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Marie- NUR 280 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What happens in the ribosomes?

A

protein synthesis

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2
Q

what happens in the mitochondria?

A

energy production

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3
Q

What is aerobic energy production

A

energy production with O2

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4
Q

anaerobic energy production

A
  • energy production without O2
  • a lot less energy is produced
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5
Q

Should Na+ ions be higher or lower OUTSIDE of the cell

A

HIGHER

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6
Q

should K+ ions be higher or lower inside the cell

A

HIGHER

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7
Q

how does the sodium potassium pump work

A
  • it uses energy to actively transport across cell membrane
  • if the pump breaks/does not work, ions will be on the wrong side of the membrane (too much in or out of cell)
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8
Q

benign cells

A
  • looks like parent cell
  • cells line up in orderly fashion
  • cells know when to stop growing
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9
Q

malignant cells

A
  • contact inhibition
  • metastasize
  • grow over other things
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10
Q

What can result from Marfan’s syndrome?

A
  • abnormal chest, heart, and lung problems
  • eye problems
  • short torso
  • tall, thin body frame
  • long arms, legs, and fingers
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11
Q

normal WBC level

A

4,000-10,000 cells/mL

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12
Q

leukocytosis

A
  • high WBC
  • greater than 11,000
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13
Q

leukopenia

A
  • low WBC
  • fewer than 4,000
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14
Q

Are CRP and ESR increased or decreased during inflammation?

A
  • increased
  • they are non specific markers that tell us if there is inflammation but not where it is
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15
Q

What are the 5 cardinal signs of inflammation

A
  • redness
  • heat
  • swelling
  • pain
  • loss of function
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16
Q

how do wounds heal properly

A
  1. hemostasis: limit blood loss
  2. inflammation
  3. proliferation, granulation tissue formation, angiogenesis, epithelization
  4. wound contraction and remodeling
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17
Q

healing by primary intention

A
  • simple reapproximation of edges of wound
  • simple reepithelialization
  • best outcome of healing
  • surgical incision type of healing
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18
Q

healing by secondary intention

A
  • gap in the tissue
  • prolonged healing involving generation of granulation tissue and more complex tissue
  • scar tissue formation/deformity
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19
Q

healing by tertiary intention

A
  • gap n the tissue
  • contaminated wound
  • temporary loose closure to allow for drainage
  • firm closure of wound after decontamination
  • skin graft often needed
  • scar tissue/deformity
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20
Q

innate immunity

A
  • born with it
  • nonspecific response
  • cannot be transferred
  • inflammatory process is part of it
  • ex. skin, cilia
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21
Q

acquired immunity

A
  • get it from contact with a pathogen
  • specific response to invasion
  • B- cells: memory, make antibodies
  • T cells: cell mediated immunity
  • recognize self vs non self
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22
Q

How does inflammation work in immunity

A
  • it is part of innate immunity
  • immunocompetence plays an important role in immune response and risk for inflammatory response
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23
Q

natural active immunity

A
  • longest lasting immunity
  • person in natural world comes in contact with antigen
  • your body actively makes the antibodies
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24
Q

artificial active immunity

A
  • vaccines, boosters
  • you artificially get the antigen but your body actively makes the antibody
  • not as long lasting but you can re up it
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25
Q

natural passive immunity

A
  • mom to baby
  • mom’s body makes the antibody and passes them to baby
  • temporary
  • given to baby through placenta or breastmilk
  • when the antibody dies, baby cannot make more
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26
Q

artificial passive immunity

A
  • antibody is artificially acquired
  • only lasts for the life of the antibody
  • given to people that are very sick
  • ex. immunoglobulin infusion
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27
Q

type 1 hypersensitivity: immediate hypersensitivity

A
  • B cell mediated
  • hives, nasal discharge, bronchial asthma, allergic gastroenteritis
  • can lead to anaphylaxis (inflammatory response so large that the airway closes, body is producing too much IgE)
  • when anaphylaxis occurs STOP ALLERGEN
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28
Q

type 2 hypersensitivity: cytotoxic hypersensitivity

A
  • Igs attack antigens on the cell surface
  • antibody-mediated cell lysis results (bc the body wants to kill it off)
  • ex. blood transfusion reaction
  • s/s blood transfusion reaction: high temp, may have itchiness, BP changes, HR changes
  • STOP INFUSION if any reaction occurs, do not flush
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29
Q

