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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
Autoimmune etiology of diabetes
: destruction of β-cells in genetically susceptible individuals
26
None-autoimmune etiology of type 1 diabetes
genetic defects of β-cell
27
Type 1 diabetes is
No insulin | Overproduction of glucagon by alpha cell
28
No insulin from type 1 diabetes can be caused by
Glucose not transported into cells | Production of glucose by liver is unopposed
29
Overproduction of glucagon by alpha cells is caused by
Increased glycogenolysis | Increased gluconeogensis
30
Hyperglycemia in type 1 diabetics
Glucose accumulates in blood
31
Polyphagia, fatigue, and weight loss in type 1 diabetes is due to
No glucose for ATP production
32
Ketoacidosis
Breakdown fat/protein stores: liver produces increased ketones
33
Increased glucose concentration in blood leads to increased osmolality of blood leads to
- osmotic diuresis (polyuria, glucosuria, hypovolemia, weight loss, fatigue) - Intracellular dehydration (polydipsia)
34
Signs and symptoms of type 1 diabetes
Polydipsia Polyuria Polyphagia
35
glycosuria
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
36
Osmotic pull of glucose caused
Polyuria
37
Are autoimmune processes involved in type 2 diabetes
NO!
38
Most powerful risk factor of type 2 diabetes
Obesity
39
Other risk factors for type 2 diabetes
sedentary lifestyle, excessive abdominal fat (central obesity), positive familial history, metabolic syndrome
40
Type 2 diabetes in becoming more prevalent in
obese adolescents and children
41
Type 2 diabetes can be characterized as
Relative lack of insulin Abnormal insulin release Increase gluconeogensis by liver
42
Insulin resistance
Requirement for more insulin than biologically necessary
43
Abnormal insulin release caused from
Decrease beta cell responsiveness
44
Increase gluconeogensis by liver cause
hyperinsulinemia | hyperglycemia
45
Clinical manifestations of type 2 diabetes
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
Complications of diabetes
Hypoglycemia Hyperglycemia Diabetic ketoacidosis (DKA) Hyperosmolar Hyperglycemic (Nonketotic) State (HHS) Microvascular & macrovascular complications Neuropathies Infection
47
Hypoglycemia is also referred to as
insulin reaction or insulin shock
48
Hyperglycemia can be caused by
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
Diabetic ketoacidosis is a
life threatening complication
50
Diabetic ketoacidosis may present as undiagnosed
type 1 DM
51
Diabetic ketoacidosis is caused by
by lack of insulin & concomitant elevations of counterregulatory hormones (catecholamines, glucagon, growth hormone & cortisol)
52
Hormonal alterations in diabetic ketoacidosis cause
(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
Clinical manifestations of diabetic ketoacidosis
- 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
Hyperosmolar hyperglycemic state most common in
elderly with type 2 diabetes
55
Hyperosmolar hyperglycemic state cause
may be caused by excessive CHO intake or increase insulin resistance
56
Hyperosmolar hyperglycemic state characterized by
Hyperglycemia Hyperosmolarity Dehydration No significant ketoacidosis
57
Hyperosmolar hyperglycemic state clinical manifestations
``` 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
Somogyi effect
-Compensatory mechanisms counteract insulin-induced hypoglycemia causing rebound hyperglycemia via gluconeogenesis (mobilization of counterregulatory hormones) **Catecholamines Glucagon Cortisol Growth hormone**
59
Dawn Phenomenon
- 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
is the Dawn Phenomenon a reaction to hypoglycemia
NO!
61
Macrovascular
Damage to large blood vessels providing circulation to brain, heart, extremities
62
Macrovascular is related to
hyperglycemia & altered lipid metabolism (causes endothelial damage)
63
Macrovascular leads to
Leads to cardiovascular disease, cerebrovascular disease, & peripheral vascular disease
64
____ is twice as common in diabetics compared with non-diabetic population
Stroke
65
What is the most common cause of death in type 2 DM
CAD
66
Microvascular
Level of microvascular disruption increases with duration of disease & with persistent hyperglycemia
67
Microvascular involves
abnormal thickening of capillary basement membrane, endothelial hyperplasia, thrombosis
68
Flow of blood slows in microcirculation
Retinopathy | Nephropathy
69
is leading cause of acquired blindness in the U.S.
Diabetes
70
retinopathy is characterized by
``` abnormal retinal vascular permeability microaneurysm neovascularization scarring retinal detachment ```
71
leading cause of end-stage renal disease (ESRD)
Diabetic nephropathy
72
Glomerular changes in diabetic nephropathy
capillary basement membrane thickening, diffuse glomerular sclerosis, nodular glomerulosclerosis
73
Initial manifestation of nephropathy
microalbuminuria
74
microalbuminuria increases with
Increase hemoglobin A1C Increase DBP or SBP Smoking
75
Neuropathy produces symptoms in 60-70% of diabetics
autonomic dysfunction | somatic dysfunction
76
Sustained hyperglycemia in neuropathy leads to
thickening of walls of vessels supplying nerves & segmental demylenization + injury to capillaries supplying nerves causing slowing of nerve conduction
77
Autonomic neuropathy
Impaired vasomotor function leads to orthostatic hypotension
78
Autonomic neuropathy increases risk for UTI because
there is incomplete voiding
79
Autonomic neuropathy GI problems
gastroparesis which is delayed gastric emptying
80
Autonomic neuropathy can cause what kind of dysfunction
erectile dysfunction
81
Somatic neuropathy commonly involves
Lower extremities
82
Somatic neuropathy can cause
- Paresthesias - Impaired pain, temperature, & vibratory sensation - Impaired position sense (increase risk of falling)
83
Individuals with diabetes are at risk for infection:
- Impaired senses (neuropathy & retinopathy) - Hypoxia - Hyperglycemia & pathogens - Blood supply - WBCs
84
Impaired senses (neuropathy and retinopathy)
Impaired vision and sensation causing increase risk of injury and decrease ability to feel injuries when they occur
85
Hypoxia in DM caused by
1. Vascular compromise decrease O2 delivery | 2. glycoslyated Hgb does not release O2 to the tissues as easily as normal Hgb
86
Hyperglycemia and pathogens in DM
certain pathogens proliferate rapidly in glucose-rich body fluids
87
Blood supply complications in DM
impaired blood supply leads to decrease delivery of WBCs
88
WBCs complications for DM
Impaired function of WBCs due to high glucose levels
89
What is the underlying cause of limb amputation
infection
90
diabetes management goals
Maintain euglycemia Prevent acute complications Promote health Reduce progression of chronic complications Patient involved as an active participant
91
The key to preventing acute and chronic complications is
good glycemic control
92
Diabetes management nutrition
balance food intake with insulin & antidiabetic agents optimal serum lipid levels weight control
93
Other ways to manage diabetes
``` 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
what does glucagon do
Prevents hypoglycemia by promoting release of glucose from liver storage sites

316 Pharmacology (19 decks)

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