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Y2S2- Genetics, Renal, Endocrine > Diabetes > Flashcards

Diabetes Flashcards

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1
Q

pathophysiology of T1 diabetes

A

Autoimmune disorder where the insulin-producing beta cells are destroyed by the immune system
This results in an absolute deficiency of insulin resulting in raised glucose levels

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2
Q

where is insulin secreted?

A

beta cells in the islets of Langerhans in the pancreas

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3
Q

common presentation of T1DM

A

Patients tend to develop T1DM in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis
- weight loss, polyuria, polydipsia, fatigue, nausea

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4
Q

prediabetes

A

fasting glucose 6.1-6.9mmol/L
HbA1c 42-47
require closer monitoring and lifestyle interventions such as weight loss

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5
Q

alpha cell in pancreas secretes

A

glucagon

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6
Q

beta cell in pancreas secretes

A

insulin

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7
Q

delta cell in pancreas secretes

A

somatostatin

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8
Q

F cell in pancreas secretes

A

pancreatic polypeptide

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9
Q

structure of insulin

A

alpha & betachains linked via disulphide bonds by C peptide

which is cleaved by B cell peptidase→ activated insulin

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10
Q

insulin secretion from beta cells in directly couple to glucose influx

A

GLUT2 allows glucose to enter from the interstitium into the cell which then increases the intracellular ATP:ADP ratio.
Closes ATP-sensitive potassium channels (SUR1), depolarising the cell.
This opens voltage-gated calcium channels, increasing intracellular calcium flux
and leading to increased exocytosis of stored insulin.

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11
Q

most common secondary causes of diabetes?

A

Long-term steroids, other endocrine conditions such as acromegaly and Cushing’s syndrome, and pancreatic damage e.g. cystic fibrosis.

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12
Q

Sulfonylurea cellular mechanism

A

bind to SUR1 channel and close it which depolarises the cell- endogenous production of insulin

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13
Q

what is a measure of endogenous insulin?

A

C peptide as exogenous insulin treatment has no C peptide

Pro-insulin is converted to insulin and C- peptide in equimolar amounts

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14
Q

biphasic response of insulin secretion

A 
1st= in response to ingestion of food, stored insulin released
2nd= release of synthesised insulin
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15
Q

route of insulin from the pancreas

A
  • Secreted into portal vein (much higher concentration here than in systemic)
  • Acts first on LIVER
  • Passes through liver into systemic circulation via hepatic vein
  • Acts on MUSCLE and FAT
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16
Q

principle actions of insulin

A

increased glucose uptake in fat and muscle + glycogen storage in liver and muscle
increased amino acid uptake, protein synthesis and lipogenesis
decreased gluconeogenesis and ketogenesis

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17
Q

insulin causes translation of – to cell membranes

A

GLUT4 in adipose and muscle tissue

This allows insulin dependant glucose uptake into cells.

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18
Q

does brain tissue have GLUT2 transporters?

A

no, brain has GLUT3 (not insulin dependant)

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19
Q

glucagon favours

A

glycogenolysis and gluconeogenesis

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20
Q

stimulatory factors in gluconeogenesis

A

adrenaline, noradrenaline, Ach

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21
Q

_ obesity leads to insulin resistance

A

central

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22
Q

glucocorticoids antagonise

A

insulin

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23
Q

fasting plasma glucose in diabetes

A

> 7

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24
Q

2hr plasma glucose in OGTT

A

> 11.1

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25
Q

random plasma glucose in diabetes

A

> 11.1

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26
Q

HbA1c in diabetes

A

> 48

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27
Q

is 1 test sufficient for a diagnosis of diabetes if a patient is asymptomatic?

A

no, the same test should be repeated to confirm diagnosis of diabetes

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28
Q

what does HbA1c reflect?

A

glycated haemoglobin

• Reflects integrated blood glucose (BG) concentrations during lifespan of erythrocyte (120 days)

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29
Q

when should HbA1c not be used as a diagnostic test?

A

rapid onset of diabetes- T1DM, children, drugs- steroids
pregnancy- hBA1c is lower and glucose levels can raise rapidly
conditions where RBC survival may be reduced/ increased eg. haemoglobinopathy/ splenectomy
renal dialysis
iron and Vit B12 deficiency

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30
Q

oral glucose tolerance test

A

a fasting blood glucose is taken after which a 75g glucose load is taken. After 2 hours a second blood glucose reading is then taken

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31
Q

impaired glucose tolerance

A

Fasting plasma glucose: <7.0 mmol/l

2 hours after 75g oral glucose load: 7.8-11.0 mmol/l

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32
Q

impaired fasting glucose (fasting hyperglcyemia)

A

Fasting plasma glucose: 6.0 – 6.9 mmol/l
• Intermediate state between normal glucose metabolism and diabetes
prevalence increases with age and increased risk of vascular complication

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33
Q

why does T2DM prevalence increase with age

A

Beta cell function and number reduces with age

• Obesity increases with age

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34
Q

main driver of progression of T2DM

A

weight

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35
Q

what can delay progression of glucose intolerance?

A

lifestyle changes with dietary modification

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36
Q

modifiable risk factors for T2DM

A

Obesity
Sedentary lifestyles
High carbohydrate (particularly refined carbohydrate) diet

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37
Q

why can T2DM patients present with blurred vison?

A

lens in eyes coated with glucose and drags interstitial fluid into eyes- refractive error

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38
Q

classical presentations of T2DM

A

Asymptomatic – found on routine screening
• Thirst, polyuria (osmotic symptoms)
• Malaise, chronic fatigue
• Infections, e.g. thrush (candidiasis); boils
• Blurred vision
• Complication as presenting problem (e.g. retinopathy, neuropathy)

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39
Q

medical disorders associated with T2DM

A

Obstructive Sleep Apnoea
Polycystic Ovarian Disease
Hypogonadotrophic Hypogonadism in men- reduced testosterone
Non-Alcoholic Fatty Liver Disease

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40
Q

risk alleles for T1DM

A

HLA haplotypes (HLA-DR and HLA-DQ) as risk alleles- genetic tendency for autoimmune disorders

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41
Q

markers of autoimmune destruction

A

GAD, IA2 and/or ZnT8

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42
Q

Destruction of pancreatic beta cells carried out by which cell?

A

cytotoxic lymphocytes

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43
Q

autoimmune disorders associated with T1DM

A 
Thyroid disease
• Pernicious anaemia
• Coeliac disease
• Addison’s disease
• Vitiligo
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44
Q

secondary diabetes- exocrine pancreas disorders

A 
Pancreatectomy
• Trauma
• Tumours
CF
chronic pancreatitis- alcohol
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45
Q

Maturity Onset Diabetes of the Young - MODY

A

A group of autosomal dominant inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis

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46
Q

glycemic control monitoring devices

A

Home Blood Glucose Monitoring
CGMS – Continuous Glucose Monitoring System
Freestyle Libre Flash Glucose Monitoring System
HbA1c
Blood Ketone Monitoring

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47
Q

Severe insulin deficiency results in

A

life-threatening metabolic decompensation (diabetic ketoacidosis)

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48
Q

incretins-

A

gut hormones released post prandially that stimulate insulin release and inhibit glucagon release

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49
Q

HbA1c targets in patients treated with lifestyle/metformin

A

48mol/mol

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50
Q

HbA1c targets in patients in treatment including any drug which may cause hypoglycaemia (e.g. lifestyle + sulfonylurea)

A

53 mmol/mol

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51
Q

glycemic index

A

measure of change in blood glucose following ingestion of a particular food

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52
Q

low GI food

A

produce a slow, gradual rise in blood glucose after ingestion
• starchy foods (rice, spaghetti, granary bread, porridge) and pulses like beans and lentils

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53
Q

oral hypoglycaemic drugs are indicated for

A

T2DM

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54
Q

oral hypoglycaemic drug in T1DM

A

Insulin sensitisers in combination with insulin in Type 1 diabetes

55
Q

sulfonylurea indication and use (glipizide)

A

used in non-obese patients (may be insulin-deficient)

• used as monotherapy or in combination with metformin, glitazone or insulin

56
Q

sulfonylurea SE

A

Weight gain
Hypoglycaemia
Increased risk of cardiovascular disease and myocardial infarction when used as monotherapy

57
Q

Metformin (biguanide) mechanism

A

decreases hepatic gluconeogenesis
• increases insulin sensitivity in muscle
weight neutral

58
Q

thiazolidinediones (pioglitazone) mechanism

A

increases insulin sensitivity and decreases liver gluconeogenesis

59
Q

GLP-1 is rapidly degraded in plasma by

A

enzyme Dipeptidyl Peptidase 4 (DPP- 4)

60
Q

Plasma GLP-1 is lower in people with

A

impaired glucose tolerance (IGT) and type 2 diabetes

61
Q

GLP-1 Physiological Effects

A
  • Stimulates glucose- dependent insulin secretion
  • Suppresses glucagon secretion
  • Slows gastric emptying
  • Reduces food intake
  • Improves insulin sensitivity
62
Q

GLP1 is secreted from

A

L cells in the intestine

63
Q

GLP-1 mimetic eg. Exenatide route and combo

A

given as a subcutaneous injection

given in combo with either metformin or sulfonylurea

64
Q

GLP-1 mimetic SE

A

GI tract upset
Weight loss
Dizziness
Low risk of hypoglycaemia

65
Q

Gliptins mechanism, route, combo

A

DDP-4 inhibitors- inhibit degradation of incretin hormones and enhance their actions
• Oral route of administration
• Taken in combination with metformin
• Produce modest reduction in HbA1c

66
Q

SE of gliptins

A

GI tract upset
Symptoms of upper respiratory tract infection
Pancreatitis

67
Q

SGLT-2 Inhibitors eg. empagliflozin mechanism

A

glucuretic to remove glucose that would otherwise be reabsorbed- increase urinary excretion of glucose

68
Q

SE of SGLT-2 Inhibitors

A

Glucoseuria (glucose in the urine)
Increased rate of urinary tract infections
Weight loss
Diabetic ketoacidosis, notably with only moderately raised glucose- rare

69
Q

indications of insulin therapy

A

T1DM (ketosis-prone)
T2DM- severe hyperglycemia
Secondary failure to anti-diabetes drugs
Severe intercurrent illness
Metabolic complications (hyperosmolar states)

70
Q

short acting insulin

A

working in around 30 minutes and last around 8 hours

soluble- actrapid, humulin-S

71
Q

intermediate acting insulin

A

start working in around 1 hour and last around 16 hours

Isophane (NPH)- Insulatard; Humulin-I

72
Q

basal bolus insulin regimen (T1)

A

Short-acting or fast- acting insulin before meals; intermediate-acting or long- acting insulin once daily

73
Q

when is twice or once daily insulin regimens used?

A

T2 diabetes

once daily with oral tablet

74
Q

routes of administration of insulin

A

SUBCUTANEOUS - syringes, pens, pumps
• intrapulmonary - inhaler (historical)
• intravenous, intramuscular - injection (emergency use)
• intraperitoneal - dialysate (renal failure)
• transplanted islets - pancreatic islets

75
Q

lipohypertrophy at insulin injection sites

A

slows insulin absorption but resolves if site avoided

76
Q

Side-Effects of Insulin Therapy

A

HYPOGLYCAEMIA
• WEIGHT GAIN
• lipodystrophy at injection sites
• peripheral oedema (salt & water retention)
• insulin antibody formation (animal insulins)
• local allergy (rare)

77
Q

why does alcohol without food cause insulin induced hypoglycemia?

A

turns off hepatic gluconeogeeneis so mismatch between plasma insulin and glucose concentrations

78
Q

treatment of mild hypoglycaemia

A

SELF- Oral fast-acting carbohydrate (10-15g)
- glucose drink
- glucose tablets, confectionery
Oral supplementary snack (starch)

79
Q

treatment of severe hypoglycaemia

A 
EXTERNAL HELP- Parenteral therapy
- i.v. 20% dextrose (25-50g)- not alert
 - i.m. glucagon (1mg)- can't get IV access
Oral therapy
- buccal glucose gel; jam, honey
80
Q

microvascular complications of diabetes

A

retinopathy, nephropathy, neuropathy, skin and connective tissue changes

81
Q

macro-vascular complications of diabetes

A

atherosclerosis, peripheral vascular disease, ischaemic heart disease, cerebrovascular disease & stroke

82
Q

risk factors for microangiopathy (capillary wall thickening)

A

diabetes duration, hyperglycaemia, hypertension, smoking

83
Q

what causes pear scented breath?

A

fat breakdown to fatty acids causing Acetyl CoA production -> ketones

84
Q

why is there a risk of hypoglycaemia with sulfonylureas?

A

endogenous insulin release even if there isn’t any glucose present

85
Q

conditions associated with T1DM that can cause hypoglycemia

A

Coeliac disease- mismatch of carbs and insulin
– Addison’s disease (cortisol important in counterregulation)
– Hypothyroidism
– (Hypopituitarism)

86
Q

autonomic symptoms of hypoglycemia

A

Sweating
Shaking
Pounding heart (palpitations)
Hunger

87
Q

neuroglycopenic symptoms of hypoglycemia

A 
Confusion
Drowsiness 
Difficulty speaking
Odd behaviour 
Incoordination
88
Q

hypoglycemia in children can manifest as

A

behavioural change- stroppy

89
Q

mimic stroke in the elderly can be a symptom of

A

hypoglycaemia

90
Q

1st defence and prolonged defence hormones in hypoglycemia

A

adrenaline and glucagon in 1st defence

GH and cortisol in prolonged hypoglycemia

91
Q

Whipples Triad:

A

Symptoms result from hypoglycaemia can be confirmed by 2 out of 3 of:
Typical symptoms
Biochemical confirmation (no agreed cut-off)- generally 4
Symptoms resolve with carbohydrate

92
Q

when treating hypo, what should rapid acting carbs be followed by?

A

slow release carbs- stops patient from going into rebound hypo

93
Q

when can someone drive after hypo?

A

45 minutes later

94
Q

one severe hypo increases the risk of

A

further severe hypos

95
Q

Pathophysiology of diabetic ketoacidosis

A

DKA is caused by uncontrolled lipolysis and ketogenesis which results in an excess of free fatty acids that are ultimately converted to ketone bodies
hyperglycaemia and hyperketonaemia cause diuresis and dehydration

96
Q

most common precipitating factors of DKA

A

infection, missed insulin doses and myocardial infarction

97
Q

Features of DKA

A

abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)

98
Q

3 main principles of DKA management

A

– Fluids: initially fast then slower, to rehydrate
– iv insulin: switch off ketone body production
– Monitor potassium: metabolic acidosis shifts K+ to extracellular
space. As you give insulin, K+ moves into the cells and K+ falls- risk of arrhythmia

99
Q

insulin after DKA

A

Swap to s/c insulin once patient eating and drinking- IV insulin has v short half life
• Ensure basal insulin given ≥ 1h before iv insulin stops

100
Q

hyperosmolar hyperglycaemic state typically presents in

A

the elderly with T2DM

101
Q

HHS onset

A

HHS comes on over many days, and consequently the dehydration and metabolic disturbances are more extreme than DKA

102
Q

Pathophysiology of HHS

A

Hyperglycaemia results in osmotic diuresis with associated loss of sodium and potassium
Severe volume depletion results in a significant raised serum osmolarity (typically >320 mosmol/kg), resulting in hyperviscosity of blood.

103
Q

why may HHS patients not look as dehydrated as they are?

A

Despite these severe electrolyte losses and total body volume depletion, the typical patient with HHS, may not look as dehydrated as they are, because hypertonicity leads to preservation of intravascular volume.

104
Q

Clinical features of HHS

A

General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in MI, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia

105
Q

Diagnosis of HHS

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
106
Q

Management of HHS

A
  1. Normalise the osmolality (gradually)- elderly patients so can’t risk flooding lungs
  2. Replace fluid and electrolyte losses- reduced in Na+
  3. Normalise blood glucose (gradually)
    Prophylactic anticoagulation- heparin
107
Q

when should metformin be stopped?

A
  • eGFR <30
  • during tissue hypoxia: shock, MI, sepsis, dehydration
  • after iodine containing contrast
  • 2 days before general anaesthetic
108
Q

triggers for lactic acidosis

A

advanced kidney failure

tissue hypoxia

109
Q

why should insulin be started as soon as possible after diagnosis?

A

Children can develop dehydration + acidosis within 24 hours of first presentation. Children < 2years old are most at risk.
avoid metabolic decompensation and DKA

110
Q

in child with diabetes vomiting is sign of

A

insulin deficiency until proved otherwise

111
Q

T1DM in children HbA1c target

A

48 or lower

112
Q

TIR target

A

time in range of target glucose range

70% target

113
Q

types of diabetes in pregnancy

A

gestational diabetes

pre-existing diabetes- T1, T2, CF relates, MODY, steroid induced

114
Q

Risk factors for gestational diabetes

A

BMI of > 30 kg/m²
previous macrosomic baby weighing 4.5 kg or above
previous gestational diabetes
first-degree relative with diabetes
family origin with a high prevalence of diabetes (South Asian, black Caribbean and Middle Eastern)

115
Q

Screening for women who’ve previously had GDM

A

OGTT should be performed as soon as possible after booking and at 24-28 weeks if the first test is normal. NICE also recommend that early self-monitoring of blood glucose is an alternative to the OGTTs

116
Q

screening for women with risk factors for GDM

A

women with any of the other risk factors should be offered an OGTT at 24-28 weeks

117
Q

gestational diabetes is diagnosed if either:

A

fasting glucose is >= 5.6 mmol/l

2-hour glucose is >= 7.8 mmol/l

118
Q

main hormone that causes GDM

A

hPL- from 2nd trimester, increasing insulin requirements

119
Q

gestational diabetes increases the risk of

A

T2DM- 50% 5 year risk

120
Q

fetal risks of diabetes in pregnancy

A
  • macrosomia (>4.5kg) - hyperglycaemia
  • stuck in birth canal (shoulder dystocia)
  • premature/ intrauterine growth retardation- placental problems bc preexisting diabetes
  • anencephaly
121
Q

target HbA1c in GDM

A

53

122
Q

maternal risks of diabetes in pregnancy

A

• Miscarriage
• Pre-eclampsia
• Preterm labour
• Intrapartum complications
• Progression of microvascular complications
Severe hypoglycaemia- 1st trim
• Ketoacidosis- inc risk of neonatal death

123
Q

pre-pregnancy screening in diabetes

A

background retinopathy

microalbuminuria

124
Q

what diabetic complication can progress in pregnancy?

A

retinopathy

125
Q

GDM includes

A

women with undiagnosed type 1, type 2 or monogenic (MODY) DM

126
Q

after birth if fetal insulin is still high, there is a risk of

A

hypoglycaemia

127
Q

Management of GDM

A

home blood glucose monitoring
metformin/insulin
induced at term
insulin stopped once delivered

128
Q

targets for self monitoring of pregnant women (pre-existing and gestational diabetes)

A

Fasting 5.3 mmol/l
1 hour after meals 7.8 mmol/l, or:
2 hour after meals 6.4 mmol/l

129
Q

what type of insulin used in GDM?

A

short acting

130
Q

aspirin in pregnancy

A

Aspirin 75mg from 12-36 weeks (reduces pre- eclampsia risk)

131
Q

Induced labour in GDM

A

Labour induced before 40 weeks
– Because of increased risk of IUD and other maternal/fetal complications
– Increased risk of instrumental delivery and C Section

132
Q

Neonatal immediate postnatal care checks for

A

hypoglycaemia, macrosomia, jaundice, resp distress syndrome

133
Q

SE of metformin

A

Diarrhoea and abdominal pain- dose dependent
Lactic acidosis
Does NOT typically cause hypoglycaemia

134
Q

SE of Pioglitazone

A 
Weight gain
Fluid retention
Anaemia
Heart failure
Extended use may increase the risk of bladder cancer
Does NOT typically cause hypoglycaemia

Y2S2- Genetics, Renal, Endocrine (6 decks)

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