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370: Pathophysiology Flashcards

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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
BANDS released by bone marrow
1. When demand of neutrophils is high Also known as Left shift
26
Leukocytes involves in the 2nd Line of Defense
Neutrophils Eosinophils Basophils Monocytes (Nice Monkeys Eat Bananas)
27
Chemical mediator
Any messenger that acts on BVs, inflammatory cells or other cells to contribute to any inflammatory response. Also involved in 2nd Line of Defense
28
Histamine
Stored in granules of basophils, last cells, platelets
29
Mechanism of action of histamine
Causes vasodilation and increased vascular permeability
30
Kinins
Arise from polypeptides that circulate in the blood in inactive form, Kininogens
31
Mechanism of action of Kinins
Cause contraction of smooth muscle and dilation of BVs —> pain
32
Complement components (C3a, C4a, C5a)
Anaphylatoxic agents generated from complement pathway activation
33
Mechanism of action of Complement components (C3a, C4a, C5a)
1. Stimulate histamine release | 2. Stimulate chemotaxis
34
Prostaglandins and Leukotrienes
Produced from arachidonic acid. Contribute to vasodilation, capillary permeability, pain and fever, leukotriene B4 stimulates chemotaxis
35
Cytokines
Secreted by various cells Effects vary
36
The characteristic vascular change at the site of an injury produce:
Increased permeability and leakage
37
3rd Line of defense
1. Adaptive immunity 2. Specific response, occurs more slowly than inflammatory response 3. Can be induced by vaccination
38
A molecule that can react with antibodies or receptors on B and T cells
Antigen
39
An antigen that can trigger an immune response
Immunogenic antigen
40
The ability of a particular substance to provoke an immune response
Immunogenicity
41
Protein made specifically against an antigen
Antibody
42
What are the 2 forms of of adaptive immune system or 3rd line of defense?
1. Humoral (antibody-mediated) immunity | 2. Cell-mediated immunity
43
What are the 3 Antibody functions?
``` Direct: 1. Neutralization 2. Agglutination Indirect 3. Opsonization ```
44
Antibody neutralization
Block binding or inactive antigen to receptor on receptor cell
45
Agglutination
Link microns together | Clumped antigen then filtered out by blood, lymph, or phagocytosis more easily
46
Opsonization
Marking for ingestion by phagocytes. | Antibodies bind to cell membrane of pathogen.
47
Antibody titres
Blood test for amoun of antibodies. | Determines if patient is vaccinated and correlated to strength of immune response.
48
IgG
1. Most prevalent 2. Most of protective activity against infection 3. Crosses the placenta
49
IgA
1. Mostly in secretions | 2. Most of protective activity in bonds secretions
50
IgE
1. Most rare 2. Mediator of many common allergic responses 3. Defends against parasitic infections
51
IgD
1. Not well known | 2. Functions as one type of B-cell antigen receptor
52
IgM
1. Largest | 2. First antibody produced during the initial, or primary, response to an antigen
53
Which antibody is most prevalent in the body?
IgG
54
Which antibody is most rare in the body?
IgE
55
Which antibody is most protective against infection and crosses the blood brain barrier?
IgG
56
Which antibody is mediator for allergic responses and defends parasitic infections?
IgE
57
Latent phase of primary immune response
B-cell differentiation
58
Which antibody is found in saliva and other body secretions?
IgA
59
Which neurotransmitter is most prevalent in the brain?
