Pharm Test 2

Front 1

What are the ways hemostasis is controlled?

Back 1

1. Vascular contraction
2. Platelet adhesion, activation, aggregation
3. Fibrin formation/reinforcement of the platelet plug

Front 2

What prompts smooth m. contraction in vessels?

Back 2

Exposure to plasma

Front 3

What is thromboxane A2 released by?

Back 3

Platelets

Front 4

What is the role of serotonin in hemostasis?

Back 4

It mediates vasospasm

Front 5

What does the loss of NO do?

Back 5

Causes vasospasm

Front 6

What normally inhibits clotting?

Back 6

Prostacyclin

Front 7

What endogenous chemicals inhibit the clotting cascade?

Back 7

-Heparin sulfate
-Antithrombin
-Protein C&S
-Tissue factor pathway inhibitor

Front 8

Prostacyclin (PGI2)

Back 8

-Metabolite of arachidonic acid
-Synthesized by endothelial cells
-Inhibits platelet aggregation and secretion

Front 9

What is the role of nitric oxide?

Back 9

-It is a vasodilator
-It also inhibits platelet activity

Front 10

What makes NO?

Back 10

Nitric oxide synthase

Front 11

What component of blood is antithrombin?

Back 11

Plasma protein

Front 12

What is antithrombin job?

Back 12

Inhibits activated clotting factors

Front 13

What synthesizes endogenous heparin?

Back 13

Endothelial cells

Front 14

What is heparin's job?

Back 14

Accelerates the activity of antithrombin

Front 15

What do Protein C&S do when they form activated protein C?

Back 15

It inhibits clotting by degrading factors 5a and 8a

Front 16

What activates Protein C&S?

Back 16

Thrombin in the presence of thrombomodulin on endothelial cells

Front 17

Where in the plasma is TFPI found?

Back 17

In the lipoprotein fraction

Front 18

What is the job of TFPI?

Back 18

Binds and inhibits factor 10a

Front 19

What are the steps to platelet adhesion and plug formation?

Back 19

1. Platelets bind to exposed collagen
2. Plates are activated, releasing thromboxane A2 and ADP
3. Platelets bind via fibrinogen and GPIIb/IIIa

Front 20

What are the steps to forming thrombin?

Back 20

VII→VIIa→X→Xa→Prothrombin→
Thrombin

Front 21

What is the aPTT used for?

Back 21

To monitor HEPARIN levels via the intrinsic pathway

Front 22

What is the PT used for?

Back 22

It is a measure of the extrinsic pathway and it used to monitor WARFARIN

Front 23

What are the steps to fibrinolysis?

Back 23

Plasminogen→Plasmin→Fibrin→
Degradation of fibrin clot

Front 24

What turns off tPA?

Back 24

Plasminogen activator inhibitor

Front 25

Warfarin (Coumadin)

Back 25

-Indications: prevents emboli, DVT, thromboembolism
-MOA: Vit K inhibitor; decreases synthesis of 2, 7, 9, 10
-Adverse rxns: bleeding, hyperthyroidism, teratogenic,

Front 26

ASA

Back 26

-Indications: emboli, MI protection
-MOA: inhibits platelet aggregation by inhibits thromboxane A2
-Adverse effects: bleeding, CI a surgery, allergy

Front 27

Clopidogrel (Plavix)

Back 27

-Indications: MI, ASA allergy
-MOA: inhibits platelet aggregation via antagonising ADP receptor; no effect on prostaglandins-less GI effect
-Adverse effects: bleeding

Front 28

Abciximab (ReoPro)

Back 28

-Indications: AMI, unstable angina, angioplasty, atherectomy, stent placement, PCI
-MOA: inhibits platelet aggregation by binding to fibrinogen and vWF
-Adverse effects: bleeding, thrombocytopenia, cost

Front 29

Heparin

Back 29

-Indications: venous thromboemboli, adjunct in STEMI/NSTEMI
-MOA: enhances action of antithrombin III
-Adverse effects: osteoporosis, allergic rxns, decrease in platelets, bleeding; CI in: hemophilia, thrombocytopenia, purpura, HTN, ICH, infective endocarditis, active TB, ulcers, threatened abortion, visceral carcinoma, hepatic/renal dz (advanced), sx, LP

Front 30

Protamine Sulfate

Back 30

-Indications: heparin antagonist
-MOA: binds to heparin
-Adverse effects: w/o heparin, can act as an anticoagulant; hypotension (histamine release), pulmonary HTN, allergic rxns

Front 31

When is Lovenox indicated?

