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Nursing 210 > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

pathology of hyperthyroidism

A

excessive production of thyroid hormone- too much energy

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2
Q

what happens to the lab values with hyperthyroidism

A

increased T3 & T4
decreased TSH

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3
Q

signs and symptoms of hyperthyroidism

A

hyper excitable
nervous
irritable
decreased attention span
increased appetite
weight loss
hair loss
goiter
exophthalmus
increase BP, HR, GI function

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4
Q

life threatening complications of hyperthyroidism

A

thyroid storm- emergency

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5
Q

Treatment for hyperthyroidism/prevent thyroid storm

A

PTU
beta blockers
iodine compounds
radioactive iodine therapy
thyroidectomy
tylenol
steroids
D5W

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6
Q

pathology for hypothyroidism

A

low production of thyroid hormone- not enough energy

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7
Q

what happens to the lab values for hypothyroidism

A

decreased T3 & T4
increased TSH

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8
Q

signs and symptoms of hypothyroidism

A

no energy
fatigue
no expressions
weight gain
cold
amenorrhea
slurred speech
dry skin
coarse hair
decreased HR, BS, GI function

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9
Q

life threatening complications of hypothyroidism

A

myxedema coma

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10
Q

treatment for hypothyroidism/prevent myxedema coma

A

hormone replacement (synthroid)
will be on medication forever
labs taken 1X a month til stable

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11
Q

what are the adrenal cortex hormones

A

Glucocorticoids (cortisol) - sugar
Mineralcorticoids (aldosterone)- salt
Androgens- sex

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12
Q

what is the pathology of cushing’s disease

A

disorder of the adrenal cortex- too many steroids

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13
Q

causes of cushings disease

A

females
overuse/prolonged use of cortisol medications
tumor in the adrenal gland

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14
Q

signs and symptoms of cushings disease

A

muscle wasting
moon face
buffalo hump
truncal obesity w/thin extremities
supraclavicular fat pads
weight gain
hirsutism (masculine characteristics)
increased glucose and sodium
decreased potassium and calcium
hypertension

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15
Q

treatment for cushings disease

A

adrenalectomy (requires life long glucocorticoid replacement)
avoid infection
administer chemo agents if adrenal tumor is present

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16
Q

what is the pathology for addisons disease

A

disorder of the adrenal cortex-not enough steroids

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17
Q

causes of addisons disease

A

surgical removal of both adrenal glands
infection of the adrenal glands
TB, cytomegalovirus, & bacterial infections

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18
Q

signs and symptoms of addisons disease

A

fatigue
n/v/d
anorexia
hypotension & hypovolemia
confusion
decreased BS
decreased sodium and water
increased potassium
hyperpigmentation of the skin
vitiligo (white areas of depigmentation)

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19
Q

complications of addisons disease

A

addisonian crisis

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20
Q

what are the signs and symptoms of addisonian crisis

A

fatigue
dehydration/shock
renal failure
vascular collapse
hyponatremia
hyperkalemia

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21
Q

treatment of addisonian crisis

A

fluid rescucitation and high dose hydrocortisone

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22
Q

treatment for addisons disease

A

administer glucocorticoid and/or mineralcorticoid
diet high in protein and carbs

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23
Q

What is SIADH caused by?

A

excessive secretion of ADH (not peeing enough)

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24
Q

High or low serum Na+, serum concentration, and urine concentration for SIADH?

A

low serum Na+ and serum concentration, high urine concentration

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25
Q

primary tx for SIADH?

A

fluid restriction

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26
Q

intravascular volume for SIADH?

A

hypervolemic

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27
Q

What happens with SIADH? (excessive release of ADH)

A

causes renal excretion of Na+ = water intoxication, cellular edema, dilutional hypona+, low serum osmolality

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28
Q

What increases risk for SIADH?

A

malignant tumors, increased intrathoracic pressure, head injury, meningitis, trauma, alcohol, meds, stress, CVA

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29
Q

Assessment findings for SIADH?

A

oliguria, dilutional hyponatremia intake greater than output
early- headache, weakness, anorexia, muscle cramps, weight gain w/o edema, crackles, JVD
later- personality changes, hostility, sluggish deep tendon reflexes, N/V/D

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30
Q

lab tests for SIADH?

