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Endocrine > DM Epidemiology and Pathophys - Exam 4 > Flashcards

DM Epidemiology and Pathophys - Exam 4 Flashcards

1
Q

**What is normal fasting glucose? ____ of glucose from meal → stored, released later as needed by the body

A

70-99

⅔

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2
Q

______ is secreted in response to postprandial serum glucose changes. How is glucose stored?

A

insulin

stored in liver and skeletal muscle as glycogen

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3
Q

What is a triglyceride made up of?

A

3 fatty acids linked by a glycerol molecule

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4
Q

Once a glycogen molecule is stored in the skeletal muscle, can it be broken down and used in the blood stream?

A

NO! once its in the skeletal muscle it can only be used for energy but the muscle

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5
Q

Once a glycogen molecule is stored in the liver, can it be broken down and used in the blood stream?

A

YES! liver glycogen can be used by the entire body

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6
Q

______ hepatic synthesis of glucose
from amino acids, glycerol, and lactic acid

A

gluconeogenesis

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7
Q

_____ is the most efficient form of fuel storage. ______ convert TGs to fatty acids and glycerol

A

Fat Metabolism

lipase

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8
Q

______ are converted to ____ by liver, then released for energy. _____ can be used by the brain for energy when glucose is not available. Can FA be made directly into glucose?

A

Fatty acids

ketones

ketones

NO!! FA cannot be made directly into glucose

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9
Q

How is excessive protein stored? When are protein broken down and used for energy?

A

limited facility for storage of excess amino acids

Excess amino acids → fatty acids, ketones, or glucose

in periods of fasting/starving. AA are broken down as substrates for gluconeogenesis when glucose is NOT available

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10
Q

What are the 2 types of Islets of Langerhan cells? What is their function?

A

alpha cell: secrete glucagon

beta cell: secretes insulin and amylin

secrete hormones into the blood

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11
Q

What are the 2 types of pancreatic acini cells? What do they secrete?

A

exocrine cells

F cell: secretes pancreatic polypeptide

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12
Q

Name 3 substances that are produced in the beta cells. What is the function of each?

A

Preproinsulin - initially synthesized polypeptide chain

Proinsulin - Created by removal of signal peptide and linkage between A and B chains

Insulin - active form; created by cleavage and removal of C-peptide chain

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13
Q

How is proinsulin created? How is insulin created?

A

by removal of signal peptide and linkage between A and B chains

active form; created by cleavage and removal of C-peptide chain

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14
Q

How is mature insulin stored and released? How can you assess insulin function?

A

Mature insulin molecule and C-peptides are co-stored in the beta cells and released together

order a C-peptide level because you cannot measure insulin directly because it is not very stable

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15
Q

What does a low C-peptide level indicate?

A

that the pancreas is NOT producing insulin

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16
Q

____ is the primary regulator of beta cell secretion of insulin. What does it bind to?

A

Glucose

binds to specific cell membrane transporter proteins known as GLUT

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17
Q

What is the role of GLUT- 2 (and/or GLUT 1)? GLUT-4?

A

GLUT-2 (and/or GLUT-1) - transport glucose into numerous body cells, including beta cells

GLUT-4 - skeletal muscle, adipose tissue - in an inactive position until stimulated by insulin

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18
Q

Once within the Beta cell, how does glucose stimulate the release of insulin? Why do we need to know this process?

A

glucose is phosphorylated → ATP generation → inhibition of an ATP-sensitive K+ channel

Inhibition of this channel leads to depolarization of the beta cell

Depolarization → opening of voltage-gated calcium channel → insulin secretion

because different medications target diff areas of the process

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19
Q

What are the 2 major actions of insulin on glucose metabolism?

A

insulin increases glucose transport into skeletal muscle and adipose tissue

insulin increases synthesis of glycogen which decreases gluconeogenesis

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20
Q

What are the 3 major effects of insulin on fat metabolism?

A

Transport - ↑ transport of fatty acids into adipose cells

Synthesis - ↑ synthesis of fatty acid and TG synthesis

Breakdown - ↓ TG breakdown

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21
Q

What are the 3 major action of insulin on protein metabolism?

A

Transport - ↑ transport of amino acids into cells

Synthesis - ↑ synthesis of proteins

Breakdown - ↓ breakdown of proteins

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22
Q

What is the function of glucagon? Where it is produced? When is glucagon the highest?

A

increased gluconeogensis
increased glycogen breaken (to pull glucose out of storage to used for energy)

increases adipose breakdown by activating lipase in adipose cells

increases transport of AA to the liver to use for gluconeogenesis

glucagon is highest during periods of not eating aka first thing in the morning

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23
Q

What is the role of amylin? Where is it produced?

A

Works with insulin to regulate plasma glucose concentrations, decreases post meal glucagon secretion, slows gastric emptying and increases satiety

secreted by beta cells along with insulin and C-peptide

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24
Q

Somatostatin secreted by _____ in the Islets of Langerhans, as well as by other cells throughout the body. What is its function?

A

delta cells

Inhibitory hormone - suppresses release of several hormones, including insulin and glucagon

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25
Q

_____ are gut-derived hormones that promote insulin release after oral nutrient load. Accounts for ____ of postprandial insulin secretion. What is another function?

A

Incretins

~50%

Slowed gastric emptying and increased satiety aka slows down appetite

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26
Q

What is the effect of epinephrine on blood glucose levels?

A

increases blood glucose during periods of stress

Increased - glycogenolysis in liver and muscle tissues; lipolysis in adipose tissues

Decreased - release of insulin by the pancreas

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27
Q

Growth Hormone is normally ____ by insulin and elevated glucose levels. What does a chronic hyper secretion of growth hormone result in?

A

insulin resistance, elevated glucose, and
increased overall risk of DM

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28
Q

Why does glucocorticoids increase blood glucose levels?

A

because it increases gluconeogenesis in the liver

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29
Q

DM is the ____ cause of death in the US

A

8 cause of death in US

30
Q

What is the breakdown in prevalence between Type 1 and Type 2 DM?

A

90-95% have Type 2 DM; 5-10% have Type 1 DM

31
Q

What is the basic root cause of T1DM? What is the basic root cause of T2DM?

A

destruction of beta cells due to an AI condition

associated with insulin resistance, inadequate insulin secretion, and increased glucose production

32
Q

What is the basis root cause of T3DM?

A

destruction of pancreas (e.g. infiltrative disease, CF, pancreatitis), genetic defects in glucose or insulin metabolism, etc.

33
Q

_____ is the MC form of “other DM”. What does it increase your risk for?

A

gestational DM: increases risk of developing DM later in life

34
Q

What is type IA DM associated with? What cell type is commonly seen? type IB? What ethnicity?

A

Autoimmune destruction of beta cells - ~95%: Associated with autoantibodies, autoreactive T lymphocytes

Type IB:
Idiopathic
No associated autoantibodies
Most patients are of Asian or African origin

35
Q

What is the deeper thought process to why type IA DM occurs? What gene? What are some environmental triggers?

A

Thought to be ⅓ due to genetics, ⅔ due to environment

HLA genes - contribute to 40-50% of risk of type IA DM 3% risk if mother, 6% risk if father

cow’s milk, hygiene hypothesis, certain viruses

36
Q

When does s/s start to appear in type IA DM? What is Latent Autoimmune Diabetes in Adults (LADA)?

A

Clinical s/s present when about 70-80% of beta cells are destroyed

very slow progression of type IA DM

37
Q

Describe the process behind the beta cell destruction in Type IA DM. Are alpha and delta cell effected? Will immunosuppressive medication help?

A

Islets of Langerhans become infiltrated by lymphocytes, cytokines are released

T cell are responsible for destruction

Other cells in Islets of Langerhans (alpha, delta, etc.) are generally spared

immunosuppressive meds are generally NOT helpful!

38
Q

What autoantibodies can you test for that make you think Type IA DM? What is the major one? What is the limitation?

A

Anti-GAD65, Anti-ZnT8, Anti-IA2, Islet Cell
Autoantibodies (ICA), and anti-insulin (IAA)

autoantibodies decline once you have had T1DM for a while, they will no longer test positive

39
Q

What is the pathogenesis of T2DM? What are the contributing factors?

A

Insensitivity (resistance) of tissues to insulin → inadequate insulin secretion

genetic and environmental factor

40
Q

What is the #1 environmental factor for T2DM?

A

visceral obesity

41
Q

What is happening early in the onset of T2DM? What starts happening over time?

A

Insulin resistance leads to compensatory hyperinsulinemia

Pancreatic beta cells are no longer able to maintain hyperinsulinemic state, causing “prediabetic” abnormalities

42
Q

Impaired glucose tolerance leads to ???? What is it caused by?

A

higher-than-expected postprandial glucose

Mainly due to decreased peripheral tissue glucose uptake and use

43
Q

impaired fasting glucose leads to ????? What is it caused by?

A

higher-than-expected fasting glucose levels

Mainly due to increased hepatic production of glucose

aka its the liver’s fault due to making too much glucose

44
Q

What is the diabetes “triumvirate”?

A

Abnormal insulin secretion
Increased hepatic glucose production
Decreased peripheral glucose uptake

the biggest 3 factors that cause DM

45
Q

What is the “Ominous Octet” of DM?

A
  1. Decreased insulin secretion
  2. Increased hepatic glucose production
  3. Decreased peripheral glucose uptake
  4. Increased lipolysis
  5. Decreased incretin effect
  6. Increased glucagon secretion
  7. Increased renal glucose reabsorption
  8. Neurotransmitter dysfunction
46
Q

Why are increased hepatic glucose production seen in T2DM?

A

resistance to insulin effects and lower insulin levels → loss of negative feedback stimulus to suppress hepatic gluconeogenesis

47
Q

Why do you see increased lipolysis in T2DM?

A

resistance to insulin’s antilipolytic effect → release of free fatty acids, which stimulate gluconeogenesis and promote further hepatic and muscle insulin resistance

48
Q

Also with↑ insulin resistance–inducing, inflammatory, and atherosclerotic-provoking ______. Also see ↓ insulin-sensitizing adipocytokines such as _____

A

adipocytokines

adiponectin

49
Q

What is the effect of incretins? Name 2 major ones.

A

stimulate insulin release, inhibit glucagon secretion, promote satiety

GLP-1: decreased secretion of GLP-1 in T2DM

GIP: tissue resistance to effects of GIP in T2DM

50
Q

What is the role of glucagon?

A

promotes gluconeogenesis, glycogenolysis, and lipolysis

51
Q

____ of glucose filtered in the kidney is reabsorbed in the proximal tubule by the _____ protein

A

90%

SGLT2 transporter

52
Q

____ normally acts as an appetite suppressant. What is normally seen as a result?

A

Insulin

high prevalence of overeating and obesity

53
Q

_______ is an autosomal-dominant; genetically mediated impaired insulin secretion in response to glucose

A

Maturity-Onset Diabetes of the Young

54
Q

What medications are common secondary causes of DM?

A

corticosteroids, thiazides, beta blockers, antipsychotics

55
Q

Describe the difference between a DM pt postprandial glucose level and a normal persons.

A

diabetic pts blood glucose peaks higher and takes longer to come back down to normal levels than a normal person’s BS

56
Q

What does metabolic syndrome increase your risk for what 7 conditions?

A

atherosclerosis, heart disease, stroke, cancer, dementia, type 2 DM, erectile dysfunction

57
Q

What are the general criteria for metabolic syndrome? How many do you need ?

A

Waist circumference: > 40 in (102 cm) in men, >35 in (88 cm) in women

Fasting triglycerides: >150 mg/dL, or on medication

HDL cholesterol: <40 mg/dL (men), or <50 mg/dL (women), or on medication

Blood pressure: >130 mm systolic or >85 mm diastolic, or on medication

Fasting plasma glucose: ≥100 mg/dL, or on medication

need 3+ of the above criteria for metabolic syndrome

58
Q

What is the overall prevalence of metabolic syndrome in the US? What ethnicity is at highest risk?

A

22% of pts (43% of pts 60+)

Mexican americans, Black

59
Q

What are the 3 MC components of metabolic syndrome? What is important to note about the _____?

A

TG - triglycerides
HDL-C -high-density lipoprotein cholesterol
BP -blood pressure

**TG must be fasting

60
Q

What are some risk factors for metabolic syndrome?

A

central obesity
physical inactivity
aging
T2DM
CVD
lipodystrophy

61
Q

____ thought to be primary contributor to metabolic derangements. Why?

A

insulin resistance

Increased circulating free fatty acids → further reduction of antilipolytic effect of insulin

62
Q

______ resistance is thought to also play a role in insulin resistance. Why?

A

leptin

reduces appetite, and promotes insulin sensitivity

63
Q

Why does insulin resistance lead to hypertension?

A

insulin resistance leads to loss of insulin’s normal vasodilatory effect, without impacting its mild sodium retention effect

aka retains sodium without dilating the vessels = higher BP

64
Q

What is the effect of hyperuricemia?

A

HTN through activation of the RAAS

65
Q

In metabolic syndrome, ______ are produced in greater amounts due to the overall increased mass of adipose tissue. Name some examples.

A

Proinflammatory cytokines

Includes IL-1, IL-8, IL-16, TNF-alpha, C-reactive protein

66
Q

_____ is an anti-inflammatory cytokine. What cell produces it? What happens to it in metabolic syndrome?

A

Adiponectin

produced exclusively by adipocytes

production of Adiponectin is reduced in DM and metabolic syndrome

67
Q

_____ velvety darkening of skin folds associated with _____

A

Acanthosis nigricans

insulin resistance

NOT present in T1DM!!!

68
Q

What is a common abdominal PE finding in metabolic syndrome?

A

Hepatic enlargement - possible if “fatty liver” (NAFLD/steatohepatitis) is present

69
Q

Name some common clinical manifestations of metabolic syndrome?

A

increased waist circumference
hypertension
Acanthosis nigricans
hepatic enlargement
Hyperuricemia
Polycystic ovarian syndrome
Obstructive sleep apnea

70
Q

What is the tx for metabolic syndrome?

A

calorie restrictive diet with restricted dietary cholesterol
exercise
anti-obesity drugs
bariatric surgery
support groups
antidiabetic medications

71
Q

What is the HTN tx of choice for metabolic syndrome? _______ can be given to improve insulin resistance

A

ACE (-pril) or ARB (-sartan)

metformin

72
Q
A

Endocrine (14 decks)

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