Back 31

In pregnancy as a safe alternative. It is lmw heparin.

Front 32

Lepirudin (Refludan)

Back 32

-Indications: heparin-induced thrombocytopenia
-MOA: specific, direct inhibitor of thrombin
-Adverse effects:

Front 33

tPA

Back 33

-Indications: thrombolytic
-MOA: converts plasminogen to plasmin; active against fibrin-bound plasminogen, making clot-selective at high doses
-Adverse effects: cost

Front 34

Streptokinase (Streptase)

Back 34

-Indications: thrombolytic
-MOA: forms complex with proactivator-activates plasminogen
-Adverse effects: allergic rxns, not fibrin specific (systemic fibrinolysis); most effective at first dose

Front 35

Aminocaproic acid (Amicar)

Back 35

-Indications: bleeding, hyperfibrinolysis, porphylaxis against re-bleeding in ICH; hemophilia adjunct
-MOA: completely inhibits plasminogen formation; inhibits fibrinolytic activity and reverses action of fibrinolytic drugs
-Adverse effects: toxic w/tranexamic acid (causes intravascular thrombosis); hypotension, myopathy, GI discomfort, nasal stuffiness

Front 36

How and when is histamine released?

Back 36

It is released by mast cells in response to stimulation by allergens.

Front 37

What receptors does histamine act upon?

Back 37

H1, H2, H3, H4

Front 38

Where are H1 receptors found?

Back 38

-Smooth muscle
-Brain
-Endothelium

Front 39

What signaling mechanism does H1 use?

Back 39

IP3-DAG (Gq)

Front 40

Where are H2 receptors found?

Back 40

-GI
-Cardiac muscle
-Mast cells
-Brain

Front 41

How do H2 receptors signal?

Back 41

cAMP (Gs)

Front 42

Where are H3 receptors found?

Back 42

Presynaptic

Front 43

Where are H4 receptors found?

Back 43

Immune cells

Front 44

How do H3/H4 receptors signal?

Back 44

Gi

Front 45

What is histamine's effect on the nervous system?

Back 45

-Uticaria
-Via H1

Front 46

What is the triple response?

Back 46

-Stimulation of these cell types that cause flare/wheal
1. Sense nerve endings (H1): px/uticaria
2. Microvascular SM (H1/H2): redness (flushing)
3. Capillary endothelium (H1): edema

Front 47

What are histamines effects on the CV system?

Back 47

-Arteriodilatory (H1/H2): direct (H2); indirect (H1) via NO; causes hypotension, flush, HA, warmth
-Increased HR (H2): direct and indirect (reflex tachycardia), direct increase in contractility
-Edema (H1): separation of post-capillary endothelial cells; uticaria/hives

Front 48

What are histamine's effects upon bronchiolar smooth muscle?

Back 48

-Bronchoconstriction (H1)
-Diagnostic use for asthma is only pharmacological use of exogenous histamine

Front 49

What are histamine's effects upon the GI tract?

Back 49

-Contraction of smooth muscle (H1)
-Increased acid secretion (H2)
-Decreased acid secretion (H3)

Front 50

Diphenhydramine (Benadryl)

Back 50

-Indications: allergic rxns, motion sickness, sleep aid, local anesthetic
-MOA: non-selective H1 antagonist; sig anticholinergic activity
-Adverse effects: sedation, anti-muscarinic effects, excitation/convulsions in peds, postural hypotension (a1 inhibition)

Front 51

Fexofenadine (Allegra)

Back 51

-Indications: allergic rxns
-MOA: metabolite of Seldane; antagonizes peripheral H1 receptors
-Adverse effects: HA, dyspepsia, cough

Front 52

Loratadine (Claritin)

Back 52

-Indications: allergic rxns
-MOA: selective peripheral H1 antagonist
-Adverse effects:

Front 53

Bradykinin

Back 53

-Vasodilatory peptide
-Dilates aa in kidney, heart, intestine, skeletal muscle, liver
-Receptors: B1/B2; B2 responsible for most effects
-Metabolized by ACE

Front 54

Are B2 receptors inducible?

Back 54

Yes

Front 55

What does serotonin do?

Back 55

In the vasculature, it contricts vessels
-Metabolized by MAO
-Mainly found in enterocromaffin cells in GI tracts; also found in platelets and CNS
-All serotonin receptors are GPCR except for 5HT3 which is Na/K

Front 56

What happens in the two phases of migrane HA?

Back 56

Phase 1: vasoconstriction of intracranial aa leading to ischemia (aura)
Phase 2: vasodilation and pulsation of dural and extracranial vessels

Front 57

Where does the px associated with migraine come from?

