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331 test 3 Flashcards

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1
Q

what disease are considered obstructive lung diseases

A

Asthma, COPD, chronic bronchitis, and emphysema

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2
Q

upper respiratory infection symptom relief

A

expectorants, antitussives, nasal decongestants, and anti-histamines

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3
Q

upper respiratory infection symptoms

A

excessive mucus production and nasal congestion

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4
Q

Empiric therapy

A

based on symptoms practitioner is making an educated guess with their knowledge and experiences

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5
Q

when histamine attaches to H1 receptors

A 
upper respiratory:
Smooth muscle of airway 
Increased vasodilation 
Increased vascular permeability
Constriction of the bronchioles in airway
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6
Q

histamine does what to parietal cells

A

directly stimulate parietal cells to increaseacidsecretion

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7
Q

when histamine attaches to H2 receptors

A

stomach (increases gastric secretions) and heart (increases HR)

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8
Q

histamine is a true

A

neurohormone

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9
Q

Pepsid targets

A

H2 receptors

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10
Q

histamine is released in response to

A

antigen exposure

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11
Q

what are found in the heart and known to release histamine

A

mast cells

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12
Q

excessive histamine release can lead to

A

anaphylaxis

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13
Q

histamine inflammatory responses

A

urticaria, angioedema, pruritus and fever

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14
Q

urticaria

A

hives

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15
Q

how does histamine produce both hives and agiokedema

A

dilating the small blood vessels in the skin causing fluid to leak

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16
Q

constant itching can be associated with

A

high temperatures

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17
Q

vasodilation and increased permeability =

A

increased body secretions and leads to hypotension and edema

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18
Q

anaphylactic shock

A

lung constriction, increased body secretions, vasodilation everywhere except in the bronchioles which constrict, increased capillary permeability

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19
Q

Palliative

A

relieving pain without dealing with the cause of the condition (treating symptoms)

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20
Q

Antiemeticdrugs are

A

types of chemicals that help ease symptoms of nausea or vomiting. – typically for motion sickness

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21
Q

contraindications of antihistamines

A

include narrow-angle glaucoma, cardiac disease, kidney disease, hyperten­sion, bronchial asthma, chronic obstructive pulmonary disease, peptic ulcer disease, seizure disorders, benign prostatic hyperplasia, and pregnancy.

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22
Q

why do you want to give antihistamines as early as possible

A

as early as possible because it will not push already bound histamine off receptors. it competes for receptor sites

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23
Q

when are antihistamines indicated

A

allergies, vertigo (anti-emetic), insomnia, cough

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24
Q

what do antihistamines do

A

have anti-emetic effects - ease nausea, sedation, has anticholinergic effects of drying secretion, causes bronchodilator and prevents vasodilation

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25
Q

Diphenhydramine

A

Benadryl

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26
Q

where does diphenhydramine work

A

peripherally and centrally

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27
Q

what does diphenhydramine do

A

antihistamine, anticholinergic, sedative, and anti-emetic

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28
Q

anticholinergic

A

blocks the neurotransmitter acetylcholine (parasympathetic) in the central and the peripheral nervous system

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29
Q

why treat Parkinson’s with diphenhydramine

A

its anticholinergic effects help relax the patient

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30
Q

what can diphenhydramine do to older adults

A

cause hangover effect which puts them at risk for falls

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31
Q

decongestants

A

shrink engorged mucosa and constrict nasal arterioles

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32
Q

expectorants

A

decrease the viscosity (thickness) of sputum and increase cough and spit to overall decrease cough in the end

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33
Q

antitussives

A

cough suppressant

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34
Q

two types of antitussives

A

opioid (watch for respiratory depression) and non-opioid (might feel numbness in throat of mouth

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35
Q

three types of nasal decongestants

A

adrenergics (sympathomimetics), which are the largest group; anticholinergics (parasympatholytics), which are somewhat less commonly used; and selected topical corticosteroids (intranasal steroids)

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36
Q

example of decongestant

A

fluticasone (Flonase)

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37
Q

example of antitussive

A

codeine (opioid) and benzonatate (Tesselon)

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38
Q

example of expectorant

A

guaifenesin (mucinex)

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39
Q

different categories of pneumonia

A
  • CAP - community-acquired pneumonia – out in the community anywhere
  • HCAP - healthcare-associated pneumonia – pt has extensive interactions with healthcare community – constant contact with healthcare workers
  • HAP - Hospital-acquired pneumonia – show signs within 48 hrs of admission into hospital
  • VAP - Ventilator-associated pneumonia – pt in ICU who require ventilator support (happens in 9-27% of people on ventilators) – proper oral care of patients can decrease risk immensely
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40
Q

Bacteremia

A

presence of bacteria in blood

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41
Q

most common nosocomial infection

A

UTI

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42
Q

risk factors of pneumonia

A

Immunosuppression
Sedentary – especially in elderly and post op
Underlying chronic heart or lung disease

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43
Q

Atelectasis

A

complete or partial collapse of the entire lung or area (lobe) of the lung

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44
Q

different things you can see in a chest x ray of the lungs

A

consolidation, interstitial, nodule, mass, atelectasis

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45
Q

malaise

A

A general sense of being unwell, often accompanied by fatigue, diffuse pain, or lack of interest in activities.

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46
Q

objective findings with pneumonia

A

tachycardia, fever, cyanosis, dullness to percussion, inspiratory crackles, and elevated WBC

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47
Q

CXR

A

chest xray

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48
Q

ABX

A

antibiotics

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49
Q

if pt presents with pneumonia what type of antibiotics would you start them on?

A

broad spectrum until blood/sputum cultures come back and pathogen is identified

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50
Q

what do you need to watch out for in a person with pneumonia

A

bacteremia and sepsis

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51
Q

what needs to be ordered for a person with pneumonia

A

Chest xray, antibiotics, blood/sputum culture, and supportive therapy

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52
Q

supportive therapy

A

treat symptoms and prevent organ hypoxia

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53
Q

hypoxia

A

decreased oxygenation of tissue - An absence of enough oxygen in the tissues to sustain bodily functions.

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54
Q

what can hypoxia lead to

A

anaerobic metabolism which will increase lactivist acid levels

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55
Q

what does sepsis present as

A

systemic inflammatory response, vasodilation which leads to low BP, and increased vascular permeability which leads to edema

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56
Q

SIRS

A

systemic inflammatory response syndrome

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57
Q

pulmonary vascular disorder

A

disorders that occlude vessels, increase pulmonary vascular resistance, and destroy vascular bed

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58
Q

pulmonary embolism

A

occlusion of vascular bed in lungs usually from a DVT but can be from foreign body or fat

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59
Q

Pulmonary embolism can be either

A

embolus with/without infarction

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60
Q

infarction

A

tissue death due to inadequate blood supply to the affected area

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61
Q

what you need to know during a pulmonary embolism

A

Extent of Blood flow obstruction
Size of vessel
Why is it there
What is the clot doing

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62
Q

obstruction leads to

A

pulmonary vasoconstriction which causes pulmonary hypertension

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63
Q

pulmonary embolism with infarction

A

if its there long enough has the ability to cause tissue death, and the fibrinolytic system does not have the ability to dissolve clot

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64
Q

pulmonary embolism without infarction

A

embolism still there, fibrinolytic system can still dissolve clot, but getting circulation from other area – such as bronchiole arteries

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65
Q

how can you test for a PE

A

D-Dimer, BNP, CT scan

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66
Q

D- Dimer

A

test for pulmonary embolism. less than 250 – if high then we have thrombus (blood clot) formation

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67
Q

BNP

A

looks at right ventricular pressure

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68
Q

CT scan

A

help visualize a pulmonary embolism

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69
Q

high V/Q ratio

A

alveoli are ventilated but not perfused. = dead space

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70
Q

normal V/Q ratio

A

0.8, 4 (ventilation) / 5 (perfusion) = 0.8

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71
Q

high V/Q ration numbers

A

V/Q > 0.8, about 4 (ventilation) / 3 (perfusion) = 1.3 - dead space - pulmonary embolus

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72
Q

V/Q low

A

V/Q < 0.8. 2 (ventilation) / 5 (perfusion) = 0.5 perfusion without ventilation = shunt - atelectasis, asthma, pulmonary edema &PNA

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73
Q

what is the V/Q ration during a pulmonary embolism

A

high

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74
Q

risk factors of PE

A

genetics, venous stasis, hyper-coagulability, oral contraceptives

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75
Q

hypoxemia

A

decreased oxygenation of arterial blood - A low level of oxygen in the blood, inadequate exchange

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76
Q

what can PE cause

A

SOB, tachypnea, hypoxemia, tachycardia

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77
Q

pulmonary embolism prevention

A

bed exercises, early ambulation, pneumatic calf compression, prophylactic low-dose anticoagulation

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78
Q

what medication can you give for anticoagulation

A

low dose lovinox

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79
Q

steps to massive PE

A

starts with venous stasis, vessel injury, or hyper coagulability which leads to thrombus formation-dislodgment of portion of thrombus- occlusion of part of pulmonary circulation - hypoxic vasoconstriction, decrease surfactant, release of inflammatory substance, pulmonary edema, and atelectasis - signs and symptoms

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80
Q

PAH

A

pulmonary artery hypertension

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81
Q

cor pulmonale

A

Right ventricular enlargement. can be hypertrophy, dilation, or both

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82
Q

hypertrophy

A

the wall itself is enlarged

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83
Q

dilated

A

stretched chamber

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84
Q

idiopathic pulmonary artery hypertension

A

endothelial dysfunction due to increase production of vasoconstrictors and decrease production of vasodilators

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85
Q

why does pulmonary artery hypertension occur

A

increase pressure from LHF, chronic lung disease or hypoxia, chronic thromboembolism

