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Anatomy and Phyisology > HLTH 2501: insulin and diabetes mellitus > Flashcards

HLTH 2501: insulin and diabetes mellitus Flashcards

1
Q

the most common cause of endocrine disorders

A

the development of a benign tumor or adenoma; can be secretory (causing excess) or destructive (causing a deficit)

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2
Q

two types of endocrine problems

A

an excessive amount of a hormone or a deficit

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3
Q

resistant target cells

A

can cause hormonal deficits, resulting from a genetic disorder, an autoimmune response, or excessive demand on the target cells

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4
Q

tropic hormones

A

hormones that have a stimulating effect on other endocrine glands

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5
Q

what must be evaluated to determine an endocrine disorder

A

levels of tropic hormones secreted by the pituitary gland and levels of hormones secreted by the target gland

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6
Q

ectopic

A

an outside source causing an excessive amount of hormone, ex. bronchogenic cancer

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7
Q

what are diagnostic tests for hormones?

A

blood tests that make use of radioimmunoassay methods or immunochemical methods, as well as urine tests, scans, ultrasounds, and MRIs

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8
Q

hormone treatment

A

can be treated with replacement therapy, ex. insulin; or adenomas can be removed when they cause excessive secretions

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9
Q

diabetes mellitus

A

is caused by a relative deficit of insulin secretion from the beta cells in the islets of langerhans or by the lack of response by cells to insulin (insulin resistance)

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10
Q

what kind of hormone is insulin?

A

an anabolic hormone, meaning it is building up of synthesis or complex substances

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11
Q

what does deficient insulin result from?

A

abnormal carbohydrate, protein, and fat metabolism because the transport of glucose and amino acids into cells is impaired, as well as the synthesis of protein and glycogen

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12
Q

what diabetes type is more severe?

A

type 1

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13
Q

different names for type 1 diabetes

A

insulin-dependent diabetes mellitus, diabetes mellitus, or juvenile diabetes

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14
Q

what is the common population for type 1 diabetes?

A

children and adolescents

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15
Q

what does type 1 diabetes result from?

A

genetic factors and an insulin deficit that results from destruction of the pancreatic beta cells in an autoimmune reaction, resulting in an absolute deficit of insulin

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16
Q

acute complications with type 1 diabetes

A

hypoglycemia, ketoacidosis, or long-term complications like vascular disease which arises from degenerative changes in the tissues

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17
Q

risk factors for those with diabetes type 1

A

strokes, heart attacks, peripheral vascular disease, amputation, kidney failure, and blindness

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18
Q

other names for type 2 diabetes

A

non insulin-dependent, type II diabetes mellitus, or mature-onset diabetes

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19
Q

what is type 2 diabetes based on?

A

a decreased effectiveness of insulin or a relative deficit of insulin, resulting from decreased pancreatic beta cells production of insulin, increased resistance of body cells to insulin, or increased production of glucose by the liver

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20
Q

how is type 2 diabetes managed?

A

regulating diet, increasing the use of glucose through exercise, reducing insulin resistance, and stimulating the beta cells of the pancreas to produce more insulin

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21
Q

who does type 2 diabetes develop in?

A

often in older adults, the majority of them overweight

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22
Q

metabolic syndrome

A

is becoming common in younger adults in which this is a complex of several pathophysiological conditions marked by obesity, cardiovascular changes, and significant insulin resistance due to increased adipose tissue

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23
Q

gestational diabetes

A

may develop during pregnancy and disappears after delivery of the child; some of these women develop

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24
Q

prediabetes

A

an early manifestation of type 2 diabetes

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25
Q

latent autoimmune diabetes

A

occurs in adults and is a slow-onset type 1 autoimmune diabetes

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26
Q

maturity-onset diabetes

A

occurs in the young and is a rare form caused by a mutation in an autosomal dominant gene

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27
Q

diabetes insipidus

A

diabetes not related to blood sugar levels, but to an oversensitivity of the kidneys to ADH

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28
Q

what events occur in an insulin deficit?

A

insulin deficit results in decreased transportation of glucose, causing blood glucose levels to rise (hyperglycemia); excess spills into the urine (glucosuria) as the kidneys cannot absorb all of it; osmotic pressures in the filtrate result in the loss of fluid and electrolytes; this results in dehydration of cells, causing thirst and stimulating appetite, and possibly diabetic ketoacidosis

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29
Q

glucosuria

A

when excess glucose spills into the urine

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30
Q

polyuria

A

large amounts of urine excreted due to high glucose levels that create osmotic pressures

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31
Q

polydispia

A

glucose levels cause dehydration which causes thirst

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32
Q

polyphagia

A

lack of nutrients entering the cells due to glucose excess causes appetite

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33
Q

what happens is the insulin deficit is prolonged and severe?