type 3 hypersensitivity: immune complex hypersensitivity

A
  • antigen-antibody (immune) complex deposited in tissues
  • tissue damage results
  • may be systemic (lupus) or localized (RA)
  • results in constant inflammatory response
  • most of the the the antigen is unknown
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30
Q

type 4 hypersensitivity: delayed hypersensitivity

A
  • previous exposure to antigen primes the T cells
  • T cell attack does not occur until days after initial exposure
  • ex. poison ivy, transplant rejection
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31
Q

where is extracellular fluid located

A

the bloodstream

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32
Q

where is intracellular fluid located

A

inside of cells

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33
Q

hydrostatic pressure

A
  • pushing force that pushes water from ECF into ICF
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34
Q

oncotic pressure

A
  • the pulling force created by albumin, which favors fluid movement from the ICF into the ECF
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35
Q

why is albumin important

A
  • when you lose albumin, oncotic pressure drops and hydrostatic pressure kicks up
  • in a constant inflammatory state albumin will leak out of cells
  • keeps fluid in the cells
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36
Q

hypotonic solution

A
  • more water than blood
  • causes shift from ECF to ICF
  • 0.45% NaCl
  • given for dehydration, for keeping veins open
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37
Q

Isotonic solution

A
  • same tonicity as blood
  • no fluid shifts or change in cell size
  • NaCl, Lactated ringers, D5 0.9% NaCl
  • given to hydrate patients who are NPO
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38
Q

hypertonic solution

A
  • more blood than water
  • causes fluid to shift from ICF into ECF, draws water out of cell
  • 3% NaCl, mannitol
  • given for cellular edema
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39
Q

Why is the RAAS system activated

A

the kidneys want more blood because they aren’t perfusing, this causes blood pressure and blood volume to go UP

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40
Q

normal Na levels

A

135-145

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41
Q

normal K+ levels

A

3.5-5.2

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42
Q

normal Ca levels

A

8.7-10

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43
Q

normal PO4 levels

A

2.5-4.5

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44
Q

normal Mg++ levels

A

1.5-2.5

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45
Q

s/s hypovolemic hyponatremia

A
  • thirst
  • hypotension
  • tachycardia
  • neurological deficits may develop
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46
Q

s/s hypervolemic hyponatremia

A
  • headache
  • lethargy
  • confusion
  • muscle cramps
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47
Q

s/s hypokalemia

A
  • anorexia
  • nausea
  • vomiting
  • sluggish bowel
  • cardiac arrhythmias
  • postural hypotension
  • muscle fatigue and weakness
  • leg cramps
  • prolonged PR interval
  • flattened T waves
  • digitalis toxicity
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48
Q

s/s hyperkalemia

A
  • numbness
  • muscle cramps all over
  • diarrhea
  • ECG changes
  • can lead to cardiac arrest
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49
Q

s/s hypocalcemia

A
  • neuromuscular excitability
  • paresthesia
  • hypotension
  • cardiac arrhythmias
  • chronic: bone pain and fragility
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50
Q

s/s hypercalcemia

A
  • decreased neuromuscular excitability
  • weakness
  • renal calculi
  • cardiac arrhythmias
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51
Q

s/s hypophosphatemia

A
  • tremors
  • muscle weakness
  • hyporeflexia
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52
Q

s/s hyperphosphatemia

A
  • same as hypocalcemia
  • neuromuscular excitability
  • paresthesia
  • hypotension
  • cardiac arrhythmias
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53
Q

s/s hypomagnesemia

A
  • usually occurs in conjunction with hypocalcemia and hypokalemia
  • anorexia
  • nausea
  • vomiting
  • sluggish bowel
  • cardiac arrhythmias
  • postural hypotension
  • muscle fatigue and weakness
  • leg cramps
  • prolonged PR interval
  • flattened T waves
  • digitalis toxicity
  • neuromuscular excitability
  • paresthesia
  • hypotension
  • cardiac arrhythmias
  • chronic: bone pain and fragility
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54
Q

s/s hypermagnesemia

A
  • too much neuromuscular relaxation
  • muscular flaccidity
  • cardiac problems
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55
Q

characteristics of arteries

A
  • carry oxygenated blood AWAY from the heart
  • pump blood themselves
  • high pressure system
  • responsible for PULSES
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56
Q

arteriosclerosis

A

hardening/narrowing of the arteries

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57
Q

atherosclerosis

A

plaque buildup in arteries

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58
Q

risk factors for peripheral artery disease (PAD)

A
  • gender (men have greater risk than women)
  • age
  • diabetes mellitus type 2
  • family hx
  • tobacco use
  • hypertension
  • obesity
  • lifestyle factors
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59
Q

What is the treatment for PAD?

