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Clin Med- P > Intro to Metabolism > Flashcards

Intro to Metabolism Flashcards

Pathophys of DM

1
Q

what part of the body converts glycogen to glucose?

A

the liver

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2
Q

insulin is important in regulating uptake of glucose into cells but what type of cells does it not regulate uptake well?

A

muscle

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3
Q

what does glucagon do?

A

stimulates glycogenolysis mainly

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4
Q

what are the 4 main target cells important for DM?

A

fat, muscle, liver, brain

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5
Q

where are the endocrine islet cells located in the pancreas compared to the acini of the exocrine cells?

A

islet cells float within the exocrine acini

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6
Q

what is the structure of proinsulin? how is this converted to insulin?

A

“A” peptide chain is connected to a “B” peptide chain by the “C” (or connecting) peptide chain; this is converted to insulin once the C peptide is removed

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7
Q

is the C peptide considered active or inactive?

A

inactive: it is stable *=(unlike A and B peptides that have a short half life); this is why it can be measured to estimate insulin synthesis

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8
Q

what is a major predisposing factor for type 2 diabetes?

A

obesity, strongly influenced by underlying family history

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9
Q

what is the fasting plasma glucose range for prediabetes? how is this measured?

A

between 100 and 126 mg/dl (measured with serum glucose)

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10
Q

what is impaired glucose tolerance? what type of diabetes is this seen in? what test measures this?

A

its a decreased ability to uptake glucose into cells following food intake (get increased plasma glucose levels); seen in prediabetes; glucose tolerance test measures this

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11
Q

what is the glucose tolerance test?

A

medical test in which glucose is given and blood samples taken afterward to determine how quickly it is cleared from the blood

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12
Q

what is prediabetes a predecessor for?

A

type 2 DM

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13
Q

what are some risks associated with developing prediabetes? what can decrease risk?

A

risks- FH, obesity, metabolic syndrome, GDM history, drugs (seizure and antipsychotics)
risks can decrease with weight loss, exercise, gastric bypass surgery, drugs(ACE-I, metformin)

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14
Q

what kind of problems are fat and gut peptides in type 2 DM?

A

central problems (not pathophys oddities)

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15
Q

what fat/gut peptides are decreased with excess adipose tissue? how about increased?

A

decreased- adiponectin

increased- interleukin 6, TNF alpha, PAI-1, leptin

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16
Q

what is adiponectin? what is significant about decreased adiponectin due to excess adipose tissue?

A

a protein hormone involved in regulating glucose and fatty acid breakdown; decreased production reduces insulin sensitivity and leads to insulin resistance

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17
Q

where is amylin released from? what does it do? what diabetes drug is this associated with?

A

released by beta cells; decreases gastric emptying and increases fullness; smylin, BID injection for type 1 or 2 patients and has weight loss side effect

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18
Q

what do GLP-1 drugs do? what are two benefits of these drugs?

A

(exenatide/byetta) incretin hormone potentiates meal-related insulin release, decreases gastric emptying, inhibits glucagon release
benefits: may promote b cell regeneration and improved CVD benefits

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19
Q

what do DPP-IV drugs do? what is the biggest side effect?

A

(ex: gliptin drugs) prolong action of endogenous incretins (prevents breakdown of GLP-1 so insulin levels inc and glucagon levels dec)
worse side effect: nausea

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20
Q

what two peptides increase food intake? what two decrease food intake?

A

increase- ghrelin, neuropeptide

decrease- pancreatic polypeptide or peptide YY

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21
Q

where is glucagon released from? what is it in response to?

A

released from alpha cells of pancreas in response to low serum glucose levels

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22
Q

describe glucagon levels in type 2 DM

A

elevated

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23
Q

what are the three major acute complications of diabetes?

A

diabetic ketoacidosis(severe high glucose), hyperglycemic hyperosmolar state (HHNK- severe high glucose), and hypoglycemia (low glucose usually therapy induced)

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24
Q

what are the two forms of transient hyperglycemia?

A

dawn and somogyi effects

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25
Q

what is the dawn effect?

A

The dawn effect is an early-morning (usually between 5 a.m. and 9 a.m.) increase in blood sugar WITHOUT preceding hypoglycemia

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26
Q

what is the somogyi effect?

A

it is a rebound response to insulin-induced low blood sugar where the body overcompensates and ends up with too high blood sugar levels in the morning

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27
Q

what are four symptoms of hyperglycemia?

A

polydipsia/polyuria, blurred vision, weight loss (more common for type 1), fatigue

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28
Q

what is DKA? what symptoms can the pt get?

A

lack of insulin (primarily type 1) results in fat metabolism and increased free fatty acids; fat metabolism produces ketones and the keto-acids cause metabolic acidosis
pt can have N/V, confusion, BG levels > 250, and end up in a coma

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29
Q

what is the tx for DKA?

