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Endorine > Type 1 Diabetes > Flashcards

Type 1 Diabetes Flashcards

1
Q

What are the 4 cell types of the islets?

A
  1. Beta (60-80%)
  2. Alpha (20-30%
  3. Delta (somatostatin, suppresses insulin and glucagon)
  4. Pancreatic polypeptide (unknown fxn)
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2
Q

What inc risk of CV dis do you have with diabets?

A

2-4X inc risk

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3
Q

Describe the processes of insulin processing

A
  1. Insulin is synth as inactive precursor form (preproinsulin)
  2. A signal sequence is removed from preproinsulin following insertion into the endoplasmic reticulum, resulting in proinsulin
  3. Proinsulin is further processed to form insulin and a byproduct C peptide, both of which are packaged into secretory vesicles (proteolytic cleavage by trypsin, chymotrypsin–>removal of basic AAs)
  4. Mature insulin is comprised of an A and B peptide chain, linked together by two disulfide bonds
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4
Q

What kind of hormone is insulin?

A

Peptide hormone

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5
Q

What does insulin do?

A

Key anabolic hormone critical for glucose uptake and utilization, lipid and protein synth, and an essential growth factor for normal development

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6
Q

What needs to be intact for insulin to do all of its jobs?

A
  • Islet b cell mass
  • insulin synthesis
  • glucose-dep insulin secretion
  • insulin signaling at target cells
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7
Q

What is often used to measure endogenous insulin production?

A

Amount of C peptide (which was cleaved during to production of insulin)

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8
Q

What is the turnover rate of insulin?

A

2-4hrs

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9
Q

What is amylin?

A

Amylin (IAPP) is a substance also in secretory granules with insulin, proinsulin, proteolytic enzymes and Zn. It inhibits glucagon secretion after a meal. In diabetics, there is less amylin and therefore inc glucagon concentrations

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10
Q

What 3 things are stimulatory for insulin secretion?

A
  1. Nutrient load (glucsoe the most, but fat and protein also stimulate its release)
  2. Autonomic NS (vagus–>stim, sympathetic–>Inhibits and cephalic phase–>stim)
  3. Hormones (GLP-1 and GIP gut hormones stim)
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11
Q

What 2 things inhibit insulin secretion?

A
  1. Starvation/hypoglycemia

2. Hormones (glucagon, epinephrine, growth hormone, cortisol)

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12
Q

How does glucose work to regulate insulin secretion?

A

Directly and by augmenting the action of other insulin secretagogues

A rise in blood glucose levels causes an immediate release of insulin from granules. If the secretory stimulus persists, a delayed response follows causing more insulin to be produced.

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13
Q

What other agents regulate normal insulin metab?

A

GLP1, leucine, arginine, sulfonylureas stim inuslin reslease

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14
Q

What is insulin necessary for?

A
  • Transmembrane transport of gluc and AAs
  • Glycogen formation in the liver and skeletal muscles
  • Glucose conversion to TGs
  • Nucleic acid synth
  • Protein synth

-Principle fxn is to inc rate of glucose transport into striated muscle cells

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15
Q

How are type 1 and type 2 different in their insulin production?

A

T1: absolute insulin def
T2: insulin resistance with relative insulin deficiency

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16
Q

How are type 1 and type 2 different in their onset of symptoms?

A

T1: Abrupt onset of hyperglycemia and propensity for dev of DKA
T2: Hyperglycemia dev gradually with progressive decline in beta cell fxn (ie initially silent)

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17
Q

How are type 1 and type 2 different in treatment?

A

T1: lifelong insulin injection required
T2: can be treated with oral meds

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18
Q

How are type 1 and type 2 different in cause?

A

T1: Associated with auto-antibodies
T2: Associated with increasing age and obesity
(hyperosmolar hyperglycemic non-ketosis (HHNK), can dev DKA)

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19
Q

How are type 1 and type 2 different in age?

A

T1: predominant type of diabetes diagnosed <30y/o

20
Q

How are type 1 and type 2 different in family hx

A

T1: rare
T2: 95%, common

21
Q

How are type 1 and type 2 different in mechanism

A

T1: autoimmune destruction of beta cells
T2: unknown

22
Q

How are type 1 and type 2 different in first functional abnormality?

A

T1: dec in insulin sec
T2: dec insulin sec and response to insulin

23
Q

How are type 1 and type 2 different in initial pathology

A

T1: insulinitis
T2: little/none

24
Q

How are type 1 and type 2 different in late pathoogy

A

T1: absence of beta cells, inc in alpha and gamma
T2: Amyloid deposition, fibrosis. Beta cell mass reduction

25
Q

What is the criteria for diagnosis of diabetes?

A
  • Symp of diabetes plus a random plasma glucose concentration of >200mg/dL
  • Fasting plasma glucose concentration >126mg/dL
  • 2-hr plasma glucose concentration >200mg/dL during an OGTT
  • A1c >= 6.5%
26
Q

What are the specific signs and symptoms of diabetes?

A
  • Polyuria/polydipsia
  • wt loss (starvation state, not abs calories)
  • polyphagia (excessive hunger)
  • diabetic ketoacidosis (more common in type 1)
  • coma
27
Q

What are the non-specific signs and symp of diabetes?

A
  • Fatigue
  • Blurred vision (lens gets distorted due to osmolar effect)
  • Dry mouth
  • Dry/itchy skin (dehydration)
  • Vaginal candidiasis
  • Poor healing of wounds (bacteria like diabetic medium)
  • Excessive/unusual infections (immunosupp due to hyperglycemia)
28
Q

When do we get glucose in the urine?

A

When we oversaturate the glucose transporters (Tm) in the glomerular filtrate due to chronically high glucose in the blood (175-200mg/dl)

29
Q

What are the peak ages of onset of T1D?

A

5-7yr and at onset of puberty. 1/3 of cases after age 18

30
Q

What time of year more likely to have the onset?

A

Cold season…maybe virus triggers it?

31
Q

Describe the incidence of T1d

A

Incidence is increasing world wide

32
Q

What are some risk factors for T1d?

A
  • Viral infections (coxsaccie, congenital rubella, enterovirus infections)
  • Diet, esp exposure to cow’s milk at early age
  • High SES
  • Obesity
  • Vit D def
  • Perinatal factors like mat age, hx of preeclampisa, neonatal jaundice. Low birth wt dec risk of dev T1D
33
Q

What serum auto-antibodies have been detected in t1d

A
  • Islet cell Abs (ICA)
  • Insulin Abs (IAA)
  • Glutamic acid decarboxylase Abs (GAD)
  • Tyrosine phosphatase-like proteins like insulinoma associated protein (IA-2)
  • Cation efflux zinc transporter (ZnT8) has been indentified as a candidate
34
Q

Describe the relationshipt betw T1 D and other autoimmune dis

A

Lots of concurrence with other autoimmunity like thyroiditis, addisons or celiac

35
Q

What is Latent Auto-Immune Diabetes of Adulthood (LADA)?

A

-Intermediate between T1 and T2. Usually presents >25 y.o masquerading as non-obese type 2 (non DKA) with pos auto antibodies seen. It can initially be controlled with meal planning, but insulin dep gradually occurs within months. They have a low peptide C concentration and are unlikely to have a fam hx of t2d.

36
Q

How do we treat T1d?

A
  • Insulin replacement therapy
  • Edu
  • Adjust doses according to carb intake, exercise, blood glucose profile
  • Test blood gluc levels
  • Screen for complications
37
Q

By how much does intensive therapy significantly reduce microvascular complications?

A
  • Retinopathy: 76%
  • Nephropathy: 50%
  • Neuropathy: 60%
38
Q

What is DKA?

A

Potentially life threatening presentation of T1D where the body perceives a state of starvation Because no insulin is being synth or detected and rallies body stores to compensate. This includes hepatic glucose produc, muscle breakdown and fat breakdown to ketones.

39
Q

What are the symptoms of DKA?

A

Nausea/vomiting, polyuria, weakness, anorexia, abdominal pain, visual disturbances, somnolence

Signs: tachycardia, hypotension, dehydration, hyperventilation, wt loss, fruity odor on breath, altered mental status

40
Q

What do we do to treat DKA?

A

Replace insulin 1st! then correct fluid and electrolyte imbalances .

41
Q

What does loss of insulin in DKA effect?

A
  1. Liver: plasma glucose inc, glucosuria, polyuria–>dehydration
  2. Muscle: inc plasma glucose and muscle wasting–>wt loss
  3. Adipose: inc plasma FFAs–>inc plasma beta hydroxybutyrate and acetoacetate–>acidosos (ketones)
42
Q

What are the urgent problems in DKA?

A

Hyperosmolar dehydration and acidosis

43
Q

What are some potential treatment adverse events of DKA?

A

-Cerebral edema and hypokalemia if convert too quickly

44
Q

What is the #1 complication of T1D or pts on insulin?

A

Hypoglycemia

45
Q

What is the basal bolus approach?

A

Tries to mimic endogenous insulin production by combining basal dose to suppress hepatic glucose production between meals and bolus dose after meals

Endorine (24 decks)

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