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N398 > Midterm > Flashcards

Midterm Flashcards

1
Q

What are three things cells can do when presented with a challenge?

A
  1. withstand and return to normal (reversible)
  2. adapt if stress removed
  3. die (irreversible)
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2
Q

Hydropic cellular response

A

an accumulation of water inside the cell; reversible; 1st manifestation of most forms of cell injury; results from malfunction of Na-K pumps (swelling of cells and organs)

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3
Q

what are 3 ways that intracellular accumulations occur?

A
  1. excessive amounts of normal intracellular substances (ex. proteins, lipids, carbs)
  2. accumulation of abnormal substances produced by cells because of issues (ex. cellular stress –> broken down parts)
  3. accumulation of pigments and particles that cell is unable to degrade (ex. hyperbilirubanemia)
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4
Q

What is atrophy and what are 3 causes?

A

cells shrink and reduce their differentiated function in an effort to reduce energy

  1. disuse
  2. ischemia
  3. nutrition/starvation
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5
Q

What is hypertrophy?

A

increase in cell size accompanied by augmented functional capacity

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6
Q

what is hyperplasia?

A

increase in number of cells by mitotic division

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7
Q

What is metaplasia?

A

replacement of one differentiated cell type with another

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8
Q

What is an example of metaplasia?

A

smokers –> chronic irritation, bronchial mucosa changes to handle stress

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9
Q

What is dysplasia?

A

disorganized appearance of cells because of abnormal variations in size, shape and arrangement

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10
Q

What happens with necrosis?

A

external injury (toxic, deathly injury, ischemia) leading to cell rupture; intracellular contents spill out leading to inflammation; ex. heart attack

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11
Q

What happens with apoptosis?

A

natural time for cell death, signal to die; no membrane rupture so no inflammatory process; organized; phagocytes eat cell fragments; ex. dementia

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12
Q

What is the difference between hypoxia and ischemia?

A

hypoxia - poor oxygenation

ischemia - interruption of blood flow

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13
Q

What does a lack of oxygen in cells lead to?

A

plasma, mitrochondrial, and lysosomal membranes critically damaged = cell death

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14
Q

What is the mechanism of action of hypoxia/ischemia?

A
  1. ATP production in cell stalls
  2. ATP-dependent pumps fail
  3. NA accumulates and brings water inside cell
  4. excess Ca in mitochondria interferes
  5. glycogen stores depleted
  6. lactate produced
  7. pH falls - cellular components more dysfunctional
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15
Q

What are three results of reperfusion injury?

A
  1. calcium overload - washes cells with calcium, triggers apoptosis
  2. formation of ROS (free radicals) - unpaired electrons steal hydrogen from another molecule (ex. diabetes, autoimmune)
  3. inflammation - days to weeks; body’s way to right the wrong
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16
Q

What is a reperfusion injury?

A

tissue damage caused when blood supply returns to tissue after period of ischemia or hypoxia

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17
Q

What are nutritional injuries to cells?

A

deficiencies (iron, vitamin D, protein, malabsorption) or excess (sodium, diabetes, obesity)

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18
Q

What are chemical injuries to cells

A

free radicals; heavy metals; toxic gases

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19
Q

WHat are physical and mechanical injuries to cells?

A

temperature extremes; atmospheric pressure changes; abrasion/trauma; electrical burns; radiation

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20
Q

What are 2 ways that radiation causes cell damage?

A
  1. directly to cell DNA

2. creates free radicals leading to necrosis

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21
Q

What are endotoxins?

A

toxins inside cell wall of bacteria that release into body when bacteria is destroyed

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22
Q

What are exotoxins?

A

produced and excreted by bacteria; protective mechanism; interferes with cell function around cell

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23
Q

What is Cox 1 responsible for?

A

found in most tissues; responsible for synthesizing prostaglandins that maintain gastric mucosa and renal function

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24
Q

What is Cox 2 responsible for?

A

normally not present in healthy cells; produced by presence of inflammation; causes pain, fever and inflammation

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25
Q

MOA of aspirin

A

nonselective, irreversible inhibitor of cox

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26
Q

therapeutic uses of aspirin

A

inflammation suppression, analgesia, anttipyretic, prevention of platelet aggregation

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27
Q

What population should not receive aspirin and why

A

pediatrics - causes Reye’s syndrome: encephalopathy and fatty liver

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28
Q

AEs of aspirin

A

GI effects, bleeding, renal impairment, salicyclate toxicity (presents with mixed metabolic acidosis), ringing in ears

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29
Q

Drug interactions of aspirin

A

NSAIDs, glucocorticoids (GI, ulcer), anticoagulants (bleeding risk)

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30
Q

mu receptor effects

A

analgesia, respiratory depression, euphoria, sedation, decreased GI motility, physical dependence

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31
Q

kappa receptor effects

A

analgesia, sedation, decreased GI motility

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32
Q

Morphine therapeutic uses

A

pain relief

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33
Q

morphine MOA

A

mimics endogenous opioid peptides primarily at mu receptor

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34
Q

morphine drug interactions

A

CNS depressants, anticholinergic drugs (urinary retention, acetylcholine/histamine/muscarinic receptors), hypotensive drugs

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35
Q

AEs of morphine

A

respiratory depression, constipation, orthostatic hypotension, urinary retention, cough suppression, biliary colic, emesis, sedation, euphoria

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36
Q

What is neonate breathing initiated by?

