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4THPLENO

Presented by :

2OC

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Scenario 4: MR. KARDOGALIS HEART

Tn. Kardogali, 50 years old came to the clinic withcomplaints of frequent headaches. These headachesover 1 year happened. Tn. Kardogali, but by takeparacetamol or mefenamic acid reduced complaints and

do not interfere with daily activities as a farmer.

Of the examination, the doctor get a blood pressure of165/105 mmHg and the cardiac examination obtained

ictus apex laterally shifted to lower and lift strong.Doctors concluded Tn. Kardogali suffering from essentialhypertension stage II, and there has been enlargement ofthe heart due to hypertension.

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The doctor asked Mr.Kardogali whether there are

parents or siblings who suffer from hypertension?Recollection of Mr. Kardogali no history ofhypertension in the family, but the father of Mr.Kardogali died suddenly at the age of 50 years.

Then the doctor gives a combination ofantihypertensive drugs captopril and HCT withadvice Mr. Kardogali must regularly and routinelytake control of the drug for the long term. Mr.Kardogali ask the doctor, whether the disease can be

cured or progress to heart failure as neighbors?

How do you explain what happened toMr.Kardogali?

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STEP 1. TERMS

Ictus cordis: beating the apex of the heart

Mefenamic acid: NSAIDs, anti-inflammatory

Paracetamol: anti-pyretic and analgesic mild-moderate

Hypertension: increasing of blood pressure>140/90 mmHg (JNC VII)

Stage II essential hypertension: Primaryhypertension (idiopathic) with blood pressure>160/100 mmHg

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Captopril: ACE inhibitor class of anti-hypertensive

HCT: hydroclorotiazid (diuretic)

Heart failure: the failure of the heart to pumpsufficient blood to tissue.

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STEP II. PROBLEM FORMULATION

1. Why is Mr. Kardogali often headache along 1year later?

2. How is relationship between sex and age to Mr.

Kardogaliscomplaint?3. How is mechanism of paracetamol and

mefenamic acid in decreasing Mr. Kardogaliscomplaints?

4. How Is interpretation of tests done onMr.Kardogali? How does that happen?

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5. Why is the Mr. Kardogalisictus cordis shiftedlaterally down?

6. Is there a relationship with family history of

hypertension with Kardogali complaint?7. Why Mr. Kardogalis father died suddenly at the

age of 50 years?

8. What is the goal of physicians providingcombination anti-hypertensive drugs?

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9. Why is Mr. Kardogali should control regularly

and routinely take medications for long term?10. Are there other therapies that can be done on

Mr. Kardogli?

11. Is Mr. Kardogali disease can progress to heart

failure?12. How does the mechanism of hypertension to be

a heart failure?

13.What are the complications that can occur inKardogali?

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STEP III. ANALYSIS OF PROBLEM

1. Why Mr. Kardogali frequent headaches

for 1 year?Increased blood pressure will cause anincreasing in intracranial pressure and vascularconstriction responses to reduce vascular and

tissue damage. This will lead cells to nutritionaland O2deficiencies.

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2. What is the relationship of sex and age on theMr. Kardogaliscomplaint?- At the advanced age occur degradation of smoothmuscle cells in vascular and decreased elasticity ofblood vessels- High risk in men and smoking

3. How does the mechanism of paracetamol andmefenamic acid may lower Mr. kardogali

complaint?drug will inhibit the action of cyclooxygenaseenzymes that play a role in prostaglandin synthesis.Decreasing will reduce the inflammatory effects ofprostaglandins (pain), so the pain is relieved.

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4. How Is interpretation of tests done on

Mr.Kardogali? How does that happen?- blood presure > 165/ 105 and the cause isunknownessential hypertension stage II

- Ictus cordis shifted laterally down

cardiomegaly (LVH)increasing blood presureincreasing cardiacactivitycardiac muscle hypertrophy

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5. Why is the Mr. Kardogalisictus cordisshifted laterally down?

increasing of blood presureincreasing ofhearts activityleft ventricular hypertrophyIctus cordis shifted laterally down

6. Is there a relationship with familyhistory of hypertension with Kardogali

complaint?someone with a family history of hypertension,risk for hypertension (25%).- family history: help diagnosis

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7. Why Mr. Kardogalis father died suddenly atthe age of 50 years?-lack of concern and knowledge about the disease- Asymptomatic disease is getting worse.ex: hypertensionstroke , MCIdeath

8. What is the goal of physicians providingcombination anti-hypertensive drugs?- Improving the effectiveness of treatment ofhypertension

- Lowering the doseHCT: lowering fluid resistance by effects of otherdrugscaptopril: no tolerance, good used for long-term

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9. Why is Mr. Kardogali should controlregularly and routinely take medicationsfor long term?

-penyebab tidak diketahui untreatable

control blood pressure-drug withdrawal rebounding hypertensivecrisis

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10. Are there other therapies that can be done

on Mr. Kardogli?there are, change your lifestyle:- Regular exercise- Foods high in fiber, low in fat, low in salt- Reduce alcohol consumption and reduce smoking

- Lose weight

11. Can Mr. Kardogali disease progress toheart failure?

yes, it can. Depending on the level of Mr. Kardogaliadherence to therapy & Mr. Kardogali lifestyle.

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12. How does the mechanism of hypertension

to be a heart failure?hypertensionmaximal cardiac activity ventricular hypertrophydecrease inventricular volumedecrease in heart strokeheart failure

13. What are the complications that can occurin Kardogali?- Eye: hypertensive retinopathy

- Brain: stroke- Renal: renal failure, nephrosclerosis- heart: MCI

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STEP IV. SKEMA

Risk factor

Increasing cardiacoutput

Increasing

peripheralresistention

Increasing bloodpresure

etiology

Vascular damageIncreasing heart

activity

heart hypertrophy

heart failure

stroke retinopathy Kidney failure

disregulasi

edema

RAAS disturbance

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HIPERTENSION

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DefinitionElevation of blood pressure of unknowncause

Epidemiology

Increase in the age over 65 years

ESENCIAL HIPERTENSION

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Therapy1 . non-pharmacologicalReducing risk factors2 . PharmacologyAntihypertensive drugs : diuretics , beta blockers , calciumantaghonist , angiotensin converting enzyme inhibitors , and ARBs .

PathogenesisMultifactorial causes of this disease which arises mainly due to the

interaction between certain factors . the factors include:1 . Risk factors : diet and salt intake , stress , race , obesity , smoking, genetic2 . Balance between vasodilation and vasocontriksi modulator :endothelial , smooth muscle , and interstisium

3 . Influence local autocrine system that plays a role in the systemrenin , angiotensin and aldosterone .

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ComplicationStroke , myocardial infarction , renal failure ,encephalopathy , and others

Diagnosis1 . History ( past medical history , family history ,

symptoms of organ damage )2 . Physical examination ( blood pressure checks )3 . Investigations ( routine blood tests , glucose , completecholesterol , serum uric acid , serum creatinine , urinalysis

, EKG , and others deemed necessary )

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Secunder Hipertension

Hipertension in PregnancyFeocromocitomaHipertension RenovascularHipertension of Renal Diseases

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Hipertension on Pregnancy

CLASSIFICATION OF HYPERTENSIVE DISORDERSOF PREGNANCY :

1. chronic hypertension

2. gestational hypertension3. pre- eclampsia

Risk Factor

Family historymultiple pregnancyagediabetesincreased body mass index

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1. Chronic hypertension

Chronic hypertension complicates 35% of pregnancies. Thediagnosis of chronic hypertension is based on a known history ofhypertension pre-pregnancy or an elevated blood pressure 140/90mm Hg before 20 weeks gestation.

2. Gestational hypertension

Hypertension occurring in the second half of pregnancy in apreviously normotensive woman, without significant proteinuriaor other features of pre-eclampsia, is termed gestational orpregnancy induced hypertension.

3. Pre-eclampsia and eclampsia

Pre-eclampsia usually occurs after 20 weeks gestation and is amulti-system disorder. It was classically defined as a triad ofhypertension, oedema, and proteinuria. Eclampsia is defined asthe occurrence of a grand mal seizure in association with pre-eclampsia, although it may be the first presentation of thecondition.

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Pathogenesis of pre-eclampsiaThe pathogenesis and manifestations of pre-eclampsia can

be considered in a two stage model. The primary stageinvolves abnormal placentation. In the first trimester, in ahealthy pregnancy, the trophoblast invades the uterinedecidua and reaches the inner layer of the myometrium.In pre eclampsia, these vascular alterations do not occuror they are limited to vessels in the decidua.

The secondary stage of pre-eclampsia involves theconversion of this uteroplacental maladaption to the

maternal systemic syndrome, which has proteanmanifestations. Failure of the normal cardiovascularchanges of pregnancy to take place results inhypertension, reduction in plasma volume, and impairedperfusion to virtually every organ of the body.

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MANAGEMENT OF HYPERTENSION IN PREGNANCY

First line agent

MethyldopaMethyldopa is a centrally acting agent and remains the drug of first

choice for treating

hypertension in pregnancy

Second line agents

1. NifedipineNifedipine is popular for the treatment of hypertension in pregnancy

and is widely used. It is safe at any gestation.The use of sublingualnifedipine

2. Oral hydralazine

Hydralazine is safe throughout pregnancy, although the occurrence ofmaternal and neonatal lupus-like syndromes have been reported.

Third line agents

1. and Adrenergic blockers

2. Thiazide diuretics

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Fecromocitoma

etiology :

Multifactorial Genetic factors Environmental factors

Defenition :an adrenal medullary tumors that secrete epinephrine andnorepinephrine in excessive amounts. Abnormal increase inlevels of these hormones trigger an increase in cardiac output

and vasoconstriction general, the two lead to hypertensionwhich is typical for this disease

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PathophysiologyPheochromocytoma , a rare cause of secondary hypertensionoccur or is very rare , a medullar adrenal tumor orsympathetic chain tumor ( paraganglioma ) that releases largeamounts of catecholamines ( epinephrine , norepinephrine ,and dopamine ) continuously or for a period of time .

Clinical manifestations1. Tachycardia2. Palpitations heart3. Headache4. Weight loss , appetite normal5. Slow growth6. Nausea7. Vomiting

8. Abdominal pain

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EXAMINATION OF pheochromocytomaBLOOD TEST Blood glucose increased . Calcium may increase. Hemoglobin increases due to haemoconcentration causedby a decrease in circulating volume .

Urine tests-24 Hour urine collection , necessary for creatinine ( toensure 24- hour specimen ) , total catecholamines ,vanillylmandelic acid ( VMA ) and metanephrines

Several inspection techniques are frequently used below :MRI can find all tumors in the adrenal .CT scans , less sensitive , risk factors

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Procedures

1. Drug beta blockers2. Operation

Prognosis5-year survival rate for non malignantPheochromocytoma more than 95 % , but formalignant phaeochromocytomas less than 50 % .

Somewhat higher risk of malignancy if the patientwas a child .

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RENOVASKULER HYPERTENSION

HYPERTENSION IS CAUSED BY A.RENALISSTENOSIS

ETIOLOGY : A.renalis atherosklerotik lession Is the most frequently (90%) Occur in family history of hypertention Fokal or advanced aortic plaques in the third

proximal a. renal

Displasia Fibromuscular young lady , 30-40 years old haventfamily history

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Pathogenesis :

Acute PhaseConstriction renal artery immediately cause increase bloodpressure, renin, and aldosteroneChronik PhaseAfter a few days, the blood pressure remained elevated butrenin and aldosterone decreased to normal valuesOne kidney Goldblatt hypertensionAlong with a decrease followed by an increase in renin plasmadue to sodium retention

Two kidney Goldblatt hypertensionMinimal sodium retention and hypertension is renindependent

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Therapy :

Simillar with essential hypertension, but need specialattention on providing ACEI and ARB.Both of these drugs on the choice of unilateral stenosis

when the contralateral kidney is working.But contraindicated if bilateral renal artery stenosis orunilateral stenosis and renal function only one (stenosis)

Diagnosis :

Symptoms and signs similar to essential hypertensionGold standard: "arteriography"

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Hipertension of Renal Disease

Renal disease is the leading secondary hypertensioncauses after contraception with 2-4% of allhypertension

*acute glomerulonephritis- glomerulonephritis happens due to allergicreaction to a streptococcal infection- clinical findings are fever, edema, albuminuria,hematuria, and acute hypertension that lead to

cardiac failure in some cases- hypertension can be treated with fluid and saltrestriction and diuretics

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*Nephrotic syndrome

- chronically damage to glomeruli with clinical findings areproteinuria, hypoproteinemia, edema.- over time the glomerular filtration will be reduced,increased blood urea and an increase in blood pressure.

