- Information
- AI Chat
Patho exam 3.pdf (1)
Pathophysiology (NSG 211)
Marian University
Recommended for you
Related Studylists
asu pathoPreview text
Exam #3 Overview
Module 9 – Blood and Lymphatic Disorders Part 1
Blood: o Functions: Transportation (O2, Glucose, Nutrients, and Hormones), Defense mechanism (WBC), promotion of homeostasis through heat distribution, clotting factors, BP, and Acid buffer system o Components: Plasma (45% total, made of 7% protein, 91% water, 2% other solutes), Platelets (<1% - normal is 150k-450k), Leukocytes (<1% - normal is 4500-9000), and Erythrocytes (45%) o Types of cells Neutrophils (40-80%): First to respond to tissue damage; when immature are called bands/stabs; if low “Left shift” suggestive of bacterial infection Lymphocytes (20-40%): T (cell-mediated) and B (humoral) cells; activated by factors from macrophages (APCs); “Right shift” suggesting a viral or fungal infection Monocytes (2-10%): Migrate into tissue Macrophages; often act as antigen- presenting cell (APC) “Bridge” to innate/adaptive immunity Eosinophils (1-6%): Allergic response (Type 1 HS allergic rxn); releases histamine; involved in activation of IgE Basophils (1-2%): Migrates into the tissue “Mast Cell” phagocyte; releases histamines and heparin, involved in vasodilation Platelets: Not cells (non-nucleated fragments from megakaryoblast break down) “Roof shingles” that become sticky once heated up 2 factors activate them: Exposed collagen and PAF Exposed collagen Von Willebrand Factor (vWF) Integrin IIb/IIIa activated on Platelet receptor Platelet Aggregation Platelet Aggregating Factor (PAF): Innate immunity/inflammation Erythrocytes: Non-nucleated biconcave disc containing hemoglobin and comprised of Iron and Globin protein (Lifespan approximately 120 days) Use: Transportation of Oxygen Prothrombin: Made in the liver “TAR” Converts to thrombin – huge role in the clotting cascade Clotting cascade “Common Pathway” 22a Fibrinogen: Made in the liver “NETTING” Converts to fibrin Clotting cascade “Common Pathway” 11a Plasminogen: Is converted to plasmin and breaks down clots o Granulocytes: Contain dark granules on microscopy: Neutrophils, basophils, eosinophils o Agranulocytes: “Without granules”: Lymphocytes (T and B) and monocytes o Erythropoietin: Released by kidneys in response to hypoxia – stimulates increase RBC production by the bone marrow
o Hematocrit (Hct): The “red percentage” of the blood Increased indicates: Dehydration or excess RBCs (high viscosity blood) Decreased indicates: Blood loss, anemia, or blood dilution (low viscosity blood) o Hemoglobin (Hgb): Major component of Hct, contains 4 globin subunits each with a ferrous iron atom for O2 attachment. Oxyhemoglobin – O2 rich RBC’s (arterial), favorable in alkalotic environment Deoxyhemoglobin – CO2 transport (venous), favorable in acidic environment Approximately 1/3 of Hematocrit o Clotting cascade: Comprised of both an intrinsic/extrinsic pathway that both lead to the common pathway and create a “plug” to stop bleeding 5A Activates the thrombin burst and causes 22a (what many medications target) Lack of factor 8 (intrinsic) Classic hemophilia (Hemophilia A) At first extrinsic pathway is initiated and once some of thrombin is made then it activates the intrinsic pathway Coumadin is used to block extrinsic pathway To monitor effectiveness check PT/INR ratio Heparins are used to block intrinsic pathway (prevent thrombin and fibrin activation) To monitor effectiveness, check the aPPT
ABO Blood typing: o Type A: RBC contains A-antigens; blood contains Anti-B antibodies o Type B: RBC contains B-antigens; blood contains Anti-A antibodies o Type AB: RBC contains BOTH A/B-antigens; blood contains NEITHER A/B-antibodies; “universal recipient” o Type O: RBC contains NEITHER A/B-antigens; blood contains BOTH A/B-antibodies; “universal donor” o Rh “+”: RBC contains Rh-antigen; blood does NOT contain Rh-antibodies; can receive Rh+ or Rh- blood o Rh “-”: RBC does NOT contain Rh-antigen; blood does contain Rh-antibodies; can receive only Rh- blood
Lymph system: o “Gutters” of circulation o 8% of interstitial fluid is reabsorbed into venous vasculature and 1-2% flows into the lymph system – blockage of this system Peripheral edema o Function: Captures unwanted material from body fluids, monitors for foreign material, initiates immune response, & nodes are helpful for determining CA spread & prognosis o Comprised of: Vessels, nodes (Immune “surveillance”), Lymphoid Tonsils (Palatine/Pharyngeal), Thymus, Spleen and Bone Marrow
Signs/Sx: Pancytopenia (global blood issues) – all normal anemia plus leukopenia causing opportunistic infections and thrombocytopenia causing bleeding tendencies Labs: CBC (diagnostic) showing low of everything Treatment: Treat underlying cause or bone marrow transplant
o Hemolytic anemias: RBC Excessive-Destruction anemias “hemolysis” Sickle Cell: Genetic amino acid RBC abnormality HgS gene inherited from parents Protective from malaria if heterozygous “Sickling” causes hypoxia and vascular occlusions painful Sx: Severe anemia sx plus hyperbilirubinemia (jaundice/icteric sclera), splenomegaly, vascular occlusions, growth and developmental delays, CHF, frequent infections. Labs: Hgb electrophoresis and DNA testing (HgS) Prevention/Treatment: Avoidance of altitudes/exercise, prevent dehydrations, acidosis, and infections. Avoid cold and take Hydrea (drug to prevent sickle cell crisis)
Thalassemia “Sea-blood”: Genetic Hbg protein abnormality (Mediterranean) Generic defect in which 1+ genes for protein portion of Hgb are missing ( missing minor, 2+ missing major) Named by which globin is affected (alpha or beta) – there are 2 of each Beta (most common): Cooley’s anemia (major) and heterozygous (minor) Alpha (less common): trait (asymptomatic), minor (similar to beta minor), or major (Hydrops fetalis – deletion of all 4 alpha) Sx: Anemia plus: Hyperbilirubinemia, Iron overload, hyperactive bone marrow (high retic count), and growth retardation Lab: microcytic/hypochromic (Fe++ not held), elevated erythropoietin levels, high Fe++ levels Tx: Blood transfusions, Iron Chelation therapy (for iron overload), splenectomy (sometimes)
Polycythemia: RBC are being both created and destroyed too quickly Etiology: JAK2 mutation, Hypoxia (secondary polycythemia), paraneoplastic syndrome (epo stimulated inappropriately). Primary = “Vera” (true). Usually idiopathic or from JAK2 Gene mutation Secondary = Acquired (Hypoxia from smoking or lung disease) or from a tumor excreting too much erythropoietin – Can create a relative polycythemia by “training” at high altitudes Manifestations: Increased production of RBCs, granulocytes, and platelets, serum erythropoietin low Sx: Abdominal pain, hepatomegaly, splenomegaly, thick skin, HTN, visual disturbances, full/bounding pulse, dyspnea, hypercoagulative state, thromboses/infarctions, and CHF Lab: Inc cell counts, Hgb, & Hct. Hyperuricemia (from RBC destruction) Tx: Periodic phlebotomy (bleeding), marrow suppression (drugs/radiation)
Blood dyscrasias (bleeding problems): o Thrombocytopenia: < 150k with Sx at <50k Etiology: Increased Platelet consumption; can be acquired (Heparin induced, viral, or from drugs like thiazides or chemo)
o Hemophilia A (classic): Etiology: Genetic deficiency of clotting factor 8. Inherited (x-link recessive) so shown only in men Sx: Prolonged bleeding after minor trauma, spontaneous hemorrhage into joints (Hemarthrosis), hematuria, hematochezia (blood in stool) and anemia Tests: PT/INR are normal, aPTT and coagulation are prolonged , low factor 8 Treatments: Blood transfusion, factor 8 infusins, and desmopressin (DDAVP) to promote vWF and activate factor 8
o Disseminated Intravascular Coagulation (DIC): Extreme use of clotting factors in one areas so that there isn’t enough to be used in another area Pathophysiology: Both excessive clotting and bleeding Etiology: Obstetric complications (Toxemia, preeclampsia, abruption), Infection (Gram -, endotoxins), septicemia, major trauma or burns Sx: Hemorrhage/thrombosis, bruising, infarctions, tachypnea, hypoxia, tissue ischemia, respiratory failure (ARDS) Tx: Frozen plasma, heparin drip (to stop formation of inappropriate clots), FFP (Fibrinogen and prothrombin)
Blood cancers: Patho process, cells effected, lab results, and signs / symptoms o Leukemia (WBC’s): High amount of leukocyte production – however they are immature and nonfunctional and decrease the amount of functioning WBCs “BLAST Cell from bone marrow” Many of them – named by affected type of cell Acute Lymphocytic Leukemia (ALL) makes up 75% of children’s cases (aggressive); Acute Myelogenous Leukemia (AML) myoblasts in the bone marrow (aggressive); CLL (chronic) is more common in adults; CML is an accumulation effect more common in adults; Acute Monocytic Leukemia & Hairy Cell Leukemia Etiology: Childhood is idiopathic; however adult leukemia is from oncogenic mutations/accumulations such as radiation, certain chemicals, viruses, chemotherapy, etc. Much harder remission in chronic than in acute Sx: Many infections, high WBC count, severe hemorrhage, anemia symptoms, bone pain, weight loss, fever, lymphadenopathy, hepatosplenomegaly, & CNS Sx (HA, visual changes, N/V)
o Lymphoma: Etiology: Genetic mutations or viral infection (EBV/Mono) Sx: Weight loss, fatigue, anemia, night sweats, recurrent infection, splenomegaly Diagnostic test: Microscopy Treatment: Radiation, chemotherapy, surgery
Conduction pathway: o SA Node: Pacemaker control from both SNS and PSN (Over the RA) SNS – “Accelerator” (Central medulla acting on B1 adrenergic receptors) PSN – “Brake” (Vagus nerve via cholinergic receptors) *If the HR needs to be raised then the first thing the body does is release the brake (PNS control) – Anticholinergic drugs combat the brake (such as Benadryl) and can cause tachycardia o AV Node: Slows the impulse (Where 1st, 2nd, and 3rd degree blocks occur) o Bundle of His: Bifurcation of the signal and sends them to the ventricles (Site of BBB) o Purkinje Fibers: Ventricular contraction pathway (damage here = heart failure) o The pathway leads to systole (Ventricular contraction) which starts at the end of the ventricles and works its way upwards to make sure that it squeezes all the blood out. 1/3 of the time (average) is spent in systole while 2/3 is spent in diastole o *Diastole is where the heart “feeds” itself through its coronary arteries
Angina: “Pain in Chest” o Process: Ischemia in heart tissue causing O2 demand > supply, especially with exercise Important to note that there is no muscle damage/necrosis Heart tries to compensate by vasodilation but in presence of atherosclerosis vessels aren’t as flexible o Sx: Intermittent episodes of substernal CP; triggered by emotional/physical stress o Stable: Occurs with activity and is relieved by rest o Unstable: Occurs without activity and often cannot be relieved – can progress to an MI!
Myocardial infarction (MI): o Process: Coronary ischemia that leads to myocardial necrosis due to hypoxia Thrombus build-up forming an atheroma and occluding arteries Vasospasms at the site of atheroma can cause total closure Embolus (part of a thrombus that breaks off) can occlude smaller vessels downstream The longer the hypoxia lasts the larger the area of Necrosis (Time = muscle) o Sx: Sudden pain – substernal that can radiate (left jaw/arm/shoulder). Described as crushing, heavy or dull – NO RELIEF with NGT (vasodilator). Diabetics and women typically have atypical symptoms (indigestion) Other sx: N/V, SOB, fatigue, dyspnea, diaphoresis, anxiety o Labs: EKG: Checking for ST elevation = STEMI Cardiac-specific enzyme CK-MB: Elevates later – released from myocardial band muscle damage Cardiac-specific enzyme Troponin-I: Elevates early (20 minutes) Lytes: Potassium (hyper) from breakdown of cells CBC: Leukocytosis and low-grade fever o Complications: Mortality 30-40% first year after MI o Treatment: MONA (Morphine, O2, NTG, ASA) antiarrhythmics, vasodilators, clot- busters, pacemakers, angioplasty, and CABG (bypass)
*Morphine sometimes contraindicated (increases the preload)
Telemetry: (You won’t have to interpret telemetry; but, what concerns do you have for your patient with the following arrhythmias? o Afib: Abnormal, irregular P waves and irregular R-R – results in decreased CO (decreased ventricular filling) risk of thrombus MI, CVA Need to convert back to normal and put on coumadin o Aflutter: P-P ratio > 1:1 (usually 3:1) Supraventricular tachycardia o Ventricular Tachycardia: Ventricles have no time to fill low SV low CO * Shock (if pulseless) and start CPR immediately o Ventricular Fibrillation: No SV (ventricles only spasm) pulseless *Shock and start CPR immediately
Coronary Artery Disease (CAD) – Not mentioned in this study guide by professor – but I think it is important to know: o “Heart Disease” – Major cause of morbidity/mortality HTN, MI, Cardiac arrhythmias, CHF, and congenital heart defects o Diagnosis: EKG ( Most Common ), Exercise stress test, CXR (cardiomegaly and Pulmonary edema CHF), Cardiac HeartScore (Calcification test), Cardiac Catherization ( gold standard) , Doppler studies (blood flow/clots), Echocardiogram (doppler of heart chambers/valves), and Blood tests (Troponin-I and CK-MB) o Arteriosclerosis: “Normal” degenerative process in arteries (decreased elasticity) o Atherosclerosis: Formation of plaque (cholesterol) causing narrowing of walls Sx: Xanthelasmas (fatty deposits around eyelids), Arcus senilis (cornea yellowing) o Cholesterol: HDL: Helpful LDL: Bad – Recruits monocytes to engulf it becomes a foam cell makes fatty streaks which are hard to remove and stick to arterial walls o Risks: Smoking is #1! Cholesterol and obesity are next Estrogen has protective factors against CAD so men are more effected
o Sx: Low grade fever, leukocytosis, malaise/anorexia, non-pruritic rash (erythema marginatum), St. Vitus Dance (jerky movements), heart murmurs *Effects the (endocardium) valves Blood swirls around the valves (Stagnant) and allow bacteria to grab hold of them and cause infection o Tests: Elevated ESR + Antistrepolysin O titer (ASO), Echocardiogram, EKG o Complications: Can lead to heart failure o **Rheumatic Fever (Acute) leads to Rheumatic Heart Disease (Chronic) where the cardiac murmur remains, and the valves are permanently damaged o Treatment: Prophylactic Antibiotics prior to dental/invasive procedures to prevent endocarditis – Valve replacement may be required
Infective Endocarditis: Bacterial invasion of the heart valves via blood-borne organisms o Can be subacute (low-grade organism) or acute (high-grade organism) o Structures effected: Valves o Risk factors: Rheumatic Fever, recent surgery/dental procedures, history of abnormal valves, or reduced host defense o Sx: Fever, Oslers nodes (painful swollen red lesions on hands/feet), Janeway lesions (Nontender, petechial lesions on palms), fatigue, splenomegaly, septic infarctions, CHF, septic shock, abscesses in other organs o Complications: The vegetation clots can break off the valves stroke, MI, or PE o Treatment: Antibiotics and Cardiac support *ST elevation seen in many leads (not indicative of specific type of MI)
Valvular abnormalities: o Stenosis vs incompetence (regurgitation): In stenosis the valve is thickened or damaged and there is turbulent flow when the valve is OPEN. In regurgitation the valve is leaky and weak and there is backflow when the valve is CLOSED. o Sounds: Stenosis is a harsh murmur while Regurgitation is a “swooshing” sound o Where you would hear it in cycle: Stenosis would be heard when the valve is supposed to be open and Regurgitation would be heard when the valve is supposed to be closed If you hear the murmur between the Lub/Dub then it is Systolic If you hear the murmur after the Lub/Dub then it is Diastolic
Pericarditis: Inflammation of the pericardium o Structures affected: The pericardium (covering) of the heart as well as the Ventricles (when they try to open and relax the pressure from the pericardium pushes on them) o Acute Risk factors: Viral infections (#1 cause), Heart surgery, MI, Autoimmune disease (SLE/RHD), Cancer o Chronic Risk factors: Chemotherapy, TB, Liver or kidney disease o Acute Sx: Sharp retrosternal chest pain, friction rub (heard), effusion o Chronic Sx: Fever, restlessness, tachycardia, CP, dyspnea, malaise, EKG ST elevation in all leads o Complications: Pulsus paradoxus (Drop in SBP >10 with inspiration) - emergency o Treatment: Aspiration of fluid
Venous Disorders: o Varicose Veins Process: Weakness of defects in the veins or valves of the veins causing blood pooling Risk factors: Predisposes to DVT! Etiology: More common in legs from crossing, restrictive clothing, prolonged standing, trauma, or genetics Sx: Edema, decreased hair growth, hyperpigmentation of skin, bulging of veins Complications: Ulcers and delayed healing Treatment: Support hose, elevating legs, avoid restrictive clothing, surgery o Thrombophlebitis: Thrombus in the presence of inflammation Etiology: Triad of Virchon Venous Stasis (age, immobility, CHF) Endothelial Damage (trauma, IV meds) Hypercoagulable state (pregnancy, malignancy, epigenetic-Factor V Leiden mutations) Sx: Aching, burning, edema, warm reddened area around inflamed vein, fever, malaise, leukocytosis, elevated D-dimer Complications: Can break loose and form a PE o Pulmonary embolus Etiology: Comes from a thrombus that breaks loose and lodges in the pulmonary arterioles Sx: Severe CP, SOB, Shock, RvCHF Complications: Can lead to a stroke or MI
Arterial Diseases: o HTN: BP > 140/90 (1/3 of adult population) Process: Plaque buildup that narrow diameter of artery and can lead to CHF Etiology: Insidious and often asymptomatic early on Sx: Morning HA and fatigue Classification: Essential HTN: Most common (idiopathic) Secondary HTN: Results from renal/endocrine dz or pheochromocytoma Malignant HTN: Uncontrollable, severe, rapidly progresses (can cause stroke) *Need to monitor protein and albumin in urine as they are signs the GFR has been damaged from the HTN
o PAD Process: Partial arterial occlusion (cumulative effect and not just one blockage) Sx: “Leg fatigue”, intermittent claudication, neuropathy, decreased pulses, stasis ulcers, pallor of legs, shiny ruddy skin, decreased leg/foot hair, gangrene Risk Factors: Smoking, Diabetes, HTN/CAD, Age (>40) *Intermittent Claudication is the tall-tale sign of PAD
Patho exam 3.pdf (1)
Course: Pathophysiology (NSG 211)
University: Marian University
- Discover more from:
