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GERR Pharmacology > Treatment of Diabetes pt1 > Flashcards

Treatment of Diabetes pt1 Flashcards

1
Q

Plainly describe what is Diabetes mellitus

A
  • a metabolic disorder due to defects in insulin secretion , action or both
  • results in chronic hyperglycaemia and disturbances to carb, fat and protein metabolism
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2
Q

What are the late associated complications of diabetes

A

1- Microvascular : kidneys & retinopathy
2- Microvascular : atherosclerosis, MI , stroke
3- Neuropathy : loss of sensation

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3
Q

List the Onset , Nutritional status , Prevalence, genetic predisposition and defect of Type 1 diabetes

A
  • childhood / puberty
  • normally malnourished
  • 10-20% worldwide
  • moderate genetic predisposition
  • defect in pancreatic B cell
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4
Q

List the Onset , Nutritional status , Prevalence, genetic predisposition and defect of Type 2 diabetes

A
  • 35 +
  • normally obese
  • 80-90% diagnosed
  • strong genetic predisposition
  • Insulin resistance , insufficient
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5
Q

How are insulin levels measured

A
  • Insulin is measured using C-peptide ( ELISA )
  • proinsulin is made of an A, B and C chain. the C chain is cleaved off to produce mature insulin
  • C chain is what’s measured to determine insulin levels because we’re only looking at level of active insulin in blood
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6
Q

Explain the phases of insulin secretion

A

Phase 1 : rapid peak trigger by increased glucose levels (meal)
Phase 2 : slow, sustained until blood glucose is back to normal : pulsatile release into portal vein

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7
Q

Where is a lot of insulin produced lost

A
  • Liver
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8
Q

What is the half life of insulin

A

5-6 minutes

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9
Q

Explain the Mechanism by which Insulin is stimulated ( 5 steps )

A

1- glucose taken up by pancreatic B cell by GLUT2 transports
2- metabolized to generate ATP
3- ATP blocks ATP sensitive K+ channel
4- membrane depolarization because K can’t get out of cell so Ca influx into cell
5- increase in Calcium ions triggers release of insulin into prepackaged vesicles

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10
Q

What happens with beta cells in type 2 diabetes

A
  • less insulin granules are being released each time the B cell depolarizes
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11
Q

Explain the mechanism of insulin secretion during low blood glucose levels

A 
1- no glucose taken up 
2- no ATP metabolized 
3- Regular K+ efflux 
4- hyper polarization 
5- decrease Ca influx 
6- decrease in Insulin secretion
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12
Q

How does insulin stimulate glucose uptake

A
  • insulin binds to insulin receptors which signal glucose uptake via GLUT4 in liver, muscle and fat
  • GLUT 4 is translocated from cytosol to membrane and then opens up to take in glucose
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13
Q

Does the heart and brain need GLUT 4

A
  • they do not require insulin for glucose uptake since they are very metabolically active
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14
Q

How insulin works In liver

A 
1-  increase Glycolysis 
2- increase glycogen synthesis 
3- decrease gluconeogenesis 
4- decrease glycogenolysis 
overall effect : increased storage of glycogen in liver
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15
Q

How insulin works in muscle

A 
1- increase glucose uptake via GLUT 4 
2- increases glycogen synthesis 
3- increase glycolysis 
4- increases amino acid uptake 
5- increases protein synthesis
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16
Q

How insulin works in Adipose tissue

A

1- Increase glucose uptake via GLUT 4
2- increase triglyceride formation ( storage of fat )
Overall effect : fat deposition / storage for when there is no food

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17
Q

How insulin works In Brain

A

1- increase Hunger
2- decrease Hepatic glucose production
3- decrease lipoprotein production

18
Q

How is insulin taken up in brain

A

via GLUT 1

19
Q

In the case of monozygotic twins where one twin develops T1DM , what is the likelihood of the other twin developing T1DM

A
  • 25 %

- not likely

20
Q

Does insulin occur in a biphasic manner

A
  • yes
21
Q

Are insulin levels measured Bia C peptide PCR

A
  • no , ELISA not PCR
22
Q

What are the medical indications of Insulin

A
  • type 1 diabetes
  • emergency keto acidosis treatment
  • type 2 diabetes control or pre-surgery
  • pregnancy
  • emergency treatment of hyperkalaemia
23
Q

Why can insulin not be given as tablet

A
  • it’s a peptide and would be degraded by GIT
24
Q

How is insulin administered by patients

A
  • subcutaneously
25
Q

What are different methods for glucose measuring other than glucometer

A
  • transdermal bluetooth glucose sensor
26
Q

Describe short acting insulin , onset and peak time

A
  • insulin pen with soluble insulin
  • commonly insulin lisper or insulin aspart are used which have a faster onset
  • injected before meal
  • onset time : 30 min
  • peak : 2-4 hrs
27
Q

Describe Intermediate acting insulin , acting time

A
  • insulin zinc suspension : zinc slows down rate of insulin absorption ( semilente )
  • injected once or twice a day
  • 16- 35 hrs
28
Q

Describe long-acting insulin

A
  • insulin zin suspension (ultralente )
  • 35+ hrs
  • used once a day
29
Q

What is Insulin Glargine

A
  • modified insulin
  • long-acting
  • reduces risk of night time hypoglycaemia
  • provides constant basal insulin supply & prolongs absorption
30
Q

What type of therapy is best for type 1 diabetes

A
  • mixture of short acting and intermediate acting before meals
31
Q

What are insulin pumps

A
  • sense blood glucose and deliver long-acting insulin when required
  • still need to deliver short acting pumps before meals
32
Q

Factors effecting subcutaneous absorption

A
  • site of injection
  • blood flow at site ( exercise )
  • depth of injection
  • concentration and dose of insulin
  • insulin degrading activity in subcutaneous tissue
33
Q

Side effects of too much insulin injected

A
  • hypoglycaemia : patients sweat , shaky , dizzy. can result in coma or brain damage
    2- allergic reactions
    3- Lipodystrophy
    4- Lipohypertrophy
34
Q

What to do in situations where diabetic goes hypoglycaemia

A

1- sweet drinks

2- if unconscious emergency glycogen or glucose gel’s put on lips

35
Q

Insulin effect on serum K+

A
  • insulin causes potassium to go into cells via NaK ATPase

- reduces serum K levels

36
Q

Dangers of IV insulin with K levels

A
  • insulin IV can result in dangerous reduction of serum K levels
  • effects heart, ex : arrhythmia
37
Q

Explain Diabetic Ketoacidosis

A
  • type 1 patient doesn’t take insulin
  • body shifts to start breaking down fat for energy
  • generates ketones which lowers PH of blood
  • patient goes into diabetic keto acidosis
38
Q

Signs of D Ketoacidosis

A
  • unconscious
  • breath smells of alcohol
  • dehydrated
  • high blood glucose and ketones
39
Q

what is the normal PH of blood

A

7.35- 7.45

40
Q

Treatment for DKA

A
  • saline : to decrease venous ketones

- IV infusion of insulin

GERR Pharmacology (9 decks)

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