Ecam 1 Pathopharm 2 Flashcards
Subjective sensation of uncomfortable breathing
–Sensory urge to breathe is greater than a respiratory system response
–Signs: flared nostrils, retractions, use of accessory muscles
Dyspnea
Dyspnea when a person is lying down
PND Paroxysmal nocturnal dyspnea
2 voice transmissions (s/sx of pulmonary dysfunction)
- Fremitus
2. Resonance
4 abnormal lung sounds
- Rales
- Rhonchi
- Wheezing
- Stridor
(Upper Pulm Dz)
- Acute Cough =
- Chronic Cough=
- AC= 2-3 weeks
2. CC= > 3 weeks
(Upper Pulm Dz)
smokers may have
chronic bronchitis
(Upper Pulm Dz)
smokers may have
asthma, postnasal drip, GERD
Coughing of blood or bloody secretions
–Bright red, alkaline pH, frothy sputum
Hemoptysis
Hypercapnia (PaCO2 >42 mm Hg)
Hypoventilation
Hypocapnia (PaCO2<36 mm Hg)
Hyperventilation
–bluish discoloration of mucous membranes and skin related to desaturated hemoglobinLow PaO2, right to left shunt, decreased cardiac output, anxiety
Cyanosis
Painless, sign of chronic hypoxemia
Clubbing
the process of exchange of air between the lungs and the ambient air
Ventilation
the exchange of oxygen and carbon dioxide
Aveoli and Cells. diffusion of oxygen from alveoli to blood and of carbon dioxide from blood to alveoli
Respiration
Normal value of dissolved oxygen Pa02
> 80 mm Hg
Normal value of oxyhemoglobin
95-97%
Normal value of dissolved carbon dioxide PaCO2
35-45 mm Hg
When you exhale you remove CO2 from your blood and also decrease the amount of carbonic acid, raising your what?
Blood pH
Lack of surfactant; infants are not strong enough to inflate their alveoli
•Protein-rich fluid leaks into the alveoli and further blocks oxygen uptake
Respiratory Distress Syndrome
6 structures of the upper resp tract
- nose and nasal cavity
- sinuses
- pharynx
- larynx
- trachea
- bronchi
(rhinotracheitis)
–Like a common cold with profound malaise
Upper resp infection
common cold, seasonal rhinitis, sinusitis, pharyngitis, laryngitis
Upper resp tract conditions
common cold, rhino sinusitis, influenza
upper resp viruses in adults
Block the cough reflex; Drugs Used to Treat Upper Respiratory Infections
Antitussives
Drugs Used to Treat Upper Respiratory Infections; Decrease the blood flow to the upper respiratory tract and decrease the overproduction of secretions
Decongestants
Drugs Used to Treat Upper Respiratory Infections;Block the release or action of histamine that increases secretions and narrows airways
Antihistamines
Drugs Used to Treat Upper Respiratory Infections;Increase productive cough to clear airways
Expectorants
Drugs Used to Treat Upper Respiratory Infections;Increase or liquefy respiratory secretions to aid clearing of airways
Mucolytics
bacteria in the alveoli
–Lobar: affect an entire lobe of the lung
–Bronchopneumonia: patchy distribution over more than one lobe
Typical Pneumonia
Viral and mycoplasma infections of alveolar septum or interstitium
Atypical Pneumonia
onset of pneumonia; 2 s/sx of systemic inflammation
- malaise
2. chills/ fever
World’s foremost cause of death from a single infectious agent
•Causes 26% of avoidable deaths in developing countries
Tuberculosis
Can stay alive in “suspended animation” for years
Tuberculosis
What happens in the initial TB infection?
Macrophages begin a cell-mediated immune response
•Takes 3–6 weeks to develop positive TB test
•Results in a granulomatous lesion
or Ghon focus containing
–Macrophages
–T cells
–Inactive TB bacteria
What is primary TB?
- Usually isolated in Ghon Foci→ bacteria are inactive, not contagious
- If immune response is inadequate, bacteria multiply in the lungs→ progressive primary TB
Nodules in lung tissue and lymph nodes
•Caseous necrosis inside nodules
•Calcium may deposit in the fatty area of necrosis
•Visible on x-rays
GHON Complex
look like grains of millet in the tissues
•Meat inspection was introduced to keep them out of the food supply
•Pasteurization of milk was introduced to keep TB out of the milk supply
Milary TB
often referred to as reactivation or reinfection TB, may occur if patients are re-exposed to TB bacilli (after a primary infection) or if they become immunocompromised (they are unable to contain the infection).
