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Pathology > study guide circulatory pathology > Flashcards

study guide circulatory pathology Flashcards

1
Q

What is the difference between exudates and transudates and which of those cause non-pitting edema?

A

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

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2
Q

What is the “newspaper test”?

A

holding newspaper up behind tube of fluid.If cloudy and cant read print, then HIGH PROTEIN–> exudate

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3
Q
  1. Normally, people do not develop edema because the ________ pressure, and the _______ pressure balance one another out.
A

hydrostatic (out) and oncotic (in)

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4
Q
  1. How does Hypoalbuminemia cause edema?
A

decreased colloid osmotic pressure pushing into capillaries causes imbalance in hydrostatic vs. oncotic and fluid leaks OUT

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5
Q

In what types of diseases does a person develop Hypoalbuminemia?

A

• Liver disease
• Nephrotic syndrome
• Protein deficiency (e.g.,
Kwashiorkor)

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6
Q
  1. What is myxedema?
A

Specialized form of tissue swelling due to increased extracellular glycosaminoglycans
• Pretibial myxedema and
exophthalmos (Graves disease)
HYPOTHYROID

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7
Q

Where do effusions collect and why? (hint: potential spaces in the body)
32.

A

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

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8
Q

What is the major cause of ascites, and why does this fluid typically only collect in the abdomen?
33.

A 
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.
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9
Q

What is the difference between hyperemia and congestion?

34.

A
  • 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
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10
Q

Be able to describe the steps of platelet adhesion and the glycoproteins involved in each

A
  1. First, vWF adheres to subendothelial collagen

2. Platelets then adhere to vWF by glycoprotein IB

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11
Q
  1. Be able to identify the disease associated with the deficiency of each glycoprotein, and describe which medication inhibits thromboxane production.
    36.
A

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

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12
Q

List the major features of ITP

A

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

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13
Q

List the pentad of characteristic signs of TTP

A

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

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14
Q

List the major features of hemolytic uremic syndrome, and what illness it typically follows?

A

Follows a gastroenteritis with bloody diarrhea

  1. thrombotic microangiopathy due to endothelial cell damage
  2. thrombotic microangiopathy due to endothelial cell damage
  3. children
    * *similar pentad to TTP (fever, thrombocytopenia, hemolutic anemia, neuro symtpms, RENAL FAILURE)
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15
Q
  1. How are the extrinsic and intrinsic pathways activated (i.e. what factor initiates each)?
A

EXTRINSIC (PT): tissue factor (trauma)
INTRINSIC (PTT): activated by contact factors. damaged surface
• Contact with subendothelial collagen
• High molecular weight kininogen (HMWK)

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16
Q
  1. What tests are used to monitor the extrinisic and intrinsic pathways?
A

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)
17
Q
  1. What test is used to determine if platelets are functioning correctly?
A
  • Platelet count (normal: 150,000 to 400,000)
  • Platelet aggregometry
  • Bleeding time
18
Q
  1. List the major features of DIC?
A

• Platelet count is decreased
• Prolonged PT/PTT
• Decreased fibrinogen
• Elevated fibrin split products (D-dimers)
• Treatment: treat the underlying disorder
microthrombi–>hemorraghes

19
Q
  1. What factors are missing in hemophilia A and B? Do these diseases produce petechiae or ecchymoses?
A 
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

20
Q
  1. What are the vitamin K dependent clotting factors?
A 
if Vit. K is deficinent--> Decreased synthesis of factors
 II, (2)
VII, (7)
IX, (9)
X, (10)
and protein C & S
21
Q
  1. Describe the major features of Von Willebrand disease.
A

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

22
Q
  1. What is Virchow’s triad, and what are examples of the diseases/conditions contributing to stasis, vascular injury, and hypercoagulability?
A

Factors involved in thrombus formation (Virchow’s Triad)

  1. Endothelial injury
  2. Atherosclerosis
  3. Vasculitis
23
Q
  1. What is the difference between an embolism and a thrombus?
A