*Pyelonephritis- is an ascending urinary tract infection that has reached thepyelum or pelvis of the kidney.- the symptoms are high fever, pain on passing urine, and

abdominal pain that radiates along the flank towards theback.- correlation between pyelonephritis with hypertension havebeen raised by wiez-janitor (1931) and longcope (1937)

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Hypertensive heart disease

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Hypertensive heart disease is the No. 1 cause of deathassociated with high blood pressure.Hypertensive heart disease refers to heart problemsthat occur because of high blood pressure.

These problems include:1. Coronary artery disease and angina2. Heart failure

3. Thickening of the heart muscle (called hypertrophy)4. Etc

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Caused by the response of myocytes to various stimuli accompanyingelevated BP => Myocyte hypertrophy can occur as a compensatoryresponse to increased afterload. =>Mechanical and neurohormonalstimuli accompanying hypertension can lead to activation ofmyocardial cell growth => LVH.

Clinical sign1)palpitate2)fatigue3)oedema4) epitaxis,hematuria, blurred vision, retinopati(if there's vascular disease)

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Examinantion:1)started from the general to the specific one, same as Standard examination inhypertension. There's atrial/ventricle gallop or both

2)Echocardiograph:Transthoracic echocardiography (TTE) may be very useful for identifying featuresof hypertensive heart disease.TTE is more sensitive and specific then electrocardiography for diagnosing thepresence of LVH (57% for mild and 98% for severe LVH). LVH issymmetrical, whereas the hypertrophy of hypertrophic cardiomyopathy is

asymmetrical.

Non drugs:Diet, monitoring weight, avoiding tobacco product and alcohol, regularmedical check up

Drugs:diuretics, beta-blockers, ACE/ARB, aldosteron antagonistinhibitors, calcium channel blockers, angiotensin II receptor blockers,and vasodilators.

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VASCULAR DISEASE

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Occlusive Arterial Disease

Classificasion :

a. Acute , etiologi : tromosis or embolism

b. Chronic , etiologi : atheroscelrosis

Occlusion of the renal artery will causerenovascular hypertension and arterialmesentrica ischemia will lead to bowel infarction

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Pathophysiology

Chronic Occlusive will progressively narrow the lumenand increase blood flow resistance -> decreased bloodflow to tissue -> ischemia

Clinical lesions will be seen when the diameter of bloodvessels reduces 50-75%, when lesions join, small lesionscan also be annoying.

Acute occlusion will cause severe ischemia, because notenough time to form collateral vessels.

Acute occlusion most often occurs on the lowerextremities.

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Signs and symptoms

intermittent claudication -> muscle ischemiaconcomitant physical exertion

Rest pain -> pain at rest, which arise in the distal part of

the foot and toes, and are worse at night Decrease in pulse

Murmur-> turbulent at lesion

changes in skin color -> pale due to the gravitational

influence of the lower elevation of arterial pressure andblood volume in the capillary

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Chronic ischemia ->

1. nails and skin trophic changes2. body hair loss3. cold (in the bad perfusion)4. muscle hypertrophy and the addition of soft

tissue5. ulceration and gangrene

Acute occlusion -> pain, pallor, pulse missing,poicilotermi, paratesia, paralysis (6P)

