331 final exam Flashcards
types on seizures
focal or tonic/clonic
focal seizure
partial seizure (used to be called petite mal)– loss of awareness
tonic/clonic seizure
convulsion (used to be called gran mal) - tonic = contraction and associated with loss of conciseness and clonic = altering contraction and relaxation
seizures can be caused by
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
epilepsy
CNS disorder with multiple seizures of idiopathic cause. there is no cure but can be treated.
seizure vs epilepsy
seizure is a single occurrence (do not need to have epilepsy) while epilepsy is a medical condition that includes seizures
which vascular diseases can lead to seizure
CVA and aneurysm
how to diagnose of seizures
want to identify and eliminate the cause, EEG, CT, MRI, serum test for electrolytes and toxins
EEG
electroencephalogram is a test with sensors placed on a patients head used to find problems related to electrical activity of the brain.
what metabolic problems can cause a seizure
hepatic failure, electrolyte abnormalities, and hypoglycemia
things that decrease seizure threshold
stress, fatigue, hypoglycemia, fever, alcohol and antipsychotic drugs, hyperventilation, increased water ingestion, menses, light, and noise
if you increase the seizure threshold
you can reduce the occurrence of seizures
why does water intoxication increase the chances of seizures
it dilutes sodium
prodroma
early manifestations that appear a few days to hours before onset of seizure. can show as anxiety, depression, and inability to think clearly.
aura
partial seizure that manifests itself as dizziness, numbness, visual or auditory experience, or just a funny feeling
phases of seizures
preictal, ictal, postictal
what is included in the preictal phase
prodroma and aura
ictal phase includes
the seizure phase which includes tonic and clonic phases
what happens during the ictal phase
muscle contractions/relaxation and increase in metabolic demand which causes decreased level of conscious, increased O2 use, decreased glucose, and increased lactic acid
what needs to be done during the ictal phase
airway maintenance needs to be ensured and there may be relaxation of bowel and urinary sphincter which causes incontinence
postictal phase
period immediately following cessation of seizure activity
what happens during the postictal phase
decreased level of consciousness, dysphagia/dysphasia, confusion, memory loss, paralysis, and deep sleep
status epilepticus
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
what do seizures do to metabolic demand
increases it
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
hypotonia
decreased muscle tone
seizure treatment
correct or control cause if possible, anti-seizure medications, dietary, surgical interventions
goals for a patient going through seizure
pharmacology, oxygenation, and to prevent injury
dietary treatment for seizure patients
keto and adkins
status epileptics can cause
progressive and irreversible brain damage and can be life threatening
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
anti epileptic drugs do what to nerve impulses
suppress transmission between nerve impulses which stabilizes cell membranes and decreases spread of impulses
anti epileptic drugs do what to nerve impulse conduction
decrease the speed of the nerve impulse conduction within a neuron
anti epileptic drugs do what to threshold
increase the threshold which decreases the neuronal response to stimuli
anti epileptic drug do what to GABA? which does what
enhance effects of GABA which helps regulate neuron excitability in the brain
besides seizures, anti epileptic drugs are also used for
psychiatric disorders, migraines, and neuropathic pain
GABA is a
inhibitory neurotransmitter
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
indications of anti epileptic drugs
long term seizure maintenance and status epilepticus
adverse effects of anti epileptic drugs
decrease level of consciousness, SI, mood, GI upset, thrombocytopenia, and many induce hepatic metabolism
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
Phenytoin (Dilantin) adverse effects
Nystagmus, ataxia, drowsiness, rash, gingival hyperplasia, pancytopenia, agranulocytosis, hepatitis, GI upset
first line prototypical drug for both tonic/clonic and partial seizures
Phenytoin (Dilantin)
Phenytoin (Dilantin) routes
capsule and IV
Phenytoin (Dilantin) MOA
stabilize neurons (Na)
Phenytoin (Dilantin) therapeutic plasma level
10-20 mcg/mL
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
what does phenytoin toxicity look like
nagstagmus, ataxia, encephalopathy (altered level of consciousness), dysarthria
nursing considerations with IV phenytoin
20 gage needle, dilute with NS and flush with Ns, filter must be used,
what is used to overcome chemical disadvantage of IV phenytoin?
IV fosphenytoin
Dose of IV phenytoin
10-15 mg/kg
risks of IV phenytoin and why
can cause extravagation because it is mixed with antifreeze at a ph of 12
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
BBW of carbamazepine
bone marrow suppression which causes pancytopenia which causes decreased immunity, oxygen, and blood clotting
therapeutic levels of carbamazepine
4-12 mcg/mL
indication of carbamazepine
generalized tonic-clonic seizures and not for myoclonic or absent seizures
what can a patient not have if taking carbamazepine
grapefruit juice
stevens-johnson syndrom
peeling of the skin. adverse effect of carbamazepine. if not controlled leads to toxic epidermal necrolysis
levetiracetam brand name
Keppra
levetiracetam (Keppra) indication
adjunct therapy for partial seizures without secondary generalization
levetiracetam (Keppra) MOA
unknown however evidence shows it inhibits simultaneous neuronal firing
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
levetiracetam (Keppra) route
PO, IV, and IR (immediate release)
valproic acid MOA
facilitates inhibitory neurotransmitter GABA
valproic acid route, onset, and peak
PO and IV onset is 15-30 mins, and peaks in 1-4 hours
valproic acid indication
generalized seizures and can be used for bipolar disorder
valproic acid adverse effects
drowsiness, N/V, tremor, weight gain, transient hair loss
Capsules with long acting valproic acid granules are called
Depakote sprinkle
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
therapeutic levels for Depakote
50-125 mcg/mL
adverse effects of Depakote
hepatotoxicity and pancreatitis
what Benzodiazepines did we learn
lorazepam and diazepam
Benzodiazepines indications
anxiolytic (decrease anxiety), ethanol withdrawal, acute seizures
therapeutic effect of Benzodiazepines? adverse effect of Benzodiazepines?
both are sedation
nursing considerations of Benzodiazepines
habit forming, can induce withdrawal seizures, risk for falls, monitor BP, assess for suicidal ideation
lorazepam trade name
Ativan
why are patients on Benzodiazepines a fall risk
because they are CNS depressants and have mind altering capabilities
Benzodiazepines reversal
flumazenil (romazicon)
flumazenil (romazicon) BBW
rebound seizures from stopping effects of benzo too fast
gabapentin (Neurontin) MOA
increases synthesis and synaptic accumulation of GABA between the neurons
gabapentin (Neurontin) indication
most commonly used for neuropathic pain
GABA does what to brain activity
inhibits it
pregabalin (Lyrica) MOA
affects calcium channels in the CNS tissue
pregabalin (Lyrica) indication
adjunct therapy for partial seizures. also commonly used for neuropathic pain, fibromyalgia, and postherpetic neuralgia
cerebrovascular disease
any abnormalities of the brain caused by a pathological process in the blood vessels
symptoms of cerebrovascular disease are
there are focal, unilateral, and global symptoms. slurred speech, difficulty swallowing, limb weakness, and paralysis
leading cause of disability
stroke, aka cerebrovascular disease
cerebrovascular disease can be
ischemic or hemorrhagic. can also be associated with hypoperfusion
severe effects of cerebrovascular disease
hemiplegia, coma, and death
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
thrombocythemia
excess platelet production
polycythemia
over production of RBC
smoking increases risk of stroke by
50%
ischemic stroke
occurs when there is obstruction to arterial blood flow to the brain from thrombus formation, an embolus, or hypoperfusion
thrombus
chronic process that may take up to 20-30 years for obstruction to develop
cerebral thrombosis develops most often from
atherosclerosis/stenosis and inflammatory disease process that damage arterial wall
what adhere to a vessel wall that is damaged
platelets and fibrin to form a clot
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
risk factors for embolic stroke
A-fib, endocarditis, and MI
hypoperfusion
decreased cardiac output
hypoperfusion can be caused by
dehydration, low volume, HF, PE
conditions causing increased coagulation or inadequate cerebral perfusion can ________ the risk of thrombus
increase
TIA
neurological dysfunction lasting less than one hour resulting from focal cerebral ischemia
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
what are you at risk for after a TIA
of having a stroke in the next 90 days
clinical manifestations of TIA
weakness, numbness, sudden confusion, loss of balance, sudden or severe headache
what should you watch with hypoperfusion stroke
hemodynamic monitoring
conditions that can cause increased coagulation or inadequate cerebral perfusion
dehydration, hypotension, prolonged vasoconstriction due to malignant HTN
bifurcation
vessel breaks into two smaller vessels which makes its lumen smaller
cerebral infarction
occurs when the brain loses its blood supply due to vascular occlusion
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
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
treatment for cerebral infarction
prompt restoration of perfusion in the penumbra by injection of thrombolytic agent, but the window of opportunity is 3 hours.
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
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
If unable to correct tissue death within the penumbra
all becomes a dark cavity
glial scarring
the scarring of the brain tissue after injury
primary causes of hemorrhagic stroke
hypertension/stimulants such as cocaine
goal of treatment of hemorrhagic stroke
stop or decrease bleeding, control ICP, and prevent rebleed
what can reduce the incidence of hemorrhagic stroke
prevention or control of hypertension
mass of blood
formed as bleeding continues into the brain tissue
what does the mass of blood do to other brain tissue
other brain tissue is compressed producing ischemia, edema, and increased intracranial pressure
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
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.
cerebral hemorrhage resolves through
reabsorption. macrophages and astrocytes clear blood from the area and a cavity surrounded by glial scarring is left
how do you know if a patient can receive tPA?
the stroke inclusion/exclusion criteria for tPA
FAST
facial droop, arm drift, slurred speech, time to call 911
stroke warning signs
sudden numbness or weakness of face, arm, or leg, confusion or trouble speaking, trouble walking, severe headache
RAS
reticular activating system
what is RAS
a large network of nuclei connecting the brain stem to the cortex. controls vital reflexes, sleep, focus, wakefulness, and attention
alterations in arousal can be caused by
structural, metabolic, or psychogenic disorders
AVPU
patient is awake, patient responds to verbal stimuli, patient responds to painful stimuli, and patient is completely unresponsive
most important function of RAS
control of consciousness
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
example of supratentorial disorders
encephalitis
extracerebral
disorders outside the brain but within the cranial vault
intracerebral
disorders within the brain substance
intracerebral disorders
hemorrhage, infarct, or emboli
extracerebral disorders
trauma with subdural bleeding, accumulation of pus in subdural space, and tumor
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
examples of infratentorial disorders
stroke, infection with accumulation of pus, tumor, demyelination disorders
metabolic alterations in arousal
hypoxic, hypoglycemia, electrolyte imbalance, toxins
toxins the can alter arousal
urea, ammonia, or drugs
why would hypoglycemia cause alterations in arousal
glucose is the brains fuel
how can we get to toxic level of ammonia
liver and renal failure
psychogenic alterations in arousal
unresponsiveness and may signal psychiatric disorders
disorientation
beginning or ALOC usually presents as disoriented to time first
confusion
inability to think clearly
what happens with decreased level of consciousness
lower brainstem regulates breathing by responding to changes in PaCO2
how can we evaluate level of brain dysfunction?
through patterns of breathing, pupillary changes, and motor responses
obtundation
mild to mederate reduction in arousal with limited response to environment and falls asleep unless stimulated
stupor
condition of deep sleep or unresponsiveness. can be aroused only by vigorous stimulation
light coma
associated with purposeful movement on stimulation
coma
associated with non purposeful movement only on stimulation
deep coma
associated with unresponsiveness or no response to any stimulus
cheyne-stroke breathing
fast breathing with gradual decrease until apnea, then fast breathing
what will pupils look like with hypoxia/ischemia
dilated and fixed
what will pupils look like with hypothermia
fixed
what will pupils look like with atropine
dilated and fixed
what will pupils look like with sedatives and hallucinogens
fixed, unequal, mid-position or dilation
what will pupils look like with opioids `
pinpoint
Area of brain stem that controls arousal it right next
the area that controls pupillary response
bilateral dilated and fixed pupils are a
ominous sign
pinpoint pupils show
pons damage or drugs
one dilated pupil can be a sign of
compressed cranial nerve 3
decorticate
position in which the arms are drawn into the core
decerebrate
position in which the arms are turned outward along the side
responses to motor response assessment can be
purposeful, inappropriate, or not present
assessment of motor response is used to determine
brainstem dysfunction and if there is unilateral damage
if medulla oblongata is compressed or diseased what reflexes will be shown
vomiting, cough, swallowing, yawning, and hiccups
breakdown of the blood brain barrier can contribute to
neuroinflammation and neurodegeneration
substances that promote coagulation
platelets, Von Willebrand factor, activated clotting factors, and tissue thromboplastin
hemophilia
a genetic disorder in which coagulation and hemostasis factors are limited or absent. the patient is a free bleeder
Von Willebrand factor
primary function is binding to other proteins, in particular factor VIII, and it is important in platelet adhesion to wound sites
substances inhibiting coagulation
prostacyclin, antithrombin 3, proteins C & S, tissue plasminogen activator
prostacyclin
prostaglandin family. inhibits platelet activation. vasodilator
tissue plasminogen activator
natural substance that dissolve already formed clots
end result of both extrinsic and intrinsic clotting pathway is
fibrin
heparin is _____ and the its for it is ______
intrinsic and use PTT
Coumadin/warfarin is ______ and the test for it is _______
extrinsic and use pt/INR
what activates thromboplastin? and what does it initiate
Thromboplastin, contained in vessel walls gets activated due to injury & then initiates the extrinsic pathway
extrinsic pathway
outside penetration activates clotting factor 7 and 10. then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin
intrinsic pathway
endothelial damage, factor 12, then enzymes (thrombin) and proteins (fibrinogen) work together to form a clot = fibrin
reduced levels of fibrinogen will do what to PT/PTT times?
prolong them
increased level of fibrinogen increases
risk for clot
normal levels of fibrinogen in adults
200-400 mg/dL
what needs to be present for fibrinolytic system to be activated
a clot and fibrin
fibrinolysis
clot regulation and reverses the clotting process
fibrin and plasminogen =
plasmin
plasmin
protein that breaks down (lyses) thrombus
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
anticoagulants
prevents formation or progression of clot but does not bust up already present clot
how do anticoagulants prevent thrombus
by decreasing blood coagulability
Adverse effect of anticoagulants
bleeding
indications for anticoagulants
CVA, MI, DVT, PE, A-fib, heart valves, PICC/central port
indications for heparin
MI, unstable angina, a-fib, mechanical heart valves
which clotting factor is most sensitive to heparin
thrombin
MOA of heparin
deactivates thrombin, factor X and IX, which prevents conversion of fibrinogen to fibrin - overall turns off the coagulation pathway
how is heparin dosed
weight based protocol. in Kg
what do you need to do before administering heparin
PTT before and 2 RN check unless given prophylactically
range of strengths of heparin
10 u/1mL to 40,000 u/1mL
prophylactic dosing of heparin is given
subQ
signs of heparin over dose
epistaxis, hematuria, melana, petechiae
epistaxis
nose bleed
what to do for a patient with heparin induced thrombocytopenia
stop heparin infusion, give protamine sulfate IV (antidote), and start on argatroban
HIT type 2
heparin induced thrombocytopenia. immune mediated drug response that destroys platelets (platelets will fall by 50%).
