Chapter 4: Hemodynamic Disorders Flashcards

1
Q

It is a possible cause of edema and effusion

a. elevated hydrostatic pressure
b. increased albumin synthesis
c. elevated colloid osmotic pressure
d. increased movement of fluid out of vessels

A

A.

possible cause of edema and effusion:

  1. elevated hydrostatic pressure
  2. decreased colloid osmotic pressure

net result: increased movement of fluid out of vessels

edema: accumulation of fluid in tissues
effusion: accumulation of fluid in cavities

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2
Q

The following are examples of non-inflammatory-related edema and effusions, except:

a. protein-poor fluids called transudates
b. often cloudy due to the presence of white cells
c. translucent and straw-colored
d. common in many disorders, including heart failure, liver failure, renal disease, and malnutrition

A

B

inflammatory-related edema and effusion:

  1. protein-rich exudates that accumulate due to increases in vascular permeability caused by inflammatory mediators
  2. often cloudy due to the presence of white cells
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3
Q

Increased hydrostatic pressure due to impaired venous return results in the following pathophysiologic conditions, except:

a. arteriolar dilation of the heart
b. constrictive pericarditis
c. thrombosis
d. lower extremity inactivity with prolonged dependency

A

A

impaired venous return:
congestive heart failure
constrictive pericarditis
venous obstruction or compression: thrombosis and external pressure
lower extremity inactivity with prolonged dependency

arteriolar dilation:
heart
neurohumoral dysregulation

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4
Q

The following are causes of reduced plasma osmotic pressure, except:

a. reduced albumin synthesis
b. severe liver disease
c. protein malnutrition
d. decreased loss from circulation

A

D - increased dapat

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5
Q

It is characterized by low plasma oncotic pressure

a. hyperproteinemia
b. hypoproteinemia
c. hyperalbuminemia
d. hypoalbuminemia

A

D

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6
Q

Pathophysiology of reduced plasma osmotic pressure

a. Reduced plasma oncotic pressure → reduced intravascular volume → renal hypoperfusion → secondary hyperaldosteronism → edema
b. Reduced plasma oncotic pressure → reduced intravascular volume → edema → renal hypoperfusion → secondary hyperaldosteronism
c. Reduced plasma oncotic pressure → edema → reduced intravascular volume → renal hypoperfusion → secondary hyperaldosteronism

A

C

Reduced plasma oncotic pressure → edema → reduced intravascular volume → renal hypoperfusion → secondary hyperaldosteronism

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7
Q

It is the resulting massive edema of the external genitalia and lower limbs due to parasites

a. Filariasis
b. Fibrosis
c. Elephantiasis
d. Thrombocytosis

A

C

Filariasis: organism induces obstructive fibrosis of lymphatic channels and lymph nodes → causes elephantiasis

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8
Q

It is a sign that occurs when a depression is left after finger pressure is applied over markedly edematous subcutaneous tissue due to displacement of the interstitial fluid

a. dependent edema
b. subcutaneous edema
c. periorbital edema
d. pitting edema

A

D

subcutaneous edema: distribution often influenced by gravity (also called dependent edema)

periorbital edema: results from renal dysfunction, parts of the body containing loose CT

pulmonary edema: lungs are 2-3x their normal weight

brain edema: narrowed sulci, distended gyri

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9
Q

These are peritoneal effusions caused by lymphatic blockages which may be milky due to presence of lipids absorbed from the gut

a. chylous effusions
b. hydrothrorax
c. hydropericardium
d. hydroperitoneum
e. ascites

A

A

Hydrothorax - involving the pleural cavity
Hydropericardium - pericardial cavity
Hydroperitoneum or ascites - peritoneal cavity

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10
Q

An active process that is characterized by arterial dilation which leads to increased blood flow

a. congestion
b. erythema
c. hyperemia
d. cyanosis

A

C

Congestion: ↓ venous outflow of blood from a tissue ○ Passive process
Erythema: affected tissues turn red due to increased delivery of oxygenated blood
Cyanosis: abnormal blue-red color of congested tissues

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11
Q

These are the central regulators of hemostasis

a. platelets
b. endothelial cells
c. clotting factors
d. collagen

A

B

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12
Q

It is mediated by reflex neurogenic mechanisms and the effect is transient

a. primary hemostasis
b. secondary hemostasis
c. clot stabilization and resorption
d. arteriolar vasoconstriction

A

D

Arteriolar vasoconstriction → Primary hemostasis → Secondary hemostasis → Clot stabilization and resorption

Endothelin: potent endothelium-derived vasoconstrictor

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13
Q

These have the adhesion molecule P-selectin on their membranes and contain proteins involved in coagulation such as fibrinogen, coagulation factor V and vWF

a. a-Granules
b. dense granules
c. B-granules
d. light granules

A

A

dense granules: contain ADP, ATP, ionized calcium, serotonin and epinephrine

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14
Q

Deficiency in GpIb

a. von Willebrand disease
b. Glanzamann thrombasthenia
c. Bernard-Soulier syndrome
d. Hemophilia B

A

C

von Willebrand disease: deficiency of vWF
Glanzamann thrombasthenia: deficiency of GpIIb-IIIa

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15
Q

It limits the size of the clot wherein plasmin breaks down fibrin and interferes with its polymerization

a. Clotting in Vivo
b. Formation of Platelet plug
c. Hypercoagulability
d. Fibrinolysis

A

D

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16
Q

It is the most important plasminogen activator

a. plasminogen activator inhibitors (PAI)
b. tissue plasminogen activator (t-PA)
c. free plasmin
d. a2-antiplasmin

A

B

17
Q

These factors inhibit platelet activation and aggregation except:

a. prostacyclin
b. NO
c. ADP
d. protein C

A

D

18
Q

Which of the following pairs is correctly paired?

a. thrombomodulin binds protein C
b. endothelial receptor C binds thrombin
c. protein C requires protein S as cofactor
d. TFPI requires protein C as cofactor

A

C

anticoagulant effects in the endothelium:

  1. thrombomodulin binds thrombin and endothelial receptor C binds protein C → thrombin loses its ability to activate coagulation factors and platelets → cleaves and activates protein C (requires protein S) → proteinC/S complex potent inhibitor of coagulation factors Va and VIIa
  2. Heparin-like molecules on the surface of endothelial cells bind and activate antithrombin III → inhibits thrombin and factors IXa, Xa, XIa, and XIIa
  3. TFPI requires protein S as cofactor → binds and inhibits tissue factor/factor VIIa complexes
19
Q

These are hemorrhages 1-2cm in size

a. petechiae
b. purpura
c. ecchymoses
d. hematoma

A

C

Platelet defects or vWF are defects of primary hemostasis
▪ Petechiae: minute 1-2 mm hemorrhages
▪ Purpura: > 3mm hemorrhages
Coagulation factor defects are defects of secondary hemostasis
Generalized defects involving small vessels
▪ Often present with palpable purpura or ecchymoses
▪ Ecchymoses - hemorrhages 1-2 cm in size
▪ Hematoma - palpable mass of blood

20
Q

The following are the 3 primary abnormalities that lead to thrombosis termed as the Virchow triad, which is the exception?

a. endothelial injury
b. abnormal blood flow
c. hypercoagulability
d. none of the options

A

D sila na yung triad

21
Q

It forms counter currents that contribute to local pockets of stasis

a. turbulence
b. stasis
c. embolization
d. propagation

A

A

stasis - major contributor to development of thrombi

22
Q

These are considered to be strong risk factors for thrombosis. except

a. prolonged bed rest
b. atrial fibrillation
c. cancer
d. smoking

A

D