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Exam 3 PP > Ecam 1 Pathopharm 2 > Flashcards

Ecam 1 Pathopharm 2 Flashcards

1
Q

Subjective sensation of uncomfortable breathing
–Sensory urge to breathe is greater than a respiratory system response
–Signs: flared nostrils, retractions, use of accessory muscles

A

Dyspnea

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2
Q

Dyspnea when a person is lying down

A

PND Paroxysmal nocturnal dyspnea

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3
Q

2 voice transmissions (s/sx of pulmonary dysfunction)

A
  1. Fremitus

2. Resonance

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4
Q

4 abnormal lung sounds

A
  1. Rales
  2. Rhonchi
  3. Wheezing
  4. Stridor
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5
Q

(Upper Pulm Dz)

  1. Acute Cough =
  2. Chronic Cough=
A
  1. AC= 2-3 weeks

2. CC= > 3 weeks

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6
Q

(Upper Pulm Dz)

smokers may have

A

chronic bronchitis

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7
Q

(Upper Pulm Dz)

smokers may have

A

asthma, postnasal drip, GERD

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8
Q

Coughing of blood or bloody secretions

–Bright red, alkaline pH, frothy sputum

A

Hemoptysis

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9
Q

Hypercapnia (PaCO2 >42 mm Hg)

A

Hypoventilation

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10
Q

Hypocapnia (PaCO2<36 mm Hg)

A

Hyperventilation

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11
Q

–bluish discoloration of mucous membranes and skin related to desaturated hemoglobinLow PaO2, right to left shunt, decreased cardiac output, anxiety

A

Cyanosis

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12
Q

Painless, sign of chronic hypoxemia

A

Clubbing

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13
Q

the process of exchange of air between the lungs and the ambient air

A

Ventilation

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14
Q

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

A

Respiration

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15
Q

Normal value of dissolved oxygen Pa02

A

> 80 mm Hg

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16
Q

Normal value of oxyhemoglobin

A

95-97%

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17
Q

Normal value of dissolved carbon dioxide PaCO2

A

35-45 mm Hg

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18
Q

When you exhale you remove CO2 from your blood and also decrease the amount of carbonic acid, raising your what?

A

Blood pH

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19
Q

Lack of surfactant; infants are not strong enough to inflate their alveoli
•Protein-rich fluid leaks into the alveoli and further blocks oxygen uptake

A

Respiratory Distress Syndrome

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20
Q

6 structures of the upper resp tract

A
  1. nose and nasal cavity
  2. sinuses
  3. pharynx
  4. larynx
  5. trachea
  6. bronchi
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21
Q

(rhinotracheitis)

–Like a common cold with profound malaise

A

Upper resp infection

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22
Q

common cold, seasonal rhinitis, sinusitis, pharyngitis, laryngitis

A

Upper resp tract conditions

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23
Q

common cold, rhino sinusitis, influenza

A

upper resp viruses in adults

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24
Q

Block the cough reflex; Drugs Used to Treat Upper Respiratory Infections

A

Antitussives

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25
Q

Drugs Used to Treat Upper Respiratory Infections; Decrease the blood flow to the upper respiratory tract and decrease the overproduction of secretions

A

Decongestants

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26
Q

Drugs Used to Treat Upper Respiratory Infections;Block the release or action of histamine that increases secretions and narrows airways

A

Antihistamines

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27
Q

Drugs Used to Treat Upper Respiratory Infections;Increase productive cough to clear airways

A

Expectorants

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28
Q

Drugs Used to Treat Upper Respiratory Infections;Increase or liquefy respiratory secretions to aid clearing of airways

A

Mucolytics

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29
Q

bacteria in the alveoli
–Lobar: affect an entire lobe of the lung
–Bronchopneumonia: patchy distribution over more than one lobe

A

Typical Pneumonia

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30
Q

Viral and mycoplasma infections of alveolar septum or interstitium

A

Atypical Pneumonia

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31
Q

onset of pneumonia; 2 s/sx of systemic inflammation

A
  1. malaise

2. chills/ fever

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32
Q

World’s foremost cause of death from a single infectious agent
•Causes 26% of avoidable deaths in developing countries

A

Tuberculosis

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33
Q

Can stay alive in “suspended animation” for years

A

Tuberculosis

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34
Q

What happens in the initial TB infection?

A

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

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35
Q

What is primary TB?

A
  • Usually isolated in Ghon Foci→ bacteria are inactive, not contagious
  • If immune response is inadequate, bacteria multiply in the lungs→ progressive primary TB
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36
Q

Nodules in lung tissue and lymph nodes
•Caseous necrosis inside nodules
•Calcium may deposit in the fatty area of necrosis
•Visible on x-rays

A

GHON Complex

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37
Q

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

A

Milary TB

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38
Q

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).

A

Secondary TB

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39
Q

Squamous cell carcinoma
–Adenocarcinoma
–Bronchioloalveolar cell carcinoma

A

Non-small cell lung cancer

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40
Q

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

A

Small cell carcinoma

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41
Q

incidence: 30%; Growth Rate: slow; Metastisis: late, lymph nodes; tx: surgery, chemo, radiation; Prognosis: Fair

A

Squamous Cell Carcinoma

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42
Q

Incidence: 35-40%; GR: moderate; Metastisis: Early, lymph nodes, pleura, bone, adrenals, brain; Tx: surgery, chemo, radiation; Prognosis: 5yr survival <15%

A

Adeno-Carcinoma

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43
Q

Incidence: 10-15%; GR: rapid; Metastisis: early, wide spread; tx: palliative surgery; Prognosis: poor

A

Large cell Carcinoma

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44
Q

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

A

Small Cell Carcinoma

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45
Q

PaO2 ≤50mm Hg or PaCO2 ≥50mm Hg with pH ≤7.25

A

Acute resp failure

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46
Q

Inadequate alveolar ventilation

–Treatment: ventilatory support

A

Hypercapnic

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47
Q

Inadequate exchange of oxygen between the alveoli and the capillaries
–Treatment: supplemental oxygen therapy

A

Hypoxemic

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48
Q

4 Postoperative causes of resp failure?

A
  1. Atelextasis
  2. Pneumonia
  3. Pulmonary edema
  4. Pulmonary emboli
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49
Q

as the collapse or closure of the lung resulting in reduced or absent gas exchange.

A

Atelectasis

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50
Q

Air enters the pleural cavity
•Air takes up space, restricting lung expansion
•Partial or complete collapse of the affected lung

A

Pneumothorax

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51
Q

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

A

Tension Pneumothorax

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52
Q

: 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.

A

Open Pneumothorax

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53
Q

Symptoms include expiratory wheezing, dyspnea, and tachypnea

•Peak flow meters, oral corticosteroids, inhaled beta-agonists, and anti-inflammatories used to treat

A

Asthma

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54
Q

Type I hypersensitivity
•Mast cells’ inflammatory mediators cause acute response within 10–20 minutes
•Airway inflammation causes late phase response in 4–8 hours

A

Extrinsic (Atopic) Asthma

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55
Q 
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
A

Intrinsic (Nonatopic) Asthma

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56
Q

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

A

Emphysema

57
Q

Chronic irritation of airways
–Increased number of mucous cells
–Mucus hypersecretion
•Productive cough

A

Chronic Obstructive Bronchitis

58
Q

Infection and inflammation destroy smooth muscle in airways, causing permanent dilation

A

Bronchiectasis

59
Q

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?

A

COPD

60
Q

what happens during primary pulmonary hypertension?

A

Blood vessel walls thicken and constrict

61
Q

Elevation of pulmonary venous pressure
º Increased pulmonary blood flow
º Pulmonary vascular obstruction
º Hypoxemia

A

Secondary Pulmonary Hypertension

62
Q

tibia clavicle and lower humerus fractures occur mostly in who?

A

young persons; result of trauma

63
Q

upper femur, upper humerus, vertebrae, and pelvis fractures occur mostly in?

A

older adults; associated with osteoporosis

64
Q

Bone is broken all the way through

A

Complete fracture

65
Q

bone is damaged but is still in one piece

A

Incomplete fracture

66
Q

fracture that is hidden or not readily discernible

A

Occult

67
Q

(formerly referred to as compound) if the skin is broken; 2 or more fragments is termed:

A

Open fracture

Comminuted fracture

68
Q

runs parallel to the long axis of the bone

A

Linear fracture

69
Q

occurs at an oblique angle to the shaft of the bone

A

Oblique Fracture

70
Q

encircles the bone

A

Spiral fracture

71
Q

occurs straight across the bone

A

Transverse fracture

72
Q

break in only one cortex of bone

A

Greenstick

73
Q

Fracture with one end wedged into opposite end of inside fractured fragment

A

Impacted fracture

74
Q

the cortex buckles but does not break

A

Torus Fracture

75
Q

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

A

Bowing Fracture

76
Q

from disease process that weakens a bone associated with tumors, osteoporosis, infections, and metabolic bone disorders

A

Pathologic fracture

77
Q

occur in normal or abnormal bone that is subjected to repeated stress, such as occurs during athletics.

A

Stress fracture

78
Q

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

A

Fatigue fracture

79
Q

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

A

Insufficiency fractures

80
Q

consistsfragmentation and separation of a portion of the articular cartilage that covers the end of a bone at a joint.

A

Transchondral fracture

81
Q

primarily associated with vertebral fractures and hip fractures
most common in women in their 50s-60s

A

Postmenopausal Osteoporosis

82
Q

Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints

A

Ankylosing spondylitis

83
Q

Early symptoms of ankylosing spondylitis

A

low back pain, stiffness, pain, rstricted motion

84
Q

Increased serum uric acid
Crystals precipitate in the joint
Inflammation results
Tophi are deposits containing monosodium urate crystals

A

Gout

85
Q

Metabolic disorder that disrupts the body’s control of uric acid production or excretion

A

Gout

86
Q

Gout manifests high levels of what?

A

uric acid in the blood and other body fluids

87
Q

“gouty arthritis” is inflammation from what/

A

when crystals occur in the synovial fluid

88
Q

gout is related to what metabolism

A

purine (adenine and guanine)

89
Q

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

A

Tophaceous gout

90
Q

problem w/ uric acid metabolism, deposit of urate salts

A

Gout

91
Q

: urate crystals in synovial fluid; acute, painful inflammation

A

Gouty Arthritis

92
Q

advanced stage; Tophi: nodules in the fingers

A

Chronic tophaceous gout

93
Q

Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane• Autoimmune disorder Antibodies against IgG fragments
Cause inflammation in the joint

A

Rheumatoid Arthritis

94
Q 
NSAIDs 
Corticosteroids 
Leflunomide
Influximab
these are tx's for what
A

Rheumatoid Arthritis

95
Q

Degenerative joint disease
Inflammation of the joints often secondary to physical damage
Damaged joint cartilage tries to heal itself
Creating osteophytes or spurs

A

Osteoarthritis

96
Q

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

A

Osteoarthritis

97
Q

2 primary forms of migraine headaches

A
  1. with aura

2. without aura

98
Q

Begin during sleep; involve sharp, steady eye pain, sweating, flushing, tearing, and nasal congestion

A

cluster headaches

99
Q

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.

A

cluster headaches

100
Q

Primary tx of cluster headaches

A

directed prophylaxis (prednisone, lithium, verapamil)

101
Q

Usually occur at times of stress; dull band of pain around the entire head

A

Tension headaches

102
Q

Most common form of headache
–Moderate, nonthrobbing pain
–Usually located in a “head band” distribution
–May be episodic or chronic

A

tension headache

103
Q

nonopioid analgesic is tx for what?

A

tension headaches

104
Q

pain is usually behind the forehead/ cheekbones

A

sinus headache

105
Q

pain is in and around one eye

A

cluster headache

106
Q

pain is like a band squeezing the head

A

tension headaches

107
Q

pain, nausea, and visual changes are typical of classic form

A

migraine

108
Q

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

A

Alpha 1

109
Q

Nerve Membranes
—Act as modulators of norepinephrine release
—Beta Cells in the Pancreas
—Help to moderate the insulin release stimulated by SNS activation

A

Alpha 2

110
Q

—Cardiac Tissue
—Can stimulate increased myocardial activity and increased heart rate
—Responsible for increased lipolysis or breakdown of fat for energy in peripheral tissues

A

Beta 1

111
Q 
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
A

Beta 2 receptors

112
Q

—Found in visceral effector organs
—Found in sweat glands
—Found in some vascular smooth muscle
stimulation→ —Pupil Constriction

A

Muscarinic receptors

113
Q

—Increased GI Motility
—Increase Salivation
—Increased Urinary Bladder Constriction
—Decreased Heart Rate

A

Muscarinic receptors

114
Q

—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

A

Nicotinic receptors

115
Q

Called sympathomimetic drugs because they mimic the effects of the sympathetic nervous system (SNS)

A

Adrenergic agonists

116
Q

uses of adrenergic agonists

A

Varies from ophthalmic preparations for dilating pupils to systemic preparations for shock

117
Q

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

A

alpha and beta adrenergic agonists

118
Q

indications for alpha and beta adrenergic agonists

A

tx of hypotensive shock, bronchospasm, and some types of asthma

119
Q

Shock; glaucoma; prolongs effects of regional anesthetic

A

Epinephrine (Adrenalin, Sus-Phrne)

120
Q

Treat shock or during cardiac arrest to get sympathetic activity

A

Norepinephrine (Levophed)

121
Q

shock

A

Dopamine (Intropin)

122
Q

CHF

A

Dobutamine (Dobutrex)

123
Q

Seasonal rhinitis; hypotensive episodes

A

Ephedrine (Pretz-D)

124
Q

Synthetic agent that is similar to norepinephrine

A

Metaraminol (Aramine)

125
Q

Drugs that bind primarily to alpha-receptors rather than to beta-receptors

A

alpha specific adrenergic agonists

126
Q

indications for alpha specific adrenergic agonists

A

HTN, constriction of topical vessels in nose

127
Q

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

A

Beta specific adrenergic agonists

128
Q

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

A

Adrenergic blocking antagonists

129
Q

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

A

Alpha and beta adrenergic blockers

130
Q

indications for alpha and beta adrenergic blockers

A

essential HTN, contra, bradycardia or heart block, shock or CHF

131
Q

Blocks postsynaptic alpha1 receptors, decreasing sympathetic tone in the vasculature and causing vasodilatation

A

alpha adrenergic blocking agent

132
Q

Competitive blocking of the beta-receptors in the SNS

—Blocking of beta receptors in the heart and in the juxtaglomerular apparatus of the nephron

A

beta-adrenergic blocking agents

133
Q

beta-adrenergic blocking agents are indicated for

A

treating cardio problems, HTN, angina, migraine headaches, preventing reinfarction after MI

134
Q

—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

A

Beta1-Selective adrenergic blocking agents

135
Q

Chemicals that act at the same site as the neurotransmitter acetylcholine (ACh)

A

Cholinergic drugs

136
Q

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

A

cholinergic drugs

137
Q

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

A

Direct-acting cholinergic agonists

138
Q

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

A

Indirect-acting cholinergic agonists

139
Q

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

A

Anticholinergic agents (Parasympatholytic)

Exam 3 PP (3 decks)

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