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97 Cards in this Set
- Front
- Back
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Severe Generalized edem with widespread subcutaneous tissue swelling
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Anasarca
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Edema caused by increased hydrostatic pressure or reduced plasma protein, protein-poor fluid
Causes? |
Transudate
HF, RF, HepF, manutrition |
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Protein rich edema from increased vascular permeability related to inflammation
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Exudate
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Why is renal compensation not effective in hypoalbuminemia?
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Increased production of RAA causes salt/water retention but does not correct primary defect of low protein
Will exacerbate edema |
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Angiogenesis causes which type of edema?
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Inflammatory, exudative
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Inappropriate increases in ADH lead to ____ and ____ but not _____
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hyponatremia and cerebral edema but not peripheral edema
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Extensive inguinal lymphatic and lymph node fibrosis resulting in edema of the external genitalia and lower limbs
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Elephantitis from filariasis parasite
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Pitting edema is seen in?
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Subcutaneous edema
(Dependent edema) |
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Microscopic characterstic of edema?
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clearing and separation of ECM with subtle cell swelling
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Periorbital edema is characteristic of?
What tissue / area of the body does this type of edema normally present? |
Renal Dysfunction
Loose CT matrix of all parts of the body |
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Suctioned fluid of PE appears?
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Frothy, blood-tinged fluid which is a mixture of air, edema, and extravasated RBCs
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Cause of death in Brain edema?
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Brain Substance herniation
Vascular supply compression |
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ACTIVE process in which arteriolar dilation leads to increased blow flood
Visual Appearance? Causes? |
Appears read (engorged +^o2 BVs)
Inflammation, Exercise |
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PASSIVE process resulting from reduced outflow from tissue
Appearance? Causes? |
Congestion
Cyanotic (^deoxy hemeoglobin) Cardiac Failure, isolated venous obstructions |
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Hemosiderin-laden macrophages are a tell-tale sign of?
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Chronic Congestion
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Morphology of Acute Pulm Congestion?
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Engorged Alveolar capillaries
Alveolar Septal Edema Focal Intra-alveolar hemorrhage |
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Characteristic Finding of Chronic Pulmonary Congestion?
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Thickened and fibrotic septae
HF cells |
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Characteristic findings of Acute Hepatic Congestion?
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Distended CV and Sinusoids
Centrilobular cells frankly ischemic Periportal Hepatocytes fatty change only |
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Nutmeg Liver?
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Centrilobular depressed red-brown regions surrounded by tan liver.
Hemorrhage, degeneration |
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Accumulation of hemorrhage
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Hematoma
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Minute 1-2mm hemorrhages into skin, mucous membranes, serosal surfaces
causes? |
Petechiae
^intravascular pressure Thrombocytopenia Defective Platelet function |
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>3mm hemorrhages on surfaces
causes? |
Purpura
Same as Petechiae Vasculitis, Trauma, Amyloidosis |
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>1-2cm subcutaneous hematomas?
Explain Color changes |
Ecchymoses
Red-blue from Hgb Blue-green from bili Gold-brown from hemosiderin |
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What % of blood loss normally leads to hemorrhagic (hypovolemic) shock
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20%
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Chronic external blood loss can lead to loss of what that is retained in chronic internal blood loss?
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Iron --> anemia
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___________ binds to thrombin and converts it from a procoagulant into an anticoagulant via its ability to activate protein C which inhibits clotting by inactivation factors ___ and ___
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Thrombomodulin
Va and VIIIa |
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Co-factor required for full activation of Protein C and its anticoagulant effects (proteolysis of Va and VIIIa)
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Protein S
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GpIIb/IIIa deficiency, preventing platelet aggregation
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Glanzmann Thrombasthenia
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GpIb deficiency, preventing adhesion of platelet to subendothelial collagen
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Bernard-Soulier
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Platelet a-granule contents
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P-selectin
Fibrinogen Fibronection Factors 5 and 8 PF4 (heparin binding chemokine) PDGF, TGF-B |
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Platelet dense granule contents?
