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359 Cards in this Set
- Front
- Back
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what are the normal ranges of RBC
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4.25-6.1
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what are the ranges of WBC
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5000-10000mm
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what is the normal range of monocytes
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2-8%
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what is the normal range of neutrophils
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45-73%
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what is the normal range of platelets
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150000-400000
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what is the normal level of HCT males
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42-52%
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what is the normal level of HCT females
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35-47%
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what is the normal level of HbB males
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13-18
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what is the normal HgB in females
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12-16
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what are 5 se of aspirin (body as a whole)
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hypersensitivity
urticaria bronchospasm anaphylactic shock laryngeal edema |
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what are the 3 se of aspirin (cns)
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dizzinesss
confusion drowsiness |
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what are the 9 se of aspirin (gi)
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nausea
vomitting diarrhea anorexia heartburn stomach pains ulceration occult bleediing |
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what are the 4 se of aspirin (hematologic)
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thrombocytopenia
hemolytic anemia prolonged bleeding time |
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what are the 3 se of aspirin (skin)
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petechiae
easy bruising rash |
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what is the 1 se of aspirin (urogenital)
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impaired renal function
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anticoagulants delay the clotting time of blood and do what else?
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prevents the extension of a thrombus after it has formed
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anticoagulants do not do what?
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dissolve a thrombus that has already been formed
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what is unfractionated heparin used to prevent
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the extension of thrombus and development on new thrombi
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unfractionated heparin is administered how?
how do you know its affective? |
by sq or continuous infusion 5-7 days
when ptt is 1.5 x control |
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what are 2 of the low molecular weight heparin
what are they used for |
enoxaprin (lovenox)
dalteparin (fragmin) pt at risk or at risk for extension |
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how do you administer LMWH?
longer or shorter half life? |
sq
longer half life |
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with LMWH you can give 1-2 sq daily but how do you have to adjust it
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adjust to weight
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LMWH has few ___ and lower risk of ___
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few bleeding complications
risk of heparin induced thrombocytopenia |
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which is more expensive LMWH or unfrac hep
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LMWH
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what is the oral form of anticoagulants
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warfarin (coumadin)
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what is coumadin
how do you tell if its affective |
a vit k antagonist used for extended therapy
pt is 1.5-2 x normal inr is 2.0-3.0 |
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meds or foods containing vit k can do what
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reduce or enhance anticoagulant effects
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coumadin has a ___ therapeutic window and a ___ onset of action
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narrow
slow |
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APPROXIMATELY 95% OF CLIENTS WITH CML ARE...
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PHILADELPHIA CHROMOSOME-POSITIVE.
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THIS REPRESENTS WHAT?
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A TRANSLOCATION OF LONG ARM OF CHROMOSOMES 9 & 22
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THE ISCHEMIA THAT CAUSES MI CAN ALS CAUSE WHAT?
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THE HEART MUSCLE TO BECOME IRRITABLE AND IRRITAED CELLS FIRE EARLY, CAUSING DYSRHYTHMIAS.
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RT. SIDED HEART FAILURE LEADS TO...
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BACKWARD VENOUS CONGESTION
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RESULTING IN...
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JUGULAR VEIN DISTENTION
PORTAL HYPERTENSION ABDOMINAL VENOUS CONGESTION RESULTING IN ASCITES. |
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LEFT VENTRICULAR EJECTION FRACTION THAT IS LOW IN A PT. WITH SIGNS OF CHF MIGHT BE...
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PUT ON HEPARIN T PREVENT THROMBUS FORMATION IN THE LEFT VENTRICLE.
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THE PRESENCE OF THE ANTIGEN H BsAG CONCLUDES WHAT?
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THAT THE CLIENT HAS AN ACTIVE FORM OF THE DISEASE SINCE HEP. B SURFACE ANTIGEN IS PRESENT.
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DEPOLARIZATION OF THE MYOCARDIUM RESULTS IN CONTRACTION (SYSTOLE) & THAT PRODUCES...
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THE PALPABLE PULSE AND THE CORRESPONDING QRS COMPLEX ON THE ELECTROCARDIOGRAM
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DECREASED BLOOD VOLUME MUST BE PREVENTED IN ORDER TO WHAT?
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DECREASE MYOCARDIAL OXYGEN DEMAND & PROMOTE CORONARY BLOOD FLOW IN PATIENTS WITH ANGINA
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MOST COMMON COMPLICATION OF MI
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ARRHYTHMIAS
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what are the diagnostic tests for anticoagulant therapy
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aPTT
PT INR ACT Hgb Hct platelet count fibrogen levels |
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what is the normal level for PT and INR and fibrin and Ptt
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pt 11-13 sec
inr 2 to 3.5 seconds fibrinogen 200-400 ptt 25-35 sec (1.5-2.5 x normal) |
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what are the 3 reasons for anemias
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loss of RBC
decreased production increased destruction |
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the medical management for anemia is directed towards doing what 3 things
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correcting
controlling replacement |
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nursing management for anemia is directed at what managing and maintaining what 2 things
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managing fatigue
maintaining nurtrition/perfusion |
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aplastic anemia decreases or damages what
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bone marrow stem cells
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what are the 7 types of anemia
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aplastic
iron deficient megaloblastic thalassemia vit b12 sickle cell |
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witch aplastic anemia (idiopathic aplastic anemia) what 3 things get decreased
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decreased RBC
WBC Platelets |
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with aplastic anemia how many RBCs lost and they may be what?
???? look up |
1 million or fewer RBCs
larger than normal (macrocytic) |
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what are the S/S of aplastic anemia
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gradual onset
weakness dyspnea (exertion) abnormal bleeding headache pallor |
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THE BEST TX OF ACUTE HEP B (NOT CHRONIC)
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ADEQUATE NUTRITION & REST
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ALDOCTONE IS WHAT KIND OF AGENT?
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ALDOSTEONE BLOCKING
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ALDACTONE IS THE FIRST LINE OF THERAPY IN PATIENTS WITH WHAT TWO THINGS
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ASCITES FROM CIRRHOSIS
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WHEN USED WITH OTHER DIURETICS ALDACTONE PREVENTS WHAT?
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POSTASSIUM LOSS
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LASIX MAY BE ADDED BUT SHOULD BE USED CAUTIOUSLY WHY?
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BECAUSE LONG TERM USE MAY INDUCE SEVERE SODIUM DEPLETION (HYPONATREMIA)
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THE ANSWER WAS GIVE THE ALDACTONE HOLD THE LASIX
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...
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FOR PATIENTS WITH ADVANCED CIRRHOSIS LACTULOSE WILL IMPROVE WHAT?
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NERVOUS SYSTEM FUNCTION (BINDING THE AMMONIA)
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MANAGEMENT OF ACUTE PANCREANTITIS IS DIRECTED TOWARD WHAT?
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RELIEVING SYMPTOMS AND PREVENTING OR TREATING COMPLICATIONS.
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WHY IS ORAL INTAKE WITHHELD?
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TO INHIBIT STIMULATION OF THE PANCREAS & ITS SECRETION OF ENZYMES.
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WHAT IS PCI
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PERCUTANEOUS CORONARY INTERVENTION
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WHAT MAY BE SUGGESTED FOR A PATIENT SUSPECTED OF HAVING AN ACUTE MI.
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PCI
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PCI MAY BE USED TO DO WHAT?
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OPEN THE OCCLUDED CORINARY ARTERY & PROMOTE REPROFUSION.
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PCI TREATS?
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ATHEROSCLEROTIC
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& SHOULD BE PERFORMED WHEN?
WHY? |
60MIN
BC THE DURATION OF OXYGEN IS RT THE NUMBER OF CELLS THAT DIED. |
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IN ORDER FOR THIS PROCEDURE TO BE DONE WHO NEEDS TO BE PRESNT?
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CARDIAC CATHERIZATION LAB & STAFF
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EARLY PCI HAS BEEN SHOWN TO BE EFFECTIVE IN PTS OF ALL AGES INCLUDING
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>75 YEARS OLD.
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TO PREVENT THE DEVELOPMENT OF HEART FAILURE IN A PATIENT WITH HYPERTENSION IT IS IMPORTANT TO WHAT?
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STRESS COMPLIANCE WITH ANTIHYPERTENSIVE THERAPY.
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BASED ON WHAT?
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KNOWLEDGE THAT SYSTOLIC FAILURE & LOW FORWARD BLOOD FLOW CAN RESULT FROM INCREASED AFTERLOAD.
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with aplastic anemia, heart failure and tachycardia are caused by what
what is aplastic anemia |
hypoxia and increased venous return
t cells attack bone marrow resulting in aplasia (reduced hematopoiesis) neurtopenia and thrombocytopenia occur |
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what is the tx for aplastic anemia
what are some complications of aplastic anemia |
-packed RBC
-platelet transfusion -bone marrow transplant (tx of choice) complications: infection, lymphadenopathy, hemorrage |
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what is iron deficient anemia
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inadequate absortption of iron or excessive loss
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what labs would you see a decrease in with iron deficient
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low hgb, rbc, mcv, mch, mchc
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with iron deficient anemia what kind of nails do you see and why
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coarsely ridged, spoon shaped, brittle thin nail
caused by decreased capillary circulation |
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what are 2 other things youd see with iron deficient
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sore, red, buring tounge
dry skin in corners of mouth |
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what is the nursing management for iron def
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iron preps
diet change |
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what are foods high in iron
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organ meats
beans leafy veggies raisings molasses |
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magaloblastic anemia is caused by deficiencies of what two things
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vit b12 and folic acid
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myelodysplastic syndroms caused by genetic factors and exposure to what two things
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chemicals or radiation
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what is myelodysplastic syndrome
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disorder of myeloid stem cells causing dysplasia or abnormal rbcs in cell line. manifested by macrocytic anemia
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what are the S/S of myelodysplastic syndromes
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pancytopenia
anemia weakness fatigue pneumonia palpitations dizziness irritability |
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what is thalassemia
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inherited people of mediterranean decent (cooleys anemia)
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what are the characteristics of thalassemia (3)
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hypochromia
microcytosis hemolysis |
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what is hypochromia
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hemoglobin in rbc less than normal
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what is microcytosis
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many microcytes in the circulating blood
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what is hemolysis
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destruction of rbc
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thalassemias are associated with defective synthesis of what; which does what
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hemoglobin;
the production of one or more globulin chains within the hemoglobin molecule is reduced |
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with the reduction, this increases the rigidity of the erythrocytes and what happens
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premature destruction of the cells
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talassemia is classified into two major groups according to which hemoglobin chain is diminished what are the 2
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alpha
beta |
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which of the two are more mild
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alpha
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with beta thalassemia the synthsis of the beta polypeptide chain is what
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defective
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how do you treat it?
