Dr. Noreen Final Revision Notes PDF
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Dr. Noreen
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Dr. Noreen's Final Revision Notes cover Histology with an emphasis on fetal asphyxia, offering insights into its causes, classifications, and management. The notes also include respiratory distress syndrome and hematopoiesis. This document provides valuable study materials for a medical subject.
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GAD Histology Final Revision Notes -Asphyxia: Impaired respiratory gas exchange (Hypoxia and Hypercapnia) accompanied by development of metabolic acidosis -Birth Asphyxia: Failure to initiate and sustain breathing at birth. -Consequences/ Etiology/ Causes of Asphyxia: Hypoxic Ischaemic Encephalopat...
GAD Histology Final Revision Notes -Asphyxia: Impaired respiratory gas exchange (Hypoxia and Hypercapnia) accompanied by development of metabolic acidosis -Birth Asphyxia: Failure to initiate and sustain breathing at birth. -Consequences/ Etiology/ Causes of Asphyxia: Hypoxic Ischaemic Encephalopathy, Organ failure & Neonatal death. -Classifications of Asphyxia:-Acute: Caused by intranatal factors only Chronic: In the background of prolonged fetal hypoxia and placental insufficiency. -Intranatal risk factors for birth asphyxia:- Fetal arterial blood oxygen tension is only 25 ± 5 mm Hg. Rate of oxygen consumption is twice that of the adult per unit weight. Fetal oxygen reserve - 1 to 2 minutes. During uterine contractions: Blood flow - momentarily interrupted. Cord compression: cord compression - during contractions. Failure to progress or dystocia: A prolonged or obstructed labour will eventually exhaust the fetus. -Causes of Fetal Hypoxia:- Maternal Placental Fetal Acute Maternal Hypotension Placental Abruption Cord Prolapse Chronic Maternal Respiratory Any Infection Infection Disease -Intrapartum Resuscitation includes:- 1- Maternal positioning to left lateral: reduces the risk of fetal heart deceleration. - Stopping the contractions (Tocolytics or uterine relaxation): Maternal blood flow to the placental villous space is reduced or altered during a contraction. 2- Intravenous fluids: to correct maternal hypovolaemia and hypotension. 3- Oxygen -Primary Apnea: With oxygen deprivation, there is a transient period of rapid breathing, and if it persists, breathing stops - termed as Primary Apnea. If oxygen deprivation and asphyxia persist, however, the newborn will develop deep gasping respirations, followed by secondary apnea. -Secondary Apnea- associated with a further decline in heart rate, falling blood pressure, and loss of neuromuscular tone. -Management of fetal distress (Resuscitation Protocol for the newborn) -Basic Measures: Warming of the newborn to minimize heat loss. The airway is cleared. The infant dried. Routine gastric aspiration. -Assessment at 30 Seconds of Life: Apnea, gasping respirations, or heart rate < 100 bpm beyond 30 seconds after delivery, perform positive-pressure ventilation with room air. -Percent of oxygen saturation monitored by pulse oximetry. GAD Histology Final Revision Notes -At this point, supplemental oxygen can be given in graduated. -Adequate ventilation is indicated by improved heart rate. -Assessment at 60 Seconds of Life: If the heart rate persists below 100 bpm beyond 60 seconds, tracheal intubation is performed. The head position should be checked, secretions cleared, and inflation pressure increased. -Clinical findings in fetal distress: Acidaemia, pH < 7 in an umbilical artery blood sample. Apgar score of 0–3 persisting for 10 minutes or longer. -Apgar Score: It is used to identify those neonates who require resuscitation and to assess the effectiveness of any resuscitative measures. -7 or greater at 1 minute - Normal -9 or 10 at 5 minutes. - Normal -A 5-minute Apgar score of 3 correlates poorly with adverse future neurological outcomes -Respiratory Distress Syndrome: Mostly seen in preterm infants, and known as hyaline membrane disease. -Due to a deficiency of surfactant, which is a complex of phospholipids and protein secreted by type II pneumocytes, reduces surface tension in the alveoli of the lung. -Preterm infant with RDS presents as tachypnea. -Corticosteroids to mothers at risk of delivery before 32–34 weeks gestation to hasten maturation of fetal organs. -Hemopoiesis (haematopoiesis): process of origin, development and maturation of all the blood cells. -Site: 1. Mesoblastic stage: (1st two months of intrauterine life, the RBCs are produced from mesenchyme of yolk sac. 2. Hepatic stage: From third month of intrauterine life, liver is the main organ that produces RBCs. Spleen and lymphoid organs are also involved in erythropoiesis. 3. Myeloid stage: During the last three months of intrauterine life- red bone marrow and liver. -In newborn babies, children and adults: only from the red bone marrow. Up to the age of 20 years: from red bone marrow of all bones (long bones and all the flat bones). After the age of 20 years: from membranous bones like vertebra, sternum, ribs, scapula, iliac bones and skull bones and from the ends of long bones. -Hemoglobin - conjugated protein, combined with an iron containing pigment. The protein part is globin and the iron containing pigment is heme. -Iron: Normally, it is present in ferrous (Fe2+), unstable or loose form. -Porphyrin: The pigment part of heme. -Globin: contains four polypeptide chains. -Types: Normal Variants: - In the fetus: Hb F (α2γ2) GAD Histology Final Revision Notes - In newborn : Hb F (α2γ2) 80% -Hb A (α2β2) 20% - In adults:-Hb A (α2β2) 95% - Hb A2 (α2δ2) 1.5 - 3.5% -Hb F 0.8% to 2% Abnormal Variants (changes in β chains): -Hb S (α2βS2) [β6 Glu>Val] sickle cell disease. -Hb C (α2βC2) [β6 Glu>lys] mild chronic hemolytic anemia. -Hemoglobinopathy: genetic disorder caused by abnormal polypeptide chains of HB. 1. Hemoglobin S: It is found in sickle cell anaemia, α-chains are normal and β-chains are abnormal. 2. Hemoglobin C: β-chains are abnormal, characterized by mild haemolytic anaemia & splenomegaly. 3. Hemoglobin E: β-chains are abnormal, characterized by mild haemolytic anemia & splenomegaly. 4. Hemoglobin M -Variations in size of red blood cells Microcytes - (iron-deficiency anemia) Macrocytes - (megaloblastic anemia) Anisocytes - (pernicious anemia) -Variations in shape of red blood cells – (Sickle cell) -Causes of leukocytosis: -Pathological (one type of leucocytes ↑ on the expense of others): A) Infection: 1. Neutrophilia → Pyogenic infection, Tissue necrosis 2. Eosinophilia → Allergic diseases, parasitic infestations 3. Basophilia → Allergic conditions 4. Lymphocytosis → Chronic infections (TB) 5. Monocytosis → Malaria. -Uterus Hyperplasia (increase in number of cells) of myometrium Hypertrophy (increase in size of the cells) of myometrium -Histological changes:- -Decidua basalis, which is the maternal part. -Decidua capsularis that surrounds fetal sac. -Decidua parietalis, which lines rest of uterine wall. -Stages of Labor First Stage of Labor: Three functional labor divisions: 1. The preparatory division: the cervix dilates little. 2. The dilatational division: dilatation proceeds at its most rapid rate. GAD Histology Final Revision Notes 3. The pelvic division: deceleration phase of cervical dilatation. Second Stage of Labor: This stage begins with complete cervical dilatation and ends with fetal delivery. Events occur (Delivery of the head, Delivery of the shoulders, clamping the cord). Third stage of labor: Delivery of the placenta. -Causes of growth failure and delayed milestones. 1. Genetic and Chromosomal Conditions 2. Nutritional Deficiencies – Malnutrition 3. Hormonal Imbalance – i) Growth Hormone Deficiency: Can delay physical milestones, such as walking or developing muscle strength. ii) Corticosteroid Use: Long-term use of steroids can interfere with growth and development iii) Thyroid Disorders: Hypothyroidism or other thyroid issues can slow down development and cause delays in physical and cognitive milestones. -Erikson’s theory: child develops sense of industry. Fails to achieve sense of industry, develops sense of inferiority. -Adolescence: period of transition from childhood to adulthood. It involves three stages: Early adolescence - (11 - 14yrs) Middle adolescence - (15 - 17yrs) Late adolescence - (18 - 20yrs) -Physical Growth: Growth Spurt: A rapid increase in height and weight, usually beginning earlier in girls (around 10–12 years) than boys (around 12–14 years). -Jean Piaget's Theory of Cognitive Development: Adolescents are in the formal operational stage. -Erik Erikson's Psychosocial Development Theory: Adolescence corresponds to the stage of Identity vs. Role Confusion. -Aging: Biological process of growing older. -Gerontology: Scientific study of aging and its effects on individuals. -Geriatrics: Medical specialty that focuses on the health care of older adults. -Common Diseases of Old Age 1. Cardiovascular Diseases: Hypertension, heart disease, and stroke. 2. Arthritis: Osteoarthritis, affecting the joints. 3. Osteoporosis: Weakened bones due to decreased bone density lead to an increased risk of fractures. -Cognitive Changes in Old Age 1. Memory: Short-term memory tends to decline with age, while long-term memory may remain intact. Conditions like Alzheimer's disease - severe memory loss. 2. Processing Speed: The speed at which the brain processes information may slow, making tasks take longer. 3. Attention and Concentration: Difficulty focusing or switching attention between tasks.