Cardiac 1 Flashcards

1
Q

Diseases of the veins

A

Varicose veins
Chronic venous insufficiency (CVI)
Superior vena cava syndrome (SVCS)

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2
Q

Diseases of the arteries

A
Hypertension
Orthostatic hypotension 
Aneurysm 
Peripheral vascular disease 
    Buerger, Raynauds 
    Atherosclerosis 
    Peripheral artery            
    disease 
Coronary artery disease 
MI
Acute coronary syndrome
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3
Q
Varicose veins 
causes 
predisposing factors 
risk factors 
clinical features
A

A vein in which blood has pooled
Damage to valve, causing malfunction
Trauma, gravity
Female, age, family hx, obesity, pregnancy, DVT, previous injury
Distended, tortuous, palpable vessels, edema

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4
Q

Varicose veins tend to happen in what veins?

A

Superficial veins

Saphenous vein

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5
Q
Chronic vein insufficiency 
leads to?
causes
risk factors 
clinical features
A

Inadequate venous return over a long period of time
Leads to venous hypertension, blood stasis, and tissue hypoxia in lower extremities
Varicose veins and valvular incompetence
Obesity
Edema up to knee, hyperpigmentation

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6
Q

Chronic venous insufficiency complications

A

Inflammation, fibrosclerotic remodeling, any trauma/pressure can lead to ulceration
Venous Stasis Ulcer
Leads to high risk of infection

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7
Q

Venous/Arterial disease examples

A

Thrombus
Thromboembolus or Embolus
Embolism
DVT

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8
Q

Thrombus

A

Blood clot attached to vessel wall

More common in venous system

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9
Q

Thromboembolus or Embolus

A

A detached/moving thrombus

Moves freely

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10
Q

Embolism

A

The obstruction of a vessel by an embolus

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11
Q

DVT

A

occurs in lower extremity

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12
Q

Venous vs. Arterial emboli

A
Venous 
    Origin: DVT, right 
    heart 
    Destination: 
    pulmonary (PE)
Arterial 
    Origin: left heart (post 
    MI, valve disease, 
    endocarditis, 
    dysrhythmias)
    Destination: lower 
    extremities, coronary 
    arteries (MI), cerebral 
    vasculature (stroke)
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13
Q

Virchow’s Triad

Etiology

A

Factors that promote thrombus formation
Stasis of blood flow
Endothelial injury
Blood hypercoagulability

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14
Q

Virchow’s Triad

Stasis of blood

A

prolonged bedrest
dependent extremities
immobilization

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15
Q

Virchow’s Triad

Endothelial injury

A

trauma (fractures)
caustic intravenous medications
previous thrombus

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16
Q

Virchow’s Triad

Blood hypercoagulability

A
inherited coagulopathy 
medications 
malignancies 
pregnancy 
oral contraceptive/HRT
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17
Q

DVT locations

A

popliteal site most common

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18
Q

DVT clinical features

A
Insidious - asymptomatic 
Swelling from venous pooling 
Edema with obstruction
Pain (most common)
   walking increases 
   Homan's sign
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19
Q

Homan’s sign

A

dorsiflexion of the foot
not a reliable test and is contraindicated
increases chance of thrombus being thrown into blood system

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20
Q

DVT complications

A
Most dissolve 
High risk of PE
   where it lodges is  
   an important factor 
   in seriousness 
   size as well
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21
Q

DVT prevention

A
Early ambulation (any possible movements)
Pneumatic devices (SCDs)
Prophylactic anticoagulation
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22
Q

DVT diagnosis

A

D-Dimer (typically high in those that have a DVT)

Doppler

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23
Q

DVT treatment

A

Anticoagulants
Thrombolytic therapy
Inferior vena cava filter

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24
Q

Superior vena cava syndrome

A

progressive occlusion of the superior vena cava that leads to venous distension in the upper extremities and head

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25
Q

Superior vena cava syndrome

causes

A

Bronchogenic cancer (tumors)
Invasive therapies (pacemakers, catheters (central venous and pulmonary artery))
Lymphomas
CA mets

