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279 Cards in this Set
- Front
- Back
How does exudate arise?
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From vascular permeability
|
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What causes transudates?
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increased hydrostatic pressure
decreased osmotic pressure (as seen in liver, kidney disease) |
|
What kind of schedule is cortisol on?
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Circadian rhythm
it has a pronounced diurnal variation |
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What is accuracy?
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reliability of the test method
|
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What is Gold Standard?
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the recognized methodology against which new tests are compared
|
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What is precision?
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reproducibility of a result
|
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What is prevalence?
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frequency of patients with a certain disease in the group tested
|
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What is incidence?
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number of patients in whom the disease develops in a one year period
|
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What is the equation for sensitivity?
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TP / (TP + FN) x 100%
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What is the equation for specificity?
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TN / (TN + FP) x 100%
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What is the equation for Positive Predictive Value?
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PPV = TP / (TP + FP)
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What is the equation for Negative Predictive Value?
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NPV = TN / (TN + FN)
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What would cause elevated BUN?
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Almost all renal disease
Poor renal perfusion Dehydration, shock, HF |
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What would cause elevated creatinine?
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Most renal disease (late)
Poor renal perfusion Dehydration |
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What would cause elevated Bilirubin?
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3 Ways:
1. Prehepatic = hemolysis 2. Intrahepatic = liver disease (cirrhosis/hepatitis) 3. Posthepatic = gallstone in bile duct |
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What would cause elevated phosphatase?
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Major sources are:
Liver Bone (osteoclasts) Placenta Intestine Some cancers |
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What would cause elevated lactate dehydrogenase?
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High levels are associated with breakdown of erythrocytes (hemolysis); platelets
|
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What are some sources of AST? When would it be elevated?
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High in hepatocytes, released in injury. Commonly elevated in cardiac and skeletal muscle injury
|
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What are some sources of ALT?
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Major source is the liver
|
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What labs are used to diagnose an MI?
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CK-MB and Troponin I (&T) (high specificity and sensitivity)
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What labs are used to diagnose liver disease?
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AST, ALT, Alkaline phosphatase, LDH, gamma glutamyl transferase
|
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What labs are used to diagnose Musculoskeletal disease?
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CK, AST, LD, Aldolase, Myoglobin, Alkaline phosphatase
|
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What would cause decreased prealbumin?
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malnutrition, alterations of liver fxn
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What would cause a decrease in albumin?
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this is very common!
Impaired synthesis: malnutrition, malabsorption, hepatic dysfunction Increased loss: renal disease (especially nephrotic syndrome), Protein losing gasteroenteropathy, ascites |
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What is alpha-1-antitrypsin?
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an acute phase reactant and the major alpha-1 globulin
|
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When would alpha-1-antitrypsin be increased?
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Deficiency in pulmonary emphysema, cirrhosis of the liver (misfolded protein)
|
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What is the big deal about increased alpha 2 globulins?
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They are altered in acute inflamation
Alpha-2-macroglobulin: Kinin inhibitor Haptoglobin - carrier of free Hb CRP - sensitive indicator of tissue necrosis, acute infection and inflammation |
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What is CRP? What are some of its uses?
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An acute phase reactant.
It reflects presence of bacterial infection. Elevated in inflammatory response to autoimmunity (RA). Predictive value for CV events such as MI or stroke |
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What do the acute phase reactants do in response to TNF?
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they all increase!
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What would you use ESR for?
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Increase ESR is a nonspecific indicator of inflammation
|
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What is the source of gammaglobulins?
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they are produced by plasma cells. (they are not acute phase reactants) They take WEEKS to make!
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What causes decreased gamma globulin?
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b-cell immunodeficiencies
|
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What are the 3 types of increased immunoglobulin and what are the causes given for them?
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Polyclonal gammopathy = autoimmune disease; chronic infections
Monoclonal gammopathy = plasma cell malignancy or premalignancy Oligoclonal gammopathy = small number of bands - CNS test |
|
What is anasarca?
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severe generalized edema
|
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What would cause a chylous effusion?
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traumatic disruption of the thoracic duct, duct disruption from a tumor.
(the milky appearance is due to increased triglycerides/chylomicrons) |
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What would cause a serosanguinous effusion?
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malignancy or trauma, pulmonary infarction
|
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What would cause a bloody effusion?
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trauma, ruptured vasculature
|
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What is hyperemia?
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it's a synonym for erythema
Active arterioledilation |
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What causes hyperemia?
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exercise
inflammation action of cytokines (TNF and others --> vasodilation) |
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What is congestion?
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impaired venous outflow from tissues. - Stasis
|
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What is the pathology of congestion?
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It is a passive process - caused by: Heart failure - damming of blood return; local venous obstruction
Commonly associated w/ edema (transudate due to increased hydrostatic pressure) |
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What causes hepatic congestion?
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RIGHT heart failure
|
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What is the morphology of a congested liver?
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Nutmeg liver*
(red-brown depressed areas due to centrolobular hemorrhagic necrosis) |
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What would you see on a lab panel with hepatic congestion?
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AST, ALT, LDH elevated due to necrosis of hypoxic hepatocytes
If it's chronic congestion, siderophages accumulate and can lead to necrosis |
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What are the causes of congestion of the spleen?
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RHF
Cirrhosis Portal Vein occlusion (the splenic vein goes through the liver via the portal vein so any congestion/backup in the liver is going to cause splenomegaly and congestion in the spleen too) |
|
What is brown induration of the legs?
|
chronic venous insufficiency due to valve defects in the legs. The brown color arises due to accumulation of siderophages in dermis.
(induration = hardening - due to fibrosis) |
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What is a complication of brown induration of the legs?
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stasis ulceration
this arises close to malleoli (for some reason) |
|
Define hematoma
|
mass of blood confined within an organ, tissue, or internal space
|
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Define contusion
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Bruise/ecchymosis - due to blunt force injury which damages small blood vessels without disruption of the tissue
|
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Define ecchymosis
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large areas (>1-2cm) of bruising (bleeding into tisue)
|
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Define petechiae
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Punctate hemorrhages, associated with thrombocytopenia, dysfunctional platelets and suffocation
|
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Define purpura
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confluent petechiae (>3cm) + vascular inflammation, trauma
|
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Define hemarthrosis
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bleeding into a joint
|
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Define laceration
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tear due to blunt force trauma (may be stellate or linear)
Bridging strands of fibrous tissue will be evident |
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Define incision
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Produced by sharp cutting object - margins are clean and there is no bridging
|
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Define epistaxis
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Nosebleed
|
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Define hematochezia
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bright red blood in stool
|
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Define melena
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Black/digisted blood in stool
|
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Define menorrhagia
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excessive menstrual bleeding
|
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Define thrombus
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blood solidified by coagulation that forms in flowing blood in an intact vascular system.
This is ALWAYS a pathological process |
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Define blood clot
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blood solidified by coagulation that forms in nonflowing blood (as opposed to thrombus which forms in a blood vessel)
|
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What does endothelin do?
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it's a locally acting, potent but short-lived vasoconstrictor
|
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What causes platelet adhesion during primary hemostasis?
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exposure of ECM and collagen
|
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What produces platelets?
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bone marrow megakaryocytes by budding off of cytoplasm
|
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What are some inherited defects of adhesion function? (primary hemostasis)
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von Willebrand disease
Bernard-Soulier syndrome (Gp1b deficiency) |
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What is one important thing calcium does for coagulation?
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calcium forms critical sites for assembly of coagulation factors
|
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What is Glansmann thrombasthenia?
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Defects of platelet function via aggregation
Hereditary defect of Gp11b111a |
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What is Bernard-Soulier Syndrome?
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Deficiency in Gp1b (von Willebrand factor receptor) results in a bleeding disorder
|
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Why is vWF-Gp1b association necessary even though platelets can adhere to other components of the ECM?
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to overcome the high shear forces of flowing blood
|
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What is thrombomodulin?
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a heparin-like molecule that have anticoagulant effects.
Thrombomodulin binds to thrombin and converts it from a procoagulant into an anticoagulant via its ability to activate Protein C, which inhibits clotting by inactivating factors Va and VIIIa |
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What is Tissue Factor Pathway Inhibitor (TFPI) and what does it do/how does it work?
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a cell surface protein that directly inhibits tissue factor - factor VIIa and factor Xa activities (leading to anticoagulation)
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What is Protein S?
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A cofactor for Protein C which is an anticoagulant
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What is noncleaved fibrinogen good for?
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Platelet aggregation!
Platelet activation by ADP triggers a nonconformational change in the platelet GpIIb-IIIa receptors that induces binding to fibrinogen, a large protein that forms bridging interactions between platelets that promote platelet aggregation |
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What does prostacyclin (PGI2) do to coagulation?
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source = endothelial cells
Vasodilation Inhibits platelet aggregation |
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What does Nitric Oxide do to coagulation?
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Source = endothelium
Vasodilation; inhibits platelet aggregation |
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What do antiplatelet drugs do?
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affect function NOT number of platelets
|
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How do NSAIDs and Aspirin work as anticoagulants?
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Block cyclo-oxygenase action on arachidonic acid to prevent production of TxA2 (thromboxane) which is a platelet aggregation mediator
|
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What are GpIIbIIIa inhibitors?
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antibodies!
|
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How do ADP receptor PY2 inhibitors work?
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prevent ADP from binding to its receptor and therefore prevents platelet shape change, which prevents degranulation, which stops the hemostasis pathway dead in its tracks!
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What can cause thrombocytopenia? (what is is first?)
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It is decreased numbers of platelets
Decreased production in bone marrow Increased peripheral destruction (autoimmune - ITP, HIV) |
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What are some lab tests for platelet disorders
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Thromboelastograph (bleeding time)
Platelet function analyzer which measures the time it takes to form a platelet plug (analogous to bleeding time) Bleeding time |
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When are bleeding times prolonged?
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von Willebrand disease
platelet dysfunction reduced platelet number |
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What is the tenase complex?
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VIII and IX
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What is the prothrombinase complex?
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Xa binding to V
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What does thrombin do?
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recruits/activates additional platelets
Converts fibrinogen (soluble) into insoluble polymerized fibrin |
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Where are plasma coagulation factors manufactured?
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in the liver
|
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What are the Vitamin K dependent zymogens?
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Factors VII, IX, X, II
Proteins C and S |
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What is Vitamin K useful for?
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allows for Calcium binding
|
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What does plasmin do?
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cuts fibrin (from fibrinogen) into peptides = fibrinolysis
Products are fibrin degradation products and D-dimer (cross linked fibrin product) |
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What does increased D-Dimer on a lab test indicate?
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that fibrinolysis has occurred which means that there WAS a thrombus there. This is the lab test for DVT!
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How does Thrombin stabilize clots?
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via activation of Factor XIII
|
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What are the sources of Tissue factor?
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Walls of blood vessels
endothelial cells monocytes cells in CT |
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Which deficiencies in clotting factors is most common?
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Factor VIII and vWF
|
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Which deficiencies in clotting factors are inherited X-linked?
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VIII and IX
(hemophilia!) |
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Which labs will be prolonged in Vitamin K deficiency?
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PT prolonged early/first
PTT prolonged in severe deficiency |
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Is petechiae seen in Hemophilia?
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NO!
|
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Which lab test will be prolonged in hemophilia?
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PTT (intrinsic pathway)
|
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Which clotting factor does heparin-like molecules inactivate?
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IIa (enzyme)
|
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What does binding of thrombomodulin do?
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inhibits thrombin
activates protein C (anticoagulant) |
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What does tissue factor pathway inhibitor do?
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inactivates factor Xa and VIIa
|
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What is tPA (Tissue plasminogen activator)
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clot buster!
Activates plasmiogen --> plasmin which lysis fibrin |
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When is recombinant tPA used therapeutically?
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in MI - coronary thrombosis
stroke - clot in cerebral artery (in first 3 hours) PE (limited to really big clots |
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Why do BC pills (or pregnancy) make a woman more susceptible to blood clots?
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they reduce ATIII (which is responsible for inhibiting thrombin and other serine proteases IXa, Xa, XIa)
|
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What is Virchow's Triad ?(Thrombosis)
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1. endothelial injury
2. stasis or turbulence of blood 3. blood hypercoagulability |
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What is going on with Factor V Leiden Mutation?
|
A single amino acid substitution results in a Factor Va that is resistant to digestion by activated Protein C. It occurs in up to 2-9% of Caucasians, up to 60% of people with recurrent DVTs
|
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What lab would indicate a Factor V Leiden mutation?
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activated protein C resistance
Genetic testing for mutation is available |
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What is prothrombin 20210A ?
|
Mutation that results in increased levels of prothrombin which leads to more cleavage of fibrinogen to fibrin which results in increased clotting. Single nucleotide change in untranslated region. 3X increased risk of venous thrombosis
|
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What is hyperhomocysteinemia?
|
Mutation in methyltetrahydrofolate reductase.
Inhibits antithrombin III activity and thrombomodulin. Contributes to formation of atherosclerosis. Acquired form: B12 or Folate deficiency |
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What is HIT?
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Heparin-Induced Thrombocytopenia
Antibodies form to heparin complexed with heparin platelet factor 4. Binding activates platelets: formation of platelet rich thrombi. Thrombocytopenia results due to platelet consumption |
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When do you suspect HIT?
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When platlets drop by 50%
|
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What is antiphospholipid antibody syndrome?
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Antibody mediated inhibition of tPA. Fatal thromboembolic events occur. Risk for recurrent venous or arterial thrombi: stroke, MI, DVT c PE, Renovascular disease, bowel infarction, repeated miscarriages, thrombocytopenia
|
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What is the most common cause of DVTs?
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Atherosclerosis
|
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What is superficial saphenous thrombophlebitis?
|
associated with varicosities, which result in stasis which results in thrombosis. Thrombi produce local congestion, pain and swelling but RARELY EMBOLIZE! They predispose to venous insufficiency and varicose ulcers of skin
|
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Define embolus.
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Detached solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
|
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What is cor pulmonale?
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hypertrophy of right ventricle due to lung disease; leads to right heart failure
|
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What is the most common cause of a pulmonary thromboemboli?
|
Most common = DVT
other source = right ventricular mural thrombus |
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What would cause a traumatic fat embolism?
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occurs with trauma, usually a fracture to a long bone (marrow).
SOB followed by confusion, coma, 1-3 days after fracture. Fatal in 10% |
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What happens in an amniotic fluid embolism?
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infusion of amniotic fluid into maternal circulation via tear
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What does LPL (lipoprotein lipase) do?
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Extracts triglyceride from VLDL for storage in fat, use in muscle
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What does the LDL receptor do?
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Mediated transport into liver
|
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How is oxidated LDL removed?
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via scavenger receptors on macrophages (xanthomas/atherosclerosis)
|
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What does LPL (lipoprotein lipase) do?
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Extracts triglyceride from VLDL for storage in fat, use in muscle
|
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What is Neimann-Pick Type C disease?
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cholesterol exits lysosomes utilizing NPC proteins
|
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What does the LDL receptor do?
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Mediated transport into liver
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What is the most common familial hyperlipidemia?
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LDL receptor defects
|
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How is oxidated LDL removed?
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via scavenger receptors on macrophages (xanthomas/atherosclerosis)
|
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What is Neimann-Pick Type C disease?
|
cholesterol exits lysosomes utilizing NPC proteins
|
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What is the most common familial hyperlipidemia?
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LDL receptor defects
|
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Describe Heterozygous LDL receptor defects
|
Plasma cholesterol increased from birth 2-3x normal.
May exhibit cutaneous xanthomas, premature atherosclerosis develops in adults |
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Describe Homozygous LDL receptor defects
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Plasma cholesterol 5-6x normal (>500mg/dL).
Skin and tendinous xanthomas in childhood. Coronary, cerebral, and peripheral vascular atherosclerosis in childhood, adolescence |
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Define endothelial activation.
|
Endothelial cells can respond to stimuli by adjusting usual (constitutive) functions and by expressing newly (inducible) acquired properties.
|
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Define endothelial dysfunction.
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Potentially reversible changes in functional state of endothelium in response to environmental stimuli
|
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What are the 2 major hemodynamic variables regulating normal blood pressure?
|
Cardiac output
Total peripheral resistance |
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What is essential/primary hypertension?
|
idiopathic
accounts for 90-95% of hypertension |
|
What is secondary hypertension?
|
secondary to renal disease (most)
5-10% of cases |
|
What is benign essential hypertension?
|
hypertension at modest level and fairly stable over years
95% of cases |
|
What is malignant hypertension?
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Systolic >200, diastolic > 120
Rapidly rising blood pressure, untreated leads to death within 2 years May develop in previously normotensive person, often superimposed on pre-existing benign HTN |
|
What is hyaline arteriolosclerosis?
|
common in diabetes
Major characteristic of benign HTN |
|
What is hyperplastic arteriolosclerosis?
|
related to acute, severe elevations of blood pressure, characteristic of malignant HTN
Onionskin, concentric, laminated thickening of walls of arterioles with progressive narrowing of lumen |
|
What is atheroslcerosis?
|
intimal fibrous plaques with lipid rich core
|
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What is Monckberg's Medial Calcific Sclerosis?
|
calcification of the media of muscular arteries (usually adult older than 50, no clinical significance)
|
|
What is arteriolosclerosis?
|
proliferation or hyaline thickening of walls of small arteries and arterioles
|
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What is a fatty streak?
|
Earliest lesion in atheroslcerosis. Multiple yellow, flat spots coalesce into elongated streaks. Lipid-filled foam cells. May appear before 1 year and always present in older than 10 years. Not a clear cut relation to atheromas
|
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What are the 3 principle components of an atherosclerotic plaque?
|
Cells (SMCs, macrophages, T lymphs)
ECM Lipids - both intra and extracellular |
|
What are the 4 major clinical consequences of atherosclerosis?
|
1. MI
2, Stroke 3. Aortic Aneurysm 4. Peripheral vascular disease |
|
What is a true aneurysm?
|
bounded by complete (but attenuated) arterial wall components. Blood remains w/in the confines of the circulatory system
|
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What is a false aneurysm?
|
Extravascular hematoma that communicates with intravascular space.
Leak at anastomosis of vascular graft with artery |
|
What is Cystic Medial Degeneration?
|
non-specific ischemia/degenerative changes --> scarring, inadequate ECM synthesis, increased amounts of amorphous ground substance.
|
|
What is Marfan Syndrome?
|
Defective synthesis of fibrillin leads to abnormal TGF-beta, progressive weakening of elastic tissue. Aorta progressive dilation, remodeling of inelastic media
|
|
What is Loeys=Dietz Syndrome?
|
Mutations in TGF-beta receptors - abnormalities of elasticn collagen I and III
Aneurysms can rupture fairly easily even if small |
|
What is Ehlers-Danlos Syndrome?
|
Defective Type III Collagen synthesis
|
|
What is Vitamin-C deficiency?
|
Scurvy
Altered collagen cross-linking |
|
What are the 2 major disorders that predispose to aortic aneurysms?
|
Atherosclerosis and Hypertension
|
|
What is a mycotic aneurysm?
|
Infection of a major artery that weakens wall
Originate from - septic embolis lodges in vessel - extension of adjacent infection - circulating organisms directly infecting |
|
Where do aneurysms associated with atherosclerosis most commonly occur?
|
Abdominal aorta
|
|
Where are AAAs usually located?
|
below renal arteries and above bifurcation of aorta into femoral arteries
|
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At or above what size are AAAs at greatest risk for rupture?
|
>5 cm
|
|
What type of aneurysm can be caused by Syphilis?
|
thoracic aortic aneurysm
|
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What 2 groups of patients do dissections occur in?
|
Men 40-60 years old (90% with HTN)
Patients with abnormality of connective tissue |
|
What is the major predisposing factor for dissections?
|
Hypertension!!!!!
|
|
What is the most frequent detectable microscopic lesion?
|
Cystic Medial Degeneration
|
|
What is Type A DeBakey classification for dissections?
|
proximal lesions, affecting ascending or both ascending & descending aorta
|
|
What is Type B DeBakey classification for dissections?
|
distal lesions, beginning distal to subclavian
|
|
What are the classical symptoms for a dissection?
|
sudden onset of excruciating pain, anterior chest, radiating to back, moving downward. Often confused with acute MI
|
|
What is the most common cause of death with dissections?
|
Rupture of dissection into any of the 3 major body cavities (pericardial, pleural, peritoneal)
|
|
What is Type A DeBakey classification for dissections?
|
proximal lesions, affecting ascending or both ascending & descending aorta
|
|
What is Type B DeBakey classification for dissections?
|
distal lesions, beginning distal to subclavian
|
|
What are the classical symptoms for a dissection?
|
sudden onset of excruciating pain, anterior chest, radiating to back, moving downward. Often confused with acute MI
|
|
What is the most common cause of death with dissections?
|
Rupture of dissection into any of the 3 major body cavities (pericardial, pleural, peritoneal)
|
|
What are the 2 most common mechanisms for vasculitis?
|
1. infectious pathogens: direct invasion
2. immune-mediated inflammation |
|
What are the common clinical findings in vasculitis?
|
Fever, Myalgias, Arthralgias, Malaise, Tissue Ischemia
|
|
What are the 3 main mechanisms which initiate noninfectious vasculitis?
|
1. immune complex disposition (SLE)
2. Antineutrophil cytoplasmic antibodies (ANCA) 3. Anti-endothelial cell antibodies |
|
What are the 2 types of ANCAs?
|
Anti-myeloperxodiase (MPO-ANA aka P-ANA)
Important in diagnosis of Wegener's granulomatosis Anti-Proteinase 3 (PR3-ANCA aka C-ANCA). Helpful in diagnosis of microscopic polyangitis, Churg-Strauss syndrome |
|
What disease is commonly associated with Giant Cell Arteritis?
|
Polymyalgia Rheumatica
|
|
What vessels are spared in PAN?
|
pulmonary!
|
|
Do PAN patients get glomerulonephritis? Why?
|
No!
Affects the medium sized vessels, not the small ones |
|
Which arteritis causes necrotizing glomerulonephritis? Why?
|
Microscopic polyangitis
b/c it affects smaller vessels |
|
What is another name for thromboangitis obliterans?
|
Buerger disease
|
|
What group of people get Buerger Disease?
|
Smokers!!!!!!!!!!!!!!!!!!
|
|
What is Raynaud phenomenon?
|
exaggerated vasoconstriction of digital arteries and arterioles
|
|
What are the clinical features of Raynauds?
|
paroxysmal pallor or cyanosis of digits. Involved features show red, white, blue color changes proximal to distal
|
|
Who gets primary Raynauds?
|
Young females
|
|
What precipitates Raynauds attacks?
|
exaggeration of normal central and local vasomotor responses to cold or emotion
|
|
What is secondary Raynaud's?
|
Vascular insufficiency of extremities, secondary to arterial narrowing from various processe. (SLE, scleroderma, atherosclerosis, & Buerger disease)
|
|
What causes superior vena caval syndrome? What do you see clinically?
|
neoplasms that compress or invade the superior vena cava.
- dusky cyanosis - marked dilation of veins of head, neck and arms |
|
What causes inferior vena caval syndrome? What do you see clinically?
|
Neoplasms compress or penetrate walls of vena cava or thrombus may propagate upward.
- marked leg edema - distention of superficial veins of lower abdomen - massive proteinuria (renal veins involved) |
|
Which 2 cancers have a tendency to grow within the lumens of veins resulting in inferior vena caval syndrome?
|
Hepatocellular carcinoma and renal carcinoma have propensity to grow within lumens of veins with ultimate extension into vena cava, may cause obstruction
|
|
When does systolic dysfunction occur?
|
Ischemic injury, pressure/volume overload, dilated cardiomyopathy
|
|
When does diastolic dysfunction occur?
|
massive LV hypertrophy, myocardial fibrosis, amyloid, constructive pericariditis
|
|
What 3 mechanisms does the cardiovascular system use to maintain pressure and perfusion in the face of damage/excess burden?
|
1. Frank-Starling
2. Myocardial hypertrophy with/without cardiac chamber dilation 3. activation of neurohumoral system |
|
What 2 features characterize CHF?
|
diminished CO
Damming back of blood |
|
What is forward failure mean in regards to CHF?
|
diminished CO
|
|
What does backward failure refer to in regards to CHF?
|
damming back of blood
|
|
What are the 3 most common underlying disease states for CHF?
|
Hypertension
MI Diabetes Mellitus |
|
What happens to the left atrium in left heart failure?
|
atrial enlargement - leads to A. Fib
|
|
Where do thrombi form in the atrium?
|
appendages!
|
|
What are the 4 most common causes of left-sided heart failure?
|
Ischemic heart disease
Hypertension Aortic & Mitral valvular disease Nonischemic myocardial diseases |
|
What are heart failure cells?
|
hemosiderin containing macrophages in alveoli
|
|
What is the most common cause of right heart failure?
|
Left heart failure!
|
|
What is pure right sided heart failure caused by? what is it called then?
|
Chronic severe pulmonary hypertension
called Cor pulmonale |
|
What 4 things happen to the liver with Right sided heart failure?
|
1. nutmeg liver (chronic passive congestion)
2. centrilobular necrosis 3. central hemorrhagic necrosis (severe, rapidly developing failure leads to rupture of sinusoids) 4. cardiac sclerosis (long standing severe failure, central areas become fibrotic) |
|
What 5 categories of heart disease account for almost all cardiac mortality?
|
1. Ischemic heart disease*** (80-90%)
2. HTN heart disease and pulmonary HTN 3. Certian valvular disease 4. Congenital heart disease 5. nonischemic myocardial disease |
|
What is another name for ischemic heart disease?
|
coronary artery/heart disease
|
|
What 4 syndromes describe the clinical manifestations of IHD?
|
1. angina pectoris
2. MI 3. Chronic ischemic heart disease 4. sudden cardiac death |
|
What is acute plaque change?
|
disruption of previously, partially stenosing atheroslcerotic plaque with
- hemorrhage - rupture and fissuring - erosion/ulceration |
|
What does a transmural infarct usually involve?
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a portion of the LV including septum
|
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What 3 other things could cause an MI that is not due to atherosclerosis?
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vasospams
emboli unexplained |
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What causes 90% of transmural infarcts?
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occlusive intracoronary thrombus overlying an ulcerated or fissured plaque
|
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How can reperfusion after an infarct occur?
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Thrombolysis (streptokinase or tissue-type plasminogen factor)
Balloon angioplasty CABG |
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What 2 lab meaurements are useful in diagnosis of an acute MI?
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Troponins (I & T)
CK-MB |
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What 4 factors are associated with poor prognosis after an MI?
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Diabetes
Female Advanced age Previous MI |
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Which type of myocardial rupture is most common? When is it most likely to happen after an MI?
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Ventricular free wall
3-7 days post MI |
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What happens with rupture of the ventricular free wall?
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hemopericardium and cardiac tamponade
|
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What happens with papillary muscle rupture?
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acute mitral regurgitation
|
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What 3 things determine complications and prognosis after an MI?
|
infarct size
site transmural extent |
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Define sudden cardiac death.
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Unexpected death from cardiac causes early (within an hour) after or without onset of symptoms
|
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What is the ultimate mechanism of death in sudden cardiac death?
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lethal arrhythmia
|
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What is the minimal criteria for diagnosing hypertensive heart disease?
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LV hypertrophy (concentric) in absence of other causative pathology.
History or pathologic evidence of hypertension |
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What is the morphology of hypertensive heart disease?
|
LV pressure overloads leads to LV circumferential hypertrophy without dilation.
Symmetric wall thickening (may exceed 2cm) Increased heart weight Stiff heart, impairs diastolic filling Decompensation occurs with dilation, thinning of wall, enlarged heart |
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What causes mitral stenosis?
|
rheumatic heart disease
|
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What causes mitral insufficiency?
|
Mitral valve prolapse (aka myxomatous degeneration)
|
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What causes aortic stenosis?
|
calcification
|
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What causes aortic insufficiency?
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HTN and aging
|
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What is the hallmark lesion of calcific aortic stenosis?
|
concentric hypertrophy
|
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What is the anatomic change in the heart associated with mitral valve prolapse?
|
myxomatous degeneration
|
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Who is at increased risk of having mitral valve prolapse?
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people with marfan's syndrome, Ehlers-Danlos
|
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What are the serious complications of mitral valve prolapse?
|
infective endocarditis
mitral insufficiency stroke arrhythmias |
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What are Aschoff bodies? Where are they seen? When?
|
collagen surrounded by lymphocytes and plump macrophages. Seen in the myocardium in rheumatic heart disease
|
|
What can cause acute bacterial endocarditis?
|
Virulent organisms such as Staphylococcus aureus in IV drug users
|
|
What can cause subacute bacterial endocarditis?
|
low virulence organisms:
- streptococcus viridans = oral source (most common 60%) - Staphylococcus epidermidis = infects prostheses - Streptococcus bovis (GI tract infections) |
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What is a Janeway lesion? When would you see one?
|
splinter hemorrhages underneath the nails
Infective endocarditis |
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Which valve is usually affected in cases of IV drug use?
|
tricuspid
|
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What happens in Nonbacterial Thrombotic Endocarditis?
|
small, sterile thrombi deposit on valves.
This is associated with debilitation: cancer, sepsis. The pathogenesis is related to hypercoagulable states (Cancer, etc - Trousseau Syndrome) Material may embolize Fibrin deposits on valve leaflets w/o destruction |
|
What is Libman-Sacks endocarditis?
|
associated with autoimmunity of SLE and antiphospholipid syndrome.
Morphology: mitral valve most commonly involved, vegetations are small and sterile. The underside of the valve is affected. May fibrose and deform the valve. |
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Which valve is usually affected in Libman-Sacks endocarditis?
|
Mitral
|
|
What causes carcinoid heart disease?
|
systemic serotonin and other agents proced and released by carcinoid tumors
|
|
What happens in carcinoid syndrome?
|
episodic flushing, cramps, nausea, vomiting, diarrhea, asthmatic episodes, cardiac lesions
|
|
What is the cardiac lesion seen in carcinoid heart disease?
|
fibrous intimal thickening of right ventricle, pulmonic/tricuspid valves. (left side is spared)
An acid mucopolysaccharide matrix is deposited. |
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What is most commonly occurring with carcinoid heart disease?
|
tricuspid insufficiency
|
|
Which type of artificial heart valve has thromboembolic disease associated with it? What is it?
|
mechanical valves
Systemic emboli cause stroke, GI infarction, etc. Risk of hemorrhage secondary to anticoagulation treatment |
|
What strain of bacteria causes the infective endocarditis seen in artificial heart valves?
|
staph epi
|
|
Define cardiomyopathy
|
Heart muscle disease resulting from a primary abnormality of the myocardium.
|
|
Define myocarditis.
|
inflammatory involvement of heart muscle characterized by a leukocyte infiltrate not secondary to ischemia. causes nonischemic degeneration of myocytes
|
|
What is the microscopic morphology of viral myocarditis?
|
lymphocytes surround individual cells
|
|
What is the microscopic morphology of hypersensitivity myocarditis?
|
eosinophils, macrophages
|
|
What is the microscopic morphology of myocarditis due to Chagas disease?
|
myofiber distention with trypanosomes
|
|
How do catecholamines and cocaine cause cardiac toxicity?
|
direct toxicity to myocytes via calcium overload or vasconstriction in the face on tachycardia
|
|
What cardiac pathology is associated with iron overload?
