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Pharm > Diabetes > Flashcards

Diabetes Flashcards

1
Q

where are GLUT 1 receptors located

A

CNS, BBB

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2
Q

where are GLUT 2 receptors located

A

renal tubular cells
liver

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3
Q

where are GLUT 3 receptors located

A

neurons, placenta

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4
Q

where are GLUT 4 receptors located

A

muscle (glucose)
adipose (triglycerides metabolised to glucose)

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5
Q

how does metformin work

A

phosphorylates GLUT4, increasing sensitivity to insulin

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6
Q

How does GLUT 4 and insulin interact

A

insulin signals cell to insert GLUT4 transporters into membrane, allowing glucose entry, stored for later use

in absence of insulin, glucose can not enter cell

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7
Q

what is basal insulin

A

insulin is secreted continously
suppresses hepatic glucose production between meals and overnight
maintain blood sugars at constant level
50% daily insulin requirements

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8
Q

Glucagon reminder

A

increases gluconeogenesis (liver and kidney)
glycogenolysis (liver)

TURNS OFF GLYCOLYSIS in liver, glycolytic intermediates shuttled off to gluconeogenesis

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9
Q

drugs that can cause diabetes

A

PIs
glucocorticoids
thiazide diuretics
atypical antipsychotics

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10
Q

how does insulin work

A

decreases plasma glucose levels through suppression of hepatic glucose production

stimulates glucose use in skeletal muscle and adipose tissue (instead of stimulating fat lipolysis for energy so that glucose blood levels may decrease)

converts glucose to glycogen (stored form)
lipogenesis
protein synthesis

reduces K and Mg

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11
Q

diabetes diagnostic criteria

A

Fasting plasma glucose _ 7.0 mmol/L or
2 hr OGTT _ 11.1 mmol/L or
HbA1c_ 6.5% or
Random plasma glucose _ 11.1 mmol/L AND symptomatic

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12
Q

impaired glucose tolerance

A

fasting glucose less than 7.0
2hr OGTT: 7.8-11.0

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13
Q

impaired fasting glucose

A

6.1 to 6.9

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14
Q

2 consequences of insulin resistance

A

hyperglycaemia
lipid excess due to lipolysis (NAFLD)

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15
Q

2 consequences of insulin resistance

A

hyperglycaemia
lipid excess due to lipolysis (NAFLD)

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16
Q

metabolic syndrome diagnosis

A

3 of following:
central obesity
high blood pressure
high blood sugar
high serum triglycerides
low serum HDL

assoc. with: increased risk Type 2 D, CVD

17
Q

how do you treat Type 1s

A

Insulin monotherapy

18
Q

Short acting insulin

A

Actrapid

Subcut

3/day

30min before meal, peak action 2-5 hrs

duration: 5-8 hrs

human insulin

19
Q

Intermediate acting insulin eg protophane?

A

subcut
1/2 times dly, usually at night but no later than 10pm

Neutral Protamine Hagedorn (NPH) insulin

onset: 1-3 hrs
peak: 6-12 hrs
duration: 16-24 hrs

20
Q

Biphasic insulin: Actraphane

A

Subcut

2 per day

Regular human insulin plus NPH in diff proportions

premixed insulin (intermediate or short acting mixture)

onset: 30 min
peak: 2-12 hrs
duration 16-24 hrs

21
Q

what is the preferred management of Type 1s

A

basal bolus

premeal short acting insulin (bolus) PLUS bedtime (not later than 10) intermediate acting insulin (Protophane/Humulin N)

total dose divided into: 40-50 % basal insulin and rest as bolus, split equally before each meal

22
Q

what is the initial total daily insulin dose for basal bolus regimen

A

0.6 units/kg body weight

23
Q

What is lipohypertrophy

A

when you inject at 1 site instead of rotating

24
Q

Metformin MOA

A

Reduces hepatic gluconeogenesis and glycogen metabolism
Improves insulin resistance via enhancing insulin-mediated glucose uptake by skeletal muscle
Decrease carbohydrate absorption from GIT
Lowers triglyceride and total cholesterol levels, raises HDL
Indicated alone in obese, mild diabetics as it does not enhance lipogenesis (unlike insulin)

taken with meals
500mg once/twice dly or 850mg once/twice dly
after 5-7 days, uptitrate to 2000mg/day (depends on GIT SEs)

if severe GIT SEs, extended-release formulation preferred

25
Q

when is metformin contraindicated

A

eGFR below 30

26
Q

Side effects of metformin

A

GIT: nausea, vom, diarrhoea

lactic acidosis (inhibited conversion lactate to glucose)

reduced Bit B12 absorption

DOES NOT CAUSE Hypoglycaemia

27
Q

sulphonyl urea examples

A

glibenclamide
gliclazide (lowest risk hypoglycaemia)
gli……

28
Q

Sulphonylurea MOA

A

requires residual beta cell functioning: NB

stimulates insulin secretion from beta cells
promotes beta cell growth
enhances beta cell sensitivity to glucose (glucose is most potent stimulus for release of insulin from b cells)
reduces glucagon release

in more detail: Beta cells possess K channels regulated by intracellular ATP. when blood glucose increases, more glucose enters beta cells, more ATP produced, closes K channels. depolarisation of beta cell initiates influx Ca through ca channels, triggers insulin release

29
Q

contraindications to using sulphonylurea

A

avoid: renal impairment eGFR below 60
do not use if: severe hepatic impairment
pregnancy

30
Q

side effects sulphonylureas

A

Hypoglycemia
0.2-0.4 severe cases in 1000 patient years
Risk factors: renal impairment, elderly patients, irregular meal schedule

Weight gain (5kg over first 6 years

31
Q

stepwise approach to diabetes type 2 management

A

Non-drug first (diet and exercise)
+Metformin  ?HbA1C target (go to Sulphonylurea if target not achieved)
+Sulphonylurea  ? HbA1C target
-Sulphonylurea (withdraw) +Insulin **adherence NB

NO oral agents in type 1

32
Q

insulin regimens Type 2

A
  1. Add on: intermediate to long-acting

10 units starting (increase in increments to 20 units)
evening, no later than 10pm

  1. Substitution: biphasic
    twice dly
    total dly dose: 15 units divided as follows:
  2. 2/3 total dly dose 20 min before bfast (10 units)
  3. 1/3 total dly dose, 30 min before supper (5 units)
33
Q

which population groups have blunting of hypoglycaemic symptoms

A

Elderly patients with neuropathy, patients with long-standing diabetes (>10 years), and patients taking β blockers

34
Q

DKA diagnosis

A

keto: serum and urine ketone conc increases

diabetic: blood glucose > 13.8, less than 40

acidosis: blood pH < 7.2

bicarb level: <18

raised anion gap (met acidosis)

serum osmolality <350

35
Q

DKA diagnosis

A

keto: serum and urine ketone conc increases

diabetic: blood glucose > 13.8, less than 40

acidosis: blood pH < 7.2

bicarb level: <18

raised anion gap (met acidosis): accumulation Beta hydroxybutyruate and acetoacetic acid

serum osmolality <350

36
Q

how are ketones produced in DKA

A

In DKA, low levels of effective circulating insulin and an increase in glucagon, suppress glucose oxidation and increase lipolysis. Lipolysis leads to increased production of ketones, especially β-hydroxybutyrate. The ratio between acetoacetate and B-OHB increases from 1:1 to 1:10. While oxidation of fatty acyl CoA and acetoacetate provides an alternative source of energy, ensuing ketonemia contributes to metabolic acidosis.

essentially: lack of insulin means that there is no inhibition of fatty acid transport into matrix of mitochondria

37
Q

DKA complications explained

A

Acidosis causes nausea and vomiting, a frequent presenting symptom of DKA. Loss of fluid in vomit exacerbates the water deficit and consequent dehydration induced by osmotic diuresis.
(osmotic diuresis: hyperglycaemia causes increase in urine output, glucose draws water across membrane)

Acidosis is a contributory factor in the development of the dangerously high plasma potassium (hyperkalemia) that is also a feature of untreated DKA, because acidosis induces an exchange of hydrogen ions for potassium ions across cell membranes with hydrogen ions passing into cells and potassium ions passing out of cells to the ECF (blood plasma).
insulin def: K doesnt enter cells (serum is normal or raised)

Hyperkalemia, however, masks the underlying whole-body potassium deficiency that occurs in DKA.

38
Q

causes of DKA

A

Infections – pneumonia, UTI, sepsis, gastroenteritis etc.
Inadequate insulin treatment or non-compliance
New onset diabetes
Infarction - Myocardial infarction, cerebral, mesenteric, peripheral
Drugs – cocaine, atypical antipsychotics, corticosteroids, glucagon, interferon etc.,
Pregnancy

39
Q

investigations in DKA

A

blood K: NORMAL/ baseline

FBC: leukocytosis, even without infection

U and E: Urea and Creat elevated

Pharm (17 decks)

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