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26
Q

Superior vena cava syndrome

symptoms

A
Edema
Venous distension in UE/face
Fullness in head 
Headache
Visual disturbance 
Changes in LOC
Skin head/neck: purple, tight, respiratory distress
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27
Q

Superior vena cava syndrome

diagnosis

A

X-ray
CT
MRI
US

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28
Q

Superior vena cava syndrome

treatment

A

Malignancy - treatment of cancer

Nonmalignancy - bypass, thrombolysis, balloon angioplasty, stents

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29
Q

Hypertension
definition
incidence

A

Consistent elevation of systemic arterial blood pressure
1 in 3 U.S. adults;
>2/3 over 60
in children

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30
Q

Hypertension

risk factors

A
Family hx
Advancing age
Black race
Gender: 
   M>W before 55
   W>M after 55
Smoking
Obesity, DM, sedentary
Diet - heavy alcohol 
Metabolic syndrome
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31
Q

Metabolic syndromes

A

Obesity
HTN
Dyslipidemia
Glucose intolerance condition that increases risk of HD, stroke, and DM

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32
Q

Types of HTN

A

Primary
Secondary
Complicated
Hypertensive Crisis

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33
Q

Primary HTN

A
Idiopathic - multiple pathologic mechanisms 
92-95% of cases 
SNS hyperactivity
Overactive RAAS
Defect in natriuresis
Insulin resistance (obesity hormones)
Inflammation and endothelial dysfunction
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34
Q

Clinical manifestations of HTN

A
Often no signs or symptoms (early) - silent disease 
Headaches 
Dizziness
Blurred vision
Tinnitus
Anxiety
Chest pain
SOB
Nausea
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35
Q

HTN evaluation

A

Diagnosis: requires measurement on 2 separate occasions
Conditions: at rest for 5 min, seated, arm at heart level, no caffeine or smoke within 30 min
May do 24 hr BP monitoring
Can keep a log and self check

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36
Q

Complicated HTN

A

Prolonged high pressure on vessel walls causes thickening and stiffening
Causes arterial smooth muscle hypertrophy and hyperplasia
Vessel lumen narrows
Vessel thickening - increases smooth muscle contraction
Vasoconstriction - increased pressure

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37
Q

HTN Heart complications

A
Increased workload
Increased afterload
LV hypertrophy
Accelerated CAD/HF
Decreased myocardial O2
Aorta - aneurysms
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38
Q

HTN Vessel complications

A

Extremities: arterial vessels of lower extremities
Accelerated atherosclerosis results in PVD/PAD
May have no symptoms then develop pain, loss of circ - amputation
Results in intermittent claudication

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39
Q

HTN Renal complications

A

Decreased renal blood flow

Increased RAA

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40
Q

HTN Brain complications

A

Reduced blood flow
Ischemia
Vessel damage/rupture

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41
Q

HTN Eye complications

A

Retinal damage

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42
Q

Hypertensive Crisis

Malignant HTN

A

Rapidly progressing HTN with DBP >140

A medical emergency

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43
Q

Hypertensive Crisis

causes

A

complication in pregnancy
cocaine/amphetamines
adrenal tumors (pheochromocytoma)
drug/alcohol withdrawal

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44
Q

Hypertensive Crisis

symptoms

A

chest pain
blurred vision
SOB

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45
Q

Hypertensive Crisis

consequences

A

HTN -> cerebral arterioles/capillaries unable to regulate blood flow -> fluid shifts = cerebral edema, dysfunction, cerebrovascular accident
Also cardiac failure, kidney failure, retinopathy

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46
Q

Hypotension

A

Decrease in SBP of at least 20 mmHg or DBP of at least 10 mmHg within 3 min of moving to standing
Neurogenic - often seen in older adults (risk for falls)
Normal compensation - arteriolar/venous constriction and increased HR
Abnormal: blood pools, BP drops
Symptoms: dizziness, blurred vision, fainting, nausea, weakness

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47
Q

Aneurysm

definition

A

Localized dilation or outpouching of a vessel wall or cardiac chamber

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48
Q

Aneurysm

weakened medial layer

A

Atherosclerosis (most common)
Genetic/congenital
HTN, smoking, diet
Collagen-Vascular disorders (Marfan)

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49
Q

Types of Aneurysms

A
True
   Involve all 3 layers  
   of the arterial wall
   Weakening of the 
   vessel wall
   Fusiform/saccular
   Can happen on 1 or 
   both sides of the wall
False
   Extravascular 
   hematoma that 
   communicates with 
   the intravascular 
   space
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50
Q

Aneurysms

affected sites

A

Abdominal aorta - 75%
Thoracic aorta
Large peripheral arteries
Cerebral

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51
Q

Aneurysms

clinical features

A

Often asymptomatic
Detected by US, CT, MRI
Sx indicate large aneurysms or rupture and depend on site
Rupture: severe pain and hypotension

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52
Q

Aneurysms

treatment

A

Meds: BP reduction

Surgery (graft)

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53
Q

Drugs for Hypertension (Angina)

A

FIRST LINE: Diuretics, ACE Inhibitors, ARBs, Calcium Channel Blockers
SECOND LINE: Beta Blockers, Adrenergic Agonists/Antagonists, Vasodilators/Nitrates

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54
Q

Monitoring for any drugs that affect BP

A
BP (both arms / lying, sitting)
HR (at home too)
Intake/Output 
Electrolytes
ECG
Weight - BMI
Report: sx of liver dysfunction - weight gain, edema, SOB
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55
Q

Review lifestyle modifications for HTN

A
Sodium restrictions
DASH diet
Alcohol restrictions
Smoking cessation
Aerobic activity
Weight loss
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56
Q

Volume x Vasoconstriction =

A

Hypertension

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57
Q

Cardiac output x Peripheral resistance =

A

Arterial pressure

58
Q

First line HTN drug classes

A
Angiotensin converting enzyme (ACE) inhibitors - prils
Angiotensin receptor blockers (ARBs) 
- sartans
Calcium channel blockers (CCBs)
- pines
Thiazide diuretics (used in combo)
59
Q

ACE inhibitors

A

reduce blood volume and is a vasodilator

60
Q

ARBs

A

reduce blood volume and is a vasodilator

61
Q

CCBs

A

vasodilator

62
Q

Thiazide diuretics

A

reduce blood volume

best at reducing BP, improving HTN related mortality, least risky, cheapest

63
Q

ACE inhibitors

MOA

A

Inhibit conversion of angiotensin I to angiotensin II:

  • Arteriole vasodilation, less effect on veins
  • Reduction of blood volume - reduction in aldosterone
  • Reduction of remodeling: cardiac and vascular hypertrophy (redistribution of mass)
64
Q

ACE inhibitor

Drugs

A

PRIL

  • Older (first drugs): captopril (Capoten), enalapril (Vasotec)
  • Newer drugs: enalapril (Vasotec),benazepril (Lotensin), fosinopril (Monopril), lisinopril (Prinivil),, moexipril, quinapril, ramipril, trandolapril
65
Q

ACE inhibitors

HTN use

A

-Vasodilation
-Reduced blood volume
-Better than adrenergic agents
-no effect on cardiac
contractility or
exercise ability
-no orthostasis, no
bronchial effects,
CNS
-reduce the risk of CV
mortality due to HTN
-Better than diuretics – no fluid and electrolyte effects

66
Q

ACE inhibitors

HF use

A

-lowers arterial resistance
-reduces afterload
-increases CO
-reduces pulmonary
congestion
-renal vessel dilation
-increased renal
blood flow
-Na/water excretion
-reduced edema and
blood volume
-Reduce pathologic wall thickening

67
Q

ACE inhibitors

MI use

A
  • Reduced mortality and heart failure after MI

- Start right after MI – low dose – remodel heart muscle

68
Q

ACE inhibitors

Diabetic and non-DM nephropathy use

A
  • Increases renal blood flow
  • Decreases glomerular filtration pressure
  • Slows progression of renal disease
69
Q

ACE inhibitors

High CV risk use

A
  • Those with stroke, CAD, DM, PVD, and a CV risk factor

- To reduce the CV event

70
Q

ACE inhibitors

Pharmacokinetics

A

-good oral absorption – most all PO but also IV
-most have long half-life
-(except captopril –
older drug)
-significant drug accumulation in renal disease
-DO NOT TAKE IF PREGNANT

71
Q

ACE inhibitors

Drug reactions

A
  • Hypotension – syncope - most often with first dose, high BP and dehydrated
  • Orthostatic hypotension
  • Nagging, dry cough; 5-10% (bradykinin)
  • Hyperkalemia – aldosterone effects, esp combined with K sparing drugs or K supplements
  • Angioedema – rare 1%, life-threatening
72
Q

ARBS

MOA

A
Block angiotensin II action (not production)
-Receptor antagonists 
   -On blood vessels – 
   causing vasodilation 
   (arterioles and veins)
   -In the heart – reduce 
   cardiac remodeling
   -In adrenal glands – 
   decrease release of 
   aldosterone – 
   promotes excretion   
   of Na and water
   -Does not increase 
   bradykinin which 
   causes the ACEI 
   cough
73
Q

ARBs

Drugs

A

-Losartan (Cozar) – prototype
-Losartan and
Hydrochlorothiazide =
Hyzaar
-Valsartan (Diovan)
-Irbesartan (Avapro)

74
Q

ARBs

Uses

A

-HTN
-HF
-small amount of data
-increases function
(ejection fraction)
-Diabetic nephropathy
-in pts with HTN and
DM
-slowed disease

75
Q

ARBs

Pharmacokinetics

A
  • First pass limits bioavailability to 30%
  • Active metabolite is more powerful than the drug
  • Highly bound to protein (99%)
76
Q

ARBs

Adverse effects

A
  • Very few cases of hyperkalemia, cough

- Angioedema

77
Q

ACE inhibitors vs ARBs

A
  • ACE inhibitors reduce overall mortality when compared to ARBs
  • ACE inhibitors are first line treatment
  • If ACE inhibitors are not tolerable due to SE, ARBs are introduced
78
Q

CCBs

original treatment

A

Treated angina, but SE was reduced BP

-Typically not used as HTN monotherapy, but good if not responsive to other anti-HTN therapies

79
Q

CCBs

MOA

A

-Cardiac and smooth muscle cells depend on influx of calcium for maintenance of contraction or tone
-inhibit Ca from
entering cell, limits
muscular contraction
and thus relaxation of
muscle

80
Q

CCBs

Classes

A
Selective and Non-selective 
-vascular selective: dihydropyridines 
   -relax arterial smooth 
   muscle = lower 
   peripheral resistance 
   -overall primary effect: 
   arterial vasodilation
-nonselective: non-dihydropyridines 
   -relax cardiac muscle 
   and arterial smooth 
   muscle 
   -overall primary effect: 
   cardiac muscle 
   relaxation
81
Q

Vascular selective CCBs

pines

A

Nifedipine (procardia)
-Vasodilation in vascular smooth muscles PRIMARILY - in peripheral arterioles and in coronary arteries
-Arteriole vasodilation PRIMARILY
-Uses – HTN and angina
-ADRs
-Reflex (baro)
tachycardia – as BP
falls, HR increases
Amlodipine (Norvasc)
-effective in cerebral vessel spasm; and for effort induced spasm of coronary vasospam
Nimodipine
-effective in cerebral vessel spasm -cerebral aneurysm
Other drugs = felodipine, amlodipine, nicardipine, isradipine

82
Q

Non-selective CCBs

A
Uses: angina and dysrhythmias 
More cardiac, less vascular 
-Diltiazem (Cardiazem) - anti-anginal
   -Blocks calcium 
   channels in the 
   myocardium
     -Decreased cardiac 
     contractility, 
     -Conduction effects
     -Used for 
     tachydysrhythmias, 
     angina, HTN 
     -ADRs – bradycardia, 
     conduction blocks, 
     depression of 
     myocardial 
     contractility, HA, 
     flushing, peripheral 
     edema, hypotension
-Verapamil – anti-dysrhythmic
   -Blocks calcium 
   channels in blood 
   vessels AND the heart
     -Arteriole vasodilation 
     (decreased BP, 
     increase flow in 
     coronary arteries)
     -Decreased cardiac 
     contractility
83
Q

Second Line

HTN drugs

A
Alpha 2-adrenergic agonists
Alpha 1-adrenergic blockers (zosins)
Beta-adrenergic blockers (olos)
Centrally acting alpha and beta blockers
Direct acting vasodilators
Direct renin inhibitors 
Peripherally acting adrenergic neuron blockers
84
Q

Parasympathetic Division

A
Rest and Digest
constricts pupil
stimulates salivation
slows heart
constricts bronchioles
stimulates digestion
stimulates gallbladder
contracts bladder
stimulates sex organs
85
Q

Sympathetic Division

A
Fight or flight
dilates pupils
inhibits salivation
accelerates heart
dilates bronchioles
inhibits digestion
stimulates glucose release
secretes epi and norepi 
relaxes bladder
inhibits sex organs
86
Q

Beta blockers

HTN

A

decrease HR and myocardial contractility

reduces CO

87
Q

Alpha2 agonists

HTN

A

decreases sympathetic impulses from CNS to heart and arterioles
causes vasodilation

88
Q

Alpha1 blockers

HTN

A

inhibits sympathetic activation in arterioles

causes vasodilation

89
Q

Direct vasodilators

A

act on smooth muscle of arterioles

causes vasodilation

90
Q

Drug indications

Beta 1 agonists

A

bradycardia
HF
shock

91
Q

Drug indications

Beta 1 antagonists

A

acute MI
angina
HTN
dysrhythmias

92
Q

Drug indications

Beta 2 agonists

A

severe allergic reactions
asthma
COPD

93
Q

Drug indications

Alpha 1 agonists

A

nasal congestion

opthalmic hyperemia

94
Q

Drug indications

Alpha 1 antagonists

A

HTN

BPH

95
Q

Drug indications

Alpha 2 agonists

A

HTN

96
Q

Drug indications

Alpha 2 antagonists

A

erectile dysfunction

97
Q

Beta 1

Normal actions

A
Increased:
   AV conduction
   Cardiac contraction
   HR
   Renin release
98
Q

Beta 2

Normal actions

A
Bronchodilation
Glycogenolysis
Relaxation:
   bladder
   eye muscle
   smooth muscle
   uterine
99
Q

Beta 2

Normal actions

A
Bronchodilation
Glycogenolysis
Relaxation:
   bladder
   eye muscle
   smooth muscle
   uterine
100
Q

Alpha 1

Normal actions

A

Vasoconstriction
Increased PVR
Constriction - bladder sphincter
Mydriasis (pupil dilation)

101
Q

Alpha 2

Normal actions

A

Controls release of NE

102
Q

Alpha 1 Blockers
Drugs
Use

A

Doxazosin (cardura)
Others: Prazosin (minipress), Terazosin
-Blocks a1 receptors on arterioles and veins
-dilation of arterioles: lower BP
-dilation of veins: decreases venous return, decreases CO, lowers BP

103
Q

Alpha 1 blockers

adverse effects

A

orthostatic hypotension
reflex tachycardia
nasal congestion
inhibition of ejaculation

104
Q

Alpha 2 agonists
Drugs
Use

A

Clonidine (catapress), Methyldopa (aldomet)

  • suppresses sympathetic outflow from CNS
  • lowers a and b adrenergic receptor peripheral activation
  • dilation of arterioles
  • slows HR conduction velocity (reducing CO)
105
Q

Alpha 2 agonists

adverse effects

A
orthostatic hypotension
dry mouth
sedation
Clonidine: rebound HTN
Methyldopa: hemolytic anemia, liver disorder
106
Q

Beta 1 blockers
Receptors
Use

A
receptors in heart and kidneys
reduced HR
decreased force of contraction
suppressed conduction through AV node
--reduce CO, lower BP
suppresses renin secretion
blocks receptors at JG app
107
Q

Beta 2 blockers
Receptors
Use

A

receptors in lungs, liver, and skeletal muscle
bronchoconstriction
inhibition of glycogenolysis in skeletal muscle and liver

108
Q

Beta 1 blockers

Adverse effects

A

bradycardia
reduced CO
HF
AV heart block

109
Q

Beta 2 blockers

Adverse effects

A

bronchoconstriction
inhibition of glycogenolysis
decreased libido and impotence

110
Q

Types of Beta blocking drugs

A
Nonselective: propranolol (inderal)
-block B1 and B2 receptors 
Cardio selective: metoprolol (lopressor)
-block B1 receptors 
-dose dependent - high doses lose selectivity
111
Q