Secondary TB
Squamous cell carcinoma
–Adenocarcinoma
–Bronchioloalveolar cell carcinoma
Non-small cell lung cancer
Strongest correlation with cigarette smoking
–Rapid growth, metastisize widely & early
•85% have metastisized by diagnosis
–Poor prognosis
–1-3 months untreated
–14% survive after 2 years if treated
Small cell carcinoma
incidence: 30%; Growth Rate: slow; Metastisis: late, lymph nodes; tx: surgery, chemo, radiation; Prognosis: Fair
Squamous Cell Carcinoma
Incidence: 35-40%; GR: moderate; Metastisis: Early, lymph nodes, pleura, bone, adrenals, brain; Tx: surgery, chemo, radiation; Prognosis: 5yr survival <15%
Adeno-Carcinoma
Incidence: 10-15%; GR: rapid; Metastisis: early, wide spread; tx: palliative surgery; Prognosis: poor
Large cell Carcinoma
Incidence: 15-20%; GR: very rapid; Metastisis: very early, mediastinum, lymph nodes, bone, brain; Prognosis: very poor, 1-3months if NO tx, 14% after 2yrs with tx
Small Cell Carcinoma
PaO2 ≤50mm Hg or PaCO2 ≥50mm Hg with pH ≤7.25
Acute resp failure
Inadequate alveolar ventilation
–Treatment: ventilatory support
Hypercapnic
Inadequate exchange of oxygen between the alveoli and the capillaries
–Treatment: supplemental oxygen therapy
Hypoxemic
4 Postoperative causes of resp failure?
- Atelextasis
- Pneumonia
- Pulmonary edema
- Pulmonary emboli
as the collapse or closure of the lung resulting in reduced or absent gas exchange.
Atelectasis
Air enters the pleural cavity
•Air takes up space, restricting lung expansion
•Partial or complete collapse of the affected lung
Pneumothorax
air enters pleural cavity through the wound on inhalation but cannot leave on exhalation. A sort of one-way valve exists— the air enters the affected side during inhalation, but is unable to leave when the patient exhales. Therefore, all of this air exerts increased pressure on the organs of the thoracic cage. CAN BE FATAL
Tension Pneumothorax
: air enters pleural cavity through the wound on inhalation and leaves on exhalation. Inhaled air compresses the affected side’s lung, but during exhalation, the lung reinflates somewhat.
Open Pneumothorax
Symptoms include expiratory wheezing, dyspnea, and tachypnea
•Peak flow meters, oral corticosteroids, inhaled beta-agonists, and anti-inflammatories used to treat
Asthma
Type I hypersensitivity
•Mast cells’ inflammatory mediators cause acute response within 10–20 minutes
•Airway inflammation causes late phase response in 4–8 hours
Extrinsic (Atopic) Asthma
Respiratory infections –Epithelial damage, IgE production •Exercise, hyperventilation, cold air –Loss of heat and water may cause bronchospasm •Inhaled irritants –Inflammation, vagal reflex •Aspirin and other NSAIDs –Abnormal arachidonic acid metabolism
Intrinsic (Nonatopic) Asthma
Enlargement of air spaces and destruction of lung tissue
•Neutrophils in alveoli secrete trypsin: Increased neutrophil numbers due to inhaled irritants can damage alveoli
•α1-antitrypsin inactivates the trypsin before it can damage the alveoli: A genetic defect in α1-antitrypsin synthesis leads to alveolar damage
Emphysema
Chronic irritation of airways
–Increased number of mucous cells
–Mucus hypersecretion
•Productive cough
Chronic Obstructive Bronchitis
Infection and inflammation destroy smooth muscle in airways, causing permanent dilation
Bronchiectasis
Air is trapped in the lower respiratory tract
•The alveoli degenerate and fuse together
•The exchange of gases is greatly impaired
these are manifestations of what?
COPD
what happens during primary pulmonary hypertension?
Blood vessel walls thicken and constrict
Elevation of pulmonary venous pressure
º Increased pulmonary blood flow
º Pulmonary vascular obstruction
º Hypoxemia
Secondary Pulmonary Hypertension
tibia clavicle and lower humerus fractures occur mostly in who?
young persons; result of trauma
upper femur, upper humerus, vertebrae, and pelvis fractures occur mostly in?
older adults; associated with osteoporosis
Bone is broken all the way through
Complete fracture
bone is damaged but is still in one piece
Incomplete fracture
fracture that is hidden or not readily discernible
Occult
(formerly referred to as compound) if the skin is broken; 2 or more fragments is termed:
Open fracture
Comminuted fracture
runs parallel to the long axis of the bone
Linear fracture
occurs at an oblique angle to the shaft of the bone
Oblique Fracture
encircles the bone
Spiral fracture
occurs straight across the bone
Transverse fracture
break in only one cortex of bone
Greenstick
Fracture with one end wedged into opposite end of inside fractured fragment
Impacted fracture
the cortex buckles but does not break
Torus Fracture
fractures usually occur when longitudinal force is applied to bone. This type of fracture is common in children and usually involves the paired radius-ulna or the fibula-tibia
Bowing Fracture
from disease process that weakens a bone associated with tumors, osteoporosis, infections, and metabolic bone disorders
Pathologic fracture
occur in normal or abnormal bone that is subjected to repeated stress, such as occurs during athletics.
Stress fracture
is caused by abnormal stress or torque applied to a bone with normal ability to deform and recover. usually occur in individuals who engage in a new or different activity that is both strenuous and repetitive
Fatigue fracture
are stress fractures that occur in bones lacking the normal ability to deform and recover, Rheumatoid arthritis, osteoporosis, Paget disease, osteomalacia, rickets, hyperparathyroidism, and radiation therapy
Insufficiency fractures
consistsfragmentation and separation of a portion of the articular cartilage that covers the end of a bone at a joint.
Transchondral fracture
primarily associated with vertebral fractures and hip fractures
most common in women in their 50s-60s
Postmenopausal Osteoporosis
Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints
Ankylosing spondylitis
Early symptoms of ankylosing spondylitis
low back pain, stiffness, pain, rstricted motion
Increased serum uric acid
Crystals precipitate in the joint
Inflammation results
Tophi are deposits containing monosodium urate crystals
Gout
Metabolic disorder that disrupts the body’s control of uric acid production or excretion
Gout
Gout manifests high levels of what?
uric acid in the blood and other body fluids
“gouty arthritis” is inflammation from what/
when crystals occur in the synovial fluid
gout is related to what metabolism
purine (adenine and guanine)
A chronic form of gout with nodular masses of UA crystals (tophi) that are deposited in different soft tissue areas of the bodye
Occur with hyperuricemia over time
It develops years after initial attack
Tophaceous gout
problem w/ uric acid metabolism, deposit of urate salts
Gout
: urate crystals in synovial fluid; acute, painful inflammation
Gouty Arthritis
advanced stage; Tophi: nodules in the fingers
Chronic tophaceous gout
Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane• Autoimmune disorder Antibodies against IgG fragments
Cause inflammation in the joint
Rheumatoid Arthritis
NSAIDs Corticosteroids Leflunomide Influximab these are tx's for what
Rheumatoid Arthritis
Degenerative joint disease
Inflammation of the joints often secondary to physical damage
Damaged joint cartilage tries to heal itself
Creating osteophytes or spurs
Osteoarthritis
local areas of damage and loss of articular cartilage, new bone formation of joint margins, subchondral bone changes, and variable degrees of mild synovitis and thickening of the joint capsule
Osteoarthritis
2 primary forms of migraine headaches
- with aura
2. without aura
Begin during sleep; involve sharp, steady eye pain, sweating, flushing, tearing, and nasal congestion
cluster headaches
may be caused by blood vessel dilation in the eye area. Inflammation of nearby nerves may give rise to the distinctive stabbing, throbbing pain usually felt in one eye. The trigeminal nerves branch off the brainstem behind the eyes and send impulses throughout the cranium and face.
cluster headaches
Primary tx of cluster headaches
directed prophylaxis (prednisone, lithium, verapamil)
Usually occur at times of stress; dull band of pain around the entire head
Tension headaches
Most common form of headache
–Moderate, nonthrobbing pain
–Usually located in a “head band” distribution
–May be episodic or chronic
tension headache
nonopioid analgesic is tx for what?
tension headaches
pain is usually behind the forehead/ cheekbones
sinus headache
pain is in and around one eye
cluster headache
pain is like a band squeezing the head
tension headaches
pain, nausea, and visual changes are typical of classic form
migraine
Blood Vessels
—Cause vasoconstriction and increase peripheral resistance, raising blood pressure
—Iris
—Cause pupil dilation
—Urinary Bladder
—Cause the increased closure of the internal sphincter
Alpha 1
Nerve Membranes
—Act as modulators of norepinephrine release
—Beta Cells in the Pancreas
—Help to moderate the insulin release stimulated by SNS activation
Alpha 2
—Cardiac Tissue
—Can stimulate increased myocardial activity and increased heart rate
—Responsible for increased lipolysis or breakdown of fat for energy in peripheral tissues
Beta 1
Smooth Muscle in Blood Vessels —Stimulation leads to vasodilatation —Bronchi —Can cause dilation —Periphery —Increased muscle and liver breakdown of glycogen and increased release of glucagon —Uterine Muscle —Results in relaxed uterine smooth muscle
Beta 2 receptors
—Found in visceral effector organs
—Found in sweat glands
—Found in some vascular smooth muscle
stimulation→ —Pupil Constriction
Muscarinic receptors
—Increased GI Motility
—Increase Salivation
—Increased Urinary Bladder Constriction
—Decreased Heart Rate
Muscarinic receptors
—Located in the CNS, adrenal medulla, the autonomic ganglia, and the neuromuscular junction
—Stimulation Causes:
—Muscle contraction
—Autonomic response
—Release of norepinephrine and epinephrine from the adrenal medul
Nicotinic receptors
Called sympathomimetic drugs because they mimic the effects of the sympathetic nervous system (SNS)
Adrenergic agonists
uses of adrenergic agonists
Varies from ophthalmic preparations for dilating pupils to systemic preparations for shock
The effects of these drug are mediated by the adrenergic receptors in target organs; heart rate increases, bronchi dilate, vasoconstriction occurs, intraocular pressure decreases, glycogenolysis occurs throughout the body
alpha and beta adrenergic agonists
indications for alpha and beta adrenergic agonists
tx of hypotensive shock, bronchospasm, and some types of asthma
Shock; glaucoma; prolongs effects of regional anesthetic
Epinephrine (Adrenalin, Sus-Phrne)
Treat shock or during cardiac arrest to get sympathetic activity
Norepinephrine (Levophed)
shock
Dopamine (Intropin)
CHF
Dobutamine (Dobutrex)
Seasonal rhinitis; hypotensive episodes
Ephedrine (Pretz-D)
Synthetic agent that is similar to norepinephrine
Metaraminol (Aramine)
Drugs that bind primarily to alpha-receptors rather than to beta-receptors
alpha specific adrenergic agonists
indications for alpha specific adrenergic agonists
HTN, constriction of topical vessels in nose
Effect is related to its stimulation of the beta-adrenergic receptors
—Increase heart rate, conductivity, and contractility, bronchodilation, increase blood flow to skeletal muscles and splanchnic bed, and relaxation of uterus
Beta specific adrenergic agonists
Called sympatholytic drugs because they lyse, or block, the effects of the SNS;
Related to their ability to react with specific adrenergic receptor sites without activating them;
Prevent norepinephrine from activating the receptor
Adrenergic blocking antagonists
Competitively block the effects of norepinephrine at the alpha and beta receptors throughout the SNS
—Prevents the signs and symptoms associated with sympathetic stress reaction and results in lower blood pressure, slower pulse, and increased renal perfusion with decreased renin levels
Alpha and beta adrenergic blockers
indications for alpha and beta adrenergic blockers
essential HTN, contra, bradycardia or heart block, shock or CHF
Blocks postsynaptic alpha1 receptors, decreasing sympathetic tone in the vasculature and causing vasodilatation
alpha adrenergic blocking agent
Competitive blocking of the beta-receptors in the SNS
—Blocking of beta receptors in the heart and in the juxtaglomerular apparatus of the nephron
beta-adrenergic blocking agents
beta-adrenergic blocking agents are indicated for
treating cardio problems, HTN, angina, migraine headaches, preventing reinfarction after MI
—Do not usually block beta2-receptor sites, including the sympathetic bronchodilation
—Preferred for patients who smoke or have asthma, obstructive pulmonary disease, or seasonal or allergic rhinitis
HTN, angina, some cardiac arrhythmias
Beta1-Selective adrenergic blocking agents
Chemicals that act at the same site as the neurotransmitter acetylcholine (ACh)
Cholinergic drugs
Often called parasympathomimetic drugs because their action mimics the action of the parasympathetic nervous system
—Not limited to a specific site; therefore associated with many undesirable systemic effects
cholinergic drugs
Occupy receptor sites for ACh on the membranes of the effector cells of the postganglionic cholinergic nerves
—Cause increased stimulation of the cholinergic receptor
Increase the tone of the detrusor muscle of the bladder and relax the bladder sphincter
Direct-acting cholinergic agonists
Blocks acetylcholinesterase at the synaptic cleft. This allows the accumulation of ACh released from the nerve endings and leads to increased and prolonged stimulation of ACh
React with the enzyme acetylcholinesterase and prevent it from breaking down the ACh that was released from the nerve
—Cause increased stimulation of the ACh receptor sites
Indirect-acting cholinergic agonists
Used to block the effects of acetylcholine
—Lyse, or block effects of the PNS; also called parasympatholytic agentsBlocks the acetylcholine receptors at the muscarinic cholinergic receptor site
Anticholinergic agents (Parasympatholytic)
