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Exam 1 Flashcards

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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
Infectious and immunologic cellular injury
Bacteria: endotoxins and exotoxins Virus Indirect immunologic response: processes of inflammation and byproducts of immune response
26
Endotoxin vs. Exotoxin
Endotoxins: toxins with the cell walls of bacteria; released when killed Exotoxins: Produced by bacteria and released while still alive
27
When presented with a challenge, cells have the following three reactions
Withstand and return to normal Adapt Die
28
Which cell reactions are reversible/irreversible?
Withstanding and adapting are generally reversible. | Dying is irreversible
29
Which form of adaptation is the least reversible?
Dysplasia
30
What are two forms of reversible cell injury?
Hydropic and intracellular accumulations
31
Hydropic injury results from the malfunction of what?
Na - K pumps
32
Generalized swelling in cells of a particular organ caused by hydropic injury is called
Megaly
33
Four cases of atrophy
Dehydration Immobilization Lack of nutrition Ischemia
34
Three cases of hypertrophy
``` Uterus/ breasts (pregnancy) Skeletal muscles (exercise) ```
35
Three cases hyperplasia
Liver Increase in RBC's at altitude Prostate enlargement
36
Two cellular adaptations in response to persistent injury
Metaplasia | Dysplasia
37
Does pH rise or fall during hypoxia and ischemia?
Falls
38
During hypoxia and ischemia, what ion is found in excess in the mitochondria?
Calcium
39
COX 1
Protective prostaglandins, stomach mucosa, and platelet stickiness
40
COX 2
Inflammatory prostaglandins leading to pain, inflammation and fever
41
What are four therapeutic uses of aspirin?
Anti-inflammatory, analgesia, antipyretic, prevention of platelet aggregation
42
Can children take aspirin?
No, risk of Reye's Syndrome, which results in encephalopathy and fatty liver
43
Adverse effects of aspirin
GI effects, bleeding, renal impairment, salicylate toxicity (4g +)
44
Major drug interaction with aspirin
Anticoagulants
45
Mu receptors affect what?
Analgesia, respiratory depression, euphoria, sedation, decreased GI motility and physical dependence
46
Kappa receptors affect what?
Analgesia, sedation, and decreased motility
47
What is tolerance?
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
48
Physical dependence
When physiologic abstinence syndrome will occur if drug is abruptly stopped
49
Addiction
Uncontrollable cravings, inability to control drug use, compulsive drug use and use despite doing harm to oneself or others
50
Three major physiologic changes that occur at birth
Oxygenation Circulation Nutrition
51
How long can neonates survive without breathing? When does brain damage occur?
10 minutes | 8 minutes
52
What can interfere with oxygenation to the fetus?
Umbilical cord compression Premature separation of placenta Excessive contraction of uterus Analgesics
53
What are three fetal shunts that close after birth?
``` Foramen ovale (bypass lungs, blood from right atrium to left) Ductus arteriosus (blood from pulmonary artery to aorta) Ductus venosus (blood away from liver) ```
54
What is the number one way to tell if the baby's circulation transition is going well?
Upper and lower pulse ox at 95%+ with near identical pulses
55
Two other factors to assess fetal circulation
Respiratory rate | Cap refill on sternum
56
How much weight loss is expected after first days after birth?
20%
57
When should a baby be back at birth weight?
Within 2 weeks
58
What is a disease causing organism called?
Agent/ microbe/ pathogen
59
Reservoir
Where a pathogen lives or reproduces
60
Mode of transmission
Mechanism by which agent is spread: contact, droplet, airborne, or animal
61
Host
Individual at risk for contracting the infection
62
Examples of breaking chain of infection at the reservoir level
Spraying for mosquitoes | Quarantine
63
Examples of breaking chain of infection at the Portal of entry/exit
Gloves and PPE | Cough etiquette
64
Examples of breaking chain of infection at mode of transmission
Sterile technique | Proper cooking and food storage
65
Examples of breaking chain of infection at host level
Vaccines | Boosting immunity through wellness techniques
66
Pathogenicity
Ability of a microbe to cause disease
67
Virulence
How severe the disease is
68
Adherence of microbe
How well it can stick to something: often using fillae or fimbrae
69
Biofilm
Sheets of microbes stuck together
70
Antiphagocytic factors
Keep a pathogen from being tagged by the immune system for destruction
71
Four types of pathogens
Bacteria Viruses Fungi Parasites
72
Bacteria
Single celled Rigid cell wall No internal organelles
73
Cocci
Spherical bacteria
74
Bacilli
Rod or comma bacteria
75
Gram positive bacteria
Stain blue
76
Gram negative bacteria
Stain pink
77
Fungi
Eurkaryotic Form complex structures Thick, rigid cell wall
78
Mycotic infections
Caused by fungi
79
Three examples of parasites
Protozoa Helminths Arthropods
80
Viruses
No metabolism Dependent on permissive host cells to make and assemble parts Develop intracellularly
81
Four clinical infectious disease stages
Incubation Prodromal Illness Convalescence
82
Most signs and symptoms during illness are from
Inflammation and immune response
83
Hallmark clinical manifestation of infection is:
Fever
84
What two groups often do not show a fever with an infection?
Elderly | Immunosuppressed
85
What can a broad spectrum antibiotic target?
Gram positive bacteria Gram negative bacteria Anaerobes
86
Bacteriocidal
Lethal to bacteria at clinically achievable concentrations
87
Bacteriostatic
Slow bacterial growth without causing cell death | Host will ultimately eliminate pathogen
88
Four mechanisms of action for antibiotics
Cell wall synthesis inhibition Protein synthesis inhibition DNA synthesis inhibition Metabolism inhibition
89
Four antibiotics that are cell wall synthesis inhibitors
Amoxicillin Piperacillin Cephalexin Ceftriaxone
90
How does Penicillin work?
Binds to penicilllin binding protein and inhibits synthesis of cell wall by interfering with transpeptidase
91
What is the result of Penicillin
Lysis of bacterial cell and death
92
Amoxicillin
Broad spectrum against both gram positive and negative bacteria adn some anaerobes
93
Major side effect for almost all antibiotics
Abdominal pain and diarrhea
94
What enzyme can make some bacteria resistant to antibiotics?
Beta-lactamase
95
Beta-lactamase inhibitor
Chemical compound that does not have antimicrobial therapy but combines with an antibiotic to prevent inactivation by beta-lactamase
96
Three beta-lactamase inhibitors
Clavulanic acid Sulbactam Tazobactam
97
Major side effect of clavulanic acid
Diarrhea
98
Which antibiotics are grouped into generations according to effectiveness against different organisms, characteristics and development?
Cephalosporins
99
What is the risk of penicillin and cephalosporin being chemically similar?
Cross sensitivity can occur in about 5% of patients
100
Cephalexin
AKA Keflex Oral first gen cephalosporin Active against skin flora
101
Ceftriaxone
Third gen cephalosporin IV or IM CNS penetration
102
Two antibiotics that are protein synthesis inhibitors
Doxycycline | Azirthromycin
103
How do doxycycline and azirthromycin work?
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
Doxycycline is effective against
Gram positive and negative bacteria Mycoplasma pneumoniae Chlamydia species Tick borne illness
105
Doxycyline belongs to what class?
Tetracyclines
106
Doxycyline should not be taken with
Milk | Antacids
107
Doxycyline associated with what type of diarrhea
C. difficile
108
Three atypical organisms covered by azithromycin
Mycoplasma Legionella Chlamydia
109
What class of protein synthesis inhibitor does azithromycin belong in?
Macrolides/ketolides
110
Azithromycin increases the risk of
QT prolongation on an EKG
111
Anemia
Deficit of RBC's
112
Two things that result in anemia
Relative-normal total RBC mass with increased plasma volume (pregnancy) Absolute decrease in RBC's
113
Pernicious anemia
Lack of Vitamin B leads to altered DNA synthesis
114
Folate deficiency anemia
Lack of folate leads to premature cell death
115
Iron deficiency anemia
Lack of iron leads to lack of hemoglobin
116
Thalassemia anemia
Impaired synthesis of hemoglobin | Congenital
117
Aplastic anemia
Bone marrow suppression leads to decreased production of RBC's
118
Sickle cell anemia
Abnormal hemoglobin molecule | Congenital
119
Post hemorrhage anemia
Blood loss leads to insufficient RBC's
120
Hemolytic disease of the newborn
Maternal antibodies cause the destruction of fetal cells
121
Signs and symptoms of anemia
``` Claudication (muscle cramps) Weakness Pallor Increased respiratory rate Dizziness, fainting, lethary Fatty changes in liver, kidneys and heart ```
122
What two hormones are elevated in anemia?
Epinephrine | Norepinephrine
123
Decreased RBC's/hemoglobin leads to
Decreased oxygen carrying capacity: hypoxia
124
Effects of anemia on cardiovascular system
Increased HR, stroke volume, and capillary dilation
125
Effects of anemia on renal system
Increased salt and water retention | Increased extracellular fluid
126
Increase of DPG in cells leads to
Increased release of oxygen from hemoglovin in tissues
127
Erythropoietin
Stimulates bone marrow to produce more RBC's
128
Most common nutritional deficiency in the world
Iron deficiency anemia
129
Possible causes of iron deficiency anemia
Low intake of iron in the diet Physiological increase in need Iron loss due to hemorrhage or heavy period Renal issues
130
What age group is at the highest risk for iron deficiency anemia
Infants and toddlers due to introduction of solid food
131
Pica
Condition in which people crave non-food or non-nutritive substances Primary sign of iron deficiency anemia
132
Thrombocytopenia
Platelet disorder of reduced quantity or increased consumption of platelets
133
Hemostasis
Physiologic process that stops bleeding at site of injury while maintaining normal blood flow elsewhere
134
Primary hemostasis
Vasoconstriction at the site Platelet plug Takes 3-7 min
135
Secondary hemostasis
Formation of fibrin clot Clotting factors activated Starts in about 3-10 min
136
Petechia
Flat, pinpoint red marks on skin
137
Purpura
lots of petechia together | Tends to be itchy
138
Ecchymosis
Bruising
139
Hemarthrosis
Collection of blood in joints
140
Hematoma
Collection of blood in tissue
141
Hematuria
Blood in urine
142
Hematochezia
Blood in stool
143
Hematemesis
Blood in vomit
144
Epistaxis
Nose bleed
145
Hemoptysis
Coughing blood
146
Menorrhagia
Heavy period
147
Hypovolemia
Low blood volume
148
Signs of hypovolemia
``` Tenting Low BP Initial increase in HR, then decrease Pallor Similar to hypoxia ```
149
Treatment for bleeding disorders
``` Avoid the cause Steroids to suppress the immune system IVIG Factor replacement Platelets Fresh frozen plasma ```
150
Assessment findings for thrombocytopenia
Petechiae Purpura Decreased platelet counts Generalized bleeding
151
Thrombus
Stationary blood clot formed within a vessel or chamber of the heart
152
What is a thrombus composed of?
Platelets, clotting factors and fibrin
153
Three major risk factors for thrombus
Vessel wall injury Circulatory stasis Hypercoagulable conditions
154
Deep vein thrombosis
Presence of a thrombus in a deep vein | Typically lower extremity
155
Assessment findings for DVT
Edema Pain and tenderness Redness or discoloration Warmth
156
D-dimer
Presence of high levels of fibrin products in the body
157
Treatments for DVT
Thrombolytic to break down clot | Anticoagulants to reduce clot formation
158
Are platelets involved in secondary hemostasis?
Yes
159
What circulatory changes are expected after the birth of an infant?
Decreased pulmonary vascular resistance | Increased systemic vascular resistance
160
Three contributing factors to formation of thrombus
Endothelial injury Circulatory stasis Hypercoagulability
161
Why should ceftriaxone be avoided in neonates?
Due to the risk of hyperbilirubinemia because ceftriaxone displaces bilirubin from albumin binding sites
162
Heparin and Enoxaparin
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
Factor Xa
Converts prothrombin into thrombin
164
Thrombin does 3 things
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
Warfarin
Vitamin K antagonist Inhibits synthesis of Vitamin K-dependent clotting factors (VII, IX, X and thrombin) PO
166
Dabigatran
Direct thrombin inhibitor | PO
167
Rivaroxaban
Direct inhibitor of Factor Xa | PO
168
Vitamin K
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
Ferrous sulfate
To treat iron deficiency anemia Reduced absorption with antacids Increased absorption with Vitamin C (but also increased adverse effects) Causes GI issues: constipation
170
Iron Dextran
Parenteral iron product Can cause anaphylactic reaction or cardiac arrest Start with small test dose
171
Vitamin B12
Cyanocobalamin Converts folic acid from inactive form to active form Can cause hypokalemia
172
Vitamin B12 deficiency
Magaloblastic anemia | Important to distinguish between B12 deficiency and Folic Acid deficiency
173
Folic Acid
Essential factor for DNA synthesis and erythropoiesis (RBC, WBC and platelets)
174
Example of a metabolism inhibitor or folate antagonist
Sulfamethoxazole/ Trimethoprim | AKA Bactrim, Septra
175
Sulfamethoxazole/ Trimethoprim
Treats UTI's Synergistic effect Interacts with Warfarin Can cause Stevens-Johnson syndrome, hyperkalemia, bone marrow suppression, increased bilirubin, renal dysfunction
176
Nitrofurantoin
Treats only UTI's Damage bacterial cell DNA Therapeutic concentrations only reached in urine
177
Name two antibiotics used to treat UTI's
Sulfamethoxazole/Trimethoprim | Nitrofurantoin
178
Pelvic inflammatory disease
Infection of oviducts, ovaries and adjacent reproductive organs Gonorrhea and Chlamydia most common causes
179
Cervicitis
Infection of the cervix
180
Endometritis
Infection of uterus
181
Salpingitis
Infection of oviducts
182
Oophoritis
Infection of ovaries
183
Blood pressure =
Cardiac output (HR x Stroke volume) x Systemic Vascular Resistance
184
BP regulation: short term
Mediated by SNS: epi and norepi | To quickly accommodate behavioral, emotional and physiologic changes
185
BP regulation: long term
Neural, hormonal and renal interactions | Connected with fluid volume homeostasis
186
RAAS
Renin angiotensin aldosterone system Normal homeostasis Body senses hypovolemia: increases BP
187
8 steps of RAAS
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
1 most effective way to treat HTN
Lose weight
189
Pharmacologic methods to lower BP (5)
``` Beta blocker (Metoprolol) ACE inhibitor (Lisinopril) ARB (Losartan) Calcium channel blocker (Amlodipine) Direct vasodilator (Hydralazine) ```
190
Metoprolol
Selective B1 inhibitor Decreases cardiac output Reduces release of renin Long term: reduces peripheral vascular resistance Adverse: bradycardia, heart block, bronchoconstriction
191
Lisinopril
ACE (Angiotensin converting enzyme; produced by lungs) inhibitor Can cause persistent cough, hyperkalemia, angioedema Teratogenic
192
Losartan
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
Main difference between adverse effects of Lisonopril (ACE-I) and Losartan (ARB)
Lisonopril can cause persistent cough, Losartan does not
194
Amlodipine
Calcium channel blocker Blocks calcium channel to induce vasodilation AE: reflexive tachycardia, peripheral edema
195
Hydralazine
Direct acting vasodilator | Can cause systemic lupus reaction
196
Clinical manifestations of preeclampsia
``` 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
Edema
Excessive accumulation of fluid within interstitial space
198
4 causes of edema with example
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
Assessment findings for edema
``` Weight gain Swelling Limited range of motion Wet lungs Bounding pulses ```
200
Treatment for edema
* Treat underlying cause Support for clinical manifestations (eg elevate swollen legs) Diet: limit sodium Diuretics
201
Clinical dehydration/ hypovolemia
Too small volume of fluid in extracellular compartment (vascular and interstitial) or body fluids too concentrated
202
Clinical manifestations of dehydration
``` Weight loss: particularly peds Lightheaded/dizzy Weak pulse Tenting Lack of tear production Decreased output Sunken fontanels ```
203
Treatment for dehydration
Stop fluid loss: treat underlying cause | Give fluids slowly: too fast can lead to cerebral edema
204
Hyponatremia
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
Hypernatremia
``` 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
Hypokalemia
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
Hyperkalemia
K > 5 mEq/L *Most dangerous condition K shifts to extracellular fluid: acidosis Increased intake/ decreased secretion
208
4 imbalances that cause cardiac dysrhythmias
Hypokalemia Hyperkalemia Hypocalcemia Hypercalcemia
209
Hypocalcemia
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
Hypercalcemia
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
Respiratory acidosis
Hypoventilation: excess of carbonic acid
212
Compensation for respiratory acidosis
Renal system | Kidneys hold on to bicarb and excrete hydrogen
