100b Flashcards

1
Q

upper air way

A
  1. Pharynx
    - Nasopharynx – nose to uvula
    - Oropharynx – Nasopharynx to epiglottis
  2. Larynx – epiglottis to glottis
  3. Thyroid cartilage
  4. Glottic opening
  5. Arytenoid cartilage – false vocal cords
  6. Pyriform fossae
  7. Cricoid ring
  8. Vallecula – base of tongue meeting epiglottis, hyoid epiglottic ligament
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2
Q

lower air way

A

Functions to exchange O2 and CO2

Trachea – glottis to bronchi bifurcation, 16-20 cartilaginous incomplete rings, carina

Bronchi

Bronchioles – smallest airway without alveoli

Alveoli

Lungs – L 2 lobes, R 3 Lobes

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3
Q

pharynx

A

nasopharynx
oropharynx
(epiglottis sits between oro and hypo)
hypopharynx

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4
Q

larynx

A

vocal cords
thyroid cartilage
cricoid cartilage

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5
Q

esophagus

A

attaches to the stomach, runs postieor to the larynx

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6
Q

minute volume

A

tidal volume x ventolations per min

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7
Q

tidal volume

A

amount of air inhaled in one breath

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8
Q

dead space

A

the air that fills the upper and lower airways but doesnt actually get used by the body simply fills the cavities
approx 150ml

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9
Q

perfusion

A

delivery of oxygenated blood to tissues

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10
Q

shock

A

lack of end organ perfusion leading to anaerobic metabolism

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11
Q

effects of anaerobic metabolism

A

cause build up of waste products acids eg. latic acid and pyruvic acid. and cell death

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12
Q

anaerobic metabolism

A
  • which can be defined as ATP production without oxygen
  • much less effective
  • occurs in 3 stages glycolysis , the Krebs cycle , and electron transport
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13
Q

fick principle

A
  • adequate supply of O2
  • on loading of O2 to RBCs
  • delivery of oxygenated RBCs to tissue
  • off loading of O2 from RBC to tissue
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14
Q

cellular respiration

A

chemical reactions breaking down food to use as energy

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15
Q

increased H+ in the body

A

causes decreased PH causing metabolic acidosis

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16
Q

brain damage
heart damage
organ damage

A

4-6 min
starts 30-60 seconds
minutes to hours depending on the organ

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17
Q

norepinephrine

A

released causing peripheral vasoconstriction

increased chrontropic, inotropic effects increasing organ perfusion

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18
Q

stroke volume

A

amount of blood pumped by the heart in one contraction

approx 70ml

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19
Q

perload

A
  • passive stretching on the walls of the heart

- more blood in, increased stretching, increased contraction, increased output

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20
Q

blood pressure

A

force that blood exerts on artery walls

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21
Q

cardiac out put

A

stroke volume x heart rate (BPM)

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22
Q

blood buffer system

A
  • almost instant
  • protects form changes in H+
  • chemical sponge absorbing H+ when there is excess and releasing H+ when levels are low
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23
Q

ratio of Bicarb to H+

A

20:1

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24
Q

respiratory buffer

A

-aids in correcting acid base imbalance by controlling CO2 levels
-CO2 in the body increase, resp rate increases to blow off CO2
-increased resp = decreased CO2 and H2CO3 = increased PH
decreased resp = increased CO2 and H2CO3 = decreased PH

