Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

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

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%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does somatostatin do?

A

inhibits insulin, glucagon and GH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how does insulin antagonize glucagons effect?

A

driving glucose uptake and thus decreasing blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how does glucagon antagonize insulins effect?

A

stimulating hepatic glucose release and increasing blood sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is a normal blood sugar

A

4-6mM = 80-100mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what things stimulate insulin?

A

glucagon
glucose (hyperglycemia)
amino acids

incretins (GIP, GLP)
sulfonylurea drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what things inhibit insulin

A

somatostatin
NE/Epi and cortisol
fasting/exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what things stimulate glucagon?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what things inhibit glucagon?

A

incretins (GIP, GLP)
insulin
somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

C-Peptide

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Sulfonylureas do what

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What maken incretins work better?

A

DPP4 antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A
  1. Insulin from Beta cells
  2. Somatostatin from Delta cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what tissue is responsible for type 2 diabetes?

A

skeletal muscle, primary glucose storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GLUT2

A

Glucose transporter in liver non-insulin dependent

Glucose transporter in Beta cell, glucose dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GLUT4

A

Insulin dependant transporter in muscle and fat cells

Myocytes and adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

OGTT

A

oral glucose tolerance test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

OGTT Levels

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is T1D?

A

loss of beta cells due to autoimmune distruction (genetic factor)

triggered by environmental factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some enviromental factors that can trigger T1D?

A
  • Viruses like Mumps, Rubella, and Coxsackie
  • Nutrients: cows milk

Babies>milk>antibodies for cow insulin>close to human insulin>autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Systemic effects of insulin deficiency problem 1

T1D issue

A

Decreased glucose uptake causes
* Hyperglycemia
* Glycosuria
* Osmotic diuresis
* Electrolyte depletion
Dehydration
acidosis
Coma
Death

Glucose is hydroscopic so it ends up in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Systemic effects of insulin deficiency problem 2

T1D issue

A

Increased protein catabolism
* Increased plasma amino acids
* Nitrogen lossed in urine
* Osmotic diuresis
Dehydration
Acidosis
Coma
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Systemic effects of insulin deficiency problem 3

T1D issue

A

Increased Lipolysis
* Increased plasma FFA
* Ketogenesis
* Ketouria
* Ketoemia
Dehydration
Acidosis
Coma
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is insulin resistance?

A

loss of insulin receptor sensitivity in the GLUT4 transporter in skeletal muscle

Less transportation of glucose into the SK

32
Q

How do we transport more glucose into skeletal muscle in an insulin resistant person?

A

We increase insulin levels which is a right shift on the insulin effectiveness curve

33
Q

how do we develop type 2 diabetes?

A

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
Q

how do we know that insulin resistance (inactivity and genetics) precede obesity for type 2 diabetes?

A

research shows that from just two weeks of inactivity insulin and glucose levels increased

35
Q

HbA1C

A

glucose that is covalently bound to hemoglobin and a test for diabetes

36
Q

HbA1C levels

A
  • 6% / 114 / Normal
  • 6-7.5% / 115-164 / Good
  • 7.6-9 / 167-214 / Poor
  • > 9 / >214 / Very Poor

% / Mean blood Glucose / Range

37
Q

what does elevated HbA1C increased the risk of

A

Morbidity and mortality
retinoplasty / neuropathy
CVD / Stroke / ESRD
* Specific for anesthesia
* Reduced lung function
* Glycosylation of joints (harder to move neck for DL)

38
Q

How to calculate Mean Plasma Glucose?

A

(33.3 x HbA1c)-86

(33.3 x 7)-86=147 (Good range)

39
Q

what does HbA1C predict preoperativly in non diabetic pts?

A

mortality

acute kidney injury

Getting good glycemic control before surgeries decreasces these

40
Q

what is the leading cause of CKD and ESRD?

A

diabetes

41
Q

DKA

A

diabetic ketoacidosis
ketones (blood acids elevated)
sugar elevated
dehydration and coma

42
Q

Quick Rundown: Insulin

A

Inhibits glucose production in liver
Promotes glucose uptake in SK and adipose

Lowers blood sugar

43
Q

Promotes Glucose production in Liver

A

T3/T4
Glucagon
Catecholamines
Cortisol
GH

44
Q

Inhibits glucose uptake in SK and adipose

A

Cortisol
GH/IGF-1

45
Q

Surgery and Anesthesia increase stress hormones

A

T3/T4
Glucagon
Catecholamines
Cortisol
GH/IGF-1

46
Q

GH

A

Anterior Pituitary hormone
Increases liver glucose production
Bind to receptors on the liver to produce another hormone - IGF-1

47
Q

GH/IGF-1

A

makes muscle and adipose tissue more insulin resistant

Increased GH usually more diabetic

48
Q

what is the major storage site for calcium and phosphate?

A

bone as hydroxyapatite (HA)

49
Q

free calcium vs protein bound calcium vs complex calcium

A

free 50%
PB 40%
complex 10%

50
Q

free phosphate vs protein bound phosphate vs complex phosphate

A

free 80%
PB 10%
complex 10%

51
Q

Ca2+ and PO4- are in dynamic equalibrium

A

Calcium excreted in feces 900 mg/d
Phosphate excreted in urine 900 mg/d

52
Q

how does thyroid regulate Calcium?

A

c cells release calcitonin and lowers calcium

53
Q

how does parathyroid regulate phosphate and calcium?

A

chief cells release parathyroid hormone and increase phosphate and calcium

By bone breakdown

54
Q

how do the skin, liver and kidney regulate phosphate and calcium?

A

skin intakes Vit D
liver converts to 25OHVitD3
kidney converts to active VitD3

55
Q

how does the bone regulate phosphate?

A

osteocytes secrete FGF23 that regulate phosphate

56
Q

what is the normal blood calcium level?

A

10mg/100mL

57
Q

what is used theraputically to prevent bone loss? shows no clinical symptoms when deficient.

A

calcitonin

58
Q

what activates PTH?

A

hypocalcemia

hyperphosptemia

59
Q

what decreases PTH?

A

hypercalcemia

increases in Vit D and FGF23

60
Q

What is 1,25(OH)2?

A

1 25 hydroxy vitamin d

AKA Calcitrol

61
Q

Pathway for Activated Vit D

AKA Calcitrol

A

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
Q

1-alpha hydroxylase is activated by what?

A

PTH

63
Q

What does PTH do?

A

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
Q

3 rapid ways PTH increases Ca2+

A
  1. Wastes phosphate via kidney
  2. Increases kidney Ca2+ reabsporbtion
  3. Breakdown bone via osteoprogenerin cells
65
Q

2 slow ways PTH increases Ca2+

A
  1. Osteoclastic bone reabsorption
  2. Increase gut absorption
66
Q

How does PTH decrease high phosphate levels?

A

PTH increases calcitrol synthesis
Promotes renal excretion

67
Q

Calcitrol is incresed by what

A

PTH via 1-alpha hydroxylase

68
Q

Calcitrol is decreased by what

A

Increased Ca2+
Increased Calcitrol
Increased FGF23

69
Q

Breadown of what controls Ca2+

A

Thyroid: Calcitonin = lowers Ca2+
Parathyroid: PTH = raises Ca2+
Vit D: helps raise Ca2+

70
Q

Breakdown of what controls Phosphate

A

Parathyroid: PTH = Increases PO4-
Bone: FGF23 = lowers PO4-
Vit D: increases PO4-

71
Q

FGF23 is increased by

A

Increased PO4-
Increased PTH
Increased Calcitrol

72
Q

FGF23 is decreased by

A

Decreased PO4-
Decreased PTH
Decreased Calcitrol

73
Q

How to remember Osterocyte types

B and C

A

OsteoBlasts = Build Bone
OsteroClasts = Consume Bone

74
Q

Difference between OPG and RANKL?

A

OPG = Maintaine bone
RANKL = Bone breakdown

75
Q

Osteolysis steps

7

A
  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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions