Pathology Topic 4 Hemodynamic Disorders Etc

Front 1

anasarca definition

Back 1

severe generalized edema in the subcutaneous

Front 2

what are three of the main ways fluid moves into and out of the vasculature

Back 2

plasma colloid osmotic pressure: fluid into vessels
hydrostatic pressure: fluid into interstitium
interstitial fluid pressure: into venules

Front 3

what is congestive heart failure?

Back 3

Congestive heart failure (CHF), or heart failure, is a condition in which the heart can't pump enough blood to the body's other organs.

Front 4

how does congestive heart failure cause edema

Back 4

if the kidney's aren't receiving enough blood = kidneys cause aldosterone to be released = aldosterone causes sodium and water retention to increase blood volume = heart can't pump blood anyway so there's "blocked venous return" = increased hydrostatic pressure = edema

Front 5

what happens edemawise when you have right ventricular failure

Back 5

edema of legs and sacrum via increased hydrostatic pressure

Front 6

what happens when you have left ventricular failure

Back 6

pulmonary edema: heavy lungs, frothy, blood tinged fluid

Front 7

what are some causes of low albumin (which in turn causes low plasma osmotic pressure)

Back 7

nephrotic syndrome (protein leaks from glomeruli); liver disease reduces albumin synthesis; protein malnutrition

Front 8

what causes lymphedema and what does it cause

Back 8

lymph obstruction due to inflammation with fibrosis, tumor, physical disruption, radiation damage or infection (gives you elephantisis like symptoms in dependent parts)

Front 9

what causes peau d'orange skin?

Back 9

lymphatic infiltration caued by cancer causes skin edema due to fine pitted accentuation of hair follicles

Front 10

what is filarisis

Back 10

elephantitis: lymphatic obstruction that causes edema of the legs and other body parts

Front 11

why does acute inflammation go along with edema

Back 11

BECAUSE EDEMA IS CAUSED BY INJURING TO HELP MEDIATE THE ACUTE INFLAMMATION THAT HELPS REPAIR THE INJURY. leaky vessels leak proteins that maintain plasma osmotic pressure, increased blood flow to the area increases hydrostatic pressure (Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid into the tissue (edema), which manifests itself as swelling (tumor). The mediator molecules alter the blood vessels to permit the migration of leukocytes, mainly neutrophils, outside of the blood vessels (extravasation) into the tissue. The neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.)

Front 12

what does edema do to wound healing?

Back 12

impairs infection clearance and wound healing

Front 13

what are two conditions that accompany edema. what do they have in common

Back 13

hyperemia and congestion (both are localized increases in blood volume that accompany edema)

Front 14

what causes hyperemia

Back 14

active increased blood flow due to arteriolar dilatation (e.g. caused by exercise, inflammation)

Front 15

what does hyperemia tissue look like?

Back 15

red, wet, engorged by oxygenated blood.

Front 16

what is congestion. what happens to congested tissue.

Back 16

passive decreased blood flow due to decreased outflow. tissue is blue-red because of lack of oxygen

Front 17

what generally causes congestion

Back 17

local venous occlusion, cardiac failure

Front 18

what does acute congestion in the lungs look like?

Back 18

transudate is present. engorged capillaries, edema in airspaces

Front 19

what does acute congestion in the liver look like?

Back 19

central veins and sinusoids become distended. central hepatocytes degenerate but periportal hepatocytes are better off.

Front 20

what does chronic congestion look like in the liver?

Back 20

nutmeg liver. centrilobular hepatocellular necrosis occurs because of ischemia.

Front 21

what does chronic passive congestion of the lungs look like?

Back 21

capillaries become congested and they rupture (=small foci of hemorrhage and hemosiderin-laden macrophages (heart failure cells)); edematous, fibrotic septa

Front 22

what is a hematoma. what are the three types of hematomas

Back 22

hemorrhage in tissue. petechiae, purpura, ecchymosis

Front 23

ecchymoses

Back 23

1-2 cm subQ hematoma

Front 24

what are the color changes in hemorrage caused by

Back 24

as RBC age, degrade and are phagocytosed

Front 25

what is shock caused by blood loss called

Back 25

hemorrhagic hypovolemic shock

Front 26

what is hemostasis? what are its steps

Back 26

complex process by which bleeding is stopped. vasoconstriction. primary hemostasis. secondary hemostasis. antithrombotic countterregulation.

Front 27

what causes the vasoconstriction step of hemostasis

Back 27

when endothelial cells are stripped away local neurogenic factors and endothelial-derived vasoconstrictor endothelin do their thing

Front 28

what is primary hemostasis

Back 28

platelets stick to endothelium and then they secrete products to recruit more platelets to form a hemostatic plug

Front 29

what is 2ndary hemostasis

Back 29

tissue factor released by endothelial cells and these act with secreted platelet factors to activate coagulation cascade, resulting in thrombin activation which causes fibrin polymerization

Front 30

what is the coagulation cascade

Back 30

series of enzymatic conversions of proenzymes into active enzymes that results in thrombin formation. thrombin then converts soluble fibrinogen to insoluble fibrin

Front 31

what does antithrombotic counterregulation do and how does it do it?

Back 31

prevents formation of thrombus. endothelium releases tissue plasminogen activator thrombomodulin to interfere with coagulation cascade.

Front 32

why do thrombuses form?

Back 32

when antithrombotic counterregulation doesn't work

Front 33

what is a thrombus

Back 33

when a coagulum forms in flowing blood

Front 34

what is the term used to describe the things that predispose to thrombus

Back 34

virchow triad: abnormal blood flow, hypercoagulability, endothelial injury

Front 35

what happens in abnormal endothelium chemicalwise to favor thrombus

Back 35

injured or activated endothelium has increased procoagulants and decreased anticoagulants; normal endothelium has a balance between the two

Front 36

what are some hard to remember causes of abnormal endothelium

Back 36

radiation, cigarette smoke, hypercholesteremia, homocysteinuria, immune injury, bacterial endotoxins

Front 37

what are the two things that abnormal flow does to cause thrombus

Back 37

stasis/turbulence

Front 38

what are some things that cause stasis and turbulence

Back 38

aneurysm, noncontractile myocardium, atherosclerotic plaques, atrial fibrillation

Front 39

what are some things that cause stasis

Back 39

varicose veins, bed rest, hyperviscosity (polycythemia, sickle cell disease)

Front 40

what is another name for hypercoagubility? what are the two types of causes?

Back 40

thrombophilia. there are primary (genetic) and secondary causes.

Front 41

what is hypercoagibility caused by, general mecanism

Back 41

weird coagulation pathways make you more susceptible

Front 42

what are some primary (genetic causes of hypercoagibility)

Back 42

1. factor V, prothrombin mutations
2. antithrombin III, Protein C, S deficiency
3. Fibrinolysis defects
4. Hyperhomocysteinemia

Front 43

what are some secondary (acquired) causes of thrombophilia?

Back 43

1. prolonged bed rest
2. atherosclerosis, MI
3. smoking
4. cancer
5. pregnancy
6. morning
7. autoimmune disorders
8. surgery, trauma

Front 44

what are the 4 fates that can happen to a thrombus?

Back 44

propagation, dissolution, organization/recanalization, embolism

Front 45

describe organization/recanalization of a thrombus.

Back 45

thrombi induce inflammation that causes endothelial, smooth muscle cells, and fibroblasts to grow into thrombus and make capillaries in thrombus to reestablish lumen and flow.

Front 46

where are thrombi attached?

Back 46

attachd to a vessel wall (arterial or venous)

Front 47

what is embolization property of arterial thrombi?

Back 47

generally obstruct more than embolize. but can embolize to extremities, brain, kidney, intestine

Front 48

what are the most common places of arterial thrombi in most common to least common

Back 48

coronary, cerebral, femoral artery

Front 49

what are some qualities of mural thrombi

Back 49

noninclusive, attached to wall of heart or aorta, often at aneurysm

Front 50

what is vegetation

Back 50

thrombus on cardiac valve

Front 51

what is the embolization potential of venous thrombi

Back 51

phlebothrombosis is usually occlusive

Front 52

what are the most common sites of venous thrombi

Back 52

superficial & deep leg vein, upper excremity, periprostatic plexus, ovarian veins

Front 53

what do venous thrombi do to you?

Back 53

cause congestion and edema in distal vascular beds

Front 54

what are two specific common types of venous thrombi

Back 54

superficial (saphenous) phlebothrombosis and deep leg vein phlebothrombosis

Front 55

describe qualities of superficial (saphenous) phlebothrombosis

Back 55

rarely embolize
occur with varicose veins
cause local edema
impaired venous drainage predisposes to varicose ulcers and skin infection

Front 56

what are some qualities of deep leg vein phlebothombosis

Back 56

CAN EMBOLIZE TO LUNGS,
half of DVTs asymptomatic until emboli occur

Front 57

clot during life and during death forms where

Back 57

clot forms external to vessels during life or in vessels after death

Front 58

what are some qualities of postmortem clots

Back 58

red jelly and chicken fat. not attached to endothelium

Front 59

what are some qualities of thrombi

Back 59

lines of zahn and attached to endothelium

Front 60

what can embolize

Back 60

vascular thrombus, fat, gas, amniotic fluid, foreign body, tumor cells

Front 61

where do pulmonary emboli usually come from

Back 61

DVT

Front 62

when do pulmonary emboli become a problem

Back 62

doesn't cause problems in NORMAL lung because of collateral circulation usually, but if 60% or more of the lung is obstructed it can cause sudden death and RV failure (cor pulmonale) and pulmonary hypertension

Front 63

what is a paradoxical embolus

Back 63

venous embolus goes into systemic circulation through heart wall defect. paradoxical cause it transports itself bypassing pulmonary circulation

Front 64

where do systemic arterial thromboemboli come from

Back 64

intracardiac mural thrombi, atherosclerotic plaques (present at heart or elsewhere), and aortic aneurysm

Front 65

what are the fates of the systemic arterial thromboemboli (location specificity)

Back 65

cause infarction in extremities > brain > intestine, kidney, spleen

Front 66

what is a fat embolism and what is it caused by

Back 66

fat from bone marrow gets into circulation because of bone break, or from a burn, trauma, liposuction

Front 67

what is a syndrome that fat embolism can cause

Back 67

fat embolism syndrome

Front 68

symptoms of fat embolism syndrome

Back 68

pulmonary insufficiency, neurological symptoms, anemia, thrombocytopenia, petechial rash

Front 69

what is air embolism caused by

Back 69

obstretic procedure, laproscopic procedure, chest trauma, decompression sickness.

Front 70

how much air do you need for an air embolism to do its damage

Back 70

more than 100 cc needed for distal ischemic injury

Front 71

the bends can cause

Back 71

periartcular pain, brain, heart, lung ischemia

Front 72

what is caisson disease

Back 72

chronic decompression sickness: gas emboli in bone persist and cause ischemic necrosis of heads of femur, tibia, humerii

Front 73

what does amniotic fluid embolism cause

Back 73

sudden severe dyspnea, cyanosis, hypotension, shock, seizures, coma, pulmonary edema, DIC.

Front 74

what is an infarction

Back 74

ischemic necrosis due to vascular occlusion

Front 75

what are the types of infarction

Back 75

arterial or venous, red or white, septic or bland. these are not mutually exclusive

Front 76

infarction capability of venous vs arterial thromboembolism

Back 76

venous usually doesn't infarct, arterial usually does infarct

Front 77

if venous thromboembolism usually don't infarct when do they do?

Back 77

infarct organs with only one venous outflow channel (e.g. testis or ovaries); otherwise they only usually cause congestion

Front 78

when do red infarcts happen

Back 78

venous occlusion (e.g. ovarian, testicular torsion) or reflow to necrotic area after venous or arterial occlusion (e.g. brain) or dual circulation allows blood from unobstructed vessel to go to necrotic area (arterial occlusion in lung and bowel which have space for extravasculated blood to go into)

Front 79

when and where do white infarcts happen

Back 79

after arterial occlusion in organs without space for extravasculated blood.

Front 80

what is another name for a white infarct

Back 80

anemic infarct

Front 81

what happens to tissues damaged by anemic aka white infarcts?

Back 81

wedge shaped white area of coagulative necrosis often at apex and periphery of organ. with red edges made by extravascalated blood. marginal inflammation incited by ischemic necrosis. it repairs by scar after the dead tissue has been handled by secondary union.

Front 82

where do anemic infarcts happen

Back 82

solid organs (heart, spleen, kidny) with little space for extravasated blood

Front 83

what are some things that influence infarct development?

Back 83

alternative vascular supply, vulnerability to hypoxia, rate of development of occlusion, oxygen content of blood

Front 84

what are some things that cause alternative blood supply that protects from an infarct

Back 84

dual blood supply (lungs [pulmonayr, bronchial arteries]; liver (hepatic artery, portal vein); anastomosing circulation (radial + ulnar arteries, circle of willis, small intestine); collateral blood supply (can prevent infarction and also make lesions develop slower)

Front 85

what are some organs that don't have an alternative blood supply?

Back 85

kidney and spleen are end-arterial therefore vessel occlusion caused an infarct

Front 86

how does oxygen content of the blood cause an infarct?

Back 86

partial obstruction of vessel in anemic or cyanotic patient can cause infarction

Front 87

neurons, myocardial cells, fibroblast tolerance to ischemia

Back 87

neurons: 3-4 min
myocardial cells: 20-30 min
fibroblasts: 1-2 hours
function of cells glycolysis, glycogen stores, rate cell used ATP

Front 88

what is shock the final common pathway for

Back 88

many lethal events: hemorrhage, trauma, MI, PE, sepsis

Front 89

definition of shock

Back 89

systemic hypoperfusion due to decreased cardiac output and/or circulating blood volume

Front 90

what does shock lead to

Back 90

hypotension causes decreased perfusion and hypoxia. this decreased perfusion and hypoxia leads to irreversible tissue injury and death (eventually).

Front 91

what are the different types of shock

Back 91

cardiogenic, hypovolemic, septic/endotoxic (severe infection), anaphylactic, neurogenic (brain damage, spinal cord injury)

Front 92

what do all types of shock lead to cardiovascularwise?

Back 92

myocardial pump failure. decreased blood volume, vasodilation,

Front 93

what is hypovolemic shock caused by and what causes those things

Back 93

blood or plasma loss because of hemorrhage, diarrhea, dehydration, burns

Front 94

what is cardiogenic shock caused by?

Back 94

pump failure, intrinsic heart damage, arrhythmia, outflow obstruction, extrinsic compression

Front 95

what is septic shock mechanism of shock

Back 95

can be caused by gram pos or neg organism. gram neg releases endotoxins that cause inflammation, complement cascade. this and other mechanism cause peripheral vasodilation nd pooling of blood; endothelial activation/injury; leukocyte-induced damage; disseminated intravascular coagulation; activation of cytokine cascades

Front 96

what can septic shock lead to?

Back 96

multiorgan dysfunction syndrome

Front 97

what organs does multiorgan dysfunction syndrome effect?

Back 97

brain, heart, kidney, lungs, GI, liver, disseminated intravascular coagulation