Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Medicine sara > diabetes > Flashcards

diabetes Flashcards

1
Q

what is diabetes?

A

a group of metabolic disorders characterised by hyperglycaemia due to lack of insulin, insulin insensitivity or both.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what causes type 1 diabetes?

A

type 1 diabetes is an autoimmune disease whereby there is destruction of B cells.
It is associated with the autoantibodies GAD65 and tyrosine phosphate.
associated with HLA DR3/4
genotype + environmental trigger leads to immune activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what causes type 2 diabetes

A

obesity and genotype leads to insulin insensitivity.
At first the pancreas produces more insulin to keep up. Eventually there is pancreatic exhaustion and insulin production falls.
eventually all insulin ceases and injections are needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

in general how can the causes of diabetes be classified? i.e. one being not enough insulin is made (T1/2)?

A

not enough insulin
insulin receptor problem
insulin molecule problem
insulin signalling problem post receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is type 1.5 diabetes

A

an autosomal dominant condition where type 1 diabetes presents later in life. it is due to autoimmunity against B cells.
often misdiagnosed for type 2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is MODY?

A

mature onset diabetes of the young.

  • T2D in the young
  • autosomal dominant cause
  • defects in B cells to produce enough insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

apparent from type 1 and 2 diabetes, list some other causes of diabetes

A

Type 1.5
MODY
leprechaunism = receptor problem
lipodystrophic diabetes = signalling problem
secondary: drugs, exocrine pancrease damage, endocrinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

name the condition that causes diabetes due to insulin receptor dysfunction

A

leprechaunism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

name the condition that causes diabetes due to post insulin receptor dysfunction ?

A

lipodystrophic diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A syndrome that leads to diabetes and deafness is caused by what?

A

mutations in mitochondrial DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what drugs induce secondary diabetes?

A

thiazides, B blockers, steroids, HIV medication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are the causes of damage to exocrine pancreas that can lead to diabetes

A

pancreatitis, infection, carcinoma, trauma, pancreatectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the endocrinopathies that can lead to diabetes?

A

cushings, hyperthyroidism

high: GH, adrenaline, glucagon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

state 2 non-diabetic hyperglycaemias.

A

prediabetes (borderline diabetes) - impaired glucose tolerance test and impaired fasting glucose test are both high but not enough for diabetes.

gestational - diabetes through pregnancy (usually 3rd trimester)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what has a stronger genetic link, T1D or T2D?

A

T2D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does the presentation of type 1 and 2 diabetes differ? (not including symptoms) i.e. age of onset, gradual/acute

A

type 1:

  • before 20/30 yrs
  • rapid onset (weeks) and rapidly fatal if not treated
  • usually in lean individual
    - less common than type 1
  • associated with other autoimmunity

type 2:

  • > 40yrs
  • slow onset and long time before diagnosis
  • usually in overweight and Asians
  • associated with obesity, lack of exercise, high calories and alcohol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do the symptoms between type 1 and 2 diabetes differ?

A

type 1 and 2: polydipsia and polyuria and lack of energy

type 1: marked weight loss. although in type 2 there is weight loss it is not as obvious because individual is over weight and there isn’t as dramatic lack of insulin

type 1:

  • symptoms of ketoacidosis
  • muscle wasting

type 2:
- vague symptoms and more variable e.g. persistent infections (thrush), visual problems and slow healing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the symptoms of ketoacidosis?

A 
acetone breath
dehydration and thirst
nausea and vomiting
abdominal pain
blurry vision 
hyperventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the two most useful ways to differentiate between type 1 and 2 diabetes?

A

weight loss more obvious in type 1

ketoacidosis: either symptoms of it or by blood test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

in an osce other than the presenting complaint, what other information would be useful in someone presenting with diabetic symptoms?

A

PMH: pancreatitis, other autoimmune, cushings, previosu stroke

FHx = diabetes, CVS disease, stroke

Drug history = thiazides, B blockers, HIV medication, steroids. also check for diuretics and lithium (other causes of polyuria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the differentials for polyuria?

A 
diuretics
UTI
nephrogenic diabetes
   - pituitary tumour
   - nephrogenic insensitivity - lithium, hypoK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

explain the cause of polyuria and polydipsia in diabetes

A

there is excess glucose in the blood and thus more gets filtered and exceeds the Tmax. Therefore glycosuria and water follows by osmosis and thus polyruria.
this leads to dehydration which acts on the thirst centre of the hypothalamus to induce polydipsia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

explain the cause of weight loss and ketoacidosis in diabetes

A

although more glucose, cells (such as liver) cannot use this because there is no insulin. Therefore the liver instead metabolises proteins (gluconeogenesis) and fats (B oxidation). this leads to muscle wasting and weight loss.
ketones build up from breakdown of fats. some ketones are acidic and thus lead to ketoacidosis

ketoacidosis only usually in T1D when insulin is very low.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

explain the complications to the microvasculature and microvasculature in diabetes

A

microvasculature: osmotic pressure of the blood damages capillaries and small vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

how are plasma proteins affected in diabetes

A

glycosylation of them disrupts their function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what happens to non-insulin dependant cells in diabetes. (don’t need to include specific organ changes)

A

glucose enters these cells/
glucose is converted to sorbitol by aldose reductase (NADPH to NADP).
Sorbitol damages the cells by increasing the osmotic pressure
less NADPH means less reducing power - cross linking of proteins.

e.g. eyes, neurons and kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the 3 types of nerves that can be affected in diabetic neuropathy

A

sensory
motor
autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

explain the problems of sensory neuropathy in diabetes

A

leads to damage of skin and thus infection and ulcers

leads to charcot arthropathy (deformity of weight bearing joints due to repeated injury and increased mechanical stress)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

explain the problem of autonomic neuropathy in diabetes

A 
postural hypotension - most common
erectile dysfunction
dry feet
urology - nephrogenic bladder - reduced emptying.
sweating
heart rate doesn't vary with resp rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

explain the problem of motor neuropathy in diabetes

A

clawing of toes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

how do diabetic foot ulcers occur?

A

poor sensensation so damage to skin
poor nutrition (poor blood supply) - therefore slow healing
poor immunity - increased risk of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are diabetic foot ulcers and what can they lead to?

A

painless punched out ulcer in area of thick callus

can lead to cellulitis, abscess or osteomyelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what are the different pathologies in diabetic eye?

A

retinopathy
-maculopathy
glaucoma
cataracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

overall what is causing damage in retinopathy?

A

increased blood pressure in small vessels leads to microaneurysms and haemorrhages. Proteins leak onto the retina and form plaques. haemorrhages lead to areas of ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what changes are seen in retinopathy?

A

micro aneurysms: weak small blood vessels dilate and are predisposed to leakage and breaking

hard exudate: lipoproteins and other protein leak out of blood vessles

haemorrhages: rupture of weak vessles

cotton wool spots: areas of axonal debris and ischaemic infarcts

neovascularisation: new blood vessels are made to re-vascularise hypoxic retina. but these are small and prone to rupture.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

describe the 3 stages of diabetic retinopathy

A

background retinopathy - microaneurysms, haemorrhage, lipid deposits
pre proliferative retinopathy - same as above + cotton wool spots
proliferative retinopathy - new blood vessel formation. in advanced disease larger vessels also proliferate and retinal detachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is maculopathy seen in diabetes?

A

when the retinopathy changes affect the macula specifically. this is more problematic as it will affect vision more greatly.

includes focal/diffuse macular oedema
ischaemic maculopathy: may actually look normal on fundoscope (but acuity will be reduced and can be seen on fluorescin angiography.
clinically significant macular oedema (CSMO): thickened retina and hard exudates - when found near fovea or big enough it is classed as CSMO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is glaucoma and how does diabetes cause it?

A

glaucoma is caused by increased pressure in the eye and this pressure compresses and damages the optic nerve and can lead to loss of vision

in diabetes there is increased pressure due to sorbitol being produced from glucose and excess water (osmosis). This pressure can lead to glaucoma.

moreover rubeosis iridis (neovascularisation of the iris) can block the angle of the eye (where fluid drains) leading to acute glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is cataracts and how does diabetes cause it?

A

cataracts is when the lens of the eye becomes cloudy.

in diabetes there is excess cross linking of proteins (less NADPH) and thus leads to cataracts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the risk factors for retinopathy in diabetics?

A 
poor glycaemic control
HTN
duration of diabetes
smoking 
high lipids 
pregnancy 
renal disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how do diabetic patients with retinopathy present usually?

A

usually asymptomatic (normal eyesight) until advanced disease

gradual decline of central vision.

haemorrhage: black painless floaters which resolve over several days
severe haemorrhage: may obscure vision completely. again painless
acute glaucoma: sudden painful reduction in vision. urgent referral needed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what is the pathyophysiology behind diabetic nephropathy?

