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316 Pharmacology > Exam 3: Pathophysiology Diabetes > Flashcards

Exam 3: Pathophysiology Diabetes Flashcards

1
Q

Alpha cells of pancreas

A

Glucagon

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2
Q

Beta cells of pancreas

A

insulin

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3
Q

Insulin and glucagon relationship effects

A

have opposite effects

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4
Q

Primary target tissue of insulin

A

Liver, skeletal muscle, fat tissue

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5
Q

Insulin action

A

Decrease glucose levels by

  • increase uptake of glucose into cells
  • increase conversion of glucose into glycogen in liver (glycogenesis)
  • — decreased glycogenolysis and gluconeogensis
  • decrease fat breakdown and increase fat storage
  • decrease protein breakdown and increase protein synthesis
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6
Q

Insulins and glucagon work in _____ to maintain ____

A

Anatogonistic fashion, euglycemia

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7
Q

Normal blood glucose levels

A

70-100 mg/dl

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8
Q

Leading cause of heart disease, stroke, adult blindness, renal disease, non-traumatic amputations

A

Diabetes mellitus

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9
Q

Which type is most common for diabetes

A

Type 2/ type 1

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10
Q

Diabetes mellitus is a group of

A

Metabolic disorders

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11
Q

Diabetes mellitus is characterized by

A 
glucose intolerance
altered metabolism of:
-CHO
-protein
-fats
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12
Q

Diabetes mellitus types

A 
Type 1
Type 2
Prediabetes
Gestational diabetes
MODY
Idiopathic diabetes
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13
Q

when should pre diabetes & type 2 diabetes testing happen

A

asymptomatic adults with BMI >25 + risk factors

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14
Q

Gestational diabetes

A

Routine testing during prenatal care

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15
Q

A cluster of clinical signs that predispose

A

Abdominal obesity
Abnormal lipid profile
Increased blood pressure
Resistance to insulin & increased fasting plasma glucose

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16
Q

Diagnosis of diabetes

A 
Clinical manifestations
Fasting plasma glucose (FPG)
Postprandial glucose tests
Glucose tolerance tests
Glycosylated hemoglobin (HbA1c)
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17
Q

A1C (HbA1c) measures

A

Plasma glucose levels over time

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18
Q

During lifespan of RBC, glucose molecules join the Hgb molecule in proportion to blood glucose levels known as

A

Gycosylated Hgb

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19
Q

Once Hgb becomes glycoslated, it

A

remains that way

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20
Q

A1C (HbA1c ) assesses the

A

effectiveness of glucose management

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21
Q

Type 1 diabetes is an

A

absolute insule deficiency

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22
Q

Type 1 diabetes is a primary ____ defect or failure

A

beta cell

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23
Q

Peak onset for type 1 diabetes

A

11-13 years of age

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24
Q

Etiology of type 1 diabetes

A

autoimmune:
non-autoimmune
chromosomes 6 & 11 implicated
epigenetics (interaction between genetic & environmental factors)

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25
Q

Autoimmune etiology of diabetes

A

: destruction of β-cells in genetically susceptible individuals

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26
Q

None-autoimmune etiology of type 1 diabetes

A

genetic defects of β-cell

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27
Q

Type 1 diabetes is

A

No insulin

Overproduction of glucagon by alpha cell

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28
Q

No insulin from type 1 diabetes can be caused by

A

Glucose not transported into cells

Production of glucose by liver is unopposed

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29
Q

Overproduction of glucagon by alpha cells is caused by

A

Increased glycogenolysis

Increased gluconeogensis

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30
Q

Hyperglycemia in type 1 diabetics

A

Glucose accumulates in blood

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31
Q

Polyphagia, fatigue, and weight loss in type 1 diabetes is due to

A

No glucose for ATP production

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32
Q

Ketoacidosis

A

Breakdown fat/protein stores: liver produces increased ketones

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33
Q

Increased glucose concentration in blood leads to increased osmolality of blood leads to

A
  • osmotic diuresis (polyuria, glucosuria, hypovolemia, weight loss, fatigue)
  • Intracellular dehydration (polydipsia)
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34
Q

Signs and symptoms of type 1 diabetes

A

Polydipsia
Polyuria
Polyphagia

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35
Q

glycosuria

A

When blood levels are sufficiently elevated, the amount of glucose filtered by the glomeruli exceeds the amount that can be reabsorbed by the renal tubules

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36
Q

Osmotic pull of glucose caused

A

Polyuria

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37
Q

Are autoimmune processes involved in type 2 diabetes

A

NO!

