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Therapeutics P2 > Exam 2 lecture 1 > Flashcards

Exam 2 lecture 1 Flashcards

1
Q

What is the second leading cause of blindness

A

glaucoma

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2
Q

Is glaucoma life long or one and done treatment

A

lifelong

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3
Q

two different types of glaucome

A

Open angle vs closed angle

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4
Q

difference between open vs closed angle glaucoma

A

Open agnle- most common (90%), happens gradually over time, painless, no vision change at first
Closed angle- Occurs when iris is very close to the lens or drainage angle and blocks it. It is a medical emergency

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5
Q

symptoms of open angle glaucoma

A

No symptoms during the early stages.
patchy blind spots in peripheral vision
Dificulty seeing in central vision

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6
Q

3 MOA to treat open angle glaucoma and the drugs to do it

A

Reduce aqueous humor production
increase aqueous humor outflow
Both

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7
Q

Which drugs can reduce aqueous humor production

A

B blockers
carbonic anhydrase inhibitors

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8
Q

Which drugs can increase aqueous humor outflow

A

prostaglandin analogs
cholinergics
RHo kinase inhibitors

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9
Q

Which drugs can reduce aqueous humor production and increase outflow

A

a-2 agonists

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10
Q

What are some 1st line options for open angle glaucome

A

prostaglandin analogs
B blockers

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11
Q

Name prostaglandin analog drugs

A

all end with prost
remember generic and brand

Bimatoprost (lumigan)
Travoprost (Travaton)
Latanoprost (xalatan)
Tafluprost (zioptan)
Bimatoprost (Latisse)

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12
Q

Which prostaglandin analog is indicated for eyelash hypotrichosis

A

Bimatoprost (latisse)

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13
Q

MOA of prostaglandin analogs

A

Increase aqueous humor outflow, (reduce IOP by 30%)

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14
Q

Dosing of prostaglandin

A

1 drop QHS

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15
Q

warnings of prostaglandin analogs

A

Darjkening of iris, increase eye lash length and number

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16
Q

side effects of prostaglandin analogs

A

Blurred vision
stinging
increased pigmentation
foreign body sensation

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17
Q

MOA of b blockers

A

decrease aqueous humor production

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18
Q

2 types of B blockers

A

non selective and selective

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19
Q

name non selective b blockers

A

Timolol (timoptic)
lartelol
levobunolol

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20
Q

name selective b blockers

A

Betaxolol (betoptic)

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21
Q

dosing of B blockers

A

1 drop daily or BID

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22
Q

contraindications of b blockers

A

sinus bradychardia
2nd or 3rd degree heart block
cardiogenic shock
uncompensated cardiac failure

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23
Q

side effects of b blockers

A

stinging
blurred vision
bradycardia
breathing problems
hypotension
diziness
fatugue
impotence

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24
Q

is betaxolol more effective than non selective

A

no

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25
Q

what is an alternative to 1st line therapy in glaucoma

A

a- agonist

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26
Q

moa of alpha agonist

A

increase aqueous humor outflow and reduce aqueous humor production

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27
Q

a-agonist drugs

A

Brimonidine (alphagan)
Aprachlonidine (iopidine)
Brimonidine (lumify)

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28
Q

dosing of a-agonist drugs

A

1 drop TID

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29
Q

Contraindication and warnings of a-agonist

A

CNS depression

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30
Q

Side effects of a-agonist

A

Dry eyes
xerostomia
blurry vision
sedation/confusion

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31
Q

Aprachlonidine clinical pearl

A

Does not have long term effects

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32
Q

xerostomia meaning

A

redness of eye

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33
Q

2nd line treatment of glaucoma

A

Carbonic anhydrase inhibitor

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34
Q

MOA of cAI

A

decrease aqueous humor production

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35
Q

Two ROA of CAI

A

opthalmic and oral

meds end with ide

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36
Q

Name opthalmic and oral CAI

A

Opthalmic- Dorzolamide (trusoft)
Brinzolamide (Azopt)

Oral- Acetazolamide
Methazolamide

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37
Q

Dosing of CAI

A

1 drop TID

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38
Q

warnings of CAI

A

sulfonamide allergy (meds end with amide )

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39
Q

side effects of opthalmic drugs

A

burning
blurred vision
blepharitis
taste disturbance

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40
Q

side effects of oral medications

A

Ataxia
Confusion
photosensitivity

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41
Q

What happens if CAI if bottles not capped

A

Can lead to crystallization

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42
Q

CAI not recommended in pts with

A

CRCL<30

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43
Q

3rd line treatment for glaucoma

A

Rho kinase inhibitor

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44
Q

MOA of rho kinase inhibitor

A

increased aqeous humor outflow

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45
Q

Rho-kinase inhibitor drugs

A

Netarsudil (rhopressin)

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46
Q

Dosing of Rho-kinase

A

1 drop QPM

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47
Q

side effects of rho kinase

A

Burning
Corneal disease
conjuctival hemorrhage
conjuctival hyperemia

remove contact lenses

48
Q

Last line glaucoma treatment

A

Cholinergic

49
Q

MOA of cholinergics

A

Increase aqueous humor outflow

50
Q

Cholinergic drugs

A

carbachol (milostat)
pilocarpine (isopto carpine)

51
Q

dosing of carbachol and pilocarpine

A

1-2 drops up to TID for carbachol
1-2 drops upto QID- pilocarpine

52
Q

contraindications of cholinergics

A

Use with caution in patients with history of retinal detachment or corneal abrasion

53
Q

Side effects of cholinergics

A

Pupil constriction
corneal clouding
hypotension
bronchospasms

54
Q

tx algorithim for glaucoma

A

1st line- prostaglandin analog and B blocker

alternative a-agonist (brimonidine)

reassess response every 2-4 weeks.

If no response try different 1st line response (prostaglandin analog or b blocker)

if only partial response- add an additional 1st or 2nd line option (CAI)

3.

if inadequate reponse
increase concentration and frequency
add 3rd or 4th line treatment
consider replacing CAI with oral CAI

  1. Inadequate response to max therapy
    laser/surgery
55
Q

if more than 1 drop of the same med, how long should we wait between drops? different meds?

A

5 mins
5-10 mins for different meds

56
Q

2 ointments

A

30 mins

57
Q

1 drop 1 ointment

A

drop 1st, 5 mins later, ointment

58
Q

when should we rule out B blocker

A

if pt has low HR and/or COPD

59
Q

when to rule out CAI

A

sulfa allergy

60
Q

sx of closed angle glaucoma

A

halos around eyes
severe pain
severe headache

61
Q

when should we treat closed angle glaucome=a

A

immediately, may cause blindness

62
Q

treatment of closed angle glaucoma

A

-Hyperosmotic agents
-Mannitol IV (1.5-2 g/kg/dose over 30 min)
-glycerin PO
1-2 g/kg/dose every 5 H
-surgery (irridotomy)

63
Q

What are some medications that increase IOP

A

anticholinergics (oxybutin, tolterodine)
Topiramate
SSRIs
sudafed

64
Q

Use of lipoprotein

A

transports cholesterol and triglyceride around the body

65
Q

structure of lipoprotein

A

Sperical particle with phospholipid, free cholesterol and protein making up the surface

66
Q

lipoprotein core made of

A

triglyceride and cholesterol ester

67
Q

How do lipoproteins determine where to go

A

Apoproteins determine where lipoproteins go

68
Q

what is lipoprotein lipase system

A

release free fatty acid from lipoprotein

69
Q

Classes of lipoproteins

A

chylomicrons
VLDL
ILDL
LDL
HDL

70
Q

chylomicrons use size and what makes it up

A

Transport dietary lipids from gut to liver and adipose tissue
biggest lipoprotein
predominantly triglyceride

71
Q

VLDL secreted by, made up of, and size

A

secreted by liver into the blood
lots of triglyceride, but less than chylomicron, more cholesterol than chylomicron.

it is big, but smaller than chylomicron

72
Q

IDL

A

intermediate between VLDL and LDL
triglyceride depleted VLDL

73
Q

LDL yse

A

main form of cholesterol in blood

74
Q

HDL secreted by, made up of, and use

A

secreted by liver
mostly protein, some cholesterol, no triglyceride
main use is reverse cholesterol transport (bring cholesterol from peripheral tissue to liver)

75
Q

when centrifuged, which lipids will be low? which will be high?

A

densest will be low
HDL will be low
Chylomicrons will be highest

76
Q

Which apoprotein are on the Lipids

A

apoprotein A1 on HDL
apoprotein B on the others

77
Q

Name important apoproteins

A

Apo A1
Apo B-100
Apo b-48
Apo C II
APO E

78
Q

Apo A1 use? what lipid is it on?

A

Mediates reverse cholesterol transport back to liver
structural in HDL

79
Q

Apo B 100 found on? produced by? use?

A

Dound on everything except HDL and chylomicro
produced in liver
ligand for LDL

80
Q

APO B 48 found on? produced by?

A

found on chylomicrons, produced by intestines

81
Q

difference between APO b 100 vs 48

A

-B 100 found on VLDL, IDL and LDL and produced by liver, bigger than B 48
-B 48 found on Chylomicron and producede by intestine

82
Q

Apo C II found on? binds to? use?

A

-Found on chylomicrons and VLDL
-Binds to enzyme called lipoprotein lipase to enhance TG hydrolysis

83
Q

APO E found in? Use?

A

found on HDL
ligand for LDL remnant receptor (helps get cholesterol into liver)

84
Q

What is LPL? where is it found?

A

Lipoprotein lipase. Found in capillaries of fat, cardiac and skeletal muscle

85
Q

What is HL? produced by? Use?

A

hepatic lipase
produced in liver
converts IDL to LDL

86
Q

2 pathways for lipid absorption and trasnport

A

Exogenous pathway
endogenous pathway

87
Q

describe the exogenous pathway

A

-eat food (dietary fat+cholesterol)
-absorbed into intestine and chylomicrons made
-chylomicrons encounter LPL (LPL break down trg into FFA, which are distributed into peripheral tissue.
-chylomicron remnants are reduced by LPL and HL and taken back up to liver through remnant receptor (APO E mediated profess)
-liver can secrete VLDLs, VLDLs encounter LPL and FFAare taken up.
-leads to reduction of VLDL into IDL
-IDL can be taken up into liver by APO E and remnant receptor OR it can be further hydrolized into LDL

88
Q

HL is key for

A

converting IDL to LDL

89
Q

What happens to IDL in exogenous pathway

A

some of the IDL gets taken up into liver and some of it gets converted to LDL

this is the way cholesterol is distrubuted in the body

90
Q

most important apoprotein on LDL is

A

B-100

91
Q

primary apoprotein for HDL? HDL importance

A

Apoprotein A1. HDLS are important for reverse transport cholesterol from peripheral tissue to liver

92
Q

What does CETP stand for? What does it do?

A

Cholesterol ester transfer protein

move cholesterol esters from HDL into IDL in exchange for triglycerides

93
Q

What is foam cell? how is it formed?

A

Foam cell is the basic unit of atherosclerotic plaque.

OXIDIED LDLs become tragets for scavenger receptors. leading to formation of foam cells.

94
Q

what is the most critical way of reducing cholesterol

A

inhibiting synthesis of choletserol by liver.

95
Q

What is the key building block for cholesterol

A

Mevalonate

96
Q

What is a key enzyme that produces mevalonate

A

HMG-COA reductase

97
Q

Lipoprotein disorders are detected by

A

measuring lipid in serum after a 10 hour fast

98
Q

Ratio of total cholesterol to HDL and risk of CVD

A

Ratio of>4,5 is associated with increased risk of CVD
Ratio of < 3.5 is desirable
<3 is optimal

99
Q

What are the two diseases associated with lipoprotein disorders

A

hyperproteinemia
Hypertriglyceridemia

100
Q

What are hyperlipoproteinemia diseases

A

-Atherosclerosis - excess accumulation of cholesterol in smooth muscle
-Premature coronary artery disease
-neurologic disease (stroke)

101
Q

What are hypertriglyceridemia diseases

A

-pancreatitis
-xanthoma
-increased risk of CHD

Atherosclerotic plaque and thrombosis are a deadly combo

102
Q

Explain atherosclerosis

A

-Presence of a high number of LDLs lead to higher levels of oxidized LDL.
-Oxidized/modified LDLs get into the area between the endothelium and vascuar smooth muscle (entema)
-this stimulates T cells and they secrete pr inflammatory cytokines, cintributing to uptake of cholesterol

103
Q

Name drugs used for high cholesterol

A

Bile acid binding resins
Inhibitors of cholesterol absorption
inhibitors of cholesterol synthesis
PCSK9 inhibitors
MTTP inhibitors

104
Q

Drugs used for high triglycerides

A

Fibrates
Niacin
Omega 3 fatty acids

105
Q

Bile acid binding resin MOA

A

inhibit reabsorption of bile acids from intestine by binding bile acids to form insoluble complex excreted in feces.

causes upregulation of LDL in liver to make more bile acids

all bile acid binding resins have positive charge

106
Q

Bile acid binding resin drugs

A

Cholestyramine (queastran)
Olestipol (colestid)

all have positive charges on them.

107
Q

What happens when liver is running low on LDL and needs to make bile (after we inhibit reabsorption of bile acids)

A

When liver is running low on cholesterol, there is an increase in LDL receptors, bringing LDL level in body to liver and away from peripheral tissues and entema.

108
Q

by sequestering bile acids with bile acid resins, we can increase excretion of bile acid by

A

10 fold

109
Q

bile acid binding resin side effects

A

Constipation and bloating

110
Q

use of bile acid? how long does it take to work?

A

Used in hypercholesterolemia
reduce LDL in 2-4 weeks
may raise it 5%
May increase TG

111
Q

Cholesterol absorption inhibitor drug

A

Ezetimebe

112
Q

Ezetimebe MOA

A

inhibits intestinal absorption of cholesterol from dietary sources and reabsorption of cholesterol excreted in bile.

113
Q

How does ezetimebe affect cholesterol in bile acid? how does it do it?

A

Binds NPCL4 and interferes with the ability of AP-2 to stimulate endocytosis of transporter

114
Q

Indication of ezetimebe

A

Reduce LDL levels
used in combo with statins

115
Q

How does ezetimebe affect statin action

A

May enhance statin action by 20%

116
Q

ezetimebe adverse effects

A

Low incidence of liver and skeletal muscle damage

Therapeutics P2 (41 decks)

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