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Clinical medicine A > diabetes patho and epidemiology > Flashcards

diabetes patho and epidemiology Flashcards

1
Q

what happens to the majority of glucose that you eat from meals

A

2/3 is stored and released later

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2
Q

if the liver and skeletal muscle are both already saturdated with glucose, what happens to it?

A

excess glucose gets turned into fatty acids and then into triglycerides

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3
Q

gluconeogenesis

A

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

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4
Q

what is the most efficient form of fuel storage

A

fat metabolism

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5
Q

what are triglycerides converted into and what is the enzyme used to do so

A

fatty acids and glycerol
enzyme used is lipase

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6
Q

how is glycerol used

A

used directly for energy or converted to glucose

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7
Q

how are fatty acids used

A

converted to ketones by the liver then released for energy

CANNOT be made directly into glucose.

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8
Q

what can be used by the brain for energy when glucose is unavailable

A

ketones (from fatty acids)

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9
Q

converted to ketones by the liver then released for energy

A

fatty acids (from TG)

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10
Q

used directly for energy or converted to glucose

A

glycerol

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11
Q

excess of this is turned into fatty acids, ketones or glucose

A

amino acids from proteins

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12
Q

secretes digestive juices into duodenum

A

pancreatic acini

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13
Q

hormone secretion portion of pancretic cells

A

islets o langerhands

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14
Q

secretes insulin

A

beta cells

also secretes amylin

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15
Q

secretes amylin

A

beta cells

also secretes insulin

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16
Q

secretes glucagon

A

alpha cells

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17
Q

initial polypeptide chain synthesized by beta cells with signal peptide present

A

preproinsulin

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18
Q

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

A

proinsulin

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19
Q

created by cleavage and removal of C-peptide chain

A

insulin

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20
Q

used to assess active insulin

A

C-peptide

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21
Q

glucose transporter for most body cells

A

GLUT 2

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22
Q

glucose transporter for skeletal muscle and adipose tissue

A

GLUT 4

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23
Q

What happens to glucose in a beta cell?

A
  1. Phosphorylation of glucose
  2. ATP generation
  3. Inhibition of ATP-sensitive K+ channel
  4. Sulfonylureas can bind to this channel to stimulate insulin release
  5. Beta cell is depolarized, resulting in opening of the voltage-gated calcium channel
  6. Insulin is released.
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24
Q

three things released from beta cells when depolarized

A

C - peptide
IAPP (amylin)

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25
Q

what channel can sulfonylureas bind to in order to depolarize beta cells and therefore stimulate insulin release

A

ATP sensitive potassium channels!

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26
Q

how does insulin affect glucose metabolism

A
  1. increases glucose transport into skeletal and adipose tissue
  2. increases glycogen synthesis
  3. decreases gluconeogenesis
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27
Q

how does insulin affect fat metabolism

A
  1. inceases transpot of FAs into adipose cells
  2. increases synthesis of FAs and TGs
  3. decreases TG breakdown
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28
Q

how does insulin affect protein metabolism

A
  1. increases transport of AAs into cells
  2. increases synthesis of proteins
  3. decreases breakdown of proteins
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29
Q

what are the effects of glucagon on glucose metabolism

A
  1. increases gluconeogenesis
  2. increases glycogen breakdown
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30
Q

what are the efects of glucoagon on fat metabolism

A
  1. increases adipose tissue breakown
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31
Q

what activates lipade in adipose tissue

A

glucagon

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32
Q

how does glucagon affect protein metabolism

A

increases transport of amino acids into liver cells for use in gluconeogenesis

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33
Q

functions of amylin

A
  1. works with insulin to regulate plasma glucose
  2. decreases postprandial glucagon secretion
  3. slows gastric emptying and increases satiety
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34
Q

secreted by delta cells

A

somatostatin

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35
Q

job of somatostatin

A

inhibition of insulin and glucagon release

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36
Q

these gut derived hormones accounts for 50% of postprandial insulin secretion

A

incretins

also slows gastric emptying/increases satiety

37
Q

what are the effects of epi on glucose

A
  1. increases glycogenolysis in liver and muscles
  2. increases lipolysis in adipose tissues
  3. decreases release of insulin
38
Q

what can result as a chronic hypersecretion of GH

A
  1. insulin resistance
  2. elevated glucose
  3. inceased DM risk
39
Q

what is the effect of glucocorticoids on glucose levels

A
  1. increases gluconeogenesis in the liver
40
Q

what does the term “diabetes” mean

A

siphon

(related to excessive urination)

41
Q

what does the word “mellitus” mean

A

sweet

42
Q

what is the estimated US pevelance of DM, what about the worldwide prevelance?

A

8.5-15.9% of adults in US
10.5% wordlwide

43
Q

what is the prevelance of patients w gestational DM? how likely are these pateints to develope DM later on?

A

7% of US pregnancies

35-60% risk of later developement of DM

44
Q

what is T1DM associated with?

A

autoantibodies
autoreactive T lymphocytes

45
Q

what form of DM is idiopathic

A

T1B DM

46
Q

what is the genetic and envrionmental contribution of T1ADM

A

genetic 1/3 - because of HLA genes

environmental 2/3 - due to cows milkl, hygiene hypothesis, certain viruses

genetic predisposition w an environmental trigger!

47
Q

at what point in T1A DM do clinical S/S begin to show

A

when 70-80% of the beta cells are destroyed

48
Q

very slow progressing T1ADM is known as

A

latent autoimmune diabetes in adults (LADA)

49
Q

What is the geneal idea of the process of beta cell destruction in T1ADM

A
  1. islets of langerhans become infiltrated by lymphocytes
  2. exact mechanism is not fully understood but T cells are to be primarily responsible.
  3. other cells are generally spared!
50
Q

what are the immunoligic abnormalities in T1ADM

A
  1. islet cell autoantibodies
  2. activated lymphocytes in islets, peripancreatic lymph nodes and systemic circulation
  3. T lymphocytes that proliferate when stimulated w islet proteins
  4. release of cytokines w/i infiltrated islets
51
Q

what type of therapy does NOT work for T1ADM

A

immunosuppression

52
Q

what autoantibodies are positive in >85% of T1ADM patients

A
  1. Anti-GAD65 (MC)
  2. Anti-ZnT8
  3. Anti-IA2
  4. Islet cell autoantibody (ICA)
  5. Anti-insulin autoantibody (IAA)
53
Q

what are the limitations to the autoantibody testing in someone with T1ADM?

A
  1. declines with increasing duratio of disease
    • in about 5% of T2DM and gestational DM
  3. low IAA levels in many pts after tx w exogenous insulin
54
Q

What is T3DM/other types of DM associated with?

A
  1. Pancreatic destruction
  2. Genetic defects in production of insulin or glucose
  3. Gestational DM (7% of pregnancies)
55
Q

what is the pathogenesis of T2DM

A

insulin insensitivity in tissues which causes inadequate insulin secretion

sufficient insulin to prevent ketosis but not enough to prevent systemic hyperglycemia

56
Q

what are the contributors to T2DM

A
  1. genetic! - family hx
  2. environmental - obesity (#1 is visceral), high/low birthweight, lack of phyiscal activity
57
Q

what are the contributors to T2DM

A
  1. genetic! - family hx
  2. environmental - obesity (#1 is visceral), high/low birthweight, lack of phyiscal activity
58
Q

what are the metabolic abnormalities seen in T2DM

A
  1. impaired insulin secretion w insulin resistance
  2. exessive hepatic glucose production
  3. abnormal fat/lipid and muscle metabolism
59
Q

what occurs in early T2DM?
what occurs over time?
what occurs as disease progresses

A

early - insulin resistance leads to compensatory hyperinsulinemia

over time -
pancreastic beta cells cant maintain hyperinsulinemia which causes pre diabetic s/s such as impaired glucose tolerance and impaired fasting glucose

progression- further decline in insulin secretion and increased insulin resistance causes worsening hyperglycemia until eventually T2DM is reached

60
Q

what is the old diabetes triumvirate theory

A

major factors contributing to glucose regulation in T2DM were thought to be:
1. abnormal insulin secretion
2. increased hepatic glucose production
3. decreased peripheral glucose uptake

these are still thought to be contributing factors but are no longer thought to be the ONLY contributing factors!

61
Q

what is the ominous octet?

A

the new theory of T2DM regarding major factors of poor glucose regulation:
1. decreased insulin secretion - d/t loss of B cell function

  1. increased hepatic glucose production - d/t insulin resistance and low insulin levels causing loss of negative feedback to suppress gluconeogenesis
  2. decreased peripheral glucose uptake - d/t insulin resistance/absence causing inability to absorb glucose into muscles/adipose tissue
  3. increased lipolysis - d/t resistance of insulins antilipolytic effect resulting in release of FA’s which stimulate gluconeogenesis
  4. decreased inccretin effect - incretins cause stimulated insulin release, inhibition of glucagon secretion and promotion of satiety
  5. increased glucagon secretion - glucagon promotes gluconeogenesis, glycolysis and lipolysis
  6. increased renal glucose absoprtion
  7. neurotransmitter dysfunction - insulin normally acts as appetite suppressant. decreased sensistivity = increased appetite.
62
Q

where in the kidney is glucose reabsorbed

A

in proximal tubule by the SGLT2 transporter protein.

63
Q

pathogenesis of gestational DM

A

insulin esistance due to metabolic changes of pregnancy

64
Q

poathogenesis of maturity onsetdiabetes of the young

A

autosomal dominant; genetically mediated impaired insulin secretion in response to glucose

64
Q

pathogenesis of gestational DM

A

insulin esistance due to metabolic changes of pregnancy

65
Q

what are the 4 main causes of secondary DM

A

hormonal rumors
liver disease
pharmacologic agents
panceatic disease

66
Q

what pharmacologic agents could cause secondary DM

A

corticosteroids
thiazides
BB
antipsychotics

67
Q

what are the 2 main incretins

A

GLP - 1
GIP

68
Q

What is metabolic syndrome

A

aka syndrome X
a criteria of three of the following:
1. waist circumference of >40 in men and >35 in women
2. fasting TG’s >150
3. HDL <40 men, <50 women
4. BP >130 systolic or >85 diastolic
5. fasting plasma glucose >100

it also counts if they are on medication for any of these.

69
Q

people with metabolic syndrome have an increased risk of…

A

atherosclerosis
heart disease
stroke
cancer
dementia
T2DM
ED

70
Q

what is prevalence of metabolic syndrrome in US

A

22% of patients
43% of patients 60+

71
Q

what are risks for metabolic sndrome

A
  1. mexican american or black
  2. women
  3. overweight (central/visceral mostly)
  4. physical inactivity
  5. aging
  6. T2DM
  7. CVD
  8. Lipodystrophy
72
Q

what has been found to raise metabolic syndrome risk by x2

A

> 4 hours a day o TV/computer time

73
Q

When does BG peak postprandial?

A

Generally around 2 hours is the peak BG before it drops down to normal.

74
Q

how does insulin resistance correlate with metabolic syndrome

A

thought to be the primary contributor of metabolic syndrmome

causes inceased circulating FFA’s

75
Q

how does glucose intolerance effect metabolic syndrome

A

increased levels of postprandial and fasting glucose

76
Q

how does hypertension effect metabolic syndrome

A

insulin resistance leads to loss of insulins normal vasodilatory effect without impacting its mild sodium retention effect.

hyperuricemia also contributes to HTN through activation of the RAAS

77
Q

how does waist circumference effect metabolic syndrome

A

increased visceral adipose tissue = greater effect of circulating FFA’s on hepatic metabolism

78
Q

dyslipidemia

A

influx of FFA’s into the liver = abnormal lipid production
TG increased
HDL decreased
LDL increased

79
Q

how do proinflammatory cytokines effect metabolisc syndrome

A

increased production due to the increased overall mass of adipose tissue.

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

80
Q

how does Adiponectin effect metabolic syndrome

A

anti-inflammatory cytokine produced exclusively by adipocytes (reduced rate of production in pts w metabolic syndrome)

81
Q

what are the PE findings of metabolic syndrome

A

increased waist circumference and HTN
acanthosis nigricans
hepatic enlargement

82
Q

what are the lab findings in metabolic syndrome

A

hyperuricemia (w gouty arthritis)
polycystic ovarian syndrome
obstructive sleep apnea

83
Q

how do you treat metabolic syndrome

A

primary approach = weight reduction

  • diet of 500 cal/day low in carbs high in veggies, whole grains and lean proteins
  • physical activity of at elast 30 min/day (60-90 is optimal for weight loss)
84
Q

what might be needed prior to physical activity in metabolic syndrome patients

A

cardiovascular evaluation

85
Q

how do you treat metabolic syndrome w dyslipidemia

A

restrict dietary cholesterol

use statins IF + DM, CVD or high 10 year CVD risk

fibrates may be considered to help reduce TGs

86
Q

how do you treat metabolic syndrome with HTN

A

sodium restricted diet
home BP monitoring
ACE/ARB

87
Q

how do you treat metabolic syndrome w hyperglycemia

A

reduce dietary carbs
TZDs and/or metformin

Clinical medicine A (32 decks)

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