A

diabetic ketoacidosis may develop

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34
Q

diabetic ketoacidosis

A

lack of glucose in cells results in catabolism of fats and proteins, leading to excessive amounts of fatty acids and their metabolites (known as ketones) in the blood

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35
Q

who does diabetic ketoacidosis occur more commonly in?

A

type 1

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36
Q

what do ketones consist of?

A

acetone and two organic acids (beta-hydroxybutyric acid and acetoacetic acid)

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37
Q

how do ketones cause low pH?

A

they bind with HCO3- buffer in the blood, leading to decreased serum HCO3- and eventually to a decrease in the pH of body fluids

38
Q

ketonuria

A

when ketoacids are excreted in the urine

39
Q

why can diabetic ketoacidosis be so dangerous?

A

because as dehydration develops, the GFR decreases and excretion of acids becomes more limited; this results in decompensated metabolic acidosis

40
Q

signs and symptoms in all diabetes types

A

hunger, fatigue, thirst, polyuria, dry mouth, itchy skin, and blurred vision; type 2 gains weight and type 1 may lose weight

41
Q

what signifies the onset of diabetes?

A

the three Ps; polyuria, polydipsia, and polyphagia

42
Q

testing for diabetes

A

fasting blood glucose level, the glucose tolerance test, and the glycosylated hemoglobin test

43
Q

what blood sugar level confirms a diagnosis of diabetes?

A

> 126 mg/dL

44
Q

how are long term blood glucose levels monitored?

A

the test for HbA1c and this should be repeated every 3 months

45
Q

how do diabetes patients check their own glucose levels?

A

with a blood sample from a portable monitoring machine, ex. glucometer

46
Q

treatment for diabetes

A

maintaining normal blood glucose levels through 3 levels of control 1. diet and exercise 2. oral medication to increase insulin secretion or reduce insulin resistance 3. insulin replacement

47
Q

diet for diabetes

A

more complex carbs with a low glycemic index, adequate protein, low cholesterol and lipids, and increased fibre

48
Q

exercise for diabetes

A

a regular moderate exercise program is important, as exercise helps to increase the uptake of glucose by muscles without an increase in insulin use; also helps to control weight, reduce stress, and improve cardiovascular health

49
Q

risk of exercise for diabetes

A

risk of hypoglycemia developing with prolonged exercise

50
Q

oral medications for diabetes

A

metformin, sulfonylureas, meglitinides, thiazolidinediones, DPP-4 inhibitors, GLP-1 receptors, and SGLT2 inhibitors

51
Q

metformin

A

aka glucophage; usually is the first medication prescribed for type 2 diabetes; it works to reduce insulin resistance and glucose production

52
Q

sulfonylureas

A

help the body to create more glucose; ex. glyburide (DiaBeta), glipizide (Glucotrol), and glimepiride (amaryl)

53
Q

meglitinides

A

includes repaglinide (Prandin_ and nateglinide (Starlix) which stimulate insulin production

54
Q

thiazolidinediones

A

reduce insulin resistance; ex. rosiglitazone (Avandia) and pioglitazone (Actos)

55
Q

DPP-4 inhibitors

A

sitagliptin (januvia), saxagliptin (Onglyza) and linagliptin (Tradjenta) which help to reduce blood sugar levels

56
Q

GLP-1 receptor agonists

A

slow digestion and help to lower blood sugar levels; ex. exenatide (Byetta) and liraglutide (Victoza)

57
Q

SGLT2 inhibitors

A

prevent the kidneys from reabsorbing sugar into the blood; ex. canagliflozin (Invokana) and dapagliflozin (Farxiga)

58
Q

how is insulin administered?

A

subcutaneously because it is a protein that is destroyed in the GI tract if taken orally

59
Q

primary form of insulin used

A

biosynthetic form which is identical to human insulin (Humulin)

60
Q

3 forms of insulin for replacement

A

rapid-onset, short-acting; intermediate-acting; and slow-onset and long-acting

61
Q

example of rapid-onset and short-acting insulin

A

lente

62
Q

example of slow-onset and long-acting insulin

A

protamine zinc or ultralente

63
Q

when may insulin dosage change?

A

during special circumstances, such as infection with a high fever or vomiting, or at the time of surgery

64
Q

what may complications associated with glucose levels arise from?

A

variations in diet and exercise, the presence of infections, and alcohol use

65
Q

what is hypoglycemia?

