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CDM core conditions > Non communicable metabolic disease > Flashcards

Non communicable metabolic disease Flashcards

1
Q

Pathology of T2DM?

A

Repeated exposure to glucose + insulin –> cells resistant to effects of insulin –> more and more insulin needed –> pancreatic beta cells become fatigued –> produce less –> so big amount glucose + insulin resistance + pancreatic fatigue = chronic hyperglycaemia –> micro/macro and infectious Cx

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2
Q

RF of T2DM (non mod +mod)

A
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3
Q

Genetic component of T2DM

A

Polygenic up to 50 genes w small effect (TCF7L2 most powerful)

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4
Q

Presentation of T2DM

A
  • Consider in anyone with RF –> often asymptomatic
  • Fatigue
  • Polydipsia + polyuria
  • Unintentional wloss
  • Opportunistic infections
  • Slow healing
  • Glucose in urine on dipstick
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5
Q

What is prediabetes and diagnostic levels?

A
  • Indication of progression to diabetes
  • Education = lifestyle changes + risk reduction
    • Don’t recommend medical tx
  • Diagnosis of prediabetic
    • HbA1c = 42-47 mmol/mol
    • Impaired fasting glucose = 6.1-6.9 mmol/l
      • Body struggles to get blood levels in normal range even after prolonged period
    • Impaired glucose tolerance = 7.8-11.1 on OGTT
      • Body struggles to cope w a carb meal
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6
Q

Diagnostic levels of T2DM?

A
  • HbA1c > 48 mmol/mol
  • Random glucose >11 mmol/l
  • Fasting glucose >7 mmol/l
  • OGTT 2 hr result >11 mmol/l

“shopped in 7-11 and cost me 48 quid!!!”

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7
Q

Gross Mx of T2DM

A
  • Patient education!!
  • Dietary modification
    • Veggies + oily fish
    • Low glycaemic high fibre diet
  • Other RF
    • Exercise + wloss // Stop smoking // Optimise Tx for HTN / hyperlipidaemia / CV disease
  • Monitoring for Cx
    • Diabetic retinopathy // Kidney disease // Diabetic foot
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8
Q

Tx targets in T2DM (newly diagnosed + other…)

A
  • 48 mmol/mol for new T2DM
  • 53 mmol/mol for diabetics that have moved beyond metformin alone
  • HbA1c measured every 3-6 months typically red top EDTA bottle
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9
Q

Medical Mx of T2DM stepwise therapy

A

1st line = metformin titrated from 500g OD as tolerated

2nd line = add sulfonylurea / pioglitazone / DPP4 inhib / SGLT-2 inhibit

Decision based on individual factors + drug tolerance

3rd line =

Triple therapy w metformin + 2 of second line drugs combined OR

Metformin plus insulin

SIGN guidelines = SGLT2 inhibits / GLP1 mimetics (liraglutide) used preferentially in pt w CV disease

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10
Q

Causes of HTN

A

Essential HTN = 95% cases

Secondary causes = ROPE

Renal

Obesity

Pregnancy induced / preeclampsia

Endocrine

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11
Q

Secondary causes of HTN:

A
  • Renal disease
    • Most common secondary type
    • If BP v high / doesn’t respond to Tx consider renal artery stenosis
  • O- Obesity
  • P- Pregnancy induced HTN / pre-eclampsia
  • E- Endocrine
    • Hyperaldosteronism (Conns syndrome)
      • Simple test for this is renin:aldosterone ratio in blood test
  • Specialist investigation if = potential secondary caused // aged 40 or under
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12
Q

Cx of HTN (5)

A
  1. IHD
  2. CVA –> stroke / haemorrhage
  3. Hypertensive retinopathy
  4. Hypertensive nephropathy
  5. HF
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13
Q

Diagnosis steps + screening of HTN

A
  • Measure BP every 5 yrs to screen
    • Every year if borderline for diagnosis
    • Every yr in people w T2DM
  • Pt with clinic BP between 140/90 and 180/120 should have ambulatory BP / home readings to confirm diagnosis
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14
Q

Stages of HTN

A
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15
Q

tests after diagnosis of HTN

A

for end organ damage!

