Pathophysiology 5 Flashcards

1
Q

Islet, Alpha cell

A

glucagon

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2
Q

islet, beta cell

A

insulin + amylin

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3
Q

islet, delta cell

A

somatostatin

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4
Q

Modifiable Causes of Diabetes

A

1) Weight/BMI
2) Central Obesity
3) Sedentary Lifestyle

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5
Q

Non-modifiable Causes of Diabetes

A

1) Age
2) Ethnicity
3) Genetics

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6
Q

Structure of Human Proinsulin

A

-one continuous polypeptide
1) C-peptide
2) A-chain
3) B-chain
A & B chain are insulin hormone, must be broken down to be activated

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7
Q

Connecting Peptide

A
  • different than C-peptide
  • have 2 Arg on 1 end and 1lys 1 arg on other end
  • not an active form
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8
Q

What are A and B chain joined by?

A

di-sulfide bonds

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9
Q

How many disulfide bonds in proinsulin?

A

3

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10
Q

How active is proinsulin?

A

1/10 as active as insulin

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11
Q

What converts pro insulin to insulin?

A

-protein synthesis

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12
Q

Biosynthesis of Insulin

A

AAs
DNA
RNA (messenger to transfer)
then peptide

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13
Q

What stimulates glucagon?

A
  • amino acids

- GIP, VIP

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14
Q

What stimulates insulin?

A
  • glucose
  • gastrin
  • FFA
  • secretin
  • gut glucagon
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15
Q

What does glucagon do?

A

-protects from hypoglycemia

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16
Q

How is Blood Glucose gotten rid of?

A
  • Fat synthesis
  • Oxidation
  • Muscle glycogen (then can go to lactic acid then hepatic glycogen)
17
Q

Gluconeogenesis

A

-production of glucose from non-carbohydrate precursor

18
Q

GLP-1

A

“glucagon like peptide”

  • secreted upon the ingestion of food
  • Beta cell is enhanced by glucose-dep insulin secretion
  • Alpha cell: dec. postprandial glucagon secretion
  • Liver: dec. glucagon reduces hepatic glucose output
  • Stomach: helps regulate gastric emptying
  • promotes satiety and reduces appetite*
19
Q

GLP-1 administration

A

-oral only

NOT IV

20
Q

How is diabetes diagnosed?

A

1) normally fasting blood sugar < 5.7%
2) impaired 126mg/dl 2 hr sample >200
Hem A1c >6.5%

21
Q

How many people does diabetes effect?

A

-25.8 million people
8.3% US population
7 million of 25.8 not undiagnosed

22
Q

Is diabetes related to obesity?

A

yes

23
Q

Mortality of Diabetes

A
  • 72,000 in 2006 direct
  • 233,000 in 2005 linked as contributing cause
  • leading cause of new blindness, chronic renal failure leading to dialysis and non-traumatic amputations
24
Q

Characteristics of Type 1 DM

A
age: less than 40
~10% of all diabetes
fall and winter
-acute or subacute
-frequent metabolic ketoacidosis
-uncommon obesity
-decreased beta cells
-decreased/absent insulin
inflammatory cells in islets are present initially
25
Q

Characteristics of Type 2 DM

A
age: greater than 40
~90% of all diabetes 
-no seasonal trend
-slow or subacute 
-common obesity
-rare metabolic ketoacidosis
-absent inflammatory cells in islets 
-common family history
-90-95% concordance in identical twins
-no HLA association
-uncommon to have abs to islet cells or insulin
26
Q

Diagnostic Criteria in Diabetic Ketoacidosis

A

-arterial pH and bicarb is distinguishing feature
-pH7.25-250
-bicarb 15 - <10
positive urine/serum ketone
anion gap of 10-12
alert to stupor/coma

27
Q

Typical total body defect of water and electrolytes in Diabetic Ketoacidosis (DKA)

A

-

28
Q

Diagnostic Criteria in Hyperglycemic Hyperosmolar State (HHS)

A
Plasma glucose >600mg/dl
pH >7.3
bicarb >15
small urine/serum ketone
serum osmolality >320mOsm/kg
variable anion gap
mental status is stupor/coma
29
Q

Typical total body defect of water and electrolytes in HHS

A

-

30
Q

Factors in Development of DKA

A

-infection
-new-onset diabetes
-discontinued insulin
unknown/

31
Q

Factors in Development of HHS

A

-infection
-new-onset diabetes
unknown/

32
Q

Hormone of fed state

A

insulin

33
Q

Hormone of fasting state

A

counter regulatory hormone

34
Q

Serum Osmolality Calculation

A

-

35
Q

Pathophysiology of DKA

A

1) Adipose Tissue - released FFA

2) Liver: increased ketogenesis

36
Q

Pathophysiology of HHS

A

1) Liver- increased hepatic glucose production

2) Peripheral tissue - decreased glucose utilization