what cant you use? |
no iron supplements
tx with desferal |
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why do you treat with desferal
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due to long term blood transfusion
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what is desferal
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antidote for iron toxicity
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anemia in renal disease and in chronic diseases are due to what 3 things
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decreased production
deficiency of erythroprotein shortened rbc span life |
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what is the patho for b12 def
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faulty absorption from gi tract, lack of intrinsic factor
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what does this lead to
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production of few deformed rbs with poor ox carrying capacity
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what are the labs seen with b12 def what happens to the megaloblasts
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low rbc, wbc, mch
high mcv and megaloblasts fewer and larger rbc |
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what test must be done for b12 def
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schilling test
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what are the S/S of b12 def
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pale
fatigue weakness smooth sore tongue mild diahrrea confusion paresthesias diff maintaining balance |
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what is the nursing management for vit b12
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vegetarians give b12
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what is the patho of sickle cells anemia
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inheritance of sickle hemoglobin gene
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what are the 2 clinical manifestations of sickle cell
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anemia
jaundice |
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what must this person avoid and what must they add
for pain control what would you give |
cold temps
treat infection high altitudes add folic acid give morphine: give droxia for risk of leukemia |
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with a sickle cell crisis what is happening
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tissue hypoxia and necrosis due to inadequate blood flow to specific region of tissue or organ
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what is the clinical manifestation of sc crisis
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severe pain
fever leukocytosis swelling of joints osteomylitis and pneumonia common |
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what are the 3 types of jaundice
what are se of jaundice |
obstructive
hepatocellular hemolytic itchy skin, dark urine |
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obstructive jaundice produces increased what
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occlusion of bile duct/inflammation
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hepatocellular jaundice results from injury or disease of what
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damaged liver doesnt allow normal bile to excrete
liver cannot excrete bili as fast as it is formed |
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what is the cause of hepatocellular
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liver cell toxic injury
viral infections cirrhosis infections mononucleosis reactions of drugs |
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what causes liver cell toxic injurjy
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acetaminophen overdose
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what is a reaction of a drug that is bad
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chlorpromazine
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what is hemolytic jaundic due to
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overproduction of bilirubin resulting from hemolytic processes that produce increased levels of unconjugated bilirubin
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what are the causes of hemolytic jaundice
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hereditary spherocytosis
sickle cell anemia thalassemia G6PD blood transfusion reactions |
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afterload refers to what
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the amount of resistance to the ejection of blood from the ventricle
(systolic outward flow) more common weakened heart muscle |
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what are the major factors that determine afterload
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diameter and distensibility of the aorta/pulmonary artery, opening and competence of semilunar valves
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what is the preload
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amount of blood presented to the ventricle before systole
(diastolic filling) characterized by stiff/noncompliant, heart muscle making it hard to fill |
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what is the major factor that determines preload
what do you see with r sided and l sided hf |
venous return
rside: lungs lside: body |
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what are some s/s of digoxin toxicity
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anorexia, n/v, fatigue, depression, malaise, changes in heart rate/rhythm, onset of irregular rhythm
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what are the ecg changes seen with digoxin toxicity
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sa or av block
ventricular dysrhythmias atrial tachy w/ block junctional tachy vent tachy |
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what are the risk factors for digoxin toxicity
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hypokalemia
antibiotics cardiac drugs impaired renal function |
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what does hypokalemia do
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increases action of digoxin
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what do antibiotics and cardiac drugs do
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slow av conduction and decreases hr
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what is monitored with renal function
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creatinine
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what are some ex of beta blockers
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carvedilol (coreg)
metoprolol (lopressor, toprol) |
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what do beta blockers do
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reduce adverse effects from constant stimulation of sympathetic nervous system (decreases myocardial oxygen demand)
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what do nitrates do
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cause venous dilation
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what is an ex of a nitrate
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isosorbide dinitrate
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what is a calcium channel blocker ex
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amlodipine (norvasc)
felodipine (plendil) |
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cal channel blockers are contraindicated for patients with what
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ssystolic dysfunction
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what do cal channel blockers do
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cause vasodilation reducing systemic vascular resistance
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what are some ex of ace inhibitors
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benazepril (lotensin)
capropril (capoten) enalapril (vasotec) |
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what is the action of ace
|
decreases the secretion of aldosterone; blocks the conversion of angiotensis 1 and angiotensis 2 (decrease afterload and improve contractility)
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with pt using ace inhibitors what needs to be monitored
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hypotension, hypovolemia
hyperkalemia, renal fx |
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what is a se of ace
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dry, persistent cough
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ace inhibitors casue kidneys to do what
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retain potassium
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beta blockers se are what 3 things
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dizziness
hypotension bradycardia |
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what do diuretics do
|
removes excess extracellular fluid by increassing the rate of urine produced
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what is an ex of thiazide
loop potassium sparing |
metolazone (zaroxolyn)
furosemide (lasix) spironolactone (aldactone) |
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what are the se of diuretics
|
hypotension
hyperuricemia ototoxicity |
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what is digitalis
|
digoxin (lanoxin)
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what is the action of digitalis
|
-increases
force of myocardium -slows conduction through av -improves contractility -increases l ventric output |
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a se of digitalis is what
|
enhanced diuresis
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herb milk thistle (silybum marianum) is used to treat what
|
jaundice
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SAM-e (adenosylmethione) does what
|
improves liver function
|
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an MI is aka what two things
|
coronary occlusion
heart attack |
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an mi is caused by reduced blood flow in coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of ___ by a ___
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artery by a thrombus
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what are some s/s of mi
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chest pain (continues w rest and meds)
sob indigestion nausea anxiety cool/pale/moist skin increased hr & r |
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with an ecg changes that evolve over time include what
|
t wave inversion
st segment elevation development of ab q wave |
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what are the lab tests; cardiac bio markers
|
ck-mb (cardiac muscle)
myoglobin troponin |
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what is the level for cpk (creatine phosphokinase) men and women
|
men 38-174
women 26-140 |
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ck mb (creatine kinase heart muscle) increases when and what time
|
increases when damage to cardiac cells
increases within few hours peaks within 24 hr |
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myoglobin lab values
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<90mcg/L
|
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what is myoglobin
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heme protein that helps transport o2
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where is myoglobin found
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cardiac and skeletal muscle
|
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when does the level increase, peak
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within 1-3 hr peaks within 12 hrs
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with a neg result of myoglobin what does that mean
|
r.o mi
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tropoin t lab value
troponin I |
<0.2ng/ml
<0.03ng/ml |
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troponin is a protein found in the myocardium that regulates what
|
myocardial contraction process
|
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an increased level of troponin can be detected within a few hours during acute mi and remains elevated for about how long
|
3 weeks
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what is the dx tests for mi
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ecg within 10 min
cxr echocardiography tee myocardial perfusion scan thallium 201 digital angiography coronary arteriography |
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what are some medications for mi
|
aspirin
nitroglycerin morphine beta blockers |
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ace inhibitors are administered when
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within 24 hours
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evaluate for PCI to used to open occluded coronary artery to permit reperfusion for what reason
|
the area has been deprived of oxygen
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continued therapy for mi is what
|
iv heparin or LMWH
clopidogrel (plavix) glycoprotein IIb/IIa inhibitor |
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what is pulmonary edema
|
acute event resulting from hf
|
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with pe the left ventricle cant handle an overload of blood volume causing pressure to___
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increase in the pulmonary vasculature
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pulmonary vasculature causes what
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fluid to move out of pulmonary capillaries and into interstitial space of lungs and alveoli resulting in hypoxemia
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when auscultating a pe what do you hear
|
crackles in the lung bases (posterior)
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where does it progress
|
toward the apices of lungs
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what is this caused by
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movement of air through alveolar fluid
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what se of pe
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frothy pink (blood tinged) sputum
tachycardia |
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chest xray reveals
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pulmonary veins engorged
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with pe what do abg labs show
|
worsening hypoxemia
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tx of pe is directed toward..
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reducing bolume overload, improving ventricular function and increasing resp exchange
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how do you position the pt
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upright and dangle legs
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morphine is given with pe; titrated iv in small doses (2-5mg) to do what
|
reduce peripheral resistance and venous return so blood can be redistributed to other pts of body
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what does morphine decrease
|
pressure in pulmonary capillaries and seepage into lung tissues
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diuretics are also used for what reason
|
to promote excretion of sodium and water from kidneys
|
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diuretics for pe causes what
|
vasodilation and pooling of blood in peripheral blood vessels which reduces amt of blood return to the heart
|
|
|
what is cirrhosis characterized by
|
replacement of normal liver tissue with diffuse fibrosis that disrupts the structure and fx of liver
|
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what are the 3 types of cirrhosis
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alcoholic
postnecrotic biliary |
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what is alcoholic cirrhosis
|
most common
scar tissue surrounds the portal areas |
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what is postnecrotic cirrhosis
|
result of previous bout of acute viral hepatits, broad bands of scar tissue
|
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|
what is biliary cirrhosis
|
reults from chronic viliary obstruction and infection; scarring occurs in the liver around the bile ducts
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|
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what is the clinical manifestations of cirrhosis
|
weakness
fatigue transient jaundic enlarged liver ruq tenderness indigestion |
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what are the later signs of cirrhosis
|
liver decreases in size
leukopenia thrombocytopenia ascites portal hypertension varices |
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what are the labs used for cirrhosis
|
increased sgot, sgpt, bilirubin
pt serum globulin level decreased albumin and serum cholinesterase |
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cardiomyopathy is a heart muscle disease ass with ___ which may lead to ___,___
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cardiac dysfunciton
severe heart failure, lethal dysrythmias |
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all cardiomyopathys involve a series of events that culminate in what
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impaired cardiac output
|
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cardiomyopathy is classified according to the what
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structural and functional abnormalities of heart muscle
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what is the most common cardiomyopathy
|
dilated cardiomyopathy
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what is the unclassified cardiomyopathy
|
arrhythmogenic right ventricular cardiomyopathy
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what are the 4 kinds of cardiomyopathys
|
dilated
hypertrophic restrictive/constrictive arrhythmogenic r ventricular |
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a physical exam may reveal what 2 things
|
tachycardia
extra heart sound (s3, s4) |
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diastolic murmurs and systolic murmurs are found in which kind of cirrhosis
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d: dcm
s: dcm, hcm |
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what are the s/s of hf
|
crackles
jugular vein distention pitting edema enlarged liver |
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what is the most helpful dx tool and why
|
echocardiogram
bc you can view structure and function of ventricles |
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ecg demonstrates what
|
dysrthymias and changes w LV hypertrophy
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a chest xray reveals what
|
heart enlargement
poss pulmonary cogestion |
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cardiac catheterization is used to..
|
r/o coronary artery disease
|
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endomyocardial biopsy is used to analyze what
|
myocardial tissue cells
|
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tx is aimed at controlling dysrthymias w...
|
antirrythmic medications and with an implanted electronic device
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enefective edocarditis prophylaxis and system anticoagulants are used to prevent
|
thromboembolic events
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if a pt has s/s of congestion what do you do
|
limit fluid intake to 2l/day
|
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pts with hcm should avoid what and they may also need what drug
|
dehydration
beta blockers to maintain cardiac output and minimize risk of LV outflow tract obstruction during systole |
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pts with hcm and rcm may need to limit what
|
physical activity to life threatning dysrythimas
|
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what are surgical interventions
|
heart transplant
lv assist device implanted with pt waits for donor |
|
|
what is disseminated intravascular coagulation
|
life threatening disorder in which bleeding and clotting occur simultaneously
|
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|
dic occurs with what pts
|
acutely ill with cancer or mothers with dead fetus
|
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what is the path of dic
|
involves over activation of clotting mechanism; massive amts of tiny clots accumulate in capillaries througout body, depleting body of supply of clotting factors
|
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microemboli interfere with blood flow causing what two things
|
ischemia and organ damage
|
|
|
once the clots begin to lysis..what happens
|
fibrin degradation products are released
|
|
|
what are fibrin degradation products
|
potent anticoagulants
|
|
|
fdp along with low levels of clotting factors lead to what
|
massive internal bleeding (brain, kidney, lungs, heart, wounds, old puncture sites)
|
|
|
with leukemia what do you see an increase of
|
neutrophils and lymphocytes
|
|
|
with leukemia what gets proliferated
|
leukocytes in bone marrow
|
|
|
what are some drugs for leukemia
|
novantrone, idamycin, cytosar, cerubidine
CHEMO |
|
|
what is angina patho
|
myocardium extracts lg amounts of oxygen from coronary circulation to meed demands
|
|
|
with increased demands what else needs to increase
|
flow through coronary artery
|
|
|
what happens when coronary artery is blocked
|
decrease oxygen supply. need for oxygen exceeds supply
|
|
|
what is the tx for angina
|
PTCA
nitro |
|
|
what does nitro do
|
decreases myocardial ox consumption and ischemia
dilates veins |
|
|
with an increased dose of nitro what happens
|
dilates arteries
|
|
|
what other class of meds relieve angina
|
beta blockers
|
|
|
what do cal channel blockers do for angina
|
dilates smooth muscle wall of arteries and decreases ox demand
|
|
|
what does of antiplatelet/anticoags is used for angina
|
160-325mg
|
|
|
what are some other drugs used
|
plavix, glycoprotein, heparin
oxygen |
|
|
ekg is done with angina when
|
within 10 min of pain
|
|
|
ekg dx what
|
dysrhythmias
injury ischemia enlargement infarction conduction abn electrolyte disturbances |
|
|
with an mi what do you see on an ekg
|
st dep
|
|
|
what are labs used for pancreatitis
|
serum lipase ^ w/in 24 hr
amylase ^ w/in 24 hr (usually returns w/in 48-72) urine amylase ^ wbc^ hypocalcemia transient hyperglycemia & gulcosurea ^ bili |
|
|
what is a myelodysplastic syndrome
|
myeloid stem cell disorder that causes dysplasia in cell ines
|
|
|
what is mds manifested by
|
macrocytic anemia
|
|
|
what does mds leave you at risk for
|
pneumonia and bleeding
|
|
|
how do you dx mds
|
bone marrow biopsy
|
|
|
what is the only cure for mds
|
bmt
|
|
|
with iron how does it need to be taken
|
on empty stomach 1 hr before or 2 hr after food w/o dairy
dark poop |
|
|
what do you take to prevent anemia
|
b12, folic acid, protein, no alcohol
|
|
|
path of cirrhosis
|
eventually scar tissue exceeds that of functioning liver tissue
|
|
|
what is the tx for cirrhosis
|
antacids
pot sparing diuretics ace glitazones inc protein in diet immunosupressants antiinflam milk thistle |
|
|
what are some meds for thyroid disorders
|
hypo: sythroid or levothroid
hyper: iodinde, propranolol, PTU, methimazole, dexamethasone |
|
|
se of coumadin
|
bleeding and necrosis of skin, headache, weakness, joint pain
|
|
|
pt w neutropenia need to be monitored for temp how often
|
q4h
|
|
|
cerebral tissue hypoxia is commonly associated with
|
dizziness
|
|
|
recognition of cerebral hypoxia is critical since the body will do what
|
attempt to shunt oxygenated blood to vital organs
|
|
|
what is the most common type of blood transfusion reaction
|
febrile transfustion
|
|
|
febrile transfusion reaction is most commonly seen in who
|
pt who have had previous transfusions and exposure to multiple antigens from blood products
|
|
|
s/s of febrile trans reaction are what
|
chills, fever (begins within 2 hr) muscle stiffness
|
|
|
how can you prevent febrile reaction
|
leukocyte reduction filter
|
|
|
why is it not suggested to give antipyretics
|
mask the beginning of a transfusion reaction
|
|
|
how does an acute hemolytic reaction occur
|
when donor blood is incompatible with that of the recipient
|
|
|
what is the most dangerous of the two
|
acute hemolytic
|
|
|
with ahr, antibodies already present in the recipients plasma combine with donor erythrocytes and what happens
|
the erythrocytes are destroyed in circulation (intravascular hymolysis)
|
|
|
the reaction can occur at how many ml
|
10ml of PRBC
|
|
|
what are the s/s of this
|
fever, chills, back pain, nausea, chest tightness, dyspnea, anxiety, hemoglobinuria
|
|
|
why does hyemoglobinuria show
|
bc as the erythrocytes are destroyed, the hmg is released from the cells and excreted by the kindeys
|
|
|
what may result if not fixed
|
hypotension, bronchospasms, vascular collapse, dic
|
|
|
what are normal heart sounds produced by
|
closure of av valves and semilunar valves;
the period between s1 and s2 corresponds with ventricular systole |
|
|
how can you prevent febrile reaction
|
leukocyte reduction filter
|
|
|
why is it not suggested to give antipyretics
|
mask the beginning of a transfusion reaction
|
|
|
how does an acute hemolytic reaction occur
|
when donor blood is incompatible with that of the recipient
|
|
|
what is the most dangerous of the two
|
acute hemolytic
|
|
|
with ahr, antibodies already present in the recipients plasma combine with donor erythrocytes and what happens
|
the erythrocytes are destroyed in circulation (intravascular hymolysis)
|
|
|
the reaction can occur at how many ml
|
10ml of PRBC
|
|
|
what are the s/s of this
|
fever, chills, back pain, nausea, chest tightness, dyspnea, anxiety, hemoglobinuria
|
|
|
why does hyemoglobinuria show
|
bc as the erythrocytes are destroyed, the hmg is released from the cells and excreted by the kindeys
|
|
|
what may result if not fixed
|
hypotension, bronchospasms, vascular collapse, dic
|
|
|
what are normal heart sounds produced by
|
closure of av valves and semilunar valves;
the period between s1 and s2 corresponds with ventricular systole |
|
|
the s1 is described as what
|
tricuspid and mitral valve closure
|
|
|
the intensity of s1 increases with what
|
tachycardia or mitral stenosis
|
|
|
the s2 is described as what
|
closure of pulmonic and aortic valves
|
|
|
where is s2 heard loudest
|
over aortic and pulmonic areas
|
|
|
s1 is heard loudest where
|
apical area
|
|
|
s3 and s4 are heard during what
|
diastole
|
|
|
s3 and s4 are created how
|
by the vibration of ventricle and surrounding strucutes as blood meeds resistance during ventricular filling
|
|
|
s3 occurs when
|
early during diastole during rapid ventricular filling
|
|
|
s4 occurs when
|
late during diastole and is generated during atrial contraction as blood enters noncompliant ventricle
|
|
|
the resistance to blood flow is due to what
|
hypertrophy caused by hypertension, cad, cardiomyopathies, aortic stenosis
|
|
|
murmurs are created by what
|
turbulent flow of blood
|
|
|
what is the cause of turbulence
|
narrowed valve, malfunctioning value that allows regurgitated blood flow, congenital defect of ventricular wall, defect bt aorta and pulmonary artery or increased flow of blood
|
|
|
hodgkin lympthoma is unicentric in orgin in that it inititaes in a what
|
single node
|
|
|
the disease spreads by contiguous extension along the __
|
lymphatic system
|
|
|
what is the malignant cell of hl
|
reed-sternberg, huge tumor cell that is morphologically unique
|
|
|
tx of hl is what
|
tx of 2-4 months of chemo followed by radiation
and chemo with doxorubicin (adriamycin) bleomycin (blenoxane) vinblastine (velban) and dacarbazine (DTIC) |
|
|
how is dx made for hl
|
excisional lymph node biopsy and findings of the reed sternberg cell
|
|
|
what is the patho of pancreatitis
|
self digestion of the pancreas by its own proteolytic enzymes, tyrpsin
|
|
|
how do you tx pancreatitis
|
npo
ng tube pain management histamine 2 tagament and zantac paracentesis |
|
|
cerebral tissue hypoxia is commonly associated with what
|
dizziness
|
|
|
recognition of cerebral hypoxia is critical since the body will do what
|
attempt to shunt oxygenated blood to vital organs
|
|
|
atenolol blocks stimulation of beta1 adrenergic receptors causing what
|
reduction in blood pressure and heart rate
|
|
|
what is a se of atenolol
|
prolongation of the PR interval (normal is 0.12-0.20)
|
|
|
continued use of the drug can cause what
|
heart block
|
|
|
nitrates and cal channel blockers are minstays of medical therapy rather than beta blocker for what
|
variant angina
|
|
|
what kind of angina is caused from cornary artery vasospasm
|
printzmetals
|
|
|
printzmetals medications choices are
|
nitrates and ccb
|
|
|
what labs would you anticipate the md ordering on your pt with chest pain
|
cardiac enzymes (ck-mb, ck-mm, ck-bb) if elevated and troponin t or i to determine if the pt had an mi
cbc metabolic/chem panel serum lipid panel pt/inr/ptt/ua |
|
|
thalassaemia, sickle cell disease and hemophilia a and b are what kind of disordes
|
hereditary
|
|
|
what kind of anemia is an acquired hemolytic anemia
|
autoimmune hemolytic
|
|
|
thalassemia major occurs from a deficiency in the synthesis of the beta chain of the hemoglobin resulting in defective hemoglobin that damages what
|
red blood cells
|
|
|
plasmapheresis would be ___ in treating thalassemia why?
|
ineffective
bc the cells are not being destroyed by toxins in the plasma |
|
|
megaloblastic anemia is caused by def of b12 or folic acid. a vegitarian can prevent a def with oral vitamiin supp or what
|
fortified soy milk
|
|
|
you should consume b12 in what form
|
crystalline
|
|
|
urine and blood cultures should be obtained before what
|
antibiotics are administered
|
|
|
CLL derives from what
|
a malignant clone of b lymphocytes and t lymphocytes
|
|
|
treatment is initiated when what happens
|
symptoms are severe (night sweats, painful lymphanopathy), or disease progresses to later stages
|
|
|
because many people are asymptomatic it is often dx how
|
during routine physical or tx of another condition
|
|
|
tx of cll includes what
|
chemo with fludarabine (fludara)
|
|
|
a major se of fludara is what
|
prolonged bone marrow suppression
|
|
|
in cll there is an accumulation of what
|
mature appearing but functionally inactive lymphocytes
|
|
|
excessive accumulation of immature lymphocytes occurs in what
|
acute lymphocytic leukemia
|
|
|
acute chest syndrome and pulmonary hypertension are two of the complications ass with what
|
sickle cell disease
|
|
|
what may help prevent complications ass with sickle cell
|
blood transfusions
|
|
|
what can decrease the permanent formation of sickled cells
|
hydroxyurea
|
|
|
what is a se of hydroxyrea
|
supression of leukocyte formation
|
|
|
what is the highest risk factor for hepatitis c
|
iv drug abuse
|
|
|
reticulocyte count along with rbc, hct, hmg may be ordered to monitor what
|
marrow function and response to tx
|
|
|
what are the 3 phases for hepatitis
|
preicteric (prodromal)
icteric convalescent |
|
|
what are the se of prodromal phase
|
flulike symptoms
malaise ha muscle pain joint pain abd pain ruq |
|
|
what are the labs for prodromal phase
|
hep a: anti-hav img
igm anti-hbc |
|
|
what are the se of icteric phase
|
tender liver
dark urine jaundice |
|
|
what are the serum labs for icteric phase
|
hep a igm
igg hep b: hbsag & hbcag & igm antic hbc |
|
|
what are the se of convalescent phase
|
gradual increase in sense of well being
appetite returns fatigability no abd pain |
|
|
what are the labs see in convolescent phase
|
hep a: igm, igg
hep b: hbsag &hbeag& igm anti hbc |
|
|
what is hepatitis
|
inflammation of liver degeneration and necrosis of liver cells
|
|
|
how do you dx hepatitis
|
bilirubin increase (0.2-1.3)
alp serum amintransferases ptt |
|
|
what is the tx for hepatitis
|
small meals
increase protein increase carbs sup iv glucose |
|
|
what is leukemia
|
bone marrow malignancy
|
|
|
what is aml (adult)
s/s? |
rapid accumulation of hematopietic stem cells
s/s:high fever |
|
|
what is the tx for aml (meds)
|
cytrabine (cystosar)
daunorubicin (cerubidine) mitoxantrone (novatrone) idarubicin (idamycin) |
|
|
what is all (children)
s/s? |
lymphoid proliferation takes over bone marrow, not allowing normal development of wbc, plat, and rbc
s/s: malaise, vomiting, confusion, sores in eyes/skin |
|
|
what is the tx for acute
|
bone marrow transplant
|
|
|
what is chronic myelogenous leukemia
tx? |
abnormal growth and increase of myelobast cells
s/s imatinib |
|
|
what is P wave
|
atrial depolarization
|
|
|
what is PR segment
|
flat line that follows p wave-percedes contraction of ventricles
|
|
|
what happens after pr
|
signal leaves atria and enters ventricles via av node
|
|
|
what is the Q wave
|
enters the bundles of HIS
|
|
|
what is R wave
|
spreads through bundle brances
|
|
|
what is S wave
|
purkinje fibers (spread depolarizing along ventricle walls, begins in septum moves from apex upwards) ca enters
|
|
|
what is the ST segment
|
ventricles depolarized; ventricular diastole
|
|
|
T wave?
|
marks ventricular repolarization
|
|
|
what is QT seg
|
time it takes for depolarization and repolarization of ventricles
|
|
|
exacerbations with sickle cell crisis is aimed at what
|
controlling pain
|
|
|
positioing the client of the right side after a liver biopsy does what
|
splints the puncture site to prevent and decrease bleeding
|
|
|
depolarization of the myocardium results in ___ and that produces the palpable pulse and the corresponding QRS complex on the electrocardiogram
|
systole (contraction)
|
|
|
left ventricular ejection fraction that is low in a pt with signs of CHF may be put on what
|
heparin to prevent thrombus formation in the LV
|
|
|
the ischemia that causes the MI can also cause the heart muslce to become irritable, which fire early causing what
|
dysrhythmias
|
|
|
intermittent claudication is what
|
arterial; shiny skin, dependent rubor
|
|
|
the presence of the antigen HBsAG concludes that the clinet has ___ form of the disease since hep b surface antigen is ___
|
active; present
|
|
|
for a pt with advanced cirrhosis what will improve nervous system function
|
lactulose by binding to ammonia
|
|
|
why is food withheld with pancreatitis
|
to inhibit stimulation of the pancreas and its secretion of enzymes
|
|
|
what is an alkylating agent used for and what does it do
|
leukemia; it interferes w rapidly reproducing cell nca
|
|
|
what are some ex of alkylating agents
|
- Busulfan (myloran)
- Cyclophoshomia (cytoxan); Report hematuria & give antimetics - Chlorambucil (CHL (Leukemia)); avoid IM injections when low - Cisplatin |
|
|
what the se of alkylating agents
|
bone marrow suppression, stomitits, alopecia, ototoxicity
|
|
|
what are antimetabolites used for
|
acute leukemia, sickle cell it stops cell division
|
|
|
what are some ex of antimetabolites
|
hydroxyurea (hydrea); Ed. Report GI symptoms immediately
- methothexate; avoid alcohol - Cytarabine; ck hepatic & renal function; force fluids - fluorouracil |
|
|
what are the se of antimetabolites
|
bone marrow dep
stomatitis, hepatic dysfunction, renal dysfunction |
|
|
what is an antitumor antibiotic used for what does it do
|
Hodgkins, Non-Hodgkins, Leukemia; Interferes w DNA & RNA synthesis
|
|
|
what are some ex of the drugs
|
Bleomycin (Blenoxane); ck pulmonary comp., treat fever w Tylenol, ck breath sounds
- Dactinomycin (Actinomycin); Give antiemetic before admin - Doxorubicin (Adriamycin); ck EKG, avoid IV infiltration, Monitor VS, ed. red urine |
|
|
what are the se of the drugs
|
bone marrow dep, stomatitis, shock (septic, hf
|
|
|
what are vinca alkaloids used for
|
Hodgkin’s ds, lymphoma, cancer; Interfers w cell division
|
|
|
what are some ex of drugs
|
- Vinblstin (Velban); give antiemetic before admin, acute bronchospasm risk for IV
- Vincristine (Oncovin; VCR); ck reflexes, motor & sensory function |