A

is an excess of insulin which causes a deficit in glucose

66
Q

who is hypoglycemia more common in?

A

type 1 diabetes individuals

67
Q

why might hypoglycemia occur?

A

due to strenuous exercise, error in dosage, vomiting, or skipping a meal after taking insulin

68
Q

what are the results of hypoglycemia?

A

the nervous system cannot function well due to neurons not being able to use fats or protein as an energy source

69
Q

why does excess insulin cause less glucose?

A

because this excess transports glucose into cells

70
Q

clinical signs of hypoglycemia

A

neulogic signs are poor concentration, slurred speech, and lack of coordination; the SNS systems are weakness, pallor, diaphoresis, tremors, and tachycardia

71
Q

hypoglycemic shock

A

hypoglycemia triggers the SNS which increased gluconeogenesis, causing glucose to not be taken up and for neurons to not function

72
Q

what may occur if hypoglycemia is left untreated?

A

loss of consciousness, seizures, and death

73
Q

treatment for hypoglycemia

A

immediate administration of a concentrated carbohydrate such as fruit juice or candy; if the person remains unconscious, glucose or glucagon may be given parenterally

74
Q

what may ketoacidosis result from?

A

infection, stress, error in dosage, or overindulgence in food or alcohol; develops over a few days

75
Q

signs of diabetic ketoacidosis

A

all signs are related to dehydration, metabolic acidosis, and electrolyte imbalances and include thirst, dry, rough oral mucosa, warm, dry skin, rapid but weak pulse, low BP, and oliguria (decreased urine output)

76
Q

what may ketoacidosis lead to?

A

rapid, deep respirations, acetone breath (fruity, sweet), lethargy, and decreased responsiveness

77
Q

when does metabolic acidosis occur?

A

as ketoacids bind with bicarbonate

78
Q

signs of metabolic acidosis

A

decreased serum HCO3- and decreased serum pH, renal compensation, and loss of consciousness; electrolyte imbalance signs are abdominal cramps, nausea, vomiting, and lethargy or weakness

79
Q

treatment of diabetic ketoacidosis

A

administration of insulin and replacing fluids and electrolytes (especially HCO3- as this reverses the acidosis)

80
Q

hyperosmolar hyperglycemic nonketotic coma

A

can develop in those with type 2 diabetes and often when the patient is elderly with an infection or has overindulged in carbohydrates, thereby using more insulin

81
Q

why might one go into a hyperosmolar hyperglycemic nonketotic coma

A

because there are dehydrated, leading to severe cellular dehydration, causing neurological deficits, muscle weakness, difficulties with speech and abnormal reflexes

82
Q

why do vascular problems occur with diabetes?

A

because generation of metabolism leads to atherosclerosis in large arteries as a result of hyperlipidemia and hypertension

83
Q

microangiopathy

A

occurs when the capillary basement membrane becomes thick and hard, causing obstruction or rupture of capillaries and small arteries, resulting in tissue necrosis and loss of function; can affect the kidneys, eyes, and the nervous system

84
Q

retinopathy

A

is the leading cause of blindness and occurs as a result of microaneurysms, neovascularization, and fibrosis

85
Q

diabetic nephropathy

A

is vascular degeneration (thickening of the capillary basement membrane) in the kidney glomeruli, eventually leading to chronic renal failure

86
Q

macroangiopathy

A

affects the large arteries, leading to a high incidence of heart attacks, strokes, and peripheral vascular disease in diabetics; if obstruction occurs in the legs, it can result in ulcers

87
Q

peripheral neuropathy

A

is a common problem for diabetics and leads to impaired sensation, numbness, tingling, weakness, and muscle wasting (can also impair autonomic nerve function like bladder incompetence); results from ischemia and altered metabolic processes

88
Q

infections and diabetes

A

are more common and severe in diabetics and this is because of vascular impairment, which decreases tissue resistance and healing time due to deficit insulin and increased glucose

89
Q

common infections in diabetics

A

tuberculosis, infections in the feet and legs (due to vascular impairment), candida fungal infections, periodontal tissue, and dental caries

90
Q

cataracts

A

clouding of the lens of the eye which results in accumulated sorbitol and water in the lens, destroying the transparency and can lead to blindness; is more common in diabetics due to abnormal glucose metabolism

91
Q

diabetics and pregnancy

A

complications for both mother and fetus may occur due to difficulty controlling the continual hormones and metabolic changes; fetus may be larger and predisposed to conditions and the mother may experience loss of the baby

Anatomy and Phyisology (71 decks)

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