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حفظكم الرحمن ايعا العالم الجليل

- Diagnosis is (Thrombotic Thrombocytopenic Purpura ) Proved by Neurological manifestations + hemolytic anemia ( Increase fragmented RBCs) + prolonged BT, FDPs Complicated by (AKI) ( as Creatinine is Increased ) and (hemolytic anemiа) - for (Distal gangrene )it's explained by microvascular occlusion of small BVs by microthrombi leading to ischemia and gangrene , there's a damage to the endothelial lining of these small BVs - DVT is explained by , hypercoagulability state ( leading to increase clots formation in the veins) And reduced venous return ( that happened in some cases as immobility) + presence of hypercoagulability state aggravates the situation 3- absence of bleeding is explained by ( 1- compensatory mechanisms as increasing clotting factors and FDPs - 2 efficient platelets despite the decrease in count - and it's an acute state, as TTP mostly lead to thrombosis rather than bleeding) 4- pathogenesis : deficiency or inhibition of ADAMTS13, leading to the formation of microthrombi, endothelial injury, resulting in hemolytic anemia, thrombocytopenia, and organ dysfunction,

Q1) Most likely diagnosis: Acquired thrombotic thrombocytopenic purpura (TTP) along with antiphospholipid antibody syndrome. Q2) Deficiency in ADAMTS13 protease which cleaves large vWF multimers into small multimers leading to its accumulation and thrombi formation. However, this explains the digital gangrene only as these multimers accumulate in the small arterioles. For the DVT, most probably it is caused by anti-phospholipid antibody syndrome as it is a common clinical condition to occur with TTP along with SLE. Q3) No bleeding as the PT and PTT in TTP are not prolonged and the patient here has mild thrombocytopenia as the platelet count is above 100,000 which is very unlikely to cause bleeding. Q4) Acquired TTP means that there is no gene defect, but it is due to antibodies against ADAMTS13 which is responsible for the cleavage of large vWF multimers to smaller ones leading to the accumulation of these multimers causing organ damage as these multimers bind to platelets within the micro vessels and they are large enough to form micro thrombo causing platelets consumption, tissue ischemia and microangiopathic hemolytic anemia (MAHA) . They accumulate in the arterioles to the CNS causing CNS manifestations, kidneys involvement, abdominal involvement and other organs such as the digital infarction in this case.

The clinical vignette exhibits Pentad of TTP CNS affection : stroke and hallucination Fever Microangiopathic hemolytic anemia with THROMBOCYTOPENIA.... (SCHISTOCYTES) RENAL AFFECTION (INCREASED SERUM CREATININE) TTP can be inhereted due to ADAMST13 gene mutation OR Secondary to autoimmune or drugs In this young female It can be triggered by lupus with antiphospholipid antibody syndrome that causes both arterial and Venous thrombosis ( Stroke - Digital gangrene and DVT) So we need to do ANA anti dsDNA anti smith ab and APLAS antibodies B2 glycoprotein 2 ab Lupus anticoagulant And anticardiolipin ab Treatment with plasmapheresis and underlying cause

1 -Diagnosis is (TTP) based on neurological signs, fever, digital gangrene, DVT, thrombocytopenia, and renal dysfunction. 2-Digital Gangrene & DVT caused by microvascular thrombosis and hypercoagulable state in TTP, Reflects excessive platelet aggregation and microthrombi formation. 3- Because of low platalets are consumed in microthrombi formation rather than causing bleeding and Thrombosis predominates over hemorrhage. 4- Pathogenesis is accumulation of large von Wilebrand factor multimers and excessive platelet aggregation and microthrombi formation which lead to RBC destruction, platelet consumption, and renal dysfunction.

د. شريف، أستاذ طب بكل معنى الكلمة، بارك الله به ونفعنا بعلمه 🤲

anti phospholibid syndrome 2 hypercogulable state with paradoxical plateletes def 3platelt more than 100000 4 form of anti phospholipid anti body

1) SLE ( lupus Nephritis and vasculitis) Due to ( sex female , autoimmune hemolytic anemia , hypercoagulable state , mild thrombocytopenia...) 2) Due to thrombosis and vascultits 3) Due to ( hypercoagulability predominance , mild decrease in platelets, normal clotting factor ) 4) Autoimmune mechanism ( genetic predisposition HLA DR2 and 3) + environmental factors Hormonal ( estrogen may have a role ) , autoantibody ( ANA and anti smith)

Most probably diagnosis is Acquired thrombotic thrombocytopenic purpra due to presence of (thrombocytopenia + microangiopathic hemolytic anemia ) , neurological manifestations, fever and kidney affection. It is classic pentad for TTP. Causes of gangrene and DVT Due to formation of microthrombi mainly by platlets Causes of absence of bleeding Due to mild thrombocytopenia Pathogensis May be inherited or acquired but in this case it is acquired Inhibitors of ADAMTS13 enzyme which results in presence of VWF Multimers ( more active ) VWF multimers induce platelet microthrombi formation which cause consumption of platelets ( thrombocytopenia ), fragmented RBCs ( shistocytes ), which are the major criteria for diagnosis Also fever, AKI, and neurological manifestation could be present to microthrombi and ischemia which cause multi organ damage.

Most probably diagnosis is Acquired thrombotic thrombocytopenic purpra due to presence of (thrombocytopenia + microangiopathic hemolytic anemia ) , neurological manifestations, fever and kidney affection. It is classic pentad for TTP. Causes of gangrene and DVT Due to formation of microthrombi mainly by platlets Causes of absence of bleeding Due to mild thrombocytopenia Pathogensis May be inherited or acquired but in this case it is acquired Inhibitors of ADAMTS13 enzyme which results in presence of VWF Multimers ( more active ) VWF multimers induce platelet microthrombi formation which cause consumption of platelets ( thrombocytopenia ), fragmented RBCs ( shistocytes ), which are the major criteria for diagnosis Also fever, AKI, and neurological manifestation could be present to microthrombi and ischemia which cause multi organ damage.

Number 1 : Antiphospholipid antibody syndrome Number 2: its a hypercoagulable state that involve BOTH veins and arteries Number 3 : its a procoagulant state , also the bleeding usually occur when the platelets are with a lower number than 100 K Number 4 : formation of procoagulatory antiphospholipids antibodies which lead to activation of platelets

TTP Hypercoagulability microthrombi formation Characterized microangiopathic hemolytic anemia and fever and thrombocytopenia >100000 appear in mild renal problems creatinine 1.9 and neurological dysfunction Deficiency of ADAMTS13 Caused by failure to cleave vWF explain the absence of bleeding because Instead, they can cause damage to organs and tissues by blocking blood

Female with Triad of thrombocytopenia ( decreased platelets) + microangiopathic hemolytic anemia + Acute kidney injury ( high Cr) could be TTP or HUS but presence of (stroke and hallucinations) neurologic symptoms + fever marks the diagnosis of TTP normal PT and PTT >> coagulation pathway is not involved Inhibition of ADAMTS13 level >> uncleaved vWF multimers >> platelet trapping & activation >> microthrombi formation and prothrombotic state. As there is not widespread activation of the clotting factors and FDP is normal unlike DIC >> no consumption of clotting factors >> no bleeding intact platelet function Treatment with plasma exchange + corticosteroids + rituximab + caplasizumab

1- Thrombosis + low plateletes + anemia (schistocytes) + high creatinine + CNS affection = Thrombotic thrombocytopenic purpra (TTP) . 2- Digital gangrene and DVT is due to thrmobus formation. 3- There is no bleeding because the plateletes count is above 100,000 (platelets count above 100,000 = asymptomatic thrombocytopenia), "the low plateletes count is due to consumption of platelets in thrombus formation". 4- The pathogenesis of TTP : mutation in ADAMS 13 >> accumulation of large vwf molecules in endothelium >> thrombus formation.

1/lupus vasculitis 2/inflammatory mediators , procagulants 3/as autoimmune disese cause micro angiopathic hemolytic anemia (MAHA) 4/lupus vasculitis causes psychogenic manifestions and induce inflammation causes stroke and dvt and autoimmune reaction causes MAHA and affect kidney

TTP Hypercoagulability Microthrombi formation Platelets count above 100,000 Inhibition or deficiency of ADAMTS13

Waiting...

First question Possible causes of pallor (anemia or pallor with normal Hb as low cop,tb toxemia,generalized edema ) Anemia may due to ACD or bone marrow suppression or malnutrition if there is history of tb before (chronic) Second question Laboratory findings in ascitic fluid : 1. Gross Appearance: The fluid is often cloudy 2. Biochemical Characteristics: High protein concentration: >3g/dL, indicating exudative ascites. Low glucose levels: <60 mg/dL, due to consumption by bacteria or inflammatory cells. Elevated LDH: Higher levels compared to serum. 3. Cellular Analysis: Lymphocytic predominance: The majority of white cells are lymphocytes, a hallmark of tuberculous ascites. White blood cell count: Typically ranges between 500-5000 cells/μL. 4. Microbiological Studies: PCR: Useful for detecting M. tuberculosis DNA with high sensitivity and specificity. 5. Microscopy and Ziehl-Neelsen Staining 6. Adenosine Deaminase (ADA): Elevated ADA levels are highly suggestive of TB 7. SAAG less than 1.1 These findings if tb is the cause of ascites (exudative) May be pericardial effusion cause transudative ascites: due to Ascites precox (not sure) Third question (treatment) First urgent pericadiocentesis to relieve dyspnea and for analysis Also treatment of ascites by paracentesis May give steroids to prevent constrictive pericarditis Second treatment of tb by standard four drug regimen Third supportive treatment Treat anemia Antipyretics Diuretics Finally monitoring and follow up

Q1-, pallor due to toxemia of TB Q2ascitic fluid is exudative due to Tuberculosis Q3-ttt of cardiac tamponade it's emergency by pericardiocetesis and ttt of congestion and edema by dieurics (Lasix) Then ttt of the cause (TB) 3 months INH. Rifampicin. Ethambitol. Pyrizolamide then continue other 6 months with INH and Rifampicin

1- anemia: Due one or mixed etiology A-ACD B-chronic toxemia -->BM - - pancyto C-pallor due low CO 2: ascites Protein>3gm or fluid serum >0.5 LDH > 200 or F/S > 0.6 Wbc>1000 And other as glu,LDL 3-urgent pericardiocentisis And stabilized the pt Then treat the cause 1-anti TB drug 2-steroid under cover of ab

Q1) Pallor due to decreased cardiac output due to cardiac tamponade and anemia of chronic disease Q2) The ascitic fluid obtained will be a transudate as it is caused by cardiac ascites: SAAG ratio greater than or equal 1.1 g/dl Q3) Treatment: 1- Careful U/S guided pericardiocentesis for the pericardial effusion 2-Corticosteroids to prevent pericarditis 3-Anti-TB drugs

Q4: causes of pallor 1- because of cardiac temponade (pericardial effusion) as the venous return is decreased so the COP is decreased 2- Because of severe toxemia of TB 3- IDA due to nutritional deficiency because of loss of appetite and may be because malabsorption syndrome because of TB enteritis common in ileocecal region which may cause ulceration and bleeding per rectum or malabsorption syndrome or may be there is because of low immunity may be associated with co-helminthic infections that causes malabsorption 3- Anemia of chronic disease because of inflammatory process as short erythrocyte life span, poor erythrocyte iron incorporation, and decreased sensitivity to or supply of erythropoietin 4- may be normocytic normochromic anemia when there's acute bleeding as hemoptysis 5- IDA in chronic bleeding as ulceration in the ileocecal region Q5: criteria of exudative fluid by light criteria -Ptn: fluid ptn/ serum ptn >.5 -Ptns >3 gm% -LDH >200 IU/L -Fluid LDH/serum LDH >.6 -Specific gravity>1016 -Cells (WBCs) >1000/cmm * Characteristics of TB effusion: * 1- exudate rich in lymphocytes and RBCs * 2- TB can be detected by staining: ZN stain * culture: Lowenstein-Jensen medium or BACTEC mor rapid * PCR for TB DNA * Adenosine deaminase : increased activity Q6: ttt 1- O2 therapy and IV fluids 2- diagnostic and therapeutic Pericardiocentesis if it massive pericardial effusion and Subxiphoid pericardial tube under general anaesthesia if the patient is stable and free not encysted fluid And if the patient is unstable it done under local anaesthesia 3- Anti-TB drugs First-line therapy for MTB is 6 months of isoniazid and rifampin, with the addition of pyrazinamide and ethambutol for the initial 2 months. 4- Corticosteroids injection

Q4) pallor is most probably due to ● anemia that may result from malabsorbtion due to intestinal congesion also may take place due to chronic disease TB ● it may be due to sympathetic stimulation due to decrease in cardiac out put due to increase pressure on heart and reduction in venous return that lead to decrease in baro receptor activity which give the upper hand to sympathetic over parathymp. So VC take place in skin that make the patient appears pallor Q2) Tapered fluid will take the exudate criteria e.g Color is turbid Elevated LDH Elevated proteins Elevated specific gravity Abundunt lymphocytes Low level glucose and by ZN stain Mycobacterium tuberculosis will detected Q3) treatment of this patient This patient have to transfere to specialized center and isolated to avoid spread of infection *Symptomatic treatment* e.g Pericardiothentesis to relieve dyspnea , intestinal congesion , ascitis Antipyeritics and analgesics TB management She will take long term regimn for at least 9 month in which the first 2 month she will take 4 drugs e.g INH + Refampicin + ethamputol + streptomycin Then for the rest of period she will take only 2 drugs And since TB affect pericardium she also needs steroids to avoid excess fibrosis Nb: because of these drugs surgeries are very very limited in management of tb and it may used in case of complications e.g strictured urethra ●for anemia we have to determine the cause of it and manage it according to its cause e.g IV iron for intestinal malabsorbtion

possible explanations of pallor in this patient:- 1 cardiac temponad cause reduction in cardiac relaxation and cardiac filling therefore it will lead to low cardiac output 2 TB infection cause toxic inhibition of bone marrow 3 animia of chronic disease 4 may heamatological spread of TB causing myelophisic animia (TB in bone marrow) 5 malnutrition (anroxia,nuesea ,vomiting) and git congestion so decreasing absorption may be due to shock so to confirm I need to count her RR and pulse lab finding of fluid obtained on tapping the ascites ascites before oedema of lower limb (ascites precox ) which is commonly accur with pericardial effusion it will be transudative proteins : low less tha 3 gm % fluid protein/ serum protein less than 0.5 specific gravity less than 1016 LDH less than 200 IU /L fluid LDH/ serumLDH less than 0.6 WBCs less than 1000/cmm but may be TB peritonitis accur and it will be exudative rich in lymphocytes and RBCs proteins : more than 3 gm % fluid protein/ serum protein more than 0.5 specific gravity more than 1016 LDH more than 200 IU /L fluid LDH/ serumLDH more than 0.6 WBCs more than 1000/cmm mainly lymphocytes and by staining ZN stain culture lowenstain- jensen medium PCR for TB DNA I will confirm I would treat this patient by :- General measures rest in bed proper nutrition antipyretics, analgesics Treat the cause 1 anti tuberculous drugs INH and Rifampicine for 9-12 months plus Ethambutol for first 2 months only 2 corticosteroids under cover of anti-TB drugs to prevent constrictive pericarditis Pericardiocentesis to relieve dyspnea and compression (withdrawal of only 50 to 75 ml eliminate tamponade in most cases ) ttt of systemic congestion diuretics (torasemide) and venodilator must be used with caution (avoid excessive preload reduction)

1) Pallor in this patient may be due to acute or chronic cause:- A: acute cause most probably due to obstructive shock caused by tamponading effect of effusion B: chronic cause most probably due to anemia of chronic disease resulting in iron trapping. 2)lab fluid of ascites most probably show: A:Grossly: exudate or may be bloody. B:Biochemical: protein >2.5gm Glucose 30:60mg SAAG <1.1 g/dl (hypoalbuminemia) C:Cytological: epithelioid multinucleated giant cells, degenerating inflammatory cells (most predominantly lymphocytes). D: C&S: will show nonmotile non-spore forming acid alcohol fast bacilli stained by Z-N stain and grow on LJ media. 3) Treatment is according to hemodynamic state: if unstable it should undergo U/S guided pericardiocentesis and IV fluid to increase RV preload. if stable it should undergo emergent pleuro-pericardial window to treat the tamponade and prevent recurrence. Pericardiectomy should be performed also to prevent recurrence. Long term anti-TB medications.

يا ريت يا دكتور تعمل محاضرات كلينيكال تفصيلية للبوستجرادويت و يا ريت تعرفنا المكان الجميل ده فين بجد ده يشجع على الجري اوي

Q4- anemia: as manifestation of TB and low COP in P.effusion. *In TB : a- anemia of chronic disease (most common) b- BM infiltration (mylopathic anemia) C-malnutrion ........................ Q5: lab.findings : * Exudate rich in lymphocytes, RBCs *Exudate: -fluid protein more than 3gm% -serum protein more than 0.5 -Specific gravity more than 1016 _fluid LDH more than 200 IU/l Serum LDH more than 0.6 -WBC: more than 1000/cmm *to detect TB : -ZN stain -Culture: Lowenstein-jensen media or Bactec -Guinae pig inoculation -increased ADA activity - PCR for TB DNA .......................... Q6: ttt a- ttt of the cause (TB) 1-antiTB drugs : -first line: INH,Rifampicin,Streptomycin,Ethambutol,Pyrazinamide -Second line: Ethionamide, Cycloserine,Para-aminosalicylic acid ,Capreonmycin, Kanamycin,Amikacin 2-Corticosteriods: to reduce inflammation and prevent constrictive pericarditis b- Pericardiocentesis: to relieve dyspnea, compression from tamponade

1- Patient has palor and toxemia with probable diagnosis of TB pleruitis and effusion Indicating anemia which is due to multifactorial causes including nutritional, gastropathy and toxemia with bone marrow supression by inflammatory cytokines like TNFalpha which causes anorexia as well 2- Pericardial fluid will be exudative ( high Protein - high LDH) lymphocytic predominant with high ADA AFB in fluid is unlikely as it represents Hypersensitivity reaction rather than infection but we can add gene xpert and IGRA tests 3- treatment includes relieving Tamponade by pericadiocentesis which is both diagnostic and theraputic in this patient as well as treatment of the cause with CAT 1 regimen 2HRZE/4 HR plus short course of corticosteroid to avoid development of constrictive pericarditis Other DD like malignancy ( lymphoma) and CTD like RA and SLE should be considered

شكرا جزيلا و نتمنى الاستمرار في عمل فيديوات الحالات المرضية و الاسئلة التفاعلية عليها

1- causes of pallor in this case may be due to * anemia especially anemia of ch. disease du to Tb * low COP * stressful event itself can lead to pallor due to vasoconstriction *congestion of neck veins also one of ddx. 2- ascetic fluid analysis in heart f. Show SAAG level (≥1.1 g/dL) and high ascites protein levels (≥2.5 g/dL). 3- firstly decompress the pericardium after confirm dx. By ECHO or even on your clinical finding By Pericardiocentesis Give O2 for patient And if the cause is TB Should be give him anti TB medications 4 drugs ( first 2 months ) rifampin, isoniazid, pyrazinamide, and ethambutol Then continue on 2 drugs only ( ifampin, isoniazid) for 4 months and steroids should be given to patient. ( Prednisolone ) 5-7 days then tapering over 6-8 wks.

1- anemia due to: A- Low COP B- T.B 2- since the cause is mostly T.B then beside an Exudate effusion it will have more lymphocytes and RBCs: > 1016 specific gravity > 3 gm protein > .5 fluid/ serum protein > 200 IU/L LDH >.6 Fluid/serum LDH >1000 WBCs 3- A- Treatment of the cause >> anti-TB drugs with corticosteroids B- Intravenous fluids to increase right-sided preload C- Drainage via pericardiocentesis or pericardial window if it is massive and recurrent

1. Anemia of chronic disease. Normal MCV with normal RDW. 2. protein is greater than 2/3 of plasma protein. Glucose is lesser than 2/3 of plasma glucose. Lympocytosis. LDH elevated. and zel Nelson stain positive. 3. treatment include pericadiocentsis if the pericardium is calcified needs pericardioctomy. Treating the underlying TB with antituberculus according to sensitivity test by PCR.

Q1) Pallor in this case is due to 2 causes (anemia and low cardiac output state) : 1) Anemia of chronic disease (ACD) dut to TB ( decrease EPO production and action on BM and low iron release from Macrophages!!) 2) Low cardiac output due to cardiac compression Q2) the ascitec fluid obtained will reveal transudative characters in the form of : a- Low protein level below 3 gm b- low LDH c- low or no WBCs Q3) Treating this patient : a- First step should be would be could be periicardiocentesis to relif dyspnea and compression b- steroids undercover of anti TB drugs to prevent fibrosis and reduce inflammation of pericardium. c- tetracyclines also can be injected in the preicardium to obliterate this potential space so reaccumulation is prevented !!! 6- Anti TB drugs for pulmonary TB مظبوط الكلام.

- Pallor causes in this case : 1- *low COP* ( causing systemic congestion) 2- Anemia *(AOCD)* that caused by TB 3 - *malnutrition* ( proved by the presence of anorexia and Wt loss ) - lab findings of the fluid obtained from the ascites : *Transudate* Ascitic fluid *protein < 3 gm* *LDH <200 IU/l* *Specific gravity <1016* *SAAG : high >1.1 g/dl* *WBCs <1000 mm3* - TTT - it's an emergency so the patient must be *resuscitated* and *pericardiocentesis* or *pericardiectomy* is performed to remove the fluid or *implantation of pericardio - peritoneal shunt* in case of refractory tamponade و دي الحقيقه شوفت انها ممكن تتعمل مع ال refractory, malignancy و الكلام ده كان ع سايت الجمعيه الامريكيه معرفش دلوقتى يمكن اتغير - after it Initial Phase (First 2 Months): Isoniazid Rifampicin Pyrazinamide Ethambutol taken daily for about two months. Continuation Phase (Next 4 to 7 Months): with: Isoniazid ,, Rifampicin This phase can last for 4 to 7 months depending on several factors, including the type of TB and the patient's response to treatment. With monitoring and following up. Thank u dr for these cases ❤️❤️ و جزاك الله خيرا و جعله في ميزان حسناتك

لو سمحت ي دكتور عايزين كيسات مهمه لانه الامتحانات قربت وجزاك الله خير

Pallor (pale skin) in a patient with tuberculous (TB) pericarditis may indicate underlying complications or associated conditions, including: 1. Anemia of Chronic Disease (ACD) • TB is a chronic infection that can cause anemia due to inflammatory cytokines interfering with iron metabolism and red blood cell production. • Common findings: • Mild to moderate anemia. • Normocytic, normochromic red blood cells on blood smear. 2. Nutritional Deficiencies • Patients with TB may experience weight loss and malnutrition due to reduced appetite, contributing to deficiencies in iron, vitamin B12, or folate. • Results in iron-deficiency anemia or megaloblastic anemia, which can cause pallor. 3. Hypoxia • In severe cases of pericardial effusion or cardiac tamponade, reduced cardiac output may lead to poor oxygen delivery to tissues, causing pallor. 4. Hemodynamic Instability • TB pericarditis with complications such as cardiac tamponade can lead to shock or low blood pressure, causing pale, cold, and clammy skin. Pericardial fluid analysis: • High protein, lymphocyte-predominant, ADA (adenosine deaminase) levels suggest TB. • Culture or PCR for Mycobacterium tuberculosis confirms diagnosis. • HIV testing (as TB is common in HIV-positive individuals). • Biopsy: Pericardial biopsy may be needed for definitive diagnosis. Treatment 1. Antitubercular Therapy (ATT): • Standard TB regimen (e.g., rifampicin, isoniazid, pyrazinamide, ethambutol for 6-9 months). • Extended duration (up to 12 months) may be needed in some cases. 2. Corticosteroids (controversial): • Used in severe cases to reduce inflammation (e.g., with significant effusion or constriction). • Example: Prednisone, gradually tapered. 3. Drainage: • Pericardiocentesis to relieve tamponade or analyze pericardial fluid. 4. Surgery: • Pericardiectomy (removal of the pericardium) for constrictive pericarditis if unresponsive to medical therapy.

Causes of anemia in case 1- d.t anorexia associated with t.b infection 2-chronic infection causing anemia Descrebtion fluid Exudative whiche appears couldy , increase LDH, increase protin , low glucose, high wBC especialy in D.C lymphocyte, +ve culture AFB Treatment : paracentasis is diagnostic and therpeutic , accroding to the cause If cause t.b Rx anti T.b for 6m

1.##Cause of pallor by: 1. Anemia of Chronic Disease (ACD) 2. Nutritional deficiency : cause malnutrition due to poor appetite. 3. Hemodynamic cause: ◦ Low cardiac output in cardiac tamponade leads to tissue hypoperfusion. 2.## The type of ascites associated with cardiac tamponade caused by tuberculosis is typically transudative ascites. But it maybe show characteristics ofexudative ascites. #Explanation: 1.Transudative Ascites: Increased systemic venous pressure due to impaired cardiac filling and reduced cardiac output. *Clear fluid in appearance. * Protein Level: Low protein content (<2.5 g/dL) *Serum-Ascitic Albumin Gradient (SAAG): High (>1.1 g/dL), consistent with venous congestion. 2. Exudative Ascites (Less common): Associated with peritoneal involvement by tuberculosis. *Cloudy in appearance * Protein Level: High protein content (>2.5 g/dL). * SAAG: Low (<1.1 g/dL). *Cell Count: May show lymphocytic predominance. *High Adenosine deaminase. 3.##Treatment: 1. Urgent Pericardiocentesis: To relieve cardiac tamponade and restore hemodynamic stability. Perform under echocardiographic guidance. Send the fluid for analysis: Biochemical analysis (protein, glucose). Cytology. Acid-fast bacilli (AFB) smear and culture. 2. Hemodynamic Support: Monitor blood pressure and manage hypotension with fluid resuscitation as needed (cautiously to avoid worsening effusion) #Definitive Treatment: 1. Antituberculous Therapy (ATT) RIPE regimen. *Intensive Phase (2 months): INH, Rifampicin , Pyrazinamide, Ethambutol. *Continuation Phase (4 months): Isoniazid and Rifampicin. *Adjust doses based on weight and monitor for drug toxicity. 2. Corticosteroids : To reduce inflammation and prevent constrictive pericarditis 3. Ascites and Lower Limb Edema: Diuretics like spironolactone and furosemide, if ascites is causing significant discomfort or dyspnea.

(1) In this case pallor may be due to : 1- Anaemia of chronic disease (TB) 2- systemic congestion ( gastroenteropathy and liver congestion ) which leads to decreased absorbtion and storage of iron . 3-Also cardiac tamponade causes decrease in cop . (2) Lab finding of the "ascitic" fluid in this case : # according to the "light's criteria " it will be a transudate : 1- Ascitic fluid protein < 3 gm 2- (Ascitic fluid/serum )protein <0.5 3 - LDH< 200 4- (Ascitic fluid /serum ) LDH < 0.6 5- Specific gravity < 1016 (3) Treatment of cardiac tamponade : ‏‪ 1- Treatment of the cause (antituberculous drugs for 9 months) 2- pericardiocentesis 3- pericardiectomy #Great benifit from these videos Thank you dr .❤

4- venous congestion due to right sided heart failure ( enlarged tender liver ) Decreased circulation volume also tb increases hepcidin production which inhibits iron absorption leading to iron deficiency anemia 5- elevated wbcs count > 1000 Elevated protein level Cloudy fluid or white Low glucose level ( due to consumption of macrophages and neutrophils for energy ) Elevated LDH 6- first tb therapy ( 4 drugs ) for 2 months ( rifampin isoniazid ethambutol pyrazinamide ) followed by 4 months of 2 drugs isoniazid rifampin then for follow up Second for pericardial effusion Pericardiocentesis with u/s Thirdly ascites Paracentesis Diuretics: mix of Lasix and spironolactone to avoid electrolyte imbalance Fourthly we can use oxygen therapy

Pallor may be due to: Edema...masks blood vessels. Anemia of chronic disease. Nutritional anemia. Tapping: Stained by Zeil_Nelsen stain...pink bacilli against blue background. TTT Supportive: Rest Very good nutrition. Antipyretic. Specific: Pericardiocentesis...to relief pericardial effusion. Diuretics for edema and ascites. Anti_tuberculous drugs.

عظيم يا دكتور❤❤

❤Thank you prof for your distinguishable sharpened knowledge ❤. ♧The first thing i do is to call for help by (cardiologist and cardiothoracic surgeon Pulmonologyeist if possible**), meanwhile i would try to make this pt a life and stable. ♧In unstable pts(like the pt above),and those in cardiac arrest or pre-cardic aresst with suspected C-tamponade, live saving pericardiocentesis therapeutic & diagnostic sample,even blindly (off course at limited set area resources)* should not be delayed for extensive diagnostic confirmation*, ♧but if hemodynamically stable pt i would confirm the Diagnosis with ECHO either (TTE *it's the Gold standard* & others,,, FAST, or foCUS with Subxiphoid view*... then manage it as conservative & treat the underlying insult (TB )+glucocorticoids( by specialist)* ,i will not forget to give analgesia 😂, i won't forget to look for and treat HF or pericarditis if co-existed, & so on😊. ♧☆☆ then i will do ECG to every pt suspected or have C-Tamponade..which can show the following; 1-Low voltage. 2- electrical alternans 3-PEA in cardiac arrest. ⊙Also cardiac enzymes may be required(peri/myo & peri-myocarditis) ♧i will do CXR not to diagnosis but to excluded other , also i may find features that support my diagnosis like: 1-Water bottle sign. 2-Posterior inferior bulge sign. 3-Pericardiac fat pad sign ♧i would do other relevant and appropriate investigations as required. □now a days they say that (Beck Traid which has Sensitivity <20%)*. ♧By so doing ICU/CCU admission will be recommended to ; °fluid resuscitation ,but i will do it cautiously °Dobutamine 0.5-1 mcg/kg/minute; i titrate it up as pt needed °i would Avoid anesthetic agents and positive pressure ventilation °i would do Continuous telemetry °Regular BP monitoring °Serial pulsus paradoxus measurement i will never forget about it😂 ❤❤❤❤❤❤❤❤❤

أعظم من شرح الباطنة وتعلمها وعلمها.

1) pale is due to anemia for chronic disease and may be due to systemic congestion which decrease blood supply to skin. 2) Ascitic fluid: SAAG >1.1 and Total protein >2.5 3) treatment should be urgent needle aspiration of fluid guided by ultrasound and anti-TB medication..

السلام عليكم جميعا / اسمي معتصم النهمي جامعة تعز (طبيب امتياز) دفعه 18 اجابة السوال الاول كالتالي / Causes of pallor in these case due to 1-Chronic inflammation suppress bone marrow function, leading to anemia of chronic disease. 2-Severe cardiac dysfunction, as in tamponade, can impair oxygen delivery to tissues, worsening the pallor. 3- مريض السل يكون فاقد الشهيه لذالك ممكن يكون ناقص حديد او vit B12،،،، ايظا اذا انتشر السل الى الامعاء ممكن يعمل git bleeding.____________________ اجابة السوال الثاني / لدينا سته اشياء نحبث عنها 1- appearance:- clear or yellow 2-SAAG :- >1.1 g/dL (high gradient) indicate portal hypertension . 3-Total protein > 2.5 g/dL, consistent with cardiac ascites . 4-Glucose :- normal. 5-LDH:-May be raised if there is associated with inflammation. 6-Cell Count:-Low WBC count (<250 cells/µL), primarily lymphocytes. --------+++------++++++-------- اجابة السوال الثالث 1-(Pericardiocentesis) 2- ttt of TB by regimen of 4*2 Then 2*4 A_ (RIF):- 10 mg/kg daily . B- (INH): 5 mg/kg daily. C-(PZA): 25 mg/kg daily. D-(EMB): 15-20 mg/kg daily.

Causes of pallor in this case is due to anemia of chronic disease (TB) that was explained that interlukins 1,6 &TNF stimulate hepcidin so that reduce iron absorption, also cytokines inhibit BM. Another cause for pallor is low cardiac output due to HF (pericardial tamponade ) Aspiration of ascitic fluid : transudate Proteins <3 gm Specific gravity <1016 WBC<1000/mm3 LDH<200IU/L Treatment: Pericardiocetesis Treatment of the cause ( ttt of TB : INH, rifambicin, ethambutol, pyrazinamide) You are completely completely completely perfect. Thank you prof

4 ) pallor is due to low cardiac output may be due to congestive heart failure , chronic TB infection, and anemia due to weight loss 5 ) laboratory findings : Turbid fluid Low protein and high SAAG Increase of lymphocytes Positive TB 6 ) Treat cause which is treat TB Treat cardiac tamponade by pericardiocentesis Or pericardial window

Q4: Potential causes of pallor? • Low COP due to ↓ S.V by the pericardial effusion • Hypotension • Anemia of chronic disease due TB • Hypoxemia due to obstructive shock Q5: Ascitic fluid analysis if TB is the cause • ↑↑ lymphocytes • Low SAAG <1.1 • Ascitic fluid total protein levels: >2.5 • Fluid color: Cloudy, turbulent • Microbiology: acid fast stain, PCR, culture • ↑ Adenosine deaminase Q6: Treatment approach to this patient • Tamponade: - Investigation: Echo (+ve pericardial effusion, Diastolic collapse of RA/RV) - Treatment: - US guided pericardiocentesis - GIVE IV fluid (careful because overfilling can worsen tamponade) - GIVE +ve inotropes: Doputamin - AVOID vasoconstrictors because will ↓ S.V - AVOID PPV because it ↓ V.R • Tuberculosis: - Investigation: Microbiological studies + CT chest - Treatment: RIPE TB regimen as Pulmonary TB

Causes of pallor in This Case: 1. Low Cardiac output due to diastolic heart failure due to Cardiac Tamponade. 2. Activation of Sympathetic system as a compensatory mechanism. 3. Anaemia due to chronic infection. Characters of ascitic fluid include: 1. Straw colored/ Bloody/ turbid , may be clear. 2. Low Sugar 3. High protein 4. High WBCs >500/mm3 with predominant lymphocytes >50% 5. Low SAAG <1.1 6. May be Positive AFB smear/ positive Culture & PCR for DNA. 7. ADA positive. Treatment: 1. Therapetic Pericardiocentesis. 2. Anti-TB medications