Glutamate
60
Negative symptoms of schizophrenia
Decreased motivation Blunted affect Poor self-care Social withdrawal
61
Positive symptoms of schizophrenia
Hallucinations Delusions Paranoia Agitation
62
Cognitive symptoms of schizophrenia
Disordered thinking Memory and learning Lack of focus
63
Pathophysiology of schizophrenia
1. Dysregulation of dopamine (up or down) | 2. Imbalance of dopamine and serotonin
64
First generation antipsychotics (FGA)
1. D2 antagonists (decrease dopamine transmission) 2. Blockade on receptors for: ``` Acetylcholine Histamine Norepinephrine Serotonin Dopamine ``` 3. Classified by potency
65
Second generation antipsychotics (SGAs) aka Atypical agents
1. Decreased serotonin transmission 2. Low affinity for D2 receptors (Serotonin has inhibitory effects on DA)
66
Medicated cooperative stage
1st week of antipsychotic action Decreased agitation, hostility
67
Improved socialization stage
2-6 week of antipsychotic action Obeys rules, attends meetings, etc
68
Elimination of thought disorder stage
2 weeks - months of antipsychotic action Decreased delusions, hallucinations, thought disturbances
69
Maintenance Stage of antipsychotic action
Achieves baseline level of functioning
70
Positive symptoms of schizophrenia
Too much dopamine in MESOLIMBIC area Treat with FGAs (D2 blockers) or SGAs
71
Negative symptoms of schizophrenia
Not enough dopamine in MESOCORTICAL area Treat with SGAs (restore balance between serotonin and dopamine)
72
Protype of First Gen Antipsychotic
Chlorpromazine
73
Low potency agents of FGA
(Low D2 affinity, non selective) Sedation, orthostatic hypotension, anticholinergic effects, weight gain
74
High potency agents of FGAs
(High D2 affinity/selectivity) Extrapyramidal symptoms, prolactin release, arrhythmias
75
Prototype of high potency agent of FGA
Haloperidol
76
Extrapyramidal Symptoms
1. Movement disorders 2. Due to blockade of D2 receptors in nigrostriatal region 3. Low DA, high Ach
77
Extrapyramidal movement disorders
High potency agents, occur early: 1. Acute dystopia 2. Parkinsonism 3. Akathisia Prolonged med use: 4. Tardive Dyskinesia
78
Severe spasm of muscles in tongue, face, neck, back
Acute dystopia Treated with anticholinergics
79
Tremor, rigidity, slow shuffling gait
Parkinsonism Treated with anticholinergics
80
Profound restlessness, pacing, movement
Akathisia Treated with anticholinergics
81
Involuntary twisting, writhing movements of face, tongue; may be irreversible, no reliable treatment
Tardive Dyskinesia Treated with anticholinergics
82
Anticholinergics
(Benztropine, diphenhydramine) Restore balance between DA and Ach
83
Neuroleptic Malignant Syndrome (NMS)
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
84
Prototype of Second Gen Antipsychotics
Olanzapine Others: Risperidobe, Clozapine Blockade of 5-HT2 receptors (restore DA/5HT balance) Side effects: weight gain
85
Side effects of Second Gen Antipsychotics
Weight gain, diabetes, increased cholesterol, prolonged QT interval
86
Clozapine
Risk of agranulocytosis
87
Agranulocytosis
Drop in blood cell counts Could be fatal due to sepsis Monitor WBC and neutrophil counts
88
Monoamine hypothesis of depression
Deficit of one or more NE, 5HT, or DA neurotransmission
89
Principal symptoms of depression
Depressed mood, loss of interest/pleasure Respond by 4 weeks
90
Somatic symptoms of Depression
Sleep pattern, changes in appetite, weight changes, fatigue Respond in 1-3 weeks
91
Antidepressant drug classes
1. SSRIs 2. SNRIs 3. TCAs 4. Atypical/Antidepressants 5. MAOIs
92
Prototype of SSRIs
fluoxetine (Prozac) 1. Blocks neuronal reuptakr of 5HT 2. Long half-life
93
SSRI Side effects
1. Sexual dysfunction 2. Nausea, HA, weight gain 3. CNS stimulation (nervousness, insomnia, anxiety) 4. Headache
94
Serotonin Syndrome
1. Altered mental status (confusion, agitation, hallucination) 2. Increased muscle tone 3. Tremor 4. Rigidity 5. Sweating 6. Fever
95
Prototype of TCA antidepressants
Amitriptyline (Elavil) 1. Blocks neuronal reuptake of NE/5HT 2. Long half-lives 3. Second-Line therapy
96
Side effects of TCAs antidepressants
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
Prototype of SNRI antidepressants
Venlafaxine (Effexor) 1. Block reuptake of NE and 5HT Side effects: nausea, HA, insomnia, weight loss/anorexia, sexual dysfunction, increased BP
98
Atypical antidepressant
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
What is the Frank-Starling Mechanism?
Increased stretch of heart -> increased force of contraction. Increased blood volume -> stretch of myocardium
100
What results in increased preload?
Increased stroke volume -> increased preload (EDV) -> increased stretch -> increased force of contraction
101
How do you calculate mean arterial pressure (MAP)?
(SBP + 2 x DBP)/3
102
Where are chemoreceptors found?
1. Medulla oblongata 2. Carotid body 3. Aortic body
103
Where are baroreceptors found?
1. Carotid sinus | 2. Aorta
104
What is Laplace’s Law?
Wall tension = intraventricular pressure x internal radius
105
What happens to arterial pressure as radius increases?
As radius increases, so does tension but Pressure remains equal
106
What happens during cardiomyopathy?
Heart becomes significantly distended. Increased radius increases tension. Heart requires more energy to pump same amount of blood.
107
What happens during myocardial hypertrophy?
Thickening and stiffening of the heart muscle. Decreased elasticity, decreases compliance and contractility.
108
What are 4 factors affecting cardiac performance?
1. Preload 2. Afterload 3. Heart rate 4. Myocardial contractility
109
What 2 primary factors that effect preload?
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
What decreases preload?
Decrease in Venous return or filling 1. Constrictive pericarditis 2. Cardiac tamponade 3. Hemorrhage 4. 3rd spacing 5. Vasodilators 6. Diuretics
111
What is afterload?
Resistance to ejection during systole. | Force to eject blood from heart.
112
What are 2 main factors that effect afterload?
1. Ventricular wall tension 2. Peripheral vascular resistance Increased afterload -> decreased cardiac output (CO)
113
What increases afterload?
Increased aortic pressure or increases SVR 1. Aortic stenosis 2. Severe HTN 3. Vasoconstriction 4. Vasopressors
114
What decreases afterload?
1. Decreased SVR 2. Vasodilation 3. Sepsis 4. Hyperthermia 5. Decreases BP 6. Nitrates 7. Arterial dilators
115
What 3 factors effect contractility of the heart?
1. Preload 2. Innervation to ventricles 3. Oxygen supply
116
What compromises intrinsic contractility of the heart?
``` 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
What increases contractility of the heart?
Ionotropes (dobutamine, dopamine, digoxin)
118
What decreases contractility of the heart?
1. Beta blockers 2. Calcium channel blockers 3. Antiarrhythmatics
119
What are the effects of aldosterone?
Hormone that promotes sodium retention, which can increase H2O reabsorption, increased blood volume, and increased CO (HTN)
120
How is blood pressure calculated?
BP = CO x SVR
121
How is cardiac output calculated?
CO = stroke volume x HR
122
What are the 2 primary causes of sustained hypertension?
1. Increased peripheral resistance | 2. Increased blood volume
123
What are natriuretic peptides?
1. Atrial natriuretic peptide (ANP) 2. Brain natriuretic peptide (BNP) 3. C-type natriuretic peptide (CNP) 4. Urodilatin Modulate renal sodium excretion
124
What do diuretics do?
Increase renal excretion of Na+, H2O, Cl-, K+ by blocking reabsorption in distal tubule. This decreases blood volume
125
What do Beta-Blockers do?
Blocks cardiac beta1-receptors to decrease HR and contractility. This reduces cardiac output.
126
What do ACE inhibitors do?
Inhibit the enzyme that converts Angiotension 1 to Angiotension 2. Blocks vasoconstriction and aldosterone mediated volume expansion.
127
What do calcium-channel blockers do?
Calcium channels regulate contraction of vascular smooth muscles. If blocked, contraction will be prevented and results in vasodilation.
128
What are complications of hypertension?
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
What are the roles of sympathetic nervous system in the circulatory system?
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
What are the primary risk factors of heart failure?
1. CAD (Coronary artery disease) | 2. Advanced age
131
What are contributing factors to heart failure?
1. Hypertension 2. Diabetes 3. Tobacco use 4. Obesity 5. High cholesterol
132
What are the 2 types of heart failure?
1. Acute | 2. Chronic
133
What are the 4 compensatory mechanisms in heart failure?
1. Frank-Starling Mechanism 2. Sympathetic NS 3. Neurohormonal responses 4. Myocardial remodeling & hypertrophy
134
What are the effects of SNS on heart failure?
1. Increase HR 2. Increased myocardial contractility 3. Peripheral vasoconstriction Increase the workload of failing myocardium
135
What are the 4 neurohormonal responses that effect heart failure?
1. RAAS system 2. ADH 3. Endothelin 4. Proinflammatory cytokines
136
How does the RAAS system effect heart failure?
Angiotensin 2 causes adrenal cortex to release aldosterone. Causes sodium and water retention. Increased peripheral vasoconstriction, increases BP.
137
How does ADH effect heart failure?
Antidiuretic hormone causes increased H2O reabsorption in renal tubules, leading to H2O retention and increased blood volume.
138
How does endothelin effect heart failure?
