Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/64

Click to flip

64 Cards in this Set

  • Front
  • Back
Causes of edema
Increased Hydrostatic Pressure
Reduced Oncotic Pressure
Lymphatic Obstruction
Sodium/Water Retention
Edema (def)
Incrased fluid in the interstitial tissue spaces.
In different body cavities:
- hydrothorax
- hydropericardium
- hydroperituneum (ascites)
- anscara: severe, generalized edame with subcutaenous tissue swelling
Transudate
Protein-poor, specific gravity less than 1.012. (Fluid leakage)
Exudate
In inflammatoy edema. Protein rich, specific gravity greater than 1.020. (Fluid and protein leakage)
INCREASED HYDROSTATIC PRESSURE
Impaired venous return
Congestive heart failure  
Constrictive pericarditis  
Ascites (liver cirrhosis)  
Venous obstruction or compression
Thrombosis    
External pressure (e.g., mass)
Lower extremity inactivity with prolonged dependency
Arteriolar dilation
Heat  
Neurohumoral dysregulation
REDUCED PLASMA ONCOTIC
PRESSURE (HYPOPROTEINEMIA)
Protein-losing glomerulopathies (nephrotic syndrome)
Liver cirrhosis (ascites)
Malnutrition
Protein-losing gastroenteropathy
LYMPHATIC OBSTRUCTION
(LYMPHEDEMA)
Inflammatory
Neoplastic
Postsurgical
Postirradiation
Na+ RETENTION
Excessive salt intake with renal insufficiency
Increased tubular reabsorption of sodium
Renal hypoperfusion --> Increased renin-angiotensin-aldosterone secretion
Congestive heart failure edema
INCREASED VENOUS PRESSURE DUE TO FAILURE

DECREASED RENAL PERFUSION, triggering of RENIN-ANGIOTENSION-ALDOSTERONE complex, resulting ultimately in SODIUM RETENTION (secondary aldosteronism)
Nephrotic vc nephrotic syndroms
Both leads to hypoalbuminemia.

NephrOtic: proteins move into urine

NephrItic: small pores in podocytes leads to loss of RBC and proteins, cause hematuria.
Peu d'orange
In breast carcinoma infiltration and obstruction of superficial lymphatics can cause edema ov overlying skin.
Subcutaneous dependent edema
Gravity dependent. Typical for cardiac failure, particularly RV.
Edema due to renal sysfunction or nephrotic syndrome
More severe than cardiac edema, and affects all parts of the body equally.
Pulmonary edema
Seen most frequently in left ventricular failure, but also in renal failure, ARDS, pulmonary infections and hypersensitivity reactions.
Weigh 2-3 times normal, on section: frothy, blood-tingled fluid (air, edema fluid and extravasated red cells)
Edema of the brain
May be localized to places of focal injury (infarct, abcsess, neoplasm) or generalized (encephalitis, hypertensive crisis, obstruction of venous outflow).
Generalized: swollen, narrowed sulci, distended gyri.
May cause herniation throug foramen magnum.
Hyperemia and congestion
Local increased volume of blood in a particular tissue.
Hyperemia
Active process resulting form augmented blood flow due to arteriolar dilation. Eg: infl, excercise
Congestion
Passice process resulting form impaired venous return out of a tissue. May be systemic (heart failure), or local (isloated venous obstruction). Leads to cyanosis. Commonly occure together with edema.
Chronic passive congestion: hypoxia, death of tissue, fibrosis. If capillary rupture --> hemociderin-laden macroph.
Morphology acute pulmonary congestion
Alveolar capillaries engorged with blood, septal edema and/or focal minute intra-alveolar hemorrhage.
Morphology chronic pulmonary congestion
Septa become thickened and fibroticHemociderin-laden macrophages (heart failure cells) in alveolar spaces
Morphology acute hepatic congestion
Central vein and sinusoids are distended with blood, mey be central hepatocyte degeneration. Periportal hepatocytes have less hypoxia, only fatty change is seen.
Morphology chronic passive congestion of the liver
Nutmeg liver: central regions of hepatic lobules are red-brown, surrounding zones are uncongested tan, sometimes fatty.
Micro: centrilobular necrosis, , hemorrhage, hemociderin-laden macroph.
Brain herniation due to edema
1. Subfalcine herniation
2. Transtenrorial herniation
3. Tonsillar herniation
Hemorrhage
Extravasation of blood from vessles into the extravascular space
Hematoma
Accumulation of blood. Insignificant; bruise. Significant; massive retriperitoenal hematoma resulting form ruptupe of a dissecting aortic aneurysm
Petechiae
Minute (1-2 mm) hemorrhages into the skin, mucous membr, serosal surf.
Associated with:
- local increase IV pressure,
- thrombocytopenia,
- defevtiv platelet function or
- clotting factor deficiencies
Purpura
3-5 mm hem
Associated with:
(- same as peteciae pluss:)
- vasculitis
- trauma
- increased vascular fragility
Ecchymoses
1-2 cm, subcutaneous (brusies)
Colour changes in hematoma due to phagocytises and degradation of RBC:
1. hemoglobin: red-blue
2. bilirubin: blue-green
3. hemosiderin: golden-brown
Large accumulations of blood in body cavities
- hemothorax
- hemopericardium
- hemoperitoneum
- hemarthrosis
Normal hemostasis(def)
Consequence of thightly regulated processes that maintain blood in a fluid, clot-free state in normal vessels while inducing tha rapid formation of a localized hemostatic plug at the site of vascular injury.
Pathologic form: thrombosis.
Involve three components: vascular wall, platelets, coagulation cascade.
Steps of normal hemostasis
A. Vasoconstriciton: after vascular injury, local neurohumoral factors (endothelin) induce transient vasoconstr.
B. Primary hemostasis: platelet adhere (via Gplb rec) to exposed ECM by binding to vWF and are activated, undergoing shape change and granule release. Released ADP and TXA2 lead to further platelet aggr (binding fibrinogen to platelet GpIIb-IIIa rec), to form primary hemostatic plug.
C. Local activation of coagulation cascade (involving tissue factor and platelet phospholipid) results in polymerization, "cementing" the platelets to definitive secondary hemostatic plug.
D. Counter-regulatory mechanism, such as release of t-PA and thrombomodulin, limit hemostatic process to the site of injury.
PLATELET ADHESION
Primarily to the subendothelial ECM
Regulated by vWF, which bridges platelet surface receptors to ECM collagen
Platelet secretion
Both granules. Agonist binds to surface receptors and initiate an IC phosphorulation cascade which leads to degranulation. Dense bodies are spesially important; ADP for platelet aggregation, calcium for coagulation cascade.
Platelet aggregation
ADP
TxA2 (Thromboxane A2)
THROMBIN from coagulation cascade also
FIBRIN further strengthens and hardens and contracts the platelet plug
Platelet events
1. ADHERENCE to ECM
2. SECRETION of ADP and TxA2
3. EXPOSE phospholipid complexes
4. Express TISSUE FACTOR
5. PRIMARY -> SECONDARY PLUG
6. STRENGTHENED by FIBRIN
Cofactors in coagulation cascade
Ca++
Phospholipid (from platelet membranes)
Vit-K dep.
Prot. S, C, Z
Vit K dependent factors in coagulation cascade
II
VII
IX
X
Virchow's triad
Three primary influences on thrombus formation
1) endothelial injury
2) stasis or turbulence of flow
3) blood hypercoagulability
Primary (genetic) hypercoagulable states
Common
- mutaion in factor V gene (Leiden)
- mut in prothrombin gene
- mut in methyltetrahydrofolate gene
Rare
- antithrobin III deficiency
- protein C def
- protein S def
Very rare
- fibrinolysis defects
Secondary (acquired) hypercoagulable states
High risk for throbosis
- prolonged immonilization
-MI
-atrial fibrillation
- tissue damage
-cancer
- prosthetic cardiac valve
- DIC
- heparin-induced thrombocytopenia
- antiphospholipid ab syndrome (lupus anticoagulant sy)
Lower risk:
- cardiomyopathy
- nephrotic sy
- hyperestrogenic states (pregnancy)
- oral contraceprive use
- sickle cell anemia
- smoking
Properties of endothelium related to thrombus formation
1. ANTI-Platelet PROPERTIES
- Protection from the subendothelial ECM
- Degrades ADP (inhib. Aggregation)
2. ANTI-Coagulant PROPERTIES
- Membrane HEPARIN-like molecules
- Makes THROMBOMODULIN --> Protein-C
- TISSUE FACTOR PATHWAY INHIBITOR
3. FIBRINOLYTIC PROPERTIES (TPA)
Arterial thrombi characteristics
- Arterial and cardiac thrombi typically begins at sites of endothelial injury or turbulence
- arterial thrombi grow retrograde
Venous thrombi characteristics
- Venous thrombi occure at sites of stasis
- extend in the direction of the blood flow
Lines of Zahn:
laminations, pale platelet and fibrin layers alternating with darker erythrocyte rich layers. Antemortem. 
Mural thrombi:
in heart chambers or in the aortic lumen. Abnormal myocardial contraction or endomyocardial injury promotes cardial mural thrombi. Ulcerated atherosclerotic plaques and aneurysmal dilation promote aortic thrombosis. 
Arteral thrombi:
frequently occlusive, produced by platelet and coagulation ativation. Meshwork of platelets, fibrin, erythrocytes, and degenerating leukocytes. White "flux" thrombus in arteries. Mixed "coral" thrombus with changing layers in big arteries, heart and aneurisms. Hyaline thrombus in capillaries.
Venous thrombosis:
(phlebothrombosis): occlusive, can create a long cast of the lumen. It is largely the result of activation of the coagulation cascade, and platelets play a secondary role. Contain more erythrocytes; red or stasis thrombi. Strands of grey fibrin.
Postmortem clots:
gelatinous with a dark red dependent portion where red cells have setteled by gravity, and a yellow supernatant. They are not attached to the vessel wall.
Vegetations
thrombi on heart valves. Bacterial or fungal blood born infecions can cause valve damage, leading to thrombothic masses (infective endocarditis). Nonbacterial thrombotic endocarditis; sterile hypercoagulative states. Sterile verrucous endocarditis (Libman-Sacks endocarditis) can occure in the setting of SLE (uncommon).
Fate of thrombus
- Propagation: thrombi accumulate platelets and fibrin, eventually causing vessel obstruction
- Embolization: Thrombi dislodge or fragment and are transported elsewhere in the vasculature
- Dissolution: Thrombi are removed by fibrinolytic activity
- Organization and recanalization;: Thrombi induce inflammation and fibrosis. These can eventually recanalize, or they can be incorporated into a thickened vessel wall.
Trousseau's syndrom
=migratory thromboplebitis
Increased risk of thromboembolic phenomena seen in disseminated cancers due to tumour-assosiated procoagulant release.
Paradoxial emboli
A small fraction of systemic emboli arise in the veins, but end up in the arterial circulations, through interatrial or interventricular defects.
Saddle embolus
Emboli in the pulmonary artery branchin point.
Types of emboli
99% dislodged from thrombi.
Fat droplets,
bubbles of nitrogen,
atherosclerotic debris (cholesterol emboli),
tumor fragments,
bits of bone marrow,
foreign bodies such as bullets
Pulmonary emboli
60-80% are clinically silent
When 60% or more of pulm circ is obstructed: Cor pulmonale (RV failure), CV collapse or sudden death.
In medium size a: Lead to hemorrhage, but normally not infarct (left-sided heart failure leads to massive infarct)
In small arterioles: infarct
Many emboli over time: pulm hypertension, RV failure
Systemic emboli
80% cardiac/20% aortic aneurysm
Embolization lodging site is proportional to the degree of flow (cardiac output) that area or organ gets, i.e., brain, kidneys, legs
Other emboli; fat, air, amniotic
FAT (long bone fx’s )
AIR (SCUBA bends)
AMNIOTIC FLUID, very prolonged or difficult delivery, high mortality
Infarct def
area of necrosis secondary to decreased blood flow
Anemic infartct
White/pale infarct.
Caused by arterial occlusions in the heart, spleen, kidney
Hemorrhagic infarct
Red infarcts; red cells goes in to necrotic tissue.
In lungs and GIT form arterial occlusion. Tissues are loose and have double blood supplies.
Can also be venous occlusion
Types of shock
1. CARDIOGENIC: (Acute, Chronic Heart Failure)
2. HYPOVOLEMIC: (Hemorrhage or Leakage)
3. SEPTIC: (“ENDOTOXIC” shock, #1 killer in ICU)
4. NEUROGENIC: (loss of vascular tone)
5. ANAPHYLACTIC: (IgE mediated systemic vasodilation and increased vascular permeability)
Septic shock events
SYSTEMIC VASODILATION (hypotension) -->
↓ MYOCARDIAL CONTRACTILITY -->
DIFFUSE ENDOTHELIAL ACTIVATION -->
LEUKOCYTE ADHESION -->
ALVEOLAR DAMAGE --> (ARDS)
DIC
VITAL ORGAN FAILURE --> CNS
Clinical stages of shock
1. NON-PROGRESSIVE
- COMPENSATORY MECHANISMS
- CATECHOLAMINES
- VITAL ORGANS PERFUSED
2. PROGRESSIVE
- HYPOPERFUSION
- EARLY “VITAL” ORGAN FAILURE
- OLIGURIA
- ACIDOSIS
3. IRREVERSIBLE
- HEMODYNAMIC CORRECTIONS of no use
Clinical progression of symproms in shock
Hypotension -->
Tachycardia -->
Tachypnea -->
Warm skin --> Cool skin --> Cyanosis
Renal insufficiency -->
Obtundance
Death