A

glomerular damage and proteinuria due to:

  • increased pressure in glomerulus (due to sugars and osmotic pressure)
    - glycosylation of the basement membrane leading to increased collagen IV and mesangial expansion. leads to nodular scleorosis (kimmelsteil Wilson lesion) and BM thickening.
  • can present as nephrotic or nephritic syndrome
  • progressive proteinuria so eventually classed as nephrotic syndrome

ischaemia due to atherosclerosis of renal artery

Damage from ascending UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

describe the progressive changes in glomerular function seen in diabetes.

A
  1. at first increased filtration simply due to increased osmotic pressure due to sugars (reversible)
  2. changes to BM lead to permanent increased GFR
  3. GFR now normal (due to beginning of nephropathy) but still microproteinuria (meaning more leaky)
  4. eGFR is low (nephropathy) and still proteinuria (leaky)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the signs and symptoms of diabetic nephropathy?

A

uncommon to have symptoms in early stage

oedema and weight gain (loss of proteins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how can we prevent diabetic nephropathy?`

A

good blood pressure and sugar control

stop smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

why does diabetes lead to infection

A

hyperglycaemia and acidaemia lead to impaired immunity

reduced healing due to poor vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what are the 2 ENT infections diabetics get?

A

malignant necrotising otitis externa

rhinocerebral mucormyocosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is malignant necrotising otitis externa?

A

infection caused by pseudomonas aeruginosa
starts in auditory canal and spreads to soft tissue, cartilage and bone
severe ear pain and ottorhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what is rhinocerebral mucormycosis ?

A

infection caused by mould fungus in the sinuses.
occurs in patients with poorly controlled diabetes or ketoacidosis.
spreads to soft tissue and bone necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what organisms cause:

  • cellulitis
  • necrotising fasciitis and diabetic foot

in diabetes

A

cellulitis:
- staphylococcus aureus and group A B haemolytic streptococcus

necrotising fasciitis and diabetic foot are caused by many organisms at once including the two above and enterobacter and anaerobes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

why do diabetics get UTIs?

what organisms are responsible?

A

neurogenic bladder - incomplete emptying
glycosuria - aids bacterial growth

E.coli and pseudomonas aeruginosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the normal plasma glucose level?

A

3.8-6.5mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are the different venous glucose blood tests available and how are they used to diagnose diabetes?

A

random venous plasma glucose >11.1mM
fasting glucose tolerance test >7mM
oral glucose tolerance test (measure after 2 hr) >11.1

need 1 positive if symptomatic
OR 2 positive results if asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is prediabetes defined using plasma glucose tests?

A

fasting 6.1-7mM

oral: 7.8-11 mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is HbA1c and how can it be used in diabetes

A

glycosylated Hb should be 4%-6%

diagnosis if >6.5%
can monitor HbA1c because it is a good predictor of glycaemic control over last 2-3 months. also linked to complications so by monitoring you can know if complications are being minimised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

when can HbA1c not be used? what can be used instead?

A

haemoglobinopathies

use fructosamine test instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

other than blood tests and HbA1c what other tests can be used to diagnosis/assess diabetics?

A

For type 1:

  • Assay for AutoAb (GAD65 and islet cell Ab)
  • check for HLA DR3/4

urine dipstick:

  • look for glucose
  • look for ketones (distinguish between T1D and T2D)

ketoacidosis: plasma ketones >3mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is plasma C peptide?

A

tells you how much endogenous insulin is being made

cleaved off endogenous insulin during production of active insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

how do we monitor CVS complications in diabetes

A

monitor cholesterol and lipid blood levels.
monitor blood pressure (aim <135/80; even lower if renal disease) - check every 6 months
check BMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what treatment is used in diabetes to reduce CVS risk?

A

statins (40mg simvastatin to all diabetics regardless of IHD)
antihypertensives if >140/90; ACEi if microalbuminuria (despite BP)
aspirin 75mg to reduce CVS events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what advice is given to reduce CVS complications of diabetes?

A

stop smoking (offer cessation service)
reduce lipids
loose weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

how can we monitor nephropathy in diabetics?

A

U&E, eGFR, ACR in urine , proteinuria by urinalysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what is the difference between macro and microproteinuria

A

macro- a lot of proteins - picked up by urine dipstick. indicates renal failure.

microalbuminuria - not picked up by dipstick but can be found by analysis of urine albumin: creatinine ratio. if ACR >3 indicates early renal disease and increased vascular risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

how do we treat microalbuminuria and why?

