Patho Ii- Exam 2

Front 1

Flow reduction in systemic circuit creates

Back 1

ischemia-leading to hypoxia

Front 2

ischemia

Back 2

lack of arterial flow

Front 3

hypoxia

Back 3

lack of oxygen in tissues

Front 4

flow reduction in venous system altering waste removal and increases systemic pressure

Back 4

venous engorgement or venous obstruction

Front 5

general mechanisms that alter flow

Back 5

1. changes in lyphatic syst.

2. blood vessel obstructions

3. blood vessel structural alterations

Front 6

lymphadema

Back 6

lymphatic flow alteration due to impairment in lymph circulation.

Primary-due to congenital abscence or decrease numbers of lymphatics

Secondary-sugical removal of lymph nodes (such as in mastectomies)

Front 7

thrombus

Back 7

clot attached to the vessel wall

Front 8

thromboembolus

Back 8

detached thrombus

Front 9

most common cause of thromboembolus in arteries

Back 9

athroschlrosis

Front 10

most common cause of thromboembolus in veins

Back 10

phlebitis

Front 11

2 secondary locations thromboembolisms can form

Back 11

1. heart valves that have been altered by acterial endocarditis

2. rheimatic heart diseases cause thrombi to form on cusps of valves inside heart.

Front 12

Shock can lead to thrombi T/F?

Back 12

True: impaired metabolisms activates the extrinsic clotting cascade and blood stasis.

Front 13

arterial thrombi-two threats:

Back 13

1. occlusion of artery

2. thromboembolus causing occlusion at distant site.

Front 14

venous thrombi threat:

Back 14

cause edema and can embolize (pulmonary)

Front 15

air embolus

Back 15

undissolved air

Front 16

embolism

Back 16

obstruciton of a vessel by an embolus

Front 17

embolus

Back 17

bolus of matter circulating in the blood stream

Front 18

amneotic fluid embolism

Back 18

forced into mother through uterine wall

Front 19

bacterial embolism

Back 19

aggregates of bacteria, most common subaccute bacterail endocarditits

Front 20

fat embolism

Back 20

caused by trauma to long bones, normally legs where large amounts of fat is stored.

Front 21

foreign matter embolism

Back 21

enters due to trauma, IV or interarterial lines

Front 22

vasospasm

Back 22

sudden invollutary constriction of arterial smooth muscle

Front 23

inflammation-vasculitis

Back 23

inflammation of intima of artery

Front 24

phlebitis

Back 24

inflimmation of intima of vein

Front 25

mechanical compression

Back 25

external forces altering blood flow

Front 26

valvular incompetence

Back 26

when intimal folds of venous valves are damaged. cause varicose veins and chronic venous insufficency

Front 27

arteriosclerosis/athroschlerosis

Back 27

complex conditions that alter the structure of the arteries.

-athro a specific type of arterio that cause an increase in the number of smooth muscle cells as the lipids collect in the intima

both narrow arterial lumen

Front 28

aneurysms

Back 28

localized dilation of arterial wall.

Usually form at biforcation of arteries

Front 29

Arteriovenous fistulas (AVF)

Back 29

abnormal communication between arteries and veins.

Most common (AVM) AV-Malformation; lack of traditional cappilaries.

Front 30

alterations in arterial blood flow

Back 30

1. arteriosclerosis/atherosclerosis

2. ateritis

3. Raynaud Syndrome

4. aneurysms

5. acute arterial occlusion

Front 31

Arteritis/Thromboangitis obliterans - Buerger Disease

Back 31

inflammatory disese of peripheral arteries. Can occlude and obliterate small and medium arteries in feet and hands

Front 32

Raynaud syndrome

Back 32

A primary vasospastic disorder of unknown origin that mainly affects young women, attacks of vasospasms in small arteries and arterioles

-red white and blue disorder

blue finger tips, white fingers, red hands

Front 33

raynaud phenomenom

Back 33

symptoms of raynaud syndrome, but secondary to systemic diseases

Front 34

true aneurysms

Back 34

all three tunics of the blood vessel

Front 35

false aneurysms

Back 35

at least one tunic unaffected, forming a hematoma

Front 36

dissectiong aneurysm

Back 36

tear in arterial wall creates blood flow channel.

Cerebral aneurysms increase ICP.

Front 37

Acute arterial occlusion (AAO)

Back 37

an embolism lodges in major artery (Augustus Klump of CatCF).

No arterial flow to extermity. Gangrene occurs without surgery

Front 38

6 Ps - symptoms of AAO

Back 38

pallor (pale), parasthesia (tingling skin), paralysis, pain, polar (cold), pulseless.

Front 39

Alterations of Venous flow

Back 39

1. Valvular incompetence

2. varicose veins

3. chronic venous insufficency

4. Deep Vein Throbosis

Front 40

causes of valvular incompetence

Back 40

1. valvular over-stretching due to excessive venous pressure

2. backflow

Standing for long periods, pregnancy & obesity leading factors

Front 41

varicose veins

Back 41

veins in which blood has pooled

Front 42

chronic venous insufficiency (CVI)

Back 42

inadequate venous return over long period.

Pathological changes due to ischemia.

can cause venous stasis ulcers.

Front 43

Deep Vein Thrombosis (DVT)

Back 43

obstruction (clot) of normal blood flow. Usually in lower extremities

Front 44

hypertension

Back 44

sustained elevation of systemic arterial pressure

Front 45

3 common hypertension diseases

Back 45

MIs, kidney disease, stroke

Front 46

causes of hypertension

Back 46

increase in cardiac output (increase in HR or SV) and/or peripheral resistance (increase blood viscosity or reduction in vessel diameter

Front 47

Primary hypertension

Back 47

essential or idiopathic HTN, no known cause. 90% of all cases.

Front 48

Secondary hypertension

Back 48

caused by altered hemodynamics associated with a primary disease.

Front 49

factors of primary HTN

Back 49

family hx, advanced age, gender, black race, high NaCl intake, glucose intolerance, smoking, obesity, alcohol intake

Front 50

patho of primary HTN

Back 50

1. genetic changes increase vascular tone and blood volume

2. mediated by SNS, RAA system, adducin natiuretic peptides.

Front 51

shift in pressure-natriuresis relationship

Back 51

person with HTN tends to secrete less salt in their urine

Front 52

SNS contribution to HTN

Back 52

activate renin-angiotension-aldosterone system increasing absorbtion of salt and contractility of blood vessels

Front 53

endothelial dysfuction

Back 53

decreased production of vasodialators and incresed production of vasocontrictors

Front 54

isolated systolic HTN

Back 54

increase in CO or total peripheral vascular resistance

-can be secondary to

dysfunction of aortic SL valve

abnormal heart opening

thyrotoxic crisis, Paget disease, beriberi

Front 55

orthostatic HTN

Back 55

decrease in BP on standing

Front 56

defined obstructive pulmonary disorders

Back 56

airway obstruction that worsens with expiration

Front 57

most common OPD

Back 57

asthma, chronic bronchitis, and emphysema

Front 58

hypoventilation

Back 58

inadiquate alviolary ventilation

Front 59

hyperventilation

Back 59

excessive alveolar ventilation

Front 60

asthma

Back 60

inflamation creating hyperresponsiveness of airway

Front 61

acute bronchitis

Back 61

acute infection or inflamation of airway or bronchi

Front 62

cause of chronic bronchitis

Back 62

increased mucus produciton