A
  • lifestyle modification: diet, exercise, no smoking
  • medications
  • peripheral arterial revascularization procedures help restore circulation
  • open surgical bypass grafting
  • dangle legs
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60
Q

what is the primary sign of PAD

A

intermittent claudication

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61
Q

characteristics of veins

A
  • thein walled, flexible
  • return “trash” blood to the heart
  • rely on skeletal muscle pump and valves
  • can stretch and hold a lot of fluid which can = edema
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61
Q

What is Virchow’s triad

A
  • venous stasis
  • vascular damage
  • hypercoagulability
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62
Q

chronic venous insufficiency

A
  • results from damage to deep veins in legs/ incompetent valves which causes impaired venous return
  • edema d/t pooling blood
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63
Q

clinical presentation CVI

A
  • thin, shiny skin
  • dusky discoloration
  • edema
  • poor healing
  • reduced/absent hair distribution
  • stasis dermatitis
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64
Q

How do we treat CVI

A
  • elevate legs
  • wear compression stockings all the time
  • SCDs
  • anticoagulant or antiplatelet meds
  • venoablation
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65
Q

normal platelet values

A

150,000-400,000

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66
Q

thrombocytopenia

A
  • low platelet count
  • less than 100,000
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67
Q

thrombocytosis

A
  • high platelet count
  • greater than 750,000
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68
Q

what is pt at risk for with platelet count too low

A

risk for bleeding

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69
Q

what is pt at risk for with platelet count too high

A

risk for clotting

70
Q

extrinsic pathway

A
  • activated when there is injury to the blood vessel from the outside in
  • Factor 7 and tissue factor only
71
Q

what lab is extrinsic pathway measured with

A

PT/INR

72
Q

intrinsic pathway

A
  • activated when there is injury to the blood vessel from inside out
73
Q

what lab is intrinsic pathway measured with

A
  • PTT (Play Table Tennis inside)
  • the higher to PTT the higher the risk for bleeding
74
Q

aspirin

A
  • most common antiplatelet drug
  • acts on platelets for the life of the platelet
75
Q

warfarin

A
  • better for venous clots
  • inhibits Vitamin K
  • interferes with vitamin K dependent clotting factors
  • monitor with PT/INR
76
Q

heparin

A
  • better for arterial clots
  • slows or stops the coagulation pathway
  • monitor with PTT
  • inhibits intrinsic pathway
77
Q

What is DIC

A
  • disorder of clot formation and bleeding episodes
  • clot formation
  • depletion of coagulation
  • elevated fibrinolysis leads to bleeding
78
Q

What type of patient does DIC happen in?

A
  • critically ill
  • develops secondary to other significant disorders, such as septic shock, massive trauma, burns, transfusion
79
Q

how is DIC diagnosed

A
  • elevated D-dimer
  • clotting times
  • RBC hemolysis
80
Q

how is DIC treated

A
  • control primary disease
  • prevent further clotting
  • transfuse with FFP (fresh frozen plasma)
81
Q

what is pyelonephritis

A
  • infection of renal pelvis
  • ascending UTI
  • stasis of urine plays a role
82
Q

what is pyelonephritis caused by

A
  • obstruction somewhere in the renal system
  • urine backs up into the kidneys
83
Q

s/s pyelonephritis

A
  • fever
  • abdominal or CVA tenderness
  • flank pain
  • dysuria
  • urinary frequency
  • microscopic hematuria
  • pyuria (WBC in urine)
    • leukocyte esterase test of urine
84
Q

treatment for pyelonephritis

A
  • abx
  • analgesics if needed
  • fluid intake greater than 3 L/day
  • remove urological obstruction, if present
85
Q

