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RCP > PHARM final > Flashcards

PHARM final Flashcards

1
Q

Corticosteriod endogenous

A

Cortisol or Glucocorticoids regulate the metabolism of carbohydrates, fats, and proteins to increase levels of glucose for body energy!
- relives

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2
Q

Corticosteriod exogenous

A

A primary reason for using Aerosolized Glucocorticoids is to minimize adrenal, or HPA axis suppression, by minimizing the dosage and localizing the site of tx.
- inhibit

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3
Q

corticosteriods intrinsic/extrinsic

A

Body cannot distinguish between endogenous and exogenous

Administration of glucocorticoid drugs raise body’s level of hormones

Inhibits hypothalamus and pituitary glands, which decreases adrenal production

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4
Q

beclomethasone dipropinate HFA

A

Qvar redihaler

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5
Q

Flunisolide hemihydrate HFA

A

Aerospan

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6
Q

Fluticasone propinate

A
  • Flovent HFA
  • Flovent diskus
    -Armonair respicklick
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7
Q

Fluitcasone furoate

A

arnuituy ellipta

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8
Q

budenoside

A
  • pulmicort flexhaler
  • pulmicort respules
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9
Q

Mometasone furoate

A
  • asmanex twisthaler
  • asmanex HFA
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10
Q

ciclesonide

A

alvesco

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11
Q

fluticasone propinate/salmaterol

A
  • advair diskus
  • wixela inhub
  • advair HFA
  • Airduo respiclick
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12
Q

budesonide/formoterol fumarate HFA

A

symbicort

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13
Q

mometasone furoate/formoterol fumarate HFA

A

dulera

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14
Q

fluticasone furoate/vilanterol

A

breo ellipta

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15
Q

fluitcasone furoate/umeclidinium bromide/vilanterol

A

treglegy ellipta

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16
Q

mast cells

A

(a type of WBC; aka: Mastocyte or Labrocyte): Connective tissue cells that contain heparin and histamine released during inflammatory and allergic reactions. When mast cells detect a germ or virus, they set off an inflammatory (allergic) response by releasing a chemical called histamine. This response protects your body from germs and infections.

Heparin: extracted from tissues rich in mast cells remains the ideal rapid anticoagulant in clinical practice.

Histamine: makes blood vessels expand and the surrounding skin itchy and swollen.

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17
Q

eosinophils

A

They attack and kill parasites andcancer cells, and help with “allergic responses”.

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18
Q

basophils

A

These small cells seem to sound an alarm when infectious agents invade your blood. They secrete chemicals, such as histamine, a marker of allergic disease, that help control the body’s immune response.

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19
Q

t-lymphocytes

A

They create antibodies to fight against bacteria, viruses, and other potentially harmful invaders

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20
Q

neutrophils

A

They kill and digest bacteria and fungi. They are the mostnumerous type of WBC and your first line of defense when infection strikes.

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21
Q

macrophages

A

A type of white blood cell that surrounds and kills microorganisms, removes dead cells, and stimulates the action of other immune system cells

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22
Q

Diurnal steroid cycle

A

Production of body’s own glucocorticoids follows rhythmic cycle; a daily rise and fall termed diurnal or circadian rhythm

  • Cortisol levels are highest in the morning at 8 a.m.
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23
Q

Alternate-day steroid therapy

A

Mimics natural diurnal rhythm by giving steroid drug early in the morning when normal tissue levels are high

Suppression of the HPA system occurs at the same time it normally would with the body’s own steroid!

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24
Q

Inflammation

A

=the response of vascularized tissue to injury

Produces redness, swelling, heat, and pain

Triple response:

Redness: Local dilation of blood vessels, occurring in seconds

Flare: Reddish color several centimeters from the site, occurring 15 to 30 seconds after injury

Wheal: Local swelling, occurring in minutes

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25
Q

Asthma

A
  • mast cells, eosinophils, lymphocytes, macrophages, neutrophils, epithelial cells
  • inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing in night or early morning
  • HYPERRESPONSIVENSS to various stimuli
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26
Q

Asthma

A

Chronic inflammation of the Aw wall causing airflow limitation and hyperresponsiveness to various stimuli

The Mast Cells and the Eosinophils are considered the be the major effector cells of the inflammatory response, regardless of whether the asthma is allergic or non-allergic

During an Asthmatic response: Aw smooth muscle contracts (bronchospasm), increased microvascular leakage and Aw wall swelling, mucus secretion, and remodeling of the Aw wall over the long term

In an Acute phase attack: pts experience wheezing, breathlessness, chest tightness, and cough

Treatment with anti-inflammatory agents such as glucocorticoids is important to reduce basal level of Aw inflammation, Aw hyperresponsiveness and predisposition to acute episodes of obstruction

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27
Q

Asthmatic reactions are Biphasic

A

Early asthmatic response caused by Immunoglobulin E (IgE)
After an insult, IgE activates Mast Cells which release inflammatory mediators such as Histamine, the Aw’s immediate response is Bronchospasm
Response peaks at 15 minutes

Late-phase reaction caused by Mast Cell mediators and release of Cytokines
- Response occurs after ~ 6-8 hours
- Can last up to 24 hours

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28
Q

Aerosolized steriods effect (systemic)

A
  1. Adrenal insufficiency may occur after transfer from systemic to inhaled steroids – Weaning may be required to allow recovery of the Adrenal Cortex and HPA Axis function
  2. Recurrence of allergic inflammation after cessation
  3. Acute Asthma may occur after transfer from systemic to inhaled steroids
  4. HPA suppression is Minimal or Absent on small doses; Increases with High Doses (dose-dependent)
  5. Growth restriction in children (dose-dependent)
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29
Q

aerosolized steriods effect (local)

A

Most common
1. Oropharyngeal fungal infections; aka: Candidiasis (Oral “Thrush”)
2. Dysphonia (hoarseness and changes in voice quality)

Less common:
1. Cough, bronchoconstriction
2. Incorrect use of MDI (inadequate dose)

What to do:
1. Use minimal dose
2. Use reservoir
3. “Rinse mouth after use”

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30
Q

steriod use in asthma

A

Clinical use of inhaled corticosteroids in “addition to” first-line β-agonist reduces morbidity and Aw hyperresponsiveness, decreased exacerbations, and improved FEV1

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31
Q

steriod use in COPD

A

Reduces symptoms, exacerbations, and mortality
Neutrophils predominate in COPD

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32
Q

steriod effect on WBC count

A

Demargination (don’t adhere): Causes depletion of neutrophil stores reducing their accumulation at inflammatory sites and in exudates

Overall increase in WBC count

Constriction of microvasculature to reduce leakage of cells and fluids into inflammatory sites

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33
Q

steriod effect on B-receptors

A

β-adrenergic agents are the most potent inhibitor of mast cell release!

Steroids restore responsiveness to β-adrenergic stimulation

Steroid action is slow, but the sooner steroids are given, the sooner the pt begins to respond to β-adrenergic drugs!

Steroids enhance β-receptor stimulation by increasing the number and availability of β-receptors on cell surfaces and by increasing the affinity of the receptor for β-agonists

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34
Q

inflammatory response

A
  1. Increased vascular permeability:
    An exudate is formed in surrounding tissues
  2. Leukocytic infiltration:
    - White Blood Cells (WBC) emigratethrough capillary walls (diapedesis)in response to attractant chemicals (chemotaxis)
  3. Phagocytosis:
    - White cells and macrophages (in lungs) ingest and process foreign material such as bacteria
  4. Mediator cascade:
    - Histamine and chemoattractant factors are released at the injury site
    - Various inflammatory mediators are generated
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35
Q

aerosolized corticosteriods

A

“targets” inflammation in the Aw with a smaller dose “reducing systemic side effects!”

Complementary interaction between Glucocorticoids and β-adrenergic Agonists (LABAs)

Steroids increase β2-adrenergic receptor transcription

Inhaled corticosteroid therapy can provide partial protection against the development of tolerance!

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36
Q

Intranasal steriods

A

Used for treatment of allergic or inflammatory nasal conditions and seasonal or perennial allergic or nonallergic rhinitis and to prevent reoccurrence of nasal polyps

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37
Q

nonsteriol indications

A
  1. Cromolyn-like drugs (aka: “Mast Cell” Stabilizers)
  2. Antileukotrienes
  3. Monoclonal antibodies
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38
Q

B2-antagonists

A

blovcks or inhibits beta 2 receptors

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39
Q

controllers

A

= to maintain exacerbations
- inhaled corticosteriods
- oral corticosteriods
- cromolyn sodium
- LABA
- leukotriene modifiers
- sustained-release thephylline
- muonoclonal antibodies

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40
Q

relivers

A

= relieve symptoms
- SABA
- systemic corticosteriod
- inhaled anticholinergic bronchodilators

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41
Q

extrinsic asthma (allergic)

A

Depends on allergy, atopy (environment)

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42
Q

Intrinsic asthma (non-allergic)

A

Shows no evidence of sensitization to common inhaled allergens (inside)

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43
Q

mast cell stabilizers

A

cromolyn sodium

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44
Q

antileukotrienes

A
  • zarfirlukast
  • montelukast
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45
Q

Cromolyn sodium

A

= Prophylactic aerosolized agent in the treatment of Asthma to prevent inflammatory responses often used in infants and young children

Anti-Asthma agent; Anti-Allergy agent; Mast Cell Stabilizer
- Prevents (inhibition of…) “Mast Cell degranulation” blocking the release of chemical mediators of inflammation

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46
Q

Pentamidine

A

type: anti-fungal

indication: active against pneumocytsis jiroveci, the organism for pneumocytsis jiroveci pneumonia

trade name: NebuPent

form: dry powder
Reconstituted with 6 mL of sterile water (Not saline - can cause precipitation)

Respirgard II Nebulizer (1-2 um)

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47
Q

pentamidine MOA/side effects

A

When given by Aerosol, Pentamindine reaches significantly higher concentration in the lung than when given via IV

MOA= UNKNOWN

Cough and bronchial irritation (36% of patients in one study)
Shortness of breath (SOB
Bad taste (bitter or burning) of aerosol impacting in oropharynx
Bronchospasm and wheezing (11% of patients
Spontaneous pneumothoraces
Conjunctivitis
Rash
Neutropenia (Neutrophil WBC)
Pancreatitis
Renal insufficiency
Dysglycemia (hypoglycemia and diabetes)
Digital necrosis in both feet
Appearance of extrapulmonary P. jiroveci infection

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48
Q

pentamidine preventing airwat effects

A

Pretreat with β-adrenergic bronchodilator
Can reduce or prevent local airway reaction!

