Exam 4 Flashcards

Question

What are the options for artificial tears?

Answer 1

Aqueous supplementing - - Carboxymethylcellulose, hydroxypropylcellulose, polyethylene glycol, propylene glycol Lipid supplementing - - DMPG propylene glycol, Mineral oil

Answer 2

Warm compress may be helpful No stye ointment Possible topical antimicrobial, need to refer

Answer 3

Happens when people wet their contacts with their own saliva

Answer 4

- Rinse the eye for at least 5 minutes - Tap water is fine - Be careful not to rinse the eye with a strong stream of fluid that directly hits the cornea - Patient needs to be referred for emergency care immediately

Answer 5

Nonpharm therapy: warm compress, increase fluid intake, use humidifier Increase tear volume: conisder artificial tears or other lubricants, punctal occlusion Decrease inflammation: 0.05% cyclosporine ophthalmic drugs, LFA-1 antagonist ophthalmic drops (xiidra), short-term ophthalmic glucocorticoids Medication changes: D/c medication, use preservative free ophthalmic drops

Answer 6

Cataracts - Surgical removal of the cataract - Alkylating agents, antiestrogens, corticosteroids, statins Floppy iris syndrome - Preop screening for previous/current use of causative agents - Alpha-1 antagonists, benzodiazepines Optic neuropathy - D/c of causative agent - Amiodarone, ethambutol, linezolid, PDE5 inhibitors Retinopathy - Monitor through regular eye exams. Vision loss is irreversible - Aminoquinolones, antiestrogens, phenothiazines, retinoids

Answer 7

Hemostasis - Stopping the bleeding from a damaged blood vessel. Platelets are activated when collagen is exposed to the blood stream. Platelets are then activated, and through secretion of other molecules and platelet adherence/aggregation, a plug is formed. In secondary hemostasis, a blood clot forms and is then degraded.

Answer 8

Platelets start out really small. Contact with the extracellular maxtrix (collagen) starts the platelet reactions. 1. Adhesion and shape change - GP Ia bind to collagen, GPIb binds to vWF that's bridged to collagen. (normally, the epithelium produces PGI2 [prostacyclin] to keep platelets in their inactivated state) 2. Secretion reaction - Degranulation occurs and platelets granules secrete ADP, thromboxane A2 (TXA2), and serotonin (5-HT). These recruit other platelets. TXA2 and 5HT are also vasoconstrictors. 3. Aggregation - GPIIb/IIIa receptors undergo a shape change to bind to fibrinogen, which crosslinks the platelets and forms a temporary hemostatic plug. As platelets contract and the fibrin stabilizes/achors aggregated platelets, a clot forms.

Answer 9

Collagen - Exposure of collagen to the blood is what triggers the platelet activation. GP Ia/IIa binds to collagen. vWF - Binds to collagen, then binds to GP Ib to activate platelets GP Ia/Ib receptors - GP Ia binds to collagen, GP Ib binds to vWF that's bound to collagen

Answer 10

ADP - Activate and recruit other platelets Thromboxane A2 (TXA2) - Activate and recruit other platelets, also vasoconstrictor Serotonin (5-HT) - Activate and recruit other platelets, also vasoconstrictor The activation of ADP, 5-HT, and TXA2 induces the conformational change of GP IIb/IIIa receptors to bind to fibrinogen, which is the start of platelet aggregation,

Answer 11

Once GP IIb/IIIa receptors are activated, they bind to fibrinogen, which crosslinks the platelets.

Answer 12

MOA: Aspirin irreversibly inhibits platelet COX-1 by acetylation. It blocks the conversion of arachidonic acid to PGG2, which inhibits the formation of TXA2. This interferes with platelet aggregation, prolongs bleeding time, and prevents arterial thrombi formation. - The main pathway for aspirin is to inhibit COX-1, but at higher concentrations, it affects the COX-2 pathway, inhibiting the formation of prostacycline (which keeps platelets inactive/vasodilates) - Indicated for prophylaxis and treatment of arterial thromboembolic disorders (ex. stroke). - Hemostasis returns to normal after 36 hours of last dose of aspirin. Prolongs bleeding time, but not PT time. - Doses above 500mg/kg can be fatal

Answer 13

The activation of both P2Y1 and P2Y12 is needed for platelet activation due to activating GP IIb/IIIa downstream. Prasugrel - Prodrug that requires esterases. It irreversibly binds to the P2Y12 receptor. It's not associated with genetic differences in 2C19. Clopidogrel - Requires metabolism by CYP2C19 to be active. It irreversibly binds to the P2Y12 receptor. It has more genetic variability than prasugrel due to relying in CYP2C19. Ticagrelor - Binds to an allosteric site, so this is a reversible inhibitor. It is not a prodrug and therefore has faster onset. Cangrelor - is IV, but binds to the same site at prasugrel and clopidogrel, but is reversible. Not a prodrug. Fast onset and short 1/2 life. **Loading doses of prasugrel or clopidogrel should only be given after cangrelor is stopped due to cangrelor blocking their active site. Ticagrelor can be given at any time because it's acting on an allosteric site.

Answer 14

Abciximab - inhibit GP IIb/IIIa receptor, which is the receptor for fibrinogen that anchors platelets to each other. This is a chimeric mouse-human monoclonal Ab - Given IV, long duration of action (increases bleeding risk) Eptifibitide - inhibit GP IIb/IIIa receptor, which is the receptor for fibrinogen that anchors platelets to each other. Synthetic peptide that selectively blocks BP IIb/IIIa, reversibly. - From snake venom - Large peptide with short duration of action delivered IV Tirofiban - inhibit GP IIb/IIIa receptor, which is the receptor for fibrinogen that anchors platelets to each other. Nonpeptide tyrosine analogue. - Given IV, 2 hour plasma life - More than 90% inhibition of platelet aggregation after 30 min infusion

Answer 15

Dipyridamole - PDE5 inhibitor. Inhibits the uptake of adenosine, which keeps local adenosine concentrations high, which activates adenosine receptors (A2) on platelets. These are Gs coupled, so this increases cAMP. Along with inhibiting PDE5 degradation of cAMP to AMP, there is a lot more cAMP in the cell. This leads to decreased intracellular calcium and therefore decreases platelet activation and aggregation. Cilostazol - PDE3 inhibitor, increasing cAMP in the cell, decreases Ca2 -> keeps platelet round and inactive.

Answer 16

Extrinsic - Requires a factor (tissue factor) that is not in the blood. - Involves Tissue factor, factor VII, and factor X - Tissue factor is on the surface of cells outside but near blood vessels. VII is usually in the blood, but TF binding to factor VII activates it. Then Factor VIIa binds and cleaves factor X. - TF + VII -> VIIa/TF causes -> X -> Xa Intrinsic - Triggered when collagen is exposed on the wall of the blood vessel - Involves factor VIII, IX, X, XI, XIII - Thrombin causes Factor XI -> XIa causes IX -> IXa -> also VIII -> VIIIa -> then IXa/VIIIa causes X -> Xa

Answer 17

As Xa is formed, Thrombin causes V -> Va; Xa/Va causes prothrombin -> thrombin; thrombin causes fibrinogen -> fibrin and XIII -> XIIIa; XIIa causes fibrin -> cross-linked fibrin Thrombin activation plays major role. Eventually factor XIII is cleaved and then cross-links fibrin to form a stable clot incorporated into platelet plug

Answer 18

Platelet count - - Thrombocytopenia: too low, could be due to bone marrow malfunction or nutritional deficiencies. - Thrombocytosis: too high Prothrombin time (PT/INR) - Mixing plasma with thromboplastin and calcium, then seeing the time to clot. - Normal is 11-14 seconds. - INR = (PT test/ PT normal) ^ISI; normal is 0.8-1.2, and therapeutic INR is ~2-3. More than 3, risk of hemmorhage aPTT - plasma + phospholipid (no TF) + activating agent - Normal is 25-40 seconds. - Used to monitor with heparin therapy Fibrinogen: range from 200-400mg/dL D-dimer: measures the products of fibrin breakdown

Answer 19

Ticlopidine (ADP receptor inhibitor) induces antibodies against ADAMTS13, which decreases the proteolytic activity of ADAMTS13. This means vWF doesn't get cleaved and excessive platelet aggregation occurs. It causes depletion of platelets, hemolytic anemia, renal impairment, neurological symptoms, fever, and can be fatal.

Answer 20

Inhibits protease activated receptor inhibitors. These are normally activated by thrombin to activate platelets downstream. Thrombin binds to the PARs that are coupled to GPCRs. The PAR1 receptors are cleaves on the platelet surface and then downstream, the platelet is activated. Vorapaxar inhibits this. - Half life is 3-4 days, so it lasts a few days after d/c - Reversible, used prophylactically

Answer 21

Increase coagulation: - Thrombin: activates factor V and VIII, enhances platelet activation - Platelet activation increases the activation of factor VII, factor X, and cleavage of prothrombin Decrease coagulation: - Antithrombin: Neutralizes procoagulant serine proteases like thrombin, Xa, and IXa. - Protein C system: Activated by thrombin binding to thrombomodulin. The activated protein C complex (APC) forms a complex with protein S to inactivate factors Va and VIIIa. - Factor Xa: activates tissue factor pathway inhibitor to block upstream activation of factor VII.