Nurs 605 Module 10 Flashcards
What is anemia?
anemia is the lack of hemoglobin in red blood cells
lacks oxygen carrying properties
What are the clinical manifestations of anemia?
usually chronic so could be asymptomatic mostly fatigue impaired congnitive function anorexia nausea chest pain dyspnea tachycardia
Describe the different types of anemia
generally classified into nutritional deficient anemias or lack of hemapoietic growth factors
In those who have nutrient deficient anemia, what important substances are missing or deficient?
iron, folate, or vitamin b12
What hematopoietic growth factor is missing in those who have anemia?
erythropoiten
What are some of the causes of anemia/
dietary deficiency medical conditions menses pregnancy blood deficient conditions ie) thalassemia infections
Which two organs are responsible for the creation and break down of red blood cells?
bone marrow-creates RBCs
spleen-destroys RBCs, converts them into waste products
Which organ is responsible for the creation of erythopoitin and why is this substance important?
kidneys create epo
epo is a hormine that stimulates RBC growth
important in the creation of RBCs
Describe the significance of iron in the production of RBCs
iron is used to produce RBC
stored in the liver
hepacidin hormone releases iron to respond to low RBC levels
lack of iron means lack of production of RBCs = anemia
What are the pharmalogical choices for iron defiency anemia?
oral iron salts such as ferrous fumarate, glucanate or sulfate
parenteral iron such as iron dextran or sucrose
What are the adverse effects of oral iron salts?
better absorption on an empty stomach but can add to adverse effects
nausea, diarrhea, abdominal cramping
Iron toxicity is possible in those taking high levels of oral iron; what is the reversal or antidote agent?
desferrioxamine
What are the adverse effects of parenteral iron?
anaphylaxis
caution in using in patients with infection as increase in iron can be a source of nutrition for pathogens
Describe the importance of folic acid and vitamin b12 in the body
folic acid-essential in diet
used in DNA synthesis
esp. important in pregnant or conceiving women as lack of folic acid can lead to neural tube defects
vitamin b12
DNA synthesis
absorbed in the duodenum and jejunum
what are the causes of folic acid deficiency?
diet
malabsorption concerns
drugs
What is the recommended pharmaceutical intervention for someone who has a folic acid deficiency?
oral folic acid
increase during pregnancy
In what condition is vitamin b12 used for?
pernicious anemia
How is vitamin b12 given?
usually parenterally through IM due to malabsorption
It is possible to have an overdose of folic acid; what is the reversal agent?
methotrexate
In what conditions are epoitien or darbepoiten recommended?
chronic kidney disease
cancer
AIDs
chronic inflammatory disease
How is EPO or Darbe given?
subq or IV
How often would you give someone EPO? Darbe? and why?
EPO has shorter half life, so may need to give 3x a week
Darbe has a longer half life so can give weekly, bi weekly or even monthly dependent on condition
What are the adverse effects of EPO or darbe?
transient flu like symptoms
hypertension
iron deficiency
increased blood viscosity
Describe hemostasis; what is it and what is its role in our body
arrests blood from being loss in our body; done by:
platelet formation and activation
fibrin formation/blood coagulation
Describe the difference between venous and arterial thrombosis
venous- RBCs with white blood cell tail end
arterial thrombosis-mostly made of platelets and fibrin
What is the Triad of virchow?
risk factors of thrombus creation
- injury to the cell wall
- disrupted/altered blood flow
- abnormal coagulation
What is the mechanism of action of heparin?
- Antithrombin III- enzyme that assists in prevention of clotting/soldification of the blood
- Activiating this enzyme=prevents clotting
- Not absorbed by the gut, must be given SQ or IV
What is the mechanism of action of warfarin?
• Prevents activation of vitamin K which assits in activation of cclotting factors 279X
prevents clotting initiation and recurrence
What is the mechanism of action of ASA?
- Inhibits platelet aggregation
- Inhibits CoX 1 and CoX 1 irreversibly
- Similar profile to an NSAID
What factors increase risk of bleeding when a person is on antithrombitics?
• Combo of ASA and clopidogrel plus warfarin (3x risk) • Age • Sex • Upper GI pain • History of ulcers, GI bleeds • NSAID use • Uncontrolled HTN Renal/hepatic dysfunction CVD etoh consumption
Formulate an appropriate prevention strategy for a patient at high risk for deep vein thrombosis;
- High risk patients: triad of Virchow – poor circulation, poor valve response, sedentary lifestyle
- DVT- elevate leg, acetaminophen for pain, compression/elastic stockings as needed
Formulate an appropriate treatment plan for a patient who develops a deep vein thrombosis or pulmonary embolism;
- DVT/PE: treatment plan
- Rest, early ambulation, elevate feet, acetaminophen for pain if needed
- Low dose heparin +/- warfarin/anticoagulants for DVT/PE
- Continue for 3 months if first episode
- Otherwise, continue until INR <2 for 24-48 hours
What are some drug interactions with warfarin; what do they do?
- NSAIDs, ASA- do not contribute directly to decreased effective of warfarin but can increase risk of bleeding
- Antimicrobials- azoles, macrolides, fluroquinolones (increase warfarin effects); ritonavir, rifampin (decrease effects)
- CV drugs- SSRIs, antiparkinson drugs
- GI drugs-cimetidine, omeprazole
- CNS- carbamzepein, barbituates (increase effects)
What are some food-drug interactions with warfarin and what do they do?
