Summary

These notes describe hemorrhage, hyperemia, and shock, covering different types, causes, and clinical effects. It includes classifications, examples, and mechanisms.

Full Transcript

Telegram : @degwaly (8) hemorrhage & Definition: It is the escape of blood outside the cvs Causes: Artery / vein rupture Capillary rupture bleeding bleeding  Trauma  Chronic venous  At...

Telegram : @degwaly (8) hemorrhage & Definition: It is the escape of blood outside the cvs Causes: Artery / vein rupture Capillary rupture bleeding bleeding  Trauma  Chronic venous  Atherosclerosis congestion  aneurysm  Hemorrhagic diathesis. - varicose veins.  Inflammation  Neoplasia Classification of hemorrhage according to size : a. Petechiae :  shape = pinpoint flat round red spots under the skin / MM / serous surface  size = 1-2 mm  cause = intradermal hemorrhage b. Purpura :  shape = round red spots under the skin / MM / serous surface  size = greater than 3 mm  colour = varies with the duration of the lesions red  darker  purple  brown yellow as it fades. c. Ecchymoses (bruise) :  shape = large , irregularly discoloration of skin due to formed hemorrhagic areas  size = 1 -2 cm d. Hematoma :  solid swelling of large blood clot accumulation in soft tissues e. g. mediastinum / retroperitoneum / muscle ‫الصفحة‬1 Telegram : @degwaly (8) internal bleeding External hemorrhage  blood accumulates within a tissue  escape of blood outside the body or in body cavities ) Example : Example : I Haemopericardium  v Hematemesis   collection of blood in  Is vomiting of bright or pericardium coffee ground like blood  cause : rupture of aorta or  Cause : upper GIT bleeding heart. v Melena  2. Haemothorax   Passage of Black tarry stools  collection of blood in pleural  cause : upper GIT bleeding cavity  causes : trauma or rupture of - Hematochezia  aorta  is the passage of fresh blood 3. haemoperitoneum  per anus.  collection of blood in  cause : lower GIT bleeding peritoneal cavity  causes: rupture of aorta, spleen or liver ‫الصفحة‬2 Telegram : @degwaly (8) 4. haemarthrosis  Epistaxis  bleeding from the  collection of blood within joint nose. space Hemoptysis  coughing of blood.  causes: bleeding disorders or Menorrhagia  heavy MC bleeding kencophil n trauma Hematuria  blood in urine. Haemorrhage from the skin 8 Clinical effects of hemorrhage Depend on: 1. Volume of blood loss 2. Rate of blood loss 3. Site of bleeding :  Rapid loss , severe bleeding : more than 20% of blood volume  hemorrhagic (hypovolemic) shock  slow loss , smaller rapid loss , mild bleeding  little effect ( except in brain  fatal ). 3 ‫الصفحة‬3 C hyperemia A -- - V -> - -- - > --- -- -> -> · XD · o-blood 2 ① excercise ↳ ex:O digestion 3 P hysiological pat h ol o gi c - ③ Menopause ⑬ Acute inflamation is Congestion - C ein obstruction · de-8-blood IVC ex: d Systemic Cong estic Telegram : @degwaly (8) Hyperemia Congestion ( passive hyperemia )  local increased volume of  local increased volume of blood blood  Cause : VD of arteriole  Cause : impaired venous return  blood accumulation in  blood accumulation in veins and arteriole & capillary capillaries.  Active process  Passive process  Color  red due to  Color  blue-red (cyanosed) engorgement with due to engorgement with oxygenated blood. deoxygenated blood  Types :  Types: 1. Physiological hyperemia  1. Systemic congestion   Exercise : hyperemia occurs  blood accumulates in all veins in skeletal and cardiac except pulmonary veins. muscles.  cause: right sided heart failure.  Digestion : hyperemia occurs 2. Pulmonary congestion  in the splanchnic area.  blood accumulates in the pulmonary veins  Menopausal flush  Causes : left sided heart failure. 3. Local congestion : Causes:  Mechanical obstruction of vein 2. Pathological hyperemia  acute  by ligature or twisting. inflammation  Venous thrombosis.  Pressure on vein - by a tumor.  Constriction of vein by scar tissue . congestion of portal area resulting from fibrosis of liver ‫الصفحة‬4 Chronic - -> Rt. HF CVC Liver IVC. Congestion Easie But Savan D - Enlarge R - ↳&Nutmeg Appearance 1 : - ~ 1 888888838 O ·O = : ↑ -.... &a 08 & ⑧0 -..... I I... -.. 88.. 80 YS Y 1 dated Normal dilated S - -> 1 - -> - Sinusoids- Sinusoids- change Central: hepatocytes - - Fatty hepatocytes E- ecursi Peripheral:Fatty (Centrall (yellow) change 8 08 ⑳ * -a /> Senttanbulasca ⑨ ⑨ E - - * ⑳6 Telegram : @degwaly (8) Pathological changes in chronic venous congestion (CVC): 1. CVC – liver 2. CVC – lung 3. CVC – spleen Cardiac Grrhusis - -> but Meg Liver Grossly : liver is enlarged , firm and its cut surface shows a "nutmeg" 5 · I I appearance ( dark areas of congestion alternating with yellow areas of fatty... change. ) Microscopically : Early : Central zones   the central veins and the sinusoids are dilated and engorged with blood  The hepatocytes between the dilated sinusoids show fatty change. Later :  Central zones  more dilated sinusoids  compress on central hepatocytes  necrosis  mid zones  peripheral hepatocytes  develop fatty change.  old cases  centrilobular fibrosis occurs and regenerative nodules of hepatic parenchyma develop (cardiac cirrhosis). ‫الصفحة‬5 Lt - HF Gang A pulmonary congestion veins Size · r. 8⑳ enlarged ↑3 - Firm heavy Color= Red Sdeep) => ↳ * own in duration p. V dilated p.c = congested * - Alveolar Thick - L wall -> - - a A I. edema Fibrosis -⑰ ⑧ sl..· RBIs alveolus Alveolar kennen -> edem Fluid macrophage Capillary, rupture -> RBC leak to IS hypertepl y shemosiderin brown) Compl i c ati o n: ↳ RBCs - A S -> engulfed by alveolar sit marphage media Fiber APF. # I intima Ruptur HTN ⑧· - ·. - called: cells GE pulmonousknering) ghyaline A this Telegram : @degwaly (8) C.V.C of lung *Grossly :  the lungs are enlarged, heavy, firm and deep red in color (brown S - induration).  The cut surface may ooze frothy blood on squeezing. Microscopically :  the pulmonary venules and alveolar capillaries are dilated and engorged with blood.  The alveolar walls are thickened due to edema and later due to fibrosis.  The alveolar spaces contain RBCs and many large macrophages with brownish hemosiderin pigment granules (heart failure cells).  Alveoli may also contain edema fluid.  Complication : pulmonary veins show medial hypertrophy and intimal fibrosis If pulmonary arterial hypertension develops, structural changes of hypertension occur in the pulmonary arterial tree (elastic hyperplasia of arteries and hyaline thickening of arterioles). ‫الصفحة‬6 Sianemia, Rt_HFs Liver CirrLeosis Congestion of Spleen Gamma Carlos Gandt Charles Size => Enlarge Firm Colour Red brown -> - Fibro Sedrotic plaques I ( ⑤ Gumna w Gandy dis Red pulp Sinusoids-> S dilated ⑮ - Congested I Wall Fibrosis brown hemosi dein e - Sdert ↳ entrapped with Fbur, File0 Sis Telegram : @degwaly (8) C.V.C of spleen Grossly : the spleen is moderately enlarged, firm and its cut surface is dark red and may show scattered brownish plaques (fibrosiderotic or Gamna- Gandi nodules). plaques *Microscopically : the red pulp sinusoids are dilated and engorged with blood and their walls are thickened due to fibrosis. The fibrosiderotic nodules are composed of fibrous tissue entrapping hemosiderin. They result from hemorrhage from engorged veins, with the hemosiderin liberated from the broken RBCs inducing the fibrosis. ‫الصفحة‬7 Lips -> Cyanosis Neck -> Pulsatina veins. Telegram : @degwaly (8) Enlarged Render Liver Liver - v Clinical features of CVC Lower Limb -> -> Edema 1. Cyanosis (blue discoloration of tissues, especially apparent in the lips) due to presence of abundant reduced hemoglobin. 2. Congested pulsating neck veins due to increased venous pressure. 3. Edema of the lower limbs mainly due to increased venous and capillary pressure and hypoxia. 4. Enlarged tender liver. Shock Definition : failure of the circulatory system to maintain adequate perfusion and - oxygenation of vital organs Types and causes of shock - bacteremia=bacteria in blood ~ Toxemia - toxin / - 1. Cardiogenic shock: due to  ↓ COP due to ~ Septicemia bacteria = toxin - - S  cardiac diseases  pulmonary embolism 2. Hypovolemic shock: due to  ↓ blood or plasma volume ( due to ):  Vomiting  Diarrhea  Burns  Hemorrhage 3. Septic shock : due to  microbial infection  gram positive bacilli, follows with gram negative one ) endotoxic shock). 4. Neurogenic shock:  due to : VD ( loss of vascular tone and peripheral pooling of blood ) due to :  anesthetic accident  spinal cord injury. 5. Anaphylactic shock: due to generalized VD due to :  Allergy ‫الصفحة‬8 T Tissue perfusion. Low (shock) Skin cool Pallov "Siena ↓ - = Compensat o r s * mechanism X X Sympathetic ① (CA) X AS ⑪ R A & Not ressive COP, PBP, ABV * perfusion to Vital prog Organs. phase Failed Reversible S No it ↑ Tissue perfusion - Very low is chemia (hypoxia C acidosis I mogussi phase ve Kidney brain & Limbs - Confused - severe b UOP. I blood DC * pooling = of to Failure of Sympathetic I - RAAS Failed No t Tissue injury -> Cells necrosis Sgets) I Kidney irreversi b l e anuria = (RF) brain - Coma phase I & Telegram : @degwaly (8) Clinical manifestation and Stages of shock A. Non progressive stage of shock  activation of neurohumoral compensatory mechanisms ( CA , RAAS ) to maintain cardiac out put and blood pressure of vital organs (e.g brain, heart) MCQ  Clinical manifestations: tachycardia, skin coolness and pallor (except = septic shock Skin may be warm & flushed due to peripheral vasodilation), Oligouria. B. Progressive stage of shock  If non progressive stage not given appropriate medical care and or unreasoned to treatment pass to progressive stage,.  Tissue hypo-perfusion and widespread tissue hypoxia leads to anaerobic respiration,  metabolic acidosis, peripheral pooling of blood and may finally reach to DIC.  Clinical manifestations:- Patient is confused , progressive falling of urine out put. C. Irreversible Stage of shock  irreversible cellular and tissue injury, bad prognosis stage may leads to death  Mechanism. :  Decrease PH, release of lysosomal enzymes  aggrevate shock state  nitric oxide synthesis  worse myocardial contractile function  ischemic bowel  allow intestinal flora to enter circulation  Septic shock may be superimposed  Clinical manifestations : anuria  Death Fate of shock : Hypovolemic and neurogenic shocks have the best prognosis (decrease mortality rate) followed by cardiogenic shock, and finally septic shock worst one ‫الصفحة‬9

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