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Nursing-Sem 1 > Patho Exam 1 > Flashcards

Patho Exam 1 Flashcards

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1
Q

Components of the hematologic system

A

bone marrow, blood (RBC, WBC, platelets), spleen, and lymphatics

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2
Q

plasma vs serum

A

serum is plasma minus clotting factors (fibrin/fibrinogen)

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3
Q

Main plasma proteins

A

albumin, clotting factors (fibrinogen), and globulins (alpha, beta, and gamma)

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4
Q

Formed elements of blood (and rough #s)

A

Platelets(250-400 thousand), erythrocytes (4.2-5.8 million), leukocytes (5-9 thousand)

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5
Q

normocytic, microcytic, macrocytic

A

normal size, small size, large size

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6
Q

normochromic, hypochromic, hyperchromic

A

normal color, pale color, vivid color

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7
Q

average life span of RBCs

A

120 days

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8
Q

what removes old RBCs from the bloodstream?

A

reticuloendothelial cells in the liver and spleen

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9
Q

what happens to hemoglobin when RBCs are destroyed?

A

some is recycled and some is broken down to form bilirubin and secreted in bile

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10
Q

what happens to iron when RBCs are destroyed?

A

it is recycled to form new hemoglobin molecules in the bone marrow

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11
Q

Normal levels hemoglobin in men, women

A

M: 13-18 g/100mL; W: 12-16 g/ 100mL

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12
Q

Normal hematocrit levels men, women

A

M: 37-49%; W: 36-46%

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13
Q

what is the mean corpuscular volume (MCV)?

A

The average size of individual RBCs

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14
Q

Normal RBC count in men, women

A

M: 4.5-5.3 million/mm3; W: 4.1-5.1 million/mm3

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15
Q

what is hematocrit?

A

% of RBCs in the plasma

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16
Q

what is hemoglobin?

A

Oxygen-carrying compound composed of a pigment (heme), which contains iron, and a protein (globin)

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17
Q

What does a decrease in plasma volume do to a person’s hematocrit level?

A

increases it–decrease in plasma volume causes increase in hematocrit.

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18
Q

Would dehydration cause increase or decrease in hematocrit?

A

Increase–loss of plasma volume would increase hematocrit

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19
Q

Increase or decrease hematocrit?

  1. decrease plasma volume
  2. deydration
  3. overhydration
  4. decrease # RBCs?
A
  1. increase
  2. increase
  3. decrease
  4. decrease
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20
Q

Hematocrit is helpful for assessing magnitude of what?

A

blood loss

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21
Q

If hematocrit is drawn immediately after blood loss, what will the results show? What about over time after loss?

A

Normal levels. RBCs and plasma lost in equal proportions. Over time the body will compensate for loss by shifting fluid from interstitial space into bloodstream, so the hematocrit will go down (RBCs will be less % of blood…can’t make them as quickly as can shift fluid from interstitial space into bloodstream)

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22
Q

What causes a decrease in hbg (hemoglobin)?

A

blood loss, hemolytic anemia, bone marrow suppression.

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23
Q

If a patient has a normal RBC level but low hbg, what does this indicate?

A

iron deficiency anemia

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24
Q

What are leukocytes?

A

Granulocyte (neutrophils, eosinophils, basophils), agranulocyte (T/B cell lymphocytes, monocytes, tissue macrophages), and platelets

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25
Q

what is erythropoiesis?

A

the production of red blood cells

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26
Q

What triggers erythropoiesis?

A

Low oxygen levels trigger the kidneys to produce erythropoietin (hormone), which stimulates myeloid stem cells in bone marrow to make red blood cells

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27
Q

What nutrients are required for erythropoiesis?

A

iron, B12, folate, B6, protein, other factors

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28
Q

A decrease in the levels of iron, B12, folate, B6, protein, or other factors would lead to..?

A

decrease in production of RBCs, anemia.

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29
Q

What impact does iron deficiency have on RBCs?

A

results in small RBCs, less iron would impact hemoglobin and ability to carry O2

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30
Q

What causes the formation/production of megaloblasts and what are they?

A

Vitamin B12 and folate deficiency. Abnormally large RBCs/erythrocytes.

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31
Q

What role do B12 and folate have in erythropoiesis? How doe people get these nutrients?

A

They;re required for the synthesis of DNA in RBCs. Derived from diet (except in vegetarians–b12 only in animal origin foods)

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32
Q

where does erythropoiesis occur?

A

bone marrow

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33
Q

what stem cells form erythrocytes?

A

hemocytoblasts

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34
Q

erythroblasts, erythrocytes….nucleus?

A

erythroblasts have nucleus, erythrocytes do not.

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35
Q

what is erythropoietin?

A

hormone produced at kidneys in response to low O2, primary regulator or erythropoiesis

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36
Q

what is anemia?

A

lack of adequate #s of mature, healthy RBCs resulting in inefficient O2 carrying capacity/delivery to cells/tissues

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37
Q

what is a reticulocyte? What does it mean if you have increased levels of them?

A

immature red blood cells. If increased # of reticulocytes, it indicates that the body is trying to compensate for anemia,

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38
Q

What are some indicators of anemia?

A

Low hbg and hct, low RBC count, increased reticulocyte count

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39
Q

What are some signs and symptoms of anemia?

A

Fatigue, SOB that worsens with exertion, dizziness, cold intolerance

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40
Q

How do you assess for anemia?

A

pallor, tachypnea, tachycardia, cold extremities, labs (RBC count, hct, hbg, reticulocyte count)

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41
Q

Difference between anemia with acute vs chronic blood loss

A

both: low hct, hbg, low RBC count
acute: high reticulocyte count
chronic: low iron-can’t recycle

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42
Q

most common cause of anemia? how does it work?

A

iron deficiency anemia. Iron is essential for the formation of heme, the part of Hgb responsible for attaching oxygen for transport. Normal erythropoiesis cannot occur

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43
Q

aplastic anemia

A

suppression of bone marrow production of RBCs.

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44
Q

most common hemoglobinopathy & inheritance

A

sickle cell anemia. autosomal recessive

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45
Q

thalassemia & inheritance

A

abnormal hbg (alpha or beta) and large amounts of RBC formed leads to deformities, weak bones. autosomal recessive.

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46
Q

polycythemia

A

excess RBCs > thick blood > increase peripheral resistance dec. blood flow > inc. clotting

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47
Q

WBCs include…

A

granulocytes and agranulocytes

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48
Q

granulocytes

A

neutrophils (mature = segmented, immature = banded) , basophils, eosinophils

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49
Q

agranulocytes

A

lymphocytes (B and T cells) and monocytes (macrophages)

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50
Q

less mature neutrophil called ________ and an increase in these indicates…

A

band cell…body is trying to fight off infection (shift to left = increase in immature neutrophils)

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51
Q

function of monocytes; where located?

A

transform into macrophages to remove debris and phagocytize bacteria@ tissues. particularly @ spleen, liver, peritoneum, alveoli.

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52
Q

Lymphocytes

A

T and B cells

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53
Q

normal range for total WBC count?

A

4500-11000/mm3

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54
Q

neutrophilia

A

increase in neutrophils and bands. often indicative of infection.

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55
Q

neutropenia

A

decrease in neutrophils and agranulocytosis (dramatic decrease in granulocytes. ANC critical @

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56
Q

thrombocytes

A

platelets

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57
Q

platelets form from _____ by _____

A

megakaryocytes by endomitosis. instead of producing daughter cells, fragments into pieces.

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58
Q

how long do platelets last in the bloodstream?

A

~10 days

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59
Q

what’s the function of platelets?

A

blood clotting/ coagulation/ control bleeding

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60
Q

describe the clotting cascade…

A

platelets adhere to injury site > extrinsic and intrinsic pathways activated to release factor X (both pathways) > prothrombin > thrombin > fibrinogen to fibrin

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61
Q

blood is ~____% water

A

90%

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62
Q

where is albumin produced?

A

liver

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63
Q

plasma minus fibrinogen/clotting factors

A

serum

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64
Q

hemostasis

A

blood clotting (stopping of blood)

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65
Q

under normal (not injured) conditions, endothelial cells secrete prostacyclin, nitric oxide, CD39 enzyme, which do…

A

prostacyclin = prostaglandin
NO = vasodilator, inhibit platelet aggregation
CD39 enzyme = breaks down ADP in blood. OVERALL: assure platelets don’t stick together or to vessel wall

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66
Q

vWf (von Willibrand factor)

A

produced by endothelial cells, helps to bind collagen and platelets together when vessel injured

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67
Q

blood clot consists of…

A

fibrin, platelets, and trapped RBCs

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68
Q

prothrombin time (PT)

A

amount of time it takes liquid portion of your blood to clot. evaluates extrinsic pathway of coagulation cascade. normal = 11 to 13.5 sec

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69
Q

INR

A

international normalized ration. normal = 0.8-1.1. Above normal = blood clotting too slowly. If on blood thinners, INR 2-3. More than 3

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70
Q

what does D-dimer measure?

A

fibrin degradation products. indicates recent clotting activity.

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71
Q

substances primarily responsible for decreasing/dissolving clots?

A

Plasmin, plasminogen, tissue plasminogen activator (tPA)

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72
Q

fibrinogen levels indicate…

A

reflect clotting activity/ability. may be elevated with inflammation, infection

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73
Q

aPTT

A

measures time to clot. evaluates intrinsic coagulation cascade.

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74
Q

platelet aggregation

A

evaluates platelet ability to adhere, form clumps. If abnormal, bleeding risk

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75
Q

ITP, TTP, vWD, DIC

A

clotting disorders

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76
Q

types of immunity

A

natural (nonspecific, 1st line), acquired (develops with exposure-humoral (B) or cellular (T))

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77
Q

humoral immunity

A

B cells detect specific antigen and produce antibodies/immunoglobilins. 2nd line defense. Operates @ humor/blood.

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78
Q

cellular immunity

A

T lymphocytes detect antigen and transform into cytotoxic T cells to “kill” infected cells. Operates @ cellular level

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79
Q

B cells differentiate into

A

effector cells (produce antibodies) and memory cells ( remember antigens/MHCs for faster response next time)

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80
Q

when cell detects foreign body/pathogen, what’s the next step?

A

Forms MHC/APC and presents “flag” on surface for B (@ blood) or T(@cell) cells to recognize/respond to

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81
Q

leukocytes vs. lymphocytes

A

leukocytes (neutrophils, eosinophils, basophils, monocytes, macrophages) and lymphocytes (B, T, and NK cells)

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82
Q

where do immune cells originate? mature?

A

all immune cells originate @ bone marrow. B cells mature @ bone marrow, T cells mature @ thymus.

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83
Q

immune system @ skin

A

1st line defense. antimicrobial proteins and protection.

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84
Q

immune system @ bone marrow

A

immune cells all produced at bone marrow

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85
Q

immune system @ bloodstream

A

immune cells circulate through blood stream looking for pathogens/infected cells

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86
Q

immune system @ thymus

A

T cells mature @ thymus

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87
Q

immune system @ lymphatic system

A

immune cells converge @ lymph nodes. travel/comm of immune cells @ lymphatic system.

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88
Q

immune system @ spleen

A

immune cells enriched @ certain parts of spleen

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89
Q

immune system @ mucosal tissue

A

prime entry points for pathogens > specialized immune hubs (Peyer’s patches where immune cells “sample” GI tract)

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90
Q

4 stages of immunity

A

recognition, proliferation (of B/T cells), response (Ab or cytotoxic Ts), effector (immune cells begin to destroy pathogens)

91
Q

How to antibodies/immunoglobulins work to destroy pathogens?

A

agglutination (clumping), opsonization (coat with sticky substance), histamine production, activate complement system

92
Q

IgG

A

most common. blood borne and tissue infections. activates complement system.

93
Q

IgA

A

body fluids. protects against respiratory, GI, and GU infections

94
Q

IgM

A

intravascular serum. 1st in bacterial infections.

95
Q

IgE

A

in serum. allergies. combats parasitic infections.

96
Q

IgD

A

role unknown.

97
Q

types of T cells and roles

A

Effector (activate when find antigen, attract other cells–B,Tc, NK, macrophages), cytotoxic T (attack cell w/ cell lysis & cytolytic enzymes), suppressor T (feedback loop. check B cell production), memory T (rec. from earlier exposure)

98
Q

complement system

A

circulating plasma proteins help fight off invading pathogens (vessel size, permeability, clotting, enhance chemotaxis). Promotes inflammatory response.

99
Q

CBC count

A

complete blood cell count (leukopenia v. leukocytosis & WBC differential)

100
Q

normal leukocyte levels (adult)

A

7400/uL

101
Q

leukemias

A

problematic B/T stem cell formation @ bone marrow.

102
Q

Characteristic sign of non-hodgkins lymphoma

A

lymphademopathy (enlarged lymph nodes)

103
Q

pathophysiology

A

biological and physical manifestations of disease and associated functional changes.

104
Q

health

A

state of complete physical, mental, and social wellbeing, not just absence of disease

105
Q

homeostasis

A

“steady state” maintenance . constantly changing to regulate and keep body at optimal levels of functioning

106
Q

constancy

A

never changing

107
Q

stress

A

challenge, threat, damage to a person’s equilibrium. a state manifested by a specific syndrome of the body developed in response to any stimuli that made an intense systemic demand on it

108
Q

adaptation / resilience

A

an individual’s unique capacity to adapt to or cope with the stressor

109
Q

types of stressors

A

physical (cold, heat), physiologic (pain, fatigue), psychosocial (isolation, fear)

110
Q

stress response 3 stages

A

alarm, resistance, exhaustion

111
Q

alarm stage of stress response

A

HPA axis, fight or flight response. defensive, anti-inflammatory. limited.

112
Q

resistance stage of stress response

A

adaptation to stressor. cortisol still increased.

113
Q

exhaustion stage of stress response

A

endocrine activity increases. negative consequences of long term stressors.

114
Q

Psychoneuroimmunology

A

Study of the interactions between our mind (consciousness, brain, and CNS) and immune function

115
Q

what does cortisol do to immune response

A

suppresses inflammatory response. relationship between stress and sickness because can’t fight off infections as well w. high cortisol levels

116
Q

sympathetic nervous system (SNS)

A

fight or flight response. epic/norepi released > shuts blood to vital areas, increases BP (in trauma, trying to return BP to normal when hypotensive/hypovolemic shock/ etc.)

117
Q

RAAS pathway

A

drop bp/bvol > kidneys release renin/angiotensin > inc. angiotensin I (kidney), II > angiotensin II (lung) stimulates vasoconstriction to inc. bp and > stimulates adrenal cortex to release aldosterone > increases reabsorption of H2O, Na > inc. blood volume > BP to normal

118
Q

cortisol release

A

Hypothalamus - CRH (corticotropin-releasing hormone) > ant. pituitary - ACTH > adrenal cortex - cortisol

119
Q

angiotensin II f’n

A

promotes vasoconstriction

120
Q

aldosterone f’n

A

promotes reabsorption of water, sodium. released @ adrenal cortex

121
Q

cortisol f’n

A

alters glucose, fat, protein metabolism (from storage to supplying…increase blood glucose); suppresses inflammatory and immunes response. Aid fight or flight response.

122
Q

antidiuretic hormone (ADH) & how works

A

vasopressin. causes vasoconstriction. Stimulates kidneys to reabsorb water from urine to blood.

123
Q

cortisol @ chronic stress, PTSD

A

cortisol elevated with chronic stress, decreased with PTSD

124
Q

Chronic stress and neuroendocrine and metabolic stress…

A

chronic stress >elevated cortisol/epi/norepi levels > insulin resistance > inc. blood glucose > link with inactivity and overeating

125
Q

positive and negative feedback loop

A

positive promotes more of activity (i.e. clotting) and negative stops activity (i.e. blood pressure return to normal w/ RAAS)

126
Q

hypertrophy

A

enlarged muscle mass that happens with increased workload

127
Q

atrophy

A

loss of muscle mass associated with loss of use, disease, dec. blood/ nerve supply, etc.

128
Q

hyperplasia, dysplasia, metaplasia

A 
hyper = increase in # new cells 
dys = abnormal cell changes
meta = change of cells to unusual former tissue where it's found
129
Q

cellular injury and common causes

A

disruption of steady state regulation. commonly caused by hypoxia, nutritional imbalances, physical agents, chemical injury, infectious agents

130
Q

inflammation and purposes

A

innate, automatic response to neutralize harmful agents, remove dead tissue, generate new growth, promote healing

131
Q

inflammatory response

A

injury > chemical signals like histamine released > increase vascular permeability > more fluids, WBC to injury site > WBCs “eat” pathogens, debris > tissue heals

132
Q

gene

A

sequence of DNA that contains instructions for making RNA molecules/proteins.

133
Q

transcription

A

DNA to RNA

134
Q

translation

A

RNA to proteins

135
Q

induction

A

turn gene “on”

136
Q

repression

A

turn gene “off”

137
Q

genotype

A

genetic makeup/material

138
Q

phenotype

A

expression of genetic makeup/physical characteristics

139
Q

polygenic

A

many genes affect one trait

140
Q

allele

A

copy of a gene. if alike, homozygous. if different, heterozygous. if only have one copy, homozygous

141
Q

interstitial fluid

A

A filtrate of the blood; located between cells and between cells and capillaries. contains water, sodium

142
Q

diffusion

A

passive transport of molecules from high conc to low conc

143
Q

osmosis

A

movement of water from less conc sol to more conc sol. Movement of WATER.

144
Q

facilitated transport

A

The passing of certain molecules through the plasma membrane with assistance from carrier proteins. i.e. glucose with carrier insulin

145
Q

active transport

A

requires energy. goes against concentration gradient. sodium potassium pump powers movement.

146
Q

sodium is more prevalent in/outside cells?

A

outside

147
Q

potassium is more prevalent in/outside cells?

A

inside

148
Q

normal sodium level

A

140 mEq

149
Q

normal potassium level

A

5 mEq

150
Q

hydrostatic pressure

A

force exerted by water in bloodstream. source: heart pumping.

151
Q

osmotic pressure

A

pressure exerted by solutes (i.e. electrolytes) in solution (bloodstream)

152
Q

Oncotic pressure

A

force exerted by albumin (plasma protein) in bloodstream.

153
Q

normal serum albumin

A

3.1-4.3 g/ dL

154
Q

total albumin levels indicate…

A

overal nutritional level of pt.

155
Q

Osmolality + normal levels

A

if take solutes out of solution and measure their mass per kg of solvent. Based on 1 mole (6.02 * 10^23). Normal = 282-295mOsmoles / kg water.

156
Q

Osmolarity

A

Osmoles per L of solute (R in osmolarity and liter). Mainly sodium. Found in extracellular space.

157
Q

What is osmolality used for in clinical practice?

A

determining hydration status

158
Q

Isotonic

A

same tonicity as blood; does not cause fluid shifts or alter body cell size

159
Q

Hypotonic

A

fewer particles and more water than blood and body fluids. Adds water to the bloodstream and causes a fluid shift from ECF to ICF, causing cells to swell.

160
Q

Hypertonic

A

contains more particles and less water than blood and body fluids. Adds solutes to the bloodstream and causes fluids to shift from ICF to ECF, causing body cells to shrink

161
Q

fluid output @ kidneys

A

1 mL urine/Kg/hr.

162
Q

fluid loss @ skin

A

perspiration, evaporation

163
Q

fluid output @ lungs

A

300mL/ day

164
Q

fluid output @ GI

A

100-200 mL/ day

165
Q

most significant factor in urine concentration

A

presence/absence of of ADH

166
Q

Natriuretic peptides

A

Three major peptides that promote natriuresis (excretion of large volumes of both sodium and water by the kidneys in response to excess ECF volume). Atrial natriuretic peptide (ANP), Brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP)

167
Q

hypovolemia

A

dehydration

168
Q

hypervolemia

A

overhydration

169
Q

Hypo/pernatremia

A

too little/much salt

170
Q

Hypo/perkalemia

A

Too little/much potassium

171
Q

hypo/percalcemia

A

too little/much calcium

172
Q

hypo/perphosphatemia

A

too litte/much phosphate

173
Q

hypo/permagensemia

A

too little/much magnesium

174
Q

s/s, assessment, tx, testing for hypovolemia

A

s/s: thirst, dry membranes, weakness

assessment: little, dark urine, turgor poor, hypotension, dry membranes
tx: oral fluids
testing: blood urea nitrogen elevated, oliguria (abn. small amt urine), hypernatremia

175
Q

s/s, assessment, tx, testing for hypervolemia

A

s/s: edema, weight gain

ass: SOB/fluid, crackles, edema/pitting, weight
tx: Diuretic
test: dilutional hypernatremia

176
Q

s/s, assessment, tx, testing for hyponatremia

A

s/s: muscle cramps, weakness, headache, confusion

ass: weakness, depression, anxiety, lethargy, confusion
tx: depends on cause
test: Serum sodium levels

177
Q

extracellular electrolytes

A

Na, Cl

178
Q

intracellular electrolytes

A

K, Mg, PO4,

179
Q

Sodium reference range

A

136-145 mEq/ L

180
Q

potassium reference range

A

3.5-5.1 mEq/ L

181
Q

calcium reference range

A

9-10.5 mg/ dL

182
Q

bicarbonate reference range

A

21-30 mEq/ L

183
Q

s/s, assessment, tx, testing for hypernatremia

A

s/s: dec. saliva, thirst, headache, agitation, seizures

ass: turgor, reflexes, tachycardia, thready pulse, vol. changes
tx: replace water if necessary
test: serum sodium >145 mEq/ L

184
Q

s/s, assessment, tx, testing for hypokalemia

A

too little potassium.
s/s: anorexia, nausea, vomiting, weakness/cramping
ass: postural hypotension, muscle weakness
tx: oral, parenteral K+
test: serum pot

185
Q

s/s, assessment, tx, testing for hypokalemia

A

too little potassium.
s/s: anorexia, nausea, vomiting, weakness/cramping
ass: postural hypotension, muscle weakness
tx: oral, parenteral K+
test: serum pot

186
Q

IV potassium: yay or nay? why?

A

nay. potassium is extremely caustic to veins, careful about infiltration. can also cause fatal dysrhythmias b/c affects muscle function. lethal injections. in emergencies can be given DILUTED via CENTRAL LINE.

187
Q

s/s, assessment, tx, testing for hyperkalemia

A 
too much potassium
s/s: nausea, cramping, diarrhea, muscle weakness/cramping
ass: muscle weakness, cramping
tx: dextrose, insulin, sodium bicarb
test: serum potassium levels
188
Q

s/s, assessment, tx, testing for hypocalcemia

A

s/s: tetany, laryngeal spasm, bone pain, fx, confusion, seizures

ass: tetany, hyperactive reflexes, Chvostek/Trousseau’s signs, hypotension
tx: admin Ca2+ and Vit D.
test: serum calcium level

189
Q

tetany

A

body-wide cramping

190
Q

Chvostek signs

A

tap facial nerve > induce lip twitches to facial spasms

191
Q

Trousseau’s sign

A

inflate BP cuff > occlude arterial BP 3-5 min > induces carpopedal spasm

192
Q

s/s, assessment, tx, testing for hypercalcemia

A

s/s: anorexia, nausea, constipation, muscle weakness, bone fx

ass: dec. muscle excitability, ataxia, loss muscle tone
tx: fluids, loop diuretics, biphosphonates, calcitonin, dialysis
test: serum calcium > 10.5 mg/ dL

193
Q

s/s, assessment, tx, testing for hypophosphatemia

A

s/s: tremor, lack coordination, confusion, joint stiffness

ass: tremor, ataxia, weakness, dec. refelxes
tx: replace PO4-
test: serum phosphorous level

194
Q

s/s, assessment, tx, testing for hypomagnesemia

A

s/s: cramps, muscle change, uncontrol mvmt

ass: + Chvostek/Trousseau, Babkinski, nystagmus, htn
tx: replace Mg2+ therapy
test: serum magnesium

195
Q

Babinski signs

A

toes fan out with “tickle” bottom of foot

196
Q

s/s, assessment, tx, testing for hypermagnesemia

A

s/s: lethary, confusion, weakness

ass: hyporeflexia, hypotension, weakness
tx: IV calcium or dialysis
test: serum magnesium level >2.5 mg/dL, arrhythmia

197
Q

acid

A

donates H+, pH

198
Q

base

A

accepts H+, pH > 7.0

199
Q

carbonic acid link

A

H2CO3 links respiratory and metabolic systems. @ lungs regulate by changing breathing rate/depth. @ kidneys regulate by absorbing/excreting acids/bases

200
Q

partial pressure of CO2 (PCO2)

A

35-45 mmHg

201
Q

describe respiratory compensation (pH)

A

receptors @ arteries sense changes in PCO2, if too low (resp alkalosis), stimulate respiratory center @ medulla to inc. breathing rate. if too high (resp acidosis), decrease rate. Compensation only moderately effective, but fast.

202
Q

describe metabolic compensation (pH)

A

kidneys control pH by regulating level of bicarb(HCO3-) reabsorption and H+ reabsorption or excretion. Slow compensation. Takes days to reach max effect.

203
Q

respiratory alkalosis

A

too much CO2 is blown off, blood become alkaline (hyperventilation)

204
Q

ABGs (arterial blood gasses)

A

measure blood acidity, partial pressure of O2 &CO2, O2CT & O2Sat, and HCO3-

205
Q

pH reference values (arterial)

A

7.35-7.45 pH

206
Q

PaCO2 reference values (arterial)

A

35-45 mmHg

207
Q

acidemia

A

pH > 7.45. 7.8+ can be fatal

208
Q

alkalemia

A

pH

209
Q

PaO2 reference range

A

80-100 mmHg

210
Q

PaO2

A

hypoxemia

211
Q

hyperventilation/hypocapnia

A

PaCO2

212
Q

hypoventilation/hypercapnia

A

PaCO2 > 45 mmHg. Hypercapnia = too much CO2 in blood. Results from breathing too low/shallow, don’t blow off enough CO2.

213
Q

what % of O2 carried by hbg molecules?

A

97%

214
Q

normal O2Sat

A

95-98%

215
Q

normal O2Sat (SaO2)

A

95-98%

216
Q

bicarbonate (HCO3-) reference range

A

21-28 mmol/L

217
Q
A

metabolic acidosis

218
Q

> 26 mEq/L HCO3-

A

metabolic alkalosis

219
Q

buffer ions

A

bicarbonate, phosphates, hbg, plasma proteins

220
Q

Low PO2

A

hypoxia, hypoemia

221
Q

elevated PCO2

A

hypercapnia

222
Q

low PCO2

A

hypocapnia

223
Q

Interpreting ABGs

A
  1. pH (acid or alkalosis)

2. PCO2 (PCO2 > 45 hypovent,

Nursing-Sem 1 (13 decks)

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