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z S1: Module > DM-2 > Flashcards

DM-2 Flashcards

1
Q

Decreased insulin secretion __________ beta cells sensitivity to glucose

A

decreased

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2
Q

What is the drug of choice for type 2 diabetes

A

metformin

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3
Q

Metformin is transported into the cells by organic _______ transporters

A

cation

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4
Q

Metformin is excreted into urine by what

A

MATE 1 and 2

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5
Q

OCT-1 and OCT-3 are in _______ for activity in the liver

A

hepatocytes

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6
Q

OCT-2 are in ____ cells for excretion

A

renal

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7
Q

Metformin has a slow onset and a long duration of action meaning it is what kind of coverage

A

basal

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8
Q

Effects of metformin in liver

A

decrease gluconeogenesis
decrease lipogenesis and increase fatty acid oxidation

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9
Q

Effects of metformin in muscle

A

increase glucose uptake
increase glycogen storage
decrease lipogenesis

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10
Q

Effects of metformin in intestine

A

decrease intestinal glucose absorption

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11
Q

MOA of metformin (biguanides)

A

-decrease cellular respiration by inhibiting mitochondrial respiratory chain complex 1
-decrease ATP by inhibiting fructose 1,6 bisphosphate
-activate AMPK causing protein phosphorylation and decrease gluconeogenesis and lipogenesis gene expression
-antagonizes the action of glucagon by inhibiting adenylate cyclase

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12
Q

Adverse effects of metformin

A

GI upset
Metallic taste
decrease Vit B12

Rare: lactic acidosis

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13
Q

Metformin drug interaction with inhibitors of _____ transporters

A

OCT

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14
Q

Metformin drug interactions with drugs that increase plasma glucose can _________ the effects

A

antagonize (corticosteroids, estrogens)

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15
Q

Cimetidine _______ renal elimination of metformin

A

decreases

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16
Q

Ranolazine ___________ metformin serum levels

A

increase

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17
Q

Iodinated contrast media can enhance _______ adverse effecrs and renal failure

A

metformin

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18
Q

Insulin secretagogues are effective in patients with functional ______ cells

A

beta

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19
Q

Sulfonylureas cover _____ insulin levels and ________ insulin

A

basal
mealtime

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20
Q

MOA of sulfonylureas

A

-Bind to SUR 1 complex in Katp channel
-activate exocytosis and release endogenous insulin independent of plasma glucose
-increase tissue sensitivity to insulin (improved metabolic control)
-decreased hepatic glucose production and increase glucose uptake

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21
Q

Sulfonylureas adverse effects

A

hypoglycemia
weight gain
(GI, hematological rxn, hypersensitivity rxns, SIADH)

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22
Q

Aspirin, sulfonamides, chlorofibrates cause increased hypoglycemic effect in which drug class

A

Sulfonylureas

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23
Q

Miconazole, chloramphenicol, warfarin decrease __________ metabolism

A

Sulfonylureas

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24
Q

Ethanol increase action of _____________

A

Sulfonylureas

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25
Q

_________ are two hormones secreted from enteroendocrine cells in the intestine in response to food intake

A

incretins

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26
Q

______ is secreted from L-cells

A

GLP-1

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27
Q

_____ is secreted from K-cells

A

GIP

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28
Q

Incretins are metabolized by

A

DPP-4

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29
Q

_______ activate insulin secretion from the pancreas in response to food intake

A

incretins

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30
Q

GLP-1 MOA

A

-insulin secretion by activation of GLP-1 GPCR on beta cells
-receptor also in other cells
-PKA phosphorylates the channel (closes it)
-increase calcium from intracellular store -> exocytosis -> insulin secretion

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31
Q

GLP-1 is secreted into circulation from endocrine L cells in ______ __________ after a meal

A

small intestine

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32
Q

GLP-1 Effects in brain, stomach, liver, pancreas

A

brain: decrease appetite
stomach: decrease gastric empty
liver: decrease glucose production
pancreas: increase insulin secretion, decrease glucagon secretion

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33
Q

What two classes of drugs can restore GLP-1 activity from decreased GLP-1 postprandial, inadequate glucagon suppression, increase glucose output

A

GLP-1 analogs
DPP-4 inhibitors

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34
Q

Short-acting GLP-1 receptor agonists (exenatide, lixisenatide) cause what

A

postprandial hyperglycemia

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35
Q

Long-acting GLP-1 receptor agonists (exenatide, dulaglutide, liraglutide, semaglutide) cause what

A

basal glycemia

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36
Q

Metabolism of GLP-1 RA

A

proteolytic degradation and beta oxidation of FA

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37
Q

Adverse effects of GLP-1 RA

A

nausea, vomiting, diarrhea
weight loss
(hypersensitivity, hypoglycemia, altered kidney function, thyroid cancer, pancreatitis)

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38
Q

Contraindications of GLP-1 RAs

A

hypersensitivity rxns
GI problems or moderate to severe kidney disease
FH of medullary thyroid cancer
pregnancy
breast-feeding

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39
Q

Drugs that affect gastric emptying and drug absorption from GI tract cause a drug interaction with what class of drugs

A

GLP-1 RAs

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40
Q

Increased risk of hypoglycemia when used with other antidiabetic drugs cause a drug interaction with what class of drugs

A

GLP-1 RAs

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41
Q

Drugs that elevate plasma glucose and antagonize effect cause drug interaction with what class of drugs

A

GLP-1 RAs

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42
Q

What class of drug is Tirzepatide and what does it treat

A

GIP/GLP-1 RA
diabetes and obesity

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43
Q

Effects of Tirzepatide

A

significantly lower blood glucose levels
improve insulin sensitivity
reduce weight
amend dyslipidemia

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44
Q

When to take DPP-4 drugs

A

mealtime

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45
Q

DPP-4 MOA

A

-inhibit DPP-4 enzyme found on cell membrane
-serine protease cleaves N-t aa to inactivate incretins
-inhibit degradation of GLP-1 and GIP increasing levels of endogenous incretins and increase insulin secretion in a glucose independent manner

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46
Q

Effects of DPP-4 I

A

increase cellular glucose uptake
decrease hepatic glucose output

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47
Q

Adverse effects of DPP-4

A

pharyngitis/upper respiratory tract infections
hypoglycemia w/ other antidiabetic agents
(pancreatitis, hypersensitivity rxn, hepatotoxicity)

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48
Q

Drugs that inhibit CYP3A4/5 will elevate plasma levels in which class of drugs

A

DPP-4

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49
Q

Corticosteroids decrease effects of which class of drugs

A

DPP-4

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50
Q

All metabolites of SGLT-2s are _______

A

inactive

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51
Q

Filtered glucose is returned to the circulation by the action what

A

SGLT 1 and 2

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52
Q

_________ is in the s1/s2 segments and is a low affinity and high capacity transporter

A

SGLT-2

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53
Q

________ is in s3 segment of the proximal convoluted tubule and has high affinity and is a low capacity transporter

A

SGLT-1

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54
Q

SGLT2 Inhibitors MOA

A

-suppress of glucose reabsorption
-insulin-dependent
-decrease hyperglycemia by increasing urinary clearance of glucose to improve glycemic control and decrease toxicity
-do not confer a risk of hypoglycemia
-efficacy is reduced in renal impaired function

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55
Q

What SGLT-2 drug is the only inhibitor that also inhibits SGLT-1

A

Invokana

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56
Q

Side effects of SGLT2

A

-genital fungal and urinary infection
-GI, nausea, constipation
-hypotension and hypovolemia
-hypersensitivity
-not used in pregnancy

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57
Q

Side effects of metformin

A

diarrhea
stomach upset
nausea
vit B12 deficiency

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58
Q

Renal considerations in metformin

A

GFR <30 Cl contraindication
GFR <45 no new start, cut dose by 50%

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59
Q

What are these other considerations drug class apart of: weight neutral and insulin sensitizer

A

Metformin

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60
Q

GLP-1 agonists and GLP/G1P agonist side effects

A

nausea
vomiting

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61
Q

Other consideration in GLP-1 agonists and GLP/G1P agonists

A

injection
weight loss
reverse/improve insulin deficiency
global shortages

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62
Q

GLP-1 RAs risk and reduction

A

benefit: CKD and ASCVD
used: clinical ASCVD and high risk, albuminuria (>300mg/g)

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63
Q

SGLT-2 Inhibitors side effects

A

genital infections (yeast and UTI)

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64
Q

Other considerations in SGLT-2 inhibitors

A

weight loss
diuresis (BP lowering)

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65
Q

SGLT-2’s risk and reduction

A

Benefits: CKD, ASCVD, heart failure
Used: clinical and high-risk ASCVD, albuminuria (>300mg/g +eGFR >25), HF

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66
Q

Sulfonylureas side effects

A

weight gain
hypoglycemia

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67
Q

Sulfonylureas other considerations

A

pancreas burn out
renal adjustment needed
mechanistically unfavorable

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68
Q

DPP-IV inhibitors side effects

A

infectious complications (URIs)
usually very well tolerated

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69
Q

Other consideration in DPP-IV Inhibitors

A

renal adjustment (except tradjenta)
weight neutral

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70
Q

What are the 5 steps in diabetes management

A

glucose control
cardiorenal risk (anti-clotting, statin, ACE, GLP-1, SGLT-2)
DRP
Monitor
Follow-up

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71
Q

What are the fasting and post-pranial goals for diabetes

A

fasting: <130
post-prandial: <180

72
Q

Statin use in diabetes

A

40-75 and low risk = moderate intensity
ASCVD or high risk = high intensity

73
Q

Anti-clotting drugs in diabetes

A

ASCVD
-ASA
-low dose rivaroxaban if low bleeding risk

74
Q

ACE/ARB in diabetes

A

UACR >30 +/- HTN

75
Q

Drug-related problems in diabetes patients

A

drugs that interfere w/ glucose control
smoking
duplicate therapy
sulfonylureas + mealtime insulin
DPP-IV plus GLP-1s
Drugs that require renal adjustment

76
Q

Monitoring of non-insulin diabetes medications

A

blood sugar checks
-bid to qid -> unstable hypoglycemia, MDI insulin
A1C
-every 3 months if not at goal, every 6 months if at goal

77
Q

What is the pharmacophore in sulfonylureas

A

benzenesulfonylurea (weak acids)

78
Q

First generation sulfonylureas have small __________ substituent on phenyl ring of _____

A

lipophilic
R1

79
Q

First generation sulfonylureas have lipophilic ____ or _______ substituent on non-sulfonyl-attached urea nitrogen on R2

A

alkyl
cycloalkyl

80
Q

Second-generation sulfonylureas are more _____ than first generation

A

potent (rapid onset and longer duration of action)

81
Q

The enhancement of glyburide activity is attributed to the strong binding affinity of that what group

A

p-beta-arylcarboxyamidoethyl

82
Q

Metformin is the only biguanides derivative and is considered to be the _____ ______ therapy for treatment of type 2 DM

A

first line (basic drug with 2 guanidine groups)

83
Q

Metformin in high doses can increase what

A

lactic acidosis

84
Q

Thiazolidenediones (TZD) are classic examples of PPAR gamma agonists and are commonly referred to as the ___________

A

glitazones (increased sensitization of cells to insulin)

85
Q

What is the pharmacophore of TZDs

A

thiazolidinedione moiety

86
Q

The ______ ring attached to the TZD ring via methylene group is essential for activity

A

phenyl

87
Q

A ___________ linker is found to be more potent than the ___________ counterpart of TZD

A

saturated
unsaturated

88
Q

__________ at either carbon adjacent to the pyridine ring leads to metabolites which appear to contribute to the biological activity of pioglitazone

A

oxidation

89
Q

GLP-1 exists in two equipotent forms of GLP-1 (__-__)-NH2 and GLP-1 (__-__)

A

2-36
7-37

90
Q

GLP-1 is rapidly metabolized by an aminopeptidase enzyme which is called what

A

DPP-IV

91
Q

One of the reasons that GLP-1 is susceptible to DPP-IV is because it contains an ____ in the penultimate N-terminal position

A

Ala

92
Q

Exenatide is a GLP-1 analogue that has a modification at position 8 of what

A

Gly instead of Ala

93
Q

Liraglutide is a GLP-1 analogue that has a modification of what

A

Lys 26
Arg 34
(best combination for albumin binding)

94
Q

Dulaglutide is a GLP-1 analogue that has a modification of what

A

fusion protein that is prepared by fusing two identical GLP-1 analogs protecting it from inactivation

95
Q

Lixisenatide is a GLP-1 analogue that has a modification of what

A

Gly at position 8
ser and lys tail
extends half-life

96
Q

Semaglutide is a GLP-1 analogue that has a modification of what

A

amino-terminal sequence on ala 8
lys 26
(fatty acid chain enhances affinity for albumin)

97
Q

The fatty-diacid section of tirzepatide is linked via a _________ acid and two acetic acids units to the side chain of the lysine residue

A

glutamic
(once weekly dosing)

98
Q

DPP-IV are peptide derivatives of alpha-aminoacyl pyrrolidines or alpha-aminoacyl thiazolidines which also take advantage of the enzyme’s high preference for ____ binding

A

Pro

99
Q

DPP-IV have an electrophilic group in the 2-position of the pyrrolidine or thiazolidine ring where ______ is the most common group present

A

cyano (Vildagliptin, Saxagliptin, and Alogliptin)

100
Q

DPP-IV have ______ _______ group in the position equivalent to the penultimate amino acid (Ala) in GLP-1 which also is important for binding through ionic interaction with Glu205 and Glu206 of DDP-IV.

A

basic amino

101
Q

The aminopiperidine’s primary amino group occupies the recognition site for the amino terminus of GLP-1, and hydrogen and ionic bonds with Glu residues. What drug class does this belong to

A

DPP-IV

102
Q

SGLT2 is expressed in the epithelial cells of the brush border of S1 and S2 segments of the proximal convoluted of renal tubule and reabsorbs ___ to ____% of filtered glucose.

A

80-90%

103
Q

Changing the O-glycoside linkage to a C-glycoside linkage has led to the development of __________ structures that are resistant to hydrolysis by b-glucosidases in the gut.

A

“Gliflozin”
UGT -> uridine glucuronyltransferases
(have an aryl moiety linked to a benzyl group pharmacophore)

104
Q

Macrovascular DM indications

A

CVD and PVD

105
Q

Microvascular DM indications

A

retinopathy
nephropathy
neuropathy
-peripheral
-autonomic

106
Q

There are slight differences between how and when complications may develop in type 1 versus type 2 diabetes

A

Most mechanisms, screening, and treatment recommendations remain the same for both

107
Q

Glycemic control is the primary prevention and treatment for all _____________ complications

A

microvascular

108
Q

Relationship between _____________ complications and glycemic control: Its complicated

A

macrovascular

109
Q

Unifying Mechanism

A

-Hyperglycemia leads to increased production of reactive oxygen species which may activate all of these pathways
-Some pathways may predominate in certain organs/areas

110
Q

Medications emphasized under CV Risk

A

statins
ASA
rivaroxaban
icosapent ethyl
ezetimbie
PCSK-9I
SGLT-2I
GLP-1
ACE/ARB
Bempidoic Acid

111
Q

How do you identify cardiovascular disease?

A

MI, PVD, CHF, CAD, angina, stroke, PCI, Stent, ACS, USA, CABG

112
Q

Additional major risk factors for CVD according to the ADA

A

Hypertension
Hyperlipidemia
Smoking
Family History
Albuminurea
Obesity
CKD

113
Q

Preventing Cardiovascular Disease

A

Glycemic Control
Weight Loss in overweight and obese patients
HTN management
Lipid management
Anti-clotting agents

114
Q

Drug classes with evidence in reducing CV events in DM patients: (HTN)

A

Beta-blockers (mask sign of hypoglycemia)
Give one antihypertensive at bedtime
ACE/ARB with albuminuria or CAD

115
Q

Primary goal of hyperlipidemia

A

LDL <70 mg/dl, <55 mg/dl if ASCVD

116
Q

Secondary Goals of hyperlipidemia

A

HDL>40 mg/dL
TG<150 mg/dL
at >500 mg/dl TG become primary target

117
Q

Screening recommendations of hyperlipdemia

A

Check lipid panel every 5 years if not on statin, yearly if on statin

118
Q

Primary Prevention (no ASCVD) 40-75 years old

A

moderate intensity statin

119
Q

Primary Prevention (no ASCVD) multiple risk factors

A

high intensity statin

120
Q

Primary Prevention (no ASCVD) ASCVD Risk >20%

A

High Intensity +/- ezetimibe to lower LDL by 50%

121
Q

Secondary Prevention (ASCVD)

A

High intensity statin for all

122
Q

Secondary Prevention (ASCVD) If LDL >70 with statin

A

consider addition of ezetimibe (cheaper) or PCSK9 inhibitor (more effective)

123
Q

Secondary Prevention (ASCVD) If 75-year-old and already on statin vs not on a statin

A

on statin: keep it
not on statin: consider risk/benefit

124
Q

DM + ASCVD + elevated TG

A

may add icosapent ethyl

125
Q

Statin + Fibrate or Niacin

A

generally not recommended

126
Q

Statins and DM Risk

A

benefit of statins outweigh the risk of use

127
Q

Statins and Cognitive Function decline

A

evidence points against this association

128
Q

If TG>500, target TG lowering to prevent what

A

pancreatitis

129
Q

Antiplatelet agents: Low-dose aspirin (ASA) therapy should be considered in what groups of patients

A

CVD
increased risk -> risk benefit discussion

130
Q

Antiplatelet agents when to use clopidogrel

A

ASA allergy

131
Q

Antiplatelet agents Add low dose rivaroxaban if what

A

CAD/PAD and low bleeding risk

132
Q

Other ASCVD Considerations: ASCVD or high risk add what two things

A

SGLT and/or GLP

133
Q

Smoking considerations in DM

A

-Nicotine increases insulin resistance
-Smokers=greater risk of CVD, microvascular complications and premature death
-Smoking may have a role in DM2 development

134
Q

PVD lead to what

A

May lead to skin ulcers, intermittent claudication and foot infections or gangrene

135
Q

PVD symptoms

A

Leg pain, especially at night
Cold feet
Decreased or absent radial or pedal pulses

136
Q

PVD treatment

A

Smoking cessation
Control blood pressure
Antiplatelet agents
Pentoxyphylline or cilostazol for symptoms

137
Q

Medications Emphasized for CKD/DKD

A

ACE/ARB
Finerenone
SGLT-2
GLP-1

138
Q

Nephropathy occurs in how many DM patients and leads to what

A

Occurs within 20-40% of DM patients and is the leading cause of end-stage renal disease (ESRD)

139
Q

Nephropathy monitoring

A

Urine albumin excretion should be measured at least annually with a Urine Albumin-creatinine ratio (Alb/Cr ratio or UACR)
SCr checked annually

140
Q

Difference between Micro-albuminurea and albuminuria

A

Micro-albuminurea 30-299 mg/g creatinine
Albuminuria is defined as >300 mg/g creatinine

141
Q

DKD vs CKD

A

DKD is CKD where DM is the cause of the CKD

142
Q

Finerenone (Kerendia®)

A

-non-steroidal mineralocorticoid receptor antagonist
-used in patients with DKD
-shows positive outcomes with DKD progression, reduce CV events and HF hospitalizations
-it increases K+

143
Q

Nephropathy - Treatment in UACR, CKD/DKD

A

UACR >30 add ACE/ARB (maxed out add finerenone)
CKD/DKD - eGFR >25 SGLT-2I
Optimize BP control

144
Q

Main risk factors neuropathy

A

Longer duration of diabetes
Poor diabetes control
Increased BMI
Smoking
(other include CVD, increase TG, HTN)

145
Q

Sensory (peripheral) Neuropathy sensory loss (feet/lower legs or hands)

A

Usually presents as numbness, tingling, sharpness or burning
Generally present at rest and worsens at night
Can be very painful but usually progresses to be complete loss of feeling over time

146
Q

Screening - yearly through physical exam and diabetic foot exam

A

Testing for loss of protective sensation
-Monofilament test
-Pinprick sensation
-Vibration perception

147
Q

Treatment of neuropathy

A

Specific treatment for underlying nerve damage not available
Duloxetine, pregabalin and gabapentin are recommended first line

148
Q

Autonomic Neuropathy

A

vary in type, severity, onset
full history and physical exam should be performed at each diabetes follow-up to screen
Individual symptoms should be treated as necessary

149
Q

Symptoms of autonomic neuropathy

A

Resting tachycardia
Exercise intolerance
Orthostatic hypotension
Constipation
Gastroparesis
Erectile dysfunction
Genitourinary tract disturbances

150
Q

Retinopathy

A

Optimize glycemic and blood pressure control
Annual dilated eye exams
Treatment
-Laser photocoagulation therapy
-Intra-corneal injections - VEGF Inhibitors

151
Q

What is diabetic ketoacidosis (DKA)

A

life-threatening state resulting from a relative or absolute deficiency of insulin (mainly Type 1)

152
Q

What is the triad in DKA

A

hyperglycemia
anion gap metabolic acidosis
ketosis

153
Q

Pathophysiology of DKA

A

Insulin deficit with increased levels of stress hormones and a precipitating factor

-Stress hormones: glucagon, cortisol, epi, growth
-Precipitating factors: insulin deficiency, undiagnosed DM1, non-compliances, stress

154
Q

What are the 5 results of insulin deficiency

A

hyperglycemia
glycogen catabolism
glycogen depletion
lipolyis
ketosis

155
Q

What is the main result of hyperglycemia

A

polydipsia*
polyuria*
weight loss*
volume depletion
electrolyte depletion
renal hypoperfusion
hypotension

156
Q

What are the 4 ketosis results

A

anion gap metabolic acidosis
compensatory alkalosis
hypotension
shock

157
Q

What are the diabetic ketoacidosis clinical course effects

A

hyperglycemia
polydipsia, polyuria dehydration
anorexia, ab pain, acidosis
Kussmaul breathing
altered consciousness
coma, death

158
Q

Diagnostic criteria for DKA

A

BS > 250
pH <7.3
Bicarb <15
Ketonuria or ketonemia

159
Q

Treatment of DKA

A

-IV Regular Insulin 0.1 u/k bolus or 0.1 u/kg/hr infusion (MONITOR potassium before starting)
-IV fluids 0.9% NS if corrected NA+ <135 or 0.45% NS if corrected NA >135
-IV potassium supplementation: K+ will be elevated then when IV given K+ returns to intracellular space and serum K+ will be low

160
Q

Before IV regular insulin is given for DKA what level does the serum K+ have to be

A

> 3.3

161
Q

When to give dextrose in DKA treatment

A

blood glucose falls <250 replace dextrose but continue IV insulin until ketones are undetectable

162
Q

When to use bicarb in DKA treatment

A

not recommended
could use when pH <6.9

163
Q

What is hyperglycemia hyperosmolar syndrome (HHS)

A

life-threatening emergency resulting from severe dehydration and hyperglycemia in Type 2 DM
-serum osmol elevates and severe dehydration occurs as result of osmotic diuresis

164
Q

HHS diagnostic criteria

A

BG: >600 mg/dl
pH >7.3
Bicarb >18 mEq/l
Serum Osmol: >320 mOsmo/L

165
Q

Treatment for HHS

A

IV fluids ~9L
IV regular insulin infusion
Electrolytes (K+, Mg)
Treat precipitating event

166
Q

DKA:
age
duration of symptoms
glucose level
potassium conc
bicab conc
ketone bodies
pH
serum osmolarity
prognosis

A

age: <40
duration of symptoms: <2 days
glucose level: <600
potassium conc: low
bicab conc: <18
ketone bodies: yes
pH: <7.3
serum osmolarity: <350
prognosis: 3-10% mortality

167
Q

HHS:
age
duration of symptoms
glucose level
potassium conc
bicab conc
ketone bodies
pH
serum osmolarity
prognosis

A

age: >60
duration of symptoms: >5 days
glucose level: >800
potassium conc: variable
bicab conc: normal
ketone bodies: no
pH: normal
serum osmolarity: >350
prognosis: 1-20% mortality

168
Q

Primary problems in DKA and HHS

A

DKA: acidosis
HHS: dehydration

169
Q

Key things to look for in DKA and HHS

A

DKA: acidosis, ketones
HHS: glucose, no ketones, no acidosis, high osmols

170
Q

Primary treatment strategies for DKA and HHS

A

IV fluids, IV insulin, IV potassium

171
Q

Monitoring for DKA and HHS

A

DKA: glucose, pH, ketones, e-lytes
HHS: glucose, osmol, e-lytes, fluid/urine output

172
Q

What is the correct sodium equation

A

measured Na + [(glucose level - 100) x 0.016]

173
Q

Daily patient responsibilities for DM

A

check feet daily
check blood sugars as recommended
medication compliance

174
Q

What should you check at each DM follow-up

A

blood sugar
blood pressure
weight
visual foot exam
physical exam and history screening for neuropathy

175
Q

Other screening tests that are needed every 3-6 months, 6 months, and annually

A

3-6: HgbA1c
6: dental
year: comprehensive foot exam, urine albumin/cr ratio, SCr, dilated eye exam

z S1: Module (8 decks)

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