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Serotonin
ADP ATP Calcium Histamine Epinephrine |
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Two diseases causing bleeding disorders via inability of platelets to adhere to collagen of subendothelium
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vW Disease (vWF)
Bernard Soilier (GpIb) |
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Critical Reactions on dense granule release? (3)
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1 - Calcium release for Coag Cascade
2 - ADP activates aggregation (and more ADP release) 3 - Appearance of negatively charged phospholipids which bind calcium and are the sites of cascade reactions |
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Three Steps of Platelet + ECM encounter and major components
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Adhesion - vWF, GpIb
Secretion - ADP, Calcium Aggregation - ADP, Thromboxane A2 |
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What triggers the conformational change in GpIIB/GpIIIa which allows for fibrinogen binding?
What drug inhibits this? |
ADP
Clopidogren |
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Clinical utility of aspirin in persons at risk for coronary thrombosis?
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permanent block of TxA2 synthesis
PGI2 can overcome block |
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Clotting of blood is prevented by?
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Calcium Chelators
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Activation of Intrinsic Pathway?
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Exposure of Hageman Factor to thrombogenic surfaces (Ex glass)
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What factors does PT test for? Unique for?
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2 5 7 10 fibrinogen
7 extrinsic |
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What factors does PTT test for? Unique for?
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2 5 8 9 10 11 12 fibrinogen
8 9 11 12 intrinsic |
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What factors does Thrombin (II) help activate?
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9
8 5 13 |
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Vitamin K dependent proteins that proteolytically inactivate f5 and f7
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Protein C + S
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Inhibits activity of thrombin and
9 10 11 12? Activated by? |
ATIII
Heparin |
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__ is produced by the endothelium and inactivates TF-VIIa complexes
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TFPI
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Elevated levels of ______ cna be used in diagnosing abnomral thrombotic states including DIC, DVT, PE
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D-Dimer (a fibrin split product)
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When is t-PA most active, why is this useful in treatment?
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When bound to fibrin, localizes fibrinolytic activity
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_____ can activate plasmin in the fluid phase
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Urokinase-PA
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Free plasmin is inactivated by ______ to prevent indiscriminant thrombus lysis
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a2-Plasmin inhibitor
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Produced by endothelial cells, inhibits t-PA binding to fibrin, producing procoagulant effects
Increased by? |
Plasminogen Activator Inhibitor (PAI)
Thrombin |
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stasis is a major contributor to the development of _____ thrombi
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venous
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Thrombophilia is?
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hypercoagulability
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How does a Factor 5 Leiden Mutation Present?
What is the mutation? |
MILD Hypercoagulability, DVT (60% of time f5 is present)
Glutamine to Arginine substitution at position 506 that renders factor 5 resistant to cleavage by protein C |
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Type of mutation in elevated prothrombin?
presentation? |
MILD
G20210A in 3'-untranslated region |
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When should inherited causes of hypercoagulability be considered?
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under 50 with thrombosis
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Common causes of genetic hypercoagulability? (4)
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Factor 5 Leiden
Prothrombin mutation (elevation) Elevated Homocysteine Increased levels of 8,9,11 or fibrinogen |
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1 Cause of hyperocag in pregnancy?
2 Cause of hypercoag in elderly? |
^estrogen^hepatic synthesis of factors
Decreased PGI2 production |
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What is the mechanism of HIT?
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HMW heparin binds with PF4 and this complex is recognized by antibodies
This triggers the activation aggregation and CONSUMPTION of the platelets |
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Presentation of Antiphospholipid AB Syndrome?
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Hypercoagulable state
Miscarraiges (*inhib of t-PA prevents trophoblast invasion of uterus) Renal Microangiopathy |
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Which hypercoagulability state commonly produces a false negative Syphilis test?
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Antiphospholipid Antibody Syndrome
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Arterial thrombi typically grow ____ from the site of insertion
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retrograde (towards heart)
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Venous thrombi typically grow _____ from the site of insertion
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Antegrade (towards heart)
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What is the appearance and importance of Lines of Zahn?
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Alternating Pale/Dark lines
ALIVE @ THROMBUS |
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Composition differences of Arterial versus Venous Thrombi?
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Arterial, under high flow, are composed of platelets, fibrin, RBCs, dead leukocytes
Venous, formed in statis, are RED, composed of RBCs and only few platelets |
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Gelatinous clot with a dark red dependent portion and a yellow upper portion which are not attached to the underlying wall
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Postmortem clots
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How is a mycotic aneurysm formed?
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Release of lysosomal enzymes from the center of a old thrombi in the setting of bacteremia. This leads to infection and an inflammatory reaction
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Where does DVT occur?
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If patient forms Pulmonary Embolism, which leg veins are likely involved
Popliteal, Femoral, Ileac |
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Syndrome caused by the release of coagulant factors and procoagulants from tumor cells leading to increased risk of thromboembolism
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Trousseau Syndrome
migratory thrombophlebitis |
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Most common targets of emobolus from the heart?
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Brain Kidneys Spleen because of rich blood supply
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Progression of DIC?
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Intitially hypercoagulable state which leads to bleeding catastrophe from depletion of platelets and coag proteins
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Discovery of a delicate bridging fibrous web in the pulmonary circulation
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Previous Embolus likely
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When can a medium sized PE become fatal?
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If it coincides with lsHF so collateral bronchial arteries cannot compensate
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MCC Systemic Emboli
MC site? |
left sided mural thrombi (LV infarcts)
Lower extemities 75% of time |
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Patient presents with pulmonary insufficiency, neurologic symptoms, anemia, and *thrombocytopenia 1-3 days after injury
Type of Embolism? Morphology? |
Fat/Marrow Embolism
Fat Vacuoles and clusters of hematopoietic precursors |
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Frothy masses that obstruct vascular flow
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Gas Embolus
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Main Composition of Decompression Emboli?
Presentation? If Chronic? |
Nitrogen
The Bends (muscles) Chokes (Lungs) Caisson Disease (Muscle ischemic necrosis) |
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Immediate Postpartum mother with sudden severe dyspnea, cyanosis, shock, and neurologic symptoms? Risk of survival?
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Amniotic Fluid Embolism
PE, DIC |
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Morphology of Amniotic Fluid Embolism?
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Whorls of fetal squamous cells
Lanugo Hair PE DAD |
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Where are infarcts caused by venous thrombi possible?
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Testis and Ovary (single efferent veins)
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In the lung, ______ infarcts are the rule
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Hemorrhagic
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In the brain, infarction results in _____ necrosis
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Liquefactive
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How long folllowing vascular obstruction does frank necrosis appear?
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4-12 hours
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Which organs present with White infarcts?
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Heart Spleen Kidney
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Cells most vulnerable to hypoxia
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Neurons, 3-4 minutes
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MCC septic shock
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Gram +s
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Major presentation of septic shock?
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DIC
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What is the effect of septic shock on insulin and glucose levels? How does this effect neutrophils?
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Increases insulin resistance and causes hyperglycemia
This decreases the effectivity of neutrophils |
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Cause of immunosupression in Septic Shock?
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Change from Th1 to Th2 cells
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End-stage of Septic Shock?
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**Multi-organ failure
DIC (waterhouse-friedrichson) Vasodilation Immunosuppression |
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Treatment of Septic Shock?
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ABs
Fluids Corticosteroids Insulin |
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Presentation of Nonprogressive Shock?
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Tachycardia
Peripheral vasoconstriction Renal Retention |
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Presentation of Progressive Shock?
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Hypoxia
Metabolic Lactic Acidosis *Pooling of microcirculation* |
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Morphology of Shock in:
1 Adrenals 2 Kidney 3 Lungs 4 Skin |
1 Lipid Depletion
2 Acute tubular necrosis 3 IF SEPTIC, DAD, none otherwise 4 Peterchial Hemorrhages |
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In _____ shock, patient presents with hypotension, weak rapid pulse, tachypnea, cool clammy cyanotic skin
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Hypovolemic and Cardiogenic
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In ____ shock, patients present with warm flushed skin from vasodilation
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Septic Shock
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Major secondary presentations of shock?
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Renal Insufficiency
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Extensive petechial hemorrhages of the white matter following trauma is indicative of?
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Fat Emboli
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What organs are typically involved in a fat embolism?
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The brain - petechiae @ white matter
Lungs - microvascular inflammation and thrombosis Thrombocytopenia also develops rapidly |
