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قناة طبيه تهتم بالكتب الطبيه واي شي۽ متعلق بالطب #BRS #pathoma @Yaqob_alsomaii
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prophylactic cholecystectomy may be performed for asymp- tomatic cholelithiasis in the following situations:
● large (>3 cm) gallstones;
● choledocholithiasis;
● chronic haemolytic conditions (sickle cell disease, heredi-
tary spherocytosis);
● gallbladder polyps >1 cm in diameter;
● suspicion/risk of malignancy (anomalous pancreatic duc-
tal drainage);
● calcifcation of the wall (porcelain gallbladder);
● some ethnic groups or subjects living in areas with a high
prevalence of gallbladder cancer associated with gallstones (some parts of northern India, Native Americans, Mexican Americans, Colombia, Chile, Bolivia);
● transplant patients (during transplantation);
● bariatric surgery.
resource : Bailey & Love's Short Practice of Surgery 28E
Naloxone has a much shorter duration of action than most opioids and so coma and respiratory depression often recur when naloxone wears off.
More naloxone is often needed, given IV, by IVI, or IM, the dose adjusted depending on the response. Observe for at least 6hr after the last dose of naloxone and up to 24hr with methadone overdose. If repeat doses are required, consider starting a naloxone infusion.
Female with proximal muscle weakness:
1) polmyalgia rheumatica " high ESR normal CK "
2) fibromyalgia normal ESR and normal CK
3) Polymyositis "high CK "
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نحنُ أحياءُ وباقون، وللحلم بقيّة ..
Features of hereditary spherocytosis include all of the
following except :
A. increase Osmotic fragility
B. Increase MCHC
C. Increase MCV
D. Decrease surface area per unit volume
Thrombocytopenia
👨⚕ What is the normal count of platelets?
🧑⚕To know palpable Purpura Vs non palpable Purpura ? Important to know the causes
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NB v
Petechiae are pinpoint, nonblanching hemorrhages and are usually a sign of a decreased platelet number and not platelet dysfunction.
assume you have injury ....
How bleeding stop ?
About the cause :
See three points above , every point have different cause
Secondary hemostasis
Definition: processes that lead to stabilization of the platelet plug (white thrombus) by creating a fibrin network
Coagulation cascade: a sequence of events triggered by the activation of the intrinsic or extrinsic pathway of coagulation that results in the formation of a stable thrombus
Coagulation factors
Substances that interact with each other to promote blood coagulation
Activated factors are designated with an “a” (e.g., activated factor VII = factor VIIa).
Extrinsic pathway of coagulation: triggered by endothelial injury
Tissue factor (factor III) activates factor VII.
Tissue factor is expressed on the surface of subendothelial muscle cells and fibroblasts.
Factor VII: vitamin K-dependent coagulation factor produced by the liver
Factor VIIa and tissue factor form a complex (TF-FVIIa). This step requires calcium (factor IV) found on the surface of fibrocytes and activated platelets.
TF-FVIIa activates factor X and factor IX.
Intrinsic pathway of coagulation
Exposed collagen, kallikrein, and kininogen (HMWK) activate factor XII.
Factor XII (Hageman factor): coagulation factor that also plays a role in inflammatory response by activating the kallikrein system, which leads to the production of bradykinin
Factor XIIa activates factor XI.
Thrombin activates factor XI and factor VIII.
Factor XIa activates factor IX.
Factors VIIIa and IXa form a complex (mediated by calcium) that activates factor X.
This causes a positive feedback loop of factor X and thrombin activation via the intrinsic pathway.
Common pathway of coagulation: The extrinsic and intrinsic pathway both end in the common pathway.
Factor Xa and factor Va form a complex (mediated by calcium) that cleaves prothrombin (factor II) to thrombin (factor IIa).
Thrombin cleaves fibrinogen (factor I) into insoluble fibrin (factor Ia) monomers.
Crosslinks of the fibrin network are stabilized by factor XIIIa → formation of a fibrin network → fibrin closely binds to the platelet plug, forming a stable thrombus (secondary thrombus or red thrombus)
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How to treat opioid poisoning
Treatment
Clear and maintain the airway. If breathing is inadequate, ventilate with O2using a bag and mask or an ET tube .
Naloxone is a specific antagonist for opioids and reverses coma and respiratory depression if given in sufficient dosage
. Give naloxone as a therapeutic trial in suspected opioid poisoning—record coma level, pupil size, and RR, and check for any response
The usual
initial dose of naloxone for adults is 0.4mg IV, followed by a further dose of 0.8mg after 60s if no response
Children, give 100mcg/kg (IV, IM or IN) up to 2mg, repeated as
necessary. Intranasal naloxone, given by dripping or spraying the IV solution into the nose over 60s, enables rapid absorption. For children at risk of opioid withdrawal, give 1–10mcg/kg every 60s,
Opioid poisoning
The opioids include morphine, diamorphine (heroin), pethidine, codeine, buprenorphine, and methadoneClinical features
Opioid poisoning causes the triad of coma, d RR, and pinpoint pupils. Cyanosis, apnoea, convulsions, and hypotension may occur. Effects of opioids are potentiated by alcohol. Non-cardiogenic pulmonary oedema may result from injecting heroin or other opioids.
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👨⚕🤨 what is the causes of palpable Purpura?
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👨⚕It's important to palpate purpuric rash or not ? Why?
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1- V.C 2- platelet 3- coagulation " if major injury"
👨⚕ What is difference between petechiae, purpura , and ecchymosis ?
🧑⚕
1- massive uncontrolled bleeding
2 - 2-bleeding from one orifice when there's no local cause
3-from two non-repeated orifice
4-uncotrolled bleeding after minor trauma
5-or after minor surgery
Primary hemostasis
Definition: processes involved in the formation of a platelet plug (white thrombus) following endothelial injury
Vascular hemostasis
Endothelial injury results in:
Neural stimulation reflexes and endothelin release → transient vasoconstriction, leading to:
Reduced blood flow
Platelet accumulation at the vessel walls
Exposure of subendothelial collagen → circulating von Willebrand factor binds to the exposed collagen
Von Willebrand factor (vWF): plasma protein that is synthesized by and stored in endothelial cells (in Weibel-Palade bodies) and platelets (in α-granules)
Mediates platelet adhesion and aggregation
Binds factor VIII (and thereby prevents its degradation)
Platelet hemostasis
Platelet adhesion: platelets bind to vWF via platelet GpIb receptor at the endothelial injury site
Ristocetin normally activates vWF to bind to glycoprotein Ib
Platelet activation: After binding to vWF, platelets change their shape and release mediators that lead to activation of more platelets (positive feedback). These mediators include:
Adenosine diphosphate (ADP): promotes adhesion of platelets to endothelium
Thromboxane A2 (TXA2): activates additional platelets and promotes vasoconstriction
Calcium: required for secondary hemostasis
Platelet-activating factor (PAF): a phospholipid mediator that is produced by platelets and inflammatory cells (e.g., neutrophils, monocytes, macrophages), involved in platelet aggregation and activation and local inflammatory response
Platelet aggregation
Mediated by GpIIb/IIIa-receptor and fibrinogen → formation of a white thrombus composed of platelets and fibrinogen
A white thrombus is transient, unstable, and easily dislodged. It stabilizes through the process of secondary hemostasis.