Test 2 Flashcards

1
Q

CWCM stands for

A

Colour
Warmth
Circulation
Movement

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2
Q

taken w meals and then w vitamin c

A

Pyrosulfate supplement

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3
Q

can stain teeth - rinse mouth out after

A

Oral liquid iron

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4
Q

When taking supplements iron will be checked, ________ will be checked
When things are back to normal continue therapy for at least 2 months after normalized

A

hemoglobin

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5
Q

-B12 deficiency, folic acid deficiency
Cobalamin deficiency is the most common
Neurological, nerve, muscle problems
Can have upset stomach, nausea, abdominal discomfort, vomiting
High alcohol intake – absorption of B12 (substance use consideration)
Wounds that don’t heal, changes in neuro, muscle weakness, thinking process impaired

A

Megaloblastic anemia

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6
Q

Rare, autoimmune
Can lead to cobalamin deficiency
Middle age
Ethnic groups - African, northern European ancestry ++ impacted
Women more than men
Can often be more severe
Lack of intrinsic factor (IF) - protein needed for cobalamin absorption **

A

Pernicious anemia

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7
Q

People w ____ have increased risk of gastric cancer

A

anemia

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8
Q

need to be on supplements parenteral, intranasal because they can’t absorb it. Won’t cure will help w blood levels. As long as they use supplement - symptoms can be reversed. Neuro problems won’t be reversed if symptoms left untreated

A

Pernicious anemia

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9
Q

part of megaloblastic anemia, some links to other diseases and deformities - deficiency could be related to diet, absorption, alcohol use, medications

A

Folic acid

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10
Q

Normal ______ levels 11-57

A

folate

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11
Q

Some anti-seizure medications in particular affect absorption - Dilantin

A

Folic acid

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12
Q

Under production of RBC
Possible underlying conditions: Chronic renal problems, chronic liver disease - on going inflammation
Thyroid problems, chronic endocrine disease
Looking for: Serum folate, iron store, cobalamin levels
Best thing to do is treat the underlying cause

A

Anemia related to disease

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13
Q

Decrease in all blood cell types - RBC, WBC, and platelets
Potential cause: malfunctioning bone marrow - stem cell transplants, repressive therapy, bone marry transplants
Lots of things cause this - even radiation, chemical stuff, chromosomal problems
Can be abrupt or gradual development

A

Aplastic anemia

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14
Q

Identify and treat ____________: Important to do for all forms anemia

A

Underlying cause

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15
Q

Gradual development is often missed until symptoms are really pronounced
Symptoms will manifest as general symptoms of anemia (fatigue, heart has to work harder, SOB, WBC decrease, neutropenia, thrombocytopenia (platelets are really decreased)

A

Aplastic anemia (Gradual Development)

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16
Q

Low neutrophil count is at risk for infection
Low platelet count is at risk for bleeding
Watch for signs / symptoms of infection (fever, chills, decreased LOC)
Thrombocytopenia - red spot rash, easy bruising, bleeding gum & nose

A

Aplastic anemia

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17
Q

can be acute or chronic

A

Blood loss

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18
Q

Trauma, cuts, heavy periods
Anything where there is a lot of blood loss - loss of RBC - decreased available oxygen

Decreased RBC will not be reflected in labs right away - reflection of actual blood loss will happen with 2-3 days, because of volume
Volume of blood has also decreased - so it will be proportionate

A

Acute Blood Loss

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19
Q

Goal: prevent shock
Replace blood volume - stop the bleeding

A

Acute Blood Loss

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20
Q

Clinical signs are key - we need to pick up clinical signs quicker than 2-3 days in order to prevent bleeding out

A

Acute Blood Loss

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21
Q

HR increase
BP decrease
As we lose more blood LOC will change, pallor/grey (noticeable)

A

Clinical signs of shock (in acute blood loss)

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22
Q

Symptoms
Pain - volume of blood pushing organs with internal bleeding, pressing on nerves

A

Acute blood loss

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23
Q

Major complication of acute blood loss is ____

A

shock

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24
Q

Need to do some kind of volume replacement
May get packed red blood cells, may need supplemental iron
As soon as we notice increase HR and decrease BP - pt heading toward shock

A

Shock prevention (blood loss)

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25
Q

Lab work will reflect blood loss
Symptoms very similar to iron deficiency
Treated w iron supplements

A

Chronic blood loss

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26
Q

Hemorrhoids, menstrual bleeding, epistaxis - identify the source
Effects are related to iron stores

A

Chronic blood loss

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27
Q

Vitamin C helps w absorption
Changes stools - not like Malena
Liquid - rinse mouth out, take w a straw
Metallic taste in mouth
Foods high in - beans, lentils, spinach, red meat

A

Iron Supplements - pt teaching

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28
Q

Destruction of erythrocytes greater than production can be caused by:

A

Hereditary problem
External factors

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29
Q

Destruction of hemoglobin or RBC is the spleen - primary site of destruction

A

Splenomegaly

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30
Q

Inherited
Abnormal form of hemoglobin
Prevent organ damage from happening
Since hereditary found in early childhood
Predominantly African descent, east Indian, Arabian

A

Sickle cell disorder

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31
Q

Antibodies are destroying RBCs

A

Acquired hemolytic

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32
Q

Iron overload
Jaundice, abdominal pain

A

Hemochromatosis

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33
Q

Goal to get rid of iron
Donate blood

A

Hemochromatosis

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34
Q

Increased production increase amount of RBC, increases thickness/viscosity of blood
Causes an Increase hyper viscosity
Thicker blood
Need to decrease thickness - increase volume and decrease thickness, look at bone marrow activity
Circulation is impaired

A

Polycythemia

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35
Q

_________ changes associated with blood disorders:
Pallor (decreased hemoglobin, blood flow to the skin)
Jaundice (increase concentration of serum bilirubin)
Bilirubin can cause skin itching as a symptom
Eyes often show jaundice, bottom of feet, palms of hands - darker skin people
Pruritus’ (increase serum and skin bile salt concentrations)

A

Integumentary changes

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36
Q

_________ changes associated with blood disorders:
Can eventually result in heart failure
Edema
Manifesting cardiopulmonary change

A

Cardiopulmonary

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37
Q

Anemia is not a normal finding in _________:
Person will have symptoms, be exhausted
Nutritional deficiencies - fixed income
Worsening cardiovascular & pulmonary problems w anemia
Pallor, confusion, fatigue, trouble walking - increase risk of falls

A

older adults

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38
Q

Organs enlarge w organs not getting enough blood

A

sickle cell

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39
Q

Changes in ________:
Eyes can be very sensitive
Erectile dysfunction

A

circulation

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40
Q

Includes RBC, WBC and platelets
Follows what is being formed in that bone marrow

A

CBC

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41
Q

Size & volume of blood cells

A

MCV

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42
Q

Ratio between CBC and MCV

A

MCH

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43
Q

A decrease in _____ can increase risk of infection.
Neutrophils are important to look at to look at

