LBM 5

Kardiovaskular
Step 1
1. Varicose : abnormality dilated vessel with a tortuos source. Usually occurs
in venous system but may also occur in atrial or lymphatic vessel
2. Varicose vein: are enlarged, swollen veins that are caused by faulty valves
in the veins or weak vein walls . It is a sign because the blood flow is
abnormal
3. Tortuous: Twisted veins
4. Vericeal area: area around varicose veins
Step 2

1. Why does woman feel pain and her right leg become swollen and redness?
2. What are the cause of varicose?

Varicose veins are caused by weakened valves and veins in your legs. Normally, one-way
valves in your veins keep blood flowing from your legs up toward your heart. When these valves
do not work as they should, blood collects in your legs, and pressure builds up. The veins
become weak, large, and twisted.

3. What are the risk factors of varicose veins?

hese factors increase your risk of developing varicose veins:

Age. The risk of varicose veins increases with age. Aging causes wear and tear on the valves
in your veins that help regulate blood flow. Eventually, that wear causes the valves to allow some
blood to flow back into your veins where it collects instead of flowing up to your heart.

Sex. Women are more likely to develop the condition. Hormonal changes during pregnancy,
premenstruation or menopause may be a factor. Female hormones tend to relax vein walls.
Taking hormone replacement therapy or birth control pills may increase your risk of varicose
veins.

Family history. If other family members had varicose veins, there's a greater chance you will
too.

Obesity. Being overweight puts added pressure on your veins.

Standing or sitting for long periods of time. Your blood doesn't flow as well if you're in the same
position for long periods.

4. What is the relation between hypertention and varicose?

5. Why the womans skin is brownish and hard when palpated?
6. What is the reation between pregnancy and varicose veins?
7. What is the relation between obese and varicose veins?
8. Where does varicose veins can be occur?
9. What is patophysiology of varicose veins?
10.What are the therapy of varicose veins?
11.How to diagnose the varicose veins?
12.What are the clinical manifestations of varicose veins?
13.What are the different between deep and superficial veins?

Step 3
1. What is the veins anatomy?
Wall: collapse
If there is injury, it will be
More elastic
It does have valves
The direction is to heart, brings CO2 except v.pulmonalis

2. What is the physiology of veins?

What can make the blood go upwards:

Muscle pumps

respiration : because there is perifer resistance

thoraco abdominalis pressure

3. What factors can cause changes in veins (vasoconstriction and

vasodilatation)?
o

Temperature: Cold temperaturevasoconstriction. So does the

reverse.

Blood volume: when the blood volume is less than normal, to make
it adequate, its needed to be vasoconstriction (body compensation)

Sympathetic and parasympathetic nerves. Vasocontriction by

sympathetic nerves, vasodilatation by parasympathetic nerves.

Hormones: vasoconstriction: vasopresin, angiotensin, adrenalin

Vasodilatation: bradikinin, histamin

Injury

4. What are the different between deep and superficial veins?

Superficial veins: near the skin.
Deep veins: far from the skin. In between of muscles.
Perforates vein: connects the superficial vein and deep veins
5. Why the womans skin is brownish and hard when palpated?
Becaus there is: penumpukan hemosiderindarah yg dipecah di limfa
tdk mengalir, tetap berada di daerah itu mengeluarkan
hemosiderinperubahan warna
The damage occurs in capillary vessel and venules erythrocyte moves
to extravasationchange in color brownish
The damage occurs in capillary vessel and venules
thrombocytesblood clothardened vessel

6. What is the relation between hypertention and varicose?

When there is a damage in veins (valve) blood flows

increasehearthypertension

Blood accumulation in inferior parts increasing back to

hearthypertension

Activity of sympathic nerves to veins increasing, blood volume

increasing, skeletal muscle pumps also increasing. Therefore,
the make the vein pressure increasingvenous return
increasingatrial pressure increasingdiastolic volume
increasingstroke volume increasinghypertension.

7. What is the relation between pregnancy and varicose veins?

Pressure in abdomen effected to leg veins pressure increasing (30
mmHg) because, the leg must have greater pressure so, it can pump
the blood back to heartdamage of vein valves

8. What is the relation between obese and varicose veins?

Less activitypumping activity decreasingblood trap in inferior
partsvalve cant opened correctlyaccumulation of blood in legs

9. Why does woman feel pain and her right leg become swollen and
redness?
Damage of valveblood cant go upwardextravasation swelling and
redness
Sweelingnerves are pressed by the swollen parts.

10.What are the cause of varicose?

Varicose veins are caused by weakened valves and veins in your legs. Normally, oneway valves in your veins keep blood flowing from your legs up toward your heart. When
these valves do not work as they should, blood collects in your legs, and pressure
builds up. The veins become weak, large, and twisted.

11.What are the clinical manifestations of varicose veins?

Varicose veins usually don't cause any pain. Signs you may have varicose veins include:
Veins that are dark purple or blue in color
Veins that appear twisted and bulging; often like cords on your legs
When painful signs and symptoms occur, they may include:
An achy or heavy feeling in your legs
Burning, throbbing, muscle cramping and swelling in your lower legs
Worsened pain after sitting or standing for a long time
Itching around one or more of your veins
Skin ulcers near your ankle, which can mean you have a serious form of vascular disease that
requires medical attention

12.What are the risk factors of varicose veins?

hese factors increase your risk of developing varicose veins:

Age. The risk of varicose veins increases with age. Aging causes wear and tear on the

valves in your veins that help regulate blood flow. Eventually, that wear causes the valves to
allow some blood to flow back into your veins where it collects instead of flowing up to your
heart.

Sex. Women are more likely to develop the condition. Hormonal changes during

pregnancy, premenstruation or menopause may be a factor. Female hormones tend to relax

vein walls. Taking hormone replacement therapy or birth control pills may increase your risk
of varicose veins.

Family history. If other family members had varicose veins, there's a greater chance you

will too.

Obesity. Being overweight puts added pressure on your veins.

Standing or sitting for long periods of time. Your blood doesn't flow as well if you're in

the same position for long periods.

13.Where does varicose veins can be occur?

Varicose veins can appear in various parts of the body, including:

Although varicose veins may occur anywhere in the human body, they are most
commonly found in the legs and feet, particularly in the calves. Experts say that
standing and walking places extra pressure on the veins of the lower limbs
Legs (most common)
Rectum
Pelvis
Vagina
Uterus (womb)
Esophagus

14.What is patophysiology of varicose veins?

In healthy veins, the blood go upwards to the leg.
Abnormal: incompetent of the valvesincreasing venous
returndisruption blood flows to heartvenous
dilatationinsufficiency
The cause are two: primary and secondary.
Primary: valvular insufficency of superficial veins, mostly in saphena
femoral junction
Secondary: anatomic congenital abnormality. E.g: avalvulia
Over th time, with more local dilatation it can be failed superficial
venous system
The circulation system - arteries and veins form part of our circulation system, with
blood flowing from the heart into the arteries and to tissues and organs, and coming
back to the heart via the veins. The returning blood has to travel against gravity in the
veins, this is done through muscle contractions and a system of valves.
The veins have one-way valves that allow blood through, but not back, so that the
blood travels in only one direction. If the walls of the vein become stretched and less
flexible (elastic), the valves may get weaker. A weakened valve may allow blood to
leak backwards, and eventually flow backwards. When this occurs, blood can
accumulate in the vein(s), which becomes enlarged and swollen.

Experts are not sure why the walls of veins stretch or why the valves become faulty.
In many cases, it occurs for no clear reason.

15.How to diagnose the varicose veins?

Anamnesis: fatigue, often feels pain, muscle cramp at night, color
changes in affected skin
physical examination: dilated vein, tortuous vein, edema, ulcus
supported examination: Brodie Trendelenburg test, Tes perban, doppler
ultrasound, duplex ultrasound, venografi/flebografi
A physical examination, mainly visual, by a qualified doctor will decide whether or not
a patient has varicose veins. The patient will be asked to stand while the doctor
checks for signs of swelling. The patient may also be asked questions about the
symptoms, whether any close relatives have/had varicose veins, and whether they
are or have been pregnant. The physician may also ask the patient whether he/she
has ever had any leg injury, such as a broken bone, and any history of deep vein
thrombosis.
In some cases, a general practitioner (GP, primary care physician, family doctor) may
refer the patient to a vascular specialist.
The following diagnostic tests may also be ordered:

Doppler test - this is an ultrasound scan to check the direction of blood flow in
the veins to see whether the valves are working properly. This test can also check
for blood clots or obstructions in the veins.
Color duplex ultrasound scan - this ultrasound test provides color images of the
structure of veins, which helps the doctor identify any abnormalities. This test can
also measure blood-flow speed.

16.What are the differential diagnose?

Cellulitis
Osler-Weber-Rendu Syndrome
Stasis Dermatitis

17.What are the therapy of varicose veins?

General treatment: analgetic, antibiotic (if needed),anticoagulant (prevent
blood clots formation), NSAID (ibuprofen. Reduces pain and inflammation),
thrombolytic (to dissolve an existing clot)

High pressureslowen the flowthrombosis

Superficial varicosities are the result of high-pressure flow into a normally low-pressure system.
Varicosities carrying retrograde flow are hemodynamically harmful because they cause
recirculation of oxygen-poor, lactate-laden venous blood back into an already congested
extremity. The primary goal of treatment is the ablation of these reflux pathways with resulting
improvement of venous circulation.
In the rare setting of deep system obstruction, varicosities are hemodynamically helpful because
they provide a bypass pathway for venous return. Hemodynamically helpful varices must not be
removed or sclerosed. This condition is encountered rarely, but when it is, ablation of these
varicosities causes rapid onset of pain and swelling of the extremity, eventually followed by the
development of new varicose bypass pathways.
Sclerotherapy, laser and intense-pulsed-light therapy, radiofrequency (RF) or laser ablation, and
ambulatory phlebectomy are the modern techniques used to ablate varicosities. Numerous
reports describe success rates of greater than 90% for less invasive techniques, which are
associated with fewer complications, with comparable efficacy.[4, 5]

Chemical sclerosis or endovenous chemoablation (sclerotherapy) is the most widely used

medical procedure for ablation of varicose veins and spider veins.[6] In this procedure, a
sclerosing substance is injected into the abnormal vessels to produce endothelial destruction
that is followed by formation of a fibrotic cord and eventually by reabsorption of all vascular
tissue layers. For most veins, a detergent sclerosing agent is agitated with air to create a foam
similar to shaving foam. A thorough diagnostic evaluation is essential prior to treatment. A high
degree of technical skill is necessary for effective sclerotherapy for the following reasons:
Local treatment of the superficial manifestations of venous insufficiency is unsuccessful if
the underlying high points of reflux have not been found and treated. Even when the patient
appears to have only primary telangiectasias and the initial treatment seems to be
successful, recurrences are observed very quickly if unrecognized reflux exists in larger
subsurface vessels.
Missing the diagnosis of superficial truncal incompetence can cause significant
complications (especially skin staining and telangiectatic matting) if spider veins and
superficial tributaries are treated while high-pressure feeders remain open.
Delivery of sclerosant to subsurface feeding vessels that are not visible is usually performed
under ultrasonographic guidance.
Missing the diagnosis of deep system disease can lead to bad outcomes in several ways.
Symptoms become immediately worse if an unrecognized bypass pathway is ablated.
Missing the diagnosis of underlying venous thrombosis can lead to fatal embolism.
Unrecognized deep venous insufficiency can lead to early or immediate recurrence of
treated superficial disease.[7]
Selection of the correct sclerosant and the correct volume and concentration of sclerosant
depends on the type and location of disease, internal volume of the vessel to be treated,
positioning of the patient, and many other factors. The minimum effective concentration and
volume should always be used because sclerosant inevitably passes into the deep venous
system, where endothelial injury can lead to disastrous consequences.
Some sclerosants (eg, hypertonic sodium chloride solution) are highly caustic.
Extravasation of even a single drop of these agents can lead to skin sloughing and a very
poor cosmetic result.
Inadvertent injection into an arteriovenous malformation (or directly into an unrecognized
underlying artery) can cause extensive tissue loss or loss of the entire limb.

Inadvertent injection of concentrated sclerosants into the deep system can cause deep vein
thrombosis, pulmonary embolism, and death.
The proper use of sclerosing agents requires special training and extended study. Specific
dosing and technique recommendations for the administration of sclerosants are beyond the
scope of this article.
The most commonly used sclerosants today are polidocanol and sodium tetradecyl sulfate,
both known as detergent sclerosants because they are amphiphilic substances that are
inactive in dilute solution but are biologically active when they form micelles. These agents
are preferred because they have a low incidence of allergic reactions, produce a low
incidence of staining and other cutaneous adverse effects, and are relatively forgiving if
extravasated.[8] These are best delivered as a foam, which is made by agitating the
solutions with air to create a frothy substance.
Sodium morrhuate is an older detergent sclerosant that is made up of a mixture of saturated
and unsaturated fatty acids extracted from cod liver oil. The agent is of variable composition
and has been associated with a relatively high incidence of anaphylaxis. The incidence of
extravasation necrosis is high with this drug.
Ethanolamine oleate, a synthetic preparation of oleic acid and ethanolamine, has weak
detergent properties because its attenuated hydrophobic chain lengths make it excessively
soluble and decrease its ability to denature cell surface proteins. High concentrations of the
drug are necessary for effective sclerosis. Allergic reactions are uncommon, but reports exist
of pneumonitis, pleural effusions, and other pulmonary symptoms following the injection of
ethanolamine oleate into esophageal varices. The principal disadvantages of the drug are a
high viscosity that makes injection difficult, a tendency to cause red cell hemolysis and
hemoglobinuria, the occasional production of renal failure at high doses, the possibility of
pulmonary complications, and a relative lack of strength compared with other available
sclerosants.
Hypertonic sodium chloride solution in a 20% or 23.4% solution can be used as a sclerosing
agent. The principal advantage of the agent is the fact that it is a naturally occurring bodily
substance with no molecular toxicity, but the disadvantages of the agent make it unsuitable
except in the hands of highly skilled practitioners.
Because of dilutional effects, achieving adequate sclerosis of large vessels without
exceeding a tolerable salt load is difficult.
It can cause significant pain on injection and significant cramping after a treatment
session.
If extravasated, it almost invariably causes significant necrosis. Seeing patients with
dozens of disfiguring scars at the sites of extravasation of hypertonic sodium chloride
solution is not uncommon.
Because it causes immediate red blood cell hemolysis and rapidly disrupts vascular
endothelial continuity, it may cause marked hemosiderin staining that is not cosmetically
acceptable.
Food and Drug Administration (FDA) approval of drug labeling is an important concern for
physicians and patients in the United States. Polidocanol is the most widely used sclerosant
in the world, but the agent has not been approved by the FDA. Sotradecol, sodium
morrhuate, and ethanolamine oleate all were developed prior to the establishment of the
FDA. These agents are available in the United States as grandfathered agents. The newest
form of Sotradecol was cleared by the FDA in 2006. It is highly purified with no
contaminants.
The safety of sclerosing agents in pregnancy has not been established.
Transcutaneous pulsed dye laser and intense-pulsed-light (IPL) therapy has proven effective
for the tiniest surface vessels (eg, those found on the face), but this modality is not generally
useful as primary therapy for treatment of spider veins of the lower extremity. This is true for
several reasons.

Because of the physics of light absorption, delivering an ablative dose of thermal energy to
the vessel without damaging the overlying skin is difficult.
The degree of patient-to-patient variability of light absorption in the skin is high. Even an
experienced practitioner may inadvertently cause painful skin burns that can lead to
permanent hyperpigmentation or hypopigmentation.
For most patients, the laser pulses are significantly more painful than the 30-gauge needles
used for microsclerotherapy.
Most spider veins have associated feeding vessels that must be treated by some other
means before the tiny surface vessels are amenable to laser or IPL treatment.
Dudelzak et al report successful treatment of facial spider veins (telangiectasias) with a 980nm diode laser. No complications were reported.

18.How can be varicose vein ulcer?

19.What is thrombophlebitis? And what is the patophysiology?
20.Complication of varicose vein?
21.What are differences between superficial varicose veins and deep
varicose veins?
Step 4
Veins
Risk factor
Elasticity
Damage valves
varicose
diagnosis therapy