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38
Q

Most powerful risk factor of type 2 diabetes

A

Obesity

39
Q

Other risk factors for type 2 diabetes

A

sedentary lifestyle, excessive abdominal fat (central obesity), positive familial history, metabolic syndrome

40
Q

Type 2 diabetes in becoming more prevalent in

A

obese adolescents and children

41
Q

Type 2 diabetes can be characterized as

A

Relative lack of insulin
Abnormal insulin release
Increase gluconeogensis by liver

42
Q

Insulin resistance

A

Requirement for more insulin than biologically necessary

43
Q

Abnormal insulin release caused from

A

Decrease beta cell responsiveness

44
Q

Increase gluconeogensis by liver cause

A

hyperinsulinemia

hyperglycemia

45
Q

Clinical manifestations of type 2 diabetes

A

Classic symptoms may be more subtle or absent in Type 2
Fatigue
Paresthesias (secondary to neuropathies)
Visual changes
Recurrent infections (secondary to increased glucose levels; glycosuria predisposes to candidia infections)

46
Q

Complications of diabetes

A

Hypoglycemia
Hyperglycemia
Diabetic ketoacidosis (DKA)
Hyperosmolar Hyperglycemic (Nonketotic) State (HHS)
Microvascular & macrovascular complications
Neuropathies
Infection

47
Q

Hypoglycemia is also referred to as

A

insulin reaction or insulin shock

48
Q

Hyperglycemia can be caused by

A

Eating too much food or the wrong foods
Exercising too little
Physical stress, such as an infection or other illness
Emotional stress, such as family conflict or workplace challenges
Forgetting to take diabetes medication
Problems with medication regimen

49
Q

Diabetic ketoacidosis is a

A

life threatening complication

50
Q

Diabetic ketoacidosis may present as undiagnosed

A

type 1 DM

51
Q

Diabetic ketoacidosis is caused by

A

by lack of insulin & concomitant elevations of counterregulatory hormones (catecholamines, glucagon, growth hormone & cortisol)

52
Q

Hormonal alterations in diabetic ketoacidosis cause

A

(1) hyperglycemia resulting from accelerated gluconeogenesis &
decreased glucose utilization

(2) increased proteolysis & decreased protein synthesis plus increased lipolysis & ketone production resulting in
(3) metabolic acidosis

53
Q

Clinical manifestations of diabetic ketoacidosis

A
  • Glucose levels: 250 – 750 mg/dl
  • Ketonemia & ketonuria
  • Metabolic acidosis (pH < 7.3)
  • Kussmaul respirations
  • “Fruity” or acetone odor to breath
  • Classic S/S of hyperglycemia
  • Osmotic diuresis & -dehydration
  • Tachycardia, hypotension
  • Electrolyte imbalances
  • Malaise, lethargy, dry mouth, headache, N/V
  • Stupor that may progress to coma
54
Q

Hyperosmolar hyperglycemic state most common in

A

elderly with type 2 diabetes

55
Q

Hyperosmolar hyperglycemic state cause

A

may be caused by excessive CHO intake or increase insulin resistance

56
Q

Hyperosmolar hyperglycemic state characterized by

A

Hyperglycemia
Hyperosmolarity
Dehydration
No significant ketoacidosis

57
Q

Hyperosmolar hyperglycemic state clinical manifestations

A 
Slower onset than DKA
Glucose levels 600 – 2000 mg/dl
Classic S/S of hyperglycemia
Profound hyperosmolarity, diuresis, dehydration
S/S intravascular volume deficit
S/S intracellular volume deficit
May progress to coma
Less favorable prognosis than DKA
58
Q

Somogyi effect

A

-Compensatory mechanisms counteract insulin-induced hypoglycemia causing rebound hyperglycemia via gluconeogenesis (mobilization of counterregulatory hormones)

Catecholamines
Glucagon
Cortisol
Growth hormone

59
Q

Dawn Phenomenon

A
  • Occurs with Type 1 or 2 DM
  • Blood glucose levels rise in the early AM
  • GH & normal circadian rhythms play a role
  • Profound hyperglycemia if combined with Somogyi effect
60
Q

is the Dawn Phenomenon a reaction to hypoglycemia

A

NO!

