2920 Pathophysiology Exam One Flashcards

1
Q

define genetics

A

study of heredity and inherited characteristics

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2
Q

define mutation

A

change or damage to a gene that alters genetic code

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3
Q

autosomal dominant genetic disease

A

abnormal allele is dominant and normal allele is recessive

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4
Q

what is the recurrence risk of autosomal dominant diseases if one parent is affected? Both parents?

A

50% chance for one parent, 75% chance if both affected

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5
Q

are males or females more affected in autosomal dominant disorders?

A

both are affected equally

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6
Q

examples of autosomal dominant disorders

A

BRCA gene cancers (breast and ovarian)
Huntington’s disease
familial hypercholesterolemia
marfan syndrome

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7
Q

autosomal recessive genetic diseases

A

abnormal allele is recessive, and the person must be homozygous for the disease to be expressed

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8
Q

what is the recurrence rate of autosomal dominant diseases if parents are heterozygous? what is the chance of children being a carrier?

A

25% risk of disease recurrence, 50% chance of child being a carrier

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9
Q

what are some examples of autosomal recessive disorders?

A

cystic fibrosis
sickle cell disease
tay-sachs disease
PKU

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10
Q

who is usually affected by x linked recessive disorders? who is usually a carrier?

A

men are usually affected because they have only one x chromosome, women can be carriers

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11
Q

can affected men transmit x linked disorders to their sons?

A

no, because they give only their Y chromosome

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12
Q

what are some examples of x linked recessive disorders?

A

duchenne muscular dystrophy
hemophilia
color blindness
wiskott-aldrich syndrome

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13
Q

Is familial hypercholesterolemia autosomal dominant or recessive?

A

dominant

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14
Q

pathophysiology: familial hypercholesterolemia

A

liver lacks production LDL receptors, so patient has increasingly high levels of LDL

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15
Q

clinical manifestations: familial hypercholesterolemia

A

cholesterol exceeding 600 mg/dL
early atherosclerosis
early adult coronary artery disease or MI

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16
Q

pathophysiology: marfan syndrome

A

gene mutation that causes connective tissue weakening, which leads to weakening and aneurysms of vascular structures that will eventually rupture

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17
Q

clinical manifestations: marfan syndrome

A
tall stature
heart murmurs
ligament hypermobility
syncope
dyspnea
joint issues
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18
Q

what is the most common lethal inherited disease in caucasians?

A

cystic fibrosis

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19
Q

pathohysiology: cystic fibrosis

A

dysfunction of gene that regulates chloride channels, leading to salt and chloride exchange issues in epithelial cells

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20
Q

clinical manifestations: cystic fibrosis

A

pancreatic enzyme deficiency
thick respiratory mucus and difficulty breathing
everything clogged with thick mucus and severe dehydration in all systems

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21
Q

pathophysiology: tay sachs disease

A

genetic mutation causing deficiency of lysozomal enzyme, leading to progressive destruction of neurons

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22
Q

clinical manifestations: tay-sachs disease

A

cherry red spots on retina
incoordination and flaccid muscles
cognitive impairment
symptoms often present in early infancy

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23
Q

pathophysiology: wilson’s disease

A

genetic disorder of copper metabolism, leading to copper deposits in the body that damage hepatocytes

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24
Q

clinical manifestations: wilson disease

A
cirrhosis
tremor
speaking issues
ataxia
clumsiness/dystonia
seizures
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25
Q

pathophysiology: kleinfelter syndrome

A

extra x or y chromosome, only affects males

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26
Q

clinical manifestations: kleinfelter syndrome

A

less puberty changes (decreased testicle development, gynecomastia)
diabetes and obesity
cognitive impairment
skeletal/heart abnormalities

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27
Q

pathophysiology: turner syndrome

A

complete or partially missing x chromosome in females

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28
Q

clinical manifestations: turner syndrome

A
webbed feet and neck
short stature
infertility
amenorrhea 
cardiovascular problems
hypothyroidism
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29
Q

pathophysiology: down syndrome

A

trisomy of chromosome 21

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30
Q

clinical manifestations: down syndrome

A
cognitive impairment
dysmorphic facial features 
heart disease
weak immune system 
only one hand crease
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31
Q

pathophysiology: prader-willi syndrome

A

mutation of chromosome 15 causing hypothalamic dysfunction

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32
Q

clinical manifestations: prader willi syndrome

A
obesity and overeating
hypotonia
low IQ
short stature
seizures 
hypogonadism
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33
Q

pathophysiology: huntington disease

A

adult onset autosomal dominant neurodegenerative disorder causing degeneration of specific neurons at basal ganglia and cortex

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34
Q

clinical manifestations: huntington disease

A
movement issues (tremors progressing rapidly to parkinsonian symptoms)
cognitive issues
dementia
depression
rapid progression to death
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35
Q

pathophysiology: COPD

A

chronic bronchitis + emphysema causing airflow limitations that lead to narrowing, excessive mucus, and loss of alveolar elasticity
airway permanently remodeled

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36
Q

what are manifestations of a COPD exacerbation?

A

worsening shortness of breath at rest
increased secretions
increased purulence of secretions

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37
Q

general manifestations of COPD?

A
dyspnea
barrel chest
cough/wheeze 
cyanosis
hypoxia
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38
Q

risk factors: COPD

A
age
smoking history
being male
asthma
AAT deficiency 
bacterial or viral infections 
inhalation of chemicals/dust/pollution
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39
Q

ARDS stands for

A

acute respiratory distress syndrome

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40
Q

pathophysiology: ARDS

A

alveolar injury triggers inflammation, which makes the capillary membrane more permeable. this increases pulmonary edema and impairs gas exchange. vasculature also narrows causing pulmonary hypertension

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41
Q

what is atelectasis?

A

alveolar collapse

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42
Q

what are the first signs of ARDS?

A

sudden onset dyspnea and being unable to catch breath

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43
Q

what are later signs and manifestations of ARDS?

A
sudden progressive pulmonary edema
restlessness
confusion
rapidly dropping O2 sats 
hypoxemia and hypercapnia
crackles in lungs
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44
Q

what is the number one cause of ARDS?

A

sepsis

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45
Q

what are some examples of things that can cause indirect lung injury leading to ARDS?

A
sepsis
drug overdose
massive transfusion 
prolonged cardiopulmonary bypass surgery 
severe head injury 
acute pancreatitis 
traumatic injury
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46
Q

what are some direct lung injury examples that can lead to ARDS?

A
aspiration of gastric contents
pneumonia
air/fat/amniotic fluid emboli 
inhalation of toxic substances 
near drowning
oxygen toxicity 
radiation pneumonitis
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47
Q

what is the pathophysiology of pre-eclampsia?

A

unknown, but it is a progressive problem that stems from the placenta

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48
Q

what is the first problem that leads to the complications of pre-eclampsia?

A

inadequate vascular remodeling of the spiral arteries (they fail to widen)

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49
Q

what problems occur because the spiral arteries fail to widen in pre-eclampsia?

A

decreased placental perfusion

hypoxia

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50
Q

what happens to the endothelial cells because of decreased placental perfusion and hypoxia in pre-eclampsia?

A

they malfunction and release toxic substances

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51
Q

what three things occur because of endothelial cell dysfunction in pre-eclampsia?

A

vasospasm
increased peripheral resistance
increased endothelial cell permeability

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52
Q

increased peripheral resistance gives rise to…

A

hypertension

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53
Q

increased endothelial cell permeability leads to..

A

edema and protein loss

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54
Q

vasospasm causes what problems in pre-eclampsia?

A

headache and visual disturbances

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55
Q

what is the end result of the pre-eclampsia disease cascade?

A

decreased tissue perfusion to all organs

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56
Q

what are some primary clinical manifestations of pre-eclampsia?

A
hypertension
headache
blurred vision
edema
increased CNS irritability
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57
Q

what are the blood pressure criteria for pre-eclampsia diagnosis?

A

BP greater than or equal to 140/90 on at least two occasions at least four hours apart

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58
Q

what will happen to hemoglobin and hematocrit levels in pre-eclampsia?

