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Y2 NnD > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Are severe insulin resistance syndromes autosomal dominant or recessive

A

Dominant

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2
Q

Causes of insulin resistance

A
  • Central adiposty
  • Acromegaly ⇒ GH resistance
  • Pheochromocytoma of adrenal glands
  • Cushing’s disease
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3
Q

Effect of visceral fat on insulin resistance

A

Produced adipokines that affect action of insulin

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4
Q

HbA1c in acute T1DM

A

NORMAL

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5
Q

Will HbA1c be higher or lower in pregnant women

A

Lower

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6
Q

When is OGTT often used for identifying T2DM

A

IN gestational diabetes

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7
Q

How does T1 DM usually progress
What are the 3 stages and when does clinical onset happen?

A

Genetic susceptibility to immune dysfunction
Stage 1-> Insulitits, inflammatory infiltration of islet, B cell destruction by T cells, autoantibodies present in blood, BGL STILL NORMAL
Stage 2-> loss of first phase insulin secretion, IGT
Stage 3- clinical onset when 80% of islets destroyed, overt diabetes

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8
Q

What antibodies can be detected for type 1 diabetes

A

GAD, IA2, ICA, ZnT8

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9
Q

What symptoms in T1DM are not common in T2DM

A

Weight loss, kussmaul breathing

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10
Q

Diagnostic tests for Type ! DM

A

High blood glucose, DKA , antibodies, elevated HbA1c in some cases

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11
Q

autoimmune disorders associated with diabetes

A

thyroid, pernicious anaemia, coeliac, addison’s, vitiligo

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12
Q

drugs that can cause hypos and what is their MOA

A

Sulphonylureas - Encourage beta cells to produce more insulin
Binds to SUR1 receptor on cell membrane which closes K+ channels and leads to depolarisation of the cell and opening of voltage dependent ca2+ channels , leading to release of insulin

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13
Q

What are the first few hormones to rise as counter regulation for hypoglycaemia

A

epinephrine and glucagon, which result in gluconeogenesis in liver ( epinephrine also stimulates kidneys and reduces glucose use in kidneys)

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14
Q

What hormones are secreted when epinephrine and glucagon fail to sufficiently raise blood glucose levels

A

Cortisol and GH

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15
Q

What are autonomic symptoms of hypoglycaemia

A

Sweating, shaking, palpitations, hunger

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16
Q

What are neuroglycopenic symptoms of hypo

A

Confusion, driwsiness, difficulty speaking, odd behaviour and incoordination

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17
Q

What are non-specific (malaise) symptoms of hypo

A

Nausea and headache

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18
Q

What is whipple’s triad and what does it do

A

Diagnosis of hypos
- Typical symptoms
- Biochemical confirmation (no agreed cut-off) but usually below 4
- Symptoms resolve with carbohydrates

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19
Q

What is the management of hypos

alert
Not alert
Follow up

A
  • If alert and has safe swallow , give oral carbs ⇒ sweet drink or dextrose tablet (20g CHO)
  • If not alert give 20% dextrose iv
  • If can’t get iv access and unsafe swallow, give 1mg im glucagon plus sweet drink (not effective in alcoholic hypo or liver disease)
  • Follow-up rapid acting carbs with slow release (complex) carbs
  • 10% glucose IV infusion if long-acting insulin or SU.
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20
Q

How often should drivers test glucose

A

Before driving (2h). every 2h while on long journey Do not drive if below FIVE

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21
Q

How long to wait before continuing driving if hypo

A

45 mins

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22
Q

When must drivers inform DVLA

A

more than 1 severe hypo while awake, impaired hypo awareness, hypo while driving

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23
Q

How does DKA develop

A

Body unable to utilise glucose, so FFA is mobilised instead and lipolysid occurs -> ketogenesis-

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24
Q

Why is glucose so high in DKA

A

profound insulin deficiency -> muscle proteinolysis->lactate and arginine gluconeogenesis

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25
Q

how does DKA affect GFR

A

decreases GFR due to osmotic diuresis and hypovolemia

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26
Q

What are the clinical signs of DKA

A

JVP, BP decreased, HR increased, 5L fluid deficit, significant electrocyte deficit, abdominal pain, nausea and vomiting due to ketone bodies, kussmaul resp, ketotic breath, muscle cramps

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27
Q

What is the management of dKA?

A

Fluids to rehydrate- fast (rapid iv fluids in firs hour)initially then slower
IV insulin in first hour to switch off ketone body production

1-4 hrs:
need to monitor K+ as hypokalaenia common as insulin given
Add 10% glucose once blood glucose is 14 or less to continue giving IV insulin

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28
Q

Treatment of DKA patient once they are eating and drinking

A

Swap to subcutaneous inulin, but must give basal insulin 1h before IV inslin ustops

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29
Q

How to deal with CVD risk in patients with T2DM

A

Statins like atorvastatin to any T1DM patient above 40yo,T2M patients with Q Risk Score above 10

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30
Q

What do monocytes form in the arteriar wall

A

Differentiate into macrophages which accumulate oxidised lipids to form foam cells

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31
Q

How do foam cells lead to atherosclerosis

A

foam cells stimulate macrophage proliferation and attraction of T lymphocytes, in turn inducing smooth muscle proliferation in the arterial walls and collagen accumulation.

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32
Q

How is platelet aggregation promoted in macrovascular complications

A

Impaired nitric oxide generation, increased free radical formation in platelets and altered calcium regulation all promote platelet aggregation

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33
Q

How is fibrinolysis impaired in macrovascular complications

A

Elevated levels of plasminogen activator inhibitor type 1 may also impair fibrinolysis

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34
Q

How to treat DKD

A

Check for microalbuminuria
ACE inhibitors and ARBS like losartan to reduce glomerular pressure and microalbuminuria

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35
Q

Treatment of diabetic foot

A
  • Antibiotics
  • Debridement ⇒ To reveal what is going on but also take away some of the infection
  • Off loading ⇒ Take away pressure from toe
  • Improved glycaemic control ⇒ To bring down Hb1Ac
  • Vascular assessment ⇒ Feeling for pulses or imaging if lack of pulse
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36
Q

pathophysiology of retinopathy

A
  • Aldose reductase may play role in development of diabetic complications
  • Initial enzyme in intracellular coil pathway = glucose converted into sorbitol
  • High glucose levels increases flux of sugar mol in the pathway and causes sorbitol accumulation in the cells.
  • Osmotic stress from sorbitol accumulation may be a causes of diabetic microvascular complications
37
Q

What is sorbitol accumulation in the eyes also linked to

A
  • Linked to microaneurysm formation, thickening of basement membranes and loss of pericytes
  • Cells are also thought to be injured by glycoproteins
38
Q

What does proliferative retina disease mean

A

New vessel formation or preretina hemorrhage or tractional retinal detatchment

39
Q

Treatment for diabetic retinopathy

A

Try to improve glycaemic control first, may use laser to improve (for proliferative diabetic retinopathy ⇒ new vessels in the eye to increase oxygen supply to the eyes)
Anti VEGF for macular oedema => treatment removes fluid

40
Q

How does diabetes lead to diabetic nephropathy

A
  • Initial constriction of the efferent arterioles and dilatation of the afferent
  • Resultant glomerular HTN and hyperfiltration
  • Gradually changes to hypotension through time
  • Thickening of basement membrane
  • Widening of podocytes
  • Increased mesangial cells
  • Eventually shutting off glomerular filtration
41
Q

Ways to halt complications with diabetic nephropathy

A
  • Improving glycaemic control
  • ACEI (reducing BP within the glomerular capillaries)
  • Haemodialysis or peritoneal dialysis
  • Kidney transplant
42
Q

What are the GI effects of diabetes and how to treat?

A

Can cause gastroparesis– vomitting, not absorbing food
Metoclopramide or gastric pacemaker for GI symptoms

43
Q

How to treat Erectile Dysfunction

A

Patient should lose weitght, can give testosterone replacement and PD 5 inhibitors like sildenafil

44
Q

What is Hyperosmolar hyperglycemic state

A

Due to relative insulin deficiency affecting the ability for peripheral glucose to be taken into tissue, results in excess glucagon secretion to raise glucose levels, resulting in increase liberation of arginine and gluconeogenesis , as well as increased glycogenolysis

45
Q

diagnoses of HHS and how to differentiate from DKA

A
  • Hyperglycaemia (>30mmol/l, but often 60-90 mmol/l))
  • Serum osmolality >320mmol/Kg
  • No / mild ketoacidosis ⇒ since it is only due to RELATIVE insulin deficiency
  • Severe dehydration (2x DKA) and pre-renal failure common
46
Q

Symptoms of HHS

A
  • nsidious onset
  • Profound dehydration (9-10L deficit) 2x DKA
  • Hypercoagulability (exclude CVA, DVT, PE)
    • Hypercoagulable due to profound dehydration and raised osmolarity
  • Confusion, coma, fits.
  • Gastroparesis, N&V, hematemesis
47
Q

Management of HHS and difference with DKA

A
    • Slower, prolonged rehydration
    • Gradual reduction in Na+
    • Gentler glucose reduction
    • Anticoagulation vital: Prophylactic sc heparin
48
Q

When should Metformin not be given to patients

A

If eGFR is less than 30 or withdrawing fast

Withdraw during tissue hypoxia but can reinstate later
- ‘Shock’
- MI, significant CCF
- Sepsis
- Dehydration
- Acute renal failure

  • Withdraw for 3 days after iodine-containing contrast medium given. Check U/E before reinstating 48h later’
  • Withdraw 2 days before general anaesthetic and reinstate once renal function stable
49
Q

What is the first line for diabetes lol

A

Metformin lmao

50
Q

What is the mechanism of action of metformin

A

Reduces hepatic glucose output through effect on AMPK - reduces synthesis and increases glucose uptake, glycolysis, fatty acid oxidation and mitchondrial biogenesis

51
Q

Is metformin weight neutral

A

Encourages weight loss/ neutral

52
Q

What diabetic drug causes hypos

A

Only Sulphonylureas – Gliclazide and glibenclamide

53
Q

How do glicazides work

A

They cause insulin secretion independent of blood glucose level

54
Q

Are sulphonylureas weight neutral

A

No, can cause modest increase in weight

55
Q

What do glitazones/thiazolidinediones do?

A

Reduce insulin resistance => Can stop the drug and still have effects for 6 months due to long lasting action

56
Q

Side effects of metformin

A

In people with renal impairment ⇒ Possible nausea, kidney interactions like lactic acidosis
- Hold metformin for patients with low GFR

57
Q

What glitazone/thiazolidinedione side effects are there and what are the contraindications

A

Cause fluid retention and may lead to CHF, affect bone mineral density, IHD is contraindication

58
Q

what do GLP 1 agonists and DDP4 agonists do

A

Increase incretins and therefore insulin secretion
GLP 1 agonists increase insulin secretion while DDP4 agonists reduce incretin breakdown

59
Q

Effect of incretin mimetics on weight loss

A

Increases as it encourages secretion of insulin as you eat, GLP 1 agonists delay gastric emptying

60
Q

Side effects of incretin mimetics

A

GI symptoms

61
Q

When should incretin mimetics be used

A

To be used in combination with other medications when other choices have failed

62
Q

Does SGLT 2 inhibitor cause hypos

A

Only if really low in blood sugar

63
Q

How do SGLT2 inhibitors reduce hyperglycaemia

A
  • Stop reabsorption of glucose through urine - may have excess glucose in urine
    • Bacterial infection, thrush, UTI
64
Q

Contraindications of SGLT2 inhibitors

A

Don’t use in patients with eGFR < 40

65
Q

What are the main causes of secondary diabetes

A

CF, diabetes secondary to pancreatitis ( alcohol intake) , acromegaly, cushing’s , Drugs like Corticosteroids eg. prednisolone ⇒ Exogenous glucocorticoids exacerbates insulin resistance

haemochromatosis ⇒ iron overload (deposited in liver)
- Primary pancreatic tumours
- Pancreatectomy
- Trauma
- Haemochromatosis

66
Q

What test to do for diabetes secondary to pancreatitis

A

C peptide

67
Q

What gene defects are there in MODY, what inheritance

A

Single gene defects, autosomal dominant

68
Q

Is MODY early onset? Insulin dependent?

A

Early onset BUT not insulin dependent

69
Q

Most common MODY>

A

HNF 1 a

70
Q

What does HNF 1B mutation lead to

A

Cystic formation in kidneys, insulin requiring diabetes and early onset kidney failure

71
Q

How to test for MODY

A

C-peptide, check if insulin is being produced, if low, is more likely to be type 1

72
Q

What hormone does the delta cell secrete

A

Somatostatin

73
Q

What kind of enzymesdoes insulin stimulate

A

Synthesis enzymes like acetyl CoA carboxylase and glycogen synthase

74
Q

What kind of hormones does glucagon stimulate

A

breakdown enzymes like TAG lipase and glycogen phosphorylase

75
Q

What channels are involved in secretion of Insulin

A

GLUT 2

76
Q

What does influx of glucose in B cells result in

A

Increase in metabolism and production of ATP which results in membrane depolarization due to closing of K+ channels causing less leakage of K+ ions. The depolarization of the channels results in opening of Ca2+ channels and exocytosis of the insulin vesicles

77
Q

What is the action of insulin when it binds to cell membranes ( and of what cells?)

A

It causes the translocation of GLUT4 to cell membranes in fat and allows insulin-dependent glucose uptake into cells

78
Q

Effect of insulin on glucose

A
  • Increased glucose uptake in fat and muscle
  • Increased glycogenesis in liver and muscle
  • Decreased gluconeogenesis from C3 precursors in Liver
  • Decreased Glycogenolysis in liver and muscle
79
Q

Effect of insulin on protein

A

Increased amino acid uptake in muscle ⇒ increased protein synthesis

80
Q

Effect of insulin on fats

A
  • Increased lipogenesis in adipose tissue
  • Decreased lipolysis in adipose tissue
81
Q

Effect of insulin on ketones

A

Decreases ketogenesis in liver from aminoacids and fats

82
Q

What is the effect of T1DM and T2DM on action of insulin

A

T1DM basically reverses it, T2DM reverses almost everything but decreases lipolysis and increases TAG

83
Q

Actions of glucagon

A
  • Glucagon favours glycogenolysis and gluconeogenesis
  • Inhibits glycolysis
84
Q

Effect of cortisol on glucos, protein and fats

A

Synergistic with glucagon and adrenalin and increases protein breakdown

85
Q

Effect of glucagon and adrenaline wrt insulin

A

bascially opp

86
Q

Difference in metabolic changes in starvation and trauma

A

Decreased BMR in starvation but increased in trauma, increase BG in trauma but not in starvation

87
Q

What are medical disorders associated with T2DM

A
  • Obstructive Sleep Apnoea
  • Polycystic Ovarian Disease
  • Hypogonadotropic Hypogonadism in men
  • Non-Alcoholic Fatty Liver Disease
88
Q

What is a renal complication of HHS

A

Pre renal failure

Y2 NnD (10 decks)

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