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Pharm: Block 3 Flashcards

1
Q

Fasting Plasma Glucose reflects the hepatic glucose output level, what are the ranges?

A

Norm= <100mg
Impaired fasting= 100-125mg
Diabetes= >126mg

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2
Q

Oral Glucose Tolerance Test is a 2hr post-load test reflecting glucose uptake by peripheral tissues (insulin sensitivity), what are the ranges?

A 
Normal= <140mg
impaired= 140-199mg
Diabetes= >200mg
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3
Q

What are the reference ranges for HbA1C?

A

Normal= <5%
Inc risk= 5.7-6.4%
Diabetes= >6.5%

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4
Q

When HbA1C is lower, _____ is the major contributor to overall hyperglycemia

A

Post-prandial glucose-

  • HbA1C <7.3, post-prandial contributes 69.7%
  • HbA1c >10.2, post-prandial contributes 30.5%
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5
Q

When HbA1C is higher, _____ is the major contributor to overall hyperglycemia

A

Fasting plasma glucose-

  • HbA1C <7.3, fasting glucose contributes 30.3%
  • HbA1C >10.2, fasting glucose contributes 69.5%
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6
Q

Diabetes is #_ leading cause of death from it’s complications which can include ?

A

Macrovascular- heart attack, stroke, PVD
Micro- retin/neuro/nephropathy
Acute- Hypoglycemia, DKA, HHS

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7
Q

Diabetic BP control reduces CV risk by _% and microvascular complications by __%
What is the general reduction assumption?

A

CVD- 33-50%
Micro- 33%
For ever 10mm SBP decrease, diabetic risks decreases by 12%
Reducing DBP from 90 to 80mm dec CVD risk by 50%

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8
Q

Glucose control in diabetes is generalized by every _% dec of A1C = ?

A

1% dec = 40% reduced risk in microvascular complications

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9
Q

When is gestational diabetes tested for?

What are the S/Sx?

A

24-28th week

Glucosuria, Polydispia, Polyuria, UTI infections, blurred vision

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10
Q

What happens in untreated gestational diabetes?

A

Large birth weight
Premature delivery
C-section
Inc risk of infant death

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11
Q

What are the gestational blood sugar goals?

A

Preprandial= <95mg
1hr postprandial= <140mg
2hr postprandial= <120mg

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12
Q

What is the therapy for pregnant women with risk factors using standard diagnostic criteria?

A

Screen for undiagnosed T2DM at first prenatal visit

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13
Q

What is the therapy for pregnant women without known prior diabetes?

A

24-28wks, 75g 2h OGTT

Diagnostic cut points

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14
Q

What is the therapy for women with gestational diabetes?

A

6-12wks, OGTT and non-pregnancy criteria

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15
Q

What is the therapy for women w/ Hx of GDM and pre-diabetes?

A

Lifestyle interventions

Metformin for diabetes prevention

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16
Q

What medication is preferred for gestational diabetes?

A

Insulin- reqs frequent titration and referral to specialists

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17
Q

All insulins are pregnancy Category __ with the exception of ____

A

Category B

Except Glargine and Glulisine- Category C

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18
Q

What types of insulin are most commonly used?

A

Regular
Rapid acting
NPH insulin

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19
Q

Characteristics of non-insulin medicaiton use in GDM?

A

Lack long term safety data and cross placenta
Glyburide
Metformin
Both Category B

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20
Q

Define Hypoglycemia

A

Blood glucose below 70mg and 10x more common in T1DM

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21
Q

What are the Sympathetic Sx of Hypoglycemia

A

Tachy, tremor, sweating, anxiety, hunger

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22
Q

What are the Neuroglycopenic Sx of hypoglycemia

A

Confusion, weak, drowsy, dizzy, blurred vision, difficulty speaking and concentration

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23
Q

Level 1 Hypoglycemic stage and treatment

A

Glucose 60-70
Adrenergic Sx
15-15-15- 15g CHO, wait 15m, treat if Sx persist

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24
Q

Level 2 Hypoglycemia stage and treatment

A

Glucose 41-59
Adrenergic and neuroglycopenic Sx
30-15-30: 30gm CHO, wait 15m, treat again

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25
Q

Level 3 Hypoglycemia stage and treatment

A

Glucose <40
Adrenergic and neuroglycopenic Sx with possible seizure/coma
Glucagon 1mg subQ or 50mls D50W IV (only give to unconscious/responsive/confused PT)

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26
Q

Characteristics of HHS

A

Hyperosmolar Hyperglycemic State- inc glucose in urine impairing concentration ability/process causing more H2O loss than Na (HyperOsmo) despite insulin presence (doesn’t red blood sugar levels)

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27
Q

When/who does HHS usually occur in?

A

Older T2DM PTs

Younger PTs with prolonged hyperglycemia and dehydration or renal insufficiency

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28
Q

What are the hallmark lab results for DKA?

A 
Hyperglycemia
Acidosis
Anion gap
Large ketonemia/ketonuria
Rapid onset in PTs that can be alert, stupor or comatose
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29
Q

What are the hallmark lab results of HHS?

A 
Similar to DKA except:
Higher plasma glucose >600
Elevated serum osmolality
pH > 7.30
Little/no ketonuria/nemia
Onset- days to weeks
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30
Q

MOA of Insulin

A

T1DM replacement/T2DM supplementation to facilitate glucose uptake in peripheral tissue while dec glucose/glucagon secretions to overall dec circulating glucose

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31
Q

What are the 3 adverse effects of Insulin?

A

Hypglycemia
Weight gain
Lipodystrophy- hypertrophy/atrophy at injection site

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32
Q

What factors affect insulin pharmacokinetics?

A

Route: IV>IM>SC
Absorption: Abd fat>Post arm>Lat thigh>Sup buttocks; exercise/massage, lower dose/concentrations absorb faster

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33
Q

How is insulin clearance altered?

A

RF- 60% exogenous cleared

LF- 30-40% exogenous cleared

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34
Q

Bolus insulin are broken into what two subcategories?

A

Rapid- Lispro, Aspart, Glulisine

Short acting- Regular: Humilin, Novolin

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35
Q

Basal insulin are broken into what two subcategories?

A

Intermediate- NPH (Neutral Protamine Hagedorn)

Long acting- Glargine
Detemir

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36
Q

What two insulin subcategories include meds that are insulin analogs?

A

Rapid acting

Long acting

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37
Q

What is the inhaled version of insulin?

A

Afrezza- in T1DM, must be used w/ long lasting insulin

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38
Q

Afrezza is NOT recommended for ?

A

DKA treatment

PTs w/ respiratory complications- smoke/quit in last 6mon, COPD, asthma or cancer

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39
Q

What type of diabetic PT uses U-500 Insulin?

A

PTs w/ severe insulin resistance used BID 30m prior to meals in U-500 or tuberculin U-100 syringes

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40
Q

What is the NPH/Regular insulin combo made up of?

