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Pharm exam 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Where is autonomic NS; draw a picture of the central, peripheral, and autonomic

A

It is in both the peripheral and central nervous system, but largely located in peripheral

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2
Q

What is the somatic nervous system apart of

A

The peripheral NS

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3
Q

Sympathetic has what and what are they close to

A

Sympathetic ganglia; and they are close to the CNS (spinal cord) and distant from the organs they are going to effect.

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4
Q

Parasympathetic has what and what are they close to? and why?

A

The ganglia are usually imbedded in the organs; really close. This system is designed for fast global responses… broadcasting signals

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5
Q

why are they called post ganglionic

A

They are postsynaptic to the pre-ganglionic with its cell body in the gray matter of spinal cord

Pre-ganglion sends process out to post ganglion

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6
Q

What kind of system is the autonomic NS

A

A two neuron system
whether sympathetic or parasympathetic

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7
Q

What kind of system is the somatic system

A

a one neuron system — skeletal muscle

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8
Q

What are the four parts of the autonomic system drawn out

A

(brain/spine)—Pre-ganglionic neuron, mylenated and part of CNS–Autonomic ganglion—-Post-ganglionic neuron, unmylenated and part of PNS—Smooth muscle

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9
Q

Draw the autonomic NS diagram with cholinergic and adernergic

A
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10
Q

sympathetic nervous system is cholinergic from pre-ganglionic to post-ganglionic

T or F

A

False

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11
Q

Where do drugs target in the autonomic NS?

A

the pre or post ganglionic or post ganglionic tissue

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12
Q

What are the two kinds of receptors in the cholinergic synapse

A

muscarnic and nicotinic

The neurotransmitter is acetycholine

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13
Q

Draw out the anatomical location of ANS neurotransmitters; with nicotinic/mucarinic, adenergic receptors

A
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14
Q

Cholernergic all throughout but nicotinic at what synapse, and what synapse is it muscarinic?

A

Draw and label

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15
Q

What are the muscarnic receptor agonist and antagonists

A

Agonist:
Bethanechol
Pilocarpine

Antagonist:
Atropine
Scopolamine
Ipratroprium

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16
Q

What does Bethanechol do/ what is it

A

Activates muscarinic but NOT nicotinic acetocholine, so it causes smooth muscle but not skeletal muscle contraction or general activation of the autonomic nervous system.

-direct agonist for all muscarinic receptors
-does nto cross bbb
-stimulates GI, bladder, eye, sweating

-resists hydrolysis by cholinesterase or butyrylcholinesterase

-is a modified version of acetylcholine (note; acetylcholine is unstable and hard to work with)

-very stable

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17
Q

What kind of receptor resides in the smooth muscle

A

M3

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18
Q

M2 receptor tissue, responses and mechanism

A

Tissue: cardiac muscle

Responses: Slow heart rate decreases atrial force, slow A-V conduction velocity

Mechanism: activation of K channels and inhibition of adenylyl cyclase through G-i

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19
Q

M3; what tissue; responses; mechanism

A

Tissue: Smooth muscle, secretory glands, blood vessels
Responses: Smooth muscle contraction, Increases secretion from secretory glands, dilation vis endothelial factors of blood vessels

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20
Q

What is one of the major effects from the M3 receptors

A

contraction of bladder; parasympathetic stimulation causes the bladder evacuation

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21
Q

Effect of M3 on vascular smooth muscle and what does it release

A

-both vascular smooth muscle and endothelial cells have m3 receptors

-stimulation of m3 in VSM causes contraction

-Stimulation of m3 in endothelial cells cause release of NO, which causes VSM to relax

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22
Q

What kind of drugs do not pass through endothelial cells

A

injected, water-soluble drugs like bethanechol do not pass through and do not impact smooth muscle directly. Even if they did; the relaxing impact from the NO would overide it. The effects of the relaxation are always present

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23
Q

How are pilocarpine and bethanechol the same/ different

A

They react the exact same on M3 receptors; not degraded by cholinesterases

Difference: Pilocarpine crosses the BBB while bethanechol does not; there is CNS arousal: hallucinations/delirium

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24
Q

Do blood vessels receive parasympathetic input?

A

no, they only receive sympathetic input which can cause them to contract (and is important for BP)

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25
Q

What creates the BBB, what are the properties, and what does it mean

A

Endothelial cells create

-Large molecules cant cross
- lipid (fat) soluble can
-Charged molecules cant cross

-Knowing if something crosses or not is a key point in deciding which drug to use for what purpose

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26
Q

How does pilocarpine alleviates glaucoma

A

M3 receptors in the eye in the iris sphincter and ciliary muscle

(local application; ex: eyedrops to have a localized effects is really good)

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27
Q

What slows the heart down/ speeds up?

