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General Medicine Block > Diabetes > Flashcards

Diabetes Flashcards

1
Q

how does acute illness affect the insulin demands of the body?

A

demands are increased

*acute illness= stress response, resulting in higher blood sugar level, and so greater need for insulin in order to reduce this?

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2
Q

examples of rapid acting insulins?

A

humalog

novorapid

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3
Q

examples of short acting insulins?

A

actrapid

humulin S

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4
Q

example of intermediate acting insulin?

A

humulin I

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5
Q

examples of long acting insulins?

A

glargine

levemir

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6
Q

what insulin would be safe to use in a pt alongside an insulin infusion?

A

a long acting basal insulin e.g. glargine or levemir

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7
Q

why can fortisip be used in pts with celiac disease, and why are these pts more at risk of hypoglycaemia?

A

it is gluten free

reduced carbohydrate intake

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8
Q

immediate tment of a pt having a hypoglycaemic episode?

A

need quick acting carb (CHO) so can give cold sugary drink e.g. lucozade 120ml, 200ml of fruit juice or 5-7 glucose tablets.

this must then be followed by a long acting carb. to ensure blood glucose is maintained within the normal range e.g. cereal, sandwich or 2 biscuits.

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9
Q

normal range of blood glucose aimed for a diabetic inpatient?

A

4-11mmol/L

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10
Q

hypoglycaemia definition?

A

plasma glucose less than 4mmol/L

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11
Q

IV fluid to be used for infusing into diabetic insulin dependent pt undergoing surgery?**

A

1L of 5% dextrose with 20mmol KCl/8h

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12
Q

what are the symptoms of hyperglycaemic hyperosmolar nonketotic coma (HONK)/ hyperosmolar hyperglycaemic state?

A

frequent need to urinate
extreme thirst, dehydration
nausea
disorientation, stupor or coma

may be evidence of underlying illness e.g. pneumonia or pyelonephritis, and hyperosmolar state may predisose to stroke, MI or arterial insufficiency in lower limbs.

occurs with blood glucose >33mmol/L in type 2 diabetes

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13
Q

management of hyperglycaemic hyperosmolar nonketotic coma?

A

IV insulin

IV fluids

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14
Q

symptoms of hypoglycaemia?

A

autonomic: sweating, pale, palpitations, tremor, dizziness
neurological: tingling around the lips, confusion, coma, difficulty concentrating, convulsions, drowsiness, visual trouble
irritability/anxiety
feeling of hunger
trembling
restlessness
personality change

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15
Q

what management follows administration of a sugary drink in hopsital to a hyoglycaemic pt?

A

recheck blood glucose after 15 mins
if now 4mmol/L or above, give a longer-acting carb snack e.g. biscuits, cereal or sandwich, or next meal if ready, and check capillary glucose in 30-60 mins. Do not omit insulin injection if due. CBG must be regularly measured over next 24-48 hrs and pt to be referred to DSN (diabetes specialist nurse) for hypoglycaemia education.

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16
Q

if pt hypoglycaemic and conscious, and able to swallow but unable to help self, what should be given?

A

dextrogel (1.5-2tubes)- put in inside of mouth
or
consider 1mg glucagon IM
and recheck blood glucose after 15 mins

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17
Q

in which pts will glucagon therapy to treat hypoglycaemia NOT be effective?

A

liver disease
glucocorticoid deficiency
have been malnourished or starved

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18
Q

what is it important to consider in administration of glucagon for hypoglycaemia?

A
  • use only once in tment of hypoglycaemic episode
  • effects wear off after 30min
  • will require larger portion of long acting carbohydrate e.g. cereal, sandwich or biscuit, to replenish glycogen stores.
  • will not be effective in those with liver disease- glucagon only mobilises liver glycogen, glucocorticoid deficiency or malnourished or starved.
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19
Q

if pt unconscious with hypoglycaemia, how should they be managed before IV access secured and when secured?

A

before secured: ABCDE- give O2, check GCS and capillary blood glucose
then IV pump 20% glucose infusion of 300mls/hour stopped after 15 mins (75 ml total dose)
then check capillary blood glucose in 10min and repeat once if necessary. if pt responds, then check blood glucose and proceed to long acting carb.
if no response, check blood glucose and do full med review to check for other causes e.g. SAH, cerebral oedema.
if CBG remains less than 4, then consider IV 20% glucose infusion 50ml over 1hr or 1mg glucagon IM

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20
Q

if pt unconscious with hypoglycaemia, and secure IV access to give glucose cannot be achieved, what should be done?

A

prescribe and administer immediate glucagon injection 1mg IM

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21
Q

how should a pt with an IV insulin infusion who experiences hypoglycaemia be managed?

