ENDO V Flashcards

1
Q

A cells/α cells -

A

Glucagon

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2
Q

B cells/β cells -

A

Insulin

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3
Q

D cells/δ cells -

A

Somatostatin

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4
Q

F Cells –

A

Pancreatic Polypeptide

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5
Q

The pancreas
contains ~–
million islets of
Langerhans.

A

1-2

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6
Q

α cells and β
constitute about
–% of the cells in
the islets.

A

85

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7
Q

he majority of the
pancreas is composed of
Acinar Cells produce

A

Digestive Enzymes

Exocrine Portion

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8
Q

Insulin secretion is associated

with

A

energy abundance.

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9
Q

Insulin is composed of

A

two amino acid
chains, connected by disulfide
linkages.

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10
Q

When A & B chains are —,
functional activity of insulin
molecule is lost

A

split

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11
Q

The proinsulin and C peptide

have virtually

A

no insulin activity

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12
Q

Insulin circulates entirely in

unbound form. T1/2 =

A

6min

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13
Q

Formation of Insulin occurs in –

cells. It is first made as proinsulin.

A

β

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14
Q

In the Golgi, proinsulin is

cleaved to form

A

C

peptide and insulin

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15
Q

Incretins are

A

hormones produced by the digestive system that work to

stimulate insulin secretion BEFORE plasma glucose is elevated.

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16
Q

incretins include (2)

A

Glucagon-like Peptide-1 (GLP-1)

Glucose-dependent Insulinotropic Polypeptide (GIP).

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17
Q
The sulfonylurea 
receptor (SUR) receptor 
(KATP channel) is the 
binding site for some 
drugs that act as
A
insulin 
secretagogues (ex. 
Glimepiride/Amaryl) for 
treatment of type 2 
Diabetes Mellitus.
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18
Q
Glucose is the key regulator 
of insulin secretion; 
glucose levels >-- mmol/L (70 
mg/dL) stimulate insulin 
synthesis.
A

3.9

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19
Q

(5) also

influence insulin secretion.

A
Amino acids, 
ketones, 
various nutrients, 
gastrointestinal peptides, 
and neurotransmitters
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20
Q

Tyrosine Kinase-linked receptor

• Target cells responses: (3)

A
1. Fast (seconds): Increased 
glucose uptake, especially by 
muscle cells and adipocytes due 
to translocation of vesicles 
containing GLUT-4 to the 
membrane. 
The membrane also becomes more 
permeable to many amino acids along with 
potassium and phosphate ions. 
  1. Slower (10-15 minutes): Change
    in enzyme activity leading to
    changes in metabolism.
  2. Slowest (hours-days): Changes
    in gene expression and growth.
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21
Q

Insulin promotes muscle glucose — and metabolism-

anabolic effect

A

uptake

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22
Q

– Resting muscle

membrane only

A

slightly

permeable to glucose

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23
Q

– Insulin stimulation

increases

A

glucose

transport

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24
Q

Effects of Insulin on Muscle

increase (2)

A
– Increases glycogen 
storage in skeletal muscle
– Increases protein 
synthesis and inhibits 
protein degradation
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25
Q

Effect of Insulin on Protein Metabolism & Growth
Promotes — — and
Storage Inhibits — —

A

Protein Synthesis

Protein Degradation

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26
Q

Lack of insulin
causes protein
depletion &
increased

A

plasma amino

acids.

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27
Q

Insulin promotes the uptake and storage of

A

glucose (as

glycogen) by the liver

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28
Q

nsulin promotes the uptake and storage of glucose (as
glycogen) by the liver
Mechanisms: (3)

A

• increases glucose uptake (glucokinase)
• increase glycogen synthase lead to increased glycogen synthesis
• decrease breakdown of glycogen by inhibiting liver
phosphorylase

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29
Q

Insulin promotes conversion of excess glucose into

A

fatty

acids

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30
Q

insulin inhibits

A

gluconeogenesis

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31
Q

Insulin Promotes Fat (2)

A

Synthesis and Storage

32
Q

Insulin Promotes Fat Synthesis and Storage:

A

· increase glucose transport into liver
-TG+ lipoprotein released from liver
· activates lipoprotein lipase in the capillary walls of adipose tissue
- splitting triglycerides into fatty acids
- absorption into adipocytes

33
Q

Essential effects of insulin for
fat storage in adipose tissue:
· Inhibits action of
· Enhances glucose transport into

A

hormone-sensitive lipase

adipocytes

  • α glycerol phosphate
  • glycerol+ fatty acids to TG
34
Q

Lack of insulin causes (2) and

increases (2)

A

lipolysis and
release of FFA (Diabetic Ketoacidosis)

plasma cholesterol
and phospholipids conc.

