4TH PLENO

Presented by : 2OC

Scenario 4: MR. KARDOGALIS HEART

Tn. Kardogali, 50 years old came to the clinic with complaints of frequent headaches. These headaches over 1 year happened. Tn. Kardogali, but by take paracetamol or mefenamic acid reduced complaints and do not interfere with daily activities as a farmer. Of the examination, the doctor get a blood pressure of 165/105 mmHg and the cardiac examination obtained ictus apex laterally shifted to lower and lift strong. Doctors concluded Tn. Kardogali suffering from essential hypertension stage II, and there has been enlargement of the heart due to hypertension.

The doctor asked Mr.Kardogali whether there are parents or siblings who suffer from hypertension? Recollection of Mr. Kardogali no history of hypertension in the family, but the father of Mr. Kardogali died suddenly at the age of 50 years. Then the doctor gives a combination of antihypertensive drugs captopril and HCT with advice Mr. Kardogali must regularly and routinely take 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 to Mr.Kardogali?

STEP 1. TERMS
Ictus cordis: beating the apex of the heart Mefenamic acid: NSAIDs, anti-inflammatory Paracetamol: anti-pyretic and analgesic mildmoderate Hypertension: increasing of blood pressure> 140/90 mmHg (JNC VII) Stage II essential hypertension: Primary hypertension (idiopathic) with blood pressure> 160/100 mmHg

 Captopril: ACE inhibitor class of antihypertensive HCT: hydroclorotiazid (diuretic) Heart failure: the failure of the heart to pump sufficient blood to tissue.

STEP II. PROBLEM FORMULATION

1. Why is Mr. Kardogali often headache along 1 year later? 2. How is relationship between sex and age to Mr. Kardogalis complaint? 3. How is mechanism of paracetamol and mefenamic acid in decreasing Mr. Kardogalis complaints? 4. How Is interpretation of tests done on Mr.Kardogali? How does that happen?

5. Why is the Mr. Kardogalis ictus cordis shifted laterally 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 providing combination anti-hypertensive drugs?

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 in Kardogali?

STEP III. ANALYSIS OF PROBLEM

1. Why Mr. Kardogali frequent headaches for 1 year? Increased blood pressure will cause an increasing in intracranial pressure and vascular constriction responses to reduce vascular and tissue damage. This will lead cells to nutritional and O2 deficiencies.

2. What is the relationship of sex and age on the Mr. Kardogalis complaint? - At the advanced age occur degradation of smooth muscle cells in vascular and decreased elasticity of blood vessels - High risk in men and smoking 3. How does the mechanism of paracetamol and mefenamic acid may lower Mr. kardogali complaint? drug will inhibit the action of cyclooxygenase enzymes that play a role in prostaglandin synthesis. Decreasing will reduce the inflammatory effects of prostaglandins (pain), so the pain is relieved.

4. How Is interpretation of tests done on Mr.Kardogali? How does that happen? - blood presure > 165/ 105 and the cause is unknown essential hypertension stage II - Ictus cordis shifted laterally down cardiomegaly (LVH) increasing blood presure increasing cardiac activity cardiac muscle hypertrophy

5. Why is the Mr. Kardogalis ictus cordis shifted laterally down?

increasing of blood presure increasing of hearts activityleft ventricular hypertrophy Ictus cordis shifted laterally down 6. Is there a relationship with family history of hypertension with Kardogali complaint? someone with a family history of hypertension, risk for hypertension (25%). - family history: help diagnosis

7. Why Mr. Kardogalis father died suddenly at the age of 50 years? -lack of concern and knowledge about the disease - Asymptomatic disease is getting worse. ex: hypertension stroke , MCI death

8. What is the goal of physicians providing combination anti-hypertensive drugs? - Improving the effectiveness of treatment of hypertension - Lowering the dose HCT: lowering fluid resistance by effects of other drugs captopril: no tolerance, good used for long-term

9. Why is Mr. Kardogali should control regularly and routinely take medications for long term? -penyebab tidak diketahui untreatable control blood pressure -drug withdrawal rebounding hypertensive crisis

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 to heart failure? yes, it can. Depending on the level of Mr. Kardogali adherence to therapy & Mr. Kardogali lifestyle.