- Drug food:
- Grapefruit juice -increases warfarin effects
- Avocado, gingseng, foods with increased amount of vitamin K
What is the INR target for NVAF? for patients with mechanical valves?
NVAF- 2.0-3.0; INR 2.5 average
VAF or with mechanical valves- 2.5-3.5
What types of conditions is warfarin used for
Afib- NVAF, VAF
atrial flutter
post MI, post stroke
DVT/PE prevention
Why does warfarin not work immediately? How long does it take to work?
body still has clotting factors so clotting factors need to pass through the liver before warfarin works
takes about 5-7 days
What is the optimal starting dose of warfarin? When would you consider going even lower?
optimal starting dose 5mg daily
consider <5mg doses if: age >70 baseline INR is 1.1 low albumin impaired nutrition CHF medications that increase risk of warfarin sensitivity to warfarin
Which clotting factors does warfarin inhibit?
clotting factors 2, 7, 9, 10
What is a normal INR (for someone who isn’t on warfarin)
0.8-1.2
Discuss key teaching points for management of INR levels
dose changes wont reflect for 4-5 days
stable doses can be monitoried q 4 hours
do not adjust dose for one out of range INR
consistent vitamin K intake, no need to change diet
routine blood work at same time of day
When would you increase testing frequency of INR levels?
q 2-4 day testing if: changes in medication that may interfere with warfarin changes to diet illness non therapuetic leves
What are some warfarin contraindications?
severe/active bleeding
pregnancy
intolerance/allergy
non adherence
When choosing an appropriate anticoagulant; what factors need to be considered/
contraindications specific patient factors (lifestyle, cognition) age renal function/hepatic function drug interactions cost heart valves? - MUST CHOOSE WARFARIN
When oral anticoagulation is required for patients with non-valvular atrial fibrillation, explain why warfarin is the initial therapy of choice for most patients
o Warfarin is first line therapy in most patients (unless contraindicated)
use in heart valves
o Extensively researched
o Ability to monitor therapeutic ranges and adjust as needed, use of INRs
o Benefits of new oral anticoagulants vs. warfarin is small
stable coronary heart disease, stent
reversal agents available
ARR 3% with warfarin in decreasing risk of stroke
Discuss the current evidence for the use of oral anticoagulants such as warfarin, dabigatran, rivaroxaban and apixaban in atrial fibrillation
non inferiority between NOACs and warfarin in decreasing stroke and bleeding
manufacturer funded
no head to head comparison between new drugs
study populations (no older populations, complex patients were ruled out, CHADs Scores <2)
ARR <1% between oral anticoagulants
What are some key concerns with the new oral anticoagulants?
no defined bleed management potential impact of missed doses lack of switching optimization unknown optimal dosing for older adult, low body weight and renal impairement little discussion on drug interactions no management with pre surgeries
When are new oral anticoagulants contraindicated?
heart valve patients those well managed on warfarin patients with coronary heart disease, or stents CYP 450 interactions CrCl <30
What types of drug interactions occur with dabigratran?
direct inhibitor vs. clotting factors
d–different
dyspepsia
drug interactions with PPIs, H2RAs, antacids
more discontinuations due to adverse effects
What is a concern with rivaroxaban and its once daily dosing?
rivaroxaban has the shortest half life, yet only one approved for once daily
implications for missed doses and what this means
What is the concern with switching from warfarin to new anticoagulants?
during this transition; increased risk of stroke and PE clots and vice versa
NOACs and warfarin-no proper switching method
What is the risk of combining antiplatelet and anticoagulants?
3x risk of bleeds with warfarin plus asa or clopidogrel
NOACs plus antiplatelets = increased risk of bleeds
When is a combination of antiplatelets and anticoagulants suggested?
NVAF plus intracoronary stent
NVAF plus acute coronary syndrome
In combo therapy with antiplatelets, which drug is preferred?
warfarin always
Describe the treatments for secondary prevention of ischemic stroke
- Modifiable therapies:
- Smoking cessation
- Dietary changes
- Increase physical activity
- Speech therapy
- Rehab/physiotherapy
- Antiplatelets or anticoagulants as preventative therapies
- Antiplaelets-antithrombitic
- Anticoagulants-cardiac evets
- ASA, clopidogrel =prevention in cerebral and cardiac events
- Vitamin K antagonists-warfardin, superior to antiplatelets
- NOACs- a fib, non valvular a firb
Discuss the significance of long QT syndrome and sudden cardiac death
prolonged “stretching” of ventricular cells
the “snap back” causes sudden cardiac death by triggering sudden arrythmia
action potential plateaus and repolarizes causes ventricular arrythmia and potential death
List commonly prescribed antibiotics antihistamines and psychiatric drugs that increase the risk for long QT
abx: macrolides (azithromycins etc); fluroquinolones (floxacins)
antihistamines: terfenedine
psych drugs: tricyclic antidepressants (amitriptaline)
Discuss alcohol and related cardiac toxicity
excess ETOH causes cardiac myopathy - dilation of ventricles, wall thinning, ventricular dysfunction, heart failure
