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# TWU FHN 2 module 1

### Module 1

Primary Care Definition integrated, accessible health care services by clinicians who are accountable for addressing a large majority of personal health care needs, developing a sustained partnership with patients, and practicing in the context of family and community.
Primary Care Conceptualized Primary care is coordinated, comprehensive, and personal care, available on both a first-contact and a continuous basis. (Groll)
Screening Tests Current state of health Identification of chronic health problems having high prevalence in the population screened Validation of being free of disease
Terminology for Test Selection Accuracy: degree of closeness of the measurement made to the true value or “gold standard” true positives + true negatives divided by the total tests
Terminology for Test Selection Precision: Ability to give nearly the same result in repeated determinations
Sensitivity: Probability that it will be positive when it is applied to a person who actually has the disease.Sensitive tests are used to confirm or rule in (true pregnancy)
Specificity: Probability that a test will be negative when it is applied to a person who actually does not have the disease. Specific tests are used to rule out or exclude (true negative)
Predicted Value The probability of the disease being present if the test is positive or not being present if the test is negaive
Positive predictive value Probability of test being positive if the condition is present
Negative predictive value Probability of test being negative if the condition/disease is not present
Differential Diagnosis Definition: Identification of a disease by comparison of the symptoms of two or more similar diseases
Guidelines for Ordering Diagnostic Tests As an additional piece of info to confirm or refute a diagnosis To stage a disease As a screening test To delineate risk factor of recurrence To monitor therapy To rule out treatable life threatening or serious disease For a research protocol.
Factors to Consider Prior to Ordering the Test Consider benefits Is the test to reassure the patient, support the diagnostic decision? Is the test for defensive medicine? Tests are measured in diagnostic, therapeutic and prognostic outcomes
Pathways for Differential Diagnosis Knowledge of the patterns of illness in the community/population being served Separation of illnesses that are self limiting versus emergent Knowledge for differentiating transient, chronic and minor illnesses
How to Generate Differential Diagnoses or Hypotheses What is probable is the key, not what is possible! Know the common causes Be aware of the more probable causes in a particular patient, in view of that patient’s known medical background
Abnormalities of Hemostasis Nurse practitioner role is to identify common disorders of hemostasis, obtain basic diagnostic testing, and to refer/consult with physician/hematologist on appropriate treatment and follow-up
Definition of Hemostasis: the prevention of blood loss achieved by: Vascular spasm Formation of platelet plug Blood coagulation Growth of fibrous tissue into clot to seal hole in the vessel permanently (Guyton)
Hemostasis dependent upon normal functioning of Vascular system Platelets Coagulation proteins
Abnormal Hemostasis Bleeding Disorders are due to: -Quantitative or qualitative abnormalities of platelets (# of or impaired function) -Quantitative or qualitative abnormalities in plasma coagulation -Vascular abnormalities (such as narrowing for instance) -Accelerated fibrinolysis
Testing for entire coagulation cascade: PT Prothrombin time Clotting activity factors VII, X, II, V, & Fibrinogen Norm: 10-13 seconds. Varies by lab NOTE: INR values should be used ONLY for orally anticoagulated patients, not for patients with coagulation defects
aPTT Activated partial thromboplastin time; synonym PTT Clotting activity factors HMWK, prekallikrein(PK), XII,XI,IX,VIII,X,V,II,& Fibrinogen Norm: 20-34 seconds
Prolongation of either PT or PTT due to coagulation factor deficiency and/or circulating antibody
Quantitative test--Platelet count Norm adult: 150,000-400,00/mm3 Norm child: 150,000-450,00/mm3
Qualitative test--Bleeding time (bedside test) Norm adult: 2-10 min Norm child:2-8 min Bleeding time is a bedside test not performed if platelet count less than 50,000 or NSAIDS taken within last 5 days
TT--Thrombin time (indirect measure of fibrinogen) Norm: Varies by lab. Clot formation in 12-18 seconds
FDP--Fibrinogen degradation products; synonym FSP--Fibrin split products Norm: <10 mcg/ml Uses: DIC , therapeutic thrombolysis, thrombosis, PE, thrombotic thrombocytic purpura (TTP)
D-dimers-Measures cross-linked d-dimers which are released from factor XIIIa reacted fibrin Norm <0.5 mcg/ml More specific for DIC than FDP test Uses: diagnosis of thrombosis, DIC, hyperfibrinolytic coagulopaties and therapeutic thrombolysis
Hemorrhagic Disorders Congenital Von Willebrand’s disease Extrinsic pathway defect Intrinsic pathway defect Common or multiple pathway defects Fibrinogen deficiency, Primary fibrinolysis XIII deficiency
Hemorrhagic Disorders Acquired Vitamin K deficiency Liver disease DIC Thrombocytopenia
Hemorrhagic Disorders Physical exam findings Petechiae--platelet defect Ecchymosis--coagulation defect Palpable spleen Other abnormalities which could indicate systemic illness associated with hemorrhagic or thrombotic disorders
Thrombocytopenia: Less than 150,000 platelets/mm3
Prolonged bleeding time: 50,000-75,000
Spontaneous bleeding: 10,000-20,000
Thrombocytopenia Pathophysiology Inadequate production Peripheral destruction
Causes of inadequate production by bone marrow: Stem cell defect Invasion of marrow by carcinoma Drug induced reduction Vitamin B12, folic acid deficiencies
Thrombocytopenia Causes of peripheral destruction: Hyperfunctioning spleen with splenomegaly Nonimmune DIC- TTP--Thrombotic thrombocytopenic purpura Both life threatening emergencies Immune--mediated by antibodies HIT--Heparin induced thrombocytopenia ITP--Idiopathic thrombocytopenic purpura
Idiopathic Thrombocytopenic Purpura ITP (An Autoimmune Disease) Etiology: Immune thrombocytopenia Acute or childhood form Chronic or adult form
ITP: Acute form Childhood Form Males: females equal Age of onset: 2-6 years Common in childhood Preceded by viral illness such as Epstein-Barr or varicella Serious bleeding uncommon Epistaxis is common Resolve w/o intervention 1-3
ITP: Acute form Physical findings Petechiae dependent extremities Splenomegaly not seen Generally, there are no other physical findings
ITP: Acute form Laboratory Platelet count <20,000
ITP: Acute form Treatment Unnecessary Corticosteroids may be given to boost platelet counts Clinical course is 2-6 weeks Consider limiting contact sports until clinical course is over
ITP: Chronic form Adult Form Age of onset: 20-50 years 2 females: 1 male Onset: Insidious onset Not associated with prior infection Serious bleeding uncommon Easy bruising, minor bleeding
ITP: Chronic form Physical findings Petechiae, ecchymoses, purpura(confluent petechiae or ecchymoses Menorrhagia, epistaxis, gingival bleeding Hematuria, melena Palpable spleen is rare
ITP: Chronic form Laboratory Platelets 20,000-80,000 Bone marrow biopsy excludes other cause for thrombocytopenia Platelet antibody assay helpful but not definitive Diagnosis is clinical diagnosis of exclusion
ITP: Chronic form Treatment-more complex than childhood form Corticosteroids Intravenous Immune Globulin Rho(D) Immune Globulin is effective in RH pos & with functional spleen Splenectomy in surgical candidates 10% will have persistent thrombocytopenia unresponsive to therapy Clinical course months to years
Deep Vein Thrombosis Pathophysiology: DVT is promoted by abnormality of any of the elements of Virchow’s triad: Blood vessel-vascular intimal injury Blood flow-stasis Blood constituents-hypercoagulability
Deep Vein Thrombosis 80-90% of clinically significant PE’s arise from deep veins of lower extremities Greatest risk for PE from proximal lower extremity Thrombi confined to calf do not cause significant PE Pelvic veins, axillary, and subclavian veins are other sites
Deep Vein Thrombosis History: Determine if risk factors for thromboembolism In many patients, significant risks converge to promote DVT development Low: <40, no other risk factors, general anesthesia<30 minutes Medium: >40, general anesthesia>30 minutes
Deep Vein Thrombosis High: Predisposing risk factors Prolonged immobilization, ICU CHF, MI Prior DVT or PE Malignancy Obesity Age>65 Hip fracture/replacement/knee replacement Pelvic/lowered extremity trauma or surgery Inherited and acquired coagulation defects
Deep Vein Thrombosis Subset has predisposition due to hypercoagulable state: Primary or congenital disorders (rare); deficiencies and gene mutations Family history of thrombosis Unexplained recurrent events Despite adequate anticoagulation poor resolution
Deep Vein Thrombosis Secondary Disorders Nephrotic syndrome Vasculitides Liver disease Peripartum period Malignancy Estrogen therapy Acquired platelet disorders Hyperviscosity syndromes
Deep Vein Thrombosis Physical exam findings Unilateral edema Calf pain Homan’s sign(only positive in 50%) Erythema Bilateral, generalized leg edema could indicate DVT obstruction of inferior vena cava Pale, cool extremity or cyanosis of skin could indicate iliofemoral venous thrombosis
Deep Vein Thrombosis High probability if >3 criteria met: Paralysis/plaster immobilization Bedridden 3 days and/or surgery Localized tenderness deep venous system Active cancer Swelling of entire leg Calf swelling >3 cm when compared to other Collateral superficial vein dilation no alternative diagnoses
Deep Vein Thrombosis Other factors to consider Hypercoagulable states Recent pregnancy Lupus
Deep Vein Thrombosis Differential Cardiac or pulmonary etiologies Severe anemia Severe hypoalbuminemia Gout Obstruction of venous return--various etiologies Malnutrition Preeclampsia or Cushing's syndrome Venous stasis disease Cellulitis Lymphedema Acute glomerulonephritis
Deep Vein Thrombosis Laboratory evaluation D-dimer test elevated in patients with thrombosis
Deep Vein Thrombosis Diagnosis Contrast venography is definitive test Cons: Invasive study, large amounts of IV contrast Impedance plethysmography (IPG) uses mild electric current and occlusive cuff to measure thigh vein impedance Cons: Calf thrombi not detected reliably
Deep Vein Thrombosis Duplex Ultrasonography/Venous compression ultrasound examination of proximal veins of lower extremity is sensitive and specific for DVT Serial testing on days 1, 2, & 8 (Preferred) If vessel is adequately visualized and cannot be compressed, diagnosis of DVT is confirmed Disadvantages: Visualization of thrombus is unreliable
Deep Vein Thrombosis MRI (recent studies)-- sensitive for proximal DVT with added benefits of visualizing inferior vena cava, pelvic veins, and pulmonary emboli
Deep Vein Thrombosis Initial Treatment Proximal DVT (thigh) Greatest risk for PE IV Heparin--immediate inhibition of thrombus formation Risk for hemorrhage Adjust using PTT q 4-6 hours Maintain PTT in 1.5 to 2.5 times control Administered for 5 days, overlapping with coumadin
Deep Vein Thrombosis Continued Treatment Continue coumadin for 3-6 months maintaining PT at INR of 2-3.0 Alternatively, low molecular weight heparin (LMWH) Enoxaparin (1mg/kg subq bid) is approved for DVT therapy: No IV administration No PTT monitoring Ease of outpatient therapy
Deep Vein Thrombosis Distal DVT (calf) To treat?? Studies show good outcomes without anticoagulation on patients with no proximal extension of thrombus as noted on serial IPG Those that are symptomatic should be anti-coagulated
Deep Vein Thrombosis Prophylaxis Principles for use of prophylactic modalities Well-defined risk group Simple and easily implemented Safe for widespread use
Deep Vein Thrombosis Prophylaxis Risk group and DVT incidence General surgery 25% Hip replacement 50% Spinal cord surgery 70-90% Neurosurgery25% MI 25% Ischemic stroke 47% ICU patients 50%
Deep Vein Thrombosis Prophylaxis Prophylactic modalities Elastic stocking Intermittent calf-thigh-compression devices Low dose heparin adjusted to high normal or 1.5 X control Low dose heparin 5000 units SC q 8-12 hrs Low molecular weight heparin Low intensity warfarin
Anemia Definition: Anemia is reduction in blood hemoglobin. Anemia is reduction in RBC mass Pallor, weakness, breathlessness, lack of color, lack of vitality
Anemia in males Hct <41, Hgb < 13.5
Anemia in females Hct <37, Hgb < 12
Anemia is the manifestation of an underlying illness
Anemia ALWAYS represents a disorder of hemopoesis
Classification of Anemia By pathophysiology Underproduction of RBC’s Hypoproliferative anemia Maturation disorders Excessive and premature destruction of RBC’s Hemolytic anemia Blood loss
Classification of anemias By morphologic appearance Size—MCV Macrocytic Microcytic Normocytic Color—MCHC Hypochromic Hyperchromic
Hereditary spherocytosis Classified as a normocytic (or slightly microcytic) hyperchromic hemolytic anemia
Iron deficiency Classified as microcytic hypochromic iron deficiency anemia
Laboratory Red cell indices--Automated calculation MCV=mean corpuscular volume MCHC=mean corpuscular hemoglobin concentration MCH=mean corpuscular hemoglobin RDW=red cell distribution width
Laboratory MCV Average size of RBC MCV=Hct/RBC
MCV<82 Microcytic anemia
MCV 82-98 Normocytic anemia
MCV>98 Macrocytic anemia
Laboratory MCHC weight of hemoglobin per volume of RBC’s MCHC=Hgb/Hct
MCHC <31.5 gm/dl Hypochromic
MCHC 32-34 gm/dl Normochromic
MCHC >36 gm/dl Hyperchromic
RDW is measure of variability in Cell Size
RDW is One of the earliest indicators of Iron Deficiency Anemia
RDW increased in conditions in which there is large variation in RBC size
Peripheral blood smear smear-imperative in evaluation of anemias Direct examination of morphology of RBC’s Diagnostic in some cases
Cell abnormalities Target cell Circular zone of pallor with peripheral and central color Liver disease, hemoglobinopathy, ** characterize thalassemia Seen after splenectomy
Spherocyte--Round, small Spherocytosis, hemolytic anemia
Schistocyte--helmet, triangular, fragmented RBC (Disrupted RBC) DIC Thrombocytopenic purpura Hemolytic Anemia Syndrome
Teardrop cell--pear Myeloproliferative diseases Thalassemia major Severe iron deficiency
Macroovalocyte--large egg-shaped B12 or folate deficiency
Peripheral smear terminology Anisocytosis-excess inequality in erythrocyte size Poikilocytosis--variation in shape of RBC
Reticulocyte count Gives indication of bone marrow’s ability to respond to anemia by increased production
Normal bone marrow can increase usual reticulocyte count by _______________ in response to blood loss or destruction 6-8 fold
If patient has low Hct or large numbers of very young reticulocytes released, the lab will report result as corrected
Ferritin Protein that indirectly reflects iron level
Normal ferritin 12-150ng/mL females
Normal Ferritin 12-300 Males
Serum iron Normal 60-170 mcg/dL
TIBC--total iron binding capacity Norm 255-450mcg/dL
% Saturation=Fe/TIBC Norm 20-50% Another way of expressing TIBC
*****Ferritin level is highly sensitive for Iron deficient anemia
Microcytic Anemias By definition MCV<82 Check MCHC-hypo or hyperchromic Microcytic hyperchromic Hereditary spherocytosis
Microcytic hypochromic anemia Iron deficiency anemia Lead poisoning Sideroblastic anemia; PZA, INH induced Anemia of chronic disease (also normocytic normochromic) Hemoglobinopathies Sickle cell Thalassemias
Lead poisoning causes anemia primarily by inhibiting enzymes important to heme synthesis. Lead may also cause hemolysis. Peripheral blood smear will show basophilic stippling of the red cells. Lead or plumbism usually results in a normocytic hypochromic anemia, although it may also cause a microcytic anemia.
INH inhibits pyridoxal kinase may cause a pyridoxine-responsive sideroblastic anemia
Sickle cell hemoglobinopathy may be microcyti but is primarily normocytic.
Thalassemia minot is 90% probable if significant microcytosis is found to accompany a mild anemia
Over ___ different abnormal human hemoglobins have been described. 350
Iron Deficiency Anemia Pathophysiology Decreased hemoglobin Maturation abnormality Decreased red cell production
Iron Deficiency Anemia Most common cause of anemia in the US Etiology Decreased dietary intake Teens, infants (cow’s milk), elderly Impaired absorption Malabsorption--inflammatory bowel disease, sprue, surgical resection of proximal bowel
Iron Deficiency Anemia Increased requirements Rapid growth Pregnancy
Iron Deficiency Anemia Blood loss Menstruating females GI loss in postmenopausal females and men Intravascular hemolysis Loss of iron via urine in case of hemolysis from malfunctioning prosthetic heart valve
Iron Deficiency Anemia Clinical Findings Common to all anemias: Fatigue Weakness Headache
Iron Deficiency Anemia Clinical Findings Specific to IDA Chelitis-cracks at corners of mouth Stomatitis-oral sores Koilonychia-spoon nails Dysphagia-esophageal webs Pica-especially ice craving
Iron Deficiency Anemia Laboratory diagnosis Anemia Microcytic hypochromic RBC’s Varying RBC size and shape leading to elevated RDW
Iron Deficiency Anemia Confirmed by Lo serum iron (Fe) High TIBC Lo serum ferritin (Key Test !!!!)
Iron Deficiency Anemia Treatment Start FeSo4 60 mg elemental iron, 1 tab daily, increasing to 2 -3 tabs daily to avoid GI upset Check reticulocyte count (should increase) in 1 week Continue iron therapy for several months Search for cause must be found and treated appropriately
The Thalassemias Pathophysiology Microcytosis out of proportion to the degree of anemia -Hereditary hemoglobinopathies -Reduction in the synthesis of the globin chains-either alpha or beta -hypochromic/microcytic results due to defective hemoglobinization of the RBC’s
The Thalassemias Hemoglobin Physiology Hemoglobin A-98% of adult hemoglobin; formed from a tetramer of 2 alpha and 2 beta chains -Alpha Globin-2 copies of this gene on chromosome 16 No Subs -Beta globin-resides on chromosome 11 next to genes that can encode “beta-like” chains-delta and gamma
The Thalassemias Alpha Thalassemia: Etiology Primarily seen in persons from China and Southeast Asia, sometimes in Afro-Americans -Disorders caused by gene deletion -Silent carrier when 3 of the 4 copies of the alpha chain are present
Alpha Thalassemia Trait Form of Thalassemia minor-2 of the 4 copies the alpha chain are present -Clinical Findings: none
Alpha Thalassemia Trait Lab Findings -Laboratory Findings: mild anemia with HCT’s between 28-40%; MCV is very low-60-75; RBC count normal; Smear shows mild abnormalities such as microcytes, hypochromia; Reticulocyte count normal -Is a diagnosis of exclusion
Hemoglobin H disease/Alpha Thalassemia Only one alpha-globin chain out of the 4 are present and there will be an excess of beta chains, thus Hemoglobin H -Clinical Findings: Pallor, splenomegaly, exacerbations of hemolytic anemia
Hemoglobin H disease/Alpha Thalassemia Laboratory Findings: HCT between 22-32%; MCV very low 60-70; Peripheral smear very abnormal-hypochromia, microcytosis, poikilocytosis; Reticulocyte count elevated; Hemoglobin electrophoresis shows HGB H
Beta Thalassemia: Etiology Seen in persons of Mediterranean origin; some Asians and Blacks beta-chain reductions or absences, excess of alpha chain, and gamma or delta chain substitutions leads to damaged RBC membranes & widespread hemolysis and overproduction of bone marrow
Beta thalassemia minor -Heterozygous for beta thalassemia Clinical Findings: None -Laboratory Findings: Mild anemia HCT between 28-40%; MCV between 55-75; RBC count normal; Peripheral smear slightly abnormal; Reticulocyte count normal or sl. elevated
Beta thalassemia major (Cooley’s or Mediterranean A Anemia. This is the severe transfusion dependent anemia that can be fatal by late childhood -Homozygous for beta thalassemia Clinical Findings: growth failure, bony deformities, hepatosplenomegaly, jaundice, heart failure, iron overload (hemosiderosis) secondary to numerous transfusions Lab Findings:HCT below 10; poikilocytosis, hypochromia, microcytosis, basophilic stipling
The Thalassemias Diagnosis Laboratory will show: -Mild Forms: Modest anemia with low MCV, abnormal peripheral blood smear, normal RBC
The Thalassemias Diagnosis Laboratory will show: -Severe Forms: Diagnosis made by hemoglobin electrophoresis to differentiate from other hemoglobinopathies
The Thalassemias Treatment: Mild Forms No treatment necessary; Identification very important to avoid inappropriate iron supplementation and to receive genetic counseling
The Thalassemias Treatment: Severe Forms: Regular blood transfusions, folate supplementation, splenectomy, Deferoxamine given as an iron-chelating agent, low iron diet, bone marrow transplant for children with beta thalassemia major, genetic counseling
Macrocytic Anemias By definition MCV>98 Megaloblastic--large red cells that result from impaired DNA synthesis More time for cell growth between cell divisions resulting in larger cells
Macrocytic Anemias Macrocytic anemia associated with megaloblastic morphology in the bone marrow, however, not all macrocytic anemias are megaloblastic
Macrocytic normochromic anemia Hypothyroidism B12 deficiency Folic acid deficiency
Hypothyroidism can cause a macrocytic anemia. More than 50 % of patients with hypothyroidism demonstrate an asociated macrocytic anemia.
Reticulocytes are larger than normal RBC’s and may raise the MCV to the macrocytic range when reticulocytosis is marked (>10-20%)
Macrocytic normochromic anemia Increased reticulocyte count as in Hemolysis Posthemorrhage Antimetabolite administration Long term sulfa drugs Myelodysplastic (refractory) anemias
Vitamin B12 and Folate Deficiency Pathophysiology Megaloblastic maturation abnormality of RBC’s Folate and B12 deficiency impairs folic acid cycle
Vitamin B12 and Folate Deficiency Etiology Inadequate intake B12--rare Folate--poor diet or long term oral antibiotics Malabsorption B12--usual cause is pernicious anemia Other --competition from bacterial overgrowth or tapeworm Folate--Sprue, celiac disease in children
Folate Deficiency Increased demand Pregnancy Chronic hemolysis Exfoliative dermatitis
Folate Deficiency Interference with metabolism Alcohol abuse Anticonvulsants Oral contraceptives Antimetabolites
Vitamin B12 and Folate Deficiency Clinical Findings Insidious onset Asymptomatic until severe anemia Folic acid stores only last 3 months B12 stores last for 3 or more years
Symptoms B12 deficiency Can occur with minor anemia Adult: Age >40, northern European descent Can occur in young black women Congenital: Rare, autosomal recessive Impaired vibratory, position sense Ataxia or spastic gait Mental status changes If untreated, irreversible
Vitamin B12 and Folate Deficiency Laboratory Diagnosis Peripheral blood smear shows oval macrocytes and hypesegmented neutrophils
Vitamin B12 and Folate Deficiency Laboratory Diagnosis Confirmed by Low B12 or Folate level Bone marrow-megaloblastic maturation of all 3 cell lines B12 deficiency-- need to determine site of malabsorption Schilling test--three parts
Vitamin B12 and Folate Deficiency Treatment Folic acid 1 mg daily Vitamin B12 1000mcg IM weekly X 4 then 100 mcg IM q month Oral forms of B12 have similar efficacy
Vitamin B12 and Folate Deficiency Treatment Caution: Must differentiate between B12 and folate deficiencies as treating with folate alone will improve the anemia of B12 but will not affect the neuro impairment that can become irreversible if untreated.
Normocytic Anemias By definition MCV 82-98 Normocytic, normochromic anemia Check the reticulocyte count (corrected) Anemia with increased production >1.5% Check peripheral smear Normal smear--anemia most likely due to blood loss somewhere Smear with hemolysis--hemolytic anemia
Normocytic Anemia Normal or decreased production<1.5% R/O dilutional anemia (proximal IV site) Inadequate marrow production Will need bone marrow aspiration to diagnose (hematologist , pathologist) Aplastic anemia Myeloma, lymphoma, leukema Granulomatous, lipid storage diseases Congenital dyserythropoietic anemias Early iron deficiency Anemia of chronic disease--normal bone marrow
Anemia of Chronic Disease Normocytic normochromic or mildly microcytic hypochromic Etiology: Chronic inflammation from Autoimmune disorders Rheumatoid arthritis Infections Cancer
Normocytic normochromic or mildly microcytic hypochromic Pathophysiology: Inflammatory mediators (poorly understood) block iron utilization by RBC precursors Storage iron tends to build up (elevated ferritin) Circulating iron is low (lo serum iron)
Anemia of Chronic Disease Clinical symptoms Fatigue, weakness, headache
Anemia of Chronic Disease Laboratory Hi ferritin Lo serum iron Lo TIBC Hct rarely below 28% May be difficult to differentiate from IDA as can occur simultaneously in the patient with chronic disease
Anemia of Chronic Disease Treatment Diagnose and treat underlying disorder Clients will need frequent rest
Hemolytic Anemias Pathyphysiologic abnormality in hemolysis Shortening of RBC survival Normal RBC survives 100-120 days Multiple causes Usual response of the bone marrow to hemolysis is an increase in erythropoiesis as seen by elevated reticulocyte count.
Hemolytic Anemias Intrinsic defects- usually congenital
Hemolytic Anemias Extrinsic defects- usually acquired
Hemolytic Anemias Clinical Findings Jaundice Cholelithiasis or splenomegaly if congenital or chronic hemolysis Similar family history Suspect hemolysis when retic count is elevated in the absence of blood loss
Hemolytic Anemias Laboratory Anemia Elevated reticulocytes Peripheral smear with hemolysis and abnormalities in cell shape Check direct Coombs Positive indicates the hemolysis due to immune system destruction Autoimmune hemolytic anemia (AIHA)
Hemolytic Anemias Negative Coombs Mechanical causes radiation, artificial heart valves, insect, snake bites, malaria, leishmaniasis, clostridia Burns, extreme temperatures, hypersplenism, RBC cell membrane abnormalities Hereditary spherocytosis Hereditary elliptocytosis
Hemolytic Anemias RBC abnormal internal structures G-6-PD deficiency--hemolysis with drugs (antimalarials, sulfonamides, Vitamin K, probenecid, chloramphenicol)
Hemolytic Anemias Hemoglobinopathies Thalassemias Sickle cell anemia
Glucose-6-Phosphate Dehydrogenase Deficiency (G6PD) Common Disease Characteristics X-linked recessive disorder -Common in Afro-american males-10-15% and some of mediterranean, middle-eastern, asian descent -Episodic hemolytic events
G6PD Pathophysiology: Hereditary enzyme defect that causes RBC’s to be vulnerable to oxidative stressors -Hemoglobin undergoes oxidative denaturation and form precipitants called Heinz bodies which causes cell damage and ultimate removal by the spleen
G6PD Clinical Findings: Female carriers rarely affected -Healthy until exposed to certain drugs, and chemicals-dapsone, quinidine, sulfa, nitrofurantoin,benzene, high doses of Vitamin C, moth balls, or have infection and then will have a hemolytic episode
G6PD Laboratory Findings: -Heinz bodies on peripheral smear -Enzyme assays may reveal low level of G6PD -Elevated reticulocyte count
G6PD Treatment: -None -Supportive and avoid certain drugs
Sickle Cell Anemia Etiology Inherited disease in African descent Trait occurs in 8-10% of Afro-Americans
Sickle Cell Anemia Pathophysiology Defective gene on the beta globin chain forming Hemoglobin S Hemoglobin S forms polymers that damage the RBC cell membrane thus causing sickling Hemolysis occurs due to abnormal rigidity of deformed cell membrane
Sickle Cell Anemia Two main forms Homozygous sickle cell anemia Severe, constant, hemolytic anemia Heterozygous sickle cell trait 20-40% RBC’s abnormal
Sickle cell variants Abnormal Hgb S plus other hemoglobinopathies Rarely, induced sickling with severe hypoxia
Sickle Cell Anemia Clinical findings Constant hemolytic anemia Vasooclusive (painful) crises infarctions of chest, abdomen, skeleton Aplastic crises Result of infection During infection, compensatory RBC production impaired
Sickle Cell Anemia Clinical findings (con’t) Avascular necrosis of the hip or shoulder Osteomyelitis (salmonella) as a sequela Cardiomegaly and pulmonary disease Priapism Acute chest syndrome Fever, pleuritic pain, lung infiltrates, hypoxemia Fatal in 2-14% of cases
Sickle Cell Anemia Clinical findings (con’t) Stroke Nephrotic syndrome Blindness, retinal detachment First symptoms at 6-12 months of age Survival beyond 30’s uncommon
Sickle Cell Anemia Laboratory Hemoglobin electrophoresis-Hgb S Peripheral smears-grossly abnormal with sickled RBC’s, nucleated RBC’s, & evidence of hyposplenism like target cells & Howell-Jolly bodies Wright-stained blood smears-easily seen sickled cells 5-50% of RBC’s
Sickle Cell Anemia Treatment Genetic counseling for those with sickle cell trait Supplementation with 1 mg Folic acid daily Prevention of infection by prompt antibiotic therapy Prevention of infection via vaccination
Sickle Cell Anemia Vasooclusive crises Analgesics, IV fluids, oxygen Partial exchange transfusions if vasooclusive crisis prolonged
Sickle Cell Anemia Pregnancy Maintain Hct at 25% Sickle cell blood closest to normal viscosity
Aplastic Anemia Essential Characteristics: -Pancytopenia -No abnormal cells -Hypocellular bone marrow
Aplastic Anemia Physiology -This anemia is the result of bone marrow failure whether from injury or the inability to produce normal stem cells. -Causes of stem cell injury or suppression: radiation, chemotherapy, toxins, drugs, pregnancy, lupus, or autoimmune
Aplastic Anemia Laboratory Findings -Pancytopenia is the hallmark sign -Always associated with decreased reticulocyte count -MCV normal -No abnormal RBC’s seen
Aplastic Anemia Treatment -Treat the cause -Mild cases blood & platelet transfusions given when necessary and antibiotics to treat infections -Severe cases-children bone marrow transplant/umbilical blood; adults treated with immunosuppression and antithymocyte globulin (ATG)
The degee of closeness a test meets to the "gold standard" is: Accuracy
probability that a test will be positive when it is applied to a person who actually has the disease? Sensitivity
Which inherited anemia is characterized by the presence of hemoglobin S? Sickle cell
Physical findings in association with a possible bleeding disorder include petechiae and ecchymoses.  Petechiae are generally associated with a __________defect, whereas ecchymoses are associated with a_____________ defect. platelet, coagulation
Spontaneous bleeding will occur with a platelet count of 10,000-20,000
Which of the following laboratory tests would be elevated in a patient with thrombosis? D-dimers
In uncomplicated HTN, the specific drug of choice is less important than the attainment of goal blood pressure
the attainment of goal blood pressure 90% lifetime risk for developing HTN.
The higher the b/p the greater the risk for ischemic heart disease, MI, heart failure, and kidney disease
Abdominal Obesity Promotes increased systemic inflammation cytokines: tumor necrosis factor, interleukins etc.
angiotensin II II-A POTENT VASOCONSTRICTOR
Sympathetic Nervous System: Often found in younger clients May exhibit tachycardia & increase in cardiac output Insensitivity of the baroreflexes may play a role with adrenergic hyperactivity
Intracellular sodium and calcium: An increase in intracellular Na may lead to increased cellular calcium causing increase in vascular smooth muscle contraction.
Hypertension-Defect in natriuresis Normally there is an increase in renal sodium excretion in response to elevations of arterial pressure. Some pt with HTN exhibit a diminished ability to excrete sodium
HTN - Exacerbating factors: Obesity: increase in intravascular volume & cardiac output sodium intake may increase HTN in some clients aerobic exercise has been shown to decrease b/p in previously sedentary clients
Alcohol: raises blood pressure possibly by increase in plasma catecholamines
Cigarette smoking: increasing norepinephrine
Polycythema: increases blood viscosity
NSAIDs: may increase B/P average of 5 mm Hg.
Potassium: Low K+ intake may be associated with B/P elevations.
Estrogen Use: A small increase in B/P is associated with oral contraceptive, occ. will have significant increase. Increase in blood pressure thought to be due to volume expansion through renin-angiotensin-aldosterone system.
Chronic sleep apnea: Now considered an identifiable cause of HTN Loud snoring, daytime sleepiness, obesity, large neck Diagnosis with a sleep study
Primary hyperaldosteronism/Cushings Excess aldosterone secretion< 0.5% cause of HTN Lesion is usually an adrenal adenoma Consider if pt also has hypokalemia Diagnosed by CT or MRI Urine aldosterone concentration is elevated-collect 24 hr urine
Guidelines from the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure The Eighth Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 8 released Dec. 18th 2013)
In the general population age at or > age 60 initiate drug therapy at or greater than 150/90. (Level A) If the patient’s blood pressure is lower than 140- for systolic based on previous guidelines, it is not necessary to adjust if patient tolerates the lower BP. Some panel debate on risk for higher BP.
In the general population patient at or < 60, initiate drug therapy to lower BP at DBP at or greater than 90. 30-59 years, strong recommendation Grade A 18-29 Grade E
In the general population younger than age 60, initiate pharmacologic treatment to low SBP of 140 or higher and to treat to goal of SBP lower than 140mm Hg. Grade E
In the population aged 18 years or older with CKD, initiate pharmacologic treatment to lower BP at SBP of 140 mm Hg or higher or DBP of 90 mm Hg. And treat to goal of SBP lower than 140 mm Hg and goal of DBP lower than 90 mm Hg. Applies to individuals younger than 70 and GFR less than 60 Grade E
In the population age 18 years or older with diabetes, initiate pharmacologic treatment to lower BP at SPB of 140 mm Hg or higher or DBP of 90 mm Hg or higher. Grade E
In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker. Did not recommend beta-blockers for initial treatment. In one study B-blockers results in higher rate of CVD events Grade B
In the general black population, including those with diabetes, initial antihypertensive treatment should include of thiazide type diuretic or CCB For general black population Grade B For general black population with diabetes Grade C
In the general population age 18 years or older with CKD and hypertension, initial or add-on antihypertensive treatment should include an ACE or ARB to improve kidney outcomes. This applies to all CKD patients with HTN regardless of race or diabetes. No evidence to support benefit in those 75 years and older, use of a thiazide-type diuretic or CCB is an option for treatment Grade B
If the goal BP is not reached within a month, increase the dose of initial drug or add on a second goal from one of the classes recommended (thiazide, CCB, ACE or ARB). Do not use ACE and ARB together If goal is not met with 3 drugs may consider referral to an HTN expert Grade E
Thorough History / Exam - htn History Family history--Important!! Personal History-Risk factors--Important Exam Fundoscopic-narrowing of vessels hemorrhages, papilledema (not always done) Carotid bruits - IMPORTANT!! Enlarged kidneys, renal bruits Peripheral edema! and pulses
HTN Laboratory Evaluation *Renal Function *Lipids to evaluate CVD *Electrolytes-serum K+ *FBS-elevated in diabetes and pheochromocytoma Uric acid level-if elevated relative contraindication for diuretic not commonly done for routine screen.
High Sensitive C-Reactive Protein Marker for inflammation Usually elevated with atherosclerosis or conditions associated with CVD, smoking, obesity, hyperglycemia Treat with eliminating risk factors, ie: smoking, increase exercise, etc Control lipids Consider ASA therapy
Lipid Profile Profiles Lipo (a): an atherogenic/prothrombotic subparticle of LDL Particle size and concentration of lipids Small size HDL and LDL are more atherogenic than large size Pattern A-Optimal with Large LDL/HDL bad small size
Who should be treated for HTN - Evaluate overall cardiovascular risk Framingham Reynolds includes family history American Heart Association http://www.heart.org/HEARTORG/Conditions/HeartAttack/HeartAttackToolsResources/Heart-Attack-Risk-Assessment_UCM_303944_Article.jsp See JNC 8 Guidelines
HTN - Lifestyle Modifications Lose weight if overweight Limit alcohol Increase aerobic exercise to 30-45 minutes 4-5 times per week - sodium intake Maintain adequate intake of dietary potassium, calcium, and magnesium. no smoking Reduce dietary saturated fat and cholesterol
American Heart Association/American College of Cardiology Joint Health y Living Clinical Practice Guidelines Fruits: 4-5 servings Vegetables: 4-5 servings Whole grains preferably high fiber: 6-8 serving Fat-free or low-fat milk and mild products: 2-3 Lean meats, poultry or fish: 6 or fewer ounces Nuts, legumes and seeds: 4-5 servings per week Fats and o
Pregnancy ACE-category D typically will use beta blocker
Diuretic Increase risk for gout exacerbation
Side Effects With Diuretics Hypokalemia Hyperuricemia (increase gout) Hyperglycemia (caution with diabetics) Hypovolemia Hyperlipoproteinemia (increase atherosclerosis) Increase in triglycerides and LDL cholesterol with thiazides
Beta 1 EFFECTS THE HEART
Beta 2 Effects the lungs
Beta Blockers Taper when stopping. Can blunt the effect of stress testing.
Calcium Channel Blockers Adverse Reactions Peripheral edema, hypotension, headache, dizziness, fatigue, constipation, muscle cramps, rash, and exacerbation of heart failure or angina. Concurrent use of B-blockers with verapamil or diltiazem can lead to cardiac depression. However, B-blockers with
Simvastatin risk New warnings with the use of amlodipine with simvastatin greater than 20mg for increase risk for muscle damage (Prescriber’s Letter Sept. 2011; Vol. 18)
High-intensity statin therapy generally results in an average LDL reduction at or greater than 50% Atorvastatin 40-80mg Rouvastatin 20-(40) mg
Moderate -intensity statin therapy generally results in an average LDL-C reduction of 30-<50% Atorvastatin 10-20 mg Rouvastatin 5-10 mg Simvastain 20-40 mg (80mg not advised due to myopathy) Pravastatin 40-80mg Fluvastatin XL 80mg Fluvastatin 40mg bid Pitavastin 2-4 mg
1st heart sound closing of mitral valve (^ LV pressure)
2nd heart sound closing of aortic valve ( decrease ventricular pressure)
preload volume of blood in ventricle at end of diastole
afterload force ventricles must contract to eject blood
Frank-Starling phenomenon as preload ^, ventricle stretches ensuring ventricular contraction becomes more rapid and forceful
Increase in afterload is R/T HTN, aortic valve stenosis, ventricular hypertrophy
Decrease in afterload ACE inhibitors, hydralzine
Contractility- + inotropic effects : digoxin, epinephrine, norepinephrine, dopamine
Contractility - inotropic effects B Blockers, CCB (work by decrease strength of ventricular contraction)
Normal Ejection Fraction 60%
Angina - ^ with exertion, cold weather, meals, stress and is relieved by rest or nitroglycerin Prinzmetal angina is not related to exertion usually lasts <2-10 minutes
MI similar to angina but usually lasts >30 min and is NOT relieved by rest or nitro
Pericarditis- sharp pain L of sternum (stabbing); lasts days/hours; aggravated by deep breathing, movement, lying supine: Pericardial Friction Rub present
Aortic Dissection- anterior chest may radiate to back, excruciating knife like tearing pain, sudden onset
PE- sharp pain that is worse with inspiration, SOB, poss pleural friction rub
Central Cyanosis- cyanosis of lips trunk and reflects R-L shunting of blood. Cyanosis in childhood-congenital heart disease with R-L shunt Epistaxis, hoarseness, hiccups, fever, chills may reflect underlying heart disease.
Congenital Heart Disease Assoc with chromosomal disorders, gene defects, teratogens, maternal metabolic disease Divided into 3 types: L-R shunt ^ pulmonary blood flow R-L shunt Obstructive Stenosis
Created by: kcorkinsnctc