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Pharma 2 > Lecture 3: Cardiac Pathology & Pharmacology > Flashcards

Lecture 3: Cardiac Pathology & Pharmacology Flashcards

1
Q

Fatty deposits (plaque) accumulate inside the artery wall: called what?

A

Atherosclerosis

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2
Q

Where does arthosclerosis start?

A

Tunica intima

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3
Q

Which layer of arteries is responsible for inflammatory responses?

A

Tunica Intima

You get plaque buildup which causes a tear in the tunica intima and causes an inflammatory response

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4
Q

What is an ischemia?

A

Reduction of blood flow (not complete blockage)

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5
Q

What diliniates myocardial infarction and ischemia?

A

Ishcemia is a partal blackage while infarction is complete

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6
Q

KNOW: Atherosclerosis causes progressive hardening and narrowing of the coronary, cerebral, and peripheral arteries
* **Its very systemic
* If you have cornary artery disease or likely have cerebral / peripheral artery disease as well (because its a systemic disease) **

A
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7
Q

KNOW: Atherosis (paste) = the fatty streak
* Consists of lipid-laden macrophages (foam cells) and smooth muscle cells

A
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8
Q

Sclerosis definition

A

Hardening

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9
Q

Does atherosclerosis indecrease or decrease blood vessel compliance?

A

Decreases

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10
Q

KNOW: Progressive hardening / narrow in atherosclerosis comes from that inflammatory response. You have those fibroblasts that are in the tunica intimia, and in order to repair itself it keeps lying down more collagen, which leads to the hardening, essentially forming a fibris cap of thrombi over advanced plaqyes that have developed on the endothelial lining

The thrombus can block the entire artery or break of

A
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11
Q

7 Recommendations for reducing the risk of coronary artery disease and cardiovasclar disease

A

1) Avoid cigarette smoking
2) Engage in appropriate PA
3) Maintain ideal body wt
4) Eat a healthy diet
5) Manage BP
6) Manage cholesterol
7) Manage fasting blood glucose

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12
Q

KNOW: Emerging risk factors for cardiovascular disease:
1) Lipid-releated biomarkers; lipoprotein(a) and high lopoprotein-associated phospholipase A2
2) Inflammatory markers; interleukin-6, C-reactive protein, and others
3) kidney related biomarkers; microalbuminuria
4) Air pollution
5) Mediastinal radiation (think cancer radiation)
6) Human immunodeficiency viral infection (HIV) - causes increase radiation
7) Elevated homocysteine levels
8) Abdominal sleep (increased infllamation)

I think really anything that causes increase inflammatory response

A
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13
Q

Atherosclerosis typically persents in one of four ways

A

1) Sudden cardiac death (typically from ventricular tachycardia –> ventricular fibriliation –> quivering of ventricle and not pumping enough blood out into body)
2) Chronic stable agina
3) Acute cornary syndrome (ACS)
* unstable angina
* ST-segment elevation myocardial infarction (STEMI)
* Non-STEMI
4) Cardiac muscle dysfunction

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14
Q

What is angina

A

Not enough blood to supply metabolic demands

Substernal pressure anywhere from epigastric area to jaw

Squeezing tightness or crushing

Imbalance in supply and demand of myocardial O2

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15
Q

How are angina symptoms controlled? (2)

A

Reducing the intensity of EX and taking sublingual nitroglycerin

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16
Q

angina that has a well established onset (I get over this HR and it starts) is called

A

Chronic stable angina

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17
Q

What is the most common syptom of acute coronary syndrome?

A

Chest discomfort for greater than 20 minutes

NOTE: its basically chest pain (kind of an umbrella term for lots of things)

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18
Q

Whats dangerous stable or unstable angina

A

unstable

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19
Q

Patient starts to have new chest pain 30 seconds into working out. What is this?

A

unstable angina

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20
Q

KNOW: Acute myocardial infarction can be STEMI or non STEMI

A
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21
Q

transient ischemic attack = stroke

aneurysm = outpocket of wall

A
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22
Q

KNOW: Coronary Artery disease = when atherosclerosis hits coronary arteries

A
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23
Q

Order of anginia that occurs w/ coronary artery disease

A

Unstable anginia –> resting anginia –> new onset anginia

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24
Q

Coronary Artery Disease causes elevation of what thing?

A

Troponin 1

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25
Q

What is peripheral vascular disease?

A

Atherosclerosis of arteries AND veins

issue to getting blood there

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26
Q

Where is PVD most common?

A

Extremities (legs mostly)

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27
Q

Why is someone w/ cornoary artery disease likely to also have peripheral vascular disease (PVD)

A

Because atherosclerosis (which causes both) is typially systemic

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28
Q

Arterial Occlusive Disease = Peripheral vascular disease

A
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29
Q

What is arteriosclerosis?

A

Atherosclerosis of arterioles

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30
Q

What do symptomes of acute coronary syndrome signify?

A

Acute mycardial infarction, as a result of insufficient supply to cardiac muscle

symptoms indicate whats coming

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31
Q

What is angina pectoris?

A

Chest pain

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32
Q

Is Angina Pectoris a symptom or a disaese? (Test)

A

Angina Pectoris is a symptom not a disease

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33
Q

What kind of ischemia is angina?

A

Transient ischemia of cardiac m

Its ischemia that omes and goes

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34
Q

Does angina cause damage to cardiac muscle

A

No

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35
Q

KNOW: Angina can be one of the first warning signs that there is a cardiac issue

A
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36
Q

4 causes of angina Test

A

1) Demand of myocardium > blood supply = ischemia (not enough blood flow) –> happens w/ EX because you need more blood supply to the heart
* With angina, the vessels narrow, meaning you have an increased demand on that tiny space it can get through but a decreased supply
2) Increase O2 needs to myocardium
3) Decreased blood flow to heart
4) Increased CO

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37
Q

Anginia equivalents (things that arent chest pain but indicate a coronary issue) TEST

A

1) Shortness of breath
2) Nausea
3) Fatigue
4) Diaphoresis - excessive sweating
5) Pain other htan chest

EX: someone exercising and sweating perfusly for the amount of EX they’re doing. Well that could indicate an angina equivalents, especially if that have any kind of cardiovascular issues in the past.

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38
Q

Exertional angina is also known as

A

Stable angina (comes on w/ EX)

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39
Q

TEST What do you do for someone with exertional (stable) angina that it comes on when they start exercising.

A

Record symptoms/vital and continue on w/ EX (maybe at a lower intensity)

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40
Q

TEST Do you continue EX w/ unstable angina?

A

Stop EX immediately.

NOTE: It could turn into stable angina, or it could lead to a myocardial infarction, we just dont know at this point. Needs to be tracked before we feel comfortable continuing EX.

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41
Q

TEST The question is essentially going to be diliniating between stable vs unstable angina, then your course of action.

A
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42
Q

Most common cause of angina?

What often triggers it?

A

Coronary artery disease (when artherosclerosis hits the coronary arteries)

Often triggered by EX or any kind of exertion because, exertion causes increased blood supply through a decreased area.

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43
Q

Remember, angina is just chest pain. However, it is typically caused by atherosclerosis. Name the different causes of angina
* How it happens w/ vessels
* How it happens w/ circulation
* How it happens w/ blood factors

A

Vessels: Atherosclerosis, hypertension, cardiomyopathy, CAD

Circulation: Arrhythmias, coronary spasms, aortic stenosis, hypotension, bleeding (trauma)

Blood factors: Anemia, hypoxia, polycythemia (wasnt really covered)

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44
Q

TEST a pt w/ chest pain doesnt always have angina. Know the differential diagnosis charts and be able to dilinate them out.

A

Probs focus mostly on s/s

pleural rub = sound w/ stethascope

RR = respiratory rate

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45
Q
A
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46
Q

TEST Reasons to stop or modify EX: - With CV Hx or angina
1) New onset of easily provoked chest pain (unstable angina)
2) Increasing episodes/intensity /duration of angina (unstable angina)
3) Discomfort elsewhere in the upper body
4) Syncope, dizziness, light-headedness
5) Severe sydden dyspnea (difficult breathing)
6) Severe fatigue or muscle pain
7) Nausea or vomiting
8) Back pain during exercise - further investigate if they’ve had cardiac risk factors that could be leading to this
9) Bone/joint pain or discomfort during or after EX
10)

A
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47
Q

TEST Symptoms of angina (15)

A

1) Temporary squeezing
2) Burning
3) Pressure
4) Heartburn
5) Indigestion
6) Chocking
7) Pallor (think turning blue_
8) Cyanosis
9) Cold
10) Moist skin
11) >6 arrhythmias (palpations or irregular beats) per hour
12) Oxygen saturation <90%
13) Resting HR 130 beats/mm (because heart rate trying to get CO back up)
14) Fall in systolic BP with increase workload (10 mmHg or more)
15) Rise in systolic BP > 250 mmHg or diastolic > 115 mmHg

** If you have any of the above + angina, discontinue exercise**

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48
Q

Angina scale

A
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49
Q

Will ECG be normal or abnormal with angina?

A

Normal, angina isnt affecting the electrical part unless its actually stopping the heart

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50
Q

For documentation what is our mnuemonic / fill in

A

OLDCART
* Onset
* Location
* Duration
* Charactersitics
* Accompanying symptoms
* Radiation
* Treatment

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51
Q

Drugs used to treat angina pectoris (4)

A
  1. Organic Nitrates = first line of defense
  2. Beta-Adrenergic Blockers
  3. Calcium Channel Blockers
  4. Anticoagulants

typically prescribed when you have something else + angina, however, you typically have angina + another pathology going on thats leading to angina
* Remember, angina is a symptom, not a pathology

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52
Q

What is the MOA for Organic Nitrates?

A

Dilate peripheral blood vessels, decreasing peripheral resistance so the afterload is decreased, making it easier for the heart to pump into the systemic vascular supply

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53
Q

How are organic nitrates typically administered and how long does it take to see affects?

A

Adminustred sublingally

Therapeutic effects within 2 minutes

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54
Q

What effect does the sublingual adminstration of organic nitrates spare the patient?

A

First pass effect

when taken orally it goes through GI system and into liver which breaks down medication

Sublingually, it just disolves and goes right into blood system, which is why its much faster than taking orally

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55
Q

Adverse effects and why nitro

A

Primary: HA, dizziness, orthostatic hypotension
* This is because the blood vessels are dilated, so, HA because increased BF, and dizziness / hypotension because blood pressure cannot be maintained w/ diliated vessels

Nausea is another possible side effect

NOTE: Transdermal is another possible application (patch on skin), however, isnt recommend because they can build a tolerance
* This is typically for people who need it all the time

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56
Q

Why would you want to sit a patient down before adminsitration of organic nitrates?

A

Because vasodilation causes hypotension, which can lead to them falling and causing some injury

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57
Q

TEST Sublingual organic Nitrates should be kept how
* Discard after how long?
* how many till you call 911

A

In OG bottle
* ROOM temp, no direct light
* Discard after 3 months

should be in original glass bottle, O2 starts breaking it down along w/ sunlight

Super important to discard after 3 months because if they have angina they need this medication to work

If they have adminstered 3 than call 911

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58
Q

What do Beta blockers do?
* How do they work?

A

Block beta-1 receports on the myocardium (act as antagonists)

Block HR and force on contractions, which decreases the workload of the heart and demand of O2

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59
Q

Beta blockers suffix

A

olol

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60
Q

What do selective beta blockers target?

What do non-selective beta receptors target?

A

Selective = Beta 1 receptors on the heart
* 1 heart –> targets the heart

Non-selective = block both beta 1 and beta 2 receptors
* 2 Lungs –> targets the lungs

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61
Q

TEST Patient taking non-selective betablockers is experienceing brochoconstriction, how can this be fixed?

A

Put them on selective beta blockers that only target the heart

go back to slide 35 and recap here

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62
Q

KNOW: If beta blockers are taken daily they will blunt HR/BP, so you can’t use BP/HR to see how they’re responding to EX. Going to have to use RPE scale (increased subjectivity)

A
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63
Q

Calcium channel blockers suffix
* 2 exceptions

A

End in Pine

Diltiazem
Verepamil

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64
Q
A
64
Q

How do calcium blockers work?
* does it cause vasodilation or constriction
* Does it increase or decrease oxygen supply

A

Block entry of calcium into the smooth muscle within the vessels, which stops that interaction between actin and myosin because the troponin is never displaysed meaning that the interaction never takes places.
* Essentailly w/ this interaction relaxion/vasodilation occurs which inxcreases oxygen supply to myocardium (because of increased BF)

65
Q

Why are whirlpools / hot tubs contraindicated when a pt is taking calcium channel blockers?

A

because calcium channel blockers cause vasodilation, and the hot tub / whirl pool also cause vasodilation, meaning there is entirely too much vasodilation occuring.
* they’re already having vasodilation on the inside, now they’re having it on the outside, and this can lead to a fall

66
Q

Adverse effects of calcium channel blockers

A

HA, flushing, feelings of warmth, dizziness, peripheral edema, nausea, disturbances in cardiac rhythm, which can lead to reflex tachycardia

67
Q

What ia reflex tachycardia?

A

HR increasing due to taking calcium channel blockers

A cardiac arrhythmia that occurs when the heart beats faster in response to decrease BP or blood flow) - and that vasodilation that calcium channel blockers cause = decrease in BP

68
Q

True or false: patients taking nitroglycerine for angina should avoid PA, as exercise can worsen their symptoms

A

False

While exercise can worsen those symptoms, PA can help manage and decreaase those symptoms.
* They just need to know how to exercise the correct way

69
Q

How should nitrogylcerine tablets be stored:
a) in the refigerator
b) in a warm and humid environment
c) in their OG container (to know when it expires [3 months]), away from light and moisture
d) in a pill cotainer

A

C

70
Q
A
71
Q

Force exerted on wall of vessels (arteries and arteroles)

A

BP

composed of systolic/diastolic

72
Q

How is BP controlled

A

Hormones

73
Q

RAS system controlled BP in short term or long term pathways?

A

Long term

74
Q

Baroreflex controlled BP in a short term or long term manner?

A

Short term

75
Q

To ways BP is controlled?

A

Baroreflex (short term)
RAS system (long term)

76
Q

What does the baroreflex respond to?

A

Change in pressure (responds mostly to peripheral vascular resistance) - this is if you have blood loss and need a quick increase in BP, to make sure all vital organs are getting blood. Its quick, which is why its short term

77
Q

Blood comes into the heart and fills the ventricle causing end diasoltic volume. What two things increase it?

A

1) Hypervolemia
2) Regurgitation of cardiac valves

78
Q

What can increase BP, preload or afterload?

A

Afterload (its the resistance taht the left ventricle must overcome to circulate blood

79
Q

What two things increase afterload?

A

1) Hypertension
2) Vasoconstriction

Basically the LV has to overcome more resistance when these two things are taking place, and it increases BP

80
Q

What external organ in affect stroke volume?

A

Stroke volume is influenced by the kidneys desire to maintain homeostasis (I think through RAS)

81
Q

Is SV affected by preload or afterload?

A

Both

82
Q

What 3 things affect SV?

A

1) Preload
2) Afterload
3) Contractility (how hard it pumps to get the blood out)

83
Q

TEST Shes going to ask about the things that affect preload/afterload/contractility. Learn the right side of this chart well

A
84
Q

4 vasoconstricting hormones

A

1) Norepinephrine
2) Epinephrine
3) Angiotensin II
4) Vasopressin

85
Q

What percent of the population is hypertensive?

A

50%

Silent killer, you don’t have symptoms until its really bad

Leading cause of lost years of quality of life

86
Q

What is the most common kidn of hypertension: Primary (essential), secondary, labile?

A

Primariy (90-95% of population has this one)

87
Q

What causes primary (essential) hypertension?

A

No known cause, idiopathic

88
Q

Which part of the vessels is increased w/ primary hypertension?

A

Increased arteriole resistance

89
Q

What causes secondary hypertension

A

Occurs in the presence of a disease

Think, the person having a stroke, or spinal cord injury, liver issue, etc… anything that has caused damage

90
Q

What is labile hypertension?

A

elevation of blood pressure with normal readings - think white coat syndrome
* might be increased now but normal later

91
Q
A
92
Q

What is malignant hypertension?
* What can it load to?

A

Same thing as a hypertensive crisis - marker of elevated BP reading of > 180 mmHG for systolic AND/OR > 120 mmHg diastolic

Leads to targeted organ damage

Stop EX here, if they’ve having symptoms they’re going straight to the ER

93
Q

KNOW: with hypertension sympathetic tone increases vasoconstriction of blood vessels
* arteriole resistance is increased

artioles regulate the pressure of blood going into capillary bloods where O2 exchange takes place. If the arterioles are constricted the blood will be flowing too quickly through it which will decrease the amount of gas exchange taking place (less O2) which will lead to an increase in the O2 demand

A
94
Q

Explain the Renin-Angiotension-Aldosterone system (RAS)
* What triggers it to turn on?
* is it a long term or short term
* Once angiotensin II is in the body what 2 things start happening

A

Turned on w/ a drop in BP

Signals kidneys to release renin (which is an enzyme)

Renin goes and splits angiotensin (which is in the liver) into angiontensin 1 (which is an inactive hormone)

Angiotensin 1 goes to the lungs and is converted to angiontesin 2 by the angiotensin converting enzyme (ACE)

Angiontesin II is a powerul vasoconstrictor

once angiontesin II is in the body the adreal gland will start producting aldosterone and pituitary gland releasing the antidirectic hormone (ADH)
* both of these help with sodium reteintion and excretion of patissum
* That sodium retetntion is going to cause increased water retention which is going to cause vasoconstriction (I think she means increased BP)

Angiotensin II being in the blood stream also leads to vascular remodeling and hypertrophy; and decreased vascular compliance

Long term pathway

95
Q

This chart is showing secondary hypertension

Impaired renal function: If kidneys arent working well they might just be producing a lot of renin which is causing increased hypertension

This renin will cause inappropriate activation of hormones that regulate salt and water excreetion by the kidney, causing increased BP

Excessive activation of the sympathetic NS can also lead tot his

Natriuresis = process of the kidneys excreting large amounts of sodium in urine, which lowers sodium levels in the blood

A
96
Q

Who is high BP most common in (race)

A
97
Q

What is the highest risk factor for cardiovascular disease mortality (thing that leads to dying of cardiovascular disease)

A

Hypertension

98
Q

KNOW: risk factors for cardiovascular disease = alcohol, obesity, oral contraceptives (women)

Primary hypertension risk factors
* Modifiable = smoking
* non modifable = age, gender, ethnicity

Secondary hypertension risk factors
* Chronic kidney disease
* Drug induced/releated

A
99
Q

S/S of hypertension

A

1) Often asymptomatic (called silent killer)
2) HA
3) Vertigo
4) Flushed face
5) Spontaneous epitaxis (nose bleed)
6) Blurred vision
7) Nocturnal urinary frequency

KNOW: If someone is taking medication for hypertension you really don’t want them stopping it because they’re typically asymptomatic and won’t see a difference even though its elevating
* NOTE: they often won’t like taking the medication and will want to stop

100
Q

Best way to take blookd pressure for someone with labile hypertension?

