Bld 204 Exam 2 (Objective Hemodynamic Derangements)

Front 1

Hemostasis

Back 1

series of regulated processes that keep blood in fluid, un-clotted state in normal circumstances while rapidly forming a "plug" when vascular

injury occurs

(letting blood flow when it should)

Front 2

thrombosis

Back 2

pathogenic version when clots form within intact vessels

(letting clot where it needs to)

Front 3

Hemostasis

3 components

Back 3

1. vascular wall

2. platelets

3. coagulation cascade

Front 4

active hyperemia

Back 4

due to increase flow of arterial blood in dilated capillaries

Front 5

passive hyperemia

Back 5

-venous congestion

-disruption of blood flow to an area

-chronic

-results from increase pulmonary and systematic venous pressure

Front 6

hyperemia

Back 6

ACTIVE increase in the volume of blood in tissues cause by arteriolar dilation

Front 7

hemorrhage

Back 7

extravasation of blood to exterior of body or into nonvascular body space due to rupture of blood vessels

Front 8

epistaxis

Back 8

nose bleeds

Front 9

hemothorax

Back 9

collection of blood in the space between the chest wall and the lung (the pleural cavity).

Front 10

hemoptysis

Back 10

coughing up blood from the respiratory tract.

Front 11

hemopericardium

Back 11

to blood in the pericardial sac of the heart

Front 12

hematemesis

Back 12

person begins to vomit blood

Front 13

hemoperitoneum

Back 13

presence of blood in the peritoneal cavity.

(peritoneal cavity contains the pelvis, stomach, spleen, gall bladder, liver and the intestines. )

Front 14

enterorrhagia

Back 14

Bleeding within the intestinal tract.

Front 15

petechiae

Back 15

Tiny purple or red spots on the skin associated with endocarditis, resulting from hemorrhages under the skin's surface.

Front 16

metrorrhagia

Back 16

uterine bleeding occurring at irregular intervals, and sometimes of prolonged duration.

Front 17

purpura

Back 17

a small hemorrhage in the skin, mucous membrane, or serosal surface.

Front 18

hematuria

Back 18

blood (erythrocytes) in the urine.

Front 19

ecchymoses

Back 19

The medical term for a bruise. Ecchymoses may develop around the eyes following a nasal fracture.

Front 20

ischemia

Back 20

Ischemia is an insufficient supply of blood to an organ, usually due to a blocked artery.

Front 21

arteriosclerosis

Back 21

a group of diseases characterized by thickening and loss of elasticity of the arterial walls, occurring in three forms: atherosclerosis,

monckeberg's arteriosclerosis, and

arteriolosclerosis

Front 22

atherosclerosis

Back 22

Atherosclerosis is the build up of a waxy plaque on the inside of blood vessels.

-can occur in several forms

-terms means hardening of arteries

Front 23

risk factors of atherosclerosis

Back 23

-raised plaque is where problems develop.

-thin caps with large lipid cores more risky

-injury to cap and release of lipid is likely

Front 24

atherosclerosis

atherosclerotic plaques

Back 24

-lipids contained within foam cells or in pools

-collagen

-ca++ deposits

Front 25

thrombi

Back 25

-solid mass or plug within

heart/arteries/veins/capillaries

from components of streaming blood

-A fibrinous clot formed in a blood vessel or in a chamber of the heart.

Front 26

thrombi

clotting

Back 26

activation of a protein cascade within the blood leading to the formation of thrombin, which convert fibrinogen to fibrin

Front 27

thrombi

thrombosis is ___ activation and ____

which occurs when...

Back 27

platelet, clotting

plaque is unstable and cap releases

Front 28

thrombi

thrombosis is ___ to get rid of

clotting is ___ because

Back 28

hard

easier because it can dissolve with enzymes

Front 29

thrombi

4 contributions of platelets to hemostasis

Back 29

-adhere to underlying vessel walls

-release pharmacologically active compounds

-aggregate (platelet and platelet binding)

-provide co-factors for clotting

Front 30

thrombi

4 contributions of platelets to hemostasis

1. Adhesion

Back 30

-bind to damaged endothelium cells

-bind to glycoprotein receptors

-collagen now exposed ->

bind glycoprotein receptors

Front 31

thrombi

4 contributions of platelets to hemostasis

2. Release

Back 31

-platelet adherences leads to shape change

-release preformed compounds

-release storage granules

-release of orchidonate used in synthesis of prostaglandins that promote and prevent