A

stop infusion
treat hypoglycaemia
restart infusion after reviewing prescribed rate when CBG >4mmol/L

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22
Q

normal glucose conc?

A

3.0-6.6mmol/L

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23
Q

what type of small haemorrhages are seen in the eye with diabetic pts?

A

dot and blot: dots=microaneurysms, and blots=haemorrhages, which occur with background retinopathy.

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24
Q

causes of charcot arthopathy other than diabetes?

A

alcohol neuropathy
syphilis (treponema pallidum)
leprosy
charcot-marie tooth syndrome

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25
Q

investigations to be undertaken in newly diagnosed diabetes pt to determine appropriate management and underlying cause?

A

HbA1c-l=if raised suggests high glucose for a while (last 3 mnths), more likely type 2
Us and Es (renal), send urine for ACR to assess for microalbuminuria, do urinalysis for ketones and proteinuria, then MSU if protein detected.
LFTs-fatty liver common
TFTs- hyperthyroidism?-graves associated with type 1 DM?
lipid profile, CVS risk profile-ECG, blood pressure, smoking status
ketones (urine or blood) and venous HCO3- to assess for DKA
calculate BMI, height and weight
check feet for diabetes complications e.g. peripheral neuropathy, PVD
consider underlying causes e.g. cushing’s syndrome-24hr urinary free cortisol, dexamethasone suppression test, phaeochromocytoma-metanephrines,
GAD autoantibodies-glutamic acid decarboxylase autoantibodies-can be used to help distinguish between type 2 DM and latent AI diabetes of adulthood
C-peptide can also be measured to distinguish between type 1 and 2

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26
Q

example of structured education in flexible insulin therapy for newly diagnosed type 1 diabetics?

A

DAFNE= dose adjustment for normal eating

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27
Q

what affects basal requirements of insulin?

A

weight
exercise
alcohol
stress

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28
Q

clinical features of neuropathic feet?

A 
warm
palpable foot pulses
dry skin-anhidrosis
no discomfort with ulcer
callus present
ulcer on sole of foot
toe clawing with motor neuropathy, pes cavus, loss of transverse arch, rocker-bottom sole-charcot arthropathy
absent ankle jerks
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29
Q

clinical features of ischaemic feet?

A

cold/cool
atrophic/often hairless
no palpable foot pulses
more often tender/painful
claudication/rest pain
skin blanches on elevation and reddens on dependency, +ve Beurger’s test
ulcers over tips of toes, heel-pressure area and lateral foot border

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30
Q

management of the charcot foot?

A

immobilisation to help prevent joint destruction
may use non-walking plaster cast of Aircast type boot for 2-3 mnths at least while bone repair/remodelling occurring.
may immobilse for up to 1 yr

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31
Q

why might an infected diabetic foot have a green tinge?

A

infection with pseudomonas aeruginosa

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32
Q

pathogenesis of Charcot foot?

A

trauma to foot
blood flow increases to foot due to sympathetic nerve loss, so OC activity increases
osteoclast activity occurs, with bone breakdown ,and osteoblasts try and repair but osteoclast activity overwhelms that of osteoblast, and disordered remodelling takes place with increased bone turnover, producing a deformed foot with bone fractures.

Charcot arthropathy can also affect other body areas e.g. knee, wrist.

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33
Q

how does diabetes increase risk of acquiring infections and delay healing?

A
  • high blood glucose- breeding ground for bacteria.
  • glucose causes thickening of capillary basement membranes, disordered chemotaxis and disrupted phagocytosis.
  • glycosylation of arterial wall proteins predisposes to atheroma formation, and PVD, so poor blood supply for healing process.
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34
Q

when should glucose levels be highest in a diabetic pt?

A

morning , ?after breakfast

as this is when greatest resistance to insulin (cortisol levels highest on a morning)

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35
Q

3 main ways in which the kidney can be damaged in diabetes?

A

glomerular damage
ischaemia resulting from hypertrophy of afferent and efferent arterioles
ascending infection

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36
Q

describe the pathophysiology of diabetic nephropathy

A

poor glycaemic control linked to renal hypertrophy associated with a raised GFR
afferent arteriole becomes vasodilated to a greater extent than efferent, increasing intraglomerular filtration pressure, further damaging the capillaries
this also increases local shearing forces, contributing to mesangial cell hypertophy and increased EC mesangial matrix material secretion
glomerular sclerosis results with BM thickening, glomerular BM maintenance carried out by mesangium, and material is deposited in BM, disrupting protein cross-linkages so progressive leak of protein into urine.

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37
Q

how can microalbuminuria be tested for?

A

radioimmunoassay

special dipsticks

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38
Q

what is microalbuminuria a predictive marker of in diabetes?

A

in type 1, predictive marker of progression to nephropathy

in type 2, of increased CV risk

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39
Q

what light microscopic changes in the glomeruli are seen with diabetic nephropathy?

A

features of glomerulosclerosis= diffuse and nodular, nodular= Kimmelstiel-Wilson lesion.
glomerulus replaced by hyaline material at later stage

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40
Q

typical bloods for pt with nephropathy?

A

normocytic, normochromic anaemia

raised ESR

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41
Q

why does ascending infection occur with diabetes?

A

bladder stasis due to autonomic neuropathy

not all glucose able to be reabsorbed by kidneys, so glycosuria- attracts bacteria- multiply, cause infection.

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42
Q

describe the natural history of nephropathy in diabetics

A

tends to occur 15yrs after diagnosis of diabetes
initially microalbuminuria, then intermittent proteinuria and then persistent proteinuria- here plasma creatinine is normal but pt likely to be 5-10 yrs away from developing end stage kidney disease. plasma creatinine subsequently rises and GFR falls.

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43
Q

why are diabetic foot ulcers debrided?

A

to reduce risk of infection tracking

to reduce pressure, which can reduce healing and predispose to further ulceration?

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44
Q

usefulness of X-rays in diabetic feet?

A

osteomyelitis can be shown by fott X-ray, but features don’t appear until a few wks after clinical features, so X-ray appearance of the disease will show what the disease was like a few wks previously.

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45
Q

albumin creatinine ratio (ACR) in healthy men and women?

A

men=less than 2.5, and less than 3.5mg/mmol in women, measured with 1st morning mid-stream urine sample

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46
Q

how can progression of diabetic nephropathy to end stage renal disease be slowed?

A

aggresive anti-hypertensive therapy

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47
Q

investigations once proteinuria detected in pt with suspected diabetic nephropathy?

A

24 hr urine collection to quantify protein loss

regular plasma creatinine and eGFR measurements

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48
Q

target BP in diabetic pts with nephropathy, retinopathy or CV damage?

A

less than 130/80mmHg

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49
Q

management of diabetic nephropathy?

A

BP lowering, target of less than 130/80 mmHg, with ACEI or AngIIRB-also use in normotensive pts with persistent microalbuminuria.
tight glycaemic control- HbA1c 6.5-7.0%
avoid oral hypoglycaemic agents partially excreted by kidney e.g. metformin and glibenclamide.
may need significant reductions in insulin dosage as insulin sensitivity increases
frequent opthalmic supervision as assoc. diabetic retinopathy tends to progress rapidly.
treat dyslipidaemia
aspirin therapy if indicated
lifestyle modif- weight loss, smoking cessation

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50
Q

what form of dialysis might be preferred in diabetic pts with end stage renal disease and why?

A

chronic ambulatory peritoneal dialysis, as vascular shunts tend to calicify rapidly.

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51
Q

name of group of drugs which are SGLUT2 inhibitors used in type 2 diabetes?

A

glifozins e.g. dapaglifozin

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52
Q

in which asymptomatic pts should HbA1c NOT be used for diagnosing type 2 diabetes?

A 
children
pregnancy
acutely ill
anaemia
altered Hbs
altered red cell lifespan
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53
Q

range for healthy BMI in south asian pts?

A

18.5-22.9

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54
Q

target HbA1c in newly diagnosed type 2 diabetics and those on up to 2 oral hypoglycaemic drugs?

A

6.5%/48mmol/mol

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55
Q

how might the toes appear in neuropathic feet?

A

clawed

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56
Q

medications that can cause peripheral neuropathy?

A

isoniazid-TB tment

metronidazole-antibiotic, may be used in hepatic encephalopathy

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57
Q

what is tested in a foot examination for diabetic neurpathy?

A

vibration-e.g. with a neurothesiometer, if can’t feel vibrating head at >25V then signif risk of neuropathic ulceration=at risk feet.
fine touch
reflexes

58
Q

tment of diabetic neuropathy?

A

r/v by podiatrist, possibly orthotist
good glycaemic control in asymptomatic pts
painful DN: duloxetine (SNRI)-main ADR=nausea but often self-limiting and pregabalin (GABA analogue). TCAs been used for many yrs but many pts unresponsive and ADRs frequent.
acupuncture
TENS
CVS RFs e.g. obesity, smoking, HTN and hyperlipidaemia are RFs for peripheral neuropathy.

59
Q

tment of existing ulcers in diabetic feet?

