331 final exam Flashcards
1
Q
types on seizures
A
focal or tonic/clonic
2
Q
focal seizure
A
partial seizure (used to be called petite mal)– loss of awareness
3
Q
tonic/clonic seizure
A
convulsion (used to be called gran mal) - tonic = contraction and associated with loss of conciseness and clonic = altering contraction and relaxation
4
Q
seizures can be caused by
A
hyperthermia, hypoxia, hypoglycemia, hyponatremia, repeated sensory stimulation, & sleep phases. increased ICP from brain tumor or injury, infection, drug withdrawal, vascular disease, metabolic problems, CNS degenerative diseases (such as Alzheimers or multiple sclerosis), and hypoxia
5
Q
epilepsy
A
CNS disorder with multiple seizures of idiopathic cause. there is no cure but can be treated.
6
Q
seizure vs epilepsy
A
seizure is a single occurrence (do not need to have epilepsy) while epilepsy is a medical condition that includes seizures
7
Q
which vascular diseases can lead to seizure
A
CVA and aneurysm
8
Q
how to diagnose of seizures
A
want to identify and eliminate the cause, EEG, CT, MRI, serum test for electrolytes and toxins
9
Q
EEG
A
electroencephalogram is a test with sensors placed on a patients head used to find problems related to electrical activity of the brain.
10
Q
what metabolic problems can cause a seizure
A
hepatic failure, electrolyte abnormalities, and hypoglycemia
11
Q
things that decrease seizure threshold
A
stress, fatigue, hypoglycemia, fever, alcohol and antipsychotic drugs, hyperventilation, increased water ingestion, menses, light, and noise
12
Q
if you increase the seizure threshold
A
you can reduce the occurrence of seizures
13
Q
why does water intoxication increase the chances of seizures
A
it dilutes sodium
14
Q
prodroma
A
early manifestations that appear a few days to hours before onset of seizure. can show as anxiety, depression, and inability to think clearly.
15
Q
aura
A
partial seizure that manifests itself as dizziness, numbness, visual or auditory experience, or just a funny feeling
16
Q
phases of seizures
A
preictal, ictal, postictal
17
Q
what is included in the preictal phase
A
prodroma and aura
18
Q
ictal phase includes
A
the seizure phase which includes tonic and clonic phases
19
Q
what happens during the ictal phase
A
muscle contractions/relaxation and increase in metabolic demand which causes decreased level of conscious, increased O2 use, decreased glucose, and increased lactic acid
20
Q
what needs to be done during the ictal phase
A
airway maintenance needs to be ensured and there may be relaxation of bowel and urinary sphincter which causes incontinence
21
Q
postictal phase
A
period immediately following cessation of seizure activity
22
Q
what happens during the postictal phase
A
decreased level of consciousness, dysphagia/dysphasia, confusion, memory loss, paralysis, and deep sleep
23
Q
status epilepticus
A
severe seizure can be multiple lasting for 5 minutes, one longer than 30 minutes, or rapidly recurring seizures before a person has fully regained consciousness from preceding seizure
24
Q
what do seizures do to metabolic demand
A
increases it
25
what does increased metabolic demand do?
uses up glucose and oxygen rapidly which leads to lactic acid accumulation in brain tissue because O2 and glucose are not available
26
hypotonia
decreased muscle tone
27
seizure treatment
correct or control cause if possible, anti-seizure medications, dietary, surgical interventions
28
goals for a patient going through seizure
pharmacology, oxygenation, and to prevent injury
29
dietary treatment for seizure patients
keto and adkins
30
status epileptics can cause
progressive and irreversible brain damage and can be life threatening
31
anti epileptic drug mechanism of action
not known but evidence has shown that it alters movement of Na, K, Mg, and Ca which stabilizes the hyper-excitable states and inhibits burst firing
32
anti epileptic drugs do what to nerve impulses
suppress transmission between nerve impulses which stabilizes cell membranes and decreases spread of impulses
33
anti epileptic drugs do what to nerve impulse conduction
decrease the speed of the nerve impulse conduction within a neuron
34
anti epileptic drugs do what to threshold
increase the threshold which decreases the neuronal response to stimuli
35
anti epileptic drug do what to GABA? which does what
enhance effects of GABA which helps regulate neuron excitability in the brain
36
besides seizures, anti epileptic drugs are also used for
psychiatric disorders, migraines, and neuropathic pain
37
GABA is a
inhibitory neurotransmitter
38
anti epileptic drug goal of therapy and how do you do that?
