final exam Flashcards
1
Q
Approx how many aveoli are in the human lung?
A
450 million
2
Q
When a person INHALES air what is the chemical makeup of Oxygen and CO2?
A
21% oxygen and 0.04% CO2
3
Q
When a person EXHALES air what is the chemical makeup of oxygen and CO2?
A
16% Oxygen and 4% CO2
4
Q
Lung disease affects the lungs ability to do what?
A
move air and exchange gas
5
Q
Name an acute respiratory disease.
A
Pneumonia
6
Q
Why is pneumonia considered acute?
A
It’s usually viral, bacterial, or fungal.
7
Q
Name a few chronic respiratory diseases.
A
Asthma, COPD, and cystic fibrosis
8
Q
Treament of chronic diseases is generally what?
A
prophylactic and not curative
9
Q
How are respiratory drugs administered?
A
Via systemic administration (oral or IV) or inhalation
10
Q
Which chronic respiratory disease is responsible for the most peds hospital visits?
A
Asthma
11
Q
How is asthma characterized?
A
Hyperactivity of airways, asthmatics only need one to two percent of muscarinic agonist to cause a 20% decrease in exhaled air compared to non asthmatics.
12
Q
What are the clinical hallmarks of asthma?
A
coughing
wheezing
SOB
Chest tightness
13
Q
What are the two main goals of asthma treatments?
A
prevent fatal acute attacks and allow normal lifestyle
14
Q
What is the MOA of short term asthma therapies?
A
bronco dilate and relax smooth muscle
15
Q
What is the MOA of long term asthma therapies?
A
control inflammation
16
Q
Name the three steps to pathogenizing asthmatic lungs.
A
- Constriction of the smooth muscle
- swelling of mucosal lining
- generation of abnormally thick mucus.
17
Q
Which step in asthma pathogenesis does acute therapies target?
A
constriction of smooth muscle
18
Q
Which step in asthma pathogenesis does chronic asthma therapies target?
A
mucosal swelling and thick muscus
OVERALL INFLAMMATION
19
Q
Explain the asthma cascade.
A
exposure to trigger
antigens and IgE’s are activated
mediators like leukotrienes and histamines are activated, leading to a late and early response.
20
Q
Explain the late response activation.
A
Leukotrines cause inflammation and bronchial hyperresponsiveness
21
Q
Explain the early response activation.
A
early response causes bronchoconstriction and symptoms
22
Q
How can a patient avoid triggering their asthma cascade?
A
avoiding triggers
23
Q
How can a patient treat their late response?
A
anti-inflammatory therapy
24
Q
How can a patient control their early response?
A
bronchodilator therapy
25
What can I use too block leukotreiens and histamines?
Steroids and anti-IgE antibodies
26
What can I use to block the late response?
steroids and LT synthesis inhibitors
27
What can I use to block the early response?
beta-agonists and muscarinic blockers
28
When it comes to the sympathetic ADRENERGIC receptors, do they dilate or constrict the lungs?
DILATE
29
When it comes to the parasympathetic cholinergic receptors do they dilate or constrict?
constrict
30
Name a nonselective adrenergic agonist.
Epinephrine
31
What are the pros and cons of epinephrine?
inexpensive
does not require a doctors visit
dangerously increases the heart rate
patients self treat asthma for a long time without controlling it
32
Where can the different adrenergic receptors be found?
beta 2: lungs, gi, uterus,skeletal muscle, smooth muscle.
Beta one: Heart
Alpha one: smooth muscle
33
Which receptors do we want agonized only?
beta-two
34
What are the endogenous ligands for adrenergic receptors?
epi and NE
35
Where do inhaled beta agonist act?
muscles of the lung
36
Name a short acting selective broncodilator.
Albuterol
37
Explain albuterol.
selective beta-2 agonist causing bronchial dilation
fast onset with inhaltion lasting 3-4 hrs.
38
Name a long acting selective beta two agonist.
Salmeterol
39
explain salmeterol.
long acting selective beta two agonist
slow onset with inhalation admin approx 20 min with 12hr persistence
40
Why wouldn't I use salmeterol for acute asthma attacks?
because it has a 20 minute onset
41
What do muscarinic antagonists cause upon binding?
dilation
42
Name a muscarinic antagonist and derivative of atropine.
Ipratropium
43
Explain Ipratoropium.
poorly absorbed
inhibits bronchial contraction ad decrease mucous secretion
used for patients who are beta agonist intolerant
combine with albuterol and
44
What does ICS stand for?
inhaled corticosteroids
45
What is the MOA of ICS's?
glucocorticosteroids bind to the glucocorticoid receptor and the receptor-ligand complex goes into the nucleus and inhibits cytokine and chemokine gene transcription and upregulates the anti-inflammatory genes.
46
Name an ICS anti-inflammitory drug for asthma.
Fluticasone
47
Will fluticasone reduce INFLAMMATION and hyperresponsiveness?
YES
48
What is the most effective long term asthma therapy?
Fluticasone
49
Can fluticasone be used for acute attacks?
NO
50
Name an anti-inflammatory LT inhibitor for asthma?
Monetelukast
51
What is the MOA of LT inhibitors?
Leukotrienes signaling involves the inflammitory response in broncoconstriction and invasion of airway walls by immune cells.
52
Explain motelukast.
LT receptor antagonist
chronic oral admin is effective for mild asthma. Good for patients that are intolerant of steroid treatment or unable to inhale.
53
What is the major con of montelukast? Why is it no longer recommended for mild asthma.
Has a black box warning due to the increased risk of serious bahavior and mood changes, specifically suicidal thoughts.
54
Name an anti-inflammatory immunotherapy treatment.
Omalizumab (Xolair)
55
Explain Omalizumab
An IgE monoclonal anitbody that prevents IgE from activiating immune cells. Decreases allergy related hospital visits by 88%!!!!
56
Can Omalizumab be used for patients with a high level for food allergies?
YES
57
Why would Omalizumab be dangerous for people outside of the U.S.?
IgE's are responsible for detecting parasites.
58
Do patients who take Omalizumab have a higher risks of developing malignant cancer?
yes bc the IgE's are turned off and cant recognize the early stages of cancer anymore.
59
What is the umbrella term for a group of inflammitory lung diseases that obstruct airflow?
COPD
60
What is chronic bronchitis?
inflammation of the lining of bronchial tubes
61
What is emphysema?
permenant loss of aveoli
62
What are the characteristic chronoic symptoms of COPD?
wheezing
cough
mucus (sputum)
difficulty breathing
63
What is the 4th leading casue of death in the U.S.?
lower respiratory disease mainly COPD.
64
What is the main cause of developing copd in developed countries?
smoking
65
What is the main reason for developing COPD in underdeveloped counteies?
SMOKE...from cooking on an open fire
66
Does environmental factors play a role in COPD development?
yes
67
Do genetic factors play a role in developing COPD?
A small role less than one percent of cases have the gene for low levels of A1AT and SERPINA1
68
How can we treat intermittent or mild copd with beta two agonist or antimuscarinics?
Short acting beta two and antimuscarinic: albuterol and ipratropium
69
How can we treat persistent copd with beta two agonist or antimuscarinics?
long acting beta two and antimuscarinic: Salmeterol and tiotropium
70
How can we treat severe copd with beta two agonist or antimuscarinics?
Long acting beta two agonist, muscarinic antagonist plus an anti-inflammatory: Salmeterol, Tiotropium, and inhaled corticosteroid.
71
What kind of drug is Acetylcysteine?
mucolytic drug
72
Acetylcysteine MOA?
Breaks the disulfide bonds in mucosal proteins
73
What is CTFR?
Cystic Fibrosis Transmembrane Conductance regulator.
74
A mutation in CTFR leads to what condition?
Cystic fibrosis
75
Is cystic fibrosis rare?
no its very common
76
What type of gene is CTFR?
Autosomal recessive
77
What is the job of wt-CTFR?
Transport Cl- ions out of the secretory epithelia
78
What does cAMP do to wt- CTFR?
Regulate on the apical side
79
What happens when the mutated CTFR is disrupting the salt / water balance of secretory epithelia?
abnormal mucus production in the lungs casuing airway clogging, decreased gas exchange
80
What is the main problem with increased thick mucus production?
increased inflammation and infection in the lungs along with pancreatic and liver disease
81
What is the most common allele for patients with cystic fibrosis?
90% have the type 2 allele
82
Explain the type three and type two allele for mutated CTFR?
Type three: has no function, the receptor is placed correctly but isnt working.
Type two: the receptor has no traffic, meaning it isnt placed on the cell membrane let alone working.
83
Name a type one CTFR potentiator.
Ivacaftor
84
Explain Ivacaftor.
first in class oral agent
used for trafficked but non functional channels (type Three)
8x more function of the G55D1 channel
85
What is the problem with Ivacaftor?
treats 4-5% of cases due to most CF patients having a type two allele and not type three allele. Ivacaftor cost 300,000 dollars a year.
86
Name the triple drug therapy that combines CTFR potentiator with CTFR corrector?
Trikafta
87
What are the three components making it a triple drug?
Elexacaftor for trafficking and correcting
Tezacaftor for trafficking and correcting
Ivacaftor for increased function and potentiation
88
Does Trikafta work well with CF type two patients?
absolutely
89
What is the downside of Trikafta?