12. How does the mechanism of hypertension to be a heart failure? hypertension maximal cardiac activity ventricular hypertrophy decrease in ventricular volume decrease in heart stroke heart failure

13. What are the complications that can occur in Kardogali? - Eye: hypertensive retinopathy - Brain: stroke - Renal: renal failure, nephrosclerosis - heart: MCI

STEP IV. SKEMA

Risk factor disregulasi RAAS disturbance Increasing cardiac output Increasing blood presure Increasing peripheral resistention heart failure etiology

heart hypertrophy

edema

Vascular damage

Increasing heart activity

stroke

retinopathy

Kidney failure

HIPERTENSION

ESENCIAL HIPERTENSION

Definition Elevation of blood pressure of unknown cause Epidemiology Increase in the age over 65 years

 Pathogenesis Multifactorial 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 , genetic 2 . Balance between vasodilation and vasocontriksi modulator : endothelial , smooth muscle , and interstisium 3 . Influence local autocrine system that plays a role in the system renin , angiotensin and aldosterone . Therapy 1 . non-pharmacological Reducing risk factors 2 . Pharmacology Antihypertensive drugs : diuretics , beta blockers , calcium antaghonist , angiotensin converting enzyme inhibitors , and ARBs .

 Diagnosis 1 . History ( past medical history , family history , symptoms of organ damage ) 2 . Physical examination ( blood pressure checks ) 3 . Investigations ( routine blood tests , glucose , complete cholesterol , serum uric acid , serum creatinine , urinalysis , EKG , and others deemed necessary )

Complication Stroke , myocardial infarction , renal failure , encephalopathy , and others

Secunder Hipertension
Hipertension in Pregnancy Feocromocitoma Hipertension Renovascular Hipertension of Renal Diseases

Hipertension on Pregnancy
CLASSIFICATION OF HYPERTENSIVE DISORDERS OF PREGNANCY : 1. chronic hypertension 2. gestational hypertension 3. pre- eclampsia Risk Factor Family history multiple pregnancy age diabetes increased body mass index

1. Chronic hypertension Chronic hypertension complicates 35% of pregnancies. The diagnosis of chronic hypertension is based on a known history of hypertension pre-pregnancy or an elevated blood pressure 140/90 mm Hg before 20 weeks gestation. 2. Gestational hypertension Hypertension occurring in the second half of pregnancy in a previously normotensive woman, without significant proteinuria or other features of pre-eclampsia, is termed gestational or pregnancy induced hypertension. 3. Pre-eclampsia and eclampsia Pre-eclampsia usually occurs after 20 weeks gestation and is a multi-system disorder. It was classically defined as a triad of hypertension, oedema, and proteinuria. Eclampsia is defined as the occurrence of a grand mal seizure in association with preeclampsia, although it may be the first presentation of the condition.

 Pathogenesis of pre-eclampsia The pathogenesis and manifestations of pre-eclampsia can be considered in a two stage model. The primary stage involves abnormal placentation. In the first trimester, in a healthy pregnancy, the trophoblast invades the uterine decidua and reaches the inner layer of the myometrium. In pre eclampsia, these vascular alterations do not occur or they are limited to vessels in the decidua. The secondary stage of pre-eclampsia involves the conversion of this uteroplacental maladaption to the maternal systemic syndrome, which has protean manifestations. Failure of the normal cardiovascular changes of pregnancy to take place results in hypertension, reduction in plasma volume, and impaired perfusion to virtually every organ of the body.

MANAGEMENT OF HYPERTENSION IN PREGNANCY First line agent Methyldopa Methyldopa is a centrally acting agent and remains the drug of first choice for treating hypertension in pregnancy Second line agents 1. Nifedipine Nifedipine is popular for the treatment of hypertension in pregnancy and is widely used. It is safe at any gestation.The use of sublingual nifedipine 2. Oral hydralazine Hydralazine is safe throughout pregnancy, although the occurrence of maternal and neonatal lupus-like syndromes have been reported. Third line agents 1. and Adrenergic blockers 2. Thiazide diuretics

Fecromocitoma
Defenition : an adrenal medullary tumors that secrete epinephrine and norepinephrine in excessive amounts. Abnormal increase in levels of these hormones trigger an increase in cardiac output and vasoconstriction general, the two lead to hypertension which is typical for this disease

etiology : Multifactorial Genetic factors Environmental factors

Pathophysiology Pheochromocytoma , a rare cause of secondary hypertension occur or is very rare , a medullar adrenal tumor or sympathetic chain tumor ( paraganglioma ) that releases large amounts of catecholamines ( epinephrine , norepinephrine , and dopamine ) continuously or for a period of time .
Clinical manifestations 1. Tachycardia 2. Palpitations heart 3. Headache 4. Weight loss , appetite normal 5. Slow growth 6. Nausea 7. Vomiting 8. Abdominal pain

EXAMINATION OF pheochromocytoma BLOOD TEST Blood glucose increased . Calcium may increase. Hemoglobin increases due to haemoconcentration caused by a decrease in circulating volume . Urine tests -24 Hour urine collection , necessary for creatinine ( to ensure 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

Procedures 1. Drug beta blockers 2. Operation Prognosis 5-year survival rate for non malignant Pheochromocytoma more than 95 % , but for malignant phaeochromocytomas less than 50 % . Somewhat higher risk of malignancy if the patient was a child .

