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Med Year 3 > diabetes > Flashcards

diabetes Flashcards

1
Q

what is diabetes mellitus

A

reduction in insulin action sufficient to cause hyperglycaemia that will result in diabetes specific, microvascular pathology over time eg of eyes, kidneys and nerves

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2
Q

what are the figures for diabetes patients plasma concentrations

A

> 7 mmol/L fasting
11.1 2h post load
HbA1c>48

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3
Q

what does HbA1c mean

A

shows glc levels over the past 3 months

=lifespan of RBC

Hb gets exposed to glc in 3 months that it is in RBC

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4
Q

what are the levels for prediabetes/impaired glc tolerance

A

between 7.8 and 11.1

HbA1c between 42 and 47

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5
Q

what causes T1DM and when does it occur

A

childhood onset, caused by insulin deficiency from auto-immune destruction of beta cells

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6
Q

what cells secrete what hormone

A 
alpha = glucagon
beta = insulin

both in IoL

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7
Q

why are T1DM patients prone to ketosis

A

bc no insulin at all = burn fat inappropriately instead of glc to form FFA = ketone bodies = acidic

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8
Q

what are the symptoms of T1DM and why

A

polydipsia - thirst - bc increased urination

polyuria - bc glc lost in urine, hence osmotic effect to draw water out

tiredness - not using energy effectively

weight loss - cells get no glucose, lipolysis attacks and breaks down fatty tissue

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9
Q

how do you treat T1DM

A

insulin injections into abdomen or thigh (subcutaneous fat)

quick acting, slow acting or bi-phasic

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10
Q

example regimen of insulin injections?

A

BD biphasic - twice daily premixed insulins by pen eg novomix (uncontrolled type 2 or t1 with reg lifestyle)

QDS regimen- before meals, ultra-fast insulin and bedtime long acting analogue aka rapid acting

OD before bed long acting analogue, good initial in moving from t2 tablets

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11
Q

what are the other types of diabetes

A
  • MODY syndromes - genetic defects b cell function or insulin
  • diseases of exocrine (secrete amylase and pancreatic juice) pancreas; cancer, pancreatitis (b cells get destroyed)

-endocrinopathies eg cushing’s (hormones antagonsitic to insulin are affected eg GH cortisol are in excess)

drug induced - steroids, anti-psychotics

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12
Q

what is type 2 diabetes

A

insulin resistance, combined with b-cell dysfunction (look on ipad for detailed pathophys)

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13
Q

what age does it occur and what is it’s link to ketosis (t2)

A

adult onset, ketosis resistant; only need a small amount of insulin to stop burning of fat

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14
Q

how does T2DM present

A
  • presence of RF
  • may be picked up on routine screening
  • may present with the same symptoms as T1DM
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15
Q

what are the risk factors for diabetes and why?

A
  • obesity:
  • as BMI increases, insulin resistance increases
  • abdominal fat affects it more
  • reduced calories improve islet function
  • socio-economic deprivation

-ethnicity

black african 3x more likely, SA 6x, bc increased amount of intrab fat

  • diet composition
  • lack of exercise, exercise improves insulin sensitivity with or without weight loss
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16
Q

what is the twin cycle hypothesis for T2DM?

A

first cycle:
-increase in liver fat = increase in VLDL triglycerides which are taken up by b cells and reduce their effectiveness = increase in blood glc

  • increase in liver fat also means insulin suppression of hepatic glucose production is impaired (insulin resistance)
  • which also increases blood glc
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17
Q

diabetic complications

A

microvascular (neuropathy, retinopathy, nephropathy)

macrovascular (ACS, stroke PVD)

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18
Q

what is the first step in treating T2DM

A

diet, exercise, weight control

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19
Q

what is the 1st line therapy for T2DM

A

standard release metformin (if GI side effects = modified-release)

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20
Q

what is the 1st line therapy for T2DM

A

standard release metformin (if GI side effects = modified-release)

dont give if eGFR is <30

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21
Q

if T2DM is not controlled with dual therapy what do you do?

A

triple therapy with:

  • metformin, SU and DPP4
  • metformin, SU and pioglitazone
  • metformin, SU, SGLT-2i
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22
Q

if triple therapy not tolerated what do you do?

A

insulin therapy
or
metformin, SU and GLP-1 mimetic

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23
Q

what are the side effects of T2 drug treatments?

A

weight gain: sulfonylureas bc increase beta cell activity

hypoglycamiea: all drugs that increase b cell activity

GI symptoms; metformin and incretins, GLP1 agonists

weight loss: metformin, incretins, SGLT-2i

osteoporosis: pioglitazone
headaches - sitagliptin
UTI’s - SGLT-2 inhibitors

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24
Q

what are incretins

A

gut hormones that decease blood glc by stimulating insulin production after eating

25
Q

how does metformin work

A

increases insulin sensitvity by increasing peripheral uptake of glc and decreases hepatic glc production

26
Q

how do sulfonylureas like gliclazide work?

A

increases insulin secretion by increasing the b cell activity

27
Q

how does pioglitazone work?

A

increases cell’s sensitivity to insulin

28
Q

how do DPP4 inhibitors work

A

blocks enzyme DPP4 which is responsible for destroying incretin hormone

sitagliptin

29
Q

how do SGLT-2’s like empaglifozin work?

A

sodium glc co-transporter

blocks reabsorption of glucose in the kidneys and promotes excess excretion of glc in urine

30
Q

how should T2DM be monitored?