|
systolic dysfunction
Interference with metal dependent enzyme systems |
|
What cardiac pathology is associated with hyperthyroidism?
|
myocardial hypertrophy
|
|
What cardiac pathology is associated with hypothyroidism?
|
myxedema heart: insterstitial mucopolysaccharide; myofiber swelling - promotes atherosclerosis
|
|
What is the cause of serous pericarditis?
|
non-infectious inflammatory conditions, viral infections
|
|
What are the 3 important causes of fibrinous pericarditis?
|
Acute MI
Postinfarction syndrome (aka Dressler's Syndrome) Rheumatic fever |
|
What causes purulent pericarditis?
|
infection
|
|
What type(s) of pericarditis develop adhesions?
|
Fibrinous
Purulent |
|
What causes caseous pericarditis?
|
TB
Cocci |
|
What is the outcome of caseous pericarditis?
|
chronic constrictive pericarditis
|
|
What gene is indicated in 22q11.2 deletion?
|
T-box transcription gene.
TBX1 in deleted region responsible for DiGeorge Syndrome and velocardiafacial syndrome |
|
What are the clinical findings in 22q11.2 deletion: DiGeorge syndrome?
|
CATCH-22
Cleft Palate Absent thymus/hypoplastic thymus Cardiac anomalies (outflow tract - truncus arterosus, double outlet RV, tetralogy of fallot) Hypoplasia of parathyroids (hypoparathyroidism - hypocalcemia) |
|
What are the causes of Right to Left shunts?
|
Tetralogy of Fallot
Transposition of the Great arteries Total anomalous pulmonary venous connection Tricuspid atresia Persistent Truncus arteriosus |
|
What is one consequence of a Left to Right shunt?
|
pulmonary hypertension due to increased pulmonary blood flow
|
|
What is Eisenmegner's syndrome?
|
"late cyanotic congenital heart disease" or cyanose tardive
- L to R shunt becomes R to L shunt due to pulmonary hypertension |
|
What are the causes of Left to Right shunts?
|
VSD
ASD AV septal defect PDA |
|
Which type of ASD is most common?
|
Septum secundum type most common (90%)
|
|
What are the frequency and significance of a patent foramen ovale in adults?
|
Fuses 80% of the time
Remaining 20% may re-open due to pulmonary HTN |
|
What is the most common location for VSD?
|
membranous septum (right below valve)
|
|
What is the frequency of VSD?
|
most common defect!
20-30% isolated defect |
|
What are the features of PDA?
|
L to R shunt, usually an isolated defect. Presentation is a machine-like murmur
Normal cardiac function at birth |
|
How is patency maintained in a PDA?
|
administration of prostaglandin E will maintain patency (which is used for survival in some defects)
|
|
How is patency closed without surgery in PDA?
|
NSAID administration
--indomethacin --ibuprofen |
|
What is the embryology and most common association of AVSD?
|
failure of fusion of endocardial cushions - 1/3 occur with Down's Syndrome
|
|
What are the components of Tetralogy of Fallot?
|
1. VSD
2. Subpulmonary stenosis 3. Aorta overrides VSD/dextroposition - shifted right 4. right ventricular hypertrophy |
|
How is the severity of Tetralogy of Fallot determined?
|
Degree of subpulmonary stenosis determines direction of shunting and outcome
|
|
What shape does the heart take on in Tetralogy of Fallot?
|
Boot shape
|
|
What the the genetics involved in Tetralogy of Fallot?
|
Notch pathway genes implicated
|
|
What is persistant truncus arteriosus?
|
R to L shunt. Early cyanosis is seen. Single great artery overriding both ventricles. Associated VSD.
Embryology: failure of separation of the truncus arteriosus into 2 vessels. Most common association is 22q11.2 deletion syndrome |
|
What are the associations of adult coarctation of the aorta?
|
Valve defects: bicuspid aortic valve
Berry aneurysm, circle of Willis |
|
What are the symptoms of coarctation of the aorta?
|
upper body HTN
Hypotension of the legs (cold/cyanotic legs, claudication intermittent) Characteristic x-ray finding = rib notching |
|
What is hypoplastic left heart syndrome?
|
Severe stenosis or atresia of aortic valve. Underdeveloped left ventricle of aorta. PDA necessary for life!
|
|
What is William's Syndrome?
|
Deletion of Chromosome 7 (elastin gene)
Thickened ascending aorta; lumen of aorta is constricted = supravalvular stenosis. Multiorgan system disorder. Facial abnormalities - elfin, flat nose. Hypercalcemia in infancy (colic, vomiting, risk for metastatic calcifications) |