A

Humulin 70/30

Novolin 70/30

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41
Q

What is the NPH/Rapid acting insulin combo?

A

Humalog Mix 75/25 (neutral protamine lispro/lispro)

Humalog Mix 50/50 (neutral protamine lispro/lispro)

Novolog Mix 70/30 (aspartate protamine suspension/aspart)

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42
Q

Characteristics of Rapid-Acting Insulins

A 
Aspart, Lispro, Glulisine, Afrezza
Onset <0.5hrs
Peak .5-2hrs
Duration 3-6hrs
Admin 15m prior to meal, less risk of post-prandial hypoglycemia than regular insulin
Approved for CSII
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43
Q

Characteristics of Short Acting Insulin 100

A

Onset .5h
Peak 2-5hrs
Duration 4-12hrs
DOC for IV, approved for CSII, must inject 30m prior to meal

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44
Q

Characteristics of Short Acting Insulin 500

A

Onset less than .5h
Peak 4-8h
Duration 13-24hrs
Inject 30m prior to meal in highly insulin resistant PT, caution w/ accidental OD

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45
Q

Characteristics of the Intermediate Acting Insulin?

A 
Onset 1-4hr
Peak 3-12hr
Duration 16-24hr
Greater risk of nocturnal hypoglycemia
Cloudy appearance combined with protamine
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46
Q

Characteristics of the Long Acting Insulin

A 
Onset 1-2hr
Peak None
Duration 7.6 > 24
Less nocturnal hypoglycemia
Daily for T2DM
BID for T1DM
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47
Q

How are syringes selected for insulin administration?

A

30u/0.3ml
50u/0.5ml
100u/1ml
U500 or Tuberculin syringe for U-500

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48
Q

Insulin syringes measures _

Tuberculin syringes measures _

A

Units

mls

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49
Q

T1DM is AKA ?

A

Insulin dependent DM

Juvenile onset DM

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50
Q

T1DM insulin physiologic regimens use insulin __

A

Analogs

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51
Q

What are the two insulin regimens for T1DM?

A

1-2 basal injections per day
w/ prandial injections
CSII therapy

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52
Q

How are T1DM insulin regiments measured out?

A

Based on weight, 0.5u/kg

Inc dose for obese, illness, sedentery or puberty

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53
Q

How much basal/bolus insulin for T1DM?

A

Basal- 40-50% of body’s daily insulin requirement

Bolus- 50-60%; 10-20% of daily requirement before/at each meal from carb intake determination

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54
Q

What is the insulin : carb ratio?

A 
Regular insulin: 450/TDD=CHO coverage dose
Rapid-Acting: 500/TDD=CHO coverage dose
1u/15gm of CHO
Obese= 1:5
Lean/insulin sensitive= 1:20
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55
Q

What is the purpose of corrective/supplemental doses?

A

Given when blood sugar is unexpectedly high and to bring pre-meal/bed glucose levels into range

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56
Q

What insulin management method provides estimate of PTs sensitivity to insulin?

A

Corrective/Supplemental Dose

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57
Q

Define the Rule of 1500 and 1800

A

Correction bolus set up after basal dose has been tested for accuracy
Regular: 1500/TDD
Rapid-Acting: 1800/TDD

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58
Q

What is the Correction Dose equation

A

CD= current BG - desired BG / correction factor

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59
Q

If pre-breakfast/lunch/supper/bedtime glucose is high/low, adjust ?

A

B- evening basal
L- next morning bolus
S- next day morning basal and/or pre-lunch bolus
Bed- adjust supper rapid/reg insulin dose next day

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60
Q

If 2hr post prandial glucose is high/low, adjust ?

A

Pre-meal rapid/reg insulin dose next day

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61
Q

If 0300 blood glucose is high/low, adjust ?

A

Evening basal insulin dose next day

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62
Q

Define Dawn Phenomenon

How is it fixed?

A

Insufficient evening basal insulin leads to AM hyperglycemia secondary normal waking process
0200-0300 SMBG shows normal/elevated blood sugar
Inc evening basal insulin

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63
Q

Define Somogyi Effect

How is it fixed?

A

Too much evening basal insulin leads to hypoglycemia in middle of night
0200-0300 blood sugar shows dec levels
Body adjusts w/ inc glycogenolysis and gluconeogenesis
Dec evening basal insulin

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64
Q

T2DM is AKA ?

A

Non-Insulin Dependent DM
Adult Onset DM
Decline B-Cell function and secretion
Characterized by insulin resistance and lack of secretion w/ lower secretion over time

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65
Q

What are the risk factors for T2DM?

A 
Inactivity
FamHx w/ 1* relative
Ethnicity
Women delivered +9lb baby
GDM Dx
PCOS
HTN
CVD Hx
Dyslipidemia
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66
Q

What are the objective glucose tests for T2DM risk factors?

A

HbA1C > 5.7%
Impaired tolerance
Impaired fasting

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67
Q

Insulin resistance is related to ___ and is proportional to _____

A

Weight

Amount of visceral adipose tissue

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68
Q

Define VAT

A

Visceral Adipose Tissue- fat cells located within abdominal cavity

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69
Q

How does VAT affect insulin resistance?

A 
Higher rate of lypolysis, inc FAs that are released into portal circulation, drain to liver and stimulate VLDL and dec insulin sensitivity in peripheral tissues
Produce cytokines (TNF-a, IL-6) which contribute to resistance
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70
Q

What is adiponectin’s role in insulin resistance?

A

Improves sensitivity but decreases with inc obesity

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71
Q

PTs w/ ____ _have 5-6x inc risk of T2DM

A 
Metabolic Syndromes- have 3 of 5 components- 
abd obesity: m40", w35"
HDL: m<40mg, w<50mg
Triglycerides: >150mg
BP: SBP>130 DBP >85 
Fasting glucose: >100mg
Any above "or on Rx"
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72
Q

What are the 4 criteria for Dx T2DM?

A

A1C > 6.5%
FPG > 126mg
2hr PG >200mg during 75g OGTT
Random PG >200mg

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73
Q

What confirmatory/validation tests are done on T2DM samples prior to final Dx?

A

Unless Dx is clear, same test is repeated using new blood sample for confirmation
2 discordant results= result above cut off needs to be repeated

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74
Q

Glycemic targets for Non-pregnant adults w/ diabetes?

A

A1C <7%
Pre-prandial PG 80-130
Post-prandial PG <180

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75
Q

T2DM targets are based off of what factors?

A 
Age/life expectancy
Comorbid conditions
Diabetes duration
Hypoglycemia status
Individual PT considerations
Known CVD
Adv microvascular issues
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76
Q

Most stringent T2DM target is ?

Less stringent T2DM target is ?

A

<6.5%

<8%

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77
Q

What are the goals of Medical Nutrition Therapy?

A

Eating pattern to improve overall health
Glycemic BP and lipid goals
Body weight goals
Delay/prevent DM complications

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78
Q

How much exercise should T2DM get?

A

+150min of aerobics across 3 days/wk with no more than 2 consecutive days w/out exercise
Resistance training x 2days/wk

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79
Q

What part of the VS needs to be assessed at every T2DM Dr visit?

A

BP
+130/80= anti-HTN treatment w/ goal of <130/80
PTs w/ BP >120/80= lifestyle mods

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80
Q

What is the lipid management criteria for T2DM?

A

All ages w/ ASCVD/10yr risk >20%= high intensity statin
+40y/o and no ASCVD= moderate statin
ASCVD and LDL is >70 on max statin= additional LDL lowering therapy

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81
Q

Can T2DM get influenza, PPSV23, HepB vaccines?

A

Influenza- >6mon old
PPSV- >2yrs old
HepB- unvaccinated adults with diabetes aged 19-59 and consider in unvaccinated adults >60yrs
Do not coadminister, minimum interval between doses- 8wks

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82
Q

MOA of Biguanides

A

Dec glucose production and enhances glucose uptake while slowing intestinal absorption of sugars

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83
Q 
What med is the first line drug of choice for T2DM?
What are two additional benefits this drug class offeres?
A

Biguanides

Impoved CV outcome

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84
Q

Two clinical uses of Biguanides?

A

T2DM

PCOS

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85
Q

How are Biguanides dosed?

What type of PT should these meds be used with caution?

A

Only labeled oral agent for use in children 10-16y/o

Geriatrics (renal dysf), don’t titrate to max dose

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86
Q

What are the adverse effects of Biguanides

A

GI upset/diarrhea
Metallic taste and dec B12 absorption
Hypoglycemia (low)
Lactic acidosis (rare)

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87
Q

What is a contraindication of using Biguanides?

A

ScR >1.4 female / 1.5 in males

Risk of lactic acidosis

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88
Q

What is are the drug interactions of Biguanides?

A

Stop Metformin if radiology iodinated contrasts are given
Resume after 2-3 days and normal renal function is proven
Cimetidine- competes for renal secretion w/ metformin and can inc metformin levels

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89
Q

What needs to be monitored for in PTs taking Biguanides?

A

Situations that increase lactic acid and decrease tissue perfusion
Liver Dz
Chronic alcohol

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90
Q

MOA of Sulfonylureas

A

Binds to sulfonylurea receptor on B-cells to stimulate insulin secretion in T2DM

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91
Q

What are the cautions for Sulfonylureas?

Why does this class need monitoring?

A

Hepatic/Renal Dysfunction

Reduced efficacy over time, 5-7% fail/year

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92
Q

Adverse effects of Sulfonylureas

A 
Hypoglycemia- esp if used with Glyburide or Chlorpropamide
Weight gain
Skin rash
GI upset/cholestasis
HypoNa
Allergic reaction w/ sulfonylurea
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93
Q

What are the drug interactions of Sulfonylureas?

A

Protein binding displacement- esp 1st gen
Hepatic metabolism 2C9 and 2C19
Avoid Chlopropamide in PTs w renal dysfunction or elderly
GLP-1 agonist/DPP-4 inhibitor- dec dose by 50% to reduce hypoglycemia risk

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94
Q

What are the drug names of the first generation Sulfonylureas?

A

Chlopropramide- highest hypoglycemic risk
Tolazamide
Tolbutamide- shortest acting

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95
Q

What are the names of the 2nd generations Sufonylurea drugs?

A

Glipizide/XL
Glyburide/micronized
Glimepiride

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96
Q

Which 2nd Gen Sulfonyurea is safe for pregnancy?

Which one is safer for PTs with renal dysfunction?

A

Glyburide

Glimepiride

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97
Q

What is the MOA of Meglitinides

A

Stimulate insulin secretion from B-cells of pancreas like Sulfonyureas but from different sites (reqs presence of glucose to stimulate insulin secretion)

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98
Q

What are the adverse effects of Meglitinides?

A 
Dizzy
URI/Flu-like Sx
Slight risk of inc serum uric acid
Hypglycemia, less than Sulfos
Weight neutral
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99
Q

Which Meglitinides have better efficacy at lowering A1C?

A

Repaglinide > Nateglinide

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100
Q

When is the use of Meglitinides preferred/inidcated?

A

2 or 3 in line w/ Metformin in place of Sulfos in PTs with irregular eating schedules or who develop late hypoglycemia while on Sulfos

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101
Q

Meglitinides can be used in conjunction with what other meds?

A

Metformin, TZD, DPP-4 inhibs, or GLP-1 Agonists but,

Use w/ Sulfonylureas won’t improve glycemic parameters

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102
Q

When are Meglitinides considered for use as a monotherapy?

A

One of the last monotherapy considerations in PTs w/ A1C less than 7.5%
Use w/ Caution

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103
Q

What are the names of the Meglitinides?

A

Nateglinide- 2CP substrate

Repaglinide- 2C8 and 3A4 substrate

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104
Q

What medication can double effects of Repaglinide?

How?

A

Gemfibrozil, inhibition of glucoronidation

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105
Q

MOA of Thiazolidinediones

A

Enhance T2DM insulin sensitivity in muscle/fat by increasing glucose transporter expression through PPAR-y binding

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106
Q

What are the adverse effects of Thiazolidinediones?

A 
Weight gain
Dilution anemia
MI
Inc Fx rate
Hep failure- d/c if LFTs > 3x
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107
Q

When is caution exercised when using TZDs?

A

NYHA Class 1/2 HF, contraindicated in 3 and 4

Bladder cancer

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108
Q

What drug interactions does TZDs have?

A

MI risk if Rosiglitazone is used w/ nitrates

CHF risk 2.5x if used in combo w/ insulin

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109
Q

What needs to be monitored when using TZDs?

A

HbA1C- not seen for 4mon
Livier- draw baseline LFT and secondary if Dz suspicion
CV- Rosigli inc LDL but Pioglit dec TG and improves lipid profile
HF- inc risk w/ Rosiglitazone

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110
Q

Characteristics of GLP-1

A

Glucagon-Like Peptide Agonist
Secreted from L cells and action is glucose dependent= low risk of hypoglycemia
Dec glucagon secretion, slows gastric emptying and inc satiety
Stimulates B cells

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111
Q

Characteristics of GIP

A

Glucose Dependent Insulinotropic Polypeptide
Augments insulin secretion and is secreted by K Cells w/ little effect if glucose is >140
No effect on gastric motility of satiety

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112
Q

What is the MOA of DPP-4 inhibitors

A

Inhibs DPP4 enzyme to prevent GLP-1 and GLP degradation to inc insulin secretion and dec glucagon secretion, no effect on satiety/gastric motility

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113
Q

What are the adverse effects of DPP4-Inhibs

A 
Weight neutral
Pancreatitis risk
Sita/Saxa- inc risk of URI/UTI
Saxa- worsen HF, dec lymphocyte counts
Modifications needed if renal impairment is present and taking Sita/Saxa and Alog.
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114
Q

What are the drug interactions of DPP-4 Inhibitors?