RENOVASKULER HYPERTENSION
HYPERTENSION IS CAUSED BY A.RENALIS STENOSIS 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 havent family history

Pathogenesis : Acute Phase Constriction renal artery immediately cause increase blood pressure, renin, and aldosterone Chronik Phase After a few days, the blood pressure remained elevated but renin and aldosterone decreased to normal values One kidney Goldblatt hypertension Along with a decrease followed by an increase in renin plasma due to sodium retention Two kidney Goldblatt hypertension Minimal sodium retention and hypertension is renin dependent

Diagnosis : Symptoms and signs similar to essential hypertension Gold standard: "arteriography" Therapy : Simillar with essential hypertension, but need special attention 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 or unilateral stenosis and renal function only one (stenosis)

Hipertension of Renal Disease

Renal disease is the leading secondary hypertension causes after contraception with 2-4% of all hypertension
*acute glomerulonephritis - glomerulonephritis happens due to allergic reaction 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 salt restriction and diuretics

*Nephrotic syndrome - chronically damage to glomeruli with clinical findings are proteinuria, 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 the pyelum or pelvis of the kidney. - the symptoms are high fever, pain on passing urine, and abdominal pain that radiates along the flank towards the back. - correlation between pyelonephritis with hypertension have been raised by wiez-janitor (1931) and longcope (1937)

Hypertensive heart disease

Hypertensive heart disease is the No. 1 cause of death associated with high blood pressure. Hypertensive heart disease refers to heart problems that occur because of high blood pressure.

These problems include: 1. Coronary artery disease and angina 2. Heart failure 3. Thickening of the heart muscle (called hypertrophy) 4. Etc

Caused by the response of myocytes to various stimuli accompanying elevated BP => Myocyte hypertrophy can occur as a compensatory response to increased afterload. =>Mechanical and neurohormonal stimuli accompanying hypertension can lead to activation of myocardial cell growth => LVH.

Clinical sign 1)palpitate 2)fatigue 3)oedema 4) epitaxis,hematuria, blurred vision, retinopati (if there's vascular disease)

Examinantion: 1)started from the general to the specific one, same as Standard examination in hypertension. There's atrial/ventricle gallop or both 2)Echocardiograph: Transthoracic echocardiography (TTE) may be very useful for identifying features of hypertensive heart disease. TTE is more sensitive and specific then electrocardiography for diagnosing the presence of LVH (57% for mild and 98% for severe LVH). LVH is symmetrical, whereas the hypertrophy of hypertrophic cardiomyopathy is asymmetrical. Non drugs: Diet, monitoring weight, avoiding tobacco product and alcohol, regular medical check up Drugs: diuretics, beta-blockers, ACE/ARB, aldosteron antagonist inhibitors, calcium channel blockers, angiotensin II receptor blockers, and vasodilators.

VASCULAR DISEASE

Occlusive Arterial Disease

Classificasion : a. Acute , etiologi : tromosis or embolism b. Chronic , etiologi : atheroscelrosis

Occlusion of the renal artery will cause renovascular hypertension and arterial mesentrica ischemia will lead to bowel infarction

Pathophysiology Chronic Occlusive will progressively narrow the lumen and increase blood flow resistance -> decreased blood flow to tissue -> ischemia Clinical lesions will be seen when the diameter of blood vessels reduces 50-75%, when lesions join, small lesions can also be annoying. Acute occlusion will cause severe ischemia, because not enough time to form collateral vessels. Acute occlusion most often occurs on the lower extremities.

