NSG 205

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chumbis
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NSG 205
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2013-03-09 18:44:50
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NSG 205
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MEd/Surg 1
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  1. ◦Beta blockers
    • Beta blockers target the beta receptor. Beta
    • receptors are found on cells of the heart muscles, smooth muscles, airways,
    • arteries, kidneys, and other tissues that are part of the sympathetic
    • nervous system and lead to stress responses, especially when they
    • are stimulated by epinephrine
    • (adrenaline). Beta blockers interfere with the binding to the receptor of
    • epinephrine and other stress hormones, and weaken the effects of stress
    • hormones.
  2. ◦ACE inhibitors
    • ACE inhibitors block the
    • conversion of angiotensin I to angiotensin II.[4]
    • They, therefore, lower arteriolar
    • resistance and increase venous capacity; increase cardiac output, cardiac index, stroke
    • work, and volume;
    • lower renovascular resistance; and lead to increased natriuresis (excretion of sodium in the urine). Renin will
    • increase in concentration in the blood due to negative feedback of conversion
    • of AI to AII. Angiotensin I will increase for the same reason. Angiotensin II
    • and Aldosterone will decrease. Bradykinin will increase due to less
    • inactivation that is done by ACE.
  3. ◦Calcium channel blockers
    Antihypertensive medication

     

    • Relax smooth muscle of arterioles
    • and decrease peripheral vascular resistance

     

    • Calcium channel blockers
    • work by blocking voltage-gated
    • calcium channels (VGCCs) in cardiac muscle and blood vessels. This
    • decreases intracellular calcium leading to a reduction in muscle contraction. In the
    • heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility.
    • In blood vessels, a decrease in calcium results in less contraction of the vascular smooth
    • muscle and therefore an increase in arterial diameter (CCBs do not
    • work on venous smooth muscle), a phenomenon called vasodilation. Vasodilation
    • decreases total peripheral
    • resistance, while a decrease in cardiac contractility decreases cardiac output. Since
    • blood pressure is determined by cardiac output and peripheral resistance, blood
    • pressure drops. Calcium channel blockers are especially effective against large
    • vessel stiffness, one of the common causes of elevated systolic blood pressure
    • in elderly patients.[2]

     
  4. ◦Angiotensin II blocker
    • These substances are AT1-receptor
    • antagonists – that is, they block the activation of angiotensin II
    • AT1 receptors. Blockage of AT1
    • receptors directly causes vasodilation,
    • reduces secretion of vasopressin,
    • and reduces production and secretion of aldosterone, amongst other
    • actions. The combined effect reduces blood pressure.

    • The specific efficacy of
    • each ARB within this class depends upon a combination of three pharmacodynamic and pharmacokinetic
    • parameters. Efficacy requires three key PD/ PK areas at an effective level; the
    • parameters of the three characteristics will need to be compiled into a table
    • similar to one below, eliminating duplications and arriving at consensus
    • values; the latter are at variance now.
  5. ◦Cholesterol lower agents
    • Statins act by competitively
    • inhibiting HMG-CoA
    • reductase, the first committed enzyme of the HMG-CoA
    • reductase pathway. Because statins are similar to HMG-CoA on a
    • molecular level, they take the place of HMG-CoA in the enzyme and reduce the
    • rate by which it is able to produce mevalonate, the next
    • molecule in the cascade that
    • eventually produces cholesterol, as well as a number of other
    • compounds. This ultimately reduces cholesterol via several mechanisms.

     

    • Drugs that inhibit HMG-CoA reductase, known
    • collectively as HMG-CoA
    • reductase inhibitors (or "statins"), are used to lower
    • serum cholesterol
    • as a means of reducing the risk for cardiovascular disease.[5]

    • These drugs include rosuvastatin (CRESTOR), lovastatin (Mevacor), atorvastatin (Lipitor), pravastatin (Pravachol), fluvastatin (Lescol), pitavastatin (Livalo), and
    • simvastatin (Zocor).
  6. ◦Aminoglycoside agents
    • Several aminoglycosides
    • function as

     

    • protein synthesis
    • inhibition of aminoglycosides

     

    • that are effective
    • against certain types of bacteria.
    • They include amikacin,
    • arbekacin, gentamicin, kanamycin, neomycin, netilmicin, paromomycin,
    • rhodostreptomycin,[2] streptomycin, tobramycin, and apramycin.[3]
  7. ◦Anti-viral
    • specific antivirals are used for specific
    • viruses

     

    • Unlike most antibiotics,
    • antiviral drugs do not destroy their target pathogen; instead they inhibit
    • their development.