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Treatment

reducing risk factors stop smoking

therapy for patients with other diseases: diabetes,hyperlipidemia , hypertension

Diet and exercise Intermittent claudication pain will be relieved with rest

rest pain in the extremities is reduced by hanging orelevate your head

analgesic administration physical exercise

prevention of gangrene

Topical antibiotics for systemic ulcer

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Aortic Aneurysms

Inciden

30-60/1000

Increasing incidence over past 3 decades

Incidence of AAAAutopsy 1.5-3.0%

U/S Screening 3.2%

Pts with CAD 5.0%Pts with PVD 10.0%

Pts with femoral and pop.aneurysms 50.0%

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Defenition

Aneurysm - Increase in diameter of 50% (1.5x)its normal diameter Focal region Ectasia - Diffuse dilatation of an artery with

increase in diameter >50%

Arteriomegaly - Diffuse enlargement of anartery, but not lg. Enough to meet criteria for ananeurysm

ClassificationPseudoaneurysm

True Aneurysm

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Etiology

Atherosclerosis

Cystic Medial Necrosis

Dissection

Syphilis

Familial Associated

MultifactorialDecrease in elastin and collagen in arterial wallElastin becomes fragmented-->arterialelongation and dilatationIncrease in the collagenase and elastase activity

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Aortic AneurysmsClinical Presentation

Asymptomatic - 70-75%

Symptoms:

Early satiety, N,V

Abd., Flank, or Back pain

1/3 of pts experience abd. And flank pain

Abrupt onset of pain -->Rupture or expansion ofaneurysm

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Ruptured Aneurysms

Small tear-> pain, followed by frank rupture

Usually occurs postero-laterally

Can rupture in Vena Cava creating Aorto-Caval

Fistula Occasionally can rupture anterior - usually fatal

Thumbnail Sketch

60-70 y/o who presents with c/o abd pain,hypotension and a pulsatile abdominal mass

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Diagnosis

Physical Exam: If

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Aortic AneurysmsDiagnosis

Arteriography: Cannot determine aneurysm size because of

mural thrombus

Indications for obtaining arteriography Suspicion of visceral ischemia Occlusive disease of iliac and femoral arteries Severe HTN, or impair renal function ? Horseshoe Kidney Suprarenal of TAAA component Femoro-Popliteal Aneurysms

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Ultrasound

Establishes diagnosis easily

Accurately measures infrarenal diameter

Difficult to visualize thoracic or suprarenalaneurysms

Difficult to establish relationship to renal arteries

Technician dependent

Widely available, quick, no risk, cheap

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Aortic AneurysmsCT Scan

Very reliable and reproducible

Can image entire aorta

Can visualize relation ship to visceral vessels Longer to obtain and is more costly than U/S

Most useful

Requires contrast agent - renal toxicity

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Aortic AneurysmsRisks

Complications of AAA

Thrombosis

Distal embolization

Rupture Size YearlyRupture Rate

5 YearRisk

5-6 cm 5-10% 25-50%

6-7 cm 7-15%% 30-75%

>7 cm 20-30% >90%

23.4% of aneurysms 4-5 cm

will rupture

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Indications for Treatment

Presence of an infrarenal aneurysm > 5cmwithout associated co-morbid medicalconditions

Repair smaller aneurysms if rate of enlargementis greater than expected

Repair all symptomatic aneurysms

If co-morbid conditions exist wait until risk ofrepair and rupture are equal (approx. 6 cm)

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Treatment-Surgical

Standard Surgical Repair

Replace diseased aorta with artificial artery

Requires 7 day hospital stay Recovery time 3-6 months

Proven method with good long term results

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Treatment - Endovascular

Repair through an incision in the groin withexpandable prosthesis under fluoroscopicguidance

Requires both surgical and radiologicalassistance

Significantly reduced m+m

Long tern result unknown Hospital stay 2 days, Recovery time 1-2 weeks

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DEEP VEIN TROMBOSISDVT invade blood vessels deep venous system.

In the United States, reported 2 million cases ofdeep vein thrombosis is treated in the hospitaland at the estimate at 600,000 cases ofpulmonary embolism occurred and 60,000deaths due to the blockage of blood vessels .

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Deep vein thrombosis is a rare illness and cancause death if not in the know and treateffectively .

Deaths occurred as a result of the loss oftrombus vein , forming emboli which can causesudden death if the blockage occurs in thearteries in the lungs ( pulmonary embolism ) .