what are complications fo pyelonephritis

A
  • chronic pyelonephritis
  • which deteriorates into chronic renal insufficiency, which may develop into end stage renal disease
86
Q

what is nephrolithiasis

A

stones in kidneys

87
Q

risk factors for nephrolithiasis

A
  • genetic susceptibility
  • dehydration
  • hypercalcemia
  • hyperparathyroidism
  • gout
  • hyperuricemia
  • urinary tract infection
  • immobility
88
Q

lower urinary tract infection

A
  • most commonly caused by E. coli, originating from bowel
  • women at higher risk
  • stagnant urine increases infection risk
89
Q

risk factors for lower UTI

A
  • female
  • poor hygiene
  • taking baths
  • BPH
  • tight clothing
  • dehydration
  • diabetes
  • sexual intercourse
  • pregnancy
  • bladder cancer, urinary catheterization (in men)
90
Q

s/s lower UTI

A
  • increased frequency, dysuria, and urgency
  • hematuria
  • fever (not always present)
91
Q

s/s lower UTI

A
  • increased frequency, dysuria, and urgency
  • hematuria
  • fever (not always present)
92
Q

How can we prevent UTIs?

A
  • patient education
  • shower rather than bathe
  • wipe from front to back
  • drink liberal amounts of fluids daily to flush out bacteria, may be helpful to drink 1 glass of cranberry juice a day
  • avoid fluids that are urinary tract irritants (coffee, tea, alcohol)
  • void every 2-3 hours and completely empty the bladder
  • take medication exactly as prescribed
  • notify PCP if symptoms persist
  • consult primary provider regularly for follow up
93
Q

potential complications of UTIs

A
  • urosepsis
  • ascending UTI becomes pyelonephritis
94
Q

chronic renal failure

A
  • characterized by dropping GFR
  • irreversible and progressive, with gradual onset
  • usually progresses to ESRD
  • hemodialysis or kidney transplant needed
  • DM, HTN are leading causes
95
Q

leading causes of CRF

A
  • DM
  • HTN
96
Q

s/s CRF

A
  • CBC, BUN, and Cr serum levels, urinalysis, albumin levels
  • renal imaging studies
97
Q

treatment for CRF

A
  • fluida and electrolyte management, along with BP management
  • GFR less than 10-20 mL/min- dialysis, kidney transplant evaluation
98
Q

potential complications of CRF

A
  • encephalopathy
  • hyperparathyroidism
  • heart failure
  • infertility
  • thrombocytopenia
  • anemia
  • electrolyte imbalance
  • high BUN
  • edema
99
Q

is asthma obstructive or restrictive

A

obstructive

100
Q

asthma

A
  • hyperreactive airway disease of bronchioles
101
Q

how is asthma diagnosed

A

PFT during an acute asthma attack

102
Q

treatment for asthma

A
  • stepwise approach
  • maintenance medications: daily
  • rescue: acute attack
  • limit exposure to allergens, know triggers
103
Q

COPD

A
  • must have in combination chronic bronchitis and emphysema, and hyperreactive airways
  • smoking is a MAJOR cause
  • genetic and environmental factors
  • SEVERE COPD results in Cor Pulmonale
104
Q

what do alveoli look like in chronic bronchitis

A

shrunken alveoli

105
Q

what do alveoli look like in emphysema

A
  • distended, nonrecoiling alveoli
  • alveoli lose elasticity
106
Q

how is COPD diagnosed

A
  • COPD assessment test
  • PFT’s
  • CBC, chest x-ray, ABG’s, ECG
107
Q

how is COPD treated

A
  • stepwise approach with medications
  • smoking cessation, pulmonary rehabilitation, vaccinations
  • oxygen therapy: continuous oxygen when PaO2 less than 55 mm Hg or SaO2 less than 88%
  • teaching pursed lip breathing
108
Q

s/s emphysema

A
  • “pink puffer”
  • SOB and scant sputum production
  • thin, cachectic, rosy skin tones
  • adventitious sounds are less common
  • sputum is scant and like evaporated milk
  • dyspnea before cough
  • barrel chest
  • use of accessory muscles
109
Q