312,000 dollars a year
90
What kind of drug is Dornase alfa?
mucolytic drug
91
Dornase alpha MOA?
Degrades the DNA buildup caused by leukocyte degredation.
92
Why is surfactant important?
it decreases surface tension allowing the small aveoli to expand during inhalation and prevents collapse during exhalation.
93
What is RDS?
Respiratory Distress Syndrom in premature infants resulting in lack of lung surfactant.
94
How can I help with RDS?
Preemies need to be above 35 weeks of gestation to receive the Surfactant replacement therapy called Colfosceril
95
Are estrogen and progesteron considered steroid hormones?
yes
96
Which molecule synthesizes estogen andprogesteron in the gonads?
cholesterol
97
Are steroid hormones only a positive modulation for certain genes?
no they can be negative or positive modulators
98
Which steroid hormones plays a role in both males and females during pubertal changes?
Estrogen
99
estrogen oral contraceptives are usually used for?
reproductive function and tissue maintenance
100
Hormone replacement therapy is usually used for?
loss of estrogen during menopause
101
How does estogen impact females during puberty?
via secondary sexual characteristics
102
How does estogen impact males during puberty?
mainly epiphyseal closure and body molding
103
What are some of the tissue maintenance that estrogen does?
sensitive tissue integrity
maintain bone mass
positive impact of lipid metabolism
104
What role does the hypothalamus have during the human menstrual cycle?
releases gonadotropin-releasing hormone aka GnRH
105
What does GnRH do?
activates the pituitary to release gonadotropins.
106
What are the gonadotropins released by the pituitary?
Luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
107
What do FSH and LH cause?
Activated the ovaries to release estrogen and progesterone
108
Is this whole thing a feedback mechanism?
yes
109
Estrogen provides a negative feedback on the pituitary leading to decreased FSH/LH
YES
110
Day one the hypothalmus releases GnRH which develops a follicle, what is happening to the estrogen?
The estrogen is increasing in levels which tells the PITUITARY to stop producing GnRH.
111
What is going down as estrogen goes up?
FSH/LH from the pituitary
112
When the estrogen levels get really high what does it do to the pituitary?
It works like a positive modulator causing a burst of LH while estrogen drops completely.
113
What is happening to the follicle when estrogen drops and LH is at its peak?
the oocyte ruptures from the follicle this is called ovulation.
114
The empty follicle is now a corpus luteum and it releases a lot of what?
progesterone
115
What does progesterone do to the hypothalamus?
decreases GnRH, LH, and FSH
116
Does the corpus luteium have a long life span?
no
117
The progesterone is capable of maintaining a uterine lining during pregnancy, what happens with no pregnancy occurs?
the corpus luteum degrades and stops producing progesterone leading to a period.
118
In case of a pregnancy what does the blastocyte release to keep the corpus luteum alive?
human chorionic gonadotropin hormone aka hCG
119
What eventually takes over the progesterone production instead of corpus luteum?
the placenta
120
What are the major physiological effects of progesterone?
matures the endometrium
decreases uterine contractions
main determinant of onset menstration
prevents rejection of fetus
121
What are progestins?
synthetic analogs of progesterone
122
Why would a patient want or need progestins?
CONTRACEPTON
dysmenorrhea
endometriosis
prevents 1st trimester misscarriage
123
Explain contraception.
contraception is the prevention of conception: sperm production, sperm motility, ovulation, sperm/ovum encounter.
124
explain interception
interferes with implantation of fertilized ovum
125
explain abortion
interception of a fertilized ovum, dislodging of blastocyte, embryo, or fetus
126
Hormonal contraceptives can come in combinatio form like progesteron + estrogen. What would this combination lead to?
prevents both FSH and LH leading to no maturation of follicle or ovulation.
127
How can progesterone decrease sperm mobility?
causes the cervix to produce a thick mucus
128
Why is the secondary interception of progesterone+ estrogen considered theoretical?
due to its high ability to block ovulation the patient doesnt get to the interception point.
129
What are the two combination hormonal contraceptives PILLS?
Combination pills are 21 days on and 7 days off. The seasonal pill is 84 days on and 7 days off
130
Is the vaginal ring aka Nuva ring a hormal contraceptive?
YES
131
How does the Nuva ring work?
releases progeesteron and estrogen locally to the vagina good for minimizing noncompliance
132
What kind of cancers are you at risk for if taking Oral contraceptives?
breast cancer and cervical cancer due to increased HPV
133
What is post-pill amenorrhea?
up to 10% of patient fail to menstration following cessation of the combination pill.
134
Does the pill have any long term effect on fecundity?
no
135
How does postcoital work?
by releasing a high level of progestin which stops ovulation and prevents sperm and ovum contact.
136
explain IUD and its Sx.
Releases low dose progestogen locally for 3-5 years. Inhibits LH and menstruation. Serious side effect includes increased ectopic pregnancy risk if a pregnancy does escape the IUD.
137
Why is RU 38486 used?
Mifepristone is used as a medical abortion and works as a competitive antagonist for the progesterone receptor.
138
When the uterus stops producing estrogen during menopause what effects can occur?
vasomotor effects and cardiovascular disease
139
Name two HTR treatments?
premarin and estratest
140
How is premarin different from estatest?
premarin is estrogen only while estatest is a combination of estrogen and adrogens.
141
What happpens to androgen levels during menopause?
it decreases by 50%
142
What does estratest do in hormone replacement therapy?
restore estrogen and androgen levels for bone health and vasomotor symptoms
143
What is the main Sx of estratest?
hirsuitism
144
What is the main Sx of estrogen only HRT?
Endometrial cancer
145
How can the increased risk of endometrial cancer be mediated?
via progesterone
146
Which HRT is recomended for woman who have a hysterectomy?
estrogen only HRT
147
Why is menopausal hormone therapy controversal?
due to the increased risk of cancer and several large scale studies have shown that MHT does not decrease incidence of stroke and heart attack.
148
What are the key takeaways from the Womens Health Initiative study?
The age of onset MHT is important.
MHT does increase risk of cancer.
149
How does estrogen inhibit bone loss?
Osteoblasts are balanced by osteoclasts that want to reabsorb bone matter. Estrogen inhibits osteoclasts.
150
Which selective estrogen receptor modulator aka SERMs is used to treat postmenopausal osteoperosis?
Raloxifene
151
Can Raloxifene relieve vasomotor symptoms?
no
152
Why is Tamoxifen used as a SERM?
used to treat breast cancer by inhibiting the proliferation of ER+ and PR+ tumors.
153
What is the Sx's of Tamoxifen?
increased risk of endometrial carcinoma, DVT, and pulmonary embolisms.
154
Which SERM can be used to help women induce ovulation is case of low endogenous estrogen levels?
Clomiphene
155
What is the definition of a hormone?
A type of chemical the goes into the bloodstream and has systemic circulation.
156
Does insulin function as a hormone?
yes
157
Before insulin how long did type one patients live?
two weeks to a year
158
What are the key players in blood glucose levels?
pancrease
159
What are the two parts of pancrease?
exocrine as a duc tand endocrine dump chemical into bloodstream
160
What do pancreatic beta cells release?
insulin
161
What do pancreatic alpha cells release?
glucagon
162
How is insulin an anabolic hormone?
by binding to kinase enzymes
163
How is insulin stimulated?
by increased levels of blood glucose and incretins.
164
What does low blood glucose stimulate?
the release of glucagon
165
Is glucagon catabolic?
yes
166
After eating we have elevated glucose and insulin is released what happens next?
Insulin generates ATP and glycogen synthesis, fat and protein synthesis.
167
When insulin stores glucose it is now called what?
glycogen
168
Glucagon is released during fasting what happens next?
glycogenolysis (stored glycogen into glucose)
ketogenesis (alternative energy source in the brain)
gluconeogenesis ( makes new glucose by degrading proteins in the liver)
169
What makes the beta cell release insulin?
Glucose is not lipid soluble so it has GLUT2 transporter. Glucose generates ATP in the beta cell via glycolysis. The atp closes the potassium channel causing depolarization and calcium influx. The calcium influx causes the vesicles to fuse to the membrane and release insulin.
170
Now we have insulin in the bloodstream and binds to kinase-associated receptor causing what?
GLUT-4 migrates to the membrane in muscle and adipose tissue exclusively.
171
T or F: Type one diabetes is autoimmune and degrades beta cells.
True
172
can type one diabetes be both enviornmental and genetic?
yes
173
Tor F: these patients dont have to have insulin therapy.
false, they must
174
Insulin resistance is called...?
type two DB
175
In type two DB what is happening to the beta cells?
They get burned out and stop releasing as much insulin.
176
DO PATIENTS WITH TYPE TWO DB PRODUCED MORE GLUCOGON?
YES
177
symptoms of hyperglycemia?
extreme thirst
dry skin
frequent urination
blurred vision
nausea
drowsiness
hunger
178
What causes the majority of DB associated problems?
damaged vessels
179
damaged capillaries can lead to?
retinopathy
nephropathy
neuropathy
impaired healing of foot ulcers
180
damage of larger vessels lead to?
angina.MI
Stroke
181
182
