Midterm Flashcards
Functions of the Conduction Zone
warm, humidify and filter air
Types of pnuemocyte
Type 1 - squamous epithelium
Type 2 - Produces surfactant
Atmospheric Pressure
Patm
-0 mmHg
Alveolar Pressure Palv
-must be negative (lower than Patm) during inspiration and higher during expiration
Transmural pressure
Palv - Pip
- the pressure difference across the alveolar wall
- as this increases alveoli size increases
Intrapleural Pressure Pip
- usually negative and keeps alveoli inflated
- decreasing this pulls on the alveoli increasing the volume
- change is generated by muscles
Compliance
delta V / delta P
with a lowered compliance you need to muscular work harder to breathe
Elasticity
Delta P / Delta V
-if lowered you need to work harder to exhale
What does surfactant do?
- inserts itself between water molecules and reduces surface tension
- increased lung V, surfactant spreads out and increases surface tension
Dynamic Compression
During forced expiration Pip becomes positive
- if Pip exceeds airway pressure than airways can narrow/collapse
- Pursed-lip breathing increases Palv to counter act this
What can cause Bronchiolar Smooth Muscle Constriction
- histamine
- PNS stimulation
- decreased PCO2
- expiration
What can cause Bronchiolar Smooth Muscle Relaxation
- epinephrine (Beta2 stim)
- increased PCO2
- inspiration
Inspiratory Reserve Volume
Top of TV to max inspiratory effort
Inspiratory Capacity
TV + IRV
Expiratory Reserve Volume
-low point of TV to the most they can expire
Residual volume
-gas that is left in the lungs that cannot be exhaled
Total Lung Capacity
IRV + TV + ERV + RV
Functional Residual Capacity
ERV + RV
FEV1
forced expiratory volume in 1 second
-should be 80% of FVC
Minute Ventilation
TV x f
Dead Space
volume of gas that fills conducting airways and doesn’t do gas exchange
Composition of Alveolar gas and pulmonary veins
100 mmHg of O2
40 mmHg of CO2
Composition of gas in pulmonary arteries and peripheral veins
40 mmHg of O2
46mmHg of CO2
Intrapulmonary Shunt
-perfusion w/o Ventilation
Alveolar Dead space
Ventilation without perfusion
Right shift of Oxygen Hemoglobin Dissociation curve
- increased PCO2
- Increased H+ ion
- increased Temp.
- exercise
- hemoglobin is giving up more O2 more readily
How does anemia affect the O2 hemoglobin dissociation curve
-anemia lowers the O2 carrying capacity of the blood and the O2 content, but not the O2 saturation
Buffering of H+ ions in venous blood
???
Dorsal Respiratory Group
- connects with skeletal muscle motor neurons
- active during inspiration
- sensitive to opiates
Pneumotaxic Center
- provides inhibitory input to the DRG
- active during expiration, allows DRG to shut off Relaxes muscles
Apneustic Center
- signals the DRG to delay the inhibitory input by the PC
- gives positive impulses to inspiratory neurons
- prolongs inspiration
Ventral Respiratory Group
-active during forced expiratory
Stretch Receptors in the lung
-found in airways and responsible for the Hering-Breuer reflex
Hering-Breuer reflex
too big of inspiration=too much stretch and inhibits DRG so you don’t continue to inspire
Irritant Receptors in the lungs
- increases rate
- decreases TV
Juxtacapillary Receptors
- in alveolar walls
- sensitive to excess fluid
- increased rate and decreased TV
Peripheral Chemoreceptors
what do they monitor and rxn
aortic and carotid bodies
- monitor arterial PO2, H+, and CO2
- decreased PO2 = increased rate and depth
Central Chemoreceptors
what do they monitor and rxn
in respiratory centers in brain stem
- sensitive to CSF H+
- increased H+ = increased rate and depth
How does exercise affect PCO2 and PO2
doesn’t change during mild to moderate exercise
What happens at anaerobic threshold
-arterial PCO2 decreases
-production of lactic acid decreases pH
-
Restrictive Dysfunction = ???
