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Y2 LCRS Endocrinology > diabetes > Flashcards

diabetes Flashcards

type 1 Diabetes Mellitus: define type 1 diabetes mellitus, recall the epidemiology, explain the aetiology, pathophysiology, clinical presentations and explain the physiological basis of treatment

1
Q

appearance of patients with T1DM compared to T2DM

A

lean, lose a lot of weight, symptomatic from high glucose vs obese and insulin-resistant

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2
Q

typical age of T1DM patient and reason; explain why may be later onset (LADA)

A

young as autoimmune leading to insulin deficiency; may be insulin deficient over 40 due to latent autoimmune diabetes in adults (LADA) because of antibodies vs pancreas

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3
Q

why is the prevalence of T2DM in children rising

A

obesity

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4
Q

common consequence of T1DM which can also be present in T2DM

A

diabetic ketoacidosis

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5
Q

why might a patient present as obese with diabetic ketoacidosis

A

insulin deficiency as irritation to pancreas in Afro-Caribbean

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6
Q

examples of monogenic diabetes which can present phenotypically as T1DM or T2DM (small proportion)

A

MODY, mitochondrial diabetes

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7
Q

diseases and circumstances which present with high glucose but not diabetic

A

pheochromocytoma, Cushing’s syndrome; drinking cause pancreatic insufficiency

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8
Q

triggers/causes and pathway of T1DM

A

may be environmental trigger (prevalence increases during winter) and/or genetic influence (less predominant than T2DM), causing autoimmune destruction of islet cells, causing insulin deficiency and hyperglycaemia

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9
Q

triggers/causes and pathway of T2DM

A

genetic influence and/or obesity causing insulin resistance, causing B-cell failure after many years of high insulin output, causing hyperglycaemia

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10
Q

pathogenesis of T1DM

A

pre-diabetes with gene interactions imparting susceptibility and resistance, environmental triggers and immune dysregulation (autoantibodies) cause variable insulitis B-cell sensitivity to injury, reducing B-cell mass and causing a loss of glucose tolerance until diabetic and low B-cell mass (complete destruction) and undetectable C-peptide

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11
Q

T1DM cyclical relationship between autoreactive effector T cells and Treg cells

A

increase in autoreactive effector T cells controlled by increase in Treg cells, but over time a gradual disequilibrium cyclical behaviour could occur, leading to autoreactive effector T cells>Treg cells, leading to declining pancreatic islet function

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12
Q

why is immune basis of T1DM important (disease and treatment)

A

increased prevalence of other autoimmune diseases, risk of autoimmunity in relatives, more complete destruction of B-cells; autoantibodies can be useful clinically, immune modulation offers possibility of novel treatments

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13
Q

genetic susceptibility to T1DM (HLA-DR allele)

A

HLA markers are on chromosome 6 and alert if more at risk (HLA DR3 and 4 significant risk); research not clinical

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14
Q

why is there a reduction in T1DM prevalence in summer

A

bacterial/viral conditions in winter lead to pancreatic failure

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15
Q

4 markers for confirming T1DM diagnosis (most patients not needed)

A

islet cell antibodies (ICA) - group O human pancreas; insulin antibodies (IAA); glutamic acid decarboxylase (GADA; widespread nuerotransmitter); insulinoma-associated-2 autoantibodies (IA-2A; receptor like family)

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16
Q

presentation of T1DM: symptoms

A

polyuia, nocturia, polydipsia, blurring of vision, thrush, weight loss, fatigue

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17
Q

presentation of T1DM: signs

A

dehydration, cachexia (if insulin-deficient for a while), hyperventilation (metabolic acidosis), smell of ketones, glycosuria, ketonuria

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18
Q

what 3 organs/tissues are important for glucose regulation

A

liver, muscles, adipose

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19
Q

effect on glucose if insulin deficient in T1DM

A

glucose excreted out of liver into circulation, and can’t be taken up by muscle, so a lot left in circulation

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20
Q

effect on amino acids if insulin deficient in T1DM

A

amino acids broken down by muscle into circulation and liver uses these to produce more glucose

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21
Q

effect on glycerol if insulin deficient in T1DM

A

glycerol comes out of adipocytes, which liver uses again to make glucose

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22
Q

effect on fatty acids if insulin deficient in T1DM

A

fatty acids come out of adipocytes then taken out circulation and converted to ketone bodies in liver; some can be uptaken by muscles but not as good as glucose uptake

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23
Q

2 aims of T1DM treatment

A

reduce early mortality, avoid acute metabolic decompensation

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24
Q

what do T1DM need to preserve life, and what defines if this is deficient

A

need exogenous insulin, and ketones define insulin deficiency

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25
Q

4 long term complications of T1DM

A

retinopathy, nephropathy, neuropathy, vascular disease

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26
Q

4 features of controlled T1DM diet to balance distribution of food over course of day (diet more important in T2DM, but still important in T1DM as glucose levels difficult to control)

A

reduce calories as fat, reduce calories as refined carbohydrate, increase calories as complex carbohydrate, increase soluble fibre

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27
Q

progression of insulin source

A

animal -> human -> insulin analogues

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28
Q

non-diabetic insulin profile, and impact on insulin treatment

A

insulin peaks with food intake (glucose), but is a basal production by B-cells all the time; attempt to mirror this by giving short action insulin when eating and background long action basal insulin

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29
Q

examples of insulin analogue acting as short acting insulin with meals

A

Lispro, Aspart, Glulisine

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30
Q

how is insulin modified to make it last longer as background insulin

A

non-c bound to zinc or protamine

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31
Q

examples of insulin analogue acting as long acting background insulin

A

Glargine, Determir, Degludec

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32
Q

when is short acting insulin injected

A

with meals (dose dependent on size of meal)

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33
Q

when is long acting insulin injected

A

1/2 times a day (e.g. evening and morning)

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34
Q

features of insulin pump

A

continuous insulin delivery to mimic programmed basal rate, plus option for bolus amount for meals; doesn’t measure glucose, so no completion of feedback loop

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35
Q

process of islet cell transplant

A

islet cells in pancreas extracted from donor -> inserted into recipient by portal vein in liver and redistribute around body; must be on immunosuppressant agents for rest of life

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36
Q

criteria for islet cell transplant as very long waiting list

A

must have very severe hypoglycaemic episodes

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37
Q

how are capillary glucose levels monitored

A

prick finger -> blood on strip -> machine reads levels, gving trend of glucose throughout day

38
Q

capillary vs venous glucose accuracy

A

capillary not as accurate

39
Q

describe continous glucose monitoring (CGM)

A

on abdomen and checks instantaneously, giving a reading and trend in real time but is less accurate; can have alarms if entering hypoglycaemia

40
Q

what is a long term marker of glucose control to show compliance

A

HbA1c (glucose molecules bound to Hb), which falls in CGM and those who use capillary monitoring more frequently (compliance)

41
Q

what does HbA1c irreverible non-covalent bonding depend on

A

Hb levels, RBC lifespand (120 days), glucose levels

42
Q

HbA1c impacted by different individuals or diseases

A

rate of glycation is faster in some individuals, with thalassaemia, renal failure etc. causing HbA1c to be unreflective as RBCs have a shorter lifespan

43
Q

HbA1c correlation with glucose, and levels for diabetes and pre-diabetes

A

positive correlation, with >6.5% diabetes and 6-6.5% pre-diabetes

44
Q

what is lowered HbA1c associated with

A

lower risk of microvascular complications

45
Q

acute complications of T1DM

A

ketoacidosis (metabolic acidosis), hyperglycaemia

46
Q

glucose utilisation and production in hyperglycaemia

A

reduced tissue glucose utilisation, increased hepatic glucose production

47
Q

what is metabolic acidosis associated with

A

osmotic dehydration and poor tissue perfusion

48
Q

why is there a slightly higher prevalence of diabetic ketoacidosis in T2DM in black

A

potential insulin deficiency in T2DM before insulin resistance

49
Q

what consequence is inevitable inevitable when treating diabetes

A

occasional hypoglycaemic events (major cause of anxiety in patients and families)

50
Q

criteria for hypoglycaemia

A

plasma glucose <3.6mmol/l

51
Q

define severe hypoglycaemia

A

any hypoglycaemic event (hypo) requiring help of another person to treat

52
Q

how is hypo risk reduced but consequence of this

A

keep glucose high, but this risks complications

53
Q

features of hypo

A

disorientation, sweaty, confused (if eat will rectify, but if, not risk of going into coma)

54
Q

hypo: what happens at <3mmol/l

A

most mental processes impaired

55
Q

hypo: what happens at <2mmol/l

A

consciousness impaired

56
Q

how might severe hypoglycaemia lead to sudden death

A

contribute to arrhythmia

57
Q

describe hypoglycaemia unawareness

A

don’t spot symptoms of sweating etc. and lose awareness, becoming unconscious, because of habituation by recurrent hypos

58
Q

who are at main risk of hypos

A

patients with low HbA1c, who strive for tight glucose control but overdo it

59
Q

when do hypos occur

A

anytime, but often clear pattern (pre-lunch, nocturnal)

60
Q

why are nocturnal hypos very common

A

patient not totally aware and has increased production of adrenaline, so higher glucose level than normal

61
Q

5 reasons why hypos occur

A

unaccustomed exercise (doesn’t eat more and keeps same amount of insulin), missed meals (e.g. psychological condition where give less insulin or miss meals so lose weight), inadequate snacks, alcohol, inappropriate insulin regime

62
Q

hypoglycaemia signs and symptoms due to increased autonomic activation

A

palpitations (tachycardia), tremor, sweating, pallor/cold extremities, anxiety

63
Q

hypoglycaemia signs and symptoms due to impaired CNS function

A

drowsiness, confusion, altered behaviour, focal neurology, coma

64
Q

how is hypoglycaemia treated if conscious

A

oral food: glucose solution or tablets, then complex carbohydrates to maintain blood glucose after initial treatment

65
Q

how is hypoglycaemia treated if consciousness impaired

A

parenteral: IV dextrose (not concentrated solutions), 1mg glucagon IM (releases glucose from liver, but if thin and fasting, then low glucose reserves in liver so IM glucagon won’t work)

66
Q

what can precipitate diabetic ketoacidosis

A

new diagnosis of T1DM, not taking insulin, intercurrent stress (pneumonia, heart attack), fasting and not taking enough insulin, infection

67
Q

what will happen with deficient [insulin]

A

high hepatic glucose output and deficient muscle glucose uptake; lipolysis rate will increase, glycerol used to produce glucose in liver; fatty acids produce ketone bodies in liver

68
Q

what will happen with high plasma [glucose]

A

glucose exceeds proximal convoluted tubule ability for reabsorption, causing glycosuria (further promoted by SGLT2 inhibitors during treatment)

69
Q

how is dehydration caused by T1DM

A

insulin deficiency and stress hormones cause hyperglycaemia -> osmotic diuresis; this and fever with sepsis, along with not drinking enough or vomiting, causes dehydration

70
Q

where are ketones produced

A

occurs in non-diabetics as well as in insulin deficiency, and produced in liver from by-products of fatty acids

71
Q

what 3 things contribute to diabetic ketoacidosis

A

insulin deficiency, stress hormones, fasting (vomiting and fasting make ketosis worse)

72
Q

why do T1DM present as lean

A

lose weight as insulin required to keep triglycerides in adipocytes

73
Q

what is HCO3- production linked to

A

H+ excretion (attempt to buffer)

74
Q

4 features of distal convoluted tubule concerning acid-base homeostasis: filtration, enzyme, Na+ excretion and ketone bodies impact

A

needs adequate GRF for acid base system to function; needs carbonate dehydratase acid base homeostasis; Na+ excretion linked to H+ or K+ excretion; acid ketone bodies require increased HCO3- buffering