What are the names of the DPP-4 Inhibitors

A

Dec Sulfonylurea by 50% if used in combo

Linagliptin
Alogliptin
Sitagliptin
Saxagliptin

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115
Q

Which DPP-4 use does not require dose adjustment if PT has renal impairment?

A

Linagliptin

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116
Q

What are the adverse effects of GLP-1 agonists

What are the GLP-1 agonists names?

A 
HA, N/Diarrhea
Lira/Dula/Exen- pancreatitis
Thyroid cancer
Renal insufficiency
Dulaglutide, Liraglutide, Exenatide
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117
Q

What are the contraindications of GLP-1 agonists?

A

T1DM

PTs with Hx of medullary thyroid cancer/nodules or elevated calcitonin

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118
Q

What are the interactions of GLP-1s?

A

Delay drug absorptions

Sulfonylurea- dec dose by 50% to dec risk of hypoglycemia

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119
Q

What needs to be monitored in TPs on GLP-1s?

A

Dec BP
Improved lipid profile
Baseline amylase/lipase for suspected pancreatitis
Dysphagia, hoarse and neck mass if suspected Thyroid cancer

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120
Q

MOA of Synthetic Anylin Analogue

A

Suppress inappropriate high postprandial glucagon secretion and increases satiety/slows gastric emptying

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121
Q

When is Synthetic Anylin Analogue used?

A

Adjunct to meal time insulin therapy in T1/2DM

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122
Q

How is Synthetic Amylin Analogue dosing determined

A

SQ prior to major meals +250kcal or +30gm of carbs in abdomen or thigh and at different site than insulin

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123
Q

What are the Synthetic Amylin Analogue adverse effects?

A

Severe Hypoglycemia

N/V/Anorexia

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124
Q

What are the Synthetic Amylin Analogue contraindications?

A

Don’t use w/ gastroparesis or PTs taking motility agents
Peds
Hypoglycemia

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125
Q

What are the Synthetic Amylin Analogue interactions?

A

2x inc hypoglycemia T1DM- dec prandial insulin dose by 50%

May delay drug absorptions

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126
Q

MOA of a-glucosidase inhibitors

A

Inhibit enzymes in small intestine to delay breakdown of sucrose/complex carbs to cause and overall dec in post-prandial blood glucose w/out effecting glucose, lactose and fructose in T2DM

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127
Q

When is a-glucosidase inhibitor use considered good?

A

PTs near target HbA1C levels with near normal FPG levels BUT have high postprandial

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128
Q

How is a-glucosidase inhibitor dosage used?

A

Taken w/ first bite of meal and titrated based on tolerability

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129
Q

What are the adverse effects of a-glucosidase inhibitor use?

A

Weight neutral

GI- gas, abd pain, diarrhea

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130
Q

What are the contraindications of a-glucosidase inhibitor use?

A

PTs w/ short bowel sydrome
IBDz
Cirrhosis

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131
Q

What is a unique characteristic of using Beano with a-glucosidase inhibitors?

A

Dec GI side effects but will decrease efficacy

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132
Q

What are the a-glucosidase inhibitor drug names?

A

Acarbose
Miglitol
Dont use either if SrCr is below 2mg

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133
Q

MOA of Selective Sodium Dependent Glucose CoTransporter 2 Inhibitors

A

Inhibits transporter which reduces reabsorption of filtered glucose and lowers renal threshold of glucose to increase urinary excretion of glucose in T2DM PTs

134
Q

What are extra benefits of using Selective Sodium Dependent Glucose CoTransporter 2 Inhibitors Empagliflozing and Canagliflozin

A

FDA approval for reducing CV risk

135
Q

What are the names of Selective Sodium Dependent Glucose CoTransporter 2 Inhibitors drugs?

A

Canagliflozin
Dapagliflozin
Empagliflozin

136
Q

What are the adverse effects of Selective Sodium Dependent Glucose CoTransporter 2 Inhibitors use?

A 
Genital Fungal infection
UTIs
Inc LDL
Weight loss
Low hypoglycemic risk if monotherapy
Dec BP
137
Q

What are the precautions of Selective Sodium Dependent Glucose CoTransporter 2 Inhibitors use?

A

Cana- inc stroke risk
Dapag- inc bladder cancer risk
Do NOT use if renal dysfunction is present

138
Q

What drug classes can cause an increase of blood glucose?

A

BBs
Diuretics- thiazides, Loop
Niacin

139
Q

What are the 3 phases of thrombus formation?

A

Adhesion
Activation
Aggregation

140
Q

What are the 5 steps of a platelet aggregation pathway and plaque rupture

A

1: homeostasis, NO and PGI2 released
2: homeostasis; NO and PGI2 induce cAMP synthesis, cAMP dec Ca and inhibs GP2b/3a activation
3: rupture; collagen, ADP, TXA2 and thrombogenics exposed, platelets recruited and activated
4: change; thrombogenics inhibit cAMP synthesis, activates the platelet
5: aggregation; platelets crosslink w/ fibrin creating thrombus

141
Q

What mediates platelet adhesion to damaged endothelial sites?

A

Von Willebrand Factor- protein secreted by endothelial cells that circulate in plasma, mediates platelet adhesion at injury site

142
Q

Function of prostaglandin

A

Modulate immune function via lymphocyte and are mediators in vascular phase of inflammation

143
Q

What is the role of PGI2 that’s released from undamaged endothelial cells?

A

Binds to platelets causing cAMP synthesis which inhibits release of granules containing aggregating agents

144
Q

Adhered platelets release what chemical mediators?

A

ADP
TXA2
5HT
Platelet activating factor

145
Q

What are the receptors on the surface of platelets that are activated by mediators?

A

Serotonin- 5HT, cause vessel spasm, inc cytosolic Ca release causing dec blood loss
Thromboxane Synthesis- liberates arachidonic acid from membrane, acid converted to PGG2 by COX to be matabolized into TXA2`

146
Q

Steps of COX pathway

A

Mem phospholipids
Arachidonic acid
Prostaglandin
Sythases- TXA2 and PGI2
TXA2- constriction, platelet aggregation, bronchonstriction
PGI2- vasodilation, platelet anti-aggregation

147
Q

Steps of platelet aggregation

A

TXA2- stims activation and aggregation of platelets and is a potent vasoconstrictor
G2b/3a- receptors for fibrin and aid in platelet activation to regulate platelet-platelet interaction and thrombus formation

148
Q

Define Extrinsic Pathway

A

Tissue Factor pathway
Vit K depedent
Inhib by Warfarin which inhibits hepatic synthesis of clotting factors

149
Q

Define Intrinsic pathway

A

Contact Activation Pathway

Inhibited by heparin

150
Q

What are the Natural Anticoagulants

A

Protein C- destroys 5a and 8a
Protein S- cofactor for Protein C
Anti-Thrombin 3- inactivates 2a, 7a, proteases, especially thrombin)

