study guide circulatory pathology Flashcards
(36 cards)
What is the difference between exudates and transudates and which of those cause non-pitting edema?
exudate:Edema fluid with high protein content and
cells
• Specific gravity >1.020
transudate: Edema fluid with low protein content
• Specific gravity <1.020
Protein-rich fluid produces non-pitting edema! EXUDATE
What is the “newspaper test”?
holding newspaper up behind tube of fluid.If cloudy and cant read print, then HIGH PROTEIN–> exudate
- Normally, people do not develop edema because the ________ pressure, and the _______ pressure balance one another out.
hydrostatic (out) and oncotic (in)
- How does Hypoalbuminemia cause edema?
decreased colloid osmotic pressure pushing into capillaries causes imbalance in hydrostatic vs. oncotic and fluid leaks OUT
In what types of diseases does a person develop Hypoalbuminemia?
• Liver disease
• Nephrotic syndrome
• Protein deficiency (e.g.,
Kwashiorkor)
- What is myxedema?
Specialized form of tissue swelling due to increased extracellular glycosaminoglycans
• Pretibial myxedema and
exophthalmos (Graves disease)
HYPOTHYROID
Where do effusions collect and why? (hint: potential spaces in the body)
32.
Fluid within the body cavities.
Serous – thin fluid derived from either serum or secretions of mesothelial cells (effusion). i.e. COLLAPSED LUNG
infarctions due to PE–> effusion in lungs
What is the major cause of ascites, and why does this fluid typically only collect in the abdomen?
33.
Inreased blood volume leads to ascites. In ABDOMEN Increased blood volume from: -Portal HTN (major)--chirrohsis -heart failure -renal Na retention/ nephrotic sundrome -kwashiorkor -peripheral artery vasodilation Stays in abdomen because of peritoneum/walled off from other cavities.
What is the difference between hyperemia and congestion?
34.
- hyperemia (active hyperemia)=active inc. in volume of blood/tissue, vasodilation. blushing, inflammation…
- congestion (passive hyperemia) =passive increase in volume, accompanied by edema. impaired venous flow. ALWAYS PATHOLOGICAL
Be able to describe the steps of platelet adhesion and the glycoproteins involved in each
- First, vWF adheres to subendothelial collagen
2. Platelets then adhere to vWF by glycoprotein IB
- Be able to identify the disease associated with the deficiency of each glycoprotein, and describe which medication inhibits thromboxane production.
36.
medication that inhibits thromboxane: ASPIRIN
-Irreversibly acetylates cyclooxygenase, preventing
platelet production of thromboxane A2
Deficiency of platelet Gp Ib: BERNARD SOULIER SYNDROME.
-defective adhesion
Deficiency of Gp IIb-IIIa: GLANZMANN THROMBASTHENIA
-defective aggregation
deficiency of VWF: VON WILLEBRANDS disease
List the major features of ITP
Immune Thrombocytopenia Purpura
-Autoimmune mediated attack (typically IgG antiplatelet
antibodies) against platelets leading to decreased platelets
(thrombocytopenia)
-Antiplatelet antibodies against platelet antigens such as Gp IIb-IIIaand Gp Ib-IX (type II hypersensitivity reaction)
-Results in petechiae, purpura (bruises), and a bleeding
diathesis (e.g. hematomas)
-platelets destroyed in spleen
List the pentad of characteristic signs of TTP
Thrombotic Thrombocytopenic Purpura
1. Fever
2. Thrombocytopenia
3. Microangiopathic hemolytic anemia (intravascular hemolysis)
4. Neurologic symptoms
5. Renal failure
***Most often affects adult women
caused by: deficiency of ADAMTS13–> cleaving large
multimers of von Willebrand factor–>fibrin-platelet thrombi
List the major features of hemolytic uremic syndrome, and what illness it typically follows?
Follows a gastroenteritis with bloody diarrhea
- thrombotic microangiopathy due to endothelial cell damage
- thrombotic microangiopathy due to endothelial cell damage
- children
* *similar pentad to TTP (fever, thrombocytopenia, hemolutic anemia, neuro symtpms, RENAL FAILURE)
- How are the extrinsic and intrinsic pathways activated (i.e. what factor initiates each)?
EXTRINSIC (PT): tissue factor (trauma)
INTRINSIC (PTT): activated by contact factors. damaged surface
• Contact with subendothelial collagen
• High molecular weight kininogen (HMWK)
- What tests are used to monitor the extrinisic and intrinsic pathways?
Prothrombin time (PT)
• Tests the EXTRINSIC and common coagulation pathways
• Tests factors VII, X, V, prothrombin, fibrinogen
• International normalized ratio standardizes
the PT test
Partial thromboplastin time (PTT)
• Tests the INTRINSIC and common coagulation pathways
• Tests factors XII, XI, IX, VIII, X, V, prothrombin, fibrinogen
Thrombin time (TT): tests for adequate FIBRINOGEN LEVELS
Fibrin degradation products (FDP): tests the FIBRINOLYTIC system (increased with DIC)
- What test is used to determine if platelets are functioning correctly?
- Platelet count (normal: 150,000 to 400,000)
- Platelet aggregometry
- Bleeding time
- List the major features of DIC?
• Platelet count is decreased
• Prolonged PT/PTT
• Decreased fibrinogen
• Elevated fibrin split products (D-dimers)
• Treatment: treat the underlying disorder
microthrombi–>hemorraghes
- What factors are missing in hemophilia A and B? Do these diseases produce petechiae or ecchymoses?
Hemophilia A (classic): 8 • Deficiency of factor VIII • X-linked recessive • No petechiae or ecchymoses • Normal PT and PROLONGED PTT • normal platelet count and bleeding time
Hemophilia B (Christmas Disease): 9
• Deficiency of factor IX
• X-linked recessive
• Clinically identical to hemophilia A
- What are the vitamin K dependent clotting factors?
if Vit. K is deficinent--> Decreased synthesis of factors II, (2) VII, (7) IX, (9) X, (10) and protein C & S
- Describe the major features of Von Willebrand disease.
LAB:
• Normal platelet count and a prolonged bleeding time
• Normal PT with often a prolonged PTT
• Abnormal platelet response to ristocetin (adhesion defect)
CLINICAL:
• Spontaneous bleeding from mucous membranes
• Prolonged bleeding from wounds
• Menorrhagia in young females
• Hemarthrosis is uncommon
- What is Virchow’s triad, and what are examples of the diseases/conditions contributing to stasis, vascular injury, and hypercoagulability?
Factors involved in thrombus formation (Virchow’s Triad)
- Endothelial injury
- Atherosclerosis
- Vasculitis
- What is the difference between an embolism and a thrombus?
THROMBUS: fibrin platelet clot. STATIONARY
EMBOLUS: moving thrombus.
carried down the bloodstream from its site of origin resulting in the occlusion of a vessel
multiple types
- Know the features of pulmonary emboli?
patient ICU, bedridden, post-op gets out of bed and BOOM
- often clinically silent and often missed
- most from DVT (pelvic plexus, right side of heart)
- can cause sudden death