     

    • Antiviral drugs are one
    • class of antimicrobials,
    • a larger group which also includes antibiotic (also termed
    • antibacterial), antifungal
    • and antiparasitic
    • drugs. They are relatively harmless to the host, and therefore can be used to treat infections. They should be
    • distinguished from viricides,
    • which are not medication but deactivate or destroy virus particles, either
    • inside or outside the body.

     

     
  8. ◦MONA- B
    • the mnemonic MONA
    • in the treatment of a patient with an MI, this stands for Morphine, Oxygen,
    • Nitrates and Aspirin.
  9. ◦nitrate
    • a vasodilator to treat heart conditions, such as angina and chronic heart
    • failure.

     

    • Nitrates cause vasodilation[1] of the venous capacitance vessels by
    • stimulating the endothelium-derived
    • relaxing factor (EDRF). Used to relieve both exertional and
    • vasospastic angina by allowing venous pooling, reducing the pressure in the
    • ventricles and so reducing wall tension and oxygen requirements in the heart.
    • Short-acting nitrates are used to abort angina attacks that have occurred,
    • while longer-acting nitrates are used in the prophylactic management of the
    • condition.
  10. Steroids
    • Corticosteroids
    • include glucocorticoids
    • and mineralocorticoids.


     

    • Glucocorticoids regulate
    • many aspects of metabolism
    • and immune function,
    • whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.

     

    Most medical 'steroid' drugs are corticosteroids.

     

    • Anabolic steroids
    • are a class of steroids that interact with androgen receptors to increase
    • muscle and bone synthesis.

     

    • There are natural and
    • synthetic anabolic steroids. In popular language, the word "steroids"
    • usually refers to anabolic steroids.

     

    • Cholesterol,
    • which modulates the fluidity of cell membranes and is the
    • principal constituent of the plaques implicated in atherosclerosis.
  11. Novolog
    Rapid acting







    Onset:  10-20 min.


    Peak:    40-50 min.


    Duration:    3-5 hours
  12. Regular (R) humulin or
    novolin
    Onset:   30 min. -1 hour


    Peak:    2-5 hours


    Duration:    5-8 hours
  13. NPH
    Onset:   1-2 hours


    Peak:    4-12 hours


    Duration:    18-24 hours
  14. Lente
    Onset:   1-2½ hours


    Peak:    3-10 hours


    Duration:  18-24 hours
  15. Lantus
    Onset:    1-1½ hour


    • No peak time; insulin is delivered at a steady
    • level


    Duration:   20-24 hours
  16. ◦anticoagulant (blood thinners):
    • Inhibits the vitamin K-dependent
    • synthesis of biologically active forms of the calcium-dependent clotting factors II, VII, IX and X, as well as the
    • regulatory factors protein C,
    • protein S, and protein Z.

     

    • The precursors of these
    • factors require carboxylation
    • of their glutamic acid
    • residues to allow the coagulation factors to bind to phospholipid surfaces
    • inside blood vessels, on the vascular endothelium.
  17. Sodium
    136 -145 mEq/L.
  18. Chloride
    98-106 mEq/L
  19. Potassium
    3.5 - 5.0 mEq/L
  20. Calcium
                9.0-10.5 mg/dL
  21. Phosphate
             3.0-4.0 mg/dl
  22. Blood urea
    nitrogen (BUN)
                10-20    mg/dl
  23. Serum creatinine
                53-106   mmol/L
  24. WBC
                5,000-10,000/mm3
  25. HGB (Hemoglobin)
    Males: 14-18 g/dl

     

    Females:12-16 g/dl
  26. HCT (Hemotocrit)
    Males: 42%- 52%

     

    Females:  37%-47%
  27. Liver
    • –Eliminate
    • metabolic waste

    • –Produce
    • bile, albumin, and clotting factor (vit.
    • K)
  28. Beta Blocker
    • }Medication
    • ending with ALOL or LOL

    • }Mechanism
    • of action:  Selective beta
    • 1-adrenergic blockers but occasional blocks beta 2.

