CH 20: integrated patho concepts Flashcards
1
Q
important sugar for making ATP, an essential energy source.
A
glucose
2
Q
anabolic hormone required for uptake of glucose
A
insulin
3
Q
key functions of insulin
A
-Promoting glucose usage, thereby decreasing blood glucose levels
-Promoting protein synthesis
-Promoting the formation and storage of lipids
-Facilitating transport of potassium, phosphate, and magnesium into the cells
4
Q
endocrine glands of the pancreas secrete:
A
hormones (insulin and glucagon)
5
Q
exocrine glands of the pancreas secrete:
A
digestive enzymes and alkaline fluids through the pancreatic duct into the duodenum.
6
Q
pancreatic islets 3 major groups of hormone-secreting cells
A
alpha cells
beta cells
delta cells
7
Q
alpha cells secrete:
A
glucagon
8
Q
beta cells secrete
A
insulin
9
Q
delta cells secrete
A
somatostatin and gastrin
10
Q
insulin secretion is increased when there are elevations in:
A
(1) blood glucose;
(2) amino acids;
(3) potassium, phosphate, and magnesium
(4) glucagon and gastrin
11
Q
insulin secretion is decreased with:
A
low blood glucose,
high levels of insulin (through negative feedback mechanisms)
stimulation of alpha cells.
12
Q
the inability to regulate the amount of glucose in the body
A
DM
13
Q
onset in puberty of childhood (10-14) because of insulin deficiency
A
Type 1 DM
14
Q
onset in adult years from insulin resistance
A
type 2 DM
15
Q
onset in pregnancy from insulin resistance
A
gestational DM
16
Q
One or a combination of the following characterizes the basic pathophysiology in the various types of diabetes:
A
- A complete destruction of pancreatic beta cells leading to a lack of insulin secretion
- Reduced insulin secretion from impaired beta cell function in response to glucose stimulation
- A peripheral resistance to insulin
17
Q
chronic problem of carb, fat and protein metabolism - insulin deficit
A
Type 1 DM
18
Q
etiology of type 1 DM
A
insulin deficiency
multifactorial and includes both genetic and environmental influences leading to autoimmune destruction of beta cells
19
Q
fat oxidation produced hyperketonemia leads to state of:
A
metabolic ketoacidosis
20
Q
condition in which excess glucose promotes the attraction of water into the kidneys causing increased urination.
A
osmotic diuresis
21
Q
blood test that determines hemoglobin and red blood cell exposure to glucose over the previous 3 to 4 months.
A
HbA1c
22
Q
clinical manifestations of type 1 DM
A
Polydipsia—excessive thirst
Polyuria—excessive urination
Polyphagia—excessive hunger
]nocturia (waking up at night to urinate),
fatigue,
lethargy,
unexplained weight loss,
blurred vision.
23
Q
diagnostic criteria of type 1 DM
A
patient history
physical
labs
presence of CM
24
Q
blood glucose expected values
A
70-120
25
blood glucose significant diagnostic findings
>200 along with CM
26
fasting blood glucose significant diagnostic findings
>126 on two occasions after fasting
27
glucose tolerance test directions
individual is given 50-100g of glucose dissolved in water
blood glucose measured at 1,2, and 3 hours
28
expected range of glucose tolerance test
120-160 at 1 hour
70-120 at 2 hours
29
significant diagnostic findings of glucose tolerance test
>190 after 1 hour
>165 after 2 hours
30
A1c expected findings
2%-6%
31
A1c significant diagnostic findings
8% and great signifies prolonged hyperglycemia
32
urinalysis expected findings
negative for glucose
negative for ketones
33
urinalysis significant diagnostic findings
glucose >15
ketones present
34
treatment for DM requires balance of:
1. Glycemic control
2. Exercise
3. Insulin replacement therapy
35
goal of treatment for DM
stabilize blood glucose levels within the expected range (70 to 120 mg/dL).
