Week 11 - Pain & Hematological Function & Pediatrics (Student) PDF

Pain and Alterations in Hematological Function SLIDES BY KARA SEALOCK EdD MEd BN RN CNCC(C) CCNE GUEST SLIDE CONTRIBUTIONS: SANDIP DHALIWAL (RN, PHD STUDENT) NOVEMBER 2024 Pain Topics for this Lecture: Pediatric Content: Structure and Fu...

Pain and Alterations in Hematological Function SLIDES BY KARA SEALOCK EdD MEd BN RN CNCC(C) CCNE GUEST SLIDE CONTRIBUTIONS: SANDIP DHALIWAL (RN, PHD STUDENT) NOVEMBER 2024 Pain Topics for this Lecture: Pediatric Content: Structure and Function of Blood Neonatal Hematology Structure and Function of Lymphoid Organs Skin Alterations Alterations in Platelet Function ▪Heparin Induced Thrombocytopenia Alterations in Coagulation ▪Disseminated Intravascular Coagulation Hematological Conditions ▪Anemia ▪Polycythemia Alterations in Leukocyte Function  By the End of this Lecture You Will: Critically reflect upon the structure and function of blood and lymphoid function leads to significant changes systemically Explain pathophysiology and effects on the body related to: ▪ Alterations in Platelet Function ▪ HIT ▪ Alterations in Coagulation ▪ DIC ▪ Hematological Conditions ▪ Anemia and Polycythemia ▪ Alterations in Leukocyte Function ▪ Neonatal hematology ▪ Skin Alterations Begin to prioritize patient conditions related to nursing assessment and clinical manifestations  Objectives for this lecture ▪You will be able to identify the elements of pain ▪You will be able to list and apply the 4 phases of nociceptive pain ▪You will be able to apply concepts of pain in the pediatric population ▪You will be able to identify the Structure and function of blood and lymphoid organs ▪You will be able to verbalize the pathophysiology associated with HIT ▪You will be able to identify at least 3 causes of DIC ▪You will be able to Alterations in erythrocyte function ▪You will be able to verbalize neonatal hematology ▪You will be able to identify skin alterations specific to the pediatric population Pain Nociceptors ▪ Processing harmful stimuli in anormal functioning nervous system is called nociception ▪Nociceptors or pain receptors are free nerve endings in the afferent peripheral nervous system→ stimulated = pain ▪3 portions of the nervous system that are responsible for the sensation, perception, and response to pain: ▪Afferent pathways ▪Interpretive centers ▪Efferent pathways  4 Phases of Nociception ▪Pain transduction ▪Pain transmission ▪Pain perception ▪Modulation Fig 14-1, p. 331, Phases of Nociceptive Pain Power-Kean et al. , (2023)  Fig 11-2, p. 182, Jarvis et al. (2019) Fig 14-1, p. 331, Power-Kean et al. , (2023)  Differences Between Acute and Persistent Pain Characteristic Acute Pain Persistent Pain Onset Sudden Gradual or sudden Duration Usually within the normal time for healing May start as acute injury to continues past the normal time for healing to occur Severity Mild to severe Mild to severe Cause of Pain A precipitating illness or event May not be known Course of Pain Decreases over time and goes away Pain persists and may be ongoing, episodic, or both Types of Physical and Reflect SNS: Predominantly behavioral: Behavioral Manifestations ▪ Increased HR, RR, and BP ▪ Changes in affect ▪ Diaphoresis, pallor ▪ Decreased physical movement and ▪ Anxiety, agitation, confusion activity ▪ Fatigue ▪ Withdrawal from other people and social interaction  Stimuli that Activate Nociceptors (Pain Receptors) Location of the Receptor Provoking Stimuli Skin Pricking, cutting, crushing, burning, freezing GI Tract Engorged or inflamed mucosa, distention or spasm of smooth muscle, traction on mesenteric attachment Skeletal Muscle Ischemia, injuries of connective tissue sheaths, necrosis, hemorrhage, prolonged contraction, injection of irritating solutions Joints Synovial membrane inflammation Arteries Piercing, inflammation Head Traction, inflammation, or displacement of arteries, meningeal structures, and sinuses; prolonged muscle contraction Heart Ischemia and inflammation Bone Periosteal injury: fractures, tumor, inflammation  Pain Assessment ▪Goals of Pain Assessment : ▪ To describe the patient’s sensory, affective, behavioral, cognitive, and sociocultural pain experience for the purpose of implementing pain management techniques ▪ To identify the patient’s goal for therapy and resources and strategies for effective self-management ▪Sensory-Descriminative Component ▪ Pattern of pain ▪ Area of pain ▪ Intensity of pain ▪ Nature of pain ▪ Motivational-Affective, Behavioral, Cognitive-Evaluative, and Sociocultural Components Pain Assessment Tools  Categories of Pain I. Neurophysiologic pain II. Neurogenic pain IV. Regional pain A. Nociceptive pain A. Neuralgia (pain in the distribution of a nerve) A. Abdominal pain D. Low back pain 1. Somatic (e.g., skin, muscle, B. Constant B. Chest pain E. Orofacial pain bone) 1. Sympathetically independent C. Headache F. Pelvic pain 2. Visceral (e.g., intestine, liver, 2. Sympathetically dependent stomach) V. Etiologic pain III. Temporal pain (time related, B. Neuropathic (non-nociceptive) duration) A. Cancer pain 1. Central pain (lesion in brain or A. Acute pain B. Dental pain spinal cord) 1. Somatic C. Inflammatory pain 2. Peripheral pain (lesion in PNS) 2. Visceral D. Ischemic pain B. Chronic E. Vascular pain  Assessment of Acute Pain in Pediatrics ▪Causes of acute pain: ▪ Medical procedures ▪ Surgical procedures ▪ Medical treatments ▪ Injury ▪ Infection ▪ Exacerbation of arthritis, sickle cell disease, cancer ▪Pain Intensity: ▪ Defined as behavioral measures, physiological measures, and measures of self-report ▪ Address domain of pain intensity ▪ Based on age of the child  Developmental Characteristics of Children’s Responses to Pain Young Infant Generalized body response of rigidity or thrashing, possibly with local reflex withdrawal of stimulated area Loud crying Facial expression of pain (brows lowered and drawn together, eyes tightly closed, mouth open and squarish) No association demonstrated between approaching stimulus and subsequent pain Older Infant Localized body response with deliberate withdrawal of stimulated area Loud crying Facial expression of pain or anger Physical resistance, especially pushing the stimulus away after it is applied  Developmental Characteristics of Children’s Responses to Pain Young Child Loud crying, screaming Verbal expressions such as “Ow,” “Ouch,” “It hurts” Thrashing of arms and legs Attempts to push stimulus away before it is applied Lack of cooperation; need for physical restraint Requests for termination of procedure Clinging to parent, nurse, or other significant person Requests for emotional support, such as hugs or other forms of physical comfort Becoming restless and irritable with continuing pain Behaviours occurring in anticipation of actual painful procedure  Developmental Characteristics of Children’s Responses to Pain School-Age Child May see all behaviours of young child, especially during actual painful procedure, but less in anticipatory period Stalling behaviour, such as “Wait a minute” or “I'm not ready” Muscular rigidity, such as clenched fists, white knuckles, gritted teeth, contracted limbs, body stiffness, closed eyes, wrinkled forehead Adolescent Less vocal protest More verbal expressions, such as “It hurts” or “You're hurting me” Increased muscle tension and body control  Videos for Extra Resources TED talk: Great overview of pain as an introduction – how the brain responds to pain. (5 mins) https://www.youtube.com/watch?v=I7wfDenj6CQ Overview of how nociceptors work – very nice A&P (12 minutes) https://www.youtube.com/watch?v=fUKlpuz2VTs Video of the gymnast who breaks his leg (42 seconds) https://www.youtube.com/watch?v=2Z9WjbwkwCg Hematology HEPARIN INDUCED ANEMIA’S THROMBOCYTOPENIA POLYCYTHEMIAS DISSEMINATED INTRAVASCULAR ALTERATIONS IN LEUKOCYTE COAGULATION FUNCTION  Structure and function Blood Composition of Blood ▪Plasma ▪Albumin ▪Globulins ▪Cellular components of the blood ▪Erythrocytes ▪Leukocytes ▪Granulocytes (neutrophil, eosinophils, basophils, mast cells ▪Agranulocytes (phagocytes or immunocytes) ▪Platelets  Structure and Function Lymphoid Organs Primary lymphoid organs ▪Thymus and bone marrow ▪Spleen ▪Golden hour to rupture ▪Lymph nodes  Platelets ▪Function: ▪ Contribute to regulation of blood flow in a damaged site by inducing vasoconstriction ▪ Initiate platelet-to-platelet interactions resulting in a platelet plug to stop further bleeding ▪ Activate the coagulation (or clotting) cascade to stabilize the plug ▪ Initiate repair processes including clot retraction and clot dissolution (fibrinolysis) ▪Damage to the vessel initiates a process of platelet activation ▪ Adhesion to damaged vascular wall ▪ Secretion of chemicals that simulate changes in platelet shape and biochemistry ▪ Aggregation of platelet to wall and platelet to platelet  Alterations of Platelet Function SYSTEMIC DISORDERS THAT AFFECT CLINICAL MANIFESTATIONS PLATELET FUNCTION ▪Spontaneous petechiae and purpura ▪Chronic renal failure ▪Bleeding from GI tract, GU tract, ▪Liver disease pulmonary mucosa and gums ▪Cardiopulmonary bypass surgery ▪Severe deficiencies of iron or folate ▪Antiplatelet antibodies associated with autoimmune disorders ▪Hematological disorders  Disorders of Platelets: Heparin Induced Thrombocytopenia ▪Occurs primarily with IV heparin but there is a small incidence associated with LMWH ▪Immune-mediated, adverse drug reaction caused by IgG Antibodies ▪Increased platelet consumption and decrease in platelet count ▪BEGINS 5-10 DAYS after administration of heparin  Disorder of Platelets: Heparin Induced Thrombocytopenia Clinical Manifestation: ▪ Thrombocytopenia * ▪ Watch the trends in the blood work!!! ▪ Venous thrombosis resulting in DVT and PE ▪ Arterial thrombosis of lower extremities, leading to limb ischemia Evaluation and Treatment ▪ Clinical observations ▪ Lab values ▪ Withdraw heparin and use alternative anticoagulants→ NO COUMADIN  Disorders of Coagulation Impaired hemostasis ▪Inability to promote coagulation and develop stable fibrin clot ▪Usually associated with liver disease ▪Examples include Vitamin K deficiency and liver disease ▪Consumptive thrombohemorrhagic disorders ▪Disseminated intravascular coagulation  Disorders of Coagulation: Disseminated Intravascular Coagulation(DIC) ▪Acquired syndrome (a cause) that activates systemic coagulation ▪Damage to the vascular endothelium ▪Fibrin clots are formed in medium and small vessels ▪Blocks blood flow to organs→ multiple organ failure ▪Consumption of platelets and clotting factors that Leads to bleeding  Disorders of Coagulation: Disseminated Intravascular Coagulation Etiology ▪Sepsis* ▪Trauma ▪ Head injury ▪Malignancy ▪ Burns ▪Infections (bacterial and viral ▪ Tissue necrosis (Necrotizing fasciitis) ▪Intravascular hemolysis ▪Liver disease ▪ Transfusion reactions ▪ Obstructive jaundice ▪ Drug induced hemolysis ▪ Prosthetic devices ▪Pregnancy complications ▪Medical devices ▪ Eclampsia or preeclampsia ▪ Placental abruption ▪Hypoxia and low blood flow states ▪ Arterial hypotension secondary to shock ▪ Amniotic fluid embolism ▪ Cardiopulmonary arrest  Disorders of Coagulation: Disseminated Intravascular Coagulation ▪Pathophysiology: ▪ Vascular damage → clotting cascade is activated to repair and protect ▪ Tissue factor is released by the endothelium ▪ Stimulation of cells such as inflammatory cytokines ▪ Proinflammatory cytokines and platelet activating factor responsible for manifestations of DIC ▪ Tissue factor binds to factor VII which converts prothrombin to thrombin and forms fibrin clots Disseminated Intravascular Coagulation Pathophysiology  Disseminated Intravascular Coagulation Pathophysiology Rate of fibrinolysis is diminished in DIC ▪ Plasminogen→ plasmin that digests clots but pAi-1 (natural inhibitor to plasmin) is produced during DIC These patients are at risk for severe bleeding→ EMERGENCY!!! Hemorrhage occurs secondary to high consumption of clotting factors and platelets which leads to thrombocytopenia Clots block blood flow → leads to hypoperfusion→ ischemia, infarction and necrosis Fig. 21-19, pg. 530, Power-Kean, et al. (2023)  Disorders of Coagulation: Disseminated Intravascular Coagulation ▪Clinical Manifestations: ▪ Symptoms related to hemorrhage or thrombosis ▪ Presents: ▪ Rapid development of hemorrhage ▪ Shock and low blood pressure ▪ Microvascular thrombosis that cannot be seen leading to organ failure ▪Presentation of multisystem failure Fig 33.9, pg. 726, Tyerman & Cobbett (2023)  Disorders of Coagulation: Disseminated Intravascular Coagulation ▪Nursing Assessment: ▪Prompt recognition of symptoms ▪Diagnosis based on clinical manifestations and combination of laboratory tests ▪Thrombocytopenia and prolonged clotting times and D-dimer ▪Treatment: ▪Treat underlying cause ▪Control ongoing thrombosis ▪Maintain organ function  Hematological Conditions Anemia’s Polycythemias Alterations in Leukocyte Function  Hematological Conditions: Anemia ▪Too few erythrocytes or insufficient volume of erythrocytes in blood ▪Classified 2 Ways: ▪Cause ▪Altered Production ▪Blood Loss ▪Increased Erythrocyte Destruction ▪Combination of all Three ▪Changes that affect the size, shape, or substance of the erythrocyte Fig 21-1, p. 501, Power-Kean et al., (2023)  Hematological Conditions: Types of Anemia's ▪Macrocytic-Normochromic Anemia ▪Characterized by large stem cells in the bone marrow that mature into erythrocytes that are unusually large in size, thickness, and voluvme ▪Result of ineffective DNA synthesis caused by deficiencies of Vitamin B12 (cobalamin) or folate (folic acid) ▪Defective erythrocytes die prematurely (eryptosis) ▪2 primary types: ▪Pernicious Anemia * ▪Folate Deficiency Anemia  Pernicious Anemia ▪Pathophysiology: ▪ Absence of intrinsic factor, a transporter required for gastric absorption of dietary Vitamin B 12, a vitamin essential for nuclear maturation and DNA synthesis in RBC ▪ Result from autoimmune gastritis (gastric atrophy results from destruction of parietal and zymogenic cells) leads to deficiency of all secretions of the stomach, HCL, pepsin, and intrinsic factor ▪ May be secondary to previous H. pylori infection ▪Clinical Manifestations: ▪ Develops slowly ▪ Early→ infections, mood swings, and GI, cardiac, and kidney ailments ▪ When Hgb drops to 70-80 g/L patient may be weak, fatigue, paresthesia of feet and fingers, difficulty in walking, loss of appetite, abdominal pains, weight loss, tongue may become sore, smooth, and beefy red secondary to atrophic glossitis, skin may become sallow or “lemon yellow” due to pallor and icterus, enlarged liver, and rt sided heart failure  Hematological Conditions: Types of Anemia's ▪Microcytic-Hypochromic Anemia ▪ Small erythrocytes that contain reduced amounts of hemoglobin ▪ Iron Deficiency Anemia ▪Siderblastic Anemia ▪ Insufficient iron uptake, that results in abnormal hemoglobin synthesis ▪ Acquired ▪ Hereditary ▪ Reversible  Anemia ▪Normocytic-normochromic anemia ▪ Aplastic ▪ Insufficient erythropoiesis likely autoimmune in nature ▪ Depletion of T-cells ▪ Presents as pancytopenia or may present as only one deficiency (ITP or RBC’s) ▪ Clinical manifestations: hypoxemia, pallor, and weakness with fever and dyspnea, bleeding in the GI tract, prolonged bleeding at other sites, menorrhagia, purpura, diminished leukocytes may result in progressive frequency and prolonged infections, paresthesias ▪Post Hemorrhagic ▪Hemolytic ▪Anemia of Chronic Inflammation  Hematological Conditions: Polycythemia ▪Excessive red blood cell production ▪Two primary kinds; ▪ Relative ▪ Absolute aka Polycythemia Vera ▪ abnormal proliferation of bone marrow stem cells with subsequent self-destructive expansion of red cells. ▪ Etiology is unknown ▪ Creates hypercoagulability  Polycythemia ▪Hereditary Hemochromatosis ▪Autosomal recessive disorder ▪Characterized by GI iron absorption with subsequent tissue iron deposition ▪Symptoms such as fatigue, malaise, abdominal pain, arthralgia's and impotence, and clinical findings of hepatomegaly, abnormal liver enzymes, bronzed skin, diabetes, and cardiomegaly Sandip Dhaliwal ☺ (RN, MN Student) Hematology and Blood & Marrow Transplant (BMT) ▪ Unit 57 at Foothills Medical Centre ▪ BMT treatment clinic at Tom Baker Cancer Centre Email: sdhali @ucalgary.ca  Leukocytes (white blood cells) Lymphoid Myeloid origin origin Mnemonic Never (Neutrophils) Let (Lymphocytes) Monkeys (Monocytes) Eat (Eosinophils) Bananas (Basophils) Alterations in Leukocytosis: increase in leukocytes in the blood Leukocyte Function Leukopenia: decrease in leukocytes in the blood Granulocyte and Monocyte Alterations: - Increased levels are due to a physiologic response to microbial invasion, or due to myeloproliferative disorders that increase stem cell proliferation in the bone marrow (polycythemia vera, chronic myeloid leukemia) - Decreased levels are due to infectious processes that deplete the supply or disorders that suppress marrow function Alterations in Granulocyte and Monocyte Function Neutrophilia Early stages of Infection or Inflammation (numerous) Neutropenia Hypoplastic of aplastic anemia, megablastic anemias, leukemia, (reduced) HIV, EBV Eosinophilia Asthma, hay fever or drug interactions Eosinopenia Cushing’s Disease, shock, surgery, burns, trauma or mental distress Basophilia Immediate response to inflammation and hypersensitivity reactions, CML, myeloid metaplasia Basopenia Hyperthyroidism, acute infection or long term steroid use Lymphocytosis Viral infections like EBV Lymphocytopenia Associated with HF, HIV  Myelodysplastic Syndrome (MDS) ▪Group of diseases in which the bone marrow doesn’t make enough healthy mature blood cells ▪Immature myeloid blood cells, called blasts, do not work properly and build up in the bone marrow and the blood ▪Clinical Manifestations: fever, frequent infections, easy bruising and bleeding, fatigue, paleness, shortness of breath, general feeling of discomfort or illness, abdominal discomfort or a feeling of fullness if the spleen or liver is enlarged  Leukemia ▪ Malignant disorder of the blood ▪ Uncontrolled proliferation of malignant leukocytes causing overcrowding in the bone marrow and decreased production and function of hematopoietic cells Acute Leukemia ▪Characterized by undifferentiated or immature cells called blast cells ▪Onset is abrupt and rapid, short survival. Chronic Leukemia ▪Cell is mature but does not function ▪Onset is gradual and survival is longer  Leukemia Predominant origin is either MYELOID or LYMPHOID Lymphoid Origin Myeloid Origin (overproduction of B-Cells/T-Cells) (overproduction of granulocytes /monocytes) Acute Lymphocytic (ALL) Acute Myelogenous (AML) Chronic Lymphocytic (CLL) Chronic Myelogenous (CML)  Pancytopenia ▪Associated when leukemia blasts take over the marrow and cause cellular proliferation ▪Characterized in aplastic anemia ▪Reduction in all cellular components of the blood ▪ Red blood cells, white blood cells and platelets ▪Priorities include oxygenation and dysfunction in immunity ▪Patients may become immunocompromised (Fevers are very serious!)  Alterations in Lymph System Lymphadenopathy is enlarged lymph nodes likely as a result of an infectious process or mass Pediatrics Neonatal Hematology Approach to Skin Alterations Marlies R. Murdoch MSc BScN RN (creator) Kara Sealock RN EdD MEd. BN CNCC(C) CCNE Class Outline Neonatal Hematology Skin Alterations Erythrocytes Most abundant cells of the blood Primarily responsible for tissue oxygenation Normal lifespan: Full term infants ________ to ______ days Children to adults _________ days Hemolytic Disease of the Newborn (HDN) Exists if mother and fetus differ in ABO blood type (1 in 10 cases) OR If the fetus is Rh+ and mother is Rh- (10% of pregnancies). The first incompatible fetus causes the mother’s immune system to produce antibodies that affect the fetuses of subsequent incompatible pregnancies.  Hemolytic Disease of the Newborn: Pathophysiology Rh factor is an antigen on the red blood cells of some people (these people are Rh +); the Rh factor is dominant; a person may be homozygous or heterozygous for Rh factor. A person who is Rh – is homozygous for this recessive trait-does not carry the antigen; develops antibodies when exposed to Rh + red blood cells through transplacental transfusion.  Hemolytic Disease of the Newborn: Pathophysiology Cont’d Following birth of an infant who is Rh +, if fetal cells enter the mother’s bloodstream, maternal antibody formation begins (IgM and then IgG); antibodies remain in the maternal circulation. At time of next pregnancy with fetus who is Rh +, antibodies (maternal IgG) will cross placenta ➔ hemolysis  Mother who is Rh –  Rh + fetal red blood cells enter the maternal circulation  Maternal antibody formation (maternal sensitization)  Antibodies (IgG) cross placenta and enter fetal bloodstream  Attack fetal red blood cells  Hemolysis  Anemia, hypoxia  Hydrops Fetalis Hydrops Fetalis  Hemolytic Disease of the Newborn: Diagnostic Evaluation Prenatal: ▪ Maternal blood type and Rh factor ▪ Indirect Coomb’s test-determine presence of Rh sensitization (titer indicates amount of maternal antibodies) ▪ Amniocentesis- as early 26 weeks of gestation-amount of bilirubin by-products indicates severity of hemolytic activity Intrapartum (observation of amniotic fluid – after membrane rupture): ▪ Straw-colored fluid-mild disease ▪ Golden fluid- severe fetal disease Postnatal: ▪ Direct Coombs’ blood test (positive test demonstrates Rh antibodies in fetal blood)  Hemolytic Disease of the Newborn: Clinical Manifestations Neonates with mild HDN may appear healthy or slightly pale, with slight enlargement of the liver or spleen. Severe anemia: pallor, splenomegaly and hepatomegaly, cardiovascular failure +/- shock. Hyperbilirubinemia (neonatal jaundice) ➔ Kernicterus ➔ cerebral damage ➔ death Skin Alterations  The Skin: The Largest Organ in the Body Fig 41-1, p. 1023, Power-Kean et al., (2023)  Skin Manifestations: Primary Skin Lesions Skin changes produced by a causative factor Table 41-2, page 1025-1026, Power-Kean et al., (2023) Macule Vesicles Papule Bulla  Skin Manifestations: Secondary Skin Lesions Changes that result from alteration in the primary lesion. Ulcer Erosion Table 41-3, page 1027-1028 Power-Kean et al., (2023) Scar Generalized Rashes Usually due to systemic exposures or illnesses, for example: ▪Drug eruptions ▪Viral illnesses ▪Toxin-mediated processes ▪Immune-mediated conditions Localized Rashes Isolated Special features ▪Part of a generalized rash ▪May help in determining the etiology  Sequence of the Rash Where did it start on the body? How did it spread and over what time? How has it evolved over time? Does it fluctuate? Associated Symptoms: Pruritus (Itch) Generalized VS Localized Distribution Timing of the Itch Associated Signs and Symptoms Fever Tongue changes (strawberry) Cough Nausea/vomiting Conjunctivitis Abdominal pain Runny nose Diarrhea Sore throat Dizziness Pain Headache Weakness Swollen extremities  Medical Hx Exposure hx Sexual hx ▪Medications Prior hx of skin disease ▪Food/drinks ▪Animals Family hx of skin disease ▪Chemicals/physical Past medical hx materials Age of the child ▪Sick contacts Allergies Immunization hx Travel hx (foreign) Approach to Describing a Rash Distribution ▪Generalized ▪Localized ▪Important locations present or absent Morphology ▪Lesion type ▪Appearance Progression over time Associated symptoms  Rules to Guide the Skin Exam #1: Look at the WHOLE tree #2:The BRANCHES involved say a lot about the rash #3: Describe the LEAVES carefully  #1: Look at the WHOLE tree Is the distribution: ▪ Generalized (whole tree)- affecting multiple body parts? ▪ Localized (one branch)- affecting only one body part? ▪ Central or peripheral? ▪ Symmetrical or asymmetrical? ▪ Involves specific sites that narrow the differential?  2. Branches = Specific Body Part (s) Involved Location may be an important diagnostic clue for a limited condition or when part of a generalized rash. Specific etiologies suggest by location in: ▪Palms and soles ▪Mouth and/or tongue ▪Eyes ▪Lower extremities ◦ Absence in certain areas may also be relevant Common Etiologies: Palms and Soles Hand-foot-mouth disease Scabies Atopic dermatitis Allergic rashes Common Etiologies: Oral Hand-Foot-Mouth Disease Varicella Kawasaki syndrome Scarlet Fever Candidiasis Measles Steven Johnson Syndrome Common Etiologies: Conjunctiva Viral: ▪Measles ▪Rubella ▪Varicella Bacterial: ▪Rocky mountain spotted fever ▪Meningococcal infection 3. Leaves = Lesions Many components of individual lesions of the rash may help with recognition. ▪Shape and morphology ▪Color ▪Presence or absence of scales, excoriation ▪Relationship to hair follicles ▪Tenderness or pruritus Skin Lesion Vocabulary: Individual (Primary) Lesion Morphology Macule Papule Vesicle Bulla Plaque Nodule Pustule Table 41-2, page 1025-1026, Power-Kean et al., (2023) Skin Lesion Vocabulary: Secondary Lesions Morphology Ulcer Keloid Ulceration Excoriation Scale Erosion Fissure Table 41-3, page 1027-1028 Scar Power-Kean et al., (2023) Other Rash Words Linear Serpiginous- twisting linear form Annular- tendency to form rings Target lesions- circular rash with mid-zone clearing  Key Points to Remember ▪Can you perform a full head to toe assessment with knowledge of physiological landmarks and anatomy and physiology related to Neuro, CV, Resp, GI and GU assessment? ▪Explain the “why” associated with head to toe assessment and connections to other systems ▪Identify and apply concepts of lab values related to hematology ▪ Do you understand the pathophysiology, clinical manifestations and nursing assessment related to : ▪ Alterations in Platelet Function ▪ Heparin Induced Thrombocytopenia ▪ Alterations in Coagulation ▪ Disseminated Intravascular Coagulation ▪ Hematological Conditions ▪ Anemia ▪ Polycythemia ▪ Alterations in Leukocyte Function ▪ Neonatal hematology and Skin Alterations