Cardio Part 3

Front 1

in normal endo, the default tension =

Back 1

relaxed

Front 2

4 things that contribute to a dysfunctional endo:

Back 2

1. atherosclerosis

2. tobacco/smoking

3. abnormal lipids

4. diabetes

Front 3

inc. wall stress =>

Back 3

inc. O2 consumption

Front 4

inc HR => shorter:

Back 4

diastolic period => less perfusion of the heart by the coronary arteries

Front 5

UA = _________ problem due to __________________________

Back 5

SUPPLY;

CLOTS forming from ruptured plaques

=> that's why treatment = anti-plats

Front 6

4 platelt inhibitors:

Back 6

1. asp

2. thienopyridines

3. GP IIb/IIIa inhibitors

4. Dipyridamole

Front 7

which of the 3 ACS conditions is aspirin given for?

Back 7

ALL of them

- chronic stable, UA/N, and STEMI

Front 8

how does aspirin work?

Back 8

it blocks COX activation of TXA2

Front 9

what does TXA2 do?

Back 9

1. activates platelets

2. enhances clot formation

Front 10

**2 major effects of aspirin:**

Back 10

1. dec. incidence of recurrent coronary event

2. dec. m/m

Front 11

main side effect of ALL anti-plats and anti-coagulants =

Back 11

bleeding

=> hemorrhagic stroke, GI bleed, etc.

Front 12

2 examples of Thienopyridines:

Back 12

1. Clopidogrel

2. Ticlopidine

Front 13

what does Clop do?

Back 13

inhibit ADP

(ADP activates P2Yr's to ultimately activate platelets)

Front 14

Clop compared to aspirin:

(2)

Back 14

1. modestly better at dec. risk of MI

2. but worse SE's than aspirin

Front 15

critical feature of Clop:

Back 15

it's *irreversible*

Front 16

Clop in combination with aspirin =>

Back 16

better outcomes than aspirin alone

Front 17

clop is used to treat:

(2)

Back 17

1. UA/N

2. STEMI

Front 18

GP IIb/IIIa inhibitors prevent:

Back 18

fibrinogen from binding

Front 19

best example of GP IIb/IIIa inhibitor =

Back 19

Abciximab

Front 20

GP IIb/IIIa inhibitors are ALWAYS given:

Back 20

IV

Front 21

what do dipyridamoles do, and when are they used?

Back 21

1. dec plat's

2. given to pts intolerant of aspirin

Front 22

UFH enhances:

Back 22

AT against thrombin, 10a

Front 23

UFH is used to treat:

(2)

Back 23

1. UA/N

2. STEMI

Front 24

LMWH only targets:

Back 24

10a

Front 25

LMWH compared to UFH:

(2)

Back 25

1. better anticoagulant,

2. less bleeding than UFH

Front 26

3 goals in treating myocardial ischemia:

Back 26

1. dec. frequency of angina

2. prevent MI

3. prolong survival

Front 27

3 routes to reaching the goals of treating myocardial infarction:

Back 27

1. improve lifestyle

2. treat *acute* episodes

3. manage recurrent episodes

Front 28

what do you use to treat *acute* ischemia?

Back 28

nitrates

Front 29

what do you give to manage recurrent episodes of myo ischemia?

(3)

Back 29

1. B-blockers

2. nitrates

3. Ca2+ chan blockers

Front 30

what do nitrates do?

Back 30

1. dilate *veins*

2. dilate both veins and arteries at higher dose

Front 31

effect of nitrates - dilation of veins =>

Back 31

dec. *ventricular preload,* dec wall stress

=> dec. O2 demand

Front 32

auxilliary effect of nitrates =

Back 32

opening up coronary reserves => supply

Front 33

nitrates are given:

Back 33

sublingual

=> rapid, avoids FPE

Front 34

2 situations in which nitrates are used:

Back 34

1. treatment of acute ischemia

2. prophylaxis before exertion

Front 35

SE's of nitrates:

(3)

Back 35

1. HA

2. hypotension

3. reflex tachy

Front 36

bottom-line efficacy of nitrates:

Back 36

improve QOL, but do NOT prolong life

Front 37

what do B-blockers do?

(3)

Back 37

1. dec. HR

2. dec. contractility

3. dec. time in systole => better coronary perfusion

Front 38

not all B-blockers are the same:

Back 38

some are nonselective

=> risk bronchospasm in asthma

- Carve, Labet, Propranolol, Nado, Tim

Front 39

some B-blockers are B1 selective, while others have:

Back 39

B-*agonist* activity

=> LESS bradycardia than other B-blockers

Front 40

3 B-blockers that have B-agonist activity:

Back 40

1. Carteolol

2. Penbutolol

3. Pindolol

Front 41

4 SE's of B-blockers:

Back 41

1. excessive brady

2. dec. LV contractile function

3. bronchoconstriction

4. fatigue/hopelessness (not all)

Front 42

**2 great ultimate effects of B-blockers:**

Back 42

1. dec. rate of recurrent infarction and mortality following acute MI

2. dec. likelihood of *first* MI if HTN

Front 43

Ca2+ blockers like dihydro cause:

Back 43

**arterial** dilation

=> dec. afterload, myocardial size

- also open up coronaries

Front 44

2 specific Ca2+ blockers:

Back 44

1. Diltiazem

2. Verapamil

Front 45

**Diltiazem and Verapamil also cause:

Back 45

1. dec. HR

2. dec. Contractility

Front 46

BUT - SE's of Diltiazem and Verapamil =

(3)

Back 46

1. hypotension

2. ankle edema

3. brady arrhythmias (if with B-blockers)

- **generally, avoid these short-acting chan blockers**

Front 47

3 effects of Ranolazine:

Back 47

1. dec. frequency of angina

2. inc. exercise capacity

3. NO effect on HR, BP

Front 48

arterial clots:

(2)

Back 48

1. white/plat-rich

2. treat with BOTH anti-plat and anticoagulants

Front 49

venous clots:

(2)

Back 49

1. red/fibrin-rich

2. treat with anticoagulants

Front 50

another name for GP IIb/IIIa =

Back 50

aIIbB3

Front 51

what is aIIbB3?

(aka GP IIb/IIIa)

Back 51

receptor on platelets for fibrinogen

=> *aggregation*

Front 52

3 plat-activating receptors:

Back 52

1. TXA2 r'

2. P2Y12

3. PAR-1

Front 53

2 platelet adhesion receptors:

Back 53

1. GPVI

2. GPIba-V-IX

- attach to VWF

Front 54

TXA2 and ADp are released by:

Back 54

activated platelets to aid in NEW plat, activation and aggregation

Front 55

**when thrombin binds PAR-1, the complex activates:

Back 55

GPIIb/IIIa

=> aggregation

(TXA2 and PAR-1 complexes also activate it)

Front 56

4 risk factors for arterial thrombosis:

Back 56

1. atherosclerosis

2. elevated CRP

3. inc. homocysteine

4. lupus

Front 57

3 major classes of anti-plats:

Back 57

1. COX inhibitors

2. P2Y12 r' antagonist

3. GP IIb/IIIa inhibitors

Front 58

be careful giving aspiring with:

Back 58

anti-coagulants,

e.g. w3's

Front 59

best example of a P2Y12 r' antagonist =

Back 59

clopidogrel

Front 60

clopidogrel prevents:

Back 60

ADP from binding

=> prevention of IIb/IIIa activation

=> prevention of aggregation

Front 61

clopidogrel is the drug-of-choice for:

Back 61

stenting

Front 62

3 druggy features of clopidogrel:

Back 62

1. oral

2. a pro-drug - requires metabolism in the liver

3. irreversible - no antidote

Front 63

clopidogrel is given to:

Back 63

ACS pts with moderate-to-high risk of MI

Front 64

main SE of clopidogrel = bleeding, esp. if given with:

(2)

Back 64

other anti-plats, PPI's

Front 65

2 emerging ADP inhibitors:

Back 65

1. Prasugrel

2. Ticangrelor

Front 66

Prasugrel:

(3)

Back 66

1. most likely successor to Clop

2. faster with less needed

3. dec. mortality vs Clop

Front 67

Ticangrelor:

(2)

Back 67

1. reversible

2. faster than Clop

Front 68

GP IIb/IIIa inhibitors prevent:

Back 68

platelet aggregation

Front 69

GP IIb/IIIa inhibitors are used in:

(3)

Back 69

1. PCI

2. UA

3. MI

Front 70

therapy for UA =

(2)

Back 70

aspirin + heparin

Front 71

most likely new PAR-1 inhibitor =

Back 71

Vasopaxar

- most likely to be used widely

Front 72

4 requirements for blood to clot:

Back 72

1. activator (TF or negative surface)

2. clotting factors

3. PL surface ( ~ plats)

4. Ca2+

Front 73

aPTT measures:

Back 73

UFH,/LMWH function

Front 74

PTT m's:

Back 74

warfarin function

Front 75

VTE = venous thromboembolism =

Back 75

DVT + PE

Front 76

9 risk factors for VTE:

Back 76

1. >40

2. surgery

3. oral contraceptives

4. preg

5. stasis

6. central line catheters

7. CHF

8. Favtor V Leiden, other anti-fibrinolytic deficiencies

9. elevated clotting factors

Front 77

VTE is diagnosed via:

Back 77

D-Dimer test

- not great: if positive, need more tests

Front 78

3 ways to find PE:

Back 78

1. CT

2. MRI

3. pulm arteriography

Front 79

short-term anticoagulants =

Back 79

heparin

- warfarin = long-term

Front 80

2 Classes of anticoagulants:

Back 80

1. Heparins

2. Vit, K antagonists

Front 81

heparins include:

Back 81

fondapurinux

Front 82

fondapurinux:

(3)

Back 82

1. targets ONLY 10a,

2. but has fewer SE's

3. yet no antidote

Front 83

UFH effects are fully reversible with:

Back 83

Protamine Sulfate

Front 84

heparin is given esp to pts with:

(2)

Back 84

1. DVT

2. CABG

Front 85

main complication of heparin =

Back 85

HIT

- AB's formed against heparin complex

=> dec. plat count

=> dec. paradoxical thrombosis

Front 86

**to anticoagulate HIT pts, give:**

Back 86

Direct Thrombin Inhibitors (DTI's)

Front 87

4 imp. DTI's:

Back 87

1. Bevalirudin

2. Argatroban

3. Dabigatran 9oral)

4. Rivaroxaban


(no antidote for any of them)

Front 88

LMWH ~~ reduced risk of:

Back 88

HIT

- also reversible with PSulfate

Front 89

best example of LMWH =

Back 89

Enoxaparin

Front 90

both fonda and LMWH are given to:

Back 90

prevent DVT's in hip/knee surgery

Front 91

make sure you're giving:

Back 91

thrombophylaxis

Front 92

anuerysm =

Back 92

localized dilation in vessel or cardiac chamber due to weakening of media

Front 93

aneuryms are most common in:

Back 93

abdominal aorta, then LV

Front 94

false aneurysm/pseudoaneurysm =

Back 94

extravascular hematoma that communicates with intravascular space

- *looks* like an aneurysm

Front 95

***7 key features of abdominal aortic aneurysm:***

Back 95

1. ALWAYS ~~ severe atherosclerosis

2. usually located between renal and iliac arteries

3. fusiform

4. ~~mural thrombus/emboli

5. ruptures are common

6. NEVER involves aortic root (rarely, aortic arch)

7. rare before 50

Front 96

***9 key features of syphilitic aneurysms:***

Back 96

1. due to obliterative endarteritis of thoracic aorta

2. ~~ ischemic injury with loss of elastic fibers, SM

3. => inflam, fibrosis of aortic media

4. ~~occlusion of coronary ostia (openings)

5. ~ aortic insufficiency

6. => LVH

7. => LV volume overload => LHF

8. ~~ aneurysm at *aortic root*

9. tree-bark appearance

Front 97

aortic dissection =

Back 97

entrance of blood into the media, forming a blood-filled channel within the aortic wall

- also called an intramural hematoma

Front 98

**2 key features of aortic dissection:**

Back 98

1. **frequently ruptures**

2. not usually associated with aneurysmal swelling

Front 99

2 groups predisposed to aortic dissection:

Back 99

1. men 40-60 years old with HTN

2. younger pts with CT disorder


~~ aging, which degenerates elastin, media

Front 100

2 degenerative CT disorders:

Back 100

1. Marfan syndrome

2. Cystic Medial Degeneration

Front 101

7 features of Marfan Syndrome:

Back 101

1. tall/slender

2. long extremities, spider fingers

3. myopia

4. weak aortic media

5. higher incidence of rupture

6. aortic regurgitation

7. mitral valve prolapse

Front 102

most common cause of death in Marfan Syndrome =

Back 102

CV disorders

Front 103

3 other features of Marfan:

Back 103

1. AD

2. ~~ FBN1 mutation

3. => fragmented elastnc fibers

Front 104

cystic medial degeneration = the most common:

Back 104

pre-existing condition before aortic dissection

~~ elastic tissue fragmentation due to small cysts of ECM within media

- freq. seen in Marfan

Front 105

aortic dissection occurs in:

Back 105

the *ascending* aorta

- dissection can occur in other vessels though

Front 106

most common cause of death wrt aortic dissection =

Back 106

extravascular rupture

- intravascular rupture may also occur in a second spot, forming a double-barrel aorta

Front 107

Type A aortic dissection =

Back 107

1. proximal internal rupture

OR

2. proximal AND distal internal rupture


(Type A = most common, most dangerous)

Front 108

Type B aortic dissection =

Back 108

*distal* rupture, *after* ascending aorta

Front 109

6 signs of aortic dissection:

Back 109

1. acute onset of severe tearing pain, radiating from anterior to back

2. loss of arterial pulses

3. aortic regurgitation/murmurs

4. MI

5. hypotension (ominus - suggests rupture)

6. cardiac tamponade

Front 110

in an arterial thrmobosis, the thrmobus is most commonly:

Back 110

superimposed on an atheroma

Front 111

atheroma =

Back 111

degeneration of walls due to accumulation of fat and scar tissue

Front 112

venous thrmobi are most often due to:

Back 112

stasis

- followed by vascular injury, old age, hypercoaguability

Front 113

common sites of arterial thromboses:

(2)

Back 113

1. large or medium arteries (aorta, carotids, coronary)

2. heart

Front 114

*DVT's are frequently:**

Back 114

asymp

Front 115

Homan sign = sign of DVT =

Back 115

calf tenderness w/ forced dorsiflexion of foot

Front 116

occlusive DVT is associated with:

(3)

Back 116

1. congestion

2. edema

3. cyanosis

Front 117

LARGE venous thrombi represent a serious hazard to life, b/c if they embolize, they =>

Back 117

acute RHF, as right heart can't push against pressure found in pulmonary arteries due to obstruction there

Front 118

an embolism can be ANY material:

(5)

Back 118

1. air

2. fat (from fracture)

3. atheromatous debris

4. tumor

5. amniotic fluid

Front 119

amniotic fluid embolism is associated with:

(4)

Back 119

DIC, ARDS

- sudden dyspnea, CV arrest

Front 120

PAD =

Back 120

peripheral artery disease

= flow-limiting lesion in an artery that prrovides blood supply to the limbs

Front 121

**top 2 causes of PAD =

Back 121

smoking, diabetes

(56% of pts with PAD have CVD)

Front 122

5 risk factors for PAD:

Back 122

1. old age

2. younger but smoking or diabetic

3. claudication upon exertion >3 blocks

4. ischemic leg pain

5. dec. pulse in lower extremities

Front 123

PAD manifests on a spectrum: 50% =

Back 123

asymp

=> atypical leg pain

=> classic claudication

=> limb ischemia

Front 124

location of PAD symptoms points to artery in trouble:

butt/hips ~~

thigh ~~

calf ~~

foot ~~

Back 124

aorto-iliac region;

common femoral

superficial femoral/popliteal

TP trunk

Front 125

5 levels of diagnosing PAD:

Back 125

1. vascular ROS

2. Phys Exam

3. ABI

4. noninvasive studies (e.g. duplex US)

5. angiography

Front 126

in the vascular ROS, look for:

(5)

Back 126

1. exertional limitation

2. wounds in legs/feet

3. pain in legs/feet when at rest

4. post-prandial abdominal pain

5. first-degree family history of AAA

Front 127

Phys Exam pulse scale, 0 - 3

Back 127

0 = absent

1 = diminished

2 = normal

3 = bounding (~aneurysm)

Front 128

ABI =

Back 128

gold standard for diagnosing PAD

Front 129

formula for ABI (ankle-brachial index):

Back 129

ankle systolic pressure / high brachial artery SP

- take the higher of the righ or left arms

Front 130

an ABI of __________ is diagnostic of PAD

Back 130

</= 0.90

Front 131

an ABI range of ___________ = normal

Back 131

1 - 1.4

Front 132

an ABI of >1.4 means you have to use:

Back 132

t0e-brachial index (TBI)

Front 133

**if PAD is confirmed, immediately:

Back 133

address lifestyle, with treatment if necessary

- have to quit smoking, lower HTN

- antiplat therapy to reduce risk

Front 134

if symptoms of PAD are limiting your life, treatment =

(4)

Back 134

1. supervised exercise

2. pharm. therapy (cilostazol)

3. angioplasty

4. surgery if indicated

Front 135

don't treat PAD if:

Back 135

they don't have claudication or any other symptoms

Front 136

cilostazol: does NOT reduce ischemic events, but does:

Back 136

improve claudication

- vice versa for Clop

Front 137

sequence of PAD treatment:

Back 137

medical therapy before endovascular surgery before open surgery

Front 138

2 non0imflammatory vascular diseases:

Back 138

1. varicose veins

2. Raynaud's phenomenon

Front 139

varicose veins =

Back 139

dilated, tortuous *superficial* veins,

esp. saphenous

Front 140

Raynaud's phenomenon =

Back 140

peripheral *arterial* vasospasm

=> color changes, paresthisia, pain

Front 141

corticosteroids tamp down:

Back 141

the immune system

Front 142

5 inflammatory vascular diseases:

Back 142

1. temporal/giant cell arteritis

2. polyarteritis nodosa

3. Kawasaki Disease

4. Takayasu Arteritis

5. Buergers Disease

Front 143

temporal/giant cell arteritis =

Back 143

most common inflam. vascular disease

Front 144

polyarteritis nodosa (PAN) =

Back 144

type 3 immune response

=>=> infarct

Front 145

Kawasaki disease is aka:

Back 145

mucocutaneous LN syndrome

Front 146

Takayasu arteritis is also called:

(2)

Back 146

1. aortic arch syndrome

2. Pulseless Disease

Front 147

Neurgers disease is also called:

Back 147

thromboangitis obliterans

Front 148

3 CV neoplasms:

Back 148

1. Hemangioma

2. Cardiac Myxoma

3. Kaposi's syndrome

Front 149

Hemangioma =

Back 149

proliferation of *endothelium,*

creating large or small vascular channels

Front 150

cardiac myxoma =

Back 150

benign neoplasm of primitive CT

Front 151

Cardiac Myxoma:

(2)

Back 151

1. most common primary neoplasm of the heart

2. LA > RA > ventricles

Front 152

Kaposi's syndrome:

(5)

Back 152

1. ~~ HHV8

2. occurs in AIDS pts

3. infected endothelial cells => unregulated growth

4. ~ skin, mucus membrane

5. ~ spindle cells, blood-filled vacular spaces

Front 153

new MI =

Back 153

black,

old MI = white