75
Q

pH, basic lesion and compensation of metabolic diabetic ketoacidosis

A

low pH, low HCO3-, so compensated by respiratory processes to increase CO2 release (hyperventilation)

76
Q

diabetic ketoacidosis: why is there a reduction in [HCO3-]

A

impaired production, increased H+ buffering

77
Q

diabetic ketoacidosis: what is pH dependent on

A

HCO3- and PCO2 levels

78
Q

diabetic ketoacidosis: anion gap

A

large anion gap (increase in single anion other than Cl-)

79
Q

why does diabetic ketoacidosis show high [K+], and why is this unreflective

A

water, Na+ and K+ lost in urine; excess H+ ions in diabetic ketoacidosis drive out K+ from IC into circulation, so high K+ in plasma but total body K+ is low

80
Q

what does diabetic ketoacidosis lead to (list all things forming cycle)

A

hyperventilation and vomiting (acid causes irritation of GI tract), which lead to dehydration -> renal hypoperfusion -> impaired H+ excretion -> acidosis

81
Q

10 clinical features of diabetic ketoacidosis

A

dehydration; insulin deficiency; hyperglycaemia; total body K+ deficiency despite high plasma [K+]; polyuria and polydipsia (osmotic diuresis); acidotic; hyperventilation (Kussmaul); risk of arrhythmia, infection and dilated stomach; abdominal pain and vomiting; coma; glycosuria and ketonuria

82
Q

9 investigations for diabetic ketoacidosis

A

capillary glucose, plasma glucose; creatine (kidney function), K+ and Na+ (electrolyte impalance; all elevated due to dehydration and acidosis, although Na+ could be low if prolonged hyperglycaemia); full blood count (high neutrophil if due to infection); arterial blood gases (through radial artery showing metabolic acidosis; for HCO3- look at venous); amylase (triglyceride; elevated e.g. due to pancreatitis causing insulin deficiency); ECG (check for MI and arrhythmias due to acidosis and low K+); chest x-ray (check for pneumonia precipitant); septic screen (urinary infection, chest infection or gut infection -> CRP high)

83
Q

4 treatments of diabetic ketoacidosis

A

fluid (aggressive rehydration with normal saline to improve renal perfusion, allowing HCO3- buffering); insulin (IV, not subcutaneous as tissues are poorly perfused); K+ replacement (insulin drives K+ into cells, causing rapid drop -> hypokalaemia and cardiac arrhythmias); HCO3- (not usual)

84
Q

diabetic ketoacidosis treatment: why is HCO3- not usual

A

danger of hypokalaemia, hypernatraemia, rebound alkalosis, CSF acidosis, impaired oxyHb dissociation

85
Q

6 other measures to monitor and treat diabetic ketoacidosis

A

cardiac monitor for arrhythmias; catheterise; antibiotics; NG tube (gastroparesis); heparin; arterial or central line

86
Q

why catheterise patients in diabetic ketoacidosis

A

as if confused, won’t be able to go to toilet; allows measurement of fluid output to ensure replacing lost fluids

87
Q

why NG tube patients in diabetic ketoacidosis

A

ac acidosis worsens vomiting, NG tube through nose into GIT prevents juices going into lungs

88
Q

why heparin patients in diabetic ketoacidosis

A

prevents coagulation, reducing risk of DVT and pulmonary embolism

89
Q

why arterial line or central line patients in diabetic ketoacidosis

A

arterial line if very acidotic; central line if very elderly or in cardia failure

90
Q

6 causes of death in diabetic ketoacidosis

A

overwhelming disease, self-neglect, social factors, delay seeking help, delay primary care, inappropriate treatment

91
Q

5 ways to prevent diabetic ketoacidosis

A

education, never stop insulin, check glucose and modify insulin if ill, admit if vomiting, determine cause of diabetic ketoacidosis (underlying condition e.g. gastroparesis)

92
Q

what 4 things are important in diabetic ketoacidosis genesis

A

insulin deficiency, other stress hormones, fasting, dehydration

Y2 LCRS Endocrinology (37 decks)

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