greatest risk of the patient with HIT
paradoxical occurrence of thrombosis. can be fatal if not treated quickly
adverse effect of heparin
Bleeding, hematoma, anemia, thrombocytopenia
argatroban
thrombin inhibitor can replace heparin if patient is effected by HIT
PTT
evaluates overall ability to produce a clot in a reasonable amount of time
higher than normal PTT
bleeding disorder
enoxaparin brand name
lovenox
advantage of lovenox
more predictable/stable response and fewer adverse effects
how does lovenox come
in profiled syringes
how is lovenox dosed
weight and indication
how is lovenox given
subQ and need to rotate sites frequently
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
are labs required for lovenox
no
which has larger molecules heparin or lovenox
heparin. lovenox is just fragments
BBW of lovernox
Spinal/Epidural Hematomas
what can lovenox be used for?
bridge therapy
what lab do you want to check with warfarin
INR
what should a patients INR be when one warfarin
2-3.5
geriatrics INR threshold
INR threshold decreases in older population
Warfarin MOA
inhibits synthesis of vitamin And clotting factors that are produced in liver which prevents clot formation
warfarin route
PO and IV. IV need to dilute with normal saline
warfarin antidote
IV vitamin K. reverses effects in 6 hours
warfarin drug interactions
amiodarone which increases INR by 50% so cut warfarin dose in half
warfarin adverse effects
Bleeding, lethargy, muscle pain, purple toes
warfarin brand name
coumadin
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
how long does lovenox take to reach therapeutic therapy
2-3 days so it should be overlapped with lovenox for those days
BBW of warfarin
fatal bleeding
PT/INR
PT= prothrombin time, INR= international normalization ratio
increased INR
blood clots too slowly - risk for bleed
decreased INR
blood clots more quickly
clopidogrel brand name
plavix
Plavix
anti platelet, ADP inhibitor
plavix MOA
prevents platelet adhesion before clotting cascade by altering platelet membrane
indication for plavix
prevention of TIA, post MI, CAD
side effects of plavix
fata intracranial bleeding, thrombotic thrombocytopenia, hepatotoxicity
BBW plavix
genetic factors leading to higher risk of CV events - CYP450
can plavix be given with aspirin?
yes - 81 mg for heart healthy dose. up to 325 mg
ADP, TXA2
stimulators released from platelets – they increase the arrival of (recruit) more platelets to site and cause vasoconstriction
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
alteplase brand name
activase
alteplase
pharmaceutically available t-PA made through recumbent DNA techniques. is fibrin specific. is a clot buster
alteplase MOA
degrades protein of fibrin and clotting factors
how to give alteplase
within 3-4.5 hours of symptoms. with heparin to prevent reocclusion. as a bolus and followed by infusion
side effect of alteplase
bleeding
disadvantages of alteplase
no antidote and short half life
what do you need to look out for when administering alteplase
repercussion injury which could lead to an acute ischemic stroke or acute MI
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
pharmacodynamics
what the drug does to the body
pharmacokinetics
what our body does to the drug - absorption, distribution, metabolism, excretion
bioavailability
amount of drug available for absorption - IV - 100%, sublingual - 100%
inactive prodrugs
inactive until in your body
pharmacogenomics
same drug but different response in different bodies
GFR
gives us an idea of how fast a drug can be metabolized - BUN test
cardinal signs of inflammation
(HEELP) heat (fever), erythema (redness), edema (swelling), loss of function, pain
what happens when inflammation is present
vasodilation, increased vascular permeability, and white blood cell infiltration
capillary hydrostatic pressure
pushing pressure inside the arterial part of the vessel where filtration is favored
interstitial oncotic pressure
pulling pressure outside the vessel on the arterial side
interstitial hydrostatic pressure
pushing pressure on venous side of vessel where reabsorption is favored
plasma oncotic pressure
pulling pressure inside the vessel on the venous side
Normal sodium levels
135-145 mEq/L