151
Q

Define Prothrombin Time

A

Screening assay for Extrinsic Pathway

152
Q

Define International Normalized Ratio

A

Prothrombin Time to account for differences in thromboplastin

153
Q

Define Activated Partial Thromboplastin Time

A

APTT- screening test for Intrinsic System and it’s factors

154
Q

Define Hypocoagulability

A

Dysfunction in natural anticoagulants: protein C and S

155
Q

What are the two categories of injectable anti-coagulants

A

Indirect Thrombin Inhib- UFH, LMWH (Enox/Dalt), Fonda

Direct Thrombin Inhib- Biva, Arga

156
Q

What are the categories of oral anti-coagulants

A

Indirect Thrombin Inhibs- Warfarin
Direct Xa inhib- Apix, Riva, Edox
Direct Thrombin Inhib- Diabigatran

157
Q

MOA of Warfarin

A

Inhibs Vit K cofactors to reduce available Vit K needed for clotting factors

158
Q

Clinical use of Warfarin

A

DVT/PE prophylaxis
A-fib heart valves
Secondary prevention after stroke/MI
Protein C/S deficiency

159
Q

If rapid anticoagulation is needed with Warfarin, what can it be combined with?

A

Heparin/LMWH until INR goal is achieved

160
Q

What are the T1/2 of Warfarin components?

A

10: 48-72hrs
2: 60hrs
9: 24hrs
S: 10
7/C: 6hrs

161
Q

What is a normal INR goal?
What is DVT prophylaxis goal?
What is artificial heart valve goal?

A

0.8 - 1.2
2-3
2.5 - 3.5

162
Q

How often is INR monitored when starting Warfarin?

A

Bi-weekly until goal is reached

4-6wks after

163
Q

Adverse reactions of Warfarin

A

Bleed/bruise
Necrosis- related to C or S
Purple Toe Syndrome
Category X

164
Q

How is Warfarin metabolized and what does it interact with?

A

2C9

Displaced by other protein binding drugs w/ higher affinity since it’s 99% protein bound

165
Q

What PT education needs to happen when giving Warfarin

A

Avoid NSAIDs

Consistent diet

166
Q

What are 3 foods with high Vit K levels and what is one with low levels?

A

Kale +500
Spinach +400
Collards +400
Asparagus 48

167
Q

How to manage high INRs with Warfarin PTs

A

Above range but below 4/5: reduce/skip dose
4.5-10: skip 1-2 doses, Vit K not routinely recommended
+10: stop Warfarin and give 2.5-5mg of Vit K regardless of bleeding

168
Q

How much Vit K is given to Warfarin PT neededing emergent surgery?

A

<5mg w/ additional 1-2mg in 24hrs

High bleed risk= 1-2/5mg

169
Q

What to do with Warfarin associated major bleeding?

A

PCC instead of FFP

Vit K 5-10mg by slow IV

170
Q

What are the two types of PCC for use during associated major bleeding

A

Kcentra: prothrombin, Factor 7, 9 and 10, Protein C and S

Profilinine: Vit K dependent clotting factors 2 7 9 10

Use to reverse Fondaparinux

171
Q

What is the Warfarin reversal agent?

A

Phytonadion
Mephyton- PO
Aquamephyton- injection

172
Q

How is Phytonadione administration preferred?

A

PO- more predictable response
If IV- slowly over 30m to watch for adverse reaction
Avoid SubQ and IM

173
Q

What does Heparin/LMWH do to the coagulation cascade?

A

Boosts Antithrombin 3

Inhibits 10a and 2a

174
Q

Characteristics of UFH

A

Macromolecule complex in histamine

Extracted from pig intestine

175
Q

What is the MOA of UFH

A

Binds to Anti-Thrombin 3 and speeds ability to inhibit thrombin

176
Q

What is the clinical use for UFH

A

Prevent expansion and prevent thrombus formation

177
Q

What are the pharmacokinetics of UFH?

A

SubQ or IV only
Not absorbed SubQ
NOT protein bound/secreted in milk/placenta crossing
Acts in minutes

178
Q

What are the adverse reactions of UFH?

A

Bleeding- reverse w/ P.Sulfate
Thrombocytopenia- -150K
(HIT): systemic hypercoag in PTs on UFH x 7 days and 50% dec of platelet count from baseline from heparin Abs
Treat w/ d/c and direct thrombin inhib if anticoag is needed
Osteoporosis
Hyper Ka

179
Q

Contrainidications for using UFH

A 
HIT/Hx of HIT
Allergy
Active bleeds
Purpura
HTN
Surgery- brain, eye, back or LP
180
Q

How much Heparin is in treatment doses?

How much is in prophylaxis?

A

50-70u/kg w/ 12-18u/kg/hr maintenance

SubQ 5Ku Q8-12hrs

181
Q

What needs to be monitored for UFH use?

A 
aPTT
Hgb
Hct
Platelet
Bleeding sings
Pregnancy Class C
182
Q

MOA of LMWH

A

Depolymerized UFH to bind to anti-thrombin 3 and inactivates 10a w/out affecting aPTT time

183
Q

When is LMWH used?

A

Reduce thrombi expansion/formation and can be used w/ aspirin and Warfarin

184
Q

Clinical use of Enoxaparin

A

Prophylaxis DVT and PE
Ischemic issue of unstable angina and Non Q-wave MI
Treat DVT/PE
Treat acute STEMI

185
Q

Clinical use of Dalteparin

A

Prophylaxis for DVT and PE

Treat Sx VTE/reduce recurrence in cancer PTs

186
Q

What LMWH is Class B and preferred use in Pregnancy?

A

Enoxaparin

Dalteparin

187
Q

Pharmacobenefit of using LMWH

A

No PT or aPTT monitoring

Long t1/2, 3-12hrs

188
Q

Adverse effects of LMWH

A

Bleeding
HIT
Not completely reversed by Protamine

189
Q

How is LMWH dosed?

A

Prevention: standard dose
Treatment: weight adjusted in mg or anti-Xa units
Only SubQ on BID schedule

190
Q

What are the advantages of using LMWH over Heparin

A

Less HIT risk
Minimal monitoring
Longer t1/2

191
Q

What is the preferred anticoagulant drug for pregnant women?

192
Q

MOA of Fondaparinux

A

SubQ administration that binds to antithrombin 3 and selectively inhibits 10a

193
Q

When is Fondaparinux used in clinic?

A

Prophylaxis of DVT for PTs having knee/hip replacement and abd surgery
DVT/PE treatment when used w/ Warfarin Sodium

194
Q

Adverse effects of Fondaparinux

A

Bleeding, don’t use if platelets are below 100K

Less likely to cause HIT, not FA approved for HIT

195
Q

MOA of Protamine Sulfate

A

Protein from fish sperm that forms stable salt complex to rapidly reverse heparin/some LMWH

196
Q

How is Protamine Sulfate administered?

A

Very slowly in IV over 10m and not to exceed 50mg

197
Q

How much Protamine Sulfate reverses how much Heparin?

A

1mg reverses 100 units of heparin

198
Q

What types of reactions can occur when doing a protamine sulfate infusion?

A

Transitory flushing, warmth, dyspnea, vomit and lassitude

HOTN/Brady

199
Q

Protamine Sulfate interacts w/ what drugs?

A

Cephalosporins

Penicillins

200
Q

What is the MOA of Direct Oral Factor Xa Inhibitors

A

Selectively block Xa w/out requiring co-factor

201
Q

D/c _____ anti-coagulant in PTs without adequate continuous anticoagulation increases risk of stroke

A

Direct Oral Xa inhibitors

202
Q

What are the clinical advantages of DOF Xa Inhibitors vs Warfarin?

A 
Non inferior
Apixaban is superior
Fewer drug interactions
Antidote- Recombinant Factor Xa Andexx w/ activated charcoal w/in 2hrs
Not monitoring needed
203
Q

What are the clinical disadvantages of DOF Xa Inhibitors vs Warfarin?

A

$$

Can’t use if PT has prostetic valves

204
Q

What are the names of the 3 direct oral factor Xa inhibitor drugs?

A

Rivaroxaban
Apixaban
Edoxaban

205
Q

What is the clinical indications for using DOF Xa INhibitors

A

Riva/Apix: stroke prevention and systemic embolism in PTs with non-valve A-fib
Prophylaxis of DVT for knee/hip surgery
DVT/PE treatment

Edox: stroke prevention and systemic embolism in PTs with non-valve A-fib; DVT/PE treatment after 5-10 days of parenteral anti-coag therapy

206
Q

What PTs is the use of DOFXaI avoided in?

A

Riva- mod/severe liver dz
Apix- don’t use in liver dz
Adeox- mod/severe liver dz or if CrCl <15ml

207
Q

Avoid using DOFXaIs with what other drugs?

A

Drugs that are both p-glycoprotein and strong 3A4 inducers and inhibitors

208
Q

Pregnancy categories for DOFXaI

A

Riva/Edox- C

Apix- B

209
Q

What are the limits for stopping Warfarin and starting DOFXaIs?

A

Riva when INR is less than 3
Apix- INR below 2
Edox- INR below 2.5

210
Q

MOA of Direct Thrombin Inhibitors

A

Bind to active site of thrombin and inhibits down stream effects of converting fibrinogen to fibrin without need of cofactor

211
Q

Clinical indication to use Bivalirudin

A

Percutaneous coronary intervention
Percutaneous transluminal corornary angioplasty
PTs w/ at risk of HIT/HITTS undergoing PCI/PTCA

212
Q

Clinical indication to use Argatroban

A

Prophylaxis/treatment of PTs w/ HIT

PT w/ HIT undergoing PCI

213
Q

How does Bivalirudin and Argatroban get metabolized?

A

Biva- renal, adjust if CrCl is below 30

Argatro- liver, dose adjust if impaired

214
Q

What needs to be monitored when using Bivalirudin or Argatroban

A

Biva- aPTT 1.5-2.5 and ACT >2.5x baseline

Argato- aPTT 1/5-3 and ACT >2.5x baseline

215
Q

How is the Warfarin bridge established w/ PTs on Bivalurdin or Argatroban

A

Over lap administration for 5 days min until INR is in target
Recheck INR after non-heparin anticoag effect is gone

216
Q

MOA of Dabigatran

A

Direct thrombin inhibitor prodrug

217
Q

When is Dabigatran used

A

Preventing stroke or systemic embolism in PTs w/ non-valvular A-fib
DVT/PE treatment/prevention

218
Q

What therapeutic considerations need to be noted when using Dabigatran?

A

If +75y/o
Poor renal function
Under weight
Req’d BID dosing

219
Q

What is the risk of discontinuing using Dabigatran?

A

PTs w/out adequate continuous anti-coag increases their risk of stroke

220
Q

What drugs does Dabigatran interact with?

A

Aspirin/Clopidogrel doubles bleeding risk
100mg or less considered
Avoid Ticagrelor

221
Q

What 4 P-Glycoprotein inhibitors may increase Dabigatran levels?

A 
Ketconazole
Verapamil
Amiodarone
Clarthromycin
P-glycoprotein inducers DEC dabigatran efficacy
222
Q

How do PTs modulate taking Dabigatran if they also take antiacids?

A

Take Dabigatran 2hrs prior to antacids

223
Q

Adverse effect of Dabigatran is bleeding, so what’s the antidote?

A

Idarucizumab and acitvated charcaol in 2hrs of admin and hemodialysis

224
Q

What are the contraindications of using Dabigatran?

A

Mechanical heart valves

Ketoconazole/strong p-glycoprotein inhibitors

225
Q

When can PTs convert from Warfarin to Dabigatran?

What is it’s Pregnancy Category?

A

Stop Warfarin and start Dabigatran at INR less than 2.0

Cat C

226
Q

Dabigatran has to be dispensed and stored in the same package and used with in ?

227
Q

How is Dabigatran dose adjusted for A-fib

A

75mg BID if CrCl is 15-30
Don’t use if below 15
DVT/PE- don’t use if below 30 or if on dialysis

228
Q

Advantages of Dabigatran over Warfarin?

A

More effective stroke/ embolism prevention
Lower intracranial bleed risk
Fewer interactions
No monitoring

229
Q

Disadvantages of Dabigatran over Warfarin?

A 
Renal elimination= renal dosing
Not for use w/ fake valves
Dyspepsia
BID dosing
\$\$
230
Q

MOA of Idarucizumab

A

Humanized monoclonal Ab that binds to Dabigatran and neutralized it

231
Q

When is Idarucizumab used

A

Reverse Dabigatran for emergency surgery in next 8hrs
Life threatening bleeds
BUT doesn’t work for Xa inhibitors

232
Q

MOA of fibrinolytics/thrombolytics

A

Dissolve clots by activating conversion of plasminogen to plasmin w/ greatest benefit in use in first 3hrs and some benefits after 12hrs

233
Q

What are the clinical uses of Fibrinolytics/Thrombolytics?

A 
STEMI
Acute Ischemic stroke
Acute PE w/ instability
Restoration CV catheter flow
Severe massive DVT
Ascending thrombophlebitis of ilofemoral vein
234
Q

MOA of thrombolytic enzymes

A

Human enzyme synthesized by kidney that directly converts uncomplexed plasminogen to active plasmin and Factors 5 and 7

235
Q

MOA of tPA

A

Activates plasminogen that is bound to fibrin in thrombus and initiating fibrinolysis

236
Q

What is the use of Alteplase

A

tPA for STEMI, PE and acute ischemic stroke within 3hrs

237
Q

Reteplase and Tenecteplase are only approved for use in ?