A

urine glucose
blood glc: self-regulation, 4x a day for T1, targeted for those with T2 and on hypoglycaemic risk medications

HbA1c = every 6 month s

31
Q

what checks should diabetes people get annually other than glc?

A
  • BP
  • lipids
  • UACR (albuminuria for kidney disease)
  • eGFR = 78
  • foot exam
  • diabetic eye screening
32
Q

what is the pathophys of the vascular changes in diabetes complications

A

high glc in lumen (in blood) = endothelial cells uptake this glc with no insulin stimulation = ROS and energy

ROS lead to production of PKC and VEGF leading to platelet aggregation and angiogenesis

increases vascular permeability

= monocytes and LDL in tunica intima

atherosclerosis and inflammation and arteriosclerosis

33
Q

what are the main complications of diabetes

A

retinopathy, nephropathy, neuropathy, peripheral vascular, CHD

34
Q

what are the 2 main eye problems

A

capillary leakage and capillary occlusion

35
Q

why does capillary leakage occur and what does it lead to

A

bc of the changes to BV = leakage of plasma into retina causing oedema

if this occurs at fovea = loss of central vision

36
Q

why does capillary occlusion occur and what does it lead to

A

retinal ischaemia, causing angiogenesis = bleed into vitreous humour = fibrosis = secondary, new vessel glaucoma

37
Q

what changes will you physically see in a diabetic patients eye

A
  • cotton wool spots (retinal ischaemia)
  • haemorrhages
  • hard exudates
  • yellow bits indicating loss of vision due to oedema
38
Q

how do you treat retinopathy

A

prevention: BG control, retinal screening

this screening: laser treatment to target new blood vessels and stop them from forming
salvage: vitrectomy

39
Q

nephropathy in diabetes; what are the stages?

A

leads to CKD and end stage kidney disease

stage 1: kidney damage with normal GFR >90, microproteinuria
stage 2: mild reduction in GFR

etc until stage 4-5 where GFR <30 and then <15 which is failure, and macroproteinuria

40
Q

why does nephropathy occur

A

growth factors, activation of RAAS, oxidative stress which lead to an increase in glomerular capillary pressure and endothelial dysfunction

41
Q

what is the first sign of nephropathy

A

albuminuria, then scarring and nodule formation and fibrosis

high BP makes it worse

42
Q

diagnosis of nephropathy?

A

microalbuminuria 3-30mg/mmol, regression still possible; not on standard dipstick

43
Q

how do you treat nephropathy

A

DM control, hba1c control
BP; ACE-I or ARBs to prevent microalbuminuria to macro
sodium restriction
statins to reduce CV risk

44
Q

what are the 3 things that you can find in a diabetic foot

A

neuropathy (decreased sensation, absent ankle jerks, swelling, etc)

ischaemia - no foot pulses, necrosis, calluses, fungal infections

foot ulceration: painless, punched out-ulcer but may be infected

45
Q

what are the symptoms of diabetic foot

A

burning, cold, tingling, stabbing, allodynia, numbness , blisters etc

46
Q

how do you get infections in diabetic foot

A

damage to skin = staph aureus can penetrate, and strep pyrogenes = cellulitis and lymphangitis = septicaemia

secondary to this can get osteomyelitis

47
Q

what is charcot foot

A

bone weakness in foot due to significant nerve damage = deformity or amputation may be necessary

48
Q

what other complications are there of diabetes

A

cheiroarthropathy - thickened skin and reduced joint motility in hands and fingers

cataracts

49
Q

gestational diabetes risks to mother and fetus

A

miscarriage, pre-term labour, pre-eclampsia and then complications of diabetes

in first trimester: congenital abnormalities

in 2nd and 3rd = accelerated growth: intrauterine growth restriction

50
Q

what are the RF for GDM

A

age>25, non-caucasion, high weight, HIV+, prev GDM

51
Q

how do you treat and prevent GDM

A

monitor BG, folic acid etc

treatment: everything but metformin should be stopped

52
Q

why would diabetics become hypoglycaemic and why is this dangerous?

A

sulfonylureas and insulin is high in the body; eg missed meal, increase in activity etc

brain death can occur

hypoglycaemia = <3mmol plasma glucose

53
Q

link between DM and CV problems

A

risk is proportional to HbA1c

multi-vessel disease and atheromatous involvement of smaller CA common with DM

54
Q

prevention of CV events in diabetes

A
  • lifestyle, control glucose, bp and lipids
  • should already be on BP control meds and statins

post angina, ACS, MI etc give aspirin, thrombolysis, beta blockers

55
Q

treatment of CV events in DM

A

revascularisation

56
Q

brand names and examples of insulin?

A

humalog - rapid acting
humulin S and actrapid: short acting
humulin I - intermediate: reaches peak after about 6 hours so can be used for basal
ultra-long acting eg lamtus and levemir: trickles in over 24 hours
humalogmix: mix of humalogue and humulin I

57
Q

how do insulin pumps work

A

SC needle which gives insulin over 24 hours, but risk of hyper or dka if pump stops working

58
Q

What is a hypo?
What causes it?
How is it managed?

A 
•	Classed when blood sugar is <4
•	ABCDE 
•	If conscious and able to swallow:
o	2-3 dextrose tablets or sweets, NOT chocolate as high in fat so will slow glucose absorption 
o	300ml of Lucozade or coke 
•	If cannot swallow, use glucogel 
•	Otherwise, use glucagon injections
•	If emergency: 20ml of 20% dextrose IV

caused if diabetic patient has taken medication/insulin but not eaten at the correct time, eaten less than usual or exercised more than usual

Med Year 3 (25 decks)

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