A
  1. sudden exposure to world

2. slight asphyxiation

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37
Q

What are 4 causes of prolonged hypoxia in neonates

A

umbilical cord compression, premature separation of placenta, excessive contraction force, aesthetics

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38
Q

What is needed to open collapsed alveoli in neonates?

A

negative intraplural pressure

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39
Q

What is the role of surfactant?

A

decreases surface tension of alveolar fluid and allows easier open

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40
Q

Pulmonary resistance needed in neonate circulation

A

decreased pulmonary vascular resistance - reduces resistance to blood flow through lungs

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41
Q

systemic resistance needed in neonate circulation

A

increased systemic vascular resistance - increased aortic pressure and pressure in left A and V

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42
Q

What is the chain of infection transmission?

A

infectious agent - reservoir - portal of exit - mode of transmission - portal of entry - host

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43
Q

What is a n agent/pathogen/microbe?

A

some disease-causing organism; ex. bacteria, parasite, virus, fungi

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44
Q

What are 5 ways to break the chain of transmission?

A

destroy reservoir, block portal of exit, block mode of transmission, block portal of entry, reduce victim’s susceptibility

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45
Q

What are three potential relationships between host and pathogen?

A
  1. symbiosis: benefit only to human, no harm to microbe
  2. mutualism: benefit to human and microbe
  3. commensalism: benefit only to microbe, no harm to human
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46
Q

What is pathogenicity?

A

potential for pathogen to cause a disease; benefits organism and harms host

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47
Q

What are some physical and mechanical barrier characteristics of a host?

A

epithelial cells in skin/respiratory/GI tract, mucous membranes, cough/sneeze/urination/defecation, mucus/sweat/tears

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48
Q

What are 5 host risk factors?

A

age, nutritional status, chronic illness, immunosuppression, chronic stress

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49
Q

What are the three lines of host defense?

A
  1. physical and mechanical barriers
  2. innate inflammatory response - vasodilation, emigration, phagocytosis
  3. acquired immunity - antigens
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50
Q

What are the microbe characteristics?

A

pathogenicity/virulence, adherence, invasion, endotoxins/exotoxins, bacterial enzymes, anti-phagocytic factors (coating), endospore protection, mobility, increased microbial resistance

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51
Q

What are the characteristics of bacteria?

A

single cell, rigid cell wall, no internal organelles, shapes (cocci, bacilli, spiral), gram stains, anaerobic or aerobic

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52
Q

Classification of amoxicillin

A

broad spectrum penicillin antibiotic

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53
Q

Major use of amoxicillin

A

G+ and G- coverage; some anaerobic coverage; renally eliminated; treats UTIs, respiratory/oral/skin infections; bacteriocidal

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54
Q

MOA amoxicillin

A

destroys bacteria by weakening the cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition of autolysins

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55
Q

AEs of amoxicillin

A

allergies, anaphylaxis, renal impairment, diarrhea

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56
Q

nursing actions of amoxicillin

A

take with food and water; additional contraception method

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57
Q

Classification of amoxicillin + clavulanic acid

A

broad spectrum penicillin antibiotic

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58
Q

major use of amoxicillin + clavulanic acid

A

G+/- and some anaerobic coverage; bacteriocidal; extends to cover organisms that are beta-lactam producing; renally eliminated

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59
Q

MOA of amoxicillin + clavulanic acid

A

aminopenicillin + beta-lactamase inhibitor; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins

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60
Q

AEs of amoxicillin + clavulanic acid

A

hypersensitivity; diarrhea (increased risk due to beta-lactamase inhibitor)

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61
Q

Nursing actions for amoxicillin + clavulanic acid

A

take with meals; additional contraception methods

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62
Q

classification of Piperacillin + tazobactum

A

antipsuedomonal penicillin antiobiotic (IV)

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63
Q

major use of Piperacillin + tazobactum

A

extended broad spectrum coverage of G+/- and anaerobes; covers more nosocomial; penicillin + beta-lactamase inhibitor; bacteriocidal

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64
Q

MOA of Piperacillin + tazobactum

A

antipseudomonal penicillin; destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins

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65
Q

AEs of Piperacillin + tazobactum

A

allergies, anaphylaxis, renal impairement, diarrhea

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66
Q

Nursing actions for Piperacillin + tazobactum

A

take with food, additional contraceptive method

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67
Q

classification of cefalexin

A

1st generation cephalosporin for PO antibiotic use

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68
Q

major use of cefalexin

A

mainly G+ skin flora; bacteriocidal; renally eliminated

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69
Q

MOA of cephalexin

A

destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins

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70
Q

AEs of cephalexin

A

hypersensitivity, nausea, vomiting, diarrhea

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71
Q

nursing actions for cephalexin

A

take with food

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72
Q

classification of ceftriaxone

A

3rd generation cephalosporin antibiotic for IM or IV (no PO

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73
Q

major use of ceftriaxone

A

some G+/- coverage; great CNS penetration (meningitis or CSF infections)

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74
Q

MOA of ceftriaxone

A

destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins

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75
Q

AEs of ceftriaxone

A

hypersensitivity, increases in bleeding

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76
Q

Nursing actions for ceftriaxone

A

avoid in neonates (displaces bilirubin); concomitant use with IV calcium-containing solutions/products in neonates; TPN contraindicated

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77
Q

classification of azithromycin

A

macrolide antibiotic

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78
Q

major use of azithromycin

A

broad spectrum bacterostasis (can become -cidal at high levels); can cover atypical organisms

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79
Q

MOA of azithromycin

A

reversibly binds to 50s subunit inhibiting protein synthesis; slows growth of microorganisms by inhibiting protein synthesis (static), but it is bacteriocidal at high doses)

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80
Q

AEs of azithromycin

A

GI discomfort, prolonged QT intervals - QT prolongation are contraindications

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81
Q

classification of doxycycline

A

tetracyclin antibiotic

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82
Q

major use of doxycycline

A

broad spectrum bacteriostatic; used to treat G+/-; tick borne illness

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83
Q

MOA of doxycycline

A

protein synthesis inhibition at 30s subunit

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84
Q

AEs of doxycycline

A

photo-toxicity, tooth discoloration in pregnancy and children under 8; associated with development of C.diff associated diarrhea

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85
Q

nursing actions for doxycycline

A

binds to cations (Mg, K) so avoid admin with milk, antacids; oral contraceptives

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86
Q

What are the four clinical infectious disease stages?

A

incubation, prodromal, illness, convalescence

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87
Q

Classification of metronidazole

A

antiprotozoal

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88
Q

major use of metronidazole

A

protozoas, anaerobic bacteria, narrow spectrum bacteriocidal

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89
Q

MOA of metronidazole

A

inhibits nucleic acid synthesis = cell death

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90
Q

drug interactions of metronidazole

A

ethanol (disulfiram reaction - facial flushing, vomiting, dyspnea, tachycardia); CYP3A4 substrate (warfarin, phenytoin)

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91
Q

AEs of metronidazole

A

N/HA, metallic taste, hypersensitivity

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92
Q

classification of fluconazole

A

antifungal

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93
Q

major use of fluconazole

A

SC/systemic; commonly used for candida infections

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94
Q

MOA of fluconazole

A

inhibition of CYP450-dependent synthesis of ergosterol (can’t continue to form fungus)

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95
Q

AEs of fluconazole

A

N/HA, rash, abdominal pain, rare - hepatic necrosis (monitor liver function)

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96
Q

drug interactions of fluconazole

A

CYP 450 - inhibition of 3A4

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97
Q

What is relative anemia?

A

normal total RBS mass with increased plasma volume; ex. pregnancy

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98
Q

What is absolute anemia?

A

decreased number of RBCs

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99
Q

What are 2 ways anemias can be classified?

A
  1. size and color

2. underlying issue

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100
Q

What are the etiologic events of anemia?

A

decrease in RBCs/hemoglobin/hypoxemia -> tissue hypoxia (low level s/s such as claudicatino, weakness, fatigue, pallor, increased RR, dizziness, lethargy, liver fatty changes) -> compensatory mechanisms SNS response of epi/norepi (increased heart rate, stimulation of bone marrow, capillary dilation, increased RAAS, increased of DPG protein which helps Hgb release O2), retain volume

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101
Q

What is the mechanism of aplastic anemia (decreased RBC production)?

A

bone marrow suppression leads to decreased production (toxic, radiant, immune injury)

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102
Q

What is the mechanism of anemia of chronic disease (decreased RBC production)?

A

chronic infection, inflammation, malignancy leads to increased demand or suppression

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103
Q

WHat is the mechanism of folate deficiency (decreased RBC production)?

A

lack of folate leads to premature cell death

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104
Q

What is the mechanism of iron deficiency (decreased RBC production)?

A

lack of iron leads to lack of hemoglobin

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105
Q

What is the mechanism of thalassemia (inherited disorder?)

A

congenital - impaired synthesis of hemoglobin chain

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106
Q

What is the mechanism of sickle cell (inherited disorder)?

A

congenital - abnormal hemoglobin molecule

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107
Q

What is the mechanism of hemolytic disease of newborn (extrinsic RBC destruction or loss)?

A

maternal antibodies case destruction of fetal cells

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108
Q

What is the mechanism of acute blood loss (extrinsic RBC destruction or loss)?

A

blood loss leads to insufficient RBC

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109
Q

What are the clinical maifestations of mild anemia?

A

no symptoms

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110
Q

What are the clinical manifestations of mild to moderate anemia?

A

fatigue, generalized weakness, loss of stamina, tachycardia, exertional dyspnea

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111
Q

What are the clinical manifestations of moderate to severe anemia?

A

orthostatic hypotension, tachycardia, transient murmor, vasocontriction/pallor, tachypnea, angina pectoris, intermittent claudication, night muscle cramps, HA/light headed/ faint,, tinnitus

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112
Q

Evaluation of anemia

A

labs (H&H, blood smear), bone marrow aspiration

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113
Q

treatment of anemia

A

erythropoitin, blood transfusion, supplements, rest/O2, fluids

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114
Q

classification of iron deficiency anemia

A

microcytic-hypochromic

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115
Q

Etiology of iron deficiency anemia

A
  1. body’s diminished capacity to absorb iron
  2. physiologic increase in general requirements
  3. excessive iron loss through blood loss
  4. renal issues
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116
Q

assessment findings for iron deficiency anemia

A

pica, pallor, fatigue, headaches

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117
Q

What are 3 types of bleeding disorder categories

A
  1. vascular disorders (vascular defect) - vascular purpura
  2. platelet disorders (abnormal quality/quantity) - thrombocytopenia
  3. coagulation disorders (clotting factor deficiency) - vitamin K, inherited, disseminated intravascular coagulation
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118
Q

WHat is hemostasis?

