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Patho Exam 3 > CH 20: integrated patho concepts > Flashcards

CH 20: integrated patho concepts Flashcards

1
Q

important sugar for making ATP, an essential energy source.

A

glucose

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2
Q

anabolic hormone required for uptake of glucose

A

insulin

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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

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4
Q

endocrine glands of the pancreas secrete:

A

hormones (insulin and glucagon)

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5
Q

exocrine glands of the pancreas secrete:

A

digestive enzymes and alkaline fluids through the pancreatic duct into the duodenum.

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6
Q

pancreatic islets 3 major groups of hormone-secreting cells

A

alpha cells
beta cells
delta cells

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7
Q

alpha cells secrete:

A

glucagon

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8
Q

beta cells secrete

A

insulin

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9
Q

delta cells secrete

A

somatostatin and gastrin

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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

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11
Q

insulin secretion is decreased with:

A

low blood glucose,
high levels of insulin (through negative feedback mechanisms)
stimulation of alpha cells.

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12
Q

the inability to regulate the amount of glucose in the body

A

DM

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13
Q

onset in puberty of childhood (10-14) because of insulin deficiency

A

Type 1 DM

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14
Q

onset in adult years from insulin resistance

A

type 2 DM

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15
Q

onset in pregnancy from insulin resistance

A

gestational DM

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16
Q

One or a combination of the following characterizes the basic pathophysiology in the various types of diabetes:

A
  1. A complete destruction of pancreatic beta cells leading to a lack of insulin secretion
  2. Reduced insulin secretion from impaired beta cell function in response to glucose stimulation
  3. A peripheral resistance to insulin
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17
Q

chronic problem of carb, fat and protein metabolism - insulin deficit

A

Type 1 DM

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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

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19
Q

fat oxidation produced hyperketonemia leads to state of:

A

metabolic ketoacidosis

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20
Q

condition in which excess glucose promotes the attraction of water into the kidneys causing increased urination.

A

osmotic diuresis

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21
Q

blood test that determines hemoglobin and red blood cell exposure to glucose over the previous 3 to 4 months.

A

HbA1c

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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.

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23
Q

diagnostic criteria of type 1 DM

A

patient history
physical
labs
presence of CM

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24
Q

blood glucose expected values

A

70-120

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25
Q

blood glucose significant diagnostic findings

A

> 200 along with CM

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26
Q

fasting blood glucose significant diagnostic findings

A

> 126 on two occasions after fasting

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27
Q

glucose tolerance test directions

A

individual is given 50-100g of glucose dissolved in water
blood glucose measured at 1,2, and 3 hours

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28
Q

expected range of glucose tolerance test

A

120-160 at 1 hour
70-120 at 2 hours

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29
Q

significant diagnostic findings of glucose tolerance test

A

> 190 after 1 hour
165 after 2 hours

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30
Q

A1c expected findings

A

2%-6%

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31
Q

A1c significant diagnostic findings

A

8% and great signifies prolonged hyperglycemia

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32
Q

urinalysis expected findings

A

negative for glucose
negative for ketones

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33
Q

urinalysis significant diagnostic findings

A

glucose >15
ketones present

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34
Q

treatment for DM requires balance of:

A
  1. Glycemic control
  2. Exercise
  3. Insulin replacement therapy
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35
Q

goal of treatment for DM

A

stabilize blood glucose levels within the expected range (70 to 120 mg/dL).

36
Q

types of insulin

A
  1. Rapid onset, short acting (also called regular)
  2. Intermediate acting
  3. Slow onset, long acting
37
Q

rapid acting insulin onset, peak and duration / when to administer and ex

A

onset = 15 min
peak = 1 hour
duration = 2-4 hours
when = immediately before a meal
ex = Lispro

38
Q

short acting insulin onset, peak and duration / when to administer and ex

A

onset = 30 min
peak = 2-3 hours
duration = 3-6 hours
when = throughout the day
ex = regular, Humulin R

39
Q

intermediate acting insulin onset, peak and duration / when to administer and ex

A

onset = 2-4 hours
peak = 4-12 hours
duration = 12-20 hours
when = throughout the day
ex = NPH

40
Q

long acting insulin onset, peak and duration / when to administer and ex

A

onset = 6-10 hours
peak = 8-12 hours
duration = 20-26 hours
when = nighttime
ex = Ultralente

41
Q

glargine insulin onset, peak and duration / when to administer

A

onset = 2-4 hours
peak = none
duration = up to 24 hours
when = nighttime

42
Q

problem of insulin resistance and a reduction in a adequate insulin secretion

A

type 2 DM

43
Q

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.

A

maturity-onset diabetes of the young

44
Q

causes of type 2 diabetes

A

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
Q

sub-adequate levels of insulin and peripheral resistance to insulin uptake leads to the following:

A
  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
Q

clinical manifestations of type 2 diabetes

A

asymptomatic

visual changes,
changes in kidney function,
coronary artery disease,
peripheral vascular disease,
recurrent infections,
neuropathy.

