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Exam 1 Flashcards

1
Q

Hemoglobin

A

12 - 16 g/dL

Protein in RBC’s responsible for carrying O2

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2
Q

Hematocrit

A

37 - 47%

Volume of RBC’s compared to total blood volume

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3
Q

Treatment for anemia

A 
Targeted to cause
Erythropoietin
Blood transfusions
Supplements: Fe
Rest, oxygen, fluids
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4
Q

Platelet counts

A

150 - 450 x 10^3

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5
Q

INR

A 
International normalized ratio
0.9 - 1.1
Standardized prothombintine
High INR = thinner blood
Low INR = thicker blood
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6
Q

Hydropic cell injury

A

Accumulation of water
Malfunction of Na-K pump (water follows salt)
Causes swelling
Reversible

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7
Q

3 types of intracellular accumulations

A

Normal substances: fatty deposits in liver from alcoholism
Abnormal substances: glucose in diabetics
Pigments and particles: billirubin in neonates

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8
Q

Cellular atrophy

A

Cells shrink and reduce function (adaptation)

Dehydration, immobilization, poor nutrition

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9
Q

Cellular hypertrophy

A

Increase in cell mass with increased functional capacity (adaptation)
Uterus and breasts in pregnancy
Skeletal muscle with exercise

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10
Q

Cellular hyperplasia

A

Increase in number of cells by mitotic division (adaptation)

Increase RBC in altitude

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11
Q

Cellular metaplasia

A

Replacement of one differentiated cell type with another
Less reversible
Smoking leads to lung changes

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12
Q

Cellular dysplasia

A

Abnormal appearance of cells because of abnormal variations in size, shape and arrangement
Less reversible
Significant probability of developing into cancer

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13
Q

Irreversible cell injury

A

Cellular death

Necrosis and apoptosis

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14
Q

Necrosis

A

Caused by toxic injury or ischemia
Cell ruptures and spills contents
Breakdown of plasma membrane
Systemic problems: shown in labs

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15
Q

Apoptosis

A

Doesn’t directly kill cell but activates chain of events that leads to cell death
Blebs separate from cell which are then destroyed by other cells
No damage to surrounding cells
No inflammation
Normal process of cell death

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16
Q

Hypoxia

A

Poor oxygenation

Most common cause of cellular injury

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17
Q

Ischemia

A

Interruption of blood flow leading to poor oxygenation

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18
Q

Steps of hypoxia/ischemia (Mechanism)

A 
ATP production slows from lack of O2
ATP pumps fail (e.g. Na-K pump)
Na accumulates and brings more H20
Excess Ca in mitochondria interferes
Glycogen depleted
Lactate produced (cramps)
pH falls: cellular components become dysfunctional
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19
Q

What are the adverse effects of reintroducing O2 during hypoxia/ischemia?

A

Reperfusion injury and reactive oxygen species

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20
Q

Reperfusion injury

A

Calcium overload: crosses cell membrane and triggers apoptosis
Forms reactive oxygen species/ free radicals
Inflammation can last days/weeks
Complement activation

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21
Q

Reactive oxygen species

A

Unpaired electron looking for a partner: steal molecules causing damage to that molecule (from cell membranes, proteins or cell chromosomes)

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22
Q

Nutritional causes of cellular injury

A

Deficiencies: iron deficiency, malabsorption
Excess: obesity

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23
Q

Chemical causes of cellular injury

A

Free radicals
Heavy metals: lead
Toxic gases: ozone, CO, poisoning

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24
Q

Physical and mechanical cellular injury

A

Temperature extremes: heat stroke, frostbite
Abrupt changes in atmospheric pressure
Abrasion: trauma
Electrical burns
Radiation: direct damage; indirect by creating free radicals

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25
Q

Infectious and immunologic cellular injury

A

Bacteria: endotoxins and exotoxins
Virus
Indirect immunologic response: processes of inflammation and byproducts of immune response

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26
Q

Endotoxin vs. Exotoxin

A

Endotoxins: toxins with the cell walls of bacteria; released when killed
Exotoxins: Produced by bacteria and released while still alive

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27
Q

When presented with a challenge, cells have the following three reactions

A

Withstand and return to normal
Adapt
Die

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28
Q

Which cell reactions are reversible/irreversible?