Nonselective Beta blockers
Drugs
Use

A
Propanolol 
Others: Timolol (blocadren), Pindolol (visken), Nadolol (corgrard), Penbutolol (levatol), Sotalol (betapace)
Use: 
-HTN - reduced CO, RAA
-Angina - decreased workload
-Dysrhythmias 
-MI
-Reduces pain, infarct size
-Reduces mortality, risk of infarction
-Migraine, stage fright
112
Q

Nonselective Beta blockers

Pharmacokinetics

A

highly lipid soluble
well absorbed PO
extensive first pass: 30% available
hepatic metabolism - renal excretion

113
Q

Nonselective Beta blockers

Adverse effects

A
bradycardia
AV heart block
CNS (depression, insomnia)
HF (decreased contraction force)
rebound cardiac excitation (abrupt drug withdrawal) 
bronchoconstriction
glycogenolysis
114
Q

Bronchoconstriction

A

block beta2 receptors in the lung

block normal bronchodilation when needed - bronchospasm

115
Q

Inhibition of glycogenolysis

A

decreases breakdown of glycogen to glucose
dangerous for diabetics who need glucose if insulin is too much
suppress early symptoms of hypoglycemia

116
Q

Cardio-selective Beta blockers
Drugs
Use

A

Metoprolol
Others: Atenolol (Tenormin), Metoprolol slow release (Toprol XL), Acebutolol (Sectral), Betaxolol (Kerlone), Carvedilol (Coreg)
Use
-HTN
-Angina, MI, HF
-helps to balance O2 supply and demand by reducing demand/workload

117
Q

Cardio-selective Beta blockers

Pharmacokinetics

A

highly lipid soluble
well absorbed PO
extensive first pass: 30% available
hepatic metabolism - renal excretion

118
Q

Cardio-selective Beta blockers

Adverse effects

A

Bradycardia
AV heart block
HF
Rebound cardiac excitation

119
Q

Direct Vasodilators

Types

A

Nitrates

Hydralazine

120
Q

Vasodilators

Action

A
On arterioles: resistance vessels
-decrease afterload
-increase CO
On veins: capacitance vessels 
-reduce force with which blood is returned to heart, reduced volume 
-decreased preload
121
Q

Vasodilators

Adverse reactions

A

postural hypotension due to vasodilation of veins
reflex tachycardia
expansion of blood volume - low kidney perfusion (RAAS)

122
Q

Vasodilators
Nitrates
MOA
Pharmacokinetics

A
Nitroglycerin 
Used for angina 
MOA:
-dilates veins (reduces pre and afterload)
-dilates coronary arteries 
-decreases workload
-reduces angina and BP
Pharmacokinetics:
-highly soluble
-given many diff ways
-PO-most destroyed on first pass
-rapid hepatic inact.
-half life: 5-7 min
123
Q

Vasodilators
Nitrates
Admin

A

Route – acute vs prophylactic therapy

  • SL – quick acting, small dose (0.3-0.6), no more than 3 in 15 min
  • Transdermal – slow release up to 14hrs
  • Spray – acute attack (0.4 mg), same as SL
  • Topical – ointment, 1-2”, release same as transdermal
  • IV – continuous infusion
  • PO – large dose to survive first pass
124
Q

Vasodilators
Nitrates
Adverse Effects
Tolerance

A

Headache, facial flush
Orthostatic Hypotension
Reflex tachycardia

happens rapidly - with high dose use
use lowest dose: long action formulations
6-12 hr nitrate free interval

125
Q

Vasodilators
Hydralazine
MOA

A

Hydralazine (apresoline)
MOA:
-acts directly on smooth muscle in arterioles to cause dilation - no effect on veins
HF AA pts: combo with isosorbide dinitrate for selective dilation

126
Q

Vasodilators
Hydralazine
Contraindication
Adverse effects

A

Lupus: sx worsen
Rheumatic heart disease, MI, angina, tachycardia

Causes reflex tachycardia (used with beta blocker to counteract tachycardia)
Na and H2O retention

