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z S1: Module > DM-1 > Flashcards

DM-1 Flashcards

1
Q

Defn of Diabetes

A

hyperglycemia resulting from defects in insulin secretion, insulin action, or both that leads to the failure of various organs

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2
Q

Morbidity of DM

A

blindless
end-stage renal disease
non-traumatic amputations

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3
Q

Type 1:
percent
cause
age
clinical presentation
body type
treatment
other

A

percent: 5%
cause: auto-immune
age: children
clinical presentation: acute, life-threatening polydipsia, polyphagia, weight loss, DKA
body type: thin
treatment: insulin
other: predisposed to other types of auto-immune disorders

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4
Q

Type 2:
percent
cause
age
clinical presentation
body type
treatment
other

A

percent: 95%
cause: lifestyle, insulin resistance, genetic
age: adult >40
clinical presentation: gradual, subtle sx., fatigue, polydipsia, polyuria
body type: overweight/obese
treatment: lifestyle, non-insulin injections, orals, insulin
other: have metabolic syndrome

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5
Q

If a patient has C-peptide what type of DM does it indicate

A

Type 2
(type 1 has zero)

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6
Q

If a patient has islet cell antibodies what type of DM does it indicate

A

Type 1

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7
Q

If a patient has antibodies to insulin what type of DM does it indicate

A

Type 1

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8
Q

Risk factors for T2DM

A

lifestyle
FH
HTN
Dyslipidemia
gestational DM or giving birth >9 lb baby
Race (Hispanic, Native, AA, Pacific)

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9
Q

Genetic defects in B-Cell function

A

can resent like type 1 or type 2 (more type 1)
usually insulin dependent
MODY (maturity-onset diabetes of youth)
LADA (latent autoimmune diabetes in adults)

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10
Q

Secondary causes of DM

A

Pancreatic disease (pancreatitis, cystic fibrosis)
Endocrinopathies (acromegaly, cushings, hyperthyroidism)

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11
Q

Most prevalent drug induced diabetes

A

steroids
atypical antipsychotics
protease inhibitors
statins

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12
Q

Imparied fasting glucose

A

> 100 mg/dl but <126 mg/dl

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13
Q

Imparied glucose tolerance

A

2 hour OGTT >140 mg/dl but <200 mg/dl

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14
Q

HgbA1C between what is pre-diabetes

A

5.7% and 6.4%

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15
Q

Oral Glucose Tolerance Test (OGTT)

A

75 gm glucose load
BS check q30 min x 2 hours
level peak at 1 hr, remain below 200 throughout return to fasting at 2 hrs

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16
Q

Diagnosis of DM

A

symptoms of DM + any glucose >200
Fasting plasma glucose >126
Plasma glucose >200 after 2 hrs of OGTT
HgbA1C >6.5%

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17
Q

Fasting BG range: normal, pre DM, DM

A

normal: <100
pre DM: 100-126
DM: >126

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18
Q

2hr PP BG range: normal, pre DM, DM

A

normal: <140
Pre DM: 140-200
DM: >200

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19
Q

A1C range: normal, pre DM, DM

A

normal: <5.7
Pre DM: <5.7-6.4
DM: >6.4

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20
Q

What stores glucose

A

adipose tissue
glycogen
triglycerides

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21
Q

How much insulin is secreted a day and how much can your body store

A

secreted: 25-50 units
store: 200 units

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22
Q

Epi stimulates what

A

glycogenolysis

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23
Q

Glucocorticosteriods stimulate what

A

gluconeogenesis

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24
Q

GLP-1 secreted from the small intestine after a meal, increases _________ secretion, inhibits _________ secretion, signals satiety in CNS, and delays gastric emptying

A

insulin
glucagon

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25
Q

BS normal range and CNS normal range of glucose homeostasis

A

BS: 70-130
CNS: >40-60

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26
Q

T1DM pre-clinical stage

A

immune markers are present but no symptoms present (B-cell destruction occurs here)

