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Pharmacology > Nurs 605 Module 10 > Flashcards

Nurs 605 Module 10 Flashcards

1
Q

What is anemia?

A

anemia is the lack of hemoglobin in red blood cells

lacks oxygen carrying properties

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2
Q

What are the clinical manifestations of anemia?

A 
usually chronic so could be asymptomatic
mostly fatigue 
impaired congnitive function 
anorexia
nausea 
chest pain
dyspnea
tachycardia
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3
Q

Describe the different types of anemia

A

generally classified into nutritional deficient anemias or lack of hemapoietic growth factors

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4
Q

In those who have nutrient deficient anemia, what important substances are missing or deficient?

A

iron, folate, or vitamin b12

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5
Q

What hematopoietic growth factor is missing in those who have anemia?

A

erythropoiten

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6
Q

What are some of the causes of anemia/

A 
dietary deficiency 
medical conditions
menses
pregnancy 
blood deficient conditions ie) thalassemia 
infections
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7
Q

Which two organs are responsible for the creation and break down of red blood cells?

A

bone marrow-creates RBCs

spleen-destroys RBCs, converts them into waste products

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8
Q

Which organ is responsible for the creation of erythopoitin and why is this substance important?

A

kidneys create epo
epo is a hormine that stimulates RBC growth
important in the creation of RBCs

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9
Q

Describe the significance of iron in the production of RBCs

A

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

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10
Q

What are the pharmalogical choices for iron defiency anemia?

A

oral iron salts such as ferrous fumarate, glucanate or sulfate
parenteral iron such as iron dextran or sucrose

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11
Q

What are the adverse effects of oral iron salts?

A

better absorption on an empty stomach but can add to adverse effects
nausea, diarrhea, abdominal cramping

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12
Q

Iron toxicity is possible in those taking high levels of oral iron; what is the reversal or antidote agent?

A

desferrioxamine

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13
Q

What are the adverse effects of parenteral iron?

A

anaphylaxis

caution in using in patients with infection as increase in iron can be a source of nutrition for pathogens

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14
Q

Describe the importance of folic acid and vitamin b12 in the body

A

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

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15
Q

what are the causes of folic acid deficiency?

A

diet
malabsorption concerns
drugs

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16
Q

What is the recommended pharmaceutical intervention for someone who has a folic acid deficiency?

A

oral folic acid

increase during pregnancy

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17
Q

In what condition is vitamin b12 used for?

A

pernicious anemia

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18
Q

How is vitamin b12 given?

A

usually parenterally through IM due to malabsorption

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19
Q

It is possible to have an overdose of folic acid; what is the reversal agent?

A

methotrexate

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20
Q

In what conditions are epoitien or darbepoiten recommended?

A

chronic kidney disease
cancer
AIDs
chronic inflammatory disease

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21
Q

How is EPO or Darbe given?

A

subq or IV

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22
Q

How often would you give someone EPO? Darbe? and why?

A

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

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23
Q

What are the adverse effects of EPO or darbe?

A

transient flu like symptoms
hypertension
iron deficiency
increased blood viscosity

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24
Q

Describe hemostasis; what is it and what is its role in our body

A

arrests blood from being loss in our body; done by:
platelet formation and activation
fibrin formation/blood coagulation

25
Q

Describe the difference between venous and arterial thrombosis

A

venous- RBCs with white blood cell tail end

arterial thrombosis-mostly made of platelets and fibrin

26
Q

What is the Triad of virchow?

A

risk factors of thrombus creation

  1. injury to the cell wall
  2. disrupted/altered blood flow
  3. abnormal coagulation
27
Q

What is the mechanism of action of heparin?

A
  • 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
28
Q

What is the mechanism of action of warfarin?

A

• Prevents activation of vitamin K which assits in activation of cclotting factors 279X
prevents clotting initiation and recurrence

29
Q

What is the mechanism of action of ASA?

A
  • Inhibits platelet aggregation
  • Inhibits CoX 1 and CoX 1 irreversibly
  • Similar profile to an NSAID
30
Q

What factors increase risk of bleeding when a person is on antithrombitics?

A 
•	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
31
Q

Formulate an appropriate prevention strategy for a patient at high risk for deep vein thrombosis;

A
  • High risk patients: triad of Virchow – poor circulation, poor valve response, sedentary lifestyle
  • DVT- elevate leg, acetaminophen for pain, compression/elastic stockings as needed
32
Q

Formulate an appropriate treatment plan for a patient who develops a deep vein thrombosis or pulmonary embolism;

A
  • 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
33
Q

What are some drug interactions with warfarin; what do they do?

A
  • 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)
34
Q

What are some food-drug interactions with warfarin and what do they do?

A
  • Drug food:
  • Grapefruit juice -increases warfarin effects
  • Avocado, gingseng, foods with increased amount of vitamin K
35
Q

What is the INR target for NVAF? for patients with mechanical valves?

A

NVAF- 2.0-3.0; INR 2.5 average

VAF or with mechanical valves- 2.5-3.5

36
Q

What types of conditions is warfarin used for

A

Afib- NVAF, VAF
atrial flutter
post MI, post stroke
DVT/PE prevention

37
Q

Why does warfarin not work immediately? How long does it take to work?

A

body still has clotting factors so clotting factors need to pass through the liver before warfarin works
takes about 5-7 days

38
Q

What is the optimal starting dose of warfarin? When would you consider going even lower?

A

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
39
Q

Which clotting factors does warfarin inhibit?

A

clotting factors 2, 7, 9, 10

40
Q

What is a normal INR (for someone who isn’t on warfarin)

A

0.8-1.2

41
Q

Discuss key teaching points for management of INR levels

A

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

42
Q

When would you increase testing frequency of INR levels?

A 
q 2-4 day testing if:
changes in medication that may interfere with warfarin 
changes to diet
illness
non therapuetic leves
43
Q

What are some warfarin contraindications?

A

severe/active bleeding
pregnancy
intolerance/allergy
non adherence

44
Q

When choosing an appropriate anticoagulant; what factors need to be considered/

A 
contraindications
specific patient factors (lifestyle, cognition)
age
renal function/hepatic function 
drug interactions 
cost 
heart valves? - MUST CHOOSE WARFARIN
45
Q

When oral anticoagulation is required for patients with non-valvular atrial fibrillation, explain why warfarin is the initial therapy of choice for most patients

A

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

46
Q

Discuss the current evidence for the use of oral anticoagulants such as warfarin, dabigatran, rivaroxaban and apixaban in atrial fibrillation

A

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

47
Q

What are some key concerns with the new oral anticoagulants?

A 
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
48
Q

When are new oral anticoagulants contraindicated?

A 
heart valve patients 
those well managed on warfarin 
patients with coronary heart disease,  or stents
CYP 450 interactions 
CrCl <30
49
Q

What types of drug interactions occur with dabigratran?

A

direct inhibitor vs. clotting factors
d–different
dyspepsia
drug interactions with PPIs, H2RAs, antacids
more discontinuations due to adverse effects

50
Q

What is a concern with rivaroxaban and its once daily dosing?

A

rivaroxaban has the shortest half life, yet only one approved for once daily
implications for missed doses and what this means

51
Q

What is the concern with switching from warfarin to new anticoagulants?

A

during this transition; increased risk of stroke and PE clots and vice versa
NOACs and warfarin-no proper switching method

52
Q

What is the risk of combining antiplatelet and anticoagulants?

A

3x risk of bleeds with warfarin plus asa or clopidogrel

NOACs plus antiplatelets = increased risk of bleeds

53
Q

When is a combination of antiplatelets and anticoagulants suggested?

A

NVAF plus intracoronary stent

NVAF plus acute coronary syndrome

54
Q

In combo therapy with antiplatelets, which drug is preferred?

A

warfarin always

55
Q

Describe the treatments for secondary prevention of ischemic stroke

A
  • 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
56
Q

Discuss the significance of long QT syndrome and sudden cardiac death

A

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

57
Q

List commonly prescribed antibiotics antihistamines and psychiatric drugs that increase the risk for long QT

A

abx: macrolides (azithromycins etc); fluroquinolones (floxacins)
antihistamines: terfenedine
psych drugs: tricyclic antidepressants (amitriptaline)

58
Q

Discuss alcohol and related cardiac toxicity

A

excess ETOH causes cardiac myopathy - dilation of ventricles, wall thinning, ventricular dysfunction, heart failure

Pharmacology (13 decks)

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