extracellular electrolytes
sodium, chloride, bicarb
intracellular electrolytes
potassium, magnesium, phosphate
signs and symptoms of hyponatremia
ALOC, seizures, ICP, coma, cerebral adema, muscle weakness, twitching, or tremors
Signs of hypernatremia
fever, flushed, increased fluid retention, edema, ALOC, coma, muscle twitching, hyperreflexion
normal levels of potassium
3.5 -5
hypokalemia signs and symptoms
irregular pulse, dysrhythmias, or arrest. everything is slow, can flatten T and U waves, muscle aches, paralysis, V/D
hyperkalemia signs and symptoms
decreased cardiac contractibility, cramps, cause peaked Ts and widened QRS, Brady dysrhythmias or arrest, hyperactive smooth and skeletal muscle
ph of less than 7.4
acidosis
ph greater than 7.4
alkalosis
regulations of ph
chemical buffers, intracellular phosphate and protein, lungs, kidneys
chemical buffers
plasma: CO2, HCO3, and hemoglobin and intracellular: phosphate and protein
uncompensated acidosis or alkalosis
CO2 or HCO3 normal
fully compensated acidosis or alkalosis
ph is normal
partially compensated acidosis or alkalosis
nothing normal
respiratory acidosis vs metabolic acidosis
respiratory acidosis has a co2>44, metabolic acidosis has a HCO3<22
respiratory alkalosis vs metabolic alkalosis
respiratory alkalosis has a CO2< 38, metabolic alkalosis has a HCO3 > 26
acidosis symptoms
headache, SOB, coughing, arrhythmia, increased HR, seizures, weakness N/V/D
alkalosis symptoms
light headedness, hand tremor, numbness or tingling, spasms N/V/D
PaO2
O2 dissolved in blood 80-100 mmHg
PaCO2
35-45 mmHg
HCO3 levels
33-36 mEq/L
acute therapy
short term
maintenance therapy
ongoing
palliative therapy
symptom relief
prophylactic therapy
preventative
supplemental therapy
replacement
supportive therapy
recovery
parasympathetic
rest and digest. cholinergic receptors
sympathetic
fight or flight. adrenergic receptors with alpha and beta receptors
what neurotransmitter is connected with parasympathetic
acetylcholine
inotropic
contractibility of the heart
chronotropic
effect heart rate
dromotropic
electrical conduction of the heart
sympathetic neurotransmitter
norepinephrine and epinephrine
increase in RAAS leads to
decreased renal salt excretion so increase salt retention which can lead to HTN
what can prolonged hypertension do to your body?
vascular remodeling, increase renin/angiotensin, renal sodium retention, and procoagulant
primary hypertension
due to genetics and environment
secondary hypertension
usually from disease process. Is reversible
complicated hypertension
leads to target organ damage such as LVH, HF, CAD
hypertensive crisis
BP 180/110+, rapid onset. can cause organ damage, CVA, or stroke
what can cause a hypertensive crisis
alcohol withdrawal, stimulant drugs, or pregnancy
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
adipokines
inflammatory mediators released by adipocytes
adipokines release
leptin and adiponectin
leptin control what in the body?
appetite suppression and increase metabolic rate
what happens to leptin and adiponectin when you are obese?
increase in leptin and decrease in adiponectin
what do adiponectins deal with
insulin
what do increased levels of leptin do?
cause resistance by increases SNS, decreasing renal sodium excretion, and causing inflammation
what does a decreased amount of adiponectin do to your body?
increases SNS, increases RAAS, and decreases nitric oxide
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
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
effects of decrease contractility
increase preload - stretching of myocardium and decrease of lumen coronary arteries - myocardial ischemia - leads right back to more decreased contractility
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
how does a patient present with left systolic heart failure
fatigue, pulmonary edema, dyspnea, orthopnea, cough with frothy sputum, S3 heart sound
orthopnea
shortness of breath while laying down
Ace inhibitors and ARBs
reduce preload and after load, decrease volume and PVR, are cardio and renal protective
treatment for heart failure
beta blocker, anti platelet, salt restriction, diuretic, ACE inhibitor or ARB
what is a first line treatment for HTN if no other comorbidities exist?