A

Withstanding and adapting are generally reversible.

Dying is irreversible

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29
Q

Which form of adaptation is the least reversible?

A

Dysplasia

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30
Q

What are two forms of reversible cell injury?

A

Hydropic and intracellular accumulations

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31
Q

Hydropic injury results from the malfunction of what?

A

Na - K pumps

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32
Q

Generalized swelling in cells of a particular organ caused by hydropic injury is called

A

Megaly

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33
Q

Four cases of atrophy

A

Dehydration
Immobilization
Lack of nutrition
Ischemia

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34
Q

Three cases of hypertrophy

A 
Uterus/ breasts (pregnancy)
Skeletal muscles (exercise)
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35
Q

Three cases hyperplasia

A

Liver
Increase in RBC’s at altitude
Prostate enlargement

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36
Q

Two cellular adaptations in response to persistent injury

A

Metaplasia

Dysplasia

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37
Q

Does pH rise or fall during hypoxia and ischemia?

A

Falls

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38
Q

During hypoxia and ischemia, what ion is found in excess in the mitochondria?

A

Calcium

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39
Q

COX 1

A

Protective prostaglandins, stomach mucosa, and platelet stickiness

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40
Q

COX 2

A

Inflammatory prostaglandins leading to pain, inflammation and fever

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41
Q

What are four therapeutic uses of aspirin?

A

Anti-inflammatory, analgesia, antipyretic, prevention of platelet aggregation

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42
Q

Can children take aspirin?

A

No, risk of Reye’s Syndrome, which results in encephalopathy and fatty liver

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43
Q

Adverse effects of aspirin

A

GI effects, bleeding, renal impairment, salicylate toxicity (4g +)

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44
Q

Major drug interaction with aspirin

A

Anticoagulants

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45
Q

Mu receptors affect what?

A

Analgesia, respiratory depression, euphoria, sedation, decreased GI motility and physical dependence

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46
Q

Kappa receptors affect what?

A

Analgesia, sedation, and decreased motility

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47
Q

What is tolerance?

A

When a larger dose is required to produce the same response as before from a smaller dose
* Can develop tolerance to sedation and respiratory depression but not constipation

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48
Q

Physical dependence

A

When physiologic abstinence syndrome will occur if drug is abruptly stopped

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49
Q

Addiction

A

Uncontrollable cravings, inability to control drug use, compulsive drug use and use despite doing harm to oneself or others

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50
Q

Three major physiologic changes that occur at birth

A

Oxygenation
Circulation
Nutrition

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51
Q

How long can neonates survive without breathing? When does brain damage occur?

A

10 minutes

8 minutes

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52
Q

What can interfere with oxygenation to the fetus?

A

Umbilical cord compression
Premature separation of placenta
Excessive contraction of uterus
Analgesics

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53
Q

What are three fetal shunts that close after birth?

A 
Foramen ovale (bypass lungs, blood from right atrium to left)
Ductus arteriosus (blood from pulmonary artery to aorta)
Ductus venosus (blood away from liver)
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54
Q

What is the number one way to tell if the baby’s circulation transition is going well?

A

Upper and lower pulse ox at 95%+ with near identical pulses

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55
Q

Two other factors to assess fetal circulation

A

Respiratory rate

Cap refill on sternum

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56
Q

How much weight loss is expected after first days after birth?

A

20%

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57
Q

When should a baby be back at birth weight?

A

Within 2 weeks

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58
Q

What is a disease causing organism called?