36
types of insulin
1. Rapid onset, short acting (also called regular)
2. Intermediate acting
3. Slow onset, long acting
37
rapid acting insulin onset, peak and duration / when to administer and ex
onset = 15 min
peak = 1 hour
duration = 2-4 hours
when = immediately before a meal
ex = Lispro
38
short acting insulin onset, peak and duration / when to administer and ex
onset = 30 min
peak = 2-3 hours
duration = 3-6 hours
when = throughout the day
ex = regular, Humulin R
39
intermediate acting insulin onset, peak and duration / when to administer and ex
onset = 2-4 hours
peak = 4-12 hours
duration = 12-20 hours
when = throughout the day
ex = NPH
40
long acting insulin onset, peak and duration / when to administer and ex
onset = 6-10 hours
peak = 8-12 hours
duration = 20-26 hours
when = nighttime
ex = Ultralente
41
glargine insulin onset, peak and duration / when to administer
onset = 2-4 hours
peak = none
duration = up to 24 hours
when = nighttime
42
problem of insulin resistance and a reduction in a adequate insulin secretion
type 2 DM
43
rare form of type 2 diabetes that has a strong genetic component (autosomal dominant inheritance) and is found to affect individuals younger than 25 years of age.
maturity-onset diabetes of the young
44
causes of type 2 diabetes
cause of type 2 diabetes is unknown; however, genetic and environmental factors appear to contribute to its development. The most significant risk factor is obesity,
45
sub-adequate levels of insulin and peripheral resistance to insulin uptake leads to the following:
1. Beta cells do not adequately respond to circulating blood glucose levels.
2. The release of glycogen from the liver coupled with the suppression of insulin by glucagon promotes excessive circulating glucose.
3. The insulin receptors in the liver, skeletal muscle, and adipose tissues are unresponsive, thereby making the tissues unable, or resistant to, using the insulin.
46
clinical manifestations of type 2 diabetes
asymptomatic
visual changes,
changes in kidney function,
coronary artery disease,
peripheral vascular disease,
recurrent infections,
neuropathy.
47
diagnosis of type 2 diabetes
random or fasting blood glucose measurements
clinical manifestations
glucose over 200
48
treatment of type 2 diabetes
weight control
oral glycemic agent
insulin replacement therapy
EXERCISE
49
act to increase insulin release by the beta cells, increase glucose production by the liver, or increase the uptake of insulin by cells.
glycemic agents
50
oral glycemic agents that slows carb digestion
alpha-glucosidase inhibitors (acarbose, migitol)
51
oral glycemic agent that prevents excessive glucose release from the liver; makes tissue more sensitive to insulin
biguanides (metformin)
52
oral glycemic agent that stimulate more secretion fo insulin from pancreas; short acting
meglitinides (repaglinide)
53
oral glycemic agent that stimulates more secretion of insulin from the pancreas
sulfonylureas
54
oral glycemic agent that increases sensitivity of tissues
thiazolidinediones
55
defined as any degree of glucose intolerance that occurs during pregnancy - usually temporary,
gestational diabetes mellitus
56
gestational diabetes can lead to:
Fetal macrosomia (abnormally large body size)
Hypoglycemia from pancreatic hyperplasia and excess insulin secretion in the newborn
Hypocalcemia
Hyperbilirubinemia
A 5% to 10% incidence of major developmental anomalies, such as spina bifida or heart defects.
57
glucose deprivation in the brain
neuroglycopenia
58
responses related to the adrenal glands
adrenergic symptoms
59
hypoglycemia can occur from:
-Hyperinsulinemia (high circulating insulin levels) as can occur with administering exogenous insulin to treat diabetes
-Inadequate food intake or vomiting, in which glucose in the body is reduced
-Frequent simple carbohydrate intake
-Strenuous exercise or infection, which uses excessive glucose
60
hypoglycemia is most commonly found in patients with:
type 1 diabetes who are undergoing insulin replacement therapy
61
clinical manifestations of hypoglycemia
poor concentration,
extreme hunger,
clammy/cool skin,
blurred vision,
dizziness and confusion,
difficulty with speech,
lack of coordination,
staggering gait,
headache.
increase in the pulse,
along with palpitations,
sweating,
anxiety,
tremors.