A

ACEi regardless of BP

ACEi will reduce glomerular pressure and thus reduce proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

is microalbuminuria reversible

A

yes with good glycaemic control, good blood pressure control, stop smoking and reduce fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are gliptins?

A

DPP4 inhibitors (DPP4 normally inhibits GLP1 by breaking it down; GLP1 acts normally to increase insulin release etc)

more GLP1, more insulin, increased satiety and reduced gastric emptying and reduced glucagon release.

67
Q

what are the ADRs of gliptins?

what are the advantages

A

GI symptoms (reflux, diarrhoea)
pancreatitis
low risk of hypoglycaemia

weight neutral. actually very good drugs and used second line to metformin and sulphonylureas but expensive.

68
Q

how can you monitor someone with diabetic neuropathy ?

A

peripheral nerve exam

  • test sensation: diabetics loose sensation over stocking distribution
  • absent ankle reflexes
  • claw toe and pes cavus
69
Q

how can we treat diabetic neuropathy?

A

give vitamin B12 to improve function
depends on the problem:
- symmetric sensory polyneuropathy: amitriptyline, gabapentin and paracetamol
- mononeuritis multiplex: if sudden corticosteroids
- postural hypotension: sometimes fludrocortisone
- amyotrophy: IV immunoglobulins

charcots joints:

  • reduce weight bearing by using crutches and bed rest.
  • bony repair
70
Q

other than diabetes, what other conditions lead to charcots joints?

A 
spina bifida
hereditary sensory motor neuropathy
leprosy
tabes dorsalis
syringomyelia
71
Q

name 4 specific diabetic neuropathies and explain what they are

A

symmetric sensory polyneuropathy: glove and stocking numbness and tingling (worse at night)

amyotrophy: painful wasting of quadriceps due to radiculopathy

mononeuritis multiplex: cranial nerves III and IV

autonomic neuropathy.

72
Q

what are GLP1 receptor agonists? what are the ADRs and advantages?

A

mimic GLP 1 and thus increase insulin release and satiety, reduce glucagon and gastric emptying.

ADRs: reflux, GI problems (diarrhoea, nausea), low risk of hypoglycaemia

advantage - weight loss.

73
Q

what are sulphonylureas’s? what are the ADRs?

A

antagonise K+ ATP sensitive channels. therefore block them so B cell depolarises and insulin is released.

ADR: weight gain, hypoglycaemia, GI disturbance

74
Q

what is metformin? what are the ADRs? what are the benefits

A

first line agent for T2D
increases insulin sensitivity - reduces gluconeogenesis and increases glucogenesis.

ADRs: 
GI symptoms (dyspepsia, flatulence, diarrhoea)
rare - lactic acidosis by reducing renal bicarbonate secretion (more likely if renal problems)
B12 deficiency - rare

benefits: no risk of hypo and weight neutral. cardio protective. (usually once started kept on it)

75
Q

how do we check the eyes of a diabetic?

A

eye examination:

- visual acuity (Snellen chart, fine print reading and ishihara plates)
- visual fields, eye movement and pupil reflexes

fundoscopy:
- best viewed when eyes dilated (but cant drive for 6hours after)
- check red flex first and then retina.

digital retinal photography with mydriasis (dilation of pupil) is gold standard for retinopathy.

76
Q

what do spots on the red reflex during fundoscopy suggest?

A

vitreous haemorrhage

77
Q

what are the diabetic guidelines for retinal screening

A

T1D/T2D aged above 12 must be offered annual retinal screening
pregnant diabetics more often.

78
Q

how do we treat diabetic eye?

A

primary prevention - educate patient how important glycaemic control is
laser photocoagulopathy - for proliferative retinopathy
intravitreal steroids for maculopathy
anti VEGF for diabetic macular oedema

surgery:
vitrectomy - after a bleed (to remove blood) and to repair any retinal detachments allows for clearer vision.
surgery for cataracts - lens replacement
surgery for glaucoma - reopen drainage system

eye drops for glaucoma

laser treatment for glaucoma.

79
Q

what eye drops are given for glaucoma?

A

B blockers, prostaglandin analogues

80
Q

what is laser photocoagulopathy?

A

stops the production of angiogenic factors on ischaemic retina. used to prevent progression of proliferative retinopathy. cannot restore vision.

81
Q

how would you monitor diabetic feet in diabetic patients?

A

peripheral nerve and peripheral vascular exam (include Doppler)
Xray for bony deformities or osteomyelitis
swab, blood cultures for infections.

82
Q

how can you distinguish between neuropathy and peripheral vascular disease

A

PVD: absent foot pulses
neuropathy: injury and infection over pressure points

mostly both are present.

83
Q

how do you manage patients with diabetic feet?

A

educate patient to look at feet regularly, wear comfortable shoes, protect any injuries and visit chiropody to remove callus before necrotic tissue forms

treat infections: flucoxacillin, benzylpenicillin and metronidazole

surgery: endovascular stenting to improve blood supply

84
Q

what are alpha glycosidase inhibitors? what are their ADRs?

A

e.g. acarbose
blocks enzyme responsible for breakdown of carbohydrates to glucose therefore reduces absorption

ADRs: diarrhoea, bloating, flatulence, abdo pain, weight loss

85
Q

what are SGLT2 inhibtors? what are the ADRs?

A

inhibit SGLT2 on renal tubules. less glucose is reabsorbed

ADRs: polyuria and polydipsia (due to loss of water by osmosis, UTI, dehydration

86
Q

what are glitazones/TZDs?
what are the ADRs?
what can we say about the half life and when the effects peak?

A

bind and activate PPARgamma nuclear receptor. increase gene expression for insulin sensitivity e.g. glucogenesis etc. so response to insulin is higher.

weight gain, fluid retention, heart failure, bladder cancer, bone metabolism

long half life - take once a day, and don’t offer fine control
effects peak after 1-2 months

no hypoglycaemias.

87
Q

what is the normal regime for treating T2D?

A
  1. diet, exercise
  2. metformin (if HbA1c is still high)
  3. add sulphonylureas (if HbA1c is still high)
  4. start insulin or other oral hypoglycaemics (glitazones, meglitidines, GLP analogs, a-glycosidase inhibitors)

.

88
Q

can T2Ds use combination therapy?

A

combination therapy: if metformin and insulin together then less insulin is needed (benefit) however more ADRs e.g. higher risk of hypoglycaemia?
Sulphonylureas and TZDs are bound to plasma proteins and thus displace eachother and levels rise

89
Q

list some common ADRs of oral hypoglycaemics?

A

weight gain - due to increased insulin sensitivity so more glucose for cells to store. (however sometimes weight loss if glucose is excreted by other means i.e. not by increasing storage /insulin sensitivity)

hypoglycaemia

GI symptoms because interfering with glucose absorption

90
Q

why cant oral hypoglycaemics be used forever?

A

initially T2D is caused by insulin insensitivity and thus drugs like metformin increase this.
sulphonylureas - increases insulin release

but eventually there is prancreatic exhaustion and no more insulin and thus insulin therapy will eventually be needed

91
Q

how is insulin released in normal physiology?

A

glucose enters B cells of islets of Langerhans.
Glucose enters glycolysis and makes ATP
ATP binds to ATP sensitive K channels to close them
Depolarisation of the cell
VG calcium channels open
Calcium is released into the cell
leads to exocytosis of insulin packaged vesicles.

insulin release is also promoted by amino acids, fatty acids, gastrin, secretin and CCK. insulin is inhibited by noradrenaline and adrenaline.

92
Q

what is the action of insulin?

A

activates GLUT4 channels in liver, muscle and adipose. therefore glucose is taken up by these cells.
inhibits gluconeogenesis, glucogenolysis and lipolysis
stimulates glucogenesis, fatty acid synthesiss

overall anabolic.

93
Q

how does glucagon work?

A

released from a cells when glucose is low.

stimulates glucogenolysis and gluconeogenesis.

94
Q

explain the normal process that occurs when glucose is ingested (relating to the parts that are pharmacologically relevant: alpha glycosidase, ATP K channels, GLP1 and DPP4)

A
  1. complex sugar eaten and digested by amylase
  2. alpha glycosidase is an enzyme that breaks down disaccharides to glucose
  3. glucose is absorbed into the blood streem
  4. glucose goes into B cells and leads to closure of ATP sensitive K channels which leads to insulin release
  5. insulin binds muscle, liver and adipose cells to allow glucose to be taken up and anabolic processes to begin.

GLP1 is a hormone released by intensines after eating to increase insulin release and inhibit glucagon and gastric emptying. also promotes fullness,

DPP4 normally breaks down GLP1

95
Q

which T2D drug is best effective at lowering HbA1c?

A

biguanides e.g. metformin

96
Q

when should metformin be stopped and why?

A

any serious/unmanageable side effects

if eGFR is less than 30 as this increases risk of lactic acidosis.

97
Q

how often is metformin given?

A

2-3 times a day due to short half life.

98
Q

what are meglitidines?

A

rapaglinide

work by same mechanism as sulphonylureases

99
Q

name 2 sulphonylureas’s

A

gliclazide, tolbutamide

100
Q

when are sulphonylurea’s usually taken?

A

before meals.

101
Q

give 1 example of a glitazones (TZDs)

A

rosiglitazone

102
Q

name a gliptin

A

sitagliptin

103
Q

how is borderline diabetes managed?

A

diet and exercise

annual reviews

104
Q

what equipment is needed for finger prick glucose monitoring?

A

lancing devise (pricks finger), needle, alcohol wipes, test strips, cotton balls, plaster and meter reading

105
Q

describe the steps for finger prick glucose monitoring

A
  1. wash hands with warm water to get blood flowing and massage finger
  2. put test strip into meter
  3. wipe finger with alcohol wipe
  4. prick finger and squeeze
  5. put strip into blood.
106
Q

how is an insulin syringe used?

A

using syringe and needle draw up correct amount of insulin (info given by GP)
wipe abdomen/thigh with alcohol wipe
pinch skin/fat and inject at 90 degrees
dispose syringe to avoid infection.

alternate injection site

107
Q

how is an insulin pen used?

A

usually have two pens, one long acting and one short acting. put cartridges into pen. dial up dose and inject at 90 degrees. change needle daily
easy but expensive

108
Q

how is urinalysis performed?

A

collect urine.
dip dipstick into it and wait for 30 seconds.
remove and place horizontally and wait for 30sec-1 min
read colours using box as a guide.

109
Q

what are the complications when treating T2D patients

A

poor compliance due to:

  • fear of weight gain
  • cant feel long term effects of hyperglycaemia
  • don’t like injections
  • fear of hypoglycaemia.
110
Q

What is classed as hypoglycaemia and what can cause this?

A

glucose <3mM

not enough glucose or too much insulin

111
Q

what are the two stages of hypoglycaemia?

A

stage 1:

  • increase in sympathetic NS - sweating, hunger, anxiety, tremor, palpitations, dizzy
  • patient should be able to recognise and eat/drink Lucozade

stage 2:
sympathetic NS crashes: confusion, drowsy, seizures, visual problems and coma

112
Q

how is hypoglycaemia treated?

A

glucose to mouth: glucogel and a long acting sugar (starch) - this is if patient is conscious and can swallow.

if they cant swallow then give IV glucose 75ml

if no IV access give glucagon IM injection

113
Q

what are the different types of insulins?

A

ultrafast acting/ bolous insulin (novorapid)
- inject just before/after meal for fine control

isophane insulin:
- variable peak 4-12 hours. cheap so favoured by NICE

premixed insulin (Novomix)
   - both long and short

long acting analogue (basal insulin):
- before bed (i.e. when not eating for a while)

114
Q

what are the different insulin regimes?

A

BD biphasic (premixed insulin used):
- twice daily of novomix
- less injections but control is less fine
QDS regime (a.k.a. basal bolus)
- before meals ultra fast and before bed long acting.
- allows more varied life style (different meal sizes, gym) but more injections required.

Once daily: i.e. long acting before bed. T2D that have recently started on insulin

115
Q

what are the ADRs of insulin?

A 
weight gain
risk of hypoglycaemia
lipohypertrophy - fat lump at site of injection if use the same place
painful injection
allergy
116
Q

what is DAFNE?

A

dose adjustment for normal eating
- it is an educational programme for patients to help them better control their diabetes. Also must complete this before they qualify for a pump.

  • teaches you how to match dose to carb input
  • teaches you how to adjust dose during illness, exercise and menstruation
117
Q

how does the insulin requirement change during a period of infection? what advice is given to patients

A

despite reduced appeptite and food intake the need for insulin actually increases.
Patients need to check their blood glucose and ketones in urine >4 times a day
They are advised to seek medical attention if vomiting, diarrhoea, pregnant or signs of DKA.

118
Q

how does insulin requirements change with exercise?

A

less insulin is required.

119
Q

what general advice is given to both T1D and T2D in helping them manage diabetes

A

life style advice (stop smoking)
educate about long term complications
tell them about HbA1c and target of 6.5-7.5
how to use equipment
record blood sugars on daily basis so GP can look at day to day control on the chart.
seek help if pregnant
check for foot ulcer and other complications.

120
Q

which diabetic patients are most likely to get
DKA
hyperglycaemic hyperosmolar nonketotic coma??

A

DKA - type 1

HONK - also known as hyperglycaemic hyperosmotic state - type 2

121
Q

biochemically how is HONK defined?

A

high glucose
high osmolality
normal ketones
no acidosis

122
Q

what can HONK lead to?

A

CNS signs
rhabdomyolysis
DIC and DVTs
leg ischaemia

123
Q

how is HONK managed?

A

ABCDE + investigations (i.e. bloods etc)
give LMWH
rehydrate slowly with 0.9% saline
may need to give insulin if glucose doesn’t drop
look for cause:
- MI, Drugs, bowel infarct, infection (pneumonia, pyelonephritis)

124
Q

other than DKA and HONK what is another acute complication of DM?

A

lactic acidosis

lactate in blood >5mM

125
Q

what is lactic acidosis in DM patients caused by ? therefore how is it managed?

A

metformin and sepsis

stop metformin and treat sepsis

126
Q

what are the different ways of having diabetes in pregnancy?

A

previous T1/2D

new onset gestation

127
Q

what are the complications of diabetes in pregnancy?

A 
miscarriage
preterm
pre-eclampsia
congenital malformations
macrosomia
128
Q

what increases the risk of gestational diabetes?

A 
over 25
family history
previous gestational diabetes
Asian
overweight
HIV positive
129
Q

when should pregnant women be screen for gestational diabetes

A

oral glucose tolerance test at 16-18 weeks

6 weeks after birth fasting glucose tolerance test to see if diabetes persist (even if negative, 50% of these women will go on to develop chronic DM)

130
Q

what advice should be given to pregnant women to reduce risk of gestational diabetes?

A

weight and glycaemic control

131
Q

which diabetic drugs should be stopped in pregnancy

A

oral hypoglycaemics except metformin

132
Q

why are elderly patients more prone to complications of diabetes

A

poor/eratic diet
reduced mental state so less able to pick up signs of complications
isolated so less able to get help
often symptoms are mistaken for other co-morbidities e.g. dementia, delirium, UTI
polypharmacy
impaired hepatic/renal metabolism
deteriorate faster

133
Q

how often are elderly patients screened for diabetes?

A

annually

134
Q

what are the main steps in managing DKA

A

ABCDE (repeat regularly)

  • Airways: if vomiting, recovery position, NG tube
  • Breathing: (probably hyperventilation) 100% O2 by face mask
  • Circulation: likely to be in shock - fluid resus if <90mmHg. insert 2 large bore cannulas. If unresponsive send to ICU
    - Disability : if patient unconscious consider cerebral oedema
    - Exposure

Get results: - regularly check

- venous blood gas: HCO3, pH 
- glucose, ketones, U&amp;Es (H+ leads to K+)
- ABG 
- ECG in case of hyperK
- CXR, blood cultures and midstream urine - in case of infection (no fever in DKA)     - urine dipstick     - FBC (WCC may be raised even if absence of infection)

cover the following:

 - correct fluid loss 
 - correct hyperglycaemia
 - correct electrolytes 
 - correct acidosis
 - treat cause e.g. infection - e.g. start broad spec Abx
 - manage complications

Monitor

135
Q

why may signs of infection be different for patients with DKA?

A

fever is masked so need to be aware of this

136
Q

why is creatinine not a good measure of renal function in DKA?

A

creatinine cross links ketones and so not true value

137
Q

what are the triggers to DKA?

A 
infection 
wrong insulin dose
antipsychotic meds/chemotherapy
MI
trauma
138
Q

how is DKA diagnosed? include criteria for severe DKA

A

DKA:

  • acidaemia <7.3
  • hyperglycaemia
  • ketonaemia

severe (one or more):

- pH <7.1
- Ketones >6mM
- HCO3 venous <5mM
- anion gap >16
- GCS <12
- O2 sats <92%
- BP <90mmHg
- tachy/bradycardia
139
Q

how can you assess dehydration (useful for DKA)?

A 
cap refil
weak pulse
sunken eyes
dry mucus membranes
hypotension 
oligiouria 
cool peripheries
140
Q

how do we correct fluid loss in DKA?

A

give 500ml 0.9% saline over 15mins. repeat up to 2 litres. if not responding seek ITU advice.
maintainance: 1L every 2 hours.

