Lecture 38: Homeostasis in Action Flashcards

1
Q

Increasing glucose level, ______ responds to high glucose by secreting _____. This causes _____, skeletal muscle, and ___ ____ to ….

A
  • Pancreas
  • Insulin
  • Liver
  • Other tissues
  • Take up more glucose
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2
Q

Control of blood glucose is mainly by _____ _____.

A
  • Negative feedback
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3
Q

Insulin can be thought of as…

A
  • Signalling that the body has been fed

- i.e promotes uptake and storage of nutrients

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4
Q

If there’s no insulin around then the body is going to act as if…

A
  • It’s “starved”
  • Breaking down stores of glycogen and releasing that glucose to other tissues in the body
  • Gluconeogenesis = liver is taking non carbohydrate sources (break down of amino acids) to make new glucose
  • Breaking down fat stores to increase lipid levels in blood
  • Increase ketone production which can be ‘glucose sparing’.
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5
Q

Diabetes derived from Greek….

Mellitus derived from Latin…

A
  • “Passing through”

- “Honey” or “Sweet”

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6
Q

Diabetes is historically referred to a disease state characterized by…

A
  • Polyuria (passing large volumes of urine)
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
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7
Q

Type 1 Diabetes Mellitus:

A
  • Little or NO INSULIN
  • Typically younger onset (children or teenagers)
  • May be associated with prior viral illness and subsequent autoimmune response that destroys pancreatic Beta Cells
    Environmental agent + genetic predisposition ^^^
  • Treatment = Insulin
  • HYPO only occurs if they’ve been overtreated with insulin
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8
Q

Type II Diabetes Mellitus:

A
  • Insulin Resistance
  • Cells aren’t responding to the insulin
  • May have higher than normal levels of insulin, because glucose ends up staying in blood, which means lots and lots of insulin
  • Eventually insulin level may drop off because pancreas has had enough
  • May be related to:
    Ageing
    Obesity
    » Reduced numbers or function of insulin receptors
    » Altered intracellular signalling in target cells
  • Other conditions (eg Cushing’s disease, PCOS)
  • Hyperglycemia but diff to Type I, insulin levels may still be adequate to suppress lipolysis and ketogenesis but not sufficient to control BGL
  • Treatment: Exercise, Weight Loss, Oral Drugs, Insulin if needed
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9
Q

Oral Hypoglycemic Drug Classes are used for ____ ____ Diabetes people. These include:

A
  • Type II
  • Sulphonylureas : increase insulin secretion by beta cells, can cause hypoglycemia if not eating or overdose
  • Metformin : reduces glucose output from liver by inhibiting gluconeogenesis
  • Thiazolidinediones : increase insulin sensitivity of cells
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10
Q

Diabetes Insipidus:

A
  • Lots of dilute urine but no glucose in it!!!
  • Due to altered secretion of ADH or decreased responsiveness to it
  • Often associated with brain injury or tumour in region of pituitary gland
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11
Q

Gestational Diabetes (important):

A
  • Can affect women during pregnancy
  • May resolve after pregnancy or not
  • Large baby increased risk of birth injuries, neonatal hypoglycemia, congenital malformations, child/adult obesity?
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12
Q

Hyperglycemia is due to:

A
  • Inability of most cells (not brain) to absorb glucose
    » glucose stays in blood, can’t enter cells, decreased production
  • Increased output of glucose by liver
    » Glycogenolysis and gluconeogenesis
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13
Q

Glycosuria is when…

A
  • Renal tubes can’t reabsorb the excessive glucose being filtered
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14
Q

Polyuria…

A
  • Excessive thirst
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15
Q

Acute Consequences…

A
  • Breakdown of protein and fat
  • (Diabetic) Ketoacidosis (DKA) : ketones are acidic and cause acidosis when produced in excess
  • Acetone-like smell on breath and can also be detected in urine
  • Acidosis causes hyperventilation
  • Acidosis can cause hyperkalemia
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16
Q

Need to be careful when administering insulin in DKA - why?

A
  • Increases uptake of amino acid and potassium

- Potassium is back in cells, total K is depleted

17
Q

Chronic hyperglycemia can predispose blood vessels and nerves to damage. This includes:

A
  • Cardiovascular disease
  • Renal failure
  • Retinal damage
  • Poor wound healing
  • Peripheral nerve damage
  • Susceptibility to infection
18
Q

Treatment of Type I Diabetes Mellitus:

A
  • Insulin : Banting + best at UOT developed methods for extracting and purifying insulin from cattle pancreases.
  • Now a much greater range of insulin types available
  • Human insulin modifies to slow absorption
19
Q

Homeostatic mechanisms restoring blood pressure and volume after haemorrhage

A
  • Activation of platelets and the coagulation cascade
  • Drop in pressure detected by sensors
  • Info sent by nerves to cardiovascular control centres in brainstem
  • Nerve impulses sent from brain to heart to increase HR and force of contraction
20
Q

Signs typically associated with physiological shock…But what about blood volume?

A
  • Looks pale and skin cool ‘clammy’
  • Vasoconstriction to blood vessels in skin and other organs
  • Decreased blood pressure detected by stretch receptors in walls of renal arterioles
  • Specialised cells in the kidney (integrator) cause the formation of a hormone (control signal) in the blood (communication pathway)
  • Hormone 1 can (1) stimulate adrenal glands –> Aldosterone –> Na+ reabsorption by kidney
    (2) stimulate ADH glands
21
Q

Blood pressure and blood volume are restored but what about the lost RBCs?

A
  • A few weeks