Chapter 11- Veins and Lymphatics Flashcards

1
Q

What together account for at least 90% of
clinical venous disease?

A
  • Varicose veins and
  • phlebothrombosis/thrombophlebitis
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2
Q

What are Varicose veins?

A

abnormally dilated, tortuous veins produced by prolonged, increased intraluminal pressure and loss of vessel wall support.

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3
Q

What veins are typically involved in varicose veins?

A

The superficial veins of the upper and
lower leg are typically involved ( Fig. 11-29 ).

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4
Q

What is the pathophysiology of varicose veins?

A

When legs are dependent for prolonged periods,

  • *venous pressures** in these sites can be markedly elevated (up to 10 times normal) and can lead
  • *to venous stasis and pedal edema**, even in essentially normal veins (simple orthostatic edema).

Some 10% to 20% of adult males and 25% to 33% of adult females develop lower extremity
varicose veins;

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5
Q

What are the risk factors for varicose veins?

A

obesity increases risk, and the higher incidence in women is a reflection of the
elevated venous pressure in lower legs caused by pregnancy. A familial tendency toward
premature varicosities has been noted.

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6
Q
A

FIGURE 11-29 Varicose veins of the leg (arrow).

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7
Q

Varicose dilation renders the venous valves what?

A
  • incompetent and leads to stasis,
  • congestion,
  • edema,
  • pain, and
  • thrombosis.
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8
Q

What is the most disabling sequelae of varicose veins?

A
  • include persistent edema in the extremity and
  • ischemic skin changes, including stasis dermatitis and ulcerations;
  • poor wound healing and superimposed infections can lead to chronic varicose ulcers.

Notably, embolism from these superficial veins is very rare. This is in sharp contrast to the relatively frequent
thromboembolism that arises from thrombosed deep vein
s (see below and Chapter 4 ).

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9
Q

Can embolism arise from superficial veins?

A

Notably, embolism

from these superficial veins is very rare.

This is in sharp contrast to the relatively frequent
thromboembolism that arises from thrombosed deep veins (see below and Chapter 4 ).

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10
Q

Varicosities that occur in two other sites deserve special mention

A
  • Esophageal varices.
  • Hemorrhoids
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11
Q

Discuss the pathophysiology of Esophageal varices

A

Liver cirrhosis (less frequently, portal vein obstruction or hepatic vein thrombosis) causes portal vein hypertension ( Chapter 18 )

. Portal hypertension
leads to the opening of porto-systemic shunts that increase the blood flow into veins at
the gastro-esophageal junction (forming esophageal varices), the rectum (forming
hemorrhoids)
, andperiumbilical veins of the abdominal wall (forming a caput medusa).
Esophageal varices are the most important, since their rupture can lead to massive (even fatal) upper gastrointestinal hemorrhage.

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12
Q

Hemorrhoids result from what?

A

Hemorrhoids can also result from primary varicose dilation of the venous plexus at the
anorectal junction
(e.g., through prolonged pelvic vascular congestion due to pregnancy or chronic constipation).

Hemorrhoids are uncomfortable and may be a source of
bleeding; they can also thrombose and get inflamed, and are prone to painful
ulceration

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13
Q

What is the site of more than 90% of cases site of more than 90% of cases?

A

Deep leg veins

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14
Q

What are thrombophlebitis and
phlebothrombosis?

A

the two terms are largely interchangeable designations for venous thrombosis and inflammation.

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15
Q

What are the additional sites for THROMBOPHLEBITIS AND PHLEBOTHROMBOSIS?

A
  • periprostatic venous plexus in males and the
  • pelvic venous plexus in females are additional sites,
  • as are the large veins in the skull and
  • the dural sinuses (especially in the setting of infection or inflammation).
  • Peritoneal infections, including peritonitis,

appendicitis, salpingitis, and pelvic abscesses, as well as certain thrombophilic conditions
associated with platelet hyperactivity (e.g., polycythemia vera, Chapter 13 ), can lead to portal
vein thrombosis

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16
Q

For deep venous thrombosis (DVT) of the legs, what is the most important predisposing condition?

A

prolonged immobilization resulting in decreased blood flow through the veins

This can occur with extended bed rest or from just sitting during extended travel in an
airplane or automobile
; thepostoperative state is another independent risk factor in DVT
formation.

Clearly, other mechanical factors that slow venous return also promote the
development of DVT; these include congestive heart failure, pregnancy, and obesity

17
Q

What are the risk factors for DVT?

A
  • extended bed rest or from just sitting during extended travel in an airplane or automobile;
  • the postoperative state is another independent risk factor in DVT formation.
  • Clearly, other mechanical factors that slow venous return also promote the development of DVT; these include congestive heart failure, pregnancy, and obesity
18
Q

What is an independent risk factor for DVT formation?

A

the postoperative state is another independent risk factor in DVT formation

19
Q

What often predisposes to thrombophlebitis?

A

Systemic hypercoagulability ( Chapter 4 )

In patients with
cancer, particularly adenocarcinomas, hypercoagulability occurs as a paraneoplastic syndrome related to elaboration of pro-coagulant factors by the tumor cells ( Chapter 7 ).

In this setting,
venous thromboses classically appear in one site, disappear, and then reoccur in other veins;
this is referred to as migratory thrombophlebitis (Trousseau sign) .

