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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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