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📘 Chapter 19: Blood – Full Simplified Study Notes (27 Slides) ⸻ Slide 1: Cardiovascular System • Cardiovascular system = heart, blood, blood vessels. • Blood’s job: • Delivers nutrients, hormones, oxygen, and chemical messages. • Carries immune cells to fight infections. • Why it matters: Without this transport system, cells would starve and toxins would build up. • Analogy: Like UPS + garbage service → delivers packages (nutrients, O₂) and removes trash (waste, CO₂). ⸻ Slide 2: Whole Blood • Whole blood = plasma + formed elements. • Hematocrit: percentage of blood volume made of cells. • Plasma: watery fluid. • Key properties of blood: • Temp: 38°C (100.4°F) → warmer than body surface. • Thickness: 5x thicker than water. • pH: ~7.4 (slightly alkaline). • Volume: Men = 5–6 L, Women = 4–5 L. • About 7% of body weight. • Example: If someone weighs 150 lbs, about 10 lbs of that is blood. ⸻ Slide 3: Blood Plasma • Plasma = liquid with proteins + solutes. • Proteins: • Albumins: keep water inside blood vessels (prevent swelling). • Globulins: antibodies → defense. • Fibrinogen: forms clots. • Other solutes: • Electrolytes: Na⁺, K⁺, Cl⁻, HCO₃⁻ (important for nerves/muscles). • Nutrients: glucose, fructose, amino acids. • Wastes: urea, uric acid. • Analogy: Plasma = soup broth carrying salt, sugar, proteins, and waste. ⸻ Slide 4: Formed Elements • Red Blood Cells (RBCs / erythrocytes): 99.9% of all blood cells. • RBC count: Men = 4.5–6.3 million/μL, Women = 4.2–5.5 million/μL. • Platelets: fragments needed for clotting. • White Blood Cells (WBCs / leukocytes): fight disease. • Think: Plasma is the liquid, formed elements are the “stuff floating inside.” ⸻ Slide 5: RBC Structure • RBCs lose their nucleus & organelles. • Consequences: • Can’t divide. • Can’t make proteins or repair. • Only use glycolysis (anaerobic metabolism) → no oxygen needed for energy. • Analogy: Like delivery trucks with no engine shop → they drive until they break down. ⸻ Slide 6: RBC Lifespan • RBCs have no nucleus, mitochondria, ribosomes → no repair. • Rely on glycolysis for energy. • Live about 120 days. • Must be recycled by spleen/liver. • Example: Like a disposable battery that runs until it dies. ⸻ Slide 7: RBC Shape & Function • Shape = biconcave disc (doughnut-like, thin middle). • Benefits: • High surface area → better oxygen exchange. • Can stack like coins → smooth flow. • Flexible → squeeze through tiny capillaries. • Analogy: Like a flexible frisbee that can bend and stack. ⸻ Slide 8: Hemoglobin • Main protein inside RBC. • Structure: • 2 alpha chains + 2 beta chains. • Each has heme group with iron atom (Fe). • Function: Iron binds oxygen → carries it around body. • Why recycle? Iron is valuable, so old RBCs get broken down to save it. • Analogy: Hemoglobin = oxygen backpack. ⸻ Slide 9: RBC Lifecycle • Starts from hemocytoblast (stem cell). • Branches into: • Myeloid stem cells: make RBCs + some WBCs. • Lymphoid stem cells: make lymphocytes. • Think: Hemocytoblast = tree trunk, RBCs and WBCs = branches. ⸻ Slide 10: RBC Production (Erythropoiesis) • Erythropoiesis = making RBCs. • Embryo: 1st 8 weeks = yolk sac → later liver, spleen, thymus, bone marrow. • Adult: red bone marrow only (vertebrae, sternum, ribs, skull, pelvis, ends of long bones). • Nutrients needed: amino acids, iron, vitamins B12, B6, folic acid. • Analogy: RBCs = cookies, bone marrow = kitchen, iron + vitamins = ingredients. ⸻ Slide 11: RBC Production Control • Controlled by erythropoietin (EPO). • Made by kidneys/liver when low oxygen (hypoxia). • Effects: • Increases stem cell division. • Speeds up hemoglobin production. • Blood doping: Athletes take EPO or reinfuse RBCs → more oxygen for muscles. • Risk: thicker blood → clots, strokes. • Analogy: EPO = coach yelling “make more RBCs!” ⸻ Slide 12: Blood Types • RBCs have antigens on membranes (A, B, AB, O). • Rh factor = + or –. • Plasma has antibodies (agglutinins): attack foreign antigens → cause clumping (agglutination). • Universal donor = O–. • Analogy: Blood type = ID card. If ID doesn’t match, antibodies attack. ⸻ Slide 13: RBC Summary • Know: • How typing works. • How RBCs are made. • What controls them. • Why they live 120 days. • How they’re broken down. • Analogy: RBCs = delivery trucks with expiration dates. ⸻ Slide 14: WBC Basics • WBCs = leukocytes. • Have nuclei, organelles, no Hb. • Functions: fight pathogens, remove wastes, destroy abnormal cells. • Only in blood briefly → then move into tissues. • Analogy: WBCs = body’s police force. ⸻ Slide 15: Neutrophils • 50–70% of WBCs. • Nucleus 2–5 lobes. • First responders → attack bacteria. • Use phagocytosis + enzymes. • Die quickly → pus = dead neutrophils + bacteria. • Analogy: Neutrophils = foot soldiers. ⸻ Slide 16: Basophils • <1% WBCs. • Release histamine (dilates vessels, causes swelling/redness). • Release heparin (prevents clots). • Trigger inflammation → work with mast cells. • Analogy: Basophils = fire alarms. ⸻ Slide 17: Eosinophils • 2–4% WBCs. • Stain red-orange. • Bi-lobed nucleus. • Kill parasites, respond to allergies. • Release toxic chemicals (nitric oxide, enzymes). • Help control inflammation. • Analogy: Eosinophils = exterminators. ⸻ Slide 18: Monocytes • 2–8% WBCs. • Largest WBC, kidney-shaped nucleus. • Become macrophages in tissue. • Eat large pathogens, dead cells. • Call fibrocytes → scar tissue. • Analogy: Monocytes = garbage trucks. ⸻ Slide 19: Lymphocytes • 20–30% WBCs. • Big nucleus, little cytoplasm. • Most live in lymph tissue. • Types: • T cells: attack infected cells. • B cells: make antibodies. • NK cells: kill cancer/virus cells. • Analogy: Lymphocytes = special forces. ⸻ Slide 20: WBC Production • From hemocytoblasts. • Myeloid stem cells: all except lymphocytes. • Lymphoid stem cells: lymphocytes. • Colony-Stimulating Factors (CSFs): • M-CSF = monocytes. • G-CSF = granulocytes. • GM-CSF = granulocytes + monocytes. • Multi-CSF = RBCs + WBCs + platelets. • Analogy: CSFs = managers assigning jobs. ⸻ Slide 21: Platelets • Fragments of cells, no nucleus. • Lifespan = 9–12 days. • Removed by spleen. • 2/3 stored for emergencies. • Analogy: Platelets = emergency patch kits. ⸻ Slide 22: Platelet Functions 1. Release clotting chemicals. 2. Form platelet plug at damage site. 3. Contract (actin + myosin) → shrink clot, close wound. • Analogy: Platelets = patch team pulling duct tape tight. ⸻ Slide 23: Hemostasis • Definition: stopping bleeding. • 3 phases: vascular, platelet, coagulation. • Analogy: Like fixing a leaking pipe step by step. ⸻ Slide 24: Vascular Phase • Vessel wall contracts (vascular spasm). • Endothelial cells: • Expose basement membrane. • Release endothelins → stimulate contraction/healing. • Become sticky → platelets attach. • Analogy: Pinch a hose to slow the leak. ⸻ Slide 25: Platelet Phase • Platelets stick to exposed collagen. • Form platelet plug (15 sec after injury). • Release chemicals: ADP, thromboxane A₂, serotonin, Ca²⁺, PDGF. • Feedback prevents over-clotting. • Analogy: Like putting your hand over a hole until repair arrives. ⸻ Slide 26: Coagulation Phase • Chain reaction of clotting factors. • Fibrinogen → fibrin (forms net). • Common pathway: 1. Factor X → prothrombinase. 2. Prothrombin → thrombin. 3. Fibrinogen → fibrin. • Clot retraction pulls vessel edges together. • Analogy: Casting a fishing net over the leak. ⸻ Slide 27: Fibrinolysis & Clotting Needs • Fibrinolysis: clot dissolves after healing. • t-PA → activates plasminogen → plasmin → digests fibrin. • Requirements for clotting: • Calcium (Ca²⁺): needed in all clotting steps. • Vitamin K: liver makes clotting factors; comes from food + gut bacteria. • Deficiency = bleeding problems. • Analogy: Once pipe is repaired, cut away the net (clot)

Updated 15d ago

1. Hyperemesis Gravidarum/ Pernicious Vomiting Definition: Excessive nausea and vomiting during pregnancy, extending beyond week 12 or causing dehydration, ketonuria, and significant weight loss within the first 12 weeks. Incidence: 1 in 200-300 women Cause: Unknown, but may be associated with increased thyroid function and Helicobacter pylori infection. Signs and Symptoms: • Decreased urine output • Weight loss • Ketonuria • Dry mucous membranes • Poor skin turgor • Elevated hematocrit • Decreased sodium, potassium, and chloride levels • Polyneuritis (in some cases) Assessment: • Hemoglobin: Elevated hematocrit concentration (hemoconcentration) due to inability to retain fluids. • Electrolytes: Decreased sodium, potassium, and chloride levels due to low intake. • Acid-base Balance: Hypokalemic alkalosis (severe vomiting, prolonged period). • Neurological Examination: Polyneuritis due to B vitamin deficiency. Effects (if left untreated): • Intrauterine Growth Restriction (IUGR): Dehydration and inability to provide nutrients for fetal growth. • Preterm birth: Due to complications caused by the condition. • Prolonged hospitalization/home care: Resulting in social isolation. Therapeutic Management: • Fluid and Electrolyte Management: Monitor input and output, blood chemistry to prevent dehydration. • Nutritional Support: Withhold oral food and fluids (usually) and administer total parenteral nutrition (TPN). • Intravenous Fluid Replacement: 3000 ml Ringer's lactate with added vitamin B to increase hydration. • Antiemetic Medication: Metoclopramide (Reglan) to control vomiting. 2. Ectopic Pregnancy Definition: Implantation of a fertilized egg outside the uterine cavity (ovary, cervix, fallopian tube - most common). Incidence: Second most frequent cause of bleeding during the first trimester. Causes: • Obstruction of the fallopian tube: ◦ Adhesions (from previous infection like chronic salpingitis or pelvic inflammatory disease). ◦ Congenital malformations. ◦ Scars from tubal surgery. ◦ Uterine tumor pressing on the proximal end of the tube. ◦ Current use of an intrauterine device (IUD). Signs and Symptoms: • Missed period/amenorrhea. • Positive hCG test. • Sharp, stabbing pain in the lower abdominal quadrants and pelvic pain (at time of rupture). • Scant vaginal spotting/bleeding. • Rigid abdomen (from peritoneal irritation). • Leukocytosis (increased WBC count due to trauma). • Decreased blood pressure and increased pulse rate (signs of shock). • Cullen's sign (bluish tinge around the umbilicus). • Tender mass palpable in the cul-de-sac of Douglas (vaginal exam). • Falling hCG or serum progesterone level (suggesting the pregnancy has ended). • No gestational sac on ultrasound. Therapeutic Management: • Non-ruptured Ectopic Pregnancy: Oral administration of methotrexate followed by leucovorin. • Ruptured Ectopic Pregnancy (emergency): Laparoscopy to ligate bleeding vessels and remove or repair the damaged fallopian tube. 3. Hydatidiform Mole (H-mole)/ Gestational Trophoblastic Disease/ Molar Pregnancy Definition: A gestational anomaly of the placenta consisting of a bunch of clear vesicles resembling grapes. This neoplasm is formed from the swelling of the chorionic villi, resulting from a fertilized egg whose nucleus is lost, and the sperm nucleus duplicates, producing a diploid number 46XX. Incidence: Approximately 1 in every 1500 pregnancies. Risk Factors: • Low socioeconomic group (decreased protein intake). • Women under 18 or over 35 years old. • Women of Asian heritage. • Receiving clomiphene citrate (Clomid) for induced ovulation. Types of Molar Growth: • Complete/Classic H-mole: All trophoblastic villi swell and become cystic. No embryonic or fetal tissue present. High risk for malignancy. • Partial/Incomplete H-mole: Some of the villi form normally. Presence of fetal or embryonic tissue. Low risk for malignancy. Signs and Symptoms: • Uterus expands faster than normal. • No fetal heart sounds heard. • Serum or urine test for hCG strongly positive. • Early signs of preeclampsia. • Vaginal bleeding (dark-brown spotting or profuse fresh flow). • Discharge of fluid-filled vesicles. Diagnosis: • Ultrasound. • Chest x-ray (lung metastasis). • Amniocentesis (no fluid). • Hysteroscopy (via cervix). Management: • Evacuation of the mole: Dilation and curettage (D&C). • Blood transfusion. • Hysterectomy (in some cases). • Monitoring hCG levels: Every 2 weeks until normal. • Contraception: Reliable method for 12 months to prevent confusion with a new pregnancy. 4. Premature Cervical Dilatation/ Incompetent Cervix Definition: Premature dilation of the cervix, usually occurring around week 20, when the fetus is too immature to survive. Incidence: About 1% of pregnancies. Causes: • Increased maternal age. • Congenital structural defects. • Trauma to the cervix (cone biopsy, repeated D&C). Signs and Symptoms: • Painless dilation of the cervix. • Pink-stained vaginal discharge. • Increased pelvic pressure. • Rupture of membranes and discharge of amniotic fluid. Therapeutic Management: • Cervical cerclage: Surgical procedure to prevent loss of the child due to premature dilation. • Bed rest: After cerclage surgery, to decrease pressure on the sutures. 5. Abortion Definition: Termination of pregnancy before the fetus is viable (400-500 grams or 20-24 weeks gestation). Types of Abortion: • Spontaneous Abortion: Pregnancy interruption due to natural causes. ◦ Threatened: Mild cramping, vaginal spotting. ◦ Inevitable/Imminent: Profuse bleeding, uterine contractions, cervical dilation. ◦ Complete: All products of conception expelled spontaneously. ◦ Incomplete: Part of the conceptus expelled, some retained in the uterus. ◦ Missed: Fetus dies in utero but is not expelled. ◦ Habitual: 3 or more consecutive spontaneous abortions. • Induced Abortion: Deliberate termination of pregnancy in a controlled setting. Complications of Abortion: • Hemorrhage. • Infection (endometritis, parametritis, peritonitis, thrombophlebitis, septicemia). Management: • Bed rest. • Emotional support. • Sedation. • D&C: Surgical removal of retained products of conception. • Antibiotics. • Blood transfusion. 6. Placenta Previa Definition: The placenta is implanted in the lower uterine segment, covering the cervical os, obstructing the birth canal. Incidence: 5 per 1000 pregnancies. Signs and Symptoms: • Abrupt, painless vaginal bleeding (bright red). • Bleeding may stop or slow after the initial hemorrhage, but continue as spotting. Types: • Total: Placenta completely obstructs the cervical os. • Partial: Placenta partially obstructs the cervical os. • Marginal: Placenta edge approaches the cervical os. • Low-lying: Placenta implanted in the lower rather than the upper portion of the uterus. Therapeutic Management: • Immediate Care: Bed rest in a side-lying position. • Assessment: Monitor vital signs, bleeding, and fetal heart sounds. • Intravenous Therapy: Fluid replacement with large gauge catheter. • Delivery: Vaginal birth (safe for infant if previa is less than 30%). Cesarean section (safest for both mother and infant if previa is over 30%). 7. Abruptio Placenta/ Premature Separation of Placenta/ Accidental Hemorrhage/ Placental Abruption Definition: Separation of a normally implanted placenta after the 20th week of pregnancy, before birth of the fetus. Incidence: Most frequent cause of perinatal death. Causes: • Unknown. • Predisposing Factors: ◦ High parity. ◦ Advanced maternal age. ◦ Short umbilical cord. ◦ Chronic hypertensive disease. ◦ PIH. ◦ Trauma (automobile accident, intimate partner abuse). ◦ Cocaine or cigarette use. ◦ Thrombophilitic conditions (autoimmune antibodies). Classification: • Total/Complete: Concealed hemorrhage. • Partial: Concealed or apparent hemorrhage. Signs and Symptoms: • Sharp, stabbing pain in the uterine fundus. • Contractions accompanied by pain. • Uterine tenderness on palpation. • Heavy vaginal bleeding (may be concealed). • Signs of shock. • Tense, rigid uterus. • Disseminated Intravascular Coagulation (DIC). Therapeutic Management: • Fluid Replacement: IV fluids. • Oxygen: Limit fetal hypoxia. • Fetal Monitoring: External fetal heart rate monitoring. • Fibrinogen Determination: IV fibrinogen or cryoprecipitate. • Lateral Position: Prevent pressure on the vena cava. • Delivery: CS is the method of choice if birth is not imminent. 8. Premature Rupture of Membranes Definition: Rupture of the fetal membranes with loss of amniotic fluid during pregnancy before 37 weeks. Incidence: 5%-10% of pregnancies. Causes: • Unknown. • Associated with: Infection of the membranes (chorioamnionitis), vaginal infections (gonorrhea, streptococcus B, Chlamydia). Signs and Symptoms: • Sudden gush of clear fluid from the vagina with continued minimal leakage. • Nitrazine paper test: Amniotic fluid turns the paper blue (alkaline), urine remains yellow (acidic). • Microscopic examination: Amniotic fluid shows ferning, urine does not. • Ultrasound: Assess amniotic fluid index. • Signs of infection (increased WBC count, C-reactive protein, temperature, tenderness, odorous vaginal discharge). Therapeutic Management: • Bed Rest: To prevent further leakage and risk of infection. • Corticosteroids: To hasten fetal lung maturity. • Prophylactic Antibiotics: To reduce risk of infection. • Intravenous Penicillin/Ampicillin: If (+) for streptococcus B. • Induction of Labor: If fetus is mature and labor does not begin within 24 hours. 9. Pregnancy-Induced Hypertension (PIH)/ Toxemia Definition: Vasospasm occurring in both small and large arteries during pregnancy, causing elevated blood pressure, proteinuria, and edema. Incidence: Rarely occurs before 20 weeks of pregnancy. Risk Factors: • Multiple pregnancy. • Primiparas younger than 20 or older than 40. • Low socioeconomic background. • Five or more pregnancies. • Hydramnios. • Underlying diseases (heart disease, diabetes). • Rh incompatibility. • History of H-mole. Categories: • Gestational Hypertension: Blood pressure 140/90 or greater, without proteinuria or edema. • Preeclampsia: Blood pressure 140/90 or greater, with proteinuria and edema. • Eclampsia: Seizures or coma accompanied by preeclampsia. Therapeutic Management: • Preeclampsia: Bed rest, balanced diet, left lateral position. • Severe Preeclampsia: Hospitalization, diazepam, hydralazine, magnesium sulfate. • Eclampsia: Magnesium sulfate, diazepam, oxygen therapy, left lateral position

Updated 184d ago

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