A

Acute STEMIs
Rete- off label DVT and PE
Tene- mutant tPA w/ longer half life

238
Q

What are the physiological steps of tPA use

A

1: tPA binds to fibrin in thromubs
2: plasminogen to plasmin
3: initiates fibrinolysis

239
Q

What platelet aggregation inhibitor drug inhibits prostaglandin synthesis

240
Q

What platelet aggregation inhibitor drug inhibits other anti-platelets

A

Dipyridamole
Aspirin
Cilostazol

241
Q

What platelet aggregation inhibitor drug inhibits ADP P2Y12 receptor inhibitors

A

Clopidogrel
Ticagrelor
Prasugreal
Cangrelor

242
Q

What platelet aggregation inhibitor drug inhibits G2b/3a receptors

A

Abciximab
Apitifibatide
Tirofiban

243
Q

What are the drug names of the Glycoprotein 2b/3a Inhibitors

A

Abciximab
Eptifibatide
Tirofiban

244
Q

MOA of Eptifibatide and Tirofiban

A

Reversibly inhibit binding of fibrin to GP receptor w/out Abs but have shorter duration of action than Abc

245
Q

Therapeutic use of Eptifibatide and Tirofiban

What caution is taken?

A

Used with heparin and aspirin for ACS and PCI to reduce thrombotic cardiac events
Special dose req’d for red renal function

246
Q

What is a benefit of using Abciximab over the other two?

A

No renal adjustment needed

247
Q

When is Abciximab used?

A

Adjunct to PCI for prevention of cardiac ischemic issues in PTs undergoing PCI or have unstable angina and PCI is planned for next 24hrs

248
Q

What antiplatelet regime is recommended for all PTs with a NSTEMI?

A

ASA
P2Y12 inhib
G2a/3b inhibitor

249
Q

All PTs with NSTEMI ACS are req’d to have anticoagulant therapy ASAP which includes ?

A

UFH/LMWH/Fondaparinux or Bivalirudin to prevent formation of fibrin and thrombus

250
Q

MOA of P2Y12 inhibitors Clopidogreal and Prasugrel

A

Irreversibly inhibits ADP binding to receptor causing inhibition of GP2b/3a for platelet aggregation

251
Q

MOA of Ticagrelor

A

Reversibly inhibits ADP binding to receptor causing inhibtion of GP2b/3a receptors

252
Q

What is the clinical use of Clopidogrel?

A

Prevent atherosclerotic event in PTs with peripheral artery dz, recent stroke/MI
Unstable angina prophylaxis
Combo w/ aspirin to reduce CV issues

253
Q

What is the clinical use of Prasugrel

A

W/ aspirin to prevent CV event in post-PCI in ACS PTs

254
Q

Clinical use of Ticagrelor is ?

A

Reduce rate of thombotic CV events in PTs with ACS: unstable angina, N/STEMI or MI

255
Q

Drug interaction of P2Y12 Inhibitor Clopidogrel

A

Prodrug

2C19 inhibitors reduce antiplatelet effect

256
Q

Drug interaction of P2Y12 Inhibitor Prasugrel

A

Prodrug w/ least drug inteactions

257
Q

Drug interaction of P2Y12 Inhibitor Ticagrelor

A

3A4 substrate

BBWarning- dec efficacy w/ aspirin +100mg

258
Q

Using P2Y12 inhibitors with ? or ? may increase bleeding risks

A

Anticoagulants Warfarin

Antiplatelets NSAIDs

259
Q

What are the adverse events and wash out period for Clopidogrel

A

Less than other 2

5-7days

260
Q

What are the adverse events and wash out period for Prasugrel

A

Don’t use +75y/o

7 days

261
Q

What are the adverse events and wash out period for Ticagrelor

A

Dyspnea

Careful in asthma/bradycardia PTs

262
Q

Clinical use of Cangrelor

A

Idjunct to PCI in PTs not treated w/ P2Y12 inhibitor or G2b/3a to reduce risk of MI, repeat coronary revascularization or stent thrombosis

263
Q

What are the adverse effects of Cangrelor

A

Bleeding but short half life leaves no antiplatelet effect after an hour of d/c

264
Q

MOA of aspirin

A

Irreversibly inhibits COX1 and 2 to dec TXA2 production from arachidonic acid that lasts 7-10 days

265
Q

What aspirin dose has shown to be effective prevention of CV events?

Complete COX1 inhibition is compelted w/ __mg of aspirin

A

50-160mg

75-150

266
Q

Top 3 uses of aspirin are ?

A

Primary prevention of CV, stroke and A-fib stroke
50-59 w/ >10%= 81mg/day
60-69 w/ >10%= smaller benefit
<50 or >70= think twice before Rx

267
Q

Avoid aspirin in what 4 previous Hx

A

High bleed risk
Previous GI bleed
On anticoagulant
Uncontrolled HTN

268
Q

Adverse events of aspirin?

A

GI
Reyes Syndrome in kids if given aspirin when they had chickenpox or flu
Stop 7-10 day prior to surgery
Pregnancy C/D

269
Q

Why are pregnant women to avoid aspirin

A

Closes ductus arteriosus

270
Q

What med is the preferred analgesic or antipyretic during pregnancy

A

Acetaminophen

271
Q

MOA of Dipyridamole

A

Stims prostacyclin synthesis and inhibits adenosine uptake to inhibit platelet aggregation

272
Q

When is Dipyridamole used?

A

W/ aspirin to prevent CV ischemia

Monotherapy has little benefit

273
Q

Adverse effects of Dipyridamole

A

HA dizzy

Coronary Steal Phenomenon in unstable angina PTs, so avoid use and allow 2-3 day wash out

274
Q

Use Dipyridamole with caution and what other drugs?

A

Anticoagulants

Could aggrevate myasthenia gravis

275
Q

MOA of Aspirin/Dipyridamole

A

Irreversibly inhibit COX 1 and 2 to dec TXA2 and stim prostacyclin synthesis and inhibit adenosine uptake to platelets

276
Q

When is used?

A

Secondary prevention to stroke post-ischemic stroke or TIA

277
Q

Therapeutic considerations for Aspirin/Dipyridamole

A

Must be taken as combo, not together but separate
Protect from moisture
BID dose

278
Q

Don’t use Aspirin/Dipyridamole with ?

A

Anticoagulatns

Children/teens w/ viral syndrome

279
Q

MOA of Cilostazol

A

PDE3 inhibitor
Vasodilator
Inhibit platelet aggregation

280
Q

Use of Cilostazol

A

Reduce Sx of Intermittent Claudication

Use w/ aspirin enhances platelet inhibition

281
Q

Contraindication for using Cilostazol

A

HF of any level
hemostatic disorder
Bleeding

282
Q

Drug interactions of Cilostazol

A

Major 3A4 and 2C19 substrate

2-3 day washout

283
Q

What is the Gold Standard for Dx PE?

