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Year 3 Human Disease > Diabetes and its treatment > Flashcards

Diabetes and its treatment Flashcards

1
Q

how is insulin made

A

beta cells of pancreas –> proinsulin –> breaks down in to C peptide and insulin

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2
Q

effects of insulin

A

decreases blood glucose

increases glucose in liver, kidneys, muscle

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3
Q

normal range of blood glucose levels

A

4-7M/m

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4
Q

define diabetes

A

metabolic disorder characterised by chronic hyperglycaemia resulting from defects in insulin secretion/ action/ both

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5
Q

difference between type 1 and type 2 insulin

A

type 1: insulin deficiency. autoimmune destruction of pancreas
type 2: insulin resistance (due to other hormones/ obesity)

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6
Q

why is obesity linked to insulin type 2 diabetes 2

A

hormones linked to obesity prevent insulin binding to receptor IRS1
mutations of 2nd messengers

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7
Q

what is cut off point for having diabetes

A

4-7m/M normal
8-10 impaired glucose tolerance
11 M/m DIABETES

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8
Q

IGT stand for and relevance to diabetes

A

impaired glucose tolerance

50% go on to develop diabetes

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9
Q

how doe HbA1c test for diabetes work

A

looks at glucose over ast 2-3 months (lifetime of current haemoglobin

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10
Q

HbA1c cannot pick up rapid changes, so do not use…

A

cannot pick up rapid changes, so do not use:

  • children/ young people
  • symptoms suggesting type 1 diabetes
  • short duration diabetes symptoms
  • pts at high risk of diabetes who are acutely ill
  • pts taking medication that may cause rapid glucose rise eg corticosteroids
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11
Q

when HbA1c can be innacurate

TABLE ON DIAGNOSIS VALUES

A
  • HIGH HbA1c 2: persistant HbF (thalassaemia), uraemia (carbamylates Hb) *high HbF Fucking High)
  • LOW HbA1c 2: haemolysis, inc red cell turnover, blood loss (HbS, HbC, Low and SexC)
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12
Q

3 types of diabetes

A

1,2, gestational

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13
Q

2 types of pre diabetes

A

impaired fasting glycaemia

impaired glucose tolerance

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14
Q

impaired fasting glycaemia:

a. cause
b. risk of diabetes
c. risk of disease
d. treatment
e. preventing progress to diabetes

A

a. cause: unknown, ?glucose sensitising
b. risk of diabetes: 50%, 50% recovery to normal
c. risk of disease: not known
d. treatment: healthy diet, yearly glucose checks
e. preventing progress to diabetes: not known

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15
Q

impaired glucose tolerance:

a. cause
b. risk of diabetes
c. risk of disease
d. treatment
e. preventing progress to diabetes

A

a. cause: insulin resistance
b. risk of diabetes: 50%, 50% return to normal
c. risk of disease: heart disease, cerebrovascular disease
d. treatment: diabetic diet, yrly glucose checks, tx of cardiac risk factors
e. preventing progress to diabetes: exercise, weight loss

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16
Q

causes other than diabetes for

a. insulin deficiency
b. insulin resistance

A

a. insulin deficiency: cancer/ alcohol –> destroy pancreas
b. insulin resistance: receptor abnormalities (leprechaunism, insulin resistance symptoms A and B)
excessive hormones (cushing’s, acromegaly)

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17
Q

type 1 diabetes:

a. incidence
b. cause
c. pathology

A

a. incidence: 1/10 000, M>F, normally

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18
Q

6 symptoms of type 1 diabetes

A
  • polyuria (bedwetting)
  • thirst esp for sugary drinks
  • weight loss
  • dehydration
  • ketoacidosis
  • coma
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19
Q

possible genes for type 1 diabetes

A

DR3, DR4

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20
Q

new options for type 1 diabetes tx

A
  • insulin pumps (continuous insulin –> less hypos but v expensive)
  • inhaled insulin (only 1/10 dose absorbed. long term safety not known)
  • islet cell transplant (beta cells)
  • pancreas transplant
21
Q

type 2 diabetes

a. incidence
b. cause
c. pathology

A

a. incidence: 1/1000 (more undiagnosed), m=f, normally >40
b. cause: genetic > environment
c. pathology: insulin resistance, insulin deficiency

22
Q

relationship between birthweight and type 2 diabetes

A

low birthweight, go on to be heavy adults –> higher risk of diabetes

23
Q

4 things which contribute to type 2 diabetes development

A

birthweight
genetics
exercise
fat distribution (upper body obesity ie in abdomen mroe risk of diabetes)

24
Q

2 step model of type 2 diabetes

A

genetic predispositon –>
insulin resistance –>
relative lack of insulin –>
hyperglycaemia

diet/ activity levels/ level of obesity all contribute to this process

25
Q

3 types of presentation of type 2 diabetes

A
  • non-symptomatic: routine screening urine/ RPG
  • metabolic: thirst, polyuria (less acute than type 1)
  • non-metabolic 8: blurred vision, intertrigo, peripheral neuropathy, angina/MI, UTI, pruitis vulvae/ balanitis, peripheral vascular disease, foot ulcers
26
Q

type 2 diabetes tx for

a. thin people
b. fat people

A

a. thin people: diet, exerise -> sulphonylureas -> +metformin -> +newer drugs -> insulin
b. fat people: diet, exercise, weight loss -> metformin -> +sulphonylureas -> +newer drug -> insulin

27
Q

what is the incretin effect

A

twice as much insulin released when glucose taken orally compared to IV due to GLP1 (glucagon like receptor 1)

28
Q

5 effects of GLP1 and what does it stand for

A

glucagon-like-receptor 1
pancreas (2):– enhances glucose-dependent insulin secretion in beta cells of pancreas
–alpha cell suppression of postprandial glucagon secretion
-reduces hepatic glucose production
-slows rate of gastric emptying
-promotes satiety, reduces appetite

29
Q

what causes GLP-1 secretion

A

ingestion of food

30
Q

what is HbA1c and its relationship with diabetes

A

glycated haemoglobin

indicates blood glucose level –> high HbA1c, high risk of diabetes

31
Q

mechanism of dapagliflozin

TABLE ON DIABETES DRUGS

A

Blocks SGLT2 in proximal tubule of kidney –> less reabsorption

32
Q

list

a. insulin sensitisers
b. insulin releasers
c. insulin replacement

A

a. insulin sensitisers: thiaolidinediones, metformin
b. insulin releasers: sulphonylureas, meglitinides
c. insulin replacement: insulin

33
Q

treatment of gestational diabetes

A

85% diet

15% diet + insulin

34
Q

4 factors increasing risk of gestational diabetes

A

obese
previous diabetes in pregnancy
asian
age >35

35
Q

when in pregnancy does gestational diabetes often occur

A

2nd/3rd trimester

36
Q

future prospect of gestational diabetes

A

50% get diabetes in next 5 yrs

15% get diabetes in next pregnancy

37
Q

complications of gestational diabetes 3

A
  • large baby
  • stillbirth
  • death of mother
38
Q

acute complications of diabetes 2

A

hypoglycaemia

diabetic comas

39
Q

chronic complications of diabetes 6

A

microvascular 3: neuropathy, retinopathy, nephropathy

macrovascular 3: IHD, CVA, PVD

40
Q

symptoms of hypoglycaemia:

a. early warning
b. mild
c. more advanced
d. unconsious

A

a. early warning: shaking, trembling, sweating, pins&needles, hunger, headache, palpation
b. mild: double vision, slurred speech, difficulty concentrating
c. more advanced: confusion, change of behaviour
d. unconscious: epileptic fits, weakness

41
Q

draw diagram of normal hormonal responses to hypoglycaemia

list whats missing in diabetes

A

see lecture

diabetes:
- no adrenaline to increase hepatic glucose production
- no glucagon to increase hepatic glucose production

42
Q

3 causes of hypoglycaemia

A
  • missed meal
  • too much insulin
  • alcohol
43
Q

treatment of hypoglycaemia if the pt is:

a. conscious
b. drowsy
c. unconscious

A

a. conscious: oral glucose
b. drowsy: hypostop
c. unconscious: s/c glucagon, IV 50% dextrose

44
Q

2 types of diabetic comas

A
  • diabetic ketoacidosis (DKA) with type 1 diabetes

- hyperosmolar non-ketoic hyperglycaemia (HONK)

45
Q

risk of these with each type of diabetes

a. retinopathy
b. neuropathy
c. nephropathy

A

a. retinopathy: 100% type 1 pts
b. neuropathy: increase with time. 70-100%
c. nephropathy: 30-40% type 1, less in type 2 pts

46
Q

are micro/ macrovascular complications present in impaired glucose tolerance (IGT)

A

macrovascular

47
Q

what reduces risk of macrovascular complications

A

metformin

48
Q

what is made in the following pancreatic cells
A cells
B cells
D cells

A

A cells: glucagon (A away, glucose away)
B cells: insulin
D cells: somatostatin

Year 3 Human Disease (28 decks)

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