Volume Limitation
Obstructive Disease = ????
Flow limitation
What is the key method to determine the type of limitation for lung disease?
ratio of FEV1 to FVC
- restrictive disease ratio doesn’t change much
- obstructive disease the ratio decreases
Flow Volume loops and disease?
- obstructive disease = scooped out shape
- restrictive disease = smaller overall
What does COPD include
- pulmonary emphysema
- chronic bronchitis
- asthma
Symptoms of COPD
- chronic cough
- expectoration of mucus
- wheezing
- Dyspnea on exertion
Characteristics of COPD
- inflammation of smaller airways
- increase mucus production
- decreased mucous clearance
- thickened mucous
- tissue destruction
- bronchial smooth muscle spasm
Definition of Chronic bronchitis
-sputum producing cough on most days for 3 months during 2 consecutive years
Emphysema
- tissue destruction (alveoli and capillaries)
- decreased elasticity
- flattening of diaphragm
Cause of alpha 1 antitrypsin deficiency
smoking
Asthma
reversible airway obstruction caused by smooth muscle spams, inflammation of mucosa and hyper secretion of mucus
Extrinsic asthma?
- most common
- reaction to allergens
Intrinsic asthma
-exposure to cold or air pollution
Asthma Mechanism
in response to triggers, mast cells, eosinophils, and macrophages release inflammatory mediators
Bonchiectasis
- abnormal dilation of medium sized bronchi
- Obstructive disease
Cystic Fibrosis
- Obstructive Disorder
- structural damage and increase mucus production
- liver cirrhosis
- decreased pancreatic secretions
- 36.8 median life expectancy
Restrictive Lung Dysfunction
- disorder of Compliance in either the chest wall or the lungs or both
- decreased TV, increased Rate
- work of breathing can increase to 25% resting energy
How do corticosteroids work?
-blocks release of arachidonic acid from epithelial cells which blocks production of pro-inflammatory agents
What is corticosteroids used for?
drug of choice in mild to moderate asthma
Sympathomimetics
epinephrine and ephedrine
- cause peripheral vasoconstriction
- tachycardia
- bronchodilation
Parasympatholytics
- anticholinergics that block the binding of acetylcholine to post synaptic membrane
- spiriva
- no improvement in survival
Diaphysis
- shaft of the bone
- compact bone
- contains marrow cavity
Epiphysis
- head of the bone
- spongy bone
Metaphysis
- area of shaft that widens towards epiphysis
- spongy bone
Compact Bone
- dense and rigid
- functional unit is the osteon
Osteon
- made of osteocytes arranged in concentric layers
- osteocytes are in extracellular fluid spaces called lacunae
- 4-20 layers surrounding a Haversian canal
Lacunae
osteocytes contained in small extracellular fluid filled spaces
Canaliculi
-protrude from lacunae and penetrate the surrounding calcified matrix
Haversian canal
contains blood vessels that carry nutrients and wastes to canaliculi
Spongy bone
- primary component of the interior of bones
- made of spicules lined with osteogenic cells
Osteogenic cells
- differentiate into osteoblasts
- active in growing bone
- may become activated in adults during fracture or worn out bone
Osteoblasts
- modified fibroblasts
- make the bone
- synthesize and secrete organic matrix during ossification
- calcification of matrix during mineralization
Osteocytes
- mature bone cells
- active in transfer of minerals from interior bone to growth surfaces
- transfer of Ca and minerals back and forth between blood and organic matrix
Osteoclasts
- derived from monocytes
- break down the organic matrix during bone resorption
- release calcium from matrix into blood
Describe the organic matrix of bones
- synthesized and secreted by osteoblasts
- made of type 1 collagen, proteoglycans and glycoproteins
- called osteoid in unmineralized state
Describe the inorganic component in matrix
- hydroxyapatites
- calcium phosphates/ flouride/ hydroxide
What are the 5 steps of bone growth
- Bone Collar Forms
- Cavitation of hyaline cartilage
- Invasion of periosteal bud
- Continuation of ossification and medullary cavity
- Ossification of epiphysis
Bone Collar formation
- periosteum forms, contains osteogenic cells
- osteogenic cells differentiate into osteoblasts
- these secrete osteoid against the shaft
Cavitation of Hyaline cartilage
- occurs in the middle of the diaphysis
- chondrocytes stop secreting collagen and mineralization starts
- chondrocytes die creating cavity
Invasion of periosteal bud
periosteal bud invades primary ossification center and forms blood/lymphatic vessels and nerves
-brings hematopoietic cells, oblasts, oclasts into cavity
Continuation of ossification center
- Oblasts use matrix to lay down osteoid forming bony trabeculae
- Oclasts break down trabeculae enlarging cavity
- secondary ossification occurs at epiphysis
Ossification at epiphysis
- this is how bones grow
- cartilage continues to proliferate but eventually stops and ossification ocurs
Describe the process of epiphyseal plate becoming bone
- chondrocytes increase in number
- older chondrocytes hypertrophy, the matrix becomes calcified
- calcification leads to chondrocyte death and matrix deteriorates
- oblasts secrete osteoid
- mineralization of osteoid and bone forms
Nutrition important for bone growth
- Calcium
- Vitamin D
- Vitamin C
Hormones for bone growth
- Growth hormone stimulates liver to produce IGF 1 to grow
- Insulin
- thyroid hormone
- testosterone and estrogen
Describe the palace of oblasts and oclasts
- osteoclasts express RANK receptor
- Oblasts secrete protein RANKL
- Oblasts also secrete osteoprotegerin an inhibitor of RANKL
- binding of RANKL to RANK activates oclasts and keeps them alive
Describe menopause’s effect on osteoclasts
- before=estrogen limits amount of RANKL produced by Oblasts and osteoprotegerin dominates
- after=RANKL increases which increases osteoclast function
What contributes to Ca homeostasis
- PTH
- calcitonin
- Vitamin D
- kidneys
- GI system
Describe Calciums effect on PTH
- there are calcium receptors on the PT gland
- when Ca decreases PTH production increases
What does increased PTH do?
- differentiates Oblasts to Oclasts
- increases Oclast activity
- Ca reabsorption in kidney and decreased Ca excretion in urine
- GI absorbs more Ca
What are the effects of calcitonin on Ca
- calcitonin is secreted by parafollicular cells of the thyroid
- the stimulus is high Ca concentration
- inhibits the release of Ca from bone
- decreases renal reabsorption of Ca
Vitamin D
-very high levels in fish liver oil
-fatty fish
-eggs
beef liver
Hypocalcemia
- increased neuronal excitability
- Trousseaus and Chvosteks sign
- neuromuscular instability
- death
- fatigue
- anxiety
- dental problems
Hypercalcemia
- depressed neuronal excitability
- decreased reflexes
- brady cardia
- most common cause is PTH dyfunction
Treatment of a fracture
- reduction
- immobilization
- restoration of function
What are the 4 stages of fracture healing
- hematoma formation
- Fibrocartilaginous callus formation
- Bony Callus Formation
- Remodeling
Describe the Hematoma Formatoin
- starts first 1-2 days
- hematoma develops from injured blood vessels
- a large clot forms days 2-5
- invasion of new blood vessels and early fibrosis begins
Describe the Fibrocartilaginous Callus formation
- soft tissue callus
- fibroblasts and osteoblasts go into fracture and secrete collage
- osteoblasts deposit osteoid
- collar forms around fracture site
- reaches max girth 2-3 weeks
- stable fracture but not load bearing
Describe the bony callus formation
- ossification of matrix 3-4 weeks
- spongy bone initially forms
- radiographic union cast can be removed sometimes
Describe the remodeling phase
- osteoclasts resorb dead and excess bone
- reestablish medullary canal
- compact bone replaces spongy bone
Timeline for fracture healing
kids 4-6 weeks
adolescents 6-8 weeks
adults 10-18 weeks
Osteomyelitis
-bacterial infection of bone
Routes of infection for osteomyelitis
- hematogenous = blood borne
- contiguous = infection that spread from adjacent tissues
- exogenous = direct traumatic intro from external environment
Hematogenous osteomyelitis
- more likely in children and sick adults
- staphylococcus aureus
Sequelae
pus limits blood flow to bone and starts necrosis
-fragmentation occurs separating from blood supply
Sequestra
devascularized necrotic bone fragments
Involcrum
new bone that forms around sequestra
Tuberculosis
infects bone from lungs or lymph
-most common in vertebrae and long bones
Osteonecrosis
-bone death from fracture, thrombus, embolism, infection, vascular compression
What is the most common consequence of metastatic bone disease
-hypercalcemia - decreased excitability
DXA scan and values
comapres BMD to BMD of 30 y/o
> 1 SD below = osteopenia
>2-2.5 = osteoporosis
Type 1 osteoporosis
caused by menopausal estrogen deficiency
- primarily spongy bone
- vertebrae and radial fractures
Type 2 Osteoprosis
- senile, occurs with aging
- both spongy and cortical bone lost
- hip, long bone, and vertebrae
Biphosphonates
-inhibit osteoclast activity
Selective estrogen receptor modulators
-raloxifene
Antigen
substance foreign to the host which can stimulate an immune response
-bacteria, pollen
Epitope
the immunologically active sites on antigens
-the portion of the antigen that interacts with the antibody
Major Histocompatibility Complex Molecules
-self recognition molecules on the surface of nucleated cells
Cytokines
proteins made during an immune response that regulate leukocytes
What is the second line of defense mechanism
inflammatory response initiated by tissue injury
How does vasodilation help with inflammatory response
-enhances delivery of neutrophils and monocytes
How does chemotaxis help with inflammatory response
WBCs are attracted to injured tissues
What happens when complement is activated?
- 5 complement proteins form a complex called the (MAC) that inserts itself into membrane of bacteria and creates a pore that causes cell lysis and death
- enhances other inflammatory responses
- can act as opsonizing agent enhancing phagocytosis
Specific Immune Defense
-typically against bacteria, viruses, and non-microbials
Antibodies
proteins in the serum
-contain a Y shaped variable that determine specificity to antigen
Where are antibodies found?
- surface of lymphocytes
- soluble antibodies are produced by plasma cells
IgA
- 15% of antibodies
- found in body secretions
- protect against microbes
IgD
- .2%
- found on surface of immature B lymphocytes
IgE
- capable of triggering the most powerful immune response
- binds to mast cells
IgG
- 75%
- most abundant
- can cross placenta
- activates complement
IgM
- 10%
- potent complement activator
Describe the antibody mediated immune response
- antigen enters blood
- recognized by B lymphocyte, and antigen binds to antibody
- antigen encounters macrophages and processes and is presented on the surface of the macrophage in a complex with class 2 MHC proteins
- macrophage presents antigen complex to CD4+ Cell
- antigen presenting cell and helped T cell triggers release of cytokines which trigger
Memory cells
ensure a more rapid response when re-exposed to antigen
What happens when a soluble antibody binds to an antigen?
- the antibody acts as a opsonizing agent to link phagocytes to antigen
- activates complement and MAC kills cells to which antibody is attached
Active immunity
- due to formation of memory cells
- developed by natural infection
- vaccination
Passive Immunity
-due to direct transfer of antibodies by
injection
placenta
breast milk
What mediates the Cell Mediated Immune Response?
- CD8+ or Cytoxic T cells in the lymphoid tissues
- they respond to virus and cancer cells
Immunodeficiencey
abnormality in the immune system that makes a person susceptible to disease that are normally preventable
Hypersensitivity/Allergic Disorders
an immune system in which responses to an environmental antigen causes inflammation and tissue damage
Acquired Immunodeficiency Syndrome
-Human immunodeficiency virus selectively attacks CD4+ lymphocytes and macrophages
IgE mediated disorder (type 1 hypersensitivity)
- immediate response within 5 mins
- allergic reaction
Antibody Mediated Disorder (type 2 hypersensitivity)
-ABO or Rh
Immune Complex Allergic Disorder (type 3 hypersensitivity)
-soluble antibody binds to antigen forming insoluble complex
Cell Mediated Hypersensitivity Disorder (Type 4)
- delayed hypersensitivity
- against TB or viruses
NRTI
- zidovudine or Retrovir
- can cause myopathy
NNRTIs
- Sustiva
- nausea and skin reactions
Protease inhibitors
- Invirase
- hyperglycemia, thrombophlebitis
Fusion inhibitors
Fuzeon
Where is the liver located?
Upper right Quadrant
-not palpable
Describe the lobule of the liver
- functional unit of the liver
- a branch of the hepatic vein is at the center of each lobule
- at each corner is bile duct, hepatic artery and portal vein
Kuppfer cells
- macrophagges in sinusoid
- consume RBC, bacteria
Stellate cells
- fat storing cells in the perisinusoidal space
- storage of Vitamin A
- regeneration after injury, deposit collagen and can cause cirrhosis
In the liver cells farthest from the central vein…
are most oxygenated
-involved in AA, gluconeogensis, and bile formation
In the liver cells closest to the central vein…
- least oxygenated,
- involved in glycolysis, lipogenesis, and drug metabolism
What supplies blood to the liver?
hepatic portal vein (60-70%)
-hepatic artery
Biotransformation
-modification of substances from the blood to return to circulation or excrete to bile
Filtration
-done by kuppfer cells
The liver and CHO metabolism (2)
- the liver stores glucose as glycogen, and can then break down to maintain blood sugar.
- Converts CHO to triglycerides for storage in tissues
What does the Liver do during fasting?
-synthesizes glucose from AA or LA (gluconeogenesis)
The liver and lipid metabolism
- almost all fat synthesis from CHO and protein occurs in liver
- synthesis of cholesterol, phospholipids occurs in liver
The liver exports cholesterol in what 2 forms?
- used to synthesize bile acids
- enters the blood as VLDL
Transamination
- how the liver metabolizes proteins
- transfer amino group to an ketoacid which allows AA to gluconeogenesis, and lipid synthesis
Bilirubin
-a product of breakdown of RBC
Describe the process of the breakdown of bilirubin
- hemoglobin is broken down into biliverdin and then converted to free bilirubin and binds with albumin
- converted to conjugated bilirubin in liver
- exported to bile (soluble)
Jaundice
- yellow discoloration of skin and sclera of eye
- excess plasma bilirubin
What can cause Jaundice
- excessive RBC lysis
- decreased hepatic BF
- limited conjugation of bilirubin
- obstruction of bile ducts
What does bile do?
-excretion of bilirubin and cholesterol
-promotes digestion and absorption of lipids
-emulsify lipids to be absorbed
-
What does the gallbladder do?
concentrates bile salts, bilirubin, and cholesterol by as much as 10-20 X
What is cholestasis
- the suppression of bile secretion backed up into the systemic circulation
- caused by cirrhosis
Cholecystitis
- inflammation of the gallbladder
- partial or complete obstruction of cystic or common duct
Signs of cholecystitis
- RUQ pain, muscle spasm and vomiting after a meal
- Jaundice 25%
Cholelithiasis
- too much cholesterol with too little bile salts
- leads to bile stasis and formation of stones
Hepatitis that are fecal-oral transmission
A, E
Hep A
- young children
- RNA virus
Hep B
- DNA virus
- transmitted through body fluids
Hep C
- most common cause of liver disease, cirrhosis
- usually asymptomatic
Pancreatitis
- release of enzymes into pancreas and tissues
- usually caused by alcohol abuse
Where are antibodies found?
- surfaces of B lymphocytes (receptors)
- circulate in plasma