127
Q

Treatment of HTN crisis

adverse effects

A
When RAPID reduction in BP is warranted
Vasodilators: Nitroprusside (arterioles and veins)
-IV admin
-rapid onset: half life is 2 min
-short term use, less than 72 hrs
-metabolized to cyanide: toxic

Adverse effects: cerebral ischemia, MI, renal failure

Preeclampisa/eclampsia: delivery, magnesium sulfate, labetolol

128
Q

Arteriosclerosis vs Atherosclerosis

A

Art: thickening and hardening of the vessel wall
Ath: form of art that is caused by accumulation of lipid-laden macrophages within the arterial wall
-leads to lesions called plaques
-leading cause of:
-CAD
-Cerebrovascular
disease

129
Q

Atherosclerosis

Pathologic process

A
  1. Injury-damaged endothelium
  2. Fatty streak
  3. Fibrous plaque
  4. Complicated lesion
130
Q

Injury: damaged endothelium

risk factors

A
Injured endothelium becomes: 
-inflamed and can't make normal antithrombic and vasodilating cytokines 
-stimulates inflammatory cascade 
Risk factors:
-HTN
-Smoking
-Hyperlipidemia 
-Hyperhomocysteinemia 
-Hemodynamic factors
-Toxins
-Viruses
-Immune reactions
131
Q

Injury: damaged endothelium

progression

A
  1. LDL enters intima (hypercholesterolemia) and is oxidized
  2. Oxidized LDL generates proinflammatory lipids that induce adhesion molecules
  3. Monocytes are recruited and phagocytize oxidized LDL and transform to foam cells
  4. Foam cells present oxidized LDL to T cells, release growth factors that stimulate smooth muscle proliferation, secrete cytokines that are proinflammatory and procoagulant (more injury)
132
Q

Fatty Streak

A

when there is an accumulation of enough foam cells they become a fatty streak

  • seen most in teens & 20s, and kids
  • leads to more T cell recruitment, more macrophages, more inflammation, more smooth muscle cells, proliferation, more damage
133
Q

Fibrous Plaque

A

fatty streaks develop into fibrous plaque
-smooth muscle cells proliferate and produce collagen
-smc and fibroblasts migrate over fatty streak
-fibrous plaques may calcify and protrude into lumen/create fissures
-stable: thick fibrous
cap
-unstable: thin fibrous
cap, thick lipid pool,
prone to rupture
-all equal: narrowing of vessel lumen = obstruction of blood flow which can produce: angina and intermittent
claudication

134
Q

Complicated lesion

A
complicated plaques: unstable and can rupture prior to occlusion
-rupture caused by immune response to endothelial injury/fissure
   -exposes underlying 
   tissue, causes 
   platelet adhesion, 
   initiates clotting 
   cascade, and rapid 
   thrombus formation
   -thrombus formation 
   can occlude; results 
   in ischemia or 
   infarction
135
Q

Symptoms of atherosclerosis

A
associated with:
-amount of narrowing/occlusion
-progression
   -acute: ischemia, pain, 
   poor perfusion
   -chronic: 
   asymptomatic, can 
   develop collateral 
   circulation
-rupture
-location: may have sx in several tissues/areas at same time
136
Q

Atherosclerotic lesion locations

A
  1. large vessels
    - coronary: MI
    - cerebral: stroke
    - renal: kidney disease/HTN
  2. at bifurcations
  3. localized, focal in distribution
  4. PAD
137
Q

Atherosclerosis

primary risk factor

A

CAD, MI, and acute coronary syndromes (infarction)

138
Q

PAD
risk factors
progression

A
atherosclerotic disease of the arteries that perfuse the limbs - particularly lower
risk:
-CAD
-advanced age, DM, smoking
progression: gradual or acute
139
Q

PAD
symptoms
diagnosis

A

sx:
-asymptomatic (2/3 case)
-intermittent claudication
-severe pain, pallor, loss of pulse, skin color change
Diagnosis: history, bruits, BP: ankle-brachial index, doppler

140
Q

PAD

treatment

A
Risk factor reduction
Exercise
Meds:
-vasodilators
-anticoagulants
-cholesterol lowering
-surgical revascularization