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Nursing - Bloomberg > 370: Pathophysiology > Flashcards

370: Pathophysiology Flashcards

1
Q

1st Line of Defense

A

Physical, Mechanical and Biochemical Barriers

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2
Q

2ns Line of Defense

A

The inflammatory response

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3
Q

3rd line of Defense

A

Adaptive immunity

  1. Cell-mediated immunity
  2. Humoral immunity
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4
Q

Physical and mechanical barriers such as skin, low temperature, mucus membranes, mechanical cleansing, and cilia.

A

1st line of Defense

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5
Q

What are the 2 biochemical barriers?

A
  1. Epithelial-Derived Chemicals (cathelicidins, defensins, and collectins)
  2. Bacteria-Derived Chemicals
    (Normal bacterial flora)
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6
Q

What are 3 main Epithelial-Derived Chemicals or antimicrobial peptides?

A
  1. Cathelicidins
  2. Defensins
  3. Collectins
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7
Q

What is the normal bacterial flora in the vagina?

A

Lactobacillus

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8
Q

What is the normal bacterial flora of the skin?

A

Pseudomonas aeruginosa

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9
Q

Why does a 3rd Degree burn increase risk for bacterial invasion?

A

1st line of Defense is removed (skin and anti-microbial)

Jump into the 2nd/inflammatory response

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10
Q

The inflammatory response

A

2nd Line of Defense

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11
Q

What are the properties of 2nd Line of Defense?

A
  • inflammatory response
  • non-specific
  • intensity depends on severity of injury
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12
Q

What are the two responses of the 2nd Line of Defense ?

A
  1. Vascular Response

2. Cellular Response

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13
Q

What causes the inflammatory response?

A
  1. Infection
  2. mechanical damage
  3. ischemia
  4. nutrient deprivation
  5. temperature extremes
  6. Radiation
    Etc
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14
Q

What are the goals of the inflammatory response?

A
  1. Neutralizes/diluted the inflammatory agent
  2. Remove necrotic material
  3. Establish environment for healing
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15
Q

What causes Redness in the 2nd Line of Defense?

A

Hyperaemia from vasodilation

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16
Q

What causes Heat in the 2nd Line of Defense?

A

Increased metabolism at inflammatory site

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17
Q

What causes Pain & tenderness in the 2nd Line of Defense?

A
  1. Change in pH
  2. Nerve stimulation by chemical mediators
  3. Increased fluid
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18
Q

What causes Edema in the 2nd Line of Defense?

A
  1. Fluid shift

2. Accumulation of fluid exudate

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19
Q

What causes loss of function in the 2nd Line of Defense?

A

Swelling and pain

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20
Q

Why does ph decrease due to cell damage?

A

Released potassium

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21
Q

Chemotaxis

A

Movement of leukocytes in response to chemical signal from area of injury

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22
Q

Margination

A

Free flowing leukocytes initiate close mechanical contact

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23
Q

Diapedesis

A

Movement of leukocytes to area of damage

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24
Q

Neutrophils

A
  1. First to arrive
  2. Phagocytosis
  3. Within 6 hours, only live for 24-48 hrs
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25
Q

BANDS released by bone marrow

A
  1. When demand of neutrophils is high

Also known as Left shift

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26
Q

Leukocytes involves in the 2nd Line of Defense

A

Neutrophils
Eosinophils
Basophils
Monocytes

(Nice Monkeys Eat Bananas)

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27
Q

Chemical mediator

A

Any messenger that acts on BVs, inflammatory cells or other cells to contribute to any inflammatory response.
Also involved in 2nd Line of Defense

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28
Q

Histamine

A

Stored in granules of basophils, last cells, platelets

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29
Q

Mechanism of action of histamine

A

Causes vasodilation and increased vascular permeability

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30
Q

Kinins

A

Arise from polypeptides that circulate in the blood in inactive form, Kininogens

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31
Q

Mechanism of action of Kinins

A

Cause contraction of smooth muscle and dilation of BVs —> pain

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32
Q

Complement components (C3a, C4a, C5a)

A

Anaphylatoxic agents generated from complement pathway activation

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33
Q

Mechanism of action of Complement components (C3a, C4a, C5a)

A
  1. Stimulate histamine release

2. Stimulate chemotaxis

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34
Q

Prostaglandins and Leukotrienes

A

Produced from arachidonic acid.

Contribute to vasodilation, capillary permeability, pain and fever, leukotriene B4 stimulates chemotaxis

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35
Q

Cytokines

A

Secreted by various cells

Effects vary

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36
Q

The characteristic vascular change at the site of an injury produce:

A

Increased permeability and leakage

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37
Q

3rd Line of defense

A
  1. Adaptive immunity
  2. Specific response, occurs more slowly than inflammatory response
  3. Can be induced by vaccination
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38
Q

A molecule that can react with antibodies or receptors on B and T cells

A

Antigen

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39
Q

An antigen that can trigger an immune response

A

Immunogenic antigen

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40
Q

The ability of a particular substance to provoke an immune response

A

Immunogenicity

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41
Q

Protein made specifically against an antigen

A

Antibody

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42
Q

What are the 2 forms of of adaptive immune system or 3rd line of defense?

A
  1. Humoral (antibody-mediated) immunity

2. Cell-mediated immunity

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43
Q

What are the 3 Antibody functions?

A 
Direct:
   1. Neutralization 
   2. Agglutination
Indirect 
   3. Opsonization
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44
Q

Antibody neutralization

A

Block binding or inactive antigen to receptor on receptor cell

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45
Q

Agglutination

A

Link microns together

Clumped antigen then filtered out by blood, lymph, or phagocytosis more easily

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46
Q

Opsonization

A

Marking for ingestion by phagocytes.

Antibodies bind to cell membrane of pathogen.

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47
Q

Antibody titres

A

Blood test for amoun of antibodies.

Determines if patient is vaccinated and correlated to strength of immune response.

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48
Q

IgG

A
  1. Most prevalent
  2. Most of protective activity against infection
  3. Crosses the placenta
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49
Q

IgA

A
  1. Mostly in secretions

2. Most of protective activity in bonds secretions

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50
Q

IgE

A
  1. Most rare
  2. Mediator of many common allergic responses
  3. Defends against parasitic infections
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51
Q

IgD

A
  1. Not well known

2. Functions as one type of B-cell antigen receptor

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52
Q

IgM

A
  1. Largest

2. First antibody produced during the initial, or primary, response to an antigen

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53
Q

Which antibody is most prevalent in the body?

A

IgG

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54
Q

Which antibody is most rare in the body?

A

IgE

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55
Q

Which antibody is most protective against infection and crosses the blood brain barrier?

A

IgG

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56
Q

Which antibody is mediator for allergic responses and defends parasitic infections?

A

IgE

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57
Q

Latent phase of primary immune response

A

B-cell differentiation

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58
Q

Which antibody is found in saliva and other body secretions?

A

IgA

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59
Q

Which neurotransmitter is most prevalent in the brain?

A

Glutamate

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60
Q

Negative symptoms of schizophrenia

A

Decreased motivation
Blunted affect
Poor self-care
Social withdrawal

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61
Q

Positive symptoms of schizophrenia

A

Hallucinations
Delusions
Paranoia
Agitation

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62
Q

Cognitive symptoms of schizophrenia

A

Disordered thinking
Memory and learning
Lack of focus

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63
Q

Pathophysiology of schizophrenia

A
  1. Dysregulation of dopamine (up or down)

2. Imbalance of dopamine and serotonin

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64
Q

First generation antipsychotics (FGA)

A
  1. D2 antagonists (decrease dopamine transmission)
  2. Blockade on receptors for:
Acetylcholine 
Histamine
Norepinephrine 
Serotonin 
Dopamine
  1. Classified by potency
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65
Q

Second generation antipsychotics (SGAs) aka Atypical agents

A
  1. Decreased serotonin transmission
  2. Low affinity for D2 receptors

(Serotonin has inhibitory effects on DA)

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66
Q

Medicated cooperative stage

A

1st week of antipsychotic action

Decreased agitation, hostility

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67
Q

Improved socialization stage

A

2-6 week of antipsychotic action

Obeys rules, attends meetings, etc

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68
Q

Elimination of thought disorder stage

A

2 weeks - months of antipsychotic action

Decreased delusions, hallucinations, thought disturbances

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69
Q

Maintenance Stage of antipsychotic action

A

Achieves baseline level of functioning

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70
Q

Positive symptoms of schizophrenia

A

Too much dopamine in MESOLIMBIC area

Treat with FGAs (D2 blockers) or SGAs

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71
Q

Negative symptoms of schizophrenia

A

Not enough dopamine in MESOCORTICAL area

Treat with SGAs (restore balance between serotonin and dopamine)

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72
Q

Protype of First Gen Antipsychotic

A

Chlorpromazine

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73
Q

Low potency agents of FGA

A

(Low D2 affinity, non selective)

Sedation, orthostatic hypotension, anticholinergic effects, weight gain

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74
Q

High potency agents of FGAs

A

(High D2 affinity/selectivity)

Extrapyramidal symptoms, prolactin release, arrhythmias

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75
Q

Prototype of high potency agent of FGA

A

Haloperidol

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76
Q

Extrapyramidal Symptoms

A
  1. Movement disorders
  2. Due to blockade of D2 receptors in nigrostriatal region
  3. Low DA, high Ach
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77
Q

Extrapyramidal movement disorders

A

High potency agents, occur early:

  1. Acute dystopia
  2. Parkinsonism
  3. Akathisia

Prolonged med use:
4. Tardive Dyskinesia

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78
Q

Severe spasm of muscles in tongue, face, neck, back

A

Acute dystopia

Treated with anticholinergics

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79
Q

Tremor, rigidity, slow shuffling gait

A

Parkinsonism

Treated with anticholinergics

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80
Q

Profound restlessness, pacing, movement

A

Akathisia

Treated with anticholinergics

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81
Q

Involuntary twisting, writhing movements of face, tongue; may be irreversible, no reliable treatment

A

Tardive Dyskinesia

Treated with anticholinergics

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82
Q

Anticholinergics

A

(Benztropine, diphenhydramine)

Restore balance between DA and Ach

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83
Q

Neuroleptic Malignant Syndrome (NMS)

A
  1. More likely with high potency antipsychotics

Sudden fever, muscle rigidity, sweating, increased HR, labile BP, altered LOC, confusion, seizures, coma, arrhythmia, death

D/c antipsychotics, no antidote

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84
Q

Prototype of Second Gen Antipsychotics

A

Olanzapine

Others: Risperidobe, Clozapine

Blockade of 5-HT2 receptors (restore DA/5HT balance)

Side effects: weight gain

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85
Q

Side effects of Second Gen Antipsychotics

A

Weight gain, diabetes, increased cholesterol, prolonged QT interval

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86
Q

Clozapine

A

Risk of agranulocytosis

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87
Q

Agranulocytosis

A

Drop in blood cell counts

Could be fatal due to sepsis

Monitor WBC and neutrophil counts

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88
Q

Monoamine hypothesis of depression

A

Deficit of one or more NE, 5HT, or DA neurotransmission

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89
Q

Principal symptoms of depression

A

Depressed mood, loss of interest/pleasure

Respond by 4 weeks

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90
Q

Somatic symptoms of Depression

A

Sleep pattern, changes in appetite, weight changes, fatigue

Respond in 1-3 weeks

91
Q

Antidepressant drug classes

A
  1. SSRIs
  2. SNRIs
  3. TCAs
  4. Atypical/Antidepressants
  5. MAOIs
92
Q

Prototype of SSRIs

A

fluoxetine (Prozac)

  1. Blocks neuronal reuptakr of 5HT
  2. Long half-life
93
Q

SSRI Side effects

A
  1. Sexual dysfunction
  2. Nausea, HA, weight gain
  3. CNS stimulation (nervousness, insomnia, anxiety)
  4. Headache
94
Q

Serotonin Syndrome

A
  1. Altered mental status (confusion, agitation, hallucination)
  2. Increased muscle tone
  3. Tremor
  4. Rigidity
  5. Sweating
  6. Fever
95
Q

Prototype of TCA antidepressants

A

Amitriptyline (Elavil)

  1. Blocks neuronal reuptake of NE/5HT
  2. Long half-lives
  3. Second-Line therapy
96
Q

Side effects of TCAs antidepressants

A
  1. Sedation (H1 receptor blockade)
  2. Orthostatic hypotension (blockade of alpha1-adrenergic receptors)
  3. Anticholinergic effects (dry mouth, blurred vision, constipation, urinary retention, tachycardia, etc) (muscarinic cholinergic receptor blockade)
  4. Weight gain (5HT2 receptor blockade)
  5. Cardiac toxicity (arrhythmias)
  6. Diaphoresis (sweating)
  7. Seizures
  8. Hypomania
97
Q

Prototype of SNRI antidepressants

A

Venlafaxine (Effexor)

  1. Block reuptake of NE and 5HT

Side effects: nausea, HA, insomnia, weight loss/anorexia, sexual dysfunction, increased BP

98
Q

Atypical antidepressant

A

Bupropion (Wellbutrin)

  1. Blocks DA and NE reuptake. Also works on nicotine receptors.
  2. Shorter half life

Side effects: agitation, HA, nausea, dry mouth, insomnia, constipation, weight loss, psychosis (rare)

99
Q

What is the Frank-Starling Mechanism?

A

Increased stretch of heart -> increased force of contraction.

Increased blood volume -> stretch of myocardium

100
Q

What results in increased preload?

A

Increased stroke volume -> increased preload (EDV) -> increased stretch -> increased force of contraction

101
Q

How do you calculate mean arterial pressure (MAP)?

A

(SBP + 2 x DBP)/3

102
Q

Where are chemoreceptors found?

A
  1. Medulla oblongata
  2. Carotid body
  3. Aortic body
103
Q

Where are baroreceptors found?

A
  1. Carotid sinus

2. Aorta

104
Q

What is Laplace’s Law?

A

Wall tension = intraventricular pressure x internal radius

105
Q

What happens to arterial pressure as radius increases?

A

As radius increases, so does tension but Pressure remains equal

106
Q

What happens during cardiomyopathy?

A

Heart becomes significantly distended. Increased radius increases tension. Heart requires more energy to pump same amount of blood.

107
Q

What happens during myocardial hypertrophy?

A

Thickening and stiffening of the heart muscle. Decreased elasticity, decreases compliance and contractility.

108
Q

What are 4 factors affecting cardiac performance?

A
  1. Preload
  2. Afterload
  3. Heart rate
  4. Myocardial contractility
109
Q

What 2 primary factors that effect preload?

A
  1. Amount of venous return to ventricle
  2. Blood left in the ventricle after systole or end-systolic volume (EDV)

Increased preload = increased cardiac output

110
Q

What decreases preload?

A

Decrease in Venous return or filling

  1. Constrictive pericarditis
  2. Cardiac tamponade
  3. Hemorrhage
  4. 3rd spacing
  5. Vasodilators
  6. Diuretics
111
Q

What is afterload?

A

Resistance to ejection during systole.

Force to eject blood from heart.

112
Q

What are 2 main factors that effect afterload?

A
  1. Ventricular wall tension
  2. Peripheral vascular resistance

Increased afterload -> decreased cardiac output (CO)

113
Q

What increases afterload?

A

Increased aortic pressure or increases SVR

  1. Aortic stenosis
  2. Severe HTN
  3. Vasoconstriction
  4. Vasopressors
114
Q

What decreases afterload?

A
  1. Decreased SVR
  2. Vasodilation
  3. Sepsis
  4. Hyperthermia
  5. Decreases BP
  6. Nitrates
  7. Arterial dilators
115
Q

What 3 factors effect contractility of the heart?

A
  1. Preload
  2. Innervation to ventricles
  3. Oxygen supply
116
Q

What compromises intrinsic contractility of the heart?

A 
1. Poor myocardial perfusion 
(Secondary to atherosclerosis) 
2. Primary disease of myocardium 
3. Degenerative changes with aging 
4. Necrosis from MI
5. Negative ionotropic drugs
117
Q

What increases contractility of the heart?

A

Ionotropes (dobutamine, dopamine, digoxin)

118
Q

What decreases contractility of the heart?

A
  1. Beta blockers
  2. Calcium channel blockers
  3. Antiarrhythmatics
119
Q

What are the effects of aldosterone?

A

Hormone that promotes sodium retention, which can increase H2O reabsorption, increased blood volume, and increased CO (HTN)

120
Q

How is blood pressure calculated?

A

BP = CO x SVR

121
Q

How is cardiac output calculated?

A

CO = stroke volume x HR

122
Q

What are the 2 primary causes of sustained hypertension?

A
  1. Increased peripheral resistance

2. Increased blood volume

123
Q

What are natriuretic peptides?

A
  1. Atrial natriuretic peptide (ANP)
  2. Brain natriuretic peptide (BNP)
  3. C-type natriuretic peptide (CNP)
  4. Urodilatin

Modulate renal sodium excretion

124
Q

What do diuretics do?

A

Increase renal excretion of Na+, H2O, Cl-, K+ by blocking reabsorption in distal tubule.
This decreases blood volume

125
Q

What do Beta-Blockers do?

A

Blocks cardiac beta1-receptors to decrease HR and contractility.
This reduces cardiac output.

126
Q

What do ACE inhibitors do?

A

Inhibit the enzyme that converts Angiotension 1 to Angiotension 2.
Blocks vasoconstriction and aldosterone mediated volume expansion.

127
Q

What do calcium-channel blockers do?

A

Calcium channels regulate contraction of vascular smooth muscles. If blocked, contraction will be prevented and results in vasodilation.

128
Q

What are complications of hypertension?

A
  1. Stroke, dementia
  2. Retinopathy-hemorrhage, blindness
  3. CAD, angina, MI, heart failure
  4. Aortic aneurysms or dissection
  5. Kidney injury, end stage renal disease
129
Q

What are the roles of sympathetic nervous system in the circulatory system?

A
  1. Increase HR and contractility
  2. Vasoconstriction
  3. Releases renin from the kidneys
  4. Increased arterial pressure due to increased CO and SVR
  5. Increased insulin resistance
130
Q

What are the primary risk factors of heart failure?

A
  1. CAD (Coronary artery disease)

2. Advanced age

131
Q

What are contributing factors to heart failure?

A
  1. Hypertension
  2. Diabetes
  3. Tobacco use
  4. Obesity
  5. High cholesterol
132
Q

What are the 2 types of heart failure?

A
  1. Acute

2. Chronic

133
Q

What are the 4 compensatory mechanisms in heart failure?

A
  1. Frank-Starling Mechanism
  2. Sympathetic NS
  3. Neurohormonal responses
  4. Myocardial remodeling & hypertrophy
134
Q

What are the effects of SNS on heart failure?

A
  1. Increase HR
  2. Increased myocardial contractility
  3. Peripheral vasoconstriction

Increase the workload of failing myocardium

135
Q

What are the 4 neurohormonal responses that effect heart failure?

A
  1. RAAS system
  2. ADH
  3. Endothelin
  4. Proinflammatory cytokines
136
Q

How does the RAAS system effect heart failure?

A

Angiotensin 2 causes adrenal cortex to release aldosterone. Causes sodium and water retention. Increased peripheral vasoconstriction, increases BP.

137
Q

How does ADH effect heart failure?

A

Antidiuretic hormone causes increased H2O reabsorption in renal tubules, leading to H2O retention and increased blood volume.

138
Q

How does endothelin effect heart failure?

A

Endothelin is stimulated by ADH, catecholines, and angiotensin 2. Causes

  1. Arterial vasoconstriction
  2. Increase in cardiac contractility
  3. Hypertrophy
139
Q

How does proinflammatory cytokines effect heart failure?

A

Released in response to cardiac injury. Depressed cardiac function by causing cardiac hypertrophy, contractile dysfunction, and death of myocytes. Leads to cardiac wasting, muscle myopathy, and fatigue.

140
Q

What are the 2 compensatory consequences of myocardial remodeling?

A
  1. Dilation

2. Hypertrophy

141
Q

What happens during compensatory dilation?

A
  1. Elevated pressure of left ventricle
  2. Chambers of heart enlarge
  3. Eventually decreases CO
142
Q

What happens during compensatory hypertrophy of the heart?

A

Increase muscle mass and cardiac wall thickness in response to chronic dilation. Results in:

  1. Poor contractility
  2. Higher O2 needs
  3. Poor coronary artery circulation
  4. Risk for ventricular dysrhythmias
143
Q

What is another name for left-sided heart failure?

A

Congestive heart failure

144
Q

What causes left-sided heart failure?

A

Left ventricular dysfunction (MI HTN, CAD, cardiomyopathy) causes backup of blood into left atrium and pulmonary veins (pulmonary congestion, edema)

145
Q

What are the subtypes of left-sided heart failure?

A
  1. Systolic: impaired contractile or pump function

2. Diastolic: impaired ventricular function

146
Q

What is the primary causes of right-sided heart failure?

A
  1. Left-sided heart failure.
  2. Pulmonary diseases resulting in high pulmonary resistance
  3. Right ventricular infarction (ineffective R ventricular contractility)
147
Q

What happens during right-sided heart failure?

A

Causes backflow of blood to the R atrium and venous circulation. Causes jugular distensión and hepatomegaly.

148
Q

Which type of heart failure is pulmonary?

A

Right-sided (Lung Disease)

149
Q

What are the symptoms of left-sided heart failure?

A
  1. Pulmonary Congestion (cough, crackles, wheezes, blood-tinged sputum, Dyspnea, orthopnea, paroxysmal nocturna dyspnea)
  2. Fatigue, activity intolerance, confusion, restlessness (reduces O2)
  3. Peripheral constriction (Cyanosis, cool, pale skin)
  4. Tachycardia (sympathetic stimulation)
  5. S3 (rapid ventricular filling)
  6. S4 (atrial contraction)
150
Q

Lung disease and right-sided heart failure

A
  1. Increased force of RV contraction
  2. Increased RV oxygen demand
  3. RV hypoxia
  4. Decrease force of RV contraction
  5. Increase RV end-diastolic pressure
  6. Increased RV preload
  7. Increased RA preload
  8. Peripheral edema
151
Q

What are the symptoms of right-sided heart failure?

A
  1. Venous congestion (jugular distension, hepatomegaly, splenomegaly)
  2. Congestion of liver and intestines (anorexia, fullness, nausea, RUQ pain)
  3. Fluid retention (ascites, dependent edema, weight gain)
152
Q

What are the symptoms of left-sided heart failure?

A

(FORCED)

Fatigue
Orthopnea 
Rales/restlessness 
Cyanosis/confusion
Extreme weakness 
Dyspnea
153
Q

What are the symptoms of right-sided heart failure?

A

(BACONED)

Bloating
Anorexia 
Cyanosis/cool legs
Oliguria
Nausea 
Edema 
Distended neck veins
154
Q

What are complications of heart failure?

A
  1. Pleural effusion (from increased pressure of pleural capillaries)
  2. Atrial fibrillation (promotes thrombus/embolus formation, increased risk of stroke)
  3. Fatal dysrhythmias (ventricular tachycardia)
    Due to cardiac enlargement altering electrical pathways
  4. Hepatomegaly (congested with venous blood)
  5. Renal insufficiency/failure (due to decreased CO and perfusion to kidneys)
155
Q

What are drug therapies for heart failure?

A
  1. Diuretics to reduce preload (thiazides/loop/potassium-sparing)
  2. Enhance contractility (digitalis, dopamine, dobutamine)
  3. Vasodilators to reduce preload (hydralazine, isosorbide dinitrate)
  4. Beta-blocking agents to reduce myocardial O2 demands
  5. ACE-inhibitors to suppress agiotensin2 (captopril)
156
Q

Chronic heart failure is associated with activation of the:

A

Renin-angiotensin-aldosterone (RAAS) system

157
Q

Heart rate is reduced by:

A

Stimulation of parasympathetic nervous system

158
Q

A patient is diagnosed with pulmonary disease and elevated pulmonary vascular resistance. Which form of heart failure may result from pulmonary disease and elevated pulmonary vascular resistance?

A

Right heart failure

159
Q

In systolic heart failure, what effect does the RAAS have on stroke volume?

A

Increases preload and increases afterload (vasoconstriction)

160
Q

Mechanism of coronary artery disease (CAD)?

A
  1. Decreased perfusion to myocardium due to occlusion (cholesterol, plaques, thrombi)
  2. Inadequate blood supply to meet myocardial O2 demand
  3. myocardial ischemia
  4. Myocardial death
161
Q

Pathophysiology of atherosclerosis

A
  1. Blood lipids irritate or damage intima of arterial vessels
  2. Fatty substances enter vessels after damaging protective barrier, accumulate and for fatty streak formation
  3. Smooth muscle cells move to intima to engulf fatty substance
  4. Fibrous tissue formation and calcification
  5. Atheroma grows, causing vessel wall to become thick, fibrotic, and calcified
  6. Lumen narrows, impedes blood flow with risk for thrombosis
162
Q

The hardening and narrowing of process of an artery

A

Atherosclerosis

163
Q

Atherosclerosis occlusion

A
  1. Plaques form in lining of artery
  2. Plaque grows, intima of artery damaged
  3. Plaque ruptures
  4. Blood clot forms, limiting blood flow
164
Q

Why might CAD remain asymptomatic until it is far advanced?

A

Collateral circulation

165
Q

Collateral circulation

A
  1. Anastomotic channels join small arteries

2. Smaller collateral vessels increase in size to provide alternative blood flow

166
Q

What are the non-modifiable risk factors of CAD?

A
  1. Age
  2. Sex (inc risk with menopause)
  3. Family history
  4. Ethnicity (lifestyle, SDH, awareness of risks)
  5. Genetics (familial hypercholesterolemia)
  6. Estrogen is cardio-protective
167
Q

What are the modifiable risk factors of CAD?

A
  1. Dyslipidemia (inc LDL, dec HDL, inc triglycerides)
  2. HTN(vascular inflammation, endothelial injury)
  3. Smoking (nicotine -> catecholamine release -> inc HR, peripheral vasoconstriction, inc BP -> inc cardiac workload and O2 consumption) (nicotine inc platelet adhesion; CO -> dec O2-carrying capacity of Hgb)
  4. Physical inactivity (cholesterol, HTN, diabetes, obesity)
  5. Diet (fat, cholesterol-> atherosclerosis)
  6. Obesity (dyslipidemia, insulin resistance, inflammation, endothelial dysfunction)
  7. Diabetes Melitis
  8. Co-morbidities (infection, renal insufficiency, HTN, insulin resistance)
  9. Lifestyle (alcohol, stress, drugs)
  10. SDH
168
Q

Which heart rhythm is shockable?

A

Ventricular tachycardia

169
Q

What are the effects of acute and chronic cocaine use on the heart?

A
  1. Suppresses myocardial contractility
  2. Reduction of coronary blood flow
  3. Electrical abnormalities
  4. Increased HR and BP
  5. Increased platelet aggregation
  6. Acceleration of atherosclerosis
170
Q

What is the normal levels of LDLs?

A

< 2.6 mmol/L

171
Q

What are the normal levels for HDLs?

A

> 1.5 mmol/L

172
Q

What are the normal levels of cholesterol?

A

<5.0 mmol/L

173
Q

What are the normal levels of triglycerides?

A

< 1.7 mmol/L

174
Q

What are the effects of HDLs?

A

Reverse cholesterol transport. Extract excess cholesterol deposited in blood vessel walls and deliver to back to the liver for elimination through GI tract.

Also reduced BV injury through antioxidant and anti-inflammatory functions

175
Q

What are the conditions of metabolic syndrome?

A
  1. Waist circumference (men >= 102cm, women >= 88cm)
  2. Triglyceride levels >= 1.7 mmol/L
  3. HDL cholesterol (men < 1mmol/L; women < 1.3)
  4. BP (>= 130/85)
  5. Fasting glucose level (>= 5.6 mmol/L)
176
Q

What is a percutaneous transluminal coronary angioplasty?

A

Balloon on end of catheter fed through artery. Balloon inflates, flattening plaque to maintain patency of vessel.

Stent may be inserted afterwards

177
Q

What is coronary atherectomy?

A

Sheets off blockage in artery with Lazer, transluminal extraction, rayarían, directional catheter.

178
Q

What is coronary artery bypass grafting (CABG)?

A

Vessels from another part of body to help normalize blood flow in heart.

Adds alternative channels.

179
Q

Myocardial ischemia under 20 minutes

A

Ischemic attract (angina)

180
Q

Myocardial ischemia over 20 minutes

A

Myocardial infarction (MI)

181
Q

What are the 3 types of angina?

A
  1. Stable angina (angina pectoris)
  2. Unstable angina
  3. Variant (Prinzmetal) angina
182
Q

Which type of angina is under 10min, and characterized by precordial discomfort provoked by exertions or stress, and how would you treat it?

A

Stable angina (angina pectoris)

Tx: rest and nitrates

183
Q

Which type of angina is due to atherosclerosis?

A

Stable angina (angina pectoris)

184
Q

Which type of angina is characterized by anginal discomfort when resting or that awakens patient from sleep?

A

Unstable angina

185
Q

Which type of angina is caused by atherosclerosis with blood clot, and CAD?

A

Unstable angina

186
Q

Which type of angina is characterized by chest discomfort with atypical characteristics, often during rest, and follows a cyclic or regular pattern?

A

Variant (Prinzmetal) angina

Due to coronary artery spasm

187
Q

Sudden coronary obstruction caused by thrombus formation from

  1. Unstable angina
  2. Myocardial infarction
A

Acute Coronary Syndrome (ACS)

188
Q

What is caused by transient ischemia due to acute coronary syndrome?

A

Unstable angina

189
Q

What is due to sustained ischemia from acute coronary syndrome (ACS)?

A

Myocardial infarction and necrosis

190
Q

What are the manifestations of myocardial ischemia?

A
  1. Chest pain (May radiate)
  2. Shortness of breath
  3. Diaphoresis, pallor, cool clammy skin (SNS stimulation)
  4. Increased BP and HR
  5. Nausea and vomiting
  6. Fever
  7. Loss of consciousness
  8. Anxiety, sense of doom, denial
191
Q

Lethal ischemic injury to which myocardium zone due to MI

A

Zone of infarction

No ECG activity from this area

192
Q

Surrounding lethal ischemic injury if myocardium

A

Zone of injury (irreversible after 2-4 hours)

ST elevation on ECG

193
Q

Area of myocardium that do not have permanent effects from MI, but function erratically.

A

Zone of ischemia

  • reversible with perfusion
  • can cause T wave inversion
194
Q

What are the 7 classifications of myocardial infarctions?

A
  1. Transmural infarcts
  2. Subendocardial infarcts
  3. Anterior MI
  4. Inferior MI
  5. Septal MI
  6. Lateral MI
  7. Combination MI
195
Q

Which type of myocardial infarction involves all 3 layers of the ventricular wall?

A

Transmural infarction

196
Q

Which type of myocardial infarction involves the inner third to half of the ventricular wall?

A

Subendocardial infarct

197
Q

Which types of myocardial infarctions are due to left ventricular failure?

A
  1. Anterior MI

2. Septal MI

198
Q

Which blood vessel is occluded during an Anterior MI?

A

Left anterior descending artery (LAD)

199
Q

Which artery is occluded during an inferior MI?

A
  1. Right coronary artery (RCA)

2. Circumflex Coronary Artery

200
Q

Which type of myocardial infarction is a result of dysrhythmias or transient AV block?

A

Inferior MI

201
Q

Which artery is occluded during a Septal MI?

A

Left anterior descending (LAD) Coronary artery

202
Q

Which coronary artery is occluded during a lateral MI?

A

Circumflex Coronary Artery

203
Q

Which myocardial infarctions are due to occlusion of the left anterior descending (LAD) coronary artery?

A
  1. Anterior MI

2. Septal MI

204
Q

Which myocardial infarctions are due to the occlusion of the circumflex Coronary artery?

A
  1. Inferior MI

2. Lateral MI

205
Q

What does the arterial gas value HCO3 indicate?

A

The bicarbonate contents in the blood plasma which indicates alkaline reserve

206
Q

What is could arterial blood gas results indicate?

A
  1. Respiratory and lung problems
  2. Efficacy of oxygen therapy
  3. Acid-base levels (kidney failure, heart failure, uncontrolled diabetes, shock, etc)
207
Q

What is a state of low blood pH?

A

Acidemia pH < 7.35

208
Q

What refers to an excess of acid in the blood that causes pH to fall below 7.35?

209
Q

What is a state of high blood pH?

A

Alkalemia pH > 7.45

210
Q

What is the normal pH range for blood?

A

7.35 - 7.45

211
Q

Which 3 systems regulate normal acid-base levels?

A
  1. Chemical Buffer System
  2. Respiratory system
  3. Renal system
212
Q

What are the 3 major chemical buffer systems in the body?

A
  1. Carbonic acid-bicarbonate buffet system (extracellular)
  2. Phosphate buffer system (intracellular)
  3. Protein buffer system (intercellular)
213
Q

What is a limitation to the carbonic acid-bicarbonate buffer system?

A

Only functions when the respiratory system is functioning normally

214
Q

What happens to the blood pH if the respiratory system is not functioning properly?

A
  1. Excess CO2 combines with H2O to make carbonic acid (H2CO3)
  2. Increase in H2CO3 cause increase depth and rate of respiration, reducing carbonic acid and increasing blood pH (alkalosis)
  3. Decreased H2CO3 causes decrease and shallow respiration, thereby retaining CO2, increasing carbonic acid and decreasing blood pH (acidosis)
  4. Activation of the lungs to compensate occurs within 1 to 3 minutes
215
Q

What is the effect of the renal system on blood pH?

A
  1. Kidneys retain or excrete bicarbonate ions (HCO3-) which neutralices excess acid in the blood
  2. As blood pH decreases, kidneys compensate by retaining HCO3-
  3. As pH rises, kidneys excrete HCO3-
  4. Kidneys can also generate additional bicarbonate ions or Elina te excess H+ to compensate during acidosis
  5. This takes hours to days to correct the imbalance
216
Q

What blood pH values are fatal?

A

pH < 6.8

pH > 7.8

217
Q

What are the manifestations if acidosis?

A
  1. pH < 7.35
  2. CNS depressions through decreased synaptic transmission
  3. Increased rate and depth of respiration
  4. Weakness and disorientation
  5. Seizures
  6. Coma and death
218
Q

What are the manifestations of alkalosis?

A
  1. pH > 7.45
  2. Over-excitability of CNS and PNS
  3. Numbness
  4. Irritability, lightheaded, nervousness
  5. Muscle spasms/tetany
  6. Cramping
  7. Convulsions
  8. Loss of consciousness and death
219
Q

What is the normal range of PaO2?

A

80 - 100 mmHg

Decreases with age:
PaO2 = 102 - 1/3age

Healthy lungs = oxygen% x 5

220
Q

What is the normal range for PaCO2?

A

35 - 45 mmHg

Elevated = acidity 
Reduced = alkalinity
221
Q

What is the normal range for HCO3- arterial blood gas values?

A

22-26 mmol/L

Increased = alkalinity
Decreased = acidity
222
Q

Condition of lowered blood pH due to decreased respiratory rate (hypoventilation) or volume

A

Respiratory Acidosis

223
Q

Condition of lowered blood pH due to reduction in bicarbonate

A

Metabolic Acidosis

224
Q

A condition of increased blood pH due to increase in bicarbonate (HCO3-)

A

Metabolic Alkalosis

Nursing - Bloomberg (52 decks)

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