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86
Q

what happens during pulmonary artery hypertension

A

hypoxic pulmonary artery vasoconstriction and increased pulmonary artery pressure

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87
Q

why does cor pulmonale occur

A

pulmonary artery hypertension and chronic pressure overload

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88
Q

what happens with cor pulmonale

A

pulmonic valve murmur and increase systemic venous pressure which causes JVD, hepatosplenomegaly, peripheral edema

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89
Q

how does PAH manifest

A

fatigue, chest discomfort, tachypnea, and dyspnea

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90
Q

most common post/op pulmonary problems

A

atelectasis, PNA, pulmonary edema, and PE

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91
Q

hypercapnia

A

inadequate alveolar ventilation

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92
Q

what can you do to prevent clots on post op patients

A

early ambulation

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93
Q

acute respiratory “failure”

A

inadequate gas exchange will be a little acidic with over 50 mm Hg CO2 and less than 60 mmHg of O2

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94
Q

acute respiratory “failure” can either be

A

hypercapnia or hypoxemia

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95
Q

hypercapnia acute respiratory “failure”

A

inadequate alveolar ventilation - use ventilator support

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96
Q

hypoxemia acute respiratory “failure”

A

inadequate exchange - use supplemental oxygen

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97
Q

ventilation

A

gas/air into and out of the lungs

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98
Q

respiration

A

exchange of CO2 and O2 during cellular metabolism

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99
Q

what do you need to oxygenate

A

both adequate ventilation and pefusion

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100
Q

tidal volume

A

amount of air coming in and going out should be 400-800 ml

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101
Q

is dyspnea subjective or objective

A

subjective

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102
Q

dyspnea

A

air hunger and labored breathing

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103
Q

dyspnea turns into objective when you see

A

pulmonary, cardiac, pain, psychogenic effects

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104
Q

psychogenic

A

anxiety or disorder

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105
Q

DOE

A

dyspnea on exertion

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106
Q

orthopnea

A

Discomfort when breathing while lying down flat

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107
Q

cough

A

protective reflex can be chronic or acute

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108
Q

acute cough

A

2-3 weeks

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109
Q

chronic cough

A

4-6 weeks - chronic bronchitis or lung cancer

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110
Q

kussmauls breathing

A

when you are trying to compensate when you are metabolic acidosis. increase rate, increase volume, no pause

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111
Q

gasping or agonal breathing

A

irregular quick inspiration, expiratory pause, severe cerebral hypoxia

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112
Q

cheyne-strokes

A

when you are dying. alternating deep, shallow, apnea- associated with decrease blood flow to brainstem

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113
Q

apnea

A

cessation of breath

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114
Q

labored breathing

A

can either by obstructive or restrictive

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115
Q

large airway labored breathing

A

decrease rate, increase volume, increase effort, prolonged inspiration and expiration, stridor or audible wheeze

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116
Q

small airway labored breathing

A

increased rate, decrease volume, increase effort, prolonged expiration and wheezing

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117
Q

hypoventilation

A

inadequate alveolar ventilation

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118
Q

potential causes of hypoventilation

A

respiratory depression, neuromuscular disease, trauma or pain, physiological dead space

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119
Q

hypercapnia

A

air sacs not ventilating properly leads to CO₂ retention, more CO2 production than CO2 removal

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120
Q

hypoventilation can lead to

A

hypercapnia, respiratory acidosis which can lead to hypoxemia and Altered level of consciousness

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121
Q

neuromuscular disease

A

conditions that impair the functioning of the muscles. can impact ability to ventilate

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122
Q

physiological dead space

A

where ventilation should be occurring but its not and example is pulmonary embolism

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123
Q

hyperventilation

A

excessive alveolar ventilation - blowing off too much CO2- leads to hypocapnia

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124
Q

potential causes of hyperventilation

A

pain, anxiety, head injury

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125
Q

hypocapnia

A

more CO2 removal than CO2 production

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126
Q

what can hypocapnia lead to

A

respiratory alkalosis

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127
Q

hypoventilation and hyperventilation is all based off

A

metabolic demand

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128
Q

deoxy hemoglobin

A

desaturated hemoglobin

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129
Q

lack of cyanosis

A

does not mean oxygenation is normal

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130
Q

O2 sat =

A

% of Hgb binding sites carrying oxygen

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131
Q

PaO2=

A

oxygen content of blood

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132
Q

O2 Sat of 90%=

A

PaO2 of 60 mmHg

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133
Q

clubbing

A

nail bed hypertrophy due to chronic hypoxemia

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134
Q

cyanosis

A

desaturated hemoglobin can show peripheral (finger tips) or central (face/mouth)

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135
Q

special circumstance of cyanosis

A

anemia, carbon monoxide, polycythemia

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136
Q

anemia

A

not enough Hgb - they will be pale

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137
Q

carbon monoxide cyanosis

A

Hgb saturated with wrong gas - will have a cherry hue

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138
Q

polycythemia

A

too many RBC- increased blood viscosity (increase risk of clot) and decreased tissue perfusion

