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PCL469 > Term Test 1 > Flashcards

Term Test 1 Flashcards

1
Q

Alendronate and Zoledronate

A

antiresorptive
bisphosphonates
rapid uptake in bone mineral
long term depot

adverse effect: atypical fractures

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2
Q

Denosumab

A

Antiresorptive
monoclonal antibody
rapid onset and reversible
anti rank L

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3
Q

Teriparatide (anabolic PTH)

A

low dose PTH increase osteoblast differentiation
and decrease osteoblast apoptosis

high does increase bone resorption

half life 5 min
excretion renal
USE RESTRICTED to 2 years

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4
Q

Romosozumab

A

block sclerostin to stimulate Wnts (osteoblast formation)

side effect: hypocalcemia, bone pain, increase heart attack and stroke risk

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5
Q

Pramlintide (amylin analogue)

A

TREAT TYPE 2 DIABETES

  1. suppress appetite
  2. slow gastric emptying
  3. inhibit glucagon release
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6
Q

Colesevelam

A

inhibit gluconeogenesis

incretins

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7
Q

Liraglutide

A 
GLP-1 receptor agonist
increase insulin (glucose dependent) will not lead to hypoglycemia
improve beta cells
slow gastric emptying
weight loss
inhibit glucagon release
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8
Q

Dapagliflozin and Canagliflozin

A 
SGLT2 inhibitors
decrease plasma glucose
kidney
decrease heart failure
lower blood pressure
diuretic

will lead to mycotic infection

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9
Q

Function of Aldosterone

A

Retain Na, H2O and Cl
excrete K

Increase blood pressure

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10
Q

11B-HSD2

A

convert cortisol to cortisone (inactive)
present in aldosterone sensitive tissue

glycyrrhetinic acid inhibit 11B-H2D2 which can lead to high cortisol

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11
Q

Addison’s Autoimmune disease

A

aldosterone insufficiency (decrease BP)

symptoms:
hyperpigmentation
salt craving
fatigue
dizziness
nausea and vomiting
weight loss
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12
Q

Dexamethasone

A

long-acting glucocorticoids
injection, oral, topical

treat acute inflammation
treats rheumatoid arthritis

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13
Q

Fludrocortisone

A

Oral
Mineralocorticoids
Treats addisons disease

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14
Q

Cushing’s disease

A

excess glucocorticoids
purple striae
muscle atrophy

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15
Q

Pasireotide

A

somatostatin receptor 5 agonist
inhibit corticotropin (CRH)
inhibit ACTH secretion

less cortisol

treats Cushing’s disease

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16
Q

L-thyroxine

A

T4

treat hypothyroidism

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17
Q

Liothyronine

A

T3
more potent than L-thyroxine
treat hypothyroidism

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18
Q

Graves’ Disease

A 
cause hyperthyroidism
autoimmune stimulation of TSH receptors
bulging eyes
heat intolerance
increase HR BP
GOITER (enlarger thyroid)
higher chance in women than men

treat with Methimazole

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19
Q

Methimazole

A

treat graves disease
treat hyperthyroidism
inhibit thyroid peroxidase

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20
Q

Plan B (Levonorgestrel)

A

inhibit ovulation, fertilization

use within 72 hours

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21
Q

RU486 (Mifepristone)

A

only available in US
terminate pregnancy
progesterone antagonist

Use with misoprostol

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22
Q

Ulipristal

A

progesterone antagonist/partial agonist
delays ovulation
antagonist at endometrium
emergency within 5 days

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23
Q

Premarin

A

long lasting estrogen
use lower dose
Hormone replacement therapy
decrease menopausal symptoms by 90%

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24
Q

Drosperinone

A

used in oral contraceptives
anti-mineralocorticoids activity
increase risk of thromboembolic disease
increase risk of hypertension

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25
Q

Stilbenes

A

estrogen antagonist

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26
Q

Tamoxifen

A 
mixed agonist/antagonist
antagonist in breast cancer
protective in uterus, bone
ENDOXIFEN more potent
CYP2D6 metabolized (poor metabolizers)
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27
Q

Aromatase inhibitors

A

depletes estrogen
adjuvant therapy
5 year use limit

side effect: bone lipids hot flashes

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28
Q

Oral contraceptive formulations

A

Use a combination of estrogen and progesterone

monophasic: all 21 pills containing the same amount of estrogen and progesterone
biphasic: two different amount of estrogen and progesterone
triphasic three different amount

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29
Q

Which 2 enzyme deactivates PGs?