35
Q

increase Insulin Secretion (9)

A

Increased blood glucose
Increased blood free fatty acids
Increased blood amino acids
Gastrointestinal hormones (gastrin, cholecystokinin,
secretin, GIP, Glucagon-like peptide-GLP-1)
Glucagon, growth hormone, cortisol
Parasympathetic stimulation; acetylcholine
β-Adrenergic stimulation
Insulin resistance; obesity
Sulfonylurea drugs (glyburide, tolbutamide

36
Q

Decrease Insulin Secretion (5)

A
Decreased blood glucose
Fasting
Somatostatin
α-Adrenergic activity
Leptin
37
Q

Glucagon

• – amino acid peptide, secreted from

A

29

pancreatic alpha cells

38
Q

Glucagon

hormone of

A

starvation

39
Q

Glucagon

secretion controlled by

A

blood glucose levels (inverse relationship)

40
Q

Glucagon

primary target tissue

A

liver

41
Q

Glucagon targets liver to increase blood glucose by (3)

A
  1. Stimulating glycogenolysis & inhibiting
    glycogen synthesis
  2. Increasing gluconeogenesis
  3. Increases blood fatty acid & ketoacid
    levels to provide more substrates for
    gluconeogenesis
42
Q

The liver functions like a

buffer for

A
blood glucose. 
Individuals with severe liver 
disease have difficulty 
maintaining a narrow plasma 
glucose range.
43
Q
Glucagon secretion is 
stimulated by (3)
A

Hypoglycemia,
Epinephrine (β2), Vagus
Nerve

44
Q
Diabetes Mellitus (DM)
Definition
A

Metabolic disorder characterized by
hyperglycemia due to insufficient insulin or
cellular resistance to insulin (or both)

45
Q

With DM, it takes longer to
reduce blood glucose levels
and glucose levels don’t
reach the

A

control level.

46
Q

DM Major classifications (2)

A
  1. Type 1 Diabetes-10% of cases-hypoinsulinemia

2. Type 2 Diabetes-90% of cases-hyperinsulinemia

47
Q

Symptoms of Diabetes Mellitus (8)

A
• Urinating often (Polyuria)
• Feeling thirsty (Polydypsia)
• Feeling hungry (Polyphagia)
• Extreme fatigue
• Blurry vision
• Cuts/bruises that are slow to heal
• Weight loss – even though you are eating more (type I 
DM)
• Tingling, pain or numbness in the hands/feet (type 2)
48
Q

These are the three
classic symptoms and
are called the 3 P’s.

A
  • Urinating often (Polyuria)
  • Feeling thirsty (Polydypsia)
  • Feeling hungry (Polyphagia)
49
Q

Approximately 25% of patients with type 1 diabetes mellitus

initially present in

A
diabetic ketoacidosis (hyperglycemia >250 
mg/dl, ketosis and metabolic acidosis with anion gap).
50
Q

Diagnosis of Diabetes Mellitus (2)

A

Casual plasma glucose ≥200 milligrams/dL (11.1 mmol/L) and

symptoms of hyperglycemia

51
Q

Diabetes Mellitus Type I

Pathophysiology (3)

A
  1. Autoimmune destruction of pancreatic beta cells
  2. Accounts for 5-10% of diabetes cases
  3. Formerly called juvenile onset diabetes or insulin dependent diabetes (IDDM)
52
Q
Diabetes Mellitus Type I
Risk Factors (3)
A

. Genetic predisposition-increased susceptibility

  1. Environmental triggers stimulate autoimmune response
    a. Viral infections (mumps, rubella)
    b. Chemical toxins
  2. Usually develops < age 40, non-obese younger patients
53
Q

Manifestations of DM Type I (3)

A
  • Beta cell destruction occurs slowly
  • Hyperglycemia occurs when 80 – 90% of cells destroyed
  • Often triggered by stressor (e.g. illness)
54
Q

Hyperglycemia leads to: (7)

A
  1. Polyuria (hyperglycemia acts as osmotic diuretic)
  2. Polydipsia (thirst from dehydration from polyuria)
  3. Polyphagia (hunger and eats more since cell cannot utilize glucose)
  4. Glycosuria (renal threshold for glucose exceeded)
  5. Weight loss (body breaking down fat and protein to restore energy source
  6. Malaise and fatigue (due to muscle & electrolyte loss)
  7. Hyperkalemia-K+ (due to lack of insulin which normally activates the Na+/K+ pump)
55
Q
Diabetic Ketoacidosis (DKA)
• Due to i
A

ncreased lipolysis to fatty acids to produce ketoacids

56
Q

DKA is a response to

A

cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (glucagon, catecholamines, cortisone and growth hormone).

57
Q

DKA Pathophysiology (3)

A
  1. Osmotic diuresis & dehydration (hyperglycemia)
  2. Metabolic acidosis (accumulation of ketones)
  3. Fluid and electrolyte imbalances (from osmotic diuresis)
58
Q

Signs and Symptoms of DKA (9)

A
– Fruity breath (due to acetone)
– Nausea/ abdominal pain
– Dehydration
– Tachycardia
– Lethargy
– Coma
– Polydipsia, Polyuria, Polyphagia
– Kussmaul respirations (deep, 
labored breathing)
• Blow off carbon dioxide to 
reverse acidosis
59
Q

There are three categories of

the severity of DKA:

A
1. Mild (pH 7.25-7.3)- the 
individual is alert
2. Moderate (pH 7.0-7.25)- the 
individual will be drowsy
3. Severe (pH less than 7.0)- 
the individual will be in a 
stupor or coma.
60
Q

Remember that acidosis
depresses neuronal function
since it blocks inward current of (2)

A

Na+ and Ca2+

61
Q

Diabetes Mellitus (DM) Type II

A

Fasting hyperglycemia despite availability of insulin-Insulin
resistance

62
Q

Diabetes Mellitus (DM) Type II was called

A

non-insulin dependent diabetes or adult onset
diabetes. Both misnomers, type II DM may require insulin
and occurs in children.

63
Q

SKIPPED

Risk Factors for DM Type II

A

• History of diabetes in parents or siblings
• Obesity (especially of upper body)
• Physical inactivity
• Race/ethnicity: African American,
Hispanic, or American Indian origin
• Women: history of gestational diabetes,
polycystic ovarian syndrome, delivered
baby with birth weight > 9 pounds
• Patients with hypertension; HDL
cholesterol < 35 mg/dL, and/or triglyceride
level > 250 mg/dl.

64
Q

Pathophysiology of T2DM
early
late

A

Hyperinsulinemia due to insulin resistance (early)

Beta cell dysfunction with impaired insulin secretion-
pancreatic exhaustion? (late)

65
Q
Pathophysiology of T2DM
Due to (2)
A

downregulation of insulin receptors in target

tissues & insulin resistance

66
Q

Insulin resistance is part of a cascade of disorders

that are called METABOLIC SYNDROME. (5)

A
  1. Obesity, especially abdominal deposition
  2. Insulin resistance
  3. Fasting Hyperglycemia
  4. Lipid Abnormalities (High TG and Low HDL)
  5. Hypertension
67
Q

ndividuals with metabolic
syndrome have increased risk
for

A
cardiovascular disease 
(CVD), particularly 
atherosclerosis and insulin 
resistance is a contributing 
factor for development of type 
2 DM.
68
Q

Pathophysiology of T2DM

similar chronic complications as

A

type 1

69
Q

Retinopathy:

A

leading causes of blindness in the

United States

70
Q

Nephropathy:

A

progressive renal dysfunction that

can lead to end-stage renal disease.

71
Q

Neuropathy:

A

peripheral loss of sensation and

dysesthesias

72
Q

Vascular disease:

A
accelerated atherosclerotic 
cerebrovascular and peripheral 
vascular diseases
may occur due to abnormal lipid 
metabolism
73
Q

Myopathies:

A

progressive weakness and

diminished exercise tolerance.

74
Q

Oral Manifestations of DM (7)

A
  • Periodontal Disease
  • Salivary and taste dysfunction
  • Oral bacterial and fungal infections (ex. candidiasis)
  • Oral mucosa lesions (geographic tongue, lichen planus, etc.)
  • Diminished salivary flow and burning mouth syndrome (with poor glycemic control)
  • Delayed mucosal wound healing
  • Xerostomia in patients on oral hypoglycemic agents
75
Q

Diabetes mellitus: linked to — disease

A

periodontal

76
Q

Periodontal disease exacerbates diabetic

complications (2)

A

– poor glycemic control
– cardiovascular complications (stroke,
ischemia, infarction)

77
Q

Control of periodontal infection may

improve — control

A

glycemic