Loss of consciousness,
seizures,
coma,
death can occur if hypoglycemia is not treated.
62
problem of deficient insulin and severe hyperglycemia leading to a state of metabolic acidosis and severe osmotic diuresis
DKA
63
clinical manifestations of DKA
polyuria
polydipsia
polyphagia,
nocturia,
weight loss
fatigue
Abdominal pain
vomiting
kussmal respirations
sweet, fruity breath
64
deep, rapid respirations that release excess acids through the lungs.
Kussmaul respirations
65
treatment focus of DKA
stabilizing blood glucose levels,
correcting acidosis,
replacing fluids and electrolytes,
improving tissue perfusion.
66
severe hyperglycemia results from increased insulin resistance and excessive carbohydrate intake
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS)
67
Hyperglycemic hyperosmolar nonketotic syndrome (HHNK) is characterized by:
Type 2
Hyperglycemia, often above 600 mg/dL
High plasma osmolarity
Dehydration
Lack of (or mild) ketosis
Changes in the level of consciousness
68
chronic complications of DM
retinopathy
cataracts
glaucoma
dizziness and syncope
hemorrhage
hypertension
ischemic heart disease
MI
D/constipation
bladder infection
ED
CKD
foot ulcers
PVD
gangrene
69
DM complication classification
1. Microvascular (relating to small vessels)
2. Macrovascular (relating to large vessels)
3. Neuropathies (relating to peripheral nerves)
70
microvascular conditions
retinopathy
nephropathy
glycosylation
aldose reductase
sorbitol
free radicals
71
education on preventing DM complications
A = advice to follow diet, weight loss, exercise program, and lifestyle modifications
B = blood pressure reduction
C = cholesterol reduction
D = diabetes hyperglycemia control
E = eye screening
F = foot care
72
macrovascular diseases
CAD
stroke
PVD
73
the buildup of fats, cholesterol and other substances in and on the artery walls. This buildup is called plaque
atherosclerosis
74
nerve degeneration that results in delayed nerve conduction and impaired sensory function.
neuropathy
75
individuals with diabetes are also at increased risk for developing __
infections
76
metabolic syndrome descriptions
*includes insulin resistance and a constellation of other metabolic problems,
*including obesity,
*high triglyceride levels,
*low high-density lipoprotein (HDL) levels,
*hypertension, and
*coronary heart disease
77
labs for type 2 DM
otwo separate fasting blood glucose measurements are needed. If both are above 126 mg/dL, type 2 diabetes may be suggested.
oA fasting plasma glucose between 110 and 125 mg/dL indicates “impaired fasting glucose” and requires close monitoring because there is a high risk of developing diabetes over time.
opresence of antibodies against the islet cells or GAD would indicate that this person does not have type 2 diabetes, but rather has type 1.
78
acute complications of DM
o Hypoglycemia
o Diabetic Ketoacidosis
o Hyperglycemic Hyperosmolar Nonketotic Syndrome
o Somogyi Effect
o Dawn Phenomenon
79
chronic complications of DM
o Microvascular
o Macrovascular
o Neuropathy
o Infection
80
hyperglycemia clinical manifestations
3 Ps
Nocturia
Weight loss
Fatigue
Kussmaul respirations
Sweet fruity breath
Decreased LOC
81
treatment for hyperglycemia
Stabilize glucose levels
Replace fluids and electrolytes
Treat any cause
82
Somogyi effect
Rebound hyperglycemia related to insulin induced hypoglycemia
83
dawn phenomenon
Glucose higher in the morning than before going to bed
Related to release of hormones and triggers insulin resistance and release of glucose from the liver
Differs hyperglycemia is not related to overnight hypoglycemia
Evening snacks and medication adjustments
84
glucagon function
which mobilizes glycogen from the liver and suppresses insulin secretion; glucagon is critical in maintaining blood glucose levels between meals.
85
insulin function
which promotes glucose utilization.
86
somatostatin and gastrin functions
which regulate alpha cell and beta cell function by suppressing the release of insulin, glucagon, and pancreatic polypeptides.