A

optimise diabetic control
reduce oedema to aid healing
regular callus debridement to reduce pressure and tracking of infection, apply dressing after and ensure change regularly
infection control- if present, commonly treat with triple therapy- flucloxacillin, amoxicillin and metronidazole, or co-amox or ciprofl, and clindamycin. IV tment initially if severe. osteomyelitis- follow local guidelines, can use ciprofloxacin or sodium fusidate for several mnths. may need resection/amputation.
reduce trauma and pressure relief- padded socks, suitable shoes, aircast boot
revascularisation

60
Q

commonest clinical consequences of neuropathy in diabetic pts?

A

neuropathic ulcers, usually on feet
altered sensation, both pain and reduced sensation
erectile dysfunction with autonomic neuropathy- also causes gastroparesis- naso-jejunostomy can be used for feeding, and postural hypotension
charcot arthropathy

61
Q

pathogenesis of neuropathy in diabetes mellitus?

A
  • increased free radical production and reduced NO- reducing nerve blood flow, due to excess glucose so increase metabolism via aldose reductase to sorbitol, which reduces glutathione levels- protection against ROS.
  • accumulation of advanced end glycation product via non-enzymatic glycosylation
  • nerve acute ischaemia

pathologically, distal axonal loss occurs with focal demyelination and attempts at nerve regenration. vasa nervorum have BM thickening, endothelial cell changes and some luminal occlusion, so nerve conduction velocities are slowed or nerve function completely lost.

62
Q

what often precipitates DKA?

A

infection

63
Q

commonest causes of death associated with DKA?

A

cerebral oedema

hypokalaemia, adult respiratory distress syndrome, co-morbid conditions e.g. pneumonia, in the elderly

64
Q

how is DKA diagnosis confirmed?

A

all of following present:
Significant ketonuria (>2+) or blood ketone >3mmol/L
Blood glucose >11mmol/L or known diabetes mellitus
Bicarbonate less than 15mmol/L or venous pH less than 7.3

65
Q

immediate actions in pt with DKA?

A

Rapid ABC with measurement of RR, temp, pulse, BP, EWS, GCS, and pulse oximetry-SpO2
Capillary blood glucose check and blood ketones
Obtain urgent IV access and commence IV fluids-0.9% sodium chloride solution
Stat dose of 10 units soluble insulin sc or im
Venous sample for - U&Es, blood ketones, bicarbonate measured by venous blood gas, FBC. Us and Es includ. venous HCO3- and K+ to be repeated at 60 mins, then 2 hrs and 2hrly therafter.
Urinalysis for ketones

66
Q

indications of severe DKA and consideration to move pt to ITU/HDU and have central venous line insertion?

A

Blood ketones above 6mmol/L
Venous bicarbonate level below 5mmol/L
Venous or arterial pH below 7.1
Hypokalaemia on admission (below 3.5mmol/L)
Anion gap above 16 [ (Na+ + K+) – (Cl- + HCO3-)]
GCS less than 12 (or abnormality on AVPU scale)
Oxygen saturation below 92% on air
(assuming normal baseline respiratory function)
Systolic BP below 90 mmHg
Pulse over 100 or below 60 bpm

67
Q

up to an hr from DKA presentation, how is insulin given?

A

After stat does of 10 U SC/IM of actrapid or insuman rapid, start fixed rate intravenous insulin infusion (IVII) 0.1unit/kg/hr based on actual or estimated weight.
Use 50units human soluble insulin (Actrapid or Insuman Rapid) in 50ml sodium chloride 0.9%.
If patient usually takes long-acting insulin analogue (Lantus or Levemir) then continue at usual dose and time

68
Q

complications arising as result of management of DKA?

A

hyper or hypokalaemia
cerebral oedema
pulmonary oedema
hypoglycaemia

69
Q

presenting symptoms of DKA?**

A 
severe abdo pain
nausea and vomiting
dehydration
prostration
hyperventilation
70
Q

2 parallel processes responsible for dehydration in DKA?

A

high glucose, so hyperglycaemia and glycosuria, producing osmotic diuresis
and increase ketones, so acidosis and vomiting
both lead to fluid and electrolyte depletion, subsequent renal hypoperfusion so impaired excretion of ketones and H+.

71
Q

following clinical assessment of DKA pt, what else is it vital to assess?

A

fluid status- monitor input and output to avoid fluid overload

72
Q

in giving IV fluids to DKA patient, what should happen if capillary blood glucose is less than 14mmol/L?

A

commence 10% glucose infusion 125ml/hour in addition to 0.9% sodium chloride solution, and reduce rate of sodium chloride infusion appropriately to avoid fluid overload.
must regularly review CVS status.

73
Q

After 1 hour of treating DKA patient, what should now be considered when reassessing the pt and monitoring?

A

urinary catheter if incontinent or not passes urine
NG tube if reduced conscious level or persistent vomiting
ABG, rpt chest X-ray and give O2 if SpO2 falling
regular vital signs and EWS charting and r/v
accurate fluid abalnce chart-min urine output of 0.5ml/kg/hr
cardiac moni
assess VTE risk and give LMWH

74
Q

After 1 hour of DKA monitoring, how often should the various metabolic parameters be assessed?