213
Respiratory alkalosis
Hyperventilation: deficit of carbonic acid
214
Compensation for respiratory alkalosis
Renal system | Kidneys conserve hydrogen and excrete bicarbonate
215
Metabolic acidosis
Relative excess of any acid except carbonic acid
216
Causes of metabolic acidosis
Increase in metabolic acid: diabetes, alcoholism, burns Decrease in base Combination
217
Compensation for metabolic acidosis
Respiration Increased rate and depth of respiration Fruity smelling breath
218
Metabolic alkalosis
Any condition causing relative deficit of acid other than carbonic acid
219
Causes of metabolic alkalosis
Increase in base: overuse of antacids, dehydration Decrease in acid: vomiting, hypokalemia Combination
220
Compensation for metabolic alkalosis
Respiration | Slow respirations to hold onto CO2 to increase acid
221
Clinical manifestations of respiratory acidosis
Headache Blurred vision Disorientation Lethargy
222
Clinical manifestations of respiratory alkalosis
Dizziness Excitation Numbness and tingling, hand and feet spasms Cerebral vasoconstriction
223
Clinical manifestations of metabolic acidosis
GI distress CNS depression Tachycardia, dysrhythmia Fruity smelling breath
224
Clinical manifestations of metabolic alkalosis
GI distress Hyper-reflexia Hypokalemia
225
Potassium chloride/ phosphate
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
Treatment options for hyperkalemia - general
``` Protect heart (calcium IV) Shift K back into cells: buys time Increase excretion of K ```
227
3 ways to shift K back into cells
Regular insulin + dextrose 50% injection Sodium bicarbonate injection Albuterol continuous inhalation
228
3 ways to increase excretion of K
Diuretic therapy: furosemide (uses kidneys) Hemodialysis Sodium polystyrene (Kayexalate): resin that exchanges Na for K in the gut (not for emergencies)
229
Difference between calcium gluconate and calcium chloride
Gluconate can be given peripherally | Chloride administered centrally: more concentrated
230
Why does insulin + dextrose move K into cell?
The Na-K adenosine triphosphate pump uses insulin and glucose for energy and works to exchange Na and K across the cell membrane
231
What should you watch for when administering insulin +dextrose?
Drops in blood sugar | Check blood sugars before and after administration
232
Sodium bicarbonate
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
Furosemide
Diureses to increase K elimination: kidneys must be fully functional
234
Kayexalate / Sodium polystyrene
Resin that exchanges Na for K in the gut: increases K elimination Can have serious GI adverse effects Not for emergencies
235
How does albuterol work?
Beta2 agonist: in lungs, causes bronchodilation | Also activates adenylate cyclase which stimulates production of cyclic adenosine monophosphate (cAMP)
236
How does albuterol move K into cell?
cAMP is used by Na-K pump to move K intracellularly
237
Adverse effects of albuterol
Tachycardia, angina, tremors
238
Role of magnesium in the body
Activates intracellular enzymes Binds the mRNA to ribosomes Plays role in regulating skeletal muscle contractility and blood coagulation
239
Magnesium hydroxide and citrate used as
Laxative
240
Magnesium sulfate (IV) treats
Hypomagnesemia Preeclampsia Migraines Status asthmaticus
241
Magnesium oxide
Oral replacement Needs to be over several days Large doses can cause diarrhea
242
Precautions with magnesium
Use caution with renal dysfunction (accumulation) | Monitor patient's cardiac and neuromuscular status
243
Treatment options for hyperkalemia
``` Sodium bicarbonate Calcium chloride Albuterol continuous inhalation Insulin + dextrose Kayexalate ```
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Cell wall synthesis inhibitors
Amoxicillin Cephalexin Ceftriaxone
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Protein synthesis inhibitor
Azithromycin | Doxycycline
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DNA synthesis inhibitor
Metronidazole
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Metabolism inhibitor
Sulfamethoxazole
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Pernicious anemia
Lack of vitamin B leads to altered DNA synthesis
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Folate deficiency anemia
Lack of folate leads to premature cell death
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Iron deficiency anemia
Lack of iron leads to lack of hemoglobin | Most common
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Thalassemia
Congenital | Impaired synthesis of hemoglobin chain
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Aplastic anemia
Bone marrow suppression leads to decrease production
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Sickle cell anemia
Congenital | Abnormal hemoglobin molecule
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Post hemorrhage anemia
Blood loss leads to insufficient RBC
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Anemia chronic disease
Chronic infection, inflammation, malignancy leads to increased demand or suppression
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Antidote to heparin
Protamine sulfate

Patho Pharm (2 decks)

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