A

WBC

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44
Q

Combined amount of iron w proteins in serum
Looking at status of what is being used and what is being stored

A

Serum Iron

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45
Q

One of the largest proteins that bonds w iron
With this one you will see a decrease in iron deficiency anemia and increase in megaloblastic

A

Transferrin

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46
Q

Platelets can be low do to virus, chronic disease
The lower this number is, the risk of bleeding
Pregnancy
Can be inherited, acquired, autoimmune, splenomegaly

A

Thrombocytopenia

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47
Q

low platelets

A

Thrombocytopenia

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48
Q

_____ disorders can be caused be cause production impaired, destruction, abnormal amount

A

Platelet

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49
Q

most common, destruction of circulating platelets

A

ITP (Immune thrombocytopenic purpura)

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50
Q

Platelets function normally till they get to spleen then the spleen mistakes them as foreign & destroys

Big goal: prevent bleeding

A

ITP (Immune thrombocytopenic purpura)

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51
Q

Platelets normally live 10 days, in _____ they live 3 days

A

ITP (Immune thrombocytopenic purpura)

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52
Q

Splenectomy is treatment, steroids in high dosages
More common

A

ITP (Immune thrombocytopenic purpura)

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53
Q

When platelet count is <____ × 109/L increase in internal bleeding
Headaches, stroke symptoms, eye sight changes, pain

A

150

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54
Q

Related to certain drugs
Not common but very serious
Increased agglutination - clotting is out of wack
Hemolytic anemia, neurological changes happening
Body will react - fever but no infection

A

TTP (Thrombotic thrombocytopenic purpura)

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55
Q

IS a medical emergency

A

TTP (Thrombotic thrombocytopenic purpura)

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56
Q

What classifies any thrombocytopenia is when platelet count drops below 150 × ____/L

A

109

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57
Q

Can start within a couple of days when someone starts on heparin
As early as 5 days
Person has a clot - shouldn’t have that with heparin

A

Heparin-Induced Thrombocytopenia

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58
Q

Pressuring about a clot, pulmonary problem
Should be zero
Measures fibrin
We would see an increase in this value w a pulmonary emboli

A

D-dimer

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59
Q

comparison of prothrombin time

A

INR

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60
Q

Genetic disorder
Defective/deficient in coagulation factor
Chronic illness
Symptoms can be mild/severe

A

Hemophilia

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61
Q

factor 8 has a problem

A

Hemophilia A

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62
Q

factor 9 has a problem

A

Hemophilia B

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63
Q

a bleeding disorder caused by the qualitative or quantitative deficiency of the pro-von Willebrand factor.

A

Von Willebrand’s disease

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64
Q

Pt needs to be educated
Preventing situations where it can be a problem
Symptoms can be mild/severe

A

Von Willebrand’s disease

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65
Q

Affected people may complain of excessive bruising, prolonged bleeding from mucosal surfaces, and prolonged bleeding after minor trauma.
Pallor, melena, hemoptysis, changes in Mental Status, headaches, joint pain, abdominal pains
Coagulation part - clots form - inhibits circulation

A

Von Willebrand’s disease

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66
Q

Bad thing to have, serious bleeding, serious clotting changes that can lead to severe hemorrhage
Always caused by something underlying
- If cause is not identified - person will die
Has to be diagnosed quickly
Bleeding, clotting (thrombotic manifestations)
Clots forming anywhere

A

Disseminated intravascular coagulation (DIC)

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67
Q

Decrease in WBC
Cancer of the blood (malignant)
Accumulation of dysfunctional cells
Bone marrow is being replaced w leukocytes that are not functional (proliferating leukocytes)
Fatal if untreated

A

Leukemia

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68
Q

Causes: chemicals, radiation, genetics, viral impact, chromosomal changes
Incidence increased in radiologists, or work in radiology
People who previously had chemo increased risk

A

Leukemia

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69
Q

Myelocytes, along with metamyelocytes and promyelocytes, are the precursors of neutrophils
High percentage of adult leukemia
Abnormal bleeding, lots of infection
Onset is abrupt
Mostly adults

A

AML - acute myelogenous leukemia

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70
Q

Most common in KIDS
20% adults
Abrupt onset of symptoms: fever, feeling sick, bleeding gums (more blood than usual - usually first sign)

A

ALL - Acute lymphocytic leukemia

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71
Q

Excess development of neoplastic granulocytes
Move into blood system, infiltrate liver, spleen
Start off more chronic then become more acute

A

CML - chronic misogynist leukemia

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72
Q

Associated w changes in genetic materials in chromosome 9 and 22

A

CML - chronic misogynist leukemia

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73
Q

Chronic phase can last for years and usually treated and well controlled - can sometimes go into remission
Often eventually progress to accelerated phase where it rapidly changes and needs aggressive treatment

A

CML - chronic misogynist leukemia

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74
Q

Mature appearing lymphocytes but functionally inactive
Common in adults
Increased risk of infection
Often disease of older people
Symptoms often related to bone marrow failure - everything is changes - thrombocytopenia, anemia, changes in WBC in production & functioning, organ enlargement, lymphopenia (enlarged lymph nodes), brain symptoms, bone pain

A

CLL - chronic lymphocytic leukemia

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75
Q

decrease in neutrophil counts

A

Neutropenia

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76
Q

lots of diff symptoms related to anemia, neutropenia, thrombocytopenia; diagnosed through bone marrow biopsy; seen in older peoples (over the age of 80); risk increases w age

A

Myelodysplastic syndrome (MDS)

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77
Q

Symptoms of bleeding, infection Labs: # of platelets are not functioning the way they should
Often diagnosed when someone is doing tests for anemia, then they do the bone marrow biopsy - more complicated at >80 yrs

A

Myelodysplastic syndrome (MDS)

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78
Q

Aggressiveness of treatment will match aggressiveness of disease
_______ prone to more side effects / complications for aggressive treatments

A

Older ppl

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79
Q

________ - cancer of the lymphocytes
- Starts in bone marrow
- Hodgkin’s lymphoma and Non-Hodgkin’s

A

Lymphomas

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80
Q

Increase in Reed Sternberg Cells - located in lymph nodes
Connection w Epstein bar virus, genetic predisposition, toxics (HIV)
Chemotherapy is done w this one
Nursing is based on management of problems that come up - like pain

A

Hodgkin’s

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81
Q

Originates outside the lymph nodes
People with this will have a progressive disease by the time it’s diagnosed meaning treatment has to be aggressive (chemo, biotherapy, radiation)

A

Non-Hodgkin’s

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81
Q

A type of non-Hodgkin’s lymphoma (NHL) that grows and spreads slowly.
Treatment is better

A

Indolent lymphoma

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82
Q

Slow and insidious
Seldom cured, remission can occur w not trace of illness
Life can be extended
Chemo is treatment
Involves bones
Bone breakdown

