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Clin Med I - Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What are the two functions of the pancreas?

A
  • endocrine gland produces hormones

- exocrine gland secretes pancreatic juices for digestion

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2
Q

What hormones are produced by the pancreas endocrine gland?

A
  • insulin

- glucagon

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3
Q

What is the functional unit of the pancreas endocrine gland?

A
  • islets of Langerhans
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4
Q

What cells make up the islet of Langerhans?

A
  • alpha
  • beta
  • delta
  • gamma
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5
Q

What do alpha cells secrete?

A
  • glucagon
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6
Q

What do beta cells secrete?

A
  • insulin
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7
Q

What doe delta cells secrete?

A
  • somatostatin
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8
Q

What do gamma cells secrete?

A
  • pancreatic polypeptide
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9
Q

What stimulates the secretion of insulin?

A
  • high glucose levels
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10
Q

What is insulins mechanism of action?

A
  • drives glucose into the cell via binding to Glut 4 transporters
  • inhibits glucagon
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11
Q

What stimulates glucagon secretion?

A
  • low glucose levels
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12
Q

What occurs to make glucagon secretion?

A
  • liver glycogenolysis (breakdown of glycogen to glucose)
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13
Q

What is the relationship between insulin & glucagon?

A
  • inverse/neg feedback
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14
Q

What cells take up glucose?

A
  • skeletal
  • cardiac
  • liver
  • adipose
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15
Q

Summarize DM

A
  • increased blood glucose levels during day
  • overall insufficient/absent insulin
  • fat, muscle, & liver unable to uptake circulating blood glucose
  • lack of glucagon inhibition d/t low insulin
  • body in “starvation mode” triggers alternative energy source
  • stimulates gluconeogenesis, glycogenolysis & lipolysis
  • results in increased FFA/ketoacidosis
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16
Q

What are the counterregulatory hormones?

A
  • glucagon

- catecholamines (i.e. E, NE, cortisol, & GH)

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17
Q

What stimulates glucagon secretion?

A
  • low glucose/hypoglycemia

- strenuous exercise

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18
Q

What inhibits glucagon secretion?

A
  • high glucose
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19
Q

What is glucagons role in the liver?

A
  • gluconeogenesis
  • glycogenolysis
  • glycolysis
  • lipolysis
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20
Q

What occurs as a result of lipolysis?

A
  • stimulates ketogenic effect

- increased acidiv enviornment/ketoacidosis

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21
Q

What is responsible for symptoms of hypoglycemia?

A
  • E
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22
Q

When _____ & _____ fail to adequately raise blood glucose levels, the body releases _____ & _____ which also work to increase blood glucose.

A
  • E & glucagon

- cortisol & GH (potent)

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23
Q

Define DM

A
  • hyperglycemia d/t inability to produce insulin, insulin resistance, OR both
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24
Q

Define DM type I

A
  • hyperglycemia d/t an absence or deficiency of insulin

- beta cell destruction ==> inability to produce insulin

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25
Q

Define DM type II

A
  • combination of insulin receptor abnormalities AND inadequate insulin secretion to compensate
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26
Q

What is DM’s rank on the list of causes of deaths worldwide?

A
  • 5th
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27
Q

At which age does DM type I most commonly present?

A
  • <30 y/o

- peak incidence during preschool & pre-puberty

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28
Q

What is the etiology of DM type I?

A
  • autoimmune
  • genetic
  • environmental (hx resp infx in infants)
  • diet (? cows milk)
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29
Q

Describe the physiology of DM type I

A
  • susceptibility gene on HLA region on chromosome 6
  • triggers autoimmune destruction of beta cells
  • loss of insulin producing beta cells leads to insulin deficiency
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30
Q

What type of immune response in DM type I?

A
  • Tcell mediated autoimmune attack
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31
Q

What antibodies are present in DM type I?

A
  • ICA
  • IAA
  • GAD
  • tyrosine phosphatases (IA2 & IA2-B)
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32
Q

How can antibody levels help patients?