Back 57

It is caused by vasodilation/inflammation due to the release of vasoactive peptides like Substance P and Calcitonin gene-related peptide

Front 58

What are the s/sx associated with cluster HA?

Back 58

-Severe unilateral, retro-orbital, burning px
-Sensitivity to movement, light, noise

Front 59

What are the s/sx associated with tension HA?

Back 59

-Mild to moderate B, band-like, non-pulsating px

Front 60

Dihydroergotamine (DHE/Migranal)

Back 60

-Indications: migrane HA
-MOA: constrict dilated aa by stimulating 5HT1 receptors; most effective/specific for acute attacks early on
-Adverse effects: powerful vasoconstrictor; not for use in preggos

Front 61

Sumatriptan (Imitrex)

Back 61

-Indications: migrane HA
-MOA: vasoconstriction via selective stimulation of 5HT1D receptors
-Adverse effects: CI: vascular/heart dz, diabetes, preggos

Front 62

Methysergide (Sansert)

Back 62

-Indications: migraine HA porphylaxis
-MOA: weak vasoconstriction via blockage of 5HT2 receptors

Front 63

What are the effects of NSAIDs?

Back 63

-Fever reduction
-Reduce chronic px
-Platelet inhibition
-Reduce inflammation

Front 64

What is ASA's MOA?

Back 64

Irreversible inhibitor of COX1 & 2

Front 65

What are the adverse effects of ASA?

Back 65

-Increased bleeding, ulcers, GI upset
-Asthma, hypersensitivity, hepatotoxicity, nephrotoxicity
-Urate excretion
-Reye's syndrome

Front 66

What are the s/sx associated with salicylism?

Back 66

-Vomiting, tinnitus, hearing loss, vertigo

Front 67

Levothyroxine

Back 67

-Indications: hypothyroidism
-MOA: synthetic T4
-Adverse effects: hyperthyroidism

Front 68

Methimazole

Back 68

-Indications: hyperthyroidism; Grave's dz
-MOA: decrease synthesis/release of T4
-Adverse effects: goiter; cretinism/goiter in fetus during preg

Front 69

Potassium Iodide

Back 69

-Indications: radiation exposure
-MOA: rapidly decreases synthesis/release of T4/T3
-Adverse effects:

Front 70

I131

Back 70

-Indications: tx hyperthyroidism
-MOA: destroys gland through radiation exposure
-Adverse effects:thyroid storm, hypothyroidism,

Front 71

Propranolol

Back 71

-Indications: symptomatic tx of hyperthyroidism
-MOA: non-selective B-blocker; blocks sympathetic activation of tissues; can also reduce peripheral conversion of T4 to T3
-Adverse effects: fatigue, dizziness, hypotension

Front 72

What do the glucocorticoids do?

Back 72

Indications: adrenal insuff, immunosuppresion, RA, asthma, dermatologic conditions, CA

Front 73

What are the adverse effects of corticoid use?

Back 73

-Increased risk of infections; can mask s/sx
-Hyperglycemia: can unmask diabetes
-Osteoporosis: this is the most limiting side effect; 30-50%
-CNS: restlessness, insomnia, psychotic rxns, euphoria, increased appetite
-Iatrogenic adrenal insufficiency: depression of the HPA due to abrupt cessation

Front 74

What are the clinical guidelines to corticosteriod tx?

Back 74

-Give sufficient amt to control problem
-Use smallest effective dose for shortest time
-Locally is better
-Alternate days
-Slowly taper withdrawal

Front 75

What are the sex steroids MOA?

Back 75

-They inhibit ovulation by stopping the LH surge
-Changes cervical mucosa to block sperm
-Changes endometrium to decrease implantation

Front 76

What are the side effects of sex steroids?

Back 76

-Wt gain, nausea, edema
-Migraine, CV probs, depression

Front 77

Tamoxifen

Back 77

-Indications: breast CA
-MOA: selective estrogen receptor modulator
-Adverse effects:

Front 78

Anastrozole

Back 78

-Indications: breast CA refractory to tamoxifen or in post-menopausal women
-MOA: aromatase inhibitor; inhibits synthesis of estrogen
-Adverse effects: can have menopausal side effects

Front 79

Finasteride

Back 79

-Indications: BPH; male pattern baldness
-MOA: converts testosterone into dihydrotestosterone; inhibts 5a-reductase
-Adverse effects:

Front 80

Lispro

Back 80

Rapid acting insulin

Front 81

Regular insulin

Back 81

Short acting insulin

Front 82

NPH

Back 82

Intermediate acting insulin

Front 83

Lantus

Back 83

Long acting insulin

Front 84

What are the adverse effects associated with insulin use?