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

24
Q
  1. Know the features of pulmonary emboli?
A

patient ICU, bedridden, post-op gets out of bed and BOOM

  1. often clinically silent and often missed
  2. most from DVT (pelvic plexus, right side of heart)
  3. can cause sudden death
25
Q
  1. What is the most common potential outcome of PE?
A 
No sequelae (75%)
• Asymptomatic or transient dyspnea/tachypnea
• No infarction (dual blood supply)
• Complete resolution
Infarctions (15%)
26
Q
  1. What is a paradoxical emboli?
A

• Any venous embolus that gains access to the systemic circulation by crossing over from the right to the left side of the heart through a SEPTAL DEFECT

27
Q
  1. Where do anemic and hemorrhagic infarcts occur, and how do they differ on gross pathology?
A

Anemic infarcts (pale or white color)
• Occur in solid organs with a single blood supply (spleen,
kidney, heart)
Hemorrhagic infarcts (red color)
• Occur in organs with a dual blood supply or collateral
circulation (lung and intestines)
• Also occur with venous occlusion (e.g., testicular torsion)
reperfused someties
Often has a wedge shape
• Apex of the wedge tends to point to the occlusion

28
Q
  1. What are the 4 major causes of shock?
A
  1. Cardiogenic (pump failure)
  2. Hypovolemic shock (reduced blood
    volume)
    3.Septic shock (bacterial infection)
  3. Neurogenic shock (generalized vasodilation)
29
Q
  1. How is hypovolemic shock classified (i.e. classes I-IV)?
A
  1. (loss of 0-15%)
    - no sig. change in vitals
  2. (loss 0f 15-30%)
    - HR >100 bpm, tachypnea, decr. pulse pressure
  3. (loss of 30-40%)
    - tachycardia, decreased systolic, oliguria
  4. (loss of >40%)
    - same,almost no urinary output. Life threatening.
30
Q
  1. What are the 3 stages of shock?
A

Stage I: • Compensation, in which perfusion to vital organs is
maintained by reflex mechanisms
-sympathetic tone, catecholamines, renin-angiotensin system
Stage II• Decompensation
acidosis, renal insuffiiency…
Stage III• Irreversible

31
Q

steps of platelet activation

A
  1. Platelets undergo a shape change and degranulation
    occurs
  2. Platelet synthesis of thromboxane A2
  3. Membrane expression of the phospholipid complex,
    which is an important substrate for the coagulation
    cascade
32
Q

steps of platelet aggregation

A
  1. Additional platelets are recruited from the bloodstream
  2. ADP and thromboxane A2 are potent mediators of
    aggregation
  3. Platelets bind to each other by binding to fibrinogen
    using Gp IIb-IIIa
33
Q

Chronic and acute ITP

A 
•Acute ITP
• Seen in children following a viral 
infection
• Self-limited disorder
Chronic ITP
• Usually seen in women in their 
childbearing years
• May be the first manifestation of SLE
• Petechiae, ecchymoses, menorrhagia, 
and nosebleeds
34
Q

lab characteristics of ITP

A

-Decreased platelet count and prolonged bleeding time
• Normal prothrombin time (PT) and partial thromboplastin time (PTT)
• Peripheral blood smear shows thrombocytopenia with enlarged immature platelets (megathrombocytes)
• Bone marrow biopsy shows increased numbers of
megakaryocytes with immature forms

35
Q

pathogenesis of TTP

A

Widespread formation of platelet thrombi with fibrin
(hyaline thrombi) leading to intravascular hemolysis (thrombotic microangiopathy)

LAB:
• Decreased platelet count and prolonged bleeding time
• Normal PT and PTT
• Peripheral blood smear shows thrombocytopenia and
schistocytes, and reticulocytos

36
Q

tissue changes after infarction

A

Ischemia –> Coagulative necrosis –>inflammation –>granulation tissue –>fibrous scar

Pathology (6 decks)

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