A
  • screen sibilings
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33
Q

At what point does a DM type I become symptomatic?

A
  • 80=90% beta cell destruction
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34
Q

What is the clinical presentation of DM type I?

A
  • 3 P’s (polyuria, polyphagia, polydipsia)
  • unexplained wt loss
  • ketonemia
  • ketonuria
  • fatigue
  • nausea
  • blurred vision
  • paresthesia
  • hypotension/orthostatic hypotension
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35
Q

Define polyuria

A
  • increased spilling of glucose in urine
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36
Q

Define polydipsia

A
  • increased plasma hyperosmolality
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37
Q

Define polyphagia

A
  • increased appetite
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38
Q

What are the values for fasting blood glucose?

A
  • normal: 70-100mg/dL
  • prediabetes: 100-125mg/dL
  • diabetes: >126mg/dL
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39
Q

What are the blood glucose values 2hs s/p eating?

A
  • normal: 200mg/dL
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40
Q

What are the values for a random blood glucose?

A
  • normal: 70-140mg/dL

- diabetes: >200mg/dL

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41
Q

What are the values for OGTT?

A
  • prediabetes: 140-199mg/dL

- diabetes: >200mg/dL

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42
Q

What can a urine dipstick test detect?

A
  • glucose
  • ketone
  • albumin
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43
Q

Define HbA1c

A
  • % Hb coated with glucose
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44
Q

What are the values of HbA1C?

A
  • normal: < 5.7%
  • risk of DM: 5.7-6.4%
  • DM: > 6.5%
  • goal for DM: <7%
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45
Q

Besides specific glucose tests, what should be ordered for DM pts?

A
  • lipid panel
  • renal function
  • EKG
  • peripheral pulse check
  • neuro, pod, & optho consults
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46
Q

What are the primary goals of DM type I tx?

A
  • prevent acute illness

- prevent long term complications

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47
Q

What does it mean to prevent long term complications?

A
  • microvascular complications

- macrovascular complications

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48
Q

What are microvascular complications?

A
  • nephropathy
  • neuropathy
  • retinopathy
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49
Q

What are macrovascular complications?

A
  • CAD
  • peripheral arterial disease
  • stroke
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50
Q

What are the types of insulin preparations?

A
  • ultra short/rapid
  • short/regular
  • intermediate
  • long
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51
Q

What are the rapid acting insulin preparations?

A
  • lispro (Humalog)

- aspart (NovoLog)

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52
Q

Discuss the use of rapid acting insulin

A
  • 5-15m prior to a meal
  • eat soon after injx
  • flexible dosing schedule
  • used with long or intermed insulin
  • subQ
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53
Q

What is a common side effect of rapid acting insulin?

A
  • hypoglycemia
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54
Q

What are the regular acting insulin preparations?

A
  • Humulin R

- Novolin R

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55
Q

Discuss the use of regular insulin preparations

A
  • 30m prior to a meal

- IV

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56
Q

What are the intermediate acting insulin preparations?

A
  • NPH (Humilin, Novolin)
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57
Q

Discuss the use of intermediate insulin

A
  • BID b/t meals

- combo with regular or lispro for tighter glucose control

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58
Q

What are the long acting insulin preparations?

A
  • glargine (Lantus)

- detemir ( Levemir)

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59
Q

What are long actin insulins best for?

A
  • basal coverage
60
Q

Discus long acting insulin use

A
  • combo with rapid acting
  • given at bedtime
  • less nocturnal hypoglycemia
61
Q

What is the preferred insulin therapy regiment?

A
  • ultrashort with long
62
Q

Why is self-monitoring required?

A
  • essential to achieve tight glycemic control
63
Q

What is the secondary line of tx for DM type I?

A
  • diet
64
Q

What is the primary line of tx for DM type II?

A
  • diet
65
Q

Why is exercise important in DM?

A
  • improves utilization of CHO & lipids
66
Q

What is a concern of DMs exercising?

A
  • predispose them to hypoglycemic episodes so start slow, check glucose, take in extra carbs, reduce insulin prior to starting
67
Q

What is the surgical intervention for DMs?

A
  • pancreas transplant
68
Q

What are the glucose level goals for DM?

A
  • preprandial & after night fast: 90-130mg/dL
  • 1hr postprandial: 180mg/dL
  • 2 hr post prandial: 150mg/dL
  • HbA1C: <7% or 8% w/ hx of hypoglycemia, short life expect, elderly, CVD, many co-morbidities
69
Q

What is a serious concern with insulin therapy?

A
  • hypoglycemia (blood glucose < 54mg/dL)
70
Q

What is stimulated at blood glucose < 54mg/dL?

A
  • ANS

i. e. tachycardia, palpitations, sweating, tremulousness, nausea, hunger

71
Q

What is stimulated at blood glucose < 50mg/dL?

A
  • neuroglycopenic

i. e. difficulty speaking, irritability, blurred vision, H/A, tiredness

72
Q

What are the treatments for insulin induced hypoglycemia?

A
  • simple sugar (IV bolus 50% or tabs dextrose)

- glucagon (1mg ampule IM or SC)

73
Q

What can patients with DM develop?

A
  • insensitivity to hypoglycemia
74
Q

How does insensitivity to hypoglycemia develop?

A
  • counterregulatory hormones fail to respond
  • loss of ability to secrete glucagon
  • repeated episodes of hypoglycemia leads to blunted E response
75
Q

What is the treatment for hypoglycemia insensitivity?

A
  • allow a few weeks of higher glucose levels to recalibrate ANS
76
Q

What are the 3 pre-breakfast hyperglycemias?

A
  1. Waning effect
  2. Dawn phenomenon
  3. Somogyi effect
77
Q

Define Waning effect

A
  • waning levels of circulating insulin at night leads to hyperglycemia
78
Q

Define Dawn phenomenon

A
  • decreased tissue sensitivity to insulin during the night
79
Q

Define Somogyi effect

A
  • nocturnal hypoglycemia which triggers counterregulatory hormones
    i. e. pt takes insulin but doesn’t eat a bedtime snack
80
Q

Describe the body changes that occur during sleep cycle

A
  • b/t 3a-8a, increase amount of counterreg hormones
  • counterreg hormones work against insulin
  • increased release of counterreg hormones when bedtime insulin is wearing out leads to prebreakfast hyperglycemia
81
Q

What is a complication of DM type I?

A
  • diabetic ketoacidosis (DKA)
82
Q

Describe the pathophysiology of DKA

A
  • lack of insulin
  • elevated glucagon
  • lipolysis
  • cerebral edema in severe cases
83
Q

What are the symptoms of DKA?

A
  • n/v
  • thirst/polyuria
  • abd pain
  • dyspnea
84
Q

What are the physical findings of DKA?

A
  • tachycardia
  • dehydration/hypotension
  • tachypnea/kussmal resp/fruity breath
  • lethargy/ obtundation/ cerebral edema/coma
85
Q

What are the labs of DKA?

A
  • glucose: 350-900mg/dL
  • blood pH: 6.9-7.2
  • serum bicarb: <15mEq/L
  • ketonemia
  • hyperkalemia (5-8mEq/L)
86
Q

What is the tx of DKA?

A
  • restore plasma vol & tissue perfusion via IV fluids
  • reduce blood glucose & osmolality via regular insulin IV
  • correct acidosis & replenish electrolytes via bicarb tx
  • ID & tx precipitating factors
87
Q

Define DM type II

A
  • metabolic disorder that is characterized by hyperglycemia d/t insulin resistance & relative lack of insulin
88
Q

What is the etiology of DM type II?

A
  • obese/overweigh
  • lack of physical activity
  • poor diet
89
Q

What are the risk factors for DM type II?

A
  • > 45 y/o
  • > 120% desirable body weight
  • increased hip:waist
  • (+) family hx in a 1st deg relative
  • hx of impaired glucose tolerance test or fasting glucose
  • HTN
  • dyslipidemia
  • hx of gestational diabetes
  • genetics
  • secondary diabetes
90
Q

What is the pathophysiology of DM type II?

A
  • body produces insulin but cell receptors have decreased sensitivity to insulin’s action
  • beta cells continue to secrete insulin –> hyperinsulinemia
  • overtime, beta cells fail –> decreased insulin
91
Q

How do many DM type II’s remain asymptomatic?

A
  • pancreas is able to keep up with body’s insulin requirement and keeps blood glucose in normal range
92
Q

What does constant state hyperglycemia + lack of insulin cause?

A
  • stimulates glucagon secretion & hyperglucagonemia as a way to supply “starving” cells with fuel via gluconeogenesis
93
Q

What is the onset of DM type I v. II?

A
  • I: sudden

- II: gradual

94
Q

What is the age at onset of DM type I v. II?

A
  • I: mostly in children

- II: mostly in adults

95
Q

What is the body habitus of DM type I v. II?

A
  • I: thin or normal

- II: often obese

96
Q

Is ketoacidosis more common in DM type I or II?

A
  • I: common

- II: rare

97
Q

Are antibodies present in DM type I or II?

A
  • usually present in I

- absent in II

98
Q

What is the level of endogenous insulin for DM type I & II?

A
  • low or absent in I

- normal, increased, or decreased in II

99
Q

What is the clinical presentation of DM type II?

A
  • initially asymptomatic
  • 3 P’s
  • fatigue
  • blurred vision
  • neuropathy
  • yeast/fungal infx
  • CVD
  • dyslipidemia
  • poor wound healing
  • acanthosis nigricans
100
Q

What is the diagnostic criteria for DM type II?

A 
- FPG > 126mg/dL (repeated 2x)
OR
- HbA1C >6.5% (repeated 2x)
- 2hPG >200mg/dL after a 75g OGTT
- random PG > 200mg/dL in pt w/ classic sx
101
Q

What are the glucose treatment goals for DM?

A
  • blood glucose near normal

- HbA1C < 7%

102
Q

What are the initial tx options for DM type II?

A
  • low CHO, low fat, CHO counting

- smoking cessation

103
Q

What is step 1 of DM type II tx?

A
  • metformin + life changes
104
Q

What is step 2 of DM type II tx?

A
  • add insulin or other oral antihyperglycemics
105
Q

What are the medications for DM type II tx?

A
  • biguanides
  • sulfonylureas
  • meglitinide derivatives
  • alpha-glucose inhibitors
  • TZDs
  • GLP-1
  • DPP-4 inhibitors
  • SGLT-2 inhibitors
106
Q

What is the first medication started for a newly dx’d DM type II?

A
  • biguanides (metformin)
107
Q

What is the MOA of biguanides?

A
  • decreases hepatic gluconeogenesis production
  • decreases intestinal absorption of glucose
  • improves insulin sensitivity
  • lowers basal & postprandial PG levels
108
Q

What are examples of sulfonylureas?

A
  • glyburide
  • glipizide
  • glimepiride
109
Q

What is the 2nd medication given to a type II DM patient?

A
  • sulfonylureas
110
Q

What is the MOA of sulfonylureas?

A
  • insulin secretagogues

- stimulates insulin release from beta cells

111
Q

What is a common side effect of sulfonylureas?

A
  • hypoglycemia
112
Q

What is the MOA of meglitinide derivatives?

A
  • short acting insulin secretagogues
113
Q

uncontrolled DM type II patient is on biguanide (metformin) with sulfonylurea allergy, what is the next tx?

A
  • meglitinide derivatives
114
Q

What is the MOA of alpha-glucosidase inhibitors?

A
  • delay sugar absorption
115
Q

What is the last resort of DM type II tx?

A
  • TZD
116
Q

What are examples of TZDs?

A
  • pioglitazaone (Actos)

- rosiglitazone (Avandia)

117
Q

What is the MOA of TZDs?

A
  • insulin sensitizers
  • increase insulin cellular transport
  • decrease tryglyceride
  • increase HDL level
118
Q

What patient population are TZDs contraindicated and why?

A
  • advanced CHF

- wt gain & fluid retention

119
Q

What is an example of GLP-1?

A
  • exenitide
120
Q

What is the MOA of GLP-1?

A
  • glucagon like peptide -1
  • increases insulin response to glucose
  • increases insulin sensitivity
  • decreases glucagon
121
Q

What is the MOA of DPP-4?

A
  • dipeptidyl-peptidase-4

- inactivates GLP1

122
Q

What is an example of DPP-4 inhibitor?

A
  • sitagliptin
123
Q

What is the EFFECT of DPP-4 INHIBITOR?

A
  • prolongs GLP-1 action
124
Q

What is the MOA of SGLT-2?

A
  • inhibit glucose reabsorption in the proximal tubule
  • increased glycosuria
  • decreased hyperglycemia
125
Q

What are examples of SGLT-2s?

A
  • Invokana (canagliflozin)

- Farxigan (dapagliflozin)

126
Q

What are side effects of SGLT-2s?

A
  • volume contraction from glycosuria & hypotension

- UTIs

127
Q

What type of insulin is used to start patients on insulin therapy?

A
  • basal or intermediate
128
Q

What is hyperosmolar hyperglycemic state?

A
  • HHS

- relative insulin deficiency

129
Q

What does HHS lead to?

A
  • volume depletion

- hemoconcentration

130
Q

What are the risk of complications of HHS?

A
  • coma

- death

131
Q

What distinguishes DKA from HHS?

A
  • level of acidosis
132
Q

What is the tx for HHS?

A
  • IV fluids
  • insulin
  • manage underlying conditions
133
Q

What are the long term microvascular complications of both types DM?

A
  • retinopathy
  • neuropathy
  • nephropathy
  • HTN
134
Q

What are the long term macrovascular complications of both types of DM?

A
  • CAD
  • cerebrovascular disease
  • peripheral vascular disease
135
Q

What ocular diseases can occur from DM?

A
  • diabetic cataracts

- diabetic retinopathy (non-proliferative & proliferative)

136
Q

What distribution will diabetic neuropathy present as?

A
  • glove & stocking
137
Q

How are diabetic neuropathy sx alleviated?

A
  • improved glycemic control

- foot protection & inspection

138
Q

What is the tx of peripheral neuropathy?

A
  • TCA (tricyclic antidepressants)
139
Q

How is diabetic nephropathy diagnosed?

A
  • urine spot >30-300mcg/mg (microablunuria)
140
Q

What is the treatment of diabetic nephropathy?

A
  • hemodialysis

- HTN control

141
Q

What is the tx of diabetic HTN?

A
  • ACE inhibitors

- ARBs

142
Q

Why are ACE inhibitors or ARBs given to patients w/o HTN?

A
  • renal protective characteristics
143
Q

What is the tx of CAD/cerebrovascular/PVD?

A
  • control HTN
  • ASA
  • statins
144
Q

What are patients with both PVD & peripheral neuropathy at risk for?

A
  • diabetic foot ulcers, poor wound healing
  • gangrene
  • digit/limb amputation
145
Q

What is diabetic foot ulcer/Charcots Foot?

A
  • d/t periarticular fx & obesity
  • decreased foot sensitivity to pain and pressure
  • osteoclastic activity
146
Q

What is the tx of Charcots Foot?

A
  • mechanical unloading
  • wound tx
  • abx
  • debridement

Clin Med I - Endocrine (6 decks)

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