A

HYDRATION, insulin, correction of electrolytes

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30
Q

what DM type is DKA more likely to be found?

A

type 1 (common presentation for new onset)

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31
Q

what is HHNK? what kinds of symptoms can the pt have?

A

type 2 DM, without ketones, but much higher glucose (over 600 mg/dl); patient primarily has neuro symptoms (mimics stroke but can have seizures, aphasia, hemiparesis, vision changes, etc)

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32
Q

what is treatment of HHNK?

A

primarily fluids, careful monitoring of K+, insulin isn’t essential

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33
Q

what are some symptoms of hypoglycemia?

A

neurologic and sympathetic (confusion/stupor, HA, seizure, inc HR, trembling, vasoconstriction, sweating)

34
Q

what type of meds are you concerned about a diabetic patient taking and why?

A

beta blockers block the symptoms of hypoglycemia (except sweating)

35
Q

what is the tx for hypoglycemia?

A

carbs/glucose PO for mild; IV glucose or glucagon for severe

36
Q

do people usually die from diabetes?

A

NOPE, they die from complications of it (heart attack-2x risk for CVD, stroke, kidney failure- leading cause, blindness- 8% of all cases, amputation- 1/2 of non traumatic cases)

37
Q

are diagnosed diabetics usually well controlled? what is the major goal in diabetes prevention?

A

nope; goal is to diagnose early and tx appropriately

38
Q

compare the at risk BMIs for diabetes in Caucasians, south Asians, Chinese, and African americans

A 
white: 30 kg/m2
south Asians: 24
Chinese: 25
African americans: 26
(overall point: lower for ethnic groups compared to whites)
39
Q

does subcutaneous fat vs intra-abdominal fat have a higher correlation with diabetes risk?

A

intra-abdominal fat has higher deposition than subcutaneous (Caucasians follow subcutaneous pattern)

40
Q

what are the two general rules of screening for diabetes?

A

1) . screen for DM2: people under 45 with BMI over 25 AND one of many risk factors (physically inactive, familial diabetes, high risk race, high BO, POS, hx of CVD, A1C over 5.7%)
2) . everyone over 45 yrs old every 3 years check FBG or A1C (if person is also at risk or has prediabetes then test every year)

41
Q

what skin marking is a sign of insulin resistance?

A

acanthosis nigricans (darkening of skin, looks dirty and might feel velvety)

42
Q

basic difference between type 1 and 2 DM?

A

1- lack of insulin secretion

2- tissue insensitivity to insulin

43
Q

basic pathophys of DM

A

increased serum glucose stimulates insulin release from pancreatic islet cells; serum insulin stimulates uptake of glucose into skeletal muscle, fat, and liver cells

44
Q

during the first phase insulin response (after an IV glucose bolus), how does a DM pts response compare to a non-DM person?

A

insulin secretion rate is decreased in a diabetic during that bolus

45
Q

what receptor is a part of the insulin resistance pathway?

A

PPAR gamma

46
Q

do insulin and glucose have the same cell receptor?

A

no

47
Q

what is insulin resistance? how are insulin levels during resistance?

A

breakdown in signaling that starts with insulin binding, which activates a 2nd messenger and causes glucose transport into cells; pts have HYPERinsulinemia which is what leads to the resistance

48
Q

what three things are increased when a patient has impaired fasting glucose?

A

insulin production, fasting plasma glucose, and insulin resistance

49
Q

when comparing pts with impaired fasting glucose vs type 2 DM, how do fasting blood glucose, insulin production, and insulin resistance compare?

A

FPG: sharp increase in type 2 DM compared to slight increase in IFG pts
Insulin production: decreased in type 2 DM vs IFG pts
Insulin resistance- higher in Type 2 DM than IFG pts but levels off/hits a threshold in type 2 pts

50
Q

according to Hadley, what type of disease is related to insulin resistance?

A

macrovascular disease (due to supranormal insulin levels)

51
Q

according to the ADA’s criteria for diabetes, what is the A1C level? fasting BS, random BS w diabetic symptoms, and OGTT?

A

A1C >6.5%
Fasting BS: > or equal to 126
Random BS: > or equal to 200 w symptoms
OGTT: 75g glucose with BS > or equal to 200 at 2 hrs

52
Q

what are normal A1C, FPG, and OGTT levels?

A

A1C < 5.7%
FPG < 100 mg/dl
OGTT <140 mg/dl

53
Q

what is hemoglobin A1C? what does this percent depend on? how often is it checked?

A

covalent modification of hemoglobin beta chain (glycosylated Hb); the % depends on overall average blood sugar over the lifespan of the RBC; therefore, its checked every 2-3 months

54
Q

after what fasting plasma glucose number is when you start seeing diabetes complications?

A

126

55
Q

for patients with increased FPG or HgA1c, what disease state has been on the rise?

A

retinopathy

56
Q

what are common diabetic symptoms? (6)

A

polydipsia, polyuria, weight loss, fatigue, nonhealing skin ulcers, blurring of vision (acute symptom that can be reversed once sugars are controlled)

57
Q

what are the 5 main disease states due to diabetic complications?

A

lipid derangements (LDL could go up or down), macrovascular disease, microvascular disease, neurological disease, integumentary/connective tissue changes

58
Q

what are the three main types of macrovascular disease?

A

1) . ATHEROSCLEROSIS (main one)
2) . CAD
3) . PVD

59
Q

what are two main types of microvascular disease?

A

1) . retinal proliferation and blindness

2) . glomerular changes leading to nephropathy and renal failure

60
Q

what lab value ratio is a good measure of nephropathy/renal failure?

A

protein/creatinine ratio

61
Q

why is neurological disease a severe diabetic complication?

A

bc there is impairment of nerve vascular supply (bad for healing and ulcers)

62
Q

based on tight control studies, how did tight control of blood sugars in DM 1 pts impact diabetic complications? what does this result suggest?

A

when these pts have good control of their sugars, they had a decreased in all diabetic complications, which suggests that glycemic control should be a primary target of tx

63
Q

what was the first study to show that glycemic control in type 1 diabetics had a beneficial effect on diabetic complications?

A

DCCT (DM complications vs glycosylated hemoglobin)

64
Q

what was the main outcome of the UKPDS (united kingdom prospective diabetes study)?

A

it was the first study to show that reducing BP (having tighter control) had just as beneficial impact in reducing diabetic complications compared to glycemic control for type 2 DM pts

65
Q

what were the two results of metformin use in the UKPDS?

A

CVD improved with intensive metformin, but not sulfonylurea/insulin tx; metformin only impacted Macrovascular things

66
Q

what type of diabetic complication is more strongly related to supranormal insulin levels?

A

macrovascular disease- atherosclerosis

67
Q

how do you best monitor Type 2 DM sugar levels?

A

hemoglobin A1c- more reliable than FPG

68
Q

Are there guidelines for monitoring type 2 DM pts with fasting blood glucose?

A

no recommendations for regular self monitoring, UNLESS on meds that can cause hypoglycemia (don’t need to monitor with metformin)

69
Q

what are 5 steps to tx approach of type 2 DM?

A

1) . diet and exercise
2) . oral therapy
3) . other insulin therapies (some non oral)
4) . insulin added to oral therapy
5) . surveillance for complications
* *most drugs are additive (can remove agents as needed too)

70
Q

nowadays what is metabolic syndrome referred to as?

A

global cardiovascular risk

71
Q

what are some risk factors of metabolic syndrome?

A

glucose intolerance/insulin resistance/high insulin levels, obesity, hypertension, dyslipidemia, endothelial dysfunction

72
Q

what are the criteria for metabolic syndrome? what is an important thing to remember about this criteria?

A

any three of the following:

1) . inc waist circumference (men>40 in, women>35 in)
2) . FPG (>100)
3) . elevated BP
4) . serum TG level (>150)
5) . dec HDL (men <40 mg/dl, women< 50mg/dl)
* *important to remember there are ethnic differences: Asians are at a higher risk than other ethnicities

73
Q

what type 2 DM drug must be taken with food? why?

A

Meglitinides; this drug stimulates beta cells to produce insulin at meal time

74
Q

what type 2 DM drug is best used to promote 1st phase insulin secretion?

A

GLP1 agonist byetta/exenatide

75
Q

what GLP1 agonist drug has a broad indication for Type 2 DM pts with preexisting CVD?

A

Liraglutide/Victoza

76
Q

What is one benefit of SGLT2 inhibitors (Type 2 DM)?

A

weight loss

77
Q

What is the purpose of intrinsic factor?

A

binds to B12 and protects it from breaking down in the gut’s acidic environment; if you don’t have intrinsic factor the you’ll be B12 deficient

78
Q

Should POS be diagnosed with an ultrasound? why?

A

no, because not all women present with visible ovary cysts

79
Q

statistically, how can advice from a provider impact obesity tx?

A

patients are 2x likely to lose 5% of body weight if they have been told that they are overweight

80
Q

describe leptin levels of obese patients

A

obese patients have high leptin levels bc the hypothalamus is insensitive to levels (therefore, hypothalamus cant provide appropriate feedback of decreasing appetite for weight loss)

Clin Med- P (124 decks)

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