61
Q

Macrovascular

A

Damage to large blood vessels providing circulation to brain, heart, extremities

62
Q

Macrovascular is related to

A

hyperglycemia & altered lipid metabolism (causes endothelial damage)

63
Q

Macrovascular leads to

A

Leads to cardiovascular disease, cerebrovascular disease, & peripheral vascular disease

64
Q

____ is twice as common in diabetics compared with non-diabetic population

A

Stroke

65
Q

What is the most common cause of death in type 2 DM

A

CAD

66
Q

Microvascular

A

Level of microvascular disruption increases with duration of disease & with persistent hyperglycemia

67
Q

Microvascular involves

A

abnormal thickening of capillary basement membrane, endothelial hyperplasia, thrombosis

68
Q

Flow of blood slows in microcirculation

A

Retinopathy

Nephropathy

69
Q

is leading cause of acquired blindness in the U.S.

A

Diabetes

70
Q

retinopathy is characterized by

A 
abnormal retinal vascular permeability
microaneurysm
neovascularization
scarring
retinal detachment
71
Q

leading cause of end-stage renal disease (ESRD)

A

Diabetic nephropathy

72
Q

Glomerular changes in diabetic nephropathy

A

capillary basement membrane thickening, diffuse glomerular sclerosis, nodular glomerulosclerosis

73
Q

Initial manifestation of nephropathy

A

microalbuminuria

74
Q

microalbuminuria increases with

A

Increase hemoglobin A1C
Increase DBP or SBP
Smoking

75
Q

Neuropathy produces symptoms in 60-70% of diabetics

A

autonomic dysfunction

somatic dysfunction

76
Q

Sustained hyperglycemia in neuropathy leads to

A

thickening of walls of vessels supplying nerves & segmental demylenization + injury to capillaries supplying nerves causing slowing of nerve conduction

77
Q

Autonomic neuropathy

A

Impaired vasomotor function leads to orthostatic hypotension

78
Q

Autonomic neuropathy increases risk for UTI because

A

there is incomplete voiding

79
Q

Autonomic neuropathy GI problems

A

gastroparesis which is delayed gastric emptying

80
Q

Autonomic neuropathy can cause what kind of dysfunction

A

erectile dysfunction

81
Q

Somatic neuropathy commonly involves

A

Lower extremities

82
Q

Somatic neuropathy can cause

A
  • Paresthesias
  • Impaired pain, temperature, & vibratory sensation
  • Impaired position sense (increase risk of falling)
83
Q

Individuals with diabetes are at risk for infection:

A
  • Impaired senses (neuropathy & retinopathy)
  • Hypoxia
  • Hyperglycemia & pathogens
  • Blood supply
  • WBCs
84
Q

Impaired senses (neuropathy and retinopathy)

A

Impaired vision and sensation causing increase risk of injury and decrease ability to feel injuries when they occur

85
Q

Hypoxia in DM caused by

A
  1. Vascular compromise decrease O2 delivery

2. glycoslyated Hgb does not release O2 to the tissues as easily as normal Hgb

86
Q

Hyperglycemia and pathogens in DM

A

certain pathogens proliferate rapidly in glucose-rich body fluids

87
Q

Blood supply complications in DM

A

impaired blood supply leads to decrease delivery of WBCs

88
Q

WBCs complications for DM

A

Impaired function of WBCs due to high glucose levels

89
Q

What is the underlying cause of limb amputation

A

infection

90
Q

diabetes management goals

A

Maintain euglycemia
Prevent acute complications
Promote health
Reduce progression of chronic complications
Patient involved as an active participant

91
Q

The key to preventing acute and chronic complications is

A

good glycemic control

92
Q

Diabetes management nutrition

A

balance food intake with insulin & antidiabetic agents
optimal serum lipid levels
weight control

93
Q

Other ways to manage diabetes

A 
Exercise
Glucose self-monitoring
A1C monitoring
Smoking cessation
Psychosocial assessment & stress reduction
Immunizations
Blood pressure & lipid screenings
Nephropathy screening
Retinopathy screening
Foot care (podiatrist) 
Pharmacological treatment:
--insulin
--oral antidibetic agents
--statins
--antiplatelet medications
94
Q

what does glucagon do

A

Prevents hypoglycemia by promoting release of glucose from liver storage sites

316 Pharmacology (19 decks)

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