  • Urine albumin:creatinine ratio for proteinuria + dipstick for microscopic haematuria to assess for kidney damage
  • Bloods for HbA1c / renal function / lipids
  • Fundus examination = hypertensive retinopathy
  • ECG for cardiac anomalies
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16
Q

Types of meds used in HTN

A

Mnemonic = ACD-ARB

  • A-ACEi = ramipril 1.25mg up to 10mg OD
  • C- CCB = amlodipine 5mg to 10mg OD
  • D- thiazide like diuretic = indapamide 2.5mg OD
  • ARB - candesartan 8mg to 32 mg OD
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17
Q

Stepwise Tx of HTN

A
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18
Q

Tx targets in HTN (with age)

A
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19
Q

Peripheral diabetic neuropathy key Fx

A

sensory loss = in glove and stocking distribution

(legs first cos length of neurons supplying area is longer)

happens cos chronic high glucose damages small blood vessels supplying nerve

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20
Q

Sx of diabetic neuropathy

A
  • Numbness / reduced abilitu to feel pain/temp
  • Tingling / bruning
  • Sharp pains + cramps
  • Muscle weakness
  • Extreme sensitivity to touch –> e.g. bedsheet hurt
  • Ulcers /infections / bone / joint damage
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21
Q

Mx of diabetic neuropathy

A

1st line = amitriptyline / duloxetine / gabapentin / pregabalin

2nd line = tramadol (rescue therapy) / topical capsaicin (localised e.g. postherpetic neuralgia) / pain management clinics

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22
Q

GI autonomic nueropathy (types and info)

A

Gastroparesis

  • erratic blood glucose / bloating / vomiting
  • Mx = metoclopramide / domperidone / erythromycin (prokinetic agents)

Chronic diarrhoea (often at night)

GORD (decreased lower oesophageal sphincter pressure)

23
Q

Diabetic nephropathy pathology

A
  • Most common cause of glomerular pathology + CKD in UK
  • Chronic hyperglycaemia causes scarring as passes through glomerulus
    • Called glomerulosclerosis
24
Q

Key Fx of diabetic nephropathy

A
  • Proteinuria
    • Damage to glomerulus –> allows protein to be filtered from blood to urine
25
Q

Screening for diabetic nephropathy

A

Diabetics should have annual urinary albumin:creatinine ratio and U+Es

  • should be early morning urinary sample
  • ACR > 2.5 = microalbuminuria
26
Q

Mx of diabetic nephropathy

A
  • optimising diabetic control + HTN
  • ACEi / ARB is Tx choice in diabetes to control BP
    • Should be starting in pts w diabetic nephropathy even if they have normal blood pressure
  • Dietary protein restriction
  • Control any dyslipidaemias e.g. statins
27
Q

HHS pathology

A
  • Hyperglycaemia results in osmotic diuresis = means loss of Na+ and K+
  • Severe volume depletion = signif raised serum osmolarity
    • So hyperviscosity of blood
  • Despite severe electrolyte losses and total body volume depletion = typical pt doesn’t look dehydrated
    • Bcos hypertonicity leads to preservation of intravascular volume
28
Q

Hyperosmolar hyperglycaemis is a ..

A

MEDICAL EMERGENCY

29
Q

Aietology of HHS

A

Elderly T2DM (but can be younger)

Can be initial presentation of T2DM

30
Q

HHS vs DKA

A

(can have mixed picture)

31
Q

Cx of HHS

A
  • MI / stroke / peripheral arterial thrombosis
  • Seizures / cerebral oedema / central pontine myelinolysis (CPM) == all are rare but documented
32
Q

CFx of HHS

A
  • General : fatigue/ lethargy / N + V
  • Neurological: altered consciousness / headaches/ papilloedema / weakness
  • Haem: hyperviscosity (may lead to MI / stroke / VTE)
  • Cardio: dehydration / hypotension / tachycardia
33
Q

Diagnosis (criteria but not official) of HHS

A
  1. Hypovolaemia
  2. Marked hyperglycaemia (>30mmol/L) without signif ketonaemia / acidosis
  3. Signif raised serum osmolarity (>320 mosmol/kg)
34
Q

Goals of Mx of HHS

A
  • Normalise osmolality gradually
    • Serum osmolarity is key to monitoring progress
    • If not available –> estimated by (2 x Na+) + glucose + urea
  • Replace fluid + electrolyte losses
  • Normalise blood glucose (gradually)
35
Q

Fluid replacement in HHS

A

1st line to restore total body fluid = 0.9% NaCl

  • aim to achieve positive balance of 3-6 litres by 12 hours*
  • Remaining replacement within next 12 hrs*

2nd line if osmolarity not gaining w positive balance of 0.9% = 0.45% NaCl

INSULIN NOT USED → corrects too quickly be harmful

36
Q

Metformin

A
  • Biguanide
  • Increase insulin sensitivity + decrease liver production of glucose
  • Considered weight neutral
  • SE
    • Diarrhoea + abdo pain = dose dependant
      • Often lowering dose improves Sx
    • Lactic acidosis (Rare)
    • Does NOT cause hypoglycaemia
37
Q

Pioglitazone

A
  • Is a thiazolidinedione
  • Increase insulin sensitivity + decrease liver production of glucose
  • SE
    • Weight gain
    • Fluid retention
    • Anaemia
    • HF!!!
    • Extended use = higher risk of bladder cancer
    • Does NOT cause hypoglycaemia
38
Q

Sulfonylureas

A
  • Most common = gliclazide
  • Stimulate insulin release from pancreas
  • Quick reduction of blood glucose
  • SE
    • Weight gain
    • Hypoglycaemia
    • Increased risk of CV disease + MI when used as a monotherapy
39
Q

What are incretins?

A
  • = hormones produced by GI tract
  • Secreted in response to large meals + act to reduce blood sugar
  • Work by
    • Increase insulin secretion
    • Inhib glucagon
    • Slow absorption by GI tract
  • Main incretin = glucagon like peptide 1 (GLP1)
  • Incretins are inhibited by enzyme = dipeptidyl peptidase 4 (DPP4)
40
Q

DPP4 inhibitors

A
  • Most common = sitagliptin
  • Inhibits DPP4 enzyme and therefore increases GLP1 activity
  • SE
    • GI tract upset
    • Sx of URTI
    • Pancreatitis
41
Q

GLP1 mimetics

A
  • GLP1 mimetics
    • Mimic action of GLP1
    • Exenatide
      • SC injection
      • BD by patient
      • OR once weekly in modifiable release form
    • Another e.g. is liraglutide
      • SC injection OD
    • Sometimes combined w metformin + a sulfonylurea in overweight pts
    • ?lower CV risk? –> liraglutie / dulaglitide / semaglutide
    • SE
      • GI tract upset
      • Wloss
      • Dizziness
      • Low risk of hypoglycaemia
    • Problem = injectables
42
Q

SGLT2 inhibitors

A
  • End w suffice -gliflozin
  • E.g. empagliflozin / canagliflozin / dapagliflozin
  • SGLT2 protein responsible for reabsorbing glucose in PCT of kidneys
    • So inhibitors block this action –> glucose excreted in wee
  • Empagliflozin
    • Shown to reduce risk fo CV disease / hosp w HF / all cause mortality in T2DM
  • Canagliflozin
    • Shown to reduce CV events e.g. MI / stroke / death / HF
  • SE
    • Glucosuria (glucose in urine)
    • Increased rate of UTI
    • Wloss
    • DKA –> with only moderately raised glucose (RARE)
    • Lower limb amputation –> appears more common in pts on canagliflozin
43
Q

INSULINS +ives and -ives

A
  • +ives
    • Effect on blood glucose
    • Improvement of glycaemic control
  • -ives
    • Injectable
    • Weight gain
    • Hypoglycaemia
    • Occupational concerns
44
Q

Rapid acting insulins

A
  • Start working at 10mins
  • Last around 4 hrs
  • E.g. novorapid / humalog / apidra
45
Q

Short acting insulins

A
  • Work in 30 mins
  • Last around 8 hrs
  • Actrapid / Humulin S / Insuman Rapid
46
Q

Intermediate acting

A
  • Start working in 1 hr
  • Last around 16 hrs
  • Insulatard / Humulin I / Insuman Basal
47
Q

Long acting insulins

A
  • Work in 1 hr
  • Last around 24 hrs
  • Lantus / Levemir / Degludec (lasts over 40 hrs!!!)
48
Q

Combination insulins

A
  • Contain a rapid acting + intermediate acting
  • Brackets mean proportion of rapid : intermediate insulin
  • Humalog 25 (25:75)
  • Humalog 50 (50:50)
  • Novomix 30 (30:70)
49
Q

Causes of hypoglycaemia

A

Diabetes + selfadminister insulin / sulfonylureas

Insulinoma

Liver failure

Addisons

Alcohol (causes exaggerated insulin secretion)

Nesidioblastosis = beta cell hyperplasia

50
Q

Physiological response hypoglycamia

A

Hormonal = decrease insulin + ^ glucagon

then GH and cortisol released

Sympathoadrenal = increase adrenergic mediated AND ACh mediated neurotransmission in PNS + CNS

51
Q

CFx of hypoglycaemia

A
  • Glucose levels and severity of Sx not always correlated
    • Esp in diabetes
  • Blood glucose <3.3 cause autonomic Sx due to release of glucagon + adrenaline
    • Sweating / shaking / hunger / anxiety / nausea
  • Blood glucos <2.8 cause neuroglycopenic Sx due to inadequate glucose supply to the brain
    • Weakness / vision changes / confusion / dizziness
  • Severe + uncommon = Coma + convulsion
52
Q

Mx of Hypoglycaemia in community

A
  • Initially oral glucose 10-20g should be given in liquid / gel / tablet form
  • OR propriety quick-acting carb may be given e.g. glucogel / dextrogel
  • ‘hypokit’ may be prescribed –> contains syringe and vial of glucagon for IM / SC injection at home
53
Q

Mx of hypoglycaemia in hosp

A
  • If pt alert = quick acting carb may be given
  • If pt unconscious / unable to swallow = SC / IM injection glucagon
  • OR IV 20% glucose solution –> give through large vein

CDM core conditions (1 decks)

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