aggregation

Front 32

thrombi

4 contributions of platelets to hemostasis

3.Aggregation

Back 32

-result of shape change

-platelet-platelet mass body forms using

fibrinogen as bridge

-fib. binds using intergrin

Front 33

thrombi

4 contributions of platelets to hemostasis

4. co-factors for clotting

Back 33

-interact with coag factors V,VIII,IX,X

-serves as surface for clotting cascade

-flipping phospholipids from interior to exterior

Front 34

thrombi

disseminated coagulation

Back 34

scattered clots

Front 35

thrombi

alpha granules are

Back 35

substrates involved with clotting

Front 36

thrombi

contents of alpha granules

Back 36

-PDGF

-thrombospondin

-platelet factor 4

-fibrinogen

-fibrinectin

-vWF

Front 37

thrombi

dense bodies are

Back 37

substrates that drive the reaction forwards

Front 38

thrombi

contents of dense bodies

Back 38

-atp, adp

-gpd, gtp

-serotonin

-calcium

-platelets contract on stimulus

-actin/myosin,

Front 39

thrombi

name three states that will promote thrombosis

Back 39

-change in intimal surface (endothelium)

-changes in blood flow

-constituent changes of the blood flow (rate of movement)

Front 40

thrombi

____ blood flow = increase chance of thrombosis

Back 40

slow

Front 41

thrombi

what changes the endothelium surface that will promote thrombosis

Back 41

-injury

-trauma

-inflammation

-changes in blood flow/pattern

Front 42

thrombi

____ can lead to atrial or cardiac thrombosis

Back 42

turbulence

Front 43

thrombi

hypercoaguable

Back 43

up regulation of vessel wall interaction in which thrombosis is favored

Front 44

thrombi

how do platelets contribute to hypercoaguable

Back 44

-increased procoagulant factors (fibrinogen)

-decreased natural anti-coagulants

-increased viscosity

-stasis (blocking blood flow)

-increased platelet vessel interaction

-atherosclerosis = most important

-deep injury to plaque cap

-increase platelet count/function

Front 45

thrombi

________ is a life long thrombosis

Back 45

protein C deficiency -->

autosomal dominant

Front 46

thrombi

4 ways thrombi can be lysed

Back 46

1. plasmin: occur naturally

2. streptokinase: dissolving thrombosis

3. plasminogen activator: genetically engineered

4. embolization: collagen plug, blocks circulation no O2 = cell death

Front 47

emboli

Back 47

mass in blood stream (solid or gaseous) and clogs vessl

Front 48

emboli

name 8 materials that can cause or be

incorporated into emboli

Back 48

-thrombus

-thrombus/clot

-air

-nitrogen

-fat

-bone marrow

-debris from base of atherosclerotic plaque

-tumor cells

Front 49

emboli

describe/recognize contribution factors to the development of pulmonary emboli

Back 49

-venous in origin

-most common/danger form (pulmonary)

Front 50

emboli

3 categories for a pulmonary emboli based on size and clinical impacts are

Back 50

-massive pulmonary emboli: acute right heart failure, from legs, straining (stool)

-medium size: localized necrosis, infarcts necrosis secondary to ischemia, block O2 = tissue die

-small size: clinically silent, multiple, hammered into vessles

Front 51

emboli

pulmonary emboli -

Back 51

right side

venous in origin

Front 52

emboli

systemic emboli

Back 52

left side

transmural myocardial infraction/congestion

cardiomyopathy

Front 53

emboli

platelet thrombi

from ____ in the ____

related to ____ ____ in the ___

deposition in the ____

Back 53

-plaques, neck

-atherosclerosis plaque, neck

-brain

Front 54

emboli

air gaseous emboli results from

Back 54

-head & neck injury

-blood transfusions

-hemodialysis

-air into fallopian tubes

-placental disruptions

Front 55

emboli

how are air gaseous emboli formed

Back 55

-air can enter into right ventricle and whipped into a frothy mess

-from the heart action, blook&air is turning causing proteins to break down and stick together

(40mL not good / 100mL fatal)

Front 56

emboli

mechanical theory

Back 56

bone marrow derived, fat globules enter the

venous system and lodge in the pulmonary

vasculature as fat emboli

Front 57

emboli

biochemical theory

Back 57

circulation free fatty acids affect cell lining the air spaces and produces abnormalities in gas exchange

Front 58

emboli

_____ plaque can lead to emboli

how...

Back 58

atherosclerosis

-ather. is hardening of veins (cause plaque). if clot/ulcer breaks off and reaches an opening it can't pass through, it will lead to embolization

-this causes a plug

-O2 blockage = cell death

Front 59

thrombi

what contributes to the generation of thrombi because they evaluate fibrinogen &

factor VIIc cencentrations

Back 59

-age

-obesity

-oral contraceptives

-cigarette smoking

-malignancy

Front 60

ischemia & infarct

ischemia -

infarct -

Back 60

-decreased perfusion, not meeting metabolic needs of the tissue

-localized ischemia due to ischemia

Front 61

ischemia & infarct

causes of local ischemia

Back 61

-atherosclerosis

-thrombosis

-emboli

-arterial smooth muscle spam

-pressure from within

-pathological change to a vessel

(drugs like heroine)

Front 62

ischemia & infarct

venous occlusion occurs when...

