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Bioscience Emily Clipston > Quiz #8 > Flashcards

Quiz #8 Flashcards

1
Q

5 mechanisms of oral agents

A
  1. increase tissue sensitivity to insulin and inhibit hepatic glucose production
  2. increase insulin secretion by the pancreas
  3. inhibit digestion and absorption of starches in the small intestine
  4. increase levels of the incretin hormone with resultant increases in pantreatic insulin production, suppression of glucagon production, and inhibition of hepatic glucose production
    (stimulate release even before even before glucose levels go up)
  5. decrease renal absorption of glucose
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2
Q

Hemoglobin A1c

A

normal= 3.9-5.5%

target for tmt of type II: less than 7%

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3
Q

TZDs

A

examples: the “glitazones” pio- and rosi-

binds to and activates receptors which act as transcription factors

enhance insulin sensitivity, inhibit hepatic glucose production

.5-1%: not that effective, used as an add on

issues with weight gain, edema, increased risk of CV events (just in rosi-)

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4
Q

Biguanides

A

metformin

enhance insulin sensitivity, inhibit hepatic glucose production

1-2%

weight neutral, GI Upset/discomfort

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5
Q

Sulfonylureas

A

glyburide, glipizide

stimulate insulin secretion by the pancreas

1-2%

weight gain, hypoglycemia
works well but is likely to lower BG too much, BG will go down regardless of where it starts/how much you eat

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6
Q

meglitinides

A

repaglinide
nateglinide

stim insulin secretion by the pancreas

1-2%

weight gain, hypoglycemia, same as sulfonyureas

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7
Q

alpha-glucosidase inhibitors

A

acarbose
miglitol

inhibit digestion and absorption of starched in the small intestine

.5-1%

GI upset, bloating, flatulence, weight issue independet of this

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8
Q

DPP4 inhibitors

A

-gliptins

inc active levels of incretin
inc in pancreatic insulin
production and supression of glucagon
production of hepatic glucose production

.5-2%

nausea/vomiting (early)
pancreatic cancer?
pancreatitis?

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9
Q

gliflozins (SGLT2 inhibitors)

A

-gliflozins

inhibits renal reabsorption of glucose

.77-1.16%

lowers BP
weight loss
inc UTI risk
elevated LDL
bone mineral density

*where glucose goes, water will follow. inc water volume in urine, lowers BP, loss of bone mineral density

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10
Q

incretin hormone

A

made by your gut in anticipation of increase in BG, signals insulin to inc, glucagon to decrease

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11
Q

injectable drugs

A

insulin

exenatide

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12
Q

insulin as a drug

A

manages type 1
long acting insulin: keeps glucose levels constant and low
combined with short acting injections before meals

best solution of type 1: pump

multiple types with range of onset and duration of action

afrazza: can be inhaled

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13
Q

exenatide

A

made of saliva of helomonsters (they eat once per month)

injection within 60 minutes prior to breakfast and dinner

synthetic version of exendin-4 and a GLP-1 agonist

stimulated insulin production, slows gastric emptying, regulates beta cell proliferation

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14
Q

SSRIs

A

cause hyper and hypoglycemia

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15
Q

things that cause hypoglycemia

A

SSRIs

fluoroquinolones

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16
Q

things that cause hyperglycemia

A 
glucocorticoids
SSRIs
SNRIs
tricyclic antidepressants
antipsychotics
protease inhibitors
glucosamine
diuretics
beta blockers
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17
Q

optimal first line drug

A

metformin

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18
Q

pts with type 2 require

A

more than one drug for glucose control

insulin in addition to oral medications

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19
Q

most likely to cause hypoglycemia

A

sulfonylureas

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20
Q

insulin causes

A

hypoglycemia

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21
Q

hemostasis

A

property of circulation whereby blood is maintained as a fluid within the vessels

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22
Q

four systems of hemostasis

A

vascular
platelets (primary hemostasis)
coagulation (secondary hemostasis)
fibrinolysis

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23
Q

vasoconstriction

A

narrowing of the vessel to minimize blood flow
mediated by serotonin and thromboxane A2

synthsized and secreted by platelets

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24
Q

vasodilation

A

widening of the vessels, inc blood flow
mediated by prostacyclin PG I2,
synthesized and secreted by mostly endothelium

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25
hemostatic plug
1. vascular injury 2. platelets adhere to exposed subendothelial tissue 3. adhesion activates platelets that signal other platelets to region 4. platelets then stick to one another - aggregation 5. plug formation 6. fibrin formation 7. clot retraction (fibrinolysis)
26
secondary hemostasis
coagulation cascade
27
coagulation factors
fibrinogen - factor I
28
coagulation cascade | intrinsic system
intrinsic system: PTT surface contact: exposure of damaged tissue blood vessel damaged, exposed tissue requires calcium and phospholipid
29
extrinsic system
PT/INR vascular injury: releases tissue factor calcium and tissue factor required to enter into common pathway
30
both extinsic and intrinsic factors
lead into common pathway, both occur together in vivo
31
common pathway
activation of factor X to Xa in presence of Ca Xa converts prothrombin (II) to thrombin (IIa) in presence of Va, Ca, and phospholipid thrombin concerts fibrinogin to fibrin - cleaves ends of fibrinogen molecule to form fibrin monomer - ends remaining are very active, allowing fibrin to polymerize spontaneously in a brick like fashion XIIIa stabilized fibrin clot
32
PT
prothrombin time: extrinsic and common pathway
33
aPTT
partial thromboplastin time | intrinsic and common pathway
34
fibrinolysis
break down of fibrin clot activation of plasmin from plasminogen via tPA, uPA, XIIa, HMWK, prekallikrein XIIa from intrinsic pathway, fibrinolysis is activated as coagulation cascade is activated
35
tPA and uPA
in endothelial cells of vessels: vessels cells themselves start breaking down clot tPA: can treat people with
36
excess levels of D-dimer in blood
indication of excess clot and fibrinolysis
37
venous thrombosis
formation of a blood clot within a vessel thromboembolism: thrombosis that then breaks free and travels to another area risk factors: acquired or inherited
38
acquired risk factors
``` age provious thrombosis immobilization surgery trauma oral contraceptives malignancy cigarette smoking ```
39
inherited
- usually present themselves by adulthood - AT III defiency (antithrombin) - protein C deficiency - protein S deficiency - APC resistance: activated protein C, mutation of factor V that makes it resistant
40
heparin
doesnt break down current clots, prevents future ones from forming monitering test: PTT IV only immediately active lasts 4 hours neutralized with protamine adverse effects: hemmorage, HIT, osteoporosis with long term therapy
41
LMWH (low molecular weight heparin)
inhibits Xa only equally effective, less bleeding, more expensive anti Xa used for monitoring routine monitering not done children, pregnant women, morbidly obese, renal disease may be monitered response more predictable: weight adjusted dosing
42
unfractioned heparin
inhibits IIa (thrombin) and Xa - mixture of different sized molecules - enhances effects of antithrombin 1000fold
43
heparin induced thrombocytopenia
1-5% of hospitalized pts exposed to heparin will develop HIT formation of antibodies to heparin and PF4 (platelet factor 4) in alpha granules of platelets platelet count decreases: platelets consumed in clot formation
44
direct thrombin inhibitors
pradaxa: oral, oral, used by patients with afib not due to valve disease major disadvantage is lack of antidote - antidote just introduced (10/15) argatroban: IV, used for patients with HIT
45
Xarelto
Xa inhibitor DVT, PE no test for activity, no antidote, probably not dialyzable
46
Apixaban
Xa inhibitor | non-valve afib
47
warfarin/coumadin
- inhibit vitamin K dependent clotting factors - clinical effect in 3-5 days - factor VII shortest half life - stable effect reached in 2 weekd
48
INR
international normal ratio normal: .7-1.4 typical target for tmt: 2-3
49
primary hemostatic disorders
bleeding disorders related to platelet function easy bruising, mucosal bleeding
50
most common inherited platelet disorder
von willebrand disease: protein that sticks platelets together, carrier protein for factor VIII
51
acquired platelet disorders
caused mostly by DRUGS
52
aspirin
dose related irreversable inhibition of platelet function platelet lifespan is 7-10 days need new platelets to overcome
53
ibuprofin and other NSAIDs
reversible | effect only lasts 24 hours
54
acetominophen
no effect on platelets
55
aggregation blockers
aspirin: blocks cyclooxygenase
56
activation inhibitors
clopidogrel: binds P2Y ADP receptors on platelets
57
fibrinolysis disorder
lots of clotting, activation of lots of factor XII, lots of conversion of plasminogen to plasmin
58
disseminated intravascular coagulation
secondary condition increased generation of thrombin begins with activation og coagulation mechanism overall decrease in fibrinogen
59
activation of fibrinolysis
increased plasmin generation lysis of clots
60
conditions associated with DIC
``` infections obstetric complications malignancies trauma snakebite ``` tmt is usually to slow fibrinolysis

Bioscience Emily Clipston (9 decks)

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