A
  1. Hydroxy prostaglandin dehydrogenase (HPGD1) at C15

2. Carbonyl reductase 1 (CBR1) at C9

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30
Q

4 types of PGE2 receptors

A

EP receptor: 1,3 = Gq

2,4 = Gs

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31
Q

Rheumatoid Arthritis

A

autoimmune disease causing destruction and inflammation of join-associated tissue

pain swelling, redness

1st line of treatment, NSAIDS
2nd line glucocorticoids

32
Q

Mechanistic of action of corticosteroids (dexamethasone)

A

Prevent PLA2 actions
cant produce prostaglandins from arachidonic acid

binds to glucocorticoids receptors
inactivates NF-KB
enable anti inflammatory transcription
inhibit inflammatory cytokines transcription

33
Q

Aspirin (ASA)

A

irreversibly inhibit COX
covalent modification of SER529
blocks AA from entry

34
Q

COX 2 selectivity

A

larger pocket in COX2 allow for selectivity

35
Q

Inhibition of COX

A

inhibit PGE2 and PGI2 formation
alter arteriosclerotic plaque formation
lead to heart attack or stroke

COX2 inhibition can increase BP and hypertension stroke, heart attack and heart failure

36
Q

Infliximab, Adalimumab, Golimumab

A

monoclonal antibody
anti TNF-a
binds to TNF-a instead of receptor
block NF-kB for inflammatory cytokines gene transcription

treats rheumatoid arthritis

37
Q

Paracetamol (Tylenol)

A 
2 distinct pathways
Cox inhibitor
1. acts as reducing agent in peroxidase site of COX
2. conjugates with AA
block PG from synthesizing
38
Q

Alprostadil

A

PGE1
second line treatment for erectile dysfunction
vasodilator and inhibits platelet aggregation
treat infants with congenital heart disease

39
Q

Misoprostol

A

synthetic PGE1
treat peptic ulceration
prevent production of gastric acid

longer half life than Alprostadil (PGE1)

40
Q

Epoprostenol

A 
PGI2
vasodilator
treat pulmonary hypertension
prevents platelet aggregation
extremely short half-life 3-5 min
Iloprost (30min)
Treprostinil (4hrs)
41
Q

Dinoprostone, Dinoprost, Carboprost

A

PGE2, PGF2a, analogue of PGF2a

carboprost have longest half life

treat postpartum hemorrhage
terminate pregnancy (promote uterine contractions)
42
Q

What cause degranulation?

A

The ligation of MULTIVALENT antigen by IgE bound to FCeRI cause clustering which promotes degranulation

43
Q

Actions of mast cell degranulation (histamine)

A

Swelling and mucus production
Increase blood flow and permeability
Increase peristalsis
vasoconstriction

44
Q

2 types of histamine receptors

A

Have a total of 4 subtypes

H1 receptor: Gq/G11 PLC, expression in immune cells (neutrophils, macrophages, dendritic cells)

H2 receptor: Gs, in gastrointestinal cells, antihistamine used in peptic ulcer, GERD

45
Q

H1 Antihistamine (inverse agonist)

A

1st generation: contain alkyl amine

2nd generation: contain piperidine (cyclic amine)

1st generation antihistamine can ligate muscarinic, adrenergic, dopaminergic serotonergic
side effects: drowsiness, tachycardia, dilation of pupils, reduction in mucus production

2nd generation: less able to cross BBB and more selective for H1 receptors.

constitutively active (inverse agonist)
antihistamine stabilize inactive state
46
Q

H2 receptor

A

histamine release by mast cell but can also release by enterochromaffin-like cells (ECL) in the stomach

47
Q

H+ production in stomach

A

Parietal, cells export H+ via H+/K+ ATPase

Histamine increase export of H+ through increase cAMP

H+ are produced by CARBONIC ANHYDRASE

48
Q

Weak base therapy

A

treat hyperacidity

acts by neutralizing stomach acid via donation of basic anions such as OH and CO3

calcium carbonate
magnesium hydroxide

49
Q

H2 receptor antagonist (Cimetidine)

A

decrease gastric secretion
some drugs are inverse agonist

longer acting compared to antacids

less cAMP production less H+ export

50
Q

Proton pump inhibitors (Omeprazole)

A

PRODRUGS (require acid to activate)

block H+/K+ ATPase pump at parietal cells

prevents acid secretion

better than H2 histamine blockers because other factors can produce histamine

conserved benzimidazole sulfoxide

51
Q

Mechanistic of action of PPIs

A

forms covalent adduct to inhibit ability of pump to export protons

prodrug only activates in acidic environment

proton pump mostly restricted to parietal cells so less side effect

52
Q

Adverse effect of using PPIs

A

Reduction in stomach acid

Hypochlorhydria (too high pH)

Polyps can be cancerous

can worsen H. Pylori infection due to increase survival cuz of higher stomach pH

53
Q

How does H. Pylori survives in stomach acid?

A

bacterial UREASE enzyme produce AMMONIA with H2O to quench HCL

can lead to destruction of stomach epithelium and ulceration

54
Q

Detection methods of H. Pylori

A

13C Assay (breath test) check to see if there is 13CO2 in breath

PCR test (stool sample)

55
Q

Inflammatory Bowel Disease (IBD)

A

inflammation of digestive tract

Crohn’s disease

Chronic diarrhea, abdominal pain, fever, weight loss

Ulcerative colitis (restricted to large intestine)

Leukocytes produce inflammatory cytokines by TLR stimulation leads to inflammation

56
Q

Mesalazine

A

first line treatment of IBD

second line treatment: glucocorticoids

57
Q

Fecal microbiota transplantation

A

Transplantation of a healthy donor’s stool to a IBD patient

altering composition of gut microbiota repertoire

58
Q

How to measure lung function?

A

Spirometry
Forced Vital Capacity (FVC)
Forced Expiratory Volume (FEV)

FEV1 = 80%FVC in 1s (normal)
reduced FEV (30% to 60% decrease)
59
Q

4 features of asthma

A

Remodeling
Edema
Immune cells
Bronchospasm (contraction of airways)

60
Q

Atropine

A

non-selective muscarinic M2 M3 antagonist

61
Q

Tiotropium (Spiriva)

A

muscarinic receptor antagonist

binds to M2 briefly but long lasting effect on M3

bronchodilation

62
Q

Ipratropium Bromide

A

Quaternary ammonium derivative: does not cross BBB or circulatory system

USED AS RESCUE MEDICATION

less effective than B2 Adrenergic Agonist

63
Q

Theophylline, Theobromine, caffeine

A

Methylxanthines
low costs
targets CNS kidney, cardiac ,skeletal and smooth muscle

4th line treatment because narrow therapeutic index (TI)

64
Q

Roflumilast

A

PDE-4 Inhibitor

lead to accumulation of cAMP

can increase signalling of B2 Adr Receptors

bronchial relaxation

65
Q

Albuterol, Terbutaline, Salmeterol, Formoterol

A

B2 Adrenergic Agonists

relax smooth muscle in bronchioles
inhibit release of bronco-constricting mediators and vascular leakage

reduce cardiac stimulation

RESCUE MEDICATION

66
Q

B2 agonist MOA

A

Gs leads to increase cAMP
decrease intracellular calcium
inhibit MLCK

vasodilation and muscle relaxation

67
Q

Beclomethasone and Ciclesonide (prodrug)

A

Corticosteroids, anti inflammatory
Most effective in treating chronic and severe asthma

inhibit production of inflammatory cytokines
inhibit eicosanoid synthesis

high does can initiate systemic effects

68
Q

Montelukast

A

Leukotriene Pathway inhibitors

second line maintenance treatment with B2 Adr agonist

block lipoxygenase to synthesize leukotrienes from arachidonic acid

69
Q

Cromolyn and Nedocromil

A

stable yet soluble salts

decrease bronchial reactivity

use prior to exercise or allergen exposure

alter function of delayed Cl- channel inhibit cell activation

Mast cell stabilizers
block degranulation
inhibit release of histamine and leukotrienes

widely prescribed in children

70
Q

Anti-IgE monoclonal antibodies

A

Omalizumab

binds to IgE and block degranulation
reduce bronchial inflammation

expensive

adverse effect: local irritation, rare anaphylaxis

reserved for chronic severe asthma sufferers inadequately controlled by inhaled corticosteroids or long lasting B2 Adr Ag

71
Q

GOLD STANDARD ASTHMA THERAPY

A

inhaled glucocorticoids and Long Acting B2 Agonist

glucocorticoids: reduce production of leukotrienes
beta agonist: cause bronchodilation

Symbicort: Budesonide + Formoterol
Advair: Fluticasone + Salmeterol

72
Q

Biased agonist

A

a drug that selectively activates one pathway while sparing another pathway

B2 agonist only activates classical signalling (relaxation) but does not activate alternative signalling (B-arrestin) desensitization

73
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

Chronic bronchitis

  • inflammation and swelling of the lining of the airways
  • increase production of mucus
  • daily cough with production of sputum for 3 months, two years in a row

Emphysema

  • permanent enlargement of alveoli due to destruction of walls between alveoli
  • decrease elasticity of the lung
  • increase dead air volume
  • destruction of alveolar walls
  • necessary to breath more often

CHRONIC IRREVERSIBLE AND PROGRESSIVE

SYMPTOMS: chronic cough. shortness of breath (dyspnea), frequent respiratory, cyanosis, pulmonary hypertension

74
Q

5 Treatment strategies for COPD

A
  1. quit smoking
  2. bronchodilators and decrease airway inflammation
  3. vaccination: influenza & pneumonia
  4. regular oxygen supplementation
  5. pulmonary rehabilitation
75
Q

Treatment for Acute Bronchitis

A
  1. Acute mucokinetic agents
    - decrease respiratory tract fluid production via atropine
  2. Mukokinetic agents (expectorants)
    - prevent drying out of secretions
    - increase productive cough (clear mucus from tract)
    - Guaifenesin (mucinex)
  3. Mucolytic agents
    -liquefy mucus
    -Acetyl cysteine
    -reduce viscosity of mucus
    -antioxidant
    usually given as aerosols

adverse effect: nausea vomiting stomatitis

76
Q

Antitussive Drugs (drugs that suppress coughing)

A

prevent chronic cough leads to fatigue

Opioid Agents: CODEINE, HYDROCODONE
cough suppression
elevates cough threshold

Non-opioid agents: Dextromethorphan

no analgesic/additive properties
half as potent as codeine
fewer adverse effect

PCL469 (10 decks)

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