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27
Q

T1DM initial hyperglycemia

A

80-90% destruction of B-cells

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28
Q

T1DM honeymoon phase

A

days to weeks after diagnosis
last for few months
BS decrease and decrease in insulin requirements

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29
Q

T1DM total destruction of b-cells

A

complete full clinical disease

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30
Q

T2DM defect in the secretion and function of hormones that regulate ____________ metabolism

A

carbohydrate

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31
Q

T2DM starts as insulin resistance and progresses to insulin _________

A

deficienct

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32
Q

Insulin resistance defn

A

excess body fat and excess glucose load cause cells to not properly recognize insulin and utilize it effectively

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33
Q

What does this describe:
-higher amounts of insulin are required to maintain euglycemia
-insulin promotes the storage of glucose as fat and results in weight gain
-pancreas is unable to keep up with demand and hyperglycemia occurs

A

insulin resistance cycle

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34
Q

Insulin suppresses glycogenolysis and gluconeogenesis in the _______

A

liver

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35
Q

Insulin __________ in hepatocytes causes the insulin suppression to be inhibited

A

resistance

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36
Q

Patho of pancreas, muscle, fat, liver, GI

A

pancreas: defective b-cell secretion
muscle: reduce glucose uptake and utilization
fat: inappropriate lipolysis
liver: excess glucose production, hepatocyte insulin resistance
GI: decreased incretin effect

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37
Q

What is fasting

A

no food for 8 hours or more

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38
Q

Post-prandial

A

1-2 hours after meal

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39
Q

Pre-prandial

A

right before a meal regard less of the time since last food

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40
Q

Goals for fasting, post-prandial, and pre-prandial

A

fasting: <130
post-prandial: <180
pre-prandial: no goal

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41
Q

What are continuous glucose monitors

A

-Device with filament inserted under the skin
-monitors blood sugars at specified intervals
-send to a smart phone
-sensor changed out every. 10-14 days

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42
Q

TIR (time in range) goal

A

aim for 70% or greater

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43
Q

TBR (time below range) goal

A

Low: <4% (<70)
Very Low: <1% (<54)

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44
Q

Who should use a CGM

A

-patients on intensive insulin therapy
-patients prone to hypoglycemia
-children as young as 2
-insurance coverage patients

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45
Q

How often should a fingerstick be if a patient is on non-insulin therapy only

A

3x/wk up to 2x qd

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46
Q

How often should a fingerstick be if a patient is on insulin therapy

A

qd up to 4x qd

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47
Q

How often should a fingerstick be if a patient has multiple daily injection insulin

A

4-6x qd

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48
Q

What is hemoglobin A1C

A

-represents percentage of total hemoglobin that has been glycosylated
-estimated average glucose over 3 months

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49
Q

How often to check a patient’s A1C if they are at goal compared to not at goal

A

goal: 6 months
not: 3 months

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50
Q

Limitation of A1C

A

-does not reflect change in blood sugar
-impacted by anything that impacts erythrocyte turnover
-does not show full tory regarding glucose excursions

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51
Q

Alternative glucose goals who fits this criteria

A

-patient w/ limited life expectancy and significant functional and cognitive impairments (A1C <8%)
-Young children
-Pregnant patients
-Patient w/ significant hypoglycemia - TIR >50%, TBR <1%

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52
Q

What is diabetic ketoacidosis (DKA)

A

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

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53
Q

What is the triad in DKA

A

hyperglycemia
anion gap metabolic acidosis
ketosis

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54
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

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55
Q

What are the 5 results of insulin deficiency results

A

hyperglycemia
glycogen catabolism
glycogen depletion
lipolyis
ketosis

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56
Q

What is the main result of hyperglycemia

A

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

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57
Q

What are the 4 ketosis results

A

anion gap metabolic acidosis
compensatory alkalosis
hypotension
shock

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58
Q

What are the diabetic ketoacidosis clinical course effects

A

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

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59
Q

Diagnostic criteria for DKA

A

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

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60
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 id 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

