Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

adv pharm > adv pharm quiz/exam 1 > Flashcards

adv pharm quiz/exam 1 Flashcards

1
Q

Pharmacokinetics

A

The study of the absorption (A), distribution (D), metabolism (M), and excretion (E) of drugs
the application of PK principles to the safe and effective therapeutic management of medications in a patient.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pharmacodynamics

A

study and relationship of the action of a drug in the body over time; relationship between the drug at site of action and resulting effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

half life

A

time required for serum concentration to decrease by 50% after absorption/distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

clearance

A

volume of blood from which drug is removed over a given time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

steady state

A

when drug concentration is considtent after each does- 5 half lives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Emax

A

maximum response of the system to drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

EC50

A

concentration of a drug that produces 1/2 maximum response; dose at which 50% of individuals exhibit specified effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Potency

A

measure referring to different doses of 2 drugs needed to produce same effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ADME- A

A

absorption

movement of drug into bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

bioavailability

A

how much of the drug is absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Routes for absorption

A

oral, rectal, IM, percutaneous, transdermal, intraosseous, peritoneal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

factors affected absorption

A

gastric pH (higher in premies)
Gastric emptying time
bile acidand bilirubin excretion
pancreatic enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

First Pass metabolism

A

drug is first metabolized by the liver and therefore decreases the bioavailability of the drug in systemic circulation
only with oral admin (sublingual goes directly into the bs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

IM admin CDC recs- site of admin

0-12 months

A

vastuls lateralis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IM admin CDC rec- 13-24 months

A

vastus lateralis, deltoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IM admin 3-adults

A

deltoid is preferred

vastus lat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How many mL can you give IM for adults, neonates and children

A

adults- 2mL
Neonates- 0.5
children- no more than 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

percutaneous absorption in children- physio differences

A

thinner stratum corneum
high water content in dermis
greater body surface area to body

by 5yo BSA normalizses; (transdermal patches);

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

pharmacokinetics percutaneous absorption

A

absorption increased in newborn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ADME- Distribution
1 compartment
2 compartment

A

movement of a drug from one compartment to another;
1- drug is immediately distrib through body
2- drug is first distributed to central compartment (heart, l lungs, kidney) and then to body (tissues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

factors affecting distribution

A 
Concentration gradient
Blood flow
Lipophilicity/ hydrophilicity 
Molecular weight
Protein binding  only unbound drugs will be able to exert pharmacologic activity 
Permeability of capillary beds
Blood brain barriers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

distribution- protein binding

A

Protein bound drugs pharmacologically inert
Only unbound drugs exert pharmacologic effects
Displacement of protein bound drugs may alter pharmacologic and toxic effects of the drug

Examples of highly protein bound drugs:
Phenytoin (80% in neonates – 95% in adults; requires serum albumin dose adjustment)
Ceftriaxone (85 – 95%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

distribution differences in children - plasma protein binding

A

Decreased in young infants> increased free drug

Fetal albumin: decreased binding affinity with acidic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Competitive binding

A

Competitive binding: bilirubin, free fatty acids and drugs competed for albumin binding sites
Highly protein bound drugs displace bilirubin from protein binding sites > kernicterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

BBB

A

blood brain barrier
Cerebral endothelial cells have tight junctions
Drugs with low lipid solubility unable to cross
Highly lipid soluble drugs cross easily
Inflammation can increase concentrations into the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Relative permeability of capillaries

A

liver, kidney, muscle, fetus (placenta), brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

distribution differences in pediatrics

A 
body composition
increasedTBW
neonates- 78%
premies- 85%
fetus- 94%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ADME-M

A

metabolism
transformation of drug into active formulation to allow for pharmacologic effect

degradation of active chemical compound
not all drugs will undergo metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Phase 1 Metabolism

A

mixed-function oxididase enzyme system
think CYP enzymes
Inc hydrophilicity of drugs to facilitate elimination of drugs by kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

phase II Metabolism

A

conjuguation reactions
enzymes which catalzye the formation of conjugates with the oxidized drug or parent compound

–where you end up with the active component in addition to inactive components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

metabolism alterations in children

A

hepatic clearance: inc during first 3 months of life, exceeds adult clearance by adolescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

drug interactions in metabolism

A

Substrate
Substance acted upon by an enzyme

Inducer
Stimulates synthesis of enzyme capacity

Inhibitor
Prevents enzyme from synthesizing drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

ADME-Excretion

A

The removal of active and inactive drugs

Renal excretion
Biliary excretion
Active or passive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Renal Excretion

A

Major route by which drugs exit the body

Rate of excretion dependent on:
Pharmacologic properties of the drug
Concentration of drug in the blood

Rate of urine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

estimating renal function

CrCl

A

Equations
CCG
Schwartz (Original, Modified, Revised)

Limitations
SCr is not a great marker (especially in kids)
Equations can vary and some can overestimate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Estimating Creatinine Clearance- equation

A 
CrCl = K x L/SCr
CrCl = Creatinine Clearance (mL/min/1.73m2)

K = constant of proportionality
Age & gender based
L = Length (height) in cm
SCr = serum creatinine (mg/dL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Biliary Excretion

A

Drugs in the liver may be secreted along with bile into the duodenum
May also be reabsorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

excretion alterations in children

A

Decreased GFR and tubular secretion at birth
Especially during first week of life
Reaches relative adult function at 6 months of age

inc risk of toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ADE associated with PK changes in pediatrics

A 
Increase risk of toxicity
Impedes linear growth
Acute dystonic reactions
Respiratory depression
Paradoxical hyperactivity
Cognitive impairments
Kernicterus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Therapeutic Drug Monitoring

A

TDM
Indications: any drug with a narrow therapeutic range
inadequate response of medication
suspected toxicities (ie serious or persistent ADE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

target concentrations
peak
trough

A

Peak – highest concentration that a certain medication reaches in the blood stream

Trough – lowest concentration that a certain medication reaches in the blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

pregnancy categories

A

A

Adequate and well-controlled studies have failed to demonstrate a risk to the fetus during pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

pregnancy-B category

A

Animal reproduction studies have failed to demonstrate a risk to the fetus and there are no adequate and well-controlled studies in humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

pregnancy-C category

A

Animal studies have shown an adverse effect on the fetus and there are no adequate and well controlled studies in humans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

pregnancy- D category

A

There is positive evidence of human fetal risk based on adverse reaction data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

pregnancy-X category

A

Studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk based on adverse reaction data

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

preload

A

Ventricular filling pressure or left ventricular end-diastolic volume (LVEDV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

afterload

A

Left ventricular wall tension or stress during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Stroke Volume (SV)

A

volume of blood ejected during systole

– Dependent on preload, afterload, & contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cardiac Output (CO)

A

volume of blood ejected
per unit of time
[CO = HR x SV]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Cardiorenal modeling

A

Na/H20 excess> think diuretics as 1st line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Cardiocirculatory

A

nadequate contractility  think (+) inotropes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Neurohormonal

A

initial insult activates sympathetic system; but
progression is mediated by neurohormones > modulate hormonal
activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

principles of pharm therapy for systolic HF

A

– Block the compensatory neurohormonal
activation caused by decreased cardiac output
– Prevent/minimize Na and water retention
– Eliminate/minimize symptoms of HF
– Slow progression of cardiac dysfunction
– Decrease mortality (prolong survival)
– Increase quality of life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

diuretics

mechanism of action

A

– Inhibits reabsorption of sodium and chloride in the renal tubules
• ↑ Na excretion>↑ volume excretion>↓ preload – Rapid improvement in edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

diuretic class: Na excretion
loop
thiazide
k-sparing

A

loop: 25-30%
Thiazide: 5-10%
k sparing- 2-5%

57
Q

ADE of diuretics

A

electrolyte depletion ( dec in Na, K, Mg and Ca and Cl)
hypotension
dizziness
dehydration

Loop: 
Nephrotoxic
sulfa allergy-caution
hyperglycemic
ototoxic

Sprironolactone-
hyperkalemia is ADE but also is often used for this effect
gynecomastia

58
Q

Beta Blockers- clinical pearls

A

clinically stable patients on CE and diuretics
should be fluid stable before starting
symptomatic for first few weeks
start low and then titrate slow

59
Q

MOA for Aldosterone Antag

A

blocks effects of aldosterone in kidneys, heart, vasculature
dec K and Mg loss–>dec in ventricular arrhythmias
-dec in Na retention–> dec in fluid retention
-dec in catecholamine potentiation–> dec in BP
-blocks direct fibrotic actions on myocardium

60
Q

Aldosterone antag– ADE

A

inc in K
Gynecomastia or breast pain
sexual dysfunction

61
Q

Why use Spiro in peds?

A

primarily for K sparing effect
only tablets are available so it requires compounding pharmacy to prepare suspension
-avoid in combination with both ACE-1 and ARB due to risk of inc. K

62
Q

benefits of Digoxin

A

improved symptoms, improved exercise tolerance, dec hospitalizations, no effect on mortality
very minimal use in children

63
Q

MOA Digoxin

A

inhibits Na-K ATPase
dec central sympathetic outflow by sensitizing cardiac baroreceptors
dec renal reabsorption of Na

64
Q

Digoxin ADE

A

Dig tox
cardiac tox- ventricular arrhythmia, heart blocks, bradycardia
CNS toxicities
Confusion, vision changes

65
Q

Risk factors for ADE-Dig

A 
low K
low Mg
High Ca
hypothyroidism
interacting meds
renal insufficiency
66
Q

Contraindications for Digoxin

A

2nd or 3rd degree heart block

67
Q

Cautions for Digoxin

A

Amiodarone, diuretics, Cholestryamine, spriro, verapamil

68
Q

Monitoring Digoxin

A 
BMP- SCr, K
serum dig levels
Ti- 0.8-1.2
HF symptoms
Signs and symptoms of dig tox
69
Q

Digoxin clinical pearls

A

NOT for acute exacerbations
loading dose not needed in HF
Low starting dose in patients with conduction abnormalities, dec renal fx, low lean body mass
dec dose by 50% for concomitant amiodarone therapy

70
Q

Nitrates & Hydralazine

MOA

A

hydralazine- Vasodilator, enhances effect of nitrates

Nitrates- stimulates nitric acid signaling in endothelium, dec. preload

71
Q

ADE Nitrates/Hydralazine

A

ADE: Headache, hypotension, dizziness

Hydra: leucopenia, thrombocytopenia, lupus-like syndrome

Nitrate- flu-like symptoms, flushing

72
Q

what to monitor for nitrates and hydralazine

A

CBC: WBC/Platelets
Vitals-BP
ANA profile (lupus)
HF symtpoms

73
Q

Calcium Channel Blockers- benefits

A

no mortality benefit
tx of htn in patients at target doses of ACE-1, BB and ARB
no observed decompensated HF with amlodipine/felodipine

74
Q

Anti-Arrhythmics in HF:

the only two that are proven safe:

A

1) Amiodarone

2) Dofetilde

75
Q

Aspirin uses

A

post Norwood/procedures requiring least amount of anticoag.

  • IVIG resistent Kawasaki disease for anti-inflamm. and aneurysm clotting
  • dose: 5-10mg/kg
  • unstable in liquid- crush and dilute w water before admin
  • reye’s syndrome- caution
76
Q

Warfarin/ Coumadin

A

MOA- inhibits VKORC1, depleting functional Vitamin K reserves
limits amount of vit K dependent coagulation factors needed for clotting

Factors: II, VII, IX, X
Protein C & S- natural anticoag
Fontan- procedures, cardiac devices

77
Q

Warfarin Dosing

A

0.2mg/kg starting dose
usually given at night for AM lab draws
may req bridge anticoag for first 304 days until therapeutic INR due to depletion of protein C and S

78
Q

monitoring Warfarin

A

Nutrition (vit K)- crucial to eat same amount of vitamin K each week
INR Goal 2-3

79
Q

reversal options for warfarin

A

vitamin K and FFP

80
Q

Enoxaparin/ Lovenox

uses

A

Procine derived low molecular weight heparin, inhibits factor Xa preventing clots

Use: DVT proph.
Tx of thrombis (PE, catheter clot)

Dosing in children: 1-2mg/kg/dose q 12
only - SC inj

81
Q

antidote for Lovenox

A

Protamine- minimally useful in reversing though

82
Q

sinus arrhythmias

A

normal physiologic variant characterized by inc HR during inspiration and a dec HR in inspiration
-caused by changes in parasympathetic input to heart

83
Q

Ventricular Premature Beats

A

(or Premature Ventricular Contractions)
Prem. depolarizations of the ventricles leading to early systolic contractions
usually folloewd by pause resulting in irregular HR and irreg patterns
occur in isolation and generally benign
may cause hemodynamic compromise

84
Q

Atrial Premature Beats-APBs

A

early depol. of atrial myocardium leading to propogation of electrical impulses through atrium
results in early systolic ventricular contractions
usually benign and rarely assoc w sustained tachyarrhythmias

85
Q

goal of therapy for Afib

A

normalize ventricular rate

86
Q

Rate Control Drugs

A

Beta blockers
Non-DHP ca ch bl
Digoxin
Amiodarone

87
Q

Rhythm Control Drugs

A 
Amiodarone
Sotalol
Propafenone
Procainamide
Quinidine
Flecainide
Dofetilide
88
Q

Inotrope:

A

hard vs soft

pos. inotrope forces heart to beat- Hard vs Soft

89
Q

Chronotrope

A

ffast vs slow
alters the rate
Pos chrono- inc HR
Neg chrono- Dec HR

90
Q

Dromotrophic

A

speed of electrical conduction from either nerve or cardiac muscle

91
Q

Rate Control Drugs:

A

Beta Blockers
Non-DHP CCBS
Dig
Amiodarone

92
Q

Beta Blockers MOA

A

block effect of sympathetic neurotrans. on heart and vasculature–>decrease ventr. arrythmias, dec impulse transmission, dec AV nodal conduction

93
Q

Beta Blockers: nonselective

A

Propranolol

94
Q

Cautions Beta Blockers

A

severe bronchospastic disease
(asthma)
symptomatic hypotension
2nd or 3rd degree HB

95
Q

Non-Dihydropyridine CCBS Moa

A

dec. influx of Ca on vasculature smoothmuscle nad myocardium; slows conduction and automaticity thru AV node
Dec impulse transmission

96
Q

ADE- CCBs

A

hypotension, dec HR, fluid retention, dizziness, flushing, constipation (verapamil)

caution- sick sinus syndrome
wolff-parkinson white synd
2ndor 3rd degree AV block

97
Q

What is agent of choice for acute rate control?

A

N-D CCB

98
Q

Digoxin MOA

A

direct inhib. of Na/K ATPase pump

99
Q

Loading dose of Dig mcg/kg/day

maintain. dose

A

loading dose is based on age, formulation, indication

Maint. Dose- 2.5-10mcg/kg q24

100
Q

therapeutic Monitoring for HF and Tox

A

HF: 0.5-.9
Tox: > 2

101
Q

ADE dig

A

3rd degree block, cardiac change (PVC, V/Vfib)
rash, N/V, D, abd. pain, anorexia, visual disturbance

INC risk of tox: hypoK, hypoMg, hyPERCa, low body weight
very long T1/2

102
Q

Digibind

A

immune antigen binding frag for dig; binds to dig and is elim thru kidneys 20-90 min resolution of symptoms

103
Q

Dofetilide

A

Classification- Class III antiarrhythmic
blocks potassium channels to inc action potential due to delayed repolarization

CAUTIONS
ADE- hypotension, dec in HR, QTc prolongation, syncope, dizziness

Caution- QTc >440 msec
CrCl < 20

104
Q

monitor Defotilide

A

Vitals-BP,HR
EKG-rhythm, QTC
BMP, ADE
prolonged QTc, req 50% dose reduction, potential for proarrythmic effects

105
Q

Flecainide

A

Class 1C antiarrythmic
Blocks Sodium Channels
Dizziness, visual, dyspnea, vent. arrythmias, worsening HF

Caution- 1st or 2nd degree HB, renal disease
Contra- congestive heart failure, post-myocardial infarction

106
Q

Sotalol

A

MOA Class II and III antiarrythmic
Beta Blocker- class II effects
B-adrenergic Blocking properties
Class III effects- blocks K+ channels at higher doses

107
Q

Sotalol ADE

A 
hypotension
Dec HR
AV block
QTc prolongation (dose reduce > 450 QTc)
bradycardia
dizziness, headache, fatigue

caution- severe bronchial asthma, 2nd or 3rd AV block, HF, renal failure

108
Q

propafenone

A

Class Ic antiarrhythmic, blocks Na challens to prolong refractor; exhib. B-Blockade activity