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139
Q

hypoxemic manifestations

A

cyanosis, confusion, tachycardia, edema, decreased urinary output

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140
Q

FiO2

A

fraction of inspired air = 21%

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141
Q

if you have hypoxemia that you have

A

pulmonary issue

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142
Q

mechanism of oxygenation

A

oxygen delivery to alveoli and diffusion of oxygen from alveoli to blood

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143
Q

how is oxygen delivered to alveoli

A

inspired air and adequate ventilation

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144
Q

diffusion of oxygen from alveoli to blood

A

includes V/Q - alveolar ventilation and alveolar perfusion

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145
Q

what do the V and Q stand for in V/Q ratio and what does V/Q overall stand for

A

V=air entering alveoli (alveolar ventilation)
Q= blood reaching capillaries (alveolar perfusion)
V/Q = ventilation perfusion

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146
Q

widespread tissue dysfunction leads to

A

organ infarction

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147
Q

two types of shunting

A

right and left shunting. can be anatomic or ventilation issues

148
Q

shunt - anatomic issue

A

deoxygenated blood bypasses the lung and goes right back into the circulation

149
Q

shunt - ventilation issues

A

alveoli collapsed - structural issue

150
Q

most common cause of hypoxemia

A

an abnormal ventilation perfusion ration

151
Q

more effort to expand the lungs =

A

increase work of breathing

152
Q

restrictive lung disease

A

decrease lung compliance due to stiff chest wall this causes increase effort to fill lungs, increase respiratory rate, and decrease tidal volume

153
Q

restrictive lung disease is expected in

A

geriatric population

154
Q

will restrictive lung disease have low or high V/Q?

A

low - can’t get air in - less ventilation - hypoxemia

155
Q

aspiration most common in

A

right lung, especially right lower lung

156
Q

PNA

A

pneumonia

157
Q

surfactant

A

keeps lungs with surface tension - if its disrupted lung can collapse

158
Q

what does CO2 do to the vessels

A

vasodilation which causes hypotension

159
Q

risks that can lead to aspiration

A

ALOC, seizures, dysphagia, NG tube

160
Q

what can aspiration lead to

A

pneumonia, damage to alveolocapillary membranes, surfactant production disrupted and lung collapsed, hypoventilation which can lead to hypercapnia and hypotension

161
Q

PEEP

A

positive and expiratory pressure (through ventilation)

162
Q

prevention of aspiration

A

semi-fowlers, assessment of swallowing/NG tube, promotility agents, avoid excessive sedation

163
Q

promotility agents

A

keep GI mobile

164
Q

aspiration pneumonitis presentation

A

choking, cough, dyspnea, fever, wheezing

165
Q

aspiration pneumonitis treatment

A

oxygen, PEEP, corticosteroids

166
Q

aspiration pneumonitis always has the risk of turning into

A

bacterial pneumonia

167
Q

atelectasis

A

collapse of lung tissue

168
Q

cause of atelectasis

A

lack of air to hyperventilated alveoli due to surfactant impairment or compression

169
Q

decrease surfactant production =

A

increased surface tension

170
Q

compression

A

tumor or fluid

171
Q

atelectasis treatment

A

deep breathing exercises, IS, position changes, early ambulation, NIPPV

172
Q

NIPPV

A

non invasive positive pressure ventilation device

173
Q

how does atelectasis present

A

dyspnea, cough, fever, leukocytosis

174
Q

pulmonary edema

A

excess water in lung, pink frothy sputum, hypoventilation, hypercapnia

175
Q

what keeps lungs dry

A

lymphatic drainage

176
Q

how does pulmonary edema occur (steps)

A

left sided heart failure creates backup into lung, pulmonary capillary injury causes increase capillary permeability and decrease surfactant, and lymphatic obstruction causes no removal of excess fluid

177
Q

ARDS

A

acute respiratory distress syndrome

178
Q

causes of pulmonary edema

A

heart failure, toxic gas, tumor, lung fibrosis, and ARDS

179
Q

what toxic gases can cause pulmonary edema

A

chloride, nitrogen dioxide, ammonia

180
Q

clinical manifestations of pulmonary edema

A

dyspnea, hypoxemia, increased work of breathing, hypercapnia, crackles and dull percussions

181
Q

diagnostic criteria from diabetes

A

HbgA1C more than 6.5%, fating glucose more than 126 mg/dL, 2-hr glucose tolerance above 200 mg/dL, or in crisis with signs and symptoms of hyperglycemia with random glucose above 200 mg/dL

182
Q

type 1 diabetes

A

t-cell mediated autoimmune - pancreas failure to produce insulin - secretion - insulin deficiency

183
Q

type 2 diabetes

A

you have insulin but insulin receptors do not work. you have a tolerance - action problem - resistance of tissue

