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200 Cards in this Set
- Front
- Back
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For a 70kg man,
Total Body Water |
40-45 L
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For a 70kg man,
Intracellular fluid |
25 L
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For a 70kg man,
Extracellular fluid |
17 L
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2 subtypes of ECF
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interstitial fluid
intravascular fluid |
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For a 70kg man,
interstitial fluid |
12 L
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For a 70kg man,
intravascular fluid (& components) |
5 L
(3L plasma fluid & 2L corpuscular elements of blood) |
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Blood
___% fine particulate matter ___% fluid plasma |
Blood
45% fine particulate matter 55% fluid plasma |
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lack of blood circulation
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hemostasis
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3 types of disturbances of laminar flow
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turbulence
eddies jet stream |
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loss of protection against blood loss -->
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hemorrhagic diathesis
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Edema
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excessive accumulation of fluid in teh CT spaces and serous sacs (i.e.: interstitial compartment)
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Dropsy
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lay term for generalized edema
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anasarca
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edema of subcutaneous tissue
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____ consitute the greates fraction of colloid osmotic pressure
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plasma proteins, especially albumin
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decrease of plasma proteins
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hypoproteinemia
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decrease in albumin
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hypoalbuminemia
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what occurs as a result of hypoproteinemia and/or hypoalbuminemia?
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+ loss of fluid in intravascular compartmen
+ gain of fluid in interstitial compartment --> edema |
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retention of sodium leads to...
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retention of water in the interstitial compartment
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the greater the permeability in the vascular wall, the greater the movement of fluid _____ the intravascular compartment
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The greater the permeability in the vascular wall, the greater the movement of fluid OUT OF the intravascular compartment
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describe fluid that moves out of intravascular compartment in venous or generalized edema
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ultrafiltrate of serum
low specific gravity (1.012) protein content 1% lacks coagulation factors |
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Compare fluids of edema and inflammation
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EDEMA:
- transudate - clear, straw-colored - hydropericardium - hydrothorax - ascites INFLAMMATION - exudate - turbid, purulent, etc. - pericarditis - pleurisy, pleuritis - peritonitis |
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Effusion
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non-specific term which refers to an accumulation of fluid, which can be transudate, lymph, exudate or blood
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removal, drainage of fluid
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paracentesis
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paracentesis of the pericardium
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pericardiocentesis
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paracentesis of the pleural sac
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thoracentesis
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paracentesis of the pleural sac
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thoracentesis
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paracentesis of the peritoneal sac
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paracentesis (abdominis)
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3 causes of LOCAL edema
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venous obstruction
lymphatic obstruction local increase in permeability of vessel wall (trauma, allergic/hypersensiviity reaction) |
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what TYPE of edema does venous obstruction cause?
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soft, pitting (yielding) edema
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5 causes of lymphatic obstruction
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Malignant neoplasms
Chronic granulomatous diseases (TB, Bunkolderia mallei) Parasitic diseases (Filariasis) Ioatrogenic causes (post surgical resection, post irradiation) compression from teh outseide (masses, tumor, aneurysms, scar tissue) |
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brawny edema
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lymphedema
swollen and indurated area peau d'orange (BRCA presentation) w/ filariasis --> elephatitis |
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presentation of lymph in serous sacs
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fluid is MILKY
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lymph accumulation in pericardial space
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chylopericarelium
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lymph accumulation in pleural sacs
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chylothorax
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lymph accumulation in peritoneal sac
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chylous ascites
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what does "chylos" mean?
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juice
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Inflammatory edema
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"tumor" sign of inflammation
exudation of fluid out of the vessel into the interstitial compartment |
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urticaria
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hives
due to increased venular permeability following the degranulation of mast cells example of local edema |
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4 types of generalized edema (by etiology)
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Cardiac
hypoproteinemia increased retention of sodium renal edema |
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etiology of cardiac edema due to LEFT HEART FAILURE
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engorgement of alveolar capillaries
increase in hydrostatic pressure & permeability of capillary wall |
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etiology of cardiac edema due to RIGHT HEART FAILURE
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aldosterone-mediated retention of sodium in the interstitial compartment & thereby, of water
distribution determined by gravity |
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3 causes of hypoproteinemia
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decreased protein intake
increased loss - gross albuminuria in nephrosis decreased hepatic metabolism |
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reversal of albumin: globulin ratio is one of the earliest signs of what?
