Term
| 1. Describe normally functioning HEMODYNAMICS? |
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Definition
| fluid is forced out of the vessel due to HYDROSTATIC PRESSURE and reabsorbed back into the veins due to OSMOTIC PRESSURE-->all fluid left in the interstitium drains via the LYMPHATICS |
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Term
| 1. what are STARLING FORCES |
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Definition
| hydrostatic and oncotic pressures |
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Term
| 1. most common representation of abnormal STARLING FORCES? what is another term for this? |
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Definition
EDEMA-->abnormal accumulation of fluid in the interstitium or body cavities
EFFUSION=fluid in the body cavities |
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Term
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Definition
local=edema
general=anasarca |
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Term
| 1. what are the two CAUSES for EDEMA? |
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Definition
INFLAMMATORY-protein rich fluid EXUDATE
NON INFLAMMATORY-salt water/low protein fluid TRANSUDATE |
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Term
| 1. what causes TRANSUDATE? clinical presentation of TRANSUDATE? |
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Definition
effusion due to MECHANICAL factors-->high hydrostatics or low plasma osmotic pressure
CLINICAL PRESENTATION=pitting edema or ASCITES |
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Term
| 1. what causes an EXUDATE? clinical presentation of EXUDATE? |
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Definition
| effusion due to damaged mesothelial lining--> neutrophil rich, swelling but NO PITTING, pus in cavities |
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Term
| 1. what are the physiological categories of edema? |
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Definition
increased hydrostatic pressure
decreased osmotic pressure
lymphatic obstruction
sodium retention
inflammation - increased vasc permeability |
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Term
| 1. what can cause high HYDROSTATIC PRESSURE? |
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Definition
1.volume overload-->too much IV
2.heart failure--> pulmonary edema (left vent) or peripheral pitting edema (right heart )
3.veinous blockage --> thrombosis, cirrhosis, pregnancy |
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Term
| 1. what causes decreased OSMOTIC PRESSURE? |
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Definition
1. decreased proteins production- hypoalbuminemia
2. malabsorption diseases - celiac
3. nephrotic syndrome-protein loss through urine
4. liver disease
5. protein deficiency - kwoshiorkor |
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Term
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Definition
*initially pitting--> eventually non pitting
1. post radical mastectomy
2. radiation following mastectomy
3. filariasis--> elephantiasis
4. lymphogranuloma venereum
5. plugging of lymphatics by tumors |
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Term
| 1. what is CHYLOUS ASCITES? |
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Definition
| cancer edema caused by METASTATIC RAFTS of cancer cells that block lymphatics |
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Term
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Definition
| Extravasation of blood due to vessel rupture--> if contained within a tissue it is a HEMATOMA |
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Term
| 3. what deficiency can a hemorrhage lead to? |
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Definition
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Term
| 3. subcutaneous hematomas commonly causes bruises called what? |
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Definition
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Term
| 1. what distinguishes PRIMARY from SECONDARY retention of Na and H2O? |
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Definition
Primary-higher intake or low clearance (glomerulonephritis)
Secondary-Renin/angio pathway due to low CO |
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Term
| 1. what are the two categories of PULMONARY EDEMA? |
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Definition
CARDIOGENIC-paroxysmal nocturnal dyspnea
NON CARDIOGENIC-signs of infection |
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Term
| 1. what is the danger with PULMONARY EDEMA in the long term? |
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Definition
| it is a perfect environment for bacterial growth--> pneumonia |
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Term
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Definition
| solid mass formed within uninterrupted blood vessel /heart, from the constituents of blood, during life |
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Term
| 2. what does a THROMBUS consist of? two types? |
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Definition
| made of platelets, coagulation factors, epithelial cells, as well as fibrin and blood cells-->venous and arterial thrombi |
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Term
| 2. what is VIRCHOW'S TRIAD? |
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Definition
predisposing factors that can cause THROMBUS FORMATION-->
*Endothelial injury-->MOST IMPORTANT
*Alterations in laminar blood flow
*Hypercoagulability of blood |
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Term
| 2. what are types of ALTERATIONS IN BLOOD FLOW? |
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Definition
turbulence--> increases collision with endothelium
stasis-->from sedentary life or following surgery |
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Term
| 2. what are the two types of HYPERCOAGULABILITY OF BLOOD? |
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Definition
INHERITED--> factor V (leiden) mutation, anticoagulant defficiency
ACQUIRED-->oral contraceptives, etc. |
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Term
| 2. causes of VENOUS THROMBI? |
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Definition
| stasis or hypercoagulability, most common in deep veins of the legs, often in hip replacements--> dangerous because can cause PULMONARY ARTERY EMBOLIZATION |
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Term
| 2. characteristics of ARTERIAL THROMBI? |
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Definition
| endothelial injury or turbulence, fewer RBCs=pale, LINES OF ZAHN |
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Term
| 2. what are LINES OF ZAHN? |
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Definition
| lines of fibroblasts, RBC, fibroblasts, RBC,etc. seen in a n arterial thrombus |
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Term
| 2. what is a VEGETATION? MURAL THROMBI? |
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Definition
VEGETATION=Thrombi which develop on heart valves *ENDOCARDITIS
MURAL THROMBI=thrombi attached to a large vessel wall *often occur after MI |
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Term
| 2. difference between a THROMBUS and a POST MORTEM CLOT? |
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Definition
THROMBUS- red, attached to the wall
POST MORTEM CLOT-dark red with yellow top, not attached to the wall |
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Term
| 2. possible sequelae of a MURAL THROMBUS? |
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Definition
| break off and go to the BRAIN or KIDNEY |
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Term
| 2. what are the different FATES of a thrombus? |
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Definition
-propogation
-embolization
-dissolve
-organization
-recanalization
-calcification
-infection |
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Term
| 2. what is the most common sequelae of pulmonary thromboemboli? |
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Definition
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Term
| 2. what is an EMBOLUS? where do the vast majority of these come from? other sources? |
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Definition
| intravascular mass in the blood stream distant from its origin that results in occlusion-->98% are from THROMBI, can also come from fat, air, bone, foreign body, etc. |
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Term
| 2. what is considered a LARGE EMBOLI? result? |
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Definition
| blocks >60% of vessel, usually causes death |
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Term
| 2. what are the clinical signs of MEDIUM EMBOLI? |
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Definition
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Term
| 2. where do ARTERIAL EMBOLI usually arise from? |
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Definition
| LEFT SIDE OF THE HEART (vegetations,mural thrombus,etc.)--> usually lead to infarct |
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Term
| 2. what are PARADOXICAL EMBOLI? |
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Definition
| arise from VENOUS SYSTEM and pass through VENTRICULAR SEPTAL DEFECTS into systemic circulation |
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Term
| 2. what is the most common cause of FAT EMBOLISM? |
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Definition
| fracture of femur or pelvis |
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Term
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Definition
| localized increase in the volume of blood in capillaries and small vessels. *Results from localized arteriolar dilation |
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Term
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Definition
| backed up venous drainage--> slow moving blood which pools in the tissue--> deO2 Hb gives bluish/purple color *is a type of HYPEREMIA |
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Term
| 3. example of ACUTE congestion? CHRONIC? |
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Definition
ACUTE-sudden right heart failure
CHRONIC-chronic passive congestion of lung, liver |
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Term
| 3. what causes CHRONIC VENOUS CONGESTION of the LUNG? what type of cells are the hallmark of this disease? |
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Definition
| LEFT SIDE HEART FAILURE--> heart failure cells |
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Term
| 3. what are HEART FAILURE CELLS? |
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Definition
| Hemosiderin laden macrophages within alveoli |
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Term
| 3. what is the PATHOGENESIS of CVC? |
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Definition
| congestion of capillary beds-->chronic congestion, hypoxia, parenchymal cell death-->capillary rupture-->hemorrhage--> red cell debris eating macrophages become haemosiderin-laden *HEART FAILURE CELLS |
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Term
| 3. what causes CVC of the LIVER? what is the characteristic appearance? |
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Definition
| right heart failure--> nutmeg liver |
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Term
| 3. along with lung congestion, what else does LHF cause? |
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Definition
| low CO-->renal perfusion-->Na and water retention |
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Term
| 3. what does large HEMORRHAGE lead to? |
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Definition
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Term
| 3. why does hemorrhage into a body cavity not lead to iron deficiency? |
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Definition
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Term
| 3. what is PETECHIA? PURPURA? |
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Definition
PETECHIA=assoc. with ↑ intravascular pressure, ↓ platelets 1-2mm
PURPURA=same causes as petechia + vasculitis or increased vascular fragility 3-4mm |
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Term
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Definition
| Ischemic necrosis of tissue distal to an area of arterial occlusion or in an area of obstructed venous outflow |
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Term
| 3. what cell types are most sensitive to HYPOXIA? |
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Definition
| neurons (most sensitive)-->myocardial cells--> skeletal muscles (most sensitive) |
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Term
| 3. what factors influence how an infart develops? |
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Definition
| amount of occlusion, rate of development, oxygen content of blood, blood supply (single or duel) |
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Term
| 3. what is a SEPTIC INFARCT? |
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Definition
| infarction related to a microbial infection--> without is a BLAND INFARCT |
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Term
| 3. where do HEMORRHAGIC INFARCTS take place? ANEMIC INFARCTS? |
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Definition
| dual blood supply organs, single blood supply organs |
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Term
| 3. what is the progression of MI up to ~ 6 weeks? |
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Definition
0-18hrs-no visible change
24-48 hrs-edema acute inflammation
3-4 days- necrosis, granulation
1-3 weeks- granulation-->fibrosis
3-6 weeks - dense fibrosis |
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Term
| 3. what are the BIOCHEMICAL MARKERS in diagnosing an MI? |
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Definition
| LDH (mostly LDH1), CPK-MB, CPK-MM, Troponin I and T |
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Term
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Definition
| hypo-perfusion of tissue --> hypooxygenation--> cellular hypoxia |
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Term
| 3. what causes HYPOVOLEMIC SHOCK? |
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Definition
| hemorrhage, loss of fluids |
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Term
| 3. pathogenesis of HYPOVOLEMIC SHOCK? findings and treatment |
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Definition
decreased CO--> decreased TPR-->decreased end diastolic left vent filling
CLINICAL FINDINGS: cold clammy skin, hypotensino, rapid weak pulse
treated with IV crystalloid solxn and whole blood |
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Term
| 3. ***what is CARDIOGENIC SHOCK? causes?*** |
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Definition
myocardial pump failure--> similar pathogenesis to hypovolemic shock
-Myocardial infarction-most common
-Ventricular rupture
-Arrhythmia
-Cardiac tamponade
-Pulmonary embolism |
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