184
Q

FPG

A

fasting plasma glucose

185
Q

tests of high risk for diabetes

A

FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%

186
Q

glycogenolysis

A

glycogen to glucose

187
Q

insulin is secreted when

A

after a meal

188
Q

the glucose that does not get used up goes to where

A

the liver

189
Q

t-cells do what

A

identify and kill a target, beta cell antigens

190
Q

insulin

A

suppresses glucagon secretion

191
Q

glucagon

A

promotes glycogenolysis and gluconeogenesis

192
Q

amylin

A

beta cell hormone - suppresses glucagon secretion

193
Q

lack of insulin and lack of glucagon suppression =

A

hyperglycemia

194
Q

there is ______ amylin production during type 1

A

less

195
Q

t-cell mediated autoimmune

A

destruction of insulin secreting beta cells, macrophages infiltration of islets, t-cells

196
Q

what happens when there is a destruction of insulin secreting beta cells

A

decreased insulin synthesis, hypoinsulinemia, hyperglycemia

197
Q

how does renal overload happen in type 1 DM

A

water moves from inside cells into bloodstream following osmotic pull of large glucose molecules, renal threshold for glucose is exceeded and glucose and water spill out, and nutrients are lost

198
Q

when water moves from inside cells into bloodstream following osmotic pull of large glucose molecules what happens

A

cellular dehydration and increase in plasma volume

199
Q

what happens when renal threshold for glucose is exceeded and glucose and water starts spilling out

A

polyuria and polydipsia

200
Q

polyphagia

A

lost nutrients

201
Q

weight loss with DM1 is due to

A

initial weight loss is due to osmotic dieresis (fluid loss) and tissue loss

202
Q

insulin can cause

A

weight gain through lipogenesis - converts glycogen to fat stores

203
Q

weight gain from DM1 can cause chronic complications associated with

A

DM2 such as MI/CVA

204
Q

diabetes type 1 patient will get what if they do not control their diabetes

A

metabolic syndrome

205
Q

warning signs of DM2 linked to increased

A

CV complications

206
Q

labs with metabolic syndrome

A

HDL less than 40 in men or less than 50 in woman, trig over 150 mg/dL, BP over 130/85, FBS over 100, waist bigger than 40 inches men and 35 inches in woman

207
Q

insulin resistance

A

during DM II. action problem- suboptimal receptor response to insulin in the liver, muscle, and adipose tissue.

208
Q

what cells try to compensate during insulin resistance

A

beta cells try to compensate by producing more insulin . once they are fatigued they will stop working at good which leads to insulin deficiency

209
Q

risk factors for DMII

A

genetic factors, sedentary lifestyle, smoking, and poor diet

210
Q

what do you end up with if you have insulin resistance

A

hyperglycemia and hyperinsulinemia

211
Q

insulin deficiency

A

decrease response of beta cells to hyperglycemia because they are fatigued and less responsive after trying to compensate during insulin resistance

212
Q

1 contributor to DM2

A

obesity

213
Q

what does obesity do to leptin and adiponectin

A

increases leptin and decreases adiponectin

214
Q

leptin resistance

A

promotes over eating and insulin resistance

215
Q

intra abdominal cytokines

A

toxic to beta cells and contribute to insulin resistance

216
Q

incretins

A

released from GI tract in response to food - increase insulin secretion, decrease glucagon secretion, delay gastric emptying, produce new beta cells, and get broken down by DPP-4

217
Q

what can intracellular deposits of triglycerides and cholesterol do

A

changes cellular insulin signaling which decreases tissue’s response to insulin, promotes inflammation, and alters incretins

218
Q

consequences of hyperglycemia

A

decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression

219
Q

acute complications of diabetes

A

hypoglycemia, DKA, and HHNKS

220
Q

somogyi effect

A

hypoglycemic episodes during the night and causes a rebound hyperglycemic period in the morning. more common in type 1 DM.

221
Q

insulin counter regulator hormones

A

growth hormone, glucagon, epinephrine, cortisol

222
Q

dawn phenomenon

A

blood sugar rises with the sun with no hypoglycemia during the night. due to growth hormone released during the night and decreases peripheral glucose uptake

223
Q

diabetic ketoacidosis

A

profound deficiency of insulin with increased stress hormones

224
Q

characteristics to DKA

A

acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated

225
Q

what will someones breath smell like if they are in DKA

A

juicy fruit due to ketones

226
Q

what type of breath do you usually see in DKA patents

A

kussmaul

227
Q

what should you do for someone in DKA

A

they need hydration, insulin, electrolyte replacement

228
Q

ketone bodies

A

produced in liver when fat is broken down for an energy source

229
Q

gluconeogenesis

A

metabolic pathway that results in the generation of glucose for the break down of fats

230
Q

without insulin

A

fat catabolism occurs and thus ketone bodies develop

231
Q

what do the accumulation of ketones do to ph

A

drop it

232
Q

insulin normally stimulates

A

lipogenesis and inhibits lipolysis

233
Q

diabetic ketoacidosis symptoms

A

Kussmauls, postrural dizziness, decreased CNS, N/V, abdominal pain, polyuria, polydipsia, anorexia, weight loss

234
Q

HHNKS

A

server dehydration with loss of electrolytes and high glucose over 600 with enough insulin to prevent ketoacidosis. High osmolarity over 320. normal ph and bicarb

235
Q

HHNKS is common in what population

A

geriatric

236
Q

what is the number one cause of HHNKS

A

infection

237
Q

high osmolarity

A

volume depletion with high concentration

238
Q

what do you need to do first for people in HHNKS

A

start on IV fluids then insulin

239
Q

main goal for pt in HHNKS

A

rehydration, electrolyte replacement, correct hyperglycemia, treat underlying disease, monitor cardio/pulmonary, renal, and CNS

240
Q

symptoms of HHNKS

A

hypotension, hypovolemia, hypoperfusion

241
Q

glucose toxicity over time does what to our bodies

A

cataracts, damage nerve conduction, and inhibits perfusion

242
Q

AGEs

A

advanced glycation end products

243
Q

what are AGEs

A

harmful compounds that are formed when protein or fat combine with sugar in the bloodstream

244
Q

decrease tissue perfusion can lead to _______ of the capillaries

A

occlusion of the capillaries which causes hypoxia and ischemia

245
Q

leading cause of blindness

A

diabetic retinopathy

246
Q

macular edema

A

blurred vision

247
Q

stages of diabetic retinopathy

A
  1. micro aneurysm formation 2. poor perfusion and ischemia 3. neovascularizaition and fibrous tissue formation within retina which may cause retinal detachment
248
Q

diabetic retinopathy increases your risk for

A

glaucoma and cataracts

249
Q

ESRD

A

end stage renal disease

250
Q

leading cause of end stage renal disease

A

diabetes

251
Q

what four things contribute to kidney injuries

A

hyperglycemia, advanced glycation end products (AGEs), activation of metabolic pathways, and inflammation

252
Q

hyperglycemia and high renal blood flow (hyper filtration) lead to

A

glomerulosclerosis

253
Q

glomerulosclerosis

A

changes in the glomerular basement membranes that becomes permeable to proteins which starts to spill out into the urine leads to decrease in filtration and blood flow to kidneys

254
Q

first manifestation of diabetic renal dysfunction

A

microalbuminuria

255
Q

microalbuminuria

A

protein in urine

256
Q

Hypoproteinemia

A

Hypoproteinemia is a condition where there is an abnormally low level of protein in the blood

257
Q

when seeing microalbuminuria what is happening in our blood

A

decreasing the amount of protein in out blood - Hypoproteinemia

258
Q

laster signs of diabetic renal dysfunction

A

Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN

259
Q

as GFR decreases to less than 10 what type of signs occur

A

uremic signs - nausea, lethargy, acidosis, anemia, and HTN from having high levels of urea in the blood

260
Q

a pt with nerve ischemia and demyelination will have

A

delayed nerve conduction

261
Q

amyotrophy

A

weakening of the hip joint and muscle

262
Q

diabetic neuropathy sensory deficits

A

footdrop, amyotrophy, temp, and pain

263
Q

diabetic autonomic neuropathy deficits

A

delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability

264
Q

steps from healthy tissue to infection in pt with diabetic peripheral neuropathy

A 
healthy tissue
capillary damage
nerve damage and loss of sensation
injury
circulation problem and infection
265
Q

68% of diabetics die from

A

CAD - coronary artery disease

266
Q

prevalence of CAD in diabetic patients increase with

A

the duration but the the severity of diabetes

267
Q

risk factors for macrovascular disease

A

HTN, hyperglycemia, hyperlipidemia, and thrombosis

268
Q

what happens during CAD

A

increased platelet adhesion, decreased fibrinolysis, and accelerated atherosclerosis

269
Q

decreased fibrinolysis

A

more likely to clot

270
Q

claudication

A

pain from reduced blood flow during exercise

271
Q

peripheral vascular disease can lead to what in diabetic patients?

A

claudication, ulcers, gangrene, osteomyelitis, amputation, and increased morbidity

272
Q

risk factors or peripheral vascular disease in diabetics

A

age, duration with DM, genetics, smoking, hyperlipidemia, HTN

273
Q

important nursing actions for diabetics

A

teaching, persevere skin integrity, promote nutrition vaccinations and exercise

274
Q

acute complications of diabetes

A

extreme fluctuations of blood glucose levels. examples: hypoglycemia, hyperglycemia, DKA, HHNKS

275
Q

chronic complications of diabetes

A

damage occurs from hyperglycemia over time. examples: microvascular (eyes, kidneys, and nerves), macrovascualr (CVA,CAD,PVD), and infection

276
Q

decreased insulin production is a characteristic of

A

type 1 DM

277
Q

alpha cells release what?