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liver failure
comorbid w/ loss of albumin into peritoneal sac in ascites |
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3 causes of renal edema
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nephritic
nephrotic chronic renal failure |
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cause of nephritic renal edema
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circumonbital edema in acute glomeronephritis
caused by immune complex deposition in vessel wall |
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cause of nephrotic renal edema
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edema in nephrotic syndrome
due to hypoproteinemia following massive loss of albumin in urine |
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cause of edema in chronic renal failure
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edema due mostly to cardiac failure
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3 important sequelae of edema
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lungs - alveoli fill with transudate, imparing hemorespiratory exchange
brain - edema causes increased pressure, forcing brain down into foramen magnum (cone phenomenon) with compression of vital centers edema glottidis - edema of larynx above the vocal cords --> encroachment of airway |
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hyperemia
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increase in the amount of blood in a tissue at a given time
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active hyperemia
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when increased inflow of blood is pumped activly into the tissue from the arterial side
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passive hyperemia
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damming back of blood being drained out of the area by the venous channels
aka: congestion |
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local congestion
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due to obstruction of venous drainage
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acute local congestion
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occurs classically in starving children - marantic thromposis:
rapid damming of blood in cortical veins --> engorgement --> rupture rapid occlusion of portal vein by hepatic cancer infiltration --> rupture of mesenteric veins --> hemorrhage into gut wall |
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chronic local congestion in limbs
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more gradual decrease in venous drainage than in acute
e.g.: variose veins, DVT --> local, pitting edema limb becomes swollen, cold and cyanosed |
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chronic local congestion in portal vein
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damming of blood in spleen and intesting
portal splenomegaly - spleen enlarges, becomes firmer and darker in color |
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Superior Mediastinal Syndrome
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compression of SVC
chronic passive congestion edema of arms, neck and head seen classically in constrictive pericarditis |
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Left heart failure leads to ____ hyperemia of the _____
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Left heart failure leads to PASSIVE hyperemia of the LUNG
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mechanism of lung congestion in left heart failure
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left heart fails
progressive damming of blood in pulmonary veins increased intravascular pressure alveolae become engorged increased pressure and permeability --> transudation into alveolar sac RBCs into alveoli by diapedesis phagocytosis of RBCs by alveolar Mphages increased venous pressure --> phlebosclerosis stagnant anoxemia --> vasoconstriction of pulmonary arterioles --> increased resistance to action of RV --> RV hypertrophy |
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heart failure cells
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siderophages
alveolar macrophages that have eaten RBCs, breaking them down into Hgb and hemosiderin |
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gross pathology of pulmonary congestion
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venous, enular and alveolar capillary engorgement
edema of interstitial tissue and alveolar sacs RBCS and siderophages in alveoli consistency of lungs increased - induration siderophages --> brown color |
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Right heart failure leads to ____ _____ hyperemia
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Right heart failure leads to generalized chronic congestion (passive hyperemia)
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Causes of right heart failure as a *pure* entity
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pulmonary stenosis
diseases of the lungs idiopathic/primary pulmonary HTN --> dimunition of RV output *NO pulmonary venous congestion |
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most important cause of right heart failure
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left heart failure
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Stasis of venous blood leads to a progressive _____ in _____ Hgb
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Stasis of venous blood leads to a progressive INCREASE in REDUCED hemoglobin
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prevalent reason for hospitalizations for heart failure
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fluid volume overload
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When the level of reduced Hgb reaches 5gm%, it causes ____
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cyanosis
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cyanotic induration
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seen in heart failure, secondary to stasis of venous blood & reduced Hgb
increased consistency of systemic viscera and cyanosis seen well in spleen - rubbery consistency and plum color of the cut surface |
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what happens to the liver in right heart failure
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affected early in right heart failure