Parasympatholytic (Ipratropium!)
Shown to prevent bronchoconstriction!

Small particle size
Reduces airway impaction and increases alveolar deposition and targeting!

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49
Q

Ribavirin

A

type: antiviral

indication: RSV, influenza viruses, herpes simplex virus

trade name: virazole

form: powder, SPAG-2 (Nebulizer)

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50
Q

ribavirin MOA/ side effects

A

= It does not prevent the attachment or penetration of RSV into the cell, which may explain why it merely reduces the severity of illness rather than prevent or abolish it altogether.

Pulmonary: Deterioration of pulmonary function and worsening of asthma or COPD; pneumothorax, apnea, and bacterial pneumonia
Cardiovascular: Cardiovascular instability, including hypotension, cardiac arrest, and digitalis toxicity
Hematological: Effects on blood cells have been reported with oral or parenteral administration but not with aerosol use
Reticulocytosis (excess of young erythrocytes in circulation) has been reported with aerosol use
Dermatological/topical: Skin irritation, rash, eyelid erythema, and conjunctivitis

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51
Q

RSV with other problems

A

Children infected with RSV results in either Bronchiolitis or Pneumonia (PNA)

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52
Q

Tobramycin

A
  • antibiotic
  • managment of chronic pseudonomonas aeruginosa infection in CF
  • liquid/dry

Blocks protein synthesis in bacteria and causes cellular death
Bactericidal

Improved pulmonary function
- Reduced need for IV antipseudomonal antibiotics and hospitalizations

May affect nebulizer performance
Environmental contamination
Incompatibility with other drugs

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53
Q

cystic fibrosis meds and treatment

A

Tobramycin (TOBI) : chronic P. aeruginosa infection in CF patient
Aztreonam (Cayston) : chronic P. aeruginosa infection in CF patient
- antibiotics, bronchohygiene, PFT, peak flow

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54
Q

Endogenous

A

Produced inside body
- relieves

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55
Q

Exogenous

A

Outside product going inside of body (medicine)
- inhibits

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56
Q

activated mast cell

A

mulitvalent antigen cross-links bind IgE antibodies, casuing degranulation

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57
Q

resting mast cell

A

resting mast cell granules contian histamine and other inflammatory mediators

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58
Q

prophylactic

A

alternative to ICS

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59
Q

zafirlukast

A

accodate
- nonsteriod antiasthma
- leukotriene receptor antagonists

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60
Q

montelukast

A

singulair
- nonsteriod antiasthma
- leukotriene receptor antagonists

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61
Q

cell mediated

A

t lymphocytes mediate immune respone by several mechanisms, including cytotoxiticy and secretion of cytokinese (helper-T)

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62
Q

antibody-mediated

A

antibodies are serum globins modified specifically to combine and react with an antigen (IgE)

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63
Q

cromolyn sodium

A

can assist in suppressing a cough
- anti-sickle cell effects
prophylactic use only –> NOT treating acute bronchospasms

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64
Q

leukotrienes

A

= potent bronchoconstrictors
- airway edema
- mucus secretion
- ciliary beat inhibition
- recruitment of other inflammatory cells

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65
Q

Antileukotriene

A

BLOCK:
- cell sources of leukotrines
- biochemical pathways
- leukotriene production

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66
Q

zileuton

A

inhibits 5-LO enzyme

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67
Q

1-5um

A

last 5-6 generations
- effect of aersol particle size on area of preferential desposition within the airway

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68
Q

bronchi conducting zone

A

5-10 generation

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69
Q

gram stain

A

= bacteria stain differently depending on the structural componets of their cell wall
+ = purple
- = pink

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70
Q

acid fast stain—acid fast bacilli (AFB)

A

rapidn diagnosis of TB

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71
Q

gram positive bacteria

A
  • MRSA
  • VISA
  • VRSA
  • pencillin-resistant streptococcus pneumoniate
  • VRE
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72
Q

gram negative bacteria

A
  • MDR nonenteric bacilli (PA, SM, A)
  • third generation cephalosporin
  • ESBLA producing ecoli and klebsiella
  • ampicillin resistant haemophilus
  • carbapanemase-producing enterobacteriaceae
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73
Q

bacteriostatic

A

drug that inhibit the growth of bacteria but do not kill them

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74
Q

bacteriocidial

A

drug that kills the bacteria

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75
Q

penicillin (B-lactams antibiotic)

A

MOA= inhibit cell wall synthesis
- bactericidal (kills bacteria)

Adverse reactions:
- hypersensitivty
- hematological reactions
- GI disturbances
CNS toxicity

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76
Q

cephalosporins (antibiotic)

A

MOA= inhibit bacterial cell wall synthesis
- bactericidal (kills bacteria)
- has activity against MRSA

Adverse reactions:
- hypersensitivty
- minor GI complaints
- hypoprothrombinemia

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77
Q

TB meds

A

= airbourne isolation

  • Isoniazid (bactericidal)
  • Rifampin/Rifabutin (bactericidal)
  • Pyrazinamide (bactericidal)
  • Ethambutol (bacteriostatic)
  • Streptomycin
78
Q

Acyclovir and valacyclovir (antiviral)

A

= Zovriax

MOA= Terminate viral replication

Clinical uses:
– Herpesvirus family
– Epstein-Barr virus (EBV)
– Cytomegalovirus (CMV)
– Varicella-zoster virus (VZV) - causes chickenpox and herpes zoster (shingles)

Adverse reactions:
– Neuropathy
– Burning, irritation if used topically

79
Q

Penciclovir and Famciclovir (antiviral)

A

= Famvir

MOA= Interfere with viral DNA synthesis and replication

Clinical uses:
– Genital Herpes Simplex Virus (HSV) and VZV

Adverse reactions:
– Considered well tolerated
– Occasional nausea, vomiting, diarrhea, headache
– Rare: neutropenia

80
Q

Ganciclovir and Valganciclovir

A

= cytovene

MOA= Terminates viral DNA synthesis and replication

Clinical uses:
– HSV, VZV, CMV

Adverse reactions:
– Bone marrow suppression
– Headache, nausea, rash, fever, and liver transaminase elevations

81
Q

Cififovir

A

= Vistide

MOA= Inhibits viral replication

Clinical uses:
– Herpesvirus, EBV, CMV

Adverse reactions:
– Dose-dependent nephrotoxicity
– Neutropenia, fever, headache, emesis, rash, diarrhea

82
Q

Foscarnet

A

= Foscavir

MOA= Inhibits viral replication

Clinical uses:
– Herpesvirus, EBV, CMV

Adverse reactions:
– Dose-dependent nephrotoxicity
– Neutropenia, fever, headache, emesis, rash, diarrhea

83
Q

Amanradine and Rimantadine

A

= Symadine/Flumadine

MOA= – Inhibit viral replication and assembly
– May inhibit uncoating of influenza virus

Clinical uses:
– Active against influenza A virus

Adverse reactions
– Well tolerated
– CNS: tremor, insomnia, light-headedness, seizure, cardiac arrhythmias, agitation

84
Q

Oseltamivir and Zanamavir

A

= Tamiflu/Relenza

MOA= Inhibits influenza A and B neuraminidase
– Prevents virus from leaving host cells

Clinical uses:
– Treatment of Influenza A and B infection

Adverse reactions :
– Nausea and vomiting in first two days of therapy

85
Q

Common cold

A

A nonbacterial upper respiratory tract infection (URI), usually characterized by mild general malaise and a runny, stuffy nose, symptoms include sneezing, cough and possibly a sore throat or some chest discomfort

86
Q

Signs/symptoms of cold

A

Sign/Symptom –> Cold
Fever –> Rare
Chills –> None
Cough –> Present
Headache –> Rare
Fatigue –> Mild
Myalgia –> None or slight
Nasal congestion –> Common
Sneezing –> Common
Sore throat –> Common

87
Q

Cold remedies

A
  1. Sympathomimetics
    ⁃ For decongestion
    -pseudoephedrine (sudafed)
  2. Antihistamines
    ⁃ To reduce (dry) secretions
  3. Expectorants
    ⁃ To increase mucus clearance
  4. Antitussives
    ⁃ To suppress cough reflex
88
Q

Sympathomimetic (adrenergic) decongestants

A

= Adrenergic agents act to reduce swelling and relieve nasal congestion based on the “α-stimulation” causing vasoconstriction causing the decongestant effect

89
Q

Antihistamines

A
  • Occur “naturally” in the body and are contained in tissue mast cells and blood basophils
  • Important mediators of local inflammatory response with effects of smooth muscle contraction, increased capillary permeability, and dilation, itching, and pain

Wheal-and-flare reaction (aka: triple response) which causes:
– Local redness, welt (wheal) formation, and reddish-white (flare) border

90
Q

Effects of antihistaminic

A

– Blocks the increased vascular permeability, pruritus, and bronchial smooth muscle constriction

– Treats allergic disorders such as rhino-conjunctivitis or allergic rhinitis

Alternative to antihistamines for rhinorrhea = Ipratropium Bromide nasal spray

91
Q

H1 receptors

A
  • Located on nerve endings, smooth muscle, and glandular cells
  • Involved in inflammation/allergic reactions, produce wheal/flare reactions, bronchoconstriction, mucus secretion, and nasal congestion and irritation
92
Q

H3 receptors

A
  • Located primarily in the CNS
  • May be auto receptors for cholinergic neurotransmission in airway
93
Q

