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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
Q

hemostatic plug

A
  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
Q

secondary hemostasis

A

coagulation cascade

27
Q

coagulation factors

A

fibrinogen - factor I

28
Q

coagulation cascade

intrinsic system

A

intrinsic system: PTT
surface contact: exposure of damaged tissue

blood vessel damaged, exposed tissue

requires calcium and phospholipid

29
Q

extrinsic system

A

PT/INR
vascular injury: releases tissue factor
calcium and tissue factor required to enter into common pathway

30
Q

both extinsic and intrinsic factors

A

lead into common pathway, both occur together in vivo

31
Q

common pathway

A

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
Q

PT

A

prothrombin time: extrinsic and common pathway

33
Q

aPTT

A

partial thromboplastin time

intrinsic and common pathway

34
Q

fibrinolysis

A

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
Q

tPA and uPA

A

in endothelial cells of vessels: vessels cells themselves start breaking down clot

tPA: can treat people with

36
Q

excess levels of D-dimer in blood

A

indication of excess clot and fibrinolysis

37
Q

venous thrombosis

A

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
Q

acquired risk factors

A 
age
provious thrombosis
immobilization
surgery
trauma
oral contraceptives
malignancy
cigarette smoking
39
Q

inherited

A
  • 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
Q

heparin

A

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
Q

LMWH (low molecular weight heparin)

A

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
Q

unfractioned heparin

A

inhibits IIa (thrombin) and Xa

  • mixture of different sized molecules
  • enhances effects of antithrombin 1000fold
43
Q

heparin induced thrombocytopenia

A

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
Q

direct thrombin inhibitors

A

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
Q

Xarelto

A

Xa inhibitor
DVT, PE
no test for activity, no antidote, probably not dialyzable

46
Q

Apixaban

A

Xa inhibitor

non-valve afib

47
Q

warfarin/coumadin

A
  • inhibit vitamin K dependent clotting factors
  • clinical effect in 3-5 days
  • factor VII shortest half life
  • stable effect reached in 2 weekd
48
Q

INR

A

international normal ratio
normal: .7-1.4
typical target for tmt: 2-3

49
Q

primary hemostatic disorders

A

bleeding disorders related to platelet function

easy bruising, mucosal bleeding

50
Q

most common inherited platelet disorder

A

von willebrand disease: protein that sticks platelets together, carrier protein for factor VIII

51
Q

acquired platelet disorders

A

caused mostly by DRUGS

52
Q

aspirin

A

dose related irreversable inhibition of platelet function

platelet lifespan is 7-10 days

need new platelets to overcome

53
Q

ibuprofin and other NSAIDs

A

reversible

effect only lasts 24 hours

54
Q

acetominophen

A

no effect on platelets

55
Q

aggregation blockers

A

aspirin: blocks cyclooxygenase

56
Q

activation inhibitors

A

clopidogrel: binds P2Y ADP receptors on platelets

57
Q

fibrinolysis disorder

A

lots of clotting, activation of lots of factor XII, lots of conversion of plasminogen to plasmin

58
Q

disseminated intravascular coagulation

A

secondary condition
increased generation of thrombin

begins with activation og coagulation mechanism

overall decrease in fibrinogen

59
Q

activation of fibrinolysis

A

increased plasmin generation

lysis of clots

60
Q

conditions associated with DIC

A 
infections
obstetric complications
malignancies
trauma
snakebite

tmt is usually to slow fibrinolysis

Bioscience Emily Clipston (9 decks)

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