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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
Insulin regimes
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
Insulin requirements
Increase in infection, pregnancy, exercise and with stress
27
Insulin SE
Leads to uptake of K+ to cells = hypokalemia, lipogenesis @ peripheral tissue unsightly swellings due to lipohypertrophy - can = infected Hypoglycaemia
28
Insulin Pumps
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
Mx T2DM
Lifestyle = reduce wt, stop smoking, increase exercise ``` 1st = metformin Adjunct = sulphonylurea Adjunct = GLP-1, SGLT-2 ```
30
Diagnosis of DKA
Ketones ++/ >3mmol/L Blood glucose >11mmol/L Venous pH < 7.3 or bicarb <15
31
PC DKA
PC = polyuria, polydipsia, N/V abdo pain low GCS, drowsiness Kassmual breathing
32
Mx DKA
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
When blood glucose <13mmol/L
GKI infusion 500ml 10% dextrose, 24 units of actrapid, 20mmol/L KCL @ 80ml/hr
34
PC hypoglycemia
PC tremor, confusion, mood changes and speech difficulty, autonomic activation = sweating, palpitations and nausea. Drowsiness leading to low GCS and coma seizures,
35
Risks for hypoglycaemia
exercise, inability to calculate insulin dose - elderly/child, illness, B-blocker blunting symptoms of hypo, pregnancy
36
Mx hypoglycemia
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
Statins MOA
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
Uses of statins
1 and 2 prevention of CVD events anyone with Q Risk >10%, hyperlipidemia disorders.
39
SE of statins
Constipation/flatulence, deranged LFT's (high ALT) Myalgia can = myositis leading to rhabdomyolysis Peripheral neuropathy
40
Interactions of statins
Metabolised by CYP450 enzymes Enzyme inhibitors such as amiodarone, clarithromycin/erythromycin, HIV protease inhibitors, grapefruit juice = increased statin levels and SE
41
Fibres (fenofibrate/benzofibrate) MOA
Increase activity of lipoprotein lipase to facilitate catabolism of VLDL's and increase cholesterol content of HDL's. Activate PPAR
42
Use of fibrates
Adjuvant to statins if TG >10mmol/L or CI statins
43
SE of fibrates
GI disturbance, cholestasis and pancreatitis, increased risk of myositis if combined with fibrates
44
PCSKL inhibitors (Evolocumab)
Monoclonal IgG antibody to PCSK9 leads to increased LDL receptor recycling promoting increased LDL receptors on surface V. expensive and SC injection
45
Pregnancy and DM
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
Causes of N/V
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
Anion gap
Anions - cations (Na+ -(HCO3 + CL)) Causes of high anion gap acidosis = DKA, lactic acidosis, paracetamol and aspirin OD
48
DKA pathogenesis
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
Causes of DKA
New T1DM, insulin pump malfunction, omission on insulin, infections, MI, PE, alcohol intoxication
50
Hypoglycaemia PC and reasons
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
Why does insulin infusion need to be stat
Crucial to stop further ketogensis, begin to reduce hypoglycaemia and treat hyperkalemia

CPTP (11 decks)

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