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Pharmocology > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

CO=

A

HR x SV

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2
Q

BP=

A

SVR x CO

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3
Q

blood flow through the heart

A

RA- tricuspid valve- RV- Pulmonary Artery- lungs pulmonary vein- LA- Mitral valve- LV- Aortic valve- body

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4
Q

Preload

A

filling and stretch just prior to contraction

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5
Q

Afterload

A

resistance in the aorta, if it increases SV/CO decrease

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6
Q

Baroreceptors

A

Sense pressure in large vessels (aorta and internal carotid artery)
Decreased stretch because of decreased volume causes increased HR and vasoconstriction

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7
Q

ADH

A

potent vasoconstriction, assists kidney water conservation

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8
Q

Renin- angiotension- aldosterone system

A

increases CO, constricts arterioles

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9
Q

ANP or BNP

A

suppress ADH and aldosterone, Ventricle stretch

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10
Q

antihypertensive classifications

A

Adrenergic Drugs= Alpha 1 blockers (antagonist), Alpha 2 agonist, Beta Blockers
Drugs that interfere with the Renin, Angiotensin, Aldosterone System (RAAS)= Angiotensin- Converting Enzyme (ACE) Inhibitor, Angiotensin II Receptor Blockers (ARB), Direct Renin Inhibitors
Calcium Channel Blockers
Diuretics
Vasodilators

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11
Q

Adrenergic drugs categories

A

Centrally and peripherally acting adrenergic neuron blockers
Centrally acting alpha2 receptor agonists
Peripherally acting alpha1 receptor blockers
Peripherally acting beta receptor blockers (beta blockers)= Cardioselective (beta1 receptors), Nonselective (both beta1 and beta2 receptors)

Peripherally acting dual alpha1 and beta receptor blockers

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12
Q

Centrally acting alpha 2 receptor agonists

A

Stimulate alpha2-adrenergic receptors in the brain
Decrease sympathetic outflow from the CNS
Decrease norepinephrine
Stimulate alpha2-adrenergic receptors
Result in decreased bp
clonidine (Catapres) methyldopa (Aldomet)
Can be used for hypertension in pregnancy

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13
Q

Peripheral alpha 1 blocker/ agonist

A

Block alpha1-adrenergic receptors
doxazosin (Cardura)
terazosin (Hytrin)
prazosin (Minipress)

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14
Q

Beta blockers

A

Reduce BP by reducing heart rate through beta1 blockade
Cause reduced secretion of renin
Long-term use causes reduced peripheral vascular resistance
nebivolol (Bystolic), propranolol (Inderal), atenolol (Tenormin)

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15
Q

Dual-action alpha 1 and beta receptor blockers

A

Reduce heart rate (beta1 receptor blockade)
Cause vasodilation (alpha1 receptor blockade)
carvedilol (Coreg)
labetalol
Result in decreased blood pressure

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16
Q

Adverse effects of Adrenergic drugs

A

*High incidence of orthostatic hypotension

Bradycardia with reflex tachycardia, Dry mouth, Drowsiness, sedation, Constipation, Depression, Edema, Sexual dysfunction (impotence)

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17
Q

ACE inhibitors

A

block conversion of angiotensin I to angiotensin II, may be combined with thiazide diuretic or calcium channel blocker, vasodilation

  • captopril (Capoten) benazepril (Lotensin) enalapril (Vasotec) fosinopril (Monopril) *lisinopril (Prinivil) moexipril (Univasc) quinapril (Accupril)
  • can be used with liver disfunction
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18
Q

ACE inhibitors adverse effects

A

Fatigue Dizziness Headache Mood changes Impaired taste Possible hyperkalemia
***Dry, nonproductive cough, which reverses when therapy is stopped
Angioedema: rare but potentially fatal

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19
Q

ARBs

A

blocks receptors that receive angiotensin, block vasoconstriction and release of aldosterone
losartan (Cozaar) eprosartan (Teveten) valsartan (Diovan) irbesartan (Avapro) candesartan (Atacand) olmesartan (Benicar) telmisartan (Micardis) azilsartan (Edarbi)

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20
Q

ARB adverse effects

A

Upper respiratory infections, Headache, May cause occasional dizziness, inability to sleep, diarrhea, dyspnea, heartburn, nasal congestion, back pain, fatigue
Hyperkalemia much less likely to occur