Back 62

blood cannot bypass obstruction which leads to intense congestion

Front 63

ischemia & infarct

venous occlusion can also be...

and decrease...

Back 63

hemorrhagic

blood flow

Front 64

ischemia & infarct

venous occlusion is seen in

Back 64

-extensive mesenteric venous thrombosis

-strangulation of hernias: intestines drop down, twisted, which then disrupts blood flow

Front 65

ischemia & infarct

capillary obstruction

what is a physical damage that can be seen

Back 65

-frost bite due to the physical damage to

capillaries

Front 66

ischemia & infarct

capillary obstruction

what kind of cells are obtained

Back 66

-abnormal red cells: sickle cell anemia

Front 67

ischemia & infarct

capillary obstruction

explain the role of fibrin

Back 67

-spread in intravascular coagulation

-little dots everywhere screwing with capillaries

-lead to small blood clots in body: use up platelets and coagulation, no more left = death

-cant really fix it

Front 68

ischemia & infarct

capillary obstruction

explain the role of antigen-antibody complexes

Back 68

-interact with basement membrane

-leads to inflammation

-make it so blood can't circulate

Front 69

ischemia & infarct

capillary obstruction

explain role of fate gaseous emboli

Back 69

-external pressure-bed sores

-must keep turning on order to prevent pressure

or cut off blood supply

Front 70

ischemia & infarct

arterial obstruction

has a wide range of ____ & ____

Back 70

- cause and effect

Front 71

ischemia & infarct

arterial obstruction

no effects result of good...

Back 71

-collateral (same tree but different branch)

circulation or insignificant reduction of blood flow

(collateral circulation = more than one entry for arterial blood to tissue)

Front 72

ischemia & infarct

functional evidence of ischemia

Back 72

-you're okay until stressed (demand of O2 ↑)

-angina (pain in chest due to insufficient supply of blood) , intermittent claudication

(weakness in legs, limping, pain), plaque build up

Front 73

ischemia & infarct

some ways to get rid of symptoms of ischemia

Back 73

stop being stressed

Front 74

ischemia & infarct

structural evidence of ischemia

lost of ___ leads to ___...

Back 74

-lost tissue leads to fibrosis from necrosis

Front 75

ischemia & infarct

if ischemia is slow...

if ischemia is sudden...

Back 75

-little damage / loss

- pulmonary emboli

Front 76

ischemia & infarct

what determines the degree of ischemia...

Back 76

- post-ischemia necrosis

(↓ damage, ↓ischemia)

Front 77

ischemia & infarct

what are interacting variable of ischemia

Back 77

-metabolic needs of the tissue

-speed: sudden=bad

-degree of blockage

-local anatomy

-state of collateral coagulation

Front 78

ischemia & infarct

ischemia

there is more damage to the body when...

Back 78

the clot causing the ischemia is closer to the heart

Front 79

ischemia & infarct

describe relationship of ischemia & infarct

Back 79

infarction: coagulative necrosis (may be bloody from congestion)

infarction is the result of ↓ arterial blood aupply aka ischemia.

tissues die off the from the lack of supply of blood that surround the area of blockage

Front 80

ischemia & infarct

given specific anatomical sites of infarct, what type of necrosis would be expected:

CNS

Back 80

necrosis is liquefaction not

coagulative (cavity formation)

Front 81

ischemia & infarct

given specific anatomical sites of infarct, what type of necrosis would be expected:

Heart

Back 81

angia, arrhythemia's, necrosis, failure of muscular activity, deterioration of a beating heart

Front 82

ischemia & infarct

given specific anatomical sites of infarct, what type of necrosis would be expected:

Lung

Back 82

wedge-shape (<10% emboli) due to circulatory

Front 83

ischemia & infarct

given specific anatomical sites of infarct, what type of necrosis would be expected:

Liver

Back 83

rare

Front 84

ischemia & infarct

given specific anatomical sites of infarct, what type of necrosis would be expected:

Intestine

Back 84

strangulating hernia

(bulge of organ thru structure)

volvus, intussusception (enfolding of one segment of the intestine within another

→ twisted = block)

Front 85

shock

define shock

Back 85

clinical syndrome characterized by systemic

underprefusion (heavy to bottom, light on top) of tissues due to prolonged

hypotension (low blood pressure)

Front 86

ischemia & infarct

2 acute myocardial infarction

Back 86

-regional

-subendocardial

Front 87

shock

3 types of shock

Back 87

1. hypovolemic: ↓ circulating blood vol., severe hemorrhage, major loss of body fluids

