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Physio II (mine) > Endocrine II: Diabetes and Pancreas / Calcium and Phosphate regulation > Flashcards

Endocrine II: Diabetes and Pancreas / Calcium and Phosphate regulation Flashcards

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1
Q

Islet of Langerhans Cell Types and %

BAD

A
  1. Beta=insulin producing (75%)
  2. Alpha=glucagon producing (20%)
  3. Delta=somatostatin producing (5%)
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2
Q

what does somatostatin do?

A

inhibits insulin, glucagon and GH

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3
Q

how does insulin antagonize glucagons effect?

A

driving glucose uptake and thus decreasing blood sugar

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4
Q

how does glucagon antagonize insulins effect?

A

stimulating hepatic glucose release and increasing blood sugar

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5
Q

what is a normal blood sugar

A

4-6mM = 80-100mg/dL

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6
Q

what things stimulate insulin?

A

glucagon
glucose (hyperglycemia)
amino acids

incretins (GIP, GLP)
sulfonylurea drugs

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7
Q

what things inhibit insulin

A

somatostatin
NE/Epi and cortisol
fasting/exercise

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8
Q

what things stimulate glucagon?

A

glucose (hypoglycemia)
amino acids
NE/Epi and cortisol
exercise and fasting

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9
Q

what things inhibit glucagon?

A

incretins (GIP, GLP)
insulin
somatostatin

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10
Q

mechanism of action of glucose binding to beta cells releasing insulin

A
  • glucose binds GLUT 2 R on pancreatic beta cell
  • closes the K-ATP channel
  • depolarizes beta cell
  • opens Ca channel
  • Ca binds to vesicles
  • insulin is released
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11
Q

C-Peptide

A

Cleaved off when endongenous insulin is made. Exogenius injectable insulin does not have this peptide.

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12
Q

Sulfonylureas do what

A

directly block the K-Atp channel in Beta cells causing insulin release

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13
Q

Incretins do what and are broken down by what?

GIP and GLP

A
  • Indirectly close the K-Atp channel in Beta cells causing insulin release
  • This insulin release directly inhibtis Alpha cells release of glucagon
  • Quickly broken down by DPP4
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14
Q

What maken incretins work better?

A

DPP4 antagonists

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15
Q

how does glucose control alpha cells in low glucose environments?

A
  1. Some glucose enters via the GLUT1
  2. Some ATP is still made inside cell
  3. Most of the K-Atp channels are closed
  4. Some depolerization occures
  5. Some VGCC open and Ca enters
  6. Ca binds to vesicles
  7. Some glucagon is released
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16
Q

how does glucose control alpha cells in high glucose environments?

A
  1. A ton of glucose enters via GLUT1
  2. A ton of ATP is made
  3. All K-Atp channels close
  4. Entire cell depolarized
  5. VDCC inactivated
  6. No Ca can enter and bind to vesicles
  7. No glucagon is released
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17
Q

What two things can inhibit glucagon release in the alpha cells?

A
  1. Insulin from Beta cells
  2. Somatostatin from Delta cells
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18
Q

What problems do diabetics have concerning alpha cells?

A

Insulin does not act upon them to inhibt glucagon release which increases resting blood sugar levels

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19
Q

is insulin anabolic or catabolic? and what does it cause in skeletal muscle, liver, and adipose tissue

A

anabolic
Skeletal muscle: increase glucose and AA uptake
Hepatic: supress glucose production
Adipose: inhibit lipolysis (breakdown of trigycerides into free fatty acids

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20
Q

is glucagon anabolic or catabolic? and what does it cause in skeletal muscle, liver, and adipose tissue

A

catabolic
Skeletal muscle: no effect
Hepatic: glycogen breakdown, sugar formation, ketone formation
Adipose: stimulates lipolysis = triglycerides into free fatty acids

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21
Q

what tissue is responsible for type 2 diabetes?

A

skeletal muscle, primary glucose storage

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22
Q

GLUT2

A

Glucose transporter in liver non-insulin dependent

Glucose transporter in Beta cell, glucose dependent

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23
Q

GLUT4

A

Insulin dependant transporter in muscle and fat cells

Myocytes and adipocytes

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24
Q

OGTT

A

oral glucose tolerance test

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25
OGTT Levels
1. Normal: After 2 hours less than 140 and never over 200 2. Insulin Resistant: more upper limits of normal (slightly over or near 200 after 2 hours) 3. Diabetes: Greater than 200 after 2 hours
26
What is T1D?
loss of beta cells due to autoimmune distruction (genetic factor) triggered by environmental factor
27
What are some enviromental factors that can trigger T1D?
* Viruses like Mumps, Rubella, and Coxsackie * Nutrients: cows milk | Babies>milk>antibodies for cow insulin>close to human insulin>autoimmune
28
Systemic effects of insulin deficiency problem 1 | T1D issue
Decreased glucose uptake causes * Hyperglycemia * Glycosuria * Osmotic diuresis * Electrolyte depletion Dehydration acidosis Coma Death | Glucose is hydroscopic so it ends up in urine
29
Systemic effects of insulin deficiency problem 2 | T1D issue
Increased protein catabolism * Increased plasma amino acids * Nitrogen lossed in urine * Osmotic diuresis Dehydration Acidosis Coma Death
30
Systemic effects of insulin deficiency problem 3 | T1D issue
Increased Lipolysis * Increased plasma FFA * Ketogenesis * Ketouria * Ketoemia Dehydration Acidosis Coma Death
31
What is insulin resistance?
loss of insulin receptor sensitivity in the GLUT4 transporter in skeletal muscle | Less transportation of glucose into the SK
32
How do we transport more glucose into skeletal muscle in an insulin resistant person?
We increase insulin levels which is a right shift on the insulin effectiveness curve
33
how do we develop type 2 diabetes?
insulin resistance (inactivity and genetics) obesity beta cell **hyperplasia** (normal glucose/high insulin) beta cell **fatigue** (high glucose/ high insulin)[last place to reverse damage] beta cell **failure** (high glucose/ low insulin)
34
how do we know that insulin resistance (inactivity and genetics) precede obesity for type 2 diabetes?
research shows that from just two weeks of inactivity insulin and glucose levels increased
35
HbA1C
glucose that is covalently bound to hemoglobin and a test for diabetes
36
HbA1C levels
* 6% / 114 / Normal * 6-7.5% / 115-164 / Good * 7.6-9 / 167-214 / Poor * >9 / >214 / Very Poor | % / Mean blood Glucose / Range
37
what does elevated HbA1C increased the risk of
Morbidity and mortality retinoplasty / neuropathy CVD / Stroke / ESRD * Specific for anesthesia * Reduced lung function * Glycosylation of joints (harder to move neck for DL)
38
How to calculate Mean Plasma Glucose?
(33.3 x HbA1c)-86 | (33.3 x 7)-86=147 (Good range)
39
what does HbA1C predict preoperativly in non diabetic pts?
mortality acute kidney injury | Getting good glycemic control before surgeries decreasces these
40
what is the leading cause of CKD and ESRD?
diabetes
41
DKA
diabetic ketoacidosis ketones (blood acids elevated) sugar elevated dehydration and coma
42
Quick Rundown: Insulin
Inhibits glucose production in liver Promotes glucose uptake in SK and adipose Lowers blood sugar
43
Promotes Glucose production in Liver
T3/T4 Glucagon Catecholamines Cortisol GH
44
Inhibits glucose uptake in SK and adipose
Cortisol GH/IGF-1
45
Surgery and Anesthesia increase stress hormones
T3/T4 Glucagon Catecholamines Cortisol GH/IGF-1
46
GH
Anterior Pituitary hormone Increases liver glucose production Bind to receptors on the liver to produce another hormone - IGF-1
47
GH/IGF-1
makes muscle and adipose tissue more insulin resistant | Increased GH usually more diabetic
48
what is the major storage site for calcium and phosphate?
bone as hydroxyapatite (HA)
49
free calcium vs protein bound calcium vs complex calcium
free 50% PB 40% complex 10%
50
free phosphate vs protein bound phosphate vs complex phosphate
free 80% PB 10% complex 10%
51
Ca2+ and PO4- are in dynamic equalibrium
Calcium excreted in feces 900 mg/d Phosphate excreted in urine 900 mg/d
52
how does thyroid regulate Calcium?
c cells release calcitonin and lowers calcium
53
how does parathyroid regulate phosphate and calcium?
chief cells release parathyroid hormone and increase phosphate and calcium | By bone breakdown
54
how do the skin, liver and kidney regulate phosphate and calcium?
skin intakes Vit D liver converts to 25OHVitD3 kidney converts to active VitD3
55
how does the bone regulate phosphate?
osteocytes secrete FGF23 that regulate phosphate
56
what is the normal blood calcium level?
10mg/100mL
57
what is used theraputically to prevent bone loss? shows no clinical symptoms when deficient.
calcitonin
58
what activates PTH?
hypocalcemia hyperphosptemia
59
what decreases PTH?
hypercalcemia increases in Vit D and FGF23
60
What is 1,25(OH)2?
1 25 hydroxy vitamin d | AKA Calcitrol
61
Pathway for Activated Vit D | AKA Calcitrol
Skin/Sun ProD3 PreD3 Vitamin D3 (we get this from diet)[aka Cholecaliferol] Liver converts to: Calcifediol(25(OH) Vit D) Kidney converts to: Calcitrol (1,25 (OH)2D2) via 1-alpha hydroxylase
62
1-alpha hydroxylase is activated by what?
PTH
63
What does PTH do?
If calcium levels drop it has 3 rapid and 2 slow ways to increase Ca2+ uptake If phosphate levels increase it helps lower them
64
3 rapid ways PTH increases Ca2+
1. Wastes phosphate via kidney 2. Increases kidney Ca2+ reabsporbtion 3. Breakdown bone via osteoprogenerin cells
65
2 slow ways PTH increases Ca2+
1. Osteoclastic bone reabsorption 2. Increase gut absorption
66
How does PTH decrease high phosphate levels?
PTH increases calcitrol synthesis Promotes renal excretion
67
Calcitrol is incresed by what
PTH via 1-alpha hydroxylase
68
Calcitrol is decreased by what
Increased Ca2+ Increased Calcitrol Increased FGF23
69
Breadown of what controls Ca2+
Thyroid: Calcitonin = lowers Ca2+ Parathyroid: PTH = raises Ca2+ Vit D: helps raise Ca2+
70
Breakdown of what controls Phosphate
Parathyroid: PTH = Increases PO4- Bone: FGF23 = lowers PO4- Vit D: increases PO4-
71
FGF23 is increased by
Increased PO4- Increased PTH Increased Calcitrol
72
FGF23 is decreased by
Decreased PO4- Decreased PTH Decreased Calcitrol
73
How to remember Osterocyte types | B and C
Osteo**B**lasts = **B**uild Bone Ostero**C**lasts = **C**onsume Bone
74
Difference between OPG and RANKL?
OPG = Maintaine bone RANKL = Bone breakdown
75
Osteolysis steps | 7
1. PTH>Vit D> osteoblasts 2. Stimulated osteoblasts release RANKL and M-CSF 3. Osteoblasts stop OPG production (allows for more osteoclast formation) 4. M-CSF binds to stem cells = osteoclast precurser formation 5. RANKL binds to precursers making pre-osteoclasts 6. The pre-osteoclast group merge into mature osteoclasts 7. Osteoclast attach to bone and begin breakdown | M-CSF: Macrophage-colony stimulating factor

Physio II (mine) (6 decks)

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