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25
decreased CO2
increased blood PH
26
increased CO2
decreased blood PH
27
renal buffer
- slowest to act but most effective | - kidneys excrete H+ and form HCO3
28
CO2 + H2O = H2CO3 = H + HCO3
uses buffer systems to shift back and forth to maintain PH (homeostasis)
29
4 types of imblances
respiratory acidosis respiratory alkalosis metabolic acidosis metabolic alkalosis
30
respiratory acidosis
- decreased resp rate causing the body to retain CO2 - increased CO2 in blood causing decreased PH and a surplus of H2CO3 - easily correctable by increasing resp rate and blowing off CO2
31
respiratory alkalosis
- increased resp rate causing excess CO2 to be exhaled | - decreased CO2 leads to increased PH and decreased H2CO3
32
metabolic acidosis
- renal impairment - decreased HCO3 increased H2CO3 - increased PH
33
metabolic alkalosis
- ingestion of alkaline products (baking soda, tums) - prolonged vomiting (decreasing acid in body) - increased HCO3 and decreased H2CO3 - decreased PH
34
3 stages of shock
compensated - < 15% blood loss decompensated - 15%-25% blood loss irreversible - > 25% blood loss
35
compensated shock (stage 1)
- body recognizes a problem and attempts to correct it by initiating a sympathetic response - norepi and epi released, increased HR, peripheral vasoconstriction, increased BP - shunting blood from limbs - decreased urine out put - increased resp rate (combat metabolic acidosis)
36
decompensated shock (stage 2)
body cant compensate forever, condition worsens and compensatory mechanisms begin to fail - BP decreased with increased HR and RR - epi is still being released in an attempt to oxygenate vital organs - peripheral cells are now hypoxic and anaerobic metabolism is the only option, this produces greater amounts of acid and increases the acidity (decreased PH) in the body. - metabolic acidosis increases and vital organs began to get affected
37
irreversible shock (stage 3)
- body can no longer compensate even with medical interventions - BP, HR, RR and perfusion decline and begin to fail - blood shunted from liver, kidneys and lungs in an attempt to oxygenate heart and brain - organs start to die - decreased LOC, feeling of impending doom
38
hypovolemic shock
- caused by fluid loss - can be blood, or fluid volume - internal or external loss
39
cardiogenic shock
-caused by heart failure, most common the left ventricle. If L ventricle is 40% damaged the heart is unable to properly pump blood
40
neurogenic shock
- disconnect between nervous system and body - unable to control blood vessels, they relax and dilate creating to large a space for the volume of blood to full - no compensated phase
41
septic shock
- caused by infection | - toxins released cause vasodilation
42
anaphylactic shock
- caused by exposure to allergen triggering a histamine release - bronchoconstriction - vasodilation
43
stage 1 vasoconstriction
15%
44
stage 2 capillary and venule opening
15%-25%
45
stage 3 disseminated coagulation
25%-35%
46
stage 4 multiple organ failure
greater than 35%
47
beta 1
increased chronotropic, inotopic and dromotropic
48
beta 2
bronchodilation | smooth muscle dilation
49
norepinephrine
- primary alpha 1 and 2 - vasoconstriction - increased PVR and afterload
50
AVP arginine vasopressin
also known as ADH released from pituitatry glad increased water absorption and decreased urine out put
51
renin-angiotensin
- renin released from kidneys - renin and angiotensin combine and produce angiotensin I - angiotensin I converted to agiotensin II by enzymes - potent vasoconstrition - sodium reabsorption - inotropic and chrontropic
52
aldosterone
defends fluid volume sodium reabsorption water retention decreased urine output
53
Drug Sources
Five major sources of drugs - Plants - Animals/humans - Minerals - Microorganisms - Chemical substances
54
Drug Names
1. Chemical - chemical make up or structure 2. Generic or Non-proprietary - Not capitalized - abbreviated chemical name 3. Trade, Brand or proprietary name - copyright name designed by selling drug company 4. Official - usually the same as generic name followed by USP or NF
55
Drug Control in Canada
- Department of health Canada – bureau of drug surveillance - Canada food and drugs act & regulation - Narcotics Control act & regulations
56
General Properties of Drugs
1-Action – what the drug does and how it goes about this 2-Indications - what the drug is used for 3-Contraindications – conditions for which the drug should not be given 4-Therapeutic effects – desirable drug actions 5-Major Side Effects – undesirable or harmful drug actions 6-Precautions – conditions or potential problems of which you should be aware 7-Preparations – how the drug comes packaged 8-Dosage – how much is given to achieve desired effects
57
Potential Reactions to Drug Therapy
- Antagonists - Contraindication - Cumulative action - Depressant - Allergy - Dependence - Interaction - Idiosyncrasy - Potentiation - Stimulant - Summation - Synergism - Therapeutic action - Tolerance - Untoward effect
58
Antagonist
agents designed to inhibit or counteract effects of other drugs or undesired effects caused by normal or hyperactive physiological mechanisms
59
contraindication
medical or physiological factors that make it harmful to admin a drug
60
cumulative action
tendency for repeated doses to accumulate in blood and organs causing increased and sometimes toxic effects
61
depressant
substance which decreases a function or activity
62
allergy
systemic reaction to a drug resulting from a previous sensitizing exposure and development of immunological mechanism. Can be initiated by drug itself or a metabolite of
63
dependance
state of which withdrawal of a drug causes intense physical or emotional disturbance
64
interacton
beneficial or detrimental modification of the effects of one drug by the prior or concurrent admin of another drug
65
idosyscrasy
abnormal or peculiar response to a drug
66
potentiation
enhancement of effects caused by concurrent admin of two drugs in which one drug increases effects of the other
67
stimulant
drug that enhances or increases body function or activity
68
Summation
combined effect of two drugs such that the total effects equals sum of individual effects (1+1=2)
69
Synergism
the combined action of two drugs such that the total effect exceeds the sum of the individual effects (1+1=3)
70
Therapeutic action
desired intended actions of drug
71
Tolerance
decreased physiological response to repeated admin of a drug
72
Untoward effect
side effect proving harmful
73
Types of Drug Reactions
Type I – Anaphylaxis, IgE antibody and antigen complexes stimulating release of histamines Type II – Cytotoxic, IgG antibody and antigen stimulating hemolysis and platelet destruction Type III – Serum Sickness, IgG antibody and antigen complexes producing inflammatory reaction Type IV – Contact dermatitis reaction – topical application stimulates T lymphocyte production causing dermatitis
74
biotransomation
- process by which the drug is chemically converted to a metabolite - liver is the primary site and aim is to "detoxify" the drug
75
agonists
drug that binds to a receptor and causes a response
76
antagonists
drug that binds to a receptor to inhibit a response or block something else from binding to that site
77
Sympathetic (adrenergic)
Parasympathetic (cholinergic)
78
Sympathetic exits from thoracic and lumbar regions of spinal cord
Parasympathetic exits from cranial and sacral portion of spinal cord
79
Sympathetic ganglia are found near spinal column
Parasympathetic ganglia are found near the effector organ
80
Types of Nerve Fibers
Visceral Afferent – Sensory – convey impulses from organs to CNS Visceral Efferent – Motor – convey impulses from CNS to organs Somatic Afferent – Sensory – Convey impulses from head, body wall and extremities to CNS Somatic Efferent – Motor -Convey impulses from CNS to striated muscle
81
preganglionic neuron
located in CNS passes between CNS and ganglia | fibers are autonomic
82
postganglionic neuron
located in the periphery, passes between ganglia and effector organ fibers are sympathetic
83
synapse
junction between 2 neurons
84
acetylcholine (ACH)
neurotransmitter | fibers that release ACH are cholinergic
85
nicotinic
excitatory response
86
muscarinic
can excite or inhibit
87
sympathetic
alpha and beta recptors
88
parapympathetic
nicotinic and muscarinic receptors
89
cholinergic is parasympathomimetic (mimic parasysmpathic)
cholinergic blocking is parasympatholytic
90
adrenergic is sympathomimetic
adrenergic blocking is sympatholytic
91
Respiration
exchange of oxygen and carbon dioxide between an organism and the environment
92
External Respiration
transfer of oxygen and carbon dioxide between inspired air and capillaries
93
Internal Respiration
Transfer of oxygen and carbon dioxide between peripheral blood capillaries and tissue cells
94
Pressure gradient (required for gas flow into lungs) produced by differences in
Atmospheric pressure Intrapulmonic pressure Intrapleural (intrathoracic pressure)
95
Inspiration and Expiration Based on
Muscles of respiration Compliance Work of breathing Pulmonary surfactant – lipoproteins reduce surface tension allowing alveoli to stay open Airway resistance Structural Changes in lungs or thorax
96
gass pressures
PaO2 - partial pressure of arterial O2, normal 80-100mmHg PO2 - partial pressure of venous O2 PaCO2 - partial pressure arterial CO2, normal 35-45mmHg PCO2 - partial pressure of venous CO2
97
Oxy-Hemoglobin Dissociation Curve
Offloading of O2 based on need, in exercising tissues percentage of saturation of hemoglobin can decrease to 25%, results in release of 75% of transported O2 Partial pressure can maintain for a while but will then drop off quick
98
`BOHR Effect
High CO2 equals drop in pH and decrease of O2 affinity for Hgb Low CO2 equal rise in pH and increase in O2 affinity for Hgb
99
6 P’s of RSI
- Preparation - Preoxygenation - Pretreatment - Paralysis with induction - Placement of tube - Postintubation management
100
Phernic nerve
responsible for moving the diaphragm
101
right upper quadrant
``` liver gallbladder pylorus duodenum pancreas head R adrenal glad top of R kidney colon- ascending and transverse ```
102
left upper quadrant
``` left lobe of liver spleen stomach body of pancreas left adrenal glad portion of left kidney transverse and descending colon ```
103
right lower
``` lower pole of kidney appendix ascending colon bladder ovary uterus ```
104
left lower
``` lower pole of kidney sigmoid colon descending colon bladder ovary uterus ```
105
cranial nerves
``` 1-Olfactory 7-Facial 2-Optic 8-Acoustic 3-Oculomotor 9-Glossopharyngeal 4-Trachlear 10-Vagus 5-Trigeminal 11-Spinal accessory 6-Abducens 12-Hypoglossal ```
106
cranial nerve 1
olfactory- sensor nerve
107
cranial nerve 2
optic- sensory nerve
108
cranial nerve 3
oculomotor- motor nerve
109
cranial nerve 4
trachlear- motor nerve
110
cranial nerve 5
trigeminal- both
111
cranial nerve 6
abducens- motor
112
cranial nerve 7
facial- both
113
cranial nerve 8
acoustic- sensory
114
cranial nerve 9
glossopharyngeal- both
115
cranial nerve 10
vagus- both
116
cranial nerve 11
spinal- motor
117
cranial nerve 12
hypoglossal- motor
118
percussion sounds
``` loudest to quietest tympany hyperresonance resonance dullnes flatness ```