s/s chronic bronchitis

A
  • “blue bloater”
  • chronic, productive cough
  • often overweight, obese
  • rhonchi and wheezes
  • copious, purulent drainage like condensed milk
  • cyanotic
  • peripheral edema
  • ** cough 3 months of year for at least 2 years
110
Q

primary pneumothorax

A

just happens , no underlying disease process

111
Q

secondary pneumothorax

A

lung collapses because of underlying disease process

112
Q

traumatic pneumothorax

A

penetrating wound to thoracic cage and pleural membrane

113
Q

tension (closed) pneumothorax

A

closed wound that allows air into the pleural cavity but not out

114
Q

iatrogenic pneumothorax

A

caused by any medical procedure complications, can often be a parting gift from central line insertion

115
Q

how are primary, secondary, traumatic, and iatrogenic pneumothorax treated

A

chest tube with suction

116
Q

how is a tension pneumothorax treated

A

needle insertion to remove air

117
Q

pleural effusion

A
  • abnormal collection of fluid in pleural space
  • results of heart failure, severe pulmonary infections
  • fluid can be exudate, transudate, purulent, lymph, blood
118
Q

s/s pleural effusion

A
  • dyspnea
  • tachypnea
  • sharp pleuritic CP
  • dullness to percussion
  • diminished breath sounds on affected side, maybe even absent over area of effusion
119
Q

treatment for pleural effusion

A

thoracentesis

120
Q

thoracic cage deformity

A
  • anything that structurally makes it hard for lungs to fully inflate
  • kyphosis, scoliosis
121
Q

treatment for cage deformity

A

orthopedic brace

122
Q

pulmonary fibrosis

A
  • may be idiopathic: repeated injury to the alveoli that we do not know the cause is
  • may be caused by environmental particles like coal, dust, asbestos, silica, anthrax
  • fibrotic changes decrease lung compliance, lungs become stiff because of repeated inflammation to the alveoli
123
Q

s/s pulmonary fibrosis

A
  • dyspnea
  • tachypnea
  • crackles
  • eventual cyanosis
  • CXR results in “ground glass” appearance
124
Q

treatment for pulmonary fibrosis

A
  • try to decrease inflammation/inflammatory response
  • may treat with O2
  • bronchodilators, corticosteroids
125
Q

pulmonary edema

A
  • edema in the pulmonary veins
  • often caused by heart failure
  • blood backs up into the veins of the lungs and increases pressure
  • when the pressure is too great, fluid is pushed in to the alveoli of the lungs
126
Q

pulmonary embolism

A

DVT dislodges and travels to lungs

127
Q

pulmonary hypertension

A
  • high blood pressure that affects arteries in the lungs, right side of heart, walls of pulmonary arteries become thick and stiff and cannot expand very well to allow proper blood flow
128
Q

what is ARDS

A
  • adult respiratory distress syndrome
  • injury to alveoli, pulmonary capillaries causes sudden, progressive pulmonary edema called flash pulmonary edema
  • arterial hypoxemia does not improve with administration of O2
129
Q

who is at risk for ARDS

A
  • critically ill patients
  • sepsis
  • trauma
  • massive transfusions
  • acute pancreatitis, aspiration
130
Q

what does ARDS require

A
  • intubation, sedation, and mechanical ventilation
  • death is common
131
Q

Crohn’s disease

A
  • lesions can be anywhere gum to bum
  • skip lesions
  • cobblestone appearance
  • RLQ abdominal pain
132
Q

What is a potential complication of Crohn’s disease

A

toxic megacolon

133
Q

ulcerative colitis

A
  • involves large intestine only
  • isolated to the colon and rectum
  • ulceration is continuous
  • LLQ abdominal pain
  • bleeding often occurs
134
Q

GERD

A
  • problem with tone of LES
  • regurgitation of stomach acid into esophagus
135
Q

selye’s stress response theory

A
  1. alarm
  2. resistance
  3. exhaustion
136
Q

binge eating

A

when you just keep eating with no intention of getting rid of food (like inducing vomiting)

137
Q

effects of immobility

A
  • atelectasis
  • bone demineralization
  • muscle deconditioning
  • decubitus ulcers
  • depression
  • decreased GI motility
  • kidney stones
  • decreased pulmonary function
  • UTI
  • venous stasis
138
Q

metabolic alkalosis

A
  • vomiting
  • diarrhea
  • NG tube suction
  • low K+
  • low Ca
    Tx: treat underlying cause
139
Q

metabolic acidosis

A
  • diabetics and ketoacidosis
  • high K+
  • high Ca
  • Tx: treat underlying cause
140
Q

respiratory alkalosis

A
  • breathing too much CO2 off
  • hyperventilation
  • high RR
  • panic attack
  • breath into paper bag
141
Q

respiratory acidosis

A
  • holding onto CO2
  • overdose
  • low RR
142
Q

normal pH levels

A

7.35-7.45

143
Q

normal PCO2 levels

A

35-45

144
Q

normal bicarb levels

A

22-26

145
Q

fasting blood glucose level for diabetes diagnosis

A

126 or greater

146
Q

OGTT result for diabetes

A

200 or greater

147
Q

random glucose level for diabetes diagnosis

A

200 or greater

148
Q

A1C level for diabetes diagnosis

A

6.5% or higher

149
Q

what will urinalysis show in diabetes

A
  • ketones
  • glucose
150
Q

hyperglycemia cause

A
  • stress
  • illness
  • eating too much
  • dehydration
  • lack of exercise
151
Q

s/s hyperglycemia

A
  • polydipsia
  • polyuria
  • polyphagia
  • blurred vision
  • electrolyte imbalances
152
Q

treatment for hyperglycemia

A
  • reverse process
  • give insulin
153
Q

hypoglycemia cause

A
  • taking too much insulin
  • not eating enough carbs
  • strenuous exercise
154
Q

hypoglycemia s/s

A
  • sweating
  • hunger
  • dizziness
  • nervousness
  • tremulousness
  • irritability
  • headache
  • heart palpitations
  • confusion
  • disorientation
  • inability to concentrate
  • seizures
  • stupor or loss of consciousness
  • blurred vision
155
Q

hypoglycemia treatment

A
  • if awake: EAT, foods high in SUGAR
  • if asleep: inject DEXTROSE
156
Q

what does the anterior pituitary secrete

A
  • growth hormone
  • adrenocorticotropic hormone
  • TSH
  • FSH
  • LH
  • prolactin
157
Q

what does the posterior pituitary secrete

A
  • oxytocin
  • ADH
158
Q

what does thyroid control

A

METABOLISM

159
Q

hypothyroidism

A
  • couch potato
  • hypercholesterolemia
  • gains wt easily
  • decreased fertility
  • delayed reflexes
  • sluggishness
  • feeling cold
  • constipation
  • lethargy
  • fatigue
160
Q

hyperthyroidism

A
  • hyperdrive
  • anxiety
  • tremor
  • tachycardia
  • feeling warm
  • wt loss
  • exophthalmos
  • atrial fibrillation
  • decreased fertility
161
Q

which electrolyte goes with parathyroid

A

calcium and albumin

162
Q

SIADH

A
  • holding onto water
  • excess ADH
  • tells kidneys not to diurese
163
Q

s/s SIADH

A
  • same as fluid overload
  • hypertension
  • swelling
  • SOB
164
Q

DI

A
  • insufficient ADH
  • kidneys are not told to stop diuresing so you get rid of all your fluid
165
Q

s/s DI

A
  • same as dehydration
  • hypotension
  • dry mouth
  • feeling thirsty
  • fatigue
  • dark urine
166
Q

diagnostics for SIADH and DI

A

check adh levels

167
Q

treatment for SIADH and DI

A

fix underlying cause- pituitary

168
Q

Addison’s disease

A
  • adrenal insufficiency
  • low sodium
  • everything low
169
Q

s/s addisons

A
  • tan skin
  • weight loss
  • fatigue
  • muscle weakness
  • light headed
170
Q

Cushing’s

A
  • too much cortisol
  • immune system depressed
171
Q

s/s cushings

A
  • wt gain
  • neck fat/humpback
  • moon facies
  • easy bruising
  • striae
  • muscle weakness
172
Q

end organ examples

A
  • bones
  • adrenal cortex
  • adrenal medulla
  • thyroid
  • parathyroid
  • testes/ovaries
  • mammary glands
  • uterus
  • kidneys

Marie- NUR 280 (12 decks)

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