diabetes physiology Flashcards

1
Q

is glucagon and insulin an anabolic or catabolic hormone?

A

glucagon = catabolic = breakdown

insulin = anabolic = building

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2
Q

glycogenolysis

A

liver breaks down glycogen into glucose

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3
Q

gluconeogenesis

A

liver converts proteins + fats into glucose

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4
Q

when is glucagon released? (in response to..)

A

low blood sugars

+ stress

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5
Q

how does glucagon increase blood sugar levels

A

glycogenolysis (glycogen -> glucose)

gluconeogenesis (proteins + fats -> glucose)

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6
Q

can ketones cross the blood brain barrier?

A

yes - brain cas use as fuel

water soluble fatty acids

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7
Q

how can ketone levels be measured?

A

urine dipstick

blood via ketone meter

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8
Q

where is insulin made?

A

rough endoplasmic reticulum of pancreatic beta cells

2 polypeptide chains linked by disulphide bonds

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9
Q

insulin creation

A

initially large single chain = preproinsulin

preproinsulin -> proinsulin + single peptide -> C-peptide + insulin

(C peptide has no function)

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10
Q

what do the 4 cell types of pancreatic islets secrete?

A
alpha = glucagon
beta(commonest) = insulin
delta = somastatin
PP-cell = pancreatic polypeptide
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11
Q

how does glucose enter beta cells?

A

through GLUT2 (glucose transporter)

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12
Q

How are thyroid hormones transported in the blood?

A

Thyroid hormones are lipophilic, and bind to thyroxine binding globulin (TBG) and thyroid binding pre-albumin (TBPA). A very small concentration of T3 and T4 travels freely in the bloodstream where it can interact with target cells.

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13
Q

How is adrenal corticosteroid production regulated?

A

When low amounts of cortisol are detected, the hypothalamus releases corticotropin releasing hormone. This stimulated production of adrenocorticotropic hormone in the anterior pituitary, which acts upon the adrenal glands to raise cortisol. Increased cortisol has a negative feedback mechanism on both the hypothalamus and anterior pituitary, to stop levels rising too high.

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14
Q

what is glucose phosphorylated by in pancreatic beta cells?

A

glucokinase

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15
Q

what can be said about the amout of insulin released vs the amount of glucose than enters the pancreatic beta cell?

A

directly proportional

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16
Q

activity of glucokinase in type 2 diabetes

A

maximmaly acitive at all times

17
Q

effect of chronic insulin secretion on mitochondria

A

mitochondrial exhaustion = reduced ATP production

18
Q

alpha cells reaction to low glucose

A

K-ATP channels open
voltage-gated sodium channels (NaV) contribute to APs
P/Q voltage gated calcium channels (CaV) enable Ca influx
glucagon exocytosis triggered

19
Q

alpha cells reaction to low glucose

A

K-ATP channels open
voltage-gated sodium channels (NaV) contribute to APs
P/Q voltage gated calcium channels (CaV) enable Ca influx
glucagon exocytosis triggered

20
Q

alpha cells reaction to high glucose

A

K-ATP channels closed - cell depolarised
presence of SGLT 2 glucose transporters contributes to non-voltage regulated sodium ion influx
NaV + CaV channels closed, glucagon not exocytosed

21
Q

relation between glucagon secretion and blood glucose

A

secretion of glucagon INVERSELY proportional to blood glucose

22
Q

mechanisms of insulin resistance (3)

A
  1. impairment of insulin signalling - skeletal muscle insulin resistance
  2. inflammation - adipose tissue insulin resitance (obesity induced inflammation)
  3. pathway-selective hepatic insulin resistance
23
Q

gold standard measurement of insulin resistance?

A

hyperinsulinemic-euglycemic clamp

initial sample taken from artery then infuse insulin into vein + keep taking artery samples

24
Q

patient is given insulin infusion and potassium is lowered, by what mechanism is insulin causing this effect?

A

stimulation of the Na/K ATPase pump

25
Q

type 2 diabetic started on steroids, what monitoring is most important after starting?

A

four times daily capillary blood glucose

-> use of corticosteroids can worsen diabetic control due to their anti-insulin effects