A

venous blood gas-pH, HCO3- and K+ at time 1hr, then 2hr and then 2hr thereafter. K+ may need checking hrly if outside ref range by venous blood gas.
hrly blood ketones-should be falling at rate of 0.5mmol/hr. Increase insulin infusion rate by 1U/hr if not satisfactory
hrly capillary blood glucose-should be falling by 3mmol/L/hr

75
Q

At 6 hrs, how is resolution of DKA defined?

A

blood ketones less than 0.3mmol/L

venous pH more than 7.3 and/or venous HCO3- more than 18mmol/L

76
Q

when is DKA pt put back on SC insulin?

A

when biochemically stable with normal blood ketones and eating and drinking
by 24hrs, if pt not E and D but ketones normal, change to IV variable rate insulin (sliding scale?)
should be overlap of 30-60mins between SC and IV insulin, so start SC insulin and stop IV 30-60 mins after starting SC

77
Q

why is there are 30-60 min overlap between restarting SC insulin and IV insulin in managing DKA pt?

A

IV insulin t 1/2 of only 3-4 mins and SC insulin may take considerably longer to be absorbed.

78
Q

duration of activity of humulin I and when is it taken?

A

intermediate acting insulin
can be taken with short acting before meal, or on its own before bed to cope with high night time and mornign blood glucose levels
must be aware of risk of hypoglycaemia, especially at night
peak activity between 1 and 8 hours after injecting, duration as long as 22 hours.

79
Q

what is HONK/hyperosmolar hyperglycaemic state characteristic of?

A

uncontrolled TYPE 2 diabetes (rather than type 1 in which DKA most commonly occurs)

80
Q

common precipitating factors to HONK?

A

consumption of glucose rich fluids
concurrent medication e.g. thiazide diuretics, steroids
intercurrent illness: infection-URTI, pneumonia, UTI
MI
stroke/TIA

81
Q

what is it thought the extreme dehydration of HONK is related to?

A

age
older people in which condition occurs, often with undiagnosed type 2 diabetes, expereince thirst less acutely and more readily become dehydrated, and mild renal impairment assoc with age means increased urinary losses of fluid and electrolytes.

82
Q

why are ketones NOT produced in HONK?

A

endogenous insulin levels sufficient to inhibit hepatic ketogenesis, but insufficient to inhibit hepatic glucose production.

83
Q

how does future management of pt after DKA differ from that after HONK?

A

DKA is an absolute indication for subsequent insulin therapy, whereas pts after HONK may do well on diet and oral agents.

84
Q

why is mortality with HONK much greater than with DKA?

A

pts more likely to be elderly and have an underlying primary pathology e.g. pneumonia.

85
Q

main causes of death in HONK?

A

aspiration of gastric contents due to gastroparesis
cerebral oedeoma
TE complications
underlying primary pathology

86
Q

how is HONK diagnosis established?

A

Undiagnosed Type 2 DM or known cases of Type 2 DM
Hyperglycaemia (blood glucose often more than 28 mmol/l)
Usually no ketones in the urine, although may be present in patient with vomiting ( Particularly trace or 1+)
No severe acidosis (pH >7.2 and HCO3
-often normal)
Hyperosmolality (serum osmolality more than 350 mosm/l)
50% of patients are hypernatraemic
± decreased conscious level and mental confusion

consider precipitating event e.g. In elderly patients, consider MI, chest infection, etc, usually underlying infection (URTI, diarrhoea and vomiting, UTI, etc, while temp and WCC unhelpful), newly presenting patient, acute abdomen.

87
Q

initial investigations in HONK?

A 
glucose
U and Es, (HCO3- if possible), amylase
Infection screen (including CXR and blood cultures)
Arterial blood gases
Calculation of serum osmolality {= 2(K+ + Na+) + urea + glucose (all in mmol/l)},
and measurement by the laboratory
Urinalysis
CXR and ECG
88
Q

initial management of HONK patient?

A

Site nasogastric tube (consider in all subjects mandatory if reduced conscious level: GCS less than 9)
IV access
insulin regime-10U human actrapid stat IM/IV, then 50 U of soluble insulin in 50 mls 0.9% sodium chloride, fixed rate insulin infusion
fluid replacement
consider Abx
stop metformin
LMWH, and consider full heparinisation if serum osmolarity more than 350 mosm/L
Catheterise if no urine output in first 3 - 4 hours of treatment, or if the patient is clinically shocked and/or has a reduced conscious level
CVP line often required, particularly in those with IHD
Monitor U and Es and glucose after 2 hours, and then at least 4 hourly until the patient is stable. Ensure adequate K+ replacement-need to replace 200mmolL in 1st 24-36 hrs, usually at 10mmol/L/hr.
Protection of pressure areas, particularly heels (Spenco boots should be considered)

89
Q

key differences between DKA and HONK?

A

Patient: DKA- young, type 1 DM
HONK- elderly, type 2 DM diagnosed/undiagnosed, underlying primary pathology
bloods: DKA- pH less than 7.2, HCO3- less than 15, ketones more than 3, Na+ normal and osmolality much less than in HONK-high osmolality more than 350, pH, HCO3- and blood ketones normal, urine may have +1 ketones, blood glucose very high, often more than 28.
both manage with IV insulin and fluids, and careful K+ replacement, BUT DKA absolute indication for future insulin therapy in contrast to HONK.

90
Q

why does excessive alcohol intake increase risk of diabetes development?

A

causes chronic pancreatitis

91
Q

what can cause hypoglycaemic awareness to reduce?

A

with time in type 1 DM due to decrease in glucagon secretion

if blood glucose control too tight

92
Q

NICE guidelines on statin tment for CVD primary prevention in type 1 diabetics?

A 
atorvastatin 20mg to adults with type 1 DM if:
older than 40 or
had DM for more than 10 yrs or
have established nephropathy or
have other CVD RFs
93
Q

importance of avoiding binge drinking in type 1 DM?

A

danger of delayed hypoglycaemia

94
Q

what do different timings of fingerprick glucose indicate in terms of insulin treatment?

A

if done before meal, inform about LA insulin doses

those done after inform about SA insulin dose

95
Q

example of pre-mixed insulin?

A

Novomix 30- 30% SA insulin, 70% LA

96
Q

NICE guidelines on statin tment for CVD primary prevention in type 2 diabetics?

A

atorvastatin 20mg to type 2 diabetics who have a 10% or greater 10yr risk of developing CVD, with risk assessed using the QRISK2 assessment tool.

97
Q

a pt with type 2 DM has recently been started on atorvastatin due to a 10% 10yr risk of CVD. he loves grapefruit juice, what must the pt be warned about?

A 
ADRs of statin more likely if continues to drink lots of grapefruit juice as this is a CYP450 inhibitor, the enzyme responsible for statin metabolism in the liver, so increased drug will be around to induce ADRs e.g. myalgia.
other drugs which may increase risk of myalgia with a statin: ODEVICES
omeprazole
disulfiram
erythromycin
valproate
isoniazid
cimetidine, ciprofloxacin
alcohol- binge drink
sulfonamides
98
Q

effect of exercise on insulin sensitivity?

A

increases sensitivity

99
Q

what is microalbuminuria?

A

urine dipstick is negative for protein, but urine albumin to creatinine ratio is 3mg/mmol or more, reflecting early nephropathy and increased vascular risk in DM patients.

100
Q

characteristics of background retinopathy?

A

dots (microaneurysms), blots (haemorrhages) and hard exudates-lipid deposits

101
Q

characteristics of pre-proliferative retinopathy?

A

cotton wool spots e.g. infarcts
hamorrhages
venous beading
these are signs of retinal ischaemia, must refer to specialist

102
Q

characteristics of proliferative retinopathy?

A

new vessels form
haemorrhages
needs urgent referral

103
Q

components of the QRISK2 assessment tool for CVD risk in next 10 years?

A 
age
gender
ethnicity
smoking status
DM status
angina or MI in 1st degree relative
104
Q

absolute indications for surgery in diabetic feet?

A

abscess or deep infection
spreading anaerobic infection
gangrene/rest pain
suppurative arthritis

105
Q

typical foot ulcers in DM?

A

painless, punched-out ulcer in area of thick callus and/or superadded infection

106
Q

the degree of what must be assessed in diabetic foot ulcers?

A

neuropathy-clinically
ischaemia- clinically, doppler, angiography
bony deformity e.g. charcot joint, clinically and xray
infection-swabs, probe down to reveal depth, blood cultures, x-ray for osteomyelitis.

107
Q

tment of cellulitis in diabetic feet?

A

should admit for IV antibiotics
staph, strep and anaerobes common
start with benzylpenicillin 1.2g/6h IV and flucloxacillin 1g/6h IV, with or without metronidazole 500mg/8h IV

108
Q

symptoms of autonomic neuropathy in diabetic pts?

A 
postural drop- feeling dizzy on standing, may respond to fludrocortisone-synthetic with mineralocorticoid actions
gastroparesis-early satiety, post-prandial bloating, nausea/vomiting, diagnosed with gastric scintigraphy with technetium labelled meal, can give antiemetics and tetracycline if bacterial overgrowth
urinary retention-atonic bladder
erectile dysfunction
diarrhoea
gustatory sweating
cardiac denervation
AV shunting
109
Q

define metabolic syndrome

A

central obesity or BMI more than 30 with any 2 of:
triglycerides 1.7mmol/l or more
HDL less than 1.03
BP of or more than 130/85
fasting glucose 5.6mmol/L or more, or type 2 DM
insulin resistance-although this is hard to measure

110
Q

In Leicester, contact of a diabetic patient in pregnancy with the diabetes care team for glycaemic control assessment should occur how often?

A

ever 1-2 weeks

111
Q

when is retinopathy and nephropathy assessed in diabetic pt in pregnancy?

A

assessment should be offered at 1st appointment with joint diabetes and antenatal clinic if not already been assessed in previous yr.
offer retinal assessment at 16 wks in pre-existing DM if signs of diabetic retinopathy at 1st antenatal appointment
to those who did not have signs of retinopathy at 1st visit, assess again at 28 weeks

both should be done 3 times during pregnancy?-at booking, 28wks and before delivery.

112
Q

why are urine tests of glucose unuseful in pregnancy?

A

renal threshold for glucose in pregnancy falls

113
Q

blood glucose targets and monitoring in diabetics in pregnancy?

A

should test blood glucose fasting and 1 hr after meals
aim for fasting glucose between 4 and 5.5mmol/L adn 1 hr post-prandial less than 7.8
don’t measure HbA1c routinely in 2nd and 3rd trimesters

114
Q

diabetic medication recommended in pregnancy?

A

oral therapy should be avoided, except for metformin which is recognised to be safe in pregnancy

115
Q

advice to women taking insulin in pregnancy?

A

insulin pump if multiple injections not adequate and experiencing significant disabling hypoglycaemia
concentrated oral glucose solution
glucagon in type 1 if partner willing to administer it

advise to check blood glucose before bed, risks of hypos and hypo unawareness , espec. in 1st trimester with part. ref. to driving
use of oral glucose solutions and glucagon

116
Q

BP aim in type 2 diabetics without kidney, eye or CVS damage?

A

less than 140/80mmHg

117
Q

what must a diabetic patients blood glucose be before driving?

A

5mmol/L or more

if less than this, must eat before driving

118
Q

if pt’s blood glucose less than 5mmol/L but pt not hypoglycaemic, how long must they wait before driving?*

A

45mins

119
Q

how does gliclazide work?

A

sulfonylurea
antagonises beta cell K+/ATP channel activity, reducing K+ current causing beta cell depolarisation as K+ accumulates. This increases Ca2+ entry which governs fusion rate of insulin vesicles with beta cell membrane and their release into circulation.

so drug increases insulin release from beta cells of islets of Langerhans in the pancreas.

120
Q

how is impaired glucose tolerance (IGT) defined with the oral glucose tolerance test?

A

plasma blood glucose between 7.8 and 11.0 mmol/L 2hr after 75g glucose load.

121
Q

how is DM diagnosed with blood glucose results?

A

if with symptoms:
fasting blood glucose of 7mmol/L or more,
or random venous 11.1mmol/L or more, or
11.1mmol/L or more 2hr after 75g oral anhydrous glucose load in OGTT

with no symptoms, must be at least 1 additional glucose test result on another day with a value in the diabetic range

HbA1c of 48mmol/L or more (6.5% or more) also diagnostic, must be repeated if pt asymptomatic, at least 2 weeks apart

122
Q

symptoms of somatic neuropathy in diabetic patients?

A

ocular palsies
CTS- pain and paraesthesia in median nerve distribution of hand, espec. at night*
small muscle wasting
amyotrophy
painful neuropathy
neuropathic foot- painless plantar ulcers, toe clawing, hair loss, pes cavus, warm foot with bounding pulses.

123
Q

frequency of blood glucose testing in pregnant women with type 1 or 2 DM?

A

at least 2-4 times daily pre- and 2hr post-prandial

124
Q

role of GLP-1 injections in DM tment?

A

stimulate glucose dependent insulin secretions, increase satiety and slow gastric emptying, prevent glucagon release after meals.
reduce fasting and post prandial glucose levels.

should be 6hr between injections
does 60min before morning and evening meals

125
Q

what should a pt taking exenatide do if they experience persistent and severe abdo pain with vomiting?

A

stop the exenatide (a GLP-1 receptor agonist)

these symptoms may indicate acute pancreatitis, and drug should not be restarted if this is confirmed.

126
Q

indications for continued use of GLP-1s?

A

HbA1c reduction of 1% and weight loss of 3% within 6mnths

127
Q

how often should diabetics have their urine checked for protein?

A

at least annually

128
Q

how often should BP be checked in diabetics?

A

at least 3mnthly until targets achieved

and then 4-6mnthly once targets achieved.

129
Q

who should be considered for lipid tment?

A

all diabetics aged 40 or over
diabetics aged 18-39 who have at least 1 of the following with poor CV risk profile:
significant retinopathy
any degree of nephropathy
HbA1c more than 9% (75mmol/mol)
requirement of antihypertensive therapy
total cholesteronl more than 5mmol/L
FH of premature CVD in 1st degree relative, under age of 55 in males or 65 in females
features of metabolic syndrome- increased waist circumference, triglycerides, HTN and decreased triglycerides.

130
Q

initial target in lipid tment in diabetics?

A

total cholesterol less than 4mmol/L
LDLs less than 2mmol/L

=statins 1st line-cheapest 1st e.g. simvastatin 40mg, then atorvastatin if not well controlled

131
Q

what blds should be monitored after statin tment started?

A

LFTs 6 wks after starting

then yearly if normal

132
Q

what additional lipid managemet should take place in diabetic pt on a statin after achieving targets of total cholesterol and LDLs?

A

consider HDLs and triglycerides- HDLs should be more than 1mmol/L in males and 1.2 in females, and triglycerides fasting less than 1.7
lifestyle- weight loss and exercise
can try fibrate-fenofibrate 160mg, don’t commence if eGFR less than 45ml/min, and discontinue with renal deterioration.

monitor lipids 6wkly until targets met, then yrly

133
Q

use of anti-platelet tment in DM?

A

aspirin 75mg daily recommended for all with any form of CVD
if hypertensive, shouldn’t start until BP 145/90 or less
use clopidogrel if aspirin not tolerate or CI

134
Q

how is higher risk urine albumin excretion in DM defined?

A

microalbuminuria- ACR from 2.5-30 in males and 3.5-30 in females, PCR less tahn 50
low proteinuria- ACR 30-70 and PCR less than 100
hgih proteinuria- ACR more than 70, PCR more than 100

135
Q

investigations to assess diabetic pt with diabetic nephropathy?

A

urinalysis-ACR
kidney function assessment- GFR, ?creatinine
FBC- exclude anaemia
kidney imaging

136
Q

when should ACEI/AngIIRB therapy in diabetic pt be stopped?

A

if serum creatinine rises by more tahn 30% or eGFR falls by more than 25%
must seek specialist advice to exclude renovascular disease.

137
Q

importance of testing ketones in pregnancy?

A

DKA in pregnancy can develop with blood glucose concentrations close to the normal range

138
Q

for women with pre-existing diabetes in pregnancy, how should renal function be assessed?

A

renal assessment at 1st contact in pregnancy if hasn’t been done in past 12 mnths
refer to nephrologist if serum creatinine 120micromol/L or more or total protein excretion more than 2g/day
thromboprophylaxis if proteinuria more than 5g/day

139
Q

how should fetal development be monitored and screened for in diabetic women in pregnancy?

A

for women with booking HbA1c 8% or more, antenatal US examination of fetal cardiac outflow tracts in addition to routine anomaly scanning at 18-22wks
US monitoring of fetal growth and amniotic fluid vol every 4 wks from 28-36wks
individualised monitoring of fetal wellbeing to women at risk of intrauterine growth restriction- those with macrovascular disease or nephropathy.

don’t offer tests of fetal wellbeing before 38wks unless risk of IGR.

140
Q

issues for people with dementia who develop diabetes?

A

incontinence as need to pass urine more often but can’t find a toilet
increased falls risk as visiting toilet more often
increased confusion if blood glucose levels high and causing dehydration
distress if usual diet changed significantly
distress, wandering, rocking movements, crying if they have pain and can’t put it into words.

141
Q

issues for people with diabetes who develop dementia?

A

forget to take meds regularly
forget have takens meds so risk of OD
forget how to do injections
unable to make dcisions about interpreting blood glucose such as adjusting insulin injections or treating hypoglycaemia.
miss meals and drinks- risk of hypos and dehydration
forget have eaten so risk of high glucose if eat again.

142
Q

points to consider in support plans for elderly with diabetes and dementia?

A

keeping them safe: if still want to administer their insulin themselves, maybe keep locked away.
be observant of symptoms of hypos.
agree appropr. blood glucose levels with pt’s diabetes team
cognitive ability: support self-care, ask GP to simplify med.s regimen e.g. OD tablets, and administration e.g. dosset box- although not helpful if don’t know time or day.
personality: hypo symptoms may be mistaken for dementia symptoms e.g. loud aggression
physical health: apparent incontinence
environment: encourage nourishing diet in calm and distraction free environment.

General Medicine Block (10 decks)

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