Focus review for Term 2 Final Flashcards
(88 cards)
Cell Mediated (delayed) Immunity
- A delayed immune response to injury or infection that does not involve antibodies.
- It involves the activation of phagocytes, T-lymphocytes, and the release of substancesthat enhance the immune response and influence the destruction of antigens.
- T cells include helper cells, supressor cells, and killer cells.
- Helper T cells enhance humoral immunity
- Suppresor T cells help to “turn off” the humoral response.
- Disease may occur when the normal ratio of helper to supressor cells (2:1) is altered.
- In AIDS, for instance, the number of helper T cellsis diminished.
- When the number of suppressor T cells is too high, infections, allergy, or immune disease develop.
- Killer T cells directly destroy antigens.
- Cellular immunity fights most viral or bacterial infections and hinders the growth of malignant cells.: This process also launches an attack on transplanted tissue or organs in the body.
Respiratory Acidosis
- respiratory acidosis occurs when the respiratory system fails to eliminate the appropiate amount of carbon dioxide to maintain the normal acid base balance.
- Carbon dioxide retained, with resultant accumulation of carbonic acid and a decrease in blood PH
- The body responds to respiratory acidosis by stimulating respirations to eliminate excess carbon dioxide.
- If that mechanism cannot restore balance , renal compensation begins.
- The kidneys attempt to help by reabsorbing more bicarbonate to balance the amount of carbonic acid in the blood.
Causesa of Acute Respiratory Acidosis
- Caused by respiratory disease such as, pneumonia, drug overdose, head injury, chest wall injury, obesity, asphyxiation, drowning, or acute respiratory failure.
- People with chronic pulmonary disease may have elecated carbon dioxide levels but a normal PH as a result of renal conpensation.
- Common clinical S/S: rapid HR, headache, sweating, lethargy and confusion.
Arterial blood Gas Values with uncompensated rspiratory and metabolic acidosis and alkalosis
see attached
Opioid Analgesics
- generaly used for moderate to severe acute pain, cancer pain, and some other types of pain.
- they vary in ptency and duration of action.
- Opioid agonists: Codeine, methadone (Dolophine), hydromorphone (Diludid), meperidine (Demerol), morphine and fentanyl.
- Opioid agonist-antagonists: buprenorphine ( Buprenex), nalbuphine, butorphanol, and pentazocine (Talwin).
- Both types relieve pain at the level of the CNS.
- Older ppl more sensitive due to delayed excetion and slower metabolism.
- Dose should be reduced 25% to 50% initially and titrated.
- Oral dosage should be larger then parenteral as it needs to pass the liver after absorption reducing the dose.
Agonist Drugs
- Agonist drugs fit into receptor sites on the cell to “turn on” the site and produce the drug effect.
- Opioid agonist bind to opioid receptors to produce analgesia but also bind to other receptors to produce unwanted side effects such as: Decreased respirations, drowsiness, and nausea.
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agonist-Antagonist Drugs
- Opioid agonist-antagonist are drugs designed to produce analgesia and block certain side effects.
- They block side effects in the same manner naxolone the effects of pure opioids.
- Drugs classified as as agonist antagonists are: pentazocine, nalbulphine, buprennorphine
- they can produce pain relieve but also block the effects of opioids such as morphine or meperidine.
- A patient receiving pure opioid agonist for pain should not be given opioid agonist antagonist because they may block analgesia, precipitate withdrawl symptoms, and increase pain.
agonist Drugs
Are drugs that block side effects at the receptor sites.
Demerol
- Demerol or Meperidine use for moderate to severe pain has declined.
- Mepedirine may cause CNS toxicity.
- normepedirine a CNS stimulant, when accumulated in the body pt exhibits: Anxiety, twitching, tremors, muscle jerking, and generalized seizures.
When an ipioid is prescribed
- frank discussion w/ PT about realistic goal for pain relief.
- plan for monotoring opioid and illicit drug use.
- plan to reduce and time frame for discontinuation.
- no more than 3-7 days for acute pain.
Side effects of opioids
- Consatipation
- Nausea
- Vomiting
- Sedation
- Respiratory depression
- Confusion
- Hypotension
- Dizziness
- Itchyness
- Urinary retention
Sedation Scale
S Sleeping but easy to arouse when called or stimulated.
- Awake and Alert.
- Slightly drowsy but easily aroused.
- Frequently drowsy, arousable but drifts off to sleep during conversation- alert the RN
- Somnolent, minimal or no response to physical stimulation- Emergency
Stages of shock
Pre Shock
- Compensatory mechanisms respond to decreased delivery of oxygen, inadequate extraction of oxygen or both, depending on the type of shock.
- Physiological responses such as tachycardia and peripheral; vasoconstriction may maintain anormal BP.
- mild to moderate elevations in lactic acid levels, tachycardia, and slight increases or decreases in BP may be the only clinical sign detectable.
- with prompt intervention, progressive deterioration may be prevented.
Stages of Shock
Shock
- S/S of organ dysfunction become apparent as compensatory mechanisms become overwhelmed.
- Neural, endocrine and chemical compensatory mechanisms are activated in effort to overcome the conswquences of anaerobic metabolism and maintain blood flow to vital organs.
- activation of baroreceptors in the carotid arteries and the aorta stimulates the sympathetic nervous system.
- sympathetic stimulation causes increased HR, constriction of peripheral blood vessels and reduced blood flow to the kidneys, lungs, muscles, skin, and GI tract.
- decreasing renal blood flow triggers the release of renin and a sequence of events that that produce angiotensin II, a potents vasoconstrictor.
- the adrenal cortex secretes aldosterone, which promotes sodium reention by the kidneys.
- antidiuretic hormone is released by the posterior pituitary, resulting in addiotional retention of water by the kidneys.
- falling blood PH and increasing arterial carbon dioxide are detected by chemoreceptorsin the carotid arteriesthat stimulate the respiratory center. increasing RR and depth to help eliminate excess carbon dioxide and normalize blood PH.
Assessment Findings in shock stage
- Mental status: anxiety, restlessness
- BP: possibly normal initially, decreasing BP later
- Pulse: slight increase progressing to tachycardia: decreasing rate (bradycardia) that may be present in neurogenic shock as a result of sympathetic stimulation.
- Respirations: Increased rate and depth
- Urine output: decreased to less than 0.5 to 1.0 mL/kg/h
- Skin: cool and pale; exceptiom: warm and dry with septic shock.
- Abdomen: decreased bowel sounds; decreased perfussion and ischemic injury can result in movement of bacteria from the intestine to the circulation with subsequent development of sepsis.
- Blood glucose: Increased
- other: thirst
Stages of shock
End organ dysfunction
- If the cause shock is not corrected or if compensatory mechanisms continue without reversing the shock, irreversible organ damage, multiple organ failure, and death ensue.
- Even though the neural, endocrine, and chemical compensatory functioned together in the earlier stages, they now begin to function independently and in opposition.
- In this decompensated stage of shock, the systemic circulation continues to constrict in the attempt to maintain blood flow to vital organs.
- The decrease of peripheral blood flow, however, leads to weak or absent pulses and ischemia of the extremities.
- As intravascular blood volume decreases, the blood becomes increasingly vicious causing clumping of red blood cells, platelets, and proteins.
- Deprived of adequate oxygen, cells resort to anaerobic metabolism, which produces lactic acid and results in metabolic acidosis, which has a depressant effects on myocardial cells.
Typical assessment findings of end stage shock
- Mental status: listlessness, confusion, loss of consciousness.
- Blood pressure: hypotension
- Pulse:: weak and thready, tachycardia, dysrhythmias.
- Respirations: increased, deep, crackles on auscultation.
- Temperature: increased or sub normal.
- Your an output: decreased, renal failure.
- Skin: cold, pale, clammy, slow capillary refill, cyanosis.
- Other: dry mouth, thirst, sluggish pupillary response, peripheral edema, muscle weakness.
Pneumonia and atelectasis in post sx
- Drug affect and immobility place the surgical patient at risk for pneumonia and atelectasis.
- Patients who are most prone to these complications are older adults, the obese, those with chronic pulmonary disease, and those who have undergone chest or abdominal surgery.
- General anesthetics and opioid analgesic depressed respiratory function.
- Anti-cholinergics cause pulmonary secretions to be drier and thicker than normal.
- Immobility limits lung expansion and allows fluid to pull in the lungs.
- Fluid provides a medium for infectious organisms to grow.
- An infection of the lungs associated with immobility is called hypostatic pneumonia.
- As a fluid accumulate, they begin to block off branches of the respiratory tree.
- When gas is Cano longer enter or leave the effect of the alveoli, they collapse.
- Atelectasis is a term used to describe collapsed Alvioli, which may affect a portion or an entire lobe of the long.
Post op gastrointestinal disturbances
- The primary G.I. problems that follow surgery or nausea, vomiting, impaired peristalsis, and constipation.
- Nausea and vomiting are most common in the early post up period.
- Causative factors include anesthesia, pain, opioids, decrease peristalsis, and resuming oral intake to soon.
- Factors that cost peristalsis to be impaired after surgery include: anesthesia, immobility, opioid analgesics, and handling of the bell during surgery.
- Patients who develop metabolic and balances, respiratory problems, or shock are also at risk for G.I. disturbances.
- Gas pains typically occur on the second or third postoperative day.
- If peristalsis stops completely, the patient said to have a paralytic ileus.
- The patient with paralytic ileus has abdominal distention that may be severe enough to impaired lung expansion and decreased blood return from the legs, causing cardiac output to fall. Distention also causes strain on an abdominal incision.
Inadequate oxygenation
post op
- Document the patient’s respiratory status every hour for the first 24 hours and once or twice per shift after that.
- The most important nursing measures to prevent pneumonia and atelectasis are frequent position changes and coughing and deep breathing exercises.
- Deep breathing inflates the lungs completely and coughing remove secretions.
- The incentive spirometer is a device used to promote lung expansion.
- It consist of a tube through which the air is inhaled and a cylinder containing a ball rises in the cylinder as a patient inales through the tube.
- The more air that is taken in, the higher the ball moves.
- Reasons why coughing is contra indicated are surgeries for hernias and cataracts as well as brain surgery.
Cerebral angiography and digital subtraction angiography
- cerebral angiography provides images of the cerebral, carotid, and vertebral blood vessels.
- A catheter is inserted into an artery usually femoral and advanced to the carotid or vertebral arteries.
- A contrast dye is injected, and a series of radiographs are taken.
- Angiography is the most definite diagnostic test and the diagnosis of cerebral aneurysms or congenital vascular disorders, such as arterial venous malformation.
- Risk: severe allergy to contrast media, embolus, hematoma, hemorrhage, renal toxicity, transit ice cream at attack, infection, and loss of consciousness.
- Digital subtraction angiography DSA: is a complementary, computer assisted radiographic procedure for visualization of cerebral vessels.
Calcium channel blockers
- nimodipine-Nimotop
- Prevents spasms and cerebral blood vessels after a hemorrhagic stroke.
- Side effects: headache, fatigue, depression, confusion, dysrhythmias, hypertension, MI, renal failure.
- Nursing interventions: monitor pulse and blood pressure, assess for edema, monitor urine output, count pulse before each dose; withhold if less than 60 bpm.
other medication is used for CVA
- Osmotic diuretics such as mannitol and hyperventilation or sometimes used.
- phenytoin-Dilantin and phenobarbital are anticonvulsants that may be ordered if the patient has seizures.
- The efficacy and safety of heparin and heparinoid drugs have been challenged and are no longer routinely used as the first line treatment with a TIA or an acute ischemic stroke unless a cardioembolic stroke is suspected.
- Small doses of this medication subcutaneously or recommended and the prevention of DVT associated with acute stroke.
- Heparin may be given via IV followed by oral to warfarin.
- Later the regimen may be changed to aspirin, which decreases the risk of thrombus by preventing platelets from clumping.
- Newer drugs such as dabigatran (pradaxa) or rivaroxaban (XARELTO) may also be considered for long-term anticoagulation instead of warfarin.
- Drugs given to prevent strokes caused by thrombi are acetylsalicylic acid (aspirin), clopidogrel (pplavix) and extended release dipyridamole (agrennox)
RT - PA
- It is important to remember that recombinant tissue plasminogen activator, which is used to dissolve clots, is most effective when given within three hours of the onset of stroke symptoms.