Path Test 2

Front 1

RV failure vs. LV failure and congestion

Back 1

RV failure- systemic congestion

LV failure- pulmonary congestion

Front 2

heart failure cells

Back 2

macrophages in alveoli eat blood cells during congestion- NOT IN LOCATED IN HEART

Front 3

brown induration

Back 3

lungs become firm and brown due to fibrous thickening of alveolar walls

Front 4

cardiac edema

Back 4

edema is not in heart but:
subcutaneous in lower extremity, -dependent edema
-sacral edema
-pitting edema

Front 5

renal edema

Back 5

not pitting but not dependent bc it starts in face

Front 6

pulmonary edema

Back 6

may be lethal
-LV failure

Front 7

transudate vs exudate

Back 7

trans- non inflammatory, loww protein, edema fluid

exudate- inflammatory- rich in protein

Front 8

nutmeg liver

Back 8

result of chronic congestion of liver in RV failure
-red-blue congested centers rimmed by yellow-tan parenchyma produce mottled appearance of liver

Front 9

repeated chronic external hemmorhange results in

Back 9

loss of Fe-iron deficiency anemia

Front 10

virchows triad

Back 10

three major influences of thrombogenesis (clot formation)
1)endothelial injury

2)changes in blood flow
stasis and turbulence disrupt blood flow and contribute to thrombogenesis

3) hypercoagulability of Blood: DONT MISS
Deficiency (protein C)
Oral contraceptive use
Nephrotic syndrome
Trauma/Thrombocytes
Malignancy
Inc platelets
Stickiness of Platelets
Syndromes

Front 11

plasminogen to plasmin will effect a clot how

Back 11

fibrinoloysis, fibrin is degraded to FDPs (Fibrin degradation products)

Front 12

mural thrombis vs occlusive thrombis

Back 12

mural-non occlusive seen in cardiac chambers and aorta

occlusive- seen in arterial tree and veins

Front 13

fate of thromus (5 steps):

Back 13

1) propagation
2) embolization
3) removal (fibrinolytic action, fibrinolysis)
4) organization- organzied by invading fibroblasts and capillaries
5) infection

Front 14

clinical significance of thrombi

Back 14

1) obstruction to blood flow (arterial obstruct coronary artery-> MI)
2) embolization (thrombi in deep veins of leg -> pulmonary embolization and infarction)

Front 15

common clinical settings for thrombosis formation:

Back 15

1) advanced age
2) bed rest and immobilization
3) heart disease
4) Tissue injury
5) cancer -> Trousseau phenomenon (multiple thrombosis in various places)
6) late pregnancy and delivery

Front 16

disseminated intravascular coagulation

Back 16

aka: consumption coagulation

pathologic activation of coagulation-> widespread thrombosis -> consumption of coagulating factors -> blood cant clot -> hemorrhage

Front 17

causes of Disseminated intravascular coagulation

Back 17

--obstetric complications
-malignancy
-infections
-massive tissue injury
-endothelial injury (immune complexes, burns, infections)

Front 18

effects of DIC

Back 18

-hemorrhage
-FDPs (Fibrin degradation products
-microangiopathic hemolytic anemia

Front 19

lab dx: DIC

Back 19

dec fibrinoge, dec platelets, inc FDP

Front 20

emboli arising in veins vs arteries

Back 20

veins- travel to impact lungs
arteries- travel to impact legs, brain viscera

Front 21

systemic embolism

Back 21

most arise from thrombi in heart

Front 22

pulmonary embolism

Back 22

arises from deep veins in legs-> large embolus may cause sudden death or right heart failure (acute cor pulmonale)

chronic cor pulmonare -> pulmonary hypertension

Front 23

fat embolism

Back 23

globules of fat circulating in blood stream with subsequent impaction

fat embolism syndrome: consists of thrombocytopoenia, petechiae in skin and conjunctivae, respiratory difficulty, mental deterioration and coma and death

Front 24

infarction factors

Back 24

protected by anastomoses (multiple ways for blood to flow) while end arteries are danegerous

slow occlusion- provides time for bypass channels to develop

Front 25

types of infarct

Back 25

may be septic, bland (aseptic)
-involve periphery of solid organs and produce a wedge-shaped area with base at external organ and apex at site of obstruction

-fate of infarcts- phagocytic removal of dead tissue followed by organization and scar (except in brain, liquefactive necrosis)

Front 26

clinical significance of infarcts

Back 26

mycardial, pulmonary and cerebral infarctions responsible for over half of all deaths

Front 27

causes of hypovolemic shock

Back 27

hemorrhage
trauma
surgery
burns
fluid loss -> vomiting/diarrhea

Front 28

causes of vasogenic shock

Back 28

(normal blood volume, but vasodilation inc size of vascular system)

neurogenic shock
anaphylaxis
septic shock

Front 29

causes of cardiogenic shock

Back 29

MI
CHF
Arrhythmias

Front 30

causes of obstructive shock

Back 30

pulmonary embolism (saddle embolism)
cardiac tamponade
cardiac tumor
tension pneumothorax (lung collapse leading to mediastinum shift putting pressure and obstructing large BV)

Front 31

hypovolemic shock: symptoms and signs

Back 31

hypotension
rapid thready pulse
cold clammy skin
tachycardia/tachypnia

inadequate perfusion of tissues-> inc anaerobic glycolysis-> inc lactic acid -> dec peripheral vascular response to catecholamines

Front 32

compensatory mechanisms for hypovolemic shock

Back 32

maintain CO and BP via -
-baroreceptor reflexes
-sympathetic stimulation
-activation of RAAS
-vasoconstriction (except brain and heart) -> cold clammy skin

low BP- chemoreceptors -> tachypnia, tachycardia

low BP- renal shutdown

Front 33

Vasogenic (distributive) shock results in

Back 33

1) hypotension
2) warm skin (initially bc of vasodilation)
3) vasodilation -> hyperdynamic circulatory state -> peripheral pooling - no hemorrhage but due to difference in volume of blood and capicity of vascular system (which is vasodilated because of vasoactice substances released after tissue destruction, allergic rxn)

Front 34

septic shock- stats risks

Back 34

most common cause of death in ICU
-major risk: use of catheter
-aka Systemic Inflammatory Response Syndrome (SIRS) which leads to Multiple Organ Dysfunction Syndrome (MODS)

Front 35

SIRS results from systemic release of cytokines such as

Back 35

TNF, IL-1, IL-6 and PAF

Front 36

Sepsis poor prognosis if

Back 36

you have hypothermia/leukopenia

Front 37

refractory shock

Back 37

severe stage of shock showing no response to treatment- leads to multiorgan failure.

Front 38

Waterhouse-Friderichsen syndrome

Back 38

disease of adrenal gland caused by meningococcal septicemia- severe septic shock- circulatory collapse

Front 39

patient presentation of shock

Back 39

hypotension- wake rapid pulse, tachypnia, cold and clammy skin (except in vasogenic shock)

3 or more organs fail -> 80-100% chance of death

Front 40

things that worsen shock

Back 40

multiorgan failure
ARDS
SEPSIS
DIC

Front 41

programmed theories

Back 41

programmed longevitiy - aging = activation and deactivation of genes

endocrine theory- senescnece results in decrease of hormone production - decrease in bodies ability to repair itself

immunologic- programmed decline in the immune system functions leads to increased vulnerability

Front 42

error theories

Back 42

wear and tear- years of damage on cells

rate of living- limited number of times a heart beats

crosslinking- with age DNA crosslink to each other and interfere with functions

free radical theory-damage tissue and normal cell components

telomere: telomeres become too short and cell can't do mitosis

misfolded protein theory: Hsp fail- misfolded proteins accumulate and interfere with cell function

Front 43

most common fluid and electrolyte disorder the elderly

Back 43

dehydration

Front 44

most common cause of hair loss in men

Back 44

genetics