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61
Q

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

A

> 3.3

62
Q

When to give dextrose in DKA treatment

A

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

63
Q

When to use bicarb in DKA treatment

A

not recommended
could use when pH <6.9

64
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

65
Q

HHS diagnostic criteria

A

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

66
Q

Treatment for HHS

A

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

67
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

68
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

69
Q

Primary problems in DKA and HHS

A

DKA: acidosis
HHS: dehydration

70
Q

Key things to look for in DKA and HHS

A

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

71
Q

Primary treatment strategies for DKA and HHS

A

IV fluids, IV insulin, IV potassium

72
Q

Monitoring for DKA and HHS

A

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

73
Q

What is the correct sodium equation

A

Measured Na + (1.6*glucose -100)/100

74
Q

Difference between hyperglycemia and hypoglycemia

A

hyper: not enough insulin, too much glucagon
hypo: not enough glucagon, too much insulin

75
Q

Risk factors for hypoglycemia

A

increased age
skip meals
exercise/weight loss
illness
alcohol ingestion
CKD
dementia

76
Q

Medications that cause hypoglycemia

A

insulin
sulfonylureas (glyburide mainly)
beta-blockers
fluoroquinolone antibiotics (cipro, levofloxacin)

77
Q

Difference between level 1 and level 2 hypoglycemia

A

Level 1: BG <70
Level 2: BG <54

78
Q

Signs and symptoms of hypoglycemia

A

hunger
paleness
fatigue
rapid heartbeat
irritability
sweating/shaking

79
Q

Severe hypoglycemia

A

loss of consciousness
seizures
coma
death

80
Q

Beta blockers can mask hypoglycemia except for what symptom

A

sweating
(they inhibit hepatic glucose production and reduce glycogenolysis)

81
Q

Relative hypoglycemia

A

-person w/ diabetes has symptoms of hypoglycemia despite >70 BG
-occur in chronic elevated BG
-hard to achieve optimal glucose control
-no harm to patient
-treat like hypoglycemia due to discomfort

82
Q

Prevention of hypoglycemia

A

patient education
setting patient-specific glycemic targets
frequent monitoring of glucose levels
flexible and rational regimens for insulin and other drugs

83
Q

How to treat inpatient conscious and inpatient unconscious hypoglycemia

A

inpatient conscious: oral meds
inpatient unconscious: IV access

84
Q

Outpatient conscious rule of 15 (hypoglycemia)

A

15 g fast acting carbs
check BS after 15 min
If <70 repeat step 1 and 2
once >70 eat a meal with protein or fiber

85
Q

Examples of 15 g of fast-acting carbs

A

4 oz of regular pop
hard candies
1 tbsp sugar
1 dose glucose gel
3-4 glucose tablets

86
Q

Outpatient unconscious treatment

A

intranasal 3 mg
prefilled syringe 1 mg
reconstituted powder kit 1 mg
call 911 or drive them to hospital

87
Q

Inpatient unable to take oral with and without IV access treatments

A

no IV: glucagon
IV: 25 g of 50% dextrose IV

88
Q

What is the first phase of glucose homeostasis

A

lasts few minutes -> small readily releasable pool of ganules
release in response to nutrients and non-nutrients secretagogues

89
Q

What is the second phase of glucose homeostasis

A

sustained second phase -> exclusive by nutrients

90
Q

When you eat what happens to your glucose levels

A

rapid burst of insulin at mealtimes and then it slowly falls back to basal levels (basal insulin between meals)

91
Q

Insulin secretion by exocytosis

A

-glucose transport by beta cells by GLUT transporter
-glucose metabolism -> produce ATP -> K+ channels close
-depolarization of beta cells -> increase Ca2+ and activate exocytosis (insulin secreted)

92
Q

What are the positive effects of insulin

A

glycogenesis
lipogenesis
active transport of glucose in muscle and adipose cells
glycolysis
protein synthesis

93
Q

What are the negative effects of insulin

A

lipolysis
gluconeogenesis
protein catabolism
glycogenolysis

94
Q

What are the three target tissues of insulin

A

liver
skeletal muscle
adipose tissue

95
Q

What are the main effects of insulin

A

decrease glucose production and increase glucose uptake and utilization by tissues

96
Q

Insulin replacement

A

-mimic secretory pattern of nondiabetic pancreas
-control basal and postprandial glucose levels
-minimize risk of hypoglycemia

97
Q

Insulin preparations differ by what

A

amino acid sequence
onset of action
peak for max impact
duration of action
solubility

98
Q

Insulin routes of administration

A

intramuscularly, IV, nasally
long term subQ or infusion
no oral (low bioavailability)

99
Q

Factors affecting absorption of insulin

A

site of injection
type of insulin
SubQ blood flow
regional muscular activity
insulin volume and concentration

100
Q

Recombinant human insulin has a ____ ______ of 30-60 minutes

A

30-60

101
Q

Since regular insulin levels are peaks are later than normal insulin made by the body there is elevated insulin after glucose has decreased causing what

A

delayed hypoglycemia

102
Q

Insulin ______ are biologically active

A

monomers
(delate in absorption triggers the development of insulin analogs, zinc takes dimers and forms hexamers)

103
Q

Human insulin analogs are made to provide a more _________ insulin profile and reduce the risk of ____________

A

physiologic
hypoglycemia

104
Q

Modifications of insulin are made to prevent _______ formation or dissociate ______ faster causing a faster onset and shorted duraction of action

A

hexamer
hexamer

105
Q

What are the 3 rapid insulins that decrease self association (decrease hexamer formation)

A

lispro (humalog)
aspart (novolog)
gluisine (aprida)

106
Q

Rapid acting insulin analogs

A

-rapid onset
-short duration of action -> decrease hypoglycemia risk
-lyumjev is the fastest
-control of blood glucose during meals and snacks

107
Q

Intermediate acting insulin analogs

A

-NPH = neutral protamine hagedorn
-onset delayed by combining native insulin with protamine (tissue enzyme degrades this) and zinc
-dissolves more slowly causing slow absorption and long duration
-can control glucose overnight, fasting, and meals, combo with short-acting insulin

108
Q

Long acting insulin analogs

A

-mimic basal insulin release -> no peak
-prolonged absorption
-need combo with something else

109
Q

What does lantus and tresiba do (long acting insulin)

A

tresiba -> bind to albumin through lipid additions slow distributions to peripheral tissues
lantus aggregates are neutral pH -> do not mix w/ short acting, stabilization of hexamers

110
Q

Adverse effects of insulin

A

common: hypoglycemia and weight gain
rare:
-hypertrophy (lipoatrophy)
-hypersensitivity reactions (swelling, heat, allergy to insulin, immune resistance causing circulation of anti-insulin antibodies)

111
Q

Decreased hypoglycemic effect of insulin

A

albuterol, diuretics, diltiazem, epi, estrogen, corticosteroids, terbutaline, thyroid estrogen

112
Q

Increase hypoglycemic effect of insulin

A

oral diabetic agents, beta-blockers, sulfonamides, clonidine, fluoxetine, alcohol, anabolic steroids

113
Q

Insulin binding to the receptor causes a cascade of events including PI3K or PKB resulting in the release of _________

A

GLUT 4

114
Q

How many amino acids is in the A and B chain of insulin

A

A has 21
B had 30

115
Q

The disulfide linkages in insulin provide chemical _________ to the structure

A

stability

116
Q

The biosynthesis of insulin occurs in the _____ cells of the pancreas from preproinsulin

A

beta

117
Q

Proinsulin is more ______ than insulin with the addition of amino acids arg, arg, lys, and arg

A

basic

118
Q

What enzyme catalyzes the cleavage of a dipeptide segment of the amino acid connector C-chain in proinsulin

A

prohormone convertases PC 1and 2

119
Q

Only the insulin ______ is able to react with the insulin receptors and is the only readily absorbable form

A

monomer

120
Q

True or False: Zinc takes dimers and creates hexamers

A

true (store insulin in beta cells)

121
Q

Insulin molecules can form dimers due to _______ bonding

A

hydrogen

122
Q

Storage of insulin at neutral pH leads to __________ reaction

A

deamidation

123
Q

Insulin analogues are classified according to their what two factors

A

rate of onset
duration of action

124
Q

Modifications of rapid-acting insulin analogues do not form ______ in solution and dissociate immediately into ______ producing a very quick onset of action

A

dimers
monomers

125
Q

Intermediate-acting insulin is prepared by combining regular insulin and zine in an ______ buffer

A

acetate

126
Q

The isoelectric point of insulin glargine is 7 causing an _____ precipitation on SC and decreased absorption rate

A

increase

126
Q

Insulin degludec has a long duration of action due to what two things

A

formation f soluble multihexamer
hexadecanoic acid side chain binding to albumin

126
Q

Insulin Glargine is more ________ causing it to be soluble in acidic formation but ________ solubility at physiological pH

A

acidic
decrease

126
Q

What are the indications of temporary use of insulin therapy

A

pregnancy
stress/surgery/hospitalization
short term steroids

127
Q

When is basal and bolus insulin doses

A

basal: once daily except for NPH
bolus: meals and bedtime
(all type 1 patients need both)

128
Q

How often do you change an insulin pump

A

q3 days

129
Q

When to use insulin therapy in Type 2 patients

A

when NI’s are no longer effective
use in combo with NIs to simplify and max treatment (add basal first)

130
Q

How to dose new start and insulin only patients

A

0.5 units for low BMI or Type 1
1 unit for high BMI, Type 2, illness, ketosis, stress, growth
70% basal and 30% bolus
divide bolus by meals a day

131
Q

How to dose new start and basal added to NI

A

start low, go slow
20% of body weight (kg)

132
Q

1700 rule defn

A

gives number of mg/dl your BS will drop with 1 unit of SHORT acting insulin

133
Q

How to calculate 1700 rule

A

1700/TDD = ISF
(Current BS - Target BS) / ISF = units needed

134
Q

On average 1 unit short acting insulin covers how many carbs

A

15 grams

135
Q

How to calculate carb counting for insulin

A

500/TDD = # of gm of CHO covered by 1 unit of insulin

136
Q

Common adverse effects of biguanides

A

diarrhea
GI upset

137
Q

What are the biguanides generic and brand names

A

Metformin (glucophase, fortamet)

138
Q

Common adverse effects of sulfonyureas

A

hypoglycemia and weight gain

139
Q

What are the sulfonylureas generic and brand names

A

Glipizide (glucotrol)
Glimepiride (amaryl)
Glyburide (micronase, diabeta)

140
Q

Common adverse effects of GLP-1 RAs

A

nausea

141
Q

What are the GLP-1 RA generic and brand names

A

Liraglutide (victoza, saxenda)
Semaglutide (ozempic, rybelsus, wegovy)
Dulaglutide (trulicity)
Tirzepatide (mounjaro)

142
Q

Common adverse effects of DPP-IV I

A

not really anything maybe upper respiratory tract infections

143
Q

What are the DPP-IV I generic and brand names

A

Sitagliptin (januvia)
Saxagliptin (onglyza)
Linagliptin (tradjenta)
Alogliptin (nisena)

144
Q

Common adverse effects of SGLT-2 I

A

genitourinary infections

145
Q

What are the SGLT-2 generic and brand names

A

Canagliflozin (invokana)
Dapagliflozin (farxiga)
Empaglifozin (jardiance)
Ertuglifozin (steglatro)
Bexagliflozin (brenzavvy)

146
Q

What are the basal insulins

A

lantus
basaglar
toujeo
semglee
tresiba
NPH

147
Q

What are the bolus insulins

A

regular
humalog
novolog
apidra
fiasp

z S1: Module (8 decks)

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