venous blood dammed back in heaptic veins & thence into central veins (terminal heaptic venule) of the lobules sinusoids of central zone (zone 3) become engorged stagnant anoxemia --> parenchymatous degeneration of peripheral zone (zone 1) --> fatty degeneration |
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nutmeg liver
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mottling of cut surface of liver
cyanotic cnetral zone & pale, yellow peripheral zone occurs with right heart failure |
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gross pathology of chronic passive congestion of the liver
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progressive atrophy and loss of centrilobular cells
condensation of supporting tissue |
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effect of chronic passive congestion in right heart failure in BRAIN & GI tract
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petechial hemorrhages
in brain, called puncta cruenta |
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In the kidney, cyanosis is most marked in the _____
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medulla
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gross pathology of cyanotic kidney
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cyanosis most marked in medulla
engorgement of gromerular capillaries --> enlargement of glomerular tuft on cut section of cortex, glomeruli bulge above cut surface --> appear like sprinkled pepper ("peppering of glomeruli") |
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rhexis
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rupture or erosion of vessel wall
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2 ways blood is lost from intravascular compartment
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rhexis
diapedesis |
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Causes of hemorrhage by rhexis
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Rupture due to weakening of the wall
- aneurysm (atherosclerosis, TB, peptic ulcer) - inflammatory process (necrotizing vasculitis) Erosion of vessel wall - infiltration of malignant tumor - physical trauma |
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Heamtoma
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localized hemorrhage
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occult bleed
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internal hemorrhage w/ no external evidence of bleeding
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hematamesis
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vomiting of blood
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melena
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blood in the stool
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hematuria
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blood in the urine
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hemothorax
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blood in pleural cavities
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hemopericardium
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blood in the pericardial sac
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hemoperitoneum
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blood in the peritoneal sac
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hemarthrosis
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blood in a joint cavity
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Large hemorrhage sequella
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loss of circulatory volume --> hypovolemia --> shock
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long, continued loss of relatively small quantities of blood
sequella |
iron deficiency = hypochromic microcytic anemia
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hemorrahge by diapedesis
due to increased permeability of vessel wall |
vitamin C deficiency
overdistension toxic damage - bacterial, chemical |
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Hemorrhage by diapediesis
due to defects of coagulation |
deficiency of platelets
defects of coagulation factors |
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Types of hemorrhage
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petechiae - minute, localized
purpura - condition characterized by presence of multiple petechiae ecchymosis - larger, localized hemorrhage |
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Definition of shock
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inadequate blood flow to vital organs
or the inability of organs to use O2 & other nutrients widespread serious reduction of tissue perfusion --> generalized impairement of cellular function |
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circulatory deficiency of shock results from...
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disparity btw vol. blood and vol.-capacity of vascular system
--> progressive and profound fall in arterial BP |
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Conditions in which shock is caused by increased volume capacity of vascular bed
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initial shock (syncope)
primary shock vasovagal shock |
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causes of increased vol. capacity of vascular bed
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anestheisa
traumatic SCI |
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organ most sensitive to limited perfusion
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brain
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cerebral anoxia -->
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LOC
--> falling, which restores blood flow to brain |
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7 causes of shock
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traumatized tissue
pain from pathological porcesses emotional reactions or stress sympathectomy-pharmalogic or surgical induction of anestheisa hermorrhage sequestration of blood in lower extremities |
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Clinical features of shock
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faintness
pallor shallow breathing N/V cold sweat signs of prostration and unconsciousness low BP weak pulse |
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Shock is usually ____ & ____, but in severe instances it may merge into _____
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Shock is usually transient and self-limiting, but in severe cases it may merge into secondary shock.