2. cardiogenic: ↓ cardiac output

3. septic shock: systemic infection,

severe hypotension, system vasodilation

Front 88

shock

hypovolemia symptoms (3)

Back 88

-severe hemorrhage

-diarrhea/vomiting

-loss of skin

Front 89

shock

acute myocardial even causes what kind of shock

Back 89

cardiogenic

Front 90

shock

systemic infection from pathogenic

microorganisms cause which shock

Back 90

redistrubutive (septic shock)

Front 91

shock

redistrubutive (septic shock)

is caused or leads to

Back 91

-DIC

- Adult Respirator Disease (ARD)

-bacterial

Front 92

shock

3 consequences of shock

Back 92

1. renal failure

2. acid-base imbalance

3. GI hemorrhage

Front 93

edema

define edema-

Back 93

Edema is a condition of abnormally large fluid volume in the circulatory system or in tissues between the body's cells (interstitial spaces).

-fluid in extravascular

Front 94

edema

hydrothorax-

Back 94

-pleural effusion contain serous fluid

-accumulation of serous fluid in one or both pleural cavities

-results from cardiac failure

Front 95

edema

anasarca-

Back 95

-An accumulation of serous fluid in various tissues and cavities of the body.

-Anasarca often occurs in congestive heart failure, liver failure, or renal disease.

Front 96

edema

ascites-

Back 96

Ascites is an abnormal accumulation of fluid in the abdomen.

Front 97

edema

pericardial effusion-

Back 97

-the escape of blood or other fluid into the

pericardium.

-escape of fluid into a part;

exudation/transudation

Front 98

edema

describe primary causes of edema

Back 98

-raised intracapillary pressure

-low plasma oncotic pressure

-retention of salt and water

Front 99

shock

explain renal failure

Back 99

hypovolemia (diminished volume of circulating blood in the body)

causes body to direct blood to more vital organs

Front 100

shock

explain acid-base imbalance

Back 100

-lactic acidosis due to continued tissue

hypoxia (reduction of oxygen supply to a tissue)

Front 101

shock

explain GI leakage

Back 101

due to ischemia causing infection in abdominal cavity

Front 102

edema

what causes fluid to leave vasculature?

(2)

Back 102

1. ↑ intravascular hydrostatic pressure

2. ↑ colloid osmotic pressure in extravascular compartment

Front 103

edema

what helps fluid remain in the vascularture?

(3)

Back 103

1. osmotic pressure of plasma proteins, especially albumin

2. the selective permeability of the endothelium

3. tissue tension

Front 104

edema

exudates

Back 104

edema due to ↑ vascular permeability

(like in inflammation)

Front 105

edema

transudates

Back 105

edema due to ↑ hydrostatic pressure

Front 106

edema

cardiac edema

Back 106

-redistribution and retention of fluids

-gravity influences the distribution

- weak pumping leads ↑ venous pressure

-*excess retention of Na+ and H2O by kidneys

Front 107

edema

renal edema: nephritic

Back 107

-associated with acute glomerulonephritis

-caused by sodium retention

-transudate characteristics

Front 108

edema

renal edema: nephrotic

Back 108

-heavy proteinuria (excess of serum proteins in the urine, as in renal disease)

-hypoalbuminaemia (losing albumin faster than liver can make)

-decreased plasma oncotic pressure

Front 109

edema

nutritional edema

Back 109

-prolonged starvation, ppl lose subcutaneous fat

-surrounding tissues are looser so theres a

decline in tissue tension

-space fills with fluid = edema

Front 110

edema

chronic liver disease edema

Back 110

-causes: ↑ intracapillary pressure, ↑ hepatic lymph, ↓ albumin/plasma oncotic pressure,

Na+ retention if cirrhotic

-edema presents as ascites

Front 111

edema

pulmonary edema

Back 111

-distribution of fluid between intravascular &

extravascular compartments

-balance of intracapillary hydrostatic pressure & capillary permeability (↑=edema)

Front 112

edema

in pulmonary edema

↑ in intracapillary pressure causes

Back 112

-IV overload

-severe anemia

-renal failure

-↑ altitude

Front 113

edema

in pulmonary edema

↑ in capillary permeability causes

Back 113

-ARDS

-aspiration

-DIC

-pneumonia

-severe trauma

-bacteremia

Front 114

edema

3 disturbance in fluid distribution

of local edema:

Back 114

1. ↑ hydrostatic pressure in the microcirculation: occlusive venous thrombsis

2. ↑ local vascular permeability: inflammation, type I hypersensitivity

3. lymphedema: obstruction of normal lymphatic flow due to surgery/inflammation