed

A

cushings 3

31
Q

Results from chronic adrenal insufficiency
-Autoimmune destruction of adrenals is most common cause (80%)
Results in chronic deficiency of the following:
-Cortisol
-Aldosterone
-Adrenal androgens
Primary – adrenal gland dysfunction (with increased ACTH)
-decrease cortisol, increase ATCH (body can’t compensate)
Secondary – inadequate secretion of ACTH from pituitary
-decrease cortisol, decrease ATCH (decrease stimulation to adrenal cortex to release hormones)
Risk factors
-Surgical removal of both adrenal glands
-Infection of adrenal glands – TB (most common cause of secondary)
-Inadequate secretion of ACTH from pituitary gland
-Corticosteroid therapy
-Clients taking anticoagulants, trauma, sepsis
-Pituitary tumor
-Clients stop taking steroids abruptly

A

Addison’s Disease

32
Q

S/S
-Slow onset
-Delayed wound healing
-Postural hypotension r/t low blood volume
-Arrhythmias
-Lethargy, confusion
-Skin pigmentation r/t increase levels of ATCH
-Emotional lability
-Weakness, muscle wasting
-Emaciation
-N, V, A, D r/t low cortisol
-Hyperkalemia-Hyponatremia r/t kidneys have trouble excreting
-Hypoglycemia
Diagnostics
-Serum Cortisol levels decrease
-Blood glucose levels decrease
-Serum Na+ decrease, K+ increase
-BUN increase
-Plasma ACTH increase in primary, decrease in secondary
-CT scans
Treatment
-Replacement of corticosteroids (cortisol) and mineralocorticoids (aldosterone)
-Hydrocortisone sodium (Solu-Cortef) for cortisol
-Fludrocortisone acetate (Florinef) for mineralocorticoids
-Increase the sodium in diet
-Steroid therapy

A

addisons disease

BUN increases in adrenal insufficiency

33
Q

Life threatening response to acute adrenal insufficiency
-Occurs in 25% of patients
Have symptoms of Addison’s Disease (look like they’re in shock) plus
-Circulatory collapse
-Shock like symptoms– rapid & weak pulse – hypotension
-Rapid respirations
-GI symptoms
-Hyperpyrexia
-Coma
Triggers = surgery, illness, trauma, abrupt stopping of steroids
Treatment
-Immediate treatment focuses on treating circulatory shock
Restore blood circulation
Administer IVF
–Administer hydrocortisone– replaces cortisol
–Monitor vital signs
–Vasopressors for persistent hypotension
–Antibiotics if precipitated by infection
–Maintain blood glucose levels

A

addisonian’s crisis / adrenal crisis

34
Q

High levels of ADH in the absence of serum hypo-osmolality (osmolality = concentration)
An increase in ADH production = increase in total body water
-increase ADH = FVE r/t too much antidiuretic
Caused by:
-Head injury
-Tumors
-Pituitary surgery
S/S:
-Water retention – fluid volume excess
-Dilutional hyponatremia and hypo-osmolality (serum) (increase FV -> decrease/diluted sodium)
–At risk for seizures due to low Na+
–When Na+ levels fall < 120 to 125 mEq/L
-Usually no edema is present
–Water is distributed between IC & EC spaces
-Aldosterone is suppressed
–Aldosterone regulates BP so it gets suppressed with increase ADH

A

Syndrome of inappropriate antidiuretic hormone SIADH

posterior pituitary disorders: SIADH and diabetes insipidus

35
Q

Treat:
-Treat underlying cause (tumors, head injury, pituitary surgery)
-Address low serum sodium and intracellular swelling
-Administer hypertonic solutions (no isotonic)
-Loop diuretics (Furosemide)
-Keep patient safe- watch electrolytes
-Restrict fluids to 1 L/day
-Democlocycline (Declomycin)
–Tetracycline antibiotic (nasal spray) (r/t increase urine output/excessive urine flow properties)
-If suspect this do a 24 hr urine analysis to check for sodium (it will be increased)
NM:
-Monitor fluid & electrolyte balance
-Evaluate I&Os: don’t reverse sodium quick - do over a period of time
-Monitor neurological status

-Fluid restrictions
-Providing good oral care

A

Syndrome of inappropriate antidiuretic hormone SIADH (2)

posterior pituitary disorders: SIADH and diabetes insipidus

36
Q

Decreased/Deficient ADH
Two Types:
1. Neurogenic from destruction of pituitary gland (issue in pituitary gland)
2. Nephrogenic where renal tubules become insensitive to ADH an cannot conserve water (renal tubule issue)
Causes: can happen after any event causing edema or direct damage to the pituitary gland
-Trauma, surgery, head injuries, tumors
S/S:
-Polydipsia –Drinking large amounts of fluid
-Polyuria – 12-20 LITERS per day of dilute UOP (large amount of diluted urine)
-Dehydration with hypernatremia (can lose up to 12 L/day)
-Hyperosmolality (serum) is present, but have dilute urine with low specific gravity*
-Urine will be pale, dilute, and high in volume
Treatment:
-Treat underlying cause (brain injury, infection, CVA, organ failure)
-Administer IV hypotonic fluids (o.45% NS) r/t pt has hypernatremia
-Increase oral fluids
-Thiazide diuretics (only for nephrogenic forms r/t conserves in renal tubule)
-Replacing ADH
–Desmopressin acetate (DDAVP) – synthetic vasopressin (nasal spray, oral)

A

Diabetes insipidus

posterior pituitary disorders: SIADH and diabetes insipidus

3 d’s in Diabetes: diabetes insipidus, decrease ADH, diuresis

37
Q

NM:

  • Monitor for fluid volume deficit/excess
  • Monitor neurological status r/t sodium imbalance
  • Monitor electrolyte imbalances
  • Monitor I&Os and weight
  • Skin turgor and mucous membranes (especially with DI r/t dehydration)

SIADH: excessive ADH, FVE, restrict fluid intake
-Treat: demeclocycline (Declomycin) causes excessive urination
Diabetes insipidus: decreased ADH, FVD, encourage fluid intake
-Treat: demopressin (DDVAP) causes increased water reabsorption

A

nm for SIADH and diabetes insipidus

38
Q

Hyperglycemia* and hyperosmolality and dehydration without ketoacidosis
Many times have undiagnosed type II diabetes
Develops slowly
Polydipsia, polyuria, and decrease in LOC*
Dehydration!!* This makes glucose higher and increases osmolality (can lose up to 9 L fluid -> triggers glucose, change in osmolality
SNS
CNS decline
Hemoconcentration
Causes
-Age 55-70
-Infection * (UTI, pneumonia)
-Acute illness (stroke, MI, pancreatitis)
-Excessive carbohydrate intake
-Medications (corticosteroids)
Assessment - thorough
-History and physical
-CNS symptoms = confusion, drosy
-S/S of dehydration = increase urination, increased thirst, tachycardia, hypotension, tachypnea*

A

Hyperglycemic hyperosmolar state (HHS)

Patients usually have just enough insulin to prevent ketoacidosis

39
Q

Labs
-Glucose- usually >600 mg/dL (2000(
-Osmolality increased
-Na increased
-Hyperkalemia (r/t insulin pushes K intracellular and not enough insulin r/t it goes extracellular so must get back intracellular)
Treatment
-Identify cause of HHS
-Rehydration (MUST BE CAUTIOUS….WHY?)
–1st give fluids, start with isotonic and after BS <250 then hypotonic/dextrose
-Hemodynamic monitoring: CVP r/t severe dehydration and rehydrate them and prevent FVE - ART for BP (they’ll be hypotensive but since giving fluid monitor it)
-Assessment: respiratory*, lungs, UO
-Insulin
-Critical care unit
-Education and sick day care (still take meds when sick)

A

Hyperglycemic hyperosmolar state (HHS) (2)

Patients usually have just enough insulin to prevent ketoacidosis

40
Q

Severe hyperglycemia
Metabolic acidosis* (low pH like 6.8, bicarb like 5, high BS)
Fluid and electrolyte imbalances (very FVD) (K will be high, Mg/P* imbalance)
Hyperventilation to compensate (blowing off CO2 and become more acidotic) (Kaussmal respirations*)
Decreased bicarbonate level
Decompensation
Can have heart vascular collapse if untreated esp in acidosis
Treatment
-Fluid replacement (isotonic until BS <250 then switch to some dextrose)
-Insulin therapy
-Electrolyte replacement (draw labs (BNP) q 2 hrs)
-Education
-Critical care unit

A

diabetic ketoacidosis

check BS q 30-60 mins and labs q 2
continuous fluid/neuro checks

41
Q

Protects our body against foreign agents and microbial pathogens
Removes damaged and dead cells
Provides surveillance and destruction of malignant cells
Antigen – any foreign substance capable of forming an immune response (bacteria, viruses, fungi, parasites, and foreign tissues)
Antibody – a blood protein produced to counteract a specific antigen in an immune response
-Also called immunoglobulins

Immune Response:
This is the body’s internal response to substances recognized as foreign (antigens) and provides the individual with protection or defense from the disease

Two main types of immunity:

  1. Innate Immunity – present at birth
  2. Adaptive Immunity (Acquired) – gained after birth
    - Active acquired – introduction of foreign antigens (vaccinations)
    - Passive acquired – introduction of preformed antibodies (breastfeeding)
A

immune system

42
Q

Innate Immunity

  • Present at birth – First line of defense against illness
  • Allows the body to resist invasion by foreign agents
  • Previous exposure is not required to activate a response
  • -Nonspecific and has no memory
  • Includes: phagocytosis, inflammatory processes, Cytokines, dendritic cells, macrophages, and neutrophils

Barriers:
1. Physical barriers prevent harmful organisms from entering the body or body cavities
Skin, mucous membranes, epiglottis, respiratory tract cilia, sphincters
2. Chemical barriers create an environment hostile to many pathogens such as antibacterial agents, antibodies, acidity
Lysozymes, lactic acid, hydrochloric acid (CHG wipes)
3. Mechanical barriers help rid the body of potentially harmful substances by an action
Intestinal peristalsis, lacrimation, urinary flow

Biological Defense:

  • Our own “normal” flora or microflora (like staph, yeast*, fungal, cellulitis)
  • The normal flora competes with more harmful substances for nutrients preventing them from colonizing
  • Also produce substances that inhibit the growth of other microorganisms

Adaptive Immunity:
-Gained after birth after exposure to multiple different foreign agents
–An immune response will occur
-In order to be effective in fighting off the foreign agent, previous exposure is required
Active Acquired: exposed to live pathogen and becomes infected and immune
Passive Acquired: transfer of antibodies from someone else

A

Immune system (2)

43
Q

At risk:
-Age
-Chronic Disease
-Immunosuppression
-Medications & Treatments
-Nutrition
-Skin Integrity
-High Risk Behaviors
Assessment
-Important to assess body’s immunocompetence
-Getting a detailed patient history and should include
–Patient history
–Nutritional status
–Chronic diseases
–Medications and Treatments
–Skin integrity
–Immunosuppressed states
Diagnostic tests:
-C-reactive protein (CRP): tells inflammation, especially with lupus and RA
-Antinuclear antibody (ANA): looks for autoimmune disorders
-Human leukocyte antigen (HLA): determines tissue compatability
-Erythrocyte sedimentation rate (ESR): indicates inflammation
-Immunoglobulins (Igs): assess immunodeficiency state (checks response to immunizations)
-Complement system: Diagnose lupus or neurologic disorders
-CT scans: check for mass or cancer or decreased immune function
-Intradermal skin testing: (tb test) determines cell mediated immunity
-Tissue & bone marrow biopsies: check malignancy vs autoimmune disorders
NM for immunocompromised
-Standard Precautions
-Neutropenic Precautions
–Neutropenic diet: unpasteurized milk/cheese, no fresh/unpeeled fruit/vegies, no salad bar, no yogurt
-Transmission Based
-Precautions
-Latex allergies

A

Immune system (3)

