NSG 205

• 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.

• 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.

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]

 

• 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.

• 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).

• 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]

• 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.

 

 

• the mnemonic MONA
• in the treatment of a patient with an MI, this stands for Morphine, Oxygen,
• Nitrates and Aspirin.

• 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.

• 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.

Rapid acting







Onset:  10-20 min.


Peak:    40-50 min.


Duration:    3-5 hours

Onset:   30 min. -1 hour


Peak:    2-5 hours


Duration:    5-8 hours

Onset:   1-2 hours


Peak:    4-12 hours


Duration:    18-24 hours

Onset:   1-2½ hours


Peak:    3-10 hours


Duration:  18-24 hours

Onset:    1-1½ hour

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

Duration:   20-24 hours

• 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.

136 -145 mEq/L.

98-106 mEq/L

3.5 - 5.0 mEq/L

            9.0-10.5 mg/dL

         3.0-4.0 mg/dl

            10-20    mg/dl

            53-106   mmol/L

            5,000-10,000/mm3

Males: 14-18 g/dl

 

Females:12-16 g/dl

Males: 42%- 52%

 

Females:  37%-47%

• –Eliminate
• metabolic waste

• –Produce
• bile, albumin, and clotting factor (vit.
• K)

• }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

• }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.

• }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.

• }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

• }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

• }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

• }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?

• }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.

• }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)

• }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

• }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

• }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?

• }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.

• }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

• }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.

• }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?

• }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

• }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

• }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

• }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

• }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

• }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

Byproduct of muscle breakdown.

• ◦Elevation
• signifies muscle injury (gen)

• ◦Peak
• 4-6 hours post injury/insult

◦Bleeding

• ◦Third
• spacing

◦Ascites and r sided heart failure

• ◦Ammonia
• accumulation

◦Protein-by product is nitrogen with turns into ammonia

◦pH imbalance (acidosis), retain more hydrogen ions

• ◦Anemia
• (less erythropoietin production)

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

• ◦Elevated
• BUN/Nitrogen

◦Protein and sodium

◦Specific to cardiac and brain injury if value is elevated

Sensitive lab value.

◦Elevationsignifies cardiac muscles injury.

◦Peak 6 hours post injury

*measure the stretch of the ventricle.

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

◦Useto determine CHF  (high value)