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Pembahasan LO 12-8-2013 & 19-8-2013

1. Gastropathy portal hypertension

Gastropathy Portal Hypertension

Definisi: Gastric vascular changes associated with portal hypertension. Etiologi: sebagai komplikasi dari portal hypertension baik yang disebabkan

oleh sirosis atau pun yang non sirosis. Pathogenesis : Belum diketahui dengan jelas dan pasti tetapi ada

beberapa hypothesis yang mungkin berkaian:

Elevated portal pressure.

Some other humoral factors (increased circulating levels ofvasodilators such as glucagon, or a reduced sensitivity toendogenous vasoconstrictors may play a significant role. Thishypothesis was sup- ported by the fact that the levels of several

vasodilators including glucagon, norepinephrine, VIP, gastrin orsecretin, were found to be increased in the plasma of cirrhotic portalhypertensive patients and/or animals).

Several endothelial factors including prostagladins, NO and vascularendothelial growth factor.

Lokasi: in the gastric fundus and upper body of the stomach although itcan affect the whole stomach and even other areas of the gastrointestinaltract, such as the small bowel or the colon.

Gambaran klinis: overt or chronic upper gastrointestinal bleeding, chronicgastric mucosal bleeding and recurrent iron deficiency anemia thatsometimes requiring blood transfusion.

Endoscopic finding classification:

Histological features:

Dilatation of the capillaries and collecting venules in the gastricmucosa.

Submucosal veins appear ectatic, ir- regular and with areas of intimalthickening.

A greater mean mucosal capillary cross-sectional area.

Absence of any significant inflammatory cell infiltrate or erosion of thegastricmucosa.

Severe PHG : the number of mucosal vessels exhibiting fibrin thrombi andectasia and spindle cell proliferation [smooth muscle cell and myofibroblasthyperplasia] in the superficial mucosa are greater.

Tatalaksana :

Beta adrenergic blockers (propanolol), addition of isosorbite 5-mononi-trate to propanolol if not efficient

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Intravenous infusion of vasopressin

Glypressin or somatostatin

Endoscopic photocoagulation or electrocoagulation

Endoscopic photocoagulation or electrocoagulation

Decompressive shunt surgery

TIPSS. DD : GAVE (Gastric Antral Vascular Ectasia)

2. Hubungan sirosis dengan gastric ulcer

Increased resistance to portal blood flow in patients with liver disease (withand without cirrhosis) and the consequent elevation in portal pressure.

Chronic endotoxemia; the mechanism of susceptibility to mucosal injury isthought to be related to an imbalance between gastric mucosal aggressiveand defensive factors.

The ability of the gastric mucosa to repair itself following injury is alsocompromised in these individuals.

Reduced delivery of oxygen to the gastric mucosa, a phenomenon related tothe modi- fied tissue architecture (vascular congestion) and blood flowregulation of the stomach and lungs in portal hypertension, has a role in thereduced resistance of gastric mucosa to irritants in patients with cirrhosisand portal hypertension.

Reduced basal or stimulated gastric acid secretion, a phenomenon probablysecondary to a compensatory adaptation to cirrhosis and portal hypertension.

An increase in gastric blood flow in response to the presence of acid or

irritants on the mucosa enables neutralization of toxins or noxious agents andis termed the gastric hyperemic response. Reduced responsiveness of thegastric microcirculation to injury is believed to be associated with diminishedgastric prostaglandin production, a phenomenon related to the significantlyincreased nitric oxide production and release associated with thehyperdynamic circulation seen in portal hypertension.

Acute or chronic administration of the prostaglandin analog misoprostolrestores the responsiveness of the rat gastric microcirculation to acid andethanol as well as to nitric oxidea critical downstream mediator of thegastric hyperemic response to irritants.

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3. Bedanya Psychosomatic dan Psychiatric

Psychosomatic= suatu kondisi terjadinya stress ataupun gangguan mentalyang menyebabkan timbulnya suatu gejala fisik (seperti migraine, tensionheadaches, sexual dysfunction, hypertension , dan gastrointestinal problems)

yang tidak berhubungan dengan suatu penyakit fisiologis.

Psychiatric = suatu kondisi yang terjadi akibat gangguan ataupun stressmental tanpa menimbulkan berbagai gejala fisik.

4. ESR yang signifikan untuk pasien TBC = >100 mm/hour(http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34)

Normal ResultsAdults (Westergren method):

Men under 50 years old: less than 15 mm/hr

Men over 50 years old: less than 20 mm/hr Women under 50 years old: less than 20 mm/hr

Women over 50 years old: less than 30 mm/hr

Children (Westergren method):

Newborn: 0 to 2 mm/hr

Newborn to puberty: 3 to 13 mm/hr

(http://health.nytimes.com/health/guides/test/esr)

5. Rasio albumin globulin normal dan pada pasien sirosis

Normal range of albumin = 3.9 to 5.1 g/dL. Normal range of globulins= 2.3 to 3.5 g/dL.(http://www.urmc.rochester.edu/encyclopedia/content.aspx?ContentTypeID=167&ContentID=total_protein_ag_ratio)Rasio Albumin/Globulin normal =1.2 - 1.5(http://www.ecopolitan.com/health-services/specific-health-conditions/291-blood-interpretation?start=27)Rasio Albumin/Globulin pada pasien Sirosis = 1

(http://www.ncbi.nlm.nih.gov/pubmed/11995477)

6. Renal and liver problems apa saja yang terdapat prolonged fever?

PROLONGED FEVER IN LIVER PROBLEMS

Occurrence of fever in a patient with liver problems should suggest thefollowing:

1. Hepatoma ( HCC )- hepatocellular carcinoma , presenting low grade feverbecause of poor liver function with increase proinflammantory cytokines andchemokines

2. Liver cirrhosis and hepatitis : Endotoxemia. Endotoxins are normally

present in portal blood; in hepatic cirrhosis they are insufficiently cleared bythe liver and their presence can be demonstrated in the systemic circulation.
http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34http://www.ncbi.nlm.nih.gov/pubmed/11995477http://www.ncbi.nlm.nih.gov/pubmed/11995477http://www.ncbi.nlm.nih.gov/pubmed/11995477http://www.ncbi.nlm.nih.gov/pubmed/11995477http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34http://www.rcpamanual.edu.au/index.php?option=com_pttests&task=show_test&id=249&Itemid=34

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Fever is one of the many consequences ascribed to the presence ofendotoxins in the blood with low grade fever. In cirrhosis / chronic liverdisease gradual destruction of liver tissue trigger proinflammantoryresponse.

3. Cholecystitisgall stone stuckin the cystic duct and in late termscauses infection in hepatic duct.

infection in bile duct

cholangits(septicaemia), sistemic infectionand fever.

PROLONGED FEVER IN KIDNEYPROBLEMS

Low grade fever is commonly seen in kidney disease. When it occurs, thepatients are usually suspected to have infections. Due to the following causes,the patients with kidney disease are more likely to have infections like urinary

tract infection, upperrespiratory tractinfection.The patients with

kidney diseaseusually have todepend on longterm use ofimmunosuppressiveagents. Thesemedications not only

suppress theinflammatoryresponse in kidneys,but also weakenimmune system.Thus, the patientsare susceptible todevelop infection.Proteins are

antibodies in ourbody and they can defeat virus, bacteria when they invade into body.

However, in some cases of kidney diseases, the patients may lose a largeamount of proteins in urine. As a result, the patients immunity will decline and

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bacteria and virus will invade into body.The above are the main causes of infection in kidney disease. When it occurs,the patients may experience low grade fever. If urinary tract infection occurs,urgent urination, painful urination etc also can occur.Therefore, if you have low grade fever, you should go to see a doctor at once

to find out if it is related to infection. Meanwhile, the patients should also takepreventive measures to reduce the risk of infection.

1. Chronic kidney failure / end stage renal disease such as causepyelonephritis chronic, renal abcess, hydronephrosis and etc. Lowgrade fever happens because poor immunity, longterm application ofimmunosuppressive agents and loss of usefull protein in urine.

2. Acute kidney failure high inflammantory response occurs such assepsis because of bad ascending infection, dehydration, damage fromlong term effect somemedicine(gentamicin,streptomycin,aspirin,ibuprofen,ACE inhibitors),

kidney stones, kidney injury cause trauma and etc.

Kidney cancer ( wilms tumor / renal cell carcinoma )Produceproinflammantory cytokines.

7. Fever of unknown origin : Fever that lasts 3 weeks or longer withtemperatures exceeding 100.9F with no clear diagnosis despite 1 week ofclinical investigation.

Normal daily protein excretion should not exceed 150mg/24 hours or10mg/100mL. Proteinuria is defined by the production of >150mg/day withnephritic syndrome producing >3.5g/day

Dipstick urinalysis detects protein with Bromphenol blue indicator dye and ismost sensitive to albumin and less sensitive to Bence-Jones protein andglobulins. Trace positive results are equivalent to 10 mg/100 ml or about 150mg/24 hours (the upper limit of normal).

True protein elevation:

o Renal: Increased renal tubular secretion,increased glomerularfiltration (glomerular disease), nephrotic syndrome,pyelonephritis, glomerulonephritis, malignant hypertension

o CVS: Benign HT, CCF, SBE

o Functional proteinuria (albuminuria): fever, cold exposure,stress, pregnancy, eclampsia, CHF, shock, severe exercise

o Other: Orthostatic proteinuria, electric current injury,hypokalaemia, Cushings syndrome

o Drugs: Aminoglycosides, gold, amphotericin, NSAID,sulphonamides, penicillins

Note: Bence Jones globulin associated with multiple myeloma, lymphoma andmacroglobulinaemia is NOTdetected by dipstick urinalysis

o False Positive:Concentrated urine (UO7.5), trace residue of bleach, aceazolomide,cephalosporins, NaHCO3

o False Negative:Dilute urine (UO >5.0 litres/day) or acidic urine(pH

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8. Uji dipstick dan konversinya pada 24-hours urinary excretion

DipstickProtein reading Protein excretion mg/24hours

Protein excretionmg/dL

Negative 1000

9. Systemic Lupus Erythematosus Criteria (DOPAMINE RASH)

Discoid rash (erythematous circular raised patches with adherentkeratotic scalling and follicular plugging; atrophic scarringmay occur)

Oral ulcers

Photosensitive

Arthritis (on two or more peripheral joints with tenderness, swelling,or effusion)

Malar rash

Immune markers (Anti dsDNA, anti-RO, anti-La, anti-Smith)

Neurologic changes (seizure or psychosis without other causes

ESR raised

Renal disease: proteinuria >0.5 g/d or 3+, or cellular cast

ANA +

Serositis (pleurisy, pericarditis)

Hematologic disease (hemolytic anemia, thrombocytopenia,leukopenia)

10. Perbedaan T3 dan T4:

Perbedaan T3 T4

Sekresi Sangat sedikit disekresi;

sebagian besardidapatkan oleh

kelenjar tiroid

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deiodinisasi peripheral

dari hormone T4

Ketersediaan Serum dalam bentuk berikatan dengan protein

atau free state

Kekuatan ikatan denganprotein

Lebih lemah sehinggalebih mudah di uptake

oleh cell

Lebih kuat

Kekuatan ikatan dengan

reseptor nuklear

Lebih cepat Lebih lamban

Keaktifan Lebih aktif secara

biologis

Kurang aktif secara

biologis

Test T4

- Ada 2 bentuk T4 : protein-bounded dan Free T4 (FT4)

- FT4bentuk aktif yang ada di organ tubuh

- Total T4 normal : 4.512.6 g/dL

- Normal FT4: 0.7 to 1.8 ng/dL

- Angka total T4or FT4yang meningkathyperthyroidism

- Angka total T4or FT4yang menurunhypothyroidism

- Normal FT4 level disaat total T4 tinggi maupun rendahkesalahan

pada binding protein, bukan pada tiroid.

Contoh : pada masa hamil dan pemakaian oral contraceptives

meningkatkan binding protein

- Penyakit yang berat dan pemakaian kortikosteroid dapat menurunkan

binding protein

Test T3

- Normal FT3 range : 0.2-0.5 ng/dL

- Test T3 tidak berguna dalam mendiagnosis hipotiroid karena hanya

akan turun ketika keadaan sudah sangat parah

- Pada beberapa keadaan FT4 normal tapi FT3 tinggi menggambarkan

hipertiroid

11. Perbedaan C3 & C4 pada pemeriksaan SLE, hasil pemeriksaan dan

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interpretasinya

The complement system helps or complements the ability of antibodiesand phagocytic cells to clear pathogens from an organism. It is part of theimmune system called the innate immune system that is not adaptable anddoes not change over the course of an individual's lifetime. However, it can berecruited and brought into action by theadaptive immune system.

The complement system consists of a number of small proteins found in theblood, in general synthesized by theliver,and normally circulating as inactiveprecursors (pro-proteins). When stimulated by one of several triggers,proteases in the system cleave specific proteins to release cytokines andinitiate an amplifying cascade of further cleavages. The end-result of thisactivation cascade is massive amplification of the response andactivation ofthe cell-killing membrane attack complex. Over 25 proteins and proteinfragments make up the complement system, includingserum proteins,serosalproteins, and cell membrane receptors. They account for about 5% of the

globulin fraction of blood serum.

Three biochemical pathways activate the complement system: the classicalcomplement pathway, the alternative complement pathway, and the lectinpathway.

The following are the basic functions of complement:

Opsonization- enhancing phagocytosis of antigens

Chemotaxis- attracting macrophages and neutrophils

Cell Lysis- rupturing membranes of foreign cells

Clumping of antigen-bearing agents

C3 and C4 complement are parts of a group of globulin proteins found in theblood. Globulins carry substances through the bloodstream. C3 and C4complement help the body's immune system react to inflammation andinfection.

Laboratory tests which measure complement levels in the blood may also behelpful to the physician in making a diagnosis of SLE.

Complement is a blood protein that destroys bacteria and also influencesinflammation.

Complement proteins are identified by the letter "C" and a number. The most common complement tests are C3, C4, and CH50.

If the total blood complement level is low, or the C3 or C4 complement valuesare low and the person also has a positive ANA, some weight is added to thediagnosis of lupus. Low C3 and C4 complement levels in individuals with apositive ANA may signify the presence of active disease, especially kidneydisease.

12. Indikasi pemberian albumin
http://en.wikipedia.org/wiki/Phagocytichttp://en.wikipedia.org/wiki/Pathogenshttp://en.wikipedia.org/wiki/Immune_systemhttp://en.wikipedia.org/wiki/Innate_immune_systemhttp://en.wikipedia.org/wiki/Adaptive_immune_systemhttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Pro-proteinshttp://en.wikipedia.org/wiki/Proteaseshttp://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/Amplification_(molecular_biology)http://en.wikipedia.org/wiki/Activationhttp://en.wikipedia.org/wiki/Membrane_attack_complexhttp://en.wikipedia.org/wiki/Blood_plasmahttp://en.wikipedia.org/wiki/Serous_membranehttp://en.wikipedia.org/wiki/Proteinshttp://en.wikipedia.org/wiki/Serum_globulinshttp://en.wikipedia.org/wiki/Metabolic_pathwayhttp://en.wikipedia.org/wiki/Classical_complement_pathwayhttp://en.wikipedia.org/wiki/Classical_complement_pathwayhttp://en.wikipedia.org/wiki/Alternative_complement_pathwayhttp://en.wikipedia.org/wiki/Lectin_pathwayhttp://en.wikipedia.org/wiki/Lectin_pathwayhttp://www.webmd.com/hw-popup/immune-system-7922http://www.webmd.com/hw-popup/immune-system-7922http://en.wikipedia.org/wiki/Lectin_pathwayhttp://en.wikipedia.org/wiki/Lectin_pathwayhttp://en.wikipedia.org/wiki/Alternative_complement_pathwayhttp://en.wikipedia.org/wiki/Classical_complement_pathwayhttp://en.wikipedia.org/wiki/Classical_complement_pathwayhttp://en.wikipedia.org/wiki/Metabolic_pathwayhttp://en.wikipedia.org/wiki/Serum_globulinshttp://en.wikipedia.org/wiki/Proteinshttp://en.wikipedia.org/wiki/Serous_membranehttp://en.wikipedia.org/wiki/Blood_plasmahttp://en.wikipedia.org/wiki/Membrane_attack_complexhttp://en.wikipedia.org/wiki/Activationhttp://en.wikipedia.org/wiki/Amplification_(molecular_biology)http://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/Proteaseshttp://en.wikipedia.org/wiki/Pro-proteinshttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Adaptive_immune_systemhttp://en.wikipedia.org/wiki/Innate_immune_systemhttp://en.wikipedia.org/wiki/Immune_systemhttp://en.wikipedia.org/wiki/Pathogenshttp://en.wikipedia.org/wiki/Phagocytic

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Usage Recommended Dosage

ALBUMIN 5%

Hypovolemia Although the volume of ALBUMIN 5% administered must be

individualized, the initial dose should be 250 to 500 mL for olderchildren and adults and 12 to 20 mL per kg of body weight forinfants and young children. It may be repeated after 30 minuteintervals if the response is not adequate.1

Hemodynamic parameters should be monitored and should be usedto check for risk of hypervolemia and cardiovascular overload.

Hypoalbumine

mia

Hypoalbuminemia is usually accompanied by a hidden extravascular

albumin deficiency of equal magnitude. This total body albumindeficit must be considered when determining the amount ofalbumin necessary to reverse the hypoalbuminemia. When usingpatient's serum albumin concentration to estimate the deficit, thebody albumin compartment should be calculated to be 80 to 100mL per kg of body weight. Daily dose should not exceed 2 g ofalbumin per kg of body weight.1

Burns When ALBUMIN 5% is administered after the first 24 hoursfollowing burns, an initial dose of 500 mL is recommended.1

Usage Recommended Dosage

ALBUMIN 25%

HypovolemicShock

The dosage of ALBUMIN 25% must be individualized. As aguideline, the initial treatment should be in the range of 100 to 200mL for adults and 2.5 to 5 mL per kg body weight for children. Thismay be repeated after 15 to 30 minutes if the response is notadequate. For patients with significant plasma volume deficits,

albumin replacement is best administered in the form of 5%Albumin.2

Upon administration of additional albumin or if hemorrhage hasoccurred, hemodilution and a relative anemia will follow. Thiscondition should be controlled by the supplemental administrationof compatible red blood cells or compatible whole blood.2

Hemodynamic parameters should be monitored and should be used

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to check for risk of hypervolemia and cardiovascular overload.

Burns The optimal therapeutic regimen for administration of crystalloidand colloid solutions after extensive burns has not beenestablished. When ALBUMIN 25% is administered after the first 24

hours following burns, the dose should be determined according tothe patient's condition and response to treatment.2

Hypoalbuminemia

Hypoalbuminemia is usually accompanied by a hidden extravascularalbumin deficiency of equal magnitude. This total body albumindeficit must be considered when determining the amount ofalbumin necessary to reverse the hypoalbuminemia. When usingpatient's serum albumin concentration to estimate the deficit, thebody albumin compartment should be calculated to be 80 to 100mL per kg of body weight. Daily dose should not exceed 2 g ofalbumin per kg of body weight.2

HemolyticDisease of the

Newborn

ALBUMIN 25% may be administered prior to or during exchangetransfusion in a dose of 1 g per kg body weight.2

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