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Pharmacology > Exam 3 sweep 2 > Flashcards

Exam 3 sweep 2 Flashcards

1
Q

osmotic diuretics are pharmacologically inert substances that are given ——-. They increase the osmolarity of ——

A

intravenously

blood and renal filtrate.

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2
Q

Loop diuretics They are primarily used in medicine to treat –

A

hypertension and edema often due to congestive heart failure or renal insufficiency.

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3
Q

While thiazide* diuretics are more effective in patients with ——-, loop diuretics are more effective in patients with ———

A

normal kidney function

impaired kidney function

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4
Q

Loop diuretics block

A

Sodium potassium CL2 pump - (Linked to kicking K+ out, inhibition by Loop diuretics can create Mg++ and Ca++ imbalances).

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5
Q

Loop diuretics should be excreted into

A

lumen

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6
Q

Thiazide diuretics block

A

sodium chloride symporter

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7
Q

Thiazides secreted by ——, work in ——

A

PCT, DCT

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8
Q

Some thiazides have weak

A

CA-I action

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9
Q

K+ sparing diuretics work on

A

sodium channels in CD, or aldosterone receptor antagonists (binding competitor)

aldosterone receptor competitor- leads to less expression of sodium channel, less Na/K atpase in basolateral membrane

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10
Q

K sparing diuretics

They are used as adjunctive therapy, together with other drugs, in the treatment of

A

hypertension and management of congestive heart failure.

Used with other diuretics that deplete K+

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11
Q

K+ sparing diuretics work to decrease K+

A

secretion***

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12
Q

CA-I specifically inhibits

A

carbonic anhydrase resorption

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13
Q

MAP =

A

CO*TPR (total peripheral resistance)

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14
Q

Blood Pressure Regulatory Systems:
Short term:
Long term:

A

Sympathetic nervous system

Renal system

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15
Q

Baroreflex regulation of blood pressure

  1. Baroreceptors send blood pressure information to the ——-
  2. Sympathetic nerves adjust ———- to regulate vasoconstriction, heart beat, and cardiac output.
A

medula

catacholamines

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16
Q

Renin converts —— to ——

A

angiotensinogen to angiotensin 1

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17
Q

ACE converts —— to ——

A

angiotensin 1 to 2

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18
Q

Angiotensinogen is produced constitutively by the —–

A

liver

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19
Q

Working through angiotensin II receptor(s), angiotensin II mediates direct and indirect

A

vasoconstiction, sodium resorption and water retention, and can produce structural remodeling

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20
Q

Angiotensin II receptor for vasoconstriction

A

AT1

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21
Q

Angiotensin II promotes —– release from the adrenal cortex

A

aldosterone

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22
Q

Sympathoplegic agents

A

Lower blood pressure by reducing peripheral vascular resistance and diminishing cardiac output

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23
Q

Direct vasodilators

Lower blood pressure by relaxing

A

vascular smooth muscle

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24
Q

Diuretics

Lower blood pressure by depleting body of

A

Na+ and reducing blood volume

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25
Q

Block angiotensin II production or activity

Lower blood pressure reducing —— and ——-

A

vascular resistance

blood volume

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26
Q

Sympathoplegic agents

(i) Act on —-
(ii) Reduce release of —— from sympathetic nerve endings
(iii) Block selective ——

A

CNS

epinephrine

adrenoreceptors

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27
Q
  1. Sympathoplegic agents activate
A

alpha 2 in CNS

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28
Q

Sympathoplegic agents Diminish —– outflow, reduced ——

A

central sympathetic

cardiac output

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29
Q

Reserpine
Blocks ——-
Guanethidine
——-

These both are

A

transmitter uptake into vesicles

Replaces transmitter in vesicles

Sympathoplegic agents

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30
Q

Block selective adrenoreceptors

A

block beta 1

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31
Q

If you block beta 1, you diminish

A

CO, renin production

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32
Q

Block selective adrenoreceptors
Block a1 receptors ——>

can cause —–

A

Block vasoconstriction

Na+ and water retention (use diuretic)

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33
Q

Decreased mean arterial blood pressure elicits compensatory sympathetic responses (orthostatic hypotension less likely because of this)
Work best in combination with other

A

drugs that oppose compensatory cardiovascular responses.

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34
Q

——-. Nitric oxide prodrug. Relaxes arterioles and venules. Emergency treatment of hypertension.

A

Sodium nitroprusside

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35
Q

——. Stimulates nitric oxide production by endothelium by unclear mechanism. Acts on arterioles. System resets if used alone.

A

Hydralazine

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36
Q

Block angiotensin II production or activity

A

(i) Angiotensin converting enzyme inhibitors
(ii) Competitive antagonists of angiotensin receptors
(iii) Renin inhibitors
(iv) Aldosterone inhibitors

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37
Q

ACE also degrades ——, which is a ——, so ACE inhibitors also promote —— this way.

A

bradykinin

vasodilator

vasodilation

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38
Q

ACE inhibitors lower blood pressure by decreasing

A

peripheral vascular resistance. Cardiac output and heart rate not affected. Stabilize kidney function (useful in kidney compromized). Useful in treating heart failure.

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39
Q

Heart failure classification

A 
Class 1, 2, 3, 4
1 - no limit
2 - some limit
3- heavy limit
4 - Physical activity = discomfort
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40
Q

Factors that contribute to how well the heart pumps blood

A
  1. Sensitivity of contractile proteins to Ca++ 2. Amount of Ca++ that is released
  2. Amount of Ca++ that is stored in the sarcoplasmic reticulum
  3. Amount of Ca++ that enters the cell upon depolarization
  4. Activity of the Na+/Ca++ Exchanger
  5. Intracellular Na+ concentration and activity of the Na+/K+ ATPase (affects Ca++ via 5.
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41
Q 
Cardiac glycosides (inhibit Na+/K+ ATPase; Ca++) b-adrenergic receptor agonists
Bipyridines
A

Positive inotropes

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42
Q

b adrenergic receptor blockers
Diuretics
Angiotensin converting enzymes inhibitors Angiotensin receptor blockers Aldosterone receptor antagonists Vasodilators

A

Drugs without positive inotropic effects used to treat heart failure

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43
Q

Digoxin is a

A

cardiac glycoside

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44
Q

Digoxin inhibits

A

Na/K ATPase, Ca++

Internal Na+ increases. This slows the Na+/Ca++ exchanger, slowing removal of Ca++

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45
Q

Bypyridines inhibit

A

cAMP degradation

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46
Q

Bipyridines are

A

phosphodiesterase-3 inhibitors

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47
Q

Suggested mechanisms for beta blockers

A

Attenuation of adverse effects of catacholamines
Up-regulation of b receptors (possibly through decreased desensitization) Decreased heart rate
Decreased catacholamine-mediated remodeling

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48
Q

People with heart failure should not

A

lie down in dental chairs for too long (lungs fill).

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49
Q

Drugs used to treat Angina

A

nitrates/nitrites
b-adrenergic receptor blockers
calcium channel blockers
aspirin, antiplatelet, and anticoagulant drugs

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50
Q

All of the organic nitrates/nitrites used to treat angina are prodrugs that spontaneously produce

A

nitric oxide

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51
Q

Nitroglycerin has extensive

A

first pass metabolism

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52
Q

Isosorbide mononitrate avoids

A

hepatic breakdown, lasts longer.

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53
Q

Cardiac depressors

A

beta blocker, calcium blocker

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54
Q

Vasodilators

A

calcium blocker, nitrates

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55
Q

Cardiac impulse pauses for 0.1seconds at

A

AV node

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56
Q

the ——- traveling through the heart creates the EKG

A

sum total of action potentials

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57
Q

P wave reflects depolarization of – node

A

SA

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58
Q

PR interval describes the time it takes for the

A

impulse to travel from sinus node through AV node

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59
Q

QRS complex reflects

A

depolarization of right and left ventricles (lots of muscle mass, big signal).

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60
Q

ST segment.

A

Ventricles depolarized.

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61
Q

J point

A

start of repolarization phase

62
Q

T wave.

A

Repolarization of ventricles

63
Q

U wave repolarization of

A

interventricular septum.

64
Q

QT interval. QTc (if

A

corrected to speed of heart beat)

65
Q

Four main types of arrhythmias

A

extra beats
Supraventricular tachycardias
Ventricular arrhythmias
bradyarrhythmias

66
Q

1o AV block:

A

PR interval lengthened beyond 0.2 seconds

67
Q

2o AV block:

A

Disturbance, Delay, Interruption of atrial impulse conduction through the AV node to the ventricles

Dropped QRS?

68
Q

3o AV block:

A

aka complete heart block. Impulse generated in SA node does not propagate to the ventricles.

69
Q

Atrial fibrillation

A

a bunch of bumps (fibrillations) between QRS

70
Q

If another part of heart starts to produce signals,

A

arrhythmia

71
Q

Classification of antiarrhythmic drugs

Class I

A

block sodium channels in Phase 0

72
Q

Classification of antiarrhythmic drugs

Class II

A

beta adrenoceptor antagonists

Class II affect duration of refractory period (phase 4)

73
Q

Classification of antiarrhythmic drugs

Class III

A

Prolong AP and refractory period (make the AP hill wider between phase 0 and 3)

Potassium channel blocker

74
Q

Classification of antiarrhythmic drugs

Class IV

A

Ca2+ channel antagonists

Increase length of phase 2, decrease phase 4 spontaneous depolarization

75
Q

Class IA: Lengthen duration of —–. Bind more selectively to the —– of the channel. Dissociate from channel with —— kinetics.

A

action potential

open state

intermediate

76
Q

Class IB: ——– duration of action potential. Bind primarily to —– state of the channel. Dissociate from the channel with —— kinetics.

A

Shorten

inactivated

rapid

77
Q

Class IC: —— on duration of action potential. Bind more selectively to the —- of the channel. Dissociate from channel with —- kinetics.

A

Minimal effect

open state

slow

78
Q

Class II useful in treating

A

tachyarrhythmias that are cuased by increased sympathetic activity. Also used for atrial flutter and fibrillation and for AV nodal reentrant tachycardia

79
Q

Class II used for

A

ventricular arrhythmia treatment, supra-ventricular tachycardia

80
Q

Drugs used to treat Dyslipidemia

A
  1. Derivatives of fibric acid
  2. Nicotinic Acid
  3. Bile Acid sequestrants
  4. Inhibitors of HMG CoA Reductase (statins) 5. Cholesterol Absorption inhibitors
81
Q

Fibric Acid derivatives

A

Increase peripheral lipolysis, decrease hepatic triglyceride production
Major net effect: Reduce levels of triglycerides

82
Q

In times of energy demand, mobilization of ——-) is good

A

free fatty acids from triglycerides (lipolysis

83
Q

RXR receptors pair with different partners to alter

A

panels of gene expression

84
Q

Mechanism of action of fibric acid derivatives: agonist of —— receptor

A

PPARa

85
Q

Peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that function as ——- regulating the expression of genes. PPARs play essential roles in the regulation of ———-, development, and ———–.

A

transcription factors

cellular differentiation

carbohydrate, lipid and protein metabolism

86
Q

PPAR

α (alpha) is expressed in

A

liver, kidney, heart, muscle, adipose, and other tissues.

87
Q

Activated PPAR a stimulates ——- in the liver by inducing the expression of genes controlling the ——–

A

fatty acid catabolism

beta- oxidation.

88
Q

Only niacin (nicotinic acid) is suitable to treat ———. Has nothing to do with —– activity and requires doses that are much higher

A

dyslipidemia

vitamin B3

89
Q

Both niacin and niacinamide are suitable as

A

vitamin B3

90
Q

Nicotinic acid molecular mechanisms of action

  1. Agonist for ——–
  2. Inhibitor of ——–
A

GPR 109A (and 109B) receptor

diacylglycerol acyltransferase

91
Q

Diacylglycerol acethyltransferase is a key step in

A

Triglyceride production

92
Q

GPR109A activation inhibits

A

lipolysis and atherogenic activity

93
Q

GPR109A – niacin receptor

G protein receptor (activates Gi), abundant in —–

A

macrophages and adipose tissue

94
Q

Fibric acid derivatives are

A

antilipemics

95
Q

In the liver, cholesterol is converted to bile acid which is excreted to the intestine through the action of —-. By preventing bile acid resorption, the sequestrants increase cholesterol metabolism to bile acid.

A

C7H

96
Q

Liver removes cholesterol by converting it to bile acid

Does more of this if bile acid is prevented from

A

recirculating

97
Q
  1. Inhibitors of HMG CoA Reductase
A

(statins)

98
Q

NPC1L1: a transport protein moving cholesterol from lumen into ——–

This transport protein is blocked by —–

A

enterocyte (and ultimately back into the blood)

ezetimibe

99
Q

Glucagon acts through a G protein coupled receptor (coupled to Gas) to elevate ———- This initiates a kinase cascade leading to liberation of glucose from glycogen, mainly in liver and skeletal muscle.

A

cAMP levels and activate protein kinase A.

100
Q

Major functions of insulin:

A

Increases glycogen synthesis
Stimulate glucose uptake
Decreases gluconeogenesis

101
Q

Three targets of insulin

A

fat, muscle, liver

102
Q

Insulin action normally suppresses breakdown of ———- in adipose cells. Increase in FA’s leads to production of ——— by the liver

A

triglycerides to fatty acids (FA’s) and glycerol

ketone bodies

103
Q

The liver will only oxidize the fatty acid to —— and will convert the —— to ——–. ——- are not good (ketoacidosis) we’ll find out why soon).

A

acetyl CoA

‘ketone’ bodies. Ketone bodies

104
Q

In times of crises, ——- gets diverted from the TCA cycle to gluconeogenesis.

A

oxaloacetate

105
Q

Insulin promotion of fat storage

A

Promotes fatty acid and triglyceride synthesis (liver) Increase fatty acid transport into adipose cells (storage) Increased conversion to triglycerides (adipose) Decreases breakdown of triglycerides (adipose)

106
Q

Hypersomolar hyperglycemic state

often in —- with ——-

A

type 2 often in the setting of physiologic stress

107
Q

Hyperosmolar hyperglycemic state - Treatment is

A

IV saline solution and insulin

108
Q

Drugs affecting this process called ——— Must have functional b cells for the drugs to work

A

secretagogues

109
Q

In general, sulfonylureas have a duration of action of —— hours. Used to generally beat down —- levels.

A

12-24

glucose

110
Q

Meglitinides

A

More rapid onset of action, shorter duration of action than sulfonylureas. Used before meals. Hypoglycemia a concern if drug is taken and person doesn’t eat. Add on drugs.

111
Q

Some subtle mechanistic distinctions between sulfonylureas and meglitinides but both work to promote insulin release by inhibiting

A

K+ efflux from ATP/ADP regulated K+ channels

112
Q

Incretins: ——- and ——– act at the —— receptor on b cells and stimulate insulin release.

A

Glucagon like peptide 1* (GLP-1)

Glucose dependent insulinotropic polypeptide* (GIP)

GLP-1

113
Q

Exenatide is a

A

GLP-1 agonist.

114
Q

—– inhibits GLP- 1 and GIP degradation.

A

Sitagliptin

115
Q

Metformin doesn’t stimulate

A

Insulin release

116
Q

Metformin first line for

A

obese patients - helps lose weight in many

117
Q

Metformin helps increase

A

muscle uptake of glucose

118
Q

Metformin Generally opposes —–
Attenuates —– signaling in response to ——
Attenuates ——-

A

glucagon*

cAMP/PKA

glucagon

hepatic gluconeogenesis

119
Q

Thiazolidinediones
Thiazolidinediones decrease ——-
These drugs are agonists of the —–

A

insulin resistance

peroxisone
proliferator-activated receptor g. (PPAR-g)

120
Q

PPAR-g regulates ——-. The genes activated by PPARg stimulate ——– by fat cells.

A

fatty acid storage and glucose metabolism

lipid uptake and adipogenesis

121
Q

These effects by PPAR-g agonists diminish ——-

A

insulin resistance.

122
Q

Formation of a clot has three steps

A
  1. Vessel constriction
  2. Platelet adhesion, activation and aggregation (platelet plug). 3. Cross-linking of fibrin through the coagulation cascade
123
Q

Platelet activation leads to a conformation change in an —— receptor that allows it to bind ——-, a plasma protein. The platelets aggregate as a result of ——–. This is the platelet plug.