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Conditions in which shock is caused by reduction of blood volume
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hypovolemic shock
oligemic shock peipheral circulatory failure |
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3 causes of blood volume reduction
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loss of blood, e.g.: hemorrhagic shock
redistribution of fluid, e.g.: anaphylaxis loss of fluid - external fluid loss or internal sequestration |
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types of eternal fluid loss
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GI tract - vomiting, diarrhea
urinary tract - diabetes insipidus, DM, excessive use fo diuretics cutaneous - burns, perspiration |
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types of internal fluid sequestration
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ascites
pleural effusion |
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pathogenesis of reduced blood volume causing shock
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peripheral circulatory failure --> hemoconcentration --> deminished venous return --> diminished cardiac output
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shock due to primary dimunition of cardiac output, aka:
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cardiogenic shock (mortality 80-90%)
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2 causes of cardiogenic shock
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impairment of myocardial contractility
obstruction of blood flow |
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causes of myocardial contractility impairment
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intrinsic myofiber insufficiency
- myocardial infarction - severe CHF abnormalities of impulse conduction - arrhythmias |
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thrombosis definition
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formation of a solid or semi-solid mass from the contituents of the blood within vascular tree
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thrombus definition
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solid and semi-solid mass in vasculature
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difference btw thrombus and coagulation
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coagulation can occur outside vascular system and in living or nonliving tissue
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crucial locus of hemostatic-thrombotic balance
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endothelial lining
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endothelium regulates ____, _____ and _____ of the vessel wall
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anti-inflammatory
mitogenic contractile activities |
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6 anti-thrombogenic properties of endothelium
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synthesis of prostacyclin from arachidonic acid
production of ADPase synthesis of plasminogen activator synthesis of heparan sulfate activation of Protein C and Protein S synthesis of tissue factor pathway inhibitor |
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molecules that stimulate synthesis of prostacyclin
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bradykinin
adenine |
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prostacyclin function
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powerful inhibitor of platelet aggregation, but not adhesion
inhibits platelet function by elevating intracellular cAMP levels smooth muscle cell relaxant --> vasodilation |
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EDRF, aka:
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NO
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plaminogen activator function
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activating plasminogen --> plasmin
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plasminogen --> plasmin
stimulated by |
NE
thrombin bradykinin vasopressin stasis shear stress |
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function of plasmin
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lyses fibrin
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function of heparan sulfate
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adhesive porperties of vessel wall for heparin
catalyzes action of antithrombin III |
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thrombin function
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reacts with thrombomodulin on surface of endothelial cell
activates Protein C activation of PRotein C and Protein S --> digestion of coagulation factors V & VIII activates fibrinolytic system |
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tissue factor pathway inhibitor
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cell surface protein
inhibits Factor VIIa and Factor Xa |
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Bacteria causing gram negative endotoxic shock
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E. Coli
Klebsiella Proteus |
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Pathogenesis of endotoxic shock
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lipid region of endotoxin combines with C1 and activates classical complement pathway
polysaccharide fraction activates alternative complement pathway PNMs --> proteases, ROIs --> endothelial injury --> stagnation in microcirculation IL-1, IL-6, TNF-a --> downrgulation of thrombomodulin and protein S receptors |
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stagnant anoxemia
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stagnation in microcirculation
seen in endotoxic shock mortality causes cellular deprivation of O2 |
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2 common complications of endotoxic shock
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DIC: disseminated intravascular coagulation
direct parnchymatous damage by anoxemia |
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gram positive exotoxic shock
organism |
S. aureus
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6 clinical features of exotoxic shock
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fever
rash desquamation hypotension involvement of 3 or more organ systems negative blood, throat, CSF cultures |
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organ systems that may be involved in exotoxic shock
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mucous membrane
muscle renal hepatic CNS |
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6 organs showing pathomorbidity in exotoxic shock
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lungs - enlarged, heavy, congested, boggy
kidneys - acute tubular necrosis adrenals - depletion of lipid, scattered necrosis of cortical cells instine - acute hemorrhage, congestion, focal necrosis of mucosa brain - hypoxic encephalopathy, usu. focal clusters of neurons heart - subendocardial hemorrhage and zonal lesions |
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mechanical function of endothelium in anti-thrombogenesis
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mechanical barrier btw circulating blood with its procoagulant factors and the subendothelial CT, which has thrombogenic properties
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most thrombogenic constituent of subendothelial tissue
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fibrillar collagen
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role of ACh in blood vessels
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In presence of intact endothelium --> vasodilation
In absence of endothelium --> vasoconstriction |
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triggers of endothelial procoagulant properties
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mechanical damage
activation of vascular cells by cytokines bacterial endotoxin hypoxia hemodynamic forces |
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proagulant properties of endothelium
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synthesis of von Willebrand factor
production of thromboplastin endothelial cells have receptors for factors IXa and Xa inhibit tissue plasminogen activator in anoxia, release endothelin (vasoconstrictor) secrete EDGF, PAF, CAM produce ACE --> aggregation of platelets |
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Platelets include which nucleic acid?
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mRNA (and translational machinery)
(lack genomic DNA) |
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4 types of platelet granules
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dense
alpha lysosome peroxisomes |
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contents of dense granules
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ADP
ATP serotonin histamine epi Ca2+ |
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contents of alpha granules
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platelet factor 4
factors V and VIII thrombospondin von Willebrand factor fibrinogen fibronectin PDGF |
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contents of lysosomes
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acid hydrolases - dissolve protein in platelet apoptosis
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peroxisome contents
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catalase
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platelet membrane receptors responsible for cell-cell adhesion
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integrins
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platelet adhesion is mediated by _____ & _____
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integrin complex GpIb V IX
von Willebrand factor |
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morphological changes in activated platelets
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formation of pseudopodia (cytoplasmic extensions)
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platelet activation agonists
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Epi
thrombin |
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Process of platelet activation
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conversion of platelet membrane receptors GpIIb/IIIa complexes --> receptors that bind fibrinogen, vonWillebrand factor & thrombospondin
addn'l platelets recruited fibrinogen binds platelets together btw GpIIb/IIIa receptors |
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arachidonic acid derivative made by platelets
function |
Thromboxane A2
powerful platelet aggregator vasoconstrictor |
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calcium ionophores ____ platelet aggregation
calcium chelators (EDTA) ____ platelet aggregation |
calcium ionophores STIMULATE platelet aggregation
calcium chelators (EDTA) INHIBIT platelet aggregation |
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primary hemostasis
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pure platelet thrombus plugging small breaches in vascular lining
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3 natural inhibitors of platelets
|
prostacycline
ADPase NO |
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secondary hemostasis
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progressive activation of coagulation factors resulting in formation of fibrin
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2 coagulation pathways
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intrinsic pathway - intravascular
extrinsic pathway - activated outside vascular system |
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describe intrinsic pathway
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initiated by damage to endothelium exposing subendothelial collagen
deposition of platelets & activation of factor XII (Hageman factor) Kallkrein activates kinins (e.g.: bradykinin) factor XI activates factor IX, which activates factor X |
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describe extrinsic pathway
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initiated by tissue factor thromboplastin (III)
factor VII + Ca2+ activate fator X |
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action of heparin
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heparin & antithrombin III bind to heparan sulfate on endothelial surfact
remove thrombin circulating in the plasma also --> inhibition of factors IXa, Xa, XIIa also --> activation of fibrinolysis |
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Protein C and Protein S are dependent on which vitamin?
|
Vitamin K
|
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Thrombocytopenia
presentation etiology (3) |
thrombocytopenia
< 100,000/cu mm platelets spontaneous bleeding petechiae on skin and mucous mb (purpura) caused by: - diminished platelet production - increased destruction/utilization - disorders of distribution |
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thrombocytosis
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> 450,000 cu/mm platelets
reactive - response to trauma or infection, or post-splenectomy hematologic disorders |
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3 hereditary forms of thrombcytopathy
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deficiency of platelet adhesion due to deficiency of adhesion factors (vonWillebrand, or Gp Ib V IX)
deficiency of platelet aggregation - deficiency of GpIIb/IIIa sotrage granule abonormality |
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2 forms of acquired thrombocytopathy
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blood plasma inhibitors in uremia, liver ds
drug induced, eg: by aspirin |
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which coagulative factors does vitamin K deficiency affect?