A

24 hour blood monitor

can also take average of two or more readings taken on separate occasions

101
Q

KNOW: labortoary tests will help more for secondary hypertension or anything else going on in the heart
* Think CBC, urinalysis, serum electrolytes, lipid profile and creatine, fasting blood glucose, thyroid stimulating hormone

A
102
Q

Most important non pharmaceutical treatment for hypertension

A

1 Physical activity or EX

  • what we do

Can also do:
* Weight contorl
* Dietary modifications
* Decreasing use of alcohol and tobacco
* Behavior modification and stress manageemnt

103
Q

What is the first line of defense for hypertension (anti-hypertensives)
* what are the other ones

A

Diuretics (help excrete the fluid) - first line of defense

sympatholytic drugs
vasodilators
Angiotensin-converting enzyme inhibitors
calcium channel blockers - these are ACE inhibitors - we want to stop that whole process to stop because it increases BP

104
Q

TEST: What is our goal BP for someone on anti hypertensives (drugs that lower BP)

A

130/80 mmHg

goal is to achieve and maintain the lowest sage arterial blooc pressure without side effects

105
Q

Antihypertensive drugs overview

A
106
Q

What drugs increase the formation and excretion of urine?

A

Directics

Ability to increase renal excretion of water and sodium, thus decreasing fluid volume within the vascular system

107
Q

Why won’t patients no want to take diuretics?

A

Increases urination (they call it their “water pill” )

108
Q

Diuretics work directly on which organ?

A

All diuretics exert their effects by acting directly on the kidney to increase water and sodium excretion
* Less water in the vessels = decreased BP

NOTE: This is the first drug used in hypertension and is inexpensive and works well in mild-to-moderate hypertension

109
Q

Diuretic drugs are subdivided into 3 categories. What are they?

which one is most common

A

1) Thiazide Diuretics (most common)
2) Loop Diuretics
3) Potassium-Sparing Dieuretics

110
Q

What is the advantage to potassium-Sparing diuretics and how does it work?

A

Advantage = reduces potassium loss and preventing hypokalemia (basically decreases cramps because it doesnt have the potassium loss that the others do)

They prevent the secretion of potassium into the distal tubule of the kidney –> which then it would be excreted into the urine

111
Q

Thiazide diuretics act primarily on which portion of the which part of the kidney? and what do they do?

A

Act primarily on the early portion of the distal tubule of the nephron, where they inhibit sodium reabsoportion.

By inhibiting reabsorption, more sodium is retained within nephrone, creating osmotic force that retains more water in the nephron –> to be excreated as urine

NOTE: This is the most common dieurteic

112
Q

Loop Diuretic
* Where does it act?
* how does it work?

A

Act primarily on the ascending limb of the loop of henle

Exert effect by inhibiting the reabsorption of sodium and chloride from the nephron, preventing reabsorption of water that follows electrolytes

113
Q

Dieuretics - however, shes going to primarily be focusing on adverse effects

what do thiazide diuretics end in?

A

Ide/One

114
Q

What is the most serious adverse effect of diuretics?
* name some others (4)

A

Fluid depletion and electrolyte imbalance (hyponatremia / hypokalemia)

Orthostatic hypotension - due to decreased fluid
GI disturbances and weakness-fatigue
Changes in mood and confusion - more applicable for older adults

115
Q

Hyponatremia

A

Sodium depletion

116
Q

Hypokalemia

A

Potassium depletion

117
Q

Patient has a sudden decrease in BP. What pathway takes over to restore BP

A

Baroreceptors

118
Q

Diuretics can cause a sudden decrease in blood volume (removed the fluid portion) and may cause a reflexive increase in cardiac output and peripheral vascular resistance because of the baroreflex activation
* The RAS system may also be activated causing further vasoconstriction

A
119
Q

What is the most commonly prescribed diuretic?

A

Thiazide

120
Q

Which two diuretics impair glucose and lipid metabolism, creating an issue for pts w/ type 2 diabetes?

A

Thiazide and Loop

So I guess prescribe potassium-Sparing Diuretics?

121
Q

TEST two main things that beta blockers do

A

Decrease HR

Decrease force of myocardial contraction (contractility)

122
Q

What do betablockers do to CO?

A

Decrease it

CO = SV*HR and both of those things are decreased w/ this drug

123
Q

which part of the autonomic NS is changed w/ beta blockers and explain the mechanism.

A

Decreases sympathetic activity

It does this via
1) A central inhibitory effect on the brainstem
2) Decreased renin release from kidneys and within CNS
3) Impaired sympathetic activity in ganglia or at presynaptic adrenergic terminals
4) increased baroreceptor sensitivity

can be any combination of the above

it can complement other antihypertensives
* A combination of 3 drugs for hypertension is typically the best

124
Q

Recent research shows a combination of which 3 drugs is best for hypertension.

A

calcium channel blockers
Anti-directs
Ace inhibitors

125
Q

How to take someones BP

A

Feet uncrossed
Arm should be at heart level - SUPPORTED

Want them to be at resting position., not right after they’ve been walking around

126
Q
A
127
Q

TEST What drug is bad for people w/ asthma and why?

A

Non selective beta blockers because they bind to the B2 receptors in the lungs and cause bronchoconstriction

128
Q

KNOW: Beta blockers are a sympathetic drug

A
129
Q

KNOW: alpha blockers = sympathetic drug

A
130
Q

How do Alpha blockers work?

A

Alpha blockers work by blocking alpha 1 adrenergic receptors on vascylar smooth muscle, will promote decrease in vascular resistance

I think its a symapthetic drug because in a sympathetic response these alpha receptors are turned on, but now they can’t be turned on, which blocks vasoconstriction from happening.

131
Q

Which drug would be recommended for BP if the pt has diabetes?

A

Alpha blockers, because they have the ability to improve blood lipid profiles (decreased triglycerides and total cholesterol, increased high density lipoprotein-cholesterol ratoi) and produce favorable effect on glucose metabolism and insulin resistance

remember, beta blockers are bad because they can impaire glucose breakdown, leaving it in the blood stream

132
Q

KNOW: There are newer alpha receptor drugs that are better because they’re slower release, keeping from having that suddent drop in BP (decrease orthostatic hypotension)

A
133
Q

What other pathology is treated w/ alpha receptors?

A

Benign prostatic hypertrophy because decreases sympathetic mediated contraction of smooth muscle in the prostate gland
* reduction of muscle decreases constriction of ureter, improving urinary flow and ability to empty bladder
* because alpha receptors get rid of some of that sympathetic tone

134
Q
A
135
Q

Adverse effects of alpha blockers

A

1) Reflex tachycardia due to a decrease in peripheral vascular resistance –> prevented by administering with a beta blocker (slows down HR)
2) Increased risk of cardiac disease, including congestive heart failure (because it can increase the workload on the heart because of that vasodilation, causing more of that preload to the heart)
3) orthostatic hypotension

136
Q

KNOW: Presynaptic Adrengeric Inhibitors = sympathetic drug

A
137
Q

How do presynaptic adrengeric inhibitors work? (for hypertension)

what are adverse effects

A

Inhibits the release of noreepinephrine from the presynaptic termins of peripheral adrenergic neurons
* without epi/nor theres decrease vasoconstriction

Adverse: - these are basically the same for the anti hypertensive medications
*Orthostatic hypotension (too much of a decrease in BP)
GI distrubances such as nausea, vomiting, and diarrhea

138
Q

KNOW: centrally acting agents = sympathetic drugs

A
139
Q

How do centrally acting agents work as an anti hypertensive drug?

A

Work on vasomotor center in your brainstem (centerally not peripherally) which is the BP regulatory center
* Stimulation results in decrease in sympathetic discharge of heart and vasculature

140
Q

Clonidine is a centrally acting agent. However, whats its other use? (2)

A

seziure / anxiety

141
Q

Adverse effects of centrally acting agents

A

Dry mouth, dizziness, and sedation (sleepy)

142
Q

Ganglionic blockers = sympathetic drugs

A
143
Q

How do ganglionic bockers work as an antihypertensive drug?
* When are they used?

A

Decrease systemic sympathetic activity

Essentially nicotinic cholinergic antagonists, which block transmission at the junction between presynaptic and postsynaptic neurons in sympathetic and parasympathitc pathways

Used to decrease BP rapidly in certain emergencies such as acute aortic dissection or autonomic crisis in spinal cord injury.

144
Q

adverse effects of ganglionic blockers

A

GI discomfort
Urinary retention
Visual disturbances
orthostatic hypotension

high doses, neuromuscular blocking activity

145
Q

vasodilaters are antihypertensive drugs. How do they work?

A

Exert an inhibitory effect directly on vascular smooth muscle cells
* causing them to dilate so more blood can get through

146
Q

Adverse effects of vasodilators?

A

1) Reflex tachycardia - due to the increased blood supply back to the heart
2) Dizziness, postural hypotension, weakness, nausea, fluid retention, and HA

147
Q

TEST Vasodilators drugs (5)

A

Diazoxide (Hyperstat)
Hydralazine (Apresoline)
Fenoldopam (Corlopam)
Minoxidil (Loniten)
Nitroprusside (Nitropress)

148
Q

How do calcium channel blockers work as anti hypertensive drugs?

A

Block calcium entry into vascular smooth muscles cells

Essentially its blocking the binding of calcium to troponin which means that actin and myosin heads cant articulate together, meaning that the sacromeres within the smooth muscle cannot contract, meaning decreased muscle tone, leading to more vasodilating = decreased BP

149
Q

KNOW: calcium channel blockers lead to vasodilation and decreased vascular resistance, heart rate, and myocardial contraction force –> which reduces cardiac workload

A
150
Q

Adverse effects of calcium channel blockers

A

1) Excessive vasodilation leads to swelling in feet and ankles - this can happen in any drug that causes vasodilation
2) Orthostatic hypotension - one of the most common side effects - make sure they’re sitting
3) Abnoramilities in HR, reflex tachycardia
4) Dizziness, HA, nausea

150
Q

What is the suffix for calcium channel blockers? except which 2

A

pine

Diltiazem
Verapamil

151
Q
A
152
Q

ACE inhibitors end in what suffix

A

Pril

153
Q

how do ACE inhibitors work

A

They keep angiotension I from converting into angiotensin II because it stops that angiotensin converting enzyme, meaning that this system cannot increase BP

154
Q

What is the name of our only direct renin inhibitor

A

Aliskiren (Tekturna)

155
Q

Angiotensin II receptor blockers end in what suffix?

A

rtan

156
Q

TEST When taking any medication that causes vasodilation (or blocks vasoconstriction) avoid activities producing widespread vasodilation (or use them very cautiously)
* think activities like whirlpool / hottub
* Exercise may cause vasodilation in skeletal musculature, which may potentiate the peripheral vasodiltion induced by antihypertensive drugs

If the patients takes beta blockers, cardiac responses to EX may be somehwat blunted becayse the myocardial repsonse to sympathetic stimulation will be deiminshed –> so you can’t use these measures to test level of exerction
* Going to have to go w/ RPE

A
157
Q

PT implications

Baseline BP should be taken and monitored
* great way to objectify interventions

PT education
* Diet
* Monitorying BP
* Fluid intake
* Stress level
* Pain could also be a stressor

Rehab concerns:
* orthostatic hypotension
* Weakness/fatigue
* confusion/mood changes
* Decreased maximal exercise capacity (beta blockers)
* edema and reflex tachycardia (vasodilators)

A

Pharma 2 (12 decks)

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