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RISK FACTORS

1. Deficiency of clotting factor

2. Operative action

a. Release of tissue plasminogen into the blood circulation

because of trauma at the time of operation.

b .Static blood flow due to immobilization during periods

preperatif , operative and post operative .

c . Decreased fibrinolytic activity , especially the first 24 hours

after surgery .

d . Operations in the leg veins directly cause damage in the area .

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3 . Pregnancy and childbirth

During the third trimester increased clotting factors VII , VIII and

IX.

At the beginning of the birth process leading to the release of

placental tissue plasminogen release into the blood circulation ,

resulting in the improvement of blood coagulation

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6 . Obesity and varices

Obesity can cause static and varices blood flow and decrease

fibriolitic activities that facilitate the occurrence of venous

thrombosis .

7. malignant process

In the malignant tissue degenerates be found " tissue thrombo

plastine - like activity " and " activiting X factor " that resultedin increased coagulation activity

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Clinic Manifestation

Deep vein thrombosis and symptomatic complaints

would have if it causes :

Dam venous flow .

Inflammation of the vein wall and perivascularnetwork .

Pulmonary embolism on circulation .

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4. . Long immobilization and limb paralysis will cause static

blood flow which facilitates the onset of venous thrombosis

5 . Oral contraception

The hormone estrogen pills cause venous dilatation , decreased

activity of anti- thrombin III and fibrinolytic processes and

increased blood clotting factors

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Complaints and symptoms of deep vein thrombosis can be:

1 . painful

Complaints of pain are varied and nonspecific , can feel pain or stiffness and

intensity ranging from light to severe .Pain will be reduced if the patient rest

in bed , especially the elevated leg position .

2 . swelling

Swelling due to edema . Edema caused by venous obstruction in the proximal

and perivascular tissue inflammation .Swelling increases if the patient walk

and will be reduced if a break in the bed with your feet slightly elevated .

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3 . Changes in skin color

Skin discoloration is not specific and not commonly

found in deep venous thrombosis than arterial

thrombosis .

Venous thrombosis in skin discoloration found only 17% -20 % of cases . Changes in skin color can change

and sometimes pale purple

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DIAGNOSES

There are 3 types of accurate examination , which canestablish the diagnosis of deep venous thrombosis ,namely :

1 . venography

Until now venography still the standard examination forvenous thrombosis .

The principle of this examination is to inject the contrastagent into in the dorsum pedis and will look picture ofthe venous system in the calf , thigh , proximal to theinguinal to v. iliaca .

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2 . Flestimografi impendans

The principle of this inspection is to observe changes in blood

volume in the legs . This examination is more sensitive to

tombosis femrlis vein and vena iliaca than in the calf

3 . Ultra sonography ( ultrasound ) Doppler

The method is carried out mainly in cases of recurrent venous

thrombosis , which is difficult to be detected by other

objective .

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Varice occurs for two reasons:1.The malfunction of the valve in the vein,2. The congestion in the vein.

Varicose veins are classified:primer (depending on the congenital pathology of

the vein wall and vascular structures)secondary (valvular damage caused by

rechannelisation after thrombosis orinflammation of the vein).

Varices

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Epidemiology

The frequency of its occurrence in female is twice

as much as in males. The deficiency of thesurface venous system of sub-extremity is apathology seen in the males 15% and 25% in thefemales. Even though the varice are regarded asa normal finding in the physical examination,they indicate meaningful venous deficiency inmost cases.

Risk FactorsObesity, constipation, trauma and occupational

factors may lead the development of venousdeficiency.

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PathogenesesVenous system is composed of deep, surface and perforancomponents. The failure of one of these components mayresult in the failure of the system. Sephanofemoral,saphenopoplital components and perforan veins lead thecirculation from the surface to the deep.

DiagnosisThe diagnosis process starts with an outpatient physicalexamination. Abdominal and pubic examination shouldnot be ignored. Diagnostic methods of non-initiativenature are golden standards. Duplex ultrasonographyapplied by an experienced expert can indicate anatomicand pathophysiological variations that will determine thetreatment methodology.

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TREATMENT OF THE VARICES

1)Sclerotherapy: injection of sclerosan substance to the relevant1mm veins

2)Epidermal Laser Treatment: Burning by laser ray on the skin

3)Burning one by one by the thermo coagulation injection

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