A 
*Pulmonary angiography*
D-Dimer
Inc Troponin
Inc NP
Electrocardiography
284
Q

Define Massive PE

A

Acute PE with sustained HOTN SBP less 90mm

Loss of pulse

285
Q

Define Acute PE with persistant brady

A

HR <40

S/Sx of shock

286
Q

Define Submassive PE

A

PE w/out Systemic HOTN
RV dysfunction
Myocardial necrosis

287
Q

Define Low Risk PE

A

PE and absence of markers of adverse prognosis

288
Q

When ar fibrinolysis considered for PE PTs?

A

Massive acute
Submassive acute
NOT for low risk or submassive w/ minor Sx
NOT for undifferentiated cardiac arrest

289
Q

Flow to determine if Submassive PE gets anticoagulant or not

A

RV dysfunction or heart necrosis
SBP <90, shock index >1, SPO2 <95%
RV dysfunction, elevated cardiac markers
If yes, alteplase 100mg over 2hrs

290
Q

What agents are used to treat bleeding

A

Transfusion
Cryoprecipitate- plasma protein from whole blood
PCC- last line for reversing Apixaban, Dabigatran, Rivaroxaban or Edoxaban
Tranexamic Acid

291
Q

Adverse effects of treating bleeding agents

A

Stroke PE DVT

HTN reaction

292
Q

MOA of Tranexamic Acid

A

Reversible comples to displace plasminogen from fibrin to inhibit fibrolysis and proteolytic plasmin

293
Q

When is Tranexamic Acid used?

A

Label: heavy menstruation, tooth extraction in PTs w/ hemophilia

Off label: trauma hemorrhage, perioperative bleeds

294
Q

What are the adverse effects of Tranexamic Acid?

How is it eliminated?

A

HA, Abd Pain, Back pain

95% renal and unchanged

295
Q

What are the precautions for using Tranexamic Acid?

A

Hx of thrombotic events

Renal dysfunction

296
Q

What 3 nutrients are essential for hematopoiesis

297
Q

What are the types of anemia?

A

Fe Def- most common
B12= megaloblastic anemia, GI Sx and neuro abnormals
B9= defective DNA synthesis and megaloblastic anemia

298
Q

Define Transferrin

Define Ferritin

A

Plasma protein that binds Fe and delivers it to tissue

Protein that binds to Fe, found in liver, spleen sk muscle and marrow

299
Q

What agents are used as oral Fe supplements

A

Ferrous Gluconate
Ferrous Sulfate- most efficiently absorbed
Ferrous Fumurate

300
Q

How long is oral Fe used

A

Continue 3-6mon after correction of iron loss

301
Q

What precautions are taken with oral Fe supplements

A

Take w/ meals
Constipation
Black stool

302
Q

When is IV iron used

A

Pts who cant tolerate/absorb PO Fe
Extensive anemia- IBD, SmBl Ressection, gastroectomy, CKD
Severe cases that need rapid correction

303
Q

What are the IV Fe supplements

A 
Iron Dextran (High- Dexferrum, Low- INfeD)
Sodium Ferric Gluconate Complex
Iron Sucrose
Ferumoxytol
Ferric Carboxymaltose
304
Q

Adverse effects of IV Fe

A

GI
Hypersensitive
Fatal at 1-10g
Antidote; Deferoxamine

305
Q

Function of Cyanocobalamin

A

Ring w/ cobalt atom that is cofactor for biochemical reactions
AKA extrinsic factor

306
Q

B12 is essential for what processes?

A

Normal DNA synthesis

Metabolize homocysteine and cysteine w/ B6

307
Q

What is required for B12 to be absorbed?

How is it transported

A

Intrinsic factor in stomach

Transported on Transcobalamin 2 and stored in liver

308
Q

When are B12 deficiency seen?

A 
Vegetarians
Dysfunctional distal ileum
Defective/absent intrinsic factor
Gastroectomy
Pernicious anemia
309
Q

What are the injectable forms of B12?

A

Hydroxocobalamin- preferred, more protein binding and remains in circulation longer
Cyanocobalamin

310
Q

If pernicious anemia refuses/can’t tolerate injections what can they take?

A

Oral B12 intrinsic factor

311
Q

Adverse effects of B12

A

Death w/ parenteral admin
CV- congestion, HF, PV thrombosis
Derm: ithcing, exantherma
Swelling of whole body

312
Q

Why is B9 required

A

Provide precursors for synthesis of aa, purines and DNA

313
Q

Where is B9 absorbed?

A

Prox SmInt
Transported on plasma binding protein
Reqs reduction by dihydrofolate reductase to it’s active metabolite methyltetrahydrofolate

314
Q

What is the clinical use for Folate

A 
Pregnancy
PTs w/ alcohol dependence
Hemolytic anemia
Liver dz
Renal dialysis
315
Q

How much folic acid is used in dose?

A

1mg/day reverses megaloblastic anemia

316
Q

What is the reduce folic acid version used for?

A

Leucovorin
Doesn’t req dihydrofolate reductase for metabolism
Antagonist OD
Folate deficient megaloblastic anemia

317
Q

What are the Hematopoietic Growth factors

A

Erythropoitin- glycoprotein that regulates RBC production/protection in renal peritubular cells

318
Q

What is the MOA of Epoetin Alfa and Darbapoetin Alfa

A

Inc rate of proliferation and differentiation in marrow to inc reticulocyte release from marrow
Reqs Fe stores

319
Q

When are Epoetin Alfa and Darbapoetin Alfa used?

A

RBC production anemia of chronic RF
Chemo
PT prep for surgery

320
Q

What are the adverse reactions of Epoetin Alfa and Darbapoetin Alfa

A

Risk REMS program
Inc risk of death and CV events
Don’t start if Hgb >10g/dL

321
Q

What form of poetin is better?

A

Darbapoetin has less frequent dosing and longer half life

322
Q

MOA of Filgrastim

When is it used

A

Stims benefits of neutrophils
Chemo Pts
Neupogen- radiation injury syndrome

323
Q

MOA of Sargramostim

When is it used

A

Stims neutrophils
Acute myeloid leukemia
Marrow/stem cell transplant

324
Q

Warning of using Filgrastim

When is it’s use d/c?

A

Alveolar hemorrhage
Nephrotoxic
ARDS

D/c at neutrophil count of +10K

325
Q

Warning of using Sargramostim

When is it d/c?

A

1st dose effect
Fluid retention
Pulmonary Sx

Inc blood counts, dec dose x 50%

326
Q

Biguanides and Thiazolidinediones are AKA ?

Sulfonylureas are AKA ?

A

Insulin Sensitizers

Insulin Secretagogues

327
Q

Characteristics of GLP-1 Agonists

A

Greater efficacy
+ weight loss
SubQ
More ADR- N/V/D

328
Q

Characteristics of DPP-4 inhibitors?

A

Less efficacy
Weigh neutral
PO
Less ADR

329
Q

Define Incretin Based Therapy

A

GLP-1 Agonists
DPP-4 Inhibitors
Greater insulin response to oral glucose than IV load

330
Q

What are the two incretin hormones?

A

GIP
GLP-1
Both degraded by DPP-4s

IPAP (212 decks)

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