NUIP 315 final Flashcards

1
Q

Define Pharmacokinetics

A
  • what the body does to the medication

- A mathematical representation of a medication’s journey through the body

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2
Q

Define Pharmacodynamics

A
  • what the medication does to the body

- The effects of a medication on the body as result of its interaction with receptors and/or biochemical actions

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3
Q

What are the related parameters for absorption?

A

Bioavailability (F) is the fraction of the dose that reaches the blood circulation

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4
Q

What are the related parameters for distribution?

A

Volume of Distribution (VD)

Elimination Half Life (T1/2)

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5
Q

What are the related parameters for metabolism?

A

Bioavailability
Elimination Half-Life (T ½ )
Clearance (CL)

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6
Q

What is the related parameters elimination?

A

Clearance (CL) is the volume of plasma that is cleared of a drug in a given time (ml/min or l/h)

Elimination Half-Life (T ½ ) is the amount of time it takes for the drug concentration in the plasma to reach half of its value

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7
Q

What is normal pH?

A

pH 7.35-7.45

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8
Q

What ph is acidosis?

A

less than 7.35

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9
Q

What is the pH of alkalosis?

A

Higher than 7.45

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10
Q

What is an example that causes metabolic acidosis?

A

DKA (diabetic ketoacidosis)

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11
Q

What is an example that causes metabolic alkalosis?

A

excessive vomiting

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12
Q

what is example that causes respiratory acidosis?

A

COPD

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13
Q

What is an example of respiratory alkalosis?

A

Panic attack (hyperventilation)

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14
Q

What does compensation mean?

A

Restoring balance in the body; if the primary imbalance is metabolic, we try to compensate for it through the respiratory system, and that respiratory compensation is faster than metabolic

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15
Q

Is acetaminophen example of an anti-inflammatory?

A

nope. it does not have anti-inflammatory properties

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16
Q

Define NSAIDS

A

NSAIDs are Non-steroidal anti-inflammatory agents (they are NOT steroids). They inhibit cyclooxygenase enzymes (COX)

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17
Q

What examples of Cox-1 medications?

A

Acetates: diclofenac, ketorolac, indomethacin

Propionates: ibuprofen, ketoprofen, naproxen

Salicylates: aspirin (acetylsalicylic acid)

Oxicams: piroxicam

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18
Q

What enzyme does coxibs inhibits? example includes a celecoxib medication

A

cox-2

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19
Q

what are the adverse effects of a COX-1 enzyme inhibitor?

A

GI bleeds/ GI problems/ increased bleeding

→ Do not give (ASPIRIN) with a hemorrhagic stroke because of increased bleeding

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20
Q

What are the adverse effects of a Cox-2 medication?

A

BLOOD CLOTS (pulmonary embolism, deep vein thrombosis)

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21
Q

What do NSAIDS inhibit the formation of?

A

PROSTAGLANDINS

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22
Q

What are the four cardinal signs of inflammation?

A

Redness
Pain
Swelling
Heat

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23
Q

What are examples of K sparing diuretics?

A

Spironolactone, triamterene

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24
Q

What are examples of Loop diuretics?

A

Furosemide (strongest)

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25
Q

What is example of a thiazide diuretic?

A

Hydrochlorizide

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26
Q

What is an example of an osmotic diuretic?

A

Mannitol (ICP)

*** this is the class of diuretic that does NOT work by specifically changing cation (sodium or potassium) reabsorption

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27
Q

What is an example of a carbonic anhydrase diuretic?

A

Acetazolamide

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28
Q

What is the 1st generation antihistamine used to help nausea?

A

promethazine and meclizine are antihistamines we use the anti-serotonin effects of to help treat nausea

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29
Q

When are histamines released?

A

during an allergic reaction

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30
Q

What is the order we give respiratory medications in an acute asthma attack? (name the beta 2 agonist medications)

A

SABAS first: Albuterol (for acute asthma), Levalbuterol (short acting; fastest thing we have)

LABAs: Salmeterol, Formoterol (long lasting; we use for maintenance)

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31
Q

List the respiratory medications that are bronchodilators

A

Beta-2 Agonist
Anticholinergics
PDE 4 Inhibitors

(BAP)

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32
Q

List the respiratory medications that are in a class of anti-inflammatories

A

Steroids (Inhaled Mostly)
Leukotriene Agents
Mast Cell Stabilizers (stops from releasing histamine and leukotrienes)

(SLaM)

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33
Q

Where does chronic bronchitis affect in the body?

A

problem is in the bronchi

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34
Q

Where does emphysema affect in the body?

A

Alveoli

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35
Q

Name the infectives that affects cell wall synthesis

A

cephalosporins, penicillins, vancomycin

remember CEll and penCELLins

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36
Q

Name the anti-infective that affects protein synthesis?

A

Protein synthesis: aminoglycosides, fluoroquinolones, macrolides, tetracyclines

(AT MF)

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37
Q

Name the anti-infective that affects folate synthesis

A

sulfonamides (SMX/TMP)

  • Sulfonamide & Trimethoprim:Folate synthesis (used for UTIs)
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38
Q

The coronavirus is a family of what…

A

a family of viruses that cause many different respiratory disorders. The specific coronavirus that causes COVID-19 is called SARS-CoV-2 (Sudden Acute Respiratory Syndrome - CoronaVirus - 2, because it was also a coronavirus responsible for SARS)

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39
Q

The pacemaker of your heart is…

A

The SA node

40
Q

what is the normal electrical activity in the heart?

A

Rate: 60-100 bpm
Rhythm : normal velocity (note this changes in different parts of the heart)
Origin: begins at the sinoatrial (SA) node - your SA node is your natural pacemaker
Sequence: Normal conduction pathway

41
Q

What type of heart dysfunction is a conduction block?

A

bradycardia

42
Q

What are the types of dysfunction in the heart?

A

Automaticity : dysfunction in spontaneous depolarization at SA node or other cells that do not spontaneously fire (tachy, brady)

Triggered activity: myocardial cell fires first outside of normal depolarization (early or delayed) (tachy)

Re-entry : signal that cannot follow normal pathway because of scarring or block, and causes circular signal (tachy)

Conduction block: (brady)

43
Q

Which is faster: afib or a flutter?

A
Afib is faster than aflutter 
Atrial fibrillation (a-fib): multiple foci >350 bpm (re-entry) (my heart beats faster if I tell a fib)
44
Q

Define Torsades de pointe

A

Polymorphic V-tach with prolonged QT interval

45
Q

Some medications, such as TCAs, can be associated with which dysrhythmia? Tricyclic antidepressants (TCAs, amiodarone

A

ventricular tachycardia

46
Q

What are the ions associated with dysrhythmias?

A

sodium, potassium, and calcium

47
Q

What are the types of anti-dysrhythmic medications that act on the nodes of the heart?

A

Class II (beta-blockers) and Class IV (NonDHP Calcium-channel blockers) act at the nodes in the heart

48
Q

What are the adverse affects of amodarone (contains iodine) * class III potassium channel blockers?

A

cyanosis

49
Q

What is the MOA of adenosine?

A

Short-acting block of AV node (think chemical defibrillator

50
Q

What is atropine used for?

A

Symptomatic bradycardia

51
Q

What is the definition of atherosclerosis?

A

Characterized by stiffening of the arterial wall and formation of lipid plaques

52
Q

Describe the types of anginas (chest pain)

A

external/stable (demand):
Unstable (supply)
variant/prinzmetal (supply)

53
Q

How are nitrate treatments used for heart disease?

A

nitrates are direct vasodilators. Sudden vasodilation can also cause drop in blood pressure, headache, dizziness (because of drop in BP), and flushing (because of vasodilation)

54
Q

Is HDL good cholesterol?

A

YES…
LDL (wants a decrease) BAD
HDL (want an increase) GOOD
TG (want a decrease) BAD

55
Q

What anti-lipidemic medications target triglycerides?

A

Fibrates, Omega-3s

56
Q

What anti-lipidemic medications works in adipose tissue?

A

niacin

57
Q

What is the anti-lipidemic medications that is shown to decrease mortality in post MI patients?

A

statins

58
Q

What are the adverse effect of statins?

A

Rhabdomyolysis

59
Q

What are the adverse effects of Fibrates and Bile Acid Sequestrants?

A

Gallstones

60
Q

What are the adverse effects of Niacin?

A

Flushing

61
Q

What are the adverse effects of PCSK9 Inhibitors?

A

neurocognitive disturbance

62
Q

What are the adverse effects if Omega 3s?

A

Fishy taste

63
Q

What is an example of Statins?

A

Atorvastatin

- statin

64
Q

What is an example of Fibrates?

A

Gemfibrozil

-fib-

65
Q

What is an example of Bile Acid sequestrants?

A

Cholstyramine

66
Q

What is an example of Cholesterol absorption inhibitors?

A

Ezetimibe

67
Q

What is an example of Niacin?

A

Nicotinic acid

68
Q

What is an example of PCSK9 inhibitors?

A

alirocumab

69
Q

what is an example of omega-3s?

A

Eicosapentaenoic acid

70
Q

Antiplatelet MOA

A

prevent platelet aggregation by acting on receptors or biochemical processes in the platelet cell or preventing the formation of compounds necessary for these processes to occur

71
Q

Anticoagulants MOA

A

prevent the activation of various clotting factors in the clotting cascade to prevent activation of fibrinogen to fibrin

72
Q

Thrombolytics MOA

A

bust up clots that are already there by activating plasminogen to plasmin, which breaks down fibrin

73
Q

What is an example NSAID?

A

Aspirin

74
Q

What is an example ADP receptors P2Y12 blocker?

A

Clopidogrel

75
Q

What is an example of GPIIb/IIIa Receptor blockers ?

A

Abciximab

76
Q

Examples of heparin

A
  • Enoxaparin

- Fondaparinux

77
Q

Antidote for heparin

A

Protamine sulfate

78
Q

What is an example Factor Xa inhibitors?

A

rivaroxaban (note the Xa in the name!)

79
Q
What is an example of 
Direct thrombin (Factor II) inhibitors?
A

argatroban

80
Q

What is an example

Vitamin K reductase inhibitor?

A

Warfarin

81
Q

Antidote for Warfarin

A

Vitamin K

82
Q

Parameters around Warfarin:

A

It has lots of DDIs, Drug-Food Interactions, narrow therapeutic window, requires close monitoring (INR)

Works on vitamin K recycling

Takes 3-5 days for effect (so is often bridged with heparin upon initiation)

83
Q

What is systole?

A

Active contraction

84
Q

What is diastole?

A

Active relaxation

85
Q

What are the immediate medications given for MIs

A

MONA

Morphine, Oxygen, nitro-glycerin, Aspirin

86
Q

What meds are shown to decrease mortality in post- MI patients

A

SAAB

statin, ace inhibitor, anticoagulant/antiplatelet, beta blocker

87
Q

Most common causes of chronic kidney disease

A
  • Hypertension, diabetes mellitus

- Long term use of medication

88
Q

Complications of chronic Kidney disease

A
  • Hyperkalemia
  • Hyperphosphatemia
  • Hypocalcemia
  • Anemia (normocytic)
  • Hypertension
89
Q

Treatments in CKD (chronic kidney disease)

A

Hyperkalemia - Kayexalate (sodium polystyrene)

Hyperphosphatemia - Calcium carbonate/acetate,
sevelamer

Hypocalemia - Calcium + Vit D3

Anemia (normocytic) - Epo/darbopoeitin alfa

Hypertension - Antihypertensives

90
Q

What complications cause complicated UTIs

A

Diabetes, Immunocompromised, pregnant, procedures, catheter, male

91
Q

Common antibiotic treatments for UTI treatment & MOA

A

TMP/SMX:Folate synthesis
Nitrofurantoin:Protein synthesis
Fosfomycin:Cell wall synthesis
Amoxicillin/K-clavulanate: Cell wall synthesis

92
Q

What urinary anesthetic is commonly used?

A

Phenazopyridine

93
Q

Most common type of urinary stone

A

Calcium oxalate

94
Q

What treatments are used for Urinary Stones and what do they do?

A

Pain medication
- NSAIDs, opioids
Alpha-blocker (tamsulosin) * alpha stimulation can cause vasodilation
- Dilate smooth muscle of urinary
tract ⚈→ ⬤
Potassium citrate 🍌
- Decreases acidity allowing stones
to dissolve, binds calcium to
prevent precipitation
Thiazide diuretics 🚰
- Preventative

95
Q

Types of incontinence and their treatments

A
  • Stress
  • Urge
    • Oxybutynin
  • Overflow
    • tamsulosin
    • prazosin
  • Neurogenic
    • Non-pharm interventions
      necessary because meds wont
      help
96
Q

What are the differences between Type I and Type II diabetes

A

Type I
- autoimmune
- body destroyed its own pancreas
(insulin producing islet cells in the pancreas are destroyed, so the body can’t produce any insulin)
→ Primary problem is destruction of insulin producing cells

Type II
- → Acquired over time
Insulin resistance eventually leading to insulin deficiency
→ the islet cells are still working but the body is resistant to insulin