control seizure activity while avoiding adverse effects. you do this by titrating to the lowest sum drug level
39
indications of anti epileptic drugs
long term seizure maintenance and status epilepticus
40
adverse effects of anti epileptic drugs
decrease level of consciousness, SI, mood, GI upset, thrombocytopenia, and many induce hepatic metabolism
41
Carbamazepine (Tegretol) adverse effects
Stevens-johnson syndrome, toxic epidermal necrolysis, Nausea, headache, dizziness, unusual eye movements, visual change, behavioral changes, rash, abdominal pain, abnormal gait, GI upset
42
Phenytoin (Dilantin) adverse effects
Nystagmus, ataxia, drowsiness, rash, gingival hyperplasia, pancytopenia, agranulocytosis, hepatitis, GI upset
43
first line prototypical drug for both tonic/clonic and partial seizures
Phenytoin (Dilantin)
44
Phenytoin (Dilantin) routes
capsule and IV
45
Phenytoin (Dilantin) MOA
stabilize neurons (Na)
46
Phenytoin (Dilantin) therapeutic plasma level
10-20 mcg/mL
47
what if a patient has decreased albumin levels with phenytoin
Phenytoin (Dilantin) is highly protein bound and if a patient has low albumin = lots of active drug circulating = drug toxicity
48
what does phenytoin toxicity look like
nagstagmus, ataxia, encephalopathy (altered level of consciousness), dysarthria
49
nursing considerations with IV phenytoin
20 gage needle, dilute with NS and flush with Ns, filter must be used,
50
what is used to overcome chemical disadvantage of IV phenytoin?
IV fosphenytoin
51
Dose of IV phenytoin
10-15 mg/kg
52
risks of IV phenytoin and why
can cause extravagation because it is mixed with antifreeze at a ph of 12
53
BBW of IV phenytoin
IV infusion should not exceed 50 mg/min in adults. incr. risk severe hypotension and cardiac arrhythmias above recommended infusion rate
54
BBW of carbamazepine
bone marrow suppression which causes pancytopenia which causes decreased immunity, oxygen, and blood clotting
55
therapeutic levels of carbamazepine
4-12 mcg/mL
56
indication of carbamazepine
generalized tonic-clonic seizures and not for myoclonic or absent seizures
57
what can a patient not have if taking carbamazepine
grapefruit juice
58
stevens-johnson syndrom
peeling of the skin. adverse effect of carbamazepine. if not controlled leads to toxic epidermal necrolysis
59
levetiracetam brand name
Keppra
60
levetiracetam (Keppra) indication
adjunct therapy for partial seizures without secondary generalization
61
levetiracetam (Keppra) MOA
unknown however evidence shows it inhibits simultaneous neuronal firing
62
adverse effects of levetiracetam (Keppra)
excessive CNS depression when used in combination with other sedating drugs, leukopenia which puts you at risk for infection, dizziness, drowsiness, behavior changes
63
levetiracetam (Keppra) route
PO, IV, and IR (immediate release)
64
valproic acid MOA
facilitates inhibitory neurotransmitter GABA
65
valproic acid route, onset, and peak
PO and IV onset is 15-30 mins, and peaks in 1-4 hours
66
valproic acid indication
generalized seizures and can be used for bipolar disorder
67
valproic acid adverse effects
drowsiness, N/V, tremor, weight gain, transient hair loss
68
Capsules with long acting valproic acid granules are called
Depakote sprinkle
69
what does depakote do to hepatic metabolism
It does induce hepatic metabolism of other drugs due to it being a highly-protein bound drug. This is of significant consequence for any individual who has liver damage or disease, especially when you take into consideration that valproic acid can cause hepatotoxicity
70
therapeutic levels for Depakote
50-125 mcg/mL
71
adverse effects of Depakote
hepatotoxicity and pancreatitis
72
what Benzodiazepines did we learn
lorazepam and diazepam
73
Benzodiazepines indications
anxiolytic (decrease anxiety), ethanol withdrawal, acute seizures
74
therapeutic effect of Benzodiazepines? adverse effect of Benzodiazepines?
both are sedation
75
nursing considerations of Benzodiazepines
habit forming, can induce withdrawal seizures, risk for falls, monitor BP, assess for suicidal ideation
76
lorazepam trade name
Ativan
77
why are patients on Benzodiazepines a fall risk
because they are CNS depressants and have mind altering capabilities
78
Benzodiazepines reversal
flumazenil (romazicon)
79
flumazenil (romazicon) BBW
rebound seizures from stopping effects of benzo too fast
80
gabapentin (Neurontin) MOA
increases synthesis and synaptic accumulation of GABA between the neurons
81
gabapentin (Neurontin) indication
most commonly used for neuropathic pain
82
GABA does what to brain activity
inhibits it
83
pregabalin (Lyrica) MOA
affects calcium channels in the CNS tissue
84
pregabalin (Lyrica) indication
adjunct therapy for partial seizures. also commonly used for neuropathic pain, fibromyalgia, and postherpetic neuralgia
85
cerebrovascular disease
any abnormalities of the brain caused by a pathological process in the blood vessels
86
symptoms of cerebrovascular disease are
there are focal, unilateral, and global symptoms. slurred speech, difficulty swallowing, limb weakness, and paralysis
87
leading cause of disability
stroke, aka cerebrovascular disease
88
cerebrovascular disease can be
ischemic or hemorrhagic. can also be associated with hypoperfusion
89
severe effects of cerebrovascular disease
hemiplegia, coma, and death
90
risk factors to cerebrovascular disease
high total cholesterol or low HDL, smoking, HTN, A-fib, DM, thrombocythemia, increased blood viscosity, insulin resistance, heart disease, peripheral vascular disease
91
thrombocythemia
excess platelet production
92
polycythemia
over production of RBC
93
smoking increases risk of stroke by
50%
94
ischemic stroke
occurs when there is obstruction to arterial blood flow to the brain from thrombus formation, an embolus, or hypoperfusion
95
thrombus
chronic process that may take up to 20-30 years for obstruction to develop
96
cerebral thrombosis develops most often from
atherosclerosis/stenosis and inflammatory disease process that damage arterial wall
97
what adhere to a vessel wall that is damaged
platelets and fibrin to form a clot
98
embolic stroke
fragments that break from a thrombus formed outside the brain usually in the heart or carotids but can also be from blood, fat, air, or bacteria
99
risk factors for embolic stroke
A-fib, endocarditis, and MI
100
hypoperfusion
decreased cardiac output
101
hypoperfusion can be caused by
dehydration, low volume, HF, PE
102
conditions causing increased coagulation or inadequate cerebral perfusion can ________ the risk of thrombus
increase
103
TIA
neurological dysfunction lasting less than one hour resulting from focal cerebral ischemia
104
Focal brain ischemia
Focal brain ischemia occurs when a blood clot has occluded a cerebral vessel. Focal brain ischemia reduces blood flow to a specific brain region, increasing the risk of cell death to that particular area
105
what are you at risk for after a TIA
of having a stroke in the next 90 days
106
clinical manifestations of TIA
weakness, numbness, sudden confusion, loss of balance, sudden or severe headache
107
what should you watch with hypoperfusion stroke
hemodynamic monitoring
108
conditions that can cause increased coagulation or inadequate cerebral perfusion
dehydration, hypotension, prolonged vasoconstriction due to malignant HTN
109
bifurcation
vessel breaks into two smaller vessels which makes its lumen smaller
110
cerebral infarction
occurs when the brain loses its blood supply due to vascular occlusion
111
most common reasons for cerebral infarction and what are the dominant underlying processes
cerebral thrombi and emboli most commonly produce occlusion but atherosclerosis and hypertension are the dominant underlying processes
112
ischemic penumbra and central core
there is a central core of irreversible ischemia and necrosis with cerebral infarction. the central core is surrounded by a zone of borderline ischemic tissue called the ischemic penumbra
113
treatment for cerebral infarction
prompt restoration of perfusion in the penumbra by injection of thrombolytic agent, but the window of opportunity is 3 hours.
114
if patient with ischemic stroke is not able to be given a thrombolytic what treatment should you use?
arterial clot retrieval, anticoagulant therapy, anti platelet therapy, and control of risk factors
115
what happens to brain tissue after ischemic infarcts
affected area softens 6-12 hours after occlusion. 48-72 hours after infarction, necrosis and swelling occur, and there is an infiltration of macrophages and phagocytosis or necrotic tissue. necrosis resolves within 2 weeks and leaves a cavity surrounded by glial scarring
116
If unable to correct tissue death within the penumbra
all becomes a dark cavity
117
glial scarring
the scarring of the brain tissue after injury
118
primary causes of hemorrhagic stroke
hypertension/stimulants such as cocaine
119
goal of treatment of hemorrhagic stroke
stop or decrease bleeding, control ICP, and prevent rebleed
120
what can reduce the incidence of hemorrhagic stroke
prevention or control of hypertension
121
mass of blood
formed as bleeding continues into the brain tissue
122
what does the mass of blood do to other brain tissue
other brain tissue is compressed producing ischemia, edema, and increased intracranial pressure
123
clinical manifestation of hemorrhagic stroke
will either have excruciating headache with a lapse into unresponsive state, headache but with consciousness maintained, or overall sudden lapse into unconsciousness
124
why does cerebral edema occur during hemorrhagic stroke
neurons surrounding ischemic or infarcted area undergo changes that disrupt the plasma membrane which causes cerebral edema.
125
cerebral hemorrhage resolves through
reabsorption. macrophages and astrocytes clear blood from the area and a cavity surrounded by glial scarring is left
126
how do you know if a patient can receive tPA?
the stroke inclusion/exclusion criteria for tPA
127
FAST
facial droop, arm drift, slurred speech, time to call 911
128
stroke warning signs
sudden numbness or weakness of face, arm, or leg, confusion or trouble speaking, trouble walking, severe headache
129
RAS
reticular activating system
130
what is RAS
a large network of nuclei connecting the brain stem to the cortex. controls vital reflexes, sleep, focus, wakefulness, and attention
131
alterations in arousal can be caused by
structural, metabolic, or psychogenic disorders
132
AVPU
patient is awake, patient responds to verbal stimuli, patient responds to painful stimuli, and patient is completely unresponsive
133
most important function of RAS
control of consciousness
134
supratentorial disorders
produce changes in arousal by either diffuse or localized dysfunction caused by disease process that affect the cerebral cortex or underlying subcortical white matter
135
example of supratentorial disorders
encephalitis
136
extracerebral
disorders outside the brain but within the cranial vault
137
intracerebral
disorders within the brain substance
138
intracerebral disorders
hemorrhage, infarct, or emboli
139
extracerebral disorders
trauma with subdural bleeding, accumulation of pus in subdural space, and tumor
140
infratentorial disorders
produces a decline in arousal by direct destruction or compression of RAS or by destruction or obstruction of blood flow to the brain stem
141
examples of infratentorial disorders
stroke, infection with accumulation of pus, tumor, demyelination disorders
142
metabolic alterations in arousal
hypoxic, hypoglycemia, electrolyte imbalance, toxins
143
toxins the can alter arousal
urea, ammonia, or drugs
144
why would hypoglycemia cause alterations in arousal
glucose is the brains fuel
145
how can we get to toxic level of ammonia
liver and renal failure
146
psychogenic alterations in arousal
unresponsiveness and may signal psychiatric disorders
147
disorientation
beginning or ALOC usually presents as disoriented to time first
148
confusion
inability to think clearly
149
what happens with decreased level of consciousness
lower brainstem regulates breathing by responding to changes in PaCO2
150
how can we evaluate level of brain dysfunction?
through patterns of breathing, pupillary changes, and motor responses
151
obtundation
mild to mederate reduction in arousal with limited response to environment and falls asleep unless stimulated
152
stupor
condition of deep sleep or unresponsiveness. can be aroused only by vigorous stimulation
153
light coma
associated with purposeful movement on stimulation
154
coma
associated with non purposeful movement only on stimulation
155
deep coma
associated with unresponsiveness or no response to any stimulus
156
cheyne-stroke breathing
fast breathing with gradual decrease until apnea, then fast breathing
157
what will pupils look like with hypoxia/ischemia
dilated and fixed
158
what will pupils look like with hypothermia
fixed
159
what will pupils look like with atropine
dilated and fixed
160
what will pupils look like with sedatives and hallucinogens
fixed, unequal, mid-position or dilation
161
what will pupils look like with opioids `
pinpoint
162
Area of brain stem that controls arousal it right next
the area that controls pupillary response
163
bilateral dilated and fixed pupils are a
ominous sign
164
pinpoint pupils show
pons damage or drugs
165
one dilated pupil can be a sign of
compressed cranial nerve 3
166
decorticate
position in which the arms are drawn into the core
167
decerebrate
position in which the arms are turned outward along the side
168
responses to motor response assessment can be
purposeful, inappropriate, or not present
169
assessment of motor response is used to determine
brainstem dysfunction and if there is unilateral damage
170
if medulla oblongata is compressed or diseased what reflexes will be shown
vomiting, cough, swallowing, yawning, and hiccups
171
breakdown of the blood brain barrier can contribute to
neuroinflammation and neurodegeneration
172
substances that promote coagulation
platelets, Von Willebrand factor, activated clotting factors, and tissue thromboplastin
173
hemophilia
a genetic disorder in which coagulation and hemostasis factors are limited or absent. the patient is a free bleeder
174
Von Willebrand factor
primary function is binding to other proteins, in particular factor VIII, and it is important in platelet adhesion to wound sites
175
substances inhibiting coagulation
prostacyclin, antithrombin 3, proteins C & S, tissue plasminogen activator
176
prostacyclin
prostaglandin family. inhibits platelet activation. vasodilator
177
tissue plasminogen activator
natural substance that dissolve already formed clots
178
end result of both extrinsic and intrinsic clotting pathway is
fibrin
179
heparin is _____ and the its for it is ______
intrinsic and use PTT
180
Coumadin/warfarin is ______ and the test for it is _______
extrinsic and use pt/INR
181
what activates thromboplastin? and what does it initiate
Thromboplastin, contained in vessel walls gets activated due to injury & then initiates the extrinsic pathway
182
extrinsic pathway
outside penetration activates clotting factor 7 and 10. then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin
183
intrinsic pathway
endothelial damage, factor 12, then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin
184
reduced levels of fibrinogen will do what to PT/PTT times?
prolong them
185
increased level of fibrinogen increases
risk for clot
186
normal levels of fibrinogen in adults
200-400 mg/dL
187
what needs to be present for fibrinolytic system to be activated
a clot and fibrin
188
fibrinolysis
clot regulation and reverses the clotting process
189
fibrin and plasminogen =
plasmin
190
plasmin
protein that breaks down (lyses) thrombus
191
tissue plasminogen activator
it dissolves already formed clots. we have it naturally and secreted by endothelial cells but it takes several days vs if we administer it (exogenous) it takes 30 minutes
192
anticoagulants
prevents formation or progression of clot but does not bust up already present clot
193
how do anticoagulants prevent thrombus
by decreasing blood coagulability
194
Adverse effect of anticoagulants
bleeding
195
indications for anticoagulants
CVA, MI, DVT, PE, A-fib, heart valves, PICC/central port
196
indications for heparin
MI, unstable angina, a-fib, mechanical heart valves
197
which clotting factor is most sensitive to heparin
thrombin
198
MOA of heparin
deactivates thrombin, factor X and IX, which prevents conversion of fibrinogen to fibrin - overall turns off the coagulation pathway
199
how is heparin dosed
weight based protocol. in Kg
200
what do you need to do before administering heparin
PTT before and 2 RN check unless given prophylactically
201
range of strengths of heparin
10 u/1mL to 40,000 u/1mL
202
prophylactic dosing of heparin is given
subQ
203
signs of heparin over dose
epistaxis, hematuria, melana, petechiae
204
epistaxis
nose bleed
205
what to do for a patient with heparin induced thrombocytopenia
stop heparin infusion, give protamine sulfate IV (antidote), and start on argatroban
206
HIT type 2
heparin induced thrombocytopenia. immune mediated drug response that destroys platelets (platelets will fall by 50%).
207
greatest risk of the patient with HIT
paradoxical occurrence of thrombosis. can be fatal if not treated quickly
208
adverse effect of heparin
Bleeding, hematoma, anemia, thrombocytopenia
209
argatroban
thrombin inhibitor can replace heparin if patient is effected by HIT
210
PTT
evaluates overall ability to produce a clot in a reasonable amount of time
211
higher than normal PTT
bleeding disorder
212
enoxaparin brand name
lovenox
213
advantage of lovenox
more predictable/stable response and fewer adverse effects
214
how does lovenox come
in profiled syringes
215
how is lovenox dosed
weight and indication
216
how is lovenox given
subQ and need to rotate sites frequently
217
what do you not want to do with lovenox
pirate or massage site, will have air bubble in syringe do not expel air bubble before injection
218
are labs required for lovenox
no
219
which has larger molecules heparin or lovenox
heparin. lovenox is just fragments
220
BBW of lovernox
Spinal/Epidural Hematomas
221
what can lovenox be used for?
bridge therapy
222
what lab do you want to check with warfarin
INR
223
what should a patients INR be when one warfarin
2-3.5
224
geriatrics INR threshold
INR threshold decreases in older population
225
Warfarin MOA
inhibits synthesis of vitamin And clotting factors that are produced in liver which prevents clot formation
226
warfarin route
PO and IV. IV need to dilute with normal saline
227
warfarin antidote
IV vitamin K. reverses effects in 6 hours
228
warfarin drug interactions
amiodarone which increases INR by 50% so cut warfarin dose in half
229
warfarin adverse effects
Bleeding, lethargy, muscle pain, purple toes
230
warfarin brand name
coumadin
231
what do patients prescribed warfarin need to be educated on
constant levels of vitamin K in diet. if they eat to much food with vitamin K in it the warfarin may not work
232
how long does lovenox take to reach therapeutic therapy
2-3 days so it should be overlapped with lovenox for those days
233
BBW of warfarin
fatal bleeding
234
PT/INR
PT= prothrombin time, INR= international normalization ratio
235
increased INR
blood clots too slowly - risk for bleed
236
decreased INR
blood clots more quickly
237
clopidogrel brand name
plavix
238
Plavix
anti platelet, ADP inhibitor
239
plavix MOA
prevents platelet adhesion before clotting cascade by altering platelet membrane
240
indication for plavix
prevention of TIA, post MI, CAD
241
side effects of plavix
fata intracranial bleeding, thrombotic thrombocytopenia, hepatotoxicity
242
BBW plavix
genetic factors leading to higher risk of CV events - CYP450
243
can plavix be given with aspirin?
yes - 81 mg for heart healthy dose. up to 325 mg
244
ADP, TXA2
stimulators released from platelets – they increase the arrival of (recruit) more platelets to site and cause vasoconstriction
245
clotting cascade
Blood vessel injury due to disruption in blood flow, trauma, or plaque rupture occurs. Collagen is exposed.
Platelets adhere and activate. Stimulators released from activated platelets. Platelets then aggregate at injury site.
Stimulators: ADP, TXA2
Call for aggregation
Vasoconstriction
fibrin plug
246
alteplase brand name
activase
247
alteplase
pharmaceutically available t-PA made through recumbent DNA techniques. is fibrin specific. is a clot buster
248
alteplase MOA
degrades protein of fibrin and clotting factors
249
how to give alteplase
within 3-4.5 hours of symptoms. with heparin to prevent reocclusion. as a bolus and followed by infusion
250
side effect of alteplase
bleeding
251
disadvantages of alteplase
no antidote and short half life
252
what do you need to look out for when administering alteplase
repercussion injury which could lead to an acute ischemic stroke or acute MI
253
nursing considerations with alteplase
neuro exam every 15 minutes, avoid invasive procedures after injection, watch for bleeding, and check PT/PTT and hemoglobin and hematocrit
254
pharmacodynamics
what the drug does to the body
255
pharmacokinetics
what our body does to the drug - absorption, distribution, metabolism, excretion
256
bioavailability
amount of drug available for absorption - IV - 100%, sublingual - 100%
257
inactive prodrugs
inactive until in your body
258
pharmacogenomics
same drug but different response in different bodies
259
GFR
gives us an idea of how fast a drug can be metabolized - BUN test
260
cardinal signs of inflammation
(HEELP) heat (fever), erythema (redness), edema (swelling), loss of function, pain
261
what happens when inflammation is present
vasodilation, increased vascular permeability, and white blood cell infiltration
262
capillary hydrostatic pressure
pushing pressure inside the arterial part of the vessel where filtration is favored
263
interstitial oncotic pressure
pulling pressure outside the vessel on the arterial side
264
interstitial hydrostatic pressure
pushing pressure on venous side of vessel where reabsorption is favored
265
plasma oncotic pressure
pulling pressure inside the vessel on the venous side
266
Normal sodium levels
135-145 mEq/L
267
extracellular electrolytes
sodium, chloride, bicarb
268
intracellular electrolytes
potassium, magnesium, phosphate
269
signs and symptoms of hyponatremia
ALOC, seizures, ICP, coma, cerebral adema, muscle weakness, twitching, or tremors
270
Signs of hypernatremia
fever, flushed, increased fluid retention, edema, ALOC, coma, muscle twitching, hyperreflexion
271
normal levels of potassium
3.5 -5
272
hypokalemia signs and symptoms
irregular pulse, dysrhythmias, or arrest. everything is slow, can flatten T and U waves, muscle aches, paralysis, V/D
273
hyperkalemia signs and symptoms
decreased cardiac contractibility, cramps, cause peaked Ts and widened QRS, Brady dysrhythmias or arrest, hyperactive smooth and skeletal muscle
274
ph of less than 7.4
acidosis
275
ph greater than 7.4
alkalosis
276
regulations of ph
chemical buffers, intracellular phosphate and protein, lungs, kidneys
277
chemical buffers
plasma: CO2, HCO3, and hemoglobin and intracellular: phosphate and protein
278
uncompensated acidosis or alkalosis
CO2 or HCO3 normal
279
fully compensated acidosis or alkalosis
ph is normal
280
partially compensated acidosis or alkalosis
nothing normal
281
respiratory acidosis vs metabolic acidosis
respiratory acidosis has a co2>44, metabolic acidosis has a HCO3<22
282
respiratory alkalosis vs metabolic alkalosis
respiratory alkalosis has a CO2< 38, metabolic alkalosis has a HCO3 > 26
283
acidosis symptoms
headache, SOB, coughing, arrhythmia, increased HR, seizures, weakness N/V/D
284
alkalosis symptoms
light headedness, hand tremor, numbness or tingling, spasms N/V/D
285
PaO2
O2 dissolved in blood 80-100 mmHg
286
PaCO2
35-45 mmHg
287
HCO3 levels
33-36 mEq/L
288
acute therapy
short term
289
maintenance therapy
ongoing
290
palliative therapy
symptom relief
291
prophylactic therapy
preventative
292
supplemental therapy
replacement
293
supportive therapy
recovery
294
parasympathetic
rest and digest. cholinergic receptors
295
sympathetic
fight or flight. adrenergic receptors with alpha and beta receptors
296
what neurotransmitter is connected with parasympathetic
acetylcholine
297
inotropic
contractibility of the heart
298
chronotropic
effect heart rate
299
dromotropic
electrical conduction of the heart
300
sympathetic neurotransmitter
norepinephrine and epinephrine
301
increase in RAAS leads to
decreased renal salt excretion so increase salt retention which can lead to HTN
302
what can prolonged hypertension do to your body?
vascular remodeling, increase renin/angiotensin, renal sodium retention, and procoagulant
303
primary hypertension
due to genetics and environment
304
secondary hypertension
usually from disease process. Is reversible
305
complicated hypertension
leads to target organ damage such as LVH, HF, CAD
306
hypertensive crisis
BP 180/110+, rapid onset. can cause organ damage, CVA, or stroke
307
what can cause a hypertensive crisis
alcohol withdrawal, stimulant drugs, or pregnancy
308
High blood pressure guidelines
Normal: Less than 120/80 mm Hg;
Elevated: Systolic between 120-129 and diastolic less than 80;
Stage 1: Systolic between 130-139 or diastolic between 80-89;
Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage
309
adipokines
inflammatory mediators released by adipocytes
310
adipokines release
leptin and adiponectin
311
leptin control what in the body?
appetite suppression and increase metabolic rate
312
what happens to leptin and adiponectin when you are obese?
increase in leptin and decrease in adiponectin
313
what do adiponectins deal with
insulin
314
what do increased levels of leptin do?
cause resistance by increases SNS, decreasing renal sodium excretion, and causing inflammation
315
what does a decreased amount of adiponectin do to your body?
increases SNS, increases RAAS, and decreases nitric oxide
316
what does higher levels of BNP mean? what is considered normal?
less than 100 = normal. higher than 100 = heart failure, increase in volume, or ventricle stretch
317
vomiting and diarrhea may cause toxicity for which drug?
digoxin cause vomit and diarrhea can make you lose potassium and hypokalemia increases potential digoxin toxicity
318
effects of decrease contractility
increase preload - stretching of myocardium and decrease of lumen coronary arteries - myocardial ischemia - leads right back to more decreased contractility
319
effects of increased afterload
increases left ventricle workload - increase RAAS and SNS which causes hypertrophy causes increases demand for oxygen causes ventricular remolding which leads to decrease in contractility which increases RAAS and SNS and leads to more vascular resistance
320
how does a patient present with left systolic heart failure
fatigue, pulmonary edema, dyspnea, orthopnea, cough with frothy sputum, S3 heart sound
321
orthopnea
shortness of breath while laying down
322
Ace inhibitors and ARBs
reduce preload and after load, decrease volume and PVR, are cardio and renal protective
323
treatment for heart failure
beta blocker, anti platelet, salt restriction, diuretic, ACE inhibitor or ARB
324
what is a first line treatment for HTN if no other comorbidities exist?
diuretic - decrease BP, CO, and preload
325
Cardiac glycosides Mechanism of actions and what do they do to inotrope, chronotrpe, and dromotrope
increase sodium and calcium (positive inotrope), augments parasympathetic stimulation (negative chronotrope), prolongs conduction (negative dromotrope)
326
what cardiac glycoside did we learn
Digoxin
327
ROME
respiratory opposite, metabolic same
328
what is a first line treatment for HTN if no other comorbidities exist?
diuretic - decrease BP, CO, and preload
329
what do alpha receptors do
vasoconstrict cardiovascular, bladder constriction, promote glycogenolysis, mydriasis
330
what do beta 1 receptors do
increase contractility in heart, increase HR, promote renin secretion
331
what do beta 2 receptors do
bronchodilate, glycogenolysis, vasodilation
332
adrenergic agonist (alpha and beta)
promote SNS. low dose beta, high dose alpha
333
cor pulmonale
Right ventricular enlargement. can be hypertrophy, dilation, or both
334
tests of high risk for diabetes
FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%
335
consequences of hyperglycemia
decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression
336
insulin counter regulator hormones
growth hormone, glucagon, epinephrine, cortisol
337
characteristics to DKA
acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated
338
laster signs of diabetic renal dysfunction
Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN
339
as GFR decreases to less than 10 what type of signs occur
uremic signs - nausea, lethargy, acidosis, anemia, and HTN from having high levels of urea in the blood
340
diabetic neuropathy sensory deficits
footdrop, amyotrophy, temp, and pain
341
diabetic autonomic neuropathy deficits
delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability
342
alpha cells release what?
glucagon
343
first line drug for type 2 diabetes
metformin (Glucophage)
344
insulin onset and duration times
rapid: 15 minutes onset of 3-5 hr duration
short: 30-60 minutes onset with 6-10 hr duration
long: 1-2 hour onset with 24 hr duration
345
hypoglycemia blood glucose level
less than 70 mg/dL
346
less sever signs on hypoglycemia
shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable
347
BUN
7-18 mg/dL
348
Creatine
0.6-1.2 mg/dL
349
albumin
3.5-6g/dL
350
normal PTT
60-70 seconds
351
normal aPTT
30-40 seconds
352
PTT/aPTT on coagulants
will be 1.5-2.5 times longer than normal
353
insulins
lispro - Humalog (rapid acting
regular - humbling R (short acting)
glargine - Lantus (long acting)
354
adrenergic beta 2 agonist short acting
albuterol - inhaler for bronchospasm and asthma
355
adrenergic beta 2 agonist long acting
salmeterol
356
anticholinergic
ipatropium (Atrovent) for COPD
357
corticosteroid
fluticasone (Flonase/Flovent)
358
leukotriene receptor blocker
Montelukast (Singulair) - for allergic rhinitus and asthma
359
Benzodiazepines
lorazepam (Ativan) and diazepam (Valium)
360
antidiabetics
metormin (Glucopage) - decreases glucose production while increases insulin sensitivity
361
sulfonylureas
glipizide (Glucotrol) stimulates pancreas to release insulin
362
DPP 4 inhibitor
sitagliptine (Januvia) increase insulin release
363
antiplatelets
clopidogrel (Plavix) and aspirin
364
thrombolytic
alteplase (Activase)
365
Anticonvulsant
phenytoin (Dilantin) - for tonic/clonic seizures
| levetriacetam (Keppra) - partial seizures
366
anti epileptic
```
carbamazepine (Tegretol)
Valpoirc acid (Depekote)
```
367
nitrates
nitroglycerin
368
cardiac glycoside
digoxin
369
anticoagulants
Heparin
Enoxaparin (Lovenox)
Warfarin (Coumadin)
370
Beta Blockers
metoprolol (Lopressor)
| Carvedilol (Coreg)
371
Calcium Channel Blockers
Diltiazem
| Amlodipine (Norvasc)
372
ACEs
Lisinopril
| Enalopril (Vasotec)
373
ARBS
Losartan (Cozzar)