    • ◦You
    • got one heart (beta 1) and two lungs (beta 2)

    • }Block
    • sympathetic nervous systems to heart and lungs

    • ◦How
    • does SNS affect heart and lungs at a cellular level?

    • }Common
    • side effects: bradycardia, hypotension, and
    • congestive heart failure(if HR too low), and brochospasm.

    • }Assessment
    • prior to giving medication

    • ◦BP
    • must be >100 or per MD

    • ◦HR
    • must be >60 or per MD

    • Assess
    • breath sound for wheezing
  29. ACE inhibitors
    • }Any
    • medication ending with pril



    • }S/E:  chronic cough, angioedema,(do
    • not know why) and hypotension.

    • }Not
    • drug of choice for black patient (not effective)

    • }Assessment:  monitor BP and assess for s/s
    • of chronic cough or angioedema (can happen at any
    • time).

    • ◦Example of patient
    • with angioedema.

    • ◦What type of patients
    • or demographic that this medication is not effective and why?







    • }Mechanism
    • of action: angiotension converting enzyme
    • inhibitors.

    • ◦Normal: Your liver
    • produces angiotensin I (mild
    • vasoconstrictor) with the present of renin angiotensin
    • it converts to angiotensin II (potent
    • vasoconstrictor) to increase blood pressure.  This medication blocks the above effects.

    • ◦  Thinking:  If your blood vessels are not vaso-constrict,
    • it must vasodilate.
  30. Angiotensin II
    blockers
    • }Any
    • medication ending with “SARTAN”


    • }MOA:
    • blocks angiotensin II, which is a vaso-constrictor.

    • }Side
    • effects: hypotension, dizziness, and syncope.

    • }Target
    • population: very effective for black people.
  31. Calcium channel
    blockers
    • }Calcium channel blockers are very nice
    • drugs

    • }Medications
    • ending in pine and the following:

    ◦Verapamil


    ◦Nifedipine


    ◦Diltiazem/cardizem


    • }MOA:
    • blocks calcium from going into cardiac muscle and causing vaso-dilation.

    • ◦Critical
    • thinking:  Calcium aide with muscle
    • contraction.

    • Less calcium =less contraction

    • ◦For
    • every contraction = heart beat

    • }Side
    • Effects:  Bradycardia,
    • hypotension, and heart failure

    • }What
    • to avoid when taking calcium channel blockers?

    • ◦Grapefruit
    • (enhanced drug absorption)

    • ◦What
    • would you use to reverse the affects of Calcium channel blockers OD?

    • –Calcium
    • Chloride/Calcium gluconate
  32. Calcium channel
    blockers
    • }Calcium channel blockers are very nice
    • drugs

    • }Medications
    • ending in pine and the following:

    ◦Verapamil


    ◦Nifedipine


    ◦Diltiazem/cardizem


    • }MOA:
    • blocks calcium from going into cardiac muscle and causing vaso-dilation.

    • ◦Critical
    • thinking:  Calcium aide with muscle
    • contraction.

    • Less calcium =less contraction

    • ◦For
    • every contraction = heart beat

    • }Side
    • Effects:  Bradycardia,
    • hypotension, and heart failure

    • }What
    • to avoid when taking calcium channel blockers?

    • ◦Grapefruit
    • (enhanced drug absorption)

    • ◦What
    • would you use to reverse the affects of Calcium channel blockers OD?

    • –Calcium
    • Chloride/Calcium gluconate
  33. Cholesterol lowering (statin)
    • }Any
    • medication ending with statin
    • except nystatin.

    • }MOA:  acts by inhibiting fat absorption and
    • inhibit cholesterol production in the liver.

    • }Critical
    • thinking:  If your body does not
    • have enough fat and cholesterol, what would your body do?

    • ◦What
    • should you avoid with the use of this medication?

    –grapefruit

    • ◦Break
    • down muscle which causes rhabomylosis.

    • ◦If
    • your body does not absorbed fat from food consumed, what would you see?

    • –
    • (fatty stool or floaters).

    • }Side
    • effects:  Flatulence, abdominal
    • discomfort, stetorrhea, muscle weakness (rhabdomyolosis).

    • }What
    • kind of complications would you get from Rhabdomyolosis?

    • ◦ARF
    • due to excess waste and caused nephrons irritation and nephrons
    • death.

    • ◦What
    • are the treatments and why?

    • –Fluid
    • and lasix
  34. Aminoglycoside (myocin)
    • }Any
    • medication ending in myocin


    • ◦Gentamyocin, vacomyocin,
    • or amikacin


    • }MOA:
    • inhibit aminoglycoside and inhibit DNA of
    • the organism.

    • }Side
    • effect:  secondary infections, nephrotoxic,
    • and ototoxic


    • }Critical
    • thinking

    ◦Assess renal fx?

    ◦How do you assess ototoxic?
  35. Anti-viral (Vir)
    • }Any
    • medication ending in Vir is an anti-viral.

    • }MOA-
    • inhibit cell wall synthesis and caused cell death.

    • }Side
    • effects: secondary infection, nausea, vomiting, and diarrhea.

    • }Why
    • these type of side effects and what can you do to prevent the severity.
  36. Treatment for
    angina-MONA-B
    • }Treatments
    • in order:

    ◦O-oxygen

    –Rationale?

    • ◦A-Asprin-anticoagulant.
    • It works by preventing platelet aggregation.

    • –Common
    • S/E: bleeding (GI etc), bruising, and tinnitus

    • ◦N-nitroglycerin-
    • nitrate

    • –Acts
    • by systemic vasodilatation and improve coronary perfusion

    • –Use
    • to decrease workload (decrease preload and after load)

    • –SE:
    • hypotension, headache (why?), and dizziness.

    • ◦Morphine:
    • opiate agonist

    • –Acts
    • by blocking opiate receptors in the brain to alter pain perception and it also
    • has vasodilatation property.

    • –S/E-
    • hypotension,  (CNS depressant)
    • lethargy, respiratory depression, and constipation

    • ◦Beta-blocker-beta
    • adrenergic block. 

    • –Use
    • to decrease workload by decreasing the BP and heart rate.

    • –This
    • medication also improve survival of patient with angina

    –


    • ◦ACE-inhibitors
    • will be added later to prevent cardiac tissue re-engineering (scar formation
    • and prevent CHF)
  37. nitrate
    • }Medication
    • ending in nitrate

    ◦Example: isosorbide dinitrate


    • }Classification:
    • systemic vasodilator

    • }MOA-
    • dilate coronary artery and blood vessels.

    • ◦Decreases preload and
    • afterload


    • }Side
    • effects:  headache (why),
    • hypotension, dizziness, syncope
  38. anticoagulant
    • }Lovenox:
    • low molecular heparin.

    • ◦MOA:
    • inhibits the conversion of prothrombin
    • to thrombin and fibrinogen to fibrin.

    ◦S/E:  bleeding & bruising

    }Heparin

    • ◦MOA:
    • inhibits the conversion of prothrombin
    • to thrombin and fibrinogen to fibrin

    • ◦Diagnostic
    • test: PTT (partial prothrombin time)

    • ◦Antidote:
    • protamine sulfate or hold
    • heparin for 6 hours (half life of heparin)

    • }Coumadin/warfarin
    • :

    • ◦MOA:
    • inhibit vitamin K in the clotting cascade.

    ◦S/E:  bleeding.

    • ◦Diagnostic
    • test: Protime (PT) and INR

    • ◦Antidote:
    • Vitamin K and/or FFP
  39. Cortico-steroid
    • }Any
    • medication ending with (ONE)

    • ◦Example
    • predisone or methylpredisolone

    • }MOA-cortico-steroid.  It acts by inhibiting immune response
    • and also anti-inflammatory.

    • }S/E-
    • cushing’s
    • syndrome (fluid retention, wt. gain, moon face, and striae).


    • }Critical
    • thinking

    • ◦Why
    • would your patient be hyperglycemic, hypertension, and hyponatremia?

    • ◦How
    • do you know if your patient has an infection?
  40. insulin
    • }Insulin-aide
    • in the transport of glucose into the cell.

    • }Why
    • are there so many types of insulin?

    • ◦Peak
    • and half life is different

    • ◦Goals:
    • maintain stable blood glucose and avoid peaks and valleys.

    • }MOA:
    • insulin binds to glucose and potassium (K) to form a perfect key in order to
    • transport glucose into the cell.

    • }What
    • type of side of effect would you most likely observe?

    • ◦Hypoglycemic
    • (stimulate SNS-tachycardia, irritability, confusion, agitation, and
    • diaphoresis)

    • ◦Hypokalemia
    • (arrhythmias)

    • }What
    • would you assess prior to giving insulin?

    • ◦Blood
    • glucose and mental status

    • ◦If
    • on large amount of insulin- potassium level.
  41. Electrolytes
    • }Sodium
    • (135-145)

    • }Chloride
    • ( )

    • }This
    • electrolyte is important in maintaining fluid in the intravascular and
    • intracellular.

    • ◦Sodium
    • and Chloride are more extracellular than intracellular and they are always go
    • in the same direction

    • }What
    • are significant, effects, and causes of hyponatremia?

    • ◦Signify
    • : hypervolemia (hemodilution)
    • and causes fluid shift from intravascular into intracellar
    • (all cells) because of high sodium content in the cell.

    • ◦Causes:
    • excessive water intake, SIADH (release excessive ADH) hormone-causes fluid
    • retention in the intravascular system.

    • ◦Effects:
    • cerebral edema (confusion or coma), fluid retention and edema

    • ◦Treatments
    • and rationales?

    • –Best-fluid
    • restriction (dry patient out)

    • –Give
    • salt tablets
  42. hypernatremia
    • }Na
    • level greater than (>145)

    • }What
    • are significant, effects, and causes of hypernatremia.

    • }significant:
    • cause fluid shift from intracellular to intravascular and causes cellular
    • dehydration (shrink)

    • }Causes:
    • by dehydration, excessive sodium intake or DI (diabetic insipidus)-lack
    • of ADH.

    }S/S:  confusion or seizure

    • }Treatments:
    • what would you do if your blood is too salty?

    • ◦Administer
    • hypotonic solution

    • ◦Increase
    • po (water) intake

    • ◦Give
    • ADH (decrease urine production) and absorbed more water.
  43. Potassium (K)
    • }Potassium
    • is more intracellular than extracellular

    • }Normal
    • values- 3.5-5.0

    • }What
    • are significant, effects, and causes of hypokalemia?

    }Significant?


    • ◦Aide
    • with cardiac muscle contractility. Less potassium will cause irritability of
    • the cell and causes arrhythmias.

    }Causes:

    • loss of acid and gain in base

    • ◦vomiting,
    • diarrhea, Nasogastric lavage,

    • ◦excessive
    • insulin usage.

    }Treatments:

    • ◦Potassium
    • po/iv

    • ◦Can
    • you crush potassium?

    • ◦How
    • fast can you give IV potassium?

    • ◦Diet
    • high in potassium? What is diet high in potassium?
  44. hyperkalemia
    • }What
    • are significant, effects, and causes of hyperkalemia?

    }significant?


    • ◦Caused
    • changes in electrical charge on the cell membrane and make the cell membrane
    • more irritable

    }Causes?

    • ◦A
    • gain in acid and a loss of base (Renal failure (absorb more hydrogen ion in the
    • kidney)

    • ◦Excessive
    • blood glucose (diabetic ketoacidosis)

    • ◦Excessive
    • potassium supplement intake without diuretic

    • }Treatments
    • to eliminate potassium?

    • ◦Give
    • kayexalate-bind with potassium
    • and eliminate through feces.

    • ◦Give
    • insulin with D50 (dextrose)-insulin acts by binding with glucose and potassium
    • and all three go into the cell- leaving less potassium in the blood stream.

    • ◦Give
    • sodium bicarbonate-acts by increasing blood pH.

    • –As
    • pH goes up, Potassium will come down.

    • –Watch
    • for s/s of volume overload and CHF
  45. BUN/CR
    • }Normal
    • BUN/CR

    ◦ratio is 10-15: 1

    • }Blood
    • urea nitrogen

    ◦Where BUN come from?

    • –Byproduct
    • of protein break down.

    • –Protein
    • break down into nitrogen.

    • ◦Why would the level
    • be high?

    • –Body’s
    • inability to eliminate nitrogen through nephrons


    • }Serum
    • creatinine (0.8-1.2)

    • ◦Best indicator for
    • kidney function
  46. Complete blood count
    (CBC)
    • }WBC
    • (white blood cell) range (4,000-11,00)

    • }WBC
    • <  or = 500, this is known as neutropenia


    • }Function:
    • kill organisms that you immune system considered it to be none self (foreign).

    • }What
    • else would you assess for when assessing for infection beside WBC?

    • }Mnemonic-Never
    • let monkey eats banana

    • ◦Neutrophil-elevation
    • (left shift) suggested acute bacterial infection

    • ◦Lymphocytes-
    • fight infection ( B-cells and T cells)

    • ◦Monocyte-
    • elevation suggested of viral infection or parasite infection

    • ◦Eosinophil-elevation
    • suggested of allergy

    • ◦Basophil-elevation
    • suggested of allergy
  47. neutropenia
    • }What
    • is neutropenia?

    • ◦Severe immuno
    • compromised.

    • }As
    • a nurse, what would you do different for patients with neutropenia vs
    • other patients in the hospital?

    ◦Reverse isolation

    • ◦All food must be
    • cooked well

    ◦No flowers

    ◦Avoid children
  48. Red blood cell
    • }RBC-produce
    • in the bone marrow with the aid of erythropoietin (produce in the kidney)

    • }Hemoglobin
    • (Hgb)-range  male 14-16 and female 12-14

    • }Hematocrit-normal
    • range – 3x hemoglobin

    • ◦Example Hgb
    • is 9 and Hct is 27

    • }What
    • is the significant of not maintain 1:3 ratio?

    • ◦Example : if Hgb
    • is 10 and Hct is 27

    –Hemodilution.

    • ◦Example: if Hgb
    • is 10 and Hct is 35

    –dehydration
  49. Platelets
    • }Normal
    • range 150,000-450,000

    }Functions?

    • ◦Aide
    • in clotting

    • ◦Fix
    • damage blood vessels or endothelia

    • }What
    • is the significant of having higher platelets?

    • ◦Clots
    • formation (DVT etc)

    • }What
    • is the significant of having lower platelets?

    • ◦Bruising
    • or bleeding

    • ◦Know
    • as thrombocytopenia
  50. CK-creatininekinase (Cardiac)
    Byproduct of muscle breakdown.

    • ◦Elevation
    • signifies muscle injury (gen)

    • ◦Peak
    • 4-6 hours post injury/insult
  51. What will happen to your patients if their liver  does not work?
    ◦Bleeding

    • ◦Third
    • spacing

    ◦Ascites and r sided heart failure

    • ◦Ammonia
    • accumulation
  52. What type of diet should liver failure patients avoid?
    ◦Protein-by product is nitrogen with turns into ammonia
  53. What will happen to your patients if their kidney does not work?
    ◦pH imbalance (acidosis), retain more hydrogen ions

    • ◦Anemia
    • (less erythropoietin production)

    • ◦Electrolyte
    • abnormality (hyperkalemia, hyponatremia, hyperphosphatemia, hypokalemia,
    • and hypomagnesimia)

    • ◦Elevated
    • BUN/Nitrogen
  54. What type of diet should kidney failure patients avoid?
    ◦Protein and sodium
  55. CK-MB (Cardiac)
    ◦Specific to cardiac and brain injury if value is elevated
  56. Troponin (cardiac)
    Sensitive lab value.

    ◦Elevationsignifies cardiac muscles injury.

    ◦Peak 6 hours post injury
  57. BNP (Cardiac)
    *measure the stretch of the ventricle.

    ◦The higher the values, the more stretch the ventricle is undergoing.

    ◦Useto determine CHF  (high value)

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