Exam 2 Flashcards
Carcinoma
Epithelial derived malignant neoplasm
Adenocarcinoma
Glad form carcinoma
Adenoma
Benign gland forming neoplasm
Leukemia
Malignant neoplasm of circulating white blood cell
Lymphoma
Malignant neoplasm of lymphocytes
Sarcoma
Malignant neoplasm arising from soft tissues
Oncogene
a gene whose activated product causes growth
Tumor suppressor gene
a gene whose product prevents
growth
Mutation
a change in the genetic pattern
Cancer cell: A cellular population that has undergone eight fundamental
changes in cell physiology
- Self-sufficiency in growth signals
- Insensitivity to growth inhibition
- Altered cellular metabolism
- Evasion of apoptosis
- Immortality
- Sustained angiogenesis
- Ability to invade and metastasize
- Ability to evade the human immune response
Telomeres
Protect the
chromosomes from
fraying –Expiration date
Telomerase
tells telomeres
to regenerate
Tumor cells evade the immune
system one of three ways
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.
Altered
Cellular
Metabolism:
Use anaerobic
glycolysis for
carbon
Sustained Angiogensis
- Tumor secretes VEGF or bFGF
- VEGF increases blood vessel expression and movement to tumor
- Tumor has increased blood supply
Respiratory System Purpose
To facilitate the uptake of oxygen from the atmosphere
To release of carbon dioxide into the atmosphere
Turbinates
Heat and moisten air
Nasal passages
Cilia to trap particulates
Throat
Contains epiglottis, laryngeal
cartilage, muscles
Secretory cells
club cell in the bronchioles
Epiglottis
Cologen that flaps down to prevent food from going into trachea
Bronchus
Cartilage rings lined with epithelial rings, no blood gas exchange
Bronchioles
Last division with cartilage
Bronchioles are lined with
Ciliated epithelial cells that help trap debris
Mucous producing cells: Mucins helps trap pathogens
Secretory cells
Parietal pleura
adheres to internal thoracic wall (rib cage)
Visceral Pleura
Adheres to lungs
Pleural space and what is it needed for
Space between parietal and visceral pleura
Filled with fluid and helps reduce friction and provide tension for lung expansion
Can cause edema or infection
Specialized lung cells
Goblet cells and club cells
Goblet cells
Secrete mucins, repair and replace mucuos layer for airway protection.
Increased when damaged
Metaplasia in goblet cells
Results in an allergic asthma symptoms increase in goblet cells, goblet cells replicate and increase mucous production
Club cells
Exocrine cells in the respiratory tract
Stem cell capabilities to adapt
produce uroglobin
Has microvili
Uroglobin
Detoxifies harmful substances
Alveoli characteristics that make them good for O2 exchange
Large SA to help come into contact with capillaries more contact helps with O2 diffusion
Type I cells
Simplified squamous epithelial lining cannot replicate
Type II cells
Surfactant producing can replicate into type one cells
Surfactant
Helps reduces surface tension and allow alveoli to pop open
can help with inflammation
help fight bacterial infection
Ventilation
Movement of air from environment into lungs into alveoli
Diffusion
Gas exchange of O2 and CO2
Capillary perfusion
How much blood is getting to gas exchange site
Muscles of ventilation
Diaphram- Primary muscle flattens to help breathing
Intercostal- Control ribcage expansion
Accessory- ab, neck, back last resort
Cerebral Cortex
Control voluntary breathing
Pons and Medula role in breathing
Controls depth and rate of breathing
Peripheral Chemoreceptors
Measure O2 CO2 and PH in carotid/aorta
Central chemoreceptors
Measure CO2 pH in brain
Send signals to ponds and medulla for CO2 levels
In the lung (alveoli) Pressure
PaO2 higher than PaCO2
In the pulm artery side of capillaries (from body) Pressure
PaO2 lower than Pa CO2
In the pulm vein side of capillaries (going to heart&body)
PaO2 higher than PaCO2
Rapid movement of CO2 off hemoglobin
Increased pH of blood –> increases affinity of hemoglobin for oxygen
Decreases temperature of blood–>increases affinity of hemoglobin for oxygen
Altitude sickness