A

physiologic process that stops bleeding at site of injury while maintaining normal blood flow elsewhere

119
Q

What is primary hemostasis?

A

initial vasospasm at site of injury; formation of platelet plug; adhere and clump in 3-7 minutes

120
Q

What is secondary hemostasis

A

coagulation; form clot made of fibrin; clotting factors activated; clot retraction (firming) around 1 hour

121
Q

What are the 2 key players in hemostasis and what are they responsible for

A
  1. platelets - primary and secondary hemostasis; complex cell fragments; on cell surface, sticky receptors to help stick and adhere; can degranulate, which triggers cascade
  2. coagulation factors - circulate; activated by platelets and each other in cascade; plasma proteins
122
Q

What is the intrinsic pathway triggered by?

A

when blood comes into contact with altered endothelium; degranulation of platelets

123
Q

WHat triggers the extrinsic pathway?

A

tissue factors (trauma)

124
Q

What are the assessments of bleeding disorders?

A

pallor, jaundice, petechia, purpura, ecchymosis, hemarthrosis, hematoma, hematuria, hematochezia, hematoemesis, epitaxis, hemoptysis, menorrhagia

125
Q

What are 4 lab evaluations of bleeding disorders

A
  1. CBC with smear
  2. bleeding time
  3. prothrombin and INR (extrinsic coagulation - factor 7)
  4. activated partial thromboplastin time (intrinsic coagulation)
126
Q

What are the treatments of bleeding disorders

A

avoid cause, steroids (suppress immune response, prevents platelet breakdown), IVIG, factor replacement, platelets, FFP

127
Q

What is the etiology of thrombocytopenia?

A

decreased production or increased consumption of platelets - decreased platelet production, decreased platelet survival, splenic sequesterization, platelet dilution

128
Q

What is the assessment of thrombocytopenia?

A

petechiae, purpura, decreased platelet count’s, bleeding

129
Q

What is the treatment of thrombocytopenia?

A

treat/remove cause, block immune response, blood and/or platelet transfusion

130
Q

What is a thrombus?

A

stationary blood clot formed within a vessel or chamber of the heart (arterial or venous); composed of aggregated platelets, clotting factors, and fibrin that adhere to vessel wall

131
Q

What is Virchow’s Triad?

A
  1. epithelial injury - ex. vessel wall injury, trauma, IVs, smoking, HTN
  2. hypercoaguable conditions - ex. oral contraceptives, pregnancy, cancer, obesity
  3. circulatory stasis - ex. immobility
132
Q

What is a DVT?

A

presence of thrombus in one of deep veins of usually lower extremities

133
Q

What is the assessment of DVT?

A

edema, pain/tenderness (general or elicited), redness or discoloration, warmth, prediction rules, ultrasound, labs (D-dimer negative or positive)

134
Q

Treatment of DVT

A

thrombolytic to break down clot (tPA), anticoagulants to decreased further clot formation

135
Q

prevention of DVT

A

anticoagulants, SCD or compression stockings, hydration, movement

136
Q

Uses of anticoagulation therapy

A

prevents clot formation and extension, prevents and treats VTE and PE, stroke prevention in Afib, does not bust clot

137
Q

Goals of anticoagulation therapy

A

thin blood, prevent more clots, allow natural system activation

138
Q

classification of unfractionated heparin

A

anticoagulation therapy - enhances effects of antithrombin through deactivation of thrombin and factor Xa

139
Q

MOA of unfractionated heparin

A

binds to antithrobin causes a conformational change allowing better binding to thrombin and Xa

140
Q

route of admin unfractionated heparin

A

IV/SC

141
Q

AEs of unfractionated heparin

A

bleeding, heparin-induced thrombocytopenia (allergic reaction)

142
Q

Labs for unfractionated heparin

A

aPTT

143
Q

contraindications for unfractionated heparin

A

active bleeding, prep for surgery

144
Q

antidote for unfractionated heparin

A

protamine sulfate

145
Q

nursing actions for unfractionated heparin

A

binds to proteins, unpredicatble bioavailability, short half-life

146
Q

classification of LMW heparin

A

anticoagulation therapy - enhances effect of antithrombin and inactivates factor Xa

147
Q

MOA of LMW heparin

A

binds to antithrombin to cause a conformational change that better allows binding to Xa

148
Q

What is the importance of factor Xa?

A

activates thrombin (factor 2a) from prothrombin (factor 2)

149
Q

WHat are 3 things that thrombin does?

A
  1. fibrinogen –> fibrin
  2. factor v –> Va (enhances 10a)
  3. VIII –> VIIIa (increases activity of IXa)
150
Q

route of LMW heparin

A

SQ

151
Q

AEs of LMW heparin

A

bleeding, heparin-induced thrombocytopenia

152
Q

labs for LMW heparin

A

none - therapeutic dose after 1 hour

153
Q

contraindications for LMW heparin

A

active bleeding, prep for surgery, weight > 150kg, renal dysfunction

154
Q

antidote for LMW heparin

A

protamine sulfate

155
Q

nursing actions for LMW heparin

A

no protein binding; more predictable bioavailability

156
Q

Classification for warfarin

A

vitamin K antagonist

157
Q

classification for dabigatran

A

direct acting oral anticoagulant - direct thrombin inhibitor

158
Q

classification for rivaroxaban

A

direct acting oral anticoagulants - factor Xa inhibitor

159
Q

MOA of warfarin

A

suppresses production of factors 2, 7, 9 , 10; CYP 450

160
Q

AEs of warfarin

A

bleeding

161
Q

labs for warfarin

A

PT and INR

162
Q

contraindications for warfarin, rivaroxaban, and dabigitran

A

bleeding, prep for surgery

163
Q

antidote foe warfarin

A

phytonadione (vitamin K)