20
Q

What is Trousseau sign?

A

In this setting,
venous thromboses classically appear in one site, disappear, and then reoccur in other veins;
this is referred to as migratory thrombophlebitis (Trousseau sign) .

21
Q

Thrombi in the legs tend to produce few, if any, reliable signs or symptoms.

True or False

A

True

Thrombi in the legs tend to produce few, if any, reliable signs or symptoms.

Indeed, local
manifestations, including distal edema, cyanosis, superficial vein dilation, heat, tenderness,
redness, swelling, and pain may be entirely absent,
especially inbedridden patients.

In some
cases pain can be elicited by pressure over affected veins, squeezing the calf muscles, or
forced dorsiflexion of the foot (Homan sign); absence of these findings does not exclude a
diagnosis of DVT .

22
Q

What is Homan sign?

A

In some

  • *cases pain can be elicited by pressure over affected** veins, squeezing the calf muscles, or
  • *forced dorsiflexion of the foot (Homan sign);**

absence of these findings does not exclude a
diagnosis of DVT .

23
Q

What is a serious complication of DVT?

A
  • *Pulmonary embolism** resulting from
  • *fragmentation or detachment of the whole venous thrombus**.

In many cases the first
manifestation of thrombophlebitis is a pulmonary embolus. Depending on the size and number
of emboli, the outcome can range from no symptoms to death

24
Q

What is the first manifestation of thrombophlebitis in many cases?

A

pulmonary embolus.

Depending on the size and number
of emboli, the outcome can range from no symptoms to death

25
Q

What is superior vena caval syndrome?

A

The superior vena caval syndrome is usually caused by neoplasms that compress or invade the
superior vena cava
, such asbronchogenic carcinoma or mediastinal lymphoma.

The resulting obstruction produces a characteristic clinical complex that includes marked dilation of the veins of the head, neck, and arms and cyanosis. Pulmonary vessels can also be compressed,
causing respiratory distress

26
Q

What is the inferior vena caval syndrome?

A

The inferior vena caval syndrome can be caused by neoplasms that compress or invade the
inferior vena cava (IVC)
or by athrombus from the hepatic, renal, or lower extremity veins that
propagates upward.

Certain neoplasms—particularly hepatocellular carcinoma and renal cell
carcinoma—show a striking tendency to grow within veins, and these may ultimately occlude the
IVC.

27
Q

What are the certain neoplasm that show a striking tendency to grow within the veins and the may ultimately occlude the IVC?

A

Certain neoplasms—particularly hepatocellular carcinoma and renal cell
carcinoma

I

28
Q

VC obstruction induceswhat symptoms?

A
  • marked lower extremity edema,
  • distention of the superficial collateral veins of the lower abdomen,
  • and—with renal vein involvement—massive proteinuria.
29
Q

Which is more common primary or secondary disorders of lymphatic vessels?

A

Primary disorders of lymphatic vessels are extremely uncommon;

secondary processes are
much more frequent and develop in association with inflammation or malignancies.

30
Q

What is Lymphangitis?

A

acute inflammation elicited when bacterial infections spread into lymphatics;

31
Q

WHat are the most common agents that cause lymphagitis

A

group A β-hemolytic streptococci, although any microbe may be
associated
.

32
Q

What is the apperance of the affeceted lymphatics in lymphangitis?

A

The affected lymphatics are dilated and filled with an exudate of neutrophils and
monocytes; these infiltrates can extend through the vessel wall into the perilymphatic tissues
and, in severe cases, produce cellulitis or focal abscesses.

Clinically, lymphangitis is recognized
by red, painful subcutaneous streaks
(the inflamed lymphatics), andpainful enlargement of
draining lymph nodes
(acute lymphadenitis).

If bacteria are not successfully contained within the
lymph nodes, subsequent passage into the venous circulation can result in bacteremia or
sepsis.

33
Q

Primary lymphedema can occur due to what?

A
  • an isolated congenital defect (simple congenital lymphedema)
  • or as the familial Milroy disease (heredofamilial congenital lymphedema) , which causes lymphatic agenesis or hypoplasia.
34
Q

Secondary or obstructive lymphedema stems from
blockage of a previously normal lymphatic; such obstruction can result from

A
  • Malignant tumors obstructing either the lymphatic channels or the regional lymph nodes
  • • Surgical procedures that remove regional groups of lymph nodes (e.g., axillary lymph nodes in radical mastectomy)
  • • Post-irradiation fibrosis
  • • Filariasis
  • • Post-inflammatory thrombosis and scarring
35
Q

What are the outcomes of lymphadema?

A

Regardless of the cause, lymphedema increases the hydrostatic pressure in the lymphatics
distal to the obstruction and causes increased interstitial fluid accumulation.

Persistence of this
edema leads to increased deposition of interstitial connective tissue, brawny induration or peau
d’orange (orange peel)
appearance of the overlying skin, andeventually ulcers due to
inadequate tissue perfusion
.

Milky accumulations of lymph in various spaces are designated chylous ascites (abdomen), chylothorax, and chylopericardium; these are caused by rupture of
dilated lymphatics, typically obstructed secondary to an infiltrating tumor mass.

36
Q
A