|
factors II, VII, IX and X
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red thrombi
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venous thrombosis
slower blood flow --> inclusion of RBCs |
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pale thrombi
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more rapidly flowing blood
process of thrombosis slower than in red & fewer RBCs |
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lines of Zahn
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aggregation of platelets forms an irregular coralline network
differentiating feature of all thrombi |
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lamination
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variation in rate of blood flow leads to alternating layers of pale and red thrombi
usu. seen in aneurysms |
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gross appearance of thrombi
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attached to vascular lining
dull, non-glistening surface (unlike clots) |
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mural thrombus
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attached to vessel wall, but not occlude lumen
common w/in heart chambers |
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vegetation thrombi
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on heart valves
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Virchow Triad
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alteration in vascular lining
stasis - alteration in flow increased amounts procoagulants or decreased amounts of anticoagulants in blood |
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most common cause of inherited hypercoagulability
|
Factor V Leiden mutation
incrases resistance to action of Protein C |
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Antiphospholipid Ab syndrome
|
predisposes to thrombus formation
Abs attack lipins, e.g.: cardiolipin |
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endothelialization
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ingrowth into thrombus of newly formed capillaries and fibroblasts
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partial ischemia
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adequate blood flow during rest state, but insufficient during muscle contraction
|
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angina
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pain on effort relieved by rest
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angina pectoris
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substernal angina pain
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intermittent claudication
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angina pain in calf - causes pt to stop walking
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In partial ischemia, which cell type is most affected
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specialized/parenchymal
results in fibroid atrophy, or replacement fibrosis, of parenchyma |
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red infarct
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blood filled infarct
seen in organs with double blood supply after arterial occlusion or with venous occlusion e.g.: lung & liver |
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pale infarct
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seen in arterial occlusion in organs with single blood supply having organized stromal tissue
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shape of infarction in tissue
|
wedge-shaped (tapers toward blood supply)
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reaction at periphery of infarct
|
compensation of surrounding vessels --> dilation --> hemorrhagic zone ringing infarct
area of infarction = foreign body --> inflammatory reaction (PMNs) |
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avascular necrosis is of the ____ type, except in the ____
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avascular necrosis is fo the COAGULATIVE type, except in the CNS
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what happens in avascular necrosis in the CNS?
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liquefaction of the necrotic tissue
|
|
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3 possible outcomes of dead tissue
|
autolysis
myomalacia cordia (autolysis in the heart) septic infarction (bacterial proliferation) |
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What kind of tissue follows the inflammatory response in avascular necrosis?
|
granulation tissue
|
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Dry gangrene
|
not true gangrene - no putrefaction
area of avascular necrosis |
|
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After macrophages have digested the liquefied brain tissue in avascular necrosis, what is formed?
|
neuroglial cyst
|
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Embolus - definition
|
any collection of solid, liquid or gas traveling in the vascular system
|
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venous embolus - most common point of origin
|
most common in deep veins of legs
|
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most common origin of arterial embolus
|
mural thrombus, atrial appendage
|
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most common sites of occlusion for atrial emboli
|
brain
kidneys spleen lower legs |
|
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infarcts occur more with venous or arterial emboli?
|
arterial
|
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6 RFs for PE
|
genetic predisposition
age - over 60 obesity smoking HTN hormones |
|
|
clinical features of medium sized embolism impacting in hilar vessels
|
CP
SOB hemoptysis (coughing blood) tachycardia tachypnea |
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atheromatous emboi
|
embolism of materal released after ulceration of atheromatous plaques
kidney = common site |
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paradoxical embolism
|
right side of heart to arterial circulation thru PFO
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fat emboli
|
fat globules in blood commonly arising from fx in long bones
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bone marrow emboli, seen often after...
|
vigorous attempts at resuscitation
|
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air embolism
|
100cc or more gas in circulation will cause death
commonly seen after surgery, catheter insertion into jugular or subclavian veins, delivery, abortion, chest wall injury |
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3 other causes of embolism
|
nitrogen (Too rapid decompression in deep sea divers)
iatrogenic - invasive procedures foreign bodies, e.g.: bullets, IV drugs |
