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
Effect of Insulin on Protein Metabolism & Growth Promotes --- --- and Storage Inhibits --- ---
Protein Synthesis | Protein Degradation
26
Lack of insulin causes protein depletion & increased
plasma amino | acids.
27
Insulin promotes the uptake and storage of
glucose (as | glycogen) by the liver
28
nsulin promotes the uptake and storage of glucose (as glycogen) by the liver Mechanisms: (3)
• increases glucose uptake (glucokinase) • increase glycogen synthase lead to increased glycogen synthesis • decrease breakdown of glycogen by inhibiting liver phosphorylase
29
Insulin promotes conversion of excess glucose into
fatty | acids
30
insulin inhibits
gluconeogenesis
31
Insulin Promotes Fat (2)
Synthesis and Storage
32
Insulin Promotes Fat Synthesis and Storage:
· 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
Essential effects of insulin for fat storage in adipose tissue: · Inhibits action of · Enhances glucose transport into
hormone-sensitive lipase adipocytes - α glycerol phosphate - glycerol+ fatty acids to TG
34
Lack of insulin causes (2) and | increases (2)
lipolysis and release of FFA (Diabetic Ketoacidosis) plasma cholesterol and phospholipids conc.
35
increase Insulin Secretion (9)
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
Decrease Insulin Secretion (5)
``` Decreased blood glucose Fasting Somatostatin α-Adrenergic activity Leptin ```
37
Glucagon | • -- amino acid peptide, secreted from
29 | pancreatic alpha cells
38
Glucagon | hormone of
starvation
39
Glucagon | secretion controlled by
blood glucose levels (inverse relationship)
40
Glucagon | primary target tissue
liver
41
Glucagon targets liver to increase blood glucose by (3)
1. Stimulating glycogenolysis & inhibiting glycogen synthesis 2. Increasing gluconeogenesis 3. Increases blood fatty acid & ketoacid levels to provide more substrates for gluconeogenesis
42
The liver functions like a | buffer for
``` blood glucose. Individuals with severe liver disease have difficulty maintaining a narrow plasma glucose range. ```
43
``` Glucagon secretion is stimulated by (3) ```
Hypoglycemia, Epinephrine (β2), Vagus Nerve
44
``` Diabetes Mellitus (DM) Definition ```
Metabolic disorder characterized by hyperglycemia due to insufficient insulin or cellular resistance to insulin (or both)
45
With DM, it takes longer to reduce blood glucose levels and glucose levels don’t reach the
control level.
46
DM Major classifications (2)
1. Type 1 Diabetes-10% of cases-hypoinsulinemia | 2. Type 2 Diabetes-90% of cases-hyperinsulinemia
47
Symptoms of Diabetes Mellitus (8)
``` • 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
These are the three classic symptoms and are called the 3 P’s.
* Urinating often (Polyuria) * Feeling thirsty (Polydypsia) * Feeling hungry (Polyphagia)
49
Approximately 25% of patients with type 1 diabetes mellitus | initially present in
``` diabetic ketoacidosis (hyperglycemia >250 mg/dl, ketosis and metabolic acidosis with anion gap). ```
50
Diagnosis of Diabetes Mellitus (2)
Casual plasma glucose ≥200 milligrams/dL (11.1 mmol/L) and | symptoms of hyperglycemia
51
Diabetes Mellitus Type I | Pathophysiology (3)
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
``` Diabetes Mellitus Type I Risk Factors (3) ```
. Genetic predisposition-increased susceptibility 2. Environmental triggers stimulate autoimmune response a. Viral infections (mumps, rubella) b. Chemical toxins 3. Usually develops < age 40, non-obese younger patients
53
Manifestations of DM Type I (3)
* Beta cell destruction occurs slowly * Hyperglycemia occurs when 80 – 90% of cells destroyed * Often triggered by stressor (e.g. illness)
54
Hyperglycemia leads to: (7)
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
``` Diabetic Ketoacidosis (DKA) • Due to i ```
ncreased lipolysis to fatty acids to produce ketoacids
56
DKA is a response to
cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (glucagon, catecholamines, cortisone and growth hormone).
57
DKA Pathophysiology (3)
1. Osmotic diuresis & dehydration (hyperglycemia) 2. Metabolic acidosis (accumulation of ketones) 3. Fluid and electrolyte imbalances (from osmotic diuresis)
58
Signs and Symptoms of DKA (9)
``` – 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
There are three categories of | the severity of DKA:
``` 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
Remember that acidosis depresses neuronal function since it blocks inward current of (2)
Na+ and Ca2+
61
Diabetes Mellitus (DM) Type II
Fasting hyperglycemia despite availability of insulin-Insulin resistance
62
Diabetes Mellitus (DM) Type II was called
non-insulin dependent diabetes or adult onset diabetes. Both misnomers, type II DM may require insulin and occurs in children.
63
SKIPPED | Risk Factors for DM Type II
• 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
Pathophysiology of T2DM early late
Hyperinsulinemia due to insulin resistance (early) Beta cell dysfunction with impaired insulin secretion- pancreatic exhaustion? (late)
65
``` Pathophysiology of T2DM Due to (2) ```
downregulation of insulin receptors in target | tissues & insulin resistance
66
Insulin resistance is part of a cascade of disorders | that are called METABOLIC SYNDROME. (5)
1. Obesity, especially abdominal deposition 2. Insulin resistance 3. Fasting Hyperglycemia 4. Lipid Abnormalities (High TG and Low HDL) 5. Hypertension
67
ndividuals with metabolic syndrome have increased risk for
``` cardiovascular disease (CVD), particularly atherosclerosis and insulin resistance is a contributing factor for development of type 2 DM. ```
68
Pathophysiology of T2DM | similar chronic complications as
type 1
69
Retinopathy:
leading causes of blindness in the | United States
70
Nephropathy:
progressive renal dysfunction that | can lead to end-stage renal disease.
71
Neuropathy:
peripheral loss of sensation and | dysesthesias
72
Vascular disease:
``` accelerated atherosclerotic cerebrovascular and peripheral vascular diseases may occur due to abnormal lipid metabolism ```
73
Myopathies:
progressive weakness and | diminished exercise tolerance.
74
Oral Manifestations of DM (7)
* 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
Diabetes mellitus: linked to --- disease
periodontal
76
Periodontal disease exacerbates diabetic | complications (2)
– poor glycemic control – cardiovascular complications (stroke, ischemia, infarction)
77
Control of periodontal infection may | improve --- control
glycemic