Back 84

-Hypoglycemia
-Lipodystrophy
-Hypersensitivity

Front 85

What is insulin's MOA?

Back 85

-It promotes entry of glucose into skeletal muscle, heart muscle, and fat tissue.
-It inhibits catabolic processes such as the breakdown of glycogen, fat, and protein; promotes an anabolic state

Front 86

Glyburide

Back 86

-Indications: NIDDM; hyperglycemia; sulfonylureas
-MOA: stimulates insulin release; reduces [glucagon], increases insulin's effects
-Adverse effects: hypoglycemia

Front 87

Metformin

Back 87

-Indications: hyperglycemia in NIDDM; biguanides
-MOA: decreases hepatic glucose output to decrease [glucose]; reduces LDL/VLDL
-Adverse effects: diarrhea, nausea, lactic acidosis

Front 88

Acarbose

Back 88

-Indications: hyperglycemia; a-glucosidase inhibitor
-MOA: decreases absorption of starch and disaccharides from intestine
-Adverse effects: cramping, diarrhea, farts

Front 89

Pioglitazone

Back 89

-Indications: hyperglycemia; thiazolidindiones
-MOA: lowers insulin resistance; decreases triglycerides over time; causes insulin effects post-receptor; increases glucose transporter synthesis in adipose
-Adverse effects: edema, CV risk

Front 90

Exenatide (Byetta)

Back 90

-Indications: hyperglycemia; NIDDM
-MOA: increases insulin; slows gastric empyting; inhibits glucagon
-Adverse effects:

Front 91

Sitagliptin

Back 91

-Indications: hyperglycemia; NIDDM
-MOA: DPP-IV inhibitor; increases the effects of endogenous incretin hormones
-Adverse effects:

Front 92

Omeprazole (Prilosec)

Back 92

-Indications: GERD
-MOA: proton pump inhibitor; binds irreversibly to pumps and inactivates it
-Adverse effects: may increase risk of osteoporosis

Front 93

H2 receptors anatagonists (Famotidine, Cimetidine)

Back 93

-Indications: GERD
-MOA: competes with histamine at H2 receptors on parietal gastric cells; inhibits basal and meal stimulated acid secretion
-Adverse effects: Cimetidine inhibits CYP450s of other drugs; anti-androgenic

Front 94

Gastric antacids (Tums, MOM)

Back 94

-Indications: symptomatic relief of upset stomach, heartburn
-MOA: neutralize acids to form salts and water;
-Adverse effects: Mg salts increase motility and cause diarrhea; Al salts relax smooth muscle and cause constipation

Front 95

Misoprostol

Back 95

-Indications: protects stomach from long term NSAID use
-MOA: inhibits acid secretion and stimulates bicarb/mucus release by stimulating prostaglandin receptors; prostaglandin E1 analog
-Adverse effects: can stimulate uterine contractions; CI in preggos

Front 96

Glucocorticoids

Back 96

-Indications: induces remission of IBD
-MOA: inhibits production of inflammatory cytokines and other proteins involved in inflammation
-Adverse effects: PR admin

Front 97

Aminossalicytes (mesalamine, asacol)

Back 97

-Indications: induces/maintains remission of IBD; not as effective w/Crohn's
-MOA: mech unk
-Adverse effects: multiple, GI related

Front 98

Immunosuppresive agents (Infliximab, Remicade)

Back 98

-Indications: maintain remission in IBD
-MOA: AB for TNFa
-Adverse effects:

Front 99

Metoclopramide (Reglan)

Back 99

-Indications: antiemetic; increases gastric motility;
-MOA: DA D2 receptor antagonist (prevents smooth muscle relaxation); increases ACh release (increases smooth muscle toneof upper GI); decreases reflux from stomach into esophagus
-Adverse effects:

Front 100

Psyllium

Back 100

-Indications: laxative
-MOA: bulk forming; stimulates peristalsis
-Adverse effects: constipation

Front 101

Docusate

Back 101

-Indications: constipation
-MOA: incorporates water into poop
-Adverse effects:

Front 102

Magnesium hydroxide

Back 102

-Indications: laxative
-MOA: attract/retain water; stimulates peristalsis
-Adverse effects: not for constipation; CI: suspected blockage

Front 103

Biscodyl

Back 103

-Indications: laxative
-MOA: act directly upon intestinal mucosa to enhance secretion and peristalsis
-Adverse effects: cramps, loss of electrolytes

Front 104

Lubiprostone

Back 104

-Indications: constipation, idiopathic
-MOA: prostaglandin E1 derivative; increases gastric motility; activates Cl C2 channels
-Adverse effects:

Front 105

Bismuth subsalicylate

Back 105

-Indications: diarrhea, infectious
-MOA: inhibits intestinal secretions
-Adverse effects:

Front 106

Loperamide, Diphenoxylate plus atropine

Back 106

-Indications: diarrhea
-MOA: stim constriction of circular and relaxation of longitudinal muscles
-Adverse effects: CNS effects, resp depression

Front 107

How does cholera cause diarrhea?

Back 107

Cholera toxin stimulates cAMP levels; this in turn results in increased secretion of water/electrolytes by intestinal mucosa

Front 108

Ondasteron

Back 108

-Indications: antiemetic
-MOA: blocks 5HT3 receptors in GI, solitary tract, and CTZ. Prevents stimulation of peripheral and central CTZ
-Adverse effects:

Front 109

How does metoclopramide and phenothiazies work to prevent emesis?

Back 109

By blocking D2 receptors in the solitary tract nucleus and CTZ.

Front 110

Aprepitant

Back 110

-Indications: antiemetic
-MOA: blocks neurokinin 1 receptors in the solitary tract
-Adverse effects:

Front 111

Scopolamine

Back 111

-Indications: antiemetic
-MOA: blocks M1 receptors in vestibular tracts, the solitary tract, and CTZ
-Adverse effects:

Front 112

Meclizine, Antivert

Back 112

-Indications: antiemetics
-MOA: blocks H1 receptors in the vestibular tract, the solitary nucleus, and CTZ
-Adverse effects:

Front 113

Dronabinol

Back 113

-Indications: antiemetic
-MOA: THC
-Adverse effects:

Front 114

Prednisone

Back 114

-Indications: severe asthma
-MOA: decrease airway inflammation; long term tx
-Adverse effects: osteoporosis, immunosuppression, hyperglycemia

Front 115

Fluticasone

Back 115

-Indications: mod to severe asthma; use w/ B2 agonists
-MOA: decrease airway inflammation; corticosteroid
-Adverse effects:

Front 116

Cromolyn (Intal)

Back 116

-Indications: asthma
-MOA: stabilizes plasma membrane (by inhibiting Ca2+ influx) of mast cells preventing degranulation; inhibits release of histamine, leukotrienes; does not affect bronchodilation or IgE binding
-Adverse effects: bad taste

Front 117

Omalizumab

Back 117

-Indications: chronic/severe asthma
-MOA: inhibits binding of IgE to mast cells; stabilizes mast cell membrane
-Adverse effects: allergic rxn

Front 118

What are leukotrienes?

Back 118

They are archidonic acid metabolites that are made by mast cells. They activate leukotriene type 1 receptors in smooth muscle, endothelial cells, and WBCs. Stim leads to inflammation and bronchoconstriction

Front 119

Zileuton

Back 119

-Indications: asthma
-MOA: inhibits 5' lipoxygenase; anti-leukotriene
-Adverse effects: hepatotoxicity

Front 120

Monotelukast

Back 120

-Indications: allergic asthma
-MOA: leukotriene antagonist
-Adverse effects: few side effects; CI in severe asthma

Front 121

Salmeterol

Back 121

-Indications: long-term tx of asthma
-MOA: B2 agonist; increase cAMP
-Adverse effects: tachycardia

Front 122

Theophylline

Back 122

-Indications: COPD, asthma
-MOA: inhibits breakdown of cAMP; antagonizes adenosine receptors in smooth muscles, causing relaxation, inhibits Ca2+; stim catecholamine release; CNS stimulant
-Adverse effects: CNS effects, GI effects, cardiac effects; [plasma] relevant

Front 123

Tiotropium, Ipratropium

Back 123

-Indications: COPD, asthma; viral/allergic rhinitis
-MOA: bronchodilation by blocking vagus stim; inhibits ACh
-Adverse effects:

Front 124

Menthol

Back 124

-Indications: antitussive
-MOA: anesthetizes afferent nerves in upper airway
-Adverse effects:

Front 125

Dextromethorphan, et al

Back 125

-Indications: antitussive
-MOA: inhibit cough center in the dorsal medulla w/o euphoria/analgesia
-Adverse effects:

Front 126

Guaifenesin

Back 126

-Indications: expectorant
-MOA: reduces surface tension and adhesiveness of lung secretion; facilitates expectoration
-Adverse effects: