Pathophysiology Exam One

Front 1

Pathology

Back 1

study of basic dz processes. Internal homeostasis is destroyed and dz exists

Front 2

Etiology

Back 2

causative agent-reason for dz. All the responses the body mounts to the dz

Front 3

Pathogenesis

Back 3

dvlpment of dz, sequential events, EX: strep gets into throat, multiplies, damage tissue, body mounts defense

Front 4

manifestations

Back 4

signs and symptoms

Front 5

subclinical manifestation

Back 5

no real s/sx, found in lab tests, happen b/c body has protective fx

Front 6

Symptoms

Back 6

subjective, patient feels something wrong

Front 7

Signs

Back 7

objective

Front 8

Lesions

Back 8

structural changes produced by dz, microscopic and gross (macroscopic)

Front 9

complication

Back 9

arises secondary to primary dz process EX: srep can lead to rheumatic fever that can lead to heart dz

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Sequel or sequelae

Back 10

outcome or end result of dz

Front 11

resolution

Back 11

recovery from dz process or possible resolution

Front 12

Extrinsic factors

Back 12

variations in environment EX: infectious agents, radiation

Front 13

Intrinsic factors

Back 13

characterisitics of the host EX: genetic factors, age, gender, disability from prev dz

Front 14

Cellular injury

Back 14

when needs of cell not met

Front 15

Cellular injury may occur due to

Back 15

oxygen deficit, nutrient def., phys injury, infectious agent, chemical agent

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exogenous chemical agents

Back 16

outside the body EX: lead, pollution

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endogenous chemical agents

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inside the body EX: build up of waste material in the body-kidney dz and inability to to get rid of urea

Front 18

sub-lethal injury

Back 18

doesn't kill cell but affects ability to fx normally

Front 19

morphological changes

Back 19

changes in appearance of cell

Front 20

cellular adaptation

Back 20

cell may adapt when stressed EX: muscle cells hypertrophy from repeated exercise, heart muscle enlarges and outgrows its O2 and nutrient supply Cell may return to prev state when noxious stimuli is removed

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common degenerative changes found in

Back 21

kidney, heart and liver cells most common

Front 22

cellular swelling

Back 22

normally cell pumps Na+ out of cellto maintain H2O balance, injured cell unable to do this and H2O enters cell and swells damaging internal cell structures-organelles Na+/K pump damage

Front 23

Lipid infiltration

Back 23

accumulate fat in cells --look yellow, fatty liver, heart

Front 24

Cellular atrophy

Back 24

decrease in cell sizeto decrease demand and achieve new equilibrium, lack of use or attemt o minimize needs

Front 25

cellular death

Back 25

if noxious or injurious stimuli is prolonged, cell can no loner compensate or adapt, process becomes irreversible and cell dies

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lytic enzymes

Back 26

released by dying cells and dissolve various cellular contituents, changes the environment around the cell which causes adj cells to mount an inflammatory resp to protect themselves

Front 27

necrotic

Back 27

dead cell

Front 28

necrosis

Back 28

loss of function of dead area, may be no immediate impact (kidney, liver) b/c they have a large reserve or may be immed impact (brain-stroke or heart-MI)

Front 29

systemic changes of necrotic tissue

Back 29

fever, increased WBC, lytic enzymes can be detected in the blood and help lab locate location of necrosis

Front 30

end result of necrosis

Back 30

dead cells demolished

Front 31

necrotic cells replaced by

Back 31

new functional cells or by scar tissue, dead cells may slough off or be replaced by ulcer or hole rarely can be surrounded and filled by calcium salts

Front 32

is scar tissue functional?

Back 32

no it is only structural

Front 33

circulatory congestion

Back 33

excess blood within the circulation of a given area, blood trapped in the capillaries

Front 34

visible hyperemia

Back 34

area looks redder than usual, microscopically vessels are dilated, full of blood

Front 35

How is circulatory congestion classified?

