Pathology Exam 2 - Fluid And Hemodynamics Derangements

Front 1

Exudate

Back 1

INflammatory fluid, protein rich, sg>1.020, many cells

Front 2

Transudate

Back 2

NONinflammatory, low in protein & colloids, sg < 1.020, few cells

Front 3

Mechanisms of edema (4 steps)

Back 3

1. increase in hydrostatic pressure (mechanical)
2. decrease in osmotic pressure
3. obstruction of lymph flow
4. increase capillary permeability

Front 4

Effects of LV failure

Back 4

pulmonary edema - left over blood in LA (because less blood pumped from LV) --> back flow thus, pulm. edema

Front 5

Effects of RV failure

Back 5

blood left in venous system

Front 6

causes of increase in hydrostatic P
1. local
2. systemic

Back 6

1. obstruction of venous drainage
2. heart failure (hypoxia + RAAA) - compensatory mechanism

Front 7

describe system cause of increase in hydostatic pressure (hypoxia + RAAA)

Back 7

heart failure -> dec blood vol -> RAAA activated -> angiotensin acts on renal cortex and inc. pressure by reabsorbing fluid and Na+

Front 8

causes of decreased osmotic pressure

Back 8

malabsorption syndrome - no protein absorption
nephrotic syndrome
cirrhosis - proteins not manufactured

Front 9

what do you notice from dependent edema?
What is distention a sign of?

Back 9

- JVD - flows into RA (RV failure due to back flow of blood into venous system)
- heart failure

Front 10

Cardiac edema causes _______ edema

Back 10

dependent - edema in all other tissues, but not heart

Front 11

Renal edema starts in?

Back 11

the face - periorbital

Front 12

pulmonary edema

Back 12

lethal; fluid in lungs; LV failure - patients drowning in own fluids

Front 13

cerebral edema

Back 13

brain swells -> no room to expand in skull -> increases intracranial pressure -> brain herniates through foramen magnum -> pushes on medulla -> respiratory arrest

Front 14

effects of edema on stomach wall

Back 14

wall thickens, patient cannot eat

Front 15

LV failure (cause)

Back 15

chronic passive congestion of lungs

Front 16

nutmeg liver

Back 16

caused by chronic passive congestion of the liver; central hemorrhagic necrosis

Front 17

LV failure and mitral stenosis

Back 17

back up -> edema -> increase pressure -> lung capillaries rupture -> hemoptosis/hemorrhage

Front 18

heart failure cells

Back 18

macrophages eat blood from hemorrhage of lung capillaries - result in the cells
** NOT in heart**
--> most likely will lead to heart failure
--> caused by LVF

Front 19

what is the detrimental effect of repeated hemorrhaging?

Back 19

overall loss of iron --> IDA - iron deficiency anemia

Front 20

effects of rupture in heart

Back 20

intrapericardial hemorrhage -> interferes w/ cardiac filling -> cardiac tamponade

Front 21

cardiac tamponade

Back 21

decreased stroke volume of heart due to percardial fluid which puts pressure on the ventricles of the heart --> acute heart failure

Front 22

endothelial injury

Back 22

important disease in atherosclerosis (atheroma)
- endotheilial injury -> release of throbatic factors -> clotting event

Front 23

laminar flow

Back 23

blood flow is in the axial stream, and the periphery is called the "clear plasma zone"

Front 24

Stasis

Back 24

slowing of blood

Front 25

turbulence

Back 25

any obstruction in BV wall causes turbulence; cell touch periphery, become sticky due to platelet activation

- turbulence induces endothelial injury

Front 26

stasis and turbulence cause:

Back 26

thrombosis

Front 27

checks and balance for getting rid of clots

Back 27

Fibrin --plasmin--> FDP (fibrin degradation products)
FDPs aka fibrin split products
--> measurement will tell if plasmin/plasminogen system is working

Front 28

causues of hypercoagulability

Back 28

DON'T MISS
1. deficiency - antithrombin III or protein C
2. Oral contraceptives
3. nephrotic syndrome
4. trauma/thrombocytes
5. Malignancy
6. Increase: platelets/prothrombin
7. Stickiness of platelets increased
8. syndromes (nephrotic, etc)

Front 29

Virchow's triad

Back 29

1. endothelial damage
2. change in blood flow
3. quality of blood (hypercoagulability of blood)

Front 30

mural

Back 30

non-occlusive, in cardiac chambers and aorta on the walls
- no obstruction of flow exists
- usually seen in mitral stenosis
- clots detached and flow out of heart to cause emboli

Front 31

occlusive

Back 31

in small arteries, especially in coronary arteries

Front 32

fate of thrombus

Back 32

1. propagation
2. embolization
3. removal
4. organization
5. infection

Front 33

propagation

Back 33

thrombus may propagate and cause obstruction of some *critical vessel/branch*

Front 34

thrombus remains attached

Back 34

retraction, recanalization (thrombus becomes organized by invading fibroblasts and capillaries); can be hyalinized, calcified

Front 35

embolization

Back 35

whole thrombus, or part of it may break away and embolize

Front 36

removal

Back 36

by fibrinolytic action; some pulmonary emboli shrink and disappear due to fibrinolysis

Front 37

what are the 2 major problems w/ thrombosis?

Back 37

1. obstruction
2. embolization

Front 38

infection

Back 38

breaking loose can cause septic embolism; portions get detached to produce septic infarction, pyemic abscesses

Front 39

what happens when a thrombus in iliac vein detaches?

Back 39

travels to lungs

Front 40

arterial thrombi are usually _______; thrombosis in deep veins usually result in _______

Back 40

obstruction (coronary arteries; MI)
emboli

Front 41

common clinical settings of thrombosis

Back 41

1. advanced age
2. bed rest & immobilization
3. heart disease
4. tissue injury
5. cancer
6. late pregnancy and delivery

Front 42

advanced age

Back 42

atheroma, hypercoagulability, decreased activity (venous stasis)

Front 43

bed rest/immobilzation

Back 43

improper circulation of blood, stasis & hypercoag: mm and heart both propagators of circulation, so lack of movement makes blood in veins stationary

Front 44

horizontal s/p sx

Back 44

bad, must move around
people die from thrombosis s/p sx

Front 45

heart disease

Back 45

MI, MS, CHF, CHD

Front 46

tissue injury

Back 46

-- fractures, burns
-- labor - 3rd trimester, platelets increase, become more sticky
-- after injury - platelets become more sticky

Front 47

cancer

Back 47

get a lot of random clots that usually dissolve

Front 48

trousseau syndrome

Back 48

multiple thrombi that eventually cause problems

Front 49

late pregnancy and delivery

Back 49

stasis
hypercoagulability
procoagulants

Front 50

causes of DIC

Back 50

- obstetric complications
- malignancy
- severe infection
- massive tissue injury
- endothelial injury due to:
1. immune complexes
2. infections
3. burns

Front 51

effects of DIC

Back 51

1. MAHA - mitroangiopathic hemolytic anemia
2. lungs - ARDS
3. kidney - renal cortical necrosis, hemorrhage in adrenals
4. cerebral infarcts
5. infarct in pituitary - sheehan syndrome
6. toxemia of pregnancy

Front 52

MAHA

Back 52

RBCs in fragments, broken down --> causing multiple infarcts and bleeding

Front 53

lab dx of DIC

Back 53

decreased platelets
increased bleeding time
increase prothrombin time
decreased fibrinogen
increased FDP

Front 54

causes of embolisms

Back 54

- DVT:
-- deep veins behind knee (popliteal, which lack movement)
-- thrombus gets detached and gets into IVC -> heart -> lungs

Front 55

large embolus

Back 55

block main pulmonary artery or become saddle embolus

Front 56

medium emboli

Back 56

occlude pulmonary branches, induce pulmonary infarct

Front 57

small emboli

Back 57

chronic cor pulmonale -> PHT and vascular sclerosis

Front 58

saddle embolus

Back 58

acute cor pulmonale, very severe and can cause damage w/in seconds
- can instantly kill w/ very large thrombus
--> ex: in plane for 12 hrs, get up to walk around, drop dead

Front 59

fat embolism syndrome

Back 59

petechiae
thrombocytopenia - platelet count used up, respiratory difficulty, coma
- occurs after severe trauma