Glossary of Adult health and illness

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Prothrombin time
Measures time to form clot after thromboplastin and Ca are added. Evaluates extrinsic path (Activation of factor x)
Normal: 11-16 seconds or 100%
Anterior cord syndrome
Caused by disruption of blood flow in spinal artery from acute compression from flexion. Mixed loss of motor and sensory function.
Central cord syndrome
Most often in C-spine, caused by hyperextension resulting in hemorrhage into the center of the cord. Upper extremities are effected more than lower because of central cord is effected more.
Barbituates and tranquilizers used preoperatively
Valium (Diazapam)
Opiates used to reduce amount of anesthesia
Demerol (Meperidine)
Anticholinergics used to reduce secretions
normal values
Percent RBC mass
Men 40-54
Women 37-47
Normal values
Blood protein used as index of O2 carrying capacity.
Men 13.6-17.2 g/dl
Women 12-15 g/dl
Pregnancy 10-15 g/dl
Activated partial thromboblastin time
Indicates effectiveness of anticoagulation therapy,
screens for bleeding tendencies
Identifies deficiencies in intrinsic and final pathways.
normal: <35 seconds
emergency: > 70 seconds
Midazolam (Versed)
Induce amd maintain anesthesia, consious sedation and sedation for procedures
Potentiates opioids.
1. Volitile liquid muscle relaxation
low incidence of NV. Bronchodilation. Given with O2.
Enflurane (Ethrane)
1. Volitile liquid muscle relaxation
low incidence of NV.
unpredictable duration of action.
Isoflurane (Forane)
1. Volitile liquid muscle relaxation
low incidence of NV. Less cardiac depression, less toxic.
Nitrous oxide
1. Advantages,
2. disadvantages and
3. interventions
1. Potentiates volatile agents, increases rate of induction. Insoluble in blood or fat.
2. Weak anesthetic. Must be used with O2 to prevent hypoxia
3. Nontoxic, so monitor for effect of volatile liquids
Propofol (Diprivan)
Sedative, hypnotic. Rapid onset and elimination. May be used for maintenance or induction of anesthesia
Spinal shock
Loss of spinal reflexes, bradycardia due to hypoxia, hypothermia and vagal stimulation. The skin is warm and dry. Hypotension results from vasodilation.
Diazapam (Valium)
1. Uses
2. Adverse effects
3. Interventions
1. Induce and maintain anesthesia, concious sedation or sedation for procedures
2. Potentiates opioids increasing respiratory depression, hypotension and tachycardia
3. Monitor LOC, cardiopulmonary status.
Fentanyl (Sublimaze)
Induce and maintain anesthesia, reduce sensory nerve impulses, and analgesia during recovery
AE: vomiting
Meperidine (Demerol)
Opioid. Induce and maintain anesthesia, reduce sensory nerve impulses, and analgesia during recovery
Inapsine (Droperidol)
Used with levodopa to treat parkinsonism.
Sinemet is the brand name for the two combined.
Benztropine (Cogentin)
Class: Anticholinergic
Treatment of Parkinson’s
Use: Antispasmodic
Brown-sequard syndrome
Damage to half of the cord. Loss of motor function, position and vibratory sense on same side as lesion. Pain and temperature sensation lost on the opposite side.
Thiopental (Pentothol)
1. Rapid induction anesthesia. ultra short acting
Not analgesic. Reduces cerebral blood flow.
Autonomic dysreflexia
(uninhibited sympathetic response to a noxious stimulus)
Epidural hematoma
Bleeding between the skull and the dura from injury to the middle meningeal artery in the temporal area. Often manifests as a loss of consciousness followed by recovery then rapid deterioration of neural status. This is an extreme emergency because it is an arterial bleed and will require decompression
Subdural hematoma
May be venous. It will bleed slowly and pressure will stop the bleed. It is sometimes called the “great imitator” because it mimics a CVA. It can be chronic, bleeding over 1-2 weeks and ICP increases and symptoms develop. High mortality.
Intracerebral hematoma
One of the causes for stroke from ruptured vessels. It is more common in elderly. Symptoms could be masked by LOC, coma or mental confusion. There is a high mortality rate.
Monroe-Kellie theory:
The cranial vault has blood, brain tissue and CSF. When one increases, the others decrease. As pressure increases CSF and venous compression causes inadequate perfusion. This creates a vicious cycle. CO2, PO2 increases, Ph decreases; this causes vasodilation and cerebral edema, increasing ICP.
Cushing’s reflex:
Opposite of shock, increased BP, decreased heart rate. Respirations may be slow or apnic. These symptoms are grave
Multiple sclerosis
Multiple areas of demyelination causing loss of impulse transmission. Management:
Adrenocorticotropic hormone, corticosteroids are used to treat exacerbations.
Parkinson's disease
Progressive dopamine depletion from degeneration of dopamine producing neurons. This disrupts the balance between dopamine and Ach in the basal ganglia. Dopamine normally inhibits Ach. With less dopamine, Ach is released which increases excitatory muscle actions.
Myasthenia gravis
It is caused by autoimmune process where antibodies attack Ach receptors. Nerve impulses fail at the neuromuscular junction.
Amyotrophic lateral sclerosis (Lou Gehrig’s) (ALS)
Myelin sheaths are destroyed on lateral tracts of the spinal cord. Nerve impulses are distorted and blocked.
Huntington’s chorea
Loss of cells in the basal ganglia possibly due to loss of Ach. There are involuntary movements, intellectual decline, tics, grimaces
Muscular dystrophies
Muscle wasting, in shoulders, hips arms and eventually hands. Speech problems, GI and eye motor problems
Alzheimer’s disease
Neurofibrillary tangles, neuritic plaques, and abnormal proteins in areas of cell loss in the brain. Neurotransmitter changes.
EKG Paper
Small square
Large square
Small square = .04 SECONDS
Large square = .2 SECONDS
Premature atrial contractions:
Early P wave with normal QRS.
Irregular rate.
Causes: Caffeine, stress, ischemia, nicotine With ischemia, could indicate atherosclerosis.
Atrial flutter
Recurring regular saw tooth pattern with 250-350 BPM.
TX: Cardioversion, medications
Atrial fibrillation:
Rapid irregular P waves over 350.
Cause: Mitral stenosis, rheumatic heart disease, hypertension.
Tx: Digitalis, quinidine, cardioversion
Atrial tachycardia
A normal sinus rhythm with a fast rate.
Caused by SNS stimulation, caffeine, nicotine
S/S: Palpations, anxiety.
TX: Usually none, but may use vagal stimulation, carotid sinus pressure.
Premature ventricular contraction:
Shows an early, wide QRS complex. When frequent, couplets, can be precursors to life threatening arrhythmias.
Caused by stress, acidosis, electrolyte imbalances, MI, digitalis toxicity.
TX: Lidocaine, quinidine
Ventricular tachycardia
No P wave, PVC like in succession, like QRS continuing at rate of over 100. Will progress into V. fib.
Cause: Drug toxicity, electrolyte imbalance, ischemia, hypoxia…
Creatinine Kinase (Creatinine phosphokinase CK, CPK)
A blood test of the cardiovascular system. An enzyme which is released into the blood when the heart muscle is damaged.
An isoenzyme to cardiac muscle. Levels increase 3-6 hours after MI. It peaks in 12-24 hours and returns to normal in 24-48 hours.
Vein segments are taken from the saphenous vein and used to replace the coronary artery.
They are controversial because the money could be better spent on prevention.
Inter aortic balloon pump.
A balloon is inserted into the aorta that provides extra blood flow into the coronary arteries.
It inflates in diastole and deflates in systole.
Pulmonary artery line
A catheter in the pulmonary artery to measure left and right heart function.
Tests for muscle damage.
Interfering factors: IM injections, exercise and surgery.
Specific marker for damaged myocardial cells, (3-6 hours)
Interfering factors: IM injections, exercise and surgery.
An abnormal protein that appears in the blood with acute inflammation. Used to follow therapeutic response to medications.
Requires fasting
An enzyme in the heart and liver. Concentrations increase with cellular damage. Associated with acute MI, angina. It isn’t a single indicator for MI since it is associated with other drugs.
Interfering factors: exercise, medications.
Released with small amounts of cardiac injury. It identifies severity of injury allowing for correct intervention
Stable angina
Ischemia provoked by exertion, short lasting and relieved by rest or nitro.
Unstable angina:
Rupture of plaque exposing thrombogenic surface. New onset, increasing in frequency and duration, and can occur at rest.
Silent ischemia:
Ischemia without pain. Associated with Diabetes mellitus and hypertension.
Prinzmetal’s angina:
Coronary vasospasm, often occurring at rest, triggered by smoking. Associated with Raynaud’s, migraine history and with or without CAD. The pain may occur during REM sleep. The pain may be relieved by some form of exercise. May be cyclic.
Nocturnal angina:
Angina occurring at night, but not necessarily when laying down.
Papillary muscle dysfunction:
Causes mitral valve regurgitation, increasing the volume of blood in the left atrium. It is detected by a systolic murmur.
Ventricular aneurism:
The infracted wall bulges out on contraction. The individual may experience CHF, angina, arrhythmias. They harbor thrombi.
Two to three days after an MI. A common complication. Chest pain on inspiration, coughing and movement may be relieved by sitting forward. Assessment may reveal a friction rub.
Dressler syndrome:
Post MI pericarditis developing 1 to 4 weeks after MI.
It may be an antigen, antibody reaction to the necrotic tissue.
S/S:Pericardial pain, friction rub, left pleural effusion, arthralgia and elevated WBC.
SCD sudden cardiac death
Disruption in cardiac function producing loss of cerebral function. The most common cause is coronary artery disease.
Heart muscle disease
Effects structure or function
Primary is where the etiology is unknown. The muscle is the only part involved.
Dilated cardiomyopathy:
Cardiomegaly and ventricular dilation,
Atrial enlargement and stasis of blood in the left ventricle.
The walls do not hypertrophy.
Hypertrophic cardiomyopathy:
Asymmetric cardiomegaly without dilation. Often genetic. More common in men. The septum becomes enlarged and obstructs blood flow.
Causes sudden death in healthy people
Restrictive cardiomyopathy:
impairs diastolic filling and stretch. Systolic function remains unaffected.
The QRS interval is:
0.04- .12 seconds.
1.5 small squares.
The P-R interval is :
0.12 – 0.2 seconds.
One large square.
CABG complications:
Pericarditis symptoms, tamponade, effusion
MOA: Increases coronary blood flow Decreases preload. Reduces myocardial O2 consumption.
Adverse effects: Dizziness, headache, hypotension, tachycardia.
Propranalol (Inderal)
Classification: Beta blocker (non-selective), Antianginal, antiarrhythmic, antihypertensive.
Nursing actions: Take apical pulse before administering. If less than 50, or arrhythmia occurs, hold and notify physician.
Calcium channel blocker, Antianginal, antiarrhythmic, antihypertensive.
Decreases SA and AV conduction and prolongs AV node refractory period. Used in management of hypertension.
Inotropic, beta-adrenergic
Effect: Increases cardiac output, BP and improves renal blood flow.
MOA: Dose dependant, stimulates dopaminergic and beta 1 adrenergic receptors producing cardiac stimulation and renal vasodilation.
Nitroprusside (Nipride)
Vasodilator, antihypertensive
Effect: Rapid lowering of blood pressure. Decreases preload and afterload.
MOA: Produces peripheral vasodilation by acting on smooth muscle.
Digoxin (lanoxin)
positive inotropic, antiarrhythmic
Effect: Increases cardiac output.
MOA: Increases the force of myocardial contraction. Prolongs refractory period Therapeutic serum levels range from 0.5-2 ng/ml.
Enalapril (Vasotec)
Angiotensin converting enzyme inhibitor, ACE inhibitor, antihypertensive
Effect: Systemic vasodilation. Lowers BP. Decreases afterload in CHF
Effect: Controls ventricle arrhythmias. Suppresses automaticity and spontaneous depolarization of the ventricles during diastole.
Classification: Thrombolytic, plasminogen activator
Effect: Lysis of thrombi
MOA: Converts plasminogen to plasmin which degrades fibrin in clots
It stimulates the production of RBC’s in bone marrow. Deficiency leads to anemia.
Vitamin D .
Requires two steps to become activated. One in the liver, and the second in the kidneys. Active vitamin D is essential for the absorption of calcium from the GI tract. A dysfunctioning kidney leads to malabsorption of calcium.
A mineralocorticoid secreted by the adrenal cortex. It increases sodium reabsorption in the kidney resulting in a regulation of blood volume, blood pressure, K, Cl, Bicarb, pH.
Urge incontinence
Involuntary urination is preceded by short warning. It occurs from overactive or uncontrolled detrusor muscle. Central inhibition is not functional? May be from CNS disturbance, bladder disorder or obstruction.
Overflow incontinence
Pressure in bladder overcomes sphincter control. Bladder distended and palpable. Cause may be from obstruction, or under active detrusor or neurogenic bladder
Reflex incontinence
Condition with no warning or stress. Urination is frequent and moderate. Cause may be spinal cord lesion above S2.
Complications of dialysis
Hypotension, muscle cramps, loss of blood, hepatitis, sepsis or disequilibrium syndrome.

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