ADE- dec HR, QTC prolong, bronchospasm, HF, edema, arrythmias, impaired Taste, dizziness

109
Q

cautions with Propafenone

A

severe bronchial asthma, CHF, liver diseases, ANA titers (elevated) - (?lupus?)

monitor vitals, EKG, LFTS, CBC, lupus, ADE

110
Q

clinical pearls Propafenone

A

Titrate no more than every 4-5 day
reduce dose by 25-50% in aptients with liver disease, HB, QRS widening, immediate release recommended for acute control, sustained release recommended for chronic control

111
Q

Amiodarone

A

fits in ALL Vaughan Williams Classifications; place in therapy- multiple arrhythmias, also helpful in retrograde electrical disorders, angina, HF

112
Q

Amiodarone ADE

A

dec bp, dec HR, QTc prolong, AV block
N/V, dec appetite, constip.
phlebitis, optic neuropathy/neuritis
dizziness, peripheral neuropathy, coordination, hep, hypo/er thyroid, blue-gray skin discolorations, photosens, pulmonary fib

113
Q

Amidoarone Caution

A

iodine allerg, 2nd or third deg HB, hepatic disease, drug interactions, QTc prolong

monitor- Vitals (BP/HR), EKG, pulmonary testing, thyroid testing, opthalmic testing, ade
*prefer IV route in sympt. patients, safe and effective in patients iwth AFIB and HF
FDA requires patients receive drug info patient education packet

114
Q

QT Interval Prolongation

A

Duration from early ventricular
depolarization to latest repolarization
• QTc = corrected QT interval accounting for
heart rate

• Standard values
– Normal: < 430 (men) & < 450 (women)
– Borderline: > 450 (men); > 470 (women)
– Prolonged: > 450 (men) & > 470 (women)

115
Q

• Risk factors for prolonged QT:

A

– Multiple prolonging agents OR high doses of
1x agent
– HypoK+, hypoCa+, HypoNa+
• So anything that can affect electrolyte balance can
potentiate the risk (ie diuretics)
– Female
– Congenital prolonged QT

116
Q

QTc =

A

QTc = QT interval ////

sq route of RR interval (in sec)

117
Q

TdP: Torsades de Pointes

A 
Life threatening
• Requires cardioversion
• Crediblemeds.org
– Class III anti-arrhythymic drugs
– Ondansetron (Zofran®), Granisetron (Kytril®)
– Methadone
– Fluoroquinolones
– Haloperidol
118
Q

Cystic Fibrosis

life expectancy

A

life expectancy is now up to 40; used to be 10, 30s

119
Q

Patho of CF

A

CFTR dysfunction alters ion permeability of cell membranes
inadequate secretin of fluid, which alters physical chemical properties of secretions
–>imbalance of ions and water in intracellular areas

CFTR gene protein- ATP-binding cassette protein; 2 ATP hydrolysis domains. fx: cAMP- dep and protein kinase C, Cl- channel

==> Loss of function results in epithelial dysfunction

120
Q

GFTR gene mutations

A 
Class I: defective protein production
class II defecive protein processing
Class III- defective channel regulation
Class IV: defective channel conductance 
most common mutation is 3-base pare deletion-->loss o phyenylanine at position 508: 508 allele
121
Q

clinical manifestations lower resp tract

A

dec FVC, forecd exp vol in 1 sec (FEV1)
bronchiectasis, chronic hypoxia, cough, chronic infection, GERD barrel chest, clubbing

ciliary dysfunction–>mucous, warm, moist environment- infection->decline

122
Q

most common CF organisms

A 
staphylococcus aureus (mrsa)
pseudomonas aeruginosa
haemophilus influenzae

other- proteus, klebsiella,etc
Fungal: Aspergillus furnigatus

123
Q

Cycle of lung disease

A

CF gene mutation>CFTR dysfx>ion transport defect>altered airway secretions, infection, tissue damage, inflammation

124
Q

Pancreatic insufficiency and CF

A

85-90% have pancreatic insuff and need supplemt
variable effects: due to defective Cl- HCO2 exchange; dec NA and HCO3 in panc duc, retention fo enzymes, malabsorption of fat, protein, nutrients
longterm- destruction of panc. tissue: firbrosis, fatty replacement, cyst form, need insulin over time, pancreatitis;