164
Q

nursing actions for Warfarin

A

long half-life, delayed onset, prolonged effects, lots of food and drug interactions (vitamin k-rich foods)

165
Q

MOA of rivaroxaban

A

factor Xa inhibitor

166
Q

AEs for rivaroxaban

A

bleeding

167
Q

labs for rivaroxaban and dabigatran

A

none - easy therapeutic dose

168
Q

antidote for rivaroxaban

A

none yet

169
Q

nursing actions for rivaroxaban

A

active immediately, less drug interactions

170
Q

MOA fo dabigatran

A

direct thrombin inhibitor (2a)

171
Q

antidote for dabigitran

A

idarucizumab - binds to dabigitran

172
Q

nursing actions for dabigitran

A

some drug interactions that inhibit p-glycoprotein which increases bleeding risk

173
Q

What is a UTI and where can it occur

A

infection/inflammation of urinary epithelium usually caused by gut flora; urethra (urethritis), prostate, bladder (cystits), ureter, kidney (pylenophritis)

174
Q

what defense mechanisms does our body have to prevent UTIs

A

acidic urine (urea), urination, sphincters, epithelial cells, secretions

175
Q

What are 4 properties of uropathogens?

A
  1. ability to attach to epithelial cells
  2. attach to latex catheters
  3. express toxins - s/s
  4. biofilms
176
Q

What are the clinical manifestations of cystitis

A

frequency, urgency, dysuria, pain, hematuria/cloudy urine

177
Q

What are the clinical manifestations of pyelonephritis

A

cystitis, fever, chills, nausea, vomiting, anorexia, CVA tenderness

178
Q

Evaluations for UTIs

A

physical and history; urinanlysis and culture (proteins, WBCs, nitrates, blood), imaging (reflex, structure)

179
Q

Treatment of UTIs

A

antibiotics, comfort care

180
Q

What is pelvic inflammatory disease

A

infection of oviducts and ovaries and adjacent reproductive organs; inflammation of cervic, uterus, oviducts (salpingitis), and ovaries

181
Q

What are the 2 stages of PID?

A
  1. vaginal/cervical infection

2. migration to upper genital tract

182
Q

WHat are the most common of PID?

A

gonorrhea and chlamydia

183
Q

What are the clinical manifestations of PID?

A

abdominal tenderness, irregular bleeding, pain with intercourse, dysuria, fever, discharge

184
Q

What are the complications of PID

A

chronic pelvic pain, infertility, ectopic pregnancy, abcess

185
Q

What is the formula for BP and what makes up each part

A

CO x SVR

Cardiac output - heart rate from B1 stimulation from vagal nerve stimulation (PSNS)

Systemic vascular resistance from stroke volume (preload volume - myocardial contractility B1 stimulation of SNS) and arterial radius (alpha stimulation, RAAS)

186
Q

How is BP regulated short term?

A

purpose - quickly accommodate behavioral, emotional, and physiologic changes
mediated by SNS, influenced by HR and SVR

187
Q

How is BP regulated long term?

A

neural, hormonal, and renal interaction; connected with fluid homeostasis; influences HR, SV, and SVR

188
Q

Long-term RAAS

A

pressure receptors cause kidneys to release renin into blood stream -> renin helps convert angiotensinogen to angiotensin 1 in liver -> angiotensin 1 converted to angiotensin 2 by ACE in lungs -> angiotensin 2 causes arteriolar constriction and aldosterone secretio from adrenal glands -> aldosterone causes Na/H2o retention -> increase in volume -> increases pressure

189
Q

What is primary and secondary HTN?

A

primary - 90%, idiopathic

secondary - 10%, underlying cause such as ingestion, sleep apnea, cardiac defect (coarctation of aorta), pregnancy

190
Q

What are the mechanisms behind preeclampsia?

A

placental ischemia and maternal vascular dysfunction

  • maternal immunologic intolerance
  • abnormal placental implantation
  • endothelial dysfucntion
  • genetic, nutritional, environmental factors
  • cardiovascular and inflammatory change (systemic effects)
191
Q

What are the clinical manifestations of preeclampsia

A

BP >140/90 on 2 occasions more than 4 hours apart AND proteinuria OR any of the following: thrombocytopenia, impaired liver function (increased liver enzymes), renal insufficiency (increased serum creatinine), pulmonary edema, new onset cerebral or visual disturbances

192
Q

Treatment of preeclampsia

A

mild: bed rest and fetal monitor
severe: deliver baby and placenta, vasodilation drugs, antihypertensives, seizure prophylaxis

193
Q

classification of SMZ/TMP

A

antimicrobial metabolism inhibitors (folate antagonists)
sulfamethoxazole - inhibitor of folate syntehesis
trimethoprim - inhibitor of folate reductase

194
Q

use of SMZ/TMP

A

G+ and G- bacteriostatic activity for UTIs, pneumocystis cabrini (causes lung infections in its with HIV, transplants, immunocompromised), bronchitis, otitis media, MRSA skin infections

195
Q

MOA of SMZ/TMP

A

sulfonamides compete with PAGA to inhibit the synthesis of dihydrofolic acid by dihydropteroate synthase; trimethoprim inhibits reduction of dihydrofolic acid to tetrahydrofolic acid by dyhydrofolate reductase; this process inhibits DNA

196
Q

Drug interactions for SMZ/TMP

A

warfarin

197
Q

AES of SMZ/TMP

A
  • hyperkalemia (TMP hangs on to K)
  • thrombocytopenia, neutropenia, megalblastic anemia
  • kernicterus (increase bilirubin): avoid in pregnancy and near term and pet <2 months
  • renal dysfunction
  • hypersensitivity reactions (stevens-johnson syndrome)
198
Q

use of nitrofurantoin

A

UTIs only (safe in pregnancy); bacteriostatic (can become bactericidal at high levels); only works in urine!! G+ and G- coverage, 3 salt forms

199
Q

MOA of nitrofurantoin

A

damages bacterial cell DNA (synthesis) - reduced by bacterial flavoproteins to reactive intermediates which activate or alter bacterial ribosomal proteins

200
Q

AEs of nitrofurantoin

A

brown urine, GI disturbances, pulmonary reactions (acute and subacute; rare- prolonged use or decrease renal function), agranulocytosis, peripheral neuropathy, hepatotoxicity

201
Q

nursing considerations for nitrofurantoin

A

avoid in patients with CrCl <40: less excreted in urine (only works in urine)

202
Q

What are the actions of alpha, beta, and calcium blockers?

A

alpha1 blockers - vasodilation, inhibit SNS
beta blockers - decrease heart rate, decrease contractility, constrict lungs
calcium channel blockers - dilate smooth muscle

203
Q

What are 4 ways to treat hypertensive disorders

A
  1. target and block alpha 1
  2. target and block beta 1 and 2
  3. target and block calcium channels
  4. RAAS and kidneys
204
Q

classification of metoprolol

A

sympatholytic beta-adrenergic blocker

205
Q

MOA of metoprolol

A
  • decreased cardia output (heart rate and contractility)
  • suppress reflex tachycardia caused by vasodilators
  • reduces release of renin (RAAS)
  • long term use reduces peripheral vascular resistance
206
Q

AEs of metoprolol

A

bradycardia, heart block, broncho-constriction (B2 blocked); not best for patients with increased BP

207
Q

classification of hydralazine

A

direct acting vasodilator

208
Q

use of hydralazine

A

PO/IV antihypertensive

209
Q

MOA of hydralazine

A

causes arterial vasodilation

210
Q

AEs of hydralazine

A

reflex tachycardia; can cause a systemic lupus erythematosus-like rash

211
Q

classification of amlodipine

A

calcium channel blocker - dihydropyradine

212
Q

use of amlodipine

A

BP drug, usually safe and effective

213
Q

AEs of amlodipine

A

peripheral edema (especially a problem if they have heart failure), can cause reflex tachycardia

214
Q

What are non-dihydropyradines used for

A

rate-control in atrial fibrillation; slows heart rate, less effective on BP

215
Q

What are two different targets for antihypertensives in the RAAS

A

ACE inhibitors and ARBs (angiotensin receptor blockers)

216
Q

classification of lisinopril

A

ACE inhibitor

217
Q

use of lisinopril

A

shown to slow progression of kidney injury in patients with diabetes (protect kidneys)

218
Q

AES of lisinopril

A

persistent cough, hyperkalemia (blocks aldosterone - less excretion of K), teratogenic, angioedema related to bradykinin

219
Q

Yes of losartan

A

do not cause ACE-I induced cough, teratogenic, angioedema, hyperkalemia

220
Q

classification of losartan

A

ARBs (angiotensin 2 receptor blocker)

221
Q

What is capillary hydrostatic pressure?

A

facilitates outward movement of water from capillary to interstitial space; affects BP

222
Q

what is capillary oncotic pressure

A

osmotically attracts water from the interstitial space back into the capillary; plasma

223
Q

what is interstitial hydrostatic pressure

A

facilitates inward movement of water from interstitial space into capillary

224
Q

what is interstitial oncotic pressure

A

osmotically attracts water from capillary into interstitial space

225
Q

What is edema/hypervolemia

A

excessive accumulation of fluid within interstitial space

226
Q

Forces involved in edema/hypervolemia

A
  • increased capillary hydrostatic pressure: renal failure, heart failure (excessive Na/H2) retention)
  • decreased plasma oncotic pressure: kidney disease, malnutrition, burns
  • increased capillary membrane permeability: immune responses, inflammation
  • lymphatic channel obstruction: lymph node removal, inflammatory process
227
Q

clinical manifestations of edema/hypervolemia

A
  • localized
  • generalized
  • other: weight gain, swelling, limited ROM, respiratory depression, lung crackles, bounding pulse, tachycardia
228
Q

what is dehydration/hypovolemia

A

too small a volume of fluid in extracellular compartment (vascular and interstitial); body fluids too concentrated

229
Q

causes of hypovolemia

A 
fluid loss (burns, vomit, diarrhea, blood loss, sweat, diabetes polyuria)
reduced fluid volume (GI bug, altered consciousness)
fluid shifts (burns)
230
Q

clinical manifestations of hypovolemia

A

poor turgor, tachycardia, dry mucous membranes, hypotension, weight changes, depressed fontanels, no tears, dark urine, oliguria, thirst

231
Q

Sodium range and function

A

135-145 mEq/L

ECF, regulates acid-base balance, facilitates nerve conduction and neuromuscular function, maintains water balance

232
Q

causes of hyponatremia

A
  • gain of water (relative to salt): inappropriate fluid resuscitation, tap water enemas, forced drinking of water, excess ADH
  • loss of salt (relative to water): diuretics, renal distress, replace water without salt
233
Q

clinical manifestations of hyponatremia

A

nonspecific CNS dysfunction, malaise, anorexia, H/N/HA, confusion, lethargy, seizures, coma, fetal cerebral herniation

234
Q

treatment of hyponatremia

A

determine cause and fix, restrict water intake, hypertonic saline solutions with caution, IV fluids

235
Q

causes of hypernatremia

A
  • gain of sodium (relative to water): tube feeding concentration, overuse of salt tablets, no access to water
  • loss of water (relative to sodium): emesis, diarrhea, diaphoresis, tube feeding concentration
236
Q

clinical manifestations of hypernatremia

A

thirst, dry mucous membranes, hypotension, tachycardia, oliguria, muscle irritability, agitation, confusion, lethargy… seizures, coma, death

237
Q

treatments of hypernatremia

A

underlying condition, oral or IV fluids (no salines), 5DW slowly

238
Q

potassium range and function

A

3.5-5 mEq/L
ICF, cell electrical neutrality, cardiac muscle contraction and electrical conductivity, neuromuscular transmission of nerve impulses, maintains acid-base balance

239
Q

causes of hypokalemia

A
  • decreased K intake (fad diet, NPO)
  • shifts into cell (alkalosis)
  • increased K excretion or loss in renal or GI (diuretics, gastric suctioning)
240
Q

clinical manifestations of hypokalemia

A

hyper polarized smooth and cardiac muscles (less reactive to stimuli), abdominal distention, diminished bowel sounds, ileum, postural hypotension, skeletal muscle weakness, paralysis, cardiac dysrhythmia

241
Q

treatment of hypokalemia

A

replace orally or IV

242
Q

causes of hyperkalemia

A
  • increased intake (blood transfusions)
  • shifts into ECF (acidosis, rush injuries)
  • decreased excretion (oliguria, pharm)
243
Q

clinical manifestations of hyperkalemia

A

hypo polarized smooth and skeletal muscle cells (can’t fire again after discharge), mild intestinal cramping and diarrhea, skeletal muscle weakness, paralysis, cardia dysrhythmias, cardiac arrest

244
Q

treatment of hyperkalemia

A

fix issue, pharm, dialysis

245
Q

calcium range and function

A

9-11 mg/dL
cell permeability, bone and teeth formation, blood coagulation, nerve impulse transmission, normal muscle contraction, cardiac action potentials and pacemaker automaticity

246
Q

causes of hypocalcemia

A
  • decreased intake/absopriotn (diet, chronic diarrhea, CKD)
  • decreased physiologic availability (alkalosis)
  • increased excretion (pancreatitis, steorrhea)
247
Q

clinical manifestations of hypocalcemia

A

increased neuromuscular excitability - muscle twitching, cramping, hyperactive reflexes, tetany, seizures, dysrhythmias

248
Q

causes of hypercalcemia

A
  • increased intake/absorption (too much vitamin D)
  • shift from bone to ECF (tumors, leukemia, immobile)
  • decrease excretion (diuretic)
249
Q

clinical manifestations of hypercalcemia

A

anorexia, nausea, emesis, constipation, fatigue, muscle weakness, decreased reflexes, HA, confusion, lethargy, cardiac dysthymia (heart block, bradycardia, kidney stones)

250
Q

3 mechanisms that regulate acid-base imbalances

A
  1. buffers
  2. respiratory system
  3. renal system
251
Q

lab values for acid-base

A

PCO2: 36-44 mmHg
HCO3: 22-26 mmHg
pH: 7/35-7.45

252
Q

What is respiratory acidosis

A

excess of carbonic acid; shallow breaths (hypoventilation) that cause a buildup of carbonic acid H2CO3 (increases PCO2) and less HCO3

  • increase PCO2
  • decrease pH
253
Q

causes of respiratory acidosis

A
  • impaired gas exchange: asthma, COPD, bacterial pneumonia
  • inadequate neuromuscular function: guillan-barre, no deep breaths
  • impairment of respiratory control in brainstem
254
Q

clinical manifestations of respiratory acidosis

A

HA, tachycardia, cardiac dysrythmias, neuro (blurred vision, tremors, vertigo, disorientation, lethargy, somnolence)