- Atmospheric pressure is lower than normal
* PO2 pressure in alveoli is < 100 mmHg
Diffusion O2 out of alveoli depends on
Partial pressure of O2 in alveoli in relation to hemoglobin
Movement of CO2 off of hemoglobin into alveoli
Diffusion of O2 into off of hemoglobin into tissues depends on
– Tissue activity
– Higher temp of blood and lowering of pH (acidosis) = right shift • Partial pressure of O2 in tissues in relation to hemoglobin
Which part of the lung has the most perfusion
Lower levels of the lungs have higher perfusion of blood compared to
upper area of lungs
V/Q Ratio
Ratio of the air that reaches the alveoli and the blood that reaches the alveoli via capillaries = 0.8 is ideal
VQ Mismatch High and Low
High V/Q: lots of ventilation but little perfusion = dead space
Low V/Q: some ventilation but lots of perfusion
Ventilation
there is a block in the airways somewhere preventing alveoli from
having air exchange
Perfusion (Q)
breathing is fine but lack of blood getting to alveoli so gas exchange isn’t happening and pulmonary arterial blood gets recirculated
Shunt
Blood vessel or cardiac malformations
Obstructive Lung Disease
Mucous, inflammation, lung tissue destruction
Have a hard time expelling air from the lungs
–Ex. Chronic obstructive pulmonary disease (COPD), asthma, cystic fibrosis
Restrictive Lung Disease
- “Restricts” the lungs from inflating
* Disease process or structural abnormality/pregnancy
Tidal Volume
amount of air moved in and out during one normal breath Approx. 500 ml
TLC (total lung capacity)
volume of air in lungs after biggest breath in Approx. 6L
VC (Vital Capacity)
volume of air that can be exhaled after biggest breath in Approx. 80% of TLC
Spirometry
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
Flail Chest
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
Pneumothorax
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
Factors of sporadic pneumothorax
Male, young, thin, smoker, rapid change in pressure. Its secondary to lung disease like COPD, Cancer, Asthma etc)
Tention Pneumothorax
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
Pleural Effusion
When there is fluid in the pleural space
Symptoms: Dyspnea, cough, pain on inspiration, fever, difficulty taking deep breaths
Dx with thoracentisis (fluid collection)
Transudative Fluid
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
Exudative Fluid
Cloudy thick high protein cells (blood, wbc, bacteria) inflammation present
Empyema
Puss in pleural space
Brochiecteisis
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
Bronchiectasis symptoms
Symptoms: cough, sputum production, dyspnea, wheezing, chest pain, clubbing, hemoptysis, fatigue, failure to thrive
► Can lead to respiratory failure, atelectasis
Bronchiolitis
Diffuse inflammation of airways smaller than terminal bronchioles. Can lead to alveolar destruction
Epiglottitis
Acute swelling of epiglottis. Higher in unvaccinated children & adults. Inspiratory stridor, change of voice dysphagia are symptoms
Atelectasis
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
Interstitial Lung Disease
Disorders that cause progressive fibrosis in terminal lung tissue. Characterized by inflammation and scar tissue to supporting
tissue (interstitium) surrounding alveoli, fatal
Interstitial Lung Disease symptoms
• Dry cough, dyspnea, weight loss, clubbing, enlarged heart, fatigue
Sarcoidosis
Auto-immune inflammatory disease. Inflammation leads to deposits of immune cells, granulomas develop and leads to scarring (fibrosis)
Pulmonary Edema (cariogenic)
High pulmonary capillary hydrostatic pressure secondary to high pulmonary venous pressure. Accumulation of fluid in interstitial and alveoli. Found in heart failure
Pulmonary Edema (Non-cardiogenic)
Increase in filtration due to increase in capillary permeability can be due to injury/inflammation/obsturction
or lymph blockage: prevents reabsorption of net filtration
Symptoms of pulmonary edema
DOE, orthopnea (difficulty breathing lying down)
Wet cough, wheezing, frothy sputum.
Thrombus
Blood clot forming that is attached to the original vein where it is growing
Embolism
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
Virchows Triad
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
Pneumonia (what happens to the breathing and HR)
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
Tuberculosis
Caused by Myocbacterium tuberculosis bacteria, granulomas form and are filled with caseous necrosis -isolate bacteria and create cavities in the lung tissue.
TB symptoms
Progressive fatigue, anorexia, chronic cough, hemoptysis, low grade temp
ALI/ARDS
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
ABG
Measures pH O2 CO2 from artery
PaO2 75-100mmHg
Asthma
Chronic inflammatory airway disease of bronchi mucosa characterized by recurrent episodes of wheezing and/or breathlessness Decreased FEV1 (obstructive)
Asthma triggers
Exposure to:
Indoor allergens including second-hand smoke, dust mites, animals,
cockroaches, mold/mildew, viral triggers
Asthma Cytokines/IGs
IL 4,5
IgE
Asthma Effects on Airways
Smooth muscle constriction, Mucous plug & accumulation, hyperinflation of alveoli, dregranulation of mast cell
COPD
Umbrella term for progressive obstructive lung diseases, can cause permanent impairment
Chronic bronchitis
Emphysema
Refractory asthma
Refractory asthma
Non-reversible with bronchodilators
Chronic Bronchitis
Cough with sputum production for at least 3 months a year for 2 years.
Chronic exposure to irritant
Blue bloater (Bronchitis)
Airway flow issue
Blue to to cyanosis
High: Sputum, CO2, Hgb, RR,
Hypoxia, clubbing, enlarged heart, right sided heart failure.
Emphysema
Alveoli destruction reducing lung surface area
Pink Puffer (Emphysema)
High Co2 retention
Purse lip breathing to increase pressure of inhaled air
Barrel chest
Accessory muscle use to breath
Why is CO2 retention a problem
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.
Pulmonary Artery Hypertension
ncreased pulmonary vasoconstrictors and decreased pulmonary vasodilators, resulting in increased pulmonary artery pressure
Hypoxemia/ acidosis makes this worse
Cor Pulmonale
Cor pulmonale develops as PAH created pressure overload on the right ventricle
Can develop secondarily to lung disease and lead to right heart failure.
Lung Cancer
Squamous cell carcinoma, Small cell carcinoma, Adeocarinoma, Large cell carcinoma
Squamous cell carcinoma
Slow growing
Metastasizes late in disease process usually to hilar lymph nodes
Small cell carcinoma
Fast growing, rapidly fatal
Metastasizes very quickly to mediastinum or distal areas of lung
Symptoms include excessive hormone production and airway obstruction
Adenocarcinoma
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
Large cell carcinoma
Rare
Fast growth with widespread metastasis dx with elimination
Epicardium
Outer smooth layer (part of pericardium)
Myocardium
Thickest layer of cardiac muscle. Muscle cells (cardiac myocytes) provide contractile force to propel blood. Thickness varies depending on heart chamber.
Endocardium
Innermost layer
Pericardium:
double‐walled membranous sac surrounding the heart
Pericardial cavity:
& what does it do (4 things)
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
Cycle of heart beats
- Atrial contract
- Isometric ventricular contract
- Ejection
- Isometric ventricular filling
- Passive ventricular filling
SA node`
Pacemaker of the heart, generates action potential for heart beat
AV Nodes
Action potentials travel through the myocardium here where they pass through the ventricles
Bundle of His
Conduct impulses to the ventricular apex
Depolarization:
electrical activation of muscle cells.
Repolarization:
deactivation of muscle cells.