A

parasympathetic outflow; there are muscarinic receptors

Sympathetic increase HR

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28
Q

What does the M2 receptor activate on cellular level

A

potassium channels and that causes a hyper polarization

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29
Q

Bethanechol and reflex tachycardia and what is the reflex tachcardia

A

-Decreases HR through M2
-causes drop in blood pressure by impacting M3 in vascular endothelial cells

-Usually, the drop in bp would trigger baroreflex, where the sympathetic output to the heart is increased. Counteracting the effect of M2 receptor activation which causes HR to go up

-The net effect of bethanechol (or OD of pilocarpine) cab be a drop in BP AND tachycardia even though there is activation of M2 cardiac receptors

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30
Q

The parasympathetic NS

A

decreases HR and increases bowl motility

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31
Q

M3 muscarinic acetylcholine receptors are activated

A

Primary by the parasympathetic nervous system

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32
Q

Bethanechol can most readily affect blood pressure by

A

activating M3 muscarinic receptors in the cells lining the arteries

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33
Q

atropine

A

“deadly nightshade”

-direct agonist for all muscarnic receptors

-crosses BBB but need a lot to do so… high dose

-rapid treatment of bradycardia

-overcoming effects of cholmesterase block following anethetic or poising

-decreased bladder spasm

Side effects:
-Urinary retention
-can exacerbate narrow-angle glaucoma

Can be treated with physostigmine which blocks the cholinesterase enzyme (CNS and peripheral)

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34
Q

Scopolamine

A

-competitive antagonist for all M3 receptors; does the same thing as atropine but readily crosses the BBB and is longer acting.

Low-dose CNS effects in inhibition of motion sickness and induction of amnesia. CNS effects at higher doses include excitation, irritability, delirium, coma

Clinical uses: Decrease motion sickness

Side effects:
Flushed dry skin, dry mouth, tachycardia, dilated pupil, uniary retention, constipation, CNS disturbances

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35
Q

Ipratropium

A

Direct antagonist for all muscarnic receptors

-really bad at crossing BBB

-can use it for local application as an inhaler, treating asthma or COPD

-Can be used as an alternative to sympathomimetic therapy
-low system absorption from lung decreases side effects

Side effects
-minimal when used as inhaler, dry mouth sometimes can occur

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36
Q

What is the nicotinic receptor made out of and what does this mean

A

various subunits; there 5; they can be 5 of the same or a combination of tissue-specific. This means that they exist in neurons; and they can be different in neurons vs skeletal muscle and you can target skeletal muscle instead of neurons

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37
Q

Where are the nicotinic receptors

A

always in postganglionic structure; it doesn’t matter if it in parasympathetic or sympathetic, they all receive acetylcholine and target nicotinic receptors

in skeletal muscle

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38
Q

Nicotine

A

Expressed in a lot of plants

It is an insecticide (kills)

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39
Q

wet and squishy think of

A

muscarinic receptor over-activation; excess saliva, bronchorrhea, diaphoresis, diarrhea, abdominal cramping

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40
Q

Sympathetic activation symptoms

A

tachycardia, hypertension

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41
Q

therapeutic use of nicotine

A

wean people off cigs

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42
Q

why can symptoms present as both sympathetic and parasympathetic

A

because nicotinic receptors are on both parasympathetic and sympathetic parts of the NS

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43
Q

Why can symptoms change from hypertension/tachycardia to hypotension and less tachycardia

A

Nicotinic receptors depolarize cells; they are very powerful. They go through 2 phases of blocking. / desensitization

Phase one: Na channel inactivation

Phase 2 block: receptor desensitization.. not fully understood

happens quickly

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44
Q

Nicotinic activation and the heart

A

First increases all autonomic outflow- HR BP

Then with excessive cholinergic activation they desensitize through Phase 1/2

Then, it decreases all autonomic outflow because the post-ganglionic neuron nicotinic receptors are less active without the output

-turning off both sympath + para

Blood vessels receive sympathetic but not parasympathetic innervation

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45
Q

what is an indirect activator of nicotinic receptors and what are it’s inhibitors

A

they target Acytycholinesterase; its inhibitors are:

Edrophonium

Neostigmine/Physostigmine

Organophosphates (sarin, isofluorane)

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46
Q

what is sevin and what does it do

A

Insecticide and it has the active ingredient methylcarbamate which is an acetylcholinesterase inhibitor; in mammals tends to be eliminated quickly