255
Q

how does the body compensate for respiratory acidosis

A

kidneys conserve HCO3 and eliminate H+ in acidic urine

256
Q

What is respiratory alkalosis

A

carbonic acid H2CO3 excess

  • decrease PCO2
  • Increase pH
257
Q

causes of respiratory alkalosis

A

hyperventilation - anxiety, crying, acute pain, brainstem injury, hypoxemia

258
Q

clinical manifestations of respiratory alkalosis

A
  • increased neuromuscular excitability: numbness and tingling, feet/hand spasms
  • excitability and/or confusion
  • cerebral vasoconstriction
259
Q

how does the body compensate for respiratory alkalosis

A

kidneys conserve H+ ions and eliminate HCO3 in alkaline urine

260
Q

What is metabolic acidosis

A

relative excess of any acid except carbonic acid

  • decreased HCO3
  • decreased pH
261
Q

causes of metabolic acidosis

A
  • increase in metabolic acid: diabetic ketoacidosis, burns, circulatory shock
  • decrease in base: severe/prolonged diarrhea, decompression of intestines
  • combination
262
Q

how does the body compensate for metabolic acidosis

A

kidneys conserve HCO3 and eliminate H+ in acidic urine

263
Q

clinical manifestations of metabolic acidosis

A

GI (N/V/D, dehydration), CNS depression (HA, confusion, lethargy, stupor, coma), cardiac (tachycardia, dysrhythmias), fruity breath

264
Q

What is metabolic alkalosis

A

relative defect of any acid except carbonic acid

  • increase HCO3
  • increase pH
265
Q

causes of metabolic alkalosis

A
  • increase in base: overuse of antacids, hypovolemia
  • decrease in acid: emesis, removal or gastric secretions
  • combination
266
Q

how does the body compensate for metabolic alkalosis

A

kidneys conserve H+ and eliminate HCo3 in alkaline urine

267
Q

clinical manifestations of metabolic alkalosis

A
  • ECF depletion: postural hypotension, N/V/D
  • tetany, tingling, seizures
  • hypokalemia with bilateral muscle weakness
  • irritability and the CNS depression
268
Q

use of potassium chloride

A

hypokalemia; salt formation

269
Q

AES for potassium chloride

A

GI issues (N/V/D, abdominal discomfort, esophagitis), IV irritation and extravasation

270
Q

nursing actions for potassium chloride

A
  • give with lots of food and water
  • quick acting: hard on stomach, dilute liquid/powder
  • long acting: slow release, less GI issues
  • maintain good IV, proper drip, monitor
271
Q

what should be monitored when administering potassium chloride

A
  • serum K levels
  • s/s of hyperkalemia
  • IV site
  • cardiac function
272
Q

contraindications for potassium chloride

A
  • monitor closely in patients with renal dysfunction and patients on meds that can increase serum K levels (trimethoprim, ACE inhibitors - also on diuretics)
273
Q

IV administrating considerations for potassium chloride

A
  • peripheral or central (bigger IV, faster)

- K may be added to maintenance fluids

274
Q

What are the treatments of hyperkalemia (3)

A
  • protect the heart: admin Ca IV (K still high)
    1. shift K back into cells (temporary - regular insulin + dextrose 50% injection, sodium bicarbonate injection, albuterol continuous inhaler
    2. increase excretion of K - kidneys (diuretic therapy), fake kidney (hemodialysis - 1st line, emergency), gut (sodium polystyrene- resist that exchanges Na–> in gut then excretes after hours)
275
Q

What IV products are used to treat hypocalcemia and hyperkalemia

A
  • calcium gluconate: less potent, peripheral admin

- calcium chloride: more potent, more caustic to vasculature, admin centrally

276
Q

How does K and insulin work to correct hyperkalemia?

A
  • Na-K adenosine triphosphatase (ATPase) pump in cell membrane maintains ICF and ECF concentrations, exchanges Na for K in a 3:2 ration, enhances movement of K into cell
  • pump uses ATP hydrolysis as energy source; activation of pump requires insulin and glucose
277
Q

use of insulin + dextrose 50%

A

diabetes and hyperkalemia

278
Q

route of admin for insulin + dextrose 50%

A

mostly IV, also SQ

279
Q

AEs of insulin + dextrose 50%

A

insulin can accumulate in renal dysfunction

280
Q

use of sodium bicarbonate

A

severe metabolic acidosis, hyperkalemia (fixes #, note problem)

281
Q

AEs of sodium bicarbonate

A

caustic to vasculature, hypokalemia, metabolic alkalosis

282
Q

MOA of sodium bicarbonate

A

shifts K back into cell by drawing H_ to intracellular space with bicarbonate

283
Q

classification of albuterol

A

short acting beta-2 agonist

284
Q

MOA of albuterol

A

binds to beta-e in lungs (bronchodilation), activates adenylate cyclase which stimulates production of cAMP which is used by Na-K ATPase pump to move K intracellulary

285
Q

AEs of albuterol

A

tahycardia, K can still appear low (in cell)

286
Q

What are 3 ways to increase K elimination

A
  1. diuresis with furosemide
  2. hemodialysis
  3. kayaxelate (sodium polystyrene)
287
Q

route of kayaxelate

A

PO or rectally

288
Q

MOA of kayaxelate

A

resin that exchanges Na for K in gun and then excretes

289
Q

AE of kayaxelate

A

associated with intestinal necrosis and other serious GI effects

290
Q

nursing considerations for kayaxelate

A

slow onset over hours - not used in emergencies

291
Q

Roles of mag in body

A
  • activates intracellular enzymes
  • binds mRNA to ribosomes
  • plays role in regulating skeletal muscle contractility and blood coagulation
292
Q

What conditions would mag sulfate IV be used for?

A
  • hypomagnesemia: slow replacement
  • preeclampsia and eclampsia
  • migraines
  • status asthmaticus: bronchodilate for asthma
293
Q

precautions for magnesium sulfate

A

use with caution in patients with renal dysfunction, monitor patient cardiac and neuromuscular status

N398 (2 decks)

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