Important ions for Myocardial action potential
Na, K, Ca, Cl
Action potential phases
- Phase 0: depolarization; rapid Na entry into cell
- Phase 1: early repolarization; slow Ca entry into cell
- Phase 2: plateau, continued repolarization; slow entry of Na and Ca
- Phase 3: later repolarization; K moves out of cell
- Phase 4: return to resting membrane potential
PQRST wave
P-atrial depolarization
QRS-Atrial repolarization & ventricle depolarization
T-ventricle repolarization
Unique characteristics of the myocardial cells
Intercalated disks with gap junctions which allow electrical impulses to spread quickly
Have more mitochondria
Increase T-tubules giving faster access to molecules
Atherosclerosis
- Endothelial injury/ inflammation
- LDL cholesterol can pentrate vessel wall and get trapped
- Macrophage with lipids inside accumulate and form a fatty streak release inflammatory cyokines
- cytokines simulate smooth muscle growth a plaque form over the fatty streak
- Plaque can calcify, obstruct blood flow or rupture
- Plaque rupture exposes the vessel underneath and a clot rapidly form which can obstruct the vessel.
Consequences of Atherosclerosis
5 things
Stroke Renal Artery Disease Aneurysms Peripheral artery disease Coronary artery disease
Chylomicrons
lipoproteins that consist mostly of triglycerides. Transport dietary fat from intestine to liver and peripheral cells
Triglycerides:
major form of lipid, used for energy
Ideal lab: less than 150
VLDL:
triglycerides and protein
LDL:
Cholesterol and protein, delivers cholesterol
Ideal lab: Less than 100
HDL
Phospholipid and protein returns excess cholesterol from cells to liver where it can be converted to bile salts.
Ideal lab: 40+
CAD risk increased with:
- High levels of LDL
- High levels of VLDL
- High levels of Triglycerides
- LOW levels of HDL
Hypertension
Sustained elevation of 130 mm Hg systolic or higher OR
80 mm Hg diastolic or higher
Dysfunction of the SNS RAAS
Insulin resistance–>Vasoconstriction–> increased peripheral resistance & Inflammation –> salt and water retention –> Inc blood volume
Ability to evade (3 ways)
Seeding of adjacent surfaces "floating to other areas" (ovarian, mesothelioma) Lymphatic spread (breast tissue) Hematgenous spread (leukemia, sarcoma, renal)
Two proteins that inactivate RAS
P10 Stops PI3K
GAP- Stops RAS
Made by tumor suppressor genes
p53
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
APC pathway
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
RAS system
Cell receives GF on Growth receptor and RAS is activated
Rass
Angina
Chest pain, a reversabile myocardial ischemia. Plaque ruptured and infarction may happen
STEMI
ST segment elevation, requires immediate intervention, smaller infarctions not associated with this.
Subendocardial infarction
Part of the wall bf cut off
Transmural
Full thickness of the whole wall bf cut off, will show stemi
Heart/vascular system in fetus is fully developed during
8 weeks gestation
Foramen ovale
Opening between the atria
Ductus Arteriosus
Joins the pulmonary artery to the aorta
Ductus Venosus
Connects IVC to umbilical vein
After birth
Fetal shunts close
- Ductus venosis closes
- Foramen ovale closes
- Ductus arteriosis closes o2 sat in
Patent ductus arteriosus
Should close on its own, if not it allows O2’d blood with non O2 blood
VSD
opening between ventricular septum
Tetralogy of fallot
VSD
Overriding aorta straddles the VSD
Pulmonary valve stenosis- less bf to pulm artery
Right ventricle hypertrophy
Symptoms of tertraology of fallot
Clubbing, feeding difficulty, squatting
Hypercyanotic spell/tet spell (blue when crying or exerting)
Coarctation of aorta
Narrowing of aorta
Clinical manifestation of high bp in kids
systolic and diastolic bp levels are greater than 95th percentile on at least 3 occasion
Heart failure
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
SNS in heart failure
Inc heart rate
vasoconstrict BV
increased afterload (pressure heart has to pump against)
Decrease CO
Kidney System in heart failure
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
Causes of heart failure 8
Cardiomyopathy Coronary artery disease HTN Heart valve disease Obesity MII Diabetes
Preload
Ventricular stretch before contraction
Afterload
Resistence to ejection of blood from the heart
Cardiac contractility
How well the heart contracts (helps in CO)
Heart rate contributing to CO
Diastolic filling is incomplete and atrial kick wont work well
Stroke volume
Volume ejected during systole
SV depends on
Preload, afterload & contractility in NS, myocardial o2 supply (contractility)