125
Q

Intestinal tract and CF

A

10-16% of CF cases are dx with meconium ileus
obstruction–gerd, DIOS: Distal Intestinal obstruction syndrome, rectal prolapse, intussesception, appendiceal abscesses;
chronic constipation

126
Q

Upper Resp tract and CF-

A

nasal polyps, sinusitis, URI

p aeruginosa, h influenzae, strept, anaerobes

127
Q

Sweat glands and CF

Bones and joints, hematologic

A

high NA and CL concentration, loss of ability of reeabsorb sodium (Na concentrations > 100)

Bones- arthritis, osteopenia, vit D def.

Hematologic- anemia, dec erythropoitin

128
Q

CF and liver

A

STFR located on apical surfaces of cells lining the bile ducts; results in bile duct obstruction, ult leads to biliary cirrhosis, dx w inc liver enzymes
long term- cholelithiasis, cirrohosis, cholestatis, hypersplenism

129
Q

Inhaled Agents, CF

A

mucolytics- Recominant human DNAse, dornase alfa
airway obstruction- B2- Agonist

airway clearance hypertonic saline (irritating cough)

inhaled antibiotics - Tobramycin, aztreonam, colistimethate

130
Q

Mechanical devices

A

PEP- Pos exp pressure
High Freq Chest wall oscillation- chest vest
PT (draining, percussion, vibration, coughing)

131
Q

endocrine tx- pancreatic enzymes

A

Panc Enzymes Lipase, Protease, amylase
dosing: based on lipase content (max 2500 units/kg/meal)

take with meals and snacks
capsules opened and mixed w food/liq
avail: pancreaze, creon, zenpep

Insulin: CFRD
Do not crush or chew
DAW
dont allow prolonged exposure to alkaline foods like pudding
give w meals
132
Q

anti-inflamm. tx for CF

A

oral: FE1 > 60%, patients 6+ to slow los of lung fx decline
Oral ibuprofen- dose; 15-30 mg/kg q 12 ADE: abd pain, epitax

Other are not usuallly rec; oral corticosteroids - inhaled corticosteroids
inc side effects

133
Q

Antibiotics for CF

A

IV: tx based on suspected org and sensitivities from sputum culture; also consider antifungals

ORAL- Macrolide antibiotics (pesudomonas)
Recommended fo anti inflam and antibiotic propertieis; studies have shown significant improvement in FEV1
Azithromycin- 500 mg TIW
Bactrim
Minocycline

134
Q

GI Tx for CF

A

DIOS- distral intestinal obst. syndroem
Polyethylene glycol 3350
Gastrograffin enemas

liver- Ursodiol reduces cholesterol, possibly reduced cytotocicity of bile and improves LFTs

lung transplant- immunosupressants

Nasal congestion- saline irrigation; saline spray OTC products

nasal corticosteroids, surgery

135
Q

Vitamin Supp Tx

A

Fat Sol- Vit ADEK

other: Ca, Fe, Zinc, Beta carotene

136
Q

CFTR gene potentiators

A

only effective in certain mutations- Kalydeco, Orkambi

137
Q

other Tx CF

A

Lung transplant, nasal congestion (saline irrig, nasal cortico, surgery)

138
Q

CF Exacerbation background precip. factors & TX

A

infection
S aureus, p aeurigoa, B capecia, h influenzia, h influenzae
TX: Maintenance therapy, continue pulm tx, pancreatic enzymes, PT; inc time and freq to 2-4x daily

*CF exac. are important marker for disease severity; they inc w age,
clinical features- dec FEV1, cough, hemopytsis, inc sputum, SOB, feber, ano, wt loss

139
Q

TX Exacerbation Tx- antib

pulm infections

A

IV for admission
S aureus, vanco, base tx on suscpeptibility
P aeruginosa, duration of therapy 14-21 days
pseudomonas always 2 drugs

Lyophilized Aztreonam- dosing 75mg q6hx28days

req unique nebulizer system; most common ADE- cough, congestion, wheezing, pyrexia, pharyngeal pain

lung tx: inhaled Tobramycin- approved in CF pts w p aeriguniosa- 300mg q 12hr
needs specific neb ulizer and air compressor

ADE- tinnitus bronchospasm

adv pharm (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions