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CPTP > Glucose and Lipid lowering > Flashcards

Glucose and Lipid lowering Flashcards

1
Q

Effects of Insulin

A

@ liver promotes glycogen, protein, VLDL, triglyceride storage and synthesis. Inhibits lipolysis, ketogensis and gluconeogensis

@ muscle increased glucose uptake into cells, glycogen and protein synthesis

@adipose triglyceride storage and inhibition of lipoprotein lipase

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2
Q

MOA of Insulin

A

Post prandial increase in blood glucose concentration leads to B islet cells in the pancreas secreting insulin. Insulin circulates in the blood stream binding to receptors. G protein mediated reaction leads to B unit phosphorylation and translocation of GLUT4 channels on to cell surface of liver, muscle and adipose tissue

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3
Q

T1DM

A

AI destruction of B islet cells in the pancreas. Due to failure in self tolerance APC internalise self antigen migrate to lymph nodes activating T cells which in turn lead to B cells producing antibodies to target pancreatic tissue. PC 85% of B islets lost often with wt loss, polydipsia, polyuria or DKA

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4
Q

T2DM

A

Insulin resistance @ peripheral tissues, despite increasing insulin production. Progressive damage to the pancreas leads to gradual reduction of insulin so levels needed to stimulate peripheral tissues cant be maintained

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5
Q

Lifestyle management DM

A

Lose wt, low calorie and refined sugar. more exercise to improve insulin sensitivity and increase calorie use

Stop smoking to prevent potentiation of complications

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6
Q

Metformin (Biguanides) MOA

A

Acts by inhibiting hepatic gluconeogensis, increasing sensitivity to insulin @ peripheral tissues hence increasing peripheral glucose usage

Targets AMPK which promotes catabolism, lower glucose and lipid synthesis

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7
Q

CI Metformin

A

Really excreted so caution in renal failure. Hold 48hrs prior to contrast imaging due to increased risk of lactic acidosis.

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8
Q

SE Metformin

A

Reduced gastric motility - nausea, loose stool and flatulence

Lactic acidosis esp in renal failure. Occasionally hypersensitivity - urticaria, puritis and erythema

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9
Q

Benefits of metformin

A

Doesn’t increase insulin secretion therefore no risk of hypos!! Wt loss. Cheap and proven

1st line for T2DM

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10
Q

Interactions of metfomin

A

Hypoglycaemic effect increased with ACEi and MOAI’s

Increased risk of lactic acidosis with alcohol intake

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11
Q

Sulphonylureas (Glicazide) MOA

A

Increase insulin secretion by binding to su receptor on surface of B islet cell. Leading to K+ channel closure, this depolarises the cell membrane allowing Ca2+ influx and insulin secretion

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12
Q

Benefits of sulphonylureas

A

1st line in T2DM BMI <25, used as an adjunct to metformin for BMI > 25

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13
Q

SE sulphonylureas

A

wt gain, increased risk of hypos, N/V
Hypersensitivity - SJS, erythema multiform
Hepatotoxic - choleostatic jaundice + hepatitis

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14
Q

CI sulphonylureas

A

Hepatic impairment, Acute porphyria

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15
Q

Interactions with sulphonylureas

A

Increased hypo glycemic effect with warfarin, alcohol, B-blockers, MOAI’s

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16
Q

Thiazolidinediones (Pioglitazone) MOA

A

Activate PPAR receptors in adipose tissue, skeletal muscle and hepatocytes. This upregulates transcription of GLUT 4 channels on the surface of tissue to increase glucose uptake

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17
Q

SE of Pioglitazone

A

wt gain, fluid retention, liver toxicity, increased risk of fractures. Can = anaemia

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18
Q

SGLT 2 inhibtiors - Dapagliflozin

A

Prevent renal reabsorption by inhibiting SGLT-2 transporter in the proximal tubule. This leads to increase glucose loss in the urine = wt loss

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19
Q

SE of SGLT-2i

A

UTI and thrush

Expensive currently

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20
Q

Benefits of SGLT-2

A

Looks very promising renal protective, reduced incidence of diabetic nephropathy, lowers BP and prevents renal inflammation and fibrosis

Wt loss

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21
Q

DDP-4 Inhibitors (Sitagliptins)

A

Inhibit DDP-4 to prevent breakdown of incretins. Incretins are serrated by intestinal endocrine cells in response to nutrient intake. The increase insulin production from the pancreas, reduce gastric emptying from the stomach, promote satiety and reduce appetite.

22
Q

SE DDP-4

A

URTI, peripheral oedema,

Hepatotoxic and pancreatitis

23
Q

GLP-1 mimics - Exenatide

A

Bind and activate GLP-1 receptor preventing excess glucagon and increased insulin production

Leads to hypoglycaemia and wt loss

24
Q

SE GLP-1

A

SC injection BD - injection size reactions

Severe pancreatitis - haemorraghic/necrotising

25
Q

Insulin regimes

A

Basal bolus = Short acting insulin (Novarapid) 4x daily with meals and basal insulin OD lever

+ve allows flexibility with meals etc. Need to be able to calculate volume of insulin and calories in meals

BD basal insulin used in T2DM

26
Q

Insulin requirements

A

Increase in infection, pregnancy, exercise and with stress

27
Q

Insulin SE

A

Leads to uptake of K+ to cells = hypokalemia, lipogenesis @ peripheral tissue unsightly swellings due to lipohypertrophy - can = infected

Hypoglycaemia

28
Q

Insulin Pumps

A

SC deliver continous insulin via cannula, measures blood glucose and calculates dose of insulin needed. Bolus function for meals.