141
Q

how is hyperglycaemia in DKA corrected?

A 
IV fluids should occur 1 to 2 hours before insulin therapy 
add actrarapid (short acting insulin) to 0.9% saline and infuse. 
continue patient on long acting insulin

avoid hypoglycaemia - when glucose <14mM start on 10% glucose infusion too

142
Q

what electrolyte abnormalities could be found in DKA? how are they solved?

A

hypo or hyperkalaemia

  • hypo: K+ replacement started immediately with IV fluids (before any insulin therapy)
  • hyper : insulin therapy will correct this

hypophosphataemic:
- KPO4 replacement but may lead to hypocalcaemia

hyponatraemia is common due to osmotic compensation for high glucose.

hypoMg

143
Q

how can the acidosis in DKA be corrected?

A

NaHCO3 is infused if the acidosis is life threatening

144
Q

what are the complications of DKA?

A

cerebral oedema
risk of VTE
aspiration pneumonia

145
Q

how is cerebral oedema in DKA managed?

A

look for signs: headache, irritable, low HR, high BP, cranial nerve palsy

ensure hypoglycaemia, haemorrhage/thrombosis are all excluded

treat with mannitol and hypertonic NaCl

elevate head of the bed

146
Q

how is risk of DVT in DKA reduced

A

LMWH and TED stockings

147
Q

how is aspiration pneumonia treated in DKA

A

Abx

148
Q

how do we monitor a patient with DKA?

A 
pulse, resp rate , BP - every hour
fluid balance
ECG 
Cap glucose - hourly
cap ketones - hourly
U&amp;Es, blood gas, FBC- 2 to 4 hrly
neurological exam for cerebral oedema
149
Q

in DKA when does cerebral oedema normally occur?

A

at initiation of treatment and gets worse throughout.

150
Q

what is the name given to describe the type of ventilation in DKA

A

kussmaul hyperventilation - deep breathing

151
Q

how is plasma osmolality calculated?

A

2 [Na] + [urea] + [ glucose]

152
Q

what are the important points to consider when managing young children with T1D?

A

educate child and family members and inform teachers:

  • how to fingerprick etc
  • insulin therapy
  • diet and exercise
  • detecting hypo/HONK/DKA
  • what to do during infection

recommend flu vaccine.

153
Q

why is it sometimes difficult to maintain glucose in adolescence?

A

non adherence due to life stresses and stigma/bullying

154
Q

When can a person come off metformin ?

A

Not usually stopped because of its benefits

Lowers sugar, weight loss and cardio protective

155
Q

what are the causes of diarrhoea in diabetes?

A

pancreatic insufficiency –> poor enzyme production i.e. steatorrhoea

enteric neuropathy

metformin side effect

156
Q

give examples of some sulphonylureas

A

Tolbutamide
Glibenclamide
glipizide

157
Q

what is DKA?

A

complication of type 1 diabetes where by there is very low/ absolute insulin deficiency where ketones build up in the blood causing acidosis.
defined by hyperglycaemia (>11mM), ketonaemia (>3mM) and acidosis (<7.3 or HCO3 <15)

158
Q

what complication is usually seen in type 2 diabetes rather than DKA?

A

hyperglycaemic hyperosmotic state

159
Q

describe the pathophysiology behind DKA?

A

low insulin
high glucose –> saturates kidneys –> dehydration
B oxidation of fats –> beta hydroxybutyrate (acidic)

160
Q

what are the complications of DKA?

A 
cerebral oedema
pulmonary oedema
hypo or hyper K
hypoglycaemia (from insulin therapy)
death
161
Q

what factors can precipitate hyperglycaemic hyperosmotic state?

A

consumption of glucose rich food
thiazides, steroids
illness

162
Q

If a diabetic patient on treatment presents with bruising and an increased INR, which diabetic medication is most likely to be the cause?

A

GLP 1 analogues

163
Q

what are the rules concerning hypoglycaemia and driving?

A

if hypoglycaemic <4mM, stop driving in a safe way. have a carbohydrate snack. wait for 45 mins and re-check blood sugars. only drive when glucose is >4mM

driving with diabetes is okay if:

  • there has not been any severe hypoglycaemic event in the previous 12 months
  • the driver has full hypoglycaemic awareness
  • the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
  • the driver must demonstrate an understanding of the risks of hypoglycaemia
  • there are no other debarring complications of diabetes

General Medicine sara (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions