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Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Carcinoma

A

Epithelial derived malignant neoplasm

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2
Q

Adenocarcinoma

A

Glad form carcinoma

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3
Q

Adenoma

A

Benign gland forming neoplasm

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4
Q

Leukemia

A

Malignant neoplasm of circulating white blood cell

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5
Q

Lymphoma

A

Malignant neoplasm of lymphocytes

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6
Q

Sarcoma

A

Malignant neoplasm arising from soft tissues

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7
Q

Oncogene

A

a gene whose activated product causes growth

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8
Q

Tumor suppressor gene

A

a gene whose product prevents

growth

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9
Q

Mutation

A

a change in the genetic pattern

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10
Q

Cancer cell: A cellular population that has undergone eight fundamental
changes in cell physiology

A
  1. Self-sufficiency in growth signals
  2. Insensitivity to growth inhibition
  3. Altered cellular metabolism
  4. Evasion of apoptosis
  5. Immortality
  6. Sustained angiogenesis
  7. Ability to invade and metastasize
  8. Ability to evade the human immune response
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11
Q

Telomeres

A

Protect the
chromosomes from
fraying –Expiration date

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12
Q

Telomerase

A

tells telomeres

to regenerate

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13
Q

Tumor cells evade the immune

system one of three ways

A 
Don’t display an antigen on it’s MHC Class I receptor
• Stop making MHC Class I
receptors
• Make immunosuppressive
cytokines that kill the T cells.
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14
Q

Altered
Cellular
Metabolism:

A

Use anaerobic
glycolysis for
carbon

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15
Q

Sustained Angiogensis

A
  1. Tumor secretes VEGF or bFGF
  2. VEGF increases blood vessel expression and movement to tumor
  3. Tumor has increased blood supply
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16
Q

Respiratory System Purpose

A

To facilitate the uptake of oxygen from the atmosphere

To release of carbon dioxide into the atmosphere

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17
Q

Turbinates

A

Heat and moisten air

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18
Q

Nasal passages

A

Cilia to trap particulates

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19
Q

Throat

A

Contains epiglottis, laryngeal

cartilage, muscles

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20
Q

Secretory cells

A

club cell in the bronchioles

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21
Q

Epiglottis

A

Cologen that flaps down to prevent food from going into trachea

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22
Q

Bronchus

A

Cartilage rings lined with epithelial rings, no blood gas exchange

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23
Q

Bronchioles

A

Last division with cartilage

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24
Q

Bronchioles are lined with

A

Ciliated epithelial cells that help trap debris
Mucous producing cells: Mucins helps trap pathogens
Secretory cells

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25
Q

Parietal pleura

A

adheres to internal thoracic wall (rib cage)

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26
Q

Visceral Pleura

A

Adheres to lungs

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27
Q

Pleural space and what is it needed for

A

Space between parietal and visceral pleura
Filled with fluid and helps reduce friction and provide tension for lung expansion
Can cause edema or infection

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28
Q

Specialized lung cells

A

Goblet cells and club cells

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29
Q

Goblet cells

A

Secrete mucins, repair and replace mucuos layer for airway protection.

Increased when damaged

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30
Q

Metaplasia in goblet cells

A

Results in an allergic asthma symptoms increase in goblet cells, goblet cells replicate and increase mucous production

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31
Q

Club cells

A

Exocrine cells in the respiratory tract
Stem cell capabilities to adapt
produce uroglobin
Has microvili

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32
Q

Uroglobin

A

Detoxifies harmful substances

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33
Q

Alveoli characteristics that make them good for O2 exchange

A

Large SA to help come into contact with capillaries more contact helps with O2 diffusion

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34
Q

Type I cells

A

Simplified squamous epithelial lining cannot replicate

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35
Q

Type II cells

A

Surfactant producing can replicate into type one cells

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36
Q

Surfactant

A

Helps reduces surface tension and allow alveoli to pop open
can help with inflammation
help fight bacterial infection

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37
Q

Ventilation

A

Movement of air from environment into lungs into alveoli

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38
Q

Diffusion

A

Gas exchange of O2 and CO2

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39
Q

Capillary perfusion

A

How much blood is getting to gas exchange site

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40
Q

Muscles of ventilation

A

Diaphram- Primary muscle flattens to help breathing
Intercostal- Control ribcage expansion
Accessory- ab, neck, back last resort

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41
Q

Cerebral Cortex

A

Control voluntary breathing

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42
Q

Pons and Medula role in breathing

A

Controls depth and rate of breathing

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43
Q

Peripheral Chemoreceptors

A

Measure O2 CO2 and PH in carotid/aorta

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44
Q

Central chemoreceptors

A

Measure CO2 pH in brain

Send signals to ponds and medulla for CO2 levels

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45
Q

In the lung (alveoli) Pressure

A

PaO2 higher than PaCO2

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46
Q

In the pulm artery side of capillaries (from body) Pressure

A

PaO2 lower than Pa CO2

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47
Q

In the pulm vein side of capillaries (going to heart&body)

A

PaO2 higher than PaCO2

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48
Q

Rapid movement of CO2 off hemoglobin

A

Increased pH of blood –> increases affinity of hemoglobin for oxygen
Decreases temperature of blood–>increases affinity of hemoglobin for oxygen

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49
Q

Altitude sickness

A
  • Atmospheric pressure is lower than normal

* PO2 pressure in alveoli is < 100 mmHg

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50
Q

Diffusion O2 out of alveoli depends on

A

Partial pressure of O2 in alveoli in relation to hemoglobin

Movement of CO2 off of hemoglobin into alveoli

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51
Q

Diffusion of O2 into off of hemoglobin into tissues depends on

A

– Tissue activity
– Higher temp of blood and lowering of pH (acidosis) = right shift • Partial pressure of O2 in tissues in relation to hemoglobin

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52
Q

Which part of the lung has the most perfusion

A

Lower levels of the lungs have higher perfusion of blood compared to
upper area of lungs

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53
Q

V/Q Ratio

A

Ratio of the air that reaches the alveoli and the blood that reaches the alveoli via capillaries = 0.8 is ideal

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54
Q

VQ Mismatch High and Low

A

High V/Q: lots of ventilation but little perfusion = dead space

Low V/Q: some ventilation but lots of perfusion

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55
Q

Ventilation

A

there is a block in the airways somewhere preventing alveoli from
having air exchange

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56
Q

Perfusion (Q)

A

breathing is fine but lack of blood getting to alveoli so gas exchange isn’t happening and pulmonary arterial blood gets recirculated

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57
Q

Shunt

A

Blood vessel or cardiac malformations

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58
Q

Obstructive Lung Disease

A

Mucous, inflammation, lung tissue destruction
Have a hard time expelling air from the lungs
–Ex. Chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis

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59
Q

Restrictive Lung Disease

A
  • “Restricts” the lungs from inflating

* Disease process or structural abnormality/pregnancy

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60
Q

Tidal Volume

A

amount of air moved in and out during one normal breath Approx. 500 ml

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61
Q

TLC (total lung capacity)

A

volume of air in lungs after biggest breath in Approx. 6L

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62
Q

VC (Vital Capacity)

A

volume of air that can be exhaled after biggest breath in Approx. 80% of TLC

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63
Q

Spirometry

A

Measures volume (L) and percent predicted of:
• FVC=forced vital capacity
• FEV1=forced expiratory volume in
the 1st second
Helps Determine Lung health
Percent predicted = compared to normal for age and height

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64
Q

Flail Chest

A

3+ ribs are broken in 2+ places.
On inspiration lungs sink in, on expiration the lung bulges out
Symptoms: Pain when breathing, anxiety, buldging and sinking

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65
Q

Pneumothorax

A

Air gets in to the pleural space and partially collapses lung. Can be due to trauma or sporadic.
Symptoms: Dyspnesa, chest ache, chest tightness, cyanosis

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66
Q

Factors of sporadic pneumothorax

A

Male, young, thin, smoker, rapid change in pressure. Its secondary to lung disease like COPD, Cancer, Asthma etc)

67
Q

Tention Pneumothorax

A

A collapse of a whole lung due to air that cannot escape in pleural cavity. Causes a mediastinal shift of heart, trachea, to undamaged side

68
Q

Pleural Effusion

A

When there is fluid in the pleural space
Symptoms: Dyspnea, cough, pain on inspiration, fever, difficulty taking deep breaths
Dx with thoracentisis (fluid collection)

69
Q

Transudative Fluid

A

Transudative fluid does not have any cells or proteins in it non inflammatory can be caused by salt/fluid retention or higher venous pressure leaking

70
Q

Exudative Fluid

A

Cloudy thick high protein cells (blood, wbc, bacteria) inflammation present

71
Q

Empyema

A

Puss in pleural space

72
Q

Brochiecteisis

A

Walls of bronchi are damaged from inflammation/infection

Bronchi lose ability to clear mucus–>Walls widen–>more airway infections–>scarring and loss of viable lung tissue

73
Q

Bronchiectasis symptoms

A

Symptoms: cough, sputum production, dyspnea, wheezing, chest pain, clubbing, hemoptysis, fatigue, failure to thrive
► Can lead to respiratory failure, atelectasis

74
Q

Bronchiolitis

A

Diffuse inflammation of airways smaller than terminal bronchioles. Can lead to alveolar destruction

75
Q

Epiglottitis

A

Acute swelling of epiglottis. Higher in unvaccinated children & adults. Inspiratory stridor, change of voice dysphagia are symptoms

76
Q

Atelectasis

A

Collapse of lung tissue.
Reduced alveolar ventilation OR air inside a plugged alveolus gets absorbed to the alveolus collapses.
Risk factors: confinement to bed, infections, disease, foreign body

77
Q

Interstitial Lung Disease

A

Disorders that cause progressive fibrosis in terminal lung tissue. Characterized by inflammation and scar tissue to supporting
tissue (interstitium) surrounding alveoli, fatal

78
Q

Interstitial Lung Disease symptoms

A

• Dry cough, dyspnea, weight loss, clubbing, enlarged heart, fatigue

79
Q

Sarcoidosis

A

Auto-immune inflammatory disease. Inflammation leads to deposits of immune cells, granulomas develop and leads to scarring (fibrosis)

80
Q

Pulmonary Edema (cariogenic)

A

High pulmonary capillary hydrostatic pressure secondary to high pulmonary venous pressure. Accumulation of fluid in interstitial and alveoli. Found in heart failure

81
Q

Pulmonary Edema (Non-cardiogenic)

A

Increase in filtration due to increase in capillary permeability can be due to injury/inflammation/obsturction
or lymph blockage: prevents reabsorption of net filtration

82
Q

Symptoms of pulmonary edema

A

DOE, orthopnea (difficulty breathing lying down)

Wet cough, wheezing, frothy sputum.

83
Q

Thrombus

A

Blood clot forming that is attached to the original vein where it is growing

84
Q

Embolism

A

Free blood clot that lodges in pulmonary vasculature
- Travels to inferior vena cava to the right side of the heart
• From right atrium to right ventricle
• From RV to pulmonary artery
• Emboli can get lodged at any point and cause venous obstruction

85
Q

Virchows Triad

A

Risk for Pulmonary
Hyper coagulable state, vascular wall injury, circulatory status

Thrombus forms and occludes pulmonary circulation, leads to hypoxic vasoconstriction less surfactant, edema, atelectasis

86
Q

Pneumonia (what happens to the breathing and HR)

A

Infection of the lung can be fungus, bacteria, viral.
Purulent fluid in alveoli can be lobar or bronchial(patches throughout both lungs)
Green, yellow, hemoptysis
Tachypnea, dyspnea, tachycardia

87
Q

Tuberculosis

A

Caused by Myocbacterium tuberculosis bacteria, granulomas form and are filled with caseous necrosis -isolate bacteria and create cavities in the lung tissue.

88
Q

TB symptoms

A

Progressive fatigue, anorexia, chronic cough, hemoptysis, low grade temp

89
Q

ALI/ARDS

A

Acute lung injury & Acute Respiratory Distress
Acute inflammation caused by trauma or infection, disruption of alveoli epithelial lining and the cap endothelial lining.
Refractory hypoxemia V/Q mismatch

90
Q

ABG

A

Measures pH O2 CO2 from artery

PaO2 75-100mmHg

91
Q

Asthma

A 
Chronic inflammatory airway disease of bronchi mucosa characterized by recurrent episodes of wheezing and/or breathlessness
Decreased FEV1 (obstructive)
92
Q

Asthma triggers

A

Exposure to:
Indoor allergens including second-hand smoke, dust mites, animals,
cockroaches, mold/mildew, viral triggers

93
Q

Asthma Cytokines/IGs

A

IL 4,5

IgE

94
Q

Asthma Effects on Airways

A

Smooth muscle constriction, Mucous plug & accumulation, hyperinflation of alveoli, dregranulation of mast cell

95
Q

COPD

A

Umbrella term for progressive obstructive lung diseases, can cause permanent impairment
Chronic bronchitis
Emphysema
Refractory asthma

96
Q

Refractory asthma

A

Non-reversible with bronchodilators

97
Q

Chronic Bronchitis

A

Cough with sputum production for at least 3 months a year for 2 years.
Chronic exposure to irritant

98
Q

Blue bloater (Bronchitis)

A

Airway flow issue
Blue to to cyanosis
High: Sputum, CO2, Hgb, RR,
Hypoxia, clubbing, enlarged heart, right sided heart failure.

99
Q

Emphysema

A

Alveoli destruction reducing lung surface area

100
Q

Pink Puffer (Emphysema)

A

High Co2 retention
Purse lip breathing to increase pressure of inhaled air
Barrel chest
Accessory muscle use to breath

101
Q

Why is CO2 retention a problem

A

Brain gets less sensitive to CO2 and peripheral chemoreceptors take over. They use O2 levels to let them know when to breath. If too much CO2 is give, then there is no stimulation of breathing.

102
Q

Pulmonary Artery Hypertension

A

ncreased pulmonary vasoconstrictors and decreased pulmonary vasodilators, resulting in increased pulmonary artery pressure
Hypoxemia/ acidosis makes this worse

103
Q

Cor Pulmonale

A

Cor pulmonale develops as PAH created pressure overload on the right ventricle
Can develop secondarily to lung disease and lead to right heart failure.

104
Q

Lung Cancer

A

Squamous cell carcinoma, Small cell carcinoma, Adeocarinoma, Large cell carcinoma

105
Q

Squamous cell carcinoma

A

Slow growing

Metastasizes late in disease process usually to hilar lymph nodes

106
Q

Small cell carcinoma

A

Fast growing, rapidly fatal
Metastasizes very quickly to mediastinum or distal areas of lung
Symptoms include excessive hormone production and airway obstruction

107
Q

Adenocarcinoma

A

Most common and has known genetic links and can occur with squamous
and small cell cancers
Moderate growth with early metastasis
PE is a symptom

108
Q

Large cell carcinoma

A

Rare

Fast growth with widespread metastasis dx with elimination

109
Q

Epicardium

A

Outer smooth layer (part of pericardium)

110
Q

Myocardium

A

Thickest layer of cardiac muscle. Muscle cells (cardiac myocytes) provide contractile force to propel blood. Thickness varies depending on heart chamber.

111
Q

Endocardium

A

Innermost layer

112
Q

Pericardium:

A

double‐walled membranous sac surrounding the heart

113
Q

Pericardial cavity:

& what does it do (4 things)

A

space between the parietal and visceral layers

  • Contains pericardial fluid (approx 20 ml under normal circumstances)
  • Prevents displacement of heart during movement
  • Protects heart from infection/inflammation from lungs and other surrounding tissues
  • Contains receptors that can control HR and BP
114
Q

Cycle of heart beats

A
  1. Atrial contract
  2. Isometric ventricular contract
  3. Ejection
  4. Isometric ventricular filling
  5. Passive ventricular filling
115
Q

SA node`

A

Pacemaker of the heart, generates action potential for heart beat

116
Q

AV Nodes

A

Action potentials travel through the myocardium here where they pass through the ventricles

117
Q

Bundle of His

A

Conduct impulses to the ventricular apex

118
Q

Depolarization:

A

electrical activation of muscle cells.

119
Q

Repolarization:

A

deactivation of muscle cells.

120
Q

Important ions for Myocardial action potential

A

Na, K, Ca, Cl

121
Q

Action potential phases

A
  1. Phase 0: depolarization; rapid Na entry into cell
  2. Phase 1: early repolarization; slow Ca entry into cell
  3. Phase 2: plateau, continued repolarization; slow entry of Na and Ca
  4. Phase 3: later repolarization; K moves out of cell
  5. Phase 4: return to resting membrane potential
122
Q

PQRST wave

A

P-atrial depolarization
QRS-Atrial repolarization & ventricle depolarization
T-ventricle repolarization

123
Q

Unique characteristics of the myocardial cells

A

Intercalated disks with gap junctions which allow electrical impulses to spread quickly
Have more mitochondria
Increase T-tubules giving faster access to molecules

124
Q

Atherosclerosis

A
  1. Endothelial injury/ inflammation
  2. LDL cholesterol can pentrate vessel wall and get trapped
  3. Macrophage with lipids inside accumulate and form a fatty streak release inflammatory cyokines
  4. cytokines simulate smooth muscle growth a plaque form over the fatty streak
  5. Plaque can calcify, obstruct blood flow or rupture
  6. Plaque rupture exposes the vessel underneath and a clot rapidly form which can obstruct the vessel.
125
Q

Consequences of Atherosclerosis

5 things

A 
Stroke
Renal Artery Disease
Aneurysms 
Peripheral artery disease 
Coronary artery disease
126
Q

Chylomicrons

A

lipoproteins that consist mostly of triglycerides. Transport dietary fat from intestine to liver and peripheral cells

127
Q

Triglycerides:

A

major form of lipid, used for energy

Ideal lab: less than 150

128
Q

VLDL:

A

triglycerides and protein

129
Q

LDL:

A

Cholesterol and protein, delivers cholesterol

Ideal lab: Less than 100

130
Q

HDL

A

Phospholipid and protein returns excess cholesterol from cells to liver where it can be converted to bile salts.
Ideal lab: 40+

131
Q

CAD risk increased with:

A
  • High levels of LDL
  • High levels of VLDL
  • High levels of Triglycerides
  • LOW levels of HDL
132
Q

Hypertension

A

Sustained elevation of 130 mm Hg systolic or higher OR

80 mm Hg diastolic or higher

133
Q

Dysfunction of the SNS RAAS

A

Insulin resistance–>Vasoconstriction–> increased peripheral resistance & Inflammation –> salt and water retention –> Inc blood volume

134
Q

Ability to evade (3 ways)

A 
Seeding of adjacent surfaces "floating to other areas" (ovarian, mesothelioma)
Lymphatic spread (breast tissue)
Hematgenous spread (leukemia, sarcoma, renal)
135
Q

Two proteins that inactivate RAS

A

P10 Stops PI3K
GAP- Stops RAS
Made by tumor suppressor genes

136
Q

p53

A

Tumor suppressor that keeps “surveillance” on the cell can trigger senescence (alive with no replication), DNA repair or growth inhibition (if this is successful the cell can live), Apoptosis if all other mechanisms fail

mutation leads to unchecked growth

137
Q

APC pathway

A

APC & Beta catenin= inactive, WENT come and separates them
when APC is made incorrectly or not made at all, B-catenin is always active and can go into the nucleus and cause unregulated growth

138
Q

RAS system

A

Cell receives GF on Growth receptor and RAS is activated

Rass

139
Q

Angina

A

Chest pain, a reversabile myocardial ischemia. Plaque ruptured and infarction may happen

140
Q

STEMI

A

ST segment elevation, requires immediate intervention, smaller infarctions not associated with this.

141
Q

Subendocardial infarction

A

Part of the wall bf cut off

142
Q

Transmural

A

Full thickness of the whole wall bf cut off, will show stemi

143
Q

Heart/vascular system in fetus is fully developed during

A

8 weeks gestation

144
Q

Foramen ovale

A

Opening between the atria

145
Q

Ductus Arteriosus

A

Joins the pulmonary artery to the aorta

146
Q

Ductus Venosus

A

Connects IVC to umbilical vein

147
Q

After birth

A

Fetal shunts close

  • Ductus venosis closes
  • Foramen ovale closes
  • Ductus arteriosis closes o2 sat in
148
Q

Patent ductus arteriosus

A

Should close on its own, if not it allows O2’d blood with non O2 blood

149
Q

VSD

A

opening between ventricular septum

150
Q

Tetralogy of fallot

A

VSD
Overriding aorta straddles the VSD
Pulmonary valve stenosis- less bf to pulm artery
Right ventricle hypertrophy

151
Q

Symptoms of tertraology of fallot

A

Clubbing, feeding difficulty, squatting

Hypercyanotic spell/tet spell (blue when crying or exerting)

152
Q

Coarctation of aorta

A

Narrowing of aorta

153
Q

Clinical manifestation of high bp in kids

A

systolic and diastolic bp levels are greater than 95th percentile on at least 3 occasion

154
Q

Heart failure

A

Decreased pumping/ filling ability of the heart which results in decreased cardiac output and fluid build up in the lungs & there isnt enough perfusion to tissues

155
Q

SNS in heart failure

A

Inc heart rate
vasoconstrict BV
increased afterload (pressure heart has to pump against)
Decrease CO

156
Q

Kidney System in heart failure

A

Increase renin & angiotensin II bc of low BV
Increase aldostreone which leads to Na H20 reabsorbtion and increases plasma volume
Increases preload (what heart gets back)
Increases the pulmonary edema

157
Q

Causes of heart failure 8

A 
Cardiomyopathy
Coronary artery disease 
HTN
Heart valve disease
Obesity
MII
Diabetes
158
Q

Preload

A

Ventricular stretch before contraction

159
Q

Afterload

A

Resistence to ejection of blood from the heart

160
Q

Cardiac contractility

A

How well the heart contracts (helps in CO)

161
Q

Heart rate contributing to CO

A

Diastolic filling is incomplete and atrial kick wont work well

162
Q

Stroke volume

A

Volume ejected during systole

163
Q

SV depends on

A

Preload, afterload & contractility in NS, myocardial o2 supply (contractility)

Pathophysiology (6 decks)

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