+ve - good for pt with loss of hypoglycaemia awareness , very flexible and easy. Proven to reduced HbA1c. Reduces hypos. Very good for children and elderly

-ve - DKA risk if sensor fails/battery low. Expensive

29
Q

Mx T2DM

A

Lifestyle = reduce wt, stop smoking, increase exercise

1st = metformin
Adjunct = sulphonylurea
Adjunct = GLP-1, SGLT-2
30
Q

Diagnosis of DKA

A

Ketones ++/ >3mmol/L
Blood glucose >11mmol/L
Venous pH < 7.3 or bicarb <15

31
Q

PC DKA

A

PC = polyuria, polydipsia, N/V abdo pain
low GCS, drowsiness
Kassmual breathing

32
Q

Mx DKA

A

ABCDE.

0.9% Nacl if BP >100 = 1L over 1 hr, <90 500ml over 15 mins. Continue to give 1L of fluid in intervals of 2hrs, 2hrs, 4hrs, 4hrs,6hrs

Insulin infusion 0.1unit/kg/hr (1unit per ml)
KCL replacement 40mmol/L aim for (3.5-5.5)

33
Q

When blood glucose <13mmol/L

A

GKI infusion 500ml 10% dextrose, 24 units of actrapid, 20mmol/L KCL @ 80ml/hr

34
Q

PC hypoglycemia

A

PC tremor, confusion, mood changes and speech difficulty, autonomic activation = sweating, palpitations and nausea. Drowsiness leading to low GCS and coma
seizures,

35
Q

Risks for hypoglycaemia

A

exercise, inability to calculate insulin dose - elderly/child, illness, B-blocker blunting symptoms of hypo, pregnancy

36
Q

Mx hypoglycemia

A

i) conscious = rapid fast acting carb = lucozade followed by long acting meal i.e. toast
ii) reduced GCS buccal glucagel or 1mg IM glucagon if unable to swallow
iii) low GCS IV 20% dextrose 20ml over 10mins

Always follow with long acting carb and try remove reason for hypo. If BM <4 = glucose bolus, if >4 = long carb

37
Q

Statins MOA

A

Inhibit HMG CoA reductase preventing conversion of mevalonic acid to cholesterol. This lowers cholesterol in the liver leading to increased LDL receptors on hepatocytes so uptake of LDL and VLDL is increased by the liver leading to lower circulation levels

38
Q

Uses of statins

A

1 and 2 prevention of CVD events anyone with Q Risk >10%, hyperlipidemia disorders.

39
Q

SE of statins

A

Constipation/flatulence, deranged LFT’s (high ALT)
Myalgia can = myositis leading to rhabdomyolysis
Peripheral neuropathy

40
Q

Interactions of statins

A

Metabolised by CYP450 enzymes

Enzyme inhibitors such as amiodarone, clarithromycin/erythromycin, HIV protease inhibitors, grapefruit juice = increased statin levels and SE

41
Q

Fibres (fenofibrate/benzofibrate) MOA

A

Increase activity of lipoprotein lipase to facilitate catabolism of VLDL’s and increase cholesterol content of HDL’s. Activate PPAR

42
Q

Use of fibrates

A

Adjuvant to statins if TG >10mmol/L or CI statins

43
Q

SE of fibrates

A

GI disturbance, cholestasis and pancreatitis, increased risk of myositis if combined with fibrates

44
Q

PCSKL inhibitors (Evolocumab)

A

Monoclonal IgG antibody to PCSK9 leads to increased LDL receptor recycling promoting increased LDL receptors on surface

V. expensive and SC injection

45
Q

Pregnancy and DM

A

5mg folic acid to reduce risk of neural tube defects
Stop B-blocker and ACEi
Aim for HbA1c <48
Monitor carefully to prevent hypoglycaemia due to increased risk in pregnancy
4 wkly measurements from 28wks
Induced @ 37 wks to prevent still birth
Retinopathy checks at 12+20wks

46
Q

Causes of N/V

A

Surgical conditions = Small bowel obstruction, appendicitis pancreatitis, cholecystitis
DKA, hypoglycaemia, HHS, Addisonian crisis
Increased ICP
Any cause of infection
Obstetric - ectopic, morning sickness, hypermeisis

47
Q

Anion gap

A

Anions - cations (Na+ -(HCO3 + CL))

Causes of high anion gap acidosis = DKA, lactic acidosis, paracetamol and aspirin OD

48
Q

DKA pathogenesis

A

Absolute insulin deficiency leads to break down of muscle and adipose tissue for an alternative glucose source. Fatty acids are processed by the liver leading to ketone production. This leads to reduced alkaline buffer = acidosis. High blood glucose levels lead to osmotic diuresis and dehydration

49
Q

Causes of DKA

A

New T1DM, insulin pump malfunction, omission on insulin, infections, MI, PE, alcohol intoxication

50
Q

Hypoglycaemia PC and reasons

A

Autonomic - sweating, palpitations, tremor
Neuroglycopenic - confusion, drowsiness, mood change
General - N/V, headache

Normal response to low glucose is to secrete insulin. In DM there is no endogenous insulin so the body used adrenaline to compensate hence the autonomic symptoms.

51
Q

Why does insulin infusion need to be stat

A

Crucial to stop further ketogensis, begin to reduce hypoglycaemia and treat hyperkalemia

CPTP (11 decks)

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