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Diabetes Mellitus Flashcards

1
Q

What is the common underlying problem with diabetes type 1&2?

A

hyperglycemia

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2
Q

What is type 1 diabetes?

A

a genetically inherited condition that creates an absolute insulin deficiency, 5-10% of cases of diabetes, destruction of pancreatic beta cells

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3
Q

What is type 2 diabetes?

A

can be genetically/environmentally related condition, insulin deficiency + insulin resistance, obesity is a big factor, some reversibility, 90-95% of cases

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4
Q

How can hyperglycemia lead to polyuria and polydipsia?

A

polyuria: increased levels of glucose in the blood causes the body to try and excrete it via urination

polydipsia: increased urine output leads to an overall decrease of volume in the blood so the body triggers thirst mechanism

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5
Q

What leads to weight loss in type 1 diabetics?

A

when their disease is not well controlled, their body will panic and start breaking down anything (like fats and amino acids) in order to provide energy for the body. But the body can’t take it up so the body just loses weight

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6
Q

Why is HgbA1c an important value to monitor in DM?

A

it gives us a big picture idea of how glucose levels have looked over a red blood cells lifetime (120 days)

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7
Q

What causes vision loss in persons with DM?

A

the polyol pathway will get glucose shunted to it causing build-up of sugar, damage to blood vessels, and eventually vision loss. This leads to retinopathy, basement membrane thickening, hemorrhages, and retinal detachment

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8
Q

Why do individuals with DM have a high risk of dying from a myocardial infarction?

A

damage in their vessels can lead to atherosclerosis (thickening and plaque build-up in blood vessels), endothelial dysfunction, arterial SM proliferation, thrombosis, inflammation, and coronary artery disease

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9
Q

How does microvascular disease cause retinopathy, nephropathy, and neuropathy as chronic complications of DM?

A

chronic hyperglycemia causes damage to the blood vessels, which leads to atherosclerosis, and then the polyol pathway will have glucose shunted to it causing further issues

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10
Q

What contributes to leg/foot/toe amputations in a person with DM?

A

macro/microvascular disease (reduced blood flow), neuropathy (reduces sensation), and infection contributes to amputation

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11
Q

What is the endocrine system?

A

a communication system that involves glands throughout the body that make and release hormones that travel to target tissues and cause an effect

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12
Q

How do hormones work?

A

hormones operate within feedback systems to affect target cells with correlating receptors

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13
Q

What does the liver do to hormones?

A

it inactivates hormones, rendering them water soluble for renal excretion

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14
Q

What does the pituitary gland do?

A

it helps regulate our hormones

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15
Q

What is upregulation of hormone receptors?

A

low concentration of hormone increases number of receptors per cell, making it easier to create a response

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16
Q

What is downregulation of hormone receptors?

A

high concentration of hormone decreases number of receptors per cell, making it harder to create a response

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17
Q

What does feedback affect?

A

the gland/creator of the hormone

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18
Q

What does regulation affect?

A

the target cell

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19
Q

What are the two types of hormones?

A

water-soluble and lipid-soluble

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20
Q

What do water-soluble hormones do?

A

they circulate freely and unbound, having a short half-life

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21
Q

What do lipid-soluble hormones do?

A

they bind to carriers and circulate in bound form, having a long half-life

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22
Q

What hormones can cross membranes?

A

fat-soluble hormones such as reproductive steroids and thyroid hormone can cross membranes freely

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23
Q

How do water-soluble hormones cross membranes?

A

they need to use membrane receptors to cross and then utilize a second messenger to initiate a response

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24
Q

What kind of hormone is insulin?

A

insulin is water-soluble

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25
What is the pancreas role in the endocrine system?
it is an endocrine and exocrine gland; houses the islet of Langerhans (where endocrine cells live)
26
What cells are found in the pancreas?
alpha (glucagon producing), beta (insulin producing), delta (somatostatin and gastrin producing) and F cells (pancreatic polypeptide producing)
27
What is insulin?
a water-soluble hormone produced by beta cells
28
What does insulin do?
it facilitates glucose uptake into many cells of the body and carries potassium into cells; it also promotes the synthesis of proteins, carbs, and lipids (anabolic processes)
29
What stimulates insulin to be made?
increases blood glucose levels promotes insulin secretion
30
What turns down insulin production?
hypoglycemia
31
What cells/tissues DO require insulin for glucose uptake?
skeletal muscle, cardiac muscle, and adipose tissue
32
What cells/tissues do NOT require insulin for glucose uptake?
RBCs, kidneys, lens of eye, brain, blood vessels, etc.
33
What is the issue in cells that don't require insulin for glucose uptake?
they can't down-regulate glucose uptake (high levels won't be facilitated and will continue to cause responses)
34
What is glucagon?
a hormone secreted by alpha cells that counterbalances insulin
35
What does glucagon do?
it stimulates glycogenolysis (breaking glycogen into glucose), gluconeogenesis (creating glucose from AAs, glycerol, and lactate) and lipolysis (catabolic processe)
36
What stimulates glucagon production?
decreased blood glucose levels and decreased insulin levels
37
The secretion of insulin from pancreatic beta cells is promoted by...?
increased blood glucose levels
38
What is insulin deficiency?
defective insulin secretion, the beta cells aren't doing their job
39
What is insulin resistance?
defects of insulin action target cells
40
What is diabetes mellitus (DM)?
the bodies inability to produce/use insulin efficiently leading to high blood glucose levels (hyperglycemia)
41
How do we diagnose DM?
we use different tests, they don't all need to be positive for a diagnosis
42
What is the normal blood glucose level?
70-120 mg/dl *somewhat variable based on person, watch symptoms
43
What is a fasting plasma glucose test (FPG)?
a test in which you have no caloric intake for 8 hours and then your levels are checked; results greater than or equal to 126 mg/dl is a positive result
44
What is oral glucose tolerance test (OGTT)?
a test in which you give the patient something sweet then see if their blood glucose goes back to normal after 2 hours; plasma glucose greater than or equal to 200 mg/dl 2 hours past eating is a positive result
45
What is a random plasma glucose?
a test where you randomly draw and test glucose levels, not widely used; greater than or equal to 200 AND symptoms of DM is a positive result
46
What is glycated hemoglobin test (HbA1C)?
a test that measures accumulation of glycated hemoglobin in RBC over the past 120 days (a RBCs lifespan); levels greater than or equal to 6.5% is a positive result
47
Why is HbA1C an especially important test for DM?
it gives us a bigger picture over a longer period of time as to a person's glucose levels
48
What is the OGTT range for prediabetes?
<200 mg/dl to > or equal to 140 mg/dl
49
What is the FPG range for prediabetes?
<126 mg/dl to > or equal to 100 mg/dl
50
What is the A1C range for prediabetes?
<6.5% to > or equal to 5.7%
51
What are the classifications of DM?
type 1 and type 2, and gestational diabetes
52
What is type 1 diabetes?
an absolute insulin deficiency, there is no/little insulin being made
53
What is type 2 diabetes?
insulin resistance + insulin deficiency, receptors have issues
54
What is gestational diabetes?
a glucose intolerance that onsets during pregnancy
55
What are islet cell autoantibodies?
two or more autoantibodies in order to get diabetes
56
What is the basic pathophysiology of type 1 diabetes?
insulin deficiency -> decreased glucose uptake into cells -> hyperglycemia -> cell starvation -> lipolysis -> increased ketone production -> altered metabolism
57
What are the clinical manifestations of type 1 diabetes?
hyperglycemia; glucosuria, POLYURIA, dehydration, POLYDIPSIA, altered metabolism; weight loss, fatigue, polyphagia, cell starvation and lipolysis; ketonemia, ketonuria, ketoacidosis, kussmaul respirations; hyperkalemia -> coma/death
58
What are some symptoms of hypoglycemia in diabetics?
hypoglycemia (insulin reaction/shock), symptoms include tachycardia, palpitations, diaphoresis, tremors, anxiety, dizziness, fatigue, visual changes, confusion, seizures, coma
59
How do we treat hypoglycemia in diabetics?
give them a fast-acting source of sugar (in liquid form if possible) and then give them something solid and long acting after
60
What are the acute complications of type 1 diabetes?
hypoglycemia, diabetic ketoacidosis, and kussmaul respirations
61
What is diabetic ketoacidosis (DKA)?
blood sugar is WAY high due to insulin deficiency/glucagon excess leading to lipolysis, ketonemia, and ketonuria
62
How do we diagnose DKA?
metabolic acidosis (pH<7.30, bicarb <18), glucose >250 mg/dl, and presence of urine and serum ketones
63
How does blood sugar level change when stressed or sick?
it increases (even if not eating) in order to get you ready to go/heal if needed
64
How do we treat diabetes type 1?
insulin supplementation REQUIRED, meal/exercise planning, optimal glucose control, preventing acute complications (hypoglycemia and DKA), and pancreas transplant
65
What is metabolic syndrome?
a syndrome that increases risk of heart disease and stroke
66
How do we diagnose metabolic syndrome?
3 of the following must be positive; central obesity, elevated triglycerides, decreased HDL, pre-hypertension and FPG
67
What central obesity range qualifies as metabolic syndrome?
waist >40 inches in men, >35 inches in women
68
What elevated triglyceride range qualifies as metabolic syndrome?
>150 mg/dl
69
What decreased HDL range qualifies as metabolic syndrome?
<40 mg/dl in men, <50 in women
70
What pre-hypertension range qualifies as metabolic syndrome?
>130/85
71
What FPG range qualifies as metabolic syndrome?
>100 mg/dl
72
What are abnormalities of insulin signaling pathway that lead to insulin resistance?
abnormal insulin molecule, alteration of glucose transporter proteins (GLUT4), and downregulation of insulin receptors
73
How does obesity contribute to insulin resistance?
it causes altered adipokines (leptin, adiponectin) which effect beta cell production, elevated serum free fatty acids which causes cell death, and increases in inflammatory cytokines which affect insulin receptors on cells
74
How is oxidative stress a consequence of hyperglycemia?
hyperglycemia causes excessive production of reactive oxygen species which increases oxidative stress while damaging large and small vessels
75
How is shunting glucose to the polyol pathway a consequence of hyperglycemia?
excess glucose is shunted through places it isn't required for glucose transport and is converted to sorbitol there to then increase osmotic pressure causing cellular edema and injury
76
How is inappropriate protein kinase C (PKC) activation a consequence of hyperglycemia?
PKC is a group of intracellular signaling proteins that will cause insulin resistance and affect blood vessels negatively
77
What is glycation?
a reversible process where glucose attaches to proteins and lipids
78
How is glycation a consequence of hyperglycemia?
glucose irreversibly binds during this process and AGEs are produced which leads to negative vascular effects and promotes beta cell death and insulin resistance
79
In short, how does hyperglycemia interact with oxidative stress?
overproduction of reactive oxygen species
80
In short, how does hyperglycemia interact with the polyol pathway?
excessive intracellular accumulation of sorbitol
81
In short, how does hyperglycemia interact with protein kinase C?
inappropriate activation of intracellular signaling proteins
82
In short, how does hyperglycemia interact with glycation?
glucose irreversibly binds to various cells/tissues
83
What are the chronic complications of DM?
microvascular and macrovascular disease
84
What is microvascular disease?
disease of the capillaries (retinopathy, nephropathy, and neuropathy); more duration/magnitude of hyperglycemia = more microvascular disease
85
What is retinopathy?
retinal capillary damage due to basement thickening, increases permeability, formation of hemorrhages, retinal ischemia/infarcts, retinal detachment, can lead to vision loss or blindness
86
What is nephropathy?
glomerular damage due to glomerular hyperperfusion and hypertension, increases permeability, glomerulosclerosis, decreased glomerular blood/filtration rate
87
What are clinical manifestations of nephropathy?
proteinuria/albuminuria, decreased GFR, increases creatinine and BUN, progression to end-stage kidney disease with symptoms of uremia, risk for hypoglycemia in type 1 DM
88
What is neuropathy?
effects of oxidative stress, polyol pathway, PKC and AGEs lead to neurovascular damage and peripheral neuron dysfunction
89
What are clinical manifestations of neuropathy?
sensory like numbness, tingling, burning, pain, "stocking and glove" pattern, and risk for injury to feet motor like weakness, gait disturbances, depressed reflexes, and risk for falls
90
What makes macrovascular disease worse?
hyperlipidemia, hypertension, and smoking
90
What is macrovascular disease?
disease of medium and large arteries; premature atherosclerosis (correlates with duration of DM)
91
What is premature atherosclerosis?
damage to blood vessels leading to endothelial dysfunction, arterial smooth muscle proliferation, thrombosis, and inflammation (stiffness and plaque build-up)
92
What are the consequences of atherosclerosis with DM?
coronary artery disease (CAD), cerebral infarct (stroke), peripheral arterial disease (PAD)
93
How can DM increase the risk of infection?
through altered senses, compromised vascular supply and hypoxia, pathogen proliferation and immunosuppression
94
What is the single most important contributing factor to the morbidity and mortality associated with diabetes?
CHRONIC HYPERGLYCEMIA
95
What is the single most important measure that can vastly improve outcomes for those with diabetes?
OPTIMAL BLOOD GLUCOSE CONTROL

Pathophysiology (8 decks)

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