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21
Q

Direct Renin inhibitor

A

Indication: hypertension
MOA: inhibits the release of renin and prevents the activation of the RAAS.
Example: aliskiren (Tekturna)

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22
Q

Calcium channel blockers

A 
Cause smooth muscle relaxation 
Decreased peripheral smooth muscle tone
Decreased systemic vascular resistance
Decreased blood pressure
 A Very Nice Drug
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23
Q

Arteriole selective drugs (dihydropyridines)

A Nice

A

Relax arterial smooth muscle
Treat hypertension and angina
Nifedipine, amlodipine

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24
Q 
Nonselective drugs (non-dihydropyridines) 
Very Drug
A

Relax arterial smooth muscle
Affect myocardial contraction and heart rate
Treat hypertension and coronary artery disease
Verapamil, diltiazem

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25
Q

Diuretics

A

Decrease plasma and extracellular fluid volumes

Overall effect= Decreased workload of the heart and decreased blood pressure

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26
Q

Diuretic drugs

A

Thiazide
Potassium sparing
Loop diuretic
osmotic diuretics

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27
Q

Thiazide

A

Most common diuretic for hypertension
Chlorthalidone (Thalitone), Hydrochlorothiazide (Microzide) (HCTZ)
Metolazone (Zaroxolyn) is a thiazide like diuretic

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28
Q

Potassium sparing

A

Triamterene (Dyrenium), spironolactone (Aldactone), amiloride (Midamor), Eplerenone (Inspra)
Not as effective as others at diuresis
Risk of hyperkalemia with renal impairment, gynecomastia
Cannot use salt substitutes
Drugs like spironolactone Amiloride (Midamor) Triamterene (Dyrenium

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29
Q

Loop diuretic

A

Usually not used for HTN, potent diuretics
Furosemide (Lasix), bumetanide (Bumex), torsemide (Demadex)
Cannot give IV furosemide faster the 10 mg/min

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30
Q

Osmotic diuretic

A

Rarely drugs of first choice
Indications= Increased intracranial pressure High intraocular pressure Renal failure
May cause fluid/electrolyte imbalance
mannitol (Osmitrol)

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31
Q

Vasodilators

A

diazoxide (Hyperstat) hydralazine HCl (Apresoline) minoxidil (Loniten) sodium nitroprusside (Nipride, Nitropress)

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32
Q

process of atherosclerosis

A

Epithelial injury- Inflammatory process- Macrophages accumulate- Action of macrophages cause more endothelial damage- Oxygen free radicals oxidize the Low Density Lipoproteins- Macrophages engulf the oxidized LDL and foam cells are formed- Foam cells form fatty streaks, Macrophages stimulate the growth of smooth muscle cells- The combination of the foam cell smooth muscle and collagen develope fibro/fatty lesion-
become fibrous plaques- fibrous plaques narrow the lumen of the arteries- Advanced fibrous lesion called atheroma are covered by a fibrous cap.

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33
Q

Plaque rupture

A

Occurs when strain is placed on fibrous cap, Characteristics of plaque likely to rupture: Large soft lipid core High macrophage count Relatively few smooth muscle cells A thin fibrous cap

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34
Q

stable plaque

A

thick fibrous caps, Partially block vessels, Do not tend to form clots or emboli

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35
Q

unstable plaque

A

thin fibrous caps, Plaque can rupture and cause a clot to form, May completely block the artery, The clot may break free and become an embolus

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36
Q

C-reactive protein

A

Nonspecific marker of inflammation
Increased in many patients with CAD
Chronic exposure to CRP triggers the rupture of plaques

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37
Q

collateral circulation CAD

A

Normally some arterial anastomoses (or connections) exist within the coronary circulation, When occlusion of the coronary arteries occurs slowly over a long period (chronic ischemia), there is a greater chance of adequate collateral circulation developing

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38
Q

HDL increase

A

decrease chance of CAD

mobilize cholesterol from the tissues

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39
Q

LDL increase

A

direct correlation with CAD

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40
Q

triglycerides increase

A

linked to CAD

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41
Q

normal serum cholesterol

A

less than 200

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42
Q

LDL normal

A

less than 100

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43
Q

HDL normal

A

greater than 60

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44
Q

serum triglycerides normal level

A

less than 149

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45
Q

drugs used to treat hyperlipidemia

A

Bile Acid Sequestrants, HMG-CoA Inhibitors, Fibrates, Niacin, Cholesterol Absorption Inhibitors

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46
Q

Drugs that restrict lipoprotein production:

A

Statins, niacin

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47
Q

Drugs that increase lipoprotein removal:

A

Bile acid sequestrants

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48
Q

Drugs that decrease cholesterol absorption:

A

Ezetimibe (Zetia)

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49
Q

bile acid sequestrants

A

increase effects of Warfarin, used for increased LDL, other meds should be taken 1 hour before or 4 hours after
cholestyramine (Questran ) colesevelam (Welchol) colestipol hydrochloride (Colestid Sequestrants)

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50
Q

HMG-CoA inhibitors

A

STATINS contraindicated with pregnancy and liver disease, risk for rhabdomylosis (muscle breakdown, effects kidneys) **check creatine kinase CK
atorvastatin (Lipitor) Fluvastatin (Lescol) Lovastatin (Mevacor) Pitavastatin (Livalo)Pravastatin (Pravachol) Rosuvastatin (Crestor) Simvastatin (Zocor)

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51
Q

cholesterol absorption inhibitors

A

lowers serum cholesterol, ezetimibe (Zetia), Must administer concurrrently with statin

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52
Q

Niacin

A

B-complex vitamin, decreased production of VLDL

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53
Q

Fenofibrates

A

decreased LDL, Increased uric acid secretion – may stimulate triglyceride breakdown, drug interactions: with statins Increased risk of myositis and rhabdomyolysis
with anticoagulants Increased risk of bleeding
with antidiabetic agents Enhanced hypoglycemic effects

gemfibrozil (Lopid) Fenofibrate (Antara, TriCor) fenofibric acid (Trilipix)

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54
Q

Chronic stable angina

A

reversible myocardial ischemia= angina

O2 demand > o2 supply

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55
Q

angina Vasospastic

A

prinzmetal’s angina, Occurs at rest usually in response to spasm of major coronary artery, Seen in patients with a history of migraine headaches and Raynaud’s phenomenon, Spasm may occur in the absence of CAD
treat with calcium channel blockers

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56
Q

silent ischemia

A

Ischemia that occurs in the absence of any subjective symptoms
Up to 80% of patients with myocardial ischemia are asymptomatic
Associated with diabetes mellitus and hypertension
Confirmed by ECG changes

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57
Q

drug therapy for angina

A

Nitrates/nitrites (acute)
Beta blockers
Calcium channel blockers

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58
Q

sublingual nitroglycerin

A

never chew swallow, NitroQuick Nitrostat Nitroglycerin

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59
Q

Long acting Oral agents nitorglycerin

A 
Isosorbide dinitrate (Dilatrate, Isordil)
Isosorbide mononitrate (Imdur, Ismo, Monoket)
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60
Q

beta blockers

A

treats stable angina and CHF, reduces HR and contractillity, for long term treatment of angina, monitor glucose

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61
Q

Calcium channel blockers

A

A Very Nice Drug
amlodipine (Norvasc) nifedipine (Procardia)
verapamil (Calan, Isoptin) diltiazem (Cardizem)
used for prinzmetal angina- coronary artery spasms, Slow HR

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62
Q

ranolazine (Renexa)

A

used for angina, has anti-ischemic and antianginal effects that do not depend upon reductions in heart rate or blood pressure

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63
Q

enzyme PDE5

A

breaks down chemicals that cause the penis to relax/ erect, causes contraction and blood leaving the penis

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64
Q

Drugs used to treat ED

A

Sildenafil (Viagra)- used to treat hypotension in women
Tadalafil (Cialis)
Vardenafil (Levitra)
Selectively inhibits PDE5 and increases nitrous oxide levels, allowing blood flow into the corpus cavernosum

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65
Q

Ejection fraction normal range

A

50-70 %

66
Q

Left-sided failure

A

pulmonary edema, Decreased CO, pink frothy sputum, increase BP (from fluid) or decrease BP (from pump fail)

67
Q

Right-sided failure

A

dependent edema, Usually the result of left ventricular dysfunction, Isolated right sided failure can occur in patients with lung disease= cor pulmonale, increase liver size, weight gain, JVD

68
Q

Systolic failure

A

Decreased contractility, Decreased ejection fraction (less than 40), symptoms of decreased CO, Volume increases because it is not moving out of the heart, Blood backs up and symptoms of pulmonary and systemic congestion develop

69
Q

Diastolic failure

A

Decreased ventricular filling, Normal ejection fraction

70
Q

tests for ejection fraction

A

Echocardiogram MUGA CT Scan Cardiac Catheterization Nuclear Stress Test

71
Q

HF compensatory mechanisms

A

increase HR, Vasoconstriction, sodium and water retention, increase blood volume, increase BNP and ANP

72
Q

treatments for HF

A

Vasodilators (ACE Inhibitors, ARBs and Nitrates)
Diuretics (Loop, thiazide, potassium sparing)
Beta blockers
Cardiac glycosides
Nesiritide
Beta-Adrenergic Agonists
Non-pharmacologic - Ultrafiltration

73
Q

acute setting HF treatments LMNOP

A

Lasix, Morphine (dilates), Nitroglycerin, Oxygen, Position (sit upright)

74
Q

Morphine for HF

A

reduces preload HR, watch for respiratory depression

75
Q

ACE inhibitors for HF

A

reduce vasoconstriction, reduce aldosterones effects (less fluid retention)

76
Q

Diuretics for HF

A

reduce blood volume, lower BP, increase CO, only use for fluid overload

77
Q

spironolactone for HF

A

k sparing, aldosterone antagonist

78
Q

beta blocker for HF

A

Block negative effects of catecholamines- Slow heart Reduce contractility Prevent tachydysrythmias
May worsen heart failure
Initially lower CO
Must be started much lower than target dose
Cardioprotective

79
Q

Vasodilators for HF

A

reduce symptoms of heart failure by reducing preload or afterload
Hydralazine with isosorbide dinitrate (BiDil)
Nesiritide (Natrecor)

80
Q

cardiac glycosides for HF

A

increase contraction CO and renal perfusion, slow HR
digoxin (Lanoxin)
must be withheld HR is less than or equal to 60 apical pulse
Need lower doses with the elderly because of decreased renal clearance
*****Hypokalemia can increase Dig toxicity
Daily weights are essential (2-5 lbs in a week be reported)
do not switch brands

81
Q

Normal blood level for cardiac glycosides

A

0.5 to 2 ng/ml

82
Q

Digoxin antidote

A

Digoxin Immune Fab= Digibind or Digifab
Used for the treatment of life threatening digoxin intoxication (serum levels > 10 ng/mL with serum potassium > 5 mEq/L)
Patient should be on a cardiac monitor
don’t check Dig levels after, will increase

83
Q

Phosphodiesterase inhibitors

A

Inamrinone (Inocor): Approved only for use in patients with HF that has not responded to digoxin, diuretics, or vasodilators
Milrinone (Primacor): Short-term management of HF in patients who are receiving digoxin and diuretics
**ventricular dysrhythmias

84
Q

Phosphodiesterase III inhibitors

A

Increase contractility, Cause vasodilation, CO increased, Multiple toxicities
For patients with resistant HF who have not responded to ACE inhibitors, digoxin, or other therapies

85
Q

Heart failure cocktail

A

Need to be on: ACEI or ARB
-If ACEI or ARB are contraindicated then
Hydralazine with isosorbide dinitrate (BiDil)
BB (Carvedilol, Metoprolol, Bisoprolol, Atenolol)
Aldosterone Antagonist (Potassium Sparing diuretic)
Diuretic plus or minus Potassium Replacement
Possibly Digoxin (Not first line therapy)

86
Q

Intrinsic pathway and Extrinsic pathway for coagulation

A 
Intrinsic pathway
Takes several minutes to complete
Extrinsic pathway 
Less complex, completed in seconds
The outcome of both pathways is a fibrin clot
87
Q

clotting factor active X —-> _____ —->_____ which turns _____ into ______

A

Prothrombin , thrombin, fibrinogen to fibrin

88
Q

normal clotting takes about

A

6 minutes

89
Q

clot dissolution

A

Tissue plasminogen activator (t-PA) released by the endothelium activates the conversion of plasminogen to plasmin (fibrinolysis)
Urokinase type plasminogen activator also activates plasminogen

90
Q

Thromboembolic Disorder

A

Conditions that predispose a person to the formation of clots and emboli
CAD, STROKE, PVD, DVT

91
Q

Hemorrhagic Disorder

A

Disorder in which excess bleeding occurs
Hemophilia (genetic lack of clotting factors)
Liver disease (clotting factors not produced)
Bone marrow disorders (lack of platelet formation) (thrombocytopenia)
Von Willebrand Disease

92
Q

PT for clotting normal

A

Normal – 9.5-11.8

Therapeutic: 1.5 to 2 times the laboratory control value

93
Q

INR for clotting

A

Normal - 1
Therapeutic: 2-3
High level therapeutic: 2.5-3.5 (4.5)

94
Q

aPTT for clotting

A

Normal : 20-36 seconds

Therapeutic: 1.5-2.5 times normal

95
Q

anti Xa for clotting

A

anti Xa

Therapeutic 0.3-0.7

96
Q

Platelet counts

A

Normal: 150,000-400,000 cells/mm3

97
Q

D-Dimer

A

measures clot formation and lysis that results from the degradation of fibrin.

98
Q

signs and symptoms of coagulation disorders

A

Elevated PT/INR, aPTT
Bleeding, Easy bruising, Petechiae, Fecal occult blood
Bleeding from surgical wounds and IV sites

99
Q

drugs the prevent clot formation

A

anticoagulants antiplatelet agents

100
Q

drugs for removal of existing clot

A

thrombolytics

101
Q

drugs that promote clot formation

A

hemostatics and clotting factor concertrates

102
Q

Anticoagulant meds

A 
Parenteral
Heparin
Low-molecular-weight heparins (No PTT monitoring)
Fondaparinux
Direct thrombin inhibitors
Oral
Warfarin
103
Q

Antidote for heparin

A

protamine sulfate

104
Q

antidote for Warfarin

A

vitamin K

105
Q

Low-Molecular-Weight Heparins

A

prevent clots, NO PTT monitoring

enoxaparin(Lovenox) tinzaparin (Innohep) dalteparin (Fragmin)

106
Q

warfarin (Coumadin)

A

Oral, Decreases the production of Vitamin K dependent clotting factors in the liver, not used in acute situation

107
Q

Rivaroxaban (Xarelto)

A

Similar to warfarin, inhibits factor Xa, No INR or aPT monitoring, Bleeding most common side effect, No specific antidote

108
Q

Direct thrombin inhibitors

A

Dabigatran (Pradaxa-U.S.)
oral
Indicated for reducing the risk of stoke and systemic embolism in patient s with non-valvular atrial fibrillation
Adverse reactions- bleeding, dyspepsia
No INR monitoring
No antidote
others: apixaban (Eliquis) lepirudin (Refludan)

109
Q

Antiplatelet drugs

A 
Interfere with platelet aggregation, Prevent clot formation
Agents include: Aspirin, ADP receptor blockers:
Ticlipidine (Ticlid)
Clopidogrel (Plavix)
Prasugrel (Effient)
Glycoprotein IIb/IIIa receptor blockers:
Abciximab (ReoPro)
Eptifibitide (Integrelin)
Trifiban (Aggrastat)
110
Q

oral antiplatelet drugs

A 
anagrelide (Agrylin)
Aspirin
cilostazol (Pletal)
clopidogrel (Plavix)
prasugrel (Effient)
Ticagrelor (Brilinta)
ticlopidine (Ticlid)
dipyridamole (Persantine) (can also be given IV)
111
Q

GP IIB/ IIIA Inhibitors

A 
All given IV
Usually in combination with ASA and heparin
Indicated for Acute coronary syndrome
Unstable angina and non-Q wave MI
Percutaneous coronary interventions
Adverse events: Bleeding
Especially from PCI or IV site
112
Q

drugs for intermittent claudication

A

is pain or cramping in the lower legs that worsens with walking or exercise
Primary symptoms of (PVD)
Pentoxifylline (Trental) cilostazol (Pletal)
Aspirin and clopidogrel are also used to manage IC

113
Q

thrombolytic agents

A

alteplase (Activase) reteplase (Retavase) Tissue plasminogen activator (t-PA) streptokinase (Streptase) urokinase (Abbokinase) Anistreplase (Eminase) Tenecteplase (TNKase)

114
Q

bleeding disorders treated with clotting factors

A

Hemophilia, Liver Disease, Bone Marrow Disorders, von Willebrand’s Disease

115
Q

von Willebrand’s Disease

A

Hereditary bleeding disorder
characterized by a deficiency of or a defect in a protein termed vonWillebrand factor
Characterized by bleeding, Epistaxis, Bleeding gums, Easy bruising, Excessive menstual bleeding

116
Q

systemic hemostatic agents

A

Aminocaporic Acid
Actions: Stop the natural plasminogen clot-dissolving mechanism by blocking its activation or by directly inhibiting plasmin.
Indications: Prevent or treat excess bleeding
Adverse effects: Excessive clotting
similar drugs: Desmopressin (DDAVP, Stimate) Thrombin, topical (Evithrom, Recothrom, Thrombinar) Tranexamic acid (Cyklokapron, Lysteda)

117
Q

Erythocytes

A

Made of Hemoglobin molecules
Made of two pairs of polypeptide chains ( the globins)
Four complexes of iron plus protoporphyrin (the heme)

118
Q

Each erythrocyte has as may as

A

300 hemoglobin molecules that carry oxygen

119
Q

Total Iron-binding capacity (TIBC)

A

TIBC provides a measurement of all proteins that act to bind or transport iron between the tissues and bone marrow

120
Q

Serum Ferritin

A

Correlates with body iron stores

121
Q

Transferrin saturation

A

Measurement of iron available for erythropoiesis (ready for use to make RBC)

122
Q

RBC count

A

men 4.2-5.4 x 10^6/uL

women 3.6-5.0 x 10^6/uL

123
Q

Hemoglobin levels

A

Men 14-16.5g/dL
Women 12-15 g/dL
O2 capacity

124
Q

Hematocrit levels

A

Men 40%-50%
Women 37%-47%
RBC mass

125
Q

most RBC break down in the

A

spleen and is processed into bilirubin

126
Q

what is needed to have RBC

A

iron, B12 and folic acid, essential amino acids and carbs

127
Q

anemia

A

Deficiency in: the number of erythrocytes (Red Blood Cells) The quantitiy of hemoglobinThe volume of the Packed RBC’s (hematocrit)
Leads to:
Tissue Hypoxia – resulting in signs and symptoms of anemia

128
Q

types of anemia

A

Macrocytic – large size of RBC
Normochormic – normal color (Hemoglobin content is normal)
Microcytic – small size of RBC
Hypochromic – reduced Hemoglobin cause a light color of the cells pale

129
Q

iron deficiency anemia

A

Hypochromic and microcytic erythrocytes

130
Q

b12 deficiency anemia

A

Megaloblastic anemia
Erythrocytes are large, often with oval shape
Poikilocytosis and teardrop shapes
Neutrophils are hypersegmented
Manifestations: smooth beefy tongue, paresthesia of hands and feet

131
Q

Erythopoietin Drugs

A

Epoetin Alfa (Epogen) (Procrit)
Treats anemia associated with renal failure, AIDS, chemotherapy, and decreases need for blood transfusions in patients undergoing surgery
Darbopoetin Alfa (Aranesp)
Treats anemia associated with chronic renal failure, including patients on dialysis
** can cause hypertension HF and thrombotic events

132
Q

normal serum iron

A

60-170 mcg/dL

133
Q

drugs for iron deficiency anemia

A

Oral Iron Preparations include:
Ferrous Fumarate (Feostat)
Ferrous Gluconate (Fergon)
Ferrous Sulfate (Feosol)
Ferrous Sulfate Exsiccated (Feratab, Slow FE)
Parenteral Iron Preparation Include:
Iron Dextran (InFed) given IM using z-track method
Used in clients with severe GI malabsoption problems

134
Q

treat vitamin B12 deficiency

A

hydroxycobalamin, cyanocobalamin (Nascobal)

135
Q

polycythemia

A

a blood disorder characterized by high red blood cell count
Primary Polycythemia Vera-neoplastic disease resulting in an increase of all blood components
Secondary Polycythemia Vera-results from a physiologic increase in the level of erythropoietin usually secondary to hypoxia

136
Q

allergic rhinitis

A

Inflammation of mucous membranes in nose, throat, and airways by allergens

137
Q

allergic rhinitis drugs

A

Drugs fall into two categories:
Preventors, used for prophylaxis
-Antihistamines, Intranasal corticosteroids, Mast cell stabilizers
Relievers, used for acute symptom relief
-Oral and nasal decongestants, usually drugs from sympathomimetic class

138
Q

antihistamines

A

Examples: chlorpheniramine, fexofenadine (Allegra), loratadine (Claritin), cetirizine (Zyrtec),diphenhydramine (Benadryl)
compete with histamine to bind to receptors

139
Q

types of decongestants

A

Three main types are used
Adrenergics- Largest group, Sympathomimetics
Anticholinergics- Less commonly used, Parasympatholytics
Corticosteroids- Topical, intranasal steroids