Back 35

by cause as either active or passive

Front 36

active circulatory congestion

Back 36

increase in blood going to an area, arterioles dilated

Front 37

Causes of ACTIVE circulatory congestion

Back 37

inflamatory response, resp to nervous system (blush), increased blood going to muscle as metabolism demands increase, heat being applied,

Front 38

describe active circulatory congestion

Back 38

normal reaction WITHOUT pathology, short lived, after stimulation is removed blood flow returns to normal

Front 39

Causes of PASSIVE circulatory congestion

Back 39

drainage of blood impaired by something compressing the veins draining that area, impairment

Front 40

local causes of PASSIVE circulatory congestion

Back 40

tourniquet, tumor, tight bandage, legs crossed, blood clot (think of a kinked hose)

Front 41

Systemic causes of PASSIVE circulatory congestion

Back 41

heart failing to pump efficiently, venous congestion may result

Front 42

if the left side of the heart is failing where does congestion occur?

Back 42

blood returning to the heart from the lungs will back up into the lungs causing congestion of the pulmonary circulation

Front 43

if the right side of the heart is failing where does congestion occur?

Back 43

blood will back up in the peripheral system or systemic circulation--congestive heart failure

Front 44

congestive heart failure

Back 44

bllod backing up in the systemic circulation--may be acute or chronic--acute can develop into chronic

Front 45

damage caused by chronic circulatory congestion

Back 45

eventually damage tissues (esp liver and lungs), veins also damaged--varicose veins, thickened walls, damage valves in veins and develop incompetence

Front 46

edema

Back 46

excess fluid outside of circulation

Front 47

types of edema

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intracellular, effusions, ascites, anasarca

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intracellular edema

Back 48

edema between cells

Front 49

efussion

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edema within body cavities--pleural effusion, cardiac effusion

Front 50

ascites

Back 50

edema in the abdominal cavity

Front 51

anasarca

Back 51

massive generalized edema

Front 52

causes of edema

Back 52

pressure changes and permeability changes--imbalance b/n forces that keep fluid within the circulatory systemand forces that allow fluid to leave the system

Front 53

explain edema with an increase in hydrostatic pressure

Back 53

hydrostatic pressure increase will push fluid out of the capillaries and into the interstitial spaces, may happen when venous drainage is obstructed EX: hypertension--heart generates higher hydrostatic pressure than normal and more fluid is pressed out and does not some back in

Front 54

explain edema with increase in capillary permeablility

Back 54

protein moliecules escape from the blood into interstitial spaces, proteins carry fluid with them, happens as part of the inflammatory process

Front 55

explain edema with a decrease of proteins in circulating blood

Back 55

decreases the oncotic pressure in the circulation, proteins 'hold' fluid so as proteins leak out so does fluid cuasing edema, caused by malnutrition, excess protein loss (kidney dz) or decreased albumin production (liver dz)

Front 56

what causes a decrease of proteins in circulating blood

Back 56

malnutrition, excess protein loss (kidney dz) or decreased albumin production (liver dz)

Front 57

pitting edema

Back 57

push down on swollen flesh (edemic area) and when pressure is removed the 'pit' remains

Front 58

dependent edema

Back 58

edema below the level of the heart, caused by gravity

Front 59

can edema be life threatening?

Back 59

yes, even a small amount if in the right are--brain, pulmonary edema--left side of heart failure, fluid fills the lungs

Front 60

hemorrhage

Back 60

escape of blood from the cardiovascular system into tissues, spaces and outside the body

Front 61

hematoma

Back 61

blood escapes into the tissues and and clots there EX: bump your shin and it swells immediately

Front 62

hemothorax

Back 62

bleeding into the pleural space

Front 63

petechiae

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bleeding into the skin or mucous membranes, can happen if inadequate platelets to heal capillaries look like pink pinpoint breaks

Front 64

ecchymosis

Back 64

bruise

Front 65

purpura

Back 65

wide spread bruising, abuse or inabilityto clot normally, senile purpura is old age bruising caused by thin subcutaneous tissue

Front 66

causes of hemorrhage

Back 66

damage to vascular wall (trauma, dz, tumors), disruption of clotting mechanisms (decreased platelets, hemophilia, liver dz)

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effects of bleeding

Back 67

local bruising, dire if in brain or pericardial sac (fills sac and keeps heart from contracting normally) or fatal from loss of circulatory volume and tissue death from decreased O2 and nutrients

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signs and symptoms of excessive blood loss

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decreased BP, increased pulse and respirations, decreased UOP, restlessness and confusion (brain not getting enough O2), anxiety, feelings of impending doom

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embolism

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movement of a mass from one area of a body to another where it lodges

Front 70

thromboembolus

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from a blood clot--most common, usually from venous circulation in legs or pelvis

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pulmpnary embolus

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blocks pulmonary circulation S/Sx--sudden dyspnea (difficulty breathing), increased respirations and pulse, cough, chest pain, hemoptysis (blood in sputum) Dx with lung scan

Front 72

air embolus

Back 72

occludes the capillary, air enters circulation through an IV, arterial line, during surgery

Front 73

fat embolus

Back 73

fat emboli from bone marrow enter circulation and travel to the lungs (or brain), usually 24-48 hrs after trauma (crushing injury), S/Sx--restless, disoriented, dyspnea, petechiae on skin (chest)

Front 74

what does a fat embolus cause?

Back 74

vessel necrosis and bleeding at the place where it lodges

Front 75

S/Sx of a fat embolus

Back 75

restless, disoriented, dyspnea, petechiae on skin (chest)

Front 76

how can you distinguish b/n a fat embolus and a thromboembolus?

Back 76

skin petechiae

Front 77

arteriosclerosis/atherosclerosis

Back 77

hardening and thickening of the arteries, formation of atheroma or plaque

Front 78

what does plaque consist of?

Back 78

fat and fibrous tissueand maybe calcium salts

Front 79

what does plaque do to a vessel?

Back 79

roughens the lining of the vessel so that thrombus formation is more likely, may occlude the vessel, vessel unable to change sizes in response to tissue demands for more/less blood

Front 80

causes of arteriosclerosis/atherosclerosis

Back 80

genetics, diet, lipid levels, diabetes, cigarette smoking, elevated BP

Front 81

effects of arteriosclerosis/atherosclerosis

Back 81

depends on size and locationof the arteries involved, coronary artery--MI, limits ability to dilate or constrict--cannot respond to signals, lose compliance

Front 82

aneurism

Back 82

plaque weakens the vessel wall causing vessel to balloon out

Front 83

thrombosis

Back 83

inappropriate formation of a clot or thrombus in the circ system, stationary

Front 84

causes of thrombosis

Back 84

abnormality or injury in lining of the vessel wall, abnormality in the flow of blood (too turbulent or too slow), increase in coaguability (dehydration, excess platelets)

Front 85

common examples of thrombosis

Back 85

IV roughens vessel wall and clumps of platelets adhere, fibrin attaches, clump catches circulating blood cells and clot enlarges, bedridden patient with poor venous returndue to decreased pumping action of the leg muscles ---DVT

Front 86

thrombosis-heart attack

Back 86

thrombus in heart valvesif valve leaflets roughened, stenosed or infected and clot moves to coronary artery

Front 87

thrombus in brain

Back 87

stroke

Front 88

thrombus in arterial circulation

Back 88

death of tissue due to decreased O2

Front 89

thrombus in venous circulation

Back 89

venous congestion

Front 90

how is a thrombus dissolved

Back 90

by itself or with meds

Front 91

ischemia

Back 91

decresed blood flow to an area, decreased O2, nutrients, and increased accumulation of waste products

Front 92

causes of ischemia

Back 92

anything that decreases blood flow

Front 93

examples of ischemia

Back 93

thrombus, embolus, arterioschlerosis, congestive heart failure, hemorrhage

Front 94

S/Sx of ischemia in heart

Back 94

angina (chest pain)

Front 95

S/Sx of ischemia in leg muscle

Back 95

cramps when walking

Front 96

S/Sx of ischemia in heart

Back 96

confusion, agitation

Front 97

infarct

Back 97

if ischemia is abrupt and severe, ischemic tissue dies

Front 98

infarction

Back 98

process of ischemic tissue dying from abrupt and severe ischemia, anything distal to the infarct will die

Front 99

conditions that effect severity of ischemia

Back 99

depends on length of time, tissue demands

Front 100

things that increase chance of tissue recovery from ischemia

Back 100

O2 demand decreased, ischemia occurs slowly and if collateral circulation develops EX: MI