Signs and symptoms

intermittent claudication -> muscle ischemia concomitant 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 and blood volume in the capillary

 Chronic ischemia -> 1. nails and skin trophic changes 2. body hair loss 3. cold (in the bad perfusion) 4. muscle hypertrophy and the addition of soft tissue 5. ulceration and gangrene Acute occlusion -> pain, pallor, pulse missing, poicilotermi, paratesia, paralysis (6P)

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 or elevate your head analgesic administration physical exercise prevention of gangrene Topical antibiotics for systemic ulcer

Aortic Aneurysms
Inciden 30-60/1000 Increasing incidence over past 3 decades

Incidence of AAA
Autopsy U/S Screening Pts with CAD Pts with PVD Pts with femoral and pop.aneurysms 1.5-3.0% 3.2% 5.0% 10.0% 50.0%

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 an artery, but not lg. Enough to meet criteria for an aneurysm

Classification Pseudoaneurysm
True Aneurysm

Etiology
Atherosclerosis Cystic Medial Necrosis Dissection Syphilis Familial Associated
Multifactorial Decrease in elastin and collagen in arterial wall Elastin becomes fragmented-->arterial elongation and dilatation Increase in the collagenase and elastase activity

Aortic Aneurysms
Clinical 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 of aneurysm

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

Diagnosis Physical Exam:

If <5cm in diameter, then cannot be detected by routine physical exam

Radiographs:
Calcified wall. Can determine size in 2/3 Cannot rule out and AAA

Aortic Aneurysms
Diagnosis 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

 Ultrasound
Establishes diagnosis easily Accurately measures infrarenal diameter Difficult to visualize thoracic or suprarenal aneurysms Difficult to establish relationship to renal arteries Technician dependent Widely available, quick, no risk, cheap

Aortic Aneurysms
CT 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

Aortic Aneurysms
Risks
Complications of AAA
Thrombosis Distal embolization Rupture

Size 5-6 cm

Yearly 5 Year Rupture Rate Risk 5-10% 25-50% 7-15%% 20-30% 30-75% >90%

23.4% of aneurysms 4-5 cm will rupture

6-7 cm >7 cm

Indications for Treatment

Presence of an infrarenal aneurysm > 5cm without associated co-morbid medical conditions Repair smaller aneurysms if rate of enlargement is greater than expected Repair all symptomatic aneurysms If co-morbid conditions exist wait until risk of repair and rupture are equal (approx. 6 cm)

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

Treatment - Endovascular
Repair through an incision in the groin with expandable prosthesis under fluoroscopic guidance Requires both surgical and radiological assistance Significantly reduced m+m Long tern result unknown Hospital stay 2 days, Recovery time 1-2 weeks

DEEP VEIN TROMBOSIS

DVT invade blood vessels deep venous system. In the United States, reported 2 million cases of deep vein thrombosis is treated in the hospital and at the estimate at 600,000 cases of pulmonary embolism occurred and 60,000 deaths due to the blockage of blood vessels .

 Deep vein thrombosis is a rare illness and can cause death if not in the know and treat effectively . Deaths occurred as a result of the loss of trombus vein , forming emboli which can cause sudden death if the blockage occurs in the arteries in the lungs ( pulmonary embolism ) .

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 .

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

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 resulted in increased coagulation activity

Clinic Manifestation
Deep vein thrombosis and symptomatic complaints would have if it causes : Dam venous flow . Inflammation of the vein wall and perivascular network . Pulmonary embolism on circulation .

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

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 .

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

DIAGNOSES
There are 3 types of accurate examination , which can establish the diagnosis of deep venous thrombosis , namely : 1 . venography Until now venography still the standard examination for venous thrombosis . The principle of this examination is to inject the contrast agent into in the dorsum pedis and will look picture of the venous system in the calf , thigh , proximal to the inguinal to v. iliaca .

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 .

Varices
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 or inflammation of the vein).

Epidemiology The frequency of its occurrence in female is twice as much as in males. The deficiency of the surface venous system of sub-extremity is a pathology seen in the males 15% and 25% in the females. Even though the varice are regarded as a normal finding in the physical examination, they indicate meaningful venous deficiency in most cases. Risk Factors Obesity, constipation, trauma and occupational factors may lead the development of venous deficiency.

Pathogeneses Venous system is composed of deep, surface and perforan components. The failure of one of these components may result in the failure of the system. Sephanofemoral, saphenopoplital components and perforan veins lead the circulation from the surface to the deep.

Diagnosis The diagnosis process starts with an outpatient physical examination. Abdominal and pubic examination should not be ignored. Diagnostic methods of non-initiative nature are golden standards. Duplex ultrasonography applied by an experienced expert can indicate anatomic and pathophysiological variations that will determine the treatment methodology.

TREATMENT OF THE VARICES

1) Sclerotherapy: injection of sclerosan substance to the relevant 1mm veins

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

3) Burning one by one by the thermo coagulation injection