140
Q

oral decongestants

A 
Prolonged decongestant effects, but delayed onset
Effect less potent than topical 
No rebound congestion
Exclusively adrenergics
Example: pseudoephedrine (Sudafed)
141
Q

topical nasal decongestants

A

Adrenergics- phenylephrine (Neo-Synephrine)

Intranasal steroids- beclomethasone dipropionate (Beconase), budesonide (Rhinocort), flunisolide (Nasalide), fluticasone (Flonase), triamcinolone (Nasacort), ciclesonide (Omnaris)

Intranasal anticholinergic- ipratropium (Atrovent)

142
Q

antitussives

A

used only for non productive cough

143
Q

opioid antitussive

A

Suppress the cough reflex by direct action on the cough center in the medulla
Examples:
codeine (Robitussin A-C, Dimetane-DC), hydrocodone

144
Q

nonopioid antitussive

A

Suppress the cough reflex by numbing the stretch receptors in the respiratory tract and preventing the cough reflex from being stimulated
Examples:
benzonatate (Tessalon Perles), dextromethorphan (Vicks Formula 44, Robitussin-DM)

145
Q

expectorants

A

Drugs that aid in the expectoration (removal) of mucus
Reduce the viscosity of secretions
Disintegrate and thin secretions
Example: guaifenesin (Mucinex)

146
Q

mucolytics

A

Loosen thick, viscous bronchial secretions
Two versions:
Acetylcysteine (Mucomyst)
Administered PO, inhalation, or IV
Not available OTC
Used in patients with cystic fibrosis, chronic bronchitis, and other diseases with large amounts of bronchial secretions

Dornase alfa (Pulmozyme)
Oral inhalation
Approved for management of cystic fibrosis

147
Q

Tidal volume

A

the volume or amount of air per breath, normal breath

148
Q

Minute volume

A

the respiratory rate X tidal volume, efficiency of breathing

149
Q

PFT (pulmonary function tests)

A

measure lung volumes and flow rates and can be used to diagnose lung disease.

150
Q

Compliance

A

Compliance is the measure of lung and chest wall dispensability

151
Q

FEV1

A

forced expiratory volume in 1 second. push out of air quickly

152
Q

FIO2

A

fraction of inspired oxygen (.21 is room air)

153
Q

right side aspiration

A

more common than left, shorter and more straight

154
Q

Cheyne-Stokes ventilations

A

alternating periods of deep and shallow breathing with apnea lasting from 15-60 seconds. impending death

155
Q

Alveolar dead space

A

area where alveoli are ventilated but not perfused.
Classic example is pulmonary embolus
Can diagnose with VQ scan (high V/Q)

156
Q

Pulmonary Embolism

A

blockage of the pulmonary artery by a thrombus, fat, air embolus, bacterial vegetation, or tumor tissue
most arise from deep vein thrombosis (DVT)
Venous thromboembolism (VTE)

Virchow triad- increased risk of PE
-Venous stasis, Hypercoagulability, Injury to the endothelial cells that line the vessels

157
Q

COPD

A

Three mechanisms of chronic obstructive pulmonary disease (chronic airflow limitation)
*Bronchospasm -Sudden contraction of smooth muscle that causes acute dyspnea, Drugs targeted at relaxing the smooth muscle
*Thick, viscous secretions- Block the airway, Treatment may involve antibiotics or mucolytics
*Edema- Caused by engorgement of pulmonary blood vessels, Treatment may include diuretics and corticosteroids
includes emphysema and chronic obstructive bronchitis

158
Q

Bronchial asthma

A

inflammation of the airways, characterized by airflow obstruction, increased bronchial responsiveness, increased mucous production, and edema of the airway

expiratory wheezing, dyspnea, tachypnea, tachycardia

159
Q

extrinsic (atopic) asthma

A

Type I hypersensitivity, Mast cells’ inflammatory mediators cause acute response within 10–20 minutes, Airway inflammation causes late phase response in 4–8 hours

160
Q

Emphysema

A

Enlargement of air spaces and destruction of lung tissue

Decreased surface area of alveoli decrease area for gas exchange

161
Q

Chronic obstructive bronchitis

A

Obstruction of small airways, the presence of excessive mucous and chronic productive cough for 3 months in each of two consecutive years in a patient for whom other causes of cough have been excluded

Pharmocology (8 decks)

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