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47
Q

carbamates… drugs + their use

A

longer acting modification but still reversible.. the two most common drugs used medically are:

Neostigmine: does not cross BBB

Physostigmine: does cross BBB

same mechanism

used to treat diseases in communication of nerve and muscle cells or the amount of nicotinic receptors and you can increase the amount by using them

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48
Q

Oganophosphates + drug and its use

A

Acts as long-term inhibitor by generating permanent non-functional phosphorylated intermediate

drug: Isofluophate

Use: isofluophate is an indirect agonist which increases the amount of natural acetylcholine at muscarinic receptors there.

pilocarpine is a direct agonist for the receptors in the ciliary in the eye, but it acts similar

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49
Q

What is a way to reverse organophosphate poisoning

A

Pralidoxime, only case where it can’t: if you wait too long

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50
Q

Organophosphates; nerve agents

A

They block acetylcholinesterase (enzyme in nerve terminals)

Exposure: inhalation, skin, ingestion

Persistence: low to high

some can be treated with pralidoxime

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51
Q

Adrenergic receptors

A

all g-protein-coupled receptors

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52
Q

Alpha 1 tissue target, responses and mechanism

A

Tissue: smooth muscle

Responses: contraction, including: blood vessels iris (has a similar effect from M3)

Mechanism: Stimulation of PLC through gq. Release of IP and DAG lead to increased CA2+. Similar to M3

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53
Q

Beta-1 tissue, responses, mechanism

A

Tissue: Cardiac muscle

Responses: increased force and rate of contraction (similar to M2)

Mechanism: Stimulation of adenylyl cyclase through Gs increases Ca2+ causes cardiac stimulation

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54
Q

Beta-2 Tissue, response, mechanism

A

Tissue: Smooth muscle in vasoculature, bronchioles, GI

Responses: Relaxation

Mechanism: Stimulation of adenylyl cyclase through Gs leads to smooth muscle relaxation

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55
Q

The adrenergic synapse

A

removal of adrenergic transmitters by re-uptake… drugs CAN target synthesis and release of adrenergic transmitters;

Releases: Norepinepherine (noradrenaline) in sympathetic NS

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56
Q

Adrenal gland

A

A post-ganglionic structure; releases 80% epinephrine and 20% norepinephrine directly into blood stream

Think of it post-ganglionic neuron with no axons

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57
Q

Epinephrine vs pilocarpine

A

ep: reduces intraocular pressure by affecting aqueous humor production from ciliary epithelium; does they by activating alpha-1 adrenergic receptors on blood vessels

pilocarpine (increases drainage) does not cause any significant muscle contraction at therapeutic doses

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58
Q

Epinephrine: low and high does and what it does

A

Low dose: B1 + B2
High dose: B1 + B2 + A1

A1: glaucoma target
(plus usual tissue, responses, and mechanism of b1/2, a)

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59
Q

is epinephrine going to increase or decrease BP at high doses

A

Increase

it can also be used to open airways

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60
Q

Norepinephrine: agonist or antagonist? what are its receptors and where is it released and what does it do

A

agonist for: a1, b1, b2
released in nerve terminals; covers blood vessels

It keeps it at constant steady state; it has a very high affinity for a1 and b1 and not as much for b2 which is good

a1 control Bp, they can cause constriction and raise bp

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61
Q

what are two endogenous NTs and what is a disadvantage

A

epinephrine and norepinephrine

acetylcholine is also one but it is never administered clinically unlike NE and E (destroyed too fast)

a disadvantage of using endogenous NT is that they are not strongly subtype-specific

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62
Q

Isoproterenol

A

non-selective beta-agonist for B1/B2

B1: increases heart function

B2: dilates bronchial smooth muscle

can be used as inhaler

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62
Q

Phenlephrine

A

Selective a1 agonist

Constricts vascular smooth muscle

It doesn’t cross BBB

can increase BP

Nasal spray + stop runny nose

Very versatile

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63
Q

Phenylephrine misuses

A

Selective a1 agonist

does not work when taken orally

Pseudoephedrine is the oral version; makes too much money to take off the market

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64
Q

Prasozin

A

selective a1 antagonist

Used for:
-open up blood vessels (treat people with heart failure)
-hypertension (decrease BP)
-improve urine flow… benign prostatic hyperplasia

-Does not readily cross BBB, but can and have mild CNS effects

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65
Q

Propanolol

A

Nonselective Beta antagonist (b1+2)

Block beta receptors

Used for:

Cardiac and BP problems, a decrease in HR and contractility…decrease oxygen the heart needs

helps arrhythmias, migraines

Possibly also for anxiety, the HR, the body thinks you’re calm

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66
Q

adrenomimetic drugs

A

can mimic effects of sympathetic nervous system

-can stimulate neurotransmitter release or block uptake

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67
Q

Pseudoephedrine/ephedrine

A

-both an agonist, but also

causes an INCREASE OF RELEASE

-helps with colds

-came from a weed

-Penetrates the BBB

controlled because it can be turned into amphetamine

68
Q

What does organophosphate nerve gas do

A

It disrupts autonomic function by indirectly hyperactivating both nicotinic and muscarinic receptors

69
Q

A patient comes into the emergency room exhibits inhibitor poisoning, excessive salivation with fluid in the lungs. The patient is being treated for a muscle disorder with physostigmine. The patient is showing signs of confusion what should you do?

A

inject scopolamine to block muscarinic receptors

69
Q

There is no connection between the airway and the sympathetic NS. However, the fight/flight response does cause an increase in the diameter of bronchial airways by relaxing bronchial smooth muscle.. what processes contribute to this?

A

Increased sympathetic outflow causes the release of epinephrine, which activates beta-2 adrenergic receptors on the bronchial smooth muscle, causing them to relax

70
Q

A patient on prazosin to treat high BP. Has a cold and wants to use an over-the-counter drug to relieve her runny nose, what should she use?

A

Pseudoephedrine taken as a nasal spray

Phenylephrine taken as a nasal spray

both work great to treat cold symptoms

71
Q

Cardiovascular system + Cardiovascular disease

A

heart, blood vessels, and blood

20% of all hospital admissions are patients over 65 have to do with heart failure

72
Q

drugs and heart failure: whats the aim

A

Decrease hospitalizations and mortality rather than improve quality of life, physical function, or symptoms

lots have severe side effects

73
Q

What is congestive heart failure what is survival rate

A

The heart can’t pump out enough blood to the body’s other organs.

symptoms: Shortness of breath (blood backs up… creates back pressure in tissue which causes fluid to leak in the lungs), fatigue, swollen ankles or legs

5-year morality, which is worse than most cancers

74
Q

Basics of human heart function; systole and diastole

A

Right side: smaller and weaker and pumps to the lungs

Left ventricle: bigger and stronger pumps to the whole body

Systole (pumping, the BP comes from contractions of left ventricle)

Diastole (filling, resting between beats, BP comes from slowly depressurizing arteries)

75
Q

Chronic/ acute heart failure

A

Chronic: long term.. if you have chronic failure, you also have… compensation by the body

Acute: rapid onset, can be immediately life-threatening

76
Q

Compensation phase in chronic heart failure; what are mechanisms one and two

A

It can fail– and lead to acute heart failure…

-in heart failure, what your body tries to do is make your heart work harder/faster

-it affects kidney function and increases BP

Compensation Mechanism 1: Sympathetic outflow increases HR and force of contraction VIA B1. It also causes vasoconstriction, increasing BP.

Compensation mechanism 2: Angiotensin (ACE): peptide hormone that causes vasoconstriction and increased BP

77
Q

Angiotensin receptors cause what

A

vasoconstriction

78
Q

Decompensation

A

failure of compensation, a sudden heart failure

79
Q

What is a positive inotropic drug

A

Any drug that increases cardiac contractility

79
Q

Catecholamines: epinephrine

A

Agonist for B1 B2 and A1 and A2

it affects A1 in the blood vessels (constricts) not really want because it increases BP and puts more work on the heart

Still best to have a drug without the vasoconstrictive effect

Adverse effects: arrhythmias, tachcardia

80
Q

Dobutamine

A

selective B1 agonist

It is used to stimulate the heart by activating to B1, which has the same side effects as epinephrine.

Issues: tolerance is likely to develop with prolonged use because of receptor desensitization

81
Q

Bipyridines: Milrinone

A

Used only within the first 48 hours… overtime it is toxic so it is only for acute heart failure

Increases stroke volume and cardiac output via two mechanisms that BYPASS the B1 receptor

Positive Inotropic agent- increases cardiac contractility but decreases of smooth muscle.

Vasodilator- reduces impedance to blood flow.

How does it do this: PDE increases cAMP

in cardiac cells: increase cAMP causes INCREASE in Ca and INCREASE cardiac contractility

82
Q

Digoxin

A

Increases Ca2+ levels within cardiac myocytes to enhance contractility

-comes from plants-

Mech of action: inhibition (not completely) of Na+/K+
leads to an increase of Na+
Increases cytosolic Ca2+ levels within cardiac
myocytes to enhance contractility
does not cross BBB

Clinical effects: decreased rate of hospitalization, decreased symptoms of heart failure, increased exercise tolerance

Does not increase survival… just makes what time is left is easier

Adverse effects:
Narrow therapeutic index…
CNS confusion, fatigue… nausea, vomiting
have vision disturbances: yellowed vision or blurred vision

83
Q

Therapies that target the angiotensin system will….

A

Do one or both of:

Ace inhibitors to reduce angii levels

AT1 receptor antagonist to reduce angii effects

ACE inhibitors: decrease mortality rates in patients with heart failure

84
Q

Captopril effects

A

Ace inhib
decreases total peripheral resistance because there is less BP

so as a result there is an increase in heart performance

Decreases water reabsorption in kidneys…

Improves survival in patients with heart failure

Side effects: Dry cough, hypotension, anaphylactoid reactions, fetal malformations

84
Q

What does it mean if it ends in pril

A

it is an ace inhibitor.. prototype is captopril

IT INHIBITS angiotensin-converting enzymes

85
Q

Angiotensin 2 receptor blockers: Losartan

A

Helps BP.. blocks effects of angiotensin 2 at the receptor.

It doesn’t impact ACE activity

Side effects: hypertension, fetal malforms

86
Q

if it ends in LOL what does it mean

A

It is a beta-blocker…

87
Q

B1 cardiac (kidney)

A

also has impacts in kidney

increases force and rate of contraction in the heart + HR

88
Q

Beneficial effects of B-blockers + adverse effects

A

decreases O2 + HR, contractility

Improved survival

Adverse effects:
Balance, fatigue, heart failure, bradycardia, asthma (blockade in lung), depression, insomnia, nightmares, impotence, tachycardia

89
Q

Propranolol

A

nonselective beta antagonist

Sir James Black

90
Q

Metoprolol and bisoprolol

A

relatively selective beta antagonist

91
Q

Carvedilol

A

combined non-selective beta and a1 antagonist

has antioxidant properties

not good for patients with asthma, or COPD

92
Q

Angina is

A

the result of ischemia, it is pain… that is the result of ischemia in the heart tissue

93
Q

Ischemia

A

reduced blood supply.. less oxygen; it is a build-up of plaque inside the blood vessels and restricts the normal flow of blood.

94
Q

Atherosclerosis

A

build-up of plaque

95
Q

what are anginas symptoms

A

Chest pain; the pain is severe and crushing.

It can accompany or be a precursor to a heart attack

96
Q

Unstable angina

A

can happen at rest it comes on and off; it is unstable because it is a plaque becoming unstable… the plaque can start to break apart. It is often a prelude to a heart attack

What helps: nitrodilators, beta-blockers

97
Q

Angina pectoris

A

can happen when sitting at rest

Caused by a spasm of the coronary arteries

Drug therapy: calcium channel blockers

98
Q

Classic/ stable angina

A

triggered by physical activity, emotional stress, something where heart is beating faster

-always there under the right circumstances

-pain isn’t super long

therapy: Nitrocasodialators, Ca2+ blockers, beta-blockers, ranolazine

99
Q

Etiology of angina + reactive hypermia

A

as cardiac work increases; need more flood flow to keep up with the O2 demand

In angina: the coronary arteries cannot widen enough to let O2

reactive hyperemia: When artery dilation occurs to match O2 supply with demand

it results in hypoxia-induced vasodilator production

100
Q

Stable angina pectoris treatments

A

exercise

invasive surgeries

Pharmacological: Organic nitrates, Ca2+, Ranolazine

101
Q

Organic nitrates how does it get into the cell; and uses; and how does it work

A

converted to nitric oxide, which can then go into the smooth muscle… which then it can activate GTP, activates cGMP and when activates PKG

In SMOOTH MUSCLE, PKG phosphorylates Ca channels, which reduces Ca entry… which reduces contraction

USE: vascular smooth muscle but not a lot of effects in the heart

Main effect: opens up the veins and the volume of the venous system; feedback is slower to the heart (decrease cardiac O2 demand through action on veins) it does also open the coronary heart arteries but it’s not the main effect

102
Q

Nitroglycerin

A

Organic nitrate drug

There is a short and long-lasting form; under tongue, transdermal is long (/ointment)

Primary use: treatment of acute angina or peaks of pain in stable angina

pretty fast onset of action

Tolerance can occur; but they change time dosing

Longest form: a chemical derivative of nitro glycerin

-long onset of time; tolerance still a problem

Side effects: headache

103
Q

anything that drops BP

A

you can have reflex tachycardia

104
Q

Nitrate interactions with sidenafil (viagra)

A

Causes a build up of cAMP

can lead to extreme low BP and can cause heart attack because of decreased perfusion of heart

105
Q

summary points of nitrovasodilators

A

treatment of angina
They do not cause dilation of coronary arteries,

Major action is decreasing myocardial oxygen demand through venodilation

106
Q

Ca2+ inhibitors

A

PKA increases increases contractility (activation of Ca2+)

PKG decreases it (Inhibits Ca2+)

contrast to smooth muscle where they both decrease contractility (both inhibit)

they are good targets

107
Q

what do you want to do to help the heart

A

decrease blood flow and decrease demand

108
Q

Ca2+ channel blockers

A

dilate coronary arteries, and peripheral dilation to decrease BP

Ca2+ in the heart: Spike in sodium, and then a huge Ca2+ spike

so blocking decreases ability of heart to generate force

They can also slow the heart

Uses: treat stable angina, heart failure

109
Q

Nifedipine

A

treatment of angina

Ca2+ channel inhibitor

vascular version; impacts without heart rhythm disruption

less impact on cardiac calcium channels

110
Q

diltiazem/verapamil

A

treatment of angina

Ca2+ channel inhibitor

similar potency on arterial and cardiac muscle

Uses: angina, hypertension, arrhythmias

111
Q

Adverse effects Ca2+ channels

A

headache, dizzy, hypotension, peripheral edema, heart failure

112
Q

Beta-blockers impact with ca2+ in treating angina

A

Activation of b1 receptors increases PKA which increases the strength of contraction; beta-blockers block this impact which then DECREASES HR and cardiac contractility to decrease oxygen demand

113
Q

Ranolazine

A

treatment of angina

inhibitor of cardiac sodium and potassium channels

opposite of digoxin

more Na+ into the cell and therefore more Ca2+ out of the cell.

The lower amounts of Ca2+ cause a decrease in cardiac muscle contractility and O2 demand

No effect on HR or BP

DOES cross BBB

Sife effects: nausea and constipation.. but not a lot

114
Q

What are the two major types of blood flow

A

systemic and pulmonary

115
Q

Systemic circulation

A

Left ventricle of the heart, Every time the heart contracts, pressure shoots up, when it relaxes it almost goes to 0.

Fluctuation is limited to 120 and 80 in the arteries

After the capillaries, pressure is less and less

116
Q

How to calculate BP

A

cardiac output X vascular resistance

Increasing either increases BP

117
Q

What can impact BP Cardiac output factors

A

Preload (pressure that fills the heart)

Afterload (Pressure the heart needs to work against)

Neuroendocrine control of cardiac function (stress (HR increase), physical activity)

118
Q

What can impact BP Peripheral vascular resistance

A

Dilation/constriction of resistance arterioles (Neuroendocrine control, hormones, local regulation (running hard- dilates for O2))

Vascular diseases (arteriosclerosis)

119
Q

the relationship of blood volume and blood pressure

A

Blood volume is regulated by kidneys by adjusting urine production

-Increases blood volume=increases preload, increases cardiac output… then peripheral blood vessels contrast to maintain normal blood flow, which then you get higher BP.

If kidneys are unable to restore this then there is hypertension; damaging heart and kindey

Cycle of: vicious cycle, hypertension, peripheral edema, pulmonary edema

120
Q

Normal BP and what an increase means

A

normal: less than120 and less than 80

any tiny changes are impactful

121
Q

Hypertension factors

A

Primary hypertension: genetic, age, Risk factors: stress, smoking, obesity, physical inactivity

secondary: renal, endocrine, hormone treatment

others: Pregnancy induced pre-eclampsia, coarctation of the aorta

121
Q

Complications of hypertension in: cardiac

A

Left ventricle hypertrophy

Heart failure

Ischemic heart disease

Arrhythmias

122
Q

Complications of hypertension in: vasular

A

Arteriosclerosis

123
Q

Complications of hypertension in: cerebral

A

stroke

transient ischemic attack

Encephalopathy

124
Q

Complications of hypertension in: Renal and eye

A

Renal: Nephropathy

Eye: Retinopathy

125
Q

Consequences of Heart failure

A

kidney failure, Na+ water retention, excess amount of extracellular fluid, increased venous pressure, peripheral and pulmonary edema

Leg edema: fluid buildup in periphery

126
Q

When does stroke mortality risk double

A

for every 20/10 hg increase above 115/75

126
Q

Diuretics

A

drugs that increase urine output by kidneys they help get rid of extra Na+ and water which helps reduce: extracellular fluid volume, blood volume, edema, and BP

BLOCKS NA+

categorized by where they act

127
Q

What is nephron

A

it is the functional unit of the kidney, starts with the glomerulus and goes to the collecting tubule which has a cortical and medullary

128
Q

What are the steps of exretion

A

Filtration: movement of water from glomerulus to tubules

reabsorption: transport from urine to blood: from the outside world to the body

secretion: Transport of blood to urine, from body to outside world

129
Q

Proximal convoluted tubule; carbonic anhydrase inhibitor: acetazolamide

A

By Lumen, there is a reabsorption of NA+ and bicarbonate.

Mild diuretic, used for GLAUCOMA, not hypertension

increases urinary excretion of bicarbonate

Side effects: Acidosis, K+ depletion, avoid in ppl with hepatic cirrhosis risk of hepatic encephalopathy

130
Q

Loop diuretics; Furosemide

A

actions: inhibits reabsorption of Na+, K+, Mg2+, Ca2+ in the thick ascending limb

oral or parenteral, FAST

MOST POTENT DIURETIC

drug of choice for acute pulmonary edema due to heart failure

SIDE EFFECTS:
hypotension, hypovolemic shock

130
Q

Distal convoluted tubule- Thiazides

A

Na+/Cl- transporter inhibitor
Chlorothiazide is blcoed
Actions: orally active

MOST COMMONLY PRESCRIBED

Drug of choice for HYPERTENSION + Heart failure

reduces Ca2+ excretion

SIDE EFFECTS: thirst, increased blood cholesterol and glucose levels

131
Q

Collecting duct- potassium-sparing diuretcs

A

The antagonist: Spironolactone– it reduces Na+ reabsorption but INHIBITS the loss of K+

Action:
Oral

inhibits reabsorption of Na+ and secretion of K+

mild effect but if used in combination with others it can prevent K+ loss

Decreases mortality of heart failure

SIDE EFFECTS:
drug interaction

tummy hurt

132
Q

Mannitol- osmotic diuretics

A

Action:
intravenous

Used to reduce intracranial pressure, and remove of renal toxins.

Osmotically active.. filtered through glomerulus, but not reabsorbed

Mannitol promotes water diuresis

Side effects: dehydration, hypoantremia

133
Q

What does a blockage of the angiotensin system do

A

It has a similar effect to potassium-sparing diuretics; increases Na+ reabsorption…

Spironolactone is an aldosterone antagonist

134
Q

Angiotensin-converting enzyme (ACE) Captopril

A

Actions: effective antihypertensive agent

-increases K+ reabsorption, decreases aldosterone, decreases hypokalemia in patients on diuretics

-decreases proteinuria and slows the progression of renal insufficiency of renal insuff especially in patients with diabetes

Side effects: Dry cough, hyperkalemia, renal failure, skin reactions, contraindicated during pregnancy, angioedema

good bioavailability, eliminated by kidneys 2 hours,

135
Q

Renin- angiotensin system (angiotensin 2 receptor blockers ARBs) LOSARTAN

A

Actions: get rid of cough

selective to actions of Ang2, no effect on bradykinin

No effect on levels

more effective blockage of Ang2–AT1R

Side effects:

Hyperkalemia
renal failure
contraindicated during pregnancy
angiodemia

136
Q

Indications and complications of ACE inhibitors and ARBs

A

Indications: hypertension, heart failure, left ventricle hypertrophy, acute MI, renal disease, diabetes

Contraindications: Hyperkalemia, pregnancy, Bilateral renal artery stenosis

137
Q

Sprint trial

A

Examine the effect of intensive high blood pressure treatment, looking at intensive treatment and standard treatment

Intensive care has a 25% lower cardiovascular disease risk

Serious adverse events: way higher chance of hypotension and syncope when there is intensive care

138
Q

Management of high blood pressure- lifestyle

A

Physical activity, healthy diet, and weight reduction, less alcohol reduction can impact and make significant changes in bp.

139
Q

Hemostasis

A

Control of blood loss from a damaged vessel

It is initiated by vasospasm

rapid platelet adhesion to collagen and platelet aggregation

Reinforcement of platelet plug by fibrin

140
Q

What is secondary hemostasis

A

Clot formation to stabilize the plug

140
Q

What is primary hemostasis

A

damaged endothelial cells

transient vasoconstriction induced by endothelium secretion from endothelium

Exposed subendothelial components con Willebrand factor and collagen

Formation of the platelet plug

141
Q

Thrombosis what is it and what are the effects

A

Happens at site

Blockage of a blood vessel by formation of a blood clot inside the lumen

It depends on where thrombosis is..

effects:
Arterial (ischemia, infarction)

Venous (congestion, edema, ischemia, infarction)

142
Q

What is an embolism

A

Blockage of a blood vessel by solid, liquid, or gas at site..

when a clots breaks off and causes a problem

143
Q

how the blockage leads to a stroke

A

clot enters blood stream and travels towards brain

Blocks blood flow to part of the brain… starved of oxygen, it leads to a stroke

It can also lead to pulmonary embolism

144
Q

Anticlotting drugs work on

A

heart failure

pulmonary embolism

myocardial infarction

ischemic stroke

145
Q

Anti-clotting drug classes

A

Anti-platelet agents

Anticoagulants

Fibrinolytic agents

146
Q

antiplatelet Aspirin… mechanism of action

A

inhibits COX-1 (cox-1 is important for synthesis of platelet thromboxane)

Irreversible inhibitor

inhibits platelet aggregation

Adverse effect: Bleeding

147
Q

antiplatelet drug: Clopidogrel

A

Inhibtsi ADP binding which leads to inhibition of platelet actatioin

Oral

Prodrug, converted to active metabolite by CYP450

Adverse effect: bleeeding

148
Q

Coagulation cascade

A

Involves a lot of blood clotting; these are all proteolytic enzymes.

They are typically inactivated but can get activated, which can amplify the reaction to activate prothrombin, which then activates thrombin.

149
Q

Anticoagulants: Heparins

A

has negative charge

Parenteral administration: cant be oral

Adverse effect: Bleeding

have to monitor aPTT

Antidote: Protamine sulfate (positive charge)

Mech of action: Binds and activates antithrombin and increases the activity by 1000x

Uses: there is a low-molecular-weight heparin can be given outside of hospital

150
Q

Oral Anticoagulants: Warfarin

A

Action: inhibits of Vitamin K

It inhibits the re-activation of Vitamin K

ORAL

Binds to albumin (99%), and clearance is slow, and onset of action is delayed

narrow therapeutic index

Adverse effect: bleeding, can cross the placenta

Reversal is done by: stop taking, vitamin K, fresh frozen plasma, prothrombin complex concentrate

Drug interactions:

Asprin and heparin enhance the effects.

CYP450 activators reduce the effects

151
Q

What is cholesterol and what are its phases of absorption

A

Waxy, sterol lipid molecule

How it is absorbed: enzymes are in the mouth, stomach, and intestines

152
Q

How does micelles impact cholesterol

A

Critical for how cholesterol is absorbed.

153
Q

What are lipoproteins and what do they do

A

They are balls that carry and store cholesterol around..

It is a structure that is made up of lipids, cholesterol, and apolipoproteins (which is just a protein)

LDL (low density) is a major store of cholesterol in the body

HDL: high density

154
Q

What are some facts about the population for cholesterol

A

Millions of deaths (4.4) every year

37% / 78 million adults have “bad” cholesterol

7% of adolescents have high cholesterol

people with high = 2x the desk of heart disease

155
Q

what is artherocslerosis

A

It is BAD

can lead to the complete closure of arteries

unstable; can rupture and cause thromboembolic event

156
Q

Drugs that treat hyperlipidemia… what is their goal/ what are the two types

A

Reduce LDL blood levels

1- lower LDL… by inhibiting de novo production in liver

2- lower LDL and triglycerides

157
Q

Drugs that inhibit de novo cholesterol synthesis

A

drugs that end in statin

main: Atorvastatin, rosuvastin, simvastatin

158
Q

how do satin drugs work

A

HMG-coA reductase is blocked.

Lower de novo synthesis

decreases synthesis of LDL receptor

no effect on HDL

they also have other benefits: reduced inflammation, plaque stabilization

Adverse effects: Stomach disturbances, rash, headache, muscle toxicity, acute renal failure, cognitive difficulties, pregnancy issues

159
Q

guidelines for cholesterol

A

GOOD:
less than 40mg is low and a major risk factor

60 mg is lowers risk

LDL: raises heart disease risk

Borderline or high (130-160…165 or higher)

160
Q

Rhabdomyolysis… what is it

A

Breakdown of skeletal muscle tissue

161
Q

What is cholesterol like in the brain

A

accounts for 1/4th of total cholesterol

brain must produce its own cholesterol… like the liver it uses HMG-coA

Statins can cross BBB and can have cognitive effects.. (simvastatin, atorvastatin)

Less cognitive effects: rosuvastatin

Pharm exam 2 (1 decks)

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