A

Agent/ microbe/ pathogen

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59
Q

Reservoir

A

Where a pathogen lives or reproduces

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60
Q

Mode of transmission

A

Mechanism by which agent is spread: contact, droplet, airborne, or animal

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61
Q

Host

A

Individual at risk for contracting the infection

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62
Q

Examples of breaking chain of infection at the reservoir level

A

Spraying for mosquitoes

Quarantine

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63
Q

Examples of breaking chain of infection at the Portal of entry/exit

A

Gloves and PPE

Cough etiquette

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64
Q

Examples of breaking chain of infection at mode of transmission

A

Sterile technique

Proper cooking and food storage

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65
Q

Examples of breaking chain of infection at host level

A

Vaccines

Boosting immunity through wellness techniques

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66
Q

Pathogenicity

A

Ability of a microbe to cause disease

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67
Q

Virulence

A

How severe the disease is

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68
Q

Adherence of microbe

A

How well it can stick to something: often using fillae or fimbrae

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69
Q

Biofilm

A

Sheets of microbes stuck together

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70
Q

Antiphagocytic factors

A

Keep a pathogen from being tagged by the immune system for destruction

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71
Q

Four types of pathogens

A

Bacteria
Viruses
Fungi
Parasites

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72
Q

Bacteria

A

Single celled
Rigid cell wall
No internal organelles

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73
Q

Cocci

A

Spherical bacteria

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74
Q

Bacilli

A

Rod or comma bacteria

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75
Q

Gram positive bacteria

A

Stain blue

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76
Q

Gram negative bacteria

A

Stain pink

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77
Q

Fungi

A

Eurkaryotic
Form complex structures
Thick, rigid cell wall

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78
Q

Mycotic infections

A

Caused by fungi

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79
Q

Three examples of parasites

A

Protozoa
Helminths
Arthropods

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80
Q

Viruses

A

No metabolism
Dependent on permissive host cells to make and assemble parts
Develop intracellularly

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81
Q

Four clinical infectious disease stages

A

Incubation
Prodromal
Illness
Convalescence

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82
Q

Most signs and symptoms during illness are from

A

Inflammation and immune response

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83
Q

Hallmark clinical manifestation of infection is:

A

Fever

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84
Q

What two groups often do not show a fever with an infection?

A

Elderly

Immunosuppressed

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85
Q

What can a broad spectrum antibiotic target?

A

Gram positive bacteria
Gram negative bacteria
Anaerobes

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86
Q

Bacteriocidal

A

Lethal to bacteria at clinically achievable concentrations

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87
Q

Bacteriostatic

A

Slow bacterial growth without causing cell death

Host will ultimately eliminate pathogen

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88
Q

Four mechanisms of action for antibiotics

A

Cell wall synthesis inhibition
Protein synthesis inhibition
DNA synthesis inhibition
Metabolism inhibition

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89
Q

Four antibiotics that are cell wall synthesis inhibitors

A

Amoxicillin
Piperacillin
Cephalexin
Ceftriaxone

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90
Q

How does Penicillin work?

A

Binds to penicilllin binding protein and inhibits synthesis of cell wall by interfering with transpeptidase

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91
Q

What is the result of Penicillin

A

Lysis of bacterial cell and death

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92
Q

Amoxicillin

A

Broad spectrum against both gram positive and negative bacteria adn some anaerobes

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93
Q

Major side effect for almost all antibiotics

A

Abdominal pain and diarrhea

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94
Q

What enzyme can make some bacteria resistant to antibiotics?

A

Beta-lactamase

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95
Q

Beta-lactamase inhibitor

A

Chemical compound that does not have antimicrobial therapy but combines with an antibiotic to prevent inactivation by beta-lactamase

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96
Q

Three beta-lactamase inhibitors

A

Clavulanic acid
Sulbactam
Tazobactam

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97
Q

Major side effect of clavulanic acid

A

Diarrhea

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98
Q

Which antibiotics are grouped into generations according to effectiveness against different organisms, characteristics and development?

A

Cephalosporins

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99
Q

What is the risk of penicillin and cephalosporin being chemically similar?

A

Cross sensitivity can occur in about 5% of patients

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100
Q

Cephalexin

A

AKA Keflex
Oral first gen cephalosporin
Active against skin flora

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101
Q

Ceftriaxone

A

Third gen cephalosporin
IV or IM
CNS penetration

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102
Q

Two antibiotics that are protein synthesis inhibitors

A

Doxycycline

Azirthromycin

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103
Q

How do doxycycline and azirthromycin work?