A

urine specific gravity greater than 1.030, blood serum sodium less than 135

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31
Q

Nursing care for SIADH?

A

monitor I/O, hypertonic IV, fluid restriction, no ETOH, seizure precautions

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32
Q

What is diabetes insipidus?

A

deficiency of ADH- reduces ability to concentrate urine, can’t hold onto fluid, peeing a lot

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33
Q

Causes of DI?

A

primary (defect in hypothalamus or pituitary), secondary-neurogenic (damage to hypothalamus or pituitary from trauma, infections, nephrogenic (don’t react to ADH), drug induced (lithium, declomycin)

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34
Q

Intravascular volume for DI?

A

hypovolemic

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35
Q

Serum Na+, serum concentration, and urine concentration for DI?

A

high serum Na+, high serum concentration, low urine concentration

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36
Q

Assessment findings for DI?

A

polydipsia- consume 2-20 L/day;
polyuria- UOP of 4-20 L/day;
nocturia, fatigue; dehydration; sunken eyes, tachycardia, hypotension, poor skin turgor, dry mucous membranes, weight loss, dizziness, constipation, weak pulses, decreased LOC

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37
Q

lab tests for DI?

A

urine specific gravity less than 1.005; serum Na+ greater than 145; water deprivation test (withhold fluids 8-12hrs, positive if kidneys are unable to concentrate urine); vasopressin test

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38
Q

tx for DI?

A

fluid resuscitation
replace ADH, replace fluids, identify and correct underlying intracranial issue, desmopressin, tegretol

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39
Q

nursing care for DI?

A

Monitor I/O, VS, labs, weight checks, IV fluids, no caffeine, no ETOH, increase bulk, skin and mouth care

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40
Q

complications with DI?

A

hypovolemia, hyperosmolarity, hypernatremia, circulatory collapse, loss of consciousness, CNS damage, seizures

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41
Q

how do you remember the three levels of preventative care?

A

Primary = Prevention
Secondary= Screening
Tertiary = Treatment

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42
Q

why is health literacy important (3 things) (( different than what her powerpoint says but she said this in class multiple times))

A

it decreases patient anxiety
it prepares patient for discharge
lower readmission rates

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43
Q

what does health literacy lead to ( 4 things)

A

longer life
reduced chronic disease
decreased health disparities
decreased health care costs

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44
Q

who is at risk for poor health literacy

A

elderly
low socioeconomic population
low eduction
african americans/multiracial adults

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45
Q

diagnostic eval for cushings disease

A

dexamethasone overnight suppression test
serum cortisol level
24 hour urine for cortisol

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46
Q

what do you teach patient with cushings

A

low sodium diet
s/s complications
medications

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47
Q

definition of ethics

A

the study or examination of morality through a variety of different approaches

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48
Q

ethical dilemma vs ethical distress

A

ethical dilemma: 2+ clear moral principles apply but support mutually inconsistent courses of action
ethical distress: the RN knows the right thing to do but either personal or institutional factors make it difficult to follow the correct course of action

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49
Q

normal levels for Na, K+, Ca, BUN, Creat

A

Na- 135-145
K+- 3.5-5
Ca 8.5-10.5
BUN- 7-20
Creat- 0.6-1.2

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50
Q

what can cause low creatinine

A

low muscle mass
hyperthyroidism
starvation
liver disease

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51
Q

what can cause high creatinine

A

AKI
CHF
dehydration

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52
Q

top 3 leading causes of death from cancer in men

A

1- lung
2 - prostate
3- colorectal

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53
Q

screening for prostate cancer

A

PSA and DRE usually beginning at age 50

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54
Q

only diagnostic test for prostate cancer

A

biopsy

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55
Q

what are the 3 types of prostate biopsy’s

A

transrectal
transurethral
transperineal

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56
Q

what do you teach patient after prostate biopsy

A

antibiotic tx
slight soreness and bleeding
blood in stools, urine or semen
CALL DOCTOR FOR
prolonged or heavy bleeding
pain that worsens
swelling near biopsy site
difficulty urinating

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57
Q

What is PST in health promotion mean?

A

Prevention (primary), Screening (secondary), Treatment (tertiary)

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58
Q

What is primary prevention?

A

focus is health promotion and prevention of illness or disease; interventions include teaching about healthy lifestyles

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59
Q

What is secondary prevention?

A

centers on health maintenance and is aimed at early detection; prompt intervention to prevent or minimize loss of function and independence; interventions include health screening

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60
Q

What is tertiary prevention?

A

Focuses on minimizing deterioration; improving quality of life

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61
Q

Why are fluids important?

A

to regulate/facilitate cellular metabolism and proper cellular functioning; facilitate digestion and elimination; help regulate temperature; needed for transport (blood, hormones, cells, blood components)

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62
Q

Aldosterone increases ______ which helps the body hold onto ______.

A

sodium; water

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63
Q

Describe the RAAS system

A

Liver releases angiotensinogen and in response to that kidney releases renin, angiotensinogen plus renin produces angiotensin 1… once it circulates to lungs, lungs release ACE.. ACE plus angiotensin 1 makes angiotensin 2… when that gets to adrenal glands it makes aldosterone… aldosterone increases reabsorption of sodium which increases fluid on board which increases bp and it also decreases potassium because it leaves through the urine have to keep in mind… angiotensin 2 (at level of kidneys) causes vasoconstriction in arterioles of kidneys which increases bp

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64
Q

To increase volume but maintain osmolarity, use _____ but not _____.

A

aldosterone, ADH

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65
Q

To increase volume regardless of osmolarity, use ______.

A

ADH and aldosterone

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66
Q

To decrease osmolarity regardless of volume, use _____.

A

ADH (aldosterone not needed)

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67
Q

To decrease osmolarity and maintain volume, decrease _____ and increase _____.

A

decrease aldosterone a smidge and increase ADH.

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68
Q

Common causes of edema?

A

increased capillary pressure, decreased colloidal osmotic pressure, obstruction of lymphatic flow, increased capillary permeability

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69
Q

What are factors affecting fluid and electrolyte balance?

A

age (pediatric/geriatric), gender, body size, environmental temp, lifestyle (stress, exercise, ETOH, diet)

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70
Q

causes of fluid volume deficit?

A

vomiting, diarrhea, GI suctioning, sweating, decreased intake, inability to gain access to fluids

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71
Q

risk factors of FVD?

A

DI, adrenal insufficiency, hemorrhage, coma

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72
Q

sx of FVD?

A

oliguria, decreased skin turgor, concentrated urine, postural hypotension, rapid weight loss, weak rapid pulse, cramps, nausea, thirst, clammy skin, increased temp, increased BUN and HCT

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73
Q

tx for FVD?

A

provide fluids to meet body requirements

74
Q

risk factors for fluid volume excess?

A

heart and renal failure

75
Q

sx of fluid volume excess?

A

edema, distended neck veins, crackles in lungs, tachycardia, increased BP, increased weight

76
Q

medical management of fluid volume excess?

A

treat cause, restrict fluids and sodium, diuretics

77
Q

normal lab value for magnesium?

A

1.3-2.1

78
Q

normal lab value for phosphorus?

A

3.0-4.5

79
Q

normal lab value for chloride?

A

100-106

80
Q

how does the blood flow through the kidneys?

A

Blood flows into the nephron through the glomerulus-> filtrate flows into the Bowman’s capsule-> proximal tubule-> loop of henle-> distal tubule(modifies filtrate by reabsorbing H2O and needed electrolytes into the bloodstream-> modified filtrate then flows into the collecting duct and drains into renal pelvis.

81
Q

what is normal specific gravity?

A

1.010-1.025

82
Q

What id RIFLE classification?

A

Risk- increased creatinine 1.5 X baseline (urine output- 0.5ml/kg/h for 6h)
Injury- increased creatinine 2X baseline (urine output- 0.5ml/kg/h for 12h)
Failure- Increase creatinine 3X baseline (urine ouput- <0.3ml/kg/hr for 24h or anuria for 12h)
Loss- Persistent ARF > 4 weeks
E- ESRD > 3 mos

83
Q

normal GFR?

A

60-120

84
Q

kidney disease GFR?

A

15-60

85
Q

kidney failure GFR?

A

0-15

86
Q

What is acute renal failure (injury)?

A

reversible syndrome that results in decreased glomerular filtration rate and oliguria

87
Q

What is chronic renal failure (injury)?

A

ends with (ESRD) is a progressive, irreversible deterioration of renal function that results in azotemia

88
Q

What happens in AKI?

A

rapid loss of renal function due to damage to kidneys; complications depend on severity; 50% or greater increase in serum creatinine above baseline; you would see sudden increase in BUN and creatinine, high potassium

89
Q

causes of AKI?

A

Hypovolemia /Hypotension /Hypertension
Reduced cardiac output and heart failure
Obstruction of renal arteries or veins
Diabetes mellitus
Chronic glomerulonephritis,
Pyelonephritis or other infections
Obstruction of urinary tract
Hereditary lesions
Vascular disorders
Medications or toxic agents
Kidney disease causing injury
Obstruction of the kidney or lower urinary tract

90
Q

AKI can be separated into what 3 groups?

A

prerenal, intrarenal, postrenal

91
Q

What are the 4 phases of AKI?

A

Initiation phase- sudden increase in BUN and creatinine
Oliguria phase- can be life threatening, less than 400ml urine per day, uric acid, potassium, BUN, nitrogen and creatinine all sky high (longer it goes on, more dangerous it is); dialysis needed
Diuresis phase- start slowly putting out urine and getting rid of metabolic waste, lab values start to stabilize naturally, can become dehydrated so strict I/O monitoring
Recovery phase- can take up to a year

92
Q

pharmacological therapies for AKI?

A

diuretics, volume expanders, IV fluids, phosphorus binding capsules, Kayexalate

93
Q

Once vascular volume and renal perfusion is restored with AKI, you ______.

A

restrict fluids and monitor fluid balance

94
Q

nutrition for AKI and CKD?

A

Limit protein to 0.5 g/kg (no urea)- normal is 1g/kg; for chronic it might be .8g/kg; end stage is 1-1 ½ g/kg
Increase carbohydrates
Parenteral nutrition as necessary

95
Q

What is hemodialysis?

A

removes electrolytes, waste products, and water

96
Q

What is disequilibrium syndrome?

A

urea pulled off too fast and end up with increased cerebral edema

97
Q

complications with renal replacement therapy?

A

Hypotension
Hemorrhage
Infection
Disequilibrium syndrome

98
Q

vascular access for hemodialysis?

A

short term- double lumen catheter; long term- AV fistula

99
Q

What is Continuous renal replacement therapy?

A

Allows gradual fluid and solute removal
Clients unable to tolerate hemodialysis
Blood continuously circulated for 12 hours
better hemodynamic tolerance

100
Q

What is peritoneal dialysis?

A

Peritoneal membrane serves as dialyzing surface
Less risk for unstable client
Fluid and solutes removed more gradually
Increased risk for peritonitis

101
Q

a disadvantage of peritoneal dialysis is _____.

A

risk of hypergylcemia

102
Q

Causes of chronic renal failure?

A

AKI untreated; older age; chronic kidney stones; HTN; DM; polycystic kidney disease; chronic glomerulonephritis; pyelonephritis; prostate cancer; meds (NSAIDS, vanco) ; toxic agents

103
Q

What is acute nephritic syndrome?

A

Post-infectious glomerulonephritis, rapidly progressive glomerulonephritis, and membranous glomerulonephritis
Manifestations include hematuria, edema, azotemia, proteinuria, and hypertension
May be mild or may progress to acute renal failure or death
Medical management includes supportive care and dietary modifications; treat cause if appropriate—antibiotics, corticosteroids, and immunosuppressants

104
Q

What is chronic glomerulonephritis?

A

causes- Repeated acute glomerularnephritis, hypertensive nephrosclerosis, hyperlipidemia, and other causes of glomerular damage
*Renal insufficiency or failure: asymptomatic for years as glomerular damage increases before signs and symptoms develop
*Abnormal laboratory test results: urine with fixed specific gravity, casts, proteinuria, electrolyte imbalances and hypoalbuminemia
*Medical management determined by symptoms

105
Q

What is nephrotic syndrome?

A

Any condition that seriously damages the glomerular membrane and results in increased permeability to plasma proteins
Results in hypoalbuminemia and edema
Causes include chronic glomerulonephritis, diabetes mellitus with intercapillary glomerulosclerosis, amyloidosis, lupus erythematosus, multiple myeloma, and renal vein thrombosis
Medical management includes drug and dietary therapy

106
Q

Nephritic sx?

A

oliguria, hematuria, non selective proteinuria, decreased GFR, increased Cr and BUN, edema, HTN, RBC and protein casts see with eye

107
Q

Nephrotic sx?

A

proteinuria, edema, hyperlipidemia, lipiduria, protein casts

108
Q

What is stage 1 CKD?

A

GFR ≥90 mL/min/1.73 m2
Kidney damage with normal or increased GFR

109
Q

What is stage 2 CKD?

A

GFR = 60–89 mL/min/1.73 m2
Mild decrease in GFR

110
Q

What is stage 3 CKD?

A

GFR = 30–59 mL/min/1.73 m2
Moderate decrease in GFR

111
Q

What is stage 4 CKD?

A

GFR = 15–29 mL/min/1.73 m2
Severe decrease in GFR

112
Q

What is stage 5 CKD?

A

GFR < 15 mL/min/1.73 m2
End-stage kidney disease or chronic renal failure

113
Q

Clinical manifestations of uremia?

A

retain sodium and water
lose water
N/V/D
high potassium
impaired buffer production- acidosis

114
Q

clinical manifestations of CKD? (to look at not memorize)

A

Uremia, Fluid and electrolyte effects (retain sodium and water, lose water, N/V/D, high potassium, impaired buffer production- acidosis), Systemic hypertension, Arrhythmias, Edema, Heart failure, Pericarditis, Increased RR, crackles in lungs, Anemia, Fatigue, weakness, depression, impaired cognition, Impaired platelet function, Risk for infection, Decreased inflammatory response, Uremic fetor, Ulcerations, Anorexia, nausea and vomiting, Gastric hypomotility, Glucose intolerance, Dry skin, Poor healing, Pruritus, Bruising and excoriations, Uremic frost, Changes in cognitive functioning, Psychosis, Seizures, Coma, peripheral neuropathy, paresthesia

115
Q

pharmacological therapies for anemia?

A

Treat w iron supplements, folic acid
Possible blood transfusion
Erythropoietin injections to stimulate production of red cells

116
Q

pharmacological therapies for calcium and phosphorus imbalance?

A

Phosphorus binders
Possibly increase calcium (oscal, phoslow)
Keep an eye on calcium and phosphorus levels

117
Q

pharmacological therapies for antihypertension (CKD)?

A

Arbs and aces
HF or pulmonary edema- digoxin or dibutamine
Treat metabolic acidosis w bicarb
Loop diuretics
Electrolyte replacement

118
Q

what to avoid with CKD?

A

salt substitutes, eggs, dairy, meat, decrease protein, increase carbs

119
Q

medications for kidney transplants?

A

prednisone, immunosuppressive agents

120
Q

what is hyperacute organ rejection and when does it take place?

A

within 48 hours after surgery;
Etiology: An antibody mediated response causing small blood clots to form in the transplanted organ (kidney) that occlude vessels and result in massive cellular destruction. This process is not reversible.
Findings: Fever, hypertension, pain at the transplant site (flank pain)
Treatment: Immediate removal of the donor kidney

121
Q

What is acute organ rejection and when does it take place?

A

days to weeks after surgery;
Etiology: an antibody mediated response causing vasculitis in the donor kidney, and cellular destruction starts with inflammation that causes lysis of the donor kidney
Findings: Oligulia, anuria, low-grade fever, hypertension, tenderness at the transplant site, lethargy, azotemia, and fluid retention
Treatment: increased doses of immunosuppressive medications

122
Q

What is chronic organ rejection and when does it take place?

A

gradually over months to years;
Etiology: Blood vessel injury from overgrowth of smooth muscles from the blood vessels causing fibrotic tissue to replace normal tissue resulting in nonfunctioning donor kidney
Findings: gradual return of azotemia, fluid retention, electrolyte imbalance and fatigue
Treatment: conservative to start (monitor kidney function status, electrolytes, continue immunosuppressive therapy) until dialysis is needed.

123
Q

Patient education on organ rejection?

A

Teach patient about S&S of rejection and to contact provider IMMEDIATELY
Teach the patient that in order to diagnose rejection & type, kidney scans and biopsies will be needed
Teach the patient the importance of medication/ pharmaceutical compliance

124
Q

s/s of hypokalemia

A

Muscle weakness
Fatigue
Nausea & vomiting
Dysrhythmias
Flat T waves (ECG)
Irritability, confusion
Decreased bowel motility
Paresthesia

125
Q

s/s of hyperkalemia

A

Muscle cramps, weakness, paralysis
Bradycardia
Dysrhythmias
Tall T waves (ECG)
Increased bowel motility

126
Q

s/s of hypernatremia

A

Sticky mucous membranes
Hallucinations
Restless, weak
Orthostatic hypotension
Muscle irritability, seizures, coma
Thirst, dry mucous membranes, fever
Swollen, dry tongue

127
Q

s/s of hyponatremia

A

Weakness
Lethargy
Confusion
Seizures
Coma
Headache, anorexia,nausea, vomiting
Muscle cramps, hypotension
Tachycardia
Weight gain, edema

128
Q

s/s of hypocalcemia

A

Tetany, cramps
Paresthesias
Dysrhythmias
Trousseau’s sign
Chvostek’s sign
Seizures
Hyperreflexia
Impaired clotting time

129
Q

s/s of hypercalcemia

A

Muscle weakness
Decreased DTR’s
Hypercalciuria/renal
stones
Dysrhythmias
Confusion
Anxiety
Lethargy/coma
Pathologic fractures
Flank pain, deep bone pain

130
Q

tx of hypercalcemia

A

isotonic iv fluids
diuretics
calcitonin
glucocorticoids
dialysis

131
Q

tx of hypocalcemia

A

iv calcium replacement
calcium supplements
vitamin d therapy

132
Q

tx for hyponatremia

A

isotonic iv fluids
loop diuretics (prevent fluid overload)
restrict oral intake

133
Q

tx for hypernatremia

A

isotonic iv fluids
D5W

134
Q

tx for hyperkalemia

A

kayexalate
calcium gluconate
loop diuretics
dialysis

135
Q

tx for hypokalemia

A

administer potassium
dietary sources of K+

136
Q

s/s low creatinine

A

low muscle mass
lack of strength
frail
liver disease
weight loss
faint/dizzy

137
Q

s/s high creatinine

A

nausea
chest pain
muscle cramps
vomitting
fatigue
changes in urinary frequency and appearance
hypertension
fluid retention
itchiness

138
Q

s/s high bun

A

urinating more frequently
fatigue
muscle cramps
swelling in legs, feet, ankles
trouble sleeping
back pain

139
Q

s/s low bun

A

frequent urination
dark discolored urine
joint/bone pain
muscle cramping
restless legs

140
Q

prostate diagnosis is measured by a ______ score

A

gleason

141
Q

3 prostate cancer surgical procedures

A

open procedure ( open up abdomen )
laparoscopic/robotic procedure ( minimally invasive )
transurethral removal of the prostate (TURP)

142
Q

what drug is used for bladder spasms regarding a TURP

A

oxybutynin

143
Q

typically how long is CBI used following a TURP

A

24 hours post op

144
Q

purpose of cbi following turp

A

prevents formation of blood clots

145
Q

with turp care there is a risk for

A

infection
hypovolemia
catheter obstruction
VTE

146
Q

what do you see with turp syndrome

A

hyponatremia
low hematocrit
hypertension
bradycardia
nausea
confusion

147
Q

what would you do if you suspected turp syndrome

A

stop irrigant
call provider
request diuretic
assess lung sounds

148
Q

alpha adrenergic blockers for benign prostatic hypertrophy

A

(relaxes bladder neck for easier urination)
doxazosin
prozosin
tamulosin
terazosin

149
Q

alpha adrenergic blockers side effects (for bph)

A

orthostatic hypotension
first dose phenomenon (severe hypotension and syncope) with prozosin
headache
dizziness

150
Q

5-alpha reductase inhibitors for bph

A

(decrease prostate size by blocking testosterone)
finasteride
dutasteride

151
Q

___ x ___ = cardiac output

A

stroke volume x heart rate

152
Q

Why is health literacy important?

A

decreases anxiety, prepares them for discharge, decreases readmission

153
Q

What is perfusion dependent on?

A

volume, vascular resistance, and cardiac output

154
Q

The foramen ovale allows blood flow…?

A

between R and L atriums

155
Q

The ductus arteriosus allows blood flow between….?

A

R and L ventricles

156
Q

normal infant HR?

A

120-130

157
Q

normal toddler HR?

A

80-105

158
Q

normal school age child HR?

A

70-80

159
Q

What are the adaptations in the fetal heart?

A

umbilical vein, umbilical artery, ductus venous, foramen ovale, ductus arteriosus

160
Q

What happens after birth?

A

placenta is removed which decreases prostaglandins, and resistance increases; once the lungs take in air the increased resistance decreases

161
Q

What happens once the lungs take in air after baby is born?

A

reduced pulmonary vascular resistance, pulmonary artery pressure drops, decreases R atrium pressure, L side heart pressure increases, CLOSES foramen ovale, drop in pulmonary artery pressure promotes CLOSURE of ductus arteriosus, ductus venosus closes due to decreased blood flow and vasoconstriction

162
Q

When do most CHD develop?

A

during first 8 weeks gestation

163
Q

congenital heart disease vs acquired heart disease

A

congenital- present at birth; acquired- after birth

164
Q

What is ASD and what to assess for atrial septal defect?

A

increased pressure on R side of heart, may be asymptomatic but frequent URIs; assess lungs, listen for murmur, monitor baby interact, input (fatigued easy when drinking?)

165
Q

Tx for ASD?

A

wait, surgery if CHF or pulmonary flow increases or if not closed by age 3; diagnosed by echo

166
Q

Tx for patent ductus arteriosus?

A

indomethacin, surgical closure, may need to keep open for prostaglandins

167
Q

What is VSD?

A

ventricular septal defect; most common CHD; associated with TORCH, Trisomy 10 & 18; asymptomatic; murmur; surgery if symptomatic or persistent after a year

168
Q

potential meds for VSD?

A

digoxin, ace inhibitor, lasix

169
Q

What happens with VSD?

A

oxygenated (left) and deoxygenated (right) blood mix together

170
Q

What is pulmonary stenosis?

A

narrowed pulmonary valve, causes hypertrophy on right ventricular wall

171
Q

What is coarctation of the aorta?

A

narrowing of the aorta

172
Q

sx of coarctation of aorta?

A

asymptomatic HTN, lower extremity claudication, syncope, epistaxis, headache, weak femoral pulses, BP higher in upper extremities

173
Q

tx for coarctation of aorta?

A

surgery, watch for restenosis or dissection or aneurism

174
Q

What tis aortic stenosis?

A

narrow aortic valve; causes hypertrophy of left ventricle wall

175
Q

What is tetrology of fallot?

A

4 problems with heart- pulmonary stenosis, R ventricular hypertrophy (due to stenosis), ventricular septal defect, overriding aorta (between R and L ventricle)

176
Q

blood flow w/ tetrology of fallot?

A

RA - ASD - LA - LV (aorta) and PDA (pulmonary artery) - VSD - RV - pulm artery - lungs

177
Q

how is tetrology of fallot diagnosed?

A

echo, EKG, CXR

178
Q

symptoms of TOF may present with ____.

A

CHF

179
Q

tx for TOF?

A

surgery

180
Q

Acyanotic 3 D’s

A

VSD, ASD, PDA

181
Q

Cyanotic 12345

A

1 trunk (truncus arteriosus), 2 vessel switch (transposition of vessels), 3 (TRIcuspid insufficiency), 4 (TETRAlogy of Falot), 5 words (total anomalous pulmonary venous return) disclaimer- I have absolutely no idea what any of this means

182
Q

Medications for child w cardiac disorder?

A

prostaglandin (alprostadil), digoxin, furosemide, heparin, indomethacin, spironolactone, penicillin, erythromycin, ace inhibitors, beta-blockers, hydralazine

Nursing 210 (2 decks)

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