Midterm Flashcards
1
Q
What are three things cells can do when presented with a challenge?
A
- withstand and return to normal (reversible)
- adapt if stress removed
- die (irreversible)
2
Q
Hydropic cellular response
A
an accumulation of water inside the cell; reversible; 1st manifestation of most forms of cell injury; results from malfunction of Na-K pumps (swelling of cells and organs)
3
Q
what are 3 ways that intracellular accumulations occur?
A
- excessive amounts of normal intracellular substances (ex. proteins, lipids, carbs)
- accumulation of abnormal substances produced by cells because of issues (ex. cellular stress –> broken down parts)
- accumulation of pigments and particles that cell is unable to degrade (ex. hyperbilirubanemia)
4
Q
What is atrophy and what are 3 causes?
A
cells shrink and reduce their differentiated function in an effort to reduce energy
- disuse
- ischemia
- nutrition/starvation
5
Q
What is hypertrophy?
A
increase in cell size accompanied by augmented functional capacity
6
Q
what is hyperplasia?
A
increase in number of cells by mitotic division
7
Q
What is metaplasia?
A
replacement of one differentiated cell type with another
8
Q
What is an example of metaplasia?
A
smokers –> chronic irritation, bronchial mucosa changes to handle stress
9
Q
What is dysplasia?
A
disorganized appearance of cells because of abnormal variations in size, shape and arrangement
10
Q
What happens with necrosis?
A
external injury (toxic, deathly injury, ischemia) leading to cell rupture; intracellular contents spill out leading to inflammation; ex. heart attack
11
Q
What happens with apoptosis?
A
natural time for cell death, signal to die; no membrane rupture so no inflammatory process; organized; phagocytes eat cell fragments; ex. dementia
12
Q
What is the difference between hypoxia and ischemia?
A
hypoxia - poor oxygenation
ischemia - interruption of blood flow
13
Q
What does a lack of oxygen in cells lead to?
A
plasma, mitrochondrial, and lysosomal membranes critically damaged = cell death
14
Q
What is the mechanism of action of hypoxia/ischemia?
A
- ATP production in cell stalls
- ATP-dependent pumps fail
- NA accumulates and brings water inside cell
- excess Ca in mitochondria interferes
- glycogen stores depleted
- lactate produced
- pH falls - cellular components more dysfunctional
15
Q
What are three results of reperfusion injury?
A
- calcium overload - washes cells with calcium, triggers apoptosis
- formation of ROS (free radicals) - unpaired electrons steal hydrogen from another molecule (ex. diabetes, autoimmune)
- inflammation - days to weeks; body’s way to right the wrong
16
Q
What is a reperfusion injury?
A
tissue damage caused when blood supply returns to tissue after period of ischemia or hypoxia
17
Q
What are nutritional injuries to cells?
A
deficiencies (iron, vitamin D, protein, malabsorption) or excess (sodium, diabetes, obesity)
18
Q
What are chemical injuries to cells
A
free radicals; heavy metals; toxic gases
19
Q
WHat are physical and mechanical injuries to cells?
A
temperature extremes; atmospheric pressure changes; abrasion/trauma; electrical burns; radiation
20
Q
What are 2 ways that radiation causes cell damage?
A
- directly to cell DNA
2. creates free radicals leading to necrosis
21
Q
What are endotoxins?
A
toxins inside cell wall of bacteria that release into body when bacteria is destroyed
22
Q
What are exotoxins?
A
produced and excreted by bacteria; protective mechanism; interferes with cell function around cell
23
Q
What is Cox 1 responsible for?
A
found in most tissues; responsible for synthesizing prostaglandins that maintain gastric mucosa and renal function
24
Q
What is Cox 2 responsible for?
A
normally not present in healthy cells; produced by presence of inflammation; causes pain, fever and inflammation
25
MOA of aspirin
nonselective, irreversible inhibitor of cox
26
therapeutic uses of aspirin
inflammation suppression, analgesia, anttipyretic, prevention of platelet aggregation
27
What population should not receive aspirin and why
pediatrics - causes Reye's syndrome: encephalopathy and fatty liver
28
AEs of aspirin
GI effects, bleeding, renal impairment, salicyclate toxicity (presents with mixed metabolic acidosis), ringing in ears
29
Drug interactions of aspirin
NSAIDs, glucocorticoids (GI, ulcer), anticoagulants (bleeding risk)
30
mu receptor effects
analgesia, respiratory depression, euphoria, sedation, decreased GI motility, physical dependence
31
kappa receptor effects
analgesia, sedation, decreased GI motility
32
Morphine therapeutic uses
pain relief
33
morphine MOA
mimics endogenous opioid peptides primarily at mu receptor
34
morphine drug interactions
CNS depressants, anticholinergic drugs (urinary retention, acetylcholine/histamine/muscarinic receptors), hypotensive drugs
35
AEs of morphine
respiratory depression, constipation, orthostatic hypotension, urinary retention, cough suppression, biliary colic, emesis, sedation, euphoria
36
What is neonate breathing initiated by?
1. sudden exposure to world
| 2. slight asphyxiation
37
What are 4 causes of prolonged hypoxia in neonates
umbilical cord compression, premature separation of placenta, excessive contraction force, aesthetics
38
What is needed to open collapsed alveoli in neonates?
negative intraplural pressure
39
What is the role of surfactant?
decreases surface tension of alveolar fluid and allows easier open
40
Pulmonary resistance needed in neonate circulation
decreased pulmonary vascular resistance - reduces resistance to blood flow through lungs
41
systemic resistance needed in neonate circulation
increased systemic vascular resistance - increased aortic pressure and pressure in left A and V
42
What is the chain of infection transmission?
infectious agent - reservoir - portal of exit - mode of transmission - portal of entry - host
43
What is a n agent/pathogen/microbe?
some disease-causing organism; ex. bacteria, parasite, virus, fungi
44
What are 5 ways to break the chain of transmission?
destroy reservoir, block portal of exit, block mode of transmission, block portal of entry, reduce victim's susceptibility
45
What are three potential relationships between host and pathogen?
1. symbiosis: benefit only to human, no harm to microbe
2. mutualism: benefit to human and microbe
3. commensalism: benefit only to microbe, no harm to human
46
What is pathogenicity?
potential for pathogen to cause a disease; benefits organism and harms host
47
What are some physical and mechanical barrier characteristics of a host?
epithelial cells in skin/respiratory/GI tract, mucous membranes, cough/sneeze/urination/defecation, mucus/sweat/tears
48
What are 5 host risk factors?
age, nutritional status, chronic illness, immunosuppression, chronic stress
49
What are the three lines of host defense?
1. physical and mechanical barriers
2. innate inflammatory response - vasodilation, emigration, phagocytosis
3. acquired immunity - antigens
50
What are the microbe characteristics?
pathogenicity/virulence, adherence, invasion, endotoxins/exotoxins, bacterial enzymes, anti-phagocytic factors (coating), endospore protection, mobility, increased microbial resistance
51
What are the characteristics of bacteria?
single cell, rigid cell wall, no internal organelles, shapes (cocci, bacilli, spiral), gram stains, anaerobic or aerobic
52
Classification of amoxicillin
broad spectrum penicillin antibiotic
53
Major use of amoxicillin
G+ and G- coverage; some anaerobic coverage; renally eliminated; treats UTIs, respiratory/oral/skin infections; bacteriocidal
54
MOA amoxicillin
destroys bacteria by weakening the cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition of autolysins
55
AEs of amoxicillin
allergies, anaphylaxis, renal impairment, diarrhea
56
nursing actions of amoxicillin
take with food and water; additional contraception method
57
Classification of amoxicillin + clavulanic acid
broad spectrum penicillin antibiotic
58
major use of amoxicillin + clavulanic acid
G+/- and some anaerobic coverage; bacteriocidal; extends to cover organisms that are beta-lactam producing; renally eliminated
59
MOA of amoxicillin + clavulanic acid
aminopenicillin + beta-lactamase inhibitor; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins
60
AEs of amoxicillin + clavulanic acid
hypersensitivity; diarrhea (increased risk due to beta-lactamase inhibitor)
61
Nursing actions for amoxicillin + clavulanic acid
take with meals; additional contraception methods
62
classification of Piperacillin + tazobactum
antipsuedomonal penicillin antiobiotic (IV)
63
major use of Piperacillin + tazobactum
extended broad spectrum coverage of G+/- and anaerobes; covers more nosocomial; penicillin + beta-lactamase inhibitor; bacteriocidal
64
MOA of Piperacillin + tazobactum
antipseudomonal penicillin; destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins
65
AEs of Piperacillin + tazobactum
allergies, anaphylaxis, renal impairement, diarrhea
66
Nursing actions for Piperacillin + tazobactum
take with food, additional contraceptive method
67
classification of cefalexin
1st generation cephalosporin for PO antibiotic use
68
major use of cefalexin
mainly G+ skin flora; bacteriocidal; renally eliminated
69
MOA of cephalexin
destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins
70
AEs of cephalexin
hypersensitivity, nausea, vomiting, diarrhea
71
nursing actions for cephalexin
take with food
72
classification of ceftriaxone
3rd generation cephalosporin antibiotic for IM or IV (no PO
73
major use of ceftriaxone
some G+/- coverage; great CNS penetration (meningitis or CSF infections)
74
MOA of ceftriaxone
destroy bacteria by weakening the bacterial cell wall; binds to penicillin-binding protein and interrupts cell wall synthesis by inhibition of transpeptidase and disinhibition (activation) of autolysins
75
AEs of ceftriaxone
hypersensitivity, increases in bleeding
76
Nursing actions for ceftriaxone
avoid in neonates (displaces bilirubin); concomitant use with IV calcium-containing solutions/products in neonates; TPN contraindicated
77
classification of azithromycin
macrolide antibiotic
78
major use of azithromycin
broad spectrum bacterostasis (can become -cidal at high levels); can cover atypical organisms
79
MOA of azithromycin
reversibly binds to 50s subunit inhibiting protein synthesis; slows growth of microorganisms by inhibiting protein synthesis (static), but it is bacteriocidal at high doses)
80
AEs of azithromycin
GI discomfort, prolonged QT intervals - QT prolongation are contraindications
81
classification of doxycycline
tetracyclin antibiotic
82
major use of doxycycline
broad spectrum bacteriostatic; used to treat G+/-; tick borne illness
83
MOA of doxycycline
protein synthesis inhibition at 30s subunit
84
AEs of doxycycline
photo-toxicity, tooth discoloration in pregnancy and children under 8; associated with development of C.diff associated diarrhea
85
nursing actions for doxycycline
binds to cations (Mg, K) so avoid admin with milk, antacids; oral contraceptives
86
What are the four clinical infectious disease stages?
