EXAM 2- DIABETES MELLITUS Flashcards

1
Q

What is glucose?

A

a simple carbohydrate, a monosaccharide

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2
Q

What is glucose involved with?

A

cellular respiration
body’s main source of energy

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3
Q

Glycogen

A

insulin allows glucose to be stored in the liver as glycogen, liver can release glucose back into circulation when glucose levels start to fall after eating a meal

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4
Q

Glycolysis

A

glucose catabolism in cells, yield 2 molecules of pyretic acid and net gain of 2 ATP

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5
Q

Gluconeogenesis

A

production of glucose from lactation and amino acids, important in starvation

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6
Q

Glycogenolysis

A

in the presence of glucagon, glycogen is released by the liver as glucose

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7
Q

Glycogenesis

A

production of glycogen in the liver when there is excess carbohydrates

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8
Q

What are the two most important organs in glucose concentration

A

1) pancreas
2) liver

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9
Q

Which macros break into glucose?

A

carbohydrates, lipids, proteins

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10
Q

How is glucose made and stored in plants?

A

made from CO2 and H2O during photosynthesis, stored as starch

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11
Q

How is glucose transported?

A

NOT diffusion, but protein carrier molecules (facilitated diffusion)
moves from HIGH to LOW
INSULIN facilitates

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12
Q

What controls glucose utilization?

A

rate of insulin secretion
glucose diffusion is increased by presence of insulin by 10x or more

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13
Q

Glucose diffusion across cell membrane is limited EXCEPT in?

A

the liver and brain

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14
Q

What is the exocrine function of the pancreas?

A

digestive enzymes

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15
Q

What is the endocrine function of the pancreas?

A

hormones

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16
Q

Alpha cells are associated with?

A

glucagon

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17
Q

Beta cells are associated with?

A

insulin and amylin

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18
Q

What is glucagon?

A

insulin antagonist
stimulated by decreased blood glucose levels
acts in liver to increase glucose

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19
Q

What is amylin?

A

delays gastric emptying, suppresses glucagon secretion, satiety

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20
Q

What is insulin secretion stimulated by?

A

increased blood glucose, parasympathetic nervous system, amino acids, GI hormones

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21
Q

When insulin binds and activates cell surface receptors, what happens?

A

promotes cellular uptake of glucose, facilitates intracellular transport of K, phosphate, and Mg

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22
Q

How is insulin an anabolic hormone?

A

glucose uptake in liver, muscle, and adipose tissue, stimulates protein and fat synthesis, decreased blood glucose

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23
Q

Which cells do not require insulin?

A

brain, RBCs, kidney, lens of eye

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24
Q

What is the expectancy for a red blood cell?

A

120 days

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25
What do hemoglobin A1c levels indicate?
2-3 month average of glucose glucose enters hbg without insulin
26
What is a normal HbA1c?
<5.7%
27
What is a prediabetic HbA1c?
5.7-6.4%
28
What is a poor HbA1c?
>7%
29
What are normal glucose levels?
<100 after fating 8 hours <140 2 hours after eating
30
What happens to the pancreas over time if there are high glucose levels?
the ability of pancreatic cells to make insulin is diminished overcompensation by pancreas = high insulin levels
31
Changes that occur with high glucose levels can lead to atherosclerosis of blood vessels including:
kidney disease, CVA, MI, vision loss, decreased IS function, nerve damage, poor circulation
32
What population is type 1 DM most common in?
pediatrics, diagnosis around 12 years, about 5-10% of DM
33
What are the two types of type 1 DM?
idiopathic, autoimmune
34
Genetic exposures to type 1 DM?
about 13% newly diagnosed with close family member w type 1 twins have 50% rate of type 1
35
Environmental exposure to type 1 DM?
drugs, food, viruses
36
Cellular and humoral immunity leads to what?
destruction of 80-90% of beta cells, decrease synthesis, hyperglycemia, decreased amylin secretion
37
Less insulin leads to?
increased glucagon
38
symptoms of DM
always tired, frequent urination, sudden weight loss, wounds that won't heal, sexual problems, always hungry, blurry vision, numb or tingling hands/feet, always thirsty, vaginal infections
39
symptoms of Type 1 DM
increased blood glucose, increased glucose in urine, no glucose for energy, feel hungry, delayed wound healing, recurrent infections, genital pruritus, visual changes, paresthesias, CV symptoms
40
normal serum osmolality
285-295
41
What will happen to your sodium level with hyperglycemia?
decrease
42
Who is mostly diagnosed with type 2 DM?
10% of US adults, native Americans, and alaskan natives
43
What are risk factors for type 2 DM?
genetics and environmental age, obesity, HTN, physical inactivity, family hx, poor diet
44
What is type 2 DM characterized by?
insulin resistance cells do not respond appropriately to insulin in the liver, muscle, or fat insulin molecule abnormal, insulin antagonists, down-regulated receptors, alteration in GLUT, increased glucagon secretion
45
What do adipokines do? obesity r/t DM
1. increase leptin 2. decrease adiponectin 3. leads to inflammation 4. increased insulin resistance
46
What do free fatty acids do? obesity r/t DM
1. decrease tissue response to insulin 2. increased intracellular triglycerides and cholesterol
47
What does inflammation do? obesity r/t DM
it is cytotoxic to beta cells
48
What happens if there is mitochondrial dysfunction? obesity r/t DM
activity is reduced
49
Type 2 risk factors you can't fix
45 yrs and older gestational diabetes high risk ethnic background close relative with diabetes other medical conditions
50
Type 2 risk factors you can improve
high weight high blood pressure low activity level cholesterol numbers
51
vague symptoms of type 2 DM
fatigue recurrent infections visual changes prolonged wound healing
52
testing done for type 2 done on those who are high risk, if you are:
overweight dyslipidemia HTN
53
in both type 1 and type 2 there is:
an excess amount of glucose in the blood that cannot be used by the cells
54
Are type 2 symptoms always evident early?
no so organ damage may occur
55
What happens to babies with gestational diabetes
they get bigger d/t increased metabolic demands they can get hypoglycemia
56
What fixes gestational diabetes?
having the baby
57
What increases in the mother during gestational diabetes?
glucose, amino acids, and lipids
58
What happens during steroid-induced diabetes?
steroids cause increase in glucose levels, so pancreas cannot produce enough insulin
59
What happens in the brain with hyperglycemia?
decreased satiety
60
What happens in the liver with hyperglycemia?
increase gluconeogenosis
61
What happens in the pancreas with hyperglycemia?
decreased insulin secretion increased glucagon secretion
62
What happens in the intestine with hyperglycemia?
decreased GLP-1 secretion
63
What happens in the kidneys with hyperglycemia?
increased gluconeogensis increased glucose reabsorption
64
What happens in the muscles with hyperglycemia?
decreased glucose uptake
65
What happens to fat with hyperglycemia?
increase free fatty acids decreased adiponectin increased inflammatory cytokines
66
acute complication of diabetes
hypoglycemia diabetes ketoacidosis (DKA) hyperosmolar hyperglycemic nonketotic syndrome
67
What is hypoglycemia related to?
treatment insulin shock or reaction greatest risk with type 1
68
symptoms of hypoglycemia
pallor, tremor, anxiety, tachycardia/palpitations, diaphoresis, headache, dizziness, irritability, fatigue, confusion, seizures, feels like you're drunk!
69
What is the treatment for hypoglycemia?
Give glucose D50 (25 gm glucose in 50 mL water) huge osmolality
70
What system would you assess for a complication of D50?
lungs d/t fluid overload
71
A person with diabetes has had good control of their glucose, HA1c would be?
5.3%
72
What happens with DKA?
decreased insulin, increased resistance increased counterregulatory hormones
73
Who typically has DKA?
type 1 DM symptoms seen before blood sugar gets too high
74
What does DKA do?
enhances break down of fatty acids - ketone bodes ketone bodies are then transported into tissues, pH goes very low (acidic)
75
What happens with acidosis?
excess hydrogen ions body tries to correct pH (shift H into cells, K out) increased urine output, lose K from kidney
76
What are patient symptoms with DKA?
breathing deep and fast, fruity breath, high glucose
77
What will happen to the measured K level in a someone in DKA?
increase
78
What will happen with the total body K level, in a patient with DKA, if their kidneys work?
decrease
79
How to treat DKA?
rehydrate (volume) give insulin
80
Who typically has HHNS?
type 2 DM (there is insulin to help prevent ketosis) high mortality rate
81
What can glucose be with HHNS?
>1000, hyperglycemia
82
symptoms of HHNS?
excessive thirst, high urine output, dry mouth, weakness, fever, warm dry skin, N/V, leg cramps, vision changes, confusion, hallucinations
83
treatment for HHNS?
volume, electrolytes, insulin
84
chronic complication sof diabetes
capillary damage (microvascular) retinopathy, nephropathy, neuropathy
85
diabetic retinopathy
retinal hypoxemia 1. capillary permeability, vein dilation, micro aneurysms 2. retinal ischemia 3. scar tissue
86
protect eyes with TRACK
t- take meds r- reach healthy weight a- add physical activity c- control a1c, bp, cholesterol k- kick smoking
87
diabetic neuropathy
most common chronic ischemia demyelination lose pain, temp, vibration sensation starts in hands/feet deteriorate weight-bearing joints
88
diabetic nephropathy
glomerular changes start early glucose bonds to protein increased renal blood flow = hyperfiltration glomerular sclerosis
89
risk factors for diabetic kidney disease
hyperglycemia, systemic HTN, obesity, oxidative stress, inflammation
90
macrovascular complications of diabetes
CVD, stroke, PVD, HF
91
infection as a complication of diabetes
diminished warning signs, tissue hypoxia, rapid proliferation of pathogens, fungal/yeast/UTI/gangrene