Exam 2 sweep 2 Flashcards

1
Q

Barbituates act as CNS depressants by ————, thus providing an ——— on synaptic transmission.

A

potentiating the activity of the GABA-A receptor

inhibitory influence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

There are three important opioid receptors named: mu (m); kappa (k); and delta (d)
They are all G protein coupled receptors They are widely distributed in the CNS
They activate —-

A

Gai

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Activation of —— leads to an inhibition of adenylate cyclase activity, a diminution in cAMP levels and a reduction in Protein Kinase A activity. The reduction of PKA activity results in a reduction of Ca++ entry from voltage sensitive Ca++ channels.

A

Gi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

opioids inhibit —— release

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Histamine-H1 receptor activity on vascular endothelium increases intracellular Ca++ - two effects of this:

A

endothelium - NO production, vasodilation in smooth muscle

vasoconstriction in capillary endothelium, now leaky.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

COX1 and 2 send ——– down to be made into

A

arachidonic acid

prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The NSAIDS all work by inhibition of ——

A

the COX enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

COX enzymes inhibit ————–

A

Thromboxane A2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Platelet aggregation is mediated in part through the ————- production of thromboxane

A

autocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Eventually, ——— leads to extension of the inflammatory tissue mass to the articular cartilage. This overgrowth is called the pannus.

A

synovitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RF) is the autoantibody (antibody directed against an organism’s own tissues) that was first found in rheumatoid arthritis. It is defined as an antibody against the ——-

A

Fc portion of IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lower dose methotrexate treatment produces

A

immuno-suppressive and anti-inflammatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

leflunomide Inhibits dihydroorotate dehydrogenase, thereby inhibiting ———

A

pyrimidine biosynthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In patients with Rheumatoid Arthritis that is not well- controlled with methotrexate, treatment with ———– is the next option

A

biologicals that disrupt TNFa signaling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

-azine: ——-

A

phenothiazine-like antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Extrapyramidal rxns include

A

parkinsonism

akathisia - restlessness, mild-moderate hyperactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  1. Block transmitter reuptake
A

There are two types of drugs working here. The tricyclic antidepressants (TCAs) are rather non-specific blockers of transmitter reuptake that are generally also muscarinic receptor antagonists. Both of these properties make for significant side effects.
The Selective Serotonin Reuptake Inhibitors (SSRIs) are more specific for serotonergic systems and also have less anti-muscarinic activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Block presynaptic autoreceptors

A

epi/norepi feedback loop in cns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Apomorphine is a

A

dopamine receptor agonist

20
Q

Some anti-convulsants potentiate the effects of GABA to ——-

A

dampen synaptic nerve impulses by hyperpolarization

21
Q

Barbituates

A

Facilitation of Cl- channel opening (GABA A)

22
Q

Blockade of T-type calcium channels

Drugs that block these channels in the thalamus are effective as ——–

A

anti- convulsants

23
Q

GABA B receptors are ———- (coupled to Gai). They hyperpolarize by activating — channels via ——-. They also diminish Ca++ entry into cells.

A

G protein receptors

K

GbGg

24
Q

Barbiturates and Benzodiazepines act by facilitating

A

GABA- mediated Cl- conductance of GABA A receptors

25
Q

Barbiturates increase the ——— of GABA -mediated channel opening

A

duration

26
Q

Benzodiazepines increase the ———- of GABA -mediated channel opening

A

frequency

27
Q

Flumazenil

A

Benzodiazepine Antagonist

1) Manage benzodiazepine overdose.
2) Recovery from benzodiazepine sedation. IV administration can reverse in 1-2 minutes.

28
Q

Th2 cells mediate an inflammatory response in (eosinophilic) asthma leading to ——– They do this by virtue of the ——— they produce

A

eosinophil infiltration of the lung

cytokines

29
Q

PKA-mediated activation of ——– contributes to attenuation of myosin light chain kinase activity

A

K+ channels

Beta 2 stimulation, hyperpolarization from this leads to less calcium.

30
Q

General Adverse Effects of b2 Agonists

A

Muscle tremor:
-stimulation of skeletal b2 receptors
Tachycardia/palpitations:
-Non-specific b1 stimulation (at high doses) -Atrial b2 stimulation
-Reflux tachycardia secondary to vasodilation
CNS (headache, restlessness, nervousness): -Stimulation of b2 receptors

31
Q

Treatment with inhalational corticosteroids are a critical component of the strategy for managing (——–) asthma

A

eosinophilic

32
Q

An important marker of the effectiveness of corticosteroid treatment is the reduction of ——– in the lung of an asthmatic after treatment.

A

eosinophils

33
Q

Glucocorticoids
1. Attenuate ——– trafficking (recruitment of leukocytes to the site of inflammation)
Reduced ability of leukocytes to adhere to ————–
Reduced expression of ——– (endothelial and immune cells)
Reduced expression of pro-inflammatory —— that affect this process

A

leukocyte

vascular endothelium and leave the circulation

adhesion molecules

cytokines

34
Q

Glucocorticoids

Neutrophils: ——– of neutrophil apoptosis? (circulating levels rise), impair ——– to inflammatory site

A

Inhibition

migration

35
Q

Glucocorticoids

Eosinophils: Promote eosinophil ===== (circulating levels fall), impair ======== to inflammatory site, inhibit eosinophil ========

A

apoptosis

migration

degranulation

36
Q

Glucocorticoids

Monocytes/Macrophages: Diminish production of M/M derived ——– and inflammatory ——–, inhibit ——— function

A

eicosinoids

cytokines

phagocytic

37
Q

Glucocorticoids

Mast cells and Basophils: Diminish ——— production and ———

A

cytokine

degranulation

38
Q

Glucocorticoids

Up-regulate —– and neutral —— enzymes that degrade bradykinin (vasodilatory peptide)

A

ACE

endopepidase

39
Q

Gluccorticoids induce transcription of IkB which goes on to

A

blcok transcription by chromatin remodeling

40
Q

Unless asthma is ——— (SABA’s used less than 3 times a week) ICS’s are usually an integral part of the daily treatment regimen

A

exercise-induced or intermittent

41
Q

• Vagal tone (Bronchial tone)

A

—> acetylcholine

42
Q

Use of ——- to treat COPD

First line of defense in maintenance therapy, used alone or in combination with SABA or LABA.

A

anti-cholinergics

43
Q

Treatment with leukotriene modifiers

A

Asthma

  1. Alternative therapy to treat mild persistent asthma. 2. Adjunctive therapy with ICS’s.
  2. Prevention of exercise-induced asthma.

Not for COPD

44
Q

Anterior serous glands (ca. 200-300) ——–

Posterior seromucous glands (100,000) ——–

A

watery non-viscous secretions

Largely responsible for nasal discharge

45
Q

Drug treatments for Allergic Rhinitis Major drug classes

A

H1 receptor antagonists (antihistamines)

a1-adrenergic receptor agonists (decongestants) intranasal corticosteroids