A

integrin

fibrinogen

fibrinogen cross-linking

124
Q

Cross-linking of fibrin through the coagulation cascade
Proteolytic cleavage of fibrinogen (by ——) to form fibrin, followed by chemical cross-linking by —— produces a blood clot. This results from a rather incredible series of well controlled events. Hold on to your seats.

A

thrombin

factor XIII

125
Q

TF (tissue factor) binds

A

Factor VII

126
Q

TF is present in the ——- (extracellular matrix of endothelial cells, subendothelium). It is not exposed to the blood unless the tissue is damaged.

A

basement membrane

127
Q

Once you have some TF-VIIa, it can activate (by proteolytic cleavage) Factors

A

IX and X, but mainly IX.

128
Q

The Xa-Va complex will cleave =——- producing the enzyme that will create a blood clot.

A

prothrombin (II) to thrombin (IIa),

129
Q

Cleavage of fibrinogen by —— exposes binding sites, resulting in the formation of a fibrin mesh.

A

thrombin (Factor IIa)

130
Q

Thrombin will also cleave and activate the clotting factors

A

V, VIII, and XI

131
Q

Finally, thrombin also activates —— an enzyme that cross links the fibrin mesh. Voila, you have a blood clot.

A

Factor XIII,

132
Q

heparin, which enhances the binding of ——- to factor

A

antithrombin

—– II (thrombin) and factor X.

133
Q

Clotting factors inhibited by AT:

A

XII, X, IX, VII, II (thrombin)

134
Q

Protein C, (also known as

A

autoprothrombin IIA and blood coagulation factor XIV

135
Q

Activated protein C (APC) performs these operations primarily by proteolytically inactivating proteins Factor

A

Vaand Factor VIIIa

136
Q

Protein C’s activation is greatly promoted by the presence of

A

thrombomodulin and endothelial protein C receptors (EPCRs).

137
Q
  1. Indirect thrombin inhibitors (act on
A

AT)

Heparin binds to AT, and increases its activity ca* 1000 fold.

138
Q
  1. Direct Thrombin Inhibitors
A

huridan, bivalirudin, Argatroban

139
Q

Argatroban

A

is an anticoagulant that is a small molecule direct thrombin inhibitor.

140
Q

Coumarin anticoagulants

A

warfarin

141
Q

In order for thrombin (and other clotting enzymes) to become catalytically competent, they must undergo a carboxylation reaction. This carboxylation requires the oxidation of vitamin K. Coumarins block the conversion of ——- back to the reduced form. Without this conversion, the body runs out of reduced vitamin K and thrombin will not become enzymically active.

A

oxidized vitamin K

142
Q

Vitamin K aqua mephyton used for

A

warfarin overdose

143
Q

Protamine sulfate used for

A

heparin overdose

144
Q

Thromboxane A2 (TXA2) is a type of —– that is produced by activated platelets and has —— properties: it stimulates activation of new platelets as well as increases platelet aggregation. This is achieved by increasing expression of the glycoprotein complex GPIIb/IIIa on the cell membrane of platelets. The same effect is also achieved by ADP in platelet stimulation,

A

thromboxane

prothrombotic

145
Q

Folic acid and vitamin B12 are necessary for —–

A

DNA synthesis

146
Q

Macrocytic anemia due to failure of

A

RBC maturation

147
Q

Vit B12 needed for

A

myelination of nerves

148
Q

—— is the most common cause of adult B12 deficiency.

A

The loss of ability to absorb vitamin B12

149
Q

Granulocyte-colony stimulating factor (G-CSF or GCSF), also known as colony- stimulating factor 3 (CSF 3), is a ——- that stimulates the bone marrow to produce ——— and release them into the bloodstream.

A

glycoprotein

granulocytes and stem cells

150
Q

Granulocyte-macrophage colony-stimulating factor (GM-CSF), also known as colony stimulating factor 2 (CSF2), is a ——- secreted by ————- that functions as a cytokine.

A

monomeric glycoprotein

macrophages, T cells, mast cells, endothelial cells and fibroblasts

151
Q

G-CSF and GM-CSF are used to treat chemotherapy induced —–

A

neutropenia

152
Q

IL-11 is a multifunctional cytokine first isolated in 1990 from bone marrow- derived stromal cells. It is a key regulator of multiple events in ———–.

A

hematopoiesis

Pharmacology (19 decks)

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