Mucokinetic

A

= medication that increases ciliary clearance of respiratory mucus secretions

94
Q

Mucolytic

A

= medication that degrades polymers in secretions

  • classic are INEFFECTIVE for the therapy of ariway diseases and NOT recommended
95
Q

Stimulants

A

= Increase production and presumably the clearance of mucus secretions
- Guaifenesin

96
Q

Expectorants

A

= Facilitate removal of mucus from the lower respiratory tract

MOA:
- Vagal gastric reflex stimulation
- Absorption into respiratory glands to directly increase mucus production
- Topical stimulation with inhaled volatile agents

  • Organidin (Iodinated Glycerol), an expectorant that appears safe and effective when used in cases of Chronic (obstructive) Bronchitis
97
Q

Mucolytic

A

= Lysing or mucolytic action
- Dornase Alfa

98
Q

Expectorant agents

A
  • Iodine products
  • Guaifenesin (Glycerol Guaiacolate) (aka: Robitussin or Mucinex)
  • Topical agents (i.e., vaporizers)
  • Parasympathomimetics (Cholinergics)
99
Q

cough suppressants (antitussives)

A

=Treatment of nonproductive, irritating, dry, and hacking coughs
* Expectorants stimulate mucus production
* Cough Suppressants depress the cough reflex

MOA= Depress the cough center in the medulla

Narcotics:
– i.e., Codeine, Hydrocodone

Nonnarcotic:
– i.e., Dextromethorphan and Benzonatate

100
Q

Diphenhydramine Hydrochloride

A

Benadrly

101
Q

Flu (influenza)

A

= Caused by the Influenza virus and associated with symptoms of fever, headache, general muscle ache, and extreme fatigue or weakness. Onset of symptoms is usually rapid

Sign/Symptom –> Influenza
Fever –> Typical, high
Chills –> Typical
Cough –> Nonproductive, may be severe
Headache –> Prominent
Fatigue –> Early, severe
Myalgia –> Usual, may be severe
Nasal congestion –> Occasional
Sneezing –> Occasional
Sore throat –> Occasional

102
Q

API alpha-1 antitrypsin (a1-AT)

A

= treatment of congenital a1-AT deficiency which leads to emphysema

103
Q

α1-AT deficiency

A

= diseased state

104
Q

α1-proteinase inhibitor

A

= deficient protein

105
Q

α1-Antitrypsin Deficiency

A

= A genetic defect that can lead to development of severe Panacinar Emphysema

  • Accounts for ~ 2% of all emphysema in the United States
106
Q

Pathogenesis of Emphysema

A

= process of alveolar wall destruction

107
Q

Centrilobular emphysema

A

occurs in the upper lobes

108
Q

Panacinar

A

= involves all lung fields, primairly in the bases

109
Q

Emphysema

A

= the alveoli at the end of the bronchioles of the lungs are destroyed

  • permenant enlargement and destruction of air sacs
  • destruction of A-C membrane
  • air trapping/hyperinflation
110
Q

Nicotine

A
  • The affinity of Nicotine stimulates acetylcholine (neurotransmitter) receptors
  • Causes HTN, tachycardia, and peripheral vasoconstriction.
  • Also binds to receptors in the CNS which causes respiratory stimulation, tremors, convulsions, nausea, and emesis
111
Q

nictoine withdrawls

A
  • Craving for nicotine
  • Nervousness
  • Irritability
  • Anxiety
  • Drowsiness
  • Sleep disturbance
  • Impaired concentration
  • Increased appetite with weight gain
112
Q

Drugs for nictoine withdrawls

A
  • Bupropion (Zyban) —> first line
  • Varenicline (chantix) –> first line
  • Clonidine (catapres) –> antihypertensive second line
113
Q

Nitric oxide (NO)

A

= a product of endothelial cells, in the respiratory tract, and acts as a Nitrovasodilator

  • pulmonary vascular relaxation

= use in neonates with hypoxic respiratory failure to reduce pulmonary artery pressure and increase oxygenation in newborns with PPHN (up to 14 days of tx)

114
Q

NO risks

A

= Risks of methemoglobinemia and elevated Nitrogen Dioxide (NO2) increase at concentrations > 20 ppm (in the bloodstream)

115
Q

Neuromuscular Blocking Agents (NMBAs)

A

= Drugs that cause skeletal muscle weakness or paralysis, preventing movement ¨Paralytics or Muscle Relaxants¨

  • Produce their effect at the neuromuscular junction by interfering with Ach
116
Q

Non depolarizing agents (antagonists) –> slow to act

A

= block Ach receptors without activating them, by preventing thebinding of Ach, nondepolarizing agents block the depolarizing effects of Ach, thereby preventing muscle contraction)

117
Q

Depolarizing agents (agonists) –> no action

A

= bind to Ach receptors and cause sustained postsynaptic membrane depolarization; the postsynaptic ending becomes refractory and unexcitable, resulting in flaccid muscles)

118
Q

depolarizing NMBAs drug

A

succinlycholine

119
Q

nondepolarizing NMBAs drugs

A
  • Cisatracurium
  • Pancuronium
  • Rocuronium
  • Vecironium
120
Q

Clincial use of NMBAs

A
  • Facilitate Intubation
  • Obtain muscle relaxation during surgery; particularly to the thorax and abdomen
  • Enhance patient-ventilator synchrony
  • Reduce intracranial pressure (ICP) in intubatedpatients with uncontrolled ICP’s
  • Reduce O2 consumption
  • Terminate convulsive status epilepticus and tetanus refractory to other therapies
  • Facilitate procedures and diagnostic studies
  • Keep pts immobile (i.e., trauma patients)
121
Q

Dendrites

A

= collect information from other neurons

122
Q

Synaptic cleft

A

= the small gap seperates the transmitting and receiving neurons

123
Q

Neurotransmitters

A

= stored in the axon terminal

124
Q

Transmitting neuron

A

= releases neurotransmitter into synaptic cleft

125
Q

Neurotransmitter

A

= bind to the receptors in the plasma membrane of the receiving cell

126
Q

Depolarization

A

= action potential occurs

127
Q

Repolarization

A

= Membrane potential returns to baseline (resting state)

  • Ach is broken down and inactivated by acetylcholinesterase (AChE), thus returning it to the resting state
128
Q

NMBA vent

A

= require muscle relaxation are pts with severe asthma, reduction of oxygen consumption in PTs with difficult-to-manage conditions, like ARDS, and PTS requiring “uncomfortable” modes of ventilations

129
Q

Succinylcholine

A
  • depolarizing agent
  • Paralysis in 60–90 seconds with a clinical duration from 10 to 15 minutes
  • No agents that reverse their blockade
  • Ideal for patients requiring intubation!
130
Q

Diurectics

A

= Main purpose is to eliminate “excess fluid” from the body

  • Drugs that increase the excretion of solutes and water by directly increasing urine output (UOP)
  • Reduce extracellular fluid volume (ECFV) in order to decrease Blood Pressure (BP) “or” rid the body of excess interstitial (tissue) fluid
131
Q

Osmotic diuretics

A

= Mannitol (Aridol), Glyerin, Isosorbide, & Urea
- Mannitol is preferred because of its lowest toxicity

  • Mannitol is the preferred agent because of lower toxicity
  • Treat and prevent Acute Renal Failure (ARF)
132
Q

Carbonic anhydrase inhibitors (CAIs)

A

= Acetazolamide, methazolamide, dichlorphenamide

Main indication:
- Effectively decrease intraocular pressure in glaucoma
- Lower HCO3– in mountain sickness
- Treat Metabolic Alkalosis
- Increase urine pH in cystinuria
* Considered to be very weak diuretics

= increased flow of alkaline urine

Adverse effect= Hypokalemia (K+)

133
Q

Loop diuretics

A

= Furosemide (Lasix), Bumetanide (Bumex), Torsemide (Demadex), Ethacrynic Acid
* Most potent diuretics called “High-ceiling” diuretics

Main indications:
- HTN, CHF, ARF, CRF, Ascites, and Nephrotic Syndrome
- Acute pulmonary edema, hypercalcemia (Ca++), renal transplant, and to enhance urinary excretion of chemical toxins

Adverse effects= may cause dose-related ototoxicity, consisting of tinnitus and clinical or subclinical hearing loss; most ototoxicity is reversible!

134
Q

Thiazide diuretics

A

= Chlorothaizidem hydrochlorothizide, chlorthalidone

= First line therapy for mild HTN
- CHF, Idiopathic Hypercalciuria (Ca++)

Other uses:
- Nephrogenic diabetes insipidus (next slide), CRF

Adverse effect= increase in serum glucose; some case of DKA have been reported

135
Q

Potassium-sparing diuretics

A

= Spironolactone (Aldactone), Eplerenone (Inspra)

Main indications:
- Most commonly used for Cirrhosis and Ascites

Other uses:
- Pt’s with elevated aldosterone

  • May cause Hyperkalemia (K+), which is a more life-threatening situation than K+ depletion
136
Q

Potassium-sparing diuretics

A

= Triamterene and Amiloride

Triamterene
⁃ Blocks Na+ channels in the collecting ducts
⁃ Short acting, but requiring multiple doses
* Poor choice for patients with liver dysfunction

Amiloride
⁃ Blocks Na+ channels in the collecting ducts
⁃ Moderately long half-life
* Coadministration of K+ supplements as well as renal dysfunction, may cause Hyperkalemia (K+), which is a more life-threatening situation than K+ depletion

137
Q

Nephron

A

= functional unit of the kidney
- maintains homeostasis between the internal volume and electrolyte status and the influences of the environment, diet and intake)

  • Kidneys can not regenerate new Nephrons
  • Renal injury, disease, and aging are associated with a gradual decrease in the number of Nephrons
138
Q

Cardiac output through renal system

A

= 20% of total blood flow through the nephron (~ 130 mL/min) is filtered through the Glomerulus
- < 1% is excreted as urine

Normal adult output = 30-60 mL/hr

139
Q

Common electrolytes

A

= Fundamental function of the Kidney is the control of buffering substances, especially, HCO3– !
- Sodium
- Potassium
- Chloride
- Bicarb
- Hydrogen
- Calcium
- Magnesium

140
Q

Cerebral edema

A

= swelling caused by abnormal accumalation of fluid in intercellular spaces of body
- TREAT WITH OSMOTIC DIURETICS

141
Q

Synergistic effect

A

= effect of two chemicals on an organism is greater than effect of either chemical individual
- Most common combination of diuretics is Loop and Thiazide!

142
Q

Midbrain

A

= Functions as a relay station for information traveling “to and from” the Cortex

  • Also integrates and modulates autonomic (involuntary system) functions, which occur primarily in the hypothalamus (involuntary eye movement)
143
Q

Brainstem (medulla)

A

= Control area for autonomic (involuntary system) functions such as breathing and cardiovascular control, and alertness

144
Q

Hypothalamus

A

= controls various homeostatic functions such as body temp, respirations, and heart beat
- directs horomone secretions of the pituitary

145
Q

Antidepressants

A

= drugs that can alter levels of certain neurotransmitters within the brain, in particular norephinephrine and serotonin
- SSRI first line medical treatment

146
Q

Antipsychotics

A

= increase dopamine in the brain
- help with hallucinations and abnormal thought process

147
Q

Benzodiazepines

A

= (CNS depressants) used to reduce anxiety

  • Little effect on cardiac function!
  • Excellent induction agents when providing general anesthesia
  • Prevent “unpleasant recall” during uncomfortable interventions
  • Terminate seizures and elevate seizure threshold
  • Can be used as a Somnific (promotes sleep)
  • Alprazolam (Xanax)
  • Diazepam (Valium)
  • Lorazepam (Ativan)
  • Midazolam (Versed)

Adverse effect:
= may augment respiratory depression induced by opioids

148
Q

Barbiturates

A

= oldest groups of sedative drugs

Ultra-short acting barbiturates are used for:
- Anesthesia induction –> Thiopental, Thiamylal, Methohexital
- Hypnotics (sleep aid meds) –> Pentobarbital, Secobarbital
- Seizures –> Phenobarbital

Adverse effects:
- Because of their toxic potential and rapid development of tolerance,
- Intentional or accidental overdose (OD) results in respiratory arrest and cardiovascular collapse
- Depress neuron activity in the brain control center
- High risk of addiction and abuse

149
Q

Opaites

A

= moderate to severe pain by binding to opioid receptors in the brain and spinal cord

Drugs:
- Morphine, Codeine, Fentanyl, Heroin, Hydrocodone (Norco, Vicodin), Hydromorphone (Dilaudid – 5-10 times stronger than Morphine), Oxycodone, Tramadol

Adverse effects:
- Tolerance develops rapidly and withdrawal is very painful and
unpleasant
- High enough doses result in loss of consciousness and respiratory
arrest

150
Q

Alcohol

A

= In excess alcohol behaves like a general anesthetic by depressing ALL BRAIN AREAS resulting in the loss of voluntary muscle control and consciousness

  • Toxic Levels 400–600 mg/dl (0.4 – 0.5%) blood alcohol level=Respiratory arrest

Withdrawls:
- Delirium Tremens (DT’s)
– hyperthermia, increased BP, muscle twitching, hallucinosis, and seizures
– If seizures occur, mortality from DT’s is 5% to 10%

151
Q

Pain scale

A

= fifth vital sign

  • many factors that alter pt responses: physiologic, social, and psychological
  • Won-Baker face pain rating scale
152
Q

Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

A

= frequently used to treat moderate pain

= Aspirin is a salicylate; OTC analgesic and cold remedy
- May cause gastric irritation and ulceration
- Renal injury can result from prolonged use and high doses
- Inhibit platelet aggregation which compounds the problem of GI bleeding

= Acetaminophen (Tylenol)
- In large doses may cause lethal hepatic (liver) necrosis
* OD of Acetaminophen reversed with N-Acetylcysteine!

153
Q

Patient-controlled analgesia (PCA) pumps

A

= PRN
- Better to keep control of pain than have to regain control
- For pts on a PCA pump it is recommended a bag-mask and naloxone be available in rooms at all times

154
Q

Naloxone

A

= Narcan, opoid antagonist
- Nasal Spray has been approved for use to combat overdoses

155
Q

Cardiac output (CO)

A

= Amount of blood leaving the heart with each contraction per unit of time
HR x SV

156
Q

Epinephrine (Adrenalin chloride)

A

= Alpha receptors cause vasoconstriction
- tachycardia effect

157
Q

Vasopressin (Pitressin)

A

= for hypotension in setting of septic shock

158
Q

Atropine

A

Anticholinergic
= symptomatic bradycardia

159
Q

Adenosine

A

Endogenous nucleotide
= treat supraventricular tachycardia

160
Q

SA node

A

= initiates electrical activity (pacemaker)
- generates action potential

161
Q

AV node

A

= links activity of the atria and ventricle

162
Q

Purkinje fibers

A

= conduction network

163
Q

Sudden cardiac death (SCD)

A
  • CPR
  • minimize time to defibrillation

MEDS:
- epinephrine
- vasopressin
- atropine
- sodium BICARBONATE
- magnesium sulfate

164
Q

NAVEL

A
  • Naloxone (narcan)
  • Atropine
  • Vasopressin
  • Epinephrine
  • Lidocaine
165
Q

Implantable cardioverter-defibrillator (ICD)

A

= used to cardiovert, terminate ventricular tachycardia (VT), and pace bradycardia

166
Q

Hypertension (HTN)

A
  • 1 billion people world wide; 1 in every 4 Americans
  • more than 140/90
  • Affects numerous organs (heart, brain, kidneys, eyes
  • increased CVD morbidity and mortality
167
Q

HTN pathophysiology

A

Arterial blood pressure= generate by interplay between blood flow and resistance to blood flow

Preload= volume of blood affected by venous capacitance
- increase in hypervolemia, regurgitation of cardiac valves, and heart failure 

After load= volume of blood flow affected by arteriolar capacitance
- increase in hypertension and vasoconstriction

168
Q

Angiotensin-converting enzyme inhibitor (ACEIs)

A

= used to suppress the renin-angiotensin-aldosterone system (RAAS)
- block the conversion of Angiotensin 1 to 2

  • antihypertensives
169
Q

Arterial blood pressure (BP)

A

= blood flow and resistance to blood flow

Elevated: 120-129, less then 80
Stage 1: 130-139, 80-89
Stage 2: more than 140, more than 80

170
Q

Diuretics used for HTN

A

= thiazide and thiazide-like agents
- mainly for vasodilation

171
Q

First line agents for HTN

A
  • Angiotensin-Converting Enzyme Inhibitors (ACEIs)
  • Angiotensin II Receptor Blockers (ARBs)
  • Calcium Channel Blockers (CCBs)
  • Thiazide-type Diuretics
172
Q

Second line agents for HTN

A
  • α2-Agonists
  • Vasodilators
  • β-Blockers
  • α-Blockers
  • Direct Renin Inhibitors (DRIs)
  • Antiadrenergics
173
Q

Myocardial ischemia

A

= lack of blood flow to the cardiac tissue which leads to poor O2 supply

174
Q

Myocardial infarction

A

= blood flow is completely cut off, resulting in cellular, death and necrosis 

175
Q

Angina pectoris signs

A
  • burning sensation
  • Shortness of breath
  • Chest tightness
176
Q

PTS with angina

A

= should receive daily aspirin 75 to 100 mg per day to prevent MI 

Nitroglycerin= reduces myocardial oxygen demand by dilating coronary arteries of collaterals
- 2.5-9mg every 12 hours

Ranolazine (Ranexa)= chronic angina
- 500mg BID

177
Q

Nitroglycerin

A

= acute TX or prophylaxis of angina, AMI, acute HF, HTN

ROA: oral, IV, mensch, transdermal, translimgual, sublingual

Adverse effect: tachycardia, palpitations, postural hypotension, dizziness, flushing, headache

178
Q

Heparin

A

= anticoagulant naturally present in the secretary granules of human mass cells inhibits the conversion of fibrinogen to fibrin

  • prevent unwanted clotting without an increased risk of hemorrhage  
179
Q

Aspirin

A

= reduce platelet irrigation by the inhibition of prostaglandin production
- Increases bleeding times

180
Q

Anticoagulant

A

= work by preventing the formation of the fibrin clot and preventing further clap formation and already existing thrombi 

181
Q

Thrombolytics

A

Indications: PE, ischemic stroke, acute ST segment elevation MI (STEMI)

Contradictions: internal bleeding, aortic, dissection, head injury, or stroke in the last three months, HTN, and anticoagulant use

Adverse effect: major and minor bleeding

182
Q

Cardiac cell contraction

A

= depend on free, intracellular calcium ion concentration

183
Q

Sleep apnea

A

OSA: occurs when the muscles in the back of your throat relax

CSA: When the brain fails to transmit signals to your breathing muscles

184
Q

Restless leg syndrome (RLS)

A

= chronic and progressive neurological disorder, characterized by unpleasant sensation and legs
- dopamine

185
Q

Narcolepsy

A

= excessive daytime sleepiness, and sleep attacks
- sodium oxybate (xyrem)

186
Q

Insomnia

A

= difficulty and falling asleep
- Benzos

187
Q

N1 (NREM)

A

= lightest sleep stage

188
Q

N3 (NREM)

A

= deepest sleep stage

189
Q

REM sleep

A
  • rapid eye movement

Tonic (persistent)= similar to N1, ECG facing increased activity in theta frequency range —> sawtooth wave
- loss in muscle strength

190
Q

Circadian rhythm

A

= 24 hour light dark cycle critical for human health and well-being

6am —> sharpest BP
10am —> highest alertness
2100 —> melatonin secretion starts


191
Q

Melatonin

A

= transition phase from wakefulness in arousal to high sleep propensity coincides with nocturnal rise and endogen melatonin

192
Q

Neurotransmitters

A

= wakefulness, and EEG arousal influenced by several excitatory neurotransmitters
- Glutamate, acetylcholine, monoamines

RCP (8 decks)

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