44
Q

Most often develops after many exposures to a protein found in rubber latex but can be an immediate reaction
-Increase of latex allergy seen in healthcare workers over the years
Contact or Airborne
Mild – Severe symptoms: rash to anaphylaxis
Symptoms:
-Hives, itching, stuffy/runny nose
-Respiratory complications – chest tightness, wheezing, difficulty breathing
Treatment:
-Antihistamines and Corticosteroids
-Severe: Epinephrine
Similar proteins found in latex are also found in foods
-Apples, bananas, kiwi, hazelnuts, carrots, avocados, pineapple, strawberries
Body responds with the same allergic reactions when these proteins are presented into the body
-Some may be allergic and some may not at all

A

Latex allergies

Immunocompromised

45
Q

Provide a private room
Positive pressure room (for neutropenia) precautions
Strict handwashing*
Restrict visitors with active infections
Cooked foods only, no fresh flowers or live plants
Have patient wear a mask when leaving the room
NOTHING per rectum (temperatures, enemas, suppositories, etc)
Neutropenic Diet: unpasteurized milk/cheese, no fresh/unpeeled fruit/veggies, no salad bar or yogurt

A

nm for immunocompromised pt

46
Q
Indications
-PRIMARY REASON: End Stage Disease
-Not treatable by other medical or surgical options
-Patient will die from complications of organ failure without a transplant
Process:
-End Stage Organ Failure
-Referral to transplant center
-Evaluation of Patient
-Wait for an available donor….
-Transplantation of new organ
-Post-op hospitalization
-Regular follow-ups with transplant coordinator
-Multidisciplinary process
Contraindications
-based upon conditions/behaviors that decrease the chance of survival
--Active infection
--Active cancer
--Other irreversible organ dysfunction
--AIDS/HIV infection
--Current substance abuse
--Age > 65 
--Psychosocial factors
--Noncompliance
A

organ transplant

47
Q
Blood Type
Body Size
How sick is the patient?
Distance from the donor
Histocompatibility testing (tissue)
Tests donor antigens against recipient antibodies
Time on the waitlist
HLA antigen testing

Want to have patient in the best condition possible prior to transplant: Nutrition, Mobility, Muscle Strength
Home health care RN, PT/OT may be involved to keep patient healthy
Inpatient RN responsible for calling organ procurement organization (OPO)

A

organ transplant 2

48
Q
NM:
-Act as patient advocate regarding donation
-Family support
-Call OPO
-Maintain hemodynamic stability: meds to increase perfusion, suctioning properly
-Optimal pulmonary management
-Monitor urine output
-Prevention of infections
Postop Phase
-Require close monitoring and care in a transplant unit or ICU
-Monitor the following:
--BP, HR, respirations, CVP, cardiopulmonary hemodynamics
--Level of consciousness
--Pain
--Dressings and drains
--Urinary catheters
--NG tubes
--Lab values
Complications
-Organ Rejection
--Hyperacute tissue rejection
--Acute tissue rejection
--Chronic tissue rejection
--Graft-versus-host disease
-Infections
-Bleeding (esp liver r/t it bleeds a lot)
-Immunosuppressive toxicity
-Organ dysfunction
-Secondary cancers
-Post-op complications
A

organ transplant 3

if liver transplant, watch for s/s of liver failure
if heart, watch s/s of heart failure

49
Q

Hyperacute

  • Occurs in operating room immediately after transplantation
  • -Rare
  • Body has preformed antibodies that immediately react against the antigens of the donor organ (humoral response)
  • No treatment so results in the need for re-transplantation
  • Prevented by pre-transplantation cross-matching

acute

  • This occurs within the first 3-6 months after transplantation
  • -MOST COMMON TYPE OF REJECTION
  • Cell mediated response
  • -Occurs when antigens on the donor organ trigger lymphocytes to mature into helper T cells
  • -Helper T cells then increase production of cytotoxic killer T cells
  • -Killer T cells bind to the transplanted organ and damage the organ
  • This type of rejection responds best to immunosuppressive therapy
  • NM: increase immunosuppressant therapy*

Chronic

  • Occurs over months – years after transplantation
  • Pathophysiology of chronic rejection not completely understood
  • Believed it is most likely a combination of cell-mediated responses to circulating antibodies
  • Accompanied by deteriorating organ function that is irreversible
  • Typically occurs after multiple acute rejections
A

tissue rejections

50
Q

liver: increased LFT, PT/INR, alk phos, total bilirubin, abd tenderness, jaundice, fatigue, fever, dark urine
-biopsy
heart: arrhythmias, increased WBC, low-grade fever, fatigue, hypervolemia
Lung: SOB, fever, cough, fatigue, tachypnea, decreased breath sounds
-biopsy
-bronch/biopsy
kidney: increased BUN/Cr, decrease UOP, weight gain, fever, edema, malaise, tenderness of graft site, increased BP
-US, biopsy
Pancreas: difficult to diagnose rejection, major cause of graft loss, elevated BG (late), flu-like S/S
-biopsy

A

s/s of rejection

51
Q
treatment
-Need to increase immunosuppression of the patient – early treatment increases success of reversal
-Change the immunosuppressive regimen
-Try different combinations of medications
-Increase dosage of medications
Add medications
-IV Solumedrol
Plasmapheresis to remove antibodies from body
-Go home on prednisone - when rejecting use solumedrol 
Immunosuppressive agents
-Calcineurin inhibitors (common) (nephrotoxic - pt taking med has to get routine lab done)
--Cyclosporine*
--Tacrolimus*
--Sirolimus (common with kidney transplant)
-Corticosteroids:
--Prednisone (wean to lowest dose)
--Methylprednisolone
-Cytotoxic: (common)
--Mycophenolate moferil
--Azathioprine
-Antibody products:
--Muromonab-CD3 (OKT3)
--Anti-thymocyte globulin
--Lymphocyte immune globulin
--Daclizumab
--Basiliximab
A

organ transplant (4)

52
Q
EDUCATE YOUR PATIENT
-Medications
-Infection Prevention
-HANDWASHING
-Compliance
Prevention of rejection is the key!
Monitor for immunosuppressive toxicity – early diagnosis important
-Nephrotoxicity
-Cyclosporine and Tacrolimus levels

How will we know if nephrotoxicity occurs? - cyco/taclo: nephrotoxic meds - tell patient it hurts kidneys and teach S/S - UO change, pain with urination, increased BUN/Cr

A

nm for organ transplants

53
Q

Unspecialized cells within the body that can:
-Divide in their unspecialized states
-Differentiate and develop into specialized cells
They can divide and replace old tissues in some of our organs
HSCT is used to treat (and even cure) malignant and nonmalignant

Hematopoietic (production of RBC/platelets) stem cell transplantation
Two Types:
1.Autologous – comes from the patient (less reactions)
2.Allogeneic – comes from a donor
Third type = Syngeneic (donor is identical twin)
Sources of hematopoietic stem cells
-bone marrow
-Cord Blood (disadvantage: insufficient amount)
-Peripheral Blood Stem Cells
Selection of donor:
-Type and stage of disease
-Age
-Comorbidities
-Availability of appropriate
-HLA and MLC matched donor
MLC matching = mixed lymphocyte culture
-Mix donor cells with recipient cells watching reactivity
-Low reactivity = greater compatibility

A

stem cell

54
Q

Process
-Harvest
–Bone Marrow most common
—Aspirate from the posterior iliac crest for bone marrow collection
—Usually takes 1-2 hours
–Pressure dressing are placed over aspiration sites
–Donor typically stays overnight for observation
–Donor will have pain for 2-7 days post procedure
Peripheral blood collection done via leukapheresis
Usually takes 3-4 hours
-Conditioning
–Refers to preparation of the recipient for transplantation
–Allogeneic goals:
—Eradicate malignancies
—Eliminate bone marrow
—Provide sufficient immunosuppression
–High doses of chemotherapy are given to patient with lots of medications used to destroy bone marrow (myeloablative) (RFI so watch for sepsis (cardiac, RR, S/S)
–Regimen is administered over 2-8 day period
–Patient allowed to REST 1-2 days
-rest
-Transplant (day 0)
–Healthy stem cells infused to patient via central line IV
–30-120 minutes
–Pre-medicated with Tylenol, Benadryl, and hydrocortisone
–Patient pre-hydrated
Diuretics may be needed after infusion
–Donated cells travel to the bone marrow and settle in the bone
-Post-transplant: give immunosuppressant’s so check for infection
Engraftment
-Occurs when progenitor cells begin to grow and manufacture healthy cells in the bone marrow (identify through labs)
-Couple of weeks for pt to develop hemopiotic cells so pt is still
-Time for engraftment varies
–Bone Marrow (2-3 weeks)
–Cord Blood (26-42 days)
–Peripheral (11-16 days)
Post transplant

A

stem cells (2)

55
Q

complications:

  • High dose chemotherapy during conditioning
  • -Infections, Bleeding, Anemia, Organ toxicity
  • Graft versus Host Disease (allogeneic)
  • Underlying diseases
  • Relapse
  • Pancytopenia
  • Malnutrition: N/V, weakness
  • Pain
  • Mucositis: sores in oral cavity and can travel down GI system (contributes to malnourishment)

GVHD: (graft: donor, host: person receiving transplant)
-When the infused donor stem cells (graft) recognize the recipient (host) as foreign tissue
-Causes an immunological response attacking the host tissues
-Targets the skin, liver, and GI tract
–Rash on palms/soles, enteritis, elevated liver function tests
–Skin: rash, itching on palms/soles, progress to sloughing skin
–liver: jaundice, increase LFT, progress to hepatic coma
GI tract: mild-mod diarrhea, severe ab. pain, GI bleeds, malabsorption
-Risk for infection* is big issue with GVHD (opportunistic): bacterial and fungal
-Must increase immunosuppression with GVHD
Prevention of GVHD:
-Finding a well matched donor: HLA matching
-Immunosuppressive Medications
-Less intensive conditioning regimen
Treatment:
-Increase immunosuppression
–Immunosuppressant’s
–Corticosteroids
-Supportive Care
–Gut rest
–Pain management (magic mouthwash)
–Skin care
–Infection prophylaxis

A

stem cells (3)

56
Q

HIV is a single stranded RNA virus
There are two known species of HIV: HIV – 1, HIV – 2
HIV is transmitted by blood, semen, vaginal fluids, and breast milk - can’t reproduce on its own
HIV virus attacks our CD4 cells (T cells)
Virus then decreases the number of CD4 cells within the body
-Decreases our immunity making us susceptible to other infections
HIV is NOT transmitted by…
-Air or water, Sweat, tears, saliva, or closed mouth kissing, Insects or pets, Sharing toileting, food, or drinks
*Transmitted via blood, semen, pre-seminal fluid (pre-cum), rectal fluids, vaginal fluids, and breast milk
Most common transmission in the United States: Sexual activity without protection and Needles/syringes (drug use)
Rare transmission seen in the following (but can still occur in certain circumstances):
-Oral sex, Blood transfusions, Being bitten by an infected person, Deep open mouthed kissing, Eating pre-chewed food from an HIV + person, Contact between broken skin/mucous membranes

A

HIV

CD4/T cells: helper cells/fight infection and tells how good IS is

57
Q

The amount of HIV in the blood of an infected person
When the viral load is very low, the risk of transmission is low
The higher the viral load, the higher the of risk transmission

Viral replication:

  • HIV is composed of nine genes that invade host cells and replicate
  • HIV enters the bloodstream and attaches to dendritic cells
  • HIV cannot replicate on its own – it needs a host
  • Once invades the cells and replicates, it causes apoptosis (cell death)
  • -They destroy cellular immune function resulting in immunosuppression
A

viral load and replication

Sero-conversion: after infection a patient doesn’t always test positive: this is the process of changing - to + once antibodies against virus develop

58
Q
Stage 1 – HIV 
-Confirmation of an HIV infection
-CD4 T lymphocyte count > 500 cells/mcL
-CD4 T lymphocyte percentage of > 29
Stage 2 – HIV (progressive)
-Confirmation of an HIV infection
-CD4 T lymphocyte count 200-499 cells/mcL
-CD4 T lymphocyte percentage of > 14-28
Stage 3 (AIDS) (conversion to AIDS)
-Confirmation of an HIV infection
-CD4 T lymphocyte count < 200 cells/mcL
-CD4 T lymphocyte percentage of < 14
Stage “Unknown”
-Confirmation of an HIV infection
-No information on CD4 t lymphocyte count or percentage
S/S:
-Flu-like symptoms: Fever, malaise, anorexia, weight loss, fatigue, myalgias
-Leukopenia
-Lymphadenopathy for at least 3 months
-Neoplasms: decrease immunity so it can't fight off new growth
-Night sweats
-Diarrhea
-Presence of opportunistic infections: Bacterial, Fungal, Protozoal, Viral
Opportunistic infections:
-Pneumocystis carinii pneumonia (PCP) (fungus)
-Herpes simplex (HSV)
-Encephalopathy
-Kaposi’s sarcoma: only seen if AIDs (its tumors on skin)
-Lymphoma
-Cervical Cancer
-Histoplasmosis: breath in spores from birds
-Cytomegalovirus (CMV) (passed through semen, saliva, etc. - transplant pts have this a lot)
-Mycobacterium avium complex	
-Tuberculosis (TB)
-Toxoplasmosis
-Salmonella
-Wasting syndrome
-Candidiasis (esophagus, bronchi, trachea, lungs)
-Cryptococcus
-Cryptosporidiosis
A

HIV

staging based on CD4 cell level
CD4 and viral load have inverse relationship
lower CD4 = lower immunity

59
Q

Diagnostics to detect HIV virus
-ELISA: detects presence of antibodies for HIV - blood/oral fluid and get reactive or nonreactive (+ or -). If + then repeat r/t other antibodies can cause false +
-Rapid HIV testing: 20 mins
-Western blot: most used and highly sensitive
-PCR test: test for genetic material instead of antibodies, can detect virus in early stage - for babies and nurses
Diagnostics to evaluate progression of HIV
-HIV nucleic acid testing (viral loading) test
-CD4 T lymphocyte count
-CBC
-Rapid plasma reagin
-Chest radiograph
-Purified protein derivative skin test (PPD)
-Hepatitis serology
-Toxoplasmosis serology
-Cytomegalovirus (CMV) antibody serology

A

HIV 2

60
Q

Treatment of virus
-Antiretroviral Therapy (ART) (either fully enforced or not at all r/t pt can become resistant)
–Nucleoside/Nucleotide Reverse Transcriptase Inhibitors (NRTIs)
–Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
–Protease Inhibitors (PIs)
–Fusion Inhibitors (FIs)
–Integrase Strand Transfer Inhibitors (INSTIs)
–Entry Inhibitors/CCR5 antagonists
-Combinations can also be used to increase effectiveness of each drug
Complications of ART therapy
-Short Term Side-Effects:
–Fatigue, N/V/D, Rash,
–Insomnia, Dry mouth
–Pain & Neuropathies
–Weight loss
-Long-Term Side-Effects:
–Hyperglycemia
–Loss of bone density
–Hyperlipidemia
–Lactic acidosis
–Fat redistribution
Treatment of Virus (2)
-In advanced AIDS, ART may not be the best option
–Can cause Immune Reconstitution Inflammatory Syndrome (IRIS) (worsening onset of infectious S?S r/t improved IS which causes inflammatory response
–Patient at greater risk for TB, CMV, herpes zoster during this time
–Provide supportive therapy and aggressive treatment of infections
-Treatment can slow or stop the progression from one stage to the next
-Treatment can also stop the transmission from one person to the next
Other treatments/prevention
-PrEP – Pre-exposure prophylaxis
–Those who have injected drugs in the past 6 months
–Partner had sex with someone else without a condom
–Partner diagnosed with an STD in past 6 months
-PeP – Post-exposure prophylaxis
–Can keep you from becoming infected
–Condom breaks
–Shared needles
–The sooner you start the better, every hour counts.

A

HIV 3 (treatment)

Goal of treatment:

  1. Decrease the plasma HIV viral load
  2. Restore and preserve immunological function
  3. Reduce HIV disease transmission
  4. Reduce HIV-associated morbidity
  5. Improve quality of life