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Renal Agents Flashcards

1
Q

ADH allows for:

A

Water permeability in the CCT

Alcohol inhibits this

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2
Q

Osmotic Diuretics

A

Mannitol
Glucose in lumen

Promotes H2O retention in the tubular fluid

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3
Q

Diuretics

A

Are natureitcs

  • loop diuretics
  • thiazides

Interfere with active or passive uptake of Na+

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4
Q

Acetazolamide

A

Carbonic anhydrase inhibitor - inhibits carbonic anhydrase, excreted in PT

Acts on the PT after the glomerulus

Effectiveness decreases after several days because there is enhanced NaCl reabsoprtion at other sites due to bicarbonate depletion

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5
Q

Acetazolamide

A

Blocks Na bicarbonate reabsorption -> decrease in NaCl reabsorption -> increase in water retention

Might result in:

  • hypercloremia
  • metabolic acidosis
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6
Q

Mannitol

A

Osmotic agent

  • expands the ECV
  • inhibits renin release

Poorly absorbed, so must be given parents rally

Acts in the Thin Descending Limb

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7
Q

Oral Mannitol

A

Eliminates toxic substances

To potential the effects of K+ binding resins

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8
Q

Furosemide

A

Loop diuretic
Acts in the Thick Ascending Limb

Blocks the NKCC2 transporter

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9
Q

Thiazides

A

Make the distal convoluted tubule impermeable to H20

Blocks the Na/Cl transporter = NCC

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10
Q

Adenosine A1 Receptor Antagonists

Caffeine, Rolofyline

A

Enhances reabsorption of the Na+, counteracts diuresis
Activates tubuloglomerular feedback (TGF)
- stimulates afferent constriction
- decreases GFR

^inhibiting these mechanisms, increase diuretic responsiveness, maintain kidney function

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11
Q

Dorzolamide

Briazolamide

A

Topical Carbonic Anhydrase Inhibitors

- used to correct for pts with metabolic alkalosis

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12
Q

Adverse effects of carbonic anhydrase inhibitors

A

Parenthesis
Somnolence
Renal K+ wasting
Allergic Rxns to those sensitive to sulfonamides

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13
Q

Contraindications of Carbonic Anhydrase Inhibitors

A

Hepatic cirrhosis

Decrease in NH4+ excretion might contribute to hepatic encephalopathy

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14
Q

Osmotic diuretics

A

Increase H20 secretion in preference to Na+ excretion

  • reduces intracranial/intraocular pressure
  • removes renal toxins (e.g. post-radio contrast agents)
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15
Q

Toxicity of Osmotic Diuretics (Mannitol)

A

ECV expansion causes hyponatremia
Headache/Nausea/vomiting
Dehydration

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16
Q

Furosemide, Bumetanide, Torsemide, Ethacrynic Acid

A

Loop diuretics

2-6 hour until it takes effect

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17
Q

Loop Diuretics

A

-mide

Blocks the NKCC cotransporter (Na+, K+, 2Cl)
Causes high Mg2+ and Ca2+ excretion!

Develop a positive lumen potential

Furosemide = less toxic, few GI problems, wider dose-response curve

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18
Q

Loop Diuretics

A

Furosemide/bumetanide/torsemide

  • block Tubuloglomerular feedback by inhibiting salt transport in macula densa
  • induces synthesis of renal prostaglandins (FGE2) by increasing COX II
    > increases blood flow and inhibits transport

NSAIDs ca interfere w/ loop diuretics by inhibiting COX

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19
Q

Uses for loop diuretics

A 
Acute pulmonary edema
Edematous conditions
Acute Hypercalcemia (Ca2+ wasting)
Hyperkalemia
Acute Renale Failure
Anion OD (bromide, fluoride, iodide)
  • not used to treat hypertension bc of short half lives
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20
Q

Thiazides

A

Block the Na/Cl cotransporter
- increases Na/Ca exchange (enhances Ca reabsorption)

Like CA inhibitors, thiazides have unsubstituted sulfoamide group

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21
Q

Hydrochlorothiazide

A

Thiazide
Increases Ca2+ absorption

Orally: less lipid like, must be given in high doses
- slowly absorbed, therefore longer duration of action

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22
Q

Indications for thiazides

A

Hypertension
HF
Neprolitiasis (bc of hypercalciuria)

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23
Q

Thiazides

A

Act on distal convoluted tubule

Some members retain significant carbonic anhydrase inhibitor activity.
Can be inhibited by NSAIDs.

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24
Q

Thiazide toxicities:

A

Hypokalemia Metabolic Alkalosis

  • Hyperuricemia: Similar to loop diuretics.
  • Impaired Carbohydrate tolerance.
  • Hyperlipidemia
  • Hyponatremia
  • Allergic reactions: Since thiazides are sulfonamides
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25
Q

Late Distal Tubule and Collecting Duct

A

Major site of K+ secretion (where virtually all diuretic-induced changes in K+ metabolism occur) and acidification of urine.

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26
Q

Loop Diuretics are used for..

A

Think Edema!

- furosemide, torsemide, bumetanide

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27
Q

Action of Loop Diuretic

A

Blocks the co-transporter NKCC2 in thick, ascending limb
- prevents Na+ absorption

Must monitor the K+ levels = low K+ can cause arrhymias

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28
Q

Action of Loop Diuretic

A

Think edema, pulmonary congestion

  1. Blocks the NKCC2 co-transporter
  2. Induces prostaglandin and NO generation from endothelial cells
    - reduces pulmonary congestion and mobilizes fluid out of lung
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29
Q

Furosemide

A

Most widely used
6 hr duration
Loop diuretic

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30
Q

Ethacrynic Acid

A

For pts allergic to sulfoamides
- can cause more otoxicity than furosemide

Decreases preload (as a loop diuretic)

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31
Q

Thiazides

A

Chlorothiazide, hydrocholorthiazide, chlorthalidone, metalazone, indapamide

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32
Q

Thiazide role

A

Blocks the Na/Cl - NCC cotransporter in the distal convoluted tubule

Used in combo with loop diuretics for those refractory to loops (furosemide)

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33
Q

Side effects of thiazides

A 
Hyperkalemia
Metabolic alkalosis
Hyponatremia
Hyperuricema
Hyperglycemia
Hypercalcemia
  • decreases afterload, therefore the BP is at level where easier pumping blood through
  • decreases pulmonary congestion
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34
Q

K-Sparing Diuretics:

Blockers of ENaC and Na+ channel

A

Trina Terence

Amiloride

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35
Q

K-Sparing Diuretics:

Aldosterone Antagonists

A

Spironolactone

Eplernone

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36
Q

Direct aldosterone antagonists

A
  • oppose aldosterone in late distal tubule and collecting duct
  • prevents myocardial and. Vascular fibrosis
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37
Q

Aldosterone Antagonists: K+ sparing diuretic

A

Reduce cardiac remodeling
Prevention Na+ retention

Side effects: spironolactone

  • gynecomastia
  • hypocholremic metabolic acidosis
  • hyperkalemia

Diuretic - decrease ECF

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38
Q

Gynecomastia

A

Endocrine abnormalities
Impotence, benign prostatic hyperplasia - reported with spironolactone

Use eplerenone instead

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39
Q

Side effects of K+ sparing diuretics:

A

Hypercholermic metabolic acidosis
They inhibit H+ secretion, therefore acidosis might occur

Hyperkalemia: oral K+ should be discontinued if aldosterone antagonists are administered

Gynecomastia - reported with spironolactone

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40
Q

ADH

A

Increase permeability of principal cells in late distal tubule to water
Increases up regulation of AQP2 channels

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41
Q

Contraindications of K+ sparing diuretics

A
  1. chronic renal insufficiency
  2. Liver disease -> dosing carefully adjusted

CYP34A inhibitors - increase the blood levels of eplerenone

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42
Q

ADH Receptor antagonists = VAPTANS

A

Treatment of euvolemic hyponatremia

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43
Q

Conivaptan

A

ADH receptor antagonist

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44
Q

Conivaptan

A

IV use

ADH receptor antagonist at V1/V2 receptors

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45
Q

Lixivaptan/Tolvaptan

A

Selective ADH antagonist for V2 receptor

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46
Q

Li+ (demeclocyline)

A

No selective agent
Decreases production of cAMP

reduces cell responsiveness to ADH
Used to treat SIADH

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47
Q

Clinical Indications of ADH antagonists

A
  1. SIADH
  2. Elevated ADH

Complications associated with diuretic pt 2-3 wks

  • initial Na+ loss
  • gradually counteracted by antinatriuetric factors (decreasing Na excretion, like aldosterone)
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48
Q

ADH antagonist toxicity

A

Might cause:

  • nephrogenic diabetes insipidus
  • renal failure: Li+.demeclocycline causes renal failure

Li+ therapy:

  • tremors
  • mental obtundation
  • cardiotoxicity
  • thyroid dysfunction
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49
Q

Spironolactone/Eplerenone

A

Competitive aldosterone antagonist
K+ sparing diuretic

Eplerenone: more selective and less side effects

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50
Q

Triamtere/Amiloride

A

Blocks ENaC Na+ channel in apical cells of the collecting duct
K+ sparing diuretic

Spironolactone/Triamtere = dependent on prostaglandin secretion, therefore might be inhibited by NSAIDs

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51
Q

Blockers of ENaC Na+ channel

K+ sparing diuretic

A

Used to treat hypertension in Liddle Syndrome (where there is an increase in ENaC activity)

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52
Q

Late distal tubule and CCT

A

Site of aldosterone

Site of K+ secretion

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53
Q

What is aldosterone?

A

Increases Na+ reabsorption

K+ and H+ secretion

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54
Q

K+ sparing diuretic

A

Useful in states of:
- mineralcorticoid excess
Primary hypersecretion- Conn Syndrome, ectopic ACTH production
Secondary Aldosteronism: HF, hepatic cirrhosis, nephrotic syndrome

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55
Q

Oral Androgens have…

A

Low oral bioavailability

  • slow and continuously absorbed form
  • chemically modified derivative that pay passes liver metabolism
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56
Q

Type A Oral Androgen

A

Esterification of the C17 hydroxyl group

  • longer the chain=more prolonged the action
  • more soluble / lipophillic
  • must be hydrolysis back to become active
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57
Q

Type B Oral Androgen

A

Alkylation of C17 alpha

  • inhibits hepatic catabolism (bypasses 1st metabolism)
  • more suitable for oral
  • can bind directly to the androgen receptor

Prolonged use = associated with liver toxicity (cholestasis, pelosis, hepatic cysts, neoplasms

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58
Q

Type C Oral Androgen

A

Modifications of A,B,C ring

  • enhances androgenic potency
  • usually occurs with C17 alpha methylation
  • increases bioavailability of drug
  • increases the half life
  • does not make a stronger Kd
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59
Q

Stanozolol, Oxandrolone

A

Pure anabolic steroids

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60
Q

GnRH androgen synthesis blockers

A 
Leuprolide
Gosenelin
Buserelin
Histrelin
“Chemical castration”
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61
Q

Estrogen Treatment - Androgen Synthesis Blocker

A

Estradiol
Diethylstilbestrol (DES)

Estradiol - negatively feedbacks to inhibit GnRH/LH “chemical castration”

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62
Q

1st generation androgen synthesis blocker

A

Ketoconazole

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63
Q

2nd generation androgen synthesis blocker

A

Abiratenone

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64
Q

Inhibitors of DHT biosynthesis

A

Finesteride

Dutasteride

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65
Q

Side effects of Androgen Therapy

A 
Increase in cholesterol
Increase in acne
Baldness
Liver damage
Polycythemia
Mood disorders

Increase in BP, fluid retention

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66
Q

Androgen Therapy Side Effects in Males

A

Decrease size of testes
Decrease sperm
Impotence
Gynecomastia

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67
Q

Androgen therapy side effects in Females

A

Infertility
Menstrual irregularities
Hisutism
Decrease in breast size

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68
Q

Anti-Androgens

A

Block the synthesis of androgen
Block the androgen receptor

Used for:

  • prostate cancer (initially dependent on androgens for survival)
  • benign prostate hyperplasia
  • male pattern hair loss
  • hirsutism (females)
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69
Q

Castration Levels cause..

A

<50ng/dL of testosterone

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70
Q

Ketoconazole

A

1st generation androgen synthesis blocker

  • potent, non selective inhibitor of steroid biosynthesis
  • inhibits 3/4 of enzymes involved in biosynthesis in Leydig cels
  • inhibits CYP3A4

Binds to cytochrome 450 active site
Blocks cortisol/aldosterone synthesis too

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71
Q

Abiraterone

A

2nd generation
Selective inhibitor of CYP17 in testes and adrenal context
Does not inhibit CYP3A4

“Pyridine moiety”

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72
Q

Androgenic Precursors

A

DHEA
Androstenedione

Inactive from the adrenal cortex

73
Q

Androgens

A

Mostly derived from testes

Testosterone - tests (potent in circulation)
DHT - androgen target cells/tissues (binds 5x more strongly than testosterone, the Kd is lower)

74
Q

Leydig Cells

A

Produce testosterone into the blood stream

  • express 17B HSD that allow conversion of DHEA and Andrestenedione -> testosterone
75
Q

How does testosterone -> DHT?

A

5 alpha-reductase - found in androgen responsive tissues

76
Q

What is CYP19?

A

Aromatase
- converts androstenedione/testosterone (the obligate precursors to estrogens) -> estrone

Estrone -> Estradiol (17HSD)

77
Q

Pituitary gland releases…

A

LH - stimulates the Leydig Cells

FSH - stimulates Sertoli cells

78
Q

Androgens are responsible for…

A

Bone resorption by osteoclasts
Bone mass by osteroblasts

Increase in protein synthesis
Increase in muscle mass

Increase in sebum production in sebaceous glands
Increase in eryhtropoiten, maturation of erythrocytes

Increase in LDL
Decrease in HDL

79
Q

Androgen therapy indicated for

A 
Male hypogonadism
Andropause
Delayed Puberty
Improved Protein Balance
Osteoporosis
Anemia
Female Hypogonadism/Hypoadarenalism
80
Q

Contraindications of androgen therapy

A

Prostate disorders
Cardiac/renal/liver disorders
Pregnant/lactating females
Infants/young children

Used as replacement in elderly men:
Mood, libido, bone density

81
Q

Synthetic Progestogen

A

As a male contraceptive
Acne
Increased libido
Mood disorders

82
Q

DHT synthesis inhibitors

A

Used to treat benign hyperplasia
Finastride
Dutasteride

83
Q

Finasteride

Dutasteride

A

Inhibit the 5alpha reductase, decreasing DHT

84
Q

1st generation AR Antagonists

A

Glutamine
Bicalutamide
Nilutamide

85
Q

2nd generation AR Antagonists

A

Enzalutamide: higher potency

Apalutamide

86
Q

1st generation AR antagonists

A

Flutamide, bicalutamide, nilutamide

  • lower potency (higher Kd)
  • imports into nucleus
  • binds DNA
  • recruits coactivators
87
Q

Inflammation

A 
Swelling
Heat
Redness
Red
Pain
88
Q

Inflammation

A

SHARP
Vasodilation
Vascular permeability
Neutrophil leukocytes to the area

89
Q

Neutrophils in Inflammation

A

1st WBC to the area

  • remove damaged tissue through phagocytosis
  • infiltrate injured tissue
90
Q

Macrophages in inflammation

A

Phagocytosis debris

91
Q

Mast Cells in inflammation

A

Mediate wound healing
Part of the immune system
Role in allergy/anaphalaxis

92
Q

Role of Kinins in Inflammation

A

Cause vasodilation
Lowers blood pressure
Stimulates pain receptors

93
Q

Role of prostaglandins in inflammation

A

Potentiate the action of bradykinin (vasodilation, lowering of BP, stimulate pain receptors)

Prostaglandins are a derivative of arachidonic acid.
Apart of the eicosanoid family

94
Q

3 members of eicosanoid family

A

Prostaglandin
Thromboxanes
Leukotrienes

95
Q

prostaglandins/thromboxanes

A

Grouped together as prostanoids

96
Q

PGE2

A

Promotes gastric mucus secretion
Inhibits gastric acid secretion (protects the stomach lining)

Main prostanoid
Increases vascular permeability

97
Q

What do mast cells and macrophages release into an area of inflammation?

A

PGE2

  • promotes gastric mucus
  • inhibits gastric acid
98
Q

The expression of COX2 is induced by what?

A

It is induced by inflammation and causes an increase in PGE2 (increased vascular permeability, mucus secretion)

99
Q

COX 1

A

More common than COX 2

Produces prostaglandins involved in “house-keeping” functions

100
Q

What is PGI2?

A

Prostacyclin

  • inhibits platelet aggregation
  • vasodilator
101
Q

What is TXA2?

A

Thromboxane A2

  • promotes platelet aggregation
  • vasoconstrictor

Opposes PGI2

102
Q

COX

A

Is responsible for converting arachidonic acid to Endoperoxides which are then converted to prostaglandins

103
Q

NSAIDs

A

Analgesics (decrease pain)
Antipyretic (decrease fever)
Anti-inflammatory effects

Reduce PGE2 = attenuating inflammatory effects

  • reduce edema/swelling
  • attenuate. Bradykinin
  • decrease in allodynia (tenderness of skin)
  • decreases fever
104
Q

NSAIDs

A 
Aspirin
Ibuprofen
Naproxen
Indomethacin
Diclofenac
  • inhibit the COX II enzyme, results obtained within a week
105
Q

NSAIDs bind to

A

COX II
Might also bind to COX I (housekeeping functions)
- COX I offers protective effects that prevent stomach upset/bleeding caused by gastric acid, therefore might have GI discomfort

106
Q

Contraindications of NSAIDs

A

Peptic ulcers
Hypersensitivity to aspirin
Coagulation defects
Severe HF

107
Q

NSAID induced asthma

A

Arachidonic Acid -> Leukotrienes (LTC, LTD, LTE)

108
Q

Aspirin

A

Prescribed for CAD pts at risk for thrombosis

  • binds covalently to COX I and II in platelets
  • inhibits TXA2 = reduces their ability to coagulate

Anti-platelet drug

109
Q

COX I

A

Released by platelet cells
Which then releases TXA2
- vasoconstrictor
- pro-aggregator

110
Q

COX II

A

Released from endothelial cells
- releases PGI2 and PGE2
Vasodilator
Anti-Aggregation

111
Q

Celebrex

A

Selective COX II inhibitor

  • inhibits pro-inflammatory prostaglandin (PGE2)
  • slightly increases MI/stroke (bc they inhibit PGI2)

Leads to excess TXA2 - negative CV effects (vasoconstrictor, pro-aggregator)

112
Q

Low Dose Aspirin is beneficial for..

A

CHD

  • inhibits COX I and COX II
  • small excess of PGI2, yielding positive CV effects
113
Q

TXA2

A

Responsible for pro-aggregation

Vasoconstrictor

114
Q

PGI2

A

Vasodilator

Anti-aggregator

115
Q

Aspirin inhibits..

A

TXA2 - reducing ability to coagulate

Binds covalently to COX I and II

116
Q

Acetaminophen

A

Tylenol
Paracetamol

NOT an NSAID, as it does not have anti-inflammatory properties

117
Q

Acetaminophen

A

Narrow therapeutic window
Anti-pyretic, Analgesic

Hepatotoxicity:

  • 2-3x of the therapeutic dose
  • creates NAPQI -> causes necrosis of the liver
118
Q

What is N-acetylcysteine (NAC)?

A

Used to treat acetaminophen OD
- promotes metabolism/excretion of the drug

7.5g = min toxic dose
<4 = toxic dose for pts with severe liver injury
119
Q

Cytochrome p450 is induced in alcoholics, therefore NAPQI is

A

Toxic

Byproduct of acetaminophen -> NAPQI

120
Q

Hydrocortisone

A

Steroidal - anti-inflammatory drugs (cortisol drugs)

121
Q

Prednisolone

A

Steroidal - anti-inflammatory drugs (cortisol drugs)

122
Q

Dexamethasone

A

Steroidal - anti-inflammatory drugs (cortisol drugs)

123
Q

Betamethasone

A

Steroidal - anti-inflammatory drugs (cortisol drugs)

124
Q

Steroid Anti-Inflammatory

A

Stress response/immune response

125
Q

Steroidal Anti-inflammatory Drugs

A

Regulate inflammation
Metabolism carbs
Protein catabolism
Immune response/stress response

126
Q

Steroidal Anti-Inflammatory Drugs (Cortisol)

A

Decrease in COX II -> Decrease in Prostaglandins
Decrease in the activity of immune cells, mast cells/macrophages
- reduces the production of histamine and inflammatory activity

127
Q

Indications for Steroid Anti-Inflammatory Drugs

A 
Asthma
Allergic Rxns
IBD
Arthritis
Bursitis
Edema
128
Q

Side effects of Steroid Anti-Inflammatory

A 
Muscle wasting
Osteoporosis
Suppression of response to infection
Cushingoid Face “moon face”
Iatrogenic Cushing Syndrome
129
Q

Metabolic Complications of Steroidal AntiInflammatory Use

A

Carbs: hyperglycemia, diabetes, wt gain, insulin need
Lipids: increase in fat distribution, deposit of fat at selected anatomical locations - buffalo hump
Proteins: osteoporosis, muscle wasting

Poor wound healing
Peptic ulcers
Insomnia
Depression
Psychosis 
Increased BP and Edema
130
Q

In asthma aerosol delivery..

A

10-20% inhaled
80-90% swallowed
- under go first pass metabolism in the liver

131
Q

To administer asthma drugs topically to lungs, increase the local concentrations and administer via:

A

Metered dose inhalers (MDI)
Nebulizers
Dry Powder Inhalers

132
Q

Asthma:

Anti-inflamm = used to?

A

Prevent symptoms

Whereas,

Bronchodilators = used to relieve acute symptoms

133
Q

Bronchodilators

A

Used to relieve acute symptoms

134
Q

Anti-inflammatory in asthma treatment

A

Used to prevent symptoms

135
Q

B2AR Agonists

136
Q

SABA and LABA

A

Short acting/Long acting Beta Agonists

137
Q

SABA

A

B2R Agonist

Lasts 3-4hrs

  • bronchodilaton occurs in 15-30 min
  • used for relief of acute symptoms/bronchospasm
138
Q

LABAs

A

Lasts 12 hours

  • administered MDI
  • lacks anti-inflammatory action
  • works well with corticosteroids
139
Q

Terbutaline, Salbuterol, Albuterol, Fenoterol

140
Q

Formoterol, Salmeterol, Indacaterol

141
Q

Adverse effects of B2AR Agonist

A

Tachycardia
Palpitations
Tremor

Do not use a B2AR agonist as monotherapy!
Black Box Warning

142
Q

Methylxanthines

A

Relaxes bronchial smooth muscle

  • reduces the release of inflammatory mediators/cytokines
  • theophylline = effective

5-20mg = improved pulmonary functioning
>20 = anorexia
>40 =Seizures

Has a narrow therapeutic index.

143
Q

Theophylline

A

Methylxanthines

CNS: increases alertness, cortical arousal
Weak diuretic
Secretes gastric acid
Improves contractility in COPD pts

144
Q

Muscarinic Receptor Antagonists (SAMRA, LAMRA)

A

Methacholine, Acetylcholine binds to the M2R

Often combined with B2 agonists to enhance dilation

145
Q

Leukotriene Modifiers for Asthma

A

Anti-inflammatory agent, anti-constrictor

Bronchoconstrictor associated in COPD/asthma with the following symptoms:

  • mucus secretion
  • increase in bronchial reactivity
  • mucosal edema
146
Q

Leukotriene Modifier = Zileuton

A

Anti-Leukotrienes

5-Lipooxygenase inhibitor (5-LOR)

147
Q

Zarilukast, Montelukast

A

Blocks LTD4

Anti-leukotriene

148
Q

Zileuton

A

Anti-leukotriene

Inhibits multiple CYPs

  • hepatitis
  • dyespepsia
149
Q

Zafirlukast

A

Anti-leukotriene

GI disturbances
Inhibits CYP2C9/3A4

150
Q

Montelukast

A

Anti-leukotriene

No CYP inhibition

151
Q

Steroid action at the Nuclear Level

A

Dimerization of steroid-receptor complex at DNA level

- leads to anti-inflammatory acativity

152
Q

Corticosteroids for Asthma

A

Inhibits eosinophilia airway mucosal inflammation

  • potentiates effects of B2 agonist
  • oral steroids for ST treatment
153
Q

Inhaled CS

A

Have very low bioavailability
Extensive first pass metabolism

Aerosol RX = most effective

154
Q

Biologics for Asthma

A

Anti-IgE
Anti-IL5
Anti-IL5R

155
Q

Omalizumab

A

Humanized antibody to IgE

  • inhibits IgE binding to receptors
  • lessens severity of asthma attacks
  • given by subcutaneous injection
156
Q

Reslizumab

A

Humanized ab to IL5

Decreases SABA use
Increases FEV1

157
Q

Mepolizumab

A

Humanized ab to IL5

Decreases # of exacerbations
Little effect on FEV1

158
Q

Benralizumab

A

Ab against IL5-receptor

159
Q

Benralizumab

A

Ab again at IL5-R

Decreases number of exacerbations
Decreases oral glucocorticoid use

160
Q

For mild-moderate asthma,

A

As needed SABA

Yet if:
Rescue therapy 2x/wk
Nocturnal symptoms 2x/mo
FEV <80% usual

…then add: ICS = budesonide or oral anti-leukotriene (monteleukast)

161
Q

For refractory or severe asthma:

A

If poor response to an ICS (fluticasone or budesonide)

-> add a LABA (salmeterol/formoterol)

162
Q

Common combo-inhalers:

A

Advair, Symbicort

If don’t respond to combo inhaler, then might be a candidate for anti-IgE, IL-5

ICS+ LABA = safe

163
Q

For pts with COPD, what is recommended as treatment?

A

Inhaled bronchodilator
Bronchodilator + steroid combo
(Fluticasone:steroid- Vilanterol:LABA)

164
Q

Acute COPD

A

SABA (albuterol)

SARA (ipratroprium) or a combo is effective

165
Q

Chronic COPD

A

LABA

LAMRA

166
Q

Chronic COPD treatments

A

LABA
LAMBRA

Corticosteroid (Fluticasone) + LABA (vilanterol)= indicated

167
Q

Statins are contraindicated for…

A

Pregnant women

168
Q

Statins are approved for use in children who have…

A

Family of hypercholerestolemia

169
Q

What drugs are for more severe Hypercholesterolemia?

A

Atorvastain
Rosuvastatin

They are more TG lowering

170
Q

What are the toxic effects of statins?

A

Elevations of ALT (3x the normal)

Liver function enzymes should be measured initially and then clinically if recommended

Medication should be discontinued if:
- anorexia, malaise, decrease in LDL

171
Q

What are adverse effects of statins?

A

Myopathy
- first in arms and legs, then the entire body
Fatigue
Effects are reversible when the drug is stopped
Rhabdomyolysis -> Myoglobinuria = can lead to renal failure
(Associated with pts with CK levels of 10x or higher)

172
Q

What drugs can statins interact with?

A

When given with other drugs that are metabolized by CYP3A4

  • grapefruit juice
  • inhibitors of organic anion transport
173
Q

Genetic variations in OATP1B1 (1B1) are associated with

A

Reduced hepatic uptake of simvastain acid

increase in simvastatin acid in plasma
Increase in risk of myopathy

174
Q

Red Yeast Rice as a LDL lowering agent

A

Statin source
Contains 14 active compounds that inhibit hepatic cholesterol synthesis

Have 12 RYR products = gives variability in monacolin content

175
Q

Monacolin K is also known as …

A

Lovastatin

176
Q

PCSK9 inhibitors

A

Monoclonal antibodies against the PCSK9 Protein

177
Q

HMG CoA reductase inhibitors (statins) side effects

A

Decreases LDL and TG

Increases HDL

178
Q

HMG CoA Reductase Inhibitors

A

Statin

Side effects:
Myopathy
Increased liver enzymes
Contraindications:
Absolute: Active or chronic liver disease
Relative: Concomitant use of certain drugs

Pharm (6 decks)

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