A

Multiple Myeloma

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83
Q

Increased filtering and capacity of circulating blood cells, which decreases amount of circulating blood cells (lol what)
Can palpate when it’s large
Sometimes you have abdominal pain / sometimes you don’t
When enlarged there is a risk of pain

A

Enlarged Spleen (splenomegaly)

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84
Q

Problems that occur w/ _______ problems:
Teaching signs and symptoms to the family as well when someone is in isolation
Impaired oral mucous membrane integrity - soft bristle toothbrush
Possible Nursing Diagnoses:
Knowledge deficit
Risk of bleeding

A

hematological

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85
Q

on an EKG is the top of the QRS

A

S1

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86
Q

on an EKG is the little T wave

A

S2

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87
Q

with this condition the U wave will be opposite direction on an EKG

A

Hypokalemia

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88
Q

baroreceptors, autonomic NS, ANS impact on heart & blood vessels, chemoreceptors, blood pressure

A

What regulates your cardiovascular system? ***

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89
Q

Kyphosis can affect placement of everything, making pumping action hard & breathing hard
Heart can enlarge, increased vascular rigidity due to this our heart’s ability to pump will increase/decrease
Ability to adapt to exercise not the same
Blood vessels - arterial stiffening
Age related - impacts blood vessels, heart
Dyspnea - is this respiratory or cardiac? Can be hard to tell w/ out diagnostics
Dizziness
Postural blood pressure changes (orthostatic hypertension/hypo?)
Claudication, erectile dysfunction is often present when there is a change in a males body, any vascular change - it is impacted
QRS can become widened - heart arrythmia problem, medications - need to be watched - regular EKG

A

Older adults

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90
Q

Objective data: vitals, chest exam, trunk-al obesity, cardiovascular system can impact way a person is thinking, Mental Status changes, confusion/fogginess

A

Older adults - important info

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91
Q

troponin, CK-MB, myoglobin

A

Cardiac biomarkers

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92
Q

big one, if MI occurs it is released, can be detected 4-6 hrs and lasts 14 hrs. Anyone who has chest pain they check this level

A

Troponin

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93
Q

creatine kinase, specific to the heart MB, elevated with any kind of injury, starts to rise anywhere between 3-6 hours, peaks 12-24 hours then goes down to baseline - has to be caught in that other time frame. Returns to baseline anywhere between 12-48 hours after MI

A

CK-MB

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94
Q

protein, comes from skeletal muscle, released whenever any kind of problem, cardiac marker but it is not specific to that

A

Myoglobin

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95
Q

released from atrium & ventricles, and released in endothelial cells (renal), used to distinguish SOB is respiratory / cardiac *

A

Cardiac natriuretic peptide markers

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96
Q

HDL, LVL, triglycerides, cholesterol is a lipid panel, often bound to proteins so sometimes call lipoproteins. Increased LDL and something risk of cardiovascular disease increased, increased HDL (protective cholesterol - gets rid of that cholesterol) the risk is lower

A

Serum lipids

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97
Q

another one that is done, inflammation in general, history of MI / chest pain they probably will have this elevated - but this alone is not enough to say it’s cardiac, but goes along w the package to support it, CRP increase can indicate further risk of cardiac problems in people w cardiac history

A

C reactive proteins

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98
Q

portion that is released w protein breakdown, at increased risk of Cardiovascular/peripheral vascular disease & stroke, can be monitored w history/family history of cardiac stuff. Tell tale sign

A

Homocysteine

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99
Q

associated phospholipase A2 - is an enzyme that is elevated when plaque in blood vessels

A

Lipoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Chest pain for _______ - some of these biomarkers might be back to normal. CK-MB could possibly still be elevated, other ones could be back to normal - that is why we try to catch them early on also to prevent damage

A

24 hours

101
Q

silent killer **

A

Hypertension

102
Q

+ hypertension (BP) = + risk of ____ = + risk of heart failure = + risk of stroke = + risk of renal disease

A

MI

103
Q

Hugely modifiable - medication, exercise, diet
Things we can do to try and prevent that
As we age high BP go up, women who have high BP are at increased risk of cardiovascular disease, Indigenous peoples, older women are at a higher risk than older men

A

Hypertension

104
Q

_______ need lower BP
Why?
High sugars already damage the vessels
High BP on top of diabetes = + risk for stroke and any other kind of cardio disease
Which is why we try and maintain that lower - important to do this
Some ppl w diabetes on medication for hypertension right away because of this

A

Diabetes

105
Q

Blood pressure = cardiac output + systemic vascular resistance
Any one of these parts is off, + BP

A

Hypertension

106
Q

the volume of blood ejected from the heart per minute

A

Cardiac output

107
Q

another term they look at, amount of normal blood volume, 60-100 ml. At rest heart pump 5-6 L per minute, increase w exercise

A

Stroke volume

108
Q

renal fluid volume control (salt impact) (Renin Angiotensin S system, naturetic peptide); cardiac wise (HR, contraction, conductivity - affect CO)
- Renal & cardiac

A

Factors influencing cardiac output

109
Q

neurohormonal stuff (vasoconstrictors (angiotensin & norepinephrine)); sympathetic nervous system; local regulation
- When one or more of these not working = + BP

A

Systemic vascular resistance

110
Q

androgenic receptors (vasoconstrictors; α1 and α2); B2 - adrenergic receptor (opens it) medications work in these specific areas *

A

Sympathetic NS

111
Q

α1- and α2- adrenergic: Vasoconstriction
β1-adrenergic: Increased HR and conduction
β2-adrenergic: Vasodilation and increased renin secretion
Dopaminergic: Vasodilation Sympathetic nervous system (SNS)
Baroreceptors Vascular endothelium
Renal system Renin–angiotensin–aldosterone system (RAAS)
Endocrine system

A

Normal Regulation of BP

112
Q

α1- and α2- adrenergic: _________

A

Vasoconstriction

113
Q

β1-adrenergic: Increased _______ and conduction

A

HR

114
Q

β2-adrenergic: __________ and increased renin secretion

A

Vasodilation

115
Q

If our BP drops then we have automatic protection (________); increase CO & vascular resistance

A

renin

116
Q

_________ tell our brain what is going on
“our BP is too high, we need to decrease” then we have communication & decrease HR by stimulating Vagus nerve to decrease CO

A

Baroreceptors

117
Q

“our BP is too high, we need to decrease” then we have communication & decrease HR by stimulating __________ to decrease CO
Neurotransmitters that are released & we have them in SA node, myocardium & vascular smooth muscle has these receptors (a1 and a2; b1 & b2; the adrenergic receptors)
B1 adrenergic receptor responds by + HR; prototrophic effect
Increases inotropic effect (when force of contraction is +)
Increase conduction - dromotropic effect

A

Vagus nerve

118
Q

__________ that are released & we have them in SA node, myocardium & vascular smooth muscle has these receptors (a1 and a2; b1 & b2; the adrenergic receptors)

A

Neurotransmitters

119
Q

______________ responds by + HR; prototrophic effect
- Increases inotropic effect (when force of contraction is +)
Increase conduction - dromotropic effect

A

B1 adrenergic receptor

120
Q

___________ work on protropin, inotropic, dromotropic

A

Medications

121
Q

β1-Adrenergic receptors in the heart respond to NE with increased HR (___________ effect), increased force of contraction (____________ effect), and increased speed of conduction (_____________ effect).

A

chronotropic; inotropic; dromotropic

122
Q

B2 receptor activated by NE; causes _____

A

dilation

123
Q

pressure receptors; sensitive to stretching in blood vessels

A

Baroreceptors

124
Q

Carotid arteries, aortic areas
Stretching - activation of Sympathetic NS, ____________ will occur
A fall in BP, sensed by the baroreceptors, leads to activation of the SNS. The result is constriction of the peripheral arterioles, increased HR, and increased contractility of the heart.

A

vasodilation

125
Q

Stimulation of vagus nerve can ________ HR

A

decrease

126
Q

has an impact of BP control (sodium increased; water retained; all increase heart stroke volume & others CO)
RAS system - pg 775
Angiotensin converting enzyme
Decrease BP we need ACE inhibitor to block that effect

A

Renal system

127
Q

HF is a progressive disease
Salt restricted
Maximize heart functioning, get rid of fluids

A

Acute interventions

128
Q
  • Automatic (start impulse and continue)
  • Excitability (heart responds to the impulse by contracting)
  • Conductivity (transmission of impulse)
  • Contractility (electrically stimulated)
A

Properties of Conduction System

129
Q

_______ nervous system controls rate of impulse, speed of conduction and strength

A

Autonomic

130
Q

Impulse starts in _______ **
- Make atrium and ventricle contract
PR interval - purkinje fibres

A

SA node

131
Q

__________ control of Heart
- Autonomic controls rate of impulse, speed of conduction & strength
- Parasympathetic - decreases force, rate
- Sympathetic - opposite; increases

A

Nervous System

132
Q
  • Most commonly used diagnostic tool
  • Hearts electrical activity
  • Each beat is seen thru one wave
A

Electrocardiogram

133
Q
  • Drug toxicity
    • Diagnostic tool
      Electrical forces in the horizontal plane
A

12 Lead EKG

134
Q

_____ - isoelectric flatline ** Important when looking at EKG
Time period where there is no electrical activity in the heart

A

QT line

135
Q

Evaluation of _______
- Stress testing
- Treadmill
- Holter monitoring
Feel like heart is skipping beats - person will wear monitor, keep a diary and say how they feel at diff times
- Take strip and see if the information matches their symptom

A

Dysrhythmias

136
Q
  • Sinus nodes fires <60 beats
  • Normal rhythm in aerobically trained athletes and during sleep
  • Starting at sinus nodes
  • Hypothyroidism can cause
  • Outside problem, not a heart problem
A

Sinus Bradycardia

137
Q

Clinical associations, responds to:
- Can get when we have carotid sinus massage
- Valsalva maneuver (pooping) - that is why sometimes people faint
- Increased intraocular pressure

A

Sinus Bradycardia

138
Q

Clinical associations, occurs in disease:
- Inferior wall MI
- Head injury/intercranial pressure
- Hypothyroidism
- Obstructive jaundice
Meds that bring this up - beta, calcium channel blockers

A

Sinus Bradycardia

139
Q

Clinically significant
Symptoms
- Hypotension
- Pale, cool skin
- Confusion
- Disorientation
- Do delirium workup to differentiate

A

Sinus Bradycardia

140
Q

Treatment
- Atropine (when serious and person is symptomatic)
- Pacemaker may be required
- Epinephrine/dopamine infusions

A

Sinus Bradycardia

141
Q

Can be normal related to stress, exercise, fever, anxiety, pain
Conduction pathway same as bradycardia; starting at SA
Greater than 100 BPM

A

Sinus Tachycardia (too fast)

142
Q

Hypotension **
Hypovolemia
Anemia
Hypoxia
MI
Heart failure
Hyperthyroidism ** she said test question lol

A

Associated w physiological & psychological stressors (Sinus Tach)

143
Q

Clinical significance
Is person symptomatic
Dizziness; hypotension due to decreased CO
Increased myocardial oxygen consumption may lead to angina

A

Sinus tach

144
Q

Stress, alcohol, tobacco, hyperthyroidism, heart disease, stress, caffeine, hypoxia, electrolyte imbalance, COPD
Originating from ECTOPIC (outside) focus in atrium location other than SA node
Travels across atria by abnormal pathway creating distorted P wave
May be stopped, delayed, or conducted normally at the atrioventricular node (AV)

A

Premature Atrial Contraction (PAC)

145
Q

ventricle movement, atrial working MORE than the rest
Can get into a saw like pattern
Not getting full ventricular conduction w it
Not normal

A

Atrial flutter

146
Q

Can lead to decreased CO, heart failure because of that, stroke
Recurring and regular
Atria is moving fast 250-350

A

Atrial flutter

147
Q

Caused by
CAD
Severe hypertension
Mitral valve disorders
Pulmonary emolus
Have to figure out WHY this is happening; could be many diff underlying conditions

A

Atrial flutter

148
Q

When happening for >48 hours can cause a stroke due to thrombus formation in the atria
Often people put on blood thinner
High ventricular rate >100 and loss of atrial “kick” can decrease CO and precipitate Heart Failure (HF), angina
Could have chest pain, really decreasing CO
Need to convert atrial flutter BACK to sinus rhythm
Calcium channel blockers
Adrenergic blockers
To try and control

A

Atrial flutter

149
Q

Disorganized
Telling you that there are different areas stimulated to produce that rhythm
Most common dysrhythmia
Increases w age
1-2% of pop live w this
Decrease consciousness
Can be intermittent
Increase risk of stroke
Ventricular rate can be from normal to abnormal - increase risk for clots (thrombus)
Not recommend doing radial pulse; do apical (manually)
Not as accurate to use automatic BP machine; doesn’t pick it up the same

A

Atrial Fibrillation

150
Q

What is a common dysrhythmia that occurs as we age?
____________
Disorganized - that is how we would identify (abnormal pattern)
QRS could be a normal pattern; but irregular pattern

A

Atrial fibrillation

151
Q

Clinical associations - usually occurs w underlying heart disease
Rheumatic heart disease
Cardiomyopathy - diseased heart
Heart failure (HF)
Pericarditis
CAD
Acute onset: caffeine use, stimulants, stress, alcohol, electrolyte disturbances - main things you look at right away

A

Atrial fib

152
Q

Clinical significance
Decrease CO (due to ineffective atrial contractions/loss of atrial kick)
Risk of stroke 3-5 x higher w _______

A

atrial fib

153
Q

Treatment
Goals
Decrease ventricular rate (improve the control)
Prevent cerebral embolic events
Long term anticoagulation therapy

A

Atrial fib

154
Q

Originates in AV node (weird because should start in SA node - this isn’t working proper; skipping this part)
SA node fails to fire; has been blocked at AV node
Diff med can start this; MI; caffeine
Digoxin can result in this as well - popular med
Lab work is done to see if you’re in the right range, toxicity can result in further abnormal rhythm
Is the person symptomatic? Can’t tell w taking a pulse
Symptoms involved usually
Will see on EKG

A

Junctional Dysrhythmias

155
Q

(first degree, second degree, third degree full heart block)

A

Junctional Dysrhythmias

156
Q

________ - quite slow; PR interval is long (lengthened)
Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged
Bradycardic - usually asymptomatic otherwise

A

First degree block

157
Q

________:
AV node prolonged
Atria and ventricles contract independently of each other
Loss of electrical activity happening - increased
Gradual lengthening of interval, gradually lose QRS
May need pacemaker to make sure heart is working evenly; not missing beats
Most often seen: HF, shock, damaged heart

A

Second-degree

158
Q

Form of AV dissociation in which no impulses from the atria are conducted to ventricles
Atria are stimulated and contract independently of ventricles
Ventricular rhythm is an escape rhythm
Seen w severe heart disease; MI; some systemic disease; lovely meds like digoxin can do this too
CO is poor
CO w ischemia
Person may be fainting (Syncope)
Ectopic pacemaker may be above / below the bifurcation of the bundle of His
Permanent pacemaker
Especially being symptomatic

A

Third Degree (Complete heart block)

159
Q

Next to no CO
Digitalis toxicity
Valve problems
Electrolyte imbalances
What is causing it? Fix it
Person can have this and have a pulse; or be considered unstable w no pulse
Pulse not normal; not pumping the heart
Decreased cerebral blood flow
V-tach - life threatening - need CPR done; defibrillation and epinephrine is drug of choice

A

Ventricular tachycardia

160
Q

They need CPR, defibrillation
All types of MI; CAD; cardiomyopathy
Hyperkalemia (high potassium) - cardiac arrest
Potassium out of wack needs to be fixed RIGHT AWAY
If untreated leads to death

A

Ventricular Fibrillation

161
Q

Cardiac Arrhythmias
_________:
Absence of contractions of heart
Flat line in EKG
Not breathing, pulseless
Not good
Advanced cardiac life support

A

Asystole

162
Q

_______:
Most effective method of terminating VF and pulseless VT
Passage of DC electrical shock through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker

A

Defibrillation

163
Q

_______ - changes associated w acute coronary syndrome
Ischemia
Injury
Infraction

A

ECG/EKG

164
Q

________ ** need to know
Brief lapse in consciousness accompanied by a loss of postural tone (fainting)
Cardiovascular causes
Neurocardiogenic syncope or “vasovagal” syncope (e.g., carotid sinus sensitivity)
Primary cardiac dysrhythmias (e.g., tachycardias, bradycardias)
Non-cardiovascular causes
Hypoglycemia
Hysteria
Unwitnessed seizure
Vertebrobasilar transient ischemic attack

A

Syncope

165
Q

Layers of the _______
Serous pericardium (visceral layer; epicardium)
Endocardium
Myocardium
Serous pericardium (parietal layer)
Pericardial space
Fibrous pericardium

A

heart

166
Q

An Infection of the heart valves or the endocardial surface of the heart.
Risk factors include previous endocarditis, prosthetic valves, acquired valvular disease other cardiac lesions, and non cardiac condition.
Symptoms are nonspecific and can involve multiple organ systems.

A

Infective Endocardium

167
Q

Inflammation of the pericardial sac
Infectious, non-infectious, and autoimmune
Symptoms of progressive, frequent, severe chest pain
Hallmark finding in acute pericarditis is the pericardial friction rub.
Complications include, pericardial effusion and cardiac tamponade
Treatment is geared identifying and treating the underlying cause.

A

Acute Pericarditis

168
Q

Inflammation of the myocardium - focal or diffuse
Clinical manifestations vary from mild to sudden cardiac death

A

Myocarditis

169
Q

Chronic condition
Inflammatory disease
Affects several connective tissues of the body especially heart, brain, joints or skin
Can involve all layers of the heart

A

Rheumatic fever

170
Q

Cardiac lesions and valvular deformities
Extracardiac lesion
Acute rheumatic heart disease can occur as a complication from strep A pharyngitis
Chest pain, excessive fatigue, heart palpation, sob, edema

A

Rheumatic heart disease

171
Q

_______ Heart Disease
The heart has
Two atrioventricular valves
Mitral
Tricuspid
Two semilunar valves
Aortic
Pulmonic

A

Valvular

172
Q

Stenosis
The valve is restricted
Forward blood flow is impeded
A pressure gradient is created across the open valve
Pressure gradient differences reflect the degree of stenosis

A

Valvular Heart Disease

173
Q

Regurgitation
Incomplete closure of valve leaflets
Results in backward flow of blood

A

Valvular Heart Disease

174
Q

The majority of adult cases result from rheumatic heart disease
Causes scarring of valve leaflets and chordae tendineae
Contractions develop w adhesions between commissures of the leaflets
Primary symptom if exertional dyspnea due to decreased lung compliance

A

Mitral Valve Stenosis

175
Q

Valve function depends on
Intact mitral leaflets
Integrity of mitral annulus
Chordae tendineae
Papillary muscles

A

Mitral Valve Regurgitation

176
Q

Valve patency depends on
Left atrium
Left ventricle
An abnormality of any of these structures can result in regurgitation

A

Mitral Valve Regurgitation

177
Q

Abnormality of mitral valve leaflets and the papillary muscle of chordae
Allows the leaflets to prolapse back into the left atrium during systole
Unknown cause

A

Mitral Valve Prolapse (MVP)

178
Q

Usually discovered in childhood, adolescence, or young adulthood
Those seen later in life usually have aortic stenosis from rheumatic fever/calcification of a normal valve
Isolated aortic valve stenosis is almost always of nonrheumatic origin
Results in obstruction of flow from left ventricle to aorta during systole
Angina
Syncope
Exertional
Dyspnea

A

Aortic Valve Stenosis

179
Q

May result from disease of aortic valve leaflets, aortic root, or both
Caused by:
Infective endocarditis
Trauma
Aortic dissection

A

Aortic Valve Regurgitation

180
Q

Myocardial contractility eventually declines
Pulmonary hypertension and right ventricular failure develop
Clinical manifestations of sudden cardiovascular collapse - constitutes a medical emergency

A

Aortic Valve Regurgitation

181
Q

Very uncommon
Tricuspid occurs almost exclusively in patients
W rheumatic mitral stenosis
IV drug users
Have had multiple myocardial biopsies, radiation treatment, anorectic medications
Treated w dopamine agonists
Pulmonic is almost always congenital
Both result in increased blood volume in right atrium and ventricle, respectively

A

Tricuspid and Pulmonic Valve Stenosis

182
Q

Diagnostic Studies for _______:
Pt history/physical exam
Echocardiography and doppler imaging
Chest radiograph
ECG/EKG
Cardiac catheterization

A

Valvular Heart Disease

183
Q

Interprofessional Care
Prevention of recurrent rheumatic fever and infection endocarditis is essential
Treatment depends on the valve involved and severity of disease
Medication therapy to treat / control HF
Digitalis (positive inotropes)
Vasodilators
Diuretics
B blockers
Other medication therapies
Anticoagulants
Antidysrhythmic
Low sodium diet
Percutaneous aortic valve replacement
Percutaneous transluminal balloon valvuloplasty (PTBV) to split open fused commissures

A

Valvular Heart Disease

184
Q

Nursing Assessment
Subjective
Objective
Fever
Hepatomegaly
Diaphoresis
Crackles, wheezes, hoarseness
Ascites
Abnormal heart sounds
Tachycardia
Dysrhythmias
Hypotension
Reduced stamina
Excess fluid volume
Decreased cardiac output

A

Valvular Heart Disease

185
Q

A group of diseases that directly affect the structural or functional ability of the myocardium
Dilated, Hypertrophic, Restrictive
A diagnosis of cardiomyopathy is made on the basis of the patient’s clinical manifestations and non-invasive and invasive diagnostic procedures.
There are two types: primary and secondary.
Symptoms may include decreased exercise capacity, fatigue, dyspnea at rest, paroxysmal nocturnal dyspnea and orthopnea, dry cough, palpitations

A

Cardiomyopathy

186
Q

__________ - Dilated
Ventricles are weaker & get larger
Heart muscle is larger and thicker
Ventricles stiffen, heart wall do not thicken

A

Cardiomyopathy

187
Q

Include disorder of the arteries, veins, and lymphatic vessels

A

Vascular Disorders

188
Q

____________ - your limbs :) - everything outside the heart and brain
Aneurysmal
Atherosclerotic
Narrowing & degeneration
Risk factors: diet, tobacco, diabetes (damages endothelial tissue in blood vessels - increased glucose levels,
Nonatherosclerotic

A

Peripheral artery disease (PAD)

189
Q

Progressive narrowing & degeneration of arteries in neck, abdomen & extremities
Strong associated w systemic atherosclerosis
Higher as age increases (85 30-50% have PAD)
Sections of arteries
Anyone w diabetes this can happen earlier
Usually a marker for systemic problems

A

Peripheral artery disease (PAD)

190
Q

What causes them and WHY
Risk factors - why? Think bigger picture
High cholesterol, increased fats and lipids, obesity, sedentary lifestyle, high BP (hypertension), genetic risk (family history)
Marker in blood - C reactive protein**
Chronic problem, it will be monitored
Homocysteine levels are sometimes elevated as well w atherosclerosis AND blood clots
Lipid monitoring ***

A

Atherosclerosis

191
Q

In diabetes, tend to be below the knee - loss of sensation, amputation
More common in aortoiliac, femoral, popliteal, tibial & peroneal arteries
Intermittent claudication (calf pain/leg pain after movement - occurs w movement & goes away in 10 mins after rest) - key for peripheral vascular pain **
Rest pain, chronic
Related to ischemia - ischemic pain
Reproducible - pain will show up for same thing that caused it over and over
Rest pain
In forefoot & toes * aggravated by limb elevation
Insufficient blood flow
More frequent at night

A

PAD of lower Extremities

192
Q

when you elevated legs it remains that grey colour

A

Elevation pallor

193
Q

Other clinical manifestation
Reactive hyperemia - foot gets redder when just sitting there
Paresthesia
Thin, shiny, and taut skin
Loss of hair on lower legs
Diminished/absent pedal, popliteal or femoral
Elevation pallor
Reactive hyperemia
Rest pain
Occurs in the forefoot or toes and is aggravated by limb elevation
Occurs from insufficient blood flow
Occurs more often at night

A

Elevation pallor

194
Q

_______ complications (at risk for the following)
Atrophy of muscles
Increased damage from minor trauma
Slowed wound healing
Increases risk of infection
Nonhealing arterial ulcers
Gangrene
Amputation

A

PAD

195
Q

_________ - gangrene, ulcers
They will have an amputation within 7 months if they have this critical limb ischemia
Ischemia is bad because - no circulation, blood flow change, tissue death (gangrene), risk will increase in diabetes
Bypass is most common treatment
Proper fitting shoes, nails
Bottom of feet need to be looked at, change in sensation

A

Critical limb Ischemia

196
Q

What can nurse do? Decrease the risk:
Education is huge to decrease risk
Tobacco
Antiplatelet side effects
Non pharmacological - walking/exercise is huge

A

Critical limb Ischemia

197
Q

Diagnosis - doppler ultrasound
Angiogram, venograms sometimes

A

Critical limb Ischemia

198
Q

Acute, sudden
Huge interruption in blood supply
Thrombus may develop within an artery & cause complete occlusion of blood flow to the tissues “downstream”
An embolus may dislodge from within an artery, travel “downstream” and completely occlude artery
Think about the 6 P’s **
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
Poikilothermia - the inability to maintain a constant core temperature independent of ambient temperature
Anticoagulation therapy, remove clot
Revascularization / amputation

A

Acute Arterial Ischemia

199
Q

Aka burgers disease
No tests for this
Non anthrosclerotic inflammatory disorder
Might have rest pain, intermittent claudification
A nonatherosclerotic, segmental, recurrent inflammatory vaso-occlusive disorder of the small and medium-sized arteries and veins of the upper and lower extremities
Sometimes ulcerations, feet hands and arms (smaller areas)
Decreasing risk - analgesics *
Lots of pain

A

Thomboangiitis Obliterans

200
Q

Spastic disorder of cutaneous arteries
Fingers & toes
Colour change
Only a few minutes sometimes for an hour or so
Triggered by stress, change in temp is a big one, emotional stress
Caffeine & tobacco
Diagnosed if persists for > 2yrs
Anything that limits vasoconstriction - caffeine, tobacco, and cold
Drug of choice - calcium channel blocker (decrease that response)

A

Raynaud’s

201
Q

Loss of elasticity of media layer of arterial wall causing thinning and bulging of aortic wall
¾ occur in abdominal aorta
Also in aortic arch, thoracic aorta
Any artery can have aneurysm
Congenital or acquired
Can be caused by infection, inflammation, trauma (mechanical - outside factor)
Men > women for risk; >65
Abdominal aneurysm - big cause of death in elderly
Tobacco - major risk factor
CAD, PAD, high cholesterol
Often asymptomatic - found in regular x ray often
High mortality rate
Surgery when around 5-5.5 cm
Unless person is symptomatic (pain); surrounding area is compressed because of the aneurysm is increasing in size
Abdominal - level of renal - that is why we listen for bruits (asymptomatic)
Biggest cause in aorta - atherosclerosis
Biggest risk, tobacco
Can even get intermittent claudication

A

Aneurysm

202
Q

A - uniform/intact, has fusiform area (bulging area), bulge is outside the wall
Thoracic aneurysm
Aorta in that area
Chest pain - into back & scapula
Mimics gallbladder & liver problems

A

Aneurysm

203
Q

__________ (AAA most common)
Present w TIAs
Hoarseness, dysphagia depending on what is compressed
Jugular distension
Decreased venous return - edema (in phase & arms)

A

Ascending Aorta aneurysm

204
Q

__________ is when you have disruption in the layers
Result of trauma
Graft didn’t hold
Leaking arterial line

A

False aneurysm

205
Q

Complications
Biggest - bleeding - rupture (serious complication related to untreated)
Rupture into retroperitoneal space Bleeding may be tamponaded by surrounding structures, thus preventing exsanguination and death.
Severe pain
May or may not have back or flank ecchymosis (Grey Turner’s sign).

A

Aneurysm

206
Q

Rupture into thoracic or abdominal cavity
Massive hemorrhage
Most patients do not survive long enough to get to the hospital.

A

aneurysm

207
Q

90% of people die if rupture - As many as 50% to 90% of people with an aneurysm rupture in their brain get a vasospasm.

A

aneurysm

208
Q

Peripheral aspect - ______ is biggest one *

A

aorta (aneurysm)

209
Q

Circulation impacted
Low BP
Tachycardic
Pale/ashen/very sick
Altered LOC
Tenderness

A

Hypovolemic shock

210
Q

___________ - like aneurysm but a tear
Tear in intimal layer of arterial wall allows bleeding into the media layer and a pool or bulge of blood results
Leads to compression & occlusion of surrounding vessels an/or rupture
Men at higher risk
Any type of aortic disease, heart disorder, connective tissue, heart problems, bowel problems
Anytime heart pumps, pressure restricted in that area, increase pressure in that area
Can impact blood flow in other areas of the body

A

Aortic Dissection

211
Q

Complication (big one)
Cardiac tamponade - blood leaking in pericardial sac
Compress heart
Life threatening
Symptoms:
Distension in jugular
Hypotension ?
Heart sounds change (muffled)
Narrow pulse pressure
Bleeding biggest boy **
Hypovolemic shock
Decreased BP (hypotension), tachycardia (trying to exert more blood by going faster), pallor/pale, fearful
Imperative that BP is not too high, increase the tear; maintain BP at lower level; lot of intense monitoring

A

Aortic Dissection

212
Q

___________ - what do they look like? Where are they usually? Symptoms are what we have been talking about. Often have punched out look (thickened area around it) - mostly over bony prominences
Typically toes, heels, prominences of foot
“Punched out” well demarcated edges
Pale, non granulating, often necrotic base
Skin dust, erythema, cool to touch
Hairless, thin, brittle skin w shiny texture
Toe nails thickened, opaque, maybe lost
Gangrene may occur
Loss or decreased pulse (dorsalis pedis or tibial arteries)

If person has this you are monitoring:
Infection
Poor healing
Any other changes in CWCM
Treating w whatever is ordered
Doppler ultrasound - to see blood flow in that area - espec. If not healing
Ankle brachial indexes
1 to 1.4 is normal number you would see

A

Arterial Leg Ulcers

213
Q

Treatment
Increase blood flow - surgery
Smoking cessation
Control diabetes, hypertension, hyperlipidemia
Head of bed raised at night may help rest pain
Excellent foot & leg care
Waling is beneficial
Treatment of infections w system antibiotics
Analgesics
Do not debride ulcers

A

Arterial Leg Ulcers

214
Q

Phlebitis
Inflammation of a vein
Can happen cause of IV or med
Redness, tenderness, warm
Pt will complain
Superficial vein (usually no clot)
Deep - as a result of a clot
Block
Can move
May have symptoms
Change in circulation, discomfort, redness
Do something before it travels
If having difficulty breathing suddenly - pulmonary emboli

A

Venous Disorders

215
Q

a condition that occurs when a blood clot forms in a vein

A

Venous thromboembolism

216
Q

Twisted, distorted, cord looking appearance
Can be uncomfortable
Achy
Caused by wall/valve damage
Spider veins appearance is more mild

A

Varicose

217
Q

Venous Thrombus / Venous disorders
_________:
Venous stasis
Damage to endothelium
Hypercoagulability of blood (elevated clot, thicker and gooey)

A

Virchow’s triad **

218
Q

At risk of clots because blood is just chillin’
________ can sit there, start to block or move
Any problem w the valve will cause stagnation
Mostly in people who are obese, heart failure, anything that causes a person to be sedentary (lengthy hospital stay), hip fractures, IV therapy (chemo - very irritating)
Estrogen based BC - increases risk of clots

A

Thrombus

219
Q

Venous Thrombosis
_________ - may palpate a hard area, euthymia, red, warm to touch, temperature (increased WBC)
Promote venous returns
NSAIDs
Venous thrombo-embolism - in deeper veins
Systemic
Lungs - chance of death (cardiac arrest)

A

Superficial

220
Q

Diagnosis of VTE
DVT
Prevention
Mobilization post op
Moving limbs
Compression stockings
Intermittent compression devices
Prevention and prophylaxis
Drug therapy: Anticoagulant therapy - inhibiting 1 component of the clotting
Vitamin K is an antagonists *** can interfere w medications
Indirect thrombin inhibitors Direct thrombin inhibitors Factor Xa inhibitors Anticoagulation therapy for VTE prophylaxis Anticoagulation therapy for VTE treatment Thrombolytic therapy for VTE treatment

A

Venous thromboembolism (VTE)

221
Q

Commonly called blood thinners - but they don’t thin
Used to treat DVT or PE
Prevent the clot from becoming larger while the body slowly reabsorbs it
Reduce the risk of further clots developing

A

Anticoagulants

222
Q

Monitor lab results (e.g., PTT)
Observe S & S of bleeding, bruising
Do not give IM’s, minimize IV - well we never do that stuff unnecessarily anyway (prone to bruising, may bleed more after)
Do not take Vit K, avoid certain herbs
Limit alcohol use
Report blood in urine/stool
Report prolonged bleeding
Do not take ASA or NSAIDs
Report severe headache, stomach ache

A

Anticoagulant Treatment

223
Q

Filter inserted inside IVC (large vein that brings blood back to heart)
Traps amolus before it reaches the lungs

A

VTE - inferior vena cava filter

224
Q

What does _____ mean
International normalized ratio
test tells you how long it takes for your blood to clot. A test called the prothrombin time (PT) actually measures how quickly your blood clots.

A

INR

225
Q

Valve damage
Backflow of venous blood
Persistent edema
Bronze-brown pigmentation (breakdown of blood, iron leaches out and browns the skin - hemocyteric)
Thick, hard, fibrous skin
Ulceration

A

Chronic Venous Insufficiency

226
Q

___________ - itchy, looks like eczema (happens w this)
Sores will ooze and crust
Treatment is compression stockings, if swelling (elevation), itching w antihistamines & moisturizers; watching for wounds that aren’t healing; infection spreading up the legs (cellulitis - redness going in direction that is increasing - mark area w pen on person & document)

A

Stasis dermatitis

227
Q

From chronic venous insufficiency
Often accompanied by stasis dermatitis & peritus
Partial thickness
Painful
Extensive drainage
Can lead to infection, cellulitis
Uncomfortable, drain lots, prone to infection

A

Venous Ulcers

228
Q

________- - Collaborative care
Compression only if no arterial disease
Moist dressings
Diet high in protein, Vit C, A, and zinc
Control of diabetes
Reduce obesity
Observe for infection
Happens w older people, antihistamines (drowsy) increase falls
Improve healing - nutrition is very important, supplements (liquid may increase pt adherence)
Obesity is a big risk factor too
Compression socks need to be measured to person leg - hard to get on, if too tight can cause skin breakdown
Need to be replaced and washed (every 4-6 months)
Bacteria

A

Leg Ulcer

229
Q

Long-term management of venous leg ulcers should focus on teaching the client about self-care measures because the ulcers often recur.
Instruct the client and caregiver to avoid trauma to the limbs and teach them proper skin care.
Demonstrate the correct application of graduated compression stockings and stress the importance of regular replacement (every 4–6 months).

A

Chronic Venous Insufficiency & Venous Leg Ulcers

230
Q

______ - Nursing Care
Careful foot & skin care
Avoid sitting, standing for long periods
Elevate leg frequently if no arterial disease
Daily walking program
Compression stockings as ordered only if not arterial

A

Leg Ulcers

231
Q

Dilated, twisted veins
Esophageal varices
Hemorrhoids
Saphenous veins in legs
Primary or secondary (valve damage from DVT)

A

Varicose Veins

232
Q

Decreased tissue perfusion and impaired cellular metabolism
Imbalance in supply/demand for O2 and nutrients

A

Shock

233
Q

Types of _______- ***
Cardiogenic (low volume)
Hypovolemic (low volume)
Neurogenic (distribution) - she said earlier that this one is different
Anaphylactic (distribution)
Septic (distribution)
Obstructive (not on there)

A

shock

234
Q

Low Blood Flow
__________:
Systolic / diastolic dysfunction
Compromised CO
Precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems
Early manifestations are similar to that of a client w decompensated heart failure
Looking at cardiac enzymes in lab work
Troponin level
EKG
Chest x ray
Echocardiogram
Person will be in ICU

A

Cardiogenic Shock

235
Q

Three things that RESULT from _______ *
Decreased cellular oxygen supply
Decreased tissue perfusion
Impaired cellular metabolism

A

shock

236
Q

Low Blood Flow
____________ - not just bleeding can be loss of other body fluids
Absolute hypovolemia: loss of intravascular fluid volume
Hemorrhage
GI loss (e.g., vomiting diarrhea)
Fistula drainage
Diabetes insipidus
Hyperglycemia
Diuresis

A

Hypovolemic Shock

237
Q

_________:
Results when fluid volume moves out of the vascular space into extravascular space (e.g., interstitial or intracavity space)
Termed third spacing

A

Relative hypovolemia

238
Q

Clinical Manifestations
Anxiety
Tachypnea
Increased in CO, heart rate
Decrease in stroke volume, PAOP, urinary output
If loss is >30%, blood volume is replaced
15-30% will be symptomatic - will see more of a response (BP, tachycardic)
Respiratory status will change too

A

Relative hypovolemia

239
Q

Distributive Shock
___________:
Hemodynamic phenomenon that can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and can last up to 6 weeks.
Can occur in response to spinal anaesthesia (spinal anesthetic)
Results in massive vasodilation, leading to pooling of blood in vessels
Lost the ability to compensate here because we lost ability to communicate and therefore change*
DECREASED HEART RATE - different

A

Neurogenic shock

240
Q

Clinical manifestations
Hypotension
Bradycardia
Temperature dysregulation (resulting in heat loss)
Dry skin
Poikilothermia (taking on the temperature of the environment) - greater risk for hypothermia ***

A

Neurogenic shock

241
Q

Distributive Shock
___________ - sudden onset
Acute, life-threatening hypersensitivity reaction
Massive vasodilation
Release of mediators Increased capillary permeability
Clinical manifestations
Anxiety, confusion, dizziness
Sense of impending doom
Chest pain
Incontinence
Swelling of the lips and tongue, angioedema
Wheezing, stridor
Flushing, pruritus, urticaria
Respiratory distress and circulatory failure

A

Anaphylactic Shock

242
Q

Distributive Shock
_________ - inflammatory response related to infection (30% do not know what caused it)
Mortality rate of 15-20% ? W severe sepsis

A

Septic Shock

243
Q

__________ =
Presence of sepsis with hypotension despite fluid resuscitation
Presence of tissue perfusion abnormalities
Clinical manifestations
Increased coagulation and inflammation
Decreased fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Clinical presentation of sepsis is complex, and no single symptom or group of symptoms is specific to the diagnosis.
Hyperdynamic state: increased CO and decreased SVR
Tachypnea/hyperventilation
Temperature dysregulation
Decreased urine output
Altered neurological status
GI dysfunction
Respiratory failure is common.
Usually quick

A

Septic Shock

244
Q

Develops when a physical obstruction to blood flow occurs, resulting in decreased CO
Abdominal compartment syndrome
Decreased CO, increased afterload, and variable left ventricular filling pressures
Jugular venous distention and pulses paradoxus
Rapid assessment and treatment are important to prevent cardiac arrest.

A

Obstructive Shock

245
Q

Coronavirus Disease 2019 - people can become _______ w COVID as well
Clinically, many patients infected by SARS-CoV-2 present with mild symptoms.
About 5% show severe lung injury and/or multiple organ dysfunction syndrome.
Many patients meet sepsis criteria; sepsis is the second leading cause of death among patients with COVID-19.

A

septic

246
Q

_________ - she doesn’t need us to know the stages; we know at beginning no symptoms (we compensate)

A

Stages of Shock

247
Q

Initial stage
Compensatory stage
Progressive stage
Refractory stage

A

Stages of shock

248
Q

Usually not clinically apparent
Metabolism changes from aerobic to anerobic
Lactic acid accumulates and must be removed by blood & broken down by liver
Process requires unavailable O2

A

Initial Shock

249
Q

Clinically apparent
Body activates neural, hormonal & biochemical compensatory mechanisms
Classic clinical sign is hypotension
Vasoconstriction while blood to vital organs maintained
Increased venous return to heart, CO, BP Impaired GI motility
Cool clammy skin from blood (except with septic)
Blood is shunting from lungs and increasing physiological dead space
Increased myocardial oxygen demands.

A

Compensatory Stage

250
Q

Begins when compensatory mechanisms fail
Multiple organ dysfunction syndrome
Cardiac problems
Liver starts to fail
Everything starts to shut down

A

Progressive Stage

251
Q

Increasing fluid leaking out
Worsening CO
More organs worsening - person won’t recover

A

Refractory Stage