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NURS 2020_Unit 1_Blood and Cardiovascular Disorders_Part 1.pdf

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NURS 2020 Advanced Pathophysiology and Microbiology Unit 1 Cardiovascular Disorders Part 1: Blood and Vascular Disorders Avinash Thadani, PhD HBNA ...

NURS 2020 Advanced Pathophysiology and Microbiology Unit 1 Cardiovascular Disorders Part 1: Blood and Vascular Disorders Avinash Thadani, PhD HBNA Content 1. Blood Disorders Patterns of Bleeding Lab Tests Hemophilia Disseminated Intravascular Coagulation (DIC) Various types of Anemias 2. Vascular Disorders Alterations in arterial flow Alterations in venous flow Readings: Unit 1 Slide Deck and the other learning resources posted on the Bb shell 2 Two Major Patterns of Bleeding 1. Mucosal bleeding reduced number or function of platelets (e.g., bone marrow failure or aspirin) von Willebrand deficiency clinical manifestations: skin: petechiae, bruises, post-surgical bleeding gum and mucous membrane bleeding fundal hemorrhage 3 Two Major Patterns of Bleeding 2. Coagulation factor deficiency e.g., hemophilia A and B, complication of warfarin therapy clinical manifestations: bleeding into joints (hemarthrosis) or muscles bleeding into soft tissues intracranial hemorrhage post-surgical bleeding 4 Hemostasis & Coagulation Assessment & Lab Tests When to evaluate hemostatic abnormality: genetics (e.g., family history of bleeding); bleeding from multiple sites, spontaneous bleeding, or excessive bleeding after injury pre-surgical screening during anticoagulation treatment 5 Lab Tests Complete Blood Count (CBC) Platelet Count Peripheral blood smear Bleeding Time Prothrombin Time (PT) International Normalized Ratio (INR) Activated Partial Thromboplastin Time (aPTT) Thrombin Time D-dimer Assay 6 Coagulation Screening Tests Test Normal Range Situations in which tests may be abnormal Platelet count 150 – 400 x 109/L Thrombocytopenia Bleeding time < 9 mins Thrombocytopenia Abnormal platelet function von Willebrand disease Prothrombin time (PT) 10 – 13 s Deficiencies of factors II, V, VII or X Severe fibrinogen deficiency Activated partial 28 – 38 s Deficiencies of factors II, V, VIII, IX, X, XI, XII thromboplastin time Severe fibrinogen deficiency Unfractionated heparin therapy Antibodies against clotting factors International Normalized 0.9 – 1.2 Used to monitor coumarin (warfarin) therapy Ratio (INR) and is not a coagulation screening test Fibrinogen concentration 1.5 – 4.0 g/L Hypofibrinogenemia, e.g., liver failure, DIC 7 Definitions Ecchymosis: larger areas of bleeding into the skin; typically resulting in a “bruise” Epistaxis: blood in nasal drainage Hemarthrosis: bleeding into a joint Hematoma: raised area of bleeding into soft tissue Hematuria: blood in urine Hemoptysis: blood in sputum (coughing up blood) Melena: tarry, very dark feces; typically indicates a lower GI bleed Menorrhagia: excessive menstrual bleeding Petechiae: small, flat hemorrhages ranging from pinpoint size or a few mm in diameter and which do not blanch on pressure; common in vascular & platelet disorders Purpura: combination of petechiae and/or ecchymosis 8 Coagulation Disorders Bleeding disorder due to: deficiency in coagulation factor(s) deficiency in vit. K liver disease inappropriate activation of coagulation cascade Examples: 1. Hemophilia 2. Disseminated Intravascular Coagulation (DIC) 9 Hemophilia most common inherited coagulation disorder deficiency of either factor VIII or IX the intrinsic pathway of coagulation is affected bleeding disorder 10 Hemophilia A Etiology: X-linked recessive pattern of inheritance ppredominantly affects males Pathogenesis: deficiency of factor VIII Clinical manifestations are variable dependent on the degree of deficiency Clinical manifestations: symptoms are variable dependent on the degree of deficiency newborns may develop bleeding at the time of circumcision spontaneous hemarthrosis (hallmark) easy bruising and hematoma formation after minor trauma severe prolonged bleeding after surgery or lacerations 11 Hemophilia B Less common than Hemophilia A; also referred to as “Christmas disease” Etiology: X-link recessive genetic disorder; predominantly affects males Pathogenesis: deficiency of Factor IX Clinical manifestations are identical to Hemophilia A 12 Disseminated Intravascular Coagulation (DIC) A syndrome characterized by inappropriate intravascular activation of coagulation (i.e., loss of localization) Simultaneous thrombosis and hemorrhage events may occur Etiology: trauma, shock, infection, malignancy, obstetric complications Clinical manifestations: spectrum of both bleeding (intracranial hemorrhage, ecchymosis, hematuria, epistaxis, massive bleeding) and thrombosis (multifocal brain infarcts, superficial gangrene, oliguria, ARDS, acute GI ulceration) if severe, can produce multiorgan dysfunction and failure and eventually death 13 Disseminated Intravascular Coagulation (DIC) 14 Anemia Definition: Hb aortoiliac Etiology: embolism (e.g., arrhythmias, valvular heart disease), thrombosis (e.g., rupture of atherosclerotic plaque, trauma) Clinical manifestations: 6 Ps Pain Pallor Paresthesia (loss of light touch first) Paralysis (most important; indicates impending loss of limb) Polar (cold) Pulselessness (helps determine site of occlusion) 29 Peripheral Arterial Disease Chronic ischemia due to inadequate arterial supply to meet metabolic needs during walking (claudification) or at rest (critical ischemia) Etiology: atherosclerosis Modifiable risk factors: smoking, DM, hyperlipidemia, HTN, obesity, sedentary lifestyle Non-modifiable risk factors: advanced age, PMHx or FMHx PAD/CAD/CVD Clinical manifestations: Claudification: pain with exertion (usually in the calves); relieved by rest (5 min); reproducible 30 Aortic Dissection Tear in the tunica intima allowing blood to dissect in to the tunica media Etiology: HTN Epidemiology: M:F=3:1; age 50-65 Clinical manifestations: sudden onset of tearing chest or pain that radiates distally to between the scapula bleeding into the pleura (hemoptysis, dyspnea) and retroperitoneum (shock) or pericardium (cardiac tamponade) can occur syncope 31 Aneurysms Localized dilatation of an artery (1.5x normal diameter; >3 cm for abdominal aorta) True aneurysm: involves all three layers (tunica intima, media, and adventitia) False aneurysm: breach in the intima/media allows blood to collect between the media and adventitia Can rupture, thrombose, embolize, erode, or fistulize Classification: (i) shape: fusiform (full circumference of wall) or saccular (only portion of wall); (ii) location (e.g., thoracic aorta; abdominal aorta) Risk factors: smoking, age, male, HTN Clinical manifestations: 75% asymptomatic; symptoms develop due to acute expansion or rupture 32 Abdominal Aortic Aneurysm (AAA) Acute expansion (>3 cm) or rupture of an aneurysm in the abdominal aorta Clinical manifestations: Syncope Pain (chest, abdominal, back, flank) Hypotension (shock) Palpable, pulsatile mass above the umbilicus Airway or esophageal obstruction Hemoptysis or hematemesis 33 Atherosclerosis Hardening of the arteries Risk factors: HTN, DM, smoking, dyslipidemia In response to endothelial injury, inflammation and LDL metabolism promote hyperplasia and the formation of a fibrous cap over lipid core: atherosclerotic plaque Stable plaques have a thick fibrous cap; unstable plaques have a vulnerable fibrous cap Rupture of plaque may lead to thrombosis, emboli formation, lumen narrowing, and wall weakening (aneurysm) 34 Atherosclerosis 35 Venous Thromboembolism Thrombus formation and subsequent inflammatory response in a superficial or deep vein Deep vein thrombosis (DVT) or pulmonary embolism (PE) Etiology: endothelial damage, venous stasis (e.g., post-MI, HF, stroke, and postoperative), hypercoagulable states (e.g., surgery, trauma, neoplasms, prolonged immobilization, OCP use, HRT, pregnancy) Clinical manifestations of DVT: Unilateral leg edema (calf circumference increased) Erythema, warmth, and tenderness Investigation: Doppler U/S Complication: Acute PE (life-threatening) Treatment: LMWH, UFH, direct thrombin inhibitors (e.g., dabigatran), direct factor Xa inhibitors (e.g., apixaban), thrombolytic drugs (e.g., tPA) 36 Chronic Venous Insufficiency Wide spectrum of chronic venous diseases with advancing symptoms of edema, skin changes, varicosities, and leg ulcers 65% of NA adults develop some degree of venous insufficiency Etiology: valvular incompetence or obstruction Risk factors: age, prolonged standing, pregnancy, obesity Clinical manifestations: Pain (fullness, tightness, aching) worst at end of day Ankle/calf edema; relieved by foot elevation Skin changes (pruritis, eczema), stasis dermatitis, brownish hyperpigmentation Ulceration Varicose veins Treatment: compression stockings, ambulation, periodic rest-elevation 37 Summary Please learn the pathophysiology (etiology, modifiable risk factors, pathogenesis (briefly), and most importantly the clinical manifestations) of the various diseases/disorders/conditions covered in this slide show and listed in the learning outcomes of Unit 1 in the syllabus You will only be assessed on the diseases/disorders/conditions that are listed in the leaning outcomes Please contact me via email ([email protected]) if you require any clarification/assistance 38 Next Lesson Blood and Cardiovascular Disorders – Part 2: Heart Disorders 39

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