A

glucagon

278
Q

metabolic syndrome is a component if type 1, 2 or both

A

both

279
Q

first line drug for type 2 diabetes

A

metformin (Glucophage)

280
Q

can metformin be combined with insulin

A

yes

281
Q

what does metformin do?

A

decreases hepatic production of cholesterol, glucose intestinal absorption, and glucose production in liver and increases peripheral glucose uptake and insulin receptor sensitivity

282
Q

black box warning of metformin

A

lactic acidosis and renal disease. renal kidney disease

283
Q

adverse effects of metformin

A

GI, weight loss, hypoglycemia

284
Q

signs and symptoms of lactic acidosis

A

tachypnea, cold/clammy, pain, dizziness, irregular HR

285
Q

metformin contraindicated in

A

renal disease. slows down GFR - drug can build up which can lead to lactic acidosis so check creatine levels before

286
Q

if you have a CT scan with contrast media you should not have

A

metformin for 48 hrs

287
Q

sulfonylureas

A

binds to receptors on beta cells to stimulate release of insulin and decreases glucagon secretion. need a working pancreas for these to work

288
Q

when should sulfonylureas be given

A

30 minutes before breakfast. has a rapid onset of action

289
Q

can you use sulfonylureas in renal patients

A

yes

290
Q

can you use sulfonylureas with insulin? what about metformin?

A

cannot be used with insulin but can be used with metformin

291
Q

adverse effects of sulfonylureas

A

hypoglycemia and weight gain

292
Q

what is an example of a sulfonylureas

A

glipizide (glucotrol)

293
Q

Dipeptidyl peptidase IV inhibitors

A

DPP-IV - inhibits breakdown of incretins

294
Q

Dipeptidyl peptidase IV inhibitors indication

A

improve glycemic control for type 2 diabetes

295
Q

Dipeptidyl peptidase IV inhibitors are associated with

A

pancreatitis

296
Q

common side effects of Dipeptidyl peptidase IV inhibitors

A

URI, headache, and diarrhea

297
Q

can you use Dipeptidyl peptidase IV inhibitors with insulin

A

yes

298
Q

example of Dipeptidyl peptidase IV inhibitors

A

sitagliptin (Januvia)

299
Q

incretin mimetics

A

stimulate insulin production, suppress glucagon, slows gastric emptying, and increased satiety

300
Q

satiety

A

declining satisfaction generated by the consumption of a certain type of food

301
Q

how and when do you give incretin mimetics

A

subcutaneous injection 60 minutes before meal. once daily

302
Q

adverse effect of incretin mimetics

A

thyroid tumors, N/V/D, hemorrhagic/necrotizing pancreatitis

303
Q

black box warning of incretin mimetics

A

thyroid carcinoma

304
Q

example of incretin mimetics

A

liraglutide (Victoza)

305
Q

FSBS

A

finger stick blood sugar

306
Q

what do you want to watch for with insulin and what do you want to check before hand

A

watch for hypoglycemia and check figure stick blood sugar (FSBS) before administration

307
Q

insulin is given

A

sub cut only! besides regular (can be given IV) fat absorbs chemicals slower than muscle

308
Q

insulin restores patient’s ability to

A

metabolize nutrients and convert glycogen to fat stores

309
Q

insulin onset and duration times

A

rapid: 15 minutes onset of 3-5 hr duration
short: 30-60 minutes onset with 6-10 hr duration
long: 1-2 hour onset with 24 hr duration

310
Q

insulin sliding scale

A

basic and basal bolus

311
Q

basic sliding scale

A

FSBS several times a day, delays treatment until hyperglycemia occurs, no research supports it

312
Q

basal bolus scale

A

mimics healthy pancreas, basal = long acting, bolus= meal coverage and corrections

313
Q

severe sign and symptoms of hypoglycemia

A

hypothermia, seizure, brain damage, and death

314
Q

hypoglycemia blood glucose level

A

less than 70 mg/dL

315
Q

less sever signs on hypoglycemia

A

shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable

316
Q

no IV access with someone in hypoglycemia

A

give them sugar tablets

317
Q

what do you do for a patient with hypoglycemia

A

give simple carbs, oral glucose, or IV dextrose (D50W)

318
Q

obstructive lung disease

A

difficulty exhaling

319
Q

restrictive lung disease

A

difficulty getting air in

320
Q

during asthma what happens to activate immune response

A

IgE binds to mast cells and crosslinks to antigen

321
Q

asthma

A

constriction and obstruction of airways

322
Q

eosinophils play a role in what with asthma

A

early (direct tissue injury) and late (release of toxic neuropeptides) inflammatory response

323
Q

activation of immune response during asthma

A

vasodilation, mucosal swelling, bronchocontriction

324
Q

what immunity is involved in asthma

A

cellular and humoral

325
Q

what happens with mast cell degranulation

A

leukotriene synthesis, histamine release, and bradykinin release

326
Q

what can happen to airways with untreated inflammation

A

airway remodeling

327
Q

hyperinflation

A

alveoli getting bigger from CO2 getting trapped

328
Q

asthma attack

A

sudden onset, severe wheezing occurs with inspiration and expiration, dyspnea, nonproductive cough, tachycardia

329
Q

if asthma attack is not resolved

A

status asthmaticus

330
Q

status asthmaticus

A

decrease expiratory volume, increased hypoxemia and CO2, respiratory acidosis

331
Q

silent chest

A

can not hear air movement in lungs. PaCO2 greater than 70 = impending death

332
Q

most common lung disease

A

COPD - 4th leading cause of death

333
Q

risk factors for COPD

A

smoking, air pollutants, genetic components

334
Q

COPD characteristics

A

prolonged expirations, air trapping and pursed lip breathing

335
Q

chronic bronchitis

A

hyper secretion of mucus leads to chronic productive cough and ciliary function impaired so mucus in not moving

336
Q

presentation of chronic bronchitis

A

bronchospasm, cough, air trapping, decrease tidal volume, hypoventilation, hypercapnia, V/Q mismatch, hypoxemia

337
Q

chronic bronchitis treatment

A

bronchodilators, expectorants, antibiotics, steroids, oxygen, and chest physiotherapy

338
Q

what receptors tell use to breathe

A

chemoreceptors

339
Q

chest physiotherapy

A

airway clearance technique (ACT) to drain the lungs, and may include percussion (clapping), vibration, deep breathing, and huffing or coughing.

340
Q

chronic bronchitis patients

A

blue bloaters

341
Q

pulmonary emphysema

A

pink puffer

342
Q

what med is used to treat neuropathy in diabetes patients

A

gabapentin

343
Q

long term control of obstructive lung disease

A

long acting beta 2 agonists, anticholinergics, and leukotriene receptor antagonists

344
Q

quick relief meds for obstructive lung disease

A

IV corticosteroids, short acting beta 2 agonist, and anticholinergics

345
Q

bronchodilating medications

A

short acting beta 2 agonist, long acting beta 2 agonist, and anticholinergics

346
Q

immune suppressant medications

A

leukotriene receptor antagonist and corticosteroids

347
Q

short acting beta 2 agonist example

A

albuterol

348
Q

short acting beta 2 agonist

A

Relax and dilate airways by stimulating the beta 2- adrenergic receptors located throughout the lungs. Cardiac stimulation and increases diuresis and gastric acid secretion . Dose dependent

349
Q

short acting beta 2 agonist indication

A

exercise-induced asthma, acute bronchospasm, bronchitis, emphysema, and other airway obstructions

350
Q

if albuterol is used too much can

A

lose beta 2 affinity and stimulate beta 1

351
Q

side effects of short acting beta 2 agonist

A

tremors, anxiety, restlessness, hypo/hypertension, dizziness

352
Q

Long acting beta 2 agonist example

A

Advair (Fluticasone)

353
Q

anticholinergic bronchodilator example

A

Ipratropium (atrovent)

354
Q

anticholinergic bronchodilator MOA

A

Block acetylcholine receptors to prevent bronchoconstriction which indirectly causes airway relaxation and dilation.

355
Q

anticholinergic bronchodilator indication

A

prevents bronchospasms in chronic bronchitis or emphysema

356
Q

Leukotriene Receptor Antagonist (LTRAs) example

A

Montelukast (Singulair)

357
Q

Leukotriene Receptor Antagonist (LTRAs) MOA

A

Alleviates asthma symptoms in the lungs by reducing inflammation, prevent smooth muscle contraction of the bronchial airways, decrease mucus secretion, and reduce vascular permeability

358
Q

most important guardians of the lung

A

alveolar macrophages

359
Q

what do alveolar macrophages do?

A

activate t and B cells, plasma protein systems (inflammation), and pattern recognition receptors (PRRs)

360
Q

widespread inflammation during pneumonia

A

damage to bronchial mucosa and capillary membranes which cause neutrophil infiltration which causes lung consolidation

361
Q

during pneumonia accumulation of exudate (consolidation) leads to

A

V/Q mismatch, hypoxemia, and hypercapnia

362
Q

treatment for anaphylactic shock

A

diphenhydramine, famotidine (Pepsid), epinephrine

363
Q

emphysema

A

loss of elastic recoil, decrease expiration, enlargement of acini, alveolar destruction without fibrosis, changes in lung tissue cause obstruction, air trapping

364
Q

air trapping leads to

A

V/Q mismatch, hypoxemia, hypercapnia

365
Q

bull and blebs

A

air blisters from alveolar destruction without fibrosis in emphysema patients - decreases ventilation

366
Q

treatment for emphysema patients

A

inhaled anticholinergics, beta 2 agonist, and avoid steroids until late/severe

NURSING School (17 decks)

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