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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
Screening for diabetic nephropathy
Diabetics should have annual **urinary** **albumin:creatinine ratio** and U+Es * should be _early morning urinary sample_ * ACR \> 2.5 = microalbuminuria
26
Mx of diabetic nephropathy
* **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
HHS pathology
* **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
Hyperosmolar hyperglycaemis is a ..
MEDICAL EMERGENCY
29
Aietology of HHS
**Elderly T2DM** (but can be younger) Can be **initial presentation** of T2DM
30
HHS vs DKA
(*can have mixed picture)*
31
Cx of HHS
* MI / stroke / peripheral arterial thrombosis * Seizures / cerebral oedema / central pontine myelinolysis (CPM) == all are rare but documented
32
CFx of HHS
* **General** : fatigue/ lethargy / N + V * **Neurological**: altered consciousness / headaches/ papilloedema / weakness * **Haem:** hyperviscosity (may lead to MI / stroke / VTE) * **Cardio:** dehydration / hypotension / tachycardia
33
Diagnosis (criteria but not official) of HHS
1. **Hypovolaemia** 2. Marked **hyperglycaemia** (\>30mmol/L) without signif _ketonaemia / acidosis_ 3. Signif raised **serum osmolarity** (\>320 mosmol/kg)
34
Goals of Mx of HHS
* 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
Fluid replacement in HHS
**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
**Metformin**
* **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
Pioglitazone
* Is a **thiazolidinedione** * **Increase insulin sensitivit**y + decrease liver production of glucose * SE * **Weight gain** * Fluid retention * Anaemia * **HF!**!! * Extended use = **higher risk of bladder cancer** * **Does NOT cause hypoglycaemia**
38
Sulfonylureas
* 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
What are incretins?
* = **_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
DPP4 inhibitors
* Most common = **sitagliptin** * Inhibits DPP4 enzyme and therefore increases GLP1 activity * SE * GI tract upset * Sx of URTI * Pancreatitis
41
GLP1 mimetics
* 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
SGLT2 inhibitors
* 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
INSULINS +ives and -ives
* **+ives** * Effect on blood glucose * Improvement of glycaemic control * **-ives** * Injectable * Weight gain * Hypoglycaemia * Occupational concerns
44
Rapid acting insulins
* Start working at **10mins** * Last around **4 hrs** * E.g. novorapid / humalog / apidra
45
Short acting insulins
* Work in **30 mins** * Last around **8 hrs** * Actrapid / Humulin S / Insuman Rapid
46
Intermediate acting
* Start working in **1 hr** * Last around **16 hrs** * Insulatard / Humulin I / Insuman Basal
47
Long acting insulins
* Work in **1 hr** * Last around **24 hrs** * Lantus / Levemir / Degludec (lasts over 40 hrs!!!)
48
Combination insulins
* 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
Causes of hypoglycaemia
Diabetes + selfadminister insulin / sulfonylureas Insulinoma Liver failure Addisons Alcohol (causes exaggerated insulin secretion) Nesidioblastosis = beta cell hyperplasia
50
Physiological response hypoglycamia
**Hormonal** = decrease **insulin** + ^ **glucagon** *then GH and cortisol released* **Sympathoadrenal** = increase adrenergic mediated AND ACh mediated neurotransmission in PNS + CNS
51
CFx of hypoglycaemia
* 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 + convulsio*n
52
Mx of Hypoglycaemia in community
* 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
Mx of hypoglycaemia in hosp
* 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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