Brainscape's Knowledge GenomeTM

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


See full index

endo > DM > Flashcards

DM Flashcards

1
Q

how does the body increase blood glucose levels

A

1) absorption of glucose from GIT
2) glycogenolysis in muscle & liver
3) gluconeogenesis in liver

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

how does body decrease blood glucose levels

A

1) uptake & utilisation of glucose by tissues
2) glycogen synthesis in muscle & liver

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

pre-DM - general

A
  • can be asymptomatic
  • predispose individuals to T2DM & cardiovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

pre-DM components

A

1) impaired fasting glucose (IFT)
2) impaired glucose tolerance (IGT)

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

nonpharmaco for pre DM

A

1) lifestyle intervention to prevent/delay progression

  • healthy diet
  • increase physical activity (150 min moderate or 75 mins vigorous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pharamco for pre DM

A

metformin

  • only used when:

1) glycaemic status X improve despite lifestyle intervention
2) X to do lifestyle intervention esp if BMI ≥ 23 kg/m^2, younger than 60, women w history of gestational DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is type 1 DM associated with

A

insufficient secretion of insulin

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

pathogenesis for type 1 DM

A

absolute deficiency of pancreatic beta cell function due to immune mediated destruction or positive antibodies

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

staging for type 1 DM

A

1) type 1, type 2

  • +ve antibodies, asymptomatic

2) type 3

  • +Ve antibodies, symptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is type 2 DM associated with

A

body resistant to insulin

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

pathogenesis for type 2 DM

A
  • progressive loss of adequate beta-cell insulin secretion on the background of insulin resistance
  • insulin resistance:
    1) glucose utilisation impaired
    2) hepatic glucose output increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is the levels of insulin and glucose like at the early stage of type 2 DM

A

high levels

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

Type 1 vs Type 2 DM

A

1) primary cause

  • type 1: autoimmune-mediated pancreatic beta cell destruction, +ve antibodies
  • type 2: insulin resistance, impaired insulin secretion, negative antibodies

2) insulin production

  • type 1: absent, type 2: normal/abnormal

3) age of onset

  • type 1: < 30 yo, type 2: often > 40 yo but increasing prevalent in obese children/younger adult

4) onset of clinical presentation

  • type 1 abrupt, type 2 gradual

5) physical appearance

  • type 1 thin, type 2 overweight

6) proneness to ketosis

  • type 1 frequent, type 2 uncommon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

signs and symptoms of hyperglycaemia

A

1) polydipsia, polyuria, polyphagia
2) decreased healing, dry skin
3) drowsiness, blur vision

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

signs and symptoms of hypoglycaemia

A

1) fast heartbeat, shaking
2) Sweating, dizziness
3) hungry, impaired vision

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

DM measuring parameters

A

1) fasting plasma glucose (FPG)

  • X calorie intake for ≥ 8 hrs

2) random/casual plasma glucose

3) postprandial plasma glucose (PPG)

  • glucose level after meal, usually after 2 hrs (time taken for glucose to be stable)
  • 75g oral glucose tolerance test (OGTT)

4) HbA1c

  • average amt of glucose over 3 months (glucose stay attached to haemoglobin over lifespan of RBC
  • 3 month average of FPG + PPG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

diagnosis of DM (MOH guidelines)

A
  • 2 abnormal test results required to diagnose DM
  • HbA1c values
    1) ≥ 7%: X further test, confirm DM

2) 6.1% - 6.9%: take second test
** FPG values: > 7 confirm DM | 6.1 - 6.9 pre DM | < 6 no DM

** OGTT: > 11.1 confirm DM | 7.8 - 11.0 pre DM | < 7.8 no DM

3) < 6% no further test, no possibility of DM

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

complications of DM

A

1) microvascular

  • retinopathy, blindness
  • nephropathy, kidney failure
  • neuropathy, amputation

2) macrovascular

  • increase cardiovascular disease

3) others

  • decrease life expectancy for 5-10 yrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

screening tests before confirming DM

A
  • recommended for asymptomatic individuals ≥ 40 yo +/- risk factors
  • FPG, HbA1c
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the 4 screening tests to do after confirming DM

A

1) Retinal fundal photography
2) urine microalbumin/creatinine ratio
3) diabetic foot screening
4) diabetic nephropathy test

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

screening test after confirmed DM - retinal fundal photography

A
  • test for diabetic retinopathy
  • within 5 yrs of onset for adults w T1DM
  • at time of diagnosis for T2DM
  • every 1-2 yrs if X evidence of retinopathy & well controlled hyperglycaemia
  • annual if any level of diabetic retinopathy present
  • pregnant ladies w DM: before pregnant/1st trimester, followed up to 1 year after giving birth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

screening test after confirming DM - urine microalbumin/creatinine ratio

A

test for diabetic nephropathy/albuminuria

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

screening test after confirming DM - diabetic foot screening

A
  • reduce risk of diabetic foot ulcer
  • at least once a year
  • process: inspection of skin, assess foot deformities, neurological assessment, vascular assessment
  • non pharmacotherapy for this (glycaemic control, quit smoking, good foot care)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

screening test after confirming DM - diabetic nephropathy test

A
  • T1DM within 5 yrs of onset
  • T2DM upon diagnosis
  • components
    1) serum Cr +/- eGFR
    2) urine albumin/creatinine ratio or protein-creatinine ratio if albuminuria heavy (≥ 300mg/g)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

monitoring cardiovascular risk factors for DM

A
  • macrovascular
    1) HbA1c: X well controlled every 3 months, controlled every 6 month
    2) lipid panel: X well controlled every 3-6 month, controlled annually
    3) BP: Every visit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

treatment goals for DM - HbA1c

A

1) less stringent: 7.5 - 8.0%

  • history of severe hypoglycaemia
  • limited life expectancy
  • advanced complications
  • extensive comorbid conditions
  • target hard to attain despite intensive SMBG, repeated counselling, effective pharmacotherapy

2) normal: < 7.0%

3) more stringent: 6.0 - 6.5%

  • short disease duration
  • long life expectancy
  • X significant cardiovascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

target for FBG & PPG

A
  • mmol/L X 18 = mg/dL
  • FBG: 4.4 - 7.2 mmol/L
  • PPG: < 10 mmol/L
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

metformin - change in lab values

A
  • 1.5 - 2.0% reduction in HbA1c
  • marked reduction FBG
  • mild reduce PPG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

metformin - non DM uses

A
  • polycystic ovarian syndrome (POS)
  • weight loss
  • improve lipid levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

metformin formulations

A
  • immediate release: 250, 500, 850, 1000mg
  • extended release: 500, 750,1000mg (BD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

metformin dosing

A

1) immediate release

  • start 500 - 850 mg OD
  • titrate 500 - 850mg every 1 - 2 wks in divided doses (OD - TDS)
  • max 2550mg per day

2) extended release

  • 500mg OD
  • increase 500mg weekly
  • max 2000mg OD, can divide into 1000mg BD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

MOA of metformin

A

1) primary

  • lower hepatic glucose production (gluconeogenesis)

2) Secondary

  • enhance tissue sensitivity to insulin
  • enhance peripheral glucose uptake & utilisation
  • increase AMP activated protein kinase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

PD for metformin

A
  • onset within days
  • duration of action 8-12 hrs
  • max effect 2 wks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

metformin PK

A
  • absorption: oral
  • elimination: renal, excreted unchanged in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

metformin AE

A

1) common: GI disturbances (V/D/indigestion), metallic taste

  • transient
  • take w food/increase dose gradually
  • diarrhoea -> weight loss

2) long term

  • increase risk of Vit B12 malabsorption -> deficiency

3) rare but fatal

  • lactic acidosis (block gluconeogenesis -> prevent lactic broken down to glucose -> increase lactate concentration -> lactic acidosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

metformin special population

A

can use for pregnant & > 10 yo

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

metformin CI

A
  • severe renal impairment (GFR < 30ml/min, worse than stage 4)
  • hypoxic state/risk of hypovolemia (HF, sepsis, respi failure, liver impairment)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

metformin drug interactions

A

1) alcohol: increase risk for lactic acidosis
2) iodinated contrast material

  • radiologic procedure
  • temporarily withhold metformin for 48 hrs after iodinated contrast administration
  • restart when renal function stable & acceptable post procedure

3) inhibitor/inducer of organic cationic transporter (OCT)

  • OCT 2 inhibitor: cimetidine, dolutegravir, ranolazine
  • increase metformin by reducing renal elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Thiazolidinediones (TZD) indication

A

1) combination to reduce HbA1c when X tolerate metformin

2) change in lab values

  • 0.5-.14% reduction HbA1c
  • moderate reduction FBG & PPG

3) good for fatty liver disease

4) CV effect: reduce stroke risk, increase HF risk

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

thiazolidinediones (TZD) - formulation

A

15, 30mg tablets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

thiazolidinediones (TZD) - MOA

A

PPARgamma agonist -> promote glucose uptake into target cells (skeletal/adipose), decrease insulin resistance & increase insulin sensitivity

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

thiazolidinediones (TZD) - PDPK

A
  • 1 month max effect
  • liver elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

thiazolidinediones (TZD) - adverse effect

A

1) hepatotox

  • monitor LFT prior initiation & after
  • X use if ALT > 3x ULN
  • if > 1.5x ULN then repeat tests
  • discontinue if sign of hepatic dysfunction

2) fluid retention (monitor HF)
3) increase fracture risk (esp women)
4) weight gain (dose-related)
5) risk of bladder cancer
6) increased risk of hypoglycaemia w insulin therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

thiazolidinediones (TZD) - CI

A

1) acute liver disease
2) symptomatic/history of HF
3) active/history of bladder cancer

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

thiazolidinediones (TZD) - drug interaction

A
  • coadministered w CYP inhibitor/inducer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

sulfonylureas (SU) - change in lab values

A
  • 1.5% reduction HbA1c
  • mild reduction FBG
  • marked reduction PPG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

types of sulfonylureas (SU)

A

1) 1st gen: tolbutamide
2) 2nd gen: glipizide, gliclazide, glibenclamide
3) 3rd gen: glimepiride

48
Q

sulfonylureas dosage

A
  • OD dosage improve adherence but $$
  • take immediately after meal, X miss/delay meal
  • caution if irregular meal schedule
49
Q

sulfonylureas MOA

A

1) primary

  • bind to SU receptor proteins of ATP sensitive potassium channels -> inhibit channel mediated K+ efflux -> trigger calcium dependent exocytosis of insulin granules from pancreatic beta cells

2) Secondary

  • decrease hepatic glucose output & increase insulin sensitivity
50
Q

sulfonylureas PD

A

onset 30 mins, duration of action 12-24 hrs

51
Q

sulfonylureas PK

A
  • oral absorption
  • highly plasma protein bound, t1/2 4h
  • hydroxylation in liver
  • < 10% excreted unchanged in urine & faeces
52
Q

AE sulfonylureas

A

hypoglycaemia (Esp elderly), weight gain

53
Q

drug interaction sulfonylureas

A
  • BB mask signs of hyperglycaemia
  • disulfiram-like reaction w alcohol (more common w 1st gen)
  • CYP2C9 inhibitor increase glimepiride & glipizide
54
Q

DPP-4i - incretin

A
  • released after eating
  • augment secretion of insulin from pancreatic beta cells in glucose-dependent manner (presence of hyperglycaemia)
55
Q

DPP-4i change in lab values

A
  • 0.5 - 0.8% decrease HbA1c
  • mild reduction FBG
  • moderate reduction PPG
56
Q

DPP-4i types

A

1) sitagliptin

  • eGFR < 30 -> 25 mg OD
  • eGFR 30 - 45 -> 50 mg OD

2) vildagliptin

  • CrCl < 50 -> 50mg daily
  • CrCl >50 -> 50mg BD

3) linagliptin

  • X dose adjustment
57
Q

DPP-4i MOA

A
  • GLP-1 make you full by

1) decrease gastric emptying
2) improve beta cell function -> increase more insulin, reduce glucagon
3) decrease food intake

  • DPP-4 inactivate GLP-1 so DPP-4i extends GLP-1 action
58
Q

DDP-4i PK

A
  • oral absorption
  • t1/2 10-12h
  • low liver metabolism
  • 80% unchanged urine, rest shit
59
Q

DDP-4i AE

A
  • severe joint pain
  • skin reaction (Rash, itch)
  • hypersensitivity
  • flu like symptoms
  • GI
  • rare: acute pancreatitis, bullous pemphigod (blister on skin)
60
Q

DDP-4i drug interaction

A

CYP3A4 inhibitor

61
Q

SGLT2-i cariorenal beneift

A
  • cana & empa
  • HF & CKD
  • discontinue when start dialysis
62
Q

SGLT2-i change in lab values

A
  • reduce HbA1c by 0.8-1%
  • moderate reduction FBG
  • mild reduction PPG
63
Q

types of SGLT2-i

A

1) Canagliflozin

  • 100, 300mg
  • X initiate if eGFR < 30ml/min

2) empagliflozin

  • 10, 25mg
  • X initiate if eGFR < 45ml/min

3) dapagliflozin

  • 5, 10 mg
  • X initiate if eGFR < 45 ml/min
64
Q

SGLT2-i MOA

A
  • inhibit SGLT2
  • reduce absorption of filtered glucose
  • reduce renal threshold for glucose & increase urinary glucose excretion
65
Q

SGLT2-i PK

A

1) absorption

  • oral, Cmax 1-2 hr

2) distribution

  • highly plasma protein bound
  • t1/2 12 hr, OD

3) minimal liver metabolism (glucuronidation)

4) excreted unchanged pee/shit

66
Q

SGLT2-i AE

A

1) hypotension (titrate anti HTN)
2) hypoglycaemia
3) increase urination
4) genital mycotic infection/UTI

  • more for female
  • check UTI/history of fungal infection in vagina
  • good toilet hygiene, drink more water

5) euglycemia diabetic ketoacidosis (DKA)

  • more common if undergoing severe stress (dehydrated, alcohol abuse, X eating well, poor oral intake)
  • hold of SGLT2-i until recover from stress

6) fournier’s gangrene

  • more for males
  • necrotising fascitis of perineum
  • good toilet hygiene, drink more water

7) canagliflozin: lower limb amputation, hyperkalaemia, fracture

67
Q

SGLT2-i CI

A

X dialysis

68
Q

MOA of insulin - liver

A

1) decrease gluconeogenesis (make glucose
2) increase glycogenesis (convert to glycogen for storage)
3) decrease glycogenolysis (reduce breakdown of glycogen to glucose)

69
Q

MOA of insulin - pancreas

A

increase insulin secretion

70
Q

MOA of insulin - muscle

A

1) increase glucose transport
2) increase glycogenesis
3) inhibit proteolysis

71
Q

MOA of insulin - adipocyte

A

1) increase glucose transport
2) increase protein synthesis
3) increase lipogenesis (make more fat cell)
4) decrease lipolysis & FFA oxidation (reduce breakdown of fat tissue)

72
Q

metabolism of insulin

A
  • exogenous: kidney
  • endogenous: liver
73
Q

insulin needle length

A
  • pen needle: 4mm - 12.7mm
  • syringe needle: 6mm - 12.7mm
74
Q

insulin gauge size (needle thickness)

A
  • 28, 29, 30, 31
  • higher gauge = finer needle - lesser pain but increase needle weakness & decrease speed of injection
75
Q

insulin syringe size

A
  • 100 IU/ml
  • 1cc: max dose 100, increment 2
  • 1/2 cc: max dose 50, increment 1
  • 3/10 cc: max dose 30, increment 1
76
Q

insulin vial size

A
  • U-100 (100 units/1mL of solution)
77
Q

stability of insulin

A

1) unopened: good till expiration if store in fridge
2) opened: good for 28 days regardless of fridge
3) insulin containing device: product insert
4) detemir: opened good for 42 days

78
Q

insulin administration sites

A
  • outer upper arms: fatty tissue area
  • abdomen: 2 inch circle around navel
  • top & outer thigh: avoid bony area above knees
  • rotate sites to prevent lipohypertrophy
  • speed of absorption: abdomen > outer upper arm > top & outer thigh > buttock
79
Q

factors that increase insulin absorption

A

1) heat
2) massage
3) exercise
4) lipoatrophy (concavity/pitting of adipose tissue)
5) IM administration

80
Q

factors that decrease insulin absorption

A

1) cold
2) lipohypertrophy (bulging of adipose tissue)

81
Q

indication for basal-prandial (basal/bolus)

A
  • T1DM w severe insulin deficiency
  • insulin deficiency - longer duration of T2DM
  • tighter glucose control (coronary artery bypass grafting, gestational DM)
82
Q

ultra short acting insulin

A
  • added excipients to increase rate of absorption & stabilise
83
Q

rapid acting insulin

A
  • e.g. aspart (novorapid), lispro (humalog)
  • target PPG (shjort action)
  • 5 mins before meals
84
Q

short acting/regular insulin

A
  • e.g. actrapid
  • target PPG, 30 mins before meals
85
Q

intermediate acting insulin

A
  • e.g. NPH (insulatard)
  • target FPG, 16 hrs (inject 2x for 24 hrs coverage)
86
Q

long acting insulin

A
  • glargine (lantus), detemir (levemir)
  • target FBG
87
Q

what insulins cannot be mixed with others (pre/self mix)

A

1) glargine (incompatible pH)
2) glulisine (only can w NPH)
3) detemir

88
Q

stable mixes for insulin

A

regular/rapid insulin + NPH

89
Q

examples of compatible insulin mixtures

A

1) Novomix 30

  • 30% short, 70% long, within 15 mins meal

2) humalog 75/25

  • 25% short, 75% long, within 15 mins meal

3) humalog 50/50

  • 50% short, 50% long, within 15 mins meal

4) mixtard 70/30

  • 30% regular, 70% intermediate, within 30 mins meal
90
Q

insulin + concurrent oral therapy

A

1) continue metformin
2) discontinue TZD or reduce dose when initiating
3) sulfonylureas

  • discontinue/reduce dose by 50% when initiate basal
  • discontinue if initiate prandial/premix
  • effectiveness decrease over time

4) continue SGLT2-i
5) discontinue DPP-4i if initiate GLP-1

91
Q

insulin dose conversion

A
  • most 1:1 (basically same AM & PM doses)
  • reduce by 10-20% if high risk of hypoglycaemia
  • if switch from BD NPH (intermediate) -> OD glargine/detemir (long acting) -> decrease by 20%
  • if switch from ultra long acting to other -> decrease by 20%
92
Q

insulin AE

A

1) hypoglycaemia (BG < 4 mmol/L)

  • S&S: blur vision, sweat, tremor, hunger, confuse, anxiety, shake, rapid heart beat, dizzy, headache, weakness & fatigue, irritability
  • management: 15-15-15 (15g fast acting carbs, 15 mins waiting time, another 15g if still BG < 4.0 mmol/L)

2) weight gain

  • dose dependent
  • management: diet, exercise, lose weight

3) lipodystrophy
4) local allergic reaction
5) rare: systemic allergy, insulin resistance

93
Q

types of GLP-1 agonist - liraglutide

A
  • SC OD regardless of meals
  • initiate 0.6 mg -> titrate 1.2 mg after 1 wk
  • max 1.8 mg
94
Q

types of GLP-1 agonist - Dulaglutide

A
  • SC injection once weekly regardless of meals
  • initiate 0.75mg -> titrate 1.5mg after 4 wks
  • max 3/4.5mg
95
Q

types of GLP-1 agonist - semaglutide (Ozempic)

A
  • SC injection once wkly regardless of meals
  • initiate 0.25 mg -> titrate to 0.5mg after 4 wks
  • max 1mg
96
Q

types of GLP-1 agonist - semaglutide (Rybelsus)

A
  • PO OD 30 mins before first meal of day
    ** empty stomach (30 mins before meal, med, drink)
    ** X more than 120ml water
  • initiate 3mg -> titrate to 7mg after 30 days
  • max 14mg
97
Q

MOA of GLP-1 agonist

A
  • activate GLP-1 receptor (GPCR) on pancreatic beta cell -> activate adenylate cyclase -> increase cAMP -> activate PKA -> phosphorylate all downstream proteins -> increase insulin secretion & decrease glucagon release
98
Q

what extra thing does liraglutide & semaglutide have

A
  • C-16 fatty acid on Lys -> Delay degradation & bind to plasma protein -> longer acting
99
Q

GLP-1 agonist PK

A
  • endogenously metabolised in similar manner to polypeptides wo specific major route of elimination
  • little/non excreted unchanged
100
Q