incubation, prodromal, illness, convalescence
87
Classification of metronidazole
antiprotozoal
88
major use of metronidazole
protozoas, anaerobic bacteria, narrow spectrum bacteriocidal
89
MOA of metronidazole
inhibits nucleic acid synthesis = cell death
90
drug interactions of metronidazole
ethanol (disulfiram reaction - facial flushing, vomiting, dyspnea, tachycardia); CYP3A4 substrate (warfarin, phenytoin)
91
AEs of metronidazole
N/HA, metallic taste, hypersensitivity
92
classification of fluconazole
antifungal
93
major use of fluconazole
SC/systemic; commonly used for candida infections
94
MOA of fluconazole
inhibition of CYP450-dependent synthesis of ergosterol (can't continue to form fungus)
95
AEs of fluconazole
N/HA, rash, abdominal pain, rare - hepatic necrosis (monitor liver function)
96
drug interactions of fluconazole
CYP 450 - inhibition of 3A4
97
What is relative anemia?
normal total RBS mass with increased plasma volume; ex. pregnancy
98
What is absolute anemia?
decreased number of RBCs
99
What are 2 ways anemias can be classified?
1. size and color
| 2. underlying issue
100
What are the etiologic events of anemia?
decrease in RBCs/hemoglobin/hypoxemia -> tissue hypoxia (low level s/s such as claudicatino, weakness, fatigue, pallor, increased RR, dizziness, lethargy, liver fatty changes) -> compensatory mechanisms SNS response of epi/norepi (increased heart rate, stimulation of bone marrow, capillary dilation, increased RAAS, increased of DPG protein which helps Hgb release O2), retain volume
101
What is the mechanism of aplastic anemia (decreased RBC production)?
bone marrow suppression leads to decreased production (toxic, radiant, immune injury)
102
What is the mechanism of anemia of chronic disease (decreased RBC production)?
chronic infection, inflammation, malignancy leads to increased demand or suppression
103
WHat is the mechanism of folate deficiency (decreased RBC production)?
lack of folate leads to premature cell death
104
What is the mechanism of iron deficiency (decreased RBC production)?
lack of iron leads to lack of hemoglobin
105
What is the mechanism of thalassemia (inherited disorder?)
congenital - impaired synthesis of hemoglobin chain
106
What is the mechanism of sickle cell (inherited disorder)?
congenital - abnormal hemoglobin molecule
107
What is the mechanism of hemolytic disease of newborn (extrinsic RBC destruction or loss)?
maternal antibodies case destruction of fetal cells
108
What is the mechanism of acute blood loss (extrinsic RBC destruction or loss)?
blood loss leads to insufficient RBC
109
What are the clinical maifestations of mild anemia?
no symptoms
110
What are the clinical manifestations of mild to moderate anemia?
fatigue, generalized weakness, loss of stamina, tachycardia, exertional dyspnea
111
What are the clinical manifestations of moderate to severe anemia?
orthostatic hypotension, tachycardia, transient murmor, vasocontriction/pallor, tachypnea, angina pectoris, intermittent claudication, night muscle cramps, HA/light headed/ faint,, tinnitus
112
Evaluation of anemia
labs (H&H, blood smear), bone marrow aspiration
113
treatment of anemia
erythropoitin, blood transfusion, supplements, rest/O2, fluids
114
classification of iron deficiency anemia
microcytic-hypochromic
115
Etiology of iron deficiency anemia
1. body's diminished capacity to absorb iron
2. physiologic increase in general requirements
3. excessive iron loss through blood loss
4. renal issues
116
assessment findings for iron deficiency anemia
pica, pallor, fatigue, headaches
117
What are 3 types of bleeding disorder categories
1. vascular disorders (vascular defect) - vascular purpura
2. platelet disorders (abnormal quality/quantity) - thrombocytopenia
3. coagulation disorders (clotting factor deficiency) - vitamin K, inherited, disseminated intravascular coagulation
118
WHat is hemostasis?
physiologic process that stops bleeding at site of injury while maintaining normal blood flow elsewhere
119
What is primary hemostasis?
initial vasospasm at site of injury; formation of platelet plug; adhere and clump in 3-7 minutes
120
What is secondary hemostasis
coagulation; form clot made of fibrin; clotting factors activated; clot retraction (firming) around 1 hour
121
What are the 2 key players in hemostasis and what are they responsible for
1. platelets - primary and secondary hemostasis; complex cell fragments; on cell surface, sticky receptors to help stick and adhere; can degranulate, which triggers cascade
2. coagulation factors - circulate; activated by platelets and each other in cascade; plasma proteins
122
What is the intrinsic pathway triggered by?
when blood comes into contact with altered endothelium; degranulation of platelets
123
WHat triggers the extrinsic pathway?
tissue factors (trauma)
124
What are the assessments of bleeding disorders?
pallor, jaundice, petechia, purpura, ecchymosis, hemarthrosis, hematoma, hematuria, hematochezia, hematoemesis, epitaxis, hemoptysis, menorrhagia
125
What are 4 lab evaluations of bleeding disorders
1. CBC with smear
2. bleeding time
3. prothrombin and INR (extrinsic coagulation - factor 7)
4. activated partial thromboplastin time (intrinsic coagulation)
126
What are the treatments of bleeding disorders
avoid cause, steroids (suppress immune response, prevents platelet breakdown), IVIG, factor replacement, platelets, FFP
127
What is the etiology of thrombocytopenia?
decreased production or increased consumption of platelets - decreased platelet production, decreased platelet survival, splenic sequesterization, platelet dilution
128
What is the assessment of thrombocytopenia?
petechiae, purpura, decreased platelet count's, bleeding
129
What is the treatment of thrombocytopenia?
treat/remove cause, block immune response, blood and/or platelet transfusion
130
What is a thrombus?
stationary blood clot formed within a vessel or chamber of the heart (arterial or venous); composed of aggregated platelets, clotting factors, and fibrin that adhere to vessel wall
131
What is Virchow's Triad?
1. epithelial injury - ex. vessel wall injury, trauma, IVs, smoking, HTN
2. hypercoaguable conditions - ex. oral contraceptives, pregnancy, cancer, obesity
3. circulatory stasis - ex. immobility
132
What is a DVT?
presence of thrombus in one of deep veins of usually lower extremities
133
What is the assessment of DVT?
edema, pain/tenderness (general or elicited), redness or discoloration, warmth, prediction rules, ultrasound, labs (D-dimer negative or positive)
134
Treatment of DVT
thrombolytic to break down clot (tPA), anticoagulants to decreased further clot formation
135
prevention of DVT
anticoagulants, SCD or compression stockings, hydration, movement
136
Uses of anticoagulation therapy
prevents clot formation and extension, prevents and treats VTE and PE, stroke prevention in Afib, does not bust clot
137
Goals of anticoagulation therapy
thin blood, prevent more clots, allow natural system activation
138
classification of unfractionated heparin
anticoagulation therapy - enhances effects of antithrombin through deactivation of thrombin and factor Xa
139
MOA of unfractionated heparin
binds to antithrobin causes a conformational change allowing better binding to thrombin and Xa
140
route of admin unfractionated heparin
IV/SC
141
AEs of unfractionated heparin
bleeding, heparin-induced thrombocytopenia (allergic reaction)
142
Labs for unfractionated heparin
aPTT
143
contraindications for unfractionated heparin
active bleeding, prep for surgery
144
antidote for unfractionated heparin
protamine sulfate
145
nursing actions for unfractionated heparin
binds to proteins, unpredicatble bioavailability, short half-life
146
classification of LMW heparin
anticoagulation therapy - enhances effect of antithrombin and inactivates factor Xa
147
MOA of LMW heparin
binds to antithrombin to cause a conformational change that better allows binding to Xa
148
What is the importance of factor Xa?
activates thrombin (factor 2a) from prothrombin (factor 2)
149
WHat are 3 things that thrombin does?
1. fibrinogen --> fibrin
2. factor v --> Va (enhances 10a)
3. VIII --> VIIIa (increases activity of IXa)
150
route of LMW heparin
SQ
151
AEs of LMW heparin
bleeding, heparin-induced thrombocytopenia
152
labs for LMW heparin
none - therapeutic dose after 1 hour
153
contraindications for LMW heparin
active bleeding, prep for surgery, weight > 150kg, renal dysfunction
154
antidote for LMW heparin
protamine sulfate
155
nursing actions for LMW heparin
no protein binding; more predictable bioavailability
156
Classification for warfarin
vitamin K antagonist
157
classification for dabigatran
direct acting oral anticoagulant - direct thrombin inhibitor
158
classification for rivaroxaban
direct acting oral anticoagulants - factor Xa inhibitor
159
MOA of warfarin
suppresses production of factors 2, 7, 9 , 10; CYP 450
160
AEs of warfarin
bleeding
161
labs for warfarin
PT and INR
162
contraindications for warfarin, rivaroxaban, and dabigitran
bleeding, prep for surgery
163
antidote foe warfarin
phytonadione (vitamin K)
164
nursing actions for Warfarin
long half-life, delayed onset, prolonged effects, lots of food and drug interactions (vitamin k-rich foods)
165
MOA of rivaroxaban
factor Xa inhibitor
166
AEs for rivaroxaban
bleeding
167
labs for rivaroxaban and dabigatran
none - easy therapeutic dose
168
antidote for rivaroxaban
none yet
169
nursing actions for rivaroxaban
active immediately, less drug interactions
170
MOA fo dabigatran
direct thrombin inhibitor (2a)
171
antidote for dabigitran
idarucizumab - binds to dabigitran
172
nursing actions for dabigitran
some drug interactions that inhibit p-glycoprotein which increases bleeding risk
173
What is a UTI and where can it occur
infection/inflammation of urinary epithelium usually caused by gut flora; urethra (urethritis), prostate, bladder (cystits), ureter, kidney (pylenophritis)
174
what defense mechanisms does our body have to prevent UTIs
acidic urine (urea), urination, sphincters, epithelial cells, secretions
175
What are 4 properties of uropathogens?
1. ability to attach to epithelial cells
2. attach to latex catheters
3. express toxins - s/s
4. biofilms
176
What are the clinical manifestations of cystitis
frequency, urgency, dysuria, pain, hematuria/cloudy urine
177
What are the clinical manifestations of pyelonephritis
cystitis, fever, chills, nausea, vomiting, anorexia, CVA tenderness
178
Evaluations for UTIs
physical and history; urinanlysis and culture (proteins, WBCs, nitrates, blood), imaging (reflex, structure)
179
Treatment of UTIs
antibiotics, comfort care
180
What is pelvic inflammatory disease
infection of oviducts and ovaries and adjacent reproductive organs; inflammation of cervic, uterus, oviducts (salpingitis), and ovaries
181
What are the 2 stages of PID?
1. vaginal/cervical infection
| 2. migration to upper genital tract
182
WHat are the most common of PID?
gonorrhea and chlamydia
183
What are the clinical manifestations of PID?
abdominal tenderness, irregular bleeding, pain with intercourse, dysuria, fever, discharge
184
What are the complications of PID
chronic pelvic pain, infertility, ectopic pregnancy, abcess
185
What is the formula for BP and what makes up each part
CO x SVR
Cardiac output - heart rate from B1 stimulation from vagal nerve stimulation (PSNS)
Systemic vascular resistance from stroke volume (preload volume - myocardial contractility B1 stimulation of SNS) and arterial radius (alpha stimulation, RAAS)
186
How is BP regulated short term?
purpose - quickly accommodate behavioral, emotional, and physiologic changes
mediated by SNS, influenced by HR and SVR
187
How is BP regulated long term?
neural, hormonal, and renal interaction; connected with fluid homeostasis; influences HR, SV, and SVR
188
Long-term RAAS
pressure receptors cause kidneys to release renin into blood stream -> renin helps convert angiotensinogen to angiotensin 1 in liver -> angiotensin 1 converted to angiotensin 2 by ACE in lungs -> angiotensin 2 causes arteriolar constriction and aldosterone secretio from adrenal glands -> aldosterone causes Na/H2o retention -> increase in volume -> increases pressure
189
What is primary and secondary HTN?
primary - 90%, idiopathic
| secondary - 10%, underlying cause such as ingestion, sleep apnea, cardiac defect (coarctation of aorta), pregnancy
190
What are the mechanisms behind preeclampsia?
placental ischemia and maternal vascular dysfunction
- maternal immunologic intolerance
- abnormal placental implantation
- endothelial dysfucntion
- genetic, nutritional, environmental factors
- cardiovascular and inflammatory change (systemic effects)
191
What are the clinical manifestations of preeclampsia
BP >140/90 on 2 occasions more than 4 hours apart AND proteinuria OR any of the following: thrombocytopenia, impaired liver function (increased liver enzymes), renal insufficiency (increased serum creatinine), pulmonary edema, new onset cerebral or visual disturbances
192
Treatment of preeclampsia
mild: bed rest and fetal monitor
severe: deliver baby and placenta, vasodilation drugs, antihypertensives, seizure prophylaxis
193
classification of SMZ/TMP
antimicrobial metabolism inhibitors (folate antagonists)
sulfamethoxazole - inhibitor of folate syntehesis
trimethoprim - inhibitor of folate reductase
194
use of SMZ/TMP
G+ and G- bacteriostatic activity for UTIs, pneumocystis cabrini (causes lung infections in its with HIV, transplants, immunocompromised), bronchitis, otitis media, MRSA skin infections
195
MOA of SMZ/TMP
sulfonamides compete with PAGA to inhibit the synthesis of dihydrofolic acid by dihydropteroate synthase; trimethoprim inhibits reduction of dihydrofolic acid to tetrahydrofolic acid by dyhydrofolate reductase; this process inhibits DNA
196
Drug interactions for SMZ/TMP
warfarin
197
AES of SMZ/TMP
- hyperkalemia (TMP hangs on to K)
- thrombocytopenia, neutropenia, megalblastic anemia
- kernicterus (increase bilirubin): avoid in pregnancy and near term and pet <2 months
- renal dysfunction
- hypersensitivity reactions (stevens-johnson syndrome)
198
use of nitrofurantoin
UTIs only (safe in pregnancy); bacteriostatic (can become bactericidal at high levels); only works in urine!! G+ and G- coverage, 3 salt forms
199
MOA of nitrofurantoin
damages bacterial cell DNA (synthesis) - reduced by bacterial flavoproteins to reactive intermediates which activate or alter bacterial ribosomal proteins
200
AEs of nitrofurantoin
brown urine, GI disturbances, pulmonary reactions (acute and subacute; rare- prolonged use or decrease renal function), agranulocytosis, peripheral neuropathy, hepatotoxicity
201
nursing considerations for nitrofurantoin
avoid in patients with CrCl <40: less excreted in urine (only works in urine)
202
What are the actions of alpha, beta, and calcium blockers?
alpha1 blockers - vasodilation, inhibit SNS
beta blockers - decrease heart rate, decrease contractility, constrict lungs
calcium channel blockers - dilate smooth muscle
203
What are 4 ways to treat hypertensive disorders
1. target and block alpha 1
2. target and block beta 1 and 2
3. target and block calcium channels
4. RAAS and kidneys
204
classification of metoprolol
sympatholytic beta-adrenergic blocker
205
MOA of metoprolol
- decreased cardia output (heart rate and contractility)
- suppress reflex tachycardia caused by vasodilators
- reduces release of renin (RAAS)
- long term use reduces peripheral vascular resistance
206
AEs of metoprolol
bradycardia, heart block, broncho-constriction (B2 blocked); not best for patients with increased BP
207
classification of hydralazine
direct acting vasodilator
208
use of hydralazine
PO/IV antihypertensive
209
MOA of hydralazine
causes arterial vasodilation
210
AEs of hydralazine
reflex tachycardia; can cause a systemic lupus erythematosus-like rash
211
classification of amlodipine
calcium channel blocker - dihydropyradine
212
use of amlodipine
BP drug, usually safe and effective
213
AEs of amlodipine
peripheral edema (especially a problem if they have heart failure), can cause reflex tachycardia
214
What are non-dihydropyradines used for
rate-control in atrial fibrillation; slows heart rate, less effective on BP
215
What are two different targets for antihypertensives in the RAAS
ACE inhibitors and ARBs (angiotensin receptor blockers)
216
classification of lisinopril
ACE inhibitor
217
use of lisinopril
shown to slow progression of kidney injury in patients with diabetes (protect kidneys)
218
AES of lisinopril
persistent cough, hyperkalemia (blocks aldosterone - less excretion of K), teratogenic, angioedema related to bradykinin
219
Yes of losartan
do not cause ACE-I induced cough, teratogenic, angioedema, hyperkalemia
220
classification of losartan
ARBs (angiotensin 2 receptor blocker)
221
What is capillary hydrostatic pressure?
facilitates outward movement of water from capillary to interstitial space; affects BP
222
what is capillary oncotic pressure
osmotically attracts water from the interstitial space back into the capillary; plasma
223
what is interstitial hydrostatic pressure
facilitates inward movement of water from interstitial space into capillary
224
what is interstitial oncotic pressure
osmotically attracts water from capillary into interstitial space
225
What is edema/hypervolemia
excessive accumulation of fluid within interstitial space
226
Forces involved in edema/hypervolemia
- increased capillary hydrostatic pressure: renal failure, heart failure (excessive Na/H2) retention)
- decreased plasma oncotic pressure: kidney disease, malnutrition, burns
- increased capillary membrane permeability: immune responses, inflammation
- lymphatic channel obstruction: lymph node removal, inflammatory process
227
clinical manifestations of edema/hypervolemia
- localized
- generalized
- other: weight gain, swelling, limited ROM, respiratory depression, lung crackles, bounding pulse, tachycardia
228
what is dehydration/hypovolemia
too small a volume of fluid in extracellular compartment (vascular and interstitial); body fluids too concentrated
229
causes of hypovolemia
```
fluid loss (burns, vomit, diarrhea, blood loss, sweat, diabetes polyuria)
reduced fluid volume (GI bug, altered consciousness)
fluid shifts (burns)
```
230
clinical manifestations of hypovolemia
poor turgor, tachycardia, dry mucous membranes, hypotension, weight changes, depressed fontanels, no tears, dark urine, oliguria, thirst
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Sodium range and function
135-145 mEq/L
| ECF, regulates acid-base balance, facilitates nerve conduction and neuromuscular function, maintains water balance
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causes of hyponatremia
- gain of water (relative to salt): inappropriate fluid resuscitation, tap water enemas, forced drinking of water, excess ADH
- loss of salt (relative to water): diuretics, renal distress, replace water without salt
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clinical manifestations of hyponatremia
nonspecific CNS dysfunction, malaise, anorexia, H/N/HA, confusion, lethargy, seizures, coma, fetal cerebral herniation
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treatment of hyponatremia
determine cause and fix, restrict water intake, hypertonic saline solutions with caution, IV fluids
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causes of hypernatremia
- gain of sodium (relative to water): tube feeding concentration, overuse of salt tablets, no access to water
- loss of water (relative to sodium): emesis, diarrhea, diaphoresis, tube feeding concentration
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clinical manifestations of hypernatremia
thirst, dry mucous membranes, hypotension, tachycardia, oliguria, muscle irritability, agitation, confusion, lethargy... seizures, coma, death
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treatments of hypernatremia
underlying condition, oral or IV fluids (no salines), 5DW slowly
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potassium range and function
3.5-5 mEq/L
ICF, cell electrical neutrality, cardiac muscle contraction and electrical conductivity, neuromuscular transmission of nerve impulses, maintains acid-base balance
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causes of hypokalemia
- decreased K intake (fad diet, NPO)
- shifts into cell (alkalosis)
- increased K excretion or loss in renal or GI (diuretics, gastric suctioning)
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clinical manifestations of hypokalemia
hyper polarized smooth and cardiac muscles (less reactive to stimuli), abdominal distention, diminished bowel sounds, ileum, postural hypotension, skeletal muscle weakness, paralysis, cardiac dysrhythmia
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treatment of hypokalemia
replace orally or IV
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causes of hyperkalemia
- increased intake (blood transfusions)
- shifts into ECF (acidosis, rush injuries)
- decreased excretion (oliguria, pharm)
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clinical manifestations of hyperkalemia
hypo polarized smooth and skeletal muscle cells (can't fire again after discharge), mild intestinal cramping and diarrhea, skeletal muscle weakness, paralysis, cardia dysrhythmias, cardiac arrest
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treatment of hyperkalemia
fix issue, pharm, dialysis
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calcium range and function
9-11 mg/dL
cell permeability, bone and teeth formation, blood coagulation, nerve impulse transmission, normal muscle contraction, cardiac action potentials and pacemaker automaticity
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causes of hypocalcemia
- decreased intake/absopriotn (diet, chronic diarrhea, CKD)
- decreased physiologic availability (alkalosis)
- increased excretion (pancreatitis, steorrhea)
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clinical manifestations of hypocalcemia
increased neuromuscular excitability - muscle twitching, cramping, hyperactive reflexes, tetany, seizures, dysrhythmias
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causes of hypercalcemia
- increased intake/absorption (too much vitamin D)
- shift from bone to ECF (tumors, leukemia, immobile)
- decrease excretion (diuretic)
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clinical manifestations of hypercalcemia
anorexia, nausea, emesis, constipation, fatigue, muscle weakness, decreased reflexes, HA, confusion, lethargy, cardiac dysthymia (heart block, bradycardia, kidney stones)
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3 mechanisms that regulate acid-base imbalances
1. buffers
2. respiratory system
3. renal system
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lab values for acid-base
PCO2: 36-44 mmHg
HCO3: 22-26 mmHg
pH: 7/35-7.45
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What is respiratory acidosis
excess of carbonic acid; shallow breaths (hypoventilation) that cause a buildup of carbonic acid H2CO3 (increases PCO2) and less HCO3
- increase PCO2
- decrease pH
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causes of respiratory acidosis
- impaired gas exchange: asthma, COPD, bacterial pneumonia
- inadequate neuromuscular function: guillan-barre, no deep breaths
- impairment of respiratory control in brainstem
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clinical manifestations of respiratory acidosis
HA, tachycardia, cardiac dysrythmias, neuro (blurred vision, tremors, vertigo, disorientation, lethargy, somnolence)
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how does the body compensate for respiratory acidosis
kidneys conserve HCO3 and eliminate H+ in acidic urine
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What is respiratory alkalosis
carbonic acid H2CO3 excess
- decrease PCO2
- Increase pH
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causes of respiratory alkalosis
hyperventilation - anxiety, crying, acute pain, brainstem injury, hypoxemia
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clinical manifestations of respiratory alkalosis
- increased neuromuscular excitability: numbness and tingling, feet/hand spasms
- excitability and/or confusion
- cerebral vasoconstriction
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how does the body compensate for respiratory alkalosis
kidneys conserve H+ ions and eliminate HCO3 in alkaline urine
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What is metabolic acidosis
relative excess of any acid except carbonic acid
- decreased HCO3
- decreased pH
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causes of metabolic acidosis
- increase in metabolic acid: diabetic ketoacidosis, burns, circulatory shock
- decrease in base: severe/prolonged diarrhea, decompression of intestines
- combination
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how does the body compensate for metabolic acidosis
kidneys conserve HCO3 and eliminate H+ in acidic urine
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clinical manifestations of metabolic acidosis
GI (N/V/D, dehydration), CNS depression (HA, confusion, lethargy, stupor, coma), cardiac (tachycardia, dysrhythmias), fruity breath
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What is metabolic alkalosis
relative defect of any acid except carbonic acid
- increase HCO3
- increase pH
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causes of metabolic alkalosis
- increase in base: overuse of antacids, hypovolemia
- decrease in acid: emesis, removal or gastric secretions
- combination
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how does the body compensate for metabolic alkalosis
kidneys conserve H+ and eliminate HCo3 in alkaline urine
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clinical manifestations of metabolic alkalosis
- ECF depletion: postural hypotension, N/V/D
- tetany, tingling, seizures
- hypokalemia with bilateral muscle weakness
- irritability and the CNS depression
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use of potassium chloride
hypokalemia; salt formation
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AES for potassium chloride
GI issues (N/V/D, abdominal discomfort, esophagitis), IV irritation and extravasation
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nursing actions for potassium chloride
- give with lots of food and water
- quick acting: hard on stomach, dilute liquid/powder
- long acting: slow release, less GI issues
- maintain good IV, proper drip, monitor
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what should be monitored when administering potassium chloride
- serum K levels
- s/s of hyperkalemia
- IV site
- cardiac function
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contraindications for potassium chloride
- monitor closely in patients with renal dysfunction and patients on meds that can increase serum K levels (trimethoprim, ACE inhibitors - also on diuretics)
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IV administrating considerations for potassium chloride
- peripheral or central (bigger IV, faster)
| - K may be added to maintenance fluids
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What are the treatments of hyperkalemia (3)
- protect the heart: admin Ca IV (K still high)
1. shift K back into cells (temporary - regular insulin + dextrose 50% injection, sodium bicarbonate injection, albuterol continuous inhaler
2. increase excretion of K - kidneys (diuretic therapy), fake kidney (hemodialysis - 1st line, emergency), gut (sodium polystyrene- resist that exchanges Na--> in gut then excretes after hours)
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What IV products are used to treat hypocalcemia and hyperkalemia
- calcium gluconate: less potent, peripheral admin
| - calcium chloride: more potent, more caustic to vasculature, admin centrally
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How does K and insulin work to correct hyperkalemia?
- Na-K adenosine triphosphatase (ATPase) pump in cell membrane maintains ICF and ECF concentrations, exchanges Na for K in a 3:2 ration, enhances movement of K into cell
- pump uses ATP hydrolysis as energy source; activation of pump requires insulin and glucose
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use of insulin + dextrose 50%
diabetes and hyperkalemia
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route of admin for insulin + dextrose 50%
mostly IV, also SQ
279
AEs of insulin + dextrose 50%
insulin can accumulate in renal dysfunction
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use of sodium bicarbonate
severe metabolic acidosis, hyperkalemia (fixes #, note problem)
281
AEs of sodium bicarbonate
caustic to vasculature, hypokalemia, metabolic alkalosis
282
MOA of sodium bicarbonate
shifts K back into cell by drawing H_ to intracellular space with bicarbonate
283
classification of albuterol
short acting beta-2 agonist
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MOA of albuterol
binds to beta-e in lungs (bronchodilation), activates adenylate cyclase which stimulates production of cAMP which is used by Na-K ATPase pump to move K intracellulary
285
AEs of albuterol
tahycardia, K can still appear low (in cell)
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What are 3 ways to increase K elimination
1. diuresis with furosemide
2. hemodialysis
3. kayaxelate (sodium polystyrene)
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route of kayaxelate
PO or rectally
288
MOA of kayaxelate
resin that exchanges Na for K in gun and then excretes
289
AE of kayaxelate
associated with intestinal necrosis and other serious GI effects
290
nursing considerations for kayaxelate
slow onset over hours - not used in emergencies
291
Roles of mag in body
- activates intracellular enzymes
- binds mRNA to ribosomes
- plays role in regulating skeletal muscle contractility and blood coagulation
292
What conditions would mag sulfate IV be used for?
- hypomagnesemia: slow replacement
- preeclampsia and eclampsia
- migraines
- status asthmaticus: bronchodilate for asthma
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precautions for magnesium sulfate
use with caution in patients with renal dysfunction, monitor patient cardiac and neuromuscular status