47
Q

diagnosis of type 2 diabetes

A

random or fasting blood glucose measurements
clinical manifestations
glucose over 200

48
Q

treatment of type 2 diabetes

A

weight control
oral glycemic agent
insulin replacement therapy
EXERCISE

49
Q

act to increase insulin release by the beta cells, increase glucose production by the liver, or increase the uptake of insulin by cells.

A

glycemic agents

50
Q

oral glycemic agents that slows carb digestion

A

alpha-glucosidase inhibitors (acarbose, migitol)

51
Q

oral glycemic agent that prevents excessive glucose release from the liver; makes tissue more sensitive to insulin

A

biguanides (metformin)

52
Q

oral glycemic agent that stimulate more secretion fo insulin from pancreas; short acting

A

meglitinides (repaglinide)

53
Q

oral glycemic agent that stimulates more secretion of insulin from the pancreas

A

sulfonylureas

54
Q

oral glycemic agent that increases sensitivity of tissues

A

thiazolidinediones

55
Q

defined as any degree of glucose intolerance that occurs during pregnancy - usually temporary,

A

gestational diabetes mellitus

56
Q

gestational diabetes can lead to:

A

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
Q

glucose deprivation in the brain

A

neuroglycopenia

58
Q

responses related to the adrenal glands

A

adrenergic symptoms

59
Q

hypoglycemia can occur from:

A

-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
Q

hypoglycemia is most commonly found in patients with:

A

type 1 diabetes who are undergoing insulin replacement therapy

61
Q

clinical manifestations of hypoglycemia

A

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
Q

problem of deficient insulin and severe hyperglycemia leading to a state of metabolic acidosis and severe osmotic diuresis

A

DKA

63
Q

clinical manifestations of DKA

A

polyuria
polydipsia
polyphagia,
nocturia,
weight loss
fatigue
Abdominal pain
vomiting
kussmal respirations
sweet, fruity breath

64
Q

deep, rapid respirations that release excess acids through the lungs.

A

Kussmaul respirations

65
Q

treatment focus of DKA

A

stabilizing blood glucose levels,
correcting acidosis,
replacing fluids and electrolytes,
improving tissue perfusion.

66
Q

severe hyperglycemia results from increased insulin resistance and excessive carbohydrate intake

A

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

67
Q

Hyperglycemic hyperosmolar nonketotic syndrome (HHNK) is characterized by:

A

Type 2
Hyperglycemia, often above 600 mg/dL
High plasma osmolarity
Dehydration
Lack of (or mild) ketosis
Changes in the level of consciousness

68
Q

chronic complications of DM

A

retinopathy
cataracts
glaucoma
dizziness and syncope
hemorrhage
hypertension
ischemic heart disease
MI
D/constipation
bladder infection
ED
CKD
foot ulcers
PVD
gangrene

69
Q

DM complication classification

A
  1. Microvascular (relating to small vessels)
  2. Macrovascular (relating to large vessels)
  3. Neuropathies (relating to peripheral nerves)
70
Q

microvascular conditions

A

retinopathy
nephropathy
glycosylation
aldose reductase
sorbitol
free radicals

71
Q

education on preventing DM complications

A

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
Q

macrovascular diseases

A

CAD
stroke
PVD

73
Q

the buildup of fats, cholesterol and other substances in and on the artery walls. This buildup is called plaque

A

atherosclerosis

74
Q

nerve degeneration that results in delayed nerve conduction and impaired sensory function.

A

neuropathy

75
Q

individuals with diabetes are also at increased risk for developing __

A

infections

76
Q

metabolic syndrome descriptions

A

*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
Q

labs for type 2 DM

A

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
Q

acute complications of DM

A

o Hypoglycemia
o Diabetic Ketoacidosis
o Hyperglycemic Hyperosmolar Nonketotic Syndrome
o Somogyi Effect
o Dawn Phenomenon

79
Q

chronic complications of DM

A

o Microvascular
o Macrovascular
o Neuropathy
o Infection

80
Q

hyperglycemia clinical manifestations

A

3 Ps
Nocturia
Weight loss
Fatigue
Kussmaul respirations
Sweet fruity breath
Decreased LOC

81
Q

treatment for hyperglycemia

A

Stabilize glucose levels
Replace fluids and electrolytes
Treat any cause

82
Q

Somogyi effect

A

Rebound hyperglycemia related to insulin induced hypoglycemia

83
Q

dawn phenomenon

A

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
Q

glucagon function

A

which mobilizes glycogen from the liver and suppresses insulin secretion; glucagon is critical in maintaining blood glucose levels between meals.

85
Q

insulin function

A

which promotes glucose utilization.

86
Q

somatostatin and gastrin functions

A

which regulate alpha cell and beta cell function by suppressing the release of insulin, glucagon, and pancreatic polypeptides.

Patho Exam 3 (3 decks)

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