A

decreased hemoglobin

increased hematocrit

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59
Q

what happens when pre-eclampsia progresses to eclampsia?

A

seizures, coma, and death

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60
Q

what is the name of the syndrome that occurs in severe pre-eclampsia?

A

HELLP syndrome

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61
Q

what is HELLP syndrome?

A

hemolysis, elevated liver enzymes, low platelets

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62
Q

is HELLP syndrome easily detected?

A

no, many women are asymptomatic and don’t know they have it

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63
Q

what are risk factors for developing preeclampsia?

A
first pregnancy 
age over 40 or under 19
family history or personal history of preeclampsia 
multifetal pregnancy 
chronic hypertension
renal disease 
diabetes or other vessel disorders
African American
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64
Q

what are the risks to the unborn infant in preeclampsia cases?

A

preterm birth
low birth weight infants
poor fetal oxygenation
decreased amniotic fluid

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65
Q

what does RSV stand for?

A

respiratory syncytial virus

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66
Q

what is RSV?

A

a lower respiratory RNA virus that primarily occurs in very young children or elderly people with lung diseases

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67
Q

what is the pathophysiology of RSV?

A

the virus invades the bronchioles and lower respiratory tract, causing airway obstruction, edema, and mucus production
the narrow airways allow air to be inhaled but exhalation is hindered, causing air trapping

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68
Q

what do the endothelial cells of the respiratory tract do in RSV?

A

they fuse together, making swollen giant cells that clog the airway and create a lot of mucus and exudate

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69
Q

what are initial manifestations of RSV?

A

cold-like symptoms

70
Q

what are progressive symptoms of RSV?

A

retractions
high RR
cyanosis
wheezing and stridor

71
Q

what are severe symptoms of RSV?

A

fever
listlessness
minimal breath sounds

72
Q

what are some of the main risk factors for RSV?

A
premature infants
infants less than one year old
crowded living conditions 
congenital heart disease 
immunodeficiency 
winter or early springtime
being male 
non-breastfed 
having a mother who smokes
73
Q

pathophysiology of malignant hyperthermia

A

autosomal dominant trait that causes a reaction to anasthesia.
it is a hypermetabolism of skeletal muscle due to altered control of intracellular calcium

74
Q

what is usually the first sign of malignant hyperthermia?

A

muscle rigidity

75
Q

what is the treatment for malignant hyperthermia?

A

dantrolene (a muscle relaxant)

76
Q

what is the pathophysiology and manifestations of anaphylaxis?

A

extreme allergic immune response causing hypotension, tachycardia, bronchospasm, and pulmonary edema

77
Q

what is the treatment for anaphylaxis?

A

subcutaneous epinephrine and fluids

if that isnt working, vasopressors can also be given

78
Q

what are some of the duties of of a preoperative nurse?

A
full patient assessment/interview/history
asking about allergies and meds
vitals and labs 
surgery teaching and informed consent
pre-op medications 
family history and medical history
pulses in all extremities
color/movement/sensation
79
Q

What are some of the roles/duties of the intraoperative nurse?

A

take report from the pre-op nurse
advocate for the patient in the surgery room
call for pause to make sure everything is correct before beginning
ensure safety and sterility
monitor vitals, blood loss, and intake and output
report off to post-op nurse

80
Q

what are some of the duties of the postoperative nurse?

A
monitor patients and ensure they are stable before moving them out of PACU
monitor ABCs/vitals/LOC
administer meds and manage pain
assess psychological status
discharge planning and education
81
Q

before what point is a birth considered premature?

A

anytime before 37 weeks

82
Q

the majority of preterm birth mortalities occurs in babies born before when?

83
Q

what is considered the age of viability (when a premature infant has a chance at survival)?

84
Q

what are some causes of preterm birth?

A
gestational diabetes
hypertension or preeclampsia
placental disorders
seizures
advanced maternal age
smoking
obesity
85
Q

what are some complications of preterm birth?

A
death
immature lungs
oxygen toxicity
apneic spells
aspiration risk
immature GI system
inability to regulate temperature
startle easily
prone to strokes due to weak vessels
86
Q

what complications can occur due to immature GI system in premature babies?

A

bowel obstruction

holes in bowels

87
Q

how can a nurse stimulate breathing in preterm babies prone to apneic spells?

A

flick their toes

88
Q

how does the suck/swallow reflex work in preterm babies?

A

they have a suck reflex but no swallow reflex

89
Q

pathophysiology of respiratory acidosis

A

decreased ventilation causes accumulation of acidic CO2 in the bloodstream

90
Q

what are some common pulmonary causes of respiratory acidosis?

A
pulmonary obstruction
respiratory depression
pneumonia
asthma/lung disease 
underventilation or hypoventilation
CF
COPD
91
Q

what are some common non-pulmonary causes of Respiratory acidosis?

A

overdose of sedatives or narcotics
neuromuscular disorders (GB, MS)
nervous system damage
cardiopulmonary arrest

92
Q

pathophysiology of respiratory alkalosis

A

usually hyperventilation causes excess CO2 elimination, so less acid than normal is in the bloodstream

93
Q

what are some common pulmonary causes of respiratory alkalosis?

A
pneumonia
overventilation/hyperventilation
pulmonary edema or embolus
lung disease with shortness of breath
asthma
94
Q

what are some common non-pulmonary causes of respiratory alkalosis?

A
anxiety
pain
liver disease 
fever/infection/sepsis
CNS disorders
alcohol or salicylate intoxication
95
Q

what is the pathophysiology/etiology of metabolic acidosis?

A

increased acid production, decreased acid excretion, or loss of base in the body

96
Q

what are some common causes of increased non-carbonic acid in the body (leading to metabolic acidosis)?

A
DKA
lactic acidosis
alcoholic or uremic acidosis
toxic substance ingestion 
shock
renal disease 
hypokalemia
hypocalcemia
hypomagnesia
97
Q

what are some common causes of bicarbonate loss (leading to metabolic acidosis)?

A

prolonged diarrhea
renal tubular acidosis
interstitial renal disease

98
Q

what electrolyte imbalance can occur as a result of compensatory mechanisms to correct metabolic acidosis?

A

hyperkalemia

99
Q

pathophysiology/etiology of metabolic alkalosis

A

depletion of hydrogen ions, which are usually lost through the kidneys or GI system

100
Q

what electrolyte imbalance can cause metabolic alkalosis, and why?

A

hypokalemia, due to hydrogen ions shifting into the intracellular space to make up for missing potassium

101
Q

what are some common causes of metabolic alkalosis?

A
bicarbonate ingestion
potassium wasting diuretics
loss of gastric fluid from suctioning or vomiting
cushing syndrome
primary or secondary hyperaldosteronism
102
Q

how will you know if an ABG is partially compensated?

A

all three values will be abnormal

103
Q

how will you know if an ABG is fully compensated?

A

pH will be normal and the other two values will be abnormal

104
Q

normal PaCO2 levels

105
Q

normal bicarb levels

106
Q

normal PaO2

107
Q

what is acute renal injury

A

a rapid decrease in renal filtration function

108
Q

what are the four phases of AKI?

A

initial
oliguric
diuretic
recovery

109
Q

initial phase of AKI

A

initial insult/injury to kidneys, usually occurs over hours to days

110
Q

oliguric phase of AKI

A

decreased urine output
decreased GFR
retention of urea, creatinine, and potassium

111
Q

diuretic phase of AKI

A

beginning of recovery, high urine output put urine is undiluted, so patient still retains waste products
fluid replacement is vital
fibrosis may begin to occur in the kidneys

112
Q

recovery phase of AKI

A
may or may not happen
if it does happen...
urine is appropriately concentrated 
inflammation goes down
renal function returns
may take months to a year to fully recover and kidneys may have scar tissue
113
Q

what does the RIFLE scale look at as pertains to AKI?

A

creatinine
urine output
GFR

114
Q

what is a red flag/emergency manifestation of AKI?

A

encephalopathy (confusion)

115
Q

what are other clinical manifestations of AKI?

A

oliguria
fluid overload
uremia, causing encephalopathy, anemia, hyperkalemia, metabolic acidosis, thrombocytopenia, and neuromuscular irritability
pulmonary edema

116
Q

what are the three categories of kidney injuries that can cause AKI?

A

prerenal
intrarenal
postrenal

117
Q

what are some examples of prerenal injuries that can cause AKI?

A

low BP
shock
hypovolemia
anything decreasing renal perfusion

118
Q

what are some examples of intrarenal injuries that can cause AKI?

A

kidney damage from nephrotoxic drugs (NSAIDs, antibiotics, radioopaque dyes)
sepsis
infection (glomerulonephritis, pyelonephritis)

119
Q

what are some examples of postrenal injuries/problems that can cause AKI?

A

obstruction of urine outflow from things like BPH, blader disorders
spinal cord injuries causing issues with bladder emptying
tubule obstruction

120
Q

what is the number one killer in AKI?

A

infection (sepsis)

121
Q

when might a cancer patient need to be put on neutropenic precautions?

A

when/if WBC levels get too low

122
Q

what is superior vena cava syndrome?

A

cancer emergency in which the SVC is obstructed by tumor or thrombosis

123
Q

clinical manifestations of superior vena cava syndrome

A

facial/periorbital edema
headache
seizures
distended neck veins

124
Q

what is spinal cord compression?

A

cancer emergency in which cancer is present in the epidural space of the spinal cord, compressing it

125
Q

clinical manifestations: spinal cord compression

A
intense localized back pain
vertebral tenderness
motor weakness 
autonomic loss
sudden immobility
126
Q

what is third space syndrome?

A

cancer emergency in which fluid shifts from the vascular space to the interstitial space. usually happens after surgery, septic shock, or immunotherapy

127
Q

why does third space syndrome not go away in cancer patients?

A

because their cells are weak/unhealthy, and unable to mobilize the fluid back into the vascular space and out of the body

128
Q

clinical manifestations: third space syndrome

A

signs of hypovolemia: hypotension, tachycardia, decreased urine output
edema

129
Q

what is SIADH?

A

syndrome of inappropriate antidiuretic hormone, a cancer emergency in which chemo or cancer cells cause the production of excess ADH, leading to fluid retention

130
Q

clinical manifestations: SIADH

A
water retention
hypotonic hypernatremia 
weight gain
weakness
anorexia/N/V
seizures
personality changes 
decreased reflexes
coma
131
Q

what is tumor lysis syndrome?

A

cancer emergency that usually occurs shortly after first chemo treatment if its going to occur. its a rapid release of intracellular contents (potassium, phosphorus, urea) into the body

132
Q

clinical manifestations: tumor lysis syndrome

A
hyperuricemia 
hyperphosphatemia
hyperkalemia
hypocalcemia 
weakness
cramps
diarrhea
nausea/vomiting
133
Q

what is cardiac tamponade?

A

cancer accumulation in which fluid accumulates in the pericardium. pericardium is typically constricted by tumor or pericarditis secondary to radation

134
Q

clinical manifestations: cardiac tamponade

A
distant/muted heart sounds (may sound like listening through a well) 
heavy feeling chest 
SOB
cough
tachycardia
dysphagia
hoarseness
N/V
sweating
decreased LOC
anxiety
135
Q

what is carotid artery rupture?

A

cancer emergency usually caused by radiation to the head or neck in which the arterial wall is invaded by a tumor or eroded by surgery/radiation

136
Q

manifestations of carotid artery rupture

A

bleeding, ranging from mild oozing to spurting blood explosion from carotid artery

137
Q

in heart failure, what four problems in the body can lead to decreased cardiac output?

A

volume overload
pressure overload
myocardial disease
rapid heart rate

138
Q

what two specific problems will result from poor cardiac output?

A

decreased renal perfusion

increased autonomic nervous system stimulation

139
Q

decreased renal perfusion will trigger the activation of what?

A

RAAS (renin-angiotensin-aldosterone system)

140
Q

what does the RAAS do?

A

causes everything to constrict and increases sodium and water retention

141
Q

what is the end result of the RAAS?

A

increased blood volume

142
Q

what will result in the body because of increased autonomic nervous system stimulation?

A
vasoconstriction
increased systemic vascular resistance
pallor
sweating
tachypnea
tachycardia
143
Q

what is the end result in the heart when the RAAS and the autonomic nervous system are activated?

A

increased diastolic pressures in the left and right ventricles, which in turn increases pressure in the atriums

144
Q

what symptoms arise from increased right atrium pressure?

A

elevated jugular venous pressure
hepatomegaly
interstitial edema
poor GI absorption

145
Q

what symptoms arise from increased left atrium pressure?

A

pulmonary edema and associated pulmonary symptoms

146
Q

what formula/calculation determines the degree of heart failure?

A

ejection fraction

147
Q

what is ejection fraction?

A

a measurement of the percent of blood leaving the left ventricle every time it contracts

148
Q

what are some signs and symptoms of left sided heart failure?

A
paroxysmal nocturnal dyspnea
restlessness
confusion 
orthopnea
tachycardia
pulmonary congestion
fatigue
cyanosis
149
Q

what specific signs and symptoms indicate pulmonary congestion?

A
cough
crackles
wheezes
blood tinged sputum
tachypnea
150
Q

what is the most common cause of right sided heart failure?

A

left sided heart failure

151
Q

what are some signs and symptoms of right sided heart failure?

A
fatigue
increased peripheral venous pressure
ascites
enlarged liver and spleen
distended jugular veins
anorexia and GI distress
weight gain
dependent edema
152
Q

what are some things that can cause cardiac arrhythmias?

A

drugs, alcohol, caffeine, infection, shock, stress

153
Q

what are some labs and diagnostics that need to be monitored related to cardiac conduction and function?

A
ECG
BNP
CKP-MB
cardiac troponin
magnesium/calcium/potassium
154
Q

what is a PVC?

A

premature ventricular contraction: the ventricle beats independently without waiting to sequential conduction of other nodes

155
Q

how does one calculate heart rate on an ECG?

A

take 300 and divide it by the number of large boxes between QRS complexes

156
Q

describe v-tach and necessary interventions

A

wide and bizarre QRS complexes because just the ventricle action is seen.
shock, CPR, and epinephrine are needed

157
Q

describe v-fib and necessary interventions

A

just random waves with no pattern, very serious problem. needs shock, CPR, and epi

158
Q

describe supraventricular tachycardia and necessary interventions

A

very fast HR (up to 200 BPM). may be transient and require no intervention, or may need adenosine and a shock

159
Q

describe sinus bradycardia and necessary interventions

A

normal heart pattern at a very slow rate. give atropine and use artificial pacing if no response can be obtained

160
Q

what should be done for a patient in asystole?

A

CPR, oxygen, IV fluids, intubation, anything to get them back

161
Q

what should be done immediately for clients with chest pain? (think MONA)

A

morphine
oxygen
nitroglycerin
asprin

162
Q

what is the most common cause of acute MI?

A

atherosclerosis

163
Q

pathophysiology of MI

A

blockage of coronary artery/arteries causes prolonged ischemia of cardiac tissue, which causes necrosis and irreversible cell damage if not treated immediately

164
Q

STEMI

A

ST elevation (on EKG) MI. this is a more serious MI as the ischemia goes all the way to the endocardial wall

165
Q

NSTEMI

A

non-ST elevation MI. ischemia hasn’t progressed as far and there is more time for interventions

166
Q

what are manifestations of MI?

A
chest pain and pressure
initial HTN, then hypotension
elevated LDL
diaphoresis
dyspnea
extreme anxiety
pallor 
radiating pain and pressure (to shoulder, arm, jaw, or back)
fatigue
weak pulses
167
Q

what is the gold standard lab test when looking for MI?

168
Q

what does troponin measure?

A

how many cardiac cells have died. drawn repeatedly to look for bell curve of cell death

169
Q

what lab test will help determine if someone is headed for heart failure?

170
Q

what are risk factors for MI?

A
atherosclerosis
angina pectoris
diabetes
elevated LDL
smoking and tobacco use
family history
being male or being a post-menopausal woman