AE of GLP-1 agonist

A

headache, N/V, acute pancreatitis, acute cholecystitis, injection site reaction

101
Q

special precaution for GLP-1 agonist

A
  • X pregnant
  • black box warning: thyroid C-cell tumour in animals -> counsel on risk of medullary thyroid carcinoma & symptoms of thyroid cancer
102
Q

insulin dosing

A

1) initiation: basal control (FPG)

  • bedtime NPH 10 units or 0.2/kg/day
  • bedtime/morning glargine/detemir/degludex but $$

2) still controlled

  • increase insulin 2 units every 3 days until FPG at goal
  • increase insulin 4 units every 3 days if FPG consistently > 10 mmol/L
  • decrease insulin by 10-0% if X clear reason for hypoglycaemia

3) uncontrolled after basal dose > 0.5 units/kg (ceiling effective dose or FPG at goal)

  • prandial dose (rapid/regular)
    ** 1 dose (4 units/10% basal) w largest meal
    ** reduce basal by 4 units/10% if A1c < 8%
  • if bedtime NPH: split dose into 2 (2/3 morn, 1/3 evening)
103
Q

treatment algorithm for DM from start to end

A

1) metformin 1st line if no CI

2) if A1c still elevated

  • history of ASCVD/HD/CKD regardless of A1c
    ** ASCVD: GLP-1 agonist or SGLT-2i
    ** HF: SGLT2i
    ** CKD: SGLT2i then GLP-1 agonist
  • other combinations
    ** glucose lowering: insulin, GLP-1
    ** minimise hypoglycaemia: avoid SU, insulin
    ** promote weight loss: GLP-1, SGLT-2
104
Q

when to initiate insulin?

A

1) ongoing catabolism (weight loss)
2) symptoms of hyperglycaemia
3) A1c > 10%
4) BG > 16.7 mmol/L

105
Q

diabetic emergency - how is ketones formed

A
  • break down fats -> produce fatty acids -> travel back to liver + glucagon -> change fatty acid into ketone (beta hydroxybutyrate measured in hospital)
106
Q

diabetic emergency - diabetic ketoacidosis (DKA)

A
  • more for type 1
  • ketones formed
  • testing: blood & urine, fruity breath, acidosis
  • usually still alert
  • BG > 14 mmol/L
107
Q

diabetic emergency - hyperglycaemic hyperosmolar state (HHS)

A
  • more for type 2
  • residual insulin so X ketones & acidosis
  • extremely dehydrated so BG can > 33
  • stupor
108
Q

why early morning blood sugar high but bedtime low?

A

1) Dawn phenomenon

  • release of cortisol in waking hours -> BG rise sharply

2) Somogyi effect

  • BG levels drop sharply at night (X eat + meds) -> body respond by releasing glucagon -> rebound increase BG
109
Q

differentiate Somogyi effect & Dawn phenomenon

A
  • consistently low sugar -> somogyi effect
110
Q

BP management for DM

A
  • target: BP < 130/80
  • 1st line: ACEi/ARB w/wo kidney disease
111
Q

lipid management in DM - primary prevention

A
  • X cardiovascular disease but T2DM + risk factors
  • 45-70 yo: moderate intensity statin
  • additional ASCVD: high intensity
  • goal: reduce LDL 50% baseline, < 70 mg/dL
112
Q

lipid management in DM - secondary prevention

A
  • already have cardiovascular disease
  • target: LDL reduction 50% from baseline, < 55 mg/dL
  • ASCVD: high intensity
  • if X achieved then + ezetimibe/PCSK9i
113
Q

CKD management in DM - primary prevention

A
  • blood glucose, BP control
114
Q

CKD management in DM - secondary prevention

A

1) ACEi/ARB for micro/macroalbuminuria
2) finerenone

  • non steroidal MRA
  • eGFR > 25
  • SE: hyperkalaemia, hypotension, lesser risk of gynaecomastia

3) SGLT-2i

  • T2DM + DKD + eGFR > 20
    • ACEi/ARB
115
Q

use of aspirin w insulin

A
  • primary preventive measure for DM + increased CV risk + counsel on benefit vs risk of bleeding
  • secondary preventive measure for DM + history of ASCVD
    ** use clopidogrel if allergic to aspirin
  • X for > 60 yo & low ASCVD risk

endo (8 decks)

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