Endothelin is stimulated by ADH, catecholines, and angiotensin 2. Causes 1. Arterial vasoconstriction 2. Increase in cardiac contractility 3. Hypertrophy
139
How does proinflammatory cytokines effect heart failure?
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
What are the 2 compensatory consequences of myocardial remodeling?
1. Dilation | 2. Hypertrophy
141
What happens during compensatory dilation?
1. Elevated pressure of left ventricle 2. Chambers of heart enlarge 3. Eventually decreases CO
142
What happens during compensatory hypertrophy of the heart?
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
What is another name for left-sided heart failure?
Congestive heart failure
144
What causes left-sided heart failure?
Left ventricular dysfunction (MI HTN, CAD, cardiomyopathy) causes backup of blood into left atrium and pulmonary veins (pulmonary congestion, edema)
145
What are the subtypes of left-sided heart failure?
1. Systolic: impaired contractile or pump function | 2. Diastolic: impaired ventricular function
146
What is the primary causes of right-sided heart failure?
1. Left-sided heart failure. 2. Pulmonary diseases resulting in high pulmonary resistance 3. Right ventricular infarction (ineffective R ventricular contractility)
147
What happens during right-sided heart failure?
Causes backflow of blood to the R atrium and venous circulation. Causes jugular distensión and hepatomegaly.
148
Which type of heart failure is pulmonary?
Right-sided (Lung Disease)
149
What are the symptoms of left-sided heart failure?
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
Lung disease and right-sided heart failure
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
What are the symptoms of right-sided heart failure?
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
What are the symptoms of left-sided heart failure?
(FORCED) ``` Fatigue Orthopnea Rales/restlessness Cyanosis/confusion Extreme weakness Dyspnea ```
153
What are the symptoms of right-sided heart failure?
(BACONED) ``` Bloating Anorexia Cyanosis/cool legs Oliguria Nausea Edema Distended neck veins ```
154
What are complications of heart failure?
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
What are drug therapies for heart failure?
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
Chronic heart failure is associated with activation of the:
Renin-angiotensin-aldosterone (RAAS) system
157
Heart rate is reduced by:
Stimulation of parasympathetic nervous system
158
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?
Right heart failure
159
In systolic heart failure, what effect does the RAAS have on stroke volume?
Increases preload and increases afterload (vasoconstriction)
160
Mechanism of coronary artery disease (CAD)?
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
Pathophysiology of atherosclerosis
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
The hardening and narrowing of process of an artery
Atherosclerosis
163
Atherosclerosis occlusion
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
Why might CAD remain asymptomatic until it is far advanced?
Collateral circulation
165
Collateral circulation
1. Anastomotic channels join small arteries | 2. Smaller collateral vessels increase in size to provide alternative blood flow
166
What are the non-modifiable risk factors of CAD?
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
What are the modifiable risk factors of CAD?
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
Which heart rhythm is shockable?
Ventricular tachycardia
169
What are the effects of acute and chronic cocaine use on the heart?
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
What is the normal levels of LDLs?
< 2.6 mmol/L
171
What are the normal levels for HDLs?
> 1.5 mmol/L
172
What are the normal levels of cholesterol?
<5.0 mmol/L
173
What are the normal levels of triglycerides?
< 1.7 mmol/L
174
What are the effects of HDLs?
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
What are the conditions of metabolic syndrome?
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
What is a percutaneous transluminal coronary angioplasty?
Balloon on end of catheter fed through artery. Balloon inflates, flattening plaque to maintain patency of vessel. Stent may be inserted afterwards
177
What is coronary atherectomy?
Sheets off blockage in artery with Lazer, transluminal extraction, rayarían, directional catheter.
178
What is coronary artery bypass grafting (CABG)?
Vessels from another part of body to help normalize blood flow in heart. Adds alternative channels.
179
Myocardial ischemia under 20 minutes
Ischemic attract (angina)
180
Myocardial ischemia over 20 minutes
Myocardial infarction (MI)
181
What are the 3 types of angina?
1. Stable angina (angina pectoris) 2. Unstable angina 3. Variant (Prinzmetal) angina
182
Which type of angina is under 10min, and characterized by precordial discomfort provoked by exertions or stress, and how would you treat it?
Stable angina (angina pectoris) Tx: rest and nitrates
183
Which type of angina is due to atherosclerosis?
Stable angina (angina pectoris)
184
Which type of angina is characterized by anginal discomfort when resting or that awakens patient from sleep?
Unstable angina
185
Which type of angina is caused by atherosclerosis with blood clot, and CAD?
Unstable angina
186
Which type of angina is characterized by chest discomfort with atypical characteristics, often during rest, and follows a cyclic or regular pattern?
Variant (Prinzmetal) angina Due to coronary artery spasm
187
Sudden coronary obstruction caused by thrombus formation from 1. Unstable angina 2. Myocardial infarction
Acute Coronary Syndrome (ACS)
188
What is caused by transient ischemia due to acute coronary syndrome?
Unstable angina
189
What is due to sustained ischemia from acute coronary syndrome (ACS)?
Myocardial infarction and necrosis
190
What are the manifestations of myocardial ischemia?
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
Lethal ischemic injury to which myocardium zone due to MI
Zone of infarction No ECG activity from this area
192
Surrounding lethal ischemic injury if myocardium
Zone of injury (irreversible after 2-4 hours) ST elevation on ECG
193
Area of myocardium that do not have permanent effects from MI, but function erratically.
Zone of ischemia - reversible with perfusion - can cause T wave inversion
194
What are the 7 classifications of myocardial infarctions?
1. Transmural infarcts 2. Subendocardial infarcts 3. Anterior MI 4. Inferior MI 5. Septal MI 6. Lateral MI 7. Combination MI
195
Which type of myocardial infarction involves all 3 layers of the ventricular wall?
Transmural infarction
196
Which type of myocardial infarction involves the inner third to half of the ventricular wall?
Subendocardial infarct
197
Which types of myocardial infarctions are due to left ventricular failure?
1. Anterior MI | 2. Septal MI
198
Which blood vessel is occluded during an Anterior MI?
Left anterior descending artery (LAD)
199
Which artery is occluded during an inferior MI?
1. Right coronary artery (RCA) | 2. Circumflex Coronary Artery
200
Which type of myocardial infarction is a result of dysrhythmias or transient AV block?
Inferior MI
201
Which artery is occluded during a Septal MI?
Left anterior descending (LAD) Coronary artery
202
Which coronary artery is occluded during a lateral MI?
Circumflex Coronary Artery
203
Which myocardial infarctions are due to occlusion of the left anterior descending (LAD) coronary artery?
1. Anterior MI | 2. Septal MI
204
Which myocardial infarctions are due to the occlusion of the circumflex Coronary artery?
1. Inferior MI | 2. Lateral MI
205
What does the arterial gas value HCO3 indicate?
The bicarbonate contents in the blood plasma which indicates alkaline reserve
206
What is could arterial blood gas results indicate?
1. Respiratory and lung problems 2. Efficacy of oxygen therapy 3. Acid-base levels (kidney failure, heart failure, uncontrolled diabetes, shock, etc)
207
What is a state of low blood pH?
Acidemia pH < 7.35
208
What refers to an excess of acid in the blood that causes pH to fall below 7.35?
Acidosis
209
What is a state of high blood pH?
Alkalemia pH > 7.45
210
What is the normal pH range for blood?
7.35 - 7.45
211
Which 3 systems regulate normal acid-base levels?
1. Chemical Buffer System 2. Respiratory system 3. Renal system
212
What are the 3 major chemical buffer systems in the body?
1. Carbonic acid-bicarbonate buffet system (extracellular) 2. Phosphate buffer system (intracellular) 3. Protein buffer system (intercellular)
213
What is a limitation to the carbonic acid-bicarbonate buffer system?
Only functions when the respiratory system is functioning normally
214
What happens to the blood pH if the respiratory system is not functioning properly?
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
What is the effect of the renal system on blood pH?
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
What blood pH values are fatal?
pH < 6.8 | pH > 7.8
217
What are the manifestations if acidosis?
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
What are the manifestations of alkalosis?
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
What is the normal range of PaO2?
80 - 100 mmHg Decreases with age: PaO2 = 102 - 1/3age Healthy lungs = oxygen% x 5
220
What is the normal range for PaCO2?
35 - 45 mmHg ``` Elevated = acidity Reduced = alkalinity ```
221
What is the normal range for HCO3- arterial blood gas values?
22-26 mmol/L ``` Increased = alkalinity Decreased = acidity ```
222
Condition of lowered blood pH due to decreased respiratory rate (hypoventilation) or volume
Respiratory Acidosis
223
Condition of lowered blood pH due to reduction in bicarbonate
Metabolic Acidosis
224
A condition of increased blood pH due to increase in bicarbonate (HCO3-)
Metabolic Alkalosis
Nursing
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