diuretic - decrease BP, CO, and preload
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)
what cardiac glycoside did we learn
Digoxin
ROME
respiratory opposite, metabolic same
what is a first line treatment for HTN if no other comorbidities exist?
diuretic - decrease BP, CO, and preload
what do alpha receptors do
vasoconstrict cardiovascular, bladder constriction, promote glycogenolysis, mydriasis
what do beta 1 receptors do
increase contractility in heart, increase HR, promote renin secretion
what do beta 2 receptors do
bronchodilate, glycogenolysis, vasodilation
adrenergic agonist (alpha and beta)
promote SNS. low dose beta, high dose alpha
cor pulmonale
Right ventricular enlargement. can be hypertrophy, dilation, or both
tests of high risk for diabetes
FPG of 100-125 mg/dL, 2 hr PG 140-199, hgbA1C- 5.7%-6.4%
consequences of hyperglycemia
decreased cognition, neuropathy, cataracts, hypertension, stroke, heart disease, gastroparesis, nephropathy, chronic kidney disease, oxidative stress, infection, cancer, immunosuppression
insulin counter regulator hormones
growth hormone, glucagon, epinephrine, cortisol
characteristics to DKA
acidosis, ketonuria, ketonemia, hyperglycemia over 250 mg/dL, tachycardia, dehydrated
laster signs of diabetic renal dysfunction
Hypoproteinemia, decrease oncotic pressure, fluid overload, anasarca, HTN
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
diabetic neuropathy sensory deficits
footdrop, amyotrophy, temp, and pain
diabetic autonomic neuropathy deficits
delayed gastric emptying, altered bladder function, impotence, orthostatic hypotension, HR variability
alpha cells release what?
glucagon
first line drug for type 2 diabetes
metformin (Glucophage)
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
hypoglycemia blood glucose level
less than 70 mg/dL
less sever signs on hypoglycemia
shaking, sweating, dizziness, hunger, fast HR, headache, weakness, irritable
BUN
7-18 mg/dL
Creatine
0.6-1.2 mg/dL
albumin
3.5-6g/dL
normal PTT
60-70 seconds
normal aPTT
30-40 seconds
PTT/aPTT on coagulants
will be 1.5-2.5 times longer than normal
insulins
lispro - Humalog (rapid acting
regular - humbling R (short acting)
glargine - Lantus (long acting)
adrenergic beta 2 agonist short acting
albuterol - inhaler for bronchospasm and asthma
adrenergic beta 2 agonist long acting
salmeterol
anticholinergic
ipatropium (Atrovent) for COPD
corticosteroid
fluticasone (Flonase/Flovent)
leukotriene receptor blocker
Montelukast (Singulair) - for allergic rhinitus and asthma
Benzodiazepines
lorazepam (Ativan) and diazepam (Valium)
antidiabetics
metormin (Glucopage) - decreases glucose production while increases insulin sensitivity
sulfonylureas
glipizide (Glucotrol) stimulates pancreas to release insulin
DPP 4 inhibitor
sitagliptine (Januvia) increase insulin release
antiplatelets
clopidogrel (Plavix) and aspirin
thrombolytic
alteplase (Activase)
Anticonvulsant
phenytoin (Dilantin) - for tonic/clonic seizures
levetriacetam (Keppra) - partial seizures
anti epileptic
carbamazepine (Tegretol) Valpoirc acid (Depekote)
nitrates
nitroglycerin
cardiac glycoside
digoxin
anticoagulants
Heparin
Enoxaparin (Lovenox)
Warfarin (Coumadin)
Beta Blockers
metoprolol (Lopressor)
Carvedilol (Coreg)
Calcium Channel Blockers
Diltiazem
Amlodipine (Norvasc)
ACEs
Lisinopril
Enalopril (Vasotec)
ARBS
Losartan (Cozzar)