A

Doxy binds at the 30S portion of bacterial ribosome
Azith binds at 50S portion of ribosome
No human interaction because humans have 40s and 60S ribosomes

104
Q

Doxycycline is effective against

A

Gram positive and negative bacteria
Mycoplasma pneumoniae
Chlamydia species
Tick borne illness

105
Q

Doxycyline belongs to what class?

A

Tetracyclines

106
Q

Doxycyline should not be taken with

A

Milk

Antacids

107
Q

Doxycyline associated with what type of diarrhea

A

C. difficile

108
Q

Three atypical organisms covered by azithromycin

A

Mycoplasma
Legionella
Chlamydia

109
Q

What class of protein synthesis inhibitor does azithromycin belong in?

A

Macrolides/ketolides

110
Q

Azithromycin increases the risk of

A

QT prolongation on an EKG

111
Q

Anemia

A

Deficit of RBC’s

112
Q

Two things that result in anemia

A

Relative-normal total RBC mass with increased plasma volume (pregnancy)
Absolute decrease in RBC’s

113
Q

Pernicious anemia

A

Lack of Vitamin B leads to altered DNA synthesis

114
Q

Folate deficiency anemia

A

Lack of folate leads to premature cell death

115
Q

Iron deficiency anemia

A

Lack of iron leads to lack of hemoglobin

116
Q

Thalassemia anemia

A

Impaired synthesis of hemoglobin

Congenital

117
Q

Aplastic anemia

A

Bone marrow suppression leads to decreased production of RBC’s

118
Q

Sickle cell anemia

A

Abnormal hemoglobin molecule

Congenital

119
Q

Post hemorrhage anemia

A

Blood loss leads to insufficient RBC’s

120
Q

Hemolytic disease of the newborn

A

Maternal antibodies cause the destruction of fetal cells

121
Q

Signs and symptoms of anemia

A 
Claudication (muscle cramps)
Weakness
Pallor
Increased respiratory rate
Dizziness, fainting, lethary
Fatty changes in liver, kidneys and heart
122
Q

What two hormones are elevated in anemia?

A

Epinephrine

Norepinephrine

123
Q

Decreased RBC’s/hemoglobin leads to

A

Decreased oxygen carrying capacity: hypoxia

124
Q

Effects of anemia on cardiovascular system

A

Increased HR, stroke volume, and capillary dilation

125
Q

Effects of anemia on renal system

A

Increased salt and water retention

Increased extracellular fluid

126
Q

Increase of DPG in cells leads to

A

Increased release of oxygen from hemoglovin in tissues

127
Q

Erythropoietin

A

Stimulates bone marrow to produce more RBC’s

128
Q

Most common nutritional deficiency in the world

A

Iron deficiency anemia

129
Q

Possible causes of iron deficiency anemia

A

Low intake of iron in the diet
Physiological increase in need
Iron loss due to hemorrhage or heavy period
Renal issues

130
Q

What age group is at the highest risk for iron deficiency anemia

A

Infants and toddlers due to introduction of solid food

131
Q

Pica

A

Condition in which people crave non-food or non-nutritive substances
Primary sign of iron deficiency anemia

132
Q

Thrombocytopenia

A

Platelet disorder of reduced quantity or increased consumption of platelets

133
Q

Hemostasis

A

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

134
Q

Primary hemostasis

A

Vasoconstriction at the site
Platelet plug
Takes 3-7 min

135
Q

Secondary hemostasis

A

Formation of fibrin clot
Clotting factors activated
Starts in about 3-10 min

136
Q

Petechia

A

Flat, pinpoint red marks on skin

137
Q

Purpura

A

lots of petechia together

Tends to be itchy

138
Q

Ecchymosis

139
Q

Hemarthrosis

A

Collection of blood in joints

140
Q

Hematoma

A

Collection of blood in tissue

141
Q

Hematuria

A

Blood in urine

142
Q

Hematochezia

A

Blood in stool

143
Q

Hematemesis

A

Blood in vomit

144
Q

Epistaxis

A

Nose bleed

145
Q

Hemoptysis

A

Coughing blood

146
Q

Menorrhagia

A

Heavy period

147
Q

Hypovolemia

A

Low blood volume

148
Q

Signs of hypovolemia

A 
Tenting
Low BP
Initial increase in HR, then decrease
Pallor
Similar to hypoxia
149
Q

Treatment for bleeding disorders

A 
Avoid the cause
Steroids to suppress the immune system
IVIG
Factor replacement
Platelets
Fresh frozen plasma
150
Q

Assessment findings for thrombocytopenia

A

Petechiae
Purpura
Decreased platelet counts
Generalized bleeding

151
Q

Thrombus

A

Stationary blood clot formed within a vessel or chamber of the heart

152
Q

What is a thrombus composed of?

A

Platelets, clotting factors and fibrin

153
Q

Three major risk factors for thrombus

A

Vessel wall injury
Circulatory stasis
Hypercoagulable conditions

154
Q

Deep vein thrombosis

A

Presence of a thrombus in a deep vein

Typically lower extremity

155
Q

Assessment findings for DVT

A

Edema
Pain and tenderness
Redness or discoloration
Warmth

156
Q

D-dimer

A

Presence of high levels of fibrin products in the body

157
Q

Treatments for DVT

A

Thrombolytic to break down clot

Anticoagulants to reduce clot formation

158
Q

Are platelets involved in secondary hemostasis?

159
Q

What circulatory changes are expected after the birth of an infant?

A

Decreased pulmonary vascular resistance

Increased systemic vascular resistance

160
Q

Three contributing factors to formation of thrombus

A

Endothelial injury
Circulatory stasis
Hypercoagulability

161
Q

Why should ceftriaxone be avoided in neonates?

A

Due to the risk of hyperbilirubinemia because ceftriaxone displaces bilirubin from albumin binding sites

162
Q

Heparin and Enoxaparin

A

Unfractionated heparin and low molecular weight heparin
Heparin: Binds to both Factor Xa and thrombin; unpredictable bioavailability r/t protein binding
Enoxaparin: only binds to Xa; no protein binding

163
Q

Factor Xa

A

Converts prothrombin into thrombin

164
Q

Thrombin does 3 things

A
  1. Conversion of fribrinogen into fibrin
  2. Conversion of Factor V into Va: enhances activity of Xa
  3. Conversion of Factor VIII into VIIIa
165
Q

Warfarin

A

Vitamin K antagonist
Inhibits synthesis of Vitamin K-dependent clotting factors (VII, IX, X and thrombin)
PO

166
Q

Dabigatran

A

Direct thrombin inhibitor

PO

167
Q

Rivaroxaban

A

Direct inhibitor of Factor Xa

PO

168
Q

Vitamin K

A

Green leafy vegetables
Warfarin patients must eat same amount each week to adjust dose
Too much Vitamin K will decrease INR (thicker blood)
Less Vitamin K will increase INR (thinner blood)

169
Q

Ferrous sulfate

A

To treat iron deficiency anemia
Reduced absorption with antacids
Increased absorption with Vitamin C (but also increased adverse effects)
Causes GI issues: constipation

170
Q

Iron Dextran

A

Parenteral iron product
Can cause anaphylactic reaction or cardiac arrest
Start with small test dose

171
Q

Vitamin B12

A

Cyanocobalamin
Converts folic acid from inactive form to active form
Can cause hypokalemia

172
Q

Vitamin B12 deficiency

A

Magaloblastic anemia

Important to distinguish between B12 deficiency and Folic Acid deficiency

173
Q

Folic Acid

A

Essential factor for DNA synthesis and erythropoiesis (RBC, WBC and platelets)

174
Q

Example of a metabolism inhibitor or folate antagonist

A

Sulfamethoxazole/ Trimethoprim

AKA Bactrim, Septra

175
Q

Sulfamethoxazole/ Trimethoprim

A

Treats UTI’s
Synergistic effect
Interacts with Warfarin
Can cause Stevens-Johnson syndrome, hyperkalemia, bone marrow suppression, increased bilirubin, renal dysfunction

176
Q

Nitrofurantoin

A

Treats only UTI’s
Damage bacterial cell DNA
Therapeutic concentrations only reached in urine

177
Q

Name two antibiotics used to treat UTI’s

A

Sulfamethoxazole/Trimethoprim

Nitrofurantoin

178
Q

Pelvic inflammatory disease

A

Infection of oviducts, ovaries and adjacent reproductive organs
Gonorrhea and Chlamydia most common causes

179
Q

Cervicitis

A

Infection of the cervix

180
Q

Endometritis

A

Infection of uterus

181
Q

Salpingitis

A

Infection of oviducts

182
Q

Oophoritis

A

Infection of ovaries

183
Q

Blood pressure =

A

Cardiac output (HR x Stroke volume) x Systemic Vascular Resistance

184
Q

BP regulation: short term

A

Mediated by SNS: epi and norepi

To quickly accommodate behavioral, emotional and physiologic changes

185
Q

BP regulation: long term

A

Neural, hormonal and renal interactions

Connected with fluid volume homeostasis

186
Q

RAAS

A

Renin angiotensin aldosterone system
Normal homeostasis
Body senses hypovolemia: increases BP

187
Q

8 steps of RAAS

A
  1. Kidneys release renin into bloodstream
  2. Renin converts angiotensinogen into angiotensin I
  3. Lungs secrete angiotensin-converting enzyme (ACE)
  4. Angiotensin I is converted to angiotensin II in lungs by ACE (potent vasoconstrictor)
  5. Angiotensin II causes arteriolar constriction and aldosterone secretion
  6. Aldosterone causes sodium and water retention
  7. Retained sodium and water increases blood volume
  8. Arteriolar constriction increases peripheral vascular resistance
    Increased blood volume + vascular resistance = High BP
188
Q

1 most effective way to treat HTN

A

Lose weight

189
Q

Pharmacologic methods to lower BP (5)

A 
Beta blocker (Metoprolol)
ACE inhibitor (Lisinopril)
ARB (Losartan)
Calcium channel blocker (Amlodipine)
Direct vasodilator (Hydralazine)
190
Q

Metoprolol

A

Selective B1 inhibitor
Decreases cardiac output
Reduces release of renin
Long term: reduces peripheral vascular resistance
Adverse: bradycardia, heart block, bronchoconstriction

191
Q

Lisinopril

A

ACE (Angiotensin converting enzyme; produced by lungs) inhibitor
Can cause persistent cough, hyperkalemia, angioedema
Teratogenic

192
Q

Losartan

A

Angiotensin II Receptor blocker (ARB): causes vasodilation and excretion of sodium and water
Does NOT cause ACE inhibitor cough
Does cause angioedema, hyperkalemia
Teratogenic

193
Q

Main difference between adverse effects of Lisonopril (ACE-I) and Losartan (ARB)

A

Lisonopril can cause persistent cough, Losartan does not

194
Q

Amlodipine

A

Calcium channel blocker
Blocks calcium channel to induce vasodilation
AE: reflexive tachycardia, peripheral edema

195
Q

Hydralazine

A

Direct acting vasodilator

Can cause systemic lupus reaction

196
Q

Clinical manifestations of preeclampsia

A 
BP > 140/90 on two occasions, 4 hours apart
Proteinuria
Thrombocytopenia
Impaired liver function
Renal insufficiency
Pulmonary edema
New-onset cerbral or visual disturbances
197
Q

Edema

A

Excessive accumulation of fluid within interstitial space

198
Q

4 causes of edema with example

A
  1. Increased capillary hyrdostatic pressure (heart failure)
  2. Decreased plasma oncotic pressure (hemorrhage)
  3. Increased capillary membrane permeability (inflammation)
  4. Lymphatic channel obstruction (removal of lymph node)
199
Q

Assessment findings for edema

A 
Weight gain
Swelling
Limited range of motion
Wet lungs
Bounding pulses
200
Q

Treatment for edema

A
  • Treat underlying cause
    Support for clinical manifestations (eg elevate swollen legs)
    Diet: limit sodium
    Diuretics
201
Q

Clinical dehydration/ hypovolemia

A

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

202
Q

Clinical manifestations of dehydration

A 
Weight loss: particularly peds
Lightheaded/dizzy
Weak pulse
Tenting
Lack of tear production
Decreased output
Sunken fontanels
203
Q

Treatment for dehydration

A

Stop fluid loss: treat underlying cause

Give fluids slowly: too fast can lead to cerebral edema

204
Q

Hyponatremia

A

Sodium < 135 mEq/L
Extracellular fluid contains too much water compared to sodium (hypotonic)
Causes water to move into cell
Caused by gaining too much water (SSRI’s, D5W)
or loss of salt (diuretics, renal disease)
IV: hypertonic saline solutions with caution
Clinical manifestations: decreased reflexes

205
Q

Hypernatremia

A 
Sodium > 145 mEq/L
Hypertonic extracellular fluid
Caused by gain of sodium (salt tablets, no access to water) or loss of water (disease conditions, vomiting, diarrhea, diaphoresis)
IV: d5W, slowly
Clinical manifestations: hyper-reflexia
206
Q

Hypokalemia

A

K < 3.5 mEq/L
Causes: decreased K intake; shifts into cell (alkalosis); increased K excretion (diuretics, black licorice)
Impairs smooth muscle contractility: vomiting, constipation
Can cause cardiac dysrhythmias, skeletal muscle weakness
Replace K orally or IV

207
Q

Hyperkalemia

A

K > 5 mEq/L *Most dangerous condition
K shifts to extracellular fluid: acidosis
Increased intake/ decreased secretion

208
Q

4 imbalances that cause cardiac dysrhythmias

A

Hypokalemia
Hyperkalemia
Hypocalcemia
Hypercalcemia

209
Q

Hypocalcemia

A

Ca < 9 mg/dL
Causes: decreased intake/absorption; decrease in physiologic availability (large blood transfusion); increased excretion (fatty stool in CF patients)
Clinical manifestations: muscle twitching, cramping, hyperactive reflexes

210
Q

Hypercalcemia

A

Ca > 11 mg/dL
Causes: increased intake or absorption; shifts from bone to ECF (cancer, immobility); decreased excretion
Clinical manifestations: muscle weakness, diminished reflexes

211
Q

Respiratory acidosis

A

Hypoventilation: excess of carbonic acid

212
Q

Compensation for respiratory acidosis

A

Renal system

Kidneys hold on to bicarb and excrete hydrogen

213
Q

Respiratory alkalosis

A

Hyperventilation: deficit of carbonic acid

214
Q

Compensation for respiratory alkalosis

A

Renal system

Kidneys conserve hydrogen and excrete bicarbonate

215
Q

Metabolic acidosis

A

Relative excess of any acid except carbonic acid

216
Q

Causes of metabolic acidosis

A

Increase in metabolic acid: diabetes, alcoholism, burns
Decrease in base
Combination

217
Q

Compensation for metabolic acidosis

A

Respiration
Increased rate and depth of respiration
Fruity smelling breath

218
Q

Metabolic alkalosis

A

Any condition causing relative deficit of acid other than carbonic acid

219
Q

Causes of metabolic alkalosis

A

Increase in base: overuse of antacids, dehydration
Decrease in acid: vomiting, hypokalemia
Combination

220
Q

Compensation for metabolic alkalosis

A

Respiration

Slow respirations to hold onto CO2 to increase acid

221
Q

Clinical manifestations of respiratory acidosis

A

Headache
Blurred vision
Disorientation
Lethargy

222
Q

Clinical manifestations of respiratory alkalosis

A

Dizziness
Excitation
Numbness and tingling, hand and feet spasms
Cerebral vasoconstriction

223
Q

Clinical manifestations of metabolic acidosis

A

GI distress
CNS depression
Tachycardia, dysrhythmia
Fruity smelling breath

224
Q

Clinical manifestations of metabolic alkalosis

A

GI distress
Hyper-reflexia
Hypokalemia

225
Q

Potassium chloride/ phosphate

A

Treatment of hypokalemia
Should be given with food and lots of water
Be careful with patients with renal dysfunction: could hold onto too much K and cause hyperkalemia

226
Q

Treatment options for hyperkalemia - general

A 
Protect heart (calcium IV)
Shift K back into cells: buys time
Increase excretion of K
227
Q

3 ways to shift K back into cells

A

Regular insulin + dextrose 50% injection
Sodium bicarbonate injection
Albuterol continuous inhalation

228
Q

3 ways to increase excretion of K

A

Diuretic therapy: furosemide (uses kidneys)
Hemodialysis
Sodium polystyrene (Kayexalate): resin that exchanges Na for K in the gut (not for emergencies)

229
Q

Difference between calcium gluconate and calcium chloride

A

Gluconate can be given peripherally

Chloride administered centrally: more concentrated

230
Q

Why does insulin + dextrose move K into cell?

A

The Na-K adenosine triphosphate pump uses insulin and glucose for energy and works to exchange Na and K across the cell membrane

231
Q

What should you watch for when administering insulin +dextrose?

A

Drops in blood sugar

Check blood sugars before and after administration

232
Q

Sodium bicarbonate

A

Treats severe metabolic acidosis and hyperkalemia
Shifts K into cell by increasing cell membrane permeability
Can be caustic, can cause hypokalemia or metabolic alkalosis

233
Q

Furosemide

A

Diureses to increase K elimination: kidneys must be fully functional

234
Q

Kayexalate / Sodium polystyrene

A

Resin that exchanges Na for K in the gut: increases K elimination
Can have serious GI adverse effects
Not for emergencies

235
Q

How does albuterol work?

A

Beta2 agonist: in lungs, causes bronchodilation

Also activates adenylate cyclase which stimulates production of cyclic adenosine monophosphate (cAMP)

236
Q

How does albuterol move K into cell?

A

cAMP is used by Na-K pump to move K intracellularly

237
Q

Adverse effects of albuterol

A

Tachycardia, angina, tremors

238
Q

Role of magnesium in the body

A

Activates intracellular enzymes
Binds the mRNA to ribosomes
Plays role in regulating skeletal muscle contractility and blood coagulation

239
Q

Magnesium hydroxide and citrate used as

240
Q

Magnesium sulfate (IV) treats

A

Hypomagnesemia
Preeclampsia
Migraines
Status asthmaticus

241
Q

Magnesium oxide

A

Oral replacement
Needs to be over several days
Large doses can cause diarrhea

242
Q

Precautions with magnesium

A

Use caution with renal dysfunction (accumulation)

Monitor patient’s cardiac and neuromuscular status

243
Q

Treatment options for hyperkalemia

A 
Sodium bicarbonate
Calcium chloride
Albuterol continuous inhalation
Insulin + dextrose
Kayexalate
244
Q

Cell wall synthesis inhibitors

A

Amoxicillin
Cephalexin
Ceftriaxone

245
Q

Protein synthesis inhibitor

A

Azithromycin

Doxycycline

246
Q

DNA synthesis inhibitor

A

Metronidazole

247
Q

Metabolism inhibitor

A

Sulfamethoxazole

248
Q

Pernicious anemia

A

Lack of vitamin B leads to altered DNA synthesis

249
Q

Folate deficiency anemia

A

Lack of folate leads to premature cell death

250
Q

Iron deficiency anemia

A

Lack of iron leads to lack of hemoglobin

Most common

251
Q

Thalassemia

A

Congenital

Impaired synthesis of hemoglobin chain

252
Q

Aplastic anemia

A

Bone marrow suppression leads to decrease production

253
Q

Sickle cell anemia

A

Congenital

Abnormal hemoglobin molecule

254
Q

Post hemorrhage anemia

A

Blood loss leads to insufficient RBC

255
Q

Anemia chronic disease

A

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

256
Q

Antidote to heparin

A

Protamine sulfate

Patho Pharm (2 decks)

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